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Whitten, James R.; Ruehter, Valerie L.; Pharm, B.

doi:10.1023/a:1026286109635

Cited by 15 publications

(4 citation statements)

References 6 publications

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“…Frequently prescribed atypical antipsychotics include risperidone (risperdal®), olanzapine (zyprexa®), and quetiapine (seroquel®). A number of case reports have suggested a possible association between atypical antipsychotics and hyponatremia [ 9 – 14 ]. Hyponatremia from older typical antipsychotics has also been observed, but their use has been declining in routine care, primarily due to their adverse side effect profile [ 7 , 15 , 16 ].…”

Section: Introductionmentioning

confidence: 99%

Atypical Antipsychotic Medications and Hyponatremia in Older Adults: A Population-Based Cohort Study

Gandhi

McArthur

Reiss

et al. 2016

Can J Kidney Health Dis

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BackgroundA number of case reports have suggested a possible association between atypical antipsychotic medications and hyponatremia. Currently, there are no reliable estimates of hyponatremia risk from atypical antipsychotic drugs.ObjectiveThe objective of this study was to examine the 30-day risk of hospitalization with hyponatremia in older adults dispensed an atypical antipsychotic drug relative to no antipsychotic use.DesignThe design of this study was a retrospective, population-based cohort study.SettingThe setting of this study was in Ontario, Canada, from 2003 to 2012.PatientsAdults 65 years or older with an identified psychiatric condition who were newly dispensed risperidone, olanzapine, or quetiapine in the community setting compared to adults with similar indicators of baseline health who were not dispensed such a prescription.MeasurementsThe primary outcome was the 30-day risk of hospitalization with hyponatremia. The tracer outcome (an outcome that is not expected to be influenced by the study drugs) was the 30-day risk of hospitalization with bowel obstruction. These outcomes were assessed using hospital diagnosis codes.MethodsUsing health administrative data, we applied a propensity score technique to match antipsychotic users 1:1 to non-users of antipsychotic drugs (58,008 patients in each group). We used conditional logistic regression to compare outcomes among the matched users and non-users.ResultsA total of 104 baseline characteristics were well-balanced between the two matched groups. Atypical antipsychotic use compared to non-use was associated with an increased risk of hospitalization with hyponatremia within 30 days (86/58,008 (0.15 %) versus 53/58,008 (0.09 %); relative risk 1.62 (95 % confidence interval (CI) 1.15 to 2.29); absolute risk increase 0.06 % (95 % CI 0.02 to 0.10)). The limited number of events precluded some additional analyses to confirm if the association was robust. Atypical antipsychotic use compared to non-use was not associated with hospitalization with bowel obstruction within 30 days (55/58,008 (0.09 %) versus 44/58,008 (0.08 %); relative risk 1.25 (95 % CI 0.84 to 1.86)).LimitationsWe could only study older adults within our data sources.ConclusionsIn this study, the use of an atypical antipsychotic was associated with a modest but statistically significant increase in the 30-day risk of a hospitalization with hyponatremia. The association was less pronounced than that described with other psychotropic drugs.Electronic supplementary materialThe online version of this article (doi:10.1186/s40697-016-0111-z) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

Atypical Antipsychotic Medications and Hyponatremia in Older Adults: A Population-Based Cohort Study

Gandhi

McArthur

Reiss

et al. 2016

Can J Kidney Health Dis

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“…The association was stronger for first-generation antipsychotics than secondgeneration antipsychotics (Falhammar et al, 2019). Several psychotropic drugs have been reported to be associated with the features of the SIADH, but without demonstration of unsuppressed plasma AVP (Peck and Shenkman, 1979;Whitten and Ruehter, 1997;Bachu et al, 2006).…”

Section: Haloperidolmentioning

confidence: 99%

The Role of Vasopressin V2 Receptor in Drug-Induced Hyponatremia

Kim

2021

Front. Physiol.

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Hyponatremia is frequently encountered in clinical practice and usually induced by renal water retention. Many medications are considered to be among the various causes of hyponatremia, because they either stimulate the release of arginine vasopressin (AVP) or potentiate its action in the kidney. Antidepressants, anticonvulsants, antipsychotics, diuretics, and cytotoxic agents are the major causes of drug-induced hyponatremia. However, studies addressing the potential of these drugs to increase AVP release from the posterior pituitary gland or enhance urine concentration through intrarenal mechanisms are lacking. We previously showed that in the absence of AVP, sertraline, carbamazepine, haloperidol, and cyclophosphamide each increased vasopressin V2 receptor (V2R) mRNA and aquaporin-2 (AQP2) protein and mRNA expression in primary cultured inner medullary collecting duct cells. The upregulation of AQP2 was blocked by the V2R antagonist tolvaptan or protein kinase A (PKA) inhibitors. These findings led us to conclude that the nephrogenic syndrome of inappropriate antidiuresis (NSIAD) is the main mechanism of drug-induced hyponatremia. Previous studies have also shown that the V2R has a role in chlorpropamide-induced hyponatremia. Several other agents, including metformin and statins, have been found to induce antidiuresis and AQP2 upregulation through various V2R-independent pathways in animal experiments but are not associated with hyponatremia despite being frequently used clinically. In brief, drug-induced hyponatremia can be largely explained by AQP2 upregulation from V2R-cAMP-PKA signaling in the absence of AVP stimulation. This paper reviews the central and nephrogenic mechanisms of drug-induced hyponatremia and discusses the importance of the canonical pathway of AQP2 upregulation in drug-induced NSIAD.

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“…A number of drugs may also cause SIADH and hyponatremia, including tricyclic antidepressants, selective serotonin reuptake inhibitors, conventional and atypical antipsychotics (e.g., haloperidol and risperidone) [17, 18], narcotics, angiotensin-converting enzyme (ACE) inhibitors, sulfonylureas used in the treatment of type-2 diabetes, thiazide diuretics, and antineoplastic agents (vincristine, vinblastine, cyclophosphamide) [16]. …”

Section: Hyponatremia: Definition Incidence and Pathophysiologymentioning

confidence: 99%

“…This distinction is relevant, as the rate at which hyponatremia develops significantly influences the severity of CNS manifestations and potential complications [1, 18]. Acute severe hyponatremia occurs when serum [Na + ] falls rapidly below 120 mEq/l in less than 48 h. Because homeostatic mechanisms in the brain cannot react with sufficient speed to compensate for this rapid change, acute severe hyponatremia, if untreated, can lead to cerebral edema, irreversible neurologic damage, respiratory arrest, brainstem herniation, and even death[1, ][21].…”

Section: Hyponatremia: Definition Incidence and Pathophysiologymentioning

confidence: 99%

Consequences of Inadequate Management of Hyponatremia

2005

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Dilutional hyponatremia is a commonly observed disorder in hospitalized patients. It represents an excess of water in relation to prevailing sodium stores and is most often associated with a high plasma level of arginine vasopressin, including that found in patients with the syndrome of inappropriate antidiuretic hormone secretion. Hyponatremia may be classified as either acute or chronic depending on the rate of decline of serum sodium concentration, and can lead to a wide range of deleterious changes involving almost all body systems. Serious complications of dilutional hyponatremia most frequently involve the central nervous system. In fact, acute severe hyponatremia is potentially life-threatening and must be treated promptly and aggressively. Chronic hyponatremia often develops in patients with nonrenal diseases and is associated with increased morbidity and mortality. In patients hospitalized for congestive heart failure, hyponatremia is linked to a poor prognosis and increased length of hospital stay. Prompt recognition and optimal management of hyponatremia in hospitalized patients may reduce in-hospital mortality and symptom severity, allow for less intensive hospital care, decrease the duration of hospitalization and associated costs, and improve the treatment of underlying comorbid conditions and patients’ quality of life. The proper treatment of dilutional hyponatremia, especially when chronic, must avoid increasing serum sodium too rapidly, which can lead to permanent or fatal neurologic sequelae. The treatment of hyponatremia may be facilitated by emerging therapies that block the actions of arginine vasopressin at V₂ and V_1a receptors to promote aquaresis, the electrolyte-sparing elimination of free water, and elevate serum sodium concentrations.

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Untitled

Cited by 15 publications

References 6 publications

Atypical Antipsychotic Medications and Hyponatremia in Older Adults: A Population-Based Cohort Study

Atypical Antipsychotic Medications and Hyponatremia in Older Adults: A Population-Based Cohort Study

The Role of Vasopressin V2 Receptor in Drug-Induced Hyponatremia

Consequences of Inadequate Management of Hyponatremia

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