Search Results
You are looking at 21 - 30 of 255 items for
- Abstract: Adrenal x
- Abstract: Addisons x
- Abstract: Adrenaline x
- Abstract: Androgens x
- Abstract: Catecholamines x
- Abstract: hyperplasia x
- Abstract: Cortex x
- Abstract: Cushings x
- Abstract: Glucocorticoids x
- Abstract: Medulla x
- Abstract: Noradrenaline x
Diabetes and Endocrine Clinic, Mediclinic Airport Road Hospital, Abu Dhabi, United Arab Emirates
Search for other papers by Salem A Beshyah in
Google Scholar
PubMed
Search for other papers by Khawla F Ali in
Google Scholar
PubMed
Search for other papers by Hussein F Saadi in
Google Scholar
PubMed
Introduction:
Appropriate dose adjustments of glucocorticoids replacement therapy for adrenal insufficiency (AI) is vital.
Objective:
We sought to scope physicians’ perceptions, and practices regarding Ramadan fasting (RF) impact on the management of AI.
Methods:
A web-based survey of a convenience sample of endocrinologists.
Results:
Nearly two-thirds of 145 respondents (64.1%) were adult endocrinologists and almost half (49%) saw more than 10 hypoadrenal patients per year. Most respondents (78.6%) prescribed hydrocortisone, while the minority prescribed other preparations. The glucocorticoid doses were reportedly divided twice daily by 70.8% and thrice daily by 22.2% of respondents. Respondents recognized RF as having potential consequences in adrenal insufficiency patients included causing hypoglycaemia, undue tiredness, and fatigue, hypotension, feeling dizzy, and light-headedness. Symptoms of under-replacement were thought to happen in the late afternoon by 59.3% of respondents. Almost half (45.5%) of respondents thought that RF has some probable or definite impact on glucocorticoid therapy that certainly warrants specific concern and possible action. Three quarters (76.4%) of respondents confirmed providing specific management recommendations during RF. The most frequently reported recommendation was taking in the usual morning dose of hydrocortisone just before pre-dawn meal (Suhor) (57.8%). A third switch patients from hydrocortisone to prednisolone/prednisone. Half reported providing patients with specific recommendations regarding breaking their fast and/or seeking help if hypoadrenal symptoms occur.
Conclusions:
There is a remarkable variation in the physicians’ perceptions and practices regarding the management of AI during Ramadan. This warrants professional effort to increase the awareness and dissemination of evidence-based guidelines.
Search for other papers by Kathrin Zopf in
Google Scholar
PubMed
Search for other papers by Kathrin R Frey in
Google Scholar
PubMed
Search for other papers by Tina Kienitz in
Google Scholar
PubMed
Search for other papers by Manfred Ventz in
Google Scholar
PubMed
Search for other papers by Britta Bauer in
Google Scholar
PubMed
Search for other papers by Marcus Quinkler in
Google Scholar
PubMed
Context
Patients with primary adrenal insufficiency (PAI) or congenital adrenal hyperplasia (CAH) are at a high risk of adrenal crisis (AC). Glucocorticoid sensitivity is at least partially genetically determined by polymorphisms of the glucocorticoid receptor (GR).
Objectives
To determine if a number of intercurrent illnesses and AC are associated with the GR gene polymorphism BclI in patients with PAI and CAH.
Design and patients
This prospective, longitudinal study over 37.7 ± 10.1 months included 47 PAI and 25 CAH patients. During the study period, intercurrent illness episodes and AC were documented.
Results
The study period covered 223 patient years in which 21 AC occurred (9.4 AC/100 pat years). There were no significant differences between BclI polymorphisms (CC (n = 29), CG (n = 34) and GG (n = 9)) regarding BMI, hydrocortisone equivalent daily dose and blood pressure. We did not find a difference in the number of intercurrent illnesses/patient year among BclI polymorphisms (CC (1.5 ± 1.4/pat year), CG (1.2 ± 1.2/pat year) and GG (1.6 ± 2.2/pat year)). The occurrence of AC was not significantly different among the homozygous (GG) genotype (32.5 AC/100 pat years), the CC genotype (6.7 AC/100 pat years) and the CG genotype (4.9 AC/100 pat years). Concomitant hypothyroidism was the highest in the GG genotype group (5/9), compared to others (CC (11/29) and CG (11/34)).
Conclusions
Although sample sizes were relatively small and results should be interpreted with caution, this study suggests that the GR gene polymorphism BclI may not be associated with the frequencies of intercurrent illnesses and AC.
Search for other papers by David J F Smith in
Google Scholar
PubMed
Search for other papers by Hemanth Prabhudev in
Google Scholar
PubMed
Department of Clinical Biochemistry, Imperial College Healthcare NHS Trust, London, UK
Department of Investigative Medicine, Division of Diabetes, Endocrinology and Metabolism, Imperial College London, London, UK
Search for other papers by Sirazum Choudhury in
Google Scholar
PubMed
Department of Investigative Medicine, Division of Diabetes, Endocrinology and Metabolism, Imperial College London, London, UK
Search for other papers by Karim Meeran in
Google Scholar
PubMed
Introduction
Patients who need glucocorticoid replacement in both primary and secondary adrenal insufficiency (AI) have the choice of either once-daily prednisolone or thrice-daily hydrocortisone. A recent European study found no difference between prednisolone and hydrocortisone users in several markers including glucose, weight, body mass index, systolic and diastolic blood pressure and waist circumference, although an increase in cholesterol and low-density lipoprotein (LDL) was suggested in a subgroup of these patients. The aim of this study was to expand the evidence base for the use of these agents as replacement therapy.
Methods
Data from 82 patients on hydrocortisone and 64 patients on prednisolone for AI at Imperial College Healthcare NHS Trust were analysed.
Results
There was no significant difference in total cholesterol, LDL levels or any other risk factors between hydrocortisone and prednisolone patients. Prednisolone was subjectively significantly more convenient than hydrocortisone (P = 0.048).
Conclusions
Prednisolone once daily is more convenient than hydrocortisone thrice daily, and there is no difference in the markers of cardiovascular risk measured. Because prednisolone mimics the circadian rhythm better than other glucocorticoids, it should be considered as an alternative to hydrocortisone for AI.
Search for other papers by Arno Téblick in
Google Scholar
PubMed
Search for other papers by Ilse Vanhorebeek in
Google Scholar
PubMed
Search for other papers by Inge Derese in
Google Scholar
PubMed
Search for other papers by An Jacobs in
Google Scholar
PubMed
Search for other papers by Renata Haghedooren in
Google Scholar
PubMed
Search for other papers by Sofie Maebe in
Google Scholar
PubMed
Search for other papers by Gerdien A Zeilmaker-Roest in
Google Scholar
PubMed
Search for other papers by Enno D Wildschut in
Google Scholar
PubMed
Search for other papers by Lies Langouche in
Google Scholar
PubMed
Search for other papers by Greet Van den Berghe in
Google Scholar
PubMed
In critically ill adults, high plasma cortisol in the face of low ACTH coincides with high pro-opiomelanocortin (POMC) levels. Glucocorticoids further lower ACTH without affecting POMC. We hypothesized that in pediatric cardiac surgery-induced critical illness, plasma POMC is elevated, plasma ACTH transiently rises intraoperatively but becomes suppressed post-operatively, and glucocorticoid administration amplifies this phenotype. From 53 patients (0–36 months), plasma was obtained pre-operatively, intraoperatively, and on post-operative days 1 and 2. Plasma was also collected from 24 healthy children. In patients, POMC was supra-normal pre-operatively (P < 0.0001) but no longer thereafter (P > 0.05). ACTH was never high in patients. While in glucocorticoid-naive patients ACTH became suppressed by post-operative day 1 (P < 0.0001), glucocorticoid-treated patients had already suppressed ACTH intraoperatively (P ≤ 0.0001). Pre-operatively high POMC, not accompanied by increased plasma ACTH, suggests a centrally activated HPA axis with reduced pituitary processing of POMC into ACTH. Increasing systemic glucocorticoid availability with glucocorticoid treatment accelerated the suppression of plasma ACTH.
Significance statement
Glucocorticoids are often administered during pediatric cardiac surgery. In critically ill children, endogenous systemic glucocorticoid availability is elevated already upon ICU admission while ACTH levels are normal. This hormonal constellation suggests the presence of active feedback inhibition of ACTH. In this study, we have documented that intraoperative administration of glucocorticoids accelerates the suppression of ACTH, resulting in low plasma ACTH already upon ICU admission. Pre-operative plasma POMC, the ACTH precursor, but not ACTH, was increased. This is compatible with a centrally activated HPA axis prior to surgery in young children but reduced processing of POMC into ACTH within the pituitary. These findings suggest that glucocorticoid treatment in the context of pediatric cardiac surgery may amplify pre-existing impaired pituitary processing of the prohormone POMC.
International Centre for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Trine Holm Johannsen in
Google Scholar
PubMed
International Centre for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Jakob Albrethsen in
Google Scholar
PubMed
Search for other papers by Vassos Neocleous in
Google Scholar
PubMed
Search for other papers by Federico Baronio in
Google Scholar
PubMed
Search for other papers by Martine Cools in
Google Scholar
PubMed
International Centre for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Lise Aksglaede in
Google Scholar
PubMed
International Centre for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Niels Jørgensen in
Google Scholar
PubMed
International Centre for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Peter Christiansen in
Google Scholar
PubMed
Pediatric Endocrinology Clinic, Department of Pediatrics, Aretaeio Hospital, Nicosia, Cyprus
Search for other papers by Meropi Toumba in
Google Scholar
PubMed
Search for other papers by Pavlos Fanis in
Google Scholar
PubMed
International Centre for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Marie Lindhardt Ljubicic in
Google Scholar
PubMed
International Centre for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
Department of Clinical Medicine, University of Copenhagen, Denmark
Search for other papers by Anders Juul in
Google Scholar
PubMed
Congenital adrenal hyperplasia (CAH) is a recessive condition that affects the adrenal glands. Despite life-long replacement therapy with glucocorticoids and mineralocorticoids, adult patients with CAH often experience impaired gonadal function. In pubertal boys and in men with CAH, circulating testosterone is produced by the adrenal glands as well as the testicular, steroidogenic cells. In this European two-center study, we evaluated the function of Leydig and Sertoli cells in 61 boys and men with CAH, primarily due to 21-hydroxylase deficiency. Despite conventional hormone replacement therapy, our results indicated a significant reduction in serum concentrations of both Leydig cell-derived hormones (i.e. insulin-like factor 3 (INSL3) and testosterone) and Sertoli cell-derived hormones (i.e. inhibin B and anti-Müllerian hormone) in adult males with CAH. Serum concentrations of INSL3 were particularly reduced in those with testicular adrenal rest tumors. To our knowledge, this is the first study to evaluate circulating INSL3 as a candidate biomarker to monitor Leydig cell function in patients with CAH.
Search for other papers by Greta B Raglan in
Google Scholar
PubMed
Search for other papers by Louis A Schmidt in
Google Scholar
PubMed
Department of Neuroscience, Georgetown University, Washington, District of Columbia, USA
Search for other papers by Jay Schulkin in
Google Scholar
PubMed
The stress response has been linked to the expression of anxiety and depression, but the mechanisms for these connections are under continued consideration. The activation and expression of glucocorticoids and CRH are variable and may hold important clues to individual experiences of mood disorders. This paper explores the interactions of glucocorticoids and CRH in the presentation of anxiety and depressive disorders in an effort to better describe their differing roles in each of these clinical presentations. In addition, it focuses on ways in which extra-hypothalamic glucocorticoids and CRH, often overlooked, may play important roles in the presentation of clinical disorders.
Search for other papers by Sandra R Dahl in
Google Scholar
PubMed
Division of Medicine, Akershus University Hospital, Lørenskog, Norway
Search for other papers by Ingrid Nermoen in
Google Scholar
PubMed
Department of Clinical Medicine, University of Bergen, Bergen, Norway
Search for other papers by Ingeborg Brønstad in
Google Scholar
PubMed
K.G. Jebsen-Center for Autoimmune Diseases, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway
Search for other papers by Eystein S Husebye in
Google Scholar
PubMed
K.G. Jebsen-Center for Autoimmune Diseases, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway
Search for other papers by Kristian Løvås in
Google Scholar
PubMed
Search for other papers by Per M Thorsby in
Google Scholar
PubMed
Immunoassays of steroid hormones are still used in the diagnosis and monitoring of patients with congenital adrenal hyperplasia. However, cross-reactivity between steroids can give rise to falsely elevated steroid levels. Here, we compare the use of immunoassays and liquid chromatography–tandem mass spectrometry (LC–MS/MS) in the monitoring of patients with classic 21-hydroxylase deficiency (21OHD). Steroid profiles in different mutation groups (genotypes) were also compared. Fifty-five patients with classic 21OHD (38 women) were studied. Blood samples were collected in the morning after an overnight medication fast. LC–MS/MS and immunoassays were employed to assay 17-hydroxyprogesterone (17OHP), testosterone and androstenedione. In addition, 21-deoxycortisol (21DF), 11-deoxycortisol (11DF), corticosterone, deoxycorticosterone, cortisone and cortisol were analyzed by LC–MS/MS. Testosterone, androstenedione and 17OHP levels were consistently lower (by about 30–50%) when measured by LC–MS/MS compared with immunoassays, with exception of testosterone in men. There was a significant correlation between 21DF and 17OHP (r = 0.87, P < 0.001), but three patients had undetectable 21DF. Subjects with no enzyme activity had significantly lower mean 11DF concentrations than subjects with residual activity. The use of LC–MS/MS gives a more specific view of adrenal steroid levels in 21OHD compared with immunoassays, which seem to considerably overestimate the levels of 17OHP and androstenedione. Falsely elevated levels of 17OHP and androstenedione could lead to overtreatment with glucocorticoids.
Search for other papers by Thomas Reinehr in
Google Scholar
PubMed
Search for other papers by Alexandra Kulle in
Google Scholar
PubMed
Search for other papers by Juliane Rothermel in
Google Scholar
PubMed
Search for other papers by Caroline Knop-Schmenn in
Google Scholar
PubMed
Search for other papers by Nina Lass in
Google Scholar
PubMed
Search for other papers by Christina Bosse in
Google Scholar
PubMed
Search for other papers by Paul-Martin Holterhus in
Google Scholar
PubMed
Objective
The underlying mechanisms of polycystic ovarian syndrome (PCOS) are not fully understood yet. The aim of the study was to get functional insights into the regulation of steroid hormones in PCOS by steroid metabolomics.
Design
This is a longitudinal study of changes of steroid hormones in 40 obese girls aged 13–16 years (50% with PCOS) participating in a 1-year lifestyle intervention. Girls with and without PCOS were matched to age, BMI and change of weight status.
Methods
We measured progesterone, 17-hydroxyprogesterone, 17-hydroxyprogenolon, 11-deoxycorticosterone, 21-deoxycorticosterone, deoxycorticosterone, corticosterone, 11-deoxycortisol, cortisol, cortisone, androstenedione, testosterone, dehydroepiandrostendione-sulfate (DHEA-S), estrone and estradiol by LC–MS/MS steroid profiling at baseline and one year later.
Results
At baseline, obese PCOS girls demonstrated significantly higher androstenedione and testosterone concentrations compared to obese girls without PCOS, whereas the other steroid hormones including glucocorticoids, mineralocorticoids, estrogens and precursors of androgens did not differ significantly. Weight loss in obese PCOS girls was associated with a significant decrease of testosterone, androstenedione, DHEA-S, cortisol and corticosterone concentrations. Weight loss in obese non-PCOS girls was associated with a significant decrease of DHEA-S, cortisol and corticosterone concentrations, whereas no significant changes of testosterone and androstenedione concentrations could be observed. Without weight loss, no significant changes of steroid hormones were measured except an increase of estradiol in obese PCOS girls without weight loss.
Conclusions
The key steroid hormones in obese adolescents with PCOS are androstenedione and testosterone, whereas glucocorticoids, mineralocorticoids, estrogens and precursors of androgens did not differ between obese girls with and without PCOS.
Search for other papers by Aneta Gawlik in
Google Scholar
PubMed
Search for other papers by Michael Shmoish in
Google Scholar
PubMed
Search for other papers by Michaela F Hartmann in
Google Scholar
PubMed
Search for other papers by Stefan A Wudy in
Google Scholar
PubMed
Search for other papers by Zbigniew Olczak in
Google Scholar
PubMed
Search for other papers by Katarzyna Gruszczynska in
Google Scholar
PubMed
Search for other papers by Ze’ev Hochberg in
Google Scholar
PubMed
Objective
Analysis of steroids by gas chromatography-mass spectrometry (GC-MS) defines a subject’s steroidal fingerprint. Here, we compare the steroidal fingerprints of obese children with or without liver disease to identify the ‘steroid metabolomic signature’ of childhood nonalcoholic fatty liver disease.
Methods
Urinary samples of 85 children aged 8.5–18.0 years with BMI >97% were quantified for 31 steroid metabolites by GC-MS. The fingerprints of 21 children with liver disease (L1) as assessed by sonographic steatosis (L1L), elevated alanine aminotransferases (L1A) or both (L1AL), were compared to 64 children without markers of liver disease (L0). The steroidal signature of the liver disease was generated as the difference in profiles of L1 against L0 groups.
Results
L1 comparing to L0 presented higher fasting triglycerides (P = 0.004), insulin (P = 0.002), INS/GLU (P = 0.003), HOMA-IR (P = 0.002), GGTP (P = 0.006), AST/SGOT (P = 0.002), postprandial glucose (P = 0.001) and insulin (P = 0.011). L1AL showed highest level of T-cholesterol and triglycerides (P = 0.029; P = 0.044). Fasting insulin, postprandial glucose, INS/GLU and HOMA-IR were highest in L1L and L1AL (P = 0.001; P = 0.017; P = 0.001; P = 0.001). The liver disease steroidal signature was marked by lower DHEA and its metabolites, higher glucocorticoids (mostly tetrahydrocortisone) and lower mineralocorticoid metabolites than L0. L1 patients showed higher 5α-reductase and 21-hydroxylase activity (the highest in L1A and L1AL) and lower activity of 11βHSD1 than L0 (P = 0.041, P = 0.009, P = 0.019).
Conclusions
The ‘steroid metabolomic signature’ of liver disease in childhood obesity provides a new approach to the diagnosis and further understanding of its metabolic consequences. It reflects the derangements of steroid metabolism in NAFLD that includes enhanced glucocorticoids and deranged androgens and mineralocorticoids.
Endocrine Disease Unit, University-Hospital of Padova, Padova, Italy
Department of Neuroscience DNS, University of Padova, Padova, Italy
Search for other papers by Filippo Ceccato in
Google Scholar
PubMed
Search for other papers by Elisa Selmin in
Google Scholar
PubMed
Laboratory Medicine, University-Hospital of Padova, Padova, Italy
Search for other papers by Giorgia Antonelli in
Google Scholar
PubMed
Endocrine Disease Unit, University-Hospital of Padova, Padova, Italy
Department of Neuroscience DNS, University of Padova, Padova, Italy
Search for other papers by Mattia Barbot in
Google Scholar
PubMed
Search for other papers by Andrea Daniele in
Google Scholar
PubMed
Search for other papers by Marco Boscaro in
Google Scholar
PubMed
Laboratory Medicine, University-Hospital of Padova, Padova, Italy
Search for other papers by Mario Plebani in
Google Scholar
PubMed
Endocrine Disease Unit, University-Hospital of Padova, Padova, Italy
Search for other papers by Carla Scaroni in
Google Scholar
PubMed
Context
The low-dose short synacthen test (LDSST) is recommended for patients with suspected central adrenal insufficiency (AI) if their basal serum cortisol (F) levels are not indicative of an intact hypothalamic–pituitary–adrenal (HPA) axis.
Objective
To evaluate diagnostic threshold for salivary F before and 30 min after administering 1 μg of synacthen, performed before 09:30 h.
Design
A cross-sectional study from 2014 to 2020.
Setting
A tertiary referral university hospital.
Patients
In this study, 174 patients with suspected AI, 37 with central AI and 137 adrenal sufficient (AS), were included.
Main outcome measure
The diagnostic accuracy (sensitivity (SE), specificity (SP)) of serum and salivary F levels measured, respectively, by chemiluminescence immunoassay and liquid chromatography-tandem mass spectrometry.
Results
Low basal serum or salivary F levels could predict AI. For the LDSST, the best ROC-calculated threshold for serum F to differentiate AI from AS was 427 nmol/L (SE 79%, SP 89%), serum F > 500 nmol/L reached SP 100%. A salivary F peak > 12.1 nmol/L after administering synacthen reached SE 95% and SP 84% for diagnosing central AI, indicating a conclusive reduction in the likelihood of AI. This ROC-calculated threshold for salivary F was similar to the 2.5th percentile of patients with a normal HPA axis, so it was considered sufficient to exclude AI. Considering AS those patients with salivary F > 12.1 nmol/L after LDSST, we could avoid unnecessary glucocorticoid treatment: 99/150 subjects (66%) had an inadequate serum F peak after synacthen, but salivary F was >12.1 nmol/L in 79 cases, who could, therefore, be considered AS.
Conclusions
Salivary F levels > 12.1 nmol/L after synacthen administration can indicate an intact HPA axis in patients with an incomplete serum F response, avoiding the need to start glucocorticoid replacement treatment.
