The risks of pancreatic and nonpancreatic cancers are increased in the course of chronic pancreatitis, the former being significantly higher than the latter. The very high incidence of pancreatic cancer in smokers probably suggests that, in addition to cigarette smoking, some other factor linked to chronic inflammation of the pancreas may be responsible for the increased risk.

The role of cigarette smoking and diabetes mellitus as risk factors for exocrine pancreatic cancer (PC) was investigated in a hospital based case-control study. Current smokers were at increased risk for PC (OR = 2.36, 95% CI 1.53-3.63): the magnitude of the risk was related to the lifetime amount of smoking (chi2(trend) = 17.00; P < 0.0001). Among former smokers, after 15 years from ceasing smoking, the risk for PC dropped to the level of a lifetime non-smoker, whichever the lifetime smoking amount. Diabetes was associated with a 2.89-fold increased risk for PC (95% CI 1.71-4.86): the risk was 4.76 (95% CI 1.99-11.53) for diabetes diagnosed up to 2 years before the diagnosis of PC and dropped to 2.07 (95% CI 1.02-4.20) for diabetes diagnosed more than 5 years before PC. The risk for PC was estimated according to the treatment used to control diabetes: it was 6.49 (95% CI 2.28-18.48) for insulin treated diabetes and 2.12 (95% CI 1.16-3.87) for diabetes treated with oral hypoglycemic drugs. The risk of PC for diabetes treated for more than 5 years before the diagnosis of PC was 6.21 (95% CI 1.61-23.96) for patients treated with insulin and 1.21 (95% CI 0.50-2.92) for those treated with oral hypoglycemic drugs: the type of treatment needed to control the disease may discriminate between the diabetes that represents a consequence of cancer from the diabetes that could represent an etiological co-factor. More studies are needed to clarify whether long-lasting insulin-treated diabetes is an etiological co-factor in PC.

The aim of this study was to clarify the influence of gastroesophageal reflux (GER) on cough threshold in patients with digestive symptoms but free from respiratory involvement. Of 57 consecutive subjects referred for 24-h esophageal pH monitoring because of digestive reflux symptoms, 29 patients free from respiratory disorders were studied. They underwent esophageal pH monitoring and manometry, upper gastrointestinal endoscopy, pulmonary function tests, and methacholine and capsaicin challenges. The methacholine test was performed by inhalation of increasing doses of methacholine up to 4,000 micrograms; the results were expressed as the dose causing a 20% decrease in FEV1 from baseline (PD20). The capsaicin threshold was evaluated by inhalation of increasing doses of capsaicin from 0.3 up to 9.84 nmol, expressing the results as the dose of capsaicin eliciting five coughs (PD5). Fifteen patients were considered refluxers on the basis of a total esophageal acid exposure time above 4.7%. Esophagitis grade 0 was found in 15 patients, grade 1 in seven patients, grade 2 in seven patients. PD5 was significantly lower in refluxers (median 0.51 micrograms, range 0.22 to 19.8) than in nonrefluxers (19.8 micrograms, range 0.31 to 19.8) (p < 0.001); there was no difference in baseline ventilatory parameters and in airway responsiveness to methacholine between the two groups. All patients with a pathologic acid exposure time but one had a low cough threshold, irrespective of the presence or absence of esophagitis.(ABSTRACT TRUNCATED AT 250 WORDS)

This long-term follow-up of 27 patients treated with conservative surgery for necrohemorrhagic pancreatitis (NHP) showed that an almost complete recovery of the exocrine function is achieved within 4 years after discharge, while about half of the patients presented still abnormal endocrine function. The morphological sequelae, pointed out by endoscopic retrograde pancreatography in almost 50% of the cases, remained unchanged during the follow-up period. Therefore, these data seem to exclude an evolution of NHP towards chronic pancreatitis.

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