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)

An autopsy case of a 67-year-old Japanese male is presented. He had been suffering from carcinoid syndrome for 5 years and showed a typical picture of carcinoid heart disease. In Japan, carcinoid heart disease is rare and we can find only four reported cases (33% of reported carcinoid syndrome). The patient had high urinary secretion of 5-HIAA and high serum serotonin, and finally he died of heart failure and bronchopneumonia. The primary site of this carcinoid tumor was of the bronchus of the right B10c , and it had large hepatic metastases. Electronmicroscopically, the tumor cells had secretory granules measuring 1500-3500 A in diameter. Immunohistochemically, the tumor cells were markedly positive for human chorionic gonadotropin (hCG) and antidiuretic hormone (ADH) and positive for serotonin, in both the primary site and hepatic metastases. Characteristic fibrous plaques were detected in the right atrium, tricuspid valve, right ventricle, and left atrium. Electron-microscopically, the fibrous plaques consisted of smooth muscle cells and myofibroblasts surrounded by basement membrane-like material. The abundant matrix of the fibrous plaques contained acid mucopolysaccharide, microfibrils and collagen fibers. The same fibrous plaques were also found in hepatic veins. Furthermore, retroperitoneal fibrosis was present, which showed proliferation of myofibroblasts, fibroblasts and immature mesenchymal cells.
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PMID:Cardiovascular lesion of carcinoid syndrome. An autopsy case of bronchial carcinoid. 673 Sep 65

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.
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PMID:Nitric oxide inhibition sustains vasopressin-induced vasoconstriction. 773 17

A 62-year-old male with small cell lung cancer (SCLC) associated with Cushing's syndrome and diabetes insipidus (DI) is reported. The patient was referred to our hospital for treatment of SCLC. A diagnosis of paraneoplastic Cushing's syndrome was made on the basis of an elevated serum ACTH (623.5 pg/ml) level, elevated excretion of urinary 17-OHCS (18.01 mg/day), obesity, hypertension, hyperglycemia, persistent hypokalemia, alkalosis, and no history of diabetes mellitus. He was also diagnosed as having DI based on polyuria and polydipsia, low specific gravity of the urine (1.007-1.010), low serum ADH (1.4 pg/ml) level, normal plasma osmolarity (29 mOsm/kg H2O), and the results of water deprivation test. DI and a left visual field defect was suggestive of metastasis to the pituitary region, but no lesion was detected by either CT scan or MRI scan. The patient failed to show a good response to intensive chemotherapy, and died of the tumor five months after commencing chemotherapy. Post-mortem examination revealed metastases to the hypothalamic-neurohypophyseal region, lungs, liver, adrenal glands, bone, bone marrow, and hilar and mediastinal lymph nodes.
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PMID:[A case of small cell lung cancer associated with diabetes insipidus and Cushing's syndrome]. 839 May 89

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

In a minority of patients with malignant tumors, signs and symptoms develop that cannot be explained on the basis of the mass effect produced by the primary tumor or its metastases, or production of a hormone normally associated with the tissue type that has given rise to the malignant tumor; these peculiar symptom complexes are known as paraneoplastic syndromes, and may be divided into endocrinologic, dermatologic, hematologic, neurologic, and osteoarticular manifestations. In the head and neck region in particular, the syndrome of inappropriate antidiuretic hormone production (SIADH, or Schwartz-Bartter syndrome) is a well-recognized form of paraneoplastic syndrome that may accompany head and neck malignancies. Most of such tumors are squamous carcinomas, with lesser numbers of olfactory neuroblastomas, small cell neuroendocrine carcinomas, adenoid cystic carcinomas, and undifferentiated carcinomas; sarcoma was reported in only a single instance. The lesions associated with the development of SIADH have most often been located in the oral cavity, and less often in the larynx, nasopharynx, hypopharynx, nasal cavity, maxillary sinus, parapharyngeal space, salivary glands, and oropharynx. Key features of SIADH include serum hypo-osmolality; an unexpectedly high urinary specific gravity; an absence of edema or dehydration; normal adrenal, thyroid, and renal function; hyponatremia; and an elevation of plasma vasopressin.
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PMID:Syndrome of inappropriate antidiuretic hormone secretion associated with head neck cancers: review of the literature. 934 88

A 44-year-old woman with Marie-Bamberger's syndrome and diabetes insipidus had a lung tumour with mediastinal metastases, but no signs of metastases to the hypothalamus or pituitary gland. A week after removal of the tumour, the joint pain, polyuria and polydipsia disappeared. The tumour was diagnosed histopathologically as a moderately differentiated adenocarcinoma with focal neuroendocrine cell differentiation and dispersed cells reacting with antisera against neurone-specific enolase, S-100 protein, neuropeptide Y, follicle-stimulating hormone, substance P, vasoactive polypeptide (VIP), adrenocorticotropic hormone and pancreatic polypeptide (PP) as well as to one of three tested antisera raised against antidiuretic hormone (ADH). It was suggested that Marie-Bamberger's syndrome might be caused by one of these immunoreactive substances or by a substance that shares an amino acid sequence with one of these neuroendocrine peptides. It was also suggested that the tumour might produce an ADH-like substance which might have an ADH-antagonist effect.
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PMID:Recovery from Marie-Bamberger's syndrome and diabetes insipidus after removal of a lung adenocarcinoma with neuroendocrine features. 956 47

The case of a previously healthy 63-year-old female with metastatic adenocarcinoma to the hypothalamus presenting with central diabetes insipidus is presented. The patient was found to have metastatic disease isolated to her hypothalamus on brain magnetic resonance imaging as well as a water deprivation test consistent with central diabetes insipidus. The patient had a decrease in symptoms of polyuria and polydypsia as well as a decrease in urine volumes after treatment with intranasal vasopressin. Even though a rare occurrence, physicians should consider metastatic adenocarcinoma in patients with recent-onset polyuria and polydypsia.
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PMID:Metastatic adenocarcinoma presenting with central diabetes insipidus. 961 23

Nephrogenic diabetes insipidus was diagnosed in a dog with an intestinal leiomyosarcoma. The diagnosis of nephrogenic diabetes insipidus was made on the basis of results of serum biochemical tests, urinalyses, and a water-deprivation test, along with a lack of response to exogenous administration of vasopressin following the water-deprivation test. The temporal association between resection of the intestinal mass and resolution of clinical signs of diabetes insipidus (i.e., polyuria and polydipsia) and between recurrence of clinical signs and detection of metastatic disease suggests that there may have been a causal relationship, and nephrogenic diabetes insipidus may have developed as a paraneoplastic syndrome in this dog.
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PMID:Nephrogenic diabetes insipidus in a dog with intestinal leiomyosarcoma. 1061 14

An autopsy case of primary small cell carcinoma (SCC) of the prostate in a 68-year-old man is reported. The patient was admitted to hospital because of a bloody stool and suspected rectal cancer. However, a diagnosis of prostate cancer was made on the basis of a digital rectal examination, the serum level of prostate-specific antigen, and a needle biopsy of the prostate. The patient also experienced a syndrome of inappropriate secretion of antidiuretic hormone. He died 29 days after admission. At autopsy, the tumor had invaded the rectum, bladder and pelvic peritoneum. Metastases to the heart, vertebrae and lymph nodes were observed. Microscopically, the tumor was composed of small round cells that showed a solid growth pattern. Rosette formations were observed. Immunohistochemically, the tumor cells were positive for a prostatic epithelial marker and neuroendocrine markers. A high level of antidiuretic hormone was detected in the tumor tissue. To our knowledge, this is the first reported case of SCC of the prostate in which both a prostatic epithelial marker and neuroendocrine markers have been found in the same tumor. This finding supports the hypothesis that SCC of the prostate originates from a multipotential stem cell of the prostatic epithelium.
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PMID:Small cell carcinoma of the prostate expressing prostate-specific antigen and showing syndrome of inappropriate secretion of antidiuretic hormone: an autopsy case report. 1462 57

We can define paraneoplastic syndromes as a combination of effects occurring far from the original location of the tumour and independently from the local repercussion of its metastases. Paraneoplastic hormonal syndromes depend on the secretion of hormonal peptides or their precursors, cytokines and, more rarely, thyroidal hormones and Vitamin D, which act in an endocrine, paracrine or autocrine way. Sometimes, paraneoplastic syndromes can be more serious than the consequences of the primary tumour itself and can precede, develop in parallel, or follow the manifestations of this tumour. It is important to recognise a paraneoplastic hormonal syndrome for several reasons, amongst which we would draw attention to three: 1) It can lead to the diagnosis of a previously undetected, underlying malign or benign neoplasia; 2) It can dominate the clinical picture and thus lead to errors with respect to the origin and type of primary tumour; and 3) It can follow the clinical course of the underlying tumour and thus be useful for monitoring its evolution. The molecular mechanisms responsible for the development of these syndromes are not well-known, but it is believed that they might be inherent to the mutations responsible for the primary tumour or depend on epigenetic factors such as methylation. In this review, we consider the following paraneoplastic hormonal syndromes: malign hypercalcaemia, hyponatraemia (inappropiate secretion of the antidiuretic hormone), ectopic Cushing's syndrome, ectopic acromegaly, hypoglycaemia due to tumours different from those of the islet cells and paraneoplastic gynaecomastia; we make a brief final reference to other hormones (calcitonin, somatostatin, and VIP).
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PMID:[Paraneoplastic hormonal syndromes]. 1615 18


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