Liver ramipril

Liver Ramipril-induced hepatotoxicity has been reported. 

Hepatic function impairment Patients with impaired liver function could develop markedly elevated plasma levels of unchanged fosinopril or ramipril. In patients with alcoholic or biliary cirrhosis, the rate, but not extent of fosinopril hydrolysis was reduced. Quinaprilat concentrations are reduced in alcoholic cirrhosis. 

Enalapril is an oral prodrug that is converted by hydrolysis to a converting enzyme inhibitor, enalaprilat, with effects similar to those of captopril. Enalaprilat itself is available only for intravenous use, primarily for hypertensive emergencies. Lisinopril is a lysine derivative of enalaprilat. Benazepril, fosinopril, moexipril, perindopril, quinapril, ramipril, and trandolapril are other long-acting members of the class. All are prodrugs, like enalapril, and are converted to the active agents by hydrolysis, primarily in the liver. 

There are no pharmakinetic data on the ACE inhibitors in the horse. In humans, enalapril is 60% absorbed following oral administration and is de-esterified in the liver to its active form enalapri-lat it undergoes renal clearance. Both the liver and kidneys eliminate the active forms of benazepril (benazeprilat) and ramipril (ramiprilat). 

The extent of oral absorption varies from 25% (li-sinopril) to 75% (captopril). The rate of absorption also varies from 0.5 h (captopril and enalopril) to 7h (lisinopril). Reported volumes of distribution range from 0.7lkg (captopril) to 1.8lkg (lisinopril). All of the ACE inhibitors, except for captopril and lisinopril, are metabolized in the liver to active metabolites. Excretion is via both the urine and the feces. The half-life ranges from 1.3 h (enalapril) to 17h (ramipril). 

Ramipril is a long-acting nonsulfhydryl ACE inhibitor. It is a prodrug that undergoes de-esterification in the liver... 

A 40-year-old man with liver cirrhosis and nephrotic syndrome who had been taking losartan for 6 weeks developed severe acute encephalopathy with unconsciousness after the addition of ramipril [31 ]. The authors surmised that dual blockade had suppressed angiotensin II at the level of the proximal tubule leading to inadequate renal excretion of ammonia, precipitating decompensation. 

Douros A, Kauffmann W, Bronder E, Ktimpel A, Garbe E, Kreutz R. Ramipril-induced liver injury case report and review of the literature. 

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