Winter Meeting 2011 - The Pathological Society of Great Britain ...

P65
Palatal Malignant Melanoma in a Middle -Aged Female
P M Samaila 1 ; SO Ajike 2
1 Department of Pathology/Morbid Anatomy, Zaria, Nigeria;
2 Department of Maxillofacial Surgery, Ahmadu Bello University Teaching
Hospital Shika, Zaria, Nigeria
Background:Malignant melanoma of the oral cavity is an uncommon aggressive tumour
that preferentially affects elderly males. Its pathological classification is unclear and the
diagnosis is often fraught with delay. Case:A 45 year old emanciated Fulani woman with
a 6-month history of left palatal swelling and loosened teeth is presented. She had no
history of pre-existing palatal or oral cavity lesion. Examination revealed a 9x4cm sessile
nodular dark grey mass involving the anterior two-thirds of the hard palate and a 5x5cm
palpable submandibular lymph node. The mass bled spontaneously and extended to the
posterior gingiva. Palatal radiogragh showed an osteolytic lesion with destruction of the
left maxillary bone. She had a hemi-maxillectomy with nodal excision. Tissue histology
of both specimens showed infiltrating sheets of tumour cells composed of spindle cells
having ovoid nuclei with prominent eosinophilic nucleolus and moderate cytoplasm
containing melanin pigments. Extensive melanin incontinence was seen within the stroma
and the resection margins showed tumour involvement. She was diagnosed as Clark’s
level IV and stage III melanoma. Conclusion:Palatal melanoma has a rapid growth rate
and commonly arises from pre-existing dysplastic lesions. It may be seen in younger
females as in the index case. Most patients present with advanced disease which has
a poorer prognosis because early disease is often asymptomatic. Its classification and
treatment is still based on the cutaneous disease and requires a combination of surgery
and chemotherapy. Awareness and knowledge of its biologic behaviour by attending
clinicians should aid early diagnosis and reduce morbidity and mortality from this
aggressive tumour.
P67
Cell Surface Markers in Alcoholic Hepatitis: A Pilot Study of
Targets for Monoclonal Antibody Therapy
P R Watts 1 ; C Keeling 2 ; S Greer 3 ; RFT McMahon 1
1 The Medical School, University of Manchester, Manchester, United
Kingdom; 2 Department of Histopathology, Manchester Royal Infirmary,
Manchester, United Kingdom; 3 Department of Gastroenterology,
Manchester Royal Infirmary, Manchester, United Kingdom
Background: Alcoholic hepatitis is a serious life-threatening condition with a shortterm
mortality of 30-50%. Current treatment is largely inadequate with controversy
surrounding the benefits of corticosteroid treatment and a shortage of donor organs for
liver transplantation. Aims: The aim of this project was to investigate the presence of
cell surface markers using immunohistochemistry in liver biopsies from patients with
clinically evident alcoholic hepatitis and compare them with normal controls. Identifying
the cell surface markers present may indicate a potential role for biological therapy in the
treatment of alcoholic liver disease. Methods: We identified 22 patients with clinically and
histologically evident alcoholic hepatitis and 20 biopsies of normal liver tissue. Sections
were stained with 4 antibodies: anti-CD20 (mouse monoclonal 1:75 Novocastra), anti-
CD52 (rat monoclonal 1:40 Serotec), anti-TNF-R1 (rabbit polyclonal 1:150 Abcam)
and anti-IL-1 R1 (rabbit polyclonal 1:50 Abcam) and staining patterns were compared
between the two groups. Results: B cells were sparsely distributed in liver tissue from both
the test and control groups. There were slightly more B cells (not statistically significant)
in diseased liver. Anti-CD52 antibody intensely stained Kupffer cells and macrophages,
which were easier to identify in normal tissue. Anti-IL-1 R1 antibody bound intracellular
Mallory’s hyaline and also produced background nuclear staining of hepatocytes. Anti-
TNF-R1 diffusely stained hepatocytes; there was no difference in staining patterns or
intensity between the test and control groups. Conclusions: Of the antibodies tested,
anti-CD52 seems to be the most promising as it intensely stained Kupffer cells, however,
a possible down-regulation of CD52 in advanced disease could be a concern. Further
studies with more patients are required.
P66
Do Papillary Carcinomas arise in Thyroglossal Cysts?
P T Grigor; J Mathews
Royal Cornwall Hospital Trust, Truro, United Kingdom
A 68 year old male presented with a longstanding, non-tender, midline swelling of his
neck that appeared to move on swallowing. Serum biochemical analysis was unremarkable
(TSH 1.15 mIU/L). Pre-operative imaging or cytological assessment were not obtained.
An excision biopsy was performed. Macroscopically the specimen comprised of scanty
fatty tissue surrounding a smooth, thin-walled 16mm diameter cyst with a smooth inner
lining containing a small amount of straw coloured fluid. Light microscopic examination
showed a typical thyroglossal duct cyst architecture. Focally there were intra-luminal
papillary projections covered by CK-19 and thyroglobulin positive cells that had
overlapping, occasionally grooved nuclei, without the typical ‘Orphan Annie’ appearance.
Intracystic aggregates of pigmented macrophages admixed with reactive fibrosis and a
lymphocytic inflammatory infiltrate were also a feature. There were two lymph nodes
in the wall of the cyst; one appeared to contain crushed epithelial cells in a sub-sinus
location that were stainable for thyroglobulin antibody. Specialist review confirmed a
diagnosis of Cystic Papillary Carcinoma arising in thyroglossal duct remnants with a
micrometastasis to a lymph node adjacent to it. This patient’s case is interesting because of
its rare and unusual mode of clinical presentation and the necessary exclusion of benign
papillary hyperplasia as a possible alternate diagnosis. Specific light microscopic features,
immunohistochemistry and the fortuitous inclusion of an adjacent 2mm lymph node
containing a micrometastasis were the keys to this case. Kusunoki et al. Thyroid. 2007 Jun;
Vol 17 (6):591-2. Carcinoma arising in thyroglossal duct remnants.
P68
Perisinusoidal and Kupffer Cell Numbers in Autoimmune
Chronic Hepatitis
P N Harris; C Pritchard; P Helliwell; J Palmer; J Mathew
Royal Cornwall Hospitals Trust, Truro, United Kingdom
Introduction: 40% of autoimmune chronic hepatitis (AICH) patients eventually develop
liver cirrhosis. Liver fibrosis, a consequence of the interaction between Kupffer cells (KC)
and perisinusoidal cell (PSC), is thought to be “irreversible” but there is evidence that
AICH-related fibrosis may regress following corticosteroid and immunosuppressant
therapy.
Aim:To determine perisinusoidal cell (PSC) and Kupffer cell (KC) numbers during the
acute (presenting) (AP) and the late (post-treatment; resolved) phase (LP) of AICH.
Method: 45 AICH AP-LP matched biopsies identified from our database using SNOMED
search criteria (T56* and D4700). 4µm sections of each phase were stained with antibodies
to Smooth Muscle Actin (SMA) (clone 1A4, Dako, dilution 1:400) and CD68 (clone KP1,
Dako, dilution 1:400) with a Bondmax ® automated immunostainer. 10 images at x400
magnification were taken from periseptal or periportal areas of each biopsy using a BX61
Olympus microscope and a DP70 camera with Cell P imaging software. PSCs and KCs
were counted using the softwares’ touch count facility in µm 2 , and converted to cells/mm 2 .
Results: The difference in the numbers of PSCs in AP (mean = 392cells/mm 2 ; 95% CI,
349.20 - 435.35) to PSCs in LP (mean = 317 cells/mm 2 ;95% CI, 283.18 - 352.03) was
significant (Wilcoxon, Z = -2.489, p=0.013). Similarly, the difference in the numbers of
KCs in AP (mean = 728 cells/mm 2 ; 95% CI, 621.18 - 835.93) to KCs in LP (mean = 439
cells/mm 2 ; 95% CI, 392.84 - 486.48) was significant (Wilcoxon, Z=-4.534 , p=