Relationship between nucleotide-binding oligomerization domain-containing protein 2 variants and severity of acute pancreatitis.

BACKGROUND AND AIM: Intestinal barrier dysfunction has been implicated in the development of infectious complications of acute pancreatitis. Nucleotide-Binding Oligomerization DomainContaining Protein 2 (NOD2) plays an important role in the proper functioning of intestinal defense mechanisms. Here, we investigated the frequency of NOD2 variants in patients with mild and severe acute pancreatitis. MATERIALS AND METHODS: Groups 1, 2 and 3 comprised healthy participants and patients with mild and severe pancreatitis, respectively. Four NOD2 variants and serum interleukin-6 (IL-6), Tumor Necrosis Factor-a (TNF-a) and lipopolysaccharide-binding protein (LBP) levels were analyzed. RESULTS: Three patients (3/32, 9.4%) in the severe pancreatitis group were positive for the p.R702W variant. This variant was negative in other groups. One, three and three patients in the healthy (1/27, 3.7%), mild (3/36, 8.3%) and severe pancreatitis (3/32, 9.4%) groups tested positive for the 1007fs variant, respectively. No significant differences in the frequencies of NOD2 variants were evident among the groups. Serum IL-6, TNF-a and LBP levels were markedly higher in the severe pancreatitis than the healthy and mild pancreatitis groups (all p<0.001). We observed no significant correlation between cytokine levels and NOD2 variants. CONCLUSION: Our results support an association between the presence of the p.R702W variant and severe pancreatitis.

Ecstasy induced acute hepatic failure. Case reports.

3,4-methylenedioxymethamphetamine (MDMA), an amphetamine derivative known as ecstasy, has stimulating and hallucinogenic properties. It has become a substance that is widely used especially by young people. Hepatotoxicity is one of the rare side effects of this substance and can be fatal. Ecstasy-induced fulminant hepatitis has been reported in case reports. The clinical course and the prognosis of the cases may differ. In this article, two cases in whom ecstasy-induced fulminant hepatic failure had developed and who were treated with liver transplantation, and one case which recovered with treatment, have been presented.

The effects of Teucrium polium on ionizing radiation-induced intestinal damage in rats.

BACKGROUND AND STUDY AIMS: Oxidative stress plays an important role in development of intestinal injury after abdomino-pelvic radiation therapy. Teucrium polium (TP) is a medicinal plant which has antioxidant and anti-inflammatory properties. The aim of this study was to investigate the effect of TP on radiation-induced intestinal oxidative damage in rats. MATERIALS AND METHODS: Group 1 (n = 8), the control group; Group 2 (n = 8), the RAD (radiation) group in which each rat received a single whole-body 800 cGy radiation performed with a LINAC ; Group 3 (n = 8), the RAD + TP group in which rats were exposed to radiation as in Group 2, followed by intragastric administration of 0.5 g/kg/daily TP extract for 7 consecutive days; and Group 4 (n = 8), the TP group, rats received only intragastric TP for 7 days. RESULTS: Radiation led to intestinal damage, which was accompanied by an increase in intestinal thiobarbituric-acid-reactive substances (TBARS) and myeloperoxidase (MPO) levels, and a decrease in reduced glutathione (GSH) levels. Although TP significantly decreased intestinal MPO levels and inflammation scores, it neither reverted intestinal TBARS and GSH levels nor ameliorated other histological parameters of the disease. CONCLUSIONS: Our results suggest that TP reduces inflammation but does not ameliorate the increased oxidative stress conditions in radiation-induced intestinal damage in rats.

The effects of Gingko biloba, vitamin E and melatonin on bacterial translocation in thioacetamide-induced fulminant hepatic failure in rats.

BACKGROUND AND STUDY AIMS: Bacterial translocation (BT) has been implicated in the development of infectious complications in many serious clinical conditions such as fulminant hepatic failure (FHF). We aimed to investigate the effects of Gingko biloba (GB), vitamin E (Vit E) and melatonin on intestinal oxidative damage and BT in thioacetamide (TAA)-induced FHF in rats. MATERIALS AND METHODS: A total of 42 rats were divided into five groups. Group 1 (n = 8) was the control group. Group 2 (n = 10) was the TAA group, in which rats received 350 mg/kg TAA daily by the intraperitoneal (ip) route for 3 days. Oral 100 mg/kg GB per day was administered to group 3 (n = 8), oral 200 mg/kg Vit E per day to group 4 (n = 8) and ip 3 mg/kg melatonin per day to group 5 (n = 8) 48 h prior to the first TAA injection and was continued for 5 consecutive days. RESULTS: When compared with the control group, serious hepatic and intestinal oxidative damage, increased Escherichia coli counts in ileal aspirates and high BT frequencies were observed in the TAA group (all p < 0.0001). Only GB treatment attenuated hepatic oxidative damage (p < 0.0001). There was no difference in intestinal oxidative damage, E. coli counts in ileal aspirates and BT frequency between TAA and the other antioxidant treatment groups (p > 0.05). CONCLUSION: Our results suggest that intestinal oxidative damage plays a major role in the development of BT by disrupting the barrier function of intestinal mucosa.

Protective effects of Gingko biloba on thioacetamide-induced fulminant hepatic failure in rats.

Gingko biloba (GB) has antioxidant and platelet-activating factor (PAF) antagonistic effects. We investigated the protective effects of GB on thioacetamide (TAA)-induced fulminant hepatic failure in rats. Fulminant hepatic failure was induced in treatment groups by three intraperitoneal (ip) injections of TAA (350 mg/kg) at 24-hour intervals. Treatments with GB (100 mg/kg per day, orally) and N-acetylcysteine (20 mg/kg twice daily, sc) were initiated 48 hours prior to TAA administration. The liver was removed for histopathological examinations. Serum and liver thiobarbituric acid-reactive substance (TBARS) levels were measured for assessment of oxidative stress. Liver necrosis and inflammation scores and serum and liver TBARS levels were significantly higher in the TAA group compared to the control group (P < 0.001, < 0.001, 0.001, < 0.001, respectively). Liver necrosis and inflammation scores and liver TBARS levels were significantly lower in the GB group compared to the TAA group (P < 0.001, < 0.001 and 0.01, respectively). GB ameliorated hepatic damage in TAA-induced fulminant hepatic failure. This may be due to the free radical-scavenging effects of GB.