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Sexual Precocity in a 16-Month-Old; }5 c+ H1 H$ h& F$ i0 S4 Y
Boy Induced by Indirect Topical
+ G3 y: ]. U- T8 LExposure to Testosterone6 n/ c' R4 Q9 z6 O0 |9 O, i( Y) Z4 n
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,26 l5 N. ?. z8 r) _$ }  V
and Kenneth R. Rettig, MD1& L7 ?! f5 G* ~  `7 h
Clinical Pediatrics9 `" |) q9 t$ H1 y9 N% N% ?& }1 p3 \
Volume 46 Number 6
" f7 x# d" D& |# i0 CJuly 2007 540-543
+ Q- C9 r* o! ~© 2007 Sage Publications
, E; T7 t% m! D* V- }( g3 u# c10.1177/0009922806296651
" o2 X3 ~  K5 phttp://clp.sagepub.com
, ~9 E0 h0 I. ^2 W8 Zhosted at% [% `7 Y) I4 O! H: F+ |
http://online.sagepub.com
& U5 r- R# Y% lPrecocious puberty in boys, central or peripheral,8 q) O* o$ a7 A& j9 D
is a significant concern for physicians. Central
; F6 P3 X% t; ~# r+ S7 pprecocious puberty (CPP), which is mediated
% z  H: I; l3 ]2 u7 x$ K2 Ethrough the hypothalamic pituitary gonadal axis, has# Q9 ~  ?) i: n) {! H* Z! Y: e: @8 G
a higher incidence of organic central nervous system
- H# @4 y$ e$ `% l2 E9 V  N9 ^lesions in boys.1,2 Virilization in boys, as manifested. j, l  a- G5 ?5 }! l( \. t
by enlargement of the penis, development of pubic. ^1 E) U' J2 S- r) h+ p' ]3 z
hair, and facial acne without enlargement of testi-( w& |. l9 i1 J7 D
cles, suggests peripheral or pseudopuberty.1-3 We) L( L! X, T% h3 H5 [* u7 b/ X$ t4 }
report a 16-month-old boy who presented with the
# X: n* U% }5 |3 ^enlargement of the phallus and pubic hair develop-
; s* b: \6 G( H7 Nment without testicular enlargement, which was due' i9 I% a0 E9 E* M. _, Y
to the unintentional exposure to androgen gel used by
. s: J9 A/ W: T! @the father. The family initially concealed this infor-
6 i7 o4 g; U! k1 A' O' h7 I; Imation, resulting in an extensive work-up for this
% f- {- ~4 d$ d, C* }( |5 }child. Given the widespread and easy availability of' \4 D& r" ?( G. p/ \' J# \
testosterone gel and cream, we believe this is proba-( {( j8 M* b! r; w
bly more common than the rare case report in the
$ P5 e* [/ Y6 I) Sliterature.4
) p. Z+ e$ J0 yPatient Report
- s& O5 I# s( o& E' e2 p( n$ RA 16-month-old white child was referred to the5 B- c; j1 |& H& |7 S' [, q* w; P
endocrine clinic by his pediatrician with the concern- z% f: R5 t9 W9 Q
of early sexual development. His mother noticed; e: U- `+ l9 _9 w7 w
light colored pubic hair development when he was
: D3 z2 K+ @+ f& FFrom the 1Division of Pediatric Endocrinology, 2University of. g6 }1 B$ k9 Q4 X0 M* b" K# l  c
South Alabama Medical Center, Mobile, Alabama.$ Z8 R( B$ D$ t0 _1 c( f2 w
Address correspondence to: Samar K. Bhowmick, MD, FACE,4 W. p9 _% }8 v2 c# p3 w4 E5 O# w
Professor of Pediatrics, University of South Alabama, College of
3 v! g- m$ Z/ `# C9 dMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
5 m; r. {* ?3 \7 ee-mail: [email protected].% P( Q& ]% P+ j$ L- E
about 6 to 7 months old, which progressively became
3 J& U+ S% g. L( g4 e; B$ _: Y; kdarker. She was also concerned about the enlarge-: u8 P1 X0 U& f5 s, J
ment of his penis and frequent erections. The child
1 i# r' ]: M- ]( v! u6 Pwas the product of a full-term normal delivery, with* j  L1 E2 j8 }' O) ^! j
a birth weight of 7 lb 14 oz, and birth length of- K- `- O, E6 Z7 `3 A) ~. ?$ ]
20 inches. He was breast-fed throughout the first year$ \/ t' A; Q0 d% ^' k4 b
of life and was still receiving breast milk along with
# `+ ^' J- n4 N8 \1 b* t9 Z- Isolid food. He had no hospitalizations or surgery,3 B1 h, O" Q- @  I' X) S
and his psychosocial and psychomotor development
( g& {4 h2 \( o( t4 S& kwas age appropriate.1 \3 _( [! Y" ?& r, \8 `) C
The family history was remarkable for the father,
6 C3 |7 k# a8 @- J9 M$ ~who was diagnosed with hypothyroidism at age 16,
0 p+ g" y7 f* {( y; B, G% [which was treated with thyroxine. The father’s$ C  y$ R" q! o) c
height was 6 feet, and he went through a somewhat* J" ^0 l  B! w
early puberty and had stopped growing by age 14.
! D8 g+ f* [& [% s9 o  Q- h/ ~) }The father denied taking any other medication. The
$ V5 }, s* T, B7 I6 N( K* \child’s mother was in good health. Her menarche) i8 @% ?3 q" L' Q! s
was at 11 years of age, and her height was at 5 feet
3 X( k* `6 j. I4 |: w5 S5 inches. There was no other family history of pre-" V$ K1 ?: _8 S5 N
cocious sexual development in the first-degree rela-3 l. U! e# a6 _% _! X
tives. There were no siblings.
3 @: a4 Y8 l$ A2 {; O; J) I* RPhysical Examination* ?$ _! [9 ~9 C4 U  S
The physical examination revealed a very active,5 h1 ?- d  t0 u8 C$ ^0 N
playful, and healthy boy. The vital signs documented
4 x  M# Q) \# v6 K2 h0 S% da blood pressure of 85/50 mm Hg, his length was8 l* T- \: h) d3 @. l  N2 X6 A
90 cm (>97th percentile), and his weight was 14.4 kg; V8 `! {9 j8 a7 C8 V
(also >97th percentile). The observed yearly growth! u/ h' i& f) D# b3 S
velocity was 30 cm (12 inches). The examination of+ Y! r$ J7 z; Y- D8 J$ \/ c9 ~- a$ r# ], m
the neck revealed no thyroid enlargement." e0 D  K" T9 D
The genitourinary examination was remarkable for
3 _8 N/ d; d# k& C& q( H( T& t4 ]7 Kenlargement of the penis, with a stretched length of7 s, I7 B1 o8 G) u  A7 V. [
8 cm and a width of 2 cm. The glans penis was very well
! x5 |( z7 G/ f; a% k# ]developed. The pubic hair was Tanner II, mostly around) s: a  c4 S) W' z
5405 t" ^& h+ I% c* t  l
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% t; c: h9 b, I7 U  q/ h# m
the base of the phallus and was dark and curled. The
- f! e3 T5 O) X9 U3 Z4 Rtesticular volume was prepubertal at 2 mL each.4 ~( \2 H  w. _& J0 R1 _4 C6 {9 ~
The skin was moist and smooth and somewhat
  {& V; |& Z9 {& ~oily. No axillary hair was noted. There were no9 Z( z; _, D. P; O) S
abnormal skin pigmentations or café-au-lait spots.
+ J9 ~0 D* L5 sNeurologic evaluation showed deep tendon reflex 2+
# t  Q  Y( `8 O# x3 X8 t: [) Wbilateral and symmetrical. There was no suggestion3 H: B  ~- L9 }4 W# r& R
of papilledema.
6 S9 k& d9 Z1 K+ l' }7 S% N9 [Laboratory Evaluation" {% |2 e( ~& u; V' M5 [  o2 G
The bone age was consistent with 28 months by% E& X6 h7 i7 q
using the standard of Greulich and Pyle at a chrono-
6 \6 C4 H# \: T/ Z% j: glogic age of 16 months (advanced).5 Chromosomal
* y6 O$ @! k: ?) f* @karyotype was 46XY. The thyroid function test
; H( W0 n0 K( W% J2 \showed a free T4 of 1.69 ng/dL, and thyroid stimu-& L% i$ K% ^! H+ h% F7 ?
lating hormone level was 1.3 µIU/mL (both normal).+ ~2 J2 o; V( P0 V
The concentrations of serum electrolytes, blood, p' {, G% F4 ?  Z, m# _
urea nitrogen, creatinine, and calcium all were
1 b* L  A" V0 c1 |within normal range for his age. The concentration. R* F6 M& y, _) r2 l3 U$ S
of serum 17-hydroxyprogesterone was 16 ng/dL! ]# A- G; o* l5 h
(normal, 3 to 90 ng/dL), androstenedione was 20
- A4 X- q0 u. f- M9 H  o. ang/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
5 s1 ]$ n2 e- i9 Uterone was 38 ng/dL (normal, 50 to 760 ng/dL),4 p7 G. |9 U9 |" A
desoxycorticosterone was 4.3 ng/dL (normal, 7 to3 _& N# s* x4 c+ _; v
49ng/dL), 11-desoxycortisol (specific compound S)+ p' A' l" W$ G! m! u) H% b* y
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-& M3 ~, _  Y, V$ o/ m" m* l
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
) i: C8 \2 p0 m5 N; Ktestosterone was 60 ng/dL (normal <3 to 10 ng/dL),$ |7 E5 J' z! k- q9 h
and β-human chorionic gonadotropin was less than
0 H# Y$ s8 _  D% k; y7 s* J5 mIU/mL (normal <5 mIU/mL). Serum follicular' `+ j$ C3 Q9 A" v; f
stimulating hormone and leuteinizing hormone
5 [9 l1 @/ O! Y. H9 Qconcentrations were less than 0.05 mIU/mL' P1 |3 V4 [; G2 I! V5 J. W
(prepubertal).
+ u& N4 ~/ }5 Z9 E) d3 iThe parents were notified about the laboratory0 `* o5 ^: l' B" B4 ^! `8 A
results and were informed that all of the tests were- r7 G0 C  d6 U( w. a! @
normal except the testosterone level was high. The
' @2 ]7 P5 j, A4 N5 }2 efollow-up visit was arranged within a few weeks to5 T9 H/ R5 `1 T# z% n9 O/ {
obtain testicular and abdominal sonograms; how-
; ?7 F& ^; B! E  Kever, the family did not return for 4 months." M2 o& l1 H7 m2 E, }8 Y
Physical examination at this time revealed that the
# B  P. J  C* m1 b4 }child had grown 2.5 cm in 4 months and had gained
* g' ^; `$ j: C2 ]: l- p2 kg of weight. Physical examination remained/ c( _, [0 P2 N
unchanged. Surprisingly, the pubic hair almost com-
/ f) ~. K7 l- R. k" v$ O) n! Gpletely disappeared except for a few vellous hairs at* j! H: U8 l5 @! @/ @" W+ s  t) a2 v
the base of the phallus. Testicular volume was still 2
- A: M: S  a0 n. vmL, and the size of the penis remained unchanged.! b9 x  ^: ]/ G* ~5 r
The mother also said that the boy was no longer hav-* v. q" ~" D4 s% U. A9 ], F
ing frequent erections.
6 e; b% q% U7 z$ f# J$ S( d* @Both parents were again questioned about use of
& y7 _, g7 F) q) u2 ~any ointment/creams that they may have applied to" D! _! K: S; `# \6 \
the child’s skin. This time the father admitted the+ l3 d4 C: Z: @- p
Topical Testosterone Exposure / Bhowmick et al 541
* y7 m8 Y; J) J9 Vuse of testosterone gel twice daily that he was apply-2 ?2 M8 }2 ]4 _* D0 K0 l/ Z
ing over his own shoulders, chest, and back area for; A; H' ?5 s0 Z* I
a year. The father also revealed he was embarrassed
" f4 O7 F) X+ W( H0 `- wto disclose that he was using a testosterone gel pre-$ o. w3 }: q1 f$ J, I, K* p( Q% u
scribed by his family physician for decreased libido
% U! T; e% v5 Csecondary to depression., N: R1 C# r& [- _7 s  y
The child slept in the same bed with parents.
; E  i4 t! A) @/ |5 p. \The father would hug the baby and hold him on his5 B  b  a/ i- Z' d9 B9 X8 Q/ u* @
chest for a considerable period of time, causing sig-- A) w3 e7 n6 f
nificant bare skin contact between baby and father.
& ]& [! c. ?1 U: iThe father also admitted that after the phone call,
3 _* n- d1 |  n1 Z9 o; k$ W$ e( F; Xwhen he learned the testosterone level in the baby
- e3 D' S: H% k( ^. y1 n3 w' u" _was high, he then read the product information8 B0 C0 k( V0 V) w9 B
packet and concluded that it was most likely the rea-& O) v2 H( e! s8 N0 u5 U8 G
son for the child’s virilization. At that time, they
! Z' I% j" Z3 {( N, Rdecided to put the baby in a separate bed, and the
8 G/ Y2 ^! E( t+ w8 Nfather was not hugging him with bare skin and had
. Y) Y1 R- H7 r8 Tbeen using protective clothing. A repeat testosterone
2 N" Q- S* G: [test was ordered, but the family did not go to the
9 v# b+ ]& k& z" ^laboratory to obtain the test.
3 E+ U9 E. a7 ~: a+ O7 p, Z& H5 X2 SDiscussion
5 s; T$ ^! l8 G  ^7 e% [Precocious puberty in boys is defined as secondary
% e2 @# O/ c+ F1 t; W" o( U5 ~sexual development before 9 years of age.1,4
4 ?: v! V5 I* K' \; z4 }Precocious puberty is termed as central (true) when
, k" M6 ]: H' ait is caused by the premature activation of hypo-
/ |) G( [7 c2 I* `thalamic pituitary gonadal axis. CPP is more com-& C% ~: P  a; U) u
mon in girls than in boys.1,3 Most boys with CPP
4 ~8 E# j0 N. Q3 P' ~' [may have a central nervous system lesion that is
% Z' ]8 f# P' ]7 Yresponsible for the early activation of the hypothal-3 Q1 K7 }6 l9 @
amic pituitary gonadal axis.1-3 Thus, greater empha-9 r/ X$ t( x& s) C
sis has been given to neuroradiologic imaging in
+ e, p! [; b' t$ |; }boys with precocious puberty. In addition to viril-
$ X' w+ Y" l" X8 n, ?; nization, the clinical hallmark of CPP is the symmet-4 H! l6 R% x6 I+ |1 F; v9 ~- q4 ^
rical testicular growth secondary to stimulation by
* Y  f+ D8 s$ X6 w4 E. d  ~gonadotropins.1,3: ?  X: O0 x, D% @( v
Gonadotropin-independent peripheral preco-
1 q5 Q. }% i; }# @* i6 Fcious puberty in boys also results from inappropriate4 B+ J, s3 ~" a( }* M2 u
androgenic stimulation from either endogenous or+ N( @& j+ j( T- n% b
exogenous sources, nonpituitary gonadotropin stim-9 s1 I& s$ ?. B; G5 c
ulation, and rare activating mutations.3 Virilizing5 R5 }* o9 X7 l# S2 b! b5 ^; h
congenital adrenal hyperplasia producing excessive
, v1 k6 q1 u5 P" v$ w7 s- w& radrenal androgens is a common cause of precocious( I/ A4 q1 \* n
puberty in boys.3,4
6 J! R' \8 a7 `4 mThe most common form of congenital adrenal
, u. i+ ?% b9 O3 v8 chyperplasia is the 21-hydroxylase enzyme deficiency.
. M% T7 Z- M* @( J: o5 a7 _# ~8 }% {The 11-β hydroxylase deficiency may also result in- c8 F( d& r. Q
excessive adrenal androgen production, and rarely,6 z. o9 N  Y) C; z
an adrenal tumor may also cause adrenal androgen4 F0 i0 v4 H; b/ g# A" ]- A3 m$ h  e
excess.1,3
; D1 o! B& z- V% Z, @' f" yat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, T. c% N$ ?: Q) f9 A
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007# _9 p5 b8 k6 Y) o- j
A unique entity of male-limited gonadotropin-; I5 l, r9 C& m' X9 d% i6 j
independent precocious puberty, which is also known, r4 O7 k/ i* k& k) U* W8 V5 _
as testotoxicosis, may cause precocious puberty at a6 Q( V0 W. {& ^) K, a% b
very young age. The physical findings in these boys& ?& @  Q0 O: |* R# L: a, g) X
with this disorder are full pubertal development,+ y' n+ ~+ R$ c
including bilateral testicular growth, similar to boys1 J) e- x9 g( I% ]/ B
with CPP. The gonadotropin levels in this disorder2 W6 f0 ~9 K( A; S
are suppressed to prepubertal levels and do not show6 G" C" S3 T2 a1 u$ w* u
pubertal response of gonadotropin after gonadotropin-
2 y) C+ V1 I' E) U9 Nreleasing hormone stimulation. This is a sex-linked9 T  K2 R% r& z: B7 D
autosomal dominant disorder that affects only1 Y0 e) b9 T- }
males; therefore, other male members of the family
( b) M7 l2 X  f% Lmay have similar precocious puberty.3! p( p$ N/ G. F8 y0 D7 ^
In our patient, physical examination was incon-2 Y: P4 d& C' u( j4 @3 F. o
sistent with true precocious puberty since his testi-
. {0 m' o$ [/ U, Q, Q/ C) a& `; ^cles were prepubertal in size. However, testotoxicosis
) [3 l; A- T& w- o! n) Nwas in the differential diagnosis because his father
6 e* d" m8 u- S" Cstarted puberty somewhat early, and occasionally,
" W" E4 p5 I; f: u+ r. mtesticular enlargement is not that evident in the) c  Q2 a) j( _# ~3 N2 w. v
beginning of this process.1 In the absence of a neg-: L5 o" s4 n8 k3 e5 Y3 Z" O/ F
ative initial history of androgen exposure, our
; q5 r7 W: j  _# r" ~. f/ c& [+ p% Vbiggest concern was virilizing adrenal hyperplasia,& Z  ~+ q, W4 y
either 21-hydroxylase deficiency or 11-β hydroxylase
+ p, o) X8 N! G, @deficiency. Those diagnoses were excluded by find-2 I: z# f2 E' G- Y
ing the normal level of adrenal steroids.$ [2 t" N+ K  n7 m
The diagnosis of exogenous androgens was strongly
, _; o& g! Z& s0 qsuspected in a follow-up visit after 4 months because
; I: B* d1 Z) N: Q( othe physical examination revealed the complete disap-
; d2 P9 z4 e4 }; m2 Kpearance of pubic hair, normal growth velocity, and
3 {6 v% v' U& x7 ^% k% V7 Y4 pdecreased erections. The father admitted using a testos-% t' L# L# t1 ~0 w+ R. r, W
terone gel, which he concealed at first visit. He was
; X1 a- K" x. x! `5 X$ c$ Rusing it rather frequently, twice a day. The Physicians’, L( x/ A2 E% n# C/ L  \
Desk Reference, or package insert of this product, gel or  k5 }2 d! z4 h% _# g7 Y9 `0 Y
cream, cautions about dermal testosterone transfer to) M# E! k6 [3 j2 c
unprotected females through direct skin exposure., S8 h  _0 B2 m
Serum testosterone level was found to be 2 times the% W1 T- J$ h3 D& C$ H, O' _
baseline value in those females who were exposed to9 h3 f9 `: n5 c6 ^  c; r1 `1 C
even 15 minutes of direct skin contact with their male4 W& B& ^1 `9 p# N0 O/ H! c) S$ l
partners.6 However, when a shirt covered the applica-
+ Y' U9 Z/ V1 i$ s6 Z4 mtion site, this testosterone transfer was prevented.+ q' u2 e. N& O0 i
Our patient’s testosterone level was 60 ng/mL,  M7 ~- s8 i: s
which was clearly high. Some studies suggest that6 Q9 Q, _8 J, _" z* J( n% L& T, _
dermal conversion of testosterone to dihydrotestos-7 u9 d8 X$ {4 Q/ z
terone, which is a more potent metabolite, is more9 Y9 J# S7 F8 w" O
active in young children exposed to testosterone6 x4 K/ e* s) _* J
exogenously7; however, we did not measure a dihy-, r* \& Z+ _  `& k
drotestosterone level in our patient. In addition to
# N2 n4 }4 B0 o. Yvirilization, exposure to exogenous testosterone in% U) e. p" Y1 Y8 ?$ `
children results in an increase in growth velocity and/ |* X) c, h7 l# b% Z1 M
advanced bone age, as seen in our patient.
) J9 o7 a" i1 z) e* oThe long-term effect of androgen exposure during: F- F/ A$ y1 V0 d, m# m
early childhood on pubertal development and final
4 m( O7 U) ?5 ^adult height are not fully known and always remain% d! ~- y" R) @' W5 `6 o+ ^
a concern. Children treated with short-term testos-
/ |: A3 r# l8 }terone injection or topical androgen may exhibit some! }+ m& |9 \2 q
acceleration of the skeletal maturation; however, after
) f; H1 l. u/ e' fcessation of treatment, the rate of bone maturation/ i* z! g# g" L1 n0 ?
decelerates and gradually returns to normal.8,9: |$ N5 f" T' o, ^, q
There are conflicting reports and controversy
1 I8 i7 @- w, {$ e) n1 S+ \  `" iover the effect of early androgen exposure on adult
( e6 m- Y* v: b; {penile length.10,11 Some reports suggest subnormal$ q1 a( U* q0 W5 `& V$ Y+ [6 I8 l: _
adult penile length, apparently because of downreg-' }0 e" `  O/ O
ulation of androgen receptor number.10,12 However,
9 [. a5 q; E6 jSutherland et al13 did not find a correlation between7 e3 [; H) S6 u% n, L* k
childhood testosterone exposure and reduced adult
+ e* C8 o1 Z& U' Z/ {  ]penile length in clinical studies.
( z' e7 ^" Y% vNonetheless, we do not believe our patient is
1 ~0 z7 h' T( G( i2 h6 Lgoing to experience any of the untoward effects from9 J0 E7 o. C8 N4 S0 c
testosterone exposure as mentioned earlier because
, }+ s8 P/ p4 T& D. j0 r$ B( Bthe exposure was not for a prolonged period of time.
7 ^& |. ~$ ^5 R& e2 b" MAlthough the bone age was advanced at the time of  p$ q+ Q/ p$ n3 \
diagnosis, the child had a normal growth velocity at
; R. i+ _" D- J8 `' }+ x0 }1 pthe follow-up visit. It is hoped that his final adult# V7 u9 I& H7 }8 l! O. Q1 T7 [% z' I! Y
height will not be affected.' [7 S( ~& A3 I- T5 b
Although rarely reported, the widespread avail-
8 y$ u  s8 d8 w  H0 C& x: Qability of androgen products in our society may
& f) ]( A- s% [  V0 T' Yindeed cause more virilization in male or female
( q( P$ ^9 w6 ]" Y& g5 Mchildren than one would realize. Exposure to andro-
5 y4 c2 D% [! c/ Q6 @gen products must be considered and specific ques-
2 |( z  O$ e) a3 ?/ a& \2 ctioning about the use of a testosterone product or
4 m9 P) L8 |" I: F' p8 ^3 Fgel should be asked of the family members during
# E& q+ B# e0 ~6 G  a, m7 uthe evaluation of any children who present with vir-$ f3 w0 e) j- [& u% m& o
ilization or peripheral precocious puberty. The diag-% O7 y6 s* n/ u' |7 G, V" R* J0 _
nosis can be established by just a few tests and by" m  t( e/ y2 i4 E. S' D
appropriate history. The inability to obtain such a
# S" o% I1 |3 V: G. vhistory, or failure to ask the specific questions, may$ y6 d: c$ j2 F% M
result in extensive, unnecessary, and expensive4 b) U& d0 o1 m1 T
investigation. The primary care physician should be6 ]0 e# `0 x- ~: _' A  s
aware of this fact, because most of these children$ H* g; g0 |3 a* Y
may initially present in their practice. The Physicians’; U% K9 B/ L( z% n& y6 _% N
Desk Reference and package insert should also put a
9 L& R( R" Z% l- `; y2 y% n5 l, Cwarning about the virilizing effect on a male or4 b% F5 g1 W- T: F- V( a
female child who might come in contact with some-
9 ?) H4 m& ?9 h9 Lone using any of these products.4 E% g. R4 t* R& [
References; a; I5 j  v( p  z8 [+ ?
1. Styne DM. The testes: disorder of sexual differentiation
' p* {  a8 \8 h. m4 ^' h$ t+ aand puberty in the male. In: Sperling MA, ed. Pediatric
1 X$ R& c* k  h/ J& HEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;( p* w8 u) Y4 C; \) n4 a
2002: 565-628.7 L+ T9 R5 m- {7 N" ]
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
! j3 i* t3 ?+ q! }puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old1 u7 y: U! _6 |( ^% ?1 w
Boy Induced by Indirect Topical. }% G( y. ~9 e1 t/ A1 A" [
Exposure to Testosterone
( U' B: \' G9 D+ u) ^9 r! JSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. D8 r8 _% [( E3 @; W& Y
and Kenneth R. Rettig, MD1! I. D8 T! z/ X8 |4 `0 ]
Clinical Pediatrics
4 h- E4 t+ L0 R+ w5 R( sVolume 46 Number 6: {; Q  A& \0 p- M' G3 t& T
July 2007 540-543/ k4 j6 c; h! a, j
© 2007 Sage Publications
5 C' Y2 q( M+ _  M8 Y10.1177/0009922806296651
/ F) ]! o- I2 d2 |: U9 xhttp://clp.sagepub.com+ q: |# M, W; q' Q
hosted at" i( b6 i- \" h. {# }% s; `
http://online.sagepub.com
1 L1 _$ T3 L2 x1 H/ e/ e/ xPrecocious puberty in boys, central or peripheral,2 t* q2 Z6 I0 o9 F
is a significant concern for physicians. Central4 b, @( p& x+ B/ h3 L
precocious puberty (CPP), which is mediated
; T; c, a' ]) O6 E; s5 V( Athrough the hypothalamic pituitary gonadal axis, has: q+ N& R9 Q8 @
a higher incidence of organic central nervous system
3 ]0 w( E, t9 ^. H5 olesions in boys.1,2 Virilization in boys, as manifested0 w) @: ~# m) v2 s8 U1 [8 `
by enlargement of the penis, development of pubic: }  H* H% {5 y6 V6 {3 ?
hair, and facial acne without enlargement of testi-
# Q' N5 J6 z9 H- s+ hcles, suggests peripheral or pseudopuberty.1-3 We* d5 x' E4 j7 L3 T2 U( `) z
report a 16-month-old boy who presented with the$ P- J& c# s" b6 y) Q0 ~" m* i- ~1 E
enlargement of the phallus and pubic hair develop-
# R8 O7 h& p0 A+ Y1 x" s1 I& sment without testicular enlargement, which was due, [" Z) P' G( c" d
to the unintentional exposure to androgen gel used by% D9 q' |! B: G* Q7 D: C1 s# e2 A
the father. The family initially concealed this infor-
" R! ]' N5 g$ v. Z& k3 y' Gmation, resulting in an extensive work-up for this, Y& Q5 W, \/ R6 `
child. Given the widespread and easy availability of
3 p7 j6 }& n3 Q6 K9 s( h$ Gtestosterone gel and cream, we believe this is proba-
7 A( G$ I: ~/ S0 j! G- qbly more common than the rare case report in the
+ r' z. Z- L9 F% ^3 A" oliterature.4
* d- N( Z3 H( y- DPatient Report( b! b9 v; X! z: d8 Z! @
A 16-month-old white child was referred to the! |/ F( b4 a- D, ~, v' d: k
endocrine clinic by his pediatrician with the concern8 M5 y% H. D( w) i$ O
of early sexual development. His mother noticed
  x) v7 e& U; b+ E( t. ]" ulight colored pubic hair development when he was
* h) y9 w% E* K8 J& u5 cFrom the 1Division of Pediatric Endocrinology, 2University of4 R9 x1 o% M4 T. z+ E: x1 Y: H
South Alabama Medical Center, Mobile, Alabama.
% {9 `& o9 p% o! p3 t9 J/ cAddress correspondence to: Samar K. Bhowmick, MD, FACE,
! o: w2 Q" a" h/ _" z: e" d9 F' ]Professor of Pediatrics, University of South Alabama, College of% Q! O' Y/ X1 R/ K* v& @* v
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
# ~0 c/ l" \( T9 Je-mail: [email protected].
& E7 r$ v: P/ c7 W7 r5 [about 6 to 7 months old, which progressively became1 s: t" D' L  G4 Q5 d3 o5 g; j
darker. She was also concerned about the enlarge-8 |( P" }' c( w$ O( o6 I/ Q# L
ment of his penis and frequent erections. The child
5 l% U$ h/ y& J( k* A$ m/ d" M( _was the product of a full-term normal delivery, with# Z( o( V7 t, i8 H* n! s
a birth weight of 7 lb 14 oz, and birth length of
8 M  V9 r: {% b2 |. l4 a20 inches. He was breast-fed throughout the first year
4 ?2 k! r- F! r9 A% Q% b1 e  ?of life and was still receiving breast milk along with& k, Z8 R4 }0 C, t
solid food. He had no hospitalizations or surgery,! U. w" R; A& a2 G3 u
and his psychosocial and psychomotor development
3 }8 l3 `  M  hwas age appropriate.
1 Y/ V) t; j$ B6 W5 n) _The family history was remarkable for the father,# v. r) Z. p" S  @6 P! j
who was diagnosed with hypothyroidism at age 16,
& w$ j; W0 N- y9 d+ cwhich was treated with thyroxine. The father’s0 X/ m% L. Q& I
height was 6 feet, and he went through a somewhat1 Y/ ]9 H1 W8 Z& a
early puberty and had stopped growing by age 14.  Q( [" w0 A# I' v
The father denied taking any other medication. The: q+ j! [& x6 M# j- U/ W
child’s mother was in good health. Her menarche2 l, k& t  B; g5 i/ i; n4 ]% w% i, x
was at 11 years of age, and her height was at 5 feet
2 F9 k6 B1 r$ {9 U8 }; n5 inches. There was no other family history of pre-
$ O0 D$ t& ]; M, w" a4 ncocious sexual development in the first-degree rela-
0 v& z: U4 H/ ptives. There were no siblings.
0 r4 @- J9 F: gPhysical Examination
; C( b( _8 I( L4 I7 iThe physical examination revealed a very active,4 {. K; X* @- j2 g
playful, and healthy boy. The vital signs documented+ H: ?6 Y# U3 D/ H8 D  P* g& A% E4 h. }
a blood pressure of 85/50 mm Hg, his length was& `* S) R6 {" J+ d! R6 n* m4 Y7 a
90 cm (>97th percentile), and his weight was 14.4 kg# z( F$ v* R. X- t
(also >97th percentile). The observed yearly growth
' t+ z3 l4 D$ X7 }velocity was 30 cm (12 inches). The examination of1 j+ l9 k' r( k8 ~% q( W8 y/ H0 {
the neck revealed no thyroid enlargement.
) g4 W/ D0 |$ j3 GThe genitourinary examination was remarkable for
! s/ ]( G9 u+ f2 Henlargement of the penis, with a stretched length of
7 ]. X/ f4 {# O8 cm and a width of 2 cm. The glans penis was very well
9 e; t5 y% ^8 h8 e2 `  @developed. The pubic hair was Tanner II, mostly around
' f4 ~2 d; j' F. q540
* a8 g( ^8 m6 A! A- T( |' I2 u# ?at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  x( @4 X6 K- k& _' }/ @
the base of the phallus and was dark and curled. The
  ~3 K% M8 f5 B7 wtesticular volume was prepubertal at 2 mL each.
8 u6 K9 Z* V8 {7 k$ CThe skin was moist and smooth and somewhat, D1 `0 v# G: V9 G+ E
oily. No axillary hair was noted. There were no; D$ Y( @1 x7 W6 }, y. b
abnormal skin pigmentations or café-au-lait spots.$ S5 }' y8 a! g/ p
Neurologic evaluation showed deep tendon reflex 2+, ]9 W6 f' r8 z6 f7 Y5 M
bilateral and symmetrical. There was no suggestion
, H/ J0 r0 ]4 q+ S- O( w9 yof papilledema.
+ ^" o* F+ X+ l- T% wLaboratory Evaluation
) K/ k4 w+ H4 _1 SThe bone age was consistent with 28 months by% `6 x- T  @! l' z
using the standard of Greulich and Pyle at a chrono-& d& l' d. M5 W- ^" o, \
logic age of 16 months (advanced).5 Chromosomal
' u% S5 N5 k& F  Nkaryotype was 46XY. The thyroid function test
/ s; [5 o$ W& {/ r  Bshowed a free T4 of 1.69 ng/dL, and thyroid stimu-+ p  ]9 U: q7 x4 C- P
lating hormone level was 1.3 µIU/mL (both normal).
3 x* z! K& p# ]The concentrations of serum electrolytes, blood
: ^7 @! g4 f7 |- h1 surea nitrogen, creatinine, and calcium all were
) X9 j  k, G* Wwithin normal range for his age. The concentration: D  E7 o5 j% J" X$ U2 \0 c
of serum 17-hydroxyprogesterone was 16 ng/dL
  [! m( F7 X, g. Q) _' n7 u. O( x% g7 D(normal, 3 to 90 ng/dL), androstenedione was 200 f* Y" [5 @5 Z# G: x1 d' N' K
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-+ D) b" z" q8 q  }( j6 a4 F; O
terone was 38 ng/dL (normal, 50 to 760 ng/dL),7 W3 R; W; y0 x5 Z# X2 k8 g
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
8 ~0 V# W$ a: \( }: E49ng/dL), 11-desoxycortisol (specific compound S), c2 G- h0 Q/ m& ?- G& I& S
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
/ q9 U, o* W5 ], M! Ctisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
( o- t/ }, l) z2 Gtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),  x, o* P/ J: s
and β-human chorionic gonadotropin was less than
0 w) k! G8 f: H2 L7 \5 mIU/mL (normal <5 mIU/mL). Serum follicular
) K/ T+ y$ n2 q( {' X$ astimulating hormone and leuteinizing hormone
+ k0 D" }& a& l$ Xconcentrations were less than 0.05 mIU/mL
6 L( g  Q" N, I2 Q1 f1 S& m(prepubertal).
4 V/ u0 Y9 o8 f3 X0 {* {The parents were notified about the laboratory
3 [0 a' n2 C5 u# qresults and were informed that all of the tests were
0 C. _# o" h6 A) }" V6 k% O: E& Jnormal except the testosterone level was high. The
& Q* _5 s- f6 b& p) ofollow-up visit was arranged within a few weeks to; S, ^" a/ j" j& c8 o% _
obtain testicular and abdominal sonograms; how-6 u6 s" R3 [; M# ]
ever, the family did not return for 4 months.
/ u. F; u0 j" bPhysical examination at this time revealed that the
) h0 Z9 O2 h8 }5 wchild had grown 2.5 cm in 4 months and had gained4 W, c' J+ K0 G& S
2 kg of weight. Physical examination remained* M0 ^$ x  Y% j6 \  Z+ f3 D" z
unchanged. Surprisingly, the pubic hair almost com-5 N$ E' f" Z' c) G* E
pletely disappeared except for a few vellous hairs at
' `1 M# f& P" Q+ W# F2 f% Rthe base of the phallus. Testicular volume was still 2
% R0 C; G7 H: K5 dmL, and the size of the penis remained unchanged.& i  Z! B8 Z  [. Y5 s2 Z
The mother also said that the boy was no longer hav-
, M( W8 o+ t* o' R! Iing frequent erections.; w) v& S/ }; P- {
Both parents were again questioned about use of7 a( E: J! G: S0 ?' \' A
any ointment/creams that they may have applied to
" R6 q# Z. G1 h7 N" s$ D# B; [the child’s skin. This time the father admitted the
* L2 X& \/ b4 T6 v0 UTopical Testosterone Exposure / Bhowmick et al 5416 B, r; H6 u! Z$ T, X$ a: b( Y
use of testosterone gel twice daily that he was apply-
* C% x; I: |9 |0 s+ sing over his own shoulders, chest, and back area for  X. L! l7 ~' a) `
a year. The father also revealed he was embarrassed3 P+ d% `2 x& P3 c; C' J5 k2 ?
to disclose that he was using a testosterone gel pre-
# t- f% C: z. A* b$ `! j/ ]2 wscribed by his family physician for decreased libido/ R/ K  W4 o2 w0 t
secondary to depression.
7 a% L2 o, I* p( _9 E/ b1 m( O. R1 P8 xThe child slept in the same bed with parents.
8 a2 I" S& S6 y9 r/ S" _3 YThe father would hug the baby and hold him on his8 u( B9 X% m! P, X  L: c; n/ Y
chest for a considerable period of time, causing sig-
$ i) I1 \( L/ L& x5 M) Hnificant bare skin contact between baby and father.
1 {9 E+ }# T6 M- L" Z9 J( I3 lThe father also admitted that after the phone call,
1 a0 P8 t' B! o: V2 C) lwhen he learned the testosterone level in the baby
; w* B% i5 ~$ F$ B9 A, K8 V" C/ rwas high, he then read the product information
) e4 h( a7 R) p- Rpacket and concluded that it was most likely the rea-
9 S$ Y1 d1 D3 ~6 n7 Y7 {son for the child’s virilization. At that time, they' \" z1 X  S0 M, d
decided to put the baby in a separate bed, and the
3 L, N' O/ A5 S$ {) vfather was not hugging him with bare skin and had9 A* O! X! h0 H7 }9 B& `+ z
been using protective clothing. A repeat testosterone
6 Q6 W7 E6 p% S5 ]% T' Wtest was ordered, but the family did not go to the3 n/ m7 Z! o, ]& Z/ \% U
laboratory to obtain the test.: V+ l( b# {  S( h  t, E
Discussion
4 G1 [# K! O8 }2 d6 D* `) [Precocious puberty in boys is defined as secondary
4 D/ x2 A6 v) Q' q9 r  `sexual development before 9 years of age.1,4: s+ C# H$ l/ U
Precocious puberty is termed as central (true) when
: z% `$ G: E/ B4 e5 W0 }it is caused by the premature activation of hypo-+ G7 j2 o! o5 G" G. x8 U/ V
thalamic pituitary gonadal axis. CPP is more com-
) o; o4 j  T  q3 [mon in girls than in boys.1,3 Most boys with CPP
* o9 N4 F7 S5 y( jmay have a central nervous system lesion that is3 Y, a! u) _7 e. T# s# d8 {
responsible for the early activation of the hypothal-  `9 i3 T; S; p; i5 `9 u: u
amic pituitary gonadal axis.1-3 Thus, greater empha-
4 a( D/ k: r/ A; b+ K# U: d/ X6 Osis has been given to neuroradiologic imaging in/ K6 K) b- H2 w7 i
boys with precocious puberty. In addition to viril-1 I3 o& G; r* m. k( h& x
ization, the clinical hallmark of CPP is the symmet-: q: c. j; ^) k# f; B# f% Y1 w  S. d
rical testicular growth secondary to stimulation by5 `: Z5 S2 j; g7 n4 g5 J  G
gonadotropins.1,3
- d3 S/ Y3 h8 q/ C3 }Gonadotropin-independent peripheral preco-
" T8 j- g  A& m- W0 x! [2 {* U3 {cious puberty in boys also results from inappropriate9 M1 _2 r5 T% Y: q
androgenic stimulation from either endogenous or
( h1 L$ m1 q) T9 B; zexogenous sources, nonpituitary gonadotropin stim-, B. [6 j; u2 p( H8 H
ulation, and rare activating mutations.3 Virilizing
# n/ t: A% |5 g4 N$ @8 W8 U9 ^congenital adrenal hyperplasia producing excessive. {' U) Y( u/ _* g* u* [
adrenal androgens is a common cause of precocious
: T5 b: u. z2 z; s0 m8 ]# j* e$ Upuberty in boys.3,4; i$ U4 Q) D$ m7 k" w' g  B, Q, @
The most common form of congenital adrenal7 W, `1 |% s  o
hyperplasia is the 21-hydroxylase enzyme deficiency.
) K" f' r/ L! L# |( M: e2 q/ nThe 11-β hydroxylase deficiency may also result in
9 G- m3 }4 ^. w: C1 u: \5 U( gexcessive adrenal androgen production, and rarely,: h4 G. l+ B% \8 B5 W
an adrenal tumor may also cause adrenal androgen
+ M' `4 x3 J5 j" |6 B0 V& yexcess.1,3
) {* J6 k( L& I2 s3 dat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% D3 u1 O2 u) f
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
+ q4 c  L, b& Q9 kA unique entity of male-limited gonadotropin-9 H6 y: X/ `9 A& }6 V/ x* s
independent precocious puberty, which is also known
/ {9 ^4 a- |! ]as testotoxicosis, may cause precocious puberty at a
9 \8 g* e3 U+ D" R) ~* every young age. The physical findings in these boys% \0 e0 n2 P/ K" |
with this disorder are full pubertal development,6 w4 a4 v+ j/ e# a- Z; g
including bilateral testicular growth, similar to boys
; v% L' O2 }- b# P) w" Y( {with CPP. The gonadotropin levels in this disorder
0 u8 N& N- \' ?# B5 Aare suppressed to prepubertal levels and do not show
$ d! Q' ]: z) i2 Ppubertal response of gonadotropin after gonadotropin-
4 R! g7 U. t' P; E8 D- m6 Lreleasing hormone stimulation. This is a sex-linked5 d; ]8 v2 u6 c1 f! \6 ]
autosomal dominant disorder that affects only
$ i: b4 [+ ]4 @  [2 @males; therefore, other male members of the family* A5 j9 P& L% N* q1 w- I! N  l  T5 h
may have similar precocious puberty.39 v, C8 Y' B% \/ [
In our patient, physical examination was incon-& O. p! \4 ]( x4 X
sistent with true precocious puberty since his testi-% n2 W% t$ W% @. X* l1 ~  F% j
cles were prepubertal in size. However, testotoxicosis8 O+ W  }8 r7 Z) i6 a  t7 {# V: o
was in the differential diagnosis because his father
' r# u- L1 ~* q& q( wstarted puberty somewhat early, and occasionally,; i" s7 G: l1 E+ p( B! S$ {8 P: Q
testicular enlargement is not that evident in the
- c% o) _: W. D2 b1 R; wbeginning of this process.1 In the absence of a neg-5 G1 }$ t& l1 V! h- w' \
ative initial history of androgen exposure, our  N; ]7 Q! d% o* y2 `0 ~+ O/ V( T
biggest concern was virilizing adrenal hyperplasia,
! D" G# y, x& zeither 21-hydroxylase deficiency or 11-β hydroxylase2 k6 ^5 K4 m( l0 H) y- y% i
deficiency. Those diagnoses were excluded by find-" k! Y9 G2 e, T: E
ing the normal level of adrenal steroids.5 R- {  M9 G$ h5 M& d
The diagnosis of exogenous androgens was strongly
/ Q4 f5 |  m; X) Msuspected in a follow-up visit after 4 months because
3 G/ U6 z) H  X; f9 w; ethe physical examination revealed the complete disap-
* l3 k  L! u* ]- _# G) f1 Cpearance of pubic hair, normal growth velocity, and
' P( F8 T: B2 Q7 _decreased erections. The father admitted using a testos-8 E) \( F$ ?% g) V
terone gel, which he concealed at first visit. He was
) L. Z7 G8 B# z7 ?0 l, z9 Husing it rather frequently, twice a day. The Physicians’
: H6 @2 s' K! I$ wDesk Reference, or package insert of this product, gel or
8 |* M& r: v2 v4 K) H2 P& y6 Y  q( Fcream, cautions about dermal testosterone transfer to6 h: u# T1 P  X( z+ I% t
unprotected females through direct skin exposure.6 S5 |& c3 }2 \; y) O7 m: O
Serum testosterone level was found to be 2 times the4 n% K- [+ S6 p' d0 p) U- s& A
baseline value in those females who were exposed to
* L7 X6 t& G5 P5 \3 o/ Reven 15 minutes of direct skin contact with their male+ p. {- M0 B% u6 K% X) S
partners.6 However, when a shirt covered the applica-: H8 z4 _' M4 q. T0 H" N
tion site, this testosterone transfer was prevented.5 M9 u: W* x) v
Our patient’s testosterone level was 60 ng/mL,4 [3 [# {) {$ U" J- |" J2 b$ n1 y
which was clearly high. Some studies suggest that+ \' e. ^% {& M5 X0 S1 _
dermal conversion of testosterone to dihydrotestos-& P" V  [/ V1 A% {) n/ V
terone, which is a more potent metabolite, is more# ?' z* R2 ]3 y' H0 B- K
active in young children exposed to testosterone
; q# f) p8 P* V7 Sexogenously7; however, we did not measure a dihy-! \! U1 E0 ?: v! i  T0 a7 k
drotestosterone level in our patient. In addition to! f& \, d9 e/ y4 J$ a  b+ k7 H
virilization, exposure to exogenous testosterone in7 H" u5 U; \; F
children results in an increase in growth velocity and; ~4 |2 X5 _; T8 L# A  v0 _
advanced bone age, as seen in our patient.5 g& V0 R0 F) a, @
The long-term effect of androgen exposure during0 L5 D2 e8 n$ n% {, c; n3 P
early childhood on pubertal development and final
# T% p( X0 ^& G+ madult height are not fully known and always remain
% A0 r+ p4 h$ F/ La concern. Children treated with short-term testos-
7 E9 G3 i" |  ?5 ?9 `; Vterone injection or topical androgen may exhibit some( b7 X( B$ o1 j' M" T$ N- H
acceleration of the skeletal maturation; however, after
0 k( i. A; M5 acessation of treatment, the rate of bone maturation
/ _  y. f( i/ M, o3 H% e, ldecelerates and gradually returns to normal.8,99 u4 M( H' o" l' s
There are conflicting reports and controversy8 d: i4 S9 s) w$ B- r- g$ A
over the effect of early androgen exposure on adult
, ~2 P/ J% T. `penile length.10,11 Some reports suggest subnormal- }% s# z) b# Z: {" b% K
adult penile length, apparently because of downreg-
8 q6 o# r& E1 Z! g$ Wulation of androgen receptor number.10,12 However,. S9 K& z' }3 O2 q* Z: h% n
Sutherland et al13 did not find a correlation between
" w2 G% h( T' O; b4 Dchildhood testosterone exposure and reduced adult, m. [% Z1 z3 v- t& V$ b( i
penile length in clinical studies.
& k4 U2 |4 R2 j+ x- o% v& w5 |Nonetheless, we do not believe our patient is* p4 _2 q' D9 R
going to experience any of the untoward effects from
6 @6 r+ y6 u6 Dtestosterone exposure as mentioned earlier because
0 q" P2 o" I& M& O: L4 qthe exposure was not for a prolonged period of time.  D, a2 d1 ?, ?5 q% z) n- n
Although the bone age was advanced at the time of! ~3 ~# L: k9 E- F9 ^, s
diagnosis, the child had a normal growth velocity at  s7 r3 s( v1 K- B" c9 y- O
the follow-up visit. It is hoped that his final adult+ M$ ]0 @2 x. J% I( L
height will not be affected.% I2 v$ ~+ M+ E# q' j* S% `
Although rarely reported, the widespread avail-6 i) W, {4 h8 k8 {
ability of androgen products in our society may
' Z1 g3 x. ?8 B7 q, h4 jindeed cause more virilization in male or female
- b! Q& x4 @4 ?+ s' \/ I( I9 lchildren than one would realize. Exposure to andro-
0 ]# Q8 k$ ]5 r! M( f( pgen products must be considered and specific ques-
% F8 w& E* o% F5 k0 [$ R' Y; N+ \& d) Ltioning about the use of a testosterone product or
( i( w7 ^/ ^' g) k9 |8 _gel should be asked of the family members during
) n9 V5 r2 w) M7 [+ H- i, uthe evaluation of any children who present with vir-
. e% U7 I  f* q7 a- S# u- r, L: b# C! dilization or peripheral precocious puberty. The diag-
+ S  q/ N0 m8 t" }% p$ A! E/ v7 jnosis can be established by just a few tests and by
7 k: a, ~  n; n. p. Yappropriate history. The inability to obtain such a$ d" [5 m, B8 @6 h3 v
history, or failure to ask the specific questions, may: T" s+ r& W5 {, g% \8 f
result in extensive, unnecessary, and expensive+ S, I: K! r- o  R
investigation. The primary care physician should be
$ x9 B0 ^( k/ _' t& k) J" uaware of this fact, because most of these children: J% m: C( t& h4 P0 Q# H3 ?
may initially present in their practice. The Physicians’
% s. K5 O$ \+ t6 cDesk Reference and package insert should also put a* N0 p8 \4 [# y& B! |4 ^# f
warning about the virilizing effect on a male or( L, X2 K4 D4 X& |8 n6 @
female child who might come in contact with some-! I* G" g: M8 b
one using any of these products.6 `# k! X6 J4 r% u7 N# M
References6 S* v- X$ i( D
1. Styne DM. The testes: disorder of sexual differentiation6 \. ?+ j0 {8 `( W% m* b* b
and puberty in the male. In: Sperling MA, ed. Pediatric! X. V4 b: B: c; z4 g8 \$ S
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, f9 P3 ~: {4 i, d$ o8 ~# S
2002: 565-628.; G. B0 @( E# `* D! U5 J
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious7 V1 O+ f8 `9 u; t( Y
puberty in children with tumours of the suprasellar pineal
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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!

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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!
累計簽到:11 天
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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

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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?
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發表於 2025-1-19 02:41:05 | 顯示全部樓層

$ ~% o% @; F" m$ G精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!

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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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