Glucocorticoids (GC) have immunosuppressive effects by the following mechanisms: (1) anti-inflammatory effects through down-regulation of pro-inflammatory factors and up-regulation of inhibitory pro-inflammatory factors; (2) changes in the number and distribution of lymphocytes through inhibition of macrophage phagocytosis and processing of antigens; (3) interference with and blockage of lymphocyte recognition, obstruction of complement components from attaching to the cell surface, and inhibition of inflammatory factor production. thereby inhibiting the antibody response. It is because of its powerful anti-inflammatory effects that it has an unassailable position in the treatment of rheumatic immune diseases, especially in patients with multi-organ damage. However, many clinicians have a love-hate relationship with GC because of its potential to cause various adverse reactions, calling it a “double-edged sword”. Therefore, it requires rheumatologists to have a more comprehensive and scientific understanding of GC. Here, we will briefly introduce the recent international research on the use of GC in rheumatologic diseases. 1. GC and polymyositis It is effective for most patients with polymyositis (PM). However, the effect of GC on catabolism can disrupt the balance of amino acid metabolism in muscle, leading to elevated serum amino acid levels, especially branched-chain amino acids, leading to steroidal myopathy, increased muscle weakness and disability, and inadequate intake due to swallowing dysfunction. Giving nutritional interventions, especially branched-chain amino acid supplementation as an adjunctive treatment against myositis, will help to improve the symptoms of muscle weakness and improve the activity of daily life. 2. GC and rheumatoid arthritis In a study of increased mortality in patients with rheumatoid arthritis (RA) in relation to the cumulative dose threshold of GC, a total of 779 patients with RA were included. The mortality rate during the study period was 3.2%, including 1.8% due to cardiovascular events. The increase in mortality was dose-dependent with GC. The lowest daily prednisone dose threshold for increased all-cause mortality was 8-15 mg compared with patients not treated with GC. for cumulative doses of GC, the lowest dosage associated with all-cause mortality was 40 g. These findings may help clinicians select more appropriate doses for treating patients with RA. In a prospective cohort (n=353) study, however, the views were quite different. Previous and current use of GC was indeed associated with cardiovascular event-relatedness, which was related to duration of use and cumulative dose. However after adjusting for disease activity and severity, this association was negated. This means that the occurrence of cardiovascular events in RA patients using GC is inseparable from disease activity. the adverse cardiovascular effects of GC may be in a balance due to its positive effect in controlling inflammation. Another study (n=76) found that methotrexate (MTX) plus low-dose hormones remained an effective treatment option for RA from a “target control” perspective. All patients with RA were given MTX 15 mg/week, folic acid 5 mg/week and prednisone (no more than 10 mg/d) orally. The main adverse reactions were liver injury, abdominal pain, bloating and acid reflux rates, nausea, alopecia, herpes zoster and lung infection; no serious adverse events were observed. In another study evaluating factors that hinder physical activity in RA patients, the effect of GC on physical activity aspects in RA patients was also evaluated. GC was identified as an independent risk factor in the multivariate analysis. Regarding the use of prednisone extended-release agents in RA, recent studies suggest that low-dose nocturnal prednisone extended-release use is effective in counteracting elevated levels of pro-inflammatory factors that contribute to disease activity. Increasing the average duration of morning stiffness was largely reduced by nocturnal prednisone extended-release therapy versus morning dosing. In an observational study of RA from a diverse population, it was found that. Prednisone extended-release treatment given at night for 12 months was generally well tolerated, similar to placebo or morning dose prednisone given at night, and no new safety concerns were identified. In the UK pharmacoeconomic model, prednisone extended-release was assessed to have better economic benefits relative to fast-acting prednisone. 3. The sensitivity of GC to SLE can be measured in vitro with lymphocyte sensitivity (LSA). However, its clinical value in systemic lupus erythematosus (SLE) has not been determined. In a recent comparative study of GC sensitivity in SLE patients, the results of the LSA assay were clinically consistent, suggesting that the LSA assay, which can help determine whether SLE patients are resistant to GC, could help in the early selection of other immunosuppressive agents to replace therapy. One study found a significantly increased risk of fracture in SLE patients compared to controls, and the risk increased further with the duration of the disease. 6 months of GC use increased the incidence of fracture. And cerebrovascular events, epilepsy and the pre-existing osteoporosis can be used as predictors of fracture. 4. GC and osteoporosis The osteoporosis caused by GC is complex, and the study of exogenous and endogenous GC can better understand this disease and guide treatment and prevention. GC has a negative impact on bone through its indirect effects on bone cells and on calcium absorption. However, much of the relevant knowledge comes from understanding patients treated with exogenous steroids. In contrast, endogenous GC overproduction or underproduction may also have an impact on osteoporosis. An in-depth understanding of the mechanisms involved would be beneficial in the use of endogenous GC for the treatment of corresponding osteoporosis. 5. GC and tendinopathy Local application of GC has significant negative effects on tendon cells in vitro, including cell viability, cell proliferation and collagen synthesis. Similar to the in vivo test results, there was also collagen destruction and necrosis. The mechanical contractile function of the tendon was also significantly reduced. The clinical evidence that has emerged suggests that intravenous GC has a significant long-term effect on tendon tissue and cells. 6. GC use and patient compliance Although it has been widely used in clinical practice since 1948, the optimal treatment regimen is still controversial. Patients also have some concerns about the side effects of GC. Many factors adversely affect adherence to treatment. In a recent survey involving 85 residents from various departments and 125 patients receiving long-term GC treatment and follow-up, it was found that physicians often consider abnormal weight gain as the most problematic adverse effect, but underestimate the presence of psychiatric adverse effects in patients receiving long-term GC treatment, which seriously affects patient compliance. In contrast, regular follow-up given during treatment, timely detection and active management of adverse reactions in all systems may improve patient compliance with treatment.