Endocrine Abstracts

Introduction: Acute and chronic alcohol intake and alcohol withdrawal induce dysfunction of neuroendocrine and other regulatory systems. The expression ‘neuroendocrine dysfunction’ alludes to an assortment of conditions brought about by imbalances in the body’s chemical creation straightforwardly connected with the pituitary, nerve center, and their tomahawks following TBI.

Aims: This study aimed to assess a possible hypothalamo-pituitary-adrenal (HPA) axis dysfunction in a population of alcoholics, using a dexamethasone suppression test (DST).

Methods: For this study, 90 participants had been selected, among whom 65% of participants were depressive and 35% of are non-depressive alcoholics.

Discussion: The serum and urinary cortisol were compared between the groups of 89 male patients (65% depressive and 36% non-depressive alcoholics) (Hamilton test), before and after DST. In non-depressive patients, 49% was non-suppressive in DST. In depressive patients, 47% was suppressive in the DST test (serum cortisol). Twenty-four hours urinary excretion in a group of non-depressive patients was suppressed in 79% of cases; depressive patients showed 50.9% non-suppressors. Basal serum cortisol secretion was significantly lower in a group of non-depressive than depressive patients. Also, serum concentrations at 16 h were significantly higher in a group of depressive non-suppressive patients. Basal urinary cortisol excretion was in the normal range in all patients, but after dividing the patients into suppressible and non-suppressible groups, significantly higher (P< 0.002) basal urinary cortisol concentrations were found in the latter.

Conclusion: Based on the DST test and the basal cortisol measurement, the findings reveal that the neuroendocrine dysfunction of alcoholic patients could be present even if the depression is pronounced.