ライフサイエンスコーパス: polyneuropathy

1 ch as L55P (associated with familial amyloid polyneuropathy).

2 peripheral neuropathy (familial amyloidotic polyneuropathy).

3 ry testing in patients with distal symmetric polyneuropathy.

4 development of dysphagia in critical illness polyneuropathy.

5 d induced a sensory and predominantly axonal polyneuropathy.

6 while undergoing prospective assessments for polyneuropathy.

7 he TTR gene are involved in familial amyloid polyneuropathy.

8 ere most and least susceptible to paclitaxel polyneuropathy.

9 n implicated in the pathogenesis of diabetic polyneuropathy.

10 of familial chylomicronemia and TTR-mediated polyneuropathy.

11 enes are the cause of rare familial forms of polyneuropathy.

12 nd Parkinson's diseases and familial amyloid polyneuropathy.

13 tic marker in transthyretin familial amyloid polyneuropathy.

14 ing amyloid fibril formation, known to cause polyneuropathy.

15 BG imaging in transthyretin familial amyloid polyneuropathy.

16 delayed gross motor development, ataxia, and polyneuropathy.

17 ation approved to treat TTR familial amyloid polyneuropathy.

18 l TTR mutants are linked to familial amyloid polyneuropathy.

19 ysis, and/or later-onset axonal sensorimotor polyneuropathy.

20 inct from chronic inflammatory demyelinating polyneuropathy.

21 drome and chronic inflammatory demyelinating polyneuropathy.

22 elial growth factor (VEGF) to treat diabetic polyneuropathy.

23 At baseline, 20% of patients had sensory polyneuropathy.

24 and 1 had chronic inflammatory demyelinating polyneuropathy.

25 sociated glycoprotein antibody demyelinating polyneuropathy.

26 e a diagnosis of a superimposed inflammatory polyneuropathy.

27 ritical in the development of distal sensory polyneuropathy.

28 verity of neuropathic pain in distal sensory polyneuropathy.

29 e detection and monitoring of distal sensory polyneuropathy.

30 tolerance is being explored as it relates to polyneuropathy.

31 ndrome or chronic inflammatory demyelinating polyneuropathy.

32 on distal symmetric sensory and sensorimotor polyneuropathy.

33 dose, and time-dependent axonal sensorimotor polyneuropathy.

34 develops a spontaneous autoimmune peripheral polyneuropathy.

35 le systemic amyloidosis and familial amyloid polyneuropathy.

36 weakness separately from overall severity of polyneuropathy.

37 ile systemic amyloidosis or familial amyloid polyneuropathy.

38 pathological changes typical of diphtheritic polyneuropathy.

39 icant beneficial effect of rhNGF on diabetic polyneuropathy.

40 diagnosed chronic inflammatory demyelinating polyneuropathy.

41 le systemic amyloidosis and familial amyloid polyneuropathy.

42 n complicated by severe photosensitivity and polyneuropathy.

43 Diabetes is a common cause of polyneuropathy.

44 the syndrome of TTR-related familial amyloid polyneuropathy.

45 educed at 7 months, which is indicative of a polyneuropathy.

46 imits its use is the onset of a sensorimotor polyneuropathy.

47 ultiple tests, and 9) estimating severity of polyneuropathy.

48 th impaired nerve function in people without polyneuropathy.

49 ctions in the course of familial amyloidotic polyneuropathy.

50 ecific components of metabolic syndrome with polyneuropathy.

51 idant that is used in patients with diabetic polyneuropathy.

52 onduction parameters in participants without polyneuropathy.

53 ic syndrome and its separate components with polyneuropathy.

54 evelopment of vincristine-induced peripheral polyneuropathy.

55 ) is an acute postinfectious immune-mediated polyneuropathy.

56 ay reduce the prevalence of critical illness polyneuropathy.

57 es: Toronto consensus definition of probable polyneuropathy.

58 tosomal dominant distal symmetric peripheral polyneuropathy.

59 gth-dependent mixed demyelinating and axonal polyneuropathy.

60 nt testing in patients with distal symmetric polyneuropathy.

61 e disease characterized by sensory and motor polyneuropathies.

62 various peripheral nerve antigens and immune polyneuropathies.

63 It is also the target of autoantibodies in polyneuropathies.

64 polyneuropathy and possibly other peripheral polyneuropathies.

65 ween CD and acute inflammatory demyelinating polyneuropathy (0.8; 0.3-2.1; P = .68).

66 Among the 2892 patients with polyneuropathy (1364 women and 1528 men; mean [SD] age,

67 ; multiple sclerosis, 2 (CI: 2, 3); diabetic polyneuropathy, 2 (CI: 1, 3); compressive mononeuropathi

68 due to muscle weakness and not to worsening polyneuropathy; (2) in multivariate analysis, duration o

69 230); shingles, 140 (CI: 104, 184); diabetic polyneuropathy, 54 (CI: 33, 83); compressive neuropathie

70 imab in patients with anti-MAG demyelinating polyneuropathy (A-MAG-DP).

71 y-somatic nervous system underlie peripheral polyneuropathy, a common complication of diabetes.

72 cases of chronic inflammatory demyelinating polyneuropathy, a concomitant axonal loss secondary to p

73 gy to halt neurodegeneration associated with polyneuropathy, according to recent placebo-controlled c

74 riants of chronic inflammatory demyelinating polyneuropathy, account for a proportion of LMN presenta

75 teria, with acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy

76 two forms: acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy

77 ages of the acute inflammatory demyelinating polyneuropathy (AIDP) pattern of Guillain-Barre syndrome

78 In acute inflammatory demyelinating polyneuropathy (AIDP), the attack appears directed again

79 ts, has been implicated in some acute immune polyneuropathies (AIP).

80 NGF influences the presentation of diabetic polyneuropathy, although metabolic or vascular abnormali

81 ents with chronic inflammatory demyelinating polyneuropathy, an autoimmune disease of the peripheral

82 The evaluation of demyelinating polyneuropathies and the data for treatment of inflammat

83 tor deficient mouse (dbdb) model of diabetic polyneuropathy and 2) superoxide dismutase 1 knockout (S

84 aluable both for diagnosis of distal sensory polyneuropathy and as a predictor of the condition occur

85 In conclusion, axonal sensory-motor polyneuropathy and autonomic neuropathy are commonly see

86 he management of diabetic distal symmetrical polyneuropathy and autonomic neuropathy but that the cli

87 the treatment of diabetic distal symmetrical polyneuropathy and autonomic neuropathy.

88 to provide a therapeutic effect in models of polyneuropathy and chronic regional pain.

89 for a patient presenting with demyelinating polyneuropathy and concurrent papilledema.

90 long-term opioid therapy among patients with polyneuropathy and controls.

91 ory and autonomic function in early diabetic polyneuropathy and correlated changes with levels of NGF

92 ogenesis of the most common familial amyloid polyneuropathy and familial amyloid cardiomyopathy mutat

93 TTR mutants lead to familial amyloidotic polyneuropathy and familial amyloid cardiomyopathy, with

94 mbalance toward inflammation predisposing to polyneuropathy and foot ulcers.

95 homechanisms underlying chemotherapy-induced polyneuropathy and for the development of novel therapeu

96 rior wall and septal thickening, reversal of polyneuropathy and gastric atony, and resolution of hepa

97 t reported in HSAN IE-large and small fibres polyneuropathy and lower limbs oedema.

98 zing the prevalence and severity of diabetic polyneuropathy and makes research into the deleterious e

99 Sensory polyneuropathy and mucositis were prominent toxicities,

100 enotype characterized by chronic progressive polyneuropathy and myopathy without hepatic or cardiac i

101 has been shown to have beneficial effects on polyneuropathy and on the parameters of oxidative stress

102 a rare plasma cell dyscrasia presenting with polyneuropathy and other systemic findings.

103 on to prevent vincristine-induced peripheral polyneuropathy and possibly other peripheral polyneuropa

104 is observed systemically in familial amyloid polyneuropathy and senile systemic amyloidosis and appea

105 deposition and the onset of familial amyloid polyneuropathy and senile systemic amyloidosis.

106 hown the relationship between distal sensory polyneuropathy and the use of neurotoxic antiretroviral

107 of long-term opioid use among patients with polyneuropathy and to assess the association of long-ter

108 cted of prescriptions given to patients with polyneuropathy and to controls in ambulatory practice be

109 nd a discharge diagnosis of critical illness polyneuropathy and/or myopathy along with adult ICU prop

110 of a discharge diagnosis of critical illness polyneuropathy and/or myopathy and the need for effectiv

111 th a discharge diagnosis of critical illness polyneuropathy and/or myopathy had fewer 28-day hospital

112 e, a discharge diagnosis of critical illness polyneuropathy and/or myopathy is strongly associated wi

113 ut a discharge diagnosis of critical illness polyneuropathy and/or myopathy, patients with a discharg

114 th a discharge diagnosis of critical illness polyneuropathy and/or myopathy, we matched 3,436 of thes

115 ve a discharge diagnosis of critical illness polyneuropathy and/or myopathy.

116 increase the diagnostic yield in late-onset polyneuropathies, and it will be tempting to explore whe

117 V30M mutant associated with familial amyloid polyneuropathy, and Abeta42 associated with Alzheimer's

118 utants exhibit hyperexcitability, peripheral polyneuropathy, and axonal degeneration reminiscent of C

119 and ICU-acquired weakness, critical illness polyneuropathy, and critical illness myopathy.

120 uropathy, chronic inflammatory demyelinating polyneuropathy, and dermatomyositis.

121 enile systemic amyloidosis, familial amyloid polyneuropathy, and familial amyloid cardiomyopathy.

122 enile systemic amyloidosis, familial amyloid polyneuropathy, and familial amyloid cardiomyopathy.

123 revalence of baseline and treatment-emergent polyneuropathy, and identify molecular markers associate

124 syndrome, chronic inflammatory demyelinating polyneuropathy, and multifocal motor neuropathy and as s

125 luding Alzheimer's disease, familial amyloid polyneuropathy, and senile systemic amyloidosis.

126 c therapies for neuropathic pain in diabetic polyneuropathy appear promising.

127 Axonal polyneuropathies are a frequent cause of progressive dis

128 Sensory polyneuropathies are the most frequent neurological comp

129 sible for chronic inflammatory demyelination polyneuropathy are broad and may include dysfunctions at

130 s of and differential diagnosis for diabetic polyneuropathy are reviewed herein.

131 ion was used to model the primary outcome of polyneuropathy as a function of the components of metabo

132 Eleven patients with demyelinating polyneuropathy associated with monoclonal IgM antibodies

133 y is that of a symmetrical, length-dependent polyneuropathy associated with sensory or autonomic symp

134 splantation is effective in familial amyloid polyneuropathy associated with variant transthyretin, be

135 he L55P transthyretin (TTR) familial amyloid polyneuropathy-associated variant is distinct from the o

136 ariant of chronic inflammatory demyelinating polyneuropathy but that multifocal motor neuropathy is d

137 idney disease prevents worsening of diabetic polyneuropathy, but neuropathic improvement is delayed a

138 n association between metabolic syndrome and polyneuropathy, but the precise components that drive th

139 Diabetes mellitus is a known risk factor for polyneuropathy, but the role of pre-diabetes and metabol

140 ogression and improves the signs of diabetic polyneuropathy by restoration of a normoglycemic state.

141 of liver transplantation on amyloid-related polyneuropathy, cardiovascular, and gastrointestinal dys

142 Indeed, small-fiber-predominant polyneuropathies cause CRPS-like abnormalities, and path

143 system which characterizes familial amyloid polyneuropathy caused by variant TTR.

144 cterized by retinitis pigmentosa, peripheral polyneuropathy, cerebellar ataxia and increased cerebros

145 myositis, paraproteinemic IgM demyelinating polyneuropathy, certain intractable childhood epilepsies

146 e the aetiology of chronic idiopathic axonal polyneuropathy (CIAP), 50 consecutive patients were comp

147 (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP) are conditions that affect periphe

148 Chronic inflammatory demyelinating polyneuropathy (CIDP) has occasionally been associated w

149 ents with chronic inflammatory demyelinating polyneuropathy (CIDP) need long-term intravenous immunog

150 ents with chronic inflammatory demyelinating polyneuropathy (CIDP) were compared with 10 healthy subj

151 ents with chronic inflammatory demyelinating polyneuropathy (CIDP), CIDP associated with human immuno

152 trophy in chronic inflammatory demyelinating polyneuropathy (CIDP), magnetic resonance neurography wi

153 n disease chronic inflammatory demyelinating polyneuropathy (CIDP).

154 disease, chronic inflammatory demyelinating polyneuropathy (CIDP).

155 drome and chronic inflammatory demyelinating polyneuropathy (CIDP).

156 mimicking chronic inflammatory demyelinating polyneuropathy (CIDP).

157 weakness and atrophy due to critical illness polyneuropathy (CIP), an axonal neuropathy associated wi

158 d in the etiology of the symmetrical sensory polyneuropathy commonly associated with diabetes.

159 enes is also associated with common forms of polyneuropathy-considered "acquired" in medical parlance

160 outcomes, and mortality among patients with polyneuropathy could influence disease-specific decision

161 ortionate contribution from critical illness polyneuropathy/critical illness myopathy and severe seps

162 dies examining patients for critical illness polyneuropathy/critical illness myopathy and those with

163 Sensory polyneuropathy developed during treatment in 64% of pati

164 esembling chronic inflammatory demyelinating polyneuropathy develops spontaneously in NOD mice with a

165 rophysiology that a progressive sensorimotor polyneuropathy does indeed segregate with the mutation,

166 erations of nerve microstructure in diabetic polyneuropathy (DPN) by magnetic resonance (MR) neurogra

167 tabolic syndrome that contribute to diabetic polyneuropathy (DPN) in type 2 diabetes mellitus (T2DM),

168 Large-fiber diabetic polyneuropathy (DPN) leads to balance and gait abnormali

169 ated the risk factors for distal symmetrical polyneuropathy (DSP) in a cohort of childhood-onset IDDM

170 factors for progression of distal symmetric polyneuropathy (DSP) in type 1 (insulin-dependent) diabe

171 Distal symmetric polyneuropathy (DSP) is a prevalent condition that resul

172 Distal symmetric polyneuropathy (DSP), associated with HIV infection, is

173 t common manifestation is distal symmetrical polyneuropathy (DSP), but many patterns of nerve injury

174 ferative retinopathy, and distal symmetrical polyneuropathy (DSP), compared with subjects who were in

175 herapy increased the risk for distal sensory polyneuropathy (DSPN) in subjects with human immunodefic

176 estingly, the L55P and V30M familial amyloid polyneuropathy (FAP) associated variants form amyloid pr

177 Familial amyloid polyneuropathy (FAP) associated with mutations in the ge

178 tetramers including two familial amyloidotic polyneuropathy (FAP) causing variants (V30M and L55P), a

179 thy is a major component of familial amyloid polyneuropathy (FAP) due to mutated transthyretin, with

180 Familial amyloidotic polyneuropathy (FAP) has a high prevalence in Portugal,

181 Familial amyloid polyneuropathy (FAP) is a neurodegenerative disorder ass

182 Familial amyloidotic polyneuropathy (FAP) is an autosomal dominant inherited

183 TR) in Indian patients with familial amyloid polyneuropathy (FAP) is described.

184 DLT using livers from familial amyloidotic polyneuropathy (FAP) patients is a well-described techni

185 ant in which a patient with familial amyloid polyneuropathy (FAP) received an orthotopic split liver

186 tations associated with familial amyloidotic polyneuropathy (FAP), a neurodegenerative disease charac

187 In the most common familial amyloid polyneuropathy (FAP), transthyretin (TTR) displays this

188 (1) transthyretin (TTR) familial amyloidotic polyneuropathy (FAP; n = 20), (2) TTR mutation carriers

189 ve regeneration, early diagnosis of diabetic polyneuropathy, followed by tight glycemic control with

190 be useful as a measure of change in diabetic polyneuropathy for purposes of medical practice, epidemi

191 ially the classic inflammatory demyelinating polyneuropathy form, seems to involve lymphocytes and ma

192 the human neurodegenerative disorder PHARC (polyneuropathy, hearing loss, ataxia, retinosis pigmento

193 1487 showed clearly symptoms associated with polyneuropathy, hearing loss, cerebellar ataxia, RP, and

194 drome, a neurodegenerative disease including polyneuropathy, hearing loss, cerebellar ataxia, RP, and

195 le systemic amyloidosis and familial amyloid polyneuropathy), immunoglobulin light chains (light-chai

196 nerve conduction studies indicated an axonal polyneuropathy in 14 percent.

197 the most prevalent cause of familial amyloid polyneuropathy in heterozygotes, whereas a Thr119 --> Me

198 y that mimics vincristine-induced peripheral polyneuropathy in humans.

199 evelopment of vincristine-induced peripheral polyneuropathy in mice.

200 ly reduces the incidence of distal symmetric polyneuropathy in patients with type 1 diabetes but not

201 a 52-year-old woman who has had progressive polyneuropathy in the setting of diabetes for the past 8

202 se studies characterized a motor and sensory polyneuropathy in transgenic diabetic mice and are the f

203 Grade </=2 polyneuropathy increased from 19% at baseline to 52% at

204 Polyneuropathy increased the likelihood of long-term opi

205 sease and chronic inflammatory demyelinating polyneuropathy indicate that the association is more fre

206 dyslipidaemia, are strongly associated with polyneuropathy, irrespective of the presence of diabetes

207 Peripheral polyneuropathy is a common and dose-limiting side effect

208 Critical illness polyneuropathy is a common disorder in the neurological

209 Chronic inflammatory demyelinating polyneuropathy is a debilitating autoimmune disease char

210 Polyneuropathy is a frequent and potentially severe side

211 Transthyretin familial amyloid polyneuropathy is a hereditary form of amyloidosis chara

212 Chronic inflammatory demyelination polyneuropathy is a heterogeneous and treatable immune-m

213 le consistent with previous critical illness polyneuropathy is almost invariable and can be found up

214 Diabetic peripheral polyneuropathy is associated with decrements in motor/se

215 Familial amyloidotic polyneuropathy is characterized by poor functional recov

216 Conclusions and Relevance: The prevalence of polyneuropathy is high in obese individuals, even those

217 prevalence of dysphagia in critical illness polyneuropathy is not known.

218 Polyneuropathy is one of the most common painful conditi

219 e incidence of HIV-associated distal sensory polyneuropathy is reduced.

220 Distal symmetrical polyneuropathy is the most common form of HIV infection-

221 eady in clinical trials for familial amyloid polyneuropathy, is a strong candidate for therapeutic in

222 gs raise the possibility that other acquired polyneuropathies may also be codetermined by genetic eti

223 Familial amyloid polyneuropathy may respond to liver transplantation.

224 h severe polyneuropathy (sDPN), 13 with mild polyneuropathy (mDPN), and 25 without polyneuropathy (nD

225 In participants without polyneuropathy, metabolic syndrome associated with lower

226 syndrome, chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropathy, and amyotro

227 syndrome, chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropathy, and some pa

228 s of amyloid fibrils of familial amyloidotic polyneuropathy mutant TTR suggest a structure similar to

229 west incidence of confirmed distal symmetric polyneuropathy (n = 123), confirmed distal symmetric pol

230 y (n = 1), gastrointestinal involvement with polyneuropathy (n = 2), and hepatomegaly (n = 1).

231 h mild polyneuropathy (mDPN), and 25 without polyneuropathy (nDPN)-along with 30 healthy control subj

232 e major expressions of varieties of diabetic polyneuropathies needing improved assessments for clinic

233 OLT was uneventful, and he developed neither polyneuropathy nor exacerbation of photosensitivity.

234 th painful mononeuropathies or an asymmetric polyneuropathy of acute or subacute onset.

235 The polyneuropathy of the GBS affects one to four humans per

236 t common example is that of familial amyloid polyneuropathy, of particular concern for the clinician

237 Inherited polyneuropathies often go undiagnosed.

238 thy was seen more commonly than motor axonal polyneuropathy on nerve conduction studies.

239 19 index case subjects diagnosed with axonal polyneuropathies or neurodegenerative conditions involvi

240 the 4 affected members of the RP-1292 had no polyneuropathy or ataxia, and the sensorineural hearing

241 Metabolic syndrome was associated with polyneuropathy (OR 1.92, 95% CI 1.09 to 3.38), with a st

242 Diabetes was associated with polyneuropathy (OR 3.01, 95% CI 1.60 to 5.65), while imp

243 The POEMS syndrome (coined to refer to polyneuropathy, organomegaly, endocrinopathy, M protein,

244 e (the acronym reflects the common features: Polyneuropathy, Organomegaly, Endocrinopathy, Monoclonal

245 uncommon syndromic disorder characterized by polyneuropathy, organomegaly, endocrinopathy, monoclonal

246 ng complications (confirmed distal symmetric polyneuropathy, overt nephropathy, or coronary artery di

247 ients were identified from the 2 ends of the polyneuropathy phenotype distribution: patients that wer

248 ns and caused a more severe distal symmetric polyneuropathy phenotype.

249 onic Coombs-negative hemolysis and relapsing polyneuropathy presenting as chronic inflammatory demyel

250 [SD] age, 67.5 [16.5] years), patients with polyneuropathy received long-term opioids more often tha

251 ortality were compared between patients with polyneuropathy receiving long-term opioid therapy (>/=90

252 utcomes were more common among patients with polyneuropathy receiving long-term opioids, including de

253 pioid therapy (>/=90 days) and patients with polyneuropathy receiving shorter durations of opioid the

254 In general, treatment options for diabetic polyneuropathy remain primarily symptomatic.

255 enesis of chronic inflammatory demyelinating polyneuropathy remain still fragmentary and insufficient

256 cdh10 overexpression in familial amyloidotic polyneuropathy represents a protective or deleterious re

257 ile systemic amyloidosis or familial amyloid polyneuropathy, respectively.

258 Chronic inflammatory demyelinating polyneuropathy results from autoimmune destruction of th

259 ican family with dominantly inherited axonal polyneuropathy reveals a phenotype similar to those in p

260 opathy (n = 123), confirmed distal symmetric polyneuropathy risk increased fivefold for those with th

261 the development of a spontaneous autoimmune polyneuropathy (SAP), which resembles the human disease

262 abetes (n = 49) were included-11 with severe polyneuropathy (sDPN), 13 with mild polyneuropathy (mDPN

263 stablishes phrenic neuropathy and peripheral polyneuropathy secondary to neurosarcoidosis as a cause

264 An acute or subacute demyelinating polyneuropathy should be considered a potential adverse

265 Objectives: To determine the prevalence of polyneuropathy stratified by glycemic status in well-cha

266 nt with the acute inflammatory demyelinating polyneuropathy subtype of the Guillain-Barre syndrome.

267 tant measure of overall severity of diabetic polyneuropathy, taking into account both symptoms and im

268 h to diagnose and grade severity of diabetic polyneuropathy than does the use of individual clinical

269 as multiple mononeuropathies or sensorimotor polyneuropathies that affect large nerve fibers; painful

270 e model of HIV-associated distal symmetrical polyneuropathy that can be used for investigating the ro

271 s on the mitochondrion may be related to the polyneuropathy that develops in these patients.

272 ment of a distal, sensory predominant axonal polyneuropathy that mimics vincristine-induced periphera

273 g of chronic symmetric sensorimotor diabetic polyneuropathy, the most common and problematic of chron

274 cy for the treatment of TTR familial amyloid polyneuropathy, the most common familial TTR amyloid dis

275 and therapeutic advances in distal symmetric polyneuropathy, the most common subtype of peripheral ne

276 To estimate severity of diabetic polyneuropathy, the results of the neurological examinat

277 rogression of transthyretin familial amyloid polyneuropathy, there are no approved pharmacologic ther

278 requent among patients with critical illness polyneuropathy treated in the ICU.

279 ress some of the challenges of past diabetic polyneuropathy trials.

280 tment of Transthyretin Type Familial Amyloid Polyneuropathy (TTR-FAP) and demonstrated a slowing of d

281 nt feature of transthyretin familial amyloid polyneuropathy (TTR-FAP).

282 Familial amyloid polyneuropathy type I is an autosomal dominant disorder

283 quately characterize and quantitate diabetic polyneuropathies using only one or two clinical or test

284 om patients with MS, Parkinson, Epilepsy and Polyneuropathy using both the aptasensor and commercial

285 prevalence of dysphagia in critical illness polyneuropathy using fiberoptic endoscopic evaluation of

286 ation of progressive spastic paraparesis and polyneuropathy, variably associated with behavioral chan

287 The prevalence of polyneuropathy was 3.8% in lean controls (n = 2), 11.1%

288 ointestinal (12%), and skin disorders (10%); polyneuropathy was infrequent (1%).

289 ities, an independent measure of severity of polyneuropathy, was not significantly worse and, in fact

290 igate the mechanism by which suramin induces polyneuropathy, we examined its effects on SH-SY5Y human

291 Diabetic patients with polyneuropathy were randomized to receive a VEGF-to-plac

292 ents, and often favour a diagnosis of axonal polyneuropathy, whereas muscle histology, where availabl

293 s, including retinopathy, renal disease, and polyneuropathy, which are the topics of this review.

294 the disease: transthyretin familial amyloid polyneuropathy, which primarily affects the peripheral n

295 Patients with polyneuropathy who were receiving long-term opioids had

296 n age 70.0, 54.5% females) were screened for polyneuropathy with a questionnaire, neurological examin

297 nt axonal, predominantly sensory, peripheral polyneuropathy with an onset in early adulthood.

298 el to investigate the association of non-CMT polyneuropathy with CMT genes.

299 genetic causes of diverse forms of inherited polyneuropathies without genetic diagnosis.

300 ter LTx, as reported to the Familial Amyloid Polyneuropathy World Transplant Registry (FAPWTR).