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Antifibrotic effect of angiotensin blockers in hypertensive hepatitis C patients

To the Editor: We read with interest the manuscript by Corey et al. (1) on the effect of angiotensin II (Ang II) blocking agents on liver fibrosis in hypertensive patients with chronic hepatitis C (HCV). Their retrospective study demonstrated that hypertensive HCV patients had a higher fibrosis stage compared with non-hypertensive patients. Fibrosis in hypertensive patients was decreased, when they received angiotensin-converting enzyme (ACE) inhibitors or Ang II receptor type 1 antagonists (AT1A) compared with other antihypertensive regimens. The authors are to be commended for their results. Angiotensin II acting via AT1 receptors on hepatic stellate cells (HSCs) can promote liver fibrosis with increased HSC proliferation, synthesis of extracellular matrix components, growth factors, cytokines and other bioactive substances (2). Beside Ang II the disparity in the production and metabolism of endothelin 1 (ET-1) in cirrhotic livers is another important factor in disease progression (3). Whereas the effect of ET-1 receptor blockers on liver fibrosis is largely unknown, there is evidence that blockade of Ang II signalling attenuates fibrosis in selected patients (4, 5). Because of the risk of acute renal failure there is concern about the administration of Ang II blockers in decompensated cirrhotics with ascites or high plasma renin activity (4). This might have an impact on patient population in the present study, but information about liver disease stage before the introduction of antihypertensive treatment and about the kind of hypertension is not provided. Is systemic hypertension the cause for more fibrosis or just its consequence? The authors demonstrated a mere relation between hypertension and fibrosis. Evidence for the role of systemic hypertension itself on the development of liver fibrosis is limited. But prevalence of hypertension among patients with cirrhosis is relatively low (3–7%) (6). In fact Henriksen et al. (6) have reported that liver function was significantly better in hypertensive cirrhotics than in their normotensive counterparts. If one assumes that systemic hypertension is associated with more fibrosis, the significant longer antihypertensive treatment in patients receiving Ang II blockers compared with patients receiving other antihypertensive drugs makes it difficult to interpret the results of the present study. Unfortunately, the authors could not evaluate the different effects of ACE inhibitors vs AT1A on liver fibrosis. The simultaneous prevention of Ang II production, bradykinin degradation and induction of angiotensin 1–7 production by ACE inhibitors could be particularly favourable regarding antifibrotic therapy and liver regeneration (7, 8). This will need to be addressed in future studies.