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Sexual Precocity in a 16-Month-Old
( N" M4 {" e$ _! n+ g+ xBoy Induced by Indirect Topical9 U& o/ G" h9 K5 G
Exposure to Testosterone6 o% U8 V$ c% L. f8 U' o
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 c" q% U2 [5 ^4 b' I7 A- oand Kenneth R. Rettig, MD12 M9 f  c. ~# G. u! e
Clinical Pediatrics0 `; s9 u! f1 \+ s
Volume 46 Number 6' Y: G+ L) G* b7 l+ H" X
July 2007 540-5434 J  x5 V& p' S7 s
© 2007 Sage Publications: N: k$ ]  F+ O0 g' W- K$ i( u; [
10.1177/0009922806296651
6 _/ f) f0 s' xhttp://clp.sagepub.com$ J$ |0 Y8 ?6 [8 x7 I
hosted at
3 x- l/ k3 Z: f; O8 ?http://online.sagepub.com/ P5 ]" l- b% Q) r- R# `
Precocious puberty in boys, central or peripheral,
/ Z! E! {0 m$ [' w/ Eis a significant concern for physicians. Central# R: G5 p7 e) L0 E2 J
precocious puberty (CPP), which is mediated
8 v7 g/ n) k# d  U: u/ J' Xthrough the hypothalamic pituitary gonadal axis, has
! l9 I8 K" ~/ X) D9 Ba higher incidence of organic central nervous system
6 d' \* ~1 e& }" d0 [+ rlesions in boys.1,2 Virilization in boys, as manifested( k1 F# ^4 |- V4 M) D( S
by enlargement of the penis, development of pubic
1 [3 A- }) R6 U6 U) Bhair, and facial acne without enlargement of testi-
5 E  d' W7 f7 [; w0 acles, suggests peripheral or pseudopuberty.1-3 We! G; n0 V) i0 V% F
report a 16-month-old boy who presented with the' `" K) C7 |5 }7 A; k9 A
enlargement of the phallus and pubic hair develop-
. q3 s% I5 O$ Jment without testicular enlargement, which was due- @# s* p5 B! \  x  t
to the unintentional exposure to androgen gel used by
; E, f7 o% w0 V; Q) w7 Othe father. The family initially concealed this infor-2 ~) A5 H  K) Z. U
mation, resulting in an extensive work-up for this
9 i, m' S! }6 T1 `3 ]9 A# Vchild. Given the widespread and easy availability of
0 G3 S0 u$ ]+ d' v% ptestosterone gel and cream, we believe this is proba-
: C. M1 h( X- lbly more common than the rare case report in the
; K# o% B5 ]9 s& Z% M# g, _' oliterature.45 m$ p+ J8 w7 ?
Patient Report
5 }, T7 |8 J) H* `A 16-month-old white child was referred to the6 G5 T# i9 K  n
endocrine clinic by his pediatrician with the concern
- Y0 n# _$ p9 Gof early sexual development. His mother noticed
% [4 H) ~- R* w+ C' flight colored pubic hair development when he was
7 x, _: Y" v" t7 |: n; D- {1 Y( r. xFrom the 1Division of Pediatric Endocrinology, 2University of+ E/ B/ k; C. [7 K- B, F
South Alabama Medical Center, Mobile, Alabama.
; W/ v% L# @2 ^. v8 ^0 e4 XAddress correspondence to: Samar K. Bhowmick, MD, FACE,
* }1 i' M; D- {, ^& V' yProfessor of Pediatrics, University of South Alabama, College of
* r4 e) e- r9 L+ {% W$ eMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;  |) ]% ~7 x1 H: c8 F! U
e-mail: [email protected].& J9 w8 ?. K& h( N
about 6 to 7 months old, which progressively became
, ^2 L$ @5 d* {( n- ydarker. She was also concerned about the enlarge-
* ?, ^- m" @6 ]) n9 M% I6 |. Iment of his penis and frequent erections. The child4 m2 _- g. I, u
was the product of a full-term normal delivery, with
+ Q# J8 ~1 U7 [1 R, t, la birth weight of 7 lb 14 oz, and birth length of1 @( _- Q) L& U: w
20 inches. He was breast-fed throughout the first year2 R9 @' r1 }9 l; Z$ _
of life and was still receiving breast milk along with1 ^# Q3 V' S1 b7 D% C$ Q' Y0 t! A
solid food. He had no hospitalizations or surgery,
5 Z  M/ F( ~2 W. `and his psychosocial and psychomotor development
( W) W- S5 s9 i6 P; kwas age appropriate.' O8 ~' |* l) U- i- P
The family history was remarkable for the father,
! M9 k; V' m, U6 ?3 X0 [who was diagnosed with hypothyroidism at age 16,- R$ o7 d. b! o
which was treated with thyroxine. The father’s
; w) H$ I* H) \! h- @1 Eheight was 6 feet, and he went through a somewhat
4 Y5 Q1 W# d: c) Z" ^4 Dearly puberty and had stopped growing by age 14.
! q) W- R5 D' t+ k7 ?The father denied taking any other medication. The
) R; n/ R. ]6 N% Uchild’s mother was in good health. Her menarche& T  U  Q  A. f
was at 11 years of age, and her height was at 5 feet
  G+ B( |& w& M- Y% h$ [( l5 B4 f5 inches. There was no other family history of pre-# b' t, u0 ?! O3 _
cocious sexual development in the first-degree rela-
9 e' b. x* S5 L# ]) @) gtives. There were no siblings.8 q+ }' I- K, o2 @* N* Q: L$ r
Physical Examination. {9 Q( `7 [, l) ]" g. g, h
The physical examination revealed a very active,
, ^9 U5 W1 u! {: b2 S2 G, vplayful, and healthy boy. The vital signs documented0 ]) a/ G: R! i3 D3 P" x7 x6 A
a blood pressure of 85/50 mm Hg, his length was
+ W, j$ [2 ]$ i+ v" P) X90 cm (>97th percentile), and his weight was 14.4 kg
' O% X& m! i8 V- M(also >97th percentile). The observed yearly growth
' `- p8 I8 L% J" hvelocity was 30 cm (12 inches). The examination of
7 ?3 Q2 r. ]  C7 Q$ f: i0 o! Y& w  zthe neck revealed no thyroid enlargement.
4 u. O% z9 z2 o, Q. j7 WThe genitourinary examination was remarkable for
+ c% o* Z. {# ?1 }- [2 S2 @" Ienlargement of the penis, with a stretched length of$ p5 {6 r( i- Q4 T; m* c! K
8 cm and a width of 2 cm. The glans penis was very well
. ^0 ?- e; r7 Mdeveloped. The pubic hair was Tanner II, mostly around
9 W/ f6 ]6 T1 K( b* J540- t+ \+ R" \+ h6 `& o
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 r5 T7 @5 o7 {1 Q/ Zthe base of the phallus and was dark and curled. The
) N* A1 A  {3 f, c' t* ctesticular volume was prepubertal at 2 mL each.) p$ W' s- x$ X  R* N- ~- T
The skin was moist and smooth and somewhat
$ I1 G8 M- ?4 d3 Koily. No axillary hair was noted. There were no
: p3 i- r5 H& S, r7 Yabnormal skin pigmentations or café-au-lait spots.; {1 G. J; b: `; k- M6 u  E
Neurologic evaluation showed deep tendon reflex 2+
' u& R+ @4 k2 U" Y$ N" mbilateral and symmetrical. There was no suggestion
$ U; j8 ~9 {2 g0 W: Q4 |of papilledema.) ~' l: p6 P$ u7 L. E5 a
Laboratory Evaluation
' a  X0 P$ n' y# |  S  AThe bone age was consistent with 28 months by- \3 }% c0 \% v' O# Z
using the standard of Greulich and Pyle at a chrono-
% L9 G3 ?( P1 i" W8 W% g; B* K: Flogic age of 16 months (advanced).5 Chromosomal" n* ?( a5 X& V4 \; B3 i/ B& q- |
karyotype was 46XY. The thyroid function test  p+ u' Z: j& O/ D; e( ~5 J
showed a free T4 of 1.69 ng/dL, and thyroid stimu-2 I' O% }! {, h; U8 j/ u
lating hormone level was 1.3 µIU/mL (both normal)." U( V; R  L" u7 a' x
The concentrations of serum electrolytes, blood+ ~- W/ m! x2 K+ [
urea nitrogen, creatinine, and calcium all were- y# ~$ M1 s; v" X
within normal range for his age. The concentration( M: ~5 i, n# z" I( d( F; U
of serum 17-hydroxyprogesterone was 16 ng/dL
9 q% L7 W9 @& J) C, H(normal, 3 to 90 ng/dL), androstenedione was 20
( ~, e0 W: l; w) |" p6 Fng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-9 y# U0 i2 ^! c7 D  m
terone was 38 ng/dL (normal, 50 to 760 ng/dL),! K3 k+ I; x# T* e
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
5 z4 {: `. s0 s4 `9 {49ng/dL), 11-desoxycortisol (specific compound S)) e/ y4 ?( d+ s4 }1 m
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-; I, j7 L3 I: b5 m
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# W; O- q  }$ [0 @' ]2 E! z
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),2 k5 }; c0 U) a* k# K8 ^
and β-human chorionic gonadotropin was less than4 W% y/ `* E" t1 C4 W9 K
5 mIU/mL (normal <5 mIU/mL). Serum follicular) W/ O. i" ?) e5 a  s+ N
stimulating hormone and leuteinizing hormone
1 O6 Y8 z- m; N$ X$ Xconcentrations were less than 0.05 mIU/mL' y. a' j0 f3 |' K' {
(prepubertal).
0 z* f$ o: a5 s7 T( D+ jThe parents were notified about the laboratory
& f$ |) m. a+ y$ Qresults and were informed that all of the tests were
% z. Y4 ]0 L9 ^! y  M* s! S# L- hnormal except the testosterone level was high. The
# i* i! d, [$ ^follow-up visit was arranged within a few weeks to; I; W( z* w, E1 @
obtain testicular and abdominal sonograms; how-
: k" [# W7 p. b7 D3 x8 Tever, the family did not return for 4 months.% v1 E/ S+ Q0 g1 n6 D/ M1 s. S4 }
Physical examination at this time revealed that the9 v+ y$ _0 j* S; E8 p/ z: w
child had grown 2.5 cm in 4 months and had gained7 T8 k7 {/ I0 n* j9 k  }& F
2 kg of weight. Physical examination remained
9 Y" t% }" W. Z2 ?9 A1 Kunchanged. Surprisingly, the pubic hair almost com-
: z$ R8 m* z+ t: A8 spletely disappeared except for a few vellous hairs at
- p9 I6 [% J% T' w2 Y" O2 @the base of the phallus. Testicular volume was still 27 t1 k+ s2 m' b9 P0 F* g9 [
mL, and the size of the penis remained unchanged.8 Q2 M  q0 e9 ^! B7 x2 N
The mother also said that the boy was no longer hav-
/ ?! U3 @, O/ v: bing frequent erections.
8 Q9 J+ k: p0 A$ V0 S5 S( ^Both parents were again questioned about use of
/ M& y1 \/ Y9 N' Pany ointment/creams that they may have applied to- r% ]* a- T1 P" N/ l
the child’s skin. This time the father admitted the
' i6 E' U' G/ X6 E4 GTopical Testosterone Exposure / Bhowmick et al 5412 ?+ E  w* F  F
use of testosterone gel twice daily that he was apply-
' E/ i! T, G) fing over his own shoulders, chest, and back area for
' o' g* c( S; a3 }/ H1 wa year. The father also revealed he was embarrassed
3 u, z- F8 K3 h/ e4 ]! ]to disclose that he was using a testosterone gel pre-
, G- ?3 N+ O! Y' Y; |1 I6 B( L6 Q8 iscribed by his family physician for decreased libido
) K% ?% I" O0 Esecondary to depression.. ~8 p- Z7 w2 W+ n+ ]( D5 C9 t
The child slept in the same bed with parents.  U( f: j$ ]# e% `+ M+ [7 G: z
The father would hug the baby and hold him on his2 s, Z1 t$ ]3 r. B! D
chest for a considerable period of time, causing sig-
  s2 e2 g, }; c8 E% r7 gnificant bare skin contact between baby and father.1 A+ L8 d9 C% {  ]5 [3 T
The father also admitted that after the phone call,) @  P! h: }8 w+ F" \
when he learned the testosterone level in the baby
  D/ i$ I% v7 {. C; W9 w* x$ xwas high, he then read the product information3 _$ a# f5 D, D. i, a) I+ D. d. W
packet and concluded that it was most likely the rea-
: c: q+ G3 a  o( C9 Bson for the child’s virilization. At that time, they6 Q% f" F; ]0 ~3 |3 g
decided to put the baby in a separate bed, and the
* T5 d' S! K) ~: [father was not hugging him with bare skin and had
& G, K  M$ c# u% V5 cbeen using protective clothing. A repeat testosterone; q1 H! _6 L* R# P
test was ordered, but the family did not go to the
* `3 N3 u6 O: L( \0 t$ Q; E; nlaboratory to obtain the test.' M6 Z/ |* D1 \
Discussion
1 j( u. n  s# `4 d+ q8 M0 YPrecocious puberty in boys is defined as secondary, a& k+ j3 @& O1 }0 ?2 C2 H5 D
sexual development before 9 years of age.1,4
9 J/ C: y0 B- @& i/ M* dPrecocious puberty is termed as central (true) when
  X- h7 C- Z0 Eit is caused by the premature activation of hypo-
+ U) a, Y4 f/ X5 W2 M. Z$ x1 y- \thalamic pituitary gonadal axis. CPP is more com-  a# C/ r, c& s4 P! G/ x# r
mon in girls than in boys.1,3 Most boys with CPP
* V) e4 Q4 n0 emay have a central nervous system lesion that is9 }. ~( L  g; j1 q$ Z
responsible for the early activation of the hypothal-; J$ _: _5 Y- m9 v( _) [8 T3 x
amic pituitary gonadal axis.1-3 Thus, greater empha-
( a* W; j- F7 q* Psis has been given to neuroradiologic imaging in
+ }  m1 C7 y. W! r. q6 p& }  Lboys with precocious puberty. In addition to viril-
2 _( Q# i9 W# u5 w3 Vization, the clinical hallmark of CPP is the symmet-
; C, `6 D$ E: J; e0 l+ `rical testicular growth secondary to stimulation by; Z/ g: I/ Z6 Y9 ^/ L& E
gonadotropins.1,3
& A1 s" R+ T, p0 F6 U3 ]+ h* x; ZGonadotropin-independent peripheral preco-1 d2 X  e) ^  |4 `2 l4 X9 U
cious puberty in boys also results from inappropriate( a- [7 b5 E* u/ D5 E
androgenic stimulation from either endogenous or& a; x6 N; [6 v* |" \' f! j, I
exogenous sources, nonpituitary gonadotropin stim-
: ]* [/ {! T0 \- S# L( D& F- _ulation, and rare activating mutations.3 Virilizing  d+ T  ]2 a3 s4 x, _5 E: J5 q: H8 p6 o
congenital adrenal hyperplasia producing excessive7 N: L# i( G- c/ a7 k
adrenal androgens is a common cause of precocious
6 _' i9 U5 W& E" Y  I: A& upuberty in boys.3,44 \4 `: L  X0 ?5 J6 b* R
The most common form of congenital adrenal8 x! r/ {  P# t1 [3 |
hyperplasia is the 21-hydroxylase enzyme deficiency.2 v1 a! p# @" T( j7 y
The 11-β hydroxylase deficiency may also result in' J; t& t. B# `! T, c7 y% L
excessive adrenal androgen production, and rarely,- ^! k  E6 O/ a) g* @8 z
an adrenal tumor may also cause adrenal androgen0 i( z9 h0 ~, e8 q
excess.1,3; |* J1 R3 x4 r6 B8 s. p9 F
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 n; u3 o, t6 V9 O4 n* R: E: _2 r542 Clinical Pediatrics / Vol. 46, No. 6, July 20070 p& j, r7 S* B$ q' T! D4 }
A unique entity of male-limited gonadotropin-
, Q/ |( z  _& D& h; G2 r3 l/ T3 [independent precocious puberty, which is also known
, Q8 w7 R2 e0 Q* ^as testotoxicosis, may cause precocious puberty at a
3 t6 G# }  ?  Q+ {9 M9 c% Dvery young age. The physical findings in these boys
2 ^. t8 f) f" _) h. H3 m# h, }' wwith this disorder are full pubertal development,5 o9 K3 L* A( b+ H
including bilateral testicular growth, similar to boys8 T7 @( K# N7 X2 i. y# M
with CPP. The gonadotropin levels in this disorder6 I- D$ O% t8 ]' w$ x& q2 f
are suppressed to prepubertal levels and do not show
: R1 D& J; ]6 f+ ]1 bpubertal response of gonadotropin after gonadotropin-: E. d; L; I. ^3 Y1 D
releasing hormone stimulation. This is a sex-linked
2 Q1 J* r7 X! f) H# A3 }! yautosomal dominant disorder that affects only+ h+ u! @# a9 X! W
males; therefore, other male members of the family
2 z; |: S# v) I! @may have similar precocious puberty.3: d! I& l1 N7 v! r1 r
In our patient, physical examination was incon-0 }( f2 ]8 H# W3 }9 T" L) W& E1 u4 v# k% c
sistent with true precocious puberty since his testi-. m9 U/ q/ q1 d4 O7 v; f
cles were prepubertal in size. However, testotoxicosis
% m$ a6 N8 r7 i& A: {/ qwas in the differential diagnosis because his father) |/ H5 b5 r. _
started puberty somewhat early, and occasionally,
) \3 e( o; i+ M/ q) b' n: \) k7 ~testicular enlargement is not that evident in the2 n9 q) {3 D0 ~' ~+ r5 W$ _- p4 K
beginning of this process.1 In the absence of a neg-
6 F8 L, d$ c* [$ M0 q+ ?+ ]' q# m' |ative initial history of androgen exposure, our& x! Z  {; ~7 z7 o" K& d0 b
biggest concern was virilizing adrenal hyperplasia,/ o. G: h- n' t0 J: g* e* {, d, z
either 21-hydroxylase deficiency or 11-β hydroxylase
$ u/ {( v) }8 P2 o" }( t! w3 _7 n- Zdeficiency. Those diagnoses were excluded by find-
$ T2 q6 k0 ]# ?ing the normal level of adrenal steroids.
' @; t# m& J: w# Q+ d; E. h& d/ p0 EThe diagnosis of exogenous androgens was strongly
; n3 Z  ]. _/ x* |9 A9 ysuspected in a follow-up visit after 4 months because& b! a1 Z1 N: G& Y: x% B1 M4 b$ i! j
the physical examination revealed the complete disap-
9 I% S+ u2 r; m. D' Q9 gpearance of pubic hair, normal growth velocity, and- _! u' H' e0 \
decreased erections. The father admitted using a testos-
9 \6 O6 r0 h4 s6 L' T4 |' A4 n% Uterone gel, which he concealed at first visit. He was
* N" `$ g2 v( f: f( gusing it rather frequently, twice a day. The Physicians’
+ R+ l- q0 N5 z$ {$ I( YDesk Reference, or package insert of this product, gel or: @1 l- r3 q3 ]( g% J+ Z
cream, cautions about dermal testosterone transfer to
  o( R) t4 d. B/ t; c* ~4 H* punprotected females through direct skin exposure.
1 G/ ^* Z' e: o" g1 W0 n3 @$ I& P. ASerum testosterone level was found to be 2 times the) R5 _' N2 E0 A: R7 k
baseline value in those females who were exposed to* D5 f0 B$ [; {
even 15 minutes of direct skin contact with their male' V6 Z2 L8 X. z6 d
partners.6 However, when a shirt covered the applica-
- f! V/ W) }. K4 ption site, this testosterone transfer was prevented.
: a# Q( h/ l  J7 J! N8 UOur patient’s testosterone level was 60 ng/mL,
- {5 O  ^; e( ?8 }# owhich was clearly high. Some studies suggest that/ ^& P* |7 {) ~1 S! u
dermal conversion of testosterone to dihydrotestos-: N6 E- W6 @1 c: [
terone, which is a more potent metabolite, is more
+ z4 e- q; s6 M$ \active in young children exposed to testosterone+ I2 f! Q/ r5 O% x) L# I0 Z
exogenously7; however, we did not measure a dihy-3 n$ N$ f2 L9 ^, i8 O/ k. h# H3 D
drotestosterone level in our patient. In addition to& X2 h3 s& ?& r. E  X) C# [
virilization, exposure to exogenous testosterone in9 q6 o' `8 a5 P& K& Z
children results in an increase in growth velocity and
# \* F. y2 a# s5 ^# \0 W2 M0 Fadvanced bone age, as seen in our patient.& T; o. k5 |/ l$ b) _
The long-term effect of androgen exposure during
/ @: g0 r5 |/ ~" _early childhood on pubertal development and final- X7 Z& K- Q$ |! `+ B3 ?) g: M  C
adult height are not fully known and always remain9 S: L# D2 A/ p7 v1 n! Y
a concern. Children treated with short-term testos-; G+ {; L4 L& ^7 f1 I$ l* M3 l
terone injection or topical androgen may exhibit some
$ P1 S7 N1 E  r3 eacceleration of the skeletal maturation; however, after
1 S/ c0 {, j* P  ccessation of treatment, the rate of bone maturation6 c5 c9 n9 K5 I+ D
decelerates and gradually returns to normal.8,9
( c& M0 I" j) e. b. e9 bThere are conflicting reports and controversy
* `& S  V8 ?% `% H0 ]4 ?over the effect of early androgen exposure on adult. m4 q5 R' u3 {" @5 N
penile length.10,11 Some reports suggest subnormal
% {6 n& }. {$ b) Madult penile length, apparently because of downreg-
9 T+ S2 ^0 X5 a/ V- u: v# R3 Oulation of androgen receptor number.10,12 However,
. f+ v$ I0 g" E" }6 R$ `Sutherland et al13 did not find a correlation between
5 u  C/ a5 b: a7 V% \1 f# y% ?childhood testosterone exposure and reduced adult5 [4 K- _2 f) b) I! k3 ?4 S
penile length in clinical studies.
6 C9 q7 A& c/ x3 k6 \% |) K0 JNonetheless, we do not believe our patient is, ]+ U& Z/ Q! y0 E
going to experience any of the untoward effects from! q' z5 r% \5 `' D4 ^
testosterone exposure as mentioned earlier because; t0 K% S& i0 E0 ~3 o
the exposure was not for a prolonged period of time.* t, C& M" ~% A8 ]
Although the bone age was advanced at the time of. |3 ^$ C" s% z0 u
diagnosis, the child had a normal growth velocity at; |( |6 \% M, b( C$ h* O% X2 M
the follow-up visit. It is hoped that his final adult
% Z/ P! Q! c, p& Aheight will not be affected.
9 Y' k) ]4 @3 r' d3 k+ Q5 m5 OAlthough rarely reported, the widespread avail-. R) t& |* q+ R
ability of androgen products in our society may" c2 L2 R, D3 T( a
indeed cause more virilization in male or female
! }/ l0 z0 q' D' l! t- |children than one would realize. Exposure to andro-
( y) w+ u, g8 C1 c' Hgen products must be considered and specific ques-% S: T- v/ R" S$ e! q
tioning about the use of a testosterone product or
$ F! m/ A0 X5 e0 sgel should be asked of the family members during7 p5 }' @3 K# u8 N9 g3 K- B, S
the evaluation of any children who present with vir-
! T4 l& E, I: uilization or peripheral precocious puberty. The diag-
- e2 k& G9 v! i/ b. r8 |* ]) j% v6 _nosis can be established by just a few tests and by
4 G! t* M3 x6 V# \, w% bappropriate history. The inability to obtain such a
9 s. q. m: r- u6 L/ y# z, w- D. {history, or failure to ask the specific questions, may- g- {+ m" X( ?" ~1 y
result in extensive, unnecessary, and expensive( ]5 b7 ?8 _+ M# U" k
investigation. The primary care physician should be
1 W$ e2 s( v1 M7 taware of this fact, because most of these children
9 M) w; `, D! r7 f2 I: U$ y$ Dmay initially present in their practice. The Physicians’
3 M* l# S3 e( I( k2 r: t. RDesk Reference and package insert should also put a0 I3 h; O( y3 x  n/ @6 r6 c
warning about the virilizing effect on a male or' P6 M$ s, E) ^$ @9 h& @
female child who might come in contact with some-
2 _& o$ \$ \  ?6 ^one using any of these products.
1 C4 R* ~' B5 P% Q' P, QReferences
3 A+ C/ C0 @' o) K! [. S7 _1. Styne DM. The testes: disorder of sexual differentiation
) u! Z* M: n* I3 tand puberty in the male. In: Sperling MA, ed. Pediatric3 C. ]" \$ }5 w' D8 M# F) s7 j3 q
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;9 B0 W* A4 N3 ^# i
2002: 565-628.
* {  m& N$ v! ?0 n2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
+ U. D% Q( h$ x4 Tpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
" E6 l7 D7 R% a) v, zBoy Induced by Indirect Topical. C2 L' E, s# t8 R3 L3 V
Exposure to Testosterone
$ I( c+ n  t- ]* A# v& ?% {Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
( X3 {/ r% W+ M8 W( m2 Tand Kenneth R. Rettig, MD1- V6 P! T+ C3 N' i6 U
Clinical Pediatrics2 _6 V8 M: w! d$ I  |! L
Volume 46 Number 6. W8 z0 s% x' ~' A$ r8 K. H
July 2007 540-543* z+ v9 E' Z$ P! e  l  D# J* }, _* w' z
© 2007 Sage Publications
2 L% L0 w! ]4 Y6 u+ ^+ v( ^10.1177/00099228062966518 ^: T" v8 i6 a; Z
http://clp.sagepub.com4 C6 b+ q" ]1 y! R' N, @1 h
hosted at
2 R  ]7 A5 [) K# V( V1 hhttp://online.sagepub.com. ~* C$ F, A8 w% e# _
Precocious puberty in boys, central or peripheral,
% D7 a- `: j& |; Wis a significant concern for physicians. Central9 A* Q" R5 ]+ k  E0 V8 U" ?
precocious puberty (CPP), which is mediated
+ P/ }5 V/ V  W0 y7 S1 Othrough the hypothalamic pituitary gonadal axis, has
- ]+ @1 }% z1 {7 F+ E$ I/ S* R9 t" ra higher incidence of organic central nervous system/ m8 ~6 [' f5 K* M3 ^+ V8 H
lesions in boys.1,2 Virilization in boys, as manifested! v& ]& p4 H3 n6 U$ q& f
by enlargement of the penis, development of pubic+ ?! [; u! R/ v+ b5 l1 |4 y
hair, and facial acne without enlargement of testi-
/ g3 Q+ g& T  h! P$ T6 Hcles, suggests peripheral or pseudopuberty.1-3 We7 b( Q6 p. \0 L9 i' ?: \; z2 ^7 W
report a 16-month-old boy who presented with the* L3 M7 C1 Q# L/ F- ^& U! D
enlargement of the phallus and pubic hair develop-
9 o' L- U1 ?% D0 B6 Kment without testicular enlargement, which was due0 Z' _9 y: r8 J0 h% M( `/ u( s! f* S
to the unintentional exposure to androgen gel used by
' b5 E! j& m  q  xthe father. The family initially concealed this infor-
8 ^- m5 m$ |9 C- J) ~& t4 Imation, resulting in an extensive work-up for this
' I: I- `$ R- X. S. ?* Qchild. Given the widespread and easy availability of
/ F/ E! v( k# X. S# K2 o, P6 Dtestosterone gel and cream, we believe this is proba-) D# A6 \$ h- b  w* s" F2 e
bly more common than the rare case report in the
5 y3 h# j; T7 C! b# H' Iliterature.4
) J2 f  s9 g/ |, fPatient Report3 Q' V" A" ^* _- C
A 16-month-old white child was referred to the
0 v  {; g6 g  ]! Bendocrine clinic by his pediatrician with the concern
& E: m& P1 \- t# q5 |4 zof early sexual development. His mother noticed5 o5 t) z( z9 {' U0 N0 L5 B, A9 l
light colored pubic hair development when he was: F  F  a" A! {; }& V
From the 1Division of Pediatric Endocrinology, 2University of& r- {$ R+ w4 x$ [# }0 |' M
South Alabama Medical Center, Mobile, Alabama.
+ w' }, {* [* S& r# c# KAddress correspondence to: Samar K. Bhowmick, MD, FACE,$ }- h& j' o- z! w! a% R/ h$ }
Professor of Pediatrics, University of South Alabama, College of1 ~- F4 x5 s; q, J2 x
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;0 W1 L4 @. `7 L$ |2 h# h& w
e-mail: [email protected].+ F2 v+ K3 Z0 T7 b1 r6 ?! e; O
about 6 to 7 months old, which progressively became8 R* Z9 y: `/ p6 M2 w
darker. She was also concerned about the enlarge-
3 ~# I+ m* o& `4 ~; w% r6 \ment of his penis and frequent erections. The child7 y4 Q7 W* |2 y1 E4 s
was the product of a full-term normal delivery, with
+ |- s& a8 u/ {- Y5 ra birth weight of 7 lb 14 oz, and birth length of
0 [2 N& J( Z% B20 inches. He was breast-fed throughout the first year8 _$ D0 A9 ~# F% m' p/ f5 J6 y" I
of life and was still receiving breast milk along with
+ g' Y' a6 |- {) Asolid food. He had no hospitalizations or surgery,
! A3 A: }: b& s2 D8 Yand his psychosocial and psychomotor development. T4 G$ o7 s* J
was age appropriate.) z$ M$ @1 ?6 J7 q; I" b! O
The family history was remarkable for the father,
6 V1 B9 l' \* q! P1 e/ a4 o0 pwho was diagnosed with hypothyroidism at age 16,
0 ?+ x2 |' c& C% O9 bwhich was treated with thyroxine. The father’s
, M" S3 ^1 q$ K7 `height was 6 feet, and he went through a somewhat# d8 O# t0 [6 ]& I, `! }
early puberty and had stopped growing by age 14.5 ?: d# A& ^5 ^. R' }
The father denied taking any other medication. The+ u$ S) ]/ R* a: @
child’s mother was in good health. Her menarche6 A1 ]$ b0 o& B
was at 11 years of age, and her height was at 5 feet
. a# f( Y! u% g5 inches. There was no other family history of pre-8 G0 s1 }; K# Z* W
cocious sexual development in the first-degree rela-
; X+ R. h0 h9 N9 O: Ltives. There were no siblings.
; G7 Q& m/ v5 f3 O5 }" `Physical Examination: f0 ~3 V5 E+ K0 n6 ]! b% Y
The physical examination revealed a very active,
' X5 D: i$ U. Jplayful, and healthy boy. The vital signs documented1 z3 m: |$ i1 Z  X& w0 m2 `
a blood pressure of 85/50 mm Hg, his length was
. u: Y) m' a$ H& H9 S90 cm (>97th percentile), and his weight was 14.4 kg
; |3 D' N4 r2 E) ^* @. x" e(also >97th percentile). The observed yearly growth
- J7 V6 j: [. [7 dvelocity was 30 cm (12 inches). The examination of; Y5 z- [7 [; G% O( P
the neck revealed no thyroid enlargement.7 b6 j" i2 ?; M6 f3 U- X$ O
The genitourinary examination was remarkable for
0 l2 e! m9 ~6 B* J) H! a7 D  N7 Penlargement of the penis, with a stretched length of
! Q( ~& I$ C+ K9 a" K$ [8 cm and a width of 2 cm. The glans penis was very well
- @* f' a' e) L2 X  Edeveloped. The pubic hair was Tanner II, mostly around% q. V' F0 `! i0 Q: w
540
7 D% u- B* }7 y9 T, E& ^( {/ H! o9 |at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 @) U9 z& a1 Zthe base of the phallus and was dark and curled. The( K8 u( w( R! n0 y2 @2 d3 p
testicular volume was prepubertal at 2 mL each.
( x* s0 i% ]  r; Q  j4 kThe skin was moist and smooth and somewhat
, u8 \4 g. W# f6 Yoily. No axillary hair was noted. There were no& |  p% @8 a4 r7 ~3 {
abnormal skin pigmentations or café-au-lait spots.8 T9 p$ s, i/ w" D2 ]
Neurologic evaluation showed deep tendon reflex 2+1 U3 G+ i- s! w0 I) F3 A
bilateral and symmetrical. There was no suggestion
; ?5 H+ v3 `- ^+ h: t7 S3 b$ Rof papilledema.
: T. {$ C, F; ILaboratory Evaluation8 [+ [8 s4 F& A' ~0 w/ {6 w
The bone age was consistent with 28 months by
1 m6 F5 q/ O; q; lusing the standard of Greulich and Pyle at a chrono-! r  a! T1 x# B. a
logic age of 16 months (advanced).5 Chromosomal3 b" `* @0 q7 x, `* k
karyotype was 46XY. The thyroid function test
( ]. ]* R9 X4 O2 \! U1 Hshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
2 G2 h- z6 z; H! E0 w- E' S" q- ulating hormone level was 1.3 µIU/mL (both normal).
9 G: a3 C! p3 w5 U% n8 YThe concentrations of serum electrolytes, blood
2 j* t4 s6 U' t/ b8 _urea nitrogen, creatinine, and calcium all were& H; b6 X. {: g+ e9 @
within normal range for his age. The concentration
& R8 |- ^) }: h4 ]1 v# C& @of serum 17-hydroxyprogesterone was 16 ng/dL) l. l8 ^) Y' l) Z2 V
(normal, 3 to 90 ng/dL), androstenedione was 20/ F# P  i  B$ P% J
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
( i- `" B1 @1 D, L% N0 Lterone was 38 ng/dL (normal, 50 to 760 ng/dL),
( j5 h& h+ ]# o9 y3 j: f: zdesoxycorticosterone was 4.3 ng/dL (normal, 7 to0 ^4 [& @/ p7 V9 j
49ng/dL), 11-desoxycortisol (specific compound S)( x4 F+ w! m. K. k9 S
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
2 L/ ]# c6 `) L1 otisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total) K3 h# w$ ^: @
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),- `6 ~: o* `- v& V, Z2 ^* r- w
and β-human chorionic gonadotropin was less than& `# R9 l* t4 L$ S& W0 t
5 mIU/mL (normal <5 mIU/mL). Serum follicular8 h' h  k/ a( y7 E
stimulating hormone and leuteinizing hormone
, \& ^1 q& i* E! ^3 @concentrations were less than 0.05 mIU/mL
- X$ o0 O/ q" s" p* H8 R$ m(prepubertal).
. e% O" S$ c/ v/ w+ GThe parents were notified about the laboratory5 D6 I: B$ N9 g
results and were informed that all of the tests were8 I5 Z3 r6 s0 y+ d. H5 g
normal except the testosterone level was high. The4 f' v. b" u' P7 @2 R. m
follow-up visit was arranged within a few weeks to2 B% i7 y8 W9 v+ x0 B
obtain testicular and abdominal sonograms; how-
2 P; A/ j  l! c) J0 A& f4 g0 D+ I+ V7 qever, the family did not return for 4 months.) G. X- {# S5 J6 e
Physical examination at this time revealed that the
. C1 O6 E% h# W5 ~+ uchild had grown 2.5 cm in 4 months and had gained
' e8 R/ A& J& ], B  a2 kg of weight. Physical examination remained3 s6 W6 a$ j. _* [
unchanged. Surprisingly, the pubic hair almost com-; D# S* k2 \! o& ~2 S* Y) A+ d
pletely disappeared except for a few vellous hairs at
1 ], ^$ Q% _9 q& V' l: ithe base of the phallus. Testicular volume was still 25 D; w; s7 Y" Q
mL, and the size of the penis remained unchanged.1 k/ u- b9 N0 G0 f/ C# F
The mother also said that the boy was no longer hav-
" R* b# C; @$ r, Iing frequent erections.3 g. v7 M& o9 E$ R
Both parents were again questioned about use of  i0 [$ Z- D, t  B, ]  S
any ointment/creams that they may have applied to
. s6 F; q' J4 `3 U+ @( F: hthe child’s skin. This time the father admitted the: P: I4 {; S3 Y+ Q
Topical Testosterone Exposure / Bhowmick et al 541- u+ I3 g, y! z& b" ~6 z3 A0 q7 M
use of testosterone gel twice daily that he was apply-
9 i+ T" }/ R7 `; u' @ing over his own shoulders, chest, and back area for
% V2 k7 V& `% Q, la year. The father also revealed he was embarrassed
$ h5 e1 ~) n3 j8 f# _' a5 g# a" qto disclose that he was using a testosterone gel pre-
3 m4 k% J' _" r1 Cscribed by his family physician for decreased libido5 v  M/ ?2 ^- n/ b0 B& J5 }
secondary to depression.1 X) W7 {  t2 M7 Q& B5 ~
The child slept in the same bed with parents.
0 p- {9 D& u" f. EThe father would hug the baby and hold him on his
/ w- S5 s$ H8 O6 g8 r$ qchest for a considerable period of time, causing sig-, _/ L5 }9 h" T
nificant bare skin contact between baby and father.: I0 z* q* X" r& x# J5 F
The father also admitted that after the phone call,7 X; N3 t- b/ D7 F3 S
when he learned the testosterone level in the baby2 h0 g+ |" C/ _. w& m+ F
was high, he then read the product information- n( P4 H1 }1 f
packet and concluded that it was most likely the rea-
! P4 G) V% ?  S5 q. }son for the child’s virilization. At that time, they4 w. U0 {2 T1 t& c- [0 _4 p" C5 B- p
decided to put the baby in a separate bed, and the+ f$ m" ^' x0 T# _. ?
father was not hugging him with bare skin and had
/ q1 v- ?% d. v9 b0 x" p" v& obeen using protective clothing. A repeat testosterone
+ n  P7 V5 K& ^  r. vtest was ordered, but the family did not go to the2 n# Y; T3 {# t9 h! A6 h6 O
laboratory to obtain the test.
. U" Z; H$ {4 L8 m  B) M! nDiscussion% ^8 Y  P# N$ A- n# \
Precocious puberty in boys is defined as secondary
$ T# D* E( q9 ksexual development before 9 years of age.1,4
( l8 g/ m) L; o8 p5 K! XPrecocious puberty is termed as central (true) when
! d" ?/ \2 @/ M; Z, fit is caused by the premature activation of hypo-; C5 Z- I/ c$ n  J. z3 C
thalamic pituitary gonadal axis. CPP is more com-4 ?9 Q6 _6 }* C1 r
mon in girls than in boys.1,3 Most boys with CPP
% c* R8 r2 h, V7 xmay have a central nervous system lesion that is
% _0 x( Q+ U$ g# `* S& rresponsible for the early activation of the hypothal-, d5 M) b8 |# G9 T& b
amic pituitary gonadal axis.1-3 Thus, greater empha-: X; t; E6 U: t. }8 F: X8 t
sis has been given to neuroradiologic imaging in
( _4 f& {; o9 ?1 m' @4 ~7 L3 nboys with precocious puberty. In addition to viril-
+ _/ X1 j) H/ R; o, C& U$ Rization, the clinical hallmark of CPP is the symmet-
! e+ G: C) W6 n5 B; [9 Urical testicular growth secondary to stimulation by5 [# g1 Q! n& m% O+ V+ M+ c; s. T
gonadotropins.1,38 d$ U" z. i0 Q: }" b
Gonadotropin-independent peripheral preco-
  _3 [$ O5 Q) n/ L* Lcious puberty in boys also results from inappropriate
6 D" B; a% u3 F4 T: wandrogenic stimulation from either endogenous or
. x4 A7 Q' o' s; [! [; _, Xexogenous sources, nonpituitary gonadotropin stim-" a& l( B# X' U* K& N* B* ~. `0 j: h
ulation, and rare activating mutations.3 Virilizing8 ]( L4 a' ]6 X4 z! U
congenital adrenal hyperplasia producing excessive
1 d# ^4 {& l. G6 d, z. D/ u2 ~adrenal androgens is a common cause of precocious1 ]9 e* ?/ W5 ^+ s3 g4 K; ~' X$ o, L
puberty in boys.3,4& K$ L9 G/ u3 l4 @
The most common form of congenital adrenal9 T' C1 u# Q2 B
hyperplasia is the 21-hydroxylase enzyme deficiency.1 s8 r+ ^7 \+ T4 l; m
The 11-β hydroxylase deficiency may also result in6 A! M- M: A- [6 h; ^3 P
excessive adrenal androgen production, and rarely,
& R0 C9 J1 F- O3 H# ean adrenal tumor may also cause adrenal androgen5 _9 S# Y( n5 Y1 K; H; o
excess.1,3
9 s  M  w8 F4 E# @5 _$ y! T2 `$ p3 A5 @' ]at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 d! t" V1 ?. x
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007! m. e, N" T3 A; w1 n. d
A unique entity of male-limited gonadotropin-! \; V  |/ }5 L2 k. J& X
independent precocious puberty, which is also known. W" y$ ^- @$ N5 {# k" U
as testotoxicosis, may cause precocious puberty at a5 ], ^+ L5 y- R7 N+ M
very young age. The physical findings in these boys+ \& y& |$ U( W  ^
with this disorder are full pubertal development,
/ n( {) K& a( U& p1 @& U: M6 t* cincluding bilateral testicular growth, similar to boys1 L% Q$ ]0 L2 A/ T, S1 X
with CPP. The gonadotropin levels in this disorder- T# i& q& I8 ^  }6 M6 U0 ~
are suppressed to prepubertal levels and do not show! J: W. D# o, g' l! e
pubertal response of gonadotropin after gonadotropin-
0 m' _# C- ?/ [; v! kreleasing hormone stimulation. This is a sex-linked
" e( Q# D3 V! }autosomal dominant disorder that affects only2 a' i6 k* |5 s% a
males; therefore, other male members of the family
: x: {1 a5 W+ F- b6 p# c) t) Kmay have similar precocious puberty.36 s" ]. m" p' \0 u
In our patient, physical examination was incon-
2 |0 s# T$ y  s8 {5 Psistent with true precocious puberty since his testi-5 @0 C9 X1 V. P' j# O* l
cles were prepubertal in size. However, testotoxicosis6 X! r6 B+ f2 X
was in the differential diagnosis because his father
# x3 @/ m2 i( e5 a& `1 bstarted puberty somewhat early, and occasionally,# l) y, u& X3 `( z% L$ Q
testicular enlargement is not that evident in the4 e$ W) H* E0 n: |7 V
beginning of this process.1 In the absence of a neg-2 l4 X1 {, c+ Y; O) p- q6 s
ative initial history of androgen exposure, our
9 c4 Y7 f* y* g$ Ibiggest concern was virilizing adrenal hyperplasia,1 ]& s. d) ]5 n# A+ b
either 21-hydroxylase deficiency or 11-β hydroxylase% ]/ i; P  b. h' s: G4 C  O
deficiency. Those diagnoses were excluded by find-* d( W$ b+ M) m; o8 v" G
ing the normal level of adrenal steroids., T1 z+ ?" v* d! C5 ^: F  s: y
The diagnosis of exogenous androgens was strongly# l+ e1 ~4 x+ _
suspected in a follow-up visit after 4 months because3 i5 Q& M0 ^0 e6 Z/ r5 m$ z
the physical examination revealed the complete disap-
3 A# G# O: X" Apearance of pubic hair, normal growth velocity, and, _% Z% T' S1 p
decreased erections. The father admitted using a testos-
1 s6 U# G# V5 V1 I9 C4 h- Dterone gel, which he concealed at first visit. He was
; ?! z9 R  n1 s0 kusing it rather frequently, twice a day. The Physicians’
" p( k: E; N; m* }6 y" jDesk Reference, or package insert of this product, gel or8 o/ Z- q) }1 I* O& w5 P$ \5 H
cream, cautions about dermal testosterone transfer to8 h  d0 P9 [  `1 u
unprotected females through direct skin exposure.
; O7 u+ W- d: {7 u% USerum testosterone level was found to be 2 times the
! ~5 K' j  M0 t  G- F: q  xbaseline value in those females who were exposed to
" ^: I- Q% C! B* T9 z( neven 15 minutes of direct skin contact with their male" X( q9 z( H3 V) S
partners.6 However, when a shirt covered the applica-
- W: C& r1 @! F% k- Ution site, this testosterone transfer was prevented.7 H2 \$ z+ g2 V, u2 B$ f
Our patient’s testosterone level was 60 ng/mL,
, U/ T  g( T: N0 |which was clearly high. Some studies suggest that
# q$ ]( t+ B' C$ ]- F% t* udermal conversion of testosterone to dihydrotestos-: y5 y$ a! Y" L( {1 n& J! q+ @
terone, which is a more potent metabolite, is more, k4 K1 D) m# \- R
active in young children exposed to testosterone
6 {& ?' [! ]+ A( r! zexogenously7; however, we did not measure a dihy-
1 h* A/ z, f9 |3 O* N9 ydrotestosterone level in our patient. In addition to6 S8 H! R: {. q+ z! m/ d$ H& v5 F  X5 E
virilization, exposure to exogenous testosterone in
7 K4 S# Y, I  x8 H  Y, A! C+ fchildren results in an increase in growth velocity and4 n/ R) i6 s6 i% G2 d' [
advanced bone age, as seen in our patient.
  ^! @7 R/ w! P) ^$ v9 X  dThe long-term effect of androgen exposure during
/ B# Z, n6 q( Learly childhood on pubertal development and final' Z# O$ K9 R8 |3 O- J; |8 h0 x5 D
adult height are not fully known and always remain
# A+ w4 w( Q6 _* va concern. Children treated with short-term testos-
. L" i% Y3 n- uterone injection or topical androgen may exhibit some
0 D. n% f9 X. T! K2 oacceleration of the skeletal maturation; however, after# C" o2 Z" H$ U) y, b2 Y& \
cessation of treatment, the rate of bone maturation
9 y! l! o4 U- W3 X: jdecelerates and gradually returns to normal.8,9/ X. k3 s# v; E  \! q
There are conflicting reports and controversy
" ^5 [3 Y/ q. G6 |5 Oover the effect of early androgen exposure on adult) \: k- J3 C: c  l: L" k
penile length.10,11 Some reports suggest subnormal! a/ L/ v3 L" L" m+ k7 E1 |
adult penile length, apparently because of downreg-9 x3 L. g" Q" r4 F
ulation of androgen receptor number.10,12 However,; B& z& R- N& D4 \
Sutherland et al13 did not find a correlation between
: b+ S/ J' Q/ @3 a; J# j2 g$ b$ V1 bchildhood testosterone exposure and reduced adult% I# q  u& Z1 v$ D' {
penile length in clinical studies.
; a* U4 K& d. a3 _Nonetheless, we do not believe our patient is5 s$ x8 f9 @4 u" i  A; L, {, o8 z8 G
going to experience any of the untoward effects from
9 M0 o" y$ C+ |" O3 Ttestosterone exposure as mentioned earlier because
1 u. S( d. P# @2 |the exposure was not for a prolonged period of time.2 X" R" V. G+ j/ |& ^
Although the bone age was advanced at the time of
1 O  p# J1 u6 [! A2 Qdiagnosis, the child had a normal growth velocity at
# L' h/ }. \! Uthe follow-up visit. It is hoped that his final adult4 L7 @  _4 r- l6 J
height will not be affected.
7 P" b7 ^; H/ Y" n7 OAlthough rarely reported, the widespread avail-
- L! S% l: b9 i9 i& Eability of androgen products in our society may
+ y, f1 w% @: `) H* zindeed cause more virilization in male or female
6 v' C# Z' y* }0 Q% l6 schildren than one would realize. Exposure to andro-
% x$ t: j$ e! y- ?2 c1 \* ?, L, agen products must be considered and specific ques-
* @2 a* l. z  _# I1 Dtioning about the use of a testosterone product or0 ^1 n6 v0 J" e5 l5 g8 a
gel should be asked of the family members during6 Y5 T6 N" U5 j4 r6 y. n- m
the evaluation of any children who present with vir-
2 [1 H4 p+ [3 N; D$ eilization or peripheral precocious puberty. The diag-0 A2 y2 j7 q5 ~( y1 d$ n
nosis can be established by just a few tests and by) _8 {: p% V" _0 s, {5 [0 ?5 R
appropriate history. The inability to obtain such a  w% d/ `* g. N4 M# p4 |
history, or failure to ask the specific questions, may
- g! e0 S; r# r7 H$ a' `6 z0 u; `result in extensive, unnecessary, and expensive
3 B! Q( E3 W, b- B# A( T. U5 kinvestigation. The primary care physician should be
  U' G9 r3 ]. Z# u2 g3 N( ~' N% eaware of this fact, because most of these children0 W* |8 ~0 @  [
may initially present in their practice. The Physicians’
/ Q$ G$ P( m# |2 u# d& S$ TDesk Reference and package insert should also put a
' @* Q* L) D3 F8 K  cwarning about the virilizing effect on a male or
' y; j2 ~$ X- N- M+ Ofemale child who might come in contact with some-
$ z0 }' w- y! hone using any of these products.
% K, M; v" p) M' H! S3 J7 D: qReferences
! w" ]8 d8 G6 V- E1. Styne DM. The testes: disorder of sexual differentiation' I, U! W$ Z9 H7 ?+ m7 A& L6 D
and puberty in the male. In: Sperling MA, ed. Pediatric
4 F4 L" {% K3 X/ a5 Q' NEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;* `9 x3 F+ i4 w- s
2002: 565-628.) L1 o$ Z' e+ f3 h9 A' T& f- r& u
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
3 u+ }& @. U) _6 y5 Wpuberty in children with tumours of the suprasellar pineal
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VIP精品區,資源無限好賺金任務區,輕松賺金幣
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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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
3 h2 ~+ V& m$ w5 H7 O
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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