Somatostatin: Influence on hemostasis—A review

The discovery in 1972 1 and the subsequent synthesis 2 of somatostatin (somatotropin release inhibiting hormone) has generated excitement in the use of this tetradecapeptide in diabetes since it was shown to inhibit the secretion of insulin and glucagon. Subsequently, interest was raised in other endocrine disorders. However, during the investigation of this substance, caution was raised by Koerker and co-workers in 1975 3 that this agent impairs platelet function. Thirteen of 19 baboons who had received multiple infusions of somatostatin through indwelling catheters, along with other drugs and materials, became sick and either died or were sacrificed. Seven of the 13 animals were autopsied, and five of the six animals studied histologically showed the presence of microscopic pulmonary hemorrhages, as well as hemosiderin deposits in the liver and lungs. Platelet counts were measured in seven animals and all but one had thrombocytopenia of varying degrees (32,000–181,000 platelets per microliter). Coagulation parameters in four of these animals, including platelet and fibrinogen survivals, were within normal limits. These findings prompted us to study the effect of infusion of this agent on platelet function in normal and diabetic volunteers. 4 This paper will first discuss normal platelet physiology 5 and then review our current understanding of the influence of somatostatin on hemostasis.