ABSTRACT
INTRODUCTION: Guanfacine, an alpha-2 adrenergic agonist, is used to treat attention deficit hyperactivity disorder (ADHD). Although cardiovascular effects including hypotension and bradycardia are common adverse effects of guanfacine, the effect of guanfacine on QT intervals remains unclear. The association between the serum concentration of guanfacine and its toxicity has also not been fully investigated. CASE REPORT: This is a case of a 21-year-old woman with ADHD who developed repeated presyncope 1 day before admission. She was taking 3 mg of extended-release guanfacine and 50 mg of sertraline. On admission, she had bradycardia and hypotension. An electrocardiogram (ECG) showed a QT interval of 0.68 s and a QTcF interval of 0.648 s. The QT intervals were manually measured and corrected by the Fridericia formula (QTcF = QT/RR1/3). Although she denied taking an overdose of guanfacine and other drugs, we suspected guanfacine toxicity. The serum guanfacine concentration was 13.0 ng/mL on admission and decreased to 3.2 ng/mL on day 1 and 0.4 ng/mL on day 2. Changes in QTcF intervals and her vital signs correlated with serum guanfacine concentrations. CONCLUSION: Supratherapeutic serum guanfacine concentrations may induce QT prolongation.
Subject(s)
Attention Deficit Disorder with Hyperactivity , Hypotension , Female , Humans , Young Adult , Adrenergic alpha-2 Receptor Agonists/toxicity , Attention Deficit Disorder with Hyperactivity/chemically induced , Attention Deficit Disorder with Hyperactivity/drug therapy , Bradycardia/chemically induced , Guanfacine/toxicity , Hypotension/chemically inducedABSTRACT
Guanfacine hydrochloride extended-release (GXR) is used to treat attention deficit hyperactivity disorder. It is a selective α2A-adrenorecepor agonist that was reported to cause QT prolongation and hypotension in the event of overdosing. We report the case of a 17-year-old man who took 226 tablets of GXR 3 mg for attempted suicide. He was found complaining of dyspnea, and emergency medical services were called. When the patient was transferred to our hospital, his Glasgow coma scale was 12 (E4V3M5). He was agitated and hypoxemic. He was intubated for invasive mechanical ventilation under sedation. His chest X-ray and computed tomography scan showed pulmonary edema. Transthoracic echocardiography showed markedly reduced cardiac function. His serum guanfacine concentration peaked on day 3 after admission. His pulmonary edema improved quickly after a decrease in serum guanfacine concentration, but cardiac decompensation persisted for about 1 month. This case reveals that the decline in cardiac function after guanfacine intoxication is prolonged even after its serum concentration has decreased.
Subject(s)
Guanfacine , Pulmonary Edema , Adolescent , Humans , Male , Adrenergic alpha-2 Receptor Agonists/adverse effects , Attention Deficit Disorder with Hyperactivity/drug therapy , Delayed-Action Preparations/adverse effects , Guanfacine/blood , Guanfacine/toxicity , Pulmonary Edema/chemically inducedSubject(s)
Adrenergic alpha-2 Receptor Agonists/toxicity , Adrenergic alpha-2 Receptor Agonists/therapeutic use , Attention Deficit Disorder with Hyperactivity/drug therapy , Guanfacine/toxicity , Guanfacine/therapeutic use , Adrenergic alpha-2 Receptor Agonists/blood , Child , Emergency Service, Hospital , Female , Guanfacine/blood , Humans , Lethargy/etiology , SleepinessABSTRACT
Guanfacine in analgesic doses of 2.0 and 4.0 mg/kg inhibits the background activity of the spinal cord posterior horn neurons and their responses to nociceptive stimulation of the receptive field in conscious rats. Naloxone (0.1 mg/kg) does not change, whereas prazosin and yohimbine (both on doses of 0.1 mg/kg) remove and partly relieve the depressant effect of guanfacine.