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Taking statins can cause increase in the level of aspartate and alanine aminotransferase. The aim of this study was to assess the usefulness of melatonin in counteracting the adverse hepatic events from statins. Methods. The research program included 60 patients (aged 47–65 years, 41 women and 19 men) with hyperlipidemia taking atorvastatin or rosuvastatin at a dose of 20–40 mg daily. The patients were randomly allocated in two groups. Group I (n=30) was recommended to take the same statin at a standardized daily dose of 20 mg together with melatonin at a dose of 2×5 mg. Group II (n=30) patients took statin with placebo at the same dose and time of the day. Follow-up laboratory tests (AST, ALT, GGT, and ALP) were evaluated after 2, 4, and 6 months of treatment. Results. In Group I the levels of all enzymes decreased after 6 months, particularly AST, 97,2±19,1 U/L versus 52,8±12,3 U/L (p<0,001); ALT, 87,4±15,6 U/L versus 49,8±14,5 U/L (p<0,001); and GGT, 84,1±14,8 U/L versus 59,6 U/L (p<0,001). Conclusion. Melatonin exerts a hepatoprotective effect in patients taking statins.

Helicobacter pyloricolonization of gastric mucosa causes pain of unknown etiology in about 15–20% of infected subjects. The aim of the present work was to determine the level of expression of enzymes involved in the synthesis of melatonin in gastric mucosa of asymptomatic and symptomaticH. pyloriinfected patients. To diagnoseH. pyloriinfection, histological analysis and the urea breath test (UBT C13) were performed. The levels of mRNA expression of arylalkylamine-N-acetyltransferase (AA-NAT) and acetylserotonin methyltransferase (ASMT) were estimated in gastric mucosa with RT-PCR. The level of AA-NAT expression and AMST was decreased inH. pyloriinfected patients and was increased afterH. pylorieradication. We conclude that decreased expression of melatonin synthesizing enzymes, AA-NAT and ASMT, in patients with symptomaticH. pyloriinfection returns to normal level afterH. pylorieradication.