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Sexual Precocity in a 16-Month-Old2 H4 O9 o6 i5 Q' j
Boy Induced by Indirect Topical
9 U* F9 c  Z4 l: n$ c5 vExposure to Testosterone  r  ?3 x5 Z, b- ~3 n* @$ ]9 \0 C
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,20 w7 V( M$ i, Q) R
and Kenneth R. Rettig, MD16 Z/ |! ^% H7 @& E2 r
Clinical Pediatrics# ~5 I% l  H" z7 ^2 Z$ v
Volume 46 Number 6
( A: h/ o& B4 t8 ~- [July 2007 540-543
. M. I/ k0 w( F8 i0 k2 _6 T© 2007 Sage Publications
7 K3 ^+ X: {) S  n/ O5 _1 V- |" Z10.1177/0009922806296651" q& ?. T3 {8 x9 r# C) y
http://clp.sagepub.com
% `! e% @3 [$ \" g& J' C. d7 f) Chosted at9 r. {% X7 _1 q
http://online.sagepub.com
9 t3 X. u: `- J$ ~! xPrecocious puberty in boys, central or peripheral,
$ B3 E7 `# ]3 _3 Yis a significant concern for physicians. Central0 T8 N4 O! ~8 p8 D- r6 d* `3 W
precocious puberty (CPP), which is mediated
# Q2 q  ]3 y: c% Hthrough the hypothalamic pituitary gonadal axis, has
* ~$ {8 R7 {/ m9 G) za higher incidence of organic central nervous system
) |+ {, W* e' o% @6 plesions in boys.1,2 Virilization in boys, as manifested
( Y& d) J' x; p3 x3 Lby enlargement of the penis, development of pubic
9 a# y. j7 l# F" ~2 bhair, and facial acne without enlargement of testi-
3 U4 u4 s! i8 C/ Q  ?0 q: scles, suggests peripheral or pseudopuberty.1-3 We
1 Y1 D7 V  z; q) mreport a 16-month-old boy who presented with the
) }! q. C; K5 j' m; h" ~$ venlargement of the phallus and pubic hair develop-
+ k# L. U: @8 j# T) Z  x, O1 bment without testicular enlargement, which was due
2 B& Q1 w; u2 X& h  {8 Y. n. Hto the unintentional exposure to androgen gel used by
7 X+ P8 O" p- j' u2 i2 R: kthe father. The family initially concealed this infor-! V3 S& `# l7 [; V6 D, [5 S
mation, resulting in an extensive work-up for this
4 V4 j$ [5 ]3 f) a6 Q; }9 }child. Given the widespread and easy availability of
- V" G! Z, a% M; Ktestosterone gel and cream, we believe this is proba-
" f4 R3 K5 q* h2 j6 J: Fbly more common than the rare case report in the/ u6 e9 I4 O( |, `
literature.4, E5 m( A' r$ T4 G/ A/ O+ h+ k& g
Patient Report
6 O5 V' n- o, sA 16-month-old white child was referred to the: p# W! y' N* l# J
endocrine clinic by his pediatrician with the concern
+ q2 N- f" r. kof early sexual development. His mother noticed, L" L# z& |4 i& |* L% G
light colored pubic hair development when he was( w$ q9 Q: `; D- f$ ~
From the 1Division of Pediatric Endocrinology, 2University of/ o& k2 g0 s0 t' c; b$ L
South Alabama Medical Center, Mobile, Alabama.: t) ^  _, z' |- D
Address correspondence to: Samar K. Bhowmick, MD, FACE,: ]9 d1 X; L0 [9 I
Professor of Pediatrics, University of South Alabama, College of
4 V# y" P( |0 i5 S: dMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;; U+ c, K! r5 \, X9 g7 p/ }
e-mail: [email protected].
7 P8 H4 k6 G0 q' E. N1 ]about 6 to 7 months old, which progressively became
: Y; s, N# `9 ~2 Jdarker. She was also concerned about the enlarge-6 g" \. H! `! D& j6 H: a# o! ?
ment of his penis and frequent erections. The child
% j+ R5 f8 Y; x8 e$ swas the product of a full-term normal delivery, with
! C8 _4 \& Y8 Q+ X4 I5 k, h' Ha birth weight of 7 lb 14 oz, and birth length of3 L: A' A8 u: W- {# h/ [
20 inches. He was breast-fed throughout the first year
( j% I. j2 s& f, c/ cof life and was still receiving breast milk along with
, v1 t3 m% ]- g* p) Ysolid food. He had no hospitalizations or surgery,
4 y: I# W2 w3 R$ |: v2 S0 land his psychosocial and psychomotor development
# _3 r" Y: j4 ~. Uwas age appropriate.# x: {' I: r, o7 z
The family history was remarkable for the father,- |9 w5 z+ Q1 M; N
who was diagnosed with hypothyroidism at age 16,
  i8 R4 i& d1 ]which was treated with thyroxine. The father’s1 N( d; P9 c# U& l3 A9 N
height was 6 feet, and he went through a somewhat
: N; x4 Z' D4 V  [, ^3 r5 Rearly puberty and had stopped growing by age 14.
6 `9 V; t' ?; w6 F4 xThe father denied taking any other medication. The# o+ Q" }3 ]0 ?; ?/ r9 s) |0 L
child’s mother was in good health. Her menarche
, r! f8 k& p2 \% V' n& f1 Swas at 11 years of age, and her height was at 5 feet( ]+ X3 Y, k0 o/ F5 H
5 inches. There was no other family history of pre-
* I$ V% ^$ v$ H& W" ^* {+ O7 mcocious sexual development in the first-degree rela-
4 _( ~$ X0 V: W8 p' h# L% u+ ytives. There were no siblings.
9 s  C4 v8 `7 {$ NPhysical Examination9 @( [% Z8 L) O% }7 C& Q
The physical examination revealed a very active,  [; \$ r/ m$ G- s( R0 q" f; D: r9 D
playful, and healthy boy. The vital signs documented: \/ ?1 l6 n& Z! ]8 ^. |
a blood pressure of 85/50 mm Hg, his length was6 b( C& A+ r% x( z
90 cm (>97th percentile), and his weight was 14.4 kg
: F9 d4 h, m2 [6 `4 d: e. U; v(also >97th percentile). The observed yearly growth
" m% ]! P3 i- f1 ~, G0 {5 G" gvelocity was 30 cm (12 inches). The examination of
1 H! v0 }: T7 }) Othe neck revealed no thyroid enlargement.- f( }# K4 Q" a7 `6 M
The genitourinary examination was remarkable for; E- G5 L2 P& Y# ?& T
enlargement of the penis, with a stretched length of
" D( j! g8 n1 _2 V/ K9 C8 cm and a width of 2 cm. The glans penis was very well
8 `4 E' Y1 t7 i* E7 v$ z* edeveloped. The pubic hair was Tanner II, mostly around; d! c$ \# o, Q1 u1 j: y" r
5409 b8 \- ^8 i0 ?3 y; j8 @
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 _6 X& F# Y5 P: q+ w8 k6 M
the base of the phallus and was dark and curled. The- s4 c- w/ \6 S4 [
testicular volume was prepubertal at 2 mL each.
, O" f- T$ I3 _/ V# GThe skin was moist and smooth and somewhat
$ ~5 @9 `) m" m/ Voily. No axillary hair was noted. There were no
, i' X- K0 r# ?6 mabnormal skin pigmentations or café-au-lait spots.: \' |, s% ~3 }6 O6 M7 f3 F
Neurologic evaluation showed deep tendon reflex 2+
  l' O9 E0 P6 O7 ^  s: Dbilateral and symmetrical. There was no suggestion
- o& R- H! e) \; ^1 Iof papilledema.
  t+ S4 g+ Q& W# N& n9 _Laboratory Evaluation
4 W4 h. F. X3 g8 YThe bone age was consistent with 28 months by
( }; P* @. u7 S, Iusing the standard of Greulich and Pyle at a chrono-
! a1 A3 G6 R. T4 y5 klogic age of 16 months (advanced).5 Chromosomal4 ]# Y0 I4 ^3 n9 F5 ]7 i
karyotype was 46XY. The thyroid function test
: ?. {, I( E  a5 V/ D) X$ ashowed a free T4 of 1.69 ng/dL, and thyroid stimu-
: u& u2 |) \# S3 v& ^# m' @lating hormone level was 1.3 µIU/mL (both normal)./ t; T/ C' c/ z) {, L
The concentrations of serum electrolytes, blood
; A: ?3 \9 x! k$ p# C/ A% W4 M; ?7 B1 curea nitrogen, creatinine, and calcium all were' f/ c% c6 ?0 @6 c( V3 c  \
within normal range for his age. The concentration+ ~& g7 b6 ?5 Q. M% b/ {0 `
of serum 17-hydroxyprogesterone was 16 ng/dL. [! {/ g- `/ [
(normal, 3 to 90 ng/dL), androstenedione was 20; `9 m- A1 V4 K* Q) H6 e
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
6 `6 a$ [5 J! M5 m( L& \% H( Lterone was 38 ng/dL (normal, 50 to 760 ng/dL),* l+ }/ K/ w5 k  k: f5 x
desoxycorticosterone was 4.3 ng/dL (normal, 7 to9 \. V. ]( N. K; Q5 l  P
49ng/dL), 11-desoxycortisol (specific compound S)2 Z% X9 F9 X+ y' w
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
7 @6 m6 S+ N, T  |8 U9 qtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total/ P; s0 }6 O2 t& }8 i, q/ G/ Y
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),* y8 g3 r3 u& q" {
and β-human chorionic gonadotropin was less than
/ ^/ A- U( g7 W' }5 mIU/mL (normal <5 mIU/mL). Serum follicular0 S. m; q$ ?5 I" ^9 ^; M
stimulating hormone and leuteinizing hormone- Z# }$ |5 m/ t0 ?; H
concentrations were less than 0.05 mIU/mL  e+ P& h" Y1 Y: `+ y5 e
(prepubertal).  I) l7 Y4 Q/ Y- t9 q! b' w
The parents were notified about the laboratory
7 \3 D9 w9 f: a4 ?3 k9 @# t) d7 rresults and were informed that all of the tests were6 {2 z* u# g6 N# t; ]# h) Y! E
normal except the testosterone level was high. The# {, E' p: e9 y  v4 U7 Q
follow-up visit was arranged within a few weeks to; t- d6 Z8 r9 i5 \1 w' D; N4 i# H
obtain testicular and abdominal sonograms; how-- z. [6 e# d' _
ever, the family did not return for 4 months.
; a- b  L3 C) Q# YPhysical examination at this time revealed that the2 |; `- H% m* Z1 f' r& \+ c% g
child had grown 2.5 cm in 4 months and had gained1 Q* X' z/ Q# l1 @, T/ y; V
2 kg of weight. Physical examination remained
( }$ b0 `: y* h# m3 I4 ^unchanged. Surprisingly, the pubic hair almost com-6 x; P# K( _8 S) M
pletely disappeared except for a few vellous hairs at
; C. X: y1 O# |' [4 d) j. T2 Lthe base of the phallus. Testicular volume was still 2% t' L7 M0 }. b4 W, u1 E, _7 G
mL, and the size of the penis remained unchanged.
9 H$ Y2 w/ J" IThe mother also said that the boy was no longer hav-/ }( L6 ^0 P! N: H
ing frequent erections.
. d: M) U( E4 l8 E4 p! b+ n* pBoth parents were again questioned about use of
2 i; b' r  F# i3 yany ointment/creams that they may have applied to
0 z, E0 N. c/ ]3 R* _the child’s skin. This time the father admitted the3 e9 |( H1 U3 Z# w! a  v
Topical Testosterone Exposure / Bhowmick et al 541
/ n$ ~8 N' N" w* o4 t5 j9 l$ {3 luse of testosterone gel twice daily that he was apply-5 F! `. M7 R8 o- V; x
ing over his own shoulders, chest, and back area for
9 ~7 L) j5 f1 n% ]" F4 La year. The father also revealed he was embarrassed
, E7 z5 Q, v7 J9 A( Y. J4 Ito disclose that he was using a testosterone gel pre-' Y2 p# p1 k( R/ \$ x* Y( g
scribed by his family physician for decreased libido
$ z& m: x! ]' U" d# k3 dsecondary to depression.7 q4 u- k: c; ?% A7 ]8 B
The child slept in the same bed with parents.
& |6 [5 Z7 O1 z$ P5 z. nThe father would hug the baby and hold him on his" T: G1 q: c3 y( D1 ]2 v' J
chest for a considerable period of time, causing sig-
, H0 ?! h+ D0 B5 T4 u  knificant bare skin contact between baby and father.
% `& n* }0 C: D: d) A! G5 l0 c! N5 BThe father also admitted that after the phone call,! K( w. Q. r3 A$ ^2 e9 S" {# d
when he learned the testosterone level in the baby
3 e7 n1 g3 W; E  O/ x8 r$ `* Vwas high, he then read the product information
8 n9 D  T. ?9 }packet and concluded that it was most likely the rea-5 u, x* _% ?1 N$ ~5 S
son for the child’s virilization. At that time, they
, N& p: [& M5 E% Adecided to put the baby in a separate bed, and the3 t* r$ G- g, k
father was not hugging him with bare skin and had4 S1 ]& J0 i4 g  |6 _
been using protective clothing. A repeat testosterone- \; R/ V" L  W; x5 z- B; h, M
test was ordered, but the family did not go to the0 }) |; h" T' x! q# i
laboratory to obtain the test.
5 h. U  s+ m/ ]; IDiscussion- u  L8 ?) L8 ?' {
Precocious puberty in boys is defined as secondary
$ K' ]7 S* b* Z* P& k4 @# c1 Isexual development before 9 years of age.1,4
9 M% R8 T1 l1 q4 K! p' X  u, i6 ]Precocious puberty is termed as central (true) when. v( n" @6 V' Y0 w2 q
it is caused by the premature activation of hypo-
7 Y5 W$ q( K0 h7 e. R/ M/ {thalamic pituitary gonadal axis. CPP is more com-
+ f1 _+ H6 T3 C6 T3 l! zmon in girls than in boys.1,3 Most boys with CPP
5 I+ V% _7 B% l' N. {3 j' ^4 a* Zmay have a central nervous system lesion that is- Y5 a) W5 [: o5 [+ Y9 A
responsible for the early activation of the hypothal-
, N* g1 @' g3 p) q  J6 k& o- @amic pituitary gonadal axis.1-3 Thus, greater empha-
8 n& i4 `7 S9 U! `0 x  |8 Tsis has been given to neuroradiologic imaging in
& T4 O; B8 h/ E; M) v- Aboys with precocious puberty. In addition to viril-
6 ^- T5 U: k+ p: b' t: z# Gization, the clinical hallmark of CPP is the symmet-
; V9 D6 v! R1 g" b/ W0 C2 ]* x; qrical testicular growth secondary to stimulation by
" ^7 C7 i# ]; g4 _6 ygonadotropins.1,3
& ^# O$ j2 [- c7 _9 gGonadotropin-independent peripheral preco-  U) N/ {5 k5 }9 s7 n* D! C! F. g
cious puberty in boys also results from inappropriate
; z. H: k* b) B# Uandrogenic stimulation from either endogenous or" p( {& A! c: @- u+ b
exogenous sources, nonpituitary gonadotropin stim-1 K5 F; D$ _- ^- J- I# I$ e$ t
ulation, and rare activating mutations.3 Virilizing! I9 z4 k! z  @( I- w! w  T  T
congenital adrenal hyperplasia producing excessive
% Q. a! Y0 l$ J4 Y1 vadrenal androgens is a common cause of precocious
5 x: O' x# @) y0 h4 K& Vpuberty in boys.3,40 v) S% `' W" _2 L# p' X9 I
The most common form of congenital adrenal$ h& I" q9 ^( r* Q6 X
hyperplasia is the 21-hydroxylase enzyme deficiency.
* k7 [4 ~3 s) {* k# q/ V5 u7 {The 11-β hydroxylase deficiency may also result in
" V" Q) L% [/ y* E# w' _' Lexcessive adrenal androgen production, and rarely,
1 }, y9 {' _3 Ran adrenal tumor may also cause adrenal androgen! l: R6 k3 m  _' n8 m9 Z" X
excess.1,33 m  |3 h( u9 j
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: U' \/ B/ a. m4 B$ u/ s542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
. u' Z  j4 B$ w# S7 TA unique entity of male-limited gonadotropin-# c2 G) C6 U/ U* n
independent precocious puberty, which is also known
2 o' R! m( d3 ^% I( F) bas testotoxicosis, may cause precocious puberty at a
  N; T! [6 f- x2 l* ?very young age. The physical findings in these boys; r6 W' v$ j- f
with this disorder are full pubertal development,# u- h$ B; s2 M; }  {5 E  R+ j  |
including bilateral testicular growth, similar to boys/ y0 L4 j0 d. X- P3 Q
with CPP. The gonadotropin levels in this disorder5 O. J$ b0 O% P
are suppressed to prepubertal levels and do not show6 z6 J3 I7 g$ X, E
pubertal response of gonadotropin after gonadotropin-
+ N& w- l' p; R! i/ U+ Kreleasing hormone stimulation. This is a sex-linked
: ?/ u0 b9 N3 b  M( @9 P+ b3 Bautosomal dominant disorder that affects only6 l9 ^$ r5 e* p+ \  b  X: m/ D" Z9 C
males; therefore, other male members of the family
& x. L5 d) B$ |" o/ ?) \% `may have similar precocious puberty.3
) m% {) Z) p9 R; V+ nIn our patient, physical examination was incon-
& h( d+ @$ O  @4 jsistent with true precocious puberty since his testi-, I" B, }# {" w- c  p4 ?
cles were prepubertal in size. However, testotoxicosis' @4 E/ ~" @! j- y
was in the differential diagnosis because his father  L! J) T& [$ I& l9 Y! n, H' U
started puberty somewhat early, and occasionally,
6 ~8 g1 k: M, N+ {3 a3 c7 i: q4 [testicular enlargement is not that evident in the5 ~: Y4 _& \% N" ]0 v5 P
beginning of this process.1 In the absence of a neg-, C) e4 R$ U8 P% D2 q
ative initial history of androgen exposure, our2 k3 I; r& P; Z# I6 U
biggest concern was virilizing adrenal hyperplasia,
1 T" \8 l4 u4 deither 21-hydroxylase deficiency or 11-β hydroxylase0 t( C" E( J/ d0 Z2 _
deficiency. Those diagnoses were excluded by find-
5 C5 f5 \7 ~1 v4 z+ G+ P8 ring the normal level of adrenal steroids.
# a8 S) a) A; e, t$ G8 [" T& mThe diagnosis of exogenous androgens was strongly% ~4 X" d/ i: S% v* e7 R% l' d$ q
suspected in a follow-up visit after 4 months because
* {. s$ Q  e) p0 x# q& `the physical examination revealed the complete disap-
$ Z6 e$ z; F' r1 B8 [& [: R( Rpearance of pubic hair, normal growth velocity, and
3 w. d. D1 R# u& I* w5 bdecreased erections. The father admitted using a testos-8 e% E7 `$ T* ?3 J
terone gel, which he concealed at first visit. He was
! E2 c' f: d+ f/ n  u) musing it rather frequently, twice a day. The Physicians’
$ h: ^% E1 |! d4 nDesk Reference, or package insert of this product, gel or- L* H% i  I6 o* M* Q# {/ [; `* m9 @
cream, cautions about dermal testosterone transfer to
) b+ i# k; \( d, R2 Eunprotected females through direct skin exposure.+ N/ E; w" N8 t8 {  k+ S" _
Serum testosterone level was found to be 2 times the
, ~" I* L' G& |; X) [baseline value in those females who were exposed to+ r* X! q: j2 F6 d& b* h( ~
even 15 minutes of direct skin contact with their male+ S9 P5 u6 P* T7 @! b1 f0 m
partners.6 However, when a shirt covered the applica-3 F. I9 c) ~( T* U
tion site, this testosterone transfer was prevented.+ M& h9 u1 C1 E' Y7 w: ^
Our patient’s testosterone level was 60 ng/mL," {0 M! w; T/ W3 o3 g
which was clearly high. Some studies suggest that
/ X2 @5 i. y8 c; u" Wdermal conversion of testosterone to dihydrotestos-
% e4 L" Z2 f7 A0 z% ?+ sterone, which is a more potent metabolite, is more, Q/ ?+ s8 C6 i: n( e- M) D4 Y
active in young children exposed to testosterone
# Z$ N& U2 ?& f: \' @3 }( ^6 Yexogenously7; however, we did not measure a dihy-
8 u) {3 ^) s5 C% n9 P) [9 f0 n7 Ydrotestosterone level in our patient. In addition to
8 M; ^3 i0 P7 x8 o" ~virilization, exposure to exogenous testosterone in% s3 u. h4 _; `' z/ i
children results in an increase in growth velocity and* e: K; t- ?4 }  E2 a5 O/ C* m; D
advanced bone age, as seen in our patient.
6 b! F4 Z8 K: wThe long-term effect of androgen exposure during
& _  ?* L: `4 n% A5 eearly childhood on pubertal development and final
1 X. G* n8 W3 B3 C% qadult height are not fully known and always remain! t. a) z1 ?. z, C* d
a concern. Children treated with short-term testos-
) Q* F$ [2 W1 I  ~; Gterone injection or topical androgen may exhibit some
! ^# K# o1 S/ R/ n  B* cacceleration of the skeletal maturation; however, after
7 e; I, ?6 @% j! L3 r/ {cessation of treatment, the rate of bone maturation( \9 H2 e! k! b! R4 C8 O
decelerates and gradually returns to normal.8,9( |1 \5 @% x% N$ a# H; x
There are conflicting reports and controversy
. r5 o9 |6 S3 O2 j! p( a2 L7 ?  Yover the effect of early androgen exposure on adult5 T9 D* w8 x& A
penile length.10,11 Some reports suggest subnormal
- n1 ]# Q! u& `8 F6 F3 h& P& ?( j: sadult penile length, apparently because of downreg-
* |4 H/ [2 _" L7 e2 I4 y9 P1 B- oulation of androgen receptor number.10,12 However,* I; ?; T& [3 P' f
Sutherland et al13 did not find a correlation between  X) _3 M: D/ S! {5 D4 F
childhood testosterone exposure and reduced adult
, }% Z+ ?8 h' @7 e/ O' openile length in clinical studies.% t# ?2 K2 Z$ B* l( o' @4 l0 w
Nonetheless, we do not believe our patient is
0 J3 b  V& G6 j9 ~4 M0 p* fgoing to experience any of the untoward effects from
8 S3 ]  ~5 S5 ltestosterone exposure as mentioned earlier because/ s; Q, _6 d% w4 r
the exposure was not for a prolonged period of time.
) w+ U8 ~) o; {* c: k  ?7 r/ aAlthough the bone age was advanced at the time of
' R- j+ ~1 p$ d7 s7 D, l- n, G3 Jdiagnosis, the child had a normal growth velocity at
0 F5 R; \- t+ z4 p2 G" ^- @the follow-up visit. It is hoped that his final adult
' _; f0 G1 ]+ r2 Q  a1 H! H7 a& x! ^height will not be affected.
3 b0 ~7 U) a( ^+ n& I: kAlthough rarely reported, the widespread avail-
2 f) }+ l+ `/ T6 H9 |' B% Eability of androgen products in our society may
% e4 d& q: x1 t! {4 J' l! Eindeed cause more virilization in male or female" v' }4 A. X) N" Q: `
children than one would realize. Exposure to andro-
7 E. W$ I3 ?% o' V, agen products must be considered and specific ques-. x) W# S6 G+ T
tioning about the use of a testosterone product or
, k9 a: }1 A- g# E4 Bgel should be asked of the family members during
8 G% y1 e+ W8 ~0 {& A5 j) ithe evaluation of any children who present with vir-6 o$ K1 s+ K* o( O7 t
ilization or peripheral precocious puberty. The diag-7 L: t& K4 z& Y) f4 s
nosis can be established by just a few tests and by% p% C1 T% I) l& P
appropriate history. The inability to obtain such a- a* f. I6 @. l, I4 p/ g& Y( w) U
history, or failure to ask the specific questions, may* p$ i$ l. N: M" r: X; }3 v
result in extensive, unnecessary, and expensive# e8 u- J, [: c* ?) F8 S, I
investigation. The primary care physician should be& Q* D3 `) E$ n4 R
aware of this fact, because most of these children, Y, t& r7 l. b: w( X8 i/ l
may initially present in their practice. The Physicians’& b  b  |' K8 |/ u/ }9 v- H  z
Desk Reference and package insert should also put a
1 q$ d/ D! L& H' N0 @' A, W6 c( Mwarning about the virilizing effect on a male or
2 V6 a  E. q8 g2 i* L9 Ofemale child who might come in contact with some-
1 ?  `' P8 B9 Ione using any of these products./ G( K0 o1 L. E! E- G6 S* h; _* B
References
+ |- T; M9 b9 a  j; Z% y& Z1. Styne DM. The testes: disorder of sexual differentiation$ O5 Z3 U$ K% Y$ k, t' x
and puberty in the male. In: Sperling MA, ed. Pediatric
6 f4 s) h$ u2 [. a) y- FEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;7 J/ a% ~/ m# B
2002: 565-628.! h( z  r6 E2 ]& b+ e
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 X# |' w0 C2 I, C; N) _
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
7 g! x/ Q% o5 D- Q! cBoy Induced by Indirect Topical
  m8 k1 O, \* U  D; {- A9 iExposure to Testosterone
. n' Z) E& Q7 WSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 ^& E" l4 B- cand Kenneth R. Rettig, MD1
' x: r! ~2 x" d& iClinical Pediatrics
6 ~1 }8 w4 [* p5 FVolume 46 Number 6! c& Z8 ~7 n: ~
July 2007 540-543
; q' I+ C  ?2 s. i- F© 2007 Sage Publications" m  v" Q9 j1 F- Z
10.1177/0009922806296651
3 ~. u$ y! q% Z9 Y; Ghttp://clp.sagepub.com. J+ w- J+ i6 Y5 W* D: p, d* g% ^% Y
hosted at1 ]' {+ J" c: d7 y2 s2 v2 }" v
http://online.sagepub.com# h. U% V) A! }- r
Precocious puberty in boys, central or peripheral,& W  W: p2 A4 r7 j
is a significant concern for physicians. Central
5 Y% R& h- c/ q3 S! Dprecocious puberty (CPP), which is mediated# I2 T0 C$ G8 U
through the hypothalamic pituitary gonadal axis, has
+ n: p: i( f0 J8 k9 E& Pa higher incidence of organic central nervous system
4 [. t7 [0 ?6 P1 b7 i9 K% H8 n4 [lesions in boys.1,2 Virilization in boys, as manifested+ P" ?! a( |! r9 p' n' Y$ ^
by enlargement of the penis, development of pubic
( s, p$ Q2 D: W' B  d: Ihair, and facial acne without enlargement of testi-
- U- h8 l8 ~& C5 t+ rcles, suggests peripheral or pseudopuberty.1-3 We
# B- v$ `" w! Y( v6 D  s) u' B6 ~report a 16-month-old boy who presented with the
( a( \8 q( [7 e% b8 h: L# a+ _  Genlargement of the phallus and pubic hair develop-9 C% k, _0 I3 V9 e! A
ment without testicular enlargement, which was due$ [# y- `# _$ d1 X; o
to the unintentional exposure to androgen gel used by4 w) U2 f3 Q. L9 }$ U2 s; r1 |# f
the father. The family initially concealed this infor-" s0 r4 U( J( I! e5 \* b
mation, resulting in an extensive work-up for this
! I- _# d+ l: g/ D  I8 gchild. Given the widespread and easy availability of
( X' K# `. [, G5 l0 A. Ltestosterone gel and cream, we believe this is proba-
- o+ w. M) h; R! t1 n1 ]+ Cbly more common than the rare case report in the
: a; d* E6 Z; y6 K% \/ @literature.44 e% a/ a3 v" F- @( f2 ^1 \
Patient Report
7 \4 ~- `4 N, h, ^# e7 a. a- c9 LA 16-month-old white child was referred to the
0 R0 F4 Y1 y( k, U' E$ Sendocrine clinic by his pediatrician with the concern
6 {, M( B& j4 a1 |" t( E$ ?5 @. tof early sexual development. His mother noticed" Z$ n9 ~9 E  g8 |
light colored pubic hair development when he was1 M5 I) E$ D+ d
From the 1Division of Pediatric Endocrinology, 2University of
# V* |1 {5 Y1 v9 e6 ySouth Alabama Medical Center, Mobile, Alabama.0 I/ F( Y* m3 v
Address correspondence to: Samar K. Bhowmick, MD, FACE," {9 y; u* W0 e) @  w4 h3 _
Professor of Pediatrics, University of South Alabama, College of/ O9 T/ k/ ^6 Q1 B4 V- l% L8 ^
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
: V  w. f3 U2 y+ Z7 oe-mail: [email protected].
% u* I& J* l! z% rabout 6 to 7 months old, which progressively became$ T9 v) L$ K# d$ f5 b* z
darker. She was also concerned about the enlarge-) O  P" g% R& c$ T. z0 T
ment of his penis and frequent erections. The child+ e( v, n. N. {+ u
was the product of a full-term normal delivery, with
2 C, J3 X5 @9 Z& g) U0 H/ Da birth weight of 7 lb 14 oz, and birth length of
2 m1 T8 S, r8 I6 ]+ G! o3 V20 inches. He was breast-fed throughout the first year) c# \+ I, U' x* U  Z
of life and was still receiving breast milk along with
$ e4 C: k! ]7 v- A* M! |" rsolid food. He had no hospitalizations or surgery,. N4 _4 ]* v! k
and his psychosocial and psychomotor development
6 u) F5 q$ D, Xwas age appropriate.# B7 E: W2 C3 h8 g5 v3 O
The family history was remarkable for the father,7 p6 e* c7 v2 G9 k
who was diagnosed with hypothyroidism at age 16,* ^, @  O$ f! ?8 n8 l
which was treated with thyroxine. The father’s
; S" E2 [3 P1 q6 r3 T3 m) kheight was 6 feet, and he went through a somewhat# d8 ^* F. ?( i( g0 b
early puberty and had stopped growing by age 14." s1 k! l. ^' O$ c
The father denied taking any other medication. The
8 D0 D8 r' o; j. lchild’s mother was in good health. Her menarche. N& v: l" @; Z
was at 11 years of age, and her height was at 5 feet
9 Y& n2 t( m- x4 h& f! S5 inches. There was no other family history of pre-( p  m. p- L% ?
cocious sexual development in the first-degree rela-
0 F. X" |0 A( {tives. There were no siblings.
! N# k* @3 ~& V! i+ Z+ }+ ~Physical Examination
  a& f3 X$ E& l) _7 T- TThe physical examination revealed a very active,
# `% M8 p  n5 y  uplayful, and healthy boy. The vital signs documented
2 x. `7 J. V7 k: T3 y0 ba blood pressure of 85/50 mm Hg, his length was* I& A; m0 J* s
90 cm (>97th percentile), and his weight was 14.4 kg+ G2 y8 T" B5 R+ Y* b2 i
(also >97th percentile). The observed yearly growth* T! ~8 X1 ^8 [: w+ W' m9 K
velocity was 30 cm (12 inches). The examination of" w' K& z3 i- S1 q
the neck revealed no thyroid enlargement.1 s$ H/ e: N3 b- {. f
The genitourinary examination was remarkable for
6 C! t2 r: r2 henlargement of the penis, with a stretched length of
$ m0 L* j# s2 W- X6 C/ ~9 a8 cm and a width of 2 cm. The glans penis was very well0 a- u* X9 |" A$ w
developed. The pubic hair was Tanner II, mostly around  C* c( K* {! n/ O
540) n' |( ?( d! ?: {- g  G5 u2 ]' I
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ V& r) a# x. Ithe base of the phallus and was dark and curled. The6 R2 G5 _5 @: \. |8 T" E) t: q
testicular volume was prepubertal at 2 mL each.; z; C2 B3 R' z2 l2 `6 P  N+ ~2 T) N
The skin was moist and smooth and somewhat- I0 O2 P1 e* d: {! D
oily. No axillary hair was noted. There were no  A- `8 F5 c; R; w! ~/ z
abnormal skin pigmentations or café-au-lait spots.
' ?' V* r8 `+ S- x6 INeurologic evaluation showed deep tendon reflex 2+
% c, j$ u  M$ {' Ubilateral and symmetrical. There was no suggestion
2 T2 ]  u1 ]1 a" x/ Sof papilledema.* r% q% c" H8 v! M: q
Laboratory Evaluation
( k# C( o* ~" i6 P0 Q1 kThe bone age was consistent with 28 months by
9 \' z  n; ~+ Z. `+ S. q1 E/ lusing the standard of Greulich and Pyle at a chrono-9 V$ ~- I7 u" S
logic age of 16 months (advanced).5 Chromosomal
  }% f0 r, R/ n2 n1 m6 ukaryotype was 46XY. The thyroid function test# Q6 A+ ~8 n1 D: h4 d' j: Y
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
9 A& d, J3 D; N. S; G- t% rlating hormone level was 1.3 µIU/mL (both normal).- V* n+ q* `. T
The concentrations of serum electrolytes, blood
$ D/ }6 b! T  q8 N" w% f# aurea nitrogen, creatinine, and calcium all were  e( q0 b6 G) Q0 q- I6 r
within normal range for his age. The concentration
; P0 Y' ?9 I& [5 i9 zof serum 17-hydroxyprogesterone was 16 ng/dL# C" t9 y4 k2 ]1 {' W
(normal, 3 to 90 ng/dL), androstenedione was 20
& T' c( K0 M4 ang/dL (normal, 18 to 80 ng/dL), dehydroepiandros-+ G2 q! s0 l% j3 u4 O& d4 ]
terone was 38 ng/dL (normal, 50 to 760 ng/dL),0 ^2 L- b* w* u! O9 [7 d
desoxycorticosterone was 4.3 ng/dL (normal, 7 to/ k0 P- T( l6 d( I& ~7 s
49ng/dL), 11-desoxycortisol (specific compound S)
/ v- e# m# X/ B* M7 ]( p" \was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-+ _; Y( H3 \1 Y6 _9 M8 N
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total: L. J; w1 r1 m1 G. T2 r; T* }+ N
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
! b; _+ l6 `7 J9 l7 b" nand β-human chorionic gonadotropin was less than
6 U3 P3 Q- c" c" S. j: Y4 m. K5 mIU/mL (normal <5 mIU/mL). Serum follicular
2 ]3 y, e- k1 y1 o8 Hstimulating hormone and leuteinizing hormone
  |$ i/ s3 G- Y$ m9 g* q- ?concentrations were less than 0.05 mIU/mL0 e" w# i: t. [" s4 |3 U9 e0 v
(prepubertal).- L  U5 Q4 W1 V
The parents were notified about the laboratory" E! z- G: t- p; ?# @
results and were informed that all of the tests were; X2 n2 E: s5 z" E  X
normal except the testosterone level was high. The
( t5 _3 W/ c' }0 ^; Pfollow-up visit was arranged within a few weeks to
/ J. ~/ \+ K+ {; x% {8 Mobtain testicular and abdominal sonograms; how-
1 V$ s1 N: j. g$ g) Yever, the family did not return for 4 months." |% m  Q0 j; G; S4 e; r
Physical examination at this time revealed that the
! X1 J" M/ H; a1 E/ s0 V0 Dchild had grown 2.5 cm in 4 months and had gained$ K, O3 w$ ~' w. n3 X
2 kg of weight. Physical examination remained
& Y: l7 H: ~1 K, p3 k0 ]unchanged. Surprisingly, the pubic hair almost com-# {. U/ D; T+ F7 z" p2 q
pletely disappeared except for a few vellous hairs at% E* _% ?0 j& v" t' i  R2 H
the base of the phallus. Testicular volume was still 2
/ f3 i* x7 P. l! W' hmL, and the size of the penis remained unchanged.
+ x8 Z# F+ S3 j+ j6 ~1 D4 C+ ?" m: nThe mother also said that the boy was no longer hav-
8 {3 D' _8 A8 d) W9 J$ U3 u+ {ing frequent erections.
8 h( C* W; Z  c% r/ MBoth parents were again questioned about use of
  ?: ?" Y0 J- u: B5 W6 @+ e9 \! Xany ointment/creams that they may have applied to) Z# _0 k5 b- s6 {- {0 t) i! X" H& V1 U
the child’s skin. This time the father admitted the
8 a/ m8 M4 ~& c. yTopical Testosterone Exposure / Bhowmick et al 541( ?3 ^/ {: B  L' @3 j9 q
use of testosterone gel twice daily that he was apply-
. x: {' B- D0 H7 ]# ~' T1 ving over his own shoulders, chest, and back area for8 T0 }1 w9 [# j. x3 o5 U" z2 [
a year. The father also revealed he was embarrassed
- @3 L$ t7 ^/ o! ?+ m! bto disclose that he was using a testosterone gel pre-
0 l1 f, l# l7 K# W5 z. U  l/ xscribed by his family physician for decreased libido7 J' J6 @" c6 z, ~6 c
secondary to depression.
( |( w4 z, X8 R3 SThe child slept in the same bed with parents.% p/ q# V* ?& G
The father would hug the baby and hold him on his
, ]: N$ P  b; C& f: kchest for a considerable period of time, causing sig-1 Z1 |  K; S4 x* L! I' r2 |, C
nificant bare skin contact between baby and father.3 M& c/ u7 S- r; c( S# ?- X
The father also admitted that after the phone call,
, q: w. u7 D! I+ z% y( Swhen he learned the testosterone level in the baby, `9 t. m  C; V2 R7 M  s) Q$ G
was high, he then read the product information9 h6 U! P0 k) W2 G: \
packet and concluded that it was most likely the rea-
: v' r  S/ g+ m9 H# X, Gson for the child’s virilization. At that time, they
5 C) O( o. v' S, W9 A& ?decided to put the baby in a separate bed, and the
" v9 A& X) |( \# D% e" j" B9 mfather was not hugging him with bare skin and had0 [/ F& p2 R2 f* B
been using protective clothing. A repeat testosterone/ m; V2 i2 |: v& U8 }
test was ordered, but the family did not go to the2 q8 B, {4 o! C: s6 S
laboratory to obtain the test.
! g$ o) w' _$ C# ADiscussion
, L+ s6 x/ Z, e2 _Precocious puberty in boys is defined as secondary4 T( T2 O# }5 j" E
sexual development before 9 years of age.1,4
3 N+ J9 c: k6 [# [% TPrecocious puberty is termed as central (true) when; H( [# P1 R- \; N8 a- p, j
it is caused by the premature activation of hypo-; M0 e9 Z) T6 {4 ~
thalamic pituitary gonadal axis. CPP is more com-' c4 o) \6 f' u' f& z% A
mon in girls than in boys.1,3 Most boys with CPP
9 R- S4 c, O( k+ q5 B0 L4 Q1 C2 \0 Vmay have a central nervous system lesion that is
4 h! p& \, |( D( }# Uresponsible for the early activation of the hypothal-# |% Y" _# a3 R+ j
amic pituitary gonadal axis.1-3 Thus, greater empha-! w: A( n1 z# ?* S7 Y, J
sis has been given to neuroradiologic imaging in' T: q6 w; C* J" ?) x6 d# k
boys with precocious puberty. In addition to viril-1 \- j7 U9 v8 ?- d& ?3 k
ization, the clinical hallmark of CPP is the symmet-: W1 T; H* m% Z* ~' }9 N
rical testicular growth secondary to stimulation by
) |7 ]3 j8 @0 r( igonadotropins.1,3, }# K! s" o- s6 |/ D
Gonadotropin-independent peripheral preco-& |. }2 [2 [5 x8 Z
cious puberty in boys also results from inappropriate" Q5 B1 i: `$ a3 X
androgenic stimulation from either endogenous or. B* q" D1 C( y* |: r1 h
exogenous sources, nonpituitary gonadotropin stim-3 w% C0 }. Q, A6 ], a) h
ulation, and rare activating mutations.3 Virilizing
" M% X, q+ z0 w* h& Wcongenital adrenal hyperplasia producing excessive8 c" |. `- n. E. \
adrenal androgens is a common cause of precocious
& v# |; F- u# D' b: i' m" w$ kpuberty in boys.3,4
7 _+ ~4 E5 b/ H& D+ `% F3 j7 `The most common form of congenital adrenal
  [' a% {9 d2 y- ]hyperplasia is the 21-hydroxylase enzyme deficiency.
& B6 P% G5 m4 H# Q5 e$ |; ]: D3 CThe 11-β hydroxylase deficiency may also result in
0 `# p, m. |$ Z( ?excessive adrenal androgen production, and rarely,' w1 Z5 {' ?- Y' |) N
an adrenal tumor may also cause adrenal androgen5 u" Y1 k& F. a6 P% w  X! K, `
excess.1,3
" F% E/ \0 ?' x/ x& C" |at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 U; A# f, `2 U2 d' @' k! A542 Clinical Pediatrics / Vol. 46, No. 6, July 2007- A8 n8 f. |, c/ k( ?* O' K" l; J/ E
A unique entity of male-limited gonadotropin-. V+ d4 P9 `; \' |
independent precocious puberty, which is also known
+ Q, C/ A( W+ J# K) w, O4 Y6 Jas testotoxicosis, may cause precocious puberty at a
9 N! k/ m; N  m9 _( Zvery young age. The physical findings in these boys. _  y% Q7 L+ ]- f9 @
with this disorder are full pubertal development,* Z- d1 i$ Z7 `7 x( r9 @
including bilateral testicular growth, similar to boys
' `* T! Q( \- s6 d  s) `with CPP. The gonadotropin levels in this disorder
& y9 X& _$ O% U6 j# p' ~  \are suppressed to prepubertal levels and do not show" m4 m0 R! Y$ _# u0 H7 P- h5 `
pubertal response of gonadotropin after gonadotropin-
: j' b3 Y6 M) creleasing hormone stimulation. This is a sex-linked
, |) ^8 z& x/ \) d0 j4 r: {  tautosomal dominant disorder that affects only: c7 G) j0 J+ t; W+ r$ L
males; therefore, other male members of the family
# B. m- ?- I" T, K1 Z& e8 [may have similar precocious puberty.3
6 W. E* b1 M7 T9 @& ^In our patient, physical examination was incon-
4 N4 _! `3 f0 s* E  z. R7 z$ Xsistent with true precocious puberty since his testi-# r( h' f) E- q" V' H3 l) p: @
cles were prepubertal in size. However, testotoxicosis
2 p" y2 }3 E  \" P* E: ^4 Jwas in the differential diagnosis because his father
) A" Y+ A2 e' g# P, _started puberty somewhat early, and occasionally,
2 W1 K, s' X  j  I% c) jtesticular enlargement is not that evident in the
9 x$ `! L/ ~3 x9 xbeginning of this process.1 In the absence of a neg-8 p# R& A- j; G5 Z6 s. A; v
ative initial history of androgen exposure, our
6 x; A% b6 W" C3 J+ U5 rbiggest concern was virilizing adrenal hyperplasia,! Y7 k# _* ?2 B  {$ N2 t. D
either 21-hydroxylase deficiency or 11-β hydroxylase
& ?7 ]/ D" I$ j4 |' q2 j/ T# mdeficiency. Those diagnoses were excluded by find-, q( a3 ]1 E2 M5 S8 l; v4 ]+ s
ing the normal level of adrenal steroids.
5 b- X/ f: R3 b: ]& A$ cThe diagnosis of exogenous androgens was strongly
0 T) \) @, f2 B* ?+ N* ~* a6 L6 qsuspected in a follow-up visit after 4 months because) p. @2 e. o/ U, v
the physical examination revealed the complete disap-; U9 X8 ^( S; Y2 Y4 o1 D
pearance of pubic hair, normal growth velocity, and
$ T& Z2 f9 T" ^$ J4 ?) [! j/ Zdecreased erections. The father admitted using a testos-4 E7 X. Y3 q5 w& s4 G: D  z% k
terone gel, which he concealed at first visit. He was3 _, A4 l8 ^6 V+ o; q( {3 C+ ?
using it rather frequently, twice a day. The Physicians’! u9 ?5 N# `' K; d/ \
Desk Reference, or package insert of this product, gel or. p8 d5 U7 W( n8 S4 S
cream, cautions about dermal testosterone transfer to) O- X2 B5 h( o6 O
unprotected females through direct skin exposure.
1 U8 r0 R9 }4 kSerum testosterone level was found to be 2 times the
4 [, v% L: |/ fbaseline value in those females who were exposed to
: J$ j" L; |4 L  L$ Jeven 15 minutes of direct skin contact with their male! |% \' R* ]) Z& v) J! ?
partners.6 However, when a shirt covered the applica-) \' K/ U; ]4 |5 w. z( ~
tion site, this testosterone transfer was prevented.+ Y; }' f3 p9 X8 r: C
Our patient’s testosterone level was 60 ng/mL,2 z+ z$ I% C9 k
which was clearly high. Some studies suggest that
" O% H/ W5 {/ ]dermal conversion of testosterone to dihydrotestos-& P) }% k' J1 B. L% I
terone, which is a more potent metabolite, is more
: V. ?% I+ P0 b$ vactive in young children exposed to testosterone
& ?" j3 t3 |. H. M& W. |" }3 nexogenously7; however, we did not measure a dihy-" o1 d! P$ b9 c3 w" v" f8 N
drotestosterone level in our patient. In addition to
6 T( `4 t3 N4 P0 N, ^virilization, exposure to exogenous testosterone in
$ l- y% B6 i  [7 qchildren results in an increase in growth velocity and/ {# c- o+ w+ x
advanced bone age, as seen in our patient.
- A: U" T& r/ LThe long-term effect of androgen exposure during" u1 m. {5 Y8 o, J9 J, Q  s% I
early childhood on pubertal development and final
1 P- N3 v* I, p+ i; |6 s8 S7 qadult height are not fully known and always remain; R0 A& T) l  I( G5 X
a concern. Children treated with short-term testos-4 `( }2 q( W7 {% b" e
terone injection or topical androgen may exhibit some
* {# e& H6 y# {8 {4 U1 [: ?; ~! Kacceleration of the skeletal maturation; however, after
' `, ?" b7 r/ e  M" k) t* ecessation of treatment, the rate of bone maturation0 d: R2 Q  E: k* a$ k/ l8 |
decelerates and gradually returns to normal.8,93 u4 K2 y- f$ p$ W! J
There are conflicting reports and controversy
- A6 Q( _: R, }% T% g! m' G, Gover the effect of early androgen exposure on adult
9 ^! S( O) U* [( Rpenile length.10,11 Some reports suggest subnormal
1 l1 t+ a# {4 k% ]0 Y$ @% E8 Nadult penile length, apparently because of downreg-
( [$ P6 H/ m# V- ~5 qulation of androgen receptor number.10,12 However,, [$ R5 U' F, x0 X+ P7 U
Sutherland et al13 did not find a correlation between! L( O) w; E" f9 Y
childhood testosterone exposure and reduced adult
% N, ^0 z" u$ wpenile length in clinical studies.' \, I! i5 P4 d4 |7 g; ~0 j& E& f
Nonetheless, we do not believe our patient is6 n" X7 C# e4 s( r, \6 J( M
going to experience any of the untoward effects from% t- K; k* P: Y4 X
testosterone exposure as mentioned earlier because
1 a: F: a- I, P2 bthe exposure was not for a prolonged period of time.
0 P9 @" ], {, Y4 P% M/ OAlthough the bone age was advanced at the time of
' [4 W4 ~. h' f* c9 ldiagnosis, the child had a normal growth velocity at
. q- U4 n) O  F' r! V7 uthe follow-up visit. It is hoped that his final adult7 D9 n/ K! ~! i7 K* W5 X
height will not be affected.
) \2 L1 [0 M# J% fAlthough rarely reported, the widespread avail-, A# V  t( _' {8 u, n
ability of androgen products in our society may
2 ]- \( V" X. w3 _+ I) o1 windeed cause more virilization in male or female# N% A4 k9 T8 w2 q+ l8 s; d
children than one would realize. Exposure to andro-
- x* g' z! P/ fgen products must be considered and specific ques-% w& T5 x1 V" [8 B
tioning about the use of a testosterone product or( ~& z8 M- z- x0 v( \% V
gel should be asked of the family members during
+ Y5 r' w8 D* Bthe evaluation of any children who present with vir-2 @; m  o! F7 ~9 a
ilization or peripheral precocious puberty. The diag-& V! N5 G4 l- K5 e4 M% ~; K
nosis can be established by just a few tests and by
5 j& H( a! @) S0 E; n% G  ]appropriate history. The inability to obtain such a7 X  M5 A" ~9 {; u& x
history, or failure to ask the specific questions, may  X; L$ \  J9 X* I8 {& k9 d
result in extensive, unnecessary, and expensive/ P% Q5 F. W( D+ E/ r
investigation. The primary care physician should be, @- ^3 {" r3 ~0 G$ c, A& ~
aware of this fact, because most of these children3 [$ L% h" _! f/ p  S6 e- L
may initially present in their practice. The Physicians’
: {6 s& d5 u, N5 @Desk Reference and package insert should also put a1 J% f  K. X7 B& u% S/ Y- v
warning about the virilizing effect on a male or6 f8 `' J- o% S
female child who might come in contact with some-1 z( K- a: a* u
one using any of these products., J" z& g7 L- d) x7 I, g
References1 O( ]5 X2 u  w' B
1. Styne DM. The testes: disorder of sexual differentiation
: N& y$ V  k8 z0 uand puberty in the male. In: Sperling MA, ed. Pediatric( o/ M, L* F; ]) {0 Z
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;) M7 J3 i* E; c* L# j6 L
2002: 565-628.
! A7 e7 K8 }" K$ N! v" c2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
9 \: V! E; a) Q' F0 W  z5 K; vpuberty 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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
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
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
" e) W/ W( H# Y- \/ {
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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