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Cannabidivarin for HIV‐Associated Neuropathic Pain: A Randomized, Blinded, Controlled Clinical Trial
Author(s) -
Eibach Luca,
Scheffel Simone,
Cardebring Madeleine,
Lettau Marie,
Özgür Celik M.,
Morguet Andreas,
Roehle Robert,
Stein Christoph
Publication year - 2021
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1002/cpt.2016
Subject(s) - medicine , neuropathic pain , placebo , adverse effect , randomized controlled trial , anesthesia , quality of life (healthcare) , crossover study , confidence interval , brief pain inventory , clinical endpoint , neuralgia , visual analogue scale , chronic pain , physical therapy , alternative medicine , pathology , nursing
HIV remains a major burden to the health care system and neuropathic pain is the most common neurological complication of HIV infection. Because current treatment strategies often lack satisfying pain relief, cannabinoids (CBs) are discussed as a new option. We investigated cannabidivarin (CBDV) as treatment for HIV‐associated neuropathic pain. We conducted a randomized, double‐blind, placebo‐controlled crossover study. Patients underwent two successive treatment phases (4 weeks each) and were treated with CBDV (400 mg/day) or placebo in a randomized order. A 3‐week washout phase was designed to eliminate potential carry‐over effects. Patients were followed up for 3 weeks after the end of the second treatment phase. The primary end point was pain intensity on an 11‐point numeric rating scale, recorded in a diary. Secondary end points were additional pain medication, pain characteristics, and quality of life. We included 32 patients. The mean pain intensity under CBDV was 0.62 points higher compared with placebo ( P  = 0.16, 95% confidence interval −0.27 to 1.51). CBDV did not influence the amount of additional pain medication, pain characteristics, or quality of life. The incidence of adverse events was similar during both treatments. No suspected unexpected adverse reactions occurred during either treatment. CBDV was safe but failed to reduce neuropathic pain in patients with HIV. This may be explained by a lack of CB receptor activation, as indicated by preclinical experiments. Although a larger patient number might be desirable, we would not expect a change in the conclusions because the present differences are far from statistical significance. Therefore, we would currently not consider CBDV as a clinically meaningful treatment option for neuropathic pain.

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