Vitamin D Deficiency in Unselected Patients from Swiss Primary Care: A Cross-Sectional Study in Two Seasons

<div><p>Background</p><p>As published data on 25-hydroxy-cholecalciferol (25(OH)D) deficiency in primary care settings is scarce, we assessed the prevalence of hypovitaminosis D, potential associations with clinical symptoms, body mass index, age, Vitamin D intake, and skin type in unselected patients from primary care, and the extent of seasonal variations of serum 25(OH)D concentrations.</p><p>Methodology/Principal Findings</p><p>25(OH)D was measured at the end of summer and/or winter in 1682 consecutive patients from primary care using an enzyme-linked immunosorbant assay. Clinical symptoms were assessed by self-report (visual analogue scale 0 to 10), and vitamin D deficiency was defined as 25(OH)D concentrations < 50 nmol/l. 25(OH)D deficiency was present in 995 (59.2%) patients. 25(OH)D deficient patients reported more intense muscle weakness (visual analogue scale 2.7, 95% confidence interval 2.5 to 2.9) and had a higher body mass index (25.9kg/m², 25.5 to 26.2) than non-deficient patients (2.5, 2.3 to 2.7; and 24.2, 23.9 to 24.5, respectively). 25(OH)D concentrations also weakly correlated with muscle weakness (Spearman’s rho -0.059, 95% confidence interval -0.107 to -0.011) and body mass index (-0.156, -0.202 to -0.108). Self-reported musculoskeletal pain, fatigue, and age were not associated with deficiency, nor with concentrations. Mean 25(OH)D concentrations in patients with vitamin D containing medication were higher (60.6 ± 22.2 nmol/l) than in patients without medication (44.8 ± 19.2 nmol/l, p < 0.0001) but still below the targeted level of 75 nmol/l. Summer and winter 25(OH)D concentrations differed (53.4 ± 19.9 vs. 41.6 ± 19.3nmol/l, p < 0.0001), which was confirmed in a subgroup of 93 patients who were tested in both seasons (p = 0.01).</p><p>Conclusion/Significance</p><p>Nearly 60% of unselected patients from primary care met the criteria for 25(OH)D deficiency. Self-reported muscle weakness and high body mass index were associated with lower 25(OH)D levels. As expected 25(OH)D concentrations were lower in winter compared to summer.</p></div

Significant difference of 25-hydroxy 25(OH)D concentrations end of summer and end of winter (53.4 ± 19.9 vs. 41.6 ± 19.3 nmol/l, p<0.0001).

<p>Significant difference of 25-hydroxy 25(OH)D concentrations end of summer and end of winter (53.4 ± 19.9 vs. 41.6 ± 19.3 nmol/l, p<0.0001).</p

Characteristics of the study populations assessed end of summer (month of September) and end of winter (month of March).

<p>No significant differences were found between variables assessed end of summer and end of winter (p > 0.05)</p><p>Characteristics of the study populations assessed end of summer (month of September) and end of winter (month of March).</p

Mean muscle pain and weakness, fatigue, body mass index (BMI), and age in 25(OH)D deficient (<50 nmol/l) and non-deficient (>50 nmol/l) patients.

<p>VAS, Visual analogue scale, BMI, body mass index;</p><p>^at test</p><p>Mean muscle pain and weakness, fatigue, body mass index (BMI), and age in 25(OH)D deficient (<50 nmol/l) and non-deficient (>50 nmol/l) patients.</p

Fecal calprotectin correlates more closely with the simple endoscopic score for Crohn's Disease (SES-CD) than CRP, blood leukocytes, and the CDAI

OBJECTIVES:Studies evaluating the correlation between the widely used Simple Endoscopic Score for Crohn's disease (SES-CD) and noninvasive markers are scarce. The aim of this study was to evaluate the correlation between the SES-CD and fecal calprotectin, C-reactive protein (CRP), blood leukocytes, and the Crohn's disease activity index (CDAI).METHODS:Crohn's disease patients undergoing complete ileocolonoscopy were prospectively enrolled and scored independently according to the SES-CD and the CDAI. SES-CD was defined as follows: inactive 0-3; mild 4-10; moderate 11-19; and high >/=20.RESULTS:Values in CD patients (n=140 ileocolonoscopies) compared with controls (n=43) are as follows: calprotectin, 334+/-322 vs. 18+/-5 mug/g; CRP, 26+/-29 vs. 3+/-2 mg/l; and blood leukocytes, 9.1+/-3.4 vs. 5.4+/-1.9 g/l (all P/=150.CONCLUSIONS:Fecal calprotectin correlated closest with SES-CD, followed by CRP, blood leukocytes, and the CDAI. Furthermore, fecal calprotectin was the only marker that reliably discriminated inactive from mild, moderate, and highly active disease, which underlines its usefulness for activity monitoring

Iron metabolism in patients with Graves’ hyperthyroidism

OBJECTIVES: Graves' hyperthyroidism (GH) interferes with iron metabolism and elevates ferritin. The precise mechanisms remain unclear. The influence of thyroid hormones on the synthesis/regulation of hepcidin, an important regulator of iron metabolism, remains uncharacterized. DESIGN: Prospective observational study. PATIENTS: We included patients (n = 31) with new-onset and untreated GH. MEASUREMENTS: Laboratory parameters indicative of iron metabolism (ferritin, transferrin, hepcidin), inflammatory markers/cytokines and smoking status were assessed at the diagnosis of GH (T0) and at euthyroidism (T1) in the same patients using multivariable analyses. Hepcidin was measured by mass spectrometry (hepcidinMS ) and ELISA (hepcidinEL ). The impact of T3 on hepatic hepcidin expression was studied in a cell culture model using HepG2 cells. RESULTS: Median ferritin levels were significantly lower and transferrin significantly higher at T1 than at T0. HepcidinMS levels were lower in males and females at T1 (statistically significant in males only). No statistically significant difference in hepcidinEL was detected between T0 and T1. Plasma levels of inflammatory markers (high-sensitive CRP, procalcitonin) and cytokines (interleukin 6, interleukin 1ß, tumour necrosis factor α) were not different between T0 and T1. Smokers tended to have lower fT3 and fT4 at T0 than nonsmoking GH patients. T3 significantly induced hepcidin mRNA expression in HepG2 cells. CONCLUSIONS: Iron metabolism in patients with GH undergoes dynamic changes in patients with GH that resemble an acute-phase reaction. Inflammatory parameters and cytokines were unaffected by thyroid status. Gender and smoking status had an impact on ferritin, hepcidin and thyroid hormones

ROC of adrenal values.

<p>Dehydroepiandrosterone (DHEA): Area 0.59, Std. Error 0.05, 95% CI 0.49–0.69, p = 0.07 Dehydroepiandrosterone-sulfate (DHEAS): Area 0.60, Std. Error 0.04, 95% CI 0.51–0.69, p = 0.048. Basal cortisol: Area 0.71, Std. Error 0.05, 95% CI 0.61–0.80, p<0.0001. Stimulated cortisol: Area 0.67, Std. Error 0.05, 95% CI 0.57–0.77, p = 0.001. Cortisol/DHEA: Area 0.70, Std. Error 0.05, 95% CI 0.61–0.79, p<0.0001. Cortisol/DHEAS: Area 0.71, Std. Error 0.05, 95% CI 0.63–0.81, p<0.0001.</p

<b>Baseline Characteristics,n = 179.</b>

<p><b>Baseline Characteristics,n = 179.</b></p

Baseline characteristics.

<p>n = 231.</p