ライフサイエンスコーパス: IRIS

1 IRIS cases were similar overall to non-IRIS cases in his

2 IRIS developed 2-12 months after starting antifungals in

3 IRIS flow cytometry data provides useful information in

4 IRIS is a simple, inexpensive, multiplexed, high-through

5 IRIS is associated with an increased risk of admission t

6 IRIS is associated with an increased risk of hospitaliza

7 IRIS offers four main advantages compared to existing te

8 IRIS presents with cerebral manifestations.

9 IRIS reflects pathogenic immune responses against opport

10 IRIS Registry patients with nAMD who received bevacizuma

11 The 2011 IRIS assessment of dichloromethane provides insights int

12 Among 3876 IRIS participants (mean age, 63 years; 65% male), 377 st

13 The study cohort was composed of 3876 IRIS participants, mean age 63 years, 65% male, 89% whit

14 Of the 3876 IRIS participants, 3398 had a 3MS score at baseline and

15 Plasma from 51 IRIS cases, including 6 stratified by preenrollment CD4

16 standard deviation for FBP (638.9 +/- 9.6), IRIS (622.7 +/- 15.2), and SAFIRE (631.4 +/- 17.6) were

17 t in 2 cases JCV persisted > 21 months after IRIS accompanied by delayed clinical improvement.

18 n a decline of CD8(+) T-cell responses after IRIS.

19 ary syndromes (MI and unstable angina) among IRIS participants.

20 n CD4 cell count at lymphoma diagnosis among IRIS cases was 173 cells/microL (interquartile range, 73

21 ncreased early mortality was suggested among IRIS cases.

22 ART initiation until week 24, the time of an IRIS event or death.

23 The primary outcome was time to an IRIS event by 24 weeks.

24 Big Data drawing on Medicare claims and IRIS Registry records can help identify additional areas

25 and significantly lower rates of relapse and IRIS than itraconazole.

26 HCS is associated with seizures and IRIS, and correlates histologically with JCV focal leuko

27 By using both approaches, IRIS can overcome with reasonable accuracy the analytica

28 onal T-cell responses by 3 months after ART, IRIS patients were strikingly monofunctional (generally

29 thout a diagnosis of tuberculosis-associated IRIS (controls), on the basis of outcomes recorded in th

30 ls and patients with tuberculosis-associated IRIS (p=0.45), were substantially lower in patients who

31 uberculosis who have tuberculosis-associated IRIS and death.

32 Patients with tuberculosis-associated IRIS had reduced pre-ART concentrations of several pro-i

33 Tuberculosis-associated IRIS has been associated with quicker recovery of cellul

34 after ART initation, tuberculosis-associated IRIS was independently associated with greater increases

35 ation with death and tuberculosis-associated IRIS, compared with controls.

36 d patients as having tuberculosis-associated IRIS, early mortality, or survival without a diagnosis o

37 sentation and survival were examined between IRIS and non-IRIS cases.

38 rall survival at 5 years was similar between IRIS (49%; 95% confidence interval [CI], 37%-64%) and no

39 centiles showed excellent agreement for both IRIS and SAFIRE with FBP (kappa = 0.975 [0.942-1.00] and

40 several ovarian cancer cell lines, and BRCA1-IRIS silencing or inactivation using a novel inhibitory

41 In a mouse xenograft model, BRCA1-IRIS inactivation using this novel inhibitory peptide re

42 varian epithelial cells overexpressing BRCA1-IRIS formed metastasis in mice when injected in the peri

43 ovarian cancer samples analyzed showed BRCA1-IRIS and survivin overexpression and lacked nuclear FOXO

44 We show that BRCA1-IRIS activates two autocrine signaling loops, brain-deri

45 ther, these data strongly suggest that BRCA1-IRIS and/or BDNF/TrkB and NRG1/ErbB2 could serve as rati

46 form tumors or metastases in mice when BRCA1-IRIS was silenced in them.

47 This study investigates whether BRCA1-IRIS is a novel treatment target for ovarian cancers and

48 on the coated silicon surface as analysed by IRIS.

49 sociated with increased risk of developing C-IRIS.

50 Patients with CM who experienced C-IRIS (N = 27) upon ART initiation were compared to CD4+

51 esponses after cART, were risk factors for C-IRIS.

52 ecrosis factor-alpha levels were higher in C-IRIS patients compared to controls (all P < .05), with I

53 , 1.96-44.0]; P = .005) were predictive of C-IRIS.

54 Patients with paradoxical C-IRIS (n = 27), compared with patients with no neurologic

55 vels of cytokines and chemokines predicted C-IRIS and are potential predictive biomarkers.

56 mune reconstitution inflammatory syndrome (C-IRIS) may be driven by aberrant T-cell responses against

57 mune reconstitution inflammatory syndrome (C-IRIS), upon initiation of antiretroviral therapy (ART).

58 nervous system may predispose patients to C-IRIS.

59 The immunological mechanisms underlying C-IRIS are incompletely defined and no reliable predictive

60 Patients with C-IRIS (n = 26), compared with those with no neurological

61 ls, both of which could be associated with C-IRIS immunopathogenesis.

62 CD4+ T-cell count-matched patients without C-IRIS (N = 27).

63 CM-IRIS was associated with an increasing frequency of CSF

64 vs 0 of 14 in the control arm experienced CM-IRIS (P=.002).

65 to more effectively treat CM and prevent CM-IRIS.

66 21) of antifungal therapy, and those with CM-IRIS (n = 10).

67 baseline CD4 count <350 cells/muL developed IRIS.

68 study, we analyzed 20 patients who developed IRIS following initiation of ART and 16 patients who did

69 During IRIS, tissues were heavily infiltrated by CD3(+), predom

70 was high, whereas serum IL-10 was low during IRIS.

71 sregulated immune response, with exacerbated IRIS and greater pulmonary function deficits than those

72 nd extends host survival during experimental IRIS.

73 were not significantly different among FBP, IRIS, and SAFIRE in paired comparisons (median Agatston

74 crosis factor blockade may be beneficial for IRIS and warrants further study in clinical trials.

75 The EC50 values for the E-screen and FT-IRIS assays were 2.29 and 2.56 ppt, respectively, indica

76 The use of FT-IRIS enabled subcellular imaging of the cells and determ

77 transform infrared imaging spectroscopy (FT-IRIS) was investigated.

78 The FT-IRIS method shows potential to be used as a rapid and se

79 The FT-IRIS method, when combined with principal component anal

80 e observed at the single cell level using FT-IRIS, are reflective of physiological changes that are o

81 In total, 64 (23%) patients had IRIS events, 33 (24%) in the maraviroc arm and 31 (23%)

82 64 (23%) patients had IRIS events, 33 (24%) in the maraviroc group and 31 (23%

83 processing correction significantly improved IRIS accuracy in both natural samples and alcohol diluti

84 To directly test the role of IL-6 in IRIS pathology, we used a model of experimentally induci

85 esponses to PPD were significantly higher in IRIS patients compared to controls during the IRIS time

86 bial translocation appear to be important in IRIS pathogenesis.

87 trol stimulation were significantly lower in IRIS patients at all time points.

88 roaches to cope with contaminated samples in IRIS: on-line oxidation of organic compounds (MCM) and p

89 we used a model of experimentally inducible IRIS in which M. avium-infected T cell-deficient mice un

90 These changes provide insight into IRIS pathogenesis and could be exploited to more effecti

91 g exchangeable single-molecule localization (IRIS) approach to SMLM, in the context of the fibrous ac

92 Detailed studies of lymphoma IRIS might identify immunologic mechanisms of lymphoma c

93 s met a uniformly applied unmasking lymphoma IRIS case definition.

94 eristics and survival for unmasking lymphoma IRIS have not been described.

95 Unmasking lymphoma IRIS was defined as lymphoma within 6 months after ART a

96 56 (12%) met criteria for unmasking lymphoma IRIS.

97 These features make IRIS an ideal candidate for clinical and diagnostic appl

98 way is not only a biomarker of mycobacterial IRIS but also a major mediator of pathology distinct fro

99 erse events in 3 patients with mycobacterial IRIS.

100 ls/muL, were analyzed and compared to 94 non-IRIS controls.

101 % confidence interval [CI], 37%-64%) and non-IRIS (44%; 95% CI, 39%-50%), although increased early mo

102 survival were examined between IRIS and non-IRIS cases.

103 Cs from paradoxical TB-IRIS patients and non-IRIS controls (HIV-TB-coinfected patients commencing ant

104 tected in patients with TBM-IRIS than in non-IRIS controls.

105 Patients with TBM-non-IRIS whose CSF cultures were positive for M. tuberculosi

106 BM-IRIS, compared with patients with TBM-non-IRIS whose cultures were positive at baseline.

107 ix metalloproteinases, compared with TBM-non-IRIS.

108 IRIS (n = 16) and those who did not (TBM-non-IRIS; n = 18).

109 IRIS cases were similar overall to non-IRIS cases in histologic distribution and clinical chara

110 Patients with TB-IRIS were compared to non-IRIS controls using chi(2) and rank-sum tests and logist

111 uberculosis-IRIS patients, compared with non-IRIS patients.

112 ses to hkH37Rv in TB-IRIS, compared with non-IRIS PBMC (p = 0.035).

113 In years 1-3 of IRIS, emergent resistance to oseltamivir in influenza vi

114 the spectrum of previously reported cases of IRIS reactions in this population.

115 t at least up to 3 months after cessation of IRIS.

116 ms, and therefore potential determinants, of IRIS are still unknown.

117 had no significant effect on development of IRIS after ART initiation.

118 n CSF tend to evolve with the development of IRIS, with increasing proportions of activated CD4(+) T

119 the challenges inherent to the diagnosis of IRIS, especially in patients without human immunodeficie

120 ned suppressed before and after emergence of IRIS.

121 The incidence of IRIS, and drug toxicity was not significantly different

122 The primary outcome was occurrence of IRIS by 24 weeks.

123 meaningful protection from the occurrence of IRIS in people with advanced HIV infection.

124 meaningful protection from the occurrence of IRIS in persons with advanced HIV infection.

125 y is not instrumental in the pathogenesis of IRIS in CWD.

126 data including seizure history, presence of IRIS, and MR imaging scans from PML patients evaluated a

127 blockade with maraviroc reduces the risk of IRIS.

128 blockade using maraviroc reduces the risk of IRIS.

129 -alpha2 were associated with greater risk of IRIS.

130 ant effect on frequency, time or severity of IRIS events after ART initiation.

131 The clinical utility of IRIS was demonstrated by detecting allergen-specific IgE

132 ariance ANOVA to investigate their impact on IRIS duration; and (3) a linear mixed model to assess th

133 azard ratio [HR] = 1.05; p = 0.92), but once IRIS emerged, its duration was significantly longer in p

134 need heightened awareness for new onset PML, IRIS, and MS relapse in evaluating neurological decline

135 tics of inflammatory NTZ-PML lesions and PML-IRIS to determine differentiating and overlapping featur

136 earliest sign of natalizumab-associated PML-IRIS with a frequent imaging pattern of contrast-enhanci

137 inflammation (90% at diagnosis, 100% at PML-IRIS).

138 nosis was similar to the pattern seen at PML-IRIS, with contrast enhancement representing the most fr

139 o investigate their impact on full-blown PML-IRIS latency; (2) an analysis of variance ANOVA to inves

140 r prophylactic use to prevent full-blown PML-IRIS seems to negatively impact on the longitudinal disa

141 ML presenting with lesions suggestive of PML-IRIS during follow-up.

142 the earliest imaging characteristics of PML-IRIS manifestation in natalizumab-treated patients with

143 e most common imaging sign suggestive of PML-IRIS, seen in 92.3% of the patients (with patchy and/or

144 were followed up until the occurrence of PML-IRIS.

145 ne reconstitution inflammatory syndrome (PML-IRIS).

146 ne reconstitution inflammatory syndrome (PML-IRIS).

147 (10%) at diagnosis, as compared with the PML-IRIS stage (40%).

148 at the time of PML diagnosis and at the PML-IRIS stage overlap but differ in their severity of infla

149 reatment with PLEX was not associated to PML-IRIS latency (hazard ratio [HR] = 1.05; p = 0.92), but o

150 nger BPI use, after accounting for potential IRIS and other factors.

151 ockade of IL-6 and IFN-gamma further reduces IRIS pathology, even after the onset of wasting disease.

152 , and enhances the resolution of PcP-related IRIS.

153 ffectively cleared Pneumocystis and resolved IRIS.

154 g in the American Academy of Ophthalmology's IRIS (Intelligent Research in Sight) Registry.

155 ometry data (Immune Response In Scleroderma, IRIS) from consented patients followed at the Johns Hopk

156 Interferometric Reflectance Imaging Sensor (IRIS) was utilized to digitally detect and size single g

157 Interferometric Reflectance Imaging Sensor (IRIS), a platform amenable to high-throughput detection

158 lmology (AAO) Intelligent Research in Sight (IRIS) Registry.

159 These capabilities improve the existing SP-IRIS technology, resulting in a more robust and versatil

160 tomatitis virus (VSV) as a model virus on SP-IRIS platform.

161 terferometric Reflectance Imaging Sensor (SP-IRIS) that allows multiplexed phenotyping and digital co

162 terferometric reflectance imaging sensor (SP-IRIS), a simple, label-free biosensor capable of imaging

163 P), iterative reconstruction in image space (IRIS), and sinogram-affirmed iterative reconstruction (S

164 h the Interface Region Imaging Spectrograph (IRIS) at the solar limb reveal a plethora of short, low-

165 ASA's Interface Region Imaging Spectrograph (IRIS) reveal a chromosphere and TR that are replete with

166 h the Interface Region Imaging Spectrograph (IRIS) reveal rapid variability (~20 to 60 seconds) of in

167 y the Interface Region Imaging Spectrograph (IRIS) reveal that it is difficult to determine what is u

168 ) or an isotope ratio infrared spectrometer (IRIS) (in this case a Delta Ray (Thermo Fisher Scientifi

169 Isotope-ratio infrared spectroscopy (IRIS) offers a cheaper alternative to isotope-ratio mass

170 nsulin Resistance Intervention after Stroke (IRIS) trial, patients with a recent ischaemic stroke or

171 immune reconstitution inflammatory syndrome (IRIS) after initiation of antiretroviral therapy at the

172 immune reconstitution inflammatory syndrome (IRIS) after successful initiation of ART.

173 immune reconstitution inflammatory syndrome (IRIS) and death soon after initiation of antiretroviral

174 immune reconstitution inflammatory syndrome (IRIS) in approximately 25% of patients.

175 Immune reconstitution inflammatory syndrome (IRIS) in human immunodeficiency virus (HIV)-infected per

176 immune reconstitution inflammatory syndrome (IRIS) in natalizumab-associated progressive multifocal l

177 immune reconstitution inflammatory syndrome (IRIS) in patients with human immunodeficiency virus (HIV

178 immune reconstitution inflammatory syndrome (IRIS) is a common cause of deterioration in human immuno

179 Immune Reconstitution Inflammatory Syndrome (IRIS) is a common complication of antiretroviral therapy

180 Immune reconstitution inflammatory syndrome (IRIS) is a common complication of antiretroviral therapy

181 Immune reconstitution inflammatory syndrome (IRIS) is a major adverse event of antiretroviral therapy

182 immune reconstitution inflammatory syndrome (IRIS) is currently unclear.

183 immune reconstitution inflammatory syndrome (IRIS) remains incompletely understood, and we know of on

184 Immune reconstitution inflammatory syndrome (IRIS) was reported in 11 patients.

185 immune reconstitution inflammatory syndrome (IRIS) were determined.

186 immune reconstitution inflammatory syndrome (IRIS), and the side-effect profile.

187 immune reconstitution inflammatory syndrome (IRIS), both Dectin-1:mIgG1 and Dectin-1:mIgG2a Fc reduce

188 immune reconstitution inflammatory syndrome (IRIS), but in 2 cases JCV persisted > 21 months after IR

189 immune reconstitution inflammatory syndrome (IRIS), but its underlying cause remains poorly understoo

190 immune reconstitution inflammatory syndrome (IRIS), is a serious complication.

191 immune reconstitution inflammatory syndrome (IRIS).

192 immune reconstitution inflammatory syndrome (IRIS).

193 immune reconstitution inflammatory syndrome (IRIS).

194 immune reconstitution inflammatory syndrome (IRIS).

195 of an immune recovery inflammatory syndrome (IRIS).

196 immune reconstitution inflammatory syndrome (IRIS).

197 via the Intelligent Retinal Imaging System (IRIS) from June 2013 to April 2014 were included.

198 EPA's Integrated Risk Information System (IRIS) completed an updated toxicological review of dichl

199 om EPA's Integrated Risk Information System (IRIS) database, Spearman rank correlation identified 68%

200 t of the Integrated Risk Information System (IRIS), the U.S. Environmental Protection Agency (EPA) co

201 t of the Integrated Risk Information System (IRIS), the U.S. Environmental Protection Agency (EPA) ha

202 TB-IRIS patients also exhibited greater upregulation of NLR

203 TB-IRIS patients and controls had similar CD4 counts, level

204 In contrast, TB-IRIS patients had significantly greater early increases

205 ntiretroviral therapy who did not develop TB-IRIS).

206 ts without TB, and patients who developed TB-IRIS exhibited the greatest increase in casp1 expression

207 ated with TB-IRIS, both before and during TB-IRIS onset.

208 d patients is increased before and during TB-IRIS, informing novel diagnostic strategies.

209 some activation, was also elevated during TB-IRIS.

210 No biomarkers for TB-IRIS have been identified and the underlying mechanisms

211 granzyme B secretion reduced in PBMC from TB-IRIS patients during corticosteroid treatment.

212 nflammasome activation, are implicated in TB-IRIS pathogenesis.

213 plicate the granule exocytosis pathway in TB-IRIS pathophysiology.

214 +)Valpha24(+)) proportions were higher in TB-IRIS patients (p = 0.004) and were a source of perforin.

215 n and T-cell subsets also were similar in TB-IRIS patients and controls.

216 els were lower both pre- and post-cART in TB-IRIS patients, providing evidence of inadequate inflamma

217 CD4(+) T cells and NK cells was higher in TB-IRIS patients, providing evidence that IL-18 is a marker

218 secretion of cytokines including IL-1 in TB-IRIS patients.

219 ome activation both pre- and post-cART in TB-IRIS patients.

220 creased IFN-gamma responses to hkH37Rv in TB-IRIS, compared with non-IRIS PBMC (p = 0.035).

221 cytokines and caspase-1/5 are elevated in TB-IRIS.

222 erence 3.587 and 2.828, respectively), in TB-IRIS.

223 ociated with a 2.8-fold increased risk of TB-IRIS (95% confidence interval, 1.1 to 7.5-fold).

224 ta provide insight on the pathogenesis of TB-IRIS and may assist the development of specific therapie

225 At the characteristic time of TB-IRIS onset (week 2), the signature is characterized by o

226 was associated with a higher incidence of TB-IRIS than delayed ART (RR, 2.31 [CI, 1.87 to 2.86]; I2 =

227 ociated with a 2-fold higher frequency of TB-IRIS.

228 strategy for prevention and treatment of TB-IRIS.

229 responses and development of paradoxical TB-IRIS on antiretroviral therapy (ART).

230 analyses of human PBMCs from paradoxical TB-IRIS patients and non-IRIS controls (HIV-TB-coinfected p

231 ssociated with development of paradoxical TB-IRIS.

232 une reconstitution inflammatory syndrome (TB-IRIS) complicates combination antiretroviral therapy (cA

233 une reconstitution inflammatory syndrome (TB-IRIS) frequently complicates combined antiretroviral the

234 une reconstitution inflammatory syndrome (TB-IRIS) remains unclear.

235 une reconstitution inflammatory syndrome (TB-IRIS), in Cape Town, South Africa.

236 une reconstitution inflammatory syndrome (TB-IRIS).

237 une reconstitution inflammatory syndrome (TB-IRIS).

238 asma mitochondrial DNA levels showed that TB-IRIS patients experienced greater cell death, especially

239 ory cytokines in patients who progress to TB-IRIS.

240 immunopathological mechanisms underlying TB-IRIS are incompletely defined, and improved understandin

241 In a secondary analysis, patients with TB-IRIS had rapid, concomitant increases in tuberculosis-sp

242 Patients with TB-IRIS were compared to non-IRIS controls using chi(2) and

243 lular matrix turnover was associated with TB-IRIS, both before and during TB-IRIS onset.

244 enced, which is greatest in patients with TB-IRIS.

245 TBM-IRIS is a frequent, severe complication of ART in HIV-as

246 ry response that manifests clinically as TBM-IRIS in most, but not all, patients with TBM.

247 s system inflammation that characterizes TBM-IRIS.

248 compared between patients who developed TBM-IRIS (n = 16) and those who did not (TBM-non-IRIS; n = 1

249 compared between patients who developed TBM-IRIS (TBM-IRIS patients) and those who did not (non-TBM-

250 ercent (16/34) of TBM patients developed TBM-IRIS, which manifested with severe features of inflammat

251 gnosis and 2 weeks after ART initiation, TBM-IRIS was associated with severe, compartmentalized infla

252 between patients who developed TBM-IRIS (TBM-IRIS patients) and those who did not (non-TBM-IRIS patie

253 RIS patients) and those who did not (non-TBM-IRIS patients).

254 transcripts, from before development of TBM-IRIS through IRIS symptom onset.

255 after ART initiation, at presentation of TBM-IRIS, and 14 days thereafter.

256 To investigate the pathogenesis of TBM-IRIS, we performed longitudinal whole-blood microarray a

257 ate immune system in the pathogenesis of TBM-IRIS.

258 n (IFN)-gamma at TBM diagnosis predicted TBM-IRIS (area under the curve = 0.91 [95% CI, .53-.99]).

259 Patients in whom TBM-IRIS eventually developed had significantly more abundan

260 s similar to those seen in patients with TBM-IRIS at both time points.

261 lammasomes was detected in patients with TBM-IRIS than in non-IRIS controls.

262 significantly increased in patients with TBM-IRIS, compared with patients with TBM-non-IRIS whose cul

263 ors at the disease site in patients with TBM-IRIS.

264 ous meningitis (TBM) are associated with TBM-IRIS.

265 The findings that IRIS in CWD mainly are mediated by nonspecific activatio

266 The IRIS algorithm population statistics were calculated.

267 The IRIS algorithm shows promise as a screening program, but

268 The IRIS trial (Insulin Resistance Intervention after Stroke

269 The IRIS trial (Insulin Resistance Intervention after Stroke

270 The IRIS-based interpretations were compared with manual int

271 sight-threatening diabetic eye disease, the IRIS algorithm positive predictive value was 10.8% (95%

272 RIS patients compared to controls during the IRIS time point, but CD4(+) and CD8(+) T-cell responses

273 RNA at lymphoma diagnosis resulting from the IRIS case definition.

274 Relating data from the IRIS Registry and NHANES could be a novel method for ass

275 Data from the IRIS Registry were used to calculate the real-world prev

276 We analyzed data from the IRIS Registry, from January 1, 2012 to December 31, 2014

277 Innovations in the IRIS assessment include estimation of cancer risk specif

278 ovement, such as in the 18.3% of eyes in the IRIS Registry having 1-month-postoperative VA worse than

279 Visual acuity (VA) in the IRIS Registry in eyes with and without postoperative end

280 In the IRIS Registry the endophthalmitis rate after cataract su

281 The sensitivity of the IRIS algorithm in detecting sight-threatening diabetic e

282 Sensitivity and false-negative rate of the IRIS computer-based algorithm compared with reading cent

283 n levels transiently rise at the time of the IRIS event in HIV-infected patients, unmasking Mycobacte

284 In the case of the IRIS system, we demonstrate that the use of two standard

285 In this large urban setting, the IRIS computer algorithm-based screening program had a hi

286 These IRIS observations not only confirm that the photosphere

287 from before development of TBM-IRIS through IRIS symptom onset.

288 ng proST versus therST was not associated to IRIS latency (HR = 0.67; p = 0.39) or duration (p = 0.95

289 riving T-cell activation and contributing to IRIS pathophysiology.

290 There was no difference in the time to IRIS events between treatment arms (HR 1.08, 95% CI (0.6

291 No difference in the time to IRIS events was noted between the treatment groups (HR 1

292 kine and immunopathology during tuberculosis-IRIS.

293 ntiinflammatory response during tuberculosis-IRIS.

294 2 (IL-22) transcript levels for tuberculosis-IRIS patients, compared with non-IRIS patients.

295 rentially induced in PBMCs from tuberculosis-IRIS patients after in vitro stimulation, and higher con

296 ed CENTRAL, CINAHL, Embase, MEDLINE, and WHO IRIS databases for publications between Jan 1, 2000, and

297 ent was more pronounced in CWD patients with IRIS than in those without IRIS.

298 Of the 20 patients with IRIS, 16 (80.0%) had HCS compared with 14 of 29 (49.3%)

299 pared with 14 of 29 (49.3%) patients without IRIS (p=0.04).

300 CWD patients with IRIS than in those without IRIS.