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。     

乙肝后肝硬化患者血清1,25(OH)2D3检测及其临床意义

采用竞争性放射受体法测定３２例乙肝后肝硬化患者血清１Ｍ２５（ＯＨ）２Ｄ３水平,并与３２例性乙型肝炎、３１例健康者对照。发现：肝硬化组血清１,２５（ＯＨ）２Ｄ３水平较肝炎组和对照组明显下降（Ｐ〈０．０１,Ｐ〈０．００１）,且与血清骨钙素、尺桡密度呈正相关（Ｐ〈０．０１,Ｐ〈０．０５）。提示：测定乙肝后肝硬化患者血清１,２５（ＯＨ）２Ｄ３水平有利于肝性骨病的早期发现。     

慢性肾功能衰竭患者铝与骨病的关系

观察了２３例慢性肾功能衰竭（ＣＲＦ）患者，血铝含量平均为１．２７８±０．６４３ｐｐｍ，发铝含量为２．３７３±０．７９３μｇ／ｇ，明显高于正常人血铝０．７３８±０．０８２ｐｐｍ，发铝１．４９５±０．５９μｇ／ｇ，Ｐ值分别＜０．０１及＜０．００１。血铝与血钙水平呈明显负相关，ｒ＝－０．６２５３，Ｐ＜０．０５。肾性骨病（ＲＯＤ）患者血铝明显高于非骨病组，Ｐ＜０．０５。提示ＣＲＦ患者存在明显铝蓄积，并且与ＲＯＤ密切相关。对ＣＲＦ患者一经确诊即应采取有效的防治铝中毒的各项措施。     

小剂量1，25（OH）_2D_3口服冲击治疗尿毒症患者继发性甲状旁腺功能亢进

目的：对２０例尿毒症继发性甲状旁腺功能亢进患者使用小剂量１，２５（ＯＨ）２Ｄ３口服冲击治疗，以比较其与常规治疗的疗效。方法：４０例尿毒症透析患者，随机分为常规治疗组（ｎ＝２０），口服罗钙全０．２５μｇ／ｄ；冲击治疗组（ｎ＝２０），口服罗钙全２μｇ／次，每周２次，８周后改为０．２５μｇ／ｄ维持１个月。结果：冲击治疗组血ＰＴＨ、ＡＫＰ、Ｐ３＋较常规治疗组下降明显，血钙上升，症状改善，无高血钙发生。结论：应用小剂量１，２５（ＯＨ）２Ｄ３，无发生高血钙的危险，是一种经济合理安全有效的治疗方法     

不同药物对糖尿病骨质疏松的短期疗效比较

把糖尿病事并骨质疏松而血糖控制满意的患者分为单纯加用钙剂组（组１）、钙剂加维生素Ｄ２组（组２）、钙剂加钙全组（组３）、钙剂加密息组（组４）及单纯尿治疗组为对照组（组５），治疗三个月后进行疗效比较。结果组１、组５治疗前后骨密度、骨代谢指标（血钙、血磷、碱性磷酸酶（ＡＫＰ）、血甲主腺激素（ＰＴＨ）、尿羟脯氨酸（均无明显变化）（Ｐ〉０．０５）。组２治疗后ＰＴＨ明显降低（Ｐ〈０．０５）。组３、组４血ＰＴＨ     

铝与肾性骨症

铝与肾性骨症［朱萍，等．中华内科杂志１９９３，３２（３）；１７６］为了研究铝与肾性骨病和关系，我们对５１倒尿毒症终末期患者进行了髂骨活检与骨铝染色，并对其中２７例进行了骨铝含量、ＰＴＨ及１，２５（ＯＨ）２Ｄ３的测定．结果发现肾性骨病的发生率为１００％...     

糖尿病患者钙磷调节激素及环核苷酸测定的临床意义

作者观察了７５例糖尿病患者血中Ｃ—肽、２５—羟维生素Ｄ３（２５—ＯＨＤ３）、降钙素（ＣＴ）、甲状旁腺激素—Ｍ（ＰＴＨ—Ｍ）及环核苷酸（ｃＡＭＰ）的变化。结果表明，糖尿病患者与正常人比较Ｃ—肽、ＣＴ、ＰＴＨ—Ｍ、ｃＡＭＰ水平相比均有显著性差异（Ｐ均＜０．０５）；２５—ＯＨＤ：水平无显著性差异（Ｐ＞０．０５）；且Ｃ—肽水平与ＣＴ、ＰＴＨ—Ｍ有显著相关性。提示ＣＴ、ＰＴＨ—Ｍ、ｃＡＭＰ的改变在糖尿病性骨质疏松的发病机理中起重要作用。     

小剂量1,25（OH）2D3口服冲击治疗尿毒症患者继发性甲状旁…

目的：对２０例尿毒症继发性甲状旁腺功能亢进患者使用小剂量１，２５（ＯＨ）２Ｄ３口服冲击治疗，以比较其与常规治疗的疗效。方法：４０例毒症透析患者，随机分为常治疗组（ｎ＝２０），口服罗钙珍０．２５μｇ／ｄ；冲击治疗组（ｎ＝２０），口服罗钙全２μｇ／次，每周２次，８周后改为０．２５μｇ／ｄ维持１个月，结果：冲击治疗组血ＰＴＨ，ＡＫＰ，Ｐ＾３＋较常规治疗组下降明显，血钙上升，症状改善，无高血症发生，结论，     

二甲基硫脲对心肌细胞抗过氧化氢损伤的实验研究

为探讨二甲基硫脲（ＤＭＴＵ）保护心肌细胞抗过氧化氢（Ｈ２Ｏ２）损伤。３２瓶培养乳鼠心肌细胞随机分４组，每组８瓶：（１）对照组；（２）Ｈ２Ｏ２（５ｍｍｏｌ）组；（３）ＤＭＴＵ（２０ｍｍｏｌ）组；（４）Ｈ２Ｏ２（５ｍｍｏｌ）＋ＤＭＴＵ（２０ｍｍｏｌ）组。在３７℃、５％ＣＯ２的ＭＥＭ培养４小时。结果发现：（１）与对照组比，Ｈ２Ｏ２组乳酸脱氢酶（ＬＤＨ，Ｕ／１００ｍｌ）释放多（２８２．３８±４７．２８比７７．２５±１８．２５，Ｐ＜０．０１）、ＴＢＡ反应物（ＴＢＡＲＳ，ｎｍｏｌ／ｍｇＰｒ．）产生多（２．２５±０．５３比０．７９±０．３６，Ｐ＜０．０１）；（２）与Ｈ２Ｏ２组比，Ｈ２Ｏ２＋ＤＭ－ＴＵ组ＬＤＨ释放少（９９．２５±４１．８８比２８２．３８±４７．２８，Ｐ＜０．０１）；ＴＢＡＲＳ产生少（０．５９±０．１８比２．２５±０．５３，Ｐ＜０．０１）；此外，我们还发现ＤＭＴＵ组超氧化物歧化酶（ＳＯＤ，μｇ／ｍｇＰｒ．）比对照组高（８．４９±３．６５比１．９２±１．４０，Ｐ＜０．０１）。ＤＭＴＵ能保护心肌细胞抗Ｈ２Ｏ２损伤，机制与灭活羟自由基（·ＯＨ）、保护ＳＯＤ活性有关     

Hyperparathyroidism and 1,25-dihydroxyvitamin D deficiency in mild, moderate, and severe renal failure

It has been postulated that hyperparathyroidism in chronic renal failure results from hypocalcemia, occurring, in part, from phosphate retention and/or deficient 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] synthesis. However, many studies have failed to demonstrate hyperphosphatemia or low 1,25-(OH)2D levels in patients with mild renal failure. We measured creatinine clearance (CCr), fractional excretion of phosphorus (FEP), and serum phosphorus, ionized calcium, and plasma N-terminal PTH, and 1,25-(OH)2D concentrations in 21 normal subjects and 51 patients with renal failure. Patients with mild renal failure (Ccr, greater than 40 mL/min.1.73 m2) had normal mean serum phosphorus and ionized calcium and decreased mean 1,25-(OH)2D levels compared with those in normal subjects. In patients with moderate renal failure (CCr, 20-40), the mean ionized calcium level was normal, plasma PTH levels and FEP were elevated, and the decrement in 1,25-(OH)2D was more pronounced. The mean ionized calcium level was decreased only in the group of patients with severe renal failure (CCr, less than 20). The 1,25-(OH)2D values correlated positively with CCr and negatively with the log of plasma PTH and serum phosphorus concentrations. Log of plasma PTH correlated negatively with CCr and positively with FEP. The ionized calcium concentration correlated very weakly with CCr and the log of the plasma PTH level. These data demonstrate the presence of hyperparathyroidism, normocalcemia, and 1,25-(OH)2D deficiency in renal failure and are consistent with a role for 1,25-(OH)2D in the suppression of parathyroid activity through as yet unidentified mechanisms.     

大鼠骨基质形态增龄性改变及其与骨代谢指标的相关性研究

目的　研究大鼠增龄过程中骨基质形态计量改变规律及与骨代谢指标相关性。　方法　 3、9、15个月龄雌性SD大鼠各 10只。第 4腰椎及右侧胫骨上段作形态计量学分析。物理密度法测定股骨及腰椎骨密度 (BMD)。第 3腰椎作抗压缩试验。自动分析仪测定血清钙、磷 ,放免法测定1,2 5 (OH) 2 D3 。　结果　与 3月龄组比较 ,15月龄组第 4腰椎骨小梁体积减小 4 3 3% (P <0 0 1) ,胫骨上段骨小梁体积减小 2 8 0 % (P <0 0 1) ,骨形成表面降低 17 2 % (P <0 0 5 ) ,骨吸收表面增加39 8% (P <0 0 1) ,腰椎、股骨BMD分别下降 7 7% (P <0 0 1)和 7 3% (P <0 0 1)。骨小梁体积与腰椎BMD、最大载荷、血清 1,2 5 (OH) 2 D3 呈明显正相关 (r =0 6 84、0 972及 0 86 6 ,P <0 0 0 1)。血清 1,2 5 (OH) 2 D3 与胫骨骨形成表面及矿化沉积率呈明显正相关 (r =0 5 87,r =0 6 2 8,P <0 0 1)。　结论　 15月龄雌性SD大鼠骨形成减弱 ,骨吸收增加 ,骨量减少 ,骨结构改变 ,生物力学性能降低。骨形态计量学指标与腰椎BMD和骨生物力学指标有明显的相关性。     

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。     

Infusions of parathyroid hormone in ruminants: hypercalcemia and reduced plasma 1,25-dihydroxyvitamin D concentrations

The relationship between infused synthetic bovine PTH-(1-34) and plasma concentrations of minerals and vitamin D metabolites was studied in eight calves (150-230 kg) and two thyroparathyroidectomized goats. Calves were infused iv with saline for 15-20 h. Then, calves were infused with one of three types of solution for an additional 35-h period. Three of the eight calves received 3 ng/kg X min (group H), three received 0.75 ng/kg X min (group L), and the remaining two calves received control saline over a 33-h period (group C). Blood samples were taken every 4-6 h. Plasma calcium, phosphorus, hydroxyproline, and 1,25-dihydroxyvitamin D [1,25-(OH)2D] remained relatively constant in control calves. PTH infusions into calves in group H resulted in an increase in plasma calcium from 2.4 to a plateau of 3.0 mmol/liter. PTH infusion caused no change in plasma phosphorus, but increased urinary excretion of phosphorus. Infusion of PTH caused a moderate increase in urinary calcium excretion, followed by pronounced calciuria after PTH withdrawal. Plasma concentrations of 1,25-(OH)2D decreased from about 30 pg/ml at the start of infusion to undetectable levels (less than 5 pg/ml) at the end of the infusion and for 30 h thereafter. Similar, but less pronounced, changes in plasma calcium and 1,25-(OH)2D concentration were observed in group L. Hypocalcemia and hypophosphatemia developed in the two lactating goats after thyroparathyroidectomy, and plasma 1,25-(OH)2D concentrations were decreased. PTH infusion (3 ng/kg X min) corrected the hypocalcemia and hypophosphatemia and markedly raised plasma 1,25-(OH)2D concentrations. When calcium chloride was infused in addition to PTH, the resulting hypercalcemia (3 mmol/liter) was associated with a marked reduction in plasma 1,25-(OH)2D. We conclude that the concentration of calcium in plasma has the major regulatory role on plasma 1,25-(OH)2D concentrations in ruminant species when potentially conflicting signals, such as hypercalcemia and high PTH concentrations, are present simultaneously.     

Relationships between bone mineral density, serum vitamin D metabolites and calcium:phosphorus intake in healthy perimenopausal women

OBJECTIVES: To determine the relationships between serum vitamin D metabolites, bone mass, and dietary calcium and phosphorus in a cohort of 510 healthy Danish perimenopausal women. DESIGN: A population-based cross-sectional study. SUBJECTS: A total of 510 healthy women aged 45-58 years, with amenorrhoea for 3-24 months. None of the women was using hormone replacement therapy. MEASUREMENTS: Measurements of total bone mineral content and regional bone mineral density were performed by dual-energy X-ray absorptiometry. Analyses of serum levels of 25-OHD and 1,25-(OH)2D, intact PTH, ionized calcium and phosphate, as well as biochemical markers of bone turnover in blood and urine. Assessment of calcium and phosphorus intake using dietary records. RESULTS: A consistent inverse relationship between serum 1,25-(OH)2D and bone mineral content/ density was found in whole-body mineral content (P = 0.001), spine (P = 0.005) and femoral neck (P<0.05). There was a positive relationship between levels of 1,25-(OH)2D and biochemical bone markers, indicating that high levels of 1,25-(OH)2D are accompanied by increased bone turnover. The dietary calcium:phosphorus ratio was inversely related to serum 1,25-(OH)2D (P = 0.04) and positively related to bone mineral density (P<0.0005). No relationships could be detected between levels of PTH, serum ionized calcium and phosphate, and serum vitamin D metabolites. CONCLUSION: Within normal physiological range, elevated levels of 1,25-(OH)2D were associated with decreased bone mineral density and content, reduced calcium:phosphorus ratio in the diet and increased bone turnover.     

The role of the vitamin D receptor in regulating vitamin D metabolism: a study of vitamin D-dependent rickets, type II

In vitro studies and animal experiments suggest that the production of 1,25-dihydroxyvitamin D [1,25-(OH)(2)D] and 24,25-(OH)(2)D is reciprocally controlled by 1,25-(OH)(2)D. To investigate the role of the vitamin D receptor (VDR) in controlling vitamin D metabolism in humans, we studied 10 patients with vitamin D-dependent rickets type II due to a defective VDR. After a period of high dose calcium therapy, 7 of the patients had normal serum calcium, phosphorus, alkaline phosphatase, and plasma PTH levels (PTH-N), and 3 showed increased serum alkaline phosphatase and plasma PTH (PTH-H). Serum calcium, phosphorus, alkaline phosphatase, PTH, vitamin D metabolites, urinary calcium/creatinine, and renal phosphate threshold concentration were compared with unaffected family members that comprised the control group. Vitamin D metabolites were measured before and after an oral load of 50,000 U/m(2) cholecalciferol. Compared with the control group, 1,25-(OH)(2)D levels were significantly higher and 24,25-(OH)(2)D levels were lower in the PTH-N group and even more so in the PTH-H group. 1alpha-Hydroxylase (1-OHase) and 24-OHase activities were estimated by the product/substrate ratio. In the PTH-N group, 1-OHase activity was higher and 24-OHase activity was lower than in controls. In the PTH-H group, 1-OHase activity was even higher, probably due to an additive effect of PTH. Thus, 1,25-(OH)(2)D-liganded VDR is a major control mechanism for vitamin D metabolism, and PTH exerts an additive effect. Assessment of the influence of 1,25-(OH)(2)D shows reciprocal control of enzyme activity in man, suppressing 1-OHase and stimulating 24-OHase activity.     

1,25-Dihydroxycholecalciferol effect on serum phosphorus homeostasis in rats.

It has recently been shown that 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) increases the serum phosphorus concentration of rats on a low-phosphorus diet. While studying the biological activity of 1,25(OH)2D3, we observed that under certain circumstances 1,25-(OH)2D3 would decrease the serum phosphorus concentration. The analysis of all data obtained in rat experiments during the past 3 years revealed highly significant linear correlations (P less than 0.001) between changes of serum phosphorus concentrations after the administration of 1,25-(OH)2-D3 (130 pmol/d for 1 or 5 days) and serum phosphorus or calcium levels in the animals before injection. Similar correlations could only be found with the higher dose of 25-hydroxycholecalciferol (130 pmol/d for 5 days). Another vitamin D3 metabolite, 24,25-dihydroxycholecalciferol, had no effect on serum phosphorus concentrations under our experimental conditions. The 1,25-(OH)2D3 effect on serum phosphorus concentration does not require the presence of circulating parathormone and/or calcitonin. We suggest that 1,25-(OH)2D3 might be an important factor in serum phosphorus homeostasis.     

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.