Mechanisms of Nonneoplastic Endocrine Hyperplasia—A Changing Concept: A Review Focused on the Thyroid Gland
1995; Oxford University Press; Volume: 16; Issue: 4 Linguagem: Inglês
10.1210/edrv-16-4-411
ISSN1945-7189
Autores Tópico(s)Neuroendocrine Tumor Research Advances
ResumoASIGNIFICANT part of clinical endocrinology concerns diseases that are caused by excessive diffuse or focal proliferation of cells within one or several endocrine glands. The ensuing hyperplastic, often nodular, expansion is commonly thought to arise by one of two pathways: 1) excessive cell growth is either considered to be the consequence of aberrant secretion of a growth-and function-stimulating hormone or, 2) a nodule may be a true tumor evolving by mechanisms analogous to those operating in the pathogenesis of any other tumor (1- 5). The former process may be called “nonneoplastic endocrine hyperplasia” (NNEH) since it is considered to be reversible upon cessation of the stimulus, while true neoplasias are generally regarded to be clonal lesions caused by known or unknown irreversible some of their genes (6–8). For the present review, the term “true neoplasia” will be applied to all nodular lesions that grow autonomously, i.e. in the absence of any known systemically active growth-stimulating agent and irrespective of a presently known genetic or cytogenetic aberration. The three basic types of NNEH are described in Table 1.
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