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Background The term adrenal incidentaloma (AI), by definition, is an adrenal mass that is unexpectedly detected through an imaging procedure performed for reasons unrelated to adrenal dysfunction or suspected dysfunction. Despite their frequent appearance, the challenge remains in recognizing and treating the small percentage of AI that poses a significant risk, either because of their hormonal activity or because of their malignant histology. The aim of this study is to study the role of MRI, specifically chemical shift imaging (CSI), against various MDCT scans (non-enhanced, enhanced, and delayed) in the characterization of incidentally discovered adrenal masses to offer a way for the patients to avoid unnecessary time and money-wasting imaging modalities used to reach a diagnosis of their incidentally discovered adrenal lesions. We examined a total number of 20 patients with total of 22 adrenal lesions. The mean age was 51.1 ± 15.27. Results In our study, we found that among CT parameters, APW and RPW showed the highest sensitivity and specificity for detection of lipid-rich adenomas. CSI has also proven to be the best MR technique. However, there is no statistically significant difference in the diagnostic capability of CSI versus the CT washout technique. Both modalities could be conducted, according to specific patient preferences and/or limitations, with comparable highly accurate outcomes. Conclusion This study demonstrates that a similar diagnostic outcome is obtained from contrast-enhanced CT (CECT) and MRI with CSI of adrenal lesions.

Hyperandrogenismus bzw. Hyperandrogenamie sind pathologische Zustande, die entsprechend durch ubermasige Androgenempfindlichkeit in der Peripherie bzw. erhohte Androgenspiegel in der Zirkulation gekennzeichnet sind. Klinische Manifestationen von Hyperandrogenismus umfassen Hirsutismus, Seborrho, Akne und androgenetische Alopezie. Im Falle einer Hyperandrogenamie konnen ein polyzystisches Ovarialsyndrom (PCOS), Morbus Cushing, spat einsetzendes Adrenogenitalsyndrom und Virilisierung auftreten. Hirsutismus, eine maximale Variante der Hypertrichose, definiert als ubermasiges Wachstum von terminalen Haaren bei Frauen in einem mannlichen Muster, ist das am haufigsten auftretende diagnostische Kriterium fur Hyperandrogenismus. Akne und Alopezie sind weitere androgenbedingte Hautveranderungen und konnen bei Frauen ohne Hirsutismus beobachtet werden. Klitorishypertrophie, Zunahme der Muskelmasse, unregelmasiger Menstruationszyklus und metabolisches Syndrom konnen mit Hyperandrogenamie einhergehen. Virilisierung ist ein relativ seltener Zustand, und sein Vorhandensein deutet haufig auf einen Androgen produzierenden Tumor hin. Die Behandlung der Symptome umfasst die Verwendung von antiandrogen wirkenden Kontrazeptiva wie Cyproteronacetat, Chlormadinonacetat, Dienogest, Drospirenon wie auch Spironolacton und Flutamid. Eine grundliche Anamnese, eine gezielte klinische Untersuchung und ein interdisziplinarer Ansatz zusammen mit Gynakologen und Endokrinologen sind auserst hilfreich bei der diagnostischen Bewertung und Therapie von Patienten mit Verdacht auf Hyperandrogenismus/Hyperandrogenamie.

Introduction: Adrenal lesions as such are very rare conditions, which are incidentally detected through an imaging procedure, performed for reasons unrelated to adrenal dysfunction or suspected dysfunction and are known as adrenal incidentalomas.1 Its prevalence ranges from 1.4% to 2.9% worldwide. We report a series of three cases of adrenal lesions received at our hospital between the years 2011 and 2016. Case series: In a series of three cases, we found that there was one case of Adrenal cortical adenoma, one case of nodular hyperplasia of adrenal gland and one case of adrenocortical carcinoma. Majority of the tumors were seen in the age group of 20-40 years with male preponderance and only 42.8% were detected coincidentally on imaging. Conclusion: The three cases are reported here for their rarity of presentation. Keywords: Adrenal tumours, Adrenal incidentaloma, Adrenocortical carcinomas.

Latent varicella zoster virus (VZV) has been detected in human adrenal glands, raising the possibility of virus-induced adrenal damage and dysfunction during primary infection or reactivation. Rare cases of bilateral adrenal hemorrhage and insufficiency associated with VZV reactivation have been reported. Since there is no animal model for VZV infection of adrenal glands, we obtained adrenal glands from two non-human primates (NHPs) that spontaneously developed varicella from primary simian varicella virus (SVV) infection, the NHP VZV homolog. Histological and immunohistochemical analysis revealed SVV antigen and DNA in the adrenal medulla and cortex of both animals. Adrenal glands were observed to have Cowdry A inclusion bodies, cellular necrosis, multiple areas of hemorrhage, and varying amounts of polymorphonuclear cells. No specific association of SVV antigen with βIII-tubulin-positive nerve fibers was found. Overall, we found that SVV can productively infect NHP adrenal glands, and is associated with inflammation, hemorrhage, and cell death. These findings suggest that further studies are warranted to examine the contribution of VZV infection to human adrenal disease. This study also suggests that VZV infection may present itself as acute adrenal dysfunction with “long-hauler” symptoms of fatigue, weakness, myalgias/arthralgias, and hypotension.

BACKGROUND: Adrenal gland ultrasonographic measurements are useful in clinical evaluation of patients with adrenal dysfunction in several species. In human healthy neonates, the ultrasonographic size of the adrenal glands decreases during the first days of life. Ultrasonography of adrenal glands was demonstrated to be feasible in neonatal foals. The aims of this study were to describe a technique for ultrasonographic measurement of adrenal gland size to test its reliability in neonatal foals, and to assess any variation of ultrasonographic measurements during the first five days of life in healthy foals.METHODS: First, measurements of the adrenal glands were retrospectively obtained by three observers in 26 adrenal gland images of 13 healthy and sick neonatal foals. The interobserver and intraobserver agreement were tested. Later, adrenal gland ultrasonographic images and measurements were acquired by one operator in 11 healthy neonatal foals at one, three and five days of life and differences among the measurements obtained at the different time points were assessed.RESULTS: Interobserver agreement ranged from fair to excellent (0.48-0.92), except for cortex width (

A systematic approach to regulating hormones is outlined within. The steps in the process for hormone balancing will be reviewed as they build upon each other. Hormones must be balanced and working in concert with one another to maintain good health. Many factors affect hormonal balance, such as food quality and poor nutrition, stress, and environmental toxins. Unfortunately, we live in an increasingly toxic world and these exposures affect our endocrine system and hormonal balance. These toxic exposures include the air we breathe, the food we eat, the water we drink, and even the thoughts we think. Endocrine active chemicals (EACs) or endocrine disruptors can cause variations in normal hormone function. Even small alterations in hormone concentrations have significant and lasting effects. Further, some EACs have the potential to impact human health at lower doses than limits set in traditional toxicity testing by regulatory agencies, which means that some effects may be overlooked.

Adrenal insufficiency (Addison's disease) and Cushing's syndrome are rare disorders characterized by abnormal secretion of adrenal hormones. All patients with adrenal insufficiency and many with Cushing's syndrome require life-long therapy with the potential to impact the quality of life. Management requires gain of a significant amount of knowledge related to treatment, self-care, and how to react quickly in critical situations. Knowledge deficits related to management may cause patients to become critically ill and may even cause death. Ongoing patient/family teaching is crucial for proper disease management and sustaining the quality of life.

Objective: To describe a case of sequential bilateral adrenal infarction and hemorrhage resulting in an unusual pattern of adrenal function over time. Methods: A 50-year-old male with autoimmune antiphospholipid syndrome (APS) presented to the emergency room with severe abdominal pain. Diagnostic studies performed included contrast-enhanced computerized tomographic (IV-CT) imaging of abdomen and pelvis, and laboratory assessment of the hypothalamic-pituitary-adrenal axis. Results: IV-CT of abdomen and pelvis on day 1 showed acute left adrenal gland infarction; cortisol level was 19.9 μg/dL and serum sodium was 133 mEq/L. The patient subsequently developed hyponatremia and hypotension. Repeat IV-CT of abdomen and pelvis on day 3 showed hemorrhagic conversion of the left infarcted adrenal gland and a new right adrenal gland infarction. Cosyntropin stimulation test (CST) confirmed primary glucocorticoid insufficiency. Plasma renin activity and the serum aldosterone level were within normal limits with normokalemia. At 7-month follow-up, CST demonstrated cortisol and aldosterone deficiency. Conclusion: Adrenal infarction is a rare complication of APS but is the most common endocrine complication. Evidence of bilateral adrenal infarction on imaging does not predict the type of adrenal dysfunction that might ensue, as demonstrated in this case. Thorough evaluation of glucocorticoid, mineralocorticoid, and androgen deficiency should be conducted both at the time of the event and in follow-up.

Opakovane, obtižně vysvětlitelne, popř. těžke hypoglykemie u pacientů s diabetes mellitus 1. typu (DM1T) mohou být vzacným, ale přesto realným přiznakem manifestace adrenalni insuficience (AI). AI se objevuje u přibližně 0,5 % těchto pacientů, větsinou několik let po vzniku diabetu, typicky ve střednim věku a castěji u žen. Plosne vysetřovani pacientů trpicich rekurentnimi, obvyklými přicinami nevysvětlitelnými hypoglykemickými epizodami na přitomnost AI se vsak neukazalo jako efektivni, a neni tedy doporucovano. Přesto je nutne na AI jako na realnou přicinu takových hypoglykemii u pacientů s DM1T pamatovat a prověřit u nich soucasnou přitomnost obvyklejsich přiznaků AI, kterými jsou předevsim slabost, nechutenstvi, hubnuti, ortostaticka hypotenze, ci hyperpigmentace, připadně poruchy mineralogramu (hyponatremie).

In the capuchin monkey (Cebus apella), a new-world nonhuman primate, maternal exposure to constant light during last third of gestation induces precocious maturation of the fetal adrenal and increased plasma cortisol in the newborn. Here, we further explored the effects of this challenge on the developmental programming of adrenal function in newborn and infant capuchin monkeys. We measured (i) plasma dehydroepiandrosterone sulphate (DHAS) and cortisol response to ACTH in infants with suppressed endogenous ACTH, (ii) plasma DHAS and cortisol response to ACTH in vitro, and (iii) adrenal weight and expression level of key factors in steroid synthesis (StAR and 3β-HSD). In one-month-old infants from mothers subjected to constant light, plasma levels of cortisol and cortisol response to ACTH were twofold higher, whereas plasma levels of DHAS and DHAS response to ACTH were markedly reduced, compared to control conditions. At 10 months of age, DHAS levels were still lower but closer to control animals, whereas cortisol response to ACTH was similar in both experimental groups. A compensatory response was detected at the adrenal level, consisting of a 30% increase in adrenal weight and about 50% reduction of both StAR and 3β-HSD mRNA and protein expression and the magnitude of DHAS and cortisol response to ACTH in vitro. Hence, at birth and at 10 months of age, there were differential effects in DHAS, cortisol production, and their response to ACTH. However, by 10 months of age, these subsided, leading to a normal cortisol response to ACTH. These compensatory mechanisms may help to overcome the adrenal alterations induced during pregnancy to restore normal cortisol concentrations in the growing infant.

Thyroid function, glucose metabolism, and an adaptive hypothalamic–pituitary–adrenal (HPA) axis are critical determinants of health and wellness. This chapter highlights the integrative physiology and interactions between these three systems and an integrative medicine approach to these conditions. Integrative medicine expands the evaluation of endocrine dysfunction through a person-centered approach. Patients’ overall symptoms and physiological function should be taken into account in evaluating thyroid function and planning treatment. Our approach to diabetes focuses on the importance of lifestyle changes and nutrition. Our perspective of the effects of chronic stress has been informed by current perspectives on neurobiology and neuroplasticity; chronic stress leaves its mark on the brain through changes in structure as well as its function in adapting to further stress. We present an integrative approach to manage and improve these three endocrine systems to address disease and improve patients’ energy and health.

There are complex dynamics involving the endocrine and immune system. Cytokines are a key component of the immune system response to infection. The hypothalamus-anterior pituitary-adrenal gland (HPA) and the hypothalamus-anterior pituitary-gonad (HPG) axis have significant dynamics with cytokines. In this paper there is a discussion on the background on the physiology of cytokines affects on the adrenal hormones and glands and on the reproductive hormones and glands. Pro- and anti-inflammatory signaling are important to understanding HPA and HPG axis responses to infection. In the second section of this research paper, effects of severe infection on production of cytokines are explored with a discussion on the negative feedback of cortisol on the production of cytokines, hence methods of treating sepsis to improve positive outcomes. The next section involved effects of cytokines during severe inflection on the adrenal axis and the reproductive axis with an interesting discussion on fertility issues with severe infection. In the last section, potential manipulations of cytokines for therapies for sepsis are investigated relating to adrenal dysfunction, neonatal sepsis and treatment for improved outcomes of critically ill patients with severe infection.

Sepsis and septic shock represent important causes of morbidity and mortality in children, and adrenal dysfunction may play a role in the cardiovascular and immunological response. According to existing reports, the incidence of adrenal dysfunction in critically ill children varies significantly between 4 and 52% of patients. This article reviews the concept of adrenal insufficiency and the role it may play in a pediatric septic shock. Also discussed are the diagnosis, prognosis, and treatment of adrenal insufficiency in septic shock in adults and children. Finally, the latest recommendations about steroid use in pediatric septic shock are summarized.

The analysis of the reasons for the children to the intensive care unit indicates that the poisoning is one of the most important cause of life-threatening conditions in childhood. The poisoning by drugs and ethanol dominates among other poisoning factors. Multiple drug poisoning is not so rare case as well as intentional self-poisoning among teenagers. It is dangerous not only toxigenic phase of poisoning by various chemical compounds but also their long-term effects. The symptoms of cerebroasthenia, minimal dysfunction of brain, vascular disorders, violation of thermoregulation, convulsions, visual impairment, hepatopathy, nephropathy, adrenal dysfunction are discussed as the effects of acute poisoning in children. Above-mentioned facts indicate the need to improve the toxicological assistance not only during resuscitation but also in a phase of long-term effects. The as early as possible elimination of the effects of acute poisoning leaves the possibility of development of the child according to age. The study of the general laws of chemical and biological interaction of poison with organs and tissues of animals in the experiment can detect adaptive and compensatory mechanisms to ensure stability of the basic functions of the organism to the damaging effects of xenobiotics. The study of the molecular and cellular mechanisms of action of exogenous chemical factors elucidates the target points to the impact of pharmacological agents. Taking into account that the mandatory pathogenetic component of the process of intoxication is hypoxia we used the ethylene glycol poisoning model to test direct antihypoxants 2 etiltiobenzimidazola hydrobromide (metaprot) and 5-ethoxy-2-etiltiobenzimidazol (etomerzol). Aim: to estimate antihypoxic and antioxidant effects of actoprotective substances as metaprot and etomerzol in the model of ethylene glycol poisoning.

We here described a case of a 38-year-old woman who was referred to our hospital for general malaise, slight fever, and palpitations after a meal for the past several years. She became hungry at approximately 3:00 or 4:00 p.m. every day, and simultaneously felt the urge to eat something sweet. During a five-hour 75g OGTT test, her blood glucose level dropped sharply twice (79 mg/dL at 60 min and 76 mg/dL at 300 min) due to the excessive secretion of insulin (29.9 µU/mL at 30 min and 43.1 µU/mL at 120 min). She was diagnosed with a mild adrenal insufficiency due to a decrease in her serum cortisol value in the early morning and an insufficient response to the rapid ACTH stress test. We speculated that the reactive hypoglycemic symptoms observed in this patient may have developed due to the inadequate secretion of serum cortisol as a counterregulation against insulin, which resulted in a relative excess of serum insulin after a meal. Her clinical manifestations and laboratory data were similar to a state called adrenal fatigue. Since the presentation of mild adrenal insufficiency is often insidious and difficult to recognize, careful

Allgrove (Triple A) syndrome is a rare autosomal recessive disorder characterized by cardinal features of adrenal insufficiency due to adrenocorticotropic hormone (ACTH) resistance, achalasia, and alacrimia. It is frequently associated with neurological manifestations like polyneuropathy. Since its first description by Allgrove in 1978, approximately 100 cases have been reported in the literature. Here we report an 18-year-old boy diagnosed as having Allgrove syndrome, with ACTH resistant adrenal insufficiency, achalasia, alacrimia, and severe motor polyneuropathy. Alacrimia was the earliest feature evident at the age of 8 years. He presented with achalasia and adrenal insufficiency at 12 and 18 years respectively and developed neurological symptoms in the form of severe muscle wasting at the age of 15 years. Patients with Allgrove syndrome usually manifest adrenal insufficiency and achalasia during first decade of life. Our patient manifested adrenal insufficiency and achalasia in the second decade and manifested neurological dysfunction before adrenal dysfunction.

Background Hepatopulmonary syndrome (HPS) is a relatively common complication in patients with decompensated cirrhosis. Our aim was to evaluate the prevalence of HPS, its clinical impact, and the possible association between HPS and characteristics of patients with decompensated cirrhosis. Methods Patients with stable decompensated cirrhosis admitted to our department and assessed for HPS were included. For each patient, several clinical, laboratory and echocardiographic parameters as well as renal function were recorded. The severity of liver disease was evaluated according to the Model for End-stage Liver Disease and Child-Pugh scores, and renal function was assessed using 51chromium complexed with ethylene diamine tetracetic acid. In addition, the short synacthen test was performed in each patient to evaluate the adrenal function. Results Sixty-three patients were enrolled, 26 (41.3%) of whom diagnosed with HPS. In multivariate analysis, the presence of hepatocellular carcinoma [odds ratio (OR) 8.1, 95% confidence interval (CI) 5.3-27.9, P=0.045] and salivary cortisol at T60 (60 min after the intravenous injection of 250 μg corticotropin) (OR 0.88, 95%CI 0.71-0.98, P=0.045) were the factors independently associated with HPS. T60 salivary cortisol had relatively good discriminative ability for the presence of HPS (area under the curve=0.73). The presence of HPS was not associated with the outcome (P=0.22). Conclusion In our cohort of patients with decompensated cirrhosis, the presence of hepatocellular carcinoma and T60 salivary cortisol were the only factors independently associated with HPS. Keywords Cirrhosis, hepatopulmonary syndrome, hepatocellular carcinoma, salivary cortisol, adrenal dysfunction Ann Gastroenterol 2017; 30 (2): 225-231

Survival of all living organisms depends on maintenance of a steady state of homeostasis, which process relies on its ability to react and adapt to various physical and emotional threats. The defense against stress is executed by the hypothalamic-pituitary-adrenal axis and the sympathetic-adrenal medullary system. Adrenal gland is a major effector organ of stress system. During stress adrenal gland rapidly respond with increased secretion of glucocorticoids and catecholamines into circulation, which hormones, in turn, affect metabolism, to provide acutely energy, vasculature to increase blood pressure and the immune system to prevent it from extensive activation. Sepsis resulting from microbial infections is a sustained and extreme example of stress situation. In many critical ill patients levels of both corticotropin-releasing hormone and adrenocorticotropin, two major regulators of adrenal hormone production, are suppressed. Levels of glucocorticoids however, remain normal or are elevated in these patients, suggesting a shift from central to local intraadrenal regulation of adrenal stress response. Among many mechanisms potentially involved in this process, reduced glucocorticoid metabolism and local intraadrenal activation of hormone production mediated by adrenocortical and chromaffin cell interactions, the adrenal vascular system and the immune-adrenal crosstalk play a key role. Consequently, any impairment in function of these systems, can ultimately affect adrenal stress response. The purpose of this mini review is to present and discuss recent advances in our understanding of the adrenal gland microenvironment, and its role in regulation of stress-induced hormone secretion.

Since the advent of modern molecular tools, researchers have extensively shown that essential cellular machineries have robust circadian (roughly 24 hours) variations in their pace. This molecular rhythmicity translates directly into time-of-day-dependent variation in physiology in most organ systems, which in turn provides the mechanistic rationale for why timing on a daily basis should matter in many aspects of human health. However, these basic science findings have been slow to move from bench to bedside because clinical studies are still lacking to demonstrate the importance of timing. Therefore, it has not been clear how physicians should incorporate knowledge of natural 24-hour rhythms into routine practice. This review is a brief summary of results from recently completed clinical studies on hypertension, myocardial infarction, diabetes mellitus, and adrenal dysfunction that highlights new evidence for the emerging importance of circadian rhythms in diagnosis, prognosis and treatment of disease.

Adrenogenital syndrome is a group of pathological conditions with autosomal recessive inheritance underlain by the deficit of one of the enzymes involved in cortisol biosynthesis. The first clinical reports of patients with adrenogenital syndrome date back to the XIXth century. The literature of the early XXth century offers comprehensive clinical characteristics of the disease along with the first attempts at its classification. The progress in biochemistry and pharmacology in the mid-XX century provided knowledge for the explanation of the nature of adrenogenital syndrome and the development of methods of pathogenetically-grounded therapy of this pathology. The advent of the era of breakthroughs in molecular genetics was marked by the elucidation of underlying causes of congenital adrenal dysfunction. At present, neonatal screening makes it possible to diagnose adrenogenital syndrome in 100% of the patients and thereby ensure prevention of mortality from salt-losing crisis. Modern techniques are used not only for prenatal diagnostics but also for preimplantation prophylaxis of adrenogenital syndrome. At the same time, extensive investigations bring to light new forms of the disorder. Recent progress in genetics gives hope that even more efficacious methods of genotherapeutic modalities will be proposed for the management of chronic pathology in question.

エリスロポエチン不応性貧血にダルベポエチンαが奏効した赤芽球癆，副腎機能不全合併の長期透析患者の1例を経験した．症例はIgA腎症を原疾患とする慢性腎不全のため1988年5月（45歳）より血液透析導入，透析中の64歳男性である．2000年（57歳），2005年（62歳）に腎癌を合併し，両側の腎臓を摘出．以後も外来維持透析されていたが，低血圧および貧血の進行が認められたため，精査加療目的に2007年9月当科入院となった．入院時Hb 5.2g/dL，Ht 15.9％で，貧血の原因については術後の副腎機能不全に加え，骨髄生検の結果，赤芽球系の減少が認められ，赤芽球癆と診断された．入院後，輸血を頻回に行い，エポエチンβ 9,000単位/週からダルベポエチンα 120μg/週投与へ変更したところ，Hb 8.1g/dL，Ht 24.4％まで改善した．本症例は長期透析患者に合併したエリスロポエチン不応性貧血および，両側腎摘出術後の副腎機能不全であり，診断，加療ともに難渋した1例であった．エリスロポエチン抵抗性貧血におけるダルベポエチンα投与の有効性についても考察する．

Proper functioning of the hypothalamic–pituitary–adrenal axis is necessary for normal homeostasis in children and especially under conditions of stress, such as critical illness. Disturbances of this axis have been classified collectively under the heading of adrenal insufficiency. Although the majority of literature has focused on children with septic shock, more recent evidence suggests that adrenal insufficiency occurs in a much broader group of critically ill children. Its etiology in pediatric critical illness remains unclear but is most likely multifactorial. Several studies have suggested possible diagnostic criteria for adrenal insufficiency in pediatric critical illness; however, to date none of these biochemical definitions have been validated. Similarly, current management of this condition in children remains based primarily on an empiric, best-practice approach. Future large-scale studies are needed to elucidate the prevalence, pathogenesis, definition, diagnosis and management of this condition.

We sought to determine whether descending thoracic aortic occlusion (DTAOC) induced ischemia results in adrenal dysfunction.Eight pigs underwent DTAOC for 45 min. Six control pigs underwent a sham procedure. Serum cortisol and adrenocorticotropic hormone (ACTH) were measured at baseline, at the end of DTAOC, 30 and 60 min after restoration of flow, and 24 hours later. Statistical analysis was performed using repeated measures ANOVA and t-test.In the study group, cortisol levels decreased during DTAOC (p=0.048) and 30 min after flow restoration (p=0.004). In the control group there was no change in serum cortisol levels. In the study group the drop in serum cortisol was associated with an increase in ACTH levels during DTAOC (p=0.040) and 30 minutes after flow restoration (p=0.070). The increase in ACTH was also significant when compared to the controls during DTAOC (p=0.030) and 30 min after blood flow restoration (p=0.040).There is a transient period of adrenal dysfunction associated with DTAOC that results in stimulation of the pituitary-adrenal axis.

Adrenal dysfunction is frequently reported in severe acute hepatitis using serum total cortisol.Because 90% of serum cortisol is bound to proteins that are altered during stress, we investigated the effect of decreased cortisol-binding proteins on serum total and free cortisol in severe acute hepatitis.43 severe and 31 non-severe acute hepatitis and 29 healthy controls were enrolled consecutively and studied prospectively. Baseline (T0) and cosyntropin-stimulated (T60) serum total and free cortisol concentrations were measured.T0 and T60 serum total cortisol did not differ significantly between severe, non-severe hepatitis and healthy controls. Conversely, serum free cortisol (T0p=0.012; T60p0.001) concentrations increased from healthy controls to severe hepatitis, accompanied by a decrease in corticosteroid-binding globulin and albumin (all p0.001). In acute hepatitis (n=74), patients with "low" corticosteroid-binding globulin (28mg/L) had higher T0 serum free cortisol than others (103.1 [61.2-157] vs. 56.6 [43.6-81.9]nmol/L, p=0.0024). Analysis of covariance showed that at equal concentration of total cortisol, the free cortisol concentration was significantly higher in severe than in non-severe hepatitis (p0.001) or healthy controls (p0.001).In severe hepatitis, the decrease in cortisol-binding proteins impairs correct diagnosis of adrenal dysfunction. This could be corrected by measuring or estimating free cortisol.

Background:There is no single test can identify hypothalamic-pituitary-adrenal dysfunction (HPAD) perfectly. The study aimed to assess the performance of measuring serum cortisol, serum dehydroepiandrosterone sulfate (DHEA-S) and plasma corticotropin (ACTH) in comparison with standard-dose short cosyntropin (250 µg) testing for the diagnosis of HPAD.Methods:This is a cross-sectional study from Al-Faiha Specialized Diabetes, Endocrine, and Metabolism Center (FDEMC) in Basrah. For all patients with suspected HAD; baseline serum cortisol, serum dehydroepiandrosterone sulfate (DHEA-S) and plasma corticotropin (ACTH) and were measured, followed by a formal short cosyntropin test as the gold standard test.Results:The total number of the study participant was 169 patients. Of them, 134 (79.3%) were women. Their age ranges from 5-80 years. The cutoff serum cortisol that predicts abnormal short cosyntropin test was less than 5.31µg/dl with maximal sensitivity and specificity of 90.4 % and 92.3% respectively. The cutoff serum DHEA-S that predict abnormal short cosyntropin test was less than 31.11 µg/dl with a sensitivity of 89.2%and specificity of 62.7%.The least reliable parameter to predict the abnormal short cosyntropin was the plasma ACTH level with a cutoff of less than 5.30 pg/ml and lowest sensitivity of 89.2% and specificity of 62.7%.Conclusion:To exclude HPAD, serum cortisol at 9-11 am having the highest predictive value, DHEA-S has the midway function and plasma ACTH is the least reliable for that. Combination of serum cortisol and serum DHEA-S yield the best performance for combinations of test. Keywords: Hypothalamic pituitaryadrenal dysfunction, short cosyntropin test, dehydroepiandrosterone sulfate, corticotropin,cortisol.