Immunoreactive Parathyroid Hormone Levels Research Articles

Elevated Bone Aluminum Content in Dialysis Patients Without Osteomalacia

In almost all dialysis patients, bone aluminum content (BAC) is elevated in comparison with levels in normal subjects. Extremely high BAC (200 micrograms or more of aluminum per gram of bone) is significantly associated with classic aluminum-related osteomalacia. We noted three patients with elevated BAC but without histologic evidence of typical osteomalacia. Two of the patients had moderately severe osteitis fibrosa (hyperparathyroidism), and one patient had mixed uremic bone disease--predominantly hyperparathyroidism but some impairment of bone mineralization as well. As has recently been reported by others, the deferoxamine infusion test yielded unusual results in these patients. On the basis of our observations, we believe that an isolated measurement of BAC to determine whether aluminum-related osteomalacia is present has certain limitations. Aluminum-related bone disease can be accurately diagnosed only with use of bone histomorphometry. Elevated levels of immunoreactive parathyroid hormone may offer protection from the toxic effects of aluminum.

Effects of parathyroidectomy on bone formation and mineralization in hemodialyzed patients

Undecalcified sections of doubly tetracycline-labeled transiliac bone biopsy specimens obtained from ten hemodialyzed patients before and 10 to 16 months after parathyroidectomy (PTX) were analyzed. Before parathyroidectomy (total PTX with autotransplant in six patients and subtotal PTX in four patients), all the patients demonstrated histological evidence of hyperparathyroidism with increased resorption parameters. A high bone formation rate (BFR) was noted in all patients but one who had both an increase in the osteoid seam thickness and a low calcification rate characteristic of osteomalacia. A significant correlation was found between immunoreactive parathyroid hormone (iPTH) levels and BFR at the tissue and at the basic multicellular unit (BMU) levels. Parathyroidectomy was associated with a dramatic drop in resorption surfaces and osteoclast number as well as in bone formation rate at the tissue, BMU, and cell-levels. After PTX, the bone formation rate at the tissue level was low or in the lower range of normal values in six patients. The thickness index of osteoid seams was significantly reduced and no evidence of osteomalacia was present even in the six patients showing bone aluminum deposits after PTX. One of the three patients, who had an iPTH level within the normal range after PTX, showed an osteoid excess associated with a low bone formation rate. These date demonstrate that increased PTH secretion is an important factor of bone formation in dialyzed patients and that excessive reduction of the PTH secretion leads to an inactive bone.

Effect of active vitamin D3 analogs on the osteoporosis of rats caused by ovariectomy.

The effects of 1, 24(R)-dihydroxyvitamin D3(1, 24(R)(OH)2D3), 1, 25-dihydroxyvitamin D3(1, 25(OH)2D3) and 1α-hydroxyvitamin D3(1α(OH)D3) on the development of osteoporosis in ovariectomized rats were investigated biochemically and histomorphologically. Vitamin D3 analogs dissoloved in corn oil were given orally to the rats for 6 months after the ovariectomy. The sham-operated control animals received the vehicle alone. Ovariectomy was followed by the development of osteoporosis after 6 months of observation. This was characterized by a reduction in ash content of the tibia and histjologically by a disappearance of the trabecular bone in tibial metaphysis. Biochemical studies showed significant decreases in serum calcium and 1, 25(OH)2D concentrations, and significant increases in serum immunoreactive parathyroid hormone (iPTH) level in ovariectomized rats. These findings suggest that ovariectomy partially impairs intestinal absorption of calcium, increases bone resorption, and results in a negative calcium balance, which may contribute to the development of osteoporosis in rats. The administration of 1, 24(R)(OH)2D3, 1, 25(OH)2D3 and 1α(OH)D3 increased dose-dependently serum and urinary calcium, but decreased serum iPTH levels to the control level and prevented the development of osteoporosis histologically. These results support the view that active vitamin D3 analogs may be valable tools for the treatment of osteoporosis.

Changes in parathyroid hormone and calcium levels after superior cervical ganglionectomy of rats.

To assess the role of peripheral sympathetic nerves in the regulation of parathyroid hormone (PTH) release rats subjected to bilateral superior cervical ganglionectomy (SCGx) 8-24 h earlier were used. SCGx did not result in significant changes of basal serum calcium (Ca) or immunoreactive PTH (iPTH) levels. The i.p. administration of EDTA every 30 min for up to 3 h brought about an impending decrease of serum Ca levels in both sham-operated and SCGx rats when assessed 23 h after surgery. The extent of hypocalcemia was significantly larger in the SCGx group. In sham-operated controls serum iPTH increased by 32-145%, 1-3 h after beginning EDTA treatment whereas such increases were considerably lower or absent in SCGx rats. In 3 out of 7 SCGx animals that survived to a double EDTA dose, iPTH increased to levels indistinguishable from controls. When SCGx rats subjected to surgery 23 h earlier and receiving d-1-propranolol (5 mg/kg) or phentolamine (10 mg/kg) 4 h and 30 min earlier were submitted to iterative EDTA injection serum iPTH increased, whereas no changes were detected in SCGx rats treated with vehicle and subjected to the same EDTA treatment. These data indicate that (1) SCGx does not affect basal release of iPTH or serum Ca concentration; (2) 23-26 h after SCGx there is a significant impairment of homeostatic iPTH responses to low Ca levels which can be overcome by suitable Ca stimulus; (3) circulating catecholamines may affect denervated parathyroid cells, as revealed by the changes in serum iPTH and Ca elicited by alpha- and beta-adrenoceptor-blocker treatment of SCGx rats.

Surgical treatment of secondary hyperparathyroidism in patients with chronic renal failure: reevaluation of indications for parathyroidectomy.

On reviewing the preoperative clinical and laboratory findings and the surgical response seen in our series of 32 patients with renal hyperparathyroidism, the indication for parathyroidectomy was reevaluated. During the 5-year period from 1975 to 1979, parathyroid resection was performed in 9 patients who had various conditions for which surgery had been thought indicated. During the following period from January 1980 to March 1985, parathyroidectomy was carried out on 23 patients all of whom had roentgenologic evidence of generalized fibrous osteitis except for two whose indication for surgery was an elevation of the serum alkaline phosphatase level more than 45 KA units. The resected parathyroid glands had increased to 1 g or more in total weight in all the 25 patients who showed distinct postoperative improvement. Laboratory evidence indicating the presence of generalized fibrous osteitis, such as subperiosteal resorption on phalanx roentgenograms and high serum alkaline phosphatase level, along with marked elevation of the plasma immunoreactive parathyroid hormone level, proved to be a good indicator for medically uncontrollable secondary hyperparathyroidism. Fracture, heterotopic calcification, pruritus or persistent hypercalcemia was not a parameter of severe hyperparathyroidism warranting parathyroid resection, unless there was concomitant evidence of fibrous osteitis. The preoperative use of the recently developed noninvasive techniques for parathyroid localization also proved to be useful in detecting the parathyroid glands large enough to fulfill the requirements for parathyroidectomy.

Prolactin and calcium metabolism: influence of hyperprolactinemia on immunoreactive parathyroid hormone levels in man and in the rat.

Serum prolactin, parathyroid hormone, P and Ca serum levels were measured in 15 patients (12 women and 3 men) with hyperprolactinemia, and in 6 normal male volunteers who underwent a TRH test (100 micrograms by rapid iv injection) in order to obtain a short-term pharmacologically-induced hyperprolactinemia. A pituitary gland graft under the kidney capsule was carried out on 26 Sprague-Dawley male rats, which became hyperprolactinemic since the transplanted pituitary was stripped of the inhibitory hypothalamic control. Another group of 10 rats was injected with L-sulpiride (0.1 mg/kg). The serum PTH levels in patients and in subjects with induced hyperprolactinemia were within the normal range and there was no correlation between serum PRL and PTH levels. The same occurred both in transplanted and L-sulpiride injected rats. Our results suggest that prolactin does not modify PTH secretion in vivo and therefore, in contrast with previous data, it should not be considered a physiologically relevant secretagogue for parathyroid hormone.

A model for malignancy-associated humoral hypercalcemia.

Tumor tissue from a patient with squamous cell carcinoma of the lung and hypercalcemia has been serially implanted into athymic mice. Tumor-bearing mice develop cachexia, hypercalcemia without bone metastases, hypophosphatemia, increased urinary cyclic adenosine monophosphate (cAMP) to creatinine ratio, and undetectable human immunoreactive parathyroid hormone levels. Radiographs of spines in the tumor-bearing mice demonstrate demineralization, suggesting skeletal resorption as the source of the hypercalcemia. Within 4-8 hours following tumor removal, hypercalcemia is reversed, suggesting that a relatively short-acting humoral substance is responsible for the hypercalcemia. The animals gain weight and become essentially normal within 4 days following tumor removal. The studies demonstrate that this animal model is similar in many aspects to human malignancy-associated humoral hypercalcemia (MAHH) and can provide a useful tool for further investigation of the pathogenesis and treatment of this syndrome.

Bioactive parathyroid hormone in canine progressive renal insufficiency.

Bioactive parathyroid hormone and hormonal actions were monitored as hyperparathyroidism evolved in a model of progressive canine renal failure. Circulating levels of bioactive and immunoreactive parathyroid hormone rose as renal insufficiency worsened, but elevations, especially in bioactivity, were most marked in the final stage of uremia. By gel filtration analysis, the major circulating bioactive moiety was similar to the major glandular form of parathyroid hormone, although a smaller-molecular-weight entity was seen in the final stage of renal failure. Renal phosphate threshold fell, urinary hydroxyproline corrected for glomerular filtration rose, and plasma 1,25-dihydroxyvitamin D fell but remained detectable, as renal function deteriorated. The results demonstrate a progressive rise in bioactive parathyroid hormone, show the appearance of a small-molecular-weight bioactive entity in severe renal disease, and correlate effects of the rising bioactive parathyroid hormone with changes in renal phosphate handling and with skeletal resorption.

Production of immunoreactive calcitonin and parathyroid hormone by embryonal carcinoma cells: Alteration with retinoic acid-induced differentiation

To determine possible ectopic production of, and altered responsiveness to, specific hormones and growth factors which may be involved in mediating embryonic differentiation and development embryonal carcinoma cells in culture have been employed to serve as an in vitro system of embryogenesis. Exposure of F9 embryonal carcinoma cells to all- trans-retinoic acid previously has been shown to induce differentiation of these undifferentiated stem cells to parietal endoderm and to markedly alter the ability of calcitonin and parathyroid hormone to stimulate adenylate cyclase activity. Evidence is presented that F9 cells secrete immunoreactive calcitonin into the culture medium (200 pg/12 hr/10 7 cells) while parietal yolk sac (PYS) cells secrete immunoreactive parathyroid hormone (800 pg/12 hr/10 7 cells). Retinoic-induced differentiation of F9 cells to endoderm results in a progressive reduction in immunoreactive calcitonin production, while there is an increase in the level of immunoreactive parathyroid hormone found in the conditioned medium. After exposure of F9 cells to retinoic acid for 5 days, little calcitonin is detectable in 12-hr conditioned medium. Changes in the intracellular levels of immunoreactive calcitonin and PTH follow a pattern similar to that noted for changes in the amount of secreted hormones. Thus, immunoreactive calcitonin is produced by undifferentiated F9 cells which possess a calcitonin responsive adenylate cyclase system, while parathyroid hormone is produced by parietal endoderm cells which respond to parathyroid hormone with increased cyclic AMP synthesis. Sephadex G50 gel filtration of F9-conditioned medium shows two peaks of immunoreactive calcitonin with M r of 3500 and 20,000. Immunoprecipitation of calcitonin from 35S-labeled F9 cells reveals a specific band of 20,000 M r. Likewise, two peaks of parathyroid hormone immunoreactive material of M r 8000 and 39,000 are noted after gel filtration of PYS cell-conditioned medium, whereas parathyroid hormone immunoprecipitation from the same cells reveals a specific band of 39,000 M r. These results raise the possibility that embryo production of these two hormones at specific stages in development may contribute to the regulation of subsequent steps of differentiation.

Evidence of increased parathyroid activity on discontinuation of high-aluminum dialysate in patients undergoing hemodialysis

High-aluminum dialysate exposure has been incriminated in the pathogenesis of vitamin D-resistant osteomalacia in patients undergoing long-term hemodialysis. Parathyroid-mediated osteitis fibrosa is rare in these patients. Thirteen patients undergoing long-term hemodialysis were transferred from a center (Unit A) where water used to prepare dialysate was high in aluminum (100 to 450 μg/liter) to a new center (Unit B) where dialysate was highly purified (aluminum concentration less than 10 μg/liter), and changes in calcium metabolism were studied over a 12-month period. After transfer of patients to Unit B, serum aluminum levels fell (p < 0.01), whereas serum immunoreactive parathyroid hormone levels rose (p < 0.01) over 10 months. Over this time, predialysis serum calcium levels did not alter significantly, whereas postdialysls serum calcium levels declined slightly (p < 0.05). Serum phosphate levels did not alter. Serum alkaline phosphatase levels rose progressively in Unit B (p < 0.001). Discontinuation of dialysate high in aluminum in patients undergoing long-term hemodialysis may facilitate a rise in parathyroid activity.

Effects of hypophysectomy and growth hormone treatment on renal hydroxylation of 25-hydroxycholecalciferol in rats.

Growth hormone stimulates intestinal calcium absorption. This action has been linked to vitamin D metabolism. We have investigated the effects of hypophysectomy and GH treatment on renal metabolism of 25-hydroxycholecalciferol (25-OH-D3). Renal hydroxylation of 25-OH-D3 was measured in vitro using the renal slice technique. Experiments were performed in young F344 rats fed a vitamin D-replete, low calcium diet for 4 weeks. In hypophysectomized rats, renal conversion of 25-OH-D3 to 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) was markedly reduced compared with sham-operated rats. Renal conversion of 25-OH-D3 to 24,25-(OH)2D3 was markedly increased in hypophysectomized rats compared with sham-operated rats. Treatment of hypophysectomized rats with rat GH (rGH) for 10 days resulted in a significant increase in renal conversion of 25-OH-D3 to 1,25-(OH)2D3 and a significant decrease in conversion to 24,25-(OH)2D3. Rat GH treatment caused no significant changes in serum levels of immunoreactive parathyroid hormone. Serum calcium concentrations were similar in all groups, and serum phosphorus was low in hypophysectomized rats. Treatment of hypophysectomized rats with ovine GH for 6 days caused changes which were much less pronounced than those induced by rGH. Renal conversion of 25-OH-D3 to 1,25-(OH)2D3 and 24,25-(OH)2D3 correlated well with growth rate (weight gain). These results suggest that GH, either directly or indirectly, modulates renal metabolism of 25-OH-D3.

Nephrogenous cyclic AMP and plasma parathyroid hormone in hypercalcaemia: the influence of renal function.

Immunoreactive parathyroid hormone (PTH) levels and nephrogenous cyclic adenosine monophosphate (cAMP) have been reported to be useful parameters in the diagnosis of hyperparathyroidism. Measurements in hyperparathyroid patients usually give values above the normal range when PTH is measured with a carboxyterminal radioimmunoassay and when nephrogenous cAMP is related to glomerular filtration rate. We tested these two parameters in two groups of hypercalcaemic patients (twelve cases of primary hyperparathyroidism and fourteen cases of hypercalcaemia of non-parathyroid origin) and in two groups of normocalcaemic subjects (twenty-one young healthy volunteers and fourteen elderly subjects without parathyroid disease). Slight impairment of renal function caused elevated values of immunoreactive parathyroid hormone in a carboxyterminal radioimmunoassay and also of nephrogenous cAMP when related to glomerular filtration rate. We found that elevated nephrogenous cAMP without parathyroid disease could be attributed to renal insufficiency and to the mode of expression generally used for the nephrogenous cAMP.

Vitamin D status after total gastrectomy.

Serum levels of 25-hydroxyvitamin D, 24,25-dihydroxyvitamin D, 1,25-dihydroxyvitamin D, immunoreactive parathyroid hormone, and urinary excretion of nephrogenous cyclic AMP were measured in 25 patients after total gastrectomy. Two types of reconstruction after total gastrectomy were also compared. Serum 25-hydroxyvitamin D levels were significantly decreased and serum 24,25-dihydroxyvitamin D levels were markedly reduced, whereas serum 1,25-dihydroxyvitamin D levels were significantly increased in the patients. Although serum levels of immunoreactive parathyroid hormone did not show a significant difference, serum alkaline phosphatase levels and urinary excretion of nephrogenous cyclic AMP were significantly increased in the patients. The results suggest that defective vitamin D storage and enhanced vitamin D action coexist in patients after total gastrectomy and that the enhanced vitamin D action, possibly derived from slightly increased parathyroid function, would be a compensatory mechanism to sustained calcium deficiency. No substantial difference of vitamin D status was observed between the two types of reconstruction which differed in passage through the duodenum.

Conjugated estrogens in the treatment of postmenopausal women with hyperparathyroidism.

Fourteen postmenopausal women with mild hyperparathyroidism were given conjugated estrogens. Serum calcium levels became normal and urinary calcium excretion was reduced for up to 2 years in ten patients taking an average dose of 1.25 mg of estrogen daily. Hypercalcemia returned quickly when therapy was interrupted. Estrogen did not systematically alter serum immunoreactive parathyroid hormone or calcitriol levels or urinary excretion of cyclic adenosine monophosphate. Significant reductions in urinary hydroxyproline and serum alkaline phosphatase activity during estrogen therapy indicate that the major effect of therapy was to decrease bone turnover. Iliac crest biopsy specimens taken before estrogen therapy showed normal trabecular bone volume and excessive osteoid seams. Follow-up biopsy specimens were taken from six patients after 1 year on therapy. Bone volume remained stable, but hyperosteoidosis had improved in only one patient. Without understanding the long-term impact of untreated mild hyperparathyroidism on bone, the benefits of estrogen therapy on bone remain uncertain. However, therapy with conjugated estrogens provides sustained control of serum and urine calcium in most women with hyperparathyroidism and is a reasonable alternative in patients who are not surgical candidates.

Calcium and sodium transport and vitamin D metabolism in the spontaneously hypertensive rat.

Serum ionized calcium levels are lower and immunoreactive parathyroid hormone levels are higher in the spontaneously hypertensive (SH) rat than in the normotensive Wistar-Kyoto (WKy) control. We postulated that there is either a defect in the regulation of vitamin D metabolism by parathyroid hormone or that the gut target organ for vitamin D in the SH rat is unresponsive. To test these hypotheses we measured serum concentrations of vitamin D metabolites and intestinal transport of calcium and sodium. Compared with that of WKy controls, in vitro calcium transport by duodenal sacs of the SH rat was decreased (P less than 0.001) at 5 wk, before the development of hypertension, and at 12 wk, after hypertension was well established. When measured in vivo in the most proximal 20 cm of small intestine, maximum velocity (Vmax) for calcium transport was decreased (P less than 0.05) and net absorption of sodium and water was increased (P less than 0.05) in SH rats as compared with WKy rats. Vmax for calcium transport was also decreased (P less than 0.05) in the most distal 20 cm of small intestine of SH rats, but net sodium and water transport were the same in SH and WKy rats. At 12 wk, serum concentration of 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] was the same in both SH and WKy groups, but its precursor, 25-hydroxycholecalciferol, was increased (P less than 0.05) in the SH rat. We conclude that in the SH rat: (a) the concentration of 1,25-(OH)2D3 is inappropriately low in relation to the elevated immunoreactive parathyroid hormone and the depressed calcium absorption, suggesting a defect in the regulation of vitamin D metabolism; and (b) the depressed calcium absorption, in the setting of normal concentrations of [1,25-(OH)2D3], demonstrates unresponsiveness of the gut to vitamin D and may explain in part the low serum ionized calcium found in earlier studies. The presence of these abnormalities before we found a significant difference in blood pressure suggests that they may be causal, not secondary, to the hypertension.

Parathyroid and bone response of the diabetic patient to uremia

AbstractParathyroid and bone response of the diabetic patient to uremia. Biochemical and radiologic indices of bone disease were assessed in 26 insulin-dependent diabetic patients and 28 nondiabetic patients with endstage kidney disease. The two groups were comparable in age, sex, duration of renal failure, and length of time on dialysis. Diabetic patients showed significantly lower serum calcium and immunoreactive parathyroid hormone (iPTH) levels than nondiabetic patients. iPTH was not related to total serum calcium, but was positively correlated with serum phosphorous (r = 0.37, P < 0.05 and r = 0.54, P < 0.005, in nondiabetic and diabetic patients, respectively). iPTH correlated with alkaline phosphatase (r = 0.59, P < 0.0009) and calcitonin (r = 0.51, P < 0.05) only in nondiabetic patients. Osteitis fibrosa was noted radio-logically in 30% of nondiabetic patients and in none of the diabetic patients (P < 0.03). Bone morphology in eight diabetic patients who underwent iliac bone biopsy was characterized by reduced trabecular and osteoid bone volume, no woven bone, and marked reduction in indices of bone formation and resorption. The small amount of bone and lack of osteomalacia are a unique feature of the diabetic patient with chronic renal disease. The long-term sequelae of low bone turnover and reduced circulating iPTH may present a special problem to the long term diabetic survivor on the current therapies of uremia.Réponses parathyroïdienne et osseuse de malades diabétiques en urémie. Les indices biochimiques et radiologiques d'ostéopathie ont été déterminés chez 26 malades diabétiques insulino-dépendants et 28 malades nondiabétiques avec une néphropathie terminale. Les deux groupes étaient comparables en âge, sexe, durée de l'insuffisance rénale, et durée de la dialyse. Les malades diabétiques avaient un calcium sérique et une hormone parathyroïdienne immuno-réactive (iPTH) significativement plus faibles que les malades nondiabétiques. iPTH n'était pas reliée au calcium sérique total, mais était positivement corrélée avec le phosphore sérique (r = 0,37, P < 0,05 et r = 0,54, P < 0,005, chez les nondiabétiques et les diabétiques, respectivement). iPTH était corrélée à la phosphatase alcaline (r = 0,59, P < 0,0009) et à la calcitonine (r = 0,51, P < 0,05) uniquement chez les malades nondiabétiques. Une ostéite fibreuse a été notée radiologiquement chez 30% des malades nondiabétiques et chez aucun des diabétiques (P < 0,03). La morphologie osseuse chez huit diabétiques qui avaient subi une biopsie de la crête iliaque était caractérisée par une réduction des volumes osseux trabéculaire et ostéoïde, l'absence d'os spongieux, et une réduction marquée des indices de formation et de résorption osseuses. La faible quantité d'os et l'absence d'ostéomalacie sont une caractéristique unique du malade diabétique atteint de néphropathie chronique. Les séquelles à long terme d'un renouvellement osseux faible et d'une diminution d'iPTH circulante pourraient constituer un problème spécial pour le diabétique survivant à long terme avec les traitements habituels de l'urémie.

Paraneoplastic Hypercalcemia Associated with Bladder Carcinoma: Report of 2 Cases

Hypercalcemia associated with bladder carcinoma is rare. We report on 2 patients with hypercalcemia and bladder tumor without bone metastases. In both patients serum calcium returned to normal after removal of the tumor. Serum immunoreactive parathyroid hormone levels were normal in both patients. In 1 case a high gradient of immunoreactive parathyroid hormone across the tumor was demonstrated but the secretion of nephrogenous cyclic adenosine monophosphate was normal. Urinary excretion of prostaglandins also was normal in this case. These data show that hypercalcemia was caused by the tumoral production of some humoral factor different from parathyroid hormone.

DIFFERENCES IN SERUM BONE GLA PROTEIN WITH AGE AND SEX

Serum bone Gla protein (BGP) was measured by radioimmunoassay in 166 healthy men and women aged 30-90 years. Serum BGP levels increased with age in both sexes and were higher in women than in men at all ages. The most striking rise occurred in women after age 40-49. BGP was significantly correlated positively with serum alkaline phosphatase and negatively with midshaft and distal bone mass in both sexes. In women only, BGP levels were significantly positively related to levels of immunoreactive parathyroid hormone (iPTH). When age was included in the multiple regression analysis BGP was still correlated with alkaline phosphatase in both sexes and iPTH in women only. Serum BGP levels were significantly higher in 13 osteoporotic patients than in age-matched controls. It is postulated that with increasing age 1,25-dihydroxyvitamin D levels fall, causing a rise in iPTH and thus in bone turnover, which is reflected by a rise in BGP levels.

Factors that influence the assessment of parathyroid graft function.

Autogenous parathyroid grafts are used in the treatment of primary and secondary parathyroid hyperplasia and for salvaging normal parathyroid glands removed during thyroid surgery. Placement of the autogenous grafts in the forearm may allow assessment of graft function by comparing the patient's background level of immunoreactive parathyroid hormone (iPTH) with the iPTH value in the antecubital vein above the parathyroid graft. Among patients who on clinical grounds seem to have functioning parathyroid tissue, significant iPTH gradients can be demonstrated in only approximately 80%. Several technical and clinical factors can prevent demonstration of an iPTH gradient in patients who in fact do have functioning parathyroid grafts. Hypercalcemia may suppress iPTH secretion. PTH secretion may be intermittent. High background levels of iPTH due to renal failure may transform a significant numerical gradient for iPTH into an insignificant percentage change in iPTH. It may be technically difficult to obtain blood from the particular vein bearing effluent from the parathyroid graft. The regional specificity of the iPTH assay employed may have an important influence on the magnitude of the apparent iPTH gradient. Knowledge of these factors should maximize the chance of documenting parathyroid graft function.

Maternal-fetal relationships in the parathyroidectomized rat. Intestinal calcium transport, serum calcium, immunoreactive parathyroid hormone and calcitonin.

We studied the role of the parathyroids in the adaptation of intestinal Ca transport that occurs during pregnancy, and whether maternal hypoparathyroidism causes fetal hyperparathyroidism. Serum Ca of pregnant parathyroidectomized (PTX) rats was significantly greater than nonpregnant, PTX animals. Intestinal active Ca transport was increased 2.1- and 2.2-fold by pregnancy in intact and PTX rats, respectively. Serum levels of immunoreactive parathyroid hormone (PTH) were nondetectable in PTX-pregnant rats. Fetuses from PTX rats appeared grossly normal. The serum PTH was not different in fetuses from PTX compared to fetuses from intact mothers and serum Ca, Mg, and P were normal. Thus, alleviation of maternal hypocalcemia during pregnancy in PTX rats may be due to an adaptive increase in intestinal Ca transport, which does not require the parathyroids. Fetuses from PTX mothers were euparathyroid and were protected from Ca deficiency during pregnancy.