Immunohistological and Serological Studies in Endomyocardial Fibrosis

Geld, H. van der; Peetoom, F.; Somers, Krishna; Kanyerezi, B R

doi:10.1016/s0140-6736(66)92300-2

Cited by 67 publications

(18 citation statements)

References 18 publications

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“…Interestingly, our previous discovery of IgM deposition and T-cell foci (CD43 and CD8 positive cells, T-cell activation) provide further support for a contributing fetal immune response (6,7). Over time, these insults may lead to ventricular dilation and hypertrophy, reduced ventricular compliance, and progressive EFE (22). Myocardial damage may be clinically manifested with the development of progressive myocardial dysfunction, which includes systolic and likely diastolic components.…”

Section: Mab-cm/efe Pathogenesismentioning

confidence: 91%

Use of Intravenous Gamma Globulin and Corticosteroids in the Treatment of Maternal Autoantibody-Mediated Cardiomyopathy

Trucco

Jaeggi

Cuneo

et al. 2011

Journal of the American College of Cardiology

109

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Section: Mab-cm/efe Pathogenesismentioning

confidence: 91%

Use of Intravenous Gamma Globulin and Corticosteroids in the Treatment of Maternal Autoantibody-Mediated Cardiomyopathy

Trucco

Jaeggi

Cuneo

et al. 2011

Journal of the American College of Cardiology

109

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“…11 The association between maternal anti-Ro and anti-La antibodies and congenital heart block (CHB) has been well documented. 12 Small case series have described infants diagnosed with both CHB and EFE, but a causative link between these 2 diseases has not yet been identified.…”

mentioning

confidence: 99%

Maternal Anti-Ro and Anti-La Antibody–Associated Endocardial Fibroelastosis

et al. 2002

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Background-Maternal anti-Ro and anti-La antibodies are associated with congenital heart block (CHB). Although endocardial fibroelastosis (EFE) has been described in isolated cases of autoantibody-mediated CHB, the natural history and pathogenesis of this disease are poorly understood. Methods and Results-We retrospectively reviewed the clinical history, echocardiography, and pathology of fetuses and children with EFE associated with CHB born to mothers positive for anti-Ro or anti-La antibodies at 5 centers. Thirteen patients were identified, 6 with a prenatal and 7 with a postnatal diagnosis. Six mothers were positive for anti-Ro and anti-La antibodies, and 7 were positive for anti-Ro antibodies only. Only 1 mother had autoimmune disease. Severe ventricular dysfunction was seen in all fetal and postnatal cases. Four fetal and 3 postnatal cases had EFE at initial presentation. However, 2 fetal and 4 postnatal cases developed EFE 6 to 12 weeks and 7 months to 5 years from CHB diagnosis, respectively, even despite ventricular pacing in 6 postnatal cases. Eleven (85%) either died (nϭ9) or underwent cardiac transplantation (nϭ2) secondary to the EFE. Pathologic assessment of the explanted heart, available in 10 cases, revealed moderate to severe EFE in 7 and mild EFE in 3 cases, predominantly involving the left ventricle.

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“…[49][50][51][52][53] An excessive immune response to the trigger (Figure 1) has been suggested to be the link between certain parasitic infections and EMF. [54][55][56][57][58][59] This has been demonstrated, for example, by increased circulating levels of IgE 53,60,61 and the occurrence of hyperimmune malaria-related splenomegaly among Rwandan immigrants affected by EMF. 62 Immunological investigations have revealed the presence of autoantibodies (IgG and IgM) directed against myocardial proteins.…”

Section: Eosinophilia Infectious Disease and Autoimmunitymentioning

confidence: 99%

“…Although several environmental/toxic factors such as magnesium deficiency, cerium toxicity, the cyanogenic glycosides, high vitamin D, serotonin toxicity, 58,59,62,[81][82][83][84][85][86][87][88][89][90][91][92][93][94][95][96] and, more recently, the potential effect of certain herbal preparations 97 have been advocated in the pathogenesis, no confirmatory evidence firmly establishes these hypotheses. It has been speculated that, in genetically predisposed people, poor diet per se may lead to a dysfunction in the regulatory and functional mechanisms of eosinophils, which, as in eosinophilic leukemia, may cause necrosis, thrombosis, and finally fibrosis.…”

Section: Environmental Factors Dietary Factors and Toxinsmentioning

confidence: 99%

Tropical Endomyocardial Fibrosis

et al. 2016

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Abstract-Tropical endomyocardial fibrosis (EMF) is a neglected disease of poverty that afflicts rural populations in tropical low-income countries, with some certain high-prevalence areas. Tropical EMF is characterized by the deposition of fibrous tissue in the endomyocardium, leading to restrictive physiology. Since the first descriptions in Uganda in 1948, high-frequency areas for EMF have included Africa, Asia, and South America. Although there is no clear consensus on a unified hypothesis, it seems likely that dietary, environmental, and infectious factors may combine in a susceptible individual to give rise to an inflammatory process leading to endomyocardial damage and scar formation. The natural history of EMF includes an active phase with recurrent flare-ups of inflammation evolving to a chronic phase leading to restrictive heart failure. In the chronic phase, biventricular involvement is the most common presentation, followed by isolated right-sided heart disease. Marked ascites out of proportion to peripheral edema usually develops as a typical feature of EMF. EMF carries a very poor prognosis. In addition to medical management of heart failure, early open heart surgery (endocardectomy and valve repair/replacement) appears to improve outcomes to some extent; however, surgery is technically challenging and not available in most endemic areas. Increased awareness among health workers and policy makers is the need of the hour for the unhindered development of efficient preventive and therapeutic strategies.

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Immunohistological and Serological Studies in Endomyocardial Fibrosis

Cited by 67 publications

References 18 publications

Use of Intravenous Gamma Globulin and Corticosteroids in the Treatment of Maternal Autoantibody-Mediated Cardiomyopathy

Use of Intravenous Gamma Globulin and Corticosteroids in the Treatment of Maternal Autoantibody-Mediated Cardiomyopathy

Maternal Anti-Ro and Anti-La Antibody–Associated Endocardial Fibroelastosis

Tropical Endomyocardial Fibrosis

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