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Hyposecretion of the adrenal androgen dehydroepiandrosterone sulfate and its relation to clinical variables in inflammatory arthritis

Hyposecretion of the adrenal androgen dehydroepiandrosterone sulfate and its relation to clinical variables in inflammatory arthritis

Hypothalamic–pituitary–adrenal underactivity has been reported in rheumatoid arthritis (RA). This phenomenon has implications with regard to the pathogenesis and treatment of the disease. The present study was designed to evaluate the secretion of the adrenal androgen dehydroepiandrosterone sulfate (DHEAS) and its relation to clinical variables in RA, spondyloarthropathy (Spa), and undifferentiated inflammatory arthritis (UIA). Eighty-seven patients (38 with RA, 29 with Spa, and 20 with UIA) were studied, of whom 54 were women. Only 12 patients (14%) had taken glucocorticoids previously. Age-matched, healthy women (134) and men (149) served as controls. Fasting blood samples were taken for determination of the erythrocyte sedimentation rate (ESR), serum DHEAS and insulin, and plasma glucose. Insulin resistance was estimated by the homeostasis-model assessment (HOMA IR ). DHEAS concentrations were significantly decreased in both women and men with inflammatory arthritis (IA) (P < 0.001). In 24 patients (28%), DHEAS levels were below the lower extreme ranges found for controls. Multiple intergroup comparisons revealed similarly decreased concentrations in each disease subset in both women and men. After the ESR, previous glucocorticoid usage, current treatment with nonsteroidal anti- inflammatory drugs, duration of disease and HOMA IR were controlled for, the differences in DHEAS
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Dehydroepiandrosterone sulfate and dehydroepiandrosterone sulfate/cortisol ratio in cirrhotic patients with septic shock: another sign of hepatoadrenal syndrome?

Dehydroepiandrosterone sulfate and dehydroepiandrosterone sulfate/cortisol ratio in cirrhotic patients with septic shock: another sign of hepatoadrenal syndrome?

Septic shock is accompanied by activation of the hypothal- amic–pituitary–adrenal (HPA) axis, which is highlighted by increased serum corticotropin and glucocorticoid [1–3]. Parallel to glucocorticoid secretion, HPA activation leads to the release of dehydroepiandrosterone (DHEA) and its sulfate (DHEAS). Both of these are adrenal andro- gens and practically all is secreted by the adrenal glands [4]. The serum concentration of DHEAS is 300–500 times higher than that of DHEA and can be considered a circu- lating reservoir [4]. In contrast to serum cortisol or DHEA concentrations, serum DHEAS levels do not exhibit a diurnal variation, as a consequence of a longer half-life [4]. Therefore, serum DHEAS levels have been proposed to serve as a potential biomarker of adrenal function in different clinical settings [5, 6]. In fact, investigators have combined adrenocorticotropic hormone (ACTH) stimula- tion tests or insulin tolerance tests with measurements of DHEAS to define normality of the HPA axis [7, 8]. Importantly, similar to that of glucocorticoid, the secre- tion of adrenal androgen is almost exclusively under the trophic effect of ACTH [4]. Normally, adrenal androgen is secreted synchronously with glucocorticoid from the adrenal cortex [9]. Although the specific physiological function of DHEA is still unclear, it has been shown that DHEA modulates the function of the immune system. DHEA plays an important role in the interaction be- tween the endocrine and immune systems [10, 11]. The immune-modulatory properties of DHEA include induction of T-cell activation and interleukin-2 pro- duction [12, 13], and enhancing cytotoxic functions of monocytes [14]. Because of these immune-enhancing effects, adrenal androgen has been considered a functional antagonist of glucocorticoids, which can be immunosup- pressive [4]. In fact, a recent study indicated that DHEA and glucocorticoids regulate the same immune-modulating genes in opposite directions [15]. Considering lines of evi- dence for activities of adrenal androgen that offset those of glucocorticoid, investigators have proposed quantification of their levels as a ratio, to serve as an alternative index of adrenal activity in different clinical settings [16, 17]. Inter- estingly, the responses of glucocorticoid and androgen demonstrate a significant discrepancy during critical illness, with adrenal androgen levels decreasing and gluco- corticoid levels increasing [18]. This phenomenon is more pronounced in most severely ill patients and nonsurvivors [18–20], suggesting that functional adap- tation of adrenal steroidogenesis may exhaust the counterregulatory mechanisms between adrenal an- drogen and glucocorticoid, thus negatively impacting the prognosis of critical illness. Indeed, an increased cortisol to DHEAS ratio was shown in nonsurvivors [19, 20], indicating that an exhausted adrenal reserve can serve as a prognostic factor.
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Effects of acute and chronic administration of neurosteroid dehydroepiandrosterone sulfate on neuronal excitability in mice

Effects of acute and chronic administration of neurosteroid dehydroepiandrosterone sulfate on neuronal excitability in mice

Moreover, following chronic DHEAS (10 mg/kg) treat- ment, we observed no significant differences compared to control group in the doses of pentylentetrazole (Figure 3A and B), picrotox[r]

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Management of Congenital Adrenal Hyperplasia Using Serum Dehydroepiandrosterone Sulfate and 17-Hydroxyprogesterone Concentrations

Management of Congenital Adrenal Hyperplasia Using Serum Dehydroepiandrosterone Sulfate and 17-Hydroxyprogesterone Concentrations

Of 34 evaluations, a definite assessment of adequacy of control could be arrived at 25 times using urinary values and 22 times using both serum DHEA-S and 17-OHP concentrations.. DHEA-S [r]

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Increased serum dehydroepiandrosterone sulfate in the first episode but not in subsequent episodes in male patients with schizophrenia

Increased serum dehydroepiandrosterone sulfate in the first episode but not in subsequent episodes in male patients with schizophrenia

Background: Many studies have investigated the relationship between blood levels of dehydroepiandrosterone (DHEA) and its sulfate ester (DHEA-S), cortisol, progesterone, and testosterone and the onset, prognosis, symptom severity, and treatment response of schizo- phrenia. In the present study, we assessed potential differences in blood levels of neurosteroids between drug-naïve first-episode patients with schizophrenia (FES), and drug-free patients with schizophrenia who were not in the first episode but were in a phase of acute exacerba- tion (DFP).

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Dehydroepiandrosterone-Sulfate, Insulin Resistance and Ovarian Volume Estimation in Patients With Polycystic Ovarian Syndrome

Dehydroepiandrosterone-Sulfate, Insulin Resistance and Ovarian Volume Estimation in Patients With Polycystic Ovarian Syndrome

Ovaries and adrenal glands share the same pathway of steroid hormone production. Dehydroepiandrosterone (DHEA) and especially its sulphate ester (DHEA-S) are mainly produced in the adrenal glands (90% of the total circulating amount). Although, approximately 40-70% of women with PCOS have increased levels of Δ4-Androstenedione and DHEA-S, the exact mechanism that triggers the production of androgens from the adrenal gland still remains unclear (10, 11). The correlation between DHEA-S with insulin resistance and glucose metabolism has not been thoroughly examined. Buyalos et al showed that acute induced hyperinsulinemia levels did not affect DHEA-S levels in obese and non-obese women with or without PCOS (12).
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Neuroprotective properties of dehydroepiandrosterone sulfate and its relationship to interleukin 6 after aneurysmal subarachnoid hemorrhage: a prospective cohort study

Neuroprotective properties of dehydroepiandrosterone sulfate and its relationship to interleukin 6 after aneurysmal subarachnoid hemorrhage: a prospective cohort study

Methods: A complete data set DHEAS and IL-6 serum levels for days 0, 1, 4, 7, 10 and 14 after aSAH and outcome assessment at discharge according to modified Rankin Scale score mRS was av[r]

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Small leucine-rich proteoglycans (SLRPs) in the endometrium of polycystic ovary syndrome women: a pilot study

Small leucine-rich proteoglycans (SLRPs) in the endometrium of polycystic ovary syndrome women: a pilot study

17-OHP: 17 α -hydroxyprogesterone; A: Androstenedione; CV: Coefficient of variation; DHEAS: Dehydroepiandrosterone sulfate; ECM: Extracellular matrix; EGFR: Epidermal growth factor receptor; FSH: Follicle-stimulating hormone; H&E: Hematoxylin and eosin; HC: Hip circumference; IGFIR: Insulin-like growth factor receptor I; LH: Lutein hormone; MET: Hepatocyte growth factor receptor; mFG: Modified Ferriman and Gallwey; PCOS: Polycystic ovarian syndrome; PRL: Prolactin; SHBG: Sex hormone-binding globulin; SLRPs: Small leucine-rich proteoglycans; TBS: Tris-buffered saline; Tfree: Free testosterone; TGF: Transforming growth factor; TKR: Tyrosine kinase receptors; TSH: Thyroid-stimulating hormone; TT: Total testosterone; WC: Waist circumference; β -hCG: β -human chorionic gonadotropin
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Neurosteroids block the increase in intracellular calcium level induced by Alzheimer&rsquo;s &beta;-amyloid protein in long-term cultured rat hippocampal neurons

Neurosteroids block the increase in intracellular calcium level induced by Alzheimer&rsquo;s &beta;-amyloid protein in long-term cultured rat hippocampal neurons

Thus, the search for substances that protect against A β P neurotoxicity is crucial. Our system for observing Ca 2+ infl ux induced by A β P has contributed to the search for such substances (Kawahara and Kuroda 2001). It requires a relatively short time for carrying out assays. The elevation of [Ca 2+ ] i is considered to be the primary event of A β P neuro- toxicity. We previously demonstrated that several lipophilic substances such as phloretin, cholesterol, and 17 β -estradiol signifi cantly inhibit the A β P-induced elevation of [Ca 2+ ] i in GT1–7 cells (Kawahara and Kuroda 2001). Phloretin, a plant-derived fl avonoid, decreases membrane potential and inhibits the electrostatic interaction between A β P and membrane lipids (Hertel et al 1997). Cholesterol decreases membrane fl uidity and inhibits channel formation by peptides (Tomita et al 1992). Cholesterol also blocks the increase in [Ca 2+ ] i induced by A β P in cultured neurons (Hartmann et al 1994). 17 β -estradiol, a female hormone, is neuroprotec- tive and affects membrane fl uidity (Schwartz et al 1996). All these compounds inhibit A β P neurotoxicity (Zhou and Richardson 1996; Hertel et al 1997; Olivieri et al 2002). Therefore, substances that modulate membrane properties such as membrane potential and fl uidity may inhibit A β P neurotoxicity. In line with the search for neuroprotective agents, we focused on neurosteroids including dehydro- epiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEA-S), and pregnenolone. These neurosteroids are steroid hormones synthesized de novo in the central nervous system from cholesterol or peripheral steroid precursors. Several lines of evidence suggest that neurosteroids modulate various functions of the brain and exhibit neuroprotective activities (Tsutsui et al 2000). For example, DHEA-S could protect neurons from NMDA-induced neurotoxicity (Chara- lampopoulos et al 2006). In addition, there is an age-related decrease in the levels of neurosteroids (Moffat et al 2000), and the levels of neurosteroids in plasma or in the brain are decreased in Alzheimer’s patients (Hillen et al 2000; Marx et al 2006). Thus, neurosteroids have been recognized as anti-aging hormones, and are widely used as supplements for improving the impaired cognitive functions of the elderly (Huppert et al 2000).
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Acne and PCOS are less frequent in women with Mayer-Rokitansky-Küster-Hauser syndrome despite a high rate of hyperandrogenemia: a cross-sectional study

Acne and PCOS are less frequent in women with Mayer-Rokitansky-Küster-Hauser syndrome despite a high rate of hyperandrogenemia: a cross-sectional study

17-OHP: 17-hydroxyprogesterone; DHEAS: Dehydroepiandrosterone sulfate; DLQI: Dermatology life quality index; GAGS: Global acne grading system; MRKH: Mayer-Rokitansky-Küster-Hauser syndro[r]

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Reliability of Serum Dehydroepiandrosterone Sulphate (DHEAs) as an Indicator of Skeletal Maturation: A Comparative study

Reliability of Serum Dehydroepiandrosterone Sulphate (DHEAs) as an Indicator of Skeletal Maturation: A Comparative study

During early infancy, plasma concentration of follicle stimulating hormone (FSH) and luteinizing hormone (LH) are greater than during childhood due to CNS restraint mechanisms (Reiter and Grumbach1982 19 , Kletch et al 1983 19 ). The onset of pubertal growth acceleration is marked by pulsatile secretion of GnRh by hypothalamus particularly during sleep (Jackacki et al 1982 19 ). This secretion occurs after the maturation of hypothalamus pituitary complex called as the gonadostat which is related to blood levels of adrenal sex steroids. The adrenal cortex secretes significant levels of androgenic hormones dehydroepiandrosterone (DHEA) and its sulfated derivative dehydroepiandrosterone sulfate (DHEAs). These androgens appear to be transformed into estrogen in peripheral fatty tissues and stimulate the gonadostat (Parker and Mehesh 1977 19 ). This phenomenon is termed as adrenarche. It occurs two years before the pubertal growth spurt.
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Hormonal status in protracted critical illness and in hospital mortality

Hormonal status in protracted critical illness and in hospital mortality

Methods: We conducted a prospective observational study in four medical and surgical intensive care units (ICUs). ICU patients who regained consciousness after 7 days of mechanical ventilation were included. Plasma levels of insulin-like growth factor 1 (IGF-1), prolactin, thyroid-stimulating hormone, follicle-stimulating hormone, luteinizing hormone, estradiol, progesterone, testosterone, dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS) and cortisol were measured on the first day patients were awake and cooperative (day 1). Mean blood glucose from admission to day 1 was calculated.
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Preservation of androgen secretion during estrogen suppression with aminoglutethimide in the treatment of metastatic breast carcinoma

Preservation of androgen secretion during estrogen suppression with aminoglutethimide in the treatment of metastatic breast carcinoma

We evaluated the comparative effects of aminoglutethimide (AG) on androgen and estrogen levels estrone ([E1], estradiol [E2], plasma dehydroepiandrosterone-sulfate [DHEA-S], testosterone [T], dihydrotestosterone [DHT], delta 4-androstenedione [delta 4-A]), follicle- stimulating hormone (FSH), luteinizing hormone (LH), and prolactin in postmenopausal patients with breast cancer randomly allocated to either AG treatment or bilateral surgical adrenalectomy as a control group. In response to either treatment, the plasma levels of E1 fell 62-75% (P less than 0.001) and urine E1 85.7-88.7% (P less than 0.001) in all study days over a 12-wk period. Similarly, the concentrations of E2 in plasma and urine fell 40- 72% without statistically significant differences between the two treatment modalities. The relatively weak androgen, DHEA-S, was reduced by 92% (877.3 +/- 184.6 to 71.8 +/- 14.5 ng/ml) at 12 wk in women treated with AG, but suppressed nearly 99% (1,151 +/- 262 to 5.8 +/- 3.3 ng/ml) in adrenalectomized women. At all time points after treatment, the DHEA-S levels were significantly higher in patients receiving AG. Plasma concentrations of the potent androgens, T and DHT, were also relatively preserved during AG treatment. T levels were never significantly reduced by AG, and DHT concentrations were decreased only at the 4th wk to a maximum of 20%. delta 4-A levels fell 56% in response to this drug only on the 12th wk of therapy […]
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ANDROGEN RELEASE AND SYNTHESIS IN VITRO BY HUMAN ADULT ADRENAL GLANDS

ANDROGEN RELEASE AND SYNTHESIS IN VITRO BY HUMAN ADULT ADRENAL GLANDS

These studies demonstrate that fresh human adult "normal," atrophic, "hypertensive," hyperplastic, adenomatous, and carcinomatous tissue slices release dehydroepiandrosterone, androstene[r]

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Binding of thrombin to subendothelial extracellular matrix  Protection and expression of functional properties

Binding of thrombin to subendothelial extracellular matrix Protection and expression of functional properties

catalytically blocked enzyme, diisofluorophosphate (DIP)-alpha-thrombin competed efficiently with 125I-alpha-thrombin, indicating that the binding was independent of its catalytic site. Moreover, high concentrations of the synthetic tetradecapeptide, representing residues 367-380 of thrombin B chain (the macrophage mitogenic domain of thrombin), competed with thrombin binding to ECM, indicating that the binding site may reside in the vicinity of "loop B" region. Thrombin binds to dermatan sulfate in the ECM, as demonstrated by the inhibition of 125I-alpha-thrombin binding to ECM pretreated with chondroitinase ABC, but not with heparitinase or chondroitinase AC. This stands in contrast to 125I-FGF (fibroblast growth factor) binding to ECM, which was inhibited by heparitinase but not by chondroitinase ABC, ECM-bound thrombin exhibits an exposed proteolytic site as
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Dehydroepiandrosterone (DHEA) supplementation in diminished ovarian reserve (DOR)

Dehydroepiandrosterone (DHEA) supplementation in diminished ovarian reserve (DOR)

We searched PubMed, Cochrane and Ovid Medline between 1995 and 2010 for all publications under the following key words: Dehydroepiandrosterone or DHEA; androgens or testosterone; ovarian reserve or diminished ovarian reserve; ovarian function or diminished ovarian function. In addition, we explored the bibliographies of all relevant publications for further relevant citations, which had not been detected via the original search. So identified publications were also in detail reviewed by the authors, including their relevant citations. A total of 114 publications were, thus, reviewed for this publica- tion, with 64 being cited in this manuscript. The 50 manuscripts reviewed but not referenced in the review either contained no relevant information in regards to the topic of this review and/or only recited data of ear- lier published manuscripts, which are included in the reference list of this manuscript.
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EVALUATION OF SEMINAL PLASMA TAC IN RELEVANCE TO SERUM DHEA,TESTOSTERONE LEVELS AS A DIAGNOSTIC VALUE IN INFERTILE MEN

EVALUATION OF SEMINAL PLASMA TAC IN RELEVANCE TO SERUM DHEA,TESTOSTERONE LEVELS AS A DIAGNOSTIC VALUE IN INFERTILE MEN

According to world health organization (WHO) infertility can be defined as the inability of a sexually active and non-contracepting couple to achieve spontaneous pregnancy after one year of regular unprotected intercourses 1 . The control of spermatogenesis is by the integration between local and systemic factors. Healthy and mature spermatozoa reflects a convenient testicular tissue function in response to reproductive hormones 2 . The male caused infertility can be found in about 50% of infertile couples 3 . The etiology of declining male fertility can be associated with oxidative stress (OS), however low levels of reactive oxygen species (ROS) can be involved in important physiological processes of spermatozoa, such as capacitation and acrosome reactions 4 . OS can be defined as the loss of balance between the amount of total antioxidant capacity (TAC) and the amount of reactive oxygen species (ROS) that are generated in the spermatozoa, either through the ROS overproduction and/ or the decreased concentration of TAC which can cause a shortage in the scavenging processes of abnormal free radicals 5 . Some studies in relevance to male infertility have suggested that the infertile men may have an impaired seminal plasma TAC, showing that the decreased TAC levels may have a pathogenic effect on male fertility 6 . The balance between free radicals production and antioxidants defense in the seminal plasma are under the influence of different urogenital diseases and damaging factors, such as smoking, varicocele, long sexual abstinence, infections and inflammations 7 . A relation between Hormones and TAC are suggested, a correlation between plasmatic TAC and reproductive hormones level has been observed 8 , levels of several other hormones (e.g., prolactin and growth hormone) have shown good correlation with several enzymatic antioxidant activities in different types of tissue 9 . Other studies reported that TAC is correlated with serum testosterone and estradiol in male 8 . However, it is not clearly understood if TAC levels are under systemic control, especially by the endocrine system. It has been observed that Dehydroepiandrosterone (DHEA) which is a derivative of C19 steroid that is mainly secreted by the adrenal cortex may play a role in the level of antioxidants. Exogenous DHEA can exert an antioxidant or prooxidant effect, depending on dose, schedule, and target tissue type 10 .
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The Binding of Androsterone Sulfate, Etiocholanolone Sulfate, and Dehydroisoandrosterone Sulfate by Human Plasma Protein

The Binding of Androsterone Sulfate, Etiocholanolone Sulfate, and Dehydroisoandrosterone Sulfate by Human Plasma Protein

The binding of androsterone sulfate A-S, etiocholanolone sulfate E-S, and dehydroisoandrosterone sulfate D-S to human plasma, serum, and two albumin preparations Tritiated steroid plus a[r]

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Natural ECM Bacterial Cellulose Wound Healing—Dubai Study

Natural ECM Bacterial Cellulose Wound Healing—Dubai Study

2.2.1. Synthesis of Bacterial Cellulose and Bacterial Cellulose/Chondroitin Sulfate/Hyaluronic Acid The acetic fermentation process was achieved by using glucose as a carbohydrate source. Results of this process are vinegar and a nanobiocellulose biomass. The modifying process is based on the addition of hyaluronic acid and chondroitin sulfate (1% w/w) to the culture medium before the bacteria is inoculated. Bacterial cellulose (BC) is produced by Gram-negative bacteria Gluconacetobacter xylinus, which can be obtained from the culture medium in the pure 3-D structure, consisting of an ultra fine network of cellulose nanofibers [19].
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Histological Changes of Cartilage Degeneration in Osteoarthritic Rabbits

Histological Changes of Cartilage Degeneration in Osteoarthritic Rabbits

Osteoarthritis is thought to be the most prevalent chronic and disabling joint disease in animals and humans and its treatment is a major orthopaedic challenge because there is no ideal drug treatment to preserve joint structure and function, as well as to ameliorate the symptomatology of the disease [1, 2]. Osteoarthritis is a chronic disease characterized by irreversible damage to joint structures, including loss of articular cartilage, osteophyte formation, alterations in the subchondral bone and synovial inflammation. It has been shown that chondroitin sulfate interferes with the progression of structural changes in joint
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