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)

This case is a report of a male, 52 year old, heavy smoker, with a history of about 10 years of alcohol abuse (he quitted in 1993), gastric resection for ulcer (Billroth II 1970), hypoparathyroidism and macroamylasemia, died for undiagnosed pancreatic carcinoma revealed at necroscopy. The only clinical evidence of carcinoma were pulmonary metastasis and paraneoplastic syndrome characterized from hyponatriemia due to inappropriate secretion of antidiuretic hormone and elevation of seric calcium caused by parathyroid hormone related protein. In patients without endocrine abnormalities, such unusual paraneoplastic syndrome could cause hypercalcemia, but in our patient, the increased calcemia did not reach abnormal levels due to the previous hypoparathyroidism. At present time, there are no clinical reports of parathyroid related protein secretion by pancreatic carcinoma and therefore, it could speculate that this modification together with ectopic secretion of antidiuretic hormone, represent a peculiar evidence of otherwise unknown and undetectable pancreatic carcinoma.
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PMID:Hypercalcemia due to ectopic secretion of parathyroid related protein from pancreatic carcinoma: a case report. 1223 76

Alteration in liver function are not typically present in patients with uremic syndrome, but varying degrees of liver dysfunction were observed in animals with experimental uremia and, to a lesser degree, in patients with chronic renal failure. This article summarizes the data obtained during the last 2 decades on protein, carbohydrate, and lipid metabolism by the liver in uremia and molecular aspects of regulation of lipids and protein synthesis. Particular attention is given to the role of cytosolic calcium ([Ca(2+)](i)) regulation and calcium signal transduction in hepatocytes in chronic renal failure. It is proposed that the parathyroid hormone (PTH)-mediated increase in the [Ca(2+)](i) of hepatocytes in chronic renal failure is a major signal for the downregulation of hepatic receptors for PTH-PTHrP, vasopressin and angiotensin II as well as as hepatic lipase. It is possible that the mRNA of other hormone receptors and various proteins of the liver cells are affected similarly by the elevated basal levels of [Ca(2+)](i) in CRF.
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PMID:Liver metabolism in CRF. 1261 69

Hormones have an influence on many tissues and organs, including the cardio-vascular system (CVS). Depending on their activity on CVS, they can be divided into 4 groups: having hypertensive or hypotensive influence and chronotropic positive or negative action. Endocrine regulation in CVS may occur in many ways. Apart from hormones usually connected with CVS regulation, other more recently, discovered ones can act on it. A few of these act directly through specific receptors in heart or vessel wall cells, whereas some act indirectly - stimulating other neuroendocrine factors. Additionally, novel mechanisms of signal transduction have been discovered for steroid and thyroid hormones, which are independent of gene transcription regulation and are - known as "nongenomic". Hormones which increase blood pressure include: urotensin II, endothelins, angiotensin II, catecholamines, aldosterone, antidiuretic hormone, glucocorticosteroids, thyroid hormones, growth hormone and leptin. On the other hand, blood pressure can be decreased by: natriuretic peptides, the calcitonin gene-related peptide (CGRP) family, angiotensin 1-7, substance P, neurokinin A, ghrelin, Parathyroid hormone-related protein (PTHrP), oxytocin, and, sex hormones. Hormones which when appearing in excess increase the heart rate are: catecholamines, endothelins, glucocorticosteroids, thyroid hormones, leptin and PTHrP. Those which decrease the heart rate include: natriuretic peptides, substance P, neurokinin A, oxytocin, angiotensin 1-7. This paper describes the contemporary view of the functions of hormones which act on the vessel tree and heart. The particular effect of mediator depends on many circumstances i.e.: hormone concentration, receptor type. It may also undergo contraregulation. The majority of those hormones play an important role in the pathogenesis of CVS diseases', which can result in the development of new medicines.
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PMID:[Hormones and the cardiovascular system]. 1897 53

The most frequent electrolytic disorders associating with tumors are hypercalcemia and hyponatremia, which should often be dealt with on an emergency basis. Hypercalcemia is observed in around 10% of metastatic solid tumors including lung, breast, head and neck and renal cancers. In hematological malignancies, hypercalcemia is observed with a relatively high incidence in malignant lymphoma. Hypercalcemia is caused by bone metastasis or PTH-rP secreted from tumors. In other cases, it is induced by calcitriol produced from tumor. Hypercalcemia sometimes results in a fatal outcome, and should be carefully monitored. Hyponatremia presented as SIADH is sometimes caused by arginine vasopressin derived from tumors. In other cases, SIADH is induced with chemotherapeutic drugs such as cyclophosphamide and cisplatin. Neither hypercalcemia nor hyponatremia has any specific symptoms. Delayed treatment often results in severe condition, such as unconsciousness or even death. Therapy for hypercalcemia is started by infusion of normal saline, and a patient with severe hypercalcemia should be treated with bisphosphonates. Zoledronic acid is the best bisphosphonate among them at this present. Treatment of SIADH is started by water restriction. In an emergency, treatment with hypertonic saline(3-5%)should be considered together with loop diuretics. Demethyl chlorotetracycline is considerable in poor response cases, and mozavaptan hydrochloride is applicable in case of vasopressin-producing tumors. In any case, inappropriate rapid correction of hyponatremia could induce severe brain damage called CPM without careful management.
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PMID:[Treatment for the electrolytic disorders in cancer patients]. 1909

The electrolyte imbalance in advanced cancer patients, including hyperkalemia, hypercalcemia and hyponatremia, can be induced by various factors. Hyperkalemia is occasionally induced by chemotherapy for very large malignant tumors, due to tumor lysis syndrome. Hypercalcemia and hyponatremia are often observed in patients with breast cancer, renal cancer, prostate cancer, and the like, as a paraneoplastic syndrome. Some part of hypercalcemia results from osteolysis, but the majority is induced by hormonal factors, such as parathyroid hormone-related protein. One of the paraneoplastic causes of hyponatremia is antidiuretic hormone-producing tumor. These disorders could be morbid or even motile, resulting from encephalopathy or arrhythmia in some cases. However, it should be kept in mind that they could be improved or cured by prompt treatment. Recently, after approval of the molecular targeted drugs for epidermal growth factor receptors, such as cetuximab and panitumumab, the incidence of hypomagnesia with use of these monoclonal antibodies, is relatively frequent. In addition, small molecular targeted drugs, such as m-TORinhibitors and ABL kinase inhibitors, also exert adverse reactions including hypomagnesia and hypophosphatemia. Careful monitoring of the serum concentration of magnesium and phosphate ions, to which little attention was paid previously, is a key issue in these cases.
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PMID:[Cancer and electrolytes imbalance]. 2056 1

Paraneoplastic syndromes are signs or symptoms that occur as a result of organ or tissue damage at locations remote from the site of the primary tumor or metastases. Paraneoplastic syndromes associated with lung cancer can impair various organ functions and include neurologic, endocrine, dermatologic, rheumatologic, hematologic, and ophthalmological syndromes, as well as glomerulopathy and coagulopathy (Trousseau's syndrome). The histological type of lung cancer is generally dependent on the associated syndrome, the two most common of which are humoral hypercalcemia of malignancy in squamous cell carcinoma and the syndrome of inappropriate antidiuretic hormone secretion in small cell lung cancer. The symptoms often precede the diagnosis of the associated lung cancer, especially when the symptoms are neurologic or dermatologic. The proposed mechanisms of paraneoplastic processes include the aberrant release of humoral mediators, such as hormones and hormone-like peptides, cytokines, and antibodies. Treating the underlying cancer is generally the most effective therapy for paraneoplastic syndromes, and treatment soon after symptom onset appears to offer the best potential for symptom improvement. In this article, we review the diagnosis, potential mechanisms, and treatments of a wide variety of paraneoplastic syndromes associated with lung cancer.
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PMID:Paraneoplastic syndromes associated with lung cancer. 2511 39

Paraneoplastic syndromes are defined as a combination of clinical disorders associated with malignant diseases that are caused by the secretion of various substances by the tumor without, however, being caused by the direct growth and infiltration of the primary tumor, or due to the development of distant metastases. Despite the fact that lung cancer represents the number one cause of death from cancer worldwide, the new methods of treatment increase patient survival and the incidence of paraneoplastic syndromes. The most important ones of these are humoral hypercalcemia of malignancy, syndrome of inappropriate antidiuretic hormone, hyponatremia of malignancy, ectopic Cushing's syndrome, carcinoid syndrome, and hypoglycemia and are usually a poor prognostic marker. Early diagnosis of those syndromes is achieved using specific criteria and may lead to early diagnosis of the underlying malignancy. It is essential to treat them with the overriding objective of improving the patients' quality of life.
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PMID:Endocrine paraneoplastic syndromes in lung cancer. 2996 34


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