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1 spondyloarthritis (also known as ankylosing spondylitis).
2 n which uveitis coincides with arthritis and spondylitis.
3 tory bowel disease, psoriasis and ankylosing spondylitis.
4 or autoimmune diseases, including ankylosing spondylitis.
5 and nonpharmacologic therapies in ankylosing spondylitis.
6 f benefit to select patients with ankylosing spondylitis.
7 arthritis, reactive arthritis, or ankylosing spondylitis.
8 nderstanding the genetic basis of ankylosing spondylitis.
9 atosus, rheumatoid arthritis, and ankylosing spondylitis.
10 fective for signs and symptoms of ankylosing spondylitis.
11 l deformities similar to those in ankylosing spondylitis.
12 be effective in the treatment of ankylosing spondylitis.
13 of the genetic susceptibility to ankylosing spondylitis.
14 le in delaying the progression of ankylosing spondylitis.
15 attenuate spinal inflammation in ankylosing spondylitis.
16 can prevent structural damage in ankylosing spondylitis.
17 effective in phase III trials in ankylosing spondylitis.
18 be asymptomatic, as in classical ankylosing spondylitis.
19 fusion protein, in patients with ankylosing spondylitis.
20 ined improvement in patients with ankylosing spondylitis.
21 a, seem not to be associated with ankylosing spondylitis.
22 a potential therapeutic target in ankylosing spondylitis.
23 siblings of female patients with ankylosing spondylitis.
24 JAK1 inhibitor, in patients with ankylosing spondylitis.
25 an TRBV9(+) T cell elimination in ankylosing spondylitis.
26 oriasis, psoriatic arthritis, and ankylosing spondylitis.
27 to be effective in patients with ankylosing spondylitis.
28 ory bowel diseases, psoriasis, or ankylosing spondylitis.
29 re associated with development of ankylosing spondylitis.
30 opathies, psoriatic arthritis and ankylosing spondylitis.
31 cukinumab in patients with active ankylosing spondylitis.
32 h the overall lack of efficacy in ankylosing spondylitis.
33 he modified New York criteria for ankylosing spondylitis.
34 isease, rheumatoid arthritis, and ankylosing spondylitis.
35 association of both molecules in ankylosing spondylitis.
36 l spondyloarthropathies, which is ankylosing spondylitis.
37 soriasis, psoriatic arthritis, or ankylosing spondylitis.
38 es differentially associated with ankylosing spondylitis.
39 ed for the development of EO, arthritis, and spondylitis.
40 y diseases, notably psoriasis and ankylosing spondylitis.
41 (1346+/-1011 pg per milliliter), ankylosing spondylitis (1368+/-1162 pg per milliliter), or liver fi
42 ents achieving the Assessments in Ankylosing Spondylitis 20% response (ASAS20) at weeks 12 and 24.
43 ignificantly after MR imaging for ankylosing spondylitis (29% vs 80%, P < .001), undifferentiated spo
45 mechanical back pain (4% vs 49%, P < .001), spondylitis (7% vs 76%, P < .001) and sacroiliitis (9% v
46 n had an even higher incidence of ankylosing spondylitis (7.2 [1.5-34], p=0.013) than did children of
47 , 48.8 [12.1] years), and 977 had ankylosing spondylitis (7.3%; 658 men [67.3%]; mean [SD] age, 42.3
48 ip between the gut microbiome and ankylosing spondylitis, a quantitative metagenomics study based on
49 Long-Term Efficacy and Safety in Ankylosing Spondylitis, a randomized controlled study, were randoml
51 tive arthritis, sacroiliitis, and ankylosing spondylitis also appear to be increased in these people,
54 PsA, a new composite measure for ankylosing spondylitis and axial SpA, the ASDAS, new measures for t
56 ious physical therapy programs in ankylosing spondylitis and identify their benefits and potential in
57 ed novel roles for these drugs in ankylosing spondylitis and in cancer prevention, accumulating evide
58 phase III trials of patients with ankylosing spondylitis and in trials conducted a decade ago in pati
60 es indicate that the morbidity of ankylosing spondylitis and PsA are considerably higher than previou
62 atoid arthritis, Crohn's disease, ankylosing spondylitis and psoriasis, confirms the importance of TN
65 or necrosis factor antagonists in ankylosing spondylitis and psoriatic arthritis has generated consid
66 ctor inhibitors for patients with ankylosing spondylitis and psoriatic arthritis has had a tremendous
67 azine is moderately effective for ankylosing spondylitis and psoriatic arthritis, although the large
75 -B27 in genetic susceptibility to ankylosing spondylitis and related spondyloarthropathies, although
76 son with originator infliximab in ankylosing spondylitis and rheumatoid arthritis; however, concerns
77 major histocompatibility complex (ankylosing spondylitis and sacroiliitis, P = 1.4E-15; OR, 2.5; 95%
78 EIMs (eg, ankylosing spondylitis [ankylosing spondylitis and sacroiliitis], primary sclerosing cholan
79 ic arthritis, reactive arthritis, ankylosing spondylitis), and osteoarthritis have characteristic app
81 dose (Ikbkb(GoF/GoF)) results in dactylitis, spondylitis, and characteristic nail changes, which are
85 ve structure-modifying effects in ankylosing spondylitis, and may thereby alter the disease course.
86 ases such as behcet's disease and ankylosing spondylitis, and ocular involvement of infectious diseas
89 one in detail, a risk allele for ankylosing spondylitis, and provide direct evidence of a non-coding
90 (psoriatic arthritis, psoriasis, ankylosing spondylitis, and rheumatoid arthritis), we tested whethe
91 lity, early onset osteoarthritis, ankylosing spondylitis, and seronegative erosive rheumatoid arthrit
92 in RA but also in Crohn disease, ankylosing spondylitis, and several other chronic inflammatory diso
93 tica (PMR), giant cell arteritis, ankylosing spondylitis, and Sjogren's syndrome, and to provide an o
94 ondyloarthritides, including PsA, ankylosing spondylitis, and the broader categories of SpA may be pr
95 -modifying role of these drugs in ankylosing spondylitis, and their use in the understudied pediatric
96 olitis, peripheral arthritis, and occasional spondylitis, and those with lower transgene copy numbers
97 ents with gout, two patients with ankylosing spondylitis, and two patients with psoriatic arthritis,
98 presence or absence of EIMs (eg, ankylosing spondylitis [ankylosing spondylitis and sacroiliitis], p
100 id arthritis, where patients with ankylosing spondylitis are offered therapy early in the disease cou
101 The spondylarthritides (such as ankylosing spondylitis) are multisystem inflammatory diseases that
102 This group includes 6 entities: ankylosing spondylitis, arthritis associated with inflammatory bowe
103 sample of two new loci related to ankylosing spondylitis, ARTS1 and IL23R, and confirmation of the pr
104 pus erythematosus (SLE) (n = 10), ankylosing spondylitis (AS) (n = 10), primary Sjogren's syndrome (n
106 ilarities and differences between ankylosing spondylitis (AS) and axial psoriatic arthritis (PsA).
107 their application in a number of ankylosing spondylitis (AS) and axial spondyloarthritis (axSpA) Reg
108 DCT) findings of 41 patients with ankylosing spondylitis (AS) and compared them with pulmonary functi
110 e inflammatory arthritis disorder ankylosing spondylitis (AS) and with other related spondylarthropat
111 Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) are chronic inflammatory diseases that
112 pproximately 40% of patients with ankylosing spondylitis (AS) but also affects patients with no evide
115 MRI-evident sacroiliitis develop ankylosing spondylitis (AS) in the long term and whether there are
121 We investigated the proposal that ankylosing spondylitis (AS) is associated with unusual ERAP1 genoty
123 of the gene-regulatory network in ankylosing spondylitis (AS) is vital for elucidating the mechanisms
126 nal inflammation in patients with ankylosing spondylitis (AS) relies primarily on magnetic resonance
127 e HLA-B27-transgenic rat model of ankylosing spondylitis (AS) suggested that macrophages develop an i
128 ong association between ERAP1 and ankylosing spondylitis (AS) was recently identified by the Wellcome
129 he spine and pelvis (for example, ankylosing spondylitis (AS)) and the eye (that is, acute anterior u
130 associated with susceptibility to ankylosing spondylitis (AS), and those reported not to be associate
131 s from 1,000 independent cases of ankylosing spondylitis (AS), autoimmune thyroid disease (AITD), mul
132 e B27 is strongly associated with ankylosing spondylitis (AS), but the pathogenic role of HLA-B27 is
133 heritability of susceptibility to ankylosing spondylitis (AS), it is only recently that the involveme
134 heral articular manifestations of ankylosing spondylitis (AS), psoriatic arthritis (PsA), and reactiv
135 of rheumatologists' diagnosis of ankylosing spondylitis (AS), psoriatic arthritis (PsA), or reactive
136 ondyloarthropathies (SpA) include ankylosing spondylitis (AS), psoriatic arthritis (PsA), reactive ar
137 reticulum aminopeptidase 1) with ankylosing spondylitis (AS), which is restricted to HLA-B27 positiv
148 revolutionized the management of ankylosing spondylitis (AS); however, the lack of notable clinical
149 the chronic inflammatory disease Ankylosing Spondylitis (AS); however, the mechanisms underlying thi
152 e conformations in differentially ankylosing spondylitis-associated subtypes) must not be excluded fr
155 ive study involving patients with ankylosing spondylitis, behcet's disease, presumed sarcoidosis, pre
156 ving the pain of axial disease in ankylosing spondylitis but these findings contradict two previous s
157 ptibility and disease activity of ankylosing spondylitis, but the effect of HLA-B27 on the activity o
158 ociation study in 2,053 unrelated ankylosing spondylitis cases among people of European descent and 5
160 the course of the disease, Stoke Ankylosing spondylitis classification Spinal Score (SASSS) is recom
162 stigated the genetic landscape of ankylosing spondylitis, Crohn's disease, psoriasis, primary scleros
164 and 45 controls: alopecia areata, ankylosing spondylitis, dermatomyositis, Graves' disease, Hashimoto
165 nd MMP-3 correlated with the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) values, but
167 ase activity assessed by the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), and functio
168 unctional Index (BASFI), the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), and the Ank
169 activity as measured by the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), pain and mo
172 y and functional parameters (Bath Ankylosing Spondylitis Disease Activity Index [BASDAI], Bath Ankylo
175 atoid arthritis, Crohn's disease, ankylosing spondylitis, familial Mediterranean fever, and Castleman
176 is; 16 had scleroderma; eight had ankylosing spondylitis; five had juvenile RA; three had discoid lup
179 nts included the BASDAI, the Bath Ankylosing Spondylitis Functional Index (BASFI), the Ankylosing Spo
180 ores for entheseal pain, the Bath Ankylosing Spondylitis Functional Index (BASFI), the Bath Ankylosin
182 ions were assessed using the Bath Ankylosing Spondylitis Functional Index (BASFI; score range 0-100,
183 ase Activity Index [BASDAI], Bath Ankylosing Spondylitis Functional Index [BASFI], and Bath Ankylosin
185 ammation and structural damage in ankylosing spondylitis has been an important focus of recent studie
189 nts with rheumatoid arthritis and ankylosing spondylitis have been reported, and generic quality-of-l
191 IL-23 receptor are associated with ankyosing spondylitis, however, it remains unclear whether IL-23 a
194 slows radiographic progression in ankylosing spondylitis in data from clinical trials may be because
195 g Pgis2 locus, inducing as high incidence of spondylitis in F2 hybrids as was found in the spondyliti
200 has relevance to diseases such as ankylosing spondylitis, in which HLA-B27 and ERAP jointly contribut
201 ic anemia, pernicious anemia, and ankylosing spondylitis), infectious (pneumonia, hepatitis, meningit
202 oL) instrument, the ASsessment in Ankylosing Spondylitis International Working Group criteria (ASAS)
207 ciation further substantiate that ankylosing spondylitis is determined to a large extent by genes out
208 w York criteria, the diagnosis of ankylosing spondylitis is made based on the presence of advanced le
209 rly half of the susceptibility to ankylosing spondylitis is provided by major histocompatibility comp
210 f the major goals of treatment of ankylosing spondylitis is to prevent or slow the development of spi
211 The prototypical type of axSpA, ankylosing spondylitis, is thought to be caused by interaction betw
212 soriasis/psoriatic arthritis, and ankylosing spondylitis) linked to newborns with periconception medi
215 this animal model of experimentally induced spondylitis might facilitate the identification of spond
216 mmune-mediated diseases including ankylosing spondylitis, multiple sclerosis, and inflammatory bowel
217 ile rheumatoid arthritis (n = 3), ankylosing spondylitis (n = 1), and psoriatic spondylarthropathy (n
218 Janus kinase (JAK) inhibitors for ankylosing spondylitis, new data on the effect of biologic DMARDs o
219 d arthritis, psoriatic arthritis, ankylosing spondylitis, non-infectious uveitis, and multiple sclero
220 led RCTs of rheumatoid arthritis, ankylosing spondylitis, optic neuritis, systemic lupus erythematosu
221 % CI, 1.03-1.72) and negative for ankylosing spondylitis (OR = 0.72; 95% CI, 0.54-0.98) and rheumatoi
222 , psoriasis, psoriatic arthritis, ankylosing spondylitis, or inflammatory bowel disease using Medicar
223 (psoriasis, psoriatic arthritis, ankylosing spondylitis, or juvenile arthritis), as an active compar
224 gnosed with rheumatoid arthritis, ankylosing spondylitis, or psoriatic arthritis and 219 healthy cont
225 , psoriasis, psoriatic arthritis, ankylosing spondylitis, or rheumatoid arthritis exhibited greater w
226 ions convincingly associated with ankylosing spondylitis (P < 5 x 10(-8) in the combined discovery an
227 presumed sarcoidosis compared to ankylosing spondylitis (p = 0.0001), behcet's disease (p = 0.0001),
228 sumed sarcoidosis with respect to ankylosing spondylitis (p = 0.0001), behcet's disease, (p = 0.0001)
237 in the pharmacological therapy of ankylosing spondylitis, physical therapy remains an essential part
238 gher significant association with ankylosing spondylitis, polymyositis, psoriasis, rheumatoid arthrit
239 the spinal cord in the course of ankylosing spondylitis, present in MRI include: bone marrow edema,
240 ed to inflammatory bowel disease, ankylosing spondylitis, primary sclerosing cholangitis and Takayasu
241 genesis or development process of ankylosing spondylitis, providing new leads for the development of
242 soriasis, psoriatic arthritis, or ankylosing spondylitis (psoriasis and spondyloarthropathies) combin
243 eria for SpA, without evidence of ankylosing spondylitis, psoriasis, inflammatory bowel disease, or p
244 sociated with the pathogenesis of ankylosing spondylitis, psoriatic arthritis and acute anterior uvei
245 reatment of rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, and juvenile idiopathi
246 diseases other than RA, including ankylosing spondylitis, psoriatic arthritis, and polymyositis, in 3
247 el disease, rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, and psoriasis are asso
249 category of spondyloarthropathy (ankylosing spondylitis, psoriatic arthritis, reactive arthritis, un
250 tis Functional Index (BASFI), the Ankylosing Spondylitis Quality of Life (ASQoL) instrument, the ASse
253 ips were scored by using the Bath Ankylosing Spondylitis Radiology Index (BASRI) by an experienced ra
254 graphs were scored using the Bath Ankylosing Spondylitis Radiology Index for the spine (BASRI-s), and
255 c diseases that primarily include ankylosing spondylitis, reactive arthritis, and the arthritis assoc
256 Previously, the diagnosis of ankylosing spondylitis required advanced changes on plain radiograp
257 gical conditions (i.e. psoriasis, ankylosing spondylitis, rheumatoid arthritis, fibromyalgia) than th
258 orders, including osteoarthritis, ankylosing spondylitis, rheumatoid arthritis, heterotopic ossificat
259 four genetic loci associated with ankylosing spondylitis risk and identifies a major role for the int
261 in, muscular back pain, radicular back pain, spondylitis, sacroiliitis, and other) and overall diagno
263 oriasis, psoriatic arthritis, and ankylosing spondylitis, sparking efforts to develop orally bioavail
266 ARDs on structural progression in ankylosing spondylitis, strategy trials on tapering or stopping TNF
267 erleukin-1 (IL-1) region genes in ankylosing spondylitis suggested the susceptibility to be conferred
268 ta-analysis of published scans of ankylosing spondylitis susceptibility has confirmed sites on chromo
269 stocompatibility complex genes in ankylosing spondylitis susceptibility, and suggests areas for futur
274 arthritis, rheumatoid arthritis, ankylosing spondylitis, systemic lupus erythematosus, and multiple
275 arthritis, rheumatoid arthritis, ankylosing spondylitis, systemic lupus erythematosus, Sjogren syndr
276 thematosus, rheumatoid arthritis, ankylosing spondylitis, systemic sclerosis, Sjogren syndrome and os
277 multiple sclerosis, psoriasis and ankylosing spondylitis that inclusion of known covariates can subst
278 fective structure modification in ankylosing spondylitis, the data strongly suggest a benefit, at lea
280 evidence that HLA-B27 operates in ankylosing spondylitis through a mechanism involving aberrant proce
281 erapy should remain a mainstay of ankylosing spondylitis treatment complementing medical therapy.
282 ay result in a paradigm shift for ankylosing spondylitis treatment similar to that undergone for rheu
283 ntial change from when the entity ankylosing spondylitis was defined by the modified New York criteri
286 identify susceptibility loci for ankylosing spondylitis, we undertook a genome-wide association stud
287 % of patients were diagnosed with ankylosing spondylitis were ascertained from a database of 4400 cas
289 major genetic loci Pgis1 and Pgis2 of murine spondylitis were homologous to chromosome regions in hum
290 atients with active, inflammatory ankylosing spondylitis were randomly assigned to receive twice-week
291 th psoriatic arthritis and 1 with ankylosing spondylitis) were isolated by positive selection and sti
292 ces spinal inflammation in active ankylosing spondylitis when compared to placebo; there was no compa
295 tolerated in patients with active ankylosing spondylitis who had an inadequate response or contraindi
296 -year-old woman with debilitating ankylosing spondylitis who was born to consanguineous parents was f
298 differ in their susceptibility to ankylosing spondylitis, with about 2.5 men affected for every woman
299 of the overall susceptibility to ankylosing spondylitis, with about half of the genetic contribution