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Backgrounds/aims: Certain statins interfere with the mechanism of the hepatitis C virus replication. We aimed at studying the effect of statins on the level of viremia and of the pro-and anti-inflammatory cytokines in the patients with chronic hepatitis C., Methodology: We took in our study all the patients with chronic hepatitis C placed in the evidence of the clinics of internal medicine of the Emergency County Clinical Hospitals of Braşov, Oradea and Sibiu, who had been identified with viremias. The patients were treated with fluvastatin 40 mg/day or lovastatin 20 mg/day for 28 days. The level of viremia, hemoleukogram, hepatic biochemical tests and the pro and anti-inflammatory hepatic cytokines were analysed before and after the treatment. The final results were compared with the initial ones, as well as between the 2 groups., Results: Regarding those 99 analysed patients, the initial average viremia was of 2376074 +/- 3427596 UI/ml, while the final one was of 1321136 +/- 1343570 UI/ml (p = 0.000987). Both, in the group treated with lovastatin, as well as in that treated with fluvastatin, the decrease of viremia was significant from the statistics point of view (p = 0.032, respectively p = 0.00092). Lovastatin administration resulted in the significant decrease of the pro-inflammatory cytokines IL-6 and TNF-alfa, while that of fluvastatin brought about the significant decrease of the serum levels of IL-6, IL-8 and TNF-alfa. There were no significant differences, statistically speaking, between the 2 determinations, regarding the levels of IL-10 (anti-inflammatory cytokine) and those of erythropoietin. Transaminases average level did not vary significantly after those 4 weeks of statins treatment., Conclusions: Lovastatin and fluvastatin, significantly decrease the level of viremia, of IL-6 and TNF-alpha in the patients with chronic hepatitis C.

Background/aims: Erythropoietin has an antiinflammatory action. We proposed to study its effects on patients with chronic hepatitis C., Methodology: We studied a group of 96 hospitalized patients. Those with viral chronic hepatitis C were divided into 2 groups: group A--41 patients with chronic renal failure, and group B--23 patients without renal failure. 32 patients without any hepatitis viruses formed the control group--C. We analyzed: the biochemical tests, the serum IL-6, IL-8, TNF-alpha, C reactive protein, and erythropoietin., Results: The levels of pro-inflammatory cytokines and of erythropoietin were higher in the patients from groups A and B, except the value of TNF-alpha from group B. The dialyzed patients had higherpro-inflammatory cytokines and lower erythropoietiin comparing with the non-dialyzed patients., Conclusions: Erythropoietin levels and some proinflammatory cytokines increasein patients with chronic hepatitis C. Erythropoietin could have an anti-inflammatory effect on thepatients without renal failure.

Globally, developed nations spend a significant amount of their resources on health care initiatives that poorly translate into increased population life expectancy. As an example, the United States devotes 16% of its gross domestic product to health care, the highest level in the world, but falls behind other nations that enjoy greater individual life expectancy. These observations point to the need for pioneering avenues of drug discovery to increase life span with controlled costs. In particular, innovative drug development for metabolic disorders such as diabetes mellitus becomes increasingly critical given that the number of diabetic people will increase exponentially over the next 20 years. This article discusses the elucidation and targeting of novel cellular pathways that are intimately tied to oxidative stress in diabetes mellitus for new treatment strategies. Pathways that involve wingless, β-nicotinamide adenine dinucleotide (NAD+) precursors, and cytokines govern complex biological pathways that determine both cell survival and longevity during diabetes mellitus and its complications. Furthermore, the role of these entities as biomarkers for disease can further enhance their utility irrespective of their treatment potential. Greater understanding of the intricacies of these unique cellular mechanisms will shape future drug discovery for diabetes mellitus to provide focused clinical care with limited or absent long-term complications. [ABSTRACT FROM PUBLISHER]