KL-6 as a potential new marker for amiodarone-induced pulmonary toxicity

Endoh, Yasuhiro; Hanai, Ritsuko; Uto, Kenta; Uno, Motoki; Nagashima, Hirotaka; Narimatsu, A; Takizawa, Takao; Onishi, Shun; Kasanuki, Hiroshi

doi:10.1016/s0002-9149(00)00864-x

Cited by 25 publications

(15 citation statements)

References 14 publications

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“…Additionally, DLco cannot be measured in the seriously ill patients such as in the present cases. KL-6has been reported to be a useful marker for the detection and evaluation of APT (3,4), and measurement of the KL-6 level is valuable for discriminating APTfrom other types of pneumonia and from CHF.However, in the present cases, the KL-6level did not reach an abnormal range, while another marker, the SP-D level exceeded twice the upper limit of normal subjects. SP-D is reported to be specific for lung disease, particularly interstitial lung disease; it reflects disease activity and is useful to predict the prognosis (6, 7).…”

Section: Discussioncontrasting

confidence: 67%

“…Although the pulmonary carbon monoxide diffusion capacity (DLco) has been measured to detect amiodarone-induced pulmonary toxicity (APT) (5), the sensitivity, specificity and applicability to acutely ill patients remain unclarified. Recently the serum KL-6 concentration had been advocated as a useful marker for APT (3,4). Here, we describe two patients with APT,whodid not demonstrate an abnormally increased serum KL-6concentration.…”

Section: Introductionmentioning

confidence: 83%

“…However, use of this drug is restricted due to concerns of adverse effects, especially pulmonarytoxicity (1)(2)(3)(4). Although the pulmonary carbon monoxide diffusion capacity (DLco) has been measured to detect amiodarone-induced pulmonary toxicity (APT) (5), the sensitivity, specificity and applicability to acutely ill patients remain unclarified.…”

Section: Introductionmentioning

confidence: 99%

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SP-D as a Marker of Amiodarone-induced Pulmonary Toxicity.

et al. 2002

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Twopatients with amiodarone-induced pulmonary toxicity (APT) showed abnormally increased serum SP-D concentrations, although their KL-6 level was within the normal range. In a 59-year-old man with ischemic heart disease, APTprogressed rapidly and required steroid pulse therapy. During the clinical course, SP-D was as high as 375 ng/ml, although the KL-6 level was only 289 U/ml. In a 58-year-old man treated for dilated cardiomyopathy, SP-D increased to 289 ng/ml, while KL-6 remained at less than 500 U/ml. These cases indicate that SP-D is a useful and early diagnostic marker for APTeven when KL-6 is not elevated. (Intrenal Medicine 41: 709-712, 2002)

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Section: Discussioncontrasting

confidence: 67%

Section: Introductionmentioning

confidence: 83%

Section: Introductionmentioning

confidence: 99%

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SP-D as a Marker of Amiodarone-induced Pulmonary Toxicity.

et al. 2002

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“…All the patients had life-threatening ventricular tachyarrhythmia due to myocardial infarction, dilated cardiomyopathy, sarcoidosis, or arrhythmogenic right ventricular cardiomyopathy (ARVC) [6], and had been monitored for serum levels of thyroid hormone and KL-6 every three months [14]. During this period, more that 40 patients with type II AIT were referred to the Institute of Clinical Endocrinology.…”

Section: Case Reportsmentioning

confidence: 99%

Mild and Short Recurrence of Type II Amiodarone-induced Thyrotoxicosis in Three Patients Receiving Amiodarone Continuously for More Than 10 Years

et al. 2006

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Abstract. Although there are two types of amiodarone-induced thyrotoxicosis (AIT), only type II AIT has been seen at our institution in Japan so far. There have been few case reports of AIT recurrence, probably because of the fact that amiodarone is immediately discontinued once AIT has developed. Our own policy is not to discontinue amiodarone in all AIT patients, unless severe adverse effects such as pulmonary fibrosis develop. Among more than 50 patients with type II AIT we have encountered, three with arrhythmogenic right ventricular cardiomyopathy showed AIT recurrence. In these patients, the first episode of AIT developed 3, 4, and 2 years after the start of amiodarone administration, and recurrence was observed 5, 6, and 8 years after the first episode, respectively. The AIT resolved spontaneously in all cases while the patients continued to take amiodarone. In comparison with the first AIT episode, the second was milder and resolved within a shorter period. These three cases suggest that recurrence of type II AIT may not be rare in iodine-sufficient areas, and that it is relatively mild and may resolve spontaneously. Furthermore, at least in Japan, it may be possible for patients with recurrent type II AIT to continue taking amiodarone.

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“…Although KL-6 has been studied as a biomarker for amiodarone pulmonary toxicity, it is nonspecific. 11 Chest radiography may reveal diffuse infiltrates, interstitial tissue thickening, nodules, masslike consolidations, pleural effusions, or pleural thickening. 5 Chest CT frequently shows patchy groundglass opacities in bilateral lobes, 2 intralobular septal thickening, intralobular reticulations, and single or multiple subpleural masses.…”

Section: Discussionmentioning

confidence: 99%

48-Year-Old Woman With Dyspnea, Cough, and Weight Loss

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Burger

2012

Mayo Clinic Proceedings

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A 48-year-old woman presented to our emergency department with progressive dyspnea, cough with clear sputum, and a 9-kg weight loss. Evaluation at an outside emergency department 6 months previously had revealed a right middle lobe infiltrate on chest radiography (CXR), and she was treated with a 10-day course of levofloxacin for presumed community-acquired pneumonia. Her symptoms continued, and 1 month later, she went to an outside pulmonologist who found bilateral alveolar infiltrates on chest computed tomography (CT).On presentation to our emergency department, the patient reported no orthopnea, fevers, chills, or night sweats. Her medical history was notable for nonischemic dilated cardiomyopathy that was treated with cardiac resynchronization therapy and an automatic implantable cardioverter-defibrillator (AICD), atrial fibrillation, and myelodysplastic syndrome. She had a 10-pack-year smoking history but had quit smoking 1 year previously. Her medications included furosemide, losartan, digoxin, coumadin, amiodarone, and spironolactone. No new medications had been added to her treatment regimen during the past 10 years.On admission, the patient's vital signs were as follows: temperature, 37.0 o C; blood pressure, 101/64 mm Hg; respiratory rate, 18 breaths/min; and oxygen saturation, 94% while the patient breathed room air. She was in no acute distress. Her sclera had a blue-grey discoloration. Cardiac examination revealed a regular rhythm, grade 1/6 systolic murmur heard at the left upper sternal border, no gallops, no jugular venous distention, and no peripheral edema. Pulmonary examination revealed crackles over the right middle lobe but otherwise normal results. Abdominal, musculoskeletal, and neurologic examination findings were unremarkable.Chest radiography showed bilateral dense consolidations that were greater on the right with clear costophrenic angles, an AICD, and cardiomegaly. Chest CT revealed asymmetric bilateral, multilobar alveolar consolidations without pleural effusions or engorgement of the intralobar space, 4-chamber cardiomegaly, and an AICD.Laboratory studies yielded the following results (reference ranges shown parenthetically): hemoglobin, 10.1 g/dL (12.0-15.5 g/dL; previous level, 10.0 g/dL); white blood cell count, 1.6 ϫ 10 9 /L (3.5-10.5 ϫ 10 9 /L); 10% segmented neutrophils; 59% lymphocytes with an absolute neutrophil count of 2.0 ϫ 10 9 /L (0.9-2.9 ϫ 10 9 /L); platelet count, 125 ϫ 10 9 /L (150-450 ϫ 10 9 /L); erythrocyte sedimentation rate, 64 mm/h (Ͻ29 mm/h); international normalized ratio, 1.7 (0.8-1.2); brain naturietic peptide (BNP), 1260 pg/mL (Ͻ71 pg/mL); digoxin, 1.59 ng/mL (0.5-2.0 ng/mL); thyroid stimulating hormone, 0.52 mIU/L (0.3-5.0 mIU/L); and human immunodeficiency virus antibody, negative. The patient was admitted to the hospital for evaluation of new neutropenia, progressive dyspnea, and undiagnosed pulmonary infiltrate.

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KL-6 as a potential new marker for amiodarone-induced pulmonary toxicity

Cited by 25 publications

References 14 publications

SP-D as a Marker of Amiodarone-induced Pulmonary Toxicity.

SP-D as a Marker of Amiodarone-induced Pulmonary Toxicity.

Mild and Short Recurrence of Type II Amiodarone-induced Thyrotoxicosis in Three Patients Receiving Amiodarone Continuously for More Than 10 Years

48-Year-Old Woman With Dyspnea, Cough, and Weight Loss

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