ライフサイエンスコーパス: spondylitis

1 and nonpharmacologic therapies in ankylosing spondylitis.

2 f benefit to select patients with ankylosing spondylitis.

3 arthritis, reactive arthritis, or ankylosing spondylitis.

4 nderstanding the genetic basis of ankylosing spondylitis.

5 atosus, rheumatoid arthritis, and ankylosing spondylitis.

6 fective for signs and symptoms of ankylosing spondylitis.

7 l deformities similar to those in ankylosing spondylitis.

8 be effective in the treatment of ankylosing spondylitis.

9 of the genetic susceptibility to ankylosing spondylitis.

10 le in delaying the progression of ankylosing spondylitis.

11 attenuate spinal inflammation in ankylosing spondylitis.

12 can prevent structural damage in ankylosing spondylitis.

13 effective in phase III trials in ankylosing spondylitis.

14 be asymptomatic, as in classical ankylosing spondylitis.

15 opathies, psoriatic arthritis and ankylosing spondylitis.

16 fusion protein, in patients with ankylosing spondylitis.

17 ined improvement in patients with ankylosing spondylitis.

18 a, seem not to be associated with ankylosing spondylitis.

19 cukinumab in patients with active ankylosing spondylitis.

20 siblings of female patients with ankylosing spondylitis.

21 he modified New York criteria for ankylosing spondylitis.

22 isease, rheumatoid arthritis, and ankylosing spondylitis.

23 association of both molecules in ankylosing spondylitis.

24 re associated with development of ankylosing spondylitis.

25 l spondyloarthropathies, which is ankylosing spondylitis.

26 soriasis, psoriatic arthritis, or ankylosing spondylitis.

27 es differentially associated with ankylosing spondylitis.

28 ed for the development of EO, arthritis, and spondylitis.

29 y diseases, notably psoriasis and ankylosing spondylitis.

30 n which uveitis coincides with arthritis and spondylitis.

31 tory bowel disease, psoriasis and ankylosing spondylitis.

32 (1346+/-1011 pg per milliliter), ankylosing spondylitis (1368+/-1162 pg per milliliter), or liver fi

33 ents achieving the Assessments in Ankylosing Spondylitis 20% response (ASAS20) at weeks 12 and 24.

34 ignificantly after MR imaging for ankylosing spondylitis (29% vs 80%, P < .001), undifferentiated spo

35 mechanical back pain (4% vs 49%, P < .001), spondylitis (7% vs 76%, P < .001) and sacroiliitis (9% v

36 n had an even higher incidence of ankylosing spondylitis (7.2 [1.5-34], p=0.013) than did children of

37 ip between the gut microbiome and ankylosing spondylitis, a quantitative metagenomics study based on

38 Long-Term Efficacy and Safety in Ankylosing Spondylitis, a randomized controlled study, were randoml

39 and valve disease associated with ankylosing spondylitis (AKS).

40 tive arthritis, sacroiliitis, and ankylosing spondylitis also appear to be increased in these people,

41 28 and 575/725 is associated with ankylosing spondylitis among HLA-B27-positive individuals.

42 nostic approach in the case of sacroiliitis, spondylitis and arthritis.

43 PsA, a new composite measure for ankylosing spondylitis and axial SpA, the ASDAS, new measures for t

44 pathic changes closely resembling ankylosing spondylitis and DISH.

45 ious physical therapy programs in ankylosing spondylitis and identify their benefits and potential in

46 ed novel roles for these drugs in ankylosing spondylitis and in cancer prevention, accumulating evide

47 es indicate that the morbidity of ankylosing spondylitis and PsA are considerably higher than previou

48 Three risk loci shared with ankylosing spondylitis and psoriasis (the MHC class I region, ERAP1

49 atoid arthritis, Crohn's disease, ankylosing spondylitis and psoriasis, confirms the importance of TN

50 atoid arthritis, Crohn's disease, ankylosing spondylitis and psoriasis.

51 ated disorders, most notably with ankylosing spondylitis and psoriasis.

52 or necrosis factor antagonists in ankylosing spondylitis and psoriatic arthritis has generated consid

53 ctor inhibitors for patients with ankylosing spondylitis and psoriatic arthritis has had a tremendous

54 azine is moderately effective for ankylosing spondylitis and psoriatic arthritis, although the large

55 reatest experience has accrued in ankylosing spondylitis and psoriatic arthritis.

56 nal status and quality of life in ankylosing spondylitis and psoriatic arthritis.

57 mor necrosis factor inhibitors in ankylosing spondylitis and psoriatic arthritis.

58 ive and safe for the treatment of ankylosing spondylitis and psoriatic arthritis.

59 healthy donors and patients with ankylosing spondylitis and psoriatic arthritis.

60 Ankylosing spondylitis and related spondylarthritides are associate

61 -B27 in genetic susceptibility to ankylosing spondylitis and related spondyloarthropathies, although

62 ith systemic lupus erythematosus, ankylosing spondylitis, and hepatic fibrosis.

63 ammation in rheumatoid arthritis, ankylosing spondylitis, and juvenile chronic arthritis.

64 ve structure-modifying effects in ankylosing spondylitis, and may thereby alter the disease course.

65 ases such as behcet's disease and ankylosing spondylitis, and ocular involvement of infectious diseas

66 one in detail, a risk allele for ankylosing spondylitis, and provide direct evidence of a non-coding

67 in RA but also in Crohn disease, ankylosing spondylitis, and several other chronic inflammatory diso

68 tica (PMR), giant cell arteritis, ankylosing spondylitis, and Sjogren's syndrome, and to provide an o

69 ondyloarthritides, including PsA, ankylosing spondylitis, and the broader categories of SpA may be pr

70 -modifying role of these drugs in ankylosing spondylitis, and their use in the understudied pediatric

71 olitis, peripheral arthritis, and occasional spondylitis, and those with lower transgene copy numbers

72 ents with gout, two patients with ankylosing spondylitis, and two patients with psoriatic arthritis,

73 Patients with juvenile-onset ankylosing spondylitis appear to have poorer functional outcomes.

74 id arthritis, where patients with ankylosing spondylitis are offered therapy early in the disease cou

75 The spondylarthritides (such as ankylosing spondylitis) are multisystem inflammatory diseases that

76 This group includes 6 entities: ankylosing spondylitis, arthritis associated with inflammatory bowe

77 sample of two new loci related to ankylosing spondylitis, ARTS1 and IL23R, and confirmation of the pr

78 pus erythematosus (SLE) (n = 10), ankylosing spondylitis (AS) (n = 10), primary Sjogren's syndrome (n

79 Ankylosing spondylitis (AS) affects 0.25-1.0% of the population, an

80 their application in a number of ankylosing spondylitis (AS) and axial spondyloarthritis (axSpA) Reg

81 DCT) findings of 41 patients with ankylosing spondylitis (AS) and compared them with pulmonary functi

82 e inflammatory arthritis disorder ankylosing spondylitis (AS) and with other related spondylarthropat

83 Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) are chronic inflammatory diseases that

84 pproximately 40% of patients with ankylosing spondylitis (AS) but also affects patients with no evide

85 e develops a phenotype similar to ankylosing spondylitis (AS) in humans.

86 MRI-evident sacroiliitis develop ankylosing spondylitis (AS) in the long term and whether there are

87 Ankylosing spondylitis (AS) is a chronic inflammatory arthritis aff

88 Ankylosing spondylitis (AS) is a common and highly familial rheumat

89 Ankylosing spondylitis (AS) is a common, highly heritable, inflamma

90 We investigated the proposal that ankylosing spondylitis (AS) is associated with unusual ERAP1 genoty

91 Ankylosing spondylitis (AS) may present with extra-articular involv

92 The clinical response in ankylosing spondylitis (AS) patients treated with biologic agents c

93 nal inflammation in patients with ankylosing spondylitis (AS) relies primarily on magnetic resonance

94 e HLA-B27-transgenic rat model of ankylosing spondylitis (AS) suggested that macrophages develop an i

95 ong association between ERAP1 and ankylosing spondylitis (AS) was recently identified by the Wellcome

96 associated with susceptibility to ankylosing spondylitis (AS), and those reported not to be associate

97 s from 1,000 independent cases of ankylosing spondylitis (AS), autoimmune thyroid disease (AITD), mul

98 e B27 is strongly associated with ankylosing spondylitis (AS), but the pathogenic role of HLA-B27 is

99 heritability of susceptibility to ankylosing spondylitis (AS), it is only recently that the involveme

100 heral articular manifestations of ankylosing spondylitis (AS), psoriatic arthritis (PsA), and reactiv

101 of rheumatologists' diagnosis of ankylosing spondylitis (AS), psoriatic arthritis (PsA), or reactive

102 reticulum aminopeptidase 1) with ankylosing spondylitis (AS), which is restricted to HLA-B27 positiv

103 ith rheumatoid arthritis (RA) and ankylosing spondylitis (AS).

104 age in patients with longstanding ankylosing spondylitis (AS).

105 e (HRQOL) in patients with active ankylosing spondylitis (AS).

106 role in the spondylarthropathy of ankylosing spondylitis (AS).

107 ine (SP), in patients with active ankylosing spondylitis (AS).

108 of osteoporosis in patients with ankylosing spondylitis (AS).

109 les due to their association with Ankylosing Spondylitis (AS).

110 ssary to establish a diagnosis of ankylosing spondylitis (AS).

111 the chronic inflammatory disease Ankylosing Spondylitis (AS); however, the mechanisms underlying thi

112 vented the subsequent onset of arthritis and spondylitis, as did transgene-induced azospermia.

113 ASsessment of Ankylosing Spondylitis (ASAS) International Working Group criteria

114 e conformations in differentially ankylosing spondylitis-associated subtypes) must not be excluded fr

115 utoimmune damage in patients with ankylosing spondylitis-associated subtypes.

116 ions in the signs and symptoms of ankylosing spondylitis at week 16.

117 ive study involving patients with ankylosing spondylitis, behcet's disease, presumed sarcoidosis, pre

118 ving the pain of axial disease in ankylosing spondylitis but these findings contradict two previous s

119 ociation study in 2,053 unrelated ankylosing spondylitis cases among people of European descent and 5

120 n in an independent cohort of 898 ankylosing spondylitis cases and 1,518 controls.

121 the course of the disease, Stoke Ankylosing spondylitis classification Spinal Score (SASSS) is recom

122 l Consortium and the Australo-Anglo-American Spondylitis Consortium (WTCCC-TASC) study.

123 stigated the genetic landscape of ankylosing spondylitis, Crohn's disease, psoriasis, primary scleros

124 ultiple sclerosis (D12S1052), and ankylosing spondylitis (D16S516).

125 and 45 controls: alopecia areata, ankylosing spondylitis, dermatomyositis, Graves' disease, Hashimoto

126 nd MMP-3 correlated with the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) values, but

127 ase activity assessed by the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), and functio

128 unctional Index (BASFI), the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), and the Ank

129 activity as measured by the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), pain and mo

130 ivity was assessed using the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI).

131 activity as measured by the Bath Ankylosing Spondylitis Disease Activity Index (P = 0.002).

132 using the PsA-modified Maastricht Ankylosing Spondylitis Enthesitis Score [MASES] index).

133 atoid arthritis, Crohn's disease, ankylosing spondylitis, familial Mediterranean fever, and Castleman

134 is; 16 had scleroderma; eight had ankylosing spondylitis; five had juvenile RA; three had discoid lup

135 oriatic arthritis, and those with ankylosing spondylitis from phase III trials of golimumab.

136 nts included the BASDAI, the Bath Ankylosing Spondylitis Functional Index (BASFI), the Ankylosing Spo

137 ores for entheseal pain, the Bath Ankylosing Spondylitis Functional Index (BASFI), the Bath Ankylosin

138 l impairment assessed by the Bath Ankylosing Spondylitis Functional Index (BASFI).

139 ions were assessed using the Bath Ankylosing Spondylitis Functional Index (BASFI; score range 0-100,

140 ammation and structural damage in ankylosing spondylitis has been an important focus of recent studie

141 Importantly, psoriatic spondylitis has been observed in the absence of sacroili

142 Medical therapy of ankylosing spondylitis has improved dramatically with the advent of

143 is, but an infectious trigger for ankylosing spondylitis has not yet been established.

144 nts with rheumatoid arthritis and ankylosing spondylitis have been reported, and generic quality-of-l

145 soriatic arthritis and uveitis in ankylosing spondylitis, have also been observed.

146 IL-23 receptor are associated with ankyosing spondylitis, however, it remains unclear whether IL-23 a

147 shown to control the symptoms of ankylosing spondylitis in a phase 2 trial.

148 ining increased susceptibility to ankylosing spondylitis in children.

149 slows radiographic progression in ankylosing spondylitis in data from clinical trials may be because

150 g Pgis2 locus, inducing as high incidence of spondylitis in F2 hybrids as was found in the spondyliti

151 Severity of spondylitis in F2 mice positively correlated with serum

152 ns in human genome, which control ankylosing spondylitis in human patients.

153 hed clinical account of a case of ankylosing spondylitis in the United States.

154 nce, severity, and duration of arthritis and spondylitis, in the absence of colitis.

155 has relevance to diseases such as ankylosing spondylitis, in which HLA-B27 and ERAP jointly contribut

156 ic anemia, pernicious anemia, and ankylosing spondylitis), infectious (pneumonia, hepatitis, meningit

157 oL) instrument, the ASsessment in Ankylosing Spondylitis International Working Group criteria (ASAS)

158 Ankylosing spondylitis is a common form of inflammatory arthritis p

159 Ankylosing spondylitis is a genetically determined and commonly fam

160 Ankylosing spondylitis is an inflammatory autoimmune disease and ev

161 Ankylosing spondylitis is associated with increased risk for vascul

162 ciation further substantiate that ankylosing spondylitis is determined to a large extent by genes out

163 w York criteria, the diagnosis of ankylosing spondylitis is made based on the presence of advanced le

164 rly half of the susceptibility to ankylosing spondylitis is provided by major histocompatibility comp

165 f the major goals of treatment of ankylosing spondylitis is to prevent or slow the development of spi

166 disease and evidence showed that ankylosing spondylitis may be a microbiome-driven disease.

167 this animal model of experimentally induced spondylitis might facilitate the identification of spond

168 ile rheumatoid arthritis (n = 3), ankylosing spondylitis (n = 1), and psoriatic spondylarthropathy (n

169 d arthritis, psoriatic arthritis, ankylosing spondylitis, non-infectious uveitis, and multiple sclero

170 , psoriasis, psoriatic arthritis, ankylosing spondylitis, or inflammatory bowel disease using Medicar

171 ions convincingly associated with ankylosing spondylitis (P < 5 x 10(-8) in the combined discovery an

172 presumed sarcoidosis compared to ankylosing spondylitis (p = 0.0001), behcet's disease (p = 0.0001),

173 sumed sarcoidosis with respect to ankylosing spondylitis (p = 0.0001), behcet's disease, (p = 0.0001)

174 wo new genes, IL23R and ARTS1, in ankylosing spondylitis pathogenesis.

175 e differentially abundant between ankylosing spondylitis patients and healthy controls.

176 A recent trial in ankylosing spondylitis patients demonstrated continuous nonsteroida

177 Specifically, the ankylosing spondylitis patients demonstrated increases in the abund

178 sis patients and in 3 of 12 (25%) ankylosing spondylitis patients.

179 in probiotics, accumulated in the ankylosing spondylitis patients.

180 ermissive genetic locus in murine PG-induced spondylitis (PGIS).

181 in the pharmacological therapy of ankylosing spondylitis, physical therapy remains an essential part

182 the spinal cord in the course of ankylosing spondylitis, present in MRI include: bone marrow edema,

183 genesis or development process of ankylosing spondylitis, providing new leads for the development of

184 soriasis, psoriatic arthritis, or ankylosing spondylitis (psoriasis and spondyloarthropathies) combin

185 eria for SpA, without evidence of ankylosing spondylitis, psoriasis, inflammatory bowel disease, or p

186 reatment of rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, and juvenile idiopathi

187 diseases other than RA, including ankylosing spondylitis, psoriatic arthritis, and polymyositis, in 3

188 category of spondyloarthropathy (ankylosing spondylitis, psoriatic arthritis, reactive arthritis, un

189 tis Functional Index (BASFI), the Ankylosing Spondylitis Quality of Life (ASQoL) instrument, the ASse

190 Form 36 (SF-36) Health Survey and Ankylosing Spondylitis Quality of Life (ASQoL) Questionnaire.

191 Activity Index (BASDAI), and the Ankylosing Spondylitis Quality of Life (ASQoL) questionnaire.

192 ips were scored by using the Bath Ankylosing Spondylitis Radiology Index (BASRI) by an experienced ra

193 graphs were scored using the Bath Ankylosing Spondylitis Radiology Index for the spine (BASRI-s), and

194 c diseases that primarily include ankylosing spondylitis, reactive arthritis, and the arthritis assoc

195 gical conditions (i.e. psoriasis, ankylosing spondylitis, rheumatoid arthritis, fibromyalgia) than th

196 four genetic loci associated with ankylosing spondylitis risk and identifies a major role for the int

197 class I presentation, only affect ankylosing spondylitis risk in HLA-B27-positive individuals.

198 in, muscular back pain, radicular back pain, spondylitis, sacroiliitis, and other) and overall diagno

199 sample of members of the National Ankylosing Spondylitis Society.

200 which were scored using the Stoke Ankylosing Spondylitis Spine Score.

201 erleukin-1 (IL-1) region genes in ankylosing spondylitis suggested the susceptibility to be conferred

202 ta-analysis of published scans of ankylosing spondylitis susceptibility has confirmed sites on chromo

203 stocompatibility complex genes in ankylosing spondylitis susceptibility, and suggests areas for futur

204 ity complex), 10q, 16q and 19q in ankylosing spondylitis susceptibility.

205 The dominant spondylitis-susceptibility allele for Pgis2 locus is der

206 litis might facilitate the identification of spondylitis-susceptibility genes in humans.

207 pondylitis in F2 hybrids as was found in the spondylitis-susceptible parent BALB/c strain.

208 multiple sclerosis, psoriasis and ankylosing spondylitis that inclusion of known covariates can subst

209 fective structure modification in ankylosing spondylitis, the data strongly suggest a benefit, at lea

210 As in human ankylosing spondylitis, the MHC was the major permissive genetic lo

211 evidence that HLA-B27 operates in ankylosing spondylitis through a mechanism involving aberrant proce

212 erapy should remain a mainstay of ankylosing spondylitis treatment complementing medical therapy.

213 ay result in a paradigm shift for ankylosing spondylitis treatment similar to that undergone for rheu

214 Autoimmune spondylitis was induced in BALB/c mice and their MHC-mat

215 Ankylosing spondylitis was more prevalent among children (odds rati

216 identify susceptibility loci for ankylosing spondylitis, we undertook a genome-wide association stud

217 % of patients were diagnosed with ankylosing spondylitis were ascertained from a database of 4400 cas

218 nd histopathologic severity of arthritis and spondylitis were evaluated.

219 major genetic loci Pgis1 and Pgis2 of murine spondylitis were homologous to chromosome regions in hum

220 atients with active, inflammatory ankylosing spondylitis were randomly assigned to receive twice-week

221 th psoriatic arthritis and 1 with ankylosing spondylitis) were isolated by positive selection and sti

222 ces spinal inflammation in active ankylosing spondylitis when compared to placebo; there was no compa

223 are few effective treatments for ankylosing spondylitis, which causes substantial morbidity.

224 omplex genes in predisposition to ankylosing spondylitis, which will be summarized here.

225 differ in their susceptibility to ankylosing spondylitis, with about 2.5 men affected for every woman

226 of the overall susceptibility to ankylosing spondylitis, with about half of the genetic contribution

227 ted arthritis progress to develop ankylosing spondylitis within 10 years after presentation.