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Background/aims: Immune responses are involved in arterial hypertension. An observational cross-sectional case control study was conducted to estimate the association between Toll-like receptor 4 (TLR4) expression and interleukin (IL)-17A serum levels in patients with controlled and non-controlled hypertension., Methods: We have enrolled 105 non-complicated otherwise healthy hypertensive patients: 53 with well-controlled blood pressure and 52 non-controlled. TLR4 peripheral monocytes expression and serum IL-17A levels were determined by flow cytometry and ELISA, respectively., Results: Non-controlled patients exhibited higher TLR4 expression than well-controlled (25.60 vs. 21.99, P=0.011). TLR4 expression was lower in well-controlled patients who were prescribed beta blockers (18.9 vs. 22.6, P=0.005) and IL-17A concentration was higher in patients using diuretics in either group (1.41 vs. 2.01 pg/ml, P<0.001; well-controlled 1.3 vs. 1.8 pg/ml, P= 0.023; non-controlled 1.6 vs. 2.3 pg/ml, P=0.001). Correlation between IL-17A concentration and hypertension duration was observed in non-controlled patients (Spearman correlation coefficient . ρ=0.566, P<0.001) whereas in well-controlled patients a correlation was found between hypertension duration and TLR4 expression (ρ=0.322, P=0.020)., Conclusions: Arterial hypertension stimulates the immune response regardless of blood pressure regulation status. Prolonged hypertension influences peripheral monocyte TLR4 expression and IL-17A serum levels. Anti-hypertensive drugs have different immunomodulatory effects: diuretics are associated with higher IL-17A concentration and beta-blockers with lower TLR4 expression., (© 2017 The Author(s)Published by S. Karger AG, Basel.)

Inflammatory bowel disease (IBD), encompassing ulcerative colitis (UC) and Crohn's disease (CD), is an uncontrolled chronic inflammation of the gastrointestinal tract caused by an interaction of diverse genes and environmental factors. There is growing evidence that cytokine production plays an important role in IBD. One of the key roles in signaling pathway in development of IBD is performed by interleukin 6 (IL-6), although molecular mechanism of this pathway is not yet fully understood. In order to assess the clinical relevance of IL-6 serum concentration in patients with CD and UC we performed cross-sectional, case-control study of IL-6 levels in patients' and healthy blood donors' sera. A total of 100 CD and UC patients and 71 healthy blood donors were investigated. Clinical activity of CD and UC was evaluated using the Crohn's disease activity index and Truelove-Witt's criteria, respectively. Quantitative assessment of serum IL-6 was performed with solid-phase, enzyme-labeled, chemiluminescent sequential immunometric assay. Our results indicate that serum IL-6 is a clinically relevant parameter for CD and UC that strongly correlates with inflammatory activity of disease. We confirmed and extended the role of cytokine production patterns for IBD presentation in Croatian population.

The Interleukin-23 signalling pathway is important for the differentiation of TH17 lymphocytes and is involved in the pathogenesis of Inflammatory bowel disease. Polymorphisms in the IL-23 receptor gene were previously found to be associated with Inflammatory bowel disease in various populations. The aim of this study was to determine whether the specific rs11209026 and rs7530511 single-nucleotide polymorphisms in the Interleukin-23 receptor gene are associated with Crohn's disease and ulcerative colitis in a Croatian patient population. A total of 50 patients with Crohn's disease and 93 patients with ulcerative colitis, as well as 99 healthy control subjects were included in the study. The results determined a significantly higher occurrence of rs11209026 in control group compared to patients with inflammatory bowel disease, suggesting a protective effect of this polymorphism. The rs11209026 variant was strongly associated with Crohn's disease, but it was absent in ulcerative colitis. However, there was no significant association between the rs7530511 polymorphism with either ulcerative colitis or Crohn's disease. Associations presented in this study give potentially important insight into the roles of specific Interleukin-23 receptor polymorphisms in Crohn's disease pathogenesis in the Croatian population.

Background: Studies have shown that 1-week triple therapy consisting of a proton pump inhibitor, amoxycillin and clarithromycin may cure Helicobacter pylori infection in the majority of patients., Aim: To establish whether pantoprazole plus amoxycillin in association with either azithromycin or clarithromycin is useful in curing H. pylori infection in patients with a duodenal ulcer., Methods: One hundred and ten patients with active duodenal ulcers and H. pylori infection were treated with pantoprazole (days 1-7, 40 mg b.d.; days 8-28 40 mg o.d.) plus amoxycillin 1 g b.d. for the first 7 days. Patients were randomly assigned to receive either azithromycin 500 mg o.d. for the first 6 days (PAAz group; n=55) or clarithromycin 500 mg b.d. for the first 7 days of treatment (PAC group; n=55). H. pylori status was determined by urease test and histology before the treatment, and again 4 weeks after cessation of any medication., Results: One hundred and three patients completed the study. H. pylori infection was eradicated in 78% (39/50) of patients in the PAAz group (ITT analysis: 71%, 95% CI: 61-83%) vs. 81% (43/53) of patients in the PAC group (ITT analysis: 78%, 95% CI: 69-90%) (N.S.). All ulcers had healed., Conclusion: Our study shows that 1-week triple therapy with pantoprazole, amoxycillin and either azithromycin or clarithromycin is not satisfactory (<80% ITT H. pylori eradication rate).

Background: The aim of our study was to establish whether one-week triple therapy regimen (omeprazole, amoxicillin, azithromycin) with low dose (2 x 20 mg/day) or high dose omeprazole (2 x 40 mg/day) is more effective in curing H. pylori infection in patients with active duodenal ulcer disease., Methods: One hundred and twenty patients with duodenal ulcer and H. pylori infection were treated with amoxicillin 2 x 1000 mg/day for the first 7 days plus azithromycin 500 mg/day for the first 6 days. Patients were randomly assigned to receive either omeprazole 2 x 20 mg/day for the first 7 days (group A; n = 60) or omeprazole 2 x 40 mg/day for the first 7 days (group B; n = 60). After 7 days all patients in both groups continued treatment with omeprazole (40 mg/day (days 8-14) and 20 mg/day (days 15-28)). H. pylori status was determined by urease test and histology before the treatment and 4 weeks after cessation of any medication., Results: One hundred and thirteen patients completed the study. H. pylori infection was eradicated in 73.2% [41/56] of patients in group A (intention-to-treat [ITT] analysis: 68.3%; 95% CI: 58.6-80.4%) vs. 82.5% [47/57] of patients in group B (ITT analysis: 78.3%; 95% CI: 67.8-87.9%; NS). All ulcers had healed after 4 weeks of omeprazole treatment. Side effects, usually minor, were recorded in 12.5% (group A) and in 14% (group B) of patients (NS), but therapy was discontinued for only one patient in group B (NS)., Conclusion: There was no statistically significant difference between one-week triple therapy regimen (omeprazole, amoxicillin, azithromycin) with high dose omeprazole (2 x 40 mg/day) and regimen with low dose omeprazole (2 x 20 mg/day) in curing H. pylori infection in patients with active duodenal ulcer disease.

Pantoprazole is a new proton pump inhibitor with a potent antisecretory activity, well defined pharmacokinetics and safety profile. The aim of this single blind, randomized clinical trial was to compare the efficacy of pantoprazole (PAN) 40 mg/day and omeprazole (OME) 20 mg/day in patients with grade I and II GERD (Savary-Miller classification). A total of 120 patients were included (PAN = 60 and OME = 60). In the per protocol/analysis, healing rates at 4 weeks were 76.3% PAN and 71.2% OME (ns), and at 8 weeks 94.7% PAN and 92.9% OME (ns). In the intention to treat analysis, healing rates at 4 weeks were 75% PAN and 70% OME (ns), and at 8 weeks 90% PAN and 86.6% OME (ns). Both pantoprazole and omeprazole were well tolerated with no serious drug related adverse events. Pantoprazole 40 mg/day was found to be safe and effective therapy comparable to omeprazole 20 mg/day in the short-term treatment for reflux esophagitis (grade I and II).

Background: Azithromycin is a new generation, acid stable, macrolide antibiotic that achieves remarkably high concentrations in gastric tissue (above the minimal inhibitory concentration for Helicobacter pylori) after oral administration., Aim: To establish whether azithromycin plus omeprazole in association with either amoxycillin or metronidazole are useful in curing H. pylori infection in patients with a duodenal ulcer., Methods: One hundred patients with active duodenal ulcers and H. pylori infection were treated with omeprazole (days 1-10, 40 mg b.d.; days 11-24, 40 mg o.m.; days 25-42, 20 mg o.m.) plus azithromycin 500 mg o.m. for the first 6 days. Patients were randomly assigned to receive either amoxycillin 1 g b.d. (OAzA group: n = 50) or metronidazole 400 mg t.d.s. (OAzM group: n = 50) during the first 10 days of treatment. H. pylori status was determined by urease test and histology before the treatment and 6 weeks after completion of therapy., Results: Ninety-seven patients completed the study. H. pylori infection was eradicated in 85% (41/48) of patients in the OAzA group (intention-to-treat analysis 82%) vs. 74% (36/49) of patients in the OAzM group (intention-to-treat analysis: 72%) (N.S.). All ulcers had healed after 6 weeks of omeprazole treatment. Side-effects, usually minor, were recorded in 13% (OAzA group) and 47% (OAzM group) of patients (P < 0.001), but therapy was discontinued for only one patient in the OAzA group (N.S.)., Conclusion: Ten days of treatment with omeprazole plus (for the first 6 days) azithromycin and either amoxycillin or metronidazole provides effective regimens to cure H. pylori infection in patients with duodenal ulcer disease.

Treatment with omeprazole (OME), azithromycin (AZI) and amoxicillin (AMO) resulted in encouraging Helicobacter pylori cure rates in pilot and control studies. The aim of this study was to establish whether OME + AZI in combination with either AMO or ACA (amoxicillin plus clavulanic acid) are effective in curing H. pylori infection. A hundred patients with active duodenal ulcer and H. pylori infection were treated with OME (day 1-10: 2 x 40 mg/day, day 11-24: 40 mg/day, day 25-42: 20 mg/day) plus AZI 500 mg/day for the first 6 days. Patients were randomly assigned to either AMO 2 x 1000 mg/day (group A, n = 50) or ACA 2 x 1250 mg/day (group B, n = 50) during the first 10 days of treatment. H. pylori status was determined by urease test and histology before and 6 weeks after completion of therapy. Ninety-five patients completed the study. H. pylori infection was eradicated in 85.4% (41/48) patients from group A (intention-to-treat (ITT) analysis: 82%) versus 91.5% (43/47) patients from group B (ITT) analysis: 86%) (NS). All ulcer had healed after 42 days of omeprazole treatment. Side effects, usually minor, were recorded in 12.5% (group A) and 14.9% (group B) of patients (NS). Therapy had to be discontinued in two patients (one in group A and one group B) only. Ten-days treatment with OME and AZI (for the first 6 days) with AMO or ACA are simple and highly effective regimens to cure H. pylori infection in patients with duodenal ulcer disease.

This prospective, single blind, randomized study was designed to compare the efficacy and tolerance of two therapeutic schedules for eradication of H. pylori in patients with duodenal ulcer. Patients were randomized into two groups. Group 1 (n = 25) was treated with omeprazole 20 mg each morning for 28 days, azithromycin 500 mg/day for 5 days and metronidazole 3 x 500 mg/day for 5 days. Group 2 (n = 25) was treated with omeprazole 20 mg/day for 28 days and azithromycin 500 mg/day for 5 days. H. pylori status was determined by rapid urease test and histology before and 1, 6 and 12 months after the therapy. After 4 weeks of treatment ulcers healed in 96% (24/25) of patients in the first group and in 92% (23/25) of patients in the second group. One and 12 months after the treatment, eradication of Helicobacter pylori was achieved in 72% (18/25) of patients in the first group and in 64% (16/25) of patients in the second group. In 12 months after the treatment ulcer recurred in 43.7% (7/16) of patients in whom H. pylori was not eradicated and in 2.9% (1/34) of patients with eradicated H. pylori. The side effects were minor and/or transitory and did not require discontinuation of the treatment.