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Please use this identifier to cite or link to this item: http://hdl.handle.net/20.500.12710/2553
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dc.contributor.authorLupasco, Iuliana
dc.date.accessioned2019-06-24T20:25:48Z-
dc.date.available2019-06-24T20:25:48Z-
dc.date.issued2015
dc.identifier.citationLupasco, Iu. Corticotropin and cortisol kinetics in chronic HBV infection. In: European Journal of Clinical Investigation. 2015, 45 (suppl.2), 69-92. (IF: 2.687).en_US
dc.identifier.issn1365-2362
dc.identifier.urihttp://onlinelibrary.wiley.com/doi/10.1111/eci.12436/epdf
dc.identifier.urihttp://repository.usmf.md/handle/20.500.12710/2553-
dc.descriptionScientific Laboratory of Gastroenterology, State University of Medicine and Pharmacy “N.Testemitanu”, Chisinau, Republic of Moldovaen_US
dc.description.abstractIntroduction: HBV infection remains enigma of hepatology despite is widespread and involves estimated 13.3 million adult people in important social and economic consequences. Aim of the study: In the context of the functioning mechanisms of adaptation to chronic stress, such as chronic HBV infection was considered important to study pituitary-adrenal axis. Material and methods: One hundred and ten patients with chronic hepatitis (CH) HBV have been evaluated during the study, in dependence on the viral infection phase were formed three groups: I – HBeAg+ (21), II – antiHBe+, minimal activity (56), III – antiHBe+, moderate/maximum activity (24). Thirty healthy individuals served the control group. The corticotropin and cortisol kinetics was studied in all groups fasting and in the dynamics of the authors’ glucose and euphylline stimulation test at 60 and 120 min. Results: Corticotropin level in patients of I group after 60 min of stimulation presented an impaired appearance without characteristic burst featured for healthy individuals, (P < 0.01). III group differed from control data from the very beginning (P < 0.05), having the exactly opposite ACTH pattern at 2 point of the test (P < 0.01). In HBeAg + group observed a significant increase in cortisol initial data (P < 0.01), with an inversion of the response to stimulation at 2 point (P < 0.01) with no return to normal values (P < 0.01). The same pattern was observed in II group, that differs in hormonal lower values at 2 and 3 points of the test (P < 0.01, P < 0.01, P < 0.01). The III group presented significantly higher cortisol values at all points of the study (P < 0.01, P < 0.01, P < 0.01). Conclusions: ACTH and cortisol kinetics impairment was found in relation to the viral infection phase and disease activity.en_US
dc.language.isoenen_US
dc.publisherEuropean Journal of Clinical Investigationen_US
dc.subjectCorticotropinen_US
dc.subjectCortisolen_US
dc.subject.meshAdrenocorticotropic Hormoneen_US
dc.subject.meshKineticsen_US
dc.subject.meshHepatitis B, Chronicen_US
dc.subject.meshInfectionen_US
dc.titleCorticotropin and cortisol kinetics in chronic HBV infectionen_US
dc.typeArticleen_US
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