Characterization of Dystrophin in Muscle-Biopsy Specimens from Patients with Duchenne's or Becker's Muscular Dystrophy — NEJM mannen louboutin

Characterization of Dystrophin in Muscle-Biopsy Specimens from Patients with Duchenne's or Becker's Muscular Dystrophy

Eric P. Hoffman, Ph.D., Kenneth H. Fischbeck, M.D., Robert H. Brown, M.D., Ph.D., Margaret Johnson, Ph.D., Rosella Medori, M.D., John D. Loire, Ph.D., John B. Harris, Ph.D., Robert Waterston, M.D., Ph.D., Michael Brooke, M.D., Linda Specht, M.D., Ph.D., William Kupsky, M.D., Jeffrey Chamberlain, Ph.D., C. Thomas Caskey, M.D., Frederic Shapiro, M.D., and Louis M. Kunkel, Ph.D.

N Engl J Med 1988; 318:1363-1368May 26, 1988DOI: 10.1056/NEJM198805263182104

christian louboutin lady peep spikesn class="title" id="d361e422">Abstract

A deficiency of the protein dystrophin has recently been shown to be the probable cause of Duchenne's muscular dystrophy. We sought to determine the relation between the clinical phenotype and the status of dystrophin in muscle-biopsy specimens from 103 patients with various neuromuscular disorders. We found very low levels (<3 percent of normal levels) or no dystrophin in the severe Duchenne phenotype (35 of 38 patients), low concentrations of dystrophin in the intermediate (outlier) phenotype (4 of 7), and dystrophin of abnormal molecular weight in the mild Becker phenotype (12 of 18). Normal levels of dystrophin of normal molecular weight were found in nearly all the patients (38 of 40) with 20 other neuromuscular disorders we studied.

These data show the clinical consequences of both quantitative alterations (in Duchenne's and intermediate dystrophy) and qualitative alterations (in Becker's dystrophy) in a single protein. The biochemical assay for dystrophin should prove helpful in delineating myopathies that overlap clinically with Duchenne's and Becker's dystrophies, and it shows promise as an accurate diagnostic tool. (N Engl J Med 1988; 318:1363–8.)

We are indebted to our supporting institutions, particularly the Muscular Dystrophy Associations of the United States and Great Britain.

Source Information

From the Division of Genetics, Children's Hospital, and the Department of Pediatrics, Harvard Medical School, Boston (E.P.H., L.M.K.), the Howard Hughes Medical Institute, Boston (L.M.K.), the Department of Neurology, Hospital of the University of Pennsylvania, Philadelphia (K.H.F.), the Neurology Service, Massachusetts General Hospital, Boston (R.H.B.), the Muscular Dystrophy Group Laboratories, Newcastle General Hospital, Newcastle-upon-Tyne, Great Britain (M.J., J.B.H.), the Division of Neurology (R.M., M.B.) and the Department of Genetics (R.W.), Washington University, St. Louis, the Department of Physiology and Cellular Biophysics, College of Physicians and Surgeons of Columbia University, New York (J.D.L.), the Departments of Neurology (L.S.), Pathology (W.K.), and Orthopaedic Surgery (F.S.), Children's Hospital, Boston, and the Robert J. Kleberg Jr. Center for Human Genetics, Baylor College of Medicine, Texas Medical Center, Houston (J.C., C.T.C.). Address reprint requests to Dr. Kunkel at the Howard Hughes Medical Institute Research Laboratories, Children's Hospital, 300 Longwood Ave., Boston, MA 02115.

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