Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 16-month-old black male infant had unusual thirst, polyuria, hyponatremia, and hypertension. His polyuria was unresponsive to vasopressin therapy, and his high blood pressure was not effectively controlled by antihypertensive drugs. Radiographic examinations revealed an occult Wilms tumor in the right kidney. After removal of the tumor, the signs and symptoms were relieved. The tumor had a renin activity about 280 times that of the adjacent renal cortex, and many intracytoplasmic secretory granules were found on electron microscopy. The pathogenesis of these clinical manifestations appears to be mediated through the physiologic pathways of renin-angiotensin II and renin-aldosterone.
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PMID:Polydipsia, polyuria, and hypertension associated with renin-secreting Wilms tumor. 20 43

Tetramethylthiourea (TMTU) was added to the diet of male and female ChR-CD rats for up to 2 years at levels of 0, 30 and 300 ppm. Fifty rats of each sex were used at each dietary level. High-level males and females and low-level males had a lower body weight and consumed less diet than did the controls. A slight anemia was found in the high-level males and females. Polyuria of a low osmolality was found in high level males and females. Serum thyroxine was lower in high-level males and females than in controls. TMTU-related gross and histologic changes were detected only in the thyroids of high-level males and females. After 3 months on test, the thyroids were enlarged and dark on gross examination. Histologically, there was an increase in follicle lumen size, loss of colloid staining, hypertrophy and hyperplasia of follicular cells, together with hyperemia. These early lesions were diffuse in distribution. Eight (28 percent) of 29 female high level rats, 18 to 24 months on test, developed follicular cell carcinomas with no such tumors in 26 comparable controls (p less than 0.005, Fisher's Exact Test, one tail). Although no metastases were found, capsular and vascular invasion by tumor cells was seen. TMTU was considered to be carcinogenic for the female rat under the conditions of this test.
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PMID:Thyroid tumors in rats from tetramethylthiourea. 42 41

Diabetes insipidus, resulting from metastatic involvement of the neurohypophysial system, is a rare complication of breast cancer. This review examined the clinical features, metastatic pattern, and radiological and postmortem findings of 39 breast cancer patients with this complication. All patients had polyuria and polydipsia, and all had evidence of advanced metastatic breast cancer. A high incidence of meningeal carcinoma carcinomatosis and/or sellar metastases was observed. In view of the anatomical proximity of the posterior pituitary to the dura mater and the sella turcica, our findings suggest that metastases to the neurohypophysis can occur not only as a result of hematogenous dissemination of malignant cells, but also from direct tumor extension and/or invasion from adjacent structures. Although satisfactory symptomatic relief can be obtained with vasopressin tannate, complete resolution of the diabetic insipidus syndrome was evident only in those patients who had achieved control of the underlying breast disease.
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PMID:Diabetes insipidus and breast cancer. 47 18

A 13-year-old boy with a teratoma in the sellar region was presented. This patient had gradually developed polyuria and polydipsia since 2 years prior to the first admission. Endocrinological examination showed a marked reduction of pituitary function. Careful neuroradiological examinations including CT failed to show any mass lesion in the sellar and suprasellar regions but a marked increase of the width of the third ventricle. CSF examination revealed only a slight increase of cell count (lymphocytes). The patient was discharged with hormonal replacement therapy. Seven months later the patient developed visual disturbance and mental disorders. On the second admission, plain skull films showed enlarged sella and CT demonstrated a mass in the suprasellar region. Preoperative diagnosis was suprasellar germinoma. At surgery a teratoma, probably arising from the pituitary fossa, was totally removed. Histopathology of the tumor showed tri-dermal tissues including melanotic progonoma and germinoma. The authors presented various problems of the patient and their solving processes.
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PMID:[Polyuria and polydipsia in a young boy--a case study (author's transl)]. 52 58

The renal reabsorption of water independent of solute is the result of the coordinated function of the collecting duct and the ascending limb of the loop of Henle. The unique juxtaposition of the ascending and descending portions of the loop of Henle and of the vasa recta permits the function of a counter-current multiplier system in which water is removed from the tubular lumen and reabsorbed into the circulation. The driving force for reabsorption is the osmotic gradient in the renal medulla which is dependent, in part, on chloride (followed by sodium) pumping from the thick ascending loop of Henle. Urea trapping is also thought to play an important role in the generation of a hypertonic medullary interstitium. Arginine vasopressin (AVP) acts by binding to receptors on the cell membrane and activating adenylate cyclase. This, inturn, results in the intracellular accumulation of cyclic adenosine monophosphate (AMP) which in some fashion abruptly increases the water permeability of the luminal membrane of cells in the collecting duct. As a consequence, water flows along an osmotic gradient out of the tubular lumen into the medullary interstitium. Diabetes insipidus is the clinical condition associated with either a deficiency of or a resistance to AVP. Central diabetes insipidus is due to diminished release of AVP following damage to either the neurosecretory nuclei or the pituitary stalk. Possible causes include idiopathic, familial, trauma, tumor, infection or vascular lesions. Patients present with polyuria, usually beginning over a period of a few days. The diagnosis is made by showing that urinary concentration is impaired after water restriction but that there is a good response to exogenous vasopressin therapy. Nephrogenic diabetes insipidus can be identified by a patient's lack of response to AVP. Nephrogenic diabetes insipidus is caused by a familial defect, although milder forms can be acquired as a result of various forms of renal disease. Central diabetes insipidus is eminently responsive to replacement therapy, particularly with dDAVP, a long lasting analogue of AVP. Nephrogenic diabetes insipidus is best treated with a combination of thiazide diuretics as well as a diet low in sodium and protein.
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PMID:The clinical physiology of water metabolism. Part II: Renal mechanisms for urinary concentration; diabetes insipidus. 54 67

We have experienced with 50 cases of parasellar tumors, four cases of which had persistent thirst, polydipsia, polyuria, and reversible temporary hyponatremia secondary to hypernatriuresis. The mechanism of the syndrome in these four cases could not be explained by either that of the syndrome of hypernatremia or of the so-called SIADH. We tentatively named this syndrome as "CEREBRAL POLYURIC HYPONATREMIA" and the criteria of this syndrome as as follows: 1) persistent thirst, polydipsia polyuria, 2) reversible temporary hyponatremia secondary to hypernatriuresis, 3) exception of the following items--administration of uretic drugs, renal and adrenal dysfunction, hyperglycemia, hyperlipemia, overadministration of water, and poor administration of NaCl. The mechanism of this syndrome is presumed as follows: 1) compression by a tumor or surgical attack to the anterior hypothalamus, 2) disturbance of the mechanism of ADH secret-on, 3) extrasecretion of natriuretic factor possibly produced in the anterior hypthalamus, and 4) preservation of the thirst center.
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PMID:[Cerebral polyuric hyponatremia--discussion of a new syndrome with disturbance of electrolyte balance of central origin (author's transl)]. 55 42

Parathyroid carcinoma accounts for 0.5 to 5% of all cases of hyperparathyroidism. We reviewed the clinical, surgical, and pathologic features observed in all patients with parathyroid carcinoma evaluated at the Mayo Clinic from 1920 through 1991. Forty-three patients (22 women, 21 men; mean age, 54 yrs, range 29-72) were identified, including 2 with familial hyperparathyroidism. Information on initial presentation was available in 40 patients: 15 (38%) presented with polydipsia or polyuria, 11 (27%) with myalgias or arthralgias, 7 (17%) with weight loss, and 4 (10%) with nephrolithiasis; 3 patients (7%) were asymptomatic at presentation. Of 31 patients in whom the initial neck examination was recorded, 14 (45%) had a palpable neck mass. The mean serum calcium and serum phosphorus levels were 14.6 mg/dl and 2.3 mg/dl, respectively. Parathyroid hormone levels were elevated in 21 of 21 patients (mean elevation, 10.2 times upper limit of normal). Complications included nephrolithiasis in 14 of 25 patients (56%), bone disease in 20 of 22 patients (91%) and both in 8 of 15 patients (53%). All patients underwent primary surgical resection of parathyroid carcinoma. Twenty-six of 43 patients (60%) required a second operation with 18 patients requiring multiple re-explorations. At the second operation, residual tumor was found in the neck (68%), mediastinum (16%), or both (12%). Six patients received radiation therapy to the neck (5 patients) or bones (1 patient) for recurrent or metastatic disease. Of these, 1 patient appeared cured of parathyroid carcinoma by radiation therapy 11 years after documented tumor invasion of his trachea. Repeated excision of tumor recurrences was an effective means of controlling hypercalcemia in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parathyroid carcinoma: clinical and pathologic features in 43 patients. 151 93

A 17 year-old boy was admitted to the hospital because of thirst, polyuria (5-61/day), delayed sexual development and muscle weakness. He appeared obese, had an eunuchoidal body habitus and was excessively tall. Chromosomal analysis revealed a 47XXY karyotype. Serum cortisol was 1.3 microgram/dl, LH, 10.4 mIU/ml, FSH, 2.0 mIU/ml, and testosterone, 10 ng/dl. Endocrinological dynamic tests indicated diabetes insipidus and hypopituitarism of a hypothalamic type. Brain CT disclosed the existence of a tumor shadow around the calcified pineal body, extending towards the suprasellar region. Replacement therapy with glucocorticoid and DDAVP was started. The patient complained of a headache and plasma AFP and hCG concentrations were 868 ng/ml and 68.6 IU/ml respectively. A hCG- and AFP- producing germ cell tumor was suspected and radiation therapy with 60Co was performed. Plasma AFP and hCG were decreased with significant clinical improvement. Soon after irradiation, he started to complain of a headache and had elevated AFP and hCG levels. Right hemiparesis and unconsciousness suddenly appeared and he died of left thalamic bleeding. This is the first case of Klinefelter's syndrome associated with intracranial germ cell tumor. Plasma testosterone levels fluctuated in parallel with the change in plasma hCG levels. This shows that the Leydig cells in this patient could respond to some extent to tumor-producing hCG.
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PMID:A case of Klinefelter's syndrome associated with hypothalamic-pituitary dysfunction caused by an intracranial germ cell tumor. 244 Jun 66

A case is reported of hydramnios due to excessive fetal urine production associated with congenital mesoblastic nephroma. Rapid growth of a right renal tumor and excessive fetal urine production were detected by measuring the size of the tumor and hourly fetal urine production during the development of hydramnios between 28-34 weeks of gestation. A female infant weighing 2200 g was born at 34 weeks' gestation. She lost 18% of her birth weight in the first 48 hours because of neonatal polyuria. Right nephrectomy and ureterectomy were performed 2 days after birth. After the operation, the neonatal polyuria improved dramatically. The right renal tumor was identified histologically as a mesoblastic nephroma. The importance is stressed of early and correct antenatal diagnosis of a renal tumor and precise estimation of urine production for postnatal management of hemodynamic change in cases of mesoblastic nephroma.
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PMID:Hydramnios associated with congenital mesoblastic nephroma: case report. 254 37

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


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