Endoscopic treatment of biliary complications after duct-to-duct biliary anastomosis in pediatric liver transplantation.

BACKGROUND: Studies reporting outcomes of endoscopic treatment methods in children who underwent liver transplantation (LT) is very limited. We present our outcomes, as a high-volume transplant center where endoscopic methods are preferred as the first choice in the treatment of biliary complications in children. METHODS: Patients who underwent endoscopic retrograde cholangiopancreatography (ERCP) as the first treatment approach for biliary complications after LT between 2005 and 2017 were included. Clinical data included patient demographics, ERCP indications (stricture or leak), and treatment outcomes, including the need for percutaneous and surgical intervention. RESULTS: ERCP was performed in 49 patients who had a duct-to-duct anastomosis (38 living donor liver transplantation (LDLT), 11 deceased donor liver transplantation (DDLT)). The most common biliary complication was stricture. Our endoscopic success rate was 66.7% (18/27) and 75% (6/8) in LDLT and DDLT patients with stricture (p > 0.05), respectively. While our endoscopic success rate was 75% (3/4) in patients with leak alone after LDLT, it was 25% (1/4) in patients with leak and stricture in this group. The endoscopic success rate was 50% in two patients who had leak alone after DDLT. CONCLUSIONS: ERCP should be considered as a preferential treatment option for the management of biliary complications in pediatric liver transplant patients with duct-to-duct anastomosis, as in adults.

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.

Endoscopic treatment of biliary complications after living donor liver transplantation in a high volume transplant center in Turkey; a single-center experience.

BACKGROUND AND AIM: Biliary complications are an important cause of mortality and morbidity after living donor liver transplantation (LDLT). We present our endoscopic treatment results after LDLT as a single center with high volume. METHODS: Patients who underwent endoscopic retrograde cholangiopancreatography (ERCP) after LDLT between 2005 and 2015 were included. Clinical data included patient demographics, ERCP indications (stricture or leak), and treatment outcomes, including need for percutaneous and surgical interventions. RESULTS: ERCP was performed in 446 (39.2%) patients with duct-to-duct anastomosis of 1136 LDLT patients. The most common biliary complication was stricture ± stone (70.6%, 315/446). Stricture and leak occurred in 60 (13.4%) patients. Only biliary leak was found in 40 (8.9%) patients. Our endoscopic treatment success rate in patients with biliary stricture after LDLT was 65.1%. Overall endoscopic success rates in our patients were 55.0% in patients with both leak and stricture, and only leak. In all, our percutaneous transhepatic biliary interventions (PTBI) and ERCP success rate was 90.6% in patients with biliary complications after LDLT. CONCLUSIONS: Endoscopic treatments are highly effective for biliary complications after LDLT. Effective use of percutaneous interventions in collaboration with endoscopic treatments significantly reduces the need for surgical treatment.

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.

Expression of claudin-4 and beta-catenin in gastric premalignant lesions.

BACKGROUND AND STUDY AIMS: Abnormal expression of claudin-4 and beta-catenin play a role in carcinogenesis. The purpose of the present study was to examine claudin-4 and beta-catenin expression in normal and precancerous gastric mucosa. PATIENTS AND METHODS: Endoscopic biopsy specimens [normal gastric mucosa (n = 22), intestinal metaplasia (n = 24), dysplasia (n = 18), Helicobacter pylori (H. pylori)-associated chronic gastritis (n = 32) and remnant gastric mucosa (n = 18)] obtained from different 114 patients were examined by immunohistochemistry. RESULTS: Claudin-4 expression was present in 94.4% of dysplasia, 87.5% of intestinal metaplasia, 62.5% H. pylori-associated chronic gastritis, and 88.9% remnant gastric mucosa but only 18.2% of normal gastric mucosa biopsies. Decreased expression of beta-catenin was present in 27.8% of dysplasia, 8.3% of intestinal metaplasia, 15.6% of H. pylori-associated chronic gastritis, and 22.2% of remnant gastric mucosa biopsies, but was not present in normal gastric mucosa. When compared with normal gastric mucosa, there was a significant difference in claudin-4 expression in all groups (P < 0.05), but a significant difference was detected in dysplasia and remnant gastric mucosa for beta-catenin (P < 0.05). CONCLUSIONS: Our results suggest that claudin-4 expression is upregulated in premalignant gastric alterations.

The effect of gastric Helicobacter pylori eradication on recurrent aphthous stomatitis.

BACKGROUND: Helicobacter pylori (H. pylori) has been suggested to be associated with recurrent aphthous stomatitis (RAS) as well as many other diseases. METHODS: We conducted a prospective study on a total of 23 patients with RAS to investigate the relationship between H. pylori and RAS as well as the effect of eradication therapy on the recurrence. All patients underwent endoscopic examination and gastric biopsy. The biopsy materials were examined histopathologically whether they contained H. pylori or not. The density of H. pylori was also noted. The patients with H. pylori infection were followed up for up to 1 year after starting the eradication therapy. RESULTS: Gastric mucosal H. pylori colonization was + in 39%, ++ in 39%, +++ in 9%, and - in 13% of the patients, respectively. There were statistically significant decreases in the recurrence rate and amelioration time of RAS by eradication therapy. There were no significant correlations among the intensity of H. pylori with the recurrence rate, number, diameter, and amelioration time of the lesions in 1-year follow-up. CONCLUSIONS: We concluded that eradication of H. pylori may have reducing effects on the recurrence and amelioration period of the RAS.

Epicardial adipose tissue, hepatic steatosis and obesity.

OBJECTIVE: Hepatic steatosis is a common companion of obesity. Moreover, the measurement of epicardial adipose tissue (EAT) has been reported to be related with both obesity and insulin resistance. Therefore, we aimed to evaluate the relationship between hepatic steatosis, EAT and insulin resistance in obese patients. METHODS: Sixty-three obese subjects were enrolled in the study. Patients were divided into 3 groups according to body mass index (BMI) as follows: 20 patients with 30 < or = BMI < 35 kg/m2 (Group 1, mean age 39.3+/-12.9 yr), 25 patients with 35 < or = BMI < 40 kg/m2 (Group 2, mean age 41.7+/-9.3 yr), and 18 patients with BMI > or = 40 kg/m2 (Group 3, mean age 36.8+/-13.9 yr). EAT and grade of hepatic steatosis were assessed sonographically. Anthropometrical measurements were assessed with the foot-to-foot bioelectrical impedance analysis. Insulin resistance was assessed according to basal insulin, quantitative insulin sensitivity check index (QUICKI) and homeostasis model assessment (HOMA) equations. RESULTS: Although EAT was similarly higher in both groups 2 and 3, these groups were found to be similar in terms of the grade of hepatic steatosis. Both EAT and the grade of hepatic steatosis were correlated with whole body fat mass, abdominal adiposity, insulin resistance, and triglyceridemia but waist circumference was the only factor affecting EAT thickness. Highly sensitive C-reactive protein (hsCRP) was the only metabolic parameter that was significantly higher in Group 3 than in Group 1 (p=0.02). CONCLUSION: Hepatic steatosis should be assessed as a valuable predictor that reflects the increments of whole body fat mass as well as abdominal adiposity. However, in an attempt to demonstrate marginal differences between patients with similar obesity levels, epicardial adipose tissue appears to be a more sensitive marker compared to hepatic steatosis.

Pancreatic pseudocyst development due to organophosphate poisoning.

BACKGROUND/AIMS: Acute pancreatitis is a serious complication of organophosphate poisoning. There is no report in the literature dealing with the development of a pancreatic pseudocyst after complication of organophosphate-induced acute pancreatitis. Therefore, we present a case who developed pancreatic pseudocyst after complication of organophosphate-induced acute pancreatitis. METHODS: A 17-year-old female patient with a history of ingestion of complication of organophosphate insecticide (DDVP EC 550, dichlorvos) was admitted with cholinergic symptoms. On admission, serum amylase and lipase levels were high and abdominal ultrasonography showed an edematous pancreas. No etiological factor for acute pancreatitis was evident. RESULTS: We diagnosed complication of organophosphate-induced acute pancreatitis. After four weeks, abdominal abdominal ultrasonography and computerized tomography revealed a pancreatic pseudocyst of 6 cm diameter. During follow-up, the pancreatic pseudocyst size regressed to 4 cm. CONCLUSION: Complication of organophosphate poisoning can cause acute pancreatitis and its complications. Early diagnosis and appropriate treatment may reduce morbidity and mortality.

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.

Spontaneous bacterial peritonitis due to Brucella Melitensis in a cirrhotic patient.

Spontaneous bacterial peritonitis is a well-known entity, with a reported incidence of 15-20% in advanced cirrhotic patients. Escherichia coli and Klebsiella pneumoniae are the most common causes of spontaneous bacterial peritonitis; Brucella is extremely rare. We aimed to present one case of such a rare condition in a cirrhotic patient who also had hepatocellular carcinoma. Routine laboratory tests, abdominal ultrasonography and peritoneal fluid examinations were studied in a cirrhotic patient with ascites. Peritoneal fluid white blood cell count was 1300/mm3, with lymphocyte predominance (80%). Peritoneal fluid and blood culture both yielded Brucella melitensis. The patient also had a mass in the right lobe of the liver confirmed as hepatocellular carcinoma by biopsy. Brucella should be suspected as a cause of spontaneous bacterial peritonitis in cirrhotic patients with no response to standard spontaneous bacterial peritonitis treatments and with immunodeficiency such as hepatocellular carcinoma.

Serum and gastric fluid levels of cytokines and nitrates in gastric diseases infected with Helicobacter pylori.

This case control study presents data on the concentrations of nitrite and nitrate and a variety of pro-inflammatory cytokines such as interleukin-1 beta (IL-1 beta), interleukin-2R (IL-2R), interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor TNF-alpha in gastric fluid and serum. Patients with gastritis, gastric ulcer and gastric cancer are studied and grouped according to infection by Helicobacter pylori. The 208 patients who underwent upper gastrointestinal endoscopic examination were classified as follows; H. pylori-positive gastritis (n = 32), H. pylori-negative gastritis (n = 32), H. pylori-positive ulcers (n = 34), H. pylori-negative ulcers (n = 34), 43 patients with H. pylori-positive gastric cancer in addition to 33 H. pylori-negative healthy control individuals. Gastric fluids and blood samples were taken concomitantly. Cytokines and nitrite and nitrate determinations were attempted as soon as possible after collection of the samples. Nitrite and nitrate levels of serum and gastric fluids of H. pylori-positive gastritis and ulcers were higher than H. pylori-negative gastritis and ulcers. The concentrations of total nitrite and nitrate and cytokines (TNF-alpha, IL-2R, IL-6, and IL-8) in gastric fluids and sera of H. pylori-positive gastric cancer patients were higher than H. pylori-negative control groups. IL-1 beta level was significantly elevated in gastric fluid of infected cancer patients but not in serum. Taken together, the results suggest that an increase in cytokine-NO combination in gastric mucosa previously reported by many studies is not restricted to local infected gastric tissue but also detected in gastric fluid and sera of H. pylori-positive subjects and may have an important role in the pathogenesis and development of common gastric diseases.

Acute pancreatitis: an obscure complication of organophosphate intoxication.

Acute pancreatitis secondary to organophosphate intoxication is a rare and generally well-course condition, but it is important to be aware of this complication for appropriate clinical management. There are a few reports about this subject in the literature, but it is believed that there are more cases than are reported for this condition. Because symptoms of toxicity can mask this severe complication, we report two cases of acute pancreatitis due to organophosphate intoxication for alerting this condition.

Use of pleural fluid C-reactive protein in diagnosis of pleural effusions.

The aims of the study were to assess whether C-reactive protein (CRP) is a sensitive marker for discriminating between transudative and exudative and pleural effusions to evaluate whether it can be used to distinguish inflammatory pleural effusions from other types of effusion. Pleural fluid and serum CRP levels were obtained in 97 patients with pleural effusion, using an immunoturbidimetric method (Olympus AU-600 autoanalyser). We compared CRP levels between transudates and exudates, inflammatory effusions and other types of effusion. According to the criteria used, 16 patients were included in the transudate group and 81 patients in the exudate group. Pleural fluid CRP levels were significantly lower in the transudate group (P<0.04; 14.9 +/- 4.9 mg l(-1) and 35.5 +/- 4.9 mg l(-1) respectively). Also, the ratio of pleural fluid to serum was significantly lower in the transudate group (P<0.009; 0.8 +/- 0.5 mg l(-1) and 2.8 +/- 0.7 mg l(-1), respectively). In the exudate group, 35 patients had neoplastic effusions, 10 chronic non-specific pleurisy, 19 tuberculous pleurisy, 16 parapneumonic effusion and one Dressler Syndrome. When these sub-groups were compared, the parapneumonic effusion subgroup CRP levels (mean 89 +/- 16.3 mg l(-1)) were significantly higher than those in the other subgroups, other exudate of neoplastic effusion, tuberculous pleurisy and chronic non-specific effusion and the transudate group (P<0.0001; P<0.0001; P<0.0004 and P<0.0001, respectively). The ratio between pleural fluid and serum CRP was significantly higher in the parapneumonic effusion subgroup than in the neoplastic subgroup (P<0.0002; 6.6 +/- 2.7 mg l(-1) and 1 +/- 0.2 mg l(-1), respectively). Pleural fluid CRP levels > 30 mg l(-1) had a high sensitivity (93.7%) and specificity (76.5%) and a positive predictive value of 98.4%. In the differential diagnosis of pleural effusions, higher CRP levels may prove to be a rapid, practical and accurate method of differentiating parapneumonic effusions from other exudate types. Although the high level of CRP obtained in the exudate group may be due to the number of patients with parapneumonic effusion who were included, the pleural CRP level may also be helpful in discriminating between exudative and transudative pleural effusions.