ABSTRACT
BACKGROUND AND AIMS: Inflammatory bowel disease (IBD) has many characteristics of autoimmune diseases. Sensorineural hearing loss has been reported in many autoimmune diseases. Little is known about hearing loss in patients with IBD. METHODS: A prospective blinded comparative study was conducted over a 3-year period. IBD patients and controls underwent a complete otorhinolaryngeal examination and eudiometry test. RESULTS: Altogether 105 participants (76 patients and 29 controls) took part in this study. Mean age was 36, 51 % were males, and 40 % of the patients were presently hospitalized due to IBD exacerbation. Audiometric examination revealed that any hearing loss (mild to severe) was found in 29 (38 %) of the IBD population, compared to 4 (14 %) of the control group (p = 0.02). Extraintestinal manifestation (EIM) was present in 33/76 (43 %) of IBD patients. Any hearing loss and moderate to severe hearing loss were found in 17/33 (52 %) and 7/33 (21 %) in the EIM-positive group compared to 12/43 (28 %) and 4/43 (9 %) in the EIM-negative group (p = 0.036 and p = 0.14, respectively). Out of patients over the age of 40 with other EIMs, all 11/11 (100 %) of patients had any hearing loss compared to 8/12 (66 %) of patients over the age of 40 without other EIMs, p = 0.035. CONCLUSIONS: Hearing loss may be another EIM of IBD. It is found in 38 % of IBD patients and in up to 52 % of patients with other EIMs and increases over the age of 40. Early hearing evaluation should be recommended to these high-risk IBD patients.
Subject(s)
Hearing Loss/complications , Inflammatory Bowel Diseases/complications , Adult , Aged , Case-Control Studies , Female , Humans , Male , Middle Aged , Prospective Studies , Young AdultABSTRACT
Adenoids are part of the MALT. In the present study, we analyzed cell surface markers and cytolytic activity of adenoidal NK (A-NK) cells and compared them with NK cells derived from blood of the same donors (B-NK). NK cells comprised 0.67% (0.4-1.2%) of the total lymphoid population isolated from adenoids. The majority (median=92%) of the A-NK cells was CD56(bright)CD16(-). A-NK cells were characterized by the increased expression of activation-induced receptors. NKp44 was detected on >60%, CD25 on >40%, and HLA-DR on >50% of freshly isolated A-NK cells. Functional assays indicated that the cytotoxic machinery of A-NK is intact, and sensitive target cells are killed via natural cytotoxicity receptors, such as NKG2D. Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1; CD66) expression was up-regulated in 23% (median) of the A-NK cells by IL-2 activation but unchanged in B-NK cells. CEACAM1 inhibited the A-NK killing of target cells. CXCR4 was expressed on more than 40% A-NK cells prior to activation. Its ligand, CXCL12, was found in endothelial cells of the capillaries within the adenoid and in cells of the epithelial lining. In addition, A-NK cells migrated in vitro toward a gradient of CXCL12 in a dose-responsive manner, suggesting a role for this chemokine in A-NK cell recruitment and trafficking. We conclude that the A-NK cells are unique in that they display an activated-like phenotype and are different from their CD16(-) B-NK cell counterparts. This phenotype presumably reflects the chronic interaction of A-NK cells with antigens penetrating the body through the nasal route.
