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Sexual Precocity in a 16-Month-Old
  k% H8 T6 t9 i( |2 W) qBoy Induced by Indirect Topical
/ f5 ^+ i8 p; t0 h6 zExposure to Testosterone
) b' m+ d7 Q1 A1 b. hSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
$ T! d3 Y0 K. U  X. T$ n# ^# Iand Kenneth R. Rettig, MD1
( o, [8 v) K, Y; x8 Q. c" PClinical Pediatrics
- _5 `# |5 r9 @- }" fVolume 46 Number 6
+ j6 J4 m2 R' T& f. {" o/ S* UJuly 2007 540-543: O, v8 v& e5 W8 t1 S, x
© 2007 Sage Publications
5 S! I8 `+ c# z! `6 S2 Z% x% z# m10.1177/0009922806296651. F; f- o( ~" j  t
http://clp.sagepub.com
" D" j8 w2 K' {  ]; o& I. dhosted at
5 W& j3 H# e3 |7 R* @3 |http://online.sagepub.com
+ C0 L* t* C; P; N7 MPrecocious puberty in boys, central or peripheral,, v- T" e# _3 e. n' ^3 W9 ?, b* t9 G
is a significant concern for physicians. Central7 \( r7 r1 i& `5 m" |1 L
precocious puberty (CPP), which is mediated
% }! ?2 M# a* gthrough the hypothalamic pituitary gonadal axis, has
) ?- g  X7 R# j, ca higher incidence of organic central nervous system
9 D% O7 y  t5 _; I" Ulesions in boys.1,2 Virilization in boys, as manifested
* x* b3 q0 v* j. |! Z! u7 nby enlargement of the penis, development of pubic( ^# f/ C: M# i8 t
hair, and facial acne without enlargement of testi-& T% n* Z9 Q. \/ u: I5 L1 V9 [
cles, suggests peripheral or pseudopuberty.1-3 We
+ l& p2 u/ W7 u9 {8 c2 c2 Ureport a 16-month-old boy who presented with the
9 W6 v/ u7 u( g' Y0 benlargement of the phallus and pubic hair develop-
2 u# j. f2 v9 J) X1 }; f; ]! Iment without testicular enlargement, which was due
4 k/ q3 F+ a7 \% ato the unintentional exposure to androgen gel used by
, I6 @5 M7 b/ g; x" L; i0 o0 z& ethe father. The family initially concealed this infor-
& e( H+ ]5 \- H% l8 @mation, resulting in an extensive work-up for this
) a& v' v# O2 w7 gchild. Given the widespread and easy availability of  J  z9 m, x; T7 ]) m: x
testosterone gel and cream, we believe this is proba-, e/ z1 Y& q2 z4 ]: e5 a' w
bly more common than the rare case report in the
8 M7 e: P5 u& pliterature.4
" y* g( @) m* C3 P: SPatient Report; T8 K4 h, |6 h' n+ `# U; j
A 16-month-old white child was referred to the5 ?7 ?4 q: r5 @- u, H0 U1 z# h. E
endocrine clinic by his pediatrician with the concern
! i& ]: q. o/ Aof early sexual development. His mother noticed
& [7 ]. f  F2 Z9 `+ @/ @- plight colored pubic hair development when he was. n, P) p1 }2 _8 K! Y& Z: g" `0 I$ k
From the 1Division of Pediatric Endocrinology, 2University of
, j1 I9 D3 s# S* g' {4 \4 N9 KSouth Alabama Medical Center, Mobile, Alabama.
) S5 q+ D# V6 V2 ^# Y3 nAddress correspondence to: Samar K. Bhowmick, MD, FACE,
5 t( `. W0 }0 w5 P) ^Professor of Pediatrics, University of South Alabama, College of) J6 {5 e) Z# I1 H# }5 E
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
2 a% L% P  o$ He-mail: [email protected]./ b- r8 g6 B1 V
about 6 to 7 months old, which progressively became# F( A1 b" A" \- ^! b2 W
darker. She was also concerned about the enlarge-/ ?) `, S" Y0 v
ment of his penis and frequent erections. The child& T" m# G0 ~. \, D
was the product of a full-term normal delivery, with8 C* M' J* }% I# N0 p
a birth weight of 7 lb 14 oz, and birth length of3 W% g' i' b( N- w* V( F
20 inches. He was breast-fed throughout the first year/ V5 V; X, j5 c. J
of life and was still receiving breast milk along with- {" o( r" P0 ?. g% ?
solid food. He had no hospitalizations or surgery,' P8 G: `3 O" n- m/ ]5 g
and his psychosocial and psychomotor development
& E5 r0 l- p! R3 R& Twas age appropriate.7 @% ~' E4 U1 N% S6 ?. {! U
The family history was remarkable for the father,
' V- J2 n! F# }) |! cwho was diagnosed with hypothyroidism at age 16,
, K  H' F4 G( s3 r3 |which was treated with thyroxine. The father’s
, Z2 Y" p" r! v# O3 e% F' [height was 6 feet, and he went through a somewhat6 D! A3 e$ k3 {& |" z' H  v
early puberty and had stopped growing by age 14.
9 O) ^: R7 ?/ ~+ _6 {# yThe father denied taking any other medication. The
- U& Z' J* @% T: L! schild’s mother was in good health. Her menarche
# x2 |$ a! |+ p, d& b) b8 a4 r' [was at 11 years of age, and her height was at 5 feet
  T! n% Y8 K4 V. F0 _5 inches. There was no other family history of pre-' J* z" p0 a" {8 X! b* |
cocious sexual development in the first-degree rela-
4 [( l% ~; r& D. qtives. There were no siblings., ?7 v5 J2 F: |0 f, y
Physical Examination1 q8 ?3 n# @. ], m# n9 B$ i
The physical examination revealed a very active,
: r- Q  b# d+ C" z& r& @playful, and healthy boy. The vital signs documented3 v8 [3 ]3 e" h4 O1 q3 |* r
a blood pressure of 85/50 mm Hg, his length was6 c! ^* Z8 Z, O
90 cm (>97th percentile), and his weight was 14.4 kg; }/ `& G2 s' B2 m- X7 V
(also >97th percentile). The observed yearly growth4 X' e* z% V* s( k
velocity was 30 cm (12 inches). The examination of
/ o! A7 ^# N) }1 ^( K- F* }the neck revealed no thyroid enlargement.+ o" I5 J. ?# r; J3 j
The genitourinary examination was remarkable for
( c5 s$ a# |- e. Q. \* ^. Renlargement of the penis, with a stretched length of
1 {7 F% Y7 {$ d$ C$ T2 ]8 cm and a width of 2 cm. The glans penis was very well
4 r- G6 A# D5 r$ E" h# A5 [' Odeveloped. The pubic hair was Tanner II, mostly around
1 s; A6 j# e+ x8 d! @540
; t9 c1 R" g# D/ V. `at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) I! d( b! w3 ]! ~6 J0 K3 h
the base of the phallus and was dark and curled. The" h6 s. v- Q0 D& O& K
testicular volume was prepubertal at 2 mL each.
/ ~4 \- R5 U1 r5 w" ~7 F: @The skin was moist and smooth and somewhat* i9 P. O4 m, w: u9 g/ k0 H" W- o3 v
oily. No axillary hair was noted. There were no
- c( t% u+ j: V& r! d. ?' l7 Zabnormal skin pigmentations or café-au-lait spots.
9 o# \* h8 `; Y" f( RNeurologic evaluation showed deep tendon reflex 2+( w! M3 X  ^6 j( z3 T
bilateral and symmetrical. There was no suggestion
" N" \( D+ @4 c! G/ Zof papilledema.% t+ O* l3 X9 O7 G) D
Laboratory Evaluation
- d* y+ s5 a- rThe bone age was consistent with 28 months by, Q9 w7 z* b; y1 Y( @
using the standard of Greulich and Pyle at a chrono-* P) [. x9 B* Z) [  T* a' _9 k; Q
logic age of 16 months (advanced).5 Chromosomal+ _( @! r( I. z; B. ]9 X
karyotype was 46XY. The thyroid function test% h' h; `/ X3 h1 I' n
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
% x- Y$ }" d* k$ j# O8 r: r% Q* y$ k' Wlating hormone level was 1.3 µIU/mL (both normal)." G" F5 a' i; \. W1 ?) O- m3 o( V
The concentrations of serum electrolytes, blood3 V, t5 t3 s. m  w
urea nitrogen, creatinine, and calcium all were
7 D7 R+ F+ u3 z, nwithin normal range for his age. The concentration
2 s. P. z3 R. _; Sof serum 17-hydroxyprogesterone was 16 ng/dL
/ |( @2 Q3 f; n2 i1 Z# @(normal, 3 to 90 ng/dL), androstenedione was 20
) ~" z. Q+ p! s8 T6 Mng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
& ~0 D. Z* O! Y# Q. C: pterone was 38 ng/dL (normal, 50 to 760 ng/dL),
+ x8 o1 G6 a# q% ?- t0 o8 L& bdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
/ H% S8 D+ G" {# g0 Z0 z2 U49ng/dL), 11-desoxycortisol (specific compound S)' ]0 q* K7 @' k# L; r
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-  J6 t! T4 s, }+ w; P9 l; ?
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total1 K# s7 F" |( N& t  g
testosterone was 60 ng/dL (normal <3 to 10 ng/dL)," `0 c, d# `& P# c& W" v3 {4 _
and β-human chorionic gonadotropin was less than
" j7 ~  ]; g! p( c5 mIU/mL (normal <5 mIU/mL). Serum follicular
5 Z" }; j% t, o) y# Vstimulating hormone and leuteinizing hormone9 M* m- r" Z/ I  u
concentrations were less than 0.05 mIU/mL
! K5 }9 }6 Y4 X; D  i7 p4 [(prepubertal).
  g5 z7 d; E/ R4 wThe parents were notified about the laboratory
, p- J  K: C8 L" v8 \; u1 P, uresults and were informed that all of the tests were
- N  }/ W3 e: m- Onormal except the testosterone level was high. The0 @  X/ z6 k5 O5 M% {" e, S( `
follow-up visit was arranged within a few weeks to1 j+ g/ N4 T3 ^/ W) k
obtain testicular and abdominal sonograms; how-
$ D" P* ]) I8 O2 {( Xever, the family did not return for 4 months.
9 P+ A" [4 W3 ?! TPhysical examination at this time revealed that the8 s5 W9 k. x# D. g
child had grown 2.5 cm in 4 months and had gained
( U5 z) @- _( H$ `2 kg of weight. Physical examination remained
/ g( {( X5 I  E& N, e! r5 eunchanged. Surprisingly, the pubic hair almost com-
4 Q+ R1 {% q4 \* Q9 Npletely disappeared except for a few vellous hairs at, O6 _2 o8 _0 i9 f
the base of the phallus. Testicular volume was still 2- u/ }* j& h& z! n( y+ ]) |
mL, and the size of the penis remained unchanged.
- o# W9 F# W0 |- bThe mother also said that the boy was no longer hav-$ V' J& B2 w' i/ D
ing frequent erections.
, _3 V8 P2 Z! k: B' VBoth parents were again questioned about use of
* e& P, ~; L! Pany ointment/creams that they may have applied to+ C/ J, n; [+ X% A% J
the child’s skin. This time the father admitted the" S  o+ w$ ~+ J4 g
Topical Testosterone Exposure / Bhowmick et al 541, X; ?7 z6 Z* W; J/ ^& g0 y! j* ?& }
use of testosterone gel twice daily that he was apply-
* O: o, m! J# K: C9 j1 Fing over his own shoulders, chest, and back area for6 B% I* i  {& }5 h: d0 n5 n
a year. The father also revealed he was embarrassed; X0 D5 X5 p  @5 J) g' X+ ]
to disclose that he was using a testosterone gel pre-0 f& Q3 X- c$ q2 k+ p% c
scribed by his family physician for decreased libido- d! M( X' ^# a$ S2 w* J
secondary to depression.3 V- K3 l: X4 H9 x; e+ E5 Y( Z
The child slept in the same bed with parents.
) l0 _, p9 X( t* V) {The father would hug the baby and hold him on his, F! u& e+ I& Q" r
chest for a considerable period of time, causing sig-# W6 k1 ?5 |; B& b
nificant bare skin contact between baby and father.
1 r0 c7 j% x6 x# V6 Q0 T; n0 pThe father also admitted that after the phone call,& b3 ^, V! x8 J/ E  r
when he learned the testosterone level in the baby  q1 q$ y7 }3 u& w$ E
was high, he then read the product information$ \) M# I$ l7 ?1 ^. s% _
packet and concluded that it was most likely the rea-
" p4 T+ \( T( b. Uson for the child’s virilization. At that time, they$ y" k% T$ {5 _' t) i8 l( g
decided to put the baby in a separate bed, and the
* j' u$ p0 F! v1 q, Dfather was not hugging him with bare skin and had( N" ^2 @' [7 L- g6 ?, i' |
been using protective clothing. A repeat testosterone
6 a6 X) @& B& f. y/ U, D3 Ztest was ordered, but the family did not go to the
$ J$ v- l8 E0 Y2 ]: O2 v  F9 slaboratory to obtain the test.' Y  d$ {- u" Y' _, B( G4 r. C
Discussion) T, T5 C* C. v& [
Precocious puberty in boys is defined as secondary4 G7 D- f5 @6 J* x3 r
sexual development before 9 years of age.1,4( F1 j/ l& M# @4 R
Precocious puberty is termed as central (true) when9 |2 ?2 h& h) d$ j/ k
it is caused by the premature activation of hypo-
4 [7 }8 I) {5 ~8 e( c4 L0 Fthalamic pituitary gonadal axis. CPP is more com-4 O- ^% ^, _7 E$ b8 Y
mon in girls than in boys.1,3 Most boys with CPP8 @! x$ Q' h1 p1 m6 H( j9 }
may have a central nervous system lesion that is! s9 W: M( I3 r/ U
responsible for the early activation of the hypothal-# O4 m4 a' k, U4 O
amic pituitary gonadal axis.1-3 Thus, greater empha-9 w' ^) Q5 j$ N2 r! m3 O
sis has been given to neuroradiologic imaging in1 e2 M2 A" F1 D8 c) ~$ U5 L
boys with precocious puberty. In addition to viril-
% C: y2 T0 Y& k( e" c& F- Y* xization, the clinical hallmark of CPP is the symmet-
# x  x7 K8 x) V6 _rical testicular growth secondary to stimulation by
( H& v) _4 Y) |3 S. Z+ Lgonadotropins.1,3) Z$ p5 E1 u7 r
Gonadotropin-independent peripheral preco-5 z; ]; a! B3 a5 @0 m# Z
cious puberty in boys also results from inappropriate/ `1 t% d* m7 _% f
androgenic stimulation from either endogenous or3 N( u% P, c; [2 r! D& F
exogenous sources, nonpituitary gonadotropin stim-
$ {% f" M1 y8 Lulation, and rare activating mutations.3 Virilizing' @( m7 c8 m$ X8 p* I3 h2 `* {0 i
congenital adrenal hyperplasia producing excessive  I: W, M5 p+ `2 B( \
adrenal androgens is a common cause of precocious
- O$ ~4 C7 p( C" Y% k* z$ kpuberty in boys.3,4
+ d& s, c; f% i1 sThe most common form of congenital adrenal
/ A9 J; S7 d( F( ?hyperplasia is the 21-hydroxylase enzyme deficiency.
* i1 D7 b( V0 ]9 f! I* MThe 11-β hydroxylase deficiency may also result in5 h2 g# p; z) F% h1 P
excessive adrenal androgen production, and rarely,4 |+ L0 o, G4 G! \( p7 S0 V' y& Y% y
an adrenal tumor may also cause adrenal androgen) ~' x5 f2 R# U7 }# h5 y
excess.1,31 n+ R* i) Y$ U8 @+ y* F/ y
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 a/ p/ k" L& o5 x/ W. H4 A8 N( c542 Clinical Pediatrics / Vol. 46, No. 6, July 2007/ V0 ^- Q+ Q. [- k9 b2 W3 ?
A unique entity of male-limited gonadotropin-
  i/ ]( ~* I, F% ?- i8 bindependent precocious puberty, which is also known: K5 a1 ^% [% \7 Q# O4 Q2 }4 m
as testotoxicosis, may cause precocious puberty at a" T2 H+ u, _/ Y7 z  x" T" B
very young age. The physical findings in these boys9 ]: H# s4 j( O; t/ j
with this disorder are full pubertal development,( R. ]* u& R' }& g: s$ N' C
including bilateral testicular growth, similar to boys  @1 p2 l) g- a# L. w# }# }
with CPP. The gonadotropin levels in this disorder
( F; O2 b6 l/ V* F" X- [are suppressed to prepubertal levels and do not show, x! [; \& v3 b  B" S
pubertal response of gonadotropin after gonadotropin-% f- ^% Z  C9 \6 s0 I& h
releasing hormone stimulation. This is a sex-linked' J; U  j; G. M# }$ E* h, ]
autosomal dominant disorder that affects only
  y4 N# g* A  ?1 z6 C, D- qmales; therefore, other male members of the family0 c- C1 c% v9 {
may have similar precocious puberty.3
7 Y4 j  V( m$ m9 G: J1 nIn our patient, physical examination was incon-3 K* }$ J6 Q. ?& }7 `" }6 h
sistent with true precocious puberty since his testi-9 l4 N6 Y/ o; C. ]3 n$ K) ]3 E: T
cles were prepubertal in size. However, testotoxicosis
4 {) q  f6 o6 d3 Q6 [' M5 hwas in the differential diagnosis because his father9 U  B3 M8 a0 W3 G/ F
started puberty somewhat early, and occasionally,
; T0 U3 V/ ]2 v5 e3 U. wtesticular enlargement is not that evident in the
7 O8 F! c$ l( N; w/ S( u% E0 sbeginning of this process.1 In the absence of a neg-
: ]5 h% o6 ]; F3 Uative initial history of androgen exposure, our
0 d+ m6 ~+ i( b. ebiggest concern was virilizing adrenal hyperplasia,
- B9 H- H9 @% ieither 21-hydroxylase deficiency or 11-β hydroxylase1 g, c+ c6 z7 V+ ?! v
deficiency. Those diagnoses were excluded by find-, s3 z, u3 j4 J$ l! S4 V% S
ing the normal level of adrenal steroids.
" ]* ^1 P1 U, T; P9 z' ?- dThe diagnosis of exogenous androgens was strongly8 J; J' v3 W' l" C6 [2 V' ?$ B1 A% ]
suspected in a follow-up visit after 4 months because8 h2 q7 N0 X; J" s0 @8 g2 t
the physical examination revealed the complete disap-
# N0 P7 o6 ^* A4 N$ Y5 W$ Rpearance of pubic hair, normal growth velocity, and
' \  A7 Y& o$ f9 S: t3 L. mdecreased erections. The father admitted using a testos-
2 y# N6 n! P: d8 @9 n$ M; d9 tterone gel, which he concealed at first visit. He was
- p# m, c1 H6 a" J# P  x4 Vusing it rather frequently, twice a day. The Physicians’/ y9 \% i8 c2 G4 Z/ Q
Desk Reference, or package insert of this product, gel or7 U' g5 T* |$ ?
cream, cautions about dermal testosterone transfer to8 S( Y% ^3 P& l; z8 x
unprotected females through direct skin exposure.
- M2 o  p1 R, ySerum testosterone level was found to be 2 times the# X+ d) ^) D7 B' G4 p
baseline value in those females who were exposed to! p2 h/ y7 [  b$ [
even 15 minutes of direct skin contact with their male8 n! O1 p  t* o% Q4 W  z
partners.6 However, when a shirt covered the applica-
' W( p5 ^4 x$ O" H, h" j2 Jtion site, this testosterone transfer was prevented.0 E* ^& D% t; v1 ?: O  u' g5 I
Our patient’s testosterone level was 60 ng/mL,
& u" x7 o9 L/ G: N( |which was clearly high. Some studies suggest that
0 E+ i1 V/ f) S: v! n/ zdermal conversion of testosterone to dihydrotestos-
: n1 p/ @# E6 [# B+ {) ~7 ?. ?; e6 }terone, which is a more potent metabolite, is more
0 ~# W6 \1 ~' c' Q6 z# H7 gactive in young children exposed to testosterone
/ X* J5 b; u* D' K% ]+ U5 e1 X4 Fexogenously7; however, we did not measure a dihy-
+ F, N) J5 \) d: zdrotestosterone level in our patient. In addition to
# T% y' U! e* J2 z7 Ovirilization, exposure to exogenous testosterone in. g! B8 H; E# k$ w1 e7 c" p1 Y
children results in an increase in growth velocity and
1 N# c  u. _2 N- f+ o( ?  |. eadvanced bone age, as seen in our patient.
- V0 p: T" f: M& }' tThe long-term effect of androgen exposure during
8 F! p3 C  J$ A! L& x) t2 `early childhood on pubertal development and final
4 c& t( U$ A& padult height are not fully known and always remain" o# c1 \$ o  c  u' B# q/ V
a concern. Children treated with short-term testos-* E3 a8 P# {- `7 c( h
terone injection or topical androgen may exhibit some
- V9 U- `+ j  E0 }. b! g2 V, Jacceleration of the skeletal maturation; however, after
; l/ a. k& F7 I  Q4 R$ _cessation of treatment, the rate of bone maturation
) m0 J; Z4 }# |4 x8 d* t2 vdecelerates and gradually returns to normal.8,9% J& h7 a1 X+ `9 l* c$ j; j
There are conflicting reports and controversy3 J% l8 m: h+ s! a/ k  x; s. a+ O
over the effect of early androgen exposure on adult
- ]: J: Q* K& @3 L6 epenile length.10,11 Some reports suggest subnormal; l, A2 R" e" j
adult penile length, apparently because of downreg-% u. _0 ^7 J1 j' F% K
ulation of androgen receptor number.10,12 However,
, Y8 N$ _* D! Z7 l1 {Sutherland et al13 did not find a correlation between) U# c- j7 D1 G! E5 {( i7 D  @  h' l
childhood testosterone exposure and reduced adult5 Z/ V! R& R  a
penile length in clinical studies.5 ~% h  Y* b0 ]
Nonetheless, we do not believe our patient is
% z  r% H5 G" Q5 M" J$ |/ f0 Ogoing to experience any of the untoward effects from- U1 _" Y- N. i9 G
testosterone exposure as mentioned earlier because; K& o/ L2 l8 J+ x! T3 \
the exposure was not for a prolonged period of time.- d' c" G- d/ X
Although the bone age was advanced at the time of
, I' t. [7 r; v. cdiagnosis, the child had a normal growth velocity at
2 C& z3 B% g+ g  ethe follow-up visit. It is hoped that his final adult3 L& N, \8 H5 j% S
height will not be affected.$ S: t3 S9 N8 w6 x2 Q
Although rarely reported, the widespread avail-
: C$ T5 {% U6 e& r. d1 nability of androgen products in our society may. x! y* ]- o! R4 i) u
indeed cause more virilization in male or female
6 e4 S! D6 [: K" ^. Q+ Hchildren than one would realize. Exposure to andro-9 n. _) p& `% M: t5 G
gen products must be considered and specific ques-8 D# g3 u$ S0 u0 F$ E" M
tioning about the use of a testosterone product or" j" E  q0 S/ O5 s9 _
gel should be asked of the family members during. j. b* \( N7 u0 W& g( X2 i3 ~
the evaluation of any children who present with vir-
8 U6 C# Z9 r7 Eilization or peripheral precocious puberty. The diag-/ U/ Q( g! D9 q' Q' W4 T
nosis can be established by just a few tests and by
; {% Y, U+ `  ?# t: c1 fappropriate history. The inability to obtain such a
& r6 I2 E  x9 R. vhistory, or failure to ask the specific questions, may
# K0 t' L4 ]# ^- X7 A" r& y# k0 e" _result in extensive, unnecessary, and expensive' J2 G* e. V, Z' ^, @3 h$ F
investigation. The primary care physician should be
3 R. |& V0 B2 ?! |, H7 e. maware of this fact, because most of these children) R  l" U2 i, f1 a, y
may initially present in their practice. The Physicians’% j# X2 }+ b! C; Z; m; }4 L0 o
Desk Reference and package insert should also put a
( `, d4 L# S- f7 x& _; Vwarning about the virilizing effect on a male or4 q# D. |, _% R- q" }8 e
female child who might come in contact with some-
8 j1 @8 W8 Q7 o! sone using any of these products.) v' @4 {1 h$ M, ~% k, W7 S
References
- w$ R" e) k; f0 f( J1. Styne DM. The testes: disorder of sexual differentiation
9 f8 K. a1 V7 I$ A) Dand puberty in the male. In: Sperling MA, ed. Pediatric
7 W$ R  x4 z3 \; `5 P: h. \Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;- Q% U) g$ X& F. e+ ~+ F/ |
2002: 565-628.
8 I7 H9 E6 N4 ]9 j2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious& q- Y  e- @% B  Z: M7 V# l
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old- s8 I' c6 F  i" Y
Boy Induced by Indirect Topical/ I# O7 [) m& L7 c# [0 U
Exposure to Testosterone$ E" ]. f5 ]: x9 Z* R# d
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2  T" r: z$ Y4 ?6 |& I5 G6 d$ A6 a
and Kenneth R. Rettig, MD10 b/ r# c2 Y# e" @  m
Clinical Pediatrics
- _, J& S5 v) i, g5 |( h8 z' bVolume 46 Number 6
/ z# e$ V( s1 f% I* q- SJuly 2007 540-543
& {4 r1 n* \+ u- d; k© 2007 Sage Publications- J0 u; g. u; ?5 S5 F: |' O
10.1177/0009922806296651
8 _$ s# H/ X7 b. chttp://clp.sagepub.com- j6 x4 r0 g! D8 n4 l) I1 |
hosted at
4 P) W* }$ ?$ I( _http://online.sagepub.com
" }. G6 x4 o3 H5 q: y2 VPrecocious puberty in boys, central or peripheral,
5 l6 e! g% k* [5 b8 D$ N: fis a significant concern for physicians. Central& J+ e" B2 v+ O# |
precocious puberty (CPP), which is mediated! f$ I* ^. w6 U/ b0 v! F1 I5 |+ U
through the hypothalamic pituitary gonadal axis, has  i  w; x' d, ?6 Y/ |
a higher incidence of organic central nervous system5 ]5 \/ T, i' Z0 o% j+ T
lesions in boys.1,2 Virilization in boys, as manifested
7 U- k; C) c6 L* J8 j/ N) ]+ Nby enlargement of the penis, development of pubic, A. g7 A! |' {$ g3 p' }
hair, and facial acne without enlargement of testi-
  q0 y3 d2 _. [% J: Kcles, suggests peripheral or pseudopuberty.1-3 We
! p3 G- B$ _7 ?' H1 h/ s/ Freport a 16-month-old boy who presented with the% t! N4 x7 @8 [# K; A2 W, X, S0 h
enlargement of the phallus and pubic hair develop-
' j! R( s8 Y9 j) [ment without testicular enlargement, which was due  D' b* H# P- M+ f$ Y; F2 i
to the unintentional exposure to androgen gel used by* M$ o* M3 d$ f
the father. The family initially concealed this infor-6 X! w) q# \" \# w8 K% o; q
mation, resulting in an extensive work-up for this
6 C$ K& S( I: l$ Y! Y' Lchild. Given the widespread and easy availability of
  A* }4 x- `* E' r$ ]" B# ttestosterone gel and cream, we believe this is proba-# e# W6 R9 \3 a4 R! {5 h' u. B& }
bly more common than the rare case report in the$ G/ z8 T  _9 k% g1 F
literature.4, q3 E+ u* {4 ]4 e1 L- x6 w; L& p! O
Patient Report
* D3 X: L: j7 L8 }, R5 BA 16-month-old white child was referred to the* E. A1 L" ~1 M" W$ u0 Q* j; j8 P
endocrine clinic by his pediatrician with the concern' H' k6 p/ I+ j- [+ v8 g
of early sexual development. His mother noticed4 v0 p: E  d7 d/ _
light colored pubic hair development when he was
" k- T+ x& }1 I$ WFrom the 1Division of Pediatric Endocrinology, 2University of" F3 E. f, s4 \; z
South Alabama Medical Center, Mobile, Alabama.
3 h! w, ^6 N2 D2 I1 ~3 J8 r- qAddress correspondence to: Samar K. Bhowmick, MD, FACE,, v* L" D# J3 Z: ]( J; z) L
Professor of Pediatrics, University of South Alabama, College of6 S5 s8 a7 L" d0 u: s5 }
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
! O+ L# [: J4 \1 h* A6 n& P: Ne-mail: [email protected].. J4 W1 T/ S$ g8 A, H, {  ]: ]
about 6 to 7 months old, which progressively became- u! I0 {/ _& F# j" z$ h. V
darker. She was also concerned about the enlarge-, L0 U8 M5 s/ ]. Y, t
ment of his penis and frequent erections. The child8 h' i& ^- [/ R
was the product of a full-term normal delivery, with
. k/ c. Y8 k$ b& t5 Ua birth weight of 7 lb 14 oz, and birth length of8 ?2 d) a, Q& [4 y. I
20 inches. He was breast-fed throughout the first year
$ W5 v" M8 J1 g5 p5 p. |  uof life and was still receiving breast milk along with
7 H( {9 Q1 K' g+ R9 _9 Asolid food. He had no hospitalizations or surgery,+ [0 j% L5 q( I7 h; h
and his psychosocial and psychomotor development. \% \( ]6 Z# _
was age appropriate.
" U' p- _2 V1 d$ y0 E% {The family history was remarkable for the father,
5 e' q/ D$ s/ Mwho was diagnosed with hypothyroidism at age 16,9 b9 }* ^0 C7 a' q7 Y
which was treated with thyroxine. The father’s7 B- h! G% e/ Y# J
height was 6 feet, and he went through a somewhat
  m4 U0 T' x- L, ~3 e1 }) E$ Hearly puberty and had stopped growing by age 14.
2 S7 ~6 P0 D# ~3 _5 R. B- r  wThe father denied taking any other medication. The
3 ]0 r! m: [4 z3 Vchild’s mother was in good health. Her menarche# R) @; w! K1 Z. q
was at 11 years of age, and her height was at 5 feet
* u2 R  A0 o# H5 l5 inches. There was no other family history of pre-
7 V3 X2 y& c- Ccocious sexual development in the first-degree rela-0 P& U# b1 b/ i
tives. There were no siblings.1 _( W2 ~4 F" S9 u
Physical Examination
! \/ N( C/ ^3 i8 T& oThe physical examination revealed a very active,
4 U, f; d- k: c( X: j. tplayful, and healthy boy. The vital signs documented  o, u* d8 p; ^0 P
a blood pressure of 85/50 mm Hg, his length was' b6 z. U+ b; Y! F" ^5 a
90 cm (>97th percentile), and his weight was 14.4 kg8 c* k4 Q2 E- K# m9 R$ T
(also >97th percentile). The observed yearly growth
  C# V: D8 ?& G8 Qvelocity was 30 cm (12 inches). The examination of7 i: e3 G) K4 [8 d% G- }
the neck revealed no thyroid enlargement.
9 p9 i2 E/ [+ {" |4 k0 RThe genitourinary examination was remarkable for
& @" h# K# V# y. }; j4 b: b3 lenlargement of the penis, with a stretched length of0 L8 l/ `. O3 ~* _4 c5 a8 E
8 cm and a width of 2 cm. The glans penis was very well7 v! p; a9 d! ?, }9 n
developed. The pubic hair was Tanner II, mostly around
' f: N/ |0 D+ e( [' k540, z2 ^, Q: P$ Y: Q7 I
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, b: p# k) r8 U" J
the base of the phallus and was dark and curled. The8 \& S5 u6 k2 |  w* M* g5 P
testicular volume was prepubertal at 2 mL each.
" j# V5 F! v% t3 X' K0 ~5 IThe skin was moist and smooth and somewhat6 r4 K) k) C+ \4 L
oily. No axillary hair was noted. There were no8 P; w% I3 c) D9 ~
abnormal skin pigmentations or café-au-lait spots.6 q5 g$ _, B# |; r2 }% t
Neurologic evaluation showed deep tendon reflex 2+
( C9 Y# G, p/ k$ ^) i' _bilateral and symmetrical. There was no suggestion; y6 |1 |- H3 b, t0 a, u
of papilledema.
# A# Z5 o, W9 g% ]" pLaboratory Evaluation' Y+ d* D# @" T4 f5 E# v" e
The bone age was consistent with 28 months by* l) ~) c8 p) z# J# ^0 a
using the standard of Greulich and Pyle at a chrono-
- V$ J; i, B/ F' x. Ilogic age of 16 months (advanced).5 Chromosomal
3 w1 l" ^) g, y4 W( n) qkaryotype was 46XY. The thyroid function test
1 k5 }1 c! Q- d+ m* |3 [showed a free T4 of 1.69 ng/dL, and thyroid stimu-
, z' F; J8 ]2 s8 d) F/ P6 Olating hormone level was 1.3 µIU/mL (both normal).$ s% C- r& J4 p6 H
The concentrations of serum electrolytes, blood
: q9 V! P2 \* B9 C6 O; _urea nitrogen, creatinine, and calcium all were  K6 H1 t* [1 Q( w% K# E
within normal range for his age. The concentration
" D" ?  _" i& O) [% K6 v3 V% Pof serum 17-hydroxyprogesterone was 16 ng/dL
) I! |; V* F  X4 |; w) P(normal, 3 to 90 ng/dL), androstenedione was 207 M2 Z- A( i: [5 P
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
4 G3 a( f& Z0 t- Y+ _' Pterone was 38 ng/dL (normal, 50 to 760 ng/dL),; g" d- j' V6 H
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
5 W" M" l% ]9 v8 @, k  J- O0 y49ng/dL), 11-desoxycortisol (specific compound S)
" T. n- O9 w/ }7 _4 dwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-) ^- x* F8 G2 Y; q  k: Z
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total% \$ R$ b+ F1 {& \! m
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
. P0 D* }- b. Z; Xand β-human chorionic gonadotropin was less than
: B* v3 j  Z5 _5 mIU/mL (normal <5 mIU/mL). Serum follicular
) s! L6 z" G( |4 [4 x0 G) c1 C; `stimulating hormone and leuteinizing hormone
, R/ r& p! v. @0 @$ ]0 D4 hconcentrations were less than 0.05 mIU/mL9 K9 _- {- F* n" p4 e2 H
(prepubertal).
7 g/ z$ A& J4 t; DThe parents were notified about the laboratory
7 Q, Y3 K1 H3 J$ Q7 Q2 T% Jresults and were informed that all of the tests were
: k" A9 [6 I6 [) @normal except the testosterone level was high. The
  s- T" o2 m2 x3 v& ~follow-up visit was arranged within a few weeks to
% u. ]6 }/ [/ a5 F+ @6 qobtain testicular and abdominal sonograms; how-
8 x7 Y) m2 P% X: O6 u7 |ever, the family did not return for 4 months.
% t, ~8 o0 e; N; q) ]! APhysical examination at this time revealed that the9 m/ d0 k6 e: L5 p4 F( I
child had grown 2.5 cm in 4 months and had gained
$ l% h' X3 h1 J0 t0 p2 kg of weight. Physical examination remained* Z+ S" U" v2 w; d
unchanged. Surprisingly, the pubic hair almost com-% Z# [; f" l8 g$ r  u( \
pletely disappeared except for a few vellous hairs at
' ]9 H0 g" ^' y' X/ F( s. g$ m6 Qthe base of the phallus. Testicular volume was still 2$ M% q5 d4 F% q  Z. h  h
mL, and the size of the penis remained unchanged.
4 d6 C: T. s2 g! OThe mother also said that the boy was no longer hav-
5 e) z0 ~0 Y! r6 P) a+ Ming frequent erections./ p2 _+ J3 [# t8 ^
Both parents were again questioned about use of9 }, U9 C9 K$ Q6 ^* s* ^
any ointment/creams that they may have applied to
7 G2 w% w9 J1 s4 @- ?% G/ Rthe child’s skin. This time the father admitted the
$ }4 \/ R* ]( V' k) E0 ?Topical Testosterone Exposure / Bhowmick et al 5414 |7 G9 {% ^+ c- ~2 T2 L6 q  h
use of testosterone gel twice daily that he was apply-9 O4 x+ Q# ~( W0 F7 V' r5 B
ing over his own shoulders, chest, and back area for  v6 Z  j7 f  m: E; H
a year. The father also revealed he was embarrassed
, g5 p/ L+ D1 u( T! f0 fto disclose that he was using a testosterone gel pre-2 h3 A. A" f* s7 w$ r9 C( H
scribed by his family physician for decreased libido2 i, L0 K9 P- \  v) Y( I
secondary to depression.* t! Z& a, L" W- p, M- j6 O6 T- L
The child slept in the same bed with parents.
& J( w) N- ]7 vThe father would hug the baby and hold him on his/ g. z) k5 a% I; b
chest for a considerable period of time, causing sig-6 T3 n+ w* ~$ M! q6 K+ d3 R, h- L
nificant bare skin contact between baby and father.! U# t* T4 _! n) S) h* c, ^+ O( e
The father also admitted that after the phone call,
* i6 y; a$ j/ m' u, `) F! ^0 wwhen he learned the testosterone level in the baby" Z& k# ?. G) ]1 C8 t3 E
was high, he then read the product information
" i1 Y) }: k! Z6 x, Q8 Hpacket and concluded that it was most likely the rea-! d* l; ?9 X6 u4 t6 ^
son for the child’s virilization. At that time, they
; D( W% `- ^( v5 Sdecided to put the baby in a separate bed, and the, F! s0 d) u( N- f' W% N
father was not hugging him with bare skin and had
. A4 H+ l9 B' B% abeen using protective clothing. A repeat testosterone
% z0 }! J0 h+ H4 M9 ^2 E' ^* Stest was ordered, but the family did not go to the( H! {# m7 q' G% f; b" Z  a
laboratory to obtain the test.; P' t8 o& N6 n9 w% |( G
Discussion
# h: c4 I+ D9 vPrecocious puberty in boys is defined as secondary+ M1 S* z: t; s; y3 T4 V
sexual development before 9 years of age.1,4
$ o3 O' z5 z/ QPrecocious puberty is termed as central (true) when
& o2 E1 B% ?8 G; m8 G% kit is caused by the premature activation of hypo-; J: ^" Z$ {7 `2 K2 e
thalamic pituitary gonadal axis. CPP is more com-9 W3 Y9 p  O5 @0 K
mon in girls than in boys.1,3 Most boys with CPP
0 D$ a$ E3 g/ Z! |0 j2 xmay have a central nervous system lesion that is
( |) P/ O' Y- C* r3 aresponsible for the early activation of the hypothal-9 p" l- A2 y' C( Q8 ~
amic pituitary gonadal axis.1-3 Thus, greater empha-
. p  R0 ]& c! h7 V/ p$ w- \sis has been given to neuroradiologic imaging in1 [& M& b& a* _9 D
boys with precocious puberty. In addition to viril-
1 s( U0 H/ d2 |8 `0 T* gization, the clinical hallmark of CPP is the symmet-1 N4 i9 J; A# t, ?6 k
rical testicular growth secondary to stimulation by1 i7 c& `# K9 }
gonadotropins.1,3
* O3 I. j2 r# s+ ]5 g! i  B+ q* ?Gonadotropin-independent peripheral preco-
- }5 ~3 T/ a# X2 a/ R( k9 _cious puberty in boys also results from inappropriate/ ^+ ?/ Y' ^8 W' Q8 y/ t6 L: v% M
androgenic stimulation from either endogenous or# R! u" C7 p4 C  z) g: [+ X
exogenous sources, nonpituitary gonadotropin stim-0 w4 w, Y. e6 ?8 W$ h
ulation, and rare activating mutations.3 Virilizing8 y9 Q$ X/ O+ h! b6 F7 b. {
congenital adrenal hyperplasia producing excessive+ E4 Q! ]4 g5 }  q9 t: s
adrenal androgens is a common cause of precocious
( @7 L0 D  E0 i( c; [  x  |3 Y) kpuberty in boys.3,4
1 T3 @. f& z9 e$ ~* R1 i. kThe most common form of congenital adrenal
; }7 J+ ^" C* `hyperplasia is the 21-hydroxylase enzyme deficiency.
! I- ?$ e* o( B; V7 x/ xThe 11-β hydroxylase deficiency may also result in1 B! ]+ @4 Y( Z9 Y' B
excessive adrenal androgen production, and rarely,
* ^6 e, Z. x) c, n) aan adrenal tumor may also cause adrenal androgen
( ]0 Q7 E+ x% _# {) v9 _6 _/ xexcess.1,3( M. Z7 r8 }' [3 n4 M- D3 ]
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% ^' h2 H; ?( b" f; Z$ }
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
5 M/ ^# w# ]. c% MA unique entity of male-limited gonadotropin-
2 r9 |/ d7 J) w* r6 T4 Y. Sindependent precocious puberty, which is also known
: `9 ^2 }. \9 v% ~, Z7 Das testotoxicosis, may cause precocious puberty at a2 f5 e$ k  G# \; r" b3 `
very young age. The physical findings in these boys
" \$ g+ S" k% T- Q' c7 pwith this disorder are full pubertal development,
. |) c0 f( d: B, |. p7 ^including bilateral testicular growth, similar to boys
& Y3 m# }: ]) ~# Y; D2 ]! \" \with CPP. The gonadotropin levels in this disorder( ~* c7 p( ^+ n
are suppressed to prepubertal levels and do not show
- a8 y5 ]% ^3 ^" S0 fpubertal response of gonadotropin after gonadotropin-0 e+ ]8 {8 T( A
releasing hormone stimulation. This is a sex-linked) z' ^2 H7 ^1 @5 Z1 o
autosomal dominant disorder that affects only9 ?$ m& g+ L8 T9 g6 n9 h8 i
males; therefore, other male members of the family7 D) E* d" E4 `- z, e  u' L% V. M
may have similar precocious puberty.3* H6 l. I8 I, u9 V2 h8 D0 A
In our patient, physical examination was incon-
9 ?- L. e* D) s& d4 C' Rsistent with true precocious puberty since his testi-
: z+ f' A& f- E/ `. b. J8 w" rcles were prepubertal in size. However, testotoxicosis
/ s+ Z" `7 P7 ^" ], s9 q6 wwas in the differential diagnosis because his father8 a9 ?$ U- o6 O" e6 |
started puberty somewhat early, and occasionally,
, v) L2 \; }3 O$ |  rtesticular enlargement is not that evident in the
% j8 F& \) Y% X. _beginning of this process.1 In the absence of a neg-. f! {: i, G' Q6 z1 N
ative initial history of androgen exposure, our2 [9 W/ @, o" X2 t2 V: k' E% x5 C
biggest concern was virilizing adrenal hyperplasia,. c) j( t8 _, N. h8 d- f
either 21-hydroxylase deficiency or 11-β hydroxylase
: t2 q' ]* ]% U1 F1 w& G. I0 Udeficiency. Those diagnoses were excluded by find-( ^# G$ n$ [& j+ h7 l! b% ?" k
ing the normal level of adrenal steroids.8 s5 R& N& M- y  |! O% j
The diagnosis of exogenous androgens was strongly# C5 P& q9 u" p' u4 }1 j
suspected in a follow-up visit after 4 months because
9 z% C) C, y% W$ ~+ D) Xthe physical examination revealed the complete disap-$ Q. b. s/ I, M4 `$ ~' }: f
pearance of pubic hair, normal growth velocity, and5 X5 s6 Z6 k) A$ I! Q# d
decreased erections. The father admitted using a testos-; d) l3 u: B% A- j5 t. \
terone gel, which he concealed at first visit. He was
7 K2 F! [+ X! K; U+ {9 }using it rather frequently, twice a day. The Physicians’, y, V& `: U- w  W
Desk Reference, or package insert of this product, gel or/ x2 |6 v/ {" c
cream, cautions about dermal testosterone transfer to
7 P6 n2 ~7 m  xunprotected females through direct skin exposure., ?2 F+ M9 f! }5 Y- m  y5 R& R
Serum testosterone level was found to be 2 times the& k, g1 }" p1 ?! C, ]
baseline value in those females who were exposed to
% i) P& B$ s7 G. I4 t7 ^even 15 minutes of direct skin contact with their male
0 m/ a! G5 D; |: ^6 O' s) ~partners.6 However, when a shirt covered the applica-/ g, o7 K, j& D- S8 ]. S
tion site, this testosterone transfer was prevented.4 Z" I# d  L7 W# d" e5 T
Our patient’s testosterone level was 60 ng/mL,
* H4 Y& |6 h3 iwhich was clearly high. Some studies suggest that
/ T/ A2 ~* ^. ^4 v5 m  Gdermal conversion of testosterone to dihydrotestos-
# Z1 ]. }: f& D: @7 P6 @terone, which is a more potent metabolite, is more1 q& [; S$ X* r' l- n. q1 h9 c; r
active in young children exposed to testosterone+ t# K* O& g7 }
exogenously7; however, we did not measure a dihy-% M% i5 x, a+ Y; b' J2 i
drotestosterone level in our patient. In addition to; D4 @4 P: A) W* p
virilization, exposure to exogenous testosterone in) ?+ u" R$ |( ~
children results in an increase in growth velocity and" ?4 e- [. \. K% ^6 J6 M
advanced bone age, as seen in our patient.
/ E; N* }- }$ E0 X4 PThe long-term effect of androgen exposure during( @! o5 p5 r3 k" r! k& s
early childhood on pubertal development and final
5 t$ g/ ]+ T) B* E1 `: Qadult height are not fully known and always remain
0 o# T  t3 F7 [a concern. Children treated with short-term testos-
4 C: E" z4 ~$ rterone injection or topical androgen may exhibit some
; q9 e3 V9 W: }0 q+ L' M( X7 s+ Aacceleration of the skeletal maturation; however, after
# E5 |) L5 I1 Y8 Tcessation of treatment, the rate of bone maturation& g) r, _" G6 b( z$ d! [
decelerates and gradually returns to normal.8,9
( R: _5 A$ f: T/ @* N1 y9 jThere are conflicting reports and controversy
! y3 Z; |7 \% ^4 ]over the effect of early androgen exposure on adult8 n* H* Y* z3 i7 T
penile length.10,11 Some reports suggest subnormal# C3 a% w7 P, I1 t. S
adult penile length, apparently because of downreg-
! o& W" _, G$ E" K3 ~- C% Q! K+ qulation of androgen receptor number.10,12 However,% p3 E! E4 u4 m  k2 H
Sutherland et al13 did not find a correlation between% ?; j' r# G. G' _$ @3 n  X
childhood testosterone exposure and reduced adult( ?: j$ ^5 H1 i
penile length in clinical studies.* i8 [0 l) E- j: W
Nonetheless, we do not believe our patient is
! ~  c1 y/ d( Q! t5 Z: g! ?6 W- kgoing to experience any of the untoward effects from
3 |4 L& o, d8 s0 r' q9 Otestosterone exposure as mentioned earlier because
# d* J! C4 n( l) nthe exposure was not for a prolonged period of time.
7 a  A& {' R# Z6 o) a# y6 u+ p( ~Although the bone age was advanced at the time of
( R( {* H1 T0 O: jdiagnosis, the child had a normal growth velocity at# H- r$ F+ B* |- M; L' T0 U
the follow-up visit. It is hoped that his final adult
+ i$ h) e2 q+ @9 E: [height will not be affected.
+ {8 v  e) t- L: n3 X  MAlthough rarely reported, the widespread avail-. U/ Z% L. @* R& E0 d/ e6 `
ability of androgen products in our society may
. c" r, a1 k/ Q; X- G: pindeed cause more virilization in male or female
) m3 U, B/ u5 P, H5 M% C0 n: f. Xchildren than one would realize. Exposure to andro-' `+ O$ C4 d! e# k; l+ M/ ~
gen products must be considered and specific ques-
; Z% X* l- d2 R# K4 i4 ]8 f$ `" M3 n% _tioning about the use of a testosterone product or- D& z. V% ~# u# _, d! O9 z: U( U
gel should be asked of the family members during6 V# I) k6 ]) ]( ?; v0 Z/ m$ q
the evaluation of any children who present with vir-  i+ k# A2 y) K' d# P
ilization or peripheral precocious puberty. The diag-9 Z# B; H- y! v1 c
nosis can be established by just a few tests and by# F: X1 s% i2 Q; Z: ]: Y
appropriate history. The inability to obtain such a
( n9 N# Q$ |" w+ M+ v) Dhistory, or failure to ask the specific questions, may7 L, c, ^& q8 ^
result in extensive, unnecessary, and expensive% t' ?! b7 R- Y$ E/ K: k
investigation. The primary care physician should be9 {2 e1 h* d* r8 Z* @3 Y1 F
aware of this fact, because most of these children
) w- Y/ E8 `/ U0 fmay initially present in their practice. The Physicians’
! L. X, d! n4 H" a( _Desk Reference and package insert should also put a
  P1 Z7 z. j, w6 l! ~2 l2 Awarning about the virilizing effect on a male or1 x2 T9 z7 D  _/ P5 ?
female child who might come in contact with some-4 Z+ B9 }4 N7 q# P1 ^
one using any of these products.
' [! b8 j; ]" K* W5 M; D& UReferences# x4 y9 H" B* z8 ^- [* ^
1. Styne DM. The testes: disorder of sexual differentiation
9 q/ M* j; j& }- E( rand puberty in the male. In: Sperling MA, ed. Pediatric
, |& Q4 v1 g, r  }, d+ t1 t7 X. gEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
  [9 i, w% p) U0 Y5 p2002: 565-628.
+ w5 p9 w$ o  E5 X2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious# [8 M* d9 d% T
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
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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

+ c% e1 |  G! F1 a5 l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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