Review
Endocrine abnormalities and outcome of ischaemic stroke

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Abstract

Multiple endocrine abnormalities have been reported in stroke patients. In the past few years, it has been claimed that some of these abnormalities may play a role in worsening the neurological deficit and the outcome of stroke. Several mechanisms have been hypothesised, including a direct effect on the development of neuronal cell death, vasospasm, and development of brain edema. In this brief review, we discuss the current knowledge concerning the role of endothelin-1, arginine vasopressin, and cortisol in the pathogenesis of stroke. Finally, we discuss the possibility that leptin, the OB gene product, may be the link of some of these endocrine abnormalities, and that its abnormal secretion during stroke may contribute to the eating disorders and poor nutritional status often seen in these patients.

Section snippets

Endothelins

Endothelins (ETs) are 21 amino-acid peptides produced in many different tissues. Discovered as products of the vascular endothelium 〚10〛, these peptides have now been shown to be produced in blood vessels by smooth muscle cells 〚11〛 and elsewhere by others cells in different tissues. Genes have been cloned for 3 ETs, ET-1, -2, -3 〚12〛, and for 2 ET receptor subtypes, ETA 〚13〛 and ETB 〚14〛. ETS, mainly ET-1, are potent and long-lasting vasoconstrictors, and it is generally accepted that

Arginine vasopressin

Experimental evidence indicates that arginine vasopressin (AVP), produced in the hypothalamic paraventricular and supraoptic nuclei, in addition to its primary physiological action as a water-retaining hormone, plays an important role in regulating brain volume and electrolyte homeostasis and microvascular resistance in ischaemic cerebral tissue 42, 43. These findings suggest that an alteration of hypothalamic AVP secretion in stroke patients may affect the severity and outcome of the cerebral

Hypothalamus-Pituitary Adrenocortical Axis

Increased activity of the hypothalamic-pituitary-adrenal axis (HPAA), as well as of the sympatho-adrenal system, is commonly seen in various forms of acute stress, including stroke 54, 55. Hypercortisolism per se has potentially serious side effects on many organ systems 〚54〛, and a higher mortality rate has been described in stroke patients with a higher stress response, as measured by plasma cortisol levels and cathecolamine excretion 〚55〛. Furthermore, cognitive disturbances have been

Leptin

Leptin, a recently identified circulating hormone secreted by the adipocytes as a product of the obese (OB) gene, seems to play a crucial role in the regulation of body weight in mammals 〚80〛. In humans, leptin is thought to act as a satiety hormone 〚81〛 in a feedback loop linking food ingestion, the hypothalamus, and adipocyte tissue mass 〚82〛. Although serum leptin levels vary considerably amongst individuals 〚83〛, several findings indicate that leptin secretion is mainly correlated with body

Conclusions

Endocrine abnormalities are common and often profound after stroke. The possibility that increased levels of some hormones, namely ET-1, AVP and cortisol, play an important role in aggravating the neurological deficit and outcome of stroke, deserves further investigation. The pathophysiological mechanisms involved may be several, including a direct effect on the development of neuronal cell death, constriction of collateral vessels with further reduction in regional blood flow, and development

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