DISCUSSION
Agranulocytosis is a severe adverse event of antithyroid agents and requires prompt diagnosis and treatment. In a 26-year study at one clinic, it occurred in approximately 0.4% of patients taking antithyroid agents.1 The possible mechanisms of agranulocytosis are the direct toxicity of drugs and immune-mediated responses.2 Older age, female sex, and some HLA genotypes are reported to be associated with susceptibility to agranulocytosis.2
Although the development of agranulocytosis tends to be dose related, a small dose of antithyroid agent can sometimes cause the condition.3,4 It usually occurs within the first 3 months of treatment initiation, but occasionally patients develop agranulocytosis after long-term therapy.5 Interruption and subsequent resumption of the same antithyroid drug treatment also can be a risk factor for agranulocytosis, as in this case.5
Treatment includes drug cessation, administration of broad-spectrum antibiotics if infection is suspected, and granulocyte-colony stimulating factor (G-CSF) therapy.5
Our patient was hospitalized, and methimazole was stopped immediately. Administration of potassium iodide 50 mg/d and G-CSF was started. Meropenem 3 g/d also was administered for neutropenic fever.
The patient’s condition improved, and her WBC count increased to 1640 cells/µL on Day 8 and 10,890 cells/µL on Day 9. G-CSF was stopped on Day 12 and meropenem on Day 13. Bone marrow aspiration was not performed because of improvement in lab values and her overall condition. Although monitoring of WBC count during methimazole therapy is controversial,5 we decided to routinely monitor this patient due to the possibility of drug cross-reactivity.
Continue to: Despite repeated explanations...