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 66-year-old woman was admitted to our hospital because of vomiting and appetite loss. For the 2 days prior to admission, she had a cold, which had developed into acute viral bronchitis on admission. Because laboratory data on admission showed hyponatremia, intravenous infusion of Ringer's lactate solution was started. However, generalized seizures appeared, and she developed a coma on the day of admission. Her plasma antidiuretic hormone (ADH) level was high in the context of a low serum osmolality on the second hospital day. The infusion rate was increased, and the patient's consciousness level returned to normal. However, her normalized serum Na level declined again as she drank much water to reduce throat discomfort. As the throat discomfort caused by the throat inflammation improved with azulene gargling, her water intake was reduced, and the serum Na concentration returned to normal. Thus, polydipsia caused by a throat inflammation partially contributed to hyponatremia in this patient. We note that increased ADH secretion has been reported in adults with acute respiratory infection. Therefore, we concluded that polydipsia caused by the throat inflammation, plus increased ADH secretion, resulted in hyponatremia in this patient. We should pay attention to the behavior of drinking extra fluid in patients with acute respiratory infections.
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PMID:Hyponatremic seizure associated with acute respiratory infection. 1789 51

A 53-year-old renal allograft recipient developed nocardial cerebral abscess. It manifested clinically with encephalitis, polycythemia, convulsions, syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and a space-occupying lesion presenting as multiple ring shadows in the left fronto-parietal lobe on computerized tomography (CT scan) of the brain. The initial clinical presentation included an afebrile patient with headache, convulsions and altered sensorium with no lateralising neurological deficit. He deteriorated later and developed coma with right hemiplegia. Purulent material was drained through left frontal craniotomy, and the culture confirmed the presence of nocardial infection. Despite aggressive therapy, the patient died a few days later. We conclude that high degree of early suspicion, diagnosis and prompt treatment should be stressed.
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PMID:Cerebral nocardiosis in a renal transplant recipient: a case report. 1820 49

Although hyponatremia occurs in most patients with severe malaria, its pathogenesis, prognostic significance, and optimal management have not been established. Clinical and biochemical data were prospectively collected from 171 consecutive Bangladeshi adults with severe malaria. On admission, 57% of patients were hyponatremic. Plasma sodium and Glasgow Coma Score were inversely related (r(s) = -0.36, P < 0.0001). Plasma antidiuretic hormone concentrations were similar in hyponatremic and normonatremic patients (median, range: 6.1, 2.3-85.3 versus 32.7, 3.0-56.4 pmol/L; P = 0.19). Mortality was lower in hyponatremic than normonatremic patients (31.6% versus 51.4%; odds ratio [95% confidence interval]: 0.44 [0.23-0.82]; P = 0.01 by univariate analysis). Plasma sodium normalized with crystalloid rehydration from (median, range) 127 (123-140) mmol/L on admission to 136 (128-149) mmol/L at 24 hours (P = 0.01). Hyponatremia in adults with severe malaria is common and associated with preserved consciousness and decreased mortality. It likely reflects continued oral hypotonic fluid intake in the setting of hypovolemia and requires no therapy beyond rehydration.
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PMID:Hyponatremia in severe malaria: evidence for an appropriate anti-diuretic hormone response to hypovolemia. 1914 52

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 incidence of water and electrolyte disturbances following traumatic brain injury (TBI) is considerable and has been attributed to a dysregulation of the hypothalamic peptide arginine-vasopressin (AVP). Copeptin, the C-terminal part of the AVP prohormone, reflects AVP activity. In 71 TBI patients we measured copeptin in serum by a sandwich immunoassay. Injury severity was assessed by Glasgow Coma Score (GCS) and computed tomography, and recovery by Glasgow Outcome Score (GOS). Neuroendocrine and osmoregulation regulation were examined on day 0, 3 and 7, and 24 months post-injury. Copeptin was highest on admission (40.0 +/- 72.3 pmol/l), stabilized on day 3 and 7 (21.2 +/- 18.3 resp. 20.3 +/- 17.1 pmol/l), and normalized at follow-up (4.2 +/- 1.7 pmol/l). On admission, there was a correlation between serum sodium and urine excretion (p = 0.003), but the correlation got lost on day 3 and 7. Copeptin did not reflect the individual 24 h urine excretion or serum sodium levels indicating an uncoupling of copeptin/AVP release and renal water excretion. High copeptin level on day 3 were correlated with a low GCS (p < 0.001), midline shift (p = 0.019), intracerebral hemorrhage (p = 0.026), SAPS score (p = 0.001), as well as with a low GOS (p = 0.031). Copeptin was significantly decreased following skullbase fracture (p = 0.016).Our data reveal a loss of hypothalamic osmoregulation following TBI. The measurement of Copeptin/AVP release reveals a significant predictive function for the severity of TBI.
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PMID:Following brain trauma, copeptin, a stable peptide derived from the AVP precusor, does not reflect osmoregulation but correlates with injury severity. 1981 53

Patients requiring CSF shunts frequently have comorbidities that can influence water and electrolyte balances. The authors report on a case involving a ventriculoperitoneal shunt in a patient who underwent intravenous hyperhydration and withdrawal of vasopressin substitution prior to scheduled high-dose chemotherapy regimen for a metastatic suprasellar germinoma. After acute neurological deterioration, the patient underwent CT scanning that demonstrated ventriculomegaly. A shunt tap revealed no flow and negative opening pressure. Due to suspicion of proximal shunt malfunction, the comatose patient underwent immediate surgical exploration of the ventricle catheter, which was found to be patent. However, acute severe hypernatremia was diagnosed during the procedure. After correction of the electrolyte disturbances, the patient regained consciousness and made a good recovery. Although rare, the effects of acute severe hypernatremia on brain volume and ventricular size should be considered in the differential diagnosis of ventriculoperitoneal shunt failure.
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PMID:Ventricular enlargement due to acute hypernatremia in a patient with a ventriculoperitoneal shunt. 1991 84

Central pontine myelinolysis (CPM) has been described in alcoholic patients and in the aftermath of rapid correction of chronic hyponatraemia. We describe a case of CPM occurring secondary to nephrogenic diabetes insipidus (DI), which developed as a consequence of severe hypokalaemia. A 63-year-old man with alcohol dependence was admitted to hospital with severe pulmonary sepsis and type 1 respiratory failure. On admission, he had euvolaemic hyponatraemia of 127 mmol/L, consistent with a syndrome of inappropriate antidiuretic hormone secondary to his pneumonia. Following admission, his plasma potassium dropped from 3.2 to a nadir of 2.3 mmol/L. Mineralocorticoid excess, ectopic adrenocorticotrophic hormone production and other causes of hypokalaemia were excluded. The hypokalaemia provoked significant hypotonic polyuria and a slow rise in plasma sodium to 161 mmol/L over several days. Plasma glucose, calcium and creatinine were normal. The polyuria did not respond to desmopressin, and subsequent correction of his polyuria and hypernatraemia after normalization of plasma potassium confirmed the diagnosis of nephrogenic DI due to hypokalaemia. The patient remained obtunded, and the clinical suspicion of osmotic demyelination was confirmed on magnetic resonance imaging. The patient remained comatose and passed away 10 days later. This is the first reported case of nephrogenic DI resulting in the development of CPM, despite a relatively slow rise in plasma sodium of less than 12 mmol/L/24 h. Coexisting alcohol abuse, hypoxaemia and hypokalaemia may have contributed significantly to the development of CPM in this patient.
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PMID:Central pontine myelinolysis secondary to hypokalaemic nephrogenic diabetes insipidus. 1994 Feb 3

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is characterized by hyponatremia, plasma hypo-osmolality, a urine sodium concentration >30-40 mmol/L, normal acid-base balance, a normal plasma potassium concentration and, frequently, hypouricemia. There are different types of SIADH: idiopathic, iatrogenic, and forms caused by central nervous system or lung disorders, neoplasia and major surgical interventions. Drug-induced SIADH is becoming the most frequent cause of hyponatremia encountered in clinical practice. Here we report the case of a 60-year-old man in a coma (I-II) and with very severe hyponatremia (99 mmol/L) due to SIADH induced by fluphenazine and amitriptyline, which he had been taking since many years as antidepressant drugs. SIADH became very quickly more severe due to the recent administration of cisplatin. There was rapid improvement of the clinical symptoms after withdrawal of the drugs involved and correction of hyponatremia. In conclusion, in rare cases like the present one hyponatremia related to SIADH may be so severe as to represent a true clinical emergency. The administration of drugs known to cause hyponatremia should be avoided, if possible; otherwise, very careful monitoring of the plasma sodium concentration is mandatory to avoid severe neurological complications which may lead to the death of the patient.
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PMID:[A case of drug-induced syndrome of inappropriate secretion of antidiuretic hormone]. 2067 38

A 77-year-old male with thoracic esophageal cancer (cT3N3M0, Stage III) received nedaplatin at 80mg/m2 for 1 day and 5-fluorouracil at 800mg/m2 for 5 days as neoadjuvant treatment. On the fifth day of treatment, he lapsed into a coma (Japan Coma Scale 30), and his serum sodium concentration was found to be decreased to 116mEq/L. We concluded hyponatremia due to SIADH (syndrome of inappropriate secretion of antidiuretic hormone) induced by chemotherapy based on the fact that the patient had no finding of dehydration, particular history of related disorders, serum hypoosmolality accompanied by urine hyperosmolality and persistent urinary sodium excretion. We treated him with fluid restriction, sodium supplement and administration of loop diuretic. Then he regained consciousness and appropriate serum sodium level. Thereafter, hyponatremia was corrected without recurrence, and the patient underwent radical esophagectomy safely. He has been in good condition without recurrence of esophageal cancer after surgery.
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PMID:[A case of SIADH developed during neoadjuvant chemotherapy using nedaplatin and 5-fluorouracil in a patient with esophageal cancer]. 2084 48

Hyponatremia is known as a complication of neurosurgical conditions or brain. The prevalence of hyponatremia in acute spinal cord injury has been known to be much higher than in the general medical or surgical patient population. We report here a case of hyponatremia, which occurred 10 days after cervical spinal cord injury. The data on sodium levels were improved under the tapered infusion volume and water intake restriction. Treatment for this case is the same as that for syndrome of inappropriate antidiuretic hormone, which have suggested that reduced extracellular volume is important to improve the hyponatremia after traumatic spinal cord injury. Uncontrolled hyponatremia may lead to lethargy, seizures, coma, cardiac arrhythmia and death. Therefore, the complication of hyponatremia should be paid attention after cervical spinal cord injury. A careful monitoring of sodium levels after the injury is required in the cases of cervical spinal cord injury.
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PMID:A case of hyponatremia after cervical spinal cord injury. 2144 2


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