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These abnormalities were previously regarded as secondary epiphenomena of metabolic dysfunction, but accumulating evidence now indicates that they arise from hyperglycaemia-driven OCTN2 impairment, insulin resistance, and oxidative stress, together forming a distinct carnitine-related metabolic signature

Conventional treatment options such as salicylates, corticosteroids, and immunosuppressants often come with severe side effects, limited bioavailability, and the development of drug resistance, which hampers their therapeutic effectiveness