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)

Proximal femur fractures in elderly people are more and more frequent. Falls and senile bone disorders are the risk factors of this fracture. In order to understand the mechanisms of these bone disorders, we studied 21 consecutive patients with this fracture using bone histomorphometry. Measurements of serum intact parathormone (PTH), 25-(OH)-vitamin D, 1,25-(OH) 2-vitamin D and osteocalcin have been performed in these 21 patients, included in a larger series. We excluded patients with renal failure (serum creatinine greater than 140 mumols/l), cancer, or previous metabolic bone disease. There were 19 female and 2 male patients, ranging from 75 to 96 years, (mean 84.9). We found a low frequency of cortical (2/21) and trabecular (3/21) osteoporosis. There was no case of clearcut osteomalacia. Following histomorphometric bone study, two patients showed a typical pattern of hyperparathyroidism, and in a third one, this condition seemed very likely. In these three patients who were among the oldest, and who had high levels of serum PTH, chronic renal failure and primary hyperparathyroidism could be excluded. High bone remodeling was frequent in our patients, as reflected by the enhancement of eroded surfaces (13 cases) and of osteoid thickness (7 cases). Intact PTH level was elevated in our series compared to normal values in adults (in accordance to the PTH elevation in the case control study in a larger series). These findings suggest a major role of a secondary hyperparathyroidism in senile bone disorders favoring proximal femur fractures. This hyperparathyroidism is probably secondary to mild calcium and vitamin D deficiency. It may lead to architectural bone changes favoring this fracture.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperparathyroidism in proximal femur fractures biological and histomorphometric study in 21 patients over 75 years old. 191 14

Until recently, the measurement of circulating parathyroid hormone (PTH) has been unsatisfactory due to poor analytical performance of immunological assays and due to interference in such assays by circulating biologically inactive fragments of PTH. The development of a two-site immunometric assay with the use of acridinium ester as label has solved these problems. This immunochemiluminometric assay (ICMA) measures the intact molecule and is capable of detecting PTH levels in normal subjects as well as suppression of PTH after oral administration of calcium. The ICMA PTH assay has been shown to be adequate in the diagnosis of primary hyperparathyroidism and it could prove useful in monitoring renal failure patients and investigating other bone diseases such as osteoporosis.
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PMID:The measurement of circulating parathyroid hormone. 218 52

Primary hyperparathyroidism is a common disorder and one that can usually (approximately 95%) be successfully treated by parathyroidectomy. PTH assays have become quite accurate for confirming the diagnosis. In patients with malignancy-associated hypercalcemia, parathyroid-like protein levels are usually increased, and radioimmunoassays being developed to quantitate serum levels of this protein will make the diagnosis easier. Treatment for a parathyroid adenoma is removal of the tumor and identification of the normal parathyroid glands. Treatment for primary or secondary hyperplasia is usually subtotal parathyroidectomy. Recurrent hyperparathyroidism is uncommon, except in patients with familial hyperparathyroidism, MEN-1 parathyroid carcinoma, or renal failure and secondary hyperparathyroidism. Persistent hyperparathyroidism is more common and is usually due to surgeon inexperience, but it is also caused by ectopically situated parathyroid glands, multiple abnormal parathyroid glands, or supranumerary parathyroid glands. Preoperative localization studies using ultrasound, thallium-technetium scanning, MRI, or CT scanning are reliable in patients with solitary parathyroid adenomas, but often fail to detect all of the abnormal parathyroid tissue in patients with multiple abnormal parathyroid glands. Intraoperative use of urinary cyclic AMP assays and rapid PTH assays have recently been used experimentally during parathyroid explorations to determine whether all hyperfunctioning parathyroid tissue has been removed, but these methods are not yet reliable or fast enough to be generally accepted. Most patients with primary hyperparathyroidism who are successfully treated by parathyroidectomy experience psychological, clinical, and metabolic benefits.
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PMID:Primary hyperparathyroidism. A surgical perspective. 267 68

We studied long-term morbidity after parathyroid surgery for primary hyperparathyroidism in 100 patients and compared it with the long-term morbidity of medical follow-up from the literature. The surgical treatment of primary hyperparathyroidism was associated with negative results of neck explorations, persistent hypercalcemia, recurrent hypercalcemia, permanent hypoparathyroidism, or recurrent laryngeal nerve damage in 13 (19%) of 68 patients followed up for five years postoperatively. A review of medical follow-up as reported in the literature showed progression of disease in 8% to 22% of patients followed up for five to ten years. There was no convincing evidence that mild primary hyperparathyroidism resulted in progressive osteoporosis or renal failure. Furthermore, no significant improvement in hypertension, peptic ulcer disease, or renal function followed successful parathyroid surgery. Unless future studies demonstrate progressive osteoporosis or renal damage in untreated, mild primary hyperparathyroidism, medical follow-up is a reasonable alternative to surgery in the compliant patient over 50 years of age.
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PMID:Primary hyperparathyroidism. A review of the long-term surgical and nonsurgical morbidities as a basis for a rational approach to treatment. 270 30

We report here the unusually difficult cases of two patients with end-stage renal failure who suffered from severe hyperparathyroidism requiring surgical correction. The first patient had previously undiagnosed primary hyperparathyroidism. A first surgical neck exploration led to the discovery of four glands, paradoxically normal in size and aspect, which were removed. Subsequently, a supernumerary gland was localized in the mediastinum by computerized tomography and removed via sternotomy. After confirming the hypoparathyroid state, parathyroid autotransplantation was performed using cryopreserved tissue. The second patient had five hyperplastic parathyroid glands removed during the first neck exploration, followed by immediate parathyroid autografting. Because of the persistence of severe hyperparathyroidism, forearm autografts were subsequently removed and a sternotomy performed. Both failed to improve parathyroid hyperfunction. Numerous localization procedures remained negative. A repeat surgical neck exploration was performed because of positive double isotope scanning but was of no success in preventing fatal outcome, as were all medical treatments. These observations of two patients illustrate the difficulties in localizing and removing ectopic parathyroid lesions. Even when relying on the presently available powerful diagnostic means, correction of severe hyperparathyroidism may be extremely difficult.
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PMID:[Severe hyperparathyroidism in 2 uremic patients. Diagnostic and therapeutic difficulties]. 271 49

Two antisera, C-52 and C-97, raised against bovine (b)PTH(1-84) in guinea pigs, were evaluated with 125I-[tyr53] human (h)PTH(53-84) as tracer and intact hPTH(1-84) and synthetic hPTH(39-84), representative of large carboxylterminal ("C") fragments found in circulation, as standards. In both assays, hPTH(39-84) was 5-6 times more potent than hPTH(1-84) on a molar basis in displacing the tracer. With both antisera, progressive deletion at the aminoterminal end of large "C" fragments, as in hPTH(53-84) and hPTH(65-84), lead to decreased immunoreactivity, hPTH(69-84) being non-immunoreactive. The mid-carboxylterminal fragments, hPTH(44-68) and hPTH(39-68), did not react in either assay. Each antiserum measured known quantities of pure hPTH(1-84) or hPTH(39-84) standards similarly. Serum PTH values obtained with antiserum C-97 were about 3 times higher in renal failure, 1.75 times higher in normal individuals and those with primary hyperparathyroidism, while similar to values measured with antiserum C-52 in individuals with secondary hyperparathyroidism without renal failure or with pseudohypoparathyroidism. When circulating PTH taken from patients with these disorders was fractionated by gel chromatography, both antisera recognized similar peaks of intact hPTH(1-84) and of large "C" fragments while antiserum C-97 further recognized a peak of smaller "C" fragments. This explained the different clinical behavior of the latter antiserum. Our findings demonstrate the existence of small late "C" fragments in circulation. They further suggest an influence of serum calcium and of renal function on the quantity of these fragments.
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PMID:Immunological evidences for the presence of small late carboxylterminal fragment(s) of human parathyroid hormone (PTH) in circulation in man. 274 18

The "N-tact" immunoradiometric assay (IRMA) from INCSTAR for parathyrin (PTH) in serum involves a 125I-labeled affinity-purified antiserum to PTH 1-34 and an affinity-purified antiserum to PTH 39-84, the latter bound to a polystyrene bead. The mean detection limit, determined in six consecutive assays, was 4 ng/L. The within-batch CV was less than 7% in the range 15 to 2135 ng/L. The between-batch CV was 11.7% and 5.3% at 30 and 371 ng/L, respectively. Serum PTH in 14 proven cases of primary hyperparathyroidism was 49-808 (median 111) ng/L, undetectable (less than 5 ng/L) in 10 cases of primary hypoparathyroidism and in 10 cases of hypercalcemia associated with malignancy, compared with 7-39 ng/L in 45 normal subjects. PTH was 9 to 19 ng/L in four patients with familial benign hypercalcemia. In 39 patients with renal failure, apparent concentrations were 14 to 857 (median 133) ng/L, but sera from these patients pre-diluted with zero standard did not parallel dilutions of the standard, PTH 1-84. PTH concentrations were not significantly decreased in blood or serum kept at 20 degrees C for up to 6 h. After successful removal of a parathyroid adenoma, the mean half-time for disappearance of PTH in vivo in five hyperparathyroid patients was 3.3 min.
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PMID:Performance and diagnostic application of a two-site immunoradiometric assay for parathyrin in serum. 277 25

Derangements in leukocyte function occur in patients with primary hyperparathyroidism and in those with uremia, which is a state of secondary hyperparathyroidism, suggesting that parathyroid hormone (PTH) may affect leukocyte function. We examined the interaction between PTH and random migration of human polymorphonuclear leukocytes (PMNL) utilizing a modified Boyden chamber. Intact 1-84 PTH but not its amino-terminal (1-34 PTH) or its carboxy-terminal (53-84 PTH) fragments produced marked and significant (p less than 0.01) stimulation of random migration in a dose-dependent manner. Inactivation of 1-84 PTH abolished its effect and other peptide hormones (calcitonin, glucagon, insulin and vasopressin) did not stimulate migration of PMNL. The effect of PTH on migration was not due to action of the hormone on chemotaxis. PTH did not enhance cAMP or cGMP production by PMNL. The stimulation of PMNL motility by PTH was independent of calcium concentration in media, was not mimicked by calcium ionophore and was not blocked by verapamil. Quinidine also produced significant (p less than 0.01) increase in random migration of PMNL and this effect was not additive to that of PTH. Prolonged exposure to PTH (16-20 h) was associated with significant inhibition of random migration of PMNL. The migration of PMNL from patients with advanced renal failure was significantly (p less than 0.01) reduced and there was a significant (p less than 0.01) inverse relationship between random migration of PMNL and serum levels of PTH. Also PTH produced only modest stimulation of random migration of PMNL in most patients with renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of parathyroid hormone on random migration of human polymorphonuclear leukocytes. 285 73

We describe a clinical study comparing the value of measurements of intact human PTH [hPTH(1-84)] and total PTH immunoreactivity [hPTH-(1-84) plus fragments]. A two-step immunochemical method was used to separate plasma hPTH-(1-84) from all circulating PTH fragments. The first step involved extraction and concentration of plasma PTH using solid phase antiamino-terminal PTH antibodies. After elution, the PTH immunoextract was analyzed using a sensitive mid- and C-region immunoassay. Complete separation in the immunoextraction step was proven by Sephadex G-75 gel filtration. hPTH-(1-84) values in fasting patients showed a clear distinction between those with primary hyperparathyroidism and those with nonparathyroid hypercalcemia, in contrast with small overlap in total immunoreactive PTH values. The hPTH-(1-84) values increased faster and more substantially in response to long EDTA and calcium infusion tests, compared with total PTH immunoreactivity, in normal subjects. Infusion of EDTA (10 mg/kg BW) in 5 min) elicited a readily measurable response of hPTH-(1-84) between 5 and 10 min after starting the infusion. Ingestion of 1000 mg calcium caused a decrease in hPTH-(1-84) in 1 h or less. More than 50% of patients with terminal renal failure had normal hPTH-(1-84) values despite elevated total immunoreactive PTH concentrations. We conclude that the two-step hPTH-(1-84) assay is more specific and sensitive than most regional PTH assays. Measurements of hPTH-(1-84) levels may identify disorders of parathyroid function at an early stage and provide a useful tool for the study of parathyroid physiology.
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PMID:Clinical implications of estimation of intact parathyroid hormone (PTH) versus total immunoreactive PTH in normal subjects and hyperparathyroid patients. 308 25

In the course of chronic renal failure, aluminium may deposit and accumulate in different tissues. The aluminium content of parathyroid glands was measured in 31 haemodialysis patients at the time of a parathyroidectomy. The values were compared with those obtained from ten control patients with primary hyperparathyroidism without renal failure, and were related to bone remodelling. Of the 31 patients, 27 had a bone biopsy after double tetracycline labelling, at the time of parathyroidectomy. Twenty-one patients had severe hyperparathyroidism, three patients had hyperparathyroidism associated with osteomalacia, three patients had mild hyperparathyroidism with reduced bone formation. Seven patients had bone aluminium deposits, associated with osteomalacia in one case. The parathyroid aluminium was 62 +/- 35.7 (mumol/g glandular dry weight) in haemodialysis patients and 14.3 +/- 6.3 in control patients (P less than 0.001). A significant positive correlation existed between parathyroid aluminium and serum aluminium (P less than 0.01). The parathyroid aluminium was not different in the patients with and without bone aluminium deposits. A weak correlation was found between parathyroid aluminium and plasma parathyroid hormone. A significant negative correlation existed between parathyroid aluminium and osteoblastic surfaces (P less than 0.05), but no correlation was found with bone formation rate at tissue and bone multicellular units levels. We conclude that aluminium accumulates in parathyroid glands of dialysed patients. Severe hyperparathyroidism may coexist with aluminium overload of parathyroid glands. A marked aluminium overload, however, may cut short the course of hyperparathyroidism and may decrease parathyroid function and cellular activity in bone.
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PMID:Aluminium overload of parathyroid glands in haemodialysed patients with hyperparathyroidism: effect on bone remodelling. 314 Jan 27


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