BackgroundThere are no determined treatment agents for the severe coronavirus disease 2019 (COVID-19); therefore, it is suggested that methylprednisolone, as an immunosuppressive treatment, can reduce the inflammation of the respiratory system.MethodsWe conducted a single-blind, randomised, controlled, clinical trial involving severe hospitalised patients with confirmed COVID-19 at the early pulmonary phase of the illness in Iran. The patients were randomly allocated in a 1:1 ratio by block randomisation method to receive standard care with methylprednisolone pulse (intravenous injection, 250 mg·day−1 for 3 days) or standard care alone. The study endpoint was the time of clinical improvement or death, whichever came first. Primary and safety analysis was done in the intention-to-treat (ITT) population.ResultsSixty-eight eligible patients underwent randomisation (34 patients in each group) from April 20, till Jun 20, 2020. In the standard care group, six patients received corticosteroids by the attending physician during treatment and excluded from the ITT population. Patients with clinical improvement were higher in the methylprednisolone group than in the standard care group (94·1% versus 57·1%), and the mortality rate was numerically lower in the methylprednisolone group (5·9% versus 42.9%; p <0·001). We demonstrated that patients in the methylprednisolone intervention group had a significantly increased survival time compared with the patients in the standard care group [Log rank test: p<0.001; Hazard ratio: 0.293; 95% CI: 0.154–0.556]. A total of two patients in each group (5·8% and 7·1% respectively) showed severe adverse events between initiation of treatment and the end of the study.ConclusionsOur results suggested that methylprednisolone pulse could be an efficient therapeutic agent for hospitalised severe COVID-19 patients at the pulmonary phase.
Aim: To calculate the epidemiology of Rheumatic Diseases in Iran. Materials and Methods:The data of Tehran, Zahedan, Sanandaj (urban) and Tuyserkan (rural) stage Community Oriented Program for the Control of Rheumatic Diseases (COPCORD) studies were gathered. The data were adjusted to the population number of the studied areas to represent Iran.Results: The population of Iran is 75 149 669 (71.5% urban areas, males 50.4%) and of the mentioned area were respectively 10 000 000, 580 071, 311 444 and 109 262. The interviewed subjects were 10 291, 1565, 2100 and 5830. Male/female ratio was 0.9/1, 0.8/1, 08/1 and 0.8/1.Musculoskeletal complaints during the past 7 days (people aged ≥ 15 years) were detected in 44.7% of subjects. They were: shoulder 15.6%, wrist 10.4%, hands and fingers 10.2%, hip 8.3%, knee 27.4%, ankle 12.3%, toes 6.2%, cervical spine 14.2% and dorsolumbar spine 23.7%. Osteoarthritis (OA) was detected in 16.9%: knee 15.5%, hands 2.9% and hip 0.32%. Low back pain was found in 15.7%, sciatica in 0.94%, and soft tissue rheumatism in 4.6% (shoulder tenosynovitis 2.5%, frozen shoulder 0.56%, tennis elbow 1.2%, golf elbow 0.48%, de Quervain tenosynovitis 0.24%, trigger finger 0.2%, carpal tunnel syndrome 1.3%). Rheumatoid arthritis was detected in 0.37%, seronegative spondyloarthropathy in 0.24%, ankylosing spondylitis in 0.12%, systemic lupus erythematosus in 0.06%, Behcet's disease in 0.08%, fibromyalgia in 0.79% and gout in 0.13%. Conclusion:Compared to other COPCORD reports (17 countries), Iran gets the following rank: musculoskeletal complaints second, low back pain fourth, osteoarthritis second, knee osteoarthritis third, soft tissue rheumatism sixth, rheumatoid arthritis tenth, seronegative spondyloarthropathies fifth, gout eleventh and fibromyalgia fifth.
Swelling and the progressive destruction of articular cartilage are major characteristics of rheumatoid arthritis (RA), a systemic autoimmune disease that directly affects the synovial joints and often causes severe disability in the affected positions. Recent studies have shown that type B synoviocytes, which are also called fibroblast-like synoviocytes (FLSs), as the most commonly and chiefly resident cells, play a crucial role in early-onset and disease progression by producing various mediators. During the pathogenesis of RA, the FLSs’ phenotype is altered, and represent invasive behavior similar to that observed in tumor conditions. Modified and stressful microenvironment by FLSs leads to the recruitment of other immune cells and, eventually, pannus formation. The origins of this cancerous phenotype stem fundamentally from the significant metabolic changes in glucose, lipids, and oxygen metabolism pathways. Moreover, the genetic abnormalities and epigenetic alterations have recently been implicated in cancer-like behaviors of RA FLSs. In this review, we will focus on the mechanisms underlying the transformation of FLSs to a cancer-like phenotype during RA. A comprehensive understanding of these mechanisms may lead to devising more effective and targeted treatment strategies.
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