1999 Resident Poster Competition
Navneet Bhullar M.D.
University of Missouri-- Columbia
Microangiopathic Hemolytic Anemia in a Patient With Diabetes Mellitus
A 40 year old white male with a 16 year history of Type 1 Diabetes mellitus (DM) presented in Dec '98 with generalized weakness and was found to have severe anemia (hematocrit 24%). Workup included an upper and lower GI endoscopy, a peripheral blood smear examination, serum B12 folate, iron studies, antinuclear antibody test, and viral serologies (Hepatitis B, Hepatitis C, CMV and EVB), all of which were normal. He remained transfusion dependent. Hypertension was detected a month later. He developed thrombocytopenia, high LDH (1639U/1), low haptoglobin (<8 mg/dl) and schistocytes in the peripheral smear. His creatinine increased from 1.3 to 1.8. Coomb's test was negative. A diagnosis of hemolytic uremic syndrome/TTP was entertained. Plasmapheresis was initiated and following 42 units of plasma exchange, hemoglobin and platelets rose marginally from 9.3 g/dl and 65000 to 10.1 g/dl and 89000 respectively. LDH fell to 735U/1. His renal function continued to deteriorate.
The renal biopsy revealed changes consistent with diabetic nephropathy, which included Kimmelsteil Wilson nodules, capsular drop lesions and mesangial expansion. A crescentic lesion in one of the glomeruli was noted. No microthrombi or fibrin deposits were seen. A retinal exam had earlier revealed diabetic changes.
Microangiopathic hemolytic anemia (MAHA) persisted and plasmapheresis and transfusions were continued. Two cycles of vincristine were administered. Splenectomy was considered but not performed. A Von Willebrand factor multimer analysis was normal. The patient did not have valvular heart disease.
Review of literature yielded prior reports of 12 cases of diabetes associated MAHA without a recognizable underlying cause. Favorable response to platelet aggregation inhibitors was suggested. Diabetes induced cell membrane abnormality was postulated to cause MAHA. Accordingly, patient was given ticlopidine nearly two months after the symptoms began. Platelet count normalized and hemoglobin improved quickly and he has remained transfusion free for the last two months. He continues to be on ticlopidine. Serum creatinine and renal function remain abnormal but stable.
Summary: This case is an illustration of diabetes associated MAHA which responded to the platelet aggregation inhibitor ticlopidine. Literature review found 4 similar cases with poor prognosis. Renal death occurred in several of them.
Return to 1999 Table of Contents
What's New
Contact Information
Alan D Forker, MD MACP
Missouri Chapter Governor
Patrick Mills
Missouri Chapter Executive Director
