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PubMed1986

[Computer tomography identification of carriers of Duchenne progressive muscular dystrophy].

Comparison of findings obtained by computed tomography of muscles of possible carriers and normal subjects demonstrated that structural changes existed in 31 out of 74 women; the certainty of the information obtained became greater with increasing age. Six of the seven genealogically definite carriers were detected by computed tomography. The present results show that the use of computed tomography is promising for future carrier diagnosis.

Adult↗
PubMed1986

[Cardiac manifestation of progressive muscular dystrophy of the Duchenne type].

Autopsy studies have shown that cardiomyopathy of Duchenne's muscular dystrophy (DMD) is characterized by fibrosis of the posterobasal and contiguous lateral wall of the left ventricle. This study was designed to determine whether stress testing would improve the sensitivity of echocardiography to detect secondary impairment of regional myocardial function. 12 patients aged 5 to 23 years with DMD were investigated. TM- and 2D-echocardiograms were performed before and during graded infusion of angiotensin (A) (0.5 to 5.0 mcg/min), and parameters of cardiac function analyzed. Satisfactory echocardiograms were obtained in all patients. Stress testing with A proved feasible in DMD and did not interfere with echocardiography. Before A all patients were in regular sinus rhythm and free of cardiac symptoms. Left ventricular function was normal in 9 patients and considered abnormal in 3 patients with hypokinesis and increased echo intensity of the posterobasal and lateral wall (2D short axis view) and/or a posterior wall to septal amplitude ratio of less than or equal to 1.1 (TM-echocardiogram). During A mean blood pressure rose and heart rate dropped significantly. 9 patients had marked supraventricular arrhythmias, 8 complained of dyspnea, cough or chest pain. Hypo- or akinesis of the posterobasal and sometimes the lateral wall was seen in 8, and a posterior wall to septal amplitude ratio of less than or equal to 1.1 in 9 patients. 3 patients, all with a muscle score of 60% or higher, remained free of symptoms and had no regional contraction abnormalities. Thus, clinical symptoms during A suggested latent congestive heart failure in many of the patients, and echocardiography identified provokable contraction abnormalities of such segments of the ventricular wall known to be most frequently involved in the dystrophic process in DMD. Stress testing revealed a correlation between clinical symptoms, abnormal echocardiographic findings and extent of the skeletal muscle disease in our study group. Physical limitation seems to protect the heart against demands that would otherwise cause earlier clinical manifestation of the cardiomyopathy in DMD.

Adolescent↗
PubMedDate not supplied

[Clinical role of lipid metabolism indices in the plasma and erythrocytes in progressive muscular dystrophies].

Patterns of lipid metabolism were studied in blood plasma and erythrocytes of patients with various forms of hereditary myopathies (Duchenn disease, Bekker-Kiner disease, Erba-Roth disease, Landuzy-Dejerin disease, Sharko-Mary neural amyotrophy). These diseases were characterized by a number of common patterns: deficiency of phospholipids, specific alterations in properties of lipoproteins and in content of cholesterol. In the Duchenn disease specific alterations typical for each step of the disease were shown. These alterations might be of prognostic significance for evaluation of the rate of myodystrophy development.

Adolescent↗
PubMedDate not supplied

[Diagnostic value of determining lactate dehydrogenase in the blood in progressive muscular dystrophy of the Duchenne type and in detection of the carrier state of this disease].

In the presented paper we failed to confirm the suggestion of a high diagnostic value of determination of blood lactic dehydrogenase isoenzymes in cases of Duchenne's dystrophy and in the detection of carriers of its gene. Determination of creatine kinase activity remains still the best biochemical test in this disease.

Clinical Enzyme Tests↗