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Introduction: Serotonin syndrome and neuroleptic malignant syndrome are caused by 2 distinct pathologies; however, the clinical presentation associated with both syndromes share many features. Methods: We describe a 56-year-old male patient who presented to our facility with seizures, leukocytosis, fevers, extremity hyperreflexia, and signs of autonomic dysfunction as evidenced by cardiovascular instability. The patient was noted to be taking vortioxetine, trazodone, lamotrigine, lurasidone, and carbidopa-levodopa as outpatient medications for his depression, an unspecified mood disorder, and Parkinson disease. Following a robust workup and failure of other therapies, all serotonergic and dopaminergic medications were held, and the patient was tried on cyproheptadine for serotonin syndrome, which led to the cessation of fevers. Bromocriptine was added to the regimen, which led to the resolution of the remainder of the patient's symptoms. Results: The overlapping symptomatology of several key diagnostic criteria for both serotonin syndrome and neuroleptic malignant syndrome as well as their nature as diagnoses of exclusion require an evaluation of the patient's aggregate improvement following targeted pharmacologic strategies for both syndromes. The efficacy of both cyproheptadine and bromocriptine when administered concomitantly support the concurrent pathologies. Discussion: Clinicians at the bedside must be cognizant of the potential for clinically relevant drug-drug interactions that may present with overlapping pathologies.
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Olanzapine is a second-generation antipsychotic (SGA) that has been shown to promote disease remission in persons with treatment-resistant depression when used in combination with fluoxetine. However, tolerability of treatment augmentation with SGAs may be limited because of common adverse effects, such as weight gain, hypertriglyceridemia, and elevated glucose. Data exist pertaining to rare localized edematous reactions or angioedema with use of SGAs, but diffuse whole-body edema has yet to be documented. A 47-year-old white female with treatment-resistant depression presented with a 5-day history of weight gain and swelling of her torso and extremities. Five days prior, she had initiated olanzapine/fluoxetine 6/50 mg daily following failure of fluoxetine 40 mg daily monotherapy. The patient was noted to have gained 3.6 kg since her last appointment and exhibited profuse pitting edema on her forearms, lower limbs, hands, and chest. Olanzapine/fluoxetine was discontinued and the patient was prescribed a 3-day course of a loop diuretic for symptomatic management. A follow-up visit 5 days later noted complete resolution of symptoms. Because of the temporal relationship of symptoms with initiation of olanzapine, we recommend monitoring for edema with initiation and/or titration of therapy.
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BACKGROUND: Generalized anxiety disorder (GAD) and major depressive disorder (MDD) are prevalent in patients with asthma. These disorders may increase asthma severity and decrease asthma control. No studies have evaluated the impact of achieving antidepressant target dose optimization compared with not achieving antidepressant target doses on asthma control in uninsured and underinsured patients. OBJECTIVE: To evaluate the impact of achieving antidepressant target dose optimization in uninsured and underinsured adult asthma patients with GAD and/or MDD on the risk of severe asthma exacerbations and number of asthma-related outcomes. METHODS: We conducted a retrospective cohort study of uninsured and underinsured adult asthma patients with GAD and/or MDD who have been initiated on a single antidepressant and maintained on a stable dose for 8 weeks (index date). Eligible patients were followed for 12-24 months after the index date and separated into those who achieved a target dose (target group) and those who did not (control group). Poisson regression was used to compare the risk of severe exacerbations, and analysis of covariance was used to compare the number of severe exacerbations and other asthma-related outcomes between the target and control groups during the 1- and 2-year post-index periods. RESULTS: A total of 61 patients (24 in the target group and 37 in the control group) met inclusion criteria. The target group had a reduced risk of severe asthma exacerbations compared with the control group during the 1-year post-index (adjusted risk reduction [RR] 0.46, 95% confidence interval [CI] 0.26-0.82) and 2-year post-index (adjusted RR 0.5, 95% CI 0.3-0.82) periods. The target group also experienced a lower number of severe asthma exacerbations and other asthma-related outcomes during the 1- and 2-year post-index periods compared with the control group after adjusting for confounders. CONCLUSIONS: Among uninsured and underinsured asthma patients with GAD and/or MDD who were initiated on a single antidepressant, those who were titrated to achieve target doses had a reduced risk of severe asthma exacerbations and a lower number of asthma-related outcomes than those who were not optimized to achieve target doses.
Asunto(s)
Antiasmáticos/uso terapéutico , Antidepresivos/uso terapéutico , Trastornos de Ansiedad/tratamiento farmacológico , Asma/tratamiento farmacológico , Pacientes no Asegurados , Adolescente , Adulto , Anciano , Antiasmáticos/administración & dosificación , Antiasmáticos/farmacocinética , Antidepresivos/administración & dosificación , Antidepresivos/farmacocinética , Trastornos de Ansiedad/complicaciones , Asma/complicaciones , Estudios de Cohortes , Femenino , Humanos , Masculino , Persona de Mediana Edad , Estudios Retrospectivos , Índice de Severidad de la Enfermedad , Adulto JovenRESUMEN
Sacubitril/valsartan is an angiotensin receptor-neprilysin inhibitor approved for the treatment of heart failure with reduced ejection fraction (HFrEF). Valsartan is well studied, but sacubitril has much left to understand. This report describes a 31-year-old African American female diagnosed with HFrEF who presented with a 7-day history of psychiatric symptoms following a dose increase in sacubitril/valsartan. Prior to the dose increase, the patient had no history of psychiatric diagnoses, but upon hospital presentation, family described instances of confabulation, paranoia, delusions, hallucinations, and sleep disturbances. Laboratory tests were unremarkable, ruling out infectious processes and illicit substance use. However, cranial computed tomography scans depicted intracranial volume loss abnormal for age with commensurate mild ventricular enlargement. Sacubitril/valsartan was discontinued inpatient, symptoms resolved, and the medication intolerance was documented. Clinical trials involving sacubitril/valsartan lack systematic documentation of cognitive symptoms, but active studies exploring the role of neprilysin inhibition may expand knowledge of possible psychiatric adverse effects.