老年原发性高血压患者血清1,25-二羟维生素D_3水平的研究

目的分析老年原发性高血压患者血清1,25-二羟维生素D3水平的变化,探讨1,25-二羟维生素D3水平与高血压的关系。方法选取老年原发性高血压患者98例(高血压组)和健康体检者90例(对照组),检测其血清1,25-二羟维生素D3水平和血浆肾素活性(PRA),并进行比较。结果与对照组比较,高血压组1,25-二羟维生素D3水平明显降低,PRA明显升高(P<0.01)。Pearson相关分析显示,1,25-二羟维生素D3水平与PRA、收缩压、舒张压呈负相关(r=-0.438、r=-0.355、r=-0.655,P<0.05)。logistic回归分析显示,PRA为高血压的危险因素,1,25-二羟维生素D3为高血压的保护因素。结论老年原发性高血压患者血清1,25-二羟维生素D3水平明显低于正常人群。1,25-二羟维生素D3是高血压的保护因素。     

2型糖尿病肾病患者血清1,25-二羟维生素D3与肾功能指标的相关性研究

目的检测不同严重程度2型糖尿病肾病患者的血清1,25-二羟维生素D3水平,并分析其与肾功能指标的相关性。方法根据尿清蛋白肌酐比值及血肌酐值将48例2型糖尿病肾病患者分为微量蛋白尿组、大量蛋白尿组及肾功能不全组。采用ELISA法测定血清1,25-二羟维生素D3水平,同时常规测定血糖、糖化血红蛋白、肌酐、血钙、血磷等指标,计算肌酐清除率。结果微量蛋白尿组、大量蛋白尿组及肾功能不全组的血清1,25-二羟维生素D3水平逐渐降低,组间比较差异均有统计学意义(P均<0.05)。血清1,25-二羟维生素D3与血肌酐值呈负相关(P<0.05),与肌酐清除率呈正相关(P<0.05)。结论血清1,25-二羟维生素D3水平可能与2型糖尿病肾病相关,并且能够在一定程度上反映其严重程度。     

正常人和绝经后骨质减少病人的血清1,25-(OH)_2D浓度及年龄、肾功能和女性素治疗的影响

大多数研究表明骨质减少病人与同龄非骨质减少者比较其肠吸收钙减少,可能与维生素 D 代谢异常有关,但对绝经后骨质减少者的血清1,25-(OH)_2D 浓度是否正常,各家意见不一。作者测定了194名正常人(15～90岁)的血清1,25-(OH)_2D 平均浓度为32.8±12.5pg/ml(M±SD),不随年龄变化,无性别差异;55例绝经后骨质减少者为26.9±13.6pg/ml,比62名同龄无骨质减少者的血清浓度32.8±11.6pg/ml 稍低,有显著性差异(P<0.02)。本研究发现23例骨质减少的妇女血清1,25-(OH)_2D 浓度与肌酐清除率呈正相关(P<0.01)。11例绝经后妇女口服雌二醇(5mg/d)1个月,其血清1,25-(OH)_2D 显著上升(P<0.05)。     

血清基质金属蛋白酶-9检测与系统性红斑狼疮活动性的关系

目的探讨血清基质金属蛋白酶-9(MMP-9)与系统性红斑狼疮(SLE)活动程度的关系和意义。方法采用双抗体夹心酶联免疫吸附测定法,检测30名健康人和36例SLE患者血清MMP-9水平,以分析其与SLE活动性变化关系。结果SLE患者血清MMP-9水平[(108±113)ng/ml]明显低于正常对照组[(352±115)ng/ml],P<0.001;糖皮质激素治疗后血清MMP-9水平[(246±196)ng/ml]与治疗前水平[(114±92)ng/ml]相比,差异有显著性意义(P<0.05);SLE患者活动期血清MMP-9水平[(72±66)ng/ml]低于非活动期[(166±146)ng/ml],P<0.05;SLEDAI>8分组[(80±72)ng/ml]低于SLEDAI≤8分组[(152±150)ng/ml],P<0.05;蛋白尿组[(82±20)ng/ml]低于非蛋白尿组[(152±43)ng/ml],P<0.05;关节炎组[(103±126)ng/ml]与非关节炎组[(117±89)ng/ml]之间差异无显著性,P>0.05。结论MMP-9可能与SLE的发病相关,血清MMP-9可作为反映SLE活动程度、肾脏损害及疾病进展或改善的一项指标。     

系统性红斑狼疮患者血清中B淋巴细胞刺激因子的检测

目的检测系统性红斑狼疮(SLE)患者血清B淋巴细胞刺激因子(BLyS)水平,并探讨其在SLE发病中的意义。方法采用双抗体夹心酶联免疫吸附试验(ELISA)法检测血清BLyS水平。结果①SLE患者血清BLyS[(9.6±2.3)ng/ml]显著高于正常人对照组[(4.0±1.5)ng/ml]。②SLE患者中,血清BLyS水平活动组[(11.1±2.2)ng/ml]高于非活动组[(8.1±1.2)ng/ml],抗dsDNA抗体阳性组[(10.9±2.2)ng/ml]高于抗dsDNA抗体阴性组[(8.1±1.4)ng/ml],高IgG组[(10.8±2.4)ng/ml]高于非高IgG组[(8.3±1.3)ng/ml],低C3组[(10.2±2.5)ng/ml]高于非低C3组[(8.3±1.3)ng/ml],低C4组[(10.1±2.3)ng/ml]高于非低C4组[(7.6±0.7)ng/ml],低血小板计数组[(10.7±2.7)ng/ml]高于非低血小板计数组[(8.8±1.7)ng/ml]。③SLE患者血清BLyS水平与SLE疾病活动指数(SLEDAI)(r=0.56,t=15.89,P<0.01)、IgG(r=0.33,t=4.20,P<0.05)呈正相关;与C4(r=-0.47,t=10.04,P<0.01)、血小板计数(r=-0.53,t=13.85,P<0.01)呈负相关。结论BLyS可能参与SLE的发病。     

血压正常高值者动脉硬化指数与肿瘤坏死因子α的相关研究

目的探讨血压正常高值者动态动脉硬化指数与TNF-α的关系。方法选择体检者352例,依据血压水平分为3组:正常血压组110例,正常高值组105例,高血压组137例。入选者进行24 h动态血压监测,计算动脉硬化指数。采用放射免疫法测定TNF-α水平,进行相关分析。结果正常高值组TNF-α及动脉硬化指数[(44.21±9.81)pg/ml,0.42±0.13]高于正常血压组[(26.91±12.35)pg/ml,0.36±0.15],低于高血压组[(59.74±23.38)pg/ml,0.49±0.12],差异均有统计学意义(P<0.01)。正常高值组血浆TNF-α水平与动脉硬化指数呈正相关(r=0.575,P<0.01)。多元线性逐步回归分析显示,动脉硬化指数与TNF-α相关(标准回归系数=0.272,P<0.01)。结论血压正常高值者动脉硬化指数与TNF-α相关,炎症参与了高血压前期动脉硬化的形成。     

急性和慢性束缚应激对大鼠内脏敏感性和神经内分泌的影响

目的了解急性和慢性部分束缚应激对大鼠内脏敏感性以及神经内分泌反应的影响特点和持续时间。方法成年SD大鼠分为对照组(无束缚应激)、急性组和慢性组,通过腹壁回撤反射(AWR)评分评估应激前后大鼠内脏对结直肠扩张(CRD)的敏感性;并通过放免法检测应激前后不同时间点大鼠血浆促肾上腺皮质激素(ACTH)以及皮质酮(CORT)水平。结果①20和40 mm Hg压力扩张时,急、慢性组的AWR评分均显著高于基础水平(0 d),P<0.05;但在应激后第7天AWR评分显著下降,P<0.05。②急性组血浆ACTH和CORT水平显著高于对照组[(25.35±6.03)ng/ml比(7.24±2.97)ng/ml,(312.47±50.76)pg/ml比(97.00±23.33)pg/ml],但束缚应激7 d后,激素浓度[(11.81±5.03)ng/ml和(113.73±24.58)pg/ml]下降至基础水平。③慢性组血浆ACTH和CORT水平[(20.84±2.19)ng/ml和(200.41±78.10)pg/ml]显著高于对照组,且激素水平在束缚7 d后[(19.95±5.31)ng/ml和(162.51±47.08)pg/ml)]仍维持在高水平。结论急性和慢性束缚应激都可导致大鼠内脏敏感性增高,但作用可能是短暂的。急性束缚应激短暂显著提高血浆ACTH和CORT水平,而慢性束缚应激可能长期提高激素水平。     

维生素D受体基因多态性对尿毒症伴继发性甲状旁腺功能亢进的影响

目的　评价维生素D受体 (VDR)基因多态性对尿毒症伴继发性甲状旁腺功能亢进( 2°HPT)严重程度的影响。方法　对 1 0 6例尿毒症维持性血液透析患者采用聚合酶链反应———限制性片段长度 (PCR RFLP)方法分析VDR基因Apa I位点多态性 ,有ApaI酶切位点的等位基因规定为a ,没有者规定为A。结果　 1 0 6例患者VDR基因ApaI多态性频率分别为AA 1 7%、Aa54 .7%、aa 2 8.3%。aa基因组患者血清iPTH浓度 [( 339.8± 357.4) pg/ml]明显高于AA基因组[( 1 51 .9± 1 6 7.3) pg/ml]和Aa基因组患者 [( 1 91 .5± 1 6 9.8) pg/ml],两组比较差异有显著性 ( P <0 .0 5)。aa基因组患者骨钙蛋白浓度 [( 36 .2± 56 .0 )ng/ml]明显高于AA基因组 [( 9.2± 6 .1 )ng/ml]和Aa基因组患者 [( 1 5.3± 2 1 .6 )ng/ml],两组比较差异有显著性 ( P <0 .0 5)。三组间血钙、磷、镁及一般情况均无明显差别 ,但aa基因组降钙素浓度明显低于Aa基因组 [( 30 .1 6± 1 7.59)vs( 73.2 2± 6 8.2 6 ) pg/ml,P <0 .0 1 ]。结论　a等位基因患者较非a等位基因患者易产生严重的 2°HPT。     

维生素D3对结肠癌增殖和凋亡的影响及机制研究

[目的]探讨维生素D3对结肠癌增殖和凋亡的影响及机制研究。[方法]通过对临床结肠癌患者样本收集,血液中维生素D含量检测、受体检测、PCR定量、蛋白质免疫印迹等分子生物学实验,研究维生素D3对结肠癌增殖和凋亡的影响和机制。[结果]ELISA结果显示结肠癌患者血液中的1,25-二羟维生素D3含量(11.54±3.15)ng/ml和2,5二羟维生素D3含量(10.67±2.31)ng/ml较健康对照组1,25-二羟维生素D3为(29.65±7.25)ng/ml,2,5二羟维生素D3为(15.34±6.98)ng/ml明显降低,且维生素D受体的mRNA水平(5.01±3.86)相对对照组(9.36±4.87)较低,免疫荧光技术结果表明维生素D3通过Wnt信号通路影响结肠癌,蛋白质免疫印迹和PCR结果显示维生素D3处理后的人结肠癌细胞SW480中Wnt信号通路相关蛋白,EMT相关蛋白和β-catenin表达量均下调。[结论]维生素D3能够有效减少结肠癌组织的增殖,从而降低结肠癌发病率和防止结肠癌复发。     

慢性肾功能衰竭患者血清中的磷酸盐、甲状旁腺素及维生素D代谢物:服用氢氧化铝的作用

慢性肾功能衰竭(肾衰)的患者可有磷酸盐潴留、继发性甲状旁腺功能亢进(甲旁亢)及1,25-(OH)_2D减少等表现。为了研究氢氧化铝对这些病人的治疗作用,作者曾给予7例非透析的慢性肾衰患者口服大剂量氢氧化铝(15～18g/d),发现患者于治疗后血清磷由6.3±1.3降至3.7±0.5mg/dl(P<0.005),血清甲状旁腺素由2.87±1.64降至1.85±1.26ngEq/ml(P<0.02),血清1,25-(OH)_2D也由19.4±6.1降至11.4±4.3pg/ml(P>0.02)。但血铝浓度则由1.7±1.0升至3.6±1.5μg/dl(P>     

Vitamin D levels in women with systemic lupus erythematosus and fibromyalgia.

OBJECTIVE: Many patients with systemic lupus erythematosus (SLE) and fibromyalgia (FM) may spend less time exposed to the sun than healthy individuals and thus might have low vitamin D levels. It is known that hydroxychloroquine (HCQ) inhibits conversion of 25(OH)- to 1,25(OH)2-vitamin D both in vitro and in patients with sarcoidosis. We assessed winter serum 25(OH)- and 1,25(OH)2-vitamin D levels in patients with SLE and FM. METHODS: We recruited 25 consecutive female SLE and 25 female FM patients in London, Ontario, between January and March 2000. Subjects completed a brief questionnaire. Serum levels of 25(OH)-, 1,25(OH)2-vitamin D, and parathyroid hormone (PTH) were measured. RESULTS: In SLE patients mean 25(OH)-vitamin D was 46.5 nmol/l and mean 1,25(OH)2-vitamin D was 74.4 pmol/l. In FM patients these means were 51.5 nmol/l and 90.1 pmol/l, respectively. Serum 25(OH)-vitamin D levels did not significantly differ between SLE and FM patients, nor after adjusting for age and vitamin D, milk consumption, and sun block use. In 14 of the SLE patients and 12 of the FM patients 25(OH)-vitamin D levels < 50 nmol/l were found. SLE patients not using vitamin D supplements had lower 25(OH)-vitamin D levels than those who did. 1,25(OH)2-vitamin D tended to be lower in the SLE compared to the FM patients. This difference could be attributed to HCQ use: HCQ users (n = 17) had lower 1,25(OH)2-vitamin D levels than nonusers (n = 33); the mean adjusted difference was 24.4 pmol/l (95% CI 2.8-49.9). CONCLUSION: Half the SLE and FM patients had 25(OH)-vitamin D levels < 50 nmol/l, a level at which PTH stimulation occurs. Our data suggest that in SLE patients HCQ might inhibit conversion of 25(OH)-vitamin D to 1,25(OH)2-vitamin D.     

Acromegaly and vitamin D metabolism: effect of bromocriptine treatment.

Fifteen acromegalic subjects were found to have elevated plasma levels of both 1,25(OH)2-vitamin D, 65 +/- 23 (SD) pg/ml [normal 33 + 15 pg/ml (SD)] and 24,25(OH)2-vitamin D, 6.8 +/- 1.6 (SD) ng/ml [normal 3.4 + 1.2 ng/ml (SD)]. Treatment with bromocriptine for 6 months reduced the plasma 1,25(OH)2-vitamin D3 level to 40 +/- 13 (SD) pg/ml, p less than 0.01 and the 24,25(OH)2-vitamin D level to 5.4 +/- 1.7 (SD) ng/ml, p less than 0.05.     

Vitamin D status affects osteopenia in postmenopausal patients with primary hyperparathyroidism

Controversy still exists about whether vitamin D status is related to the severity of primary hyperparathyroidism (pHPT), although vitamin D insufficiency is frequent in pHPT. The present study was therefore performed to examine the relationships between vitamin D status and various parameters in 30 postmenopausal pHPT patients. BMD values were measured by dual-energy x-ray absorptiometry at the lumbar spine (L(2-4)), femoral neck (FN) and distal one third of the radius (Rad 1/3). Serum levels of 25 hydroxy-vitamin D(3) [25(OH)D] and 1,25-dihydroxy vitamin D(3) [1,25(OH) (2)D(3)] were 15.8 +/- 3.5 microg/l and 69.3 +/- 33.3 ng/l in pHPT patients, respectively. Serum levels of calcium and PTH seemed to be negatively correlated to serum 25(OH)D levels, although the differences were not significant. However, when subjects with the highest serum PTH levels (PTH>1000 pg/ml) were excluded from the analysis, the correlation was significant between serum 25(OH)D levels and PTH, indicating that vitamin D status affects the severity of pHPT when severe cases were excluded. In addition, serum levels of 1,25(OH)(2)D(3) were significantly and negatively correlated to serum 25(OH)D levels. On the other hand, serum levels of 25(OH)D were significantly and positively correlated to BMD (Z-score) at the lumbar spine, but not at the radius and femoral neck; however, serum 25(OH)D levels were not correlated to the levels of any bone metabolic indices measured. Moreover, serum levels of 25(OH)D were not related to urinary calcium and the tubular reabsorption rate of phosphorus, and they were similar in groups with and without renal stones. In conclusion, vitamin D status seemed to be related to the severity of disease in postmenopausal patients with pHPT. In particular, the relationship between serum 25(OH)D level and BMD at the lumbar spine was predominant.     

Premenopausal osteoporosis associated with vitamin D-responsive calcium malabsorption. A case report

A premenopausal woman with severe osteoporosis was found to have impaired calcium absorption, without other evidence of intestinal malabsorption. Although circulating levels of 25-OH-vitamin D and 1,25-(OH)2-vitamin D were normal, calcium absorption improved markedly following two weeks of treatment with synthetic 1,25-(OH)2-vitamin D. This suggests that a partial intestinal resistance to the actions of 1,25-(OH)2-vitamin D contributed to the development of her osteoporosis. This case report demonstrates the feasibility of using the calciuric response to a standard oral calcium load to screen for impaired calcium absorption in osteoporotic patients.     

A case of X-linked hypophosphatemic rickets: complications and the therapeutic use of cinacalcet

In hypophosphatemic rickets, there are both inherited and acquired forms, where X-linked dominant hypophosphatemic rickets (XLH) is the most prevalent genetic form and caused by mutations in the phosphate-regulating endopeptidase (PHEX) gene. XLH is associated with growth retardation and bone deformities. The renal tubular cells have an important role in calcium and phosphate metabolism, where the 1alpha-hydroxylase enzyme metabolizes the conversion of 25 (OH)-vitamin D to potent 1,25 (OH)2-vitamin D, whereas the sodium-phosphate transporter controls tubular phosphate reabsorption. The pathophysiological defect in XLH is speculated to cause an increase in a circulating phosphate regulating hormone termed phosphatonin (fibroblast growth factor 23 is the primary phosphatonin candidate), which leads to inhibition of 1alpha-hydroxylase, and simultaneously to inhibition of the sodium-phosphate transporter domain NPT2c leading to parathyroid hormone-independent phosphaturia. Hence, current treatment of XLH is 1,25 (OH)2-vitamin D or the vitamin D analog alfacalcidol and elementary phosphorus. Unfortunately, patients with XLH may develop nephrocalcinosis, secondary or tertiary hyperparathyroidism, and in some situations also hypertension and cardiovascular abnormalities. We describe a patient with XLH caused by a novel missense mutation in the PHEX gene, who on treatment with alfacalcidol and oral phosphate had normal growth and minimal bone deformities, but who subsequently developed moderate nephrocalcinosis, significant hyperparathyroidism, hypercalcemia, renal failure, and hypertension. We also report the use of the calcimimetic drug cinacalcet in the successful treatment of hypercalcemia and hyperparathyroidism.     

COMPARISON OF INTESTINAL CALCIUM ABSORPTION AND CIRCULATING 1,25-DIHYDROXYVITAMIN D LEVELS IN MALIGNANCY-ASSOCIATED HYPERCALCAEMIA AND PRIMARY HYPERPARATHYROIDISM

The relation between circulating 1,25-dihydroxyvitamin D (1,25(OH)2D) levels and intestinal calcium absorption--as determined by an oral calcium load test--was studied in 16 patients with hypercalcaemia of malignancy (HM) and 16 with hypercalcaemic primary parathyroidism (HPT). In the HPT group serum calcium rose significantly after the oral calcium load and the increment correlated significantly with 1,25(OH)2D levels. While 1,25(OH)2D levels were raised to within the hyperparathyroid range in a number of HM patients, there was no correlation between change in serum calcium and 1,25(OH)2D level in the HM group and serum calcium did not rise significantly after the oral calcium load. HM patients with detectable or raised 1,25(OH)2D levels typically had few, or no, bone metastases in association with squamous lung cancers. A high proportion of these patients exhibited other aspects of hyperparathyroid-like activity such as increased renal tubular calcium reabsorption, depressed renal tubular phosphate reabsorption and elevated urinary cyclic AMP excretion. Conversely, HM patients with undetectable 1,25(OH)2D levels typically had extensive metastatic bone disease in association with breast carcinoma and were less likely to exhibit other hyperparathyroid-like features. It is postulated that in the former, the 'inappropriately' detectable or raised 1,25(OH)2D levels may have been due to enhanced renal 1 alpha-hydroxylase activity stimulated by the parathyroid hormone (PTH)-like effect of a non-PTH ectopic humoral mediator. In the latter the suppressed 1,25(OH)2D levels would be the predicted result of a non-humorally mediated hypercalcaemia. It is currently unclear why intestinal calcium absorption was depressed in all HM patients when 1,25(OH)2D levels were normal or raised in some cases. It is possible, however, that in HM there is 'end organ' resistance to the effects of 1,25(OH)2D due to a generalized malabsorptive process.     

Elevated serum parathyroid hormone concentration in eucalcemic patients after parathyroidectomy for primary hyperparathyroidism and its relationship to vitamin D profile

Elevation of serum parathyroid hormone (PTH) level in eucalcemic patients after parathyroidectomy for primary hyperparathyroidism has been described in up to 40% of patients, but little is known about its etiology or clinical significance. To better understand the cause of this phenomenon, we studied 49 patients without renal dysfunction or osteomalacia who underwent parathyroidectomy for primary hyperparathyroidism. Patients were categorized into 2 groups based on their serum PTH and calcium levels after parathyroidectomy: (1) elevated PTH with eucalcemia (n = 21), (2) normal PTH with eucalcemia (n = 28). Elevation of serum PTH with eucalcemia after parathyroidectomy occurred in 43% of patients. Patients in group 1 had significantly higher preoperative and postoperative mean serum PTH levels and significantly lower postoperative serum levels of 1,25(OH)(2)D(3), 1,25(OH)(2)D(3)/25(OH)D(3) ratio, and 1,25(OH)(2)D(3)/PTH ratio compared with patients in group 2. Serum PTH in group 1 patients normalized as early as 3 months, but remained elevated in some patients for more than 4 years, and was not associated with development of recurrent hypercalcemia. Normalization of serum PTH in group 1 patients was associated with significant increase in 1,25(OH)(2)D(3) and 1,25(OH)(2)D(3)/PTH ratio. Our data suggest that elevation of serum PTH in eucalcemic patients after parathyroidectomy is a frequently reversible state of resistance of the kidneys to PTH-mediated 1-alpha hydroxylation of 25(OH)D(3) and does not signify subsequent recurrence of hyperparathyroidism.     

Hypocalcemic Crisis in Alcoholic Fatty Liver: Transient Hypoparathyroidism due to Magnesium Deficiency

Hypocalcemic crisis developed in a patient with acute alcoholic fatty liver. In addition to jaundice and marked hepatomegaly, the patient presented with hypocalcemic crisis associated with hypomagnesemia, low plasma 1,25(OH)2-vitamin D and undetectable plasma parathyroid hormone (PTH) concentration. Subsequent computerized tomographic scan and liver biopsy showed the presence of severe fatty liver. With the improvement of liver function, the serum calcium level increased, and was accompanied by normalization of plasma PTH, serum magnesium, and plasma 1,25(OH)2-vitamin D levels. Serial ethylenediaminetetraacetic acid infusion tests demonstrated the reversal of the impaired PTH secretion. Thus, hypocalcemic crisis in this patient appeared to result from transient hypoparathyroidism induced by magnesium deficiency.     

血清25羟维生素D3或1,25二羟维生素D3水平与慢性阻塞性肺疾病关系的Meta分析

目的：系统评价血清25(OH)D3或1,25(OH)2 D3与 COPD 相关病例对照研究,进一步明确血清维生素 D 水平与 COPD 之间的关系。方法计算机检索 PubMed、EMBASE、The Cochrane Library、中国生物医学文献数据库(CBM)、中国知网(CNKI)数据库、万方数据库、维普数据库,并辅以文献追溯的方法,收集国内外发表的相关病例对照研究,检索时间均从建库至2015年11月。2位研究者按纳入排除标准筛选文献并评价纳入研究质量,应用 RevMan 5.2软件进行 Meta 分析。结果共纳入15篇病例对照研究,包含1948例 COPD患者及1549例健康对照者。25(OH)D3浓度水平结果：Meta分析结果表明无论是急性加重期 COPD还是稳定期 COPD,与健康对照组相比,其25(OH)D3浓度水平差异均有统计学意义,COPD组25(OH)D3浓度低于健康对照组。急性加重期组vs对照组,WMD=-14.28,95%CI =(-23.82~-4.73),Z=2.93,P <0.01;稳定期组vs对照组 WMD=-4.46,95%CI =(-7.36~-1.57),Z=3.02,P <0.01;急性加重期与稳定期相比,25(OH)D3浓度水平差异亦有统计学意义[WMD=-2.66,95%CI =(-4.19~-1.12), Z=3.38,P<0.01,见图2];1,25(OH)2 D3浓度水平结果：Meta分析结果表明无论是急性加重期COPD还是稳定期 COPD,与健康对照组相比,其1,25(OH)2 D3浓度水平差异均有统计学意义, COPD组1,25(OH)2 D3浓度低于健康对照组。急性加重期组vs对照组,WMD=-15.09,95%CI =(-17.97~-12.22),Z =10.3,P <0.01;稳定期组 vs 对照组,WMD=-9.62,95%CI =(-12.55~-6.70),Z=3.02,P<0.01。结论 COPD患者体内25(OH)D3与1,25(OH)2 D3浓度水平均显著降低,维生素D缺乏可能参与COPD的发生、发展,并影响COPD患者的预后。     

Serum vitamin D metabolites and their binding protein in patients with liver cirrhosis

Serum parameters of calcium metabolism were measured in 32 consecutive patients with biopsy-proven cirrhosis due to either hepatitis (n = 13), alcohol abuse (n = 11), Wilson's disease (n = 3), or primary or secondary biliary cirrhosis (n = 5). All measurements were normal in the small group of patients with Wilson's disease. The serum concentrations of albumin, vitamin D-binding protein, total calcium, phosphorus, and 1,25-dihydroxyvitamin D3 (1,25-(OH2)D3) were decreased in the other patients with cirrhosis, but their mean serum concentrations of ionized calcium, 25-hydroxyvitamin D3 (25-OHD3) and free 1,25-(OH2)D3 index were normal. A slight but significant increase in the serum PTH measured using a carboxyl-terminal antiserum was found. A significant correlation was found between the serum concentration of either albumin or vitamin D-binding protein and the serum concentrations of total calcium, 25-OHD3, 1,25-(OH2)D3, and PTH but not with ionized calcium or free 1,25-(OH2)D3 index. The observed abnormalities of calcium metabolism in unselected patients with cirrhosis were mainly due to decreased protein synthesis. Only the patients with severe cirrhosis had decreased concentrations of 25-OHD3 but they were nevertheless able to maintain a normal ionized serum calcium and free 1,25-(OH2)D3 level, possibly by means of compensatory hyperparathyroidism.