A 45-year-old man was admitted to our department, with the symptoms of gastric outlet obstruction. A gastric adenocancer metastatic to the liver had been diagnosed at an another institute 10 days previously. Endoscopy revealed pyloric obstruction due to advanced carcinoma of the gastric antrum. Abdominal computed tomography showed the gastric malignancy and liver metastases, and no lesions of the small or large bowel. An uncovered, 20 mm × 12 cm, self-expandable metallic stent (Ultraflex; Boston Scientific, Ireland) was deployed without any complication ([Fig. 1] a). The patient began to feed orally the next day, and we referred him to the medical oncology department for evaluation for chemotherapy.
Poststenotic aneurysm of the paraumbilical collateral vein: Doppler sonography findings.R M Killi, I Günhan, O Ozütemiz and N ElmasAudio Available | Share
The aim was to reveal the mechanism of hemolysis-induced acute pancreatitis and to evaluate the role of heme and heme oxygenase activity in inducing pancreatic inflammation in an experimental hemolysis model.Hemolytic anemia was induced in rats by intraperitoneal injection of 60 mg/kg acetylphenylhydrazine (APH). To evaluate the toxic effect of free heme after hemolysis, heme oxygenase inhibitor (HOI) was used to inhibit the enzyme which decreases the free heme concentration after hemolysis. One hundred and fifty rats were divided into two treatment and three control groups. Rats in the hemolysis group were given APH intraperitoneally. Rats in the HOI+hemolysis group were given Cr(III)mesoporphyrin IX chloride as HOI and then APH intraperitoneally. Serum amylase and lipase levels as well as pancreatic tissue cytokine content were determined and histological examination performed.No hemolysis or pancreatitis was seen in the control groups. Massive hemolysis was seen in 22 of the 30 rats of the hemolysis group and 20 of the 30 rats of the HOI+hemolysis group. The total pancreatitis rates were 60% and 76.6% in the hemolysis and HOI+hemolysis groups, respectively (p<0.05). Pancreatic cytokine levels were significantly higher in the HOI+hemolysis and hemolysis groups than in all control groups. The highest ICAM-1 and MCP-1 levels were in the HOI+hemolysis group. Histological signs of acute pancreatitis were also more severe in this group.Acute massive hemolysis can induce acute pancreatitis. Excess of free vascular heme seems to be an inducer of inflammation by modulating ICAM-1 and MCP-1.
NOD2/CARD15 gene variants may be associated with distinct phenotypic expressions of Crohn’s disease, however, this association may change according to the ethnic and regional variation. The aim of this study was to analyze the impact of NOD2/CARD15 gene mutations on disease phenotype in Turkish Crohn’s disease patients. Fourty-five Crohn’s disease patients (32 males, 13 females) with a mean age of 38,7 ± 12,1 (range: 19-78) were enrolled into this prospective study. The three major polymorphisms (R702W, G908R, 3020insC) on NOD2/CARD15 gene were studied from the peripheral blood genomic DNA. R702W and G908R mutations were studied by PCR-RFLP method, and 3020insC mutation was studied by DNA sequencing. No homozygous mutation was detected. Heterozygous R702W, G908R, and 3020insC mutations were detected in 4, 3, and 4 patients, respectively. The frequency of R702W, G908R, and 3020insC mutations was found to be 4.4, 3.3, and 4.4%, respectively. The overall mutation frequency was found to be 12.2%. There was no statistically difference between the clinical course of the patients with (n = 11) and without (n = 34) mutations (p>0.05). NOD2/CARD15 gene polymorphisms do not have impact on disease phenotype in Turkish Crohn’s disease patients.
Key words: NOD2/CARD15 gene, Crohn’s disease, phenotype.
The literature indicates that acute pancreatitis is a complication of massive hemolysis with a prevalence of about 20%. We describe an experimental model of hemolysis-induced acute pancreatitis. Hemolytic anemia was induced in rats by a single ip injection of 60 mg/kg of 20 mg/ml acetylphenylhydrazine (APH) in 20% (v/v) ethanol on the first experimental day (day 0). One hundred and fifty Wistar albino rats weighing 180-200 g were divided into three groups of 50 animals each: groups 1, 2 and 3 were injected ip with APH, 20% ethanol, and physiological saline, respectively. Ten rats from each group were sacrificed on study days 1, 2, 3, 4 and 5. Serum amylase, lipase levels and pancreatic tissue tumor necrosis factor-alpha (TNF-alpha) and platelet-activating factor (PAF) contents were determined and a histological examination of the pancreas was performed. No hemolysis or pancreatitis was observed in any of the rats in groups 2 and 3. In group 1, massive hemolysis was observed in 35 (70%) of 50 rats, moderate hemolysis in seven (14%), and no hemolysis in eight (16%). Thirty-three of 35 (94.2%) rats with massive hemolysis had hyperamylasemia, and 29 of these rats (82.8%) had histologically proven pancreatitis. The most severe pancreatitis occurred on day 3, as demonstrated by histology. Tissue TNF-alpha and PAF levels were statistically higher in group 1 than in groups 2 and 3. Acute massive hemolysis induced acute pancreatitis, as indicated by histology, in almost 80% of cases. Hemolysis may induce acute pancreatitis by triggering the release of proinflammatory and immunoregulatory cytokines.
Abstract Introduction Bronchobiliary fistula is an uncommon complication secondary to hepatobiliary surgery. Bilioptysis is a pathognomic finding for bronchobiliary fistulas. Diagnosis may be easily established in the light of clinical history, which can be aided by imaging studies to pinpoint the exact location. Some diagnostic procedures such as endoscopic retrograde cholangiopancreatectomy are also useful for treatment. Case presentation We present three Turkish patients with bronchobiliary fistula secondary to previous hepatic surgery due to hydatid cyst in two, a 19-year-old and a 47-year-old man, and iatrogenic trauma of the common bile duct by endoscopy in a 35-year-old man. All of the patients were successfully treated by minimally invasive methods including percutaneous drainage and endoscopic retrograde cholangiopancreatography. Conclusion We suggest that bronchobiliary fistula could be managed through conservative treatment methods which do not require in-hospital follow-up, particularly in uncomplicated cases. Otherwise, surgical management can be unavoidable.
