title: [Diagnostic usefulness of KL-6 measurements in patients with pulmonary complications after administration of amiodarone].
abstract: Amiodarone-induced pulmonary toxicity is one of the major complications in patients receiving administration of amiodarone. KL-6 is a useful indicator to evaluate the activity of interstitial pneumonitis. We studied the clinical utility of KL-6 as a marker for amiodarone-induced pulmonary toxicity. We investigated 6 patients in whom chest radiography revealed abnormal consolidations after administration of amiodarone from 1997 to 1999. All patients were male aged 56 to 76 years (mean 66 +/- 7 years). The indications for amiodarone included sustained ventricular tachycardia in 5 patients and atrial fibrillation in one patient with refractory heart failure. The mean left ventricular ejection fraction was 31 +/- 12% (22-52%). KL-6 levels were measured by a sandwich type enzyme immunoassay using a murine monoclonal antibody (KL-6 antibody), and the cutoff level was determined at 520 U/ml. Complications occurred from 17 days to 45 months after treatment with amiodarone. The KL-6 levels were abnormally high (2,100 and 3,000 U/ml) in 2 patients with amiodarone-induced pneumonitis but under the cutoff level in the non-pneumonitis patients. In one patient with amiodarone-induced pneumonitis, the KL-6 level increased from 695 to 2,100 U/ml concurrently with worsening interstitial changes shown by high resolution computed tomography. We conclude that KL-6 has practical uses as a marker for the detection and evaluation of amiodarone-induced pulmonary toxicity.
authors.affiliation: Department of Cardiology, Saisei-kai Kurihashi Hospital, Saitama.
authors.forename: Y
authors.initials: Y
authors.lastname: Endoh
authors.forename: R
authors.initials: R
authors.lastname: Hanai
authors.forename: K
authors.initials: K
authors.lastname: Uto
authors.forename: M
authors.initials: M
authors.lastname: Uno
authors.forename: H
authors.initials: H
authors.lastname: Nagashima
authors.forename: T
authors.initials: T
authors.lastname: Takizawa
authors.forename: A
authors.initials: A
authors.lastname: Narimatsu
authors.forename: S
authors.initials: S
authors.lastname: Ohnishi
authors.forename: H
authors.initials: H
authors.lastname: Kasanuki
mesh_terms: D000368:Aged; D000638:Amiodarone / Q000009:adverse effects*; D000889:Anti-Arrhythmia Agents / Q000009:adverse effects*; D000941:Antigens; D000951:Antigens, Neoplasm; D001281:Atrial Fibrillation / Q000188:drug therapy; D015415:Biomarkers / Q000097:blood*; D006023:Glycoproteins; D006801:Humans; D007124:Immunoenzyme Techniques; D008297:Male; D008875:Middle Aged; D018396:Mucin-1; D009077:Mucins; D010446:Peptide Fragments / Q000097:blood*; D011014:Pneumonia / Q000139:chemically induced* / Q000175:diagnosis*; D011347:Procollagen / Q000097:blood*; D013318:Stroke Volume; D017180:Tachycardia, Ventricular / Q000188:drug therapy
chemical_list: D000889:Anti-Arrhythmia Agents; D000941:Antigens; D000951:Antigens, Neoplasm; D015415:Biomarkers; D006023:Glycoproteins; C060192:MUC1 protein, human; D018396:Mucin-1; D009077:Mucins; D010446:Peptide Fragments; D011347:Procollagen; C041876:procollagen Type III-N-terminal peptide; D000638:Amiodarone