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BACKGROUND: The COVID-19 pandemic poses a particular threat to patients suffering from immunoinflammatory rheumatic diseases. New coronavirus infection has been found to be accompanied by the development of a wide range of extrapulmonary clinical and laboratory manifestations, which are characteristic of a number of immunoinflammatory rheumatic diseases. AIM: To evaluate the features of the clinical course of immunoinflammatory rheumatic diseases in patients who underwent new coronavirus infection. MATERIALS AND METHODS: The clinical course of immunoinflammatory rheumatic diseases was analyzed in 324 patients who underwent new coronavirus infection from March 2020 to February 2021 and were treated at the Clinical Rheumatology Hospital No. 25, Saint Petersburg, for exacerbation of the underlying disease. RESULTS: Analysis showed that the risk factors for severe new coronavirus infection in patients with immunoinflammatory rheumatic diseases were: age over 60, comorbidities, use of prednisolone in a dose greater than 12,5 mg, and ESR values 40 mm/hour before the development of new coronavirus infection. There was no effect of immunosuppressive and biological therapy on the severity of the course of viral infection. There was no effect of immunosuppressive therapy and biological therapy on the severity of the course of viral infection in patients with immunoinflammatory rheumatic diseases. The development of the postinfectious syndrome was observed in 1/4 of patients, which was characterized by the formation of postinfectious arthritis in 3,6% of patients, transformation of undifferentiated arthritis into various rheumatic diseases in 49% of patients (more often into early rheumatoid arthritis), as well as exacerbation of the underlying disease in 83,4% of patients with an advanced stage of rheumatoid arthritis. In patients with mixed connective tissue disease, there was a significant increase in immunologic activity due to antinuclear factor (up to a maximum of 1:163 840). Clinical cases of the development of arthritis associated with viral infection and the debut of rheumatoid arthritis after an new coronavirus infection are presented. CONCLUSIONS: New coronavirus infection in the cohort of patients with immunoinflammatory rheumatic diseases observed in the Clinical Rheumatology Hospital No. 25, Saint Petersburg, proceeded in the variant of medium severity in half of patients, initiated the development of lung lesions in 68,6% of patients, arthritis associated with viral infection in 3,6% of patients, immunoinflammatory rheumatic diseases which transformed from undifferentiated arthritis in 49% of cases and exacerbation of the main disease in an overwhelming number of patients. Patients with immunoinflammatory rheumatic diseases have a high risk of adverse outcome of new coronavirus infection, especially in cases of unstable course of the disease or exacerbation of this group of diseases.

The article presents the relevance of the problem of postmenopausal osteoporosis (OP) in modern medicine, due to the social and economic consequences of fractures. The pathogenetic mechanisms of its formation are highlighted, indicating that during postmenopausal women amid estrogen deficiency, there is a violation of bone remodeling processes with increased bone resorption and decreased bone formation. Modern recommendations of the pathogenetic therapy of OP are presented, in which it is noted that the drugs of the first choice are drugs of the bisphosphonate class (BF). The ability of BF to suppress the pathological resorption of bone tissue and stimulate bone formation determines their therapeutic effect in OP. One of the drugs of the BF class is alendronate. In the treatment with alendronate, the processes of resorption by osteoclasts are suppressed and the processes of bone metabolism are restored to the premenopausal level, microarchitectural disturbances and bone loss are prevented. It has been demonstrated that the processes of bone metabolism remain stable during prolonged treatment with alendronate for 10 years, while the accumulation of the drug in the bone does not lead to excessive suppression of bone metabolism, but rather remains at the premenopausal level. The data of international and Russian randomized placebo-controlled trials (RCTs) are presented, which indicate the high effectiveness of alendronate at a dose of 70 mg 1 time / week in the treatment of primary OP in postmenopausal women: it had a positive effect on bone mineral density (BMD), reduced pain and, as a result, reduced the restriction of physical activity of patients. Quite good tolerability of the drug was noted, side effects in the treatment group were comparable to those in the placebo group. An analysis of the action of alenadronate shows that it has an aftereffect within a 12-month period after the end of treatment in relation to the BMD of the spine.

α1-Antitrypsin (α1-AT) deficiency is a common genetic disorder characterized by low serum α1-AT levels and a clinical manifestation of pulmonary emphysema and liver disease. In addition to its classical manifestations, α1-AT deficiency frequently accompanies granulomatosis with polyangiitis (GPA); in this case the role of α1-AT deficiency in the clinical course of GPA has not been defined. Objective: to estimate the prevalence of pathological α1-AT phenotypes in GPA and other systemic vasculitides (SV) and to determinate their impact on the clinical course of GPA. Subjects and methods. The investigation enrolled 86 patients with SV, including GPA (n=47), microscopic polyangiitis (MPA) (n=16), eosinophilic granulomatosis with polyangiitis (EGPA) (n=12), and polyarteritis nodosa (PAN) (n=11). A control group included 46 healthy donors. Isoelectric focusing was used to phenotype α1-AT in blood samples and its concentrations were determined. The phenotypes of α1-AT were compared with the overall SV activity index using the Birmingham Vasculitis Activity Score (BVAS), the vasculitis damage index (VDI), the nature of an organ lesion, and the markers of immune inflammation (proteinase 3-antineutrophil cytoplasmic antibodies, total IgG, and C3 and C4 fractions of the complement system). Results and discussion. Pathological α1-AT phenotypes were detected in 17% (8/47) of the patients with GPA, 6.25% (1/16) of those with MPA and absent in EGPA and PAN. Patients with GPA had PiZZ (n=1), PiMZ (n=4), PiMF (n=2), and PiMS (n=1) phenotypes; those with MPA had a PiMS-phenotype. The detection of a pathological α1-AT phenotype in patients with GPA was characterized by the high values of BVAS and VDI (p

The deficiency of alpha-1 protease inhibitor, or alpha-1-antitrypsin (A1AT), predisposes to chronic lung diseases and extrapulmonary pathology. Besides classical manifestations, such as pulmonary emphysema and liver disease, alpha-1-antitrypsin deficiency (A1ATD) is also known to be associated with granulomatosis with polyangiitis (GPA or Wegener’s granulomatosis). The aim of our study was to evaluate the frequency of allelic isoforms of A1AT and their clinical significance among GPA patients. Detailed clinical information, including Birmingham Vasculitis Activity Score (BVAS), incidence of lung involvement, anti-proteinase 3 (PR3) antibodies concentrations, and other laboratory data were collected in 38 GPA patients. We also studied serum samples obtained from 46 healthy donors. In all collected samples A1AT phenotyping by isoelectrofocusing (IEF) and turbidimetric A1AT measurement were performed. Abnormal A1AT variants were found in 18.4% (7/38) of cases: 1 ZZ, 4 MZ, 2 MF, and only 1 MZ in control group (2%). The mean A1AT concentration in samples with atypical A1AT phenotypes was significantly lower (P=0.0038) than in normal A1AT phenotype. We found that patients with abnormal A1AT phenotypes had significantly higher vasculitis activity (BVAS) as well as anti-PR3 antibodies concentration. We conclude that A1AT deficiency should be considered in all patients with GPA.