Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 17-year-old woman manifested fever, abdominal pain, headache, and hypertension caused by a solitary, benign pheochromocytoma. She also had hypercalcemia and elevated plasma immunoreactive calcitonin levels. After removal of the pheochromocytoma, calcium and calcitonin levels returned to normal. Studies of peripheral and tumor venous blood showed no excess or ectopic parathyroid hormone secretion, but the tumor contained and secreted calcitonin. Sporadic pheochromocytoma may secrete calcitonin and cause hypercalcemia by non-parathyroid hormone-mediated mechanisms. The potential is clearly present for confusion with multiple endocrine neoplasia, type 2 (medullary thyroid carcinoma, pheochromocytoma, and primary hyperparathyroidism).
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PMID:Pheochromocytoma associated with hypercalcemia and ectopic secretion of calcitonin. 46 64

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

We report a 9-year-old girl who had massive bone marrow infiltration of tumor cells at the onset of alveolar rhabdomyosarcoma. She was admitted to a surgical hospital because of abdominal pain and tumor in the buttock. Computerized tomographic scans of the pelvis revealed an abnormal mass. She was referred to our department. Hematological examination showed pancytopenia. Blood chemistry revealed hypercalcemia and hyperuricemia. Bone marrow was occupied with 100% tumor cells. Chromosome analysis of tumor cells in bone marrow revealed a specific translocation, t(2;13) (q37;q14). This finding enabled the diagnosis of a disseminated alveolar rhabdomyosarcoma to be established. She was treated with vincristine, cyclophosphamide and epirubicin, achieved a complete remission, but died of relapse 3 months after diagnosis.
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PMID:[Alveolar rhabdomyosarcoma with massive bone marrow involvement and 2;13 chromosome translocation]. 163 76

Reports of adults with Williams syndrome (WS) have been rare. We have evaluated 13 adult WS patients and reviewed 16 case reports of WS in patients older than age 16 years. Adults in our study had progressive multisystem medical problems. Cardiovascular complications were common (12/13) including hypertension (8), supravalvular aortic stenosis (9), aortic hypoplasia (3), pulmonic artery stenosis (4), peripheral stenoses (3), and mitral valve prolapse (2). Joint limitation (12/13) was progressive, often accompanied by kyphoscoliosis and lordosis. Recurrent urinary tract infections in 6 individuals led to radiologic studies showing urethral stenosis in 2, and bladder diverticula and vesicoureteral reflux in 3. Gastrointestinal problems included obesity (5), chronic constipation (7), diverticulosis (3), and cholelithiasis (4). Hypercalcemia was documented in 5 patients, although others had hypercalcemic symptoms (abdominal pain, polyuria, and constipation). One 45-year-old man had parathyroid hyperplasia. Previous reports likewise document significant morbidity. Thus, Williams syndrome in an adult appears to dictate aggressive evaluation and monitoring. Investigation of calcium metabolism should be undertaken in each adult WS patient.
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PMID:Adults with Williams syndrome. 189 83

We describe a patient with CML who developed hypercalcemia in his course of blast crisis. A 25-years-old man was diagnosed as CML with priapism in April 1985, and controlled with BHAC-DVP, VMP, busulfan therapy. In December 1987, he readmitted to our hospital with abdominal pain. Investigations at that time showed: white blood cell count 11600/microliters (blast cells 9%); hemoglobin 8.4 g/microliters; platelets 19.0 X 10(4)/microliters; serum calcium 13.2 mg/dl; BUN 44 mg/dl; creatinine 2.7 mg/dl. Treatment with predonine, 6-MP and vincristine was begun. But serum calcium level rose gradually up to 16.5 mg/dl. So we tried middle dose Ara-c therapy, serum calcium decreased to 6.8 mg/dl. At once he was in a chronic phase, but he relapsed and died of heart failure. Necropsy showed extensive leukemic blast-cell infiltration of the bone marrow, liver, spleen, lung, and kidney. The cause of hypercalcemia in our case was suspected of local osteolytic hypercalcemia, because multiple bone destruction was found.
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PMID:[Hypercalcemia associated with blast crisis of chronic myeloid leukemia]. 218 69

A patient with hypercalcemia and newly diagnosed multiple myeloma developed acute pancreatitis. Other etiologic factors for pancreatitis were excluded. Hypercalcemia secondary to hyperparathyroidism is associated with acute pancreatitis. In English literature, only one other case has been published where the hypercalcemia of multiple myeloma may have caused pancreatitis. Pancreatitis should be considered in patients with hypercalcemia and multiple myeloma who develop nausea/vomiting, and abdominal pain.
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PMID:Acute pancreatitis in a case of multiple myeloma with hypercalcemia. 248 50

A 57-year-old female was admitted to our hospital with general lassitude, loss of appetite, nausea, upper abdominal pain, thirst, polydipsia and polyuria. On admission, she had an asymmetrical pear-shaped tumor in the right supraclavicular region and severe hypercalcemia. Plasma C-PTH was elevated to 22.72ng/ml. Plasma calcitonin was also elevated to 336 pg/ml. She died of respiratory and cardiac failure of two weeks after admission without any positive response to the treatment, including hemodialysis. Pathohistologically, the tumor was a parathyroid adenoma. The concentrations of C-PTH, intact PTH and calcitonin in the tumor tissue were markedly high: 4.56 micrograms/g wet, 13.9 ng/g wet and 50.7 ng/g wet, respectively. Immunohistologically, the tumor cells and the fibrous stroma were stained strongly positive to rabbit anti-human calcitonin antibody and rabbit anti-human N-PTH antibody by indirect immunoperoxidase staining. Calcitonin-producing tumors, except for medullary thyroid carcinoma are rarely reported. To our knowledge, this is the first report of such a calcitonin-producing parathyroid adenoma associated with primary hyperparathyroidism.
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PMID:A case of calcitonin-producing parathyroid adenoma with primary hyperparathyroidism. 258 94

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

Over a period of 42 years, 581 patients with presumed hyperparathyroidism underwent an initial cervical exploration. Abnormal parathyroid glands were removed from 495 patients (85.2%). There was a greater probability of operative success in women, patients over 50 years of age, and patients with hypercalcemia, hypertension, or nonspecific abdominal pain. There was no association of operative outcome with some of the "classic" manifestations of hyperparathyroidism--peptic ulcer disease, neuropsychiatric symptoms, pancreatitis, bone disease, or urolithiasis. The probability of surgical success improved with time, increasing from 56 per cent in the 1950s to 97 per cent in the present decade. This improvement appears to be related to greater operative experience, since all four parathyroid glands were more likely to be found with increased experience, and there was a strong correlation between finding four parathyroids and achieving persistent normocalcemia. The most common causes of operative failure were inaccurate calcium assays (the patient was not truly hypercalcemic), an inappropriate diagnosis ("normocalcemic hyperparathyroidism"), and surgical inexperience. These three factors accounted for at least three fourths of all negative explorations. More accurate diagnostic studies, and careful exploration by an experienced surgeon should maximize the probability of a successful operation for primary hyperparathyroidism.
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PMID:Causes of the failed cervical exploration for primary hyperparathyroidism. 341 98

Acute recurrent pancreatitis in the absence of alcoholism and gallstones is a frustrating illness for both the patient and the physician. Over a 10 year period, 33 patients were operated on and found to have a duct of Wirsung entering the duodenum through the fibers of the sphincter of Oddi. Recurrent pancreatitis of sufficient intensity to require hospitalization had occurred an average of 4.2 times per patient, and each had experienced numerous episodes of abdominal pain of lesser severity. At least two attacks of pancreatitis that required hospitalization had occurred in all patients. All known causes of pancreatitis, including alcoholism, gallstones, hypercalcemia, hyperlipidemia, drug reactions, and pancreas divisum were excluded. Endoscopic retrograde cholangiopancreatography showed no ductal abnormalities. Twenty-eight of the patients had previously undergone cholecystectomy 8 months to 20 years before operation. A sphinteroplasty of the common bile duct and duct of Wirsung resulted in elimination of attacks of pancreatitis in all except two patients. Follow-up has been more than 5 years in 16 patients, more than 4 years in 10 patients, and more than 1 year in 5 patients. There have been no deaths. It appears that the entrance of the duct of Wirsung into the duodenum through a separate orifice through the fibers of the sphincter of Oddi causes recurrent acute pancreatitis. It seems likely that the problem is one of intermittent pancreatic duct obstruction. Normal pancreatic duct caliber is attributed to the intermittent nature of the obstruction. Enlargement of the orifice of the duct of Wirsung and division of the sphincter of Oddi relieved attacks of recurrent pancreatitis.
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PMID:Misplaced pancreatic duct orifice as a cause of recurrent acute pancreatitis. 381 90


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