Vitamin D status and the risk of neuromyelitis optica spectrum disorders: A systematic review and meta-analysis.

BACKGROUND: Previous studies have linked vitamin D deficiency with autoimmune diseases, and recent research has found low vitamin D levels in neuromyelitis optica spectrum disorder (NMOSD) patients. We aimed to determine the variances in serum 25(OH)D levels between NMOSD patients and healthy controls. METHODS: We searched English and Chinese databases (PubMed, Embase, Cochrane Library, Web of Science, CBM, CNKI, WanFang Med, VIP) for observational studies related to serum 25(OH)D levels in NMOSD patients published up to August 24, 2023. We included studies with healthy controls and compared serum 25(OH)D levels between NMOSD patients and controls. We computed the mean difference (MD) and 95% confidence interval (CI) for continuous variables to evaluate serum 25(OH)D levels and combined odds ratios (ORs) and 95% CIs for dichotomized 25(OH)D data. RESULTS: Six papers were selected for meta-analysis, including 794 participants (347 in the NMOSD group and 447 in the healthy control group). Meta-analysis showed significantly lower serum 25(OH)D levels in the NMOSD group (MD: -7.83, 95 % CI: -10.99 to -4.68). The risk of 25(OH)D deficiency was 23.36 times higher in the NMOSD group (OR: 23.36, 95 % CI: 0.85 to 640.76, p = 0.06>0.05), with a 94 % occurrence rate. There was no significant difference in the risk of having sufficient 25(OH)D between the groups (p = 0.12>0.05). CONCLUSION: NMOSD patients have lower serum 25(OH)D levels than healthy controls. However, the current research results do not provide evidence for a causal relationship between serum 25(OH)D levels and the onset of NMOSD. Routine vitamin D supplementation may be advantageous for patients with NMOSD.

Changes and Influencing Factors of Urinary Phosphorus Excretion in Patients with Different Stages of Chronic Kidney Disease.

BACKGROUND: The aim of the study was to explore the changes and the possible influencing factors of phosphorus excretion in chronic kidney disease (CKD) patients. METHODS: A database with 204 patients who met the CKD diagnostic criteria was established. Clinical data, including 24-hour urine phosphorus excretion (24-hour UPE), were collected. The demographic and clinical characteristics of CKD patients in different stages and the changes in serum phosphorus (P) and 24-hour UPE with renal function were studied. After exploring the factors influencing 24-hour UPE by multiple linear regression analysis, the effects of gender on 24-hour UPE was assessed. RESULTS: Among 204 patients, there were significant differences in serum calcium (Ca), P, 24-hour UPE, intact parathyroid hormone (iPTH), and 25-hydroxyvitamin D [25(OH)-VD] among different CKD stages. Twenty-four-hour UPE fluctuated greatly, but serum P was relatively stable, which was > 1.46 mmol/L at an estimated glomerular filtration rate (eGFR) < 10 mL/minute/1.73 m2. Male gender (ß = 3.42, p < 0.00) and eGFR (ß = 0.06, p < 0.00) were related to 24-hour UPE, while age, body weight, albumin (ALB), iPTH, and serum P were not related to 24-hour UPE according to regression analysis. There were significant differences in 24-hour UPE and serum P between males and females. CONCLUSIONS: Urinary phosphorus excretion decreased with decreasing renal function in CKD patients. Urinary phosphorus excretion might be affected by eGFR and gender.

Prevalence and influencing factors of vitamin D deficiency in chronic kidney disease: A cross-sectional study.

BACKGROUND AND OBJECTIVES: Very few studies have investigated vitamin D deficiency of Chinese chronic kidney disease (CKD) patients. Our main aims were to measure 25(OH)D levels and to explore the possible correlated factors contributing to vitamin D deficiency. MATERIALS AND METHODS: 207 patients who came from north China and were not receiving vitamin D supplementation were included in this study from February 2013 to April 2015. We collected blood samples to determine levels of serum creatinine (Scr), blood urea nitrogen (BUN), uric acid (UA), serum phosphate (P) and calcium (Ca), intact parathyroid hormone (iPTH), albumin (ALB), as well as urinary protein within 24 hours (24hUPr). Total 25(OH)D was measured via electrochemiluminescence immunoassay. Vitamin D deficiency should be defined as a 25(OH)D < 15 ng/mL. RESULTS: Of the 207 patients, only 20.3% had a circulating 25(OH)D level > 15 ng/mL. The concentrations of 25(OH)D were 11.73 ± 6.75 ng/mL, 10.44 ± 6.03 ng/mL, 10.05 ± 5.57 ng/mL, 9.10 ± 5.00 ng/mL, 7.13 ± 3.99 ng/mL (p < 0.001) according to estimated glomerular filtration rate (eGFR) (89 - 60, 59 - 45, 44 - 30, 29 - 15, < 15 mL/min/1.73m2). The prevalence of 25(OH)D deficiency was significantly high in each group (70.1%, 70.8%, 76.5%, 81.6%, 91.4%, p < 0.001). 25(OH)D concentration decreased with the decline of renal function. The difference of 25(OH)D levels between the 24hUPr ≥ 3.5 g group and the 24hUPr < 3.5 g group was statistically significant. Multivariate linear regression analysis showed that 25(OH)D concentration was associated with 24hUPr and serum Ca. The 25(OH)D concentration was lower, and the prevalence of 25(OH)D deficiency was higher in diabetes mellitus (DM) patients compared with patients without DM. CONCLUSION: This study shows a high prevalence of 25(OH)D deficiency in CKD patients from north China, and the deficiency is dependent on eGFR. Urinary protein and serum Ca might be associated with 25(OH)D concentration. DM patients have lower 25(OH)D concentrations than non-DM patients.

Metabolic changes of H2S in smokers and patients of COPD which might involve in inflammation, oxidative stress and steroid sensitivity.

Oxidative stress and inflammation play crucial role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Most patients with COPD show a poor response to corticosteroids. Hydrogen sulfide (H2S ) has been implicated in the pathogenesis of COPD, but its expression and effects in lung tissue from COPD patients are not clear. In peripheral lung tissue samples from 24 patients, we found that compared with nonsmokers, the protein level of cystathionine-γ-lyase (CSE) was decreased in smokers and COPD patients. CSE mRNA increased but cystathionine-ß-synthase (CBS) mRNA decreased in COPD patients. H2S donors increased glutathione and superoxide dismutase in CS exposed U937 cells and inhibited CS-induced TNF-α and IL-8 secretion. Dexamethasone alone had no effect on lipopolysaccharide (LPS) induced TNF-α release by alveolar macrophages from CS exposed rats, however the combination of dexamethasone and H2S donor significantly inhibited TNF-α release. Thus, H2S metabolism is altered in lung tissue of smokers and COPD patients. Supplementation of H2S protects against CS-induced oxidative stress and inflammation in macrophages and H2S on steroid sensitivity deserves further investigation.