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The aim of our study was to analyse the serum interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta) and interferon-gamma (IFN-gamma) levels in patients with AS and their relationship with disease activity. An ELISA test was used to analyse serum cytokine (IL-6, TNF-alpha, IL-1 beta and IFN-gamma) levels in 69 patients with AS. Results were compared with those from 43 patients with RA and 36 patients with non-inflammatory back pain. The relationship between serum concentrations of the different cytokines and parameters of disease activity and severity in AS patients was also evaluated. IL-6 and TNF-alpha serum levels, but not IL-1 beta and IFN-gamma, were significantly higher in AS than in NIBP. However, patients with RA showed higher serum levels of IL-6, TNF-alpha and IFN-gamma than both AS and NIBP patients. In AS, IL-6 correlated with clinical parameters of disease activity with significant correlation being observed with laboratory parameters of inflammation such as ESR, CRP, platelet count and clinical parameters of severity such as vertebral mobility. TNF-alpha did not correlate with laboratory or clinical parameters of activity. Macrophagic cytokines (TNF-alpha and IL-6), are increased in AS patients and IL-6 closely correlated with the activity of the disease.

Several studies of DNA restriction fragment length polymorphism (RFLP) in ankylosing spondylitis (AS) have been carried out. The association between a recently identified class I HLA 9.2 kb PvuII RFLP and AS remain controversial. In order to evaluate this possible association in an Euro-Caucasian population, the genomic DNA of 42 AS patients and 18 patients with Reiter's syndrome (RS) and 42 healthy controls was analysed. Non-association between 9.2 kb PvuII RFLP and AS or RS was observed. As described previously, a strong association between this fragment and HLA-A3 and/or HLA-A9 antigens was demonstrated. A study of two families showed that this RFLP segregates with HLA-A3 and/or HLA-A9 and independently of the HLA-B27. Our findings support the view that the 9.2 kb PvuII fragment is not universally associated with AS.