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Complement activation occurs in patients with acute pancreatitis (AP) and may contribute to the development of organ failure. Because a number of enzymes are released during AP that could influence the complement inhibitor CD59, the purpose of this study was to examine serum levels of CD59 in relation to severity of AP.Twelve patients with severe AP had organ failure (referred to as the grade 2 group). For each of them, we found 2-3 age-matched AP patients who served as controls (n=27). Of these, a total of 13 had mild AP (grade 0 group) and 14 severe AP without organ failure (grade 1 group). Blood samples were collected at admission and on days 1 and 3-7 post-admission. Grade 2 patients were compared with grade 0 and grade 1 patients. CD59 levels were measured by a sandwich enzyme immunoassay.At admission, median CD59 levels were significantly higher (p = 0.002) in grade 2 patients (median 104.2 ng/ml, range 26.1-186.3) than in grade 0 patients (37.3, range 30.3-75.9) and grade 1 patients (38.6, range 19.9 96.1). CD59 levels remained higher in grade 2 patients than in grade 0 and 1 patients on day 1 (p = 0.001) and days 3-7 (p = 0.002). The CD59 levels correlated significantly (p0.05) with C-reactive protein (CRP) levels (R = 0.40) and APACHE II scores (R = 0.32) on admission.Organ failure and severity of AP are associated with elevated serum levels of CD59.

Immune suppression plays a role in the pathogenesis of acute pancreatitis. The purpose was to describe plasma anti-inflammatory cytokines and blood monocyte human leucocyte antigen (HLA)-DR expression, a cellular marker of immune suppression, in relation to clinical outcome in acute pancreatitis.We studied 74 patients with acute pancreatitis admitted within 72 h after symptom onset; 27 had mild disease and 47 severe disease, of whom 20 developed organ failure. Plasma cytokine concentrations and monocyte HLA-DR density were determined at admission and 1, 2, 3, 7, 14 and 21 days later.The levels of interleukin-1 receptor antagonist, interleukin-6 and interleukin-10 correlated inversely to monocyte HLA-DR expression; each marker correlated with disease severity. Interleukin-4, -11 and -13 levels were low. Organ failure occurred at median 36 h (range 8 to 158) after admission and was predicted at admission by the combination of interleukin-6 and interleukin-10 with sensitivity of 95%, specificity of 88% and positive likelihood ratio of 7.6 (95% confidence interval 3.3 to 17). Patients with secondary infections had a lower proportion of HLA-DR positive monocytes than did controls at day 14 (median: 32% versus 65%; n = 7) and at day 21 (median: 49% versus 83%; n = 6), P0.05 each. In the organ failure group, HLA-DR expression did not differ between survivors and non-survivors.Determining the severity of anti-inflammatory reaction at admission and monitoring the course of immune suppression provide a means for predicting clinical outcome in acute pancreatitis.

Although jejunal diverticulosis is a rare entity and usually asymptomatic, it may cause chronic symptoms and acute complications. Because of the rarity of the entity, diagnosis is often delayed, resulting in unnecessary morbidity and mortality. The purpose of this study was to draw attention to jejunal diverticula and their complications. The medical records of 8 consecutive patients with complications due to small-bowel diverticula treated at our department during the past 4 years were reviewed. All diverticula were located in the jejunum. Seven patients had acute complications, 3 patients had an intra-abdominal abscess, 2 had free perforation with diffuse peritonitis, 1 had a bowel occlusion and 1 patient had concomitant bleeding and occlusion. One patient presented with chronic symptoms. A preoperative diagnosis of jejunal diverticula, before explorative laparotomy, was not reached in any of the 7 patients with acute symptoms. In the patient with chronic symptoms, multiple jejunal diverticula complicated by a jejuno-colic fistula and foreign body were found at laparotomy. On patient died of multiorgan failure. Small-bowel diverticulosis is a rare entity, but it should not be regarded as a clinically insignificant finding. It may be difficult to make a preoperative diagnosis. Patients with incidentally detected proximal jejunal diverticula, at imaging studies or at laparotomy, warrant close observation and awareness that the diverticula may cause serious complications.

Obesity is a known risk factor for severe acute pancreatitis (AP), but the mechanism by which it affects the severity of AP is not fully understood. The main objective of this study was to investigate the relationship between obesity and inflammatory markers in AP.Thirty patients with AP who developed organ failure (Group I) and 87 patients with AP who survived without organ failure (Group II) were studied. Patients' height and weight were measured at admission for calculation of body mass index (BMI). Blood samples were taken at admission for measurement of plasma interleukin (IL)-1beta, IL-6, IL-10, IL-1 receptor antagonist, procalcitonin, C-reactive protein (CRP) and monocyte human leucocyte antigen (HLA)-DR expression.Group I patients had higher BMI values (median 26.2 kg/m2) than Group II patients (25.2 kg/m2), p =0.033. Both CRP values and monocyte HLA-DR expression showed a significant correlation with BMI (Spearman's rank correlation r=0.32, p =0.003 and r= -0.33, p = 0.002, respectively). The correlation between BMI and monocyte HLA-DR expression was significant in Group II patients (r = -0.34, p =0.002) but not in Group I patients (r = -0.02, p0.05). There was no correlation between BMI and IL-1beta, IL-6, IL-10, IL-1 receptor antagonist or procalcitonin.BMI did not affect either proinflammatory or anti-inflammatory cytokine levels in early AP. However, in patients with mild AP, BMI correlated positively with CRP levels and inversely with monocyte HLA-DR expression, which might reflect an amplified inflammatory response in these patients. Taken together, acute inflammatory response in AP, which ultimately determines the severity of AP, was little affected by BMI.

Few data are available on cellular markers of systemic inflammation and immune suppression in early acute pancreatitis. The aim of this study was to describe the cellular immune inflammatory status of patients with acute pancreatitis in relation to development of organ failure.Prospective study including 89 patients who presented within 72 h of onset of pain. Fifty-eight of them had mild disease (Grade I group), 19 had severe disease with no organ dysfunction (Grade II group) and 12 had severe disease with organ dysfunction (Grade III group). Serial blood samples were collected on admission and following 2 days. Phagocyte surface markers were analysed using flow cytometry.The proportion of HLA-DR-positive monocytes, a marker of immune suppression, and CD11b expression level on neutrophils and monocytes, a marker of systemic inflammation, were related to Grades I-III (P for trend0.001). In Grade III patients, the proportion of HLA-DR-positive monocytes was low on presentation, or decreased rapidly during follow-up, whereas CD11b expression levels were persistently high. L-selectin and monocyte CD14 expression levels were not related to disease severity.Immune suppression develops early, rapidly and unexpectedly in patients with acute pancreatitis. Monitoring immune inflammatory status may provide the means by which to identify patients who benefit from biological response modifier therapy.

Background Trypsinogen-2 and the trypsin-2-alpha1-antitrypsin complex are recently introduced new laboratory markers for acute pancreatitis. They show high sensitivity and specificity for acute pancreatitis on admission, but little is known on their time course profiles. Methods The serum concentrations of trypsinogen-2 and trypsin-2-alpha1-antitrypsin were monitored in 92 patients with verified acute pancreatitis. The follow-up period was 42 days in patients with severe acute pancreatitis (N = 73) and 9 days in mild disease (N = 19). Results On admission the mean serum concentration of trypsinogen-2 was 2880 microg/l in severe and 920 microg/l in mild acute pancreatitis. These values were 32- and 10-fold the upper reference limit, respectively. Trypsin-2-alpha1-antitrypsin concentrations were 1250 microg/l (100-fold the upper reference limit) and 635 microg/l (52-fold), respectively. The differences were statistically significant (P = 0.026-0.001). The concentrations of trypsinogen-2 and trypsin-2-alpha1-antitrypsin decreased gradually during the follow-up period, but they remained elevated for the entire study period in patients with severe and mild disease. Conclusions The time course profile of trypsinogen-2 and trypsin-2-alpha1-antitrypsin is favorable for diagnosing acute pancreatitis. The elevation starts within hours after the onset of the disease and it is very steep. Both markers remain elevated longer than amylase and the magnitude of the elevation correlates with the severity of the disease. This is further evidence to support the use of trypsinogen-2 and trypsin-2-alpha1-antitrypsin for the evaluation of patients suspected of having acute pancreatitis.

Background: The accuracy of serum trypsinogen-2 in predicting the severity of acute necrotizing pancreatitis (ANP) was prospectively evaluated in 52 consecutive patients. Methods: A new sensitive immunofluorometric assay was used for serum trypsinogen-2. Results: Mean values during the first 24 h were 42.1 μg/l in control patients, 1435 μg/l in uncomplicated cases, and 4090 μg/l in complicated or fatal cases. There was a significant difference in serum trypsinogen-2 values between patients with uncomplicated and complicated disease (p = 0.002) already on admission. When a cutoff level of 1000 μg/l was used, patients with uncomplicated ANP were differentiated from patients with complicated ANP with a sensitivity of 91% and with a specificity of 71%. Conclusions: The immunofluorometric assay of serum trypsinogen-2 is a sensitive and specific method for prediction of the severity of the disease in necrotizing pancreatitis.