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)

This study was performed in order to evaluate the clinical usefulness of the measurement of total serum alkaline phosphatase activity (AP), serum osteocalcin (BGP) and urinary hydroxyproline (OHPr) in assessing bone remodelling in primary hyperparathyroidism. Thirty-two patients with primary hyperparathyroidism were included in the study. No statistically significant differences were observed between the mean values of Z-scores obtained for each marker. Furthermore, an inverse correlation was found between percentage of bone mineral content at the distal radius and both BGP (r = -0.57; p less than 0.05) and AP (r = -0.49; p less than 0.05). The results obtained demonstrate that, contrary to other metabolic bone diseases (e.g. Paget's disease of bone), all three markers examined may be used in clinical practice to evaluate the entity of skeletal turnover in primary hyperparathyroidism.
J Endocrinol Invest 1989 Sep
PMID:Clinical value of the measurement of bone remodelling markers in primary hyperparathyroidism. 259 39

60 patients suffering from primary hyperparathyroidism were operated during the period from 1980 till september 1988. The operation was successful in 55 cases. Most patients had single adenomas of the parathyroid glands. There was only one case with a four-gland-hyperplasia and one case with a parathyroid carcinoma. Rare observations were: one woman with a truly recurrent primary hyperparathyroidism, two patients with a papillary carcinoma of the thyroid gland in addition to the hyperparathyroidism and one patient with a large cystic parathyroid adenoma. Most of the patients had severe clinical symptoms of the primary hyperparathyroidism, mainly renal stones, in some cases bone changes. Only three patients were asymptomatic.
Exp Clin Endocrinol 1989 Sep
PMID:Clinical aspects of surgery in primary hyperparathyroidism. 259 16

In order to obtain a useful screening index for primary hyperparathyroidism (PHPT), seven patients with PHPT and fifty-one patients with nonparathyroid hypercalcemia (NPHC) were studied retrospectively. Serum calcium, inorganic phosphate (IP), alkaline phosphatase, albumin (Alb), chloride (Cl), total protein, urea nitrogen and creatinine (Cre) were analyzed at the same time. Discriminant analysis using a stepwise variable select method was applied to these patients. A discriminant function (F 1) was derived from three laboratory tests; F 1 = -0.660 x [IP] + 0.142 x [Cl] + 0.564 x [Alb] - 14.4 (PHPT: F 1 greater than 0.641). F 1 had sensitivity of 100% and specificity of 72.5% (14 false positives) in diagnosing PHPT. Next, another discriminant function (F 2) was derived from PHPT and the false positive patients; F 2 = -2.61 x [IP] + 0.286 x [Cl] - 4.24 x [Cre] - 19.3 (PHPT: F 2 greater than 0.412). When F 2 was applied to positive patients by F 1, final sensitivity was 100% and specificity was 98%. This screening method was tested prospectively in fifty-six consecutive samples of hypercalcemia (PHPT 4, NPHC 52), resulting in sensitivity of 100% and specificity of 98%. It was proved that our screening method using two step discriminant functions was very useful to diagnose PHPT.
Rinsho Byori 1989 Sep
PMID:[A screening index for primary hyperparathyroidism using discriminant functions]. 260 57

Psychiatric symptoms are well recognized as a feature of patients with primary hyperparathyroidism. We have applied a standardized psychiatric interview to 15 patients before and after surgery. Thirteen had a lower 'psychiatric score' (less psychiatric morbidity) after surgery and improvements were particularly seen in symptoms of fatigue, depression, irritability, sleep disturbance and lack of concentration. The levels of intellectual impairment and of anxiety were unchanged after surgery. The 'psychiatric scores' in an additional group of 21 hyperparathyroid patients, in whom a decision to treat conservatively had been made independently, were similar to those in the surgically treated patients after surgery. Among all the untreated patients no relationship was found between overall 'psychiatric score' and serum levels of calcium or parathyrin.
Postgrad Med J 1989 Sep
PMID:Psychiatric morbidity in primary hyperparathyroidism. 260 90

Interpretation of serum immunoreactive PTH measurements requires an understanding of the secretion, metabolism, and heterogeneity of circulating immunoreactive PTH. Both intact hormone and biologically inactive carboxyl fragments containing the middle and C-terminal regions are secreted by the parathyroid glands. Inactive fragments also are produced peripherally by metabolism of intact hormone by liver and kidney. Inactive fragments represent 75 to 95% of the total immunoreactivity in serum, a consequence of their long half-life in vivo as compared with intact hormone. Immunoassays for PTH can be divided into those measuring intact hormone (N-terminal, intact) and those measuring both inactive fragments and intact hormone (mid-region, C-terminal, polyvalent). The latter principally measures inactive fragments because of their greater concentration as compared with intact hormone in peripheral serum. The clinical utility of PTH assays varies considerably because of differences in their specificity and sensitivity. Serum PTH levels have been more often observed to be elevated in individuals with primary hyperparathyroidism with the use of research quality radioimmunoassays that recognize both inactive fragments and intact hormone than with conventional N-terminal or intact assays. Homologous mid-region assays have provided exceptional clinical sensitivity in confirming primary hyperparathyroidism. Comparison of a sensitive mid-region radioimmunoassay with a recently developed two-site, noncompetitive chemiluminescent immunoassay for intact PTH indicated that both methods were highly useful in the differential diagnosis of hypercalcemia. The mid-region assay provided the best diagnostic sensitivity in primary hyperparathyroidism with more elevated levels of PTH. The sensitivity of the intact assay was good, a significant improvement over conventional N-terminal and intact assays. The specificity of the intact assay was clearly superior, with measured PTH levels found to be suppressed to below normal in most subjects with hypercalcemia associated with malignancy. In contrast, measured levels were primarily normal with the mid-region assay. The higher levels of immunoreactive PTH observed in nonparathyroid hypercalcemia with the mid-region assay are in agreement with the measurement of biologically inactive carboxyl fragments, which continue to be secreted in hypercalcemia.
Endocrinol Metab Clin North Am 1989 Sep
PMID:Measurement of parathyroid hormone. 267 65

Primary hyperparathyroidism becomes increasingly common with age and affects females four times more commonly than males. We now know that the majority of patients are asymptomatic of the disease and the commonest symptoms are fatigue and lethargy. Because of these facts, it is now appropriate to consider conservative management of primary hyperparathyroidism in the older patient who is asymptomatic or who has only mild symptoms. Further studies are indicated to ascertain whether such a conservative policy is correct.
Endocrinol Metab Clin North Am 1989 Sep
PMID:Primary hyperparathyroidism. Clinical presentation and factors influencing clinical management. 267 66

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.
Endocrinol Metab Clin North Am 1989 Sep
PMID:Primary hyperparathyroidism. A surgical perspective. 267 68

Although surgery remains the only curative treatment for primary hyperparathyroidism, interest continues in developing alternative therapy for patients who reject or cannot undergo an operation. For the majority of patients (who are menopausal women), estrogen or progestin therapy may control hypercalcemia and calciuria and reduce the rate of bone turnover. Whether the long-term clinical outcome of hyperparathyroidism is improved by hormone replacement remains to be established.
Endocrinol Metab Clin North Am 1989 Sep
PMID:Estrogens and progestins in the management of primary hyperparathyroidism. 267 69

Familial benign hypercalcemia, or hypocalciuric hypercalcemia, may be defined as a dominantly inherited disorder of calcium and magnesium metabolism, characterized by lifelong hypercalcemia and hypermagnesemia (both of variable degree), that usually is not associated with any symptoms, physical signs, reduced vitality, or ill health. Chondrocalcinosis, pancreatitis, gallstones, and neonatal primary hyperparathyroidism are possible rare associations, but findings differ among various studies. The biochemical findings are bland, with "normal" values for serum PTH by many techniques, modest hypophosphatemia, and other findings usually normal. A low calcium:creatinine clearance ratio is suggestive of, but not diagnostic for, FBH; urinary calcium excretion less than 100 mg per day may be just as helpful. The diagnosis should not be made casually or without family screening, because the findings in a given patient may be identical to those in mild primary hyperparathyroidism. The major rationale for careful evaluation is to diagnose the syndrome of FBH and to help affected family members avoid needless expense and the risk of further evaluation and treatment.
Endocrinol Metab Clin North Am 1989 Sep
PMID:Familial benign (hypocalciuric) hypercalcemia. A troublesome mimic of mild primary hyperparathyroidism. 267 70

Success in the treatment of primary hyperparathyroidism rest in the accurate localization and removal of the diseased gland or glands. Computerized tomography and nuclear imaging scans are being used to localize abnormal parathyroid tissue. In the present study, fifteen consecutive patients undergoing surgery for primary hyperparathyroidism were all subjected to these ancillary studies. Results were not revealed to the operating team. In all instances an adenoma was localized during neck exploration. CT Scan failed to localize 73% of the affected glands. Nuclear scans missed almost fifty percent of the parathyroid adenomas. The low yield of these ancillary localizing tests makes them unnecessary in the routine evaluation of patients undergoing surgery for primary hyperparathyroidism.
Bol Asoc Med P R 1989 Sep
PMID:Localization of parathyroid lesions: blind study for surgeons. 268 94


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