Manca Alessandra, Valz Cristina, Chiara Francesco, Palermiti Alice, Mula Jacopo, Soloperto Sara, Antonucci Miriam, De Nicolò Amedeo, Luxardo Nicola, Imperiale Daniele, Vischia Flavio, De Cori David, Cusato Jessica, D'Avolio Antonio
Laboratory of Clinical Pharmacology and Pharmacogenetics, Department of Medical Sciences, University of Turin, Amedeo di Savoia Hospital, 10149 Turin, Italy.
SC Terapia del Dolore, ASL Città di Torino, 10144 Turin, Italy.
J Xenobiot. 2025 May 7;15(3):66. doi: 10.3390/jox15030066.
L. shows potent anti-inflammatory activity, resulting in an interesting pharmacological option for pain management. The aim of the study was to evaluate the association between pharmacogenetics, neurological and inflammatory biomarkers, and cannabinoid plasma exposure in patients treated with cannabis. A total of 58 patients with a diagnosis of neuropathic and chronic pain treated with medical cannabis were analyzed. Cannabis was administered as a decoction (n = 47) and as inhaled cannabis (n = 11): 30 patients were treated with cannabis with high THC, while 28 patients were treated with cannabis with reduced THC (plus CBD). Cannabinoid plasma concentrations were obtained with UHPLC-MS/MS. Allelic discrimination was assessed by real-time PCR. Inflammation biomarkers (e.g., interleukin-10) were analyzed by ELISA, neurofilaments light chain (NFL), and brain-derived neurotrophic factor (BDNF) by Single Molecule Array. A statistically significant difference in IL-10 ( = 0.009) and BDNF ( = 0.004) levels was observed comparing patients treated with decoction and inhaled cannabis. BDNF and NFL results correlated with cannabinoid concentrations. Concerning genetics, the 680 T>C genetic variant influences cannabinoid plasma levels, including Δ9-THC ( = 0.017). Conclusions: This study shows a possible impact of some genetic variants on cannabinoid plasma exposure, other than a possible role of medical cannabis on inflammation-related and neuronal impairment factor levels. Further studies in larger cohorts are required.
L.显示出强大的抗炎活性，为疼痛管理带来了一种有趣的药理学选择。本研究的目的是评估药物遗传学、神经学和炎症生物标志物与接受大麻治疗患者的大麻素血浆暴露之间的关联。共分析了58例诊断为神经性和慢性疼痛并接受医用大麻治疗的患者。大麻以煎剂形式给药（n = 47）和吸入大麻形式给药（n = 11）：30例患者接受高THC大麻治疗，而28例患者接受低THC（加CBD）大麻治疗。用超高效液相色谱-串联质谱法测定大麻素血浆浓度。通过实时聚合酶链反应评估等位基因鉴别。通过酶联免疫吸附测定法分析炎症生物标志物（如白细胞介素-10），通过单分子阵列分析神经丝轻链（NFL）和脑源性神经营养因子（BDNF）。比较接受煎剂和吸入大麻治疗的患者，观察到IL-10（P = 0.009）和BDNF（P = 0.004）水平存在统计学显著差异。BDNF和NFL结果与大麻素浓度相关。关于遗传学，680 T>C基因变异影响大麻素血浆水平，包括Δ9-THC（P = 0.017）。结论：本研究表明一些基因变异可能对大麻素血浆暴露有影响，此外医用大麻可能对炎症相关和神经元损伤因子水平有作用。需要在更大队列中进行进一步研究。
