1  abnormalities in Koa mice, a mouse model of hypertrichosis.

2 s, hypoplasia of mammillae, and dorsal acral hypertrichosis.

3 lood pressure, and an increased incidence of hypertrichosis and paresthesia, were observed in the pat

4 ardiomegaly, hyperflexibility of the joints, hypertrichosis, and craniofacial dysmorphology.

5  family with X-linked congenital generalized hypertrichosis cosegregating with deafness and with dent

6 omplex multi-organ disorder characterized by hypertrichosis, craniofacial dysmorphology, osteochondro

7  identified a cohort of six individuals with hypertrichosis cubiti associated with short stature, int

8 e growth of terminal hair around the elbows (hypertrichosis cubiti) has been reported both in isolati

9 tion allograft recipients is associated with hypertrichosis, gingival hyperplasia, and hypercholester

10 acterized by scleroderma, hyperpigmentation, hypertrichosis, hepatomegaly, cardiac abnormalities and

11 es TRPS1 expression as the probable cause of hypertrichosis in AS in humans and the Koa phenotype in

12 d severe midface hypoplasia, body and facial hypertrichosis, microphthalmia, short stature, and short

13                         Twelve patients with hypertrichosis noted rapid improvement.

14 asic additional history elements (eg, fever, hypertrichosis, oligomenorrhea) were important, they reg

15              X-linked congenital generalized hypertrichosis (Online Mendelian Inheritance in Man 3071

16                      Photographs documenting hypertrichosis were taken before conversion and 1 year l

17 s syndrome (AS) is a rare form of congenital hypertrichosis with excessive hair on the shoulders, fac