The scorpion envenoming syndrome: a different perspective. The physiological basis of the role of insulin in scorpion envenoming

Abstract

Death caused by scorpion envenoming (Buthidae family) is a common event in tropical and subtropical countries. Severe scorpion envenoming causes an autonomic storm resulting in a massive release of catecholamines, angiotensin II, glucagon, cortisol, and changes in insulin secretion. As a consequence of these changes in the hormonal milieu, scorpion envenoming results in a syndrome of fuel energy deficits and an inability of the vital organs to utilize the existing metabolic substrates, which causes myocardial damage, cardiovascular disturbances, peripheral circulatory failure, pulmonary oedema, and many other clinical manifestations alone or in combination, producing multi-system-organ-failure (MSOF) and death. Insulin-glucose infusion or antivenom administration through the release of insulin seems to be the physiological basis for the control of the metabolic response when that has become a determinant to survival of scorpion sting victims

Effects of Androctonus crassicauda (Olivier, 1807) (Scorpiones: Buthidae) venom on rat metabolism

“…Many studies have emphasized that blood glucose levels increase after envenomation resulting in hyperglycemia in animal models (10,16,22,(27)(28)(29)(30)(31)49) and patients (2,11,12,47). In the present study, hyperglycemia was seen after A. crassicauda venom administration.…”

“…In the present study, hyperglycemia was seen after A. crassicauda venom administration. Several studies have reported that this might be due to a massive release of catecholamines, increased glucagon and cortisol levels, changes in thyroid hormone levels, and changes in insulin secretion (20,(27)(28)(29)(30).…”

Non-cardiogenic mechanisms for the pulmonary edema induced by scorpion venom

“…Insulin has been used to reverse the pathophysiology of envenomation [14]. It has been explained on the basis of insulin resistance resulting from autonomic storm and massive release of free fatty acids [14].…”

“…It has been explained on the basis of insulin resistance resulting from autonomic storm and massive release of free fatty acids [14]. In addition, increased levels of TNFα and other inflammatory cytokines (IL 1β and IL 6) also produce insulin resistance [2].…”

“…In addition, increased levels of TNFα and other inflammatory cytokines (IL 1β and IL 6) also produce insulin resistance [2]. Lack of insulin effect results in energy deficiency that causes metabolic disregulation and adds to the dysfunctioning of multi-systems [2,14]. In our earlier study, we have shown the development of insulin resistance after envenomation in experimental animals [15].…”