Pancreatic toxicity endocrine

Recommended dosage and monitoring requirements PEG-Intron is administered once weekly for 1 year. The dose should be administered on the same day of each week. Initial dosing should be based on body weight. Serum hepatitis C virus (HCV) should be assessed after 24 weeks of treatment. Discontinuation of treatment should be considered in patients who have not achieved HCV RNA below the limit of detection after 24 weeks of therapy. Patients should be monitored for neuropsychiatric events, bone marrow toxicity, endocrine disorders, cardiovascular events, colitis, pancreatitis, autoimmune disorders, pulmonary disorders, and hypersensitivity. 

The initial hazard identification of pancreatic toxicity in a prechnical study is always concerning because of the potentially serious human health risks, which may include fulminant, hfe-threatening cases of DIAP or a lifelong iUness, such as CP, type 1 diabetes, or pancreatic neoplasia. Because both the exocrine and the endocrine pancreas have enormous reserve capacities and there are limited sensitive and specific biomarkers to detect pancreatic injury in both animals and humans, there is always the concern that subclinical DIAP may initially go undetected in humans. Further, AP may progress until a threshold of severity is evident in minimally or asymptomatic healthy human volunteers exposed to drug candidates with unknown risks and/or in previously healthy patients that receive standard-of-care agents with marked... 

Microvascular In addition to analysis of endocrine and exocrine cell systems in the pancreas, additional cell types may play a role in the development of a drug candidate-induced pancreatic toxicity. The dense... 

Other Inflammatory Muscle Disorders Endocrine Myopathies Thyroid Disorders Adrenal Disorders Pituitary Disorders Parathyroid Disorders Pancreatic Disorders Drug-Induced and Toxic Myopathies Management of Muscle Disease... 

Other possible examples of endocrine disruption due to selenium exposure include pancreatic damage in sheep and rats fed selenium as sodium selenite, sodium selenate, or seliniferous wheat (Halverson et al. 1966 Harr et al. 1967 Smyth et al. 1990) and decreased plasma glucose (an insulin-like effects) in rats injected with sodium selenate. However, these are isolated reports and it is not clear what relevance they have for selenium toxicity in humans. 

No studies were located regarding toxicity mediated through the endocrine axis in humans after exposure to ammonia. Two studies examined the effects of induced hyperammonemia (with infusion of ammonium chloride) in steers on circulating and portal-drained visceral flux of metabolites and on pancreatic hormones (Fernandez et al. 1988, 1990). Plasma glucose increased 12% during infusion of ammonium chloride (Fernandez et al. 1988, 1990). Plasma insulin decreased up to 46% during ammonium chloride infusion, and then increased up to 122% after infusion was halted (Fernandez et al. 

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