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Myocarditis
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
Drug-induced hypersensitivity reactions and systemic hypereosinophilic syndromes can cause a specific eosinophilic myocarditis. Numerous medications, including anticonvulsants, antibiotics and antipsychotics have been implicated. Among the most common drugs that cause hypersensitivity reactions are clozapine, penicillin, ampicillin, hydrochlorothiazide, methyldopa and sulfonamide drugs. Eosinophilic myocarditis is characterized by a predominantly eosinophilic infiltrate (Fig. 6.16). It may occur in association with systemic diseases, such as the hypereosinophilic syndrome, the Churg-Strauss syndrome, cancer, parasitic, helminthic or protozoal infections. This syndrome is associated with peripheral eosinophilia, fever and rash. Eosinophilic myocarditis has been reported after vaccination for several diseases, including smallpox. The clinical presentation of myocarditis associated with hypereosinophilic syndrome tends to be more indolent, usually with less arrhythmia. Peripheral blood eosinophilia is an important laboratory finding but may be absent. Mural thrombosis may occur if the eosinophilic inflammation involves the endocardium. If so, Loeffler endomyocardial disease, in which restrictive physiology is the result of thrombotic obliteration of ventricular cavities, may evolve.
Dopamine in the Immune and Hematopoietic Systems
Published in Nira Ben-Jonathan, Dopamine, 2020
Eosinophils are responsible for combating multicellular parasites and certain infections. Along with mast cells and basophils they are associated with the occurrence of allergy and asthma. Once generated during hematopoiesis in the bone marrow, eosinophils migrate into blood as terminally differentiated cells that do not multiply. There are no published records as to their ability to synthesize DA, but they express on their membrane all five DARs [42]. Older studies with rats have showed that treatment with L-Dopa or apomorphine causes a biphasic effect on eosinophil counts. At low concentration, the eosinophil count was increased, while it was decreased at high concentrations. Administration of DA in patients awaiting heart transplant caused a reduction in the explanted heart of eosinophilic myocarditis and peripheral eosinophilia [43].
Hypereosinophilic syndrome
Published in Biju Vasudevan, Rajesh Verma, Dermatological Emergencies, 2019
Seen in nearly 60% of patients with HES, with endomyocardial fibrosis being most common [18,19]. Endocardial clot formation often leads to valve dysfunction, reduced cardiac output, and embolization to brain, viscera, and limbs.Presence of splinter hemorrhages in the nail beds indicates ongoing embolization [1].Any patient with marked eosinophilia who satisfies the criteria for HES, and splinter nail bed hemorrhages should be considered a medical emergency and aggressively treated.Eosinophilic myocarditis is a major cause of morbidity and mortality among patients with HES.Platelet-derived growth factor receptor alpha (PDGFRA)–associated HES has an increased incidence of incapacitating and potentially lethal cardiac involvement in the absence of therapy.Although cardiac involvement is best diagnosed by means of endomyocardial biopsy, this technique can have a high morbidity and mortality and be difficult to perform. Instead, a noninvasive procedure such as transesophageal echocardiography is valuable for detecting thrombus formation.Significant arrhythmia with chronic heart failure is often found in the late stages of HES.The development of cardiac disease in HES is unpredictable.Cardiac involvement does, however, appear to be more common in patients with the Fip1-like1-platelet-derived growth factor receptor alpha (FIP1L1-PDGFRA) fusion.
Letter Regarding “Fatal Eosinophilic Myocarditis in a Healthy 17-Year-Old Male with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2)”
Published in Fetal and Pediatric Pathology, 2020
Until the emergence of COVID-19, the family of coronaviruses were not commonly associated with myocarditis. Literature on myocarditis due to coronaviruses is scant. Instead, cardiotropic viral etiologies such as enteroviruses (primarily Coxsackie A and B virus), adenoviruses, parvovirus B19, and human herpesvirus 6 are historically linked to myocarditis. Other etiologies include HIV, Chagas disease, toxins, medications, and autoimmune phenomena [4]. Investigative mechanisms of myocarditis revealed that both immune-mediated and direct viral cytotoxic mechanisms are at work resulting in the destruction of myocardial tissue. The typical cellular infiltrate seen in myocarditis usually includes mononuclear cells such as lymphocytes, macrophages, dendritic cells and natural killer cells [6]. Prominent eosinophils in the cardiac autopsy specimen [5] represents an eosinophilic myocarditis, but his evaluation lacked any supporting evidence for other known causes of a primary eosinophilic myocarditis. Infective myocarditis with a prominent eosinophilic infiltration result in more life-threatening disease with fatality approaching 50% [7], therefore, given the lack of associated systemic eosinophilic disease, the histology findings likely represent an immune response that heralded progressive severe disease.
Fatal Eosinophilic Myocarditis in a Healthy 17-Year-Old Male with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2c)
Published in Fetal and Pediatric Pathology, 2020
Randall Craver, Samantha Huber, Marrianna Sandomirsky, Dwight McKenna, John Schieffelin, Leron Finger
Eosinophilic myocarditis is defined histologically as inflammation containing prominent eosinophils along with myocyte necrosis. EM is not thought to represent a single entity but can be seen with different diseases. Ten percent of EM affect children. Etiologies include hypersensitivity reactions (most often drug exposure related), eosinophilic granulomatosis with polyangiitis, hypereosinophilia syndromes, infections, malignancies, and idiopathic [15]. In this 17-year-old, there was no history of drug exposure, and caffeine and naloxone only were detected from postmortem blood. The inflammatory infiltrate was limited to the heart, was not angiocentric, not granulomatous, and not associated with vasculitis. Tissues from other organs, including the bone marrow, or within the vasculature did not show frequent eosinophils, suggesting this was not a hypereosinophilia syndrome or an eosinophilia associated with a myeloproliferative disorder. There was no increased interstitial fibrosis, suggesting this was an acute event. There was no increased subendocardial fibrosis as with Loeffler’s endocarditis. The conclusion was that this was either an idiopathic or infection related eosinophilic myocarditis.
Chronic cough and an atypical pattern of peripheral pulmonary opacities: A case report secondary to suspected drug onset
Published in Journal of Asthma, 2018
Ronnie Alas, Mark Tony Williams, Ghiam Yamin, Mohsen Rofoogaran
Our patient may have had an eosinophilic asthma phenotype [10], which works through the Th2 cell pathway. However, because he also had psoriasis, primarily a Th1 cell pathway disease, it is possible his asthma was masked most of his life. Upon starting adalimumab for psoriasis, the Th1 response was suppressed and the Th2 pathway was unmasked revealing itself clinically as asthma. Several case reports link adalimumab to asthma, pulmonary eosinophilia, and interstitial lung disease in those with rheumatologic conditions [11]. A growing compendium of cases suggest that TNF-targeted therapies potentially predispose to pulmonary complications, including asthma-like symptoms, chronic pneumonitis, chronic pneumonitis/fibrosis, systemic lupus erythematous-like reactions, and exacerbations of underlying lung disease [12–14]. One case report even suggests the link between TNF therapy and acute necrotizing eosinophilic myocarditis [15].