1,25(OH)2D3口服冲击与血液灌流对维持性血液透析患者继发甲状旁腺功能亢进的疗效对比与护理

目的:比较1,25(OH)2D3口服冲击与血液灌流对维持性血液透析患者继发甲状旁腺功能亢进(SHPT)的疗效与护理。方法:将维持性血液透析SHPT患者42例随机分成A组[1,25(OH)2D3口服冲击组]及B组(血液灌流组)各21例。A组在1周3次血液透析治疗基础上给予1,25(OH)2D3口服冲击;B组给予1周3次血液灌流串联血液透析治疗。比较治疗后两组血清全段反应性甲状旁腺激素(iPTH)和皮肤瘙痒等改善情况,并探讨护理要点。结果:治疗12周后两组患者iPTH与治疗前相比具有显著性(P0.01),但B组下降程度较A组更为显著(P0.01)。结论:血液灌流对维持性血液透析患者SHPT的疗效比1,25(OH)2D3口服冲击更明显,且皮肤瘙痒等症状好转,值得临床推广。     

骨化三醇治疗血液透析患者继发性甲状旁腺功能亢进症的临床观察

目的观察骨化三醇注射液治疗血液透析患者继发性甲状旁腺功能亢进症(secondary hyperparathyroidism,SHPT)的疗效。方法随机选择维持性血液透析患者30例,根据血清全段甲状旁腺激素(intact parathyroid hormone,iPTH)水平,确定骨化三醇注射液的剂量,比较治疗前及治疗后2、4、8周的iPTH、血钙和磷的变化及临床症状的缓解程度。结果①30例患者治疗前血清iPTH为(1218±295)pg/ml,治疗8周后iPTH降至(437±152)pg/ml,总达标率86.7%;②治疗过程中部分患者的血磷水平有一过性升高,高磷血症发生率40%,血钙水平未见明显升高;③临床症状如骨痛、四肢无力、皮肤瘙痒和关节痛等有不同程度改善,症状缓解较明显者占76.7%。结论骨化三醇注射液治疗血液透析患者SHPT安全、有效,临床症状改善较明显,但长期疗效和安全性有待进一步观察。     

术中及围手术期血清iPTH监测对501例继发性甲状旁腺功能亢进患者手术效果的精准诊断研究——“Diagnostic Accuracy Study of Intraoperative and Perioperative Serum Intact PTH Level for Successful Parathyroidectomy in 501 Secondary Hyperparathyroidism Patients”的二

目的甲状旁腺切除术(parathyroidectomy,PTX)是继发性甲状旁腺功能亢进患者(secondary hyperparathyroidism,SHPT)的有效治疗方式,然而由于甲状旁腺位置和数目异常的存在,部分患者术后SHPT仍持续存在。本研究探讨PTX患者术中及围手术期血清全段甲状旁腺激素(intact parathyroid hormone,iPTH)监测对手术效果精准诊断的意义。方法记录501例行甲状旁腺全切+自体前臂移植术(不伴胸腺切除)的慢性肾脏病患者的术中及围手术期血清iPTH值。术后一周内患者血清iPTH≤50 pg/ml为手术成功;若50 pg/ml则在6月内进行随访,随访血清iPTH300 pg/mL即为手术成功,否则为SHPT持续存在。结果 433例(86.4%)患者手术成功,49例(9.8%)患者SHPT持续存在,19例(3.8%)患者缺乏有效随访归为手术效果未知组。肝炎(n=204)与非肝炎(n=297)患者比较,基线血清iPTH水平及术中血清iPTH下降百分比无显著统计学差异(P0.05)。受试者工作特征(receiver operating characteristic,ROC)曲线结果表明术后20分钟血清iPTH下降≥88.9%提示手术成功(曲线下面积0.909,敏感度78.6%,特异度88.5%)。术后4天血清iPTH≥147.4 pg/ml提示SHPT持续存在(曲线下面积0.998,敏感度100%,特异度99.5%)。结论甲状旁腺切除术中血清iPTH监测能提示甲状旁腺切除是否彻底,避免对患者不必要的探查,降低手术并发症的发生率。围手术期血清iPTH监测提示SHPT是否持续存在,对此类患者需密切随访、及时开始药物治疗或必要时再次手术。     

维持性血液透析患者继发性甲状旁腺功能亢进的治疗观察

目的研究低钙透析联合1，25（0H）2D3及碳酸钙治疗维持性血液透析患者继发性甲状旁腺功能亢进的有效性和安全性。方法选择山东省千佛山医院肾脏病血液净化中心23例血液透析患者，校正血钙≥8．00mg／dl，iPTH〉300pg／ml，分为Ⅰ组[iPTH（300-600）pg／ml]和Ⅱ组（iPTH600-1000pg／ml），起始量分别给予1，25（OH）2D32～3μg／w和4～6μag／w，分2～3次较大剂量间断口服治疗，配合碳酸钙日服降磷，并联合低钙透析（透析液钙浓度为1．25mmol／L），总观察期20周。监测治疗前后患者血钙、磷、钙磷乘积、iPTH、碱性磷酸酶（hKP）等指标及药物用量变化情况。结果为期20周的治疗显著降低血液透析患者血磷、钙磷乘积、iPTH水平，血钙水平在治疗过程中保持稳定。不良反应较小且均可耐受。结论合理调整活性维生素D用量，配合碳酸钙及低钙透析可有效控制血液透析患者继发性甲状旁腺功能亢进，并且在治疗的早期疗效更显著，安全性良好。     

口服冲击剂量α- D3治疗慢肾衰伴严重继发性甲旁亢的疗效评价

目的评价口服α-D3冲击剂量对尿毒症维持性血液透析(HD)伴严重继发性甲旁亢(2°HPT)患者的疗效,包括对骨密度(BMD)的影响.方法20例上述患者每周口服α-D3 2次,每次2μg,疗程5个月,每4周测血清钙(SCa)、磷(SP)、碱性磷酸酶(AKP)及血清全段甲状旁腺素(iPTH),12例治疗前后测定BMD及治疗前超声多普勒测定甲状旁腺体积.结果与治疗前相比,iPTH从第1个月后明显下降(691±340vs 476±279 pg/ml,P＜0.05),第3个月后下降更加明显(691±340 vs 370±217 pg/ml,P＜0.03),但治疗后iPTH水平仍高于正常,下降幅度最大为46%;AKP第2个月下降明显(305±126 vs 223±114 IU/L,P＜0.05),第4个月下降更加明显(305±126 vs 200±110 IU/L,P＜0.03);SCa第4、5月上升明显(2.19±0.20vs 2.43±0.31,2.39±0.30mmol/L,P＜0.03),但其均值仍在正常范围内;SP第4、5个月上升明显(1.76±0.24 vs 2.15±0.33,2.85±0.76 mmol/L,P＜0.05);股骨颈及腰椎骨密度有明显增高(股骨颈0.720±0.137 vs 0.754±0.113 g/cm2,P＜0.03;腰椎(L1-L4)1.052±0.117 vs 1.074±0.113g/cm2,P＜0.05).结论口服α-D3冲击剂量能有效治疗2°HPT,但伴有SCa、SP增高,而SCa仍在正常范围以内,并能改善BMD.     

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.     

骨化三醇治疗继发甲状旁腺功能亢进临床观察

目的 评价骨化三醇冲击和每日治疗对继发甲状旁腺功能亢进(SHPT)的疗效.方法 选择肾功能不全72例血液透析患者,血甲状旁腺激素(iPTH)水平>300 pg/ml,随机分为冲击组和每日组,分别采用骨化三醇2 μg 1周2次和0.5 μg,1次/d,观察24周,检测治疗前后血PTH及钙磷代谢相关指标.结果 血清iPTH均发生变化,冲击组AKP(碱性磷酸酶),iPTH指标明显下降,钙,磷两组治疗前后无明显差异,均不良反应轻微.结论 骨化三醇能有效控制SHPT,安全性好,冲击法对SHPT患者疗效更显著.     

西那卡塞治疗维持性血液透析患者不同甲状旁腺激素水平长期疗效评估CSCD

目的观察并评价西那卡塞对不同全段甲状旁腺激素(intact parathyroid hormone,iPTH)血液透析合并继发性甲状旁腺功能亢进(secondary hyperparathyroidism,SHPT)的患者长期疗效,为临床治疗提供依据。方法回顾性分析2010年5月~2019年8月好大夫在线张凌医生网站线上诊疗及北京市垂杨柳医院肾内科血液透析室的47例SHPT患者,根据治疗起始iPTH值分为A组(iPTH<800pg/ml)和B组(iPTH≥800pg/ml),观察应用西那卡塞治疗12月后,2组患者在血钙、血磷、iPTH控制方面的差异。疗效评价标准:iPTH下降≥50%定义为治疗显效:iPTH下降≥30%定义为治疗有效。结果2组患者基线情况除了iPTH和超声检查甲状旁腺增大腺体数目不同以外,其他指标无差异;随着治疗时间延长,血钙达标率在6月A组高于B组(χ^(2)=3.632,P=0.029),在治疗12月时2组无差异(χ^(2)=1.362,P=0.243);血磷达标率逐渐上升,但无统计学差异(χ^(2)=5.158、6.000,P=0.076、0.050);iPTH均值在A组和B组治疗6月及12月时都明显下降(Z=-2.728、-1.852,P=0.003、0.032);在治疗6月及12月时2组的显效率、有效率无统计学差异(χ^(2)=0.011、0.084、0.869、0.254,P=0.917、0.772、0.351、0.614);在治疗6月时iPTH≤250 pg/ml比例A组高于B组(χ^(2)=5.887,P=0.015),在治疗12月时A组和B组无差异(χ^(2)=0.510,P=0.475)。结论西那卡塞对于不同iPTH水平的血液透析患者都有疗效,其中iPTH<800pg/ml组更易达标,iPTH≥800pg/ml组随着治疗时间延长达标率获益。     

血液灌流对维持性血透患者血清甲状旁腺素的清除作用

[摘要] 目的 观察血液透析(HD)和血液透析串联血液灌流(HD+HP)对维持性血液透析患者血清甲状旁腺素(PTH)的清除效果。方法 将20例稳定的维持性血液透析患者随机分为2组：HD组及HD+HP组，治疗前、后分别抽静脉血测定血清肌酐（Scr）、尿素氮（BuN）血清磷及PTH。结果 HD组治疗后PTH及血清磷分别由 987.86±445.31pg/ml，2.40±0.31mmol/L降至973.29±424.36pg/ml, 1.87±0.10mmol/L，PTH清除率为 7.33±2.89%，治疗前后无明显差异（P＞0.05），血清磷治疗前后差异显著（P＜0.05）；HD+HP组治疗后PTH由 998.38±431.96pg/ml降至749.13±543.13pg/ml，单次治疗清除率为39.73±27.53% ，治疗前后差异显著(P＜0.05)，血清磷由治疗前2.39±0.37mmol/L降至1.34±0.12mmol/L，差异显著并明显高于HD组（P＜0.05）。结论 HD+HP可以有效清除PTH及磷，HD可以有效清除血清磷但不能有效清除PTH。     

1,25(OH)2D3对尿毒症患者胰岛素分泌低下及胰岛素抵抗的影响

目的了解1,25(OH)2D3对尿毒症血液透析患者的糖耐量异常、胰岛素分泌低下及胰岛素抵抗的影响.方法将24名尿毒症血液透析患者[平均年龄(37±1)岁],分为2组,每组12人,治疗组(第一组)口服1,25(OH)2D3,对照组(第二组)口服无活性的维生素D.另设健康对照组6人.在治疗前和治疗4周后对血中以下指标进行检测糖耐量;胰岛素浓度;胰岛素分泌时相;胰岛素敏感度;甲状旁腺素(iPTH).结果两组治疗前后iPTH无变化. 两组治疗前均存在糖耐量异常、胰岛素分泌低下、胰岛素敏感度下降、 1,25(OH)2D3浓度下降及甘油三脂升高.第一组治疗4周后上述指标均有明显改善而第二组无明显变化.结论 1,25(OH)2D3可改善尿毒症血液透析患者的胰岛素分泌低下及胰岛素抵抗同时缓解高甘油三脂血症.     

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.     

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++.     

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.     

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.     

Size at birth, adult intestinal calcium absorption and 1,25(OH)(2) vitamin D

BACKGROUND: Adult bone mineral status is modified by early environmental influences, but the mechanism of this phenomenon is unknown. Intestinal calcium absorption and vitamin D metabolism are integrally involved in bone metabolism and may be programmed during early life. AIM: To examine the early-life influences on calcium absorption and its control in 322 post-menopausal female twins. METHODS: Intestinal calcium absorption was assessed by the stable strontium (Sr) method. Serum PTH, 25(OH) and 1,25(OH)(2) vitamin D were measured and recalled birth weight recorded. RESULTS: Fractional intestinal Sr absorption (alpha Sr) was correlated with serum 1,25(OH)(2) vitamin D (p<0.001), but not with 25(OH) vitamin D. Birth weight was inversely associated with serum 1,25(OH)(2) vitamin D (p=0.04), the association being independent of serum calcium, phosphate, creatinine and PTH. Birth weight was inversely correlated with alpha Sr (p=0.03), this association being independent of age, season, customary calcium intake and serum 25(OH) vitamin D; however, when serum 1,25(OH)(2) vitamin D was added into the model, the association became non-significant, suggesting that the association was partially mediated via serum 1,25(OH)(2) vitamin D. DISCUSSION: We found a significant inverse association between birth weight and intestinal calcium absorption that is partially explained by an association between serum 1,25(OH)(2) vitamin D and birth weight. This suggests a mechanism whereby the intra-uterine environment might affect adult skeletal status.     

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.     

Reversal of skeletal resistance to parathyroid hormone in uremia by vitamin D metabolites: evidence for the requirement of 1,25(OH)2D3 and 24,25(OH)2D3.

This study evaluates the role of vitamin D metabolites in the genesis of the skeletal resistance to the calcemic action of PTH in uremia. The changes in serum calcium after infusion of 2 U of PTE per kilogram per hour for 8 hr were evaluated in thyroparathyroidectomized dogs before and after 1 and 3 days of acute uremia produced by bilateral nephrectomy. The animals received vitamin D metabolites during the 3 days of uremia. Supplementation of 0.68 microgram/day 1,25(OH)2D3 and 24R,25(OH)2D3 restored the calcemic response to PTE to normal. This is in contrast to only partial correction of the response to PTE by 1,25(OH)2D3 alone. Administration of 1.36 microgram/day 24R,25(OH)2D3 did not improve the calcemic response to PTE. The results indicate that (1) both 1,25(OH)2D3 and 24R,25(OH)2D3 are necessary for the complete reversal of the impaired calcemic response to PTE, (2) this effect is not due to the increase in the amount of the dihydroxylated compounds of vitamin D, since equivalent amounts of these compounds in the form of 24R,25(OH)2D3 alone had no effect, and (3) the better effect of the combination of 1,25(OH)2D3 and 24R,25(OH)2D3 is most probably due to an interaction between these two metabolites of vitamin D permitting an intact calcemic action of PTH.