Orally given gastroprotective capsaicin does not modify aspirin-induced platelet aggregation in healthy male volunteers (human phase I examination).

Capsaicin is a well-known component of red pepper. Recent studies have shown that capsaicin could prevent gastric ulcer provoked by various NSAID-s like acetylsalicylic acid (ASA). Primary objective of this human clinical phase I trial was to investigate whether two different doses of capsaicin co-administered with ASA could alter the inhibitory effect of ASA on platelet aggregation. 15 healthy male subjects were involved in the study and treated orally with 400 µg capsaicin, 800 µg capsaicin, 500 mg ASA, 400 µg capsaicin+500 mg ASA and 800 µg capsaicin+500 mg ASA. Blood was drawn before and 1, 2, 6 and 24 hours after the drug administration. After that epinephrine induced platelet aggregation was measured by optical aggregometry. Between treatments, volunteers had a 6-day wash-out period. Our results showed that capsaicin had no effect on platelet aggregation, while as expected, ASA monotherapy resulted in a significant and clinically effective platelet aggregation inhibition (p ≤ 0.001). The combined ASA-capsaicin therapies reached equivalent effectiveness in platelet aggregation inhibition as ASA monotherapy. Our investigation proved that capsaicin did not influence the inhibitory effect of ASA on platelet aggregation, thus the capsaicin-ASA treatment would combine the antiplatelet effect of ASA with the possible gastroprotection of capsaicin.

Participation of capsaicin-sensitive afferent nerves in the gastric mucosa of patients with Helicobacter pylori-positive or-negative chronic gastritis.

Capsaicin-sensitive afferent nerves (CSANs) are involved in the protection of gastric mucosa. To clarify the role of CSANs in human Helicobacter pylori-negative or -positive chronic gastritis, after bacterium detection by rapid urease test, (14)C urea breath test, and specific histological staining, the immunodistribution of capsaicin receptor, calcitonin gene-related peptide (CGRP), and substance P (SP) was studied in 21 H. pylori-positive and 30 H. pylori-negative patients with chronic gastritis and 20 patients with functional dyspepsia (as histologically healthy controls). The expression of capsaicin receptor, CGRP, and SP was significantly higher in the mucosa of patients with chronic gastritis than in controls, however, no significant difference was obtained in the immunodistribution in patients with H. pylori-negative versus H. pylori-positive gastritis. In conclusion, CSANs participate in the development of human gastritis, however, their participation does not depend on the presence of Helicobacter pylori as a causative factor.

Co-infections with hepatitis G and TT virus in patients with chronic hepatitis C in Hungary.

The significance of co-infections with novel hepatitis viruses Hepatitis G (GBV-C, HGV) and TT virus (TTV) in chronic hepatitis C is not clear. We determined the prevalence of HGV RNA and TTV DNA in chronic hepatitis C patients and in asymptomatic hepatitis C virus (HCV) carriers, and assessed the influence of these agents on the course of HCV infection. Seventy-seven patients with chronic hepatitis C--50 of them treated with interferon (IFN)--and 33 HCV carriers with normal alanine aminotransferase have been investigated. Previous HBV infection was detected by testing serum HBsAg and aHBc. HGV RNA and TTV DNA were detected by PCR. In the healthy population, the prevalence of anti-HCV was 0.3%, HGV RNA 8.0% and TTV DNA 18.5%. In chronic hepatitis C HGV RNA occurred in 9.09% and TTV DNA in 40.25% of cases. In IFN-treated patients with sustained remission, the frequency of TTV was 20% vs. 45.7% found in non-responders. Among asymptomatic HCV-carriers, the prevalence of HGV RNA was 9.09% and TTV DNA 75.7%. Neither HGV RNA nor TTV DNA had apparent effect on the HCV infection. TTV was detected with the lowest frequency in persons with sustained remission due to IFN, suggesting antiviral effect of IFN on TTV.