Mukund

And his platelets are now down to 688, which is at his baseline.

I also vitamin K challenge him and the INR, I think I said PT last time, sorry, which was 2.8 is now 1.4.

Really curious, Vale, what you make of this information, particularly Asaidi's fluid studies, but also his clinical course and the change in his status over time.

Yeah, I totally think this changed our framework as well.

Vale touched on some of the key points of tension that I think I was looking at as well.

In particular, is this low sag ascites from, frankly, secondary bacterial peritonitis?

Is this from a biliary leak or ruptured cholecystitis?

Or are we actually seeing portal hypertensive ascites that has been bled into, thereby contaminating the

the ascites fluid albumin to serum albumin ratio and making it falsely appear as though it was a low sag ascites.

This is the last aliquot and it involves some invasive data.

We got a liver biopsy because I think without tissue, it was impossible for us to decide whether this was cirrhotic ascites, whether this was non-cirrhotic ascites with a hemorrhaging component or whether this was some other diagnosis entirely.

So

We asked our colleagues in interventional radiology to do an IR-guided transjugular liver biopsy, and we asked for gradient measurements as well.

Radial pressure was measured at 10, and a normal value is less than 7 or 8.

A hepatic venous free pressure was measured at 11.

The hepatic venous wedged pressure was measured at 18.

And therefore, the hepatic venous pressure gradient, or the wedged minus the free pressure, was 7.

Technically, greater than 5 is defined as portal hypertension.

We also got a liver biopsy, benign hepatic parenchyma with a nodular contour.

fibrous expansion of most portal tracts with patchy zone 1 and zone 3 perisinusoidal fibrosis, but without definitive bridging fibrosis appreciated.