Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-three cases of primary hyperparathyroidism were experienced at Wakayama Medical College Hospital and affiliated hospitals between January, 1969 and December 1985. Histopathological findings were adenoma in 22 cases, hyperplasia in 1 case. On the clinical diagnosis of this disease, the most sensitive laboratory test was serum calcium level, which was elevated in 21 patients (91%), and in 87.8% of all samples measured. Serum ionized calcium and phosphorus were also sensitive measures. The positive rate of serum PTH was 67% in 18 cases. Tl-chloride scintigraphy identified preoperatively the site of the adenomas in 8 out of 10 cases, and computed tomography in 10 out of 15 cases. Both methods are non-invasive, and are beneficial for the preoperative examination of the localization of parathyroid adenoma. After parathyroidectomy, serum calcium and ionized calcium levels recovered rapidly within the normal limit in 12 hours. On the other hand, serum phosphorus level increased gradually up to the normal limit in about 1 week.
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PMID:[Primary hyperparathyroidism in 23 cases]. 367 33

Parathyroid allotransplantation was performed in a 25-year-old woman with idiopathic hypoparathyroidism that had been diagnosed at age 4 years. Long-term medical management of the primary condition with vitamin D and oral calcium supplementation was complicated by multiorgan calcinosis and renal failure. At the age of 21 years she received a successful cadaver renal allograft. Four years later she developed calcinosis cutis with widespread skin necrosis. Medical control of calcium and phosphate metabolism was unsatisfactory and the skin necrosis became progressive and life threatening. A parathyroid allograft that was performed with tissue from a parathyroid adenoma resulted in normalization of the serum calcium and phosphorus levels with arrest and subsequent healing of the skin necrosis. Later failure of the parathyroid allograft was followed by successful retransplantation of normal parathyroid tissue from a cadaver organ donor.
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PMID:Parathyroid allotransplantation in the treatment of complicated idiopathic primary hypoparathyroidism. 407 84

A retrospective study of the case-reports of 263 patients explored surgically for primary hyperparathyroidism demonstrated the cause to be: an adenoma (206 cases), a primary hyperplasia (29 cases), or a cancer (3 cases), exploration was negative in 25 cases. Presenting symptoms were mainly urinary, but 15 p. 100 of patients seen during the last two years had been asymptomatic. Nine patients required emergency surgery and 29 had a primary normocalcemic hyperparathyroidism. The two most useful laboratory examinations, apart from measurement of blood calcium and phosphorus levels, were parathormone assay (elevated levels were present in 80 p. 100 of cases) and quantitative bone biopsy (positive in over 80 p. 100 of patients). The surgical approach was mainly cervical, except for repeat operations when ten sternotomies were performed with successful results in 4 cases. Immediate postoperative mortality was quite high (3 p. 100), particularly in the acute forms or those with multiple adenomas, and in patients over 70. Morbidity (hypocalcemia, recurrent nerve palsy) was increased after repeat surgery. Analysis of long-term results, particularly with respect to urinary symptoms, showed marked differences between lesions of single glands (adenoma) and hyperplasia. The most difficult problem to resolve with this surgery is the importance to attach to excision of the parathyroids when lesions are present in several glands.
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PMID:[Surgical treatment of primary hyperparathyroidism. Evaluation of 263 cases]. 614 97

Patients who have cutaneous and osseous neurofibromatosis, especially those with pathologic fractures, bone pain, roentgenographic evidence of cystic lesions, or hypercalcemia, should be evaluated carefully for the presence of a hormonally active parathyroid adenoma. They may have a reversible cause of osteitis fibrosa cystica. Palpation of the neck, serum and urine collections for measuring calcium and phosphorus levels, PTH determinations, bone roentgenograms, and bone biopsy help to establish the diagnosis.
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PMID:Neurofibromatosis and primary hyperparathyroidism. 642 38

The whole body content of sodium, potassium, chlorine, calcium, phosphorus and nitrogen was measured by neutron activation analysis in 13 patients with untreated primary hyperaldosteronism (Conn's syndrome; aldosterone-secreting adenoma). Concurrently, exchangeable sodium and potassium were estimated by isotope dilution. Results were compared with values in the same patients during treatment with potassium-conserving diuretics and again after removal of the adenoma; and also with those in a series of 30 patients having untreated essential hypertension. Both total body and exchangeable sodium were high in Conn's syndrome before treatment and were reduced by spironolactone or amiloride and by subsequent surgery. There was no evidence of alteration in the proportion of non-exchangeable sodium in this disease, in contrast to earlier reports. Total body and exchangeable potassium were low in untreated Conn's syndrome and increased to normal after therapy: the proportion of non-exchangeable potassium was similar before and after treatment, and also similar to that in essential hypertension. Total body chlorine was increased before treatment in Conn's syndrome and returned to normal with therapy; body calcium, phosphorus and nitrogen were normal throughout.
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PMID:Body elemental composition, with particular reference to total and exchangeable sodium and potassium and total chlorine, in untreated and treated primary hyperaldosteronism. 653 85

A review of 30 cases of acromegaly has confirmed the limited diagnostic interest of serum phosphorus determination as it was elevated in 40% of cases only; urine hydroxyproline excretion was more useful, since it was high in 80% cases. As for the baseline plasma concentration of somatotropin, it was at or above 10 ng/ml in 80% cases. Among dynamic tests meant to evaluate the responsiveness of the growth hormone-secreting adenoma, inhibition after L-Dopa ingestion and/or stimulation after T.R.H. injection occurred in 2/3 cases. Lack of inhinition after a glucose load was noted in half of the cases only. An abnormal (yet typical for acromegaly) response can be obtained for anyone of these tests, which points at the variable degree of (de) differenciation of the adenoma cells from one case to the other.
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PMID:[Assessment of biological and hormonal diagnostic criteria in acromegaly (author's transl)]. 677 58

Four patients with milk-alkali syndrome (MAS) presented with many of the characteristics of primary hyperparathyroidism including hypercalcemia, low or normal serum phosphorus levels, normal or increased urinary calcium levels, and inappropriately high or elevated serum parathyroid hormone levels. These laboratory findings differ from those classically described in MAS, i.e., hypercalcemia without hypercalciuria and a normal or high plasma phosphate level. Because the serum calcium level failed to return to normal after two weeks of hydration and a low calcium diet, and because of the inability to distinguish this syndrome from primary hyperparathyroidism, two of the four patients underwent neck exploration. Four normal parathyroid glands were histologically proven in each, and at autopsy in a third patient, there was no evidence of parathyroid hyperplasia or adenoma. Hypercalcemia eventually resolved in all patients with a low-calcium diet for as long as six months. Of the several features of MAS, hypercalcemia, alkalosis in the presence of azotemia, a history of increased calcium and alkali intake, and a response to dietary calcium restriction are helpful in differentiating this syndrome from primary hyperparathyroidism. Laboratory tests in patients with MAS may be confusing and the return to normocalcemia in response to a calcium deficient diet may be delayed.
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PMID:Milk alkali syndrome. Does it exist and can it be differentiated from primary hyperparathyroidism? 683 Mar 49

With miniature semiconductor electrodes of high sensitivity and special shape it is possible to charakterize diverse tissues during operation. The measured radioactivity of phosphorus reflects its enrichment and storage in the parathyroid tissue. The findings of 5 patients in whom clinically hyperparathyroidism was strongly suspected and who underwent surgery are reported. We have successfully localized parathyroidea adenomas in 3 patients, in 2 cases no adenoma could be found the storage of phosphorus 32 was normal. In all measurements we achieved a complete agreement with histological findings.
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PMID:[Intraoperative detection of parathyroid tissue by semiconductor electrodes (author's transl)]. 746 6

Fahr's disease associates various degrees of neuropsychological impairment and calcium deposits in the basal ganglia. We report 3 cases. The first case was a 54-year-old man with hemichorea of one-year duration. Laboratory results demonstrated idiopathic hypoparathyroidism. In the second case, a 23-year-old man treated for epilepsia for 8 years was hospitalized for subintrant episodes and hemichorea. Dysmorphism and laboratory results led to the diagnosis of pseudo-hypothyroidism. The third case was a 62-year-old woman with generalized seizures of epilepsia and dementia of two-month duration. Physical examination revealed extra-pyramidal rigidity. Hyperparathyroidism due to an adenoma was confirmed histologically. In all three patients, correction of phosphocalcium levels led to clinical improvement, particularly with disappearance of the epileptic seizures and abnormal movements. Clinical expression of Fahr's syndrome varies greatly. Symptoms include psychiatric disorders, epileptic seizures, extra-pyramidal syndrome and various neurological conditions. Diagnosis requires CT brain scan which identifies calcium deposits in the basal ganglia. The main cause is hypoparathyroidism, whether primary or post-operative. Cases due to other causes of dysparathyroidism are rare. The pathophysiology of this condition remains unknown and results of treatment are often unsatisfactory. Since correcting the impaired calcium phosphorus metabolism often leads to considerable improvement, it is essential to systematically search for dysparathyroidism in patients presenting with neuropsychologic manifestations associated with calcifications of the basal ganglia.
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PMID:[Fahr syndrome and dysparathyroidism. 3 cases]. 750 22

Antituberculous chemotherapy agents, particularly rifampicin and isoniazid, affect vitamin D metabolism and can create biochemical evidence of vitamin D deficiency. Vitamin D deficiency induces a state of resistance to parathyroid hormone. This study sought to explain the temporary resolution of hypercalcaemia and hypercalciuria, during antituberculous chemotherapy with rifampicin and isoniazid, in a subject with a surgically proven parathyroid adenoma and coincidental spinal tuberculosis. Serum ionized calcium, 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, plasma parathyroid hormone, and 24-hour urine excretions of calcium, inorganic phosphorus and hydroxyproline were sequentially measured over a 3-year interval that included 18 months of antituberculous chemotherapy. Initial serum ionized calcium was 1.52 mmol/l (normal 1.20-1.35 mmol/l), 24-hour urine calcium excretion was 9.40 mmol/day (normal 1.25 to 7.50 mmol/day) and plasma intact PTH was 9.2 pmol/l (normal 0.0-4.5 pmol/l). During antituberculous chemotherapy the serum ionized calcium and 24-hour urine calcium excretion were normal but the plasma PTH rose to higher levels. Following completion of the chemotherapy, hypercalcaemia and hypercalciuria returned with levels similar to those observed pretreatment. Serum 25-hydroxyvitamin D was low at 6.25 nmol/l (normal 20 to 90 nmol/l) during antituberculous chemotherapy, but was normal before and after. Serum 1,25-dihydroxyvitamin D was normal throughout the 3-year interval. We conclude that the antituberculous chemotherapy induced relative vitamin D deficiency and resistance to parathyroid hormone action, thereby masking the hyperparathyroidism and hypercalcaemia until the chemotherapy was completed.
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PMID:Primary hyperparathyroidism masked by antituberculous therapy-induced vitamin D deficiency. 764 6


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