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Hyponatremia caused by water intoxication: successful treatment of psychiatric disturbances with olanzapine and fluoxetine.

ABSTRACT: Hyponatremia is a frequent, yet often unrecognized result of water intoxication caused by psychogenic polydipsia in patients with psychiatric disorders such as schizophrenia and anorexia nervosa. The consequences of hyponatremia may include cerebral edema with tonic-clonic seizures and, in extreme cases, death. In cases of hyponatremia seen in psychiatric practices, the use of psychotropic drugs is often necessary to address both the underlying psychiatric problem and reduce the hyponatremia. Therefore, a patient's clinical condition, the risk of side effects, the possible effect of the medication on hyponatremia and a history of prior medication use should be considered when selecting appropriate psychotropics. The present clinical case details the beneficial effects of olanzapine and fluoxetine in treating a patient with anorexia nervosa and body dysmorphic disorder experiencing acute hyponatremia, and the stable effect the medications achieved over a period of 2.5 years of maintenance therapy.

SUBMITTER: Taube M

PROVIDER: S-EPMC7846081 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature

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Hyponatremia caused by water intoxication: successful treatment of psychiatric disturbances with olanzapine and fluoxetine.

Taube Maris M

Oxford medical case reports 20210123 1

Hyponatremia is a frequent, yet often unrecognized result of water intoxication caused by psychogenic polydipsia in patients with psychiatric disorders such as schizophrenia and anorexia nervosa. The consequences of hyponatremia may include cerebral edema with tonic-clonic seizures and, in extreme cases, death. In cases of hyponatremia seen in psychiatric practices, the use of psychotropic drugs is often necessary to address both the underlying psychiatric problem and reduce the hyponatremia. Th ...[more]

PMID: 33542829

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Project description:Treatment-resistant depression (TRD) occurs in many patients and causes high morbidity and mortality. Because TRD subjects are particularly difficult to study especially longitudinally, biological data remain very limited. In a preliminary study to judge feasibility and power, 25 TRD patients were referred from specialty psychiatric practices. All were severely and chronically depressed and mostly had comorbid psychiatric disorders as is typical in TRD. Nine patients were able to complete all required components of the protocol that included diagnostic interview; rating scales; clinical magnetic resonance imaging; medication washout; treatment with maximally tolerated olanzapine-fluoxetine combination for 8 weeks; and pre- and post-treatment fluorodeoxyglucose positron emission tomography. This drug combination is an accepted standard of treatment for TRD. Dropouts arose from worsening depression, insomnia, and anxiety. One patient remitted; three responded. A priori regions of interest included the amygdala and subgenual cingulate cortex (sgACC; Brodmann area BA25). Responders showed decreased metabolism with treatment in the right amygdala that correlated with clinical response; no significant changes in BA25; better response to treatment the higher the baseline BA25 metabolism; and decreased right ventromedial prefrontal metabolism (VMPFC; broader than BA25) with treatment which did not correlate with depression scores. The baseline metabolism of all individuals showed heterogeneous patterns when compared to a normative metabolic database. Although preliminary given the sample size, this study highlights several issues important for future work: marked dropout rate in this study design; need for large sample size for adequate power; baseline metabolic heterogeneity of TRD requiring careful subject characterization for future studies of interventions; relationship of amygdala activity decreases with response; and the relationship between baseline sgACC and VMPFC activity with response. Successful treatment of TRD with olanzapine-fluoxetine combination shows changes in cerebral metabolism like those seen in treatment-responsive major depression.

Project description:BACKGROUND:We examined the efficacy of olanzapine/fluoxetine combination (OFC) in improving health-related quality of life (QoL) in the treatment of bipolar depression in children and adolescents. METHODS:Patients aged 10-17 years with bipolar I disorder, depressed episode, baseline children's depression rating scale-revised (CDRS-R) total score ?40, Young Mania Rating Scale (YMRS) total score ?15, and YMRS-item 1 ? 2 were randomized to OFC (6/25-12/50 mg/day olanzapine/fluoxetine; n = 170) or placebo (n = 85) for up to 8 weeks of double-blind treatment. Patients and parents completed the revised KINDL questionnaire for measuring health-related QoL in children and adolescents (KINDL-R) at baseline and endpoint. The mean change in CDRS-R total and item scores were used to compare improvement in symptomatology in patients taking OFC and placebo. Tests were 2-sided using a Type I error cutoff of 0.05, and no adjustments for multiple comparisons were made. RESULTS:Baseline QoL as measured by the KINDL-R was substantially impaired relative to published norms for a healthy school-based sample. OFC-treated patients demonstrated an improvement over placebo at endpoint with respect to mean change from baseline in the patient-rated KINDL-R Self-esteem subscale score (p = 0.028), and in the parent KINDL-R ratings of emotional well-being (p = 0.020), Self-esteem (p = 0.030), and Family (p = 0.006). At endpoint, OFC-treated patients still had a lower QoL compared to the normative population. OFC showed significant improvement (p ? 0.05) versus placebo on the CDRS-R total score and on 7 of the 17 CDRS-R items. CONCLUSIONS:Patients aged 10-17 years with an acute episode of bipolar depression and their parents reported greater improvements (parents noticed improvements in more areas than did their offspring) on some aspects of QoL when treated with OFC compared with placebo. However, after 8 weeks of treatment, KINDL-R endpoint scores remained lower than those of the, presumably healthy, control population. Clinical trial registration information A Study for Assessing Treatment of Patients Ages 10-17 with Bipolar Depression; http://www.clinicaltrials.gov; NCT00844857.

Project description:Background and objectivesCurrent therapies for hyponatremia have variable effectiveness and tolerability, and in certain instances, they are very expensive. We examined the effectiveness, safety, and tolerability of urea for the treatment of inpatient hyponatremia.Design, setting, participants, & measurementsWe identified all patients hospitalized at the University of Pittsburgh Medical Center between July 2016 and August 2017 with hyponatremia (plasma sodium <135 mEq/L) who received urea, including a subgroup of patients who received urea as the sole drug therapy for hyponatremia (urea-only treated). We matched urea only-treated patients to a group of patients with hyponatremia who did not receive urea (urea untreated) and compared changes in plasma sodium at 24 hours and the end of therapy as well as the proportion of patients who achieved plasma sodium ?135 mEq/L. We abstracted data on adverse events and reported side effects of urea.ResultsFifty-eight patients received urea (7.5-90 g/d) over a median of 4.5 (interquartile range, 3-8) days and showed an increase in plasma sodium from 124 mEq/L (interquartile range, 122-126) to 131 mEq/L (interquartile range, 127-134; P<0.001). Among 12 urea only-treated patients, plasma sodium increased from 125 mEq/L (interquartile range, 122-127) to 131 mEq/L (interquartile range, 129-136; P=0.001) by the end of urea therapy. There was a larger increase in plasma sodium at 24 hours in urea only-treated patients compared with urea-untreated patients (2.5 mEq/L; interquartile range, 0-4.5 versus -0.5 mEq/L; interquartile range, -2.5 to 1.5; P=0.04), with no difference in change in plasma sodium by the end of therapy (6 mEq/L; interquartile range, 3.5-10 versus 5.5 mEq/L; interquartile range, 3-7.5; P=0.51). A greater proportion of urea only-treated patients achieved normonatremia, but this difference was not statistically significant (33% versus 8%; P=0.08). No patients experienced overly rapid correction of plasma sodium, and no serious adverse events were reported.ConclusionsUrea seems effective and safe for the treatment of inpatient hyponatremia, and it is well tolerated.

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Hyponatremia caused by water intoxication: successful treatment of psychiatric disturbances with olanzapine and fluoxetine.

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Hyponatremia caused by water intoxication: successful treatment of psychiatric disturbances with olanzapine and fluoxetine.

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