Introduction Ankylosing spondylitis (AS) is a long-term rheumatic disease characterized by inflammatory back pain (Khan, 2002). AS, formerly known as Bechterew's disease and Marie-Stümpell disease, is of unknown origin, but dysfunction of immune mechanisms is thought to play a crucial role (Braun and van der Heijde 2007). This disease usually affects the sacroiliac joints and the spine, leading to possible fusion (ankylosing) of the involved joints (Khan 2002 and Zhang et al. 2003). This disease affects up to 0.1-1.1% of the Caucasian adult population worldwide. Patients with AS also show higher rates of work disability, unemployment (Boonen 2002), and higher mortality rates (Braun and Pincus 2002). Although the exact etiology of AS is unknown, HLA-B27, a rare allele of the HLA-B gene, is found in approximately 90% of patients with the disease, indicating a strong genetic association (Khan 1995). 1-2% of individuals with the HLA-B27 genotype developed the disease (1995). Erdesz et al. (1997) suggest that several B27 subtypes may be involved in the pathogenesis of spondylitis. Tiwana et al. (2001) suggested that AS results from a synergism between HLA-B27 and antigens from the bacterial genus Klebsiella. Sieper et al. (2011) then argued that the elimination of the main nutrients of Klebsiella (starches) would decrease the presence of the antigen in the blood and improve musculoskeletal symptoms. However, as Khan (2002) argues, the evidence for a correlation between Klebsiella and SA is so far limited. There is no cure for AS, although treatments and medications can reduce symptoms and pain (Williams et al. 2007). Symptoms appear gradually, starting around age 23 (Feldtkeller et al. 2003). Treatment of the AS acute phase reactants mentioned in the paper appears to benefit most from continuous treatment with NSAIDs. This is the first study to show a possible disease-modifying effect of continuous treatment and requires further investigation. Following a review of the literature, van den Berg et al. (2012) described how two studies demonstrated that all NSAIDs have statistically significant, moderate to good effects on disease activity and pain. Furthermore, no signs of NSAID toxicity were found in this review. However, NSAIDs at certain doses may cause an increased risk of gastrointestinal (GI) bleeding. This bleeding can be reduced with the use of gastoprotective agents (Zochling et al 2005). Analgesics, such as paracetamol and opioids, may be considered for pain control in patients in whom NSAIDs are insufficient, contraindicated and/or poorly tolerated (Lewis et al.. 2002)..