Adrenocortical atrophy

Regimens for prevention of adrenocortical atrophy. Cortisol secretion is high in the early morning and low in the late evening (circadian rhythm). Accordingly, sensitivity to feedback inhibition must be high in the late evening. 

Interestingly, while peripheral neuroendocrine function appears normal in patients with panic disorder, decreased basal cortisol concentrations have been reported in most studies in PTSD patients. This relative hypocortisolism occurs in the context of increased feedback inhibition of the HPA axis (see Yehuda, 2000). However, a dissociation between central and adrenocortical (re)activity has been found in animal models of severe early-life stress as well as in abused children and women, suggesting that adrenal dysfunction may, at least in part, contribute to hypocortisolism in PTSD. In the face of hypocortisolism, it seems surprising that hippocampal atrophy is one of the most prominent findings in patients with PTSD, including adult survivors of childhood abuse with PTSD (see Newport and Nemeroff, 2000). While increased glucocorticoid sensitivity of hippocampal cells may play a role in the development of hippocampal atrophy, another potential mechanism may involve toxic effects of markedly increased cortisol responses to everyday stress in patients with PTSD. 

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... 

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. ... 

Addison s disease is a rare, potentially fatal condition due to insufficient production of both aldosterone and cortisol caused by atrophy of the adrenal glands. It is characterised by low blood pressure, loss of sodium, weight loss and pigmentation of mucosal membranes. Adrenocortical insufficiency also results from pituitary failure with loss of adrenocorticotrophic hormone (ACTH) production. 

The simple experiment of removing the pituitary and from the sella turcica to another site of the body also demonstrated the role of the hypothalamus in the control of anterior pituitary function. When the transplanted tissue is placed in a site remote from the sella turcica, for example, the anterior chamber of the eye, the kidney capsule or temporal lobe of the brain, partial or complete atrophy of the ovaries, testes, reproductive tracts, thyroid gland and adrenal cortices is observed together with a reduction in the rate of body growth. When, however, the transplanted tissue is placed in the vicinity of the hypothalamus and pituitary stalk, regeneration of the hypophysial portal vessels occurs and anterior pituitary function is restored as shown by the maintenance of reproductive, thyroid and adrenocortical activity [5]. 

Peltola [495] reported that large repeated doses of cortisone inhibits the thyroxine potentiation of the anaphylactoid reaction. Spencer and West [579, 580] then presented evidence that the action of the thyroid hormone is mediated through a temporary adrenocortical deficiency. These workers found that maximum sensitivity occurred only after prolonged treatment with the thyroid hormone, after which a return to normal in association with a compensatory adrenal hypertrophy occurred. On the other hand, hypothyroidism caused a temporary excess of the adrenal cortical hormones in the tissues followed by a homeostatic adrenal atrophy. 

---