Oertelt-Prigione et al. Journal of Medical Case Reports 2010, 4:141 http://www.jmedicalcasereports.com/content/4/1/141 Page 3 of 4 Table 1: Blood exams and gas analysis upon admission and during the two episodes of encephalopathy Presentation After 1st adverseevent After 2nd adverse event Normal range AST (U/L) ALT (U/L) Bilirubin (mg/dL) Creatinine (mg/dL) Urea (mg/dL) Albumin (g/dL) Haemoglobin (g/dL) WBC (103/μL) Platelets (103/μL) CRP (mg/L) PT (INR) Na+ (mEq/L) K+ (mEq/L) pH HCO3 (mmol/L) 112 71 1.7 0.8 46 1.5 9.4 3.9 61 15 1.2 139 4.7 7.43 23.6 115 81 2.8 0.9 55 1.6 11 4.9 73 11 1.2 139 5.0 7.43 22.1 137 84 2.7 0.8 50 1.6 10 5.0 78 12 1.2 140 4.2 7.50 24.6 5-41 7-41 <1 0.7-1.3 10-50 3.6-4.8 13-17 4.0-10.0 150.0-450.0 <5 0.8-1.2 135-145 3.6-5.2 7.35-7.45 21-23 AST: aspartate aminotransferase; ALT: alanine aminotransferase; WBC: white blood cell; PT: prothrombin time; INR: international normalized ratio; Na+: sodium, K+: potassium, HCO3: bicarbonate. serum ammonia levels of a pharmacological block by the renin-angiotensin system in humans are still undefined, our case suggests an overall reduction of renal excretion through the kidneys. In turn, this could have accounted for the abrupt rise in ammonia levels detected in a patient with increased susceptibility due to the concomitant liver cirrhosis and severe portal hypertension (Figure 1). We suggest a careful clinical follow-up and, possibly, moni- toring of blood ammonia concentrations when ACEI and ARB combination therapy is administered to patients with liver cirrhosis and portal hypertension. The inci- dence of this serious side-effect associated with a com- Figure 1 In healthy controls the excretion of ammonia is mediated by two mechanisms: liver detoxification and renal excretion. Renal excre- tion is modulated by angiotensin II (ATII) at the level of the proximal tubule. In our patient the hepatic mechanism is impaired, due to the liver cirrhosis, making the renal route essential for elimination of ammonia. Suppression of ATII activity through a combination of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers prevented adequate renal excretion, leading to an abrupt rise in serum ammonia concentration and the described neurological complications.