Serum levels of soluble Fas, nitric oxide and cytokines in acute decompensated cirrhotic patients

AIM: To evaluate plasma levels of nitrite/nitrate (NOx), soluble Fas (sFas) antigen, tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) in patients with com- pensated and acute decompensated cirrhosis and to evaluate mediators causing acute decompensation in liver cirrhosis. METHODS: This prospective study was conducted in the medical intensive care unit of an academic tertiary center. Fifty-five patients with acute decompensation (gastrointestinal hemorrhage, encephalopathy, hydropic decompensation) and twenty-five patients with compen- sated liver cirrhosis were included. Blood samples were taken for analyses of sFas, Nox, IL-6, TNF-α. Liver en- zymes and kidney functions were also tested. RESULTS: In patients with acute decompensation, plas- ma sFas levels were higher than in non-decompensated patients (15 305 ±4646 vs 12 458 ±4322 pg/mL,, P < 0.05). This was also true for the subgroup of patients with alcoholic liver cirrhosis (P < 0.05). The other media- tors were not different and none of the parameters pre- dicted survival, except for ALT (alanine-aminotransfer- ase). In patients with portal-hypertension-induced acute hemorrhage, NOx levels were significantly lower than in patients with other forms of decompensation (70.8 ± 48.3 vs 112.9 ± 74.9 pg/mL, P < 0.05). When NOx lev- els were normalized to creatinine levels, the difference disappeared. IL-6, TNF-α and sFas were not different between bleeders and non-bleeders. In decompensated patients sFas, IL-6 and NOx levels correlated positively with creatinine levels, while IL-6 levels were dependent on Child class. CONCLUSION: In acute decompensated cirrhotic pa- tients sFas is increased, suggesting a role of apoptosis in this process and patients with acute bleeding have lower NOx levels. However, in this acute complex clinical situa-tion, kidney function seems to have a predominant influ- ence on mediator levels.

Risk factors for colonic diverticular bleeding:A Westernized community based hospital study

AIM:To evaluate the risk factors-other than nonsteroidal anti-inflammatory drugs-for colonic diverticular bleeding in a westernized population. METHODS:One hundred and forty patients,treated for symptomatic diverticular disease in a community based hospital,were included.Thirty(21%) had signs of diverticular bleeding.Age,gender,and the results of colonoscopy were collected and compared to a group of patients with nonbleeding symptomatic diverticulosis.Records were reviewed for comorbidities,such as obesity,alcohol consumption,smoking habits and metabolic diseases.Special emphasis was put on arterial hypertension,cardiovascular events,diabetes mellitus,hyperuricemia and hypercholesterinemia. RESULTS:There was no difference between patients with diverticular hemorrhage and those with nonbleeding symptomatic diverticulosis regarding gender ratio(male/female 9/21 vs 47/63) and diverticular localisation.Bleeding patients differed in respect to age(73.4±9.9 vs 67.8±13.0,P<0.013) . Significant differences were found between both groups regarding the presence of hyperuricemia and use of steroids and nonsteroidal anti-inflammatory drugs.Patients with three concomitant metabolic diseases were also identified as being at risk of bleeding.A forward stepwise logistic regression analysis revealed steroids,hyperuricemia and the use of calcium-channel blockers as independent risk factors of bleeding.CONCLUSION:Beside nonsteroidal anti-inflammatory steroid drug use,antihypertensive medication and concomitant arteriosclerotic diseases are risk factors for colonic diverticular hemorrhage.Our results support the hypothesis of an altered arteriosclerotic vessel as the source of bleeding.

Alcohol binging causes peliosis hepatis during azathioprine therapy in Crohn's disease

Patients with inflammatory bowel disease have normal life expectancy and, due to modern immunosuppressive therapies, also a normal quality of life. Since mostly young people are affected, their social behaviour suits this environment. Alcohol binging is an increasingly disturbing factor among young people. We describe a patient with Crohn's disease, treated with azathioprine, who developed peliosis hepatis after three epsiodes of alcohol binging. Liver toxicity was not observed previously during the course of the treatment. Azathioprine-induced peliosis hepatis is thought to be idiosyncratic in humans. From animal studies, however, it is clear that hepatic depletion of glutathione leads to azathioprine toxicity to the sinusoidal endothelial cells. Damage of these cells causes peliosis hepatis. Since alcohol binging leads to hepatic glutathione depletion, we conclude that in our patient the episodes of binging have reduced liver gluathione content and therefore this has increased azathioprine toxicity causing peliosis hepatis. The problem of alcohol binging has not yet been addressed in IBD patients undertaking immunosuppressive therapy. This should be reviewed in future considerations regarding patients advice.