Individualized care for portal hypertension: Not quite yet

A consensus on management of portal hypertension was lacking prior to 1990, and perhaps not surprisingly, results reported on response to interventions were quite heterogenous. The Baveno meetings presented structured protocols for the management of the acute variceal bleeding episode and a consensus on both primary and secondary prophylaxis. What is evident with the passage of time from the first Baveno workshop (1990) to Baveno VI (2015), the subject of this editorial [1], is the significant impact the adoption of these consensus documents has had on bleeding related mortality, greater than 30–40% in the early 1980s to 7–12% in recent times [2,3] (Fig. 1). However, the overall one and five-year all-cause mortality in patients presenting with variceal bleeding still remains high. To address this discrepancy, one needs to assess a number of factors that impact on portal hypertension in cirrhosis, which in turn may help better management of the individual patient. Portal hypertension is inextricably linked with all the principal complications of cirrhosis including variceal bleeding, renal dysfunction, hepatic encephalopathy and susceptibility to infection and multi-organ dysfunction, from which these patients succumb. Common to all these organ manifestations of portal hypertension is an underpinning of heightened inflammatory response and the individual’s tolerance to this. For example, it has been shown that markers of bacterial translocation are increased in over 40% patients with cirrhosis [4]. Furthermore, the severity of portal hypertension has been shown to predict the occurrence of SBP and is correlated with levels of bacterial DNA [5,6], and might actually suggest that portal hypertension plays a key role in the development of bacterial translocation. Given this knowledge, perhaps unsurprisingly, several markers of systemic inflammation are elevated in advanced cirrhosis, and these correlate with portal hypertension and mortality, including serum C-reactive protein (CRP) and IL-6 levels, highlighting the importance of exploring further the role of selective gut decontaminants and anti-inflammatory strategies in the treatment of portal hypertension [7,8]. Indeed, we can draw upon cues from the cardiovascular literature where a relationship