Historical Background
The use of cannabis (hemp) as a useful and medicinal plant has a tradition dating back thousands of years. The use of cannabis was mentioned as early as nearly 5,000 years ago in Chinese medicine as a medicinal plant and was described in Egyptian, Greek, Indian, and Middle Eastern cultures (1). In Western medicine, William O’Shaughnessy published works in the mid-19th century on the effects of Indian hemp on healthy animals and in humans with conditions such as rheumatism, hydrophobia, cholera, tetanus, and infantile convulsions (2).
Chemical Composition and Pharmacological Effects
There are three subspecies of cannabis: Cannabis sativa, Cannabis indica, and Cannabis ruderalis. Cannabis sativa is the most widespread plant, cultivated for both commercial and pharmaceutical purposes (3).
Over 104 phytocannabinoids have been identified as active substances in the plant. The plant also contains terpenoids, flavonoids, nitrogen-containing compounds, and other complex plant molecules (4). Of pharmacological interest and well-studied are the plant’s two main constituents, delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD). In addition to THC and CBD, cannabinol and cannabichromene (CBC), cannabidivarin, delta-9-tetrahydrocannabivarin, and cannabigerol (CBG) are known and scientifically studied as additional phytocannabinoids. THC and CBD are poorly soluble in water but have good solubility in most organic solvents (5).
In recent decades, there has been widespread scientific interest in THC, which is characterized by high lipophilicity and rapid distribution in highly vascularized tissues (6).
THC is responsible for the psychoactive effects, as it acts as a partial agonist for type 1 cannabinoid receptors (CB1). CB1 receptors represent the largest group of ligand binding sites in the central nervous system, with expression in the cerebellum, brainstem, and limbic system (7), as well as in the gastrointestinal tract, on macrophages, mast cells, and keratinocytes (8).
CBD, on the other hand, exhibits very low affinity for CB1 and CB2 cannabinoid receptors (CBR1 and CBR2) (9). Experimental studies suggest that CBD can both activate and inhibit CBR1 via various mechanisms (10,11). CBD is also a agonist of serotonin 5-HT1A receptors (12) and Transient Receptor Potential Vanilloid Type 1 (TRPV1) receptors (13).
CBD is capable of enhancing the signaling effect of adenosine receptors by inhibiting the inactivation of adenosine, suggesting a potential therapeutic role in pain and inflammation (14).
Following the discovery of the skin’s endocannabinoid system (ECS), the two cannabinoid receptors CB1 and CB2 were found in epidermal keratinocytes, melanocytes, dermal cells, mast cells, sweat glands, hair follicles, and skin nerve fibers (15). These findings suggest that the ECS plays a crucial role in maintaining homeostasis, the skin’s barrier function, and the regulation of neuro-immuno-endocrine skin functions (16,17). Disruptions in the ECS appear to contribute to the development of skin diseases (18). Studies involving cannabinoid receptors, selective agonists, antagonists, and other regulatory agents capable of modulating endocannabinoid levels and effects in inflammatory processes have provided extensive evidence for the numerous immunomodulatory and anti-inflammatory effects of the ECS (19). The positive effects of topical cannabis application in dermatology cannot be attributed solely to phytocannabinoids. It is known that hemp seed oil, due to its high content of polyunsaturated fatty acids (PUFAs) (20) and its high levels of vitamins and minerals, such as vitamin E, provides good skin protection, reduces dryness, and slows the skin’s natural aging process (21).
Medical Applications
Definitions: Medical cannabis refers to preparations made from the constituents of the cannabis plant that are used for medical purposes. Cannabinoids are a heterogeneous group of substances that act on cannabinoid receptors. In addition to the plant’s natural constituents, this group also includes synthetic cannabinoids and endocannabinoids. Until now, the use of cannabinoids has been governed by the so-called “Cannabis Act” (Act Amending Narcotics and Other Regulations). It covers the prescription of cannabis in the form of dried flowers or extracts of standardized quality, as well as medications containing the active ingredients dronabinol or nabilone (Section 31(6), Sentence 1 of the German Social Code, Book V). With the current legal situation, a new situation has arisen since April 1, 2024, due in part to the removal of the classification as a narcotic (BTM) and the elimination of the associated regulations. Only nabilone (pure synthetic THC) remains subject to BTM regulations. The rules regarding the eligibility of cannabinoids for reimbursement have not changed:
Section 31(6) of Book V of the Social Code (SGB V) in full (excerpt)1:
Insured individuals with a serious illness are entitled to receive cannabis in the form of dried flowers, oral preparations, tea infusions, inhalation via a vaporizer (vaporizer), or extracts of standardized quality, as well as medications containing the active ingredients dronabinol or nabilone, provided that
1. a generally recognized treatment that meets medical standards
a) is not available, or
b) in individual cases, according to the reasoned assessment of the treating panel physician, cannot be used after weighing the expected side effects and taking into account the insured person’s medical condition,
2. there is a reasonable prospect of a noticeable positive effect on the course of the disease or on severe symptoms.
Any group of medical specialists may prescribe medical cannabis under these conditions. The following are approved for medical use:
Nabiximols (Sativex®): 2.5 mg CBD + 2.7 mg THC per spray, for the treatment of moderate to severe spasticity in adults with multiple sclerosis
Cannabidiol (Epidyolex®): 1 mL of solution = 100 mg CBD, for the adjunctive treatment of seizures associated with Lennox-Gastaut syndrome (LGS) or Dravet syndrome in combination with clobazam in patients aged 2 years and older.
Nabilone (Canemes®, Cesamet®): Synthetic THC, for the treatment of chemotherapy-induced emesis and nausea in cancer patients who do not respond adequately to other antiemetic treatments.
Dronabinol (Marinol®, Syndros®): Synthetic THC, used for cachexia/anorexia and loss of appetite in cancer or AIDS (approved in the U.S. and Canada).
Available over the counter:
Cannabis preparations, e.g., CBD oil in various concentrations (1–40%). Ointments or gels for topical application enriched with CBD.
A PubMed search (as of July 7, 2023) for scientific publications using the keyword “medical cannabis” yielded 13,219 references, of which 537 were clinical studies. The use of medical cannabis is primarily investigated for pain (including fibromyalgia syndrome, FMS), in palliative care, for insomnia, and for psychiatric disorders. There are 10 systematic reviews available under the keyword “medical cannabis AND fibromyalgia,” of which 6 deal with the use of cannabinoids in FMS. A search using the keywords “medical cannabis AND rheumatoid arthritis” yielded 44 results, including no clinical trials but two systematic reviews, one of which addresses chronic pain associated with rheumatic diseases (22). A literature analysis examines the use of cannabinoids in rheumatic diseases (23).
The keyword search “medical cannabis AND psoriatic arthritis” yielded two results. One of these is a review that addresses the use of complementary medicine in psoriatic arthritis, including the use of medical cannabis (24). The second publication addresses the use of phytocannabinoids in psoriasis vulgaris (25).
Further experimental studies have shown that cannabinoids have analgesic and anti-inflammatory effects in vitro and in vivo, which is of interest for their use in inflammatory rheumatic diseases. While some clinical studies have investigated the analgesic effects of cannabidiol (CBD), the anti-inflammatory effects have mainly been demonstrated in in vitro studies and preclinical animal models: The best data are available for CBD-induced suppression of cytokine production in vitro (26), for example: TNF-α (27), IFN-γ, IL-1α (28) (29), IL-6, and IL-17A (30,31). Other studies suggest reduced activity of NF-kB, which regulates the expression of pro-inflammatory genes, as well as upregulation of the STAT3 signaling pathway, which plays a role in anti-inflammation. In addition, a reduction in INF-β production and release has been reported for CBD and THC, which could be particularly significant in systemic lupus erythematosus (SLE) (32).
Early animal studies on collagen-induced arthritis report that CBD has immunosuppressive and anti-arthritic effects. The study by Malfait et al. demonstrated significant anti-arthritic effects in animal experiments following oral administration of 25 mg/kg of CBD per day; however, this would represent an unreasonably high daily dose for humans. An analysis of mouse knee synovial cells showed a reduction in interferons (IFN) and tumor necrosis factor (TNF) in cytokine assays (33). The anti-inflammatory and anti-arthritic effects were confirmed by further animal studies. The effect was considered promising, particularly because no psychoactive effects were detected (34).
A small clinical trial involving 58 patients shows that the use of an oral solution of a standardized cannabis medication containing CBD/THC (Sativex®) in patients with rheumatoid arthritis led to a significant improvement in pain during movement and at rest, as well as in the disease activity score (DAS28) (35). However, the CBD dose in this study was low compared to CBD doses used as monotherapy, e.g., for epilepsy. Therefore, the main effects in this study are likely mediated primarily by the THC component.
Further high-quality clinical studies are necessary to confirm the anti-inflammatory effects demonstrated in in vitro experiments in clinical settings. A meta-analysis published in 2021 in the * * evaluated 15 observational studies involving 10,873 rheumatology patients (RA, lupus, “arthritis,” FMS). The study determined the number of patients who had ever used cannabis or who continued to use it. These criteria applied to one in six patients. Six studies evaluated the effects of cannabis on pain (n = 1,079 patients). Compared to baseline, cannabis use was associated with a significant reduction in pain, as measured by the visual analog scale (VAS) (36). Two of the evaluated studies reported a significant improvement in quality of life and depression-related symptoms in FMS patients. Sleep disturbances also improved after cannabis use, though only significantly in one of these two studies. A systematic review evaluated studies on the use of cannabinoids for pain associated with FMS between 2015 and 2019. After critical evaluation, only five articles (in English, observational studies, and cohort analyses) were deemed relevant. Although the results suggest that medical cannabis could provide a safe and effective treatment for FMS pain, serious methodological limitations in the studies examined prevented a definitive recommendation for the use of cannabinoids in pain management for FMS patients (37). A recent review from 2023 confirms the previous findings. The analysis included four randomized controlled trials (RCTs) and five observational studies (a total of 564 patients) that examined the effects of cannabis on FMS symptoms. This systematic review found low-quality evidence supporting short-term pain relief from medical cannabis in FMS. The authors noted potential positive effects on quality of life, sleep quality, mood, libido, and appetite, but called for further studies to substantiate these findings (38).
An experimental randomized, placebo-controlled crossover study involving 20 FMS patients examined the short-term analgesic effects of inhaled medical cannabis with varying THC and CBD content. The study recorded pressure and electrical pain thresholds, spontaneous pain scores (on an 11-point visual analog scale, ranging from 0 = no pain to 10 = worst pain imaginable), and psychotropic effects over a 3-hour period. This study shows that inhaled cannabinoids produce only minor analgesic responses in chronic pain patients following a single inhalation. However, a higher proportion of subjects who received the cannabis strain Bediol (13.4 mg THC, 17.8 mg CBD; Bedrocan International BV, Veendam, the Netherlands) showed a 30% reduction in pain scores (90% versus 55% of placebo patients, P = 0.01) (39).
This study highlights the complex behavior of inhaled cannabinoids and the interaction between THC and CBD. Further studies are needed to determine the long-term effects of cannabinoid treatment and its psychotropic effects on pain relief.
A Canadian publication from 2023 reported that medical cannabis use among rheumatology patients in routine clinical care was twice as high as in the general population of similar age. This use was associated with more severe disease, pain, and prior recreational use (40).
There are no clinical studies on psoriatic arthritis (PsA), spondyloarthritis, or systemic rheumatic diseases. Analyses of a Canadian data collection involving 151 PsA patients show that 30% had used over-the-counter cannabis within the past year, with slightly more than half of them doing so for pain relief from arthritis. Compared to non-users, cannabis users were younger, had a shorter duration of PsA, and had poorer mental health, as measured by the SF-36. Respondents cited the benefits of cannabis use in aiding sleep and relieving arthritis pain (41).
It should be noted, however, that the duration of treatment, adverse effects, long-term follow-up, and potential for dependence require further investigation. Various forms of medical cannabis administration were examined in the different studies; therefore, no specific recommendation can (yet) be made regarding which form of administration is most suitable.
The German Cannabis Companion Survey (04/2017–03/2022), published in 2022, included 16,809 complete data sets in its analysis (42). In 73% of cases, medical cannabis was prescribed for pain; in 10% for the treatment of spasticity; in 6% for the treatment of wasting/anorexia; and in 10% for other conditions. Malignant neoplasms were present in 18% of patients. The documented proportion of diagnoses involving explicitly inflammatory rheumatic diseases is small at 2.6% (FMS n=307, ankylosing spondylitis n=53, RA n=82). Nearly 75% of patients reported an improvement in their symptoms following the use of cannabis-based medications. Side effects were common but generally mild. Fatigue and dizziness (especially in women) occurred very frequently. In one-third of patients, treatment was discontinued before one year had elapsed, mainly due to a lack of effect (38.5%). In just under 26% of cases, side effects were the reason for discontinuation, and in 20%, the death of the patient. In 70% of cases, an improvement in quality of life was reported. Patients treated with cannabis flowers generally rate the success of the therapy higher, discontinue treatment less frequently, and report side effects less often than when using conventional cannabis-based medications, such as Sativex®. When using cannabis flowers, the side effect “euphoric effect” was reported three times more frequently than with cannabis-based medications2.
Data from clinical trials using high-dose CBD (Epidyolex®) for the treatment of epilepsy and psychiatric disorders indicate CBD-induced drug interactions, liver abnormalities, diarrhea, fatigue, vomiting, and drowsiness (43). Drugs such as rifampicin, carbamazepine, or St. John’s wort can lower plasma levels of CBD by inducing CYP3A4/2C9. Furthermore, the Epidyolex® prescribing information notes clinically significant interactions when CBD is used concomitantly with, for example, warfarin, omeprazole, propofol, and lorazepam3. The prescribing information for Sativex® also notes potential drug interactions, e.g., with ketoconazole, ritonavir, clarithromycin, or fluconazole, and recommends corresponding dose titration.
Data from clinical use are available for neurological indications such as multiple sclerosis. A systematic literature review (41 clinical studies, n=4,550) evaluates the efficacy and safety profile of medical cannabis (44).
Furthermore, prolonged use of cannabinoids has been associated with the development of dependence. In predisposed individuals, an increased risk of psychotic disorders (somatization, depression, anxiety, phobic anxiety, irritability, paranoid thoughts, and psychosis) was observed (45,46). The review analysis was limited by the fact that only a minority of the studies recorded serious adverse events.
Medical cannabis also has a potential for dependence, similar to opioids used in analgesic therapy (46,47). In their long-term observational study involving 180 chronic pain patients, Takakuwa et al. (2020) found that medical cannabis can reduce the use of prescription opioids and serves as the preferred alternative to prescription opioids for more than half of the patients (48).
There is insufficient scientific evidence from clinical trials regarding medical cannabis to justify explicit prescription for a defined inflammatory rheumatic disease for disease modification or symptomatic therapy. Positive data are available from the treatment of patients with chronic pain and neurological disorders regarding its use for (primarily neuropathic) pain, sleep disorders, and improving quality of life. In individual cases, these may justify its use in selected patients with rheumatic diseases as part of a comprehensive therapeutic approach. Prescription may then be considered within the legal framework governing prescribability (Section 31(6) of Book V of the Social Code).
It should be noted, however, that data on dosage, long-term effects, and side effects are insufficient. The potential for dependence should be taken into account. In cases of chronic pain, opioid reduction can be achieved with medical cannabis. Prescribing physicians and patients should be informed about the side effect profile and drug interactions.
1. Friedman D, Sirven JI. Historical perspective on the medical use of cannabis for epilepsy: Ancient times to the 1980s. Epilepsy Behav 2017;70:298–301.
2. O’Shaughnessy WB. Extract from a memoir on the preparations of Indian hemp, or gunjah, [Cannabis indica], their effects on the animal system in health, and their utility in the treatment of tetanus and other convulsive diseases. J Asiat Soc Bengal 1839;93:732–45.
3. Andre CM, Hausman JF, Guerriero G. Cannabis Sativa: The Plant Of The Thousand And One. Front Plant Sci. 2016 Feb 4;7:19. Front Plant Sci. 2016 Feb 4;7:19.
4. El Sohly, M. A., and W. Gul. 2014. Constituents of Cannabis sativa. In Handbook of Cannabis. Oxford, UK: Oxford University Press. P. 20.
5. Hanus, L.O.; Meyer, S.M.; Munoz, E.; Taglialatela-Scafati, O.; Appendino, G. Phytocannabinoids: A unified critical inventory. Nat. Prod. Rep. 2016, 33, 1357–1392.
6. Bloomfield, M.A.P.; Hindocha, C.; Green, S.F.; Wall, M.B.; Lees, R.; Petrilli, K.; Costello, H.; Olabisi Ogunbiyi, M.; Bossong, M.G.; Freeman, T.P. The neuropsychopharmacology of cannabis: A review of human imaging studies. Pharmacol. Ther. 2019, 195, 132–161.
7. Pertwee RG. The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: delta-9-tetrahydrocannabinol, cannabidiol, and delta-9-tetrahydrocannabivarin. Br J Pharmacol. 2008 Jan;153(2):199-215. doi: 10.1038/sj.bjp.0707442. Epub 2007 Sep 10.
8. Mackie, K. 2006. Cannabinoid receptors as therapeutic targets. Annual Review of Pharmacology and Toxicology 46:101–122.
9. Thomas, A., G. L. Baillie, A. M. Phillips, R. K. Razdan, R. A. Ross, and R. G. Pertwee. 2007. Cannabidiol displays unexpectedly high potency as an antagonist of CB1 and CB2 receptor agonists in vitro. British Journal of Pharmacology 150(5):613–623.
10. Laprairie, R. B., A. M. Bagher, M. E. Kelly, and E. M. Denovan-Wright. 2015. Cannabidiol is a negative allosteric modulator of the cannabinoid CB1 receptor. British Journal of Pharmacology 172(20):4790–4805.
11. De Petrocellis L, Ligresti A, Moriello AS, Allarà M, Bisogno T, Petrosino S, Stott CG, Di Marzo V. Effects of cannabinoids and cannabinoid-enriched Cannabis extracts on TRP channels and endocannabinoid metabolic enzymes. Br J Pharmacol. 2011 Aug;163(7):1479-94. doi: 10.1111/j.1476-5381.2010.01166.x. PMID: 21175579; PMCID: PMC3165957.
12. Sonego, A.B.; Gomes, F.V.; Del Bel, E.A.; Guimaraes, F.S. Cannabidiol attenuates haloperidol-induced catalepsy and c-Fos protein expression in the dorsolateral striatum via 5-HT1A receptors in mice. Behav. Brain Res. 2016, 309, 22–28.
13. Hassan, S.; Eldeeb, K.; Millns, P.J.; Bennett, A.J.; Alexander, S.P.; Kendall, D.A. Cannabidiol enhances microglial phagocytosis via transient receptor potential (TRP) channel activation. Br. J. Pharmacol. 2014, 171, 2426–2439.
14. Carrier EJ, Auchampach JA, Hillard CJ. Inhibition of an equilibrative nucleoside transporter by cannabidiol: a mechanism of cannabinoid immunosuppression. Proc Natl Acad Sci U S A. 2006 May 16;103(20):7895-900. doi: 10.1073/pnas.0511232103. Epub 2006 May 3. PMID: 16672367; PMCID: PMC1472541.
15. Ständer, S.; Schmelz, M.; Metze, D.; Luger, T.; Rukwied, R. Distribution of cannabinoid receptor 1 (CB1) and 2 (CB2) on sensory nerve fibers and adnexal structures in human skin. J. Dermatol. Sci. 2005, 38, 177–188.
16. Scheau, C.; Badarau, I.A.; Mihai, L.-G.; Scheau, A.-E.; Costache, D.O.; Constantin, C.; Calina, D.; Caruntu, C.; Costache, R.S.; Caruntu, A. Cannabinoids in the pathophysiology of skin inflammation. Molecules 2020, 25, 652.
17. Cintosun, A.; Lara-Corrales, I.; Pope, E. Mechanisms of cannabinoids and potential applicability to skin diseases. Clin. Drug Investig. 2020, 40, 293–304.
18. Bíró, T.; Tóth, B.I.; Haskó, G.; Paus, R.; Pacher, P. The endocannabinoid system of the skin in health and disease: Novel perspectives and therapeutic opportunities. Trends Pharmacol. Sci. 2009, 30, 411–420.)
19. Sheriff, T.; Lin, M.J.; Dubin, D.; Khorasani, H. The potential role of cannabinoids in dermatology. J. Dermatolog. Treat. 2020, 31, 839–845.
20. Callaway, J.C. Hempseed as a nutritional resource: An overview. Euphytica 2004, 140, 65–72.
21. Vaughn, A.R.; Clark, A.K.; Sivamani, R.K.; Shi, V.Y. Natural oils for skin-barrier repair: Ancient compounds now backed by modern science. Am. J. Clin. Dermatol. 2018, 19, 103–117.
22. Fitzcharles MA, Baerwald C, Ablin J, Häuser W. Efficacy, tolerability, and safety of cannabinoids in chronic pain associated with rheumatic diseases (fibromyalgia syndrome, back pain, osteoarthritis, rheumatoid arthritis): A systematic review of randomized controlled trials. Schmerz. 2016 Feb;30(1):47-61. doi: 10.1007/s00482-015-0084-3. PMID: 26767993.
23. Fitzcharles MA, Ste-Marie PA, Häuser W, Clauw DJ, Jamal S, Karsh J, Landry T, Leclercq S, Mcdougall JJ, Shir Y, Shojania K, Walsh Z. Efficacy, Tolerability, and Safety of Cannabinoid Treatments in Rheumatic Diseases: A Systematic Review of Randomized Controlled Trials. Arthritis Care Res (Hoboken). May 2016;68(5):681-8. doi: 10.1002/acr.22727. PMID: 26548380.
24. Roberts JA 4th, Mandl LA. Complementary and Alternative Medicine Use in Psoriatic Arthritis Patients: a Review. Curr Rheumatol Rep. 2020 Sep 28;22(11):81. doi: 10.1007/s11926-020-00956-x. PMID: 32989481.
25. Wroński A, Jarocka-Karpowicz I, Stasiewicz A, Skrzydlewska E. Phytocannabinoids in the Pharmacotherapy of Psoriasis. Molecules. 2023 Jan 25;28(3):1192. doi: 10.3390/molecules28031192. PMID: 36770858; PMCID: PMC9920113.
26. Watzl B, Scuderi P, Watson RR. Marijuana components stimulate human peripheral blood mononuclear cell secretion of interferon-gamma and suppress interleukin-1 alpha in vitro. Int J Immunopharmacol. 1991;13: 1091-1097.
27. Hobbs JM, Vazquez AR, Remijan ND, Trotter RE, et al. Evaluation of pharmacokinetics and acute anti-inflammatory potential of two oral cannabidiol preparations in healthy adults. Phytotherapy Research. 2020;1-8.
28. Kaplan BL, Springs AE, Kaminski NE. The profile of immune modulation by cannabidiol (CBD) involves deregulation of nuclear factor of activated T cells (NFAT). Biochem Pharmacol. 2008;76:726737.
29. Ki Hoon Han, Sunny Lim, Jewon Ryu, Cheol-Whan Lee, Yuna Kim, Ju-Hee Kang, Soon-Suk Kang, Yeong Ki Ahn, Chan-Sik Park, Jae Joong Kim. CB1 and CB2 cannabinoid receptors differentially regulate the production of reactive oxygen species by macrophages. Cardiovascular Research, Volume 84, Issue 3, December 1, 2009, pp. 378–386.
30. Nichols MJ, Kaplan Barbara LF. Immune Responses Regulated by Cannabidiol. Cannabis and Cannabinoid Research. Volume 5, Number 1, 2020, pp. 12–31.
31. Kozela E, Juknat A, Kaushansky N, Rimmermann N, Ben-Hun A, Vogel Z. Cannabinoids decrease the TH17 inflammatory autoimmune phenotype. J Neuroimmune Pharmacol (2013) 8:1265-1276.
32. Kozela E, Pietr M, Rimmerman AJ, Levy R, Vogel Z. Cannabinoids Delta-9-Tetrahydrocannabinol and Cannabidiol Differentially Inhibit the Lipopolysaccharide-activated NF-KB and Interferon-γ/STAT - Proinflammatory Pathways in BV-2 Microglial Cells. The Journal of Biological Chemistry. Vol. 285, No. 3, pp. 1616–1626, January 15, 2010.
33. Malfait A. M., Gallily R., Sumariwalla P. F., Malik A. S., Andreakos E., Mechoulam R., Feldmann M.. The nonpsychoactive cannabis constituent cannabidiol is an oral anti-arthritic therapeutic in murine collagen-induced arthritis. Proceedings of the National Academy of Sciences Aug 2000, 97 (17) 9561-9566; DOI: 10.1073/pnas.16010589.
34. Sumariwalla PF, Gallily R, Tchilibon S, Fride E, Mechoulam R, Feldmann M. A novel synthetic, nonpsychoactive cannabinoid acid (HU-320) with anti-inflammatory properties in murine collagen-induced arthritis. Arthritis Rheum. 2004 Mar;50(3):985-98. doi: 10.1002/art.20050. PMID: 15022343.
35. Blake DR, Robson P, Ho M, Jubb RW, McCabe CS. Preliminary assessment of the efficacy, tolerability, and safety of a cannabis-based medicine (Sativex) in the treatment of pain caused by rheumatoid arthritis. Rheumatology 2006; 45: 50–2.
36. M Guillouard et al., Cannabis use assessment and its impact on pain in rheumatologic diseases: a systematic review and meta-analysis, Rheumatology, Volume 60, Issue 2, February 2021, Pages 549– 556, doi.org/10.1093/rheumatology/keaa534https://doi.org/10.1093/rheumatology/keaa534
37. Cameron EC, Hemingway SL. Cannabinoids for fibromyalgia pain: a critical review of recent studies (2015–2019). J Cannabis Res. 2020 May 29;2(1):19. doi: 10.1186/s42238-020-00024-2. PMID: 33526114; PMCID: PMC7819299.
38. Strand NH, Maloney J, Kraus M, Wie C, Turkiewicz M, Gomez DA, Adeleye O, Harbell MW. Cannabis for the Treatment of Fibromyalgia: A Systematic Review. Biomedicines. 2023 Jun 2;11(6):1621. doi: 10.3390/biomedicines11061621. PMID: 37371716; PMCID: PMC10295750.
39. van de Donk T, Niesters M, Kowal MA, Olofsen E, Dahan A, van Velzen M. An experimental randomized study on the analgesic effects of pharmaceutical-grade cannabis in chronic pain patients with fibromyalgia. Pain. 2019 Apr;160(4):860-869. doi: 10.1097/j.pain.0000000000001464. PMID: 30585986; PMCID: PMC6430597.
40. Rampakakis E, Thorne C, Cesta A, Movahedi M, Li X, Mously C, Ahluwalia V, Brophy J, Ciaschini P, Keystone E, Lau A, Major G, Pavlova V, Pope JE, Bombardier C. Medical cannabis use by rheumatology patients in routine clinical care: results from The Ontario Best Practices Research Initiative. Clin Exp Rheumatol. 2023 Jan;41(1):118-125. doi: 10.55563/clinexprheumatol/b85xu5. Epub 2022 May 23. PMID: 35616591.
41. Tsang, J., Silverberg, O., Machhar, R. et al. Exploring cannabis use and perspectives among patients with psoriatic disease. Clin Rheumatol 41, 1431–1437 (2022). doi.org/10.1007/s10067-022-06066-6
42. Schmidt-Wolf, G., Cremer-Schaeffer, P. 3 Years of Cannabis as Medicine – Interim Results of the Cannabis Companion Survey. Bundesgesundheitsbl 64, 368–377 (2021). doi.org/10.1007/s00103-021-03285-1.
43. Huestis MA, Solimini R, Pichini S, Pacifici R, Carlier J, Busardò FP. Cannabidiol Adverse Effects and Toxicity. Curr Neuropharmacol. 2019;17(10):974-989. doi: 10.2174/1570159X17666190603171901. PMID: 31161980; PMCID: PMC7052834.
44. Amato L, Minozzi S, Mitrova Z, Parmelli E, Saulle R, Cruciani F, Vecchi S, Davoli M. Systematic review of the therapeutic efficacy and safety of cannabis in patients with multiple sclerosis, chronic neuropathic pain, and in oncology patients undergoing chemotherapy. Epidemiol Prev. 2017 Sep-Dec;41(5-6):279-293. Italian. doi: 10.19191/EP17.5-6.AD01.069. PMID: 29119763.
45. Hall W, Degenhardt L. Adverse health effects of non-medical cannabis use. Lancet 2009;374(9698):1383-91.
46. Schlag AK, Hindocha C, Zafar R, Nutt DJ, Curran HV. Cannabis-based medicines and cannabis dependence: A critical review of issues and evidence. Journal of Psychopharmacology. 2021;35(7):773-785. doi:10.1177/0269881120986393
47. Edlund MJ, Martin BC, Russo JE, et al. (2014) The role of opioid prescription in incident opioid abuse and dependence among individuals with chronic noncancer pain: The role of opioid prescription. Clin J Pain 30: 557–564.
48. Takakuwa K, Hergenrather J, Shofer F, et al. (2020) The impact of medical cannabis on intermittent and chronic opioid users with back pain: How cannabis diminished prescription opioid usage. Cannabis Cannabinoid Res 5: 263–270.
1 www.gesetze-im-internet.de/sgb_5/__31.html (accessed on 04/14/2024)
2 www.bfarm.de/cannabis-begleiterhebung (accessed on April 29, 2024)
3 www.epidyolex.de/sites/default/files/documents/14394_EDY_GER_LD_XX_Fachinformation. pdf (accessed on April 29, 2024)
4 pp.jazzpharma.com/pi/sativex.ch.PI-de.pdf (accessed on April 29, 2024
Last updated: September 28, 2024