ADA试剂对镁离子测定结果干扰的评价

目的：探讨腺苷脱氨酶（ADA）试剂对全自动生化分析仪镁离子测定的影响。方法测定ADA 试剂中的镁离子浓度;单独比较测定混合血清中的镁离子和先测定ADA再测定镁离子的检测结果;将不同浓度ADA 试剂加入标本中测定其镁离子浓度的变化。结果 ADA试剂中镁离子含量为0．739 mmol/L。单独测镁离子与先测ADA 再测镁离子的结果比较差异有统计学意义（P＜0．05）。镁离子结果增加的幅度与ADA试剂的量呈直线相关。结论 ADA试剂对镁离子测定有正干扰。     

全自动生化分析仪上胱抑素C试剂对血清钙测定的影响

目的研究在全自动生化分析仪上胱抑素C试剂对血清钙测定的影响。方法单独测定血清钙,在测定胱抑素C后再测定血清钙,比较两结果的异同;将混合血清用不同浓度的胱抑素C试剂I稀释,测定血清钙浓度,观察试剂I对结果的影响。结果单独测定血清钙浓度是（2．56±0．056）mmol／L,在测定胱抑素c后测得的血清钙浓度是（2．28±0．053）mmol／L,差异有统计学意义（t=22．97≥t0.05．19=2．093,P〈0．05）;混合血清用不同浓度的胱抑素c试剂I稀释后,血清钙检测结果减少的幅度与胱抑素C试剂I的浓度呈直线正相关（r=0．982）。结论胱抑素C试剂对血清钙测定有负干扰,在生化分析仪上检测时应放在不同检测单元中进行。     

四种生化分析试剂对生化分析仪测定血清镁结果的影响

目的 探讨肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、高密度脂蛋白胆固醇(HDL-C)、甘油三酯(TG)4种分析试剂对奥林帕斯AU2700全自动分析仪测定血清镁结果的影响.方法 4个项目各检测后再测镁与单测血清镁结果作比较;混合血清加入生理盐水和4种分析试剂1,制成5份标本,每份均重复测定10次;混合血清单测镁10次作为对照,分别测定每一项目5次后,再连续测定混合血清镁10次.结果 CK或CK-MB、HDL-C、TG测定后再测镁与单测镁结果比较,差异均具有统计学意义(P＜0.01);4种分析试剂1对血清镁测定结果均有明显的正干扰;测CK或CK-MB、TG后再测镁对结果影响持续到第2管,测HDL-C后再测镁对结果影响持续到第3管.结论 自动生化分析仪测定CK或CK-MB、TG后再测定血清镁,中间间隔至少要有2个、测定HDL-C后再测定血清镁,中间间隔至少要有3个对镁离子测定无干扰的分析项目或启用试剂针特殊的清洗程序,如为高级生化分析仪应将该实验的项目置于不同的分析模块,以避免试剂针携带污染对测定结果的影响.     

四种生化分析试剂对生化分析仪测定血清镁结果的影响

目的探讨肌酸激酶（CK）、肌酸激酶同工酶（CK-MB）、高密度脂蛋白胆固醇（HDL-C）、甘油三酯（TG）4种分析试剂对奥林帕斯AU2700全自动分析仪测定血清镁结果的影响。方法4个项目各检测后再测镁与单测血清镁结果作比较;混合血清加入生理盐水和4种分析试剂1,制成5份标本,每份均重复测定10次;混合血清单测镁10次作为对照,分别测定每一项目5次后,再连续测定混合血清镁10次。结果CK或CK-MB、HDL-C、TG测定后再测镁与单测镁结果比较,差异均具有统计学意义﹙P〈0.01﹚;4种分析试剂1对血清镁测定结果均有明显的正干扰;测CK或CK-MB、TG后再测镁对结果影响持续到第2管,测HDL-C后再测镁对结果影响持续到第3管。结论自动生化分析仪测定CK或CK-MB、TG后再测定血清镁,中间间隔至少要有2个、测定HDL-C后再测定血清镁,中间间隔至少要有3个对镁离子测定无干扰的分析项目或启用试剂针特殊的清洗程序,如为高级生化分析仪应将该实验的项目置于不同的分析模块,以避免试剂针携带污染对测定结果的影响。     

四种分析试剂对生化分析仪测定血清镁结果的影响

摘要 目的 探讨肌酸激酶（CK-MB）、肌酸激酶同工酶（CK-MB）、高密度脂蛋白胆固醇（HDL-C）、甘油三酯（TG）四种分析试剂对奥林帕斯AU2700全自动分析仪测定血清镁结果的影响。方法 单测血清镁分别与四个项目检测后再测镁结果做比较；混合血清分别加入生理盐水和四个项目分析试剂1，制成5份标本，每份均重复测定10次；混合血清单测镁10次作为对照，分别测定四个项目3次后，各重复测定混合血清镁10次。结果 凡CK、CK-MB、HDL-C、TG测定后再测镁与单测镁结果比较，差别均有非常显著性意义﹙P＜ 0.01﹚；四种分析试剂1对血清镁测定结果均有明显的正干扰；四种试剂对镁测定结果影响：CK、CK-MB、TG持续到第3管，HDL-C持续到第4管。结论 自动生化分析仪测定CK还是CK-MB、TG后再测定血清镁，中间间隔至少要有三个项目分析试剂，测定HDL-C后再测定血清镁，中间间隔至少要有四个项目分析试剂对镁离子测定无影响的分析项目或启用试剂针特殊的清洗程序，如为高级生化分析仪应将相互有影响的项目置于不同的分析模块，以避免试剂携带污染对测定结果的影响。     

卤族和类卤族元素对氯化物测定的干扰研究

[目的]研究卤族元素溴、碘和氟离子以及类卤族元素硫氰酸和迭氮离子对不同测定氯离子方法的干扰情况。[方法]使用混合血清建立对照组和加入不同浓度可疑干扰物质的实验组，分别使用酶法、硫氰酸汞比色法、离子选择电极法和硝酸汞滴定法测定血清氯化物，计算干扰百分率进行比较。[结果]样品中加入可疑干扰物终浓度达10mmol／L的溴化钾、83．3mmol／L的碘化钾、50．0mmol／L的氟化钠或100．0mmol／L的氟化钾、10mmol／L的硫氰酸钾和15．87mmol／L的迭氮钠对酶法测定氯化物无干扰：氟化物对测定氯化物的4种方法均无干扰；上述浓度的溴、碘、硫氰酸和迭氮离子对硫氰酸汞比色法和硝酸汞滴定法具有显著的正干扰作用；溴、碘和硫氰酸离子对离子选择电极法亦具有显著正干扰。[结论]卤族元素氟的化学性质与其它卤族元素：氯、溴、碘离子和类卤族元素：硫氰酸和迭氮离子不同，对氯化物测定无干扰，酶法测定血清氯化物在抗卤族元素和类卤族元素干扰方面具有显著的优越性。     

肌酐酶法试剂对总胆汁酸测定的干扰作用

目的探讨肌酐酶法试荆对总胆汁酸测定的干扰,指导全自动生化分析仪测试项目顺序的编排。方法①取lO管血清,每管血清均平分为2份,测试组为血清＋肌酐酶法试剂,对照组为血清＋生理盐水,比较两组血清的总胆汁酸测定结果。②取1份血清,首先连续10次单独测定其总胆汁酸,然后连续10次交替测定肌酐与总胆汁酸．比较单独测定组与交替测定组的总胆汁酸测定结果。结果①测试组的总胆汁酸测定结果显著大于对照组,两组比较差异有统计学意义（P〈0．01）。②交替测定组的总胆汁酸测定结果显著大于单独测定组,两组比较差异有统计学意义（P〈0,01）。结论在全自动生化分析仪上编排测试项目时应注意肌酐酶法试剂总胆汁酸测定的干扰,可将总胆汁酸设置在肌酐之间,或者在肌酐与总胆汁酸之间插入其他项目。     

糖化血清蛋白酶法试剂对总胆汁酸测定的影响

目的探讨糖化血清蛋白酶法试剂对日立7600—010全自动生化分析仪测定总胆汁酸结果的影响。方法取混合血清,按照先测定糖化血清蛋白再测定胆汁酸的顺序．观察糖化血清蛋白试剂对胆汁酸测定的影响,并与对照组比较;将糖化血清蛋白的R1试剂、R2试剂及混合工作试剂加入血清中,确定试剂的干扰因素;应用仪器的特殊清洗程序使用不同的清洗液,观察仪器特殊清洗排除试剂间干扰的效果。结果与单独测定胆汁酸的对照组比较．显示糖化血清蛋白酶法试剂对胆汁酸结果有较大的影响．引起胆汁酸测定结果明显升高的主要干扰试剂为R1试剂．采用碱性液作为特殊清洗后．能明显减少糖化血清蛋白酶法试剂对总胆汁酸测定的交叉污染。结论糖化血清蛋白酶法试剂对日立7600—10全自动生化分析仪测定总胆汁酸的结果有明显的正干扰．因此实验室在设定项目程序时．应将有干扰的项目间的顺序错开,并在进行项目组合时予以考虑,以避免相邻间的交叉污染。     

酶法测定血清钾,钠离子的评价

测定血清钾、钠离子的常规方法是离子选择性电极法和火焰光度法。酶法为近几年发展起来的,Berry等首先研制成功了酶法测定血清钾、销离子的新技术[1,2]。本文就用德国（BM）公司提供的钾、钠酶法测定试剂盒,在全自动生化分析仪上进行测定,并与离子选择性电极法进行比较,现报道如下。1材料与方法1．1材料1．1．1仪器日立7170A型生化分析仪,DSI系列903型电解质分析仪。1．1．1试剂德国BM公司钾、钠酶法试剂盒（批号为1298011和1298054）,德国BM公司的高低值定标液（分别为钾2．5mmol／L和8．0mmol/L,钠140mmol/L和175mmol/L）,…     

血清钙EDTANa_2滴定法中测定管和标准管颜色不一致的处理

血清钙用乙二胺四乙酸二钠（EDTANa2）滴定法，测定时标准管和测定管变色不一致，滴定终点难以掌握，影响测定结果。我们在标准管中另外加入任意混合血清0．1ml，指示剂0．05ml，再进行简定则变色一致，而且终点明显易掌握。标准管加混合血清，并准确测定其EDTANa2用量（滴定数次取均值），然后按测定管EDTANa2用量（ml）／（混合标准管EDTANa2用量一混合血清EDTANa。量）计算。血清钙EDTANa_2滴定法中测定管和标准管颜色不一致的处理@杨兰泽$洛阳医学高等专科学校生化教研室!471003@李伟$洛阳医专附属医院…     

Renal magnesium wasting and hypocalciuria in chronic cis-platinum nephropathy in man

1. The renal handling of calcium and magnesium was studied in six patients with persistent hypomagnesaemia after cis-platinum treatment for testicular tumours. 2. In comparison with normal subjects, the patients showed hypomagnesaemia (mean 0.54 mmol/l), which was associated with a normal urinary magnesium excretion (mean 4.83 mmol/24 h). Urinary calcium excretion was significantly lower in the patients than in the normal subjects (mean 2.05 vs 5.15 mmol/24 h, respectively; P less than 0.01), despite slightly higher total serum calcium levels (2.53 vs 2.38 mmol/l, respectively; P less than 0.05). During magnesium chloride infusion, when serum magnesium levels were comparable in patients and controls, urinary calcium excretion remained lower in the patients, indicating that hypomagnesaemia was not the cause of the hypocalciuria. 3. Dietary magnesium supplementation resulted in a significant increase in the serum magnesium levels in the patients, while dietary magnesium deprivation resulted in a comparable decrease in urinary magnesium excretion in patients and controls (to 1.46 and 2.00 mmol/day, respectively), although the serum magnesium level fell further (to 0.46 mmol/l) in the patients. 4. The dissociation of renal calcium and magnesium excretion appears to be part of the intrinsic tubular defect caused by cis-platinum. This dissociation of urinary calcium and magnesium excretion, which resembles that seen in Bartter's syndrome, may result from a lesion in the distal convoluted tubule.     

腹膜透析对尿毒症患者QT离散度的影响

目的探讨持续不卧床腹膜透析对尿毒症患者QT离散度的影响,并分析导致QT离散度延长的原因。方法:以首次进入透析并进行标准、规则腹膜透析六个月的患者为研究对象,共28例。于透析前后检测血清钾、镁、钙、磷、肌酐、尿素氮以及血HCO3-,血浆白蛋白等,做心脏彩超检查,测算出左心室重量指数;做标准十二导联心电图检查,测出QT离散度(QTd)及校正的QT离散度(QTcd),并对结果进行统计学分析。结果经过透析后,患者血清钾、磷、镁、肌酐和尿素氮水平均较透析前明显降低,具有显著意义。血钙、HCO3-较前升高,也具有显著意义。左心室重量指数较前增加,但差异无显著性,QTd较前延长,无显著意义,QTcd较前延长,有显著差异。对透析前数据进行多元相关分析显示:透析前尿毒症患者QT离散度的增加与左心室重量指数和血清肌酐水平呈显著正相关,而与血钙水平呈显著负相关。透析后患者QT离散度的增加与左心室重量指数和血清肌酐水平呈显著正相关。结论腹膜透析可能导致QT离散度延长,出现这种结果的原因与透析使左心室肥厚进一步加重有密切关系,而且本研究还发现透析后尿毒症状态改善的程度对QT离散度也有显著影响。     

Placebo-controlled study of intravenous magnesium supplementation during large-volume leukapheresis in healthy allogeneic donors

BACKGROUND: Marked decreases in ionized magnesium (iMg) levels occur during large-volume leukapheresis (LVL); however, the effect of intravenous (IV) magnesium supplementation in this setting has not been carefully studied. STUDY DESIGN AND METHODS: Thirty healthy allogeneic peripheral blood progenitor cell donors receiving citrate anticoagulant with IV calcium prophylaxis were randomized to receive either IV magnesium (0.2 mg Mg per mL acid citrate dextrose-A) or placebo during LVL, with a double-blind design. RESULTS: Thirty subjects underwent 75 LVL pro- cedures, 37 with magnesium and 38 with placebo. Group characteristics were similar for sex, weight, citrate infusion rate (1.36 mg/kg/min vs. 1.37 mg/kg/min), and volume processed (16 L vs. 17 L). Serum iMg levels remained within the reference range with magnesium supplementation, but decreased 39+/-11 percent below baseline (p<10(-10)) after placebo, with greater decreases after consecutive procedures. Subjects receiving magnesium had more vigorous parathyroid hormone responses and higher glucose levels and also tended to have higher serum potassium and ionized calcium levels. Mild paresthesias, coldness, and nausea occurred in 28, 20, and 7 percent of donors, respectively, with no significant differences between groups. Severe symptoms (chest tightness) occurred in only one subject receiving placebo. CONCLUSION: IV magnesium supplementation exerts a significant impact on serum magnesium levels, but does not reduce the frequency or severity of the relatively mild citrate-related effects observed in LVL performed with continuous IV calcium prophylaxis.     

Serum magnesium concentrations after repetitive magnesium cathartic administration

Severe hypermagnesemia has been reported by several authors after multiple doses of magnesium-containing cathartic are administered during management of a toxic ingestion. To evaluate the frequency and magnitude of serum magnesium elevations after the use of repetitive magnesium catharsis, we prospectively evaluated 102 patients who received multiple doses of magnesium citrate as a part of treatment of an overdose. Commonly ingested substances for which repetitive cathartic was administered were tricyclic antidepressants in 47%, aspirin in 17%, and phenytoin in 10%. For each case, serial electrolytes, blood urea nitrogen, creatinine, calcium and magnesium were obtained. Mean initial serum magnesium concentration was 1.8 +/- .03 mEq/L. After a mean 960 mL of magnesium citrate (9.22 g magnesium), final mean serum magnesium concentration was 2.5 +/- .05 mEq/L. Forty-seven patients (47%) developed an elevated (greater than 2.4 mEq/L) serum magnesium concentration, with 12 greater than 3.0 mEq/L. No correlation was found between total quantity of magnesium citrate administered and the increment in serum magnesium concentration. Our data indicate that serum magnesium concentrations consistently rise after repetitive magnesium citrate use. However, the magnitude of this rise appears modest. The elevation in serum magnesium concentration does not correlate with the quantity of magnesium administered. We conclude that with close monitoring, repetitive magnesium citrate can be administered without inducing severe hypermagnesemia (serum magnesium concentration greater than 5.0 mEq/L).     

Hyperoxaluria or hypercalciuria in nephrolithiasis: the importance of renal tubular functions

The role of the kidney in states of hyperoxaluria and hypercalciuria was investigated in seven patients with hyperoxaluria after jejunoileal bypass (JIB) and six patients with idiopathic hypercalciuria (IHC). Eight apparently healthy persons formed a control group. Besides hyperoxaluria, the patients with JIB displayed an elevated plasma concentration of oxalate and the oxalate clearance was increased and higher than creatinine clearance, indicating a net tubular secretion of oxalate. The JIB patients had lower 24-h urinary excretions of calcium, phosphate, magnesium and citrate and higher serum parathyroid hormone (PTH) than controls, indicating increased secretion of PTH to compensate for calcium malabsorption. IHC patients exhibited increased fasting urinary calcium even though their serum values were similar to those in the controls. These results indicate a reduced tubular calcium reabsorption, which was most pronounced in patients with highest PTH values. We conclude that hyperoxaluria in JIB patients is associated both with intestinal hyperabsorption and with enhanced tubular secretion of oxalate, and that in some patients with IHC hypercalciuria is due to reduced tubular reabsorption of calcium.     

Seasonal variations in the composition of urine in relation to calcium stone-formation.

1. A retrospective cross-sectional study was carried out on data derived from single 24 h urine collections from 246 male idiopathic calcium stone-formers. 2. The daily urine volume and pH and the exretions of calcium, oxalate, phosphate, creatinine and magnesium were related to the time of year when the urine was collected, and the saturation of urine with calcium oxalate and octocalcium phosphate calculated for each month. 3. There were significant seasonal variations in the urinary excretion of calcium and oxalate, each showing a maximum during the summer months and a minimum in the winter. There was no significant seasonal variation in urinary pH, volume, creatinine, phosphate or magnesium. 4. There was a significant increase in the saturation of urine with calcium oxalate and a trend towards higher saturation levels of octo-calcium phosphate in the summer. These changes were dependent only on the seasonal variation in urinary calcium and oxalate and not on urine volume. 5. A retrospective study of the seasonal incidence of stone episodes among these 246 stone-formers showed that the rate of stone passage per month was 50% higher in the summer than in the winter. There was no significant seasonal variation in the incidence of stones removed surgically.     

Induction of de novo bone formation in the beagle. A novel effect of aluminum.

To define the primary effects of aluminum on bone in the mammalian species, we examined the dose/time-dependent actions of aluminum in normal beagles. Administration of low dose aluminum (0.75 mg/kg) significantly elevated the serum aluminum (151.7 +/- 19.9 micrograms/liter) compared with that in controls (4.2 +/- 1.35 micrograms/liter) but did not alter the calcium, creatinine, or parathyroid hormone. After 8 wk of therapy, bone biopsies displayed reduced bone resorption (2.6 +/- 0.63 vs. 4.5 +/- 0.39%) and osteoblast covered bone surfaces (2.02 +/- 0.51 vs. 7.64 +/- 1.86%), which was indicative of low turnover. In contrast, prolonged treatment resulted in increased bone volume and trabecular number (38.9 +/- 1.35 vs. 25.2 +/- 2.56% and 3.56 +/- 0.23 vs. 2.88 +/- 0.11/mm) which was consistent with uncoupled bone formation. Administration of higher doses of aluminum (1.20 mg/kg) increased the serum aluminum further (1242.3 +/- 259.8 micrograms/liter) but did not affect calcium, creatinine, or parathyroid hormone. However, after 8 wk of treatment, bone biopsies displayed changes similar to those after long-term, low-dose therapy. In this regard, an increased trabecular number (3.41 +/- 0.18/mm) and bone volume (36.5 +/- 2.38%) again provided evidence of uncoupled bone formation. In contrast, in this instance poorly mineralized woven bone contributed to the enhanced bone volume. High-dose treatment for 16 wk further enhanced bone volume (50.4 +/- 4.61%) and trabecular number (3.90 +/- 0.5/mm). These observations illustrate that aluminum may stimulate uncoupled bone formation and induce a positive bone balance. This enhancement of bone histogenesis contrasts with the effects of pharmacologic agents that alter the function of existing bone remodeling units.     

Multicentre evaluation of an enzymatic method for creatinine determination using a sensitive colour reagent

A new enzymatic colorimetric method for the determination of creatinine in serum and urine (Creatinine PAP, Cat. No. 839434 and 836885, Boehringer Mannheim GmbH, Mannheim, FRG) was evaluated in 16 clinical chemistry laboratories and the manufacturer's testing laboratory. The test is based on the enzymatic degradation of creatinine and its reaction products by creatininase, creatinase and sarcosine oxidase. The H2O2 produced by the oxidation of sarcosine is determined using a modified Trinder reaction. The test can be carried out either manually or in mechanized analysers which enable the pipetting of a starter reagent to be made. The following results were obtained: Depending on the analyte concentration (range 40 to 1240 mumol/l), medians for the coefficients of variation were: 4.6-0.9% within-run and 6.4-2.8% between-day. At 546 nm the linear measuring range extended from 13 mumol/l (detection limit) to 1780 mumol/l, at 510 nm from 9 to 890 mumol/l. Recoveries in aqueous and human serum based standards as well as method comparisons with Fuller's earth methods and an enzymatic UV test indicate a high accuracy of this new enzymatic method in serum and urine. No interference was observed with haemolysed and lipaemic sera. This also applied to anticoagulants and to 36 drugs at therapeutic concentrations, with the exception of calcium dobesilate, which led to decreased values. Icteric samples containing 120-310 mumol/l bilirubin invariably led to decreased creatinine values (10-50 mumol/l lower). In a collaborative study substantially better interlaboratory agreement was observed with the new colorimetric enzymatic test than with the comparison methods (enzymatic UV test and various Jaffe procedures). In conclusion, this new enzymatic colorimetric test permits a precise and specific determination of creatinine in serum and urine. It makes a considerable contribution to improving the interlaboratory comparability of creatinine determinations and is suitable for routine use.