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 Missouri Resident Poster Competition 1999
Navneet Bhullar M.D
University of Missouri-- Columbia
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.
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