ライフサイエンスコーパス: alopecia

1 xicity; more rash, pruritus, neuropathy, and alopecia).

2 fe, his skin showed erosions, dry scale, and alopecia.

3 Chemotherapy may induce alopecia.

4 cular inflammation and widespread persistent alopecia.

5 for the treatment of hair disorders such as alopecia.

6 hair density, consistent with a nonscarring alopecia.

7 He did not have alopecia.

8 ride over the past 3 months for androgenetic alopecia.

9 ralgia, rash, photosensitivity, fatigue, and alopecia.

10 deficiency rickets even without evidence of alopecia.

11 en reentry decreases, leading to progressive alopecia.

12 the hair follicle plays a role in autoimmune alopecia.

13 ation in the nursing neonates, manifested as alopecia.

14 unctional, leading to HVDRR, with absence of alopecia.

15 ockout mice were viable but developed severe alopecia.

16 for leucopenia, neutropenia, infection, and alopecia.

17 signaling mediator, results in a progressive alopecia.

18 a hair follicle-cycling defect resulting in alopecia.

19 in and hair phenotype that emulates scarring alopecia.

20 sebum control and treatment of androgenetic alopecia.

21 n of the VDR, in humans and mice, results in alopecia.

22 ermal thickening, dermal cyst formation, and alopecia.

23 ocesses associated with chemotherapy-induced alopecia.

24 20CC (OR 3.2, P < 0.01) were associated with alopecia.

25 strophy associated with chemotherapy-induced alopecia.

26 disruption of the hair cycle and subsequent alopecia.

27 and source population as those patients with alopecia.

28 l design, and understanding the triggers for alopecia.

29 tor (VDR) mutations in humans and mice cause alopecia.

30 lcium diet leads to transient noncicatricial alopecia.

31 to mothers fed a normal diet do not develop alopecia.

32 , low-calcium (0.47%) diet develop transient alopecia.

33 , mainly represented by acne, hirsutism, and alopecia.

34 enting both IR- and cyclophosphamide-induced alopecia.

35 adhesions, defective follicle structure, and alopecia.

36 as acne vulgaris, hirsutism, and androgenic alopecia.

37 phase of the hair cycle, resulting in cyclic alopecia.

38 ia totalis or alopecia universalis vs patchy alopecia.

39 nt scarring, disfiguration, and irreversible alopecia.

40 k late-stage disease with permanent scarring alopecia.

41 ndition we named enteropathy-lymphocytopenia-alopecia.

42 One hundred twenty-five (82%) reported alopecia.

43 lead to conditions such as aging-associated alopecia.

44 vel, low-risk therapeutic approach for scalp alopecias.

45 rops for glaucoma, may be relevant for scalp alopecias.

46 had significantly fewer events of grade 1-4 alopecia (12 [10%] vs 42 [36%]) and peripheral neuropath

47 [26%] of 189), rash (19 [20%] vs 18 [10%]), alopecia (18 [19%] vs eight [4%]), and erythema (18 [19%

48 19%); hyperbilirubinemia (10% and 22%); and alopecia (18%).

49 Of those, 13 had reported no alopecia, 18 had reported moderate alopecia, and 11 had

50 rhoea (267 [57%] vs 111 [47%] patients), and alopecia (221 [47%] vs 125 [53%]).

51 enic disorders (182 [25%] vs 334 [47%]), and alopecia (23 [3%] vs 254 [36%]) were most common.

52 grades) included nausea (43% oral; 42% IV), alopecia (26% oral; 30% IV), fatigue (31% oral; 36% IV),

53 ns occurred in 6 patients (86%) and included alopecia (29%), dysgeusia (29%), muscle cramps (29%), an

54 quently in cyclosporine patients (p < 0.01); alopecia (30%) occurred more frequently in tacrolimus pa

55 findings, including cosmetically significant alopecia (30%), periorbital hyperpigmentation (30%), dee

56 most common were muscle spasms (317 [64%]), alopecia (307 [62%]), dysgeusia (269 [54%]), weight loss

57 peripheral edema (52.7%), diarrhea (35.4%), alopecia (33.9%), and nausea (33.3%).

58 ce intervals]) in patients with androgenetic alopecia (37.3 128.4, 46.1]) and alopecia areata (24.9 [

59 emotherapy than with chemotherapy alone were alopecia (60 [74%] of 81 vs 44 [59%] of 75), nausea (56

60 ot skin reaction (76.3%), diarrhoea (68.6%), alopecia (67.1%), and rash or desquamation (50.2%).

61 4%]), photosensitivity reaction (994 [31%]), alopecia (826 [26%]), and nausea (628 [19%]).

62 patients), weight loss (10), dysgeusia (9), alopecia (9), decreased appetite (5), and fatigue (4).

63 ciency, and, in some cases, autoimmunity and alopecia, a condition we named enteropathy-lymphocytopen

64 Other adverse events included hot flushes, alopecia, abdominal pain, and back pain.

65 ic myelogenous leukemia, reportedly produces alopecia according to the package insert, but clinical a

66 For those patients who reported alopecia, additional questions about reversal of hair lo

67 Androgenetic alopecia (AGA) is a common heritable and androgen-depend

68 Early androgenetic alopecia (AGA) is patterned hair loss occurring before a

69 ude that finasteride treatment of androgenic alopecia (AGA) is safe but do not assess quality of safe

70 Presence of androgenetic alopecia (AGA) might be such a predictor.

71 la cells (DPCs) taken from male androgenetic alopecia (AGA) patients undergo premature senescence in

72 Androgenetic alopecia (AGA), a hereditary disorder that involves the

73 Androgenetic alopecia (AGA), also known as common baldness, is charac

74 ential for the treatment of skin conditions (alopecia, allergic skin diseases, hyperpigmentation, pso

75 onsequence, the nursing neonates suffer from alopecia, anaemia and growth retardation owing to elevat

76 fore explored the association of early-onset alopecia and ALS in the Health Professionals Follow-up S

77 versus-host-like condition, characterized by alopecia and blepharitis.

78 ults, viable KRT8bc replacement mice develop alopecia and chronic skin lesions, indicating that the s

79 Restoration of Gsdma3 expression in AE (alopecia and excoriation) mouse skin rescues hair follic

80 Older mice develop mild alopecia and hyperplasia of sebaceous glands, particular

81 ermine whether an association exists between alopecia and iron deficiency in women.

82 n to bone marrow failure, he had evidence of alopecia and mucositis.

83 Alopecia and nail changes are not commonly reported side

84 Alopecia and nail changes were common adverse effects as

85 were eligible to complete a survey regarding alopecia and nail changes.

86 t Pparg(Delta/Delta) mice developed scarring alopecia and severe perifollicular inflammation.

87 cornifelin deficiency contributes to cyclic alopecia and skin abnormalities in Zdhhc13(skc4) mice.

88 Alopecia and skin lesions were induced in CD200-deficien

89 rexpressing IL-31 developed severe pruritis, alopecia and skin lesions.

90 hombencephalosynapsis with parietal/temporal alopecia and sometimes trigeminal anaesthesia, towering

91 vitamin D resistant rickets (HVDRR) without alopecia and successful management of this condition wit

92 s effective at reducing chemotherapy-induced alopecia and to assess adverse treatment effects.

93 ported no alopecia, 18 had reported moderate alopecia, and 11 had reported extensive alopecia at age

94 hracycline regimens, longer-term measures of alopecia, and adverse effects.

95 lescence are telogen effluvium, androgenetic alopecia, and alopecia areata.

96 verse events with chemotherapy were fatigue, alopecia, and dyspnea.

97 thrombocytopenia, gastrointestinal symptoms, alopecia, and fatigue were the most common adverse event

98 kin, joint contractures, bone abnormalities, alopecia, and growth impairment in all 15 patients; card

99 on of this "toxic milk" causes inflammation, alopecia, and growth retardation in the nursing neonates

100 25; peripheral neuropathy, peripheral edema, alopecia, and nail disorders were more frequent with D75

101 ses severe phenotypes including amyloidosis, alopecia, and osteoporosis.

102 diposity, decreased Scd-1 expression, facial alopecia, and osteoporosis.

103 oliferative potential, stem cell exhaustion, alopecia, and premature aging.

104 resulting in cardiac hypertrophy, dwarfism, alopecia, and prenatal mortality.

105 Other symptoms of DM, including rash, alopecia, and reduced forced vital capacity, improved ma

106 Clinical features such as weight loss, alopecia, and skin ulcers, and histologic features with

107 associated with protection from early-onset alopecia, another sexually dimorphic condition.

108 clinical and histologic descriptions of the alopecia are lacking.

109 ostasis, the actions of the VDR that prevent alopecia are ligand-independent.

110 Because treatments for alopecia are not curative, helping affected patients cop

111 Acne and androgenic alopecia are prevalent but unreliable markers of biochem

112 ndrogenetic alopecia (37.3 128.4, 46.1]) and alopecia areata (24.9 [17.2, 32.6]) were statistically s

113 We aimed to determine the risk of alopecia areata (AA) and vitiligo associated with atopic

114 Treatments for alopecia areata (AA) have evolved over the decades from

115 However, vitiligo and alopecia areata (AA) have not been well characterized in

116 t has long been appreciated that episodes of alopecia areata (AA) have occurred after severely stress

117 Alopecia universalis is an uncommon form of alopecia areata (AA) involving hair loss over the entire

118 Alopecia areata (AA) is a common autoimmune disease resu

119 Alopecia areata (AA) is a common T cell-mediated disorde

120 Alopecia areata (AA) is a genetically determined, immune

121 Alopecia areata (AA) is a non-scarring inflammatory hair

122 Alopecia areata (AA) is among the most highly prevalent

123 Alopecia areata (AA) is an autoimmune disease of the hai

124 Alopecia areata (AA) is an autoimmune disease that attac

125 Alopecia areata (AA) is an autoimmune disease that targe

126 Alopecia areata (AA) is an autoimmune disorder of the ha

127 Alopecia areata (AA) is characterized by hair loss in pa

128 Characterizing blood profile of alopecia areata (AA) is important not only for treatment

129 Alopecia areata (AA) is one of the most common forms of

130 Alopecia areata (AA), a non-scarring inflammatory hair l

131 eg) cells was reported to play a key role in alopecia areata (AA).

132 ) is increased in patients with vitiligo and alopecia areata (AA).

133 phenotype and functional status in extensive alopecia areata (EAA) scalp skin.

134 um (n = 30), androgenetic alopecia (n = 52), alopecia areata (n = 17), and alopecia areata totalis/un

135 utpatients clinic, 2 to 16 years of age with alopecia areata affecting at least 10% of scalp surface

136 ese therapeutic techniques for patients with alopecia areata and further refine which subtypes of the

137 heumatic disease, thyroid disease, vitiligo, alopecia areata and inflammatory bowel disease) were sel

138 mice expressing this TCR develop spontaneous alopecia areata at nearly 100% incidence.

139 One patient with extensive alopecia areata experienced skin atrophy that resolved s

140 Few treatments for alopecia areata have been well evaluated in randomized t

141 characterize a new high-incidence model for alopecia areata in C57BL/6J mice, the first to our knowl

142 , a gene that is known to be associated with alopecia areata in humans.

143 a(+)NKG2D(+) T effector memory cells mediate alopecia areata in part through Janus kinase (JAK) signa

144 Alopecia areata is accompanied by Th2/Tc2 activation in

145 Alopecia areata is among the most prevalent autoimmune d

146 Alopecia areata is an idiopathic cause of hair loss with

147 Alopecia areata is an immune-mediated, nonscarring form

148 or efficacy of currently used treatments for alopecia areata is lacking.

149 Alopecia areata is less common, but may be distressing,

150 Alopecia areata is one of the most frequent organ-restri

151 y loci have been implicated, the genetics of alopecia areata is still unclear.

152 ating question regarding the pathogenesis of alopecia areata is the potential linkage with the brain.

153 hrough Janus kinase (JAK) signaling and that alopecia areata might be treated with JAK inhibitors.

154 In addition, although alopecia areata often results in significant psychologic

155 h telogen effluvium (50.1 [33.9, 66.33]) and alopecia areata totalis/universalis (52.3 [23.1, 81.5])

156 ecia (n = 52), alopecia areata (n = 17), and alopecia areata totalis/universalis (n = 7).

157 rticaria, pruritus, scabies, cellulitis, and alopecia areata were underrepresented in CDSR when match

158 be associated with Crohn disease, psoriasis, alopecia areata, and leprosy.

159 eczema, psoriasis, acne vulgaris, pruritus, alopecia areata, decubitus ulcer, urticaria, scabies, fu

160 the case of dermatological diseases such as alopecia areata, vitiligo, psoriasis and atopic dermatit

161 acne," "vitiligo," "seborrheic dermatitis," "alopecia areata," and "lichen planus." Diverse study pop

162 irst-line agent for limited patchy childhood alopecia areata.

163 gs regarding the use of these treatments for alopecia areata.

164 a novel high-incidence model for spontaneous alopecia areata.

165 ivilege as a key step in the pathogenesis of alopecia areata.

166 a contributing factor in the development of alopecia areata.

167 elogen effluvium, androgenetic alopecia, and alopecia areata.

168 ma, 0.03% for decubitus ulcer, and 0.01% for alopecia areata.

169 rthritis, juvenile idiopathic arthritis, and alopecia areata.

170 have a role in precipitating and maintaining alopecias as well.

171 wn to develop severe hair growth defects and alopecia, as a tool for defining pathways of hair follic

172 ermine the prevalence and characteristics of alopecia associated with this agent.

173 rate alopecia, and 11 had reported extensive alopecia at age 45 years.

174 anges in the hair cycle underlie age-related alopecia, but the causative mechanisms have remained unc

175 was made to at least one form of cicatricial alopecia, but the role lipids play in other follicular p

176 benign prostatic hyperplasia and androgenic alopecia, but the role of 5alpha-dihydrotestosterone (DH

177 Primary cicatricial or scarring alopecias (CA) are a group of inflammatory hair disorder

178 arring alopecia resembling human cicatricial alopecias (CAs), particularly the central centrifugal CA

179 bone and muscle loss, excess fat deposition, alopecia, cataracts, deafness, increased anxiety, and se

180 calp cooling to prevent chemotherapy-induced alopecia, conclusions have been limited.

181 f starting therapy, although facial hair and alopecia continue to develop after 1 year.

182 (gastrointestinal event, headache, lethargy, alopecia, cough, or dyspnea).

183 Alopecia developed a mean (standard deviation) of 75 (54

184 Alopecia developed more commonly among TAC-treated patie

185 Alopecia development is associated with CD8(+) T cell ac

186 er treatment group (any grade) were fatigue, alopecia, diarrhoea, decreased appetite, and nausea.

187 ated adverse events included diarrhea, rash, alopecia, dry skin, and nausea.

188 eratinocytes and leads to the development of alopecia due to a defect in keratinocyte stem cells.

189 The alopecia, dwarfism and cardiac abnormalities were allevi

190 ore than 30% of patients were muscle spasms, alopecia, dysgeusia (taste disturbance), weight loss, an

191 oling devices have been used to prevent this alopecia, efficacy has not been assessed in a randomized

192 -WASP deficiency in mouse skin led to severe alopecia, epidermal hyperproliferation, and ulceration,

193 We show that the alopecia exhibited by both the Hoxc13(tm1Mrc) and Foxn1(

194 deficient mice had hypothyroidism, dwarfism, alopecia, goiter and cardiac abnormalities including hyp

195 v 1.4%), sensory neuropathy (4.1% v 0%), and alopecia (grade 1 or 2; 36.8% v 6.6%) occurred with PacC

196 Those who reported extensive alopecia had an almost 3-fold increased risk of ALS comp

197 gularly thickened interfollicular epidermis, alopecia, hair follicle dystrophy, claw dystrophy, and a

198 The transgenic Cbs-/- animals exhibit facial alopecia, have moderate liver steatosis and are slightly

199 2-Tax expressing mice, developed progressive alopecia, hyperkeratosis, and skin lesions containing pr

200 e tissue, reduced muscle strength, kyphosis, alopecia, hypothermia and shortened lifespan.

201 genome-wide association study for androgenic alopecia in 1,125 men and identified a newly associated

202 leads to a phenotype characterized by cyclic alopecia in addition to the dramatic skin and mucocutane

203 The most common forms of alopecia in adolescence are telogen effluvium, androgene

204 treatment, which causes chemotherapy-induced alopecia in mice and man, induces distinct defects in fe

205 y infiltrate, dysmorphic hair follicles, and alopecia in perinatal mice.

206 led to anemia, decreased growth, and truncal alopecia in pups which was restored following weaning.

207 Keratin 17 (K17)-null mice develop alopecia in the first week post-birth, correlating with

208 s (66.3%; 95% CI, 56.2%-75.4%) evaluable for alopecia in the scalp cooling group vs 0 of 16 patients

209 oea, palmar-plantar erythrodysaesthesia, and alopecia in the sorafenib arm.

210 VDR-mediated PPARgamma suppression underlies alopecia in VDR(-/-) mice.

211 (VDR)-mediated PPARgamma suppression causes alopecia in VDR-null mice.

212 Alopecia in women is a common problem, and conflicting o

213 hat seen in primary cicatricial, or scarring alopecias in which immune targeting of hair follicle ste

214 enzyme specifically in the epidermis causes alopecia, indicating that the regulation of RA homeostas

215 Alopecia, injection site erythema, and pruritus were 13%

216 ic myelogenous leukemia developed widespread alopecia involving scalp and body hair within weeks afte

217 Chemotherapy-induced alopecia is a common and distressing adverse effect.

218 Chemotherapy-induced alopecia is a major problem in clinical oncology.

219 Autoimmune alopecia is characterized by an extensive epidermal T ce

220 Understanding the impact of alopecia is important for care providers who see adolesc

221 Male pattern baldness (MPB) or androgenetic alopecia is one of the most common conditions affecting

222 mage determines whether chemotherapy-induced alopecia is reversible.

223 nciples and explain why chemotherapy-induced alopecia is so challenging to manage.

224 e (Propecia) for the treatment of androgenic alopecia is unknown.

225 vemurafenib were arthralgia, rash, fatigue, alopecia, keratoacanthoma or squamous-cell carcinoma, ph

226 bited palmoplantar keratosis and progressive alopecia, leading to alopecia totalis, associated with a

227 tion during postnatal development as well as alopecia, lethargy, and ataxia.

228 follicles, during the inflammatory permanent alopecia, lichen planopilaris.

229 or-like nutritional abnormalities, including alopecia, liver toxicity, and runting.

230 Androgenetic alopecia may begin in adolescence, and topical minoxidil

231 Hair loss, or alopecia, may occur as a primary skin disorder or becaus

232 the syndrome mandibulofacial dysostosis with alopecia (MFDA) who have de novo missense variants in ED

233 Using a murine autoimmune alopecia model, we observed an increase in early-activat

234 Mice homozygous for the juvenile alopecia mutation (jal) display patches of hair loss tha

235 mptoms (n = 9), mild stomatitis (n = 5), and alopecia (n = 4).

236 ith telogen effluvium (n = 30), androgenetic alopecia (n = 52), alopecia areata (n = 17), and alopeci

237 81 [48.8%]), back pain (n = 54 [32.5%]), and alopecia (n = 53 [31.9%]).

238 more than 10% of administered doses included alopecia, neutropenia, fatigue, nausea, anemia, thromboc

239 d sporadic hair loss resembling the cyclical alopecia observed in mice with keratinocyte-specific del

240 rasae, epidermal expression does not lead to alopecia or other skin abnormalities typically seen in h

241 has a sevenfold-increased odds of androgenic alopecia (OR = 7.12, P = 3.7 x 10(-15)).

242 universalis compared with those with patchy alopecia (OR, 1.22; 95% CI, 1.01-1.48, P = .04).

243 The odds of having skin damage, alopecia, or diabetes were at least 5 times higher in Af

244 No grade > 1 nausea, vomiting, alopecia, or neuropathy events and no cardiac effects re

245 increased risk of congenital malformations, alopecia, or skin disorders.

246 rong biological phenotypes, including facial alopecia, osteoporosis, endoplasmic reticulum (ER) stres

247 e typified by premature death, hair graying, alopecia, osteoporosis, type II diabetes and cataracts.

248 epidermal stem cell compartments, results in alopecia owing to defective hair development.

249 of Dlx3 in the epidermis results in complete alopecia owing to failure of the hair shaft and inner ro

250 cycling in the scalp including androgenetic alopecia (pattern hair loss).

251 obiology of primary cicatricial ("scarring") alopecia (PCA) remains poorly understood and underinvest

252 In primary cicactricial alopecia (PCA), the hair follicle itself is the key targ

253 hea were more common with erlotinib; emesis, alopecia, peripheral neuropathy, and fatigue were more c

254 ease in bone density and entirely lacked the alopecia phenotype observed in age-matched Cbs(-/-) mice

255 parts in the degree of hair-follicle damage, alopecia phenotype, and hair-regrowth pattern.

256 illed in evaluating the most common forms of alopecia presenting in adolescence and should be aware o

257 undesired effects and risks including acne, alopecia, reduced HDL cholesterol, increased triglycerid

258 k of ALS compared with those who reported no alopecia (relative risk = 2.74, 95% confidence interval:

259 nagement strategies for chemotherapy-induced alopecia remain elusive.

260 Chemotherapy-induced alopecia represents one of the major unresolved problems

261 C57BL/6 mice develop dermatitis and scarring alopecia resembling human cicatricial alopecias (CAs), p

262 r fibroadiposis, palmoplantar keratosis, and alopecia, resembling the human cardiocutaneous syndromes

263 Cicatricial (scarring) alopecia results from irreversible damage to epithelial

264 e-wide association studies on early balding (alopecia) revealed single nucleotide polymorphism varian

265 In conclusion, men with early-onset alopecia seem to have a higher risk of ALS.

266 ients), decreased appetite (nine [19%]), and alopecia (seven [15%]).

267 12 months of age, indicators of senescence (alopecia, skin atrophy, kyphosis, osteoporosis, testicul

268 cterized by features of normal aging such as alopecia, skin wrinkling, and osteoporosis, patients wit

269 econdary end points included safety (with an alopecia-specific study) and overall survival (OS).

270 transgenic mice led to increased autoimmune alopecia susceptibility relative to nontransgenic litter

271 nimal model for at least some forms of focal alopecia that have their primary defect in the hair foll

272 hair follicles, linking the pathogenesis of alopecia to that of depigmentation disorders.

273 outcome was the evolution of the Severity of Alopecia Tool (SALT) score, evaluated by 2 independent i

274 audocephalic direction, resulting in truncal alopecia totalis by 20-23 days, with spontaneous recover

275 ies found higher odds of AD in patients with alopecia totalis or alopecia universalis compared with t

276 ed for childhood vs adult-onset vitiligo and alopecia totalis or alopecia universalis vs patchy alope

277 ially early-onset disease, or AA, especially alopecia totalis or alopecia universalis, have significa

278 y immunodeficiency characterized by athymia, alopecia totalis, and nail dystrophy.

279 ratosis and progressive alopecia, leading to alopecia totalis, associated with accelerated proliferat

280 d 4-10 years) with multiple scaly patches of alopecia underwent scalp dermoscopy, direct microscopic

281 s of AD in patients with alopecia totalis or alopecia universalis compared with those with patchy alo

282 IMPORTANCE Alopecia universalis is an uncommon form of alopecia are

283 en AA in patients.We report herein a case of alopecia universalis successfully treated with adalimuma

284 adult-onset vitiligo and alopecia totalis or alopecia universalis vs patchy alopecia.

285 sease, or AA, especially alopecia totalis or alopecia universalis, have significantly increased risk

286 chanism.OBSERVATIONS A woman in her 30s with alopecia universalis, refractory to multiple treatment m

287 s and regrowth, and ultimately progresses to alopecia universalis.

288 ents including Sjogren's syndrome, vitiligo, alopecia, uveitis, and others.

289 evere clinical symptoms, including diarrhea, alopecia, vasculitis, and fibrosis of the skin and visce

290 Grade 2 alopecia was absent.

291 Further analysis revealed that the observed alopecia was likely the result of a progressive and ulti

292 Alopecia was low in both the PLD and vinorelbine groups

293 Alopecia was more common in the DOX arm.

294 After course 1 of treatment, grade 3-4 alopecia was reported in 23 (23%) of 98 patients in the

295 After course 2 of treatment, grade 3-4 alopecia was reported in 25 (28%) of 89 patients in the

296 molecular mechanisms of Smad4 loss-mediated alopecia, we examined expression levels of key molecules

297 e (end-stage scarring), and controls with no alopecia were also studied.

298 dverse effects such as nausea, vomiting, and alopecia were more common with CMF, whereas symptoms of

299 ces of peripheral neuropathy/paresthesia and alopecia were significantly higher in patients treated w

300 cal toxicities (mild enophthalmos and eyelid alopecia) were observed only at the highest dose tested