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Sexual Precocity in a 16-Month-Old& ?, ^7 r: T0 |6 N
Boy Induced by Indirect Topical
+ t/ A/ T* Y' t5 |Exposure to Testosterone
$ I( ]6 p- x8 R+ _* g" b& e3 U" l  QSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
" X& R8 C* ]6 L  v$ [! ?! q: `2 U: fand Kenneth R. Rettig, MD19 l) ~$ C6 _# k( f
Clinical Pediatrics
" k- l- Y, V" R" y. O3 K0 o; QVolume 46 Number 6. E* G# l* M' m0 c! C
July 2007 540-5430 e( L' p4 Y% ~8 U+ s
© 2007 Sage Publications
/ r8 t9 D( G) }3 v( |% W10.1177/0009922806296651
3 h1 a' Q7 j' ?' n' C0 dhttp://clp.sagepub.com
; b/ ~. G4 `( E: ~/ Rhosted at
; [; A, H& [  b( M* O9 Nhttp://online.sagepub.com
, x) r( l! D5 V1 PPrecocious puberty in boys, central or peripheral,
6 i* P+ e+ B7 T1 His a significant concern for physicians. Central
) d- a) l' \3 ?7 I8 ]precocious puberty (CPP), which is mediated
2 e; V1 G) m) d3 \- @  s2 sthrough the hypothalamic pituitary gonadal axis, has
6 m- O  G( X- z/ U) l, b2 T& }; D' Ra higher incidence of organic central nervous system
2 g8 m  O  `# s9 t" ^2 ?/ m" ^( llesions in boys.1,2 Virilization in boys, as manifested
3 g0 F) m7 v9 l8 tby enlargement of the penis, development of pubic
: E0 X, n2 ^& \, fhair, and facial acne without enlargement of testi-
; i% R  o9 }+ q. s$ `9 D8 _cles, suggests peripheral or pseudopuberty.1-3 We8 R9 E& f; K* T' O  K
report a 16-month-old boy who presented with the
, F4 W# `7 O& U2 Denlargement of the phallus and pubic hair develop-
' ^( g; J6 X. s1 Y! D) q6 G3 zment without testicular enlargement, which was due
" G+ N  h: d% a. }4 N( z* Ito the unintentional exposure to androgen gel used by) P8 q1 x5 ?  N: u) Z
the father. The family initially concealed this infor-$ L4 o" X" i, i% i
mation, resulting in an extensive work-up for this/ U; m& y% Q' I; H
child. Given the widespread and easy availability of! {% _1 J* [" k4 G
testosterone gel and cream, we believe this is proba-# _" R8 ?+ i) _4 u! R- {
bly more common than the rare case report in the# {! @9 t+ s7 Y7 R
literature.40 t! W- s' K3 N* U$ m: f8 Z  E4 ^5 U$ w
Patient Report  A% Q8 i1 K9 P* n. l- W5 r% ?
A 16-month-old white child was referred to the
4 T3 U+ @* {+ j6 l, y2 J& b/ ^- hendocrine clinic by his pediatrician with the concern
5 p9 p  n, U& O  d6 P' p8 R- u4 K5 ^" pof early sexual development. His mother noticed
0 p) d  B+ ~! q7 ], |4 {light colored pubic hair development when he was8 B" T4 O( i* N% v) L; H) E
From the 1Division of Pediatric Endocrinology, 2University of
5 ]. s3 S5 P2 S! L7 p5 i# W! XSouth Alabama Medical Center, Mobile, Alabama.5 x: o5 K7 U3 L4 @; p% e
Address correspondence to: Samar K. Bhowmick, MD, FACE," k3 _; j% ^, S- {  H# ?
Professor of Pediatrics, University of South Alabama, College of) g( l# j. \# ^3 H5 H  I
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;% v; U2 w" f% t6 t8 U. D
e-mail: [email protected].
& W# c$ B( \/ G7 V  W- O4 _5 R) jabout 6 to 7 months old, which progressively became
* Q0 J, `. T" M3 D, mdarker. She was also concerned about the enlarge-
4 {& P2 g2 u6 V4 f! s7 u9 q6 Ament of his penis and frequent erections. The child9 d/ `$ w6 L) n3 A" {
was the product of a full-term normal delivery, with
: g& z/ f3 L; M  l3 Ga birth weight of 7 lb 14 oz, and birth length of4 E- k5 e6 S5 @9 ]/ E1 ~5 o  }
20 inches. He was breast-fed throughout the first year( H7 m2 u8 G& s: O* K3 r# g( F
of life and was still receiving breast milk along with' U7 Y/ K: {  I9 r
solid food. He had no hospitalizations or surgery,) ~7 {' q! K& a. Z5 \
and his psychosocial and psychomotor development( F8 ~& Z* {# W) S) b/ A+ X+ S0 p
was age appropriate.
5 ^+ W2 `! ^7 C8 F# B) j" m) l% jThe family history was remarkable for the father,
7 R# {2 [7 j9 i: }+ @. O' Jwho was diagnosed with hypothyroidism at age 16,: F8 R: R* `2 s% D; a
which was treated with thyroxine. The father’s
! {1 d1 P. J* D* Z& f( t$ O# xheight was 6 feet, and he went through a somewhat
$ u) I( M7 V2 F) g0 Aearly puberty and had stopped growing by age 14.* j7 P* D0 B0 ?, Z
The father denied taking any other medication. The
- ^1 h. ]& m5 f/ vchild’s mother was in good health. Her menarche
3 s  }$ C. V- A0 p  Qwas at 11 years of age, and her height was at 5 feet
) C: X4 z/ |* t+ W5 inches. There was no other family history of pre-  C: t( x% U0 g7 U* s7 b
cocious sexual development in the first-degree rela-, W' g3 _4 C  B% a7 q6 C( `9 a7 J+ M
tives. There were no siblings.; K& ?; r: r' g# i
Physical Examination
# ~9 {2 h( }2 S7 @% K- k' PThe physical examination revealed a very active,8 o5 `+ f4 B# o) e7 r
playful, and healthy boy. The vital signs documented
" W6 s) p& g. G  r% p2 O/ Y. _! H: Ja blood pressure of 85/50 mm Hg, his length was9 {; Y( W' [# o0 j: p
90 cm (>97th percentile), and his weight was 14.4 kg
) S1 p! m3 g9 T! [% ~3 e(also >97th percentile). The observed yearly growth/ g5 P- G% Q1 ^. c
velocity was 30 cm (12 inches). The examination of
" Q$ ?3 x! A) ^' A+ V" ethe neck revealed no thyroid enlargement.
0 |$ N  H2 [+ }) BThe genitourinary examination was remarkable for! l" x7 A2 p- R' F0 ~6 M
enlargement of the penis, with a stretched length of: G. G# A6 l+ e; R4 w9 w* ?+ E( ?
8 cm and a width of 2 cm. The glans penis was very well% b9 O1 a2 M( S1 S, g5 l1 M
developed. The pubic hair was Tanner II, mostly around
1 G: X; D/ q/ m, j5400 l/ D# A3 q$ n3 r5 j
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- ?  e; X1 D6 }( z% p+ |: Y  ~the base of the phallus and was dark and curled. The6 H* E) t9 m1 W3 E( P
testicular volume was prepubertal at 2 mL each.
5 W) V' K; }3 MThe skin was moist and smooth and somewhat! V& e, Y9 H- Z8 O2 W( U/ `5 ^6 r
oily. No axillary hair was noted. There were no
" P+ L. l) e2 G$ R" uabnormal skin pigmentations or café-au-lait spots.
% G+ ?8 d. ^  S! P2 B; |Neurologic evaluation showed deep tendon reflex 2+
+ w: ?: i, J; W' G5 _bilateral and symmetrical. There was no suggestion0 v3 w4 ]: L/ a" Y7 D6 ?) g
of papilledema.% P; c4 p1 {4 I8 b  R
Laboratory Evaluation4 d9 w2 N1 z: l! K/ J' V
The bone age was consistent with 28 months by
9 e, F- R2 B# J) n, kusing the standard of Greulich and Pyle at a chrono-; q0 |% [: d5 B5 b- k, U
logic age of 16 months (advanced).5 Chromosomal: x5 R7 Y, i6 X7 B- ~- E$ o% K
karyotype was 46XY. The thyroid function test
" x6 o& l1 K) P& C# g1 Dshowed a free T4 of 1.69 ng/dL, and thyroid stimu-4 r( O- y2 \6 l3 ^- g# s
lating hormone level was 1.3 µIU/mL (both normal).8 `! @$ m$ ]1 T( C) [3 _. F
The concentrations of serum electrolytes, blood
/ L" p5 }8 p- K' Yurea nitrogen, creatinine, and calcium all were
% x. v. d2 i( q! n- T7 R( [within normal range for his age. The concentration( w( e2 I5 N: D* s
of serum 17-hydroxyprogesterone was 16 ng/dL( L. C* G: q+ \* `! D  V' z
(normal, 3 to 90 ng/dL), androstenedione was 20
( ?( j5 Y& e6 M0 i* G' ?ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
" O/ B  \( _( `# E* m4 pterone was 38 ng/dL (normal, 50 to 760 ng/dL),
  ^3 T! v( g, e# z; Q# I3 G0 bdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
- u  d1 N5 f2 i5 y4 K& x49ng/dL), 11-desoxycortisol (specific compound S); W) G# J4 a) e" I# Z/ J8 q8 f) K4 ^
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-/ O1 K, V' b4 f
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total; W6 F! r4 N- s& O
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),3 x6 h# ]1 T# H
and β-human chorionic gonadotropin was less than
, F/ P& v4 R2 O& F3 M( d2 W. V, P5 mIU/mL (normal <5 mIU/mL). Serum follicular( [# V& C0 k7 L6 q! ~
stimulating hormone and leuteinizing hormone
: t4 a8 _2 m  I" E+ `0 Cconcentrations were less than 0.05 mIU/mL0 e6 x9 h0 Z) ^# [" S2 U
(prepubertal)./ b; y; k2 b6 g4 Q4 [+ e
The parents were notified about the laboratory5 L8 X5 }* A5 X2 I$ `5 V( b
results and were informed that all of the tests were
! F, a' _. L% k; n  \: ]normal except the testosterone level was high. The5 _% ?" h, ^8 C4 D6 w: e
follow-up visit was arranged within a few weeks to
; Q) l! Y0 ]! ~+ S7 tobtain testicular and abdominal sonograms; how-. K' f# _" x* X) B& h
ever, the family did not return for 4 months.
- o3 _) |# E$ x. ~% m% BPhysical examination at this time revealed that the6 n/ ?" N0 f! f; B" D/ _
child had grown 2.5 cm in 4 months and had gained
3 C$ ~. R" H" p7 |, _2 kg of weight. Physical examination remained3 @/ l  q+ x* P0 o2 R5 j# l$ K
unchanged. Surprisingly, the pubic hair almost com-
- K0 {% \0 e- T0 hpletely disappeared except for a few vellous hairs at
' J/ Z  C( N; ~6 k  ~the base of the phallus. Testicular volume was still 2
3 M, w; @' o; Y6 E  e; ^. d5 V0 ImL, and the size of the penis remained unchanged.
. u4 Q# e, J" {* oThe mother also said that the boy was no longer hav-
( ?3 Z" n  }0 R/ h" L6 R$ l. Ting frequent erections.
  u0 ^& K! k& i  S& mBoth parents were again questioned about use of
2 v, Y( p; x' O( ]: H: R  Hany ointment/creams that they may have applied to
( _5 h7 ~! M. V* q4 M! o* D+ Pthe child’s skin. This time the father admitted the
, Q5 G7 s+ c5 g8 }9 |Topical Testosterone Exposure / Bhowmick et al 541
+ r' ~1 G1 o2 |  Q9 ^use of testosterone gel twice daily that he was apply-5 a7 ?: @* J. K, `6 t
ing over his own shoulders, chest, and back area for5 h9 N+ @1 p5 ?" V3 [
a year. The father also revealed he was embarrassed
' H4 Y2 S4 ^& u1 |to disclose that he was using a testosterone gel pre-/ M2 s0 b1 w. o% B5 L
scribed by his family physician for decreased libido, o- ^2 p4 Q1 o  S: p: K
secondary to depression.
5 i6 F5 x  z3 N; }6 \8 ^. z& xThe child slept in the same bed with parents.; ]9 X9 t5 V6 Z* h
The father would hug the baby and hold him on his5 V5 l" X+ g3 f* x
chest for a considerable period of time, causing sig-- B. Y7 O4 Y9 m
nificant bare skin contact between baby and father.
' X3 O4 T* a* b; k6 w" zThe father also admitted that after the phone call,+ F; E. x9 O" H6 Z2 n" W
when he learned the testosterone level in the baby
% `# j* ?, _7 m7 g0 [was high, he then read the product information
! K# e) ]0 c9 ~9 C5 {# N3 upacket and concluded that it was most likely the rea-
- Z  X6 P+ p- ~/ T  Xson for the child’s virilization. At that time, they
( y+ C4 [" k# g2 V' I  ~* ^decided to put the baby in a separate bed, and the
% H. C& P' k" |; Ffather was not hugging him with bare skin and had
) R$ O3 W5 `5 t8 |+ Ubeen using protective clothing. A repeat testosterone- ?: k; u& F9 L9 n; `
test was ordered, but the family did not go to the. n! K4 z+ b9 Z6 F/ x
laboratory to obtain the test.
- q, T2 v, n/ H9 H3 uDiscussion+ l% q, M; d% @6 o; ]9 w0 r
Precocious puberty in boys is defined as secondary. p: p1 Z$ {# d" |7 c$ K  x
sexual development before 9 years of age.1,4
7 t$ z7 k5 A2 Z( _# q5 a5 jPrecocious puberty is termed as central (true) when, r$ g4 y4 L5 a/ O9 |
it is caused by the premature activation of hypo-
. y5 z; ]. c& c/ G5 Kthalamic pituitary gonadal axis. CPP is more com-
" ?' w/ s- \  [- `6 s9 k2 }2 x# Fmon in girls than in boys.1,3 Most boys with CPP% p  ?: @* c0 E! ]$ X2 F2 H
may have a central nervous system lesion that is% ]5 g3 D, h0 G) g8 f0 B
responsible for the early activation of the hypothal-
4 I6 `5 }- p5 }# j9 Y# S9 X7 Bamic pituitary gonadal axis.1-3 Thus, greater empha-
8 f1 @7 r) |- dsis has been given to neuroradiologic imaging in% |, T$ n7 ^2 \# b7 c
boys with precocious puberty. In addition to viril-
6 f5 ^3 O* L5 N1 q0 q6 ^ization, the clinical hallmark of CPP is the symmet-
$ T, k+ b6 _5 o/ ~4 E7 c  urical testicular growth secondary to stimulation by
! \$ ~- b( E; d, }+ w4 ~( T- Xgonadotropins.1,3$ e6 H& g1 D: n7 r  f" V
Gonadotropin-independent peripheral preco-/ e( ~- B' |3 {; M
cious puberty in boys also results from inappropriate
  s9 ?* e2 e) H2 [! g* {& m$ K1 Randrogenic stimulation from either endogenous or5 p( g6 N' n7 x( K
exogenous sources, nonpituitary gonadotropin stim-% S1 U: _) U2 `$ f: t  [
ulation, and rare activating mutations.3 Virilizing
9 \, W4 y3 }2 C4 [( Kcongenital adrenal hyperplasia producing excessive) C; A( d1 c4 s. S% N3 s1 L: P, ]6 h/ A
adrenal androgens is a common cause of precocious
4 c3 X! M# @6 [* r& L% n$ Opuberty in boys.3,4& R1 F9 v) y3 o
The most common form of congenital adrenal
3 Q1 w4 }% k" Rhyperplasia is the 21-hydroxylase enzyme deficiency.
! M% Y1 ^  f/ w8 b/ jThe 11-β hydroxylase deficiency may also result in
! ~1 A  w% W4 u4 oexcessive adrenal androgen production, and rarely,
2 g+ r/ H) y7 fan adrenal tumor may also cause adrenal androgen
, H2 P, `8 L1 P/ t# a3 S$ Zexcess.1,3
8 v6 d- |' j' ?8 j8 O" ]. Eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 W4 s9 v% P7 L/ c: U" Q- a542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
- ^% _+ z) _# c# |/ ^' Z  k, aA unique entity of male-limited gonadotropin-
: W& M. C+ R& A( F6 X" X' eindependent precocious puberty, which is also known, B4 j% @$ t2 M1 s) W' Q4 W! P6 i
as testotoxicosis, may cause precocious puberty at a
- T" ]. ?4 ?. |) s# ?# v, Xvery young age. The physical findings in these boys
% g/ r( o7 \( K+ C$ ]# |with this disorder are full pubertal development,0 L+ I, C! u; ]
including bilateral testicular growth, similar to boys+ {; ?7 t9 Z. [! {# I$ y
with CPP. The gonadotropin levels in this disorder4 X& d$ \$ a& d0 z2 p8 g! }0 a
are suppressed to prepubertal levels and do not show, p" C* |" l* T
pubertal response of gonadotropin after gonadotropin-! j( o% X) B0 K
releasing hormone stimulation. This is a sex-linked
: \% f- J% B3 u) b0 V* W. Kautosomal dominant disorder that affects only3 G# ]7 m  v, Z' Y
males; therefore, other male members of the family6 X2 e; v+ m. {/ z
may have similar precocious puberty.3. N0 L2 @. A+ {( }
In our patient, physical examination was incon-4 j( H' ]$ ^+ {0 m- d/ I  V& i  v! `: T
sistent with true precocious puberty since his testi-- B" c7 n* T4 B4 ^4 B
cles were prepubertal in size. However, testotoxicosis4 l" J* b2 Z0 {6 R8 {6 f8 y, m, J
was in the differential diagnosis because his father
4 P7 J& ^& ^# r) j- d2 f2 k3 Lstarted puberty somewhat early, and occasionally,
$ o) l* P2 c+ p/ ytesticular enlargement is not that evident in the
, P+ x" c% k* ^) V2 Jbeginning of this process.1 In the absence of a neg-6 j9 E0 G# L4 i$ P
ative initial history of androgen exposure, our- j1 G) M( w6 T5 z  i
biggest concern was virilizing adrenal hyperplasia,0 y, x& I! P3 C9 M, d
either 21-hydroxylase deficiency or 11-β hydroxylase8 a- o+ s3 Y( a/ s1 [- f, K
deficiency. Those diagnoses were excluded by find-  [4 p4 `9 ~  F2 j* `' E
ing the normal level of adrenal steroids.
% i& m8 j' o+ V$ m. g( jThe diagnosis of exogenous androgens was strongly8 }# U- _( U+ t$ B
suspected in a follow-up visit after 4 months because
: ]; r; `; Z1 s, e- y  [" Mthe physical examination revealed the complete disap-* [/ V  G+ {4 W7 e0 _: O' R
pearance of pubic hair, normal growth velocity, and! w) I/ v' A* U& M7 D2 D
decreased erections. The father admitted using a testos-+ i: E* ^/ I0 A3 h
terone gel, which he concealed at first visit. He was' H' V# H& B3 Y" G# X5 s
using it rather frequently, twice a day. The Physicians’) \* n. P0 e/ u; r; D: V  B
Desk Reference, or package insert of this product, gel or
+ ]4 Q3 t; b! q2 m1 ]! u/ Hcream, cautions about dermal testosterone transfer to0 y4 ?+ C; M' }2 d) }0 p% Q2 K
unprotected females through direct skin exposure.9 G; K- r1 L+ \* A
Serum testosterone level was found to be 2 times the
, K" w/ Q7 B" d" i1 x9 ubaseline value in those females who were exposed to
( i+ d6 [' N& I2 |even 15 minutes of direct skin contact with their male# H( k! Z# d; ~# s/ ^# x1 s5 N
partners.6 However, when a shirt covered the applica-
1 m! K3 i, Z& y+ V0 z9 x7 e8 u2 ction site, this testosterone transfer was prevented.
7 `) L2 i' |, R1 @Our patient’s testosterone level was 60 ng/mL,& x5 d/ g7 }6 {8 Z$ [9 D" C7 v
which was clearly high. Some studies suggest that+ O# [5 D4 l$ i
dermal conversion of testosterone to dihydrotestos-
( @9 Q- T: C" ?* l6 Tterone, which is a more potent metabolite, is more
$ ?8 B, @7 J" m$ x0 M7 nactive in young children exposed to testosterone
6 E9 a! x% c$ t& N5 u/ K6 Jexogenously7; however, we did not measure a dihy-
& `, X9 v: e/ Z% B6 s/ Y( adrotestosterone level in our patient. In addition to
8 }8 m, m  c. x) A1 O1 Yvirilization, exposure to exogenous testosterone in
  e6 b( Z$ n8 ~4 E4 Tchildren results in an increase in growth velocity and
5 \, X2 h) Q+ w+ z0 L6 |advanced bone age, as seen in our patient.) X8 e: D7 Q  H( d+ B, e$ M
The long-term effect of androgen exposure during& }6 N9 \/ p5 A
early childhood on pubertal development and final
; k6 P5 N6 {5 j' w3 _5 qadult height are not fully known and always remain( W% S" w% o' H
a concern. Children treated with short-term testos-* d* N2 e8 q7 k$ K2 u/ D  i
terone injection or topical androgen may exhibit some
3 _2 u0 U4 y4 N) Cacceleration of the skeletal maturation; however, after
0 I% h% o& \5 Ucessation of treatment, the rate of bone maturation5 K6 ]' ^: I) E& K" J& H
decelerates and gradually returns to normal.8,9% J* I; }" l$ q5 K
There are conflicting reports and controversy
: W& I& W9 }( r6 t" F+ eover the effect of early androgen exposure on adult
: G7 f8 B# Z- F. G% T, x8 dpenile length.10,11 Some reports suggest subnormal
* {5 i* c0 c/ W$ E% n: ]adult penile length, apparently because of downreg-
" d, K2 F# q+ U# ^% h1 w; fulation of androgen receptor number.10,12 However,
5 K( g4 t/ N+ Q. HSutherland et al13 did not find a correlation between
4 S- h" I# {* K7 `9 U. s) f$ P' dchildhood testosterone exposure and reduced adult
7 W3 i& F9 y  ?" w' o. fpenile length in clinical studies.
: a: J& J7 e. v# v! UNonetheless, we do not believe our patient is* B7 l& w" ?. x  M
going to experience any of the untoward effects from2 `: R% J4 p- R8 J" o' {0 `: f
testosterone exposure as mentioned earlier because$ J+ m4 n3 r! K8 V
the exposure was not for a prolonged period of time.
# X2 x: d3 n# m; B" L5 n) n( mAlthough the bone age was advanced at the time of5 ]9 h" N- X8 p- `
diagnosis, the child had a normal growth velocity at, v1 j/ A4 K" n: A% d, d
the follow-up visit. It is hoped that his final adult
" R5 U5 Z1 R1 O/ h0 u  \height will not be affected.
& g4 c; m) j' k3 e! `) qAlthough rarely reported, the widespread avail-
* l9 Q6 S: u$ v6 Zability of androgen products in our society may8 O7 I9 C* k1 {% w  h# |8 s
indeed cause more virilization in male or female
2 m  F% u* l. r& G4 ]' ichildren than one would realize. Exposure to andro-
' V0 T! ~7 ?/ [* V5 Kgen products must be considered and specific ques-8 J3 @+ y9 a2 ?1 @) G7 H3 Z
tioning about the use of a testosterone product or
$ L. |. O7 Z; X; n! Cgel should be asked of the family members during
6 Y" c' y4 q2 M8 \# Q2 K! I+ h' _the evaluation of any children who present with vir-" s  `2 r: s/ n; Y! ?1 [$ X
ilization or peripheral precocious puberty. The diag-
7 C# ?- K0 K$ anosis can be established by just a few tests and by
: i; O7 _  |2 J+ Q/ H- f& R! {appropriate history. The inability to obtain such a
4 n4 z: O% V2 u; S2 g( ?5 U0 J$ Ohistory, or failure to ask the specific questions, may8 N& C2 N. N. H* N% L+ _" m
result in extensive, unnecessary, and expensive
9 l8 h& r& v# linvestigation. The primary care physician should be
3 `# P' Y, F8 i7 n4 \aware of this fact, because most of these children
- G4 V/ C3 Q, j: omay initially present in their practice. The Physicians’( E- R% A) P4 c( G
Desk Reference and package insert should also put a! E+ S  l3 @2 W# N& x# I
warning about the virilizing effect on a male or1 R) O% u8 h3 c* k. ~  E+ G5 D( j
female child who might come in contact with some-
. [- G' ~# h% @2 ^one using any of these products.
9 ~( s$ b0 X6 [: ^References/ |- Z% e" a0 K% `
1. Styne DM. The testes: disorder of sexual differentiation
( ?- b! H( B' A; mand puberty in the male. In: Sperling MA, ed. Pediatric
: x/ F3 x0 a; B( h8 JEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;  E6 }- e4 K& z* o; L
2002: 565-628.1 m0 [1 z. G3 }1 M2 T
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
# d/ O/ B3 s2 @8 Qpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old& G8 @  c" c# D3 z. \
Boy Induced by Indirect Topical  p* q7 w" r! N& a1 H$ I
Exposure to Testosterone7 c* {6 F1 ?8 v5 j. s* U& m$ A" L
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
" V3 q8 w. p( x; C! h; aand Kenneth R. Rettig, MD1
; w  o( j" `8 y" {8 U( c( G9 {Clinical Pediatrics- [# ^1 R1 X! j. w2 H6 A
Volume 46 Number 6/ |9 q. e" h" S  ?' k/ p
July 2007 540-543% e4 {$ K1 v& l' T" [1 ^5 _. \
© 2007 Sage Publications
9 D2 U/ |* `  h$ V* ^. s2 a3 I+ B10.1177/0009922806296651
' ^  x% ^( \1 Vhttp://clp.sagepub.com  E) h1 M3 n5 `. d/ t& d
hosted at
- H+ H( e8 N& W% uhttp://online.sagepub.com. f) F7 T( Z/ }3 d* l8 k1 ?; h
Precocious puberty in boys, central or peripheral,6 u: ~+ }% D3 x! O, R
is a significant concern for physicians. Central! a& w* {: X. i8 p2 M
precocious puberty (CPP), which is mediated& a" e' W! e! V: U" N, Z
through the hypothalamic pituitary gonadal axis, has$ n) N7 A( Z2 |; C& I/ K
a higher incidence of organic central nervous system- {, B% ?1 c; r8 D, U- ?
lesions in boys.1,2 Virilization in boys, as manifested
- [1 ]0 n( I6 P1 o8 |6 M  I# r+ K; ~8 tby enlargement of the penis, development of pubic; @" r$ `% t/ k2 ]$ E$ |
hair, and facial acne without enlargement of testi-$ [: Q% R6 ~3 L/ c8 |! @
cles, suggests peripheral or pseudopuberty.1-3 We: x/ a; A1 z% l% @$ s1 f8 A: m0 f
report a 16-month-old boy who presented with the
. H# v% g3 }5 Y; uenlargement of the phallus and pubic hair develop-) L9 L+ A" l( i! f( [" ?
ment without testicular enlargement, which was due
0 H. Q  s0 H( o; z8 p! {to the unintentional exposure to androgen gel used by
/ |7 u4 J7 `( A+ G! b6 T8 Zthe father. The family initially concealed this infor-
& Y' E) q1 I' p& s4 cmation, resulting in an extensive work-up for this3 @: C0 V  m. V$ W6 t1 `: X" d
child. Given the widespread and easy availability of
9 M. k7 _+ `) gtestosterone gel and cream, we believe this is proba-
2 d' c& |# f- C7 U7 o1 ibly more common than the rare case report in the: v" O# a6 p1 P+ e
literature.4: y4 l' k6 _6 q) B3 z% z# `& R( T6 W* |- x
Patient Report
$ C, e" E4 o1 b' mA 16-month-old white child was referred to the, F0 w1 [6 H$ g* a* B
endocrine clinic by his pediatrician with the concern) }9 v* g( v" \' a
of early sexual development. His mother noticed
- F3 H4 r8 K: l6 _+ N7 ulight colored pubic hair development when he was) |$ g* B9 d9 v; T( F! N5 H
From the 1Division of Pediatric Endocrinology, 2University of
- A0 W, u/ z2 S  P; ^South Alabama Medical Center, Mobile, Alabama.0 g" g+ ], `& W( _/ l1 N& a& u! U
Address correspondence to: Samar K. Bhowmick, MD, FACE,
% k# P/ V8 k, O/ C: |+ ~1 ]Professor of Pediatrics, University of South Alabama, College of
! g7 r0 e0 J( Y8 z4 fMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
; q( r, m2 x7 A( y8 r1 f; K# [e-mail: [email protected].
- D- Q, o+ P  Q8 Mabout 6 to 7 months old, which progressively became
5 s, v- F6 h  I0 p, c! ?darker. She was also concerned about the enlarge-
& A( A1 p5 Q% mment of his penis and frequent erections. The child$ O4 r: `$ T, i8 a% U) b2 s! ]- Y
was the product of a full-term normal delivery, with
/ G9 f9 P* b1 q* f3 Ma birth weight of 7 lb 14 oz, and birth length of$ r: u! J) g! J8 n, s+ ?- x" M
20 inches. He was breast-fed throughout the first year
+ Y6 K- {9 |$ M7 {$ z) S) ~3 tof life and was still receiving breast milk along with2 [  y* _7 Q1 A- J# _
solid food. He had no hospitalizations or surgery,% R  L+ l( s' Q6 J1 z5 l6 @
and his psychosocial and psychomotor development% C6 \- d: C4 G; i1 B! Z
was age appropriate.
" f5 p/ f( x( r! yThe family history was remarkable for the father,
$ q% Q- s& j1 H; gwho was diagnosed with hypothyroidism at age 16,
/ R6 t# H. U- _9 U5 dwhich was treated with thyroxine. The father’s
6 Y) H; o1 q) r+ P6 Xheight was 6 feet, and he went through a somewhat
7 H( N! K. T5 ~; wearly puberty and had stopped growing by age 14.
6 E( }" D; ^0 ?! D6 iThe father denied taking any other medication. The, f0 H+ O3 U8 V, H) W2 q" n3 g- ?
child’s mother was in good health. Her menarche- i: I1 Q, [/ U, n+ i0 n
was at 11 years of age, and her height was at 5 feet8 m0 o9 Y7 P* j
5 inches. There was no other family history of pre-
6 N5 h# o6 V& V& {, }% L6 M( }cocious sexual development in the first-degree rela-" z7 d5 P( P" f7 h( u# c
tives. There were no siblings.
: p# \$ z1 ?* ?) e8 u. \Physical Examination1 B. I( v8 M" o9 J7 ]1 W
The physical examination revealed a very active," C" b* h9 n# b( v
playful, and healthy boy. The vital signs documented
/ ]2 \, \- G% ^! R% P0 X9 fa blood pressure of 85/50 mm Hg, his length was6 n1 S/ y2 V/ A) B# G) F
90 cm (>97th percentile), and his weight was 14.4 kg  w, d) O" I/ y0 o
(also >97th percentile). The observed yearly growth
  @5 u! `2 n9 ?4 O, \velocity was 30 cm (12 inches). The examination of# u" \- D1 b- a# _8 P3 T$ y9 `
the neck revealed no thyroid enlargement.
: @% t/ ~: f# E+ m  y) uThe genitourinary examination was remarkable for% j4 D. h" Q, s1 v4 b/ o. b
enlargement of the penis, with a stretched length of/ i0 q! P/ y' X! m; q5 t+ v  E
8 cm and a width of 2 cm. The glans penis was very well/ Z5 |3 j; I0 q1 E, c/ y" M" d
developed. The pubic hair was Tanner II, mostly around
6 b5 U. _. P0 D4 C, u5 N4 t540
. c, G( \' t0 g7 d- qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 j5 i& Y1 C" }& m# bthe base of the phallus and was dark and curled. The
; X. t5 _9 c/ Ktesticular volume was prepubertal at 2 mL each.1 [2 q' @% O& J1 J' F
The skin was moist and smooth and somewhat7 T; T# J: y+ E9 @
oily. No axillary hair was noted. There were no
6 A  s& [0 U; X9 n9 m4 K  habnormal skin pigmentations or café-au-lait spots.
5 A$ p3 {: U* X' M  r3 Z6 u5 {Neurologic evaluation showed deep tendon reflex 2+
. O) B! M  F9 u+ dbilateral and symmetrical. There was no suggestion
! s# M/ U' c& B! W9 c* aof papilledema.3 a, {' t, d" Y8 }- P$ D# a: B/ u- A
Laboratory Evaluation. K& I$ X& w% g& G
The bone age was consistent with 28 months by
- e0 L" ~/ x) N( dusing the standard of Greulich and Pyle at a chrono-
" j1 Z+ A3 A" s: O1 Y: Xlogic age of 16 months (advanced).5 Chromosomal* p7 U1 j1 ]# g  |% W: M- b! m
karyotype was 46XY. The thyroid function test
; j" f( ?* t3 l2 kshowed a free T4 of 1.69 ng/dL, and thyroid stimu-$ P" ^7 p& b  _" e5 d4 G: a
lating hormone level was 1.3 µIU/mL (both normal).
9 X9 j: I( v+ Q2 y7 uThe concentrations of serum electrolytes, blood
0 k; a# a( D6 Nurea nitrogen, creatinine, and calcium all were& b; D+ q# v: I! t9 t5 ^9 p
within normal range for his age. The concentration  U; r& ]' G$ b
of serum 17-hydroxyprogesterone was 16 ng/dL  d8 c. M5 s+ A
(normal, 3 to 90 ng/dL), androstenedione was 20) S* @: v7 Y* p4 e  _7 C* J
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-; x# k8 W. W5 m, H# s2 ?; F8 B
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
! I9 T6 S7 G; B- X& ydesoxycorticosterone was 4.3 ng/dL (normal, 7 to  X. C/ e3 z9 @7 N, {: J9 Q" J
49ng/dL), 11-desoxycortisol (specific compound S)- R( E( o  N( i& R
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-6 c2 x% w; S& D
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
- l8 R: ]1 M$ C+ dtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
7 [5 Y$ ~+ r& Z) c# ?and β-human chorionic gonadotropin was less than% Y2 i4 X9 \9 k! c4 ^0 O
5 mIU/mL (normal <5 mIU/mL). Serum follicular; {8 r3 s" w% c- S9 d4 C, P% U
stimulating hormone and leuteinizing hormone4 U6 E2 d4 L4 W& Z) W
concentrations were less than 0.05 mIU/mL/ r6 U! l8 q+ ~1 M8 Q6 n7 t
(prepubertal).
& A' W1 t3 L2 o0 gThe parents were notified about the laboratory& @2 Y/ F' Q. N& K# D2 K$ q
results and were informed that all of the tests were
) {. |1 K, ~* \0 O4 Snormal except the testosterone level was high. The" @, I$ J" l4 ~6 T' o2 t3 L& m6 h
follow-up visit was arranged within a few weeks to- S" k% h/ p2 N2 P: L' R+ q* e" I
obtain testicular and abdominal sonograms; how-
0 u1 P) r. N% E! {ever, the family did not return for 4 months.0 e- j( F* t. i0 {2 R4 l
Physical examination at this time revealed that the
6 y& y3 R7 K: X) _/ \; {3 Cchild had grown 2.5 cm in 4 months and had gained' {* R; r/ ?0 ?" q( C# o" m% n
2 kg of weight. Physical examination remained
6 z  u; C, Z* n3 v9 @5 Z* {unchanged. Surprisingly, the pubic hair almost com-# o6 F- w/ i4 v2 h8 J& w# C0 c- L
pletely disappeared except for a few vellous hairs at5 w0 |4 M' G# z0 l
the base of the phallus. Testicular volume was still 2# \+ P! k; \- @
mL, and the size of the penis remained unchanged.2 S+ [" {; y; c1 I
The mother also said that the boy was no longer hav-, F0 K& g4 T7 u8 H( V7 l
ing frequent erections.
/ }. ?& o- l6 P3 X; g# MBoth parents were again questioned about use of
) {2 Y' R- ?- ?7 l2 Sany ointment/creams that they may have applied to
7 j/ u2 }9 V5 p+ ~3 q1 bthe child’s skin. This time the father admitted the4 W9 z1 H4 k. q. k) ^8 q
Topical Testosterone Exposure / Bhowmick et al 541$ w  X# N0 [: J3 d
use of testosterone gel twice daily that he was apply-
4 W+ t7 u2 J+ g2 X" T" n8 ring over his own shoulders, chest, and back area for8 S; x6 t! X! [* \# f
a year. The father also revealed he was embarrassed9 R2 {9 N: J# Y9 d9 e; o) f2 a, i  y0 I
to disclose that he was using a testosterone gel pre-
2 G* g' j2 W6 Q) wscribed by his family physician for decreased libido( ]" B& {$ L: S, w# t- t! P. y+ R
secondary to depression.
, y# G- ~0 E7 o5 r" WThe child slept in the same bed with parents.' ^$ j# o0 h  c) o
The father would hug the baby and hold him on his3 J; x  q" ~( M5 i3 t4 e! v9 _
chest for a considerable period of time, causing sig-* |, e& X. i$ X# @
nificant bare skin contact between baby and father./ h! Z3 h: ?, r; O
The father also admitted that after the phone call,3 s, `, p% Y! u3 c# _" x' r( \4 ]
when he learned the testosterone level in the baby% l- o+ s( g& X0 W2 j$ a
was high, he then read the product information# f# K  V, ^1 p1 N7 V
packet and concluded that it was most likely the rea-
$ P/ a# v4 M# _9 c  Yson for the child’s virilization. At that time, they
3 C1 P6 f! j; L6 Mdecided to put the baby in a separate bed, and the
2 l5 F( ?* X  p- ofather was not hugging him with bare skin and had
# j( W) x: H6 Ubeen using protective clothing. A repeat testosterone
. q) t: _" V: ~3 F; ^/ @4 Z* ]test was ordered, but the family did not go to the
/ O7 m* o0 e* ?$ B$ x. elaboratory to obtain the test.
9 m2 a8 N2 K2 o' H# pDiscussion. e# G) a8 E0 `; U- @, h1 _
Precocious puberty in boys is defined as secondary
; s/ d* K9 n" |sexual development before 9 years of age.1,4
. g- U* o% F$ U6 a- |" |Precocious puberty is termed as central (true) when
6 M2 m7 ~# {& r  }  l: n. Tit is caused by the premature activation of hypo-
- c5 M* Y( h, A8 ithalamic pituitary gonadal axis. CPP is more com-* F9 s' ]. G5 o) Q7 p% ]$ f
mon in girls than in boys.1,3 Most boys with CPP1 z: {7 s* w% X! R$ _7 k8 ]
may have a central nervous system lesion that is7 O/ U: ]7 S1 \1 R
responsible for the early activation of the hypothal-
2 m( O0 ?$ ^- O  @amic pituitary gonadal axis.1-3 Thus, greater empha-
' q) |* r' D5 C$ \6 fsis has been given to neuroradiologic imaging in
# ^. O5 K5 |! u4 d) Aboys with precocious puberty. In addition to viril-1 X2 Y) f6 X: D2 O
ization, the clinical hallmark of CPP is the symmet-% n! K) O( `7 P1 u& i' i3 Q/ m5 Z' I
rical testicular growth secondary to stimulation by
5 k, \1 E' Y% ~, f" u! Pgonadotropins.1,3
' H  c5 n! D5 V, R( g( H; T0 l( XGonadotropin-independent peripheral preco-
- K. \' r7 p" O& Ocious puberty in boys also results from inappropriate' w' Q( n: e# C: M; [6 k
androgenic stimulation from either endogenous or& ^3 k( ~) C& O
exogenous sources, nonpituitary gonadotropin stim-$ C: o/ s4 d; ^3 R1 p
ulation, and rare activating mutations.3 Virilizing
- H9 G! D( S3 Dcongenital adrenal hyperplasia producing excessive2 c0 w' i, }$ b  `
adrenal androgens is a common cause of precocious
  o9 l& h- {) q* k* `puberty in boys.3,47 }  o( X  i3 _( Z
The most common form of congenital adrenal! h% I  m$ ?6 l! ^# P) b7 R
hyperplasia is the 21-hydroxylase enzyme deficiency., I6 v  T+ G& i$ }6 j: O
The 11-β hydroxylase deficiency may also result in
& ^" p9 {. R! D. g5 W, L, z/ Hexcessive adrenal androgen production, and rarely,% {6 Y' _* A: `: P4 u# }" C
an adrenal tumor may also cause adrenal androgen: w4 y% z- D; L! z) |
excess.1,3* c2 P" @; ?5 W. |* Z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 V5 O& I+ M$ P
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
  h; M/ G4 y/ Q. @- J/ f3 x& \# P2 F6 mA unique entity of male-limited gonadotropin-
7 T2 D) T: ^, F; j* o& x: Sindependent precocious puberty, which is also known
5 i8 ~* `* `' p: k) h/ Uas testotoxicosis, may cause precocious puberty at a
2 K( n( q! [1 l8 Q" T" `very young age. The physical findings in these boys/ S# o- G; j  g0 d, t. ]- \
with this disorder are full pubertal development,$ n4 d0 `7 ?/ Y  H6 o. {3 n
including bilateral testicular growth, similar to boys
( M9 T! H1 U# D  ^& M: mwith CPP. The gonadotropin levels in this disorder3 C5 C) v; n1 K, x
are suppressed to prepubertal levels and do not show/ j9 T9 A  G; B
pubertal response of gonadotropin after gonadotropin-! L1 \" Q; `- B) r- }
releasing hormone stimulation. This is a sex-linked
. Y$ u- A( h+ hautosomal dominant disorder that affects only/ M' v% p+ R/ }4 n$ v( w" a
males; therefore, other male members of the family
/ [+ Z7 r4 P, V7 J- ^& `; O8 i0 S: m' n; Mmay have similar precocious puberty.3
  _" S. y- P  QIn our patient, physical examination was incon-
# y& W7 j; g/ Ksistent with true precocious puberty since his testi-
) k+ ?6 I$ D' H  m1 A9 r' M) ^cles were prepubertal in size. However, testotoxicosis/ C* P& d3 s- C! G7 X7 F
was in the differential diagnosis because his father
3 D$ o: s: M8 V! ]; s/ O' Wstarted puberty somewhat early, and occasionally,
; P% l+ n  u- D$ L( \! {4 n" Btesticular enlargement is not that evident in the
- I* `) _: u% c* B+ ^beginning of this process.1 In the absence of a neg-
: u; r8 O! p6 V) }6 lative initial history of androgen exposure, our! q# {, H- o8 X7 C3 V
biggest concern was virilizing adrenal hyperplasia,5 r- J. h, d, W! i% l! e9 n
either 21-hydroxylase deficiency or 11-β hydroxylase
$ T4 y' x: n5 I2 c5 F. Z# odeficiency. Those diagnoses were excluded by find-
9 s/ i" n4 S' h4 v- G2 J* Ging the normal level of adrenal steroids.
  w6 O5 @' g- m% N& KThe diagnosis of exogenous androgens was strongly4 o2 s" ]8 J( m9 S$ y3 W
suspected in a follow-up visit after 4 months because( E$ w4 Y( x8 S& `, J2 e
the physical examination revealed the complete disap-" ?: A7 |' |! F8 |" b
pearance of pubic hair, normal growth velocity, and
! L" k. w1 u2 j# r' Rdecreased erections. The father admitted using a testos-
) `4 Z5 q- ?. h  {terone gel, which he concealed at first visit. He was4 U3 I- ?; n$ S! @. W
using it rather frequently, twice a day. The Physicians’
! b  q7 }# J# H+ e3 tDesk Reference, or package insert of this product, gel or
9 B1 b6 X" f* h+ [9 X5 p+ ]cream, cautions about dermal testosterone transfer to# p4 W' h8 y6 s- \
unprotected females through direct skin exposure.
6 j' v& k9 K/ T3 O" n  zSerum testosterone level was found to be 2 times the, ^, r' }6 Z. A7 r' M/ }. j* S1 K7 `
baseline value in those females who were exposed to$ y& p  F& J2 u) ?: A- }; _
even 15 minutes of direct skin contact with their male
: ~4 c3 f1 E- ?) Cpartners.6 However, when a shirt covered the applica-
* D# j% h2 `' e' r5 Ttion site, this testosterone transfer was prevented.+ k* C  ]& C. n4 t* w, x
Our patient’s testosterone level was 60 ng/mL,0 r2 ^/ t8 h3 e& o& ?, S
which was clearly high. Some studies suggest that
) k; |" e; C! p/ a8 `. n3 V0 [dermal conversion of testosterone to dihydrotestos-7 j: F7 b9 V4 n% Y, t3 V
terone, which is a more potent metabolite, is more
7 G' @6 i5 f. h4 A$ \: tactive in young children exposed to testosterone5 W) q* G4 [. B
exogenously7; however, we did not measure a dihy-: n' j% Q: G* Y2 \. \7 ?" Y
drotestosterone level in our patient. In addition to8 f4 k5 W+ e. F( Y( m0 N7 C
virilization, exposure to exogenous testosterone in$ Y# k! u1 D& s1 x
children results in an increase in growth velocity and
' {6 n+ f* A2 d0 m. M: L8 Madvanced bone age, as seen in our patient.
3 k# ^9 v3 D1 f/ K' eThe long-term effect of androgen exposure during* _, x# t) t# D; e# K5 W
early childhood on pubertal development and final
8 u' k9 X+ b) \adult height are not fully known and always remain% B2 T9 D+ y5 J' r& a' R
a concern. Children treated with short-term testos-9 u) U. Q3 P0 v" u1 l' v
terone injection or topical androgen may exhibit some% J1 M8 T- T- I  M! ?0 Y* J
acceleration of the skeletal maturation; however, after5 |: |( M# Y, s, ]$ M- C6 S
cessation of treatment, the rate of bone maturation
7 i' S3 _4 w- hdecelerates and gradually returns to normal.8,9# o0 X5 R7 U# s5 p4 ~
There are conflicting reports and controversy, R, L- z- P1 k7 W5 g$ f5 d
over the effect of early androgen exposure on adult4 h. p6 n( C! y* [- t
penile length.10,11 Some reports suggest subnormal! X* B) J  F2 k
adult penile length, apparently because of downreg-
# B  J, C% k- H) @! b! }5 Qulation of androgen receptor number.10,12 However,8 _# x; N" o' O  P! ?( f7 M" z
Sutherland et al13 did not find a correlation between
) ~+ p+ H: ]* c$ m; C: X: P8 kchildhood testosterone exposure and reduced adult
" A  A8 l; g% E! o# Lpenile length in clinical studies.: H. b6 A$ d: W4 u1 p2 ~
Nonetheless, we do not believe our patient is( F, ^2 n# R- K: C. X9 G
going to experience any of the untoward effects from, G3 Z% T2 v4 m* d
testosterone exposure as mentioned earlier because
5 h+ R2 o: b; s$ E1 Rthe exposure was not for a prolonged period of time.7 S5 n+ r/ q4 A9 t& ~6 w
Although the bone age was advanced at the time of
% ~2 h" N$ {" N  sdiagnosis, the child had a normal growth velocity at3 W8 f& q4 l) O! X* O
the follow-up visit. It is hoped that his final adult
& k) J7 ~) B% X# y- A8 zheight will not be affected.! T, E: a" i$ |: m" M' q
Although rarely reported, the widespread avail-+ y0 y, N5 U3 ]* }5 ?) s1 B7 w
ability of androgen products in our society may, S$ h3 U  d/ z1 w
indeed cause more virilization in male or female
4 R; f; L/ K! A5 ?( _2 B& v3 Tchildren than one would realize. Exposure to andro-
- D3 B- b8 G: A- b7 Ogen products must be considered and specific ques-
7 h/ C* j% d! s: vtioning about the use of a testosterone product or, K# F: _& y3 y
gel should be asked of the family members during
( b, w5 V' D0 `8 b/ P; I) fthe evaluation of any children who present with vir-
7 w9 x/ n# T+ n- I6 H1 p) \/ Hilization or peripheral precocious puberty. The diag-& _4 _. q1 Q% O6 p
nosis can be established by just a few tests and by: c& Y, i/ u, h2 \. w0 {* [
appropriate history. The inability to obtain such a# D2 Q# ?  E8 a4 C. m( c
history, or failure to ask the specific questions, may
4 I1 r, _) S0 x' m( b& W1 g1 cresult in extensive, unnecessary, and expensive
2 b* o/ M8 |" H* _2 r) O8 Oinvestigation. The primary care physician should be
" i, I# u5 X1 l9 P3 q$ c, uaware of this fact, because most of these children
. D! @' l7 ?2 `' `9 Zmay initially present in their practice. The Physicians’5 c4 g% v4 ~3 Z. x
Desk Reference and package insert should also put a; d  R. n8 C' @- A9 y) c" o
warning about the virilizing effect on a male or
1 H6 h0 T. X0 Z( J5 tfemale child who might come in contact with some-
  N7 o' M! q! ^' Ione using any of these products.6 ?' H$ T; q) ?7 G
References
8 ?) K3 o. |* ]! W" Q& x1. Styne DM. The testes: disorder of sexual differentiation
7 }( K( C4 Q4 ?  v5 D& `and puberty in the male. In: Sperling MA, ed. Pediatric
5 B+ i0 O- d! uEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;' p# _) p) u7 x! r" w$ _/ ?
2002: 565-628.
: c3 }4 ~9 [1 L$ E# X( l. g. [+ f2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious' B' [9 g  h2 I7 [) j6 y2 {
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
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
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
; H4 H- @/ J, G: M. Z* [
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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