Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pamidronate (aminopropylidene diphosphonate, APD) is known to be an effective agent in lowering plasma calcium in cancer associated hypercalcaemia and in primary hyperparathyroidism. Combined therapy with pamidronate and calcitonin has proved efficient in the treatment of severe cancer-associated hypercalcaemia. A 66-year-old woman in hypercalcaemic crisis caused by primary hypreparathyroidism was successfully treated with this combined therapy. Albumin corrected plasma calcium was 5.26 mmol/l on arrival and the PTH level was very high. The combined therapy lowered the plasma calcium to normal and made it possible to perform elective parathyreoidectomy. A 5.8 g parathyroid adenoma was removed. It is recommended to consider combined therapy with pamidronate and calcitonin in the emergency management of hypercalcaemic crisis.
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PMID:[Combination therapy with pamidronate and calcitonin in hypercalcemic crisis caused by primary hyperparathyroidism]. 146 41

The treatment of hypercalcaemia with low-dose salcatonin (100 U/d), administered either as a single intramuscular bolus or as a continuous intravenous infusion for five days, was examined in two groups of 10 patients with primary hyperparathyroidism, in a randomized open parallel study. Both the peak (0.31 +/- 0.035 mmol/L v 0.13 +/- 0.034 mmol/L) and overall (0.073 +/- 0.016 mmol/L v 0.018 +/- 0.016 mmol/L) hypocalcaemic responses were greater in the infusion group. The peak reduction in serum calcium occurred on day 2 of treatment after which there was a progressive attenuation of response. All the differences between the two methods of administration wer due to renal rather than bony effects of salcatonin. Possible causes of progressive resistance to treatment included reductions in sodium excretion and serum phosphate. It is concluded that low-dose salcatonin administered as a continuous infusion was more effective than the same dose given as a bolus. The kidney played a pivotal role both in the cause of the hypercalcaemia and in the response to treatment, including the rapid development of resistance which limits the use of salmon calcitonin in primary hyperparathyroidism to short-term reduction of serum calcium.
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PMID:Comparison of low-dose intramuscular and intravenous salcatonin in the treatment of primary hyperparathyroidism. 163 74

This study was conducted in order to establish whether C cells, which are responsible for secretion of calcitonin within the thyroid gland, change either in volume or morphology under conditions of chronic hypercalcemia in primary hyperparathyroidism. Out of 106 primary hyperparathyroid patients undergoing surgery, in 11 cases the thyroids were excised and examined for changes in the C cell. As a control group we used thyroids removed in another 14 cases undergoing thyroidectomy or laryngectomy. Calcitonin in the C cell was observed by optical microscope after immuno staining using the indirect peroxidase-labeled antibody technique. C cells are not evenly distributed within the thyroid. However, there is excellent positive correlation (p less than 0.001) between the C-cell index, which is the average of two tissue samples excised from the area at the border between the upper 1/3 and middle 1/3 of the thyroid lobe (the area where most C cells are found), and the total number of C cells. The C-cell index can thus be used as an indicator of the total number of C cells in the thyroid. The number of C cells decreased (p less than 0.01) as the level of calcium in serum increased. In patients with primary hyperparathyroidism, this decrease in C cells was significantly greater (p less than 0.025) than in the controls. Focal C cell hyperplasia and diffuse C cell hyperplasia were present in both the control group and primary hyperparathyroid group, but there was no significant difference between the two groups as to the frequency of occurrence. For both these conditions the rate of occurrence was considered within normal ranges for C cell morphology. We concluded that the decrease in C-cell count in primary hyperparathyroidism patients with chronic hypercalcemia is due to consumption of calcitonin in the C cell.
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PMID:[Immunohistochemical studies on the thyroid C-cells in primary hyperparathyroidism]. 176 Nov 42

In hospitalized patients primary hyperparathyroidism (HPT) and neoplasms account for more than 90% of all hypercalcemias. Measurements of parathyroid hormone, particularly when combined with dynamic tests using calcitonin and EDTA have a high specificity and sensitivity in the differential diagnosis of hypercalcemia but are time-consuming and costly for screening purposes. Most chemical autoanalyzers beside serum calcium also measure serum chloride, phosphate and albumin. In order to evaluate how these simple variables could differentiate between HPT and hypercalcemia due to malignant disorders, 110 measurements from HPT subjects and 111 measurements from cancer patients with hypercalcemia were used. Serum chloride was best among the simple variables to separate the two disorders and classified 84% of the hypercalcemic subjects correctly. When serum phosphatase and albumin were added giving the formula (serum chloride-84) x (albumin-15)/phosphate, only 3% of the cancer and 4% of the HPT subjects were misclassified when borderline values (400-500) were excluded (5% of the sample). In conclusion, while other more sensitive and expressive tests exist to establish the cause of hypercalcemia the above mentioned formula is a cheap and easy screening test for a preliminary diagnosis.
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PMID:Serum chloride in the differential diagnosis of hypercalcemia. 177 37

The hypocalcemic and hypophosphatemic effect of salmon calcitonin (sCT) given by intranasal (i.n.) spray to 12 patients with histological confirmed primary hyperparathyroidism (1 degree HPT) was studied. The concentration of ionized calcium in whole blood (B-Ca++), serum phosphate (S-P), magnesium (S-Mg), plasma sCT (Pl-sCT), and endogenous CT (hCT) was followed during five 24-hour periods with at least three days between. After period I (control day), 100 IU sCT was given intramuscularly (i.m.) in period II. In periods III-V, either 110, 200, or 400 IU of sCT were given intranasally (i.n.) in randomized order. Although B-Ca++ decreased from the baseline value with all four sCT treatments and at 4.5 hour on the control day (p less than 0.05-0.001), the i.n. sCT treatments had no significant hypocalcemic effect, as the change of the area under the B-Ca++ curve (delta AUC B-Ca++) for the three i.n. treatments was not significantly different from the control period (p less than 0.001, ANOVA). Only the i.m. injection of calcitonin had a calcium-lowering effect (p less than 0.001, ANOVA). Three subjects were considered nonresponders with a decrease in B-Ca++ less than 0.06 mmol/L. S-P decreased within three hours after 200 IU sCT i.n. and 100 IU i.m., but the S-Mg levels showed no consistent changes. The area under the curve for the Pl-sCT levels did not correlate with delta AUC B-Ca++ except for i.m. given sCT.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Salmon calcitonin treatment by nasal spray in primary hyperparathyroidism. 178

The problems encountered in the diagnosis and treatment of primary hyperparathyroidism were studied in 69 cases. The accuracy of imaging for hyperplasia was less than that for adenoma or carcinoma and the major causes for multiple operations were a failure to locate the four glands and mediastinal adenoma. The intravenous administration of high doses of calcitonin could reduce the serum calcium level of patients in hypercalcemic crisis. Carcinoma required ipsilateral modified radical neck dissection because of lymph node metastases, and non-medullary thyroid carcinoma was often associated with primary hyperparathyroidism. We found removal of the parathyroid adenoma and biopsy or extirpation of only one macroscopically normal gland to be a fully satisfactory procedure after bilateral neck exploration and attempting to identify at least four glands.
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PMID:The problems encountered in the surgical management of primary hyperparathyroidism. 178 12

After introductory remarks concerning the pathophysiologic activities of osteoclasts and osteoblast, the author considers the three main pathologies: primary hyperparathyroidism, osteomalacia, and Paget's disease. These pathologies represent an excellent model for the pathophysiologic and clinico-therapeutic evaluation of some calciotropic hormones, viz. parathormone, calcitriol, and calcitonin.
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PMID:[Evaluation of physiological and pathological activity of osteoclasts and osteoblasts with special reference to calciotropic hormones: parathyroid hormone, calcitonin and calcitriol]. 183 7

We studied the relationship between the bone mass and biochemical parameters in 175 normal premenopausal, 72 normal postmenopausal and osteoporotic postmenopausal women, between 20 and 88 years old, and in 40 patients with hyperthyroidism, and 23 patients with primary hyperparathyroidism, between 13 and 64 years old. The bone mineral density (BMD) of the spine (L2-L4) and proximal femur (femoral neck) was measured by dual-energy X-ray absorptiometry using a QDR-1000, Hologic. The bone mineral content (BMC) of the radius was measured by single photon absorptiometry (SPA) using a model 2780, Norland. Serum PTH, BGP and calcitonin (CT) were determined by radioimmunoassay. The BMD of the spine (L2-L4), and the proximal femur in postmenopausal women were negatively correlated with age. The mean BMD in patients with postmenopausal osteoporosis was significantly lower than that in normal postmenopausal women. In postmenopausal women, age was positively correlated with BGP, PTH, CT and negatively correlated with P. In patients with osteoporosis, the BMD of the spine was negatively correlated with serum BGP. The BMC of radius in patients with hyperthyroidism decreased significantly compared with that in the controls, and was negatively correlated with F-T3. The BMC of the radius in patients with primary hyperparathyroidism was significantly lower than that in the controls, and was negatively correlated with serum BGP and serum calcium. The measurements of biochemical parameters such as serum BGP, ALP and PTH may be useful in the assessment of metabolic bone diseases.
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PMID:[Bone mass and biochemical parameters in metabolic bone diseases]. 194 67

The roles of parathyroid hormone (PTH) and calcitonin (CT) in the pathogenesis of familial benign hypercalcemia (FBH, or hypocalciuric hypercalcemia) are uncertain. Thus we performed studies in 26 patients with FBH, 12 patients with primary hyperparathyroidism (HPT), and 20 normal volunteers, to answer these questions: are plasma levels of intact or biologically active PTH frequently elevated in FBH? Is plasma intact PTH nonsuppressible during calcium infusion? Is there blunting of the C cell CT response to calcium infusion as occurs in primary HPT? We used three methods for measurement of PTH: a mid region-specific radioimmunoassay (iPTH, antiserum GP-1M), an extraction-concentration bioassay (bioPTH, stimulation of cAMP generation in osteoblastlike cells), and a two-site immunoradiometric assay (IRMA) for intact PTH. PTH levels were significantly elevated in primary HPT by all three methods, but mean PTH was normal in FBH and 85-92% of values overlapped the normal range. During 5 minute calcium infusions (2 mg Ca2+ per kg) iPTH values fell little, but bioPTH and intact PTH fell sharply in all three groups. Mean calcium-induced decreases of intact and bioPTH were indistinguishable from normal in FBH, but PTH levels generally remained elevated at 5 minutes in primary HPT. In FBH basal and postinfusion CT levels were normal. The data show that, in the majority of patients with FBH, PTH concentrations and bioactivity in blood are within the normal range and are suppressed rapidly to very low levels with further increases of calcium. The data suggest that the abnormality of parathyroid function in FBH differs from that in primary HPT.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium regulation of parathyroid and C cell function in familial benign hypercalcemia. 202 33

Severe acute hypercalcemia (4.03 mmol/l) developed in a 50 years old woman after head and intraabdominal trauma (and splenectomy). After failure to correct the calcium levels by intravenous saline, furosemide, steroids and calcitonin, two hemodialyses were performed; definitive control of hypercalcemia was obtained by intravenous (3-amino-1-hydroxypropylidene)-1.1-bisphosphonic acid (APD). APD is a new drug analog of pyrophosphate; its main property is to block bone resorption, irrespective of its stimulus. As suspected by clinical and laboratory data and confirmed by arteriographic findings, surgery and pathologic examination, the underlying pathology was a mild primary hyperparathyroidism which was acutely worsened (parathyroid crisis) in the course of the trauma. Definitive treatment consisted of the removal of the adenoma responsible of the hyperparathyroidism.
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PMID:Posttraumatic parathyroid crisis and severe hypercalcemia treated with intravenous bisphosphonate (APD). Case report. 236 Mar 92


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