Effects of Postmenopausal Hormone Replacement Therapy With and Without Vitamin D3 on Circulating Levels of 25-Hydroxyvitamin D and 1,25-Dihydroxyvitamin D

The effects of postmenopausal hormone replacement therapy (HRT) and vitamin D₃ on vitamin D metabolites (25OHD and 1,25(OH)₂D) were studied in a population-based prospective 1-year study. The serum concentrations of intact parathyroid hormone (PTH), calcium, and phosphate were also studied. A total of 72 women were randomized into four treatment groups: HRT group (sequential combination of 2 mg estradiol valerate and 1 mg cyproterone acetate), Vit D₃ group (vitamin D₃ 300 IU/day + calcium lactate 500 mg/day), HRT + Vit D₃ group (both above) and placebo group (calcium lactate 500 mg/day). Serum samples were taken in March–April, when vitamin D formation from sunlight in Finland is minimal after the dark winter. Serum concentrations of 25OHD increased in the Vit D₃ group (33.5%, P < 0.001) and in the HRT + Vit D₃ group (38.2%, P < 0.001) but had not changed significantly in the HRT and placebo groups at the 1-year follow-up examination. Serum concentrations of calcitriol (1,25(OH)₂D) increased, however, only in the HRT group (23.7%, P < 0.05), and remained unchanged in other groups. Serum concentrations of PTH decreased by 23.2% (P < 0.05) in the placebo group, but did not change significantly in the other three groups. The concentrations of serum calcium increased in the nonhormone groups (P < 0.001), whereas serum phosphate concentrations decreased in the hormone groups (P < 0.05 and 0.001). Our results confirm the positive effect of 1 year of HRT on serum calcitriol. Vitamin D₃ supplementation increased 25OHD concentrations, but did not affect calcitriol concentrations even though the initial levels were low. Interestingly, the combination of HRT and vitamin D₃ did not increase serum calcitriol concentrations as much as HRT alone. Received: 14 June 1996 / Accepted: 17 June 1997     

Correlations between Vitamin D Status and Biochemical/Clinical and Pathological Parameters in Primary Hyperparathyroidism

Background To determine the prevalence of vitamin D deficiency and the effects of vitamin D status on parathyroid adenoma weight, clinical and biochemical indices in patients with primary hyperparathyroidism (pHPT) were studied. Methods Eighty patients with pHPT who underwent surgical treatment and in whom the presence of parathyroid adenoma were confirmed histopathologically were studied retrospectively from recorded data files. Patients were divided into three groups: patients with 25-hydroxyvitamin D (25-OHD) concentrations < 15 ng/ml (group 1, n = 44), patients with 25-OHD concentrations > 15–25 ng/ml (group 2, n = 9), and patients with 25-OHD concentrations > 26 ng/ml (group 3, n = 27). Serum calcium, phosphate, alkaline phosphatase, creatinine, and albumin levels and urinary calcium excretion were determined by auto-analyzer. Plasma 25-OHD and parathyroid hormone (PTH) levels were determined by immunoradiometric assay using commercially available kits. Results No statistically significant differences were observed with respect to serum calcium, phosphorus, albumin, and creatinine concentrations between these groups. Serum PTH, alkaline phosphatase concentrations, urinary calcium excretion, parathyroid adenoma weight, and postoperative sixth month PTH concentrations were significantly higher in group 1 patients than in group 2 and group 3 patients. Significant correlations were observed between parathyroid adenoma weight and serum 25-OHD concentrations (r = −0.348, P = 0.020); parathyroid adenoma weight and urinary calcium excretion (r = 0.348, P = 0.021). Multiple regression analysis revealed that parathyroid adenoma weight, serum 25-OHD, and preoperative PTH concentrations correlated independently and significantly with postoperative sixth month PTH concentrations. Conclusions Vitamin D deficiency leads to more severe bone disease, increased parathyroid tumor growth, and delayed postoperative recovery of parathyroid function in patients with primary hyperparathyroidism.     

Effect of immobilization upon renal synthesis of 1,25-dihydroxyvitamin D in disabled elderly stroke patients

A 1,25-dihydroxyvitamin D [1,25-(OH)2D] deficiency and immobilization-related increased serum calcium concentration have been observed in hemiplegic stroke patients. To elucidate the influence of increased serum calcium concentration on bone metabolism, we measured serum biochemical indices and bone mineral density (BMD) in the second metacarpals of 170 elderly subjects with hemiplegic stroke and 72 age-matched healthy controls. Serum concentrations of 25-hydroxyvitamin D [25-(OH)D], 1,25-(OH)2D, ionized calcium, intact parathyroid hormone (PTH), intact bone Gla protein (BGP), and pyridinoline cross-linked carboxyterminal telopeptide of type I collagen (ICTP) were measured. An increased serum calcium concentration (mean 2.543 mEq/L) was observed in this population and correlated negatively with the Barthel index (mean 66), indicating immobilization-induced bone resorption with consequent increased serum calcium. Decreased serum concentrations of 1,25-(OH)2D (mean 25.0 pg/mL) and serum 25-OHD concentration (mean 11.6 ng/mL) were noted. Serum PTH was not increased (mean 34.8 pmol/L). Serum levels of BGP were decreased significantly, whereas serum ICTP concentrations were elevated (mean 15.2 ng/mL). A strong negative correlation was seen between the serum calcium concentration and 1,25-(OH)2D (p < 0.0001). BMD of the second metacarpal in patients was decreased significantly compared with control subjects and highly correlated with 25-(OH)D and 1,25-(OH)2D concentrations. Immobilization-related increased serum calcium levels may inhibit PTH secretion, and thus 1,25-(OH)2D production. In addition, 25-(OH)D insufficiency also may contribute to decreased concentration of 1,25-(OH)2D.     

Altered divalent ion metabolism in early renal failure: role of 1,25(OH)2D

The present study evaluates the role of 1,25(OH)2D in the pathogenesis of abnormal mineral metabolism in patients with early renal failure (ERF). This was accomplished by examining the calcemic response to PTH and the handling of an oral phosphate load both before and after 6 weeks of therapy with 1,25(OH)2D. Twelve patients with ERF and six normal volunteers were studied. Patients with ERF as compared with normal subjects have low serum phosphate, low urinary calcium, low serum 1,25(OH)2D, and high plasma PTH and urinary cyclic AMP (cAMP). With EDTA infusion, an impaired calcemic response to PTH is observed in patients with ERF. The phosphate load test shows that these patients have an increased ability to excrete phosphate. After 1,25(OH)2D therapy a significant increase in serum phosphate, urinary calcium, and a decrease in urinary cAMP is observed only in ERF patients. In addition, the impaired calcemic response to PTH improves significantly, the renal handling of phosphate becomes normal, and the low baseline level of 1,25(OH)2D increases to normal. A significant correlation between levels of 1,25(OH)2D and creatinine clearance is observed in both patients and normals. In summary, the present data suggest that a mild deficiency of 1,25(OH)2D is present in ERF patients. The pathophysiological consequence of such a deficiency in patients with ERF may be important.     

Renal function and 25-hydroxyvitamin D concentrations predict parathyroid hormone levels in renal transplant patients.

BACKGROUND: Recent guidelines suggest supplementation with ergocalciferol (vitamin D(2)) in chronic kidney disease stages 3 and 4 patients with elevated parathyroid hormone (PTH) levels and 25-hydroxyvitamin D (25OHD) levels <75 nmol/l. These guidelines are also applied to renal transplant patients. However, the prevalence rates of 25OHD deficiency and its association with PTH levels in renal transplant populations have not been extensively examined. We aimed to document the prevalence rates of 25OHD deficiency [defined by serum levels <40 nmol/l (<16 ng/ml)] and insufficiency [<75 nmol/l (<30 ng/ml)] in a single renal transplant centre, and examine its relationship with PTH levels. METHODS: Serum 25OHD and PTH concentrations were measured in 419 transplant patients attending a single renal transplant clinic over a 4-month period. Demographic and biochemical data were also collected, including serum creatinine, calcium, phosphate and albumin. Simple and multiple linear regression analysis were performed. RESULTS: In 27.3% of the patients, 25OHD deficiency was present, and 75.5% had insufficiency. On univariate analysis, 25OHD, serum albumin and estimated glomerular filtration rate (eGFR) were significantly associated with PTH levels (P < 0.0001, P = 0.004 and P < 0.0001, respectively). Multiple linear regression demonstrated that only 25OHD, eGFR and serum phosphate were significantly predictive of PTH levels (R(2) = 0.19, P < 0.0001). In this model, a 75 nmol/l increase in 25OHD will only result in a maximal reduction in PTH of 2.0 pmol/l. CONCLUSIONS: We conclude that 25OHD deficiency and insufficiency are common in renal transplant patients and may exacerbate secondary hyperparathyroidism. However, 25OHD, eGFR and phosphate only account for 19% of the variability in PTH levels. In addition, even a large increase in serum 25OHD levels is likely to result in only a small reduction in PTH. Therefore, alternative approaches to managing hyperparathyroidism in renal transplant recipients rather than supplementation with ergocalciferol are warranted.     

Hyperparathyroidism and vitamin D deficiency after laparoscopic gastric bypass

Hyperparathyroidism (HPT) can occur after gastric bypass because of the alteration in vitamin D and calcium absorption. Adequate serum vitamin D concentrations have not been clearly defined in this patient population. Vitamin D (Vit D) and parathyroid hormone (PTH) were assessed 1 year after laparoscopic gastric bypass (LGB). The prevalence of HPT and Vit D deficiency were determined and their association was evaluated using Fisher's exact test. Ninety-three patients (aged 44 +/- 1.1 years, 49.6 +/- 0.67 Kg/m2 body mass index, 79.6% female, 69.6% white) were evaluated. The prevalence of Vit D deficiency (less than 20 ng/mL) and HPT (greater than 65 pg/mL) was 23.6 per cent (n = 22) and 25.7 per cent (n = 28), respectively. Among patients with HPT, only eight of 28 (28.6%) had Vit D deficiency, and of those with Vit D deficiency, only eight of 22 (36.4%) had HPT. There was a weak inverse correlation (r = -0.37) between PTH and Vit D. Blacks are at higher risk for Vit D deficiency. There was no significant association between Vit D deficiency and HPT, Vit D deficiency and Roux limb length, or HPT and Roux limb length. After LGB, Vit D deficiency and hyperparathyroidism occur commonly. Body mass index and Roux limb length are not associated with these two conditions, but racial differences do exist. There is a weak inverse correlation between Vit D and PTH. Further research is needed to elucidate the causes, treatments, and significance of HPT after LGB.     

The effects of menopause and estrogen replacement therapy on the renal handling of calcium

Mineral metabolism was studied in 99 premenopausal and 80 postmenopausal women both before and after 9–14 months of treatment with 50 µg/day transdermal estradiol. In estrogen-repleted subjects (premenopausal women and postmenopausal women on estrogen replacement therapy) total serum calcium was significantly lower (0.065 mmol/l;p<0.001) than in those who were estrogen-depleted (untreated postmenopausal women). This difference was smaller but still significant for calculated ultrafiltrable calcium (UFCa: 0.02–0.03 mmol/l;p<0.001). However, ionized calcium (both calculated and measured) was not different in the two groups of women. This finding explains why estrogen repletion does not induce changes in the serum level of intact parathyroid hormone (PTH), despite lower total or ultrafiltrable serum calcium. In a parallel study we have shown that intravenous administration of aminobutane bisphosphonate, a powerful inhibitor of bone resorption, produces similar decreases in serum calcium which were associated with significant increases in intact PTH.Estrogen-depleted women had, on the one hand, significantly higher serum levels of bicarbonate, anion gap, complexed calcium, pH, phosphate and alkaline phosphatase, and higher rates of tubular reabsorption of phosphate and urinary excretion of calcium and hydroxyproline. On the other hand they had lower serum chloride levels and lower rates of tubular reabsorption of calcium.Altogether these findings might indicate that estrogen deficiency decreases renal sensitivity to PTH. This is responsible for the higher serum phosphate and bicarbonate levels, the resulting mild metabolic alkalosis leading to higher serum levels of complexed ultrafiltrable calcium and higher rates of urinary excretion of calcium, but unchanged serum levels of ionized calcium and PTH.     

高校大学生循环骨钙素水平及其相关因素分析

目的分析高校大学生循环骨钙素水平及其与选择的钙调节激素、骨及糖脂代谢指标之间的相关性。方法通过问卷调查和血液指标检测,从某大学筛选出103名符合试验要求的非体育专业在校大学生。将受试者按照性别分为男性组和女性组,采用简单和多重线性回归分析两组受试者血清骨钙素水平的相关因素。结果男大学生血清骨钙素水平显著高于女大学生。Pearson相关分析结果表明,男大学生血清骨钙素水平与年龄和体质量指数(body mass index,BMI)呈负相关,而与血清甲状旁腺激素(parathyroid hormone,PTH)和碱性磷酸酶(alkaline phosphatase,ALP)水平呈正相关。经身体形态学指标校正后,与胰岛素水平和稳态模型评估胰岛素抵抗指数呈正相关;女大学生血清骨钙素水平与体重和BMI呈负相关,而与血清PTH、ALP、磷和空腹血糖(fasting blood glucose,FBG)水平呈正相关。经身体形态学指标校正后,与血清25羟维生素D [25-hydroxyvitamine D,25(OH) D]、钙、高密度脂蛋白胆固醇和FBG水平呈正相关。多重线性回归分析进一步表明,男大学生血清骨钙素水平与年龄和BMI独立负相关,而与血清PTH水平独立正相关;女大学生血清骨钙素水平与FBG水平独立正相关。结论高校大学生循环骨钙素水平及其与年龄、BMI、PTH和FBG水平的独立相关性具有性别差异。     

Sevelamer controls parathyroid hormone-induced bone disease as efficiently as calcium carbonate without increasing serum calcium levels during therapy with active vitamin D sterols

Little is known about the impact of various phosphate binders on the skeletal lesions of secondary hyperparathyroidism (2 degrees HPT). The effects of calcium carbonate (CaCO3) and sevelamer were compared in pediatric peritoneal dialysis patients with bone biopsy-proven 2 degrees HPT. Twenty-nine patients were randomly assigned to CaCO3 (n = 14) or sevelamer (n = 15), concomitant with either intermittent doses of oral calcitriol or doxercalciferol for 8 mo, when bone biopsies were repeated. Serum phosphorus, calcium, parathyroid hormone (PTH), and alkaline phosphatase were measured monthly. The skeletal lesions of 2 degrees HPT improved with both binders, and bone formation rates reached the normal range in approximately 75% of the patients. Overall, serum phosphorus levels were 5.5 +/- 0.1 and 5.6 +/- 0.3 mg/dl (NS) with CaCO3 and sevelamer, respectively. Serum calcium levels and the Ca x P ion product increased with CaCO3; in contrast, values remained unchanged with sevelamer (9.6 +/- 01 versus 8.9 +/- 0.2 mg/dl; P < 0.001, respectively). Hypercalcemic episodes (>10.2 mg/dl) occurred more frequently with CaCO3 (P < 0.01). Baseline PTH levels were 980 +/- 112 and 975 +/- 174 pg/ml (NS); these values decreased to 369 +/- 92 (P < 0.01) and 562 +/- 164 pg/ml (P < 0.01) in the CaCO3 and the sevelamer groups, respectively (NS between groups). Serum alkaline phosphatase levels also diminished in both groups (P < 0.01). Thus, treatment with either CaCO3 or sevelamer resulted in equivalent control of the biochemical and skeletal lesions of 2 degrees HPT. Sevelamer, however, maintained serum calcium concentrations closer to the lower end of the normal physiologic range, thereby increasing the safety of treatment with active vitamin D sterols.     

Calcitriol deficiency with retained synthetic reserve in chronic renal failure

Serum calcitriol and the free calcitriol index together with factors considered to regulate calcitriol production were measured in eleven patients with moderate chronic renal failure (MCRF) and eleven age- and sex-matched normal subjects. Although the serum dialysable calcium levels were similar in the two groups, there was depression of calcitriol levels and an elevation of PTH and nephrogenous cyclic AMP (NcAMP) levels in the MCRF patients. Furthermore, plasma phosphate levels were higher and the renal phosphate threshold was depressed in this patient group. When all subjects were grouped together calcitriol was positively correlated with GFR. When calcitriol levels were factored for GFR, to permit an assessment of calcitriol production per unit functioning renal mass, there was no significant difference between normal and MCRF subjects. To determine whether reserve for calcitriol production existed, six of the MCRF patients and six of the age- and sex-matched normal subjects received a low calcium diet for one week supplemented by cellulose phosphate to bind calcium within the gut. In both groups there was a significant rise in calcitriol, although the absolute levels were much lower in the MCRF patients than the normal subjects. These results suggest that calcitriol deficiency is a major feature of MCRF despite marked hyperparathyroidism. The rise in calcitriol levels in MCRF suggests persistent reserve secretory capacity in this condition. Therefore, the low serum calcitriol concentration may be due not only to structural renal damage, but also to suppression of calcitriol formation perhaps due to altered renal phosphate handling.     

A 6-hour human parathyroid hormone (1–34) infusion protocol: Studies in normal and hypoparathyroid subjects

Summary Parathyroid hormone (PTH)-resistant states are usually diagnosed by the failure of an acute PTH injection to elicit a rise in urinary cAMP and phosphate or, less commonly, by the failure of repeated PTH injections to raise serum calcium. We have established a 6 hour infusion of human PTH (1–34) which identifies PTH-resistant hypoparathyroid subjects on the basis of serum 1,25-dihydroxyvitamin D (1,25(OH)₂D) and calcium responses. 1.25-Dihydroxyvitamin D levels increased by at least 58 pmol/liter and serum calcium by at least 0.1 mmol/liter in PTH-responsive hypoparathyroid subjects (n=6), whereas in pseudohypoparathyroid subjects (n=5) these levels rose by less than 22 pmol/liter and 0.06 mmol/liter respectively. The responsiveness of urinary phosphate excretion, expressed as the renal threshold phosphate concentration (TmPO₄/GFR), to PTH also clearly separated the pseudohypoparathyroid patients from the other subjects. Differences in urinary calcium responses were observed though this parameter was less reliable in the identification of individual PTH-resistant or PTH-sensitive hypoparathyroid patients. Nephrogenous cAMP did not discriminate between groups when this protocol was used. This test has the potential to facilitate and extend the classification of PTH-resistant states.     

Relationship between serum parathyroid hormone, vitamin D sufficiency, age, and calcium intake

Vitamin D deficiency is extremely common among elderly subjects and it has been associated with poor bone health, and to a number of other conditions. The ideal 25-hydroxy-vitamin D [25(OH)D] concentration, reflecting the size of vitamin D deposits, are generally retained those not associated with any marginal increase in serum parathyroid hormone (PTH). These threshold values vary considerably and this may be due to the interaction of other factors. The aim of the study is to assess whether age and calcium intake interact with the relationship between 25(OH)D and PTH. Data from a survey on the prevalence of hypovitaminosis D in elderly women in Italy were analysed in order to verify whether age and calcium intake were interfering on the 25(OH)D/PTH relationship. A total of 697 women were available for analysis. Serum PTH levels were significantly correlated with age, 25(OH)D and calcium intake (p<0.001) and in a multivariate model they all significantly contributed to explain PTH variance (R(2)=24.4%). In 39 elderly osteoporotic women on a low calcium intake and given vitamin D supplements (2000-3000 IU daily for >8 months) able to increase 25(OH)D levels above 110 nMol/l, PTH levels were maintained below 35 pg/mL. The minimum 25(OH)D levels to be recommended depends largely on the age and the calcium intake. In elderly individuals not taking calcium supplements in order to keep serum PTH levels strictly within the normal range 25(OH)D serum levels should be maintained above ca. 120 nMol/L.     

Hip fracture patients in India have vitamin D deficiency and secondary hyperparathyroidism

Summary

This study evaluated the parameters of bone mineral homeostasis including 25(OH)D and PTH in 90 Indian patients with hip fracture and 90 controls. Hypovitaminosis D, secondary hyperparathyroidism, and biochemical osteomalacia was present in 77, 69, and 50 % patients, respectively, significantly higher compared to controls. Vitamin D deficiency is an important risk factor for hip fracture.

Introduction

The prevalence of vitamin D deficiency is not well known in hip fracture patients from India. Therefore, the present study was conducted to evaluate the parameters of bone mineral homeostasis including 25(OH)D and intact PTH in hip fracture from North India.

Methods

Ninety consecutive patients with hip fracture and similar number of age- and sex-matched controls were enrolled in the study. The fasting venous samples were analyzed for 25-hydroxyvitamin D (25-OHD), intact parathyroid hormone (PTH), alkaline phosphatase (ALP), calcium, and phosphorus. Vitamin D deficiency was defined as serum 25-OHD of <20 ng/dl.

Results

The mean age of hip fracture subjects was 65.9?±?12.6 which was comparable in men and women. Majority of study subjects were women (70 women and 20 men). The serum 25(OH)D and calcium levels were significantly lower, whereas the intact PTH and ALP levels were significantly higher in patients compared to controls. There was significant negative correlation between serum 25(OH)D and PTH. In the hip fracture group, 76.7 % of the subjects had vitamin D deficiency, and 68.9 % had secondary hyperparathyroidism. In the control group, vitamin D deficiency and elevated PTH levels were seen in 32.3 and 42.2 %, respectively.

Conclusion

About three fourths of hip fracture patients have vitamin D deficiency, and two thirds have secondary hyperparathyroidism. Therefore, the serum 25-OHD level may be a useful index for the assessment of risk of hip fracture in India.     

Vitamin D insufficiency defined by serum 25-hydroxyvitamin D and parathyroid hormone before and after oral vitamin D3 load in Japanese subjects

Vitamin D insufficiency is a risk for both skeletal and nonskeletal health. However, some ambiguity remains about threshold serum 25(OH)D for vitamin D insufficiency. To determine the threshold serum 25(OH)D to maintain normal calcium availability without elevation in serum parathyroid hormone (PTH) among Japanese subjects with various calcium intakes, we conducted a multicenter prospective open-labeled study. We recruited 107 ambulatory subjects without disorders affecting vitamin D metabolism to whom oral vitamin D₃ 800?IU/day for 4?weeks or 1,200?IU/day for 8?weeks was given. Serum 25(OH)D, PTH, calcium, phosphate, and magnesium were measured before and after vitamin D₃ supplementation. Calcium intake was assessed by questionnaires. When all the data were combined, serum 25(OH)D was negatively correlated with PTH. The cubic spline curve between serum 25(OH)D and PTH indicated PTH reached its plateau between 35 and 40?pg/ml at 25(OH)D between 25 and 30?ng/ml. Vitamin D₃ supplementation increased serum 25(OH)D and decreased PTH. Change in PTH correlated positively with baseline serum 25(OH)D. From the regression analyses, baseline serum 25(OH)D above 28?ng/ml corresponded to the threshold level without reduction in PTH after vitamin D₃ supplementation. In multivariate regression analyses, age but not calcium intake was a significant determinant of PTH. We concluded that a serum 25(OH)D level of 28?ng/ml was identified as a threshold for vitamin D insufficiency necessary to stabilize PTH to optimal levels.     

Vitamin D status among patients with fractured neck of femur in Hong Kong

Vitamin D deficiency leads to secondary hyperparathyroidism initially and then to mild osteomalacia, both of which conditions may be aymptomatic and may predispose to bone fracture. To assess the importance of vitamin D deficiency in predisposing to fractured neck of femur, we studied the vitamin D status, dietary intake and socio-economic characteristics in 69 patients with fractured neck of femur (group A), 28 normal subjects with age above 60 (group B), and 101 normal volunteers (group C). Patients with fractured neck of femor had significantly lower levels of serum 25-hydroxy-cholecalciferol compared with subjects of groups B and C. There is no statistically significant difference in other biochemical parameters, including calcium, phosphate, and alkaline phosphatase. Patients with fractured neck of femur and with 25-hydroxycholecalciferol below 20 ng/mL were characterized by a home-bound and/or institutionalized life-style, smaller living place, and limited access to open space. To conclude, hypovitaminosis D is a common problem among elderly patients with fractured neck of femur in Hong Kong. The fact that such vitamin D deficiency is associated with muscle weakness may contribute to falls, and thus indirectly account for an increased rate of hip fractures over the normal control.     

慢性乙肝性肝硬化症男性患者血清性激素、钙调节激素和骨转换指标的变化

目的　慢性严重肝脏损害常合并肝性骨病。为了探讨终末期肝病患者的钙调节激素变化和骨转换率状态 ,我们回顾性分析了 17例乙肝后肝硬化失代偿的男性患者 ,并和年龄、身高、体重相匹配的健康男性进行对照研究。方法　肝硬化组和对照组均检测其血清性激素 [雄激素 (T)、雌激素 (E2 ) ],钙调节激素 [甲状旁腺素 (PTH)、降钙素 (CT)和 2 5羟维生素D3(2 5 -OHVD3) ]和骨转换指标 [血清骨钙素 (BGP)和尿脱氧吡啶啉 肌酐比值 (Dpd Cr) ]以及钙 (Ca2 + )、磷 (PO3- )和碱性磷酸酶 (ALP)。结果　显示与对照组相比 ,肝硬化组血清T明显降低、E2 水平和E2 T比值显著升高 ;血清PTH显著升高、2 5 -OHVD3明显降低 ,而CT差异不大。其中E2 升高和 2 5 -OHVD3降低有极显著意义。肝硬化组血清BGP和Ca2 + 水平明显降低、尿Dpd Cr比值和尿Ca2 + Cr比值明显升高。而血清CT和PO3- 差异不大。结论　我们认为慢性严重肝硬化患者骨量减低 ,呈现出骨形成降低、骨吸收增强之特征 ,与维生素D和性激素代谢异常有关 ,而PTH升高乃继发性改变     

Aspects of juvenile rickets/osteopenia in black children

Juvenile rickets or osteopenia in rural black children is thought to be due to low calcium intake. Characteristic findings include mild calcium deficiency, normal serum phosphate levels, increased alkaline phosphatase concentrations and normal plasma vitamin D levels. The present series consisted of 62 black children (average age 6.82 years), 41 males and 21 females. Low levels of serum calcium and phosphate were present in 34 (54%) and 18 (29%) of the patients respectively. Alkaline phosphatase concentrations were raised (greater than 350 IU/l) in 38 (61%). Serum sodium, potassium, chloride, total bicarbonate, magnesium, ceruloplasmin and albumin levels were generally within normal limits. Urinary acidification was normal and barium studies were reported as normal in all but 4 children. Malabsorption was not an important feature. Serum vitamin D levels were not determined. All 18 patients with hypophosphataemia improved. Eleven children showed no clear response after at least 8 weeks in hospital--8 remained hypocalcaemic and 2 of the 3 patients with normal biochemical values showed no radiological improvement of osteopenia after 2 and 4 months in hospital, while the 3rd showed only very slight improvement after 7 months in hospital. It is not clear why these patients did not respond and whether even longer hospitalisation would have been effective.     

Absence of effect of 24,25-dihydroxycholecalciferol on serum immunoreactive PTH in patients with persistent hyperparathyroidism after renal transplantation

Three hypercalcemic renal transplant recipients with stable, excellent renal function (creatinine clearance 74 +/- 11.8 ml/min) were treated with 60 micrograms 24,25(OH)2D3 by mouth daily for three months. Immunoreactive c-terminal PTH, intact PTH, 1,25(OH)2D3, 25(OH)D3, 24,25(OH)2D3, and serum and 24 h urine calcium, phosphate, magnesium and creatinine were obtained before, at one week, one month and three months of treatment, and at six weeks post-treatment. Significant elevations in serum levels of 24,25(OH)2D3 were induced by therapy (1.32 +/- .16 ng/ml to 30.06 +/- 5.18 ng/ml at one month). Moderate elevations of c-terminal PTH and normal levels of intact PTH remained unchanged throughout the study. Serum calcium remained elevated, serum phosphate and magnesium remained depressed and creatinine clearance and urinary excretion of calcium, phosphate, and magnesium remained unchanged. Furthermore, 1,25(OH)2D3 and 25(OH)D3 remained in the normal range throughout the study. We conclude that 24,25(OH)2D3 did not have a suppressant effect on levels of iPTH in the clinical setting of persistent hyperparathyroidism after successful renal transplantation.     

Long-term Follow-up of Patients with Elevated PTH Levels following Successful Exploration for Primary Hyperparathyroidism

Several studies have documented elevated parathyroid hormone (PTH) levels after seemingly successful exploration for primary hyperparathyroidism (pHPT). It is not known if this is a transient phenomenon after pHPT surgery or if it predisposes to recurrent disease. A series of 99 consecutive patients with pHPT who had solitary parathyroid adenomas were followed for 5 years. Serum levels of PTH and biochemical variables reflecting PTH activity were measured before operation, at 8 weeks postoperatively, and then yearly for 5 years. All patients were normocalcemic after exploration. At 8 weeks after operation 28% of the patients had elevated serum PTH levels; at 5 years this figure decreased to 16%. During the 5-year follow-up one group of patients normalized their PTH levels, another groups PTH levels fluctuated, and still another group had consistently normal PTH levels. Patients with fluctuating PTH levels had increased levels of serum calcium and phosphate. Some of these patients (15%) showed signs of impaired renal function. Two patients with consistently elevated PTH levels showed signs of mild renal dysfunction, and one of them developed recurrent HPT. Elevated PTH levels after successful parathyroid surgery is not a transient phenomenon. An increased risk for recurrent disease is postulated for some of the patients who do not normalize their PTH levels postoperatively, and long-term surveillance of these patients is suggested.     

Comparative effects of vitamin K and vitamin D supplementation on prevention of osteopenia in calcium-deficient young rats

The aim of this study was to clarify the difference in the effects of vitamin K and vitamin D supplementation on the development of osteopenia in young rats under mild calcium deficiency. Sixty female Sprague-Dawley rats, 6 weeks of age, were randomized by stratified weight method into six groups with 10 rats in each group: baseline control, 0.5% (normal) calcium diet, 0.1% (low) calcium diet, 0.1% calcium diet + vitamin K (30 mg/100 g, food intake), 0.1% calcium diet + vitamin D (25 microg/100 g, food intake), and 0.1% calcium diet + K + D. After 10 weeks of feeding, serum calcium, 25-hydroxyvitamin D(3) [25 (OH) D(3)], 1,25-dihydroxyvitamin D(3) [1,25 (OH)(2) D(3)], and parathyroid hormone (PTH) levels were measured, and intestinal calcium absorption and renal calcium reabsorption were evaluated. Bone histomorphometric analyses were performed on cortical bone of the tibial shaft and cancellous bone of the proximal tibia. Calcium deficiency induced hypocalcemia, increased serum PTH and 1,25 (OH)(2) D(3) levels with decreased serum 25 (OH) D(3) level, stimulated intestinal calcium absorption and renal calcium reabsorption, and reduced maturation-related cortical bone gain as a result of decreased periosteal bone gain and enlarged marrow cavity but did not significantly influence maturation-related cancellous bone gain. Vitamin K supplementation in calcium-deficient rats stimulated renal calcium reabsorption, retarded the abnormal elevation of serum PTH level, increased maturation-related cancellous bone gain, and retarded the reduction in maturation-related cortical bone gain. On the other hand, vitamin D supplementation in calcium-deficient rats stimulated intestinal calcium absorption via increased serum 1,25 (OH)(2) D(3) level with prevention of the abnormal elevation of serum PTH level, prevented hypocalcemia, reduced the maturation-related cancellous bone gain, and prevented the reduction in periosteal bone gain and enhanced enlargement of the marrow cavity with no significant effect on the reduction in maturation-related cortical bone gain. However, no synergistic effect of vitamin K and vitamin D on intestinal calcium absorption, renal calcium reabsorption, and cancellous and cortical bone mass was found. This study shows the differential effects of vitamin K and vitamin D supplementation on the development of osteopenia in young rats under mild calcium deficiency. Vitamin K supplementation stimulates renal calcium reabsorption, increases maturation-related cancellous bone gain, and retards the reduction in maturation-related cortical bone gain, whereas vitamin D supplementation stimulates intestinal calcium absorption and prevents the reduction in maturation-related periosteal bone gain by inducing accumulation of calcium from cancellous and endocortical bone.