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Sexual Precocity in a 16-Month-Old
+ N4 ?! f& ^. f. E# ABoy Induced by Indirect Topical- z' v  R" M6 ?6 A4 ^
Exposure to Testosterone% C: P* q( r5 w4 m, k" B* c
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
, \+ B+ ~3 _+ p, |! j$ e6 \( _+ e; jand Kenneth R. Rettig, MD1
7 P* |9 R) Y, g% DClinical Pediatrics3 r! _9 I3 U# s2 c  u9 [- N
Volume 46 Number 6
' _% z0 `. q0 E4 h2 W" ZJuly 2007 540-543
. @! O! m4 `) w3 c" x' _© 2007 Sage Publications
, V; F0 S0 l/ |5 Y. Y6 V10.1177/0009922806296651
" G- M8 L9 T! j+ s- N3 G" ahttp://clp.sagepub.com
5 T( N2 m% H5 z) Vhosted at
1 E9 ?/ ^% S9 ^. K- X3 e% X' D( }http://online.sagepub.com
3 g0 |( b2 b3 }Precocious puberty in boys, central or peripheral,
  M& a) B7 v$ U3 Y& Xis a significant concern for physicians. Central
: u& c4 ?* K0 C: C, n  q7 B9 I$ D, hprecocious puberty (CPP), which is mediated
2 `8 k) C- t/ {) F- Z: ithrough the hypothalamic pituitary gonadal axis, has
: k0 A% Y: l9 q, m: ]  ~# w1 ?a higher incidence of organic central nervous system( {9 [1 @; y9 W/ W3 v' o1 _9 d
lesions in boys.1,2 Virilization in boys, as manifested
- M6 F4 ]$ m. a* ~' m! [" p& d# [by enlargement of the penis, development of pubic
9 q$ y! ~! q6 R# N, xhair, and facial acne without enlargement of testi-
+ G. i; r' N1 h* K) \2 P: m& Fcles, suggests peripheral or pseudopuberty.1-3 We- _  u+ F$ b$ C# n
report a 16-month-old boy who presented with the1 E0 a5 E2 T5 l) Z5 F
enlargement of the phallus and pubic hair develop-2 ]" l7 v5 w2 m& O. l3 [
ment without testicular enlargement, which was due1 A, j& x. w# ]' C
to the unintentional exposure to androgen gel used by1 ^# K! D1 J9 S1 C
the father. The family initially concealed this infor-% c$ G5 b- ^! T4 x5 |2 z+ I
mation, resulting in an extensive work-up for this  v. b7 ?' g( I9 T: n! T- Q
child. Given the widespread and easy availability of
3 `$ l. b0 M- X& [+ Btestosterone gel and cream, we believe this is proba-
( u4 P  w. d& W" kbly more common than the rare case report in the
, m6 Q8 D+ @! x" N& y" xliterature.4% H/ N, w! e4 a: i$ f' D
Patient Report
+ y: o9 a1 c6 K5 R4 xA 16-month-old white child was referred to the
* O  d  _5 k& M) p6 Hendocrine clinic by his pediatrician with the concern( m! o. g' [3 k4 v* g' X
of early sexual development. His mother noticed
# l3 N6 }  q/ \7 Plight colored pubic hair development when he was. p6 @4 m3 e4 k
From the 1Division of Pediatric Endocrinology, 2University of
* ]4 S2 Q+ P9 {4 y3 H# ?! l: uSouth Alabama Medical Center, Mobile, Alabama.
+ r/ u9 H% Z0 R" O/ T( ^  y) rAddress correspondence to: Samar K. Bhowmick, MD, FACE,: B% U& U" g4 m2 x  I, ?1 ^! v
Professor of Pediatrics, University of South Alabama, College of; \- H, V; F; P1 _: @% B* G: R
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 p* o3 f9 l& l& u
e-mail: [email protected].
, d" |6 ~$ F+ k/ g8 `3 V6 X' K4 P" Eabout 6 to 7 months old, which progressively became
; H1 w1 V6 M0 k' fdarker. She was also concerned about the enlarge-
, S7 j4 K) i8 g2 `ment of his penis and frequent erections. The child
" P  [0 L/ ]9 `/ Xwas the product of a full-term normal delivery, with* n# x5 `* [& {; a" B8 G; O" y
a birth weight of 7 lb 14 oz, and birth length of: ?) t5 U0 U+ M. E5 f
20 inches. He was breast-fed throughout the first year
1 g/ G# {7 s0 Tof life and was still receiving breast milk along with0 r2 ~( D% n; E* V! p3 ~% Q
solid food. He had no hospitalizations or surgery,
" G5 f2 L' E/ T9 I5 @" Oand his psychosocial and psychomotor development: ^4 }- E+ P) P: n* _+ ~! }
was age appropriate.
/ Z) [' u2 R+ T" E! A/ J' d. sThe family history was remarkable for the father,
8 j7 n. C  w; S: D1 q* q& F7 {who was diagnosed with hypothyroidism at age 16,
' I) X$ @0 K( s3 f4 w7 Wwhich was treated with thyroxine. The father’s
: U! c/ ]# e" W! N, B' dheight was 6 feet, and he went through a somewhat1 m9 c7 u5 e& y
early puberty and had stopped growing by age 14.
( P, w3 [/ ?/ @- q$ kThe father denied taking any other medication. The' i# K5 V% n) U9 C
child’s mother was in good health. Her menarche/ f* n8 H1 H1 ~& P# [6 I
was at 11 years of age, and her height was at 5 feet
# ?8 e$ Q# H  x6 d5 inches. There was no other family history of pre-
; o) P, P/ ~+ P7 E4 ^: O4 y% K! Ncocious sexual development in the first-degree rela-* ?' C* ]* I$ `
tives. There were no siblings.
2 {0 G. b; v, |: G  o1 V$ j6 dPhysical Examination, }* Q8 W9 U, A# ~' d9 s
The physical examination revealed a very active,
+ |. I& k% }( k5 @5 \6 N0 bplayful, and healthy boy. The vital signs documented
# \1 r  C0 ]% W# U) Ba blood pressure of 85/50 mm Hg, his length was9 Y& y) g- f+ q) H0 `, K3 f
90 cm (>97th percentile), and his weight was 14.4 kg" p! p. R* R# }# V6 p& c
(also >97th percentile). The observed yearly growth
' T. w5 X1 D  K8 @velocity was 30 cm (12 inches). The examination of
; m  y8 ^1 j5 E# Wthe neck revealed no thyroid enlargement.9 P8 w0 c7 F7 O/ J+ h( G, R3 I
The genitourinary examination was remarkable for2 n7 ~8 O( z* P9 e$ b6 l
enlargement of the penis, with a stretched length of0 a/ b, M$ _1 s$ k- l$ S- q
8 cm and a width of 2 cm. The glans penis was very well
6 f8 D" Z8 C7 M5 k8 n* Z& sdeveloped. The pubic hair was Tanner II, mostly around
0 A0 J) i" G( l, Y; u7 @) m540
! @' d' r: w6 q; u! s: V) A; u, Fat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: k) y# |" Z3 w' u% `9 ^% _6 E$ [, Bthe base of the phallus and was dark and curled. The! B+ u& A4 Z5 t, F
testicular volume was prepubertal at 2 mL each.
' b/ N# ?$ A9 _2 j3 [' MThe skin was moist and smooth and somewhat
. n. ]) Q- K2 R3 L" C/ i; \oily. No axillary hair was noted. There were no
& Z$ v7 L& h$ r: D5 @abnormal skin pigmentations or café-au-lait spots.. V+ r/ w. ~8 _+ z- V
Neurologic evaluation showed deep tendon reflex 2+; L" s/ |/ X2 u
bilateral and symmetrical. There was no suggestion& u, I3 N& B8 i8 B2 j6 h# z
of papilledema.
# F& v# b7 c) @: A8 V  n# MLaboratory Evaluation5 a4 w( O! N. X6 b
The bone age was consistent with 28 months by
2 n" j' Q+ t6 X5 ?$ [! ~using the standard of Greulich and Pyle at a chrono-
& l: X/ B# R( I- qlogic age of 16 months (advanced).5 Chromosomal3 N: a# y6 V( l- U: w5 U
karyotype was 46XY. The thyroid function test3 j" {. V$ M( o- X) a2 u
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ O4 e3 a$ m/ t$ G: R9 H8 q, }lating hormone level was 1.3 µIU/mL (both normal).
) O" j  c3 B2 N; N% t' yThe concentrations of serum electrolytes, blood
9 d" C; _* ]. e- P% Curea nitrogen, creatinine, and calcium all were( c: `0 T+ A* U8 r, j3 h: V
within normal range for his age. The concentration
$ J( s( z& V$ t0 g9 k# h4 W8 Bof serum 17-hydroxyprogesterone was 16 ng/dL
) U8 O5 g  T$ {% B( v- M(normal, 3 to 90 ng/dL), androstenedione was 20
+ E! r/ d+ ^6 Y: n2 eng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
7 i9 F9 i8 b$ w* r6 l# \terone was 38 ng/dL (normal, 50 to 760 ng/dL),
- H1 x8 v$ E7 [2 g; n6 adesoxycorticosterone was 4.3 ng/dL (normal, 7 to
+ \- D& Z% F6 i49ng/dL), 11-desoxycortisol (specific compound S)
0 S# Q3 K; X3 f6 H7 k8 Cwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-, w! e% I+ {0 x! W, A; Q  o. R
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
& N; J/ U1 \! m" @7 ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
1 Q" B' d( `/ H# t& R, e- ~and β-human chorionic gonadotropin was less than
! b0 K; N- t- e* J5 }' D5 mIU/mL (normal <5 mIU/mL). Serum follicular# R  F  j3 d+ u- b& ?% F, ~' n
stimulating hormone and leuteinizing hormone
) ?9 w" [5 G+ B4 ]concentrations were less than 0.05 mIU/mL
5 ~$ E. Q2 g  h(prepubertal).( @% S1 R, R4 k  G
The parents were notified about the laboratory
: s  y; h. |8 z+ a3 d* Wresults and were informed that all of the tests were
2 L0 q7 P6 T% `$ o% inormal except the testosterone level was high. The
3 X1 e" @' Y& ~2 Jfollow-up visit was arranged within a few weeks to
2 S- K! S& L+ |obtain testicular and abdominal sonograms; how-
% _* N/ v8 d+ w  n% ], J: fever, the family did not return for 4 months.
3 f/ y/ @( f4 t5 ?+ kPhysical examination at this time revealed that the1 D7 e4 h& B9 f/ [- P
child had grown 2.5 cm in 4 months and had gained
) l  K$ Z' h8 P- ~  D# m2 kg of weight. Physical examination remained7 U# n6 m3 |/ a) I( _# g. }4 i
unchanged. Surprisingly, the pubic hair almost com-
% ]; s" C% \  G0 n( y0 `' ypletely disappeared except for a few vellous hairs at
. b% T9 J0 u6 ^& u% P- @the base of the phallus. Testicular volume was still 2
3 f/ C( a1 E, W2 `/ K9 ymL, and the size of the penis remained unchanged.% F7 j9 x, Z+ k1 v
The mother also said that the boy was no longer hav-& c5 P5 C% K( o* K0 F
ing frequent erections.- N6 m. @8 W: K3 S7 |
Both parents were again questioned about use of- q" [) `1 t+ t/ t- C/ E
any ointment/creams that they may have applied to
6 t* p, a" \1 C3 Y% F9 y; N. wthe child’s skin. This time the father admitted the
- m2 N& I$ R, g6 ATopical Testosterone Exposure / Bhowmick et al 541+ q! h4 s" w0 R6 A# c9 I) l
use of testosterone gel twice daily that he was apply-
/ `0 B( p0 x  d' I) b  D) Fing over his own shoulders, chest, and back area for
2 x: D& P, h' m7 ]8 v5 Fa year. The father also revealed he was embarrassed
; [' P: d; R) h( K( ]/ Mto disclose that he was using a testosterone gel pre-4 u  r6 I% m0 V: E. k
scribed by his family physician for decreased libido& d( \0 ~. f, e$ j5 J
secondary to depression.
" n# `) @; n. g) xThe child slept in the same bed with parents.
! B  l# b3 ^6 R; B* S4 qThe father would hug the baby and hold him on his
) a- U. b( Q4 }+ }3 I( o. ]chest for a considerable period of time, causing sig-- I/ n$ z/ Z4 M& i# I
nificant bare skin contact between baby and father.: ^* x. G7 J* C. }9 f( j; o
The father also admitted that after the phone call,( }0 S# B4 N7 x" W0 A
when he learned the testosterone level in the baby
# }! I. L* {9 j/ _: s( Pwas high, he then read the product information
, U, p% s) H5 r0 g; k9 Hpacket and concluded that it was most likely the rea-2 d$ k; H( S0 K" h: E3 U  t% S
son for the child’s virilization. At that time, they+ d% w$ E+ d: j, c5 f
decided to put the baby in a separate bed, and the
4 b- k2 Q; z0 |: m( V/ U; Qfather was not hugging him with bare skin and had
  K# j+ [( H2 b7 l1 {  j% ubeen using protective clothing. A repeat testosterone
' w$ N2 [5 z( e0 ztest was ordered, but the family did not go to the8 R/ E. s4 z9 z6 Z
laboratory to obtain the test.
" h9 f3 B& s; F. l3 x. v3 JDiscussion
- X  k9 h4 J. G" b& p2 E8 xPrecocious puberty in boys is defined as secondary- K& k' U. F% e2 z
sexual development before 9 years of age.1,41 @+ ]1 S; B9 Y- a. }% {0 B! {. m
Precocious puberty is termed as central (true) when
" E6 N. E6 X/ ]: jit is caused by the premature activation of hypo-
; s7 S1 J1 w( ~: P& Dthalamic pituitary gonadal axis. CPP is more com-
: T, G% m$ M, F- S: X" E8 p0 a+ vmon in girls than in boys.1,3 Most boys with CPP4 _; T' W# f, E. v! z
may have a central nervous system lesion that is% b4 s! c, @5 b6 F$ W7 \
responsible for the early activation of the hypothal-0 v/ _" D! S- @7 w
amic pituitary gonadal axis.1-3 Thus, greater empha-$ z$ w. t( B7 e) w7 P
sis has been given to neuroradiologic imaging in6 C0 h, p  w0 N9 n# k
boys with precocious puberty. In addition to viril-
8 Y6 F5 p1 Q- ?. G) r8 jization, the clinical hallmark of CPP is the symmet-8 K* b  ~( y; ~4 S* n* q4 u
rical testicular growth secondary to stimulation by
. X8 \( h$ v" S) }# f/ n0 l# vgonadotropins.1,3+ I4 S. H, C) s4 r( Z# Y
Gonadotropin-independent peripheral preco-
: g* B% E% K; P/ s1 dcious puberty in boys also results from inappropriate; S1 l7 @2 v/ m2 d8 ~
androgenic stimulation from either endogenous or
: t9 Y' R; E) Q3 T/ H. \9 w7 pexogenous sources, nonpituitary gonadotropin stim-. p' U, G& v% ]$ Q2 l5 J
ulation, and rare activating mutations.3 Virilizing
+ I) D) ]; |0 P5 \8 xcongenital adrenal hyperplasia producing excessive
9 e! I; S3 x5 A$ e2 nadrenal androgens is a common cause of precocious( u4 P8 p9 }' w. |' A( i
puberty in boys.3,4
: i5 W4 T# U* ~The most common form of congenital adrenal) g/ ^, `0 h+ K6 v
hyperplasia is the 21-hydroxylase enzyme deficiency.9 j$ R" a7 `* L9 e2 [  N
The 11-β hydroxylase deficiency may also result in
# L" o- B$ y  ]6 e6 r0 G, \- Xexcessive adrenal androgen production, and rarely,
& u4 y- `2 P) [8 b! p) o# M* A# \2 @% ean adrenal tumor may also cause adrenal androgen# `. @+ x& S; \, V4 a
excess.1,37 s' i% n' a6 s) K8 A) f
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 P5 o) `) l" R$ [; g
542 Clinical Pediatrics / Vol. 46, No. 6, July 20079 e- V7 I% s8 o0 |
A unique entity of male-limited gonadotropin-* b5 C% y$ a$ O! c
independent precocious puberty, which is also known: i0 ^, ]7 }' V8 f& G' Z
as testotoxicosis, may cause precocious puberty at a3 M7 F& u( C3 M  i4 R) h6 e
very young age. The physical findings in these boys" w' ]1 H2 f5 I0 g8 e$ g5 A1 N
with this disorder are full pubertal development,
  F- h' v2 F% S3 w* ~including bilateral testicular growth, similar to boys
2 W8 E; E$ \  N' `6 C  a! M/ Qwith CPP. The gonadotropin levels in this disorder
1 S0 G  a: n9 g, ^1 R4 |8 }are suppressed to prepubertal levels and do not show
8 B2 u+ V  [6 d, c' w! fpubertal response of gonadotropin after gonadotropin-/ ?5 ~9 b2 n2 h4 r' ~
releasing hormone stimulation. This is a sex-linked
! A6 E6 u2 q- m' Zautosomal dominant disorder that affects only
/ s( x* C- G: ?4 R- ~1 n" L: }males; therefore, other male members of the family
' {! D6 b( y' b( V  Z3 dmay have similar precocious puberty.3# n6 X, J# {! U
In our patient, physical examination was incon-1 y8 ]. ]& [  ~# D! q; K% C2 D1 l
sistent with true precocious puberty since his testi-' O7 F9 ~7 y, M+ h
cles were prepubertal in size. However, testotoxicosis) X" u0 X% d: `  K$ C  A+ q
was in the differential diagnosis because his father
6 T. m# ?: w6 O0 T4 W6 D% _started puberty somewhat early, and occasionally,& A  _) Q0 O- \2 S
testicular enlargement is not that evident in the' |- v6 B5 H. A' @$ [( T
beginning of this process.1 In the absence of a neg-
! u& T6 W! i6 z9 n. j1 V2 L" Uative initial history of androgen exposure, our  D0 u) \7 q& i5 u/ E  J
biggest concern was virilizing adrenal hyperplasia,
5 f% h9 K+ G. l# b6 N6 ^: X3 @either 21-hydroxylase deficiency or 11-β hydroxylase$ q6 @" O. a; \/ s: {7 O+ ]
deficiency. Those diagnoses were excluded by find-  @  g$ t( g8 K6 @% b
ing the normal level of adrenal steroids.
. i& I9 V7 _% U$ ^' aThe diagnosis of exogenous androgens was strongly$ f& X$ Z2 y2 S, ]2 r# f6 w. F
suspected in a follow-up visit after 4 months because
* M$ H* [! d$ Nthe physical examination revealed the complete disap-
( C0 v; v6 k1 j8 Qpearance of pubic hair, normal growth velocity, and0 _9 i) q# W2 `% J
decreased erections. The father admitted using a testos-
! `9 x" s# r0 K0 U& xterone gel, which he concealed at first visit. He was8 y6 x2 u1 U9 \. H" F/ F) k# E
using it rather frequently, twice a day. The Physicians’
7 @# w2 u" u/ U0 ]- [2 P! IDesk Reference, or package insert of this product, gel or
/ `1 p& Q7 c1 |cream, cautions about dermal testosterone transfer to+ e2 t$ m8 U5 Z) r
unprotected females through direct skin exposure.
# u; o0 A2 o5 z, S( [4 ]8 p( l8 JSerum testosterone level was found to be 2 times the  K/ d4 i8 X* r1 C2 `
baseline value in those females who were exposed to
) O; K* P8 o) Y# Peven 15 minutes of direct skin contact with their male! v9 b  L4 @. O% \! x5 L
partners.6 However, when a shirt covered the applica-
3 u  o! A+ N% A& btion site, this testosterone transfer was prevented.! S2 Y7 y4 ~2 W
Our patient’s testosterone level was 60 ng/mL,
( G# m8 Z- |" |: V) |1 E* z: kwhich was clearly high. Some studies suggest that
; }7 }" u" s" C, D7 g0 a( ~dermal conversion of testosterone to dihydrotestos-
6 @. U2 b' B9 z. t" L; i3 a8 g, `terone, which is a more potent metabolite, is more
' w+ Z; v' R; Eactive in young children exposed to testosterone9 c: K* g) r4 Y2 u
exogenously7; however, we did not measure a dihy-
: G7 g1 [7 V( H8 @drotestosterone level in our patient. In addition to
2 a& `. x8 @3 z. t# u' J( Tvirilization, exposure to exogenous testosterone in
5 ]. q$ F' T/ T  \! `; Cchildren results in an increase in growth velocity and
) ?! `, E' {! i4 }advanced bone age, as seen in our patient.2 F8 r5 n6 X' U$ d
The long-term effect of androgen exposure during# s$ v. y7 H5 }# D
early childhood on pubertal development and final+ b4 m- o) d0 D/ S
adult height are not fully known and always remain: E9 \  w/ w) U! f+ z# m8 Q
a concern. Children treated with short-term testos-
1 Y) V4 d! n+ ]$ u: jterone injection or topical androgen may exhibit some: Y9 C7 V  t$ J' i& l, Y. I
acceleration of the skeletal maturation; however, after. U$ {4 `- n- ~+ K
cessation of treatment, the rate of bone maturation
$ d: r( }+ l/ z' A6 Pdecelerates and gradually returns to normal.8,9
  o' r- {) r. _6 O) GThere are conflicting reports and controversy
# J5 `/ D: Q- Q9 W0 `9 i1 Qover the effect of early androgen exposure on adult
6 l) V& i2 g8 [" k' zpenile length.10,11 Some reports suggest subnormal
  J8 N( B6 d1 B/ P0 l3 radult penile length, apparently because of downreg-
6 }( Y/ b" F; S* w. Wulation of androgen receptor number.10,12 However,! Z' {4 |! u! u( Z. U, }- X0 r
Sutherland et al13 did not find a correlation between
" ~8 ~% ~8 r" T" h1 Ochildhood testosterone exposure and reduced adult" X3 A1 n4 A; F9 Y0 f7 C! I3 ~
penile length in clinical studies.
* z0 d' Z+ p, [# H$ \" \Nonetheless, we do not believe our patient is
0 f8 F' q7 A6 ?9 ?going to experience any of the untoward effects from1 L1 `  j% [/ [9 `! i( @1 {7 _
testosterone exposure as mentioned earlier because
! @# `+ [+ ?* n) Z! j" j9 v0 _- Fthe exposure was not for a prolonged period of time.
% P4 D. y2 e3 W# F' I" JAlthough the bone age was advanced at the time of
2 b  T, d/ l/ G) Z  Wdiagnosis, the child had a normal growth velocity at' `( u9 f, J0 \. `! c( q
the follow-up visit. It is hoped that his final adult
4 g# c! k9 }# a/ |4 g5 vheight will not be affected.
. A6 k' g2 W) Q; a# I* KAlthough rarely reported, the widespread avail-
, \* M3 M- s7 jability of androgen products in our society may
6 f* J" w. i2 R- X3 h/ Xindeed cause more virilization in male or female
% ~7 H7 z: V( ?( Lchildren than one would realize. Exposure to andro-7 C  v/ R4 U/ i6 T+ j
gen products must be considered and specific ques-
) m/ I4 O7 U7 N( F/ Q- g6 Rtioning about the use of a testosterone product or
5 v2 [; D+ G4 x1 e8 agel should be asked of the family members during' a/ L: N: p  G/ Y. C: V
the evaluation of any children who present with vir-
7 S( Z# x% |+ ?ilization or peripheral precocious puberty. The diag-. {( p$ }2 ?. i5 w5 h9 ^6 C4 i7 D3 P7 `$ t
nosis can be established by just a few tests and by# N9 J/ q" u  e6 t
appropriate history. The inability to obtain such a
0 v. v! M6 k5 ihistory, or failure to ask the specific questions, may+ ^5 M0 X8 J+ B* N5 A+ Z+ s
result in extensive, unnecessary, and expensive6 z' @# o* i" N8 _! u& }! t
investigation. The primary care physician should be
( T( ^" `6 l1 U6 n" s$ Xaware of this fact, because most of these children) D# U1 s/ h' n" c+ j" z$ K4 d. h
may initially present in their practice. The Physicians’
. \, i( D3 T/ ^. H9 I2 A4 V; YDesk Reference and package insert should also put a2 _7 G6 \! [5 {* E
warning about the virilizing effect on a male or
7 [4 ?: N6 `; ]) o. S; `4 ]4 \female child who might come in contact with some-
/ C0 h/ A6 m7 ?8 i5 M+ G8 J: Ione using any of these products.
2 v3 o# a& x+ z  p3 V' J3 ~References
- m/ C; b$ ?  `% Q% f1. Styne DM. The testes: disorder of sexual differentiation
$ a0 |: x8 K/ h$ wand puberty in the male. In: Sperling MA, ed. Pediatric
, S% W7 a. z" V6 D% i  {0 iEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
; G+ y1 [5 B+ a2002: 565-628.
) \! L/ i7 n  Q2 d1 n2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious& l- O9 j& o- y9 o9 b& H6 P5 S
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
! t" E5 M9 S% k: o: R# c4 u! HBoy Induced by Indirect Topical
( e0 b+ D. _3 E& t8 y7 M' N* kExposure to Testosterone- t) y* T9 g- x, I8 G# z; Q, ~
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2$ ~" g1 |( T0 R. a# @
and Kenneth R. Rettig, MD19 A) E1 O9 i# I+ j" j% o6 K- Q) v! w
Clinical Pediatrics. t2 f& z+ Z1 V4 h( o
Volume 46 Number 65 N1 q, S  n& z( C1 {; S
July 2007 540-543/ r; V( P% G  Q5 s; x& h* f
© 2007 Sage Publications  u. u: x& a- v+ ]4 s' P
10.1177/0009922806296651
/ F* u' b& F' u5 C8 b# S+ hhttp://clp.sagepub.com4 a$ B/ Q' u2 t) I- P! ]8 e# l; C! `
hosted at
/ {5 t8 F* ?6 @8 Khttp://online.sagepub.com
, q5 ?  O* S! S- _/ |% OPrecocious puberty in boys, central or peripheral,
3 E8 H% O- J, o0 {- iis a significant concern for physicians. Central( |% w/ r* i8 Z$ _9 `8 U  P
precocious puberty (CPP), which is mediated
+ i, m9 h, R, s2 r+ e7 N9 Zthrough the hypothalamic pituitary gonadal axis, has
$ l4 E* i* i+ `$ s' N8 g5 _1 ja higher incidence of organic central nervous system
) I$ D8 F7 l7 l( g7 O' w$ b8 K* Alesions in boys.1,2 Virilization in boys, as manifested, n9 D( Z; _* j: k; C/ h
by enlargement of the penis, development of pubic
( {6 X2 O7 g8 P4 Q, I9 ^; v4 yhair, and facial acne without enlargement of testi-
& ?  h) X, G. Z4 h% F( g) ccles, suggests peripheral or pseudopuberty.1-3 We9 Y1 g: k2 ~/ s+ p* j3 n! W5 X* b
report a 16-month-old boy who presented with the
% L, j. [4 y) r' \" W7 menlargement of the phallus and pubic hair develop-
4 i1 V) {- C; |5 f7 v  h% cment without testicular enlargement, which was due
5 W! v/ k8 W, D! g& Kto the unintentional exposure to androgen gel used by
+ p6 g' |2 Z2 e0 `' Hthe father. The family initially concealed this infor-
) m$ W' A2 b( \& E" }, Bmation, resulting in an extensive work-up for this
7 v/ ^" L( Y: O$ {9 Vchild. Given the widespread and easy availability of' F; X- [" ^( v) R7 @% p
testosterone gel and cream, we believe this is proba-9 }& M: H# ~5 Y4 U0 R( ~  T
bly more common than the rare case report in the8 @  a* W$ k( U: ^7 i+ X, W
literature.42 h8 ~" E6 I; g$ G+ M7 r
Patient Report2 f* I& C/ n  u* ~7 U' s: G5 Y$ q6 d
A 16-month-old white child was referred to the
5 _  ?$ u4 z( H* f& l1 K- X7 Vendocrine clinic by his pediatrician with the concern4 z7 J6 Y# [* l; u% f- `* K
of early sexual development. His mother noticed& h7 i; R' j: W6 i2 |- n) @
light colored pubic hair development when he was
$ F, y' b! ]* _. f# \From the 1Division of Pediatric Endocrinology, 2University of
* Z  E0 X" _, ^! nSouth Alabama Medical Center, Mobile, Alabama.
3 j: E; {( R! ~3 X# _0 w5 GAddress correspondence to: Samar K. Bhowmick, MD, FACE,% e9 y! l; p! [" m2 g, t
Professor of Pediatrics, University of South Alabama, College of
' [$ S% J1 p' f& K0 j  ^Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;4 [8 a. R. M' \# L0 m
e-mail: [email protected]./ o# S9 ~( U2 I8 k9 i4 X) i
about 6 to 7 months old, which progressively became
5 E+ ~  m5 b' J5 B2 |9 Ydarker. She was also concerned about the enlarge-. J9 ^& j4 x3 _$ D' N
ment of his penis and frequent erections. The child
- r3 q2 C1 l5 f) t$ ]& jwas the product of a full-term normal delivery, with
: s( W; W) ?1 m7 g5 ]3 g. C9 k3 Za birth weight of 7 lb 14 oz, and birth length of
4 c, g7 P) }, D7 f6 \20 inches. He was breast-fed throughout the first year
4 Q- i$ n! r( |2 Z# _of life and was still receiving breast milk along with
0 Z. S. b) @% k8 u. `9 fsolid food. He had no hospitalizations or surgery,
4 y/ W' k6 t: z! v, C% vand his psychosocial and psychomotor development
* ?' Q1 ?% H( Q( m$ v# _2 Y" J1 awas age appropriate.1 o2 _$ B9 O! A3 @3 g: ]
The family history was remarkable for the father,! v) u. Q$ m' l8 @! D
who was diagnosed with hypothyroidism at age 16,
: |4 l% t8 z) twhich was treated with thyroxine. The father’s9 V' k4 n. J# @$ Z7 ~
height was 6 feet, and he went through a somewhat
1 z2 `1 P# n( Iearly puberty and had stopped growing by age 14.5 `4 B% ^$ B4 A( k7 h3 l/ T. s
The father denied taking any other medication. The) w+ E* n% g/ z) F1 V; `8 S! Y
child’s mother was in good health. Her menarche" G- |) m0 F, a& H# `1 {3 Z  i
was at 11 years of age, and her height was at 5 feet
( f/ V9 ]1 a3 _3 I1 H5 inches. There was no other family history of pre-
* {, F' q, G- j' Jcocious sexual development in the first-degree rela-
8 d* j+ _, V* ztives. There were no siblings.  F2 ^+ X+ a! _& i: s
Physical Examination% l6 w6 \1 U) {- t5 S& Z- R
The physical examination revealed a very active,
4 b2 E6 Q. n: @) D8 k0 h; pplayful, and healthy boy. The vital signs documented
) C1 O$ {- D' Q' ~a blood pressure of 85/50 mm Hg, his length was+ n% g) V1 r- {% H8 H
90 cm (>97th percentile), and his weight was 14.4 kg
+ R- U% T" {; q( [! o(also >97th percentile). The observed yearly growth
  K& g7 N, Z% vvelocity was 30 cm (12 inches). The examination of4 p  y) o  [' y9 M7 a' {
the neck revealed no thyroid enlargement.
" }3 Y9 ^( s) t( m+ c$ uThe genitourinary examination was remarkable for
- t9 C: l; G/ T+ c! i* v0 renlargement of the penis, with a stretched length of
7 T& W8 g5 q8 g7 p8 cm and a width of 2 cm. The glans penis was very well1 m4 E5 |7 f6 i
developed. The pubic hair was Tanner II, mostly around. R+ a. _( U9 _$ y0 l: ?. K/ T
540
- z# b7 `& w- s5 Zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- b% s7 k$ ~9 A% z6 r; ?" h* Nthe base of the phallus and was dark and curled. The8 i. p- B3 g/ w0 f7 L8 o$ v# J6 `0 `
testicular volume was prepubertal at 2 mL each.
: ^/ f# m" k+ v( W4 oThe skin was moist and smooth and somewhat
1 t) ], b, U9 Q7 G, _! ?$ e& xoily. No axillary hair was noted. There were no0 x3 |, o/ w; q( A5 T
abnormal skin pigmentations or café-au-lait spots.
0 _8 i4 W$ v' w- V1 Y9 w( hNeurologic evaluation showed deep tendon reflex 2+
# t  A2 ?0 C% T' ~* Ybilateral and symmetrical. There was no suggestion
4 O+ y; V' c# L* b/ h- t! Q, Kof papilledema.  q6 a+ }5 V% D; X/ s
Laboratory Evaluation. @" P1 O6 }8 S
The bone age was consistent with 28 months by* N8 @  ^! a% k8 B" M0 g. x% S
using the standard of Greulich and Pyle at a chrono-: h; S2 l1 [, A0 z3 k
logic age of 16 months (advanced).5 Chromosomal
" L7 V. a1 I1 L1 Ckaryotype was 46XY. The thyroid function test* y: Y$ n- P! w" ?% X6 T$ i, b
showed a free T4 of 1.69 ng/dL, and thyroid stimu-9 Z' L; q3 l- J+ w: h% m
lating hormone level was 1.3 µIU/mL (both normal).: Y" V7 ~. Y2 l% J
The concentrations of serum electrolytes, blood9 h8 m& l5 |! x8 Z# C, H3 `
urea nitrogen, creatinine, and calcium all were
, Y0 k' s% K5 b0 Q) Q. B& dwithin normal range for his age. The concentration# o. b1 K8 c* u
of serum 17-hydroxyprogesterone was 16 ng/dL
: E3 A9 h7 ^$ T# j' ](normal, 3 to 90 ng/dL), androstenedione was 20
# C" d! N, I3 r% u+ ?2 q$ Eng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-3 y. c/ d8 T0 {+ F/ \5 h2 b
terone was 38 ng/dL (normal, 50 to 760 ng/dL),+ i. ?  _. p& Z# v
desoxycorticosterone was 4.3 ng/dL (normal, 7 to% F& ^1 X! D3 z0 k7 A% q4 v! X$ t$ K6 [
49ng/dL), 11-desoxycortisol (specific compound S)2 N+ d! c" R6 {; A; Y, A$ F1 j( M7 \
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
4 @5 N% h2 D* X; mtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
, \8 y# d; X" ltestosterone was 60 ng/dL (normal <3 to 10 ng/dL),0 `0 E6 q$ d; X1 P% j8 y
and β-human chorionic gonadotropin was less than
% T9 m. K0 f( R1 y0 w7 R( U" u3 A5 mIU/mL (normal <5 mIU/mL). Serum follicular
+ I1 R& d: n+ Y0 ]7 ystimulating hormone and leuteinizing hormone$ h5 [( [# {% {
concentrations were less than 0.05 mIU/mL8 p* ?% q# g0 q1 E
(prepubertal).
3 E3 j7 O' o/ a8 s, OThe parents were notified about the laboratory/ _8 o1 c& M7 C6 j
results and were informed that all of the tests were
$ ^! Q  e$ {8 n% anormal except the testosterone level was high. The8 |# h1 o3 T- u, _1 F
follow-up visit was arranged within a few weeks to# p" R% h) Z/ |
obtain testicular and abdominal sonograms; how-
- o. e5 ^( d/ Y3 @2 G. jever, the family did not return for 4 months.) m4 w# W3 p0 Y0 {6 b3 b6 ~
Physical examination at this time revealed that the
7 C+ c1 f% N6 \! ochild had grown 2.5 cm in 4 months and had gained- J! O2 q  E' v/ G- X3 f
2 kg of weight. Physical examination remained+ |5 S- U( H6 D0 k  g+ i
unchanged. Surprisingly, the pubic hair almost com-
2 E/ B8 a* Q" `+ X4 zpletely disappeared except for a few vellous hairs at
+ Z0 K5 D6 ]* B1 f/ jthe base of the phallus. Testicular volume was still 2& j6 O# s9 J6 |+ G8 R! ^
mL, and the size of the penis remained unchanged.
' h5 \  c- Q1 @+ @/ ~. j9 iThe mother also said that the boy was no longer hav-
9 _- X) m/ C* y) w9 R1 Ring frequent erections./ [& ]' a; N- `& a; z
Both parents were again questioned about use of1 z4 _" A8 |& n! z( s( J
any ointment/creams that they may have applied to0 C7 m3 Q6 |% u* E
the child’s skin. This time the father admitted the4 W$ B# T! q! p
Topical Testosterone Exposure / Bhowmick et al 541
5 A! ]  Y1 u2 B& ^8 @) C/ Muse of testosterone gel twice daily that he was apply-8 S6 F! j. V0 G2 m  a+ m' B; Z8 K4 `- N
ing over his own shoulders, chest, and back area for4 c. t: |; L/ X) T( A. Z/ n
a year. The father also revealed he was embarrassed
( F, B0 @  \. E/ |to disclose that he was using a testosterone gel pre-5 G: L. L9 H8 q! S6 f6 c$ Z& t
scribed by his family physician for decreased libido4 S6 l1 A- D+ S9 w7 k. |: c
secondary to depression.% h' h8 R9 z" x" L: a6 I
The child slept in the same bed with parents.
$ E- \( K( l  v" iThe father would hug the baby and hold him on his
* _+ G6 j, @2 v* Z" S" M$ j" bchest for a considerable period of time, causing sig-
( s& S/ [2 m' C3 J2 _) h. ?  K* Z: unificant bare skin contact between baby and father.1 I  }# j9 x5 u% I, ~* f
The father also admitted that after the phone call,
5 ~4 k" [$ y" w- Iwhen he learned the testosterone level in the baby+ d, Z/ s6 e, `" n3 G7 t# M
was high, he then read the product information
5 }  w- W6 b: l+ l8 J8 E, Apacket and concluded that it was most likely the rea-* P3 u9 \+ w8 |8 ?. X
son for the child’s virilization. At that time, they( \6 o% j9 z( \3 F  M. x1 f. s
decided to put the baby in a separate bed, and the1 f5 W$ L: v/ ]! l7 |9 u. ~
father was not hugging him with bare skin and had3 e( `+ t" D% P% C9 O' Q
been using protective clothing. A repeat testosterone7 d) {- e& x% S, s6 g
test was ordered, but the family did not go to the  M& u2 U& `8 f" a) A% h/ t/ u
laboratory to obtain the test.( j7 g! n, }1 q% \2 o
Discussion# C  ?! p) W3 b( J2 e, @
Precocious puberty in boys is defined as secondary2 ?+ d- S, [' U8 p
sexual development before 9 years of age.1,4% c0 t& D+ n+ i& e6 e1 ^
Precocious puberty is termed as central (true) when0 t$ s  ~. |! n
it is caused by the premature activation of hypo-+ u6 [* e- U! b5 O$ L/ h1 T
thalamic pituitary gonadal axis. CPP is more com-
1 R" d; S1 {  y" h, ]mon in girls than in boys.1,3 Most boys with CPP# x; `0 a5 p0 l/ E/ \8 C
may have a central nervous system lesion that is
) B3 J: m6 N; J/ Y5 l9 Uresponsible for the early activation of the hypothal-" l1 V  g$ H/ o1 ^$ c1 G- H
amic pituitary gonadal axis.1-3 Thus, greater empha-
* |5 e) s1 b9 Tsis has been given to neuroradiologic imaging in% T8 _5 ?/ P5 ^, J7 g
boys with precocious puberty. In addition to viril-# H* j  {! b4 e+ f
ization, the clinical hallmark of CPP is the symmet-4 C  ]+ T/ K3 P) Q, l$ Z( l, O
rical testicular growth secondary to stimulation by
7 L. w. l3 e( Q! U( \9 Q2 Sgonadotropins.1,3
9 ^9 y7 M% F: RGonadotropin-independent peripheral preco-
- H; v  K# T  S& r$ h/ pcious puberty in boys also results from inappropriate
, C8 G8 Z7 I9 C; f. L; Oandrogenic stimulation from either endogenous or
/ {. N8 z+ @- l2 yexogenous sources, nonpituitary gonadotropin stim-  F; q; H/ a- Z
ulation, and rare activating mutations.3 Virilizing8 s7 R* W- N; w! m* A& E
congenital adrenal hyperplasia producing excessive
4 @5 k! v8 `( K; x8 k  i  }# f9 H* `4 ?5 Dadrenal androgens is a common cause of precocious! {0 H1 B0 ?' ]5 T5 z, y0 ?
puberty in boys.3,4" P, ~) x8 W8 ^) H6 C& \
The most common form of congenital adrenal
7 q" O8 q  R$ n$ Ehyperplasia is the 21-hydroxylase enzyme deficiency.
2 M" k* X. S6 |; iThe 11-β hydroxylase deficiency may also result in
6 V* F! j( J" H- s' q: ]1 D% j* \excessive adrenal androgen production, and rarely,# F! e1 @+ b* ^* k, Z7 z
an adrenal tumor may also cause adrenal androgen4 z7 P! x8 q2 T4 M8 j8 j
excess.1,3
: o6 q4 }5 b% [( |( Pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 T; F6 @5 J  N; k& W1 N- S7 ~
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
. }4 ]( h2 q& zA unique entity of male-limited gonadotropin-6 e6 N! A" Q7 U! |2 j
independent precocious puberty, which is also known1 M" m- x& |1 c/ `% P
as testotoxicosis, may cause precocious puberty at a8 k: @6 p* u/ `" [1 u
very young age. The physical findings in these boys
, `, R  Q  V, i& J- s3 [with this disorder are full pubertal development,
4 {5 m# A) d* g- N* v$ z  ?1 hincluding bilateral testicular growth, similar to boys
3 `7 b7 X* J9 Hwith CPP. The gonadotropin levels in this disorder
" k. D$ K: J3 Y; a, d2 bare suppressed to prepubertal levels and do not show
8 o5 E4 H) S( l9 Jpubertal response of gonadotropin after gonadotropin-
! y/ p2 \! O  q2 O5 Q/ j* D2 Hreleasing hormone stimulation. This is a sex-linked5 \- m+ M' q9 V1 q% M- b
autosomal dominant disorder that affects only
$ E+ Q4 g. M1 J8 jmales; therefore, other male members of the family4 K$ h$ X7 s7 P* v! t# i. t2 d2 ]
may have similar precocious puberty.35 K2 O1 a* V5 e) x/ R5 W
In our patient, physical examination was incon-5 T$ ^7 ]( O9 |
sistent with true precocious puberty since his testi-
4 ~* _8 q( ?- w$ ~1 X6 Mcles were prepubertal in size. However, testotoxicosis
; v" R' x, F' ]5 _7 Cwas in the differential diagnosis because his father" ?3 }0 x/ ?0 K! A
started puberty somewhat early, and occasionally,& r. ]( ~  k$ g) O* p+ j
testicular enlargement is not that evident in the
7 g! X, M" p" ~% d; t9 {- obeginning of this process.1 In the absence of a neg-
2 ]$ t1 [' M0 n( ]ative initial history of androgen exposure, our  N# s. m5 e5 j6 T8 C/ d1 W" h
biggest concern was virilizing adrenal hyperplasia,  ]4 O+ e; a+ W  V/ o
either 21-hydroxylase deficiency or 11-β hydroxylase/ O7 z* {" z: K+ S/ h% ^* G6 ^
deficiency. Those diagnoses were excluded by find-4 Z8 |0 B  ?. a9 e: N' U. |( z, T
ing the normal level of adrenal steroids.7 o, G+ C1 @& m) U- |. {1 x# W2 F
The diagnosis of exogenous androgens was strongly
/ v# o3 I& ~9 b& O( M( _& tsuspected in a follow-up visit after 4 months because
; t7 e3 m5 e! g0 t0 Z" Dthe physical examination revealed the complete disap-
. W" H5 H# d. T9 U& J. t' d: Apearance of pubic hair, normal growth velocity, and- ~+ `: ~$ q; z, W8 G2 O+ D
decreased erections. The father admitted using a testos-
( A6 ]) H2 d' Q; i2 x9 Sterone gel, which he concealed at first visit. He was" [" q: N0 `2 `8 k. k6 F  R
using it rather frequently, twice a day. The Physicians’
% p, u, Z# y$ ~, @7 |* i1 V! H% FDesk Reference, or package insert of this product, gel or/ G+ _" D( w6 S9 g  t& t) v
cream, cautions about dermal testosterone transfer to3 ~/ B5 t8 M0 \: b* F; }) u
unprotected females through direct skin exposure.
* p3 S0 T/ ~4 Z" g3 \Serum testosterone level was found to be 2 times the$ e; Y. Z4 d' O4 q$ Y; q# z5 v
baseline value in those females who were exposed to% ]) J9 i2 l5 u( F
even 15 minutes of direct skin contact with their male/ o( A1 v- c* v/ ]; ?+ X5 Y& h1 _
partners.6 However, when a shirt covered the applica-
+ d1 N: L3 B4 l* ]4 E9 Y2 qtion site, this testosterone transfer was prevented." P4 o& ~4 y" [+ d) L7 w8 R$ [
Our patient’s testosterone level was 60 ng/mL,8 H, Z, B, q) I* ?
which was clearly high. Some studies suggest that- @7 `5 j! J+ c. f$ j6 C7 Z$ K
dermal conversion of testosterone to dihydrotestos-
& J( v: t9 B! Z! S7 H! |  @5 Sterone, which is a more potent metabolite, is more
% z0 o3 U+ Z) P" M( K8 d4 ~/ U/ F7 cactive in young children exposed to testosterone
4 k4 ^( d; X/ p. Kexogenously7; however, we did not measure a dihy-0 {- c  V) \* s, w* \. d
drotestosterone level in our patient. In addition to- t: t2 l/ b! k+ t3 J8 [* H
virilization, exposure to exogenous testosterone in. [7 g8 l" c# ~+ L6 U) q
children results in an increase in growth velocity and& J2 c2 Z+ L8 a0 R9 {( l: j: p* {
advanced bone age, as seen in our patient.
. p+ y4 w3 C: |. b/ U0 s0 OThe long-term effect of androgen exposure during3 x! v# L  r6 Q7 d% z9 p# J
early childhood on pubertal development and final) h7 ]- {" v3 Q* n* S
adult height are not fully known and always remain$ t4 @' O! M8 o  O3 `) K6 `3 @3 {
a concern. Children treated with short-term testos-
& S6 Z3 N2 ~9 q7 mterone injection or topical androgen may exhibit some1 d$ r. E/ l, z) W
acceleration of the skeletal maturation; however, after2 r  c' z4 ]  r, B4 U+ \, G
cessation of treatment, the rate of bone maturation
5 G* {8 p6 v! C# Z" N7 U, {decelerates and gradually returns to normal.8,9& _+ i' }8 Q" n# E4 g
There are conflicting reports and controversy
( G; F$ n# o( s" k+ fover the effect of early androgen exposure on adult7 M" {6 k6 B5 B0 u: ~
penile length.10,11 Some reports suggest subnormal
7 I9 K1 [! }8 k* ], v5 dadult penile length, apparently because of downreg-2 Z3 {5 G; F- i. u3 ]
ulation of androgen receptor number.10,12 However,
. x1 i# Y! c1 Z. DSutherland et al13 did not find a correlation between
; V$ I4 y! c6 e% j' V6 U- ~childhood testosterone exposure and reduced adult9 p$ l( a3 x% `
penile length in clinical studies./ ?  D$ p" s: m
Nonetheless, we do not believe our patient is$ V- y: A; |' I$ @
going to experience any of the untoward effects from
  e- l) W* i" l* d) }% stestosterone exposure as mentioned earlier because' n* T/ S3 n0 A6 E0 M
the exposure was not for a prolonged period of time.
, D, L7 s  \7 |8 h3 p3 \/ rAlthough the bone age was advanced at the time of
+ v* r/ _- [% Bdiagnosis, the child had a normal growth velocity at" O$ y' O2 _, _
the follow-up visit. It is hoped that his final adult
. T  g) v+ O5 E! w$ jheight will not be affected.
0 `& o( o0 x+ m- }4 FAlthough rarely reported, the widespread avail-
3 G2 a% B# }' W  vability of androgen products in our society may: H# |9 G; ?1 b7 z5 F, u
indeed cause more virilization in male or female  {$ Q: t1 {1 U6 x3 J+ M: x
children than one would realize. Exposure to andro-% q2 i! C; Y0 c5 W' X
gen products must be considered and specific ques-
, O) K- d7 n% ]! H5 s; e9 itioning about the use of a testosterone product or) U) T9 H5 R7 v3 X! p
gel should be asked of the family members during: w/ Z$ f# R/ n- W0 U+ O7 R, A
the evaluation of any children who present with vir-
' |5 o% Z7 }/ o+ }, J- K, k7 yilization or peripheral precocious puberty. The diag-
1 }3 G; R4 D' d8 pnosis can be established by just a few tests and by
# S/ S1 n% s  R# T4 xappropriate history. The inability to obtain such a2 L3 v/ b7 k. Y1 _
history, or failure to ask the specific questions, may
: e- C8 \3 @- B+ ?& \result in extensive, unnecessary, and expensive/ Z" b* y2 N/ e
investigation. The primary care physician should be
- L1 a' Y! e) o8 E8 Z0 caware of this fact, because most of these children: B* K* {1 \! r, u5 J4 L
may initially present in their practice. The Physicians’1 J- {$ M7 `. I! k
Desk Reference and package insert should also put a; E/ N, A3 I" Z  U. ^
warning about the virilizing effect on a male or$ X% V. X# `9 r5 S
female child who might come in contact with some-# g$ f6 t4 ^& E! [2 p2 o
one using any of these products., j; L7 G6 n. Q
References
) f' T; d1 x+ D' T1. Styne DM. The testes: disorder of sexual differentiation. N# `# g& g( j! h3 d( p& q, o, y
and puberty in the male. In: Sperling MA, ed. Pediatric8 J  ~. i* l$ M0 v
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
* X4 O5 {8 m$ q) @6 ^2002: 565-628.
, ~, i) K, B! l. t7 U& J2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
- \+ @( s  J/ F& \1 c" c% r$ v* Cpuberty 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

1 A8 c: A3 Y7 W1 O4 J, W, y- L' R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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