"Genetics "
"The prevalence of AS varies significantly by geographic region, largely due to the genetic makeup of local populations 36, ranging from 0.02% up to 0.35% 37. Traditionally, it was thought there was a male predilection of 3:1 or more; however, the gender predilection of the disease is a matter of ongoing research, as females may be underdiagnosed. According to some research, men tend toward more severe disease 28. The disease usually presents in young adults, with the first symptoms typically appearing in the third decade, although up to 18% of cases present in the second decade."
"Patients are rheumatoid factor (RF) negative, hence seronegative. HLA-B27 is the gene with the strongest association. Other possibly contributing genes include ERAP-1, IL23R and TNF-associated genes 22. Although ~90% of individuals with ankylosing spondylitis have the HLA-B27 gene, it is important to note this gene is present in 8-9% of people of Northern European ancestry 5. Overall, ~5% of people positive for HLA-B27 develop ankylosing spondylitis."
"First-line therapy is primarily focused on NSAIDs and non-pharmacological measures, including education, exercise, physiotherapy and group therapy. Together, these treatments can lead to substantial clinical improvement in 70-80% of patients. Local steroid injection and DMARDs (sulfasalazine and methotrexate) can also help with peripheral manifestations. Second-line therapy includes TNF-alpha blockers (etanercept, infliximab, adalimumab, certolizumab, golimumab), IL17 inhibitors (secukinumab, ixekizumab, bimekizumab) and targeted synthetic DMARDs (JAK inhibitors: upadacitinib, tofacitinib) 24,35. Whether TNF-alpha blockers can inhibit radiographic disease progression has been the subject of some debate and remains under investigation 23."
"First-line therapy is primarily focused on NSAIDs and non-pharmacological measures, including education, exercise, physiotherapy and group therapy. Together, these treatments can lead to substantial clinical improvement in 70-80% of patients. Local steroid injection and DMARDs (sulfasalazine and methotrexate) can also help with peripheral manifestations. Second-line therapy includes TNF-alpha blockers (etanercept, infliximab, adalimumab, certolizumab, golimumab), IL17 inhibitors (secukinumab, ixekizumab, bimekizumab) and targeted synthetic DMARDs (JAK inhibitors: upadacitinib, tofacitinib) 24,35. Whether TNF-alpha blockers can inhibit radiographic disease progression has been the subject of some debate and remains under investigation 23."
"First-line therapy is primarily focused on NSAIDs and non-pharmacological measures, including education, exercise, physiotherapy and group therapy. Together, these treatments can lead to substantial clinical improvement in 70-80% of patients. Local steroid injection and DMARDs (sulfasalazine and methotrexate) can also help with peripheral manifestations. Second-line therapy includes TNF-alpha blockers (etanercept, infliximab, adalimumab, certolizumab, golimumab), IL17 inhibitors (secukinumab, ixekizumab, bimekizumab) and targeted synthetic DMARDs (JAK inhibitors: upadacitinib, tofacitinib) 24,35. Whether TNF-alpha blockers can inhibit radiographic disease progression has been the subject of some debate and remains under investigation 23."
"How would you describe the overall level of AS neck, back, or hip pain you have had?"
"Patients are rheumatoid factor (RF) negative, hence seronegative. HLA-B27 is the gene with the strongest association. Other possibly contributing genes include ERAP-1, IL23R and TNF-associated genes 22. Although ~90% of individuals with ankylosing spondylitis have the HLA-B27 gene, it is important to note this gene is present in 8-9% of people of Northern European ancestry 5. Overall, ~5% of people positive for HLA-B27 develop ankylosing spondylitis."
"Andersson lesion: inflammatory spondylodiscitis that occurs in association with ankylosing spondylitis and results in a disc pseudarthrosis"
"How would you describe the overall level of fatigue/tiredness you have experienced?"
"How would you describe the overall level of AS neck, back, or hip pain you have had?"
"How would you describe the overall level of pain/swelling in joints other than the neck, back, or hips you have had?"
"How would you describe the overall level of discomfort you have had from any areas tender to touch or pressure?"
"How would you describe the overall level of morning stiffness you have had from the time you wake up?"
"How long does your morning stiffness last from the time you wake up?"
"Bath Ankylosing Spondylitis Disease Activity Index (BASDAI)"
Expected headings
"Genetics "
"Associations"
"Sacroiliac joints"
"Spine"
"Hips"
"Pelvis"
"Knees"
"Hands"
"Shoulders"
"Chest"
"Cardiac"
"Bone scintigraphy"
"Complications"
"Bath Ankylosing Spondylitis Disease Activity Index (BASDAI)"
"Although in routine clinical practice the term ankylosing spondylitis is still widely used, contemporary rheumatological classifications use the broader term 'axial spondyloarthritis' to encompass both ankylosing spondylitis (i.e. radiographic axial spondyloarthritis; those with plain film findings) and non-radiographic axial spondyloarthritis. This is important, as patients may be eligible for specific drugs based on imaging findings 35. As such, ideally, the term ankylosing spondylitis should be reserved for patients with plain-film evidence of disease."
"The prevalence of AS varies significantly by geographic region, largely due to the genetic makeup of local populations 36, ranging from 0.02% up to 0.35% 37. Traditionally, it was thought there was a male predilection of 3:1 or more; however, the gender predilection of the disease is a matter of ongoing research, as females may be underdiagnosed. According to some research, men tend toward more severe disease 28. The disease usually presents in young adults, with the first symptoms typically appearing in the third decade, although up to 18% of cases present in the second decade."
"may have a role in early diagnosis of sacroiliitis; MRI is more sensitive than CT or plain radiography in detecting inflammatory changes (which precede structural changes) such as bone marrow oedema (best demonstrated on STIR sequences), synovitis and capsulitis (on gadolinium enhanced T1 weighted sequences) 16,18, 38"
"qualitative assessment of the accumulation of radionuclide in the SI joints may be difficult due to normal uptake in this location; thus, quantitative analysis may be more useful"
"patients with ankylosing spondylitis have a 4x higher chance than the general population of spinal fracture; the overall risk of fracture is 5-15% 30"
"Patients are rheumatoid factor (RF) negative, hence seronegative. HLA-B27 is the gene with the strongest association. Other possibly contributing genes include ERAP-1, IL23R and TNF-associated genes 22. Although ~90% of individuals with ankylosing spondylitis have the HLA-B27 gene, it is important to note this gene is present in 8-9% of people of Northern European ancestry 5. Overall, ~5% of people positive for HLA-B27 develop ankylosing spondylitis."
"sacroiliitis is usually the first manifestation, 5 and is symmetrical and bilateral"
"ossification of spinal ligaments, joints and discs (with fatty marrow within the ossified disc, best seen on MRI)"
"First-line therapy is primarily focused on NSAIDs and non-pharmacological measures, including education, exercise, physiotherapy and group therapy. Together, these treatments can lead to substantial clinical improvement in 70-80% of patients. Local steroid injection and DMARDs (sulfasalazine and methotrexate) can also help with peripheral manifestations. Second-line therapy includes TNF-alpha blockers (etanercept, infliximab, adalimumab, certolizumab, golimumab), IL17 inhibitors (secukinumab, ixekizumab, bimekizumab) and targeted synthetic DMARDs (JAK inhibitors: upadacitinib, tofacitinib) 24,35. Whether TNF-alpha blockers can inhibit radiographic disease progression has been the subject of some debate and remains under investigation 23."
"First-line therapy is primarily focused on NSAIDs and non-pharmacological measures, including education, exercise, physiotherapy and group therapy. Together, these treatments can lead to substantial clinical improvement in 70-80% of patients. Local steroid injection and DMARDs (sulfasalazine and methotrexate) can also help with peripheral manifestations. Second-line therapy includes TNF-alpha blockers (etanercept, infliximab, adalimumab, certolizumab, golimumab), IL17 inhibitors (secukinumab, ixekizumab, bimekizumab) and targeted synthetic DMARDs (JAK inhibitors: upadacitinib, tofacitinib) 24,35. Whether TNF-alpha blockers can inhibit radiographic disease progression has been the subject of some debate and remains under investigation 23."
"First-line therapy is primarily focused on NSAIDs and non-pharmacological measures, including education, exercise, physiotherapy and group therapy. Together, these treatments can lead to substantial clinical improvement in 70-80% of patients. Local steroid injection and DMARDs (sulfasalazine and methotrexate) can also help with peripheral manifestations. Second-line therapy includes TNF-alpha blockers (etanercept, infliximab, adalimumab, certolizumab, golimumab), IL17 inhibitors (secukinumab, ixekizumab, bimekizumab) and targeted synthetic DMARDs (JAK inhibitors: upadacitinib, tofacitinib) 24,35. Whether TNF-alpha blockers can inhibit radiographic disease progression has been the subject of some debate and remains under investigation 23."