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)

Meningitis is often associated with hyponatremia due to inappropriate secretion of antidiuretic hormone, and diabetes insipidus is associated with bacterial meningitis. This article describes a patient with acquired immunodeficiency syndrome who experienced recurrent episodes of central diabetes insipidus in association with recurrent fungal meningitis. Desmopressin was effective in controlling the polyuria until the episodes of meningitis resolved.
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PMID:Recurrent central diabetes insipidus secondary to cryptococcal meningitis. 958 72

For almost 20 years, fluid restriction has been applied in the management of bacterial meningitis. This recommendation was based upon the findings of elevated plasma levels of arginine vasopressin in children with bacterial meningitis and their interpretation as evidence for inappropriate secretion of antidiuretic hormone. Recent data indicate that this interpretation was erroneous and that elevated levels of arginine vasopressin is the consequence of hypovolemia in the majority of cases of bacterial meningitis. In addition, fluid restriction appears to worsen the prognosis. As a consequence, not only fluid restriction must not be systematically applied in the management of bacterial meningitis, but appropriate fluid and sodium intakes are necessary to compensate hypovolemia and dehydration. Only a small number of cases with evidence of inappropriate secretion of antidiuretic hormone will require fluid restriction.
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PMID:[Hydration and meningitis]. 1007 90

The E. coli endotoxin 0111 B4, a lipopolysaccharide (LPS), in a dose of 200 ng/kg body weight/50 microl artificial cerebrospinal fluid (CSF) was given intracisternally to 14-day-old rats. Four hours later CSF, blood and urine were sampled, and consecutive brain sections from the hypothalamic area of the brain were prepared for in situ hybridization. The LPS treatment resulted in a significant (p<0.001) pleocytosis and an elevation of the protein content of the CSF. There were no changes observed in the chemical parameters of the CSF, plasma, blood or urine, i.e. vasopressin (VP) levels, osmolality, Na+ and K+ concentrations, glucose level, pH, bicarbonate or PaCO2, PaO2 values. LPS injection, however, resulted in a significantly (p<0.01) increased VP mRNA level (121% of the control value) in the supraoptic nuclei (SON), but not in the paraventricular nuclei (PVN), as compared to controls. Our findings suggest an early effect of LPS on VP gene expression selectively in the SON of 14-days-old rats. This animal model might be suitable for studying the regulation of VP gene expression and the role of this peptide in the pathogenesis of bacterial meningitis in pediatric patients.
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PMID:Differential regulation of vasopressin gene expression in the hypothalamus of endotoxin-treated 14-day-old rat. 1042 32

Although disorders of ADH secretion associated with meningitis are usually consistent with the Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH), central diabetes insipidus (DI) is an exceptional complication of meningitis. Transient DI as a complication of Escherichia coli (E. coli) meningitis due to ventriculoperitoneal shunt in an 18-month-old boy is presented. Blood and spinal fluid cultures yielded E. coli, sensitive to cefotaxime. The DI arose on the day 3 after admission and continued to the day 20. Treatment comprised cefotaxime, dexamethasone, fluid adjustment and vasopressin. The course of our case supports that in cases of bacterial meningitis, initial fluid restriction may occasionally result in dangerous conditions. Therefore, all children with bacterial meningitis should be followed closely not only in terms of SIADH but also DI. To our knowledge this is the first transient DI associated with E. coli-caused meningitis case reported.
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PMID:Transient diabetes insipidus following Escherichia coli meningitis complicated by ventriculoperitoneal shunt. 1061 31

Neisseria meningitidis and Streptococcus pneumoniae are the most frequent causes of bacterial meningitis. The incidence of Haemophilus meningitis in the Netherlands is low due to successful Haemophilus influenzae type b vaccination. This implies that there is no need to take account into this microorganism in using initial empiric antimicrobial therapy for bacterial meningitis. Vomiting (especially children), headache, fever, and a stiff neck characterize acute bacterial meningitis. However, even without these signs a patient may still have acute bacterial meningitis. The characteristics in neonates are less specific. An emergency lumbar puncture should be performed in all patients with meningeal irritation or other signs of bacterial meningitis. Examination of the CSF is not indicated for convulsive children (between the ages of 6 months and 6 years) who do not exhibit other clinical signs. In patients who respond adequately to the treatment, it is not necessary to examine the CSF again. Papilloedema or focal neurological symptoms contraindicate a lumbar puncture in patients with bacterial meningitis, until CT results justify that it can be performed safely. Antibiotic treatment should not be delayed until after the CT. General practitioners should treat their patients with suspected meningococcus infection by admitting them to the hospital without first injecting antibiotics. In the Netherlands, patients with suspected pneumococcus meningitis may still be treated with benzylpenicillin. Patients with bacterial meningitis have no fluid restrictions; only in case of the syndrome of inadequate secretion of antidiuretic hormone is fluid reduction indicated. The physician is responsible for prescribing prophylaxis to family members. The Regional Health Services organize chemoprophylaxis for classmates. The latter is only indicated if at least 2 related cases occur in one month.
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PMID:[CBO-guideline 'Bacterial meningitis']. 1143 68

In patients with meningitis, fluid restriction is recommended to counter the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and to reduce cerebral oedema. However, any effects of an increased plasma level of ADH upon cerebral oedema would be due not to fluid retention but to hypoosmolality. In a literature review of fluid and electrolyte disturbances and the effect of fluid therapy in bacterial/tuberculous meningitis, the prevalence of hyponatraemia, hypoosmolality and SIADH varied considerably; apparently, non-osmotic stimuli for the secretion of ADH, e.g. intracranial hypertension and hypovolaemia, were present in most patients. Neither clinical nor experimental studies have confirmed that fluid restriction reduces the cerebral oedema in meningitis. Furthermore, compared with maintenance therapy, fluid restriction did not improve outcome in a randomized controlled study. Thus, we find no evidence to support the use of fluid restriction in patients with meningitis. Fluid therapy in acute bacterial meningitis should aim at avoiding hypovolaemia and hypoosmolality based on the assumptions that (i) ADH is increased by non-osmotic stimuli; (ii) elevated ADH is less important for cerebral oedema than severe hypoosmolality, which may in itself induce or aggravate oedema; (iii) maintenance fluid therapy aiming at isoosmolality will not worsen neurological outcome; and (iv) hypovolaemia is difficult to detect, and detrimental for cerebral perfusion, in these patients.
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PMID:The syndrome of inappropriate secretion of antidiuretic hormone and fluid restriction in meningitis--how strong is the evidence? 1123 73

Subarachnoid hemorrhage is the most common cause of cerebral salt wasting syndrome. There are few reports of this condition in infectious meningitis. We describe a patient with hyponatremia and bacterial meningitis. Hyponatremia rapidly improved after administration of sodium chloride. The purpose of this report is to alert clinicians to the fact that hyponatremic patients with central nervous system disease do not necessarily have a syndrome of inappropriate secretion of antidiuretic hormone (SIADH), but may have cerebral salt wasting syndrome. By contrast with SIADH, the treatment requires saline administration.
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PMID:[Cerebral salt wasting syndrome in bacterial meningitis]. 1788 8

Strongyloidiasis is an infection by the intestinal parasite Strongyloides Stercoralis, which usually stays asymptomatic. In some situations a hyperinfection or disseminated disease can occur. We report a case of a 49-year-old Congolese man with a medical history of 5 episodes of bacterial meningitis, who presents himself with a paralytic ileus and a low serum sodium. A Strongyloides hyperinfection with a syndrome of inappropriate secretion of the antidiuretic hormone (SIADH) was diagnosed. After treatment with ivermectine the abdominal symptoms subsided and the serum sodium returned to normal values. In comparison to other case reports our patient had no respiratory or gastrointestinal symptoms during the episodes of bacterial meningitis. Screening for Strongyloides stercoralis is indicated in patients with unexplained SIADH, bacterial meningitis or bacterial septicaemia, who originally come from endemic countries.
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PMID:Strongyloides Stercoralis infection associated with repititive bacterial meningitis and SIADH: a case report. 1931 85

Listeria monocytogenes is an uncommon cause of bacterial meningitis beyond the neonatal period. Patients with immunosuppression or neoplastic disease are at increased risk of developing serious invasive disease, particularly meningitis. L. monocytogenes meningitis in two previously healthy, immunocompetent children aged 7 years and 18 months is described. One of them was successfully treated with ampicillin and amikacin. In the other there was resistance to ampicillin, and meropenem, vancomycin and amikacin were given. One patient developed unilateral abducens paralysis and inappropriate antidiuretic hormone secretion. L. monocytogenes should be suspected in children with bacterial meningitis who fail to respond to empirical antibiotic therapy.
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PMID:Listeria monocytogenes meningitis in two immunocompetent children. 1968 66

Cerebral salt wasting syndrome (CSW-cerebral salt wasting) was first described in 1950 by Peters. This syndrome can occur in patients who have sustained damage to the central nervous system (e.g. patients with subarachnoid bleeding, bacterial meningitis or after neurosurgery). Patients present with excessive natriuresis and hyponatremic dehydration. Differentiating this syndrome with the syndrome of inappropriate antidiuretic hormone secretion (SIADH-syndrome of inappropriate antidiuretic hormone secretion), which may occur in the same group of patients, is necessary in order to administer the correct treatment which consists of fluid restriction and sodium replacement in SIADH and fluid and sodium replacement as well as occasional mineralocorticoid therapy in CSW.
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PMID:Cerebral salt wasting in a postoperative period. 2503 96


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