Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2008
A case of severe neuropathy associated with hypertriglyceridemia.
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Hou Runhua, Goldberg Anne Carol, Tobin Garry Stuart
Аннотация
OBJECTIVE: To describe a case of severe neuropathy associated with hypertriglyceridemia.
METHODS: We describe the clinical and laboratory findings of the study patient and review the relevant literature.
RESULTS: A 45-year-old woman presented to the emergency department with recurrent abdominal pain and severe peripheral neuropathy. Her laboratory data revealed elevated lipase and a very high triglyceride concentration (>10,000 mg/dL), consistent with a diagnosis of recurrent hypertriglyceridemia-induced pancreatitis. Workup for peripheral neuropathy showed normal concentrations of thyrotropin, fasting blood glucose, vitamin B(12), and creatinine, as well as a normal hemoglobin A(1c) level, serum protein electrophoresis, and urine protein electrophoresis. Rapid plasma reagin antibodies, antinuclear antibodies, and lyme antibodies were not detected. In the absence of other identifiable causes, hypertriglyceridemia was deemed the likely etiology of severe neuropathy in this patient.
CONCLUSIONS: Peripheral nerve conduction abnormalities can be identified in patients with mild hypertriglyceridemia in the absence of symptoms. Early recognition and aggressive management of hypertriglyceridemia may prevent the complications of severe peripheral neuropathy.
METHODS: We describe the clinical and laboratory findings of the study patient and review the relevant literature.
RESULTS: A 45-year-old woman presented to the emergency department with recurrent abdominal pain and severe peripheral neuropathy. Her laboratory data revealed elevated lipase and a very high triglyceride concentration (>10,000 mg/dL), consistent with a diagnosis of recurrent hypertriglyceridemia-induced pancreatitis. Workup for peripheral neuropathy showed normal concentrations of thyrotropin, fasting blood glucose, vitamin B(12), and creatinine, as well as a normal hemoglobin A(1c) level, serum protein electrophoresis, and urine protein electrophoresis. Rapid plasma reagin antibodies, antinuclear antibodies, and lyme antibodies were not detected. In the absence of other identifiable causes, hypertriglyceridemia was deemed the likely etiology of severe neuropathy in this patient.
CONCLUSIONS: Peripheral nerve conduction abnormalities can be identified in patients with mild hypertriglyceridemia in the absence of symptoms. Early recognition and aggressive management of hypertriglyceridemia may prevent the complications of severe peripheral neuropathy.