Adrenal cortex insufficiency

The reabsorption of NaCl is under hormonal control by the adrenal cortex insufficient activity of the gland results in drastic losses of Na and Cl . The chief mineral corticoid is aldosterone it also controls K excretion, but in the opposite sense. The Na+ K+ ratio of the urine, therefore, is an indicator of adrenal cortex function. 

Primary adrenal insufficiency (Addison s disease) most often involves the destruction of all regions of the adrenal cortex. There are deficiencies of cortisol, aldosterone, and the various androgens. Medications that inhibit cortisol synthesis (e.g., ketoconazole) or accelerate cortisol metabolism (e.g., phenytoin, rifampin, phenobarbital) can also cause primary adrenal insufficiency. 

Desoxycorticosterone causes an increase in reabsorption of sodium ions and excretion of potassium ions from the renal tubules, which leads to increased tissue hydrophilicity. This facilitates an elevated volume of plasma and increased arterial pressure. Muscle tonicity and work capability are increased. It is used for an insufficiency of function of the adrenal cortex, myasthenia, asthenia, adynamia, and overall muscle weakness. Synonyms of this drug are percorten, docabolin, cortitron, and others. 

Corticosteroids Adrenal insufficiency, antiinflammatory agents, immunosuppressants Adrenal cortex... 

Adrenal insufficiency may result from hypofunction of the adrenal cortex (primary adrenal insufficiency, Addison s disease) or from a malfunctioning of the hypothalamic-pituitary system (secondary adrenal insufficiency). In treating primary adrenal insufficiency, one should administer sufficient cortisol to diminish hyperpigmentation and abolish postural hypotension these are the cardinal signs of Addison s disease. 

The rate of aldosterone secretion is subject to several influences. ACTH produces a moderate stimulation of its release, but this effect is not sustained for more than a few days in the normal individual. Although aldosterone is no less than one third as effective as cortisol in suppressing ACTH, the quantities of aldosterone produced by the adrenal cortex and its plasma concentrations are insufficient to participate in any significant feedback control of ACTH secretion. 

Ascorbic acid depleted in adrenal cortex on stimulation by ACTH Biotin and vitamin A adrenocortical insufficiency noted in biotin and vitamin A deficiency... 

Ascorbic acid may be required for steroid hormone biosynthesis depleted from adrenal cortex on cortical secretion Biotin adrenocortical insufficiency noted in biotin deficiency... 

All of Ihese hormones arc synthesized from cholesterol in the adrenal cortex, by ait extended scries of reaelions. which include many related compounds. Although these hormones have widespread effects throughout the organism, their primary mechanism is not known, so that many of the effects may be indirect. Much of the knowledge t l their action arises from studies of insufficiency or hyperactivity of the adrenal cortex, which produces a wide variety of pathological condilioiis. See Table I. 

Withdrawal symptoms disappear if the glucocorticoid is resumed, but as a rule they will in any case vanish spontaneously within a few days. More serious consequences can ensue, however, in certain types of cases and if adrenal cortical atrophy is severe. In patients treated with corticoids for the nephrotic syndrome and apparently cured, the syndrome is particularly likely to relapse on withdrawal of therapy if the adrenal cortex is atrophic (SEDA-3,305). In some cases, acute adrenocortical insufficiency after glucocorticoid treatment has actually proved fatal. It is advisable to withdraw long-term glucocorticoid therapy gradually so that the cortex has sufficient opportunity to recover. Table 5 lists methods of... 

Of 62 initially autoantibody-negative patients treated with interferon alfa for chronic hepatitis C for a mean of 8 months, three developed antibodies to 21b-hydroxylase, a sensitive assay of adrenocortical autoimmunity (528). However, there were no cases of Addison s disease or subclinical adrenal insufficiency. This study suggested that the adrenal cortex is another potential target organ of autoimmune effects of interferon alfa, along with thyroid and pancreatic islet cells. 

Drugs with mineralocorticoidlike activity (aldosterone agonists) are frequently administered as replacement therapy whenever the natural production of mineralo-corticoids is impaired. Mineralocorticoid replacement is usually required in patients with chronic adrenocortical insufficiency (Addison disease), following adrenalectomy, and in other forms of adrenal cortex hypofunction. These conditions usually require both mineralocorticoid and glucocorticoid replacement. 

Adrenocorticotropin is a peptide hormone produced in the anterior pituitary. Its primary endocrine function is to stimulate synthesis and release of cortisol by the adrenal cortex. Corticotropin can be used therapeutically, but a synthetic derivative is more commonly—and almost exclusively—used to assess adrenocortical responsiveness. A substandard adrenocortical response to exogenous corticotropin administration indicates adrenocortical insufficiency. 

Replacement therapy for secondary or tertiary adrenocortical insufficiency These deficiencies are caused by a defect either in CRF production by the hypothalamus or corticotropin production by the pituitary (see p. 247). [Note Under these conditions, the adrenal cortex synthesis of mineralocorticoids is less impaired than that of glucocorticoids.] The adrenal cortex responds to corticotropin administration by synthesizing and releasing the adrenal corticosteroids. Hydrocortisone is also used for these deficiencies. 

It is felt, however, that true adrenocortical exhaustion is a very uncommon condition (C3) and low plasma values imresponsive to ACTH are found in only a minority of very ill people (M6). The adrenal cortex usually responds to prolonged stress by hypertrophy and measurements of cortisol after prolonged stress show that they are frequently high (C12). True adrenal exhaustion or insufficiency can be diagnosed only when the plasma cortisol levels are constantly low and do not respond to ACTH stimulation. 

Cortisol. Cortisol, secreted by the adrenal cortex in response to adrenocorticotropic hormone (ACTH), stimulates gluconeogenesis and increases the breakdown of protein and fat. Patients with Cushing s syndrome have increased cortisol owing to a tumor or hyperplasia of the adrenal cortex and may become hyperglycemic. In contrast, people with Addisons disease have adrenocortical insufficiency because of destruction or atrophy of the adrenal cortex and may exhibit hypoglycemia. ... 

The use of corticosteroids in the treatment of septic shock has been a topic of controversy for many years. A meta-analysis of early studies of steroids in sepsis demonstrated a lack of benefit and potential harm in sepsis and septic shock. There is a renewed interest in corticosteroid use because of the increased awareness of adrenocortical insufficiency in critically ill patients with septic shock. Relative adrenal insufficiency has been defined as a poor adrenal response [<250 nmol/L (9 mcg/dL) irrespective of the initial serum cortisol level] to a dose of synthetic adrenocorticotropic hormone (ACTH), indicating a low fnnctional reserve of the adrenal cortex. Although absolute insufficiency is rare, relative adrenocortical insufficiency in the presence of normal or high cortisol concentrations at baseline is present in 30% to 50% of patients with septic shock and is associated with a poor outcome. ... 

Addison s disease (primary adrenal insufficiency) is a defi- ciency in cortisol, aldosterone, and various androgens resulting from the loss of function of all regions of the adrenal cortex. 

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