活性维生素D和低钙透析液治疗血液透析患者继发性甲状旁腺功能亢进的疗效观察

目的探讨新进入血液透析的13例患者使用活性维生素D和低钙透析液（含钙1.25mmol/L）治疗继发性甲状旁腺功能亢进的疗效及不良反应.方法选择北京医院肾内科13例患者首先使用低钙透析液透析,根据继发性甲状旁腺功能亢进的程度给予活性维生素D治疗;观察7～18个月,记录血钙、磷、钙磷乘积和iPTH的变化及其它不良反应.结果治疗2个月时,13例患者血钙明显升高,iPTH水平显著降低（P＜0.05）;钙磷乘积和血磷有所增高（P＞0.05）;在结束观察时,钙磷乘积和血磷较治疗前显著增高（P＜0.05）,血钙、磷和钙磷乘积较治疗2个月时增高（P＞0.05）;11例患者的iPTH在150～320pg/ml范围波动,2例患者iPTH出现反弹.13例患者对低钙透析液的耐受性良好.结论活性维生素D和低钙透析液对新进入血液透析患者的继发性甲状旁腺功能亢进治疗效果良好,对于透析前磷高而钙不低的患者,推荐使用低钙透析液,可减少因服用含钙的磷结合剂所致体内钙负荷增加的危险,达到降低血钙磷乘积和减少心血管钙化的目的.     

骨化三醇联合低钙透析液治疗血液透析患者继发性甲状旁腺功能亢进的疗效观察

[目的]探讨血液透析患者使用骨化三醇（钙三醇）和低钙透析液（含钙1.25 mmoI/L）治疗继发性甲状旁腺功能亢进的疗效及不良反应.[方法]选择本院血液透析中心维持性血液透析患者12例,首先使用低钙透析液透析,根据继发性甲状旁腺功能亢进的程度给予骨化三醇治疗;观察6个月,记录血钙、磷、钙磷乘积和全段甲状旁腺素（iPTH）的变化及其他不良反应.[结果]治疗2个月时,12例患者血钙明显升高,iPTH水平显著降低（P〈0.05）,钙磷乘积和血磷有所增高（P〉0.05）;在结束观察时,钙磷乘积和血磷较治疗前显著增高（P〈0.05）,血钙、磷和钙磷乘积较治疗2个月时增高（P〉0.05）;10例患者的iPTH在150～320 pg/mL范围波动,2例患者iPTH出现反弹.12例患者对低钙透析液的耐受性良好.[结论]骨化三醇和低钙透析液对血液透析患者的继发性甲状旁腺功能亢进治疗效果良好,对于透析前血钙不低的患者,推荐使用低钙透析液,可减少因服用含钙的磷结合剂所致体内钙负荷增加的危险,达到降低钙磷乘积和减少心血管钙化的目的.     

低钙透析在维持性血透患者继发甲状旁腺功能亢进治疗中的应用

目的探讨低钙透析在维持性血液透析继发甲状旁腺功能亢进（甲旁亢）患者骨化三醇冲击治疗中的作用及安全性。方法采用稀释后浓度为1．25mmol/L低钙透析液,观察50例维持性透析继发甲旁亢患者在骨化三醇冲击治疗中应用低钙透析3个月的血清钙、磷、钙磷乘积、iPTH指标变化。结果所有病例血钙维持正常水平,血磷下降明显,PTH下降明显。透析过程中出现肌痉挛10％（5／50）,低血压反应4％（2／50）,心悸2％（1／50）,经处理均缓解。结论维持性血液透析患者继发甲状旁腺功能亢进在骨化三醇冲击治疗中同时应用低钙透析是安全有效的。低钙透析提高了对活性维生素D3和碳酸钙治疗的耐受性,避免了高钙血症和转移性钙化的出现。     

比较血液透析患者在不同PTH状态下低钙透析液的疗效

目的通过观察不同甲状旁腺激素(PTH)状态下合并高钙血症的血液透析患者应用低钙透析液的疗效,以肯定其实用性。方法选择27例维持性血液透析合并高钙血症患者,根据iPTH水平分为三组:I组血iPTH<120pg/ml,考虑低转运骨病(lowturnoverbonediease,LTBD),共6例;II组血iPTH不相识120～600pg/ml,即PTH合适或轻度甲状旁腺功能亢进组,共13例;III组血iPTH600～1000pg/ml,重度继发甲旁亢需活性维生素D冲击治疗组,共8例;三组患者应用低钙透析液(1.25mmol/L)三个月后比较血清钙、磷、钙磷乘积及血iPTH的变化。结果应用低钙透析液后,三组患者透析前、后血钙都有明显下降(P<0.05),尤其透析后血钙下降更明显(P<0.01);透析前、后血磷变化不大;透析前、后钙磷乘积全部下降(P<0.05);LTBD组iPTH明显升高(P<0.05),其余二组iPTH虽有所升高,但无显著性差异(P>0.05)。观察中不良反应的发生率为6/27(22.2%),主要有肌痉挛、低血压和心律失常,除1例肌痉挛不能耐受而退出以外,余5例经对症处理后尚能坚持完成3个月的观察。结论对不同原因导致的血液透析患者高钙血症,包括活性维生素D冲击治疗及LTBD患者,都适宜个体化的低钙透析液进行透析,可以降低高钙血症及钙磷乘积,但要定期监测血清钙、磷及PTH的变化。     

低钙透析在血液透析继发性甲旁亢25例治疗中的应用和护理

目的探讨低钙透析在血液透析患者继发性甲状旁腺功能亢进进行骨化三醇冲击治疗中的临床应用。方法采用浓度1.25 mmol/L低钙透析液,观察25例维持性血液透析继发甲旁亢患者在骨化三醇冲击治疗中血清钙、磷、钙磷乘积,血清全段甲状旁腺素(iPTH)等指标变化。结果所有患者治疗期间的血钙与治疗前比较差异无统计学意义(P>0.05),血磷、钙磷乘积,iPTH水平均较治疗前降低(P<0.05)。结论维持性血液透析继发甲旁亢患者在骨化三醇冲击治疗中同时应用低钙透析是安全有效的,避免了高钙血症,降低了骨外软组织钙化的风险。     

低钙透析液对钙磷代谢及甲状旁腺素的影响

目的：探讨应用低钙透析液对血液透析患者钙磷代谢及甲状旁腺功能的影响。方法：15例有高磷血症的血液透析患者，应用1．25mmol／L钙浓度透析液透析8个月，比较透析前与4个月、8个月后血清钙、磷、钙磷乘积及甲状旁腺激素的变化。结果：应用低钙透析液4个月后，患者血钙、血磷及钙磷乘积均明显下降，甲状旁腺激素下降，但差异无统计学意义。8个月后，与实验前比较，血钙及钙磷乘积明显下降，血磷下降，甲状旁腺激素升高。与透析4个月比较，血钙无明显下降，血磷升高，甲状旁腺激素明显升高。结论：短期使用低钙透析液可降低血钙和钙磷乘积水平，降低甲状旁腺激素，长期应用，可能加重继发性甲状旁腺功能亢进。     

1,25（OH）2D3治疗终末期肾病84例分析

目的探讨1,25（OH）2D3治疗终末期肾病患者继发性甲状旁腺功能亢进症有效性和安全性。方法分析血液净化中心84例患者服用1,25（OH）2D3、含钙磷结合剂后血钙、磷、钙磷乘积,iPTH变化。结果血钙、磷、钙磷乘积,iPTH发生变化。结论终末期肾病患者合理活性维生素D3等治疗后血钙、磷、钙磷乘积可达到正常动态平衡。     

骨化三醇联合低钙透析在维持性血液透析老年患者中的应用——附17例报告

目的:探讨骨化三醇联合低钙透析对老年维持性血液透析患者继发性甲状旁腺功能亢进(secondary hyperparathyroidism,SHPT)的临床疗效及安全性.方法:17例SHPT患者,根据其全段甲状旁腺素(intact parathyroid hormone,iPTH)水平分为轻度组(iPTH 300～600 ng/L)和中度组(iPTH 601～1 000 ng/L),在低钙透析(透析液钙浓度为1.25 mmol/L)的基础上,轻度组予骨化三醇1 μg,中度组患者予骨化三醇2 μg,均于透析后当日20:00～22:00口服,连续20周.治疗过程中,骨化三醇用量根据钙磷乘积进行调整.观察治疗前后患者血钙、血磷、钙磷乘积、iPTH、血清白蛋白(serum albumin,SAB)等指标及药物用量变化情况.结果:所有患者均能完成疗程.17例患者治疗期间的血钙和SAB水平与治疗前比较,差异无统计学意义(P＞0.05),钙磷乘积、iPTH水平均较治疗前降低(P＜0.05～0.01).2例出现高血压、1例出现肌痉挛,经处理后症状均消失.结论:骨化三醇联合低钙透析可有效控制老年维持性血液透析患者的SHPT,安全性良好.     

低甲状旁腺激素水平的血液透析患者应用1.25mmol/L钙浓度透析液的临床观察

目的探讨应用1.25mmol/L钙浓度透析液对于低甲状旁腺激素(iPTH)水平的血液透析(HD)患者钙磷代谢及甲状旁腺功能的影响。方法选择北京医院血液净化中心26例血清全段iPTH水平低于100pg/ml的HD患者,应用1.25mmol/L钙浓度透析液,同时停用活性维生素D治疗。观察12个月,比较观察前与3个月、6个月和12个月后血清钙、磷、钙磷乘积及iPTH的变化。结果应用低钙透析液3个月后患者血钙显著下降[(2.63±0.29)mmol/Lvs(2.38±0.13)mmol/L,P<0.05],此后保持稳定,不再继续下降。血磷浓度呈逐渐下降趋势,但差异无显著性。钙磷乘积在进入观察后3个月时已有显著下降[(53.14±13.6)mg2/dl2vs(46.74±9.47)mg2/dl2,P<0.05],此后仍呈下降趋势,但较3个月时差异无显著性。6个月时血清iPTH由观察前的(57.79±36.61)pg/ml升高至(131.12±76.17)pg/ml(P<0.05),此后继续保持此水平。结论1.25mmol/L钙浓度透析液可以降低血钙和钙磷乘积水平,改善被过度抑制的甲状旁腺功能;在维持血钙正常的情况下,较少发生甲状旁腺的过度刺激,适合应用于有高血钙倾向、且钙化危险性增加的低iPTH水平的透析患者。     

改变透析液钙浓度对血液透析患者血清钙、磷及甲状旁腺素的影响

钙磷代谢紊乱，继发甲状旁腺机能亢进及骨病是肾衰竭血液透析患的重要并发症之一，随着含钙的磷结合剂及针剂对甲状旁腺功能亢进的活性维生素D的广泛应用，血液透析患常出现高钙血症，而使用钙浓度1．75mmol／L的透析液透析后，加重高钙血症，使钙磷乘积增加，血管壁、脏器、软组织钙化的危险性增加。因此设法维持适当的钙磷平衡至关重要。北京世纪坛医院血液透析中心将透析液钙浓度由1．75mmol／L降至1．50mmol／L，并观察血钙、血磷、钙磷乘积、iPTH等蛮化。[第一段]     

Relative bioavailability of calcium from calcium formate, calcium citrate, and calcium carbonate

Calcium is an essential nutrient required in substantial amounts, but many diets are deficient in calcium making supplementation necessary or desirable. The objective of this study was to compare the oral bioavailability of calcium from calcium formate, a new experimental dietary calcium supplement, to that of calcium citrate and calcium carbonate. In a four-way crossover study, either a placebo or 1200 mg of calcium as calcium carbonate, calcium citrate, or calcium formate were administered orally to 14 healthy adult female volunteers who had fasted overnight. After calcium carbonate, the maximum rise in serum calcium ( approximately 4%) and the fall in serum intact parathyroid hormone 1-84 (iPTH) (approximately 20-40%) did not differ significantly from placebo. After calcium citrate, the changes were modestly but significantly (p < 0.05) greater, but only at 135 to 270 min after ingestion. In contrast, within 60 min after calcium formate serum calcium rose by approximately 15% and serum iPTH fell by 70%. The mean increment in area under the plasma concentration-time curve (0-270 min) for serum calcium after calcium formate (378 mg . min/dl) was double that for calcium citrate (178 mg . min/dl; p < 0.01), whereas the latter was only modestly greater than either placebo (107; p < 0.05) or calcium carbonate (91; p < 0.05). In this study, calcium formate was clearly superior to both calcium carbonate and calcium citrate in ability to deliver calcium to the bloodstream after oral administration. Calcium formate may offer significant advantages as a dietary calcium supplement.     

Meta-analysis of calcium bioavailability: a comparison of calcium citrate with calcium carbonate

OBJECTIVE: To perform a meta-analysis of data from available published trials comparing the bioavailability of calcium carbonate with that of calcium citrate. DATA SOURCES: The whole set was comprised of 15 studies involving 184 subjects who underwent measurement of calcium absorption from calcium carbonate and calcium citrate. Category A excluded four studies for lack of physiological relevance, use of a mixed preparation with low content of calcium carbonate, or wide variability in results. Category B was comprised of five studies (from Category A) involving 71 subjects who took calcium supplements on an empty stomach. Category C was comprised of six studies (from Category A) involving 65 subjects who took calcium preparations with meals. METHOD: The meta-analysis of calcium absorption data from calcium carbonate and calcium citrate, with calculation of effect size and 95% confidence intervals. RESULTS: Calcium absorption from calcium citrate was consistently significantly higher than that from calcium carbonate by 20.0% in the whole set, by 24.0% in Category A, by 27.2% on an empty stomach, and by 21.6% with meals. CONCLUSION: Calcium citrate is better absorbed than calcium carbonate by approximately 22% to 27%, either on an empty stomach or co-administered with meals.     

Comparison of serum total calcium, albumin-corrected total calcium, and ionized calcium in 1213 patients with suspected calcium disorders

The correlations between serum ionized calcium, serum total calcium, total calcium corrected for albumin and calculated ionized calcium were investigated in a prospective multicentre investigation of 1213 patients suspected of having calcium metabolic disease. Diagnostic discordance between serum total calcium and measured ionized calcium was found in 31% of the patients. With the calculation of albumin-corrected total calcium or calculated ionized calcium the discordance decreased to 17.9%. The diagnostic discordance which could be ascribed to the analytical imprecision (CV = 1.5%) amounted to only 6.7%. Although we found highly significant correlations between the parameters, a considerable scatter around the regression line made prediction of ionized calcium from albumin-corrected total calcium unreliable in many patients.     

Cerebral calcium embolism

A new‐onset neurological deficit after calcified aortic valve replacement and an hyperdense image on the computed tomography raised suspicion of an stroke of unusual etiology.     

Receptor-regulated calcium entry

A wide variety of hormones and neurotransmitters activate cellular responses by mobilizing cellular Ca2+. In general, this Ca2+ mobilization response is comprised of a release of Ca2+ from intracellular stores, as well as increased entry of Ca2+ into the cytoplasm from the extracellular space. The mechanism for release of intracellular Ca2+ results from the Ca2(+)-mobilizing actions of a second messenger, D-myo-inositol 1,4,5-trisphosphate. Inositol polyphosphates appear also to be involved in the activation of Ca2+ entry, but the mechanism by which this is accomplished is less clear. According to the capacitative model for Ca2+ entry, the depletion of the agonist-regulated intracellular Ca2+ pool by the action of D-myo-inositol 1,4,5-trisphosphate is somehow coupled to the activation of Ca2+ entry. The evidence for this model comes from the demonstration, by diverse strategies, that the same Ca2+ entry mechanism normally activated by Ca2(+)-mobilizing agonists can be equally well triggered by depletion of the intracellular Ca2+ pool, even in the absence of receptor activation or elevated cellular levels of inositol polyphosphates.