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Sall A. et al: Flower-Like Plasma Cell Nuclei in Multiple MyelomaTurk J Hematol 2021;38:153-154A 43-year-old Senegalese man with no known past medicalhistory was referred to our hospital for asthenia and bone pain.The blood count showed moderate leukocytosis (12x10 9 /L),severe anemia (hemoglobin: 53 g/L), and a normal plateletcount (315x10 9 /L), while the blood smear examination showedmarked rouleaux formation. Protein electrophoresis showed amonoclonal gamma peak (82 g/L, Figure 1F). Immunofixationrevealed a monoclonal immunoglobin G kappa band.The diagnosis of multiple myeloma was confirmed by bonemarrow aspiration. Giemsa-stained marrow smears showedhypercellularity with a large majority of very atypical plasmacells, namely medium-sized to large cells with nuclearabnormalities (budding: Figure 1A), flower-shaped nucleithat are quite uncommon in myeloma (Figures 1B-1E), andprominent nucleoli (Figure 1D, red arrow). Lymphoplasmacyticcells were also present, as well as several mitotic events (Figure1D, black and blue arrows).On flow cytometry the plasma cells expressed weak CD45, CD38,CD138, and CD56 (Figures 1G and 1H) and cytoplasmic kappalight chain. CD19, CD20, CD79a, and CD10 were negative. HIV,HBV, HCV, and HTLV-1 serology were negative. FISH was notavailable; thus, we could not calculate the Revised InternationalStaging System score. However, the International StagingSystem result was stage III (β2 microglobulin = 5.9 mg/L).Multiple myeloma is becoming more and more frequent inAfrican populations. The key difference between African andCaucasian populations is the age of onset: 45-50 years inAfrican populations and more than 60 years in Caucasians [1]. Inaddition, we note the presence of many poor prognosis factorsin African patients resulting in earlier death. Delayed diagnosisand unavailability of new therapeutic agents and autograftingcould contribute to the poor outcome. However, geneticbackground and environmental factors could play a critical roleand merit further studies [2].Keywords: Plasma cell, Morphologic abnormalities, MultiplemyelomaAnahtar Sözcükler: Plazma hücresi, Morfolojik anormallikleri,Multipl myelomAuthorship ContributionsSurgical and Medical Practices: M.S., B.F., S.D.; Concept: A.S.,A.O.T.; Design: A.S., B.F.; Data Collection or Processing: A.S., M.S.;Analysis or Interpretation: A.S., A.O.T.; Literature Search: A.S.,D.S., M.G.; Writing: A.S., M.S., D.S., A.O.T.Conflict of Interest: No conflict of interest was declared by theauthors.Financial Disclosure: The authors declared that this studyreceived no financial support.References1. Kazandjian D. Multiple myeloma epidemiology and survival: a uniquemalignancy. Semin Oncol 2016;43:676-681.2. Smith CJ, Ambs S, Landgren O. Biological determinants of health disparitiesin multiple myeloma. Blood Cancer J 2018;8:85.154
LETTERS TO THE EDITORLETTERS TO THE EDITORTurk J Hematol 2021;38:155-174Immune Thrombotic Thrombocytopenic Purpura in a Patientwith Suspected COVID-19: Hydroxychloroquine Culprit or JustHappenstance?COVID-19 Şüpheli Bir Hastada İmmün Trombotik Trombositopenik Purpura: HidroksiklorokinSuçlu mu Yoksa Sadece Rastlantı mı?Tajamul H. MirKhyber Medical Institute Srinagar, Department of Nephrology and Lupus/Vasculitis Centre, Srinagar, IndiaTo the Editor,I read with great interest the recently published letter tothe editor by Arıkan et al. [1] about hydroxychloroquine(HCQ)-associated thrombotic thrombocytopenic purpura(TTP) together with some queries raised by Sookaromdee andWiwanitkit and the original authors’ reply [1,2]. There are somepertinent points to note. First and foremost, HCQ-induced TTPis an extremely rare but nevertheless recognized entity withonly a few cases reported in the literature, which have notbeen thoroughly evaluated. Most of the data regarding thiscomplication have been extrapolated against the backgroundof HCQ’s parent compound, quinine. Quinine-induced andpresumably HCQ-induced TTP is characterized by generationof antiplatelet antibodies, which cross-react with theendothelium and cause TTP. However, typical drug-inducedTTP, including quinine-induced TTP, is not associated witha critical drop in ADAMTS13 levels or with the presence ofan ADAMTS13 inhibitor, but the patient presented by Arıkanet al. had both. This is an important differentiating featureof quinine-induced TTP from immune TTP (iTTP) and it callsinto question the diagnosis made by Arıkan et al. [1] or evensuggests iTTP after HCQ as a novel complication [3]. I wouldnot straight away repudiate the observation made by Arıkanet al. [1] because, first of all, there is a definite temporalprofile that links the medicine with iTTP, and, furthermore,some drugs like the thienopyridine group of antiplateletshave been associated with classic iTTP leading to a criticaldrop in ADAMTS13 levels and the presence of an inhibitor[4]. At least five cases of thrombotic microangiopathy of iTTP/HUS (hemolytic uremic syndrome) in coronavirus disease-19(COVID-19) have been reported in the literature with anobvious temporal relation between HCQ and the developmentof iTTP, which seems to have been ignored by most authors inlight of COVID-19 infection and everything being attributedto this novel virus [5,6,7,8]. It needs to be emphasized thatquinine-induced thrombotic microangiopathy can occurhours, days, or months after exposure to the drug and HCQhas a very long elimination half-life of 40 days after asingle dose. The typical COVID-19-induced TTP-like illness issecondary to diffuse endothelial damage secondary to virusinducedendotheliitis further aggravated by complementoveractivity, causing an over-spilling of von Willebrand factor(vWF) from the damaged endothelial network overwhelmingthe ADAMTS13 protease and producing the relative ADAMTSdeficiency typically seen as an ADAMTS13/vWF ratio of <10,but without a critical drop in ADAMTS13 levels and in theabsence of a circulating ADAMTS inhibitor [9]. Nevertheless,some cases of classic iTTP have occurred in associationwith COVID-19 infection, possibly due to some novelmechanism triggered by the virus or maybe the unmaskingof a latent disease with the virus possibly acting as a secondhit. Differentiating primary from secondary thromboticmicroangiopathy is not always easy since many genetic or evenacquired variants could be clinically silent, becoming manifestlater in life following a second hit such as an infection, drug,surgical stress, or pregnancy. In the case presented by Arıkanet al. [1], I feel that at least immunoglobulin G anti-COVIDantibodies should have been examined and, if possible, novelin vitro HCQ sensitization testing should be performed as well[10]. Although re-exposure to the drug could easily solve thediagnostic dilemma, it would be absolutely unethical and riskysince the second exposure could be more devastating if thedrug were in fact the culprit. The initial illness in the patientcould have been any trivial infection or maybe a mild COVIDcase (though not documented). I am sure the authors musthave thoroughly evaluated the patient for other mimickersand ruled them out, and systemic lupus erythematosus seemsvery unlikely. The role of HCQ in causing iTTP in the given casecannot be absolutely ruled out.Keywords: COVID-19-induced iTTP, HydoxychloroquineinducedTTP, ADAMTS13, Von Willebrand factor, Thromboticmicroangiopathy155
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