Clinical evidence linking allergy to increased risk of
middle ear inflammation
From a clinical point of view, it is extremely important to distinguish
among different phenotypes of otitis media, AOM, RAOM and OME. Clinical
evidence from the literature seems to be in favor of an association
between allergic rhinitis/atopic status and OME; whereas results about a
hypothetical correlation with AOM and RAOM are contradictory and
inconclusive because one of the major critical points is that some
authors fail to distinguish among the different phenotypes of middle ear
inflammation in children (articles included in the qualitative analyses
are reported in table 2). Salah et al. did not find evidence linking
atopy or allergy to AOM/RAOM26, whereas other
authors10, 27, 28 demonstrated that children with AR
had a significantly higher risk of otitis, even if they did not
distinguish among different phenotypes of OM. Accordingly,
authors29,30 demonstrated that atopic children may
have a significantly increased risk of recurrent or persistent OM
needing repeated tympanostomy tube insertions without distinguishing
between AOM and OME. Finally, in a recent study authors demonstrated
that RAOM was significantly associated with turbinate hypertrophy in
children suffering from allergic rhinitis.31
On the other hands most authors seem to be in agreement with
experimental data confirming also a significant clinical association
between allergy and OME. Several manuscripts32-35suggested that AR may specifically influence the onset of OME. Authors
demonstrated that AR prevalence was notably higher among OME patients
than in the controls, with remarkable differences in eosinophil counts
and serum IgE concentrations in the allergic rhinitis patients, compared
to other OME patients.36 Cheng et al. in a metanalysis
including cross-sectional and case-controlled studies confirmed that OME
and AR are prevalent in pre-school and school-aged children and that
allergy is a risk factor for OME.32Roditi et al.
interestingly demonstrated that allergic rhinitis was significantly
associated to OME even age was demonstrated as an effect modifier of the
association; indeed a significant relationship was observed in children
6 years of age and older, whereas there was no significant association
in younger children.37Furthermore, studies have
documented thatAR patients have a higher risk of ET dysfunction,
particularly during childhood, than non-allergic
ones.27, 38Therefore, AR seems to be a common risk
factor in children with OME and there is significant hearing loss
compared to non-AR children with OME; in addition, the hearing
levelimproved significantly with medical therapy.10
Recently, Torretta et al.39 demonstrated that allergy
or atopy were significantly higher in otitis-prone children with OME
than in those with simple RAOM: atopy was found in 73% of the children
with both RAOM and OME versus 39.5% of those with simple RAOM, while
allergy was found in 60% and 36%, respectively. The
authors39 suggested that children with both RAOM and
OMEare clinically different from children with simple RAOM, as they have
a more complex clinical presentation that may be sustained by underlying
allergy or atopy. Interestingly, in the same manuscript, children with
both RAOM and OME were more frequently affected by adenoidal hypertrophy
(AH) (p = 0.016). This is the second critical point that makes it
difficult to analyze data in this regard, since ET dysfunction and AH
are frequently associated with OME. Quaranta et
al.40analyzed children with AH showing that 60% had
OME and that AR was rarely present in this group. AH may constitute a
concomitant clinical entity associated with allergy that exponentially
promotes the development of OME and may be a confounding factor in the
analysis. Accordingly, some authors demonstrated that adenoid tissue and
middle ear mucosa share the same inflammatory pattern in allergic
children affected by OME.33
Most relevant clinical articles33-37,39-42investigating specifically association between OME and allergy and
included in the qualitative analyses are summarized in table 3.