ライフサイエンスコーパス: oedema

1 -2 standard deviation [SD]; MUAC >= 12.5; no oedema).

2 endothelial barrier and increasing pulmonary oedema.

3 tina homeostasis thus preventing retina from oedema.

4 such as diffuse capillary leak and pulmonary oedema.

5 arge hemispheric stroke at risk for cerebral oedema.

6 erapy for the management of diabetic macular oedema.

7 or ACE inhibitor (ACE-I) treatment and angio-oedema.

8 tegrity, but also to inflammation-associated oedema.

9 small fibres polyneuropathy and lower limbs oedema.

10 nsferase, influenza, insomnia and peripheral oedema.

11 schaemia, paralleling the onset of cytotoxic oedema.

12 low, most probably as a result of developing oedema.

13 nic day (E)17.5, associated with generalized oedema.

14 mildly injected conjunctiva with 1+ corneal oedema.

15 on of intraretinal fluid, indicating macular oedema.

16 hoea, constipation, vomiting, and peripheral oedema.

17 who did not have another reason for macular oedema.

18 ith FTY-720 (fingolimod) may exhibit macular oedema.

19 ocyte velocity, and yolk sac and pericardium oedema.

20 of T regulatory cells and reduced pulmonary oedema.

21 ity in the absence and presence of vasogenic oedema.

22 rmacological prevention and/or resolution of oedema.

23 such as haematomas, contusions and cerebral oedema.

24 Os) led to bent body axes, hydrocephalus and oedema.

25 nagement of glioblastoma-associated cerebral oedema.

26 rt, pneumothorax, and re-expansion pulmonary oedema.

27 tment for cancer, stroke, osteoarthritis and oedema.

28 ylaxis, survival, or symptoms other than leg oedema.

29 ther cerebral consequences such as vasogenic oedema.

30 s including hypopigmentation and pericardial oedema.

31 case of RDD associated with cystoid macular oedema.

32 tients' cerebellar defects, microcephaly and oedema.

33 which result in vascular leakage and retinal oedema.

34 nhibitor for prophylaxis of hereditary angio-oedema.

35 f swelling and low frequency of perilesional oedema (10%) at diagnosis, as compared with the PML-IRIS

36 uring the double-blind period was peripheral oedema (11 [26%] in the macitentan group and five [12%]

37 e most common adverse events were peripheral oedema (12 [27%] of 44 patients) and fatigue (nine [20%]

38 n (16.7%), diabetic retinopathy with macular oedema (15.8%), and AMD (11.0%).

39 e most common adverse events were peripheral oedema (16 [22%] of 73 in the riociguat group vs seven [

40 ents after emactuzumab treatment were facial oedema (16 [64%] of 25 patients), asthenia (14 [56%]), a

41 29 [33%]), myalgia 21 [24%]), and peripheral oedema 20 [23%]).

42 hy (21 [39%] of 54 patients), and peripheral oedema (21 [39%] of 54 patients).

43 cytopenia in nine [11%] vs none), peripheral oedema (22 [27%] vs three [8%]), and venous thromboembol

44 pokalaemia (28 [1%]), and fluid retention or oedema (23 [1%]).

45 [6%], respectively) and higher incidences of oedema (294 [64%] patients had any-grade oedema in the t

46 ue (six [18%] of 33 patients) and peripheral oedema (4 [12%]).

47 ents in the macitentan group were peripheral oedema (9 [23%] of 40 patients) and decreased haemoglobi

48 ogical department due to unilateral blepharo-oedema, abrupt pain and vision disturbances; in 5 cases,

49 d pancreatitis features including pancreatic oedema, acinar cell vacuolization, intrapancreatic tryps

50 Angio-oedema affecting the gastrointestinal tract or abdominal

51 multiple sclerosis with microcystic macular oedema also had higher Multiple Sclerosis Severity Score

52 episodes progressed to bilateral optic nerve oedema and a subsequent left sided optic neuropathy.

53 nly used perioperatively to control cerebral oedema and are frequently continued throughout subsequen

54 l cancer, who developed bilateral optic disc oedema and associated left sided optic neuropathy is des

55 To report a case of bilateral optic disc oedema and associated optic neuropathy in the setting of

56 High lysine alone resulted in vasogenic oedema and blood-brain barrier breakdown within the stri

57 ic disorders, including especially pulmonary oedema and cardiorespiratory collapse.

58 ation, production of oxidative stress, brain oedema and degenerating neurons.

59 sm presenting with life-threatening cerebral oedema and dysmyelination in affected individuals.

60 There was no correlation between fat pad oedema and each of the pathologies.

61 ugular lymph sacs/primordial thoracic ducts, oedema and embryonic lethality.

62 Both bone oedema and erosions on MRI have been confirmed as repres

63 on episodes were characterized by reversible oedema and erythema of the graft.

64 h multiple sclerosis for microcystic macular oedema and examined correlations between macular oedema

65 t in the classic triad of heavy proteinuria, oedema and hypoalbuminaemia.

66 of infarcts showed well demarcated zones of oedema and hypoxic-ischaemic neuronal injury, consistent

67 irculation congestion, leading to bowel wall oedema and impaired intestinal barrier function.

68 helial junctions, thereby suppressing tumour oedema and metastatic spread, may be preferable to full

69 grade 3-4 adverse events include generalised oedema and myalgia (each in two [1%] patients) in those

70 aetiology of neuroleptic associated cerebral oedema and neuroleptic malignant syndrome.

71 IL-1beta/IL-1R actions account for oedema and neutrophil recruitment to the lungs, leading

72 nts, and two (1%) died (one due to pulmonary oedema and one due to pleural effusion and pneumonitis).

73 ic approaches for the treatment of pulmonary oedema and other diseases caused by abnormal vascular pe

74 Haemorrhaging, oedema and other severe vascular defects are a central a

75 itted to the Internal Diseases Clinic due to oedema and pain of the right shoulder joint.

76 erexpressing glioblastoma results in reduced oedema and partial restoration of the integrity of the b

77 Astrocytes were swollen indicating oedema and remained swollen during the next 24 h through

78 ups, except for a slight excess of pulmonary oedema and respiratory failure in the lower magnesium ta

79 arrived with deep vein thrombosis DVT, pain, oedema and rubor of right lower limb and drug abuse.

80 signal abnormalities suggestive of vasogenic oedema and sulcal effusions (ARIA-E) and microhaemorrhag

81 correlation between the presence of fat pad oedema and the presence of at least one of the pathologi

82 tected against ALI and ameliorated pulmonary oedema and total protein in BALF.

83 is (one); pain associated with severe tongue oedema and trismus occurred twice; and non-cardiac chest

84 ma and examined correlations between macular oedema and visual and ambulatory disability in a cross-s

85 factors has been linked to haemorrhaging and oedema and we find widespread expression of VEGF-D, rigf

86 sis lesions include size >2 cm, mass effect, oedema and/or ring enhancement.

87 y with associated development of pericardial oedemas and cardiac damage.

88 height, mid-upper arm circumference [MUAC], oedema) and haemoglobin (Hb) were measured in children a

89 he placebo group (septic shock and pulmonary oedema) and one patient in the ripretinib group (cause o

90 tion of ionic oedema, formation of vasogenic oedema, and catastrophic failure with haemorrhagic conve

91 zures, optic nerve/cerebellar atrophy, pedal oedema, and early death.

92 anoxia, reduces reperfusion injury, prevents oedema, and metabolically supports the energy requiremen

93 larging pneumothorax, asymptomatic pulmonary oedema, and the device malfunctioning, leaking, or dislo

94 tients had no major MRI diagnosis other than oedema, and they were classified as the symptomatic grou

95 , influenza, diarrhoea, headache, peripheral oedema, and wrong drug given.

96 nd glucose uptake, and supervening vasogenic oedema; and (3) a chronic stage of striatal atrophy.

97 ental hypoxia, hypertension, proteinuria and oedema are the principal clinical features of this disea

98 Subcutaneous and muscle oedema are very common loco-regional post-treatment chan

99 uch as haemorrhagic transformation and angio-oedema, are reviewed.

100 vents were reported, and no cases of macular oedema arose.

101 re evaluated for types of bipartite patella, oedema around the synchondrosis, bipartite fragment heig

102 esulted in occurrence of microcystic macular oedema as recognized from experimental data.

103 galy or splenomegaly (52/67), fever (33/64), oedema, ascites, anasarca, or a combination (29/37), ele

104 ver, the increased cellularity and vasogenic oedema associated with inflammation cannot be detected o

105 There was oedema at the bipartite area in 35 patients.

106 reductions in frequency of hereditary angio-oedema attacks and was well tolerated.

107 s with chronic kidney disease was peripheral oedema (benazepril plus amlodipine, 189 of 561, 33.7%; b

108 odality of treatment for refractory cerebral oedema, but the only form of treatment known to improve

109 inhibitor deter attacks of hereditary angio-oedema, but the prophylactic effect of recombinant human

110 onociception was assessed by aesthesiometry, oedema by plethysmometry, clinical severity by scoring,

111 reover, it is not a specific finding because oedema can also be seen in some other conditions, such a

112 12% of the angio-oedema cases were severe (1% of all patients treated wit

113 acute haemorrhage or massive posterior fossa oedema causing obstructive hydrocephalus or brainstem co

114 on of the alveolar epithelial function (lung oedema clearance), epithelial cell repair, innate immuni

115 study is to report a case of cystoid macular oedema (CME) associated with Rosai-Dorfman Disease (RDD)

116 To report the rate of cystoid macular oedema (CMO) as detected by spectral-domain optical cohe

117 protocol of aflibercept for cystoid macular oedema (CMO) secondary to central retinal vein occlusion

118 evated intraocular pressure, cystoid macular oedema (CMO), cataract and posterior capsule opacificati

119 y was used in parallel as an alternative for oedema control.

120 Quadriceps fat pad oedema detected in MRI examinations should warn the radi

121 Oedema develops quickly after trauma, raising intracrani

122 acular degeneration (nAMD), diabetic macular oedema (DME) or branch/central retinal vein occlusion (B

123 abetic retinopathy (DR) and diabetic macular oedema (DMO) (542 cases, 66.0%), followed by retinal vei

124 New clinical trials for diabetic macular oedema (DMO) are being designed to prove superiority ove

125 treatment for recalcitrant diabetic macular oedema (DMO).

126 of treating DR, focusing on diabetic macular oedema [DMO] after anti-vascular endothelial growth fact

127 [6%]), fatigue (six [2%] vs 19 [5%]), brain oedema (eight [2%] vs 11 [3%]), seizure (nine [2%] vs ei

128 ated adverse events included arm swelling or oedema (eight [32%] patients), and vein hardening (seven

129 maging (MRI) for location, size, mass effect/oedema, enhancement, multifocality and fulfilment of Bar

130 erwise thought to be associated with macular oedema except in the context of comorbid clinical uveiti

131 vent in lesion pathogenesis, predisposing to oedema, excitotoxicity, and ingress of plasma proteins a

132 CH and PHO volume on CT; PHO was measured by oedema extension distance.

133 included nasal blockage, rhinorrhoea, eyelid oedema, facial sweating/flushing and ear flushing.

134 zymatically active Lethal Factor (LF) and/or Oedema Factor (EF) bound to Protective Antigen 63 (PA63)

135 ntities of the toxins lethal factor (LF) and oedema factor (EF), leading to widespread vascular leaka

136 n catalytic moieties, lethal factor (LF) and oedema factor (OF), are internalized into the host-cell

137 wo enzyme components, lethal factor (LF) and oedema factor (OF).

138 ive pore, and translocates lethal factor and oedema factor are not well defined without an atomic mod

139 es translocate the enzymes lethal factor and oedema factor into the cytosol of target cells.

140 Oedema factor is an adenylate cyclase that impairs host

141 ising protective antigen, lethal factor, and oedema factor, is the major virulence factor of Bacillus

142 in the placebo group), symptomatic cerebral oedema (five [2%] vs four [2%]), and major haemorrhage (

143 normalities may be associated with cytotoxic oedema following mechanical forces, resulting in changes

144 er cranial autonomic features include eyelid oedema, forehead/facial sweating, sense of aural fullnes

145 cerebral capillary dysfunction, resulting in oedema formation and haemorrhagic conversion.

146 y reduces infarct size, neuronal cell death, oedema formation and neutrophil infiltration in H/I mice

147 e of Starling's principle, which states that oedema formation is determined by the driving force and

148 atic vessel function and thereby exacerbates oedema formation is unknown.

149 ponse resulting in increased vasoreactivity, oedema formation, and microvascular obstruction.

150 laries into three phases: formation of ionic oedema, formation of vasogenic oedema, and catastrophic

151 umonitis (four [8%] and none, respectively), oedema (four [8%] and none, respectively), dyspnoea (thr

152 risks of retinal detachment, cystoid macular oedema, glare, halos and posterior capsule opacification

153 aled clinical signs of esophagitis including oedema, granularity, white spots, and furrowing, while h

154 n sickness (AMS), and high altitude cerebral oedema (HACE), and the genetics, molecular mechanisms, a

155 multiple sclerosis with microcystic macular oedema had significantly worse disability [median Expand

156 Hereditary angio-oedema (HAE) with normal C1 inhibitor is associated with

157 Oedema, haemodilution, and weight gain occurred in a dos

158 e Pdgfrb-Cre transgenic mouse line, leads to oedema, haemorrhage and increased levels of embryonic le

159 alveolitis associated with massive pulmonary oedema, haemorrhage and rapid destruction of the respira

160 of the blood-brain barrier, which can cause oedema, haemorrhage, and cell death.

161 n sickness (AMS) and high-altitude pulmonary oedema (HAPE) were diagnosed using clinical questionnair

162 for treatment of uveitis and uveitic macular oedema has a limited duration of action and is associate

163 pathways, and patients with hereditary angio-oedema have intermittent cutaneous or mucosal swellings

164 Adverse events were peripheral oedema, hypotension, or orthostatic hypotension.

165 the acute onset of noncardiogenic pulmonary oedema, hypoxaemia and the need for mechanical ventilati

166 Progressive encephalopathy with oedema, hypsarrhythmia and optic atrophy (PEHO) syndrome

167 Progressive encephalopathy with oedema, hypsarrhythmia, and optic atrophy (PEHO) syndrom

168 ots, and furrowing, while histology revealed oedema, immune cell infiltration, and basal zone hyperpl

169 F) mice display reduced vascular leakage and oedema, improved response to chemotherapy and, important

170 lesions demonstrated mass effect in 45% and oedema in 77%.

171 jections of bevacizumab to treat the macular oedema in a case of arteriovenous malformation.

172 mmation-associated cellularity and vasogenic oedema in addition to accounting for partial volume effe

173 inflammatory cell recruitment and pulmonary oedema in aged mouse lung during infection.

174 ht values is a suspected cause of optic disc oedema in astronauts.

175 t it is responsible for preventing embryonic oedema in birds, a role previously thought to be played

176 287 significantly inhibited hyperalgesia and oedema in both models.

177 ges in infants and interstitial white matter oedema in children and adults.

178 agents may play a role in wealing and tissue oedema in CSU so representing novel targets in therapy.

179 elial growth factor antagonists for managing oedema in glioblastoma patients.

180 The presence of microcystic macular oedema in multiple sclerosis suggests that there may be

181 nd this led to the development of optic disc oedema in one-half of the subjects.

182 t is frequently prescribed to treat cerebral oedema in patients with glioblastoma-generated circulati

183 adiological findings such as muscle atrophy, oedema in peripheric soft tissue and bone marrow, joint

184 24%) in the placebo group, including macular oedema in six (2%) versus six (1%), and basal-cell carci

185 ween groups, but more patients had pulmonary oedema in the intervention group (94 [11%] of 840) than

186 ncrease in striatal water content, vasogenic oedema in the perihaematomal region presented as increas

187 lated; two resulted in death (from pulmonary oedema in the placebo group and a pre-existing unspecifi

188 nduced significant ulceration, bleeding, and oedema in the stomach or small intestine of wild-type (W

189 of oedema (294 [64%] patients had any-grade oedema in the trebananib group vs 127 [28%] patients in

190 activities of EDP were assessed in mouse paw oedema induced by lambda-carrageenan (Carr).

191 icant correlation between quadriceps fat pad oedema intensity and its dimensions, but it was signific

192 ed Fisher scale, rebleeding, global cerebral oedema, intracranial pressure crisis, pneumonia and seps

193 Cerebral oedema is a near-universal occurrence in patients afflic

194 Orolingual angio-oedema is a recognised complication of tissue plasminoge

195 Hereditary angio-oedema is a recurrent, oedematous disorder caused by def

196 Hereditary angio-oedema is caused by a heterozygous deficiency of C1 inhi

197 Perilesional oedema is common and associated with episodic seizure ac

198 Transient perilesional brain oedema is seen around the calcified foci but its importa

199 The commonest side-effect, peripheral oedema, is attributed to a larger arterial than venous d

200 of NPSLE brains reveals presence of cerebral oedema, loss of neurons and myelinated axons, microglial

201 Five serious adverse events (periorbital oedema, lupus erythematosus [occurring twice], erythema,

202 non-restricted isotropic diffusion fraction (oedema marker) correlated with magnetization transfer ra

203 Microcystic macular oedema may also contribute to visual dysfunction beyond

204 Angio-oedema may be delayed and progress to life-threatening a

205 le range 3-6)] than patients without macular oedema [median Expanded Disability Score Scale 2 (interq

206 e of disease progression, than those without oedema [median of 6.47 (interquartile range 4.96-7.98) v

207 modal MRI, and that perihaematomal vasogenic oedema might be attributable to microglial activation, i

208 Microcystic macular oedema (MMO) of the retinal inner nuclear layer (INL) ha

209 g loss of aquaporin-4 expression, glial cell oedema, myelin breakdown and axonal injury, but little i

210 y-tract infection (n=17, 10%) and peripheral oedema (n=13, 8%) were the most frequent events with pio

211 roup were dizziness (n=10 [12%]), peripheral oedema (n=9 [11%]), urinary tract infections (n=9 [11%])

212 as the number of attacks of hereditary angio-oedema observed in each 4 week treatment period.

213 Microcystic macular oedema occurred more commonly in eyes with prior optic n

214 ease in corneal thickness (caused by corneal oedema) occurred at 1-day post-treatment but resolved in

215 perpigmentation, pain, hypopigmentation, and oedema) occurred in 943 (93%) of 1015 participants in th

216 Angio-oedema occurs more frequently than previously reported a

217 ic skin Na(+) excess, reflecting subclinical oedema, occurs in hypertensive patients and in associati

218 a significant independent predictor of angio-oedema (odds ratio (OR) 2.3; 95% CI 1.1 to 4.7).

219 ce values, the presence of bilateral pitting oedema of nutritional origin, or a mid-upper-arm circumf

220 ateral infiltrates consistent with pulmonary oedema on frontal chest radiograph.

221 cute kidney injury (one [2%]), and pulmonary oedema (one [2%]).

222 the five serious adverse events-periorbital oedema (one [4%]), lupus erythematosus (one [4%]), and d

223 iosis OR 11.24, 95% CI 3.21 to 41.34; eyelid oedema OR 5.79, 95% CI 2.57 to 13.82; rhinorrhoea OR 2.6

224 with diabetic retinopathy, diabetic macular oedema or age-related macular degeneration.

225 sease characterized by pruritic weals, angio-oedema or both occurring for at least 6 weeks.

226 biotics and related to cholestatic jaundice, oedema or erythema of the extremity associated with desq

227 raphically might show few areas of vasogenic oedema or even normal brain imaging in some rare cases.

228 Oedema or fluid retention occurred in 67 (27%) patients

229 Any associated oedema or haemorrhagic changes may alter the prognosis a

230 Neurological complications, such as brain oedema or haemorrhagic transformation, occur earlier tha

231 [95% CI 1.14-1.99]), and presumed pulmonary oedema (OR 1.58 [95% CI 1.04-2.39]).

232 he search terms "neurogenic" with "pulmonary oedema" or "pulmonary edema," "experimental neurogenic p

233 for patients presenting with osteomyelitis, oedema, or multifocal or large lesions.

234 Presentation with oedema, osteomyelitis, or large (>/=15 cm in diameter),

235 Sixty-one knees with quadriceps fat pad oedema out of 457 knee MRI examinations were included.

236 e mean number of attacks of hereditary angio-oedema over 4 weeks was significantly reduced with recom

237 barrier damage, microvascular failure, brain oedema, oxidative stress, and by directly inducing neuro

238 ion size, and presence of mass effect and/or oedema (P < 0.001).

239 by 15% in nine astronauts without optic disc oedema (P < 0.005).

240 patients showed post-treatment subcutaneous oedema (p = 0.002 to 0.03), muscle oedema (p = 0.02), an

241 cutaneous oedema (p = 0.002 to 0.03), muscle oedema (p = 0.02), and seroma, respectively.

242 eks for any reason (p=0.003), and lower limb oedema (p=0.009) independently predicted deep vein throm

243 In addition to orofacial angio-oedema, painless swellings affect peripheries, which cau

244 of four or more attacks of hereditary angio-oedema per month for at least 3 months before study init

245 ll unknown whether subsequent perihaematomal oedema (PHE) formation further increases the odds of an

246 000999 with haematoma volume, perihaematomal oedema (PHO) volume, functional outcome and mortality af

247 y intramedullary damage such as haemorrhage, oedema, post-traumatic cystic cavities, and tissue bridg

248 stemic reaction that culminates in pulmonary oedema, potentially leading to death.

249 The microcystic oedema predominantly involved the inner nuclear layer of

250 rrelated with occurrence of diffuse cerebral oedema, presence of subdural and extradural hematoma; ho

251 bone formation, bone marrow and soft tissue oedema, presence of synovial effusion, muscular atrophy

252 The patient's symptoms and oedema regressed with discontinuation of chemotherapy.

253 Hepatic encephalopathy and cerebral oedema remain important and life-threatening complicatio

254 ; two patients in each group developed brain oedema requiring osmotherapy.

255 Macular oedema responded to intravitreal treatment with triamcin

256 ions (misapposition, granuloma, haemorrhage, oedema, retraction or necrosis), and postoperative sympt

257 : 2.06 kg, 95% CI: 1.11 to 3.01) and risk of oedema (RR: 2.21, 95% CI: 1.48 to 3.31), though the risk

258 Macular oedema secondary to retinal vein occlusion (RVO) can cau

259 cacies of widely used treatments for macular oedema secondary to RVO and the feasibility of conductin

260 orehead/facial sweating, itching eye, eyelid oedema, sense of aural fullness and periaural swelling,

261 (eight [17%]; all grade 1-2), and peripheral oedema (seven [15%] grade 1-2, one [2%] grade 3).

262 luded seizure (18 [5%] vs 22 [6%]) and brain oedema (seven [2%] vs 12 [3%]).

263 o grave consequences in the form of cerebral oedema, severe neurological impairment and even death.

264 with diseases with BRB breakdown and macular oedema such as diabetic retinopathy (DR).

265 at could account for the presence of macular oedema, such as uveitis, diabetes or other retinal disea

266 esults of the two astronauts with optic disc oedema suggest that both increases and decreases in nICP

267 cantly in nine astronauts without optic disc oedema, suggesting that the cephalad fluid shift during

268 ructural ocular changes including optic disc oedema that resemble signs of intracranial hypertension.

269 e bilateral regions of subcortical vasogenic oedema that resolve within days or weeks.

270 [3%] patients vs two [1%] patients), macular oedema (three [1%] vs two [1%]), infections (11 [3%] vs

271 two exotoxins: anthrax lethal toxin (LT) and oedema toxin (ET).

272 Here we demonstrate that oedema toxin (PA + OF) induces an increase in ANTXR expr

273 ce of resistance to anthrax lethal toxin and oedema toxin action.

274 Macular oedema typically results from blood-retinal barrier disr

275 in died as a result of catastrophic cerebral oedema unrelated to either treatment.

276 We unexpectedly observed microcystic macular oedema using spectral domain optical coherence tomograph

277 veloped to determine the effect of admission oedema volume on outcome.

278 The incidence of SAM by WLZ, MUAC, or oedema was 190 (513/2,704) per 1,000 children-years.

279 a nested case-control substudy, perilesional oedema was assessed by MRI at the time of seizure in sym

280 No macular oedema was identified in 52 healthy controls assessed ov

281 Although oedema was increased, typical anti-VEGF associated adver

282 Mild-to-moderate pulmonary oedema was more common in patients given albumin than in

283 patients with chronic kidney disease, angio-oedema was more frequent in the benazepril plus amlodipi

284 Orolingual angio-oedema was observed in 42 patients (7.9%; 95% CI 5.5% to

285 reas peripapillary retinal nerve fibre layer oedema was observed in affected eyes (P = 0.008) and sub

286 A microcystic pattern of macular oedema was observed on optical coherence tomography in 1

287 Angio-oedema was retrospectively classified as mild, moderate

288 ion within 5 days of the event; perilesional oedema was seen in 12 patients (50%) compared with two (

289 s had congestive heart failure, frequency of oedema was similar to placebo (one case at 50 mug, two a

290 Erythema and oedema were more frequent with avotermin than with place

291 breast shrinkage, telangiectasia, and breast oedema were significantly less common normal tissue effe

292 reast induration, telangiectasia, and breast oedema were significantly less common normal tissue effe

293 with dysarthria, fatigue, paraesthesias, and oedema, whereas gait problems, disequilibrium, dyskinesi

294 atment, there was complete regression of the oedema with a significant improvement in visual acuity t

295 include haematoma expansion, perihaematomal oedema with increased intracranial pressure, intraventri

296 se events were skin rash (five patients) and oedema with weight gain (six).

297 iagnosis, and management of hereditary angio-oedema, with specific emphasis on the new treatments ava

298 Cases were defined as those developing angio-oedema within 24 h of initiation of tPA.

299 motor regression, characterized by cytotoxic oedema within the basal ganglia, cerebral oligemia, and

300 e urticarias, idiopathic histaminergic angio-oedema without weals as a presentation of CU and omalizu