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Updated: Jun 1, 2026

ALS - Motor Neuron Disease: Mechanism and Development of New Therapies
Published on: July 29, 2007
Lactic acidosis associated with severe neuromuscular weakness and stavudine therapy
Pongpat Vorasayan1, Kammant Phanthumchinda
1Division of Neurology, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Abstract:
Nucleoside analogue reverse-transcriptase inhibitors (NRTIs) especially stavudine, used for the treatment of HIV infection have been rarely associated with lactic acidosis syndrome (LAS) and severe neuromuscular weakness mimicking Guillain Barre syndrome. A 36-year-old man presented with a one-week history of nausea, vomiting, epigastric pain, dyspnea associated with progressive muscle weakness and numbness in glove and stocking pattern. He had symptomatic HIV infection, diagnosed 2 years before the admission and was treated with GPOvir (lamivudine, stavudine and nevirapine). Physical examination revealed afebrile dyspnic drowsy man with crepitation in both lungs and hepatomegaly. Neurological examination showed areflexic symmetrical weakness of both extremities and decreased pin-prick sensation in glove and stocking pattern as well as loss of vibration and touch sensation in both hands and feet. He developed cardiopulmonary arrest and was intubated. Investigations revealed severe lactic acidosis (lactic acid = 21.1 mg/dl). Electrophysiological studies revealed severe sensorimotor axonopathy predominantly involved the lower extremities. Stavudine was discontinued. Severe LAS dramatically improved and polyneuropathy gradually recovered with symptomatic as well as supportive interventions. Monitoring of LAS and neuromuscular weakness is advocated in HIV patient who receive stavudine therapy. Immediate discontinuation of the medication after detection of these complications may prevent this fatal complications.
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