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Sexual Precocity in a 16-Month-Old% A4 t6 c% Q6 F. V
Boy Induced by Indirect Topical, g* l+ |: d0 S+ p1 P+ j
Exposure to Testosterone
# d1 b& l3 ?' R/ r. tSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
/ G) F$ ?/ I8 e5 |; D) e0 E5 oand Kenneth R. Rettig, MD1$ v) b- A; p+ h1 `3 Y& k, C
Clinical Pediatrics
6 E9 x/ b( t9 F! J- xVolume 46 Number 69 g! p* q" f# {# u
July 2007 540-543, d; o/ X( S% a# O  U
© 2007 Sage Publications
4 a) `+ i* _) u+ t9 m* N, y3 S10.1177/0009922806296651
0 v& }0 |" q7 D- b. G  \http://clp.sagepub.com
; j+ h0 E% [8 ?$ l) R0 Z* `hosted at
4 q: \; b7 \" m, r& Q, khttp://online.sagepub.com
" M, F6 S8 k9 q9 O! @6 KPrecocious puberty in boys, central or peripheral,) z" s& e% T9 |3 \7 O% C
is a significant concern for physicians. Central* m& a8 B( v5 E- E
precocious puberty (CPP), which is mediated
. z3 \: p% S; P% l8 Cthrough the hypothalamic pituitary gonadal axis, has% l/ {$ s& O  V! |* r3 `& O" C$ p
a higher incidence of organic central nervous system6 ~& y9 A+ I/ L! c5 D
lesions in boys.1,2 Virilization in boys, as manifested
, P+ Y) y) n7 {9 Pby enlargement of the penis, development of pubic2 ~- a6 g; |5 b; X
hair, and facial acne without enlargement of testi-
6 O/ Q+ n5 L" p, \" t  @4 ycles, suggests peripheral or pseudopuberty.1-3 We
  q% O# j" P- ireport a 16-month-old boy who presented with the
6 r7 p) |+ B9 r) t* d4 jenlargement of the phallus and pubic hair develop-
6 h6 Y& K/ ~- R7 A& M- O! Hment without testicular enlargement, which was due) {9 w) s  E+ H$ K2 B9 Y
to the unintentional exposure to androgen gel used by
% x# A, J; D; u" W0 _' mthe father. The family initially concealed this infor-
+ E1 T" w& N( U5 _8 h% smation, resulting in an extensive work-up for this
, s, I! u4 J" X/ R7 B4 tchild. Given the widespread and easy availability of
( K  k% v) R* L8 ^% t& vtestosterone gel and cream, we believe this is proba-( N9 o  n/ k. A1 K8 h% U. ]* e
bly more common than the rare case report in the
  k( y, V+ E3 ?$ s7 |( n- xliterature.4
( {! V5 h& S& w& o! i. MPatient Report
! y+ ]! g$ a2 O- c; rA 16-month-old white child was referred to the- G" ^& V+ o" b
endocrine clinic by his pediatrician with the concern. W, F' |9 w: P2 Q
of early sexual development. His mother noticed
) E) e! C! N# z& o; F6 Llight colored pubic hair development when he was: l9 q  C$ f9 R( Z4 x
From the 1Division of Pediatric Endocrinology, 2University of) x) x2 g8 m% l/ P/ S! ^- H2 w2 E) b
South Alabama Medical Center, Mobile, Alabama.
2 C* d& x3 r  G, XAddress correspondence to: Samar K. Bhowmick, MD, FACE,
  ^8 q  P! `- r: gProfessor of Pediatrics, University of South Alabama, College of
7 Z* A" `. f( x( S: ]Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;* G$ D* L/ W+ S) t2 W' e% z( P6 U
e-mail: [email protected].
6 ^* X6 Y* F) ^9 \about 6 to 7 months old, which progressively became) N8 S4 N% G7 b4 g  t
darker. She was also concerned about the enlarge-
  H* ^" V* j- e( r+ i6 qment of his penis and frequent erections. The child
6 m! u8 z! O+ r; B( P% Rwas the product of a full-term normal delivery, with
, h5 k1 Z2 ]; A4 Q/ y' ja birth weight of 7 lb 14 oz, and birth length of8 n( |0 Y' t+ D
20 inches. He was breast-fed throughout the first year
0 p, N+ m4 K# Wof life and was still receiving breast milk along with2 U: t+ A) d+ d
solid food. He had no hospitalizations or surgery,. o% u1 o% t) j2 O" L# i8 i
and his psychosocial and psychomotor development5 f  L* I/ D( N$ `( f
was age appropriate.
% l  T% O9 m8 s" m' CThe family history was remarkable for the father,
1 a3 w6 P. I! x* M' o0 qwho was diagnosed with hypothyroidism at age 16,
1 R4 `/ ]# g. bwhich was treated with thyroxine. The father’s* q9 W0 J+ e) V- L+ N3 t7 p
height was 6 feet, and he went through a somewhat
3 Z' D8 m3 T3 ~$ t" U" qearly puberty and had stopped growing by age 14.4 @7 s0 @3 Y* v* K+ N5 e. g4 Q
The father denied taking any other medication. The
' U( [7 k0 f/ w# v! o9 Cchild’s mother was in good health. Her menarche! H( b! y3 q7 T2 A5 r2 ^. ^
was at 11 years of age, and her height was at 5 feet4 U3 ]1 x* L1 R9 l; Y' ?* J
5 inches. There was no other family history of pre-
  L  J  u2 i* M/ ecocious sexual development in the first-degree rela-
7 \- R# r+ _: \% T! y- ttives. There were no siblings.
/ U. O1 v# \! \3 ePhysical Examination
. m  y, K6 u5 p9 b! j2 ]& e  R/ |- OThe physical examination revealed a very active,0 e8 M5 s5 d" |" i* L& [
playful, and healthy boy. The vital signs documented
2 d9 k0 K# z  y# u. ]a blood pressure of 85/50 mm Hg, his length was
3 Y* u4 ]9 i. B2 n' @9 E' r' b8 T7 t90 cm (>97th percentile), and his weight was 14.4 kg
2 J- _/ h$ @7 Y(also >97th percentile). The observed yearly growth
( J7 ]  c! f7 E  K6 lvelocity was 30 cm (12 inches). The examination of% l6 }, F3 R3 |- a5 {5 L
the neck revealed no thyroid enlargement.8 X( f" t) J# [3 ~: v: G
The genitourinary examination was remarkable for; Q' C4 G1 H  v( u$ A
enlargement of the penis, with a stretched length of
( j7 v2 v9 n- s0 u8 ?/ _+ ?2 E8 cm and a width of 2 cm. The glans penis was very well5 O+ J2 |, L# B. D% t7 Q% h
developed. The pubic hair was Tanner II, mostly around; R/ p$ z+ R9 b, b
540
+ S1 L/ {- V0 F8 v  sat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* z& n) f6 J; k; g6 J% u1 F6 i. p$ {; ~
the base of the phallus and was dark and curled. The/ C0 c8 v) m( X7 m$ g& p; x' H8 J
testicular volume was prepubertal at 2 mL each.
4 {4 G( j1 H4 v3 k% QThe skin was moist and smooth and somewhat& m/ K2 h* D8 X5 w( O
oily. No axillary hair was noted. There were no1 `8 m! |# e8 v+ D( U
abnormal skin pigmentations or café-au-lait spots.
% Y  ~3 K- b- m$ p0 |Neurologic evaluation showed deep tendon reflex 2+1 h8 v! z/ F) w9 [5 l% g# B
bilateral and symmetrical. There was no suggestion7 {0 E5 k$ u3 d! z3 ]' s$ s$ \
of papilledema.8 P( F2 d' T/ }+ b6 Z; X) z4 _
Laboratory Evaluation- i8 F6 h+ N+ W( j5 F) s3 Y: }
The bone age was consistent with 28 months by
: O# V; e9 ?  O" Musing the standard of Greulich and Pyle at a chrono-/ x: f# }( U/ @/ N+ r8 t
logic age of 16 months (advanced).5 Chromosomal( H! |5 W9 \2 E2 }0 _
karyotype was 46XY. The thyroid function test
5 ^: W+ P0 M  `+ Rshowed a free T4 of 1.69 ng/dL, and thyroid stimu-1 `6 H) |3 h7 W6 D2 ]
lating hormone level was 1.3 µIU/mL (both normal).; T" u# Y( D3 `6 E! J" g$ {
The concentrations of serum electrolytes, blood
" V: F# Z5 m8 j- Burea nitrogen, creatinine, and calcium all were- n9 H0 V/ r) T! T; ?: R
within normal range for his age. The concentration, S- g8 c; B% A+ L2 J
of serum 17-hydroxyprogesterone was 16 ng/dL
! p9 ~* ~  @6 j$ Z1 x  C2 z( U(normal, 3 to 90 ng/dL), androstenedione was 20
0 B- e4 f  m4 e. a0 Y9 a/ ]ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-; L) N; r( J: _7 @: c% B2 V! g% p
terone was 38 ng/dL (normal, 50 to 760 ng/dL),- r: i7 z' u7 ~4 M' r# C& d
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
. V" t$ o! q7 \1 z49ng/dL), 11-desoxycortisol (specific compound S)
+ _% N  b+ V, z" J8 _! r# gwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- Y! F0 \. U  l( K
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total9 g7 I* a( }/ m1 T4 I
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
/ g; n4 A3 D; y2 Q9 x% dand β-human chorionic gonadotropin was less than* f& t3 o3 g3 O, v7 o
5 mIU/mL (normal <5 mIU/mL). Serum follicular
+ _2 o) E# d- ~7 w: ostimulating hormone and leuteinizing hormone
+ D0 a" p! [, P; `% ^( f: `concentrations were less than 0.05 mIU/mL
' y% t2 M1 C4 i6 p0 I3 R, E(prepubertal).* r6 n7 S; f" g1 ~
The parents were notified about the laboratory
- C1 _: G0 ~+ l7 C2 ?& C  `: s5 Nresults and were informed that all of the tests were0 [' g5 q& G0 D0 K
normal except the testosterone level was high. The
# T' |7 n# w; K' u  e! }# @follow-up visit was arranged within a few weeks to
: k' D1 k% N2 E" i' uobtain testicular and abdominal sonograms; how-
) U$ ]4 c3 Y. s$ {; P6 e0 wever, the family did not return for 4 months.& b( {4 D/ P$ [: \
Physical examination at this time revealed that the
5 r5 n+ X+ p6 \8 G: Zchild had grown 2.5 cm in 4 months and had gained+ M2 l/ Z( B% S$ t0 [1 ]
2 kg of weight. Physical examination remained
: L  x' D9 z$ Nunchanged. Surprisingly, the pubic hair almost com-
6 K* t3 W1 Q( D9 R; n- F1 Npletely disappeared except for a few vellous hairs at; R" |& Q" Q5 e; q, _7 M: ~9 \
the base of the phallus. Testicular volume was still 24 ]& W+ n* X3 f8 O, t3 N# {
mL, and the size of the penis remained unchanged.# O% v* W6 p) `; @
The mother also said that the boy was no longer hav-, O3 @7 i5 G  E0 m" D
ing frequent erections.4 f) H7 \( w4 y* W% S' U/ I
Both parents were again questioned about use of
4 I) W$ S/ p3 Eany ointment/creams that they may have applied to
2 l, _5 ?- X1 Y; w4 t1 Tthe child’s skin. This time the father admitted the* H. Q% R4 e- K2 B
Topical Testosterone Exposure / Bhowmick et al 541
5 o; C8 x% x: m& muse of testosterone gel twice daily that he was apply-
3 J+ W2 G5 B: x" {9 Aing over his own shoulders, chest, and back area for4 o, T9 L5 P$ v
a year. The father also revealed he was embarrassed( k8 u" q$ k* Q% B+ w
to disclose that he was using a testosterone gel pre-
2 ~6 s8 [/ q+ kscribed by his family physician for decreased libido( V1 c/ r" m- t' B# u. Z9 X
secondary to depression.
& c# ]9 t7 u2 c+ G' BThe child slept in the same bed with parents.
8 z' P* w, r( H% _' C. i$ gThe father would hug the baby and hold him on his$ J/ S, Z4 z% u' ]
chest for a considerable period of time, causing sig-4 ?- R* g& h* [. t
nificant bare skin contact between baby and father.
8 v( B. @; K5 J1 H+ V& @The father also admitted that after the phone call,4 k+ s, W/ V  c( P, u) p
when he learned the testosterone level in the baby! j, v' ]& K$ Q7 ?1 e7 |/ n. i
was high, he then read the product information3 N" t8 C7 ~9 j% B
packet and concluded that it was most likely the rea-/ R; Y0 z! k  d' `$ H# I* N1 B
son for the child’s virilization. At that time, they& t, s! R. c  O
decided to put the baby in a separate bed, and the
* n6 t# K% L) N$ H4 {father was not hugging him with bare skin and had% ~9 z; l8 j. m$ f/ B
been using protective clothing. A repeat testosterone
* \% p, n. a" O3 K! q4 ptest was ordered, but the family did not go to the0 k! x  r) \8 M
laboratory to obtain the test.
. h$ }. ^3 t% l' @+ I: z8 ADiscussion
9 o# q1 O1 m& l/ `% XPrecocious puberty in boys is defined as secondary
% I1 b( v/ m1 ?3 Csexual development before 9 years of age.1,4
: ]( x! W0 g" ?6 x& J% z9 ^Precocious puberty is termed as central (true) when
! H3 y$ X$ K8 \# E  Y' ?3 b4 jit is caused by the premature activation of hypo-, O8 l- d- g) [3 O' d/ p
thalamic pituitary gonadal axis. CPP is more com-
: _6 X+ x( ]4 v( D4 }mon in girls than in boys.1,3 Most boys with CPP
) l, C# B+ x- g  g4 O* nmay have a central nervous system lesion that is4 D5 R" @* H( f/ ?& s) {6 ]
responsible for the early activation of the hypothal-
' N7 e+ p" L( V6 E$ Yamic pituitary gonadal axis.1-3 Thus, greater empha-% x: K4 c7 J' p7 |+ k
sis has been given to neuroradiologic imaging in4 g9 v! `" z) ?+ B
boys with precocious puberty. In addition to viril-& p: I& r" \! `5 C. L6 |
ization, the clinical hallmark of CPP is the symmet-
$ ]* H0 C) r$ ^% }# V( Zrical testicular growth secondary to stimulation by4 [- ]+ R0 f1 B6 x" g. g1 H% a
gonadotropins.1,3! M3 c! }+ z4 o3 I
Gonadotropin-independent peripheral preco-
: c1 x. P* Q- H9 u* [cious puberty in boys also results from inappropriate
7 W: w; A1 M7 t" B. ~androgenic stimulation from either endogenous or8 J+ J0 T# A/ N2 v6 k# E
exogenous sources, nonpituitary gonadotropin stim-* Z+ T$ _: P/ ]5 s8 @
ulation, and rare activating mutations.3 Virilizing* H4 Y9 ~# y( p3 p" X
congenital adrenal hyperplasia producing excessive' f: I, p5 b: M  S
adrenal androgens is a common cause of precocious$ {0 O0 ^% B/ i1 W% d* Y
puberty in boys.3,4( s; `" O7 r/ @9 `- `3 L
The most common form of congenital adrenal7 g) X7 ?# n; Z8 ?8 w
hyperplasia is the 21-hydroxylase enzyme deficiency.
) J; e( s; n6 c! `# B/ E. BThe 11-β hydroxylase deficiency may also result in
. m6 Z$ r8 i- T1 d& C# B, N( vexcessive adrenal androgen production, and rarely,
% k9 Z2 j' y0 j+ Zan adrenal tumor may also cause adrenal androgen
, b; b7 r% ~# |3 {0 h. u- ^4 nexcess.1,3: [8 c7 q6 O. V- J; F* o8 e
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 {) D7 I, o! Z2 J& n& @542 Clinical Pediatrics / Vol. 46, No. 6, July 2007- }& Q' \& `4 K! t3 P6 t5 I
A unique entity of male-limited gonadotropin-
3 o$ N* X# w1 [4 kindependent precocious puberty, which is also known- }' Q( c' p, ]! X( x
as testotoxicosis, may cause precocious puberty at a
# N5 K5 x4 i. j7 `' \6 p" g- tvery young age. The physical findings in these boys
! R7 V( I. D% ]with this disorder are full pubertal development,
, m# z* x7 s4 oincluding bilateral testicular growth, similar to boys
% {& j4 j) y  q- a( ~with CPP. The gonadotropin levels in this disorder
1 f* }, w. f0 M4 |7 G1 x4 _4 Kare suppressed to prepubertal levels and do not show" N( ]% A* t0 p( o, Z( n
pubertal response of gonadotropin after gonadotropin-" x8 [: z' R1 s: C1 A+ z' m$ s9 G
releasing hormone stimulation. This is a sex-linked
" J6 |* h% k! D3 s/ e) s) g. ]autosomal dominant disorder that affects only
0 H/ {+ E, X0 Z8 P- Rmales; therefore, other male members of the family
2 P7 v: t1 t. u& Kmay have similar precocious puberty.3- _  V3 @- Y" S  u; b
In our patient, physical examination was incon-
% c8 n# J( m* c& Zsistent with true precocious puberty since his testi-
/ N6 a+ r+ ~* e6 _7 o8 wcles were prepubertal in size. However, testotoxicosis. \# d+ V$ \& r" ~
was in the differential diagnosis because his father+ J$ U2 l4 _8 J0 @9 g2 u7 a
started puberty somewhat early, and occasionally,* R% V( |) L* x5 }, [. r
testicular enlargement is not that evident in the
; C7 \( [. Q/ F% V# t& Ebeginning of this process.1 In the absence of a neg-: G4 B: g7 ^# W1 j3 u
ative initial history of androgen exposure, our) H$ K2 P- j) A9 B0 b/ ?$ l8 ]
biggest concern was virilizing adrenal hyperplasia,
$ P1 M( p  U  g) g4 O  B3 _either 21-hydroxylase deficiency or 11-β hydroxylase% d8 y/ ~2 v& {4 }$ u
deficiency. Those diagnoses were excluded by find-
0 _" i0 v2 d) k2 y5 \ing the normal level of adrenal steroids.
, {2 s3 R- r* [, JThe diagnosis of exogenous androgens was strongly9 ]- }/ G' _% q0 |9 s* p8 N
suspected in a follow-up visit after 4 months because
" Q" _' k; f3 S; v; l- [" M1 S8 Fthe physical examination revealed the complete disap-3 O! P9 _* |' |9 i% f% }) o5 H
pearance of pubic hair, normal growth velocity, and
  O. i6 `2 q/ N! H1 bdecreased erections. The father admitted using a testos-- E" g8 h1 {. }0 {& e0 V
terone gel, which he concealed at first visit. He was9 {/ ~* u& W1 x! M
using it rather frequently, twice a day. The Physicians’
6 {- r& |% \' j0 |9 E. b# o$ r0 WDesk Reference, or package insert of this product, gel or
" @. f3 {4 K4 i7 K4 zcream, cautions about dermal testosterone transfer to
- }5 v* f: i" d+ ?2 N# P( A" L6 B( Tunprotected females through direct skin exposure.( p' n& _1 P5 H: ^. r
Serum testosterone level was found to be 2 times the
+ y7 f/ ]6 X; r" ]baseline value in those females who were exposed to
: s# q) L, b; Z2 v1 }% H, d" ~. f$ B$ Peven 15 minutes of direct skin contact with their male
! i% P( @/ W: J$ ^partners.6 However, when a shirt covered the applica-2 @! H+ ^* x! @0 ]; X
tion site, this testosterone transfer was prevented.
) K* K1 Q1 _$ b8 x7 \. n! N5 D6 HOur patient’s testosterone level was 60 ng/mL,
) X+ Z( O1 j! X3 i8 p  R9 mwhich was clearly high. Some studies suggest that0 H0 H" k7 t9 K( f3 r" z  u
dermal conversion of testosterone to dihydrotestos-9 f; J7 f! p% H7 t, z* w  j
terone, which is a more potent metabolite, is more% B9 w; I3 L0 w3 A! P
active in young children exposed to testosterone8 e: u" |, N3 N: C  l7 m: _: }
exogenously7; however, we did not measure a dihy-
5 W9 t: J4 s9 C8 a( xdrotestosterone level in our patient. In addition to
1 d) U, D# j1 h, B  T0 D6 Yvirilization, exposure to exogenous testosterone in
$ i# @+ v; M. Z& l0 D( @children results in an increase in growth velocity and
5 J; r& K* b4 A7 i* _9 K, zadvanced bone age, as seen in our patient.
. j4 ^. e. E5 }2 k) a3 x. PThe long-term effect of androgen exposure during
- U& x- {+ o5 `# a5 H+ [  b+ q) fearly childhood on pubertal development and final& W+ t7 n0 G$ c0 U/ L0 m7 L3 X
adult height are not fully known and always remain
+ W- I9 L) R0 |* s% Va concern. Children treated with short-term testos-7 S5 D7 S* q2 L4 l3 Q$ d- ~" W
terone injection or topical androgen may exhibit some
* Z4 b+ @5 A4 Y2 @7 Nacceleration of the skeletal maturation; however, after& G  Y" Y! @, t2 n: B1 K% C
cessation of treatment, the rate of bone maturation
2 H  p! U  |8 v) f/ N7 J5 Kdecelerates and gradually returns to normal.8,9: M+ n/ M' \8 j. X% v# {: u
There are conflicting reports and controversy9 x1 w; C" T; ?7 k
over the effect of early androgen exposure on adult
0 R) O+ z3 j) ppenile length.10,11 Some reports suggest subnormal
( S# R% l5 U% F, i' l6 D$ P* _1 Yadult penile length, apparently because of downreg-
4 T) T* U; d! Yulation of androgen receptor number.10,12 However,
7 h  O" Q. S% oSutherland et al13 did not find a correlation between
7 D6 C9 s: V0 {% o; X7 \childhood testosterone exposure and reduced adult# S; M+ s( T3 H" z- G
penile length in clinical studies.8 C4 ^. \" I+ f6 f
Nonetheless, we do not believe our patient is
  c! d* O/ a5 ~" sgoing to experience any of the untoward effects from8 v: T5 E9 y. Q$ I" t/ P
testosterone exposure as mentioned earlier because+ Y- i7 K( E! u( N3 s2 x+ C
the exposure was not for a prolonged period of time.- j/ ?7 G2 R5 b9 y( _
Although the bone age was advanced at the time of
1 g; g% U# G% U: Tdiagnosis, the child had a normal growth velocity at9 Q- a  l7 J, K( V! M) b
the follow-up visit. It is hoped that his final adult9 I  e4 @; b6 N1 q6 y/ Z  `2 P
height will not be affected.
- o' K5 b! h/ M, x5 B* w* {( bAlthough rarely reported, the widespread avail-2 O1 n, ]4 R% F# J
ability of androgen products in our society may
, E) Y5 B- l9 k. M5 }indeed cause more virilization in male or female
9 H% d5 u, v! B5 m7 ^children than one would realize. Exposure to andro-2 x& @) y+ n/ [8 p$ l
gen products must be considered and specific ques-2 n! Y/ N) `) {* ^9 s: B4 [% r) {
tioning about the use of a testosterone product or
1 U( E. Q$ B) ngel should be asked of the family members during: }. y* Y8 w" n7 j$ l$ v  x7 j. g
the evaluation of any children who present with vir-5 [7 r! J8 a* y1 Y$ W* I( {2 c
ilization or peripheral precocious puberty. The diag-- M8 A- ?* I2 h" R. X: F2 m- _8 u
nosis can be established by just a few tests and by1 [6 v" W6 f. S; }% O
appropriate history. The inability to obtain such a
* @9 P$ d) R! O% @- V. Phistory, or failure to ask the specific questions, may; V3 c. x% ^5 ^/ r
result in extensive, unnecessary, and expensive
. s" c; a  p- L+ |investigation. The primary care physician should be
6 T) @1 y- j' M$ ~3 Daware of this fact, because most of these children
; d) g, u* P% q# q, M3 H* ]may initially present in their practice. The Physicians’8 L0 N& t  K" J2 t+ N
Desk Reference and package insert should also put a% @/ b1 O+ g. H# p
warning about the virilizing effect on a male or
/ Q! x: n4 ~' P/ cfemale child who might come in contact with some-
& }% u+ O( l- d# wone using any of these products.4 C* e7 t3 J+ D1 t+ j0 q8 `$ w
References
$ @+ ^1 ^, Y+ R/ l$ A) `1. Styne DM. The testes: disorder of sexual differentiation) g3 O$ u! f0 M# S
and puberty in the male. In: Sperling MA, ed. Pediatric4 Y% `- g! `; n% j# D. C
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
9 `; _4 W8 ^0 x0 ]# v* _, z& q# s2002: 565-628.
' _5 q% u1 R, l3 g( W* e2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
* v% b9 I6 E) P  a: b5 j2 _9 ^  \+ _, {puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old% t' R9 [; \3 V( X, L
Boy Induced by Indirect Topical
$ A6 ~1 O0 z& k. s6 ^) eExposure to Testosterone
. ]& ]1 O1 G% s# `, WSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2! X  A- d7 V! m
and Kenneth R. Rettig, MD13 P; t) P7 ?. V! f7 H; q+ B9 K
Clinical Pediatrics
4 u0 {6 D4 x2 v; LVolume 46 Number 6! M2 n1 Y+ r6 c5 G! ?: Y
July 2007 540-543
+ |8 X" j0 z5 {  B; i© 2007 Sage Publications- F5 a, N! C, ^, `" @" ^& T- y% K
10.1177/0009922806296651
# U& S6 ]1 |1 ?( I7 Ihttp://clp.sagepub.com. }: _! [# D8 v, T+ n3 B
hosted at  b) L+ `4 D% t0 g
http://online.sagepub.com  K2 N3 `1 d3 U* n/ ?5 X8 r
Precocious puberty in boys, central or peripheral,
1 r: p0 N$ }3 e: [. C) Yis a significant concern for physicians. Central$ G' V) L9 j3 U2 J/ a
precocious puberty (CPP), which is mediated
3 `4 a3 t9 R( Jthrough the hypothalamic pituitary gonadal axis, has
' w0 _1 r" C7 X: q- e& Ma higher incidence of organic central nervous system: c2 m3 G& z9 Z' L7 o3 R* a
lesions in boys.1,2 Virilization in boys, as manifested* Y* V+ j& p$ t3 X2 i" v% t! }& u
by enlargement of the penis, development of pubic& m! @/ k4 M5 }, P1 d
hair, and facial acne without enlargement of testi-
. u  m. `# l3 O2 L3 ^5 Xcles, suggests peripheral or pseudopuberty.1-3 We( @0 ?: v5 V# D* E
report a 16-month-old boy who presented with the( l' c3 ~. w2 X! P' z: ~( o
enlargement of the phallus and pubic hair develop-; V. ]3 S9 X* S# s3 P1 m
ment without testicular enlargement, which was due( \! N) ^! w! U" i- B! d$ s
to the unintentional exposure to androgen gel used by9 ~+ j+ R, p0 ~0 g9 D# C, ~
the father. The family initially concealed this infor-" N+ w2 z4 C+ t2 K# L; t. h
mation, resulting in an extensive work-up for this
: w/ n- Z; w6 lchild. Given the widespread and easy availability of: l5 P* J1 q. C  l
testosterone gel and cream, we believe this is proba-' p* m! T3 O& J) D
bly more common than the rare case report in the. h, s& f9 ^( ]' H
literature.4
& G6 @8 \' P- V2 f  B  sPatient Report
2 C8 E( w8 n' f9 KA 16-month-old white child was referred to the/ v$ [% o! R9 r5 v
endocrine clinic by his pediatrician with the concern
; T9 N- ]4 H* @1 K6 K3 Bof early sexual development. His mother noticed% q' Q! v- r. A+ O+ _
light colored pubic hair development when he was4 e( s0 t- T: m! r
From the 1Division of Pediatric Endocrinology, 2University of; P- J% J# H5 F# U
South Alabama Medical Center, Mobile, Alabama.
# W3 V" I: H2 b0 r; @! UAddress correspondence to: Samar K. Bhowmick, MD, FACE,2 V/ F* K( w# J7 Y
Professor of Pediatrics, University of South Alabama, College of
- Z) B* p9 b& m6 p5 }' iMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
! W) [) r0 O1 x8 J( g1 re-mail: [email protected]./ O- s: S" u( n5 m5 R
about 6 to 7 months old, which progressively became9 i) s* S  d+ z5 G
darker. She was also concerned about the enlarge-- |: v6 W* S2 O" J
ment of his penis and frequent erections. The child( o, u9 ~- d9 {: v8 I0 p5 I0 g
was the product of a full-term normal delivery, with: ^- \/ M3 i! O4 g! w5 U2 G4 E: c
a birth weight of 7 lb 14 oz, and birth length of' w2 U' E$ l: M
20 inches. He was breast-fed throughout the first year3 T/ `6 \% I7 H% ]$ h
of life and was still receiving breast milk along with
. q1 s9 w7 J, C/ Asolid food. He had no hospitalizations or surgery,# S) y. L- E) n. y
and his psychosocial and psychomotor development
5 V! e4 `9 V3 \9 R: D$ twas age appropriate.
0 \: M) x$ C. z: [1 G" y( oThe family history was remarkable for the father,: Y1 J5 Y/ I: [3 w$ R% |2 u
who was diagnosed with hypothyroidism at age 16,
( H# Z  W7 O, C9 F, S8 @1 Nwhich was treated with thyroxine. The father’s
' Y, o' ?' r1 \height was 6 feet, and he went through a somewhat
* M: q( D- F5 g8 iearly puberty and had stopped growing by age 14.
3 O' `- C1 I3 N! SThe father denied taking any other medication. The6 z8 {) o. p/ h2 U
child’s mother was in good health. Her menarche+ i! X: A+ s3 A4 r( j' F; L
was at 11 years of age, and her height was at 5 feet
* R8 `" |& W1 t$ H9 d5 inches. There was no other family history of pre-
  b7 X9 L, u4 e5 X7 k- A6 M5 u" Jcocious sexual development in the first-degree rela-
9 {# i/ z' F! d" O3 \. ctives. There were no siblings.
( F/ Z+ t% a4 j2 _* k* fPhysical Examination3 W8 A2 G5 x! T9 A6 J6 H
The physical examination revealed a very active,8 H2 l7 @; x! _, \7 A- k) h
playful, and healthy boy. The vital signs documented4 S& T0 R6 s( x4 e
a blood pressure of 85/50 mm Hg, his length was+ b3 S- N, w0 r5 F7 U
90 cm (>97th percentile), and his weight was 14.4 kg: H1 C) h+ Z* M" U  X' d2 y
(also >97th percentile). The observed yearly growth
7 @- |8 u( |9 \  x$ xvelocity was 30 cm (12 inches). The examination of
' |, W9 D6 z( M3 ]& @6 Rthe neck revealed no thyroid enlargement.
( |1 l3 j  k) ^2 |; aThe genitourinary examination was remarkable for  _, a2 O+ l" U* U  z* I- z& R( @
enlargement of the penis, with a stretched length of7 a7 K9 @  Z( q. U0 H$ R& h1 N
8 cm and a width of 2 cm. The glans penis was very well, ?& l0 {' w4 C! H" X( _" ]! k
developed. The pubic hair was Tanner II, mostly around
  c# n+ N# \- d3 T9 j. x$ z4 u540' o" A: G& h) }* j! r3 i( Z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, z: q" p. J9 U& M
the base of the phallus and was dark and curled. The0 y! ?5 O1 T$ n# G3 @
testicular volume was prepubertal at 2 mL each.
  B% a/ f/ v$ A, P- MThe skin was moist and smooth and somewhat
1 @; X1 y; p; S( U- L5 \! v& i8 M' |oily. No axillary hair was noted. There were no$ _$ o% X! l. h9 U9 _
abnormal skin pigmentations or café-au-lait spots.! L: v7 A$ X" _- L+ G. A
Neurologic evaluation showed deep tendon reflex 2+  Q+ t# @2 w, A; C7 X" ^
bilateral and symmetrical. There was no suggestion; i0 h+ r+ V$ x1 n; ~) j
of papilledema.  n( c5 `! ~7 ]* a
Laboratory Evaluation
7 S0 `" f9 s/ x6 c9 P7 ?1 s' fThe bone age was consistent with 28 months by
; X7 e" o/ m! m- N8 a9 @/ z1 L! Qusing the standard of Greulich and Pyle at a chrono-
; }" B$ i  z7 a0 g1 W# \) nlogic age of 16 months (advanced).5 Chromosomal
+ V/ p# {* k& s/ V- Q; M  q4 r0 ~karyotype was 46XY. The thyroid function test( X6 e% ?+ b; m, F! C9 T0 q
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
7 N& O. w0 Q. i: {; y2 Klating hormone level was 1.3 µIU/mL (both normal).; b% v1 @, e, Z1 e/ y$ u) r3 G
The concentrations of serum electrolytes, blood
& b# v; j9 D$ N3 P' b4 ?9 g6 v  N! G/ g; Uurea nitrogen, creatinine, and calcium all were/ A  v5 Y; p6 j6 ]2 f8 T% ?
within normal range for his age. The concentration9 q, f+ i! x- T9 [
of serum 17-hydroxyprogesterone was 16 ng/dL
3 E5 ?  f, J- Z. c0 Y* k(normal, 3 to 90 ng/dL), androstenedione was 20
4 i, E1 L: N, B& Tng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-0 I0 B' i2 l% q2 l! s  c- s3 e
terone was 38 ng/dL (normal, 50 to 760 ng/dL),5 I5 O& k4 _/ z! C, V  j" e
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
: N8 e- N. ?5 O# a49ng/dL), 11-desoxycortisol (specific compound S)
; c% g0 @; M, [- h7 ywas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-0 V& R3 Q/ ~5 k2 ^# [
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
# {2 a+ ^% ^- g4 ytestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
4 h) K$ j/ _& {and β-human chorionic gonadotropin was less than
- _, {  \1 f1 j! _! V2 F% S5 mIU/mL (normal <5 mIU/mL). Serum follicular0 U8 b! \% H# [( v0 [* ~
stimulating hormone and leuteinizing hormone: N8 \* n1 N: N( u/ \0 J
concentrations were less than 0.05 mIU/mL
" u5 d7 z# r, _: p8 z(prepubertal).0 G6 o9 H8 x3 |# s
The parents were notified about the laboratory, \. X3 U% c: `- T0 u( P
results and were informed that all of the tests were* T. R( a8 b" K' O
normal except the testosterone level was high. The+ ]7 J4 F" I' |! |/ b
follow-up visit was arranged within a few weeks to6 p/ b2 H' u$ z* E( z. x2 \
obtain testicular and abdominal sonograms; how-
3 }8 `& Q/ v+ X2 Q9 I# aever, the family did not return for 4 months.
6 s8 c% `5 B) P( N- o8 oPhysical examination at this time revealed that the
2 |- Q" k% q% H# ?# e. g; @# x; Wchild had grown 2.5 cm in 4 months and had gained. [8 K! E' `4 Q+ L5 \- c# W- D, u
2 kg of weight. Physical examination remained/ A& T+ G$ V5 @. L- ~; O! I
unchanged. Surprisingly, the pubic hair almost com-, B0 K. E5 ?: U6 p3 M& t% l; G
pletely disappeared except for a few vellous hairs at1 S. Y$ e: Z( R4 e
the base of the phallus. Testicular volume was still 2
, r; y- H2 J0 `8 Z4 s  [mL, and the size of the penis remained unchanged.: _- r* i3 h2 q! Q
The mother also said that the boy was no longer hav-
7 V; [( E& y6 {% Z" {6 w1 sing frequent erections.# G$ A6 w4 O7 @8 k3 U
Both parents were again questioned about use of2 g3 Z& n+ l! M/ P7 K9 m- r7 x
any ointment/creams that they may have applied to
% x6 U2 a# u3 r) Q8 T3 N% rthe child’s skin. This time the father admitted the; V; p/ H* H4 j0 l/ m  h* G
Topical Testosterone Exposure / Bhowmick et al 541- H; M( k; a5 v# |/ M8 \/ k. Q
use of testosterone gel twice daily that he was apply-& a* `+ M8 {* r% L" @
ing over his own shoulders, chest, and back area for
8 C* W1 K& x! \1 ea year. The father also revealed he was embarrassed6 @4 L, t3 J3 d) O* O! `
to disclose that he was using a testosterone gel pre-" {$ U- _+ ~7 c) G4 Q' }) r4 v
scribed by his family physician for decreased libido
% K' g/ d5 K/ f* x) k8 j1 Nsecondary to depression.8 P' s% p0 @( p2 R. {% o3 I2 |
The child slept in the same bed with parents.
: Y" o7 b. w. C! wThe father would hug the baby and hold him on his! ]" b6 ?* f: O8 Y2 w* X$ B
chest for a considerable period of time, causing sig-
& P% z' X8 v% O& L8 H: m/ Wnificant bare skin contact between baby and father.3 Q. Y1 d- X6 n6 F+ o& v
The father also admitted that after the phone call,3 O. _" }8 G: P, ?" y2 Z
when he learned the testosterone level in the baby
7 E# `0 m, ]3 G9 `( Uwas high, he then read the product information2 N) _7 ?/ J: l4 C) q+ {
packet and concluded that it was most likely the rea-. K7 k: g' L6 T6 n6 M8 ~% `
son for the child’s virilization. At that time, they
. d9 s% t7 N3 `" hdecided to put the baby in a separate bed, and the
7 B$ [* z8 x+ r; C4 rfather was not hugging him with bare skin and had
" T8 T' F+ I) {been using protective clothing. A repeat testosterone( i7 z" T4 }! J) a3 e) R
test was ordered, but the family did not go to the
% W1 j4 s& t/ c! a4 e: e9 H# s5 z. rlaboratory to obtain the test.. r+ y& `9 g( w3 Y% K: A  Y
Discussion
  q: y; w' l! X- ~3 L5 U. PPrecocious puberty in boys is defined as secondary
' k( B/ q+ C5 v, s1 _* D/ N! c( {sexual development before 9 years of age.1,42 f8 t- O! N0 T  W" q+ F9 H. n
Precocious puberty is termed as central (true) when$ |5 G! g2 n' p& T
it is caused by the premature activation of hypo-2 j7 |" N, m: N$ o
thalamic pituitary gonadal axis. CPP is more com-: Z# G) L% E9 O* ^0 f4 e* o
mon in girls than in boys.1,3 Most boys with CPP' L+ J1 p" F+ J; V; h
may have a central nervous system lesion that is( J/ J. x# c+ w- }' F$ c* u
responsible for the early activation of the hypothal-( m3 l% U4 [% T* `" x) F* u/ s1 N
amic pituitary gonadal axis.1-3 Thus, greater empha-& \. S& j4 g5 ]7 _
sis has been given to neuroradiologic imaging in
/ @) k: n5 a! Z- A# x' H9 nboys with precocious puberty. In addition to viril-* u* Y  w  F# O2 H* S  o
ization, the clinical hallmark of CPP is the symmet-; t9 ^3 a5 p7 b9 S3 ?
rical testicular growth secondary to stimulation by8 i/ A% U( q  N- p3 r
gonadotropins.1,3
3 z' c, u: }4 j! ~: QGonadotropin-independent peripheral preco-6 V2 @  X* C# _$ g
cious puberty in boys also results from inappropriate+ {% a# [/ `9 e
androgenic stimulation from either endogenous or# k% X2 c; X8 a' D  t# X
exogenous sources, nonpituitary gonadotropin stim-
: R/ _9 U" A+ @; wulation, and rare activating mutations.3 Virilizing( ~$ ^! w+ K; ~0 @# s
congenital adrenal hyperplasia producing excessive
' {2 n2 @- w1 H' Z% Kadrenal androgens is a common cause of precocious" V* O; `1 ^( ]9 O) \
puberty in boys.3,4
6 x$ l1 F. l0 p' @5 m+ {( E2 B6 KThe most common form of congenital adrenal
4 v1 J& J7 I" E2 F, f3 v1 qhyperplasia is the 21-hydroxylase enzyme deficiency.
! @5 o( b; o( K" k' R  y& oThe 11-β hydroxylase deficiency may also result in2 }+ X+ U! I; L. V2 e9 d/ f2 m
excessive adrenal androgen production, and rarely,- {' V  m" P0 {6 i( t8 e8 y+ r3 B
an adrenal tumor may also cause adrenal androgen
  g% j, g) i. ^0 ?  }5 qexcess.1,3
8 I/ [0 q  X& [' z3 _( Y( r, [# ]at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# B5 ~8 `% ~3 c( X4 i6 [. S+ Q
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
$ o0 b/ ?& `; D% h  k! S, V6 oA unique entity of male-limited gonadotropin-
6 u4 g; Q& N0 f  Y' ]) D0 X- q( y* [independent precocious puberty, which is also known2 e+ X& a" x6 N- V# m9 L
as testotoxicosis, may cause precocious puberty at a
  Z2 R# N: g5 W( f) Wvery young age. The physical findings in these boys" w6 P" H9 d# X: C) k2 K
with this disorder are full pubertal development,
  v1 n1 ^, V# j3 kincluding bilateral testicular growth, similar to boys1 d( y/ y( r5 J* r, F% r& ]5 B
with CPP. The gonadotropin levels in this disorder  n' r; A+ L; H6 j
are suppressed to prepubertal levels and do not show
" S; {& |: W* B8 T. Mpubertal response of gonadotropin after gonadotropin-- i. d: V: g; m- S, Y# D7 O
releasing hormone stimulation. This is a sex-linked
( B- u) R% I9 ]5 S; @$ C( M, @3 C" Aautosomal dominant disorder that affects only- Y9 b, _9 v! x) e! F5 I
males; therefore, other male members of the family
9 T" Y  j' C- Xmay have similar precocious puberty.3
4 R) S! Q- q7 C' ~' \) B3 u  ^In our patient, physical examination was incon-0 u' f9 m: J. Q, h8 W6 f  r
sistent with true precocious puberty since his testi-. B% k6 {+ l5 I4 N6 j2 l: ^' G+ |/ ]
cles were prepubertal in size. However, testotoxicosis
3 Z/ D6 L: i  e0 p9 k# A" Lwas in the differential diagnosis because his father
: M& D) w2 b" T3 c) astarted puberty somewhat early, and occasionally,* }" s+ ~4 P4 |: i9 y$ t+ V
testicular enlargement is not that evident in the3 S/ S2 y: I& \1 ~- E# ^! l
beginning of this process.1 In the absence of a neg-( @# ?! @7 o, F" W3 q0 k  O
ative initial history of androgen exposure, our
9 M7 J+ h, k. ^7 w8 H6 k4 `9 Ebiggest concern was virilizing adrenal hyperplasia,' G2 B! W: H0 L: C! V
either 21-hydroxylase deficiency or 11-β hydroxylase, w8 `8 d$ a- H7 I% i3 [
deficiency. Those diagnoses were excluded by find-" K; |2 o, t6 \! P. Z
ing the normal level of adrenal steroids.' ?5 j" A% B2 Z
The diagnosis of exogenous androgens was strongly
' x. I0 E' |2 A$ D( lsuspected in a follow-up visit after 4 months because* D/ q1 e( X$ X# a, `% e! ~8 a* v5 ^
the physical examination revealed the complete disap-2 s* v% C! S8 a0 E# M
pearance of pubic hair, normal growth velocity, and5 U6 D; X. P$ \; U, l: _) l% m# V+ B
decreased erections. The father admitted using a testos-! E, R3 L7 k1 o+ p$ g
terone gel, which he concealed at first visit. He was& i8 `# ~* v7 U8 T. u* x+ @8 ~
using it rather frequently, twice a day. The Physicians’( l8 l. L# ~! [9 P* l0 G+ H' G
Desk Reference, or package insert of this product, gel or
# e+ _. O3 |, T5 F3 Ycream, cautions about dermal testosterone transfer to
; d6 U* A, l5 }- [* s+ Gunprotected females through direct skin exposure.- Z! Y/ e# c- a  b) T3 M& D
Serum testosterone level was found to be 2 times the
. b4 \7 t8 s2 B1 k  }baseline value in those females who were exposed to0 ]/ z; r/ M' U1 l0 G
even 15 minutes of direct skin contact with their male# g. M9 U5 R2 \1 o, f
partners.6 However, when a shirt covered the applica-6 R2 ]6 A- T! e% p$ _. d$ h
tion site, this testosterone transfer was prevented.3 E" z+ I1 O2 k( ~" D, {
Our patient’s testosterone level was 60 ng/mL,
5 }1 j1 w* V0 P& ]which was clearly high. Some studies suggest that' t! u9 H) W1 a
dermal conversion of testosterone to dihydrotestos-
$ V1 W  }7 k& q8 z5 ]; Y0 Q5 a; b* sterone, which is a more potent metabolite, is more1 D4 E) v0 a' o
active in young children exposed to testosterone, E. g5 e8 d/ g! ~. B
exogenously7; however, we did not measure a dihy-3 ^1 p$ x* P2 t
drotestosterone level in our patient. In addition to$ s# e! m* S+ |# w' f8 J! x1 {
virilization, exposure to exogenous testosterone in
' A: Z( x8 m! [6 a: z2 D- W! tchildren results in an increase in growth velocity and/ s4 z$ ]% p0 C0 ~& h1 O: _6 c
advanced bone age, as seen in our patient.# Y( k6 X+ D* j$ L2 Q! N) D
The long-term effect of androgen exposure during
8 R2 ?1 e' |" R0 F) Aearly childhood on pubertal development and final* d& _+ ?4 l1 n7 }
adult height are not fully known and always remain% I  s4 E7 V! u) M% A+ e
a concern. Children treated with short-term testos-
1 G+ A$ O7 f" x$ Bterone injection or topical androgen may exhibit some
/ o8 H5 l, D1 ~acceleration of the skeletal maturation; however, after6 B8 j7 D5 Z) f7 _1 p2 `; J+ c7 `
cessation of treatment, the rate of bone maturation" `1 e/ [- ]$ X/ y9 W' S0 V7 Y
decelerates and gradually returns to normal.8,9
: Y' l5 g4 k7 [2 K! D  UThere are conflicting reports and controversy
& B/ d. u( K, l( V0 o; x. aover the effect of early androgen exposure on adult
: l$ _+ s- U8 L3 q9 p3 _penile length.10,11 Some reports suggest subnormal& V, L, ~" X- P- s5 I' p+ a
adult penile length, apparently because of downreg-
1 Z" O: X/ M+ y  E+ t" L. N0 kulation of androgen receptor number.10,12 However,6 A$ Z( R6 ~% E; C+ P- i7 H
Sutherland et al13 did not find a correlation between
: K- A6 o0 S9 ochildhood testosterone exposure and reduced adult
) ]4 v2 D- o! ^3 Rpenile length in clinical studies.1 |: q4 H$ ], w) z1 |7 e# k
Nonetheless, we do not believe our patient is
5 D* L9 j; }( H8 Agoing to experience any of the untoward effects from
; i5 s% q7 h# O9 ^testosterone exposure as mentioned earlier because
9 e( `! M" r; p% Y; Qthe exposure was not for a prolonged period of time.( R% `' q$ D8 t1 g, K$ u% J* |  R; t' q
Although the bone age was advanced at the time of1 z  s6 z, g, ]$ t3 r
diagnosis, the child had a normal growth velocity at  O* b! x9 y; Y# r+ c3 i  u
the follow-up visit. It is hoped that his final adult
8 A3 o& g1 l  Jheight will not be affected.+ S2 i: i& v/ Z  a! J4 d
Although rarely reported, the widespread avail-. }1 V1 W1 B0 o, o) e; W, D; t; a
ability of androgen products in our society may
' b# o- Y! S0 {; R5 a4 }indeed cause more virilization in male or female
, e7 |  t- D& dchildren than one would realize. Exposure to andro-# Z+ c: {. X9 h- S4 |* U* n
gen products must be considered and specific ques-
% |& X. W9 j2 ~# mtioning about the use of a testosterone product or
! s1 Y4 ^/ g# [& ^- D4 ~- Zgel should be asked of the family members during: [! u8 d' F- H/ b. N) B
the evaluation of any children who present with vir-4 C. s$ y+ b! Q- d; Y+ ^8 X
ilization or peripheral precocious puberty. The diag-" k- A  `8 q& l
nosis can be established by just a few tests and by9 `! E' u) g* l4 m' i& V
appropriate history. The inability to obtain such a
: i3 W6 ]& I! j# X3 Qhistory, or failure to ask the specific questions, may5 P0 [0 c; m6 n, ?& M; ~% n
result in extensive, unnecessary, and expensive
- D+ c* V& B; |8 xinvestigation. The primary care physician should be
* ~' s5 p, V- b# }3 c; naware of this fact, because most of these children3 a' e. E  C5 Y* a+ c
may initially present in their practice. The Physicians’
. ^5 t1 P$ R) C# @3 h7 PDesk Reference and package insert should also put a# T- A6 a5 F1 N: ~+ D& S
warning about the virilizing effect on a male or, M1 l! ^" ^3 i4 F0 N9 E
female child who might come in contact with some-
7 z  h: F: w7 O* B1 Xone using any of these products.
* I2 M2 W/ L  |, u3 dReferences
# H# C3 O! l* x1. Styne DM. The testes: disorder of sexual differentiation" E6 \4 s' a6 \% |' Z
and puberty in the male. In: Sperling MA, ed. Pediatric
3 x/ e8 k  q4 _% n* C' @Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;& w+ i9 R8 m% @' p4 k( z5 z
2002: 565-628.
9 N; ~" \& z% ]# {. o2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
/ A# m7 e  d) r: S% c* A; @1 Vpuberty 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
8 V+ I( D* a  k, `, q" @; J, D
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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