Whether or not the incidence of ulcer relapse varies according to the drug used to produce initial healing is a controversial matter. We tackled this problem using data from 15 eligible trials from 25 published controlled trials in patients followed up for six to 12 months. Pooled estimates of differences in ulcer relapse incidence between patients initially healed with H2-antagonists and patients initially healed with non-H2-antagonist drugs were calculated. The overall incidence of relapse in patients healed with comparator drugs is 11 percentage units lower at six and 12 months, than that observed in H2-antagonist-healed patients. The confidence intervals are +/- 8% at six months and +/- 7% at 12 months. These data suggest the existence of a different effect on relapse incidence for the entire class of comparator drugs taken as a whole, compared with H2-antagonists. On considering the non-H2-antagonists singly, this conclusion holds good only in the case of tripotassium dicitrato bismuthate.

We report the cases of one patient with the acquired immunodeficiency syndrome as a result of human immunodeficiency virus type 1/lymphadenopathy associated virus type 1/human T-cell lymphotrophic virus type III (HIV-1/LAV-1/HTLV-III) infection and of another patient with AIDS related complex caused by human immunodeficiency virus type 2/lymphadenopathy associated virus type 2 (HIV-2/LAV-2) infection, who were suffering from cholangitis. The manifestations and possible mechanisms for cholangitis in these patients and in 10 previously reported similar cases are reviewed.

Familial giant hypertrophic gastritis involving three generations is reported. A review of the literature, where approximately 200 cases are described, showed only few cases of familial occurrence of this disease, and only in siblings. Our findings suggest dominant heredity, but considering the sparsity of familial occurrence reported earlier, heredity seems to be of only minor pathogenetic significance.

This paper reviews recent psychological studies of patients with the irritable bowel syndrome (IBS) or 'functional abdominal pain'. Many studies have used unreliable or invalid methods of assessment and some have confused personality with treatable psychiatric illness. Reliable and valid measures have indicated that 40-50% of patients with recently diagnosed functional abdominal pain have demonstrable psychiatric illness; these patients have a worse prognosis than those who are psychologically normal. When psychiatric disorder is diagnosed in a patient with IBS there are three possibilities: (1) The patient may have developed abdominal and psychiatric symptoms simultaneously in which case treatment of the latter may relieve the bowel symptoms. (2) Psychiatric disorder may precipitate increased concern about bowel symptoms, and consequent attendance at the gastroenterology clinic, of those with chronic mild symptoms. In this case it is illness behaviour, rather than abdominal symptoms, that is caused by the anxiety/depression. (3) Those with chronic neurotic symptoms as part of their personality must be screened for organic disease if they have a fresh onset of bowel symptoms; but they are at high risk of becoming persistent clinic attenders. Further research is needed to clarify when psychological abnormalities play a role in the aetiology of IBS and when they are coincidental, but lead to illness behaviour. The role of psychological factors in the aetiology of the irritable bowel syndrome (IBS) is far from clear, but a review of the literature suggests that some consistent patterns are emerging in spite of methodological problems. There have been three major defects with studies that have linked IBS with neurotic symptomatology. First, the measurement of psychological factors has generally been imprecise. Second, most studies have considered IBS patients as a single group, without making allowance for differing symptom patterns. Third, conclusions have been drawn about hospital samples and extrapolated to all IBS subjects, without taking account of factors which affect consulting behaviour. Most studies have been concerned with psychological factors so these will be considered in most detail.

During growth and differentiation the plasma membrane has a key role not only in the reception and transmission of extracellular signals such as hormones and growth factors, but also in communicating cellular response to the cellular microenvironment. Cellular response to trophic stimuli includes alterations of cell shape and cell surface antigenicity, of cell-cell recognition and cellular adhesion, of cell matrix binding and the adaptation of cell surface receptors. The plasma membrane is therefore regarded as a 'central agency' for the integration of a single cell into the complex system of a tissue or of an organism. The numerous functions of the plasma membrane are mainly mediated by membrane integrated glycoproteins or glycolipids both sharing the common feature of covalently bound oligosaccharide side chains. Specific alterations of oligosaccharide structure and metabolism associated with growth, differentiation and various pathologic conditions suggest a specific role for the oligosaccharide moieties in the regulation of cell surface functions (Table 1). This review intends to focus on the role of plasma membrane glycoproteins describing briefly principles of glycoprotein structure and function, and characteristics of their biosynthesis and degradation.

The adaptive changes of hypertrophy and hyperplasia are diffuse and reversible responses of the pancreas to growth promoting stimuli. Early stages of neoplastic growth in the pancreas have been studied in carcinogen treated animals and preneoplastic lesions including atypical acinar cell foci and nodules, tubular ductal complexes and intraductal hyperplasia were identified. Neoplastic growth is clonal rather than diffuse and involves multiple steps through preneoplastic stages to produce a tumour. The individual steps are commonly regarded as reflecting a series of changes in the genome of the cells. Although the changes are likely to be irreversible, completion of the sequence usually requires a major portion of the lifespan of the host. The rate of progression of preneoplastic lesions to cancer may be modulated by the same factors that control adaptive growth. It follows that such factors will influence the probability that a carcinoma will develop. Cholecystokinin (CCK) seems to provide one example of a hormone/growth factor that can stimulate normal, adaptive, and neoplastic growth, and it is to be expected that other such hormones will be identified.