George Margantinis

Can somatostatin prevent post‐ERCP pancreatitis? Results of a randomized controlled trial

Background:  Acute pancreatitis is the most common complication of endoscopic retrogade cholangiopancreatography (ERCP), occurring in 1–10% of patients. Several substances have been used, with negative results, in an attempt to prevent this complication.

Esomeprazole versus omeprazole for the eradication of Helicobacter pylori infection: Results of a randomized controlled study

Background: Esomeprazole has higher oral bioavailability and increased antimicrobial activity against Helicobacter pylori than omeprazole. Goals: To compare 7 days esomeprazole with 7 days of omeprazole based triple therapies for the eradication of H. pylori, and to assess whether the administration of higher dose of esomeprazole leads to improved eradication rates. Study: One hundred and fifty-six dyspeptic patients with H. pylori received either: (1) 1-week treatment including esomeprazole 40 mg once daily, amoxicillin 1 g, and clarithromycin 500 mg, both twice daily (EAC1 group, n = 52); (2) 1-week treatment of omeprazole 20 mg, amoxicillin 1 g, and clarithromycin 500 mg, all administered twice daily (OAC group, n = 52); or (3) 1-week treatment with esomeprazole 40 mg, amoxicillin 1 g, and clarithromycin 500 mg, all given twice daily (EAC2 group, n = 52). Results: H. pylori was eradicated in 37 of 52 patients in the OAC group (Intension to treat [ITT] 71%), and in 42 patients in the EAC1 group (ITT 81%). High eradication rate was achieved by the EAC2 regimen (ITT; 96%), but more patients reported unwanted effects. Conclusion: Seven days of esomeprazole based triple therapy is a satisfactory eradication regimen for H. pylori infection. Higher doses of esomeprazole have excellent eradication rates, but they may lead to increased side effects.

Omeprazole plus azithromycin and either amoxicillin or tinidazole for eradication of Helicobacter pylori infection

Goals To establish whether omeprazole plus azithromycin in association with either amoxicillin or tinidazole is effective in curing Helicobacter pylori infection in dyspeptic patients. Background Many antibiotics in combination with antisecretory drugs have been used in an attempt to find the optimal regimen for eradication of H. pylori. Azithromycin is a macrolide that achieves high concentrations in gastric tissue after a single 500-mg oral dose. Study A total of 160 consecutive symptomatic patients with H. pylori received omeprazole 20 mg twice daily for 1 week, azithromycin 500 mg/d for 3 days, and were randomly assigned to either amoxicillin 1 g twice daily (OAzAm group, n = 80) for 1 week or tinidazole 500 mg twice daily for 3 days (OAzT group, n = 80). H. pylori status was assessed by rapid urease test and histology at entry and by histology and 13C-urea breath test after the end of the therapy. Results H. pylori was eradicated in 62.5% of patients in the OAzAm group (intention to treat [ITT] 62.5%) and in 71.2% of patients in the OAzT group (ITT 71.2%). Conclusions Although the compliance was excellent and the side effects negligible, the regimens used were partially effective for the eradication of H. pylori.

Budd-Chiari syndrome and portal vein thrombosis due to right atrial myxoma

Budd-Chiari syndrome is a rare disorder characterized by hepatic venous outflow obstruction. Atrial myxomas account for 35% to 50% of primary cardiac tumors and are usually located in the left atrium. We describe a patient who presented with hepatic inferior vena cava and portal vein thrombosis due to a large myxoma of the right atrium. After the successful removal of the tumor, ascites resolved completely. We conclude that right atrial myxoma is a rare but potentially curable cause of Budd-Chiari syndrome.

Early (mucosal) gastric cancer with synchronous osteosclerotic bone metastases: a case report.

Early gastric cancer (EGC) is defined as an adenocarcinoma confined to the gastric mucosa or submucosa, regardless of the presence of lymph node metastases. Early gastric cancer carries an excellent prognosis, with a 5-year survival rate at least 85% in most series. However, there are rare cases where distant metastases exist. Bone metastases are rare in gastric cancer; osteoblastic bone metastases are even rarer. We report a patient with EGC (mucosal) and synchronous osteosclerotic bone metastasis. To our knowledge, this is the first reported case of submucosal EGC with synchronous bone metastases. The patient was operated and he received adjuvant chemotherapy and radiotherapy. He died 18 months after gastric surgery from generalized disease.

Fulminant pancreatitis associated with ramipril therapy.

To the Editor: The use of ACE-inhibitors for the treatment of heart failure and arterial hypertension is increasing. ACE-inhibitors are rare causes of acute pancreatitis. The offending agents have, so far, included captopril, enalapril, lisinopril, quinapril, and benzanepril. We report a case of a patient who developed acute pancreatitis with a fatal outcome, while receiving ramipril. A 75-year-old man presented at the emergency room with complaints of epigastric pain radiating to the back for 2 days. The pain was accompanied with nausea and vomiting. There was no history of alcohol ingestion or previous abdominal surgery. Medication used regularly prior to admission was only ramipril 2.5 mg bid for arterial hypertension. The patient admitted that he had been using ramipril since 1 month, and that from the 1st days of the therapy, he noticed a mild abdominal pain radiating to the back for a few hours after receiving the drug. The last 7 days the pain was getting worse and he consulted his physician who prescribed an oral proton pump inhibitor and did not correlate the symptoms with the drug used. Vital signs on admission were temperature 37.3°C orally, pulse 102 beats/min, respirations 22/min and blood pressure 180/105 mm Hg. The abdomen was mildly distended with hypoactive bowel sounds and diffuse tenderness which was maximal in the epigastrium. Laboratory data on admission included: hematocrit 60.7%; WBC 21,700/mm; platelets 233,000/mm; amylase 1615 U/L; creatinine 2.1 mg/dL; blood sugar 478 mg/dL; calcium 8.3 mg/dL; LDH 605 IU/L; albumin 3.4 g/dL; ALT 30 U/L; AST 33 U/L, bilirubin 0.8 mg/dL, and triglycerides 151 mg/dL. Arterial blood gases on room air revealed a pH 7.46, pCO2 38.9 mm Hg, pO2 63.7 mm Hg and bicarbonate 28.2 mmol/lt. The patient was admitted to the intensive care unit of our hospital where restoration of intravascular volume, nasogastric decompression, and intravenous antibiotic treatment was instituted. Laboratory data 48 hours after admission included: Ht 33.4%, WBC 34,000/mm, platelets 155,000/mm, amylase 1282 U/L, blood glucose 198 mg./dl, creatinine 2.6 mg/dL, and LDH 1768 U/L. During this period, abdominal ultrasound examination showed a diffusely edematous pancreas while the biliary tree was not dilated and no gallstones were seen. Computerized tomography of the abdomen demonstrated changes consistent with acute necrotizing pancreatitis. One day after his admission the patient underwent endotracheal intubation due to progressive hypoxemia and ventilatory support was instituted. Additionally, continuous intravenous infusion of vasoconstrictors was required to maintain adequate blood pressure and a marginal urine output. Despite our support adult respiratory distress syndrome and renal failure developed. The patient became hemodynamically unstable and died 6 days after admission to the hospital. No autopsy was performed. Time intervals between the start of ACE-inhibitor treatment and the onset of acute pancreatitis varies and ranges between 1 day and 2 years, but generally it occurs early in the course of therapy. The severity of acute pancreatitis is usually mild, but fulminant pancreatitis due to lisinopril has been described. There is little information about the mechanism by which ACE-inhibitors cause acute pancreatitis. Some investigators suggest that ACE-inhibitors lead to elevated bradykinin levels in the pancreatic tissue. Bradykinin has been demonstrated to be involved in the increase of vascular permeability and local vasodilatation in the early stage of pancreatitis induced by the cholecystokinin agonist cerulein. Experimental studies in mammals have confirmed the role of bradykinin in the aggravation of pancreatitis and the protective role of bradykinin antagonists. Therefore, increased vascular permeability leading to localized angioedema and induction of pancreatic duct obstruction is a possible explanation for ACE-inhibitors induced pancreatitis. Additionally, because ACEinhibitors can cause hypoglycemia, these drugs may have a toxic effect on pancreatic cells. Our patient started experiencing epigastric pain after taking the drug, from the first days of his therapy. His physician did not correlate his symptoms with the medication used. Ramipril had not, so far, been associated with acute pancreatitis. Since all other possible causes of acute pancreatitis were excluded, our case report strengthens the association between ACE-inhibitors and pancreatitis. Despite the low incidence of druginduced pancreatitis, all patients with acute pancreatitis of unknown etiology should be carefully questioned on drugs possibly responsible for the induction of the disease. As the use of ACEinhibitors is increasing, physicians should consider the diagnosis of acute pancreatitis in patients who develop abdominal pain that is not explained by another process, while taking these medications. If pancreatitis is suspected, the drug should be stopped and replaced to reduce the possibility of further episodes of pancreatitis.

Postinfantile giant-cell hepatitis associated with ulcerative colitis and autoimmune hepatitis.

Postinfantile giant cell hepatitis (PGCH) is rare. It is characterized by the presence of multinucleated giant cells in liver biopsy, and although it has been associated with several etiological agents, in many cases its etiology remains unclear. The case is presented herein of an adult woman with PGCH in the setting of ulcerative colitis and autoimmune hepatitis. The presence of autoimmune hepatitis in the patient is consistent and supports the autoimmune pathogenesis of PGCH in a subgroup of patients. Furthermore, this finding, along with others, suggests that PGCH may be included in the list of hepatic complications of inflammatory bowel disease.

Cholecystocolic fistula demonstrated by endoscopic retrograde cholangiopancreatography

Cholecystocolic fistulas comprise between 10% and 20% of all biliary intestinal fistulas. In the majority of cases they are a sequel of cholecystitis but are reported to complicate only 0.13% of cases.1 A 72 year old man was admitted in our hospital for evaluation of unexplained pneumobilia demonstrated on a routine ultrasound examination of the abdomen. The patient admitted that in previous years he had recurrent episodes of biliary-type …