Serum Immunoreactive Parathyroid Hormone Levels Research Articles

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.

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.

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.

Cardiovascular responsiveness to parathyroid hormone (PTH) and PTH-related protein in genetic hypertension.

Hypertension is often accompanied by abnormalities of calcium homeostasis, including hyperparathyroidism with reduced target organ responses to PTH in kidney and bone. Due to this association between PTH and hypertension and since PTH and the paracrine factor PTH-related protein (PTHrp) have both been shown to exert marked changes in cardiovascular activity, these actions of PTH and PTHrp were examined in spontaneously hypertensive rats (SHR) and in control normotensive Wistar-Kyoto rats (WKY). Fourteen-week-old SHR [systolic blood pressure (SBP), 201 +/- 4.4 mm Hg] and WKY (SBP, 141 +/- 2.5 mm Hg) were studied. Renal cortical membranes were prepared and assayed for radioligand binding with [125I]PTH-(1-34) and [125I]PTHrp-(1-34). There was no apparent alteration in the affinity of the binding sites to either peptide in the SHR, but specific binding in SHR renal tissue was only 60% of that observed in WKY tissue for both peptides. Serum immunoreactive PTH levels were 4-fold higher in SHR than WKY, while serum total calcium and 1,25-dihydroxyvitamin D3 levels were not different. The iv administration of both PTH and PTHrp produced dose-dependent reductions in SBP and increases in heart rate in conscious unrestrained SHR and WKY. Both peptides caused greater absolute reductions in blood pressure in SHR than in WKY. However, when the hypotensive response was normalized for the higher baseline pressure in the SHR, the blood pressure reductions caused by PTH and PTHrp were not different in SHR and WKY. Conversely, the chronotropic responses to PTH and PTHrp were lower in SHR compared to WKY. These findings indicate that the SHR exhibits elevated PTH levels, with a reduced number of renal PTH/PTHrp receptors and a depressed chronotropic response to either PTH or PTHrp. In contrast, the hypotensive response to PTH or PTHrp was not altered, indicating possible tissue-specific receptor subclasses or tissue-specific regulation of PTH and PTHrp receptors.

Coexisting hyperparathyroidism with thyrotoxicosis

The coexistence of hyperparathyroidism complicating thyrotoxicosis is quite rare. We report the case of one patient who presented with thyrotoxicosis, (total thyroxine of 15.1 micrograms/dl (5-13), free thyroxine index of 18 (4-15) and triiodothyronine by RIA of 305 ng/dl (70-230) and asymptomatic hypercalcemia of 15 mg/dl (8.5-10.6), who was also initially noted to have an elevated (C-terminal) serum immunoreactive parathyroid hormone (iPTH) level of 8,800 pg/ml (50-340). With propylthiouracil and propranolol, however, this patient became normocalcemic with a decrease in iPTH values to 714 pg/ml. As the patient was tapered from medication, after being rendered euthyroid, a recurrence of hypercalcemia with rising iPTH levels occurred. PTH levels should be helpful in defining coexisting hyperparathyroidism in patients with thyrotoxicosis since in the latter iPTH is usually suppressed. Our findings support the recommendation that in patients suspected of having both hyperparathyroidism and hyperthyroidism, a diagnosis of the former can only be made with certainty after the patient has been rendered euthyroid with persistently elevated serum calcium and iPTH levels. While there are no clinical features which permit the easy identification of patients who present with dual lesions, the determination of iPTH values may be the most consistently helpful test initially, whereas other parameters such as vitamin D, serum phosphate are less reliable.

The effects of oophorectomy on skeletal metabolism

The effects of oophorectomy on the biological indices of bone remodelling and the time-course of their changes are described. In the first few months following surgical menopause the measurement of the markers of bone remodelling indicates that the increase in osteogenesis is delayed compared with that of bone resorption; this prevalence of destruction over new bone depositon justifies the deficiency of skeletal balance, shortly after acute oestrogen deficiency. The changes in bone remodelling are accompanied by an increase in serum calcium while serum immunoreactive parathyroid hormone levels remain unchanged or even decrease, suggesting a shift to right of the parathyroid gland set-point. The reasons for the negative skeletal balance after oophorectomy might be sought therefore at bone tissue level, even if changes in responsiveness and/or of the parathyroid gland set-point could also be contributory.

Clinical Experience with Desferrioxamine&lt;xref ref-type="fn" rid="fn1"&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/xref&gt; in Dialysis Patients With Aluminium Toxicity

A desferrioxamine (DFO) infusion test, using a DFO dose of 36.9 +/- 11.2 mg/kg (mean +/- SD), was performed in 50 consecutive dialysis patients undergoing diagnostic bone biopsy. In 30 patients whose bones stained positively for aluminium the serum aluminium level increased by an average of 373 +/- 250.4 ng/ml. The increase in 20 aluminium-negative patients was 231 +/- 179.2 ng/ml (p less than 0.05). Aluminium-positive patients had lower levels of immunoreactive parathyroid hormone (336 +/- 442 muleq/ml) than aluminium-negative patients (1278 +/- 1400 muleq/ml; p less than 0.05). A change in serum aluminium level of greater than 200 ng/ml after the administration of DFO was 73 percent sensitive and 50 percent specific, and had a positive predictive value of 69 percent for detecting positive bone aluminium staining. The combination of a baseline immunoreactive parathyroid hormone level less than 200 muleq/ml and a change in serum aluminium of greater than 200 ng/ml after DFO was 90 percent specific and had a positive predictive value of 85 percent. In the second phase of our study, 28 dialysis patients with aluminium toxicity received long-term therapy (11.0 +/- 4.3 months) with DFO at an average starting dose of 41.7 +/- 17.1 mg/kg, administered once weekly. The four deaths which occurred during this treatment involved the only patients who had advanced dialysis dementia. Seven patients with less severe neurological symptoms responded favourably. Fractures decreased from 1.7 fractures/patient/year to 0.1 fracture/patient/year. Muscular strength and overall functional class were improved or stable in 25 patients; myalgias and arthralgias were also stable or improved in 19 patients. After 5-7 months of treatment, serum aluminium levels decreased from 401 +/- 262 ng/ml to 245 +/- 217 ng/ml (p less than 0.01); erythrocyte mean corpuscular volume increased from 86.3 +/- 10.91 fl to 94.1 +/- 9.23 fl (p less than 0.02); and serum calcium decreased from 10.4 +/- 0.94 mg/dl to 9.9 +/- 0.70 mg/dl (p less than 0.02). Serum immunoreactive parathyroid hormone levels remained stable in 25 patients, but severe hyperparathyroidism developed rapidly in three patients. Eight patients with transfusional iron overload had no change in serum ferritin levels. Iron depletion developed in six patients, with a decrease in serum ferritin from 251 +/- 229.8 micrograms/l to 45 +/- 29.3 micrograms/l, and they required parenteral iron supplementation. Significant side-effects occurring during long-term DFO administration were hypotension (11 patients), gastrointestinal upset (seven patients), porphyria cutaneous tarda-like lesions (three patients), and transient visual disturbance (one patient). There was a decrease in stainable bone aluminium in all nine patients with paired bone biopsy specimens (pre- and post-DFO).(ABSTRACT TRUNCATED AT 400 WORDS)

Hyperparathyroidism and portacaval shunt: A syndrome or a coincidence?

This is a report of six patients with cirrhosis of the liver in whom primary hyperparathyroidism occurred due to a solitary parathyroid adenoma 3 months to 9 years after undergoing emergency portacaval shunt for hemorrhage from esophageal varices. The presenting symptoms in all six patients were weakness and bone pain. Three patients had a bone fracture after insignificant trauma, one and probably two passed kidney stones, and a duodenal ulcer developed in two. Bone x-ray films showed generalized osteoporosis in all patients. Renal function and arterial blood pH were within normal limits in every patient. The diagnosis of primary hyperparathyroidism in each patient was based on repeated demonstrations of hypercalcemia, hypophosphatemia, and markedly elevated serum immunoreactive parathyroid hormone concentrations. In all six patients, removal of the parathyroid adenoma resulted in disappearance of symptoms; normalization of serum calcium, phosphorus, and immunoreactive parathyroid hormone levels; and, in four of the six, improvement in radiographic evidence of osteoporosis during follow-up of from 1 to 6 years. The association of cirrhosis, portacaval shunt, and primary hyperparathyroidism has not been documented previously. Our six patients with primary hyperparathyroidism constitute 3.4 percent of 174 survivors of emergency portacaval shunt in a series of 264 unselected, consecutive patients with cirrhosis and bleeding esophageal varices. Hepatic osteodystrophy is known to have occurred in only 11 of these 174 survivors. Primary hyperparathyroidism may be a more common cause of hepatic osteodystrophy than has been previously recognized, and should be considered in patients with cirrhosis in whom weakness, bone pain, and bone demineralization develop, particularly if they have a portacaval anastomosis.

Stereological studies of the parathyroids in the young rat with hypercalcemia induced by severe phosphate depletion.

In order to suppress the parathyroid glands by inducing hypercalcemia, young rats were fed a diet containing a low (0.02%) phosphate content. After 28 days blood samples were taken for estimation of serum calcium, phosphate and immunoreactive parathyroid hormone levels. Both parathyroids from each animal were subjected to serial sectioning so that the total glandular volume could be calculated by light microscopy. Volume and surface densities of cells and organelles were measured according to conventional stereological principles, so that the total volumes and surface areas could be estimated. Phosphate depletion caused marked growth retardation. The animals also developed hypophosphatemia, but in spite of pronounced hypercalcemia the levels of circulating immunoreactive parathyroid hormone remained unchanged. The volume of the parathyroids was reduced, but only to an extent commensurate with the reduced body mass. In the experimental group the volume density of cells was unchanged, but that of nuclei was increased; the volume density of Golgi complexes was reduced. The densities of the other cell components measured, namely the volume density of mitochondria and the surface densities of secretory cells, nuclear membranes and rough endoplasmic reticulum were unchanged. When the volumes and surfaces were expressed in absolute terms and related to total body mass, no differences between the groups were apparent.(ABSTRACT TRUNCATED AT 250 WORDS)

Serum parathyroid hormone (PTH) in pregnant women determined by an immunoradiometric assay for intact PTH.

Most studies of circulating PTH levels using traditional RIAs have supported the concept of physiological hyperparathyroidism of pregnancy, with pregnant women having serum immunoreactive PTH levels significantly higher than those in nonpregnant subjects. However, such RIAs are insensitive and often detect inactive PTH fragments, so that the correlation between PTH immunoreactivity and bioactivity is poor. Employing a new intact PTH immunoradiometric assay (Allegro-Nichols), we reassessed the effects of pregnancy on parathyroid function. The mean serum PTH level in 81 pregnant women was 14.4 +/- 6.3 (+/- SD) compared to 24.8 +/- 9.0 ng/L in 11 normally cycling nonpregnant women (P less than 0.001). The mean serum total and ionized calcium levels in the 2 groups were similar. In 5 of the pregnant women, serum bioactive PTH, determined by cytochemical bioassay, was slightly lower (7.7 +/- 3.4 ng/L) than in normal individuals (11.1 +/- 1.9 ng/L). Our findings suggest, in contrast with the results of most previous studies, that serum intact PTH may decline during pregnancy.

Hyperparathyroidism, cirrhosis, and portacaval shunt: A new clinical syndrome

This is a report of six patients with cirrhosis of the liver in whom primary hyperparathyroidism occurred due to a solitary parathyroid adenoma 3 months to 9 years after undergoing emergency portacaval shunt for hemorrhage from esophageal varices. The presenting symptoms in all six patients were weakness and bone pain. Three patients had a bone fracture after insignificant trauma, one and probably two passed kidney stones, and a duodenal ulcer developed in two. Bone x-ray films showed generalized osteoporosis in all patients. Renal function and arterial blood pH were within normal limits in every patient. The diagnosis of primary hyperparathyroidism in each patient was based on repeated demonstrations of hypercalcemia, hypophosphatemia, and markedly elevated serum immunoreactive parathyroid hormone concentrations. In all six patients, removal of the parathyroid adenoma resulted in disappearance of symptoms; normalization of serum calcium, phosphorus, and immunoreactive parathyroid hormone levels; and in four of the six, improvement in radiographic evidence of osteoporosis during follow-up of from 1 to 6 years. The association of cirrhosis, portacaval shunt, and primary hyperparathyroidism has not been documented previously. Our six patients with primary hyperparathyroidism constitute 3.4 percent of 174 survivors of emergency portacaval shunt in a series of 264 unselected, consecutive patients with cirrhosis and bleeding esophageal varices. Hepatic osteodystrophy is known to have occurred in only 11 of these 174 survivors. Primary hyperparathyroidism may be a more common cause of hepatic osteodystrophy than has been previously recognized, and should be considered in patients with cirrhosis in whom weakness, bone pain, and bone demineralization develop, particularly if they have a portacaval anastomosis.

Abnormal regulation of parathyroid hormone secretion by serum calcium level in myotonic dystrophy

Although the presence of bone abnormalities has been well known in myotonic dystrophy (MyD), details about calcium metabolism in this condition remain unclear. We already reported that the intestinal calcium absorption is increased in MyD patients due to the elevation of plasma 1,25(OH)2D level. We also reported that serum immunoreactive parathyroid hormone (iPTH) levels and Nephrogenous cyclic AMP (NcAMP) levels are increased in MyD patients. This study was designed to elucidate the mechanism of hyperparathyroid state in MyD patients. Intravenous calcium tolerance test was performed in 7 patients with MyD and 7 control subjects, 3 patients with other neuromuscular disorder and 4 healthy subjects. Calcium was infused stepwise at the concentration of 0, 104.7, 194.9 and 235.5mg every hour. The basal plasma calcium levels were significantly higher in MyD (9.79 +/- 0.27 mg/dl, Mean +/- SD) as compared with control subjects (9.50 +/- 0.19; p less than 0.05). Basal serum iPTH levels were also significantly higher in MyD (514.0 +/- 188.9 pg/ml) than those in control subjects (333.7 +/- 113.5; p less than 0.05). After calcium infusion, serum calcium levels were increased in both groups, but the levels of serum calcium remained significantly higher in MyD than those in control subjects. On the other hand, urinary calcium excretion levels were not different between the two groups. At the same time, %TRP and calcium clearance were significantly lower in MyD than control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Biochemical picture accompanying sclerotic bone metastases of prostatic origin.

This study was carried out to evaluate the metabolic consequences of osteosclerotic skeletal metastases of prostatic origin in a homogeneous group of patients. We found significantly increased mean values of serum alkaline phosphatase activity and significantly reduced mean values of serum phosphate, 24-h urinary calcium, fasting calcium excretion and TmP/GFR in cancer patients with respect to age-matched controls. Mean serum immunoreactive parathyroid hormone (iPTH) levels were raised, with two patients showing increased values of the hormone above our normal limits. Our findings indicate that mild secondary hyperparathyroidism is a feature of these patients. However, it cannot be excluded that both the reduced serum phosphate and TmP/GFR values may be related, at least in some cases, to the effects of the tumour itself on tubular reabsorption of phosphate.

Parathyroid hormone radioimmunoassays in the differential diagnosis of hypercalcemia due to primary hyperparathyroidism or malignancy.

Brief Reports1 April 1987Parathyroid Hormone Radioimmunoassays in the Differential Diagnosis of Hypercalcemia Due to Primary Hyperparathyroidism or MalignancyEDWARD G. LUFKIN, M.D., PAI CHIH KAO, Ph.D., HUNTER HEATH III, M.D.EDWARD G. LUFKIN, M.D.Search for more papers by this author, PAI CHIH KAO, Ph.D.Search for more papers by this author, HUNTER HEATH III, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-106-4-559 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe determination of serum immunoreactive parathyroid hormone (iPTH) levels remains the most useful laboratory study in the differential diagnosis of hypercalcemia. The iPTH assay has been particularly valuable in distinguishing the two commonest hypercalcemic disorders, primary hyperparathyroidism and malignancy, which together account for more than 80% of cases of persistent hypercalcemia (1-3). The importance of distinguishing these two disorders lies in the great differences in their treatment and prognosis.There are differences in predictive value among commercially available iPTH assays, and some confusion persists concerning the terms used to describe these assays. When Raisz and coworkers (4) submitted aliquots of...

Parathyroid hormone secretion: Effect of estradiol and progesterone

Previous studies have shown that estrogen therapy in postmenopausal women results in an increase in serum immunoreactive parathyroid hormone (iPTH) levels. It has been assumed that this effect of estrogen on PTH secretion is indirect, being mediated via mild hypocalcemia resulting from an inhibition of bone resorption. We evaluated the direct effect of 17 β-estradiol (E 2) and of progesterone (Prog) on secretion of PTH from bovine parathyroid tissue in vitro. Both E 2 and Prog caused a significant stimulation of PTH secretion within one hour, which was progressive for the three-hour observation period. The responses were dose-related from 10 −7 to 5 × 10 −10 mol/L. There was no PTH response to 10 −7 mol/L α-E 2, 3-methoxy estriol, estrone, testosterone, or 20-α-hydroxy progesterone, indicating specificity of the responses to E 2 and Prog. There was a minimal PTH secretory response to 10 −8 mol/L cortisol and 10 −6 mol/L estrone. The E 2 receptor antagonist tamoxifen did not inhibit the E 2 effect on PTH secretion. This observation plus the rapid PTH response suggests that this hormonal effect may not be via the conventional intracellular E 2 receptor. Therefore, E 2 and Prog can stimulate PTH secretion by rapid, direct, and specific effects on parathyroid cells. These gonadal hormones may, therefore, be important in calcium homeostasis via their direct stimulatory effect on PTH secretion.