ABSTRACT
Background: Inflammatory bowel disease [IBD], Crohn's disease [CD], and ulcerative colitis [UC] are autoimmune inflammatory diseases of the alimentary tract, which seems to be caused by the interaction of environmental and genetic factors as well as diet and nutritional factors such as vitamin D. The aim of this study was to assess the vitamin D status and its associations with erythrocyte sedimentation rate [ESR], and high-sensitivity C-reactive protein [hs-CRP] as inflammatory markers in patients with UC
Methods: In this analytical cross-sectional study 90 patients with mild to moderate UC who were resident of Tehran were assessed. 25[OH]D, parathyroid hormone [PTH], ESR and hs-CRP were measured. Dietary intake was assessed by 3-day 24h diet recall. Statistical analyses were performed using STATA [Version 12]
Results: The average serum 25-OH-vitamin D3 was 33.1+/-8.3 ng/mL and 38.9 % of the patients were vitamin D deficient or insufficient [37.3 % of men and 41% of women]. No significant correlation between serum 25[OH]D and hs-CRP, ESR, body mass index [BMI], and disease duration was found. There were no significant differences in serum 25[OH]D between men and women. Mean daily dietary vitamin D and calcium intakes were 189.5 Iu [95% CI: 176.0-203.1] and 569.5 mg [95% CI: 538.8-600.2] respectively
Conclusion: In this cross-sectional study 38.9% of the patients with mild to moderate UC were vitamin D deficient or insufficient and vitamin D level was not correlated to ESR and/or hs-CRP. More studies are needed to investigate the effect of vitamin D in the pathogenesis of UC or as a part of its treatment
ABSTRACT
Findings have shown that low serum 25-hydroxy vitamin D level is a possible risk factor for incidence of preeclampsia during pregnancy. Vitamin D has important effects on multiple biological pathways, including angiogenesis. Some studies have shown that vitamin D deficiency is highly prevalent among women suffering from preeclampsia, influencing immune modulation and vascular function. Evidence has shown that an imbalance of pro-antigenic and anti-angiogenic proteins can be considered as a possible etiological factor in the development of preeclampsia. Besides, there is a series of studies linking the renin-angiotensin aldosterone system [RAAS] with preeclampsia. In this article, we review the current studies evaluating the association between maternal vitamin D status and vascular health, metabolism, placental immune function and the risk of preeclampsia. We provided evidence of the different factor involved in the metabolism of vitamin D and vitamin D receptor [VDR] expression, gene regulations, immune function, and chronic disease when vitamin D is used optimally
ABSTRACT
Background: Oxidative stress plays a major pathogenic role in liver injury following chronic hepatitis B. Glutathione peroxidase [Gpx] has a central role in regulating the oxidative state. Hepatitis B virus [HBV] results in down-regulation of Gpx. On the other hand, iron homeostasis is disrupted in HBV infected patients. Therefore, the objective of this study was to assess the interplay of Gpx and serum iron on clinical and virological characteristics of patients with chronic HBV infection
Method: One hundred and fifty adult, treatment-naïve, patients with chronic hepatitis B were randomly selected from an ongoing cohort of patients with HBV. Plasma Gpx1 concentration and HBV DNA quantity were measured. Liver stiffness was measured by transient elastography
Results: Serum iron had a positive association with HBV DNA count in the total population. Serum iron was not associated with liver stiffness. However, HBV DNA was significantly associated with liver stiffness only in male patients. Serum Gpx was inversely associated with liver stiffness. Serum iron and Gpx had indirect effects on liver stiffness via HBV DNA count. We observed distinct effects of serum iron on HBV DNA and Gpx on liver stiffness in male and female patients
Conclusion: We identified interplay of serum iron and Gpx1 in relation to level of liver fibrosis in patients with chronic hepatitis B. Our results suggest that oxidative stress and serum iron are differentially implicated in the progression of chronic hepatitis B in male and female patients