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)

Many hormones initiate their biologic actions by augmenting the intracellular concentrations of 3',5'-adenosine monophosphate (cyclic AMP). The nucleotide has been found in body fluids; its determination in plasma and urine can be performed by a rapid, simple and specific method: the cyclic AMP assay kit of the Radiochemical Centre (Amersham, England). The assay is based on the competition between unlabelled cAMP and a fixed quantity of the tritium labelled compound for binding to a bovine muscle protein which has a high specificity and affinity for cAMP. Different factors must be considered in evaluating the 24 h urinary content of the nucleotide: the renal or extrarenal origin of cAMP and the functional status of the kidneys. In basal conditions the urinary cAMP excretion is significantly correlated with creatinine excretion (n = 67; r = 0.47; p less than 0.001) thus confirming that the most part of cAMP excreted is derived from the plasma by glomerular filtration. Parathyroid hormone (PTH) stimulates adenylate cyclase predominantly in the renal cortex, whereas vasopressin (ADH) stimulated the enzyme in the medulla; thus PTH and ADH could increase the amount of cAMP in the urine from the renal source. In a case of diabetes insipidus and infusion of ADH caused a prompt rise in cAMP urinary excretion. In 5 normals an infusion of bovine synthetic parathyroid hormone caused an increased excretion of cAMP that preceded the phosphaturic response. An infusion of salmon synthetic calcitonin caused a rise in phosphate excretion and no increase in cAMP urinary content. As it concerns the two calciotopic hormones, PTH and CT, it is reasonable to assume that renal receptors are distinct. The 24 h urinary excretion of cAMP in 55 control subjects (3613 +/- 1460 D.S. n moles) was contrasted with the lower excretion in 25 elderly subjects (70-93 years: 1804 +/- 699 n moles), with the high cAMP excretion in a patient with hyperparathyroidism (that fell to normal values following removal of the parathyroid adenoma) and with the low cAMP excretion in patients with primary or surgical hypoparathyroidism. The mean 24 h cAMP excretion in patients with renal insufficiency was significantly decreased when compared to control subjects. These findings and recent reports confirm that the 24 h urinary output of cAMP may be considered an useful index of pharathyroid function in man.
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PMID:[The diagnostic value of the determination of cyclic 3',5'-adenosine monophosphate (cAMP) in urine]. 19 Jun 33

A 65-year-old woman with a history of a left heminephrectomy for renal carcinoma developed hypercalcaemia 11 years after the operation. The same kidney was found to contain a recurrent renal carcinoma. After the radical nephrectomy of the left kidney, hypercalcaemia remitted but reappeared 11 months later. The right kidney was small but functioned at a level of creatinine clearance of 10--15 ml/min. Metastatic work-up was negative, and secondary causes of hypercalcaemia were excluded. A neck exploration revealed a parathyroid adenoma. With parathyroid resection the serum calcium declined to normal, and the risk of hypercalcaemic nephropathy in the remaining kidney was precluded.
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PMID:Hypercalcaemia due to hyperparathyroidism in a patient with chronic renal failure and renal carcinoma. 42 90

A study is presented of 14 patients with hyperparathyroid crisis treated at the Massachusetts General Hospital between 1964 and 1978. These patients showed diverse clinical manifestations that were indistinguishable from those in patients with pseudohyperparathyroidism. Their symptoms varied from progressive fatigue, malaise, and weakness to those related to the gastrointestinal and urinary tracts. The one biochemical alteration commonly found among these patients was the rapid increase in the serum calcium. There was a concomitant rise in the BUN in 50% of the patients and in the creatinine in 80%. The diagnosis was established by an elevated immunoreactive parathyroid hormone (PTH) level in all eight patients (100%) who had the radioimmunoassay; by the presence of subperiosteal resorption of the phalanges in six of the eight patients (75%); and in three of four patients (75%) by the loss of the lamina dura of the teeth. The 12 patients who had surgery all survived; the two who did not died. Thirteen patients (93%) had a neoplasm--an adenoma in 12 and a carcinoma in one. One patient had hyperplasia (7%). Nine patients (64%) received hypocalcemic drug therapy. The serum calcium temporarily fell to 12 mg/100 ml in five patients (56%) but failed to budge in four (44%). Simultaneous treatment with saline infusion, furosemide and with hypocalcemic drugs over a prolonged period compounded the difficulty at operation by increasing interstitial edema. Our findings from this study show prompt surgical intervention as the ideal treatment for hyperparathyroid crisis, preferably, within 72 hours of the acute onset of symptoms.
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PMID:Hyperparathyroid crisis: clinical and pathologic studies of 14 patients. 51 79

The urodynamic relevance of benign prostatic hyperplasia (BPH) is determined by evaluation of the symptoms of prostatism, the degree of infravesical obstruction and the size of adenoma. The combination of all three findings, but also the presence of at least of two of these findings suggest a diagnosis of clinical BPH. Standard diagnostic procedures consist in elicitation of the history, evaluation of symptoms, physical examination, urinalysis and laboratory examination of serum creatinine; with evaluation of residual urine and uroflowmetry in addition, surgical therapy can be expected to be successful in 93%. Urinary flow rates exceeding 15 ml/s and/or discrepancies between symptoms and findings need further assessment by synchronous pressure-flow studies for differential diagnosis between unobstructed flow and high-flow outflow obstruction. Complete videourodynamic investigation is indicated both in patients with combined BPH and urinary incontinence without residual urine and in patients with BPH and suspected or known neurological disorder. Surgical treatment of BPH involves the risk of postoperative incontinence in patients with detrusor hyperreflexia combined with a functional or morphological lesion of the external urinary sphincter.
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PMID:[Value of functional examination techniques for the assessment of the clinical aspects of benign prostatic hyperplasia]. 137 31

During the last years interest has focused on the trophic effect of gastrin in colorectal carcinomas. Some reports indicated an increased serum level of gastrin in patients with colorectal adenomas or carcinomas. In a prospective study in 261 patients submitted to colonoscopy fasting serum gastrin concentrations were determined. 91 patients served as control, 89 patients had one or more adenomas, 55 patients suffered from a colorectal carcinoma, 17 had a benign, postoperative stenosis of the colon, and 9 had a chronic inflammatory bowel disease. All patients fulfilled the following criteria: No regular drug intake, no previous gastric or small bowel operation, no known ulcer disease, no abnormalities in serum calcium, creatinine, triglycerides, cholesterol and blood urea. Mean gastrin level was 86.63 +/- 23.8 pg/ml in the control, 84.57 +/- 25.1 pg/ml in the adenoma group and 84.6 +/- 24.4 pg/ml in the carcinoma group. No difference of serum gastrin levels were observed regarding sex, age, tumor stage and localisation.
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PMID:[Serum gastrin level in patients with colorectal adenoma or carcinoma]. 141 56

Hypertension in primary hyperparathyroidism (HPT) was previously attributed to hypercalcemia per se or to impaired kidney function. Of 441 consecutive patients operated on for HPT over 24 years, 57% were hypertensive. Preoperative blood pressure remained fairly constant during the study period, despite otherwise markedly changing clinical picture with, latterly, more asymptomatic patients. The preoperative systolic blood pressure (SBP) was significantly correlated to both serum calcium (p less than 0.001) and serum creatinine (p less than 0.05), but not when the influence of age was taken into account in a multiple regression analysis. Other pathogenetic factors in hypertension were therefore probable. When the statistical analysis was adjusted for differences in age and serum calcium, blood pressure was lower in the HPT patients with parathyroid hyperplasia than in those with adenoma (153 +/- 31/90 +/- 14 vs. 163 +/- 29/91 +/- 14 mmHg, p less than 0.01 for SBP). The concept that parathyroid hyperplasia represents a mild (early) form of HPT that may precede adenoma formation is corroborated by our observations, which also indicate that there is no simple cause-and-effect relationship accounting for hypertension in primary HPT.
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PMID:Hypertension in primary hyperparathyroidism in relation to histopathology. 168 31

Serum beta 2-microglobulin concentrations were determined in 21 untreated hyperthyroid patients (12 with Graves' disease, and nine with toxic nodular adenoma) and in 20 healthy controls. All subjects had normal serum creatinine concentrations and urine analysis. Both total and free thyroid hormones were significantly higher in the hyperthyroid groups than in controls. Beta 2-microglobulin concentrations were significantly increased in both groups of hyperthyroid patients compared with controls. No difference was found in the thyroid hormone and beta 2-microglobulin concentrations between both sets of patients. The beta 2-microglobulin and thyroid hormone concentrations were not correlated. These data show that hyperthyroidism is another cause of increased beta 2-microglobulin production along with viral infections, immunologically mediated diseases, and malignant neoplasms. The increased serum beta 2-microglobulin concentration in thyroid hyperfunction is probably related to metabolic rate, even if autoimmunity might contribute to its overproduction.
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PMID:Increased serum beta 2-microglobulin concentrations in hyperthyroid states. 199 37

The aim of this study was to produce large liver tumors reliably, and to diagnose the tumors during development. Therefore, New Zealand white rabbits were treated with N-nitrosodiethylamine orally three times per week by gavage and were examined by clinical-chemical assay at regular intervals during the average treatment period of 14 months. The total cumulative dose was 1200 mg N-nitrosodiethylamine over 14 months. After a short treatment period the initial dose of 3 mg/kg had to be reduced to 1.5 mg/kg. In all 11 treated animals (100%) liver tumors were seen at the end of the study. Four control animals did not show any neoplastic changes. Clinical parameters investigated were for an assessment of liver function, total protein, urea, creatinine, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, albumin and neuraminic acid as well as some serum electrolytes. The in vivo diagnosis of liver tumors based on changes in these parameters proved to be relatively unreliable. The liver enzyme tests and urea concentration only yielded significant changes when the liver tumors were very large. Changes in neuraminic acid levels were the most reliable indicator for the presence of a liver tumor in this animal model. In the 11 treated animals, serum values of this marker increased towards the end of the study by an average of 300 mg/dl. The induced tumors were mainly hepatocellular carcinomas. Only in 1 animal was a hepatocellular adenoma found. Further primary tumors diagnosed were six adenomas in the kidneys and two uterus adenomas, as well as nasal cavity tumors (two papillomas, one carcinoma, one adenoma and one adenocarcinoma). In 70% of the treated rabbits the hepatocellular carcinomas had metastasized to the lungs.
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PMID:Diethylnitrosamine-induced metastasizing hepatocellular carcinomas in New Zealand white rabbits. A tumor model for clinical investigations. 200 10

In order to evaluate the role of calcium metabolism in blood pressure regulation, 15 patients with primary hyperparathyroidism and 9 healthy control subjects were studied before and during angiotensin II infusion. The patients were re-investigated 2-5 months after removal of the parathyroid adenoma. Blood pressure, plasma levels of angiotensin II, aldosterone, arginine vasopressin, and atrial natriuretic peptide, and creatinine clearance were determined. Blood pressure and the blood pressure response to angiotensin II infusion were both the same before and after the operation. Angiotensin II and arginine vasopressin during basal conditions were significantly higher before than after the operation (angiotensin II: 17 (median) to 10 pmol/l, P less than 0.02; arginine vasopressin: 2.9 to 1.9 pmol/l, P less than 0.01), whereas aldosterone, atrial natriuretic peptide, and creatinine clearance were unchanged. During angiotensin II infusion, aldosterone, arginine vasopressin, and atrial natriuretic peptide increased to approximately the same levels before and after the operation. Blood pressure was not correlated to any of the hormones measured. Thus, patients with primary hyperparathyroidism have elevated plasma levels of angiotensin II and arginine vasopressin which may be compensatory phenomena counteracting volume depletion owing to a decreased renal concentrating ability induced by hypercalcemia, and owing to PTH-induced inhibition of renal sodium reabsorption.
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PMID:Elevated angiotensin II and vasopressin in primary hyperparathyroidism. Angiotensin II infusion studies before and after removal of the parathyroid adenoma. 252 5

Bone status, calcium and phosphate metabolism were prospectively evaluated in 98 renal transplant recipients with stable renal function. Aseptic necrosis of bone was found in 30 patients, leading to arthroplasty in 12 patients. Plasma parathyroid hormone and nephrogenic cyclic adenosine monophosphate (cAMP) values were greater and the duration of pre-transplant chronic renal failure longer in patients with aseptic necrosis of bone than in those who were not affected. Cumulative oral corticosteroid doses and the number of acute rejection episodes treated by intravenous methylprednisolone pulses were similar in patients with or without aseptic necrosis of bone. Hyperparathyroidism was confirmed histologically in 14 patients, comprising 4 cases of adenoma and 10 of diffuse hyperplasia. Serum parathyroid hormone correlated positively with serum creatinine (r = 0.47; P less than 0.001) and with cumulative corticosteroid dose (r = 0.30; P less than 0.003). This study suggests that hyperparathyroidism is a factor in the pathogenesis of aseptic bone necrosis. The frequency and severity of bone necrosis may be decreased by early detection and treatment of post-transplant hyperparathyroidism.
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PMID:Aseptic necrosis of bone following renal transplantation: relation with hyperparathyroidism. 254 Apr 58


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