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Newborn guinea pigs (less than 24 hours old) are highly susceptible to the lethal effect of endotoxin and susceptibility decreases with age. The vulnerability to endotoxin has not been attributed to hypofunction of either the adrenal gland or the reticuloendothelial system of the newborn, since prior injection of corticosteroids provides only partial protection to endotoxin and newborn guinea pigs can efficiently remove colloidal substances from the circulation. In contrast to adults, newborns do not develop a delayed inflammatory reaction following intradermal injection of endotoxin, and after intravenous challenge frequently fail to display neutropenia and sustained fever.
Two cases of asymptomatic adrenocortical insufficiency are reported. Both patients had a normal cortisol and increased ACTH. The cortisol response to ACTH was impaired, although not absent, in both cases. One case was associated with autoimmune polyglandular syndrome type II (Graves' disease and vitiligo), and the other was possibly associated with an early stage of Hashimoto's thyroiditis, suggesting autoimmune pathogenesis of their adrenocortical insufficiency. CT of the abdomen revealed unilateral enlargement of the adrenal glands in one case, but no enlargement of the adrenal glands in another case. Adrenal hypofunction seemed to be compensated for by increased trophic hormone (ACTH), as in subclinical hypothyroidism. However, prolonged ACTH stimulation increased urinary 17-OHCS in both cases, and normalized cortisol response to ACTH in one case. In both cases, the plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were normal, and adrenal autoantibodies were negative, suggesting that neither negative adrenal autoantibodies nor normal PRA can exclude asymptomatic adrenocortical insufficiency. The results suggest that a rapid ACTH test should be performed in cases with increased ACTH, especially those associated with other autoimmune endocrine disorders.
Sarcoidosis is a multisystem disorder of unknown etiology that frequently involves the lymph nodes, lungs, eyes, and skin. The disease can involve any organ system, and noncaseating granulomas are characteristically present. Synthesis of 1,25-dihydroxyvitamin D, the most biologically active form of vitamin D, occurs in granulomatous tissue and may give rise to increases in its concentration in the peripheral circulation and to hypercalcemia and hypercalciuria. Infiltration of endocrine organs also occurs. Involvement of the hypothalamus and pituitary can cause primary polydipsia and disordered regulation of thirst; diabetes insipidus, impaired secretion of anterior pituitary hormones (with clinically apparent hypothyroidism, hypogonadism, hypoadrenalism, or impaired growth), and increases in serum prolactin may also result. Galactorrhea, however, seldom occurs. Involvement of the thyroid and adrenal glands rarely leads to hypofunction. Involvement of the pancreas rarely occurs but does not produce diabetes mellitus. Involvement of the male reproductive system results in epididymitis and hypogonadism, and involvement of the uterus causes abnormalities in menstrual function.
Maintenance of the balance of electrolytes and hormones within their normal range is necessary for normal myocardial metabolism. Open heart surgery involving cardiopulmonary bypass produces metabolic disturbances which affect normal metabolic homeostasis. Several studies have suggested that pulsatile cardiopulmonary bypass causes less severe metabolic disturbance than non-pulsatile bypass and that non-pulsatile bypass causes hypofunction of the anterior pituitary and adrenal glands. The present study, however, with non-pulsatile flow showed that there was no evidence of hypothalamo-pituitary-adrenal axis hypofunction when the hormonal values of corticotrophin (ACTH), cortisol and cortisone were corrected for the hemodilution involved in cardiac surgery. Electrolytes, particularly calcium, play an important role in myocardial contractility. The levels of ionized calcium are normally controlled by parathyroid hormone (PTH) with a negative feedback of calcium controlling the system. However, this study showed that significant increases in bioactive PTH during cardiopulmonary bypass were not related to the calcium concentration, but appeared to be influenced by low blood pH values and by the degree of hypothermia.
In a morphological study of thyroid glands and adrenal cortex of large fetuses compared to the controls the authors revealed a significant increase of the thyroid gland functional activity, as well as of glomerular and fascicular zones of adrenal cortex. The functional tension of the thyroid gland appeared to be reduced in large fetuses with obesity. Hyperfunction of all zones of the adrenal cortex was also revealed in them. In medium height fetuses with obesity hypofunction of the thyroid gland, as well as hyperfunction of the fascicular and fetal adrenal cortex zones were present. Correlation-regression analysis has revealed close interrelations between the functional state of the thyroid gland, adrenal cortex and fetal mass.
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The diagnosis of adrenal hypofunction is suggested by clinical features and confirmed by biochemical testing. The characteristic features of acute primary adrenal insufficiency include orthostatic hypotension, fever, and hypoglycemia. By contrast, patients with chronic primary adrenal insufficiency have a longer history of malaise, as well as fatigue, anorexia, diarrhea, weight loss, joint and back pain, and darkening of the skin. While the clinical presentation of secondary adrenal insufficiency is similar to that of primary adrenal insufficiency, there is no hyperpigmentation, and hypotension and orthostasis are less pronounced. As a result, patients often present with vague, non-specific symptoms and the diagnosis may not be entertained. There is considerable debate regarding the best dynamic test for the diagnosis of adrenal hypofunction. Optimally, a screening test would be economic, convenient and safe. It would have high sensitivity and specificity based on consensus criteria for interpretation. Unfortunately, to date no test meets all of these criteria. Measurement of basal cortisol is an inexpensive and convenient screening test that can include (< 3 microg/dl; 83 nmol/l) or exclude (> 19 microg/dl; 524 nmol/l) adrenal insufficiency. However, most patients will have intermediate values and will require dynamic testing. This review discusses the use of metyrapone, insulin, CRH and synthetic ACTH 1-24 as provocative agents for cortisol secretion. Although the insulin and metyrapone stimulation tests have the advantage of testing the entire hypothalamic-pituitary-adrenal axis, they are cumbersome and carry more risk than the other tests. The 250 microg ACTH test works well to identify primary adrenal hypofunction, but can only detect secondary adrenal hypofunction when there is sufficient time for the glands to atrophy because of reduced endogenous ACTH stimulation. The 1 microg ACTH test has been advocated in the setting of possible secondary adrenal insufficiency, but its widespread use has been mitigated by the lack of a commercial preparation of this small dose and controversy regarding diagnostic criteria. Ultimately, the choice of test should be individualized for each patient, with knowledge of the available reference assays and the vagaries of each test.
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To elucidate factors producing destructive changes in the adrenal cortex under severe stress, the following experiments were performed: 1) severe combined stress (KC) including unilateral adrenalectomy and fixation in supin position for 24 h (control group); 2)hypophysectomy KC; 3) thyroidectomy KC; 4) bilateral orchiectomy KC; 5) injection of vitamine "E" for 14 days + KC. The adrenals were studied by a complex of morphometrical and histochemical methods. Hypophysectomy prevented estructive changes in the adrenal cortex under KC. This effect was not connected with hypofunction of the thyroid gland and the testes, as their excision (in rats without hypophysectomy) did not prevent the development of necrobiotic changes in the adrenal cortex. A suggestion is made on a "corticolytic" effect of ACTH which reveals itself under severe stress. Destruction of adrenocorticocytes is supposed to result from activation of peroxide oxidation of lipids. This is indirectly supported by a large number of lipofuscin containing cells, by decrease in the activity of alkaline phosphatase and ATPh-ase, by activation of acid phosphatase and also by decreasing alterative phenomena at the injection of vitamine "E".
The actions and interactions of the pituitary gland and the nervous system constitute a regulatory system whereby the physiologic activity of the thyroid, adrenals, and gonads is controlled. Damage to or interference with the pituitary gland may cause hyper- or hypofunctional states resulting in devastating changes in a person's body and life. This article limits its discussion to several of the more frequently encountered pathological states, their diagnostic work-up, evaluation, and treatment.
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We report a case of painful ophthalmoplegia (Tolosa-Hunt syndrome), which was complicated with diabetes insipidus (DI) and pituitary-adrenal axis hypofunction. A 42-year-old man hospitalized for left orbital pain and impairment of left cranial nerves III, IV, V, VI, developed diabetes insipidus during the corticosteroid treatment. Neuroimaging studies disclosed a thickened, highly contrast-enhanced pituitary stalk, swollen pituitary gland and widened left cavernous sinus up to the superior orbital fissure, which were accompanied by diabetes insipidus and hypofunction of the pituitary-adrenal axis. These were indicative of an extension of granulomatous inflammation of the cavernous sinus to the pituitary portal system and the gland itself.
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No inclusive or satisfactory biomedical explanation for chronic fatigue syndrome (CFS) has as yet been forwarded. Recent research suggests that a dysregulated hypothalamic-pituitary-adrenal axis (HPA) may be contributory, and in particular that there may be diminished forward drive and adrenal under-stimulation. In this preliminary study we wished to examine a cohort of CFS patients in whom evidence for such hypofunctioning was found. Our aim was to establish whether these patients had altered adrenal gland size. Patients were recruited from a fatigue clinic. Those who fulfilled the Centre for Disease Control and Prevention (CDC) criteria underwent a 1 microgram adrenocorticotropin (ACTH) stimulation test, a test of adrenal gland functioning. Eight subjects (five females, three males) with a subnormal response to this test underwent a computer tomography (CT) adrenal gland assessment. Measurements were compared with those from a group of 55 healthy subjects. The right and left adrenal gland bodies were reduced by over 50% in the CFS subjects indicative of significant adrenal atrophy in a group of CFS patients with abnormal endocrine parameters. This is the first study to use imaging methods to measure adrenal gland size in CFS. It is a limitation of this study that a selected CFS sample was employed. A future larger study would optimally employ an unselected cohort of CFS patients. This study has implications not only for the elucidation of CFS pathophysiology, but also for possible therapeutic strategies.
In the present study, we investigated the influence of dietary protein restriction stress on adrenal steroidogenic function of the domestic turkey. Immature male turkeys (2 weeks old) were fed isocaloric synthetic diets containing either 28% (control) or 8% (restriction) soy protein for 4 weeks. Trunk plasma was processed for the determination of adrenocorticotropin (ACTH), corticosterone, aldosterone, and total 3, 5, 3'-triiodothyronine (T3). In addition, adrenal glands were processed for the isolation of defined, density-separable, adrenal steroidogenic cell subpopulations: three low-density adrenal steroidogenic cell subpopulations [LDAC-1 (rho = 1.0350-1.0490 g/ml). LDAC-2 (rho = 1.0490-1.0570 g/ml), and LDAC 3 (rho = 1.0370-1.0585 g/ml)] and a high-density subpopulation [HDAC (rho = 1.0590-1.0720 g/ml)], and the steroidogenic function of these cell subpopulations was evaluated. Protein restriction did not influence plasma ACTH However, it increased relative adrenal weight (mg/100 g body wt) (+37.8%) and plasma corticosterone (+317%). By contrast, it depressed plasma aldosterone (-51.2%). In addition, it caused a modest depression in plasma T3 (-25.9%). At the cellular level, protein restriction induced panhypofunction. Basal corticosteroid (aldosterone and corticosterone) production values of LDAC-1, -2, and -3 and HDAC from protein-restricted birds were, respectively, 42.9, 47.9, 30.8, and 57.5% less than those of corresponding cell subpopulations from control birds. In addition, maximal corticosteroid production values of LDAC-1, -2, and -3 and HDAC from protein-restricted birds, in response to ACTH, angiotensin II (AngII), and 25-hydroxycholesterol support, were depressed by 56.8, 55.1, 22.7, and 42.9%, respectively. Interestingly, LDAC-3 was relatively refractory to the influence of this stressor. By contrast, there was the lack of a concentration-dependent aldosterone response of LDAC-1 and -2 to AngII with protein restriction. This was not due to a failure in cell function since aldosterone responses of these cell subpopulations to ACTH and to 25-hydroxycholesterol support were apparent. In addition, the concentration of AngII receptors of cell subpopulations from protein-restricted turkeys, if anything, was greater than that of cell subpopulations from control turkeys. Protein restriction also altered the cell subpopulation composition of the adrenal gland: compared to control, it decreased the proportion of LDAC-2 by 42.3% and increased the proportion of LDAC-3 and HDAC by 68.7 and 302%, respectively. Thus, dietary protein restriction induces adrenal steroidogenic hypofunction in turkeys. In addition, the present study suggests that this nutritional stressor induces marked remodeling of the steroidogenic tissue in the turkey adrenal gland.