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Liver Int. 2009 May;29(5):748-53. doi: 10.1111/j.1478-3231.2009.01973.x. Epub 2009 Feb 9.

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

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Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.



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.


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


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.


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).


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.

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