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 patient initially showed symptoms of peptic ulcer disease in 1953 and was later found to have hypercalcemia and hyperparathyroidism. Peptic ulcer symptoms persisted after parathyroidectomy, and results of studies provided evidence of the Zollinger-Ellison syndrome. Evaluation of the patient's family showed a classic pattern of multiple endocrine adenomatosis type 1. The patient underwent total gastrectomy and excision of a gastrin cell adenoma in 1971 with relief of symptoms, but with persistent hypergastrinemia. He remained in good health until January 1976, when symptoms of hypoglycemia developed. Results of laboratory studies were compatible with the diagnosis of a pancreatic beta-cell adenoma. At the time of operation, an adenoma of the head of the pancreas was found. The tumor was excised; no other metastatic tumors were found. The tumor was compatible with a beta-cell adenoma and was found to contain high concentrations of insulin; there was no important amount of gastrin. Symptoms of hypoglycemia have entirely disappeared.
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PMID:Separate pancreatic gastrin cell and beta-cell adenomas: report of a patient with multiple endocrine adenomatosis type 1. 3 17

After removal of two large pancreactic insulinomas, although the presenting spontaneous hypoglycaemia was eliminated, severe and persisting haematemesis and melaena supervened with a rise in serum gastrin. The patient had multiple endocrine adenopathy (pituitary, parathyroids and islet cells), but no evidence of a pancreatic gastrin-producing tumour. After emergency gastric operation for the bleeding, the serum gastrin remained high until the hypercalcaemia and hyperparathyroidism had been corrected by subtotal parathyroidectomy. Immunofluorescence studies showed gastrin in the parathyroid tissue.
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PMID:Possible parathyroid origin of gastrin in a patient with multiple endocrine adenopathy type I. 16 52

After description of the central-nervous signs due to hypoglycemia, hypoxia, hypo- and hypercalcemia there are discussed several internal diseases with prominent neurologic symptoms like endocrine disorders of thyroid, adrenal and pituitary gland, malignant diseases especially regarding the hematopoietic system, disorders of the joints and connective tissue and metabolic disorders as acute intermittent porphyria, uremic and hepatic coma. The principal differential diagnostic considerations in this relation are being described in order to avoid severe diagnostic errors.
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PMID:[Leading neurological symptoms of internal diseases]. 96 30

A review of 106 patients with multiple endocrine neoplasia (MEN) type 1 reported between 1966-1989 in Japan was conducted in order to clarify the natural history of this disease. Sporadic MEN 1 was found in 61 patients, and familial MEN 1 was found in 45 patients from 15 families. The mean ages at diagnosis of the two groups were 46.2 and 41.3 years, respectively, and the male to female ratio was 3:4. With regards to the involvement of the pituitary, parathyroid and endocrine pancreas, the combination of three endocrine glands was 31%, and that of two was 48%, in which the pituitary, parathyroid and endocrine pancreas had tumorous lesions in 60%, 88% and 63%, respectively. The first clinical manifestations of MEN 1 were the symptoms of hyperparathyroidism (32%), pituitary tumors (26%), peptic ulcer (28%) and hypoglycemia (13%). These symptoms appeared between 6 and 57 years of age (mean 34 years). The main clinical symptoms of the pituitary tumors were acromegaly and gigantism (37%), galactorrhea-amenorrhea syndrome (20%), Cushing's disease (10%) and visual disturbance due to compression of the tumor (20%). The clinical manifestations of hyperparathyroidism were mainly asymptomatic hypercalcemia (41%), nephrolithiasis (42%) and osteitis fibrosa (5%). In the patients with pancreatic tumor, Zollinger-Ellison syndrome (52%) and hypoglycemic symptoms (42%) were found. Tumors in the adrenal cortex, thyroid, carcinoid and lipoma were detected in association with MEN 1 in the frequencies of 28%, 21%, 9% and 5%, respectively. Death was reported in 37 patients between 9 and 86 years of age (mean 50.0 years). The cause of death was gastrointestinal bleeding and perforation (45%), surgery (24%) and disseminated carcinomatosis (18%). Recently, the gene predisposing to this syndrome has been assigned to chromosome 11 (11q13) in non-Japanese cases but not yet in Japanese MEN 1 patients.
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PMID:[Clinical characteristics in multiple endocrine neoplasia type 1 in Japan: a review of 106 patients]. 167 21

Tumors of the female genital tract may be associated with a variety of unusual clinical manifestations. Uncommon endocrine and paraendocrine syndromes include production of human chorionic gonadotropin by tumors other than those of germ cell origin, hyperthyroidism associated with struma ovarii and gestational trophoblastic disease, the carcinoid syndrome, the Zollinger-Ellison syndrome, hypercalcemia, Cushing's syndrome, hypoglycemia, hypertension related to renin or aldosterone production, hyperprolactinemia, inappropriate secretion of antidiuretic hormone, and virilization associated with Nelson's syndrome and placental site trophoblastic tumor. Paraneoplastic syndromes associated with gynecological tumors include disorders of the nervous system, connective tissue, and skin, as well as hematologic abnormalities and the nephrotic syndrome. Heritable and other congenital syndromes associated with these tumors are the Peutz-Jeghers syndrome, the nevoid basal-cell carcinoma syndrome, Ollier's disease and Maffucci's syndrome, hereditary leiomyomatosis, ataxia-telangiectasia, von Hippel-Lindau's disease, thyroid abnormalities associated with Sertoli-Leydig cell tumors, and Carney's complex. Other syndromes associated with tumors of the female genital tract include Meigs' syndrome, hyperamylasemia, uveal melanocytic lesions, and pyrexia.
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PMID:Clinical syndromes associated with tumors of the female genital tract. 175 57

Metabolic disturbances of Na, K, Ca and glucose as paraneoplastic syndrome were reviewed on the basis of recent progress of such areas. These abnormalities usually occur due to the production of hormones or other physiologically active substances by tumor tissues. Hyponatremia is the most common abnormality of Na metabolism in patients with cancers such as lung cancer, malignant lymphoma, thymoma and so on. Usual cause of hyponatremia as paraneoplastic syndrome is inadequate secretion of Antidiuretic Hormone (SIADH), which brings dilution hyponatremia associated with water intoxication. Recently hyponatremia due to abnormal secretion of atrial natriuretic peptide has been noted. Ca metabolism disturbance associated with cancer is usually observed as hypercalcemia and it is said that such hypercalcemia is seen in about 10% of cancer patients. Main cause of hypercalcemia associated with cancer is local osteolytic hypercalcemia (LOH) due to bone metastasis or humoral hypercalcemia of malignancy (HHM). The most common etiology of HHM is the production of Parathormone (PTH) related peptide (PTH-rP) massively secreted from cancer tissues. PTH-rP has been recently well investigated and its molecular, mRNA and gene structure have been already determined. The progress of this area is very rapid and PTH-rP will be assayed in the clinical laboratory in near future. As for glucose metabolism disturbance as paraneoplastic syndrome, hypoglycemia is the most common abnormality. This type of hypoglycemia has been noted in relation with excessive production of somatomedin.
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PMID:[Metabolic disturbance as paraneoplastic syndrome]. 182 8

A 26-year-old woman, gravida 1, para 0, having episodes of confusion, slurred speech, and blurred vision in pregnancy was documented to have severe hypoglycemia with elevated serum insulin and C-peptide levels. Emergency treatment for hypoglycemia was necessary several times during pregnancy. A healthy female infant was delivered after oxytocin induction of labor. Post partum the patient had numerous episodes of severe hypoglycemia in spite of constant intravenous glucose. Computerized tomographic scan of the pancreas failed to show a lesion, whereas pancreatic arteriography revealed a 2 cm mass in the tail of the pancreas. Partial pancreatectomy was performed 6 days after delivery. Microscopic examination of the tissue confirmed the presence of an insulinoma. Hypercalcemia developed together with elevated parathyroid hormone levels. The presence of an insulinoma, hypercalcemia, and a history of hyperparathyroidism in two relatives indicates that this is a case of multiple endocrine adenomatosis type I first diagnosed during pregnancy.
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PMID:Multiple endocrine adenomatosis type I in pregnancy. 197 95

In this problem-oriented review of abnormalities associated with cancer, we have emphasized distinctive diagnostic points related to pathogenesis for each condition and outlined how the approach to management is determined by pathogenesis. For abnormalities of the complete blood count, it is important to distinguish between abnormalities directly related to marrow malignancy and abnormalities associated with extramarrow malignancy. Hemopoietic tumors consist of developmentally deficient blood cells produced by a clonal population of malignant stem cells. Tumors infiltrating marrow cause overcrowding in the limited marrow microenviroment. Extramarrow malignancies cause blood abnormalities, but the potential for normal marrow function is present. Abnormalities of blood cells secondary to therapy are usually clearly identified by consideration of clinical history. The initial differential diagnosis for hypercalcemia is malignancy. An aggressive diagnostic approach may be needed to identify the neoplasm, and therapy should incorporate measures to prevent renal failure. Hypoproteinemia and hyperproteinemia may be caused by neoplasia. Monoclonal gammopathies should be identified and may be associated with hyperviscosity syndrome. Hypoglycemia in the adult animal is most frequently caused by insulin-secreting tumors, but it has also been associated with hepatic and other tumors. Increased blood urea nitrogen, creatinine, lipase, amylase, and liver enzyme activities may also be caused by malignancy. Inadequate urine concentrating ability may be caused by hypercalcemia or malignancy-associated renal insufficiency. Hematuria in older animals is suggestive of urinary tract neoplasia. Exfoliated tumor cells may be identified in the urine sediment of these patients.
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PMID:Laboratory abnormalities in patients with cancer. 219 37

The physical and metabolic characteristics of a Dark Agouti rat mammary adenocarcinoma and its effects on host metabolism are described. The tumour was characterized by a lack of glandular differentiation, tetraploidy, a rapid mitotic index and a high rate of glycolysis. The adenocarcinoma was readily maintained in tissue culture and could be passaged through the host by inoculating either cell suspensions or tissue explants. In the rat, tumour growth resulted in a loss of adipose tissue at a tumour mass of less than 5% body weight indicating that increased energy expenditure was already present at that stage. In addition the tumour caused anaemia, hypercalcaemia and hypoglycaemia. Hyperketonaemia was also observed in fasted tumour-bearing rats. Methotrexate arrested tumour growth in vivo. These aspects of the tumour model make it useful for investigations into host-tumour competition and mechanisms of cachexia.
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PMID:Biochemical manifestations of a rat mammary adenocarcinoma-producing cachexia: in vivo and in vitro studies. 222 29

As antineoplastic therapy improves, patients with cancer will have the potential for prolonged survival. Tumor products may produce metabolic complications, such as hypercalcemia, hyponatremia, and hypoglycemia, and these conditions must be promptly recognized so that treatment can be initiated before severe or life-threatening symptoms occur. Tumor-lysis syndrome is a metabolic complication that occurs most frequently when effective treatment for rapidly proliferating tumors is initiated. It is a syndrome that can be prevented or ameliorated with appropriate anticipatory treatment. Recognition of metabolic emergencies common to cancer patients will improve quality of life and improve survival, allowing patients to benefit from definitive cancer treatment.
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PMID:Metabolic emergencies in clinical oncology. 268 10


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