Ww. Deherder et Swj. Lamberts, IS THERE A ROLE FOR SOMATOSTATIN AND ITS ANALOGS IN CUSHINGS-SYNDROME, Metabolism, clinical and experimental, 45(8), 1996, pp. 83-85
The effects of somatostatin and its analogs have been studied in diffe
rent subclasses of patients with Cushing's syndrome (due to Cushing's
disease, ectopic corticotropin [ACTH]- and/or corticotropin-releasing
hormone [CRH]-secreting tumors, or ACTH-independent Cushing's syndrome
) and in patients with Nelson's syndrome. In most patients with untrea
ted Cushing's disease, octreotide does not suppress ACTH release, a fi
nding that is supported by in vitro studies. However, octreotide or so
matostatin inhibits pathological ACTH secretion in Nelson's syndrome.
Short-term octreotide treatment has caused a significant initial respo
nse (decreased serum cortisol, ACTH, and cortisoluria) in 24 of 38 (64
%) patients with ectopic ACTH/CRH Cushing's syndrome, and long-term tr
eatment caused a persistent response in 10 of 14 (71%) cases. Pentetre
otide scintigraphy may help to identify those patients with ectopic AC
TH/CRH tumors who will have an initial response to octreotide, and is
useful for locating ectopic ACTH/CRH-secreting tumors and their metast
ases. To date, octreotide has been shown to temporarily suppress gastr
ic inhibitory peptide (GIP)-induced cortisol secretion in GIP-dependen
t (ACTH-independent) Cushing's syndrome, but has not shown any therape
utic benefit in other forms of ACTH-independent Cushing's syndrome. Co
pyright (C) 1996 by W.B. Saunders Company