Search

Background Diagnosis and curative treatment of cholangiocarcinoma (CC) often comes too late due to the lack of reliable tumour markers especially in patients with primary sclerosing cholangitis (PSC). The authors recently introduced bile proteomic analysis for CC diagnosis. Nevertheless, bile collection depends on invasive endoscopic retrograde cholangiography. The authors therefore evaluated urine proteomic analysis for non-invasive CC diagnosis. Methods Using capillary electrophoresis mass spectrometry the authors established a CC-specific peptide marker model based on the distribution of 42 peptides in 14 CC, 13 PSC and 14 benign biliary disorder (BBD) patients. Results In cross-sectional validation of 123 patients, the urine peptide marker model correctly classified 35 of 42 CC patients and 64 of 81 PSC and BBD patients with an area under the curve value of 0.87 (95% CI 0.80 to 0.92, p=0.0001, 83% sensitivity, 79% specificity). Evaluation of 101 normal controls resulted in 86% specificity. All 10 patients with CC on top of PSC were correctly classified. The majority of sequence-identified peptides are fragments of interstitial collagens with some of them also detected in blood indicating their extra-renal origin. Immunostaining of liver sections for matrix metallopeptidase 1 indicated increased activity of the interstitial collagenase in liver epithelial cells of CC patients. Conclusion The urine test differentiates CC from PSC and other BBD and may provide a new diagnostic non-invasive tool for PSC surveillance and CC detection.

A longterm review (median follow up 11 years) of the postoperative course of pancreatic pseudocysts was undertaken in 55 patients with chronic pancreatitis. While 96% of the patients were free of pain immediately after the operation this figure fell to 53% subsequently. Alcohol abstinence did not significantly reduce pain. Endocrine pancreatic deterioration (60%) was significantly (p = 0.0059) more frequent than exocrine (38%). Unemployment increased from 2 to 41%; retirement rose from 0 to 33%, mainly as a result of pancreatitis. Twenty one (38%) patients died. Chronic pancreatitis related death rate was 14%. Three patients died of extrapancreatic carcinomas.

BACKGROUNDIn most treatment studies on acute pancreatitis, pancreatologists base their diagnosis on amylase/lipase levels more than three times above the upper limit of normal (>3n) and thus exclude patients with smaller enzyme level increases. The recommendations derived from the results of treatment studies do not take into account such patients. Non-pancreatologists frequently believe that only patients with high enzyme levels have a serious prognosis.AIMSTo question the assumption that high enzyme levels indicate severe, and conversely low enzyme levels indicate mild, acute pancreatitis.PATIENTS/METHODSThis retrospective study includes 284 consecutive patients with a first attack of acute pancreatitis. The cause was biliary in 114 (40%) patients, alcoholism in 83 (29%), other in 21 (7%), and unknown in 66 (23%). Patients were divided into two groups according to their serum enzyme levels (amylase: ⩽3n, n = 88; >3n, n = 196; lipase: ⩽3n, n = 51; >3n, n = 233). Renal impairment, indication for dialysis and artificial ventilation, development of pseudocysts, necessity for surgery, and mortality were taken as parameters of severity.RESULTSThe incidence of severity was the same for both the ⩽3n and >3n groups.CONCLUSIONSThe severity of acute pancreatitis is independent of the elevation in serum amylase/lipase level (⩽3n or >3n) on admission. Patients with only a slight increase can also have or develop severe acute pancreatitis. Patients with ⩽3n elevated enzyme levels on admission represent a substantial group that treatment studies have frequently overlooked. This is especially true for patients with alcohol induced acute pancreatitis whose amylase levels are lower than in other aetiological groups.

Background: Smoking is a recognised risk factor for pancreatic cancer and has been associated with chronic pancreatitis and also with type II diabetes. Aims: The aim of this study was to investigate the effect of tobacco on the age of diagnosis of pancreatitis and progression of disease, as measured by the appearance of calcification and diabetes. Patients: We used data from a retrospective cohort of 934 patients with chronic alcoholic pancreatitis where information on smoking was available, who were diagnosed and followed in clinical centres in five countries. Methods: We compared age at diagnosis of pancreatitis in smokers versus non-smokers, and used the Cox proportional hazards model to evaluate the effects of tobacco on the development of calcification and diabetes, after adjustment for age, sex, centre, and alcohol consumption. Results: The diagnosis of pancreatitis was made, on average, 4.7 years earlier in smokers than in non-smokers (p = 0.001). Tobacco smoking increased significantly the risk of pancreatic calcifications (hazard ratio (HR) 4.9 (95% confidence interval (CI) 2.3–10.5) for smokers v non-smokers) and to a lesser extent the risk of diabetes (HR 2.3 (95% CI 1.2–4.2)) during the course of pancreatitis. Conclusions: In this study, tobacco smoking was associated with earlier diagnosis of chronic alcoholic pancreatitis and with the appearance of calcifications and diabetes, independent of alcohol consumption.

To determine the incidence and severity of drug induced acute pancreatitis, data from 45 German centres of gastroenterology were evaluated. Among 1613 patients treated for acute pancreatitis in 1993, drug induced acute pancreatitis was diagnosed in 22 patients (incidence 1.4%). Drugs held responsible were azathioprine, mesalazine/sulfasalazine, 2',3'-dideoxyinosine (ddI), oestrogens, frusemide, hydrochlorothiazide, and rifampicin. Pancreatic necrosis not exceeding 33% of the organ was found on ultrasonography or computed tomography, or both, in three patients (14%). Pancreatic pseudocysts did not occur. A decrease of arterial PO2 reflecting respiratory insufficiency, and an increase of serum creatinine, reflecting renal insufficiency as complications of acute pancreatitis were seen in two (9%) and four (18%) patients, respectively. Artificial ventilation was not needed, and dialysis was necessary in only one (5%) case. Two patients (9%) died of AIDS and tuberculosis, respectively; pancreatitis did not seem to have contributed materially to their death. In conclusion, drugs rarely cause acute pancreatitis, and drug induced acute pancreatitis usually runs a benign course.

Editor,—I read with interest the recent paper by Lankisch et al ( Gut 1998; 42 :551–4). The authors studied faecal elastase 1 and faecal chymotrypsin in 30 patients with chronic pancreatitis and concluded that the estimation of faecal elastase 1 is not helpful in diagnosing mild and moderate exocrine pancreatic insufficiency and that this enzyme is not superior to faecal chymotrypsin in the diagnosis of exocrine pancreatic insufficiency. As various studies have already been published on this subject, I believe that it is useful to report the results of these studies, mainly because they clearly show that Lankisch et al ’s conclusions cannot be substantiated. Dominguez-Munoz and colleagues,1 in 20 patients with chronic pancreatitis (six mild, four moderate and 10 severe), found that the sensitivity of faecal elastase 1 was 0%, 100% and 100%, and that of faecal chymotrypsin 0%, 75% and 70%, in the three groups, respectively. Glasbrenner and colleagues2 studied 63 patients with chronic pancreatitis (19 mild, 14 moderate and 30 severe) and found that faecal elastase 1 had a sensitivity of 47%, 79% and 100%, and faecal chymotrypsin a sensitivity of 32%, 36% and 63%, respectively. Loser et al ,3 in 44 patients with …

Because somatostatin (SRIF) reduces exocrine pancreatic secretion, its effect on acute pancreatitis was investigated in rats. Linear SRIF reduced serum amylase and lipase but had no effect on pancreatic necrosis, oedema, leucocyte infiltration, and enzyme content. The mortality rate was not reduced. These results do not recommend the use of SRIF in the treatment of acute pancreatitis.