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)

The purpose of this report is to alert the clinician that hyponatremic patients with CNS disease do not necessarily have a syndrome of inappropriate secretion of antidiuretic hormone. We describe a patient with hyponatremia and carcinomatous meningitis whose volume contraction resulted from striking urinary sodium losses. Although no longer even alluded to in reviews of hyponatremia, cerebral salt wasting appears to be a real clinical entity that warrants further investigation.
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PMID:Cerebral salt wasting in a man with carcinomatous meningitis. 663 41

Patients with intracranial disorders are prone to develop hyponatremia with inability to prevent the loss of sodium in their urine. This was originally referred to as "cerebral salt wasting," but more recently is thought to be secondary to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Blood volume determinations were made in 12 unselected neurosurgical patients with intracranial disease who fulfilled the laboratory criteria for SIADH. Ten of the 12 patients had significant decreases in their red blood cell mass, plasma volume, and total blood volume. The finding of a decreased blood volume in patients who fulfill the laboratory criteria for SIADH is better explained by the original concepts of cerebral salt wasting than by SIADH. The primary defect may be the inability of the kidney to conserve sodium.
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PMID:Hyponatremia in intracranial disease: perhaps not the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). 729 68

Renal phosphate wasting related to a tumor (oncogenous osteomalacia) is a rare disorder usually associated with benign mesenchymal tumors. In this article, the authors describe a man with renal phosphate wasting and the syndrome of inappropriate antidiuretic hormone associated with small cell carcinoma. Chemotherapy markedly reduced tumor burden and was associated with normalization of renal phosphate handling and serum sodium. With recurrence, renal phosphate wasting and the syndrome of inappropriate antidiuretic hormone developed again, with the additional complication of hypercortisolism secondary to ectopic corticotropin production. The authors report the rare occurrence of renal phosphate wasting with small cell carcinoma (5 previously reported cases) and the unique co-existence of this paraneoplastic syndrome with the syndrome of inappropriate antidiuretic hormone and ectopic corticotropin production.
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PMID:Case report: renal phosphate wasting, syndrome of inappropriate antidiuretic hormone, and ectopic corticotropin production in small cell carcinoma. 760 39

Cisplatin is an antineoplastic agent. Several nephrotoxic effects are associated with its use including chronic and acute renal failure, renal magnesium wasting, and polyuria. We have investigated polyuria in groups of rats treated with cisplatin at doses of 2.5 and 5 mg/kg body weight given once weekly for 3 weeks to determine possible mechanisms of this impairment. After cisplatin administration, glomerular filtration rate was reduced and significant increases in sodium and water loss were also seen. These changes were associated with decreases in urinary cAMP. Inner medullary collecting duct (IMCD) cells were removed from these animals and were stimulated with graded doses of vasopressin. Cells from cisplatin-treated rats showed an impaired response in cAMP generation to vasopressin stimulation as compared to cells from normal animals. To determine more precisely the site of impairment, the adenylate cyclase complex of the IMCD cells was further studied with forskolin and NaF. Forskolin was used to probe the catalytic unit activating adenylate cyclase, and NaF the guanine nucleotide regulatory protein (G protein). In response to forskolin, cells from cisplatin-treated rats and normal rats responded similarly in generating cAMP. However, following NaF, the cAMP response was blunted in the cells from the cisplatin rats. These results suggested that the catalytic unit was not injured by cisplatin (forskolin study) but the G protein was (NaF). In conclusion, the present study suggests that the polyuria seen following cisplatin administration is associated with an end-organ resistance to vasopressin manifested by reduced cAMP generation, secondary in part or whole to a defect at the level of the G protein.
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PMID:Mechanism of polyuria after cisplatin therapy. 830 21

Hyponatremia is frequently seen in neurosurgical patients and is often attributed to inappropriate secretion of antidiuretic hormone. A number of studies in recent years have shown that hyponatremia in many patients with intracranial disease may actually be caused by cerebral salt wasting, in which a renal loss of sodium leads to hyponatremia and a decrease in extracellular fluid volume. The appropriate treatment of cerebral salt wasting fluid and salt replacement, is opposite from the usual treatment of hyponatremia caused by inappropriate secretion of antidiuretic hormone. This review summarizes the evidence in favor of cerebral salt wasting in patients with intracranial disease, examines the possible mechanisms responsible for this phenomenon, and discusses methods for diagnosis and treatment.
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PMID:Cerebral salt wasting syndrome: a review. 883 89

Symptoms and other abnormalities associated with serum sodium imbalance were studied in bedridden elderly and healthy elderly subjects. 1. A significantly higher number of the bedridden elderly suffered from chronic wasting disease. 2. The average serum sodium concentration in bedridden elderly subjects was significantly lower than in healthy subjects, as was the sodium intake and the sodium content in urine, which indicate that the bedridden elderly subjects suffered from chronic sodium deficiency. 3. The bedridden elderly subjects had high levels of plasma PRA and antidiuretic hormone, and their aldosterone levels were low, which indicate that their condition was associated with a decrease in available circulating plasma, hypersecretion of antidiuretic hormone, and a decline in the ability to retain sodium. 4. Measurement of 24-hr creatinine clearance, albumin, and beta 2-microglobulin in urine revealed that bedridden elderly subjects had high levels of renal dysfunction, the result of which may a disturbance in water excretion. Abnormalities in serum sodium levels in the bedridden elderly subjects were related to a chronic deficiency in sodium intake, which reduced their ability to maintain sodium levels and impaired their renal function. Iatrogenic factors are likely to play an important role in the genesis of this condition, and should be taken into account in during management.
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PMID:[Serum sodium imbalance in the bedridden elderly. Part One: Realities and problem of management]. 879 57

Hyponatremia is a common potential complication in cancer patients. It can be related to anticancer medical therapy. Vincristine, vinblastine, cisplatin and cyclophosphamide are the chemotherapeutic agents most frequently associated with hyponatremia. More recently, analogs such as carboplatin and ifosfamide have also been incriminated. Hyponatremia is also associated with new immunomodulators (interferon, interleukin-2 and levamisole) and monoclonal antibodies. The mechanism by which all these drugs act on the sodium steady state is only partially known. The syndrome of inappropriate antidiuretic hormone secretion is described secondary to vinca alkaloids and cisplatin and possibly with alkylating agents. Renal salt wasting is described with platinum compounds.
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PMID:Hyponatremia related to medical anticancer treatment. 888 27

A prospective observational study of the pathophysiology of sodium and water disorders in patients with pituitary region tumours after surgical excision was carried out in 20 patients. Serial pre-operative and post-operative fluid and sodium balance, plasma and urine elctrolyte biochemistry and their derived parameters, and circulating hormones associated with fluid balance, atrial natriureic peptide (ANP) and antidiuretic hormone (ADH) were documented to correlate with the patients' clinical conditions. Ten out of these twenty cases developed diabetes insipidus (DI) requiring ADH replacement therapy, although in the majority (6 cases), this way only a transient event. Of the nine patients who developed hyponatraemia, six had symptoms such as impaired consciousness and convulsions. Four patients developed alternating hypoatraemia and hypernatraemia, which constituted a difficult group, where appropriate sodium and fluid management, and ADH replacement therapy were based upon twice daily plasma and urine biochemistry and their derived parameters. Whilst DI in this group of patients was the result of a low circulating ADH level, hyponatraemia was not associated with an exaggerated ADH activity (6.0 +/- 2.3 vs 7.4 +/- 2.3 pmol/ml, mean +/- SEM). Rather, hyponatraemia was strongly associated with an elevated circulating ANP concentration (82.4 +/- 10.5 vs 30.0 +/- 3.1 pmol/ml, mean +/- SEM, p < 0.001), resulting in salt wasting and hypovolaemia.
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PMID:Water and sodium disorders following surgical excision of pituitary region tumours. 889 Sep 88

Electrolyte abnormalities are common medical complications of traumatic brain injury (TBI). Hyponatremia is the most common of these disorders. The syndrome of inappropriate antidiuretic hormone and cerebral salt-wasting are the most well known causes of hyponatremia following TBI. In the presence of polydipsia and polyuria, psychogenic polydipsia should be included in the differential diagnosis. It is important to distinguish among these entities because treatment differs to such an extent that improper diagnosis may lead to a worsening of the patient's condition. We present a patient who presented with a new onset of polyuria and polydipsia after sustaining a TBI. Evaluation, including monitoring of fluid intake and output, serum and urine sodium and osmolarity, as well as a fluid deprivation test revealed the cause to be psychogenic polydipsia. The patient's symptoms improved after institution of a behavioral program and fluid restriction. Various models of drinking behavior have been used to identify the site of dysregulation. Dopaminergic, cholinergic, and hippocampal etiologies have been implicated in this abnormality of fluid homeostasis. If disorders of these systems can lead to psychogenic polydipsia, it is reasonable to believe that a person who has sustained a TBI would be at higher risk of developing psychogenic polydipsia.
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PMID:Psychogenic polydipsia after traumatic brain injury. A case report. 920 12

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


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