Heterogeneous Responses to the Long-Term Treatment of Active Acromegaly with Octreotide.

Abstract

Abstract. To study GH response to the long-acting somatostatin analogue, we treated 11 actively acromegalic patients with octreotide (Sandostatin),100 µg, sc, tid, for six months. Their endocrinological outcomes and clinical improvements varied. The 11-h GH secretory profiles on pretreatment day confirmed the hypersecretion of GH in all patients. Three hours after the first dose of octreotide, serum GH declined rapidly to levels below 5 ng/ml in all but two patients who failed to normalize their serum GH. In spite of the subsequent doses, there was no further suppression in serum GH. Drug resistance with GH rebound developed in some patients after three months of continued treatment.The paradoxical serum GH rises in response to oral glucose or iv TRH detected before the treatment in all patients attenuated or disappeared after the 6-month octreotide therapy; an exceptional case was one of the above-mentioned two patients, whose serum GH was stimulated more than before by glucose and TRH at the end of therapy. Serum insulin-like growth factor I (IGF-I) levels of all patients showed a significant reduction after 6-month treatment, but their mean values remained abnormally high. There were no intolerable adverse side effects; some patients, however, experienced pain at the injection site, passage of loose stool, and incidence of new gall stone or intrahepatic lesions on octreotide therapy. We concluded that octreotide was a useful long-term adjunctive therapeutic agent for patients with active acromegaly, but that a high degree of response heterogeneity including total refractoriness would be expected.

Treatment of acromegaly with octreotide‐LAR: extensive experience in a Brazilian institution

“…The real meaning of our observation regarding the morbi‐mortality of acromegaly remains unclear, but its finding might be associated to an intermediate response to OCT‐LAR as a result of more elevated basal IGF‐I levels, irregular absorption of the medication or reduction in efficacy along the treatment. In fact, there are some reports, albeit sporadic, showing an ‘escape’ of the inhibitory effect of octreotide 25–27 . This finding could be explained by the loss of octreotide activity, as one aspect of the dysregulation process, resulting from the decreased somatostatin receptor (SSTR) expression or changes at the receptor or postreceptor level.…”

“…In fact, there are some reports, albeit sporadic, showing an 'escape' of the inhibitory effect of octreotide. [25][26][27] This finding could be explained by the loss of octreotide activity, as one aspect of the dysregulation process, resulting from the decreased somatostatin receptor (SSTR) expression or changes at the receptor or postreceptor level. Alternatively, development of OCT antibodies could be the reason.…”

Rebound Hypersecretion of GH Following Octreotide Withdrawal due to Liver Dysfunction in an Acromegalic Patient.

“…Arosio et al [6] also reported that several acromegalic patients showed GH concentrations 60-120% higher than baseline after octreotide therapy. Chang et al [7] showed the atypical case of GH rebound within two weeks after therapy. We also report here a similar case showing rebound phenomena of GH and IGF-1 for 10 days after stopping octreotide.…”

“…It has been shown to induce long-acting inhibition of GH secretion without rebound hypersecretion [3,4]. We report a case of GH rebound elevation after octreotide withdrawal due to liver injury in a patient with active acromegaly, since very few acromegalics are reported to exhibit rebound phenomena [5][6][7]. Case report In 1996, a 45-year-old man was referred to us because of hypertension and acromegaly.…”