World Journal of Radiology (World J Radiol

World Journal of 

Radiology 

World J Radiol 2011 December 28; 3(12): 279-305 

www.wjgnet.com 

ISSN 1949-8470 (online)

W J R 

PRESIDENT AND EDITOR-IN- 

CHIEF 

Lian-Sheng Ma, Beijing 

STRATEGY ASSOCIATE 

EDITORS-IN-CHIEF 

Ritesh Agarwal, Chandigarh 

Kenneth Coenegrachts, Bruges 

Mannudeep K Kalra, Boston 

Meng Law, Lost Angeles 

Ewald Moser, Vienna 

Aytekin Oto, Chicago 

AAK Abdel Razek, Mansoura 

Àlex Rovira, Barcelona 

Yi-Xiang Wang, Hong Kong 

Hui-Xiong Xu, Guangzhou 

GUEST EDITORIAL BOARD 

MEMBERS 

Wing P Chan, Taipei 

Wen-Chen Huang, Taipei 

Shi-Long Lian, Kaohsiung 

Chao-Bao Luo, Taipei 

Shu-Hang Ng, Taoyuan 

Pao-Sheng Yen, Haulien 

MEMBERS OF THE EDITORIAL 

BOARD 

Australia 

Karol Miller, Perth 

Tomas Kron, Melbourne 

Zhonghua Sun, Perth 

Austria 

Herwig R Cerwenka, Graz 

Editorial Board 

2009-2013 

The World Journal of Radiology Editorial Board consists of 319 members, representing a team of worldwide experts 

in radiology. They are from 40 countries, including Australia (3), Austria (4), Belgium (5), Brazil (3), Canada (9), 

Chile (1), China (25), Czech (1), Denmark (1), Egypt (4), Estonia (1), Finland (1), France (6), Germany (17), Greece 

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WJR|www.wjgnet.com 



Daniela Prayer,Vienna 

Siegfried Trattnig, Vienna 

Belgium 

Piet R Dirix, Leuven 

Yicheng Ni, Leuven 

Piet Vanhoenacker, Aalst 

Jean-Louis Vincent, Brussels 

Brazil 

Emerson L Gasparetto, Rio de Janeiro 

Edson Marchiori, Petrópolis 

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Canada 

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Mark Otto Baerlocher, Toronto 

Martin Charron, Toronto 

James Chow, Toronto 

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Weiguang Yao, Sudbury 

Chile 

Masami Yamamoto, Santiago 

China 

Feng Chen, Nanjing 

Ying-Sheng Cheng, Shanghai 

Woei-Chyn Chu, Taipei 

Guo-Guang Fan, Shenyang 

Shen Fu, Shanghai 

Gang Jin, Beijing 

Tak Yeung Leung, Hong Kong 

Wen-Bin Li, Shanghai 

Rico Liu, Hong Kong 

Yi-Yao Liu, Chengdu 

Wei Lu, Guangdong 

Fu-Hua Peng, Guangzhou 

Li-Jun Wu, Hefei 

Zhi-Gang Yang, Chengdu 

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Czech 

Vlastimil Válek, Brno 

Denmark 

Poul Erik Andersen, Odense 

Egypt 

Mohamed Abou El-Ghar, Mansoura 

Mohamed Ragab Nouh, Alexandria 

Ahmed A Shokeir, Mansoura 

Estonia 

Tiina Talvik, Tartu 

Finland 

Tove J Grönroos, Turku 

I December 28, 2011

France 

Alain Chapel, Fontenay�Aux�Roses �Aux�Roses Aux�Roses 

Nathalie Lassau, Villejuif 

Youlia M Kirova, Paris 

Géraldine Le Duc, Grenoble Cedex 

Laurent Pierot, Reims 

Frank Pilleul, Lyon 

Pascal Pommier, Lyon 

Germany 

Ambros J Beer, München 

Thomas Deserno, Aachen 

Frederik L Giesel, Heidelberg 

Ulf Jensen, Kiel 

Markus Sebastian Juchems, Ulm 

Kai U Juergens, Bremen 

Melanie Kettering, Jena 

Jennifer Linn, Munich 

Christian Lohrmann, Freiburg 

David Maintz, Münster 

Henrik J Michaely, Mannheim 

Oliver Micke, Bielefeld 

Thoralf Niendorf, Berlin�Buch 

Silvia Obenauer, Duesseldorf 

Steffen Rickes, Halberstadt 

Lars V Baron von Engelhardt, Bochum 

Goetz H Welsch, Erlangen 

Greece 

Panagiotis Antoniou, Alexandroupolis 

George C Kagadis, Rion 

Dimitris Karacostas, Thessaloniki 

George Panayiotakis, Patras 

Alexander D Rapidis, Athens 

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Virginia Tsapaki, Anixi 

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Hungary 

Peter Laszlo Lakatos, Budapest 

India 

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Iran 

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Ireland 

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Israel 

Amit Gefen, Tel Aviv 

Eyal Sheiner, Be’er�Sheva 

Jacob Sosna, Jerusalem 

Simcha Yagel, Jerusalem 

Italy 

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Tommaso Bartalena, Imola 

Filippo Cademartiri, Parma 

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Laura Martincich, Candiolo 

Mario Mascalchi, Florence 

Roberto Miraglia, Palermo 

Eugenio Picano, Pisa 

Antonio Pinto, Naples 

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Lidia Strigari, Rome 

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Japan 

Shigeru Ehara, Morioka 

Nobuyuki Hamada, Chiba 

Takao Hiraki, Okayama 

Akio Hiwatashi, Fukuoka 

Masahiro Jinzaki, Tokyo 

Hiroshi Matsuda, Saitama 

Yasunori Minami, Osaka 

Jun-Ichi Nishizawa, Tokyo 

Tetsu Niwa, Yokohama 

Kazushi Numata, Kanagawa 

Kazuhiko Ogawa, Okinawa 

Hitoshi Shibuya, Tokyo 

Akira Uchino, Saitama 

Haiquan Yang, Kanagawa 

Lebanon 

Aghiad Al-Kutoubi, Beirut 

Libya 

Anuj Mishra, Tripoli 

Malaysia 

R Logeswaran, Cyberjaya 

Kwan-Hoong Ng, Kuala Lumpur 

Mexico 

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Netherlands 

Jurgen J Fütterer, Nijmegen 

Raffaella Rossin, Eindhoven 

Paul E Sijens, Groningen 

Willem Jan van Rooij, Tilburg 

New Zealand 

W Howell Round, Hamilton 

Norway 

Arne Sigmund Borthne, Lørenskog 

Saudi Arabia 

Mohammed Al-Omran, Riyadh 

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Volker Rudat, Al Khobar 

Serbia 

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Singapore 

Uei Pua, Singapore 

Lim CC Tchoyoson, Singapore 

Slovakia 

František Dubecký, Bratislava 

South Korea 

Bo-Young Choe, Seoul 

Joon Koo Han, Seoul 

Seung Jae Huh, Seoul 

Chan Kyo Kim, Seoul 

Myeong-Jin Kim, Seoul 

Seung Hyup Kim, Seoul 

Kyoung Ho Lee, Gyeonggi�do 

Won-Jin Moon, Seoul 

Wazir Muhammad, Daegu 

Jai Soung Park, Bucheon 

Noh Hyuck Park, Kyunggi 

Sang-Hyun Park, Daejeon 

Joon Beom Seo, Seoul 

Ji-Hoon Shin, Seoul 

Jin-Suck Suh, Seoul 

Hong-Gyun Wu, Seoul 

II December 28, 2011

Spain 

Eduardo J Aguilar, Valencia 

Miguel Alcaraz, Murcia 

Juan Luis Alcazar, Pamplona 

Gorka Bastarrika, Pamplona 

Rafael Martínez-Monge, Pamplona 

Alberto Muñoz, Madrid 

Joan C Vilanova, Girona 

Switzerland 

Nicolau Beckmann, Basel 

Silke Grabherr, Lausanne 

Karl-Olof Lövblad, Geneva 

Tilo Niemann, Basel 

Martin A Walter, Basel 

Thailand 

Sudsriluk Sampatchalit, Bangkok 

Turkey 

Olus Api, Istanbul 

Kubilay Aydin, İstanbul 

Işıl Bilgen, Izmir 

Zulkif Bozgeyik, Elazig 

Barbaros E Çil, Ankara 

Gulgun Engin, Istanbul 

M Fatih Evcimik, Malatya 

Ahmet Kaan Gündüz, Ankara 

Tayfun Hakan, Istanbul 

Adnan Kabaalioglu, Antalya 

Fehmi Kaçmaz, Ankara 

Musturay Karcaaltincaba, Ankara 

Osman Kizilkilic, Istanbul 

Zafer Koc, Adana 

Cem Onal, Adana 

Yahya Paksoy, Konya 

Bunyamin Sahin, Samsun 

Ercument Unlu, Edirne 

Ahmet Tuncay Turgut, Ankara 

Ender Uysal, Istanbul 


United Kingdom 

K Faulkner, Wallsend 

Peter Gaines, Sheffield 

Balaji Ganeshan, Brighton 

Nagy Habib, London 

Alan Jackson, Manchester 

Pradesh Kumar, Portsmouth 

Tarik F Massoud, Cambridge 

Igor Meglinski, Bedfordshire 

Robert Morgan, London 

Ian Negus, Bristol 

Georgios A Plataniotis, Aberdeen 

N J Raine-Fenning, Nottingham 

Manuchehr Soleimani, Bath 

MY Tseng, Nottingham 

Edwin JR van Beek, Edinburgh 

Feng Wu, Oxford 

United States 

Athanassios Argiris, Pittsburgh 

Stephen R Baker, Newark 

Lia Bartella, New York 

Charles Bellows, New Orleans 

Walter L Biffl, Denver 

Homer S Black, Houston 

Wessam Bou-Assaly, Ann Arbor 

Owen Carmichael, Davis 

Shelton D Caruthers, St Louis 

Yuhchyau Chen, Rochester 

Melvin E Clouse, Boston 

Ezra Eddy Wyssam Cohen, Chicago 

Aaron Cohen-Gadol, Indianapolis 

Patrick M Colletti, Los Angeles 

Kassa Darge, Philadelphia 

Abhijit P Datir, Miami 

Delia C DeBuc, Miami 

Russell L Deter, Houston 

Adam P Dicker, Phil 

Khaled M Elsayes, Ann Arbor 

Steven Feigenberg, Baltimore 

Christopher G Filippi, Burlington 

Victor Frenkel, Bethesda 

Thomas J George Jr, Gainesville 

Patrick K Ha, Baltimore 

Robert I Haddad, Boston 

Walter A Hall, Syracuse 

Mary S Hammes, Chicago 

John Hart Jr, Dallas 

Randall T Higashida, San Francisco 

Juebin Huang, Jackson 

Andrei Iagaru, Stanford 

Craig Johnson, Milwaukee 

Ella F Jones, San Francisco 

Csaba Juhasz, Detroit 

Riyad Karmy-Jones, Vancouver 

Daniel J Kelley, Madison 

Amir Khan, Longview 

Euishin Edmund Kim, Houston 

Vikas Kundra, Houston 

Kennith F Layton, Dallas 

Rui Liao, Princeton 

CM Charlie Ma, Philadelphia 

Nina A Mayr, Columbus 

Thomas J Meade, Evanston 

Steven R Messé, Philadelphia 

Nathan Olivier Mewton, Baltimore 

Feroze B Mohamed, Philadelphia 

Koenraad J Mortele, Boston 

Mohan Natarajan, San Antonio 

John L Nosher, New Brunswick 

Chong-Xian Pan, Sacramento 

Dipanjan Pan, St Louis 

Martin R Prince, New York 

Reza Rahbar, Boston 

Carlos S Restrepo, San Antonio 

Veronica Rooks, Honolulu 

Maythem Saeed, San Francisco 

Edgar A Samaniego, Palo Alto 

Kohkan Shamsi, Doylestown 

Jason P Sheehan, Charlottesville 

William P Sheehan, Willmar 

Charles Jeffrey Smith, Columbia 

Monvadi B Srichai-Parsia, New York 

Dan Stoianovici, Baltimore 

Janio Szklaruk, Houston 

Dian Wang, Milwaukee 

Jian Z Wang, Columbus 

Liang Wang, New York 

Shougang Wang, Santa Clara 

Wenbao Wang, New York 

Aaron H Wolfson, Miami 

Gayle E Woloschak, Chicago 

Ying Xiao, Philadelphia 

Juan Xu, Pittsburgh 

Benjamin M Yeh, San Francisco 

Terry T Yoshizumi, Durham 

Jinxing Yu, Richmond 

Jianhui Zhong, Rochester 

III December 28, 2011

W J R 

Contents 

EDITORIAL 

REVIEW 

BRIEF ARTICLES 




279 Chest neoplasms with infectious etiologies 

Restrepo CS, Chen MM, Martinez-Jimenez S, Carrillo J, Restrepo C 

289 Multidetector computed tomography imaging of congenital anomalies of 

major airways: A pictorial essay 

Monthly Volume 3 Number 12 December 28, 2011 

Sundarakumar DK, Bhalla AS, Sharma R, Gupta AK, Kabra SK, Jagia P 

298 Image of tumor metastasis and inflammatory lymph node enlargement by 

contrast-enhanced ultrasonography 

Aoki T, Moriyasu F, Yamamoto K, Shimizu M, Yamada M, Imai Y 

December 28, 2011|Volume 3| ssue 12|

Contents 

ACKNOWLEDGMENTS 

APPENDIX 

ABOUT COVER 

AIM AND SCOPE 

FLYLEAF 

EDITORS FOR 

THIS ISSUE 

NAME OF JOURNAL 

World Journal of Radiology 

LAUNCH DATE 

December 31, 2009 

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Volume 3 Number 12 December 28, 2011 

I Acknowledgments to reviewers of World Journal of Radiology 

I Meetings 

I-V Instructions to authors 

Restrepo CS, Chen MM, Martinez-Jimenez S, Carrillo J, Restrepo C. Chest 

neoplasms with infectious etiologies. 

World J Radiol 2011; 3(12): 279-288 

http://www.wjgnet.com/1949-8470/full/v3/i12/279.htm 

World Journal of Radiology (World J Radiol, WJR, online ISSN 1949-8470, DOI: 10.4329) is 

a monthly peer-reviewed, online, open-access, journal supported by an editorial board 

consisting of 319 experts in radiology from 40 countries. 

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ISSN 1949-8470 (online) 

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doi:10.4329/wjr.v3.i12.279 

Chest neoplasms with infectious etiologies 

Carlos S Restrepo, Melissa M Chen, Santiago Martinez-Jimenez, Jorge Carrillo, Catalina Restrepo 

Carlos S Restrepo, Melissa M Chen, Santiago Martinez- 

Jimenez, Jorge Carrillo, Catalina Restrepo, Department of 

Radiology, The University of Texas Health Science Center at San 

Antonio, Mail Code 7800, 7703 Floyd Curl Drive, San Antonio, 

TX 78229, United States 

Author contributions: Chen MM, Restrep CS reviewed and 

summarized the literature that provided the basis of the manuscript. 

Martinez-Jimenez C, Carrillo J and Restrepo C contributed 

to the conceptual design of the manuscript and data interpretation. 

Correspondence to: Carlos S Restrepo, M�, M�, Assistant �ro- �ro- 

fessor, Department of Radiology, The University of Texas Health 

Science Center at San Antonio, Mail Code 7800, 7703 Floyd Curl 

Drive, San Antonio, TX 78229, United States. crestr@gmail.com 

Telephone: +1-210-5676488 Fax: +1-210-5676418 

Received: May 4, 2011 Revised: September 19, 2011 

Accepted: October 11, 2011 

�ublished online: December 28, 2011 

Abstract 

A wide spectrum of thoracic tumors have known or suspected 

viral etiologies. Oncogenic viruses can be classified 

by the type of genomic material they contain. Neoplastic 

conditions found to have viral etiologies include 

post-transplant lymphoproliferative disease, lymphoid 

granulomatosis, Kaposi’s sarcoma, Castleman’s disease, 

recurrent respiratory papillomatosis, lung cancer, malignant 

mesothelioma, leukemia and lymphomas. Viruses 

involved in these conditions include Epstein-Barr virus, 

human herpes virus 8, human papillomavirus, Simian 

virus 40, human immunodeficiency virus, and Human 

T-lymphotropic virus. Imaging findings, epidemiology 

and mechanism of transmission for these diseases are 

reviewed in detail to gain a more thorough appreciation 

of disease pathophysiology for the chest radiologist. 

© 2011 Baishideng. All rights reserved. 

Key words: Acquired immunodeficiency syndrome; Castleman’s 

disease; Kaposi’s sarcoma; Thoracic imaging; 

Thoracic lymphoma; Thoracic malignancies; Malignant 

mesothelioma 




Peer reviewer: Patrick K Ha, MD, Assistant Professor, Johns 

Hopkins Department of Otolaryngology, Johns Hopkins Head 

and Neck Surgery at GBMC, 1550 Orleans Street, David H Koch 

Cancer Research Building, Room 5M06, Baltimore, MD 21231, 

United States 

Restrepo CS, Chen MM, Martinez-Jimenez S, Carrillo J, Restrepo 

C. Chest neoplasms with infectious etiologies. World J 

Radiol 2011; 3(12): 279-288 Available from: URL: http://www. 

wjgnet.com/1949-8470/full/v3/i12/279.htm DOI: http://dx.doi. 

org/10.4329/wjr.v3.i12.279 

INTRODUCTION 

Approximately 12% of cancers worldwide can be linked 

to a viral infection [1] . Oncogenic viruses that have been 

identified include Epstein-Barr virus (EBV), human herpes 

virus 8 (HHV8), human papillomavirus (HPV), Simian 

virus 40 (SV-40), Human T-lymphotropic virus, and 

human immunodeficiency virus (HIV) [1,2] . Viruses can be 

categorized into several families and sub-families according 

to the type of genomic material they contain (DNA 

or RNA), symmetry of the capsid, presence or absence 

of an envelope, dimension, and the viral genome replication 

mechanisms. Tumor viruses belong to a number of 

families including the DNA virus families: Hepadnaviridae, 

Herpesviridae, and Papillomaviridae and the RNA 

virus families: Retroviridae and Flaviviridae [3] . 

This article focuses on thoracic tumors with viral 

etiologies, which include post-transplant lymphoproliferative 

disease, lymphomatoid granulomatosis, Kaposi’s 

sarcoma (KS), Castleman’s disease, recurrent respiratory 

papillomatosis (RRP), lung cancer, malignant mesothelioma, 

leukemia and lymphomas. The participation of the 

viral infection in the pathogenesis of these tumors as well 

as their most common imaging findings will be discussed. 

EBV 




EDITORIAL 

EBV was first discovered in 1964 by Epstein and Barr 

279 December 28, 2011|Volume 3|Issue 12|

A 

C 

Restrepo CS et al . Infectious chest tumors 

B 

D 

Figure 1 Hodgkin’s lymphoma. A 23-year-old woman with a four-mo history of dry cough and chest pain. A: Chest X-ray shows mediastinal widening and upper lobe 

parenchymal opacities; B and C: Contrast-enhanced computed tomography confirms lymphadenopathy involving the mediastinum and infiltrative masses in the bilateral 

upper lobes; D: Photomicrograph (HE stain). Nodular sclerosing HL lymph node. Fibrous bands divide the lymphoid infiltrate into nodules and contain Hodgkin 

cells. 

from a cell line derived from Burkitt lymphoma (BL) [4] . 

The virus is a DNA double-stranded virus which belongs 

to the γ herpesvirus subfamily. More than 95% of 

the healthy population worldwide carries the virus and 

transmission usually occurs during childhood via saliva. 

Children under the age of 10 usually have an asymptomatic 

primary infection. Primary infection occurring over 

the age of 15 leads to the clinical syndrome of infectious 

mononucleosis in 30%-40% of cases [5] . 

EBV infection develops when virions (the infective 

form of a virus which consists of a DNA or RNA core 

with a protein shell or capsid) transit across the epithelial 

cells in the oropharnynx to infect B cells in the mucosa. 

The virus has two phases of replication, a lytic and a latent 

cycle. The virus initiates a latent infection by shutting 

down viral protein expression. It is this latent infectious 

state that is responsible for malignant transformation [6] . 

The virus remains in the B cell memory pool, recirculating, 

and is found predominantly in the blood and pharyngeal 

lymphoid tissue [3,7] . 

EBV is known to be associated with several different 

malignancies in humans, including Hodgkin’s lymphoma 

(HL), BL, nasopharyngeal carcinoma, and post-transplant 

proliferative disease (PTLD), in which the malignant cells 

are characterized by unique viral and cellular phenotypes, 

as well as unique viral antigen expression [8] . 

More than 30% of HL cases are EBV-associated, with 

the clonal virus localized inside the malignant cells. In developing 

countries this number is higher with 90% of HL 


being EBV positive. Similarly, the association between 

EBV and HL is even higher in patients with acquired 

immunodeficiency syndrome (AIDS) in whom 95% are 

EBV positive HL. The histology of these tumors also 

has some distinctive features since HL positive for EBV 

is more often a mixed cellular type. The clinical presentation 

also differs from that of the EBV negative counterpart 

in that this form is more commonly seen in either 

children younger than 10 years of age or in adults older 

than 45 years old. Additionally, the prognosis of EBV 

positive HL in the elderly and immunocompromised is 

poor, compared with that of patients with EBV negative 

HL [8] . 

HL is currently classified by two distinct types: nodular 

lymphocyte predominant HL and classical HL (CHL). 

The latter is further categorized into three subgroups: 

nodular sclerosis, lymphocyte rich, and mixed cellularity 

(MCCHL) [9] . There is significant overlap in the imaging 

manifestations of the different types and subtypes of 

lymphomas, which in the chest may involve the mediastinum, 

lung, pleura and chest wall, but some differences 

should be highlighted. First, primary pulmonary lymphoma 

is rare in Hodgkin’s disease. Pulmonary involvement 

in HL is more commonly seen either in advanced 

stages (secondary involvement) or in recurrent disease [10] . 

Second, even though HL is the most common lymphoma 

presenting with mediastinal lymphadenopathy, MCCHL, 

the type most commonly seen in association with EBV 

involvement, typically spares the thymus gland and medi- 


A 

Figure 2 Burkitt lymphoma in a 38-year-old male with a left axilla mass. Contrast-enhanced computed tomography, axial (A) and coronal (B) images demonstrates 

a bulky soft tissue mass involving the axilla, subpectoral and subscapular spaces. 

Figure 3 Post-transplant proliferative disease in a 50-year-old male postright 

lung transplant. Contrast-enhanced computed tomography shows an 

infiltrative right hilar mass surrounding the right lower lobe bronchus and involving 

the subcarinal region. Ipsilateral small pleural effusion is also noted. 

astinum [9] (Figure 1). 

The association between EBV infection and BL varies 

depending on the subtype of the disease. The endemic 

form (eBL) is associated with EBV infection in 

over 95% of cases. Only half of AIDS-related BLs are 

associated with this viral infection, while the sporadic 

form of (sBL) is rarely associated with it [11,12] . Thoracic 

involvement in BL is less common than the more typical 

facial or abdominal disease, and is more commonly 

seen in HIV positive (10%) than in HIV negative (2%) 

patients [13] . The most common thoracic manifestations 

of BL include mediastinal mass and lymphadenopathy 

followed by pleural and chest wall involvement. Isolated 

pleural effusion and pulmonary parenchymal disease are 

rare [14,15] (Figure 2). 

Another infectious disease associated with BL is malaria. 

It is currently thought that the association between 

malaria and BL arises from a combination of multiple 

factors including immunosuppression, B-cell activation 

directly by the malarial parasite Plasmodium falciparum and 

EBV, since the viral loads for EBV are higher in areas endemic 

for malaria [11] . 

EBV and KS virus (KSV) in a complex interaction 

with the HIV, and the immunosuppression status have 


B 


also been implicated in the pathophysiology of non- 

HLs in AIDS, typically B-cell lymphomas. AIDS-related 

lymphomas remain an important cause of morbidity and 

mortality in HIV-infected individuals, often occurring in 

extranodal locations (e.g. bone marrow, brain, viscera) and 

have an aggressive clinical course [16] . On imaging examinations 

the extranodal location of these tumors manifest as 

pleural effusion, interstitial and alveolar lung disease, and 

pulmonary nodules [17] . 

PTLD is made up of a heterogeneous group of EBV 

diseases with malignant lymphoproliferation occurring after 

hematopoietic or solid organ transplantation secondary 

to iatrogenic suppression of T-cell function [18] . EBVinfected 

B cells in the germinal centers, which should be 

destroyed, persist in the absence of cytotoxic T cells [6] . 

Approximately 2% of all allograft recipients are afflicted 

with PTLD, and it is more likely to develop in 

patients who are seronegative for EBV before transplantation. 

Onset of the disease can occur at variable intervals 

with the mean at 2-5 mo after bone marrow, lung or 

heart-lung transplantation and at a mean of 22-32 mo 

after kidney, or liver transplantation [19] . 

PTLD involvement of the lung is more common 

after heart-lung transplantation than after liver or renal 

transplant. The most common intrathoracic findings of 

PTLD include well-circumscribed, often bilateral peripheral 

pulmonary nodules, patchy air space consolidation 

and mediastinal and hilar lymphadenopathy [19] . Pleuralbased 

masses, chest wall masses, pleural and pericardial 

effusion, and thymic enlargement have also been reported 

[20] (Figures 3 and 4). 

Positron Emission Tomography with Fluoro-2-deoxy- 

D-glucose (FDG-PET) has replaced gallium-67 scintigraphy 

in the functional and metabolic imaging evaluation 

of lymphomas. FDG-PET, in particular, is recommended 

before treatment in typically FDG avid lymphomas like 

diffuse large B cell lymphoma (DLBCL) and HL [21] . 

FDG-PET has also proven useful for the diagnosis, staging 

and therapy monitoring of PTLD both in infants 

and adult patients, revealing foci of increased uptake, not 

seen by other imaging techniques [22-24] . 

Lymphomatoid Granulomatosis is a B-cell lymphop- 


A 

Figure 4 Post-right lung transplant post-transplant proliferative disease in a 68-year-old male with pulmonary fibrosis. Non-contrast computed tomography, 

axial (A) and sagittal images (B) demonstrates an irregular mass in the right lung involving the middle lobe and lower lobe extending across the major fissure. 

A 


roliferative disease that is angiocentric and angiodestructive. 

It is comprised of predominantly reactive T cells and 

some neoplastic EBV-positive B cells. The pathogenesis 

of the disease is hypothesized to be similar to that of 

PTLD, in which infected B cells proliferate in the absence 

of an adequate number of cytotoxic T cells [25] . Malignant 

transformation to lymphoma occurs in 12%-47% of patients 

with a mortality rate between 53% and 63.5% [26] . 

The most common site of involvement for lymphomatoid 

granulomatosis is the lung [27] . Imaging findings 

include poorly marginated pulmonary nodules and lung 

masses distributed along the bronchovascular bundle and 

interlobar septa [26] . On computed tomography (CT), the 

nodular lesions may present with surrounding groundglass 

density (halo sign) or central ground-glass surrounded 

by a denser rim (the reverse halo sign) [28] . Rapid 

progression, central necrosis and cavitation masquerading 

as a lung abscess are other imaging features [29,30] . The 

presence of migratory nodules in the lung parenchyma 

mimicking the imaging findings of pulmonary vasculitis 

has also been reported [30] (Figure 5). 

HHV8 

HHV8 or KS herpes virus was first isolated in a patient 

with AIDS-associated KS and subsequently isolated in 


B 

B 

Figure 5 Lymphomatoid granulomatosis in a young adult male with acquired immunodeficiency syndrome. Initial chest computed tomography (CT) (A) demonstrates 

a round solid mass in the right lower lobe. After surgical resection follow-up CT (B) 4 mo later shows recurrent disease with new multiple nodules and cavitation 

in the right lower lobe. 

KS patients without HIV [31] . HHV8 is a γ2-herpes virus 

and similar to EBV has two different life cycles: lytic and 

latent. Viral proteins produced in both phases of viral 

replication are responsible for oncogenesis [32] . 

The virus has been identified in association with KS, 

primary effusion lymphomas (PEL) and Multicentric 

Castleman’s Disease [33] . Epidemiologically, the virus is 

widespread in most of sub-Saharan Africa with 50% of 

the population having antibodies to HHV8. It is also relatively 

frequent in the Mediterranean region. In endemic 

countries, transmission of the virus occurs in childhood 

from mother to child or among peers. In non-endemic 

countries, HHV8 is a sexually transmitted disease [34] . 

PEL is a rare type of AIDS non-HL that predominantly 

grows in the pleural, pericardial and peritoneal 

cavities. They are characterized clinically and on imaging 

examination by the presence of neoplastic effusions in 

complete absence of a contiguous solid mass, and are 

considered to develop from HHV8/KSV infection [35] . 

KS is a low-grade mesenchymal tumor involving 

blood and lymphatic vessels and is considered one of the 

major complications of AIDS. Four variants of KS are 

recognized: classic KS, endemic (African) KS, iatrogenic 

(organ transplant-related) KS, and AIDS-related KS [36] . 

In two of the forms of KS (AIDS and iatrogenic), the 

HHV8 causes a reactive polyclonal angioproliferative re- 


A 

sponse in the presence of host immunosuppression. The 

polyclonal cells become an oligoclonal cell population 

which proliferates and undergoes a malignant transformation 

[37] . 

KS with pulmonary involvement is found in approximately 

45% of patients with cutaneous AIDS-related 

KS [37] . Pulmonary involvement in KS is usually secondary 

to profound immunosuppression. Pulmonary KS was 

found to be associated with a low CD4 cell count and 

may be related to late presentation of HIV [38] . Following 

the introduction of highly active antiretroviral therapy 

(HAART), thoracic disease has become less frequent [38] . 

The most common presenting symptoms of pulmonary 

KS are progressive dyspnea, non-productive cough 

and fever. Other symptoms reported include pleural 

effusion with chest pain, hypoxemia, and acute respiratory 

failure requiring mechanical ventilation [37] . KS may 

involve the tracheobronchial tree, the lung parenchyma 

and pleura. Imaging manifestations in the chest include 

reticular and nodular opacities with a bronchovascular 

distribution, consolidation and adenopathies (Figure 6). 

Enlarged lymph nodes in the chest and abdomen may 

demonstrate significant contrast enhancement. Chest wall 

involvement with skin lesions and subcutaneous nodules 

or masses as well as osteolytic bone lesions involving the 

sternum, ribs and spine are not uncommon [36] . 

Castleman’s Disease was identified in a series of 13 

cases of localized mediastinal lymph node hyperplasia 

resembling thymoma described in 1956 by Dr. Benjamin 

Castleman [39] . Histologically, the disease is characterized 

by expanded germinal centers with B-cell proliferation 

and vascular proliferation. Castleman’s disease can be 

classified histologically as either hyaline-vascular or plasma 

cell variant, and clinically as either localized or multicentric 

[33] . Castleman’s disease in the HIV population is 

usually of the multicentric and plasma cell variant [40] . 

It is hypothesized that the active viral lytic replication 

cycle of HHV8 in lymphoid tissue can lead to Multicentric 

Castleman’s Disease [34] . HIV-related Multicentric Castleman’s 

disease is associated with Kaposi sarcoma. In fact, 

in a clinical series, 71% of HIV positive patients with 

Castleman’s Disease had Kaposi sarcoma [40] . Clinical fea- 


B 

tures include fever, weight loss, respiratory symptoms such 

as dyspnea and cough, hepatomegaly and splenomegaly. 

Prognosis is poor with a median survival of 14 mo [40] . 

There is an increased risk of progression to large B-cell 

plasmablastic lymphoma and other lymphomas [33] . The 

most common location for the localized form of Castleman’s 

disease, typically the hyaline vascular type, is in the 

chest, where the characteristic imaging manifestation on 

CT is as a mediastinal or hilar mass, with diffuse homogeneous 

enhancement after contrast injection [41] . Pleural, 

pericardial and intrapulmonary forms of Castleman’s 

disease, which are considered atypical presentations, have 

also been reported [42] . The multicentric type of Castleman’s 

disease associated with AIDS, typically the plasma 

cell type, more commonly manifests as diffuse pulmonary 

involvement with acute reticular and nodular opacities 

in patients who also present mediastinal and peripheral 

lymphadenopathy [43] (Figure 7). 

HPV 


Figure 6 Kaposi sarcoma in a 37-year-old male with acquired immunodeficiency syndrome. Contrast enhanced computed tomography of the chest, mediastinal 

window (A) and lung window (B) images demonstrate innumerable peribronchovascular and peripheral pulmonary nodules throughout the bilateral lungs. Enhancing 

skin lesions and bilateral pleural effusion are also noted. 

HPV is a non-enveloped double-stranded DNA virus 

with more than 200 types isolated [44] . The virus infects 

the basal layers of cutaneous and mucosal epithelium and 

enters the cell via a receptor. E6 and E7 proteins are the 

portions of the viral genome that encode viral oncoproteins 

expressed in HPV-positive cancers. E6 interferes 

with p53, a tumor suppressor protein that regulates the 

G1/S and G2/M cell cycle checkpoints. The main function 

of E7 is the binding and degradation of the Rb family 

of proteins, which are the major regulators of the cell 

cycle [45] . 

RRP is a benign lesion commonly found in the larynx 

with rare pulmonary involvement. The disease is difficult 

to treat because of frequent recurrence and spread 

throughout the respiratory tract. Ororespiratory exposure 

during vaginal birth is thought to be the origin of the disease 

and is often associated with HPV types 6 and 11 [46] . 

HPV 11 is thought to be associated with more aggressive 

disease than HPV 6 [47] . Pulmonary papillomatosis affecting 

the bronchi and lung parenchyma occurs in 1.8% of 

patients with RRP. Spread to the lower airways is usually 


A 


Figure 7 Multicentric Castleman’s disease in a 40-year-old male with acquired immunodeficiency syndrome. Contrast-enhanced chest computed tomography, 

axial images at two different levels (A, B) reveal numerous enhancing abnormally enlarged lymph nodes in the axillae and mediastinum. 

A B 

C 

Figure 8 Recurrent respiratory papillomatosis in a 27-year-old patient. Contrast-enhanced computed tomography, axial (A, B) and coronal (C) images. Numerous 

nodules and cystic lesion are seen in the bilateral lungs as well as a large lobulated mass partially obstructing the distal trachea (arrows). 

caused by tracheotomy performed in a child with laryngeal 

papillomatosis. Prognosis of pulmonary papillomatosis 

is poor with a mortality rate of 57.1% [47] . Malignant 

transformation in RRP can develop in 10% to 13% of 

affected patients [48,49] . 

Radiographic findings of RRP in the lungs include 

bilateral, multiple, thin-walled cysts and nodular papillomas 

with predominant lower lobe distribution. Cysts are 

usually less than 5 cm in size with air-fluid levels. Pulmonary 

nodules are usually small, but occasionally may be 

as large as 3 cm in diameter (Figure 8). Chest CT can be 

more sensitive in detecting small cysts and nodules. Virtual 

bronchoscopy is a non-invasive technique that can 

be used to evaluate the tracheobronchial tree and reduces 

the risk of downward spread of the virus that can occur 

during an endoscopic exam [46] . 

The association of lung cancer and HPV was first 

suggested by Syrjanen in 1979, who described epithelial 

changes in bronchial carcinomas similar to those of exophytic 

condylomas of the genital tract seen with HPV [50] . 

It has been theorized that HPV can infect the lungs hematogenously 

from other sites such as the cervix [51] . HPV 

types 16, 18, 31, 33 and 35 have been associated with lung 

cancer and both adenocarcinoma and squamous cell carcinoma 

have been seen with HPV infections [44] . HPV DNA 

has been identified in more than 20% of lung cancers [52] . 

SV-40 

SV-40 is a double-stranded DNA polyoma monkey virus. 


B 

It is believed that the most likely route of transmission of 

SV-40 from monkey to human was through contaminated 

polio vaccines produced between 1955 and 1978 [53] . Expression 

of the oncogenes, large T antigen and small T 

antigen, causes a high rate of malignant transformation. 

The large T antigen binds and inhibits p53 and pRB tumor 

suppressor proteins. Human mesothelial cells are susceptible 

to SV-40 infection and allow the virus to replicate 

without lysing leading to malignant transformation [2] . 

Malignant mesothelioma is an aggressive tumor that 

arises from mesothelial cells lining the pleura, peritonea 

and pericardia. SV-40 DNA is found in up to 60% of 

mesothelioma [54] . There is solid evidence linking SV-40 

either alone or with asbestos exposure as a contributing 

factor in the malignant transformation of mesothelial 

cells and subsequent development of malignant mesotheliomas 

[55,56] . Affected patients typically present with 

pleural effusion associated with chest wall pain. Prognosis 

is poor with an average survival of just 12 mo 

after diagnosis [54] . Characteristic imaging findings on CT 

include unilateral pleural effusion; nodular pleural thickening 

that may completely encase the affected lung; and 

pleural thickening extending into the pulmonary fissures 

(Figure 9). Given the association with asbestos exposure, 

calcified pleural plaques are seen in approximately in one 

fifth of affected patients [57] . 

HUmaN T-CEll-lymPHOTROPIC VIRUS 1 

Human T-cell-lymphotropic virus 1 (HTLV-1) is an RNA 


A 

Figure 9 Malignant mesothelioma in a 60-year-old male with progressive chest pain. Contrast-enhanced computed tomography, axial (A) and sagittal (B) images 

show an irregular and slightly lobulated soft tissue density mass extensively involving the pleural surface of the left lung including the major fissure (arrows). 

A 

virus belonging to the deltaretrovirus genus. It is the first 

human retrovirus linked to human malignancy [58] . It was 

isolated from peripheral blood samples of a patient with 

cutaneous T-cell lymphoma in the 1980s [59] . HTLV-1 is 

endemic to Japan, South America, Africa and the Caribbean 

[3] . Based on a number of studies, it appears that the 

viral regulatory factors, TAX and HBZ, are the malignant 

transforming factors. TAX modulates gene expression 

and induces genomic instability. HBZ stimulates T-lymphocyte 

proliferation [58,60] . 

Adult T cell leukemia/lymphoma (ATLL) is a mature 

T cell neoplasm of post-thymic lymphocytes that has 

been linked to HTLV-1. Although worldwide, 20 million 

people are infected with HTLV-1, it is estimated that 

only 2%-6% will develop ATLL. Patients with ATL have 

atypical lymphoid cells with multilobulated nuclei [58] . ATL 

is divided into 4 subcategories based on the diversity of 

clinical features and prognosis of patients: acute, lymphoma, 

chronic and smoldering. The acute form is aggressive 

with poor prognosis due to multidrug-resistant malignant 

cells. Chronic and smoldering types have an indolent 

course and do not require chemotherapy [61] . Thoracic 

involvement in Adult T-cell leukemia and lymphoma is 

common, with abnormal imaging findings in two thirds 

of affected patients. The most common abnormalities on 

CT include ground-glass opacities and thickening of the 


B 

B 

peribronchovascular interstitium with predominant peripheral 

distribution. Pleural effusion and enlarged lymph 

nodes are less common findings [62] (Figure 10). 

HIV 


Figure 10 Adult T cell leukemia in a 24-year-old male. Contrast-enhanced computed tomography at the level of the aortic arch (A) and mid-ventricular level (B) 

demonstrates a large mediastinal mass with extensive pericardial involvement and bilateral pleural effusions. 

Patients with HIV have an increased risk of developing 

cancer compared to the general population. Defined 

by the Center for Disease Control (CDC, Atlanta GA, 

USA), some of the AIDS-defining malignancies include 

KS, non-HL and invasive cervical cancer. Some of the 

non-AIDS defining malignancies that patients with HIV 

have an increased risk of developing include: HL, leukemia, 

lung cancer, invasive anal carcinoma, and multiple 

myeloma [63] . An increased risk of primary liver cancer 

has also been reported [64] . The mechanisms for the development 

of these malignancies are multifactorial and 

include a complex interaction between the HIV and 

other oncogenic viruses (e.g. EBV and HPV), immunosuppression 

and dysregulation of the immune system 

and environmental factors [65] . 

While the incidence of KS has decreased with the advent 

of HAART, HIV patients continue to be at risk for 

non-HL [66] . The most common AIDS-related lymphomas 

among patients include: DLBCL and Burkitt’s lymphoma, 

representing 90% of all lymphomas. The pathogenesis of 


A 

these lymphomas include: HIV-induced immunosuppression, 

chronic antigenic stimulation, genetic abnormalities, 

cytokine release and dysregulation, dendritic cell impairment, 

and the role of EBV and HHV8 [63] . 

Compared to the general population with NHL, AIDS 

patients with NHL tend to have advanced disease and 

present with B symptoms. The AIDS patients also have 

extranodal disease including bone marrow involvement 

and have disease in unusual locations such as body cavities, 

jaw, rectum, and soft tissues. In addition, patients 

have frequent plasmacellular differentiation and the disease 

is commonly associated with EBV and HHV8 [63] . 

The respiratory system is the most common extranodal 

site (70%) involved in individuals with AIDS-related 

NHL. Pleural effusion and mediastinal lymphadenopathy 

are the most common findings on CT (60%), followed by 

pulmonary nodules in half of them, and lobar opacities 

or consolidation in one fourth [67] . Cavitation of a lung 

or mediastinal mass is not an uncommon imaging finding 

[68,69] (Figure 11). 

Patients with HIV/AIDS also have an elevated risk 

for developing lung cancer. The incidence of HIV-related 

lung cancer has significantly increased, independent of 

smoking history, after the introduction HAART from 

0.8% (pre-HAART) to 6.7% (post-HAART). The major- 


B 

Figure 11 Non-Hodgkin lymphoma in two different patients with acquired immunodeficiency syndrome. A: Contrast-enhanced computed tomography (CT) at 

the level of the AP window demonstrates a large mediastinal mass with areas of cavitation with air-fluid levels (arrows); B: Contrast-enhanced CT reveals a large mediastinal 

mass with low-density foci consistent with tumoral necrosis. There is small left sided pleural effusion in both cases. 

A 


B 

Figure 12 Non-small cell lung cancer in a 39-year-old male with acquired immunodeficiency syndrome. Contrast enhanced chest CT. A: Mediastinum window, 

axial image at the level of the pulmonary arteries demonstrates a soft tissue density mass with air-bronchogram in the right lung; B: Lung window image at the same 

level shows the spiculated contour of the lung mass. 

ity of these cancers (94%) are non-small cell lung cancers 

with adenocarcinoma as the most common subtype 

(34%). Mortality is high (97%) with a median survival of 

3 mo [70] (Figure 12). 

Marginal zone lymphomas, a subtype of B-cell non- 

Hodgkin lymphoma has also been associated with bacterial 

infection (e.g. Helicobacter pylori, Campylobacter jejuni, 

Borrelia burdoferi, and Chlamydia psittaci) and viral infection 

(HIV, EBV and hepatitis C virus) [71] . 

CONClUSION 

A significant number of malignancies, many of which 

originate or manifest in the thoracic region, are known to 

be associated with viral infections. The pathophysiology 

for the development of these neoplastic processes are 

extremely complex and in some cases not yet completely 

understood. Multiple variables in addition to the initial viral 

infection including immunosuppression and dysregulation 

of the immune system, co-infection with another 

virus, as well as genetic and environmental factors come 

into play and interact. CT, with its capability for imaging 

the lung, mediastinum, pleural and chest wall, remains the 

most common imaging modality used for the diagnosis, 

staging and follow-up of these lesions. 


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AL, Taylor GP, Yamaguchi K, Utsunomiya A, Tobinai K, 

Watanabe T. Definition, prognostic factors, treatment, and 

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from an international consensus meeting. J Clin Oncol 

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62 Okada F, Ando Y, Kondo Y, Matsumoto S, Maeda T, Mori H. 

Thoracic CT findings of adult T-cell leukemia or lymphoma. 

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emerging challenges in the era of highly active 

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JJ. Cancer risk in people infected with human immunodeficiency 

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with AIDS. J Natl Cancer Inst 2007; 99: 962-972 

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sarcoma and non-Hodgkin’s lymphoma with potent 

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Duvivier C, Meyohas MC, Girard PM, Mayaud C, Cadranel 

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S- Editor Cheng JX L- Editor Webster JR E- Editor Zheng XM 


W J R 



doi:10.4329/wjr.v3.i12.289 

Multidetector computed tomography imaging of congenital 

anomalies of major airways: A pictorial essay 

Dinesh Kumar Sundarakumar, Ashu Seith Bhalla, Raju Sharma, Arun Kumar Gupta, Susheel Kumar Kabra, 

Priya Jagia 

Dinesh Kumar Sundarakumar, Ashu Seith Bhalla, Raju 

Sharma, Arun Kumar Gupta, Department of Radiodiagnosis, 

All India Institute of Medical Sciences, New Delhi 110029, India 

Susheel Kumar Kabra, Department of Pediatrics, All India Institute 

of Medical Sciences, New Delhi 110029, India 

Priya Jagia, Department of Cardiac Radiology, All India Institute 

of Medical Sciences, New Delhi 110029, India 

Author contributions: Sundarakumar DK reviewed and summarized 

the literature that provided the basis of the manuscript; 

Bhalla AS, Sharma R, Gupta AK, Kabra SK and Jagia P contributed 

to the conceptual design of the manuscript and case input. 

Correspondence to: Dr�� Dr�� Ashu Seith Bhalla, Department of 

Radiodiagnosis, All India Institute of Medical Sciences, New 

Delhi 110029, India. ashubhalla1@yahoo.com 

Telephone: +91-11-26588500 Fax: +91-11-26588641 

Received: May 17, 2011 Revised: September 7, 2011 

Accepted: October 11, 2011 

Published online: December 28, 2011 

Abstract 

Congenital airway anomalies can be asymptomatic or 

may cause severe respiratory distress requiring immediate 

treatment�� These anomalies can present early in 

life, or may be just incidental findings. It is important 

to recognize these entities to realize their clinical significance 

and to avoid false diagnosis. In this article, 

the various congenital airway anomalies and their imaging 

features by multidetector computed tomography 

(MDCT) are reviewed in order of occurrence during 

the embryological timeline�� This pictorial essay reviews 

the various distinct congenital airway lesions and their 

MDCT manifestations. It also provides insight into the 

embryological basis of the congenital airway lesions encountered�� 

© 2011 Baishideng�� All rights reserved�� 

Key words: Airway; Anomalies; Computed tomography; 

Congenital 




Peer reviewer: Patrick K Ha, MD, Assistant Professor, Johns 

Hopkins Department of Otolaryngology, Johns Hopkins Head 

and Neck Surgery at GBMC, 1550 Orleans Street, David H Koch 

Cancer Research Building, Room 5M06, Baltimore, MD 21231, 

United States 

Sundarakumar DK, Bhalla AS, Sharma R, Gupta AK, Kabra SK, 

Jagia P. Multidetector computed tomography imaging of congenital 

anomalies of major airways: A pictorial essay. World J 



org/10.4329/wjr.v3.i12.289 

INTRODUCTION 

Imaging modalities for pediatric tracheo-bronchial lesions 

have vastly improved over time. Frontal and lateral 

neck and chest X-rays were the radiological investigations 

used in the past which provided limited diagnostic yield [1] . 

With the advent of multidetector computed tomography 

(MDCT) scanners and continued refinement in the 3-D 

reconstruction software algorithms, newer options for 

non-invasive imaging of these lesions have become available. 

These high resolution images demonstrate exquisite 

details of the airways down to the segmental bronchi, 

can depict the adjacent mediastinal structures, and result 

in an improvement in diagnostic confidence. In addition, 

decreased scan time, and therefore decreased need for 

prolonged sedation in the pediatric population, are advantageous 

in scanning children, where motion artifact is 

an issue. 

TECHNIQUES 




REVIEW 

In this pictorial essay, congenital airway lesions are depicted 

using axial MDCT images and reconstructed imaging 

techniques such as multiplanar reformatted images, minimal 

intensity projection images, and virtual bronchoscopy 

images. 


A 

Figure 2 Foregut duplication cyst. Axial images in the mediastinal (A) and lung (B) window and coronal multiplanar reformatted images (C) showing a fluid-attenuating 

lesion (long arrows) in the mediastinum compressing the left main bronchus (short arrow) with hyperinflation of left lower lobe. Hydropneumothorax in the left 

side was due to post-surgical change. 

A 

A 

B 

B 

C 

Figure 4 Subglottic stenosis Sagittal (A) and coronal (B) minimal intensity projection images and sagittal multiplanar reformatted images images (C) 

show segmental narrowing of the subglottic trachea (arrow). Virtual bronchoscopy images from the proximal (D) and distal perspective(E) show the glottis (black 

arrow) and the subglottic tubular narrowing (red arrow). 


B 

C 

Figure 3 Congenital subglottic web. A, B: Sagittal multiplanar reformatted images (A) and coronal minimal intensity projection images (B) show the short segment 

and circumferential narrowing of the subglottic region; C: Virtual bronchoscopy image shows the narrowing to be annular and is located below the vocal cords 

(arrow). 

abnormal shape of the cricoid cartilage (Figure 4). Congenital 

tracheal stenosis can be generalized as follows: hypoplasia, 

funnel-shaped stenosis or segmental stenosis [5] . 

DISORDERS OF MESENCHYME 

Tracheomalacia 

Tracheomalacia is a common cause of stridor and respi- 

Sundarakumar DK et al �� MCDT imaging of congenital airway lesions 

D 

C 

ratory distress in neonates and infants, second only to 

laryngomalacia. Tracheomalacia is caused by abnormal 

collapsibility of the C-cartilages of the trachea. CT imaging 

features include opposition of the tracheal wall and 

widening of the C-cartilage with buckling of the posterior 

wall during the expiratory scan, i.e. the “expiratory frown 

sign”. Often, imaging may not reveal the narrowing due to 

the dynamic nature of the narrowing [6] (Figure 5). 

291 December 28, 2011|Volume 3|Issue 12| 

E

A 

DISORDERS OF TRACHEOESOPHAGEAL 

SEPTUM 

Tracheoesophageal fistula 

Tracheoesophageal fistula (TEF) is due to an incomplete 

separation of pulmonary and esophageal anlage during 

early embryogenesis. There are five types of esophageal 

atresia (EA) and TEF, the most common abnormality being 

EA with a distal TEF (84%). Isolated atresia without 

a fistula is the next most common finding (8%), followed 

by H-type TEF without atresia (4%). EA with proximal 

and distal fistulas (3%) and EA with a proximal fistula 

(1%) are less common [7] (Figure 6). 

DISORDERS OF TRACHEAL BUD 

BRANCHING 

Tracheal bronchus 

Tracheal bronchus refers to an aberrant bronchus arising 

from the tracheal wall above the carina, usually on the 

right side, caused by abnormal additional branching in 

early embryonic life. The incidence of tracheal bronchus 

is reported to be between 0.1% and 5%. Rarely, it might 

cause recurrent infection of the involved upper lobe [8] 

(Figure 7). 


B 

Figure 5 Tracheomalacia. Axial image (A) in the lung window and virtual bronchoscopy image (B) shows widening of the tracheal ‘C’- cartilage and decreased 

antero-posterior dimension of the trachea. 

A 


B 

Figure 6 Tracheo-esophageal fistula ‘H’- type. Axial image in the mediastinal (A) and lung window (B) shows the presence of tracheo-esophageal ��stula ��stula (arrows) 

and consolidation in the right upper lobe. Nasogastric tube is present in the esophageal lumen; C: Coronal multiplanar reformatted images depicts the ‘H’- shaped 

��stula (arrow) between the trachea and esophagus. 

Tracheal trifurcation 

Tracheal trifurcation develops when there is an abnormal 

division of tracheal segments into three segments instead 

of the normal two divisions [9] (Figure 8). 

Tracheal diverticulum 

Congenital tracheal diverticula are rare developmental lesions 

which are due to abnormal supernumerary branches 

arising from the trachea during development. The 

diverticulum is lined by respiratory mucosa and usually 

communicates with the tracheal lumen. The most common 

location of the lesion is the right postero-lateral wall 

of the trachea at the cervicodorsal junction [10] (Figure 9). 

Pulmonary isomerism 

Pulmonary isomerism is an anomaly of the number of 

lung lobes. In this anomaly, the right lung has 2 lobes, 

whereas the left has three. This condition may be associated 

with situs inversus, asplenia, polysplenia, and/or 

anomalous pulmonary venous drainage (Figure 10). 

DISORDERS OF BRONCHIAL BUD 

DEVELOPMENT 

C 

Spin: -4 

Tilt: 0 

Pulmonary agenesis, aplasia, and lobar agenesis 

The absence of development of bronchial buds leads to 


A 

these conditions may give rise to airway symptoms due to 

extrinsic compression. 

Vascular compression 

The left main bronchus can be compressed by an anteriorly 

placed descending aorta or enlarged pulmonary artery 

[16] . Tracheal compression can be due to a pulmonary 

arterial sling (Figure 7) or aortic ring [17] (Figure 16). 

Peribronchial hamartomas 

Pulmonary hamartomas are generally seen sub-pleurally 

in the peripheral lung parenchyma. Occasionally, they 

may arise from the mesenchyme of the bronchial wall 

causing bronchial narrowing or intraluminal growth and 

can lead to hyperinflation, collapse, pneumonia and hemoptysis 

[18] ( Figure 17). 

CONCLUSION 

Congenital major airway anomalies differ in their stage 

of development in the embryological sequence, severity 

of symptoms, time of presentation, and prognosis. 

MDCT is a valuable adjunct to bronchoscopy, especially 

in patients with suboptimal bronchoscopy examination. 


B 

Figure 16 Compression of left main bronchus between enlarged pulmonary artery and descending aorta. Axial images in the mediastinal window (A and B) 

show enlarged pulmonary artery in this case of atrial septal defect. Axial image (B) and coronal multiplanar reformatted images in the lung window (C) show narrowing 

of the mid segment of the left main bronchus (arrows) and the resultant hyperinflation in the left lung. 

A 


B 

Figure 17 Peribronchial hamartoma. A: Coronal multiplanar reformatted images in the mediastinal window shows eccentric narrowing of the right main bronchus 

by a lesion with dense calci��cation (arrow) and resultant distal bronchiectasis and volume loss; B: Fiberoptic image of the carina shows distortion of the antero-lateral 

wall of the right main bronchus (arrow). Histological analysis revealed the lesion to be a peribronchial hamartoma. 

C 

In this review, the utility of MDCT in the diagnosis of 

congenital airway anomalies is highlighted. 

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JC. Tracheal agenesis. Am J Roentgenol Radium Ther Nucl Med 

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3 Madhusudhan KS, Seith A, Srinivas M, Gupta AK. Esophageal 

duplication cyst causing unilateral hyperinflation of the 

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4 Cohen SR. Congenital glottic webs in children. A retrospective 

review of 51 patients. Ann Otol Rhinol Laryngol Suppl 

1985; 121: 2-16 

5 Cantrell JR, Guild HG. Congenital stenosis of the trachea. 

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6 Boiselle PM, Ernst A. Tracheal morphology in patients with 

tracheomalacia: prevalence of inspiratory lunate and expiratory 

“frown” shapes. J Thorac Imaging 2006; 21: 190-196 

7 Holder TM, Ashcraft KW, Sharp RJ, Amoury RA. Care of 

infants with esophageal atresia, tracheoesophageal fistula, 

and associated anomalies. J Thorac Cardiovasc Surg 1987; 94: 

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8 Barat M, Konrad HR. Tracheal bronchus. Am J Otolaryngol 


1987; 8: 118-122 

9 Beigelman C, Howarth NR, Chartrand-Lefebvre C, Grenier 

P. Congenital anomalies of tracheobronchial branching patterns: 

spiral CT aspects in adults. Eur Radiol 1998; 8: 79-85 

10 Goo JM, Im JG, Ahn JM, Moon WK, Chung JW, Park JH, Seo 

JB, Han MC. Right paratracheal air cysts in the thoracic inlet: 

clinical and radiologic significance. AJR Am J Roentgenol 1999; 

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11 Tsunezuka Y, Oda M, Ohta Y, Watanabe G. Congenital 

absence of the right upper lobe of the lung. Ann Thorac Surg 

2002; 74: 571-573 

12 Braimbridge MV, Keith HI. Oesophago-bronchial fistula in 

the adult. Thorax 1965; 20: 226-233 

13 Lucaya J, Strife J. Pediatric chest imaging: chest imaging in 

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14 Zylak CJ, Eyler WR, Spizarny DL, Stone CH. Developmental 

lung anomalies in the adult: radiologic-pathologic correlation. 

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15 CH’IN KY, TANG MY. Congenital adenomatoid malformation 

of one lobe of a lung with general anasarca. Arch Pathol 

(Chic) 1949; 48: 221-229 

16 Hungate RG, Newman B, Meza MP. Left mainstem bronchial 

narrowing: a vascular compression syndrome? Evaluation by 

magnetic resonance imaging. Pediatr Radiol 1998; 28: 527-532 

17 Park CD, Waldhausen JA, Friedman S, Aberdeen E, Johnson 

J. Tracheal compression by the great arteries in the mediastinum. 

Report of 39 cases. Arch Surg 1971; 103: 626-632 

18 Jain V, Goel P, Kumar D, Seith A, Sarkar C, Kabra S, Agarwala 

S. Endobronchial chondroid hamartoma in an infant. J 

Pediatr Surg 2009; 44: e21-23 

S- Editor Cheng JX L- Editor Webster JR E- Editor Zheng XM 


W J R 



doi:10.4329/wjr.v3.i12.298 

Image of tumor metastasis and inflammatory lymph node 

enlargement by contrast-enhanced ultrasonography 

Takaya Aoki, Fuminori Moriyasu, Kei Yamamoto, Masafumi Shimizu, Masahiko Yamada, Yasuharu Imai 

Takaya Aoki, Fuminori Moriyasu, Kei Yamamoto, Masafumi 

Shimizu, Masahiko Yamada, Yasuharu Imai, Department of 

Gastroenterology and Hepatology, Tokyo Medical University, 

6-7-1, Nishishinjuku, Shinjyuku-ku, Tokyo 160-0023, Japan 

Author contributions: All authors contribute equally to this article. 

Correspondence to: Fuminori Moriyasu, MD, PhD, Department 

of Gastroenterology and Hepatology, Tokyo Medical University, 

6-7-1 Nishi-Shinjuku Shinjukuku Tokyo 160-0023, 

Japan. moriyasu@tokyo-med.ac.jp 

Telephone: +81-3-53256838 Fax: +81-3-53256840 

Received: March 12, 2011 Revised: May 1, 2011 

Accepted: July 4, 2011 

Published online: December 28, 2011 

Abstract 

AIM: To compare the difference between tumorinduced 

lymph node enlargement and inflammationinduced 

lymph node enlargement by contrast-enhanced 

ultrasonography and pathological findings. 

METHODS: A model of tumor-induced lymph node 

metastasis was prepared by embedding a VX2 tumor 

into the hind paws of white rabbits. A model of 

inflammation-induced enlargement was prepared by 

injecting a suspension of Escherichia coli into separate 

hind paws of white rabbits. Then, a solution of Sonazoid 

(GE Healthcare, Oslo, Norway) was injected 

subcutaneously in the proximity of the lesion followed 

by contrast-enhanced ultrasonography of the enlarged 

popliteal lymph nodes. 

RESULTS: In the contrast-enhanced ultrasonography 

of the tumor-induced metastasis model, the sentinel 

lymph node was imaged. An area of filling defect was 

observed in that enlarged lymph node. In the histology 

examination, the area of filling defect corresponded to 

the metastatic lesion of the tumor. Contrast-enhanced 

ultrasonography of the model on inflammation-induced 

lymph node enlargement, and that of the acute inflam- 




mation model performed 3-7 d later, revealed dense 

staining that was comparatively uniform. The pathological 

findings showed acute lymphadenitis mainly due 

to infiltration of inflammatory cells. Contrast-enhanced 

ultrasonography that was performed 28 d post-infection 

in the acute inflammation model showed speckled 

staining. Inflammation-induced cell infiltration and fiberization, 

which are findings of chronic lymphadenitis, 

were seen in the pathological findings. 

CONCLUSION: Sentinel lymph node imaging was made 

possible by subcutaneous injection of Sonazoid. Contrast-enhanced 

ultrasonography was suggested to be 

useful in differentiating tumor-induced enlargement and 

inflammation-induced enlargement of lymph nodes. 


Key words: Lymph node enlargement; Sentinel lymph 

node; Contrast-enhanced ultrasonography; Subcutaneous 

injection; Sonazoid 

Peer reviewer: Ragab Hani Donkol, Professor, Radiology Department, 

Aseer Central Hospital, 34 Abha, Saudi Arabia 

Aoki T, Moriyasu F, Yamamoto K, Shimizu M, Yamada M, Imai 

Y. Image of tumor metastasis and inflammatory lymph node 

enlargement by contrast-enhanced ultrasonography. World J 



org/10.4329/wjr.v3.i12.298 

INTRODUCTION 




BRIEF ARTICLE 

Sonographic imaging eliminates the variations in scattered 

intensity that occur due to differences in acoustic 

impedance of various body tissue interfaces. Gaseous 

impedance is very small compared to impedance by body 

tissues that consists of liquids and solids. Thus, by using 

gaseous microbubbles, a strong contrast effect such as 


an echo source can be achieved. This is the principle of 

contrast-enhanced ultrasonography and its development 

has made microvascular diagnosis possible. 

When the acoustic pressure (amplitude) of the bombarding 

ultrasound wave is low, the microbubbles are 

comparatively stable, resonance occurs as scatter and reflector, 

and a non-linear signal is obtained. However, when 

the acoustic pressure of the bombarding ultrasonic wave 

is high, the microbubbles burst. With Sonazoid, the 

threshold value of the resonating acoustic pressure when 

the MI value ranges from 0.2 to 0.4 is high compared 

to when SonoVue is used [1] . Sonazoid is a contrast 

agent that can be observed continuously with moderate 

acoustic pressure and without the microbubbles bursting. 

The sentinel lymph node is a lymph node that cancer 

cells first reach if there is tumor metastasis to lymph 

nodes. The status of cancer cells reaching the subsequent 

lymph nodes that are downstream is judged based on the 

status of metastasis to this lymph node. It is also an important 

lymph node for decision making about the need 

for lymph node dissection. In various malignant tumors 

such as breast cancer, colon cancer and skin cancer, identification 

of the sentinel lymph node is now known to 

affect the choice of treatment [2-6] . 

Sentinel node navigation surgery (SNNS) is becoming 

the focus of attention as a lowly invasive form of treatment 

of early cancer. In SNNS, the site of the sentinel 

lymph node is different from that of the tumor. In addition, 

there are inter-individual variations, thus accurate 

identification of the sentinel lymph node is essential. To 

achieve this, substances that cause lymph node metastasis 

in the periphery of tumors are administered and the dynamics 

monitored to detect the direct inflow to the sentinel 

lymph node from the tumor lesion. 

Radio-isotope (RI) procedures [4,7] and pigmentation 

techniques [8,9] are being used to identify sentinel lymph 

nodes such as those found in breast cancer and gastric 

cancer. The pigmentation techniques are inexpensive but 

need expertise. In addition, pigments can be administered 

during surgery of the lymphatic system where the rate of 

metastasis is high. The flow of lymph can be observed 

directly in real time. However, spreading of the pigment 

to distal lymph nodes is faster than to the sentinel lymph 

node, therefore, it is not necessarily the best procedure to 

identify the sentinel node. In addition, administration of 

pigments has been reported to cause anaphylaxis [10] . 

The RI procedure uses radioisotopes, therefore precision 

is high and quantitative identification is possible [11] . 

However, the equipment is massive and moreover, radioactive 

exposure of subjects and the examiner is a concern. 

On the other hand, local injection of microbubble, 

which is a contrast agent, reveals the sentinel lymph node 

in ultrasonography [11-15] . Here, imaging performance in 

an animal model of malignant tumor-induced sentinel 

lymph node metastasis was investigated using the contrast 

agent Sonazoid. In addition, a model of tumorinduced 

and a model of inflammation-induced swelling 


Aoki T et al . Ultrasonography imaging of lymph node 

of lymph nodes were prepared to comparatively investigate 

the differences between tumor-induced enlargement 

and inflammation-induced enlargement of lymph nodes. 

MATERIALS AND METHODS 

Animal model 

A total of 11 Japanese white rabbits (Clea Japan, Tokyo, 

Japan) weighing 2.5-3.5 kg (mean 2.9 kg) were used in the 

study. The rabbits were cared for by the Tokyo Medical 

University Animal Study Center staff and experimental 

protocols were approved by the Animal Ethical Committee 

of Tokyo Medical University. 

The animals were kept in a room maintained in a 

day/night environment of alternate 12 h of light and 

darkness at a room temperature of 21℃. 

Tumor-induced lymph node enlargement model 

A model of VX2 tumor-induced metastatic lymph node 

enlargement was prepared in six animals. The VX2 tumor 

was embedded by injecting it into the femoral muscle of 

rabbit and from day 14 to 21, each muscle was excised. 

The isolated tumor was shredded and filtered under 

pressure using a commercial fine meshed filtering device 

while adding a small amount of physiological saline. After 

centrifugation at 700 r/min, the residue was suspended in 

physiological saline to make a cell concentration of about 

2 × 10 6 cells/mL. 

A total of 1 mL of that suspension was divided into 

several aliquots and each aliquot injected directly into the 

subcutaneous connective tissue of the hind paw of rabbit 

using an 18G injection needle. After 7-35 d had passed 

since the injection, VX2 tumors that had increased to 

30-50 mm were found in the hind paws. The popliteal 

lymph nodes of these animals had enlarged from 12-18 mm 

and were used as the tumor-induced lymph node enlargement. 

Coliform inflammation model 

A coliform inflammation-induced lymph node enlargement 

model was prepared using five animals. Cultured 

colonies of coliform bacteria [Escherichia coli (E. coli), 

verotoxin non-producing] of 10 × 10 mm that had been 

collected from human clinical specimens were taken and 

dispersed in 10 mL physiological saline at 30℃ to prepare 

a coliform solution at a cell concentration of about 10 6 

cells/mL. 

For the inflammation-induced lymph node enlargement 

model, a total of 1 mL of this coliform solution 

was divided into several aliquots and each aliquot subcutaneously 

injected into the connective tissue of the hind 

paw of a white rabbit using an 18 gauge needle. From 

3 to 28 d after the injection, tumors that had enlarged 

by 10 to 30 mm or connective tissue inflammation (cellulitis) 

were found in the hind paw. The popliteal lymph 

nodes of these rabbits had enlarged by 8 to 17 mm. The 

enlarged popliteal lymph nodes were confirmed with an 

ultrasound device and were used as the inflammation- 



induced lymph node enlargement model. 

Prior to observation, hair on the entire legs of the 

rabbits was shaved off and cleaned using commercial hair 

removing cream to make them hairless. This facilitated 

the observation by ultrasound. 

The protocol of the study was performed in accordance 

with the specifications of the Ethics Committee 

on Animal Studies of Tokyo Medical University. 

Ultrasound diagnostic device 

The ultrasound device used was AplioXV (SSA-770A 

ultrasound diagnostic system AplioXV, Toshiba Medical 

Systems Co., Otawara, Japan) that was commercialized 

by Toshiba Medical Systems Corp for clinical use. 

A 7.5 MHz linear type (PLT-704AT) probe was used. 

The contrast mode was Pulse Subtraction Imaging (PSI ® ), 

which is phase invasion harmonic. The acoustic pressure 

for the MI value was set at 0.2-0.4. The frame rate was 

set at 15 fps. 

Dose of contrast and observations 

The study was performed by intravenous injection under 

intravenous anesthesia. A 24G indwelling needle (BD 

Insyte Autoguard Winged, Becton Dickson Japan Co. 

Ltd., Fukushima, Japan) was placed in the ear vein of rabbit, 

through which was administered physiological saline 

by drip infusion at a rate of 60 mL/h. The anesthetic used 

was Nembutal (pentobarbital 50 mg/mL, Dainippon 

Pharmaceutical Co. Ltd., Osaka, Japan). Nembutal was 

diluted 10-fold in physiological saline and administered 

intravenously at an initial rate of 2 mL. Additional Nembutal 

was then appropriately administered by drip infusion 

at the rate of 1 mL each time such that the animal 

remained anesthetized without spontaneous respiration 

being suppressed. 

The primary tumor, other tumors and lymph nodes 

were identified by normal B mode (basic ultrasound tomography) 

and recorded, and the size was measured. 

The contrast agent Sonazoid is supplied as a lyophilized 

powder in vials and is reconstituted in 2 mL of 

distilled water prior to use. A total volume of 1 mL of 

Sonazoid was administered in aliquots of 0.25 mL to 

the subcutaneous tissues within the surroundings of the 

primary lesion or 5 mm of the tumor periphery in four 

locations (0, 3, 4, 6, and 9 o’clock). A 21G needle was 

used to make the subcutaneous injection. Then, a probe 

was placed in the direction of the long axis from the tumor 

or primary lesion of the hind paw towards the knee 

while massaging the tumor or tumor periphery. Imaging 

of the lymph duct was observed and a video recording 

and still images were recorded. In addition, a video recording 

and still images of the popliteal lymph node were 

observed and recorded. 

The captured images were stored on the hard disk in 

the ultrasound device and the data was later extracted. 

Histological examination 

After the ultrasound observation, a total of 0.5 mL of 

blue dye (Patent Blue V sodium dye, Guerbert, Roissy, 


France) in aliquots of 0.125 mL was administered subcutaneously 

in almost the same four locations as the 

contrast agent. Then, the tumor or tumor periphery was 

massaged. 

Fifteen minutes later, the rabbits were sacrificed by 

administering an overdose of Nembutal intravenously. 

The skin of the legs was opened and subcutaneous 

tissue isolated. After confirming the blue stained lymph 

nodes, they were extracted. The extracted lymph nodes 

were fixed in 10% formaldehyde. Pathological specimen 

slides were then prepared. The specimens were stained 

with hematoxylin-eosin dye and observed microscopically. 

The contrast-enhanced sonographic images and 

pathological tissue images that were obtained above were 

compared. 

RESULTS 

Contrast-enhanced ultrasonography of lymph ducts and 

lymph nodes 

Sonazoid solution was injected subcutaneously and 

massage performed. Immediately after, both the tumorinduced 

and inflammation-induced enlargement models 

and the lymph ducts from the site of injection of the 

contrast agent in the hind paw to the popliteal lymph 

nodes were imaged (Figure 1). Imaging of the lymph 

ducts continued over several minutes. When imaging of 

the lymph ducts included the lymph node, the contrast 

agent entered the lymph nodes from the afferent duct 

and soon all the lymph nodes could be imaged. For some 

of the lymph nodes, the contrast agent leaked from the 

afferent duct (Figure 2). 

Tumor-induced lymph node enlargement model 

Models 1-6 are metastatic lymph node enlargement that 

was achieved by implanting VX2 tumor in hind paw of 

rabbits. Lymph node imaging was performed for all six 

animals that underwent contrast-enhanced sonography 

following implantation of the tumor. The period from 

the tumor transplant to the contrast-enhanced ultrasonography 

was 7-35 d. Enlarged popliteal lymph nodes 

with diameters of 12-18 mm were confirmed in the images 

taken by basic B mode (Figures 3A and 4A). 

In model 1 (Table 1), only the periphery was enhanced. 

The central area was notably defective (Figure 3B). The 

histopathological images showed that most of the central 

area had changed into tumor while lymph tissue remained 

in the periphery (Figure 3C). 

In model 2 (Table 1), only part of the periphery was 

enhanced and so most sites were not enhanced. The histopathological 

images showed that almost the entire area 

had changed into tumors while lymph tissue remained in 

only part of the periphery. 

In models 3-5 (Table 1), a comparatively small defect 

was seen internally. The histopathological images showed 

that the site of that defect coincided with the site that 

had changed into tumor. 

In model 6 (Table 1), the entire lymph nodes could 


A 

1 cm 


B 

1 cm 

Figure 1 Ultrasound image of lymph ducts. Model of tumor-induced lymph node enlargement at 21 d after VX2 tumor was implemented (model 3). A: Sonazoid 

that was administered subcutaneously in the tumor lesion periphery of the hind paw. The arrowhead is the site where the contrast agent was injected; B: The lymph 

duct (arrowheads) towards the top part from the injection site that is shown in the form of a line. 

A 

B 

C 

1 cm 

1 cm 

1 cm 


Figure 2 Lymph node imaging (dynamics study). The model of inflammation-induced lymph node enlargement at 3 d after Escherichia coli was implanted (model 8). 

A: The image of the lymph hilum 9 s later, showing flow of the contrast agent from the afferent lymph duct; B: The contrast agent reached the center of the lymph node 

from the lymph hilum 12 s later; C: The entire lymph node was imaged 15 s. 


A 

B 

C 


1 cm 

Figure 3 Contrast-enhanced ultrasonography image and histopathological 

image of the tumor-induced lymph node enlargement model. This is 

the tumor-induced lymph node enlargement model at 28 d after VX2 tumor was 

implanted (Model 1). A: The enlarged popliteal lymph node with a diameter of 

18 mm that was seen in the B mode ultrasound image. This lymph node shown 

hypoechoic mass; B: Image of the popliteal lymph node that was imaged after 

the contrast agent was administered in the periphery of the primary tumor lesion. 

The central area is large and defective and so only the periphery of the 

lymph node was imaged; C: Histopathological image (hematoxylin-eosin stain) 

of the lymph node that was extracted. A large metastatic tumor lesion was seen 

in the center. 

be enhanced by contrast-enhanced ultrasonography. The 

histopathological images showed swollen inflammationinduced 

lymph nodes with no metastatic tumor lesions. 

Inflammation-induced lymph node enlargement model 

Models 7-11 (Table 1) are swollen inflammation-induced 

lymph nodes that were obtained by implanting E. coli into 

the hind paw of rabbits. The period from the infection to 

the contrast-enhanced ultrasonography was 3-18 d. Enlarged 

popliteal lymph nodes of diameter 8-17 mm were 

found during sonography. Images of these lymph nodes 


1 cm 

A 

B 

C 

1 cm 

1 cm 

Figure 4 The contrast-enhanced ultrasonography image and histopathological 

image of the acute inflammation-induced lymph node enlargement 

model. The model of inflammation-induced lymph node enlargement at 7 d 

after Escherichia coli was implanted (model 9). A: The enlarged popliteal lymph 

node with a diameter of 13 mm that was seen in the B mode ultrasound image. 

This lymph node showed up as a hypoechoic mass; B: Image of the popliteal 

lymph node that was imaged after the contrast agent was administered in 

the periphery of the primary lesion. The entire lymph node was imaged; C: 

Histopathological image (hematoxylin-eosin stain) of the lymph node that was 

extracted. Invasion of inflammatory cells, mainly nucleocytes, was seen. These 

are findings of acute lymphadenitis. 

in basic B mode showed a flat condition compared to the 

VX2 tumor-induced metastasis model. 

In models 8-10 (Table 1), contrast-enhanced ultrasonography 

showed that the entire lymph nodes were enhanced 

(Figure 4B). The contrast agent entered the lymph 

nodes from the afferent lymph duct. The lymph nodes 

were uniformly imaged gradually towards the trunk. Imaging 

of the efferent duct was minimal. The histopathological 

images showed strong infiltration of inflammatory 

cells, mainly of the mononuclear cells. In particular, follicular 

formation was seen in the central area. These were 


Table 1 List of experimental models 

Model 

No. # 

Implanting Days after 

implanting 

findings of acute lymphadenitis (Figure 4C). 

In models 7 and 11, the entire lymph nodes were enhanced 

non-uniformly by contrast-enhanced ultrasonography. 

In model 7, a defective star-like image was seen. In 

the histopathological image, inflammation-induced cell 

invasion and fiberization in the entire lymph nodes were 

seen while in model 11, there was lymph tissue in the periphery 

and inflammation-induced cell invasion as well as 

strong fiberization. 

In sum, contrast-enhanced sonography of the tumor 

metastatic model revealed defective shadows in the lymph 

nodes. The one animal that had no defective part did not 

have tumor metastasis in the lymph nodes but was rather 

a case of enhanced inflammation (model 5). The contrastenhanced 

ultrasonography of the five animals used for the 

inflammation-induced enlargement model showed that 

the short period that elapsed after staining contributed to 

the uniform staining trend while a long period resulted 

in non-uniform staining, which was consistent with the 

histopathological findings of chronic lymphadenitis with 

fiberization. 

DISCUSSION 

Contrast-enhanced ultrasonography was first reported 

by Gramiak in 1968 [16] . Rapid intravenous injection of 

physiological saline enhanced the ultrasound signal in the 

right atrium [16] . The basic principle of contrast-enhanced 

ultrasonography lies on the separation of the ultrasound 

signals from tissues from ultrasound signals from the microbubbles. 

The ultrasound signal from organs is almost 

the same form as transmission pulses, whereas bubbles 

that have been bombarded with ultrasound waves behave 

in a complicated manner such as vibration, disappearance 

and fragmentation. The ultrasound signal released 

from the bubbles is of a different form compared to 

that of the transmission pulse, and is said to be a nonlinear 

signal. Extraction of this non-linear signal is the 

basic principle of contrast-enhanced ultrasonography. To 


Size of 

lymph node 

Imaging findings 

in B mode 


Imaging findings in contrast enhanced ultrasonography 

1 VX2 28 18 × 11 Hypoechoic Only the periphery was enhanced 

The central area was notably defective 

2 VX2 28 18 × 10 Iso-hypoechoic Only part of the periphery was enhanced. Most sites were not enhanced 

3 VX2 21 15 × 10 Isoechoic A comparatively small defect was seen internally 

4 VX2 35 16 × 10 Hypoechoic A comparatively small defect was seen internally 

5 VX2 21 17 × 6 Hypoechoic A comparatively small defect was seen internally 

6 VX2 7 12 × 7 Iso-hypoechoic The entire lymph node could be enhanced 

7 E. coli 28 17 × 8 Iso-hypoechoic The entire lymph node was enhanced (a defective star-like image was seen) 

8 E. coli 3 8 × 3 Isoechoic The entire lymph node was enhanced 

9 E. coli 7 13 × 5 Iso-hypoechoic The entire lymph node was enhanced 

10 E. coli 3 9 × 3 Hypoechoic The entire lymph node was enhanced 

11 E. coli 3 8 × 3 Isoechoic The entire lymph node was enhanced 

The list of the tumor-induced and inflammation-induced lymph node enlargement models is shown. Models 1 to 6 are tumor-induced lymph node 

enlargement that was obtained by implanting VX2 tumor. Models 7 to 11 are inflammation-induced lymph node enlargement that was obtained by 

implanting Escherichia coli (E. coli). 

visualize information on microvascular flow that cannot 

be detected by power Doppler, a technique that is more 

effective at extracting the non-linear signal is necessary. 

Recent advances in devices have led to the appearance of 

non-linear imaging techniques such as second harmonic 

imaging and pulse inversion that are now being used 

clinically [11,17,18] . 

The active ingredient of Sonazoid is perflubutane 

(PFB) microbubble that was stabilized using hydrogenated 

egg phosphatidyl serine sodium (H-EPSNa), which is 

a phospholipid [19] . PFB is chemically stable and insoluble 

in water. Therefore, it has a long lifespan in the body because 

it hardly dissolves in the blood. 

When the microbubble is bombarded with ultrasound 

waves with an acoustic pressure that is normally used 

clinically, it bursts easily. Sonazoid uses a single layer 

of H-EPSNa membrane, therefore it has superior ultrasound 

wave tolerance and has been designed such that 

non-linear ultrasound signals are produced consistently. 

Sonazoid is classed as one of the second generation 

contrast agents. Compared to Definity, it can be visualized 

at a comparatively high acoustic pressure. Therefore, 

it is classed as a moderate acoustic pressure contrast agent. 

It is comparatively hard, as fluorocarbon is enclosed in a 

shell and so has a comparatively long lifespan in the body. 

The diameter of Sonazoid is 2-3 μm while the diameter 

of lymph ducts in subcutaneous tissue is normally 

0.2-0.5 mm. Therefore, Sonazoid can easily move into 

lymph ducts. In addition, lymph ducts can be contrasted 

because hydrophobic bases are arranged on the membrane 

of the H-EPSNa shell and the shell is highly elastic. 

Goldberg et al [13] extracted the sentinel lymph node 

following contrast-enhanced ultrasonography and observed 

it by electron microscopy. They confirmed the 

presence of spherical vacuoles in the cytoplasm of histiocytes 

(i.e. macrophages). The size of the vacuoles ranged 

from 1.07 to 1.99 μm. These vacuoles were not found 

anywhere else apart from the lymph node cells of the 



histiocytes. In addition, they were not found in the histiocytes 

of the control lymph nodes. Therefore, it was concluded 

that the vacuoles that were seen in the histiocytes 

of the cytoplasm were the Sonazoid microbubbles that 

were phagocytosed. The fact that placing the Sonazoid 

microbubbles into lymph ducts is simple and that they are 

phagocytosed by macrophages in lymph nodes has led to 

the suggestion that the mechanism whereby the microbubbles 

are maintained is by their uptake by the sentinel 

lymph node. In addition, when Sonazoid is injected, 

it accumulates in reticuloendothelial organs such as the 

liver and spleen maintaining the actual contrast over long 

hours. This is called Kupffer imaging. The mechanism 

is suggested to be phagocytosis of the microbubbles by 

macrophages present in the endodermis of the liver and 

spleen [20] . 

Basically, lymphocytes, plasma cells and histiocytes 

make up the parenchyma and reticular fiber, blood vessels, 

lymphatic sinus endothelium, beam-columns and 

capsules make up the stroma. In addition, lymph nodes 

are modified according to the quality and quantity of immune 

stimulation they receive and individual responses, 

which are influenced by factors such as age and nutrition. 

Lymphocyte proliferation takes place in the lymph nodule 

aggregates present in lymphocytes. The filtering device 

used to process the lymphatic sinuses was bacterial and 

foreign body phagocytosis. Antibodies were produced. 

When foreign bodies such as pathogens enter lymph 

nodes, they become reddened and swollen in response 

resulting in increased weight [21] . 

Shope first reported that “Shope papilloma” is a tumor 

that proliferates in papilla that could be seen in cottontailed 

rabbits. It is caused by the virus Parvoviridae (Shope 

papilloma virus) and even when rabbits are infected with 

this virus, the same proliferation is induced. Of these 

tumors, the VX2 tumor, which has a high rate of malignancy 

is a successively transplanted stock that was established 

from epidermoid carcinoma [22,23] . 

Contrast-enhanced ultrasonography of the tumor metastatic 

model showed imaging and continued staining of the 

sentinel lymph nodes. Contrast-enhanced ultrasonography 

also revealed a region of defective shadows in that enlarged 

lymph node and was suggested to be the metastatic lesion. 

The minimum size of the lesion was 2-3 mm. Histological 

examination confirmed that the imaged area corresponded 

to the remaining lymph tissue while the area of the defective 

shadows was confirmed to be the metastatic lesion of 

the tumor. 

In the inflammation-induced enlargement model, there 

was uniform staining but non-uniform imaging. Contrast 

imaging that was performed shortly after the infection 

showed comparatively uniform staining but the staining 

tended to be non-uniform in chronic-phase lymph nodes. 

Investigation of the histopathological images of the 

chronic lymph node enlargement model showed chronic 

lymphadenitis with fiberization. This was suggested not to 

be a reflection of non-uniform staining. 

The above findings suggested that contrast-enhanced 

ultrasonography is useful in distinguishing tumor-induced 


and inflammation-induced lymph node enlargements. 

Omoto et al [11] reported a sentinel node detection method 

using contrast-enhanced ultrasonography with Sonazoid 

in a human breast cancer patient. The contrast-enhanced 

ultrasonography with Sonazoid for liver tumors has 

come to be generally performed in Japan [24,25] . The safety 

of Sonazoid in humans has been established. We want 

to continue with further study that compares tumorinduced 

and inflammation-induced lymph node enlargements 

using contrast-enhanced ultrasonography. 

COMMENTS 

Background 

By using gaseous microbubbles, a strong contrast effect such as an echo 

source will be achieved. Sentinel node navigation surgery is becoming the 

focus of attention as a lowly invasive form of treatment for early cancer. Local 

injection of microbubble, which is a contrast agent, reveals the sentinel lymph 

node in ultrasonography 

Research frontiers 

A model of tumor-induced and a model of inflammation-induced swelling of 

lymph nodes were prepared to compare the differences between tumor-induced 

enlargement and inflammation-induced enlargement of lymph nodes using by 

contrast-enhanced ultrasonography. 

Innovations and breakthroughs 

Contrast-enhanced ultrasonography also revealed a region of defective shadows 

in the enlarged lymph node and this was suggested to be the metastatic 

lesion. In inflammation-induced swelling of lymph nodes models, contrast imaging 

that was performed shortly after the infection showed comparatively uniform 

staining but the staining tended to be non-uniform in chronic-phase lymph 

nodes. 

Applications 

Our study suggested that contrast-enhanced ultrasonography is useful in distinguishing 

tumor-induced and inflammation-induced lymph node enlargements. 

Terminology 

Sonazoid is a contrast agent that can be observed continuously with moderate 

acoustic pressure and without the microbubbles bursting. 

Peer review 

The paper can be accepted for publication in World Journal of Radiology after 

correction of many spelling and grammar mistakes. 

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12 Goldberg BB, Merton DA, Liu JB, Thakur M, Murphy GF, 

Needleman L, Tornes A, Forsberg F. Sentinel lymph nodes 

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S- Editor Cheng JX L- Editor O’Neill M E- Editor Zheng XM 


W J R 




ACKNOWLEDGMENTS 

Acknowledgments to reviewers of World Journal of 


Many reviewers have contributed their expertise and time 

to the peer review, a critical process to ensure the quality 

of World Journal of Radiology. The editors and authors of 

the articles submitted to the journal are grateful to the 

following reviewers for evaluating the articles (including 

those published in this issue and those rejected for this 

issue) during the last editing time period. 

Mohamed Abou El-Ghar, MD, Radiology dep, Urology and Ne- 




World J Radiol 2011 December 28; 3(12): I 



phrology center-Mansoura University, 72 El-gomhoria st, Mansoura 

35516, Egypt 

Ritesh Agarwal, MD, DM, MAMS, Assistant Professor, Department 

of Pulmonary Medicine, Postgraduate Institute of Medical 

Education and Research, Sector-12, Chandigarh 160012, India 

Mario Mascalchi, MD, PhD, Professor, Radiodiagnostic Section, 

Department of Clinical Physiopathology, University of Florence, 

Viale Morgagni 50134, Florence, Italy 

I December 28, 2011|Volume 3|Issue 12|

W J R 




Events Calendar 2011 

January 23-27 

Radiology at Snowbird 

San Diego, Mexico 

January 24-28 

Neuro/ENT at the Beach 

Palm Beach, FL, United States 

February 28-29 

MIAD 2011 - 2nd International 

Workshop on Medical Image 

Analysis and Description for 

Diagnosis System 

Rome, Italy 

February 5-6 

Washington Neuroradiology Review 

Arlington, VA, United States 


MI11 - SPIE Medical Imaging 2011 

Lake Buena Vista, FL, United States 


2nd National Conference Diagnostic 

and Interventional Radiology 2011 

London, United Kingdom 

Februrary 17-18 

VII National Neuroradiology Course 

Lleida, Spain 

February 18 

Radiology in child protection 

Nottingham, United Kingdom 

Februrary 19-22 

COMPREHENSIVE REVIEW OF 

MUSCULOSKELETAL MRI 

Lake Buena Vista, FL, United States 

March 2-5 

2011 Abdominal Radiology Course 

Carlsbad, CA, United States 

March 3-7 

European Congress of Radiology 

Meeting ECR 2011 Vienna, Austria 

March 6-9 

World Congress Thoracic Imaging - IV 

Bonita Springs, FL, United States 

March 14-18 

9th Annual NYU Radiology Alpine 

Imaging Symposium at Beaver Creek 

Beaver Creek, CO, United States 


March 20-25 

Abdominal Radiology Course 2011 

Carlsbad, CA, United States 

March 26-31 

2011 SIR Annual Meeting 

Chicago, IL, United States 

March 28-April 1 

University of Utah Neuroradiology 

2nd Intensive Interactive Brain & 

Spine Imaging Conference 

Salt Lake City, UT, United States 

April 3-8 

1st Annual Ottawa Radiology 

Resident Review 

Ottawa, Canada 

April 3-8 

43rd International Diagnostic Course 

Davos on Diagnostic Imaging and 

Interventional Techniques 

Davos, Switzerland 

April 6-9 

Image-Based Neurodiagnosis: 

Intensive Clinical and Radiologic 

Review, CAQ Preparation 

Cincinnati, OH, United States 

April 28-May 1 

74th Annual Scientific Meeting 

of the Canadian Association of 

Radiologists CAR 

Montreal, Canada 

May 5-8 

EMBL Conference-Sixth 

International Congress on Electron 

Tomography 

Heidelberg, Germany 

May 10-13 

27th Iranian Congress of Radiology 

Tehran, Iran 

May 14-21 

Radiology in Marrakech 

Marrakech, Morocco 



May 21-24 

European Society of Gastrointestinal 

and Abdominal Radiology 2011 

Annual Meeting 

Venice, Italy 

May 23-25 

Sports Medicine Imaging State of 

the Art: A Collaborative Course for 

Radiologists and Sports Medicine 

Specialists 

New York, NY, United States 

May 24-26 

Russian Congress of Radiology 

Moscow, Russia 

May 28-31 

International Congress of Pediatric 

Radiology (IPR) 

London, United Kingdom 

June 4-8 

58th Annual Meeting of the Society 

of Nuclear Medicine 

San Antonio, 

TX, United States 

June 6-8 

UKRC 2011 - UK Radiological 

Congress 

Manchester, United Kingdom 

June 8-11 

CIRA 2011 - Canadian Internventinal 

Radiology Association Meeting 

Montreal, QC, Canada 

June 9-10 

8th ESGAR Liver Imaging Workshop 

Dublin, Ireland 

June 17-19 

ASCI 2011 - 5th Congress of Asian 

Society of Cardiovascular Imaging 

Hong Kong, China 

June 22-25 

CARS 2011 - Computer Assisted 

Radiology and Surgery - 25th 

International Congress and 

Exhibition Berlin, Germany 

June 27-July 1 

NYU Summer Radiology 

Symposium at The Sagamore 

Lake George, NY, United States 

July 18-22 

Clinical Case-Based Radiology 

Update in Iceland 

Reykjavik, Iceland 

August 1-5 

NYU Clinical Imaging Symposium 

in Santa Fe 

Santa Fe, NM, United States 

World J Radiol 2011 December 28; 3(12): I 



MEETINGS 

September 22-25 

European Society of Neuroradiology 

(ESNR) XXXV Congress and 19th 

Advanced Course 

Antwerp, Belgium 

October 12-14 

International Conference Vipimage 

2011 - Computational Vision and 

Medical Image Processing 

Algarve, Portugal 

October 15-16 

Essentials of Emergency and Trauma 



October 23-29 

2011 IEEE NSS - 2011 IEEE Nuclear 

Science Symposium and Medical 

Imaging Conference 

Valencia, Spain 

October 25-28 

NYU Radiology in Scottsdale - Fall 

Radiology Symposium in Scottsdale 

Scottsdale, AZ, 

United States 

October 28-30 

Fourth National Congress of 

Professionals of Radiological 

Techniques Florianópolis, Brazil 

October 28-30 

Multi-Modality Gynecological & 

Obstetric Imaging 


November 3-4 

9th ESGAR Liver Imaging Workshop 

Taormina, Italy 

November 15-19 

EANM 2011 - Annual Congress of 

the European Association of Nuclear 

Medicine 

Birmingham, 

United Kingdom 


NSS/MIC - Nuclear Science 

Symposium and Medical Imaging 

Conference 2011 Valencia, Spain 


8th Asia Oceaninan Congress of 

Neuro-Radiology Bangkok, 

Thailand 


W J R 




GENERAL INFORMATION 

World Journal of Radiology (World J Radiol, WJR, online ISSN 

1949-8470, DOI: 10.4329), is a monthly, open-access (OA), peerreviewed 

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We insist on strengthening our team cultivation and construction so 

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World J Radiol 2011 December 28; 3(12): I-V 



ticles, thereby realizing the maximization of the personal benefits 

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The major task of WJR is to rapidly report the most recent improvement 

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research, and make suggestions for future work; (8) Original Articles: 

To report innovative and original findings in radiology; (9) Brief 

Articles: To briefly report the novel and innovative findings in radiology; 

(10) Case Report: To report a rare or typical case; (11) Letters to 

the Editor: To discuss and make reply to the contributions published 

in WJR, or to introduce and comment on a controversial issue of 

general interest; (12) Book Reviews: To introduce and comment on 

quality monographs of radiology; and (13) Guidelines: To introduce 

consensuses and guidelines reached by international and national 

academic authorities worldwide on the research in radiology. 

Name of journal 


ISSN 


Indexed and Abstracted in 

PubMed Central, PubMed, Digital Object Identifer, and Directory 

of Open Access Journals. 

Published by 

Baishideng Publishing Group Co., Limited. 

INSTRUCTIONS TO AUTHORS 

SPECIAL STATEMENT 

All articles published in this journal represent the viewpoints of the 

authors except where indicated otherwise. 


Instructions to authors 

Biostatistical editing 

Statisital review is performed after peer review. We invite an expert in 

Biomedical Statistics from to evaluate the statistical method used in 

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points include: (1) Statistical methods should be described 

when they are used to verify the results; (2) Whether the statistical 

techniques are suitable or correct; (3) Only homogeneous data can be 

averaged. Standard deviations are preferred to standard errors. Give 

the number of observations and subjects (n). Losses in observations, 

such as drop-outs from the study should be reported; (4) Values such 

as ED50, LD50, IC50 should have their 95% confidence limits calculated 

and compared by weighted probit analysis (Bliss and Finney); 

and (5) The word ‘significantly’ should be replaced by its synonyms (if 

it indicates extent) or the P value (if it indicates statistical significance). 

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Statement of human and animal rights 

When reporting the results from experiments, authors should follow 

the highest standards and the trial should conform to Good Clinical 

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Clinical Practice in FDA-Regulated Clinical Trials; UK Medicines 

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Generally, we suggest authors follow the lead investigator’s national 

standard. If doubt exists whether the research was conducted 

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If human participants were involved, manuscripts must be accompanied 

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Manuscripts should be typed in 1.5 line spacing and 12 pt. Book 


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start each of the following sections on a new page: Title Page, Abstract, 

Introduction, Materials and Methods, Results, Discussion, 

Acknowledgements, References, Tables, Figures, and Figure Legends. 

Neither the editors nor the publisher are responsible for the 

opinions expressed by contributors. Manuscripts formally accepted 

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put onto our website accepted manuscripts. Authors should follow 

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papers on clinical trial results if the trial was not recorded in a 

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that other registers become available you will be duly notified. A 

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Authors should retain one copy of the text, tables, photographs 

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Online submissions 

Manuscripts should be submitted through the Online Submission 

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highly recommended to consult the ONLINE INSTRUCTIONS 

TO AUTHORS (http://www.wjgnet.com/1949-8470/g_info_ 

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System may send an email describing the problem to wjr@ 

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online submission for the same manuscript is strictly prohibited. 

MANUSCRIPT PREPARATION 

All contributions should be written in English. All articles must be 

submitted using word-processing software. All submissions must be 

typed in 1.5 line spacing and 12 pt. Book Antiqua with ample margins. 

Style should conform to our house format. Required information 

for each of the manuscript sections is as follows: 

Title page 

Title: Title should be less than 12 words. 

Running title: A short running title of less than 6 words should be 

provided. 

Authorship: Authorship credit should be in accordance with the 

standard proposed by International Committee of Medical Journal 

Editors, based on (1) substantial contributions to conception and 

design, acquisition of data, or analysis and interpretation of data; (2) 

drafting the article or revising it critically for important intellectual 

content; and (3) final approval of the version to be published. Authors 

should meet conditions 1, 2, and 3. 

Institution: Author names should be given first, then the complete 

name of institution, city, province and postcode. For example, Xu- 

Chen Zhang, Li-Xin Mei, Department of Pathology, Chengde 

Medical College, Chengde 067000, Hebei Province, China. One author 

may be represented from two institutions, for example, George 

Sgourakis, Department of General, Visceral, and Transplantation 

Surgery, Essen 45122, Germany; George Sgourakis, 2nd Surgical 

II December 28, 2011|Volume 3|Issue 12|

Department, Korgialenio-Benakio Red Cross Hospital, Athens 

15451, Greece 

Author contributions: The format of this section should be: 

Author contributions: Wang CL and Liang L contributed equally 

to this work; Wang CL, Liang L, Fu JF, Zou CC, Hong F and Wu 

XM designed the research; Wang CL, Zou CC, Hong F and Wu 

XM performed the research; Xue JZ and Lu JR contributed new 

reagents/analytic tools; Wang CL, Liang L and Fu JF analyzed the 

data; and Wang CL, Liang L and Fu JF wrote the paper. 

Supportive foundations: The complete name and number of supportive 

foundations should be provided, e.g., Supported by National 

Natural Science Foundation of China, No. 30224801 

Correspondence to: Only one corresponding address should be 

provided. Author names should be given first, then author title, affiliation, 

the complete name of institution, city, postcode, province, 

country, and email. All the letters in the email should be in lower 

case. A space interval should be inserted between country name and 

email address. For example, Montgomery Bissell, MD, Professor of 

Medicine, Chief, Liver Center, Gastroenterology Division, University 

of California, Box 0538, San Francisco, CA 94143, United States. 

montgomery.bissell@ucsf.edu 

Telephone and fax: Telephone and fax should consist of +, country 

number, district number and telephone or fax number, e.g., Telephone: 

+86-10-85381892 Fax: +86-10-85381893 

Peer reviewers: All articles received are subject to peer review. 

Normally, three experts are invited for each article. Decision for 

acceptance is made only when at least two experts recommend 

an article for publication. Reviewers for accepted manuscripts are 

acknowledged in each manuscript, and reviewers of articles which 

were not accepted will be acknowledged at the end of each issue. 

To ensure the quality of the articles published in WJR, reviewers of 

accepted manuscripts will be announced by publishing the name, 

title/position and institution of the reviewer in the footnote accompanying 

the printed article. For example, reviewers: Professor 

Jing-Yuan Fang, Shanghai Institute of Digestive Disease, Shanghai, 

Affiliated Renji Hospital, Medical Faculty, Shanghai Jiaotong University, 

Shanghai, China; Professor Xin-Wei Han, Department of 

Radiology, The First Affiliated Hospital, Zhengzhou University, 

Zhengzhou, Henan Province, China; and Professor Anren Kuang, 

Department of Nuclear Medicine, Huaxi Hospital, Sichuan University, 

Chengdu, Sichuan Province, China. 

Abstract 

There are unstructured abstracts (no more than 256 words) and 

structured abstracts (no more than 480). The specific requirements 

for structured abstracts are as follows: 

An informative, structured abstracts of no more than 480 

words should accompany each manuscript. Abstracts for original 

contributions should be structured into the following sections. AIM 

(no more than 20 words): Only the purpose should be included. 

Please write the aim as the form of “To investigate/study/…; 

MATERIALS AND METHODS (no more than 140 words); 

RESULTS (no more than 294 words): You should present P values 

where appropriate and must provide relevant data to illustrate 

how they were obtained, e.g. 6.92 ± 3.86 vs 3.61 ± 1.67, P < 0.001; 

CONCLUSION (no more than 26 words). 

Key words 

Please list 5-10 key words, selected mainly from Index Medicus, which 

reflect the content of the study. 

Text 

For articles of these sections, original articles and brief articles, the 

main text should be structured into the following sections: INTRO- 



DUCTION, MATERIALS AND METHODS, RESULTS and 

DISCUSSION, and should include appropriate Figures and Tables. 

Data should be presented in the main text or in Figures and Tables, 

but not in both. The main text format of these sections, editorial, 

topic highlight, case report, letters to the editors, can be found at: 

http://www.wjgnet.com/1949-8470/g_info_20100313183720.htm. 

Illustrations 

Figures should be numbered as 1, 2, 3, etc., and mentioned clearly 

in the main text. Provide a brief title for each figure on a separate 

page. Detailed legends should not be provided under the 

figures. This part should be added into the text where the figures 

are applicable. Figures should be either Photoshop or Illustrator 

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can be found at: http://www.wjgnet.com/1007-9327/13/4520. 

pdf; http://www.wjgnet.com/1007-9327/13/4554.pdf; http:// 

www.wjgnet.com/1007-9327/13/4891.pdf; http://www. 

wjgnet.com/1007-9327/13/4986.pdf; http://www.wjgnet. 

com/1007-9327/13/4498.pdf. Keeping all elements compiled is 

necessary in line-art image. Scale bars should be used rather than 

magnification factors, with the length of the bar defined in the legend 

rather than on the bar itself. File names should identify the figure 

and panel. Avoid layering type directly over shaded or textured 

areas. Please use uniform legends for the same subjects. For example: 

Figure 1 Pathological changes in atrophic gastritis after treatment. 

A: ...; B: ...; C: ...; D: ...; E: ...; F: ...; G: …etc. It is our principle 

to publish high resolution-figures for the printed and E-versions. 

Tables 

Three-line tables should be numbered 1, 2, 3, etc., and mentioned 

clearly in the main text. Provide a brief title for each table. Detailed 

legends should not be included under tables, but rather added into 

the text where applicable. The information should complement, 

but not duplicate the text. Use one horizontal line under the title, a 

second under column heads, and a third below the Table, above any 

footnotes. Vertical and italic lines should be omitted. 

Notes in tables and illustrations 

Data that are not statistically significant should not be noted. a P < 

0.05, b P < 0.01 should be noted (P > 0.05 should not be noted). If 

there are other series of P values, c P < 0.05 and d P < 0.01 are used. 

A third series of P values can be expressed as e P < 0.05 and f P < 0.01. 

Other notes in tables or under illustrations should be expressed as 

1 F, 2 F, 3 F; or sometimes as other symbols with a superscript (Arabic 

numerals) in the upper left corner. In a multi-curve illustration, each 

curve should be labeled with ●, ○, ■, □, ▲, △, etc., in a certain sequence. 

Acknowledgments 

Brief acknowledgments of persons who have made genuine contributions 

to the manuscript and who endorse the data and conclusions 

should be included. Authors are responsible for obtaining 

written permission to use any copyrighted text and/or illustrations. 

REFERENCES 

Coding system 

The author should number the references in Arabic numerals according 

to the citation order in the text. Put reference numbers in 

square brackets in superscript at the end of citation content or after 

the cited author’s name. For citation content which is part of the 

narration, the coding number and square brackets should be typeset 

normally. For example, “Crohn’s disease (CD) is associated with 

increased intestinal permeability [1,2] ”. If references are cited directly 

in the text, they should be put together within the text, for example, 

“From references [19,22-24] , we know that...” 

When the authors write the references, please ensure that the 

order in text is the same as in the references section, and also ensure 

the spelling accuracy of the first author’s name. Do not list the same 

citation twice. 

III December 28, 2011|Volume 3|Issue 12|


PMID and DOI 

Pleased provide PubMed citation numbers to the reference list, e.g. 

PMID and DOI, which can be found at http://www.ncbi.nlm.nih. 

gov/sites/entrez?db=pubmed and http://www.crossref.org/SimpleTextQuery/, 

respectively. The numbers will be used in E-version 

of this journal. 

Style for journal references 

Authors: the name of the first author should be typed in bold-faced 

letters. The family name of all authors should be typed with the initial 

letter capitalized, followed by their abbreviated first and middle 

initials. (For example, Lian-Sheng Ma is abbreviated as Ma LS, Bo- 

Rong Pan as Pan BR). The title of the cited article and italicized 

journal title (journal title should be in its abbreviated form as shown 

in PubMed), publication date, volume number (in black), start page, 

and end page [PMID: 11819634 DOI: 10.3748/wjg.13.5396]. 

Style for book references 

Authors: the name of the first author should be typed in bold-faced 

letters. The surname of all authors should be typed with the initial 

letter capitalized, followed by their abbreviated middle and first 

initials. (For example, Lian-Sheng Ma is abbreviated as Ma LS, Bo- 

Rong Pan as Pan BR) Book title. Publication number. Publication 

place: Publication press, Year: start page and end page. 

Format 

Journals 

English journal article (list all authors and include the PMID where applicable) 

1 Jung EM, Clevert DA, Schreyer AG, Schmitt S, Rennert J, 

Kubale R, Feuerbach S, Jung F. Evaluation of quantitative contrast 

harmonic imaging to assess malignancy of liver tumors: 

A prospective controlled two-center study. World J Gastroenterol 

2007; 13: 6356-6364 [PMID: 18081224 DOI: 10.3748/wjg.13. 

6356] 

Chinese journal article (list all authors and include the PMID where applicable) 

2 Lin GZ, Wang XZ, Wang P, Lin J, Yang FD. Immunologic 

effect of Jianpi Yishen decoction in treatment of Pixu-diarrhoea. 

Shijie Huaren Xiaohua Zazhi 1999; 7: 285-287 

In press 

3 Tian D, Araki H, Stahl E, Bergelson J, Kreitman M. Signature 

of balancing selection in Arabidopsis. Proc Natl Acad Sci USA 

2006; In press 

Organization as author 

4 Diabetes Prevention Program Research Group. Hypertension, 

insulin, and proinsulin in participants with impaired glucose 

tolerance. Hypertension 2002; 40: 679-686 [PMID: 12411462 

PMCID:2516377 DOI:10.1161/01.HYP.0000035706.28494. 

09] 

Both personal authors and an organization as author 

5 Vallancien G, Emberton M, Harving N, van Moorselaar RJ; 

Alf-One Study Group. Sexual dysfunction in 1, 274 European 

men suffering from lower urinary tract symptoms. J Urol 

2003; 169: 2257-2261 [PMID: 12771764 DOI:10.1097/01.ju. 

0000067940.76090.73] 

No author given 

6 21st century heart solution may have a sting in the tail. BMJ 

2002; 325: 184 [PMID: 12142303 DOI:10.1136/bmj.325. 

7357.184] 

Volume with supplement 

7 Geraud G, Spierings EL, Keywood C. Tolerability and safety 

of frovatriptan with short- and long-term use for treatment 

of migraine and in comparison with sumatriptan. Headache 

2002; 42 Suppl 2: S93-99 [PMID: 12028325 DOI:10.1046/ 

j.1526-4610.42.s2.7.x] 

Issue with no volume 

8 Banit DM, Kaufer H, Hartford JM. Intraoperative frozen 

section analysis in revision total joint arthroplasty. Clin Orthop 

Relat Res 2002; (401): 230-238 [PMID: 12151900 DOI:10.10 

97/00003086-200208000-00026] 


No volume or issue 

9 Outreach: Bringing HIV-positive individuals into care. HRSA 

Careaction 2002; 1-6 [PMID: 12154804] 

Books 

Personal author(s) 

10 Sherlock S, Dooley J. Diseases of the liver and billiary system. 

9th ed. Oxford: Blackwell Sci Pub, 1993: 258-296 

Chapter in a book (list all authors) 

11 Lam SK. Academic investigator’s perspectives of medical 

treatment for peptic ulcer. In: Swabb EA, Azabo S. Ulcer 

disease: investigation and basis for therapy. New York: Marcel 

Dekker, 1991: 431-450 

Author(s) and editor(s) 

12 Breedlove GK, Schorfheide AM. Adolescent pregnancy. 

2nd ed. Wieczorek RR, editor. White Plains (NY): March of 

Dimes Education Services, 2001: 20-34 

Conference proceedings 

13 Harnden P, Joffe JK, Jones WG, editors. Germ cell tumours V. 

Proceedings of the 5th Germ cell tumours Conference; 2001 

Sep 13-15; Leeds, UK. New York: Springer, 2002: 30-56 

Conference paper 

14 Christensen S, Oppacher F. An analysis of Koza's computational 

effort statistic for genetic programming. In: Foster JA, 

Lutton E, Miller J, Ryan C, Tettamanzi AG, editors. Genetic 

programming. EuroGP 2002: Proceedings of the 5th European 

Conference on Genetic Programming; 2002 Apr 3-5; 

Kinsdale, Ireland. Berlin: Springer, 2002: 182-191 

Electronic journal (list all authors) 

15 Morse SS. Factors in the emergence of infectious diseases. 

Emerg Infect Dis serial online, 1995-01-03, cited 1996-06-05; 

1(1): 24 screens. Available from: URL: http://www.cdc.gov/ 

ncidod/eid/index.htm 

Patent (list all authors) 

16 Pagedas AC, inventor; Ancel Surgical R&D Inc., assignee. 

Flexible endoscopic grasping and cutting device and positioning 

tool assembly. United States patent US 20020103498. 2002 Aug 

1 

Statistical data 

Write as mean ± SD or mean ± SE. 

Statistical expression 

Express t test as t (in italics), F test as F (in italics), chi square test as 

χ 2 (in Greek), related coefficient as r (in italics), degree of freedom 

as υ (in Greek), sample number as n (in italics), and probability as P (in 

italics). 

Units 

Use SI units. For example: body mass, m (B) = 78 kg; blood pressure, 

p (B) = 16.2/12.3 kPa; incubation time, t (incubation) = 96 h, 

blood glucose concentration, c (glucose) 6.4 ± 2.1 mmol/L; blood 

CEA mass concentration, p (CEA) = 8.6 24.5 mg/L; CO 2 volume 

fraction, 50 mL/L CO 2, not 5% CO 2; likewise for 40 g/L formaldehyde, 

not 10% formalin; and mass fraction, 8 ng/g, etc. Arabic 

numerals such as 23, 243, 641 should be read 23 243 641. 

The format for how to accurately write common units and 

quantums can be found at: http://www.wjgnet.com/1949-8470/ 

g_info_20100313185816.htm. 

Abbreviations 

Standard abbreviations should be defined in the abstract and on 

first mention in the text. In general, terms should not be abbreviated 

unless they are used repeatedly and the abbreviation is helpful 

to the reader. Permissible abbreviations are listed in Units, Symbols 

and Abbreviations: A Guide for Biological and Medical Editors and 

Authors (Ed. Baron DN, 1988) published by The Royal Society of 

Medicine, London. Certain commonly used abbreviations, such as 

DNA, RNA, HIV, LD50, PCR, HBV, ECG, WBC, RBC, CT, ESR, 

CSF, IgG, ELISA, PBS, ATP, EDTA, mAb, can be used directly 

without further explanation. 

IV December 28, 2011|Volume 3|Issue 12|

Italics 

Quantities: t time or temperature, c concentration, A area, l length, 

m mass, V volume. 

Genotypes: gyrA, arg 1, c myc, c fos, etc. 

Restriction enzymes: EcoRI, HindI, BamHI, Kbo I, Kpn I, etc. 

Biology: H. pylori, E coli, etc. 

Examples for paper writing 

Editorial: http://www.wjgnet.com/1949-8470/g_info_20100313 

182341.htm 

Frontier: http://www.wjgnet.com/1949-8470/g_info_2010031318 

2448.htm 

Topic highlight: http://www.wjgnet.com/1949-8470/g_info_201003 

13182639.htm 

Observation: http://www.wjgnet.com/1949-8470/g_info_20100313 

182834.htm 

Guidelines for basic research: http://www.wjgnet.com/1949-8470/ 

g_info_20100313183057.htm 

Guidelines for clinical practice: http://www.wjgnet.com/1949- 

8470/g_info_20100313183238.htm 

Review: http://www.wjgnet.com/1949-8470/g_info_20100313 

183433.htm 

Original articles: http://www.wjgnet.com/1949-8470/g_info_2010 

0313183720.htm 

Brief articles: http://www.wjgnet.com/1949-8470/g_info_201003 

13184005.htm 

Case report: http://www.wjgnet.com/1949-8470/g_info_20100313 

184149.htm 

Letters to the editor: http://www.wjgnet.com/1949-8470/g_info_20 

100313184410.htm 

Book reviews: http://www.wjgnet.com/1949-8470/g_info_201003 

13184803.htm 

Guidelines: http://www.wjgnet.com/1949-8470/g_info_20100313 

185047.htm 

SUBMISSION OF THE REVISED MANUSCRIPTS 

AFTER ACCEPTED 

Please revise your article according to the revision policies of WJR. 

The revised version including manuscript and high-resolution image 

figures (if any) should be re-submitted or uploaded online. The 

author should send copyright transfer letter, and responses to the 

reviewers and science news to us via email. 

Editorial Office 


Editorial Department: Room 903, Building D, 



Ocean International Center, No. 62 Dongsihuan Zhonglu, 

Chaoyang District, Beijing 100025, China 



Telephone: +86-10-8538-1892 

Fax: +86-10-8538-1893 

Language evaluation 

The language of a manuscript will be graded before it is sent for 

revision. (1) Grade A: priority publishing; (2) Grade B: minor language 

polishing; (3) Grade C: a great deal of language polishing 

needed; and (4) Grade D: rejected. Revised articles should reach 

Grade A or B. 

Copyright assignment form 

Please download a Copyright assignment form from http://www. 

wjgnet.com/1949-8470/g_info_20100313185522.htm. 

Responses to reviewers 

Please revise your article according to the comments/suggestions 

provided by the reviewers. The format for responses to the reviewers’ 

comments can be found at: http://www.wjgnet.com/1949-8470/ 

g_info_20100313185358.htm. 

Proof of financial support 

For paper supported by a foundation, authors should provide a 

copy of the document and serial number of the foundation. 

Links to documents related to the manuscript 

WJR will be initiating a platform to promote dynamic interactions between 

the editors, peer reviewers, readers and authors. After a manuscript 

is published online, links to the PDF version of the submitted 

manuscript, the peer-reviewers’ report and the revised manuscript will 

be put on-line. Readers can make comments on the peer reviewer’s 

report, authors’ responses to peer reviewers, and the revised manuscript. 

We hope that authors will benefit from this feedback and be 

able to revise the manuscript accordingly in a timely manner. 

Science news releases 

Authors of accepted manuscripts are suggested to write a science 

news item to promote their articles. The news will be released rapidly 

at EurekAlert/AAAS (http://www.eurekalert.org). The title for 

news items should be less than 90 characters; the summary should 

be less than 75 words; and main body less than 500 words. Science 

news items should be lawful, ethical, and strictly based on your 

original content with an attractive title and interesting pictures. 

Publication fee 

WJR is an international, peer-reviewed, Open-Access, online journal. 

Articles published by this journal are distributed under the 

terms of the Creative Commons Attribution Non-commercial 

License, which permits use, distribution, and reproduction in any 

medium, provided the original work is properly cited, the use is 

non commercial and is otherwise in compliance with the license. 

Authors of accepted articles must pay a publication fee. The related 

standards are as follows. Publication fee: 1300 USD per article; 

Reprints fee: 350 USD per 100 reprints, including postage cost. 

Editorial, topic highlights, book reviews and letters to the editor 

are published free of charge. 

V December 28, 2011|Volume 3|Issue 12|

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