Patients were divided into 3 groups according to the serum cortisol response to the rapid ACTH test; those with a peak serum cortisol level of <15 μg/dL were defined as the adrenal insufficiency (AI) probable group, ≥15 μg/dL and <18 μg/dL as the AI suspected group, and ≥18 μg/dL as the non-AI group.
<b>ABSTRACT</b><b>Objective:</b> To evaluate the performance of morning serum cortisol (MSC) compared to a 10 μg ACTH stimulation test in the diagnosis of adrenal insufficiency (AI).
In both groups, none of the patients who had sufficient preoperative ACTH without hydrocortisone supplementation (n=15) showed hypocortisolism in the immediate postoperative measurement.
Primary AI is defined by the inability of the adrenal cortex to produce sufficient amounts of glucocorticoids and/or mineralocorticoids despite normal or increased adrenocorticotropin hormone (ACTH).
The subsequent evidence of low plasmatic and urinary cortisol and increased ACTH required the start of Hydrocortisone replacement therapy and it defined a clinical picture of adrenal insufficiency.
We compared AI determination in cirrhotic patients with the ACTH test using these SaC thresholds versus established TSC thresholds (TSC-T<sub>0</sub>< 9 <i>μ</i>g/dl [248 nmol/L], TSC-T<sub>60</sub> < 18 <i>μ</i>g/dl [497 nmol/L], or ΔTSC<9 <i>μ</i>g/dl [248 nmol/L]).SaC correlated well with TSC.
On an outpatient visit, serum ACTH and cortisol levels were normal despite the discontinuation of fludrocortisone and so the patient had been evaluated as partial adrenal insufficiency secondary to PD-related peritonitis.
It is important to recognize that relative adrenal insufficiency (AI) is the most common cause of low cortisol levels and failedACTH challenge in ill patients.
In previous reports, most cases of immune checkpoint inhibitor (ICI)-induced hypophysitis were diagnosed based on adrenal insufficiency symptoms or hyponatremia with low ACTH and cortisol.
Our systematic literature search revealed 9 studies (n = 371) that evaluated AI using adrenocorticotropic hormone stimulation testing, with measures of serum cortisol levels at baseline and following at least 2 weeks of TCS application.
Mutations in the POMC gene were linked with a clinical phenotype of adrenal insufficiency, red hair pigmentation, early onset and rapidly progressive obesity, early onset type 2 diabetes, hypothyroidism, hypogonadism and growth hormone deficiency.
Despite widespread use of the 250-mcg Cosyntropin test (ACTH test) for the diagnosis of adrenal insufficiency (AI), the effect of time of day and the utility of performing both 30- and 60-min serum cortisol values remains unclear.
We therefore decided to assess adrenal reserve and the value of salivary cortisol during ACTH stimulation in the diagnosis of adrenocortical insufficiency in adult patients with β-thalassemia major.
We investigated the potential role of measuring salivary cortisol when adrenal insufficiency (AI) is suspected, to reduce the numbers of ACTH stimulation tests.
Here, we reported a 12-year-old female patient that was initially presented with unusual skin darkening and low serum level of adrenocorticotropic hormone and diagnosed as having adrenocortical insufficiency.
By protocol, the first group received steroids in step 3 of the treatment according to the current international guidelines (group A), and the second group was managed as group A and was tested for AI by adrenal stimulation test using intramuscular adrenocorticotropic hormone (cosyntropin) (group B).
The models of (i) 1-mg DST >138 nmol/l or (ii) >61 nmol/l with the presence of one among low levels of ACTH and dehydroepiandrosterone-sulphate had the highest accuracy (89·9%, P < 0·001) and odds ratio [OR 111·62, 95% confidence interval (CI) 21·98-566·74, P < 0·001] for predicting postsurgical hypocortisolism.
Homozygous mutations in the POMC gene is associated with hyperphagia, severe and early-onset obesity, adrenal insufficiency, hypopigmentation of the skin and red hair.
Adrenal insufficiency is characterised by inadequate -glucocorticoid production owing to destruction of the adrenal cortex or lack of adrenocorticotropic hormone stimulation.