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)

Fluid, electrolyte and mineral perturbations are prevalent features of tropical disease. Hemodynamic alterations, fever, nitrogen wasting, and changes in membrane transport and acid-base balance contribute to these perturbations. Models of malaria and leptospirosis have been used to show that common hemodynamic changes in tropical disease include decreased systemic vascular resistance, increased cardiac output and increased renal vascular resistance. Blood volume is initially increased, but it decreases as disease progresses. Response to fluid loading is decreased. Diabetes insipidus is occasionally observed in malaria. Hyponatremia occurs frequently in tropical diseases, as a result of increased levels of antidiuretic hormone (vasopressin), entry of sodium into cells, sodium loss and resetting of osmoreceptors. Natriuresis and kaliuresis are observed in patients with leptospirosis. Large amounts of sodium and potassium are lost in stool as a result of diarrhea. Hypernatremia is uncommon, whereas hypokalemia caused by hyperventilation is often observed (more frequently in patients with leptospirosis and kaliuresis). During severe tropical infective episodes, hyperkalemia results from intravascular hemolysis or rhabdomyolysis, and occasionally from decreased activity of Na+,K+-ATPase. Hypocalcemia, hypomagnesemia and hypophosphatemia are common features of both malaria and leptospirosis. Loss of magnesium in the urine is uniquely associated with leptospiral nephropathy. Hypozincemia and hypocupremia can also develop during tropical infection, and might interfere with a patient's immune response. These electrolyte and mineral perturbations are transient and quickly resolve when the disease is controlled.
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PMID:Altered fluid, electrolyte and mineral status in tropical disease, with an emphasis on malaria and leptospirosis. 1822 2

The complexity of hyponatremia as a clinical problem is likely caused by the opposite scenarios that accompany this electrolyte disorder regarding pathophysiology (depletional versus dilutional hyponatremia, high versus low vasopressin levels) and therapy (rapid correction to treat cerebral edema versus slow correction to prevent osmotic demyelination, fluid restriction versus fluid resuscitation). For a balanced differentiation between these opposites, an understanding of the pathophysiology of hyponatremia is required. Therefore, in this review an attempt is made to translate the physiology of water balance regulation to strategies that improve the clinical management of hyponatremia. A physiology-based approach to the patient with hyponatremia is presented, first addressing the possibility of acute hyponatremia, and then asking if and if so why vasopressin is secreted non-osmotically. Additional diagnostic recommendations are not to rely too heavily of the assessment of the extracellular fluid volume, to regard the syndrome of inappropriate antidiuresis as a diagnosis of exclusion, and to rationally investigate the pathophysiology of hyponatremia rather than to rely on isolated laboratory values with arbitrary cutoff values. The features of the major hyponatremic disorders are discussed, including diuretic-induced hyponatremia, adrenal and pituitary insufficiency, the syndrome of inappropriate antidiuresis, cerebral salt wasting, and exercise-associated hyponatremia. The treatment of hyponatremia is reviewed from simple saline solutions to the recently introduced vasopressin receptor antagonists, including their promises and limitations. Given the persistently high rates of hospital-acquired hyponatremia, the importance of improving the management of hyponatremia seems both necessary and achievable.
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PMID:Hyponatremia revisited: translating physiology to practice. 1831 6

Dysregulation of the neuroendocrine system is a frequent complication after traumatic brain injury (TBI). Symptoms of these hormonal abnormalities might be subtle and thus easily ignored. Hyponatremia usually indicates underlying disorders that disrupt fluid homeostasis. In most patients with TBI, hyponatremia is a feature of the syndrome of inappropriate antidiuretic hormone (SIADH) secretion due to pituitary dysfunction after head injury. Usually TBI-associated hyponatremia is transient and reversible. We report the case of a 48-year-old man with TBI-associated hyponatremia with delayed recovery and recurrent hyponatremia precipitated by subsequent surgery. In this report, we emphasize the importance of identifying patients with slow recovery of the injured brain, which could complicate with SIADH and acute hyponatremia. Differentiating TBI-associated SIADH from other important causes of hyponatremia such as cerebral salt wasting, and hypocortisonism are also reviewed. Prevention of its recurrence by avoiding further risk is mandatory in managing patients with TBI.
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PMID:Recurrent hyponatremia after traumatic brain injury. 1848 Jun 58

Although the syndrome of inappropriate antidiuretic hormone secretion (SIADH) is commonly observed in patients with acute or chronic central nervous system (CNS) disorders, cerebral salt wasting (CSW) that results in hyponatremia has rarely been reported in children. Both SIADH and CSW result in increased urinary sodium excretion and hyponatremia. However, the management protocols for these two conditions are quite different; volume restriction is used in treating SIADH, while volume expansion is necessary for the treatment of CSW. We present a case of CSW in a child with cervicothoracic hematoma secondary to head and cervicothoracic trauma, without evidence of brain edema. The child was diagnosed on the basis of high urinary sodium excretion resulting in hyponatremia and low serum osmolarity. Improvements in serum sodium levels after saline hydration confirmed this diagnosis. We believe that potentially dangerous cases of hyponatremia should be carefully evaluated in children with cervicothoracic hematoma secondary to trauma, including situations in which brain edema is absent.
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PMID:Cerebral salt wasting in a child with cervicothoracic hematoma. 1878 Jun 5

Cerebral salt-wasting (CSW), or renal salt-wasting (RSW), has evolved from a misrepresentation of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) to acceptance as a distinct entity. Challenges still confront us as we attempt to differentiate RSW from SIADH, ascertain the prevalence of RSW, and address reports of RSW occurring without cerebral disease. RSW is redefined as 'extracellular volume depletion due to a renal sodium transport abnormality with or without high urinary sodium concentration, presence of hyponatremia or cerebral disease with normal adrenal and thyroid function.' Our inability to differentiate RSW from SIADH lies in the clinical and laboratory similarities between the two syndromes and the difficulty of accurate assessment of extracellular volume. Radioisotopic determinations of extracellular volume in neurosurgical patients reveal renal that RSW is more common than SIADH. We review the persistence of hypouricemia and increased fractional excretion of urate in RSW as compared to correction of both in SIADH, the appropriateness of ADH secretion in RSW, and the importance of differentiating renal RSW from SIADH because of disparate treatment goals: fluid repletion in RSW and fluid restriction in SIADH. Patients with RSW are being incorrectly treated by fluid restriction, with clinical consequences. We conclude that RSW is common and occurs without cerebral disease, and propose changing CSW to RSW.
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PMID:Is it cerebral or renal salt wasting? 1964 85

Hyponatremia is the most frequent electrolyte disorder in critically ill neurological patients. The major differential diagnoses in this situation are the syndrome of inappropriate antidiuretic hormone secretion, marked by inappropriate retention of free water, and cerebral salt wasting, characterized by excessive urinary loss of sodium and resulting in polyuria and extracellular volume contraction. Cerebral salt wasting is a syndrome of hyponatremia due to increased urine output and excessive natriuresis described in patients with central nervous system disease. Although cerebral salt wasting has been well described in neurosurgical patients, data regarding pediatric patients is sparse. We present a 34-month-old boy with lissencephaly who developed cerebral salt wasting after brain biopsy. The patient was treated with hypertonic saline and multiple antiepileptic drugs. Fludrocortisone supplementation effectively treated cerebral salt wasting.
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PMID:The treatment of cerebral salt wasting with fludrocortisone in a child with lissencephaly. 2006 33

Cerebral salt wasting (CSW) is a syndrome of hypovolemic hyponatremia caused by natriuresis and diuresis. The mechanisms underlying CSW have not been precisely delineated, although existing evidence strongly implicates abnormal elevations in circulating natriuretic peptides. The key in diagnosis of CSW lies in distinguishing it from the more common syndrome of inappropriate secretion of antidiuretic hormone. Volume status, but not serum and urine electrolytes and osmolality, is crucial for making this distinction. Volume and sodium repletion are the goals of treatment of patients with CSW, and this can be performed using some combination of isotonic saline, hypertonic saline, and mineralocorticoids.
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PMID:Cerebral salt wasting: pathophysiology, diagnosis, and treatment. 2038 Sep 74

Cisplatin was the first platinum compound to be introduced as a chemotherapeutic agent with antineoplastic activity against a wide variety of solid tumors. Renal impairment with a decline in glomerular filtration has been the classical nephrotoxicity of cisplatin. Renal salt wasting syndrome is yet another, though it is not common. Previous studies were identified by searching the Pubmed database using the following keywords: cisplatin, cisplatin nephrotoxicity, renal salt wasting, and salt loosing nephropathy. Renal salt wasting syndrome has been described in 17 case reports since 1984. It is a rare side effect of cisplatin that manifests with polyuria, hypovolemia, and hyponatremia, and, because of similarities in clinical settings and laboratory values, it is frequently misdiagnosed as a syndrome of inappropriate antidiuretic hormone. Other causes of polyuria and hyponatremia should be excluded. Treatment aims at restoring the lost water and salt. Substituting cisplatin with carboplatin depends on individual clinical settings. Prognosis is excellent, as recovery was the rule in all the reported cases.
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PMID:Cisplatin-induced renal salt wasting syndrome. 2062 42

Hyponatremia is one of the most common electrolyte disorders encountered in clinical practice of medical anticancer treatment. Cisplatin (CDDP) is a well-known chemotherapeutic agent that associates with hyponatremia. We retrospectively studied clinical features of hyponatremia CDDP administration. The incidence of hyponatremia at the first administration was 64. 1%. The significant risk factors of hyponatremia are body weight less than 60 kg, creatinin clearance less than 60mL/min, and sodium depletion and intake loss due to treatment-induced anorexia, nausea, vomiting and diarrhea. The mechanism of hyponatremia induced by CDDP is thought to be mainly renal salt wasting, and sometimes the syndrome of inappropriate secretion of antidiuretic hormone(SIADH).
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PMID:[Hyponatremia with cisplatin administration in head and neck cancer patients]. 2116 Feb 61

Hyponatremia is the most common electrolyte disorder encountered in neurosurgical patients. The aggressive treatment of hyponatremia in this group is critical, as hyponatremia can lead to mental status changes, seizures, vasospasm, cerebral edema, and even death. When it occurs, it represents a failure of one of several homeostatic mechanisms that tightly regulate serum sodium. In these patients, hyponatremia is most commonly due to the syndrome of inappropriate antidiuretic hormone (SIADH) or cerebral salt wasting (CSW). It can be problematic to differentiate between these 2 as they share key features, including low serum sodium, low serum osmolality, a higher urine osmolality than serum osmolality, and an elevated urinary sodium concentration. Furthermore, distinctions between CSW and SIADH, namely extracellular fluid (ECF) volume and total sodium balance, are often difficult to establish. Syndrome of inappropriate antidiuretic hormone is characterized by a volume-expanded state, whereas CSW is characterized by a volume-contracted state. Determining the exact cause remains a clinical imperative as the treatment for each is different. The rate at which serum sodium is corrected must be attended to, as rapid shifts in serum sodium pose potential risk of cerebral pontine myelinolysis.
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PMID:Etiology and management of hyponatremia in neurosurgical patients. 2134 81


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