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Datensatz: duchenne:15118904
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba
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Nur Publikationshinweis. Kein zur Wiederverwendung freigegebener Textauszug in HealthOS.
FindZebra
Datensatz: duchenne:15118904
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba
Cardiac amyloidosis (CA) is a rare systemic disease determined by the extracellular deposition of amyloid protein in the heart. The protein can accumulate in any part of the heart: myocardium, vessels, endocardium, valves, epicardium and parietal pericardium. The types of CA include the following types: light chain (AL), amyloidosis AA (Amyloid A) and transthyretin (ATTR). The detection of specific subtypes remains of great importance to implement the targeted treatment. We present the case of a 65-year-old woman, who was admitted with severe deterioration of exercise capacity, a bilateral reduction of physiological vesicular murmur, ascites and edema of lower extremities. CA was suspected due to echocardiographic examination results, which led to further examination and final diagnosis. The aim of this study is to improve the disease awareness among clinicians and shorten the delay between the first symptoms and the diagnosis establishment resulting in a better outcome.
Auszug in der Originalsprache. Kozak S, Ulbrich K, Migacz M, Szydło K, Mizia-Stec K, Holecki M. · Lizenz: cc by. Für den vollständigen Kontext die Originalpublikation öffnen.
FindZebra
Datensatz: fac:34066321
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba
The etiologic determinants of cryptogenic stroke remain a diagnostic challenge in clinical practice. Fabry disease (FD) is one of the monogenic causes of stroke that may remain unrecognized as a potential contributing causative factor, because of its rarity and difficulty in diagnosis. We report a case with rare bilateral medial medullary infarction manifesting as "heart appearance" who was diagnosed with FD. A 51-year-old Chinese man presented with acute dysarthria and mild tetraparesis. In the 24 h following admission, the patient rapidly developed progressive flaccid quadriplegia and tongue weakness, necessitating ventilator support. Immediate magnetic resonance imaging of the brain showed heart-shaped appearance of bilateral medial medullary infarction. The patient suffered two new subcortical infarcts 40 days after the first. Detailed Family history and physical examination indicated symptoms consistent with FD, which was confirmed by very low alpha galactosidase A levels and a missense mutation of the alpha-galactosidase A gene. We report what appears to be the first case of FD manifesting as bilateral medial medullary infarction. Our case suggests that clinicians should consider the possibility of FD in patients with cryptogenic stroke, especially when combined with infarction in the vertebrobasilar artery system, renal insufficiency, or cardiomyopathy. A detailed analysis of subtle historical clues and performing a complete physical examination on stroke patients would help promote earlier diagnosis of FD.
Auszug in der Originalsprache. Jiang S, Wang L, Yan Y, Zhu Q, Wan J, Sun J, Wu B. · Lizenz: cc by. Für den vollständigen Kontext die Originalpublikation öffnen.
FindZebra
Datensatz: fabry:32397962
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba
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FindZebra
Datensatz: duchenne:23444294
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba
We describe a young adult male presenting with cardiac failure necessitating cardiac transplantation 7 months after presentation. Skeletal muscle biopsy showed mosaic immunostaining for dystrophin. DNA studies showed somatic mosaicism for a nonsense mutation in the dystrophin gene (Arg2905X). The frequency of normal versus mutant genes were determined in blood/DNA (50:50), muscle/DNA (80:20) and muscle/mRNA (90:10). These data are consistent with genetic normalization processes that may biochemically rescue skeletal muscle in male somatic mosaic patients mitigating muscle symptoms (gradual loss of dystrophin-negative skeletal muscle tissue replaced by dystrophin-positive stem cells). To our knowledge, this is only the second reported case of a clinically ascertained patient showing somatic mosaicism for Duchenne muscular dystrophy (DMD). We hypothesize that many somatic mosaic males for DMD exist, yet they are not detected clinically due to genetic normalization. Somatic mosaicism for DMD should be considered in acute heart failure with dilated cardiomyopathy, as genetic normalization in heart is unlikely to occur.
Auszug in der Originalsprache. Kesari A, Neel R, Wagoner L, Harmon B, Spurney C, Hoffman EP. · Lizenz: cc by. Für den vollständigen Kontext die Originalpublikation öffnen.
FindZebra
Datensatz: duchenne:19530190
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba
Nur Publikationshinweis. Kein zur Wiederverwendung freigegebener Textauszug in HealthOS.
FindZebra
Datensatz: duchenne:16738009
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba
Nur Publikationshinweis. Kein zur Wiederverwendung freigegebener Textauszug in HealthOS.
FindZebra
Datensatz: gaucher:8461327
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba
Duchenne muscular dystrophy (DMD) is one of the most common and severest muscular dystrophies. Although it can be a cause of death when associated with cardiac muscle and/or respiratory muscles, no cases of sudden deaths in the setting of undiagnosed DMD with cardiac involvement have been reported in the literatures. Previous studies showed that N-terminal-proBNP (NT-proBNP) was a robust laboratory biomarker to diagnose and monitor cardiac failure in clinical situations, suggesting that it may be used as an auxiliary indicator for diagnosis on left ventricular dysfunction in sudden cardiac deaths in forensic settings. Here, we reported a case of 29-year-old man who died suddenly. Autopsy revealed that muscles of the body were almost replaced by fatty and fibrotic tissues. The heart was enlarged with disarray and degeneration of cardiomyocytes in cardiac muscle. Total absence of dystrophin was detected by immunohistochemical staining, which confirmed DMD. Postmortem biochemical test of pericardial fluid revealed a high level of NT-proBNP, indicating dysfunction of the left ventricle before death. The cause of death was certified as an early dilated cardiomyopathy (DCM)/dysfunction of the left ventricle secondary to DMD, suggesting that sudden cardiac death with cardiac dysfunction could be identified by immunohistochemical method in combination with pericardial fluid NT-proBNP determination after systemic autopsy.
Auszug in der Originalsprache. Zhang M, Zhao R, Yu T, Li J, Zhang M, Jiang S, Wang L, Zhang G, Li R, Zhu B, Guan D. · Lizenz: cc by. Für den vollständigen Kontext die Originalpublikation öffnen.
FindZebra
Datensatz: duchenne:32939432
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba
Fabry disease is an X-linked inherited, progressive disorder of lipid metabolism resulting from the deficient activity of the enzyme α-galactosidase. Enzyme replacement therapy (ERT) with recombinant agalsidase, with intravenous infusions of either agalsidase beta or agalsidase alfa, is available and clinical experience now exceeds 15 years. There are very few randomised, placebo-controlled clinical trials evaluating the outcomes of ERT. Data are often derived from observational, registry-based studies and case reports. Pooled analysis of data from different sources may be limited by the heterogeneity of the patient populations, outcomes and treatment. Therefore, comprehensive systematic literature reviews of unpooled data are needed to determine the effects of ERT on disease outcomes. A systematic literature search was conducted in the Embase and PubMed (MEDLINE) databases to retrieve original articles that evaluated outcomes of ERT in patients with Fabry disease; the outcome data were analysed unpooled. The literature analysis included the full range of published literature including observational studies and case series/case reports. Considerable heterogeneity was found among the studies, with differences in sample size, statistical methods, ERT regimens and patient demographic and clinical characteristics. We have demonstrated the value of performing an unpooled systematic literature review of all published evidence of ERT outcomes in Fabry disease, highlighting that in a rare genetic disorder like Fabry disease, which is phenotypically diverse, different patient populations can require different disease management and therapeutic goals depending on age, genotype, and disease severity/level of organ involvement. In addition, these findings are valuable to guide the design and reporting of new clinical studies.
Auszug in der Originalsprache. Elliott PM, Germain DP, Hilz MJ, Spada M, Wanner C, Falissard B. · Lizenz: cc by. Für den vollständigen Kontext die Originalpublikation öffnen.
FindZebra
Datensatz: fabry:31195166
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba