Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.

Correction of main manifestations of metabolic syndrome

Currently, there is no doubt that all components of the metabolic syndrome (MS) (abdominal obesity, impaired glucose tolerance, hypertension and dyslipidemia) are risk factors for cardiovascular disease. Liver is the key link in the impaiment of lipid and carbohydrate metabolism, and at the same time one of the main targets of MS. The variety of metabolic changes in the liver manifest themselves in nonalcoholic fatty liver disease (NAFLD), which is recognized as the sixth MS criterion and one of the major risk factors for cardiovascular diseases and their complications

Detoxification therapy for chronic gastrointestinal diseases

Enterosorption, as one of the methods of detoxification therapy, has become widespread in clinical practice and is successfully used in the treatment of various diseases of the gastrointestinal tract (GI tract). Safety and ease of use, absence of contraindications and the possibility of combination with other medicines allow individualizing therapeutic tactics, avoiding the side effects of therapy and achieving high treatment effectiveness while reducing its duration

Depressive disorders and their correction in complex treatment of metabolic syndrome patients

Aim. To study clinical and metabolic effects of selective serotonin re‑uptake inhibitor (SSTI) sertraline in complex treatment of metabolic syndrome (MS) patients. Material and methods. Thirty‑six MS patients were divided into two groups, according to treatment program and psychological symptoms. Intervention group received basic therapy and, in case of depressive disorders (DD) diagnosed, sertraline (50 mg/d), once per day in the morning, for 8 weeks. Control group received basic therapy only. In all participants, clinical, biochemical, and psycho‑physiological parameters were assessed. Results. DD of varying severity were diagnosed in 77,8% of MS patients. Clinical and metabolic MS symptoms correlated with depression severity. Adding sertraline to complex treatment was associated with hemodynamics stabilization, clinical and psychopathological symptom regression, glucose and serum lipoprotein level normalization. Conclusion. Adding sertraline to complex treatment of MS associated with DD improved therapy effectiveness and demonstrated beneficial clinical and metabolic effects