Risk of mortality from cardiovascular and respiratory causes in patients with chronic obstructive pulmonary disease submitted to follow-up after lung resection for non-small cell lung cancer.

AIM: Considerable controversy surrounds mortality from non-neoplastic diseases during the postoperative follow-up of patients with non-small cell lung cancer (NSCLC) and chronic obstructive pulmonary disease (COPD). This study investigated the incidence of mortality from cardiovascular and respiratory (CVR) causes in patients with COPD submitted to follow-up after lung resection for NSCLC, and identified preoperative and postoperative risk factors. METHODS: A total of 398 patients with mild or moderate COPD were followed up in our department after lung resection for NSCLC (median follow-up 61 months). Statistical analysis of the data was carried out to determine the incidence and the prognostic factors of postoperative death from CVR causes. RESULTS: Of the 398 resected patients, 186 survived without tumor recurrence; 24/186 (12.9%) died of CVR causes (acute respiratory failure, pneumonia, pulmonary embolism, acute pulmonary edema, acute myocardial ischemia or stroke). These 24 patients had a higher frequency of pre-existing coronary artery disease or heart failure (P=0.0003), predicted postoperative FEV1 <1000 mL (P=0.0008), exertional dyspnea (P=0.0000), and 30-day operative cardiopulmonary complications (P=0.001). Protective features were young age (<40 years), early stage disease, and minor resection (lobectomy). Independently significant adverse prognostic factors were stage III-IV disease (cumulative CVR death rate 47% at 5-10 years; P=0.028 vs. stage I-II) and completion pneumonectomy or partial resection of the other lung for a second primary tumor (cumulative CVR death rate 50% and 57%, respectively, at 5-10 years; P=0.0016 vs. all other resections). Older age and tumor histology were significant risk factors only in patients with advanced stage disease. CONCLUSION: The findings suggest that postoperative CVR death may be expected in patients with COPD and advanced stage NSCLC or in those undergoing completion pneumonectomy or partial resection of the other lung for a second primary tumor. Other risk factors are previous coronary artery disease and/or heart failure, exertional dyspnea and predicted postoperative FEV1 <1000 mL.

Immunologic evidence of no harmful effect of oats in celiac disease.

BACKGROUND: It was recently shown that antiendomysial antibodies (EMAs), which are highly sensitive and specific for celiac disease, are produced by intestinal mucosa. Furthermore, EMAs were detected previously in supernatant fluid from cultured duodenal mucosa specimens collected from untreated celiac disease patients and in culture media of biopsy specimens collected from treated celiac disease patients after an in vitro challenge with gliadin. Moreover, it was recently shown in vivo that oats are not toxic to celiac disease patients, suggesting the safety of oats in a gluten free-diet. OBJECTIVE: The objective was to better define the controversial role of oats in celiac disease to determine whether oats can be safely included in a gluten-free diet. DESIGN: We used an in vitro model to test whether oats induce EMA production in supernatant fluid from cultured duodenal mucosa specimens collected from 13 treated celiac disease patients. The biopsy specimens were cultured with and without peptic-tryptic digest (PT) of gliadin and avenin (from oats) and in medium alone. Samples from 5 of the 13 patients were cultured with the C fraction of PT-avenin. Indirect immunofluorescence was used to detect EMAs. RESULTS: EMAs were detected in specimens from all 13 patients after the challenge with gliadin but not after culture in medium alone. By contrast, no EMAs were detected in any of the specimens cultured with PT-avenin and its C fraction. CONCLUSIONS: Because the in vitro challenge with PT-avenin and its C fraction did not induce EMA production in treated celiac disease patients, it appears that oats have no harmful effect on celiac disease. Therefore, oats can be safely included in a gluten-free diet.

Identification of a new coeliac disease subgroup: antiendomysial and anti-transglutaminase antibodies of IgG class in the absence of selective IgA deficiency.

OBJECTIVE: The aim of the present study was to increase the sensitivity of the antiendomysial antibody (EMA) test by evaluating also EMAs of IgG1 isotype. DESIGN AND SUBJECTS: Over the last 2 years, serum EMAs IgA and IgG1 were determined in 1399 patients, referred to our gastrointestinal unit due to clinical suspicion of malabsorption. Serum anti-tissue transglutaminase (tTG) antibodies IgA and IgG, as well as total IgA levels, were also investigated. Furthermore, EMAs IgA and IgG1 were evaluated in biopsy culture supernatants. Biopsy specimens were also admitted to histological and immunohistochemical evaluation. Twenty-six patients with gastroenterological disease other than coeliac disease (CD) were used as a disease control group. Ninety-nine blood donors were used as a healthy control group. RESULTS: Diagnosis of CD was based on histological findings in the 110/1399 patients showing EMA IgA positivity, and in a further 56/1399 patients presenting both EMA IgA and IgG1 positivity in sera as well as in culture supernatants. Of the remaining 1233 EMA IgA-negative patients, 60 showed only EMA IgG1 positivity both in sera and in culture supernatants. It is noteworthy that anti-tissue transglutaminase antibodies IgG (anti-tTG) were positive in all 60 EMA IgG1-positive patients as well. By contrast, a selective IgA deficiency was found in only 11 out of the 60 EMA IgG1-positive patients. Villous height/crypt depth ratio was < 3:1 in 38 of the 60 EMA IgG1-positive patients (63.3%), whilst overexpression of ICAM-1 and CD25 was observed in all these patients. CONCLUSIONS: In this study, we observed a group of CD patients who were EMA IgG1-positive even in the absence of EMA IgA positivity and IgA deficiency. The diagnosis was based on the finding of the gluten-dependent clinical and histological features typical of CD. Data emerging from the present investigation thus suggest that the prevalence of CD should be reassessed and that the determination of EMA IgG1 could offer a new tool in the diagnostic armamentarium of CD.