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Wheat-dependent exercise-induced anaphylaxis (WDEIA) is a special form of adult food allergy when allergic symptoms are elicited when triggering factor such as exercise is added after ingestion of wheat. Besides the molecular characteristics of wheat proteins, the gastric function is decisive for the allergenic potential. Alterations in the gastric milieu are frequently experienced during a lifetime either physiologically or as a result of gastrointestinal pathologies. Helicobacter pyloriinfection can lead to hypoacidity and enhance the sensitization risk for food allergens in adults. Gastric transit of food proteins and alterations in the gastric secretion can be disturbed after bariatric surgery such as the laparoscopic adjustable gastric binding (LAGB) procedure used commonly as therapy for morbid obesity. We report a case of WDEIA in a 42-year-old man with H. pyloripositive gastritis, 2 years after bariatric surgery and no history of allergy previously. Our presented case strongly suggests that H. pylori-associated gastritis and gastric anatomy and functional changes after adjustable gastric banding lead to the alterations in gastric milieu and may contribute to a development of food allergy in previously non-sensitized patients.

Smoking is the main risk factor for the development of chronic obstructive pulmonary disease (COPD) that has been recently defined as a systemic pulmonary inflammatory disease. However, the impact of smoking itself on systemic inflammation in COPD patients has not yet been well established. The aim of our study was to investigate the association between inflammatory markers and smoking status. We compared 202 current smokers, 61 ex-smokers and 57 never-smokers, all COPD patients. Assessments included medical history, spirometry, alpha-1 antitrypsin (AAT) genotyping, serum AAT, C-reactive protein (CRP), tumor necrosis factor (TNF)-α, and soluble tumor necrosis factor receptor (sTNFR)-1 and sTNFR-2 concentrations. AAT and CRP concentrations in smokers (1.75 ± 0.51 g/L and 14.4 [9.5-20.5] mg/L) and ex-smokers (1.69 ± 0.43 g/L and 12.3 [8.7-16.3] mg/L) were higher than in never-smokers (1.49 ± 0.38 g/L and 5.1 [2.5-8.7] mg/L; p < 0.05). sTNFR-1 level was higher in smokers than ex-smokers or never-smokers (241.2 pg/mL [145.3-349.4] vs. 213.7 pg/mL [147.1-280.3] and 205.2 pg/mL [125-275]; p < 0.05). Our data confirm that smoking is associated with increased levels of AAT, CRP, and sTNFR-1 in COPD patients, an array of systemic inflammation markers that continue to be active even after smoking cessation. Il fumo è la principale causa della broncopneumopatia cronica ostruttiva (BPCO), patologia che è stata recentemente definita come una malattia infiammatoria sistemica. Tuttavia, i dati relativi all'influenza del fumo sull’infiammazione sistemica per i malati di BPCO non sono sufficienti. Scopo della ricerca è quello di stabilire i collegamenti tra i marcatori dell'infiammazione e l'abitudine al fumo. Sono stati presi in esame 320 malati di BPCO: 202 fumatori, 61 ex fumatori, 57 non fumatori. Sono stati valutati: anamnesi, spirometria, genotipo di alfa-1 antitripsina (AAT), concentrazioni seriche di AAT, proteina C reattiva (CRP), fattore di necrosi tumorale alfa (TNF-α) e delle frazioni solubili dei recettori per il fattore di necrosi tumorale (sTNFR-1, sTNFR-2). I livelli di AAT e di CRP dei fumatori (1,75 ± 0,51 g/l e 14,4 mg/l [9,5–20,5]) e negli ex-fumatori (1,69 ± 0,43 g/l e 12,3 mg/l [8,7–16,3]) sono risultati più alti dei non fumatori (1,49 ± 0,38 g/l e 5,1 mg/l [2,5–8,7]; p < 0,05). I livelli di TNFR-1 sono risultati più alti nei fumatori rispetto agli ex-fumatori e ai non fumatori (241,2 pg/ml [145,3–349,4] versus 213,7 pg/ml [147,1–280,3] e 205,2 pg/ml [125–275]; p < 0,05). L’aumento delle concentrazioni di AAT e CRP nel siero dei pazienti fumatori ed ex-fumatori con BPCO, rispetto ai non fumatori, indica che l’infiammazione sistemica si prolunga anche dopo la cessazione del fumo, anche se le concentrazioni di sTNFR risultano inferiori dopo la cessazione.