Objective To correlate renal calculi and other clinical factors with urinary biochemical analytes in patients with inflammatory bowel disease, and to investigate the relative importance of hyperoxaluria (associated with fat malabsorption) or reduced stone inhibitors in the development of calculi in these patients. Patients, subjects and methods Samples were obtained from 25 patients with Crohn's disease (CD), 15 with ulcerative colitis (UC) and 17 normal subjects (controls). Evidence for the presence of renal calculi was obtained from plain films, ultrasonography or intravenous urography. Urine oxalate and citrate were analysed using commercial enzymatic assays; magnesium was measured using atomic absorption and other analytes assayed using standard methods on automated analysers. Results Renal calculi were found in two patients with CD and in none with UC. Hyperoxaluria was present in 36% of patients with CD but was absent in those with UC. Analysis of covariance showed an association between low urinary citrate/creatinine ratio and renal stones (P=0.02), and between a combined urinary citrate and magnesium deficit relative to calcium, as expressed in the CMC index ((citrater magnesium)/calcium), and renal stones (P=0.017). Changes in urinary calcium, oxalate, urate, magnesium or the calcium oxalate index were not associated with the presence of stones. There was no independent relationship between any clinical factor and the presence of stones. Conclusion Lower urinary concentrations of magnesium and citrate (stone inhibitors), relative to calcium (stone promoter; the CMC index) may be more important in lithogenesis in inflammatory bowel disease than is hyperoxaluria. In patients with a functioning colon, a low CMC index may predict likely stone-formers; this requires a prospective evaluation. Avoiding low urinary levels of magnesium and citrate may aid in preventing and treating renal calculi.

SUMMARY The influence of endoscopic forceps variables (size, design, and make) on biopsy specimen weight, depth, and diagnostic adequacy has been studied in vitro on normal human stomach, and in vivo at endoscopy in dog and in patients. Greater pressure during the biopsy procedure yielded significantly heavier, deeper, and histologically more acceptable specimens. Standard sized forceps (diameter 2A4 mm) and those with ellipsoid cups consistently produced larger specimens than the smaller 'paediatric' forceps (1-8 mm) and those with round cups. Deeper specimens were also obtained using the standard forceps. In vitro and in vivo in the dog, the standard sized forceps also produced specimens of greater diagnostic adequacy than the paediatric forceps. At endoscopy in patients, however, we could not detect any influence of the size, shape, and presence of forceps spike or fenestration on the diagnostic adequacy of the specimens.Gastrointestinal endoscopy is now used routinely in most general hospitals, and endoscopic biopsy specimens constitute a significant proportion of the material handled by routine histopathology laboratories. Most instrurmients for upper gastrointestinal endoscopy have biopsy channels which permit the use of forceps 2-4 mm in diameter. The specimens are of necessity small, and concern has been expressed about their adequacy. Such concern has been highlighted by the use of even smaller 'paediatric' fibrescopes, some of which have a channel which permits the use of forceps, only 18 mm in diameter. Apart from their size, endoscopic biopsy forceps vary in their precise design; the endoscopist is faced with a bewildering variety.Two small studies have addressed part of the problem -the size of the forceps. Siegel and colleagues1 showed that forceps with 4 mm bite size yielded larger specimens than 3 and 2 5 mm forceps; Neuhaus and Hintze2 showed that 2 mm forceps provided specimens inferior to those obtained with experimental 3-5 mm and 5 mm forceps.We have compared the weight (as a measure of

Angiodysplasia of the colon was diagnosed in 31 out of 1,050 patients (3%) presenting with rectal bleeding or anaemia, among 10,000 colonoscoped at St. Mark's Hospital. The lesions were identified in 16 out of 879 (2%) patients with rectal bleeding, in 15 out of 171 (9%) patients with anaemia, and in a further three patients without features of blood loss. The angiodysplasia lesions were predominantly in the right colon (76%) and occurred with a similar frequency (12%) in the transverse and the left colon. Affected patients (59% male and 41% female) were in the older age group (53-89 years; mean age 69.5 years) but only one patient had known aortic valve disease. Angiodysplasia is an important diagnosis to consider in patients presenting with colonic bleeding or anaemia because it can be treated in the majority of cases by endoscopic electrocoagulation. However in our experience it is less common (3%) than previously suggested by other authors (40-67%). Endoscopic over-diagnosis is possible when intramucosal capillaries with no bleeding tendency on local traumatisation or biopsy are included in the diagnosis but these lesions are not true angiodysplasia.

Summary: We have encountered five cases of chronic iron deficiency anaemia due to bleeding from gastric antral vascular ectasia (watermelon stomach). Two cases were associated with a lymphoma and in three cases there was evidence of portal hypertension. Two patients were treated conservatively by blood transfusions. The other patients required either surgery or tranexamic acid or endoscopic laser therapy to control the chronic haemorrhage.