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)

Forty-one patients with newly diagnosed small cell anaplastic lung cancer were evaluated for abnormalities in water homeostasis. Each patient underwent a standard water load (SWL) test. Overall, 68% had abnormalities in the SWL test. Abnormalities were found in 47% of the patients with carcinoma clinically limited to one hemithorax and in 86% of the patients with more extensive carcinoma. The determination of urinary antidiuretic hormone levels was available for 27 patients. Abnormally elevated levels were found in 44% of those patients. Forty-six patients had clinically detectable syndrome of the inappropriate secretion of antidiuretic hormone (SIADH); in 12% of patients water restriction was necessary. The incidence of detectable abnormalities in water homeostasis in this study was higher than has been previously recognized. The SWL test is a sensitive and useful means of determining the presence of impaired water handling in patients with small cell carcinoma of the lung.
Cancer 1980 May 01
PMID:Abnormalities in water homeostasis in small cell anaplastic lung cancer. 737 38

The clinical syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with malignancy cannot be distinguished from a similar metabolic abnormality found in patients with non-malignant conditions. It is, nevertheless, widely accepted that SIADH associated with malignancy is due to the "ectopic" tumour production of arginine vasopressin (AVP). This view is challenged after scrutiny of available data. Since some malignant or non-malignant tissues may produce neurophysins, the presence of "ectopic" AVP in tumour tissue may be explained by active binding of AVP from the circulation by neurophysins. On the other hand, the absence of detectable AVP in tumour accompanied with SIADH suggests excess AVP secretion from the posterior pituitary or hyponatraemia due to other, as yet unidentified, antidiuretic factors. The concept of "ectopic" AVP may be false.
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PMID:Is the evidence for ectopic antidiuretic hormone watertight? 739 18

The incidence of SIADH (the syndrome of inappropriate antidiuretic hormone secretion) was analyzed retrospectively in 43 children who received marrow-ablative chemotherapy before autografts with peripheral blood stem cells for lymphoid malignancies. SIADH was documented in three children (ages 3, 13, and 13 years) who received chemotherapy, which included high-dose methyl 6-[3-(chloroethyl)-3-nitrosoureido]-6-deoxy-alpha-D-glucopyranoside (MCNU) and cyclophosphamide, under a concomitant overhydration protocol. SIADH was manifested as frequent vomiting in two patients and as generalized seizure in one. Hyponatremia (< 125 mEq/L), hypo-osmolality (< 260 mOsm/kgH2O), and continued urinary excretion of sodium (> 30 mEq/L) were used to diagnose SIADH in these three patients. All signs and symptoms subsided within 24 hours either by fluid restriction alone (n = 1) or by supportive care including anticonvulsant and D-mannitol, or hyperhydration with saline plus 5% glucose and diuretic. None of the patients died. Careful monitoring of the serum sodium level, as well as the osmolality of plasma and urine, should be incorporated into the patient management protocol for this type of high-dose chemotherapy.
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PMID:Syndrome of inappropriate antidiuretic hormone secretion (SIADH) in children undergoing high-dose chemotherapy and autologous peripheral blood stem cell transplantation. 757 88

We describe the case of a patient with multiple paraneoplastic syndromes, six in total, associated with a non-small-cell cancer of the lung. In this single patient we found hypertrophic pulmonary osteoarthropathy, hyperkeratosis of palms and soles, erythema annulare centrifugum, syndrome of inappropriate secretion of antidiuretic hormone (SIADH), and ectopic andrenocorticotrophic hormone (ACTH) and calcitonin production.
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PMID:Non-small-cell lung cancer with multiple paraneoplastic syndromes. 758 10

The first clinical case of a patient with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) was presented by Schwartz et al. in 1957 (Am J Med 1957; 23: 529-42), describing two patients with lung cancer who developed hyponatraemia associated with continued urinary sodium loss. They postulated that the tumours led to the inappropriate release of antidiuretic hormone (ADH), later discovered to consist of arginine-vasopressin (AVP). This suggestion was later confirmed in several studies. The clinical description of the syndrome has changed little since the original observation, and the cardinal findings of SIADH are as follows: (i) hyponatraemia with corresponding hypo-osmolality of the serum and extracellular fluid, (ii) continued renal excretion of sodium. (iii) absence of clinical evidence of fluid volume depletion, (iv) osmolality of the urine greater than that appropriate for the concomitant osmolality of the plasma, i.e. urine less than maximal diluted, and (v) normal function of kidneys, suprarenal glands and thyroid glands. Measurement of AVP in plasma is not a part of the definition of SIADH. SIADH may be caused by a variety of malignant tumours, but may also be caused by various other conditions, such as disorders involving the central nervous system, intrathoratic disorders such as infections, positive pressure ventilation and conditions with decrease in left atrial pressure. Also, a large number of pharmaceutical agents have been shown to produce SIADH, including a number of cytotoxic drugs such as vincristine, vinblastine, cisplatin, cyclophosphamide, and melphalan. A broad spectrum of malignant tumours has been reported to cause SIADH; however, most of these observations have been in case reports including very few patients. This includes a number of primary brain tumours, haematologic malignancies, intrathoracic non-pulmonary cancers, skin tumours, gastrointestinal cancers, gynaecological cancer, breast-and prostatic cancer, and sarcomas. Larger series of patients have revealed that SIADH occurs in 3% of patients with head and neck cancer (47 cases out of 1696 patients), in 0.7% of patients with non-small-cell lung cancer (three cases out of 427 patients), and in 15% of cases of small-cell lung cancer (214 cases out of 1473 patients). The optimal therapy for SIADH is to treat the underlying malignant disease. If this is not possible, or if the disease has become refractory, other treatment methods are available such as water restriction, demeclocycline therapy, or, in severe cases, infusion of hypertonic saline together with furosemide during careful monitoring.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in malignant disease. 762 92

Hepatic parenchymal vasoconstriction increases cytotoxic drug uptake into hepatic metastases by increasing the tumour to liver blood flow ratio. Prolonged infusion of the vasoconstrictor vasopressin does not result in sustained vasoconstriction, and this may limit the benefit of vasopressin in infusional chemotherapy. We have assessed whether loss of vasopressin-induced vasoconstriction is mediated by nitric oxide. Hepatic and tumour blood flow were continuously monitored, in an animal hepatic tumour model, by laser Doppler flowmetry. The response to regionally infused vasopressin and the nitric oxide inhibitor N-nitro-L-arginine methyl ester (L-NAME) were assessed over a 30 min infusion period. The vasopressin-induced vasoconstrictor effect diminished after 15 min despite continued infusion. Vasoconstriction was significantly prolonged when L-NAME was infused in addition to vasopressin. The increase in tumour to normal blood flow ratio was greater over the infusion period when L-NAME was co-administered with vasopressin. Our results suggest that the loss of vasopressin-induced vasoconstriction seen in liver parenchyma after regional infusion is prevented by the nitric oxide synthase inhibitor L-name and may be mediated by nitric oxide.
Br J Cancer 1995 May
PMID:Nitric oxide inhibition sustains vasopressin-induced vasoconstriction. 773 17

Many cancers and complications of cancer treatment may cause major critical care problems. Cardiopulmonary complications include pericardial effusion, cardiac tamponade, superior vena cava syndrome, pleural effusion, pulmonary embolism, radiation pneumonitis, and toxicities related to chemotherapy. Syndrome of inappropriate antidiuretic hormone (SIADH), Cushing's disease, and hypercalcemia are common endocrine complications associated with solid tumors. Astute nursing assessment plays an important role in preventing or reducing morbidity related to these complications.
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PMID:Heart, lung, and endocrine complications of solid tumors. 780 Sep 72

A transgenic mouse model has been developed to test the involvement of ectopic neuropeptide production as a secondary factor in cancer. Mice bearing a mouse mammary tumor virus-vasopressin (MMTV-VP) fusion transgene synthesized authentic vasopressin in mammary ducts and alveoli, but this had no effect on mammary gland development and growth. Mice bearing the MMTV-VP transgene were then mated with mice bearing the MMTV-Wnt-1 transgene to produce bitransgenic animals. Two types of mammary tumor develop in MMTV-Wnt-1 mice; type A mammary adenocarcinomas are uniform with fine acinar structure composed of small epithelial cells arranged to form round cavities and elongated tubules, while adenocarcinoma type B tumors have acinar areas, cystic spaces filled with blood or fluid, intracystic papillary projections, and cords as well as sheets of cells. Compared to the MMTV-Wnt-1 mice, the bitransgenic animals developed proportionally less type B tumors. Further, type B mammary adenocarcinomas from bitransgenic mice exhibited increased proliferation and growth, as judged by mitotic index and argyrophilic nucleolar organizer region counts, compared to type B tumors from MMTV-Wnt-1 mice. These data provide evidence that ectopic neuropeptide production can modulate the development of tumors in vivo.
Cancer Res 1994 Dec 15
PMID:Ectopic vasopressin expression in MMTV-Wnt-1 transgenic mice modifies mammary tumor differentiation and pathology. 798 39

Bromocriptine, a dopaminergic agonist, inhibited the growth of human small cell lung cancer (SCLC) implanted as tumor xenografts in athymic nude mice; the effect was dose dependent. In mice bearing a SCLC with ectopic vasopressin production, plasma levels of human vasopressin-associated neurophysin decreased concomitantly. Electron microscopy of tumor tissues revealed marked degenerative changes, including pyknosis, densely aggregated chromatin masses, and vacuolization of cytoplasm after bromocriptine treatment. When a SCLC cell line, NCI-H69, was grown in semisolid medium, bromocriptine inhibited its clonal growth in a dose-related manner. Coincubation with dopamine D2 receptor antagonist, metoclopramide, or domperidone, completely blocked the inhibitory effect of bromocriptine. Receptor studies with a dopamine D2 receptor ligand, [125I]iodosulpride, showed high affinity binding sites on the membranes of SCLC cells. These results indicate that SCLC cells are enriched with dopamine D2 receptors, which may mediate the growth-inhibitory effect of bromocriptine on SCLC. Dopaminergic agonists may be useful in the medical treatment of SCLC.
Cancer Res 1994 Jul 01
PMID:Inhibition of growth of human small cell lung cancer by bromocriptine. 801 64

We found that thapsigargin (Tg), a non-phorbol ester type tumor promoter that specifically inhibits endoplasmic reticulum Ca(2+)-ATPase, transiently increased the level of cytosolic free calcium ([Ca2+]i) and subsequently induced chromatin condensation, nuclear fragmentation, and internucleosomal DNA cleavage in cultured PLC/PRF/5 human hepatoma cells. These alterations were followed by the loss of plasma membrane integrity and by cell death. Epidermal growth factor (EGF) and vasopressin similarly elevated [Ca2+]i without causing DNA fragmentation which is characteristic of apoptosis. Consequently, the elevation of [Ca2+]i itself was not sufficient for causing Tg-induced cell death. On the other hand, preculturing the cells with Tg completely suppressed Ca2+ mobilization induced by EGF and vasopressin; a result that strongly suggests that Tg depleted the endoplasmic reticulum Ca2+ pool. Such depletion is hypothesized to induce apoptotic cell death in this hepatoma cell line by changing the nuclear Ca2+ levels which probably produce a structural change in chromatin.
Cancer Lett 1994 May 16
PMID:Thapsigargin-induced persistent intracellular calcium pool depletion and apoptosis in human hepatoma cells. 801 72


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