AIM:Adrenomedullin (ADM) is a potent vasodilator peptide.ADM and nitric oxide (NO) are produced in vascular endothelialcells.Increased ADM level has been linked to hyperdynamiccirculation and arterial vasodilatation in cirrhotic portalhypertension (CPH).The role of ADM in non-cirrhotic portalhypertension (NCPH) is unknown,plasma ADM levels werestudied in patients with NCPH,compensated anddecompensated cirrhosis in order to determine itscontribution to portal hypertension (PH) in these groups.METHODS:There were 4 groups of subjects.Group 1consisted of 27 patients (F/M:12/15) with NCPH due toportal and/or splenic vein thrombosis (mean age:41±12years),group 2 consisted of 14 patients (F/M:6/8) withcompensated (Child-Pugh A) cirrhosis (mean age:46±4),group 3 consisted of 16 patients (F/M:6/10) withdecompensated (Child-Pugh C) cirrhosis (mean age:47±12).Fourteen healthy subjects (F/M:6/8) (mean age:44±8) wereused as controls in Group 4.ADM level was measured byELISA.NO was determined as nitrite/nitrate level bychemoluminescence.RESULTS:ADM level in Group 1 (236±61.4 pg/mL) wassignificantly higher than that in group 2 (108.4±28.3 pg/mL)and group 4 (84.1±31.5 pg/mL) (both P<0.0001) but waslower than that in Group3 (324±93.7 pg/mL) (P=0.002).NOlevel in group 1 (27±1.4 μmol/L) was significantly higher thanthat in group 2 (19.8±2.8 μmol/L) and group 4 (16.9±1.6μmol/L) but was lower than that in Group 3 (39±3.6 μmol/L)(for all three P<0.0001).A strong correlation was observedbetween ADM and NO levels (r=0.827,P<0.0001).CONCLUSION:Adrenomedullin and NO levels were highin both non-cirrhotic and cirrhotic portal hypertension andwere closely correlated,Adrenomedullin and NO levelsincreased proportionally with the severity of cirrhosis,andwere significantly higher than those in patients with NCPH.Portal hypertension plays an important role in the increaseof ADM and NO.Parenchymal damage in cirrhosis maycontribute to the increase in these parameters. AIM: Adrenomedullin (ADM) is a potent vasodilator peptide. ADM and nitric oxide (NO) are produced in vascular endothelial cells. Increased ADM level has been linked to hyperdynamic circulatory and arterial vasodilatation in cirrhotic portal hypertype (CPH). The role of ADM in non- cirrhotic portal hypertension (NCPH) is unknown, plasma ADM levels were staged in patients with NCPH, compensated and depensated cirrhosis in order to determine its contribution to portal hypertension (PH) in these groups. METHODS: There were 4 groups of subjects.Group 1consisted of 27 patients ( F / M: 12/15) with NCPH due toportal and / or splenic vein thrombosis (mean age: 41 ± 12 years), group 2 consisted of 14 patients (F / M: 6/8) with compensated (Child- Pugh A) cirrhosis (mean age: 46 ± 4), group 3 consisted of 16 patients (F / M: 6/10) with decompensated (Child-Pugh C) cirrhosis (mean age: 47 ± 12) / 8) (mean age: 44 ± 8) were used as controls in Group 4. ADM level was measured by ELISA.NO was determined as nitrite / nitrate level by chemoluminescence. RESULTS: ADM level in Group 1 (236 ± 61.4 pg / mL) wassignificantly higher than that in group 2 (108.4 ± 28.3 pg / mL) and group 4 (84.1 ± 31.5 pg / mL) <0.0001) but waslower than that in Group 3 (324 ± 93.7 pg / mL) (P = 0.002) .NOlevel in group 1 (27 ± 1.4 μmol / L) was significantly higher thanthat in group 2 (19.8 ± 2.8 μmol / L) and group 4 (16.9 ± 1.6 μmol / L) was lower than that in Group 3 (39 ± 3.6 μmol / L) for all three P <0.0001. A strong correlation was observed between ADM and NO levels (r = 0.827, P <0.0001). CONCLUSION: Adrenomedullin and NO levels were highin both non-cirrhotic and cirrhotic portal hypertension and closely correlated, Adrenomedullin and NO levels established with the severity of cirrhosis, and significantly higher than those in patients with NCPH. Portal hypertension plays an important role in the increaseof ADM and NO.Parenchymal damage in cirrhosis maycontribute to the increase in these parameters.