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Results on hernia surgery from numerous centers confirm that tensionless repair with various meshes reduces the complication rates and the frequency of recurrences. Some evidence on incisional hernias suggests, however, that the use of mesh seems to transfer the onset of recurrences by several years. Persistent pain and other discomfort is also an unpleasant complication of otherwise successful surgery in a number of patients. Thus, improved, slowly degrading, mesh materials, with strong connective tissue-inducing action, might be more optimal for hernia surgery. Accumulating evidence also suggests that recurrent hernias appear in patients having inherited weakness of connective tissues. Numerous tissue specific collagens, in addition to the classical fibrillar I-III collagens and numerous substrate specific matrix proteinases, have recently been described in biochemical literature, and their roles as possible causes of tissue weakness are discussed.

Gut hypoperfusion has a major role in the pathogenesis of multiple organ failure, which is the main cause of death in severe acute pancreatitis. The effects of experimental acute pancreatitis on splanchnic and pancreatic perfusion and oxygenation were studied to find out whether gut hypoperfusion occurs already at the same time as changes in pancreatic perfusion.Twenty-four domestic pigs weighing 21-27 kg were randomized to severe or mild acute pancreatitis or control groups. Eight anaesthetized and mechanically ventilated pigs were intraductally infused with taurocholic acid to induce severe acute pancreatitis and eight received intraductal saline to induce mild acute pancreatitis. Eight pigs served as controls.Intraductally infused taurocholic acid rapidly induced severe necrotizing acute pancreatitis as assessed macroscopically and histologically. Histological changes of mild acute pancreatitis were seen in animals after intraductal saline infusion. After the induction, pancreatic tissue oxygen tension decreased promptly in severe acute pancreatitis and increased in mild acute pancreatitis. Laser-Doppler red cell flux decreased in severe acute pancreatitis. Gut pH gap and pCO2 gap decreased in 2 h after the induction of severe acute pancreatitis. Central haemodynamics were fairly stable throughout the study period in all groups.In experimental severe acute pancreatitis, splanchnic malperfusion seems to begin with pancreatic hypoperfusion before disturbances in gut microcirculation.

The present study aimed to determine the role of leucocyte count and C-reactive protein (CRP) measurements in the diagnosis of acute appendicitis in children. In particular, children with acute appendicitis but normal leucocyte count and CRP level were sought. The present study protocol was identical to those used in earlier studies on adult patients with suspected acute appendicitis. The mean preoperative leucocyte count and CRP value in 100 consecutive children with an uninflamed appendix at appendicectomy (group A) and in 100 consecutive patients with acute appendicitis (group B) were calculated. The numbers of patients with (i) both values normal, (ii) only leucocyte count raised, (iii) only CRP level raised, and (iv) both values raised were calculated in both groups A and B. Leucocyte count effectively (p0.001) separated children with uninflamed appendix (mean +/- SEM 10.2 +/- 0.4 x 10(9) l(-1)) from those with acute appendicitis (15.0 +/- 0.4 x 10(9) l(-1)), but the CRP value was of no use in this respect (p = 0.866; 31 +/- 4 mg l(-1) and 30 +/- 4 mg l(-1)). The most conspicuous finding was that in children with acute appendicitis, both values were normal in 7 out of 100 patients.Contrary to adult patients, normal leucocyte count and CRP value do not effectively exclude acute appendicitis in children.

An uninflamed appendix at appendectomy represents a misdiagnosis. In fertile-aged women, the diagnostic accuracy in acute appendicitis is usually lower than 60%. We studied the role of preoperative leukocyte count and C-reactive protein (CRP) measurements in the diagnosis of acute appendicitis in fertile-aged women with a clinical suspicion of acute appendicitis. In particular, what is the clinical value of unelevated leukocyte count and CRP in excluding acute appendicitis in these patients?We calculated the mean leukocyte count and CRP values in (1) 100 consecutive fertile-aged women operated on for a clinical suspicion of acute appendicitis but with an uninflamed appendix found at appendectomy, and (2) 100 consecutive fertile-aged women operated on for a clinical suspicion of acute appendicitis and acute appendicitis found at appendectomy. The percentages of patients with (1) both values unelevated, (2) only leukocyte count elevated, (3) only CRP value elevated, or (4) both values elevated were calculated within the groups A (uninflamed appendix) and B (acute appendicitis).The mean leukocyte value was significantly (P0.001) higher in patients with acute appendicitis (13.7x10(9)/l) than in those with an uninflamed appendix (10.6x10(9)/l). Similarly, the mean CRP value was significantly (P0.05) higher in patients with acute appendicitis (42 mg/l) than in those with an uninflamed appendix(29 mg/l). Taken together, 24 patients were operated on for a clinical suspicion of acute appendicitis, although preoperative leukocyte count and CRP values were unelevated. An uninflamed appendix was found in all these patients at appendectomy.Although clinical symptoms and signs indicated acute appendicitis, unelevated leukocyte count and CRP values excluded it, with a 100% predictive value in the current study of fertile-aged women. In our patients, 24% (24 of 100) of unnecessary appendectomies could have been avoided by trusting in this finding.

Increased mucosal concentration of bactericidal/permeability-increasing protein (BPI) has been shown in inflammatory bowel diseases. The purpose of the present study was to investigate the relationship between the mucosal concentration of BPI and the grade of mucosal inflammation in ulcerative colitis.Samples of colonic mucosa from 12 patients with ulcerative colitis and from 8 control patients were studied. The concentration of BPI in tissue extracts was measured by a time-resolved fluoroimmunoassay. The concentration of BPI was compared between samples with histological inflammatory changes of different severity. BPI was localized in tissue sections by immunohistochemistry.The concentration of BPI was higher (p0.001) in samples of colonic mucosa from patients with ulcerative colitis (median: 3.2 micrograms/g, range: 0.3-22.6 micrograms/g) than in control samples (0.4 microgram/g, 0.1-0.6 microgram/g,). Moreover, the concentration of BPI was higher (p = 0.015) in samples with severe inflammation (2.5 mu/g, 0.3-22.6 micrograms/g) than in those with mild inflammation (0.5 mu/g, 0.3-2.5 micrograms/g). The concentration of BPI in mucosal samples correlated well with the degree of histological inflammation (Spearman R = 0.70, p = 0.01). BPI was localized in polymorphonuclear leukocytes in the mucosa and stroma of the colonic wall.The concentration of BPI is increased in the colonic mucosa of patients with ulcerative colitis. The increase in the concentration of BPI in colonic mucosa seems to be closely associated with the inflammatory activity of ulcerative colitis.

The role of surgical procedures in the treatment of acute pancreatitis is still unclear. The aim of the present study was to analyze the mortality in acute pancreatitis in Turku University Central Hospital during the last quarter century with special reference to the prevailing surgical treatment trends.A total of 3921 patients with acute pancreatitis were treated 1971-1995. We analyzed the mortality in acute pancreatitis and the number of patients treated in the intensive care unit as well as the number of various surgical procedures used in the treatment of acute pancreatitis in each year 1971-1995.The most conspicuous finding was that the mortality in acute pancreatitis has not decreased any more during the last 15 years. Neither pancreatic resections nor peritoneal lavages seem to decrease the mortality.We conclude that despite various surgical procedures used in the treatment of acute pancreatitis the mortality in acute pancreatitis has not decreased any more during the last 15 years. Because of the retrospective nature of the current study the present results do not justify drawing any strict conclusions concerning the treatment of acute pancreatitis. However, the present results support the view that conservative treatment in the intensive care unit is justified as an initial therapy even in the fulminant attacks of acute pancreatitis.

Group II phospholipase A2 has been proposed to play an important role in the pathophysiology of inflammatory bowel diseases. This enzyme has also been linked to host defence mechanisms against bacteria. The current study aimed at measuring the mass concentrations of group II phospholipase A2 in serum and colonic mucosa of patients with Crohn's disease of different severity and of appropriate control patients without any inflammatory disease. The activity of the disease was determined by clinical factors (the simple index score) and endoscopic and histological scoring. The mass concentration of group II phospholipase A2 was measured by a time-resolved fluoroimmunoassay. The mass concentrations of group II phospholipase A2 in serum and colonic mucosa were significantly higher both in patients with active and inactive Crohn's disease when compared with controls. There was statistically significant difference in the mass concentration of group II phospholipase A2 in colonic mucosa but not in serum between inactive and active Crohn's disease. The current results indicate that the mass concentration of group II phospholipase A2 is increased in serum and colonic mucosa of patients with Crohn's disease and that the latter is associated with the degree of the inflammatory activity in the intestinal wall. These results support the idea that group II phospholipase A2 is involved in the local and generalised pathological processes of Crohn's disease.

Phospholipase A2 values increase in serum in various inflammatory states, infections, and postoperatively in surgical patients. Several organs, including the liver and spleen have been suggested as sources of circulating phospholipase A2. The purpose of the present work was to examine the possible role of the spleen as a source of elevated serum concentrations of phospholipase A2 after surgery. Pre- and postoperative serum samples of patients undergoing splenectomy were studied for group I phospholipase A2, group II phospholipase A2, and C-reactive protein mass concentrations and catalytic activity concentration of phospholipase A2. The catalytic activity concentration of phospholipase A2 and the mass concentrations of group II phospholipase A2 and C-reactive protein increased postoperatively (8.08 +/- 1.40 U/l vs. 3.96 +/- 0.89 U/l (mean +/- SEM) for phospholipase A2 catalytic concentration (p0.03), and 154.8 +/- 32.1 micrograms/l vs. 47.5 +/- 14.7 micrograms/l (mean +/- SEM) for group II phospholipase A2 mass concentration (p0.02, n = 7). The mass concentration of group I phospholipase A2 remained unchanged. The catalytic concentration of phospholipase A2 correlated well with the mass concentration of group II phospholipase A2 (p0.001, r = 0.846, n = 43). The concentration of C-reactive protein correlated well with the mass concentration of group II phospholipase A2 (p0.001, r = 0.566, n = 43) in serum. The results indicate that group II phospholipase A2 is released into the circulation after splenectomy, and the spleen seems not to be the source of circulating group II phospholipase A2.

It has been suggested that group II phospholipase A2 (PLA2-II) plays an essential role in inflammation, but the cellular source(s) of the enzyme is (are) largely unknown.Expression of PLA2-II was analyzed in human gastrointestinal tract at both protein and mRNA levels. Both normal tissues and specimen from patients with a few different common gastrointestinal disorders were analyzed.Expression of PLA2-II mRNA was seen in the Paneth cells but not in any other cell type of the intestinal tract. Blood vessel walls showed PLA2-II immunoreactivity but were negative in in situ hybridization for PLA2-II mRNA.It was concluded that nonpancreatic group II PLA2 is synthesized and stored by Paneth cells, whereas other cell types of the gastrointestinal tract seem incapable of synthesis of this enzyme. The positive immunoreaction in vascular structures may reflect the entry of circulating PLA2-II into vessel walls rather than local production of the enzyme.

We compared the predictive value of determining group II phospholipase A2 (PLA2) in serum for diagnosing acute appendicitis with the predictive values of white blood cell count (WBC) and measurement of C-reactive protein (CRP). In this prospective study, we included 186 patients who were undergoing appendectomy after clinical diagnoses of acute appendicitis. The performance of each test was measured by receiver-operating characteristic curves. WBC was the test of choice in diagnosing uncomplicated acute appendicitis. However, in contrast to CRP and PLA2, which increased in patients with protracted inflammation, there was not a concomitant increase in WBC. Therefore, especially CRP, but also PLA2, were better indicators of appendiceal perforation or abscess formation than was WBC. Increased WBC, CRP, and PLA2 values did not unequivocally corroborate the clinical suspicion of appendicitis, but if all three values were within normal limits, acute appendicitis could be excluded with a 100% predictive value. PLA2 values showed a highly significant correlation with CRP but not with WBC values, which supports the view that PLA2 represents an acute-phase reactant.

The most important fatal complications of acute pancreatitis are respiratory dysfunction and anuria. Phospholipase A2 has been postulated to be associated with pathologies of various diseases, such as acute pancreatitis, septic shock and multiple injuries. We have recently developed immunoassays for the measurement of pancreatic and nonpancreatic synovial-type phospholipase A2. The present prospective study on 35 consecutive patients with acute pancreatitis indicated that the concentration of synovial-type phospholipase A2, the catalytic activity of phospholipase A2 and the concentration of C-reactive protein in serum were significantly higher in those patients suffering from acute pancreatitis who needed respirator treatment than in those who managed with spontaneous breathing, while there was no difference between these groups in the concentration of pancreatic phospholipase A2. The only significant difference between patients whose highest creatinine concentration rose up to 140 mumol/l and those whose highest creatinine concentration remained below this cutoff value was in their synovial-type phospholipase A2 values. The increased concentration of nonpancreatic synovial-type phospholipase A2 in serum was associated with pulmonary and renal complications. These results emphasize the role of synovial-type phospholipase A2 in the pathophysiology of acute pancreatitis.