Adrenal insufficiency with chronic hyponatraemia and normal basal cortisol level: time to review the investigation of hyponatraemia

Author(s):  
Mansukhbhai Shekhda Kalyan ◽  
Maria Darda ◽  
Syed Bitat ◽  
Ali Rathore ◽  
Taofeek Ojewuyi ◽  
...  
PLoS ONE ◽  
2019 ◽  
Vol 14 (11) ◽  
pp. e0225255 ◽  
Author(s):  
Worapaka Manosroi ◽  
Mattabhorn Phimphilai ◽  
Jiraporn Khorana ◽  
Pichitchai Atthakomol

2009 ◽  
Vol 16 (10) ◽  
pp. 1283-1286 ◽  
Author(s):  
Chi-Wei Huang ◽  
Chun-Chung Lui ◽  
Weng-Neng Chang ◽  
Cheng-Hsien Lu ◽  
Ya-Ling Wang ◽  
...  

1997 ◽  
pp. 172-175 ◽  
Author(s):  
G Dickstein ◽  
D Spigel ◽  
E Arad ◽  
C Shechner

There are many suggestions in the literature that the adrenal gland is more sensitive to ACTH in the evening than in the morning. However, all these studies in humans were conducted when the basal cortisol level was not suppressed, and were based on the observation that, after stimulation, the increases in cortisol differed, though the peak values were the same. To examine this, we established the lowest ACTH dose that caused a maximal cortisol stimulation even when the basal cortisol was suppressed, and used a smaller dose of ACTH for morning and evening stimulation. The lowest ACTH dose to achieve maximal stimulation was found to be 1.0 microgram, with which dose cortisol concentration increased to 607.2 +/- 182 nmol/l, compared with 612.7 +/- 140.8 nmol/l with the 250 micrograms test (P > 0.3). The use of smaller doses of ACTH (0.8 and 0.6 microgram) achieved significantly lower cortisol responses (312 +/- 179.4 and 323 +/- 157.3 nmol/l respectively; both P < 0.01 compared with the 1 microgram test). When a submaximal ACTH dose (0.6 microgram) was used to stimulate the adrenal at 0800 and 1600 h, after pretreatment with dexamethasone, no difference in response was noted at either 15 min (372.6 +/- 116 compared with 394.7 +/- 129.7 nmol/l) or 30 min (397.4 +/- 176.6 compared with 403 +/- 226.3 nmol/l; P > 0.3 for both times). These results show that 1.0 microgram ACTH, used latterly as a low-dose test, is very potent in stimulating the adrenal, even when baseline cortisol is suppressed; smaller doses cause reduction of this potency. Our data show that there is probably no diurnal variation in the response of the adrenal to ACTH, if one eliminates the influence of the basal cortisol level and uses physiologic rather than superphysiologic stimuli.


1993 ◽  
Vol 136 (1) ◽  
pp. 167-172 ◽  
Author(s):  
S. Crowley ◽  
P. C. Hindmarsh ◽  
J. W. Honour ◽  
C. G. D. Brook

ABSTRACT We compared the reproducibility and repeatability of the acute adrenal response to low doses (90 and 500 ng/1·73 m2) of Synacthen (ACTH(1–24)) with that of the standard dose (250 μg/1·73 m2). We also examined the effect of basal cortisol levels on peak values achieved after stimulation with a low dose. ACTH(1–24) was given to six male volunteers: 90 ng/1·73 m2 twice at 90-min intervals on day 1, and 90 and 500 ng/1·73 m2 once on day 2 and 250 μg/1·73 m2 once on day 3. The rise in serum cortisol concentration with repeated low doses of ACTH was not attenuated (161 ± 49 (s.d.) nmol/l on initial vs 150 ± 41 nmol/l on repeat stimulation; P = 0·5) and this was reproducible (161 ± 49 nmol/l on day 1 vs 148 ± 15 nmol/l on day 2; P = 0·6). A dose of 500 ng ACTH(1–24)/1·73 m2 produced a maximal adrenal response in that the rise in serum cortisol concentration at 20 min was identical with that produced at the same time by the standard dose of 250 μg/1·73 m2. There was a strong positive correlation between the basal cortisol level and peak cortisol concentration after low-dose ACTH stimulation (r = 0·93, P < 0·001) but not between the basal cortisol level and the incremental rise (r= −0·1, P = 0·69). These results suggest that the cortisol response to low-dose ACTH stimulation is reproducible and not attenuated by repeat stimulation at 90-min intervals. The incremental rise in serum cortisol concentration after ACTH stimulation appears constant in these situations and is not influenced by the basal cortisol level. When there is concern that the standard dose may be excessive and mask subtle but important changes in adrenal function, the low dose (500 ng) of ACTH should be used. Journal of Endocrinology (1993) 136, 167–172


Author(s):  
Hany Khairy ◽  
Yara Eid ◽  
Iman Zaky ◽  
Merhan Samy ◽  
Mohammed Omar

2017 ◽  
Vol 7 (2) ◽  
pp. 150-153 ◽  
Author(s):  
Hali Rakici

ABSTRACT Aim Adrenal insufficiency (AI) in cirrhosis is an issue that has recently gained momentum. It can be seen in both stable and critically ill (sepsis, septic shock, and gastrointestinal system bleeding) cirrhotic patients. Its prevalence exists in a wide range since standardization of diagnostic methods is lacking. We aimed to scrutinize this issue in a 108 case series. Materials and methods We studied the presence of AI and its stage in patients with cirrhosis and its complications by using cross-sectional study. Standard-dose short synacthen test (SD-SST) was performed in 108 patients that had Child C decompensated cirrhosis without critical illness and it was aimed to determine the prevalence of AI based on basal cortisol, peak cortisol, and delta cortisol (basal total cortisol minus peak cortisol after stimulation) levels. Results The prevalence of AI in cirrhosis was found to be 25% based on basal cortisol level of <140 nmol/L, 22.2% based on delta cortisol level of <250 nmol/L, and 29.6% based on peak cortisol level of <500 nmol/L. Conclusion Prevalence of AI shows variation in decompensated cirrhosis without critical illness depending on different measures used. More definite results can be obtained when more standardized criteria are widely put into use. How to cite this article Rakici H. Adrenal Insufficiency in Cirrhosis Patients: Evaluation of 108 Case Series. Euroasian J Hepato-Gastroenterol 2017;7(2):150-153.


2019 ◽  
Vol 3 (10) ◽  
pp. 1837-1846 ◽  
Author(s):  
Chika Kyo ◽  
Takeshi Usui ◽  
Rieko Kosugi ◽  
Mizuki Torii ◽  
Takako Yonemoto ◽  
...  

Abstract Context Primary macronodular adrenal hyperplasia (PMAH) is a rare type of Cushing or subclinical Cushing syndrome and is associated with bilateral multinodular formation. ARMC5 is one of the responsible genes for PMAH. Objectives This study was performed to identify the genotype-phenotype correlation of ARMC5 in a cohort of Japanese patients. Patients and Methods Fourteen patients with clinically diagnosed PMAH and family members of selected patients were studied for ARMC5 gene alteration and clinical phenotype. The associated nonadrenal tumor tissues were also studied. Results Of fourteen patients with PMAH, 10 had pathogenic or likely pathogenic variants of ARMC5. We found two variants. Five unrelated patients had identical variants (p.R619*). In two patients, the variant was found in offspring with the asymptomatic or presymptomatic state. Six of ten patients who tested positive for the ARMC5 pathogenic or likely pathogenic variant carried nonadrenal tumors; however, no loss of heterozygosity (LOH) or second hit of the ARMC5 gene was evident. The ARMC5 variant–positive group showed a significantly higher basal cortisol level. Furthermore, age-dependent cortisol hypersecretion was seen in the ARMC5 variant–positive group. Conclusions ARMC5 pathogenic variants are common (71%) in Japanese patients with PMAH. p.R619* might be a hot spot in Japanese patients with PMAH. Asymptomatic or presymptomatic pathogenic variant carriers were found among the family members of the patients. Although 50% of ARMC5 variant carriers had nonadrenal neoplastic lesions, no LOH or second hit of ARMC5 in the tumor tissues was evident. The ARMC5 variant–positive mutant group showed a higher basal cortisol level than the negative group.


IBRO Reports ◽  
2019 ◽  
Vol 6 ◽  
pp. S389-S390
Author(s):  
Dongil Min ◽  
Seung Yeon Baik ◽  
Aeran Kwon ◽  
Min Jin Jin ◽  
Yourim Kim ◽  
...  

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