Glucocorticoids (GCs) are hormones that are released in response to stressors and exhibit many activities, including immunomodulatory and anti-inflammatory activities. They are primarily synthesized in the adrenal gland but are also produced in peripheral tissues via regeneration of adrenal 11-oxo metabolites or by de novo synthesis from cholesterol. The present study investigated the influence of the microbiota on de novo steroidogenesis and regeneration of corticosterone in the intestine of germ-free (GF) and specific pathogen-free mice challenged with a physical stressor (anti-CD3 antibody i.p. injection). In the small intestine, acute immune stress resulted in increased mRNA levels of the proinflammatory cytokines IL1β, IL6 and Tnfα and genes involved in de novo steroidogenesis (Stard3 and Cyp11a1), as well as in regeneration of active GCs from their 11-oxo metabolites (Hsd11b1). GF mice showed a generally reduced transcriptional response to immune stress, which was accompanied by decreased intestinal corticosterone production and reduced expression of the GC-sensitive marker Fkbp5. In contrast, the interaction between stress and the microbiota was not detected at the level of plasma corticosterone or the transcriptional response of adrenal steroidogenic enzymes. The results indicate a differential immune stress-induced intestinal response to proinflammatory stimuli and local corticosterone production driven by the gut microbiota.

• Klíčová slova
• 11β-hydroxysteroid dehydrogenase, anti-CD3 antibody, extra-adrenal steroidogenesis, glucocorticoids, intestine, microbiome,
• MeSH
• 11-beta-hydroxysteroiddehydrogenasy genetika   metabolismus   MeSH
• kortikosteron metabolismus   MeSH
• kvantitativní polymerázová řetězová reakce MeSH
• myši MeSH
• steroidy metabolismus   MeSH
• střevní mikroflóra fyziologie   MeSH
• tandemová hmotnostní spektrometrie MeSH
• tenké střevo metabolismus   MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• 11-beta-hydroxysteroiddehydrogenasy MeSH
• kortikosteron MeSH
• steroidy MeSH

The commensal microbiota affects brain functioning, emotional behavior and ACTH and corticosterone responses to acute stress. However, little is known about the role of the microbiota in shaping the chronic stress response in the peripheral components of the hypothalamus-pituitary-adrenocortical (HPA) axis and in the colon. Here, we studied the effects of the chronic stress-microbiota interaction on HPA axis activity and on the expression of colonic corticotropin-releasing hormone (CRH) system, cytokines and 11β-hydroxysteroid dehydrogenase type 1 (11HSD1), an enzyme that determines locally produced glucocorticoids. Using specific pathogen-free (SPF) and germ-free (GF) BALB/c mice, we showed that the microbiota modulates emotional behavior in social conflicts and the response of the HPA axis, colon and mesenteric lymph nodes (MLN) to chronic psychosocial stress. In the pituitary gland, microbiota attenuated the expression of Fkbp5, a gene regulating glucocorticoid receptor sensitivity, while in the adrenal gland, it attenuated the expression of genes encoding steroidogenesis (MC2R, StaR, Cyp11a1) and catecholamine synthesis (TH, PNMT). The pituitary expression of CRH receptor type 1 (CRHR1) and of proopiomelanocortin was not influenced by microbiota. In the colon, the microbiota attenuated the expression of 11HSD1, CRH, urocortin UCN2 and its receptor, CRHR2, but potentiated the expression of cytokines TNFα, IFNγ, IL-4, IL-5, IL-6, IL-10, IL-13 and IL-17, with the exception of IL-1β. Compared to GF mice, chronic stress upregulated in SPF animals the expression of pituitary Fkbp5 and colonic CRH and UCN2 and downregulated the expression of colonic cytokines. Differences in the stress responses of both GF and SPF animals were also observed when immunophenotype of MLN cells and their secretion of cytokines were analyzed. The data suggest that the presence of microbiota/intestinal commensals plays an important role in shaping the response of peripheral tissues to stress and indicates possible pathways by which the environment can interact with glucocorticoid signaling.

• Klíčová slova
• 11β-hydroxysteroid dehydrogenase, Adrenal gland, CRH system, Chronic psychosocial stress, Colon, Cytokines, Immune system, Local metabolism of glucocorticoids, Mice, Microbiome,
• MeSH
• 11-beta-hydroxysteroiddehydrogenasa typ 1 metabolismus   MeSH
• adrenokortikotropní hormon metabolismus   MeSH
• chování zvířat fyziologie   MeSH
• cytokiny metabolismus   MeSH
• exprese genu fyziologie   MeSH
• glukokortikoidy genetika   fyziologie   MeSH
• hormon uvolňující kortikotropin metabolismus   MeSH
• hypofýza MeSH
• kortikosteron metabolismus   MeSH
• mikrobiota fyziologie   MeSH
• myši inbrední BALB C MeSH
• myši MeSH
• nadledviny MeSH
• psychický stres genetika   metabolismus   MeSH
• psychologie MeSH
• receptory glukokortikoidů metabolismus   MeSH
• regulace genové exprese fyziologie   MeSH
• sociální chování MeSH
• systém hypofýza - nadledviny mikrobiologie   MeSH
• systém hypotalamus-hypofýza mikrobiologie   MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• 11-beta-hydroxysteroiddehydrogenasa typ 1 MeSH
• adrenokortikotropní hormon MeSH
• cytokiny MeSH
• glukokortikoidy MeSH
• hormon uvolňující kortikotropin MeSH
• kortikosteron MeSH
• receptory glukokortikoidů MeSH

The bioavailability of glucocorticoids is modulated by enzyme 11β-hydroxysteroid dehydrogenase type 1 (11HSD1), which catalyzes the conversion of inactive 11-oxo-glucocorticoids to active 11-hydroxy-glucocorticoids cortisol and corticosterone and is regulated by pro-inflammatory cytokines. Our aim was to assess the effect of colitis on the expression of 11HSD1 in specific microanatomical compartments of the mucosal immune system. Using qRT-PCR we quantified the expression of 11HSD1 and cytokines in the colon, mesenteric lymph nodes (MLN) and spleen of mice with colitis. Microsamples of the MLN cortex, paracortex and medulla, colonic crypt epithelium (CCE), lamina propria and isolated intestinal lymphoid follicles (ILF) were harvested by laser microdissection, whereas splenic and MLN lymphocytes by flow cytometry. Colitis increased 11HSD1 in the CCE, ILF, and MLN cortex but not in the lamina propria and the MLN paracortex and medulla. Expression of IL-4, IL-21 and TNFα was increased in both the cortex of MLN and ILF, whereas IL-1β and IL-10 were only increased in the follicles. No positive effect was observed in the case of IFNγ and TGFβ. 11HSD1 was positively correlated with TNFα and less strongly with IL-21, IL-1β, and IL-4. Colitis also upregulated the 11HSD1 expression of T cells in the spleen and MLN. The study demonstrates the stimulatory effect of inflammation on local glucocorticoid metabolism only in particular compartments of the mucosal immune system. The correlation between cytokines and 11HSD1 in the ILF and MLN cortex indicates that pro-inflammatory cytokines may amplify glucocorticoid signals in inductive compartments of the mucosal immune system.

• Klíčová slova
• Colon, Cytokine microenvironment, Dextran sodium sulfate colitis, Lymphoid organs, Metabolism of glucocorticoids,
• MeSH
• 11-beta-hydroxysteroiddehydrogenasa typ 1 genetika   metabolismus   MeSH
• cytokiny metabolismus   MeSH
• kolitida enzymologie   genetika   imunologie   MeSH
• myši inbrední BALB C MeSH
• myši MeSH
• regulace genové exprese enzymů MeSH
• střevní sliznice imunologie   MeSH
• zánět enzymologie   genetika   imunologie   MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• 11-beta-hydroxysteroiddehydrogenasa typ 1 MeSH
• cytokiny MeSH

Numerous chemicals in the environment have the ability to interact with the endocrine system. These compounds are called endocrine disruptors (EDs). Exposure to EDs represents one of the hypotheses for decreasing fertility, the increased risk of numerous cancers and obesity, metabolic syndrome and type 2 diabetes. There are various mechanisms of ED action, one of which is their interference in the action of 11β-hydroxysteroid dehydrogenase (11βHSD) that maintains a balance between active and inactive glucocorticoids on the intracellular level. This enzyme has two isoforms and is expressed in various tissues. Inhibition of 11βHSD in various tissues can have different consequences. In the case of EDs, the results of exposure are mainly adverse; on the other hand pharmaceutically developed inhibitors of 11βHSD type 1 are evaluated as an option for treating metabolic syndrome, as well as related diseases and depressive disorders. This review focuses on the effects of 11βHSD inhibitors in the testis, colon, adipose tissue, kidney, brain and placenta.

• Klíčová slova
• 11β-hydroxysteroid dehydrogenase, Adipose tissue, Brain, Colon, Endocrine disruptor, Inhibitor, Placenta, Testis,
• MeSH
• 11-beta-hydroxysteroiddehydrogenasa typ 1 antagonisté a inhibitory   metabolismus   MeSH
• 11-beta-hydroxysteroiddehydrogenasa typ 2 antagonisté a inhibitory   metabolismus   MeSH
• diabetes mellitus chemicky indukované   enzymologie   patologie   MeSH
• endokrinní disruptory farmakologie   MeSH
• glukokortikoidy metabolismus   MeSH
• inhibitory enzymů farmakologie   MeSH
• kolon účinky léků   enzymologie   MeSH
• lidé MeSH
• metabolický syndrom chemicky indukované   enzymologie   patologie   MeSH
• mozek účinky léků   enzymologie   MeSH
• nádory chemicky indukované   enzymologie   patologie   MeSH
• obezita chemicky indukované   enzymologie   patologie   MeSH
• orgánová specificita MeSH
• placenta účinky léků   enzymologie   MeSH
• těhotenství MeSH
• testis účinky léků   enzymologie   MeSH
• tuková tkáň účinky léků   enzymologie   MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• těhotenství MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• 11-beta-hydroxysteroiddehydrogenasa typ 1 MeSH
• 11-beta-hydroxysteroiddehydrogenasa typ 2 MeSH
• endokrinní disruptory MeSH
• glukokortikoidy MeSH
• inhibitory enzymů MeSH

Dehydroepiandrosterone (DHEA) and its 7-oxo- and 7-hydroxy-metabolites occurring in the brain are considered neurosteroids. Metabolism of the latter is catalysed by 11β-hydroxysteroid dehydrogenase (11β-HSD) which also interconverts cortisol and cortisone. The concurrent metabolic reaction to DHEA 7-hydroxylation is the formation of 16α-hydroxy-DHEA. The LC-MS/MS method using triple stage quadrupole-mass spectrometer was developed for simultaneous quantification of free DHEA, 7α-hydroxy-DHEA, 7β-hydroxy-DHEA, 7-oxo-DHEA, 16α-hydroxy-DHEA, cortisol and cortisone in human plasma and cerebrospinal fluid (CSF). The method employs 500 μL of human plasma and 3000 μL of CSF extracted with diethyl ether and derivatized with 2-hydrazinopyridine. It has been validated in terms of sensitivity, precision and recovery. In plasma, the following values were obtained: limit of detection: 2-50p g/mL; limit of quantification: 5-140 pg/mL; within-day precision 0.58-14.58%; between-day precision: 1.24-13.89% and recovery: 85-113.2%). For CSF, the values of limit of detection: 2-28 pg/mL; limit of quantification: 6-94 pg/mL; within-day precision; 0.63-5.48%; between-day precision: 0.88-14.59% and recovery: 85.1-109.4% were acquired. Medians and concentration ranges of detected steroids in plasma and CSF are given in subjects with excluded normal pressure hydrocephalus (n=37; 65-80 years). The method enables simultaneous quantification of steroids important for the estimation of 11β-HSD activity in human plasma and CSF. It will be helpful in better understanding various degenerative diseases development and progression.

• Klíčová slova
• 11β-Hydroxysteroid dehydrogenase, Cerebrospinal fluid, Dehydroepiandrosterone metabolites, LC–MS/MS,
• MeSH
• 11-beta-hydroxysteroiddehydrogenasy metabolismus   MeSH
• dehydroepiandrosteron analogy a deriváty   mozkomíšní mok   MeSH
• imunologické faktory mozkomíšní mok   MeSH
• lidé MeSH
• neurotransmiterové látky mozkomíšní mok   MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• 11-beta-hydroxysteroiddehydrogenasy MeSH
• dehydroepiandrosteron MeSH
• imunologické faktory MeSH
• neurotransmiterové látky MeSH

The local concentration of glucocorticoids is intensively regulated by 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD 1). Human 11beta-HSD 1 also reversibly catalyzes the inter-conversion of 7alpha-hydroxy- and 7beta-hydroxy-dehydroepiandrosterone (DHEA) into 7-oxo-DHEA. The cohort of 282 obese adolescents, 154 girls (median age 15.31 years, range 14.17-16.68 years) and 128 boys (median age 14.95 years, range 13.87-16.16 years), BMI (Body Mass Index) >90th percentile was examined. In samples collected before and after one month of reductive diet therapy, circulating levels of steroids were analyzed by liquid chromatography-tandem mass spectrometry and radioimmunoassay methods. The model of the treatment efficacy prediction was calculated. A significant reduction in circulating levels of cortisone, E2 and increased levels of 7beta-hydroxy-DHEA after the reductive treatment was observed. Levels of cortisol, DHEA, DHT sustained without any significant change. The predictive Orthogonal Projections to Latent Structures (OPLS) model explained 20.1 % of variability of BMI, z-score change by the basal levels of 7alpha-hydroxy-DHEA, DHEA, cortisol and E2 as the strongest predictors. Reduced levels of circulating cortisone and reduced ratios of oxygenated/reduced metabolites reflect increased reductase activity of 11beta-HSD 1 with reduced BMI, z-score. We hypothesize whether these changes can be attributed to the altered activity of 11beta-HSD 1 in the liver.

• MeSH
• 11-beta-hydroxysteroiddehydrogenasa typ 1 krev   MeSH
• biologické markery krev   MeSH
• dehydroepiandrosteron krev   MeSH
• játra metabolismus   MeSH
• kohortové studie MeSH
• lidé MeSH
• mladiství MeSH
• obezita krev   terapie   MeSH
• redukční dieta trendy   MeSH
• výsledek terapie MeSH
• Check Tag
• lidé MeSH
• mladiství MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• 11-beta-hydroxysteroiddehydrogenasa typ 1 MeSH
• biologické markery MeSH
• dehydroepiandrosteron MeSH

The aim of the present work was to study the influence of variable stress on the expression of 11β-hydroxysteroid dehydrogenase type 1 (11HSD1) and the neuropeptides corticotropin-releasing hormone (CRH), urocortins 2 and 3(UCN2, UCN3), arginine vasopressin (AVP), oxytocin (OXT) and adenylate cyclase-activating polypeptide (PACAP) in two inbred rat strains: stress hypo-responsive Lewis (LEW) and hyper-responsive Fisher 344 (F344) rats. We found site-specific and strain-dependent differences in the basal and stress-stimulated expression of 11HSD1, CRH, UCN2, UCN3 and PACAP. In LEW rats, stress upregulated 11HSD1 in the prefrontal cortex and lateral amygdala, whereas in F344 rats 11HSD1 was upregulated in the central amygdala and hippocampal CA2 and ventral but not dorsal CA1 region; no effect was observed in the paraventricular nucleus, pituitary gland and adrenal cortex of both strains. The expression of glucocorticoid receptors did not parallel the upregulation of 11HSD1. Stress also stimulated the expression of paraventricular OXT, CRH, UCN3 and PACAP in both strains but amygdalar CRH only in LEW and UCN2/UCN3 in F344 rats, respectively. The upregulation of PACAP and CRH was paralleled only by increased expression of PACAP receptor PAC1 but not CRH receptor type 1. These observations provide evidence that inbred F344 and LEW rats exhibit not only the well-known phenotypic differences in the activity of the HPA axis but also strain- and stress-dependent differences in the expression of genes encoding 11HSD1 and neuropeptides associated with the HPA axis activity. Moreover, the differences in 11HSD1 expression suggest different local concentration of corticosterone and access to GR in canonical and noncanonical structures of the HPA axis.

• Klíčová slova
• 11β-Hydroxysteroid dehydrogenase type 1, Brain, Fisher rat, Lewis rat, Neuropeptides, Stress,
• MeSH
• 11-beta-hydroxysteroiddehydrogenasa typ 1 genetika   metabolismus   MeSH
• amygdala metabolismus   MeSH
• arginin vasopresin genetika   metabolismus   MeSH
• hipokampus metabolismus   MeSH
• hormon uvolňující kortikotropin genetika   metabolismus   MeSH
• hypofýza metabolismus   MeSH
• hypofyzární adenylátcyklázu aktivující peptid genetika   metabolismus   MeSH
• krysa rodu Rattus MeSH
• kůra nadledvin metabolismus   MeSH
• messenger RNA metabolismus   MeSH
• mozek metabolismus   MeSH
• nucleus paraventricularis hypothalami metabolismus   MeSH
• oxytocin genetika   metabolismus   MeSH
• potkani inbrední F344 MeSH
• potkani inbrední LEW MeSH
• prefrontální mozková kůra metabolismus   MeSH
• psychický stres genetika   metabolismus   MeSH
• receptory glukokortikoidů genetika   metabolismus   MeSH
• stanovení celkové genové exprese MeSH
• systém hypofýza - nadledviny metabolismus   MeSH
• systém hypotalamus-hypofýza metabolismus   MeSH
• urokortiny genetika   metabolismus   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• srovnávací studie MeSH
• Názvy látek
• 11-beta-hydroxysteroiddehydrogenasa typ 1 MeSH
• arginin vasopresin MeSH
• hormon uvolňující kortikotropin MeSH
• hypofyzární adenylátcyklázu aktivující peptid MeSH
• messenger RNA MeSH
• oxytocin MeSH
• receptory glukokortikoidů MeSH
• urokortiny MeSH

Primary adrenal insufficiency (PAI) is a rare condition in childhood which is either inherited (mostly) or acquired. It is characterized by glucocorticoid and maybe mineralocorticoid deficiency. The most common form in children is 21-hydroxylase deficiency, which belongs to the steroid biosynthetic defects causing PAI. Newer forms of complex defects of steroid biosynthesis are P450 oxidoreductase deficiency and (apparent) cortisone reductase deficiency. Other forms of PAI include metabolic disorders, autoimmune disorders and adrenal dysgenesis, e.g. the IMAGe syndrome, for which the underlying genetic defect has been recently identified. Newer work has also expanded the genetic causes underlying isolated, familial glucocorticoid deficiency (FGD). Mild mutations of CYP11A1 or StAR have been identified in patients with FGD. MCM4 mutations were found in a variant of FGD in an Irish travelling community manifesting with PAI, short stature, microcephaly and recurrent infections. Finally, mutations in genes involved in the detoxification of reactive oxygen species were identified in patients with unsolved FGD. Most mutations were found in the enzyme nicotinamide nucleotide transhydrogenase, which uses the mitochondrial proton pump gradient to produce NADPH. NADPH is essential in maintaining high levels of reduced forms of antioxidant enzymes for the reduction of hydrogen peroxide. Similarly, mutations in the gene for TXNRD2 involved in this system were found in FGD patients, suggesting that the adrenal cortex is particularly susceptible to oxidative stress.

• MeSH
• 11-beta-hydroxysteroiddehydrogenasy nedostatek   MeSH
• adrenální insuficience diagnóza   etiologie   metabolismus   terapie   MeSH
• dítě MeSH
• glukokortikoidy nedostatek   MeSH
• hirzutismus komplikace   vrozené   terapie   MeSH
• kojenec MeSH
• lidé MeSH
• poruchy sexuálního vývoje s karyotypem 46, XX komplikace   terapie   MeSH
• předškolní dítě MeSH
• steroidy biosyntéza   MeSH
• vrozené poruchy metabolismu steroidů komplikace   terapie   MeSH
• Check Tag
• dítě MeSH
• kojenec MeSH
• lidé MeSH
• předškolní dítě MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• 11-beta-hydroxysteroiddehydrogenasy MeSH
• glukokortikoidy MeSH
• steroidy MeSH

Although the effects of glucocorticoids on proliferation, differentiation and apoptosis are well known, and steroid hormones have been identified to play a role in pathogenesis and the development of various cancers, limited data are available regarding the relationship between the local metabolism of glucocorticoids and colorectal adenocarcinoma (CRC) formation. Glucocorticoid metabolism is determined by 11β-hydroxysteroid dehydrogenases type 1 and 2 (11HSD1, 11HSD2), which increase the local concentration of cortisol due to the reduction of cortisone, or decrease this concentration due to the oxidation of cortisol. The objective of this study was to evaluate the extent of 11HSD1 and 11HSD2 mRNA in pre-malignant colorectal polyps and in CRC. The specimens were retrieved from patients by endoscopic or surgical resection and the expression of 11HSD1 and 11HSD2 was measured by real-time PCR. The polyps were of the following histological types: hyperplastic polyps and adenomas with low- or high-grade dysplasia. The neoplastic tissue of CRC obtained during tumor surgery was also studied. It was found that 11HSD2 was not only downregulated in CRC but already in the early stages of neoplastic transformation (adenoma with low-grade dysplasia). In contrast, the level of 11HSD1 was significantly increased in CRC but not in pre-malignant polyps. The results demonstrate that the downregulation of 11HSD2 gene expression is a typical feature of the development of colorectal polypous lesions and their transformation into CRC.

• MeSH
• 11-beta-hydroxysteroiddehydrogenasa typ 1 analýza   biosyntéza   MeSH
• 11-beta-hydroxysteroiddehydrogenasa typ 2 analýza   biosyntéza   MeSH
• adenokarcinom enzymologie   MeSH
• adenomové polypy enzymologie   MeSH
• dítě MeSH
• dospělí MeSH
• down regulace MeSH
• kolorektální nádory enzymologie   MeSH
• kvantitativní polymerázová řetězová reakce MeSH
• laserová záchytná mikrodisekce MeSH
• lidé středního věku MeSH
• lidé MeSH
• mladiství MeSH
• mladý dospělý MeSH
• nádorové biomarkery analýza   MeSH
• polymerázová řetězová reakce s reverzní transkripcí MeSH
• prekancerózy enzymologie   MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• transkriptom MeSH
• Check Tag
• dítě MeSH
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mladiství MeSH
• mladý dospělý MeSH
• mužské pohlaví MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• 11-beta-hydroxysteroiddehydrogenasa typ 1 MeSH
• 11-beta-hydroxysteroiddehydrogenasa typ 2 MeSH
• nádorové biomarkery MeSH

The aim of our study was to investigate adrenocortical function in the context of disease activity and inflammatory status in premenopausal RA females. Adrenal glucocorticoid and androgen responses to the 1 microg ACTH 1-24 test were investigated in 23 premenopausal RA and in 15 age- and BMI-matched healthy females. Twelve RA patients were on low-dose prednisone (<8.5 mg/day). Patients with DAS28>3.2 had lower (p<0.05) total plasma cortisol, 17-hydroxyprogesterone, dehydroepiandrosterone and androstenedione responses in the ACTH test compared to healthy controls. Patients with DAS28>3.2 had lower (p<0.05) dehydroepiandrosterone response in the ACTH test compared to patients with DAS28

• MeSH
• 11-beta-hydroxysteroiddehydrogenasa typ 1 metabolismus   MeSH
• 17-alfa-hydroxyprogesteron krev   MeSH
• adrenokortikotropní hormon MeSH
• androgeny metabolismus   MeSH
• dospělí MeSH
• hormony kůry nadledvin krev   MeSH
• kůra nadledvin patofyziologie   MeSH
• lidé MeSH
• premenopauza krev   MeSH
• revmatoidní artritida krev   patofyziologie   MeSH
• studie případů a kontrol MeSH
• stupeň závažnosti nemoci MeSH
• tuková tkáň metabolismus   MeSH
• Check Tag
• dospělí MeSH
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• 11-beta-hydroxysteroiddehydrogenasa typ 1 MeSH
• 17-alfa-hydroxyprogesteron MeSH
• adrenokortikotropní hormon MeSH
• androgeny MeSH
• hormony kůry nadledvin MeSH