慢性肾脏病患者维生素D缺乏与胰岛素抵抗的关系

目的通过比较不同时期慢性肾脏病（chronickidneydisease,CKD）患者的血清1,25-二羟维生素D3[1,25（0H）2D3]水平,探讨血清1,25（0H）2D3水平与CKD患者胰岛素抵抗的关系。方法选择98例CKD2～3期患者,均测量身高、体质量及血压。ELISA法测定血清1,25（OH）2D3,同时常规测定空腹血糖、胰岛素、血肌酐,超敏C反应蛋白、白细胞介素6（IL-6）、24h尿蛋白定量、高密度脂蛋白胆固醇（HDL-C）、收缩压,计算稳态模型胰岛素抵抗指数（HOMA-IR）,分析维生素D缺乏与上述指标的关系。结果CKD3期组的体质量指数、空腹胰岛素水平、血肌酐、24h尿蛋白定量、超敏C反应蛋白、IL-6、收缩压及胰岛素抵抗指数均明显升高（P〈0．05或P〈0．01）。而CKD3期组患者有明显降低的肾小球滤过率（GFR）,1,25（OH）2D3及HDL-C均显著降低（P〈0．05或P〈0．01）。相关分析表明,血清1,25（OH）2D3与HOMA-IR、IL-6、24h尿蛋白定量、收缩压、血肌酐呈负相关水平（r=-0．357、-0．207、-0．241、-0．187、-0．141,P〈0．05或P〈0．01）,与CKD患者胰岛素抵抗的多元线性逐步回归分析示有显著相关性（r=-0．458,P〈0．01）。结论CKD患者维生素D缺乏可导致胰岛素抵抗。     

活性维生素D在慢性肾脏病继发性甲旁亢中的应用

活性维生素D是慢性肾脏病(CKD)继发性甲状旁腺功能亢进症的主要治疗药物.种类繁多,应用广泛,疗效显著.现就其在CKD中的适应症、其作用机制和分类、其在CKD治疗中的作用及其治疗中给药方法和治疗效果做一综述.     

活性维生素D在慢性肾脏病继发性甲旁亢中的应用

活性维生素D是慢性肾脏病(CKD)继发性甲状旁腺功能亢进症的主要治疗药物.种类繁多,应用广泛,疗效显著.现就其在CKD中的适应症、其作用机制和分类、其在CKD治疗中的作用及其治疗中给药方法和治疗效果做一综述.     

维生素D在慢性肾脏病治疗中的作用

慢性肾脏病（chronic kidney disease,CKD)是一个全球性的公共健康问题,维生素D缺乏是CKD患者常见的临床并发症之一,而近年的研究提示维生素D缺乏反过来又会加速肾脏病的进展,进一步增加CKD患者的死亡率。本文拟就维生素D在CKD一体化治疗中的最新进展作一综述。     

维生素D在慢性肾脏病中的传统和非传统作用

活性维生素D是治疗慢性肾脏病患者继发性甲状旁腺功能亢进的主要药物.新近的研究发现除了传统的在钙/磷稳态的调节方面发挥中枢性调控作用外,活性维生素D还通过维生素D受体(VDR)介导的机制直接在转录水平调控一系列维生素D依赖基因的表达,从而在促进细胞分化、抗细胞增殖等方面发挥独立于钙磷代谢的非传统作用.本文就维生素D的代谢、维生素D受体、维生素D在慢性肾脏病中的传统和非传统作用作一综述.     

慢性肾脏病5期患者25-羟维生素D3不足与缺乏

目的 评估慢性肾脏病(CKD)5期患者25-羟维生素D3[25 (OH) D3]不足与缺乏的患病率及其影响因素.方法 对本院96例CKD 5期患者的病史、实验室检查结果等进行回顾性分析.纳入研究的变量包括:血25 (OH) D3检测值,血白细胞(WBC)、血红蛋白(Hb)、血清尿素氮(BUN)、血清肌酐(Scr)、二氧化碳结合力(CO2CP)、血清白蛋白(Alb)、碱性磷酸酶(ALP)、总胆固醇(TCH)、高密度脂蛋白(HDL-C)、低密度脂蛋白(LDL-C)、甘油三脂(TG)、钙、磷、全段甲状旁腺激素(iPTH)等.分析25 (OH) D3水平与各项观察指标间的关系.结果 96例CKD 5期患者的25 (OH) D3平均水平为33.25(24.85～ 44.30) nmol/L,显著低于正常值(P＜0.01);非透析患者、维持性血液透析(以下简称血透)患者、维持性腹膜透析(以下简称腹透)患者25-羟维生素D3水平分别为32.70(25.30～43.70) nmol/L、37.00(29.20～ 48.65)nmoL/L和27.05(19.20 ～ 35.37) nmol/L.CKD5期患者的25 (OH) D3不足患病率为32.29％;在非透析、血透、腹透患者中分别为27.91％、45.45％和20％;CKD5期患者25 (OH) D3缺乏患病率为64.58％,在非透析、血透、腹透患者中分别为67.44％、51.52％和80％;25 (OH) D3缺乏及不足患病率为96.88％,非透析、血透、腹透患者中分别为95.35％、96.97％和100％,各患病率三组间差异无统计学意义.单因素相关分析结果显示,25 (OH) D3水平与Hb(r=0.222)、Alb(r=0.398)相关(P＜0.05).多元线性回归分析结果显示,Alb水平与25 (OH) D3水平呈正相关.结论 CKD5患者的维生素D缺乏和不足患病率高,普遍存在.Alb是CKD5期患者维生素D水平不足或缺乏的独立影响因素.     

慢性肾脏病患者维生素D缺乏与动脉僵硬度的相关性

目的 探讨慢性肾脏病患者维生素D缺乏与动脉僵硬度的相关性.方法 选取慢性肾脏病(CKD l～5期)患者300例,根据血25(OH)D3浓度分为维生素D缺乏组[25 (OH)D3＜20 μg/L]和维生素D非缺乏组[25(OH)D3≥20 μg/L].采集临床资料数据,测定动脉僵硬度指标肱踝脉搏波传导速度(baPWV).对血25(OH)D3水平与baPWV间的关系进行单因素相关分析及多元线性回归分析. 结果 维生素D缺乏组188例(62.7％),维生素D非缺乏组112例(37.3％).全部CKD患者25(OH)D3平均浓度为(17.62±8.54) μg/L,维生素D缺乏组和非缺乏组分别为(12.38±4.55) μg/L与(26.44±6.05) μg/L(P＜0.01).维生素D缺乏组baPWV值高于非缺乏组[(1 827.34±429.11) cm/s比(1 555.31±353.14) cm/s,P＜0.01].单因素相关分析显示全体CKD患者(r=-0.38,P＜0.01)以及CKD 2～5期患者[r=-0.30,P＜0.05;r=-0.26,P＜0.05;r=-0.46,P＜0.01;r=-0.57,P＜0.01]血25(OH)D3浓度与baPWV均呈负相关.多元线性回归分析显示血25 (OH)D3浓度下降与baPWV的增加独立相关(模型1:β=-0.18,P＜0.01;模型2:β=-0.17,P=0.01),回归模型1与模型2均可解释baPWV变化的50％.结论 CKD患者普遍存在维生素D缺乏,维生素D缺乏与动脉僵硬度增加相关.维生素D替代治疗可能影响CKD患者的心血管预后,但有待未来研究的进一步明确.     

活性维生素D与慢性肾脏病

为了改善慢性肾脏病（CKD）患者骨及矿物代谢的生物学指标，活性维生素D、钙剂、不含钙的磷结合剂、拟钙剂（calcimimet—ics）一直被临床广泛使用。其中活性维生素D化合物一直被用于治疗继发性甲状旁腺功能亢进。本文的目的在于评价维生素D是否能够改善CKD患者钙磷代谢的生化指标、心血管并发症及生存率。     

活性维生素D3对透析前慢性肾脏病患者肾脏保护作用研究

目的：探讨活性维生素D3对透析前慢性肾脏病（CKD）患者的肾保护作用及安全性。方法：选择透析前3～4期慢性肾脏病患者200例,随机分为治疗组和对照组各100例。对照组给予优质低蛋白饮食、α-酮酸、血管紧张素转换酶抑制剂（ACEI）和（或）血管紧张素Ⅱ受体拮抗剂（ARB）和（或）钙通道拮抗剂以及抗血小板集聚等常规治疗,治疗组在常规治疗的基础上加用骨化三醇（0.5μg/d,疗程1年）。分别在治疗前和治疗后3,6,9和12月检测患者肾功能、血清白蛋白、甲状旁腺素、血钙、磷及24h尿蛋白定量等指标,并观察其副作用。结果：两组治疗后3月血肌酐、尿素氮、血尿酸和24h尿蛋白均明显下降（P〈0.05）,估算肾小球滤过率和血清白蛋白显著上升（P〈0.05）。治疗组治疗12月后肾功能进一步改善（P〈0.05）,尿蛋白进一步减少（P〈0.05）,而对照组治疗12月后肾功能和尿蛋白与治疗3月相比无明显改变。对照组患者血钙降低,血磷升高,甲状旁腺素水平明显升高（P〈0.05）。治疗组患者血钙升高,血磷降低,甲状旁腺素水平明显下降（P〈0.05）,但无明显高钙血症等副作用。结论：骨化三醇能显著改善透析前CKD患者的肾功能,减少蛋白尿,抑制继发性甲状旁腺素分泌,具有明显的肾脏保护作用,且无明显副作用。     

1,25-二羟维生素D3的免疫调节作用与肾脏病的研究进展

1,25-二羟维生素D3[1,25-dihydmxyvitamin D3,1,25-(OH)2D3]是维生素D3的活性形式,是第二甾体类激素,它除了调节机体的钙和骨代谢外,还参与免疫系统的分化与调节.1,25-(OH)2D3是通过与它的特定受体-维生素D受体(vitamin D receptor,VDR)相互作用来实现它的大部分基因效应的,抗原提呈细胞和T细胞是它作用的靶细胞,它的作用主要是诱导产生基因耐受性树突状细胞,抑制具有致病作用的T淋巴细胞,促进调节性T细胞(regulatory T cells,Treg)的增生.研究证实,1,25-( OH)2D3对多种自身免疫性疾病均有免疫调节作用,本文着重探讨其在肾脏病中的免疫调节作用.     

High prevalence of vitamin D deficiency in north Indian adults is exacerbated in those with chronic kidney disease

Aim:   Vitamin D is being increasingly recognized as an important player in disease. Hypovitaminosis D is widespread in chronic kidney disease (CKD) populations around the world. The vitamin D status of Indian CKD patients is not known.
Methods:   Levels of 25(OH) vitamin D and parathyroid hormone (PTH) were measured in adult north Indian male patients with newly diagnosed stage IV–V CKD and matched control subjects drawn from the same population. A total of 100 (34 stage IV and 66 stage V) patients with CKD and 72 controls were studied.
Results:   Only 4% control and 1% of CKD subjects had normal (>30 ng/mL) vitamin D levels. Approximately 68% of control and 77% of the CKD population had vitamin D deficiency (<15 ng/ml) whereas the remaining 38% control and 22% CKD patients had insufficient (15–30 ng/mL) vitamin D levels. Levels were lower in CKD subjects compared to their family members, and the CKD patients were significantly more likely to have severe vitamin D deficiency (<5 ng/mL). A strong negative correlation was noted between vitamin D and PTH. No significant correlation was found between vitamin D levels and body mass index, bodyfat percentage, serum albumin or calcium levels.
Conclusion:   Vitamin D deficiency is highly prevalent in north Indians, and this is more pronounced in CKD subjects. There is a significant inverse correlation between the vitamin D and PTH levels. The clinical significance of this deficiency and the potential benefits to be derived from vitamin D supplementation in this population merits further studies.     

早期慢性肾脏病患者肾组织甲状旁腺激素的表达及其作用

目的 探讨早期慢性肾脏病(CKD)患者肾组织甲状旁腺激素(PTH)表达和分布,以及其在CKD进展中的可能作用.方法 选取2009年至2012年间本科收治并经肾活检确诊的CKD 1期及2期的肾小球肾炎患者82例为研究对象.另取8例肾移植配型不符或肾肿瘤患者的正常肾组织作对照.受试者均检测Scr、BUN、血钙、磷、PTH及25(OH) VitD3等.以Cockcroft-Gault (CG)公式计算肌酐清除率(Ccr),双血浆99mTc-DTPA清除率法检测GFR.根据肾间质炎性细胞浸润程度,将患者分为轻、中、重组,用免疫组化方法观察肾组织PTH表达和分布;用Image-Pro Plus图像分析软件计算各例肾组织PTH阳性染色吸光度(A)值,并比较PTH表达强度差异.结果CKD1期及2期的肾小球肾炎患者的外周血钙、磷、25(OH) VitD3及PTH水平均处于正常范围,PTH与上述其他指标间无相关.不同病理类型肾小球肾炎患者肾组织均可见PTH表达,主要位于肾小管,而肾小球及肾间质也有少量分布,其表达强度均显著高于对照组(P＜0.01),且随肾间质炎性细胞浸润增多,PTH表达增强.各病理类型间肾组织PTH表达强度差异无统计学意义.结论 早期CKD(1期及2期)患者肾组织PTH表达增强,且早于外周血PTH的改变及矿物质和骨代谢紊乱,可能与局部炎性反应程度相关.     

慢性肾脏病患者甲状旁腺激素水平对肾性贫血的影响

目的 探讨慢性肾脏病（CKD）患者甲状旁腺激素（PTH）升高致红细胞寿命缩短的机制。 方法 以住院初治的CKD患者75例（按eGFR分为1～2期、3～4期和5期）和健康对照组30例为对象。免疫发光法测全段甲状旁腺激素（iPTH）;流式细胞术测红细胞表面磷脂酰丝氨酸（PS）外翻水平及红细胞内钙离子浓度（[Ca2+]i）。 结果 （1）随着肾功能的减退,CKD3～4期及5期患者 iPTH、[Ca2+]i及红细胞表面PS外翻水平逐渐升高、贫血逐渐加重,明显高于CKD1～2期和对照组（均P < 0.05）。（2）CKD3～4期或5期患者Hb与iPTH和红细胞表面PS外翻水平呈负相关（r = -0.830和-0.791,均P < 0.01）;iPTH与 [Ca2+]i和红细胞表面PS外翻水平呈正相关（r = 0.882和0.924,均P < 0.01）,与血钙浓度呈负相关（r = -0.544, P < 0.01）;红细胞表面PS外翻水平与 [Ca2+]i呈正相关（r = 0.923,P < 0.01）,与血钙浓度无相关（r = -0.138,P = 0.365）。（3）[Ca2+]i（Y）对iPTH（X）的直线回归方程：Y=3.327+0.213X（F=21.529,P < 0.05）;红细胞表面PS外翻水平（Y）对iPTH（X1）及[Ca2+]i（X2）的多元线性回归方程：Y=-0.303+0.283X2+0.139X1（F = 6.59,P < 0.01）。 结论 iPTH增加红细胞内钙离子浓度,引起红细胞表面PS外翻增多,致红细胞寿命缩短而加重肾性贫血。     

Vitamin D deficiency, CD4+CD28null cells and accelerated atherosclerosis in chronic kidney disease

Aim: Cardiovascular disease (CVD) is the leading cause of death among chronic kidney disease (CKD) patients. The role of vitamin D remains controversial in this process. We evaluated the relationship between 25‐hydroxyvitamin D, abnormal T helper cells (CD4+CD28null cells), systemic inflammation and atherosclerosis in CKD patients. Methods: A total of 101 stage 4–5 non‐dialysis CKD patients and 40 healthy controls were studied. Common carotid artery intima media thickness (CCA‐IMT) was measured with an ultrasound system. 25(OH) vitamin D and highly sensitive C‐reactive protein (hsCRP) were measured in serum by enzyme linked immunosorbent assay. The frequency of circulating CD4+CD28null cells was evaluated by flowcytometry. Results: CKD subjects exhibited higher CCA‐IMT (0.71 ± 0.01 vs 0.56 ± 0.01 mm, P < 0.0001), hsCRP (90.7 ± 5.8 vs 50.1 ± 8.6 µg/mL, P < 0.0001), CD4+CD28null cell frequency (9.1 ± 0.9 vs 3.6 ± 0.5%, P < 0.0001) and lower 25(OH) vitamin D levels (17.9 ± 1.9 vs 26.9 ± 3.5 ng/mL, P < 0.0001). In CKD subjects, serum 25 (OH) vitamin D level showed a strong inverse correlation with CCA‐IMT (r = ?0.729, P < 0.0001) and correlated with CD4+CD28null cell frequency (r = ?0.249, P = 0.01) and hsCRP (r = ?0.2, P = 0.047). We also noted correlation of IMT with patient age (r = 0.291, P = 0.004) and CD4+CD28null cells (r = 0.34, P = 0.001). On multiple regression analysis, 25(OH) vitamin D level, diabetic status and CD4+CD28null cell frequency exhibited independent association with IMT in CKD subjects. Conclusions: Vitamin D deficiency, inflammatory activation and higher frequency of CD4+CD28null T lymphocyte population correlate with preclinical atherosclerotic changes in CKD population. These findings suggest possible linkage between vitamin D metabolism and T cell modulation – abnormalities that may contribute to development of atherosclerosis in CKD.     

Vitamin D insufficiency and hyperparathyroidism in children with chronic kidney disease

Chronic kidney disease (CKD) is associated with altered calcium-phosphate homeostasis and hyperparathyroidism due to decreased activity of 1alpha-hydroxylase and impaired activation of 25-hydroxyvitamin D3 [25(OH)D3]. In some patients these problems start earlier because of vitamin D deficiency. A retrospective review of patients followed in the chronic renal insufficiency clinic at Children's Hospital of Michigan assessed the prevalence of vitamin D deficiency in CKD stages 2-4 and evaluated the effect of treatment with ergocalciferol on serum parathormone (PTH). Blood levels of 1,25 dihydroxyvitamin D3, 25(OH)D3, and parathormone (PTH) were examined in 57 children (40 boys; mean age 10.6 years). Of 57 subjects, 44 (77.2%) had 25(OH)D3 levels 30 ng/ml was 67.84 +/- 29.09 ng/ml and in the remaining patients was elevated, at 120.36 +/- 86.42 ng/ml (p = 0.05). Following ergocalciferol treatment (22), PTH decreased from 122.13 +/- 82.94 ng/ml to 80.14 +/- 59.24 ng/ml (p < 0.001) over a period of 3 months. We conclude that vitamin D deficiency is common in children with CKD stages 2-4 and is associated with hyperparathyroidism in the presence of normal 1,25 dihydroxyvitamin D3. Its occurrence before significant renal impairment is noteworthy. Early diagnosis and appropriate treatment is emphasized.     

慢性肾脏病患者成纤维细胞生长因子23与肾功能及钙磷代谢的关系

目的 探讨慢性肾脏病（CKD）患者随着肾功能的变化,其成纤维细胞生长因子23（FGF23）与钙磷代谢的关系。 方法 研究对象为2008年8月至2009年4月在上海交通大学附属第一人民医院肾内科住院的初诊CKD患者72例,按照肾小球滤过率（GFR）水平分为5组,另设健康对照组20例。抽取受试者静脉血并分离血清,以酶联免疫法检测FGF23、25（OH）VitD3、1,25（OH）2VitD3;全自动生化分析仪测量钙（Ca）、磷（P）、血肌酐（Scr）、尿素氮（BUN）、白蛋白（Alb）水平;免疫放射法测定全段甲状旁腺激素（iPTH）。 结果 CKD患者血清FGF23水平随GFR降低逐渐升高,在CKD4期和5期时,血FGF23、P、iPTH上升明显,1,25（OH）2VitD3显著下降,与CKD1期差异有统计学意义（均P < 0.05）。CKD2~3期与CKD1期的FGF23、P、Ca、iPTH、活性维生素D水平差异均无统计学意义。血Ca、25（OH）VitD3随着肾功能下降有降低趋势,但各期间差异均无统计学意义。Pearson相关分析显示,CKD1~5期logFGF23与P、logiPTH呈正相关（r = 0.653,P < 0.01;r = 0.800,P < 0.01）,与GFR、1,25（OH）2VitD3呈负相关（r = -0.753,P < 0.01;r = -0.265,P < 0.05),与Ca、25（OH）VitD3无相关。CKD1~3期logFGF23与logiPTH呈正相关(r = 0.374,P < 0.05),而与Ca、P、25（OH）VitD3、1,25（OH）2VitD3、GFR均无相关。CKD4~5期log FGF23与P、logiPTH呈正相关（r = 0.381,P < 0.05;r = 0.515,P < 0.01）,与GFR呈负相关（r = -0.654,P < 0.01）,与Ca、25（OH）VitD3、1,25（OH）2VitD3无相关。 结论 随着肾功能减退,血清FGF23、P、iPTH水平逐渐升高,活性维生素D水平逐渐下降,尤以CKD4~5期明显。在肾脏病早期阶段（CKD1~3期）血iPTH水平与FGF23有关。当GFR<30 ml/min时,肾功能状态、血磷、血iPTH均可影响血FGF23水平。     

Vitamin D deficiency,insulin resistance,and ventricular hypertrophy in the early stages of chronic kidney disease

Background: Chronic kidney disease (CKD) is associated with markedly increased cardiovascular (CV) risk. This increase is not fully explained by traditional CV risk factors but may in part be mediated by nontraditional risk factors, such as inadequate vitamin D (vit D) levels and insulin resistance (IR). Although IR is shown in nondiabetic CKD, its association with vit D deficiency and vascular disease in this population is unknown and what this study aims to investigate. Materials and methods: The study comprised 67 patients with CKD (eGFR?≥?30?mL/min) and 15 healthy controls matched for age and sex. The phlogosis indexes, vit D levels, IR, carotid intima-media thickness (cIMT), and left ventricular mass index (LVMI) were measured. Results: In our study, the mean value of LVMI and cIMT was significantly higher in patients with eGFR?≥?30?mL/min compared with controls (p?=?0.037 and p?p?=?0.044, p?=?0.012, p?=?0.038). A positive correlation was found between LVMI and IR (r?=?0.704, p?=?0.041) and a negative correlation was found between IR and vit D levels (r?=??0.238, p?=?0.031). Conclusions: In our study, IR and vit D deficiency were found to be independent predictors of left ventricular hypertrophy and atherosclerotic disease. Vitamin D deficiency and IR are thus associated with increased CV risk. More novel approaches to improving IR and vit D supplementation in the CKD population might lead to potential strategies for preventing excess CV mortality.     

Vitamin D levels, bone turnover and bone mineral density show seasonal variation in patients with chronic kidney disease stage 5

AIM: Many patients with chronic kidney disease (CKD) have reduced levels of 25-hydroxyvitamin D (25(OH)D). Although renal conversion of 25(OH)D to calcitriol is reduced or absent in CKD stage 5 (GFR < 15 mL/min per 1.73 m(2) or on dialysis), 25(OH)D may have direct skeletal and non-skeletal paracrine actions. The aim of this study was to assess seasonal variation in levels of 25(OH)D, bone turnover markers and bone mineral density, which would support a direct physiological role for 25(OH)D. METHODS: Vitamin D levels, bone turnover markers and bone mineral density were measured and assessed for seasonal variation in 257 patients about to undergo kidney or kidney pancreas transplantation. RESULTS: The mean age was 43 +/- 11 years; 62% were on haemodialysis, 24% on peritoneal dialysis and 34% had type 1 diabetes. Serum 25(OH)D was less than 50 nmol/L in 39% and lower levels were associated with female sex, diabetes and peritoneal dialysis (P < 0.0001 for each). Levels of 25(OH)D varied by season (P = 0.018; anova) peaking in autumn with a nadir in spring and calcitriol levels followed a similar seasonal trend. Bone mineral denisty Z-scores differed between summer and winter at the lumbar spine (P = 0.009) with a similar trend at the hip. Osteocalcin levels also showed seasonal periodicity (P = 0.0142) and together with alkaline phosphatase were higher in summer than winter. CONCLUSION: In summary, these data suggest direct effects of 25(OH)D on bone parameters in CKD stage 5 and support the need for prospective studies to establish the effect of treatments that increase 25(OH)D levels in all stages of CKD.     

Vitamin D deficiency and insufficiency among patients with prostate cancer

OBJECTIVE

To assess the frequency of vitamin D deficiency among men with prostate cancer, as considerable epidemiological, in vitro, in vivo and clinical data support an association between vitamin D deficiency and prostate cancer outcome.

PATIENTS, SUBJECTS AND METHODS

The study included 120 ambulatory men with recurrent prostate cancer and 50 with clinically localized prostate cancer who were evaluated and serum samples assayed for 25‐OH vitamin D levels. Then 100 controls (both sexes), matched for age and season of serum sample, were chosen from a prospective serum banking protocol. The relationship between age, body mass index, disease stage, Eastern Cooperative Oncology Group performance status, season and previous therapy on vitamin D status were evaluated using univariate and multivariate analyses.

RESULTS

The mean 25‐OH vitamin D level was 25.9 ng/mL in those with recurrent disease, 27.5 ng/mL in men with clinically localized prostate cancer and 24.5 ng/mL in controls. The frequency of vitamin D deficiency (<20 ng/mL) and insufficiency (20–31 ng/mL) was 40% and 32% in men with recurrent prostate; 28% had vitamin D levels that were normal (32–100 ng/mL). Among men with localized prostate cancer, 18% were deficient, 50% were insufficient and 32% were normal. Among controls, 31% were deficient, 40% were insufficient and 29% were normal. Metastatic disease (P = 0.005) and season of blood sampling (winter/spring; P = 0.01) were associated with vitamin D deficiency in patients with prostate cancer, while age, race, performance status and body mass index were not.

CONCLUSIONS

Vitamin D deficiency and insufficiency were common among men with prostate cancer and apparently normal controls in the western New York region.