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studies demonstrate the focal absence of peripheral heterochromatin in areas between the nuclear pores, irregular and uniform thickening of the nuclear lamina, and compaction of heterochromatin in areas of irregular thickening of the nuclear lamina and areas where the peripheral heterochromatin does not adhere to the nuclear lamina25 Diagnosis can be con rmed by immunostaining muscle or skin tissue for emerin or by immunoblot analysis of leukocytes
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Molecular Genetics and Pathogenesis
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EDMD is caused by mutations in a gene (STA) located on chromosome Xq28, which encodes for emerin (Table 24 1)223 Emerin is located on the inner nuclear membranes of skeletal, cardiac, and smooth muscle bers as well as skin cells23,24 Its carboxy-terminal tail anchors the protein to the inner nuclear membrane, while the remainder of the protein projects into the nucleoplasm Emerin is a member of the nuclear LAP family23 25 The nuclear lamina is composed of intermediate-sized laments (eg, lamins A, B, and C) associated with the nucleoplasmic surface of the inner nuclear membrane These lamins bind to various LAPs, including LAP1, LAP2, and lamin B receptor, which are located on the inner nuclear membrane LAP2, lamin B receptor, and the lamins also bind to chromatin and thereby promote its attachment to the nuclear membrane Mutations in emerin conceivably lead to disorganization of the nuclear lamina and heterochromatin that is apparent on EM and immunohistochemistry25
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mutations are responsible for 76% of cases; therefore, mutations in LMNA should be considered in all familial and sporadic cases of EDMD and familial dilated cardiopathy27 Marked variability in the clinical phenotype can be seen within and between families with speci c mutations in the LMNA gene Lamins A and C are produced by alternative splicing of the lamin A/C RNA transcript As discussed in the Pathogenesis discussion regarding X-linked EDMD, these lamins are important in the organization and integrity of the nuclear membrane Muscle biopsies demonstrate variation in ber size, increased endomysial connective tissue, normal emerin expression, and usually normal lamin A/C expression EM reveals nuclear alterations similar to X-linked EDMD in 10% of muscle bers23,26 There are loss of peripheral heterochromatin or detachment from the nuclear envelop, alterations in interchromatin texture, and fewer nuclear pores compared to normal
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AUTOSOMAL-RECESSIVE EDMD3 Clinical Features
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This is a rare autosomal-recessive muscular dystrophy, with contractures and severe rigidity of the spine reported in ve unrelated children (three boys and two girls)226 Onset was in the rst 2 years of life, and the children were unable to walk by the age of 8 years However, they had no cardiac abnormalities
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We obtain yearly electrocardiograms on all our patients (as well as on possible female carriers) and obtain 24-hour Holters and cardiology consultations on those with signi cant abnormalities (eg, atrioventricular block) or cardiac symptoms Affected individuals may require pacemakers, and some authorities have even recommended prophylactic pacemakers222 Physical therapy is aimed at minimizing contractures
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Serum CK was moderately elevated226
Histopathology
Muscle biopsies revealed nonspeci c dystrophic changes with normal expression of emerin, dystrophin, the sarcoglycans, and laminins 2, 5, 1, 1 chains226
Molecular Genetics and Pathogenesis AUTOSOMAL-DOMINANT EDMD2/LGMD 1B
The clinical, laboratory, and histopathological features of this LGMD 1B are identical to those described above for typical X-linked EDMD1, except for autosomaldominant inheritance and equal frequency of affected females27,28,89 Thus, as noted previously, autosomaldominant EDMD2 and LGMD 1B are allelic disorders caused by mutations in the lamin A/C gene (LMNA) located on chromosome 1q11 2327,80,89,224 Mutations in the rod domain of LMNA cause hereditary dilated cardiopathy and conduction defects with or without an underlying skeletal muscle involvement27,28,89,225 De novo Autosomal recessive EDMD is also caused by mutations in LMNA
OTHER EDMD
In over 60% patients with EDMD do not have mutations in the genes encoding emerin or lamin A/C (Zhang et al, 2007) Recently, mutations were identi ed in genes that encode for nesprin-1 and -2, in several sporadic cases and autosomal dominant families with EDMD-like phenotypes (Zhang et al, 2007) Nesprin-1 and -2 (nuclear envelope spectrin repeat proteins) are spectrin-repeat containing proteins that are anchored in the outer and
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