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Biomedical subjects

E Kemppainen

Publications and source records attributed to E Kemppainen.

At least 19 recordsLinked to original sources
PubMed2006

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.

Abdominal Abscess↗
PubMed2005

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.

Abdominal Cavity↗
PubMed2005

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.

APACHE↗
PubMed2005

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.

Acute Disease↗
PubMed2005

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.

Acute Disease↗
PubMed2004

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.

APACHE↗
PubMed2004

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.

Acute Disease↗
PubMed2004

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.

Aged↗
PubMed2003

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.

Acute Disease↗
PubMed2002

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.

Abdominal Pain↗
PubMed2001

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.

Acute Disease↗
PubMed2001

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.

Acute Disease↗
PubMed2001

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.

Acute Disease↗
PubMed2001

The ratio of trypsin-2-alpha(1)-antitrypsin to trypsinogen-1 discriminates biliary and alcohol-induced acute pancreatitis.

BACKGROUND: Rapid determination of the etiology of acute pancreatitis (AP) enables institution of appropriate treatment. We evaluated the ability of trypsinogen-1, trypsinogen-2, trypsin-1-alpha(1)-antitrypsin (AAT), and trypsin-2-AAT in serum to identify the etiology of AP. METHODS: The study consisted of 67 consecutive patients with AP admitted to Helsinki University Central Hospital. Forty-two had alcohol-induced AP, 16 had biliary AP, and 9 had unexplained etiology. Serum samples were drawn within 12 h after admission. Trypsinogen-1, trypsinogen-2, trypsin-1-AAT, and trypsin-2-AAT were determined by time-resolved immunofluorometric assays. Logistic regression was used to estimate the ability of the serum analytes to discriminate between alcohol-induced and biliary AP. The validity of the tests was evaluated by ROC curve analysis. RESULTS: Patients with alcohol-induced AP had higher median values of trypsin-1-AAT (P = 0.065), trypsinogen-2 (P = 0.034), and trypsin-2-AAT (P <0.001) than those with biliary AP, who had higher values of amylase (P = 0.002), lipase (P = 0.012), and alanine aminotransferase (P = 0.036). The ratios of trypsin-2-AAT to trypsinogen-1, lipase, or amylase efficiently discriminated between biliary and alcohol-induced AP (areas under ROC curves, 0.92-0.96). CONCLUSIONS: Trypsinogen-2 and trypsin-2-AAT are markedly increased in AP of all etiologies, whereas trypsinogen-1 is increased preferentially in biliary AP. The trypsin-2-AAT/trypsinogen-1 ratio is a promising new marker for discrimination between biliary and alcohol-induced AP.

Acute Disease↗
PubMed2001

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.

Acute Disease↗
PubMed2000

Fatal cardiac tamponade after emergency tension-free repair of a large paraesophageal hernia.

Paraesophageal hernia is an unusual disorder of the esophageal hiatus that may be associated with life-threatening mechanical problems. We report a case of a large paraesophageal hernia that presented with acute thoracic herniation and incarceration of the stomach. The patient underwent laparoscopic operation, including reduction of an intrathoracic stomach, hernial sac removal, and tension-free repair of the hiatus with polytetrafluoroethylene (PTFE) mesh. The mesh was fixed with a straight hernia stapler. Postoperatively the patient developed a fatal cardiac tamponade secondary to a coronary vein laceration due to fixation of the mesh with the stapler. Different operative techniques and possibilities for prevention of the complication are discussed.

Aged↗
PubMed2000

Detection of severe acute pancreatitis by contrast-enhanced magnetic resonance imaging.

The aim of the study was to assess the ability of MRI to differentiate between the two forms of severity of acute pancreatitis (AP), which is important for the detection of patients who require intensive monitoring and therapy. The second objective was to evaluate whether the distinction would be possible regardless of the MRI equipment. Magnetic resonance imaging was performed before and after intravenous administration of a gadolinium (Gd) chelate at 1.0 T using the breath-hold multislice rapid gradient-echo turbo fast low-angle shot (FLASH) sequence in 14 patients, and at 1.5 T with the 2D FLASH(50) sequence with fat saturation in 18 patients with acute pancreatitis early in the course of the disease. The patients were classified according to the Atlanta classification system as having the mild (MAP) or severe (SAP) form of the disease. At 1.0 T with use of a body coil, contrast-enhanced MRI failed to distinguish mild from severe pancreatitis. At 1.5 T with a phased-array body coil, the signal intensities of the patients with SAP were statistically significantly lower than those of the MAP group. Our initial clinical experience suggests that MRI with a sufficient magnetic field gradient strength may be useful for separating the two forms of acute pancreatitis in their early phases.

Acute Disease↗