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1  abnormalities in Koa mice, a mouse model of hypertrichosis.
2 s, thereby promoting hair growth and causing hypertrichosis.
3 s, hypoplasia of mammillae, and dorsal acral hypertrichosis.
4 rse effects in the oral minoxidil group were hypertrichosis (22 of 45 [49%]) and headache (6 of 45 [1
5 me (CS), a genetic disorder characterized by hypertrichosis and cardiovascular abnormalities.
6                                Its effect on hypertrichosis and cardiovascular features in humans wit
7 lood pressure, and an increased incidence of hypertrichosis and paresthesia, were observed in the pat
8         The most frequent complications were hypertrichosis and refractive errors in 71% (95%CI 61.1-
9 ardiomegaly, hyperflexibility of the joints, hypertrichosis, and craniofacial dysmorphology.
10 l enlargement, intellectual disability (ID), hypertrichosis, and hypoplasia or aplasia of nails and t
11 , characterized by coarse facial appearance, hypertrichosis, and multiple cardiovascular abnormalitie
12                                              Hypertrichosis, cardiac function, and edema were evaluat
13  family with X-linked congenital generalized hypertrichosis cosegregating with deafness and with dent
14 omplex multi-organ disorder characterized by hypertrichosis, craniofacial dysmorphology, osteochondro
15  identified a cohort of six individuals with hypertrichosis cubiti associated with short stature, int
16 e growth of terminal hair around the elbows (hypertrichosis cubiti) has been reported both in isolati
17 tations in subjects with facial dysmorphism, hypertrichosis, epilepsy, ID, and gingival overgrowth, w
18 lpebral (e.g., eyelash trichomegaly, eyelash hypertrichosis, eyelid erythema, eyelid edema, eyelid hy
19 tion allograft recipients is associated with hypertrichosis, gingival hyperplasia, and hypercholester
20 acterized by scleroderma, hyperpigmentation, hypertrichosis, hepatomegaly, cardiac abnormalities and
21 f mesomelic dysplasia, S for seizures, H for hypertrichosis, I for intellectual disability, and P for
22 es TRPS1 expression as the probable cause of hypertrichosis in AS in humans and the Koa phenotype in
23 , namely drug-induced excessive hair growth (hypertrichosis), is insufficiently understood.
24 d severe midface hypoplasia, body and facial hypertrichosis, microphthalmia, short stature, and short
25                     Eyelash trichomegaly and hypertrichosis (n = 22, 76%), high upper eyelid crease (
26                         Twelve patients with hypertrichosis noted rapid improvement.
27 asic additional history elements (eg, fever, hypertrichosis, oligomenorrhea) were important, they reg
28              X-linked congenital generalized hypertrichosis (Online Mendelian Inheritance in Man 3071
29      By investigating congenital generalized hypertrichosis terminalis (CGHT), a rare genetic disorde
30 normalities, and dysmorphic features such as hypertrichosis, thick eyebrows, thin upper lip vermilion
31 wever, in the clinical trial, the effects on hypertrichosis were mixed, and there were no significant
32                      Photographs documenting hypertrichosis were taken before conversion and 1 year l
33 s syndrome (AS) is a rare form of congenital hypertrichosis with excessive hair on the shoulders, fac