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Elucidating mechanisms of drug induced toxicity, mechanisms and Risk Factors for Drug-Induced Dysglycemia

Mechanisms and Risk Factors for Drug-Induced Dysglycemia

Not only was the analysis of the two enzymes critical, but the new two-enzyme mass spectrophotometric assay facilitated the evaluation of greater numbers of samples. Gatifloxacin has since been withdrawn from the market. The authors postulate, based on the report of Hwa et al.

Exposure to these agents may reduce or block bile flow and precipitate liver injury, in part due to the toxicity of bile acids and other bile constituents. Extrahepatic cholestasis can be caused by bile duct tumors, strictures, cysts, diverticula, and various forms of injury. The simultaneous evaluation of both enzymes using the new assay was a major breakthrough in and of itself. These analyses were achieved by employing a mass spectrophotometric method developed in their laboratory for the simultaneous and rapid assay of the two enzymes Ndong-Akoume et al. Symbols within the gray box indicate data reported for the first time in the highlighted paper Akoume et al.

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Difficulties are associated with elucidating the mechanisms responsible for drug-induced side effects in clinical settings. Therefore, mechanisms underlying and risk factors for drug-induced dysglycemia need to be determined in order for these drugs to be used more safely. These findings will be useful for establishing safer drug therapies. The authors also raise an important consideration in their discussion of the possibility that perturbations in biliary lipid membrane transporters, high school story dating times such as multidrug resistance P-glycoproteins e.

This question was answered in a subsequent investigation Duguay et al. Furthermore, diabetes mellitus is considered one of the risk factors for hyperglycemia. Or, in other words, is the elevated cholesterol derived from the existing cellular pool or from an increase in the de novo synthesis of cholesterol? Thus, prior to the present highlighted study, confounding data sets existed that could not explain the accumulation of newly synthesized cholesterol. The investigators address this important question in the highlighted paper.

Intrahepatic cholestasis can be caused by drugs, sepsis, total parenteral nutrition, lymphomas, tuberculosis, sarcoidosis, and amyloidosis. Some drugs have been shown to induce severe dysglycemia, and this side effect continues to be a major issue for patients being treated with these drugs. Furthermore, the mechanism responsible for olanzapine-induced elevations in serum epinephrine levels differed from that by fluoroquinolone antimicrobial agents. We developed a pharmacokinetic-pharmacodynamic model of cibenzoline an antiarrhythmic agent -induced hypoglycemia. This approach will be useful for the identification of variable factors related to drug-induced hypoglycemia.

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