Hepatitis: Torres S

Marques A, Torres S, Davis JM. · Department of Surgery, Robert Wood Johnson Medical School, New Jersey, USA. · Surg Infect (Larchmt). · Pubmed #19284354 No free full text.

Abstract: BACKGROUND: Red blood cell transfusions have been widely associated with the transmission of human immunodeficiency virus (HIV) especially prior to 1985 when testing for HIV was not available. Currently the blood supply is much safer because of very sensitive testing for HIV as well as hepatitis C. However, new infectious agents emerge constantly and pose a threat to our blood supply. Current and potential threats are reviewed in this manuscript. METHODS: Review of pertinent English language literature. RESULTS: Transmission of infectious agents from blood transfusion is rare. Protozoans pose one the greatest threats because there are no assays available that can reliably detect their presence and because of worldwide travel. Viruses potentially pose a significant threat to the blood supply. The West Nile virus has recently been transmitted by a blood transfusion that was negative by assay for WNV. Severe acute respiratory syndrome (SARS) poses a threat to the blood supply but has never been transmitted in a transfusion. Prions also have been transmitted by a blood transfusion. CONCLUSIONS: Several infectious agents pose potential threats. The current risk of a blood transfusion is very low but the potential threat is ever present.

Boada LD, Zumbado M, Torres S, López A, Díaz-Chico BN, Cabrera JJ, Luzardo OP. · Department of Clinical Sciences, Health Sciences Center and Faculty of Veterinary Medicine, University of Las Palmas de Gran Canaria, Spain. · Arch Toxicol. · Pubmed #10650918 No free full text.

Abstract: Stanozolol (ST) is a 17alpha-alkyl anabolic-androgenic steroid (17alpha-AAS) often misused by athletes and bodybuilders. The use of anabolic-steroids by sportsmen and teenagers has increased dramatically, thus raising the question about their hepatotoxicity, specially those such as ST which are orally administered. Previously, we have reported diverse in vivo effects exerted by this steroid and published the existence of a highly specific ST-binding site in male rat liver microsomes. The existence of this binding site, the reported hepatic effects exerted in humans, and the very limited information about its potential hepatotoxicity led us to treat adult male rats acutely and chronically with ST and study different parameters that could indicate liver damage: serum levels of transaminases, concentration of monooxygenase enzymes in liver, liver membrane lipid peroxidation products, liver histopathology, and cell cycle/ploidy status of liver cells. In our study, no changes in serum transaminases or lipid peroxidation levels were obtained. However, acute stanozolol treatment significantly decreased the levels of cytochrome P450 (Cyt. P450) and cytochrome b5 (Cyt. b5) during the first 48 h of treatment, while subsequently, at 72 and 96 h, these microsomal enzymes underwent a significant increase in their levels. In sharp contrast with this response to acute treatment, the content of these two enzymes during chronic treatment showed an important decrease. Interestingly, acutely and chronically ST-treated livers showed slight to moderate inflammatory or degenerative lesions in centrilobular hepatocytes. Flow cytometric analysis demonstrated that both acute and chronic ST treatment were capable of increasing the percentage of S-phase fraction (%SPF) of liver cells. These findings taken together clearly show that this steroid is capable of altering the liver capacity for metabolizing xenobiotics and indicate that high doses of ST could exert a proliferative effect on liver cells. Such data should be considered in risk evaluations for this compound.