M. Demoro

Silent colon carcinoma presenting as a hepatic abscess

Penetration and abscess formation in an adjacent parenchymal organ as presentation of a colon cancer is very uncommon. We report a rare case of pyogenic liver abscess as the first manifestation of an infiltrative and penetrating hepatic flexure colon carcinoma without liver metastases. A 50-year-old woman was admitted with right abdominal pain, fever and chills. The initial diagnosis was a pyogenic liver abscess. Subsequent CT scan and colonoscopy evidenced a hepatic flexure colon cancer abscessed within segment 6 of the liver. Eight months after a right colectomy and liver resection there was no evidence of disease. The occurrence of a pyogenic liver abscess should raise the suspicion of a silent colon cancer.

Gastric Cancer Precursor Lesions and Helicobacter pylori Infection in Patients with Partial Gastrectomy for Peptic Ulcer

The mucosa of the gastric stump is considered at greater risk of dysplastic and neoplastic changes than that of the intact stomach. The combination of enteric reflux and Helicobacter pylori infection may have a synergistic damaging effect on the mucosa of the gastric remnant, both producing and increasing mucosal proliferation. The aim of this study was to assess whether the occurrence of H. pylori infection in the remnant mucosa of partially gastrectomized subjects for peptic ulcer disease is associated with an increase of the mucosal precursor lesions of malignancy. A series of 151 subjects who underwent partial gastrectomy for peptic ulcer disease were submitted to upper digestive endoscopy for long-term surveillance. Biopsy specimens of the gastric stump were tested for the occurrence of H. pylori infection and for the presence of precancerous mucosal lesions. The prevalence of H. pylori colonization in the remnant stomach was less than 30% and similar in subjects with different time intervals between gastrectomy and endoscopy. Age at surgery (χ2: p = 0.03) and H. pylori infection (χ2: p = 0.002) were significantly associated with the grading of mucosal lesions. The prevalence of normal mucosa was 10 times higher in H. pylori-negative patients as in H. pylori-positive ones (22.0% vs. 2.4%), and the prevalence of intestinal metaplasia was four times higher in H. pylori-positive patients than in H. pylori-negative ones (19.6% vs. 4.6%). We concluded that H. pylori infection may play a causal role in the development of gastric lesions in the operated stomach.

Screening of Helicobacter pylori infection after gastrectomy for cancer or peptic ulcer: Results of a cohort study

BACKGROUND Gastric cancer commonly follows a long-standing inflammation, mainly due to Helicobacter pylori (HP) infection. After resection, the stump develops precancerous alterations. DESIGN Prospective study of patients undergoing endoscopy from April 1, 2000, through March 31, 2006. SETTING University departments of Surgery and Experimental Medicine and Pathology. PATIENTS One hundred eighty-seven patients receiving upper gastrointestinal tract endoscopy many years after surgery for duodenal ulcer or gastric cancer. Ten to 12 postoperative endoscopic biopsy samples were taken from the remnant stomach. MAIN OUTCOME MEASURE The risk of gastric cancer precursor lesions associated with HP infection. RESULTS The gastric cancer precursor lesions were more common in the entire HP-positive population (odds ratio [OR], 2.37; 95% confidence interval [CI], 1.25-4.49; P = .007). However, HP-positive patients undergoing resection for cancer had a higher risk of the precursor lesions compared with HP-negative patients in the same diagnostic group (OR, 4.20; 95% CI, 1.10-15.96) and all patients undergoing resection for duodenal ulcer (OR, 1.59; 95% CI, 0.44-5.73). CONCLUSION The results of this investigation support the role of HP in gastric carcinogenesis and suggest that the HP eradication therapy might prevent the development of metachronous gastric cancer after gastric resection.

Bilateral ovarian mucinous cystadenoma in an adolescent presenting as abdominal compartment syndrome

an invasive adenocarcinoma originating in a tubulovillous adenoma. A subsequently performed sigmoidectomy revealed no residual tumour. In the pathology report, there was a description of an extensive black area in the mucosa and the serosa of the colon. The black colour was caused by the used Indian ink. Retrospectively, it is clear that the black lesions were spots of Indian ink derived from the intial marking of the resected adenoma. The pigmentation was probably not due to spilling but rather to migrating macrophages who absorbed the Indian ink and died on their journey. This case illustrates that ‘‘tissue is still the issue’’. In doubtful cases it is mandatory to take a biopsy.