原发性甲状旁腺功能亢进39例诊断及治疗分析

目的探讨原发性甲状旁腺功能亢进症(primary hyperparathyroidism,PHPT)的诊断与治疗方法。方法回顾性分析39例PHPT患者临床资料。结果 (1)39例中骨型10例,肾型2例,肾骨型3例,高钙型16例,无症状型8例;(2)初诊时患者血钙[(3.47±0.67)mmol/L]、血甲状旁腺激素(parathyroid hormonr,PTH)[(820.62±622.09)ng/L]及血碱性磷酸酶[(311.02±323.38)u/L]水平显著增高,血磷[(0.96±0.29)mmol/L]为正常值下限;(3)术前彩超、CT及MRI、99mTC-MIBI核素显像分别诊断14、5、24例;(4)12例合并高钙危象者,术前经"水疗法"和鲑鱼降钙素治疗4~8d,血钙水平[(3.22±0.43)mmol/L]较治疗前[(4.07±0.50)mmol/L]明显降低(P0.05);(5)术后7d,血钙[(2.05±0.24)mmol/L]、PTH[(66.81±114.57)ng/L]水平与术前[(3.49±0.69)mmol/L、(1 275.45±1046.42)ng/L]比较差异有统计学意义(P0.05)。结论高血钙及高PTH是PHPT的特征性指标,99mTC-MIBI检查有助于定位诊断;手术是治疗PHPT的有效方法,"水疗法"及鲑鱼降钙素治疗有助于血钙的稳定。     

血清25羟维生素D水平与2型糖尿病非骨质疏松症患者胰岛素抵抗和骨代谢的关系

目的探讨血清25羟维生素D [25(OH)D]水平与2型糖尿病(T2DM)非骨质疏松症患者胰岛素抵抗和骨代谢指标的关系。方法选取本院收治的T2DM患者150例为研究对象,根据受试者25(OH)D水平分为3组:25(OH)D20ng/ml者为G1组(n=40),25(OH)D在20ng/ml～30ng/ml之间者为G2组(n=78),25(OH)D30ng/ml者为G3组(n=32)。比较各组间血清25(OH)D、血糖代谢指标、胰岛素抵抗指数(HOMA-IR)及骨代谢相关指标水平,分析25(OH)D与HOMA-IR、骨代谢指标的关系,分析HOMA-IR与骨代谢指标的关系。结果各组间血清25(OH)D、空腹血糖、空腹C肽、空腹胰岛素及HOMA-IR水平间差异有统计学意义(P0.05);血清25(OH)D与HOMA-IR呈负相关(r=-0.440,P0.05);各组间甲状旁腺激素(PTH)水平差异有统计学意义(P0.05),血钙、血磷、钙磷乘积及碱性磷酸酶(ALP)水平间比较,差异无统计学意义(P0.05);血清25(OH)D与血钙、血磷、钙磷乘积及ALP无显著相关性(r=-0.041, r=-0.038, r=-0.011, r=-0.048, P均0.05),与PTH呈负相关(r=-0.597, P0.05);HOMA-IR与血钙、血磷、钙磷乘积及ALP无显著相关性(r=0.039, r=0.030, r=0.015, r=0.044, P均0.05),与PTH呈正相关(r=0.298, P0.05)。结论血清25(OH)D水平与T2DM非骨质疏松症患者胰岛素抵抗、骨代谢指标PTH呈负相关,胰岛素抵抗与PTH呈正相关,维生素D缺乏易引起T2DM及骨质疏松的发生。     

急性肾损伤危重患者血清1,25二羟维生素D水平对其预后的影响

目的观察血清1,25二羟维生素D[1,25(OH)_2D]水平与急性肾损伤(AKI)危重患者预后的相关性。方法回顾性分析2014年12月至2015年12月入住上海交通大学附属第六人民医院45例AKI患者的临床资料,按预后结果分为存活组和死亡组。检测患者血清1,25(OH)_2D、甲状旁腺激素、25-OH维生素D、钙和磷等对预后的影响。结果 45例患者中10例住院死亡,病死率为22.2%。存活组与死亡组AKI患者的血清1,25(OH)_2D水平间差异有统计学意义[(63.2±41.5)pg/mL vs.(33.8±24.1)pg/mL,P=0.043];死亡组患者血清磷水平高于存活组,且差异有统计学意义[(6.3±2.1)mg/dL vs.(4.5±1.6)mg/dL,P=0.019]。多因素Logistic回归分析显示,高急性生理与慢性健康评分(APACHEⅡ评分)以及高水平1,25(OH)_2D为AKI患者预后的危险因素(OR=1.191,95%CI:1.154~1.233,P=0.008;OR=1.281,95%CI:1.067~1.538,P=0.018)。结论1,25(OH)_2D与AKI患者死亡具有相关性,临床上可作为判断AKI患者预后的指标。     

血清25羟基维生素D与初诊2型糖尿病患者血糖控制及酮症酸中毒的关系

目的探讨初诊2型糖尿病(type 2diabetes mellitus,T2DM)患者血清25羟基维生素D[25-hydroxy vitamin D,25(OH)D]水平与血糖控制及酮症酸中毒的关系。方法 140例初诊T2DM患者为T2DM组,同期130例体检健康者为对照组,检测2组血清总胆固醇(total cholesterol,TC)、三酰甘油(triacylglycerol,TG)、高密度脂蛋白胆固醇(high-density lipoprotein cholesterol,HDL-C)、低密度脂蛋白胆固醇(low-density lipoprotein cholesterol,LDL-C)、糖化血红蛋白(hemoglobin A1c,HbA1c)、25(OH)D水平,Pearson法分析初诊T2DM患者血清25(OH)D与TC、TG、HDL-C、LDL-C、HbA1c的相关性;将T2DM患者依据HbA1c水平分为A组(HbA1c≥9%)75例和B组(HbA1c9%)65例,比较A、B组血清25(OH)D水平;选取同期住院10例酮症酸中毒起病T2DM患者(酮症酸中毒组),再按照配对方法从140例T2DM患者中选取10例非酮症酸中毒起病患者(非酮症酸中毒组),比较2组血清HbA1c、25(OH)D水平。结果 T2DM组血清TG[(2.43±1.35)mmol/L]、LDL-C[(2.88±0.68)mmol/L]、HbA1c[(9.24±1.91)%]水平均高于对照组[(1.19±0.63)mmol/L、(2.41±0.54)mmol/L、(5.31±1.51)%],25(OH)D水平[(11.51±3.12)μg/L]低于对照组[(19.03±4.96)μg/L](P0.05),TC[(5.22±1.53)mmol/L]、HDL-C[(1.01±0.32)mmol/L]水平与对照组[(4.68±0.98)、(1.31±0.31)mmol/L]比较差异无统计学意义(P0.05);T2DM组血清25(OH)D水平与BMI、HbA1c呈负相关(r=-0.213,P=0.042;r=-0.405,P=0.005),与HDL-C呈正相关(r=0.229,P=0.039),与LDL-C、TG无明显线性相关(r=-0.152,P=0.078;r=-0.135,P=0.729);A组血清25(OH)D水平[(10.44±3.63)μg/L]低于B组[(12.97±3.53)μg/L](P0.05);酮症酸中毒组血清25(OH)D水平[(5.52±2.61)μg/L]低于非酮症酸中毒组[(9.01±3.29)μg/L](P0.05),HbA1c[(11.71±2.12)%]与非酮症酸中毒组[(11.62±1.96)%]比较差异无统计学意义(P0.05)。结论初诊T2DM患者血清25(OH)D水平降低与血糖控制有关,且酮症酸中毒T2DM患者血清25(OH)D水平相对较低。     

上海老年男性血清维生素D水平状况调查

目的:调查上海老年男性血清维生素D水平及其缺乏程度。方法:收集2009年5月至9月上海瑞金医院老年病科体检和门诊的老年男性847例,平均年龄为76岁,测定其血清25-羟基维生素D[25-(OH)D]、肝肾功能、血钙(Ca)、磷(P)、血糖、血脂,部分测定甲状旁腺激素(PTH)、尿Ⅰ型胶原N端肽(NTX)、骨钙素(BGP)和骨碱性磷酸酶(BAP)。结果:①老年男性的血清25-(OH)D水平为(48.7±24.5)nmol/L,其中维生素D缺乏者(75 nmol/L者仅99例,占11.7%。②血清25-(OH)D水平与年龄呈负相关(r=-0.215,P<0.05),90岁以上组与其他组比较差异均有统计学意义(P0.05)。GFR<0.05)。结论:上海老年男性血清维生素D水平普遍较低,缺乏和不足者高达60.2%,且血清维生素D水平随年龄增高呈降低趋势。关注老年男性维生素D营养状况与关注绝经后女性同等重要。     

桥本甲状腺炎甲状腺功能减退患者血清1,25-二羟维生素D_3及白细胞介素-8水平变化及意义

目的探讨桥本甲状腺炎(Hashimoto's thyroiditis,HT)甲状腺功能减退(甲减)患者应用左甲状腺素钠片治疗前及治疗5个月后血清1,25-二羟维生素D_3[l,25 2-hydroxyvitamin D_3,1,25(OH)_2D_3]、白细胞介素-8(interleukin-8,IL-8)水平变化及意义。方法 HT甲减患者58例为观察组,同期体检健康者58例为对照组。观察组给予左甲状腺素钠片150~200μg/d,连续口服5个月,对照组不作处理。对照组于入组时,观察组于治疗前及治疗5个月后采用光化学分析法检测血清游离三碘甲状腺原氨酸(free triiodothyronine,FT3)、游离甲状腺素(free tetraiodothyron,FT4)、促甲状腺激素(thyroid stimulating hormone,TSH)水平,采用放射免疫分析法检测血清促甲状腺素受体抗体(thyrotropin receptor antibody,TRAb)、甲状腺过氧化物酶抗体(thyroid peroxidase antibody,TPOAb)、甲状腺球蛋白抗体(thyroglobulin antibody,TgAb)水平,采用ELISA法检测血清IL-8、1,25(OH)_2D_3水平,并与对照组进行比较;Pearson法分析观察组血清IL-8、1,25(OH)_2D_3水平与FT_3、FT_4等指标的相关性。结果观察组治疗前血清FT_4[(9.55±5.27)pmol/L]、1,25(OH)_2D_3[(22.61±7.28)μg/L]均低于对照组[(19.70±6.20)pmol/L、(33.62±6.19)μg/L],血清TSH[(5.86±1.28)u/L]、TPOAb[(558.65±89.96)u/mL]、TgAb[(203.26±16.08)%]、IL-8[(114.62±16.78)ng/L]均高于对照组[(2.73±0.17)u/L、(45.12±0.85)u/mL、(38.23±12.39)%、(90.36±18.24)ng/L](P0.05),血清FT3[(5.26±1.57)pmol/L]、TRAb[(0.15±0.05)u/L]与对照组[(4.98±1.04)pmol/L、(0.12±0.07)u/L]比较差异均无统计学意义(P0.05);治疗5个月后,观察组血清FT_4[(17.14±3.22)pmol/L]、1,25(OH)_2D_3[(31.14±8.32)μg/L]均高于治疗前(P0.05),血清TSH[(3.18±1.04)u/L]、TPOAb[(61.24±13.29)u/mL]、TgAb[(42.98±11.84)%]、IL-8[(93.16±12.34)ng/L]均低于治疗前(P0.05),血清FT_3[(5.11±1.14)pmol/L]、TRAb[(0.13±0.08)u/L]与治疗前比较差异均无统计学意义(P0.05);Pearson相关性分析结果显示,观察组血清IL-8与TSH、TPOAb水平呈正相关(r=0.520,P=0.002;r=0.398,P=0.025),血清1,25(OH)_2D_3与TSH、TPOAb水平呈负相关(r=-0.408,P=0.021;r=-0.415,P=0.020)。结论HT甲减患者血清IL-8水平升高,1,25(OH)_2D_3水平降低,且与TSH和TPOAb水平相关。     

成纤维细胞生长因子23与慢性肾脏病患者钙磷代谢关系的探讨

目的探讨慢性肾脏病患者血清成纤维细胞生长因子-23(FGF-23)与血钙、血磷的关系。方法通过酶联免疫分析(ELISA)方法检测151例CKD 1~5期非透析慢性肾脏病患者和14名健康对照组全段FGF-23和1,25二羟维生素D3[1,25(OH)2D3]的水平,同时测定血清肌酐(CREA)、钙(Ca)、磷(P)、碱性磷酸酶(ALP)、尿酸(UA)、甲状旁腺素(PTH)等指标,分析FGF-23与各指标的关系。结果 (1)CKD 1期、CKD 2~3期、CKD 4~5期者血清FGF-23水平逐渐升高,CKD 2~3期、CKD 4~5期与对照组比较,CKD 4~5期与CKD 1期、CKD 2~3期比较有统计学差异(P<0.05)。(2)相关分析结果显示:CKD 1~5期患者血清FGF-23与CREA、P、PTH存在显著正相关关系(r分别为0.971、0.650、0.536,均P<0.01);与估算的肾小球滤过率(e GFR)、1,25(OH)2D3存在显著负相关关系(r值分别为-0.578、-0.586,均P<0.01)。(3)多元回归结果显示:CREA、1.25(OH)2D3、PTH是血清FGF-23水平的独立影响因素。结论 CKD1~5期患者血清FGF-23显著升高,CREA、P、1.25(OH)2D3、PTH可能是血清FGF-23水平的影响因素。     

TPTX联合AT对SHPT患者血钙及甲状旁腺激素水平的影响

目的 探讨甲状旁腺全切术(TPTX)联合前臂自体移植术(AT)对继发性甲状旁腺功能亢进症(SHPT)患者血钙及甲状旁腺激素(PTH)水平的影响。方法 选择2019年5月至2021年4月在萍乡市人民医院及南昌大学第二附属医院治疗的72例SHPT患者作为研究对象,按照随机数字表法将其分为TPTX组与TPTX联合AT组,各36例。TPTX组采用TPTX治疗,TPTX联合AT组采用TPTX联合AT治疗,观察至术后6个月。比较两组血钙、血磷、PTH、碱性磷酸酶(ALP)水平及并发症发生情况。结果 术后TPTX联合AT组血钙、PTH水平[(1.96±0.31)mmol/L、(116.38±12.58)ng/L]高于TPTX组[(1.35±0.22)mmol/L、(62.85±8.57)ng/L],TPTX联合AT组并发症发生率[8.33%(3/36)]低于TPTX组[27.78%(10/36)],差异有统计学意义(P<0.05);两组术后血磷、血钙、PTH、ALP水平低于术前,差异有统计学意义(P<0.05)。两组术后血磷水平比较,差异无统计学意义(P>0.05)。结论 在SHP...     

超声引导下经皮激光消融治疗原发性甲状旁腺功能亢进症

目的:探讨超声引导下经皮激光消融治疗原发性甲状旁腺功能亢进症(primary hyperparathyroidism,PHPT的可行性、安全性及治疗价值。方法:对3例PHPT患者行激光消融,功率3 W,采用多点、移动消融法,术后即刻超声造影评估消融范围。术前、术后检测全段甲状旁腺素(intact parathyroid hormone,iPTH)、血钙、血磷、碱性磷酸酶(alkaline phosphatase,ALP)等,并测量甲状旁腺结节容积的变化率。密切随访12个月。结果:3例PHPT结节经超声造影证实均一次性彻底消融。术后12个月,iPTH由术前(578.37±568.66)ng/L降为(92.62±19.83)ng/L,血钙由(3.20±0.43)mmol/L降为(2.35±0.03)mmol/L(P0.05),ALP由(303.53±188.29)U/L下降为(99.70±7.86)U/L,血磷由术前(0.830±0.098)mmol/L上升为(0.923±0.120)mmol/L;术后iPTH显著下降,血钙、血磷及ALP测值均持续正常。PHPT结节容积缩小率95.73%。术后1例发生"骨饥饿综合征",予以口服补钙后好转,未发生喉返神经损伤等严重并发症。结论:超声引导下经皮激光消融治疗PHPT是一种微创、安全、有效的方法,可显著降低iPTH、血钙值,并显著缩小PHPT结节,有望成为治疗PHPT的新方法之一。     

类风湿关节炎患者血清25-羟基维生素D水平与亚临床动脉粥样硬化的关系及活性维生素D治疗的作用

目的探讨类风湿关节炎(rheumatoid arthritis,RA)患者血清25-羟基维生素D[25-hydroxyvitamin D,25(OH)D]水平与亚临床动脉粥样硬化的相关性,并观察活性维生素D干预治疗对RA患者亚临床动脉粥样硬化的影响。方法 110例RA患者依据颈动脉内中膜厚度(intima-media thickness,IMT)分为动脉粥样硬化组76例和无动脉粥样硬化组34例,同期体检健康者110例为对照组。记录3组年龄、体质量指数(body mass index,BMI)等一般资料及血清学检测结果,计算RA患者28个关节的疾病活动评分(disease activity score in 28joints,DAS28)评分;采用ELISA法检测血清25(OH)D水平;将血清25(OH)D缺乏(20μg/L)的68例患者随机分为干预组35例和非干预组33例,干预组口服阿法骨化醇0.5μg/d连续24周,非干预组不作治疗;分别于干预前、干预24周后检测血清25(OH)D水平及行颈动脉IMT;Pearson法分析各指标的相关性,多元逐步回归分析颈动脉IMT的影响因素。结果动脉粥样硬化组、无动脉粥样硬化组血清25(OH)D[(12.84±1.54)、(17.27±3.01)μg/L]水平均低于对照组[(38.72±9.45)μg/L],且动脉粥样硬化组低于无动脉粥样硬化组(P0.05);动脉粥样硬化组DAS28评分[(4.18±1.40)分]与无动脉粥样硬化组[(3.99±1.87)分]比较差异无统计学意义(P0.05);Pearson相关分析结果显示,RA患者血清25(OH)D水平与DAS28评分(r=-0.594,P=0.001)、颈动脉IMT(r=-0.586,P=0.001)呈负相关;多元逐步回归分析结果显示,血清25(OH)D(OR=0.637,95%CI:0.486~0.788,P=0.006)是颈动脉IMT的影响因素;干预组干预前血清25(OH)D、DAS28评分及颈动脉IMT与非干预组比较差异均无统计学意义(P0.05),干预24周时血清25(OH)D[(28.73±6.51)μg/L]较非干预组[(13.45±4.01)μg/L]高,DAS28评分[(4.04±1.82)分]较非干预组[(4.78±1.98)分]低,颈动脉IMT[(1.78±0.76)mm]较非干预组[(2.12±0.74)mm]小(P0.05)。结论血清25(OH)D水平降低是RA患者发生亚临床动脉粥样硬化的危险因素,活性维生素D干预对RA患者亚临床动脉粥样硬化的发展有明显的改善作用。     

Evidence that blood ionized calcium can regulate serum 1,25(OH)2D3 independently of parathyroid hormone and phosphorus in the rat.

This study asks whether arterial blood ionized calcium concentration (Ca++) can regulate the serum level of 1,25-dihydroxy-vitamin D3 [1,25(OH)2D3] independently of serum phosphorus and parathyroid hormone (PTH). We infused either PTH (bovine 1-34, 10 U/kg body wt/h) or saline into awake and unrestrained rats for 24 h, through a chronic indwelling catheter. PTH raised total serum calcium and arterial blood ionized calcium, yet serum 1,25(OH)2D3 fell from 35 +/- 6 (mean +/- SEM, n = 10) with saline to 12 +/- 3 pg/ml (n = 11, P less than 0.005 vs. saline). To determine if the decrease in serum 1,25(OH)2D3 was due to the elevated Ca++, we infused PTH into other rats for 24 h, along with varying amounts of EGTA. Infusion of PTH + 0.67 micron/min EGTA reduced Ca++, and 1,25(OH)2D3 rose to 90 +/- 33 (P less than 0.02 vs. PTH alone). PTH + 1.00 micron/min EGTA lowered Ca++ more, and 1,25(OH)2D3 increased to 148 +/- 29 (P less than 0.01 vs. saline or PTH alone). PTH + 1.33 micron/min EGTA lowered Ca++ below values seen with saline or PTH alone, and 1,25(OH)2D3 rose to 267 +/- 46 (P less than 0.003 vs. all other groups). Thus, during PTH infusion lowering Ca++ with EGTA raised 1,25(OH)2D3 progressively. There were no differences in serum phosphorus concentration or in arterial blood pH in any group infused with PTH. The log of serum 1,25(OH)2D3 was correlated inversely with Ca++ in all four groups infused with PTH (r = -0.737, n = 31, P less than 0.001), and also when the saline group was included (r = -0.677, n = 41, P less than 0.001). The results of this study indicate that serum 1,25(OH)2D3 may be regulated by Ca++ independent of PTH and serum phosphorus levels in the rat. Since 1,25(OH)2D3 regulates gastrointestinal calcium absorption, there may be direct feedback control of 1,25(OH)2D3, by its regulated ion, Ca++.     

老年男性2型糖尿病患者甲状旁腺素、维生素D与骨密度的关系

目的 探讨老年男性2型糖尿病患者主要钙调激素甲状旁腺素(PTH)和维生素D的变化对骨密度的影响.方法 应用双能X线骨密度仪测定60例老年男性2型糖尿病患者的腰椎和髋部骨密度,检测血清中骨代谢及血糖相关的指标,并根据骨密度测定结果将60例老年男性2型糖尿病患者分为骨量减少组(32例)、骨质疏松组(12例)、正常组(16例),测定3组的血清PTH和25羟维生素D3,分析其与患者不同部位骨密度的相关性.结果 依据患者腰椎或髋部的骨密度值,骨质疏松的检出率为20.0％(12/60),骨量减少的检出率为53.3％(32/60).3组的血清PTH比较差异有统计学意义(F=3.32,P=0.043),骨量减少组、骨质疏松组与正常组相比,PTH水平明显上升[(44.87±10.62)、(50.24±20.32)μg/L与(36.96±12.36)μg/L,P均＜0.05].但25羟维生素D3浓度3组比较差异无统计学意义(P＞0.05).相关分析显示,PTH水平与髋部骨矿面密度(BMD)呈显著负相关(r=-0.224,P ＜0.05),与腰椎BMD无显著相关性(r=-0.187,P＞0.05).结论 老年男性2型糖尿病患者的髋部BMD与血清PTH浓度负相关.     

Serum 1,25 dihydroxy vitamin D (1,25(OH)2D3), 25 hydroxy vitamin D (25(OH)D) and parathormone levels in diabetic retinopathy

OBJECTIVES: To investigate whether there is a relationship between serum 1,25 dihydroxy vitamin D3 [1,25(OH)2D3], which is an inhibitor of angiogenesis, concentrations and severity of diabetic retinopathy (DR). DESIGN AND METHODS: Serum 1,25(OH)2D3, 25 hydroxy vitamin D [25(OH)D] and parathormone (PTH) concentrations were measured in diabetic patients (n = 66) and nondiabetic healthy subjects (n = 20). RESULTS: The mean serum 1,25(OH)2D3 concentration in diabetic patients was lower than that in nondiabetics (57.3+/-21.44 vs. 89.4+/-18.01 pmol/L, p<0.001); mean 1,25(OH)2D3 concentrations fell with increasing severity of DR [being 63.4+/-17.26 pmol/L for background DR (BDR), 47.7+/-13.27 pmol/L for preproliferative DR (pre-PDR), and 43.1+/-19.45 pmol/L for proliferative DR (PDR)]. Compared with the control group, serum 25(OH)D concentrations were found to be decreased in diabetic patients (p<0.001).There were negative correlations between 1,25(OH)2D3 and age (r = -0.331, p<0.01) and duration of diabetes (r = -0.255, p<0.05). CONCLUSION: From these findings, it was found that there was an inverse relationship between the severity of the retinopathy, i.e., neovascularization, and serum 1,25(OH)2D3 concentrations, being the lowest in PDR and the highest in diabetic patients without retinopathy (NDR) patients. The measurement of serum 1,25(OH)2D3 concentrations might be helpful to predict severity of DR in patients with diabetes mellitus.     

Regulation of parathyroid hormone gene expression by hypocalcemia, hypercalcemia, and vitamin D in the rat.

In vivo in the rat 1,25(OH)2D3 decreases and a low calcium increases PTH mRNA levels. We now report the effect of 3 and 8 wk of changes in dietary vitamin D and calcium on PTH mRNA levels. PTH mRNA levels were increased by 3 wk of calcium deficiency (five times), a vitamin D-deficient diet (two times), and combined deficiency (10 times), but not changed by high calcium. Vitamin D-deficient-diet rats' PTH mRNA did not decrease after a single large dose of 1,25(OH)2D3, but did decrease partially after repeated daily doses of 1,25(OH)2D3. Rats after a vitamin D-, calcium-deficient (-D-Ca) diet did not respond to changes in serum calcium at 1 h. Flow cytometry of isolated cells from parathyroid-thyroid tissue separated the smaller parathyroid from the larger thyroid cells and allowed an analysis of parathyroid cell number. In normal vitamin D/normal calcium (NDNCa) rats the parathyroid cells were 24.7 +/- 3.4% (n = 6) of the total cell number, whereas in -D-Ca rats they were 41.8 +/- 6.6% (n = 6) (P less than 0.05). That is, -D-Ca rats had 1.7 times the number of cells, whereas they had 10 times the amount of PTH mRNA, indicating the major contribution (6 times) of increased PTH gene expression per cell. Moreover, a calcium-deficient, more so than a vitamin D-deficient diet, amplifies the expression of the PTH gene, and vitamin D is necessary for an intact response of PTH mRNA to 1,25(OH)2D3 or calcium.     

Effects of active vitamin D3 and parathyroid hormone on the serum osteocalcin in idiopathic hypoparathyroidism and pseudohypoparathyroidism.

Serum osteocalcin was measured in patients with idiopathic hypoparathyroidism or pseudohypoparathyroidism, before or during the treatment with active vitamin D3 (1,25(OH)2D3 or 1 alpha OHD3). Serum osteocalcin and plasma 1,25(OH)2D were decreased in 11 patients with idiopathic hypoparathyroidism before treatment (2.8 +/- 1.27 ng/ml, P less than 0.001 and 14.3 +/- 4.27 pg/ml, P less than 0.001, respectively). In 24 patients with idiopathic hypoparathyroidism during the treatment, serum osteocalcin and plasma 1,25(OH)2D were within the normal range (4.5 +/- 0.74 ng/ml and 25.7 +/- 5.69 pg/ml, respectively). In five patients with pseudohypoparathyroidism before treatment, plasma 1,25(OH)2D was decreased (15.6 +/- 10.6 pg/ml, P less than 0.001) but serum osteocalcin was normal (7.8 +/- 1.66 ng/ml). In nine patients with pseudohypoparathyroidism during the treatment with active vitamin D3, serum osteocalcin and plasma 1,25(OH)2D were normal (6.8 +/- 1.47 ng/ml and 27.2 +/- 6.0 pg/ml, respectively). Serum PTH in pseudohypoparathyroidism was increased before treatment (0.70 +/- 0.34 ng/ml, P less than 0.05) and was normal during the treatment (0.50 +/- 0.13 ng/ml). In idiopathic hypoparathyroidism, the active vitamin D3 increased serum osteocalcin without PTH. In pseudohypoparathyroidism, PTH may increase serum osteocalcin or modulate the effect of active vitamin D3 on serum osteocalcin.     

老年糖尿病患者维生素D与握力和肌肉质量相关性研究

目的研究老年2型糖尿病(type 2 diabetes mellitus,T2DM)患者维生素D水平与肌肉质量和握力的相关性。方法选取2016年5月至2018年1月入住宣武医院内分泌科年龄≥60岁的2型糖尿病患者201例进行前瞻性研究,根据25羟维生素D[25-hydroxyvitamin D,25(OH)D]水平分为维生素D缺乏组[25(OH)D<20μg/L]140例和非缺乏组[20μg/L≤25)(OH)D<70μg/L]61例,测定患者握力、步速及上下肢肌肉质量。并进行体格检查和实验室检查。结果两组患者实验室各项指标比较差异均无统计学意义(P均>0.05)。维生素D非缺乏组患者的握力、上肢及下肢肌肉含量显著高于缺乏组[(33.49±9.43)kg与(29.59±10.30)kg、(4.99±1.09)kg与(4.57±1.11)kg、(15.69±3.10)kg与(14.54±3.03)kg,P值分别为0.010、0.015、0.017]。多因素Logistic回归分析显示维生素D缺乏与握力减低及下肢肌肉质量下降独立相关(OR=1.286,95%CI:1.197~1.346,P<0.01;OR=1.231,95%CI:1.102~1.283,P<0.05)。结论维生素D缺乏是老年2型糖尿病患者握力减低及下肢肌肉质量下降的危险因素。     

Marked suppression of secondary hyperparathyroidism by intravenous administration of 1,25-dihydroxy-cholecalciferol in uremic patients

Current evidence suggests that administration of 1,25(OH)2D3 to patients with chronic renal insufficiency results in suppression of secondary hyperparathyroidism only if hypercalcemia occurs. However, since the parathyroid glands possess specific receptors for 1,25(OH)2D3 and a calcium binding protein, there is considerable interest in a possible direct effect of 1,25(OH)2D3 on parathyroid hormone (PTH) secretion independent of changes in serum calcium. Recent findings indicate substantial degradation of 1,25(OH)2D3 in the intestine, therefore, it is possible that while oral administration of the vitamin D metabolite increases intestinal calcium absorption, the delivery of 1,25(OH)2D3 to peripheral target organs may be limited. We therefore compared the effects of orally or intravenously administered 1,25(OH)2D3 on the plasma levels of 1,25(OH)2D3 and the effects of these two modes of treatment on PTH secretion. Whereas oral administration of 1,25(OH)2D3 in doses adequate to maintain serum calcium at the upper limits of normal did not alter PTH levels, a marked suppression (70.1 +/- 3.2%) of PTH levels was seen in all 20 patients given intravenous 1,25(OH)2D3. Temporal studies suggested a 20.1 +/- 5.2% decrease in PTH without a significant change in serum calcium with intravenous 1,25(OH)2D3. In five patients the serum calcium was increased by the oral administration of calcium carbonate, the decrement in serum i-PTH was only 25 +/- 6.65% when compared with 73.5 +/- 5.08% (P less than 0.001) obtained by the administration of intravenous 1,25(OH)2D3. Thus, a similar serum calcium achieved by intravenous 1,25(OH)2D3 rather than calcium carbonate has a greater suppressive effect in the release of PTH. These studies indicate that 1,25(OH)2D3 administered intravenously rather than orally may result in a greater delivery of the vitamin D metabolite to peripheral target tissues other than the intestine and allow a greater expression of biological effects of 1,25(OH)2D3 in peripheral tissues. The use of intravenous 1,25(OH)2D3 thus provides a simple and extremely effective way to suppress secondary hyperparathyroidism in dialysis patients.     

中国北方地区老年人冬季维生素D缺乏与骨量丢失

背景：中国北方地区老年人维生素D营养状态存在季节变化,冬春季维生素D缺乏严重。目的：分析沈阳市老年人冬季维生素D缺乏对骨量丢失的影响。方法：随机选择沈阳市60岁以上汉族健康老年人100名,于2000-03检测受试者血浆中25羟维生素D、甲状旁腺激素、钙和磷,清晨空腹2h尿中脱氧吡啶、钙、磷、肌酐,2000-03/2005-03两次检测髋部骨密度。结果与结论：基线时,血浆25羟维生素D浓度为（31.0±12.30）nmol/L,40%受试者低于25nmol/L;血浆甲状旁腺激素水平为（29.4±11.5）ng/L,血浆25羟维生素D浓度低于25nmol/L者甲状旁腺激素水平为（34.6±13.5）ng/L,血浆25羟维生素D浓度与甲状旁腺激素呈负相关（r=-0.479,P〈0.0001）。5年后股骨颈骨丢失率为（3.05±4.07）%,大转子为（1.46±5.02）%,经体质量和身高变化率校正后,股骨颈骨丢失率与基线血浆25羟维生素D浓度呈负相关（r=-2.3,P=0.02）,股骨颈骨丢失率基线血浆25羟维生素D浓度≤25nmol/L者高于浓度〉25nmol/L者103%（F=7.2062,P=0.0085）。其他检测指标与骨丢失无显著相关性。说明老年人群冬季维生素D缺乏严重,维生素D缺乏促进骨量丢失,影响骨健康。     

Assessment of vitamin D and calcium status in healthy adult Austrians

BACKGROUND: Because there is reason to assume that also in Austria calcium and vitamin D malnutrition is wide-spread, we initiated a comprehensive study on calcium and vitamin D status in relation to bone health in a large group of the normal adult population. SUBJECTS AND METHODS: We assessed dietary calcium and vitamin D intake, serum concentrations of Ca2+, phosphate, alkaline phosphatase, 25(OH)D, 1,25(OH)2D, parathyroid hormone (PTH), follicle-stimulating hormone (FSH), sex hormones and bone mineral density (BMD) by double-energy X-ray absorptiometry at five different skeletal sites in 648 females and 400 males (age 21-76 years). RESULTS: Mean daily intake of vitamin D (101 IU, range 0.2-320) and calcium (569 mg, range 40-2170) was significantly less than the respective recommended dietary allowances. Two hundred and seventy-one (26%) individuals had hypovitaminosis D with serum 25(OH)D < 12 ng mL(-1), while serum Ca2+ was less than normal in 82 (7.8%) subjects. Multiple regression analysis revealed significant correlations between mean calcium intake and BMD in the femoral region in the men (r = 0.13, P < 0.05) though not in the women. No consistent data could be obtained for associations between BMD and vitamin D status, except for 25(OH)D and BMD at the spine in the men (r = 0.10, P < 0.05). 25(OH)D correlated negatively (P < 0.05) with age in the women (r = -0.11) and with PTH in the women (r = -0.11) and men (r = -0.16). Inversely, a significant (P < 0.001) age-related increase in PTH was observed in both sexes (men, r = 0.19; women, r = 0.14). CONCLUSIONS: Prevalence of hypovitaminosis D in adult Austrians is an imminent risk for development of secondary hyperparathyroidism with advancing age, and requires timely correction of nutritional deficits.     

Parathyroid hormone suppression by intravenous 1,25-dihydroxyvitamin D. A role for increased sensitivity to calcium.

Numerous in vitro studies in experimental animals have demonstrated a direct suppressive effect of 1,25-dihydroxyvitamin D (1,25(OH)2D) on parathyroid hormone (PTH) synthesis. We therefore sought to determine whether such an effect could be demonstrated in uremic patients undergoing maneuvers designed to avoid changes in serum calcium concentrations. In addition, the response of the parathyroid gland in patients undergoing hypercalcemic suppression (protocol I) and hypocalcemic stimulation (protocol II) before and after 2 wk of intravenous 1,25(OH)2D was evaluated. In those enlisted in protocol I, PTH values fell from 375 +/- 66 to 294 +/- 50 pg (P less than 0.01) after 1,25(OH)2D administration. During hypercalcemic suppression, the "set point" (PTH max + PTH min/2) for PTH suppression by calcium fell from 5.24 +/- 0.14 to 5.06 +/- 0.15 mg/dl (P less than 0.05) with 1,25(OH)2D. A similar decline in PTH levels after giving intravenous 1,25(OH)2D was noted in protocol II patients. During hypocalcemic stimulation, the parathyroid response was attenuated by 1,25(OH)2D. We conclude that intravenous 1,25(OH)2D directly suppresses PTH secretion in uremic patients. This suppression, in part, appears to be due to increased sensitivity of the gland to ambient calcium levels.