Hypovitaminosis D and its relation to demographic and laboratory data among hepatitis C patients

Background. The relationship between 25-hydroxyvitamin D [25(OH)D] serum levels and response to antiviral therapy and laboratory data in HCV infection remains unclear. The aim of this study was to determine pre-treatment 25(OH)D serum level among HCV infected individuals and to evaluate the association between vitamin D status, virological response, and laboratory data.Material and methods. Baseline serum 25(OH)D levels were measured in 237 chronic HCV infected patients (139 female, age 53.7 ± 11.2 years) using chemiluminescence immunoassay. Correlations between serum 25(OH)D levels, virological and laboratory data regarding HCV infection as well as sustained virological response (SVR) to antiviral therapy were evaluated.Results. Mean serum values of 25(OH)D was 26.2 ± 12 ng/mL and prevalence of vitamin D deficiency (< 30 ng/mL) was 66.2%. Advanced age (> 55 years), high mean values of LDL, total cholesterol, HDL and low mean values of alkaline phosphatase and hemoglobin were statistically associated to vitamin D deficiency. Antiviral treatment was underwent by 133 HCV patients and 44.3% of them achieved SVR. Most of individuals that presented SVR also presented 25(OH)D level higher than 30ng/mL (55.9%). SVR was associated to low mean values of LDL, total cholesterol and platelets; high mean values of ALT, AST and low fibrosis grade. Conclusions: In conclusion, low vitamin D levels were observed among HCV infected patients and was associated to laboratory findings, however baseline 25(OH)D level is not independently associated with SVR.     

Complementary role of vitamin D deficiency and the interleukin-28B rs12979860 C/T polymorphism in predicting antiviral response in chronic hepatitis C

The widely accepted interleukin-28B (IL-28B) rs12979860 C/T polymorphism and the more recently proposed vitamin D serum concentration are two novel predictors of the response to antiviral treatment in chronic hepatitis C virus (HCV) infection. This study aimed to verify whether the IL-28B rs12979860 C/T polymorphism and pretreatment serum vitamin D levels have independent or complementary roles in predicting the rates of sustained viral response (SVR). The present study included 211 consecutive, treatment-na?ve chronic HCV patients who had their pretreatment serum 25-OH vitamin D level and IL-28B rs12979860 C/T genotype determined. Overall, SVR was achieved by 134/211 (63.5%) patients and by 47/110 (42.7%) patients infected with difficult-to-treat HCV genotypes. On multivariate analysis, SVR was predicted by the HCV genotype, the IL-28B rs12979860 C/T polymorphism, and gamma-glutamyl transpeptidase, HCV RNA, cholesterol, and 25-OH vitamin D serum levels, with an area under the receiver operating characteristic (ROC) curve of 0.827. When difficult-to-treat HCV genotypes were analyzed separately, the SVR was predicted by the IL-28B rs12979860 C/T polymorphism, viral load, and serum vitamin D level, with an area under the ROC curve of 0.836. Moreover, by categorizing these latter patients into four groups-C/C homozygotes with vitamin D levels >20 ng/mL (group A) or ≤20 ng/mL (group B) and C/T heterozygotes or T/T homozygotes with vitamin D levels >20 ng/mL (group C) or ≤20 ng/mL (group D)-a significant linear trend was observed, with SVR rates in the following descending order: group A, 18/21 (85.7%); group B, 6/11 (54.5%); group C, 14/38 (36.8%); and group D, 9/40 (22.5%) (P < 0.0001). CONCLUSION: Vitamin D serum levels are complementary to the IL-28B rs12979860 C/T polymorphism in enhancing the correct prediction of the SVR in treatment-na?ve chronic hepatitis C.     

No relationship between vitamin D status and insulin resistance in a group of high school students

Objective: To investigate the effects of vitamin D deficiency on both insulin resistance and risk of metabolic syndrome in children. Methods: The study group consisted of 301 children and adolescents with a mean age of 14.2±1.8 years. Serum 25-hydroxyvitamin D [25(OH)D] levels and insulin resistance indices were evaluated. According to serum 25(OH)D levels, the subjects were classified in 3 groups. Those with levels ≤10 ng/mL were labeled as the vitamin D deficient group (group A), those with levels of 10-20 ng/mL as the vitamin D insufficient group (group B) and those with ≥20 ng/mL as having normal vitamin D levels (group C). Metabolic syndrome was defined according to the International Diabetes Federation consensus. The participants with and without metabolic syndrome were compared in terms of 25(OH)D levels.Results: Mean 25(OH)D level of the total group was 18.2±9.3 (2.8-72.0) ng/mL. Distribution of individuals according to their vitamin D levels showed that 11.6% were in group A, 53.5% in group B, and 34.9% in group C. The proportions of boys and girls in these categories were 22.9% and 77.1% in group A, 36.6% and 63.4% in group B, 54.3% and 45.7% in group C, respectively. There were no significant differences in 25(OH)D levels in the individuals with and without impaired fasting glucose or impaired glucose tolerance. No relationship was observed between insulin resistance/sensitivity indices and vitamin D status (p>0.05). Metabolic syndrome was diagnosed in 12.3% (n=37) of the children. There was also no difference in mean 25(OH)D levels between individuals who had and those who did not have the metabolic syndrome.Conclusion: In our study, no correlations were found between insulin measurements during oral glucose tolerance test and vitamin D deficiency. Nonetheless, more extended studies including vitamin D supplementation and evaluating insulin sensitivity via clamp technique are needed to further elucidate this relationship.Conflict of interest:None declared.     

Normal vitamin D levels are associated with spontaneous hepatitis B surface antigen seroclearance

AIM: To investigate a possible association between serum vitamin D levels and spontaneous hepatitis B surface antigen (HBsAg) seroclearance.METHODS: Fifty-three patients diagnosed with chronic inactive hepatitis B and spontaneous HBsAg seroclearance were followed up in two Israeli liver units between 2007 and 2012. This retrospective study reviewed medical charts of all the patients, extracting demographic, serological and vitamin D rates in the serum, as well as medical conditions and current medical therapy. Spontaneous HBsAg seroclearance was defined as the loss of serum HBsAg indefinitely. Vitamin D levels were compared to all patients who underwent spontaneous HBsAg seroclearance.RESULTS: Out of the 53 patients who underwent hepatitis B antigen seroclearance, 44 patients (83%) had normal levels of 25-hydroxyvitamin vitamin D compared to 9 patients (17%) who had below normal levels. Multivariate analysis showed that age (> 35 years) OR = 1.7 (95%CI: 1.25-2.8, P = 0.05), serum vitamin D levels (> 20 ng/mL) OR = 2.6 (95%CI: 2.4-3.2, P = 0.02), hepatitis B e antigen negativity OR = 2.1 (95%CI: 2.2-3.1, P = 0.02), low viral load (hepatitis B virus DNA < 100 IU/mL) OR = 3 (95%CI: 2.6-4.2, P = 0.01) and duration of HBsAg seropositivity (> 8 years) OR = 1.6 (95%CI: 1.15-2.6, P = 0.04) were also associated with spontaneous HBsAg seroclearance.CONCLUSION: We found a strong correlation between normal vitamin D levels and spontaneous HBsAg seroclearance.     

High-Dose Vitamin D: Helpful or Harmful?

If the optimal serum 25(OH)D level for skeletal health is 30 ng/mL or greater, then vitamin D insufficiency is widespread, affecting about 75% of adults based on a recent survey of more than 20,000 Americans. However, after a comprehensive analysis of existing research studies, the Institute of Medicine recently concluded that nearly all individuals are vitamin D replete when their 25(OH)D levels are 20 ng/mL or greater. Furthermore, two recent publications challenge the belief that 25(OH)D levels greater than 30 ng/mL are optimal for bone health. In a randomized, placebo-controlled trial, high-dose, once-yearly vitamin D therapy increased the incidence of fractures and falls. The second study reported that high-dose vitamin D did not reduce levels of parathyroid hormone or bone resorption among adults with 25(OH)D levels less than 32 ng/mL at baseline. It is time to question whether serum 25(OH)D levels of 30 ng/mL or greater are necessary for all individuals.     

基线维生素D与慢性丙型肝炎持久病毒学应答相关性的Meta分析

目的：探讨基线维生素D水平与HCV基因1、4型感染者对标准抗病毒治疗持久病毒学应答（SVR）的关系。方法检索数据库中有关基线维生素D水平与HCV基因1、4型慢性感染者接受抗病毒治疗后SVR相关性的文献,meta分析比较SVR组和非SVR组的基线维生素D水平。结果共检索到210篇相关文献,其中符合纳入标准5篇,meta分析结果显示,基线维生素D水平在SVR组（32．9 ng/mL）与非SVR组（28．3 ng/mL）的加权均数差（WMD）为6．759（95％ CI：1．786,11．733）,两组的基线维生素D水平差异有统计学意义（Z＝2．66,P＝0．008）。结论 HCV 基因1、4型慢性感染者接受标准抗HCV治疗获得SVR者的基线维生素D水平高于未获得SVR者。     

Pre-treatment prediction of response to peginterferon plus ribavirin in chronic hepatitis C genotype 3

AIM: To evaluate pre-treatment factors associated with sustained virological response(SVR) in patients with hepatitis C virus(HCV) genotype 3 treated with peginterferon and ribavirin(RBV). METHODS: We retrospectively analyzed treatment naive, mono-infected HCV genotype 3 patients treated with peginterferon and RBV. Exclusion criteria included presence of other liver disease, alcohol consumption and African American or Asian ethnicity. The variables collected and compared between patients who achieved an SVR and patients who did not were as follows: gender, age, fibrosis stage, diabetes, body mass index,steatosis, INFL3 polymorphism, pre-treatment HCVRNA, type of peginterferon, RBV dose and adherence. RESULTS: A total of 107 patients treated between June, 2004 and March, 2013 were included. Mean treatment duration was 25.1(± 1.8) wk. Overall, 58%(62/107) of the patients achieved an SVR and 42%(45/107) did not. In the multivariate logistic regression analysis, pre-treatment HCV-RNA ≥ 600000 UI/m L(OR = 0.375, 95%CI: 0.153-0.919, P = 0.032) and advanced fibrosis(OR = 0.278, 95%CI: 0.113-0.684,P = 0.005) were significantly associated with low SVR rates. In patients with pre-treatment HCV-RNA ≥600000 UI/m L and advanced fibrosis, the probability of achieving an SVR was 29%(95%CI: 13.1-45.2).In patients with pre-treatment HCV-RNA 600000UI/m L and mild to moderate fibrosis, the probability of achieving an SVR was 81%(95%CI: 68.8-93.4).CONCLUSION: In patients with HCV genotype 3infections the presence of advance fibrosis and high pre-treatment viral load might be associated with poor response to peginterferon plus RBV. These patients could benefit the most from new direct antiviral agentsbased regimes.     

Lack of effect of subtherapeutic vitamin D treatment on glycemic and lipid parameters in Type 2 diabetes: A pilot prospective randomized trial

Background: Epidemiological studies suggest a higher prevalence of metabolic syndrome and its components among individuals with vitamin D deficiency. The aim of the present study was to determine whether vitamin D treatment improves glucose control and insulin sensitivity in Type 2 diabetes mellitus (T2DM). Methods: Subjects with T2DM and serum 25‐hydroxyvitamin D (25(OH)D) concentrations <25 ng/mL were randomized to receive 400 IU (Group 1) or 1200 IU (Group 2) cholecalciferol for 4 months. Fasting plasma glucose, glycosylated hemoglobin (HbA1c), Quantitative Insulin Sensitivity Check Index (QUICKI), serum lipid levels and serum adiponectin were measured at baseline and at 4 months. Results: Mean 25(OH)D levels increased in both groups (from 17.6 ± 1.5 to 25.5 ± 1.8 ng/mL in Group 1 and from 15.6 ± 1.4 to 27.4 ± 2.4 ng/mL in Group 2; P ≤ 0.001 vs baseline for each group). No significant differences were noted in fasting plasma glucose, HbA1c, QUICKI, serum adiponectin, and lipid levels compared with baseline within groups or between the two groups. Conclusions: In the present pilot study, conventional vitamin D treatment at a level improving, but not optimizing, serum 25(OH)D did not improve glycemia, insulin sensitivity, or lipid profile. However, diabetes and lipids were relatively well controlled at baseline. Future studies should be designed to achieve optimal concentrations of serum 25(OH)D (at least >32 ng/mL) and should include subjects showing more abnormal parameters of glycemia, lipid, and insulin sensitivity at baseline.     

Vitamin D deficiency and vitamin D therapy in chronic hepatitis C

Background. Vitamin D has immunomodulatory properties, exerts an anti-hepatitis C virus (HCV) effect in vitro and improves response to interferon-based therapy in patients with chronic hepatitis C (CHC). Low serum levels of 25(OH) vitamin D [25(OH)D] are frequently found in CHC patients and seem to be related to more advanced stages of liver fibrosis. The study aims to establish the incidence of vitamin D deficiency in Spanish patients with CHC, its possible relation with features of liver damage and with the IL28B gene polymorphism, and the immediate effect of vitamin D therapy on CHC-related analytical variables.Materials and methods. Baseline serum 25(OH)D levels were measured in 108 consecutive CHC patients (60 men, age 54.3 ± 10.5 yrs). Results of transient elastography and of IL28B rs12979860C/T genotype were available in 89 and 95 patients, respectively. Forty one patients with insufficient levels of 25(OH)D received vitamin D supplements and were re-evaluated thereafter.Results. Deficiency of vitamin D (< 20 µg/dL) and suboptimal levels (20–30 µg/mL) were detected in 36.1% and 40.9% of patients, respectively. No relationships were found between 25(OH)D levels and biochemical liver tests, fibrosis stage and IL28B genotype. Vitamin D therapy normalized 25(OH)D levels in all treated patients, but did not modify significantly HCV-RNA serum levels or biochemical tests.Conclusions. Vitamin D deficiency is common in Spanish patients with CHC but it is related neither to biochemical and virological variables nor with the fibrosis stage and IL28B polymorphism. Vitamin D therapy has no immediate effect on HCV-RNA serum levels.     

Vitamin D deficiency in children and adolescents

Objective Vitamin D deficiency is an important health problem in both developed and developing countries. Recent reports on the extraskeletal effects of vitamin D have led to increased interest in prevalence studies on states of deficiency/insufficiency of vitamin D. The aim of this study was to determine the frequency of vitamin D deficiency and insufficiency in children and adolescents residing in Ankara, Turkey and to investigate the factors associated with low vitamin D status. Methods: A total of 440 children and adolescents aged between 0 and 16 years were enrolled in this study. The subjects were divided into three groups according to their vitamin D status (deficiency ≤15 ng/mL; insufficiency: 15-20 ng/mL; sufficiency ≥20 ng/mL) and also according to their age (preschool<5 years; middle childhood: 5-10 years; adolescence: 11-16 years). Results: Overall, 40% of the subjects were found to have 25 hydroxy vitamin D [25(OH)D] levels of less than 20 ng/mL. The levels indicated a deficiency state in 110 subjects (25%) and insufficiency - in 66 (15%). The rate of vitamin D deficiency was higher in girls, regardless of age. 25(OH)D levels correlated negatively with age (r=-0.48, p<0.001), body mass index (BMI) (r=-0.20, p=0.001) and intact parathyroid hormone (iPTH) level (r=-0.31, p=0.001). A positive correlation was observed between 25(OH)D and serum ferritin levels (r=0.15, p=0.004). Conclusions: The high frequency of vitamin D deficiency in childhood (especially among adolescent girls) indicates a need for supplementation and nutritional support. Conflict of interest:None declared.     

Positive association between serum 25-hydroxyvitamin D level and bone density in osteoarthritis

OBJECTIVE: To describe the association between serum 25-hydroxyvitamin D (25[OH]D) level and bone mineral density (BMD) in persons with primary knee osteoarthritis (OA). METHODS: We conducted a population-based survey of the Framingham Study. A total of 228 subjects with primary radiographic knee OA were identified. For vitamin D status, 25(OH)D levels < or =15 ng/ml were classified as vitamin D deficient, 25(OH)D levels 16-32 ng/ml were classified as hypovitaminosis D, and 25(OH)D levels >32 ng/ml were classified as vitamin D replete. We compared average BMD between categories of 25(OH)D levels in subjects with OA using a linear regression model while adjusting for sex, age, body mass index (BMI), knee pain, physical activity, cohort, and disease severity. RESULTS: Mean age was 74.4 years and 36% were men. Of 228 individuals, 15% were vitamin D deficient, 51% had hypovitaminosis D, and 34% were vitamin D replete. Compared with subjects with vitamin D deficiency, those with hypovitaminosis D had a 7.3% higher BMD (adjusted percent difference; P = 0.02) and vitamin D replete subjects had an 8.5% higher BMD (adjusted percent difference; P = 0.02; test for trend across categories: P = 0.04). CONCLUSION: We observed a significant positive association between serum 25(OH)D and BMD in individuals with primary knee OA, independent of sex, age, BMI, knee pain, physical activity, and disease severity. Given the high prevalence of low 25(OH)D status in persons with knee OA and the positive association between 25(OH)D and BMD, vitamin D supplementation may enhance BMD in individuals with OA.     

Investigating the Efficiency of Vitamin D Administration with Buccal Spray in the Treatment of Vitamin D Deficiency in Children and Adolescents

Objective:The aim of this study was to evaluate the efficiency of a buccal spray form of vitamin D compared to single oral dose (stoss therapy) and oral drops therapy in the treatment of vitamin D deficiency.Methods:Ninety healthy children and adolescents (3-18 years) with vitamin D deficiency [serum level of 25-hydroxyvitamin D (25(OH) D) <12 ng/mL] were randomized to receive vitamin D3 buccal spray (2000 U, n=30, group 1) for six weeks, oral drops (2000 U, n=30, group 2) for six weeks and a single oral dose (300 000 U) vitamin D3 (n=30, group 3). Serum calcium, phosphorus, alkaline phosphatase, parathyroid hormone and 25(OH)D levels of the patients were measured at baseline and after the treatment on the 42^nd day.Results:All three groups had a significant increase in serum 25(OH)D concentrations (p<0.001). In group 1, baseline mean 25(OH)D was 8.0±0.41 ng/mL, which rose to 22.1 (17.8-28.2) ng/mL after treatment with a mean increase of 15.6±1.3 ng/mL. Similarly in group 2, baseline, post-treatment and mean increase in 25(OH)D concentrations were 7.9±0.45 ng/mL, 24.4 (20.6-29.6) ng/mL and 17.3±1.1 ng/mL while for group 3 these values were 7.6±0.47 ng/mL, 40.3 (29.4-58.4) ng/mL and 34.3±3.2 ng/mL, respectively.Conclusion:We conclude that vitamin D3 supplementation with buccal spray and oral drops is equally effective in terms of raising vitamin D concentrations in short-term treatment of vitamin D deficiency.     

Plasma 25-hydroxyvitamin D levels and risk of incident hypertension

Hydroxylation of 25(OH)D to 1,25-dihydroxyvitamin D and signaling through the vitamin D receptor occur in various tissues not traditionally involved in calcium homeostasis. Laboratory studies indicate that 1,25-dihydroxyvitamin D suppresses renin expression and vascular smooth muscle cell proliferation; clinical studies demonstrate an inverse association between ultraviolet radiation, a surrogate marker for vitamin D synthesis, and blood pressure. We prospectively studied the independent association between measured plasma 25-hydroxyvitamin D [25(OH)D] levels and risk of incident hypertension and also the association between predicted plasma 25(OH)D levels and risk of incident hypertension. Two prospective cohort studies including 613 men from the Health Professionals' Follow-Up Study and 1198 women from the Nurses' Health Study with measured 25(OH)D levels were followed for 4 to 8 years. In addition, 2 prospective cohort studies including 38 388 men and 77 531 women with predicted 25(OH)D levels were followed for 16 to 18 years. During 4 years of follow-up, the multivariable relative risk of incident hypertension among men whose measured plasma 25(OH)D levels were <15 ng/mL (ie, vitamin D deficiency) compared with those whose levels were >or=30 ng/mL was 6.13 (95% confidence interval [CI]: 1.00 to 37.8). Among women, the same comparison yielded a relative risk of 2.67 (95% CI: 1.05 to 6.79). The pooled relative risk combining men and women with measured 25(OH)D levels using the random-effects model was 3.18 (95% CI: 1.39 to 7.29). Using predicted 25(OH)D levels in the larger cohorts, the multivariable relative risks comparing the lowest to highest deciles were 2.31 (95% CI: 2.03 to 2.63) in men and 1.57 (95% CI: 1.44 to 1.72) in women. Plasma 25(OH)D levels are inversely associated with risk of incident hypertension.     

Vitamin D deficiency and hepatitis viruses-associated liver diseases:a literature review

The secosteroid hormone vitamin D has, in addition to its effects in bone metabolism also functions in the modulation of immune responses against infectious agents and in inhibiting tumorigenesis. Thus, deficiency of vitamin D is associated with several malignancies, but also with a plethora of infectious diseases. Among other communicable diseases, vitamin D deficiency is involved in the pathogenesis of chronic liver diseases caused by hepatitis B and C viruses(HBV, HCV) and high prevalence of vitamin D deficiency with serum levels below 20 mg/mL in patients with HBV and HCV infection are found worldwide. Several studies have assessed the effects of vitamin D supplementation on the sustained virological response(SVR) to interferon(IFN) plus ribavirin(RBV) therapy in HBV and HCV infection. In these studies, inconsistent results were reported. This review addresses general aspects of vitamin D deficiency and, in particular, the significance of vitamin D hypovitaminosis in the outcome of HBVand HCV-related chronic liver diseases. Furthermore,current literature was reviewed in order to understand the effects of vitamin D supplementation in combination with IFN-based therapy on the virological response in HBV and HCV infected patients.     

Vitamin D supplementation improves sustained virologic response in chronic hepatitis C （genotype 1）-nave patients

AIM: To determine whether adding vitamin D, a potent immunomodulator, improves the hepatitis C virus (HCV) response to antiviral therapy.METHODS: Seventy-two consecutive patients with chronic HCV genotype 1 were randomized into two groups: the treatment group (n = 36, 50% male, mean age 47 ± 11 years) received Peg-α-2b interferon (1.5 μg/kg per week) plus ribavirin (1000-1200 mg/d) together with vitamin D3 (2000 IU/d, target serum level > 32 ng/mL), and the control group (n = 36, 60% male, mean age 49 ± 7 years) received identical therapy without vitamin D. HCV-RNA was assessed by real-time polymerase chain reaction (sensitivity, 10 IU/mL). The sustained virologic response (SVR) was defined as undetectable HCV-RNA at 24 wk post-treatment.RESULTS: Clinical characteristics were similar in both groups. The treatment group had a higher mean body mass index (27 ± 4 kg/m² vs 24 ± 3 kg/m²; P < 0.01), viral load (50% vs 42%, P < 0.01), and fibrosis score (> F2: 42% vs 19%, P < 0.001) than the controls. At week 4, 16 (44%) treated patients and 6 (17%) controls were HCV-RNA negative (P < 0.001). At week 12, 34 (94%) treated patients and 17 (48%) controls were HCV-RNA negative (P < 0.001). At 24 wk post-treatment (SVR), 31 (86%) treated patients and 15 (42%) controls were HCV-RNA negative (P < 0.001). Viral load, advanced fibrosis and vitamin D supplementation were strongly and independently associated with SVR (multivariate analysis). Adverse events were mild and typical of Peg-α-2b/ribavirin.CONCLUSION: Adding vitamin D to conventional Peg-α-2b/ribavirin therapy for treatment-naïve patients with chronic HCV genotype 1 infection significantly improves the viral response.     

Serum vitamin D and vitamin-D-binding protein levels in children with chronic hepatitis B

BACKGROUND Vitamin D is an essential fat-soluble secosteroid hydroxylated by the liver to form the intermediate metabolite calcidiol{25-hydroxy vitamin D[25(OH)D]},which is a reliable indicator to investigate individual vitamin D status.Vitamin-D-binding protein(VDBP)is a multifunctional glycoprotein mainly synthesized in the liver and the major transport protein for vitamin D and its metabolites.Serum vitamin D and VDBP are both associated with hepatitis B.However,few studies have reported the relationship and clinical significance of vitamin D and VDBP with hepatitis B virus(HBV)replication and hepatic fibrosis in children with chronic hepatitis B(CHB).AIM To explore vitamin D and VDBP serum levels in children with CHB and the association of vitamin D and VDBP with HBV replication and hepatic fibrosis.METHODS We enrolled 204 children with CHB admitted to Hunan Children’Hospital in summer and autumn between 2018 and 2019 and 170 healthy controls.CHB patients included:164 hepatitis B e antigen(HBeAg)positive and 40 HBeAg negative;193 hepatitis B surface antigen(HBsAg)positive and 11 HBsAg negative;164 with detectable HBV deoxyribonucleic acid(DNA)and 40 with undetectable HBV DNA;131 with HBV genotype B and 23 with HBV genotype C;and 27 without hepatic fibrosis and 97 with hepatic fibrosis.Serum levels of 25(OH)D,VDBP,liver function markers,and other clinical parameters were collected to analyze their association with vitamin D and VDBP.Mann-Whitney U test,Kruskal-Wallis H test,or t test was used to analyze serum 25(OH)D and VDBP levels in different groups.Spearman rank correlation test was utilized to analyze the correlation of 25(OH)D and VDBP with other markers.Statistically significant factors determined by univariate analysis were further analyzed by binary multivariate logistic regression analysis.P<0.05 was considered statistically significant.RESULTS Children with CHB had lower serum 25(OH)D(56.64±17.89 nmoL/L)and VDBP[122.40(70.74-262.84μg/L)]levels than healthy controls had(P<0.001).Serum 25(OH)D and VDBP levels were significantly different among the different grades of hepatic fibrosis(P<0.05).VDBP levels in children with HBV genotype C,HBsAg,HBeAg,and detectable HBV DNA were significantly lower than those in children with HBV genotype B,no HBsAg,no HBeAg,and undetectable HBV DNA(P<0.05).Serum 25(OH)D level was negatively correlated with age and serum total bilirubin level(r=-0.396 and-0.280,respectively,P<0.001).Serum VDBP level was negatively correlated with HBV DNA(log10 IU/mL)(r=-0.272,P<0.001).Serum 25(OH)D level was not correlated with VDBP level(P>0.05).Univariate(P<0.05)and multivariate logistic regression analysis showed that low level of 25(OH)D(odds ratio=0.951,95%confidence interval:0.918-0.985)and high level of HBV DNA(odds ratio=1.445,95%confidence interval:1.163-1.794)were independently correlated with hepatic fibrosis(P<0.01).CONCLUSION Serum levels of 25(OH)D and VDBP are decreased in children with CHB.Serum VDBP level is negatively correlated with HBV replication.Low level of 25(OH)D is independently associated with hepatic fibrosis in children with CHB.There is no significant association between serum levels of 25(OH)D and VDBP.     

Effect of spleen operation on antiviral treatment in hepatitis C virus-related cirrhotic patients

AIM: To investigate the impact of spleen operation (SO) on interferon-α (IFN-α)-based antiviral treatment in patients with hepatitis C virus (HCV)-related cirrhosis.METHODS: Studies were systematically identified by searching electronic databases including MEDLINE, Cochrane Library, Elsevier, and Embase up to September 30, 2013, and relevant clinical studies were reviewed. Sustained virological response (SVR) rate and adherence to therapy were taken as the endpoints of interest.RESULTS: A total of 603 patients from 16 studies were included in the systematic review. Of 372 patients who underwent SO followed by antiviral treatment, the total SVR rate was 39.5%. SVR was associated with HCV genotypes 2/3 (OR = 10.84; 95%CI: 5.47-21.47; P < 0.00001). IFN-α dose needed to be reduced in 29.4%, and IFN-α-based therapy was discontinued in 11.5% of patients. Analysis of controlled studies showed that SVRs were achieved in 34.1% of patients with SO and 31.1% of patients without SO. SO had no effect on the SVR rate in cirrhotic patients with genotype 1 HCV infection (OR = 1.28; 95%CI: 0.51-3.22; P = 0.60), but improved the SVR rate in patients with genotypes 2/3 infection, though the difference was not significant (OR = 0.36; 95%CI: 0.13-1.02; P = 0.05).CONCLUSION: SO combined with IFN-α-based antiviral therapy may be suitable in cirrhotic patients with genotypes 2/3 HCV infection, but not in those with genotype 1 infection.     

Association of serum vitamin D levels with inflammatory response following hip fracture: the Baltimore Hip Studies

BACKGROUND: Vitamin D, known for its role in calcium homeostasis, may also regulate immune function. Whether vitamin D deficiency at the time of hip fracture is associated with the inflammatory response postfracture is not known. METHODS: In a cohort from the Baltimore Hip Studies, women aged >or= 65 years were evaluated at baseline and 2, 6, and 12 months after hip fracture repair. Serum at baseline was analyzed for 25-hydroxyvitamin D [25(OH)D], and serum from all time points was analyzed for interleukin-6 (IL-6). Participants were divided into two groups based on their baseline 25(OH)D levels. Vitamin D deficiency was defined as a 25(OH)D level of 相似文献   

Vitamin D levels: its relationship to bone mineral density response and disease activity in premenopausal Malaysian systemic lupus erythematosus patients on corticosteroids

Aim: To determine if baseline vitamin D levels would influence the gain in bone mineral density (BMD) in female systemic lupus erythematosus (SLE) patients on corticosteroids (CS) taking bone‐active medication. Method: Premenopausal SLE patients participating in a trial assessing the efficacy of calcium alone, calcitriol and calcium, and alendronate and calcium, on BMD in patients on CS, were studied. Patients were randomly allocated to the treatment groups at the start of the study and followed up for 2 years. Serum 25‐hydroxy vitamin D [25(OH)D] was measured at baseline. Results: Thirty‐eight patients were studied. One (2%) patient had osteoporosis, nine (24%) had osteopenia and all others had normal BMD. The mean baseline 25(OH)D levels were 21.6 ± 4.6 ng/mL (± 1 SD). Twelve (32%) patients had vitamin D deficiency [25(OH)D < 20 ng/mL]. There was a significant negative correlation between SLEDAI scores and 25(OH)D levels, that is, patients with high SLEDAI scores had significantly lower 25(OH)D levels (P = 0.033). Left femoral neck BMD was significantly lower in the deficient compared to insufficient group (P = 0.042). There was a trend toward better BMD gain at 2 years in the vitamin D insufficient compared to the deficient group, which did not reach statistical significance. Conclusion: This study showed that in female SLE patients, low vitamin D levels are associated with higher disease activity and suggests that patients who have higher vitamin D levels have a better BMD response during treatment with bone‐active agents.