Infliximab

Infliximab Reactions 1680, p178 - 2 Dec 2017 Various toxicities: case report A 58-year-old woman developed hypereosinophilic syndrome (HES), myocarditis and associated complications including pericardial and pleural effusion, heart failure, and fibrotic restrictive cardiomyopathy during treatment with infliximab [route, dosage and time to reaction onset not stated]. The woman presented with bilateral lower extremity oedema and progressively deteriorating shortness of breath. Previously, she received treatment with infliximab for rheumatoid arthritis and developed HES with myocarditis. At that time, she also experienced a significant hypereosinophilia and an acute myocarditis with mild pericardial and pleural effusions. Because of its chronological relation to the disease development, her condition was attributed to the infliximab therapy. The woman’s infliximab therapy was discontinued and she received treatment with unspecified steroids. There were no recurrences or residual symptoms of the disease until months before the current presentation when she developed dyspnoea. An ECG revealed left atrial enlargement, first-degree atrioventricular block and non-specific ST and T-wave changes. Transthoracic echocardiogram revealed thickened mitral valve (MV) leaflets and severe right atrial (RA) enlargement with poor visualisation of the right ventricle (RV). Cardiac MRI revealed diffuse endocardial late gadolinium enhancement suggestive of fibrosis, bowing of the interventricular septum toward the left in the diastole compatible with increased right-heart filling pressure pressures, obliteration of the RV apex, severe RA enlargement with thrombus and MV leaflet obliteration. Her heart failure symptoms continued to become progressively more debilitating despite increased doses of furosemide. She underwent RV endocardial stripping involving decortication of the fibrosed tissue to decrease the RV filling pressures. The fibrotic peel in the RV was resected which led to damage to the sub-valvular area needing tricuspid valve replacement. She underwent the MV replacement after the MV examination revealed an involvement of the leaflets in the Loeffler process. A degenerative disease with obliteration of the mitral leaflets was revealed by pathology. From the findings, she was deemed to have Loeffler endocarditis and fibrotic restrictive cardiomyopathy that were progressed from the HES and myocarditis. After the surgery, she was found to be in complete heart block because of damage to the conduction system. Hence, a permanent pacemaker was inserted. Six months after the operation, echocardiography and right heart catheterisation revealed noticeable improvement in the RA and RV size, with normalisation of the RV diastolic pressure. At a follow-up after 1 year of the operation, asymptomatic improvement was observed without any complaints of dyspnea on exertion, shortness of breath or other heart failure symptoms. Author comment: "The patient had a past medical history significant for [hypereosinophilic syndrome] with myocarditis 9 years prior, supposed to be secondary to infliximab used in the management of rheumatoid arthritis." "The anti–tumor necrosis factor agent was thought to be the responsible due to its chronological relation to disease development." Alam A, et al. Loeffler Endocarditis: A Unique Presentation of Right-Sided Heart Failure Due to Eosinophil-Induced Endomyocardial Fibrosis. Clinical Medicine Insights: Case Reports 10: 1-4, 30 Aug 2017. Available from: URL: http:// doi.org/10.1177/1179547617723643 - USA 803285066 0114-9954/17/1680-0001/$14.95 Adis © 2017 Springer International Publishing AG. All rights reserved Reactions 2 Dec 2017 No. 1680 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Reactions Weekly Springer Journals

Infliximab

Reactions Weekly , Volume 1680 (1) – Dec 2, 2017
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Publisher
Springer International Publishing
Copyright
Copyright © 2017 by Springer International Publishing AG, part of Springer Nature
Subject
Medicine & Public Health; Drug Safety and Pharmacovigilance; Pharmacology/Toxicology
ISSN
0114-9954
eISSN
1179-2051
D.O.I.
10.1007/s40278-017-39109-9
Publisher site
See Article on Publisher Site

Abstract

Reactions 1680, p178 - 2 Dec 2017 Various toxicities: case report A 58-year-old woman developed hypereosinophilic syndrome (HES), myocarditis and associated complications including pericardial and pleural effusion, heart failure, and fibrotic restrictive cardiomyopathy during treatment with infliximab [route, dosage and time to reaction onset not stated]. The woman presented with bilateral lower extremity oedema and progressively deteriorating shortness of breath. Previously, she received treatment with infliximab for rheumatoid arthritis and developed HES with myocarditis. At that time, she also experienced a significant hypereosinophilia and an acute myocarditis with mild pericardial and pleural effusions. Because of its chronological relation to the disease development, her condition was attributed to the infliximab therapy. The woman’s infliximab therapy was discontinued and she received treatment with unspecified steroids. There were no recurrences or residual symptoms of the disease until months before the current presentation when she developed dyspnoea. An ECG revealed left atrial enlargement, first-degree atrioventricular block and non-specific ST and T-wave changes. Transthoracic echocardiogram revealed thickened mitral valve (MV) leaflets and severe right atrial (RA) enlargement with poor visualisation of the right ventricle (RV). Cardiac MRI revealed diffuse endocardial late gadolinium enhancement suggestive of fibrosis, bowing of the interventricular septum toward the left in the diastole compatible with increased right-heart filling pressure pressures, obliteration of the RV apex, severe RA enlargement with thrombus and MV leaflet obliteration. Her heart failure symptoms continued to become progressively more debilitating despite increased doses of furosemide. She underwent RV endocardial stripping involving decortication of the fibrosed tissue to decrease the RV filling pressures. The fibrotic peel in the RV was resected which led to damage to the sub-valvular area needing tricuspid valve replacement. She underwent the MV replacement after the MV examination revealed an involvement of the leaflets in the Loeffler process. A degenerative disease with obliteration of the mitral leaflets was revealed by pathology. From the findings, she was deemed to have Loeffler endocarditis and fibrotic restrictive cardiomyopathy that were progressed from the HES and myocarditis. After the surgery, she was found to be in complete heart block because of damage to the conduction system. Hence, a permanent pacemaker was inserted. Six months after the operation, echocardiography and right heart catheterisation revealed noticeable improvement in the RA and RV size, with normalisation of the RV diastolic pressure. At a follow-up after 1 year of the operation, asymptomatic improvement was observed without any complaints of dyspnea on exertion, shortness of breath or other heart failure symptoms. Author comment: "The patient had a past medical history significant for [hypereosinophilic syndrome] with myocarditis 9 years prior, supposed to be secondary to infliximab used in the management of rheumatoid arthritis." "The anti–tumor necrosis factor agent was thought to be the responsible due to its chronological relation to disease development." Alam A, et al. Loeffler Endocarditis: A Unique Presentation of Right-Sided Heart Failure Due to Eosinophil-Induced Endomyocardial Fibrosis. Clinical Medicine Insights: Case Reports 10: 1-4, 30 Aug 2017. Available from: URL: http:// doi.org/10.1177/1179547617723643 - USA 803285066 0114-9954/17/1680-0001/$14.95 Adis © 2017 Springer International Publishing AG. All rights reserved Reactions 2 Dec 2017 No. 1680

Journal

Reactions WeeklySpringer Journals

Published: Dec 2, 2017

References

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