Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypouricemia in coexistence with hyponatremia often differentiates the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) from most other causes of hyponatremia. We report clearance studies in 5 cases of hyponatremia and hypouricemia that were not due to SIADH. One had metastatic pancreatic carcinoma with ascites, edema, hypoalbuminemia and hypophosphatemia. Two had adenocarcinoma of the lung with metastasis to the brain in 1, 1 had disseminated cryptococcus and 1 had Hodgkin's disease. None received radiation or known nephrotoxins at least 4 months prior to study. None had serum creatinine greater than 106.1 mumol/l (1.2 mg/dl). Two had postural hypotension and hyponatremia that responded to saline therapy. Fluid restriction corrected the hyponatremia in all patients, but the hypouricemia, high fractional excretion (FE) of urate, and high urine sodium concentration persisted. In 2 patients studied, ADH was appropriately suppressed after volume repletion but there was a defect in free water clearance due to high renal solute excretion. In contrast to patients with SIADH who correct their defect in renal urate transport with correction of hyponatremia by water restriction, our patients appear to have a persistent renal urate transport defect and abnormality in sodium conservation. Elevated FE urate of greater than 10% after correction of hyponatremia can thus differentiate these patients from SIADH. The diametrically opposing goals of fluid therapy emphasize the importance of differentiating one group from the other.
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PMID:Hyponatremia and hypouricemia: differentiation from SIADH. 235 Sep 4

In this study, the author intended to examine the validity of the inhaled hydrogen gas clearance method (i-H2) for determination of the hepatic blood flow (HBF), and also to show some applicabilities of the method in experimental animals and patients with liver diseases. Simultaneous determinations of HBF by i-H2 and electromagnetic flowmetry in rabbits revealed an excellent correlation between the values obtained by the two methods. Moreover, HBF in rabbits measured by i-H2 varied in parallel with that by thermocouple flowmetry or laser Doppler velocimetry after administration of norepinephrine, propranolol or glucagon. In carbon tetrachloride-treated rats, HBF measured by i-H2 correlated better with the severity of damage in the sinusoidal structure than the severity of hepatic cell injury or the serum levels of transaminases. HBF as determined by i-H2 was significantly decreased in acute hepatitis (AH), chronic inactive hepatitis (CIH), chronic active hepatitis (CAH), liver cirrhosis (LC) and fatty liver. Reduced HBF in AH returned to normal during recovery of the disease. The ratio of HBF in tumor/normal tissue was greater than 1.0 for hepatocellular carcinoma in contrast to the ratio of less than 1.0 for metastatic liver carcinoma. Propranolol caused a decrease in HBF by 31%, and vasopressin by 39% in patients with CIH or LC. In contrast, glucagon induced its increase by 65%, 35% and 17%, respectively, in patients with CIH, AH and LC.
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PMID:[Measurement of hepatic blood flow by the hydrogen gas clearance method. Experimental and clinical observations]. 236 96

Small cell carcinomas of the prostate gland are rare, and their histogenesis and clinical behavior remain poorly defined. We report a case with antidiuretic hormone secretion, which demonstrates direct transformation of the adenocarcinoma into the small cell component. The adenocarcinoma reacted positively for prostatic antigen, and negatively for carcinoembryonic antigen and neuron specific enolase, whereas the small cell component was negative for prostatic antigen, and positive for carcinoembryonic antigen and neuron specific enolase. At biopsy this was interpreted as denoting 2 separate tumors: one of prostatic and the other of nonprostatic origin. The clinical course was rapidly fatal but otherwise manifested the metastatic pattern of prostatic carcinoma. We caution that immunohistochemical reactions may be misleading if not interpreted in the context of other findings in the case. This case is labeled as a small cell carcinoma rather than a poorly differentiated adenocarcinoma of the ordinary type because the tumor exhibited morphological, immunohistochemical and biological features typical for that neoplasm.
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PMID:Small cell carcinoma of the prostate gland with inappropriate antidiuretic hormone secretion: morphological, immunohistochemical and clinical expressions. 242 10

Surgical hypophysectomy performed in 18 cases with hormone-dependent carcinoma resulted in tumour regression in 38.8% of the cases, and pain relief in 88%. Neuroadenolysis performed 170 times on 130 cases resulted in pain relief in 94% with hormone-dependent carcinoma, and 70% with non-dependent carcinoma. The clinical investigations, following performance of neuroadenolysis, indicate suppressed pituitary function, significant increase of ACTH, thyrotropin-releasing hormone and vasopressin in the cerebrospinal fluid (CSF), delay of long latencies in somatosensory evoked potential and increased pain threshold of C-fibres. Increase of beta-endorphin in CSF was very brief. Though the exact physiological activity in pain sensation of those peptides other than endorphins still remains obscure, increase of the peptides which are mainly synthesized in the hypothalamopituitary axis, along with suppressed pituitary function, is considered to exert a long-lasting suppressive effect on the mediation and perception of cancer pain through C-fibres and the central nervous system.
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PMID:The pituitary as a target of antalgic treatment of chronic cancer pain: a possible mechanism of pain relief through pituitary neuroadenolysis. 243 39

A case of Eaton-Lambert myasthenic syndrome associated with inappropriate secretion of antidiuretic hormone is reported. This case included a demyelinizing peripheral neuropathy and was related to a small-cell carcinoma of the lung. Twelve similar cases appeared in the literature, most of them associated with small-cell carcinoma or undifferentiated lung tumors. Etiologic and diagnostic aspects of these syndromes are discussed. When isolated, their causes are various, including the classic context of the paraneoplastic syndromes. Their association is highly suggestive of a lung carcinoma and must enable to make an early diagnosis by use of all possible means of detection.
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PMID:[Lambert-Eaton and Schwartz-Bartter syndromes and peripheral neuropathies associated with bronchial carcinoma: apropos of a case]. 284 May 62

Review of clinical data from 350 patients with small-cell lung cancer (SCLC) revealed hyponatremia (sodium less than 130 mEq/L) attributable to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in 40 patients (11%). Although hyponatremia was severe in most instances (median, sodium 117 mEq/L), symptoms attributable to water intoxication were identified in only 27% of hyponatremic episodes. Development of SIADH showed no correlation with clinical stage, distribution of metastatic sites, sex, or histologic subtype of small-cell carcinoma. SIADH occurred most often with initial presentation (33 of 40), and resolved promptly (less than 3 weeks) with initiation of combination chemotherapy in 80% of evaluable patients. The presence of SIADH did not influence response to chemotherapy or overall survival as an independent variable. However, in five patients profound hyponatremia developed immediately following primary cytotoxic therapy (range, one to five days). Despite initial control of SIADH, dilutional hyponatremia recurred in 70% of patients with tumor progression. Our findings suggest that development of clinically demonstrable SIADH in patients with SCLC is dependent on functional properties of the neoplastic cells, rather than tumor burden or metastatic site. The potential for development of clinically significant hyponatremia early in the course of cytotoxic therapy emphasizes the need to closely monitor patients, particularly those receiving chemotherapy regimens requiring substantial intravenous hydration.
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PMID:The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in small-cell lung cancer. 301 6

In the early 1980s, the French pharmaceutical firm Roussel-Uclaf developed a strong progesterone antagonist called RU-486, which exhibits strong antiglucocorticoid and weak antiandrogenic effects. The use of RU-486 in the middle to late luteal phase causes uterine bleeding after exogenous addition of human chorionic gonadotropin hindering nidation. Thus, progesterone antagonists could be used as once-a-month contraceptives. During pregnancy, RU-486 binds to decidua and leads to bleeding because of the release of trophoblasts resulting in luteolysis. The release of prostaglandins increased the contractility of the myometrium, induces the dilatation of the cervix, and prevents implantation. Women aborted in 85% of cases when RU-486 was used within 10 after missed menstruation. By the 7th to 8th week of pregnancy, the rate dropped to 70%. In advanced pregnancy after premedication with RU- 486, uterine susceptibility to prostaglandins is increased. RU-486 induces negative feedback in corticotropine releasing factor (CRF) and in the ACTH-system, leading to increased ACTH-cortisone-and arginine- vasopressin-(AVP-) values in serum. Although RU-486 was successfully used in doses of 5-20 mg/kg for the treatment of a patient with Cushing's syndrome, it did not lead to increased ACTH- cortisone-, aldosterone- or PRA serum values in normal women with doses up to 100 mg/day. It is possible that RU-486 can treat mammary tumors, since it inhibits the in vitro growth of progesterone-sensitive cell lines of mammary carcinoma (MCF 7 and T 470), as indicated by the transplantation of progesterone receptor positive tumors in naked mice.
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PMID:[Antigestagens]. 306 62

We treated 34 patients with breast carcinoma metastatic to the liver and refractory to prior chemotherapy with sequential hepatic arterial infusion of cisplatin and vinblastine in an attempt to enhance their antitumor activity. Following the administration of cisplatin at 100 mg/m2 i.v., the patients received a continuous arterial infusion of vinblastine at 1.7 mg/m2 daily for 5 consecutive days. Of 33 patients evaluable for response, eleven (33%) achieved partial responses and eight (24%) had minor responses. Median time to progression for responding patients was 31 weeks (range, 6+ to 74), and median survival was 11 months (range, 5-19). The adverse effects of the regimen were considerable, and seven failures were related to treatment intolerance or major toxicity. One patient who received vinblastine 2.0 mg/m2 daily developed a transient inappropriate secretion of antidiuretic hormone. Percutaneous hepatic arterial infusion of cisplatin and vinblastine has significant activity in the treatment of breast cancer metastatic to the liver, but subjective and objective treatment intolerance hamper the therapeutic value.
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PMID:Percutaneous hepatic arterial infusion of cisplatin-vinblastine for refractory breast carcinoma metastatic to the liver. 327 74

We report the occurrence of the syndrome of inappropriate antidiuretic hormone secretion in 3 patients with breast carcinoma metastatic to the liver who received hepatic arterial infusion of vinblastine at lower doses than those previously associated with this effect. Leukopenia was severe in all patients, who additionally experienced hypokalemia with excessive kaliuresis. The etiology of the observed hypokalemia is unclear. We suspect that vinblastine may induce renal tubular dysfunction. These toxicities appear dose-related.
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PMID:Syndrome of inappropriate antidiuretic hormone secretion associated with hepatic arterial infusion of vinblastine in three patients with breast cancer. 368 84

There has been longstanding interest in the characteristics of "feeder vessels" to tumors. To develop a convenient model for assessing the determinants of the responsiveness of the arterial blood supply to tumors, we assessed by arteriography the response of the spermatic artery to norepinephrine, vasopressin, and ergonovine after implantation of Walker carcinoma in the testis of the rat. Loss of response to norepinephrine of the spermatic artery supply to the tumor occurred by the fourth day of tumor growth in this model, along the entire length of the spermatic artery. As expected, there was sustained vasoconstriction of the contralateral spermatic artery to the normal testis in response to norepinephrine. Vasopressin and ergonovine exerted no effect, so that the specificity of the loss of response to norepinephrine remains unclear. The spermatic artery provides an accessible and convenient model for studying the blood supply to tumors.
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PMID:Autonomy extends to the arterial supply of rapidly growing tumors. Studies on the feeder vessel to carcinoma in rat testis. 372 1


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