ABSTRACT
Pseudoephedrine is a sympathomimetic α- and ß-adrenergic receptor agonist that causes vasoconstriction and reduction in edema throughout the nasal passages. Coronary vasospasm associated with pseudoephedrine has been reported in the literature. We discuss the case of a patient with new-onset atrial fibrillation receiving metoprolol for rate control on a background of pseudoephedrine use for allergic rhinitis leading to acute myocardial infarction from multivessel coronary vasospasm. This case illustrates the importance of understanding the pharmacology of potential drug-drug interactions when managing patients with acute cardiovascular syndromes.
Subject(s)
Asthma/drug therapy , Atrial Fibrillation/drug therapy , Coronary Vasospasm , Metoprolol , Myocardial Infarction , Nitroglycerin/administration & dosage , Pseudoephedrine , Anti-Arrhythmia Agents/administration & dosage , Anti-Arrhythmia Agents/adverse effects , Asthma/complications , Atrial Fibrillation/complications , Atrial Fibrillation/diagnosis , Bronchodilator Agents/administration & dosage , Bronchodilator Agents/adverse effects , Coronary Angiography/methods , Coronary Vasospasm/chemically induced , Coronary Vasospasm/diagnostic imaging , Electrocardiography/methods , Female , Humans , Metoprolol/administration & dosage , Metoprolol/adverse effects , Middle Aged , Myocardial Infarction/diagnosis , Myocardial Infarction/etiology , Myocardial Infarction/physiopathology , Myocardial Infarction/therapy , Pseudoephedrine/administration & dosage , Pseudoephedrine/adverse effects , Treatment Outcome , Vasodilator Agents/administration & dosageABSTRACT
Multiple sclerosis (MS) is a central nervous system inflammatory disorder with evidence of peripheral immune dysregulation. Abnormalities of the immune suppressive cytokine TGF-ß have been reported, but not fully defined, in MS. Through a pathway-focused expression profiling of the peripheral blood, we found abnormalities of TGF-ßRII, SMAD4 and SMAD7 expression in subjects with MS, and reduction in the levels of TGF-ß regulated genes, indicating an overall reduction in TGF-ß signaling in MS. The response to exogenous TGF-ß was intact, however, indicating an extrinsic defect of TGF-ß signaling in MS. These results indicate that TGF-ß control is diminished in MS.
