The effects of the somatostatin analogue, octreotide, on postural hypotension, before and after food ingestion, in primary autonomic failure

Abstract

The effects of the somatostatin analogue, octreotide on postural hypotension have been compared with placebo, before and after food ingestion in two groups with primary autonomic failure; patients with pure autonomic failure, and patients with additional neurological involvement as part of multiple system atrophy. After placebo, supine blood pressure was unchanged, but after octreotide, it rose in both groups. Octreotide reduced pre-prandial postural and supine post-prandial hypotension in both pure autonomic failure and multiple system atrophy patients. Postural hypotension post-prandially was considerably worse after placebo; this was reduced after octreotide. Plasma noradrenaline and adrenaline levels remained unchanged. Plasma glucose levels rose higher and faster after placebo. Insulin levels were similar in both groups at rest, but rose higher in patients with pure autonomic failure after placebo. After octreotide, the insulin response in both groups was suppressed. We conclude that octreotide prevents post-prandial hypotension in both groups with primary autonomic failure and additionally reduces postural hypotension both before and after food ingestion. The greater rise in insulin levels in patients with pure autonomic failure suggests that insulin may be a contributing factor to the more severe post-prandial hypotension observed in this group of patients.

Severe Hypertension Induced by the Long-Acting Somatostatin Analogue Sandostatin LAR in a Patient with Diabetic Autonomic Neuropathy

“…In patients with autonomic failure, octreotide has been reported to prevent alcohol-induced hypotension (16) and exert a rapid, but brief, pressor effect. Octreotide has also been used in the management of autonomic failure for relieving both postprandial and postural hypotension (9,10,17). The pressor effects of the somatostatin analogues could result from an imbalance of vasomodulatory agents, with a resultant increase of vasoconstricting tone reflecting a decrease of vasodilatory gut peptides and a relative preservation of norepinephrinemediated vasoconstriction.…”

Pharmacotherapy of Cardiovascular Autonomic Dysfunction in Parkinson Disease

“…A study reported no changes in plasma norepinephrine after octreotide suggesting no effect on NE pool. [75] Octreotide use is limited by the need for parenteral administration, and by gastrointestinal symptoms such as abdominal pain, nausea and vomiting in susceptible patients. The effective dose is 12.5 ug SQ; in patients with refractory nOH, doses of 25 ug SQ may be more appropriate in refractory cases.…”

Dysautonomia

“…Excessively high doses may cause nausea or altered gastrointestinal motility. Gastrointestinal side effects are particularly prominent in patients with diabetes mellitus who can rarely tolerate octreotide for this reason 26;29 .…”