Stump appendicitis: a rare but important entity.

A case of right lower quadrant pain in a 35-year-old male who underwent an appendicectomy 14 years previously is presented. Recurrent appendicitis with perforation was noted in an appendiceal stump on exploratory laparotomy. Although rare, inlammation of the appendiceal stump can occur and is still an important clinical entity. It is difficult to diagnose pre-operatively. A wide spectrum of causes in the differential diagnosis of right lower quadrant pain of the abdomen and a previous appendicectomy in a patient's history may delay the diagnosis. Knowledge of the condition should permit the physician to make an early diagnosis and, thus, limit the resultant morbidity.

A case of giant cell myocarditis and malignant thymoma: a postmortem diagnosis by needle biopsy.

This paper reports a case of fulminant giant cell myocarditis arising in association with a malignant thymoma causing death in a 46-year-old woman. Although the diagnosis was suspected in life, postmortem examination was required for confirmation of giant cell myocarditis. Consent was obtained only for percutaneous needle biopsy of the heart. In order to respect the family's wishes and harvest sufficient diagnostic myocardium, a simple needle-based biopsy technique was devised. A bone marrow trephine needle was attached to a 20 ml syringe and, with suction, multiple passes were used to fill 15 tissue cassettes. The cores were placed immediately in formalin and B5 fixatives. High-quality tissue preservation was obtained without crush artefact. Immunohistochemical studies of the biopsy tissue confirmed that the giant cells were of macrophage derivation.

Monozygotic twins with Crohn's disease and ulcerative colitis: a unique case report.

BACKGROUND: A large number of monozygotic and dizygotic twin pairs with inflammatory bowel disease have been reported. To date no twin pair has developed phenotypically discordant inflammatory bowel disease. This case report is the first documented occurrence of discordant inflammatory bowel disease occurring in monozygotic twins. CASE REPORT: Twenty two year old identical male twins presented within three months of each other with inflammatory bowel disease that proved to be discordant in overall disease type, disease distribution, clinical course, and histopathological findings. Twin 1 developed a severe pancolitis necessitating total colectomy while twin 2 developed a predominantly distal patchy colitis with frequent granulomas, controlled by aminosalicylates. Twin 1 was antineutrophil cytoplasmic antibody (ANCA) negative at the time of testing while twin 2 (Crohn's disease) was ANCA positive. Significantly, the twins possessed the HLA type DR3-DR52-DQ2 previously associated with extensive colitis. CONCLUSION: This case report confirms the important role played by genetic factors in the development of inflammatory bowel disease. It also highlights the crucial role of undetermined environmental agents in dictating disease expression and phenotype.

Gastric epithelial cell kinetics in the progression from normal mucosa to gastric carcinoma.

Increased epithelial cell proliferation is associated with an increased risk of adenocarcinoma and is associated with Helicobacter pylori infection. The aim of this study was to assess both gastric epithelial cell proliferation and the influence of H pylori infection on cell kinetics in the progression from normal mucosa to gastric carcinoma. One hundred and forty four subjects were assigned to study groups based on diagnosis and H pylori status: microscopically normal mucosa and H pylori negative (n = 28); chronic active gastritis and H pylori positive (n = 83); atrophic gastritis (n = 9); intestinal metaplasia (n = 19); gastric carcinoma (n = 12). Gastric antral epithelial cell proliferation was assessed using the in vitro bromodeoxyuridine immunohistochemical technique and expressed as the labelling index per cent (LI%). Subjects with chronic atrophic gastritis, intestinal metaplasia or gastric cancer have increased gastric epithelial cell proliferation compared with normal mucosa (LI% mean (SEM): 5.14 (0.6), 4.68 (0.3), 6.50 (0.5) v 3.08 (0.2), p < 0.001). This increase in gastric epithelial cell proliferation was not influenced by H pylori status. Gastritis associated with H pylori had an increased LI% compared with normal controls or subjects with H pylori negative gastritis (4.98 (0.2) v 3.08 (0.2), 3.83 (0.2), p < 0.01). H pylori infection although associated with an increased epithelial cell proliferation in subjects with chronic gastritis, does not influence the increased epithelial cell proliferation seen in subjects with precancerous lesions or gastric carcinoma. This is further evidence that H pylori may be an initiating step in gastric carcinogenesis.

Effect of eradication of Helicobacter pylori infection on gastric epithelial cell proliferation.

Helicobacter pylori infection has been linked with gastric carcinoma. Epithelial cell proliferation is an indicator of cancer risk. The aim of this study was to assess gastric epithelial cell proliferation before and after eradication therapy and to assess the efficacy of treatment of H. pylori infection using lanzoprazole and clarithromycin. Twenty-three patients with H. pylori-associated gastritis were treated with lanzoprazole 30 mg daily for four weeks and clarithromycin 500 mg three times a day for two weeks. Antral mucosal biopsies were taken for gastric epithelial cell proliferation analysis using the in vitro bromodeoxyuridine (BrdU) immunohistochemical technique before and four weeks after eradication therapy. Labeling index percent (LI%) was calculated as the percent ratio of proliferating cells to the total number of cells in the gastric pit. Efficacy of treatment was assessed in 16 subjects. Eight were negative for H. pylori infection 28 days after therapy and in eight patients H. pylori infection was not eradicated. The eradication rate for the regime was 50%. Cell kinetics were assessed in 19 subjects who completed treatment. Patients with H. pylori infection had a significantly higher LI% compared to normal (N = 19, LI%: 5.01 +/- 0.3 vs 3.2 +/- 0.2, N = 29). Eradication of H. pylori infection significantly reduced epithelial cell proliferation (N = 9, LI%: 5.2 +/- 0.4 to 3.2 +/- 0.8, P < 0.001), whereas it was unaltered in those whose infection was not eradicated (N = 10, LI%: 4.8 +/- 0.4 to 5.5 +/- 0.5, P = 0.18).(ABSTRACT TRUNCATED AT 250 WORDS)