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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This is a report of six patients with cirrhosis of the liver in whom primary hyperparathyroidism occurred due to a solitary parathyroid adenoma 3 months to 9 years after undergoing emergency portacaval shunt for hemorrhage from esophageal varices. The presenting symptoms in all six patients were weakness and bone pain. Three patients had a bone fracture after insignificant trauma, one and probably two passed kidney stones, and a duodenal ulcer developed in two. Bone x-ray films showed generalized osteoporosis in all patients. Renal function and arterial blood pH were within normal limits in every patient. The diagnosis of primary hyperparathyroidism in each patient was based on repeated demonstrations of hypercalcemia, hypophosphatemia, and markedly elevated serum immunoreactive parathyroid hormone concentrations. In all six patients, removal of the parathyroid adenoma resulted in disappearance of symptoms; normalization of serum calcium, phosphorus, and immunoreactive parathyroid hormone levels; and in four of the six, improvement in radiographic evidence of osteoporosis during follow-up of from 1 to 6 years. The association of cirrhosis, portacaval shunt, and primary hyperparathyroidism has not been documented previously. Our six patients with primary hyperparathyroidism constitute 3.4 percent of 174 survivors of emergency portacaval shunt in a series of 264 unselected, consecutive patients with cirrhosis and bleeding esophageal varices. Hepatic osteodystrophy is known to have occurred in only 11 of these 174 survivors. Primary hyperparathyroidism may be a more common cause of hepatic osteodystrophy than has been previously recognized, and should be considered in patients with cirrhosis in whom weakness, bone pain, and bone demineralization develop, particularly if they have a portacaval anastomosis.
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PMID:Hyperparathyroidism, cirrhosis, and portacaval shunt. A new clinical syndrome. 325 57

Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
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PMID:Magnesium metabolism in health and disease. 328 51

A statistical association between hypertension and hyperparathyroidism has been repeatedly reported, but the underlying pathogenetic mechanism has not been elucidated. A 51-year-old woman was hospitalized because of increasing motor disability caused by multiple bone and muscle aches with generalized weakness. She was found to have marked hypercalcemia and hypophosphatemia, increased parathyroid hormone secretion, but normal renal function and blood pressure level. After the identification and removal of a single parathyroid adenoma, the calcium/phosphate metabolism normalized in a relatively short time during which, however, hypertension developed in the absence of any other endocrine or renal dysfunction. A positive, highly significant relationship was observed between the progressive rise in blood pressure and the gradual increase in serum phosphate concentration occurring after the operation, suggesting that, in the hyperparathyroid phase, an underlying trend to hypertension could have been masked by the phosphate depletion, probably through its effects on cardiac and vascular smooth muscle function.
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PMID:Development of hypertension after correction of primary hyperparathyroidism. 335 May 90

Two dogs were examined because of anorexia, lethargy, muscle tremors, weakness, and seizures that were associated with an acute onset of hypocalcemia. Both dogs had histories of chronic hypercalcemia. Examination of the parathyroid glands revealed infarction of focal parathyroid adenomas, with atrophy of the remaining parathyroid glands. It was concluded that the acute onset of hypocalcemia was caused by infarction of functional parathyroid adenomas that were previously responsible for the cause of persistent hypercalcemia. Infarction of a parathyroid adenoma should be included in a list of differential diagnoses of acute hypocalcemia in the dog, especially if hypercalcemia has been diagnosed previously.
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PMID:Acute hypocalcemia associated with infarction of parathyroid gland adenomas in two dogs. 335 Jul 46

In a consecutive series of 100 neck explorations for primary hyperparathyroidism, 42 patients were 60 years of age or older; in this group of elderly patients the surgical cure rate was 100%. These patients were reviewed retrospectively by means of a structure interview. Twenty-one patients had had preoperative neuromuscular symptoms that ranged from coma to subjective muscular weakness. These patients had significantly-higher preoperative serum calcium and parathyroid hormone levels than did 21 patients without neuromuscular symptoms (P = 0.003 and P = 0.046, respectively). Most of the neuromuscular symptoms improved in the postoperative period. In particular, 15 of 17 patients with muscle weakness reported a significant improvement, while 14 of 15 patients who suffered from fatigue and lethargy reported an improvement. An improvement also occurred in the level of day-to-day function in eight patients. While surgery for primary hyperparathyroidism generally is undertaken for a specific indication, such as severe hypercalcaemia or renal stones, it appears from this study that neuromuscular symptoms also may improve, particularly in elderly patients.
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PMID:Neuromuscular symptoms in elderly patients with hyperparathyroidism: improvement with parathyroid surgery. 339 14

Case records from 21 dogs with hypercalcemia and hyperparathyroidism were evaluated. The dogs were greater than or equal to 7 years old, and 6 were Keeshonds. The most common clinical signs were polydipsia/polyuria, listlessness, and muscle weakness. The serum calcium concentrations were 12.1 to 19.6 mg/dl. Serum phosphorus concentrations were low in 5 dogs, within the reference range in 13 dogs, and high in 3 dogs that also had high concentrations of BUN. Twenty dogs had a parathyroid adenoma, and 1 had a parathyroid carcinoma. Nineteen dogs had their parathyroid tumor surgically removed. Within 5 days of tumor removal, 11 of the 19 dogs became hypocalcemic and the remaining 8, normocalcemic. Nine of the 11 hypocalcemic dogs developed clinical signs. Iatrogenic hypercalcemia was induced in 7 of 16 dogs treated orally with calcium carbonate plus vitamin D. Only 1 of 19 dogs that had their parathyroid tumor excised died in hypocalcemic tetany. Two additional dogs died within 2 weeks of surgery, one because of pancreatitis, the other due to renal failure. Eight dogs died 9 to 37 months after surgery of unrelated problems. Eight dogs were alive for at least 7 to 28 months after surgery.
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PMID:Primary hyperparathyroidism in dogs: 21 cases (1976-1986). 365 3

In hyperparathyroidism associated with endstage renal failure, either subtotal, or total parathyroidectomy with autotransplantation have been advocated as potentially curative for those patients non-responsive to medical therapy. Seventeen such patients managed by the Wellington renal unit were reviewed as to indications for, and responses to, surgery. Itch, psychiatric symptoms, joint ache, muscular weakness, gritty eyes and thirst were the major symptoms for which surgery was recommended. Hypercalcaemia (universal in women) and deterioration in bone radiology were additional indications for operation. All showed remarkable postoperative improvement. Symptomatic hypocalcaemia was significant in 41%. This observation has led to intensified pre- and postoperative vitamin D and calcium therapy. Postoperative radiologic improvement at three months was apparent in 80% of patients. We advocate subtotal parathyroidectomy as the effective surgical treatment of choice for uraemic hyperparathyroidism.
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PMID:Parathyroid surgery in chronic renal failure. 386 72

Dialysis osteomalacia is characterized by distinctive, although not pathognomonic, clinical and biochemical features. Symptoms and signs may include musculoskeletal pain, arthralgias, proximal muscle weakness, and spontaneous fractures. Biochemical characteristics may be hypercalcemia and normal serum alkaline phosphatase activities. Vitamin D administration may induce early severe hypercalcemia. Plasma phosphate and immunoreactive parathyroid hormone concentrations may be at any level. Only bone histology allows to establish the diagnosis of dialysis osteomalacia with certainty. Diphosphonate bone scan, however, enables to distinguish between severe osteitis fibrosa and dialysis osteomalacia. The diagnostic value of desferrioxamine administration with subsequent measurement of plasma aluminium remains to be determined. The complex interactions existing between parathyroid hormone and aluminium are not yet fully understood.
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PMID:Dialysis osteomalacia: clinical aspects and physiopathological mechanisms. 391 57

Dysphagia is an uncommon feature of thyrotoxic myopathy, and is usually associated with other signs of bulbar weakness, such as dysarthria and nasal regurgitation. We report a case of thyrotoxicosis presenting with dysphagia due to diminished oesophageal motility associated with significant hypercalcaemia; both abnormalities resolved rapidly following treatment.
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PMID:Disordered oesophageal motility in thyrotoxic myopathy. 402 94

A patient with many symptoms and signs of primary hyperparathyroidism had hypocalcaemia when first seen. Bone section histology showed osteomalacia and osteitis fibrosa, and the hyperparathyroidism at this stage was considered to be secondary to osteomalacia with postgastrectomy steatorrhoea. On treatment with vitamin D (with disappearance of her bone pains and weakness) she developed hypercalcaemia. She regained her health after removal of a 6-g. parathyroid adenoma. Normal histology was shown in another parathyroid gland.We believe that the initial hypocalcaemia was due to vitamin-D deficiency, which produced ineffective hyperparathyroidism until it was corrected. A review of the few reports of patients with autonomous hyperparathyroidism with steatorrhoea and osteomalacia does not support the argument that these patients had "tertiary" disease. It suggests that most of them, like our patient, had primary hyperparathyroidism.
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PMID:Hypocalcaemic primary hyperparathyroidism. 541 47


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