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Quantitative Liver Function

HEPATIQ: Hepatic Function Predicts Survival after Hepatocellular Carcinoma (HCC)

John Hoefs, M.D
Depts of Medicine, Divs of GI & Hepatology, University of California Irvine, Irvine, California
Hepatology, Liver Specialty Center, Irvine, CA, United States
DIGESTIVE DISEASE WEEK, 2020.

ABSTRACT

Background and Aims:

HCC can be difficult to diagnose and to treat. Outcomes from HCC are related to many factors including tumor factors (size, number, mets) and tolerance of treatment determined by hepatic function. Hepatiq is an image processing technique for the quantitative sulfur-colloid liver spleen scan resulting in a quantitative measure of hepatic function (perfused hepatic mass: PHM), functional spleen volume (fSV) and functional liver volume (fLV).  PHM correlates with the functional mass of the liver (AmJGastro;92:2054). Both PHM and fSV correlate with clinical outcomes (Hepat;55:1019). We hypothesized that PHM should correlate with treatment outcomes from HCC and would also help determine how aggressive one could treat, being more aggressive in patients with better function and, therefore, improving patient survival.

Method:

Patients: 17 patients had treatable HCC (confined to liver) diagnosed during screening with AFP and ultrasound for HCC Rx between 1/2011 - 12/2017.  All patients with HBV or HCV were treated to HBVDNA <20 and SVR. 4 of these patients were on the liver transplant (LT) list were and referred after removal from the list: 1 had a 9 cm HCC at surgery and 1 had 10 cm HCC discovered only after LT. 2 with delayed Rx by >1 year, one on LT list awaiting HCC to grow > 2 cm (sudden PV HCC thrombosis) and one without insurance and 2 with minimal Rx. 9 patients had early Rx, 8 for single lesions and 1 multifocal HCC. 1 patient had a second lesion 1 year after TCA and Rx Y90, but the rest had no recurrence including 1 with multifocal HCC. Patients were treated until there was no recurrence of HCC or a steady decline in PHM and/or fLV. Method: Hepatiq was performed on a fed sulfur-colloid QLSS with calculation of PHM (N100-110), fSV (n<2.5 cc/lb IBW) and fLV (7-12 cc/lb IBW). Blood tests and clinical data were abstracted from the clinical records at the time of HCC diagnosis.

Results:

Cause of CLD: HCV 15, HBV 3, NASH 1 (see figure for clinical). Treatment was surgical resection (3), TCA (16 in 12 patients), RFA (8) and Y90 (9).  9 patients had 1 treatment and the rest multiple treatments. 7 patients died (D), 2 were alive with known tumor (A+HCC), and 8 were alive with no known tumor (A-HCC).  Baseline PHM was significantly (p <.05) worse in those who D (69+/-15) vs A+HCC (83+/-7) vs A-HCC (99+/-4) and fSV greater D (5+/-2) vs A+HCC (4+/-2) vs A-HCC (2+/-1). Time to D was 3+/-2 yr (2/7 live >3 yr). A+HCC survived 16 and 3 yr. A-HCC alive 3+/-2 yr (5/9 >3 yr and 4/9 followed < 3 yr). Survival after Dx HCC correlated with baseline PHM (figure).

Conclusion:

1. PHM correlates with the time to death. 2. Patient alive without HCC recurrence post diagnosis had good PHM baseline supporting the role of better liver function in tolerance of both HCC and treatment of HCC. 3. Baseline hepatic function is an important test to predict outcomes from HCC.



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