Prevalence and predictors of vitamin D insufficiency in supplemented and non-supplemented women with systemic lupus erythematosus in the Mediterranean region

It has been previously reported that vitamin D deficiency is more prevalent among SLE patients than in the general population. We sought to determine the prevalence of vitamin D insufficiency and deficiency and their related factors, its relationship to SLE symptoms and disease activity on a group of supplemented and non-supplemented female SLE patients from the Mediterranean region. We performed a cross-sectional study including female SLE patients who regularly attended the outpatient Lupus Unit at Parc de Salut Mar-IMAS in Barcelona, from January 2012 to May 2014. Collected data were sociodemographics, vitamin D supplementation, fatigue degree visual analog scale, pharmacological treatment, main SLE serological markers, indexes, scales and plasma levels of 25-hydroxyvitamin D. One hundred and two consecutive female SLE patients were included. Vitamin D overall insufficiency and deficiency were exhibited by 46 and 22.5 % of patients, respectively. Vitamin D insufficiency was found in 50 % of supplemented and 60 % of non-supplemented patients. Among non-supplemented female SLE patients, it was found that patients with vitamin D insufficiency showed more fatigue (p = 0.009) and received more oral corticosteroids (p = 0.02) than those with normal levels. Patients with vitamin D insufficiency (supplemented and non-supplemented) received more oral corticosteroids than those without insufficiency (p = 0.008). Vitamin D insufficiency is highly prevalent among female SLE patients, even in southern regions. Non-supplemented female SLE patients showed more fatigue and received more oral corticosteroids than those with normal levels of vitamin D. These data were not found in supplemented patients although having a high prevalence of vitamin D insufficiency (up to 50 %). Further studies with longer follow-up and larger population are needed to confirm our observations.     

Clinical significance of vitamin D deficiency and receptor gene polymorphism in systemic lupus erythematosus patients

Introduction

The vitamin D receptor (VDR) gene is a candidate for susceptibility to autoimmune disorders.

Prevalence of vitamin D deficiency in pre-type 1 diabetes and its association with disease progression

Aims/hypothesis

Vitamin D deficiency is common in people with type 1 diabetes, but its role in disease progression is unclear. Our aim was to assess the prevalence of vitamin D deficiency in prediabetes (defined as the presence of multiple islet autoantibodies), and investigate whether or not progression to type 1 diabetes is faster in children with vitamin D deficiency and multiple islet autoantibodies.

Methods

Levels of 25-hydroxyvitamin D [25(OH)D] were measured in 108 children with multiple islet autoantibodies within 2 years of islet autoantibody seroconversion, in 406 children who remained islet autoantibody-negative and in 244 patients with newly diagnosed type 1 diabetes. Children with multiple islet autoantibodies were prospectively followed for a median of 5.8 years (interquartile range 3.4–8.6 years) to monitor progression to type 1 diabetes.

Results

In the cross-sectional analysis, 25(OH)D levels were lower and the prevalence of vitamin D deficiency (<50 nmol/l) was higher in children with prevalent multiple islet autoantibodies than in islet autoantibody-negative children (59.9?±?3.0 vs 71.9?±?1.5 nmol/l; p?<?0.001; 39.8% vs 28.3%; p?=?0.021). The differences in vitamin D levels between the groups were greatest in summer. The cumulative incidence of type 1 diabetes at 10 years after seroconversion was similar between children with vitamin D deficiency and those with sufficient vitamin D levels (51.8% [95% CI 29.3, 74.3] vs 55.4% [95% CI 35.5, 72.3], p?=?0.8).

Conclusions/interpretation

Vitamin D levels were lower in children with multiple islet autoantibodies and in children with type 1 diabetes than in autoantibody-negative children. However, vitamin D deficiency was not associated with faster progression to type 1 diabetes in children with multiple islet autoantibodies.     

Association Between Vitamin D Status and COPD Phenotypes

Background

It has been suggested that identifying phenotypes in chronic obstructive pulmonary disease (COPD) might improve treatment outcome and the accuracy of prediction of prognosis. In observational studies vitamin D deficiency has been associated with decreased pulmonary function, presence of emphysema and osteoporosis, upper respiratory tract infections, and systemic inflammation. This could indicate a relationship between vitamin D status and COPD phenotypes. The aim of this study was to assess the association between vitamin D levels and COPD phenotypes. In addition, seasonality of vitamin D levels was examined.

Methods

A total of 91 patients from a Danish subpopulation of the “Evaluation of COPD Longitudinally to Identify Predictive Surrogate End-points” cohort took part in a biomarker substudy. Vitamin D concentration was measured from blood samples taken at two visits, approximately 6 months apart. The participants were 40–75-year-old patients with COPD and had a smoking history of >10 pack-years.

Results

Fifty-six patients had 25-hydroxyvitamin D measured from blood samples from both visits. In the final model of the multivariate analyses, the factors that were associated with vitamin D deficiency at the first visit were age (OR: 0.89, p = 0.02) and summer season (OR: 3.3, p = 0.03). Factors associated with vitamin D level also at the first visit were age (B: 0.9, p = 0.02) and 6 min walking distance (B: 0.05, p = 0.01).

Conclusion

Vitamin D was not associated with COPD phenotypes and season did not seem to be a determinant of vitamin D levels in patients with moderate to severe COPD.     

Vitamin D Deficiency Is Associated with Ulcerative Colitis Disease Activity

Purpose

Previous studies on experimental mouse models have suggested a role of vitamin D in immune system regulation and IBD disease severity. In this study, we examine the relationship between vitamin D levels and clinical disease activity in human subjects with ulcerative colitis (UC). We hypothesized that patients with vitamin D deficiency will display increased UC disease activity as compared to patients with normal vitamin D levels.

Methods

A cross-sectional study was performed by querying the outpatient electronic medical record of our health system for patients seen in the gastroenterology clinic from January 2007 to October 2009 who carried both a diagnosis of UC and a documented 25-OH vitamin D level within 30 days of their clinic visit. Demographic and clinical variables were collected. Clinical disease activity was calculated using the six-point partial Mayo index. Active disease was defined as a six-point index score of ≥1. Vitamin D deficiency was defined as a 25-OH D level below 30 ng/ml. Data were analyzed using the chi-square distribution test.

Results

Thirty-four patients met inclusion criteria (53 % female, mean age 45.7 ± 24.7 years). Fifteen patients had normal vitamin D levels and 19 patients were vitamin D deficient. Twelve patients had vitamin D levels <20 ng/ml. Vitamin D deficient patients were statistically more likely to have increased disease activity than patients with normal vitamin D levels (p = 0.04), with 68 % of deficient patients displaying active disease compared with 33 % in the sufficient group. There was also a statistically significant association between vitamin D status and need for treatment with steroids, with a higher percentage of vitamin D deficient patients (47 %) requiring such treatment compared with 7 % in the sufficient group (p = 0.02). There was no association between season of visit and disease activity.

Conclusion

Vitamin D deficiency is common among patients with active UC, particularly those requiring corticosteroids. Further investigation is needed to determine the clinical utility of vitamin D monitoring in patients with UC and whether there is a role for vitamin D as a treatment for UC.     

Vitamin D deficiency in patients with either rheumatic diseases or inflammatory bowel diseases on biologic therapy

Vitamin D deficiency has been reported in patients with chronic inflammatory conditions, such as rheumatic and inflammatory bowel diseases (IBD). We evaluated the role of biologic therapy on vitamin D, calcium and parathormone (PTH) levels. This cross-sectional study enrolled consecutive patients with either rheumatic diseases or IBD who underwent an ambulatory visit. Patients receiving vitamin D/calcium supplementation were excluded. Vitamin D deficiency or insufficiency was diagnosed when values were <20 ng/mL and 21–29 ng/ml, respectively. Patients were sub-grouped according to biologic therapy. A multivariate analysis was performed. Two-hundred patients, including 136 with a rheumatic disease (M/F 37/99; mean age 60.7 ± 12.9 years) and 64 with IBD (M/F 41/23; Mean age 49.6 ± 13.1 years) were enrolled. Vitamin D deficiency/insufficiency was detected in as many as 63.5 % patients, being 61.8 and 67.2 % in patients with either rheumatic diseases or IBD, respectively. The prevalence of vitamin D deficiency/insufficiency was higher in those receiving biologics than other therapies (78.3 vs 43.2 %; p < 0.0001), in either rheumatic diseases (78.7 vs 41 %; p < 0.0001) or IBD (75 vs 50 %; p = 0.03) group. At multivariate analysis, only biologic therapy was independently associated with vitamin D deficit (OR 4.61; p = 0.001). Patients with vitamin D deficiency/insufficiency had hypocalcemia more frequently than controls (22.8 vs 10.9 %; p = 0.03), while PTH values did not differ significantly. This study finds that the prevalence of vitamin D deficiency/insufficiency was very high in patients with either rheumatic diseases or IBD receiving a biologic therapy.     

Vitamin D deficiency and the associated factors in children with type 1 diabetes mellitus in southern Iran

Type 1 diabetes mellitus (T1DM) is a chronic autoimmune disorder caused by destruction of beta cells of the pancreas. Several reports have suggested a connection between vitamin D deficiency and T1DM and the possible role of dietary vitamin D supplementation in reducing the risk of T1DM. There is little knowledge about the prevalence of vitamin D deficiency among Iranian children with T1DM. Serum 25-hydroxy vitamin D (25OHD) was assayed by high performance liquid chromatography in 8–18-year-old diabetic patients referred to pediatric diabetes clinics in Shiraz, Iran, during a period of 14 months. The age of the onset of T1DM, daily insulin usage, weight, height, and BMI of each patient were recorded along with levels of physical activity and sun exposure. The patients’ body composition was determined by DEXA and used in further analysis. This study was conducted on 39 diabetic boys and 46 diabetic girls aged 12.4 ± 4.2 years. Mean serum 25(OH)D3 was 18 ± 12.2 ng/dl. Serum levels of 25(OH)D3 were higher in boys than girls. 7.7 % of the boys and 30.4 % of the girls had severe vitamin D deficiency. There was a negative correlation between the age of the onset of T1DM and serum concentration of 25(OH)D3 (p = 0.006, r = ?0.17). Girls with T1DM showed a higher prevalence of severe vitamin D deficiency than boys with T1DM. Moreover, vitamin D deficiency was more prevalent in individuals with earlier onset of the disease and in those with higher fat mass index.     

No Significant Association Between Vitamin D and Nonalcoholic Fatty Liver Disease in a Chinese Population

Background

Some research evidence from Western populations suggests that lower vitamin D is associated with the prevalence and histologically assessed severity of nonalcoholic fatty liver disease (NAFLD).

Aims

To investigate the associations of serum 25-hydroxyvitamin D [25(OH)D] concentrations and vitamin D status (deficiency <20 ng/ml; insufficiency 20–30 ng/ml; sufficiency >30 ng/ml) with the prevalence of NAFLD in study population of Chinese.

Methods

Serum 25(OH)D, parathyroid hormone, lipids, liver enzymes, and anthropometric characteristics were measured in 1,248 subjects aged ≥20 years. NAFLD was diagnosed using abdominal ultrasound examination.

Results

The prevalence of NAFLD was 30.3 % in the total study population, 37.9 % in the male subjects, and 20.8 % in the female subjects (P < 0.0001). Subjects with NAFLD had a significantly higher body mass index, higher levels of fasting blood glucose and liver enzymes, and a more atherogenic lipid profile. However, serum 25(OH)D concentrations were not significantly different between subjects with and without NAFLD (22.1 vs. 22.8 ng/ml, respectively; P = 0.21). In addition, a 10 ng/ml higher serum 25(OH)D concentrations [odds ratio (OR) 1.02, 95 % confidence interval (CI) 0.84–1.25, P = 0.82] or vitamin D status (vs. sufficiency: deficiency OR 0.86, 95 % CI 0.54–1.37, P = 0.52; insufficiency OR 0.96, 95 % CI 0.61–1.52, P = 0.87) were not significantly associated with the presence of NAFLD in the multivariate logistic regression analyses.

Conclusions

Serum 25(OH)D concentrations or vitamin D status were not significantly associated with the presence of NAFLD. More studies are needed to elucidate the relationship between vitamin D and the occurrence of NAFLD in Chinese.     

Vitamin D Deficiency and Corticosteroid Use Are Risk Factors for Low Bone Mineral Density in Inflammatory Bowel Disease Patients

Background

As several factors can contribute to low bone mineral density (BMD), we investigated the role of vitamin D in low BMD while controlling for other risk factors in inflammatory bowel diseases (IBD) patients.

Methods

We conducted a prospective cross-sectional study between 2008 and 2012 in adult IBD patients. Demographic data including age, gender, ethnicity, BMI, along with disease type and location, vitamin D levels, prior corticosteroid use, and anti-TNF use were recorded and evaluated with DEXA results.

Results

A total of 166 patients [105 Crohn’s disease (CD), 61 ulcerative colitis (UC)] qualified for the study. Low BMD was found in 40 %, twice as frequently in CD than in UC (p = 0.048). Higher prevalence of low BMD was associated with those of male gender (p = 0.05), Asian ethnicity (p = 0.02), and history of corticosteroid use (p = 0.001). Age, body mass index, or disease location did not increase the risk of low BMD. The overall prevalence of low vitamin D was 60 %, with insufficiency (25-hydroxy levels between 20 and 30 ng/mL) found in 37 % and deficiency (levels <20 ng/mL) found in 23 % of the patients. Vitamin D insufficient and deficient patients were two times (p = 0.049) and almost 3 times (p = 0.02) as likely to have low BMD, respectively.

Conclusions

Low vitamin D, male gender, Asian ethnicity, CD, and corticosteroid use significantly increased the risk of having low BMD, while age and disease location did not affect BMD in our IBD population. It remains important to evaluate for vitamin D nutritional deficiency and limit corticosteroid use to help prevent low BMD in IBD patients.     

Increased expression of Bruton’s tyrosine kinase in peripheral blood is associated with lupus nephritis

Systemic lupus erythematosus (SLE) is an autoimmune disease manifested by multiorgan impairment. It is reported that B cells participate in the onset of SLE. Bruton’s tyrosine kinase (Btk), as a downstream signaling molecule of B cell antigen receptor (BCR) signaling pathway, is involved in the development, activation, and survival of B cells. The aim of our study was to explore the specific role of Btk in lupus nephritis (LN). We determined the percentages of Btk+ B cells in peripheral blood mononuclear cells (PBMCs) from SLE patients by flow cytometry and analyzed the correlation between the percentage of Btk+ B cells and lupus-related clinical indexes. Immunohistochemistry was used to detect the Btk expression in kidney from LN patients and tumor surrounding tissues. Compared with controls, the frequency of Btk+ B cells in SLE patients was upregulated (p < 0.01), and it was significantly correlated with the SLE Disease Activity Index (SLEDAI) (p < 0.01), levels of plasma anti-dsDNA antibody (p < 0.05), the amount of 24-h urine protein (p < 0.05), and levels of plasma C3 (p < 0.05). The frequency of Btk+ B cells in the patients with LN was significantly higher than those without LN (p < 0.05). Although the Btk expression in glomerulus of LN patients was significantly increased compared with controls (p < 0.001), but it had no correlation with the renal pathology activity index, SLEDAI, or 24-h urine protein. In conclusion, the increased expression of Btk in peripheral blood was correlated with LN, indicating that it may be a therapeutic target for SLE.     

Vitamin D in “early” primary Sjögren’s syndrome: does it play a role in influencing disease phenotypes?

Beyond its well-established role in the maintenance of mineral homeostasis, 25-OH-vitamin D deficiency seems to be involved in the development and severity of several autoimmune diseases. To date, contrasting data have been reported regarding the presence of hypovitaminosis D in primary Sjögren’s syndrome (pSS). To assess the prevalence of hypovitaminosis D in pSS at an early stage of the disease and to evaluate its impact on pSS clinical manifestations and disease activity, unselected consecutive subjects with recent onset dry mouth and/or dry eyes who underwent a comprehensive diagnostic algorithm for pSS (AECG criteria) were prospectively included in the study. The levels of 25[OH]-D3 were measured by monoclonal antibody immunoradiometric assay. Conditions of 25[OH]-D3 severe deficiency, deficiency, and insufficiency were defined as levels <10, <20, and 20–30 ng/ml, respectively, and their frequencies were investigated in pSS patients and controls. The levels of 25[OH]-D3 were also correlated with patients’ demographic, clinical, and serologic features. Seventy-six consecutive females were included: 30/76 patients fulfilled the AECG criteria for pSS. The remaining 46/76 patients represented the control group. No statistical differences were found in the serum levels of 25[OH]-D3 between pSS patients [median levels = 20 ng/ml (IQR 9.3–26)] and controls [median levels = 22.5 ng/ml (IQR 15.6–33)]. In particular, the frequency of 25[OH]-D3 severe deficiency was not significantly different in patients with pSS when compared to controls (23 vs. 17.4 %, p value = 0.24). We found a significant correlation between serum 25[OH]-D3 levels and white blood cells count (r = 0.29, p = 0.01). More specifically, leukocytopenia was significantly associated with 25[OH]-D3 severe deficiency, being documented in 40 % of the subjects with a 25[OH]-D3 severe deficiency and in 11 % of the subjects without a severe vitamin D deficiency (p = 0.02). We did not observe any further association or correlation between hypovitaminosis D and pSS glandular and extra-glandular features. Although the role of hypovitaminosis D in pSS pathogenesis remains controversial, the results of this study encourage the assessment of vitamin D in specific pSS subsets that could mostly benefit from a supplementation.     

Vitamin D deficiency is associated with digital ulcer but not with atherosclerosis or arterial stiffness in patients with systemic sclerosis: a pilot study

The objective of this study was to investigate the association of vitamin D deficiency with digital ulcers (DUs) that result from microvasculopathy, carotid intima-media thickness (CIMT) as surrogate markers of atherosclerosis, and brachial-ankle pulse wave velocity (baPWV) representing arterial stiffness in patients with systemic sclerosis (SSc). In this cross-sectional study, 40 female SSc patients and 80 healthy controls matched for sex, age, and blood sampling season were recruited. Vitamin D deficiency was defined as serum 25-OHD levels <30 ng/mL. “DUs ever” included active and healed DUs. CIMT and carotid plaque were examined using high-resolution ultrasonography, and baPWV was measured using an automatic waveform analyzer. Vitamin D deficiency was more prevalent in SSc patients than in controls (30 vs. 11.3%). Regarding SSc patients, 9 (22.5%) had DUs ever, and the mean CIMT and baPWV were 0.68 mm and 1561.1 cm/s, respectively; carotid plaque was detected in 13 (34.2%) patients. The frequency of DUs ever was significantly higher for SSc patients with vitamin D deficiency than those without this feature (50 vs. 10.7%, p = 0.012), but the median CIMT and baPWV and the frequency of carotid plaque did not differ according to the presence of vitamin D deficiency. Multivariable logistic regression analysis showed that vitamin D deficiency was an independent risk factor for DUs ever (OR = 7.72, p = 0.024). Vitamin D deficiency was associated with DUs, but not with atherosclerosis or arterial stiffness, potentially indicating that vitamin D may have different effects on the microvascular and macrovascular involvement in SSc pathophysiology.     

Vitamin D Deficiency Is an Independent Risk Factor for Urinary Tract Infections After Renal Transplants

Vitamin D deficiency is frequently found in patients with renal transplants (RTxs). Because vitamin D plays indispensable roles in the immune system, there may be an association between vitamin D deficiency and infection in these patients, but this has not been fully elucidated. Therefore, this study investigated the impact of pre-RTx vitamin D deficiency on urinary tract infection (UTI) development after RTx.We measured 25-hydroxyvitamin D3 (25(OH)D3) levels in 410 patients 2 weeks before they underwent RTx. Vitamin D deficiency was defined as 25(OH)D3 <10 ng/mL. The primary outcome was UTI occurrence after RTx. Cox proportional hazard analysis determined whether vitamin D deficiency was independently associated with UTI.The mean 25(OH)D3 level was 12.8 ± 6.9 ng/mL, and 171 patients (41.7%) were vitamin D deficient. During a median follow-up duration of 7.3 years, the UTI incidence was significantly higher in vitamin D-deficient patients (52 patients, 30.4%) compared with vitamin D-nondeficient patients (40 patients, 16.7%) (P = 0.001). Moreover, multivariate Cox proportional hazard analysis showed that vitamin D deficiency was an independent predictor of UTI after RTx (hazard ratio 1.81, 95% confidence interval 1.11–2.97, P = 0.02).Vitamin D deficiency was an independent risk factor for UTI after RTx; hence, determining 25(OH)D3 levels might help to predict infectious complications after RTx.     

维生素D缺乏与系统性红斑狼疮的相关性研究

目的 探讨系统性红斑狼疮（SLE）患者维生素D缺乏现象与疾病活动性的相关性.方法 选取60例SLE患者及30例健康志愿者,收集研究对象临床资料;ELISA法检测血清25-羟基维生素D[25-（OH）D]水平;采用Pearson相关分析法分析血清25-（OH）D水平与SLE疾病活动指数（SLEDAI）、抗ds-DNA抗体滴度、补体C3、补体C4、尿蛋白定量、血清免疫球蛋白G（IgG）的相关性.结果 （1）SLE患者血清25-（OH）D水平[36.8（23.4,53.2）nmol/L]较健康志愿者[58.8（51.1,65.3） nmol/L]明显降低（P＜0.01）;（2）SLE患者中维生素D缺乏比例为53.3％,严重维生素D缺乏比例为15.0％,健康志愿者中维生素D缺乏比例为23.3％,严重维生素D缺乏比例为6.7％,两组比较差异具有统计学意义（P＜0.01）.（3）SLE患者血清25-（OH）D水平与SLEDAI（r=-0.35,P＜0.05）及抗ds-DNA抗体滴度（r=-0.42,P＜0.05）呈负相关,与补体C3（r=0.25,P＜0.05）、补体C4（r=0.28,P＜0.05）呈正相关,与尿蛋白定量、血清IgG水平无明显相关性（P＞0.05）.结论 SLE患者中维生素D缺乏现象普遍存在,血清维生素D水平与疾病活动性具有一定相关性.     

Association of serum 25-hydroxyvitamin D and diabetes-related factors in Korean adults without diabetes: The Fifth Korea National Health and Nutrition Examination Survey 2010–2012

Aims

Vitamin D is associated with diabetes mellitus (DM) occurrence by affecting insulin secretion and resistance. However, variations exist due to differences in vitamin D sensitivity among individuals. We investigate the relationship between serum 25-hydroxyvitamin D [25(OH)D] status and various indices of DM in a Korean population without DM.

Vitamin D may not be a good marker of disease activity in Korean patients with systemic lupus erythematosus

Vitamin D is a pleiotrophic hormone with immunoregulatory properties. Low levels of vitamin D have been discovered in various autoimmune diseases. Here, we investigated serum vitamin D levels in Koreans with systemic lupus erythematosus (SLE) and examined whether levels correlate with disease activity of SLE. Blood samples were prospectively collected from patients with SLE (n = 104) and normal controls (NC, n = 49) during the spring from March to May 2008. The level of serum 25-hydroxyvitamin D (25(OH)D3) was measured by radioimmunoassay. The serum 25(OH)D3 levels of patients with SLE (42.49 ± 15.08 ng/ml) were significantly lower than NC (52.72 ± 15.19 ng/ml, P < 0.001). Additionally, 17 patients with SLE (16.3%) had vitamin D insufficiency, while two NC had vitamin D insufficiency (4.1%). The risk of vitamin D insufficiency was 4.6-fold increased in SLE (P = 0.032). The serum 25(OH)D3 levels, adjusted with BMI, were positively correlated only with hemoglobin (β = 0.256, P = 0.018) and serum complement 3 (β = 0.365, P = 0.002). Serum vitamin D levels were lower, and vitamin D insufficiency was more common in Korean patients with SLE, however, our study demonstrated that vitamin D levels might not be a good marker of disease activity.     

Longitudinal assessment of monocyte chemoattractant protein-1 in lupus nephritis as a biomarker of disease activity

Urinary MCP-1 (uMCP-1) levels reflect lupus nephritis (LN) disease activity. However, long-term prospective studies evaluating it as a biomarker are lacking. SLE patients with active nephritis (AN), active disease without nephritis (ANR), and inactive disease (ID) were enrolled. AN patients were followed up every 3 months for 1 year. Urine and serum samples were collected at baseline from all and at follow-up visits in AN group. Urine samples from healthy subjects (HC), rheumatoid arthritis (RA), and diabetic nephropathy (DM) patients (20 each) served as controls. Serum (sMCP-1) and uMCP-1 was measured using ELISA. Urinary values were normalized for creatinine excretion. Nonparametric tests were used. A total of 121 SLE patients were enrolled. Baseline uMCP-1 was significantly higher in AN as compared to ANR, ID, HC, and RA (p < 0.001), but it was not different from DM and showed good correlation with rSLEDAI and SLEDAI (r = 0.52 and 0.47, p < 0.001) but not with sMCP-1. On ROC analysis to differentiate between AN and ANR, uMCP-1 performed better than sMCP-1, anti-dsDNA antibodies, C3 and C4. uMCP-1 and not sMCP-1 decreased significantly at all follow-up visits (p < 0.001). uMCP-1 remained persistently elevated in a patient who developed CKD and rose before conventional markers in two patients with relapse of LN. uMCP-1 correlates well with LN disease activity and helps differentiate between AN and ANR patients. Its levels fall with treatment and may have a potential to predict poor response and relapse of LN. uMCP-1 is most likely generated locally in the kidney.     

Potential role of vitamin D deficiency on Fabry cardiomyopathy

Patients with Fabry disease frequently develop left ventricular (LV) hypertrophy and renal fibrosis. Due to heat intolerance and an inability to sweat, patients tend to avoid exposure to sunlight. We hypothesized that subsequent vitamin D deficiency may contribute to Fabry cardiomyopathy. This study investigated the vitamin D status and its association with LV mass and adverse clinical symptoms in patients with Fabry disease. 25-hydroxyvitamin D (25[OH]D) was measured in 111 patients who were genetically proven to have Fabry disease. LV mass and cardiomyopathy were assessed by magnetic resonance imaging and echocardiography. In cross-sectional analyses, associations with adverse clinical outcomes were determined by linear and binary logistic regression analyses, respectively, and were adjusted for age, sex, BMI and season. Patients had a mean age of 40?±?13 years (42 % males), and a mean 25(OH)D of 23.5?±?11.4 ng/ml. Those with overt vitamin D deficiency (25[OH]D?≤?15 ng/ml) had an adjusted six fold higher risk of cardiomyopathy, compared to those with sufficient 25(OH)D levels >30 ng/ml (p?=?0.04). The mean LV mass was distinctively different with 170?±?75 g in deficient, 154?±?60 g in moderately deficient and 128?±?58 g in vitamin D sufficient patients (p?=?0.01). With increasing severity of vitamin D deficiency, the median levels of proteinuria increased, as well as the prevalences of depression, edema, cornea verticillata and the need for medical pain therapy. In conclusion, vitamin D deficiency was strongly associated with cardiomyopathy and adverse clinical symptoms in patients with Fabry disease. Whether vitamin D supplementation improves complications of Fabry disease, requires a randomized controlled trial.     

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.     

Vitamin D levels in patients with small and medium vessel vasculitis

ObjectivesTo determine the prevalence of vitamin D deficiency in patients with small and medium vessel systemic vasculitis.MethodsIn this cross-sectional study, 25-hydroxy (OH) vitamin D3 levels were measured in adult patients with systemic small and medium vessel vasculitis including antineutrophil cytoplasmic antibody-associated vasculitis (AAV), cryoglobulinaemic vasculitis (CryV), IgA vasculitis (IgAV) and polyarteritis nodosa (PAN), and age- and sex-matched healthy subjects (HS) and patients with rheumatoid arthritis (RA) as control groups. 25OH vitamin D3 levels < 30 ng/ml and <20 ng/ml were regarded as insufficiency and deficiency, respectively.ResultsFifty-seven patients (42 AAV, 2 CryV, 8 IgA vasculitis, 5 PAN) with systemic vasculitis, 101 HS, and 111 RA patients were included. The mean 25OH vitamin D3 level was 21.8 ± 14.2 ng/mL in patients with vasculitis, 42.7 ± 27.6 ng/mL in HS (p < .001) and 20.1 ± 18.47 ng/mL in patients with RA (p = .54). Vitamin D insufficiency and deficiency were significantly higher in patients with systemic vasculitis compared to HS (75.4% vs 33.7%, p < .001; %50 vs 21.8%, p < .001, respectively). Vitamin D status was not different in patients with systemic vasculitis compared to RA. There was a negative correlation between vitamin D status and CRP levels (=?.364, p = .007). The multivariate logistic regression analysis showed that renal involvement was significantly associated with vitamin D deficiency/insufficiency in patients with vasculitis (OR 22.5 [95% CI 1.6–128.9].ConclusionVitamin D deficiency and insufficiency are more frequent in patients with systemic small and medium vessel vasculitis and RA than HS. Renal involvement is one of the factors associated with vitamin D deficiency/insufficiency in patients with vasculitis.