Current Opinion in Rheumatology

An increasing number of patients with rheumatoid arthritis (RA) are using cannabis to treat their symptoms, although systematic studies regarding efficacy in RA are lacking. Within this review we will give an overview on the overall effects of cannabinoids in inflammation and why they might be useful in the treatment of RA.

Peripherally, cannabinoids show anti-inflammatory effects by activating cannabinoid type 2 receptors (CB₂) which decrease cytokine production and immune cell mobilization. In contrast, cannabinoid type 1 receptor (CB₁) activation on immune cells is proinflammatory while CB₁ antagonism provides anti-inflammatory effects by increasing β₂-adrenergic signaling in the joint and secondary lymphoid organs. In addition, the nonpsychotropic cannabinoid, cannabidiol (CBD) demonstrated antiarthritic effects independent of cannabinoid receptors. In addition to controlling inflammation, cannabinoids reduce pain by activating central and peripheral CB₁, peripheral CB₂ receptors and CBD-sensitive noncannabinoid receptor targets.

Cannabinoids might be a suitable treatment for RA, but it is important to target the right receptors in the right place. For clinical studies, we propose a combination of a CB₂ agonist to decrease cytokine production, a peripheral CB₁ antagonist to prevent detrimental CB₁ signaling and to support anti-inflammatory effects of CB₂ via activation of β₂-adrenergic receptors and CBD to induce cannabinoid-receptor-independent anti-inflammatory effects.

The purpose of this review is to provide an update concerning recent advances in the evidence- based study of serious infections in patients with rheumatoid arthritis (RA) treated with biological drugs or conventional disease-modifying antirheumatic drugs (DMARDs), concentrating on studies published in the last 18 months.

New studies have further strengthened existing evidence relating the use of biological drugs to serious infections. The risk does not seem to be any different with short-term or long-term use. There is still a lack of conclusive studies identifying biomarkers, but it is plausible that the drugs have direct effects on cytokines and cell activity and then serious infections.

The frequent infections of patients with RA may be due to the disease itself (altered immunological function, disability, immobility, joint surgery), extra-articular manifestations or DMARDs, immunosuppressants and steroids. The use of biological drugs lead to the development of serious infections including tuberculosis. Patients should be informed of their increased risk, and physicians need to be aware of these complications and how to treat them.

The purpose of this review is to highlight recent studies of osteoarthritis epidemiology, including research on prevalence, disease impact, and potential risk factors.

Osteoarthritis is highly prevalent in the United States and around the globe. It is a leading cause of disability and can negatively impact people's physical and mental well being. Healthcare resources and costs associated with managing the disease can be substantial. There is increasing evidence that there are different osteoarthritis phenotypes that reflect different mechanisms of the disease. Various person-level risk factors are recognized, including sociodemographic characteristics (e.g. female sex, African-American race), genetic predispositions, obesity, diet-related factors, and high bone density/mass. Joint-level risk factors include specific bone/joint shapes, thigh flexor muscle weakness, joint malalignment, participation in certain occupational/sports activities, and joint injury. Recent studies have enhanced our understanding of preradiographic lesions associated with osteoarthritis.

Application of these new findings may allow us to develop innovative strategies and novel therapies with the purpose of preventing new disease onset and minimizing disease progression.

To give an overview of recently published articles covering therapeutic drug monitoring (TDM) of biological DMARDs (bDMARDs) in rheumatoid arthritis.

In the last 18 months, two clinical studies and nine reviews were found after a systematic literature search. Most (narrative) reviews conclude that TDM should be used to improve biological treatment in rheumatoid arthritis patients, whereas most of the clinical studies (including 13 studies identified earlier) whenever scrutinized do not support this conclusion. This disconnect between sobering data from prediction studies and test-treatment diagnostic studies and optimistic TDM beliefs in reviews is caused by failure to recognize incorrect study designs, false positives because of lack of validation after explorative multiple testing, cherry picking of studies, and incorrect interpretation of test characteristics.

Serum (anti)-drug level monitoring has been extensively studied in rheumatoid arthritis, but correctly designed and executed interventional prediction studies or test-treatment intervention studies are sparse and mostly negative. In contrast, many reviews advocate use of biological TDM in rheumatoid arthritis. On the basis of current evidence, therapeutic drug monitoring of biologicals cannot be recommended in the treatment of rheumatoid arthritis patients, although two clinical scenarios deserve further study.