Procalcitonin in early prediction of acute severe pancreatitis.

OBJECTIVE: The aim of the study was to analyze the prognostic potential of procalcitonin in acute pancreatitis complicated by ascites-peritonitis. PATIENTS AND METHODS: Materials and methods: The study analyzed the results of a comprehensive examination and treatment of 18 patients with acute pancreatitis complicated by enzymatic ascites-peritonitis, including 13 patients who were treated in the surgical department of KP "Poltava Regional Clinical Hospital. MV Sklifosovsky POR ", and 5 patients of other emergency hospitals in Poltava, in the period from 2017 to 2019. In addition to standard screening methods, these patients were additionally tested for procalcitonin to predict an adverse course in the early period. RESULTS: Results: To assess the relationship between the presence of elevated procalcitonin levels at the time of hospitalization of 0.5 ng / ml and above and unsatisfactory treatment results, differences were assessed using an accurate Fisher test. When comparing differences in the development of infectious complications in the dynamics of the disease in patients of the study group depending on the presence of elevated concentrations of procalcitonin or its absence at the time of hospitalization, a significant difference was found (p <0.05). CONCLUSION: Conclusions: In our opinion, the use of procalcitonin as a predictor of infectious complications in the dynamics of the disease will determine the category of patients in whom reducing the risk of flora translocation through the use of early oral antibiotic prophylaxis and parenteral drugs tropic to pancreatic tissue may reduce the incidence of purulent complications. In another category of patients, antibacterial therapy is not advisable due to the low risk of purulent-septic complications.

Anti-inflammatory and endothelium protective effect of long-term pioglitazone intake in patients suffering from bronchial asthma concurrent with ischemic heart disease.

INTRODUCTION: Treatment of co-morbidities, including bronchial asthma (BA) and coronary heart disease (CHD), is a relevant issue of modern therapy. The aim of the research is to study the impact of long-term intake of pioglitazone on the development of inflammation and ED in patients with BA concurrent with CHD. MATERIAL AND METHODS: The clinical study involved 50 people aged 40-75 who suffered from asthma concurrent with CHD. On the first day of the study, blood samples were collected and clinical examinations were performed, after which patients were randomized and divided into the control group who continued to receive only the standard therapy, and the study group, who received pioglitazone (Pioglar, Ranbaxy, India) 15 mg once a day along with comprehensive therapy. Re-examination was carried out in 6 months. RESULTS: It has been found that inclusion of pioglitazone in the course of standard therapy in patients with asthma concurrent with coronary heart within 6 months is a more efficient scheme than the course of standard therapies. According to the data obtained from the patients, there was a significant decrease in respiratory rate (p<0.01), levels of systolic blood pressure (p<0.001) and diastolic blood pressure (p<0.001). Administering pioglitazone contributed to the improvement of respiratory function and airflow obstruction, increased FEV1 performance (p<0.01) and Tiffeneau index (p<0.05). In patients of the study group, intake of pioglitazone helped to reduce angina. Intake of pioglitazone showed a significant decrease in the frequency of angina pectoris FC II (p<0.05) and a significant increase in the frequency of angina FC I (p<0.05), increase in the rate of threshold load power (p<0.05). In assessing endothelium-dependent vasodilation of the brachial artery, it has been noted that intake of pioglitazone by patients with asthma concurrent with coronary heart disease resulted in a statistically significant increase in the diameter of the brachial artery by an average of 4% (p<0.0001), the maximum blood flow velocity (TAMX) by an average of 40 % (p<0.0001), Δ% diameter increase in the brachial artery (p<0.0001), and achieved positive indicators of RI (p<0.0001). In assessing endothelium-dependent vasodilation of brachial artery in patients treated with pioglitazone, there was a significant increase in the diameter of brachial artery on average by 5% (p<0.0001) after taking nitroglycerin, an increase in ?% diameter of brachial artery (p<0.0001) and RI (p<0.0001). Inclusion of pioglitazone in the complex therapy for 6 months resulted in a significant decrease in the index of systemic inflammation hs-CRP (p<0.0001) and adhesion marker sVCAM-1 (p<0.0001), total cholesterol (p<0.001), triglycerides (p<0.001). CONCLUSION: Thus, these data demonstrate the anti-inflammatory and endothelium protective effects of pioglitazone against the background of standard therapy in patients with BA concurrent with CHD within 6 months, which may enhance the clinical efficacy in the treatment of these diseases.

Liraglutide exerts an anti-inflammatory action in obese patients with type 2 diabetes.

INTRODUCTION: Liraglutide (L) is the analogue of human glucagon-like peptide 1 which stimulates glucose-dependent insulin secretion and can modify the level of inflammatory biomarkers. L can influence NF-kB inflammatory cascade, but the mechanisms of anti-inflammatory activities of L remain to be determined. In animal models L influenced an activity of Sirtuin 1(SIRT1). Moreover, recent evidences strongly suggest that SIRT1 up-regulation may serve as a potent therapeutic approach against development and progression of diabetic complications. The aim of this study was to investigate L effects directed on the pro-inflammatory NF-kB pathway and expression of SIRT1 in obese patients with type 2 diabetes mellitus (DM). MATERIALS AND METHODS: 15 obese patients with type 2 diabetes were studied, all using metformin (1-2 g/day) and sulfonylurea (glimiperide). All patients received L 1.2 mg daily add-on to stable therapy for 6 weeks. Blood samples were collected before, 6 weeks after start of treatment and after an overnight fast 6 weeks after stopping L, mononuclear cells (MNC) were isolated. The mRNA expressions of TNF-α, TLR2, TLR4, NOD1, IL-2 and SIRT1 were measured in MNC by RT-PCR. Ceruloplasmin concentration was measured in plasma by photometric method. RESULTS: In this add-on pilot clinical investigation we received new data that L can inhibit proinflammatory NF-kB pathway by increased SIRT1 expression in obese patients with type 2 DM improving metabolic profile. The mRNA expression in MNC of TNF-α, IkB, TLR2, TLR4, and plasma ceruloplasmin fell after 6 weeks of L. Expressions of IL-2 and NOD-1 were stable. There was a significant increase of SIRT1 mRNA expression. The mRNA expression in MNC of TNF-α, IkB, TLR2, TLR4, NOD1, SIRT1 and ceruloplasmin concentrations did not reverse to baseline levels after 6 weeks stopping of L treatment. IL-2 expression decreased in comparison with basic level. CONCLUSIONS: L has a potent anti-inflammatory effect as do GLP-1 agonists due to inhibition of NF-kB pathways and up-regulate SIRT1 expression, down-regulating pro-inflammatory factors including cytokines (TNF-α), extra- and intracellular receptors (TLR2, TLR4), and inflammation markers such as ceruloplasmin. Long lasting effects of L can be mediated by epigenetic regulation of NF-kB pathway by SIRT-1.