Fear conditioning is impaired in systemic kainic acid and amygdala-stimulation models of epilepsy.

PURPOSE: The lateral nucleus of the amygdala is critical for fear conditioning, a paradigm of emotional learning, which requires recognition of an unconditioned stimulus as aversive and association of conditioned stimuli with an unconditioned stimulus. Some patients with temporal lobe epilepsy have amygdaloid damage associated with impaired emotional learning. Fear conditioning also is impaired at least in some animal models of epilepsy. We studied whether contextual or tone-cued fear conditioning is impaired in two status epilepticus models of epilepsy and whether impairment correlates with the extent of damage in the lateral nucleus of the amygdala. METHODS: We induced epilepsy in rats by either systemic kainic acid administration or electrical amygdala stimulation. Behavioral reactions in all phases of fear conditioning were analyzed from videotapes. Damage to the lateral nucleus of the amygdala was analyzed from thionin-stained sections both histologically and by volumetry. RESULTS: Immediate reflexive responses to unconditioned and conditioned stimuli were preserved, whereas the freezing response to an unconditioned stimulus was reduced. Contextual conditioning was severely impaired, whereas tone-cued conditioning was better preserved. The lateral nucleus pathology did not correlate with impaired fear conditioning. CONCLUSIONS: These data suggest that processing of complex contextual stimuli is severely affected in experimental epilepsy, whereas conditioning to simple cues is better preserved.

Intra-abdominal abscess in a patient with tumour necrosis factor receptor-associated periodic syndrome.

Tumour necrosis factor (TNF) receptor-associated periodic syndrome (TRAPS) is an autoinflammatory disorder characterized by periodic attacks of fever and inflammation, due to mutations in the gene coding for the TNF type I receptor (TNFRSF1A). A 16-year-old patient with the diagnosis of TRAPS was admitted to hospital because of fever and abdominal pain. Initially, the symptoms were interpreted as manifestations of another TRAPS attack, but the patient's condition worsened, despite treatment with corticosteroids and antibiotics. A repeated computer tomography revealed an intra-abdominal abscess, which necessitated urgent surgical intervention. This case stresses the importance of differential diagnostic vigilance when dealing with patients with rare genetic diseases.

Clinical value of severity markers in acute pancreatitis.

Acute pancreatitis is a common digestive disease of which the severity may vary from mild, edematous to severe, necrotizing disease. An improved outcome in the severe form of the disease is based on early identification of disease severity and subsequent focused management of these high-risk patients. However, the ability of clinicians to predict, upon presentation, which patient will have mild or severe acute pancreatitis is not accurate. Prospective systems using clinical criteria have been used to determine severity in patients with acute pancreatitis, such as the Ranson's prognostic signs, Glasgow score, and the acute physiology and chronic health evaluation II score (APACHE II). Their application in clinical practise has been limited by the time delay of at least 48 h to judge all parameters in the former two and by being cumbersome and time-consuming in the latter. Contrast-enhanced computed tomography is presently the most accurate non-invasive single method to evaluate the severity of acute pancreatitis. It cannot, however, be performed to all patients with acute pancreatitis. Therefore, considerable interest has grown in the development of reliable biochemical markers that reflect the severity of acute pancreatitis. In this article we critically appraise current and new severity markers of acute pancreatitis in their ability to distinguish between mild and severe disease and their clinical utility.

Vasodilatory shock in severe acute pancreatitis without sepsis: is there any place for hydrocortisone treatment?

BACKGROUND: Hydrocortisone (HC) has been reported to rapidly improve hemodynamics and reduce the time to vasopressor cessation in septic shock, but none has focused on this effect in acute pancreatitis. We therefore performed a study to assess the effects of hydrocortisone on catecholamine-dependent shock among patients with severe acute pancreatitis. METHODS: A retrospective, case-controlled study among 10 patients with severe acute pancreatitis and HC treatment for catecholamine-dependent shock was performed. The control group comprised 11 conventionally treated patients with the same severity of pancreatitis and circulatory shock according to the norepinephrine support required. In focus were the first 48 h from the start of HC administration in the HC group and from the reference point in the control group, respectively. The reference point for the control group was the time point at which doses of norepinephrine exceeded 0.3 microg kg(-1) min(-1). RESULTS: Patients in the HC group were weaned off norepinephrine in a significantly shorter time (61 h in HC group vs. 141 h, P = 0.016). The HC group received significantly less norepinephrine (area under curve of norepinephrine dose, P = 0.041). The reduction in norepinephrine dose was comparable at 24 h, being -0.051 (-0.208-0.022) microg kg(-1) min(-1) in the HC group vs. -0.026 (-0.150-0.030) microg kg(-1) min(-1) in the controls (P = 0.307), and at 48 h with respective figures of -0.206 (-0.317 to -0.102) microg kg(-1) min(-1) and -0.103 (-0.178-0.029) microg kg(-1) min(-1) (P = 0.072), from the start of HC administration. CONCLUSION: According to our data it seems reasonable to formulate a hypothesis that low doses of HC shorten the time to vasopressor cessation and rapidly reduce the need for norepinephrine support in patients with shock associated with severe acute pancreatitis without sepsis.

The endoscopic management of pancreatic fistulas.

BACKGROUND: Interest in the use of therapeutic endoscopy for the treatment of pancreatic diseases has been on the increase for several years. Our aim was to assess the efficacy of endoscopic retrograde cholangiopancreaticography (ERCP) in the treatment of pancreatic fistulas. METHODS: We evaluated the results of therapeutic ERCP in 50 patients with pancreatic fistula treated at the Helsinki University Central Hospital from 1998 to 2003. RESULTS: The success rate of fistula closure after therapeutic ERCP was 82%. Five patients required operative treatment when ERCP was unsuccessful. There was little morbidity and no procedure-related mortality. Four patients died because severe illnesses made them unfit for any further procedures. CONCLUSION: ERCP is a safe and effective modality and should be considered as first-line therapy in the management of pancreatic fistula.

Early prediction of organ failure by combined markers in patients with acute pancreatitis.

BACKGROUND: Several biological markers and clinical scoring systems have been used to predict the course of acute pancreatitis. Because organ failure is the most severe complication of the disease, prognostic markers and their combinations that would predict organ failure on hospital admission were sought. METHODS: Some 351 consecutive patients with acute pancreatitis were studied. Blood samples were taken within 12 h of admission. This case-control study included all 33 patients with organ failure and 99 matched controls without organ failure. Measurements included 19 prognostic markers and Acute Physiology And Chronic Health Evaluation (APACHE) II score. RESULTS: Plasma interleukin 10, serum glucose and serum calcium were identified as independent predictors of organ failure by logistic regression analysis. Calcium level correlated with clinical onset of organ failure. The combination of interleukin 10 (more than 50 pg/ml) or calcium (less than 1.65 mmol/l) was a significantly better predictor than any single marker or APACHE II score, with a sensitivity of 88 per cent, specificity 93 per cent and diagnostic odds ratio 94. CONCLUSION: Organ failure in acute pancreatitis can be predicted with high accuracy at hospital admission using a combination of plasma interleukin 10 and serum calcium measurements.

Jejunal diverticulosis: a potentially dangerous entity.

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.

Urinary trypsinogen activation peptide as a marker of severe acute pancreatitis.

BACKGROUND: Trypsinogen activation peptide (TAP) may be an early marker of severe pancreatitis. Previous studies have included all patients with organ failure in the group with severe pancreatitis, although patients with transient organ failure may have a good prognosis. The aim of this study was to determine the value of urinary TAP estimation for prediction of severity of acute pancreatitis, and to validate use of several markers of prediction of severity against a new, stringent definition of severity. METHODS: Patients with acute pancreatitis were recruited within 24 h of onset of symptoms. Urine and blood samples were collected for 24 h, and Acute Physiology And Chronic Health Evaluation (APACHE) II (24 h), Ranson (48 h) and Glasgow (48 h) scores were calculated. Severe acute pancreatitis was defined by the presence of a local complication or the presence of organ failure for more than 48 h. RESULTS: Urinary TAP levels were significantly greater in patients with severe pancreatitis than in those with mild disease during the first 36 h of admission. The highest of three estimations of TAP in the first 24 h was as effective as APACHE II at 24 h in predicting severity. At 24 h after admission, urinary TAP was better than C-reactive protein (CRP) in predicting severity. The combination of TAP and CRP at 24 h allowed identification of high- and low-risk groups. The new definition of severity excluded 24 of 190 patients with transient organ failure; none of these patients died. CONCLUSION: Use of TAP improved early prediction of the severity of acute pancreatitis. Organ failure that resolves within 48 h does not signify a severe attack of acute pancreatitis.

Plasma anti-inflammatory cytokines and monocyte human leucocyte antigen-DR expression in patients with acute pancreatitis.

BACKGROUND: 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. METHODS: 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. RESULTS: 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), P < 0.05 each. In the organ failure group, HLA-DR expression did not differ between survivors and non-survivors. CONCLUSIONS: 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.

Sequential changes in pancreatic markers in acute pancreatitis.

BACKGROUND: Trypsinogen activation within acinar cells plays a crucial role in the pathogenesis of acute pancreatitis (AP). Our aim was to characterize temporal changes of trypsinogen-1, trypsinogen-2, complexes of trypsin-1-alpha1-antitrypsin (T1-AAT) and trypsin-2-alpha1-antitrypsin (T2-AAT), trypsinogen activation peptide (TAP) and pancreatic secretory trypsin inhibitor (PSTI) in patients with AP. METHODS: The study comprised 64 consecutive patients with AP (19 with severe disease) and 32 controls. The concentrations of trypsinogen-1 and -2, PSTI, T1-AAT and T2-AAT were determined by time-resolved immunofluorometric assays (IFMA), and TAP was measured using a competitive enzyme immunoassay from serum and urine. RESULTS: The concentrations of trypsinogen-1 and -2 in serum reflected similar patterns, but excretion of trypsinogen-1 into urine was markedly lower than that of trypsinogen-2, the concentration of which correlated strongly with disease severity. The concentrations of T1-AAT were no higher in severe AP than in mild AP, while T2-AAT concentrations were significantly higher in severe than in mild disease. PSTI increased over the course of several days, showing strong correlation with disease severity. The concentrations of plasma and urinary TAP decreased rapidly to undetectable levels. During the early phase of AP, TAP correlated with the disease severity in plasma and urine but there was no difference between controls and patients with mild AP. CONCLUSION: More pronounced changes in trypsinogen-2 and its complex with AAT than in those of trypsinogen-1 were demonstrated, suggesting that trypsinogen-2 might play a more important role in the pathogenesis of AP than earlier believed. Urinary PSTI showed features warranting further investigations as a marker of disease severity.

Comparison of urine trypsinogen-2 test strip with serum lipase in the diagnosis of acute pancreatitis.

BACKGROUND/AIMS: The accuracy of a new rapid urinary trypsinogen-2 test strip (actim Pancreatitis) was compared with that of serum lipase for detection of acute pancreatitis in patients with acute abdominal pain. METHODOLOGY: A prospective study was conducted which consisted of 237 consecutive patients with acute abdominal pain admitted to the emergency unit at Helsinki University Central Hospital. The patients were tested on admission with the actim Pancreatitis test strip. Serum amylase, serum lipase, and urine trypsinogen-2 concentrations were also determined quantitatively. RESULTS: The actim Pancreatitis test strip result was positive in 27 out of 29 patients with acute pancreatitis (sensitivity 93%) and in 16 of 208 patients with non-pancreatic abdominal pain (specificity 92%). This was superior to that of serum lipase (sensitivity 79% and specificity 88%). With a cut-off > 3x the upper reference limit, the sensitivity of serum lipase was only 55% while the specificity was 99%. The high sensitivity for the actim Pancreatitis test strip resulted in a very high negative predictive value of 99%. All six patients with severe acute pancreatitis were detected by the dipstick. With a higher cut-off value (> 3x upper reference limit) for lipase, two patients with severe acute pancreatitis remained undetected. Combining the actim Pancreatitis dipstick with serum lipase a positive predictive value of 94% was obtained. CONCLUSIONS: Acute pancreatitis can be excluded with a higher probability with the actim Pancreatitis strip than with serum lipase determination, and therefore appears to be more suitable for screening of acute pancreatitis. With its high specificity with a cut-off > 3x the upper reference limit, serum lipase is suitable as a confirmatory test for pancreatitis when a positive dipstick result is obtained.

Serum amyloid A is a better early predictor of severity than C-reactive protein in acute pancreatitis.

BACKGROUND: Serum amyloid A (SAA) is an early and sensitive marker of the extent of tissue trauma and inflammation. The aim of this study was to compare the early prognostic accuracy of SAA with that of serum C-reactive protein (CRP) in acute pancreatitis. METHODS: In a prospective multicentre trial, plasma SAA and CRP levels were measured in patients with severe and mild acute pancreatitis, and in a control group with acute abdominal pain. Plasma samples were collected on admission and at 6-h intervals for 48 h, every 12 h between 48 and 72 h, then daily for 5 days. Plasma SAA was measured by a new enzyme-linked immunosorbent assay and CRP was measured by immunoturbidometry. RESULTS: There were 137 patients with mild and 35 with severe acute pancreatitis, and 74 control patients. SAA levels were significantly higher in patients with severe acute pancreatitis than in those with mild acute pancreatitis, on admission, at 24 h or less after symptom onset, and subsequently. Whereas plasma CRP concentration was also significantly higher in patients with severe acute pancreatitis on admission, it failed to distinguish mild from severe acute pancreatitis until 30-36 h after symptom onset. SAA levels predicted severity (sensitivity 67 per cent, specificity 70 per cent, negative predictive value 89 per cent, mean(s.d.) area under curve 0.7(0.05)) significantly better than CRP (57 per cent, 60 per cent, 84 per cent, 0.59(0.06) respectively) on admission (P = 0.02) and at 24 h following symptom onset (area under curve 0.65(0.09) versus 0.58(0.09) respectively; P < or = 0.02). CONCLUSION: Plasma SAA concentration is an early marker of severity in acute pancreatitis and is superior to CRP estimation on hospital admission and at 24 h or less after symptom onset. This study suggests that plasma SAA concentration is clinically useful, with the potential to replace CRP in the management of acute pancreatitis.

Predicting the severity of acute pancreatitis by rapid measurement of trypsinogen-2 in urine.

BACKGROUND: Early identification of patients at risk of developing a severe attack of acute pancreatitis (AP) is of great importance because rapid therapeutic interventions improve outcome. At a cutoff of 50 microg/L, trypsinogen-2 measured by a rapid urinary dipstick is a sensitive and specific diagnostic test in AP. The trypsinogen-2 concentration correlates with the severity of the disease, and a test with a higher cutoff might therefore be useful for prediction of disease severity. METHODS: We increased the detection limit of the urinary trypsinogen-2 test strip (Actim Pancreatitis) from 50 microg/L to 2000 microg/L and evaluated the prognostic value of this test. The results were compared with those obtained with serum C-reactive protein and the acute physiology and chronic health evaluation II (APACHE II) score. The study population consisted of 150 consecutive patients with AP (42 with severe disease). RESULTS: The sensitivity of the rapid urinary test strip (detection limit, 2000 microg/L) for prediction of severe AP, both on admission and at 24 h, was 62%; specificities were 87% and 85%, respectively, positive predictive values were 65% and 62%, and negative predictive values were 85% and 85%. C-Reactive protein had a sensitivity of only 38% on admission, but at 24 h, it was 83%; specificities were 90% and 70%, respectively, whereas positive predictive values were 59% and 52%, and NPVs were 79% and 91%, respectively. On admission the positive-likelihood ratio for the urinary trypsinogen-2 test strip was 4.8, and at 24 h it was 4.2; for C-reactive protein, the values were 3.7 and 2.7, respectively. CONCLUSIONS: The urinary trypsinogen-2 dipstick is a simple and rapid method for prediction of severe acute pancreatitis.

Expression of group II phospholipase A2 in the liver in acute pancreatitis.

BACKGROUND: A number of distinct secretory phospholipases A2 (PLA2) have been characterized in the human. Elevated group II PLA2 serum levels are associated with inflammatory diseases such as infections, septic shock, rheumatoid arthritis, multiple organ failure and acute pancreatitis. The cellular source of circulating group II PLA2 has not been defined unequivocally. The possible role of the liver as a source of circulating group II PLA2 in acute pancreatitis was studied using liver biopsies from five patients operated on for necrotizing acute pancreatitis and from two control liver samples. METHODS: Reverse transcription polymerase chain reaction (RT PCR), northern hybridization and in situ hybridization were used to study the expression of group II PLA2. Immunohistochemistry was used to study the localization of the group II PLA2 protein in liver cells and time-resolved fluoroimmunoassay to measure the plasma group II PLA2 content. RESULTS: Expression of group II PLA2 was found in the livers of patients with acute pancreatitis by RT PCR and confirmed by northern hybridization. Group II PLA2 mRNA was localized in hepatocytes by in situ hybridization. Faint immunopositivity was found in Kupffer cells. Time-resolved fluoroimmunoassay revealed elevated concentration of group II PLA2 in plasma samples. Only low levels of expression were found in the control livers. CONCLUSIONS: Group II PLA2 is expressed in the livers of patients suffering from acute pancreatitis but not in the livers of patients without pancreatic disease. The current results support the idea that hepatocytes are an important source of circulating group II PLA2 in inflammatory diseases.

Cellular markers of systemic inflammation and immune suppression in patients with organ failure due to severe acute pancreatitis.

BACKGROUND: 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. METHODS: 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. RESULTS: 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 trend <0.001). 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. CONCLUSIONS: 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.

A comparison of serum trypsinogen-2 and trypsin-2-alpha1-antitrypsin complex with lipase and amylase in the diagnosis and assessment of severity in the early phase of acute pancreatitis.

OBJECTIVE: The aim of the study was to compare the recently introduced laboratory markers trypsinogen-2 and trypsin-2-alpha1 antitrypsin complex (trypsin-2-AAT) in serum with lipase and amylase in the diagnostic and prognostic evaluation of patients with acute pancreatitis (AP). METHODS: The analytes were measured on admission in 64 consecutive patients with AP and in 30 controls with acute abdominal disease of extrapancreatic origin. Twenty-one patients had severe and 43 mild AP. As reference methods we used serum amylase and C-reactive protein. RESULTS: In subjects with AP, elevated trypsinogen-2 values (> or = 90 microg/L) were observed in 63 patients (98%), trypsin-2-AAT values (> or = 12 microg/L) in 64 patients (100%), lipase values (> or = 200 U/L) in 64 patients (100%), and amylase values (> or = 300 IU/L) in 62 patients (97%). The diagnostic accuracy of the markers was evaluated by receiver operating characteristic (ROC) analysis. On admission, trypsinogen-2, trypsin-2-AAT, lipase, and amylase differentiated patients with AP from controls with high accuracy and ROC analyses showed similar areas under the ROC curves (AUC) for trypsinogen-2 (AUC 0.960), trypsin-2-AAT (0.948), lipase (AUC 0.947), and amylase (AUC 0.930). For differentiation between severe and mild AP, trypsin-2-AAT (AUC 0.805) was slightly better than trypsinogen-2 (AUC 0.792), and they were both clearly better than lipase (AUC 0.583), C-reactive protein (AUC 0.519), or amylase (AUC 0.632) (p < 0.05). CONCLUSIONS: All the markers studied showed high accuracy for differentiating between AP and extrapancreatic diseases. However, trypsinogen-2 and trypsin-2-AAT displayed the best accuracy for predicting a severe AP already at admission, which makes these markers superior for clinical purposes.

Procalcitonin, soluble interleukin-2 receptor, and soluble E-selectin in predicting the severity of acute pancreatitis.

OBJECTIVE: To investigate whether marker(s) of systemic inflammation detect, at an early stage of acute pancreatitis, patients who may ultimately develop severe disease. DESIGN: Prospective study. SETTING: University hospital emergency unit. PATIENTS: Thirty patients with mild acute pancreatitis (SEV0 group) and 27 with severe acute pancreatitis. Of the latter, 11 did not develop organ failure (SEV1 group), whereas the other 16 patients developed acute respiratory failure and 9 of them also developed renal failure (SEV2 group). INTERVENTIONS: Blood samples were collected at admission to the hospital (T0), and at 12 hrs (T12) and 24 hrs (T24 after admission. MEASUREMENTS AND MAIN RESULTS: The plasma concentrations of procalcitonin (PCT), soluble E-selectin (sE-selectin), soluble interleukin-2 receptor (sIL-2R), and the serum concentration of C-reactive protein (CRP) were monitored. PCT levels at T0 were significantly higher in the SEV1 group (median 0.4 ng/mL, range 0.2-2.3) and the SEV2 group (0.8 ng/mL, 0.2-73.5) than in the SEV0 group (0.3 ng/mL, 0.1-3, p < .05 and p < .001, respectively). At T12, PCT level in the SEV2 group was significantly higher than that in the SEV1 group (2.2 ng/mL, 0.2-86.6 vs. 0.4 ng/mL, 0.3-2.8, p = .05), as it also was at T24 (2.2 ng/mL, 0.4-73.3 vs. 0.5 ng/mL, 0.3-4, p < .01). Among SEV2 patients, PCT concentration correlated negatively with the time elapsed between admission and the diagnosis of organ failure. At T12, sIL-2R levels of the SEV1 group (1,011 U/mL, range 334-2,211) and the SEV2 group (1,495 U/ml, range 514-4,526) both differed significantly from the SEV0 group (636 U/ml, range 356-1,678, p < .05 and p < .001, respectively) as they also did at T24. Although CRP level in the SEV1 group at T12 did not differ from the SEV0 group, the difference between SEV2 (272 microg/mL, range 46-462) and SEV0 was significant (53 microg/mL, range 5-243, p < 0.01). sE-selectin levels did not differ between groups. CONCLUSIONS: At admission to hospital, concentrations of PCT, but not those of CRP, sE-selectin, or sIL-2R, are higher in patients with severe acute pancreatitis than in patients with mild pancreatitis. PCT test had sensitivity of 94% and specificity of 73% for development of organ failure. PCT may be useful to identify the patients who benefit from novel therapies aimed at modifying the course of systemic inflammation.

Procalcitonin strip test in the early detection of severe acute pancreatitis.

BACKGROUND: Early identification of patients who subsequently develop severe acute pancreatitis would enable the selection of patients who may benefit from early intensive management. Because severe acute pancreatitis is characterized by the development of systemic inflammation the authors studied whether procalcitonin, a marker of systemic inflammation, differentiated between patients with mild and severe acute pancreatitis. METHODS: On admission and 24 h thereafter, serum procalcitonin level was measured by a rapid, semiquantitative PCT-Q test and serum C-reactive protein (CRP) by an immunoturbidimetric method in a consecutive series of 162 patients with acute pancreatitis. There were 38 severe and 124 mild cases. The accuracy of procalcitonin and CRP in predicting severe acute pancreatitis was compared with that of Ranson and Acute Physiology and Chronic Health Evaluation (APACHE) II scores. RESULTS: The PCT-Q test was more accurate in predicting severe acute pancreatitis (sensitivity 92 per cent and specificity 84 per cent at 24 h) than CRP, APACHE II score and Ranson score. Its negative predictive value was high (97 per cent at 24 h), and it detected each patient who developed subsequent organ failure (n = 22). CONCLUSION: The PCT-Q test was a useful screening method for detecting severe acute pancreatitis. It is simple and quick to perform and, unlike currently available multiple factor scoring systems, can easily be adopted into routine clinical practice.