Clonidine Suppression Test

Author(s):  
Ahmet Bahadir Ergin ◽  
Amir H. Hamrahian ◽  
A. Laurence Kennedy ◽  
Manjula K. Gupta
Keyword(s):  
2019 ◽  
Vol 25 ◽  
pp. 19
Author(s):  
Ravinder Jeet Kaur ◽  
Shobana Athimulam ◽  
Molly Van Norman ◽  
Melinda Thomas ◽  
Stefan K. Grebe ◽  
...  

1973 ◽  
Vol 12 (03) ◽  
pp. 218-224
Author(s):  
Elli Lakka - Papadodima ◽  
Constantin Ntalles ◽  
Denis Ikkos

Des mesurages répétés de la fixation thyroïdienne de 10 minutes du 132I injecté intraveineusement on été effectués sur 55 malades euthyroïdiens sans et avec goitre et sur 16 malades hyperthyreoïdiens par 4 jours consécutifs. Immédiatement après le premier mesurage tous les malades recevaient une dose unique oral de 100 μg de Triiodothyronine (T3). Les valeurs de fixation 24, 48 et 72 heures après le T3 (moyen ± déviation standard) étaient de 75 ± 1,7, 64 ± 1,8, et 67 ± 1,9 dans le groupe euthyroïdien et le 106 ± 2,6, 104 ± 2,2 et 108 ± 4,0 dans le groupe hyperthyroïdien, exprimés en pourcentage du groupe controle. 48 heures après T3 tous les personnes euthyroïdiens, sauf une, avaient des valeurs en dessous de 88% tandis que la valeur la plus basse des personnes hyperthyroïdiens ce jour était de 93%. La séparation des valeurs 48 heures des deux groupes était complète après avoir respecté l’influence de la première fixation sur la valeur 48 heures. On peut donc supposer q’un test thyroïdien de suppression utilisable en clinique peut-être effectué en 48 heures après une administration oral de 100 μg de T3 et mesurage de la fixation 10 minutes après l’injection du radioisotope.


1972 ◽  
Vol 11 (04) ◽  
pp. 317-323
Author(s):  
R. Höschl ◽  
T. M. D. Gimlette

SummaryA total of 132 triiodothyronine suppression tests were performed using 100 μg of T3 for 7 days. Radioiodine uptake at four hours, serum thyroxine [T4(D)], T3 binding coefficient [RT3U ratio] and free thyroxine index [T4-RT3 index] were estimated before and after a course of triiodothyronine.T4(D) decreased significantly in only 38.4% of T3 suppression tests assessed as positive by the decrease in radioiodine uptake; it did not change or increased significantly in 84.7% of tests negative by radioiodine uptake.RT3U ratio showed little change in all groups. The changes in T4-RT3 index were similar to those of T4(D).The correlation of changes in T4(D) with 4 hour radioiodine uptake is poor (r = 0.34).Agreement between changes in radioiodine uptake and T4(D) was observed only in 54% of tests; between changes in uptake and T4-RT3 index in 69.4%.Estimation of serum thyroxine or free thyroxine index in the T3 suppression test cannot substitute for the radioiodine uptake for reasons which are discussed.


1969 ◽  
Vol 61 (2) ◽  
pp. 219-231 ◽  
Author(s):  
V. H. Asfeldt

ABSTRACT This is an investigation of the practical clinical value of the one mg dexamethasone suppression test of Nugent et al. (1963). The results, evaluated from the decrease in fluorimetrically determined plasma corticosteroids in normal subjects, as well as in cases of exogenous obesity, hirsutism and in Cushing's syndrome, confirm the findings reported in previous studies. Plasma corticosteroid reduction after one mg of dexamethasone in cases of stable diabetes was not significantly different from that observed in control subjects, but in one third of the insulin-treated diabetics only a partial response was observed, indicating a slight hypercorticism in these patients. An insufficient decrease in plasma corticosteroids was observed in certain other conditions (anorexia nervosa, pituitary adenoma, patients receiving contraceptive or anticonvulsive treatment) with no hypercorticism. The physiological significance of these findings is discussed. It is concluded that the test, together with a determination of the basal urinary 17-ketogenic steroid excretion, is suitable as the first diagnostic test in patients in whom Cushing's syndrome is suspected. In cases of insufficient suppression of plasma corticosteroids, further studies, including the suppression test of Liddle (1960), must be carried out.


1968 ◽  
Vol 57 (1) ◽  
pp. 23-32 ◽  
Author(s):  
Hironori Nakajima ◽  
Mitsunori Murala ◽  
Masumitsu Nakata ◽  
Takeshi Naruse ◽  
Seiji Kubo

ABSTRACT The in vitro resin uptake of 3H-prednisolone was used for the determination of blood cortisol after addition of radioactive prednisolone followed by Amberlite CG 400 Type 1 to the test serum, and incubation of the mixture. The radioactivity of the supernatant was compared before and after the addition of the resin. The principle of this method is similar to that of the 131I-triiodothyronine resin uptake for the thyroid function test. The tests for the specificity, reproducibility and sensitivity gave satisfactory results. The mean basal value ± SD of the 3H-prednisolone resin uptake was 35.3 ± 9.2% in normal subjects, and 27.1 ± 4.8% in pregnant women. This method was valid in various adrenal function tests, i. e. the adrenal circadian rhythm, corticotrophin (ACTH) test, dexamethasone suppression test and the adrenal response to lysine-8-vasopressin. It proved to be a sensitive indicator of the adrenal function. These results suggest that this method should be useful for a routine adrenal function test.


2019 ◽  
Vol 4 (1) ◽  
pp. 58
Author(s):  
Aimi Fadilah Mohamad ◽  
Fatimah Zaherah Mohamed Shah ◽  
Nur Aisyah Zainordin ◽  
Ur 'Aini Eddy Warman ◽  
Nazimah Ab Mumin ◽  
...  

Primary aldosteronism (PA) causes a persistently elevated blood pressure (BP) due to excessive release of the hormone aldosterone from the adrenal glands. Classically, it is called Conn’s syndrome and is described as the triad of hypertension and hypokalemia with the presence of unilateral adrenal adenoma. It can be cured with surgical resection of the aldosterone-secreting adenoma leading to resolution of hypertension, hypokalemia and increased cardiovascular risk associated with hyperaldosteronism. We present a case of a man with previous ischemic heart disease (IHD) who presented with resistant hypertension. Investigations for secondary causes of hypertension revealed an elevated aldosterone level and saline suppression test confirmed the diagnosis of PA. Radiological examination revealed a left adrenal adenoma and a normal right adrenal gland. However, adrenal venous sampling showed lateralization of aldosterone secretion towards the right. He subsequently underwent a laparoscopic right adrenalectomy which improved his BP control promptly. This case highlights the importance of recognizing the need to investigate for secondary causes of hypertension. It also underscores the importance of dynamic tests, which may not be easily accessible to most clinicians but should pursue, to allow a definitive diagnosis and effective treatment.


Author(s):  
Florian K. Zeugswetter ◽  
Alejandra Carranza Valencia ◽  
Kerstin Glavassevich ◽  
Ilse Schwendenwein

2021 ◽  
Vol 22 (11) ◽  
pp. 5495
Author(s):  
Felipe Borges Almeida ◽  
Graziano Pinna ◽  
Helena Maria Tannhauser Barros

Under stressful conditions, the hypothalamic-pituitary-adrenal (HPA) axis acts to promote transitory physiological adaptations that are often resolved after the stressful stimulus is no longer present. In addition to corticosteroids (e.g., cortisol), the neurosteroid allopregnanolone (3α,5α-tetrahydroprogesterone, 3α-hydroxy-5α-pregnan-20-one) participates in negative feedback mechanisms that restore homeostasis. Chronic, repeated exposure to stress impairs the responsivity of the HPA axis and dampens allopregnanolone levels, participating in the etiopathology of psychiatric disorders, such as major depressive disorder (MDD) and post-traumatic stress disorder (PTSD). MDD and PTSD patients present abnormalities in the HPA axis regulation, such as altered cortisol levels or failure to suppress cortisol release in the dexamethasone suppression test. Herein, we review the neurophysiological role of allopregnanolone both as a potent and positive GABAergic neuromodulator but also in its capacity of inhibiting the HPA axis. The allopregnanolone function in the mechanisms that recapitulate stress-induced pathophysiology, including MDD and PTSD, and its potential as both a treatment target and as a biomarker for these disorders is discussed.


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