Demodex infestation and density changes remain one of the main challenges in some clinical settings. Tumour necrosis factor-α (TNF-α) inhibitors have been recommended as a first-line treatment for ankylosing spondylitis (AS). However, there have been no studies investigating the impact of TNF-α inhibitor adalimumab on changes in the Demodex density in patients with AS. The aim of this study was to investigate Demodex density changes before and after adalimumab treatment and analyse the relationship between the Demodex density and clinical characteristics in AS. It was found that the Demodex density was positively correlated with age and C-reactive protein levels and the number of Demodex mites could increase after adalimumab treatment in AS.

Objectives: We conducted a meta-analysis of recently published randomized controlled trials (RCTs) to identify the most effective and safe etanercept dosing regimen and duration of therapy for the treatment of patients with ankylosing spondylitis (AS).

Methods: We systematically reviewed PubMed, Embase, Cochrane Library, and Web of Science databases for RCTs. The proportion of patients attaining 20 percent improvement (according to the Spondyloarthritis International Society response criteria [ASAS 20]) was evaluated as a primary outcome. Secondary outcomes included 50 percent increase in the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI 50) used for evaluating efficacy, as well as the BASDAI/Bath Ankylosing Spondylitis Functional Index (BASFI) scores and adverse events.

Results: ASAS 20 indicated that the efficacy of etanercept did not differ amongst dosing regimens (25 mg twice-weekly versus 50 mg once-weekly: relative risk [RR], 2.18, 95 percent confidence interval [CI], 1.78–2.67 versus RR, 2.00, 95 percent CI, 1.70–2.37). The ASAS 20 reported subgroup differences among treatment durations of less than 12 weeks (RR, 2.70; 95 percent CI, 2.09–3.49); 12 weeks (RR, 1.74; 95 percent CI, 1.37–2.22); and more than 12 weeks (RR, 2.56; 95 percent CI, 1.88–3.48). Other outcomes included BASDAI, BASDAI 50, and BASFI. Drug safety differed according to the treatment regimen and duration.

Conclusion: Our meta-analysis found that there was no significant efficacy difference between 50 mg once-weekly and 25 mg twice-weekly dosing for the treatment of AS, and a dosing duration of less than 12 weeks was more effective for treating AS patients.

Objectives: To compare the cost-effectiveness of the treatment of ankylosing spondylitis (AS) with infliximab in the United Kingdom over lifetime estimated from two different clinical trials and adjusted for clinical practice guidelines.

Methods: A cost-effectiveness model was developed to incorporate clinical, epidemiological, and economic data and allow extrapolation of trial results and incorporation of long-term treatment. Assumptions regarding treatment beyond the trials were based on open extensions from the trials and treatment guidelines by the British Society for Rheumatology. Results are presented for both the societal perspective and the perspective of the National Health Service (UK £, discounted 3.5 percent).

Results: Under the assumption that disease activity would be controlled and functional capacity would remain stable while on drug, treatment with infliximab (5 mg/kg every 6 weeks) dominates standard treatment in the societal perspective. In the National Health Service perspective, the cost per quality-adjusted life-year (QALY) gained over lifetime was £28,300 and £26,800 for the two trials. If functional capacity were to deteriorate at half the rate of untreated patients, the cost per QALY gained would be £35,300 and £34,100, respectively. The results are sensitive to the dosing regimen adopted, the discontinuation rate, and assumptions concerning disease progression while on treatment.

Conclusions: The two clinical trials yield the same cost-effectiveness results and the cost per QALY gained with treatment was found to be in the acceptable range.

We present an unusual cause of rhinolalia clausa secondary to an oropharyngeal mass. A 69-year-old male presented to the otorhinolaryngology clinic with a one year history of a ‘plummy’ voice. He had a longstanding history of severe ankylosing spondylitis. Examination revealed an obvious hyponasal voice and a smooth hard mass in the midline of the posterior nasopharyngeal and oropharyngeal walls. Subsequent computed tomography scans and lateral plain neck X-ray showed a fracture dislocation of the odontoid peg, secondary to ankylosing spondylitis, which had eroded through the body of the C1 vertebra to lie anteriorly, resulting in the aforementioned impression into the pharyngeal mucosa. The radiological images, the role of the nasal airways in phonation and the causes of hyponasal speech are discussed.

Aims: The aim of this study was to investigate hearing loss in patients with ankylosing spondylitis.

Study design: Prospective, case–control study.

Methods: Fifty-nine ankylosing spondylitis patients (118 ears) and 52 healthy control subjects (104 ears) were included. Pure tone audiometry at 250, 500, 1000, 2000, 4000 and 6000 Hz and immittance measures, including tympanometry and acoustic reflex tests, were performed in the patients and controls.

Results: Sensorineural hearing loss was found in 21 patients (35.5 per cent), bilateral in 15 patients and unilateral in six. Pure tone thresholds significantly differed between patients and controls at all frequencies (p<0.05). There was no statistically significant difference between the right and the left ears' thresholds at all frequencies, except at 4000 Hz in ankylosing spondylitis patients. The right ears' thresholds were higher than those of the left ears. Patients' pure tone average (PTA) thresholds were significantly different from those of controls in all three PTA groups (i.e. 250 Hz; 500, 1000 and 2000 Hz; and 4000 and 6000 Hz) (p<0.05). The differences were most prominent in the higher frequencies.

Conclusion: Our findings suggest a decreased hearing level in ankylosing spondylitis patients, mostly at high frequencies, although the pure tone thresholds of patients and controls significantly differed at all frequencies.

Ankylosing spondylitis (AS) is a chronic inflammatory disease. The aim of this investigation was to study the relationship between AS and hearing loss. This study compared 28 patients with AS with 23 age-matched controls. All subjects underwent ENT examination, audiological and acoustic immittance measurements, and auditory brainstem response (ABR) tests. Sensorineural hearing loss was found in 28.6 per cent of the AS patients and in 4.35 per cent of the control group. For hearing levels at 250–500 Hz and 4000–8000 Hz, there was a statistically significant difference between the two groups. Acoustic reflex was not obtained in both ears of four patients and the left ear of one patient. There was a correlation between increase of tympanic volume and limitation in neck movement, between extension of 1–3 interpeak latency and limitation in the neck movement. In conclusion, AS affects the inner ear more than the middle ear.

The human leukocyte antigen class I allele HLA-B27 is a major histocompatibility complex (MHC) antigen that is strongly associated with the spondyloarthritic group of human rheumatic diseases, the most commmon of which is ankylosing spondylitis. Although the mechanism underlying this disease association remains unknown, numerous theories have been proposed. Much more is known of the natural role of HLA-B27 in binding and presenting antigenic peptides to T cells. The ‘arthritogenic peptide hypothesis’ suggests that the role of HLA-B27 in disease relates to its specificity for binding certain peptides. Recently, it has also been shown that HLA-B27 has an unusual cell biology and can adopt a novel homodimeric structure. In this review, a molecular model of the HLA-B27 homodimer is presented and the possible pathogenic significance of such a structure is discussed.

The 2 major categories of idiopathic inflammatory arthritis are rheumatoid arthritis and the seronegative spondyloarthropathies. Whilst the synovium is the primary site of joint disease in the former, the primary site in the latter is less well defined. However, it has recently been proposed that enthesitis-associated changes in the spondyloarthropathies are primary and that all other joint manifestations are secondary. Nevertheless, some of the sites of disease localisation have not been adequately explained in terms of enthesitis. This article summarises current knowledge of the structure, function, blood supply, innervation, molecular composition and histopathology of the classic enthesis (i.e. the bony attachment of a tendon or ligament) and introduces the concept of ‘functional’ and articular ‘fibrocartilaginous’ entheses. The former are regions where tendons or ligaments wrap-around bony pulleys, but are not attached to them, and the latter are synovial joints that are lined by fibrocartilage rather than hyaline cartilage. We describe how these 3 types of entheses relate to other, and how all are prone to pathological changes in spondyloarthropathy. We propose that the inflammatory responses characteristic of spondyloarthropathies are triggered at these seemingly diverse sites, in genetically susceptible individuals, by a combination of anatomical factors which lead to higher levels of tissue microtrauma, and the deposition of microbes.