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Two Cases of Lacquer(rhus) Induced Delayed Hypersen- sitivity Reaction: Toxic Epidermal Necrolysis and Acute Generalized Exanthematous Pustules

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The Korean Journal of Internal Medicine Vol. 29, No. 5 (Suppl. 1)

WCIM 2014 SEOUL KOREA 383

Poster Session

PS 1493 Allergy

Two Cases of Lacquer(rhus) Induced Delayed Hypersen- sitivity Reaction: Toxic Epidermal Necrolysis and Acute Generalized Exanthematous Pustules

Byeonghak Cho1, Miyeong Kim1, Youngseok Lee1, Yousang Ko1, Hyunkyung Lee1, Youngmin Lee1

Department of Internal Medicine, Inje University Busan Paik Hospital, Korea1

Lacquer(rhus) could induce delayed hypersensitivity reactions, mainly contact dermati- tis in sensitized patients. We experienced two cases of toxic epidermal necrolysis and acute generalized exanthematous pustules which were induced after ingesting food including lacquer. A 51-year-old man suffered from generalized rash with Nikolsky sign and fever during 3 days before visit. Hemorrhagic oral mucositis and conjunctival injection were observed. Hepatic enzyme and bilirubin were elevated. He ingested chicken cooked with lacquer 2 weeks ago. He experienced itching sense after that, and he also has twice history of itching after ingested same food. We diagnosed him as lacquer induced toxic epidermal necrolysis. With treatment of intravenous systemic corticosteroid and dressing, he recovered without severe complication. A 53-year-old woman suffered from generalized itching and rash during 6 days. 2 weeks ago, she ingested sprout of lacuquer. Itching was developed from chin in next day to general body in one week. Dermatitis at right fl ank, erythematic rash on back and multiple pustules on anterior chest were observed when she visited hospital. We diagnosed her as acute generalized exanthematous pustules. With treatment of oral systemic corticosteroid and antihistamine, she recovered without severe complication. All of two patients rejected patch test with lacquer and we educated the patients to avoid lacquer and lacquer including materials and food. Mango also should be taken care for cross-reaction.

PS 1494 Allergy

A Case of Acute Generalized Exanthematous Pustulosis Induced by Acetaminophen

Byung Sung Koh1, Mi jung Oh1, So Ya Baik2, Jung Wha Suh3

Department of Internal Medicine, Pundang Jesaeng Hospital, Korea1, Department of Pathology, Pun- dang Jesaeng Hospital, Korea2, Department of Dermatology, Pundang Jesaeng Hospital, Korea3

Background: Acute generalized exanthematous pustulosis (AGEP) is a severe and rare disease mostly related to drug eruption. It is characterized by a fever and a pustular eruption on the erythematous skin with an acute onset and without follicular localiza- tion. We report a case of AGEP probably induced by acetaminophen.

Case report: A 79-year-old woman, with a diabetes mellitus, was admitted for gener- alized pustular lesions with a high fever and facial edema. She had no previous history of drug allergies. She took acetaminophen for her lower back pain since 4 days ago.

The eruption appeared two days after taking acetaminophen. Physical examination of the patient revealed an erythematous, maculopapular eruption with small, non-fol- licular pustules that mainly affected the trunk. The eruption became more confl uent with widespread pustulation on the scalp, face and extremities. A laboratory exami- nation revealed a leukocytosis with a neutrophil predominance and a raised C-reac- tive protein. No microrganism was identifi ed in blood cultures. The histopathological examination of the skin biopsy specimen showed intraepidermal pustule formation with superfi cial perivascular lymphocytic infi ltration including eosinophils. The patient discontinued acetaminophen and was treated with systemic corticosteroids and an- tihistamines, which resulted in a gradual improvement of skin lesions. A patch test is scheduled to be performed later.

Conclusion: Physicians should bear in mind that AGEP can be induced by acetami- nophen because acetaminophen is commonly used as an antipyretics and analgesics.

PS 1495 Allergy

A Case of Cycloserine-Induced Lichenoid Drug Eruption Confi rmed with a Lymphocyte Transformation Test

Hyucki Kwon1, Shinyoung Park2, Chee Won Oh3, Woo Jin Kim1, Jae-Woo Kwon4 Department of Internal Medicine, Kangwon National University College of Medicine, Korea1, The Re- search Department, Kangwon Regional Cancer Center, Kangwon National University Hospital, Korea2, Department of Dermatology, Kangwon National University College of Medicine, Korea3, Department of Allergy and Clinical Immunology, Kangwon National University College of Medicine, Korea4

Lichenoid drug eruption is a rare form of delayed type drug eruptions. Among antitu- berculosis drugs, ethambutol is one of the most common causative drugs to induce lichenoid drug eruptions and cycloserine has been reported known as a rare causative drug of the lichenoid drug eruptions. The lymphocyte transformation test (LTT) is a safe and reliable diagnostic procedure for drug allergy, but it is rarely used for diagno- sis of lichenoid drug eruptions. In the current case, we performed an LTT and success- fully confi rmed cycloserine as the offending drug in the patient who were treated with many antituberculosis drugs. This suggests that the cycloserine should be considered as a possible causative drug of lichenoid drug eruption and an LTT could be an option for the diagnosis of lichenoid drug eruption due to cycloserine.

PS 1496 Allergy

A Case of Fixed Drug Eruption Due to Mefenamic Acid Simultaneously with Angioedema

Tae Hoon Yim1, Jee Seon Kim1, Byung Chul Kim1, Hak Ro Kim1, Sungjin Choi1 Good Samaritan Hospital, Korea1

Background: Mefenamic acid is a widely used nonsteroidal anti-infl ammatory drug and its hypersensitivity reaction such as bronchial obstruction, wheals and angioedema is well known, but few cases of fi xed drug eruption due to mefenamic acid have been reported. Here we report a case of fi xed drug eruption simultaneously with angioede- ma after exposure to mefenamic acid.

Case: A 34-year-old female came to our hospital with complaints of itching and ery- thematous skin lesions on her right axillar and left foot with diffuse swelling of upper lip. She took medicines 3 days ago for fl u-like symptoms and experienced fi xed drug eruption and angioedema simultaneously the next day. Past medical history revealed that she had allergic rhinitis and similar experiencies twice over three year. Laboratory test including serum total IgE and allergen-specifi c IgE using the ImmunoCAP was unremarkable. We reviewed the drugs she was prescribed and performed oral provo- cation test using aspirin and mefenamic acid. Mefenamic acid was the causative drug of fi xed drug eruption and angioedema without cross-reactivity with aspirin. she was informed about the use of mefenamic acid.

Conclusion: The fact that the patient do not show cross reactivity with aspirin sug- gests that immunological mechanism mediated by IgE may be involved in the develop- ment of angioedema not by COX inhibition mechanism. We report a rare case of fi xed drug eruption due to mefenamic acid simultaneously with angioedema which might be mediated with immunological mechanism.

Key words: fi xed drug eruption, angioedema, mefenamic acid, immunological mecha- nism

참조

관련 문서

1 Division of Infectious Diseases, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea, 2 Asia Pacific Influenza Institute, Korea University

1 Department of Internal Medicine, Seoul National University College of Medicine and Liver Research Institute, Seoul, Korea, 2 Department of Internal Medicine,

1 Department of Internal Medicine, Seoul National University College of Medicine, 2 Institute of Allergy and Clinical Immunology, Seoul National University

1 Division of Rheumatology, Department of Internal Medicine, Yonsei University College of Medicine, 2 Department of Diagnosti Radiology, Yonsei University, College of

1 Department of Internal Medicine, Pusan national University Hospital Medical Research Institute, Busan, 2 Department of Internal Medicine, Seoul Asan

Department of Medicine, Jeju National University Hospital, Jeju University School of Medicine, Korea 1 , Department of Medicine, University of Ulsan College of Medicine,

Department of Internal Medicine and Liver Research Institute, Seoul National University College of Med- icine, Korea 1 , Department of Internal Medicine and

Department of Internal Medicine, Chonbuk National University Medical School, Korea 1 , Division of Rheu- matology, Department of Internal Medicine, Chonbuk National