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Sexual Precocity in a 16-Month-Old" F! [8 x/ C# }; n, f
Boy Induced by Indirect Topical
2 m, V2 L; R: a0 u# oExposure to Testosterone7 c* q7 B3 Q5 V  O
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2: M/ |" ]6 c$ h# o
and Kenneth R. Rettig, MD1; ?7 |3 k! M9 K( s5 G- r- `+ W3 S( I
Clinical Pediatrics. H+ |. x6 @+ H. D/ e9 F& O
Volume 46 Number 6* \. M* {/ y) S. y
July 2007 540-543! V1 x, A4 K8 w$ a2 B
© 2007 Sage Publications! ]# J6 @. c6 x. g" O; y
10.1177/0009922806296651
) r- v: M! g0 ~! g6 D* y" F: D( Ahttp://clp.sagepub.com
+ m$ q+ A5 ~) G! n6 ~0 Ghosted at
( i1 n: n, C! O1 c/ Y: k5 l" ]http://online.sagepub.com7 U, P2 c  b2 P6 a, n: N; G
Precocious puberty in boys, central or peripheral,
  D$ k8 p# D, T% ]5 Q, ]2 Dis a significant concern for physicians. Central
+ |3 g4 V$ ?& z! }; Q3 rprecocious puberty (CPP), which is mediated
, @! {3 V, ~, O- P5 e( e  Z; Ithrough the hypothalamic pituitary gonadal axis, has* J. E& I' a2 B, e7 o
a higher incidence of organic central nervous system
4 p9 S4 e6 T+ t* Klesions in boys.1,2 Virilization in boys, as manifested4 U3 t0 _$ [7 e: Z$ B5 H6 ^% t- P
by enlargement of the penis, development of pubic
- y; d* S. G8 {9 k; ohair, and facial acne without enlargement of testi-
2 Z! t: _7 I7 a+ K1 s2 n$ ^cles, suggests peripheral or pseudopuberty.1-3 We; n( M6 z+ A$ i+ N2 m* }6 |
report a 16-month-old boy who presented with the
4 Q; G, H9 e6 L# q8 yenlargement of the phallus and pubic hair develop-
, \+ B: v2 }" iment without testicular enlargement, which was due
7 \" f* q; n) y8 u; p% R! T4 {7 jto the unintentional exposure to androgen gel used by* t) C- |! r/ x4 d
the father. The family initially concealed this infor-$ a+ v) r2 t3 g7 s3 P
mation, resulting in an extensive work-up for this( @# S  I- N- s
child. Given the widespread and easy availability of
, `6 A3 D# ?3 \0 C2 |! h8 H9 vtestosterone gel and cream, we believe this is proba-
3 `9 f" L5 f& ?2 F# e9 K5 U( s# ubly more common than the rare case report in the$ e: x8 @- w/ y; C( o  Q
literature.4
  H" D8 G! z. v$ @# VPatient Report. B% d# k/ a7 s1 V" Y: B
A 16-month-old white child was referred to the
! G& `& a' R- u% {6 z" k* e* ^' gendocrine clinic by his pediatrician with the concern
& B! U' F7 j: b; F8 ?0 Xof early sexual development. His mother noticed" r" o6 F1 w- S1 O* H/ `
light colored pubic hair development when he was
8 ~5 g' T& {+ O& IFrom the 1Division of Pediatric Endocrinology, 2University of6 f% E: s7 Q0 \' Z, u, i  o4 }/ ]/ ~
South Alabama Medical Center, Mobile, Alabama.
6 i: q  b" X# O) Q: h4 oAddress correspondence to: Samar K. Bhowmick, MD, FACE,& T1 P8 @: y3 G8 x
Professor of Pediatrics, University of South Alabama, College of: a8 a7 h6 C0 B5 e! j7 G! w3 }
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
- q# e' ]/ E  H4 d/ x( _e-mail: [email protected].
4 g% S3 M7 d: H0 _3 C0 Vabout 6 to 7 months old, which progressively became
8 \! F; ]% B3 s! kdarker. She was also concerned about the enlarge-; D" r) }/ A/ ~- V; b' A% n6 K% g1 [  X) U
ment of his penis and frequent erections. The child( k. n  L! q- O& G9 L
was the product of a full-term normal delivery, with
6 k4 r8 v: E2 U5 D7 y* f$ ba birth weight of 7 lb 14 oz, and birth length of5 p6 r3 s0 _/ t5 V: X
20 inches. He was breast-fed throughout the first year
( o/ j, L7 K7 \2 Zof life and was still receiving breast milk along with
. h2 Z7 F9 G8 x, bsolid food. He had no hospitalizations or surgery,
7 s6 R, M( b' dand his psychosocial and psychomotor development: G4 H* A) `8 A' i7 ~( [+ l0 P
was age appropriate.
1 o6 D1 r: V( g- |; rThe family history was remarkable for the father,
$ F3 }* x& D6 w' t8 h2 h; {8 Zwho was diagnosed with hypothyroidism at age 16,7 [7 s7 W6 u  f. N
which was treated with thyroxine. The father’s
$ N, C& [2 `8 \# Cheight was 6 feet, and he went through a somewhat
, h  G! F* y2 Bearly puberty and had stopped growing by age 14.
+ \% c, o$ _$ o/ l9 Z; R! pThe father denied taking any other medication. The
& Z, g* T' k5 I) `$ [child’s mother was in good health. Her menarche
1 s/ Y8 C, L: l* Z" Q) W1 Ewas at 11 years of age, and her height was at 5 feet
' W% ]/ |/ K5 C1 l4 \5 inches. There was no other family history of pre-
% I+ f( R* w1 x- F) J  E; P' qcocious sexual development in the first-degree rela-
- G) X' D+ U9 R& P- S1 J) S, x' f' etives. There were no siblings.% b. F. l* Q8 N" _" I9 f0 s( f$ f
Physical Examination
. e1 g( I! w# N* e4 r* r( eThe physical examination revealed a very active,8 V" O3 D: @; j7 o
playful, and healthy boy. The vital signs documented' t( i7 F  Z8 U8 E" R, {- v& E! h, Q
a blood pressure of 85/50 mm Hg, his length was* _8 p1 s! K7 y& X$ Z
90 cm (>97th percentile), and his weight was 14.4 kg  P: V" r3 }1 X) y( H1 ~
(also >97th percentile). The observed yearly growth4 |# f% ?2 Y: e0 K! K7 v$ ~8 U
velocity was 30 cm (12 inches). The examination of
" w( f2 I5 R% B' j" t% @4 fthe neck revealed no thyroid enlargement.
) r! c! j4 E/ A  ^+ f6 }3 GThe genitourinary examination was remarkable for; j; Z* W+ w4 i+ z9 G' Y7 O
enlargement of the penis, with a stretched length of0 a. w8 K# B5 y9 L$ R; i
8 cm and a width of 2 cm. The glans penis was very well3 a/ {- ^0 x  ?9 b4 z
developed. The pubic hair was Tanner II, mostly around3 T4 D! l# i: C! e6 _# G
540( C* ^2 k; F; }
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ N  g" X0 R9 f8 ^; [7 w* a* ithe base of the phallus and was dark and curled. The
" |* ~8 x3 {! u- o$ r! `: P7 Vtesticular volume was prepubertal at 2 mL each.
: v! i# c) C. |) {0 L( SThe skin was moist and smooth and somewhat  u2 W7 _1 o" k' g2 {: l6 z$ |
oily. No axillary hair was noted. There were no
4 V- ^( G0 C+ _) k8 v+ nabnormal skin pigmentations or café-au-lait spots." h. ?6 k4 ^$ w* e2 ~9 x8 M( d
Neurologic evaluation showed deep tendon reflex 2+
, A1 X5 t6 Y: M& obilateral and symmetrical. There was no suggestion
) p$ T0 X+ p1 k: s4 [9 B, nof papilledema.
& [* ?- X/ f4 X. y  i* {( LLaboratory Evaluation& p9 N7 \" J* k2 o/ ?; N
The bone age was consistent with 28 months by
1 A% E$ T3 z' e: _using the standard of Greulich and Pyle at a chrono-, G& X) Y0 M/ V3 s3 \  a
logic age of 16 months (advanced).5 Chromosomal$ B, G4 U5 E& f5 q* r8 J) w5 O% r
karyotype was 46XY. The thyroid function test8 p, E* S$ x) R5 k
showed a free T4 of 1.69 ng/dL, and thyroid stimu-# k% n( Y; J# ]  T0 [
lating hormone level was 1.3 µIU/mL (both normal).
# g+ K* e2 S4 {5 u* m- u4 Z5 L2 ?3 sThe concentrations of serum electrolytes, blood9 \7 P& k$ @% T2 f
urea nitrogen, creatinine, and calcium all were
5 C+ E% I0 |% Rwithin normal range for his age. The concentration* x0 ?3 O+ w6 x3 f! A. d
of serum 17-hydroxyprogesterone was 16 ng/dL
* u0 Z1 {# N  a8 q(normal, 3 to 90 ng/dL), androstenedione was 204 |; K* X; j  X# h% P( ?) j; `
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
7 h' e$ Y: T) ~" c# Cterone was 38 ng/dL (normal, 50 to 760 ng/dL),% i- ?* J$ k& A( }. _2 |
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
7 H/ w4 r( \  M1 _  P- f49ng/dL), 11-desoxycortisol (specific compound S)$ i0 m9 N& _4 Z& P4 E
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
/ i+ a; S! w% Ctisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
1 e4 c( N3 w# }" y) s, f- wtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),6 V! k2 l& F' R# s# M) V& h
and β-human chorionic gonadotropin was less than7 ~5 W! r, G' f- g! j+ g4 Z
5 mIU/mL (normal <5 mIU/mL). Serum follicular& W1 Z# ~' e1 Y# _3 V9 y- F
stimulating hormone and leuteinizing hormone
% Q, ]6 {1 V" \' b) bconcentrations were less than 0.05 mIU/mL" W2 {' v) L. h- Y
(prepubertal).7 m) c/ M- L* S& M0 r% H3 B1 J
The parents were notified about the laboratory
' T. U5 k8 z) [results and were informed that all of the tests were2 h0 W5 j' g  I' y
normal except the testosterone level was high. The" n4 B. F6 D& T, i; {5 Y! {
follow-up visit was arranged within a few weeks to3 D7 V0 e8 A0 E0 D! S
obtain testicular and abdominal sonograms; how-' B" ^7 H9 i/ R$ O/ t+ M
ever, the family did not return for 4 months.
2 B0 U' {# \0 S% m: A" tPhysical examination at this time revealed that the* D3 k! ~6 H0 A; ^
child had grown 2.5 cm in 4 months and had gained
. g- [& P. z' O3 o: ~2 kg of weight. Physical examination remained
7 x" x# J1 V9 E# @, i. Yunchanged. Surprisingly, the pubic hair almost com-" q: ^" M7 n4 M
pletely disappeared except for a few vellous hairs at/ s0 E- N% L# x; Y# r
the base of the phallus. Testicular volume was still 26 s' x8 @$ D! {
mL, and the size of the penis remained unchanged.
0 ^8 U8 N4 J% n' a2 q6 LThe mother also said that the boy was no longer hav-; e9 g/ B& `- t9 e/ G5 P  o
ing frequent erections.! y, R5 Q- f( C7 p$ a
Both parents were again questioned about use of4 [* g2 U  H- M* A3 ~" `
any ointment/creams that they may have applied to* q+ @4 m( O7 u6 l
the child’s skin. This time the father admitted the
) P7 K: F/ t" J) B2 o/ z% T6 VTopical Testosterone Exposure / Bhowmick et al 541' h; |% A1 B1 H! l' D; W# Z
use of testosterone gel twice daily that he was apply-. Y% s2 E+ W( w, U9 N7 a) x
ing over his own shoulders, chest, and back area for+ |: _1 I/ R1 C
a year. The father also revealed he was embarrassed3 j8 ^& G4 M$ e4 a9 ^
to disclose that he was using a testosterone gel pre-
: t: E# e. }0 [8 G" yscribed by his family physician for decreased libido+ C& S' U* F* h0 C: K5 K, r% k
secondary to depression.
9 F7 |4 I. V- I/ f% F: o& O$ Q$ xThe child slept in the same bed with parents./ H" j( X- q; j' G, w
The father would hug the baby and hold him on his' v+ o+ Q; X3 X7 o7 p- P9 c6 z+ q7 s: _3 M
chest for a considerable period of time, causing sig-* w3 Z" m& B4 `! P
nificant bare skin contact between baby and father.: X5 ]3 {2 k# H1 P' b4 M0 o
The father also admitted that after the phone call,
( i0 o$ F, {& i& |) Y+ n) dwhen he learned the testosterone level in the baby0 d4 _$ r) j, v" ?
was high, he then read the product information. C3 V0 v# S! e. @* y" j& }
packet and concluded that it was most likely the rea-
  F( u( K" M1 B9 u0 e" i8 mson for the child’s virilization. At that time, they4 p  h% n/ s/ h3 C& i% B
decided to put the baby in a separate bed, and the+ E, @3 R3 C% R
father was not hugging him with bare skin and had
1 L4 m; G; e- a/ _$ G+ Xbeen using protective clothing. A repeat testosterone/ j2 S: h% [. X6 O6 F& ?! C9 o0 }
test was ordered, but the family did not go to the/ V6 k: s, {' g+ k# S/ S% I
laboratory to obtain the test.! F0 q2 r4 T. D
Discussion" B5 n7 |' i7 U# G; Q% W+ C
Precocious puberty in boys is defined as secondary2 T2 f! Y$ ?* E4 m
sexual development before 9 years of age.1,4
& @$ e, Q& x. [, E1 s, K5 g; RPrecocious puberty is termed as central (true) when
/ D  e3 a% [) pit is caused by the premature activation of hypo-
* `/ z3 V* i( g# l' {6 f1 G; U# _thalamic pituitary gonadal axis. CPP is more com-
2 T5 l, u7 Y# p8 A2 s  f$ omon in girls than in boys.1,3 Most boys with CPP; z# P, ~  r9 M) c: m
may have a central nervous system lesion that is
9 }( |- p' ?: X, `responsible for the early activation of the hypothal-
9 E0 w6 x3 r9 v, Uamic pituitary gonadal axis.1-3 Thus, greater empha-( @/ {" p" {7 P9 n
sis has been given to neuroradiologic imaging in8 S2 z; a1 h  K) m6 l
boys with precocious puberty. In addition to viril-" O+ o. I  ]+ ^5 [% }
ization, the clinical hallmark of CPP is the symmet-
/ R0 q; N! S5 h6 Crical testicular growth secondary to stimulation by) j& F( C0 w0 m/ }3 |- \
gonadotropins.1,3
2 D( i( C! l& f/ a* R. c# B( Q9 kGonadotropin-independent peripheral preco-
! Z+ m! O/ M6 R) |  E- }cious puberty in boys also results from inappropriate
( b0 D. {5 j* E( ]% d7 wandrogenic stimulation from either endogenous or# O1 P7 D+ g4 Y' ^
exogenous sources, nonpituitary gonadotropin stim-8 u& ]# W8 }) |, [3 y  X& h
ulation, and rare activating mutations.3 Virilizing
/ K1 W) \1 V! \7 l8 n1 G6 Icongenital adrenal hyperplasia producing excessive3 R4 D8 z  g. m4 ^) a: g  x2 `
adrenal androgens is a common cause of precocious. M/ X) Y% Q3 k7 ]4 r7 Z
puberty in boys.3,4
- l# t- N8 O4 c0 S% gThe most common form of congenital adrenal
( U! I+ [+ B" ^: yhyperplasia is the 21-hydroxylase enzyme deficiency.
( G; W: h- o! z3 xThe 11-β hydroxylase deficiency may also result in
( w! y- J9 N5 U/ E% wexcessive adrenal androgen production, and rarely,3 X% v7 p" U7 I$ s4 `
an adrenal tumor may also cause adrenal androgen" q( Y0 p5 l! h( A
excess.1,3
# ]; n( ]: U! Jat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from( p( @" k% x5 m# u4 `  l3 A
542 Clinical Pediatrics / Vol. 46, No. 6, July 20078 o. H6 W6 f1 q- {: Q
A unique entity of male-limited gonadotropin-
, j, A! c/ V. \' |% f- E+ iindependent precocious puberty, which is also known0 J& i6 X. v6 l/ b: M9 H
as testotoxicosis, may cause precocious puberty at a! K$ e3 w4 V" U# _% \! F7 w# C
very young age. The physical findings in these boys, r# K$ q# _6 n7 U7 X" H  s, u" v
with this disorder are full pubertal development,
) W% _: i& a2 T7 T9 R0 v% {! t# Gincluding bilateral testicular growth, similar to boys
- E7 O. _& I- R1 b: d) n0 j' G$ Owith CPP. The gonadotropin levels in this disorder! y' [0 f) g/ [6 J, P" w3 u
are suppressed to prepubertal levels and do not show+ z5 w0 w) N/ J3 b
pubertal response of gonadotropin after gonadotropin-
3 \$ X9 Z5 J7 ^! Q# r: L+ greleasing hormone stimulation. This is a sex-linked
0 r  n, d4 V' T5 w' b! E# n# Eautosomal dominant disorder that affects only
8 a) u# X! T3 T, ^4 |/ E' I9 S/ N  Jmales; therefore, other male members of the family
) c  n+ n1 c- f% @may have similar precocious puberty.3
2 S- ?% g) b. a" uIn our patient, physical examination was incon-+ C8 u0 e. ?' `8 J! e% G
sistent with true precocious puberty since his testi-% ~9 L' S& ~/ I
cles were prepubertal in size. However, testotoxicosis
; l  f$ y5 p0 x( g# @+ Pwas in the differential diagnosis because his father
5 P5 j5 j2 H% ]. q" J- n% l5 q  }; Sstarted puberty somewhat early, and occasionally,7 z) z  T  _8 {- F: j+ Z2 B
testicular enlargement is not that evident in the1 t5 T# p7 y2 ?# `0 {
beginning of this process.1 In the absence of a neg-
: H5 w: Z$ v# |3 J/ jative initial history of androgen exposure, our
1 k' Z6 v+ ], N9 N5 u' _biggest concern was virilizing adrenal hyperplasia,
4 Z3 Z! g6 z0 o2 reither 21-hydroxylase deficiency or 11-β hydroxylase
; s" r0 o) v- v% J2 N! m  h! t+ c1 O- bdeficiency. Those diagnoses were excluded by find-6 H, O$ i( \% `
ing the normal level of adrenal steroids.
7 {  p8 F0 J9 H, J  aThe diagnosis of exogenous androgens was strongly& ^& u/ K2 g) q' L
suspected in a follow-up visit after 4 months because
* {  W# p; y0 _5 l8 D4 c+ C8 \the physical examination revealed the complete disap-& v1 ^) T$ I+ X* s1 @: t
pearance of pubic hair, normal growth velocity, and
5 r) n, J9 c1 w2 x4 ?decreased erections. The father admitted using a testos-5 e" n0 V; x5 ]2 w
terone gel, which he concealed at first visit. He was+ k% Z  d4 \, g6 {) X
using it rather frequently, twice a day. The Physicians’. a; d3 e& ?& I
Desk Reference, or package insert of this product, gel or3 q& \. v2 f" {1 w) g3 U
cream, cautions about dermal testosterone transfer to; ^/ M" R4 h: H9 f- v  g$ @
unprotected females through direct skin exposure.
$ ]6 }, V5 |* K1 x0 Z1 Q3 B/ RSerum testosterone level was found to be 2 times the! F8 U" w; k% q( u- b( q
baseline value in those females who were exposed to, E4 B- u: L. o% i, ]5 p4 V5 g( t
even 15 minutes of direct skin contact with their male
! {* O6 w8 x$ Spartners.6 However, when a shirt covered the applica-1 S3 v$ C. Q! G9 D1 l, |& G
tion site, this testosterone transfer was prevented.3 p: {: d6 P4 j$ x2 g! S
Our patient’s testosterone level was 60 ng/mL,( T4 c* n3 D" v
which was clearly high. Some studies suggest that: y/ F6 a# u1 i2 f
dermal conversion of testosterone to dihydrotestos-8 ?$ x6 E2 p" l
terone, which is a more potent metabolite, is more
$ r8 G" ^8 i2 u$ I% J9 K9 Y# }active in young children exposed to testosterone
9 s2 E* o( d1 s. w, d4 {exogenously7; however, we did not measure a dihy-
( F% w- i( I  A, ^' [* udrotestosterone level in our patient. In addition to! T; `& X6 w4 y& T
virilization, exposure to exogenous testosterone in0 ?  l3 f: [& n$ k- Z/ ^8 [/ U
children results in an increase in growth velocity and% w6 X" |2 D/ ?* }5 X* P6 n3 p
advanced bone age, as seen in our patient.! [6 N/ w6 n% \) Z& O: j9 D3 r
The long-term effect of androgen exposure during
* ]$ |+ Y+ B" U$ q& v9 x5 \early childhood on pubertal development and final. [1 \$ ?9 p. Q8 [' y3 i- O6 c& f
adult height are not fully known and always remain
" n$ d) x5 v' k) L! J) Ya concern. Children treated with short-term testos-$ g% H' ^/ g5 ?4 n
terone injection or topical androgen may exhibit some
# o7 a: Y% i7 M; v) gacceleration of the skeletal maturation; however, after2 |- q# O( X: A  {% A
cessation of treatment, the rate of bone maturation) K2 Y. U5 i6 X; M- e
decelerates and gradually returns to normal.8,9
4 z/ q! |" x0 ~" \- u- a, e; G& u4 LThere are conflicting reports and controversy
1 v; C5 G) k2 n8 Uover the effect of early androgen exposure on adult
# `2 B( {' ~% i/ I7 V5 [7 Rpenile length.10,11 Some reports suggest subnormal
; _& k' p! k5 N; S( Vadult penile length, apparently because of downreg-& ?- [) s: l3 [, |
ulation of androgen receptor number.10,12 However,/ }" N3 z2 W! K7 |! Y/ p& w
Sutherland et al13 did not find a correlation between7 s8 y. a6 L: s% U
childhood testosterone exposure and reduced adult
1 Q. ]8 ?( ~1 q' g* G; W7 Lpenile length in clinical studies.
8 b- k/ }2 t3 n* I! t, s6 m$ ]Nonetheless, we do not believe our patient is
; h3 R4 F, |$ u; I! tgoing to experience any of the untoward effects from
1 q* J& p. h2 F' I( |' ?0 [9 j: ntestosterone exposure as mentioned earlier because8 ]" D9 Q% O4 B& N. j6 I, E5 t/ D
the exposure was not for a prolonged period of time.1 n% \" ]9 Q6 r& p* g
Although the bone age was advanced at the time of
( k& E# T% s- O8 E; u% k8 f( [diagnosis, the child had a normal growth velocity at
& [& l5 A/ f1 W+ X3 }$ }the follow-up visit. It is hoped that his final adult7 Y# S; g  t6 q1 H7 L& g  j" p0 |
height will not be affected.$ W8 `! F. T; H
Although rarely reported, the widespread avail-. b( u* ~; v( e! U# Y$ \
ability of androgen products in our society may' r6 Y, u9 I( e, m0 @
indeed cause more virilization in male or female- H3 Y; G: a0 t3 D6 g6 i; ?! P9 Y
children than one would realize. Exposure to andro-
) p/ A$ N$ H! u* R! sgen products must be considered and specific ques-4 [7 L# q) k5 j* v+ b& N( R
tioning about the use of a testosterone product or: L0 B) W; ^8 I# s
gel should be asked of the family members during% D: E1 X0 k# a5 O* ^6 e
the evaluation of any children who present with vir-
( I; P0 _$ ~, k) Y% Milization or peripheral precocious puberty. The diag-# L, e8 @! t$ h' Y9 K& Z
nosis can be established by just a few tests and by, K, o7 D9 f: I) u. @# q2 A/ w, x
appropriate history. The inability to obtain such a* m/ E; L3 B) O, f% j
history, or failure to ask the specific questions, may6 e; y# ?; ^- t1 `6 S/ d
result in extensive, unnecessary, and expensive
, y" O  k9 F- _. ^/ n  [investigation. The primary care physician should be* L% L9 F  v: ]2 [7 L: r8 Y7 h' q
aware of this fact, because most of these children+ Y2 g1 u+ ?- f4 H3 x. }
may initially present in their practice. The Physicians’9 N/ ~/ ^% F+ y0 r, r$ W2 `
Desk Reference and package insert should also put a) w$ t" L, Y# M2 x6 f) `2 Y
warning about the virilizing effect on a male or/ K* ]8 V3 B4 S  \. _! Z
female child who might come in contact with some-% Z9 \. m! I- n8 J, X; E- j
one using any of these products.
" N0 a+ o0 H  w4 O; x6 ]References
, c2 t3 }) j9 @1. Styne DM. The testes: disorder of sexual differentiation
9 {/ t: p2 g* R+ f4 u0 Band puberty in the male. In: Sperling MA, ed. Pediatric
2 z2 |# V5 y, t) X! H& R( HEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;3 X, U% {" b* g7 u- c6 u
2002: 565-628., r% w$ w/ p! \- f  S" V3 D3 R
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
9 j0 B1 O  u. A& b7 ^& B; Mpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old- N0 d, X% P* d9 _6 K+ |- ?5 R, @8 C! _
Boy Induced by Indirect Topical
7 V1 k% w" J) I: N( q0 J  @Exposure to Testosterone
- P; V: H$ Z4 _3 r9 s- m  c1 F- jSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
0 R2 K- e, @5 ~" L4 vand Kenneth R. Rettig, MD1* [& k3 ^. v0 C& Y
Clinical Pediatrics
7 l. T/ O) _9 S3 |# U( o( y6 [Volume 46 Number 6- y5 Z7 |7 d' w+ G- Y* @
July 2007 540-543; e  Q  x& y& T9 N
© 2007 Sage Publications. g* N' ]0 g+ b% k
10.1177/0009922806296651. K* }$ Y4 a* n$ z0 i5 s) M
http://clp.sagepub.com+ A# C0 @9 Z) S8 }6 |
hosted at
3 z. t: z/ M/ b1 E; Rhttp://online.sagepub.com, v' J7 ?5 l' u
Precocious puberty in boys, central or peripheral,
' i# R; a; y. V$ n# h1 ]is a significant concern for physicians. Central5 l9 X) e$ f) k/ V" B; T
precocious puberty (CPP), which is mediated! {7 r' a, e! m) n
through the hypothalamic pituitary gonadal axis, has3 A- e$ E, I% y; j8 \
a higher incidence of organic central nervous system" n1 i. W- i3 V
lesions in boys.1,2 Virilization in boys, as manifested* Z- S7 o$ H; e3 N8 Q* E: h8 y
by enlargement of the penis, development of pubic; t# k$ `' d" o0 l9 X
hair, and facial acne without enlargement of testi-
8 C, k/ W& V, ^  lcles, suggests peripheral or pseudopuberty.1-3 We5 Y! K/ j; R! P: W. Y
report a 16-month-old boy who presented with the
: P. n  V, s: X, d& a0 z  menlargement of the phallus and pubic hair develop-; c; D3 D* |6 X) T( ?2 C
ment without testicular enlargement, which was due
* A1 J3 q" |7 B; j0 vto the unintentional exposure to androgen gel used by0 F+ H; Z6 L; L( z# {
the father. The family initially concealed this infor-
) V7 ?' ^, ~) B) |& Omation, resulting in an extensive work-up for this: O' l3 K& Y  \( E* \
child. Given the widespread and easy availability of
6 H; l! r  s: i& l  k" }2 Ztestosterone gel and cream, we believe this is proba-
: L0 ~) v9 `8 Q* j- ^bly more common than the rare case report in the
4 G6 D/ e( M) |/ @: Pliterature.41 w# W5 ]/ W5 {+ U
Patient Report8 v/ L' W$ _4 s/ y0 S! R; V
A 16-month-old white child was referred to the
, q1 |: T. K& L6 p4 `endocrine clinic by his pediatrician with the concern7 n; P% O' j9 r+ G9 h$ @
of early sexual development. His mother noticed
# n5 ~- i5 S0 N' L& J2 D! Y8 hlight colored pubic hair development when he was
; d/ A# O5 d2 P, i6 e0 _From the 1Division of Pediatric Endocrinology, 2University of* w: l+ Q0 o% k' @8 S( [* g
South Alabama Medical Center, Mobile, Alabama./ k. g" F* I% t: x2 O; E3 x& W
Address correspondence to: Samar K. Bhowmick, MD, FACE,$ R5 P: K* N) j; F6 e/ i
Professor of Pediatrics, University of South Alabama, College of% j5 }( v! p6 O2 X
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;6 ~) t* K/ y3 g2 y
e-mail: [email protected].( t4 c; m7 s( Z8 [6 g/ {3 v
about 6 to 7 months old, which progressively became
1 t" J: \6 C" n" T' u9 u6 o6 ?1 odarker. She was also concerned about the enlarge-5 T. N6 F1 L2 U9 h1 c! m) o9 M) ^
ment of his penis and frequent erections. The child0 K6 q9 ]+ f1 M, _1 T
was the product of a full-term normal delivery, with
1 p( d" J1 g, q0 E% Ia birth weight of 7 lb 14 oz, and birth length of
0 L% v$ e) H7 i$ L. i" w- S20 inches. He was breast-fed throughout the first year
. I6 Q- ~4 K& D- Nof life and was still receiving breast milk along with
" B5 [; e) a- w2 u: }# D3 }solid food. He had no hospitalizations or surgery,
/ A, o  R1 O8 v( m2 @and his psychosocial and psychomotor development3 z. ?* B, M; R' u
was age appropriate.4 i7 p  e! O3 b! X# T% V) g& e2 a
The family history was remarkable for the father,
3 V* P& l7 K8 gwho was diagnosed with hypothyroidism at age 16,
4 [( Y  i$ c! k& Jwhich was treated with thyroxine. The father’s
5 z0 B& r, i1 R" S* x$ ~height was 6 feet, and he went through a somewhat
  z% L5 V) \% h: ~6 B, j: g9 ]3 Iearly puberty and had stopped growing by age 14.2 O" O2 @  F8 W# l3 R% Z
The father denied taking any other medication. The
' |7 W6 {  W) K' c! o( ichild’s mother was in good health. Her menarche
! N) ?5 r* C/ Z& zwas at 11 years of age, and her height was at 5 feet
2 U9 Q! b0 G: i5 o  k2 [5 inches. There was no other family history of pre-6 ^+ Z: o) Q; {7 N; d5 n! B  ?6 g
cocious sexual development in the first-degree rela-7 ?; s# p( u' P! G
tives. There were no siblings.: r0 {! ^8 b; v$ Z; j
Physical Examination
# ]6 F9 f5 o' Q8 _/ t1 g! _The physical examination revealed a very active,
6 W2 N. X- n  |) C$ [/ {playful, and healthy boy. The vital signs documented. e2 j" N: L9 r# |
a blood pressure of 85/50 mm Hg, his length was
9 u/ b! J( t# t3 @5 w2 ]90 cm (>97th percentile), and his weight was 14.4 kg
- v* g' N' V$ m) _3 M) @(also >97th percentile). The observed yearly growth
) X) }1 |: P2 ~# G" W! A* pvelocity was 30 cm (12 inches). The examination of: o1 b" ^' R4 o: X4 \" }+ A
the neck revealed no thyroid enlargement.% o+ e7 Z3 B3 z# f
The genitourinary examination was remarkable for- ~3 [4 V+ n- v$ m, P) T% {6 L: D2 L
enlargement of the penis, with a stretched length of
  E& l; K# q8 W  ?! J8 cm and a width of 2 cm. The glans penis was very well/ D6 l, b. |. u/ j0 C  s1 p
developed. The pubic hair was Tanner II, mostly around
2 H, e8 A" J8 q8 S9 s8 u* M" v0 Y2 h540
/ j8 X" J6 P4 Y9 p% uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! {  D4 c+ X/ c8 q
the base of the phallus and was dark and curled. The% G1 M. |, l1 E/ U2 Y' C
testicular volume was prepubertal at 2 mL each./ T. d( g. C! m
The skin was moist and smooth and somewhat% Y- p0 k5 T2 \
oily. No axillary hair was noted. There were no( q3 }* Z6 [, `. r' p4 S9 G9 Z! m
abnormal skin pigmentations or café-au-lait spots.
7 A6 \% P: t) {. b  p. G$ zNeurologic evaluation showed deep tendon reflex 2+
9 Z) i2 U( d$ h0 j, lbilateral and symmetrical. There was no suggestion
- i. U8 F: r" r$ ^8 Pof papilledema.
5 w: |$ s2 e* R4 p- y, K2 gLaboratory Evaluation
- x: q! F2 G7 A2 A) p7 Y4 ~4 Z3 yThe bone age was consistent with 28 months by+ J  F+ }% G. L; d2 U
using the standard of Greulich and Pyle at a chrono-
! s9 G0 ~% U6 }5 \logic age of 16 months (advanced).5 Chromosomal( \( q) _3 b! U
karyotype was 46XY. The thyroid function test
! \+ U4 E: k0 F$ N$ Jshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
; h" l& z4 o' O2 r1 Vlating hormone level was 1.3 µIU/mL (both normal).& @8 z2 U7 V6 t4 W3 Z
The concentrations of serum electrolytes, blood4 W4 T0 J/ A' G0 U9 Y+ o9 I- M
urea nitrogen, creatinine, and calcium all were
4 _8 D" y4 v9 s2 W: E5 N3 C2 |within normal range for his age. The concentration* T5 h) y" U, {
of serum 17-hydroxyprogesterone was 16 ng/dL" d* J% U( q$ s! e! k. F
(normal, 3 to 90 ng/dL), androstenedione was 20
2 _% i$ X# X) F! ]# H' Q6 \ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 x9 r! Y$ h) g, B- [# dterone was 38 ng/dL (normal, 50 to 760 ng/dL),! @  H8 O+ t% t9 k2 n* y6 E5 J
desoxycorticosterone was 4.3 ng/dL (normal, 7 to7 {2 j' Q2 b9 C1 h" a; G$ |; j
49ng/dL), 11-desoxycortisol (specific compound S)
/ F" @( b; f( e* _6 pwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-; J* m4 ?7 G* [5 E/ }
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total+ u9 M9 `$ t( l+ ]3 D$ f
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
' T0 ?, N% F8 }5 [; @and β-human chorionic gonadotropin was less than+ m( F2 N  J; I
5 mIU/mL (normal <5 mIU/mL). Serum follicular
0 A0 S8 H- F" F& a* J" rstimulating hormone and leuteinizing hormone
& q5 ]6 O3 o9 s/ I* Rconcentrations were less than 0.05 mIU/mL
+ r9 A* L& w" I0 g(prepubertal).
% }+ Z0 F/ g9 r* B. I& IThe parents were notified about the laboratory
4 i6 l7 v1 F1 J, Y6 n4 P1 }9 K$ O7 ?  @, Aresults and were informed that all of the tests were# `3 s( E% ?8 u8 m( U7 Q4 v
normal except the testosterone level was high. The
2 z# y/ O7 q/ s& Z9 Sfollow-up visit was arranged within a few weeks to- i) q' o( q# \* t1 Y* g
obtain testicular and abdominal sonograms; how-
0 N' Y+ T$ _7 T% N$ ~) Y" yever, the family did not return for 4 months." D1 ?4 m$ V* I# p. ]- {% v
Physical examination at this time revealed that the/ v4 W" @4 S0 U- c
child had grown 2.5 cm in 4 months and had gained
$ F7 l1 X4 {6 A) {5 i3 Y$ E% E5 u2 kg of weight. Physical examination remained
+ n$ |- ~; P& n3 d( s& T# ?; Eunchanged. Surprisingly, the pubic hair almost com-( f4 ~- e/ @+ I) W5 |4 G& ^0 i
pletely disappeared except for a few vellous hairs at! o4 U! k! w5 \, p6 w& l6 y
the base of the phallus. Testicular volume was still 2
) J+ o. I  s* M2 O  y, P& amL, and the size of the penis remained unchanged.8 Y+ J+ u/ W. @5 \* Z& K
The mother also said that the boy was no longer hav-
5 x* n! \+ P* s: b+ cing frequent erections.
/ J; n: k% @: G% t5 h8 {) Z( P7 \Both parents were again questioned about use of
  K( ~5 G( u' z  F  hany ointment/creams that they may have applied to
" B( U7 m+ s" i1 P  V+ k) H$ }the child’s skin. This time the father admitted the* y. ]6 A4 N5 C1 w
Topical Testosterone Exposure / Bhowmick et al 541; x" C) `( I% Q+ ~" j* `: b
use of testosterone gel twice daily that he was apply-
( B) u; V' A1 c- Hing over his own shoulders, chest, and back area for; A, @5 k: }! w" _: r
a year. The father also revealed he was embarrassed
/ J' m! s( v/ A/ Kto disclose that he was using a testosterone gel pre-$ m% Z4 W6 i( P; Y9 d8 j
scribed by his family physician for decreased libido: ?9 |5 W3 p& X: ?: k0 N4 C
secondary to depression.
  |# I$ T7 ^) U$ ]8 r- yThe child slept in the same bed with parents.- s- c! R0 z) h+ V
The father would hug the baby and hold him on his* [+ R# U/ X! n' j: v: F
chest for a considerable period of time, causing sig-3 j9 r8 H3 X) }9 n4 O
nificant bare skin contact between baby and father.
! @% b4 K4 K7 m- |' @" ]( ~# [The father also admitted that after the phone call,
5 h$ e' @2 H/ Ywhen he learned the testosterone level in the baby
. r1 G9 R% Q9 f  U' c0 }6 Pwas high, he then read the product information
2 j5 x. X# w) m" h7 tpacket and concluded that it was most likely the rea-( g4 w4 O9 O" q& Y7 G' T+ Q# ^
son for the child’s virilization. At that time, they
" A1 K+ ^  {7 U6 s9 G' ddecided to put the baby in a separate bed, and the
4 |' o- a" @0 g. `7 _5 l1 [father was not hugging him with bare skin and had8 w4 w" B4 ~- {/ @% ]7 A
been using protective clothing. A repeat testosterone
7 K+ T4 N) w9 ~( d$ n# Ktest was ordered, but the family did not go to the% c0 h3 C: ]$ |1 u3 `
laboratory to obtain the test.
/ I- ]& A3 t3 k" ?. ODiscussion
& F4 f/ r, G8 t6 _Precocious puberty in boys is defined as secondary( J$ P$ r0 f8 P. I( v- |
sexual development before 9 years of age.1,4. A' m0 E  b6 Z4 I2 s$ w# F
Precocious puberty is termed as central (true) when  Y5 q$ X: B. M4 h% i
it is caused by the premature activation of hypo-2 J" z$ r. g$ D, F( g% z
thalamic pituitary gonadal axis. CPP is more com-
0 l: M4 y/ B, |% e! q+ P: H& \mon in girls than in boys.1,3 Most boys with CPP
# W7 D5 p0 |3 E9 F4 h' l" imay have a central nervous system lesion that is
6 ?8 |( j0 h# p8 Z. b+ ]/ J/ u* vresponsible for the early activation of the hypothal-
! M* S9 r) M& I0 F  ~; o6 l+ ?amic pituitary gonadal axis.1-3 Thus, greater empha-
; Q# @6 s2 j% @+ ~7 y2 esis has been given to neuroradiologic imaging in
' W/ B& M; ]$ ~8 L0 @boys with precocious puberty. In addition to viril-
! i% D& u; X) G7 S. O+ sization, the clinical hallmark of CPP is the symmet-) Z' L+ T3 \+ p8 o% R6 H
rical testicular growth secondary to stimulation by
. ~% S" L8 m; E+ v" P; M) Kgonadotropins.1,38 B* C' T" ?$ T# J7 K% k
Gonadotropin-independent peripheral preco-
5 f3 p! _8 A- A2 E. D, Scious puberty in boys also results from inappropriate+ R1 f8 d- v8 ?1 l0 u- R: k* J4 I
androgenic stimulation from either endogenous or
4 H/ `8 }' q. V6 a3 [7 oexogenous sources, nonpituitary gonadotropin stim-$ i& C( |0 A) M
ulation, and rare activating mutations.3 Virilizing
" [+ k  G# H; C9 Kcongenital adrenal hyperplasia producing excessive
* g5 t2 A' C6 o, v. M+ w. E1 Dadrenal androgens is a common cause of precocious5 f2 m3 g- `; ]1 Q8 ?8 S( C! r
puberty in boys.3,4
* T8 S: k( |2 l  p* _4 M! rThe most common form of congenital adrenal" a" Y2 L1 q- [, Y' u
hyperplasia is the 21-hydroxylase enzyme deficiency.5 W/ I& [$ r2 M4 y
The 11-β hydroxylase deficiency may also result in! Q# H7 I6 b. N0 k. f) K* _
excessive adrenal androgen production, and rarely,- i  E+ U: g4 F1 R
an adrenal tumor may also cause adrenal androgen/ _) J* H, |' C; p$ |
excess.1,3
7 |" D4 S( x7 V# Y- F; Z8 Lat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 r7 q& l7 K# e3 B0 W; q542 Clinical Pediatrics / Vol. 46, No. 6, July 2007# |. W; f+ W0 @7 j( c/ t+ j
A unique entity of male-limited gonadotropin-7 E/ m0 Z. L, f' |# x" P" c
independent precocious puberty, which is also known
$ P! U% b. C! U" @1 \as testotoxicosis, may cause precocious puberty at a7 x. Z9 g1 j0 W: Y2 M
very young age. The physical findings in these boys
( h' ~' \! d' E" ~0 |! q4 Zwith this disorder are full pubertal development,
8 j( G$ I, M# r8 L4 l/ V% Vincluding bilateral testicular growth, similar to boys
1 p. K& j0 Z: c" c! Hwith CPP. The gonadotropin levels in this disorder' k1 y3 ?" Q/ S+ _
are suppressed to prepubertal levels and do not show
3 D3 R! \3 Q4 wpubertal response of gonadotropin after gonadotropin-7 B/ Y% a0 [! V- Y, O$ n  j8 Y/ ~
releasing hormone stimulation. This is a sex-linked. ?) \6 W/ a: t1 m
autosomal dominant disorder that affects only- P# x/ q; c( J/ s
males; therefore, other male members of the family3 P+ ?7 G* T, Y' E+ a* `8 J
may have similar precocious puberty.3
0 j; T$ v. G4 m$ z6 O- l$ qIn our patient, physical examination was incon-1 e) K" S) n' j# h+ g
sistent with true precocious puberty since his testi-# I& q1 ?  x# z1 v
cles were prepubertal in size. However, testotoxicosis
1 ~% i4 c' j  s) Cwas in the differential diagnosis because his father
. z8 Y' [" h, }( q$ xstarted puberty somewhat early, and occasionally,2 O) Y0 s) K. U2 @$ F; d
testicular enlargement is not that evident in the8 ~  U0 w# ^: d# q/ W! N
beginning of this process.1 In the absence of a neg-
9 H; H  ~) D6 Y0 F' r4 y9 Qative initial history of androgen exposure, our
! i; ^* s) U8 v9 t  g4 ?; j- g( Xbiggest concern was virilizing adrenal hyperplasia,) Z( d0 p2 o! i. u" S* y4 `
either 21-hydroxylase deficiency or 11-β hydroxylase
$ _9 g6 k5 T6 a9 _" B; jdeficiency. Those diagnoses were excluded by find-
$ i4 U3 k% y% ~- G, k- E0 wing the normal level of adrenal steroids., ?6 E& z9 i% S7 O) b
The diagnosis of exogenous androgens was strongly" _3 r% }% E! O. Y8 ?' Y
suspected in a follow-up visit after 4 months because, o$ m6 i7 n$ c* P2 d8 e
the physical examination revealed the complete disap-9 T1 I  [! O+ L/ v
pearance of pubic hair, normal growth velocity, and# t9 U6 b+ j3 W' ]; L6 ]
decreased erections. The father admitted using a testos-7 r/ z9 ?& x4 f; T$ ^: ]% u+ f$ s2 T
terone gel, which he concealed at first visit. He was
/ k" F* m+ P6 h6 T+ t) c" vusing it rather frequently, twice a day. The Physicians’  U4 T0 ^9 C4 g/ M) z# X8 i
Desk Reference, or package insert of this product, gel or
6 b; H2 S% u8 A1 B' O5 pcream, cautions about dermal testosterone transfer to" u! g- _6 S# Y$ ]# \" m6 ^
unprotected females through direct skin exposure.
% T8 N; t; p. P6 X) V3 G# ESerum testosterone level was found to be 2 times the
. n, ?9 C, P7 D6 f0 z1 ~baseline value in those females who were exposed to; r+ L! a# |+ f: d6 E8 g+ F
even 15 minutes of direct skin contact with their male
" M. m0 }5 N7 L! d  c4 |- Fpartners.6 However, when a shirt covered the applica-$ a$ Y  Z- M/ L% e# ]& p- G; h
tion site, this testosterone transfer was prevented.
- q: A; x% s: B, LOur patient’s testosterone level was 60 ng/mL,
, V+ O: y* f' X8 jwhich was clearly high. Some studies suggest that6 a) m) r. M, p* X! L
dermal conversion of testosterone to dihydrotestos-
+ k+ i0 |( ?9 p% N' p* X9 X$ X/ zterone, which is a more potent metabolite, is more
& W0 @% T/ s6 Zactive in young children exposed to testosterone, y% c# N7 I. N# a/ Q  b+ i
exogenously7; however, we did not measure a dihy-2 P7 _: x  R/ ~; M( |( K3 T
drotestosterone level in our patient. In addition to
1 ?" H0 x1 s/ O2 X2 svirilization, exposure to exogenous testosterone in
- z( R2 n- s# \' ?0 {5 E; b2 uchildren results in an increase in growth velocity and! G" ~; W7 D" s" i2 X/ j) Q
advanced bone age, as seen in our patient.
. l/ n, `2 j, ?The long-term effect of androgen exposure during
& g/ \9 `; D$ j7 J( N/ ^1 J. zearly childhood on pubertal development and final) E- M* Z7 n1 }. J4 i* O) _9 s! `; M0 i
adult height are not fully known and always remain
1 B, j: r# R% Q1 A: _. Sa concern. Children treated with short-term testos-
& o: I% A3 e+ f4 z6 mterone injection or topical androgen may exhibit some. O3 E& Y! i. f+ N
acceleration of the skeletal maturation; however, after" T+ `8 z- f. t9 Y- n5 R2 {
cessation of treatment, the rate of bone maturation
9 k0 B5 `! q0 q$ X5 `decelerates and gradually returns to normal.8,98 o5 I6 I1 {# u' V
There are conflicting reports and controversy
/ A8 ^- G+ e# y2 @8 n- y- d: R$ J& @over the effect of early androgen exposure on adult
$ a+ \4 Y: ~! ~* I& i" R$ s+ \penile length.10,11 Some reports suggest subnormal
& t; I: j- n4 I" a$ [adult penile length, apparently because of downreg-
5 I8 R8 D  q  r0 V$ x$ eulation of androgen receptor number.10,12 However,5 O: R9 E3 p' e9 J" q- _
Sutherland et al13 did not find a correlation between
3 K' s* t5 D. V/ t* g/ \childhood testosterone exposure and reduced adult
0 y5 w% V5 p4 N+ o( mpenile length in clinical studies.3 o/ @, _. E+ }
Nonetheless, we do not believe our patient is- Y  h: d, ?2 f3 }9 R/ X! A4 N
going to experience any of the untoward effects from6 N. S' [( g! n
testosterone exposure as mentioned earlier because
% o; B, p) b. p" T0 J) `7 {- {the exposure was not for a prolonged period of time.! t& f. t4 m* d. e+ C4 @
Although the bone age was advanced at the time of
* K1 k7 K& G; ], R! Hdiagnosis, the child had a normal growth velocity at
& ?, F9 H0 i: l4 ^$ z6 z' W: a1 r3 ]the follow-up visit. It is hoped that his final adult& R. `$ I* X. A' r
height will not be affected.
! s9 M: l5 F! V4 v6 }Although rarely reported, the widespread avail-
, m7 f) {" s/ \' Y# wability of androgen products in our society may
3 m) H2 l" J$ A8 d- N* ]! X. findeed cause more virilization in male or female0 L% }! L1 a4 b! ]' F
children than one would realize. Exposure to andro-' h) l# I: ]9 i3 g
gen products must be considered and specific ques-
, Y9 u, T& a$ X+ ctioning about the use of a testosterone product or) n0 [" H) n) i, ^/ H2 Q
gel should be asked of the family members during9 f2 N" _/ a  P. E' j
the evaluation of any children who present with vir-# H  y9 c: E; ]. }$ S
ilization or peripheral precocious puberty. The diag-
4 V6 K4 c. s$ G: ~8 `nosis can be established by just a few tests and by" q+ r# K* k4 _. W* M* c! A6 v2 K. A% Z
appropriate history. The inability to obtain such a
! N  U9 o1 ]3 q5 j8 `. nhistory, or failure to ask the specific questions, may
+ l5 A8 t$ v% A1 J7 U4 P/ b. Xresult in extensive, unnecessary, and expensive
4 T5 u# q4 @  [7 Z& T; D# B7 Yinvestigation. The primary care physician should be
5 u: J1 d! ]) s5 Eaware of this fact, because most of these children
# q  s: P3 h! Q/ j0 ^0 @6 Pmay initially present in their practice. The Physicians’
7 f: D; E" {5 j4 u6 L' BDesk Reference and package insert should also put a
/ M5 U% ]" n% k$ {9 ~warning about the virilizing effect on a male or
0 t1 ~3 M/ S  V+ |6 F9 t6 ffemale child who might come in contact with some-5 r4 Y1 M0 s% [5 O  l
one using any of these products.' ~" M# O: k' U
References
' J& Z, ~, R) m1. Styne DM. The testes: disorder of sexual differentiation, {( ~; s$ {, c  V; Q6 l' S& `
and puberty in the male. In: Sperling MA, ed. Pediatric+ r$ x& q5 _# k  \3 X' x+ v
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, S- |2 X! t4 _7 N# O; G  t  F
2002: 565-628." n- u7 L& t* X9 O# E
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious4 a; w, L+ d9 Y& `, i
puberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
" |! ?. U& t$ 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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