Association of FcγRIIa R131H polymorphism with idiopathic pulmonary fibrosis severity and progression

<p>Abstract</p> <p>Background</p> <p>A significant genetic component has been described for idiopathic pulmonary fibrosis (IPF). The R131H (rs1801274) polymorphism of the IgG receptor FcγRIIa determines receptor affinity for IgG subclasses and is associated with several chronic inflammatory diseases. We investigated whether this polymorphism is associated with IPF susceptibility or progression.</p> <p>Methods</p> <p>In a case-control study, we compared the distribution of FcγRIIa R131H genotypes in 142 patients with IPF and in 218 controls using allele-specific PCR amplification.</p> <p>Results</p> <p>No differences in the frequency of FcγRIIa genotypes were evident between IPF patients and control subjects. However, significantly impaired pulmonary function at diagnosis was observed in HH compared to RR homozygotes, with evidence of more severe restriction (reduced forced vital capacity (FVC)) and lower diffusing capacity for carbon monoxide (D<smcaps>L</smcaps>_CO). Similarly, increased frequency of the H131 allele was observed in patients with severe disease (D<smcaps>L</smcaps>_CO< 40% predicted) (0.53 vs. 0.38; p = 0.03). Furthermore, the H131 allele was associated with progressive pulmonary fibrosis as determined by > 10% drop in FVC and/or > 15% fall in D<smcaps>L</smcaps>_COat 12 months after baseline (0.48 vs. 0.33; p = 0.023).</p> <p>Conclusions</p> <p>These findings support an association between the FcγRIIa R131H polymorphism and IPF severity and progression, supporting the involvement of immunological mechanisms in IPF pathogenesis.</p

EOSINOPHILIC ESOPHAGITIS AFTER SPECIFIC ORAL TOLERANCE INDUCTION (SOTI) FOR EGG PROTEIN: A CASE REPORT

Eosinophilic Esophagitis (EE) is an emerging condition where patients commonly show symptoms of gastroesophageal reflux disease and fail to react to anti-reflux therapy. Food allergy is currently recognized as the main immunological cause of EE but it also associated with other atopic illnesses. The standard treatment of food allergy is removal of incriminated foods from diet. This approach could appear problematic expecially for some foods, such as hen’s egg (HE), since they are widely used in processed foods. Specific Oral Tolerance Induction (SOTI) seems to be an alternative promising approach for a causal treatment; it can be induced by oral administration of the offending food, starting with very low dosages, gradually increasing towards a level equivalent to a usually relevant dose for a daily intake. Up to now, it is uncertain whether the tolerance achieved is transient or persistent. SOTI’s pros are the safety for an unintentional intake of the offending food and the increased Quality of Life, SOTI’s cons are the requirement for a regular intake and the potential negative impact in the long run. Our findings show: 1) a more complex or mixed allergic mechanism for EE, pointing to the need to evaluate for non IgE mediated allergies. 2) that it is possible that SOTI does not alter the natural outcome of food allergy but substantially increases the threshold dose necessary to elicit allergic symptoms resulting in clinical tolerance and this phenomenon depends on a number of variables, such as the patient’s individual course of disease. 3) when a patient with a history of severe food allergy begins a SOTI, they might be observed not only for allergic side effects but also for the onset of eosinophilic esophagitis. 4) the dosage of IgG4 specific for HE before and after SOTI would be an useful tool to evaluate the achivement of tolleranc