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 case of primary hyperparathyroidism presented several unusual features: (1) The only presenting symptoms were two gingival giant cell lesions (brown tumors), (2) Bone changes occurred early in the disease, but apparently affected only the mandible and maxilla, (3) No renal disease could be detected. The diagnosis, treatment and postoperative course of this unusual case has been described.
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PMID:Primary hyperparathyroidism detected by gingival biopsy. 27 4

Seventy-seven patients with nephrocalcinosis as revealed by X-ray studies over a 10-year period are reviewed. A programmed clinical and metabolic study was performed on each case; the author's criteria included the different pathogenic factors considered in the etiologic definition of the disease. There were 22 cases with primary hyperparathyroidism, 19 with spongy kidney, nine with tubulointerstitial nephropathy, five with hyperoxaluria, five with distal renal tubular acidosis, four with esential hypomagnesemia, and three cases of miscellaneous etiology (vitamin D intoxication, Fanconi's syndrome, Bartter's disease). Ten other cases were classified as idiopathic nephrocalcinosis since no definite cause could be found. The clinical characteristics (symptoms, associated diseases, diet and medication intake, family history) and the biochemical findings are analysed for each group. The physiopathologic mechanisms, comparisons between each etiologic group, treatment, clinical course, and prognosis are commented on. The conclusion drawn is that nephrocalcinosis is a clinical syndrome of various etiologies which in most cases arises from an underlying metabolic disease.
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PMID:[Nephrocalcinosis as a clinical syndrome. Study of 77 cases (author's transl)]. 52 25

Twenty-five patients with end-stage renal disease, nine of whom were receiving pharmacologic doses of vitamin D, and seventeen patients with primary hyperparathyroidism underwent bone biopsy following a three-day course of tetracycline administration. The mean width of the fluorescent tetracycline bands were significantly greater in the bones of patients with uremia than in those with primary hyperparathyroidism. This difference was due to wide labels present in the patients with uremia who had not been treated with vitamin D, as no differences existed in mean label widths of patients with uremia who had received this compound and the patients with primary hyperparathyroidism. Comparison of the maximum label widths distinguished not only primary hyperparathyroid patients from those with uremia, but uremic patients who had recieved vitamin D from those who had not been so treated. Quantitative microscopy of standard, nonfluorescent histologic features failed to make this latter distinction. These data are consistent with the presence of a wide zone of instantaneously fluorescing material in uremic bone following tetracycline administration, which does not relate to bone apposition occurring during antibiotic administration. This phenomenon probably represents a delay in mineral maturation which is normalized by vitamin D. Furthermore, it is apparent that the use of a continuously administered (single) tetracycline label will result in an overestimation of bone formation rates, particularly in osteomalacic states.
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PMID:Tetracycline fluorescence in uremic and primary hyperparathyroid bone. 60 25

Twenty-one patients with hyperpara-thyroidism were studied to determine the outcome of surgical treatment by a variety of surgeons using a variety of techniques. Primary surgical treatment was excision of an adenoma in 11 patients with primary hyperparathyroidism. One patient (7%) had a true recurrence. One patient (7%) had persistent disease. Subtotal parathyroidectomies were carried out in three patients with primary diffuse hyperplasia and in five patients with chronic renal disease. Total parathyroidectomy and autotransplantation were performed in two more recent patients with chronic renal disease. Permanent hypoparathyroidism was not seen postoperatively in patients with primary hyperparathyroidism. Identification of all four glands at the operating table is essential. The low recurrence rate following selective excision of diseases parathyroid glands in this series suggests that the approach can be undertaken safely in most instances.
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PMID:Surgical management of hyperparathyroidism. 62 6

A 25-year-old white woman with sporadic hypophosphatemic rickets presented with a 7 year history of chronic mild hypercalcemia, osteitis fibrosa cystic and hypercalcemic nephropathy. Serum immunoreactive parathyroid hormone was elevated by greater than 100-fold and a 3.5 g parathyroid tumor was found at operation. Survey of the literature reveals that of 9 previous cases in which hypercalcemic hyperparathyroidism occurred in association with hypophosphatemic rickets, only two had classical x-linked familial hypophosphatemic rickets. It appears more than likely that this unusual combination of skeletal diseases represents the chance occurrence of primary hyperparathyroidism in patients with underlying x-linked familial hypophosphatemic rickets rather than a complication of phosphate therapy.
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PMID:Hypercalcemic hyperparathyroidism in hypophosphatemic rickets. 87 68

A study of 92 patients operated on for primary hyperparathyroidism revealed that the condition was secondary to renal disease, thyrotoxicosis or malignancy in 35. Review of the literature revealed no reports of experimental studies on the relationship between hyperparathyroidism and thyrotoxicosis or malignancy. In renal disease, however, the author's own investigations show that the traditional concept of hypocalcemia as the most important factor in the development of parathyroid hyperfunction should be rejected. The parathyroid glands probably can be stimulated by various factors in "primary" hyperparathyroidism. Recent studies on the etiology of primary hyperparathyroidism are discussed and it is concluded that the term "primary" should be avoided as the disease is so often secondary.
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PMID:On the etiology of "primary" hyperparathyroidism. 94 14

The quartary and quintary hyperparathyroidism is observed following a primary hyperparathyroidism, in which the removal of the adenoma of the parathyroid did not lead to a reduction of the process of the disease. The nephropathy which developed during the basic disease and continued to exist after the operation leads to repeated consequences for the mineral metabolism which cause a condition of parathyroidal load and after this again an adenomatous process. The author adopts a definite attitude to the problems of heuristic biochemical parameters and generally to the question of such consecutive reactions.
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PMID:[Quintary hyperparathyroidism]. 96 Aug 60

The term "renal osteodystrophy" is used to include skeletal disorders of patients with chronic renal failure: osteitis fibrosa, osteomalacia, osteosclerosis, osteoporosis and the frequently associated extraskeletal calcifications. It is the chronic glomerular disease with phosphate retention and resultant hyperphosphatemia on one hand and deficient 1,25 (OH)2 D3 and resultant hypocalcemia on the other to induce secondary hyperparathyroidism. The three most common causes of chronic renal failure in our patients are chronic glomerulonephritis, diabetic nephropathy, hypertensive nephropathy in decreasing frequency, polycystic renal disease occurs in five patients. Other miscellaneous causes include nephrotic syndrome, chronic pyelonephritis, systemic lupus erythematosus, periarteritis nodosa, interstitial nephritis and renal stones. The bone changes are similar in primary and secondary hyperparathyroidism and the incidence of brown tumor is about 3% in the former and 1.5 to 1.7% in the latter. We present one among the 94 dialyzed patients who has long-standing severe chronic renal failure from polycystic kidney disease and develops brown tumor in the mid ulna after 7 years on maintenance hemodialysis. The incidence of brown tumor in our series is about 1.1%. Because of increased longevity of the dialyzed patients, brown tumor from secondary hyperparathyroidism is now more commonly observed. Hyperphosphatemia with serum calcium-phosphate products exceeding plasma solubility of 60 to 75 mg/dl may induce soft tissue and vascular calcification. This explains the much higher incidence of soft tissue calcification in secondary than primary hyperparathyroidism; two of our patients with generalized Monckeberg's type arterial calcification and multiple periarticular calcifications in five patients have been observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal osteodystrophy. 164 77

Over the last 25 years, the perceived clinical spectrum of primary hyperparathyroidism (HPT) has changed dramatically from a disorder characterized by severe bone and renal disease to one typically manifested by few or mild symptoms and little evidence of organ damage. Reasons for this change in spectrum include changing demographics (primary HPT is primarily a disease of the middle-aged and elderly), diffusion of medical knowledge leading to a higher index of suspicion, and improved clinical laboratory technology (especially inexpensive and accurate determination of serum calcium and parathyroid hormone). In the first 343 cases of primary HPT seen at the Massachusetts General Hospital, 57% had renal stones, 23% had hyperparathyroid bone disease, and less than 1% had no symptoms. By contrast, studies dating from the availability of automated serum calcium measurement found renal stones and hyperparathyroid bone disease in less than 5% of cases, and about half of cases had few or no symptoms. Most patients with primary HPT today have mild, nonspecific symptoms, such as weakness, fatigue, and mental depression, and such signs as arterial hypertension and osteopenia, and detection of their hypercalcemia is generally serendipitous. The mildness and slow progression seen in many cases of primary HPT has resulted in much controversy about appropriate management.
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PMID:Clinical spectrum of primary hyperparathyroidism: evolution with changes in medical practice and technology. 176 71

Since the introduction of routine automated measurements of serum calcium levels in the 1970s, the detection of primary hyperparathyroidism has risen considerably. Nevertheless, the severe bone changes described by von Recklinghausen are still quite rare. The apparent rise in incidence is accounted for by the discovery of a large group of predominantly asymptomatic elderly patients who have mild primary hyperparathyroidism. Because the diagnosis is most often confirmed through laboratory tests, radiologic studies are now most useful in assessing the severity of the disease. The presence of bone changes is an accepted indication for parathyroid surgery in primary hyperparathyroidism. For patients with asymptomatic disease in whom nonsurgical treatment may be considered, radiographic evaluation is one of several techniques that may be used to assess progression. High resolution radiographs of the hands are most valuable in this regard. Accelerated bone mineral loss, as measured by quantitative techniques, will probably play a significant role in the future. Radiographic follow-up of patients with renal disease and secondary hyperparathyroidism is equally important, as increased bone or soft tissue changes may indicate a need for therapeutic change. Radiographically identifiable changes of hyperparathyroidism consist mainly of various types of accelerated bone resorption. Multifocal subperiosteal resorption is generally considered to be pathognomonic of hyperparathyroidism. Subligamentous, subchondral, endosteal, and intracortical resorption are also important manifestations of accelerated bone turnover. The earliest bone changes are visible in the hands and should be searched for especially carefully in the phalanges and terminal tufts. Only occasionally will changes be found elsewhere in the skeleton when hand changes are not present.
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PMID:Hyperparathyroidism. 198 31


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