老年男性2型糖尿病患者各种钙调激素与骨密度改变的关系

目的测定老年男性2型糖尿病患者各种钙调激素及骨密度,探讨老年男性2型糖尿病患者骨质疏松的发病机理,为其防治提供理论依据。方法用双能X线吸收法测定70例老年男性2型糖尿病患者及60例年龄、体重指数相匹配的对照者的腰椎及髋部骨密度,并采用放免法测定血清骨钙索(BGP)、抗酒石酸酸性磷酸酶(TRAP)、甲状旁腺素(PTH)、降钙素(CT)、1,25(OH)2D3、25(OH)D3、尿羟脯氨酸(HOP)等,两组进行比较。结果 老年男性2型糖尿病患者较对照组骨密度显著降低。血BGP、CT、1,25(OH)2D3浓度低于对照组(P<0.05).TRAP、PTH、尿HOP显著高于对照组(P<0.05)。结论老年男性2型糖尿病患者PTH、CT、1,25(OH)2D3等钙调激素分泌及代谢失常,影响骨代谢,出现糖尿病性骨质疏松,表现为骨吸收增加,骨形成减少与缓慢,骨吸收过程大于骨形成。     

Effect of haemodialysis on markers of bone turnover in children

‘Intact’ parathyroid hormone (iPTH) assays are used to measure serum PTH levels in haemodialysis patients to diagnose and monitor secondary hyperparathyroidism and consequent renal osteodystrophy (ROD); these assays exhibit cross-reactivity with long carboxyl-terminal PTH fragments (C-PTH) that accumulate in end stage renal failure (ESRF) and antagonise the biological activity of the whole molecule, 1–84 PTH. The effects of haemodialysis on C-PTH are not known. We investigated how haemodialysis affects serum concentrations of calcium, iPTH, 1–84 PTH, C-PTH, and other markers of bone turnover; bone-specific alkaline phosphatase (BALP) and type 1 collagen cross-linked telopeptide (CTx). Fifteen patients, mean (range) age 13.9 (4.3–17.6) years, haemodialysed for a median of 16.3 (4–41) months, had pre- and post-dialysis serum samples collected for routine biochemistry, BALP, CTx, iPTH and 1–84 PTH assays. Changes to serum concentrations and relationships between these biochemical surrogate markers of ROD were investigated. Serum phosphate and PTH levels (measured by both assays) fell significantly during dialysis, whereas serum calcium, C-PTH, the 1–84 PTH: C-PTH ratio and BALP and CTx concentrations were not significantly changed. 1–84 PTH levels were related to pre but not post dialysis serum calcium levels and changes to 1–84 PTH levels during dialysis were related to changes in serum calcium levels. 1–84 PTH and iPTH were reduced by haemodialysis, whereas levels of BALP and CTx remained stable post-dialysis. The relationship between BALP and CTx and bone histology requires investigation to determine whether they are more useful markers of bone turnover in this patient group.     

Parathyroid hormone-independent osteoclastic resorptive bone disease: a new variant of adynamic bone disease in haemodialysis patients.

BACKGROUND: Osteitis fibrosa cystica (OFC) caused by secondary hyperparathyroidism is the pre-eminent form of uraemic osteodystrophy. In recent years, however, new bone abnormalities have been described. Among them adynamic bone disease (ABD) has become a focus of growing interest. Marked suppression of dynamic bone measurements with normal or near-normal static bone-forming parameters are the hallmarks of this disorder. Depressed parathyroid hormone (PTH) levels, frequently evident in this entity, have been linked causally with low bone turnover. METHODS: We reviewed bone biopsy specimens from 96 patients with end-stage renal disease undergoing chronic haemodialysis. RESULTS: We found OFC in 50% of our patients, 20% had mixed bone disease, 24% showed bone morphology of ABD and a minority (6%) had osteomalacia, mostly due to aluminium accumulation. In the patients that were affected by ABD there was a distinct subgroup with bone morphology featuring a striking increase in osteoclast number and osteoclast surface, whereas the osteoid volume, osteoid thickness, osteoblast surface, tetracycline uptake and bone formation rates were diminished as in ordinary ABD. Similarly the PTH levels in this subgroup were low or undetectable. CONCLUSION: We describe patients undergoing chronic haemodialysis with static and dynamic bone forming parameters, indistinguishable from that of ABD, but differing from the classic ABD by the presence of increased osteoclastic bone resorption. The suppressed PTH levels in this subgroup suggests that factors other than PTH activate osteoclasts in some patients on chronic haemodialysis. Uraemic cytokines and/or toxic metabolites, including beta-microglobulin, may be involved in this disorder. The precise nature of this bone abnormality remains to be defined by further studies.     

Serum osteoprotegerin and renal osteodystrophy.

BACKGROUND: Numerous growth factors and cytokines are known to modulate bone turnover. An important, recently discovered complex involved in osteoclastogenesis is the osteoprotegerin/osteoprotegerin-ligand (OPG/OPGL) cytokine complex, which is produced by osteoblasts. Many factors, including parathyroid hormone (PTH), appear to affect bone turnover through this pathway. In this disorder, the role of the OPG/OPGL system in the pathogenesis of renal osteodystrophy, a disease with either low or high bone turnover, has not been investigated so far. METHODS: Thirty-nine chronic haemodialysis patients had bone biopsies, including histomorphometric and histodynamic examinations. In addition, the following serum biochemistry parameters were measured: serum OPG, intact PTH, PTH 1-84, total PTH, osteocalcin, total and bone alkaline phosphatases, 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol. RESULTS: On average, serum OPG levels were above the normal range. They were lower in adynamic bone disease (ABD) patients, than in patients with predominant hyperparathyroidism (HP) or mixed osteodystrophy (MO). Significant negative correlations were found between serum OPG and PTH levels, and between serum OPG and parameters of bone resorption (ES/BS) and bone formation (ObS/BS and BFR/BS) in HP and MO patients with PTH values < or =1000 pg/ml. For intact PTH levels < or =300 pg/ml, serum OPG was significantly lower in the group with ABD than in those with HP or MO (P<0.05). CONCLUSION: In renal osteodystrophy the OPG/OPGL system is involved in the regulation of bone turnover induced by PTH. The determination of serum OPG levels could be of use in the diagnosis of low turnover bone disease, at least in association with PTH levels < or =300 pg/ml.     

Are PTH serum levels predictive of coronary calcifications in haemodialysis patients?

BACKGROUND: Cardiac calcifications are a frequent occurrence in uraemic subjects and are probably connected to the increased cardiovascular mortality of haemodialysis patients. There is substantial support to the hypothesis that low levels of serum PTH in haemodialysis patients are associated with increased vascular and cardiac calcium deposits, due to decreased buffering capacity of bone in low turnover osteodystrophy. The present study has been carried out on a cohort of patients on haemodialysis, with exclusion of previously parathyroidectomized patients, with the aim to evaluate the association between PTH serum levels and coronary calcifications. METHODS: The study has been carried out in a cohort of 197 haemodialysis patients. There were 133 males and 64 females. Twenty-two patients had diabetes mellitus. Average age was 58.6 +/- 12.9 years. Patients were divided into groups of intact PTH levels, 0-150 (A), 150-300 (B), 300-600 (C) and >600 (D) pg/ml. RESULTS: The values of coronary scores in the PTH groups were as follows: (A) 624.7 +/- 939, (B) 866.4 +/- 1080, (C) 1202.8 +/- 1742.3 and (D) 1872.7 +/- 2961.9. The difference between coronary calcium scores was significant (P < 0.01). A general linear model identified serum calcium and dialysis age as independent factors of calcium deposits in the high PTH group. CONCLUSIONS: No prominent association between low PTH serum levels and the severity of coronary calcium deposits in haemodialysis patients was found while increased levels of PTH, with special regard to very elevated levels, associated with more frequent hypercalcaemia and hyperphosphataemia, should be considered a major risk factor of coronary calcifications and cardiac events.     

End-stage renal failure in New Zealand Maori: an analysis of circulating transforming growth factor-β1

SUMMARY: There is a high incidence of end-stage renal disease in New Zealand Maori. Reasons for this have not been established. Transforming growth factor-β, (TGF-β₁) is a profibrogenic cytokine, which stimulates the secretion of extracellular matrix components, and has been implicated in the pathogenesis of kidney failure. the aim of this study was to examine TGF-β₁ in the serum of haemodialysis patients at our institution, in order to determine whether there was an upregulation of TGF-β₁ in Maori. A TGF-Prspecific sandwich enzyme-linked immunosorbant assay was used to measure active TGF-β from the sera of 74 haemodialysis patients, and 19 healthy Maori without renal disease, diabetes or hypertension. In addition, clinical and laboratory markers were examined in the haemodialysis patients studied. There was no association between TGF-β₁ and ethnicity in the groups studied. Transforming growth factor-β₁ protein appeared to be inversely related to age. but was not associated with parameters of survival on dialysis such as serum albumin or measures of dialysis adequacy. Although there was a significantly higher incidence of type II diabetes mellitus in the Maori ( P < 0.001) in comparison to European patients, the glycaemic control was comparable between the groups, as were all other laboratory and clinical parameters studied. This is the first study to examine the fibrogenic growth factor TGF-β₁ in New Zealand Maori. Thus, an endogenous increase in TGF-β₁ in Maori does not appear to be implicated in the increased incidence of end-stage renal disease in this population.     

Relationship between serum 25-hydroxyvitamin D and bone resorption markers in vitamin D insufficiency

It is known that nursing-home patients with vitamin D insufficiency have elevated serum parathyroid hormone (PTH) as well as raised serum alkaline phosphatase (ALP). Although it is well known that vitamin D insufficiency and secondary hyperparathyroidism are common among the elderly in western countries, there is continuing controversy over the level of serum 25-hydroxyvitamin D [25(OH)D] necessary for bone health. We approached this issue by examining the relationships between serum 25(OH)D, ionized calcium, PTH, and ALP and the urinary bone resorption markers hydroxyproline, pyridinoline, and deoxypyridinoline, corrected for creatinine (OHPr/Cr, Pyd/Cr, and Dpd/Cr, respectively), in 486 postmenopausal women of mean age 63 (SD 9.5) years, who were referred to our osteoporosis and menopause clinics for investigation. When the patients were divided into two groups with 25(OH)D above and below 20 nmol/L, 30 nmol/L, 40 nmol/L, 50 nmol/L, 60 nmol/L, or 70 nmol/L, the most significant differences between the two groups thus derived was found at a serum 25(OH)D level of 60 nmol/L (P < 0.001 for all markers). The most significant difference between groups for serum PTH was found when the patients were divided at a serum 25(OH)D of 50 nmol/L. PTH, OHPr/Cr, Pyd/Cr, and ALP were inversely related to serum 25(OH)D. PTH was inversely related to serum ionized calcium. There was a trend for ionized calcium to be positively related to 25(OH)D, but this did not reach statistical significance. We conclude that rises in three bone resorption markers and ALP can be detected in postmenopausal women when the serum 25(OH)D level falls below 60 nmol/L. Levels above this may be required for optimal bone health.     

Intravenous 1,25(OH)2 vitamin D3 therapy in haemodialysis patients: evaluation of direct and calcium-mediated short-term effects on serum parathyroid hormone concentration

Eleven patients on chronic haemodialysis treatment thrice weekly received 1 microgram 1,25(OH)2D3 i.v. after each dialysis for 3 weeks. Phosphate binders were mainly CaCO3, supplemented in a few patients by moderate amounts of Al(OH)3. Ionised calcium was measured by ion-selective electrode, normal values being 1.28-1.42 mmol/l. PTH was estimated by an N-terminal-sensitive assay; normal values are less than 0.25 ng/ml. Results before and after 1,25(OH)2D3 were: ionised calcium before haemodialysis, 1.19 +/- 0.12 and 1.17 +/- 0.14; ionised calcium after haemodialysis, 1.33 +/- 0.07 and 1.30 +/- 0.09; PTH before haemodialysis, 1.39 +/- 0.71 and 1.38 +/- 0.69; PTH after haemodialysis, 0.64 +/- 0.22 and 0.60 +/- 0.17; Phosphate before haemodialysis, 1.85 +/- 0.48 and 2.18 +/- 0.43 (P less than 0.05). No change of PTH concentration and ionised calcium before and after haemodialysis treatment could be documented after i.v. 1,25(OH)2D3 treatment. Mild and severe hyperparathyroidism were indistinguishable. Increased serum calcium concentrations therefore appear to be required for the suppression of PTH secretion by i.v. 1,25(OH)2D3 therapy.     

Parathyroid hormone changes during phosphorus load in patients with chronic renal insufficiency with low serum parathyroid hormone or adynamic bone disease

Adynamic bone disease (ABD) is frequently associated with low serum parathyroid hormone (PTH) concentrations. Many clinical and therapeutic conditions have been associated with ABD, and recently, a low phosphorus intake accompanied by low serum concentration of phosphorus and PTH has been described. AIM: To evaluate the parathyroid gland response of chronic renal insufficiency patients (CRI) with low serum PTH or ABD to a phosphorus load. METHODS: We examined the effects of 0.5 and 1.0 g/d of phosphorus load over a period of 60 days in 18 patients with mild CRI with a bone biopsy showing ABD (n = 7) or with low serum PTH (serum intact PTH < or = 40 ng/l) and serum phosphorus < 4.5 mg/dl (n = 11). RESULTS: Serum intact PTH increased significantly only after 1 g of phosphorus (58.5 to 83 ng/l) with a median percent increase of 72%. PTH secretion increased more in patients with lower basal PTH levels (81%). Serum phosphorus did not change significantly and urinary phosphorus increased from 487 to 1,062 mg/dl (p < 0.05). Significant decreases in serum ionized calcium (from 1.26 to 1.19 mmol/l) and calcitriol (from 34.5 to 24.9 pg/ml) were observed. Changes in PTH were inversely correlated with changes in serum ionized calcium (r = -0.54, p < 0.05) and the final PTH concentrations were positively correlated with changes in serum phosphorus (r= 0.52, p < 0.05). CONCLUSIONS: The parathyroid glands of chronic renal insufficiency patients with "relative hypoparathyroidism" or ABD responded to a phosphorus load with an increase in serum PTH levels. The decrease in serum ionized calcium and calcitriol as well as minimal changes in serum phosphorus appeared to be involved in this response.     

甲状腺功能异常患者血生化、骨代谢及骨密度特点的临床研究

目的观察甲状腺功能减退症及甲状腺功能亢进症对骨密度以及骨代谢相关指标的影响。方法纳入甲状腺功能减退症女性37例为甲减组,甲状腺功能亢进症女性41例为甲亢组,健康体检女性人员40例为对照组。观察3组甲状腺功能指标血游离三碘甲状腺原氨酸(FT_3)、游离甲状腺激素(FT_4)和高敏感促甲状腺激素(TSH);骨代谢指标血Ca~(2+)、血P~(3+)、1,25-(OH)_2D_3、甲状旁腺激素(PTH)、碱性磷酸酶(ALP)、血清Ⅰ型胶原羧基端吡啶并啉交联肽(ICTP)以及血清骨钙蛋白(BGP)以及左侧股骨颈、正位腰椎1-4(L_(1-4))的骨密度情况。结果甲亢组血清FT_3、FT_4、ALP、BGP、ICTP水平高于对照组(P0.05),甲亢组血清TSH水平低于对照组(P0.05)。甲减组血清TSH水平高于对照组(P0.05),而血清FT_3、FT_4、ALP、BGP、ICTP水平显著低于对照组(P0.05)。甲亢及甲减组L1-4及左股骨颈骨密度显著低于对照组(P0.05)。3组受试者PTH、CT、Ca~(2+)、P~(3+)、1,25-(OH)_2D_3比较无统计学意义(P0.05)。结论甲亢及甲减都可以引起骨量丢失,骨密度降低;主要通过影响骨转化来实现的;应该重视甲状腺功能异常引起的骨密度及骨代谢异常。     

How to manage mineral metabolism disorders in renal failure

Mineral metabolism abnormalities are frequently observed in patients with chronic kidney disease (CKD). The bone and cardiovascular consequences should lead to the implementation of some adapted strategies for the prevention and treatment on the basis of the physiopathology of the disease and international recommendations. Biological bone markers such as serum parathyroid hormone (PTH) and alkaline phosphatase (ALP) are necessary to classify bone diseases without the need for bone biopsy. Elevated levels of bone markers are detected in cases of secondary hyperparathyroidism (SHPT), whereas decreased levels are observed in cases of adynamic bone disease (ABD). Bone mineral density, however, is not useful for the diagnosis. Vitamin D supplementation and reducing hyperphosphataemia by dietary phosphate-intake restriction, phosphate binders, and dialysis, are the main steps for the prevention of SHPT. Calcitriol analogs and calcimimetics should be used in second line in cases of SHPT. For the treatment of ABD, excess use of calcium salts and calcitriol analogs need to be avoided. Managing these therapies adequately can help maintain the main biological values (i.e. serum PTH, calcium, phosphorus, and ALP) within their recommended ranges.     

骨质疏松症患者血清骨代谢标志物分析与相关性研究

目的对西安地区部分骨质疏松症患者血清骨代谢标志物进行统计及相关性分析。方法纳入2018年4月至2019年3月经西安市红会医院诊治的原发性骨质疏松症患者295例,检测受试者血清钙(Ca)、磷(P)、碱性磷酸酶(ALP)、维生素D(vitamin D,维生素D)、甲状旁腺素(PTH)、I型前胶原N端肽(P1NP)、β-胶原特殊序列(β-Cross)的水平,运用R统计语言进行统计学处理及Pearson相关性分析。结果在大多数骨质疏松症患者中血清Ca、P是正常的;有20%~30%患者ALP升高;绝大多数患者维生素D缺乏或不足;PTH异常者以升高为主,少数女性患者PTH降低;大多数绝经前女性P1NP、β-Cross正常,在少数绝经前女性及1/3男性中出现升高,小部分绝经后女性出现下降,在小部分绝经后女性中升高。女性骨质疏松症患者中,血清ALP与P1NP、ALP与PTH、维生素D与β-Cross呈正相关(P<0.05),血清Ca与β-Cross、P与ALP、P与β-Cross、P与PTH、ALP与维生素D、ALP与β-Cross、维生素D与P1NP、维生素D与PTH、P1NP与β-Cross呈负相关(P<0.05)。男性骨质疏松症患者中,血清维生素D与β-Cross呈正相关(P<0.05),血清Ca与PTH、ALP与维生素D、维生素D与P1NP、维生素D与PTH、P1NP与β-Cross呈负相关(P<0.05)。结论骨质疏松症患者维生素D缺乏或不足情况严重,了解骨代谢标志物间的相关性有助于更好地理解骨质疏松症骨代谢异常机制。     

血清骨代谢指标对慢性肾脏病患者骨质量的评价作用

[摘要]目的：探讨血清骨代谢指标对慢性肾脏病（CKD）患者骨质量好坏的评价意义。方法：收集2012年1月～2013年11月上海市第六人民医院肾内科首次住院的CKD患者95例,将患者按GFR分为CKD3期组、CKD4期组及CKD5期组。测定各组患者血清钙（ca2＋）、磷（P3-）、骨代谢指标碱性磷酸酶（ALP）、骨钙素N端中分子（N—MID）、13胶原特殊序列（B—CTX）、25-羟维生素D[25-（OH）VD]和甲状旁腺激素（PTH）水平。结果：CKD三组患者随着GFR的逐渐下降,血ca2＋、25（OH）D呈下降趋势,血P”、PTH、N—MID、B—CTX则呈逐渐上升趋势,组间差异有统计学意义（P〈0．05）;血ALP组间差异总体无统计学意义（P〉0．05）;Pearson直线相关分析显示GFR分别与血P3-（r=-0．494）、N—MID（r=-0．577）、B—CTX（r=-0．518）呈负相关（P＜0．001）,与25（OH）D（r=0.289,P=0.008）呈正相关;血P3-与N—MID（r=0.5）、B—CTX（r=0．497）、PTH（r=0．528）分别呈正相关（P＜0.001）,与25（OH）D呈负相关（r=-0．276,P=0．012）;PTH、N—MID、B—CTX三者互为正相关,PTH与N—MID（r=0．532）、PTH与B—CTX（r=0．551）、N—MID与β-CTX（r=0．641）分别呈正相关（P＜0．001）。结论：CKD患者血清Ca2＋、P3-、PTH、AKP、N—MID、B—CTX、25（OH）D相互作用影响骨质量。血清骨代谢生化指标在评估CKD患者骨质量方面具有重要有益作用。     

甲状旁腺激素(1-34)联合伊班膦酸钠治疗严重骨质疏松症的临床研究

目的甲状旁腺激素(parathyroid hormone,PTH)(1-34)联合伊班膦酸钠治疗严重骨质疏松症效果临床观察。方法98例严重绝经后骨质疏松症合并骨骼疼痛患者随机分为治疗组和对照组,治疗组使用PTH联合伊班膦酸钠治疗,对照组单纯予以伊班膦酸钠治疗,为期12个月。分别检测两组受试者腰椎及髋部骨密度、血清骨代谢指标治疗前后的改变。结果药物治疗6个月后两组患者腰椎L1~4及股骨粗隆、左侧股骨颈、Ward三角区的骨密度明显增加,且12个月后骨密度进一步增加,显著高于对照组(P0.05);药物治疗12个月后两组血清及碱性磷酸酶(ALP)、血清Ⅰ型胶原C末端肽(s-CTX)、血清抗酒石酸酸性磷酸酶-5b(TRACP-5b)、血清骨源性碱性磷酸酶(BAP)及血清骨钙素(OC)水平均显著改变,且治疗组对ALP及s-CTX、BAP、OC及TRACP-5b影响更明显(P0.05),而两组血钙(Ca)及血磷(P)治疗前后无明显差异(P0.05)。结论PTH联合伊班膦酸钠使用能有效提高严重骨质疏松症患者髋部及腰椎骨密度,改善骨代谢。     

Serum levels of alpha-1 microglobulin and beta-2 microglobulin in bone marrow transplant recipients treated with cyclosporin A

Abstract. The levels of alpha-1 microglobulin (α₁m) and beta-2 microglobulin (β₂m) in serum were estimated in 77 bone marrow transplant recipients. In comparison to pretransplant levels, the highest levels of α₁m and β₂m were found during impairment of renal function, i. e., during cyclosporin-induced nephrotoxicity and during treatment with other nephrotoxic drugs ( P < 0.001). The α₁m levels were less elevated during infections and acute graft-versus-host disease ( P < 0.01), while β₂m levels were markedly elevated during the same conditions ( P < 0.001). The linear correlations between serum creatinine and α₁m and creatinine and β₂m were r = 0.7 and 0.8, respectively ( P < 0.001). The overall correlation between α₁m and β₂m was 0.4 ( P < 0.001). It is concluded that α₁m might be a complement to serum creatinine levels in monitoring renal function after bone marrow transplantation.     

In vitro suppression of parathyroid hormone secretion by 22-oxa-calcitriol in human parathyroid hyperplasia due to uraermia

SUMMARY: 22-oxa-calcitriol (OCT), a vitamin D analogue, suppresses parathyroid hormone (PTH) secretion and has less calcaemic activity than 1,25-dihydroxyvitamin D₃ [1,25(OH)₂D₃] in vivo. In this study, we evaluated the effect of OCT on PTH secretion in vitro using human hyperplastic parathyroid tissue obtained during surgery for advanced renal hyperparathyroidism and normal bovine parathyroid glands to compare the effects of 1,25(OH)₂D₃. 22-oxa-calcitriol suppressed PTH secretion by nodular hyperplastic parathyroid tissue and normal bovine tissue in a dose dependent manner, the same as 1,25(OH)₂D₃. We showed the additive effect of extracellular calcium level on suppression of PTH secretion by OCT and 1,25(OH)₂D₃. These results suggest that OCT suppresses PTH secretion, the same as 1,25(OH)₂D₃ not only in normal parathyroid cells but also on hyperplastic parathyroid cells.     

Reversal of adynamic bone disease by lowering of dialysate calcium

Adynamic bone disease (ABD) is increasingly recognized, especially in dialysis patients treated with oral calcium carbonate, vitamin D supplements, or supraphysiological dialysate calcium. We undertook this study to assess the effect of lowering dialysate calcium on episodes of hypercalcemia, serum parathyroid hormone (PTH) levels as well as bone turnover. Fifty-one patients treated with peritoneal dialysis and biopsy-proven ABD were randomized to treatment with control calcium, 1.62 mM, or low calcium, 1.0 mM, dialysate calcium over a 16-month period. In the low dialysate calcium group, 14 patients completed the study. This group experienced a decrease in serum total and ionized calcium levels, and an 89% reduction in episodes of hypercalcemia, resulting in a 300% increase in serum PTH values, from 6.0+/-1.6 to 24.9+/-3.6 pM (P<0.0001). Bone formation rates, all initially suppressed, at 18.1+/-5.6 microm2/mm2/day rose to 159+/-59.4 microm2/mm2/day (P<0.05), into the normal range (>108 microm2/mm2/day). In the control group, nine patients completed the study. Their PTH levels did not increase significantly, from 7.3+/-1.6 to 9.4+/-1.5 pM and bone formation rates did not change significantly either, from 13.3+/-7.1 to 40.9+/-11.9 microm2/mm2/day. Lowering of peritoneal dialysate calcium reduced serum calcium levels and hypercalcemic episodes, which resulted in increased PTH levels and normalization of bone turnover in patients with ABD.     

The effect of 24,25 dihydroxyvitamin D3 on calcium efflux: the role of protein kinase C

SUMMARY: 24,25 dihydroxyvitamin D₃ (24,25(OH)₂D₃) is more abundant than 1,25(OH)₂D₃ in the serum. 1,25 dihydroxyvitamin D₃, a potent calciotropic metabolite of vitamin D, has been shown to induce calcium efflux from bone. This action is probably mediated, in part, by protein kinase C (PKC). to determine whether 24,25(OH)₂D₃ affects calcium flux in bone, neonatal rat calvaria were cultured and the effect of 24,25(OH)₂D₃ on calcium flux and signal transduction pathways were evaluated. Compared with a control, 24,25(OH)₂D₃ (10⁸ mol/L) inhibited basal net calcium efflux. 24,25 dihydroxyvitamin D₃ also inhibited net calcium efflux induced by the phorbol ester 12 Myristate 13-Acetate (PMA). Translocation of PKC from the membrane to the cytosolic fraction was rapidly and transiently induced by 24,25(OH)₂D₃. However, 24,25(OH)₂D₃ had no effect on cyclic AMP (cAMP) production. In conclusion, 24,25(OH)₂D₃ has a direct effect on bone by inhibiting net calcium efflux which is probably mediated by the deactivation of PKC.     

Changes of serum calcium, phosphorus, and parathyroid hormone concentrations and ocular findings among patients undergoing hemodialysis

There are various reports of ocular abnormalities in metabolic disorders. This study was done with the aim to investigate the relationships between the amounts of serum calcium, phosphorus, and parathyroid hormone concentrations and ocular findings in patients undergoing hemodialysis. Fifty eight patients with end stage renal failure undergoing hemodialysis were randomly selected and enrolled in this prospective study. Demographic data, history of diabetes mellitus and hypertension, and duration of hemodialysis were recorded. Serum calcium, phosphorus, alkaline phosphatase (ALP), and parathyroid hormone (PTH) concentrations were measured. Also, blood urea nitrogen (BUN) and weight of the patient was measured just before and three minutes after the hemodialysis. Patients also underwent a complete ocular examination including visual acuity, intraocular pressure (IOP), biomicroscopic examination, and fundoscopy. In univariate analysis, adverse relationships were found between the ocular hypertension and ALP concentration (P = 0.017) and also between the visual acuity and phosphorus concentration (P = 0.033). However, in multivariate regression analysis and with regard to the patients' characteristics and medical history in a multivariate model, no relationships were found between ocular findings and serum calcium, phosphorus, ALP, and PTH concentrations. No relationships were found between the serum concentrations of calcium, phosphorus, ALP, and PTH and ocular findings in patients with end stage renal failure undergoing hemodialysis.     

血清前列腺特异性抗原与碱性磷酸酶测定在判断前列腺癌骨转移中的价值

目的:探讨血清前列腺特异性抗原(PSA)和碱性磷酸酶(ALP)水平与前列腺癌骨转移的关系。方法:回顾性分析96例前列腺癌患者的临床资料(其中29例伴有骨转移,67例不伴有骨转移)及患者血清PSA、ALP水平和骨扫描情况。结果:骨扫描阳性患者的血清PSA和ALP平均浓度均明显高于骨扫描阴性者(P<0.01)。PSA>20μg/L时骨扫描的阳性率明显高于PSA<20μg/L时骨扫描的阳性率(P<0.01)。ALP>90 U/L时骨扫描的阳性率明显高于ALP<90 U/L时骨扫描的阳性率(P<0.01)。结论:伴有骨转移的前列腺癌患者血清PSA和ALP水平均明显高于无骨转移者。当血清PSA>20μg/L和(或)ALP>90 U/L时应行骨扫描检查。