Immunoreactive Parathyroid Hormone Levels Research Articles

A retrospective study of end-stage kidney disease patients on maintenance hemodialysis with renal osteodystrophy-associated fragility fractures

BackgroundNephropathy associated metabolic disorder induces high incidence of fragility fracture in end-stage renal disease (ESRD) patients. As the risk factors and prognosis of fragility fracture in ESRD patients are unclear, more research is needed. This study aimed to evaluate various risk factors for ESRD-related fragility fractures, explore factors affecting the prognosis of patients with such fractures, and provide information for prevention and treatment of renal osteopathy to improve the prognosis of patients.MethodsIn this retrospective case-control study, the case notes of 521 ESRD patients who received maintenance dialysis for at least 3 months were examined. Finally, 44 patients diagnosed with fragility fractures were assigned to the fragility fracture (FF) group and 192 patients were included in the control group (CG). Demographic information, underlying diseases, nutritional, bone metabolism, and renal function parameters, along with the number and causes of any deaths, were recorded for multiple statistical analysis.ResultsThe FF group had increased incidences of essential hypertension and diabetes mellitus and higher serum calcium, corrected calcium, alkaline phosphatase, and hemoglobin levels. Immunoreactive parathyroid hormone (iPTH), total cholesterol (TC), and low density lipoprotein (LDL) levels were higher in the CG. Multivariate Cox regression analysis revealed that fragility fracture was an independent risk factor for all-cause mortality in ESRD patients (P < .001, RR: 4.877, 95% CI: 2.367–10.013).ConclusionsEssential hypertension and diabetes, high serum calcium and alkaline phosphatase levels, and reduced iPTH levels were risk factors for fragility fracture in ESRD patients. Maintaining iPTH and serum TC levels may protect against fragility fractures in them. Fragility fractures may yield poor prognosis and shorter lifespan. The presence of fragility fracture was an independent predictor of all-cause death in ESRD patients.

Calcium and Vitamin D Metabolism in Pediatric Nephrotic Syndrome; An Update on the Existing Literature

Minimal Change Disease (MCD) is the leading cause of childhood Nephrotic Syndrome (NS). Therefore in pediatrics nephrotic syndrome, most children beyond the first year of life will be treated with corticosteroids without an initial biopsy. Children with NS often display a number of calcium homeostasis disturbances causing abnormal bone histology, including hypocalcemia, reduced serum vitamin D metabolites, impaired intestinal absorption of calcium, and elevated levels of immunoreactive parathyroid hormone (iPTH). These are mainly attributed to the loss of a variety of plasma proteins and minerals in the urine as well as steroid therapy. Early diagnosis and management of these abnormalities, could prevent the growth retardation and renal osteodystrophy that affects children with nephrotic syndrome. Here we reviewed the literature for changes of calcium and vitamin D metabolism in nephrotic syndrome and its consequences on bones, also the effect of corticosteroid and possible preventive strategies that could be done to avoid long term outcomes in children. Although the exact biochemical basis for Changes in levels of calcium and vitamin D metabolites in patients with NS remains speculative; Because of the potential adverse effects of these changes among growing children, widespread screening for vitamin D deficiency or routine vitamin D supplementation should be considered.

Balance impairment in chronic antiepileptic drug users: A twin and sibling study

Patients taking antiepileptic drugs (AEDs) have an increased incidence of fractures. This study investigated chronic AED use and physical contributors to falls risk using an AED-discordant, twin and sibling matched-pair approach, and assessed clinically relevant subgroups: AED polytherapy; longer-duration AED; and falls history. Twenty-nine same-sex (mean age 44.9 years, 59% female), ambulatory, community-dwelling twin and sibling pairs, discordant for AED exposure (and AED-indication), were recruited. Validated clinical and laboratory tests of strength, gait, and balance were performed. Relevant AED levels, and fasting serum samples for 25-hydroxyvitamin D (25OHD), 1,25-dihydroxyvitamin D [1,25(OH)(2)D], and immunoreactive parathyroid hormone (iPTH) levels were taken. There were significant mean within-pair differences in tests of static and dynamic balance, with the AED user having poorer balance function than the AED nonuser. No difference was seen in lower limb strength or gait measures. Increased duration of AED therapy and AED polytherapy were independent predictors of increased sway. No significant within-pair differences were seen in fasting serum levels of 1,25(OH)(2)D, 25OHD and iPTH after Bonferroni correction. Balance performance is impaired in AED users compared to their matched nonuser siblings. Pairs where the AED users took AED polytherapy, or had a longer duration of AED use, had more impaired balance performance. These balance deficits may contribute to the increased rate of fractures in this population.

Acute Hypocalcemia Enhances Prolactin Levels : A Study before and after Oophorectomy

The effect of acute hypocalcemia on serum prolactin values was investigated in 13 female subjects before and after oophorectomy. An infusion of disodium-EDTA (50 mg/kg b.w., for 120 min) was administered to each patient. Ionized calcium, immunoreactive parathyroid hormone and prolactin serum levels were determined 15 min prior to the infusion, at the beginning of each infusion and thereafter at every 30 min interval. The decrease in serum ionized calcium induced by Na2-EDTA infusion was not influenced by surgery. Serum prolactin and parathyroid hormone values before and after oophorectomy showed a significant (p less than 0.01) increase at 90 and 120 min. The maximum serum prolactin increase was achieved at 120 min and was not influenced by oophorectomy. The results demonstrate that acute hypocalcemia increases serum prolactin levels in female subjects and suggest a possible role for parathyroid hormone and dopaminergic system, even if their interaction remains speculative.

A Case of Pseudohypoparathyroidism Type I

Pseudohypoparathyroidism (PHP) is a rare clinical type of hypoparathyroidism. The patients with PHP show classic clinical and biochemical features of hypoparathyroidism, but elevated serum level of parathyroid hormone (PTH) and characteristic physical appearances termed ‘Albright's hereditary osteodystrophy’ (AHO). PHP is classified into types Ia, Ib, Ic and II according to the presence of AHO phenotype and the mechanism of PTH resistance. We experienced a case of PHP in a 12 year-old girl with carpopedal spasm, syncope and partial AHO. She showed very low serum calcium level (1.4 mmol/L), high phosphorus level (3.62 mmol/L) and high immunoreactive PTH level (186.6 ng/L). In the Ellsworth-Howard test, urinary cyclic adenosine monophosphate and phosphorus levels after an exogenous PTH injection remained unchanged. Therefore, we were able to classify the patient as either PHP type Ia or Ic. After the patient had been treated with daily calcium carbonate (1 g), cholecalciferol (250 IU) and calcitriol (0.5 μg), her neurological signs and symptoms as well as her biochemical abnormalities of hypocalcemia and hyperphosphatemia were improved. (J Kor Soc Endocrinol 21:338~344, 2006)

Radioguided Thoracoscopic Mediastinal Parathyroidectomy With Intraoperative Parathyroid Hormone Testing

Primary hyperparathyroidism is the leading cause of hypercalcemia in the United States. The goal of this study was to evaluate the feasibility of radioguided thoracoscopic mediastinal parathyroidectomy and intraoperative immunoreactive parathyroid hormone (iPTH) level testing to guide completeness of resection. Mediastinal parathyroidectomy was performed thoracoscopically with intraoperative radioguidance using a hand-held gamma probe after injection of 10 mci of TC-99m sestamibi. Parathyroid excision was confirmed by ex vivo measurement of specimen radioactivity greater than 20% of background. Complete resection was confirmed by a greater than 50% decrease in serum iPTH level at 5 minutes postresection. Four patients had mediastinal parathyroid glands successfully localized and resected thoracoscopically. Mean weight of the excised parathyroid adenoma was 1,714 mg (range, 425 to 4,400 mg). Baseline iPTH levels decreased from a mean of 202 to 39 pg/dL 5 minutes postresection. One patient underwent radioguided resection of a second enlarged cervical parathyroid adenoma at the same setting when his intraoperative iPTH levels failed to fall below 50% of baseline, despite resection of a 440 mg mediastinal parathyroid gland. Median hospital stay was one day. All mediastinal parathyroid glands resected were confirmed adenomas on final histologic examination. All patients were normocalcemic at follow-up (mean, 25 months), indicating cure. Thoracoscopic mediastinal parathyroidectomy with intraoperative iPTH level monitoring is safe and effective. Radioguidance facilitates parathyroid localization. Ex vivo specimen radioactivity of greater than 20% of background confirms parathyroid resection and obviates the need for costly, time-consuming frozen section analysis. A 50% decrease in baseline iPTH level 5 minutes postresection confirms complete resection of parathyroid adenomas.

Effect of Parathyroidectomy on Renal Graft Function

Some authors have reported acute impairment of renal transplant function after parathyroidectomy (PTx). Since 1996 PTx has been performed in 22 renal transplant recipients (follow-up, 24.2 ± 15 months; serum creatinine concentration (SCr) pre-PTx, 1.26 ± 0.4 mg/dL). We analyzed the serum levels of immunoreactive parathyroid hormone, calcitriol, calcium, phosphate, alkaline phosphatase, SCr, and hemoglobin, as well as proteinuria, blood pressure, and immunosuppressive treatment at several times: before PTx and at 7 days, 1 month, and then every 3 months post-PTx. After PTx we observed acute renal function deterioration until the third post-PTx month, when SCr levels returned to baseline values. We found no changes in blood pressure, although there was a trend toward a reduced dosage of antihypertensive drugs. We compared the patients who showed more significant increases (>30% from baseline) in SCr (group A, n = 7) with those who did not (group B, n = 15). Group A had higher SCr levels pre-PTx. We observed no other significant differences, either pre-PTx or post-PTx. In 2 patients in group A, SCr returned to baseline at the third month after PTx, but in the other 5 the renal function impairment persisted. Taking into account this risk and that severe hyperparathyroidism does not revert after transplantation, it would seem more appropriate in such cases to perform PTx while the patient is on the waiting list. The causes of this renal functional impairment are not clear, but the patients who showed worse deterioration also had a worse renal function pre-PTx.

A Case of Primary Hyperparathyroidism Caused by Cystic Parathyroid Adenoma, Diagnosed during Intra-Operative PTH Monitoring

Primary hyperparathyroidism is the most frequent cause of hypercalcemia, and its prevalence is increasing due to the routine examination of serum calcium levels. Primary hyperparathyroidims is most commonly caused by an adenoma or hyperplasia of the parathyroid gland. A cystic parathyroid adenoma is an extremely rare cause of primary hyperparathyroidism. In our case, a-79-year old female presented with lower back pain and constipation. Her serum calcium, phosphate and immunoreactive parathyroid homone levels were 15.6, 1.8 mg/dL and 371.8 pg/mL, respectively. Neck CT revealed a cystic mass and a contour bulging heterogeneous mass in the left inferior right thyroid gland, respectively. These mass lesions were removed, and the intra-operative parathyroid hormone levels monitored, to confirm the complete resection. After removing the left cystic mass to the inferior thyroid, the serum calcium and immunoreactive parathyroid hormone levels quickly returned to normal. We report a case of primary hyperparathyroidism, caused by a cystic parathyroid adenoma, with a brief review of the literature (J Kor Soc Endocrinol 20:278～282, 2005).

Secondary Causes of Osteoporosis

Secondary Causes of Osteoporosis

Spectrum of renal osteodystrophy in children on continuous ambulatory peritoneal dialysis.

The prevalence of different types of bone disease in chronic renal failure (CRF) has changed significantly during the last decade. The aim of the present study is to evaluate the spectrum of bone disease in children with CRF undergoing continuous ambulatory peritoneal dialysis (CAPD). Seventeen children with CRF on CAPD aged 7-20 years were evaluated. All patients had received regular vitamin D and calcium carbonate therapy during the 6 months preceding the bone biopsy. Serum calcium, phosphate, alkaline phosphatase and immunoreactive parathyroid hormone (iPTH) levels were measured and hand X-rays were performed. Transiliac bone biopsies were analyzed for histologic diagnosis. High turnover renal osteodystrophy (ROD) was the most common bone disease, present in eight patients (47%). Five patients (29%) had low turnover bone disease, and four (24%) had mixed ROD. The mean age of the high turnover ROD group was higher than that of the low turnover group (14 +/- 3 vs. 11 +/- 3 years, P < 0.05). Seven of the nine patients who had tubulo-interstitial nephritis were found to have high turnover bone disease. In contrast, none of the patients with glomerulonephritis exhibited high turnover bone lesions. Mean serum calcium levels were found to be significantly higher in the low turnover group compared with the patients with high turnover bone disease (P < 0.001). A serum iPTH level > 200 pg/mL was 100% sensitive and 66% specific in identifying patients with high turnover ROD. The spectrum of bone disease of the children with CRF undergoing CAPD seems to depend on the rate of CRF and primary disease. The risk of developing overt hyperparathyroid bone disease is high in children with slowly progressing forms of renal pathology and especially in those with tubulo-interstitial disease. In contrast, children with glomerular diseases who had a more rapidly progressive course may have a lesser risk of developing high turnover bone disease. The results of the present study indicate that even routinely prescribed regular vitamin D therapy early in the course of disease may lead to low turnover bone lesion in small children who have CRF due to rapidly progressive forms of renal pathology.

Pregnancy decreases immunoreactive parathyroid hormone level in rats with chronic renal failure

Pregnancy decreases immunoreactive parathyroid hormone level in rats with chronic renal failure

Pregnancy decreases immunoreactive parathyroid hormone level in rats with chronic renal failure

Normal pregnancy is associated with an increase in serum parathyroid hormone and 1,25-dihydroxyvitamin D3 (calcitriol). The effect of pregnancy on these hormones in chronic renal failure (CRF) is unknown. The present work was undertaken to study the changes of serum immunoreactive parathyroid hormone (iPTH) and calcitriol in pregnant rats with CRF. The following experimental groups were studied: CRF1 (5/6 nephrectomized virgin female rats), CRF2 (5/6 nephrectomized pregnant rats at day 20-21 of pregnancy), CRF3 (5/6 nephrectomized rats 2 weeks after delivery) and their respective sham-operated control groups: N1, N2 and N3. The 5/6 nephrectomy (CRF1) resulted in renal failure with very high serum iPTH (100+/-18 pg/ml) and low calcitriol levels (10.6+/-4.3 pg/ml) compared with normal rats [N1: 14+/-2.5 pg/ml (P<0.001) and 18.2+/-4.2 pg/ml (P<0.01) respectively]. The pregnancy in CRF rats (CRF2) resulted in normalization of serum iPTH levels (18.2+/-5.41 pg/ml), which was associated with a parallel increase in serum calcitriol (29.4+/-8.0 pg/ml) similar to that in pregnancy of normal rats (N2). Two weeks after delivery the CRF rats (CRF3) once again had high serum iPTH (87+/-17 pg/ml) and low calcitriol levels (9.3+/-1.2 pg/ml), similar to those observed in non-pregnant uraemic rats (CRF1). It is concluded that pregnancy decreases serum iPTH in 5/6 nephrectomized CRF rats most probably by the increased level of calcitriol synthesized by the feto-placental unit.

Combined therapies with calcitonin and corticosteroids, or bisphosphonate, for treatment of hypercalcemia of malignancy

Thirty-four patients with hypercalcemia of malignancy were studied in three randomized prospective clinical studies. In study 1, 10 patients with solid tumors and in study 2, 10 patients with multiple myeloma, received calcitonin alone or combined calcitonin and corticosteroids. In study 3, 14 hypercalcemic patients with solid tumors received either pamidronate alone or pamidronate and calcitonin. Patients with solid tumors had at least one bony metastasis at the time of the study. Serum immunoreactive parathyroid hormone (PTH) levels in all patients were either undetectable or below the lower limit of the normal range, suggesting that the hypercalcemia is secondary to malignancy and not caused by an underlying primary hyperparathyroidism. The calciumlowering effect of calcitonin was rapid, but disappeared in 3–4 days. Corticosteroids significantly prolonged the duration of normocalcemia in patients with hematological malignancies but not in patients with solid tumors. After a single dose of 60 mg of pamidronate, serum calcium was lowered within 2–3 days, and normocalcemia was maintained for an average of 14 days. The addition of calcitonin lowered serum calcium within 24 h and led to a rapid improvement in hypercalcemic symptoms. Except in patients with hypercalcemia caused by hematological malignancies, the calcium-lowering effect was not enhanced by adding steroids to calcitonin therapy. In patients with moderate to severe symptomatic hypercalcemia, infusions of pamidronate every 2 weeks and calcitonin therapy for the first 2–3 days rapidly reduced serum calcium levels and sustained normocalcemia.

Truncation of the amino terminus of PTH alters its anabolic activity on bone in vivo

In vitro studies of parathyroid hormone (PTH) structure and function have suggested that the anabolic effect of PTH on bone requires the presence of amino acid residues 28–34 (domains for protein kinase C activation and mitogenic activity), but not amino acid residues 1–7 (adenylate cyclase activation domain). We have tested this hypothesis with in vivo studies of human PTH (hPTH) analogs. Serum biomarkers and selected histomorphometric parameters of bone formation and resorption were assessed in adult, female, Sprague-Dawley rats following 19 daily injections of vehicle, 10 μg/kg body weight (bw) of hPTH(1–38), or a dose range of 10, 40, and 100 μg/100 g bw of hPTH(2–38) or hPTH(3–38). Treatment with hPTH(1–38) increased serum osteocalcin, the percentage of osteoblast surface, percentage of osteoid surface, percentage of bone volume, trabecular thickness, and bone formation rate, while it decreased the percentage of osteoclast surface. The hPTH(2–38) fragment exhibited 10% -25% of the in vivo anabolic activity of hPTH(1–38), while it had no effect on the percentage of osteoclast surface. The hPTH(3–38) fragment exhibited no biological activity on bone. In contrast, serum INS-PTH (intact-N-terminal specific PTH) levels were similarly and significantly increased above control in rats treated with hPTH(1–38), hPTH(2–38), or hPTH(3–38) at the same dose. This preliminary finding suggests that the differential activity of these peptides on bone is not due to differences in the circulating level of immunoreactive PTH (intact and amino-terminal fragments of PTH from endogenous and exogenous sources) several hours after PTH injection. However, we can draw no conclusion regarding the relative clearance rates of these peptides. Last, because hPTH(3–38) was without any detectable biological activity on rat bone in vivo, its mitogenic activity was confirmed in two osteoblast-like cell lines. In summary, the anabolic effect of hPTH(1–38) on bone in vivo was (1) diminished by removal of amino acid residue 1, and (2) abolished by the removal of amino acid residues 1 and 2. Although these findings suggest that the therapeutic benefits of exogenous PTH administration may depend upon activation of not only protein kinase C, but also adenylate cyclase, they do not rule out a differential PTH response due to other causes, e.g., metabolic inactivation.

New aspects in the control of parathyroid hormone secretion

Ca2+ binds to a parathyroid cell Ca2+ receptor, which is G protein-coupled and activates inositol triphosphate production. Mutations in the Ca(2+)-sensing receptor gene cause familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism. Chronic hypocalcemia increases parathyroid hormone messenger RNA levels and parathyroid cell hyperplasia. Parathyroid cells in vitro are heterologous in their response to Ca2+. The concept of a higher Ca2+ set-point in secondary hyperparathyroidism is controversial. Calcitriol is more effective than the less hypercalcemia analogues in decreasing parathyroid hormone messenger RNA and immunoreactive parathyroid hormone levels, and its kinetics are well established. Phosphate and estrogens regulate the parathyroid independently of 1,25 dihydroxyvitamin D3 and Ca2+. The physiology of the effects of endothelin and insulin-like growth factors on the parathyroid need to be established. Important advances are being made in understanding the regulation of parathyroid hormone synthesis and secretion, which are relevant to both normal physiology and the pathogenesis and treatment of diseases such as the secondary hyperparathyroidism of renal failure and osteoporosis.

Hypercalcaemia in a patient with fatal adenosquamous carcinoma of the colon

To report a rare manifestation of metastatic adenosquamous carcinoma of the colon in a patient presenting with humoral hypercalcaemia of malignancy mediated by parathyroid hormone related peptide (PTHrP). A 58-year-old man with metastatic adenosquamous carcinoma of the colon presented with hypercalcaemia. A technetium bone scan excluded osteolytic bone secondaries. A negative parathyroid subtraction scan and a low serum immunoreactive parathyroid hormone level (1-34 [amino acid fragment]) made the diagnosis of primary hyperparathyroidism unlikely. The diagnosis of humoral hypercalcaemia of malignancy was considered on the basis of an elevated serum PTHrP level and positive tumour immunoreactivity to PTHrP antiserum. The hypercalcaemia was effectively treated on two occasions with intravenous administration of aminohydroxy propilidene diphosphonate. Despite interventional chemotherapy, the patient died of progressive carcinomatosis. Hypercalcaemia is an extremely rare occurrence in carcinoma of the colon. This is the first documented case of humoral hypercalcaemia of malignancy associated with adenosquamous carcinoma of the colon mediated by PTHrP.

Significant developmental elevation in serum parathyroid hormone levels in a large kindred with familial benign (hypocalciuric) hypercalcemia

Abstract purpose: A large kindred with familial benign hypercalcemia (FBH) is described because of the new observation of developmental increases in serum immunoreactive parathyroid hormone (iPTH) levels in affected individuals that lead to significantly elevated values in adults. patients and methods: After identification of the proposita, 46 kindred members spanning 5 generations, ages 1.5 to 91 years, were surveyed biochemically and/or studied by chart review. Two hypercalcemic adults underwent biopsy of the iliac crest following tetracycline labeling for histomorphometric study. results: Of the 46 individuals studied, 19 were found to be affected. Serum iPTH levels, determined in three separate immunoassays, became supranormal by about age 30 years in the group of 15 hypercalcemic subjects examined biochemically and appeared to increase further thereafter. Serum alkaline phosphatase activity and creatinine levels were normal in these individuals, but inorganic phosphate levels were lower than in unaffected kindred members. Three of five affected adults older than age 40 years who were studied radiographically had changes suggestive of osteomalacia. Biopsy of the iliac crest of one of the subjects, a 51-year-old woman, confirmed the presence of defective skeletal mineralization. conclusions: In this kindred, FBH in adults can be especially difficult to distinguish from primary hyperparathyroidism because serum iPTH levels may be elevated. Furthermore, the disorder may not be totally benign. Osteomalacia, perhaps due to mild hypophosphatemia, can develop during adulthood. Review of data from other kindreds for evidence of developmental elevations in serum iPTH levels with careful search for skeletal disease in late adult life will help to clarify if we have observed an unusual variant of FBH.

Detection of Subtle Aluminum-Related Renal Osteodystrophy

We compared the sensitivity of aurin tricarboxylic acid (ATA) or acid solochrome azurine (ASA) for detecting bone aluminum histochemically in 87 biopsy specimens obtained between 1983 and 1987 from 84 patients receiving dialysis therapy. Two consecutive biopsy sections were stained, one with ATA and the other with ASA, and then interpreted independently by two experienced observers. Three groups were established: group 1 (N = 61) had positive results of both ATA and ASA staining, group 2 (N = 25) had negative ATA but positive ASA sections, and group 3 (N = 1) had negative results of both ATA and ASA. No significant differences existed between groups 1 and 2 for age of the patients or serum calcium or immunoreactive parathyroid hormone levels. Patients in group 1 had significantly higher bone aluminium content (110 versus 61 micrograms/g dry ash weight), higher serum aluminum levels (151 versus 26 ng/ml), and longer duration of dialysis (85 versus 30 months) than did patients in group 2. Bone biopsy diagnoses (group 1 versus group 2) included low-turnover bone disease, 8 versus 7; osteomalacia, 26 versus 0; mixed uremic bone disease, 10 versus 1; hyperparathyroidism, 12 versus 14; and mild uremic bone disease, 5 versus 4. On the basis of ATA staining, 7 of 15 patients with low-turnover and 1 of 11 patients with mixed uremic bone disease may have been incorrectly diagnosed as having non-aluminum-related bone disorders. The levels of bone and serum aluminum were lower in group 2 than in group 1 but still much higher than normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Significant developmental elevation in serum parathyroid hormone levels in a large kindred with familial benign (hypocalciuric) hypercalcemia

purpose: A large kindred with familial benign hypercalcemia (FBH) is described because of the new observation of developmental increases in serum immunoreactive parathyroid hormone (iPTH) levels in affected individuals that lead to significantly elevated values in adults. patients and methods: After identification of the proposita, 46 kindred members spanning 5 generations, ages 1.5 to 91 years, were surveyed biochemically and/or studied by chart review. Two hypercalcemic adults underwent biopsy of the iliac crest following tetracycline labeling for histomorphometric study. results: Of the 46 individuals studied, 19 were found to be affected. Serum iPTH levels, determined in three separate immunoassays, became supranormal by about age 30 years in the group of 15 hypercalcemic subjects examined biochemically and appeared to increase further thereafter. Serum alkaline phosphatase activity and creatinine levels were normal in these individuals, but inorganic phosphate levels were lower than in unaffected kindred members. Three of five affected adults older than age 40 years who were studied radiographically had changes suggestive of osteomalacia. Biopsy of the iliac crest of one of the subjects, a 51-year-old woman, confirmed the presence of defective skeletal mineralization. conclusions: In this kindred, FBH in adults can be especially difficult to distinguish from primary hyperparathyroidism because serum iPTH levels may be elevated. Furthermore, the disorder may not be totally benign. Osteomalacia, perhaps due to mild hypophosphatemia, can develop during adulthood. Review of data from other kindreds for evidence of developmental elevations in serum iPTH levels with careful search for skeletal disease in late adult life will help to clarify if we have observed an unusual variant of FBH.

Calcium acetate as a phosphorus binder in hemodialysis patients.

Much interest is currently centered on the use of calcium acetate as a phosphorus binder in patients with renal failure. Therefore, this compound in subjects previously stable on calcium carbonate and undergoing high-efficiency hemodialysis with a dialysate calcium of 2.5 mEq/L was evaluated. Twenty subjects were switched from generic calcium carbonate to a single calcium carbonate preparation for a period of 2 months. This was followed by a phase (1 month) in which calcium acetate was substituted for calcium carbonate at a dose containing half the amount of elemental calcium. Subjects then continued calcium acetate for 6 months. It was found that calcium acetate allowed comparable control of immunoreactive parathyroid hormone, calcium, and phosphorus levels compared with calcium carbonate. This occurred with half the amount of elemental calcium ingested in the form of calcium acetate (349 +/- 25 versus 699 +/- 75 mmol/day; P less than 0.001). With this lower dose, the overall incidence of hypercalcemia was the same with each formulation. In the eight subjects concurrently receiving i.v. calcitriol, the incidence of hypercalcemia was significantly higher during the first month of calcium acetate compared with that in those not receiving this compound (P less than 0.05). Of those four subjects receiving the high dose of calcitriol (2 micrograms thrice weekly), all required either reduction in the dose or discontinuation of the drug. Thus, mineral metabolism could be controlled adequately with calcium acetate despite using half as much elemental calcium compared with calcium carbonate. This, however, did not result in a lower incidence of hypercalcemia, particularly in those receiving i.v. calcitriol.