Endoscopic treatment of biliary complications in donors after living donor liver transplantation in a high volume transplant center.

BACKGROUND/AIMS: Although living donor liver transplantation (LDLT) has been accepted as a primary treatment for adults with end-stage liver disease, concerns about donor health have been emerged. As LDLT is technically complex, it creates perioperative morbidity and mortality risk in donors. Biliary complications such as stricture and leakage are seen most frequently in donors after liver transplantation. While some of these complications get treated with conservative approach, endoscopic, surgical, and percutaneous interventions may be required in some others. We aimed to present endoscopic retrograde cholangiography (ERC) results in donors who developed biliary complications after LDLT. MATERIALS AND METHODS: Between June 2010 and January 2018, a total of 1521 donors (1291 right lobe grafts, 230 left lobe grafts) of patients who underwent LDLT, were retrospectively reviewed. 63 donors who underwent ERC due to biliary complication, were included in the study. RESULTS: Biliary stricture was found in 1.6% (25/1521), biliary leakage in 2.1% (33/1521), and stricture and leakage together in 0.3% (5/1521) donors. Our endoscopic success rates in patients with biliary leakage, biliary stricture, and stricture and leakage were 85% (28/33), 92% (23/25), and 80% (4/5), respectively. Surgical treatment was performed on 12.6% (8/63) donors who failed ERC. CONCLUSION: We found that ERC is a successful treatment for post-LDLT donors who have biliary complications.

A mitochondrial neurogastrointestinal encephalomyopathy with intestinal pseudo-obstruction resulted from a novel splice site mutation.

Mitochondrial neurogastrointestinal encephalopathy (MNGIE) is an autosomal recessive disorder characterized by gastrointestinal dysmotility, cachexia, ptosis, peripheral neuropathy and leukoencephalopathy. The diagnosis is often not made until 5-10 years after the onset of symptoms. MNGIE is caused by mutations in thymidine phosphorylase gene TYMP. Here, we present a 19-year-old boy with MNGIE who had a chronic intestinal pseudo-obstruction, and we describe his family history. Genetic analysis revealed a novel homozygous c.765+1G>C intronic mutation which is expected to disrupt splicing of TYMP in the patient. Family screening revealed that the brother was also affected and the mother was a carrier. MNGIE should be considered and genetic testing instigated if individuals with cachexia have neuromuscular complaints or symptoms of chronic intestinal pseudo-obstruction.

Predictive Value of Mean Platelet Volume in Variceal Bleeding due to Cirrhotic Portal Hypertension.

AIM: To investigate whether mean platelet volume (MPV) is a predictor of variceal bleeding in patients with cirrhotic portal hypertension. MATERIALS AND METHODS: This prospective cohort was performed in the internal medicine department of our tertiary care center. Cirrhotic patients were allocated into two groups: Group I consisted of 31 cases without a history of variceal bleeding, whereas group II was made up of 31 patients with a history of variceal bleeding. Data derived from medical history, physical examination, ultrasonography, gastrointestinal system endoscopy, complete blood count, hepatic, and renal function tests were recorded and compared between two groups. On physical examination, encephalopathy and ascites were evaluated and graded with respect to Child-Pugh-Turcotte classification. RESULTS: There was no significant difference between the two groups in terms of age, duration of the disease, and gender of the patient. The only remarkable difference was that hemoglobin (p = 0.02) and hematocrit (p = 0.02) values were lower in group II. Neither the etiology of bleeding was different between groups nor did MPV seem to have a noteworthy impact on bleeding. Interestingly, risk of variceal bleeding increased in parallel to the higher grade of varices. CONCLUSION: Our results imply that there is a correlation between the grade of varices and esophageal vari-ceal bleeding in cirrhotic patients. However, association between MPV and variceal bleeding could not be demonstrated. Utilization of noninvasive tests as predictors in these patients necessitates further controlled trials on larger series.How to cite this article: Erdogan MA, Benli AR, Acmali SB, Koroglu M, Atayan Y, Danalioglu A, Kayhan B. Predictive Value of Mean Platelet Volume in Variceal Bleeding due to Cirrhotic Portal Hypertension. Euroasian J Hepato-Gastroenterol 2017;7(1):6-10.

Albendazole Induced Recurrent Acute Toxic Hepatitis: A Case Report.

INTRODUCTION: Drug induced acute toxic hepatitis can be idiosyncratic. Albendazole, a widely used broad spectrum antiparasitic drug is generally accepted as a safe drug. It may cause asymptomatic transient liver enzyme abnormalities but acute toxic hepatitis is very rare. Case Report : Herein, we present the case of 47 year old woman with recurrent acute toxic hepatitis after a single intake of albendazole in 2010 and 2014. The patient was presented with symptoms and findings of anorexia, vomiting and jaundice. For diagnosis, other acute hepatitis etiologies were excluded. Roussel Uclaf Causality Assessment Method (RUCAM) score was calculated and found to be 10, which meant highly probable drug hepatotoxicity. Within 2 months, all pathological findings came to normal. RESULT: There are a few reported cases of albendazole induced toxic hepatitis, but at adults, there is no known recurrent acute toxic hepatitis due to albendazole at this certainty according to RUCAM score. CONCLUSION: Physicians should be aware of this rare and potentially fatal adverse effect of albendazole.

Effects of dexpanthenol on acetic acid-induced colitis in rats.

While the pathogenesis of acetic acid (AA)-induced colitis is unclear, reactive oxygen species are considered to have a significant effect. The aim of the present study was to elucidate the therapeutic potential of dexpanthenol (Dxp) on the amelioration of colitis in rats. Group I (n=8; control group) was intrarectally administered 1 ml saline solution (0.9%); group II [n=8; AA] was administered 4% AA into the colon via the rectum as a single dose for three consecutive days; group III (n=8; AA + Dxp) was administered AA at the same dosage as group II from day 4, and a single dose of Dxp was administered intraperitoneally; and group IV (n=8; Dxp) was administered Dxp similarly to Group III. Oxidative stress and colonic damage were assessed via biochemical and histologic examination methods. AA treatment led to an increase in oxidative parameters and a decrease in antioxidant systems. Histopathological examination showed that AA treatment caused tissue injury and increased caspase-3 activity in the distal colon and triggered apoptosis. Dxp treatment caused biochemical and histopathological improvements, indicating that Dxp may have an anti-oxidant effect in colitis; therefore, Dxp may be a potential therapeutic agent for the amelioration of IBD.

Incidence and clinical presentation of portal vein thrombosis in cirrhotic patients.

BACKGROUND: Portal vein thrombosis (PVT) is due to many risk factors, but its pathogenesis is still not clearly understood. To identify the risk factors for PVT, we analyzed the clinical characteristics and complications associated with PVT in cirrhotic patients. METHODS: We studied patients with liver cirrhosis who were admitted to our unit from April 2009 to December 2014. The patients were divided into the PVT and non-PVT groups, and were compared by variables including gender, age, the etiology of cirrhosis, stage of cirrhosis, complications, imaging, and treatment. RESULTS: PVT was found in 45 (9.8%) of 461 cirrhotic patients admitted to our hospital. Most patients (45.9%) had hepatitis B virus (HBV)-related cirrhosis, with a similar distribution of etiologies between the groups. However, there was no positive relationship between PVT and etiologies of cirrhosis. Most patients (71.5%) were in the stage of hepatic decompensation. No statistically significant differences were found in complications including esophageal varices, ascites, and hepatic encephalopathy between the groups. However, there was a significant positive correlation between hepatocellular carcinoma (HCC) and PVT (P<0.01). In 30 patients with PVT, thrombosis occurred in the portal vein and/or portal branches, 37.8% were diagnosed on ultrasound. CONCLUSIONS: The incidence of PVT was 9.8%, mainly in patients with HBV-related cirrhosis. The development of PVT was associated with the severity of liver disease and HCC.

Lighter Ingestion as an Uncommon Cause of Severe Vomiting in a Schizophrenia Patient.

Background. Foreign bodies in the gastrointestinal tract are important morbid and mortal clinical conditions. Particularly, emergency treatment is required for cutting and drilling bodies. The majority of ingested foreign bodies (80-90%) leave gastrointestinal tract without creating problems. In 10-20% of cases, intervention is absolutely required. Less than 1% of cases need surgery. In this paper, we present a schizophrenia patient who swallowed multiple lighters. Case. A 21-year-old male schizophrenic patient who uses psychotic drugs presented to the emergency department with the complaints of abdominal pain, severe vomiting, and inability to swallow for a week. His physical examination revealed epigastric tenderness. A plain radiograph of the abdomen revealed multiple tiny metallic densities. Gastroscopy was performed. The lighters were not allowing the passage, and some of them had penetrated the gastric mucosa, and bezoars were observed. One lighter was extracted with the help of the polypectomy snare. Other lighters as a bezoar were removed by surgery. Conclusion. Excessive vomiting of swallowed foreign bodies in the etiology of psychotic patients should be kept in mind. Endoscopic therapy can be performed in the early stages in these patients, but in the late stage surgery is inevitable.

Nucleotide-Binding Oligomerization Domain-Containing Protein 2 Variants in Patients with Spontaneous Bacterial Peritonitis.

BACKGROUND: The occurrence of spontaneous bacterial peritonitis (SBP) is significantly increased in carriers of nucleotide-binding oligomerization domain-containing protein 2 (NOD2) variants, suggesting that local immune alterations might be implicated in bacterial translocation (BT). AIMS: We aimed to assess the role of the NOD2 gene in conferring susceptibility to SBP. We also sought to determine whether levels of serum interleukin-6 (IL-6), lipopolysaccharide-binding protein, and soluble TNF-α receptor, along with the presence of bacterial DNA (bactDNA) in ascitic fluid, are appropriate markers for BT in patients with liver cirrhosis and SBP. METHODS: A cohort of 171 patients was divided into two groups: patients with SBP (n = 82) and those without SBP (n = 89). The presence of the most common NOD2 variants (p.R702W, p.G908R, and c.3020insC) was determined in these patients. RESULTS: We detected the p.G908R variant in four patients (4.9 %) of the SBP group. No significant difference was observed between the SBP and non-SBP groups for NOD2 risk variants. The frequency of bactDNA in ascitic fluid was higher for patients with NOD2 variants than for patients without variants (p = 0.021). Serum IL-6 levels in the SBP group were higher than those in the non-SBP group. CONCLUSIONS: The frequent detection of bactDNA in ascites of patients with the p.G908R variant suggests there is a strong association between NOD2 risk variants and BT in SBP patients. In addition, increased serum IL-6 levels and bactDNA in ascitic fluid could be considered surrogate markers for BT in patients with cirrhosis.

Beneficial effects of dexpanthenol on mesenteric ischemia and reperfusion injury in experimental rat model.

BACKGROUND AND AIM: It has been reported that intestinal ischemia-reperfusion (I/R) injury results from oxidative stress caused by increased reactive oxygen species. Dexpanthenol (Dxp) is an alcohol analogue with epitelization, anti-inflammatory, antioxidant, and increasing peristalsis activities. In the present study, the aim was to investigate protective and therapeutic effects of Dxp against intestinal I/R injury. MATERIALS AND METHODS: Overall, 40 rats were assigned into five groups including one control, one alone Dxp, and three I/R groups (40-min ischemia; followed by 2-h reperfusion). In two I/R groups, Dxp (500 mg/kg, i.m.) was given before or during ischemia. The histopathological findings including apoptotic changes, and also tissue and serum biochemical parameters levels, were determined. Oxidative stress and ileum damage were assessed by biochemical and histological examination. In the control (n = 8) and alone Dxp (n = 8; 500 mg/kg, i.m. of Dxp was given at least 30 min before recording), groups were incised via laparotomy, and electrical activity was recorded from their intestines. In this experiment, the effect of Dxp on the motility of the intestine was examined by analyzing electrical activity. RESULTS: In ileum, oxidant levels were found to be higher, while antioxidant levels were found to be lower in I/R groups when compared with controls. Dxp approximated high levels of oxidants than those in the control group, while it increased antioxidant values compared with I/R groups. Histopathological changes caused by intestinal I/R injury and histological improvements were observed in both groups given Dxp. In the Dxp group, electrical signal activity markedly increased compared with the control group. CONCLUSIONS: Here, it was seen that Dxp had protective and therapeutic effects on intestinal I/R injury and gastrointestinal system peristaltism.

Protective Effects of Apocynin on Cisplatin-induced Hepatotoxicity in Rats.

BACKGROUND AND AIMS: Despite it being a highly potent antineoplastic drug, cisplatin has important toxic adverse effects limiting its use such as nephrotoxicity, neurotoxicity and ototoxicity. It is thought that cisplatin-induced hepatotoxicity is caused by oxidative stress resulting from increased reactive oxygen species (ROS). Apocynin (APO) exerts its antioxidant effect by reducing ROS production via inhibition of NADPH oxidase. The present study intended to demonstrate effects of cisplatin on hepatic pro-oxidant/antioxidant systems and to investigate protective effects of APO against cisplatin-induced hepatotoxicity. METHODS: Rats were randomly assigned into four groups (n = 8 each): a) control group; b) single dose of cisplatin (5 mg/kg); c) APO group (20 mg/kg on three consecutive days; i.p.); and d) APO plus cisplatin group. Liver tissue was assessed in all groups by biochemical and histopathological means. Also, serum alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase levels were studied in all groups. RESULTS: When cisplatin group was compared to controls, it was seen that lipid peroxidation product, total oxidant status and ALT levels were markedly increased, whereas superoxide dismutase and glutathione peroxidase levels were overtly decreased. APO therapy markedly prevented cisplatin-induced harmful changes in liver. Our histopathological findings such as central vein dilatation, perivenuler and periportal sinusoidal dilatation, parenchymal inflammation, vacuolar changes in hepatocytes, biliary duct proliferation and caspase-3 positive hepatocytes were in accordance with the biochemical changes. CONCLUSION: In light of these results, it is our thought that APO has a protective role against cisplatin-induced hepatotoxicity at both biochemical and histopathological levels.

The relation between pathogenesis of liver cirrhosis, hepatic encephalopathy and serum cytokine levels: what is the role of tumor necrosis factor α?

BACKGROUND/AIMS: Hepatic encephalopathy (HE) is a major complication of acute or chronic liver disease characterized by neuropsychiatric symptoms. It's etiology and pathogenetical mechanisms are not clearly understood and probably it is multifactorial. In this study, we aimed to investigate the relation between pathogenesis of HE and TNF-alpha, IL-1beta, IL-2R, IL-6, IL-8 and IL-10, and between the severity of HE and the levels of these cytokines. METHODOLOGY: Eighty patients with liver cirrhosis [50 patients with clinical findings of HE (group 1) and 30 without any symptoms of HE (group 2)] and 30 healthy controls (group 3) were included into the study. Serum TNF-alpha, IL-1beta, IL-2R, IL-6, IL-8 and IL-10 levels of patients and control subjects were studied with the chemiluminescent method. RESULTS: There were statistically significant difference between serum TNF-alpha, IL-1beta, IL-2R, IL-6 and IL-8 levels of patients with liver cirrhosis and healthy subjects (p<0.05), and between patients with and without HE (p<0.05). There was a correlation between the severity of liver cirrhosis according to Child-Pugh classification and cytokine levels. The severity of HE (grade 1-4) was closely related with cytokine levels, especially TNF-a. On the other hand, there was no relation between cytokine levels and the etiological factors. CONCLUSION: We found a positive correlation between serum inflammatory cytokine levels (TNF-alpha, IL-1beta, IL-2R, IL-6, IL-8) and the severity of liver cirrhosis. In addition, our findings suggested that this relation is independent from etiological factors.