DETERMINATION OF TRANSAMINASES AND CREATINE KINASE LEVELS IN PATIENTS WITH MUSCULAR DYSTROPHY AND MUSCULOSKELETAL DISEASES
Keywords:
Ceratine Kinase, Alanine Transminase, Aspartate Transminase, Muscular Dystrophy, Mypathy, RegressionAbstract
BACKGROUND
The transaminases, ALT and AST (alanine and aspartate transaminases, respectively), that are generally considered to be the hepatic enzymes, also found in skeletal muscles. Continual elevated levels of both enzymes in patients with several forms of muscular dystrophy and musculoskeletal diseases have been documented in several studies.
AIM AND OBJECTIVES
The present study is undertaken to examine the possibility of highlighting transaminases elevation in muscular dystrophy as an indicator of concomitant muscular damage, rather than hepatic injury due to medications, and relate its significance with underlying myofibrillar damages.
MATERIALS AND METHODS
Data of a total of 52 patients (males = 38, females = 14) were obtained during December 2006 to December 2011 and complied as per criteria. Plasma CK enzyme and transaminases (AST and ALT) levels were performed by enzymatic methods on Hitachi 912. A specific hepatic marker gamma glutamyl transpeptidase (GGT) was also measured to assess the extent or presence of hepatic damages. All enzymatic data were analyzed using regression correlation analyses with significance level of P < 0.05.
RESULTS
Cumulative as well as individual data analysis showed significant correlation of transaminases with CK, which is the distinct indicator of muscle damage. ALT R2 correlation with CK showed linear regression correlation of R2 = 0.796 and for AST R2 = 0.814. Cumulative mean of CK was 406.83 ± 20.15 IU/L; ALT = 70.86 ± 10.21 IU/L, AST = 68.78 ± 8.30 IU/L and GT = 20.13 ± 4.30 IU/L.
CONCLUSION
The present study describes the elevated level of transaminase, ALT and AST in patients of muscular dystrophy and myopathies. It was also exhibited that both transaminases concentration linearly correlated with muscle marker CK. No hepatic damage was noted in all patients as manifested by normal levels of GGT, a distinct marker of hepatic origin.