Normal Hypothalamic-pituitary-adrenal Axis Research Articles

Recovery of the hypothalamic-pituitary-adrenal (HPA) axis in patients with rheumatic diseases receiving low-dose prednisone

purpose: To assess the status of the hypothalamic-pituitary-adrenal (HPA) axis in corticosteroid-treated patients whose prednisone dose had been tapered to physiologic doses. patients and methods: The design of the study was a retrospective chart review of 50 consecutive patients receiving 10 mg or less of prednisone daily at a university teaching hospital rheumatology clinic. Patients were given a rapid adrenocorticotropic hormone stimulation test, with cortisol levels obtained at baseline and after intravenous administration of cosyntropin. Charts were reviewed for duration of therapy, highest, current, and total cumulative steroid dose, and average daily steroid dose in each month of the preceding 2 years. results: Current steroid dose was the only significant indicator of HPA axis function. Patients receiving less than 5 mg of prednisone daily had a normal HPA axis response, whereas those receiving 5 mg or more had widely varied responses. Neither the total, the highest prednisone dose, nor the duration of therapy was a significant indicator of HPA axis recovery. conclusions: Spontaneous recovery of the HPA axis is usual for patients who are taking prednisone at daily doses of 5 mg or less. Return of normal HPA axis function can be achieved without alternate-day therapy in patients whose disease allows tapering to daily prednisone doses of 5 mg or less.

Hypothalamic-Pituitary-Adrenal Function in Non-AIDS Patients with Advanced HIV Infection

Patients with acquired immune deficiency syndrome (AIDS) are reported to have increased basal cortisol and reduced stimulated cortisol release, but the dysfunction in the hypothalamic-pituitary-adrenal (HPA) axis is not yet understood in patients with human immunodeficiency virus (HIV) infection during the advanced stage of disease that precedes the development of AIDS. To understand the status of the HPA axis during this phase of HIV infection, 25 non-AIDS ambulatory patients with advanced HIV infection and without evidence of adrenal or pituitary insufficiency were studied. Ovine corticotropin-releasing hormone was administered (1 microgram/kg BW) intravenously and plasma cortisol and adrenocorticotropin (ACTH) were measured over the following 120 minutes. Based on a standard response curve, obtained from CRH testing of 10 HIV negative volunteers with no HPA abnormalities, 13 patients were found to have normal response (group 1), 6 patients had reduced ACTH and cortisol response (group 2) and 6 patients had normal ACTH with reduced cortisol response (group 3). Basal cortisol and basal ACTH were comparable for control subjects and groups 1, 2, and 3. This suggests that, in advanced non-AIDS HIV patients with no clinical evidence of pituitary or adrenal disease, about 25% (group 2) have reduced pituitary reserve with high basal ACTH and cortisol, and about 25% (group 3) have reduced adrenal reserve with high basal cortisol and inappropriately normal basal ACTH, whereas about 50% (group 1) maintain normal HPA axis activity with increased basal cortisol secretion. The exact physiopathologic mechanism is not yet known, but an enhanced CRH production by the hypothalamus may explain the alterations in the HPA axis in advanced HIV disease.

Short-term, high-dose, systemic steroids in children with asthma: The effect on the hypothalamic-pituitary-adrenal axis

Children with chronic asthma frequently receive "bursts" (less than 7 days) of short-term, high-dose prednisone (1 to 2 mg/kg/day) for acute exacerbations of their disease. Certain of these patients may also require inhaled corticosteroids (IC) for control. The effect of these "bursts" on the hypothalamic-pituitary-adrenal axis (HPAA) is unclear. To test the integrity of the HPAA in such patients, we measured plasma cortisol (F) in response to serial administration of insulin-induced hypoglycemia (nadir = 34 +/- 1.2 mg/dl; mean +/- SE), followed by 250 micrograms/1.73 m2 of synthetic ACTH in the following children with asthma: group I, seven patients who received no more than one "burst" per year (0.71 +/- 0.2); group II, six individuals who received more than one "burst" per year (3.6 +/- 0.2) and no IC; and group III, 10 subjects who received more than one "burst" per year (4.7 +/- 0.3) plus IC. All patients received daily theophylline and beta-agonists; seven patients were taking sodium cromolyn. No patients received troleandomycin. Compared to group I (control subjects), 16% of group II had a subnormal response of F to hypoglycemia. In addition, a subnormal response of F to hypoglycemia or ACTH was documented in 20% and 10% of group III, respectively. All individuals with a subnormal response of F to either hypoglycemia or ACTH received four or more "bursts" per year. We conclude that as a group, children affected by asthma treated with "bursts" alone or "bursts" plus IC appear to have a normal HPAA.(ABSTRACT TRUNCATED AT 250 WORDS)

Long-term intramuscular administration of triamcinolone acetonide.

To the Editor.— In their article ( Arch Dermatol 111:1585, 1975), Carson et al erred when they used the metyrapone test to assess hypothalamic-pituitaryadrenal (HPA) axis responsiveness to stress in patients still receiving triamcinolone acetonide therapy intramuscularly. Certain precautions should be taken in a metyrapone test. First, the patient should not simultaneously receive drugs that suppress ACTH secretion (exogenous glucocorticosteroids). . 1 That is, the metyrapone test seeks to create stress by blocking the endogenous production of cortisol, thus creating a deficiency in circulating glucocorticosteroids. Then the normal HPA axis response is to sense the deficiency, increase the release of ACTH, and, ultimately, increase measurable plasma 11-deoxycortisol. However, if the patient is already receiving significant doses of triamcinolone acetonide, no deficiency can develop and hence no stress can occur because metyrapone has no effect on exogenous circulating glucocorticosteroids. Therefore, in the patient receiving treatment, the HPA axis will fail to respond, not