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f-Hb is related to severity of colorectal neoplastic disease. This has ramifications for the selection of the appropriate cut-off concentration adopted for bowel screening programmes.

In summary, this evaluation of the FIT supports the introduction of FIT as a first-line test, even when colonoscopy capacity is limited.

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The effects of longstanding non-steroidal antiinflammatory drug (NSAID) treatment on gastric mucosal synthesis of leukotriene B4 (LTB4), leukotriene C4 (LTC4), and prostaglandin E2 (PGE2) was studied. Gastric antral biopsies in 65 patients with arthritis taking NSAIDs and 23 control patients were taken and eicosanoid concentrations, stimulated by vortex mixing or calcium ionophore, were measured by radioimmunoassay. Median gastric mucosal synthesis of LTB4 was increased in patients taking NSAIDs compared with non-users: (0 9 (0 2-2 5) pg/mg v 0 (0-0.6) pg/mg (p<0001)). These differences persisted when subgroups of patients were analysed according to Helicobacter pylon colonisation or degree of mucosal injury. Synthesis of LTB4 was strongly associated with the presence of type C (chemical) gastritis. Increased synthesis of LTC4 was associated with Helicobacter pylori colonisation but not NSAID use. Synthesis of PGE2 was decreased in patients taking NSAIDs compared with control patients (p<0001). Enhanced gastric mucosal synthesis of LTB4 in patients taking NSAIDs may represent a primary effect of these drugs and could be implicated in the pathogenesis of gastritis and ulceration associated with NSAIDs.

Colonisation with Helicobacter pylori may influence susceptibility to gastroduodenal injury and ulceration in patients taking nonsteroidal anti-inflammatory drugs (NSAIDs). The aim of this study was to determine if Helicobacter pylori colonisation altered eicosanoid synthesis by gastric musoca in these patients. Sixty five patients with longstanding NSAID intake and 23 control subjects underwent endoscopy.

Three patients with a recently described tumor of neuronal origin, intraventricular neurocytoma, are presented. These tumors occur as intraventricular lesions in young patients, and the prognosis after surgical treatment is favorable. The initial pathological diagnosis of intraventricular neurocytoma may be difficult because of the striking resemblance of these tumors to oligodendroglioma and, to a lesser extent, ependymoma on light microscopic examination. Despite the use of wide-ranging panels of monoclonal antibodies, previous authors have not found any characteristic immunohistochemical staining patterns, but in our three patients, the use of synaptophysin, glial fibrillary acidic protein, and Leu-7 demonstrated staining patterns that may be useful in the diagnosis of this tumor. The monoclonal antibody Ki-67 was used to stain one tumor and showed a low cell proliferation rate. We have reviewed the clinical, radiological, and pathological features of these 3 patients and 17 previously described patients in an attempt to determine the important diagnostic features of intraventricular neurocytoma. Intraventricular neurocytoma should be considered in any young patient with symptoms of raised intracranial pressure and radiological evidence of an intraventricular lesion. Pathological diagnosis requires the use of electron microscopy to show features of neuronal differentiation; however, immunohistochemical demonstration of a neuronal phenotype is also a useful adjunct to diagnosis. Failure to use specialized techniques for pathological diagnosis will lead to misdiagnosis of these lesions as oligodendrogliomas, as was the initial diagnosis in 2 of our patients before review.