There are many causes of<unk>  that may underlie<unk> . These causes are classified as primary (i.e. a defect intrinsic to the<unk> ell line), secondary (induced by an underlying disorder that stimulates the proliferation and activation of eosinophils), or idiopathic (i.e. unknown cause). Non-idiopathic causes of the disorder are sub-classified into various forms of allergic, autoimmune, infectious, or malignant diseases and hypersensitivity reactions to drugs, vaccines, or transplanted hearts. While virtually any cause for the elevation and activation of blood eosinophils must be considered as a potential cause for<unk> , the following list gives the principal types of<unk>  known or thought to underlie the disorder. Primary conditions that may lead to<unk>  are: * Clonal hypereosinophilia. * Chronic<unk>  leukemia. * The idiopathic hypereosinophilic syndrome. Secondary conditions that may lead to<unk>  are: * Infections agents: * Parasitic worms: various Ascaris, Strongyloides, Schistosoma, filaria, Trematoda, and Nematode species. Parasitic infestations often cause significant heart valve disease along with<unk>  and the disorder in this setting is sometimes termed Tropical endomyocardial fibrosis. While commonly considered to be due to the cited parasites, this particular form of<unk>  may more often develop in individuals with other disorders, e.g. malnutrition, dietary toxins, and genetic predisposition, in addition to or in place of round worm infestation. * Infections by protozoa: various Toxoplasma gondii, Trypanosoma cruzi, trichinella spiralis, Entamoeba, and Echinococcus species. * Viruses: While some viral infections (e.g. HIV) have been considered causes of<unk>  endocarditis, a study of 20 patients concluded that viral<unk>  lacks the characteristic of eosinophil-induced damage in hearts taken during cardiac transplantation. * Allergic and autoimmune diseases such as severe asthma, rhinitis, or urticarial, chronic sinusitis, aspirin-induced asthma, allergic bronchopulmonary aspergillosis, chronic<unk>  pneumonia, Kimura's disease, polyarteritis nodosa,<unk>  granulomatosis with polyangiitis (i.e. Churg–Strauss syndrome), and rejection of transplanted hearts. * Malignancies and/or premalignant hematologic conditions not due to a primary disorder in eosinophils such as Gleich's syndrome, Lymphocyte-variant hypereosinophilia Hodgkin disease, certain T-cell lymphomas, acute myeloid leukemia, the myelodysplastic syndromes, systemic mastocytosis, chronic myeloid leukemia, polycythemia vera, essential thrombocythemia, myelofibrosis, chronic myelomonocytic leukemia, and T-lymphoblastic leukemia/lymphoma-associated or myelodysplastic–myeloproliferative syndrome-associated<unk> s; IgG4-related disease and Angiolymphoid hyperplasia with<unk>  as well as non-hematologic cancers such as solid tumors of the lung, gastrointestinal tract, and genitourinary tract. * Hypersensitivity reactions to agents include: * Antibiotics/anti-viral agents: various penicillins (e.g. penicillin, ampicillin), cephalosporins (e.g. cephalosporin), tetracyclins (e.g. tetracycline), sulfonamides (e.g. sulfadiazine, sulfafurazole), sulfonylureas, antituburcular drugs (e.g. isoniazid, 4-aminosalicylic acid), linezolid, amphotericin B, chloramphenicol, streptomycin, dapsone, nitrofurantoin, metronidazole, nevirapine, efavirenz, abacavir, nevirapine. * Anticonvulsants/Antipsychotics/antidepressants: phenindione, phenytoin, phenobarbital, lamotrigine, lamotrigine, clozapine, valproic acid, carbamazepine, desipramine, fluoxetine, amitriptyline, olanzapine. * Anti-inflammatory agents: ibuprofen, indomethacin, phenylbutazone, oxyphenbutazone, acetazolamide, piroxicam, diclofenac. * Diuretics: hydrochlorothiazide, spironolactone, chlortalidone. * ACE inhibitors: captopril, enalapril. * Other drugs: digoxin, ranitidine, lenalidomide, methyldopa, interleukin 2, dobutamine, acetazolamide. * Contaminants: Unidentified contaminants in rapeseed oil cause the toxic oil syndrome and in commercial batches of the amino acid, L-tryptophan, cause the<unk> –myalgia syndrome. * Vaccinations: Tetanus toxoid, smallpox, and diphtheria/pertussis/tetanus vaccinations. DRESS syndrome The DRESS syndrome is a severe immunological drug reaction. It differs from other drug reactions in that it: a) is caused by a particular set of drugs; b) typically occurs after a delay of 2 to 8 weeks following intake of an offending drug; c) presents with a specific set of signs and symptoms (i.e. modest or extreme elevations in blood eosinophil and atypical lymphocyte counts; acute onset of a skin rash; lymphadenopathy; fever; neuralgia; and involvement of at least one internal organ such as the liver, lung, or heart; d) develops in individuals with particular genetic predispositions; and e) involves reactivation of latent viruses, most commonly human herpesvirus 6 or more rarely human herpes virus 5 (i.e. human cytomegalovirus), human herpesvirus 7, and human herpesvirus 4 (i.e. Epstein–Barr virus). These viruses usually become dormant after infecting humans but under special circumstances, such as drug intake, are reactivated and may contribute to serious diseases such as the DRESS syndrome.
Eosinophilic myocarditis
Idiopathic giant-cell myocarditis
Coxsackievirus-induced cardiomyopathy
Viral cardiomyopathy
Amyloid cardiomyopathy
Alcoholic cardiomyopathy
HIV associated cardiomyopathy
Tuberculous pericarditis