Acetyl‐l‐carnitine in the treatment of painful antiretroviral toxic neuropathy in human immunodeficiency virus patients: an open label study

Abstract

Antiretroviral toxic neuropathy causes morbidity in human immunodeficiency virus (HIV) patients under dideoxynucleoside therapy, benefits only partially from medical therapy, and often leads to drug discontinuation. Proposed pathogeneses include a disorder of mitochondrial oxidative metabolism, eventually related to a reduction of mitochondrial DNA content, and interference with nerve growth factor activity. Carnitine is a substrate of energy production reactions in mitochondria and is involved in many anabolic reactions. Acetyl carnitine treatment promotes peripheral nerve regeneration and has neuroprotective properties and a direct analgesic role related to glutamatergic and cholinergic modulation. The aim of this study was to evaluate acetyl-l-carnitine in the treatment of painful antiretroviral toxic neuropathy in HIV patients. Twenty subjects affected by painful antiretroviral toxic neuropathy were treated with oral acetyl-l-carnitine at a dose of 2,000 mg/day for a 4-week period. Efficacy was evaluated by means of the modified Short Form McGill Pain Questionnaire with each item rated on an 11-point intensity scale at weekly intervals and by electromyography at baseline and final visit. Mean pain intensity score was significantly reduced during the study, changing from 7.35 +/- 1.98 (mean +/- SD) at baseline to 5.80 +/- 2.63 at week 4 (p = 0.0001). Electrophysiological parameters did not significantly change between baseline and week 4. In this study, acetyl-l-carnitine was effective and well tolerated in symptomatic treatment of painful neuropathy associated with antiretroviral toxicity. On the contrary, no effect was noted on neurophysiological parameters.

Limited Brain Metabolism Changes Differentiate between the Progression and Clearance of Rabies Virus

“…The increase in carnitine levels could be one of the mechanisms by which TriGAS exerts its protective activity against a lethal RABV infection. These biochemicals have been shown to be protective in animal models of ischemia, neurodegeneration and viral-induced encephalitis [22], [23].…”

Antinociceptive Effect of Salvia Extract on Cisplatin-Induced Hyperalgesia in Mice

“…There are extensive publications demonstrating the effects of PB cancer chemotherapies on the mitochondrial function [60][61][62][63][64]; the role of the mitochondria was demonstrated in models of other forms of painful peripheral neuropathy, as well as in patients with such neuropathy [43,65,66]. Joseph et al [11] showed that reactive oxygen species (ROSs) are the main mitochondrial mechanism implicated; a contribution of mitochondrial electron transport chains (mETCs), which drive ROS production in the mitochondria, was estimated.…”

Chemotherapy-Induced Peripheral Neuropathy

“…116 ALCAR also reversed the chemotherapeutic-induced swelling and dysfunction of mitochondria. 116,131,179 These preclinical data and evidence that ALCAR have therapeutic effects on neuropathy in patients with diabetes 192 and HIV, 193,194 prompted clinical trials to examine the effects of ALCAR on paclitaxelinduced neuropathy in patients. In a phase II study with 25 patients, the effects of ALCAR were promising, providing improvement of sensory neuropathy in 60% of patients.…”