The risk of pancreatic cancer is significantly elevated in subjects with chronic pancreatitis and appears to be independent of sex, country, and type of pancreatitis.
This article deals with cystic echinococcosis (CE) and alveolar echinococcosis in humans caused by the cestode parasites Echinococcus granulosus and Echinococcus multilocularis. The life cycles of these parasites and their epidemiologic aspects are briefly discussed, and a detailed review is presented on clinical aspects of the diseases, including diagnosis and therapy. Considerable progress has been made in chemotherapy but the results are not yet satisfactory. A new alternative for treatment of CE is puncture of cysts, aspiration of fluid, injection of ethanol, and reaspiration of fluid (PAIR).
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 nonsmokers (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.
Chronic pancreatitis is a common inflammatory disease of the pancreas. Mutations in the genes encoding cationic trypsinogen (PRSS1) and the pancreatic secretory trypsin inhibitor (SPINK1) are associated with chronic pancreatitis. Because increased proteolytic activity owing to mutated PRSS1 enhances the risk for chronic pancreatitis, mutations in the gene encoding anionic trypsinogen (PRSS2) may also predispose to disease. Here we analyzed PRSS2 in individuals with chronic pancreatitis and controls and found, to our surprise, that a variant of codon 191 (G191R) is overrepresented in control subjects: G191R was present in 220/6,459 (3.4%) controls but in only 32/2,466 (1.3%) affected individuals (odds ratio 0.37; P = 1.1 x 10(-8)). Upon activation by enterokinase or trypsin, purified recombinant G191R protein showed a complete loss of trypsin activity owing to the introduction of a new tryptic cleavage site that renders the enzyme hypersensitive to autocatalytic proteolysis. In conclusion, the G191R variant of PRSS2 mitigates intrapancreatic trypsin activity and thereby protects against chronic pancreatitis.
To the Editor: I have several concerns about the metaanalysis by Dr Gould and colleagues 1 about positron emission tomography (PET) imaging for diagnosis of pulmonary nodules. First, the prevalence of malignancy in the articles that they included was extremely high (55%-100%; mean, 72%), suggesting that the types of lesions that have been evaluated thus far with PET imaging are those with a very high likelihood of malignancy. The accuracy of PET imaging may be far lower in a population in whom the risk of malignancy is lower. The sensitivity might be lower because of a milder spectrum of disease in patients with a lower risk of malignancy, and the specificity might be lower because of more overlapping PET findings in small lesions of varying etiologies. 2 Thus, the results of their review are only applicable to a population of patients with a very high prevalence of cancer. Until additional studies provide evidence that PET imaging is accurate in a population with a low prevalence of cancer, it is premature to suggest application of PET imaging in this group, as the authors have done.Second, Gould et al did not sufficiently address the issue of heterogeneity of the different studies in their meta-analysis. The data appear fairly consistent with respect to sensitivity but appear extremely variable with respect to specificity, and it is not appropriate to average the specificity estimates when the results are so inconsistent. While I believe that specificity is less important if patients would otherwise proceed to surgery in the absence of PET imaging, if PET imaging were applied to a low-risk population as the authors suggest, the false-positive rate would become quite important.Finally, the authors apply receiver operating characteristic (ROC) curve methods to the data, but it does not appear that the different accuracy reported by the different studies has much to do with threshold differences. Was there truly a significant correlation between the sensitivity and the false-positive rate? I would guess that sorting the studies in Figure 1 by sensitivity would not show an inverse relationship between sensitivity and specificity but rather would confirm that there is simply a lot of heterogeneity with respect to specificity. ROC curve methodology is complex and difficult to understand, and I think it is best used to compare the results of more than 1 test. In this case, the ROC curve does not provide accurate information for the clinician who would like to know what performance they can hope to obtain from this test. It seems clear that the sensitivity of PET imaging (in a high-risk population) is high but that the specificity is more difficult to estimate.
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