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Sexual Precocity in a 16-Month-Old$ [: ^! m" w7 ^
Boy Induced by Indirect Topical8 {8 k  a6 j- Z( [  h# M$ }
Exposure to Testosterone
7 b& v% j9 X8 p" t  X9 @, HSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,20 R$ B1 |$ X8 Y4 |  }
and Kenneth R. Rettig, MD18 V7 L, u1 Z' B9 e8 H5 ]4 A
Clinical Pediatrics" X, a& D: V- v0 b" g4 a
Volume 46 Number 6' v0 e9 x# }9 B, d  _) F, T# C; d6 l
July 2007 540-543
: w; w2 l5 e2 y. v( L6 I+ x' R1 n© 2007 Sage Publications# _. j5 g6 N' s# X, X
10.1177/0009922806296651
! b3 i* y8 B/ I. l$ ?$ R2 I* Whttp://clp.sagepub.com; u3 ?2 {8 Q1 t# K8 g" Z
hosted at
/ Z9 L  b% G$ O( d: Zhttp://online.sagepub.com
7 W$ z: R$ E# T7 |# `Precocious puberty in boys, central or peripheral,
3 [) V6 i, S" X4 n9 X/ J/ @is a significant concern for physicians. Central& @3 o2 b6 Y' K% O
precocious puberty (CPP), which is mediated$ R8 y% L' p2 i( I0 E
through the hypothalamic pituitary gonadal axis, has$ T  ~: K' w' P9 U
a higher incidence of organic central nervous system% ~7 g3 d) V! V/ r/ d! B
lesions in boys.1,2 Virilization in boys, as manifested
- @; |  R, Z! H7 mby enlargement of the penis, development of pubic
7 m2 w! K: g# m9 T8 H+ i! Q2 Nhair, and facial acne without enlargement of testi-
' u2 R& x& e; Z. acles, suggests peripheral or pseudopuberty.1-3 We) P* a6 s" _1 h2 `* ], i; t
report a 16-month-old boy who presented with the
- m2 I/ v/ l0 [6 w4 E. |. Fenlargement of the phallus and pubic hair develop-
. \6 ~0 d" N8 R1 ]8 L6 e* D7 l4 _ment without testicular enlargement, which was due% ]0 S( v  J* H
to the unintentional exposure to androgen gel used by  G" a5 A$ F% F  Y! p! _
the father. The family initially concealed this infor-
3 q6 e) G( j8 G  ]3 B1 i0 Mmation, resulting in an extensive work-up for this
- S) ^/ ^3 j9 @4 V' E8 t8 V  J0 P* }child. Given the widespread and easy availability of
% Y# Z/ x1 Q$ {$ J' ]; d9 j8 Vtestosterone gel and cream, we believe this is proba-# R( [0 ^  ?; j* J4 |# V( L
bly more common than the rare case report in the' O( o, E/ u2 p' ~. f; {/ @4 {
literature.4
/ V2 l3 E  D' Q& k# ~* EPatient Report. ]# y" K2 i7 C4 M# {7 K1 l+ r8 C
A 16-month-old white child was referred to the' G+ W4 B6 P& W% q
endocrine clinic by his pediatrician with the concern
' l0 L# b$ D: h- iof early sexual development. His mother noticed, |9 n( y/ B" {: T2 ~& E) l
light colored pubic hair development when he was
5 a0 W: r, P* w# j6 Y+ m- gFrom the 1Division of Pediatric Endocrinology, 2University of
& c2 s: d* ]1 i$ q- ^; r, v- D0 rSouth Alabama Medical Center, Mobile, Alabama.
1 {. z0 [% C4 k* p, a. YAddress correspondence to: Samar K. Bhowmick, MD, FACE,7 p( r% w7 V, G+ @( ~' X3 q5 K
Professor of Pediatrics, University of South Alabama, College of
: e9 B' R" T  _  ^8 D# b2 ZMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;5 ]/ j- U: b* Z0 t# ^
e-mail: [email protected].
9 }3 p5 R+ }% ]about 6 to 7 months old, which progressively became
; w: ]; G5 o4 j2 N0 o' v  Pdarker. She was also concerned about the enlarge-$ h! P) `# h# B2 ?+ o  u
ment of his penis and frequent erections. The child5 @; m$ d& a: A: F, m
was the product of a full-term normal delivery, with
1 D8 j( O" B  `; U) `+ ha birth weight of 7 lb 14 oz, and birth length of/ b/ z8 R, \9 W
20 inches. He was breast-fed throughout the first year
8 _* e. I5 R) l; l* \! \7 f  nof life and was still receiving breast milk along with
1 M- c# W: a" t; L5 E7 o, ?8 `solid food. He had no hospitalizations or surgery,
$ Z1 q5 [$ Y7 U+ vand his psychosocial and psychomotor development
/ _  l3 F, w' f7 _# y: u5 d: T  k. Fwas age appropriate.
* J* Q- d% n$ S' n' q) V9 m5 [The family history was remarkable for the father,
3 b+ W0 j2 l5 T& }- ?who was diagnosed with hypothyroidism at age 16,/ f. i9 r( y* ^$ k! i
which was treated with thyroxine. The father’s
% D5 _" q' I# j1 [! c. e+ Kheight was 6 feet, and he went through a somewhat7 T! k8 ^  E; ?* ?  M% {
early puberty and had stopped growing by age 14.- {; I( @" Z' s$ N" h
The father denied taking any other medication. The
- B0 J: r; B2 h( k( m9 Ychild’s mother was in good health. Her menarche% @* Y  L' X6 p1 a" J
was at 11 years of age, and her height was at 5 feet
' z# \5 c9 ~% @3 a  j5 inches. There was no other family history of pre-
+ j* \1 I% n, y8 Y9 |* Dcocious sexual development in the first-degree rela-8 E  m6 M: c' ]
tives. There were no siblings.% i1 J# V1 f% v# {+ f! W3 x4 }( w" Z% L
Physical Examination: Y1 ^9 s/ m; c/ ]4 y
The physical examination revealed a very active,6 _; j7 C" l& q, @; x' k: `6 T
playful, and healthy boy. The vital signs documented1 H$ c& u1 C. v
a blood pressure of 85/50 mm Hg, his length was, [% f1 \( d, U
90 cm (>97th percentile), and his weight was 14.4 kg
  u  U8 H, [4 i! k(also >97th percentile). The observed yearly growth
! d  G* Q. p: R1 J% `velocity was 30 cm (12 inches). The examination of
# A% R; k( X2 i/ O* @0 m  `the neck revealed no thyroid enlargement.
8 w  {9 m, n4 B, O; J+ iThe genitourinary examination was remarkable for
+ `8 B7 z$ x3 C+ V4 p* Xenlargement of the penis, with a stretched length of* i$ [2 E* n/ @
8 cm and a width of 2 cm. The glans penis was very well
5 a% Y; y0 `! @5 c1 `  @developed. The pubic hair was Tanner II, mostly around
) j) C9 v9 \( ^' K7 C, N5409 m) L& N8 s) x9 g, Y5 ~
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
. U+ P! Q, z, D* ]the base of the phallus and was dark and curled. The
( |) A, E8 Q$ J4 M# o$ K8 }testicular volume was prepubertal at 2 mL each.9 s/ k, L- [" V. V
The skin was moist and smooth and somewhat
9 V) H. v. z) P' d' w1 G4 G- ]' aoily. No axillary hair was noted. There were no, d6 f* x# F7 z$ u
abnormal skin pigmentations or café-au-lait spots.
# k7 w# n) m3 ^; qNeurologic evaluation showed deep tendon reflex 2+' b' r" G3 L2 B5 u: I
bilateral and symmetrical. There was no suggestion# ~$ m8 V6 _- B! p& t+ @2 M/ Y" b3 ~
of papilledema.
1 T# `# O3 ~; c) ~: nLaboratory Evaluation
8 A7 T/ L! s5 Y/ }  LThe bone age was consistent with 28 months by# y% Y; B1 @$ g& a
using the standard of Greulich and Pyle at a chrono-
4 M* ^2 h6 q5 E0 I) t, k1 E7 ologic age of 16 months (advanced).5 Chromosomal2 S$ ^- F9 x* q4 O3 t
karyotype was 46XY. The thyroid function test
, ~' X, B1 ~" s2 R3 D- _+ f- N' ?showed a free T4 of 1.69 ng/dL, and thyroid stimu-
( r6 c! e( r! y9 o( s3 x& |- a/ @4 xlating hormone level was 1.3 µIU/mL (both normal).: G7 W& Z- n4 _& Z/ |. s5 u
The concentrations of serum electrolytes, blood' M: h* M, t; |4 P- [4 \# t  }5 u
urea nitrogen, creatinine, and calcium all were  o2 Z1 y/ X  |* L3 C* Y
within normal range for his age. The concentration
# J5 l6 S8 j8 U5 q$ W7 zof serum 17-hydroxyprogesterone was 16 ng/dL
! r3 W/ m+ G  x1 o- o! a+ o(normal, 3 to 90 ng/dL), androstenedione was 20
2 _% h- l. O& wng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
0 q5 T% b. a( o1 oterone was 38 ng/dL (normal, 50 to 760 ng/dL),
& X' c- F$ S1 P0 c$ sdesoxycorticosterone was 4.3 ng/dL (normal, 7 to# R" X' g, k2 j" t5 a
49ng/dL), 11-desoxycortisol (specific compound S)6 ?4 b7 S2 `$ D6 E1 t+ ]. j
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-" `- a7 v4 s7 d
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' m* |7 e# @3 ^+ |
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),- F8 S+ d2 `; X' z4 D2 \) u2 @- h
and β-human chorionic gonadotropin was less than
& V+ h; k% m+ b5 mIU/mL (normal <5 mIU/mL). Serum follicular* l4 H  w0 A! P% h% }3 c
stimulating hormone and leuteinizing hormone5 q. w+ u7 L& ]2 `' I
concentrations were less than 0.05 mIU/mL2 l) h1 @5 U" {% `% X- o5 q# G
(prepubertal).5 h! B& P9 [9 V9 ]
The parents were notified about the laboratory* `/ M8 ^& n, j# c
results and were informed that all of the tests were
' D' }$ ]% G( T+ E% D! _+ ^normal except the testosterone level was high. The
8 C5 p# ]" ^( J7 W2 kfollow-up visit was arranged within a few weeks to
) c. ]& d* \8 I! Qobtain testicular and abdominal sonograms; how-
/ C- X; b% e. {" K& W# Iever, the family did not return for 4 months.: q9 R, _( B9 ^, ^) G& H
Physical examination at this time revealed that the1 c+ k! R. ~. R5 O" a) r2 ~" D
child had grown 2.5 cm in 4 months and had gained
  Z) j( R8 b1 F- s/ m# D2 kg of weight. Physical examination remained4 K# |  W! @+ M4 w
unchanged. Surprisingly, the pubic hair almost com-$ {8 o7 M  G4 c* W
pletely disappeared except for a few vellous hairs at
0 Q! S' q' E4 n0 y6 F4 i9 j" sthe base of the phallus. Testicular volume was still 2+ I$ D7 {8 e; I7 e1 d2 Q7 [
mL, and the size of the penis remained unchanged.
6 j9 e: l9 A% E" ]7 cThe mother also said that the boy was no longer hav-
& L' B* v5 M1 O3 I" f. z4 u* d) D5 _8 Ling frequent erections.
0 ^- _4 _$ w% B& w4 E! j$ w7 zBoth parents were again questioned about use of
  a1 s& ]8 n7 |7 j. H- y  Rany ointment/creams that they may have applied to$ h$ l2 G( u( H1 p4 R3 x% R
the child’s skin. This time the father admitted the
5 f9 O1 t8 E  VTopical Testosterone Exposure / Bhowmick et al 541  ~; f9 g# o0 H2 N* b6 g
use of testosterone gel twice daily that he was apply-9 x, I1 }/ e( E3 a& H
ing over his own shoulders, chest, and back area for/ }& S  m: ]' e2 N* R
a year. The father also revealed he was embarrassed8 m; f# K  b/ s
to disclose that he was using a testosterone gel pre-+ W: n2 I' A  l1 T7 i" c
scribed by his family physician for decreased libido
$ s! K) }6 z/ J5 R/ ^$ x* wsecondary to depression.
$ j5 e" d% b- r$ f- Y* {The child slept in the same bed with parents.8 |2 ]) E6 g9 T% r
The father would hug the baby and hold him on his
( y% b* s  _0 r' l+ zchest for a considerable period of time, causing sig-
4 x5 |# |" y/ Z: {5 n" K: jnificant bare skin contact between baby and father.
# ]8 j  Q+ j9 S; ~/ i3 o+ j: z8 z5 FThe father also admitted that after the phone call,2 S, p, a. s: K8 [0 t; I2 A
when he learned the testosterone level in the baby
: X" O- U* q! z% q1 H. Swas high, he then read the product information8 ], s8 _  O1 D) A  o
packet and concluded that it was most likely the rea-
' O8 X. z  _0 _: a( r; bson for the child’s virilization. At that time, they  }/ f5 C3 f) B: r8 L7 |( G: y. y
decided to put the baby in a separate bed, and the& ^  s" z) I0 o; {0 c
father was not hugging him with bare skin and had
* v! ~  q$ }" V3 Fbeen using protective clothing. A repeat testosterone
5 u" Z. X" T8 P  P6 _+ e" ]/ Wtest was ordered, but the family did not go to the7 }% N0 `$ e: \' s* R
laboratory to obtain the test." a& o8 l) l2 v4 ?# L* L) N. `" L- p
Discussion
# \: Z/ m' G: a0 k0 ]9 NPrecocious puberty in boys is defined as secondary
: z7 M0 x  W! T5 @, H+ d7 Esexual development before 9 years of age.1,4' Z5 W) J4 x3 o# @8 l
Precocious puberty is termed as central (true) when/ s4 e% E( Q) e4 s
it is caused by the premature activation of hypo-
6 K$ g0 L4 _% s- pthalamic pituitary gonadal axis. CPP is more com-+ z" p7 Y* s2 C( t/ N
mon in girls than in boys.1,3 Most boys with CPP
3 i0 z( h0 Z7 d/ h* Kmay have a central nervous system lesion that is
0 j" M" g) V  `- s* j+ yresponsible for the early activation of the hypothal-( L7 }; ~" j) y3 O7 _0 c
amic pituitary gonadal axis.1-3 Thus, greater empha-$ W2 l  v2 G  T8 U! q
sis has been given to neuroradiologic imaging in7 f1 k# d7 E- P% [; O0 D( f, O
boys with precocious puberty. In addition to viril-0 g: E% q0 v( O! t
ization, the clinical hallmark of CPP is the symmet-
( \. d5 S7 I& k& Q8 {rical testicular growth secondary to stimulation by
8 D0 Q, Z" v- Dgonadotropins.1,3
, z+ V$ i, P$ @6 fGonadotropin-independent peripheral preco-- q! H  n% s' n6 _) {
cious puberty in boys also results from inappropriate, B! e+ K( u0 B* k+ m6 v
androgenic stimulation from either endogenous or0 @& I* v9 m$ u/ L
exogenous sources, nonpituitary gonadotropin stim-
" U: d- C( E, P- [7 @0 W$ pulation, and rare activating mutations.3 Virilizing
2 b7 L, P4 d  `9 l! L' X5 t# |congenital adrenal hyperplasia producing excessive# |2 }# T; c# h" D* K' V
adrenal androgens is a common cause of precocious4 @3 l' d, ]: @7 X4 }9 f
puberty in boys.3,4' b/ h# Q5 G; T! j2 P9 A/ S
The most common form of congenital adrenal' ^7 U* e) S& o# D0 Q7 |( S
hyperplasia is the 21-hydroxylase enzyme deficiency.9 t" ^# B; c3 C) C
The 11-β hydroxylase deficiency may also result in; D$ |  f- ~$ a! T
excessive adrenal androgen production, and rarely,
! A* S1 k5 V4 uan adrenal tumor may also cause adrenal androgen
" G7 r2 e% Z5 j/ W; Sexcess.1,3- V: ?) A5 c" h# R4 t- ]
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ U, Z* X& f3 ]
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007$ ^$ j! ~; _% k# p& U  R
A unique entity of male-limited gonadotropin-
' Q5 w% ]! e% uindependent precocious puberty, which is also known
" _0 b' a- R& Bas testotoxicosis, may cause precocious puberty at a# J1 b, a* Y) n( k- A' r0 t
very young age. The physical findings in these boys7 E5 S  z+ n8 h" k+ r- ~
with this disorder are full pubertal development,
; F5 U. i1 ]: Uincluding bilateral testicular growth, similar to boys( [- o" x7 Y3 W% H  q; z
with CPP. The gonadotropin levels in this disorder% ^9 z" X; ?8 E
are suppressed to prepubertal levels and do not show6 W& U* f/ i( E3 \& k2 }. b7 b1 x
pubertal response of gonadotropin after gonadotropin-
) X. T/ H9 T" l7 F* w$ Areleasing hormone stimulation. This is a sex-linked
$ |& m8 D( L# Mautosomal dominant disorder that affects only
  v! A$ }# a6 g8 _' Q8 q' {# dmales; therefore, other male members of the family
1 H" V4 q( P/ e" p! Kmay have similar precocious puberty.3
# O' `9 g0 D: M( CIn our patient, physical examination was incon-" ~' R# D0 R) X7 z. r' V
sistent with true precocious puberty since his testi-# w/ t7 {! E( v. k) Z
cles were prepubertal in size. However, testotoxicosis, g3 r8 f1 z. e* Z- P9 b
was in the differential diagnosis because his father
, k, J$ M/ c1 u' y* Y( {, i. kstarted puberty somewhat early, and occasionally,6 k1 h% P( D5 R5 ?
testicular enlargement is not that evident in the
( u" _2 s- k0 _3 M* xbeginning of this process.1 In the absence of a neg-! q; q3 ?" {- l0 V6 b
ative initial history of androgen exposure, our
5 h$ a! ~2 [6 f% m4 X; Z# Ebiggest concern was virilizing adrenal hyperplasia,6 L7 g; {) e/ v7 A9 [
either 21-hydroxylase deficiency or 11-β hydroxylase5 K0 Z3 s8 l6 U& }. t
deficiency. Those diagnoses were excluded by find-* ?: L* M4 j5 M$ Y1 _! h1 |7 P
ing the normal level of adrenal steroids.
- p- P! w+ a& JThe diagnosis of exogenous androgens was strongly
" {" ~" Q* |$ T$ l$ qsuspected in a follow-up visit after 4 months because. A' S0 ]  D- W- R
the physical examination revealed the complete disap-3 N- u. S% I5 C, W  {$ {
pearance of pubic hair, normal growth velocity, and
/ T/ v+ S0 G; ^+ I# K' I+ k9 ^decreased erections. The father admitted using a testos-0 n) K* m( K+ x) |0 p* S  `' b
terone gel, which he concealed at first visit. He was
( f; c* V7 ]7 j) [5 Musing it rather frequently, twice a day. The Physicians’
0 k5 x' U) A5 m$ c+ r7 W: D7 O9 eDesk Reference, or package insert of this product, gel or
7 ?' \* R5 C, }& Z# L( Qcream, cautions about dermal testosterone transfer to! P1 l' V3 K; N" Y
unprotected females through direct skin exposure.. J! D. M  J; A. ]- P9 Z# j
Serum testosterone level was found to be 2 times the
, D' A  t# p% r1 Xbaseline value in those females who were exposed to; I, F: u( [1 q1 Q" J0 f
even 15 minutes of direct skin contact with their male5 m9 e/ z# H+ P+ j
partners.6 However, when a shirt covered the applica-
! Y5 g7 `& }  T% n/ n- x4 otion site, this testosterone transfer was prevented.: T8 K& j! S! `  @4 B( U: V
Our patient’s testosterone level was 60 ng/mL,' Q7 x- w) m+ ]7 V1 S" _/ e+ S& R8 E9 N
which was clearly high. Some studies suggest that
  D4 B+ R2 ~$ Fdermal conversion of testosterone to dihydrotestos-
) u7 {( T) ~. b: _terone, which is a more potent metabolite, is more. F1 ]! t& E& |3 m; v9 o$ g
active in young children exposed to testosterone4 y2 D7 I& x6 m: U
exogenously7; however, we did not measure a dihy-
8 Z' y9 T0 l! I/ ?0 t; z! H  J1 Kdrotestosterone level in our patient. In addition to! I8 r. K  [9 V& l- w2 {6 b
virilization, exposure to exogenous testosterone in& B# i! v/ H- F- K5 C; O3 s4 d
children results in an increase in growth velocity and
% L1 q& z* w9 N9 Sadvanced bone age, as seen in our patient.; j2 \9 f. o9 K7 G) p
The long-term effect of androgen exposure during
- e3 g/ f' l: @early childhood on pubertal development and final
' Q2 A* r0 Y/ Wadult height are not fully known and always remain
  Q6 s% }1 [  \4 e) xa concern. Children treated with short-term testos-0 ?  _8 A+ y: t
terone injection or topical androgen may exhibit some
; y# b% O4 U4 y& j. r. Bacceleration of the skeletal maturation; however, after
0 q  ~' O, A2 w4 F# Acessation of treatment, the rate of bone maturation
& ?. Q) d* x! ~0 g6 ^8 Udecelerates and gradually returns to normal.8,9( u8 i3 J* e$ q2 O
There are conflicting reports and controversy- v/ P( }+ s) ]* G+ O& a
over the effect of early androgen exposure on adult
% w2 c  i3 @- H' v3 Y5 _# j# U; ^1 A" vpenile length.10,11 Some reports suggest subnormal
; r: o4 `# f' X3 eadult penile length, apparently because of downreg-
6 b3 \! d8 U9 P! bulation of androgen receptor number.10,12 However,
9 K7 w. |6 p  H. Q: K+ R' U8 JSutherland et al13 did not find a correlation between
1 L# T. [( x0 K% B8 Gchildhood testosterone exposure and reduced adult; V: O5 y& ?7 `" V5 ?+ R
penile length in clinical studies.
( g3 h5 N0 G/ a3 ^Nonetheless, we do not believe our patient is+ K3 \1 M2 [3 M- a) m  s& t
going to experience any of the untoward effects from1 Q- R2 ?& O2 h1 |! k
testosterone exposure as mentioned earlier because
' l3 f/ r/ y3 fthe exposure was not for a prolonged period of time.
8 v& ]2 ]# m( g5 f. \Although the bone age was advanced at the time of8 J; y0 r8 n( f/ T- i; m, m9 q$ {
diagnosis, the child had a normal growth velocity at) X/ {# E% v. ~; G* Z
the follow-up visit. It is hoped that his final adult1 w  I* _( d9 {7 }& X
height will not be affected.
2 E8 R9 k9 Y; P3 a/ F6 g$ BAlthough rarely reported, the widespread avail-( G8 K$ T4 v" O3 D$ v
ability of androgen products in our society may, G5 k3 x9 _! L/ O3 p
indeed cause more virilization in male or female8 T; P' N6 k2 H8 Q- }4 t0 u
children than one would realize. Exposure to andro-# ~( o3 _  _) g
gen products must be considered and specific ques-8 ]- m, u; x6 T' @  `: w
tioning about the use of a testosterone product or
& h3 U. F4 @8 e  A7 ggel should be asked of the family members during
- f6 l7 ?5 k- y9 U7 qthe evaluation of any children who present with vir-# c) ~+ F  y* g
ilization or peripheral precocious puberty. The diag-8 c! M/ i# |& {; a
nosis can be established by just a few tests and by
0 \1 ?8 `$ W) h( ]6 z/ ~appropriate history. The inability to obtain such a
& m) ~0 D. S, S( Y. B* uhistory, or failure to ask the specific questions, may
2 P& k4 x, p% K- {  w% [result in extensive, unnecessary, and expensive. e1 h2 x7 R. Y; ?
investigation. The primary care physician should be
7 q. m! O6 N* t/ ?& |3 U" laware of this fact, because most of these children" J6 x6 _; j* t$ o% \6 |$ e% U
may initially present in their practice. The Physicians’9 t; G8 v* ~; \
Desk Reference and package insert should also put a
! {* s( Y8 A, {4 a% ^' vwarning about the virilizing effect on a male or' R) b& x9 c: v; C
female child who might come in contact with some-
( D& a1 o" N' u3 lone using any of these products.
1 I8 x4 L/ H1 T. `" BReferences( f: w0 n# T. j  W: n0 `( G6 b- _
1. Styne DM. The testes: disorder of sexual differentiation
* K5 {, Q( K4 V5 m8 B9 wand puberty in the male. In: Sperling MA, ed. Pediatric, l6 {  P/ T5 n' V% A$ d7 M
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;) v/ b. @) f' I8 T* S0 s4 B4 j. y. d
2002: 565-628.# k* q$ X6 C6 F5 I
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
% C  t, M7 ?; o) M; hpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
: s5 E+ N# u; ^0 {& JBoy Induced by Indirect Topical
: f2 ~5 J9 U- j' ]Exposure to Testosterone9 S* U; s" m% ^) X
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
- ~1 s/ _& Q* g0 `2 L6 Iand Kenneth R. Rettig, MD1" s9 F& r' T: l0 n2 h
Clinical Pediatrics; }) D  _) A$ U1 B
Volume 46 Number 6  T6 a* a& p; ~( R) \  t6 P
July 2007 540-543; W5 E' h& U. {0 e- D" P% e
© 2007 Sage Publications$ d& M. n' u) r( @+ e
10.1177/00099228062966516 C" B& x% f& d# J1 r  N
http://clp.sagepub.com/ `- K) u9 ], `$ J
hosted at
6 W1 l4 @/ F1 W, _http://online.sagepub.com
5 S0 A& z5 ~( v3 B% `Precocious puberty in boys, central or peripheral,
2 X* \. ~0 M  U8 s; j4 eis a significant concern for physicians. Central
: m8 G  Z8 |! S+ tprecocious puberty (CPP), which is mediated
, p! R1 j% {5 n& v* `; ]7 othrough the hypothalamic pituitary gonadal axis, has
: i* `. q- c) b3 F& J+ O; _3 _5 Ua higher incidence of organic central nervous system8 v" w: |; l4 N% {) V* Y/ Q
lesions in boys.1,2 Virilization in boys, as manifested
: S7 F% y8 N# A7 ?1 L  xby enlargement of the penis, development of pubic: S- S2 w' p% o5 R9 c! W9 p
hair, and facial acne without enlargement of testi-
; W' I' e' N9 hcles, suggests peripheral or pseudopuberty.1-3 We" t" E1 h/ n4 R" q0 I
report a 16-month-old boy who presented with the5 B2 i+ p( U  f7 ?# g+ p
enlargement of the phallus and pubic hair develop-# q: ?# n9 F) k: @6 o: F
ment without testicular enlargement, which was due8 V4 t3 R4 B7 O: o6 R1 D/ b3 B
to the unintentional exposure to androgen gel used by$ e5 ?9 b( W5 w2 t; s' Y  j
the father. The family initially concealed this infor-
* c9 P0 }/ H0 Qmation, resulting in an extensive work-up for this% u3 n" ?& W  i+ S2 L: e
child. Given the widespread and easy availability of# l8 L6 L5 p0 ^5 c
testosterone gel and cream, we believe this is proba-% }1 h5 H: X: C9 `( Y
bly more common than the rare case report in the
" v$ g4 m+ X6 J! i3 e5 B+ y8 Eliterature.4: s7 V1 I4 ?9 ?% p* Q' N" |. z
Patient Report" n& D& ~  h! F3 [# N+ l$ i6 {
A 16-month-old white child was referred to the9 U/ A, J$ K+ l) f: ?3 z% N: f. v% ?
endocrine clinic by his pediatrician with the concern
7 T$ S/ E4 J/ B$ |0 _of early sexual development. His mother noticed
# a4 O( `. y8 F1 H/ G. Y  clight colored pubic hair development when he was) E5 P; a, S* v' Q( c& s% @
From the 1Division of Pediatric Endocrinology, 2University of
; H- {, f+ [% y# z8 }# F+ CSouth Alabama Medical Center, Mobile, Alabama.
- D( @* G8 s7 vAddress correspondence to: Samar K. Bhowmick, MD, FACE,
% W( I7 D. M0 Y8 T. Y! u. ]Professor of Pediatrics, University of South Alabama, College of
+ c# [5 W2 t+ `$ f9 F8 cMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
2 l! I) n. J: [1 m3 j$ e+ ]. Pe-mail: [email protected].; \: K! g. a" T# B9 m- t% r
about 6 to 7 months old, which progressively became
# u* l) Y( q7 e7 O+ ~0 Fdarker. She was also concerned about the enlarge-0 C, o  F9 w8 m9 p( n  `6 W
ment of his penis and frequent erections. The child
7 v( ~0 j% B0 _was the product of a full-term normal delivery, with
2 \7 `5 r; n+ Ba birth weight of 7 lb 14 oz, and birth length of$ Y( R* Y. ], x- H4 _) s
20 inches. He was breast-fed throughout the first year
! B. H! k+ D- s" hof life and was still receiving breast milk along with
! f8 p) c( ^: o4 ?solid food. He had no hospitalizations or surgery,
# b% l' W4 G( l$ I' @( M2 J* _1 p, Eand his psychosocial and psychomotor development% P5 _/ b# v9 A. i( Y* \+ U& u9 Z
was age appropriate.
0 X' Q5 n4 q; B$ P$ sThe family history was remarkable for the father,7 B2 B# ^: Z5 x3 |
who was diagnosed with hypothyroidism at age 16,# \+ \7 b8 f* x* U) J
which was treated with thyroxine. The father’s
8 H1 L0 B4 P  g5 |5 J! S( aheight was 6 feet, and he went through a somewhat0 {2 y; R) M# S
early puberty and had stopped growing by age 14.
" O$ z. Q( J4 r' m2 G4 f9 i: aThe father denied taking any other medication. The
7 @- z% `: H; F; }0 V: f& Xchild’s mother was in good health. Her menarche" r. ?* |9 a! ^3 e6 u% |
was at 11 years of age, and her height was at 5 feet
' ^1 V: l2 j) {5 k: O  I% ~5 p5 inches. There was no other family history of pre-
+ |+ I  z+ ^6 |8 H0 u* m; G. y1 l) O3 Pcocious sexual development in the first-degree rela-- J( U3 s6 q/ [& m! a% a& n5 p
tives. There were no siblings.0 s5 |3 c& d  Y
Physical Examination
4 r( B: I6 Y1 X5 ?2 NThe physical examination revealed a very active,
: p7 ]: z/ l7 z1 i: A* E' ~playful, and healthy boy. The vital signs documented% u4 f/ s) y, L/ X
a blood pressure of 85/50 mm Hg, his length was  C4 y/ G9 i. s9 f/ w" N
90 cm (>97th percentile), and his weight was 14.4 kg  q7 j8 [( X5 z: y  J: b/ T
(also >97th percentile). The observed yearly growth
; o7 U2 t! {+ C; Y1 o0 R) I2 H4 yvelocity was 30 cm (12 inches). The examination of. y( y9 r9 k0 _( _( E+ q
the neck revealed no thyroid enlargement.7 c- b! ?* q/ D5 U' S( H3 w
The genitourinary examination was remarkable for
. d! u1 H5 |  F9 o, Jenlargement of the penis, with a stretched length of
4 g2 X) v, F" p, ]& j( i8 cm and a width of 2 cm. The glans penis was very well! Y9 d6 I+ ^6 c5 [
developed. The pubic hair was Tanner II, mostly around- R5 E" V6 p1 z; H: R2 f' H
540
1 p7 P1 o3 {8 d: a% p3 c. o2 tat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' c' ~, D* \; r9 j
the base of the phallus and was dark and curled. The8 l  i& r( W% d7 M3 s1 s
testicular volume was prepubertal at 2 mL each.' G$ z! ~1 M  w
The skin was moist and smooth and somewhat, @6 b* D* R5 I4 u' ^6 o
oily. No axillary hair was noted. There were no
$ q: n0 |7 Z; kabnormal skin pigmentations or café-au-lait spots./ X9 y( B" m# i) a0 \
Neurologic evaluation showed deep tendon reflex 2+
# K) r9 |6 K7 }& fbilateral and symmetrical. There was no suggestion9 Y: p# [+ |7 @" D
of papilledema.2 {, H& W1 n( B) [
Laboratory Evaluation. _- t9 V/ z; x; f$ B# a& ~' ?
The bone age was consistent with 28 months by; J3 }" p. b5 B
using the standard of Greulich and Pyle at a chrono-
, w$ D: C2 ~. p  B5 t4 C* Zlogic age of 16 months (advanced).5 Chromosomal3 }# O3 Y( W6 a* r- @5 a
karyotype was 46XY. The thyroid function test
( ^# s/ Y' Y# Y0 i0 @1 @showed a free T4 of 1.69 ng/dL, and thyroid stimu-
8 \+ b- o4 V8 E! Y8 m2 Ulating hormone level was 1.3 µIU/mL (both normal).
7 G0 l# F) \3 T5 l& zThe concentrations of serum electrolytes, blood% T6 b9 N- b& ]- _
urea nitrogen, creatinine, and calcium all were
! a& H% R) _/ v  ]within normal range for his age. The concentration
* O: D# g( V1 |/ Mof serum 17-hydroxyprogesterone was 16 ng/dL
( K+ R* B# Y9 K6 P. c(normal, 3 to 90 ng/dL), androstenedione was 20# b- _0 C$ ^2 B7 A7 Y
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
# y0 ?8 P( ?/ _' r" Tterone was 38 ng/dL (normal, 50 to 760 ng/dL),+ W/ @  e! O* ~, w& m, S+ G
desoxycorticosterone was 4.3 ng/dL (normal, 7 to! ?0 p4 w2 B2 e' n. k  w5 f
49ng/dL), 11-desoxycortisol (specific compound S)7 W# {7 F% F4 P7 Q$ l% ]/ d6 C3 Z# V0 b
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
$ h1 g3 \+ R2 U: u' ?tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
' a* U6 M8 r; T8 h* k' Xtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),$ u( a5 G" j0 F* V/ }
and β-human chorionic gonadotropin was less than$ R6 ~3 _# y+ O* A6 m# d
5 mIU/mL (normal <5 mIU/mL). Serum follicular( F, L; I" `! K# r5 B0 I
stimulating hormone and leuteinizing hormone
5 W& H0 M  _2 z( \# Y3 Kconcentrations were less than 0.05 mIU/mL! p" N) u- G6 ]! ?, _  _
(prepubertal).
6 b: F# m" [3 s# S7 WThe parents were notified about the laboratory
  T3 ^, L8 z4 K. Vresults and were informed that all of the tests were; x' }% ?& p! U% Q# w
normal except the testosterone level was high. The' @# T* U0 J, ?6 a+ B
follow-up visit was arranged within a few weeks to/ j( T* p" d2 j5 y
obtain testicular and abdominal sonograms; how-! r* O( Y& V3 l7 k5 I
ever, the family did not return for 4 months.2 Y2 H* f1 S  _0 D5 _
Physical examination at this time revealed that the, G. Z6 b  ?% X( x
child had grown 2.5 cm in 4 months and had gained5 j) L: R& L; i7 T" e% M1 e
2 kg of weight. Physical examination remained
2 T1 ^# {6 j# [7 q% J- bunchanged. Surprisingly, the pubic hair almost com-# d5 U+ G) c/ l: u* J
pletely disappeared except for a few vellous hairs at
1 C8 }" k4 N" a1 W; f9 x7 a$ O. tthe base of the phallus. Testicular volume was still 2, Q4 [( l: |$ T5 M( U
mL, and the size of the penis remained unchanged.
( a' V! r9 f; K5 {The mother also said that the boy was no longer hav-, ^* o; t2 U8 C6 ^4 x, J
ing frequent erections.
5 L; |/ J& q& ?) m: j4 q5 t; t1 ~Both parents were again questioned about use of
7 U, c+ ]$ U7 B+ m, g( e, Q3 Oany ointment/creams that they may have applied to
( B1 u4 R$ S* A  H- T% ]7 v" mthe child’s skin. This time the father admitted the# ^7 Y& g. a; d2 a" o
Topical Testosterone Exposure / Bhowmick et al 541
3 R7 T/ J  Y5 N  O, f1 _- \use of testosterone gel twice daily that he was apply-
& B, Q1 D3 d' Cing over his own shoulders, chest, and back area for8 G  Z0 w; m5 k3 O; o
a year. The father also revealed he was embarrassed
* y# s/ A* s* O# U6 }to disclose that he was using a testosterone gel pre-
& F1 J( ~* I) f# z4 I* `9 `7 sscribed by his family physician for decreased libido+ Q. I  P, |. N9 m
secondary to depression.
' `, F  k' `! C6 E! W( Y1 R$ d& r9 M) JThe child slept in the same bed with parents.: }) \. P5 i0 X
The father would hug the baby and hold him on his  |% K# t% V) S; Q
chest for a considerable period of time, causing sig-
1 t4 q2 z1 F: pnificant bare skin contact between baby and father.* G1 |2 {7 }1 y3 q) M
The father also admitted that after the phone call,
& {0 t2 T& i; }5 A/ gwhen he learned the testosterone level in the baby
. k$ Q3 V& [* h  [was high, he then read the product information4 A! k# E2 L% A& F3 K* \) ]
packet and concluded that it was most likely the rea-# S7 z5 a- C( P8 m' L
son for the child’s virilization. At that time, they1 b& h7 `) Q9 T$ a0 p) ~
decided to put the baby in a separate bed, and the
1 E: h5 ?% ]; X, S" i4 ?8 d1 [  ~father was not hugging him with bare skin and had* k# W, X' u7 ?3 T4 ?
been using protective clothing. A repeat testosterone% n2 o" Z$ P. g! ^( B( u
test was ordered, but the family did not go to the
0 F9 @, h: G9 Y5 b" x  _laboratory to obtain the test.
: I4 ~" a: P! m# j3 Q: N4 D% B2 v4 cDiscussion* ]+ m1 Q1 C2 h
Precocious puberty in boys is defined as secondary  h( u  J; q& o* p
sexual development before 9 years of age.1,4
# J" e# O5 z6 m2 o, l3 G. GPrecocious puberty is termed as central (true) when* r9 {0 ^& m4 A, W! d. ]8 I
it is caused by the premature activation of hypo-9 v9 T/ c! i! Y  a; |
thalamic pituitary gonadal axis. CPP is more com-6 U) c- D& P  V. I
mon in girls than in boys.1,3 Most boys with CPP
+ {* ~' t" P! e! l4 j3 Smay have a central nervous system lesion that is$ L2 O7 m' w* s  p$ g
responsible for the early activation of the hypothal-( x3 Y/ M% Q2 f$ o6 B# X# g
amic pituitary gonadal axis.1-3 Thus, greater empha-
8 m& m7 o! t& y* asis has been given to neuroradiologic imaging in0 m6 A! i2 x- U. _/ @% [! M) p
boys with precocious puberty. In addition to viril-7 v2 R; b+ @! e& e$ u7 I& S
ization, the clinical hallmark of CPP is the symmet-
9 F' w& K- ~5 L, z8 |rical testicular growth secondary to stimulation by/ o0 E. p. _+ p( ~8 y$ T
gonadotropins.1,3( _- @) d1 R* W- u( Q
Gonadotropin-independent peripheral preco-# r9 l( R" _$ m$ K6 F: o( x: K
cious puberty in boys also results from inappropriate
* ~1 K8 C! T1 q. Z) Q* D/ S' Wandrogenic stimulation from either endogenous or& g9 B( I# x+ ?( W: c$ B7 L
exogenous sources, nonpituitary gonadotropin stim-3 u& X: j7 d& a1 L$ _7 U
ulation, and rare activating mutations.3 Virilizing
5 m& n$ N. J0 Y. j+ Q) jcongenital adrenal hyperplasia producing excessive$ i+ \' t8 s! t6 w6 U+ `
adrenal androgens is a common cause of precocious
) a0 Y- ]! X9 H9 }% [8 i1 bpuberty in boys.3,4% V9 s0 k( b* v6 [6 {/ U
The most common form of congenital adrenal
( i. Y8 o+ U/ V: dhyperplasia is the 21-hydroxylase enzyme deficiency.
  U8 `; g: `1 y: Y( IThe 11-β hydroxylase deficiency may also result in1 Z) y' M; l0 o& N/ Z9 l8 }9 f& o
excessive adrenal androgen production, and rarely,8 D) L8 F" Y% ]0 F- J1 Y
an adrenal tumor may also cause adrenal androgen
: Z3 i* V  x# R! ~# Y# nexcess.1,3
) l: v; \" A9 ]  @3 ?at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& B6 p' M6 k  \6 e/ \
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007. L9 G4 ~3 Q0 h6 h. B
A unique entity of male-limited gonadotropin-9 [( _" \; _. N2 F, j
independent precocious puberty, which is also known
  B& w1 t/ D7 Y* O8 F* S9 w0 b) vas testotoxicosis, may cause precocious puberty at a& w& Y+ D( R& O) B2 {  T
very young age. The physical findings in these boys5 `0 ^$ ?5 W8 U  i4 k
with this disorder are full pubertal development,8 J) m  c. e4 [3 |
including bilateral testicular growth, similar to boys
+ r: E! @2 M: ^9 Jwith CPP. The gonadotropin levels in this disorder
: z/ @2 F; ]( @; g- v! jare suppressed to prepubertal levels and do not show
8 ^, f, P* m- u: }1 qpubertal response of gonadotropin after gonadotropin-
' s0 U( c+ m/ p: `- H5 \# D5 Vreleasing hormone stimulation. This is a sex-linked) O8 ^- J! w1 ^
autosomal dominant disorder that affects only6 b( i$ |  O8 p/ K( ~  v  E5 g6 B
males; therefore, other male members of the family! R- H* q$ A* C- |: u
may have similar precocious puberty.3
+ Y* R' ?3 G; u+ r4 x: AIn our patient, physical examination was incon-
4 Q, v# n9 t) z$ w9 Fsistent with true precocious puberty since his testi-
# T: O0 w+ s9 U3 Z4 bcles were prepubertal in size. However, testotoxicosis
5 K2 j. w5 F- pwas in the differential diagnosis because his father( X$ e6 A* T2 p5 c) `& W& n: U5 V0 }
started puberty somewhat early, and occasionally,+ ?) k% m. R( O+ W6 @
testicular enlargement is not that evident in the" {7 v% V1 S. `: V- ]* \4 V* w; ~. D
beginning of this process.1 In the absence of a neg-
. x2 ^+ E/ ^$ J$ }: ~9 Z' Oative initial history of androgen exposure, our
2 g6 X# j4 w( N. P  V6 `4 _  Tbiggest concern was virilizing adrenal hyperplasia,
. P2 y' H7 e1 W; Geither 21-hydroxylase deficiency or 11-β hydroxylase3 c& ~. h3 f$ y/ J* K* m8 \
deficiency. Those diagnoses were excluded by find-
1 m; ]6 S( U# u  b+ C0 o" c$ Ming the normal level of adrenal steroids.8 O3 ?" N. m' B" ^! F2 \
The diagnosis of exogenous androgens was strongly
: j% W  @' P$ a% V& v( l. O1 Ysuspected in a follow-up visit after 4 months because* d1 h! S6 P" b2 H- g& J* _
the physical examination revealed the complete disap-
: u7 z8 |* ^, A" T1 Xpearance of pubic hair, normal growth velocity, and! B  Y+ m4 M6 T% L2 l
decreased erections. The father admitted using a testos-
2 P) ?& F8 `, _: `terone gel, which he concealed at first visit. He was
9 [! I+ A; j& K; N5 j; E0 susing it rather frequently, twice a day. The Physicians’% N  _$ y+ k: h) {0 e" V
Desk Reference, or package insert of this product, gel or
2 P4 n1 u3 Q! w2 H4 o5 Tcream, cautions about dermal testosterone transfer to
* t! b5 E, L6 {) @& ^: xunprotected females through direct skin exposure.
4 x1 t( e% C; {- o2 qSerum testosterone level was found to be 2 times the
! j# \) l% ?% ebaseline value in those females who were exposed to
  w1 k% l6 g6 z* A5 `# p& Weven 15 minutes of direct skin contact with their male
1 h7 I1 _$ D4 k+ U1 c0 npartners.6 However, when a shirt covered the applica-) Z+ g$ H5 s. s5 d/ Y" H. q  U7 q
tion site, this testosterone transfer was prevented.0 l5 A0 a/ e( q* i7 R1 y& D
Our patient’s testosterone level was 60 ng/mL,' G+ B$ _( C; {
which was clearly high. Some studies suggest that
$ M3 o7 e9 r" R! mdermal conversion of testosterone to dihydrotestos-. d* |" B9 Z. r, b, P
terone, which is a more potent metabolite, is more
9 o. `& x8 p! B0 l3 Vactive in young children exposed to testosterone
/ c2 U  |6 H! k: w, X% wexogenously7; however, we did not measure a dihy-6 `( `. W/ e' y: M, \+ `
drotestosterone level in our patient. In addition to* P% N# g6 ^1 m+ ?. N/ K% Z
virilization, exposure to exogenous testosterone in3 s9 g; n- c9 G" a  F
children results in an increase in growth velocity and$ n# l! Y/ `$ F5 q# \& }% |
advanced bone age, as seen in our patient.
0 R2 N7 H( `( h" {The long-term effect of androgen exposure during
$ X( |, @3 e+ D. h. oearly childhood on pubertal development and final
5 X% K5 f9 V$ e" s7 Eadult height are not fully known and always remain/ ?% T7 @( B9 M- P' W6 M2 ~( w
a concern. Children treated with short-term testos-
6 Z9 m+ F) d2 ^$ Zterone injection or topical androgen may exhibit some1 o0 A; }3 }; l: s0 ~1 P- u% X
acceleration of the skeletal maturation; however, after
" g, f7 U* ~; s' \% `: Ccessation of treatment, the rate of bone maturation
: z& ^9 K% B" l  y6 p/ qdecelerates and gradually returns to normal.8,9& ]. D! s0 G5 G
There are conflicting reports and controversy! {! p3 A. b% A: |! o) |  ]9 y  U
over the effect of early androgen exposure on adult( a, l% ~; I* T$ c; ^, |
penile length.10,11 Some reports suggest subnormal3 Q; M* k$ }, ?' k+ p8 p9 r
adult penile length, apparently because of downreg-; I1 W2 V- {2 O$ }/ e- F; u
ulation of androgen receptor number.10,12 However,
8 `$ K+ U- U0 \; q& [# D' ySutherland et al13 did not find a correlation between
- E5 W# P; a$ U4 D! z& \childhood testosterone exposure and reduced adult$ e( f/ F5 q  K4 ]; A
penile length in clinical studies./ G. Y+ M9 a3 @! w- J
Nonetheless, we do not believe our patient is0 j, s) l$ D. N6 L% j
going to experience any of the untoward effects from" j0 l9 m: B! Z: L% P4 F6 m8 E  i
testosterone exposure as mentioned earlier because/ N. L0 _5 f" C% }* I9 j; L9 b
the exposure was not for a prolonged period of time.7 K1 h( l1 X4 q4 K' _% I' k) L
Although the bone age was advanced at the time of) g/ A) D9 Q) ]* Y. J* w
diagnosis, the child had a normal growth velocity at9 F. r* N# ]2 ~% Q+ X) n" i
the follow-up visit. It is hoped that his final adult
2 E" ~) a# o" ~height will not be affected.
9 u, f+ A9 J! KAlthough rarely reported, the widespread avail-
7 d6 ]+ A; k9 l8 \: |ability of androgen products in our society may
% `0 p/ k3 A" G$ h) [$ f6 Dindeed cause more virilization in male or female
0 V! H$ t4 d' i6 hchildren than one would realize. Exposure to andro-
# {7 G8 x- A- X( i. jgen products must be considered and specific ques-( D% Q9 I( Y/ {& g' h8 G
tioning about the use of a testosterone product or* f6 X8 G( x0 x9 j* U
gel should be asked of the family members during& r+ ^0 d$ ~, v" `1 V! t4 g  X1 {
the evaluation of any children who present with vir-' E# x* l+ `% O5 D' m" ~. _3 |
ilization or peripheral precocious puberty. The diag-
3 v- S: T5 {  X$ Z( s( G. hnosis can be established by just a few tests and by
$ G+ d* l$ l- h/ p1 z- x$ T! C1 Uappropriate history. The inability to obtain such a
' m: [$ R/ c9 q4 s+ f; Q5 O3 D5 h: D. Zhistory, or failure to ask the specific questions, may
4 R: O: u! ~  m$ ]( Q+ X1 V3 `/ v4 v- mresult in extensive, unnecessary, and expensive
: m& L3 C0 `6 Z: C6 Jinvestigation. The primary care physician should be
3 @" ]3 X9 _" K4 |& A8 vaware of this fact, because most of these children
1 y6 B: y* v% S# w" t# t! v2 _may initially present in their practice. The Physicians’2 a3 o& v& k9 r. g) m  m' c
Desk Reference and package insert should also put a
- R% W, m- ~4 z. i# p+ e; v' Zwarning about the virilizing effect on a male or% T( X( a& k6 b8 P
female child who might come in contact with some-/ Y- x/ @, n* Y
one using any of these products.
4 i. u. O' k+ \References9 G3 a0 w9 v+ [& n4 j
1. Styne DM. The testes: disorder of sexual differentiation
; S9 M3 b- d: c2 {" `and puberty in the male. In: Sperling MA, ed. Pediatric
( }4 Y" N) D- S( u9 v6 h  bEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;  p" ~/ @% ?! j- `
2002: 565-628.: w; I& y7 t$ G) {
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
  z; ^% f) C( Dpuberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

- ~  ]6 r; y# H5 v8 v精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!
發表於 2025-3-8 22:04:50 | 顯示全部樓層
絕對的好貼!謝謝啊!逐字逐圖地看完這個帖子以後,我的心久久不能平靜,感恩啊!
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