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Sexual Precocity in a 16-Month-Old3 Z! G8 u% G- n1 T+ m# R
Boy Induced by Indirect Topical
7 i, g" U4 @/ }& sExposure to Testosterone
: z" J1 C4 n5 _& lSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2! N/ R; l  C9 h1 `. ?" O1 \
and Kenneth R. Rettig, MD1. z( o& d$ S2 j) k9 v0 T/ U# D; M
Clinical Pediatrics
& O9 W/ @4 t$ w& mVolume 46 Number 6" u# y- C" ], N& @3 q
July 2007 540-543; A1 M6 h$ V( C1 S
© 2007 Sage Publications4 y. R8 P% J& b% J
10.1177/0009922806296651
4 T, v/ q, P2 Chttp://clp.sagepub.com& T8 i* a+ O* K0 g3 o3 k" N4 A# A
hosted at
( h3 P/ S/ V% r% _$ d8 k% K( khttp://online.sagepub.com3 B/ h, D% i" i; h: J2 d
Precocious puberty in boys, central or peripheral,
! r1 q" g  j, ]( n/ r2 }$ R7 V+ Eis a significant concern for physicians. Central
* P; N" X0 K! p; z% n( u! `precocious puberty (CPP), which is mediated
( R) _; i' l/ F' N" N) ~through the hypothalamic pituitary gonadal axis, has8 n! F+ s5 D8 P; ^
a higher incidence of organic central nervous system
: W: @: T' p8 l" G8 [lesions in boys.1,2 Virilization in boys, as manifested
: F0 `/ @, m4 g$ dby enlargement of the penis, development of pubic3 `$ O5 @! k" G2 H
hair, and facial acne without enlargement of testi-3 a5 c4 w" ~6 [* c: b/ _  L
cles, suggests peripheral or pseudopuberty.1-3 We
% _3 ~( ]; E, i0 o0 w9 Sreport a 16-month-old boy who presented with the& m2 E" m. |: b. Z8 V! `; F
enlargement of the phallus and pubic hair develop-$ ^6 X- Y/ ^/ b! a( a
ment without testicular enlargement, which was due
1 g& f" ]7 x* O8 `to the unintentional exposure to androgen gel used by
) @+ r& w6 r6 j7 N/ v: X; W- Y; Qthe father. The family initially concealed this infor-
0 p2 h6 W7 J6 Y2 rmation, resulting in an extensive work-up for this
( I6 i" u. c  uchild. Given the widespread and easy availability of
4 k0 A1 g2 c) @9 ftestosterone gel and cream, we believe this is proba-
4 `, E. a2 L1 S2 q* G2 r: Wbly more common than the rare case report in the/ b# P% u0 g) u- m
literature.4  X1 N* r, b5 C! ~& ^
Patient Report
& c: T! O# R- }5 a+ SA 16-month-old white child was referred to the- I3 D0 T7 O* O' ^% O
endocrine clinic by his pediatrician with the concern! t* m( L3 z: C/ K2 Z$ o7 I
of early sexual development. His mother noticed& g# ^4 c5 D- e7 |3 |$ @% M
light colored pubic hair development when he was
/ {/ ~0 e$ r+ C9 W0 j2 CFrom the 1Division of Pediatric Endocrinology, 2University of  ?9 t& i5 C$ G6 ~3 ^1 l/ E
South Alabama Medical Center, Mobile, Alabama.
* \  e6 z- u  D) N( i; XAddress correspondence to: Samar K. Bhowmick, MD, FACE,, g4 b# K* M1 x$ q* h
Professor of Pediatrics, University of South Alabama, College of. c3 V, ]& ?- B7 J9 U( @4 Q# V7 }
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
; m2 g1 J4 s- O' Te-mail: [email protected].
, _1 @) ^. ~4 b2 {about 6 to 7 months old, which progressively became# M( \. }! [" m& X; z
darker. She was also concerned about the enlarge-4 B3 Y  N+ r4 [7 l; c9 c7 `
ment of his penis and frequent erections. The child6 S& {( \1 Q5 W- x- ]7 ?2 A# ]
was the product of a full-term normal delivery, with
) n; f" t* i0 D. c; F2 pa birth weight of 7 lb 14 oz, and birth length of
- M0 N, B0 D6 C20 inches. He was breast-fed throughout the first year/ C1 j6 a6 R9 j1 D" J: I/ o9 k) P
of life and was still receiving breast milk along with  _: {1 O( I/ e9 _
solid food. He had no hospitalizations or surgery,  F: R, T, V* @; d/ ^
and his psychosocial and psychomotor development, ?! G  K; v1 K3 V0 b9 w! c+ p! b8 n! g
was age appropriate.# z4 z6 ^- R: o4 s3 I/ ~/ W% C
The family history was remarkable for the father,# D. ]5 j: S+ o9 I( ^
who was diagnosed with hypothyroidism at age 16,
/ h7 S8 g  k! R! Cwhich was treated with thyroxine. The father’s. [  r$ V$ X& J9 k; w* ?4 \
height was 6 feet, and he went through a somewhat
8 s$ m/ ~8 D+ t! F- @" mearly puberty and had stopped growing by age 14.
1 j: C1 k# I; R( ^The father denied taking any other medication. The1 r7 U$ A' `* t  a
child’s mother was in good health. Her menarche1 z8 Y8 i! f9 E$ i8 K: G
was at 11 years of age, and her height was at 5 feet1 m& m7 u( T! Z& |  a) @% q1 M+ b% K
5 inches. There was no other family history of pre-3 c# {* s+ {  d: d+ w& w! Y
cocious sexual development in the first-degree rela-
" S$ V4 z3 U; ]1 w% P( _' T& ^tives. There were no siblings.9 ^$ I' a2 V/ H. L( q( U" N+ K
Physical Examination3 ]0 a1 s6 a& ]1 T$ Y+ D/ j
The physical examination revealed a very active,7 y/ L' x5 v+ D) p% s
playful, and healthy boy. The vital signs documented4 S9 F1 B* B. N% r9 b% d3 m1 p
a blood pressure of 85/50 mm Hg, his length was9 L/ ~% j5 I7 c8 {* D
90 cm (>97th percentile), and his weight was 14.4 kg
  H. P: d6 S7 B! d- ^+ n(also >97th percentile). The observed yearly growth
( H; ?' y1 L5 vvelocity was 30 cm (12 inches). The examination of& M* t* X% ?! M0 g  `& B) K
the neck revealed no thyroid enlargement.
% O) m9 B. Q: q; w: R/ mThe genitourinary examination was remarkable for
) m) C- T1 Q- x3 I$ f% uenlargement of the penis, with a stretched length of
  t/ ]$ h. J7 a" s: e) y8 cm and a width of 2 cm. The glans penis was very well
& c3 b% Y1 ~8 u: ~$ odeveloped. The pubic hair was Tanner II, mostly around! }6 V, H' C% W' y4 x" `. \$ b9 @
540" O1 M  v1 x1 T% I# \+ C6 j
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 I# S/ v+ S4 C& @
the base of the phallus and was dark and curled. The
2 b! A0 i3 x5 m0 Z& Rtesticular volume was prepubertal at 2 mL each.
4 Q- E0 |* H& T3 Z# ~* FThe skin was moist and smooth and somewhat
3 c7 W7 t/ ]( }" h6 j- M( yoily. No axillary hair was noted. There were no
; _8 H+ [, r) g" S$ k1 ~$ k$ m$ N4 aabnormal skin pigmentations or café-au-lait spots.3 ?6 [; I3 a0 o1 _6 }& P
Neurologic evaluation showed deep tendon reflex 2+
7 n% q* z3 W5 H9 G7 B% v5 |bilateral and symmetrical. There was no suggestion5 k* n3 Z! L3 c% a- \$ i) n/ f; m
of papilledema.
; r) w# m! m- H4 Y# NLaboratory Evaluation
# L6 l8 s4 ?3 W% `The bone age was consistent with 28 months by4 b/ [2 K. x: Z7 l4 S8 g' b1 P8 U- w
using the standard of Greulich and Pyle at a chrono-8 o& r$ `% z/ k  Y( ^! {
logic age of 16 months (advanced).5 Chromosomal
$ H2 B* y: E3 q& O  |karyotype was 46XY. The thyroid function test4 n1 r: i  o( w) n  [/ Z! j
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
# J& J' i% \# H5 rlating hormone level was 1.3 µIU/mL (both normal).+ E; U! k8 [) V% K
The concentrations of serum electrolytes, blood
( {7 ^9 X, W8 O/ I0 xurea nitrogen, creatinine, and calcium all were
1 M) Z8 X6 s) B' F" E$ {  Z& Qwithin normal range for his age. The concentration
; y7 l$ m% }$ p: L+ ?: Y+ n( nof serum 17-hydroxyprogesterone was 16 ng/dL
( ~8 t; W5 v1 G& j( o(normal, 3 to 90 ng/dL), androstenedione was 20
  f9 ]8 U  x7 U! _" |0 `ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-* W' ]3 j& f0 e" i! p; }/ |
terone was 38 ng/dL (normal, 50 to 760 ng/dL),, {# N( L* V- z1 S, ?* C* U4 H
desoxycorticosterone was 4.3 ng/dL (normal, 7 to! E7 h& y7 l3 v5 F. x
49ng/dL), 11-desoxycortisol (specific compound S)( F+ `; W* V% S  z5 C
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
, X! D6 Q/ d& N$ ?( D- Ktisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
" r, v. v" S' H1 u" ]/ h$ Ntestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
( [- h  P, c1 w7 {4 I. k6 ?and β-human chorionic gonadotropin was less than
3 {  i/ f8 A3 U6 `1 N' u5 j; q4 h6 [5 mIU/mL (normal <5 mIU/mL). Serum follicular
! m% K, ^1 U" ^% f. ~# r8 r6 i; Wstimulating hormone and leuteinizing hormone' l- W; e! f6 n. g# O: c. ?
concentrations were less than 0.05 mIU/mL; Y' d: V# \& r) u. p& Y! {0 ]: U
(prepubertal).) g  R; F! P" D
The parents were notified about the laboratory
8 t$ o- U4 G. o8 e7 _/ Presults and were informed that all of the tests were- y& v0 O1 N$ L& \
normal except the testosterone level was high. The
# v! _, Z& w6 q8 Ofollow-up visit was arranged within a few weeks to% z# t' i  H: i1 t) [
obtain testicular and abdominal sonograms; how-- R9 l/ n6 [$ M, J+ o
ever, the family did not return for 4 months.
! b  G. `9 Y8 V6 {2 xPhysical examination at this time revealed that the9 G& ]! x2 V2 d0 X
child had grown 2.5 cm in 4 months and had gained9 S/ K. j& _  @: N/ h/ K  S
2 kg of weight. Physical examination remained
% i+ d- S6 w: |& Q9 @unchanged. Surprisingly, the pubic hair almost com-
5 c' q$ b" X; t+ M' _! j9 npletely disappeared except for a few vellous hairs at9 i) I5 U5 K1 w  F2 w6 l& @6 M% ^  R
the base of the phallus. Testicular volume was still 20 \+ \" u# p7 @) h
mL, and the size of the penis remained unchanged.
& M$ Q, Y9 Q8 H" V" oThe mother also said that the boy was no longer hav-; f# S0 z) h& I4 z% l- M* a  g
ing frequent erections.
3 P& _9 I1 X( G7 b' |1 ?9 D5 L& g0 GBoth parents were again questioned about use of
" i- s" J" p  j7 y# rany ointment/creams that they may have applied to5 b& Y# Q& q& d( E+ Z) [9 m/ J
the child’s skin. This time the father admitted the
" e! [, K$ e4 {5 K. A1 OTopical Testosterone Exposure / Bhowmick et al 541: U% W0 s9 @4 R9 M3 }+ _5 Z: I* r
use of testosterone gel twice daily that he was apply-8 S$ }3 ]4 u$ {* s6 ]0 H9 ^8 G. q
ing over his own shoulders, chest, and back area for3 ^( D" `; l, u7 q7 K. k
a year. The father also revealed he was embarrassed
; Q7 q* d+ G. x: A1 Y+ \% Kto disclose that he was using a testosterone gel pre-
( F' b2 f, w. a7 e/ Oscribed by his family physician for decreased libido" V5 D' \9 t& g/ Z
secondary to depression.
$ k& t9 ^- e: bThe child slept in the same bed with parents.
& y5 h1 x5 n3 U2 B3 CThe father would hug the baby and hold him on his
" z( k8 c6 o  b9 `chest for a considerable period of time, causing sig-/ E3 q6 v8 @/ D' X7 z, H
nificant bare skin contact between baby and father.
* D( j% ~( K5 _/ kThe father also admitted that after the phone call,0 m1 l0 G& n1 G
when he learned the testosterone level in the baby
+ t7 y! J2 E) _$ mwas high, he then read the product information( X" ~6 {0 c( {8 ?
packet and concluded that it was most likely the rea-
4 u# D6 {2 t1 Y3 Lson for the child’s virilization. At that time, they; g! z4 h, |6 {) i- C5 c
decided to put the baby in a separate bed, and the
- }9 P0 H0 l$ m/ B$ U0 p+ ~% k+ Rfather was not hugging him with bare skin and had
& r9 j" e; F: q: t/ q" ]0 N0 bbeen using protective clothing. A repeat testosterone9 t2 T6 _1 W4 y9 u
test was ordered, but the family did not go to the
  V7 k. I% G7 @laboratory to obtain the test.# t3 o7 F/ X+ f% @6 B' u
Discussion
4 a! [2 V5 ]/ ]% T. F9 z. UPrecocious puberty in boys is defined as secondary& F8 z( N; T  y  q+ W: z. Z
sexual development before 9 years of age.1,4
% x& x1 j8 n9 qPrecocious puberty is termed as central (true) when0 ~, \. `+ D) d
it is caused by the premature activation of hypo-" H" z. U) T6 S# P; k/ U4 I
thalamic pituitary gonadal axis. CPP is more com-% k$ g& v, ?- u7 M
mon in girls than in boys.1,3 Most boys with CPP
/ O1 }+ V' P8 J- u  umay have a central nervous system lesion that is
+ Y, R* L1 o$ e$ M) Kresponsible for the early activation of the hypothal-7 H7 }& H% U9 H- j' R( x
amic pituitary gonadal axis.1-3 Thus, greater empha-, z( t( u5 ]# Q* a  ^5 g
sis has been given to neuroradiologic imaging in
6 Q" {) j% }! f; \4 Sboys with precocious puberty. In addition to viril-6 k3 P/ S* b/ I- ~0 R5 X9 C8 H
ization, the clinical hallmark of CPP is the symmet-
  r% u) i0 @9 \4 Mrical testicular growth secondary to stimulation by" N+ b8 v! ]+ h$ F
gonadotropins.1,3% a- x3 k* C: \
Gonadotropin-independent peripheral preco-. I6 I& i, f+ x. r" B6 z% H8 Q. X' ]
cious puberty in boys also results from inappropriate
; [! w0 F- _$ V6 jandrogenic stimulation from either endogenous or
3 x7 c6 v+ r* Z+ \; \exogenous sources, nonpituitary gonadotropin stim-
' \, [' i- P1 b8 C: [2 R& E7 Eulation, and rare activating mutations.3 Virilizing
" s# P: p9 i; e& K; Z7 _congenital adrenal hyperplasia producing excessive) s5 \; e5 l- S; v' C% P5 G5 }
adrenal androgens is a common cause of precocious
$ l# X/ J+ p3 [( I0 K+ hpuberty in boys.3,4& W% T- q6 r! v  C1 j
The most common form of congenital adrenal& a8 o0 m/ q% [# E
hyperplasia is the 21-hydroxylase enzyme deficiency.
) M( x9 Q2 L: d0 @/ h: mThe 11-β hydroxylase deficiency may also result in6 e) C3 q5 t- w* j& U+ Q; V
excessive adrenal androgen production, and rarely,) a& k7 X4 C8 C0 A6 ]0 N) B, ~
an adrenal tumor may also cause adrenal androgen9 p7 {  `5 l( w$ ^
excess.1,37 c. \: w& [# T- B  P2 Z2 m# C
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& }: ]$ s1 x8 @542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
. B+ i& j$ r: H* X1 `" ~7 |A unique entity of male-limited gonadotropin-4 h3 G5 ]& e/ s; Z4 q3 Z1 \+ a
independent precocious puberty, which is also known) S1 @: s) G( I1 m
as testotoxicosis, may cause precocious puberty at a
! ?( H' l: B- l! H( e9 ^8 pvery young age. The physical findings in these boys
" v# w" ]6 y7 d5 Q- [- C- S8 rwith this disorder are full pubertal development,- @* x; c4 m1 ]
including bilateral testicular growth, similar to boys/ W$ k: H% \4 g1 H( c. a+ c8 V9 b
with CPP. The gonadotropin levels in this disorder
4 K$ g0 x7 t! l2 E; [4 l& kare suppressed to prepubertal levels and do not show
& F! Z! x& o" ^6 y! z! o5 }1 l4 Z3 _pubertal response of gonadotropin after gonadotropin-: i% g( c% E. p; E0 e3 Q- w
releasing hormone stimulation. This is a sex-linked
& ]& ]5 B! z+ w% G5 _autosomal dominant disorder that affects only
6 C  [% V% y! d6 |males; therefore, other male members of the family
! X2 j$ v/ Q& ?  b8 e* K4 zmay have similar precocious puberty.3
3 P* ]/ t9 }! S. |+ y: a" OIn our patient, physical examination was incon-
4 j" V" p( u8 c8 F. Nsistent with true precocious puberty since his testi-
2 P5 |5 Y1 D  i, ]9 R( P9 o1 vcles were prepubertal in size. However, testotoxicosis
# s9 [$ T  U8 _; M* A  Jwas in the differential diagnosis because his father
+ n) w5 T# _/ `) \) Ostarted puberty somewhat early, and occasionally,1 |4 c+ [; x, n* R& l* i7 S  o# q: F
testicular enlargement is not that evident in the0 R0 Z* h9 Y- S" p7 o
beginning of this process.1 In the absence of a neg-' Z- |1 `& Y& p4 T7 C' E! k
ative initial history of androgen exposure, our
  U3 }* E: B# @& _- {; V5 ~biggest concern was virilizing adrenal hyperplasia,
, Z# r/ t6 k3 ~+ U9 w. h5 H, Geither 21-hydroxylase deficiency or 11-β hydroxylase
- j* }5 j) u/ y6 [# kdeficiency. Those diagnoses were excluded by find-/ U$ e9 \8 s$ r- |
ing the normal level of adrenal steroids.) g+ x0 h/ u6 u9 v& d9 x5 m
The diagnosis of exogenous androgens was strongly
3 U8 r3 g, o% m9 I' I. L& jsuspected in a follow-up visit after 4 months because
; X$ |# _" k; {6 w$ @1 gthe physical examination revealed the complete disap-
- I; q+ C7 I+ T3 P! \: ~pearance of pubic hair, normal growth velocity, and
4 e9 Z3 }  i3 m6 g- p8 B5 W7 S2 ^decreased erections. The father admitted using a testos-
- u1 f+ u- d5 f: Z7 D; a9 w6 Dterone gel, which he concealed at first visit. He was7 V( b4 x% `6 t/ Z
using it rather frequently, twice a day. The Physicians’
& S! D, ^1 p$ z) p6 bDesk Reference, or package insert of this product, gel or
* `. }$ l) m& m6 Ccream, cautions about dermal testosterone transfer to
5 y" R$ B3 \5 q& ^0 M8 `unprotected females through direct skin exposure.1 ]$ V5 h+ R2 N' P# Y% k
Serum testosterone level was found to be 2 times the8 Q1 y. }! h$ c0 m' c4 O* n
baseline value in those females who were exposed to
( M$ E! s, g8 Y& g4 I% @even 15 minutes of direct skin contact with their male8 Z: Z; \( S; p- w, P
partners.6 However, when a shirt covered the applica-
5 b1 O! j% _3 w. Ntion site, this testosterone transfer was prevented.
/ ~" j! r( @' G" z8 v  W; l$ WOur patient’s testosterone level was 60 ng/mL,
9 P7 M# Q: d/ h' K, zwhich was clearly high. Some studies suggest that
: P1 W- p$ Y# `6 [4 f8 l. m: i$ l6 Bdermal conversion of testosterone to dihydrotestos-  ^+ R' p6 |  w
terone, which is a more potent metabolite, is more- T/ J% M# _1 a3 x
active in young children exposed to testosterone
, m: ^- w8 u5 q8 u) }exogenously7; however, we did not measure a dihy-! f# ]- G& M& O2 |$ a$ o8 r
drotestosterone level in our patient. In addition to. d1 G5 K* l. Q! a* ?% u
virilization, exposure to exogenous testosterone in
# n& n6 u5 @8 @- ?+ `children results in an increase in growth velocity and2 |* |) i( @& Z- e
advanced bone age, as seen in our patient.
; C# V' c) [1 a# jThe long-term effect of androgen exposure during
9 e" x8 T0 K& m6 Vearly childhood on pubertal development and final
- v/ v  [8 g1 M- b) m6 ~% l% P0 I5 vadult height are not fully known and always remain
+ e# J: M+ O' j4 |" Q5 ia concern. Children treated with short-term testos-
! i8 f6 u" I4 mterone injection or topical androgen may exhibit some
& L1 ?+ v! F) Q* V  {7 macceleration of the skeletal maturation; however, after- _* G( \4 N- }
cessation of treatment, the rate of bone maturation
) U2 g% u. v. d, Wdecelerates and gradually returns to normal.8,9
0 H8 y  l, x, f, {5 h9 Q, fThere are conflicting reports and controversy
0 Y9 m5 R( z0 O3 b! tover the effect of early androgen exposure on adult4 S+ t  T% h7 k) u/ K5 ^
penile length.10,11 Some reports suggest subnormal% A1 d9 q! m8 }: o+ F7 P
adult penile length, apparently because of downreg-% r4 S& R' [  i% A+ x: W& E
ulation of androgen receptor number.10,12 However,
( j* S8 Z  F. ESutherland et al13 did not find a correlation between% |& x6 B6 \- v+ I
childhood testosterone exposure and reduced adult
' z7 h; W/ w# c9 J# Xpenile length in clinical studies.
/ d" F$ M) f" p* l+ B6 J2 t1 wNonetheless, we do not believe our patient is. W) c+ S' {( N$ j
going to experience any of the untoward effects from
0 F9 o/ \: c. O" F; S( atestosterone exposure as mentioned earlier because
8 h6 I# v; |9 \+ ?0 V6 I% \/ G% athe exposure was not for a prolonged period of time.
+ H" {9 H1 E0 v7 F. \0 kAlthough the bone age was advanced at the time of
) _3 g$ V2 d& _' u5 S/ mdiagnosis, the child had a normal growth velocity at# J4 s' r/ i: W' V7 q6 I
the follow-up visit. It is hoped that his final adult
% R- q* T1 E: A: w: p! \% Yheight will not be affected.7 [, d2 [6 }/ G' U
Although rarely reported, the widespread avail-
  P  _5 `2 A, J5 F# Pability of androgen products in our society may2 o  R' b" R. `& v
indeed cause more virilization in male or female
, c/ @; b8 S  g" e& k/ f3 Ychildren than one would realize. Exposure to andro-) [5 k3 ?1 r8 u0 {
gen products must be considered and specific ques-
! |3 ?! I2 K" a; D) Mtioning about the use of a testosterone product or
  j; Z, J6 ^/ \+ B2 @gel should be asked of the family members during
/ Y4 j" I( ~. s, T; e, Tthe evaluation of any children who present with vir-
+ v4 z  n$ J6 V& F+ C8 X& G/ C8 K) q. Filization or peripheral precocious puberty. The diag-; R9 o( r9 u1 @1 |  H9 L
nosis can be established by just a few tests and by& ?/ w8 X( U, Q' n4 l6 N
appropriate history. The inability to obtain such a
: F) f1 X' s+ `history, or failure to ask the specific questions, may
7 `4 T, l* p8 w0 uresult in extensive, unnecessary, and expensive3 E3 G5 U4 U# t7 e1 W6 C
investigation. The primary care physician should be
% u+ W8 Y$ Z7 l' yaware of this fact, because most of these children
  H8 v4 e. y# f7 imay initially present in their practice. The Physicians’
% T# ]# H! @" c; Z- x1 QDesk Reference and package insert should also put a$ }& M9 ]( \) ?
warning about the virilizing effect on a male or
" n% u) T8 ~- u# i0 Y1 P0 Q5 Xfemale child who might come in contact with some-5 a6 V- G1 n' i# [$ C" W
one using any of these products.
% p& A& Z" y& C8 q& D- e) @: y7 QReferences" Y6 G7 x" E+ n( ]3 i, u- y
1. Styne DM. The testes: disorder of sexual differentiation
7 {' X7 P- o4 _! f* u6 x; Cand puberty in the male. In: Sperling MA, ed. Pediatric
0 ]* q( T4 @( M1 e/ yEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
) r, R2 f) y" }, S- B2002: 565-628.
# d0 h) t# b  C2 o% C2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
( J8 j8 S2 ~* q* q# Z0 X& Y3 Epuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
& r; P2 b0 E# |# N% tBoy Induced by Indirect Topical$ w# t0 @' B( m, P. h* ^' J! [
Exposure to Testosterone
4 }0 n- b+ t2 X8 BSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2/ r. j4 G3 `4 g( T) }. k3 s
and Kenneth R. Rettig, MD1
* r1 Q  ]+ C( @$ cClinical Pediatrics6 _6 S5 Q9 `: j' _
Volume 46 Number 6
1 h' J' h6 f6 `, IJuly 2007 540-543
( ?9 M. u  b* `1 c© 2007 Sage Publications% G3 n9 d. p/ M, \
10.1177/0009922806296651
! h6 Q% F( T# _$ l3 \% {http://clp.sagepub.com
/ }% F- t+ K' w6 C- Shosted at2 q9 Z% }; ]0 |( G' F
http://online.sagepub.com
! L$ B/ |1 q# MPrecocious puberty in boys, central or peripheral,# l9 o3 P1 S! c' ^
is a significant concern for physicians. Central
/ G1 C* X8 R$ G9 ^5 V% i% Vprecocious puberty (CPP), which is mediated1 ]# B" ], ]  n8 S( a8 f
through the hypothalamic pituitary gonadal axis, has& g, F( V+ E) M* Z3 I8 \
a higher incidence of organic central nervous system' i0 e- ?1 z. ~4 r
lesions in boys.1,2 Virilization in boys, as manifested
) t, `' H& r! k2 Aby enlargement of the penis, development of pubic
* \% z5 D- b: j* J( N: O6 _hair, and facial acne without enlargement of testi-4 D6 h5 E1 |# z2 j# w' \1 j, {
cles, suggests peripheral or pseudopuberty.1-3 We' N5 R  j7 B% n  ]3 J- ?, K
report a 16-month-old boy who presented with the
0 w' N- t4 p" z9 ~+ r1 W6 kenlargement of the phallus and pubic hair develop-+ |) n# \) Z2 N! |: p# h
ment without testicular enlargement, which was due* N) B& ^6 @- x: f% ]4 h
to the unintentional exposure to androgen gel used by
+ @* X6 l6 c' x. j& A9 b5 jthe father. The family initially concealed this infor-. o: Q5 G9 s' k+ [! m6 d( b( g% K
mation, resulting in an extensive work-up for this; O. N2 i0 R  \# x
child. Given the widespread and easy availability of
/ v  B$ R, R# m0 U+ t; I6 xtestosterone gel and cream, we believe this is proba-! c9 T' p! z4 J# l
bly more common than the rare case report in the% E& N6 P6 e, E" K
literature.4
* J& C! t0 |1 f: z9 F+ {Patient Report
, K4 k# w3 W" B! a$ HA 16-month-old white child was referred to the
& [8 j5 d' z! l1 mendocrine clinic by his pediatrician with the concern: P* x( ^4 S3 n* H! A# J* m, B
of early sexual development. His mother noticed
8 ~/ b2 T1 j, ], ~* hlight colored pubic hair development when he was
. f! R. P! j$ g2 H( N; pFrom the 1Division of Pediatric Endocrinology, 2University of
. l! Y7 H: B8 tSouth Alabama Medical Center, Mobile, Alabama.) f; l6 I/ T' I. @
Address correspondence to: Samar K. Bhowmick, MD, FACE,
, v0 K. T3 F1 W+ Y3 M, @Professor of Pediatrics, University of South Alabama, College of
' p* l8 P* h5 `3 W5 s# U) OMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
; y$ \, a/ H# K& ^$ x1 xe-mail: [email protected].
. N! E. F8 o9 d  S4 E8 Xabout 6 to 7 months old, which progressively became
! L7 l1 a' d4 A/ ddarker. She was also concerned about the enlarge-7 z0 L+ E/ R# v8 }8 L
ment of his penis and frequent erections. The child& u( d: c* r  x- h
was the product of a full-term normal delivery, with
+ v1 e; ]2 P9 j( A' w+ ~a birth weight of 7 lb 14 oz, and birth length of$ R' I/ L# C1 o7 I7 u2 Y7 m" p
20 inches. He was breast-fed throughout the first year
" \: Q& {4 J& L9 ^+ h4 v+ _+ jof life and was still receiving breast milk along with
0 x6 W5 h6 q2 ^( Y0 hsolid food. He had no hospitalizations or surgery,
6 r2 {" L+ Q" _4 N# w; e) }4 I8 Land his psychosocial and psychomotor development1 `4 `# ]( t' P) r9 a% z6 l& C
was age appropriate.
# r6 q$ ]0 q# ~& H7 dThe family history was remarkable for the father,
5 h: n7 b1 ~/ n: L) Lwho was diagnosed with hypothyroidism at age 16,
8 @" }$ s, `# lwhich was treated with thyroxine. The father’s# w) T# }: `0 G3 ~& I
height was 6 feet, and he went through a somewhat* V" J$ [7 n' i! K6 m7 W
early puberty and had stopped growing by age 14.
% p/ U/ i  |' xThe father denied taking any other medication. The
% d; p3 T' E- \- b* Uchild’s mother was in good health. Her menarche! q) Y2 J0 b3 \
was at 11 years of age, and her height was at 5 feet
8 w3 }) v! u. j7 W1 }6 T" ^5 inches. There was no other family history of pre-2 P3 W& ?& V7 f
cocious sexual development in the first-degree rela-# O& S1 \# }& D/ b9 e' M1 L
tives. There were no siblings.
" M3 m. |, F( q( S3 V# _: Z! pPhysical Examination
6 w8 X$ C5 U$ |* a* X/ P! |* R1 ]The physical examination revealed a very active,4 q$ j/ C7 X/ J7 q: ]
playful, and healthy boy. The vital signs documented
) ~$ P* a: r0 m7 g; i$ Aa blood pressure of 85/50 mm Hg, his length was$ T! t/ E( K: U1 V3 r
90 cm (>97th percentile), and his weight was 14.4 kg( i" q) @4 ]( O  V0 W$ z
(also >97th percentile). The observed yearly growth
1 Z: G1 X6 ]& @velocity was 30 cm (12 inches). The examination of, v  I# X5 \' W% Q
the neck revealed no thyroid enlargement.
1 V# E( m0 a6 W+ T3 XThe genitourinary examination was remarkable for  @' ~0 _: {% ^' Q0 u3 n) |" I
enlargement of the penis, with a stretched length of
/ R( e, c$ H* ~% @: u' r# E0 t8 cm and a width of 2 cm. The glans penis was very well9 A- G7 n5 o$ q' @. u
developed. The pubic hair was Tanner II, mostly around# B- b0 S# p# m& a7 Y
540! c4 D2 O; d( a& Z. g
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( \+ }8 ^: h8 Y6 D! [' ^the base of the phallus and was dark and curled. The) r8 n. A4 m7 M6 {' C  s
testicular volume was prepubertal at 2 mL each.
4 |" g  }! d# A: j$ }The skin was moist and smooth and somewhat( e2 \% |5 G* H3 j
oily. No axillary hair was noted. There were no
7 i$ M3 v0 ?( d4 }. F- O. d0 u$ v# Labnormal skin pigmentations or café-au-lait spots.
. i" M% M  q5 a; Q% iNeurologic evaluation showed deep tendon reflex 2+6 r5 E5 |; I6 p  H6 T  m
bilateral and symmetrical. There was no suggestion
. m5 v" q7 Z4 J- H# \3 mof papilledema.
: C$ F, i* {3 X& h: B0 bLaboratory Evaluation
& ?( t+ X5 y7 K, X( x/ kThe bone age was consistent with 28 months by
4 s1 C3 P# s0 ^- z6 p$ N8 Iusing the standard of Greulich and Pyle at a chrono-
; M& `3 f  j4 y3 J% mlogic age of 16 months (advanced).5 Chromosomal
6 l4 J5 E" b  {. ?karyotype was 46XY. The thyroid function test) f3 s" H( {( i$ c5 m! p7 F* J
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
6 a- V% U' u0 ~5 o& k) \lating hormone level was 1.3 µIU/mL (both normal).
7 S7 E# @) m& N8 M0 U* S+ T# l3 ?The concentrations of serum electrolytes, blood( i9 N9 p- a* @; N, b" V6 ~8 o
urea nitrogen, creatinine, and calcium all were2 O3 F# s8 p" t" I7 ?
within normal range for his age. The concentration
9 V! E) Q+ U0 Rof serum 17-hydroxyprogesterone was 16 ng/dL
0 r) E, z# a* Q' O4 _2 e(normal, 3 to 90 ng/dL), androstenedione was 20
9 |" ?. o9 j* G( Y; d( T2 `) U7 Kng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
. k) L4 d" U. b: k+ t" Lterone was 38 ng/dL (normal, 50 to 760 ng/dL),* \! X; X( E6 J$ }  {$ p
desoxycorticosterone was 4.3 ng/dL (normal, 7 to- C" e4 _# A. D! s4 R
49ng/dL), 11-desoxycortisol (specific compound S)
; S) w9 |' t% L6 ?) b' h6 R5 D3 j5 [2 Uwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-8 R: X$ S- Y- F
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
" D2 v) d7 x( U, J  jtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),4 X5 V6 b0 P( u2 d4 s: H0 x; T
and β-human chorionic gonadotropin was less than& ]3 m; }4 ~# X2 ]8 _1 D/ F* M
5 mIU/mL (normal <5 mIU/mL). Serum follicular8 s5 G& \8 x8 S
stimulating hormone and leuteinizing hormone
- x1 G1 e" |4 gconcentrations were less than 0.05 mIU/mL# J/ m  V, O! e+ x. W7 w% z# f1 h1 H
(prepubertal).
% O# F( ]$ |$ J1 D2 nThe parents were notified about the laboratory/ R5 G7 R' o& e  Z! J
results and were informed that all of the tests were
; O" C5 [8 u0 E( ^& z9 \2 h2 ~normal except the testosterone level was high. The! R" Z: Y- R0 K) h9 k' D
follow-up visit was arranged within a few weeks to
# n8 \+ \2 S: o2 gobtain testicular and abdominal sonograms; how-1 j5 r5 Z& Z) d  K
ever, the family did not return for 4 months.
6 ?" U- a, X8 n6 j* QPhysical examination at this time revealed that the$ B% p: q9 a8 E& q
child had grown 2.5 cm in 4 months and had gained
- E/ j8 m. w' }! ~  d2 kg of weight. Physical examination remained
8 F- B+ g. G- Z: Q, runchanged. Surprisingly, the pubic hair almost com-+ X1 G: Z- `- @% s1 g
pletely disappeared except for a few vellous hairs at
0 T+ D1 `# `; {, T0 S: Fthe base of the phallus. Testicular volume was still 2- w+ v. p0 c' Y6 @% t
mL, and the size of the penis remained unchanged.
( L" \# n: y" \) W* S( k( C5 JThe mother also said that the boy was no longer hav-0 S# ?1 d4 @+ m. F4 ~
ing frequent erections.5 `7 _' X, I% v" Y& ]5 [% e9 x) c1 |
Both parents were again questioned about use of
2 W$ B* k2 [; M$ \5 i) h: r5 pany ointment/creams that they may have applied to
2 D" \& ~. ^' C% A9 a$ athe child’s skin. This time the father admitted the3 l$ z# X* w4 U& z
Topical Testosterone Exposure / Bhowmick et al 541
9 N1 X) r. x  i' \$ Vuse of testosterone gel twice daily that he was apply-& ^4 x& W- `5 t% s. y9 S9 z% I9 h" \
ing over his own shoulders, chest, and back area for+ u9 W7 Y5 ]9 n- Y. }2 T; ]* D
a year. The father also revealed he was embarrassed( t8 L- Q" x) s7 K$ v
to disclose that he was using a testosterone gel pre-
9 E& G7 g- k  e+ }  {# Ascribed by his family physician for decreased libido
; l, h: j  w) O! t4 e5 Vsecondary to depression.
6 x$ B) q7 @# u6 wThe child slept in the same bed with parents.& x7 j  C/ f! O3 V
The father would hug the baby and hold him on his8 z+ V( F/ d! P% h& u& O* _* H  s2 W
chest for a considerable period of time, causing sig-
# _& I$ x; g" p$ N! Y  C% |( s5 Jnificant bare skin contact between baby and father.
7 Q7 P2 Q+ Z5 l( k) pThe father also admitted that after the phone call,: Y' ^+ m. L( ^. j
when he learned the testosterone level in the baby' z% W) G1 ]: |; B( j
was high, he then read the product information9 U  r# v" k* P* H$ b: J( f
packet and concluded that it was most likely the rea-
+ g' d$ d5 c4 V3 ^6 json for the child’s virilization. At that time, they
$ k9 M% \$ y( {7 L7 Q1 Adecided to put the baby in a separate bed, and the
0 B7 O+ h. _1 x0 z/ O) M$ Efather was not hugging him with bare skin and had- z3 Z2 I6 L4 U7 S4 g! g* |
been using protective clothing. A repeat testosterone3 D1 z/ n0 n& O
test was ordered, but the family did not go to the% `6 a/ G. G% Y! ^) k, N4 R
laboratory to obtain the test.$ ?8 E5 z: _1 O' n+ E9 Y
Discussion
: A3 k. a% Z; x' _( S" {Precocious puberty in boys is defined as secondary
2 T* {2 O1 p2 Bsexual development before 9 years of age.1,47 p4 T& _! x" m% m) _. C, F
Precocious puberty is termed as central (true) when
5 C6 Z$ l7 E9 m4 T3 dit is caused by the premature activation of hypo-
+ N" {7 M8 Y! J3 @5 {thalamic pituitary gonadal axis. CPP is more com-
9 v3 S( T3 ?% ]- W- x# D: rmon in girls than in boys.1,3 Most boys with CPP
, r8 \$ Y5 I( P0 f! u1 y5 Bmay have a central nervous system lesion that is
; o( x7 T0 o+ k5 K1 uresponsible for the early activation of the hypothal-
2 e) W5 C8 c& W8 u% R1 iamic pituitary gonadal axis.1-3 Thus, greater empha-( O. p/ E* a6 f" B
sis has been given to neuroradiologic imaging in- u" }4 I( c6 s" ?
boys with precocious puberty. In addition to viril-' K3 [' k) |1 d3 V6 o7 ?$ s
ization, the clinical hallmark of CPP is the symmet-+ i5 \% g  t5 p+ ?! i7 p, L
rical testicular growth secondary to stimulation by3 |6 c. h: v' s% a3 C
gonadotropins.1,32 D7 ?# _3 B! l8 e* k7 y7 J; u& @
Gonadotropin-independent peripheral preco-
5 `; q; j/ D3 G4 acious puberty in boys also results from inappropriate2 K: h  n+ K9 P
androgenic stimulation from either endogenous or
2 |2 D+ j& c* [0 ?' }exogenous sources, nonpituitary gonadotropin stim-! {2 i8 j; c2 P& {: }
ulation, and rare activating mutations.3 Virilizing5 G$ ]! x. [4 M6 d
congenital adrenal hyperplasia producing excessive
' k9 M" S! I, X7 d  {2 i: vadrenal androgens is a common cause of precocious5 d/ h3 O4 R1 }$ t4 g0 e
puberty in boys.3,4: O( P% S# Y# B$ j: Z
The most common form of congenital adrenal
7 J0 {8 \9 I- K% H# ^hyperplasia is the 21-hydroxylase enzyme deficiency.
  \+ ~  A+ p% n" l& QThe 11-β hydroxylase deficiency may also result in* \1 ^# |# g  i9 u: h+ s4 P8 N8 _
excessive adrenal androgen production, and rarely,
5 R5 y, B: ~# o: n0 u) ran adrenal tumor may also cause adrenal androgen0 i  w+ p( y; r2 p; T4 @  y2 Z
excess.1,35 l+ y) m$ T; Y! F7 t5 Q3 a
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' C' @- c. g1 Z. _3 Z; `% Z542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
+ s/ U$ h4 k. ^, QA unique entity of male-limited gonadotropin-& q; K+ a* [% \, h8 b1 Y3 C3 u
independent precocious puberty, which is also known  ~& f. j9 B7 u- |* u0 H- ?
as testotoxicosis, may cause precocious puberty at a( D  |/ m# i/ Z9 g' M: G
very young age. The physical findings in these boys
8 L0 W& e% g- R1 [with this disorder are full pubertal development,3 O% R% E8 ], Y* z6 I3 Q, G" l
including bilateral testicular growth, similar to boys
% G' d# N" c1 c8 E! @' u: u  N1 owith CPP. The gonadotropin levels in this disorder7 d$ \7 ^$ _. F2 z0 q: Z
are suppressed to prepubertal levels and do not show/ N- g: `7 L" F4 B: j# k
pubertal response of gonadotropin after gonadotropin-1 I1 V9 H9 o2 }0 x, J
releasing hormone stimulation. This is a sex-linked
) `6 u% M' c8 u* r: oautosomal dominant disorder that affects only
9 n. Z  `' D5 P6 d/ _$ q5 y3 lmales; therefore, other male members of the family/ `# Z0 U* M9 R; L* o
may have similar precocious puberty.3% ]  g1 s) T" a4 H8 M+ b. G
In our patient, physical examination was incon-
- g0 C) n' n' Wsistent with true precocious puberty since his testi-
8 Y0 n1 a5 K& b4 K0 C2 y$ \) u6 pcles were prepubertal in size. However, testotoxicosis
  A8 ^0 F; q$ i1 h, h4 @was in the differential diagnosis because his father  T. Z  K0 K6 i: Z& ?
started puberty somewhat early, and occasionally,
0 R8 W" i# L2 n- R; Qtesticular enlargement is not that evident in the5 G! l9 w3 s! V. H" Q" @/ F& e
beginning of this process.1 In the absence of a neg-/ n3 {/ S! W* S( c
ative initial history of androgen exposure, our
9 Z. `" G* V2 H1 _# N. g2 e+ xbiggest concern was virilizing adrenal hyperplasia,7 L! A5 n; a7 r2 N
either 21-hydroxylase deficiency or 11-β hydroxylase
6 f3 T& X% I4 u. u' Rdeficiency. Those diagnoses were excluded by find-
' n' w) |0 u2 g" cing the normal level of adrenal steroids.5 g9 u  T# h" D) I: V7 Z* D
The diagnosis of exogenous androgens was strongly
0 D& j' Y' x3 @# u% h7 Tsuspected in a follow-up visit after 4 months because) @) S1 F' d& d6 t# N2 _" Q% k& m
the physical examination revealed the complete disap-
) _/ }: |. ]! G$ xpearance of pubic hair, normal growth velocity, and9 p2 b) R+ x- K2 o
decreased erections. The father admitted using a testos-
1 K; C9 q8 ]$ `3 i  Yterone gel, which he concealed at first visit. He was
7 @. B' h5 Z/ p/ q& X# `  ?8 lusing it rather frequently, twice a day. The Physicians’/ j6 r2 ^  X, X; x) K2 |
Desk Reference, or package insert of this product, gel or
+ @/ `; |% P, \cream, cautions about dermal testosterone transfer to
  U: r7 y$ U. @* N4 Y; [- {: Kunprotected females through direct skin exposure.
! d) S( n6 {! D0 R, ^% W" sSerum testosterone level was found to be 2 times the* K0 |: {% x$ [$ D" j
baseline value in those females who were exposed to5 p0 r/ r4 \, }; h; L4 X
even 15 minutes of direct skin contact with their male) I8 b) m3 ^4 N
partners.6 However, when a shirt covered the applica-; d1 H6 G- m$ G1 S) D/ b
tion site, this testosterone transfer was prevented.: O' i3 J; @& r
Our patient’s testosterone level was 60 ng/mL,7 }, |$ D" H8 _$ I# b3 K9 V
which was clearly high. Some studies suggest that$ P) d  J+ E0 J2 f  M- g
dermal conversion of testosterone to dihydrotestos-' i- o. I& D/ G9 N' e6 d7 K6 M
terone, which is a more potent metabolite, is more
* v& i/ y- G/ P% ?$ Factive in young children exposed to testosterone
7 q2 t: B, @5 X4 qexogenously7; however, we did not measure a dihy-4 c, a. o  q' t6 u( G: o
drotestosterone level in our patient. In addition to& X8 r8 ]) ~+ Y; @% y2 j2 ]2 B
virilization, exposure to exogenous testosterone in3 s' J: K" v. \6 R
children results in an increase in growth velocity and
8 f, [% z% w, h4 R; iadvanced bone age, as seen in our patient.
, ]* D) e' S& i' A2 ?- `# IThe long-term effect of androgen exposure during8 ]( e5 S* D3 @1 ]2 ^
early childhood on pubertal development and final
. N5 r# K0 u( _/ Z2 D5 Ladult height are not fully known and always remain8 P/ D. R2 e0 [( \0 V/ j
a concern. Children treated with short-term testos-# Y$ P1 B' d) W6 ]$ R1 U% G
terone injection or topical androgen may exhibit some* v5 H" N3 y1 P! u4 C
acceleration of the skeletal maturation; however, after
9 R4 M4 o* J1 Q  K9 H& mcessation of treatment, the rate of bone maturation
, t' q8 Z, ]  ]decelerates and gradually returns to normal.8,9# G+ x5 C( h& e5 p$ S" Y
There are conflicting reports and controversy
2 j: }3 ]4 @( Q2 V6 Z, S; Qover the effect of early androgen exposure on adult+ Q$ ^9 }* e6 n5 W: e1 N
penile length.10,11 Some reports suggest subnormal$ m. I, a* x4 ~3 s" N) m( P
adult penile length, apparently because of downreg-
1 g, Y. _: e' n0 Zulation of androgen receptor number.10,12 However,
8 c# ?) k; W' X* s5 iSutherland et al13 did not find a correlation between
+ i9 o4 O3 a7 C1 T+ Uchildhood testosterone exposure and reduced adult+ c# t8 [& \1 N7 [+ {
penile length in clinical studies.# {$ l3 J/ w) A/ [. l: j
Nonetheless, we do not believe our patient is( b/ J9 J; c6 K1 N
going to experience any of the untoward effects from
/ j) m$ O: a1 D! atestosterone exposure as mentioned earlier because
3 l7 Y2 \- S+ fthe exposure was not for a prolonged period of time.
& s; \0 w( U  u& b: T& {( ~Although the bone age was advanced at the time of1 x( }" k' r8 i8 A
diagnosis, the child had a normal growth velocity at
  l/ d4 i. |; R3 f" vthe follow-up visit. It is hoped that his final adult# v6 H$ R6 Q4 O, D1 k; }- J
height will not be affected., y$ x! I8 _: M. b2 }: S) }$ d
Although rarely reported, the widespread avail-- a3 K" A$ y+ U, A
ability of androgen products in our society may
0 c' v7 I/ P, _; }3 P' G9 aindeed cause more virilization in male or female
/ a) o( z+ f! i3 a# Hchildren than one would realize. Exposure to andro-- B. J9 R' R, K) _5 t0 c' t) [
gen products must be considered and specific ques-1 }% P6 t& o2 Z4 N
tioning about the use of a testosterone product or
/ W; K% p0 L7 @  z2 `gel should be asked of the family members during
" O4 A- J# V; [8 h$ {' [the evaluation of any children who present with vir-
% }: a1 W. S  `3 qilization or peripheral precocious puberty. The diag-5 n5 {* z6 {' ]- z3 m+ {
nosis can be established by just a few tests and by
7 S6 e8 T( }1 oappropriate history. The inability to obtain such a
8 G8 d: I; U! N2 r3 ohistory, or failure to ask the specific questions, may$ ?" {! U$ j# `% o
result in extensive, unnecessary, and expensive
3 g7 ]) J! E- S& I, Y1 E' D7 x2 Ginvestigation. The primary care physician should be! T  C& i; n& [  M6 v& Y
aware of this fact, because most of these children1 j3 Y: ~9 r7 V% h8 \
may initially present in their practice. The Physicians’
2 R/ A( D  K9 g3 B: z0 ^8 t8 nDesk Reference and package insert should also put a3 L1 h% ~; b: n5 N# b3 R( h
warning about the virilizing effect on a male or& X8 B6 e/ d) I. C
female child who might come in contact with some-  a' a; N- r. N: C
one using any of these products." f/ b; L5 a! L" ~0 ~& z9 Y4 b
References
  M: A" r; R2 r; p1. Styne DM. The testes: disorder of sexual differentiation1 N: z6 a# E2 R( L( F& h2 @
and puberty in the male. In: Sperling MA, ed. Pediatric9 A2 V5 `5 a" {3 e8 t" b" i3 V
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;. a' o, Z5 g5 D+ `+ ?
2002: 565-628.7 i( h# d4 Z% |) G3 `- b
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
4 l8 l% \: u! P/ M4 r9 _puberty in children with tumours of the suprasellar pineal
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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
+ S9 N8 U0 h0 ?8 ]3 N
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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