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      Cannabis medicinal y cáncer: beneficios en dolor oncológico y otros síntomas relacionados Translated title: Medical cannabis and cancer: benefits for cancer pain and other related symptoms

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          Abstract

          RESUMEN El cannabis tiene el potencial de modular algunos de los síntomas más prevalentes en el cáncer, ya sean derivados del propio tumor o de los tratamientos antitumorales. Sin embargo, la escasez de evidencia científica sobre su eficacia y el estigma histórico ocasiona un problema para que los profesionales médicos puedan elegirlo como una opción terapéutica para sus pacientes. Esta revisión refleja la influencia del cannabis medicinal en los síntomas más prevalentes y debilitantes en cáncer, incluyendo el dolor, las náuseas y los vómitos inducidos por quimioterapia, la neuropatía periférica inducida por quimioterapia, y la anorexia y la pérdida de apetito. Asimismo, se repasa la evidencia actual del cannabis como agente anticanceroso.

          Translated abstract

          ABSTRACT Cannabis has the potential to modulate some of the most common symptoms of cancer, either from the tumour itself or from its treatments. However, the paucity of scientific evidence for its effectiveness and the historical stigma causes a problem to clinicians for choosing it as a therapeutic option for their patients. This review reflects the influence of medical cannabis on the most common and debilitating symptoms in cancer, including pain, chemotherapy-induced nausea and vomiting, chemotherapy-induced peripheral neuropathy, and anorexia and loss of appetite. Additionaly we do a review of the medical cannabis as an anticancer agent.

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          Most cited references39

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          Incidence, prevalence, and predictors of chemotherapy-induced peripheral neuropathy: A systematic review and meta-analysis.

          Chemotherapy-induced peripheral neuropathy (CIPN) is a disabling pain condition resulting from chemotherapy for cancer. Severe acute CIPN may require chemotherapy dose reduction or cessation. There is no effective CIPN prevention strategy; treatment of established chronic CIPN is limited, and the prevalence of CIPN is not known. Here we used a systematic review to identify studies reporting the prevalence of CIPN. We searched Embase, Medline, CAB Abstracts, CINAHL, PubMed central, Cochrane Library, and Web of Knowledge for relevant references and used random-effects meta-regression to estimate overall prevalence. We assessed study quality using the CONSORT and STROBE guidelines, and we report findings according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidance. We provide a qualitative summary of factors reported to alter the risk of CIPN. We included 31 studies with data from 4179 patients in our analysis. CIPN prevalence was 68.1% (57.7-78.4) when measured in the first month after chemotherapy, 60.0% (36.4-81.6) at 3months and 30.0% (6.4-53.5) at 6months or more. Different chemotherapy drugs were associated with differences in CIPN prevalence, and there was some evidence of publication bias. Genetic risk factors were reported in 4 studies. Clinical risk factors, identified in 4 of 31 studies, included neuropathy at baseline, smoking, abnormal creatinine clearance, and specific sensory changes during chemotherapy. Although CIPN prevalence decreases with time, at 6months 30% of patients continue to suffer from CIPN. Routine CIPN surveillance during post-chemotherapy follow-up is needed. A number of genetic and clinical risk factors were identified that require further study.
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            Management of Chronic Pain in Survivors of Adult Cancers: American Society of Clinical Oncology Clinical Practice Guideline

            To provide evidence-based guidance on the optimum management of chronic pain in adult cancer survivors.
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              Endocannabinoid levels in rat limbic forebrain and hypothalamus in relation to fasting, feeding and satiation: stimulation of eating by 2-arachidonoyl glycerol.

              Endocannabinoids are implicated in appetite and body weight regulation. In rodents, anandamide stimulates eating by actions at central CB1 receptors, and hypothalamic endocannabinoids may be under the negative control of leptin. However, changes to brain endocannabinoid levels in direct relation to feeding or changing nutritional status have not been investigated. We measured anandamide and 2-arachidonoyl glycerol (2-AG) levels in feeding-associated brain regions of rats, during fasting, feeding of a palatable food, or after satiation. Endocannabinoid levels were compared to those in rats fed ad libitum, at a point in their daily cycle when motivation to eat was absent. Fasting increased levels of anandamide and 2-AG in the limbic forebrain and, to a lesser extent, of 2-AG in the hypothalamus. By contrast, hypothalamic 2-AG declined as animals ate. No changes were detected in satiated rats. Endocannabinoid levels in the cerebellum, a control region not directly involved in the control of food intake, were unaffected by any manipulation. As 2-AG was most sensitive to variation during feeding, and to leptin regulation in a previous study, we examined the behavioural effects of 2-AG when injected into the nucleus accumbens shell, a limbic forebrain area strongly linked to eating motivation. 2-AG potently, and dose-dependently, stimulated feeding. This effect was attenuated by the CB1 receptor antagonist SR141716. These findings provide the first direct evidence of altered brain levels of endocannabinoids, and of 2-AG in particular, during fasting and feeding. The nature of these effects supports a role for endocannabinoids in the control of appetitive motivation.
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                Author and article information

                Journal
                dolor
                Revista de la Sociedad Española del Dolor
                Rev. Soc. Esp. Dolor
                Inspira Network Group, S.L (Madrid, Madrid, Spain )
                1134-8046
                2022
                : 29
                : suppl 1
                : 14-19
                Affiliations
                [1] Madrid orgnameOncológico Hospital HM Sanchinarro orgdiv1Unidad de Dolor España
                Article
                S1134-80462022000200004 S1134-8046(22)02900000004
                10.20986/resed.2022.4026/2022
                d766df00-3ff8-41ab-a95a-45c3399531e1

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

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                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 39, Pages: 6
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                SciELO Spain

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                Artículos

                neuropathy,anorexia,neuropatía,vómitos,náuseas,quimioterapia,tumor,cáncer,CBD,THC,cannabis medicinal,Cannabinoides,vomiting,nausea,chemotherapy,tumour,cancer,medical cannabis,Cannabinoids

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