Recently we came across two cases of high plasma ICG retention and normal BSP. Histologyof both cases showed chronic hepatitis (inactive form). On electronmicroscopy incase 1, modification of mitochondria, increase of “lipofuscin-like” lysozome and lipid dropletswere observed.
We also found mild plasma ICG retention in father and a brother of case 1, and so didhigh plasma ICG retention and normal BSP in two sisters and a brother of case 2. Laboratoryfindings showed low grade bilirubinemia (total Bil. 3.5, direct Bil. 1.8) in case 1, and not remarkableabnormality n other cases except high plasma ICG retention.
Using column chromatography containing Sephadex G-200 and preparative ultracentrifugalflotation method, we obtained three distinct peaks on the ICG curve and these threepeaks corresponded to 19S, 7S and 4S protein peaks in control group. Ist ICG peak boundto VLDL and LDL, and 2nd ICG peak bound to HDL.
In chronic liver disease 2nd ICG peak (HDL) transfered to heavier protein, stillmorethis transfer rate correlated well to plasma ICG retention (r=-0.703, p<0.001). In these5 cases, 3 cases showed increase in 1st ICG peak, on the other hand 2 cases showed transferenceof 2nd ICG peak to heavier protein.
From these results it suggested that this discrepancy was congenital or constitutional, and thc abnormality of serum lopoprotein was one of a cause of this discrepancy.
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