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This review summarizes the pathology, molecular genetics, diagnostics, and treatment of primary pigmented nodular adrenocortical disease and its association with Cushing's syndrome.
This review summarizes the pathology, molecular genetics, diagnostics, and treatment of primary pigmented nodular adrenocortical disease (PPNAD).
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Provides PPNAD-Cushing's synthesis for clinicians; extends genetic and diagnostic literature but leaves open prospective validation.
Primary pigmented nodular adrenocortical disease (PPNAD) is a form of bilateral adrenocortical hyperplasia that is often associated with corticotrophin (ACTH)-independent Cushing's syndrome (CS) and is characterized by small to normal-sized adrenal glands containing multiple small cortical pigmented nodules (1,2). PPNAD may occur in an isolated form or associated with a multiple neoplasia syndrome, the complex of spotty skin pigmentation, myxomas, and endocrine overactivity, or Carney complex, in which Cushing's syndrome is the most common endocrine manifestation (3). Molecular studies have led to the identification of several genes, defects in which may predispose PPNAD formation; all of these molecules play important role for the cAMP signaling pathway. This review intends to present the most recent knowledge of the pathology and molecular genetics of the benign bilateral adrenocortical lesions, as well as to discuss the modern tools for diagnostics and treatment of this condition.
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Horvath et al. (2007) conducted a review in Primary pigmented nodular adrenocortical disease (PPNAD) and Cushing's syndrome. This review summarizes the pathology, molecular genetics, diagnostics, and treatment of primary pigmented nodular adrenocortical disease and its association with Cushing's syndrome.
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