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Sexual Precocity in a 16-Month-Old/ b& X0 B' d) @3 x
Boy Induced by Indirect Topical7 c0 n- ]7 \& f
Exposure to Testosterone
+ b4 Y0 f$ _6 Q# }0 [2 vSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
. n8 _6 F0 I7 y" t6 ]" sand Kenneth R. Rettig, MD1' G5 \. L. O6 S  _4 _
Clinical Pediatrics% M7 X4 [0 d9 Z/ n
Volume 46 Number 6& P$ _0 D# Z# j, w7 E7 S$ N
July 2007 540-543
/ L$ {$ }7 @: R9 H7 c; {6 J© 2007 Sage Publications
, G2 o  U5 u6 i% D& J10.1177/0009922806296651/ j+ C; O, ~8 f( w
http://clp.sagepub.com' ?7 l& i) @- C5 Z3 w& \
hosted at
: ^, B! }4 v  R2 ?, t6 C3 a7 l/ K1 zhttp://online.sagepub.com
6 ^$ \" e1 B  Q) {0 [3 q) \% mPrecocious puberty in boys, central or peripheral,2 M8 P( i) K6 ?" z
is a significant concern for physicians. Central
- s* k3 y  ~" [, e% q. e! Rprecocious puberty (CPP), which is mediated
3 F8 z: h/ |  K! e" ^. D# O% N& J8 xthrough the hypothalamic pituitary gonadal axis, has) V2 x; ?( _% z, E+ \( Z- J
a higher incidence of organic central nervous system+ U- V' N: J4 ^7 T
lesions in boys.1,2 Virilization in boys, as manifested
$ W0 z/ H  O* w- r: @4 fby enlargement of the penis, development of pubic6 E. o1 e# h& L- R
hair, and facial acne without enlargement of testi-2 l# s$ I; B" p% d, m$ n5 N# K
cles, suggests peripheral or pseudopuberty.1-3 We$ a- t$ Q' |- y# v
report a 16-month-old boy who presented with the6 E( I: Y+ }; ?- Z
enlargement of the phallus and pubic hair develop-
% F' n! n  u3 ]7 d. \4 H' zment without testicular enlargement, which was due- M( r! t2 o' L8 N/ [( S
to the unintentional exposure to androgen gel used by7 O2 W4 d+ _/ g1 d5 s8 E( r# ]$ N
the father. The family initially concealed this infor-
! x3 {& r8 I' i& P: f5 t' ~8 b7 O2 }mation, resulting in an extensive work-up for this
. h5 ]- E3 |: S- `child. Given the widespread and easy availability of1 Q+ ~5 B& m  y
testosterone gel and cream, we believe this is proba-: l2 a$ L$ L3 n8 t2 J4 Y
bly more common than the rare case report in the! t* I& P' n' _4 }1 k, M
literature.4
) |, N- G0 c4 }% qPatient Report
! C: A4 Z2 a4 b( O8 T3 y# qA 16-month-old white child was referred to the
3 a. N* i! U7 y1 Z1 z: Cendocrine clinic by his pediatrician with the concern
% ^2 R' J3 {1 [1 R* C. Cof early sexual development. His mother noticed
: B8 x  e6 v! n7 R/ {# olight colored pubic hair development when he was  O) [2 z$ |8 v+ k1 g* V
From the 1Division of Pediatric Endocrinology, 2University of9 F+ e  Q$ W+ O& j" v# T
South Alabama Medical Center, Mobile, Alabama.
' p7 a1 c# E! w* g! L4 V  X" Q/ tAddress correspondence to: Samar K. Bhowmick, MD, FACE,
1 A; y1 F+ [/ ?  N$ [: O, SProfessor of Pediatrics, University of South Alabama, College of$ Z# `% g' |: b+ O* p# @' I& K
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;2 s! Z+ V" y+ s* q! U. i% H
e-mail: [email protected].- W% f! T% G& `9 h$ n
about 6 to 7 months old, which progressively became
! P: X% |/ K& `darker. She was also concerned about the enlarge-
: `9 f! W& R! r& \0 o# U$ r" lment of his penis and frequent erections. The child
5 F' o* L( U, u+ W; Z# E' \( P8 gwas the product of a full-term normal delivery, with
/ U+ u" s' {2 `- W/ ^; Aa birth weight of 7 lb 14 oz, and birth length of
( N2 E, D5 |2 \7 f0 e& q20 inches. He was breast-fed throughout the first year9 z( x2 g9 D5 r
of life and was still receiving breast milk along with0 e; l9 \' `2 J- v, `. k3 j
solid food. He had no hospitalizations or surgery,
0 F7 c  a3 a, u) Hand his psychosocial and psychomotor development
4 c, R4 l! ]5 P, H# w2 `was age appropriate.
; }7 e# _1 N& L* dThe family history was remarkable for the father,# b% Y8 ~$ O5 m" _
who was diagnosed with hypothyroidism at age 16,. G' i( I+ U7 v9 I. _
which was treated with thyroxine. The father’s
+ |  o( M' O2 a+ D! z2 oheight was 6 feet, and he went through a somewhat  b, k% ~5 {4 Q! M: |- Y
early puberty and had stopped growing by age 14.
2 K% i* i  b" J: _4 C2 c' F+ N4 CThe father denied taking any other medication. The
: @/ `" J; Q& M/ cchild’s mother was in good health. Her menarche
5 g! `6 t/ b, S* U1 i/ b# f0 c- bwas at 11 years of age, and her height was at 5 feet
! _. Y' \- N1 B$ l% [6 M( x0 Z  [, ~5 inches. There was no other family history of pre-
# x2 C8 Y* G8 N  p+ w: r1 ccocious sexual development in the first-degree rela-2 X8 f. }& s3 l
tives. There were no siblings.
. i. _7 u: e/ x" C5 b0 APhysical Examination
3 \9 z( u& c0 _/ \7 C# p2 V! gThe physical examination revealed a very active,
0 H/ x4 ?/ A1 [+ M" Gplayful, and healthy boy. The vital signs documented
. \+ D! O2 L6 _+ {a blood pressure of 85/50 mm Hg, his length was  e- M# d6 j3 G$ |+ i( H
90 cm (>97th percentile), and his weight was 14.4 kg4 _5 |: J3 k' W4 w' i0 @& o" w
(also >97th percentile). The observed yearly growth; T7 y; L( g/ H
velocity was 30 cm (12 inches). The examination of) I: O% K! N& F: h* Q) X6 p$ a  o
the neck revealed no thyroid enlargement.
& {" g/ Q8 t+ D. T- e! z0 U0 L% oThe genitourinary examination was remarkable for
! _; I4 E/ U# w2 Xenlargement of the penis, with a stretched length of
" Z7 V/ a) ?3 T' u2 S# e/ T8 cm and a width of 2 cm. The glans penis was very well
/ P: D1 l' m1 `developed. The pubic hair was Tanner II, mostly around. h" e9 k+ H  I
540- M" K9 j8 n( k3 d  v+ B8 {; H8 d( X
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 }* u& U' T; r8 z8 K$ @4 {the base of the phallus and was dark and curled. The
7 P3 ^) T; j$ S, W; I& {! `' ftesticular volume was prepubertal at 2 mL each.
. Z' a/ L' V9 @9 g$ [The skin was moist and smooth and somewhat
* N+ [. p/ u: F' toily. No axillary hair was noted. There were no$ q0 z) y' M( f
abnormal skin pigmentations or café-au-lait spots.7 j# H1 k' |) M5 q& J/ a
Neurologic evaluation showed deep tendon reflex 2+9 i8 N$ [9 z* i3 e) Z
bilateral and symmetrical. There was no suggestion
" v0 N: z5 e& A* ^" Hof papilledema.
) `: c: H0 J! j3 O, mLaboratory Evaluation
0 h% o8 A2 ]4 D+ N; l8 e9 kThe bone age was consistent with 28 months by
1 K+ L3 B  E) Y  ^* xusing the standard of Greulich and Pyle at a chrono-
# C2 f8 Q, A7 g" A5 ?" V2 s: h; plogic age of 16 months (advanced).5 Chromosomal! J4 b! v) P2 T! F  T
karyotype was 46XY. The thyroid function test# @( C0 W! i+ M5 `/ M" u  n
showed a free T4 of 1.69 ng/dL, and thyroid stimu-$ B( I) U- A  S3 M( b& W
lating hormone level was 1.3 µIU/mL (both normal).
1 H' Z1 s! G/ R& L6 ^6 q7 VThe concentrations of serum electrolytes, blood4 D) X& H& [$ V8 y0 ?; u
urea nitrogen, creatinine, and calcium all were
# {1 u/ s8 R! M7 ewithin normal range for his age. The concentration
7 B+ P7 [1 Y1 z9 T$ yof serum 17-hydroxyprogesterone was 16 ng/dL
$ k1 h' t) p/ H5 g( q# e1 o(normal, 3 to 90 ng/dL), androstenedione was 20! O) N7 x, R3 v7 E% o0 {4 k
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
! `) T! g6 m. _- s3 H0 pterone was 38 ng/dL (normal, 50 to 760 ng/dL),; t5 F# W% `5 D8 q* L0 [
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
  i7 d% _& @, k) K49ng/dL), 11-desoxycortisol (specific compound S)
  [$ |' y5 u( w& [+ |( ~! swas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-7 r7 S2 x+ s: p* u  V
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total- \1 h2 K# E$ I1 L
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),' a* u. Z9 n4 X; z# g" Y% L" D& u
and β-human chorionic gonadotropin was less than, Z+ e7 V7 `- _; y" L) a* ^/ }) c
5 mIU/mL (normal <5 mIU/mL). Serum follicular
6 e) b) ?, h8 f+ nstimulating hormone and leuteinizing hormone. W! U7 T4 p; S2 @9 D
concentrations were less than 0.05 mIU/mL
! b5 W: M' Z" \(prepubertal).& H1 ~- s: ~5 u' w) K; ^1 _
The parents were notified about the laboratory
! ?* x/ T* r/ U3 G" presults and were informed that all of the tests were% f, U4 [  w4 l
normal except the testosterone level was high. The
8 f- G0 Z  M2 y( I  ~! G2 [follow-up visit was arranged within a few weeks to$ o2 l: F5 |3 T. }+ E2 L: M
obtain testicular and abdominal sonograms; how-
1 |( F/ c# g1 q6 e# J- Gever, the family did not return for 4 months.
  L6 V- V) A( |* cPhysical examination at this time revealed that the
. y' h% T! B7 p( w/ z5 i4 s; qchild had grown 2.5 cm in 4 months and had gained2 ^' j4 |$ ?+ c3 F
2 kg of weight. Physical examination remained
* s# _/ ]2 y+ _unchanged. Surprisingly, the pubic hair almost com-# s/ z5 _2 t+ Q9 C3 H
pletely disappeared except for a few vellous hairs at' h! D" O* o- P
the base of the phallus. Testicular volume was still 2( x8 B/ P4 @; }+ @4 l( R7 M1 P. [6 g
mL, and the size of the penis remained unchanged.
' w* O# d* q# K0 R$ V, f- X3 EThe mother also said that the boy was no longer hav-
; ^/ H2 J( P+ d0 L* g1 \& Ning frequent erections.' U  f- j* X  b+ ]4 }7 O6 v
Both parents were again questioned about use of8 Z( o! `" }; j9 T: E* _
any ointment/creams that they may have applied to  ~4 P/ z. z3 O, a
the child’s skin. This time the father admitted the
( i  h# Q. \- l) v1 cTopical Testosterone Exposure / Bhowmick et al 541
" @3 Y7 T0 T# H. ]use of testosterone gel twice daily that he was apply-
" ?; n8 ]0 {6 s! b# ning over his own shoulders, chest, and back area for6 I7 E0 V! X$ |0 S' R3 A
a year. The father also revealed he was embarrassed) D6 E2 c. Y& M& W+ P! L- p  C
to disclose that he was using a testosterone gel pre-
6 r: L* u2 t- z- N% P% V# T8 U* gscribed by his family physician for decreased libido
* {; g9 L$ [) `- B% W) vsecondary to depression.
8 ?, z2 X" j2 R' C# zThe child slept in the same bed with parents.
$ C* D" H+ T1 r- DThe father would hug the baby and hold him on his# W" o# m- B0 M1 G+ f
chest for a considerable period of time, causing sig-
1 b4 v' e1 F: u( x+ tnificant bare skin contact between baby and father.
2 n8 {9 U7 B& Y8 G" IThe father also admitted that after the phone call,) ?/ @# H' N" s
when he learned the testosterone level in the baby: T' j' C* V* u; [8 a; _) T
was high, he then read the product information
" d+ ]! C* g2 s  Ipacket and concluded that it was most likely the rea-0 ?! R5 X/ n0 G6 M3 t" w' U( E
son for the child’s virilization. At that time, they5 n/ }/ u6 ?' Q( d& `" F3 @0 t
decided to put the baby in a separate bed, and the4 g6 b- m& K0 e6 C) |
father was not hugging him with bare skin and had9 t0 s' X; }7 h0 {* d
been using protective clothing. A repeat testosterone
. P! ?6 m5 O1 J8 Mtest was ordered, but the family did not go to the1 v. ?! y" ~7 L
laboratory to obtain the test.
: n9 Y, r; |  W4 |Discussion1 Y/ Y5 M+ g6 B% b* [
Precocious puberty in boys is defined as secondary( p9 B- C0 M. o' y  c
sexual development before 9 years of age.1,46 f# Y$ {' ?. u% F+ v! _
Precocious puberty is termed as central (true) when- ?; A% G1 N7 `/ |1 m2 K
it is caused by the premature activation of hypo-7 u1 l1 t' G" H1 |4 n
thalamic pituitary gonadal axis. CPP is more com-1 `6 M. L: @9 y% c* X2 M
mon in girls than in boys.1,3 Most boys with CPP+ `% y+ A" g' d/ q% D
may have a central nervous system lesion that is
" @2 }; [* B$ i" \responsible for the early activation of the hypothal-& Q1 ^& h! f* e, W+ ~
amic pituitary gonadal axis.1-3 Thus, greater empha-2 S) D$ c' I; i: K: n
sis has been given to neuroradiologic imaging in; h/ y5 x- a7 L, ]$ [
boys with precocious puberty. In addition to viril-
' Y) H1 M! R0 c9 }ization, the clinical hallmark of CPP is the symmet-
/ c& `. A7 f  |. [; b( f" Orical testicular growth secondary to stimulation by, C5 T, f( R0 f
gonadotropins.1,3
6 L0 b( k( m/ j4 R+ NGonadotropin-independent peripheral preco-6 e! N; i" Z% G/ h( Z; p
cious puberty in boys also results from inappropriate5 i% e0 D, Q3 v6 ~9 D! o/ o8 P; d
androgenic stimulation from either endogenous or
2 g& o5 D! M( W, C& Y$ U4 s/ Kexogenous sources, nonpituitary gonadotropin stim-
' u; Z' f! I, D4 h7 O* h- E- W$ Qulation, and rare activating mutations.3 Virilizing
1 ]+ v; @7 o1 V8 D) S0 wcongenital adrenal hyperplasia producing excessive
- B! M, O; d( ladrenal androgens is a common cause of precocious
# M/ H9 X0 m/ P6 R9 p) Q0 F5 _puberty in boys.3,44 {- Y! Q. E/ b( S- S8 ~- e4 u
The most common form of congenital adrenal6 `* C5 K2 X4 z
hyperplasia is the 21-hydroxylase enzyme deficiency.
% V2 o2 ?* m/ v' ?The 11-β hydroxylase deficiency may also result in8 B& f" x' h6 @
excessive adrenal androgen production, and rarely,
: ~% W) q7 p8 s4 s: l* fan adrenal tumor may also cause adrenal androgen' [1 l% {  G% w$ A
excess.1,3
( Z3 t% q) i  u8 Bat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; L9 B7 V4 v8 N/ t0 j! w
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
6 O/ Y9 H* F3 H5 |& ~A unique entity of male-limited gonadotropin-3 p# c8 D0 \+ A1 b% }7 @( e
independent precocious puberty, which is also known/ j* X" y- F/ C
as testotoxicosis, may cause precocious puberty at a
: S% U7 b# ~7 l$ J) qvery young age. The physical findings in these boys
+ s  F6 c3 G% E- @( Y& qwith this disorder are full pubertal development,
  V  j  f# o: k0 Oincluding bilateral testicular growth, similar to boys
  g. F, t; t+ C$ j- Vwith CPP. The gonadotropin levels in this disorder
. ?& h+ ~' o  v* H9 i' j6 C& yare suppressed to prepubertal levels and do not show
7 {, o3 B7 r$ V- I; _pubertal response of gonadotropin after gonadotropin-. `) F, v3 J+ w0 A
releasing hormone stimulation. This is a sex-linked7 D9 D4 B1 k6 ^+ Y8 V( F8 T+ k8 O
autosomal dominant disorder that affects only
- F& Q5 f0 J* g* H. d$ m& v+ O2 e: Cmales; therefore, other male members of the family
$ C9 f+ n$ e( A. @" Z8 \may have similar precocious puberty.3& R1 c6 O" ^$ O! m
In our patient, physical examination was incon-, ~4 E- S5 c4 g. @( s
sistent with true precocious puberty since his testi-
; j. g+ J+ H4 \) S* Q- ycles were prepubertal in size. However, testotoxicosis) ?4 N8 j# d: |" z$ Z1 A
was in the differential diagnosis because his father
9 X% g; D( L& E1 `0 @- Fstarted puberty somewhat early, and occasionally,
/ Q' {9 f1 p: a- e: v" H$ etesticular enlargement is not that evident in the1 T1 A) L  A1 t8 |, m
beginning of this process.1 In the absence of a neg-+ A  l. O, {: ^% G$ U& D
ative initial history of androgen exposure, our
2 a" @1 Q5 i: ybiggest concern was virilizing adrenal hyperplasia,& h8 P9 V7 M' g9 ]
either 21-hydroxylase deficiency or 11-β hydroxylase' ]5 A2 Z, Z  g% Q1 H4 p7 }
deficiency. Those diagnoses were excluded by find-
: f5 m' @" u# J1 F! eing the normal level of adrenal steroids.$ T* s3 {- n# T# A, r; z
The diagnosis of exogenous androgens was strongly
) F3 A5 @+ \9 s- [' ?6 ?+ zsuspected in a follow-up visit after 4 months because
, a  S; j9 i7 H6 m; n% j( [the physical examination revealed the complete disap-! F; ]6 s4 T: k6 n" G7 }) O
pearance of pubic hair, normal growth velocity, and  P- I1 Y# q7 c" r% L1 x
decreased erections. The father admitted using a testos-
9 T. @4 O1 b3 y  a" yterone gel, which he concealed at first visit. He was
* L1 |: W0 B0 o5 s  l# Xusing it rather frequently, twice a day. The Physicians’
0 K5 r: r2 l& Y1 |% c/ g$ RDesk Reference, or package insert of this product, gel or
" i9 X3 K$ T+ n& F  e2 R8 Fcream, cautions about dermal testosterone transfer to
  D, b# y. _& |unprotected females through direct skin exposure.
* a' v1 x2 o) ?Serum testosterone level was found to be 2 times the% g& Q  L. i# O0 F7 r7 u9 P
baseline value in those females who were exposed to, b+ A( X! n" h+ U0 V9 d
even 15 minutes of direct skin contact with their male
* P  g. E8 a. [partners.6 However, when a shirt covered the applica-/ l2 r% L1 s# _6 H: o# B1 v% s
tion site, this testosterone transfer was prevented.
6 P' ?+ R& l2 s! ~Our patient’s testosterone level was 60 ng/mL,
3 O) h( n  s  a% R# `which was clearly high. Some studies suggest that) h( D+ P( M+ r# C" C( x1 L2 e! S
dermal conversion of testosterone to dihydrotestos-9 k; `4 I) P; @& Z: {; b
terone, which is a more potent metabolite, is more4 R! j, }4 l) C" `4 a
active in young children exposed to testosterone8 F5 G2 x2 D3 R1 g! `4 X) c, l
exogenously7; however, we did not measure a dihy-
/ O7 z7 c: H  U! X' x8 R8 Ndrotestosterone level in our patient. In addition to
: o/ s3 p5 h' f; Wvirilization, exposure to exogenous testosterone in- I" I- f2 R$ j3 i5 s) t
children results in an increase in growth velocity and" b( W- G* Q- @* P$ F
advanced bone age, as seen in our patient., [. x( v& c" i- T9 |
The long-term effect of androgen exposure during- u6 C6 H) N4 B) Z; W2 w
early childhood on pubertal development and final
' D6 `  h  j/ Cadult height are not fully known and always remain2 Q0 Y$ `+ [6 N# B1 |4 w0 v, K6 e9 y
a concern. Children treated with short-term testos-
4 Y1 f( H4 a# z  P: _4 Uterone injection or topical androgen may exhibit some- G8 V2 Y6 Q) ~' S
acceleration of the skeletal maturation; however, after
: o$ j9 J$ C5 X) k9 R2 _cessation of treatment, the rate of bone maturation7 q2 T, c. r1 E
decelerates and gradually returns to normal.8,9
: s5 k. I* x* k; F% n/ Z9 C2 TThere are conflicting reports and controversy
$ j. C8 j0 S, bover the effect of early androgen exposure on adult# v9 ?% w+ O* x  G/ w. ~
penile length.10,11 Some reports suggest subnormal9 c% I0 u, _8 z+ g( g2 t
adult penile length, apparently because of downreg-
; J9 y$ Q. K/ yulation of androgen receptor number.10,12 However,) K. [' t1 \+ l; g3 r- }2 _" U
Sutherland et al13 did not find a correlation between
# B  \& H5 k! n; ^# O* Ochildhood testosterone exposure and reduced adult* ]" Z5 g2 x" b% e
penile length in clinical studies.% Y# V$ [0 ]1 {* L5 W
Nonetheless, we do not believe our patient is
$ ^6 r7 r( e3 M& Z7 @1 e) c# Fgoing to experience any of the untoward effects from
$ S0 E: s, e1 Q- p2 K0 ~1 K7 x1 Qtestosterone exposure as mentioned earlier because' D# A  ?. }- p. }2 q/ t7 ~
the exposure was not for a prolonged period of time.  [% b/ Y7 F9 g! E: Y
Although the bone age was advanced at the time of( U6 T1 m7 @3 G( l+ ^) u
diagnosis, the child had a normal growth velocity at
* R  x1 K/ Z/ T7 \0 v# |& sthe follow-up visit. It is hoped that his final adult  W- A' |4 T0 H2 Q7 s# A% c; i
height will not be affected.
( N$ R/ n" Y" F, w3 F* L3 QAlthough rarely reported, the widespread avail-' ]; K- }" K- L$ s- o% A
ability of androgen products in our society may
( f7 e( S& j& b- e- s* vindeed cause more virilization in male or female
, j3 I% h' d( w$ A4 J, Wchildren than one would realize. Exposure to andro-# r& s6 s7 A( l' X/ B
gen products must be considered and specific ques-
- y, l( r; ]8 }7 F9 n( q; ntioning about the use of a testosterone product or: z( `4 `1 O- ~) a$ c
gel should be asked of the family members during6 i* j4 X9 q+ A9 O/ q$ }2 d! L' x
the evaluation of any children who present with vir-
; \* A& J$ Z& O2 Uilization or peripheral precocious puberty. The diag-9 n# _; {! Q- ?6 c
nosis can be established by just a few tests and by( p% X; @6 x, H, f! g
appropriate history. The inability to obtain such a
* d/ f% w. \! z: ~0 A$ Dhistory, or failure to ask the specific questions, may
7 B/ x0 J2 V! @) X% ]) kresult in extensive, unnecessary, and expensive3 S4 {# N0 O6 M$ h7 U' w: i
investigation. The primary care physician should be
' G0 z: C  D+ L, W3 a$ x( \aware of this fact, because most of these children
& K+ H; r- k* c6 h% ]( Bmay initially present in their practice. The Physicians’
" l0 L! R/ |2 p+ e) m3 iDesk Reference and package insert should also put a+ ^/ d, f9 x8 \1 o; @( d# i, |
warning about the virilizing effect on a male or
' J+ |, D  N: Z8 F% L  jfemale child who might come in contact with some-& E6 t4 e& `" W" t9 R- A  t6 T# u
one using any of these products.
, V5 W1 z. l2 IReferences3 x9 p& j: v6 P1 Z* i. u+ C
1. Styne DM. The testes: disorder of sexual differentiation
& M, e3 E7 k" k* t0 [and puberty in the male. In: Sperling MA, ed. Pediatric
0 b) U+ f0 `+ u* T5 q; U' R; c  i; fEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;3 \7 i0 _+ }1 ~2 R
2002: 565-628.
/ z6 d/ f1 K" W9 }9 f2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious) r" Q1 Z8 B% W( H1 a- y$ f
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
& |  z( J- {3 |$ g/ O+ X6 KBoy Induced by Indirect Topical7 \2 c# Y& A, [% G+ N
Exposure to Testosterone
* r/ W/ I5 p- k( h6 d/ w4 }Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. i" e; {- L* ?) D, Z: {5 K' @
and Kenneth R. Rettig, MD1" l/ X1 G) y9 N
Clinical Pediatrics
5 N# e+ M: g% z6 ?  G$ y$ Z; ?Volume 46 Number 6, {) R# k' m9 p4 W2 s8 s; y" j
July 2007 540-543
$ f5 J, Z2 s6 Z3 G8 C. N© 2007 Sage Publications
. y- C( z! D' T' ]4 ^# ~* ?10.1177/00099228062966519 Q7 W8 E9 O4 W4 B8 `
http://clp.sagepub.com, e0 v: _) c# G% w
hosted at2 u: a/ \6 ~! ^( k; O" x
http://online.sagepub.com( |; b( q" S9 U
Precocious puberty in boys, central or peripheral,
. ~7 w9 z; P' `- [8 s1 Z; Vis a significant concern for physicians. Central  `0 W1 D; ?, E
precocious puberty (CPP), which is mediated
  I; }, \9 G$ Y* p9 ythrough the hypothalamic pituitary gonadal axis, has' e- g  Z/ p( ~+ Y/ l& G2 w
a higher incidence of organic central nervous system% f  _& d/ c* O* r
lesions in boys.1,2 Virilization in boys, as manifested' t. b  h+ o* ~' {7 @
by enlargement of the penis, development of pubic8 n5 a1 D# F7 C$ ], e1 ]6 j5 W0 u
hair, and facial acne without enlargement of testi-
0 B- l: k8 T6 S" M8 Xcles, suggests peripheral or pseudopuberty.1-3 We. m. V3 O/ q) j6 b& @4 T
report a 16-month-old boy who presented with the
& W# v: v0 @0 ^3 menlargement of the phallus and pubic hair develop-
* c, D" |3 D' O' U$ pment without testicular enlargement, which was due
/ u6 L" O6 U' E  k$ u" G8 c& r' G7 xto the unintentional exposure to androgen gel used by
# a( U. y3 V) Z8 Z) x2 Kthe father. The family initially concealed this infor-
8 N6 C# e2 ^" C5 K2 F( ~$ s4 emation, resulting in an extensive work-up for this
* R. i* q3 `% a( R6 ^7 n) ychild. Given the widespread and easy availability of
2 W; A% d0 p6 ~$ b$ ctestosterone gel and cream, we believe this is proba-; `0 W, n4 r. \
bly more common than the rare case report in the
+ ^0 N* M% Z' _3 Oliterature.4
  E3 U5 S. I6 m  qPatient Report1 M" X+ _* h4 ?- Z' V) w; Z3 f
A 16-month-old white child was referred to the
: ]: X( L5 \7 `$ ]  Rendocrine clinic by his pediatrician with the concern; b; N: H  y5 O' E
of early sexual development. His mother noticed
! }/ m  L3 V) v" `light colored pubic hair development when he was1 `7 B# r, p6 i( Z3 ^3 ]
From the 1Division of Pediatric Endocrinology, 2University of5 S3 q* P/ z  D. h' o
South Alabama Medical Center, Mobile, Alabama./ s8 @- q1 M4 ^" l
Address correspondence to: Samar K. Bhowmick, MD, FACE,
2 D7 P' h- \: IProfessor of Pediatrics, University of South Alabama, College of; O- [$ t: J  a1 }: c. X% B
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
( N( m9 u) Z1 n! qe-mail: [email protected].
: S* `  E/ H$ N. b5 _about 6 to 7 months old, which progressively became
  z, B# }# {' O+ Q3 Q5 v& d  Edarker. She was also concerned about the enlarge-3 h2 `7 U: h3 _% W9 t
ment of his penis and frequent erections. The child4 V* `' M0 a8 w1 ?, t
was the product of a full-term normal delivery, with# l' {1 N* g1 U* R2 U" S
a birth weight of 7 lb 14 oz, and birth length of* u+ l- i: w; Y
20 inches. He was breast-fed throughout the first year( Y3 z6 z4 {/ g; X& x/ o4 Z
of life and was still receiving breast milk along with7 w8 X+ F8 c4 R, P( D# U
solid food. He had no hospitalizations or surgery,
4 I/ ?( u3 _9 f& H; Z  yand his psychosocial and psychomotor development
4 w% m9 y( K3 o/ m; d0 B( owas age appropriate.
7 J, E8 z* g- }& e$ |3 eThe family history was remarkable for the father,$ }3 Q2 }/ {) P) R4 y! S
who was diagnosed with hypothyroidism at age 16,$ {; w0 s' F$ B1 J) B6 W6 v
which was treated with thyroxine. The father’s5 T" F7 w" |8 V7 L/ D0 T
height was 6 feet, and he went through a somewhat
7 Y! E* V7 o' h0 x: Z  ]early puberty and had stopped growing by age 14./ L/ v% S+ H2 M2 L$ m4 d9 H
The father denied taking any other medication. The
/ Y: g4 o9 i5 [. X+ Z% }! hchild’s mother was in good health. Her menarche
  L( U. X. q- r( I) e/ y* s2 uwas at 11 years of age, and her height was at 5 feet0 i- C* L9 G+ K5 d6 t. `) t
5 inches. There was no other family history of pre-& r' y$ U1 i6 @4 N( v
cocious sexual development in the first-degree rela-4 n0 k" O# m1 j0 H, I
tives. There were no siblings.
& X  B2 c7 Z$ m' NPhysical Examination
- ~! \3 y( a5 `8 i1 IThe physical examination revealed a very active,
9 c. T" P& W3 t- dplayful, and healthy boy. The vital signs documented
' L$ Z/ I& t# P. X7 qa blood pressure of 85/50 mm Hg, his length was
6 K2 K" v6 i4 D, F90 cm (>97th percentile), and his weight was 14.4 kg, b* e) p% F  {4 R
(also >97th percentile). The observed yearly growth2 ]' J4 O& F4 h( ~
velocity was 30 cm (12 inches). The examination of4 P2 }5 l* b$ H3 y; {! F# u0 x; P8 n  j
the neck revealed no thyroid enlargement.+ Q% d! h' x0 u' {3 N! m
The genitourinary examination was remarkable for% M: ^5 v- p' @' E
enlargement of the penis, with a stretched length of
& X- F  r* F/ Q6 b1 R7 l8 cm and a width of 2 cm. The glans penis was very well8 W5 p% N) v( |0 i* W4 q
developed. The pubic hair was Tanner II, mostly around
# f: D* \7 c- d- H9 Q( {540" v7 P  ^$ V- C1 H: w4 C  A! E# \
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: }5 x4 N- V/ O% V) d/ |9 p- lthe base of the phallus and was dark and curled. The6 l3 I0 q, X) k
testicular volume was prepubertal at 2 mL each.
. _! Z- K  n8 g. t# C+ PThe skin was moist and smooth and somewhat4 b+ m. L0 y1 z* `1 A
oily. No axillary hair was noted. There were no
" T  k" \; @: ~" P( T0 \! G; Sabnormal skin pigmentations or café-au-lait spots.4 @. z. A1 K& x% E
Neurologic evaluation showed deep tendon reflex 2+* {. |& a. f1 ~7 s+ B5 j7 j1 X
bilateral and symmetrical. There was no suggestion# A$ h" g. I6 I; d
of papilledema.
* H% q8 V% N( K- vLaboratory Evaluation; w" D% M: t7 l2 N
The bone age was consistent with 28 months by' I$ `/ r9 ~" w, Z& k1 K8 {6 W
using the standard of Greulich and Pyle at a chrono-% f" N! Y' w2 `$ O# C# o+ }& k$ s
logic age of 16 months (advanced).5 Chromosomal
- G+ }  b! `8 Akaryotype was 46XY. The thyroid function test
4 V+ D$ {4 d: D" w( x3 ashowed a free T4 of 1.69 ng/dL, and thyroid stimu-7 n8 K, G3 [, _/ E" y
lating hormone level was 1.3 µIU/mL (both normal).7 n3 h: {- v- s6 i" {+ \. Q2 N  P
The concentrations of serum electrolytes, blood
  L7 i) x+ ?+ b! U) R* burea nitrogen, creatinine, and calcium all were
% m& I% D4 C  w6 B- j, z, d9 iwithin normal range for his age. The concentration
  D$ `: g2 h' q8 Dof serum 17-hydroxyprogesterone was 16 ng/dL" r* P/ }% Q& m# c1 W  j/ V
(normal, 3 to 90 ng/dL), androstenedione was 20$ t( f; S! t1 l+ Q
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-, w2 e4 v( Q/ C* g" C
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
0 g4 `" Y( D; r5 c1 K; xdesoxycorticosterone was 4.3 ng/dL (normal, 7 to" i5 t3 Z$ [) P% G- p0 W! ?
49ng/dL), 11-desoxycortisol (specific compound S)& T1 K! H5 j. R! O: J) [
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
8 R3 P3 H5 m& A' |tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
9 L, a% z! ?2 Jtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),  V% S! C2 ?! {$ ]! c, m" T* u
and β-human chorionic gonadotropin was less than" S! c" w9 l0 b
5 mIU/mL (normal <5 mIU/mL). Serum follicular3 n( s% o2 X  f6 i( Y- K
stimulating hormone and leuteinizing hormone  g: j# Z2 Z: e) f% j+ H* l8 _
concentrations were less than 0.05 mIU/mL
1 P; P- l# c  u% t) h(prepubertal)./ s# j7 u" }6 W  ?
The parents were notified about the laboratory' E* T/ D2 V% s+ y0 z  [' ~
results and were informed that all of the tests were2 ?% S# z7 @5 z# \$ k5 o# K! L
normal except the testosterone level was high. The
( Q1 u  v9 `/ e. B! ]* H7 mfollow-up visit was arranged within a few weeks to9 n# Q% y' r1 c) n0 o2 k
obtain testicular and abdominal sonograms; how-) D" D6 ^/ Z% O+ t! i" M* B
ever, the family did not return for 4 months.
7 _3 S# p" x) RPhysical examination at this time revealed that the/ _: c5 h' j2 o2 W! w# ]- \, t2 X- z
child had grown 2.5 cm in 4 months and had gained0 ]3 \+ p  V; l8 y1 ?( J# s
2 kg of weight. Physical examination remained; J' v( E2 c# `) n0 t, Q) [
unchanged. Surprisingly, the pubic hair almost com-
6 X( N( ~- f# @2 k) `+ z! Npletely disappeared except for a few vellous hairs at$ S' P9 P, r& z% [5 n
the base of the phallus. Testicular volume was still 2
- O* \" L$ Y" \  c* DmL, and the size of the penis remained unchanged.
1 G! o5 Z  z3 z& ^The mother also said that the boy was no longer hav-
" s& X3 i1 [- l$ ?9 @' Ring frequent erections." I* S0 c9 w0 ~3 `
Both parents were again questioned about use of
8 `* ~6 S6 m0 J( m4 d3 Qany ointment/creams that they may have applied to
/ E8 ^$ f: c; E' \( ~$ }* Fthe child’s skin. This time the father admitted the( s3 N2 E3 C* |2 z' S% X3 h
Topical Testosterone Exposure / Bhowmick et al 5416 ]( K& S# L" E* J! n- h9 U% \$ Q
use of testosterone gel twice daily that he was apply-$ o) E/ B0 L4 k6 A) c7 i
ing over his own shoulders, chest, and back area for
9 h3 _* a9 j* [3 Q$ d. b( ya year. The father also revealed he was embarrassed9 K) z* Q1 U* c; K# H, d7 ^
to disclose that he was using a testosterone gel pre-% q1 d% w* h, j1 \
scribed by his family physician for decreased libido
% B( Z% u, d$ l9 t# u5 A8 Z7 Lsecondary to depression.
0 ]1 L! U! r( k8 q5 g$ a0 ?* h# PThe child slept in the same bed with parents.
2 x- y( [  q0 w5 V& GThe father would hug the baby and hold him on his) d1 }- J. ?+ i7 ]
chest for a considerable period of time, causing sig-
4 ?+ r5 W" [! P3 E) W1 ?# wnificant bare skin contact between baby and father.
2 [9 E3 |- E! ~+ f; o! I4 p5 [The father also admitted that after the phone call,; g1 C4 c- I: o$ y# C% @% V2 q! e
when he learned the testosterone level in the baby% C' a$ w2 C' w0 v" l) W( S+ Z
was high, he then read the product information. c' D) W$ }; B0 ]* W& H
packet and concluded that it was most likely the rea-
% I0 w0 O/ R' o! B( A- h& e. d" u! Dson for the child’s virilization. At that time, they
1 ?* ^! ^* Y8 T" h, ~2 B+ A  Jdecided to put the baby in a separate bed, and the0 }; M  Y- F: k5 a+ {: q6 _$ Y
father was not hugging him with bare skin and had
# X% K2 k! v, p. Q3 Vbeen using protective clothing. A repeat testosterone- N5 E) m5 ]6 [/ X, j
test was ordered, but the family did not go to the
7 b5 a1 C" `" Q, G: B/ dlaboratory to obtain the test.
9 d" H7 |) ^- ]! }Discussion* {$ D/ O. `1 J' K+ b+ B
Precocious puberty in boys is defined as secondary
  @+ O) E- X" j, Msexual development before 9 years of age.1,4
3 R" G" y( A, K; _Precocious puberty is termed as central (true) when
' W. W* S& f* C7 e+ u/ ~; d: w1 uit is caused by the premature activation of hypo-
: B0 v" n; i  ]0 P2 Q  Othalamic pituitary gonadal axis. CPP is more com-
% s7 q* c) f( J' y0 n7 p2 Zmon in girls than in boys.1,3 Most boys with CPP
) o% p8 M2 L3 y8 u  @, ~8 wmay have a central nervous system lesion that is
- P" E0 R& _/ \% i1 \: yresponsible for the early activation of the hypothal-: v4 M- G, r: }; Z4 w- o8 c
amic pituitary gonadal axis.1-3 Thus, greater empha-
  ]7 Y( a, J# v! Isis has been given to neuroradiologic imaging in+ j% U# r9 f3 L! H
boys with precocious puberty. In addition to viril-
& z% n5 n$ x( u3 B3 [* Sization, the clinical hallmark of CPP is the symmet-
3 y6 Q6 N5 R0 f( _4 H& Frical testicular growth secondary to stimulation by
- T0 ?# z2 z$ j3 [! ~- ~6 X% Y. c0 vgonadotropins.1,3
  |4 _5 ^/ V, j% O+ [! Q: |" xGonadotropin-independent peripheral preco-8 y) v0 a# o2 b' x0 ]) R
cious puberty in boys also results from inappropriate
0 ~% H2 @6 V% l& G. k1 Handrogenic stimulation from either endogenous or
2 T8 r% v$ n( Sexogenous sources, nonpituitary gonadotropin stim-
2 R  b5 ?) V' I( fulation, and rare activating mutations.3 Virilizing
$ [3 Z1 ~* z# c- Gcongenital adrenal hyperplasia producing excessive
# q. m4 m" h. M5 u8 L, H2 cadrenal androgens is a common cause of precocious
: D- I5 O4 r. o' ?) zpuberty in boys.3,4
- z" p5 v1 @- @. N. W% e$ WThe most common form of congenital adrenal0 E/ D0 J3 V& V, ]; D. N/ f6 v6 R
hyperplasia is the 21-hydroxylase enzyme deficiency.1 Y% m; Z5 @  z* A: ^$ r  U% J4 S0 v
The 11-β hydroxylase deficiency may also result in
3 M8 |7 X( Q6 r# [8 Vexcessive adrenal androgen production, and rarely,% Y2 Q7 I7 j8 C$ d8 j0 L9 y
an adrenal tumor may also cause adrenal androgen* r  S, P4 S. W2 p1 Z9 z+ Y- S
excess.1,3
5 P& M+ s8 Z5 |; ~' `at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% G2 R/ K( y5 Q: ?& q7 A' X
542 Clinical Pediatrics / Vol. 46, No. 6, July 20075 A' [, W  M# _8 t3 _" \" G/ l' K
A unique entity of male-limited gonadotropin-
# T2 v' G9 q% |independent precocious puberty, which is also known
; B, A1 B1 p" n7 Jas testotoxicosis, may cause precocious puberty at a/ `0 p9 m$ \2 g" t+ `7 Z
very young age. The physical findings in these boys; n) t" T- L+ i. w2 K0 l/ l2 f$ J; a  \
with this disorder are full pubertal development,
3 m6 {/ S  N3 Z- |6 z' s, dincluding bilateral testicular growth, similar to boys3 b4 }5 _6 P( u
with CPP. The gonadotropin levels in this disorder& {. w% h& B# b0 K  ^3 C6 E$ O
are suppressed to prepubertal levels and do not show0 H( m) N/ K5 e/ i$ P) o' U
pubertal response of gonadotropin after gonadotropin-8 t% v: C, e6 e
releasing hormone stimulation. This is a sex-linked! g" a  k  K" y9 u  V. ]( w+ I4 ]1 j$ }" Z
autosomal dominant disorder that affects only0 Q( N2 r9 S* ^. A) L6 ]' s0 f2 [
males; therefore, other male members of the family
5 t; d# a( w6 O; Ymay have similar precocious puberty.3
) u3 ~7 `0 n" W5 b  a' N1 wIn our patient, physical examination was incon-
: X9 `: N5 f- `" F9 |1 P  L- Zsistent with true precocious puberty since his testi-- q% P1 A, J7 \9 E6 C
cles were prepubertal in size. However, testotoxicosis3 f' G- @6 I$ A8 p: ?+ A
was in the differential diagnosis because his father: u3 j2 T# k( K" @' d
started puberty somewhat early, and occasionally,
5 M' _& `' w2 J. Y4 n7 D; ]testicular enlargement is not that evident in the
* l; [3 Z6 ^# b& t% Ubeginning of this process.1 In the absence of a neg-8 _  A2 v. ~4 X" Q( I9 X8 v: e+ F
ative initial history of androgen exposure, our8 H4 w3 |. Z* K+ h1 c
biggest concern was virilizing adrenal hyperplasia,9 J) H/ \5 H5 t/ N
either 21-hydroxylase deficiency or 11-β hydroxylase
  Y5 q& J  G2 u  H5 |* K2 odeficiency. Those diagnoses were excluded by find-
: F$ L* K! b4 }ing the normal level of adrenal steroids.
3 j1 g" g  V) B1 v: K% AThe diagnosis of exogenous androgens was strongly
& d! ~# j/ L! b+ gsuspected in a follow-up visit after 4 months because7 a( m- f7 H# \+ }4 ^; F9 Q, v5 q( l
the physical examination revealed the complete disap-
9 D9 F9 e9 K( |" ~: @5 Jpearance of pubic hair, normal growth velocity, and# ]7 F4 F' u4 N5 M1 v! k4 W, h
decreased erections. The father admitted using a testos-
' E; v  C' V; q/ w3 d0 hterone gel, which he concealed at first visit. He was
/ L5 E1 ^% g: A( F* x1 Gusing it rather frequently, twice a day. The Physicians’% U2 ]% W2 u- K% t& I0 i$ p/ z
Desk Reference, or package insert of this product, gel or
4 f" G$ I: q, w2 v7 k5 jcream, cautions about dermal testosterone transfer to  H; q" W( a. {- q
unprotected females through direct skin exposure.
; |" [# Q# E0 [6 X+ fSerum testosterone level was found to be 2 times the
. _9 B5 y. T5 g, |6 w4 Qbaseline value in those females who were exposed to; u# P- X  c* {9 [: D, y8 T( q# s
even 15 minutes of direct skin contact with their male' |) _3 n+ A, T0 D3 G8 u2 e. K
partners.6 However, when a shirt covered the applica-
- K4 }' u+ @( ^  P: [( ttion site, this testosterone transfer was prevented.$ L; y$ N# m8 `: Y8 G" C
Our patient’s testosterone level was 60 ng/mL,
/ l# d/ k( i/ w+ u  v) V! Ywhich was clearly high. Some studies suggest that& a7 J$ y3 z7 `/ L
dermal conversion of testosterone to dihydrotestos-
* m, ]) ?' [' I8 i, D- Rterone, which is a more potent metabolite, is more, W" z/ G3 K* G2 L) h9 r
active in young children exposed to testosterone" `5 S$ _  O! H4 \& a$ k; ~
exogenously7; however, we did not measure a dihy-) ~' L; v0 W! t: X
drotestosterone level in our patient. In addition to/ r2 Z0 g" S$ q* f3 w
virilization, exposure to exogenous testosterone in! F- I3 @) C9 `; j$ i
children results in an increase in growth velocity and: U9 F0 a! q& O9 o6 r
advanced bone age, as seen in our patient.
/ Y7 J2 P# k9 }# eThe long-term effect of androgen exposure during
9 |( Z  |5 }5 v$ C7 Qearly childhood on pubertal development and final4 ~. Y0 w5 m- Q* {9 [: y
adult height are not fully known and always remain
" ~& _0 S. k5 Q( Q! Q0 }# Ya concern. Children treated with short-term testos-# q; A7 P( L' H
terone injection or topical androgen may exhibit some
5 r8 e" G9 V& z  B) h) S" I4 V, Cacceleration of the skeletal maturation; however, after
7 H0 D# J, K" Gcessation of treatment, the rate of bone maturation/ {! l: V% ?: L5 o/ Z5 W6 M: y
decelerates and gradually returns to normal.8,9
: L6 I* B9 ]* }  VThere are conflicting reports and controversy
& [8 @& Q5 u2 O& u# x) ^over the effect of early androgen exposure on adult) o, c# j  I* G" b! }/ G) ?
penile length.10,11 Some reports suggest subnormal+ N4 s0 W- ?0 D, R5 f( t1 o2 V* P
adult penile length, apparently because of downreg-
! m, p* |$ e8 P, Oulation of androgen receptor number.10,12 However,+ R( W5 E5 N/ Q+ p- f* S, L
Sutherland et al13 did not find a correlation between1 i6 J( V9 h4 E  Z, Z- @: C5 p
childhood testosterone exposure and reduced adult; H2 ?8 N+ z  t$ r- Q$ \% ]
penile length in clinical studies.1 b) b- z6 F1 S3 l# n: ^
Nonetheless, we do not believe our patient is
' M* t$ ^- ~8 Wgoing to experience any of the untoward effects from
' q5 t4 B! K. ~% G) M$ btestosterone exposure as mentioned earlier because4 z& g/ Y- K' h7 v
the exposure was not for a prolonged period of time.. c3 p: j. S/ S5 ?4 }3 y! o5 Z, `# i
Although the bone age was advanced at the time of
& }, F& H9 r. q+ W. F$ g3 y2 gdiagnosis, the child had a normal growth velocity at
% \9 p+ d7 W$ P" J, D1 I! S! xthe follow-up visit. It is hoped that his final adult
6 P( z: n# P  C2 r" `8 Fheight will not be affected.4 H1 Q, F) z1 O( I+ q# G& \& L
Although rarely reported, the widespread avail-
4 ^! _8 T3 {% U3 k5 s1 C9 g  uability of androgen products in our society may# [! n2 u- T; ?
indeed cause more virilization in male or female& ?0 r# s. \% V3 }) s' Z9 d
children than one would realize. Exposure to andro-8 ^0 f6 j" u* V- r. ~' i1 ^. [
gen products must be considered and specific ques-- e7 d, i6 E+ s
tioning about the use of a testosterone product or7 i' Q- S. q$ @; Z5 D9 J* [
gel should be asked of the family members during
3 ]1 T- ~& X3 ]6 e8 ~  W, dthe evaluation of any children who present with vir-
. Y) a! Z: m. `. T9 [ilization or peripheral precocious puberty. The diag-
3 T- R, R2 w; d+ i/ Znosis can be established by just a few tests and by- Y# N, n" g; b( |/ Y
appropriate history. The inability to obtain such a
5 p' w) i) u0 hhistory, or failure to ask the specific questions, may' B2 v* X2 s1 ?: q
result in extensive, unnecessary, and expensive0 W3 @7 k$ d1 R& R" U- Z* L
investigation. The primary care physician should be
% ]& u, l9 g# T, @aware of this fact, because most of these children0 L0 o, W3 p% @) L4 u3 |, W' c
may initially present in their practice. The Physicians’
, H7 h; K. r9 a+ kDesk Reference and package insert should also put a
8 U, _. h  W2 h, ~) l! p; |( R- J) owarning about the virilizing effect on a male or
4 r5 M0 H/ [  X8 E1 J$ [female child who might come in contact with some-
% _5 l# S8 j. r& f) ]& T5 R- a; Rone using any of these products.  |* f1 i+ v* d, M
References) G# ]7 v; ~& A
1. Styne DM. The testes: disorder of sexual differentiation& p& }4 L" l/ i* _0 \/ w3 J: M
and puberty in the male. In: Sperling MA, ed. Pediatric
. U8 {3 ?/ F3 ]) {# \% XEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;0 p# a) P6 T/ S1 s: m# V; Z. I" T
2002: 565-628., ~) ~3 @9 j5 w% a, l2 w
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious, o6 R; [- a" k" B4 A% `
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
. Y/ D5 ?9 T7 g/ t8 n9 z& w
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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