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)

The findings of 152 patients with proven primary hyperparathyroidism are reportedmthe purpose of the analysis was to find difference between the various clinical manifestations of the disease. Furthermore the occurrence of acute hyperparathyroid crisis in our series as well as in the literature are described. 65.8% of the patients were females, 34.2% were males. The leading symptom in 98 patients (group I) were kidney stones and in 23 patients (group II) cystic bone disease. Both manifestations of the disease occurred in only 7 patients (group III) and no symptoms related to the kidneys or to the bones occurred in 24 patients (group IV). Because of the difference of the clinical manifestations the additional data were analyzed for each group separately and compared with each other. There was no difference in the mean serum calcium levels for all four groups, however, patients of group I were on the average younger, the duration of the disease was longer and the weight of the parathyroid adenoma was lower compared to the other three groups, Data are presented regarding calcium excretion, phosphate clearance and tubular reabsorption of phosphate for each group. At operation single or multiple adenoma formation was present in 133 patients, whereas diffuse hyperplasia was found in 17 and carcinoma in 2 other patients. 46 of the adenomas were found in an atypical anatomical localisation. This observation is responsible for the many unsuccessful or second explorations of the neck; The weight of the adenomas varied between 0.1 and 23.5 g. The most difficult diagnosis was that of diffuse hyperplasia. The sucess of the surgical intervention was usually established in over 80% of the cases within 24 to 48 hours after the operation with a significant fall of serum calcium. There ist still no definite explanation for the variability of the clinical manifestations of primary hyperparathyroidism. Parathyroid hormone determinations on larger numbers of patients are not yet published. The assumption, that different hormones or peptide fragments are reposible for the different action on bone and kidney is discussed; In our series of 152 patients acute hyperparathyroid crisis occurred eight times. Our findings are compared to the other well documented cases in the literature. Main symptoms were nausea, vomiting, abdominal pain and different states of cerebral dysfunction. Most of the patients had calcium levels over 16 mg/100 ml. Partial renal insufficiency with elevated blood urea and phosphate retention was found in over 50% of the cases. Overall mortality of all cases with acute parathyroid crisis is 52.5%. The pathogenesis of acute hyperparathyroidism and the implications of high calcium levels are discussed. According to our own experience hypercalcenia can be controlled with an intensive therapeutic program and emergency operation for acute parathyroid crisis is no longer necessary.
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PMID:[Primary hyperparthyroidism. Analysis of 152 patients with special reference to acute life threatening complications (acute hyperparathyroidism)]. 20 39

Hypophosphatemia is common in hospitalized patients and occurs under a variety of circumstances other than parathyroid hormone excess. Charts of 100 inpatients with hypophosphatemia were reviewed and the patients divided into five groups on the basis of serum phosphate level: 18, 2.1 to 2.4 mg/dL; 49, 1.6 to 2.0 mg/dL; 20, 1.1 to 1.5 mg/dL; 12, 0.6 to 1.0 mg/dL; 1, 0.1 to 0.5 mg/dL. The effect of glucose ingestion on serum phosphate level was shown in one normal patient. Whenever carbohydrate was administered intravenously (45 cases), this was considered the primary cause of the hypophosphatemia. Other causes were as follows: diuretics, hyperalimentation, alcoholism, respiratory alkalosis, dialysis, insulin, corticosteroids, diabetic ketoacidosis, vomiting, phosphate-binding antacid, Gram-negative sepsis, primary hyperparathyroidism, saline, epinephrine, gastrointestinal malabsorption, and unknown. Hypophosphatemia in hospitalized patients may have multiple causes.
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PMID:Hypophosphatemia in hospitalized patients. 44 90

Tthe findings of 150 patients with proven primary hyperparathyroidism are reported. The purpose of the analysis was to find differences between the various clinical manifestations of the disease. Furthermore the occurrence of acute hyperparathyroid crisis in our series as well as in the literature are described. 65.8% of the patients were females, 34.2% were males. The leading symptom in 98 patients (group I) were kidney stones and in 23 patients (group II) cystic bone disease. Both manifestations of the disease occurred in only 7 patients (group III) and no symptoms related to the kidneys or to the bones occurred in 24 patients (group IV). Because of the difference of the clinical manifestations the additional data were analyzed for each group separately and compared with each other. There was no difference in the mean serum calcium levels for all four groups, however, patients of group I were on the average younger, the duration of the disease was longer and the weight of the parathyroid adenoma was lower compared to the other three groups. Data are presented regarding calcium excretion, phosphate clearance and tubular reabsorption of phosphate for each group. At operation single or multiple adenoma formation was present in 133 patients, whereas diffuse hyperplasia was found in 17 and carcinoma in 2 other patients. 46 of the adenomas were found in atypical anatomical localisation. This observation is responsible for the many unsuccessful or second explorations of the neck. The weight of the adenomas varied between 0.1 and 23.5 g. The most difficult diagnosis was that of diffuse hyperplasia. The success of the surgical intervention was usually established in over 80% of the cases within 24 to 48 hours after the operation with a significant fall of serum calcium. There is still no definite explanation for the variability of the clinical manifestations of primary hyperparathyroidism. Parathyroid hormone determinations on larger numbers of patients are not yet published. The assumption, that different hormones or peptide fragments are responsible for the different action on bone and kidney is discussed. In our series of 152 patients acute hyperparathyroid crisis occurred eight times. Our findings are compared to the other well documented cases in the literature. Main symptoms were nausea, vomiting abdominal pain and different states of cerebral dysfunction. Most of the patients had calcium levels over 16 mg/100 ml. Partial renal insufficiency with elevated blood urea and phosphate retention was found in ov er 50% of the cases. Overall mortality of all cases with acute parathyroid crisis is 52.5%. The pathogenesis of acute hyperparathyroidism and the implications of high calcium levels are discussed. According to our own experience hypercalcemia can be controlled with an intensive therapeutic program and emergency operation for acute parathyroid crisis is no longer necessary.
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PMID:[Primary hyperparathyroidism. An analysis of 152 patients with special references to acute life threatening complications (acute hyperparathyroidism)]. 79 28

A female with premary hyperparathyroidism and secondary renal lesions, as well as lesions of the stomach and pancreas is described. The initial illness was manifested by repeated renal crises. Later, gastroenterological complaints appeared--epigastralgia, vomiting, frequent hematemesis with melena. That was the cause for a gastric resection, diffuse erosive gastritis being found. After the operation, the pains and the vomiting of hematin matter repeatedly recidivated. Clinically and at the laboratory, data were formed for a chronic recidivating pancreatitis with the presence of primary hyperparathyroidism. The postoperative treatment of the parathyroid adenoma led to an improvement of the gastroenterological complaints.
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PMID:[Chronic recurrent pancreatitis with erosive gastritis in a patient with primary hyperparathyroidism]. 101 31

A 12-year-old girl was admitted to our hospital with signs of an acute abdomen with paralytic ileus. The previous and family history were without abnormalities. Abdominal pain and vomiting had started two days earlier. On palpation the swollen abdomen was painful and there was an increased tension in the left upper part. The clinical diagnosis of acute pancreatitis was confirmed by an increased serum level of lipase (4480 U/l). Clinical chemical investigations further revealed a permanent hypercalcemia in the range of 6.4 to 8.3 mval/l. This, together with concomitantly reduced levels of serum phosphate and a threefold increased level of parathyroid hormone (343 pg/ml, upper limit of reference = 100 pg/ml) were consistent with a hyperparathyroidism. In fact, sonography of the cervical organs revealed a solitary adenoma of the parathyroid glands. After surgery serum levels of calcium returned to normal. Hypercalcemia as a consequence of primary hyperparathyroidism has to be included in the differential diagnosis of acute pancreatitis in childhood.
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PMID:[Acute pancreatitis as an initial manifestation of hypercalcemia in primary hyperparathyroidism in childhood]. 265 77

An adult Keeshond had clinical signs associated with hypercalcemia, including inappetence, polyuria, polydipsia, and vomiting. Blood biochemical findings and urinary clearance studies were consistent with a diagnosis of primary hyperparathyroidism. Histomorphometric analysis of trabecular bone in an iliac crest biopsy indicated increased bone remodeling activity. Surgical exploration of the neck revealed an oval mass, which was removed by blunt dissection. Histologic diagnosis was parathyroid gland adenoma. The dog died because of renal failure on the eighth postoperative day. This report defines primary hyperparathyroidism in the dog, thus facilitating diagnosis for the veterinary clinician.
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PMID:Primary hyperparathyroidism in a dog: biochemical, bone histomorphometric, and pathologic findings. 380 43

Hypercalcaemia can be caused by many disorders, but is most commonly due to primary hyperparathyroidism in outpatients, and to malignant disease in hospital inpatients. When mild (less than 3 mmol/L) it does not cause symptoms, but can have long term effects such as renal calculi. It is important that the aetiology of the hypercalcaemia be established, as it can reflect serious disease. In most patients the correct diagnosis can be suspected from clinical history and examination, and confirmed by laboratory tests and x-rays. The most difficult diagnostic problem is the patient with negative clinical findings, mild hypercalcaemia and mild renal impairment, when the parathyroid hormone level is normal or slightly elevated. When hypercalcaemia is severe (greater than 3.5 mmol/L), it can cause vomiting, polyuria, dehydration and renal impairment, and is then an important therapeutic problem. Therapy includes treatment of the cause, such as radiotherapy for malignant disease or surgery for primary hyperparathyroidism. In addition, it is usually necessary to treat the hypercalcaemia itself, and the initial step is always rehydration. If the plasma calcium concentration remains high, drug treatment must be added, the most effective and reliable agent being intravenous mithramycin. Aminohydroxypropylidene diphosphonate (APD), though less studied, may be equally useful in this situation. Glucocorticoids are not always effective, and phosphate may cause renal damage, particularly when given intravenously. For long term treatment of malignant hypercalcaemia, oral glucocorticoids and phosphate are often effective, and can be given in combination. When primary hyperparathyroidism cannot be corrected surgically, the hypercalcaemia (and hypercalciuria) are probably best treated with a low calcium diet and cellulose phosphate, a regimen also effective for the hypercalcaemia of sarcoidosis.
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PMID:Hypercalcaemia. What does it signify? 394 Aug 49

To determine the frequency of gastrointestinal symptoms in primary hyperparathyroidism, we retrospectively analyzed 100 consecutive patients seen at Emory University Hospital from Jan 1, 1977 through March 1, 1979. At the time of diagnosis, 28 patients complained of nausea, 19 of vomiting, 29 of abdominal pain, and 33 of constipation. One patient presented with acute pancreatitis and 14 had ulcer disease (two gastric and 12 duodenal ulcers). Hypercalcemia increases gastric acid secretion and may account for associated ulcer disease and the ulcer-like pain in primary hyperparathyroidism. The mechanisms causing the other gastrointestinal symptoms in hypercalcemia remain to be elucidated. These symptoms abate on correction of hyperparathyroidism.
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PMID:Primary hyperparathyroidism and the gastrointestinal tract. 746 39

A 9-year-old castrated male domestic shorthair cat with dysuria, anorexia, vomiting, and lethargy was admitted to the veterinary teaching hospital. A large, firm mass was palpable in the ventral cervical region. Hypercalcemia, azotemia, and nonregenerative anemia were evident on serum biochemical analysis and CBC, and multiple uroliths were detected by abdominal radiography. At necropsy, light microscopy of the ventral cervical mass revealed a parathyroid adenocarcinoma. Light microscopy of sections of the kidneys revealed multifocal, chronic, lymphocytic/plasmacytic, tubulointerstitial nephritis, as well as moderate multifocal acute tubular necrosis. On quantitative analysis, the uroliths were composed of calcium oxalate. Determination of serum calcium concentration is indicated in cats with calcium oxalate urolithiasis to aid in detection of primary hyperparathyroidism.
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PMID:Calcium oxalate urolithiasis in a cat with a functional parathyroid adenocarcinoma. 775 34

This article report a study of 23 cases of hypercalcemia crisis resulting from primary hyperparathyroidism (18 cases), carcinoma (4 cases) and vitamin D intoxication (1 case). In addition to the symptoms of primary diseases, the patients with hypercalcemia crisis often had anorexia, nausea, vomiting, polydipsia, polyuria, psychoneurotic symptoms, arrhthmia. The severity of the symptoms was proportional to the degree of hypercalcimia. Serum calcium concentration of patients in hypercalcemia crisis should be equal or higher than 3.75 mmol/L (15 mg/dl) or serum ionized calcium higher than 1.88 mmol/L. Treatment hypercalcemia crisis consisted of rapidly lowering the serum calcium level by various measures while actively treating the primary diseases. Our experience is to supply normal saline intravenously or orally to increase the extracellular fluid and to enhance excretion of the urine calcium by administrating furosemide. In this paper, serum calcium concentration of 5 patients with hypercalcemia crisis treated with salmen calcitonin was reduced in varying degrees. The above mentioned treatment would be beneficial to the alleviation of the crisis and the preparation for operative treatment.
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PMID:[The preliminary experiences of diagnosis and treatment for hypercalcemia crisis--clinical analysis of 23 cases]. 798 37


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