ライフサイエンスコーパス: peripheral neuropathy

1 lines of chemotherapy left him with chronic peripheral neuropathy.

2 e for monocyte traffic and activation in HIV peripheral neuropathy.

3 y were reversed with treatments that prevent peripheral neuropathy.

4 naire for patients with chemotherapy-induced peripheral neuropathy.

5 olecular intermediates of paclitaxel-induced peripheral neuropathy.

6 index, gastrointestinal manifestations, and peripheral neuropathy.

7 ed by cerebellar vermis atrophy, ataxia, and peripheral neuropathy.

8 vide novel insights into the pathogenesis of peripheral neuropathy.

9 Smoking was associated with peripheral neuropathy.

10 c polyneuropathy, the most common subtype of peripheral neuropathy.

11 llowing treatments that prevent experimental peripheral neuropathy.

12 sed risk and severity of vincristine-related peripheral neuropathy.

13 th delayed time to resolution/improvement of peripheral neuropathy.

14 ue among mycobacterial diseases in producing peripheral neuropathy.

15 iabetes but instead triggers an inflammatory peripheral neuropathy.

16 ith diabetes duration, cigarette smoking and peripheral neuropathy.

17 racterized by cerebellar atrophy and lack of peripheral neuropathy.

18 hly sensitive technique for the detection of peripheral neuropathy.

19 se mutations of Nav1.9 as a cause of painful peripheral neuropathy.

20 ations of Nav1.9 in individuals with painful peripheral neuropathy.

21 No patient in our series had peripheral neuropathy.

22 ith progressive external ophthalmoplegia and peripheral neuropathy.

23 sease type 1A is the most frequent inherited peripheral neuropathy.

24 e chief dose-limiting side effect of painful peripheral neuropathy.

25 f these, 16 patients (21%) had a large-fibre peripheral neuropathy.

26 contribute to the pathophysiology of painful peripheral neuropathy.

27 mising anti-myeloma effects and low rates of peripheral neuropathy.

28 cle atrophy lead to hindlimb dysfunction and peripheral neuropathy.

29 to focus future work to ameloirate risks of peripheral neuropathy.

30 l weakness, developmental delay and possible peripheral neuropathy.

31 ted the role for this phenomenon in diabetic peripheral neuropathy.

32 nd pathological features of copper-deficient peripheral neuropathy.

33 Only 1 patient had grade 3 peripheral neuropathy.

34 neration, glaucoma diabetic retinopathy, and peripheral neuropathy.

35 production on the pathogenesis of autoimmune peripheral neuropathy.

36 treatments for painful chemotherapy-induced peripheral neuropathy.

37 ganglia and contribute to the characteristic peripheral neuropathy.

38 athy and associated mild axonal sensorimotor peripheral neuropathy.

39 tochondrial dysfunction is a common cause of peripheral neuropathy.

40 ilar in age, gender, ethnicity, and baseline peripheral neuropathy.

41 mutations of Na(v)1.8 contribute to painful peripheral neuropathy.

42 primary cancers, thromboembolic events, and peripheral neuropathy.

43 s dosing to minimize adverse events, such as peripheral neuropathy.

44 etely fail to myelinate, resulting in severe peripheral neuropathy.

45 22 (PMP22) and is the most common hereditary peripheral neuropathy.

46 nal impairment, cardiac and GI symptoms, and peripheral neuropathy.

47 urpura, skin ulcers, glomerulonephritis, and peripheral neuropathy.

48 n-Barre syndrome (GBS) is an immune-mediated peripheral neuropathy.

49 isodic CNS clinical syndromes in addition to peripheral neuropathy.

50 tion of these cells causes motor and sensory peripheral neuropathy.

51 model of CMT1X that develops a demyelinating peripheral neuropathy.

52 s of the development of chemotherapy-induced peripheral neuropathy.

53 on by physicians including an assessment for peripheral neuropathy.

54 Leprosy is the most common form of treatable peripheral neuropathy.

55 nglia (DRG) is critical for pathology in HIV peripheral neuropathy.

56 a that implicate HARS mutations in inherited peripheral neuropathies.

57 se of many neurological disorders, including peripheral neuropathies.

58 ective in relieving the pain associated with peripheral neuropathies.

59 in axonal sorting results in dysmyelinating peripheral neuropathies.

60 hological mechanisms in mitochondria-related peripheral neuropathies.

61 emyelination and reduced nerve conduction in peripheral neuropathies.

62 nsight to understanding and treating sensory peripheral neuropathies.

63 ventions not only for FD, but also for other peripheral neuropathies.

64 l-mediated neurotrophic support in models of peripheral neuropathies.

65 in, can be linked to phenotypically distinct peripheral neuropathies.

66 d to identify axonal degeneration in several peripheral neuropathies.

67 ease is a genetically heterogeneous group of peripheral neuropathies.

68 portunity for the treatment of demyelinating peripheral neuropathies.

69 egeneration in the CNS and in the context of peripheral neuropathies.

70 for retinopathy (HR 1.39, 95% CI 1.09-1.76), peripheral neuropathy (1.40, 1.19-1.66), and nephropathy

71 d neutropenia (38%), thrombocytopenia (22%), peripheral neuropathy (11%), and cardiologic events (11%

72 gent carfilzomib elicited a low incidence of peripheral neuropathy-17.1% overall (1 grade 3; no grade

73 y of Life Questionnaire-Chemotherapy-Induced Peripheral Neuropathy 20 tool.

74 ) C30 and the EORTC QLQ Chemotherapy-Induced Peripheral Neuropathy 20.

75 The main toxicity was peripheral neuropathy (20% grade 2 and 7% grade 3).

76 t of Cancer (EORTC) QLQ-chemotherapy-induced peripheral neuropathy-20 (CIPN20) instrument] and the 1-

77 rtriglyceridaemia (21 [39%] of 54 patients), peripheral neuropathy (21 [39%] of 54 patients), and per

78 mmon including neutropenia (57.5% vs 53.3%), peripheral neuropathy (23.1% vs 24.8%), and diarrhea (20

79 0 [27%]), headache (27 [33%] vs seven [9%]), peripheral neuropathy (25 [31%] vs 14 [19%]), and dyspep

80 rade 1-4 alopecia (12 [10%] vs 42 [36%]) and peripheral neuropathy (27 [23%] vs 60 [51%]), but more g

81 Raynaud phenomenon (11.6% v 21.4%; P < .01), peripheral neuropathy (29.2% v 21.4%; P = .02), and obes

82 nd 60 [72%] vs four [5%], respectively), and peripheral neuropathy (35 [12%] after PAD, and none vs n

83 Baseline manifestations were purpura (75%), peripheral neuropathy (52%), arthralgia or arthritis (44

84 95 patients were (in decreasing frequency): peripheral neuropathy, 53%; cerebellar ataxia, dysmetria

85 henia or fatigue (91 [24%] vs 45 [12%]), and peripheral neuropathy (67 [18%] vs 55 [15%]).

86 y was a sensory predominant length-dependent peripheral neuropathy (71%).

87 Grade 2 or 3 peripheral neuropathy (8.1% vs 2.4%) was more frequent w

88 patients who experienced treatment-emergent peripheral neuropathy, 88% experienced either resolution

89 ielded promising results in animal models of peripheral neuropathy, a condition involving aberrant ne

90 al neurodevelopment in addition to optic and peripheral neuropathy across the life span.

91 biomarkers of risk for developing persistent peripheral neuropathy after completion of cancer treatme

92 tive burden of retinopathy, nephropathy, and peripheral neuropathy among individuals with no history

93 Thirty-three patients experienced peripheral neuropathy, among whom, the majority (30 of 3

94 or organomegaly, symptomatic hyperviscosity, peripheral neuropathy, amyloidosis, cryoglobulinemia, co

95 repair and is a powerful system for studying peripheral neuropathies and cancer.

96 velopment of neuropsychological deficits and peripheral neuropathies and may help unveil the genetic

97 Fluoroquinolone-induced peripheral neuropathies and tendinopathies are well docu

98 apnoea, possibly through the development of peripheral neuropathy and abnormalities of ventilatory a

99 countries, where it remains a major cause of peripheral neuropathy and disability.

100 y demonstrates the role of HARS mutations in peripheral neuropathy and expands the genetic and clinic

101 tin in rodent models of chemotherapy-induced peripheral neuropathy and explored its mechanism of acti

102 iculum stress in the development of diabetic peripheral neuropathy and identify a potential new thera

103 Peripheral neuropathy and insensate limbs and digits cau

104 ee survival, and response rate, but rates of peripheral neuropathy and myelosuppression were increase

105 vel independent association between diabetic peripheral neuropathy and OSA.

106 ws access proximal to all potential sites of peripheral neuropathy and overcomes many of the limitati

107 FA maps can accurately depict even mild peripheral neuropathy and perform better than the curren

108 Ulcers are deemed neuroischaemic if peripheral neuropathy and peripheral artery disease are

109 ssed the cross-sectional association between peripheral neuropathy and physical functioning and how t

110 type 1A (CMT1A) is the most common heritable peripheral neuropathy and results from a duplication on

111 otential to diagnose and monitor HIV-induced peripheral neuropathy and to set the stage for introduci

112 Rates of peripheral neuropathy and venous thromboembolism were lo

113 ients who were referred for possible painful peripheral neuropathy, and confirmed the diagnosis of sm

114 n 4 patients, including febrile neutropenia, peripheral neuropathy, and hypertension.

115 ormance status 0-2, and no grade 2 or higher peripheral neuropathy, and treated them with oral ixazom

116 nervous system-most commonly causing axonal peripheral neuropathy-and usually manifest later in life

117 Inherited peripheral neuropathies are a genetically heterogeneous

118 Peripheral neuropathies are highly prevalent and are mos

119 Inherited demyelinating peripheral neuropathies are progressive incurable diseas

120 Multiple treatments for painful diabetic peripheral neuropathy are available.

121 mial logistic regression analysis identified peripheral neuropathy as the only independent predictor

122 llular misfolding of which is known to cause peripheral neuropathies associated with Charcot-Marie-To

123 ction potentials in peripheral nerves showed peripheral neuropathy associated with degeneration and d

124 This balance may help determine risk for peripheral neuropathy associated with diabetes or metabo

125 DeltaPOZ mice acquired behavioral signs of a peripheral neuropathy at the age of 3 months.

126 erally well tolerated, with a higher rate of peripheral neuropathy but no apparent increase in risk o

127 modifying therapies for chemotherapy-induced peripheral neuropathies, but these side effects of chemo

128 nd in developing new strategies for treating peripheral neuropathy by targeting SC function.

129 anding the molecular basis for prevention of peripheral neuropathy by testing the effects of addition

130 myelin perturbations.SIGNIFICANCE STATEMENT Peripheral neuropathies can result from damage or dysreg

131 ith upper airway tract and lung involvement, peripheral neuropathy, cardiac and skin lesions.

132 Diabetic kidney disease, retinopathy, peripheral neuropathy, cardiovascular autonomic neuropat

133 ons and establish baseline clinical data for peripheral neuropathies caused by mutations in the myeli

134 he critical role of HDAC1/2-NuRD activity in peripheral neuropathies caused by ZEB2 mutations.

135 ie-Tooth disease type 1A (CMT1A), a dominant peripheral neuropathy caused by a 1.4 Mb recurrent dupli

136 a devastating developmental and progressive peripheral neuropathy caused by a mutation in the gene i

137 Peripheral neuropathy caused by cytotoxic chemotherapy,

138 rotein) neuropathy is a disabling autoimmune peripheral neuropathy caused by monoclonal IgM autoantib

139 cking Zeb2 in Schwann cells develop a severe peripheral neuropathy, caused by failure of axonal sorti

140 axonal, length-dependent sensory predominant peripheral neuropathy causing sensory ataxia is characte

141 (CMT2B) is one of the most common inherited peripheral neuropathies characterized by severe terminal

142 se type 4B1 (CMT4B1), a severe demyelinating peripheral neuropathy characterized by myelin outfolding

143 61T, and V162M) cause the autosomal dominant peripheral neuropathy Charcot-Marie-Tooth type 2B (CMT2B

144 The demyelinating peripheral neuropathy Charcot-Marie-Tooth type 4B (CMT4B

145 Dominant optic atrophy (DOA) and axonal peripheral neuropathy (Charcot-Marie-Tooth type 2, or CM

146 the pathophysiology of chemotherapy-induced peripheral neuropathy (CIPN) and may be important for de

147 cal model of bortezomib chemotherapy-induced peripheral neuropathy (CIPN) and to test whether this is

148 Chemotherapy-induced peripheral neuropathy (CIPN) arises from collateral dama

149 Chemotherapy-induced peripheral neuropathy (CIPN) is a common adverse effect

150 Chemotherapy-induced peripheral neuropathy (CIPN) is a common adverse effect

151 Chemotherapy-induced peripheral neuropathy (CIPN) is a common dose-limiting s

152 Chemotherapy-induced peripheral neuropathy (CIPN) is a debilitating side effe

153 Chemotherapy-induced peripheral neuropathy (CIPN) is a debilitating side effe

154 Chemotherapy-induced peripheral neuropathy (CIPN) is a major cause of disabil

155 Chemotherapy-induced peripheral neuropathy (CIPN) is a severe and painful adv

156 Chemotherapy-induced peripheral neuropathy (CIPN) is common and leads to subo

157 Purpose Chemotherapy-induced peripheral neuropathy (CIPN) may persist after treatment

158 Chemotherapy-induced peripheral neuropathy (CIPN) occurs commonly in cancer p

159 Chemotherapy-induced peripheral neuropathy (CIPN), characterized by pain and

160 a preclinical model of chemotherapy-induced peripheral neuropathy (CIPN), the most common treatment-

161 phenotypes in the most common demyelinating peripheral neuropathy, CMT1A.

162 /ZH3) mice developed a chronic demyelinating peripheral neuropathy, confirming the crucial involvemen

163 reasingly being used to diagnose and monitor peripheral neuropathies, corneal nerve alterations have

164 tically investigated whether the presence of peripheral neuropathy could predict the underlying genet

165 ephalopathy with a central myelin defect and peripheral neuropathy, demonstrating that defects of ala

166 The proportions of retinopathy, nephropathy, peripheral neuropathy, diabetic foot, and ischemic heart

167 Diabetic peripheral neuropathy (DPN) is the most common complicat

168 etes-associated comorbidities such as distal peripheral neuropathy (DPN) might be influenced by obesi

169 stography (SWE) in the detection of diabetic peripheral neuropathy (DPN) of the tibial nerve.

170 Diabetic peripheral neuropathy (DPN) often leads to neurotrophic

171 Rates of peripheral neuropathy during induction were 34% versus 1

172 eutic target in chemotherapy-induced painful peripheral neuropathy, establish a mechanistic insight i

173 The incidence of grade 3 peripheral neuropathy events was relatively high (30% ov

174 s, and human samples from a familial form of peripheral neuropathy (familial amyloidotic polyneuropat

175 mial logistic regression analysis identified peripheral neuropathy, family history and hearing loss a

176 CMT) diseases are the most common hereditary peripheral neuropathies, for which there are no effectiv

177 at can compromise quality of life, including peripheral neuropathy from vincristine treatment.

178 ogical phenotypes, including pain behaviors, peripheral neuropathy, glial reactivation, synapse degen

179 ibility, vincristine dose >/=39 mg/m(2) with peripheral neuropathy, glucocorticoid (prednisone equiva

180 Of these variables, peripheral neuropathy had the highest specificity (91%),

181 Concurrent peripheral neuropathy has been recognised in association

182 including ataxia, upper-motor-neuron damage, peripheral neuropathy, hearing loss, and cerebral atroph

183 , methotrexate-related stroke-like syndrome, peripheral neuropathy, high-dose methotrexate-related ne

184 tient with a late-onset, sensory-predominant peripheral neuropathy; however, the genetic evidence was

185 of expectations due to side effects such as peripheral neuropathy, hypotension, and hypersensitivity

186 776C-->G polymorphism and folate intake with peripheral neuropathy in elders with normal plasma conce

187 utations segregating with autosomal dominant peripheral neuropathy in four unrelated families (p.Thr1

188 Charcot-Marie-Tooth 1B (CMT1B) demyelinating peripheral neuropathy in human and mouse.

189 ention and treatment of chemotherapy-induced peripheral neuropathy in humans.

190 ful small fibre neuropathy, the aetiology of peripheral neuropathy in many cases remains unknown.

191 y required for the development of autoimmune peripheral neuropathy in NOD.Aire(GW/+) mice.

192 n comorbid conditions and the development of peripheral neuropathy in patients treated with taxane-ba

193 In this review, we discuss the approach to peripheral neuropathy in patients with cancer and addres

194 orphism is associated with increased odds of peripheral neuropathy in the elderly, even with a normal

195 Peripheral neuropathies included axonal and demyelinatin

196 Pirenzepine and MT7 also prevented peripheral neuropathy induced by the chemotherapeutic ag

197 Peripheral neuropathy, interstitial nephritis, and vascu

198 In a model of peripheral neuropathy, intrathecal (i.th.) administratio

199 emia, severe insulin resistance and diabetic peripheral neuropathy involving sensory and motor neuron

200 Peripheral neuropathy is a common finding in patients wi

201 Chemotherapy-induced peripheral neuropathy is a common, dose-limiting side ef

202 A major cause of peripheral neuropathy is a copy number variant involving

203 Chemotherapy-induced peripheral neuropathy is a dose-limiting side effect of

204 Peripheral neuropathy is a highly prevalent and morbid c

205 S and support the contention that congenital peripheral neuropathy is a key feature of this disorder.

206 Peripheral neuropathy is a major dose-limiting side effe

207 Peripheral neuropathy is a prevalent condition that usua

208 These results indicate that peripheral neuropathy is a rare finding in patients with

209 Peripheral neuropathy is a serious, dose-limiting side e

210 Peripheral neuropathy is also a frequent manifestation o

211 Peripheral neuropathy is dose limiting in paclitaxel can

212 Recognition of rare localizations of peripheral neuropathy is essential given the implication

213 Peripheral neuropathy is the most frequent neurological

214 In diabetic patients, an early index of peripheral neuropathy is the slowing of conduction veloc

215 Peripheral neuropathy is underappreciated as a potential

216 rcot-Marie-Tooth (CMT) disease, an inherited peripheral neuropathy, is GDAP1.

217 gical disease, such as dementia, stroke, and peripheral neuropathy, is large and growing consequent t

218 neuropathies, including chemotherapy-induced peripheral neuropathy, is the result of subacute/chronic

219 es, and radiculoplexus neuropathies are rare peripheral neuropathy localizations that often require e

220 Peripheral neuropathy may play a role in physical functi

221 more common in patients treated for AMR; and peripheral neuropathy, more common in patients treated f

222 ERK1/2 activity in demyelinating disease or peripheral neuropathies must be approached with caution.

223 Peripheral neuropathy occurred in 11 (11%) of 104 patien

224 Grade 1/2 drug-related peripheral neuropathy occurred in 12% (no grade >/=3).

225 Peripheral neuropathy occurred in 46% (grade >/=3 in 7%)

226 as associated with a decreased proportion of peripheral neuropathy (odds ratio, 0.3; 95% CI, 0.07-0.9

227 ocytopenia (five patients, 8%); drug-related peripheral neuropathy of grade 3 or higher occurred in f

228 or phosphatidylcholine curcumin improves the peripheral neuropathy of R98C mice by alleviating endopl

229 We previously showed that peripheral neuropathy of the bone marrow was associated

230 Painful peripheral neuropathy often occurs without apparent unde

231 However, rare localizations of peripheral neuropathy often require more extensive diagn

232 es peripheral neuropathy (paclitaxel-induced peripheral neuropathy or PIPN) that negatively affects c

233 , indicating that the results are not due to peripheral neuropathy or some other primary afferent mec

234 (OR, 2.24; 95% CI, 1.11-4.50; P = .02), and peripheral neuropathy (OR, 2.52; 95% CI, 1.43-4.43; P =

235 tes (OR:1.07), current smoking (OR:1.67) and peripheral neuropathy (OR:1.72) all were significantly a

236 diabetes, ataxia, upper-motor-neuron damage, peripheral neuropathy, or hearing loss.

237 chemotherapeutic agents, paclitaxel produces peripheral neuropathy (paclitaxel-induced peripheral neu

238 treated with BR (P < .05), and incidences of peripheral neuropathy/paresthesia and alopecia were sign

239 ochondrial myopathy, sensorineural deafness, peripheral neuropathy, parkinsonism, and/or cognitive im

240 medications are needed to prevent and treat peripheral neuropathy, particularly in type 2 diabetes.

241 , and hematuria were more frequent with C25; peripheral neuropathy, peripheral edema, alopecia, and n

242 ce and severity of nephropathy, retinopathy, peripheral neuropathy, peripheral vascular disease, and

243 Chemotherapy-induced peripheral neuropathy persists after completion of cance

244 frequently produces severe treatment-related peripheral neuropathy (PN) in Waldenstrom's macroglobuli

245 On the other hand, the rate of peripheral neuropathy (PN) was significantly higher in t

246 The mechanisms leading to paclitaxel-induced peripheral neuropathy remain elusive, and therapies that

247 Painful peripheral neuropathy represents a significant public he

248 l results, which demonstrated a high rate of peripheral neuropathy resolution, and durable remissions

249 Here, we investigate a mouse model of peripheral neuropathy secondary to SC mitochondrial dysf

250 taneous copper deficiency (<0.78 mug/mL) and peripheral neuropathy seen at the Mayo Clinic from 1985

251 e [2%]), diarrhoea (18 [4%] vs 39 [9%]), and peripheral neuropathy (six [1%] vs 28 [6%]).

252 ly; two [2%] vs three [3%] postoperatively), peripheral neuropathy (six [4%] vs one [1%] preoperative

253 aplegia with thin corpus callosum and axonal peripheral neuropathy (SPG7/PGN, SPG15/ZFYVE26, SPG21/AC

254 nted behavioral and histologic indicators of peripheral neuropathy, stimulated tissue NAD recovery, i

255 the large number of acquired and hereditary peripheral neuropathies, such as diabetic neuropathy or

256 rinic drugs prevented or reversed indices of peripheral neuropathy, such as depletion of sensory nerv

257 cyl-tRNA synthetases have been implicated in peripheral neuropathies, suggesting that these tRNA char

258 sted whether there is an association between peripheral neuropathy symptoms [evaluated by the Europea

259 Peripheral neuropathy symptoms after systemic chemothera

260 sciatic nerve oxidative-nitrative stress and peripheral neuropathy than the wild-type (C57Bl6/J) mice

261 Marie-Tooth disease is a group of hereditary peripheral neuropathies that share clinical characterist

262 events was 2.1 per 1000 patient-weeks, with peripheral neuropathy the most frequent severe adverse e

263 g patients with painful chemotherapy-induced peripheral neuropathy, the use of duloxetine compared wi

264 in the pathology of acquired, inflammatory, peripheral neuropathies.The identification of new target

265 ; n = 20), (2) TTR mutation carriers without peripheral neuropathy (TTR-noPN; n = 10), (3) healthy co

266 p), neutropenia (41 [10%] vs 125 [31%]), and peripheral neuropathy (two [<1%] vs 15 [4%]).

267 Peripheral neuropathy typically follows a length-depende

268 ith multiple myeloma (MM) with no history of peripheral neuropathy using quantitative sensory tests (

269 otypes mediated by immune complexes, such as peripheral neuropathy, vasculitic lesions, and hypocompl

270 ation disrupts myelin homeostasis and causes peripheral neuropathy via a combination of toxic gain-of

271 The observed rate of peripheral neuropathy was 20%, with only 1 grade 3 event

272 The incidence of peripheral neuropathy was 27% in the ixazomib group and

273 Vincristine-induced peripheral neuropathy was assessed at clinic visits usin

274 rombocytopenia (17%), and neutropenia (17%); peripheral neuropathy was limited to grade 1/2 (23%).

275 Peripheral neuropathy was limited to grades 1 and 2 (9%)

276 Peripheral neuropathy was measured in 2008 and defined a

277 Peripheral neuropathy was measured subjectively through

278 Grade 3 peripheral neuropathy was more frequent with VTD (29% v

279 Grade 1 to 2 peripheral neuropathy was observed in 65% of patients (9

280 41% (POM+LoDEX) and 48% (POM); no grade 3-4 peripheral neuropathy was reported.

281 Peripheral neuropathy was seen in 44 (67%) of 66 patient

282 The prevalence of peripheral neuropathy was significantly lower in patient

283 Peripheral neuropathy was the most common adverse event.

284 Peripheral neuropathy was uncommon and limited to grade

285 logic and nonhematologic toxicity, including peripheral neuropathy, was increased with nab-paclitaxel

286 been found mutated and aggregated in several peripheral neuropathies, we predicted that an increase i

287 From this cohort of 393 patients with peripheral neuropathy, we sequenced SCN11A in 345 patien

288 phism (SNP) analysis and vincristine-induced peripheral neuropathy were assessed in 321 patients from

289 sease conditions potentially associated with peripheral neuropathy were evaluated: diabetes, hypothyr

290 One hundred one cases of amyloidosis with peripheral neuropathy were identified, 60 primary and 41

291 at least 5 cm and without grade 2 or greater peripheral neuropathy were included in the study.

292 Grade 3/4 venous thromboembolism and peripheral neuropathy were rare (1.6% each).

293 The rates of grade 3 or 4 peripheral neuropathy were similar in the two groups.

294 ference between the genotypes in the odds of peripheral neuropathy when folate intake was </=800 mug

295 r arthralgia, vomiting, nausea, fatigue, and peripheral neuropathy, whereas edema was more frequent a

296 contribute to chemotherapy- induced painful peripheral neuropathy, which can be a critical dose-limi

297 Sensory motor axonal peripheral neuropathy, which is another rare association

298 ll patients with defined amyloid subtype and peripheral neuropathy who completed autonomic testing an

299 YP2U1), as well as for the causative gene of peripheral neuropathy with or without agenesis of the co

300 howed that they prevented paclitaxel-induced peripheral neuropathy without blocking paclitaxel's abil