High plasma levels of endothelin-1 in untreated Addison's disease

1996 ◽  
Vol 135 (6) ◽  
pp. 696-699 ◽  
Author(s):  
Claudio Letizia ◽  
Marco Centanni ◽  
Luigi Scuro ◽  
Gianluca Canettieri ◽  
Sabrina Cerci ◽  
...  

Letizia C, Centanni M, Scuro L, Canettieri G, Cerci S, De Ciocchis A, D'Ambrosio C, Scavo D. High plasma levels of endothelin 1 in untreated Addison's disease. Eur J Endocrinol 1996;135:696–9. ISSN 0804–4643 The aim of this study has been to investigate the plasma endothelin-1 (ET-1) levels in adult patients with proven Addison's disease (AD). Plasma ET-1 levels were measured in 29 subjects (17 males and 12 females, aged between 20 and 54 years): 15 of them were patients with AD and 14 were sex- and age-matched normal subjects, used as a control group. All patients with AD have been studied under basal conditions and nine of them also after 2 weeks on oral corticosteroid therapy (individual cortisol dosage ranging from 25 to 37.5 mg/day and 0.1 mg/day 9α-fluorohydrocortisone). Extracted plasma ET-1 was determined by a specific radioimmunoassay using rabbit endothelin antisera. Mean ET-1 values in the patients with AD were three times higher than in normal subjects (21.09 ± 4.38 pg/ml vs 6.72 ± 1.74 pg/ml; p < 0.0001). Plasma ET-1 levels assayed in the patients with AD after 2 weeks of corticosteroid therapy were significantly decreased (14.47 ± 3.7 pg/ml vs 22.8 ± 5.2 pg/ml; −37%; p < 0.001) compared to values in untreated patients. However, the plasma ET-1 values obtained following corticosteroid therapy were still significantly higher (p < 0.001) than those detected in the control subjects. These results clearly indicate that patients with untreated AD have increased circulating ET-1 levels that may be reduced by short-term corticosteroid therapy. Claudio Letizia, Policlinico Umberto I, II Clinica Medica, 00185 Roma, Italy

PEDIATRICS ◽  
1958 ◽  
Vol 21 (4) ◽  
pp. 660-660

Adrenal steroids exert a depressant effect on the release of pituitary adrenocorticotrophic hormone. It is therefore of interest to ascertain whether there is an increased secretion of ACTH in Addison's disease because of the deficiency of adrenal steroids in the plasma in this condition. The concentration of ACTH was determined by measuring the production of corticosteroids in the hypophysectomized dog as a measure of the amount of ACTH in plasma obtained from humans. In normal adults the amount of ACTH circulating in the plasma is so small that 20 to 31 ml of plasma does not contain sufficient ACTH to cause a significant increase in adrenal corticosteroids in adrenal venous blood collected from the test animal. Fifty-one determinations in 32 patients with adrenal insufficiency revealed a mean concentration of ACTH in the plasma which was significantly elevated over that found for plasma from 16 controlled samples obtained from normal subjects. The increased concentration of ACTH found in 10 patients with Addison's disease was significantly reduced by the intravenous infusion of hydrocortisone. It was not possible to correlate the increased concentration of ACTH in the plasma of patients with Addison's disease with the clinical manifestations or duration of the disease. The relative suppressive effect of various amounts and kinds of corticosteroids was studied.


Blood ◽  
1949 ◽  
Vol 4 (5) ◽  
pp. 646-652 ◽  
Author(s):  
JACQUES L. GABRILOVE ◽  
MARIO VOLTERRA ◽  
MILDRED D. JACOBS ◽  
LOUIS J. SOFFER

Abstract Ten normal subjects and 11 patients with Addison’s disease were studied as to their leukocyte response following the subcutaneous administration of epinephrin. The pattern of response was found to be similar in both groups, diphasic curves being noted. In general, the patients with Addison’s disease differ from normal individuals in having: (1) a lower and less labile white count, (2) a lower and less labile neutrophile count, (3) a higher lymphocyte count, (4) a slightly lesser percentage fall in absolute number of lymphocytes, and (5) a higher lymphocyte percentage. The use of this method to demonstrate adrenal cortical destruction is not feasible with the dosage of epinephrin employed in this study.


2009 ◽  
Vol 117 (8) ◽  
pp. 293-303 ◽  
Author(s):  
Rolf P. Engelberger ◽  
Daniel Teta ◽  
Hughes Henry ◽  
Olivier De Senarclens ◽  
Benoît Dischl ◽  
...  

End-stage renal disease patients have endothelial dysfunction and high plasma levels of ADMA (asymmetric ω-NG,NG-dimethylarginine), an endogenous inhibitor of NOS (NO synthase). The actual link between these abnormalities is controversial. Therefore, in the present study, we investigated whether HD (haemodialysis) has an acute impact on NO-dependent vasodilation and plasma ADMA in these patients. A total of 24 patients undergoing maintenance HD (HD group) and 24 age- and gender-matched healthy controls (Control group) were enrolled. The increase in forearm SkBF (skin blood flow) caused by local heating to 41 °C (SkBF41), known to depend on endothelial NO production, was determined with laser Doppler imaging. SkBF41 was expressed as a percentage of the vasodilatory reserve obtained from the maximal SkBF induced by local heating to 43 °C (independent of NO). In HD patients, SkBF41 was assessed on two successive HD sessions, once immediately before and once immediately after HD. Plasma ADMA was assayed simultaneously with MS/MS (tandem MS). In the Control group, SkBF41 was determined twice, on two different days, and plasma ADMA was assayed once. In HD patients, SkBF41 was identical before (82.2±13.1%) and after (82.7±12.4%) HD, but was lower than in controls (day 1, 89.6±6.1; day 2, 89.2±6.9%; P<0.01 compared with the HD group). In contrast, plasma ADMA was higher before (0.98±0.17 μmol/l) than after (0.58±0.10 μmol/l; P<0.01) HD. ADMA levels after HD did not differ from those obtained in controls (0.56±0.11 μmol/l). These findings show that HD patients have impaired NO-dependent vasodilation in forearm skin, an abnormality not acutely reversed by HD and not explained by ADMA accumulation.


2014 ◽  
Vol 15 (9) ◽  
pp. 696-701 ◽  
Author(s):  
Giuseppina Novo ◽  
Angela Sansone ◽  
Manfredi Rizzo ◽  
Francesco P. Guarneri ◽  
Claudio Pernice ◽  
...  

1979 ◽  
Vol 91 (4) ◽  
pp. 674-679 ◽  
Author(s):  
Jens Faber ◽  
Dorte Cohn ◽  
Carsten Kirkegaard ◽  
Morten Christy ◽  
Kaj Siersbæk-Nielsen ◽  
...  

ABSTRACT Fourteen patients with Idiopatic Addison's disease (IAD) were studied in order to detect a possible subclinical hypothyroid state. All were clinically euthyroid with normal serum thyroxine (T4) and serum 3,5′,3′-triiodothyronine (T3). Eleven had circulating thyroid microsomal antibodies in blood. The mean basal serum TSH was significantly higher than that of the control group but only three patients had values above the upper normal range. The mean value of serum T4 was decreased as compared to that of the normal persons, while serum 3,3′,5′-triiodothyronine was elevated. 7.5 mU bovine thyrotrophin per kilogram body weight injected intravenously caused a rise in serum T3 not different from the response in normals. However, as well increasing serum TSH as increasing microsomal antibody titer correlated significantly to decreasing thyroidal release of T3. Our results suggest that clinically euthyroid patients suffering from IAD might have a beginning thyroidal insufficiency because of a progressive immunological damage of the thyroid.


1983 ◽  
Vol 102 (1) ◽  
pp. 111-115
Author(s):  
P. Loli ◽  
F. Frascatani ◽  
D. Gelli ◽  
M. Maggioni ◽  
F. Muratori ◽  
...  

Abstract. In 14 patients with Addison's disease plasma levels of ACTH were studied after administration of a single oral dose (16 mg) of cyproheptadine. The drug administration was followed by an inhibition of ACTH release. These results support the view that cyproheptadine may exert an inhibitory effect on ACTH secretion in subjects whose corticosteroid feedback mechanism is normal. We hypothesize that the effect of cyproheptadine might be related to its anti-serotonin or anti-histaminergic action.


1974 ◽  
Vol 15 (1) ◽  
pp. 21-31 ◽  
Author(s):  
J.C. Gillin ◽  
L.S. Jacobs ◽  
F. Snyder ◽  
R.I. Henkin

1989 ◽  
Vol 12 (3) ◽  
pp. 205-207 ◽  
Author(s):  
F. P. Cappuccio ◽  
N. D. Markandu ◽  
M. G. Buckley ◽  
A. L. Sugden ◽  
G. A. Sagnella ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document