The idiopathic inflammatory myopathies are characterized by chronic muscle inflammation and involvement of internal organs, which contribute considerably to the morbidity and mortality of the disease. We conducted the current study to determine the survival data for patients with idiopathic inflammatory myopathies according to the presence of extramuscular clinical manifestations. We also determined the cumulative survival probability and the long-term prognosis and analyzed the causes of death at a single clinical immunology center.A survival analysis was performed using data for 162 patients diagnosed between 1976 and 1997 according to Bohan and Peter's criteria. Patients were followed up for a minimum of 5 years (median, 101.5 mo) or to date of death. Cumulative survival probability was calculated by the Kaplan-Meier method. The influence of extraskeletal and extramuscular involvement was analyzed as prognostic factors for death by Cox proportional hazards survival model. Eighteen disease-specific deaths occurred; pulmonary and cardiac complications were the most frequent causes of death. Global survival rates were 95%, 92%, and 89% for 1, 5, and 10 years, respectively. Analysis for clinicopathologic subgroups revealed that cancer-associated myositis had the worst prognosis, while juvenile and overlap myositis had the best prognosis. Five- and 10-year survival rates were 94.2% and 89.4% for patients with primary polymyositis and 90.1% and 86.4% for primary dermatomyositis patients, respectively. In the whole group of patients with idiopathic inflammatory myopathy, cardiac (p < 0.01) and respiratory muscle involvement (p = 0.045) were significant prognostic factors for death. In the group of patients with primary polymyositis/dermatomyositis, cardiac involvement was the main prognostic factor for death (p < 0.01). Myositis patients described in this study have higher survival rates than reported previously worldwide. We examine the reasons for the differences between the data in the current study and the available survival data in the relevant literature.

Vitamin D, besides having well‐known control functions of calcium and phosphorus metabolism, bone formation and mineralization, also has a role in the maintenance of immune‐homeostasis. The immune‐regulatory role of vitamin D affects both the innate and adaptive immune system contributing to the immune‐tolerance of self‐structures. Impaired vitamin D supply/regulation, amongst other factors, leads to the development of autoimmune processes in animal models of various autoimmune diseases. The administration of vitamin D in these animals leads to improvement of immune‐mediated symptoms. Moreover, in human autoimmune diseases, such as multiple sclerosis, or rheumatoid arthritis the pathogenic role of vitamin D has been described. The review aims at describing the complex immune‐regulatory role of vitamin D from the cellular level through autoimmune animal models and depicting the known contribution of vitamin D in the pathogenesis of human autoimmune diseases.

There is an impairment of endothelium-dependent vasodilatation indicated by low FMD in SSc. At the same time, the endothelium-independent dilatation assessed by NMD is still preserved giving an opportunity of nitroglycerine therapy. Carotid atherosclerosis indicated by ccIMT may occur at higher ages and after longer disease duration. Thus, the assessment of FMD in the pre-atherosclerotic stage may have a beneficial diagnostic, prognostic and therapeutic relevance.