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At least 829 records · Page 46Linked to original sources
PubMed1990

[Regulation of vasopressin release in primary hypothyroidism and Addison's disease as well as in central diabetes insipidus].

The osmoregulation of arginine-8-vasopressin (AVP) was investigated in 14 patients with primary hypothyroidism, in 6 with Addison's disease, and in 21 with central diabetes insipidus (CDI). In the latter disease the effect of histamine stimulus was also evaluated. Plasma AVP was measured by radioimmunoassay (RIA). Patients with primary hypothyroidism were classified into subgroups with elevated or normal basal levels of plasma AVP. A decreased osmotic threshold was found in hypothyroid patients with augmented basal AVP levels. Patients with Addison's disease exhibited an increased basal level of plasma AVP and a decreased osmotic threshold. CDI patients according to their AVP responses on osmotic stimulus fell into two groups: CDI I gave no response at all, while CDI II responded subnormally. CDI II exhibited blunted AVP release to histamine. The AVP reactions of the CDI I patients fell into two subgroups: CDI I/A had undetectable plasma AVP, whereas histamine evoked AVP release in CDI I/B. Patients with CDI II suffer from a partial CDI, while those with CDI I/A represent a complete form of the disease and CDI I/B presumably have an osmoreceptor failure.

Addison Disease↗
PubMed1990

[Effect of rifampin on the metabolism of glucocorticoids in Addison's disease].

To investigate the effect of rifampicin on the metabolism of hydrocortisone, we measured serum sodium level and blood glucose concentration before lunch in a patient with Addison's disease when treated with hydrocortisone 30 mg/day alone and together with rifampicin 450 mg/day for more than two weeks. We also studied the area under the plasma cortisol curve (AUC), half-life (T 1/2) and clearance rate (CLs) of hydrocortisone after both oral ingestion and intravenous injection of 20 mg hydrocortisone. The results showed that rifampicin increased the metabolism of cortisol by shortening of its T 1/2, increasing its CLs and decreasing its AUC. It decreases the blood sodium level and glucose concentration and makes the patient liable to have hypoglycemic symptoms before lunch. We conclude that the increase of metabolism of cortisol after simultaneous taking of rifampicin may induce adrenal crisis in Addison's disease.

Addison Disease↗
PubMed1986

Effects of ovine corticotropin-releasing hormone and FK 33-824 (met-enkephalin analogue) on the secretions of proopiomelanocortin-derived N-terminal peptide, beta-lipotropin, beta-endorphin and adrenocorticotropin in patients with Addison's disease.

The responses of plasma immunoreactive (IR) proopiomelanocortin (POMC)-derived N-terminal peptide (Nt), IR-beta-endorphin (Ep), IR-beta-lipotropin (LPH) and IR-ACTH levels to ovine corticotropin-releasing hormone (CRF) and FK 33-824 (Met-Enkephalin analogue) were studied in nine patients with Addison's disease. The basal plasma levels (mean +/- SE) of IR-Nt, IR-Ep, IR-LPH and IR-ACTH were significantly higher in patients with Addison's disease (4459 +/- 975 pg/ml, 132 +/- 25 pg/ml, 4425 +/- 1030 pg/ml, 553 +/- 89 pg/ml, respectively) than in the normal controls (202 +/- 38 pg/ml, 7 +/- 2 pg/ml, 101 +/- 18 pfi/ml, 53 +/- 16 pg/ml, respectively). Ovine CRF produced rapid and concomitant increases in plasma levels of IR-Nt, IR-Ep, IR-LPH and IR-ACTH. Ep and ACTH levels reached a peak at 30 min. On the other hand, Nt and LPH levels reached a peak at 60 min and these levels gradually decreased up to 120 min. The molar concentrations of these IR-peptides in plasma were changed in close parallel fashion to one another. FK 33-824 produced a pronounced and concomitant fall in IR-Nt, IR-EP, IR-LPH, and IR-ACTH levels. These results support the theory that Nt, Ep, LPH and ACTH are produced simultaneously from POMC as a common precursor in the pituitary gland and are secreted concomitantly under various conditions such as stimulation by CRF and inhibition by FK 33-824 in patients with Addison's disease.

Addison Disease↗
PubMed2003

GH-releasing peptide (GHRP-6)-induced ACTH release in patients with addison's disease: effect of glucocorticoid withdrawal.

GH releasing peptide (GHRP-6) is a synthetic hexapeptide with potent GH releasing activity both in man and in animals. This peptide is also able to stimulate ACTH and cortisol (F) release. It has been suggested that the ACTH responsiveness to GHRP-6 is modulated by circulating glucocorticoid levels. To further clarify this hypothesis, we studied the effect of GHRP-6 (1 ug/kg, iv) on ACTH and F release in patients with Addison's disease (no.=6) during replacement therapy and after 72 h of glucocorticoid withdrawal. Seven controls were also submitted to a single GHRP-6 test. In control subjects, ACTH values (pmol/l; mean +/- SE) increased from 2.9 +/- 0.8 to 4.7 +/- 1.4 (peak). AUC (pmol.min/l) values were 170.3 +/- 48.8. F (nmol/l) values increased from 257.0 +/- 42.9 to 367.0 +/- 50.8. In patients with Addison's disease there was an increase in ACTH levels from 38.1 +/- 17.1 to 174.9 +/- 79.4 after GHRP-6 administration. AUC values were 5490.4 +/- 2269.1. After 72 h withdrawal of glucocorticoid, there was an increase in basal ACTH values (191.2 +/- 97.3), and a trend toward an increase in ACTH levels after GHRP-6 (p=0.053). Patients with Addison's disease on therapy showed a significantly higher ACTH response to GHRP-6 when compared to controls. Our results show that in patients with Addison's disease on replacement there is an increased ACTH release after GHRP-6 administration, compared to controls. After 72 h glucocorticoid withdrawal, this enhanced responsiveness is not maintained. Our data suggest that circulating glucocorticoids modulate GHRP-6-induced ACTH release and that multiple mechanisms may be involved in this process.

Addison Disease↗
PubMed2000

[Evaluation of corticosteroid replacement therapy and its effect on bones in Addison's disease].

Assessment of patients on steroid replacement therapy is important to avoid the consequences of overtreatment such as osteoporosis. The aim of this prospective study is to evaluate the severity and the etiology of osteopenia in 24 patients (15 women, 9 men) with Addison's disease receiving 30 mg hydrocortisone. Mean age of patients was 55 15 years. Osteoporosis, diagnosed by the measurement of bone mineral density (BMD) at the level of lumbar spine and right hip, was found in 58% of patients, i.e. in 10 women and 4 men. The latter had normal testosterone levels while seven women had an early menopause, the etiology of their Addison's disease being autoimmune. Three were on hormonotherapy. Correlations were found between BMD in the femoral neck and hip and the dose of hydrocortisone (mg/m(2)/day; mg/kg/day), the duration of treatment and 24 hr-cortisoluria/g creatinine. Multivariate analysis shows that 24-hr cortisoluria/g creatinine is a good predictor of BMD values. Thus, osteoporosis is frequent in Addison's disease and cortisoluria could be a useful tool to predict this complication.

Addison Disease↗