The relationship between bone marrow characteristics and the clinical prognosis of antithyroid drug-induced agranulocytosis

Yang, Jing; Zhong, Jing; Xiao, Xinhua; Zhou, Leocadia; Chen, Yajun; Liu, Jianghua; Cao, Renxian; Ge, Wen

doi:10.1507/endocrj.ej12-0332

Cited by 20 publications

(18 citation statements)

References 24 publications

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“…Such patients should be quickly assessed for an imminent sepsis and should receive appropriate treatment for febrile neutropenia. Bone marrow examination and culture studies can be very helpful in the initial evaluation of a patient with MMIinduced agranulocytosis [23]. In our case, the follow-up bone marrow study was especially helpful because we could document an increase in myeloid precursors by flow cytometry and colony studies, although morphologically this was not immediately evident.…”

Section: Discussionmentioning

confidence: 87%

Methimazole Induced Total Myeloid Aplasia with Delayed Recovery Despite Granulocyte Colony Stimulating Factor (G-CSF): Marrow Progenitor Recovery Kinetics

Sarker

Özgönenel

Gadgeel

et al. 2015

Indian J Hematol Blood Transfus

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An eighteen-year-old female with Graves thyrotoxicosis presented with methimazole-induced agranulocytosis and total myeloid aplasia. The bone marrow at presentation showed complete absence of myeloid precursors and striking plasmacytosis. 16 days later, myeloid precursors were still absent morphologically; however bone marrow flow cytometry and cell culture detected an improvement in myelogenesis, which was soon followed by clinical recovery of agranulocytosis. Neutrophil recovery was delayed until day 22 after cessation of methimazole despite G-CSF use, consistent with a direct toxic effect on committed myeloid cells. Our findings suggest that cell culture and flow cytometric evaluation of bone marrow myeloid progenitors can be used as a guide to anticipate neutrophil recovery.

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Section: Discussionmentioning

confidence: 87%

Methimazole Induced Total Myeloid Aplasia with Delayed Recovery Despite Granulocyte Colony Stimulating Factor (G-CSF): Marrow Progenitor Recovery Kinetics

Sarker

Özgönenel

Gadgeel

et al. 2015

Indian J Hematol Blood Transfus

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“…Methimazole is the commonest ATD used, and it can cause fatal complications like agranulocytosis (0.1%-0.3%). Two major hypotheses for the pathophysiology of ATD-induced agranulocytosis are explained by Jing Yang and Jing Zhong et al (5) and include direct toxic effects and immunological reactions. As a genetic background of ADT-induced agranulocytosis, the following alleles were found to be associated: single-nucleotide polymorphisms of HLA alleles HLA-b*38:02; HLA-drb1*08:03, which is more prevalent in the Asian population, and HLA-b*27:05 on chromosome 6, which is more prevalent in the Caucasian population (4, 6, 7).…”

Section: Discussionmentioning

confidence: 99%

Methimazole-Induced Febrile Neutropenia

Varışlı¹,

Yıldırım²,

Karacam³

et al. 2018

J Emerg Med Case Rep

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Introduction: Antithyroid drugs (ATD) are commonly used for the treatment of thyrotoxicosis, particularly for the treatment of Grave's disease. Methimazole is the first line ATD. A major fatal adverse effect of ATDs, if unrecognized and not treated on time, is agranulocytosis, which is defined as an absolute neutrophil count of <500/μL. The incidence of ATD-induced agranulocytosis is 0.1%-0.3% (1). In this study, we report on a patient who developed granulocytopenic febrile neutropenia at 3 months after treatment with methimazole (5 mg twice a day per os (BID PO)). Case report: A 51-year-old female patient presented to the emergency department with complaints of fever, fatigue, and productive cough. Her body temperature was 38.5°C; rales were heard on the mid and basal part of the left lung. Drug history revealed methimazole use (10 mg per day over the last 2 months). The WBC count was 1020/μL, and the neutrophil count was 200/μL. The patients' baseline WBC differential count and immune status were normal. Following inpatient antibiotic treatment and discontinuation of methimazole, the patient became afebrile within 2 days. After 2 weeks of discontinuation of methimazole, we performed CBC and observed the following: WBC, 5180/μL and neutrophil count, 3280/μL. Conclusion: Patients visiting the emergency department with symptoms of a systemic infection and known to use ATDs should be thoroughly evaluated, and the possibility of drug-induced agranulocytosis developing because of the use of these medications should be considered. It is very important for emergency physicians to recognize this rare patient population and act in a timely manner.

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“…In one pattern (type 1), the bone marrow is usually hypercellular with adequate neutrophil precursors, Amitriptyline-Induced Agranulocytosis but there is an arrested neutrophil maturation, with few or no mature forms of neutrophils beyond myelocytes. 8,9 In the second pattern (type 2), there is a severe reduction or complete absence of granulocytic precursors with normal or increased erythropoiesis and megakaryocytes. The latter was seen in the present patient and is reportedly associated with higher mortality 8 and a longer duration of fever and time to neutrophil recovery.…”

Section: Discussionmentioning

confidence: 99%

“…The latter was seen in the present patient and is reportedly associated with higher mortality 8 and a longer duration of fever and time to neutrophil recovery. 9 Although experimental data are not available, a correlation between the bone marrow pattern and the mechanism of toxicity may be speculated. Type 1 is thought to be a result of immune complexes selectively attaching to granulocytes and their precursors, resulting in intravascular complement-mediated granulocyte destruction (peripheral destruction).…”

Section: Discussionmentioning

confidence: 99%

“…Type 1 is thought to be a result of immune complexes selectively attaching to granulocytes and their precursors, resulting in intravascular complement-mediated granulocyte destruction (peripheral destruction). 8,9 Type 2 is speculated to be a result of direct toxic suppression of granulopoietic precursors, leading to underproduction, but it affects only granulocytes, leaving other cell types unaffected. 8 The suspected diagnosis of drug-induced agranulocytosis requires a careful review of the patient's medication history.…”

Section: Discussionmentioning

confidence: 99%

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