Significant progress related particular to the use of interleukin (IL)-6 and IL17 inhibitors has been made in the pharmacotherapy of rheumatic diseases. IL-6 is a cytokine that has a wide range of biological activity and affects different types of cells. There is evidence for the important role of IL-6 hyperproduction not only in rheumatoid arthritis (RA), but also in other immune inflammatory rheumatic diseases (systemic lupus erythematosus (SLE), scleroderma system
atica, idiopathic inflammatory myopathies, giant cell arteritis, etc.). IL-6 inhibition primarily with humanized monoclonal antibodies against IL-6 receptors (tocilizumab – TCZ)) is considered as one of the promising areas of pharmacotherapy for these diseases. The successful results of TCZ use have created pre requisites for the design of other medicaments that can form a novel class of IL-6 inhibitors, genetically engineered biological agents, in the future. There is another new area in the treatment of immune inflammatory rheumatic diseases, which is the inhibition of the cytokine IL17A that provides interaction between innate and acquired immunity and is synthesized by a wide range of immunocompetent cells, the socalled Th17 ones in particular. IL-17A is implicated in the immunopathogenesis of a broad spectrum of immune inflammatory diseases, including RA, psoriasis, psoriatic arthritis, inflammatory bowel diseases, SLE, allergic diseases, transplantation immunity, obesity, carcinogenesis, etc. Elevated IL-17A concentrations correlate with the activity and severity of a pathological process. The pathogenetic effects of IL-17 in RA may be associated with its involvement in the development of synovial inflammation and joint destruction. The therapeutic efficiency of inhibition of Th17 cells and IL-17A synthesis in autoimmune diseases was first indirectly demonstrated in psoriasis. This provided
the basis for the elaboration of therapeutic approaches associated with the direct inhibition of IL-17 effects in these patients. Thus, the use of IL-6 inhibitors (primarily TCZ) and, probably, IL-17 will make significant progress in the treatment of not only RA, but other severe potentially deadly immune inflammatory rheumatic diseases in the future.

Autoinflammatory syndromes (AISs) are a group of predominantly hereditary diseases associated with the spontaneous uncontrolled production of proinflammatory cytokines. Most diseases are known to have molecular mechanisms and an inheritance pattern. The paper describes major AISs, such as familial Mediterranean fever; cryopyrin-associated periodic syndrome (familial cold urticaria, Muckle – Wells syndrome, CINCA/NOMID syndrome); tumor necrosis factor-α receptor-associated periodic syndrome; hyperimmunoglobulinemia D syndrome; periodic fever, aphthous stomatitis, pharyngitis, cervical adenitis syndrome. An inheritance pattern and molecular defects are characterized for each disease. The principles of diagnosis and therapy are described. The role of interleukin-1 blockers in the therapy of AIS is defined. The most important symptoms that can be used to detect the major forms of AIS are identified. The Gaslini score, a special formula using the clinical symptoms to identify patients at high risk for AIS who need genetic typing and those at low risk for AIS, is described. A clinical diagnostic algorithm is presented, which can be used to detect patients with AIS and to determine indications to and the time of molecular genetic typing, and to choose priority genes.

Differential diagnosis in muscle pains often presents great difficulties so all existing signs of the disease should be carefully considered to make its diagnosis and to prescribe adequate therapy. The paper considers the causes of muscle pains, laboratory and instrumental studies (immunological tests, determination of the level of specific muscular enzymes, primarily creatine phosphokinase – CPK, etc.), and the main reasons for enhanced plasma CPK activity. It also describes acute and chronic mialgias associated with enhanced plasma CPK activity, as well as diseases in which mialgias are related to the normal level of CPK, myofascial syndrome (MFS) and fibromyalgia (FM) in particular. The characteristic features of MFS are given in its diagnostic criteria. It is stated that a differential diagnosis should be made between MFS and major muscle pain-associated abnormalities, such as polymyalgia rheumatica, FM, etc. Diagnostic
criteria for polymyalgia rheumatica are given. A MFS treatment algorithm is presented. Local exposure methods applied to altered musculoligamentous structures in combination with myorelaxants and non-steroidal anti-inflammatory drugs assume paramount importance in MFS.

Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease. Coronary vascular events caused by atherosclerosis are one of the leading causes of death in RA. The review gives the results of studies of the role of interleukin-6 (IL-6) in the development of autoimmune inflammation and cardiovascular diseases. The link between IL-6, inflammation, and blood lipid spectrum is considered. Attention is focused on the lipid-lowering and pleiotropic effects of statins. There is information of the effects of IL-6 receptor inhibitors (Tocilizumab – TCZ)) on blood lipid levels in RA. The implication of IL-6 in the pathogenesis of atherosclerosis in RA and the effects of TCZ on the development and progression of atherosclerosis need future investigations.

Systemic lupus erythematosus (SLE) is a prototype for chronic autoimmune disease. Its prevalence is 20 to 70 cases per 100,000 women and varies by race and ethnicity. Despite considerable progress in traditional therapy, many problems associated with the management of these patients need to be immediately solved: thus, 50-80% are found to have activity signs and/or frequent exacerbations and about 30% of the patients have to stop work; Class IV lupus nephritis increases the risk of terminalrenal failure. In the past 20 years great progress has been made in studying the pathogenesis of SLE: biological targets to affect drugs have been sought and fundamentally new therapeutic goals defined. Belimumab is the first genetically biological agent specially designed to treat SLE, which is rightly regarded as one of the most important achievements of rheumatology in the past 50 years.

Objective: to evaluate the effect of infliximab (INF) on quality of life (QL) in patients with ankylosing spondylitis (AS), by analyzing the results of a SF-36 questionnaire survey. Subjects and methods. Sixty-six male patients, diagnosed with AS (according to the 1984 modified New-York criteria) in its extensive or end stage with a high activity (BASDAI ≥4.0), were followed up. All the patients were divided into 2 groups according to the option of disease-modifying antirheumatic drug therapy: 1) 16 patients who received combination therapy with INF given as a standard regimen at 0, 2, and 6 weeks followed by a regimen of 5 mg/kg body weight and nonsteroidal anti-inflammatory drugs (NSAIDs) in standard doses every 8 weeks; 2) 50 patients who had monotherapy with NSAIDs in the same doses. QL was assessed using the Short-Form 36 (SF-36) questionnaire in patients with AS. Results. The scales evaluating physical health showed the greatest group differences in pain intensity (38.42%; p<0.0001) and the least in the general health status (24.48%; p<0.001). Those assessing mental health displayed statistically significant group differences in vital activity (24.78%; p<0.01).
Conclusion. The patients receiving monotherapy with NSAIDs were found to have lower scores in all SF-36 scales than those on combination therapy with INF and NSAIDs.

Objective: to establish whether long-term combination therapy with a tumor necrosis factor (TNF) α inhibitor and a disease-modifying antirheumatic drug (DMARD) (methotrexate – MTX) may lead to sustained rheumatoid arthritis (RA) remission and its maintenance even after discontinuation of genetically engineered biological agents (GEBA). Subjects and methods. Moscow City Clinical Hospital Four had been following up 5 patients (4 women and 1 man) receiving certolizumab pegol (CZP, Cimzia) since 2005. Their treatment was performed in the CDP 879-027/28 study until August 2011; thereafter the patients continued to receive the drug at the department until February 2011. The patients’ mean age was 49.2±8.58 years; the average duration of RA was 4.4±2.3 years. The reason for using the medicament was ineffective previous standard DMARD therapy (sulfasalazine, leflunomide; when using CZP, all the patients took MTX
in a dose of 10-15 mg/week; 2 patients had it in combination with prednisolone 5-7.5 mg/day). In all the patients, the disease activity remained high (mean DAS28, 6.33±0.52). Quality of life (QL) was also assessed using overall HAQ, EQ-5 questionnaires. The mean EQ-5D and HAQ QL scores were 50±7.9 and 1.825±0.17, respectively. The patients received either CZP 400 or 200 mg, or placebo in a blind study in October to December 2005; in an open-label study they took 400 mg CZP subcutaneously once two weeks since 2006 and 200 mg of this agent subcutaneously once two weeks (the dose was reduced according to the protocol after data on the efficiency of this dosage regimen were accumulated) since February 2008. Results. By the end of CZP treatment, 3 patients achieved sustained (1-year or more) remission (DAS28<2.6); 2 patients had low disease activity (DAS28<3.2), as confirmed by QL indicators according to the HAQ and EQ-5D questionnaires. It was decided that 3 patients would not resume GEBA therapy. They continued to take MTX 12.5-15 mg/week as DMARD therapy. One patient with a maximum DAS28 score of 3.16 by the end of the protocol continued to be treated with CZP (200 mg subcutaneously once two weekly). Another female patient with moderate RA activity at the end of therapy herself completed the treatment with a TNF-α inhibitor.  Following a year, 2 patients remained in sustained RA remission and did not need a GEBA. RA activity increased in a female patient who had stopped treatment; she was recommended to resume therapy with the TNF-α inhibitor. Another female patient was stated to have a low RA activity and her follow-up was continued Conclusion. The findings are evidence in favor of the fact that long-term combination therapy with a TNF-α inhibitor in combination with MTX may lead to not only sustained RA remission, but also its maintenance even after a GEBA was discontinued. The use of CZP for 6.5 years induced remission and promoted stability in some patients during a year after drug discontinuation.

The paper gives the results of an investigation of quality of life (QL) in patients with ankylosing spondylitis. It shows the implication of chronic pain syndrome in lowering QL and considers the issues of combination therapy with nimesulide (nise) and tizanidine (sirdalud) for pain syndrome.

Parathyroid diseases cause serious musculoskeletal problems. The major function of parathyroid hormone (PTH) is to regulate calcium levels in the body, which is closely related to vitamin D. PTH exerts a double (anabolic and catabolic) effect on the human skeleton, which accounts for its heterogeneous action on the bone and for the major clinical manifestations of diseases associated with its hyper- and hypoproduction. The paper considers the main causes of hypoparathyroidism (HPT) that is considered to mean inadequate PHT activity and/or secretion; moreover, the level of ionized calcium falls below the reference range. It describes two HPT cases that show the clinical picture resembling ankylosing spondylitis.

The paper analyzes the role of therapeutic exercises in the therapy of patients with juvenile chronic arthritis. The author discusses the time of, indications for, and contraindications to their use and states her belief that it is advisable for a rheumatologist to prescribe this therapy option. The data available in the literature and the author’s data on the efficiency of this therapy are given.

The paper gives an update on the pathogenesis of osteoarthrosis, the role of anti-inflammatory cytokines in the destruction of cartilage and subchondral bone, and the possibility of targeted diacerein therapy.

Glucosamine sulfate or hydrochloride and chondroitin sulfate belong to the natural components of cartilage intercellular substance. In osteoarthrosis, they exert a pronounced symptom-modifying effect and, when used long, are also able to suppress the X-ray progression of the disease. Multi-ingredient medications containing glucosamine and chondroitin have benefits over each of them when used alone. These drugs include teraflex. The efficacy of pharmacological agents appears to be associated not so much with the stimulation of cartilage matrix synthesis as with their anti-inflammatory properties.

The meeting of the Russian Council of Experts for the use of the novel anabolic agent Forsteo®(teriparatide) to treat osteoporosis (OP) was held in Moscow on June 29, 2013. The meeting was attended by leading Russian OP specialists, including the members of the Russian Osteoporosis Association and its Presidium.  The participants of the Council of Experts noted the great social importance of severe OP, which was associated primarily with its consequences, such as fractures causing an increase in disability and mortality rates in elderly people, and discussed the possibilities and benefits of the new approach to treating OP with teriparatide, the first drug permitting the formation of new bone tissue. The experts have recommended teriparatide for use within the registered indications in the following groups of patients: those who have severe OP (≥1 vertebral fractures, hip fracture of vertebral bodies or a fracture of the proximal femur, multiple recurrent fractures of skeletal bones) as first-line therapy; those who had ineffective previous antiosteoporotic therapy (new fractures occurring during the treatment and/or a continuing decline in bone mineral density), those who are intolerant to other medications for OP, or who have contraindications to their use.