Exercise-induced anaphylaxis (EIA) and food-dependent, exercise-induced anaphylaxis (FDEIA) are rare but potentially life-threatening clinical syndromes in which association with exercise is crucial. The range of triggering physical activities is broad, including as mild an effort as a stroll. EIA is not fully repeatable (ie, the same exercise may not always result in anaphylaxis in a given patient). In FDEIA, the combined ingestion of sensitizing food and exercise is necessary to precipitate symptoms. Clinical features and management do not differ significantly from other types of anaphylaxis. The pathophysiology of EIA and FDEIA is not fully understood. Different hypotheses concerning the possible influence of exercise on the development of anaphylactic symptoms are taken into consideration. These include increased gastrointestinal permeability, blood flow redistribution, and most likely increased osmolality. This article also describes current diagnostic and therapeutic possibilities, including changes in lifestyle and preventive properties of antiallergic drugs as well as acute treatment of these dangerous syndromes.

Alternaria alternata is mainly an outdoor fungus whose spores disseminate in warm, dry air, so in temperate climates, their count peaks in the summers. Alternaria may also be found in damp, insufficiently ventilated houses, where its allergenic properties cocreate the sick building syndrome. Mold-induced respiratory allergies and research on Alternaria both have a lengthy history: the first was described as early as 1698 and the second dates back to 1817. However, the two were only linked in 1930 when Alternaria spores were found to cause allergic asthma. The allergenic extracts from Alternaria hyphae and spores still remain in use but are variable and insufficiently standardized as they are often a random mixture of allergenic ingredients and coincidental impurities. In contrast, contemporary biochemistry and molecular biology make it possible to obtain pure allergen molecules. To date, 16 allergens of A. alternata have been isolated, many of which are enzymes: Alt a 4 (disulfide isomerase), Alt a 6 (enolase), Alt a 8 (mannitol dehydrogenase), Alt a 10 (alcohol dehydrogenase), Alt a 13 (glutathione-S-transferase), and Alt a MnSOD (Mn superoxide dismutase). Others have structural and regulatory functions: Alt a 5 and Alt a 12 comprise the structure of large ribosomal subunits and mediate translation, Alt a 3 is a molecular chaperone, Alt a 7 regulates transcription, Alt a NTF2 facilitates protein import into the nucleus, and Alt a TCTP acts like a cytokine. The function of four allergenic proteins, Alt a 1, Alt a 2, Alt a 9, and Alt a 70 kDa, remains unknown.

One of the theories which explain, why gastroesophageal reflux disease (GORD) may provoke cough, is the occurrence of aspiration of gastric content into the airways. The aim of the study was to assess the presence of aspiration markers: pepsin and bile acids (BA) in induced sputum in gastroesophageal reflux-related (GOR-related) chronic cough (CC) patients. Forty-one CC patients and 20 healthy controls were enrolled in the study. GORD as cause of CC was diagnosed by presence of GORD-related symptoms, gastroscopy and/or improvement of cough upon treatment with proton pump inhibitors (PPI). Patients were divided into two groups based on the response to PPI treatment. In all patients and healthy controls induced sputum was obtained and differential cell counts were calculated. Levels of pepsin and BA were measured in sputum supernatants. Pepsin was detectable in 48.8% samples in CC patients and in 60% healthy controls (p = NS). In pepsin positive samples no significant difference in pepsin concentration could be found between CC patients and control subjects. Pepsin levels in pepsin positive samples were significantly decreased in patients treated with PPI compared to non-treated patients. BA were detectable in 56% samples of CC patients and in 70% healthy controls (p = NS). BA concentration in BA positive samples in CC group was not different from healthy controls. There was also no difference when comparing patients who took PPI and those who did not. Patients characterized as PPI-responders and PPI-non-responders had similar pepsin and BA concentrations. Airway cellularity was not significantly different between groups of patients with or without pepsin or BA in induced sputum. Our results demonstrated the lack of differences in gastric content aspiration between patients with probable GOR-related CC and healthy control subjects. This might imply that the reflex cough theory may be more relevant than the reflux-associated aspiration theory in the pathophysiology of GORinduced chronic cough.

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