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Deficiency of Adrenocorticoid Hormones: Addison's Disease

For the effects of the adrenocorticoid hormones, see p. 268.

Glucocorticoid deficiency frequently leads to hypoglycemia as a result of disinhibited glycolysis and reduced gluconeogenesis A1). This is especially marked in secondary deficiency of adrenocorticoid hormones due to pituitary insufficiency, because it is associated with decreased somatotropin secretion, the hyperglycemic effect of which will be absent (^ p. 262). The hypoglycemia activates the sympathetic nervous system and inhibits the release of insulin, and thus also of its influence on lipolysis and protein breakdown. The reduced lipolytic and proteolytic action of cortisol is more than compensated by a decreased insulin and an increased epinephrine effect. Li-polysis and protein breakdown are thus stimulated. Further effects of the raised epinephrine release are tachycardia and sweating (^A2). The reduced sensitivity to catecholamines of the heart and blood vessels leads to a fall in blood pressure despite the release of epineph-rine. Due to the diminished secretion of hydrochloric acid, pathogens that have been swallowed will be less effectively killed in the stomach and more commonly cause gastrointestinal infections (^ A6). Diarrhea and vomiting occur with corresponding loss of water and electrolytes. The lack in glucocorticoid effect on blood-forming cells results in anemia, neutropenia, eosinophilia, and lymphocytosis (^A4). Other symptoms are fatigue and weakness. Furthermore, depression is caused by the lack of glucocorticoid action on the brain. However, while cortisol deficiency persists, sensitivity of the target cells is raised and they thus delay the onset of symptoms.

In primary adrenocorticoid insufficiency (Addison's disease) the diminished negative feedback from cortisol leads to a massive rise in the synthesis of pro-opiomelanocortin (POMC), the precursor of ACTH. This increases formation not only of ACTH, but also of a-me-lanotropin (a-MSH or melanocortin). a-MSH as well as ACTH itself cause brown discoloration of the skin (^ A3), because of which Addison's disease has been called "bronze disease". If one adrenal cortex is absent, ACTH causes hypertrophy of the intact adrenal cor tex. If both adrenals are absent, ACTH can even cause the ectopic formation of adreno-corticoid hormones, but this is usually inadequate. In secondary adrenocorticoid insufficiency skin pigmentation is decreased because of a lack of a-MSH and ACTH.

Mineralocorticoid deficiency leads to renal salt loss and renal retention of K+, Mg2+, and H+ (^A5). Na+ reabsorption in the sweat glands and gut is also impaired. This results in salt deficiency, hypotonic dehydration, hypo-volemia, drop in blood pressure, and in the increase of intracellular volume (^p. 122ff.). This can lead to a decrease in renal perfusion and glomerular filtration rate, causing an increase of plasma creatinine concentration. Also, due to the impaired renal perfusion the release of renin and angiotensin I-II will be raised. As angiotensin II stimulates ADH release and ADH leads to renal water retention the release of angiotensin II contributes to hy-poosmolarity. The retention of K+, Mg2+, and H+ leads to reduced neuromuscular excitability as well as abnormalities of action potential formation and conduction in the heart due to hyperkalemia, hypermagnesemia, and acidosis (^A8 and p.124ff.). In combined mineralo-corticoid and glucocorticoid deficiency, the increased fat and protein breakdown and loss of fluid cause weight loss, and arterial hypotension and anemia reduce physical fitness.

A lack of androgens manifests itself especially in sparse pubic hair as well as muscle wasting and loss of libido (^A7). However, lack ofadrenal androgens is ofno consequence in men, as long as testosterone production in the testes is normal.

Acute worsening of the symptoms leads to Addisonian crisis with extreme weakness, fall in blood pressure, tachycardia, diarrhea, hypo-glycemia, hyponatremia, hyperkalemia, and oliguria. It is frequently the consequence of an infection that normally, but not in patients with Addison's disease, leads to an increase in cortisol release.

|— A. Effects and Symptoms of Adrenocortical Hormone Deficiency

Proopiomelanocortin f

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