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Zanima me predvsem, če se Medrol in hormon DHEA izključujeta v zdravljenju neplodnosti zaradi avtoimunih boleznih.
5. ENDOCRINOLOGICAL CHANGES IN AUTOIMMUNE DISEASES
HYPOTHALAMIC-PITUITARY-ADRENAL AND ADRENOMEDULLARY FUNCTION IN PREMENOPAUSAL FEMALES WITH SYSTEMIC SCLEROSIS
Jozef Rovensky1, Jozef Lukac1, Richard Imrich2, Zofia Radikova2, Adela Penesova2, Richard Kvetnansky2, Miroslava Huckova2, Milan Vigas2, Ladislav Macho2, Marco Matucci Cerinic3
1 - National Institute of Rheumatic Diseases, Piestany, Slovakia; 2 - Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Slovakia; 3 - Servizio di Reumatologia, Dipartimento di Medicina Interna, Ospedale Careggi, Firenze, Italy
OBJECTIVES: To evaluate function of the hypothalamic-pituitary-adrenal axis and adrenomedullary hormonal system (AMHS) in premenopausal females with systemic sclerosis (SSc).
METHODS: Insulin-induced hypoglycaemia (0.1 IU/kg) was performed in 17 long-term, glucocorticoid-naive SSc patients with low disease activity and in 18 healthy females matched for age and body mass index (BMI). Concentrations of glucose, adrenocorticotrophic hormone (ACTH), cortisol, D4-androstenedione (ASD), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS), 17a-hydroxyprogesterone (17OHP), epinephrine (EPI), norepinephrine (NE), interleukin 1a (IL-1a), IL-6, and tumor necrosis factor a (TNFa) were analyzed in plasma.
RESULTS:Basal plasma levels of cortisol, ASD, 17OHP, DHEAS, IL-1f, IL-6, and TNFa? were not significantly different in SSc compared to controls. Patients had higher basal ACTH (6.76 (1.0) in SSc v 4.14 (0.45) in controls; p < 0.05), lower basal DHEA (9.02 (1.64) nmol/l in SSc v 17.0 (2.8) nmol/l in controls; p < 0.05) and lower basal NE (1.61 (0.26) nmol/l in SSc v2.57 (0.38) nmol/l in controls; p < 0.05). Patients had comparable responses of glucose and ACTH to hypoglycaemia. General linear model for repeated measurements with BMI and age as covariates revealed that the responses of 17OHP (p < 0.05), ASD (p < 0.05), DHEA (p < 0.01), EPI (p < 0.001), NE (p < 0.001) to hypoglycaemia were lower in SSc compared to controls. Cortisol response to hypoglycemia tended to be lower in SSc patients (p = 0.06) compared to controls.
CONCLUSIONS: The present data indicate decreased adrenocortical and AMHS functions in premenopausal females with SSc. Whether or not the observed changes in the neuroendocrine system are secondary due to chronic disease will deserve further investigation.
PROLACTIN LEVELS IN PATIENTS WITH EARLY RHEUMATOID ARTHRITIS
Zelmira Macejova, Dusan Trejbal, Ivica Lazurova
Internal Clinic, University Hospital, Kosice, Slovakia
INTRODUCTION: Prolactin (PRL) has been found to affect immunological system which leads to hypothesis about its role in ethiopathogenesis of autoimmune diseases. The increased levels of PRL were found also in patient with rheumatoid arthritis (RA).
AIM: to investigate diurnal secretion of prolactin in patient with early RA.
PATIENTS AND METHODS: 15 patients were evaluated, 11 women with average age of 42.3 yaers and 4 men with average age of 39.4 years.Duration of the disease: 2.32 months. As controls we evaluated 6 volunteers, average age 41.3 years. Blood was collected at 4 hours intervals. PRL was analysed by chemiluniniscence-immunochemical reaction with monoclonal antibody using Imunolite.
RESULTS: Compared to the control group, higher levels of PRL were found in patients with RA. Mean levels of PRL in the group of RA patients: at 8.00 a.m.:9.64 ng/ml, at 12.00 p.m.: 9.47 ng/ml, at 4.00 p.m.: 12.34 ng/ml, at 8.00 p.m.: 14.77 ng/ml, at 12.00 a.m.: 18.89 ng/ml, at 4.00 a.m.: 18.94 ng/ml. Statistically significant differences between control group and RA patients were found at 4.00 p.m.(*p < 0.05) and at 8.00 p.m., 12.00 a.m., 4.00 a.m. (*p < 0.01). If we took the lowest cortisol levels measured at these times into account reciprocal ratio of prolactin/cortisol might then be involved in alteration of daily activity of the disease with maximum of difficulties in the morning.
CONCLUSION: Better understanding to interactions between neuroendocrine and immune system will help to reveal the ethiology of autoimmune disease and will contribute to search for new therapeutic strategies in the future.
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