Primary polydipsia, or psychogenic polydipsia, is a condition that results in considerable morbidity and mortality. In psychiatric patients, psychogenic polydipsia and the syndrome of inappropriate antidiuretic hormone secretion may cause hyponatremia. In the 1970s, it was recognized that antipsychotics such as tiotixene and haloperidol could impair the excretion of a free water load. There are also several case reports of drug-induced hyponatremia in patients using atypical drugs suggesting that these probably can also impair water balance and induce hyponatremia. Case report and review of relevant literature are reported in this article. Psychogenic polydipsia is a common cause of hyponatremia among individuals with chronic mental illness. A case of severe hyponatremia caused by psychogenic polydipsia is described involving a female patient with an adult lifelong history of chronic mental illness diagnosed as schizoaffective disorder. After switching her antipsychotic medication to clozapine water ingestion was normalized as well as sodium levels and her psychotic symptoms improved. Primary polydipsia occurs commonly with schizophrenia and other mental diseases and can cause hyponatremia. PPD may present as an acute psychotic state or as inexplicable emergence of seizures. Appropriate, timely clinical assessment with special attention to thirst, fluid intake, and urine output is essential. Proper treatment may include drug withdrawal and fluid and saline restriction. Once corrected, some pharmacological agents can be tried. The article illustrates the importance of the diagnosis of psychogenic polydipsia given its electrolyte disturbances and life threatening situations.
Haloperidol decanoate is a first generation antipsychotic drug used to treat patients with schizophrenic disorder who require prolonged parenteral antipsychotic therapy. Cases of oral haloperidol decanoate are rare, and only one has been reported in foreign literature. In this report, we present a case of an oral ingestion of haloperidol decanoate of a male with schizophrenic disorder who presented to the emergency department following an oral ingestion of 1 ampoule of haloperidol decanoate 100 mg. At presentation he was hemodynamically stable. He was maintained on vigilance for 12 hours after what was discharged to the outpatient unit for psychiatric follow-up. The bioavailability and pharmacokinetic of oral intake of haloperidol decanoate are unknown. Although there is a report of treatment with oral activated charcoal in this case there was no need of intervention.
IntroductionIntricate interactions between the immune system and the brain might have important etiological and therapeutic implications for neuropsychiatric brain disorders. A probable association between schizophrenia and the immune system was postulated over a century ago, and is supported by epidemiological and genetic studies pointing to links with infection and inflammation.ObjectiveTo describe some important areas of research regarding immune response in schizophrenia and related psychotic disorders and discuss potential mechanisms and therapeutic implications of these findings.AimsAssociations between immune response, inflammation and schizophrenia and related psychotic disorders are reviewed.MethodsA literature review of the theme is surveyed. Several articles were search on MEDLINE with the keywords: schizophrenia, psychosis, inflammation, immunity, infection.ResultsSchizophrenia is a multifactorial disease. It is associated with multiple genetic loci that confer risk, in addition to developmental and postnatal risk factors. Antipsychotic-naive first-episode psychosis and acute psychotic relapse seems to be associated with increased serum concentrations of interleukin 6 and other proinflammatory cytokines, which are normalized after remission of symptoms with antipsychotic treatment.ConclusionsInflammation and immune dysfunction might contribute to cognitive, negative, and positive symptoms in schizophrenia. Identification of specific inflammatory pathways for neuropsychiatric symptoms would provide novel targets for therapeutic intervention.Disclosure of interestThe authors have not supplied their declaration of competing interest.
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