Secondary Hypoparathyroidism Research Articles

Fahr's Disease and Schizophrenia in a Patient With Secondary Hypoparathyroidism

Fahr's Disease and Schizophrenia in a Patient With Secondary Hypoparathyroidism

Secondary hypoparathyroidism attributed to hypomagnesemia in a dog with protein-losing enteropathy

Severe hypomagnesemia (0.8 mg/dl; reference range, 1.6 to 2.3 mg/dl), hypocalcemia, and protein-losing enteropathy were identified in a 5-year-old castrated male 3-kg (6.6 lb) Shih Tzu examined because of anorexia, lethargy, paresis, and abdominal distention. Histologic examination of intestinal biopsy specimens revealed lymphangiectasia and lymphocytic, plasmacytic, neutrophilic infiltrates. Initial treatment included administration of magnesium (0.80 mEq/kg [0.36 mEq/lb]) of body weight in a balanced electrolyte solution. This treatment resulted in normalization of the serum magnesium concentration (1.7 mg/dl); resolution of the lethargy, paresis, and tachycardia; and an increase in the serum parathyroid hormone and ionized calcium concentrations. Findings were consistent with secondary hypoparathyroidism attributable to hypomagnesemia. Magnesium concentration should be monitored in all dogs with gastrointestinal tract disease, especially those with protein-losing enteropathy, anorexia, and weakness.

Niceritrol decreases serum phosphate levels in chronic hemodialysis patients

Since phosphorus retention in hemodialysis (HD) patients is known to be an important factor in the development of secondary hyperparathyroidism and renal osteodystrophy, phosphate binders have been needed for the control of serum phosphate levels (P). However, the calcium-containing phosphate binders that have been used widely can cause a rise in serum calcium levels and cause secondary hypoparathyroidism. We have recently experienced decreases in P after the administration of niceritrol (NT), a prodrug of nicotinic acid, for the treatment of low HDL-cholesteremia (HDL-C) in HD patients. The aim of the present study was to assess the mechanism of the P-lowering effect of NT in comparison with nicomol (NC), another prodrug of nicotinic acid. NT (750 mg/day) or NC (600 mg/day) was given orally to 10 or 14HD patients respectively. Blood samples were collected before the first dialysis of each week for the determination of serum urea nitrogen (UN), Cr, Ca, P, total cholesterol (TC), triglyceride (TG) and HDL-C. Serum nicotinic acid concentration (NAC) by gas chromatograph mass-spectrometry method was determined before, 4 weeks and 8 weeks after the administration of these drugs. After NT administration, P was decreased from 6.2 +/- 0.4 mg/dl to 5.1 +/- 0.4 mg/dl (1st week, p < 0.001, Mean +/- SE) and 4.5 +/- 0.3 mg/dl (2nd weeks, p < 0.001) with no change in UN, Cr or Ca levels; these significant decreases in P lasted for 8 weeks. NAC increased significantly after NT administration from 25.5 +/- 1.3 ng/ml to 549.8 +/- 102.2 ng/ml (4 weeks, p < 0.01) and 431.7 +/- 51.4 ng/ml (8 weeks, p < 0.01). HDL-C also increased (33.6 +/- 4.0 mg/dl vs 42.7 +/- 4.6 mg/dl, p < 0.05), but TC and TG did not change. In contrast, no significant changes were observed in P, NAC and HDL-C after NC administration. These discrepancies could be ascribed to the differences in serum NAC levels. These data suggest that NT could be useful for the control of P in HD patients. However further studies are needed to confirm the mechanism of the P-lowering effect of NT.

The effect of clodronate on bone in metastatic prostate cancer. Histomorphometric report of a double-blind randomised placebo-controlled study

57 patients with advanced prostate cancer and a failure of prior hormonal treatment were selected for a double-blind placebo-controlled trial, in which they were randomly allocated to receive either clodronate (C) or placebo concomitantly with the basic cancer treatment, estramustine phosphate (E) (560 mg daily). The treatment was started intravenously with 300 mg of C or placebo in 5 consecutive days, and thereafter maintained orally with 1600 mg of C or identical placebo daily for 3 months. Bone biopsies were taken at admission and at 3 months. Measurements of serum calcium, phosphate, alkaline phosphatase, prostate-specific antigen and creatinine were made at the time of both bone biopsies and at 1 month. Serum intact parathyroid hormone and vitamin D metabolites were measured at admission and at 3 months. Because of several discontinuations, the study groups at final analysis comprised 20 patients taking E+C and 19 patients taking E and placebo. Bone resorption, as judged by eroded surface and osteoclast number, was markedly increased especially in biopsies taken from tumour-involved bone. Treatments with E+C or E both induced a significant decrease in bone resorption, but were associated with the development of hypocalcaemia, secondary hypoparathyroidism, hypophosphataemia and severe impairment of mineralisation of newly formed bone, i.e. osteomalacia. Since the patients were not vitamin D deficient, we conclude that osteomalacia resulted from a relative deficiency of calcium and phosphate. The transiency of pain relief achieved with anti-resorptive agents in the treatment of bone metastases from prostate cancer may be due to the development of osteomalacia.

Immunoradiometric assay of parathyrin with polyclonal and monoclonal region-specific antibodies

In this immunoradiometric assay (IRMA) of parathyrin (PTH) a polyclonal anti-amino-PTH(1-34) is the capture antibody and a radiolabeled monoclonal anti-hPTH(44-68) is the second antibody. Gel filtration of serum from a hyperparathyroid patient yielded only a single peak of PTH, corresponding to the elution position of synthetic PTH(1-84). Healthy elderly individuals (ages 78 +/- 5 y, mean +/- SD, n = 45) had PTH concentrations (21 +/- 13 ng/L) not significantly higher than those from healthy younger (38 +/- 11 y) adults (20 +/- 8 ng/L, n = 94). Assay results agreed well with those obtained with a carboxyl-terminal PTH assay both in normal subjects (r = 0.63, P less than 0.001) and in patients with primary hyperparathyroidism (r = 0.59, P less than 0.001). Both assays equally discriminated patients with surgically confirmed primary hyperparathyroidism from normal individuals, but the PTH(1-84) IRMA also allowed a nearly absolute discrimination between normal subjects and patients with primary hypoparathyroidism (undetectable serum PTH in 18 of 21 cases) and secondary hypoparathyroidism (caused by hypercalcemia that was caused by a malignant tumor, PTH 1.3 +/- 1.3 ng/L, n = 32). Moreover, the PTH(1-84) IRMA is more sensitive (detection limit in serum, 0.8 ng/L) and easier and quicker to perform than the carboxyl-terminal assay.

Relationship between parathyroid hormone and magnesium in sera of the dementia patients

The dementia patients with central nervous or neuro-cerebro vascular disorders seemed to be decreased serum Mg due to abnormal Mg uptake in diet. An increment of PTH level was paralleled with a rise of serum Mg and hypomagnesemic group was shown to have a lower PTH level in these patients. Our results suggested that secondary hypoparathyroidism was likely to be induced by normo-calcemic hypomagnesemia.

Transient Neutral Fat Steatorrhea, Elevated Sweat Chloride Concentration, and Hypoparathyroidism in a Child with Celiac Disease

A patient with celiac disease and the unusual features of transiently elevated sweat chlorides, reversible exocrine pancreatic insufficiency, symptomatic hypocalcemia/hypomagnesemia, and transient secondary hypoparathyroidism is presented along with a brief discussion of the physiologic mechanisms thought to underlie their development.

Radioimmunoassay for the middle region of human parathyroid hormone: comparison of two radioiodinated synthetic peptides

Two synthetic peptides were evaluated to develop radioligands for midregionspecific radioimmunoassay (RIA) of human parathyroid hormone (hPTH). Both contained the 44–68 sequence of hPTH (no tyrosine residues); one contained a tyrosine residue added to the amino-terminus, (Tyr43)hPTH(43–68). The purified radioligands showed similar chemical properties (stability to storage, efficient phase separation with dextran-coated charcoal, low adsorption to glassware). Both radioligands were tested using three anti-PTH sera of proven clinical utility. While each of these midregion-directed antisera showed unique specificity, they all reacted with high affinity with both radioligands and none of them discriminated significantly between the two synthetic midregion peptides. 125 I-(Tyr43)hPTH(43–68) gave RIAs that were 15–50% more sensitive to hPTH(1–84) and the unlabelled synthetic midregion peptides than RIAs using 125I-hPTH(44–68) with all three antisera examined. 125I-(Tyr43)hPTH(43–68) was more susceptible than 125I-hPTH(44–68) to degradation from plasma or serum; this susceptibility was reduced by the peptidase inhibitor aprotinin (500 KIU/ml). Simultaneous RIAs of a series of patient plasmas using either of the two radioligands with antiserum NG5/5 produced indistinguishable discrimination between samples ( r = 0.984). Analysis of data on the relation of serum calcium and hPTH midregion immunoreactivity showed a useful separation of groups (all nonazotemic) with primary hyperparathyroidism, secondary hyperparathyroidism, primary hypoparathyroidism and secondary hypoparathyroidism.

Lack of effect of chronic hypocalcaemia on serum prolactin response to chlorpromazine.

The effects of chronic hypocalcaemia on serum basal and chlorpromazine-stimulated prolactin (Prl) levels were studied in 16 patients with idiopathic or secondary hypoparathyroidism. These results were compared with the results of other chlorpromazine stimulation tests which were made in the normocalcaemic state after treatment with vitamin D, and in normal subjects. In hypocalcaemic and normocalcaemic states (mean serum Ca 5.8 +/- 0.24 mg/dl and 9.5 +/- 0.11 mg/dl, respectively) basal Prl levels were within the normal range and during stimulation the maximal stimulated levels in each state were not significantly different from each other. Also, the mean serum Prl levels obtained from a control group were not different from values in the normocalcaemic state. It is concluded that chronic hypocalcaemia does not inhibit Prl secretion and low serum parathyroid hormone levels do not affect basal and chlorpromazine-stimulated Prl secretion.

Vitamin D metabolism in hyperthyroidism.

The serum concentrations of 25-hydroxycholecalciferol (25 OH D3), 24,25-dihydroxycholecalciferol [24,25(OH)-2D3] and 1,25-dihydroxycholecalciferol [1,25(OH)2D3] were measured in twenty-one patients with untreated hyperthyroidism. Compared with control subjects, 25 OH D3 concentrations were not altered, 24,25(OH)2D3 concentrations were increased, although not significantly and 1,25(OH)2D3 concentrations were decreased (P = 0.01). Following oral carbimazole therapy, 24,25(OH)2D3 concentrations fell (P less than 0.01), 1,25(OH)2D3 concentrations increased (P less than 0.01) and 25 OH D3 concentrations were unchanged. The altered 1,25(OH)2D3 and 24,25(OH)2D3 concentrations found in hyperthyroidism are probably due to the effects of thyroid hormone on bone and mineral metabolism. Increased serum calcium and phosphate concentrations with secondary hypoparathyroidism result in stimulation of the renal 24-hydroxylase and suppression of the 1-hydroxylase enzymes. In addition, serum 24,25(OH)2D3 concentrations were significantly correlated with serum triiodothyronine levels (T3) (r = 0.66, P less than 0.002) before treatment. This may indicate a direct stimulatory effect of T3 on 24-hydroxylase activity. No relationship was found between serum 1,25(OH)2D3 concentrations before therapy and serum T3.

Glucagon secretion in patients with hypoparathyroidism: effect of serum calcium on glucagon release.

The aim of the present study was to evaluate the influence of changes in the serum calcium concentration upon glucagon secretion in man. For this purpose, a group of subjects with either idiopathic (four cases) or secondary (two cases) hypoparathyroidism was submitted to an arginine test (0.5 g/kg) before and after the correction of hypocalcemia. In the presence of hypocalcemia, the glucagon response to the amino acid was modest and delayed (glucagon peak, 150 +/- 28 pg/ml). The acute correction of hypocalcemia produced a striking increase in basal glucagon levels (125 +/- 24 vs. 75 +/- 15 pg/ml; P less than 0.01) and restored the glucagon peak in response to arginine (270 +/- 50 pg/ml; P less than 0.01). The increase in plasma glucose triggered by arginine was augmented under normocalcemic conditions, while the pattern of plasma insulin response was quite similar. These results indicate that glucagon secretion in man is critically dependent on the serum calcium concentration.

Effects of chronic hypocalcaemia on plasma renin activity in man.

Abstract. A study was carried out to investigate the role of serum calcium in the regulation of renin secretion. The subjects for this study comprised of two groups. Group 1 consisted of 10 patients with primary or secondary hypoparathyroidism. Blood samples for basal PRA (plasma renin activity) were drawn at 8 a.m. when the patients were recumbent and on a normal sodium intake. Then all the patients were given a constant diet containing 10 mEq sodium for 4 days and were given 80 mg of Furosemid orally every day. On the morning of the fifth day blood samples were drawn after the patients had been upright for 4 h. These patients were treated with vitamin D2 and when normocalcaemic states were achieved the same study was repeated. Group 2 (control group) consisted of 10 normal, healthy subjects of both sexes. They were prepared for the experiment in the same way as for group 1. In the hypocalcaemic state mean serum calcium level was 5.6 ± 0.3 mg/100 ml. After treatment with vitamin D2, the mean serum calcium level was increased to 9.6 ± 0.1 mg/100 ml (P &lt; 0.001). There was no significant difference in the mean serum sodium and potassium levels in either hypocalcaemia or normocalcaemia. But the mean stimulated PRA (12.12 ± 1.13 ng/ml/h) was found to be decreased in hypocalcaemia compared to in normocalcaemia and in the control group (22.87 ± 1.18 and 23.83 ± 0.86 ng/ml/h, respectively). The difference of means was significant (P &lt; 0.001). There were no significant differences between basal PRA in hypocalcaemic and normocalcaemic state as well as in the control group. (P&gt; 0.5, P &gt; 0.2 and P&gt; 0.5, respectively). Our results indicate that serum calcium plays an important role in the regulation of renin secretion.

Die Diurese von zyklischem Adenosin-3'5'-monophosphat (cAMP) bei primären und sekundären Funktionsstörungen der Nebenschilddrüsen*

The diuresis of cAMP in primary hyperparathyroidism was significantly higher at 7.3 +/- 2.5 mumol/g creatinine X 24 h (P less than 0.005) than that in healthy subjects (3.5 +/- 0.7 mumol/g creatinine X 24 h). After successful operation on the parathyroid gland, cAMP diuresis usually decreased within 24 hours to normal or subnormal values. In primary or secondary hypoparathyroidism subnormal amounts of cAMP (P less than 0.005) were excreted. The method gives false-negative results in functional disorders of the parathyroid glands accompanied or caused by renal failure.

Electroencephalographic Findings in 76 Patients Treated for Secondary Hypoparathyroidism

Electroencephalographic Findings in 76 Patients Treated for Secondary Hypoparathyroidism

Observations on the effects of vitamin D in man, including the relation to cortisone.

ABSTRACT In order to study the effects of vitamin D in man, metabolic balance studies were performed in 6 normal Bantu subjects, 5 patients with various types of rickets, 2 patients with secondary hypoparathyroidism, and 4 patients with sarcoidosis. Attempts were also made to provide evidence concerning the theory that cortisone and its analogues are antagonists of vitamin D in man. An increase in the intestinal absorption of calcium due to administration of vitamin D was observed only in cases of rickets; it was not found when vitamin D was given to normal subjects or to the other patients, except occasionally as a late and possibly secondary phenomenon. Vitamin D exerted the primary actions of increasing both serum and urinary calcium, largely independently of each other. This indicates withdrawal of calcium from bone. A further independent action was the raising of the serum phosphorus level. This led to an elevated urinary excretion of phosphorus which could not have been produced by changes in renal ...