ACR Meeting Abstracts

ACR Meeting Abstracts

Abstract Number: 2063

Serum Glutamate Dehydrogenase in Idiopathic Inflammatory Myopathy Patients

Nantakarn Pongtarakulpanit1, Tanya Chandra1, shiri keret2, Vladimir Liarski1, Dana Ascherman3, Siamak Mogahadam1, Chester Oddis1 and Rohit Aggarwal4, 1Division of Rheumatology and Clinical Immunology, University of Pittsburgh, Pittsburgh, PA, 2Rheumatology unit, Bnai-Zion medical center and the faculty of Medicine, Technion - Israel Institute of Technology, Haifa, Israel., Atlit, Israel, 3Division of Rheumatology and Clinical Immunology, University of Pittsburgh Medical Center, Pittsburgh, PA, 4Division of Rheumatology and Clinical Immunology, University of Pittsburgh, Pittsburgh, PA, USA, Pittsburgh, PA

Meeting: ACR Convergence 2024

Keywords: ,

Session Information

Date: Monday, November 18, 2024

Title: Muscle Biology, Myositis & Myopathies – Basic & Clinical Science Poster III

Session Type: Poster Session C

Session Time: 10:30AM-12:30PM

Background/Purpose: Diagnosing hepatocellular injury in idiopathic inflammatory myopathy (IIM) patients with active myositis is challenging due to the lack of liver specificity of the transaminase enzymes. Glutamate dehydrogenase (GLDH) is a liver-specific biomarker capable of detecting hepatocellular injury in patients with muscle injury or degeneration. This study aims to validate serum GLDH levels as a biomarker for liver injury in IIM patients and to help differentiate serum transaminase enzyme elevation due to active myositis.

Methods: We measured serum GLDH levels in stored frozen (-80oC) serum from prospectively enrolled patients in the University of Pittsburgh Medical Center (UPMC) myositis registry and correlated these levels with traditional liver enzyme data collected on the same dates. Hepatocellular liver injury was assessed through clinical judgment based on a review of clinical data, hepatic investigations, and longitudinal changes in liver enzyme patterns over time.

Results: We analyzed 115 serum samples collected at different times from 68 IIM patients (1 – 6 samples per patient). Most of the patients were white (94.8%) and female (62.6%), with a median (IQR) age of 57.0 (45.0 – 65.0) years. Fatty liver was documented in 25.2%. Alcohol use was reported by 42.2% of the patients, and 46.6% had received hepatotoxic drugs. The most common IIM subtype was anti-synthetase syndrome (36.2%), followed by dermatomyositis (20.7%) and immune-mediated necrotizing myopathy (19.0%).
The median (IQR) levels of ALT, AST, and CPK were 32.5 (18.0 – 62.5) IU/L, 31.0 (21.0 – 52.8) IU/L, and 306.0 (66.3 – 1,123.8) IU/L, respectively. The median (IQR) fold increases above the upper limits normal (ULN) for ALT, AST, and CPK were 0.51 (0.29 – 0.97), 0.76 (0.51 – 1.29), and 1.51 (0.33 – 5.71), respectively. Log-transformed fold increases above ULN values of ALT and AST showed a good correlation with CPK (Spearman’s correlation coefficients 0.596 and 0.764, respectively; P < 0.01). In contrast, Log-transformed fold increases above ULN values of GLDH showed a poor correlation with CPK (Spearman’s correlation coefficient 0.258, P < 0.01). There were linear relationships between Log-transformed folds increases above ULN values of CPK and transaminase enzymes but not between the CPK and GLDH. The longitudinal plots demonstrated that GLDH is more specific to liver injury than transaminase enzymes.

Conclusion: In IIM patients, GLDH shows a poor correlation with CPK, confirming its specificity for liver injury independent of muscle inflammation in myositis. GLDH is a specific biomarker for evaluating hepatocellular injury in IIM patients with concurrent myositis.

Supporting image 1

Table 1 Correlations between Log10 of the folds increase from the upper limit of normal of serum CPK, AST, ALT, GLDH (all serums, n = 115)

Supporting image 2

Figure 1. Scatterplots with reference lines between serum levels of CPK and ALT (Figure 1A), AST (Figure 1B), and GLDH (Figure 1C). The value of each data point is presented as the Log10 of the folds increase from the upper limit of normal (ULN) observed in healthy subjects. There are linear relationships between the CPK and transaminase enzymes (Figure 1A and 1B) but not between the CPK and GLDH (Figure 1C).

Supporting image 3

Figure 2. Comparison of ALT, AST, CPK, and GLDH levels at different time points in four myositis patients with elevated CPK but without liver injury. The values are presented as the Log10 of the folds increase from the upper limit of normal (ULN) observed in healthy subjects. A value of 0.00 corresponds to the ULN value of each parameter (Log10 of 1-fold change of ULN value equals to 0.00).

Disclosures: N. Pongtarakulpanit: None; T. Chandra: None; s. keret: None; V. Liarski: None; D. Ascherman: None; S. Mogahadam: None; C. Oddis: Abcuro, 5, Alexion, 5, Argenx, 5, Boehringer Ingelheim, 5, CSL Behring, 5, EMD Serono, 5, Janssen, 5, Pfizer, 5, Priovant, 5; R. Aggarwal: Alexion, 2, ANI Pharmaceuticals, 2, Argenx, 2, AstraZeneca, 2, Boehringer-Ingelheim, 2, 5, Bristol-Myers Squibb(BMS), 2, 5, CabalettaBio, 2, Capella Bioscience, 2, Capstanx, 2, Corbus, 2, CSL Behring, 2, EMD Serono, 2, 5, Galapagos, 2, Horizon Therapeutics, 2, I-Cell, 2, Immunovant, 2, Janssen, 1, 2, 5, Kezar, 2, Kyverna, 2, Lilly, 2, Mallinckrodt, 5, Manta Medicines Corporation, 2, Merck, 2, Novartis, 2, Nuvig Therapeutics, 2, Octapharma, 2, Pfizer, 2, 5, Q32, 5, Roivant, 2, Sanofi, 2, Teva, 2.

To cite this abstract in AMA style:

Pongtarakulpanit N, Chandra T, keret s, Liarski V, Ascherman D, Mogahadam S, Oddis C, Aggarwal R. Serum Glutamate Dehydrogenase in Idiopathic Inflammatory Myopathy Patients [abstract]. Arthritis Rheumatol. 2024; 76 (suppl 9). https://acrabstracts.org/abstract/serum-glutamate-dehydrogenase-in-idiopathic-inflammatory-myopathy-patients/. Accessed .

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