Enzyme replacement therapy with agalsidase alfa leads to significant clinical benefits in patients with Fabry disease, and treatment is likely to alter the natural history of this disorder.
Our data provide evidence that IFN-gamma protects mice from lethal autoimmune myocarditis by inducing the expression of inducible nitric oxide synthase followed by the downregulation of T-cell responses.
Three cases, one each of native valve, prosthetic valve and composite graft endocarditis caused by Rothia dentocariosa are described. The first patient presented with multiple brain abscesses and severe congestive heart failure due to destructive endocarditis with large vegetations on the mitral valve. He died shortly after emergency valve replacement. Gram-positive coccoid rods were identified in the vegetations of the excised mitral valve. The second patient had a R. dentocariosa endocarditis of a prosthetic aortic valve that was treated empirically with netilmicin and teicoplanin, due to an allergy to penicillin. Both antibiotics were replaced according to susceptibility testing in vitro with rifampin and ciprofloxacin, and the endocarditis was cured within 9 weeks. The third patient presented with a circular root abscess of an aortic composite graft that was successfully treated with rifampin and ceftriaxone without surgery. All patients had extensive periodontal disease which was thought to be responsible for hematogenic spread and seeding of the microorganism. The microbiological identification and antibiotic resistance pattern of the isolates, as well as therapeutic implications are discussed.
Our Anderson-Fabry cohort had successful long-time ERT with impressive amelioration of subjective symptoms. Although there was not much improvement in cardiac changes apart from a slight improvement of diastolic function, at least, there was no progression of cardiac disease. For complete reversibility of cardiac changes in Anderson-Fabry disease, ERT might have to be started earlier in life and/or prescribed for a longer time.
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