Sudden Onset Agranulocytosis and Hepatotoxicity after Taking Methimazole

Abstract

Agranulocytosis is a rare adverse effect of methimazole. The usual duration of treatment prior to the onset of agranulocytosis is approximately 1 to 4 months, and can be as long as 1 year. Agranulocytosis together with hepatotoxicity is an extremely rare idiosyncratic side effect of methimazole treatment. We present an unprecedented case of a Grave's disease patient who showed a strong reaction to methimazole with obvious agranulocytosis and hepatotoxicity which developed only six days after administration. This case, along with a literature review, is offered with the aim to increase the awareness of physicians of sudden onset agranulocytosis and hepatotoxicity from methimazole.

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

“…ANC, absolute neutrophil count; G-CSF, granulocyte-colony stimulating factor; -X±s, mean ± standard deviation patients developed sudden onset agranulocytosis and hepatotoxicity after taking methimazole within 6 days. This is the first case of agranulocytosis and hepatotoxicity induced by methimazole in less than 6 days [20]. The data from our study also revealed that the onset age, period of drug exposure, associated drugs (MMI or PTU) and neutrophil count on admission have no significant effect on the types of bone marrow.…”

Maternal transfer of methimazole and effects on thyroid hormone availability in embryonic tissues

“…It has been shown in humans and rats that MMI is rapidly metabolised and that a major part is excreted via urine (Skellern & Steer 1981, Hengstmann & Hohn 1985, Cooper 2005, Kusmierek & Bald 2007. Nevertheless, MMI treatment sometimes induces severe side effects such as agranulocytosis and hepatotoxicity (Cooper 2005, Yang et al 2012, indicating that a significant amount of MMI and/or its metabolites is present in extra-thyroidal tissues. We measured the levels of reduced MMI and its oxidised metabolites in hens following 16 weeks of treatment.…”

Propylthiouracil-induced mitochondrial dysfunction in liver and its relevance to drug-induced hepatotoxicity

“…36,37 There is several human cases of PTU-induced hepatotoxicity. 15,[38][39] The mechanism(s) of PTU hepatotoxicity is obscure. In this study, we found that PTU caused mitochondrial dysfunction both in vitro and in vivo.…”

“…[8][9][10] Several cases of PTU-induced hepatotoxicity have been reported. 4,[11][12][13][14][15][16] Pediatrics seems to be more vulnerable to PTU-induced hepatotoxicity. 17 There is no precise mechanism for PTU-induced liver injury.…”