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Many other cofactors can act synergically with hyperammonemia, to produce or aggravate HE, but experts do not consider them to be exclusive causes of HE, on their own or in isolation, i.e., in the absence of hyperammonemia.10 Patients with portosystemic shunts (PSSs) and no liver disease can also present with hyperammonemia-associated brain dysfunction despite having a functional or normal liver11

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This regulatory endorsement further underscores the broader applicability of GLP-1 agonists beyond diabetes management