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PATHOPHYSIOLOGY The pathophysiology of hyperbilirubinemia in GS is multifactorial[11,12], involving disruptions in bilirubin production, hepatic uptake glucuronidation, and transport, all influenced by genetic factors (Figure 1)

However this technique has some disadvantages such as: this technique relatively high cost, leakage of ligands may accur from the column and sometimes the desorption procedure results in partial denaturation of the bound protein [24]

The published thresholds for ELF (9.8 and 11.3) and FIB4 (1.3 and 3.25) for advanced fibrosis were validated for their ability to predict both all LRE and LRE related to portal hypertension (PHTN-LRE)

doi:10.1007/s00422-010-0401-y

The results still havent been published