RESUMO
Vitamin D deficiency has been related with metabolic alterations in polycystic ovary syndrome (PCOS). As well, hyperactivation of adrenal axis can be programmed early in life and could be related later with PCOS development. Our aim was to establish the relationship between vitamin D and adrenal parameters with metabolic alterations and inflammation markers in PCOS. In 73 patients and 33 controls, 25-hydroxyvitamin D (25-OH-D), total and bioavailable testosterone (TT and bioT), androstenedione (A4), SHBG, cortisol, insulin, and C-reactive protein (hs-CRP) were determined; HOMA and lipid accumulation product (LAP) index were calculated. All parameters were higher in patients than in controls, except for SHBG and 25-OH-D which were lower. Binary regression analysis showed that differences in TT, bioT, A4, insulin and HOMA were independent of body mass index and waist circumference but SHBG, hs-CRP, LAP and 25-OH-D were related to body weight and fat distribution. Binary logistic regression analysis showed that cortisol and 25-OH-D could be associated to PCOS development. Correlations found between LAP and insulin, HOMA and hs-CRP confirm it is a good indicator of metabolic complications. Vitamin D and cortisol association to PCOS development justifies future research to understand the role of vitamin D in PCOS and analyze patient's perinatal history and its possible relationship with hyperactivation of adrenal axis in adult life.
Assuntos
Glândulas Suprarrenais/metabolismo , Biomarcadores/metabolismo , Inflamação/metabolismo , Síndrome do Ovário Policístico/metabolismo , Vitamina D/metabolismo , Adolescente , Corticosteroides/metabolismo , Adulto , Índice de Massa Corporal , Estudos de Casos e Controles , Feminino , Humanos , Masculino , Obesidade/metabolismo , Deficiência de Vitamina D/metabolismo , Circunferência da Cintura/fisiologia , Adulto JovemRESUMO
Blood samples of pigs infected with a moderately virulent African swine fever virus (ASFV) isolate, obtained from the Dominican Republic (DR-II), were monitored temporally for viremia, infective ASFV association with major blood components, differential changes in blood cell composition, and plasma antibodies to ASFV. After intranasal/oral virus inoculation, pigs underwent acute infection and illness that resolved. Acute illness began on postinoculation day (PID) 4 and continued to PID 11, and pigs were febrile, with maximal infective ASFV titers detected in blood. By PID 11, initial antibody titers to ASFV antigens were detected in plasma. The WBC numbers were maintained near preinoculation counts; however, lymphocyte counts decreased slightly with a compensatory increment in neutrophil and monocyte numbers. From PID 11 to PID 25, rectal temperatures gradually returned to preinoculation values, titers of viremia began to decrease, plasma antibody to ASFV antigens increased to peak titers, and WBC numbers increased slightly. Percentages of lymphocytes returned to preinoculation values, neutrophil percentages decreased to slightly below preinoculation values, monocyte percentages were mildly increased, and eosinophil percentages were unaffected. From PID 25 to PID 46, titers of viremia further decreased, and plasma titers of antibodies to ASFV antigens remained high. In pigs with DR-II viremia (PID 4 to PID 46), most viral infectivity (greater than 95%) was RBC associated. Plasma contained less than 1% infectivity, and less than 0.1% of virus was in the WBC fraction (monocytes, lymphocytes, and granulocytes). After PID 46, viremia was no longer detectable.