ライフサイエンスコーパス: peripheral neuropathy

1 neuropathy (five [11%] patients had grade 3 peripheral neuropathy).

2 ld be developed to prevent cisplatin induced peripheral neuropathy.

3 high-fat diet rich in SFAs developed robust peripheral neuropathy.

4 the somatosensory cortex and severity of the peripheral neuropathy.

5 Neuropathic pain is common in peripheral neuropathy.

6 significant hearing loss, nephrotoxicity and peripheral neuropathy.

7 iate ALS from lumbar spondylosis disease and peripheral neuropathy.

8 iate ALS from lumbar spondylosis disease and peripheral neuropathy.

9 gent against multiple indices of central and peripheral neuropathy.

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

11 22 (PMP22) and is the most common hereditary peripheral neuropathy.

12 isodic CNS clinical syndromes in addition to peripheral neuropathy.

13 vide novel insights into the pathogenesis of peripheral neuropathy.

14 ue among mycobacterial diseases in producing peripheral neuropathy.

15 nd pathological features of copper-deficient peripheral neuropathy.

16 primary cancers, thromboembolic events, and peripheral neuropathy.

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

18 ny forms of cancer, but frequently result in peripheral neuropathy.

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

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

21 There was no grade 3 to 4 peripheral neuropathy.

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

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

24 model of CMT1X that develops a demyelinating peripheral neuropathy.

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

26 on by physicians including an assessment for peripheral neuropathy.

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

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

29 lines of chemotherapy left him with chronic peripheral neuropathy.

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

31 y were reversed with treatments that prevent peripheral neuropathy.

32 sed chemotherapeutic agent, produces painful peripheral neuropathy.

33 naire for patients with chemotherapy-induced peripheral neuropathy.

34 olecular intermediates of paclitaxel-induced peripheral neuropathy.

35 index, gastrointestinal manifestations, and peripheral neuropathy.

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

37 2 (PMP22) causes multiple forms of inherited peripheral neuropathy.

38 Smoking was associated with peripheral neuropathy.

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

40 ant dose-limiting neurotoxicity resulting in peripheral neuropathy.

41 mutated in familial dysautonomia (FD) causes peripheral neuropathy.

42 First, missense alleles cause dominant peripheral neuropathy.

43 art failure preserved ejection fraction, and peripheral neuropathy.

44 acular telangiectasia type 2, as well as for peripheral neuropathy.

45 ie-Tooth disease (CMT) is a length-dependent peripheral neuropathy.

46 ures, two had polymicrogyria, and four had a peripheral neuropathy.

47 h type 2A (CMT2A), a dominant axonal form of peripheral neuropathy.

48 r of degenerated axons and hence a very mild peripheral neuropathy.

49 nction in high-fat diet-fed murine models of peripheral neuropathy.

50 n event associated with chemotherapy-induced peripheral neuropathy.

51 s were required in 38% of patients, most for peripheral neuropathy.

52 performed routinely in patients with various peripheral neuropathies.

53 eostasis unbalance is a central component of peripheral neuropathies.

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

55 nsight to understanding and treating sensory peripheral neuropathies.

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

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

58 d to identify axonal degeneration in several peripheral neuropathies.

59 ease is a genetically heterogeneous group of peripheral neuropathies.

60 portunity for the treatment of demyelinating peripheral neuropathies.

61 a that implicate HARS mutations in inherited peripheral neuropathies.

62 d postprocedural pain (2.2% [seven of 320]), peripheral neuropathy (0.9% [three of 320]), and tempora

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

64 HP group and 33 [15%] in the CHOP group) and peripheral neuropathy (117 [52%] in the A+CHP group and

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

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

67 0 [27%]), headache (27 [33%] vs seven [9%]), peripheral neuropathy (25 [31%] vs 14 [19%]), and dyspep

68 [8%] of 437 patients in the placebo group), peripheral neuropathy (25 [6%] vs 12 [3%]), decreased ne

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

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

71 , diarrhoea (44 [30%]), vomiting (42 [29%]), peripheral neuropathy (33 [22%]), dry eye (32 [22%]), an

72 vs 34 [6%]), diarrhoea (23 [5%] vs 16 [3%]), peripheral neuropathy (44 [8%] vs four [<1%]), dyspnoea

73 lated adverse events were fatigue (50%), any peripheral neuropathy (50%), alopecia (49%), any rash (4

74 The most common adverse events were peripheral neuropathy (50%), not customarily associated

75 95 patients were (in decreasing frequency): peripheral neuropathy, 53%; cerebellar ataxia, dysmetria

76 Common adverse events were peripheral neuropathy 7/14 (50%), not customarily associ

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

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

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

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

81 and tumour uptake of NCPs and the absence of peripheral neuropathy allow for repeated dosing to affor

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

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

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

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

86 support to the heterogeneity of EGR2-related peripheral neuropathies and provides strong functional e

87 Fluoroquinolone-induced peripheral neuropathies and tendinopathies are well docu

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

89 inal findings identify novel contributors to peripheral neuropathy and emphasize the fundamental depe

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

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

92 ess of peripheral nerves and the severity of peripheral neuropathy and its underlying condition.

93 rves and the spinal cord (SC) contributes to peripheral neuropathy and motor deficits.

94 of ARSs have been previously associated with peripheral neuropathy and multisystem disease in heteroz

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

96 and other entrapment neuropathies, diabetic peripheral neuropathy and peripheral neuropathy associat

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

98 es, we developed a novel strategy to predict peripheral neuropathy and subsequently adjust the vincri

99 verse reactions including, migraine, several peripheral neuropathies, and visual and auditory neurose

100 RS was identified in a patient with a severe peripheral neuropathy, and a mouse model precisely recre

101 cephaly, neurodevelopmental delay, seizures, peripheral neuropathy, and ataxia, with de novo heterozy

102 rse events (the most common being cytopenia, peripheral neuropathy, and heart failure) were more comm

103 ous CMT2-associated mutations exhibited mild peripheral neuropathy, and homozygous expression resulte

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

105 he treatment of cancer, chemotherapy-induced peripheral neuropathy, and neurodegenerative disease.

106 ophic lateral sclerosis, spinal cord injury, peripheral neuropathy, and stroke.

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

108 Inherited peripheral neuropathies are a genetically heterogeneous

109 Peripheral neuropathies are highly prevalent and are mos

110 Inherited demyelinating peripheral neuropathies are progressive incurable diseas

111 Paclitaxel induces peripheral neuropathy as a side effect of cancer treatme

112 s mice lacking the Sarm1 gene do not develop peripheral neuropathy as evaluated by both behavioral or

113 e, and provide a basis for the evaluation of peripheral neuropathy as part of the clinical developmen

114 ) and GFAP-gp120 transgenic (tg) mice caused peripheral neuropathy, as indicated by nerve conduction

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

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

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

118 Charcot-Marie-Tooth (CMT) disease is a peripheral neuropathy associated with gene duplication a

119 opathies, diabetic peripheral neuropathy and peripheral neuropathy associated with other systemic dis

120 sed to predict a patient's susceptibility to peripheral neuropathy at different time points during th

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

122 Ps associated with severe bortezomib-induced peripheral neuropathy (BiPN) in patients with multiple m

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

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

125 gene replacement therapy after the onset of peripheral neuropathy can provide a therapeutic benefit

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

127 graphy can accurately diagnose many types of peripheral neuropathies (carpal tunnel syndrome and othe

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

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

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

131 nt to reduce gene expression and phenocopy a peripheral neuropathy caused by the HNPP-associated dele

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

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

134 rmally thin, unstable myelin, resulting in a peripheral neuropathy characterized by hypomyelination a

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

136 result in several subtypes of the inherited peripheral neuropathy Charcot-Marie-Tooth disease; howev

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

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

139 in DRG is associated with cisplatin-induced peripheral neuropathy (CIPN) in mice.

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

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

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

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

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

145 Chemotherapy-induced peripheral neuropathy (CIPN) is a major adverse effect o

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

147 .SIGNIFICANCE STATEMENT Chemotherapy-induced peripheral neuropathy (CIPN) is a major side effect in c

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

149 Chemotherapy-induced peripheral neuropathy (CIPN) remains a pressing clinical

150 Chemotherapy induced peripheral neuropathy (CIPN), a toxic side effect of som

151 In chemotherapy-induced peripheral neuropathy (CIPN), agents such as paclitaxel

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

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

154 RT2 protected mice against cisplatin-induced peripheral neuropathy (CIPN).

155 using animal models of chemotherapy-induced peripheral neuropathy (CIPN).

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

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

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

159 trol reduced the risk of developing diabetic peripheral neuropathy (DPN) and cardiovascular autonomic

160 Diabetic peripheral neuropathy (DPN) is a common complication of

161 Diabetic peripheral neuropathy (DPN) is a complication of diabete

162 Painful diabetic peripheral neuropathy (DPN) is difficult to manage, as t

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

164 Diabetic peripheral neuropathy (DPN) often leads to neurotrophic

165 Diabetic Peripheral Neuropathy (DPN) typically is accompanied by

166 d to be involved in the etiology of diabetic peripheral neuropathy (DPN), but their identity remains

167 Diabetic peripheral neuropathy (DPN), diabetic kidney disease (DK

168 level, collectively referred to as diabetic peripheral neuropathy (DPN).

169 healthy Schwann cells (SC-Exos) on diabetic peripheral neuropathy (DPN).

170 Distal sensory peripheral neuropathy (DSPN) is a complication of human

171 rie-Tooth disease (CMT) type 2A is a form of peripheral neuropathy, due almost exclusively to dominan

172 [10%]), vomiting (seven [5%] vs seven [5%]), peripheral neuropathy (eight [6%] vs five [4%]), and pai

173 commended phase 2 dose, 19 (27%) had grade 1 peripheral neuropathy, eight (11%) grade 2, and two (3%)

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

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

176 Rash, peripheral neuropathy, fatigue, alopecia, and nausea wer

177 22 (48%) of 46 patients had peripheral neuropathy (five [11%] patients had grade 3 p

178 previously unrecognized cofactor along with peripheral neuropathy for the development of Guillain-Ba

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

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

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

182 Grade >=2 peripheral neuropathy (grouped term) during induction wa

183 Concurrent peripheral neuropathy has been recognised in association

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

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

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

187 (mental retardation, enteropathy, deafness, peripheral neuropathy, ichthyosis, and keratoderma) is a

188 comotor defects, dopaminergic neuronal loss, peripheral neuropathy, impaired respiratory chain comple

189 in treating leukemia, it can lead to severe peripheral neuropathy in a subgroup of the patients.

190 s associated with the risk of taxane-induced peripheral neuropathy in breast cancer patients.

191 776C-->G polymorphism and folate intake with peripheral neuropathy in elders with normal plasma conce

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

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

194 regulation also underlies paclitaxel-induced peripheral neuropathy in mammals, indicating that epider

195 These data demonstrate that TDF causes peripheral neuropathy in mice and alterations in inflamm

196 Ep400 absence causes peripheral neuropathy in mice, characterized by terminal

197 cronized PEA (PEA-m) formulation on diabetic peripheral neuropathy in mice.

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

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

200 c variations, can enable early prediction of peripheral neuropathy in pediatric leukemia patients.

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

202 neuronal cells and prevented development of peripheral neuropathy in-vivo.

203 ntly, there are no established predictors of peripheral neuropathy incidence during the early stage o

204 Peripheral neuropathies included axonal and demyelinatin

205 al nerves would benefit patients affected by peripheral neuropathies, including Charcot-Marie-Tooth d

206 structural indices of small and large fiber peripheral neuropathy, increased hippocampal neurogenesi

207 wth and fracture healing in a mouse model of peripheral neuropathy induced by paclitaxel treatment.

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

209 Peripheral neuropathy, interstitial nephritis, and vascu

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

211 Inherited peripheral neuropathies (IPNs) represent a broad group o

212 Peripheral neuropathy is a common finding in patients wi

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

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

215 Peripheral neuropathy is a debilitating and painful side

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

217 Peripheral neuropathy is a major dose-limiting side effe

218 Peripheral neuropathy is a prevalent condition that usua

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

220 Chemotherapy-induced peripheral neuropathy is among the most common dose-limi

221 Peripheral neuropathy is associated with an increase in

222 Peripheral neuropathy is dose limiting in paclitaxel can

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

224 Platinum-based chemotherapy-induced peripheral neuropathy is one of the most common causes o

225 While peripheral neuropathy is the most common complication of

226 for preventing or slowing the progression of peripheral neuropathy is to maintain close glycemic cont

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

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

229 in adulthood, such as multiple sclerosis and peripheral neuropathies, lead to severe pathologies, ill

230 Peripheral neuropathy, likely related to PrP(Sc) deposit

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

232 result, patients who are not susceptible to peripheral neuropathy may receive sub-therapeutic treatm

233 ogic disorders known as chemotherapy-induced peripheral neuropathy, mechanistic understanding and tre

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

235 penia (n = 9), thrombocytopenia (n = 3), and peripheral neuropathy (n = 3).

236 oss doses (once every 3 weeks) were fatigue, peripheral neuropathy, nausea, constipation, anorexia, d

237 complement-mediated myopathies, myasthenia, peripheral neuropathies, neuromyelitis and other CNS dis

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

239 The expected linezolid toxic effects of peripheral neuropathy (occurring in 81% of patients) and

240 Peripheral neuropathy of grade 2 or above was less frequ

241 r, led to axonal degeneration in the CNS and peripheral neuropathy of the axonal type.

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

243 Intrathecal gene delivery after the onset of peripheral neuropathy offers a significant therapeutic b

244 nSIRT1OE was activated after mice developed peripheral neuropathy on a HFD.

245 s for YARS p.Pro167Thr showed no evidence of peripheral neuropathy on electromyography, in contrast t

246 ularly those related to chemotherapy-induced peripheral neuropathies or CNS diseases in which axonal

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

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

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

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

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

252 Chemotherapy-induced peripheral neuropathy persists after completion of cance

253 llion people worldwide and is accompanied by peripheral neuropathy (PN) and an associated poorer qual

254 Growing evidence indicates that peripheral neuropathy (PN) is common even in the absence

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

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

257 f SC-Exos to type 2 diabetic db/db mice with peripheral neuropathy remarkably ameliorated DPN by impr

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

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

260 g Schwann cells in order to characterize the peripheral neuropathy seen in Krabbe disease.

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

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

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

264 chwann cells or their myelin sheaths lead to peripheral neuropathies such as Charcot-Marie-Tooth dise

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

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

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

268 Peripheral neuropathy symptoms after systemic chemothera

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

270 nduced high response rates with low rates of peripheral neuropathy, the main dose-limiting toxicity o

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

272 rs that may predispose to paclitaxel-induced peripheral neuropathy (TIPN).

273 ss of sensory feedback from the limbs due to peripheral neuropathy to result in motor impairments in

274 including chemotherapy-induced and diabetic peripheral neuropathies, traumatic brain injury, and amy

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

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

277 Peripheral neuropathy typically follows a length-depende

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

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

280 Peripheral neuropathy was common and was independently a

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

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

283 Peripheral neuropathy was uncommon and limited to grade

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

285 To establish the potential for impact on peripheral neuropathy, we first showed that NSI-189 enha

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

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

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

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

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

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

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

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

294 ion in adult SCs caused a rapidly-developing peripheral neuropathy with abundant demyelination.

295 hepatomegaly without imaging abnormalities; peripheral neuropathy with distal sensory symptoms, such

296 Exclusion criteria included peripheral neuropathy with grade greater than 1, major s

297 ase model developing early onset progressive peripheral neuropathy with hypo- and demyelination, slow

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

299 gene, cause autosomal recessive early-onset peripheral neuropathy with or without intellectual disab

300 reported to cause a heterogenous spectrum of peripheral neuropathy with wide variation in both severi