В статье рассмотрены современные сведения о биологически активных добавках (БАД), подчеркнута их роль в нормализации и/или улучшении функционального состояния органов и систем, в том числе микрофлоры желудочно-кишечного тракта, снижении риска заболеваний и др. Представлены данные о потреблении и оборотах БАД, определения и классификации этой группы веществ, основные документы, регламентирующие контроль их производства и продвижения в разных странах и в России. В качестве примера БАД, соответствующего правилам надлежащей медицинской практики, рассмотрен неденатурированный коллаген II типа, который вырабатывается из хряща грудины цыплят (UC-II ® ) и входит в состав препарата Сустафлекс. Терапевтические свойства неденатурированного коллагена II типа подтверждены клиническими испытаниями. Описаны механизм его действия, доказательства эффективности и безопасности, возможность использования для профилактики и комплексной терапии остеоартрита (ОА) коленных суставов, а также в качестве альтернативного средства лечения ОА.Ключевые слова: биологически активные добавки; болезни костно-мышечной системы; остеоартрит коленных суставов; механизм оральной толерантности; неденатурированный коллаген II типа (UC-II ® ).

Background:Systemic sclerosis (SSc) is an autoimmune disease characterized by endothelial dysfunction, immunological disorders, and excessive synthesis of collagen and its deposition in various tissues and organs. The juvenile onset SSc before the age of 16 is very rare, with annual incidence of 0.27-0.5 cases per million children according to English and Finnish authors [1,2].Objectives:To present a clinical case of juvenile onset SSc, manifesting from the childhood predominantly with fibrous contractures.Methods:Patient K., 30 yo. Clinical presentation on admission to the Institute of Rheumatology in September 2020: thickening of the trunk and limbs skin (mRSS 10 scores), pronounced induration of subcutaneous tissues and muscles; contractures of the elbow, shoulder, hip and knee joints, short stature (height 142 cm) with proportional shortening of the limbs. ANA (HEp-2) 1/320, a-Scl-70, a-RNP-70 and ACA tests were negative. Ultrasonography revealed left-sided coxitis, esophagogastroduodenoscopy - Barrett’s esophagus. Chest CT, echocardiography, electrocardiography and capillaroscopy yielded no specific findings.The patient has been ill since the age of 3, when SSc manifested with skin thickening, “dry” arthritis and rapid development of contractures of the large joints. Thorough diagnostic elaboration ruled out such potential causes as phenylketonuria, glycogenosis, mucopolysaccharidoses, primary amyloidosis, and porphyria. Histological findings (2007) of a biopsied skin specimen containing subcutaneous fat and muscle tissue included focal vacuolization of keratinocytes, poor perivascular lymphocytic and histiocytic infiltration, fibrosis and hyalinosis of collagen fibers of varying intensity in the in mid- and deep dermis, infiltration of collagen fibers by fibroblasts, skin appendages atrophy – all of them representing a pattern of morphological changes characteristic of SSc. Therapeutic regimens including prednisone at 5-15 mg/day and D-penicillamine were ineffective.Results:In this case, in view of fibrotic arthropathy, a differential diagnosis was made with deep morphea and stiff skin syndrome. Visceral involvement, immunological disorders and biopsy findings substantiated a diagnosis of juvenile onset SSc. Oral MTX was initiated at 15 mg to target skin lesion and osteoarticular symptoms.Conclusion:Predominance of fibrotic arthropathy in presented case caused difficulties in establishing SSc diagnosis, as this patient did not have such inherent features as the Raynaud’s phenomenon, interstitial lung disease or pulmonary hypertension. Juvenile onset SSc manifesting before the age of 16 has its own clinical features, usually persisting through the adulthood, and therefore, such one-of-a-kind appearances of juvenile onset SSc should not be missed or misinterpreted.References:[1]Herrick AL, Ennis H, Bhushan M et al. Incidence of childhood linear scleroderma and systemic sclerosis in the UK and Ireland. Arthritis Care Res. 2010 Feb;62(2):213-8. doi: 10.1002/acr.20070.[2]Pelkonen PM, Jalanko HJ, Lantto RK et al. Incidence of systemic connective tissue diseases in children: a nationwide prospective study in Finland. J Rheumatol. 1994 Nov;21(11):2143-6Disclosure of Interests:None declared

Depending on the presence of laboratory biomarkers: rheumatoid factor IgM and anti-cyclic citrullinated peptide antibodies (ACCP), “seropositive” and “seronegative” variants of rheumatoid arthritis (RA) are distinguished. Immunological subtypes differ in risk factors, immunopathogenesis, and the course of the disease. A review of data concerning immunology and clinical features of ACCP-negative rheumatoid arthritis is presented. The presence of ACCP in the peripheral blood reflects the progressive erosive process with a predominance of the inflammatory component and involvement of the B cells. Proliferative changes predominate in the ACCPnegative subtype; disorders associated with the T-cell link, primarily with CD4+ T-lymphocytes, play an important role in pathogenesis. This variant of the disease is characterized by a less pronounced erosive process, but the inflammatory activity in both subtypes of RA can be comparable. Early diagnosis, regular monitoring of the disease activity and the «treat to target» strategy are recommended for both positive and negative ACCP RA, however, the effectiveness of individual drugs in these subtypes may vary significantly.

Aim – to analyze long-term results of intensive treatment initiated at rheumatoid arthritis (RA) onset in real clinical practice.Material and methods. 93 RA patients were included. Subcutaneous MTX was initiated at 10–15 mg per week with further dose escalation up to 20–30 mg per week. If MTX monotherapy did not allow to achieve treatment target of remission or low disease activity, biologics were added.Results. Against the background of observation, there was a significant decrease in the activity of diseases and the level of acute phase indicators, after 12 months of treatment, the values of the DAS28-ESR indices were 2.76 [2; 3.7], SDAI – 5.34 [1.8; 9.7], CDAI – 5 [1.5; 9.5], corresponded to low disease activity; remission was achieved in 48.6%, low activity – in 17.5%, moderate activity remained in 31%, high activity – in 2.7% of patients. After 6 years the median age of patients was 58 [49; 66] years, the disease duration – 84 [79; 89] months, the low disease activity was documented in 21.3%, and remission – in 7.8% of patients. After 6 years, the value of the activity indices was: DAS28 – 4 [3.4; 4.59], SDAI – 15.06 [9.32; 21], CDAI – 15 [9; 21]; remission – in 7.7%, low disease activity – in 21.1%, moderate activity – in 60%, high activity – in 11.1% of patients.Conclusion. Intensive therapy initiated at RA onset demonstrates high effectiveness, allowing to achieve remission/low disease activity in about 30% of patients. Adherence to this strategy allowed to discontinue biologics in and synthetic DMARDs after achieving treatment target.

The review presents data on new biomarkers for the diagnosis of rheumatoid arthritis, considers the diagnostic parameters of antibodies to carbamylated proteins, antibodies to peptidyl arginine deaminase, antibodies to homocysteinylated α1-antitrypsin, 14-3-3η, macrophage soluble scavenger receptor A. The use of new biomarkers can improve the diagnosis of RA in the early stages, as well as stratify patients based on the prognosis of the disease and provide a rational selection of therapy.