UC can be characterized as being in remission (time when the symptoms get better) or mildly, moderately or severely active
Ketoacidosis would support one of the following etiologies: Inadequate carbohydrate intake (see #2/4 above) most strongly suggested, especially if beta-hydroxybutyrate levels are highly elevated
The body downregulates its basal metabolic rate to conserve energy, matching the lower caloric intake induced by the medication
Apoptosis, another consequence of oxidative damage and mitochondrial dysfunction, was evaluated using Annexin-V staining, which detects early apoptotic changes by binding to phosphatidylserine exposed on the outer leaflet of the plasma membrane
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