Circoli collaterali porto-sistemici all'eco-color-Doppler addominale in pazienti con ipertensione portale cirrotica: correlazione con il gradiente porto-epatico e valore prognostico

Background. Abdominal porto-systemic collaterals (APSC) on Color-Doppler ultrasound are a frequent finding in portal hypertensive cirrhotic patients. In patients with cirrhosis, an HVPG ≥ 16mmHg has been shown to be associated with increased mortality in two studies. Non-invasive indicators of HVPG ≥ 16 mmHg might define a subgroup of high-risk patients, but data on this aspect are lacking. Aims. We aimed to investigate whether HVPG predicts mortality in patients with clinically significant portal hypertension, and if APSC may predict a severe portal hypertensive state (i.e. HVPG≥16mmHg) in patients with cirrhosis and untreated portal hypertension. Methods. We analysed paired HVPG and ultrasonographic data of 86 untreated portal hypertensive cirrhotic patients. On abdominal echo-color-Doppler data on presence, type and number of APSC were prospectively collected. HVPG was measured following published guidelines. Clinical, laboratory and endoscopic data were available in all cases. First decompensation of cirrhosis and liver-disease related mortality on follow-up (mean 28±20 months) were recorded. Results. 73% of patients had compensated cirrhosis, while 27% were decompensated. All patients had an HVPG≥10 mmHg (mean 17.8±5.1 mmHg). 58% of compensated patients and 82% of decompensated patients had an HVPG over 16 mmHg. 25% had no varices, 28% had small varices, and 47% had medium/large varices. HVPG was higher in patients with esophageal varices vs. patients without varices (19.0±4.8 vs. 14.1±4.2mmHg, p<0.0001), and correlated with Child-Pugh score (R=0.494,p=0.019). 36 (42%) patients had APSC were more frequent in decompensated patients (60% vs. 35%, p=0.03) and in patients with esophageal varices (52% vs. 9%,p=0.001). HVPG was higher in patients with APSC compared with those without PSC (19.9± 4.6 vs. 16.2± 4.9mmHg, p=0.001). The prevalence of APSC was higher in patients with HVPG≥16mmHg vs. those with HVPG<16mmHg (57% vs. 13%,p<0.0001). Decompensation was significantly more frequent in patients with HVPG≥16mmHg vs. HVPG<16mmHg (35.1% vs. 11.5%, p=0.02). On multivariate analysis only HVPG and bilirubin were independent predictors of first decompensation. 10 patients died during follow-up. All had an HVPG≥16 mmHg (26% vs. 0% in patients with HVPG <16mmHg,p=0.04). On multivariate analysis only MELD score and HVPG ≥16mmHg were independent predictors of mortality. In compensated patients the detection of APSC predicted an HVPG≥16mmHg with 92% specificity, 54% sensitivity, positive and negative likelihood ratio 7.03 and 0.50, which implies that the demonstration of APSC on ultrasound increased the probability of HVPG≥16mmHg from 58% to 91%. Conclusions. HVPG maintains an independent prognostic value in the subset of patients with cirrhosis and clinically significant portal hypertension. The presence of APSC is a specific indicator of severe portal hypertension in patients with cirrhosis. Detection of APSC on ultrasound allows the non-invasive identification of a subgroup of compensated patients with bad prognosis, avoiding the invasive measurement of HVPG.