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LETTERS TO THE EDITORTurk J Hematol 2021;38:155-174the GI system [1]. Among the 4 cases with stomach involvement,only 1 case showed symptoms of upper GI bleeding witha mass of 4x10 cm [1]. Second, this patient seemed to havewell-controlled myeloma with decreased M protein compatiblewith a very good partial response (VGPR) [3] and normalizationof hemoglobin. It would be even rarer if a patient sufferedfrom a rare manifestation of myeloma with well-controlleddisease. Third, MM could be accompanied by second primarymalignancies and the reported rate (3.5%-4.52%) was higherthan that of gastric involvement (0.93%) in MM patients [1,4].However, pathology showed plasmacytoma, which indicatedprogression of MM [3]. Moreover, despite a negative 24-h urinelight chain level at baseline and marked decrease of intact serumM protein compared to baseline (31.2 g/L decreased to 2.2 g/L),significantly elevated urine light chain levels also suggesteddisease progression. This phenomenon was termed “light chainescape,” and clinicians should examine urine light chain even inpatients with normal 24-h urine light chain level at baseline [5].Previous studies showed that extramedullary plasmacytomaat relapse had the worst prognosis (progression-free survivalof 13.6 months and overall survival of 11.4 months) [6] andpatients who progress within 18 months of initial therapyhave particularly poor outcomes [7]. Considering the age, poorgeneral condition, possible outcomes, and wishes of the patientand his family members, palliative care was given. Despitesufficient supportive treatment, the patient died soon.We report a case of GI hemorrhage rarely seen in MM. Due tospatial heterogeneity, malignant cells at different anatomicallocations may display different levels of sensitivity.Keywords: Multiple myeloma, Gastrointestinal plasmacytoma,Gastric hemorrhageAnahtar Sözcükler: Multipl myelom, Gastrointestinalplazmasitom, Mide kanamasıAuthorship ContributionsData Collection or Processing: B.P.; Analysis or Interpretation:L.Z.; Writing: W.M.Conflict of Interest: No conflict of interest was declared by theauthors.Financial Disclosure: The National Natural Science Foundationof China (81900202, for ZL) and the Fundamental ResearchFunds for the Central Universities (3332018036, for ZL).References1. Talamo G, Cavallo F, Zangari M, Barlogie B, Lee CK, Pineda-Roman M, KiwanE, Krishna S, Tricot G. Clinical and biological features of multiple myelomainvolving the gastrointestinal system. Haematologica 2006;91:964-967.2. Pasmantier MW, Azar HA. Extraskeletal spread in multiple plasma cellmyeloma. A review of 57 autopsied cases. Cancer 1969;23:167-174.3. Kumar S, Paiva B, Anderson KC, Durie B, Landgren O, Moreau P, MunshiN, Lonial S, Bladé J, Mateos MV, Dimopoulos M, Kastritis E, BoccadoroM, Orlowski R, Goldschmidt H, Spencer A, Hou J, Chng WJ, Usmani SZ,Zamagni E, Shimizu K, Jagannath S, Johnsen HE, Terpos E, Reiman A, KyleRA, Sonneveld P, Richardson PG, McCarthy P, Ludwig H, Chen W, Cavo M,Harousseau JL, Lentzsch S, Hillengass J, Palumbo A, Orfao A, RajkumarSV, Miguel JS, Avet-Loiseau H. International Myeloma Working Groupconsensus criteria for response and minimal residual disease assessment inmultiple myeloma. Lancet Oncol 2016;17:e328-e346.4. Popova JG, Nenov I, Spasova M, Yaneva M, Beleva E, AnanoshtevetN. Multiple myeloma in association with second malignancy. J BUON2013;18:448-452.5. Hobbs JA, Drayson MT, Sharp K, Harding S, Bradwell AR, Mead GP. Frequencyof altered monoclonal protein production at relapse of multiple myeloma.Br J Haematol 2010;148:659-661.6. Beksac M, Seval GC, Kanellias N, Coriu D, Rosiñol L, Ozet G, Goranova-Marinova V, Unal A, Bila J, Ozsan H, Ivanaj A, Balić LI, Kastritis E, BladéJ, Dimopoulos MA. A real world multicenter retrospective study onextramedullary disease from Balkan Myeloma Study Group and BarcelonaUniversity: analysis of parameters that improve outcome. Haematologica2020;105:201-208.7. Shah N, Chari A, Scott E, Mezzi K, Usmani SZ. B-cell maturation antigen(BCMA) in multiple myeloma: rationale for targeting and currenttherapeutic approaches. Leukemia 2020;34:985-1005.EthicsInformed Consent: Informed consent for publication wasobtained from the patient.©Copyright 2021 by Turkish Society of HematologyTurkish Journal of Hematology, Published by Galenos Publishing HouseAddress for Correspondence/Yazışma Adresi: Lu Zhang, M.D., Peking Union Medical College Hospital, ChineseAcademy of Medical Sciences and Peking Union Medical College, Department of Hematology, Beijing, ChinaPhone : +86-010-69155001E-mail : pumczhanglu@126.com ORCID: orcid.org/0000-0002-0860-9625Received/Geliş tarihi: October 28, 2020Accepted/Kabul tarihi: February 8, 2021DOI: 10.4274/tjh.galenos.2021.2020.0645170
Turk J Hematol 2021;38:155-174LETTERS TO THE EDITORProlonged Severe Watery Diarrhea in a Long-Term MyelomaSurvivor: An Unforeseen Infection with Cystoisospora belliUzun Süredir Myelom Tanısıyla Takipli Hastada Uzamış Sulu İshalin Öngörülemeyen Nedeni:Cystoisospora belliTarık Onur Tiryaki 1 , Kadir Uluç Anıl 2 , Melek Büyük 3 , Ahmet Yasir Yıldırım 3 , Alp Atasoy 4 , Aslı Çiftçibaşı Örmeci 4 ,Sevgi Kalayoğlu Beşışık 11İstanbul University İstanbul Medical Faculty, Department of Internal Medicine, Division of Hematology, İstanbul, Turkey2İstanbul University İstanbul Medical Faculty, Department of Internal Medicine, İstanbul, Turkey3İstanbul University İstanbul Medical Faculty, Department of Pathology, İstanbul, Turkey4İstanbul University İstanbul Medical Faculty, Department of Internal Medicine, Division of Gastroenterohepatology, İstanbul, TurkeyTo the Editor,The parasite Cystoisospora belli (formerly known as Isosporabelli), referred to as coccidian, infects the epithelial cells ofthe small intestine and is one of the least common intestinalcoccidia that infect humans. Infections have been sporadicallyreported in a wide variety of immunocompromised patients,including patients with concurrent Hodgkin’s disease, non-Hodgkin’s lymphoma, and acute lymphoblastic leukemia, andcan sometimes be fulminant in immunocompromised patients[1,2]. Chronic diarrhea is the major clinical manifestation,sometimes associated with headache, fever, malaise, abdominalpain, vomiting, dehydration, and weight loss. Extraintestinalinfections with tissue cyst-like stages have been observed in thelymph nodes, liver, and spleen of patients with AIDS. Infectionsof immunosuppressed patients with C. belli have been reportedin association with viral infections other than HIV, especiallyhuman T-cell leukemia virus type 1 (HTLV-1) [3].Multiple myeloma (MM)-related immunodeficiency involvesB-cell dysfunction, such as hypogammaglobulinemia, as wellas T-cell, dendritic cell, and NK-cell abnormalities [4,5,6,7]. Inaddition to the disease-related inherent immunodeficiency,some studies have described a changing spectrum ofinfections in MM, possibly related to the more intensive orimmunomodulating treatment approaches of recent years.Among MM cases, infections are a significant cause of morbidityand a leading cause of death. We present here a case of C. belliinfection in a MM patient who developed persistent diarrhea inthe late responsive period.A 66-year-old male patient was diagnosed as havingimmunoglobulin (Ig) G kappa-type MM of Durie-Salmon stageIIIA in 2007. He underwent autologous stem cell transplantation(ASCT) following high-dose melphalan (200 mg/m 2 ) aftersecond-line treatment. A bortezomib-based regimen was usedagain due to progression in the first year after ASCT. A secondASCT was performed for consolidation, this time followed bylenalidomide maintenance. He achieved complete response, butat the 24 th month of maintenance, he relapsed. Pomalidomide,cyclophosphamide, and dexamethasone were started. Treatmentregimens and disease characteristics are summarized in Table 1.In the 4 th month of this treatment, he developed severe waterydiarrhea with abdominal pain, which became persistent despitesupportive measures. MM disease status showed biochemicalremission. Infectious causes were excluded by variable testsincluding ova and parasite screening. Acute phase markerswere not remarkable. Metronidazole (500 mg orally, every 8 hfor 5 days) and ciprofloxacin (500 mg orally, b.i.d.) were startedempirically. There was no fat, blood, or leukocytes in the stool.Accompanying viral infection was not detected in our patient,such as HIV or HTLV-1. Anti-tissue transglutaminase IgA andanti-gliadin IgA antibodies were negative. Thyroid hormonelevels, vasoactive intestinal peptide, and urine 5-HIAA levelswere within normal ranges. Gastroscopy showed non-erosiveantral gastritis and edematous and erythematous duodenum.He continuously lost weight and became pale, but had no fever.There was no gross pathology in colonoscopy except distinct thinvascular structures. Multiple biopsies were obtained randomly toevaluate amyloidosis. Contrast-enhanced abdominal CT did notreveal any abnormality. Endoscopic biopsy samples demonstratedmild duodenitis and colitis characterized by increased numbersof plasma cells and lymphocytes but no villous atrophy or crypthyperplasia (Figure 1B). Amyloid staining proved to be negative.No inclusion bodies were found, pointing to viral infection. Inthe duodenal epithelium, beneath the nuclei, a different imagewas striking. There were PAS-stained granules (Figure 1D) andoocysts were identified, which were consistent with C. belli.Several developmental stages of C. belli parasites in duodenalepithelial cells were identified (Figures 1A-1C). Treatment withtrimethoprim (TMP)-sulfamethoxazole (160 mg of trimethoprimand 800 mg of sulfamethoxazole [STX]) as one double-strengthtablet b.i.d. orally for 10 days improved the clinical picture171
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