The effect of angiotensin-blocking agents on liver fibrosis in patients with hepatitis C

Abstract

Background: Multiple studies implicate the renin-angiotensin system in hepatic fibrogenesis. Few studies have examined the effects of angiotensin blockade on liver fibrosis via human histology.

Aims: We studied the histological effect of angiotensin II blocking agents in chronic hepatitis C patients.

Methods: This was a retrospective study of 284 chronic hepatitis C patients from 2001 to 2006 who underwent a liver biopsy. Group I was comprised of 143 hypertensive patients who received angiotensin-blocking agents. Group II was comprised of 91 hypertensive subjects who received hypertensive agents other than angiotensin blockers. Group III was comprised of 50 non-hypertensive subjects.

Results: The groups were similar in age, sex, hepatitis C genotype, viral load and disease duration. They varied significantly in total diabetic patients (Group I, 43; Group II, 10; Group III, 1; P=0.0001), consistent with recommended use of angiotensin-converting enzyme inhibitors in hypertensive diabetics. Non-hypertensive patients had significantly less fibrosis than hypertensive patients, regardless of antihypertensive medications (Group I, 3.20; Group II, 3.73; Group III, 2.5; P=0.0002). Group I had significantly less fibrosis than Group II (P=0.02). This finding persisted in a non-diabetic subgroup of Groups I and II (Group I, 3.07; Group II, 3.69; P=0.0129).

Conclusion: Patients with hepatitis C and hypertension have increased fibrosis compared with non-hypertensive patients. Hypertensive patients receiving angiotensin-blocking agents had less fibrosis than hypertensive patients who did not receive angiotensin-blocking agents. This suggests an association with hypertension, possibly via the renin-angiotensin system in the fibrosis development and suggests a beneficial role of angiotensin II blockade in hepatitis C virus-related fibrosis.

Conflict of interest statement

No conflicts of interest exist.

Figures

Fig. 1

Comparison of fibrosis stage between Groups I and III.

Fig. 2

Comparison of steatosis scores between Groups I and III.

Fig. 3

Comparison of fibrosis stage between Groups I and III in non-diabetic patients.

Fig. 4

Comparison of steatosis scores between Groups I and III in non-diabetic patients.