Effect of chronic octreotide treatment on intestinal absorption in patients with acromegaly

Abstract

The adverse gastrointestinal effects of octreotide, a synthetic analog of somatostatin, have not been fully elucidated. Low-dose octreotide frequently causes adverse gastrointestinal symptoms in normal individuals. We investigated the adverse gastrointestinal effects of high-dose octreotide, which is required for the normalization of growth hormone hypersecretion in some patients with acromegaly. Patients with acromegaly (N = 8) were treated with octreotide, 450 micrograms/day, then 1500 micrograms/day for two months at each dosage. Carbohydrate absorption was assessed using the D-xylose test, and fat absorption using fecal fat excretion and serum carotene concentrations, at baseline, at each dosage of octreotide, and after one month of washout. Ultrasonography was used to monitor for cholelithiasis. Growth hormone and insulin-like growth factor-I concentrations were significantly suppressed at both dosages. Adverse gastrointestinal symptoms were mild and transient. D-Xylose absorption remained normal at each dosage and after one month of washout. Fecal fat excretion increased from 7 +/- 2 to 12 +/- 2 g/24 hr (P < 0.05) after the higher dosage and resumed baseline levels after the washout. Mean fasting serum carotene levels remained normal, and carotene loading test (15,000 units three times a day for three days) was unreliable in identifying patients with high fecal fat. No new cholelithiasis was detected by ultrasonography. One of two patients with preexisting cholelithiasis developed biliary colic several days after the treatment period. Although steatorrhea was common, small intestinal absorptive capacity was otherwise unchanged by four months of high-dose octreotide treatment, which significantly suppressed growth hormone secretion in acromegalic patients.

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

“…In addition, octreotide suppressed cholecystokinin and pancreatic peptide releases and impaired fat absorption from the gut [24,27]. We also confirmed this sideeffect of octreotide in our patients who complained frequently with steatorrhea.…”

Adverse events associated with somatostatin analogs in acromegaly

“…Therefore, endogenous somatostatin and its synthetic analogs inhibit all three peptides known to stimulate pancreatic fluid secretion. In support of this is the efficacy of pancreatic enzyme therapy in alleviating most of the GI side effects of octreotide during the initial weeks of therapy [69].…”

“…During subcutaneous octreotide therapy, fecal fat excretion has been demonstrated to significantly increase after the administration of high octreotide dosage (1500 micrograms/day for 2 months at each dosage), inducing steatorrhea, and to resume baseline levels after washout [69]. Although steatorrhea is common, small intestinal absorptive capacity seems to be unchanged by 4 months of high-dose octreotide treatment, as demonstrated by a normal D-Xylose test that reflects the functional absorptive capacity of the proximal small intestine [69].…”

“…Although steatorrhea is common, small intestinal absorptive capacity seems to be unchanged by 4 months of high-dose octreotide treatment, as demonstrated by a normal D-Xylose test that reflects the functional absorptive capacity of the proximal small intestine [69].…”

Therapeutic Principles in the Management of Metastasising Carcinoid Tumors: Drugs for Symptomatic Treatment

“…Pancreatic function is impaired by a decreased secretion of CCK and gallbladder sensitivity to CCK as well as by a suppression of pancreatic exocrine functions. D-Xylose absorption, serum calcium and alka line phosphatase concentrations, however, remain normal and no change in circulating fat-soluble vitamins have been consistently reported [25]. Patients may receive sub stitution with pancreatic enzymes to reduce malabsorptive diarrhea which occasionally improves the extent of steatorrhea [26], Altogether, steatorrhea does not seem to be a problem in long-term treatment because there seems to be an adaptive mechanism, the nature of which is unclear.…”