ライフサイエンスコーパス: achalasia

1 compression and pseudorelaxation, or spastic achalasia.

2 e the most effective therapeutic options for achalasia.

3 prospective studies of treatment efficacy in achalasia.

4 literature search of articles on esophageal achalasia.

5 ), 209 patients underwent Heller myotomy for achalasia.

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

7 scopic myotomy is the preferred treatment of achalasia.

8 enteric neuronal hyperplasia and esophageal achalasia.

9 undergoing myotomy as secondary treatment of achalasia.

10 hown to be an effective primary treatment of achalasia.

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

12 +/- 1.5 years) with manometrically confirmed achalasia.

13 LES hypertension and impaired relaxation in achalasia.

14 rtension with impaired relaxation resembling achalasia.

15 in a population of patients with idiopathic achalasia.

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

17 sidered the primary treatment for esophageal achalasia.

18 lasting relief of dysphagia in patients with achalasia.

19 nomic nervous system, have been described in achalasia.

20 mechanism in the pathogenesis of idiopathic achalasia.

21 uding contractions) of patients with type II achalasia.

22 nvasive surgical methods to treat esophageal achalasia.

23 have replaced cardiomyotomy for treatment of achalasia.

24 cardiomyotomy and partial fundoplication for achalasia.

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

26 ical features that are distinct from classic achalasia.

27 geal pressurization in patients with type II achalasia.

28 he currently available robust treatments for achalasia.

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

30 copic HM for safe and effective treatment of achalasia.

31 me for patients treated by cardiomyotomy for achalasia.

32 might be a safe and effective treatment for achalasia.

33 that LHM is the most effective treatment for Achalasia.

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

35 ith comorbidities and as salvage therapy for achalasia.

36 an established therapy for the treatment of achalasia.

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

38 ification, have increased the recognition of achalasia.

39 tulinum toxin injection in the management of achalasia.

40 onsidered first-line treatment of esophageal achalasia.

41 ure for evaluating efficacy of treatment for achalasia.

42 ning efficacy of treatment for patients with achalasia.

43 ical and symptomatic outcomes after POEM for achalasia.

44 ysiology: DES with short latency and spastic achalasia.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 8 with type 2 (47%), and 4 with type 3 (80%) achalasia after myotomy.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

82 patients undergoing operative management of achalasia are collected prospectively.

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

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

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

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

87 patients undergoing laparoscopic myotomy for achalasia at our institution.

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

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

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

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

92 Achalasia can be categorized into 3 subtypes that are di

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

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

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

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

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

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

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

100 Achalasia, diffuse esophageal spasm, and nutcracker esop

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

102 assification to supplement prediction of the achalasia disease course.

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

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

105 In patients with achalasia, EGJ distensibility correlated with esophageal

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

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

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

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

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

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

112 Vigorous achalasia has pathological features that are distinct fr

113 Patients with achalasia have a variable prognosis after endoscopic or

114 Although the diagnosis of achalasia hinges on demonstrating impaired esophagogastr

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

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

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

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

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

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

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

122 Achalasia is a chronic esophageal motility disorder char

123 Idiopathic achalasia is a motility disorder of the esophagus charac

124 Achalasia is a rare motility disorder of the oesophagus

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

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

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

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

129 Esophageal achalasia is most commonly treated with laparoscopic myo

130 Manometry should be performed if achalasia is suspected.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

149 Eighteen achalasia patients underwent POEMs between October 2010

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

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

152 Achalasia remains the most investigated and understood m

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

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

155 Achalasia should be considered when dysphagia is present

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

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

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

159 Achalasia significantly affects patients' quality of lif

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

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

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

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

164 treatment response were compared among the 3 achalasia subtypes.

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

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

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

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

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

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

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

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

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

174 76 patients who participated in the European achalasia trial.

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

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

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

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

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

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

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

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

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

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

185 Variants of achalasia were defined by finding manometric features th

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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