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)

A 22-year-old woman was admitted to intensive care with severe hyponatraemia. She suffered from lower abdominal pain, vomiting and irritability since one week. Physical findings showed euvolemia and an altered mental status with severe agitation and slurred speech. Abdominal examination was painful but there were no signs of peritonitis. Laboratory data were compatible with the diagnosis of syndrome of inappropriate secretion of antidiuretic hormone. Since patient was in a premenstrual phase, recently started to take an oral contraceptive and since no abnormalities were seen on an abdominal CT scan, the presentation was considered suggestive of an acute porphyria attack. A urinary sample indicated markedly increased levels of delta-aminolevulinic acid, porphobilinogen and uroporphyrin. A low activity of the porphobilinogen deaminase enzyme confirmed the diagnosis of acute intermittent porphyria. The present case demonstrates the need for a high level of suspicion in order to diagnose this disorder in unexplained syndrome of inappropriate antidiuretic hormone secretion and prevent life-threatening complications.
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PMID:An unusual cause of syndrome of inappropriate antidiuretic hormone secretion. 1904 8

Acute and severe hyponatremia causes a metabolic encephalothy. It is physiopathologically based on the cerebral edema, and its fatal symptoms include seizures and coma. We present a case of an extreme hyponatremia of multifactorial etiology in a schizophrenic patient with potomania. Potomania does not usually cause hyponatremia, unless it coexists with other trigger factors. This patient had a syndrome of inappropriate antidiuretic hormone (SIADH), and a deep hypokaliemia, due to vomiting and a treatment with indapamida, which perpetuates the deficit of extracellular sodium. In the patient's treatment, aripiprazole was the only recently introduced drug with which cases of inappropriate vasopressin secretion have been reported. Management of a severe hyponatremia must be considered a vital emergency, independent of the cause, and 3% hypertonic saline must be administered. The increase of the sodium level must not be higher than 25 mmol/L in the first 24-48 hours, to avoid a secondary brain injury.
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PMID:[Severe and acute hyponatremia in a schizophrenic patient with potomania]. 1943 May 20

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH)/syndrome of inappropriate antidiuresis is characterized by a hypotonic hyponatremia, with an insufficiently diluted urine given the plasmatic hypoosmolality, in the absence of hypovolemia (with or without a third space), hypotension, renal or heart failure, cirrhosis of the liver, hypothyroidism, adrenal insufficiency, vomiting, or other non-osmotic stimuli of ADH secretion. The response of ADH to the infusion of hypertonic saline divides SIADH into 4 different types. In type D, there is no alteration in ADH secretion. Rather, the defect is the maintained permeability of kidney aquaporin-2 channels to water. Activating mutations of the V2 receptor have been identified. The most frequent cause of SIADH is the use of drugs that induce secretion of the hormone. Old age is per se a risk factor for its development. SIADH is underdiagnosed, and hospitalization often worsens the clinical situation, due to an iatrogenic excess in the use of oral and i.v. liquids, often hypotonic, together with a reduction in salt intake. Treatment is directed towards normalization of natremia when possible, together with the avoidance of both hyponatremic encephalopathy as well as the osmotic demyelinization syndrome. Cases of "appropriate" secretion of ADH with normovolemic hyponatremia and high mortality rates should be treated with the same urgency as SIADH--such is the case of post-surgical hyponatremia.
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PMID:[Current considerations in syndrome of inappropriate secretion of antidiuretic hormone/syndrome of inappropriate antidiuresis]. 2113 Sep 59

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

Desmopressin, a synthetic analog of the antidiuretic hormone, is used in the treatment of enuresis nocturna in children and increasingly also in adults. Nocturia in the elderly causes sleeping disorders and is associated with a higher risk of falling and increased mortality. Desmopressin leads to a significant decrement of nocturia and consequently, a better sleep quality and is for this reason increasingly prescribed in the old. Desmopressin causes borderline hyponatremia (130-135 mmol/l) in 15% and severe hyponatremia in 5% of all adult users. Factors that predispose to hyponatremia are a higher dose, age > 65 years, a low-normal serum sodium, a high 24-hour urine volume and co-medication (thiazide diuretics, tricyclic antidepressants, serotonin-reuptake-inhibitors, chlorpromazine, carbamazipine, loperamide, Non-Steroidal-Anti-Inflammatory-Drugs). Hyponatremia is associated with headache, nausea, vomiting, dizziness, and can cause somnolence, loss of consciousness and death. We present two cases where initiation of desmopressin led to hyponatremia, requiring hospitalization. In view of the high risk of desmopressin-associated hyponatremia in the older population, alternative treatment strategies for nocturia must be considered first. If desmopressin is prescribed, strict follow-up of serum sodium levels is necessary.
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PMID:[Desmopressin for nocturia in the old: an inappropriate treatment due to the high risk of side-effects?]. 2122 78

A 60-year-old woman with no previous history of chronic disease or malignancy presented with intense back and left leg pain and sleep disturbances. The patient had been treated unsuccessfully for the past 6 months with analgetics. Magnetic resonance imaging showed a soft tissue tumor in the L5-S1 region that involved the spinal canal, and a pathohistological analysis of the tumor specimen confirmed the presence of non-Hodgkin, diffuse large B cell lymphoma. After the diagnosis was confirmed, malaise, nausea, and vomiting developed. Multislice computed tomography of the endocranium showed focal infiltration of the hypothalamus and lateral ventricle; dissemination of a systemic lymphoma was excluded. Therapy was initiated as per the De Angelis protocol. After intravenous and intrathecal administration of metotrexate, the patient developed signs of central diabetes insipidus, which responded to therapy with an antidiuretic hormone analog. Despite the obvious infiltration of the hypothalamus, we cannot exclude an idiosyncratic effect of methotrexate on the central diabetes insipidus.
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PMID:Hypothalamic dysfunction in a patient with primary lymphoma of the central nervous system. 2182 93

Sodium, the most important extracellular fluid electrolyte, is the focus of several homeostatic mechanisms that regulate fluid and electrolyte balance. Hyponatremia is a common electrolyte abnormality caused by an actual sodium deficiency or extracellular compartment fluid excess. Clinical symptoms are related with acuity and speed with which this abnormality is established. The symptoms are mainly neurological and neuromuscular disorders (headache, confusion, stupor, seizures, coma) due to brain cells edema. Hyponatremia due to sodium deficiency is caused by sodium loss from kidney (nephritis, diuretics, mineralocorticoid deficiency) and / or extrarenal (vomiting, diarrhea, burns). Hyponatremia due to water excess seems to be the most common and it is attributable to cirrhosis, nephrotic syndrome, heart failure, infusion 5% glucose solutions and drugs that stimulate ADH secretion. It was recently highlighted the role of inflammation and IL-6 in the non-osmotic ADH release. Hyponatremia is considered also marker of phlogosis. Acute (<48 h) and severe (<125 mEq/ L) hyponatremia is a medical emergency that requires prompt correction. Patients with chronic hyponatremia have a high risk of osmotic demyelination syndrome if rapid correction of the plasmatic sodium occurs. In combination with conventional therapy, a new class of drugs, vasopressin receptors antagonists (AVP-R antagonists) would be able to increase the excretion of electrolyte-free water and the serum sodium concentration.
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PMID:[Hyponatremic syndrome]. 2236 42

A 50-year-old Asian Indian female with known hypertension presented with persistent vomiting but no other symptoms of meningism. Clinical examination and basic laboratory parameters were entirely normal except for significant hyponatremia. Further investigation was suggestive of the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Subsequently, despite steady correction of hyponatremia, the patient developed generalised seizures. Cerebrospinal fluid (CSF) analysis performed was inconclusive. Screening for a chronic meningitis underlying SIADH, yielded positive blood and CSF titres for venereal disease research laboratory (VDRL), which were confirmed by Treponema pallidum haemagglutination (TPHA). The patient was treated for neurosyphilis and made a complete recovery. Hyponatremia resolved and she had no further episodes of seizures. She was tested for HIV infection which was negative. On follow-up, she remained TPHA positive but VDRL titres became negative.
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PMID:An unusual cause for hyponatremia with seizures. 2260 98

Hyponatremia, a common electrolyte abnormality in oncology practice, may be a negative prognostic factor in cancer patients based on a systematic analysis of published studies. The largest body of evidence comes from small-cell lung cancer (SCLC), for which hyponatremia was identified as an independent risk factor for poor outcome in six of 13 studies. Hyponatremia in the cancer patient is usually caused by the syndrome of inappropriate antidiuretic hormone (SIADH), which develops more frequently with SCLC than with other malignancies. SIADH may be driven by ectopic production of arginine vasopressin (AVP) by tumors or by effects of anticancer and palliative medications on AVP production or action. Other factors may cause hypovolemic hyponatremia, including diarrhea and vomiting caused by cancer therapy. Hyponatremia may be detected on routine laboratory testing before or during cancer treatment or may be suggested by the presence of mostly neurological symptoms. Treatment depends on several factors, including symptom severity, onset timing, and extracellular volume status. Appropriate diagnosis is important because treatment differs by etiology, and choosing the wrong approach can worsen the electrolyte abnormality. When hyponatremia is caused by SIADH, hypertonic saline is indicated for acute, symptomatic cases, whereas fluid restriction is recommended to achieve a slower rate of correction for chronic asymptomatic hyponatremia. Pharmacological therapy may be necessary when fluid restriction is insufficient. The orally active, selective AVP receptor 2 (V(2))-receptor antagonist tolvaptan provides a mechanism-based option for correcting hyponatremia caused by SIADH or other conditions with inappropriate AVP elevations. By blocking AVP effects in the renal collecting duct, tolvaptan promotes aquaresis, leading to a controlled increase in serum sodium levels.
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PMID:Diagnosis and management of hyponatremia in cancer patients. 2261 70

A 61-year-old woman was admitted with history of vomiting, diarrhoea and severe hyponatraemia (Na(+) 109). The cause of the hyponatraemia was due to intravascular volume depletion resulting in a non-osmotic release of antidiuretic hormone (ADH) with the added effects of a thiazide diuretic. She was also on fluoxetine which may induce inappropriate secretion of ADH. Despite cautious fluid replacement, the patient's serum sodium increased by 12 mmol/l over the first 18 h (and by 10 mmol/l over 12 h). This trajectory, coupled with the rapid decrease in urine osmolality, suggested that this patient was at risk of significant brain injury due to rapid correction of serum sodium. The use of desmopressin slowed the rise in serum sodium allowing brain adaptive mechanisms time to protect against osmotic demyelination.
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PMID:Preventing overcorrection of hyponatraemia with desmopressin. 2267


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