937 resultados para 25-hidroxivitamina D 2
Resumo:
The purpose was to determine the prevalence and related factors of vitamin D (VitD) insufficiency in adolescents and young adults with perinatally acquired human immunodeficiency virus. A cohort of 65 patients (17.6 ± 2 years) at the Federal University of Rio de Janeiro, Brazil, were examined for pubertal development, nutrition, serum parathormone and serum 25-hydroxyvitamin D [s25(OH)D]. s25(OH)D levels < 30 ng/mL (< 75 nmol/L) were defined as VitD insufficiency. CD4+ T-cell counts and viral load, history of worst clinical status, immunologic status as nadir, current immunologic status, and antiretroviral (ART) regimen were also evaluated as risk factors for VitD insufficiency. Mean s25(OH)D was 37.7 ± 13.9 ng/mL and 29.2% had VitD insufficiency. There was no difference between VitD status and gender, age, nutritional status, clinical and immunological classification, and type of ART. Only VitD consumption showed tendency of association with s25(OH)D (p = 0.064). Individuals analysed in summer/autumn season had a higher s25(OH)D compared to the ones analysed in winter/spring (42.6 ± 14.9 vs. 34.0 ± 11.9, p = 0.011). Although, the frequency of VitD insufficiency did not differ statistically between the groups (summer/autumn 17.9% vs. winter/spring 37.8%, p = 0.102), we suggest to monitor s25(OH)D in seropositive adolescents and young adults, especially during winter/spring months, even in sunny regions.
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BACKGROUND: To perform a comprehensive study on the relationship between vitamin D metabolism and the response to interferon-α-based therapy of chronic hepatitis C. METHODOLOGY/PRINCIPAL FINDINGS: Associations between a functionally relevant polymorphism in the gene encoding the vitamin D 1α-hydroxylase (CYP27B1-1260 rs10877012) and the response to treatment with pegylated interferon-α (PEG-IFN-α) and ribavirin were determined in 701 patients with chronic hepatitis C. In addition, associations between serum concentrations of 25-hydroxyvitamin D(3) (25[OH]D(3)) and treatment outcome were analysed. CYP27B1-1260 rs10877012 was found to be an independent predictor of sustained virologic response (SVR) in patients with poor-response IL28B genotypes (15% difference in SVR for rs10877012 genotype AA vs. CC, p202;=202;0.02, OR202;=202;1.52, 95% CI202;=202;1.061-2.188), but not in patients with favourable IL28B genotype. Patients with chronic hepatitis C showed a high prevalence of vitamin D insufficiency (25[OH]D(3)<20 ng/mL) during all seasons, but 25(OH)D(3) serum levels were not associated with treatment outcome. CONCLUSIONS/SIGNIFICANCE: Our study suggests a role of bioactive vitamin D (1,25[OH](2)D(3), calcitriol) in the response to treatment of chronic hepatitis C. However, serum concentration of the calcitriol precursor 25(OH)D(3) is not a suitable predictor of treatment outcome.
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QUESTIONS UNDER STUDY: To update the prevalence of vitamin D insufficiency and to identify factors associated with vitamin D status in the Swiss adult population. METHODS: Data from the 2010-2011 Swiss Study on Salt intake, a population-based study in the Swiss population, was used. Vitamin D concentration in serum was measured by liquid chromatography- tandem mass spectrometry. Major factors that influence vitamin D levels were taken into account. Survey statistical procedures were used to estimate means and prevalences of vitamin D levels and status. Monthly-specific tertiles of vitamin D and ordinal logistic regression were used to determine the associations of covariates of interest with vitamin D status. RESULTS: The prevalences of vitamin D insufficiency (serum 25-hydroxyvitamin D: 20-29.9 ng/ml) and deficiency (<20 ng/ml) were the highest in the January-March period; 26.4% (95%CI: 21.6-31.7) and 61.6% (95%CI: 56.0-67.0), respectively. In the same period, more than 9 of ten men were vitamin D insufficient or deficient. Each unit increase of Body Mass Index was associated with an 8% decreased likelihood of being in a higher vitamin D tertiles. Oral contraceptive, altitude, urinary excretion of calcium, use of vitamin D supplement or treatment, high wine consumption, physical activity were associated with vitamin D tertiles. Compared to the French-speaking region, the Italian-speaking region was independently associated with a higher likelihood of being in higher vitamin D tertiles (OR: 1.66, 95%CI: 1.14-2.43). CONCLUSIONS: Low levels of vitamin D are common among Swiss adults, in particular during winter months and outside the Italian-speaking region.
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BACKGROUND: Vitamin D insufficiency has been associated with the occurrence of various types of cancer, but causal relationships remain elusive. We therefore aimed to determine the relationship between genetic determinants of vitamin D serum levels and the risk of developing hepatitis C virus (HCV)-related hepatocellular carcinoma (HCC). METHODOLOGY/PRINCIPAL FINDINGS: Associations between CYP2R1, GC, and DHCR7 genotypes that are determinants of reduced 25-hydroxyvitamin D (25[OH]D3) serum levels and the risk of HCV-related HCC development were investigated for 1279 chronic hepatitis C patients with HCC and 4325 without HCC, respectively. The well-known associations between CYP2R1 (rs1993116, rs10741657), GC (rs2282679), and DHCR7 (rs7944926, rs12785878) genotypes and 25(OH)D3 serum levels were also apparent in patients with chronic hepatitis C. The same genotypes of these single nucleotide polymorphisms (SNPs) that are associated with reduced 25(OH)D3 serum levels were found to be associated with HCV-related HCC (P202;=202;0.07 [OR202;=202;1.13, 95% CI202;=202;0.99-1.28] for CYP2R1, P202;=202;0.007 [OR202;=202;1.56, 95% CI202;=202;1.12-2.15] for GC, P202;=202;0.003 [OR202;=202;1.42, 95% CI202;=202;1.13-1.78] for DHCR7; ORs for risk genotypes). In contrast, no association between these genetic variations and liver fibrosis progression rate (P>0.2 for each SNP) or outcome of standard therapy with pegylated interferon-α and ribavirin (P>0.2 for each SNP) was observed, suggesting a specific influence of the genetic determinants of 25(OH)D3 serum levels on hepatocarcinogenesis. CONCLUSIONS/SIGNIFICANCE: Our data suggest a relatively weak but functionally relevant role for vitamin D in the prevention of HCV-related hepatocarcinogenesis.
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BACKGROUND: Obesity is associated with vitamin D deficiency, and both are areas of active public health concern. We explored the causality and direction of the relationship between body mass index (BMI) and 25-hydroxyvitamin D [25(OH)D] using genetic markers as instrumental variables (IVs) in bi-directional Mendelian randomization (MR) analysis. METHODS AND FINDINGS: We used information from 21 adult cohorts (up to 42,024 participants) with 12 BMI-related SNPs (combined in an allelic score) to produce an instrument for BMI and four SNPs associated with 25(OH)D (combined in two allelic scores, separately for genes encoding its synthesis or metabolism) as an instrument for vitamin D. Regression estimates for the IVs (allele scores) were generated within-study and pooled by meta-analysis to generate summary effects. Associations between vitamin D scores and BMI were confirmed in the Genetic Investigation of Anthropometric Traits (GIANT) consortium (n202;=202;123,864). Each 1 kg/m(2) higher BMI was associated with 1.15% lower 25(OH)D (p202;=202;6.52×10⁻²⁷). The BMI allele score was associated both with BMI (p202;=202;6.30×10⁻⁶²) and 25(OH)D (-0.06% [95% CI -0.10 to -0.02], p202;=202;0.004) in the cohorts that underwent meta-analysis. The two vitamin D allele scores were strongly associated with 25(OH)D (p≤8.07×10⁻⁵⁷ for both scores) but not with BMI (synthesis score, p202;=202;0.88; metabolism score, p202;=202;0.08) in the meta-analysis. A 10% higher genetically instrumented BMI was associated with 4.2% lower 25(OH)D concentrations (IV ratio: -4.2 [95% CI -7.1 to -1.3], p202;=202;0.005). No association was seen for genetically instrumented 25(OH)D with BMI, a finding that was confirmed using data from the GIANT consortium (p≥0.57 for both vitamin D scores). CONCLUSIONS: On the basis of a bi-directional genetic approach that limits confounding, our study suggests that a higher BMI leads to lower 25(OH)D, while any effects of lower 25(OH)D increasing BMI are likely to be small. Population level interventions to reduce BMI are expected to decrease the prevalence of vitamin D deficiency.
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BACKGROUND & AIMS: Vitamin D is an important immune modulator and preliminary data indicated an association between vitamin D deficiency and sustained virologic response (SVR) rates in hepatitis C virus (HCV) genotype 1 patients. We, therefore, performed a comprehensive analysis on the impact of vitamin D serum levels and of genetic polymorphisms with functional relevance within the vitamin D cascade on chronic hepatitis C and its treatment. METHODS: Vitamin D serum levels, genetic polymorphisms within the vitamin D receptor and 1α-hydroxylase were determined in a cohort of 468 HCV genotype 1, 2, and 3 infected patients who were treated with interferon-alfa based regimens. RESULTS: Chronic hepatitis C was associated with a high incidence of severe vitamin D deficiency compared to controls (25(OH)D(3)<10 ng/ml in 25% versus 12%, p<0.00001). 25(OH)D(3) deficiency correlated with SVR in HCV genotype 2 and 3 patients (50% and 81% SVR for patients with and without severe vitamin D deficiency, respectively, p<0.0001). In addition, the CYP27B1-1260 promoter polymorphism rs10877012 had substantial impact on 1,25-dihydroxyvitamin D serum levels (72, 61, and 60 pmol/ml for rs10877012 AA, AC, and CC, respectively, p=0.04) and on SVR rates in HCV genotype 1, 2, and 3 infected patients (77% and 65% versus 42% for rs10877012 AA, AC, and CC, respectively, p=0.02). CONCLUSIONS: Chronic hepatitis C virus infection is associated with vitamin D deficiency. Reduced 25-hydroxyvitamin D levels and CYP27B1-1260 promoter polymorphism leading to reduced 1,25-dihydroxyvitamin D levels are associated with failure to achieve SVR in HCV genotype 1, 2, and 3 infected patients.
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We assessed the effect of chronic hyperglycemia on bone mineral density (BMD) and bone remodeling in patients with type 2 diabetes mellitus. We investigated 42 patients with type 2 diabetes under stable control for at least 1 year, 22 of them with good metabolic control (GMC: mean age = 48.8 ± 1.5 years, 11 females) and 20 with poor metabolic control (PMC: mean age = 50.2 ± 1.2 years, 8 females), and 24 normal control individuals (CG: mean age = 46.5 ± 1.1 years, 14 females). We determined BMD in the femoral neck and at the L2-L4 level (DEXA) and serum levels of glucose, total glycated hemoglobin (HbA1), total and ionic calcium, phosphorus, alkaline phosphatase, follicle-stimulating hormone, intact parathyroid hormone (iPTH), 25-hydroxyvitamin D (25-OH-D), insulin-like growth factor I (IGFI), osteocalcin, procollagen type I C propeptide, as well as urinary levels of deoxypyridinoline and creatinine. HbA1 levels were significantly higher in PMC patients (12.5 ± 0.6 vs 7.45 ± 0.2% for GMC and 6.3 ± 0.9% for CG; P < 0.05). There was no difference in 25-OH-D, iPTH or IGFI levels between the three groups. BMD values at L2-L4 (CG = 1.068 ± 0.02 vs GMC = 1.170 ± 0.03 vs PMC = 1.084 ± 0.02 g/cm²) and in the femoral neck (CG = 0.898 ± 0.03 vs GMC = 0.929 ± 0.03 vs PMC = 0.914 ± 0.03 g/cm²) were similar for all groups. PMC presented significantly lower osteocalcin levels than the other two groups, whereas no significant difference in urinary deoxypyridine was observed between groups. The present results demonstrate that hyperglycemia is not associated with increased bone resorption in type 2 diabetes mellitus and that BMD is not altered in type 2 diabetes mellitus.
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The purpose of this study was to investigate the effect of supplementary vitamin D therapy in addition to amitriptyline on the frequency of migraine attacks in pediatric migraine patients. Fifty-three children 8-16 years of age and diagnosed with migraine following the International Headache Society 2005 definition, which includes childhood criteria, were enrolled. Patients were classified into four groups on the basis of their 25-hydroxyvitamin D [25(OH)D] levels. Group 1 had normal 25(OH)D levels and received amitriptyline therapy alone; group 2 had normal 25(OH)D levels and received vitamin D supplementation (400 IU/day) plus amitriptyline; group 3 had mildly deficient 25(OH)D levels and received amitriptyline plus vitamin D (800 IU/day); and group 4 had severely deficient 25(OH)D levels and was given amitriptyline plus vitamin D (5000 IU/day). All groups were monitored for 6 months, and the number of migraine attacks before and during treatment was determined. Calcium, phosphorus alkaline phosphatase, parathormone, and 25(OH)D levels were also determined before and during treatment. Results were compared between the groups. Data obtained from the groups were analyzed using one-way analysis of variance. The number of pretreatment attacks in groups 1 to 4 was 7±0.12, 6.8±0.2, 7.3±0.4, and 7.2±0.3 for 6 months, respectively (all P>0.05). The number of attacks during treatment was 3±0.25, 1.76±0.37 (P<0.05), 2.14±0.29 (P<0.05), and 1.15±0.15 (P<0.05), respectively. No statistically significant differences in calcium, phosphorus, alkaline phosphatase, or parathormone levels were observed (P>0.05). Vitamin D given in addition to anti-migraine treatment reduced the number of migraine attacks.
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Vitamin D deficiency is common in the chronic kidney disease (CKD) population. CKD has been recognized as a significant public health problem and CKD patients are at increased risk of total and cardiovascular morbidity and mortality. There are increasing epidemiological data suggesting that vitamin D deficiency may play a role in overall morbidity and mortality associated with CKD. The vitamin D hormonal system is classically implicated in the regulation of calcium homeostasis and bone metabolism but there is ample evidence to support the claim that extra renal conversion of 25(OH)D to 1.25(OH)2 has significant biological roles beyond those traditionally ascribed to vitamin D. Based on the current state of evidence this review intends to give an update on novel biological and clinical insights with relevance to the steroid hormone vitamin D specifically in patients with kidney disease.
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Contient : 1 Lettre de M. « DE SORBIES DES PRUNEAUX,... à monsieur de Bellievre, de ce qui s'est passé... à l'entreprise d'Anvers... D'Anvers, ce 26e jour de janvier 1583 ». Copie ; 2 Lettre de M. « LES PRUNEAUX,... à monseigneur... le prince d'Orange,... A Termonde, ce XXIe febvrier 1583 » ; 3 Lettre de M. « LES PRUNEAUS,... A Termonde, ce XXIe jour de febvrier 1583 » ; 4 « Ampliation sur l'ouverture proposée et mise en avant par Son Altesse... Françoys [duc d'Alençon]... à messieurs les Estatz generaulx des provinces unies des Païs Bas... Faict à Terremonde, le XXVIe jour de fevrier 1583 » ; 5 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaux,... A Terremonde, le IIe jour de mars 1583 » ; 6 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaux,... A Terremonde, le IIIe mars 1583 » ; 7 « Articles envoyés aus Estats » par « FRANÇOYS [duc D'ALENÇON]... Fait à Terremonde, le VIIe de mars 1583 » ; 8 « Instruction à monseigneur Des Pruneaux, envoyé par monseigneur... Françoys[duc d'Alençon]...vers messieurs les Estatz generaux des provinces unies des Païs Bas... Fait à Derremonde, le XVIIIe de mars 1583 » ; 9 Lettre de « FRANÇOYS [duc D'ALENÇON]... à messieurs les Estatz generaux des provinces unies des Païs Bas... A Termonde, le XXe jour de mars 1583 » ; 10 Lettre de M. DE « BELLIEVRE,... à monsieur... Des Pruneaux,... De Terlemonde, le XXIIe jour de mars 1583 » ; 11 Lettre de « FRANÇOYS [duc D'ALENÇON]... à messrs les Estatz generaulx des provinces unies des Païs Bas... A Termonde, le XXIIIe mars 1583 » ; 12 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaux,... A Terremonde, le XXIIIe mars 1583 » ; 13 « Articles accordez entre... Françoys... duc d'Allençon,... et les Estatz generaulx des provinces unies des Pays Bas... A Termonde, le XXVe jour de mars, l'an mil cinq cens quatre vingtz et trois... par le Sr Des Pruneaux » ; 14 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaulx,... A Termonde, le XXIIIe mars 1583 » ; 15 « Instruction de monseigneur... FRANÇOYS [duc D'ALENÇON]... à monsieur Des Pruneaux, allant... vers messieurs les Estatz generaux des provinces unies des Païs Bas... Faict à Termonde, le XXVIIIe mars 1583 » ; 16 Deux lettres de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaulx,... A Termonde, le IIe jour d'avril 1583 » ; 17 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaulx,... A Termonde, le IIIIe jour d'avril 1583 » ; 18 Lettre de M. DE « BELLIEVRE,... à monsieur... Despruneaux,... De Terlemonde, le IIIe jour d'avril 1583 » ; 19 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monseigneur Despruneaulx,... De Terremonde, le cinquiesme apvril 1583 » ; 20 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monseigneur... Despruneaulx,... De Terremonde, le VIe apvril 1583 » ; 21 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaux,... A Termonde, le VIe avril 1583 » ; 22 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaux,... A Termonde, le VIIe jour d'avril 1583 » ; 23 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON », à M. Des Pruneaux. « Du camp, le VIII apvril 1583 » ; 24 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaulx,... A Dunquerque, le XIe jour d'avril 1583 » ; 25 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monseigneur... Despruneaulx,... D'Inguen, le XVIIe apvril 1583 » ; 26 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monseigneur... Despruneaulx,... Du camp d'Inguen, le XIXe apvril 1583 » ; 27 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaulx,... A Dunkerque, le XXIe jour d'apvril 1583 » ; 28 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaux,... A Dunkerque, le XVIIe jour d'avril 1583 » ; 29 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monseigneur... Despruneaulx,... Du camp devant Versel, le XXIII apvril 1583 » ; 30 Lettre du maréchal DE BIRON à monseigneur Des Pruneaux. « Du camp, ce XXIIe d'avril 1583 » ; 31 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monseigneur... Despruneaulx,... Du camp de Wildeques, ce XXII apvril 1583 » ; 32 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monseigneur... Despruneaulx,... Du camp du Sehel, le XXIIIIe apvril 1583 » ; 33 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaux,... A Dunkerque, le XXVe jour d'avril 1583 » ; 34 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaulx,... A Dunkerque, le XXVe jour d'avril 1583 » ; 35 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaulx,... A Dunkerque, le XXVe jour d'avril 1583 » ; 36 Lettres closes de « FRANÇOYS [duc D'ALENÇON]... à nos... Srs des Estats generaulx des provinces unies des Païs Bas... A Dunkerque, le XXVe jour d'avril 1583 » ; 37 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monseigneur... Despruneaulx,... Du camp de Rozandal, le XXVIIIe apvril 1583 » ; 38 Lettre de FRANÇOIS, duc D'ALENÇON, « à monseigneur Des Pruneaulx,... A Dunkerque, le XXVIIIe jour d'avril 1583 » ; 39 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaux,... A Dunkerque, le XXVIIIe avril 1583 » ; 40 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monseigneur... Despruneaulx,... Du camp de Rozandal, le XXIXe apvril 1583 » ; 41 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monseigneur... Despruneaulx,... Du camp de Rozandal, le XXIXe apvril 1583 » ; 42 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monseigneur... Despruneaulx,... Du camp de Rozandal, le premier may 1583 » ; 43 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monseigneur... Despruneaulx,... Du camp de Rozandal, le troisiesme jour de mai 1583 » ; 44 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monsieur... d'Espruneaux,... Du camp de Rozandal, le IIIIe mai 1583 » ; 45 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaux,... A Dunkerque, le Vme jour de may 1583 » ; 46 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monsieur... d'Espruneaux,... Du camp à Rosendal, le Ve may 1583 » ; 47 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monsieur d'Espruneaux,... De Rosendal, le XIIe de may 1583 » ; 48 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monsieur d'Espruneaux,... Du camp à Rosendal, le XIIIe de may 1583 » ; 49 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monsieur... Despruneaulx,... Du camp de Rozandal, ce XIIIIe jour de may 1583 » ; 50 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monsieur... d'Espruneaux,... Du camp à Rosendal, le XIIIIe de may 1583 » ; 51 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monsieur... d'Espruneaux,... De Rosendal, le XVe de may 1583 » ; 52 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monseigneur... Despruneaulx,... Du camp de Rozandal, le XVIe jour de may 1583 » ; 53 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaux,... A Dunkerque, le XXe jour de may 1583 » ; 54 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaulx,... A Dunkerque, le XXVIIe jour de may 1583 » ; 55 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monseigneur... Despruneaulx,... Du camp de Rozandal, le XXIXe may 1583 » ; 56 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monseigneur... Despruneaulx,... Du camp de Rozandal, le XXXe may 1583 » ; 57 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monsieur... Despruneaulx,... De Rozandal, le IIIe jung 1583 » ; 58 Lettre d'ARMAND DE GONTAUT, maréchal DE « BIRON,... à monseigneur... Despruneaulx,... De Rozandal, le IIIIe jung 1583 » ; 59 « Estat signé de Son Altesse... FRANÇOYS [duc D'ALENÇON], pour le fait des vivres... Faict à Anvers, le IXe jour de jung 1583 » ; 60 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monsr Des Pruneaulx,... A Dunquerque, le XVIIIe juing 1583 » ; 61 Lettres closes de « FRANÇOYS », duc D'ALENÇON, aux « Estatz generaulx des provinces unies des Pays Bas... A Dunkerque, le XXVIIIe jour de juing 1583 » ; 62 « Instruction à monsieur Des Pruneaux,... de la part de monseigneur... FRANÇOYS [duc D'ALENÇON]... Faict à Dunkerque, le XXVIIIe jour de juing 1583 » ; 63 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaux,... A Calais, le dernier jour de juing 1583 » ; 64 Lettre de « FRANÇOYS [duc D'ALENÇON],... à monseigneur Des Pruneaux,... A Abbeville, le IIIIe jour de juillet 1583 » ; 65 Lettre de « GUILLAUME DE NASSAU [prince D'ORANGE]... à monsieur Des Pruneaux,... Ce IIIIe de jullet 1583 » ; 66 Deux lettres du Sr « CORMONT,... à Son Excelance [le duc d'Alençon]... De Winetzberge... 11 » et « 12 juliet 1583 » ; 67 Mémoire pour secourir Dunkerque. « Faict ce VIIIe de juillet 1583, en Anvers » ; 68 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaulx,... A Chaune, ce XVe juillet 1583 » ; 69 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaulx,... A Nesle, le XXme jour de juillet 1583 » ; 70 Lettres closes de « FRANÇOYS », duc D'ALENÇON, aux « Estatz generaulx des provinces unies des Pays Bas... A Nesle, le XXme jour de juillet 1583 » ; 71 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Despruneaux,... A St Quentin, le XXIIe jour de juillet 1583 » ; 72 Lettre de M. DE « PIBRAC,... à monsieur... de Pruneaux,... De Melle, ce XXIe julle[t] » ; 73 Lettre de M. « P. DE DAMPMARTIN,... à monseigneur [le duc d'Alençon]... D'Anvers, ce 27me juillet » ; 74 Deux lettres de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Des Pruneaux,... A Cambray, le IIIIe jour de septembre » et « le IXe jour d'octobre 1583 » ; 75 Lettre de « FRANÇOYS [duc D'ALENÇON]... à monseigneur Despruneaux,... A Chasteau Thierry, le XVe jour de novembre 1583 », suivie d'une note relative à une proposition faite au duc d'Alençon par le Sr de Gougnies ; 76 Mémoire au duc d'Alençon sur la conduite qu'il doit tenir avec Henri III, son frère. « Fait au moys de novembre 1583 »
Resumo:
Vitamin D metabolites are important in the regulation of bone and calcium homeostasis, but also have a more ubiquitous role in the regulation of cell differentiation and immune function. Severely low circulating 25-dihydroxyvitamin D [25(OH)D] concentrations have been associated with the onset of active tuberculosis (TB) in immigrant populations, although the association with latent TB infection (LTBI) has not received much attention. A previous study identified the prevalence of LTBI among a sample of Mexican migrant workers enrolled in Canada's Seasonal Agricultural Workers Program (SA WP) in the Niagara Region of Ontario. The aim of the present study was to determine the vitamin D status of the same sample, and identify if a relationship existed with LTBI. Studies of vitamin D deficiency and active TB are most commonly carried out among immigrant populations to non-endemic regions, in which reactivation of LTBI has occurred. Currently, there is limited knowledge of the association between vitamin D deficiency and LTBI. Entry into Canada ensured that these individuals did not have active TB, and L TBI status was established previously by an interferon-gamma release assay (IGRA) (QuantiFERON-TB Gold In-Tube®, Cellestis Ltd., Australia). Awareness of vitamin D status may enable individuals at risk of deficiency to improve their nutritional health, and those with LTBI to be aware of this risk factor for disease. Prevalence of vitamin D insufficiency among the Mexican migrant workers was determined from serum samples collected in the summer of 2007 as part of the cross sectional LTBI study. Samples were measured for concentrations of the main circulating vitamin D metabolite, 25(OH)D, with a widely used 1251 250HD RIA (DiaSorin Inc.®, Stillwater, MN), and were categorized as deficient «37.5 nmoI/L), insufficient (>37.5 nmollL, < 80 nmol/L) or sufficient (2::80 nmoI/L). Fisher's exact tests and t tests were used to determine if vitamin D status (sufficiency or insufficiency) or 25(OH)D concentrations significantly differed by sex or age categories. Predictors of vitamin D insufficiency and 25(OH)D concentrations were taken from questionnaires carried out during the previous study, and analyzed in the present study using multiple regression prediction models. Fisher's exact test and t test was used to determine if vitamin D status or 25(OH)D concentration differed by LTBI status. Strength of the relationship between interferongamma (IFN-y) concentration (released by peripheral T cells in response to TB antigens) and 25(OH)D concentration was analyzed using a Spearman correlation. Out of 87 participants included in the study (78% male; mean age 38 years), 14 were identified as LTBI positive but none had any signs or symptoms of TB reactivation. Only 30% of the participants were vitamin D sufficient, whereas 68% were insufficient and 2% were deficient. Significant independent predictors of lower 25(OH)D concentrations were sex, number of years enrolled in the SA WP and length of stay in Canada. No significant differences were found between 25(OH)D concentrations and LTBI status. There was a significant moderate correlation between IFN-y and 25(OH)D concentrations ofLTBI-positive individuals. The majority of participants presented with Vitamin D insufficiency but none were severely deficient, indicating that 25(OH)D concentrations do not decrease dramatically in populations who temporarily reside in Canada but go back to their countries of origin during the Canadian winter. This study did not find a statistical relationship between low levels of vitamin D and LTBI which suggests that in the presence of overall good health, lower than ideal levels of 2S(OH)D, may still be exerting a protective immunological effect against LTBI reactivation. The challenge remains to determine a critical 2S(OH)D concentration at which reactivation is more likely to occur.
Resumo:
L'allergie au lait de vache (ALV) représente l'allergie alimentaire la plus fréquemment rencontrée durant l'enfance. Cette allergie a longtemps été reconnue comme transitoire mais des données récentes révèlent que celle-ci est persistante chez environ 15% des enfants qui en sont touchés durant l'enfance, posant ainsi un risque à leur santé. La présente étude examine 26 enfants avec ALV et 12 enfants contrôles recrutés au CHU Sainte-Justine durant l’hiver 2011-2012. L'objectif étant de comparer la densité minérale osseuse (DMO) et les niveaux sériques de 25(OH)D d'enfants prépubères avec ALV non résolue à un groupe contrôle d'enfants avec autres allergies alimentaires, en plus d'évaluer les apports en calcium et en vitamine D ainsi que l'adhérence à la supplémentation chez cette population. La DMO lombaire (L2-L4) ne diffère pas significativement entre les groupes. Cependant, une faible densité osseuse, caractérisée par un score-Z entre -1,0 et -2,0 pour l'âge et le sexe, est détectée chez plus de 30% des enfants avec ALV et plus de 16% du groupe contrôle, sans allergie au lait. Tel qu'attendu, les apports en calcium sont significativement moins élevés chez les enfants avec ALV comparé au groupe contrôle, avec près de 90% de tous nos participants ne rencontrant pas les besoins pour l’âge en vitamine D. Plus de la moitié des enfants avec ALV présentent une concentration de 25(OH)D inférieure à 75 nmol/L. Cependant, notre étude n'a décelé aucune différence entre les niveaux sériques de 25(OH)D des enfants avec ALV comparativement au groupe contrôle. Enfin, l'adhérence à la supplémentation est jugée adéquate chez plus de 75% de notre groupe d'enfants avec ALV, soit ≧ 4 journées par semaine, un facteur aussi associé à une meilleure atteinte de leurs apports nutritionnels en calcium et en vitamine D. Enfin, ces résultats soulignent l'importance de suivre la santé osseuse d'enfants avec ALV ainsi qu'avec allergies multiples, qui présentent un risque de faible densité osseuse. L'intervention nutritionnelle devrait suivre l'adhérence à la supplémentation chez les enfants avec ALV non résolue, afin d'optimiser les apports nutritionnels insuffisants en calcium et en vitamine D