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DOI: 10.1080/019262301301418829 Overview of Structural and Functional Lesions in Endocrine Organs of AnimalsDepartment of Veterinary Biosciences, The Ohio State University, Columbus, Ohio 43210, capen.2{at}osu.edu The objective of this review is to summarize the pathogenic mechanisms responsible for perturbations of endocrine function and development of structural lesions that result in important diseases in domestic and laboratory animals. For each major category, several specifi c disease problems have been selected to illustrate the functional and morphologic lesions that are characteristic for either a naturally occurring endocrinopathy or endocrine disturbances induced by the administration of large doses of xenobiotic chemicals. The major pathogenic mechanisms responsible for disruption of endocrine function include primary hyperfunction, secondary hyperfunction, primary hypofunction, secondary hypofunction, endocrine hyperactivity secondary to other conditions, hypersecretion of hormones by nonendocrine tumors, failure of target cells to respond to a hormone, failure of fetal endocrine function, abnormal degradation (increased or decreased rate) of hormone, and iatrogenic syndromes of hormone excess (direct and indirect). Disorders of the endocrine system are encountered in a wide variety of domestic and laboratory animal species and often present challenging diagnostic problems. The development of proliferative lesions, usually hyperplasia and benign tumors, in endocrine organs and hormone-responsive tissues are common findings in chronic studies with high doses of many nongenotoxic xenobiotic chemicals administered to sensitive rodent species and may have limited significance for human safety assessment.
Key Words: Endocrine lesions hormonal imbalances hyperthyroidism hyperparathyroidism congenital goiter hypothyroidism panhypopituitarism testicular Leydig cell adenomas tubulostromal tumors of ovary humoral hypercalcemia of malignancy parathyroid hormone—related protein prolonged gestation hormone degradation iatrogenic syndromes of hormone excess
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