Lysol: a substance for potential abuse.
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Cresols↗
Biomedical subjects
M W Kelly
Publications and source records attributed to M W Kelly.
Bruising associated with the use of fluoxetine.
OBJECTIVE: To report a case of suspected fluoxetine-induced bruising and review the literature surrounding this rare adverse effect. CASE SUMMARY: A 31-year-old white woman was diagnosed with depression and treated with fluoxetine. After fluoxetine 20 mg/d for 6 weeks, she reported bruising that was disproportionate to any trauma incurred. Her prothrombin time, partial thromboplastin time, and complete blood cell count were within normal limits. Fluoxetine was suspected to be the cause of this bruising. The patient did not want to discontinue the medication and has continued to bruise while continuing fluoxetine therapy. DISCUSSION: Frequently encountered adverse effects caused by fluoxetine use include nausea, nervousness, and insomnia, but hematologic effects have also been reported. These include bleeding or bruising with prolonged bleeding time, increased prothrombin time and partial thromboplastin time, and thrombocytopenia. The mechanism behind these adverse effects is the prevention of serotonin-induced amplification of platelet aggregation by fluoxetine. Blockade of 5-hydroxytryptamine uptake in the platelets by fluoxetine reduces or depletes the platelet serotonin stores, thereby predisposing a patient with a mild underlying platelet disorder to a fluoxetine-induced hematologic disorder. CONCLUSIONS: Fluoxetine has been reported to produce bruising, bleeding, and other hematologic disorders. It should be used with caution when treating patients with thrombocytopenia or with proven or suspected platelet dysfunction.
Antidepressive Agents, Second-Generation↗
Sudden cardiac death with clozapine and sertraline combination.
OBJECTIVE: To report a case of sudden cardiac death in a patient receiving combination therapy with clozapine and sertraline. CASE SUMMARY: A 26-year-old white man was discovered dead at his residence. His medical history included chronic paranoid schizophrenia, obsessive-compulsive disorder, major depressive disorder, obstructive sleep apnea, and akathisia. He had no prior history of cardiovascular disease. His medication regimen included clozapine 100 mg twice daily (started 4 y prior to his death), risperidone 3 mg twice daily, sertraline 200 mg once daily, atenolol 50 mg twice daily, and lorazepam 0.5 mg four times daily. Autopsy and toxicology studies revealed cardiomegaly suggestive of idiopathic cardiomyopathy, single-vessel coronary artery disease, sertraline and clozapine blood concentrations in the expected range, undetectable lorazepam and risperidone blood concentrations, obesity, and moderate fatty changes to the liver. The most likely cause of death was sudden cardiac death due to acute cardiac arrhythmia. DISCUSSION: Clozapine is structurally similar to the tricyclic antidepressants, which have type 1 A antiarrhythmic properties. Case reports have described electrocardiographic abnomalities, cardiomyopathy, and fatal myocarditis associated with its use. Unexplained death in patients on clozapine therapy has also been reported. Sertraline appears to have less cardiac effect; however, one report has observed clinically significant QT prolongation during sertraline therapy. CONCLUSIONS: Clozapine-induced cardiomyopathy and cardiac arrhythmia from clozapine and/or sertraline use may have contributed to this man's death.
Adult↗
Current perspectives on the management of seasonal affective disorder.
OBJECTIVE: To concisely review the etiology and current treatment modalities of seasonal affective disorder (SAD). DATA SOURCES: A MEDLINE search (1966-1999) was performed using the search term "seasonal affective disorder." The search was subsequently focused to "drug therapy" with limits of human studies and English-language papers. The search term "light therapy" was combined with "seasonal affective disorder." STUDY SELECTION AND DATA EXTRACTION: Articles discussing the epidemiology and treatment of SAD were independently examined by each author. Additional literature was reviewed from selected references identified by the original articles. DATA SYNTHESIS: SAD most likely results from a deficiency in serotonin. Light therapy remains the therapeutic intervention with the most experience and success. Selective serotonin reuptake inhibitors (SSRIs) have also shown benefit in treating the disorder. CONCLUSION: SAD is an important subtype of major depressive disorder. Clinicians should remain vigilant for signs and symptoms of the illness. Successful treatment may include light therapy or antidepressants, particularly SSRIs.
Antidepressive Agents↗
Mibefradil, a pharmacologically distinct calcium antagonist.
Mibefradil is the prototype of a new class of calcium antagonists that selectively block T-type voltage-gated plasma membrane calcium channels in vascular smooth muscle. The drug is structurally and pharmacologically different from traditional calcium antagonists. It does not have negative inotropism at therapeutic concentrations, and is not associated with reflex activation of neurohormonal and sympathetic systems. In clinical studies of hypertension, mibefradil 50 and 100 mg/day reduced trough sitting diastolic and systolic blood pressures in a dose-related manner. Dosages exceeding 100 mg/day generally did not result in significantly greater efficacy, but were associated with a higher frequency of adverse events. No first-dose hypotensive phenomenon was observed. Mibefradil has antiischemic properties resulting from dilation of coronary and peripheral vascular smooth muscle, and a slight reduction in heart rate. In clinical studies of chronic stable angina pectoris, dose-related increases in exercise duration, time to onset of angina, and time to 1-mm ST-segment depression during exercise tolerance tests occurred. Mibefradil reduced the number and duration of ischemic events recorded by 48-hour ambulatory electrocardiograph (ECG) monitoring, as well as number of anginal episodes and nitroglycerin consumption. Favorable hemodynamic and clinical profiles are reported, including high trough:peak ratios (> 80%), high oral bioavailability, and long elimination half-life (17-25 hrs) permitting once/day dosing. Dizziness, headache, leg edema, and lightheadedness are frequently reported, but overall the agent is well tolerated. First-degree atrioventricular block and sinus bradycardia are the most frequent ECG changes caused by the drug. In vitro studies indicate mibefradil inhibits cytochrome P450 1A2, 2D6, and 3A4, resulting in elevated plasma concentrations of drugs metabolized by those isoenzymes. Therefore, it is contraindicated in patients receiving terfenadine, astemizole, cisapride, lovastatin, or simvastatin.
Angina Pectoris↗