Urinary cyclic 3',5'-adenosine monophosphate responses to exogenous and endogenous parathyroid hormone in familial benign hypercalcemia and primary hyperparathyroidism

FBH is characterized by symptomless hypercalcemia, low urinary calcium excretion, normal iPTH values, generally normal parathyroid histology, and failure of subtotal parathyroidectomy is normalize serum calcium. We studies six patients with FBH from three kindreds, six patients with sporadic 1 omicron HPT, and six healthy volunteers. To characterize the renal response to PTH, 14 of the subjects had infusions of bovine PTE (300 U intravenously over 15 min) and, separately, stimulation of endogenous PTH release by infusion of disodium EDTA (50 mg/kg over 2 hr). PTE induced striking increases of UcAMP (nM/100 ml of GF) that were indistinguishable between controls and subjects having FBH. However, the rise of UcAMP in 1 omicron HPT was significantly reduced (p < 0.001) compared to controls or the FBH group. EDTA-induced hypocalcemia raised serum iPTH and UcAMP in all three groups; the increases of iPTH (two assays of differing specificity) were greatest in 1 omicron HPT and least in FBH. In contrast, increases of UcAMP were greatest in FBH and 1 omicron HPT and indistinguishable from one another. The increase of UcAMP considered as a function of the increase in PTH showed significantly greater UcAMP responses in FBH than in the other groups. These results are consistent with primary or secondary alterations of renal responsiveness to PTH in both FBH and 1 omicron HPT, which may in part explain the different renal tubular calcium handling in the two conditions.     

Evidence for Secondary Hyperparathyroidism in Idiopathic Hypercalciuria

Circulating levels of immunoreactive parathyroid hormone (PTH) were measured in 40 patients with idiopathic hypercalciuria (IH) before and during reversal of hypercalciuria with thiazide, and in four normal subjects before and during induction of hypercalciuria with furosemide. 26 patients with IH had elevated serum PTH levels. The remaining patients had normal levels. Although the correlation was not complete, high PTH levels were generally found in patients who had more severe average urinary calcium losses. When initially elevated. PTH levels fell to normal or nearly normal values during periods of thiazide administration lasting up to 22 months. When initially normal, PTH levels were not altered by thiazide. Reversal of hyperparathyroidism by thiazide could not be ascribed to the induction of hypercalcemia, since serum calcium concentration failed to rise in a majority of patients. Renal hypercalciuria produced by furosemide administration elevated serum PTH to levels equivalent to those observed in patients with IH.The findings in this study help to distinguish between several current alternative views of IH and its relationship to hyperparathyroidism. Alimentary calcium hyperabsorption cannot be the major cause of IH with high PTH levels, because this mechanism could not elevate PTH. Idiopathic hypercalciuria cannot be a variety of primary hyperparathyroidism, as this disease is usually defined, because PTH levels are not elevated in all patients and, when high, are lowered by reversal of hypercalciuria. Primary renal loss of calcium could explain the variable occurrence of reversible hyperparathyroidism in IH, since renal hypercalciuria from furosemide elevates serum PTH in normal subjects. Consequently, a reasonable working hypothesis is that IH is often due to a primary renal defect of calcium handling that leads, by unknown pathways, to secondary hyperparathyroidism.     

Hypocalcemia increases and hypercalcemia decreases the steady-state level of parathyroid hormone messenger RNA in the rat.

To examine the effects of serum calcium concentrations on PTH biosynthesis, rats were made hyper- (serum total calcium, approximately 3.5 mM) or hypocalcemic (approximately 1.25 mM) and steady-state levels of PTH mRNA in parathyroid cells were measured by the primer extension method using a 32P-labeled synthetic oligomer. PTH mRNA levels increased about twofold in the rats made slightly hypocalcemic by infusion of calcium-free solution and decreased slightly in those made hypercalcemic by CaCl2 infusion (120-150 mumol/h) compared with the levels present in nonfasting control rats. Infusion of calcitonin (0.5 U/h) or EGTA (90 mumol/h) with calcium-free solution increased PTH mRNA levels further (two- to sevenfold) above the levels present in animals infused with calcium-free solution alone. These changes in PTH mRNA levels were observed after 48- but not 24-h infusion, and there was an inverse correlation between PTH mRNA levels and serum calcium concentrations. The results suggest that changes in serum calcium concentrations in the near physiological range regulate the biosynthesis of PTH by affecting steady-state levels of PTH mRNA when hypercalcemia or hypocalcemia continues for a relatively long period.     

Nephrogenous Cyclic Adenosine Monophosphate as a Parathyroid Function Test

Nephrogenous cyclic AMP (NcAMP), total cyclic AMP excretion (UcAMP), and plasma immunoreactive parathyroid hormone (iPTH), determined with a multivalent antiserum, were prospectively measured in 55 control subjects, 57 patients with primary hyperparathyroidism (1 degrees HPT), and 10 patients with chronic hypoparathyroidism.In the group with 1 degrees HPT, NcAMP was elevated in 52 patients (91%), and similar elevations were noted in subgroups of 26 patients with mild (serum calcium 相似文献   

MHD人群慢性肾脏病矿物质和骨异常单中心横断面研究

目的了解维持性血液透析（maintenance hemodialysis,MHD）患者的慢性肾脏病-矿物质和骨异常（CKD-MBD）的患病情况,并分析其相关危险因素。方法对2010年7月至2011年3月在四川省人民医院血液透析中心进行规律MHD的患者217例进行调查,收集患者的一般资料,测定血钙、血磷、血iPTH,行腹部侧位、骨盆正位、双手正位X线摄片,采用Kauppila评分进行血管钙化评分。分析CKDMBD各指标在血透患者中患病率、达标率以及相关危险因素。结果本次217例MHD患者中,高磷血症患病率为45.16%,低钙血症患病率为31.8%,高钙血症患病率为21.66%,高iPTH患病率为48.85%,低iPTH患病率为20.74%。X片显示有血管钙化的患者有154人（占70.97%）,有钙磷代谢异常、PTH、血管钙化1项或多项异常,符合KDIGO关于CKD-MBD诊断的患者比例高达96.31%。本组MHD患者血钙、血磷、PTH达标率分别为45.16%、44.7%、30.88%。血钙、磷、PTH均达标仅有20人（占9.22%）。血钙和血磷的达标率低于DOPP4。多因素Logistic回归分析显示高PTH的危险因素有高磷血症、低钙血症。低PTH的危险因素有年龄、透析龄和活性维生素D服用史。血管钙化的危险因素有高龄、高ALP、高磷血症和高CRP。结论 CKD-MBD在MHD患者中普遍存在,与DOPP4比较,存在CKD-MBD各项指标达标率较低。     

The value of serum 25-hydroxyvitamin D measurements in hypoparathyroid and pseudohypoparathyroid patients treated with calciferol

In 23 patients with hypoparathyroidism or pseudohypoparathyroidism treated with vitamin D, and in whom the dosage was adjusted downward or upward in response to hypercalcemia or hypocalcemia respectively, assays of serum 25-hydroxyvitamin D (25-OHD) were carried out in addition to the usual serum calcium assays. In 120 assays there was a significant correlation between serum 25-OHD levels and serum calcium levels (corrected for serum albumin). There was, however, no clear distinction between the 25-OHD levels of patients who were hypocalcemic, normocalcemic or hypercalcemic. The highest serum 25-OHD level found in a hypocalcemic patient was 1193 nmol/L and the lowest serum 25-OHD level found in a hypercalcemic patient was 605 nmol/L. It was not possible to predict subsequent episodes of hypocalcemia or hypercalcemia from the serum 25-OHD levels. The 25-OHD assay was found to be useful only in checking compliance. We conclude that the assay of serum 25-OHD is of no more value than serum calcium alone in the management of compliant patients.     

A case of severe hypercalcemia with acute renal failure in sarcoidosis: a diagnostic challenge for the emergency department.

We present and discuss the case of a man admitted to our emergency room because of severe hypercalcemia and renal failure with maintained diuresis. We diagnosed a relapse of sarcoidosis, manifesting as hypercalcemia and renal failure, based on a history of lung sarcoidosis. This is a rare complication of sarcoidosis, due to granulomatous production of vitamin D. This mechanism may have been exacerbated by exposure of sunlight. The initial treatment of the patient was directed towards lowering the circulating calcium level through hyperhydration and forced diuresis, with secondary control of granulomatous activity using corticosteroid therapy. The patient was discharged after 7 days with normal levels of serum calcium, urinary calcium excretion and serum creatinine. Recognition of this rare cause of hypercalcemia is a challenge for the emergency physician.     

The Hypercalciurias CAUSES, PARATHYROID FUNCTIONS, AND DIAGNOSTIC CRITERIA

The causes for the hypercalciuria and diagnostic criteria for the various forms of hypercalciuria were sought in 56 patients with hypercalcemia or nephrolithiasis (Ca stones), by a careful assessment of parathyroid function and calcium metabolism. A study protocol for the evaluation of hypercalciuria, based on a constant liquid synthetic diet, was developed. In 26 cases of primary hyperparathyroidism, characteristic features were: hypercalcemia, high urinary cyclic AMP (cAMP, 8.58+/-3.63 SD mumol/g creatinine; normal, 4.02+/-0.70 mumol/g creatinine), high immunoreactive serum parathyroid hormone (PTH), hypercalciuria, the urinary Ca exceeding absorbed Ca from intestinal tract (Ca(A)), high fasting urinary Ca (0.2 mg/mg creatinine or greater), and low bone density by (125)I photon absorption. The results suggest that hypercalciuria is partly secondary to an excessive skeletal resorption (resorptive hypercalciuria). The 22 cases with renal stones had normocalcemia, hypercalciuria, intestinal hyperabsorption of calcium, normal or low serum PTH and urinary cAMP, normal fasting urinary Ca, and normal bone density. Since their Ca(A) exceeded urinary Ca, the hypercalciuria probably resulted from an intestinal hyperabsorption of Ca (absorptive hypercalciuria). The primacy of intestinal Ca hyperabsorption was confirmed by responses to Ca load and deprivation under a metabolic dietary regimen. During a Ca load of 1,700 mg/day, there was an exaggerated increase in the renal excretion of Ca and a suppression of cAMP excretion. The urinary Ca of 453+/-154 SD mg/day was significantly higher than the control group's 211+/-42 mg/day. The urinary cAMP of 2.26+/-0.56 mumol/g creatinine was significantly lower than in the control group. In contrast, when the intestinal absorption of calcium was limited by cellulose phosphate, the hypercalciuria was corrected and the suppressed renal excretion of cAMP returned towards normal. Two cases with renal stones had normocalcemia, hypercalciuria, and high urinary cAMP or serum PTH. Since Ca(A) was less than urinary Ca, the hypercalciuria may have been secondary to an impaired renal tubular reabsorption of Ca (renal hypercalciuria). Six cases with renal stones had normal values of serum Ca, urinary Ca, urinary cAMP, and serum PTH (normocalciuric nephrolithiasis). Their Ca(A) exceeded urinary Ca, and fasting urinary Ca and bone density were normal. The results support the proposed mechanisms for the hypercalciuria and provide reliable diagnostic criteria for the various forms of hypercalciuria.     

Laboratory screening for hyperparathyroidism

INTRODUCTION: The clinical syndrome produced by excess parathyroid hormone (PTH) is referred to as hyperparathyroidism (HPT). Autonomous growth of PTH producing cells is defined as primary hyperparathyroidism (pHPT). In its classic form pHPT is characterized by painful bones, kidney stones, abdominal groans, psychic moans, fatigue overtones and hypercalcemia. Chronic stimulation of the parathyroid glands secondary to low circulating calcium level results in secondary hyperparathyroidism (sHPT). Tertiary hyperparathyroidism (tHPT) results from prolonged secondary hyperparathyroidism when the glands take on an autonomous function manifested by hypercalcemia and high PTH levels despite resolution of the original stimulus. REVIEW: The paper reviews the physiologic regulation of PTH secretion and types and forms of HPT. Calcium homeostasis is discussed, emphasizing interactions of PTH, PO4 and vitamin D that can lead to HPT. In addition, the paper reviews the contribution of serum calcium, chloride, phosphorus and PTH levels to the diagnosis of HPT, the role of urinary calcium in the diagnosis of familial benign hypocalciuric hypercalcemia (FBHH), and the role of alkaline phosphatase and bone mass measurements as markers of severity of hyperparathyroid bone disease. CONCLUSIONS: It is concluded that the diagnosis of hyperparathyroidism can be made with a very high confidence rate by documenting an increased serum PTH level with an increased ionized or total calcium level in pHPT, increased serum PTH level with low or normal calcium level and an underlying renal failure or vitamin D deficiency in sHPT. Early management of HPT is important because many of the nonspecific complains, or classic symptoms, or metabolic conditions often improve after proper control of hyperparathyroidism.     

Phosphorus and calcium metabolism and its hormonal regulation in chronic kidney failure

In order to elucidate the blood serum calcium, inorganic phosphorus, parathyroid hormone (PTH) and calcitonin (CT) content in the course of the development of chronic renal failure (CRF), 80 patients with chronile glomerulonephritis were examined. Of these, in 24 glomerular filtration (GF) was normal, whereas 56 had CRF of varying degree. Thirty-three out of the 80 patients had the nephrotic syndrome (NS). The parameters enumerated were also determined in 45 patients with CRF treated by hemodialysis. In patients without the NS, hypocalcemia was discovered only at the final predialysis stage of CRF, while in the presence of the NS, it was detectable in normal GF and was aggravated as CRF progressed. The PTH level ascended if GF was lower than 40 ml/min, not correlating with calcium concentration in the serum. A direct correlation was disclosed between the PTH level and that of inorganic phosphorus. The role of the latter in stimulation of PTH and CT secretion in CRF is discussed. In patients treated by hemodialysis, the PTH level significantly rose with treatment time increase. There was also a tendency toward elevation of CT concentration. The activity of the osseous fraction of blood serum alkaline phosphatase in patients treated by hemodialysis was increased in 61-84% of cases depending on the treatment period.     

Hyperoxaluria or hypercalciuria in nephrolithiasis: the importance of renal tubular functions

The role of the kidney in states of hyperoxaluria and hypercalciuria was investigated in seven patients with hyperoxaluria after jejunoileal bypass (JIB) and six patients with idiopathic hypercalciuria (IHC). Eight apparently healthy persons formed a control group. Besides hyperoxaluria, the patients with JIB displayed an elevated plasma concentration of oxalate and the oxalate clearance was increased and higher than creatinine clearance, indicating a net tubular secretion of oxalate. The JIB patients had lower 24-h urinary excretions of calcium, phosphate, magnesium and citrate and higher serum parathyroid hormone (PTH) than controls, indicating increased secretion of PTH to compensate for calcium malabsorption. IHC patients exhibited increased fasting urinary calcium even though their serum values were similar to those in the controls. These results indicate a reduced tubular calcium reabsorption, which was most pronounced in patients with highest PTH values. We conclude that hyperoxaluria in JIB patients is associated both with intestinal hyperabsorption and with enhanced tubular secretion of oxalate, and that in some patients with IHC hypercalciuria is due to reduced tubular reabsorption of calcium.     

甲状旁腺全切除术加前臂移植治疗尿毒症难治性继发性甲状旁腺功能亢进

[目的]研究甲状旁腺全切除术加自体前臂移植对于尿毒症引起的难治性继发性甲状旁腺功能亢进的效果.[方法]总结分析本院12例因慢性肾脏疾病长期接受规律性血液透析的患者发生继发性甲状旁腺功能亢进(SHPT),因持续性高血钙及高甲状旁腺素(parathyroid hormone,PTH),药物治疗无效,予行甲状旁腺全切除术加前...     

Studies on Mechanisms of Hypocalcemia of Magnesium Depletion

Studies were carried out to evaluate the mechanism of hypocalcemia in magnesium depletion. Day old chicks fed a magnesium deficient diet developed marked hypocalcemia, with a direct relation between serum calcium (y) and magnesium (x): y = 2.68 x + 4.24, r = 0.84 (both in mg/100 ml). Injections of parathyroid extract that increased serum calcium 2-3 mg/100 ml in normals had no effect in Mg-depleted birds. Very large dietary supplements of calcium or vitamin D(3) increased mean serum calcium only from 5.3 to 7.7 and 7.8 mg/100 ml, respectively, while a normal magnesium diet for 3 days increased calcium from 5.3 to 9.9 mg/100 ml despite absence of dietary calcium. Intestinal calcium transport, studied in vitro, and the calcium concentration of the carcass was significantly increased in magnesium-depleted chicks, making it unlikely that reduced intestinal absorption of calcium caused the hypocalcemia. In magnesium-deficient chicks, the bone content of magnesium was decreased by 74%, the calcium content was unchanged, and the cortical thickness of bone was markedly increased. After 3 days of magnesium-repletion, cortical thickness was reduced with increased endosteal resorption. There was an increase in unmineralized osteoid tissue in the magnesium-depleted chicks. Parathyroid gland size and histology did not differ in magnesium-depleted and control birds. The results suggest that hypocalcemia develops due to altered equilibrium of calcium between extracellular fluid and bone, favoring increased net movement into the latter. Failure of parathyroid gland function could also exist, and unresponsiveness to parathyroid hormone (PTH) may also contribute to the hypocalcemia. However, failure of PTH action is probably due to the presence of excess osteoid tissue rather than a primary event leading to hypocalcemia.     

Evaluation of a chemiluminescence immunoassay for the determination of intact parathyroid hormone using the ADVIA Centaur

We tested a new chemiluminescence immunoassay for intact parathyroid hormone (PTH) (ADVIA Centaur intact PTH-serum assay). It is a two-site sandwich immunoassay using direct chemiluminescence technology. We investigated precision with serum pools at three levels of the analyte, analyzed in duplicate for 12 days. Total coefficients of variation (CVs) were between 4.6 and 14.4%. The intra-assay precision was between 4.4 and 6.1%. Day-to-day reproducibility was between 1.5 and 13.1% for pools with a PTH concentration between 10 pg/ml and 70 pg/ml (about 1 to 7 pmol/l). The analytical sensitivity was 3.1 pg/ml. The functional sensitivity did not differ from 3 SD minimal detectable concentration (MDC). The linearity was good in the range from 3.1-1930 pg/ml. Comparison with the IRMA used in our laboratory was analyzed by Passing-Bablok and Bland-Altman plots and revealed a proportional bias of +/-60% (slope: 1.58; IC: 1.53 to 1.63) and a systematic bias of -3.3 pg/ml which should not have any clinical consequence in the interpretation of the results. We established a reference range based on our hospital population. We evaluated 87 subjects without abnormality of calcium metabolism and with normal vitamin D supply. Three groups of patients were also analyzed: 57 patients with vitamin D insufficiency, 17 with renal failure and 15 with hypercalcemia (7 due to primary hyperparathyroidism and 8 due to another etiology). Reference ranges were from 10.2 to 93 pg/ml for CLIA measurement and from 6.4 to 68 pg/ml for IRMA measurement. PTH values measured by CLIA varied from 6 to 142 pg/ml in patients with vitamin D insufficiency. By CLIA measurement, intact PTH was between 26 and 892 pg/ml in renal failure, between 54 and 201 pg/ml in primary hyperparathyroidism and between 0 and 29 pg/ml in patients with another etiology of hypercalcemia. The results of PTH measurements in EDTA plasma did not differ significantly from those performed in serum (Passing Bablock).     

Immunochemiluminometric and immunoradiometric determinations of intact and total immunoreactive parathyrin: performance in the differential diagnosis of hypercalcemia and hypoparathyroidism

Parathyrin (parathyroid hormone; PTH) was measured with three immunoassays: a two-site immunochemiluminometric (ICMA) and a two-site immunoradiometric (IRMA) method for intact PTH, and a sensitive radioimmunoassay for mid-region or "total" PTH, measuring both intact hormone and inactive fragments. Single specimens from normal subjects and from individuals with primary hyperparathyroidism, hypercalcemia associated with malignancy, and hypoparathyroidism were analyzed with all three methods. All individuals with primary hyperparathyroidism showed absolutely above-normal concentrations with the mid-region RIA, 28 of 29 did with the ICMA, and 21 of 29 did with the IRMA. PTH concentrations in primary hyperparathyroidism were most increased relative to normal subjects with the mid-region assay (10.4 times), less so with the intact assays (ICMA 5.5 times; IRMA 5.3 times). Concentrations of intact PTH were suppressed below normal in nearly all patients with hypercalcemia associated with malignancy, as measured with the ICMA (26 of 30) and the IRMA (28 of 30) assays. In marked contrast, results for mid-region PTH were normal or slightly above normal, consistent with studies suggesting that the parathyroids secrete both intact hormone and inactive fragments, the former being more sensitive to suppression by hypercalcemia. In hypoparathyroidism PTH concentrations were detectable but below normal in all patients by the intact assays and in all but one patient by the mid-region assay. These low concentrations are probably due to a nonspecific serum effect that could be resolved with selection of a more appropriate standard matrix. Although all three assays are useful in the differential diagnosis of hypercalcemia, two-site intact assays are more convenient and more specific in patients with compromised renal function.     

2013年昆山地区血液透析患者现状的单中心调查

目的 通过对2013年8月昆山第一人民医院患者的横断面调查,了解MHD患者的现状.方法 收集2013年8月在江苏大学附属昆山医院血透室透析龄大于3个月的患者共242例,分析患者年龄、性别、透前肌酐、透析龄、血红蛋白、血清钙、磷水平、钙磷乘积、全段甲状旁腺激素（iPTH）结果,并进行统计分析.结果 242例患者中,男134例（占55.4％）,女108例（占44.6％）,男女比例为1.24∶1;原发病构成上,前3位分别为慢性肾小球肾炎132例（54.54％）,糖尿病肾病25例（10.33％）,高血压肾损害19例（7.85％）,其中不能明确原发病因者39例（16.11％）;Hb＜110 g/L 148例（61.16％）;206例（85.12％）存在钙磷代谢紊乱（包括高钙、低钙、高磷、低磷的患者）,96例（39.66％）钙磷乘积＞4.52mmol2/L2.在接受iPTH检查的236例患者中,iPTH＜150 ng/L有78例（33.05％）,PTH＞600 ng/L有32例（13.56％）.结论 本中心患者男性略多于女性,尿毒症发病年龄趋于年轻化,慢性肾小球肾炎仍是终末期肾脏病（end stage renal disease,ESRD）的第1位原因;Hb达标率低,相当多的MHD患者存在钙磷代谢紊乱及继发性甲状旁腺激素机能亢进.     

脓毒症患者血清甲状旁腺激素及钙水平与疾病严重程度及预后的关系

目的：研究甲状旁腺激素（PTH）及血清钙水平与ICU脓毒症患者疾病严重程度和预后的关系。方法：将ICU20例脓毒症患者分为生存组和死亡组进行回顾性研究。在SIRS发生48h内开始监测PTH及血钙水平。并在1周内每天检测两组PTH及血钙水平。病情严重程度用急性生理和慢性健康评分（APACHEⅡ）来评估。将两组PTH和血钙水平进行比较,并分析APACHEⅡ评分与PTH、血钙水平的相关性。结果：第1天PTH平均水平生存组患者66.7%高于正常,死亡组患者100%高于正常;血钙平均水平生存组患者77.8%低于正常,死亡组100%低于正常。死亡组PTH水平在第1～6天显著高于生存组（P〈0.05）,死亡组血钙水平在第1～5天显著低于生存组（P〈0.05）。并且APACHEⅡ评分与PTH水平（r=0.969,P〈0.05）呈正相关,与钙水平（r=-0.827,P〈0.05）呈负相关。结论：低钙血症及高PTH水平在脓毒症患者中很常见,且与疾病严重程度相关,并可能提示预后较差。     

Discovery of a calcimimetic with differential effects on parathyroid hormone and calcitonin secretion

Calcimimetics are positive allosteric modulators to the calcium-sensing receptor (CaSR). Activation of the CaSR inhibits the secretion of parathyroid hormone (PTH), stimulates the secretion of calcitonin, and decreases serum calcium (Ca(2+)). Cinacalcet, a second-generation calcimimetic, is used therapeutically to control PTH in patients with chronic kidney disease who are on dialysis with secondary hyperparathyroidism. A calcimimetic that displays increased separation of PTH versus Ca(2+) lowering in patients would potentially allow the use of calcimimetics to treat patients in earlier stages of renal disease because hypocalcemia can develop in this population. Toward this end, we developed a third-generation calcimimetic, determined the molecular pharmacological properties of it using an operation model of allosteric modulation/agonism, and measured the compound effects on PTH, serum ionized Ca(2+), and calcitonin levels in 5/6 nephrectomized rats. We found the new molecule effectively reduced PTH levels without promoting calcitonin secretion or hypocalcemia. Furthermore, our third-generation molecule was less efficacious at promoting calcitonin secretion from human thyroid carcinoma cells compared with 3-(2-chlorophenyl)-N-((1R)-1-(3-methoxyphenyl)ethyl)-1-propanamine (R-568), a first-generation calcimimetic. These data provide evidence that calcimimetics with increased potency can be used to lower PTH without production of significant hypocalcemia because the threshold for inhibition of PTH secretion is much lower than the threshold for calcitonin secretion.     

Total and ultrafiltrable plasma magnesium in hyper- and hypoparathyroidism, and in calcium-related metabolic disorders

Serum total, ultrafiltrable and protein-bound magnesium, and urinary fractional excretion of magnesium were studied in patients with primary hyperparathyroidism (before and after surgery) and in patients with hyperparathyroidism, malignant hypercalcemia and chronic renal failure with or without hemodialysis. Whereas serum total Mg was unchanged in patients with primary hyperparathyroidism, the ultrafiltrable magnesium concentration was higher than in the control group and higher before than after surgery. The total and the ultrafiltrable magnesium concentrations were highly correlated in the overall patients with Ca-related metabolic disorders, suggesting that renal function had no influence on the relation between these two parameters. Moreover, in malignant hypercalcemia, our results suggested that PTH-like peptides might be less effective than PTH in renal handling of Mg as previously described for Ca.