激素和血生化在肾性骨病中的变化

我们观察了５５例尿毒症肾性骨营养不良症（简称肾性骨病，包括甲状旁腺功能亢进性骨病、低转化软骨病、混和性骨病）中血甲状旁腺激素（ＰＴＨ）、１．２５（ＯＨ）＿２Ｄ＿３、血钙、磷、ＡＫＰ、血铝及骨铝的变化。结果发现：各型肾性骨病血ＰＴＨ显著高于正常（Ｐ＜０．００１），血１．２５（ＯＨ）＿２Ｄ＿３和血钙显著低于正常（Ｐ＜０．００１）。在低转化软骨病组，血１．２５（ＯＨ）＿２Ｄ＿３显著低于甲旁亢骨病组（Ｐ＜０．０５）；血磷与正常对照无显著性差异，而显著低于甲旁亢骨病组及混合性骨病组（Ｐ＜０．０５）。ＰＴＨ与１．２５（ＯＨ）＿２Ｄ＿３呈线性负相关（Ｐ＜０．０５），而与ＡＫＰ呈线性正相关（Ｐ＜０．０５）。ＰＴＨ与血透时间、血钙、血铝及骨铝不相关。１．２５（ＯＨ）＿２Ｄ＿３与血透时间、血磷、血铝及骨铝不相关。骨铝染色阳性组与阴性组之间，ＰＴＨ、１．２５（ＯＨ）＿２Ｄ＿３及ＡＫＰ升高率均无显著性差异。     

肝硬化患者血清1,25（OH）2D3对骨代谢的影响

分别采用竞争性放射受体法及入免法测定３２例肝硬化患者血清１，２５（ＯＨ）２Ｄ３、ＰＴＨ水平，并与３２例慢性乙型活动性肝炎、３１例健康者对照。发现：肝硬化组血清１，２５（ＯＨ）２Ｄ３较肝炎组和对照组明显下降（Ｐ〈０．０１，Ｐ〈０．００１），并与血钙、尺桡骨密度呈下相关（Ｐ〈０．０１，Ｐ〈０．０５）；肝硬化组血清ＰＴＨ较肝炎组和组明显升高（Ｐ〈０．０５，Ｐ〈０．０５），但与血钙、尺桡骨密度无相关性。提     

腹膜透析患者1,25二羟基D3冲击治疗的疗效观察

为了探讨口服１，２５（ＯＨ）２Ｄ３冲击治疗对腹膜透析患者钙磷代谢及甲状旁腺功能的影响，我们给予３２例ＣＡＰＤ患者口服１．２５（ＯＨ）２Ｄ３大剂量冲击治疗（２－４μｇ／次，每周２次）．另２９例为常规治疗组（０．２５－０．５ｕｇ／ｄ）作为对照组。结果显示，两组患者血钙均明显升主，血磷及血ＡＫＰ均明显降低；ＰＴＨ和ＣＴ在常规治疗组有轻度降低，但无统计学差异；而口服冲击治疗组，ＰＴＨ和ＣＴ则明显降低，且临床症状明显改善，用药过程中未发现明显副作用。上述结果表明，１，２５（ＯＨ）２Ｄ３口服冲击治疗是纠正钙磷代谢紊乱和甲状旁腺功能亢进的较佳疗法，值得推荐。     

月见草油治疗十二指肠溃疡的研究

目的研究月见草油对十二指肠溃疡（ＤＵ）的治疗作用．方法选经内镜确诊为ＤＵ的住院患者１２０例，随机分为治疗组（ｎ＝６０）和对照组（ｎ＝６０）．治疗组服用月见草油１５ｇ，４次／ｄ，对照组服用西味替丁２００ｍｇ，４次／ｄ，两组均为４周１疗程．治疗前及治疗４周后各做胃镜１次，观察溃疡的愈合情况，同时，治疗前及治疗４周后用放免法分别测定血浆内的ＰＧＥ２含量．结果治疗组与对照组患者的消化道症状均较服药前明显减轻（Ｐ＜００１），两组间无显著性差异（Ｐ＞００５）．４周溃疡愈合率和有效率，治疗组为７６６％和８６６％，对照组分别为７００％和８３３％，两组间无显著性差异（Ｐ＞００５），对照组于治疗前后血浆ＰＧＥ２水平无显著性差异，而治疗组于治疗前后的血浆ＰＧＥ２水平却有显著性差异（９４５ｎｇ／Ｌ±３７ｎｇ／Ｌ→１７２３ｎｇ／Ｌ±５７ｎｇ／Ｌ，Ｐ＜００５）．结论月见草对ＤＵ的近期疗效较好，可用于治疗ＤＵ．     

卡托普利与美托洛尔治疗轻、中度高血压疗效比较

本文比较了血管紧张素转换酶抑制剂卡托普利（开搏通）与选择性β１受体阻滞剂美托洛尔（倍他乐克）治疗轻中度高血压即时和短程疗效。眼药后１ｈ，卡托普利组收缩压和舒张压明显下降（Ｐ＜０．０１），而美托洛尔组仅收缩压下降（Ｐ＜０．０５）。服药后３ｈ，两药均达最大降压疗效，两组降压比较无统计学差异。服药后１２ｈ美托洛尔组收缩压和舒张压仍有降压作用（Ｐ＜０．０５），而卡托普利仅对舒张压有作用（Ｐ＜０．０５）。服药后２１天，卡托普利和美托洛尔组总有效率分别是８７．５％和８３．３％（ｘ２＝４．２２，Ｐ＞０．０５）。     

采用不同防治方案控制蛲虫病流行的比较研究

应用两硫咪唑在蛲虫感染率高于３０％的幼儿园，分别实施选择性化疗（Ａ１）、选择性化疗辅以健康教育（Ａ２）、集体化疗（Ｂ１）、集体化疗辅以健康教育（Ｂ２）、扩大化疗（Ｃ１）与扩大化疗辅以健康教育（Ｃ２）６种防治方案，结果Ａ１、Ａ２、Ｂ１、Ｂ２、Ｃ１与Ｃ２组感染率分别由防治前（１９９１）的３４．５％、３３．８％、３５．５％、３４．８％、３４．１％与３６．６％降至防治后（１９９３）的１３．６％、９．９％、４．４％、２．１％、３．５％与３．１％。其中两Ｂ组下降率明显高于两Ａ组（Ｐ均＜０．０１），而与两Ｃ组相近（Ｐ均＞０．０５）。两Ｂ组中，Ｂ２组下降率又明显高于Ｂ１组（Ｐ＜０．０５）．同期Ｂ１与Ｂ２组环境虫卵检出率亦由防治前的３．４％与３．６％降至防治后的０．８％与０．３％，分别下降了７６．４％与９１．７％，Ｂ２组下降幅度高于Ｂ１组．综上表明实施集体化疗辅以健康教育防治方案，既可快速控制传染源，又能较好地巩固防治效果，方法简便，适用于现场防治．     

中晚期肝细胞癌的化学免疫疗法

目的和方法对７４例无手术切除指征的中晚期肝细胞癌（ＨＣＣ）患者采用化学免疫治疗（ＣＩＴ），即经肝动脉化学栓塞治疗后１～２周，序贯地施行ＬＡＫ或ＣＤ３ＡＫ过继免疫治疗，并以同期单用经肝动脉化学栓塞治疗的４１例相同患者作对比。结果化学免疫治疗组和经肝动脉化学栓塞治疗组的Ⅱ、Ⅲ期ＨＣＣ患者的缓解率差异显著，分别为７２．４％与４０．４％（Ｐ＜０．０５）和４８．９％与１４．３％（Ｐ＜０．０５）。化学免疫治疗和经肝动脉化学栓塞治疗组相比，Ⅲ期ＨＣＣ患者的半年、１年生存率和Ⅱ期患者的２年生存率差异也显著，分别为６２．２％与２３．８％（Ｐ＜０．０５）、４６．０％与９．５％（Ｐ＜０．０５）以及４８．３％与１５．０％（Ｐ＜０．０５）。化学免疫治疗组１年内肝外转移发生率为２５．９％（１５／５８），明显较经肝动脉化疗栓塞治疗组（５８．１％，１８／３１）为低（Ｐ＜０．０５）。结论化学免疫治疗这一有机序贯结合在治疗中晚期肝细胞癌患者方面属合理、有效的综合治疗方案。     

高血压病患者盐敏感性与高胰岛素血症之间的关系

目的：探讨高胰岛素血症（ＨＩＳ）与盐敏感性高血压病肾脏排钠障碍间的关系。方法：根据盐敏感性（盐负荷试验Ｓｕｌｉｖａｎ标准），将５３例高血压病患者分为２组：盐敏感型（ＳＳ）组２２例、盐不敏感型（ＳＲ）组３１例。测定患者在盐负荷试验中血糖和血胰岛素浓度变化，计算胰岛素抵抗。结果：ＳＳ组与ＳＲ组相比较，基础状态、盐负荷和服呋喃苯胺酸（速尿）后各时点血糖及血胰岛素变化明显（血糖：５．１２±１．２５、５．９７±１．５９、５．２１±１．２８ｍｍｏｌ／Ｌ比４．９６±１．１４、５．４８±１．３８、５．０７±１．２３ｍｍｏｌ／Ｌ，Ｐ＞０．０５；血胰岛素：１２．４６±４．１４、３１．６８±１２．２１、１４．３５±４．４５ｍＵ／Ｌ比１０．１５±３．６２、２２．１４±８．６４、１０．８９±３．９１ｍＵ／Ｌ，Ｐ＜０．０１），ＳＳ组中胰岛素抵抗发生率显著高于ＳＲ组（６３．６％比３２．３％，Ｐ＜０．０５）。结论：ＳＳ高血压病肾脏排钠障碍与高胰岛素血症有关。     

射频消融房室旁路的复发原因分析

总结了１２２例１２４条房室旁路（ＡＰ）射频消融术（ＲＦＣＡ）的复发率，并对复发的可能原因作了初步分析。结果为：１２４条ＡＰ经２～２５（１３．５±７．１）个月随访５条复发，复发率为４．０３％（５／１２４）。其中显性与隐性ＡＰ复发率分别为１．２３％（１／８１）和９．３０％（４／４３），Ｐ＜０．０５；左游离壁与间隔分别为２．５％（２／８０）和７．５％（３／４０），Ｐ＞０．０５；左侧与右侧分别为３．３％（３／９０）和３．１％（１／３２），Ｐ＞０．０５。复发时间为０．５～６０（１５．４±２５．４）天。复发可能与消融点不够精确、ＡＰ粗大位置深在、ＡＰ功能特性与部位、消融能量不足、观察时间不够等因素有关。提示需对行ＲＦＣＡ患者进行随访。     

老年尿毒症患者血液透析滤过临床疗效

目的探讨老年尿毒症患者对血液透析滤过（ＨＤＦ）的耐受性及临床疗效。方法回顾性分析２０例老年尿毒症患者１６６例次ＨＤＦ，并与其常规血液透析（ＨＤ）治疗进行比较。结果患者对ＨＤＦ治疗的耐受性显著优于ＨＤ，且ＨＤＦ对小分子及中分子尿毒性物质的清除显著优于ＨＤ，ＨＤＦ治疗前血β２微球蛋白（β２－ＭＧ）值６０．７±１２．９ｍｇ／Ｌ、甲状旁腺素（ＰＴＨ）２．０±１．３ｐｇ／Ｌ，治疗后分别为４９．９±１１．０ｍｇ／Ｌ，及１．１±０．９ｐｇ／Ｌ，治疗前、后差异均有非常显著性（Ｐ＜０．０１及＜０．００１）；而ＨＤ治疗前后β２－ＭＧ分别为５２．８±１２．７及５１．７±１１．９ｍｇ／Ｌ（Ｐ＞０．０５），ＰＴＨ１．９±１．６及１．９±１．８ｐｇ／Ｌ（Ｐ＞０．０５）。结论老年尿毒症患者ＨＤＦ未发生ＨＤ时发生的顽固性高血压、严重的低血压、心律失常、心绞痛、心力衰竭、体腔积液等，提高了对透析治疗的耐受性，透析效果显著提高     

Insulin modulates the stimulation of renal 1,25-dihydroxyvitamin D3 production by parathyroid hormone

Previous studies have shown that there is an impairment in renal production of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), the major biologically active metabolite of vitamin D3, in diabetes. This impairment is not due to a deficiency in the parathyroid hormone (PTH), a major stimulator of renal 1,25(OH)2D3 production. Therefore, we have investigated the capacity of PTH to stimulate 1,25(OH)2D3 production in insulin deficiency and with insulin replacement. Experiments were performed in rats fed a 0.6% calcium, vitamin D sufficient diet for 2 weeks. Thyroparathyroidectomy was performed on all rats. Rats to be rendered diabetic were injected with streptozotocin immediately after surgery. In non-diabetic rats, PTH administration significantly increased renal 1,25(OH)2D3 production (11 +/- 2 vs 46 +/- 5 pg/min/g; P less than 0.05). In diabetic rats, however, PTH caused only a modest increase in 1,25(OH)2D3 production (11 +/- 1 vs 19 +/- 4 pg/min/g; P less than 0.05). With insulin replacement, PTH stimulation of 1,25(OH)2D3 production was markedly increased over that seen in diabetic rats (48 +/- 12 vs 19 +/- 4 pg/min/g; P less than 0.05). PTH was equally effective in raising serum calcium, depressing serum phosphorus and tubular reabsorption of phosphate in non-diabetic as well as in diabetic rats. These results demonstrate that insulin is necessary for the maximal stimulation of renal 1,25(OH)2D3 production by PTH. However, insulin is not necessary for PTH action in terms of renal handling of phosphate and inducing hypercalcaemia. These results suggest multiple pathways for the action of PTH, only some of which are insulin requiring.     

Ⅱ型糖尿病肾病和非肾病患者甲状旁腺激素和钙磷代谢关系的初步探讨

测定４６例Ⅱ型糖尿病患者（肾病２５例，非肾病２１例）和２４例正常人血清甲状旁腺激素（ＰＴＨ）、钙（Ｃａ）、磷（Ｐ）、碱性磷酸酶（ＡＫＰ）、肌酐（Ｃｒ）和尿白蛋白（Ａｌｂ），发现糖尿病患者血ＰＴＨ、ＡＫＰ和尿Ｐ浓度较正常人增高，血Ｃａ、Ｐ浓度较正常人降低，其中肾病患者ＰＴＨ值又较非肾病组增高，差异有显著性。相关分析示糖尿病肾病的ＰＴＨ值与血Ｃｒ、ＡＫＰ和尿Ｐ有较好的相关性。作者认为糖尿病患者存在钙、磷代谢异常，体钙缺乏，这种代谢异常在糖尿病肾病患者尤为明显，血清ＰＴＨ值、ＡＫＰ和尿Ｐ浓度是反映糖尿病肾病钙、磷代谢异常的有意义指标。     

Regulatory mechanisms of circulating fibroblast growth factor 23 in parathyroid diseases

Fibroblast growth factor-23 (FGF-23) is a circulating factor regulating phosphate and vitamin D homeostasis. Phosphate intake and an administration of 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) increase circulating FGF-23 levels, and elevated FGF-23 prevents hyperphosphatemia and vitamin D toxicity by hyperphosphaturia and suppression of circulating 1,25(OH)(2)D level, comprising a feedback loop to maintain phosphate and vitamin D homeostasis. Excess secretion of parathyroid hormone (PTH), another phosphaturic factor, elevates the serum calcium level in primary hyperparathyroidism. PTH also elevates circulating FGF-23 level, which cooperatively enhances the phosphaturia, resulting in hypophosphatemia. The circulating FGF-23 level increases as renal function declines in chronic kidney disease (CKD), and it exhibits significant and positive correlations with serum phosphate, calcium, and PTH in CKD patients on maintenance hemodialysis, suggesting that these parameters regulate circulating FGF-23 level. Tight associations between circulating FGF-23 and calcium levels were observed both in patients with primary hyperparathyroidism and in CKD patients on maintenance hemodialysis, suggesting the role of serum calcium on FGF-23 regulatory mechanisms. FGF-23 may have a physiological role in preventing tissue damage such as ectopic calcifications, partly via suppressing the serum calcium x phosphate product by accelerating urinary phosphate excretion and suppressing vitamin D activation.     

1,25-Dihydroxycholecalciferol deficiency: the probable cause of hypocalcemia and metabolic bone disease in pseudohypoparathyroidism.

Pseudohypoparathyroidism (PsH) is a genetic disease characterized by hypocalcemia, hyperphosphatemia, and metabolic unresponsiveness to parathyroid hormone (PTH). The administration of PTH elicits neither a significant rise in serum calcium (calcemic response) nor a decrease in the renal tubule reabsorption of phosphorus (phosphaturic response). The diminished phosphaturic response is due to an inability of PTH to generate cyclic AMP in renal tubule cells. We investigated the question of whether hypocalcemia and deficient calcemic response to PTH are due to a similar cyclic AMP defect in bone or to an acquired vitamin D deficiency. Four patients were studied. The active form of vitamin D (1,25-dihydroxycholecalciferol) was measured in 3 and was low. Treatment with vitamin D2 restored the serum calcium and the calcemic response to PTH to normal without changing the impaired renal response. Bone biopsy was performed in 2 patients and showed morphologic evidence of increased osteoclastic activity and osteomalacia. The data indicate that the hypocalcemia and bone disease in PsH are due to active vitamin D deficiency, possibly resulting from the genetic renal lesion.     

NF-κB对急性坏死性胰腺炎大鼠甲状旁腺激素受体表达和低钙血症的影响

目的 探讨NF-κB对ANP大鼠甲状旁腺激素受体(PTH1R)表达及低钙血症的影响.方法 将雄性SD大鼠24只按完全随机法分为对照组、ANP组和四氢化吡咯二硫代氨基甲酸脂预处理组(PDTC组),各8只.以5%牛磺脱氧胆酸钠逆行胰胆管注射建立ANP模型.观察6 h后各组血清钙浓度以及胰腺组织病理改变,蛋白免疫印渍法检测肾脏和骨组织NF-κB、PTH1R蛋白表达,RT-PCR检测肾脏和骨组织FTH1R mRNA表达.结果 对照组、ANP组和PDTC组血钙浓度分别为(2.31±0.03)mmol/L、(2.01±0.03)mmol/L和(2.12±0.05)mmol/L,3组间差异显著(P<0.05).ANP组肾脏和骨组织的NF-κB蛋白表达量分别为1.53±0.08和0.47±0.19;PDTC组分别为0.61±0.13和0.36±0.06,两组差异显著(P<0.05).ANP组肾脏和骨组织PTH1R mRNA的表达量分别为0.27±0.08和0.29±0.06,PTH1R蛋白表达分别为0.87±0.07和0.31±0.09;PDTC组分别为0.57±0.27和0.37±0.11,1.13±0.17和0.68±0.15,两组差异显著(P<0.05).ANP组NF-κB活性较对照组明显升高,PTH1R表达明显下降;与ANP组比较,PDTC组NF-κB活性降低,血清钙水平明显升高,PTH1R的表达上调(P<0.05).结论 NF-κB可能通过间接下调组织PTH1R的表达,致血清钙显著下降.PDTC对改善ANP低钙血症有一定意义.     

Early treatment of secondary hyperparathyroidism in moderate renal insufficiency: low-phosphorus diet versus calcium carbonate

Calcitriol deficiency and phosphorus retention are mechanisms involved in the pathogenesis of renal hyperparathyroidism. The aim of this study was to evaluate the effect of dietary phosphorus restriction versus calcium carbonate treatment for one month on PTH and calcitriol levels in patients with mild renal failure. We studied two groups of patients: Group I: 21 patients (14M/7F); mean age 61 years old; mean glomerular filtration rate 51 ml/min. Their diet contained phosphorus 700 mg/day. Group II: 30 patients (21M/9F); mean age 58; mean glomerular rate 56 ml/min. They were divided in two subgroups: 18 patients treated with calcium carbonate 2.5 g/day and 12 patients with 5 g/day. Serum PTH, calcitriol, 25(OH)D3, calcium, phosphorus and urinary excretion of calcium and phosphorus were measured before and after a 30 day period. The low phosphorus diet (Group I) resulted in a significant decrease in PTH levels (81.3 +/- 35 vs 71 +/- 39 pg/ml, p < 0.05) and significant increase in calcitriol levels (22.4 +/- 4.4 vs 33.4 +/- 7.5 pg/ml, p < 0.05). In our study calcium carbonate treatment (Group II) had no effect on PTH and calcitriol levels.     

Effects of intravenous and oral OCT on secondary hyperparathyroidism in dogs with chronic renal failure

In this study, we compare the relative potency of single intravenous OCT (IV OCT) and 1,25 (OH) (2)D(3) [IV 1,25 (OH) (2)D(3)] on serum PTH and ionized calcium (ICa) in dogs with chronic renal failure (CRF). In addition, we examine the efficacy of intermittent IV OCT. A single dose of OCT (5 microg/kg) to uremic dogs suppressed PTH by 81% without a statistical significant change in serum I Ca. On the other hand, any of the effective doses of 1,25 (OH) (2)D(3) on PTH suppression were hypercalcemic. The intermittent administration of OCT (0.1 microg/kg) or 1,25 (OH) (2)D(3) (0.025 microg/kg), 3 times per week IV suppressed serum PTH by 83% or 77%, relatively without hypercalcemia. To evaluate OCT as an oral drag, it was given intermittently (3 times per week) to a group of 6 uremic dogs for a period of 4 weeks. Subsequently it was changed to a daily administration (0.05 microg/kg) for a period of 2 weeks. Finally the dose was reducted to 0.025 microg/kg. Daily OCT 0.05 microg/kg suppressed serum PTH by 67%. Subsequently 0.025 micro/kg maintained serum PTH within the normal range without hypercalcemia for 4 weeks. OCT seems to be promising as a useful agent not only for hemodialysis patients but also for predialysis and CAPD patients. In conclusion, our results suggest that OCT is a useful vitamin D(3) analogue, which has a potentially larger therapeutic window than that of 1,25 (OH) (2)D(3) and which is available for IV/oral, for the management of secondary hyperparathyroidism.     

慢性肾功能不全患者血清甲状旁腺素、钙、磷之间的关系

为了解慢性肾功能不全患者血清中钙、磷、甲状旁腺素（PTH）水平变化,藉以推测继发性甲状腺腺亢进的原因,观察了92例不同阶段段功能不全患者的血清、钙、磷、PTH水平。结果显示,PTH与内生肌酐清除（Ccr)呈负相关（P＜0．05）,与血清磷水平呈正相关（P＜0．05）,与血清钙水平无相关必.性肾功能不全早期,随着Ccr降低,PTH逐渐升高,但血磷、血钙水平并无显著改变,慢性肾功能不全后期（肾功能衰竭期）血磷水平才明显升高,血钙水羡明显降低。