An 82-yr-old man was presented with fever and cough accompanied by generalized erythematous rash. He had taken mexiletine for 5 months, as he had been diagnosed with dilated cardiomyopathy and ventricular arrhythmia. Laboratory studies showed peripheral blood eosinophilia and elevated liver transaminase levels. Chest radiographs showed multiple nodular consolidations in both lungs. Biopsies of the lung and skin lesions revealed eosinophilic infiltration. After a thorough review of his medication history, mexiletine was suspected as the etiologic agent. After discontinuing the mexiletine and starting oral prednisolone, the patient improved, and the skin and lung lesions disappeared. Subsequently, mexiletine was confirmed as the causative agent based on a positive patch test. Drug-induced hypersensitivity syndrome is a severe adverse reaction to drugs and results from treatment with anticonvulsants, allopurinol, sulfonamides, and many other drugs. Several cases of mexiletine-induced hypersensitivity syndrome have been reported in older Japanese males with manifestation of fever, rash, peripheral blood eosinophilia, liver dysfunction without other organ involvement. Here, we report a case of mexiletine-induced hypersensitivity syndrome which presented as eosinophilic pneumonia in a Korean male.
Aged, 80 and over ; Anti-Arrhythmia Agents/*adverse effects ; Arrhythmias, Cardiac/drug therapy ; Cardiomyopathy, Dilated/drug therapy ; Drug Hypersensitivity/*diagnosis/etiology ; Exanthema/pathology ; Humans ; Lung/pathology/radiography ; Male ; Mexiletine/*adverse effects ; Pulmonary Eosinophilia/*chemically induced/*diagnosis ; Syndrome ; Tomography, X-Ray Computed

Levocetirizine is a second-generation nonsedative antihistaminic agent that has been demonstrated to be safe and effective for treating allergic disease. There was only one case report of levocetirizine-induced liver toxicity, but a liver biopsy was not performed. In this article, we present the first case of levocetirizine-induced liver injury with histologic findings. A 48-year-old man was hospitalized with jaundice and generalized pruritus that had developed after 2 months of therapy with levocetirizine for prurigo nodularis. Laboratory findings revealed acute hepatitis with cholestasis. A liver biopsy demonstrated portal inflammation and hepatitis with apoptotic hepatocytes. The patient fully recovered 3 weeks after withdrawing levocetirizine. Although levocetirizine is safe and effective, physicians should be aware of its potential hepatotoxicity.
Cetirizine/*adverse effects/therapeutic use ; Chemical and Drug Induced Liver Injury/*diagnosis/pathology ; Histamine H1 Antagonists, Non-Sedating/*adverse effects/therapeutic use ; Humans ; Hypersensitivity/drug therapy ; Jaundice/etiology ; Liver/pathology ; Male ; Middle Aged ; Pruritus/etiology

Trimethoprim-sulfamethoxazole (TMP-SMZ) is a commonly used antibiotic that has been associated with drug rash with eosinophilia and systemic symptoms (DRESS) syndrome. DRESS syndrome is characterised by fever, rash, lymphadenopathy, eosinophilia and one or more major organ involvement. Although rare, TMP-SMZ is a recognised cause of fulminant hepatic failure. We report a 17-year-old Chinese male adolescent who presented with fever, myalgia, generalised maculopapular rash and lymphadenopathy after taking TMP-SMZ for acne vulgaris. He subsequently developed hepatic encephalopathy and was worked up for urgent liver transplantation. He responded well to extracorporeal liver dialysis (originally intended as a bridging therapy) and subsequently recovered without the need for liver transplantation. This case report highlights the importance of early recognition of TMP-SMZ-induced DRESS syndrome and the need for early discontinuation of the drug in the affected patient. Extracorporeal liver dialysis and transplantation should be considered in the management of TMP-SMZ-induced fulminant hepatic failure.
Acne Vulgaris ; complications ; drug therapy ; Adolescent ; Anti-Infective Agents ; adverse effects ; Biopsy ; Drug Eruptions ; etiology ; Drug Hypersensitivity Syndrome ; diagnosis ; etiology ; Fever ; etiology ; Humans ; Liver Failure, Acute ; etiology ; therapy ; Lymphatic Diseases ; etiology ; Male ; Myalgia ; etiology ; Renal Dialysis ; methods ; Skin ; pathology ; Treatment Outcome ; Trimethoprim, Sulfamethoxazole Drug Combination ; adverse effects

INTRODUCTIONA 22-year-old Malay soldier developed dapsone hypersensitivity syndrome 12 weeks after taking maloprim (dapsone 100 mg/pyrimethamine 12.5 mg) for anti-malarial prophylaxis.

CLINICAL PICTUREHe presented with fever, rash, lymphadenopathy and multiple-organ involvement including serositis, hepatitis and thyroiditis. Subsequently, he developed congestive heart failure with a reduction in ejection fraction on echocardiogram, and serum cardiac enzyme elevation consistent with a hypersensitivity myocarditis.

TREATMENTMaloprim was discontinued and he was treated with steroids, diuretics and an angiotensin-converting-enzyme inhibitor.

OUTCOMEHe has made a complete recovery with resolution of thyroiditis and a return to normal ejection fraction 10 months after admission.

CONCLUSIONIn summary, we report a case of dapsone hypersensitivity syndrome with classical symptoms of fever, rash and multi-organ involvement including a rare manifestation of myocarditis. To our knowledge, this is the first case of dapsone-related hypersensitivity myocarditis not diagnosed in a post-mortem setting. As maloprim is widely used for malaria prophylaxis, clinicians need to be aware of this unusual but potentially serious association.

Abdominal Pain ; drug therapy ; Adult ; Anti-Inflammatory Agents, Non-Steroidal ; adverse effects ; therapeutic use ; Biopsy ; Dapsone ; adverse effects ; therapeutic use ; Diagnosis, Differential ; Drug Hypersensitivity ; complications ; pathology ; Echocardiography ; Electrocardiography, Ambulatory ; Fever ; drug therapy ; Follow-Up Studies ; Humans ; Male ; Myocarditis ; diagnosis ; etiology ; Radiography, Thoracic ; Skin ; pathology ; Thyrotoxicosis ; diagnosis ; etiology

Myocarditis often occurs due to viral infections and postviral immune-mediated responses. Hypersensitivity myocarditis is a rare form of myocarditis. Numerous drugs can induce myocarditis, which is typically reversible after withdrawal of the causative agent. Here, we report a case of hypersensitivity myocarditis that was probably triggered by amoxicillin and that resolved completely with heart failure management as well as discontinuation of the drug. A 68-year-old woman presented with acute chest pain mimicking acute coronary syndromes, but the coronary angiography was normal. A recent history of taking medications, skin rash, and peripheral eosinophilia suggested a diagnosis of hypersensitivity myocarditis, which was confirmed by cardiac magnetic resonance imaging and endomyocardial biopsy.
Aged ; Amoxicillin/*adverse effects ; Anti-Bacterial Agents/*adverse effects ; *Biopsy ; Drug Hypersensitivity/*diagnosis/drug therapy/etiology/pathology ; Electrocardiography ; Female ; Glucocorticoids/therapeutic use ; Humans ; *Magnetic Resonance Imaging ; Myocarditis/chemically induced/*diagnosis/drug therapy/pathology ; Myocardium/*pathology ; Predictive Value of Tests ; Prednisolone/therapeutic use ; Risk Factors ; Treatment Outcome

Alopecia ; chemically induced ; diagnosis ; Antirheumatic Agents ; administration & dosage ; adverse effects ; Arthritis, Rheumatoid ; drug therapy ; Biopsy ; methods ; Cyclosporine ; administration & dosage ; Dermatologic Agents ; administration & dosage ; Drug Hypersensitivity Syndrome ; diagnosis ; etiology ; physiopathology ; therapy ; Humans ; Male ; Middle Aged ; Prednisolone ; administration & dosage ; Skin ; pathology ; Sulfasalazine ; administration & dosage ; adverse effects ; Symptom Flare Up ; Treatment Outcome ; Vitiligo ; chemically induced ; diagnosis

Plastic bronchitis is an uncommon disorder characterized by the formation of bronchial casts. It is associated with congenital heart disease or pulmonary disease. In children with underlying conditions such as allergy or asthma, influenza can cause severe plastic bronchitis resulting in respiratory failure. A review of the literature showed nine cases of plastic bronchitis with H1N1 including this case. We report a case of a child with recurrent plastic bronchitis with eosinophilic cast associated with influenza B infection, who had recovered from plastic bronchitis associated with an influenza A (H1N1) virus infection 5 months previously. To the best of our knowledge, this is the first case of recurrent plastic bronchitis related to influenza viral infection. If patients with influenza virus infection manifest acute respiratory distress with total lung atelectasis, clinicians should consider plastic bronchitis and early bronchoscopy should be intervened. In addition, management for underlying disease may prevent from recurrence of plastic bronchitis.
Administration, Inhalation ; Adrenal Cortex Hormones/therapeutic use ; Antiviral Agents/therapeutic use ; Bronchitis/complications/*diagnosis/drug therapy ; Bronchoscopy ; Child ; DNA, Viral/analysis ; Dyspnea/etiology ; Humans ; Hypersensitivity/pathology ; Influenza A Virus, H1N1 Subtype/*genetics/isolation & purification ; Influenza B virus/genetics/isolation & purification ; Influenza, Human/complications/*diagnosis/drug therapy ; Male ; Oseltamivir/therapeutic use ; Pulmonary Atelectasis/drug therapy/radiography ; Real-Time Polymerase Chain Reaction ; Tachypnea/etiology ; Tomography, X-Ray Computed

Adult ; Anti-Inflammatory Agents, Non-Steroidal ; adverse effects ; therapeutic use ; CD3 Complex ; metabolism ; Colitis, Ulcerative ; drug therapy ; Diagnosis, Differential ; Drug Hypersensitivity ; etiology ; metabolism ; pathology ; Female ; Gastrointestinal Agents ; adverse effects ; therapeutic use ; Humans ; Immunoblastic Lymphadenopathy ; metabolism ; pathology ; Ki-1 Antigen ; metabolism ; Lymphadenitis ; chemically induced ; metabolism ; pathology ; Lymphoma, Large-Cell, Anaplastic ; metabolism ; pathology ; Lymphoma, T-Cell ; metabolism ; pathology ; Receptors, Complement 3d ; metabolism ; Sulfasalazine ; adverse effects ; therapeutic use