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Sexual Precocity in a 16-Month-Old. z  n" ^% u4 J( p7 x/ V
Boy Induced by Indirect Topical
0 a( ~& n  Q' S1 W3 j  k% T) s! f( fExposure to Testosterone9 L/ H0 K1 a- I4 ?
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2/ y/ o6 f: f) b  C: O- s
and Kenneth R. Rettig, MD1
$ A  d$ a; t# w5 J% u' NClinical Pediatrics
- A1 h- O: q+ H2 h2 VVolume 46 Number 6
8 z0 Z* W' s+ R! B# W* uJuly 2007 540-543
# V! g: S  C6 ~© 2007 Sage Publications
# `" |3 Z1 {5 D10.1177/0009922806296651
. c! A9 y5 k+ j/ j5 z/ Zhttp://clp.sagepub.com
( [  W* l+ g6 ?5 qhosted at/ [+ r  ~! n8 |
http://online.sagepub.com
9 q4 e% p) d" I6 B+ {( r& rPrecocious puberty in boys, central or peripheral,1 {9 m$ o5 V0 X1 C3 C' i
is a significant concern for physicians. Central& a3 y7 V- x9 G/ h
precocious puberty (CPP), which is mediated8 ]( U" ]/ A$ ?$ b7 C
through the hypothalamic pituitary gonadal axis, has: A! U# V6 z0 n, f+ B- |0 x6 D
a higher incidence of organic central nervous system7 G( Y6 l6 q& L) A2 F/ ~; a
lesions in boys.1,2 Virilization in boys, as manifested% @& Z! _7 F) I, s( i: R" c5 r* q- P
by enlargement of the penis, development of pubic% G$ ?5 i' ~7 R+ u7 r( S
hair, and facial acne without enlargement of testi-
1 g/ m1 ?1 L( n3 z; Lcles, suggests peripheral or pseudopuberty.1-3 We
6 X7 ]; B% M! P3 ?5 Creport a 16-month-old boy who presented with the( {+ j0 E$ t+ J! u  s; Y2 L
enlargement of the phallus and pubic hair develop-' F3 J0 c" Q% E; v: q+ X
ment without testicular enlargement, which was due
# @- \/ H  `3 U+ P' b$ C9 Qto the unintentional exposure to androgen gel used by
9 v( l7 L. t$ L* zthe father. The family initially concealed this infor-) M5 {/ y5 G2 j  |  F
mation, resulting in an extensive work-up for this4 _) S! D; U7 o, a! p6 @
child. Given the widespread and easy availability of
: H5 o7 c- l) _testosterone gel and cream, we believe this is proba-
) U, b9 w0 K: P3 u% U. fbly more common than the rare case report in the
" A9 ]7 E+ e5 `4 ^" B2 ^' Xliterature.4. O! _" ]: p0 n4 I& i" S! S$ f7 w2 g
Patient Report7 x8 J" d3 \- ?/ q" W
A 16-month-old white child was referred to the# w; `8 n" `% ~" @
endocrine clinic by his pediatrician with the concern1 P9 a& u, R  ?: A; B0 u6 \
of early sexual development. His mother noticed) e6 @1 W- N" l1 A6 L
light colored pubic hair development when he was
1 p5 Q: c- _; q' \7 Z, @; oFrom the 1Division of Pediatric Endocrinology, 2University of
2 t: C8 I4 `8 v  P0 MSouth Alabama Medical Center, Mobile, Alabama.
& P/ K7 Z! u# @5 `% |2 G+ NAddress correspondence to: Samar K. Bhowmick, MD, FACE,! D4 w; ]4 C9 f# y, x- p3 \5 C9 _
Professor of Pediatrics, University of South Alabama, College of/ P+ W& L/ L, A- C; p2 i3 U/ r( w% F
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;" F3 Z* x+ j" X8 ^% _) |3 f9 `& ^
e-mail: [email protected].
  V( _. p+ Z% I9 _$ ?6 a# Aabout 6 to 7 months old, which progressively became
/ y, N( |2 K( odarker. She was also concerned about the enlarge-9 p5 n2 r1 i* E. i
ment of his penis and frequent erections. The child
; g$ m+ S) q! m) g2 J, R. dwas the product of a full-term normal delivery, with+ K7 w9 _6 R4 }% a# R
a birth weight of 7 lb 14 oz, and birth length of/ W7 o8 B& o0 N- q8 x* i! u# P
20 inches. He was breast-fed throughout the first year7 }" D  Z& \, a/ @6 b
of life and was still receiving breast milk along with
! [4 N. N' y. Q: j/ w5 M; ysolid food. He had no hospitalizations or surgery,
' e8 \5 S$ `1 sand his psychosocial and psychomotor development
; M# d, ?0 [  F" uwas age appropriate.
0 V2 [& V1 O5 }! X* P( pThe family history was remarkable for the father,
* k' O7 }2 {7 w7 E2 ~; twho was diagnosed with hypothyroidism at age 16,
1 j. g8 c  |6 y# S8 S* k, Cwhich was treated with thyroxine. The father’s
, P8 z7 C5 z0 q! {) Nheight was 6 feet, and he went through a somewhat
; ], y1 D" z* Nearly puberty and had stopped growing by age 14.) w$ M5 H0 P1 i% ]+ h, y
The father denied taking any other medication. The
: M* T6 z. f2 ]( V! D) j  N; Xchild’s mother was in good health. Her menarche
9 ~5 v1 L+ S- X) ^  B- y, Gwas at 11 years of age, and her height was at 5 feet9 [* P. A* F4 U" `7 v
5 inches. There was no other family history of pre-
0 p' b# A7 I1 {2 @  b* Q4 D" J# J$ Fcocious sexual development in the first-degree rela-
7 c8 P5 P. \' Q( h5 |tives. There were no siblings.
% _: Y' ]+ A' J: x6 u# hPhysical Examination- J) ]1 j( p: u7 g6 v3 O# \$ M
The physical examination revealed a very active,
+ W0 z  \% _- e5 L, fplayful, and healthy boy. The vital signs documented
- c* j# O& @& S5 Ma blood pressure of 85/50 mm Hg, his length was
) f1 T3 z- _: O- K* j7 z# R' V5 D3 {90 cm (>97th percentile), and his weight was 14.4 kg
# L6 O% V# m: ]) |! z' ?8 ](also >97th percentile). The observed yearly growth5 K) f$ `9 L6 `; b$ Z
velocity was 30 cm (12 inches). The examination of
  f) I, B: `5 q& \) P: I. ~the neck revealed no thyroid enlargement.
- M* u/ V/ b: \$ yThe genitourinary examination was remarkable for! B. [0 u9 K- S9 Y* T) F4 a" i) W+ t
enlargement of the penis, with a stretched length of5 v$ u) G9 E- B& H/ C  _# [
8 cm and a width of 2 cm. The glans penis was very well, T; i4 c  V/ d+ D) A* e8 c& F
developed. The pubic hair was Tanner II, mostly around$ E7 M8 c9 Z5 c1 r/ N3 P
540) ^3 x4 P' U5 G  v# ?' R' D! z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 ]5 |. A/ V9 h
the base of the phallus and was dark and curled. The
, a/ Y8 j% {7 I& R1 ]7 G  otesticular volume was prepubertal at 2 mL each.6 x, \0 h& ]) {) Z" r0 @
The skin was moist and smooth and somewhat* X% k0 w' J" t2 R' x
oily. No axillary hair was noted. There were no7 K" r7 h; Z! F: D5 v
abnormal skin pigmentations or café-au-lait spots.
5 |- X4 e' ?" d# N- d* k+ \Neurologic evaluation showed deep tendon reflex 2+; q% l" f- r% Z
bilateral and symmetrical. There was no suggestion
* D/ b( K( M4 Z% J8 sof papilledema.& K0 ]* d6 v# j9 r6 J6 ?$ m/ z
Laboratory Evaluation( X9 E5 C4 q7 G! t' e
The bone age was consistent with 28 months by
/ I% Z0 l1 _$ z3 fusing the standard of Greulich and Pyle at a chrono-* E$ ]7 D: h, z, v  d
logic age of 16 months (advanced).5 Chromosomal
+ m0 E5 O8 Z+ N: L/ r: o$ [& xkaryotype was 46XY. The thyroid function test
, R  X! G- z, _! f: H) P# e1 H6 Nshowed a free T4 of 1.69 ng/dL, and thyroid stimu-1 f- A- m/ G) _  G) ?( b2 y
lating hormone level was 1.3 µIU/mL (both normal).
& e8 k4 b. r9 k' t8 \; JThe concentrations of serum electrolytes, blood5 n, ^; e* M! x
urea nitrogen, creatinine, and calcium all were- O& s! N$ u) Y6 u
within normal range for his age. The concentration
2 V: C, e2 w5 P$ {5 ?! ~3 f7 xof serum 17-hydroxyprogesterone was 16 ng/dL
+ L6 l  U# H. W  n* s(normal, 3 to 90 ng/dL), androstenedione was 20
! i( W2 }4 R1 `7 H7 Z5 N2 F" i* @3 z2 kng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-% ?$ _% t3 U, x) t
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
) j* L+ J0 P. x: m& i! Qdesoxycorticosterone was 4.3 ng/dL (normal, 7 to( k, k: L! \5 j) v
49ng/dL), 11-desoxycortisol (specific compound S)0 ^& _0 S  I. i. A" F( o( o  s
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
9 E* ~) y* r' F4 ytisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
* w+ M/ k! b5 S) `testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
: y% ^8 X+ j0 z3 _and β-human chorionic gonadotropin was less than
# l( G: \7 P  _; S* u2 _3 K) `5 mIU/mL (normal <5 mIU/mL). Serum follicular/ {" e* \" @- }
stimulating hormone and leuteinizing hormone
& ]3 |5 m+ {, c! \" p( S- tconcentrations were less than 0.05 mIU/mL: k% m5 k& W1 _. O* S; k# F1 y5 r
(prepubertal).; q# z/ O% l- n: g
The parents were notified about the laboratory
* X( Y& i8 D  E4 U/ S0 |results and were informed that all of the tests were& P# B: W; R7 H8 T2 z/ `
normal except the testosterone level was high. The- b2 D1 c, d2 [+ \$ H0 k9 _4 A
follow-up visit was arranged within a few weeks to
7 I9 m4 U! H* _+ V& R6 {4 {, }obtain testicular and abdominal sonograms; how-
* x" \; S3 f4 I0 T7 M2 q& e. v5 Q+ `) oever, the family did not return for 4 months.+ J% Y% V6 N7 p8 _3 F; ^6 D9 S
Physical examination at this time revealed that the
9 P5 M) e: P8 ~; V6 R- b% N* S8 jchild had grown 2.5 cm in 4 months and had gained3 }$ I6 ?1 e7 J! o( {" x" Z2 H( F
2 kg of weight. Physical examination remained
2 `/ s  A' r1 r5 U1 P2 Aunchanged. Surprisingly, the pubic hair almost com-1 \) u& h; j6 v) O) `. I
pletely disappeared except for a few vellous hairs at& X8 I* W4 W* A
the base of the phallus. Testicular volume was still 2% l% _9 d6 b4 E" L* d
mL, and the size of the penis remained unchanged.
8 V% X, K/ N: a% x6 `3 V. B/ f$ K6 VThe mother also said that the boy was no longer hav-
& U/ }. L; s/ ]' aing frequent erections.. K$ n3 s/ f' w4 t
Both parents were again questioned about use of7 O; k( |# N& B" W! y
any ointment/creams that they may have applied to5 n2 B; A$ T' V3 u* p3 j1 T
the child’s skin. This time the father admitted the
* }# K# ]* V  F4 W. E9 g; oTopical Testosterone Exposure / Bhowmick et al 541
5 j& t, ^9 k8 o: ]% e* G# yuse of testosterone gel twice daily that he was apply-7 J. e! `; v9 e4 z) u$ g" R' ]
ing over his own shoulders, chest, and back area for
( ]% T& `. u3 T; L" g* f" }a year. The father also revealed he was embarrassed& Q( Q. S( \% L- K$ g% J9 ^! y7 T
to disclose that he was using a testosterone gel pre-$ [# A  u( [' v: h" h2 @) @
scribed by his family physician for decreased libido* S1 K; E$ l  o3 A' E- d. M
secondary to depression.4 x7 e" ^3 ~- P' U1 D
The child slept in the same bed with parents.8 O) j7 n( W6 O6 Y5 @2 z  u: e
The father would hug the baby and hold him on his
8 M& h% O  W% Q; C1 r" uchest for a considerable period of time, causing sig-
( \7 s) Z3 P& z; v* D) T: U% ^nificant bare skin contact between baby and father.
- p) A  b7 H' LThe father also admitted that after the phone call,. Q) g2 c' H  R4 d
when he learned the testosterone level in the baby* v0 i3 n; }0 K2 t& |8 K
was high, he then read the product information( H7 P' H/ L/ e8 T9 b
packet and concluded that it was most likely the rea-# d, I9 V( D6 O2 z
son for the child’s virilization. At that time, they
2 L; S$ g' j6 [% Fdecided to put the baby in a separate bed, and the3 J1 j0 x5 x- R5 b) _6 V
father was not hugging him with bare skin and had. J5 S+ h# d7 F1 ?2 ^4 j  q
been using protective clothing. A repeat testosterone
2 l9 O# U! b2 G! P. r8 q- T1 S' D) _test was ordered, but the family did not go to the0 H0 p6 T, {' L
laboratory to obtain the test.- B1 p/ D0 f* N! g0 n
Discussion
1 e1 C& Z$ K  e$ m' J0 {- CPrecocious puberty in boys is defined as secondary& h. m* A6 w- V5 i7 A2 s4 i
sexual development before 9 years of age.1,4: S# j+ C. O2 D5 o2 M7 Z+ M7 F
Precocious puberty is termed as central (true) when. b; [7 V0 U5 K& p/ S7 z% H& \% ~
it is caused by the premature activation of hypo-6 {9 r: }) r7 c+ i9 U1 Y
thalamic pituitary gonadal axis. CPP is more com-% S, m( _: ]$ m8 w  }( K1 c
mon in girls than in boys.1,3 Most boys with CPP
7 R# E/ h; |1 pmay have a central nervous system lesion that is/ R* ?; Y9 S/ H; }% k) w! @) {
responsible for the early activation of the hypothal-
- G( u& @+ |& famic pituitary gonadal axis.1-3 Thus, greater empha-
( k, M8 K' {% G0 k) v  Asis has been given to neuroradiologic imaging in/ G) E% Z0 t; y# Z) g- Y, b, ?) d: b
boys with precocious puberty. In addition to viril-3 j. d2 I, i8 q! B6 y6 G- s
ization, the clinical hallmark of CPP is the symmet-
; n( K& ^- `* [' A. W8 z4 b1 Jrical testicular growth secondary to stimulation by+ F" T5 e) F% P* K% ^9 r; q3 t' X
gonadotropins.1,3
+ g  O% {. A2 w! e; l8 a/ YGonadotropin-independent peripheral preco-
( k/ `, {) ]: K: E  i, ]3 ocious puberty in boys also results from inappropriate& m: I, ?6 U9 y
androgenic stimulation from either endogenous or$ C0 t- U. D) F6 f- k. P# E1 ]
exogenous sources, nonpituitary gonadotropin stim-. W7 U: m) d8 Y7 |) s7 F1 V$ q- U
ulation, and rare activating mutations.3 Virilizing
' k1 @+ U% N. [/ ?0 kcongenital adrenal hyperplasia producing excessive
3 I; f. r2 Z* o, Z0 |) {# o0 q/ ]6 Padrenal androgens is a common cause of precocious$ ~2 x$ n: i! \9 x
puberty in boys.3,43 B' A3 ~1 [, `" z2 ]
The most common form of congenital adrenal
; \' R/ ?$ D6 y2 jhyperplasia is the 21-hydroxylase enzyme deficiency.
5 @% @* ?+ H* qThe 11-β hydroxylase deficiency may also result in# Z& {, U2 U! l/ d* }! N1 T
excessive adrenal androgen production, and rarely,
; W9 p9 e- x7 l. j. B) ]  b8 Pan adrenal tumor may also cause adrenal androgen# X1 O6 l3 S' H0 M% z/ a" n
excess.1,39 u4 S& k; ~/ N- A' x' G1 T
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
% k! y7 t% y8 o6 V2 h# a542 Clinical Pediatrics / Vol. 46, No. 6, July 2007' c! \' G0 q3 S
A unique entity of male-limited gonadotropin-4 R5 J5 R' \& N1 a+ N% ?8 P/ z
independent precocious puberty, which is also known
7 Q0 H( C  j" J8 [$ yas testotoxicosis, may cause precocious puberty at a) r5 ?% a* M! o
very young age. The physical findings in these boys
' n$ [, X% G, R1 V2 Hwith this disorder are full pubertal development,2 Q* p! v& ~$ |' {! {$ i
including bilateral testicular growth, similar to boys8 R. r* ~2 H) l' l% k' l  _' I
with CPP. The gonadotropin levels in this disorder( s* D/ s! K& @$ b
are suppressed to prepubertal levels and do not show, L  ^4 r2 I8 T
pubertal response of gonadotropin after gonadotropin-
) F; C0 u/ E% ]releasing hormone stimulation. This is a sex-linked  D3 l, R8 @4 Z/ @
autosomal dominant disorder that affects only
) P$ q  K9 o' x# z! dmales; therefore, other male members of the family1 {* r5 B. l7 W% P0 z: J; k6 t
may have similar precocious puberty.3( G! F5 G1 Z- L5 K3 ?" \
In our patient, physical examination was incon-4 G/ z3 k- P% N8 {
sistent with true precocious puberty since his testi-( N+ }. H  N9 t# q; u4 |  l
cles were prepubertal in size. However, testotoxicosis+ P% ~0 w- A& M0 Y$ V
was in the differential diagnosis because his father- n" z& {  P' E
started puberty somewhat early, and occasionally,
: B& E9 h' Z2 B8 k4 Q+ T5 F- `2 |% Y, xtesticular enlargement is not that evident in the
( Q% F& {1 E1 }* V8 @beginning of this process.1 In the absence of a neg-
4 j# S: P2 T. K) D% B4 @ative initial history of androgen exposure, our
9 B( r3 a' o- C* vbiggest concern was virilizing adrenal hyperplasia,' _! M5 I7 X9 e  e/ h, v( _8 q9 j
either 21-hydroxylase deficiency or 11-β hydroxylase
) o; z: u* C0 Hdeficiency. Those diagnoses were excluded by find-3 j0 f5 B+ o6 P: Q
ing the normal level of adrenal steroids.
: o- D  }" f- H) o& }' c! ZThe diagnosis of exogenous androgens was strongly
+ Y5 b* W* x9 N4 Z! wsuspected in a follow-up visit after 4 months because
+ C, J5 @+ q+ B# i3 Ythe physical examination revealed the complete disap-
: O- A$ d9 B. O5 y* z% A/ W5 spearance of pubic hair, normal growth velocity, and# G; `9 r0 H! D  U% h9 W
decreased erections. The father admitted using a testos-# Z6 y4 Q; y; R% O' W2 T
terone gel, which he concealed at first visit. He was
6 f5 l/ Y7 U* p* @5 dusing it rather frequently, twice a day. The Physicians’
, H3 C4 @: W, G4 P9 S" yDesk Reference, or package insert of this product, gel or
, X1 O' h& T9 Q, V! j; jcream, cautions about dermal testosterone transfer to
* H" ]  k* ]" N" }9 C+ |5 Q8 Bunprotected females through direct skin exposure.
+ v0 e  E  T; `% ^; o# @Serum testosterone level was found to be 2 times the
( \# o) }  U* B( _# z0 ?6 Cbaseline value in those females who were exposed to6 |) L! Z% l( D
even 15 minutes of direct skin contact with their male7 v6 _5 r( I; G
partners.6 However, when a shirt covered the applica-- }) T( D' U# p6 n  x$ o
tion site, this testosterone transfer was prevented.; K% h) t5 g+ Y* A
Our patient’s testosterone level was 60 ng/mL,3 i( w  x' ?* w  f3 M8 v
which was clearly high. Some studies suggest that4 j# Z! i7 _$ g; X$ a
dermal conversion of testosterone to dihydrotestos-5 X5 T3 ~, F5 T4 V) {7 S0 j
terone, which is a more potent metabolite, is more0 }8 [* I5 d+ l! p2 Y2 y1 I! _
active in young children exposed to testosterone
" R1 ]! Q; \) J6 t# B% X" Kexogenously7; however, we did not measure a dihy-& ?9 Y- q7 W4 u7 a! Z8 d
drotestosterone level in our patient. In addition to+ a! T. w/ _# _$ y" t# U2 H
virilization, exposure to exogenous testosterone in
1 r, U( A2 M; ^# k2 A: f' nchildren results in an increase in growth velocity and# P& S6 V, j4 o) P7 [- @. ?
advanced bone age, as seen in our patient.
3 v* V3 U" I& `. K) s3 }6 AThe long-term effect of androgen exposure during
2 N7 n+ I  w3 L- Iearly childhood on pubertal development and final; I' B* {$ E  E' D; D0 A
adult height are not fully known and always remain
- L) P' t3 z8 ~0 Ba concern. Children treated with short-term testos-7 W* ^$ w# W9 J
terone injection or topical androgen may exhibit some
, P+ g; D! Q" W. \0 O0 M$ dacceleration of the skeletal maturation; however, after. m) Z/ `3 _# A- i5 m* f9 V5 ~! e
cessation of treatment, the rate of bone maturation
( G1 L) g3 t% q1 L/ T% ~decelerates and gradually returns to normal.8,9
0 L+ P5 X/ f! C, h. |( R+ iThere are conflicting reports and controversy8 I3 C0 a( E* Y, F# |  }# g
over the effect of early androgen exposure on adult  o' N* c1 @" s1 s' K
penile length.10,11 Some reports suggest subnormal* T- P) m- y( d/ q* K4 x4 k
adult penile length, apparently because of downreg-( b5 i9 l& M; d/ c4 i/ @4 A0 v
ulation of androgen receptor number.10,12 However,
/ ]( N2 v6 N  H  C+ T. K4 q* zSutherland et al13 did not find a correlation between
$ o  e, I" @+ @9 hchildhood testosterone exposure and reduced adult' S3 w- s7 ]& `
penile length in clinical studies.
" `% p$ v5 E5 C  H2 s) jNonetheless, we do not believe our patient is
4 Z( s' w( K! L: k5 W' Rgoing to experience any of the untoward effects from
3 |5 z7 e( E; b0 l  g" s- }testosterone exposure as mentioned earlier because' r% f+ \4 g/ U1 p/ V: L9 y( `
the exposure was not for a prolonged period of time.
2 b% P  z" [3 ^' RAlthough the bone age was advanced at the time of
; @; e% J' d2 S6 A3 pdiagnosis, the child had a normal growth velocity at8 P3 [2 X1 e. [$ ^) X; ?8 `
the follow-up visit. It is hoped that his final adult' a5 ^3 D8 e9 f' J! r$ j% R: o9 ?
height will not be affected.
( B" I5 X9 B) ~, S4 L& AAlthough rarely reported, the widespread avail-! a* _! j4 D) V6 r) y+ h" X
ability of androgen products in our society may4 T9 Q% D. H3 ]  U  S+ ^4 z
indeed cause more virilization in male or female
) c/ u, M! j4 L- [& Kchildren than one would realize. Exposure to andro-
; u: ?" v/ B8 C6 Jgen products must be considered and specific ques-, {9 T! I5 M/ J$ C
tioning about the use of a testosterone product or% B0 k6 X' c6 h
gel should be asked of the family members during: U1 Z5 \: w; c
the evaluation of any children who present with vir-3 |, z! @1 Z! R7 x6 I9 B, c
ilization or peripheral precocious puberty. The diag-
! _9 }$ T# E/ o% ?nosis can be established by just a few tests and by" b8 |  X- W! y0 m
appropriate history. The inability to obtain such a- z7 k  h' M( E! v
history, or failure to ask the specific questions, may
3 Y0 W4 l3 k2 o6 Z; e4 sresult in extensive, unnecessary, and expensive
, n; l8 |5 N; i, ]3 R; O6 {investigation. The primary care physician should be$ Z" U: d8 m' l8 Q" p
aware of this fact, because most of these children
/ i$ a/ R7 X& o  g/ ^may initially present in their practice. The Physicians’2 U$ J, i8 N" t
Desk Reference and package insert should also put a
& @1 b9 d2 y9 b1 iwarning about the virilizing effect on a male or
% v- T/ X2 s" ^- f, H- X5 cfemale child who might come in contact with some-
1 ]$ l4 n: J6 x/ Z' S  bone using any of these products.
! U2 E) d, o' w& SReferences
# l5 W( B  U, o& _1 S6 e1. Styne DM. The testes: disorder of sexual differentiation+ G8 y+ T7 E- r
and puberty in the male. In: Sperling MA, ed. Pediatric/ @& ^, L/ H6 x; }( H  Y& W
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
6 v  ~, a- }  X) p3 V% L$ e2002: 565-628.0 B( h: d# ^6 p
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
2 ]# \# T: T' I/ I( `puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
( v0 j6 _( B# S* u, i* Y) FBoy Induced by Indirect Topical! W+ \9 d: c; R) Y
Exposure to Testosterone0 J# d' Z# @4 s8 p7 v
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 q; r( h: k) r" y& q3 @* sand Kenneth R. Rettig, MD17 o! F) K9 X! ~7 W
Clinical Pediatrics
% M7 {- c$ ], R2 K5 \Volume 46 Number 6
- Z7 s7 h" r7 Z5 E# |July 2007 540-543: i( |2 X; ^! M, u
© 2007 Sage Publications" K2 Y( [" m- _% v( o$ d* |* Z: _
10.1177/0009922806296651+ D7 y, W! ?  [0 s
http://clp.sagepub.com
: J8 h! Z5 Q6 ?9 thosted at
0 @! L3 {5 O1 x3 x  N! |http://online.sagepub.com
0 ]8 k6 O: K- m. u9 TPrecocious puberty in boys, central or peripheral,
1 N3 m' o0 e* f5 y" Dis a significant concern for physicians. Central5 Q$ O4 ~- G5 a1 L, `4 S
precocious puberty (CPP), which is mediated
% B4 g( b$ R" ]  Othrough the hypothalamic pituitary gonadal axis, has) E# q; ?9 B; j8 a
a higher incidence of organic central nervous system
/ E$ G$ o$ \2 B  J, e1 y- a$ |lesions in boys.1,2 Virilization in boys, as manifested
1 H5 \, M' ^9 n' q4 Tby enlargement of the penis, development of pubic' B5 `+ P1 o+ B8 ]8 |  i1 V
hair, and facial acne without enlargement of testi-
, X! ~' m; a# t. h" X: n/ Ncles, suggests peripheral or pseudopuberty.1-3 We& {- _5 I, u8 n- i
report a 16-month-old boy who presented with the
. S# p7 W! C8 @. Z# senlargement of the phallus and pubic hair develop-
# n2 Y/ }- N) E% j' [( ement without testicular enlargement, which was due
9 R7 I$ `" n: {6 a7 I4 s8 M* g3 yto the unintentional exposure to androgen gel used by
" c* U" g7 n' S& N) dthe father. The family initially concealed this infor-: D2 c* E% y2 ?
mation, resulting in an extensive work-up for this
$ H" a' M& B( g+ \1 O9 c# achild. Given the widespread and easy availability of
8 Y! n8 Y& M0 T- c' z, n; O3 \) mtestosterone gel and cream, we believe this is proba-
8 O9 L  n3 ]* N5 Wbly more common than the rare case report in the
& }% Y$ H( ^- I: v* G( i7 pliterature.4- ~9 _4 n9 K# ~. B1 P! Y
Patient Report6 {6 e) o; \6 X2 c5 M; ]: b
A 16-month-old white child was referred to the
7 n  f- K2 {, Y7 o9 uendocrine clinic by his pediatrician with the concern
3 T6 e+ P' T- y( O7 G1 zof early sexual development. His mother noticed5 D$ a/ J8 ]- W( l3 s& F6 N
light colored pubic hair development when he was
2 ]+ _8 f; V5 B# B9 M( v" I' kFrom the 1Division of Pediatric Endocrinology, 2University of) ]  R- S( [+ U8 r* B1 ^
South Alabama Medical Center, Mobile, Alabama.
2 [) ~6 n8 B- u: X( G; c1 n2 T9 _Address correspondence to: Samar K. Bhowmick, MD, FACE,
  K# `$ ^1 q( p9 A; X: ]" mProfessor of Pediatrics, University of South Alabama, College of+ G  ~; }, T( b$ H( ~# F/ d- A! X
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;' O" ^0 `/ c, U" t
e-mail: [email protected].5 f* i9 ]! K7 \) F% r2 f) K
about 6 to 7 months old, which progressively became8 u9 o) F4 o1 C( i
darker. She was also concerned about the enlarge-
7 Q3 ]2 g% u. qment of his penis and frequent erections. The child
! |5 N+ r0 Q+ e0 N* s2 t" F5 r" [! ^, Rwas the product of a full-term normal delivery, with
! p- b! g. B) C: I( G9 v6 Ka birth weight of 7 lb 14 oz, and birth length of  G9 ]8 @( g! T- ^
20 inches. He was breast-fed throughout the first year
* s: c$ c$ G  C; Sof life and was still receiving breast milk along with; p+ |% J" T+ B1 G6 b9 O
solid food. He had no hospitalizations or surgery,9 Q0 e- m' U% ?9 C4 a( \& p
and his psychosocial and psychomotor development2 d# K% G: P6 ]$ m
was age appropriate.2 U" A, h, g& q5 f" V( e
The family history was remarkable for the father,
7 V, m' C' m' l. `) @. {who was diagnosed with hypothyroidism at age 16,
( c$ Y5 T& {) S5 V( vwhich was treated with thyroxine. The father’s" r: @3 Q) Q$ d; ^8 J; ~
height was 6 feet, and he went through a somewhat4 v" K; M+ L* B1 T/ ~& a+ h4 n* {
early puberty and had stopped growing by age 14., h! w) N, I4 v4 p$ }5 C
The father denied taking any other medication. The: P# _/ }7 k" X% O- q) A5 U# Q0 c' ~
child’s mother was in good health. Her menarche" s+ N& k& E/ ~1 F( d) y" c
was at 11 years of age, and her height was at 5 feet* P/ \  g4 X3 J/ h4 y
5 inches. There was no other family history of pre-
: P" b) y4 E, c* F- e1 ncocious sexual development in the first-degree rela-! {$ y" r( {+ p7 V0 ^8 `
tives. There were no siblings.
9 h7 |. ?! ~" O: z7 H% A- ?Physical Examination
. I/ A1 s& e$ \; J, J) hThe physical examination revealed a very active,
$ o8 [8 `0 ^4 p. D, Cplayful, and healthy boy. The vital signs documented( \4 Z  k% j8 R: q5 Z( A
a blood pressure of 85/50 mm Hg, his length was
' U5 ]% C: M; }, ]4 x+ Q5 J90 cm (>97th percentile), and his weight was 14.4 kg
7 d! r! h2 J- l1 a! h(also >97th percentile). The observed yearly growth6 s, Z! g2 ?0 M! v$ s1 N
velocity was 30 cm (12 inches). The examination of* ~: w# z+ E% }
the neck revealed no thyroid enlargement.: J' i& Z) U/ c. \$ W! n0 z0 b
The genitourinary examination was remarkable for. A# J1 c1 ~) s2 |3 P8 Z! e  {
enlargement of the penis, with a stretched length of
* F! `$ H9 n( ~1 j8 cm and a width of 2 cm. The glans penis was very well
8 O- L3 h$ E0 ^1 xdeveloped. The pubic hair was Tanner II, mostly around  [  u7 ?! T0 h- `# H5 f4 {
540" F. q8 u5 H1 l( i3 Z2 b/ y4 ^
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' Y( E& T2 L) S3 P% v, Ythe base of the phallus and was dark and curled. The
4 s7 F) T! i5 l8 `( Ltesticular volume was prepubertal at 2 mL each.5 L3 b9 W& n# A# c+ Y. P; C5 ?* d8 h
The skin was moist and smooth and somewhat
. i& _0 G* U- P# @oily. No axillary hair was noted. There were no, m' }0 T0 v! P7 ~& h( `
abnormal skin pigmentations or café-au-lait spots.
, m. b* \( _0 O2 kNeurologic evaluation showed deep tendon reflex 2+
% _( E- \+ }! c, Hbilateral and symmetrical. There was no suggestion
$ [) F7 X; s6 d9 D) D; r7 `of papilledema.  y- f: [) z) c% y1 V
Laboratory Evaluation) F; c! ]6 w; j4 l
The bone age was consistent with 28 months by) A1 g  b8 l7 t
using the standard of Greulich and Pyle at a chrono-4 D4 b8 g9 W8 ~  q  N! J% D0 k% Z, P
logic age of 16 months (advanced).5 Chromosomal! ~0 e& ^$ z& B- R
karyotype was 46XY. The thyroid function test
+ W; H& K3 M) l) f+ Wshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
) t& w* {0 O9 a" B; Q* r6 Qlating hormone level was 1.3 µIU/mL (both normal).
3 V. S" }" h7 MThe concentrations of serum electrolytes, blood
) ]* Q6 i5 t2 g) R- p  }urea nitrogen, creatinine, and calcium all were- w8 a# i! ]% O  U1 k  Y. y7 f
within normal range for his age. The concentration* V. c4 H! E- Z5 A1 R
of serum 17-hydroxyprogesterone was 16 ng/dL
& i$ |( q/ ^) L- u. d# |(normal, 3 to 90 ng/dL), androstenedione was 205 r6 M! X4 M3 k; z6 }
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
* `: x& w. a. U/ d# d  ?% U( @terone was 38 ng/dL (normal, 50 to 760 ng/dL),& @% h5 \- A; v3 R% Z
desoxycorticosterone was 4.3 ng/dL (normal, 7 to7 `( g, O& A$ {# B7 R  b: L
49ng/dL), 11-desoxycortisol (specific compound S)) U) y1 q9 o% I4 W
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-7 M% q( F6 e8 ]
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
9 A9 M& G" y9 d' Utestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
; g! K+ o! L2 g5 p( Fand β-human chorionic gonadotropin was less than- y4 M1 U" S& }# k
5 mIU/mL (normal <5 mIU/mL). Serum follicular
& y  L9 G$ I$ h  Y7 b% E6 Y2 X- hstimulating hormone and leuteinizing hormone
0 c4 p% \5 j! ?. k8 Dconcentrations were less than 0.05 mIU/mL: I6 s" _3 K/ F  Z: _9 i( m* H
(prepubertal).
: m, n3 o% t0 u8 y  j2 S5 zThe parents were notified about the laboratory
9 ^! I+ P' m& `$ J4 R9 Z" Gresults and were informed that all of the tests were) `% E8 i2 r1 {1 A0 h
normal except the testosterone level was high. The
8 D$ j3 a6 L1 l* P& P' ~follow-up visit was arranged within a few weeks to- l. J; }, P/ U* l3 [
obtain testicular and abdominal sonograms; how-
1 Y& u% P' Y) c  ]ever, the family did not return for 4 months.
3 w0 i7 l) _3 qPhysical examination at this time revealed that the+ Z# e' Q6 U2 Q- [% r9 i
child had grown 2.5 cm in 4 months and had gained" U2 \' Q5 R% U/ t& t+ M
2 kg of weight. Physical examination remained
* v" ~. R5 @- H3 ~& q  [unchanged. Surprisingly, the pubic hair almost com-
/ E0 ^: q% s9 u7 T. spletely disappeared except for a few vellous hairs at
" b8 Q" \7 E' I( q$ @' [the base of the phallus. Testicular volume was still 2' C; K& b% ~0 i8 E: M- g( B
mL, and the size of the penis remained unchanged.) r3 F6 f2 B; }$ V7 r
The mother also said that the boy was no longer hav-
% J: e7 p/ m* r9 ^ing frequent erections.
1 s" u9 p( }/ I7 N+ _/ ]7 MBoth parents were again questioned about use of) y. R/ y5 h. S
any ointment/creams that they may have applied to8 K% i* L8 I: o+ V# c! {6 o( q3 m
the child’s skin. This time the father admitted the
+ I, o+ z6 r& g9 CTopical Testosterone Exposure / Bhowmick et al 541
* u% y9 O+ X0 _6 I! [/ n0 |( f5 g- ?use of testosterone gel twice daily that he was apply-& [1 q" H2 U5 O! M4 _& t% V
ing over his own shoulders, chest, and back area for% ]$ y& M5 o5 Z
a year. The father also revealed he was embarrassed
+ \0 Z) c% v. y& Lto disclose that he was using a testosterone gel pre-
' p: L2 J1 N, s+ z- `: \1 \scribed by his family physician for decreased libido3 A4 o1 M# Y- S3 I* v
secondary to depression.
6 \6 \$ _7 ^( p; |* F9 wThe child slept in the same bed with parents.
: {1 r! j9 a5 M. m& WThe father would hug the baby and hold him on his! c) j9 @* W7 k$ E& S
chest for a considerable period of time, causing sig-
8 g* Z% D3 g; V7 h# [& dnificant bare skin contact between baby and father.
8 n6 W* r8 _: e1 I3 V& B8 pThe father also admitted that after the phone call,' u$ c, r% j- d( c* D/ l% [
when he learned the testosterone level in the baby
7 X* d% y/ ]& c0 U" P' qwas high, he then read the product information
& e7 V6 i& `+ k! p3 z; G$ M0 Epacket and concluded that it was most likely the rea-
, h( {6 q; p3 r8 Tson for the child’s virilization. At that time, they7 N( l( k* v0 C  L/ n( r1 K. G
decided to put the baby in a separate bed, and the
+ U# l5 L# U: Q! O# o" M5 Vfather was not hugging him with bare skin and had
! ]2 S) t3 K3 M% z* V0 }8 p) V; ?been using protective clothing. A repeat testosterone
8 s9 r# b3 e5 p% M6 }) T6 F4 htest was ordered, but the family did not go to the, }& q, P3 Z  \& s% A$ k2 n, J
laboratory to obtain the test.
" z& D; B+ H( J% B8 R& tDiscussion% F0 S8 k. z- d
Precocious puberty in boys is defined as secondary
2 B) s; J5 h; e: t9 }sexual development before 9 years of age.1,4- N) Q. f& R, i0 V  z% X% M5 c
Precocious puberty is termed as central (true) when' I$ b# e  p, i! i8 D+ T4 }( c
it is caused by the premature activation of hypo-& L- ~, D5 Q! `% k; N
thalamic pituitary gonadal axis. CPP is more com-2 C9 C/ L! q: `+ [1 [
mon in girls than in boys.1,3 Most boys with CPP! o# H# I! m' c* B1 `" Z6 N' H
may have a central nervous system lesion that is. e/ o  ^7 U2 E+ n  G7 y& r+ Z
responsible for the early activation of the hypothal-' ?( O1 `) S* c, |# G, p
amic pituitary gonadal axis.1-3 Thus, greater empha-' S6 c4 {- h1 k' ]
sis has been given to neuroradiologic imaging in7 m9 o' j9 @$ S- ?/ X: S- F6 D
boys with precocious puberty. In addition to viril-
6 S+ a# t% Z9 \0 q% t# E3 Tization, the clinical hallmark of CPP is the symmet-
/ V6 k3 U. e6 L* t3 b- V/ Urical testicular growth secondary to stimulation by, H: C  g$ x- U4 N
gonadotropins.1,38 p; U7 Y% V2 w1 q! S
Gonadotropin-independent peripheral preco-
+ h: w4 o. ^! r4 P2 B9 B' Ecious puberty in boys also results from inappropriate
1 h% g) Q- j/ z! s9 \' nandrogenic stimulation from either endogenous or4 I4 f9 t3 d% J0 ?- ?$ W
exogenous sources, nonpituitary gonadotropin stim-
7 P( r2 ?; g5 Wulation, and rare activating mutations.3 Virilizing5 W0 _9 x+ B9 M1 v
congenital adrenal hyperplasia producing excessive
1 p' w/ N1 d! y7 M! z( T# @  C' Nadrenal androgens is a common cause of precocious
1 p8 x0 Q7 E* F( Q6 ~puberty in boys.3,4
* Z0 z  R: k' l0 uThe most common form of congenital adrenal1 W# n: b" k' R) v
hyperplasia is the 21-hydroxylase enzyme deficiency.
1 {) ^$ ^. W! n! F, V$ ^2 VThe 11-β hydroxylase deficiency may also result in; _  J- u' Z. M5 P
excessive adrenal androgen production, and rarely,
: h2 b8 c6 O; W) N6 j4 l! Ian adrenal tumor may also cause adrenal androgen$ V1 @, d3 `. t& f/ Q* G
excess.1,3; ]8 P) A$ [8 U) m* R  Y' i
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ s9 b& V/ f1 Q" g6 K" ?" A542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
, {7 ?# O( f6 G3 sA unique entity of male-limited gonadotropin-
) R* |' \8 m! }. b% f  I/ k3 uindependent precocious puberty, which is also known
& j' g) _$ K1 y+ c. I8 B9 las testotoxicosis, may cause precocious puberty at a
/ f" h# H! O0 M- q. K; x, l( ?very young age. The physical findings in these boys* y7 I' @& X. v- O" f
with this disorder are full pubertal development,; r' U7 H# J3 @# S
including bilateral testicular growth, similar to boys
4 B: L" e0 G+ f/ N- \0 Z. Kwith CPP. The gonadotropin levels in this disorder
( {- W4 g/ b4 Uare suppressed to prepubertal levels and do not show
3 g  m% n5 p. t# Z- E! q0 ]- a" vpubertal response of gonadotropin after gonadotropin-3 U6 |1 Q! U2 D
releasing hormone stimulation. This is a sex-linked
# h7 @+ C8 [% ]" w* eautosomal dominant disorder that affects only" ~0 }8 D2 \) j
males; therefore, other male members of the family
1 e+ U  n; X# i( N; Fmay have similar precocious puberty.3
. w/ I: C) p( c9 ~3 D6 FIn our patient, physical examination was incon-
+ |  a3 R9 E% z# ]7 jsistent with true precocious puberty since his testi-
% n5 \* ?- `2 dcles were prepubertal in size. However, testotoxicosis; w. l0 s9 P) |* ?  R
was in the differential diagnosis because his father
7 Y! n2 _8 Y. w- M: H! m# Astarted puberty somewhat early, and occasionally,0 d0 x* d, z) g; w. C5 F: B
testicular enlargement is not that evident in the4 c" X7 V3 |* Y# o% H' c; Z# Z
beginning of this process.1 In the absence of a neg-4 n1 ?) n: D, _
ative initial history of androgen exposure, our- ?2 S; I5 T, w
biggest concern was virilizing adrenal hyperplasia,$ @( q! E+ |) }& \+ H8 }- a, ]
either 21-hydroxylase deficiency or 11-β hydroxylase
+ U; |, {5 @6 O* tdeficiency. Those diagnoses were excluded by find-
9 i. \2 p/ @% i+ ?! t, Hing the normal level of adrenal steroids.
1 E: Y) }& W& ^+ ~/ g! dThe diagnosis of exogenous androgens was strongly
. A* }& G/ T, X, _  ]8 [2 V7 Asuspected in a follow-up visit after 4 months because9 Z8 P: l" `9 n, i
the physical examination revealed the complete disap-
! ]9 M! `0 h+ V: G. W4 Npearance of pubic hair, normal growth velocity, and
# G) u, j" M  _1 z3 Qdecreased erections. The father admitted using a testos-; O* }4 h- d, k. }
terone gel, which he concealed at first visit. He was
- f, j: d6 L) {; M( I+ ?. busing it rather frequently, twice a day. The Physicians’1 W' r4 `5 n# r  m* D+ Y0 d
Desk Reference, or package insert of this product, gel or2 @7 {# q1 g) ]% j% x8 w& k! |8 ?  U
cream, cautions about dermal testosterone transfer to1 o5 S1 G0 F5 C
unprotected females through direct skin exposure.
$ q, n7 m7 O: S; K9 n9 r! rSerum testosterone level was found to be 2 times the. D" Q' O9 [8 y
baseline value in those females who were exposed to1 }/ _# B( N  T# r
even 15 minutes of direct skin contact with their male0 [* W6 |* \# S9 E- F
partners.6 However, when a shirt covered the applica-4 ?% s8 @' q$ V# {6 l
tion site, this testosterone transfer was prevented.
# r0 Q& y) G. }5 ~* a, ~Our patient’s testosterone level was 60 ng/mL,) K8 e" O3 Y% {1 g2 ]
which was clearly high. Some studies suggest that
) V) N8 f8 T& q+ d: }* hdermal conversion of testosterone to dihydrotestos-9 {4 h- R3 F7 f9 f3 `6 H
terone, which is a more potent metabolite, is more
# \. ?8 L1 E( Q" qactive in young children exposed to testosterone% q0 G. M8 t: ~) x& C4 j
exogenously7; however, we did not measure a dihy-& }# ^5 H# Z: g2 ^/ c8 ^
drotestosterone level in our patient. In addition to" j- [  X# S+ [7 x8 x) ?
virilization, exposure to exogenous testosterone in6 O$ }3 q! h3 |4 ?+ s
children results in an increase in growth velocity and
; U; r" B1 B" N9 P3 A* Sadvanced bone age, as seen in our patient.; E) c# D/ K& c; z
The long-term effect of androgen exposure during
+ p* h: G5 Q; G8 R2 ]& \early childhood on pubertal development and final
8 i3 z0 m% r$ B3 {5 Q! Eadult height are not fully known and always remain
$ ]. J3 ]# F6 `a concern. Children treated with short-term testos-
" z7 _4 U& r6 g. d/ U% R# n) z$ tterone injection or topical androgen may exhibit some
. X8 j( l/ _5 c0 o; n& Nacceleration of the skeletal maturation; however, after1 t/ G/ V2 \/ t9 p7 g+ ?
cessation of treatment, the rate of bone maturation
' b/ e0 x1 G1 L5 @) rdecelerates and gradually returns to normal.8,9
6 y$ N6 I4 `* ~. }- J/ r9 rThere are conflicting reports and controversy7 T" a9 G! X8 C8 t2 e
over the effect of early androgen exposure on adult
% d- H6 p2 @: e7 S: |penile length.10,11 Some reports suggest subnormal
- J0 }8 e8 c0 V0 X# q- x" {- x+ O/ Eadult penile length, apparently because of downreg-$ ~: @; |5 [  c: ^& M* j% X4 |7 U3 {
ulation of androgen receptor number.10,12 However,
- F2 }/ k! N) F4 R. w2 n) g% ?- HSutherland et al13 did not find a correlation between
0 S6 E* p0 _! g9 r$ t/ C1 [childhood testosterone exposure and reduced adult
9 e  n4 J! q) x8 E0 |+ c2 E, s! upenile length in clinical studies.7 u1 r* G# o: i+ E0 i
Nonetheless, we do not believe our patient is
. V' A$ b: n7 k. Bgoing to experience any of the untoward effects from8 u1 [* d" @& h( S7 T+ M1 {
testosterone exposure as mentioned earlier because$ {0 Q4 l, o3 l- \9 \# r7 t
the exposure was not for a prolonged period of time.
, g; A& |2 X% V# ?2 xAlthough the bone age was advanced at the time of' [  [) t) Y4 I7 m5 B$ e, Y* p
diagnosis, the child had a normal growth velocity at
8 Q: M6 r% Y4 P" m7 `& Bthe follow-up visit. It is hoped that his final adult
# r3 j7 Q) t) V/ I2 Eheight will not be affected.' _6 l7 x2 w  g, u# f
Although rarely reported, the widespread avail-7 r: t# f' j: @8 ?  _0 Q  a
ability of androgen products in our society may9 ?4 j2 r6 ]* Q- R: y* l- r1 `8 f
indeed cause more virilization in male or female
4 U% u4 Q2 j  O# k, schildren than one would realize. Exposure to andro-( p7 {; b: X" R
gen products must be considered and specific ques-" e' Y% P5 H, ?6 X, T" s9 t' T
tioning about the use of a testosterone product or
5 s( u' i8 i0 w7 V# u: Ngel should be asked of the family members during
4 j' ?& b0 l6 a0 t  c7 ]; ]the evaluation of any children who present with vir-( F! Q. ~+ @' x
ilization or peripheral precocious puberty. The diag-* ], ?: O' H: {& L. g
nosis can be established by just a few tests and by
+ @; L' p0 m: ?# B' \appropriate history. The inability to obtain such a
& M% @' w6 Y/ [8 `- nhistory, or failure to ask the specific questions, may; q$ B2 f  j$ Y, [- _8 [9 c
result in extensive, unnecessary, and expensive2 q, L% C  w2 L7 w: v
investigation. The primary care physician should be  m" x1 i  p( i; u$ D: s& M
aware of this fact, because most of these children
: k4 J/ J  I! p$ ?' `may initially present in their practice. The Physicians’
' k/ c! |+ z) t* u8 QDesk Reference and package insert should also put a
7 M& g9 c! G5 O# f" Owarning about the virilizing effect on a male or
: G. K0 M, Y, H; o6 }4 i; `: xfemale child who might come in contact with some-3 }8 T/ I: g* d9 r6 s) T
one using any of these products.2 l' q9 b* g" Q! O; O! I+ X4 J
References9 e% \# D" }# J" T
1. Styne DM. The testes: disorder of sexual differentiation
# ?( }/ K& H) B( nand puberty in the male. In: Sperling MA, ed. Pediatric
! _4 L# S0 U  J* H/ t) s' rEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;& r1 q- o* @. z9 X# R
2002: 565-628.8 \+ @6 e6 K% |& v2 N( [2 V# G5 o0 w
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
+ V9 C" U4 S1 v( g( m% 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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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

) K6 U* D  y: `8 a$ g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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