ライフサイエンスコーパス: malabsorption

1 unting), and abnormal function (for example, malabsorption).

2 2-hydroxybutyrate (a known marker of glucose malabsorption).

3 , narrow anastomoses, excluded segments, and malabsorption.

4 , 17 puppies presented with intestinal lipid malabsorption.

5 150 cm, the procedure is believed to induce malabsorption.

6 t of vitamin A under conditions of bile acid malabsorption.

7 utations are the basis for hereditary folate malabsorption.

8 osomal recessive disorder, hereditary folate malabsorption.

9 ue to a low intake of animal source foods or malabsorption.

10 ase did not appear to have a role in the fat malabsorption.

11 d of Pakistani origin with hereditary folate malabsorption.

12 e 1 is a poor test for diagnosing pancreatic malabsorption.

13 osomal recessive disorder, hereditary folate malabsorption.

14 cose to the body and avoidance of intestinal malabsorption.

15 asal ion secretion and corrected the glucose malabsorption.

16 by increased basal ion secretion and glucose malabsorption.

17 ns, which indicated appreciable carbohydrate malabsorption.

18 ents with electrolyte imbalance and nutrient malabsorption.

19 ing in chronic diarrhea and life-threatening malabsorption.

20 to be a poor test for diagnosing pancreatic malabsorption.

21 vels > or =30 ng/mL, suggesting selective Ca malabsorption.

22 oblastic anemia (MGA1), owing to vitamin B12 malabsorption.

23 ntion studies suggest supplemental vitamin E malabsorption.

24 ssociated with three severe disorders of fat malabsorption.

25 m bile acid concentrations, itching, and fat malabsorption.

26 bile and pancreatic secretions to induce fat malabsorption.

27 deficiencies may develop because BPD causes malabsorption.

28 ormally, were fertile and showed no signs of malabsorption.

29 t on parenteral nutrition because of chronic malabsorption.

30 ed with ADfat of zero, consistent with lipid malabsorption.

31 tive intestinal vitamin B12 (B12, cobalamin) malabsorption.

32 and human diseases such as primary bile acid malabsorption.

33 um absorption and reversed water and glucose malabsorption.

34 tic-enzyme supplements to control intestinal malabsorption.

35 ndicated the likely occurrence of intestinal malabsorption.

36 c cycling of bilirubin occurs with bile salt malabsorption.

37 1 was identified in the subject with global malabsorption.

38 f them was associated with acquired fructose malabsorption.

39 for patients with severe malnutrition due to malabsorption.

40 itamin B-12 status may indicate vitamin B-12 malabsorption.

41 iated with intestinal dysbiosis and nutrient malabsorption.

42 tions that protect the body against nutrient malabsorption.

43 genetic predisposition of acquired fructose malabsorption.

44 with apoptosis, increased cell turnover and malabsorption.

45 in the small intestine, leading to nutrient malabsorption.

46 maladaptive bladder remodeling and gut lipid malabsorption.

47 itive for fructose malabsorption and fructan malabsorption.

48 ion and 91 (48.9%) were positive for fructan malabsorption.

49 gnosing children with suspected carbohydrate malabsorption.

50 lucose control but is not accompanied by fat malabsorption.

51 resulting in villous degeneration and lipid malabsorption.

52 re akin to that of starvation and intestinal malabsorption.

53 bypass (RYGB) is generally attributed to fat malabsorption.

54 r patients with significant maldigestion and malabsorption.

55 es small bowel transit, which may exacerbate malabsorption.

56 ity of some stressed individuals to fructose malabsorption.

57 over 8 d in healthy adults without fructose malabsorption.

58 ted after procedures that result in the most malabsorption.

59 supplementation, and enteral causes such as malabsorption.

60 sion but no improvement of symptoms/signs of malabsorption.

61 re the molecular basis for hereditary folate malabsorption.

62 functional hormones resulted in generalized malabsorption.

63 uodenum, avoiding blind loops and minimizing malabsorption.

64 You find no evidence of malabsorption.

65 astrointestinal inflammatory disease, 15.4%; malabsorption, 5.9%; granulomatous disease, 9.7%; liver

66 peripheral neuropathy and ataxia, is usually malabsorption-a result of fat malabsorption or genetic a

67 On average, malabsorption accounted for approximately 6% and 11% of

68 Rapid weight loss and malabsorption after bariatric surgery in patients with N

69 eficiency as a result of iatrogenic maternal malabsorption after BPD.

70 the caecum and colon, consistent with severe malabsorption, along with a unique adaptive up-regulatio

71 transporter is mutated in hereditary folate malabsorption, an autosomal recessive disorder, the mole

72 c insufficiency, dietary lactose or fructose malabsorption, anal sphincter dysfunction causing fecal

73 ients, 71 (38.2%) were positive for fructose malabsorption and 91 (48.9%) were positive for fructan m

74 essive disorders characterized by severe fat malabsorption and a failure to thrive in infancy.

75 essive disorder characterized by generalized malabsorption and a paucity of enteroendocrine cells.

76 patients frequently sustain severe nutrient malabsorption and are dependent on PN for life.

77 Aging of this organ causes malabsorption and associated illnesses, yet its aging me

78 demonstrate the necessity of coordinated Na+ malabsorption and barrier dysfunction in TNF-induced dia

79 he basis of a diagnosis code of postsurgical malabsorption and billed charges for a neonatal intensiv

80 TR transgenic animals ameliorated intestinal malabsorption and concomitantly led to an increase in CF

81 shift in intestinal function leads to lipid malabsorption and decreased deposition of body fat.

82 , displaying systemic inflammation, nutrient malabsorption and decreased expression of intestinal and

83 mmalian small intestine, leading to nutrient malabsorption and diarrhea but rarely causing inflammati

84 ice) or 2 weeks (rats), indices of bile salt malabsorption and enterohepatic cycling of bilirubin wer

85 ients, 42 (22.6%) were positive for fructose malabsorption and fructan malabsorption.

86 virus (HIV)-infected patients often develop malabsorption and increased intestinal permeability with

87 d correlated with fecal measures of nutrient malabsorption and inflammation, suggesting that E. coli

88 s gastrointestinal disease includes nutrient malabsorption and intestinal inflammation.

89 Food malabsorption and intolerance is implicated in gastroint

90 Malabsorption and malnutrition are prevalent in survivor

91 gery (BS) may be associated with significant malabsorption and nutritional deficiencies.

92 ed risk of vitamin D deficiency owing to fat malabsorption and other factors.

93 These conditions include intestinal malabsorption and primary neural cell neoplasia.

94 kindreds with selective intestinal cobalamin malabsorption and proteinuria and that normal brush-bord

95 ized by intestinal cobalamin (vitamin B(12)) malabsorption and proteinuria.

96 h age in the pancreas to such an extent that malabsorption and rapid weight loss occurred in a subset

97 ality, diarrhea, and biochemical features of malabsorption and refeeding syndrome.

98 crine insufficiency that results in nutrient malabsorption and requires oral pancreatic enzyme replac

99 epithelial cell dysplasia leading to severe malabsorption and significant morbidity and mortality.

100 Carbohydrate malabsorption and subsequent gastrointestinal symptoms a

101 icotropin-releasing factor (CRF) on fructose malabsorption and the resulting volume of water in the s

102 s show that loss of Atp8b1 in IEC causes LPC malabsorption and thereby hepatic choline deficiency.

103 it in arising only infrequently from severe malabsorption and thus being less likely to progress, co

104 pulations are needed to inform screening for malabsorption and treatment strategies.

105 This is accompanied by fat malabsorption and weight loss, which complicates studyin

106 PCFT gene in subjects with hereditary folate malabsorption and, more recently, by the Pcft-null mouse

107 amylase activity (which causes carbohydrate malabsorption), and (3) if the inhibitor alters pancreat

108 tal/malabsorptive RYGB, 12 restapled without malabsorption, and 5 loop bypasses revised to standard R

109 infantile disease characterized by diarrhea, malabsorption, and acid/base instability, requiring inte

110 elated to folate uptake in hereditary folate malabsorption, and delivery of PCFT-targeted chemotherap

111 hibition prevented NHE3 internalization, Na+ malabsorption, and diarrhea despite continued barrier dy

112 Bone loss is influenced by diet, malabsorption, and disease-related imbalances in bone tu

113 cts observed in mutant mice caused diarrhea, malabsorption, and early death.

114 of the small bowel mucosa, villous atrophy, malabsorption, and increased intestinal permeability, is

115 phangiectasia, edema due to hypoproteinemia, malabsorption, and less frequently, bowel inflammation,

116 n result in intestinal mucosal inflammation, malabsorption, and numerous secondary symptoms and autoi

117 Reduced food intake, impaired digestion, malabsorption, and poor growth rate are frequently obser

118 , resulting in severe diarrhea, dehydration, malabsorption, and potentially death.

119 atory bowel disease, pancreatitis, motility, malabsorption, and radiation enteropathy.

120 Diarrhea, carbohydrate malabsorption, and refeeding syndrome may contribute to

121 should be assessed in patients with fructose malabsorption, and vice versa.

122 ias, liver dysfunction, portal hypertension, malabsorption, and weight loss).

123 c steatosis, despite impaired intestinal fat malabsorption, and why very severe hypocholesterolemia d

124 as defined by recurrent pseudo-obstruction, malabsorption, and/or need for artificial nutrition (Med

125 hol-dependent individuals, and patients with malabsorption are at higher risk of inadequate intake or

126 e common, data on gut and pancreatic-related malabsorption are scant.

127 The survivors had fat malabsorption as newborns and as adults, but only when f

128 with a long thread of interest in folic acid malabsorption as one of the determinants of nutritional

129 risk for vitamin A deficiency because of fat malabsorption as well as for the inflammatory stresses o

130 ents with IFM and in one subject with global malabsorption, as compared with 15 healthy parents of su

131 ricts the small bowel and increases fructose malabsorption, as shown by increased ascending colon vol

132 Bile acid malabsorption (BAM) and bile acid-related diarrhea repre

133 Bile acid malabsorption (BAM) was identified in patients with diar

134 not be used clinically to diagnose cobalamin malabsorption because of overlap with normal values.

135 In older persons, food-bound cobalamin malabsorption becomes the predominant cause of deficienc

136 mbination of osmotic sensitivities, nutrient malabsorption, bowel dilatation and dysmotility, and cha

137 and gastrointestinal disease with or without malabsorption, but not with bronchiectasis, autoimmunity

138 Severe malabsorption by the gastrointestinal (GI) tract was the

139 viduals with presumed lactose intolerance or malabsorption can tolerate 12 to 15 g of lactose.

140 Intestinal damage and malabsorption caused by chronic environmental enteropath

141 The impact of nutrient malabsorption caused from untreated celiac disease is we

142 sociated with the disorder glucose-galactose malabsorption, characterized by severe diarrhea.

143 USP U of pancreatin with meals decreased fat malabsorption compared with placebo.

144 ins has been implicated in glucose/galactose malabsorption, congenital hypothyroidism, Bartter's synd

145 Antibiotic treatment abolished fructose malabsorption-dependent induction of cecal Cck mRNA expr

146 By causing bile salt malabsorption, dietary UDCA and cholesterol induce enter

147 Short bowel syndrome (SBS) is a serious malabsorption disorder, and dietetic management of patie

148 Those with fat malabsorption disorders malabsorb vitamin D and thus mus

149 A bile acid malabsorption-driven increase in cholesterol synthesis u

150 Decreased nutrient intake, malabsorption, drug-nutrient interactions, anorexia, and

151 ealthy infants and is common in infants with malabsorption due to cystic fibrosis (CF).

152 negatively affect nutritional status include malabsorption, dumping syndrome, kidney stones, altered

153 ion of cobalamin than does the more complete malabsorption engendered by disruption of intrinsic fact

154 trast, suckling PLRP2-deficient mice had fat malabsorption evidenced by increased fecal weight, incre

155 ay have severe gastrointestinal symptoms and malabsorption, extraintestinal symptoms or have no sympt

156 reath hydrogen (an indicator of carbohydrate malabsorption), flatus frequency, and abdominal symptoms

157 rocedure for diagnosing fructose and lactose malabsorption (FM/LM) but test accuracy and reliability

158 a course of parenteral ivermectin because of malabsorption from severe gastrointestinal strongyloidia

159 Glucose-Galactose Malabsorption (GGM) is caused by a defect in SGLT1.

160 ause or are associated with gastrointestinal malabsorption has led to extensive investigation into th

161 Hereditary folate malabsorption (HFM) is a rare autosomal recessive disord

162 Hereditary folate malabsorption (HFM) is a rare, autosomal recessive disor

163 osomal recessive disorder, hereditary folate malabsorption (HFM).

164 Children were considered to have malabsorption if they had chronic diarrhea, weight loss

165 with clinical evidence of isolated fructose malabsorption (IFM) has stimulated interest in possible

166 is the molecular basis for hereditary folate malabsorption in a family with this disease.

167 plementation does not completely correct fat malabsorption in CF patients.

168 small-intestinal mucosal injury and nutrient malabsorption in genetically susceptible individuals in

169 r fructose may explain the high incidence of malabsorption in infants and cause problems in adults un

170 ate responses to oral vaccines, and nutrient malabsorption in millions of children worldwide.

171 s the most likely cause for intestinal lipid malabsorption in the Australian Kelpie.

172 capillariasis is one of the common causes of malabsorption in the East.

173 Although fat malabsorption in the short-bowel syndrome is caused in p

174 l pathophysiological changes such as glucose malabsorption, increased chloride ion (Cl(-)) secretion,

175 Fructose malabsorption induces cholecystokinin expression in the

176 mptoms including pruritus, pancreatitis, fat malabsorption, intestinal inflammation, and failure to t

177 L-thyroxine (L-T4) malabsorption is a potential concern in patients with au

178 udies support previous reports that fructose malabsorption is associated with unexplained gastrointes

179 Thus, calcium malabsorption is inherent to gastric bypass.

180 at underpins SIBO as a cause of maldigestion/malabsorption is lacking in regard to its purported role

181 Ileal bile acid malabsorption is present in Crohn's ileitis.

182 rded as a pediatric illness characterized by malabsorption, it is now better viewed as an immune illn

183 question, a mouse model of moderate fructose malabsorption [ketohexokinase mutant (KHK)(-/-)] and wil

184 lial cell dysfunction occur in the pancreas (malabsorption), liver (biliary cirrhosis), sweat glands

185 Lactose malabsorption (LM) is a major cause of digestive discomf

186 low lactase expression, resulting in lactose malabsorption (LM).

187 least commonly performed because of greater malabsorption, longer operative duration, and higher tec

188 If hyperoxaluria is indeed caused by fat malabsorption, magnitudes of hyperoxaluria and steatorrh

189 ortant worldwide cause of diarrheal disease, malabsorption, malnutrition, delayed cognitive developme

190 Fructose absorption and malabsorption may alter the microbiota and could be medi

191 Vitamin D deficiency resulting from malabsorption may be a factor in the etiology of low bon

192 pancreatitis (8) Early treatment of pain and malabsorption may improve life quality (9) Antifibrogene

193 ct, including inflammation, maldigestion and malabsorption, may promote intestinal dysbiosis(4,5).

194 deficiency is associated with food-cobalamin malabsorption more often than with pernicious anemia.

195 rier dysfunction characterized by epithelial malabsorption, mucus depletion, altered mucin glycosylat

196 In patients with primary bile acid malabsorption, mutations in the ileal bile acid transpor

197 Malabsorption not responding to antibiotic therapy shoul

198 Bile acid malabsorption occurs in a high proportion of patients su

199 Bile acid malabsorption occurs in up to one third of patients with

200 ulose suggested that the tea extract induced malabsorption of 25% of the carbohydrate.

201 ealthy subjects, examining the effect on the malabsorption of a 40-g fructose test meal and its trans

202 ounts of vitamin D can normalize the calcium malabsorption of aging.

203 HIV infection may lead to malabsorption of anti-TB drugs and acquired rifamycin re

204 Ileal malabsorption of bile salts is observed in Crohn's ileit

205 Although calcitriol corrects the malabsorption of calcium, it remains to be seen whether

206 lem of osteomalacia, but it does not correct malabsorption of calcium.

207 ck, green, and mulberry tea leaves to induce malabsorption of carbohydrate and triacylglycerol in hea

208 sorder characterized by selective intestinal malabsorption of cobalamin (vitamin B12) and urinary los

209 obalamin) deficiency is caused by intestinal malabsorption of cobalamin.

210 s, we conclude that virulence factor-induced malabsorption of dietary amino acids in the small intest

211 murium invasion of the ileal mucosa triggers malabsorption of dietary amino acids to produce downstre

212 ng celiac sprue is usually attributed to the malabsorption of dietary iron or the loss of iron from t

213 Malabsorption of fat-soluble vitamins is a major complic

214 In contrast to the malabsorption of fructose, Glut5(-/-) mice did not exhib

215 hamnose ratio were used to test for possible malabsorption of glucose after surgery.

216 his was due to restriction of food intake or malabsorption of ingested macronutrients.

217 Anemia secondary to malabsorption of iron, folic acid, and/or vitamin B12 is

218 These alterations result in malabsorption of iron, vitamin B(12) (pernicious anaemia

219 Conditions associated with malabsorption of macronutrients and gastrointestinal dis

220 Bile acid (BA) malabsorption of moderate severity is reported in 32% of

221 lorhydric patients were found to have severe malabsorption of nonheme iron, which persisted after the

222 ually due to the large mass of the bezoar or malabsorption of nutrients.

223 markers for colonic fermentation, because of malabsorption of oligosaccharides (e.g., lactose or fruc

224 Malabsorption of partially digested food causes bloating

225 idered, because such individuals suffer from malabsorption of vitamin B-12 rather than from an inadeq

226 ing exons 1-4 of human AMN lead to selective malabsorption of vitamin B12 (a phenotype associated wit

227 (IGS), which is characterized by intestinal malabsorption of vitamin B12 and in some cases proteinur

228 duction of gastric acid and thus may lead to malabsorption of vitamin B12.

229 Hereditary folate malabsorption (OMIM 229050) is a rare autosomal recessiv

230 We investigated the impact of fructose malabsorption on intestinal endocrine function and addre

231 ced persistent alteration of bowel habits or malabsorption; only 1 minor wound complication has occur

232 he tea extract did not cause triacylglycerol malabsorption or any significant increase in symptoms.

233 neonatal cholestasis and fat-soluble vitamin malabsorption or as late onset chronic liver disease.

234 ia, is usually malabsorption-a result of fat malabsorption or genetic abnormalities in lipoprotein me

235 onutrients that were not absorbed because of malabsorption or restricted food intake.

236 of nutritional dyshomeostasis (oral failure, malabsorption, or both), and to quantify the effects of

237 e to discernable changes in food intake, fat malabsorption, or heat production, although intestinal l

238 ases of cholestasis and other forms of lipid malabsorption, oral administration of TPGS is the treatm

239 Primary bile acid malabsorption (PBAM) is an idiopathic intestinal disorde

240 increased permeability, dysbiosis, nutrient malabsorption, potentially higher susceptibility to infe

241 The partial nature of this form of malabsorption produces a more slowly progressive depleti

242 Features of FPE are nonbloody diarrhea, malabsorption, protein-losing enteropathy, hypoalbuminem

243 sclerosis (SSc) patients, and may result in malabsorption, pseudo-obstruction, hospitalization, and

244 that diarrhea in IBD is due to TNF-mediated malabsorption rather than to secretory processes.

245 Five months after bypass, malabsorption reduced absorption of combustible energy b

246 Fourteen months after bypass, malabsorption reduced energy absorption by 172 +/- 60 kc

247 ated intrahepatic cholestasis and intestinal malabsorption, reduced C27-bile acid intermediate produc

248 transplant diarrhea may lead to dehydration, malabsorption, rehospitalization, immunosuppression, non

249 ctrolyte disturbances with regard to enteral malabsorption, renal compensation, and the influence of

250 ty of <55% of predicted; 4) in the GI tract, malabsorption, repeated episodes of pseudoobstruction, o

251 Severe malabsorption required parenteral nutrition support for

252 Treatment of fat malabsorption requires 90,000 USP U of lipase with meals

253 limb edema, serosal effusions, and vitamin D malabsorption resulting in osteoporosis.

254 Fructan malabsorption should be assessed in patients with fructo

255 , early stage Crohn's disease, and bile salt malabsorption should be excluded, as should colon cancer

256 on of the enteric nervous system, as well as malabsorption, suggesting that common mechanisms of path

257 activation of the enteric nervous system and malabsorption, suggesting that common mechanisms of path

258 iarrhea, bloating, and nausea in addition to malabsorption symptoms such as weight loss and micronutr

259 was 100.00 (95% CI, 98.68-100.00) when only malabsorption symptoms were used instead of any symptom

260 These include the typical malabsorption syndrome (classic symptoms) and a spectrum

261 serves as a model for the hereditary folate malabsorption syndrome and is the most accurate animal m

262 SIBO was added to the list of causes of the malabsorption syndrome and the pathophysiology of its co

263 n has become less common, with diarrhea or a malabsorption syndrome as the mode of presentation in fe

264 glt1(-/-) mice developed a glucose-galactose malabsorption syndrome but thrive normally when fed a gl

265 A rare autosomal recessive hereditary folate malabsorption syndrome is attributable to human SLC46A1

266 a new murine model of the hereditary folate malabsorption syndrome that we developed through targete

267 phenotypes were classified as: 1) classical (malabsorption syndrome); 2) non-classical (extraintestin

268 d is mostly misdiagnosed in many patients as malabsorption syndrome, inflammatory bowel disease, anor

269 ted to iron deficiency, clinically confirmed malabsorption syndrome, previous hypersensitivity to any

270 d in patients with steatorrhea caused by the malabsorption syndrome.

271 refore lead to an erroneous diagnosis of the malabsorption syndrome.

272 patient include inadequate dietary intakes, malabsorption syndromes (especially owing to cholestatic

273 tions for the prevention and/or treatment of malabsorption syndromes and diet-related disorders inclu

274 tamin D supplementation to patients with fat malabsorption syndromes as well as patients with other m

275 nadequate copper intakes, in prematurity, in malabsorption syndromes, and in conditions predisposing

276 novel treatments for obesity, diabetes, and malabsorption syndromes.

277 al intestine causes unremitting diarrhea and malabsorption that can lead to chronic and sometimes fat

278 re small-bowel villus atrophy, diarrhea, and malabsorption that is reversible with drug discontinuati

279 Because of the malabsorption that results from BPD, patients need lifel

280 though sorbitol intolerance is attributed to malabsorption, the underlying mechanism remains unresolv

281 acid (UDCA) and cholesterol causes bile salt malabsorption; the former by competition for and the lat

282 clinical manifestations, ranging from severe malabsorption to minimally symptomatic or non-symptomati

283 orptive disorders, especially food-cobalamin malabsorption, underlie about half of all cases of precl

284 s with a history of TB, five had evidence of malabsorption (vomiting and/or diarrhea), versus none of

285 Fat malabsorption was a prominent feature.

286 Therefore, glucose-galactose-malabsorption was assumed.

287 A new mechanism for carbohydrate malabsorption was discovered: in sucrase-isomaltase defi

288 Malabsorption was evident in 73% of patients, of whom 44

289 No evidence of glucose malabsorption was found.

290 Lactose malabsorption was not an important factor.

291 rations, such as Cl(-) secretion and glucose malabsorption, was studied using tissues derived from ma

292 ients, 35 individuals with acquired fructose malabsorption were identified based on pathological fruc

293 Signs of malabsorption were rare.

294 iciency or with HIV infection and intestinal malabsorption were very similar to those of the B cell-d

295 ntestinal graft absorption capacity with fat malabsorption, which necessitates energy intakes of at l

296 A more frequent problem is food-cobalamin malabsorption, which usually arises from atrophic gastri

297 d on a unique proband with glucose-galactose malabsorption who was investigated 30 years ago, and the

298 cted to present with fat/fat soluble vitamin malabsorption with minimal cholestasis.

299 etic basis of selective intestinal cobalamin malabsorption with proteinuria was investigated in a can

300 y and effectively in patients in whom severe malabsorption would preclude the effective use of oral f