SUMMARY To assess the course of recovery ofgluten sensitive enteropathy in adults, histological and functional recovery was studied in 22 patients, aged 20-79 years. Biopsy specimens taken at the time of diagnosis were studied in 20; after adhering to a gluten free diet for nine to 19 (mean 14) months in 14; and after adhering to the same diet for 24-48 (mean 34) months in 10 patients. Histological recovery was assessed morphometrically in the proximal jejunum. Mucosal linings significantly improved over time, but did not completely return to normal with a gluten free diet: at diagnosis the surface:volume ratio was 22% of normal, increasing to 48% and 66% after nine to 19 and 24-48 months, respectively, ofa gluten free diet. Disaccharidase activities progressively increased. After 24-48 months maltase, sucrase, and isomaltase had returned to normal in the proximal jejunum; they were still significantly decreased in the distal duodenum. Duodenal and jejunal lactase activities were both below normal after 24 to 48 months.It is concluded that recovery of the intestinal mucosa of adults with gluten sensitive enteropathy during a gluten free diet continues beyond nine to 19 months and is still incomplete after two to four years. The recovery of disaccharidase activities extends from the distal to the proximal part of the small intestine, and is aligned to histological recovery.Gluten sensitive enteropathy or coeliac sprue is characterised by severe villous atrophy of the small intestinal mucosa; it responds favourably to the withdrawal of dietary gluten. Gross villous architecture and absorptive cells are severely damaged, and many enzymes, necessary for the digestive-absorptive process, are severely depleted. This is especially true for brush border enzymes like the disaccharidases maltase, sucrase, isomaltase, and lactase. To what degree the mucosa will recover during a gluten free diet is still a matter ofcontroversy: morphological changes occur and disaccharidases increase after gluten withdrawal. Most investigators have found that although some patients show complete histological and functional recovery during the diet, most still show some degree of histological and functional damage, even after adhering to the diet for several years.'Within days or weeks of starting a gluten free diet a clinical response can be detected. This is also true for some of the histological and functional abnormalities: soon after gluten withdrawal the height ofthe mucosal surface cells increases6 and partial return to normal of organelles is observed.7 The recovery of the villous Accepted for publication 17 March 1988 architecture is known to occur much more slowly, but so far no studies have emphasised the course of this slow recovery. Little is known with certainty about the rate and course of recovery of the disaccharidases and other brush border enzymes.There is good evidence to suggest that the most severe histological damage is found in the proximal small intestine in untreated coeliac disease28 and that during treatment, t...

Locally advanced cancer of the cardia and fundus might be cured by surgical resection. Poor results after surgery in stage IIIB and stage IV disease prompted a study of neoadjuvant chemotherapy. Treatment included four cycles of high doses of methotrexate (1.5 g/m2) and high doses of 5-fluorouracil (1.5 g/m2) followed by surgery in those patients with lesions then found to be resectable. Twenty patients with tumours staged as IIIB or IV were entered; 17 patients completed the four courses of chemotherapy and 14 underwent re-exploration. Eight patients achieved tumour reduction enabling resection. Five patients underwent total gastrectomy with distal pancreatectomy and splenectomy en bloc and three patients had an oesophagogastrectomy. There were no treatment-related deaths and toxicity was tolerable. Two patients were alive 54 and 41 months after chemotherapy with no evidence of disease. Locoregional recurrence developed in five patients and metastatic disease in one. Their median survival was 22 months.

Generalized peritonitis causes a reduction in abdominal fibrinolytic activity, resulting in persistence of intraabdominal fibrin with subsequent adhesion and abscess formation. The activities of tissue plasminogen activator (tPA) and plasminogen activator inhibitor (PAI) were measured in the peritoneal fluid of rats with faecal peritonitis and correlated with the extent of peritoneal damage to determine the cause of decreased fibrinolysis. Activity of tPA was low during the study period of 8 days, but higher in rats with peritonitis than in controls. The activity of PAI in rats with peritonitis was significantly increased compared with that of controls during the whole study period (P < 0.001). Histological signs of damage to the peritoneum were similar in rats with peritonitis and controls. There was no correlation between the extent of peritoneal damage and tPA or PAI activity. The increased activity of PAI in the peritoneal fluid of rats with faecal peritonitis may be the main cause of reduced fibrinolysis in the abdominal cavity. Activities of tPA and PAI may originate not only from the mesothelium but from other sources.

Mesangial cell (MC) proliferation and extracellular matrix (ECM) formation are hallmarks of chronic glomerular disease. The present in vitro study examined the effects of the vasoactive agents angiotensin II (Ang II), arginine vasopressin (AVP), and serotonin (5-HT) on growth and protein biosynthesis of cultured rat MCs after 72 hours of incubation. AVP and 5-HT (10(-6) M) significantly increased DNA synthesis and growth of quiescent subconfluent MCs to levels of 25 and 45%, respectively, of the optimal stimulatory effect of 10% fetal calf serum (FCS) (both P less than 0.001). The mitogenic effect of Ang II was 10% of the 10% FCS effect (P less than 0.01). ECM production was studied by ELISA assay for fibronectin (FN) secreted into the culture medium (SeFN) and cell-associated FN, that is, intra- and pericellular FN (CaFN). In all incubations, highly significant negative linear relationships were found between the numbers of MCs per well and quantities of both SeFN and CaFN after normalization of the data by logarithmic transformation (SeFN: r values greater than -0.9705; CaFN: r greater than -0.9620; P less than 0.001). Thus, increasing cell densities progressively suppressed ECM formation by MCs. The ECM production was found to be independent of growth activity. AVP significantly increased SeFN (P less than 0.05) and decreased CaFN (P less than 0.001) in subconfluent cultures; Ang II and 5-HT had no effect. Metabolic labeling with 35S-methionine (18 hr, 200 microCi/ml medium) and 2-D electrophoresis of MC lysates resulted in resolution of greater than 500 different radiolabeled intracellular proteins in molecular weight from 110 to 20 Kd over an isoelectric interval of 5.0 to 7.0.(ABSTRACT TRUNCATED AT 250 WORDS)

T stage, localization, and patient age were predictive for the number of nodes examined. A higher number of examined nodes was associated with an increase in node positivity. The survival benefit can be explained by stage migration. Eventually this may lead to an overall survival benefit, as more patients are classified as node-positive, and therefore will receive adjuvant therapy.