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Liver stiffness, controlled attenuation may predict decompensation

AMSTERDAM — Assessment of liver stiffness and controlled attenuation parameter may be useful as a novel predictor of decompensation, according to data presented at the International Liver Congress.

“Until recently, a sensitive diagnosis and quantification of liver steatosis was only possible through liver biopsy until the development of controlled attenuation parameter, or CAP,” Cristina Margini, MD, of the Department of Hepatology at UVCM, Inselspital, at the University of Bern, in Switzerland, said in her presentation. “CAP involves a non-invasive standardized numerical quantification of liver fat content based on the degree of ultrasound attenuation.”

Margini and colleagues hypothesized that CAP equal to or greater than 220 dB/m could predict clinical decompensation in compensated advanced chronic liver disease.

The study included 193 patients with liver stiffness equal to or greater than 10 kPa and available CAP measurements who were analyzed between September 2013 and September 2015. Margini highlighted the BMI of the cohort, which was 27.4 ± 4.6, and the Child-Pugh score of 5.4 ± 0.8.

Results indicated that 9.3% of the cohort decompensated, with nine of those events occurring from infection, seven from ascites and one each from variceal bleeding and hepatic encephalopathy. Three of those 18 patients died.

The remainder of the cohort (n = 175; 90.7%) remained compensated, with four fatalities in this group.

At baseline, liver stiffness was 33.6 ± 19.2 in the decompensated group and 19.8 ± 13.0 in those who remained compensated (P < .001).

When the researchers assessed if decompensation was associated with liver stiffness, results showed that 81 patients had stiffness equal to or greater than 13.6 kPa, 48 had stiffness between 13.6 and 21 kPa and 64 had stiffness equal to or greater than 21 kPa (K-W test P = .006). Margini reported a strong association between liver stiffness and decompensation (P < .001).

Similarly, decompensation occurred in just one patient (1.6%) among 61 patients with CAP less than 220 dB/m, and this patient had a BMI of 38 kg/m2. Among 132 patients with CAP equal to or greater than 220 dB/m, 17 (12.9%) developed decompensation.

Among 15 patients with liver stiffness equal to or greater than 21 kPa and CAP less than 220, none developed decompensation. Conversely, however, 12 of 49 patients with both liver stiffness equal to or greater than 21 kPa and CAP equal to or greater than 220 decompensated (P = .03).

Multivariable analysis results showed that among patients with liver stiffness, CAP higher than 220 dB/m significantly increased decompensation risk compared with CAP less than 220 (P = .012).

“Similar results were seen in a multivariate analysis with a CAP cutoff of 235,” Margini said.

At baseline, the researchers evaluate patients for etiology of liver disease, age, gender, BMI, laboratory tests, liver stiffness and CAP. They assessed patients for decompensation, which included ascites, variceal bleeding, jaundice, hepatic encephalopathy, hepatorenal syndrome and severe bacterial infections, along with mortality. Margini noted that 58 patients in the cohort had a viral etiology of liver disease.

“In our cohort of patients with compensated advanced liver disease, liver stiffness was strongly associated with decompensation,” Margini concluded. “CAP value over 220 in our population was significantly associated with clinical decompensation independent of liver stiffness value.” – by Rob Volansky

Reference: Margini C, et al. LBO-05. Presented at: International Liver Congress; April 19-24, 2017; Amsterdam.

Disclosure: Margini reports no relevant financial disclosures.