Marie Rohlenová, Kateřina Machová, Jana Baranová, Lenka Mokrá, Livie Mensová, Radim Mazanec, Lenka Juříková, Jan Staněk, Petra Fuchsová, Barbora Lauerová, Markéta Kumhera, Jana Haberlová
{"title":"杜氏和贝克尔肌营养不良症患者血清肌酸激酶和转氨酶水平。","authors":"Marie Rohlenová, Kateřina Machová, Jana Baranová, Lenka Mokrá, Livie Mensová, Radim Mazanec, Lenka Juříková, Jan Staněk, Petra Fuchsová, Barbora Lauerová, Markéta Kumhera, Jana Haberlová","doi":"10.1002/mus.28431","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction/aims: </strong>The distinction between hepatic and muscular origin of transaminases in Duchenne (DMD) and Becker (BMD) muscular dystrophy is challenging. We aimed to describe the relations between creatine kinase (CK), lactate dehydrogenase (LDH), myoglobin, and alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma glutamyltransferase (GGT), and their evolution with age, the severity of the disease, and its complications (corticosteroid therapy, cardiac ejection fraction, body mass index [BMI]).</p><p><strong>Methods: </strong>Multiple regression analysis of the studied markers was performed in three cohorts: 1. Retrospective data of 212 DMD and BMD boys available in the national registry of muscular dystrophies (REaDY), and 2. Cross-sectional study supplemented by retrospective data of A. 64 DMD boys and B. 18 adults with either BMD or B/DMD carriers.</p><p><strong>Results: </strong>The estimation of normal levels of transaminases from CK levels was: ALT [UI/L] = 228.508 + 0.011*CK [UI/L] ± 341.822for DMD, and ALT [UI/L] = 124.498 + 0.011*CK [UI/L] ± 341.822for BMD. AST [UI/L] = 167.436 + 0.012*CK [UI/L]-6.323*Age ± 249.804 for both (all p < 0.001). In the smaller cohort, ALT was best predicted by LDH and physical performance, whereas AST was defined by CK and LDH combined (all p < 0.001). In DMD, all AST, ALT, CK, LDH, and myoglobin decreased with age (p < 0.001), while GGT increased with age and BMI (both p < 0.001).</p><p><strong>Discussion: </strong>Transaminases are dependent on CK and LDH in dystrophinopathy. There is an increase in GGT in DMD connected to BMI.</p>","PeriodicalId":18968,"journal":{"name":"Muscle & Nerve","volume":" ","pages":"240-249"},"PeriodicalIF":3.1000,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Serum Creatine Kinase and Transaminase Levels in Duchenne and Becker Muscular Dystrophies.\",\"authors\":\"Marie Rohlenová, Kateřina Machová, Jana Baranová, Lenka Mokrá, Livie Mensová, Radim Mazanec, Lenka Juříková, Jan Staněk, Petra Fuchsová, Barbora Lauerová, Markéta Kumhera, Jana Haberlová\",\"doi\":\"10.1002/mus.28431\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction/aims: </strong>The distinction between hepatic and muscular origin of transaminases in Duchenne (DMD) and Becker (BMD) muscular dystrophy is challenging. We aimed to describe the relations between creatine kinase (CK), lactate dehydrogenase (LDH), myoglobin, and alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma glutamyltransferase (GGT), and their evolution with age, the severity of the disease, and its complications (corticosteroid therapy, cardiac ejection fraction, body mass index [BMI]).</p><p><strong>Methods: </strong>Multiple regression analysis of the studied markers was performed in three cohorts: 1. Retrospective data of 212 DMD and BMD boys available in the national registry of muscular dystrophies (REaDY), and 2. Cross-sectional study supplemented by retrospective data of A. 64 DMD boys and B. 18 adults with either BMD or B/DMD carriers.</p><p><strong>Results: </strong>The estimation of normal levels of transaminases from CK levels was: ALT [UI/L] = 228.508 + 0.011*CK [UI/L] ± 341.822for DMD, and ALT [UI/L] = 124.498 + 0.011*CK [UI/L] ± 341.822for BMD. AST [UI/L] = 167.436 + 0.012*CK [UI/L]-6.323*Age ± 249.804 for both (all p < 0.001). In the smaller cohort, ALT was best predicted by LDH and physical performance, whereas AST was defined by CK and LDH combined (all p < 0.001). In DMD, all AST, ALT, CK, LDH, and myoglobin decreased with age (p < 0.001), while GGT increased with age and BMI (both p < 0.001).</p><p><strong>Discussion: </strong>Transaminases are dependent on CK and LDH in dystrophinopathy. 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Serum Creatine Kinase and Transaminase Levels in Duchenne and Becker Muscular Dystrophies.
Introduction/aims: The distinction between hepatic and muscular origin of transaminases in Duchenne (DMD) and Becker (BMD) muscular dystrophy is challenging. We aimed to describe the relations between creatine kinase (CK), lactate dehydrogenase (LDH), myoglobin, and alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma glutamyltransferase (GGT), and their evolution with age, the severity of the disease, and its complications (corticosteroid therapy, cardiac ejection fraction, body mass index [BMI]).
Methods: Multiple regression analysis of the studied markers was performed in three cohorts: 1. Retrospective data of 212 DMD and BMD boys available in the national registry of muscular dystrophies (REaDY), and 2. Cross-sectional study supplemented by retrospective data of A. 64 DMD boys and B. 18 adults with either BMD or B/DMD carriers.
Results: The estimation of normal levels of transaminases from CK levels was: ALT [UI/L] = 228.508 + 0.011*CK [UI/L] ± 341.822for DMD, and ALT [UI/L] = 124.498 + 0.011*CK [UI/L] ± 341.822for BMD. AST [UI/L] = 167.436 + 0.012*CK [UI/L]-6.323*Age ± 249.804 for both (all p < 0.001). In the smaller cohort, ALT was best predicted by LDH and physical performance, whereas AST was defined by CK and LDH combined (all p < 0.001). In DMD, all AST, ALT, CK, LDH, and myoglobin decreased with age (p < 0.001), while GGT increased with age and BMI (both p < 0.001).
Discussion: Transaminases are dependent on CK and LDH in dystrophinopathy. There is an increase in GGT in DMD connected to BMI.
期刊介绍：
Muscle & Nerve is an international and interdisciplinary publication of original contributions, in both health and disease, concerning studies of the muscle, the neuromuscular junction, the peripheral motor, sensory and autonomic neurons, and the central nervous system where the behavior of the peripheral nervous system is clarified. Appearing monthly, Muscle & Nerve publishes clinical studies and clinically relevant research reports in the fields of anatomy, biochemistry, cell biology, electrophysiology and electrodiagnosis, epidemiology, genetics, immunology, pathology, pharmacology, physiology, toxicology, and virology. The Journal welcomes articles and reports on basic clinical electrophysiology and electrodiagnosis. We expedite some papers dealing with timely topics to keep up with the fast-moving pace of science, based on the referees'' recommendation.
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