Etano anabolico

A very typical case of severe cholestasis due to anabolic steroid use.  Because the steroids were being used without medical supervision, the dose and actual duration of use of each preparation was unclear, but cholestasis usually arises within 4 to 12 weeks of starting a C-17 alkylated androgenic steroid.  The jaundice can be severe and prolonged and accompanied by severe pruritus and marked weight loss.  The serum enzymes are typically minimally elevated except for a short period immediately after stopping therapy.  The pattern of enzyme elevations can be hepatocellular, cholestatic or mixed.  Liver biopsy shows a “bland” cholestasis with minimal inflammation and hepatocellular necrosis.  Ma Huang has also been implicated in cases of drug induced liver injury, but is associated with an acute hepatocellular pattern of injury.

AB - Traditional medicinal literature and previous studies have reported the possible role of Cissus quadrangularis (CQ) as an anti-osteoporotic agent. This study examines the effectiveness of CQ in promoting osteoblast differentiation of the murine pre-osteoblast cell line, MC3T3-E1. Ethanolic extract of CQ (CQ-E) was found to affect growth kinetics of MC3T3-E1 cells in a dosage-dependent manner. High concentrations of CQ-E (more than 10μg/ml) have particularly adverse effects, while lower concentrations of and 1μg/ml were non-toxic and did not affect cell viability. Notably, cell proliferation was significantly increased at the lower concentrations of CQ-E. CQ-E treatment also augmented osteoblast differentiation, as reflected by a substantial increase in expression of the early osteoblast marker ALP activity, and at later stage, by mineralization of extracellular matrix compared to the control group. These findings suggest dose-dependent effect of CQ-E with lower concentrations exhibiting anabolic and osteogenic properties.

Results and Conclusions: EtOH consumption completely abolished the anabolic bone rebuilding that occurred after lactation. Decreased BMD and BMC were associated with decreased bone formation and not with increased osteoclast activity. Furthermore, EtOH-fed rats showed greater proportion of fat volume/bone volume and expression of adipocyte-specific genes. EtOH-induced skeletal effects were mitigated by the dietary antioxidant, N -acetyl cysteine or by blocking TNF-α signaling. These data suggest EtOH consumption in the period immediately postweaning may significantly impair the mother's skeletal health and lead to long-term osteopenia.

EtOH consumption significantly impaired anabolic rebuilding of bone after lactation. Lower BMD and BMC in EtOH‐fed rats were associated with decreased bone formation in the proximal tibia, increased proportion of adipocytes, and increased expression of TNF‐α. EtOH‐induced skeletal deficits were prevented by treatment with either NAC or sTNFR1. These data suggest that postlactational anabolic rebuilding is influenced by EtOH consumption and may affect the long‐term risk of osteopenia. Introduction: Despite significant loss of bone during lactation, BMD is restored by a powerful anabolic rebuilding process after weaning. A significant number of women resume alcohol consumption after weaning their offspring from breast feeding. The objectives of this study were to examine the consequences of chronic ethanol (EtOH) consumption on the postlactational rebuilding process and to investigate the underlying mechanisms by which EtOH mediates its detrimental effects. Materials and Methods: Female Sprague‐Dawley rats (n = 7–9 per group) were fed EtOH‐containing diets (13 g/kg/d) for 1, 2, or 4 wk after weaning of their offspring. Skeletal parameters in the proximal tibia were examined using pQCT, μCT, and histomorphometric techniques, and interventional studies were performed on the mechanistic roles of EtOH‐induced oxidative stress and TNF‐α. Results and Conclusions: EtOH consumption completely abolished the anabolic bone rebuilding that occurred after lactation. Decreased BMD and BMC were associated with decreased bone formation and not with increased osteoclast activity. Furthermore, EtOH‐fed rats showed greater proportion of fat volume/bone volume and expression of adipocyte‐specific genes. EtOH‐induced skeletal effects were mitigated by the dietary antioxidant, N‐acetyl cysteine or by blocking TNF‐α signaling. These data suggest EtOH consumption in the period immediately postweaning may significantly impair the mother's skeletal health and lead to long‐term osteopenia.

Etano anabolico

etano anabolico

EtOH consumption significantly impaired anabolic rebuilding of bone after lactation. Lower BMD and BMC in EtOH‐fed rats were associated with decreased bone formation in the proximal tibia, increased proportion of adipocytes, and increased expression of TNF‐α. EtOH‐induced skeletal deficits were prevented by treatment with either NAC or sTNFR1. These data suggest that postlactational anabolic rebuilding is influenced by EtOH consumption and may affect the long‐term risk of osteopenia. Introduction: Despite significant loss of bone during lactation, BMD is restored by a powerful anabolic rebuilding process after weaning. A significant number of women resume alcohol consumption after weaning their offspring from breast feeding. The objectives of this study were to examine the consequences of chronic ethanol (EtOH) consumption on the postlactational rebuilding process and to investigate the underlying mechanisms by which EtOH mediates its detrimental effects. Materials and Methods: Female Sprague‐Dawley rats (n = 7–9 per group) were fed EtOH‐containing diets (13 g/kg/d) for 1, 2, or 4 wk after weaning of their offspring. Skeletal parameters in the proximal tibia were examined using pQCT, μCT, and histomorphometric techniques, and interventional studies were performed on the mechanistic roles of EtOH‐induced oxidative stress and TNF‐α. Results and Conclusions: EtOH consumption completely abolished the anabolic bone rebuilding that occurred after lactation. Decreased BMD and BMC were associated with decreased bone formation and not with increased osteoclast activity. Furthermore, EtOH‐fed rats showed greater proportion of fat volume/bone volume and expression of adipocyte‐specific genes. EtOH‐induced skeletal effects were mitigated by the dietary antioxidant, N‐acetyl cysteine or by blocking TNF‐α signaling. These data suggest EtOH consumption in the period immediately postweaning may significantly impair the mother's skeletal health and lead to long‐term osteopenia.

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