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Sexual Precocity in a 16-Month-Old
1 N2 f; [2 @- j" pBoy Induced by Indirect Topical
4 l8 G) D6 s0 x, c0 F; MExposure to Testosterone, ^  A$ Q$ e: }" f9 u
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. ]' ]- r. r& J7 X& B
and Kenneth R. Rettig, MD1
. s1 O; A: I+ cClinical Pediatrics4 Z4 V3 F# D9 ?
Volume 46 Number 6: w- C3 d, o8 ~% \7 u- u* g6 z. K' G
July 2007 540-543. F  \3 I1 \2 ]4 P& S/ n
© 2007 Sage Publications' P- `0 ]$ F# x7 P/ u& T0 a7 f1 j% v
10.1177/0009922806296651
* A& k3 n3 S2 U7 e' Ehttp://clp.sagepub.com9 W2 v# s/ P6 h! J  }5 a: `
hosted at
8 |2 E" \1 R: U1 {http://online.sagepub.com
; l% _3 H9 S9 i* P' GPrecocious puberty in boys, central or peripheral,
2 v  V- X9 M: r5 D( uis a significant concern for physicians. Central2 A+ t# s5 R: p  M; p
precocious puberty (CPP), which is mediated# S; }' X, y! i; Q/ z
through the hypothalamic pituitary gonadal axis, has  t. w, C: L! R: f( A
a higher incidence of organic central nervous system# U  g& b9 H7 z+ m% F: k
lesions in boys.1,2 Virilization in boys, as manifested/ L8 T2 Y- `$ S6 q9 j
by enlargement of the penis, development of pubic
! ^6 y  l$ V' x: ahair, and facial acne without enlargement of testi-
5 s* H: B/ K1 A) w" Q$ vcles, suggests peripheral or pseudopuberty.1-3 We
- s4 h+ [2 V3 I6 j& F$ l: Lreport a 16-month-old boy who presented with the
) k4 U. V8 p; o9 benlargement of the phallus and pubic hair develop-" f- U7 j: W4 }9 u0 p% h1 p
ment without testicular enlargement, which was due) J# b3 T2 E# z5 M6 X
to the unintentional exposure to androgen gel used by7 i, b  k( @( h: T7 y' b
the father. The family initially concealed this infor-
5 M: W6 g5 ]6 [- w+ wmation, resulting in an extensive work-up for this
& O" t3 D3 ]4 s6 W6 }( s. [9 Pchild. Given the widespread and easy availability of1 i9 `& f+ @+ x% u% S! i
testosterone gel and cream, we believe this is proba-* [# R$ T3 a5 x) ?
bly more common than the rare case report in the, r& Y9 r  u2 Z) C  w5 T
literature.4
  T4 U8 h+ ~$ ~2 f; ]Patient Report' ]% W+ J! D6 m( c
A 16-month-old white child was referred to the( ]0 y, W7 h: k( c/ Q. V. L: q
endocrine clinic by his pediatrician with the concern  F, Z: X' k7 k. T9 o" M4 l
of early sexual development. His mother noticed6 e% A2 E- D! \* C" h; y
light colored pubic hair development when he was
" r; @9 C! g7 G$ {/ ]From the 1Division of Pediatric Endocrinology, 2University of, E5 E6 t4 ]9 A, R; B# }
South Alabama Medical Center, Mobile, Alabama.
1 J4 Q' Y; G4 F  rAddress correspondence to: Samar K. Bhowmick, MD, FACE," H* f% u+ ^% O2 Q5 [, @7 u
Professor of Pediatrics, University of South Alabama, College of3 U2 t) c. ~) R+ P! v
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;' B' x; a, s5 K4 c
e-mail: [email protected].
* b, \5 d4 H- @9 vabout 6 to 7 months old, which progressively became
: `2 ~) W7 [3 R7 S( g8 Vdarker. She was also concerned about the enlarge-
$ |$ ]1 C0 A+ N0 k( [ment of his penis and frequent erections. The child3 }. j0 |# E7 b
was the product of a full-term normal delivery, with
% w; C- L" D( w$ s) d$ ]3 za birth weight of 7 lb 14 oz, and birth length of
& f1 D8 W( v0 q& F) `! }20 inches. He was breast-fed throughout the first year3 h2 i  l( c9 k; `6 k' Z$ X
of life and was still receiving breast milk along with7 V- O" f1 X! Y  G" n2 q
solid food. He had no hospitalizations or surgery," _; C8 n% H4 N8 s8 S
and his psychosocial and psychomotor development
6 {. T, H4 }5 K3 `: \6 r! D. Qwas age appropriate.
/ R( v7 z8 s2 j- DThe family history was remarkable for the father,9 w3 U1 R1 _* N5 S- J; X
who was diagnosed with hypothyroidism at age 16,( H% q6 v& j/ E$ v
which was treated with thyroxine. The father’s
9 c4 ~% }2 ~- i# r! `height was 6 feet, and he went through a somewhat9 U9 c( S3 W% ^3 R! j8 y9 m
early puberty and had stopped growing by age 14.
" ~3 R1 c# A& O  D) m2 ^  Y2 aThe father denied taking any other medication. The
- N& C4 m/ \& U, f* Uchild’s mother was in good health. Her menarche
) ^% A# n) g% ]$ v! rwas at 11 years of age, and her height was at 5 feet
2 L, _4 `& z  O# x0 a" L5 inches. There was no other family history of pre-
8 u4 b3 p! `3 l& A. J5 `# ?/ qcocious sexual development in the first-degree rela-7 A# p5 W1 ]' Y/ F6 ?) y
tives. There were no siblings.0 e8 i- W. K! w( g0 s1 k# c8 L
Physical Examination
# P4 n6 m; V5 W+ i+ d- cThe physical examination revealed a very active,
* v" k) K) t6 W8 I. p1 `  Aplayful, and healthy boy. The vital signs documented, O+ ?% V+ s/ a* K) |
a blood pressure of 85/50 mm Hg, his length was' N* k" \  e) ^/ [; S3 T% M
90 cm (>97th percentile), and his weight was 14.4 kg5 x: y1 U0 X# H0 W/ N9 Q% u
(also >97th percentile). The observed yearly growth
# J6 K* ^# c, V! t( g5 V# |+ cvelocity was 30 cm (12 inches). The examination of
3 g0 j4 m. f4 t& L: Lthe neck revealed no thyroid enlargement.
) n/ U" ?/ h, eThe genitourinary examination was remarkable for( M* u" N% K$ M  ~
enlargement of the penis, with a stretched length of
+ g6 s  G9 E/ m- H2 m3 e0 _# r8 cm and a width of 2 cm. The glans penis was very well0 G0 F$ V! u  Z2 h; X* v
developed. The pubic hair was Tanner II, mostly around& l" i! D1 a, m( K, b
540) m" l1 y* v' ], q3 h
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" f+ T  x2 K! `) h3 |( S9 Zthe base of the phallus and was dark and curled. The
2 ^# ~- ?; d5 T* dtesticular volume was prepubertal at 2 mL each.
  \) Z, |2 A( N4 ^- L% OThe skin was moist and smooth and somewhat
6 D; `  t5 ~* a2 e7 C) _/ l) Toily. No axillary hair was noted. There were no
& i# c8 p2 [) }" ]0 uabnormal skin pigmentations or café-au-lait spots.3 G4 F7 g- ^6 l
Neurologic evaluation showed deep tendon reflex 2+6 t. p! r9 q, f' R$ {: U. p9 K# H
bilateral and symmetrical. There was no suggestion
' e2 q2 a& k- q7 f; n$ rof papilledema.
/ {" u0 T1 s3 J1 oLaboratory Evaluation
) z' i! M, X2 uThe bone age was consistent with 28 months by
! H& ?  `' g& |& i# wusing the standard of Greulich and Pyle at a chrono-
9 g& t5 c  P$ p1 F2 y. Vlogic age of 16 months (advanced).5 Chromosomal  `0 v" d- p( g& ~
karyotype was 46XY. The thyroid function test: l5 N3 \" n* B- ~
showed a free T4 of 1.69 ng/dL, and thyroid stimu-" w' I' R3 q( g# E- u
lating hormone level was 1.3 µIU/mL (both normal).
8 e) ]& @) t& A: ~$ o: HThe concentrations of serum electrolytes, blood8 v5 w/ z" Q( V0 g, D
urea nitrogen, creatinine, and calcium all were
3 D3 o: A) Z" ~  u' [" \8 P+ Dwithin normal range for his age. The concentration
5 c. }0 [! |: Vof serum 17-hydroxyprogesterone was 16 ng/dL
9 z) M2 S* ?+ V+ A; ?- p2 A1 Y( P(normal, 3 to 90 ng/dL), androstenedione was 204 V0 {$ t, J) K
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
! t# j3 F9 G. I4 V, B9 {1 z5 Bterone was 38 ng/dL (normal, 50 to 760 ng/dL),
' ~9 }2 D8 z% L6 }: kdesoxycorticosterone was 4.3 ng/dL (normal, 7 to; N+ j6 O- b; N3 u9 X! M. C
49ng/dL), 11-desoxycortisol (specific compound S)) p  x$ p, q' J- H8 N
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-8 I  l+ N  F% w# U4 v+ _
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
/ f2 T: g# t5 itestosterone was 60 ng/dL (normal <3 to 10 ng/dL),+ P0 L$ \; L* h: f- j  w$ f) u& |4 d, d  s
and β-human chorionic gonadotropin was less than' C" `: Y* ^1 V
5 mIU/mL (normal <5 mIU/mL). Serum follicular6 R' W2 H5 N: r4 ?' e3 E* c
stimulating hormone and leuteinizing hormone- {4 k: k* N5 {+ U2 D8 g4 U4 ?
concentrations were less than 0.05 mIU/mL2 I9 X( ?0 s) I$ U
(prepubertal).7 j- j# T- B, O0 F2 P1 z
The parents were notified about the laboratory+ b/ _+ ?) F/ A* N2 b7 j& z7 k
results and were informed that all of the tests were- \! X& o, j. s
normal except the testosterone level was high. The, L. k+ s% b- H  S; e! c, r9 @
follow-up visit was arranged within a few weeks to# i3 a- \/ @- u8 W) W3 \
obtain testicular and abdominal sonograms; how-$ z: ?( q3 [7 f6 ?
ever, the family did not return for 4 months.: }$ `# k; r! T! E
Physical examination at this time revealed that the! O: E9 T' W1 |- J: f% s  \& C
child had grown 2.5 cm in 4 months and had gained
4 R4 j% {) [& ]# t. t% k2 kg of weight. Physical examination remained
$ ?# ]5 {; r4 i" V$ D# @' o) Hunchanged. Surprisingly, the pubic hair almost com-
6 d1 H0 k6 ]3 Q$ V2 Y. ^# ^8 qpletely disappeared except for a few vellous hairs at% U1 a, ~1 ?' V  l* k2 R4 r
the base of the phallus. Testicular volume was still 2
5 w- W9 n: T( n+ n) E1 }mL, and the size of the penis remained unchanged.' T6 h, \' j/ L. z+ ?
The mother also said that the boy was no longer hav-
; C2 e& E6 h! a: ^* jing frequent erections.
+ K6 `( S7 j: w( ~9 _' L% n7 S3 p2 TBoth parents were again questioned about use of9 F7 _9 m- r( f& P9 _
any ointment/creams that they may have applied to1 j1 k8 Y' ~! K3 z/ Y$ d
the child’s skin. This time the father admitted the0 @+ b5 I( b/ _, y. ~! E$ J; L  x
Topical Testosterone Exposure / Bhowmick et al 541$ x1 A: t) a6 h: }  [' J# z
use of testosterone gel twice daily that he was apply-* C- a4 x  w9 n3 S/ b
ing over his own shoulders, chest, and back area for$ u+ v; Q8 f7 \+ j
a year. The father also revealed he was embarrassed
; `' u" ~5 L7 W7 n% bto disclose that he was using a testosterone gel pre-
6 `3 `# M$ G4 i3 ^5 G5 U6 qscribed by his family physician for decreased libido
3 S, i9 G- z) R  ~1 Q, Ksecondary to depression.
5 @0 y9 Y7 E. K) `The child slept in the same bed with parents.% k" F" v) L' _; _
The father would hug the baby and hold him on his5 W$ h0 O6 l8 c  \' V3 B
chest for a considerable period of time, causing sig-
! L2 x% {5 P( ?0 j1 ?$ Jnificant bare skin contact between baby and father.0 q: n0 y7 d! H& l& K5 c% E
The father also admitted that after the phone call,
1 V* u% Y) V, ~  |when he learned the testosterone level in the baby( o) W4 [# g; `1 H2 C* L9 K
was high, he then read the product information* z5 R. e& E4 j/ V* _0 l
packet and concluded that it was most likely the rea-
# Z  d0 F: @5 n1 |9 B* z  L7 wson for the child’s virilization. At that time, they' k4 q8 R" K6 Y, F$ b) ^) z
decided to put the baby in a separate bed, and the& O2 l' F( d1 @! g! q
father was not hugging him with bare skin and had
1 e8 |5 H1 j6 |" l, @2 b) sbeen using protective clothing. A repeat testosterone
! V* Z: g* t, K. dtest was ordered, but the family did not go to the" e. Q1 {1 b# ~
laboratory to obtain the test.
4 L- w$ A8 @  K1 U3 CDiscussion
% [, x% z% v( x0 k8 l) i2 }Precocious puberty in boys is defined as secondary
2 _' E" g) W0 D. k: vsexual development before 9 years of age.1,4$ }% x9 B2 O9 P
Precocious puberty is termed as central (true) when3 x, B. |& R1 E3 D6 D
it is caused by the premature activation of hypo-9 e" I+ P" y& J# c
thalamic pituitary gonadal axis. CPP is more com-
6 Q9 s0 G! M( `/ n0 P4 }5 _& Rmon in girls than in boys.1,3 Most boys with CPP3 L  x4 Q9 ^+ U; F& j' l* U
may have a central nervous system lesion that is
# n* X8 s) L% uresponsible for the early activation of the hypothal-
' Z! [2 l' l4 \% U' Y& j$ pamic pituitary gonadal axis.1-3 Thus, greater empha-  p1 f$ _- z1 S! j% O
sis has been given to neuroradiologic imaging in. W8 k0 P" g* Z& }; I: v7 Y
boys with precocious puberty. In addition to viril-
" ?' F; z* |4 x/ N- W* n" i9 i& tization, the clinical hallmark of CPP is the symmet-! e3 }1 K2 e6 O+ \6 h$ R
rical testicular growth secondary to stimulation by
, U; p& g( A$ m, Z8 \gonadotropins.1,3
$ z* Y- I- o8 T! k$ HGonadotropin-independent peripheral preco-7 e, Z' Y# x& _7 g5 m2 s: \1 F
cious puberty in boys also results from inappropriate, S0 W2 d4 M: H) V3 C8 _! E9 |+ Z4 y
androgenic stimulation from either endogenous or/ V. p- n3 ^) M2 H
exogenous sources, nonpituitary gonadotropin stim-
3 _8 J2 J. J: X# kulation, and rare activating mutations.3 Virilizing
( N/ g+ }0 v5 t  zcongenital adrenal hyperplasia producing excessive+ `8 O$ q6 z+ I
adrenal androgens is a common cause of precocious
2 f+ k' x; q8 c4 e$ N  {. \puberty in boys.3,4# d) X, p9 z4 Y/ I
The most common form of congenital adrenal
( |. [7 {  j1 ~( e- X# Shyperplasia is the 21-hydroxylase enzyme deficiency.# V$ E4 ~2 x! |% |# ^, k; k% K
The 11-β hydroxylase deficiency may also result in7 s2 r; p& N! O& n1 T; W
excessive adrenal androgen production, and rarely,
2 y) l; k' _! R$ i5 p: Wan adrenal tumor may also cause adrenal androgen
6 c! s+ @  x! v& t3 z5 Z! T! M/ Aexcess.1,3  l( ^- ]0 Q7 ?- _8 _* `* J
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* u  ]% d: ^2 a
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007' m: d, Q& Z- F7 O0 v* j! h
A unique entity of male-limited gonadotropin-
7 _; h6 j9 {6 |/ rindependent precocious puberty, which is also known
8 B$ d' X4 o# ~; y1 b0 K5 e8 pas testotoxicosis, may cause precocious puberty at a, {4 p& z" l0 Q+ J6 h
very young age. The physical findings in these boys  ?# \3 O4 P: V& q
with this disorder are full pubertal development," G* E3 _2 E& ~; B- a) e
including bilateral testicular growth, similar to boys% A' a9 k# P9 i5 F% J4 y
with CPP. The gonadotropin levels in this disorder
  F  e% D4 z, V. l6 |6 bare suppressed to prepubertal levels and do not show3 h5 V, {6 }) R4 B/ A
pubertal response of gonadotropin after gonadotropin-+ m! m7 g8 q) E
releasing hormone stimulation. This is a sex-linked9 y$ g# U+ P  q, k0 S
autosomal dominant disorder that affects only  e8 R; R& N9 m' W6 ~+ g) q3 x
males; therefore, other male members of the family' S+ w$ r* i" d7 m6 b' I: Y. x
may have similar precocious puberty.3! |: M% H1 T& W5 j+ o4 v2 _
In our patient, physical examination was incon-* ]$ q. O; p' @: `( c
sistent with true precocious puberty since his testi-  z4 X4 b3 j  S! Q- ~% V
cles were prepubertal in size. However, testotoxicosis
: J/ p% a$ }! ~was in the differential diagnosis because his father+ L; O. x! B2 H% ~; o# @
started puberty somewhat early, and occasionally,. I+ ?; m9 e- o. g4 P% _2 \, ^" y
testicular enlargement is not that evident in the! m- [: b+ M) A0 c. ?4 A" C* a, y" J
beginning of this process.1 In the absence of a neg-
) t- x$ [% ]* B7 ^4 Uative initial history of androgen exposure, our
  T6 p- E- f. s! F9 hbiggest concern was virilizing adrenal hyperplasia,: v, I4 ]$ m! ~* P$ s% X& Z! l
either 21-hydroxylase deficiency or 11-β hydroxylase
# c/ p$ e, d* N& P8 g  f9 @deficiency. Those diagnoses were excluded by find-
3 N* d+ J3 h$ j$ }- z4 z) n$ oing the normal level of adrenal steroids." t. ~( M/ s( T* H! l
The diagnosis of exogenous androgens was strongly
5 K/ U2 H% ~1 \# m% l0 Csuspected in a follow-up visit after 4 months because
, V- m4 y  T$ L: g# a1 K5 x2 Uthe physical examination revealed the complete disap-9 X$ O. i6 V4 g# [
pearance of pubic hair, normal growth velocity, and
: z( H. l' w: B2 mdecreased erections. The father admitted using a testos-' l' G3 t+ G% k% F5 N- ~
terone gel, which he concealed at first visit. He was! c/ u7 y6 f- j2 o
using it rather frequently, twice a day. The Physicians’
) K5 s6 z) J2 q! y7 J8 J4 xDesk Reference, or package insert of this product, gel or
  ?6 x' y, }' c5 Fcream, cautions about dermal testosterone transfer to
- Y' B. ?- |; u+ A* Q, Eunprotected females through direct skin exposure.
0 H. }7 J% {1 z/ B! {Serum testosterone level was found to be 2 times the
2 i# Z' u/ f6 L' n+ \baseline value in those females who were exposed to& D+ }: ^8 i8 |& f) ~
even 15 minutes of direct skin contact with their male
6 W/ ~& _5 x6 b1 H7 b1 Opartners.6 However, when a shirt covered the applica-
3 g* z. b) M( Ztion site, this testosterone transfer was prevented.1 \2 O: x4 t* x' S* y  o4 O" B" ^
Our patient’s testosterone level was 60 ng/mL,
8 M$ k8 y5 }3 a) C4 v# N/ Ywhich was clearly high. Some studies suggest that* U, |; X3 W$ P4 F( C# n3 c: {
dermal conversion of testosterone to dihydrotestos-
& [( W! P) ]( lterone, which is a more potent metabolite, is more
$ p& y! B" v" h2 tactive in young children exposed to testosterone
9 {) L$ w) z3 C1 O' p! ^exogenously7; however, we did not measure a dihy-& w" B- j& H( E. \- c
drotestosterone level in our patient. In addition to
' n; j% c+ Q. t" N* Ivirilization, exposure to exogenous testosterone in% k# j# R  a& w2 a6 d8 B, M
children results in an increase in growth velocity and
6 X3 E* |5 H* Y. K0 j( {9 sadvanced bone age, as seen in our patient.$ H. l) ?9 O8 I) R2 v# d% j
The long-term effect of androgen exposure during' G" a" S+ q( _) V
early childhood on pubertal development and final! N' f0 a. W5 p. ]
adult height are not fully known and always remain9 x. ^- x0 Y8 _. p  h% B
a concern. Children treated with short-term testos-: n7 t' @7 x4 ^6 Q# J3 A- ]) f
terone injection or topical androgen may exhibit some1 d6 o1 R) }* k  m; u* e
acceleration of the skeletal maturation; however, after" ?( K5 u' }; O7 ~* t
cessation of treatment, the rate of bone maturation
1 n& D) u- H, d! e+ gdecelerates and gradually returns to normal.8,9
1 F& i3 |, M% ^8 t9 \" I7 l( |# wThere are conflicting reports and controversy
+ L5 ~% i" ?2 `2 Qover the effect of early androgen exposure on adult
' d5 A) V. Y) c0 Kpenile length.10,11 Some reports suggest subnormal7 H7 @6 Q- M2 D- b( k, X; _
adult penile length, apparently because of downreg-
0 C- q1 W5 Q& y! |: e3 d! T- M! ]ulation of androgen receptor number.10,12 However,: T( W( M9 S: E2 I2 _, a" J9 b8 z
Sutherland et al13 did not find a correlation between4 }# w, P1 x7 D3 H
childhood testosterone exposure and reduced adult% }- |  b% n% ^& Y
penile length in clinical studies.
5 Z, w  U) u4 l) m2 `. d  jNonetheless, we do not believe our patient is
2 d& d6 m3 p% k4 q& y; sgoing to experience any of the untoward effects from
& [' h+ h; B% ~  r3 f- ptestosterone exposure as mentioned earlier because
( {8 o5 o- @. Y; \- s& @the exposure was not for a prolonged period of time., m! O$ P: d3 P6 q& c+ X8 d
Although the bone age was advanced at the time of
" J: J+ O" p# `0 z$ idiagnosis, the child had a normal growth velocity at
, s0 A1 ~* W7 I2 f0 q* _( l% R$ jthe follow-up visit. It is hoped that his final adult/ N$ r* z4 y0 I
height will not be affected.% \* t- Z- j( U7 Z9 G  f/ p" P
Although rarely reported, the widespread avail-
1 P& ?' k1 D! A- I& t4 fability of androgen products in our society may4 {) k6 e  Z' E' W6 d9 M* `" N
indeed cause more virilization in male or female" [; P! T2 f! x0 [  B" J
children than one would realize. Exposure to andro-
4 ]+ D3 S0 g. x1 H! dgen products must be considered and specific ques-
) r% ?6 p) g' F& \tioning about the use of a testosterone product or7 p1 C' X+ S9 D. j( ~
gel should be asked of the family members during: U- U/ E2 o' N& T9 O, ~3 w
the evaluation of any children who present with vir-
) y3 }- V. M! g1 I1 D* @0 i' O4 pilization or peripheral precocious puberty. The diag-
( o$ K, f% v) ~! v8 L, Inosis can be established by just a few tests and by
2 [. Q& P2 v6 w3 x: W7 u1 [appropriate history. The inability to obtain such a3 W8 Q. y. Z& c* W* t' ?0 k% V3 F
history, or failure to ask the specific questions, may
! _1 E* W+ g& N, d% M1 d0 E* zresult in extensive, unnecessary, and expensive
0 f6 B; ]% k8 sinvestigation. The primary care physician should be
  j7 g  s4 d& q0 H) h+ paware of this fact, because most of these children9 ]- l/ \- G1 A5 C1 R, V0 \
may initially present in their practice. The Physicians’
  T* d( O9 \8 j% h0 O! WDesk Reference and package insert should also put a
0 u* G1 G, t4 D, p+ E& b. lwarning about the virilizing effect on a male or
. ~% \& m* i: i9 o8 Z  e  ]! f5 @$ Lfemale child who might come in contact with some-
- O; Y2 _8 m1 @; K5 O. Vone using any of these products.! p- w/ X! Z" O& `. e- c
References
) s( p$ X- u. J, c" i  P1. Styne DM. The testes: disorder of sexual differentiation
. v# `$ U& Q' S/ J, Uand puberty in the male. In: Sperling MA, ed. Pediatric) ~9 a8 C& W$ f" i) x1 \% \, l8 I" I
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;& _( c8 ?0 W8 _. B2 E
2002: 565-628.4 _/ G( y$ W6 r# N- F
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
; C) I/ Y: j0 n5 L6 |( Spuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
/ V4 v; Z7 I, P4 ]# m! n6 OBoy Induced by Indirect Topical/ U0 A  S! v+ X* c; O
Exposure to Testosterone. o" E  {+ d& G* @4 ]  J
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 J9 j3 [9 ~( R2 z* mand Kenneth R. Rettig, MD1, `. f' u+ B- j+ t6 M
Clinical Pediatrics3 ^) ~& W$ y3 o" {9 A
Volume 46 Number 6  e. Q- v3 Y; D9 [  z) i
July 2007 540-543- k& j% @3 J) |3 P# E! I  R( ~
© 2007 Sage Publications4 F2 m, K* u! ?& B* a; K
10.1177/0009922806296651
6 g, w8 D& H( Q% K0 v( Ohttp://clp.sagepub.com
* R9 \- v) c; thosted at
  [; L' z7 u" {5 ahttp://online.sagepub.com
: m3 `8 W! F  M7 t$ ?Precocious puberty in boys, central or peripheral,
$ C0 e- p+ k% c0 T3 Vis a significant concern for physicians. Central
% r8 J; H0 b! u+ X6 F* Z2 Sprecocious puberty (CPP), which is mediated
! O& X  v6 H! ^through the hypothalamic pituitary gonadal axis, has
8 q) \6 d) x7 @9 [6 O' U' la higher incidence of organic central nervous system
, A9 r: X9 {2 H+ }; wlesions in boys.1,2 Virilization in boys, as manifested" u+ R  h0 Z- e) Q! c! O
by enlargement of the penis, development of pubic4 ^  M8 _) F0 p$ k
hair, and facial acne without enlargement of testi-
$ c8 r3 O0 k& I, c; R6 ecles, suggests peripheral or pseudopuberty.1-3 We" ]7 K: p* t- Q9 @1 k' h
report a 16-month-old boy who presented with the
) G$ `$ y( H2 L' ^8 {: D/ u4 P+ penlargement of the phallus and pubic hair develop-  \1 H* q- R3 Q
ment without testicular enlargement, which was due
* C. V& U/ Z: \/ N: t2 {3 e1 [to the unintentional exposure to androgen gel used by/ W2 ^0 [$ W) y) N( L% X
the father. The family initially concealed this infor-6 i# L. B' k; }0 f  e& y5 L& d
mation, resulting in an extensive work-up for this
4 l! _& d  e+ B. achild. Given the widespread and easy availability of- v# k2 B! p( c- v) E7 z
testosterone gel and cream, we believe this is proba-8 V* x5 K! [. a. Y/ Z
bly more common than the rare case report in the
. O0 x7 n# H! d8 C0 t$ G2 G, dliterature.41 z+ t1 O2 C& ^3 I# _4 W0 a, U) [
Patient Report
$ l$ o) w9 q) w. ~: L+ [0 d( [A 16-month-old white child was referred to the$ K% A0 }. u0 i$ v0 e! h$ D- A( {
endocrine clinic by his pediatrician with the concern
' d" i' |7 `* E1 V. j  ~( rof early sexual development. His mother noticed/ Z: {1 ~# F# h0 P4 m& @& C
light colored pubic hair development when he was
7 N! G1 B8 ]  `From the 1Division of Pediatric Endocrinology, 2University of
9 @) ?2 x$ y& v& n! J& cSouth Alabama Medical Center, Mobile, Alabama.0 G, z8 w: S' z: R& J' I; m4 \- z
Address correspondence to: Samar K. Bhowmick, MD, FACE,
$ M9 }' q* ^5 O& K# K& dProfessor of Pediatrics, University of South Alabama, College of
) @# C6 B; V- @4 e+ zMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;% e7 o5 d( j8 \( W4 q! i) V0 O. E
e-mail: [email protected].) X, C( V3 [6 p1 T
about 6 to 7 months old, which progressively became7 D7 u% X% w- R5 n. \) y
darker. She was also concerned about the enlarge-
! K6 d+ ~* w/ oment of his penis and frequent erections. The child
. W& x' [+ D! s4 ?. o4 J) d/ `was the product of a full-term normal delivery, with" r) U( k# p: q7 V: h3 T
a birth weight of 7 lb 14 oz, and birth length of
* K& e$ _$ m$ s, W2 c2 _8 p" s' T# v20 inches. He was breast-fed throughout the first year
, G7 S; R' m& G( h9 p9 kof life and was still receiving breast milk along with4 b+ e& ]; K) }$ F( d
solid food. He had no hospitalizations or surgery,
- |4 A, w/ t1 k# _% H3 Qand his psychosocial and psychomotor development
' U0 i' n; K( p$ H) L- iwas age appropriate.
2 i! \6 Y' Z) `* S+ \The family history was remarkable for the father,& x+ T0 }. w( x. c6 G
who was diagnosed with hypothyroidism at age 16,/ B* C+ W. W9 k5 T/ g- Y+ s; h
which was treated with thyroxine. The father’s
& g3 g) J5 v) pheight was 6 feet, and he went through a somewhat
1 [+ p3 H' L+ H+ E0 M$ X0 Iearly puberty and had stopped growing by age 14.
: X* z) g* d2 l! P( `# ZThe father denied taking any other medication. The
+ s# i8 M7 w8 pchild’s mother was in good health. Her menarche9 |) Q0 r! D2 n. s
was at 11 years of age, and her height was at 5 feet' _6 x8 i$ }' |/ v$ e
5 inches. There was no other family history of pre-
& P/ ]3 `3 ?! F% S% s! w) bcocious sexual development in the first-degree rela-9 p9 w: d9 B2 t2 j1 |: U1 k
tives. There were no siblings.
1 C: k, n! u7 ^2 W4 z7 FPhysical Examination
! A! K, E+ O9 bThe physical examination revealed a very active,$ E7 f+ ~( h  d+ \7 H
playful, and healthy boy. The vital signs documented2 H- |6 h* E% G$ k0 ?
a blood pressure of 85/50 mm Hg, his length was
3 ~' o  j7 G1 c) C! `' B' c8 [9 s90 cm (>97th percentile), and his weight was 14.4 kg5 M+ A+ G3 t+ q. l4 o
(also >97th percentile). The observed yearly growth
1 V! C4 y/ p2 J$ q5 Hvelocity was 30 cm (12 inches). The examination of0 j% `# V, J/ r6 b' s- q
the neck revealed no thyroid enlargement.* Q7 x" l$ N6 b8 k& s5 D' [
The genitourinary examination was remarkable for
7 ?& m- _9 O' yenlargement of the penis, with a stretched length of* }8 U7 H+ s% ^7 g, L1 A5 z0 p0 f
8 cm and a width of 2 cm. The glans penis was very well7 j, C$ U( o* j# Y
developed. The pubic hair was Tanner II, mostly around
" q' Q2 ^6 L: F/ u540
: _. j6 _1 p+ u4 e3 M& Q7 kat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& K' A( Y2 m3 a% dthe base of the phallus and was dark and curled. The3 Q- e0 \, ?) A$ ?5 u9 B
testicular volume was prepubertal at 2 mL each.' s+ [# R+ q5 T0 S
The skin was moist and smooth and somewhat
- E8 f& ?, E+ D2 eoily. No axillary hair was noted. There were no, Z. j1 u* k& {0 n: p/ W
abnormal skin pigmentations or café-au-lait spots.; ~2 W3 V2 ?# m/ }! U! t
Neurologic evaluation showed deep tendon reflex 2+
/ {' I' M" N9 c! Mbilateral and symmetrical. There was no suggestion
4 L( a4 ]4 l! x6 ~9 qof papilledema.
: N6 J. H) [4 ]8 OLaboratory Evaluation6 \; |1 b+ a9 w% U
The bone age was consistent with 28 months by/ c2 ^, N7 N' T* r1 w; J
using the standard of Greulich and Pyle at a chrono-; g3 \* n9 W3 C3 d3 E: ^
logic age of 16 months (advanced).5 Chromosomal+ l3 M" y. r/ I, v
karyotype was 46XY. The thyroid function test3 z  r7 H8 P9 N! ~: T
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
, L0 p& W- [% r4 z5 d8 T) rlating hormone level was 1.3 µIU/mL (both normal)./ e' t. g( d5 q, ?2 E( N4 g) f" r1 |
The concentrations of serum electrolytes, blood
) a/ p* h8 V) d! A% k) N, Uurea nitrogen, creatinine, and calcium all were7 j: r: A/ B$ `" y% q5 \& W
within normal range for his age. The concentration
: Y1 O+ o0 F' L7 ?  q9 a. bof serum 17-hydroxyprogesterone was 16 ng/dL2 K: \4 h0 u4 M& ~% @: |, `1 P5 _3 S3 ?
(normal, 3 to 90 ng/dL), androstenedione was 20  {: a0 j9 ?% C6 r
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-+ O7 Y  b3 y' u0 f0 A$ D6 V) i1 ~5 N+ q
terone was 38 ng/dL (normal, 50 to 760 ng/dL),2 l2 w# ?, q+ O& G* c  S: n' J& n
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
! r; w5 v( t1 u8 a49ng/dL), 11-desoxycortisol (specific compound S)# S6 q8 y+ O  e# e* F. q3 _
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
! b+ c7 H) t3 l. t! j6 K% Itisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
0 v( f$ d  \6 {' @: J* Utestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
( J1 Z8 x) x  E4 `6 U) D# cand β-human chorionic gonadotropin was less than& A' Q3 ?5 |# G5 ~* N
5 mIU/mL (normal <5 mIU/mL). Serum follicular% J: i2 R8 \6 \
stimulating hormone and leuteinizing hormone5 R, q- e. T+ p2 g1 W( V9 G
concentrations were less than 0.05 mIU/mL
6 q) V1 Z# ]3 P(prepubertal).
  ]3 |$ V- A! U  I5 dThe parents were notified about the laboratory
: `# I) I) s' _1 ?, J  @2 uresults and were informed that all of the tests were! ~; l, g0 E& p9 o9 H4 d  ^% X
normal except the testosterone level was high. The* c& o5 f3 B& @
follow-up visit was arranged within a few weeks to
5 k  i  Y. L- f/ C5 {" U* kobtain testicular and abdominal sonograms; how-
7 R. y) [# C  |4 i8 yever, the family did not return for 4 months.8 p' B" k) K) _
Physical examination at this time revealed that the9 x' x3 ~! P2 K% t  m
child had grown 2.5 cm in 4 months and had gained2 n! c  o, u" L4 [3 ^0 \. v
2 kg of weight. Physical examination remained' ], K( r9 `5 p
unchanged. Surprisingly, the pubic hair almost com-% t2 u9 \1 s6 {  p$ |. j. z
pletely disappeared except for a few vellous hairs at
1 z# h( a  r. Q+ ?# S: o. A! Ethe base of the phallus. Testicular volume was still 2; D! ^" ~8 s. v
mL, and the size of the penis remained unchanged.2 \; m. t- D) M/ X. a- o2 Y1 ?
The mother also said that the boy was no longer hav-
' H. S8 p6 l) }" Bing frequent erections.
6 F0 }! [2 f  |- aBoth parents were again questioned about use of& G% B. v  }0 S* o* ]  h
any ointment/creams that they may have applied to2 {3 v, p) s  e  Q" Z4 m" P
the child’s skin. This time the father admitted the
/ ?: X2 [7 B9 q7 {5 kTopical Testosterone Exposure / Bhowmick et al 541
5 R1 d' W) H1 f  Duse of testosterone gel twice daily that he was apply-8 N& E0 e$ h8 z2 X. L( f! k$ \+ N( v
ing over his own shoulders, chest, and back area for
, c& R9 u1 s6 {% w4 g2 p) Ea year. The father also revealed he was embarrassed
' u6 ]. ^$ S$ eto disclose that he was using a testosterone gel pre-
3 F% e/ g4 i+ I4 @8 Qscribed by his family physician for decreased libido0 v; N' k, V) \. P1 B0 j
secondary to depression.
" ], B2 W, l- ]7 s& ^/ z, CThe child slept in the same bed with parents.7 b+ n3 ^, X; A) ]
The father would hug the baby and hold him on his' E/ @1 Z1 M' n6 ~9 i2 f
chest for a considerable period of time, causing sig-# t. v# B. q/ A8 o9 e0 i7 z9 ]) {0 p" p
nificant bare skin contact between baby and father.  \' ^9 V4 m0 S3 b, h2 [1 v
The father also admitted that after the phone call,! S0 o! H4 {( D( U- P* u( X5 |
when he learned the testosterone level in the baby
! U! j5 w( _' h$ M% U3 H2 |was high, he then read the product information
/ M8 y1 [! J, }$ Dpacket and concluded that it was most likely the rea-$ F8 \1 R. y6 d6 M# [/ J' |6 b
son for the child’s virilization. At that time, they7 }. k& b& O% c. U2 Q& R
decided to put the baby in a separate bed, and the
5 p! Z: K% O/ M- _father was not hugging him with bare skin and had3 n( G4 ]. s+ U( t) R0 X" T) `+ @
been using protective clothing. A repeat testosterone
2 a4 P: E% P' {1 Z  x8 e# Z5 ^( xtest was ordered, but the family did not go to the; b+ p1 v* ]" V" z
laboratory to obtain the test.7 g) T3 s# d0 X5 O6 f
Discussion
" a) ~1 _) q3 U, \8 l2 JPrecocious puberty in boys is defined as secondary6 D  S7 k( M" {5 u
sexual development before 9 years of age.1,48 X+ Z) B) [( ]% B0 V: @0 x
Precocious puberty is termed as central (true) when+ l$ D& k! R) u0 q- N
it is caused by the premature activation of hypo-1 t: _; H7 W. h5 l, n
thalamic pituitary gonadal axis. CPP is more com-
  t% t6 i' W' G  ?9 J, imon in girls than in boys.1,3 Most boys with CPP( N& [  d+ ?; I0 ~
may have a central nervous system lesion that is/ F8 D! z# a( x3 Q3 A5 R
responsible for the early activation of the hypothal-
3 o; i( e9 A3 c8 T2 I! Wamic pituitary gonadal axis.1-3 Thus, greater empha-
2 N" o* e6 H+ F8 s% n  r$ xsis has been given to neuroradiologic imaging in7 B# l3 g7 L3 T) Y8 ?5 E
boys with precocious puberty. In addition to viril-
4 H. F9 d5 U2 t& `2 r+ n# j5 Iization, the clinical hallmark of CPP is the symmet-
* A( g$ L' e/ v' Mrical testicular growth secondary to stimulation by
4 X9 ~8 I+ V  }) n1 Q" sgonadotropins.1,3
' D  t& d. Z8 R% G& U2 SGonadotropin-independent peripheral preco-& ]4 B2 N1 P1 y9 E( ]( h; N
cious puberty in boys also results from inappropriate
' G% Z7 x* n5 k0 Fandrogenic stimulation from either endogenous or
& c) [, S5 M8 ?exogenous sources, nonpituitary gonadotropin stim-
- U0 x0 u% z, w4 q" g1 xulation, and rare activating mutations.3 Virilizing
) X* G* W3 o# [  p8 U6 ccongenital adrenal hyperplasia producing excessive" T2 D0 W; G" ?# X
adrenal androgens is a common cause of precocious
3 d2 X4 ~; E* }, z' q: cpuberty in boys.3,4+ y" z3 |& K# u, H
The most common form of congenital adrenal5 }# Z2 N* q7 u" I1 b! q: }4 ~
hyperplasia is the 21-hydroxylase enzyme deficiency.! \( j8 e" }1 T6 U
The 11-β hydroxylase deficiency may also result in- R5 S5 R5 L$ p
excessive adrenal androgen production, and rarely,
5 ?+ J3 D% d. Q( P3 _an adrenal tumor may also cause adrenal androgen1 f" V2 M6 y7 h+ \" }# U$ P: {
excess.1,3' m( h2 v+ i$ @5 o5 K
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* R4 i* |) k# U/ L+ q- t# v542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
4 l1 J: E& H( f$ e0 J7 wA unique entity of male-limited gonadotropin-
7 A) p4 b2 l' c+ B1 v" C. Rindependent precocious puberty, which is also known! l+ K4 s7 V8 R4 t& H4 i
as testotoxicosis, may cause precocious puberty at a
4 P1 X. d6 D2 Q4 Cvery young age. The physical findings in these boys
  U  Q1 t! u6 D/ b8 x6 V$ n( K3 Bwith this disorder are full pubertal development,  }6 z7 b9 ]5 t7 ~8 y" R
including bilateral testicular growth, similar to boys
/ ^+ Z4 t) i! O/ C) Zwith CPP. The gonadotropin levels in this disorder
' L5 q, c1 L$ H- m* h3 gare suppressed to prepubertal levels and do not show: f- B9 T/ B* ]2 p) j. h
pubertal response of gonadotropin after gonadotropin-1 y4 w3 d" ~* a( K& O
releasing hormone stimulation. This is a sex-linked: j6 v3 U( _# V
autosomal dominant disorder that affects only
, I( B5 @0 u6 e) A% bmales; therefore, other male members of the family, W6 {% ]5 Q$ ~# a/ s0 _9 |- s! M
may have similar precocious puberty.32 \. Z) `% h+ G, x0 d
In our patient, physical examination was incon-# k# p+ [1 m: i+ Y
sistent with true precocious puberty since his testi-
) s! X. j. u/ Q4 i' v+ m5 `' Kcles were prepubertal in size. However, testotoxicosis
3 i( s/ S2 p2 k% d% ?1 E. l3 uwas in the differential diagnosis because his father9 G( V4 h! N: v! u0 I7 D0 K  o
started puberty somewhat early, and occasionally,
" E5 V# Q9 R3 R( B$ c: [/ Q+ [testicular enlargement is not that evident in the
9 r6 \; u3 {' n6 `3 L' Dbeginning of this process.1 In the absence of a neg-! [  b, ^( ^, Z
ative initial history of androgen exposure, our
- y3 B* g/ @  Abiggest concern was virilizing adrenal hyperplasia,9 t: o$ Z8 ~  j: M! p
either 21-hydroxylase deficiency or 11-β hydroxylase
: \7 A- ?1 G& Q( v2 |4 e4 hdeficiency. Those diagnoses were excluded by find-0 U& P' o) v7 l$ U9 O) V
ing the normal level of adrenal steroids.- x! W* a7 F8 {+ ^
The diagnosis of exogenous androgens was strongly
, @1 b* f& p) @1 f# N9 X; ~suspected in a follow-up visit after 4 months because) c8 F' O; g# P0 M; a; L
the physical examination revealed the complete disap-4 D' W1 y- E  S7 I; D
pearance of pubic hair, normal growth velocity, and1 ~' g: C4 J; F8 Q$ A
decreased erections. The father admitted using a testos-) {3 m# \1 f' {9 j: ?% }& G, C- F
terone gel, which he concealed at first visit. He was+ |  a9 n; I" w9 i0 Z, W6 H2 G( X! e# b
using it rather frequently, twice a day. The Physicians’) q' I  j3 ^2 N/ C' f7 r- g
Desk Reference, or package insert of this product, gel or3 o- X* ^5 B$ o& u/ ]2 z8 [) C
cream, cautions about dermal testosterone transfer to/ R' s) }" {2 N9 Q0 k' C  J- k
unprotected females through direct skin exposure.
7 p( }- @& i1 l$ j" W( H5 }Serum testosterone level was found to be 2 times the( ?; w) y- {8 K, }7 O% z0 d) W
baseline value in those females who were exposed to& P. n9 _+ l  g; {: W" i, G
even 15 minutes of direct skin contact with their male1 P% O  o( F0 h9 F1 \
partners.6 However, when a shirt covered the applica-0 E8 O0 y+ e1 h. c8 u3 Q4 e9 N% ?
tion site, this testosterone transfer was prevented.
& z2 K' [( A' I4 DOur patient’s testosterone level was 60 ng/mL,* Q( U0 O$ h& h0 c9 D+ s' ?; a5 n2 ]
which was clearly high. Some studies suggest that
: f# e! [: V. X$ O* ddermal conversion of testosterone to dihydrotestos-
& I: L8 M. C4 s$ gterone, which is a more potent metabolite, is more
3 s6 U) v0 Q3 T  Iactive in young children exposed to testosterone
3 P& O( ^, P% W2 m( R* J. lexogenously7; however, we did not measure a dihy-1 G4 P3 p0 I  s# T1 d5 F- s" g2 U6 G
drotestosterone level in our patient. In addition to
% u4 C) F$ o  E$ Gvirilization, exposure to exogenous testosterone in
2 w4 e  M) p/ Z# Lchildren results in an increase in growth velocity and
$ M- n) N+ x( L4 c1 q! E+ }9 gadvanced bone age, as seen in our patient.
  O$ j9 z0 m0 M6 ?- QThe long-term effect of androgen exposure during
2 N) d3 [9 M' E- x6 e, [  @early childhood on pubertal development and final
& i7 J* R, I* Padult height are not fully known and always remain" ^' p& p. v) V8 I2 S
a concern. Children treated with short-term testos-
  x' V2 o9 ?3 L2 gterone injection or topical androgen may exhibit some
7 U" j; N! y* |% dacceleration of the skeletal maturation; however, after7 |- S% X6 H2 S! G: c
cessation of treatment, the rate of bone maturation
) c; B& L6 B' Y) z" Odecelerates and gradually returns to normal.8,9* G4 U7 f* H, l( [& ~3 J) l
There are conflicting reports and controversy6 ?& _; J6 {8 q
over the effect of early androgen exposure on adult, k  |6 Y+ [% b
penile length.10,11 Some reports suggest subnormal
( c+ s! a; P3 c( y  ~8 Uadult penile length, apparently because of downreg-; a  G1 q! W6 E$ l; a5 L. q
ulation of androgen receptor number.10,12 However,
- i9 ~6 ^' A- g! @' Y7 N, WSutherland et al13 did not find a correlation between. Y9 A8 \  j* `# u) A" l2 N' D
childhood testosterone exposure and reduced adult
+ g# U" ^' J4 M) {penile length in clinical studies.) j4 H  K2 X( i" ~% Y: P
Nonetheless, we do not believe our patient is7 g" j" R4 w0 ~' e8 h* \: q4 c2 k
going to experience any of the untoward effects from
+ s, N8 T2 j( @. a6 d" r, vtestosterone exposure as mentioned earlier because
, x- O( m0 ~: v1 `3 Q1 `the exposure was not for a prolonged period of time.3 D$ r9 V& O) d, A) T, z
Although the bone age was advanced at the time of
3 ?# {! Y  e' a5 Ediagnosis, the child had a normal growth velocity at9 @- d6 q4 n$ X) }0 R
the follow-up visit. It is hoped that his final adult
3 [' Q1 [, s: ^( [/ Eheight will not be affected.9 C' y, E& b- a
Although rarely reported, the widespread avail-8 f' ^* e2 [* T: ]% q/ F5 V
ability of androgen products in our society may
. J9 A3 P: e* qindeed cause more virilization in male or female
/ K' E" `% _9 D( j$ c8 T. @1 X8 y2 Ichildren than one would realize. Exposure to andro-- ~9 R) U! O, F. @
gen products must be considered and specific ques-
: w  T3 H& w! L  ^5 j8 O; Qtioning about the use of a testosterone product or
. m: `0 M1 e2 t/ r8 p! S: U" jgel should be asked of the family members during( U, k$ t( o) ^
the evaluation of any children who present with vir-
  n. c, \$ v9 k/ C! ^$ j! B2 Q- Oilization or peripheral precocious puberty. The diag-
! n) c% x! T4 m( Y4 K6 e4 ?nosis can be established by just a few tests and by
( n( F! k) l% ^# w- ]; _% eappropriate history. The inability to obtain such a8 N. P4 B: B, r9 R9 q6 V6 o) J
history, or failure to ask the specific questions, may
, c' y! [* _; c5 l! \result in extensive, unnecessary, and expensive
2 [- s; Z/ W% ~  D0 m) oinvestigation. The primary care physician should be8 q2 w1 @" M8 Y- q
aware of this fact, because most of these children6 N+ Y. E  T9 ]2 P0 O
may initially present in their practice. The Physicians’
9 z7 |: c- h) J- `/ o1 m  q- LDesk Reference and package insert should also put a
" n0 R' ?8 j. Y1 I2 q1 T- _. u: N) Bwarning about the virilizing effect on a male or, ?, Q% A: O+ L! _+ L
female child who might come in contact with some-
- a. n0 f9 O' g+ F8 E+ u/ P3 sone using any of these products.' m& t1 Z: J$ P: e6 [' r9 Q
References: S; x. Z% h, J% M8 o
1. Styne DM. The testes: disorder of sexual differentiation* n) V) h" |) L, O: x
and puberty in the male. In: Sperling MA, ed. Pediatric
* ~6 N$ O  N: B' Y9 W6 c0 WEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
5 ]- k5 j$ P3 z2002: 565-628.
+ W" ~2 H; J- a5 [1 H1 i2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
/ W, p+ R0 z) \- upuberty 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
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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
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
$ _+ S( L/ g" b2 r" F+ Z0 n3 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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