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)

Although the majority of colorectal carcinomas express carcino-embryonic antigen (CEA), systemic anti-CEA antibody administration is an ineffective treatment for colorectal liver metastasis. A xenograft model of human colorectal carcinoma in the rat was used to determine anti-CEA antibody uptake into liver metastases. The influence of systemic (iliolumbar vein) or regional (gastroduodenal artery) delivery and effects of regional delivery of histamine, angiotensin II and vasopressin on anti-CEA antibody uptake by metastases were examined. Systemic antibody delivery achieved a median tumour:liver antibody uptake ratio of 1.60 (interquartile range (i.q.r.) 1.02-2.51). Regional delivery resulted in a similar median ratio of 1.61 (i.q.r. 1.22-2.46). Histamine and antibody delivered regionally produced a median tumour:liver ratio of 3.15 (i.q.r. 2.50-4.27), which was significantly greater than that obtained with systemic delivery (P = 0.004). Regional infusion of angiotensin resulted in a median (i.q.r.) ratio of 2.23 (1.58-2.49) and vasopressin in 2.15 (1.41-2.60), values that were not significantly different from those found with systemic or regional delivery alone. When both angiotensin and histamine were infused with antibody, the median tumour:liver ratio was 3.09 (i.q.r. 2.22-4.31), significantly greater than for systemic delivery (P = 0.01) but not significantly different from that obtained following the addition of histamine alone (P = 0.94). Histamine significantly increases antibody uptake in a model of liver metastasis and may improve the effectiveness of targeted immunotherapy in the treatment of colorectal liver metastasis.
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PMID:Histamine but neither angiotensin nor vasopressin increases antibody uptake into xenograft colorectal liver metastases. 842

Cushing's syndrome occurs rarely; in analyzing 50 cases studied at our institution we discuss the following aspects: syndromatic diagnosis, etiologic differentiation into the 3 categories of the syndrome, and therapeutic strategies for each variety. We postulate that non-endocrinologists should be responsible for the syndromatic diagnosis, easily done by using 2 simple tools: the measurement of basal free urinary cortisol and the performance of an overnight suppression of the adrenal axis with 1 mg of dexamethasone (Nugent's test). In contrast, the etiologic diagnosis and the therapeutic interventions should be strictly restricted to highly specialized institutions having well seasoned endocrinologists, a reliable endocrine laboratory, easy access to computed tomographies of the brain and abdomen as well as to nuclear resonance imaging of the brain. The usefulness of our in-house devised vasopressin challenge following overnight dexamethasone suppression for the etiologic diagnosis is highlighted. Neurosurgical expertise in the transsphenoidal approach to the pituitary gland as well surgeons well experienced in adrenal surgery are a must to offer a reasonable chance of success to patients with the syndrome. Forty one (82%) of the series were female patients, 78% were pituitary-dependent and 22% pituitary-independent Cushings. Six out of 8 (75%) of the adrenal tumors were carcinomas. Only 3 patients (6%) qualified as ectopic ACTH syndromes. The easiest variety to diagnose and treat was the adrenal adenoma (2 cases); adrenal carcinomas were always incurable. The ectopic ACTH syndrome was amenable to successful medical treatment with ketoconazole or surgical resolution with complete resection of the offending tumor (1 of 3 cases) or bilateral adrenalectomy (2 of 3 cases) Pituitary-dependent Cushings are quite tricky to diagnose and difficult to treat. Transsphenoidal resection of the offending microadenoma was successful in only 43.5% (10/23) of cases and we experienced 3 recurrences of the syndrome even after 8 years of successful removal of the pituitary adenoma. The remainder had to be cured by bilateral adrenalectomy. Seven out of 39 patients with Cushing's disease (18%) ultimately died for a variety of reasons; six out of 6 patients (100%) with adrenal carcinoma died of dissemination; two out of 2 adrenal adenomas cured and 1 out of the 3 ectopic ACTH syndromes died of dissemination of a malignant thymic carcinoma. We conclude that Cushing's syndrome is a serious, underdiagnosed disorder, which should be suspected and diagnosed by the non specialized physician and then referred to a specialized center for expert etiologic diagnosis and surgical therapy.
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PMID:[Cushing's syndrome: review of a national caseload]. 852 77

A case of syndrome of inappropriate antidiuretic hormone secretion (SIADH) in a patient with suboptimally cytoreduced stage III papillary serous surface carcinoma of the peritoneum is described. After the primary surgery, the patient refused further therapy. Within a month bilateral pleural effusions and abdominal ascites compelled the patient to accept treatment with carboplatin and cyclophosphamide. Ten days following the chemotherapy, she was admitted in a disoriented state with serum sodium of 117-mEq/L. During the evaluation, treatment, and subsequent follow-up, the diagnosis of SIADH was confirmed. Numerous disease processes have been associated with the development of SIADH; however, there have been few reports in gynecologic malignancies. Possible etiology and clinical management of this patient are briefly discussed.
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PMID:Syndrome of inappropriate antidiuretic hormone secretion in papillary serous surface carcinoma of the peritoneum. 854 63

In a 59-year-old woman suffering from the syndrome of inappropriate antidiuretic hormone secretion, a small cell carcinoma of the uterine cervix was detected. The tumor was immunoreactive for antidiuretic hormone as well as for neuron specific enolase, chromogranin A, and Leu-7, but not vimentin. Electron microscopic examination of the tumor revealed neurosecretory granules. To our knowledge, this is only the second report of the syndrome of inappropriate antidiuretic hormone secretion with small cell carcinoma of the uterine cervix and the first one confirmed immunohistopathologically.
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PMID:Small cell carcinoma of the uterine cervix with syndrome of inappropriate antidiuretic hormone secretion. 872 79

A 58-year-old postmenopausal woman with primary ovarian serous carcinoma presented with the syndrome of inappropriate antidiuresis (SIAD). Preoperative workup showed serum sodium level of 110 mEq/liter and antidiuretic hormone level of 3.3 pg/ml. The serum and urine osmolarity were 239 and 371, respectively. Antidiuretic hormone was demonstrated in tumor cells by immunohistochemistry. To the best of the authors' knowledge, this represents the first case of SIAD due to primary ovarian tumor.
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PMID:Syndrome of inappropriate antidiuresis in ovarian serous carcinoma with neuroendocrine differentiation. 881 40

We report an 8-year-old boy with a primary intrasellar mixed germ-cell tumor who underwent the trans-sphenoidal approach for tumor removal. Initially he suffered from diabetes insipidus. Precocious puberty and left abducens nerve palsy were also observed. Elevation of serum testosterone, beta-human chorionic gonadotropin (HCG), and alpha-fetoprotein (AFP) were found on admission. The histological study revealed mixed cellular types of tumor including germinoma, choriocarcinoma, embryonic cell carcinoma, and teratoma. Postoperative radiation to a total of 5000 cGy was performed. Adjuvant chemotherapy was administered before and after radiation. The boy was disease-free during a 6-month follow-up period. Follow-up magnetic resonance imaging showed no presence of tumor. The signs of precocious puberty disappeared, and the diabetes insipidus was easily controlled. The abducens nerve regained normal function. Serum HCG, AFP, and testosterone levels all returned to normal. Serum antidiuretic hormone increased to reach the lower limit of the normal range.
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PMID:Primary intrasellar mixed germ-cell tumor with precocious puberty and diabetes insipidus. 908 1

The syndrome of inappropriate secretion of antidiuretic hormone (ADH) or SIADH has been reported in various disorders. We report a pediatric patient with nasopharynx carcinoma who may have developed a clinical SIADH with severe hyponatremia and generalized seizure during the administration of intravenous hydration. We propose that the inappropriately high plasma level of ADH led to the inability to excrete sufficient amounts of free water during a hyperhydration protocol with a relatively hypotonic fluid, which resulted in acute hyponatremia and central nervous system involvement. To avoid this complication, intravenous hydration before chemotherapy in children with nasopharynx carcinoma should be performed at a slower infusion rate and with a sodium chloride concentration of more than half isotonic.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone in nasopharynx carcinoma. 926 Feb 57

Melanin concentrating hormone (MCH) is a cyclic peptide which regulates a broad array of functions in the mammalian brain and it may act as a paracrine factor in peripheral organs. In these studies a radiolabeled MCH derivative, the [125I]-[Phe13, Tyr19]-MCH, was synthesized and used as a tracer to perform binding experiments. A number of human or rodent cell lines displayed specific binding with [125I]-[Phe13, Tyr19]-MCH, the highest binding capacity being observed with human SVK14 keratinocytes. Saturation binding analysis with SVK14 cells indicated about 10,000 MCH binding sites per cell and a Kd of 0.7 nM for [125I]-[Phe13, Tyr19]-MCH. Surprisingly, the iodinated [Phe13, Tyr19]-MCH displayed about 10-fold higher affinity (Ki approximately 3.0 nM) for the putative MCH receptor than the noniodinated form (Ki approximately 25-30 nM). Competition binding analyses comparing various MCH-related peptides revealed a similar low binding potency for all these peptides (Ki approximately 65-160 nM). Strikingly, rat ANP and rat/human CNP but not rat BNP displaced [125I]-[Phe13, Tyr15]-MCH with Ki approximately 210-365 nM and may be due to topological similarities instead of partial sequence identities between MCH and some of the natriuretic peptides. However, other peptides such as CRF, alpha MSH, Arg-vasopressin, and MGOP-peptide I did not compete with the radioligand. Finally, the molecular mass of the MCH binding sites on SVK14 cells was estimated to be 47 kDa by crosslinking and SDS-PAGE experiments. Taken together, our data revealed the widespread expression of MCH binding sites on mammalian cells, particularly on skin carcinoma cells. However, the low affinity of these sites for the native MCH and MCH-related peptides as well as competitivity with ANP and CNP indicates that further biochemical and functional characterizations are needed to validate them as genuine physiological MCH receptors.
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PMID:Melanin-concentrating hormone binding sites in human SVK14 keratinocytes. 943 58

We describe a patient who had metastatic carcinoma of the stomach and severe headaches, weakness, and diplopia. The patient had meningeal carcinomatosis that was confirmed by examination of the cerebrospinal fluid after computed tomography of the brain was normal. Weakness was explained by the finding of hyponatremia due to the syndrome of inappropriate antidiuretic hormone (SIADH). We believe this is the first reported case of meningeal carcinomatosis in which stomach carcinoma caused SIADH. The differentiation between SIADH and cerebral salt wasting due to malignant tumors is emphasized.
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PMID:Meningeal carcinomatosis and syndrome of inappropriate antidiuretic hormone in a patient with metastatic carcinoma of the stomach. 982 97

We have investigated the effects of desmopressin (DDAVP), a synthetic analog of the natural hormone vasopressin, on experimental lung colonization of mammary tumor cells using a syngeneic BALB/c mouse model. Coinjection of DDAVP (1-2 microg/kg body weight) at the time of i.v. inoculation of F3II carcinoma cells or LM3 adenocarcinoma cells significantly inhibited the formation of experimental lung metastases. In both cases, the number of pulmonary nodules was reduced about 70%. Inhibition of metastasis was also obtained with i.v. administration of DDAVP 24 h after tumor cell inoculation. Interestingly, the inhibition of lung metastasis was not due to direct cytotoxic effects of DDAVP on mammary tumor cells. The in vitro formation of multicellular aggregates in the presence of citrated plasma from control and DDAVP-treated mice was also examined. Control plasma rapidly induced a significant tumor cell aggregation. In contrast, in the presence of plasma from DDAVP-treated mice, tumor cells remained as a single cell suspension. DDAVP may help to dissolve the protective fibrin shield of circulating tumor cells. Our data suggest, for the first time, that adjuvant DDAVP therapy may impair successful implantation of circulating mammary tumor cells.
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PMID:Antimetastatic effect of desmopressin in a mouse mammary tumor model. 1061 3


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