Abstract

Introduction:Recently, controversy has surrounded a 2011 Food and Drug Administration warning against using citalopram at doses >40 mg/day due to QTc prolonging effects.

Methods:Patients ≥18 years old at the VA North Texas Health Care System were included in this retrospective review if they had received at least 1 prescription for a 30-day supply of citalopram between January 1, 2007, and February 29, 2012, and had a baseline electrocardiogram (ECG) within 1 year before initiation or dose increase of citalopram and at least 1 repeat ECG within 3 months after citalopram initiation or dose increase. The primary endpoint was the prevalence of QTc prolongation (QTc interval ≥470 ms for men and ≥480 ms for women) after initiation or a dose increase of citalopram. For secondary objectives, Fisher exact tests were used determine if there was a dose-dependent difference in prevalence of QTc prolongation among the whole study sample and among the subgroup of patients ≥60 years old.

Results:Among the entire study sample, QTc prolongation was identified in 12 patients (16.4%) after initiation or a dose increase of citalopram. In the subgroup of patients ≥60 years old, QTc prolongation was identified in 7 patients (21.9%). Prevalence of QTc prolongation increased with dose in the entire study population (P = .016) and in patients ≥60 years (not significant).

Discussion:This retrospective study suggests that citalopram produces a dose-dependent increase in QTc interval.

Abstract

Introduction: Many psychotropic medications carry a risk of prolonging the QT interval and increasing the risk of developing Torsade de pointes (TdP). The goal of this study was to evaluate whether patients taking psychotropic agents with a known risk of TdP are being monitored at a community hospital through the use of electrocardiograms (EKGs).

Methods: This was a retrospective chart review of 100 adult patients—50 from general medicine floors and 50 from psychiatric units—who were taking at least one psychotropic agent with a known risk of TdP during hospitalization.

Results: The mean number of medications with QT-prolongation risk administered to the psychiatric and general medicine patients was 4.2 ± 1.7 and 3.9 ± 2.0, respectively (P = .7484). Thirty-two of the psychiatric patients (64%) and 48 of the general medicine patients (96%) received EKGs during their hospitalization (P < 0.0001). Of those newly starting the target medications, 58% (18 of 31) of the psychiatric patients and 71% (5 of 7) of the general medicine patients received a baseline EKG. The difference was not statistically significant (P = .6807). Overall, 8 patients (8%) had corrected QT (QTc) intervals >500 ms. Four had repeat EKGs performed, and none had medication changes made to decrease TdP risk.

Discussion: Many inpatients on psychiatric medications received multiple medications with a risk of TdP, but not all received monitoring through baseline or repeat EKGs when warranted. Patients with QTc intervals >500 ms were not appropriately managed to lower their risk of TdP. Pharmacists thus can help improve the monitoring and management of QT prolongation.

Abstract

Introduction: Excessive weight gain, glucose intolerance, and dyslipidemia are well-known physical side effects of the metabolic syndrome commonly associated with atypical antipsychotic (AAP) treatment. We review these side effects of AAPs and their monitoring and management strategies.

Methods: A literature search was conducted to identify articles published on the prevalence, monitoring, and management of cardiometabolic side effects of AAPs.

Results: Comparative risk of AAPs on weight gain, hyperlipidemia, glucose intolerance, and QT interval corrected for heart rate prolongation varies across the AAPs currently available. Likewise, pharmacologic and nonpharmacologic options investigated for management of these side effects, and monitoring those at appropriate intervals, differ based on the clinical condition and risk factors identified.

Discussion: Atypical antipsychotics in general have little difference among them in short-term efficacy; however, the prevalence of their physical side effects substantially distinguishes them. It is of importance that clinicians carefully select AAPs bearing in mind the presence of risk factors, initiating patients directly on AAPs with a low risk of cardiometabolic side effects, and monitoring and managing those side effects at appropriate intervals.

Abstract

Introduction: Antipsychotics represent a large portion of the psychotropics that may induce hyperprolactinemia. Clinical psychiatric pharmacists must be adept in stratifying the relative risk of hyperprolactinemia among psychotropics, identifying patient risk factors, recognizing differential diagnoses, and recommending therapeutic alternatives and treatment strategies. High-potency, typical antipsychotics are more likely to elevate prolactin although exceptions to the rule exist.

Methods: A literature search of PubMed and Google Scholar was performed to identify English language articles on the treatment of antipsychotic-induced hyperprolactinemia in humans. Methodological rigor is summarized for compiled studies in addition to feasibility and limitations of application to clinical practice.

Results: There is an absence of robust evidence for the management of antipsychotic-induced hyperprolactinemia. Among the pharmacological treatments studied, aripiprazole (switching or augmentation) possessed the strongest evidence. Pharmacological treatments with less evidence encompassed dose reduction, switching to lower potency antipsychotics, and adding dopamine agonists. To date, no head-to-head studies have been published on the above approaches.

Discussion: Atypical antipsychotics with low affinity for dopamine (D2) receptors, such as olanzapine, are logical alternatives for the patient experiencing drug-induced hyperprolactinemia. When augmentation is clinically preferred to switching, a viable option is the addition of a full or partial dopamine agonist, such as bromocriptine or aripiprazole, respectively. Patient-specific risk of psychiatric decompensation and the severity of symptomatic hyperprolactinemia should be weighed when formulating treatment strategies.

Abstract

Sexual dysfunction is an underdiscussed adverse effect to selective serotonin reuptake inhibitors (SSRIs) and may increase the risk for discontinuation and nonadherence to antidepressant pharmacotherapy. Given the prevalence of depression, health care providers should educate patients about SSRI-associated sexual dysfunction in order to promote patient awareness and medication adherence. This study evaluated primary literature from 1997 to 2015 to identify SSRI-related sexual side effects, therapeutic alternatives, and treatment strategies. The results indicate that paroxetine is associated with the greatest rate of sexual dysfunction among the SSRIs. Potential alternatives to SSRI treatment include bupropion, mirtazapine, vilazodone, vortioxetine, and serotonin-norepinephrine reuptake inhibitors. In the event that a subject responds solely to SSRIs but experiences unwanted sexual side effects, bupropion may be added as an adjunctive medication. Some limited evidence also suggests that saffron may reduce some aspects of sexual dysfunction, excluding ability to reach orgasm.

Abstract

Antidepressant medications are associated with a variety of genitourinary and adverse sexual effects, such as urinary hesitation, priapism, and delayed ejaculation. Here, we report a case of priapism and renal colic following initiation of duloxetine in a patient with history of tolerated selective serotonin reuptake inhibitor treatment. To our knowledge, this represents the first report of priapism and renal colic associated with duloxetine use. This case contributes to the current body of evidence describing adverse genitourinary and sexual effects associated with antidepressant medications.

Abstract

Introduction: Cardiovascular agents can be associated with a negative effect on cognition, especially in older adults, critically ill people, and those with baseline cognitive impairment. Negative effect on cognition is commonly reported as uncomplicated acute confusion and delirium and, less commonly, chronic cognitive changes due to drug-induced depression and/or dementia.

Methods: A literature review of case reports, case series, prospective cohort studies, clinical trials, and literature reviews were included in this study. Articles were located using online databases PubMed and Medline using the following keywords: antiarrhythmic agents, anticholinergic burden, antihypertensive agents, beta-blockers, cardiovascular agents, cognitive impairment, delirium, cognition, dementia, depression, digoxin, diuretics, and drug-induced cognitive impairment.

Results: In general, use of all antihypertensives, especially in the case of polypharmacy or inappropriate dosing, can lead to hypotension and/or bradycardia, and thus lead to mental/cognitive status change due to decreased cerebral perfusion. Use of diuretics can be associated with fluid/electrolyte and/or acid-base imbalance, resulting in the onset of confusion and delirium. In addition, cardiovascular agents with central bioavailability, such digoxin and select antiarrhythmics, and antihypertensives may carry a risk for cognitive impairment due to various mechanisms proposed, such as antagonism of central muscarinic acetylcholine receptors, neurotransmission imbalance in the brain, and disruption of physiologic function of sodium/potassium ATPase in the neuronal cells.

Discussion: When dealing with an individual who presents with acute, subacute, and chronic changes in cognitive function, one should perform a thorough medication history as the first step in order to aid in the identification of drug-induced cognitive impairment.

Abstract

Introduction: Antimicrobial-induced cognitive side effects are often overlooked or underreported. Literature often reports symptoms of antimicrobial-induced cognitive impairment under more general blanket terms, such as neuropsychiatric side effects, neurotoxicity, or drug-induced delirium or encephalopathy.

Methods: A PubMed search using terms including antibiotics, antifungals, antivirals, antimalarials, side effects, cognitive, neurotoxicity, encephalopathy, and delirium was conducted. Respectively, symptoms of cognitive impairment were teased out of the multiple neurologic complications presented for each case and reported based on antimicrobial class. Articles were excluded if they focused solely on neuropsychiatric side effects such as seizures, psychosis, hallucinations, or mood disturbances, were conducted in animals, or involved antiretroviral medication therapies.

Results: Of over 50 case reviews, case reports, retrospective chart reviews, and prospective cohort studies analyzed, 25 were deemed appropriate for purposes of this review. Common antimicrobial-induced cognitive side effects for all antimicrobial classes included confusion, delirium, encephalopathy, and impaired concentration or attention. Recurring risk factors included, but were not limited to, older age and renal impairment. Mechanisms of cognitive impairment were relatively specific to each antimicrobial class.

Discussion: Awareness of the potential for antimicrobial-induced cognitive side effects, including the general time frame of symptom onset and symptom presentation, is critical in challenging patient cases. This review article aims to summarize the risk factors, clinical symptoms, mechanisms, and management of antimicrobial-induced cognitive side effects. Pharmacists can play a key role in prevention through adjustment of medications for renal or hepatic dysfunction, avoidance of polypharmacy, and knowledge of critical drug interactions that may precipitate cognitive decline.