Post by Max on Jun 13, 2005 18:29:26 GMT -5
Statistically significant elevatation of plasma homocysteine levels have been seen in repeated independent studies of human subjects exposed to (Ro)accutane [1 and more]. It is suggested that the elevated Hcy levels in patients after 45 days on Iso therapy could be due either to the 'inhibition' of cystathionine-beta-synthase by the drug and/or their liver dysfunction [1]. Hoffman la Roche itself has admitted to these findings [0]. Significantly lower levels of thyroxine and triiodthyronine have been found in human acne-subjects exposed to the toxin after exposure, indicating a (Ro)accutane induced clinical hypothyroidism [2]. The relationship between hypothyroidism and a variety of cardiovascular risk factors is now well established [3 and more].
Significantly elevated GGT (gamma-glutamyltranspeptidase) by retinoic acid, a recently clarified risk factor for CVD
The relation of GGT to the risk of death from CVD was examined in a cohort of 163 944 Austrian adults that was monitored for up to 17 years. To evaluate GGT as an independent predictor, Cox proportional hazards models were calculated, which adjusted for established risk factors. In both men and women, high GGT was significantly (P<0.001) associated with total mortality from CVD, showing a clear dose-response relationship [4].
Retinoic acid increased the level of the GGT mRNA and this enhancement was progressive, depending on the duration of exposure and on the concentration of retinoic acid in the culture medium. When retinoic acid was removed from cultures which had been exposed to it for 4 days, the induced GGT activity remained unchanged. In contrast to transformed cell lines, retinoic acid did not induce the activity of GGT in normal/non-transformed rat liver epithelial cells [5].
Significantly elevated GGT (gamma-glutamyltranspeptidase) by retinoic acid, a recently clarified risk factor for CVD
The relation of GGT to the risk of death from CVD was examined in a cohort of 163 944 Austrian adults that was monitored for up to 17 years. To evaluate GGT as an independent predictor, Cox proportional hazards models were calculated, which adjusted for established risk factors. In both men and women, high GGT was significantly (P<0.001) associated with total mortality from CVD, showing a clear dose-response relationship [4].
Retinoic acid increased the level of the GGT mRNA and this enhancement was progressive, depending on the duration of exposure and on the concentration of retinoic acid in the culture medium. When retinoic acid was removed from cultures which had been exposed to it for 4 days, the induced GGT activity remained unchanged. In contrast to transformed cell lines, retinoic acid did not induce the activity of GGT in normal/non-transformed rat liver epithelial cells [5].
