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Sexual Precocity in a 16-Month-Old3 d4 N7 e4 T$ M
Boy Induced by Indirect Topical7 u( a  i3 g9 U) L% O, B2 A8 d& s
Exposure to Testosterone
. i  h7 e6 u  r4 m6 ~Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
! E* U* m9 X( ?. t" l0 Fand Kenneth R. Rettig, MD1
5 ]+ [$ E2 Z1 [  f3 n5 gClinical Pediatrics
2 j5 X# _0 O$ y- w# B) TVolume 46 Number 6
! l) C1 u" \% O; t" D9 MJuly 2007 540-5430 m0 Q; y) {/ {1 p8 T
© 2007 Sage Publications
! h+ {8 s  Z; z( d9 I10.1177/0009922806296651
3 w- @  a8 g$ ghttp://clp.sagepub.com# s1 e; Y; k8 H2 L- t+ O1 J1 Y( X: P
hosted at* Q8 i9 C8 i2 h: b/ k
http://online.sagepub.com
+ {6 F/ }& c0 H6 U2 A% I) f) DPrecocious puberty in boys, central or peripheral,
4 V0 }' N3 n7 N$ f+ Dis a significant concern for physicians. Central
8 r, }2 H+ K# G' H$ tprecocious puberty (CPP), which is mediated
" o( h  j" o' Q& Y3 xthrough the hypothalamic pituitary gonadal axis, has: w* L9 H6 c! w* x$ u
a higher incidence of organic central nervous system
/ f3 [; b) x& v9 u# ^- Alesions in boys.1,2 Virilization in boys, as manifested, C* D4 i4 U2 B0 s8 S
by enlargement of the penis, development of pubic
) p+ y! X6 m5 t6 O4 rhair, and facial acne without enlargement of testi-# r' q! k/ |: i% v
cles, suggests peripheral or pseudopuberty.1-3 We
% |5 @8 x; x$ q  q. I( Ureport a 16-month-old boy who presented with the3 A) R$ I; n7 r& e# ~3 J
enlargement of the phallus and pubic hair develop-
+ j1 l2 T! X$ p( ^1 x2 g8 S8 ^ment without testicular enlargement, which was due3 n+ m; X) R4 s, x9 x% C
to the unintentional exposure to androgen gel used by) J" I; _/ ^2 W( O4 z: F( U9 x
the father. The family initially concealed this infor-; |/ H- {$ W# }
mation, resulting in an extensive work-up for this- \; A) z8 X3 \+ s- Y
child. Given the widespread and easy availability of
% C& h4 n. }. j2 S/ v- @# c1 itestosterone gel and cream, we believe this is proba-
, ~( n! G3 m# `& O6 V( z: zbly more common than the rare case report in the- v9 h. \  T7 m) j! k
literature.4: ?6 C6 K- v9 a9 G- q
Patient Report8 z* x; H; b3 h/ f2 G3 [
A 16-month-old white child was referred to the" G/ Y+ H% y% X; ^% x; Y
endocrine clinic by his pediatrician with the concern
4 J+ e8 {+ X! `of early sexual development. His mother noticed2 I  y. u7 v: ^+ v) X( d% g
light colored pubic hair development when he was
4 O9 H+ }9 O3 l7 V( jFrom the 1Division of Pediatric Endocrinology, 2University of
; _- m6 y: ]4 Z7 bSouth Alabama Medical Center, Mobile, Alabama.
: `& l7 x, ~1 J* }" PAddress correspondence to: Samar K. Bhowmick, MD, FACE,
4 W, h3 }: m2 ~) u) H2 RProfessor of Pediatrics, University of South Alabama, College of" G" e/ c5 M. B9 r
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
$ X3 y5 `. @6 ]0 }3 g8 T9 se-mail: [email protected].) Q1 ^* X( y3 X3 c
about 6 to 7 months old, which progressively became
' b) [( A1 _) W' ydarker. She was also concerned about the enlarge-, ]6 t  K+ [- V' E; P% i1 [
ment of his penis and frequent erections. The child) W; R; Y) d* a! |" U" A& ~, [
was the product of a full-term normal delivery, with* V) {& u$ Q4 L) N9 z% M
a birth weight of 7 lb 14 oz, and birth length of( C4 B1 H* I% ~, Y# @; U  S
20 inches. He was breast-fed throughout the first year
4 w9 W/ M& `7 `8 N# Mof life and was still receiving breast milk along with4 j1 r$ \5 ?* l8 X5 M
solid food. He had no hospitalizations or surgery,
9 x& y" `% I' Z5 b  ]( Y% a4 Mand his psychosocial and psychomotor development  d7 |. M4 j- g) |
was age appropriate.
) w( J; p  w8 E& tThe family history was remarkable for the father,+ v8 o/ S$ W) s
who was diagnosed with hypothyroidism at age 16,! R) s8 w) d% H* W
which was treated with thyroxine. The father’s6 Y, E  A# P3 B
height was 6 feet, and he went through a somewhat
! y* Y/ c1 Z6 i1 ]+ p+ t  }early puberty and had stopped growing by age 14.
( r: E8 U+ J) Q) K4 BThe father denied taking any other medication. The
9 c- J: n+ c* z" ?2 Wchild’s mother was in good health. Her menarche5 t8 \. w4 A5 O* `3 h; E) Q+ p8 {
was at 11 years of age, and her height was at 5 feet. w' h: N: K3 o$ K$ R$ S( o3 X7 I
5 inches. There was no other family history of pre-5 _/ x0 }$ L6 {1 A$ B( r6 u8 q
cocious sexual development in the first-degree rela-: J( H/ p. r, C. t" O9 \0 S+ I3 U  ~
tives. There were no siblings.4 q& c- j! [: ^$ T
Physical Examination% ~8 Y, i/ P) ~9 m+ [7 ^% p
The physical examination revealed a very active,$ W) ^5 Q) M$ I! ?+ d3 J
playful, and healthy boy. The vital signs documented. o9 \. K+ ~/ t% u2 g" b, ~
a blood pressure of 85/50 mm Hg, his length was
& T# w1 q# \! c& c+ J9 l90 cm (>97th percentile), and his weight was 14.4 kg  a. Q0 y! T1 h2 d  M& i
(also >97th percentile). The observed yearly growth$ m  `) q6 V, D4 S
velocity was 30 cm (12 inches). The examination of# d" Z' K6 z- N
the neck revealed no thyroid enlargement.
. G) A2 d7 {5 i6 f$ n4 y0 s2 UThe genitourinary examination was remarkable for
: M3 n9 w# Z- \/ O% ienlargement of the penis, with a stretched length of
6 W3 e# u5 e8 Z1 x8 cm and a width of 2 cm. The glans penis was very well
: L2 C! j+ F- k, z( Q( V7 s  E# d  Xdeveloped. The pubic hair was Tanner II, mostly around
" m# V  W7 f4 n540- @+ K  j/ X5 P; p$ f
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
% s7 t& y. s2 \  s6 @0 j, Kthe base of the phallus and was dark and curled. The
( \4 _' w8 i4 q6 Wtesticular volume was prepubertal at 2 mL each.- s7 ]( `$ @- v* m! P* C
The skin was moist and smooth and somewhat
6 Z8 T* x" w5 x  C& Z* E. [6 [& xoily. No axillary hair was noted. There were no
1 q" T3 j5 z9 v6 y. ]% Gabnormal skin pigmentations or café-au-lait spots.- f  s# Y% R+ C
Neurologic evaluation showed deep tendon reflex 2+
4 N6 H0 Y4 L% p* {bilateral and symmetrical. There was no suggestion
/ d8 l4 z# x8 V* v" D' Aof papilledema.
# B9 a0 A! m( y7 _( mLaboratory Evaluation
/ Q, U! K5 x; W) t! {( CThe bone age was consistent with 28 months by% N5 w- v4 b; P% p7 G( n
using the standard of Greulich and Pyle at a chrono-) B* `7 w( V9 b
logic age of 16 months (advanced).5 Chromosomal
8 m0 \9 H- \' c3 z( P  Skaryotype was 46XY. The thyroid function test
" S+ o; d: M6 X& V5 @- `showed a free T4 of 1.69 ng/dL, and thyroid stimu-
: f0 o2 k/ F$ e; ]) H0 K* Y$ O* ylating hormone level was 1.3 µIU/mL (both normal).
! v; s( ^3 I3 K, e% V# YThe concentrations of serum electrolytes, blood# a8 l$ [! p- `& R
urea nitrogen, creatinine, and calcium all were) m2 h# c6 t/ T. \' ~4 G- J
within normal range for his age. The concentration
2 t) l( t" f. @/ yof serum 17-hydroxyprogesterone was 16 ng/dL
8 B+ Y. a, R  f8 L$ H, W(normal, 3 to 90 ng/dL), androstenedione was 20$ y. T2 g+ e: F# ?3 ^5 R  v
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
; N9 q# A9 [6 I' s! ~" Cterone was 38 ng/dL (normal, 50 to 760 ng/dL),- B8 Z1 L. ?0 G7 z6 o
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
" T! r8 ~1 \& k- i" l. H- c0 f  I49ng/dL), 11-desoxycortisol (specific compound S)
# ?# M2 J8 O- L5 p( g: h. C1 w- O' ~was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
3 t; n1 w7 h' V2 v& }* btisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total" D) o$ I* x  ]
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),$ V4 _5 E, J8 f. `% d
and β-human chorionic gonadotropin was less than; Y5 q/ \5 K7 V) _- V2 T: a
5 mIU/mL (normal <5 mIU/mL). Serum follicular1 }, R5 A% F  R1 H0 v5 J
stimulating hormone and leuteinizing hormone8 h3 l6 q! a5 v8 J
concentrations were less than 0.05 mIU/mL+ ?, e3 U) F% A, N
(prepubertal).# u# k0 q2 ~' W
The parents were notified about the laboratory! ?% p4 A9 A' v+ U/ \
results and were informed that all of the tests were
( u# c" e  e# E/ D0 Y0 C/ ^) W: ~normal except the testosterone level was high. The
7 j2 R+ ]/ F, d) o: Gfollow-up visit was arranged within a few weeks to
- \- F3 g' {5 k; ]; U8 Xobtain testicular and abdominal sonograms; how-
. |$ u; w3 U$ U2 x( j& U2 Iever, the family did not return for 4 months.
5 `6 `7 G/ I9 \  D2 A2 @Physical examination at this time revealed that the
3 k3 A5 p; d$ a% Z5 e* ^+ P' J' tchild had grown 2.5 cm in 4 months and had gained: W) F$ s% r/ e; M' w: L, J
2 kg of weight. Physical examination remained
5 ]# D7 E8 ]( [2 v3 J* @; N4 A. aunchanged. Surprisingly, the pubic hair almost com-
- J, L8 I) o2 S# |pletely disappeared except for a few vellous hairs at& S+ P% E9 `; ^' J: L( X
the base of the phallus. Testicular volume was still 2
, R: @- ~! C. o  X% W& i, QmL, and the size of the penis remained unchanged.- z" i( R" |/ {% N& _/ v
The mother also said that the boy was no longer hav-
4 P& x+ p, a9 Fing frequent erections.3 Q9 i8 C4 ^  G" h$ a
Both parents were again questioned about use of
" o3 P+ j( S+ a, w; P+ Z+ [any ointment/creams that they may have applied to8 A% @9 O! j. u. E* Z; q* J
the child’s skin. This time the father admitted the% q7 [3 u. W" {, t- L$ E
Topical Testosterone Exposure / Bhowmick et al 541
# k" S- W( {; V: E- ^) _5 Cuse of testosterone gel twice daily that he was apply-, m0 Z8 k) h. L; j  v4 f: s" {' W
ing over his own shoulders, chest, and back area for( K1 @% o4 M' u+ M9 m. I
a year. The father also revealed he was embarrassed
7 c# L8 x# `& J3 A& N: {8 U: {to disclose that he was using a testosterone gel pre-+ A/ f/ I- N. [: {) b: R
scribed by his family physician for decreased libido
% r* s) J% i# d2 M& nsecondary to depression.
9 e: _. [: k9 U& OThe child slept in the same bed with parents.( H2 b$ t. s2 b
The father would hug the baby and hold him on his
7 I9 c6 W- Z7 E6 E1 @8 O& }# y$ q1 Cchest for a considerable period of time, causing sig-
: q1 `' G  |+ g; ^, {nificant bare skin contact between baby and father.9 @; i& t3 Z* [- l+ q3 u* V' n
The father also admitted that after the phone call,
2 f6 `- h* o, J( D' h, g! Qwhen he learned the testosterone level in the baby
$ b2 v* K5 H, w1 M4 p- T3 {/ p( Twas high, he then read the product information% e% j4 W  `4 U2 ^2 x; V, r, G
packet and concluded that it was most likely the rea-
0 l$ I8 c: Z' }1 T" v$ M6 D( Y! \son for the child’s virilization. At that time, they( `, ^4 P% x* t7 l
decided to put the baby in a separate bed, and the# }. f2 Q) m6 Q; [- t
father was not hugging him with bare skin and had
8 j( f3 r8 Q! X6 q7 E5 ]been using protective clothing. A repeat testosterone: S' e; D* s/ I9 d+ f6 {- G  g- i! c
test was ordered, but the family did not go to the! Z3 `9 a- J# q, V. \! J6 C" g
laboratory to obtain the test.* I& R# Z4 |6 p
Discussion
8 S! `* W2 ?# O5 y- y- N6 jPrecocious puberty in boys is defined as secondary( u/ N$ z) q5 d; X1 \* ]
sexual development before 9 years of age.1,4
  H( a, P' T, V. gPrecocious puberty is termed as central (true) when
: M* Q! y/ L( r5 p9 w7 Lit is caused by the premature activation of hypo-+ I  ]" ]0 j0 D! `
thalamic pituitary gonadal axis. CPP is more com-" Q" Z: l+ D5 T$ s' `  f5 I) T9 t
mon in girls than in boys.1,3 Most boys with CPP# h. o- z# @( o' o+ F: o
may have a central nervous system lesion that is$ Z# c. o4 U, ]5 m9 d. Z
responsible for the early activation of the hypothal-
5 G7 o  E) g/ U+ @amic pituitary gonadal axis.1-3 Thus, greater empha-! u+ f# q4 D$ g; |; t" R" F
sis has been given to neuroradiologic imaging in
8 k* K: o/ O# b% k0 }$ iboys with precocious puberty. In addition to viril-
9 E, \3 v8 B: i1 xization, the clinical hallmark of CPP is the symmet-" O  p0 ]+ F  D
rical testicular growth secondary to stimulation by0 G* t: h, P9 f, _
gonadotropins.1,3
6 m/ x0 ]0 m/ ^- C6 cGonadotropin-independent peripheral preco-3 W2 t7 R1 M+ S2 H, l
cious puberty in boys also results from inappropriate
0 C/ S. `/ e' f9 o! Y: I  x0 Nandrogenic stimulation from either endogenous or
4 S5 d& v! r7 qexogenous sources, nonpituitary gonadotropin stim-
  T* @: ]/ b& H) u1 E; Rulation, and rare activating mutations.3 Virilizing$ J7 s# P4 z- I) h- a" t. J, L8 ]
congenital adrenal hyperplasia producing excessive
4 P8 C4 U6 m* \7 h% Q7 L% ~adrenal androgens is a common cause of precocious0 h7 v& |8 |/ A' Y: G
puberty in boys.3,4  b7 S4 E! y+ q0 V1 ]
The most common form of congenital adrenal3 a- Q6 p1 s$ p" b4 q8 r  e
hyperplasia is the 21-hydroxylase enzyme deficiency.
9 r/ u! I0 n+ q9 PThe 11-β hydroxylase deficiency may also result in, k+ E2 s9 q( `& _
excessive adrenal androgen production, and rarely,/ m* L4 h" _, C" y( l
an adrenal tumor may also cause adrenal androgen
6 e* B6 F3 f( t1 f: m/ Xexcess.1,3
$ W5 f6 ~& ]7 Mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; r; Y! s& O- j
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
5 L! ?) ?$ u& f1 {A unique entity of male-limited gonadotropin-% E/ d  Y* z5 |1 n6 ^% K  v+ b
independent precocious puberty, which is also known0 D. C/ c* E* U5 M4 D
as testotoxicosis, may cause precocious puberty at a
% C( X' h: ~" M5 P7 b4 overy young age. The physical findings in these boys
- b; F9 `& q2 {" X7 Z; s) v& zwith this disorder are full pubertal development,3 x& N1 I3 m" m" v) q
including bilateral testicular growth, similar to boys& v( s+ ^% y& J$ Y) m6 a! {5 `
with CPP. The gonadotropin levels in this disorder
) Z1 [6 E! b: L+ A& i3 L6 ~are suppressed to prepubertal levels and do not show$ l! [2 `' x3 V( L- B. e
pubertal response of gonadotropin after gonadotropin-
& ^; h, L- z3 [" xreleasing hormone stimulation. This is a sex-linked+ I0 U% n: D3 ~
autosomal dominant disorder that affects only
) o0 ?% G" f4 j* H: b. a  T+ hmales; therefore, other male members of the family
* R( r% X* ^& d; {1 }% ]7 imay have similar precocious puberty.3
# M: z$ I4 w9 v. A& L9 L6 C' T0 K8 KIn our patient, physical examination was incon-
& B% z$ M$ A5 M0 @" ~sistent with true precocious puberty since his testi-
# ?: [- O7 u; N8 p0 Gcles were prepubertal in size. However, testotoxicosis+ U( p8 x9 D: U; ~3 k
was in the differential diagnosis because his father" o# x( r* v1 P1 ]& r
started puberty somewhat early, and occasionally,. K/ ]1 B3 {  c+ A& G& J4 C
testicular enlargement is not that evident in the
+ _0 P4 X4 q/ S0 G4 S. `/ [  x% u6 {beginning of this process.1 In the absence of a neg-
* w" c( g: M: W2 ?' ]2 jative initial history of androgen exposure, our
2 X" u. q; g+ c1 E2 I# ]biggest concern was virilizing adrenal hyperplasia,
* H, _6 o2 F8 o4 X, P7 W4 keither 21-hydroxylase deficiency or 11-β hydroxylase
! J' w, _/ d1 I# I- \! [deficiency. Those diagnoses were excluded by find-0 @1 V; [1 D& y9 C$ U
ing the normal level of adrenal steroids.
% ?0 B0 {# E2 gThe diagnosis of exogenous androgens was strongly( E  e" V  d  K! t9 G# A, O
suspected in a follow-up visit after 4 months because
% O- q$ C) F. Q1 zthe physical examination revealed the complete disap-) t) P! j: b* |( B& e2 }
pearance of pubic hair, normal growth velocity, and- Z0 n; _% `) L4 u& B
decreased erections. The father admitted using a testos-$ R; l# Q  Q8 u9 p$ W3 ~! ?) X
terone gel, which he concealed at first visit. He was
, B6 y. K2 }6 B7 d# q" G4 ^' u, dusing it rather frequently, twice a day. The Physicians’/ m$ u+ w% q: B- k
Desk Reference, or package insert of this product, gel or
  Z5 D( u, L8 p5 n  f; bcream, cautions about dermal testosterone transfer to
! t- N: E3 [% B4 ]: Aunprotected females through direct skin exposure.6 _$ q2 P) c1 q1 w, `
Serum testosterone level was found to be 2 times the" T& G3 y! u5 q. @  j- ~; [
baseline value in those females who were exposed to, _1 J/ |( V0 [( e" J
even 15 minutes of direct skin contact with their male
$ H3 }0 S8 {6 p: Q* U# Y5 qpartners.6 However, when a shirt covered the applica-4 W1 B/ k- n4 g
tion site, this testosterone transfer was prevented.
% g1 B2 A/ Y" I8 X3 bOur patient’s testosterone level was 60 ng/mL,
" K" C& k$ i# o0 M4 E  P1 w& L: H1 @which was clearly high. Some studies suggest that
: h. t4 R4 j5 v* }! ~dermal conversion of testosterone to dihydrotestos-2 }8 r' p! l' \9 l& f4 L
terone, which is a more potent metabolite, is more- Q! K$ Z  m1 b3 V$ l/ s& M1 K
active in young children exposed to testosterone
( t) {9 i" A/ Q  j0 \exogenously7; however, we did not measure a dihy-2 M: A3 `% C2 m: R  O1 N( X( t
drotestosterone level in our patient. In addition to3 d5 c- c* Q" A
virilization, exposure to exogenous testosterone in
: h- P/ f. x. S  w2 X  o( Ochildren results in an increase in growth velocity and
1 u; A( W. S8 {, kadvanced bone age, as seen in our patient.( i4 p" _  M+ m: _4 P* D6 X2 Z
The long-term effect of androgen exposure during9 f; ?" _. d2 [2 \7 o
early childhood on pubertal development and final! G6 j* W& o9 ?% O% W
adult height are not fully known and always remain
8 X* X, u% X2 N. w7 P# fa concern. Children treated with short-term testos-
0 ?3 i* v" e! sterone injection or topical androgen may exhibit some
& j; R* @- b, x/ U5 e$ Xacceleration of the skeletal maturation; however, after
2 e4 {5 V; r4 B* W! z0 R- Mcessation of treatment, the rate of bone maturation
/ J: o2 q% ?" S* T4 H% f* sdecelerates and gradually returns to normal.8,9  q' D7 L: e7 D4 `- z$ V3 ~
There are conflicting reports and controversy4 f5 r0 d  R4 l) Q' Q) T9 F, b
over the effect of early androgen exposure on adult1 j8 n. ]: v& J! X
penile length.10,11 Some reports suggest subnormal8 ], W2 h: t) S
adult penile length, apparently because of downreg-, E5 i7 W7 x. h2 Q/ r, P
ulation of androgen receptor number.10,12 However,
3 K# w- m$ d9 e5 }: E. dSutherland et al13 did not find a correlation between8 n! d* }8 [; V
childhood testosterone exposure and reduced adult' C4 ^; x8 e1 a% R5 l
penile length in clinical studies.8 _5 z9 I: w% v, O$ v
Nonetheless, we do not believe our patient is
0 l4 b2 ^7 J: y" l& mgoing to experience any of the untoward effects from6 c& G( o# r8 O$ J. m
testosterone exposure as mentioned earlier because
+ R% H( h# M# Q& Y% jthe exposure was not for a prolonged period of time.
8 Q2 J/ N" ~+ {7 _Although the bone age was advanced at the time of2 l- w. `! Z0 f: R2 K6 m) p0 ?
diagnosis, the child had a normal growth velocity at5 }: p( F3 p" y  \7 [
the follow-up visit. It is hoped that his final adult
" H$ G1 F$ r6 H) qheight will not be affected.1 ?1 B7 h- t3 D9 K0 F
Although rarely reported, the widespread avail-
  A4 p5 U: n& R1 S( t& B* K3 Oability of androgen products in our society may
/ Y& R6 y4 `4 L. @indeed cause more virilization in male or female: j7 }& B. }( J$ g) @- [
children than one would realize. Exposure to andro-: w3 O6 U* {3 K9 b2 }
gen products must be considered and specific ques-" |, ?. I+ ]  y( {' V: G
tioning about the use of a testosterone product or, U8 w7 n. \& h4 x+ T
gel should be asked of the family members during: [- ]- `: r: Q# J% w
the evaluation of any children who present with vir-8 F! [1 N: C3 C9 \2 G& c
ilization or peripheral precocious puberty. The diag-1 u; n. F6 s" D+ b: g6 k" [
nosis can be established by just a few tests and by
6 \1 R6 u, f+ D+ T2 ~appropriate history. The inability to obtain such a3 F" v' [' @5 T. g
history, or failure to ask the specific questions, may% m7 J0 I+ c8 T( a3 x) }4 w2 u
result in extensive, unnecessary, and expensive6 f& o9 y1 c8 s$ G9 c/ P
investigation. The primary care physician should be
! }6 q  }; D- y! ^- t2 j( raware of this fact, because most of these children4 L' k6 v2 d0 h+ Y9 y' f& t
may initially present in their practice. The Physicians’
" x/ G& O7 P0 T* I, M; E' s& _9 _Desk Reference and package insert should also put a1 A5 R# N  m  K) \6 T2 c
warning about the virilizing effect on a male or
+ Z5 v2 h8 [- a- z5 |; O$ lfemale child who might come in contact with some-
$ s% j3 @3 Z7 ~, H: E6 R+ Fone using any of these products.
) K5 {+ N9 Z1 N* w/ Z, p/ uReferences  l: o5 b5 @+ T. O( _
1. Styne DM. The testes: disorder of sexual differentiation% i4 d4 Z$ u4 H
and puberty in the male. In: Sperling MA, ed. Pediatric
$ B6 @( X: N: E' e+ W% P! REndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;. [7 y$ m. \( \) t- Z
2002: 565-628.
6 @4 l. H+ \5 ?* u% x( Z2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious( u' q' v8 ~! B5 W2 D5 y: w) R
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
# ^* P7 L* I3 f8 j9 QBoy Induced by Indirect Topical
  D. L7 \" N$ [( d, M5 CExposure to Testosterone
% `6 k. b* X4 Q+ U: h" j- [Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2" e, r1 l* y) [3 P4 E* ~& Y  ^
and Kenneth R. Rettig, MD1+ n1 J/ F5 v8 [' W
Clinical Pediatrics
8 `0 D" p8 t' h/ `9 F$ ?# YVolume 46 Number 6  A/ X8 r0 p1 x6 r7 |
July 2007 540-5435 a; n! `2 c8 ?- g# ]( p  v
© 2007 Sage Publications
% J. z8 ?; z  b10.1177/0009922806296651
0 \& L) l' D- T# w) S$ Qhttp://clp.sagepub.com
) f$ a: t# L5 T! ]# c+ B0 Y! _hosted at
' T" |; k+ |7 H. j2 b5 g4 Khttp://online.sagepub.com1 U$ B; h+ p9 S& A' T& E
Precocious puberty in boys, central or peripheral,
5 t& M  N( w8 O. w5 `% Wis a significant concern for physicians. Central( ~+ t, t5 A2 Y7 H% G" \9 `/ x. M
precocious puberty (CPP), which is mediated
- }7 V* H( C! B2 Jthrough the hypothalamic pituitary gonadal axis, has
  ?" S% w# X! ~1 Pa higher incidence of organic central nervous system2 R+ [* y: A2 E
lesions in boys.1,2 Virilization in boys, as manifested
+ \( X' S) H7 @* |) t! V/ dby enlargement of the penis, development of pubic
/ ?8 a' k# k  G6 ^7 M( e9 Dhair, and facial acne without enlargement of testi-
% p& u% I( v9 f- M3 o, ~cles, suggests peripheral or pseudopuberty.1-3 We2 @0 _6 d& x4 X- `0 G% [2 x" h
report a 16-month-old boy who presented with the( X. R# b9 P" v0 z
enlargement of the phallus and pubic hair develop-
, F3 t8 f4 x" o# n$ x! Qment without testicular enlargement, which was due
9 R1 l3 U; _1 M6 R9 ]# zto the unintentional exposure to androgen gel used by
, N) q7 C4 F9 G9 ?; Y: E; ^; k& X+ xthe father. The family initially concealed this infor-
8 Z/ D- G$ y7 I# A  lmation, resulting in an extensive work-up for this
& P+ V  c& v$ }4 p. @& achild. Given the widespread and easy availability of
3 v0 a+ F% j  P+ |testosterone gel and cream, we believe this is proba-  c/ W  z3 X& S" r( W) g
bly more common than the rare case report in the9 U, }: j2 ]) b$ c
literature.4! W5 W8 {" j# @* [
Patient Report
) k' N8 U$ ]; Z3 U9 h' o/ J" RA 16-month-old white child was referred to the4 F+ L! u# J9 Q
endocrine clinic by his pediatrician with the concern0 o( \7 G% ^# i# Z
of early sexual development. His mother noticed5 [% p9 S9 x  @7 ]- z2 W- I
light colored pubic hair development when he was
' x/ a. S6 m% O, x* s7 @From the 1Division of Pediatric Endocrinology, 2University of
0 Z) e! t$ d7 n. Y* |4 |South Alabama Medical Center, Mobile, Alabama.2 x: R. P! [0 l; K8 B( G
Address correspondence to: Samar K. Bhowmick, MD, FACE,
) x; y9 E' A+ u. L5 B8 V% }2 a$ l1 uProfessor of Pediatrics, University of South Alabama, College of
, K2 @! a. x4 p) FMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;. ~# w0 D# s! x, P" A% f
e-mail: [email protected].
& d8 }/ s  r. V# m8 Jabout 6 to 7 months old, which progressively became
0 ?4 P: I7 Q1 idarker. She was also concerned about the enlarge-" y: M; ^7 ^: j3 j8 \7 ^! O; g
ment of his penis and frequent erections. The child
- L+ o2 C7 N+ K5 J7 m5 E$ r- Lwas the product of a full-term normal delivery, with- @- U( }  b$ b' v% p1 b; U
a birth weight of 7 lb 14 oz, and birth length of+ O9 b- [/ x% q1 `0 c# g
20 inches. He was breast-fed throughout the first year* g- ]' p/ g! u) i+ c5 i9 {! m2 g  J
of life and was still receiving breast milk along with
% _( M' G5 ~5 Gsolid food. He had no hospitalizations or surgery,
& t& r8 H- n* E0 P2 oand his psychosocial and psychomotor development
+ _' [, q# K/ u' p4 Y  Xwas age appropriate.8 h, z4 G+ `* _; V# l3 K5 X5 Z
The family history was remarkable for the father,
7 C9 D7 m0 U" f3 twho was diagnosed with hypothyroidism at age 16,
! R1 ^: d  V: W& b9 E$ g- M/ p1 swhich was treated with thyroxine. The father’s
  p& u2 A! A% z+ J" B& x0 [height was 6 feet, and he went through a somewhat( I! j4 ]2 ?% k. P: y: q
early puberty and had stopped growing by age 14.
! D& |  R9 \0 l' ~. D1 [& NThe father denied taking any other medication. The! R8 Y- z% T1 b9 F% F5 ]7 b
child’s mother was in good health. Her menarche8 o& h! D: Y: P( m; V3 U0 W  k
was at 11 years of age, and her height was at 5 feet% w1 R' y2 \% j* s4 |( q9 F, h
5 inches. There was no other family history of pre-
: w, f* c1 Z5 @: V1 g* [cocious sexual development in the first-degree rela-8 L. g  f/ R% B: a
tives. There were no siblings.7 M& J) l6 U) U
Physical Examination
) j) z9 }7 p! r- X& F( C, nThe physical examination revealed a very active,9 X$ d5 u+ C# e! u, g
playful, and healthy boy. The vital signs documented
2 w' B/ Z( d3 G4 i5 `- t$ w5 ua blood pressure of 85/50 mm Hg, his length was
( I7 }  P2 l) y" J$ u0 r90 cm (>97th percentile), and his weight was 14.4 kg
/ Q. ]& g# d9 d  O(also >97th percentile). The observed yearly growth
; A. c: m: T) f. B) _$ mvelocity was 30 cm (12 inches). The examination of6 j& f7 f$ p1 D# x
the neck revealed no thyroid enlargement.
9 g7 g2 V  P# L! kThe genitourinary examination was remarkable for2 l3 }2 {# \' {% d; z( h' i
enlargement of the penis, with a stretched length of
+ k! S2 i* C4 w1 j8 cm and a width of 2 cm. The glans penis was very well" ]% ^+ W  |0 a* C" h' D% W
developed. The pubic hair was Tanner II, mostly around
& F, t1 k2 L" \9 H540
) j  \4 G. p' f  oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& D$ P" p1 E  h# [9 X: u% c4 [$ Sthe base of the phallus and was dark and curled. The2 D. O9 H" I' F+ x" l3 R+ E
testicular volume was prepubertal at 2 mL each.
- s+ e- J' S2 a2 p  DThe skin was moist and smooth and somewhat% l2 V7 I* u. }
oily. No axillary hair was noted. There were no9 X7 n! Y2 F4 o. V
abnormal skin pigmentations or café-au-lait spots.
+ c. S$ j6 X; FNeurologic evaluation showed deep tendon reflex 2+3 m% t+ b3 O9 b
bilateral and symmetrical. There was no suggestion
) l+ n$ |  C; N6 L4 m0 Eof papilledema.% r* ~0 q( x0 v
Laboratory Evaluation
, E$ O9 n4 f2 e* Z. {) H% }2 }The bone age was consistent with 28 months by
+ ^0 C$ Q3 R* N* ^$ L8 R! lusing the standard of Greulich and Pyle at a chrono-
: f8 F- }* n5 j' plogic age of 16 months (advanced).5 Chromosomal
1 g$ T0 E3 ?. ~0 }, P& Bkaryotype was 46XY. The thyroid function test! d2 j( `% t1 Y4 {8 D* K1 G* g
showed a free T4 of 1.69 ng/dL, and thyroid stimu-' f) k5 Q1 o  a0 l4 w
lating hormone level was 1.3 µIU/mL (both normal).
& H; Q' R' }" kThe concentrations of serum electrolytes, blood$ A7 f4 K# e0 h" p# r  J
urea nitrogen, creatinine, and calcium all were
& @9 E8 ^" n) T7 u& f1 p5 _( Hwithin normal range for his age. The concentration* u; f2 `) x+ D" @" }! Y9 F! ]
of serum 17-hydroxyprogesterone was 16 ng/dL
) H2 k) n, }1 y) w+ t) m9 S6 i(normal, 3 to 90 ng/dL), androstenedione was 20
+ d9 m) v* M$ Fng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 ?! D! M! X: I" B. Q: Tterone was 38 ng/dL (normal, 50 to 760 ng/dL),/ N# a7 G% W2 V4 {
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
' J' B6 v* e; }49ng/dL), 11-desoxycortisol (specific compound S)
, O8 w( x' `0 i9 e8 E( A% Lwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-2 L+ l6 I: O. N1 m/ }: E7 w
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
: \$ M$ Q: @$ x7 w" ntestosterone was 60 ng/dL (normal <3 to 10 ng/dL),% S9 n% n1 ?; s+ Z
and β-human chorionic gonadotropin was less than: @1 _$ t5 E8 }. a1 B
5 mIU/mL (normal <5 mIU/mL). Serum follicular3 p( K$ y$ W& k7 n( n4 _
stimulating hormone and leuteinizing hormone
9 G4 y% }# E7 f& u3 U) K; tconcentrations were less than 0.05 mIU/mL3 Y0 X& [4 @- w* b0 V
(prepubertal).
# o1 w7 L5 z1 o/ vThe parents were notified about the laboratory: b! J! }) d! u- x8 J
results and were informed that all of the tests were1 `$ g/ O+ Z- o3 f, m+ _2 @
normal except the testosterone level was high. The
  G0 C; [/ W2 rfollow-up visit was arranged within a few weeks to
+ o$ w4 l$ ]2 r2 j9 Hobtain testicular and abdominal sonograms; how-
( ^% {4 G( ~, e* k" ]# Dever, the family did not return for 4 months.9 h/ u0 y! K# H* J6 [5 ^
Physical examination at this time revealed that the' t1 o4 B2 W7 g& k0 Z/ a: Z9 t
child had grown 2.5 cm in 4 months and had gained4 Z/ N, z0 G$ F5 D, ]' y
2 kg of weight. Physical examination remained1 z8 Z4 T; B! ~
unchanged. Surprisingly, the pubic hair almost com-
( O  x' J2 @2 q. H& ?6 {pletely disappeared except for a few vellous hairs at
1 S& r0 L0 M/ h7 q8 |the base of the phallus. Testicular volume was still 2
& y; C) S0 g' k9 D- WmL, and the size of the penis remained unchanged.  E; J3 f: \4 k  F0 ~
The mother also said that the boy was no longer hav-
4 c# m4 N8 b* T0 O  N1 Uing frequent erections.5 f; }( q# r2 Q9 q$ U) m7 q
Both parents were again questioned about use of+ K) J9 ?$ V: S5 m- m" A3 C
any ointment/creams that they may have applied to
) K$ v8 ^* a1 K( i0 _! {the child’s skin. This time the father admitted the/ a+ T/ n$ i% P
Topical Testosterone Exposure / Bhowmick et al 541* G! u' F0 w* `6 W$ c0 V- M
use of testosterone gel twice daily that he was apply-
* u, U4 s0 S) O& R2 l! G' Ting over his own shoulders, chest, and back area for8 D% y! [: X2 c: b
a year. The father also revealed he was embarrassed% f6 Z7 a9 ^  E  F9 ]2 |
to disclose that he was using a testosterone gel pre-
4 O9 G3 v# r/ L, lscribed by his family physician for decreased libido; `! p5 w6 O1 p' ~) h! |4 E5 V
secondary to depression.
4 Z7 a7 A" y. O/ [# W# W0 k  |The child slept in the same bed with parents.
# F- y5 A! M2 L% ^/ s/ ~The father would hug the baby and hold him on his1 K$ a/ `; Y' |2 W4 Q! V. @; b
chest for a considerable period of time, causing sig-
4 m+ W; Z; ^9 _. a6 ^: o+ z! inificant bare skin contact between baby and father.0 J+ D, L7 Y& e: H* V
The father also admitted that after the phone call," J' o1 i# \& j- a, B# q3 E1 }3 _+ G$ G
when he learned the testosterone level in the baby1 R+ Z1 B+ p1 n8 w# d' t- G
was high, he then read the product information
% r, ~6 F1 n3 C2 P: p- f" Ypacket and concluded that it was most likely the rea-
# b, k/ |9 @' G- v6 r+ Wson for the child’s virilization. At that time, they/ ^4 L! _  I& U2 _" R
decided to put the baby in a separate bed, and the
* b- ]. x. q9 mfather was not hugging him with bare skin and had3 f% J% R2 q8 F' @$ Z2 R
been using protective clothing. A repeat testosterone2 [$ p* X9 I/ ^
test was ordered, but the family did not go to the
. a% d" }* o2 V. m' g* m" Jlaboratory to obtain the test.
4 F6 V" P6 c% I" DDiscussion' e: @% O3 V2 R# E! k9 t( H, J
Precocious puberty in boys is defined as secondary
& K) X% m- g4 f* E' Z8 gsexual development before 9 years of age.1,4
! ]2 g: f& Q* `1 w5 e+ wPrecocious puberty is termed as central (true) when5 l8 T8 Y6 I3 M6 U3 r$ ]2 S
it is caused by the premature activation of hypo-- L6 F  X4 o/ k) }# E) B2 ^1 |
thalamic pituitary gonadal axis. CPP is more com-
- M1 i) h+ j  H5 a& kmon in girls than in boys.1,3 Most boys with CPP7 W  \3 P1 `; |0 r& o; {
may have a central nervous system lesion that is
( ~  i3 k: Q! q0 yresponsible for the early activation of the hypothal-
/ Q2 n& a' @* I  B3 o1 t4 {amic pituitary gonadal axis.1-3 Thus, greater empha-* ?5 f/ P% f3 i* K* {
sis has been given to neuroradiologic imaging in. ^8 Z. e! M5 E. S0 F3 K. [
boys with precocious puberty. In addition to viril-- h5 J" x. W6 ~7 p' E7 c+ k
ization, the clinical hallmark of CPP is the symmet-
1 a2 i3 A6 M4 G) Mrical testicular growth secondary to stimulation by
# k1 F5 J% y5 M' rgonadotropins.1,3
% N4 l, T# S2 L' uGonadotropin-independent peripheral preco-
% X9 d& Y" s" ]cious puberty in boys also results from inappropriate
4 |7 u% _1 x! U! Pandrogenic stimulation from either endogenous or
' L* |/ n1 P: ~. c* I6 Xexogenous sources, nonpituitary gonadotropin stim-
; V( U7 o  D2 N$ [! H: Q- c) K. xulation, and rare activating mutations.3 Virilizing
) ~2 ]: |' N6 {2 P6 f* R$ Ocongenital adrenal hyperplasia producing excessive3 v  L* `4 K6 S* ~, V5 u
adrenal androgens is a common cause of precocious/ P) d- ^6 f* a: ^& [  u/ e, a8 h
puberty in boys.3,4* K. Z3 c) n) j# _4 d( N5 m: {
The most common form of congenital adrenal
  O/ L4 X, m. n5 F7 uhyperplasia is the 21-hydroxylase enzyme deficiency.
0 g/ O# X  X( r/ p- T7 G2 PThe 11-β hydroxylase deficiency may also result in( I% X  d1 q0 f' u; A% M- Q% |
excessive adrenal androgen production, and rarely,5 A! D: ]( t  z+ [
an adrenal tumor may also cause adrenal androgen7 S, q; [7 V# I# J7 {
excess.1,3- B0 f, \' g1 Z- x
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 K* z  M' R# Q- A
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007" O* ?+ g% {+ X6 H8 M  `" u, k! f
A unique entity of male-limited gonadotropin-1 t4 y5 B1 o# y0 Q1 ?7 f
independent precocious puberty, which is also known
6 ?9 c" j+ Q1 o* r. e; xas testotoxicosis, may cause precocious puberty at a
: r) s5 m( T6 Y/ q2 Fvery young age. The physical findings in these boys' A) e7 E# _! y, v
with this disorder are full pubertal development,  R' I/ L3 Z& a6 l" m
including bilateral testicular growth, similar to boys
1 t$ V% C" o. X2 a/ {with CPP. The gonadotropin levels in this disorder
* j+ R7 u2 E2 [* w- Z# M% Zare suppressed to prepubertal levels and do not show
/ ]1 G' c. t  O, y( ~" D+ y; |pubertal response of gonadotropin after gonadotropin-
! M9 k2 p' @/ V1 T1 u0 \, e$ qreleasing hormone stimulation. This is a sex-linked
+ L0 E- `! x" n5 i$ T9 t! w; sautosomal dominant disorder that affects only
# G4 {0 R$ r9 h* o3 f4 x0 hmales; therefore, other male members of the family
+ {- \0 k! u& ]- K6 Fmay have similar precocious puberty.3
- d  @' F. E$ J* DIn our patient, physical examination was incon-
$ a; h( k1 L( S; x  w8 s" [sistent with true precocious puberty since his testi-. R9 D9 b3 K1 k  l, }1 K5 u" W
cles were prepubertal in size. However, testotoxicosis
7 x$ w7 \" d) ]' q- c: J7 Xwas in the differential diagnosis because his father$ I9 I# t* K) O7 ^# |7 t
started puberty somewhat early, and occasionally,* y3 o+ F4 R* y/ ^8 H" o- l. |
testicular enlargement is not that evident in the7 J) k: v: i7 Z' n/ O
beginning of this process.1 In the absence of a neg-
+ |: B, Q  M; j: [% Dative initial history of androgen exposure, our
2 z  a3 S7 o* w+ J9 R5 Zbiggest concern was virilizing adrenal hyperplasia,
$ j0 H, K# T5 r2 \* p& }) y# F5 teither 21-hydroxylase deficiency or 11-β hydroxylase" o  Z# h4 d1 u8 W8 a" s1 n
deficiency. Those diagnoses were excluded by find-
$ G% C8 ~( \1 {# ning the normal level of adrenal steroids.
' d0 ^* S9 J8 z1 s+ g$ ^The diagnosis of exogenous androgens was strongly
7 n* [! l- R/ A+ v# ~suspected in a follow-up visit after 4 months because
  W; S7 T; R' N8 l2 @6 Gthe physical examination revealed the complete disap-- w) v: f6 x' z+ R
pearance of pubic hair, normal growth velocity, and& @3 r& x" |6 s! N7 h
decreased erections. The father admitted using a testos-
$ [. M. _- n) o( J3 s, cterone gel, which he concealed at first visit. He was$ Z* L, u! L. F' m' K! J
using it rather frequently, twice a day. The Physicians’
5 Y: f$ k9 y2 O) B. q5 ^8 LDesk Reference, or package insert of this product, gel or' @: [0 E% Z, [" z7 f. i* c* E+ r- U* c- H
cream, cautions about dermal testosterone transfer to) v$ k% M8 S3 C6 C9 F+ @6 F
unprotected females through direct skin exposure.
3 Z) a$ b# G. y6 v/ FSerum testosterone level was found to be 2 times the! I3 O) S- `  ^! N9 y
baseline value in those females who were exposed to( ]" @& _  c' v) m, p: x7 V( l2 r2 B0 t$ {
even 15 minutes of direct skin contact with their male
* i& q  h( a& opartners.6 However, when a shirt covered the applica-
* G7 h; n! X# X8 S# p3 Mtion site, this testosterone transfer was prevented.
% P1 n- z; G* p, I, R- i; GOur patient’s testosterone level was 60 ng/mL,
* X% M: Y+ t  ~! twhich was clearly high. Some studies suggest that% {! E! Z# R( @0 x: w. \" O8 u
dermal conversion of testosterone to dihydrotestos-
2 n) M( ~+ _" V( zterone, which is a more potent metabolite, is more
% @3 _+ E( u1 c! c# j+ g7 q$ bactive in young children exposed to testosterone' j5 b% s7 P# N7 t: U" F& C/ J
exogenously7; however, we did not measure a dihy-' [6 s* R( @9 ~; u/ R5 G
drotestosterone level in our patient. In addition to7 U: q5 l1 C  y3 }6 @# N$ Y
virilization, exposure to exogenous testosterone in
  H2 Z% J" Q1 F' V" ~/ Jchildren results in an increase in growth velocity and1 u6 Z  y: ]; j' i2 R9 x/ {& N
advanced bone age, as seen in our patient.: w: l! f% Q* z, W
The long-term effect of androgen exposure during5 M) ^9 O. d+ ?  {# w" T
early childhood on pubertal development and final, t. Q( \4 L2 X3 R) ?' A
adult height are not fully known and always remain
' l5 O  i+ f# ]  q( Ta concern. Children treated with short-term testos-, |5 x1 y3 B# a9 H' t9 `3 k" ^$ w
terone injection or topical androgen may exhibit some
/ I# z. f7 s$ @7 Q- p: Cacceleration of the skeletal maturation; however, after2 s( ^; A# B" f4 p0 w
cessation of treatment, the rate of bone maturation
8 q& u9 E6 h# {% Jdecelerates and gradually returns to normal.8,9
. [" g% V% R* R& N# g/ e0 qThere are conflicting reports and controversy$ b+ n. h( n; t  f
over the effect of early androgen exposure on adult
  X, G% {5 R& \/ e0 X0 Zpenile length.10,11 Some reports suggest subnormal
% n( Z% T+ \# R' z7 p+ Z3 Yadult penile length, apparently because of downreg-4 p/ f. z- U6 z* J+ E
ulation of androgen receptor number.10,12 However,) J" l5 q7 R  G1 r1 t) S( Q
Sutherland et al13 did not find a correlation between' u/ S5 \8 s3 T
childhood testosterone exposure and reduced adult, p% U# ?, z8 I) B" W" A
penile length in clinical studies.& q7 p2 z  P8 V
Nonetheless, we do not believe our patient is8 L7 b8 F/ o7 \, p1 [$ \
going to experience any of the untoward effects from/ c) Y; o% b  O$ w! o- @) ?* p1 a
testosterone exposure as mentioned earlier because
' [) S" I4 D$ q' p  e5 [the exposure was not for a prolonged period of time.
, L  J( @% C5 J& c$ cAlthough the bone age was advanced at the time of6 W7 c( v, @7 J7 c2 k( C0 [1 d" z
diagnosis, the child had a normal growth velocity at
) D* _2 x" M0 dthe follow-up visit. It is hoped that his final adult" y9 h$ g$ B+ Q8 z* B$ u
height will not be affected.
2 F: I  X9 F4 f+ L7 ]9 ?: {+ hAlthough rarely reported, the widespread avail-
6 Z& o" E: F# @. o! t; W: dability of androgen products in our society may
: X0 V' _# g6 i; Yindeed cause more virilization in male or female4 M& B+ g( F8 R) G0 {
children than one would realize. Exposure to andro-
6 B4 r6 x# m. i3 E; qgen products must be considered and specific ques-
( X" r1 ~: s+ c; n9 {% A& l, F* Itioning about the use of a testosterone product or# q" h1 D0 l& B% a; p' B
gel should be asked of the family members during$ b; U/ N% R  j3 s/ Z
the evaluation of any children who present with vir-
9 r3 V! f: F3 Z& L- }1 q9 Silization or peripheral precocious puberty. The diag-
8 z% Q- ^2 z: V9 x* i7 A) j% \nosis can be established by just a few tests and by$ ~% m: }- A& A, q; A: g) S+ q
appropriate history. The inability to obtain such a$ _6 y8 u0 {8 r. C
history, or failure to ask the specific questions, may
9 q- e% u6 N+ v0 o$ }" ]result in extensive, unnecessary, and expensive- l& K- ~: J8 `* p$ }6 N% T, z. T
investigation. The primary care physician should be2 j& M; L# B( t6 @
aware of this fact, because most of these children/ I' t) C3 ?3 {) H8 B7 k8 h
may initially present in their practice. The Physicians’
& `* e4 F4 A& bDesk Reference and package insert should also put a! }/ l# K& P& i
warning about the virilizing effect on a male or% M, Z- e; M' f1 h& i0 r
female child who might come in contact with some-2 s% w4 V+ U2 c- u% M- j
one using any of these products.' X$ n3 J9 S& M9 `
References
3 ?+ j9 n) `" ^2 |  b6 X/ v1. Styne DM. The testes: disorder of sexual differentiation+ X, y, \* ]1 s, s3 c
and puberty in the male. In: Sperling MA, ed. Pediatric4 b  @  A6 N  b4 S* `
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
, F$ Y0 @. g) H# [4 _2002: 565-628.
1 U# n, P2 c" w- I% J* H2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious: ~/ F8 c% h2 B+ K7 c
puberty 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
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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
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
. W( k: Q) v3 h! H2 r+ P
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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