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CLINICAL PERSPECTIVE: Acromegaly and Cancer: Not a Problem?

2001; Oxford University Press; Volume: 86; Issue: 7 Linguagem: Inglês

10.1210/jcem.86.7.7635

1945-7197

Shlomo Melmed,

Neuroendocrine Tumor Research Advances

Acromegaly is usually caused by a GH-secreting pituitary adenoma. Somatic growth and metabolic dysfunction occur subsequent to unrestrained GH secretion and elevated insulin-like growth factor (IGF)-I and IGF-binding protein (IGFBP)-3 levels (1) (Fig 1). Classic clinical features of acromegaly include acral overgrowth, sweating, headaches, menstrual disturbances, and glucose intolerance (Table 1) (2). Well-documented clinical risks of long-term tissue exposure to uncontrolled GH hypersecretion include cardiac disease and hypertension, diabetes, respiratory disorders, joint disease, and neuropathy (Table 2) (3). The degree of risk for malignancy in these patients is unresolved; and acromegaly, representing an experiment of nature, could answer the question of whether or not elevated GH and IGF levels provide a permissive growth advantage for neoplasms, resulting in more aggressive malignant disease and/or increased cancer-associated mortality (4). Analysis of the determinants for mortality outcome in acromegaly indicates that approximately 60% of patients succumb to cardiovascular disease; 25% from respiratory disease; and in 15% of patients, the cause of death is attributed to malignancy (Table 2). Nevertheless, absolute circulating GH values seem to constitute the most significant single determinant of survival, regardless of the cause of death (5–14). Several recent compelling studies support the critical role of GH, suggesting that GH control is associated with reversal of adverse mortality rates, regardless of the nature of associated comorbidity (13). Thus, suppression of GH to less than 1 ng/mL, during an oral glucose tolerance test, and normalization of IGF-I levels portend a favorable mortality outcome (15).