Severe thrombocytopenia due to repaglinide in a patient with type 2 diabetes.

Repaglinide is an insulin secretagogue with a rapid onset and short duration of action. Several studies have proposed repaglinide to be a safe and effective treatment for patients, including elderly people with type 2 diabetes (1–3). Here we report a case subject with type 2 diabetes who showed severe thrombocytopenia due to repaglinide.

A 71-year-old man was referred and admitted to our hospital due to poor glycemic control in July 2012. His plasma glucose (350 mg/dL) and HbA1c (7.6%) levels were significantly elevated. The intensive insulin therapy promptly ameliorated his blood glucose, which was 91–151 mg/dL, by using 6 and 8 units of insulin glulisine before lunch and dinner, respectively. We stopped the insulin therapy and started to use repaglinide (0.75 mg/day) and miglitol, α-glycosidase inhibitor (225 mg/day), on July 25 and August 2, respectively. The counts of leukocytes and platelets were 7,800/μL and 15.1 × 104/μL, respectively, and serum C-reactive protein (CRP) level was 2.52 mg/dL (normal, <0.3 mg/dL) on July 24. He showed fever, and the count of leukocytes and serum CRP level increased to 9,000/μL and 18.88 mg/dL, respectively, and the count of platelets significantly decreased to 2.5 × 104/μL on August 6. Urinary counts of bacteria and leukocytes significantly increased, and culture of urine grew Serratia marcescens. We considered that his thrombocytopenia was due to severe urinary tract infection. We stopped repaglinide and miglitol and started antibiotic therapy; we also restarted the intensive insulin therapy because he was critically ill. His fever disappeared, and the count of leukocytes and serum CRP level decreased to 3,000/μL and 0.18 mg/dL, respectively. The count of platelets increased to 15.8 × 104/μL on August 15, and we restarted repaglinide and miglitol. The count of platelets decreased to 14.9 × 104/μL, 10.2 × 104/μL, and 7.3 × 104/μL, on August 17, 20, and 22, respectively. We stopped the use of miglitol on August 22; however, the count of platelets continuously decreased to 6.4 × 104/μL and 4.8 × 104/μL on August 24 and 27, respectively. After we stopped the use of repaglinide, the count of platelets promptly increased to 5.9 × 104/μL, 7.2 × 104/μL, 8.7 × 104/μL, and 9.1 × 104/μL on August 30 and September 3, 9 and 10, respectively. Antiplatelet antibody was not detected.

In summary, we experienced a patient with type 2 diabetes who showed severe decrease of platelets due to repaglinide use and showed prompt elevation of platelets due to discontinuation of the use of repaglinide. To our knowledge, this is the first report of thrombocytopenia due to repaglinide.