Introduction

Hypopituitarism is the clinical syndrome which results from failure of the anterior pituitary gland to secrete adequately one or more of its hormones. In contrast with the posterior pituitary, the anterior lobe is an endocrine gland. Prolactin, growth hormone, corticotropin, thyrotropin, and the gonadotropins (luteinizing hormone and follicle-stimulating hormone) are all primarily under control of regulatory hormones secreted by the hypothalamus and released into the hypothalamic-pituitary portal system. The somatotropic, thyrotropic, and gonadotropic axes are key determinants of normal growth and anabolism. Prolactin, the pituitary-adrenal axis (cortisol and dehydroepiandrosterone sulphate (DHEAS)), and growth hormone play important roles in immunological homeostasis.

Hypopituitarism can result from intrinsic hypothalamic lesions, intrinsic pituitary lesions, or extrinsic extrasellar disease which impinges on, infiltrates, or destroys the hypothalamus, the pituitary stalk, or the pituitary gland. All disorders can have an 'organic' or 'functional' origin; the latter has the potential for reversibility ( Table,. .1).

Table 1 Etiology of hypopituitarism

A critical care specialist may have to deal with hypopituitarism as a recognized pre-existing disease that requires appropriately continued therapy during intercurrent illness, an acute exacerbation of an undiagnosed insufficiency evoked by surgery or disease, the sequela of recent neurosurgery, cerebral trauma, infection, or shock, or a temporary dysfunction induced by the stress of the critical condition itself and/or its therapy.

The clinical impact of acquired hypopituitarism in critical care conditions depends on which axes are involved in the lesion and on the severity and duration of the pituitary failure.

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