ライフサイエンスコーパス: achalasia

1 elops into type II achalasia and then type I achalasia.

2 ification, have increased the recognition of achalasia.

3 tulinum toxin injection in the management of achalasia.

4 outcomes among treatment-naive patients with achalasia.

5 onsidered first-line treatment of esophageal achalasia.

6 ure for evaluating efficacy of treatment for achalasia.

7 ning efficacy of treatment for patients with achalasia.

8 ical and symptomatic outcomes after POEM for achalasia.

9 ysiology: DES with short latency and spastic achalasia.

10 option to consider as first-line therapy for achalasia.

11 compression and pseudorelaxation, or spastic achalasia.

12 e the most effective therapeutic options for achalasia.

13 prospective studies of treatment efficacy in achalasia.

14 literature search of articles on esophageal achalasia.

15 ), 209 patients underwent Heller myotomy for achalasia.

16 scopic myotomy is the preferred treatment of achalasia.

17 enteric neuronal hyperplasia and esophageal achalasia.

18 undergoing myotomy as secondary treatment of achalasia.

19 hown to be an effective primary treatment of achalasia.

20 +/- 1.5 years) with manometrically confirmed achalasia.

21 LES hypertension and impaired relaxation in achalasia.

22 rtension with impaired relaxation resembling achalasia.

23 in a population of patients with idiopathic achalasia.

24 ients (23 white and 9 black) with idiopathic achalasia.

25 sidered the primary treatment for esophageal achalasia.

26 lasting relief of dysphagia in patients with achalasia.

27 nomic nervous system, have been described in achalasia.

28 mechanism in the pathogenesis of idiopathic achalasia.

29 nvasive surgical methods to treat esophageal achalasia.

30 have replaced cardiomyotomy for treatment of achalasia.

31 PD is a safe, durable treatment for achalasia.

32 cardiomyotomy and partial fundoplication for achalasia.

33 ical features that are distinct from classic achalasia.

34 clinicians may use FLIP findings to diagnose achalasia.

35 better understanding regional differences in achalasia.

36 ed with gastro-oesophageal reflux disease or achalasia.

37 a such as gastroesophageal reflux disease or achalasia.

38 t neurological disorders, such as esophageal achalasia.

39 omy, with superiority for type III (spastic) achalasia.

40 certain clinical scenarios such as type III achalasia.

41 were not different in the three subtypes of achalasia.

42 sidered the preferred treatment for type III achalasia.

43 ed as a standard intervention for esophageal achalasia.

44 increasingly utilized endoscopic therapy for achalasia.

45 atients had symptoms suggestive of an active achalasia.

46 tion with EC development among patients with achalasia.

47 treat a host of esophageal diseases such as achalasia.

48 r optimizing the monitoring of patients with achalasia.

49 ith increased risk of EC among patients with achalasia.

50 hagogastric junction outflow obstruction and achalasia.

51 M) are established treatments for idiopathic achalasia.

52 fundoplication in patients with symptomatic achalasia.

53 he currently available robust treatments for achalasia.

54 tic analysis of 2 siblings with infant-onset achalasia.

55 hought to have a role in the pathogenesis of achalasia.

56 tentional weight loss initially diagnosed as achalasia.

57 uding contractions) of patients with type II achalasia.

58 oxide synthase 1-deficient mice, which have achalasia.

59 hat are often indistinguishable from primary achalasia.

60 geal pressurization in patients with type II achalasia.

61 long-term follow-up after cardiomyotomy for achalasia.

62 copic HM for safe and effective treatment of achalasia.

63 try and endoscopy was suggestive for primary achalasia.

64 me for patients treated by cardiomyotomy for achalasia.

65 might be a safe and effective treatment for achalasia.

66 that LHM is the most effective treatment for Achalasia.

67 PD or LHM than patients with types I and III achalasia.

68 ith comorbidities and as salvage therapy for achalasia.

69 an established therapy for the treatment of achalasia.

70 r than that of LHM for patients with type II achalasia (100% vs 93%; P < .05), but LHM had a higher s

71 nts; P = 0.03) and in patients with vigorous achalasia (100% vs. 52% with classic achalasia; P = 0.03

72 spine-LES angle was smaller in patients with achalasia (104 degrees ) compared with controls (124 deg

73 e 209 patients undergoing Heller myotomy for achalasia, 154 received endoscopic therapy before being

74 age, 40 +/- 4.1 years) and 30 patients with achalasia (16 male; age, 51 +/- 3.1 years).

75 nety-nine patients were newly diagnosed with achalasia (21 type I, 49 type II, 29 type III), and 83 o

76 Thirty patients had previous therapy of achalasia, 21 with pneumatic dilation, 1 with BOTOX, 6 w

77 Plasma from 53 patients with achalasia, 22 with EoE, and 20 with GERD (symptoms plus

78 e considered as primary therapy for type III achalasia; 4) if the expertise is available, POEM should

79 ia (81%; P < .01, log-rank test) or type III achalasia (66%; P < .001, log-rank test).

80 5 +/- 2) and 12 patients with a diagnosis of achalasia (7 male; mean age, 63 +/- 13 years; mean body

81 as detected in all 10 patients with type III achalasia; 8 of these patients had a pattern of contract

82 nts with type II achalasia (96%) than type I achalasia (81%; P < .01, log-rank test) or type III acha

83 cess rate than PD for patients with type III achalasia (86% vs 40%; P = .12, difference was not stati

84 ificantly higher among patients with type II achalasia (96%) than type I achalasia (81%; P < .01, log

85 does not demonstrate findings supportive of achalasia, abnormal esophagogastric junction opening on

86 eproducibly subtyping achalasia into classic achalasia, achalasia with pressurization, or spastic ach

87 lder patients with a manometric diagnosis of achalasia, additional investigation to rule out pseudoac

88 y at this locus and called ALADIN (alacrima, achalasia, adrenal insufficiency neurologic disorder).

89 M was found to be an effective treatment for achalasia after a mean follow-up period of 10 months.

90 8 with type 2 (47%), and 4 with type 3 (80%) achalasia after myotomy.

91 tions had the classical triple A syndrome of achalasia, alacrima, adrenal abnormalities and a progres

92 le A (Allgrove) syndrome is characterized by achalasia, alacrima, adrenal abnormalities and a progres

93 in the 0.5% once daily group had oesophageal achalasia), all of which were unrelated to study treatme

94 ic recordings of 58 patients with idiopathic achalasia and 43 control subjects were analyzed with reg

95 RNA-sequencing on esophageal mucosa from 14 achalasia and 8 healthy subjects.

96 ic relief in 94% of patients with nonspastic achalasia and 90% of patients with type 3 achalasia/spas

97 at are specific for individual phenotypes of achalasia and away from the one-size-fits-all approach.

98 ant for assessing motility disorders such as achalasia and diffuse esophageal spasm.

99 there was no association between idiopathic achalasia and DQB1*0602 or DRB1*15, but a trend was foun

100 escribed as minimally invasive therapies for achalasia and gastrointestinal subepithelial tumors orig

101 f any of the measured biomarkers between the achalasia and GERD groups suggesting that luminal stasis

102 y has improved the sensitivity for detecting achalasia and has also enhanced our understanding of spa

103 treatments of infectious diarrhea with zinc; achalasia and Hirschsprung's disease with botulinum toxi

104 uncovered a previously unknown dysfunction (achalasia and impaired gut motility) that explains the g

105 ted in 27% (4 of 15) of patients with type I achalasia and in 65% (18 of 26, including 9 with occludi

106 gly encouraged for patients with symptomatic achalasia and is efficacious even after failures of dila

107 t in patients with diffuse esophageal spasm, achalasia and patients with normal manometry.

108 y, the frequency and severity of symptoms of achalasia and reflux significantly decreased.

109 Idiopathic achalasia and the broad HLA-DQ1 allele were not signific

110 a significant association between idiopathic achalasia and the DQB1*0602 allele (OR, 3.10; chi2 = 7.3

111 d peristalsis and then develops into type II achalasia and then type I achalasia.

112 art review of patients who underwent HCM for achalasia and were followed up postoperatively for at le

113 distensibility is impaired in patients with achalasia and, in contrast to LES pressure, is associate

114 t pH-abnormal GERD, 93 without GERD, 18 with achalasia, and 15 with eosinophilic esophagitis.

115 cally inactive homolog GMPPA cause alacrima, achalasia, and mental retardation syndrome (AAMR syndrom

116 , these mice invariably developed esophageal achalasia, and the enteric neurons and nerve fibers in g

117 e, Cdo(-/-) mice displayed megaesophagus and achalasia, and their lower esophageal sphincter was resi

118 patients undergoing operative management of achalasia are collected prospectively.

119 sults after minimally invasive treatment for achalasia are equivalent to historical outcomes with ope

120 Patients with achalasia are treated with either pneumatic dilation (PD

121 Some, such as achalasia, are diseases with a well defined pathology, c

122 less important than systematically excluding achalasia, as the vague and variable presentations of th

123 's fundoplication in controlling symptoms of achalasia at 2 years.

124 patients undergoing laparoscopic myotomy for achalasia at our institution.

125 A higher percentage of patients with type II achalasia (based on manometric tracings) are treated suc

126 ts were evident only in patients with type 3 achalasia before treatment, intact, weak, or frequent fa

127 ew of patients with an ICD-9 or - 10 code of achalasia between 2005 and 2017 was performed.

128 often billed as a "short term" treatment for achalasia but anecdotally can last years.

129 ed as a new minimally invasive treatment for achalasia, but there have not yet been any randomised cl

130 different surgical treatment modalities for achalasia by Heller's cardiomyotomy (HCM) helps to choos

131 rs) who had laparoscopic esophagomyotomy for achalasia by our group between August 1995 and January 2

132 Achalasia can be categorized into 3 subtypes that are di

133 gical training/skills are needed for optimal achalasia care.

134 utoimmune enteropathy, autoimmune gastritis, achalasia, celiac disease, inflammatory bowel disease, G

135 demonstrates findings strongly supportive of achalasia, clinicians may use FLIP findings to diagnose

136 ificantly reduced in untreated patients with achalasia compared with controls (0.7 +/- 0.9 vs 6.3 +/-

137 displaced 45 to 90 degrees in patients with achalasia compared with controls.

138 The many processes that can mimic idiopathic achalasia continue to be exposed.

139 ever, many physicians treating patients with achalasia continue to offer endoscopic therapies before

140 Fifty-one treatment-naive patients with achalasia, defined and subclassified by high-resolution

141 yotomy specimens from 11 patients with early achalasia, defined as minimal to moderate esophageal dil

142 Although successful treatment of achalasia depends on alleviating the obstruction at the

143 men, nine women; mean age, 52.4 years) with achalasia depicted on barium esophagograms who had under

144 spective cohort study included patients with achalasia diagnosed at or referred for treatment and mon

145 years can pass between symptom onset and an achalasia diagnosis.

146 Achalasia, diffuse esophageal spasm, and nutcracker esop

147 dently diagnose esophageal disorders such as achalasia, direct therapy and predict outcomes.

148 assification to supplement prediction of the achalasia disease course.

149 stinctions objectifies the identification of achalasia, distal esophageal spasm, functional obstructi

150 or hemifundoplication to esophagomyotomy for achalasia does not improve or worsen clinical results.

151 t al. in a group of patients with esophageal achalasia (EA).

152 In patients with achalasia, EGJ distensibility correlated with esophageal

153 2, IL-17, IL-22, and IL-23) of patients with achalasia, eosinophilic esophagitis (EoE), and gastroeso

154 final literature review addressing facets of achalasia epidemiology, pathophysiology, diagnosis, trea

155 n between healthy subjects and patients with achalasia esophagus.

156 the crural diaphragm muscle in patients with achalasia esophagus.

157 Patients with achalasia face a higher risk of developing esophageal ca

158 TBE can accurately identify achalasia/FLIP+ EGJ outflow obstruction when using multi

159 TBE accuracy for predicting achalasia/FLIP+ esophagogastric junction (EGJ) outflow o

160 Data on consecutive HMs and POEMs for achalasia from 2007 to 2012 were collected.

161 ns is linked to severe conditions, including achalasia, gastroparesis, intestinal pseudo-obstruction

162 ll 21 patients with radiographic findings of achalasia had aperistalsis at manometry.

163 One patient with type 3 achalasia had distal esophageal spasm after treatment.

164 Three patients with vigorous achalasia had normal ganglion cell numbers (0.79-0.91 ga

165 Five of the 10 subjects with achalasia had physical breaks in the left crus of the di

166 between the HLA-DQ1 phenotype and idiopathic achalasia has been found, suggesting a possible immunoge

167 Vigorous achalasia has pathological features that are distinct fr

168 Patients with achalasia have a variable prognosis after endoscopic or

169 We enrolled 29 patients with achalasia having a mean age of 24 +/- 16 years and predo

170 Although the diagnosis of achalasia hinges on demonstrating impaired esophagogastr

171 Any of these phenotypes could indicate achalasia; however, without a disease-specific biomarker

172 become apparent that the cardinal feature of achalasia, impaired lower esophageal sphincter relaxatio

173 l methods of managing Zenker diverticula and achalasia, important disorders associated with these pre

174 otulinum toxin is an effective treatment for achalasia in about two thirds of patients, with a durati

175 ppears to be involved in the pathogenesis of achalasia in humans.

176 ay become one of the first-line therapies of achalasia in the next future.

177 Achalasia incidence and prevalence increase with age, bu

178 hies, such as Hirschsprung's disease (HSCR), achalasia, intestinal neuronal dysplasia (IND), chronic

179 By reproducibly subtyping achalasia into classic achalasia, achalasia with pressur

180 Achalasia is a chronic esophageal motility disorder char

181 Idiopathic achalasia is a motility disorder of the esophagus charac

182 Achalasia is a rare disorder of the oesophageal smooth m

183 Achalasia is a rare esophageal disease with potentially

184 Achalasia is a rare motility disorder of the oesophagus

185 Laboratory studies indicate that achalasia is an autoimmune disease in which esophageal m

186 Achalasia is an esophageal motility disorder characteriz

187 Idiopathic achalasia is associated with HLA alleles in a race-speci

188 n relaxation pressure achieved by myotomy in achalasia is associated with partial recovery of perista

189 Achalasia is diagnosed late in this resource-limited set

190 The surgical gold standard for achalasia is laparoscopic Heller myotomy (HM) and partia

191 Esophageal achalasia is most commonly treated with laparoscopic myo

192 Manometry should be performed if achalasia is suspected.

193 Although rare, esophageal achalasia is the best described primary esophageal motil

194 Although the underlying cause of idiopathic achalasia is unknown, the diffuse neuronal effects found

195 oesophageal reflux after esophagomyotomy for achalasia, it may also lead to persistent dysphagia in t

196 surgical myotomy are effective therapies for achalasia; laparoscopic Heller myotomy is emerging as th

197 For type I achalasia, LHM and PD had similar rates of success (81%

198 e significance in defining these variants of achalasia lies in the recognition that these sometimes c

199 OS(-/-)) and W/W(v) mice lacking ICC-IM have achalasia-like LES dysfunction.

200 Some gene changes observed in the mucosa of achalasia may be associated with esophagitis.

201 enoscopy (EGD), patients with a diagnosis of achalasia may receive endotracheal intubation (EI) to re

202 This study included 234 patients with achalasia (median [IQR] age at diagnosis, 45 [32-63] yea

203 e most common initial endoscopic therapy for achalasia, most likely due to its safety and ease of adm

204 y 1976 and September 2011 using the keywords achalasia, myotomy, antireflux surgery, and fundoplicati

205 riasis vulgaris (ncases = 3,089), idiopathic achalasia (ncases = 727) and celiac disease (ncases = 11

206 The focus of attention remains with achalasia, not because of pathophysiologic developments

207 dance is a safe and successful treatment for achalasia of the cardia.

208 rural diaphragm dysfunction in patients with achalasia of the esophagus.

209 results of medical and surgical treatment of achalasia of the esophagus.

210 overall) were ultimately managed as spastic achalasia or DES.

211 ation of inflammatory cytokines is unique to achalasia or occurs with other diseases involving the es

212 New developments in the understanding of achalasia or reports of therapeutic efficacy in either c

213 an in patients without GERD or patients with achalasia (P < .001).

214 igorous achalasia (100% vs. 52% with classic achalasia; P = 0.03).

215 In certain cases of achalasia, particularly those in early stages with minim

216 advances in diagnosis, our understanding of achalasia pathogenesis at the molecular level is very li

217 nduce symptom remission in a treatment-naive achalasia patient.

218 At our institution, all achalasia patients are instructed to avoid solid oral in

219 ial leukocytes were seen in the mucosa of 38 achalasia patients compared to 12 controls.

220 levation of serum inflammatory biomarkers in achalasia patients compared with controls recently was d

221 nificant elevations in IL- 6 (p = 0.0158) in achalasia patients compared with EoE patients.

222 Despite history of myotomy, treated achalasia patients frequently receive EI on follow-up EG

223 Eighteen achalasia patients underwent POEMs between October 2010

224 We identified achalasia patients who underwent POEM from September 202

225 In post-POEM achalasia patients, follow-up TBE at 3-6 months demonstr

226 significantly differed from the remainder of achalasia patients, such that the diagnosis might be que

227 ussed and compared with the remainder of the achalasia population and with controls.

228 ifferent gastrointestinal diseases including achalasia, refractory gastroparesis, and other esophagea

229 Achalasia remains the most investigated and understood m

230 lower esophageal sphincter of patients with achalasia results in effective short-term relief of symp

231 Age and type of achalasia seem to be important predictors of response.

232 Achalasia should be considered when dysphagia is present

233 A diagnosis of achalasia should be considered when patients present wit

234 Endoscopic therapy for achalasia should not be used unless patients are not can

235 l features of esophagi resected for endstage achalasia showed marked depletion of myenteric ganglion

236 Achalasia significantly affects patients' quality of lif

237 Peroral endoscopic myotomy (POEM) for achalasia (sometimes also referred as E-POEM to distingu

238 ive treatment alternatives for patients with achalasia, spastic esophageal disorders and upper gastro

239 ic achalasia and 90% of patients with type 3 achalasia/spastic esophageal motility disorders, with a

240 meal-related chest pain) after treatment of achalasia spectrum disorders.

241 ere found in the distal esophageal mucosa of achalasia subjects and 120 DEGs were identified in proxi

242 Responses to treatment vary based on which achalasia subtype is present.

243 (FLIP) could improve the characterization of achalasia subtypes by detecting nonocclusive esophageal

244 Achalasia subtypes have management and prognostic implic

245 treatment response were compared among the 3 achalasia subtypes.

246 e same plasma cytokine profiles in the three achalasia subtypes.

247 ve been reported in the esophageal mucosa of achalasia, suggesting its involvement in disease pathoge

248 h laparoscopic Heller myotomy for any of the achalasia syndromes; and 5) post-POEM patients should be

249 tients with typical radiographic findings of achalasia, the barium study can be used to guide treatme

250 Controversy concerning the management of achalasia, the best-understood distal motor disorder, is

251 sponses associated with subclassification of achalasia, the use of distal latency in the diagnosis of

252 e effective therapies for type I and type II achalasia; the decision between these treatment modaliti

253 ed for prospective studies on interventional achalasia therapy with predefined exclusion criteria.

254 ommendations: 1) in determining the need for achalasia therapy, patient-specific parameters (Chicago

255 arifying some aspects of the pathogenesis of achalasia, they bring about many more questions that req

256 we performed tissue typing in patients with achalasia to determine their specific HLA phenotypes.

257 Thirty-one patients with achalasia treated with botulinum toxin were followed up

258 treated with either PD or LHM (the European achalasia trial).

259 76 patients who participated in the European achalasia trial.

260 Forty-four patients had achalasia type I (25%), 114 patients had achalasia type

261 had achalasia type I (25%), 114 patients had achalasia type II (65%), and 18 patients had achalasia t

262 achalasia type II (65%), and 18 patients had achalasia type III (10%).

263 h manometry can be detected in patients with achalasia using FLIP topography.

264 uring volumetric distention in patients with achalasia using FLIP topography.

265 lower esophageal sphincter was impaired and achalasia was confirmed in vivo by manometry.

266 Diagnosis of achalasia was established with clinical, radiologic, and

267 The same disorder, achalasia, was observed in genetically modified mice tha

268 nogenetics in the pathogenesis of idiopathic achalasia, we performed tissue typing in patients with a

269 phagomyotomy specimens from 11 patients with achalasia were analyzed and compared with the findings o

270 board-approved clinical trial, patients with achalasia were assigned to undergo Heller myotomy or Hel

271 Variants of achalasia were defined by finding manometric features th

272 roportion of annual procedures performed for achalasia were evaluated over time.

273 ghts into the molecular changes occurring in achalasia were generated in this transcriptomic study.

274 cusing on endoscopic or surgical therapy for achalasia were included (734 total patients).

275 atients with manometric diagnosis of primary achalasia were included.

276 elapsed since laparoscopic cardiomyotomy for achalasia, were identified from a prospective database.

277 sing manometric findings are consistent with achalasia when combined with additional clinical data su

278 ment in the sensitivity for the diagnosis of achalasia when compared with conventional manometry.

279 POEM is an effective and safe procedure for achalasia when performed by experienced operators with a

280 POEM is a recently developed treatment of achalasia, which combines the efficacy of surgical myoto

281 t the opposite extreme is type III (spastic) achalasia, which has no demonstrated neuronal loss but o

282 The most common underlying disorder was achalasia, which was detected in nine (43%) patients.

283 End-stage achalasia with a dilated, non-functioning oesophagus may

284 POEM is an endoscopic therapy for achalasia with a shorter hospitalization than HM.

285 a, achalasia with pressurization, or spastic achalasia with differential responses to treatment, HRM

286 years, who underwent index intervention for achalasia with either LHM, PD, or POEM in the US between

287 esophageal pressurization (type I, classic), achalasia with esophageal compression (type II), achalas

288 s labeled distal esophageal spasm is in fact achalasia with esophageal compression and pseudorelaxati

289 These were categorized into 4 groups: achalasia with minimal esophageal pressurization (type I

290 ressive plexopathy, which likely arises from achalasia with preserved peristalsis and then develops i

291 subtyping achalasia into classic achalasia, achalasia with pressurization, or spastic achalasia with

292 n appears to provide definitive treatment of achalasia with rapid rehabilitation and few complication

293 lasia with esophageal compression (type II), achalasia with spasm (type III), and functional obstruct

294 er scores indicating more severe symptoms of achalasia) without the use of additional treatments, at

295 ial first-line therapy for the management of achalasia, yet payers remain hesitant to reimburse for t