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Sexual Precocity in a 16-Month-Old
' D* Q2 p# G6 r0 E0 X6 G1 sBoy Induced by Indirect Topical  R- T3 `8 I; A3 f( d; E+ k
Exposure to Testosterone
! m4 l1 P) d4 ^5 ]3 ]& [Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
/ n: i+ m9 R# |* Uand Kenneth R. Rettig, MD1
& b) r7 i/ f  e1 d) s5 dClinical Pediatrics
9 R+ k. ]7 C: G/ y, }Volume 46 Number 6
! F  W! t4 Q) `! V! h7 sJuly 2007 540-543  C+ x% i# |2 ]7 U! h$ d
© 2007 Sage Publications
2 R! G: P+ d. e7 F0 W: O7 ~" G10.1177/0009922806296651* W: n% A( [8 O# M. F5 N
http://clp.sagepub.com( |5 e  |/ S( i* W- H
hosted at: }* }4 X! m7 O6 u. L
http://online.sagepub.com
/ d8 c1 b& P) t0 _' X% Z: \Precocious puberty in boys, central or peripheral,
8 @& i( _% [. @' Y- Pis a significant concern for physicians. Central
% X1 N. x5 f/ zprecocious puberty (CPP), which is mediated$ |4 x: M$ x/ v6 B& d3 F
through the hypothalamic pituitary gonadal axis, has
( `' Z- S; o) f9 C" w! C+ |1 l% Na higher incidence of organic central nervous system4 v0 ~1 R7 g4 S0 n
lesions in boys.1,2 Virilization in boys, as manifested4 _2 U8 j" H$ b7 v! X! Z
by enlargement of the penis, development of pubic
& c, _& F" V2 Y) C* P6 V- qhair, and facial acne without enlargement of testi-/ |3 `( r6 H" o3 U# S7 H8 M
cles, suggests peripheral or pseudopuberty.1-3 We% K5 X- a' o7 z  o& g
report a 16-month-old boy who presented with the8 y/ X6 h5 ?  x) ~/ y7 i: V
enlargement of the phallus and pubic hair develop-
! B$ u( O. s. y  h- O' i3 Jment without testicular enlargement, which was due4 \' N! ~# Y7 c7 n6 S+ e
to the unintentional exposure to androgen gel used by/ z! u) r  u# R+ Q7 H: H% q9 G( w
the father. The family initially concealed this infor-1 p- O1 @& ~* N. b* p
mation, resulting in an extensive work-up for this' N4 N5 e0 {: U! f
child. Given the widespread and easy availability of
, C, J- i, b+ O" Ftestosterone gel and cream, we believe this is proba-
5 R- ?- r1 i5 U: |7 hbly more common than the rare case report in the
4 h! B7 M- I+ O* {2 fliterature.4
, i& B6 O' S& w& z! b2 b' d" d( TPatient Report
  a# T' y/ i! h5 `& _A 16-month-old white child was referred to the, Q" t' H+ N6 N6 K, U  L) h
endocrine clinic by his pediatrician with the concern
- r3 b6 ^) O0 o* c9 i7 ~" oof early sexual development. His mother noticed3 ]( K6 W. i+ p# }2 K* X! U
light colored pubic hair development when he was. h4 k# U0 V4 |( T  K+ Y  [
From the 1Division of Pediatric Endocrinology, 2University of4 \9 I4 v7 |! b
South Alabama Medical Center, Mobile, Alabama.# |0 n& r; S' n. p- R
Address correspondence to: Samar K. Bhowmick, MD, FACE,
8 _" B0 l! K. T. W9 `7 i" TProfessor of Pediatrics, University of South Alabama, College of
+ F1 z: a  X( o" _Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;8 T( z% b! X# F, l! t, o; L
e-mail: [email protected].
; J  \% V8 l* e0 ]3 a( j. Pabout 6 to 7 months old, which progressively became
3 x5 B. {2 \: j) M, Idarker. She was also concerned about the enlarge-
& `6 D8 F0 `( Qment of his penis and frequent erections. The child3 ~, A, M+ p5 q, f# B
was the product of a full-term normal delivery, with0 J' _1 N$ ?+ \* r
a birth weight of 7 lb 14 oz, and birth length of
$ |, T. I8 y+ c20 inches. He was breast-fed throughout the first year5 m# g3 _* s0 L- ]5 d4 ^" K
of life and was still receiving breast milk along with6 t5 ?# T, v' }' K
solid food. He had no hospitalizations or surgery,, A' Z& n, \/ ~2 |- c$ z6 Y
and his psychosocial and psychomotor development
% I. q) V" V6 z1 T, C/ W  {was age appropriate.$ q# c2 c! |2 D6 V8 k- y% W
The family history was remarkable for the father,
& b6 s. N7 M3 T8 Y8 }who was diagnosed with hypothyroidism at age 16,% }/ u2 t& y) O) O+ s) b
which was treated with thyroxine. The father’s
# O  T- ], x1 v# \) Eheight was 6 feet, and he went through a somewhat  H. ]; W: g7 u1 \
early puberty and had stopped growing by age 14.0 {7 N5 N+ c2 S) j: F# u
The father denied taking any other medication. The* D) @2 @; s( C
child’s mother was in good health. Her menarche
2 v" V4 Q9 ?! {7 o7 q- owas at 11 years of age, and her height was at 5 feet& g. [7 M6 v" Z& Z7 G+ U5 @
5 inches. There was no other family history of pre-; ^6 A3 [: m2 J2 ~( ]% G- I5 B
cocious sexual development in the first-degree rela-7 d$ \- q3 B$ w, r" h# l3 [
tives. There were no siblings.) f! |1 ?$ k1 \1 b7 m0 U
Physical Examination' _* B2 ]% s- l' A; U4 `$ B, L" v
The physical examination revealed a very active,2 [* t2 h* c' ]$ C& w6 X9 U2 i& t3 T" X
playful, and healthy boy. The vital signs documented
7 Q- `; P/ r1 k4 I0 fa blood pressure of 85/50 mm Hg, his length was4 |8 s; K% Y9 y! Y, w* g
90 cm (>97th percentile), and his weight was 14.4 kg  U, V: W- U9 p) i8 q
(also >97th percentile). The observed yearly growth
% O# a. A3 ~7 _  Svelocity was 30 cm (12 inches). The examination of
' g% K; l3 j2 Z  \+ G. v, s; Pthe neck revealed no thyroid enlargement.
0 P- G: d7 }- I) ?9 t  V9 pThe genitourinary examination was remarkable for4 L/ u  T3 K4 @; `+ }
enlargement of the penis, with a stretched length of2 ~; A" U1 |' `4 P! V. }4 r
8 cm and a width of 2 cm. The glans penis was very well
/ J4 P3 z2 F6 u1 T. Sdeveloped. The pubic hair was Tanner II, mostly around/ g: }- f% N1 s  F* L# W( ~# b1 n% Y
540
; U& z7 x9 A: z8 H$ L7 u: w) nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 q. r, S# V8 o, @3 A2 m3 Fthe base of the phallus and was dark and curled. The9 u+ P: t4 `0 n
testicular volume was prepubertal at 2 mL each.: Z1 w- J$ \; J* M
The skin was moist and smooth and somewhat+ ?0 }. f# \6 J0 |% k& ~' a
oily. No axillary hair was noted. There were no
  L! K; h0 v% @/ iabnormal skin pigmentations or café-au-lait spots.8 S5 {4 X1 m: y+ U8 t# |
Neurologic evaluation showed deep tendon reflex 2+. X8 t  `7 H$ |! N( D
bilateral and symmetrical. There was no suggestion
* Y+ D9 D) f8 I$ C+ f+ wof papilledema.
  d/ k& _5 {# k! H/ KLaboratory Evaluation) A9 ^, v' H2 a) M. d% {
The bone age was consistent with 28 months by8 y6 z  l. ^' v, I5 @6 C5 k6 ~
using the standard of Greulich and Pyle at a chrono-
. Y; r6 V4 K) p+ c9 B% \logic age of 16 months (advanced).5 Chromosomal+ p% P0 y  p1 Q+ C0 E
karyotype was 46XY. The thyroid function test
  v( i7 z8 m( F* E6 n& Jshowed a free T4 of 1.69 ng/dL, and thyroid stimu-- f% Z' q3 f; {) {+ }
lating hormone level was 1.3 µIU/mL (both normal).
3 {- b: R! }8 F  EThe concentrations of serum electrolytes, blood4 P1 _, f5 _3 z4 F. g
urea nitrogen, creatinine, and calcium all were/ }9 G6 p% G# D- e
within normal range for his age. The concentration. M/ D6 \/ h2 m, C: l
of serum 17-hydroxyprogesterone was 16 ng/dL5 [5 o0 R! i; p, }" k1 _1 I
(normal, 3 to 90 ng/dL), androstenedione was 20
  y( J* y% t2 ~5 ]ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
. U$ n* D5 v/ O2 I. z# t0 F  {* Bterone was 38 ng/dL (normal, 50 to 760 ng/dL),
- M1 j: {5 T3 V3 Q5 idesoxycorticosterone was 4.3 ng/dL (normal, 7 to) a7 _- t& ]7 U! T
49ng/dL), 11-desoxycortisol (specific compound S)
0 \! a) c9 A' Q' C" Swas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- g9 g# D% v$ [
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total& J( K1 [0 f) a$ \7 L$ z( g
testosterone was 60 ng/dL (normal <3 to 10 ng/dL)," Z3 Q! P8 @. C  h
and β-human chorionic gonadotropin was less than
3 V. h/ v/ q" |- @& W2 a! I1 @5 mIU/mL (normal <5 mIU/mL). Serum follicular
6 B4 R4 [* e( Estimulating hormone and leuteinizing hormone8 {6 b$ V" Y! r$ P5 d5 y
concentrations were less than 0.05 mIU/mL6 W" ?0 m9 i) Q
(prepubertal).
* l' s5 i) q1 t( A7 S3 q' cThe parents were notified about the laboratory/ i1 k& z  ^6 b; C1 Z8 b
results and were informed that all of the tests were0 t' C, L0 t/ y  [6 l- k
normal except the testosterone level was high. The9 Q1 O( w1 {2 E) E, t
follow-up visit was arranged within a few weeks to
9 m) z* V) E6 C0 sobtain testicular and abdominal sonograms; how-/ l5 ^2 g0 F  M/ ]* B0 h- K
ever, the family did not return for 4 months.
' W( }; j  h7 L& |Physical examination at this time revealed that the4 s8 q' {% ^8 _8 n, Y
child had grown 2.5 cm in 4 months and had gained
5 Y/ t8 Z" _9 s' L8 I4 Q! z2 kg of weight. Physical examination remained
4 w1 O, `% z8 D1 V2 Runchanged. Surprisingly, the pubic hair almost com-
1 j$ W. \) z3 M' Z3 d# a! Hpletely disappeared except for a few vellous hairs at
' {. m( F( ^; R! X6 F  m! lthe base of the phallus. Testicular volume was still 26 I/ X3 {& d5 S) g0 T& f! T
mL, and the size of the penis remained unchanged.* `" h5 G: V3 w% b
The mother also said that the boy was no longer hav-- R  F5 E- a4 a
ing frequent erections.
' a  u! z, V& N6 t% d; ]4 q% {% \1 mBoth parents were again questioned about use of4 j9 H! R; m8 f! L* [; M$ }. D" J; h
any ointment/creams that they may have applied to
# z7 i4 W9 W( J9 l- [1 I$ S! i; vthe child’s skin. This time the father admitted the: r. B) \* b0 O/ c6 R: Z' ~0 b* C3 z: k
Topical Testosterone Exposure / Bhowmick et al 541. s! Q" @/ ~2 Y6 F# j& y2 Q7 ^
use of testosterone gel twice daily that he was apply-8 v9 @$ S" l) f  h; T
ing over his own shoulders, chest, and back area for
5 T. w' K- b* Ha year. The father also revealed he was embarrassed
) \/ c; U  f7 ?* Qto disclose that he was using a testosterone gel pre-
7 p) m' F4 G! f& m$ j% |+ Wscribed by his family physician for decreased libido9 R, C4 {; |/ r
secondary to depression.
3 G' {# O) O) }, R. E9 |The child slept in the same bed with parents.9 K: j$ ^; C8 z
The father would hug the baby and hold him on his
$ q6 q5 R4 v1 Z5 r' K# n, n* R6 Ichest for a considerable period of time, causing sig-
6 G4 x- e6 Z5 }nificant bare skin contact between baby and father.
7 p9 H. E8 O' [. pThe father also admitted that after the phone call,. b$ u. E* [4 b" k3 K% Y% M9 ~
when he learned the testosterone level in the baby; m0 p  h" w3 e0 s7 M8 z; m  u0 R) Y
was high, he then read the product information
3 I# J) X! v; y) P1 a9 H) Xpacket and concluded that it was most likely the rea-
$ h8 R2 o" U6 A1 H) Ison for the child’s virilization. At that time, they5 i$ w6 o4 m8 j
decided to put the baby in a separate bed, and the
" Z! K* ~5 _- R) f# bfather was not hugging him with bare skin and had
" g5 k, F; ?1 p3 Wbeen using protective clothing. A repeat testosterone0 i  q7 y: m& F4 z% g
test was ordered, but the family did not go to the) v, a5 L8 B. s/ a. n. t' Y0 K
laboratory to obtain the test.+ x8 L* ^! D3 w1 B+ N6 T  a
Discussion4 J; d' o0 A5 c9 I4 `
Precocious puberty in boys is defined as secondary, A2 {6 M8 Q2 {& N" L' l) K
sexual development before 9 years of age.1,4$ }. d' b( T4 N
Precocious puberty is termed as central (true) when  X  ~: b8 y0 \' P4 l1 h  s! a( w
it is caused by the premature activation of hypo-
5 _9 S: l# f& _9 Ythalamic pituitary gonadal axis. CPP is more com-
- q4 ^% ^! n1 h7 l, f" L4 Z! Q* emon in girls than in boys.1,3 Most boys with CPP
1 S1 ]5 O; D5 T" b8 n2 Amay have a central nervous system lesion that is" x  A: K9 p6 d6 S- N  Q( K; A
responsible for the early activation of the hypothal-
9 Q4 N  ~& }/ j: \7 ?amic pituitary gonadal axis.1-3 Thus, greater empha-
) ]' a8 w. N4 vsis has been given to neuroradiologic imaging in
  ?& H& n0 N5 {) s$ e: fboys with precocious puberty. In addition to viril-4 Q" p3 Q( z, w9 J1 E! k5 K
ization, the clinical hallmark of CPP is the symmet-+ o2 E4 D% Y* l1 O  w
rical testicular growth secondary to stimulation by
7 s- ~  J* _* U, }gonadotropins.1,34 B) M' c9 o& P. R) X% x$ L
Gonadotropin-independent peripheral preco-1 n. F9 `8 X/ s/ R' e) T2 }
cious puberty in boys also results from inappropriate
$ z: ?# o) Y- K! Z. mandrogenic stimulation from either endogenous or
+ |( s$ s. v: G: pexogenous sources, nonpituitary gonadotropin stim-8 X4 C9 h8 k7 u
ulation, and rare activating mutations.3 Virilizing$ H3 v/ E9 t5 n3 z
congenital adrenal hyperplasia producing excessive; x/ G$ M" D0 Q, u0 V' b% \
adrenal androgens is a common cause of precocious
$ k3 ?8 M- D. C0 u/ J; s" opuberty in boys.3,46 v/ X. g$ R! Y; a" K' |$ N! k
The most common form of congenital adrenal
) ]; J" w4 w8 i5 Shyperplasia is the 21-hydroxylase enzyme deficiency.
( w3 v0 m. j/ w  YThe 11-β hydroxylase deficiency may also result in
; ^8 P* U; f. N5 \) s) nexcessive adrenal androgen production, and rarely,
4 l" B  T( m, j" m7 B% _# }+ Oan adrenal tumor may also cause adrenal androgen5 ~( l2 v4 _3 Q0 e  s) S
excess.1,38 X. C: z, U1 N
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ M- N, _. i* h542 Clinical Pediatrics / Vol. 46, No. 6, July 2007) J0 l( M" i$ `6 g% l9 q/ v) w
A unique entity of male-limited gonadotropin-3 C# N! ?: @) P& `3 [
independent precocious puberty, which is also known
, W! O( `, v1 M0 z5 ias testotoxicosis, may cause precocious puberty at a
9 X+ r" a0 v: [/ E( tvery young age. The physical findings in these boys, v" M% b4 X! Y8 f7 I2 z
with this disorder are full pubertal development,
# y3 @) ^; J* t1 }including bilateral testicular growth, similar to boys
# t1 i/ G% ]5 D/ B" ^with CPP. The gonadotropin levels in this disorder
6 ^9 u: h: s& m8 G" v, nare suppressed to prepubertal levels and do not show
3 ?2 r# v7 a4 Kpubertal response of gonadotropin after gonadotropin-
& z" q  O- m  Y7 treleasing hormone stimulation. This is a sex-linked& q0 j0 u2 X* _. y6 `, X
autosomal dominant disorder that affects only3 K# a& Z* F. ]. L$ M/ ]5 R* `3 c
males; therefore, other male members of the family
* I; g8 k, _) Jmay have similar precocious puberty.3
7 I9 c' R$ e* B- b! q! S# ]# ZIn our patient, physical examination was incon-
( A$ S* b1 j& `* tsistent with true precocious puberty since his testi-. Z7 l( w: j/ @5 n# Y0 q( e0 a  [
cles were prepubertal in size. However, testotoxicosis. E, |* C5 t2 ]
was in the differential diagnosis because his father
( J3 t7 |- O; h3 Xstarted puberty somewhat early, and occasionally," V# W) b( x1 B  e5 k% I9 R
testicular enlargement is not that evident in the6 ^6 u5 L0 t' V
beginning of this process.1 In the absence of a neg-
, a6 }- `# F* _9 `6 R( Xative initial history of androgen exposure, our
( E+ Q* Q9 H- ^# q- f, Rbiggest concern was virilizing adrenal hyperplasia,; M7 s, M5 M7 Q* I' N8 }- {" |7 L
either 21-hydroxylase deficiency or 11-β hydroxylase
' D! Q, a1 V9 I7 h: T. Tdeficiency. Those diagnoses were excluded by find-
! K7 |, J) S5 e& e# C' V3 p. Hing the normal level of adrenal steroids.
$ f  [5 E4 E" Z4 _8 w3 YThe diagnosis of exogenous androgens was strongly, F0 |7 y) X$ y$ o" X1 B3 {2 S
suspected in a follow-up visit after 4 months because
' I/ V# [: a3 d1 R/ M" ]the physical examination revealed the complete disap-! u9 m, k' a) A6 n3 t, ?
pearance of pubic hair, normal growth velocity, and
# V% z- ^. G/ h( _decreased erections. The father admitted using a testos-- I  e. \! O% ?+ S
terone gel, which he concealed at first visit. He was
# K7 b# C5 i1 m0 r. k0 {using it rather frequently, twice a day. The Physicians’
/ C9 ^" d+ L/ p# L; q2 i- wDesk Reference, or package insert of this product, gel or
# J8 G  S+ T  m; r  s% U1 `+ B. `cream, cautions about dermal testosterone transfer to; F5 I! E! s9 Q& Y
unprotected females through direct skin exposure.
, z% l& V% d/ f: L' m5 T1 ISerum testosterone level was found to be 2 times the; t5 \* m& x; w  ?
baseline value in those females who were exposed to
0 m3 ~, k; O) M  N2 J4 K( D9 qeven 15 minutes of direct skin contact with their male/ j- h  N1 D% p7 v
partners.6 However, when a shirt covered the applica-
' s+ q( T4 Y; b& y7 ^: t6 f9 qtion site, this testosterone transfer was prevented.
( h) L) y) K+ F/ W4 {2 e0 Z$ ?Our patient’s testosterone level was 60 ng/mL,  Z8 x  K* u- `  y
which was clearly high. Some studies suggest that2 B/ n5 E' a1 d+ L6 P
dermal conversion of testosterone to dihydrotestos-! l9 _1 G/ K, L& C
terone, which is a more potent metabolite, is more# m7 U! B/ v! Y* D6 z2 I2 n
active in young children exposed to testosterone: P1 s0 y7 S; r3 J$ u% m
exogenously7; however, we did not measure a dihy-) p( [* Q9 e$ `1 o, k4 j" c
drotestosterone level in our patient. In addition to  v7 E) X0 v) K  }" W- X
virilization, exposure to exogenous testosterone in. q) z0 N1 ~3 e7 j2 P
children results in an increase in growth velocity and) ]# a9 S9 u: ]$ [9 z6 G
advanced bone age, as seen in our patient.
: P3 u9 `) I1 l- U) h6 fThe long-term effect of androgen exposure during
( \+ w, D5 w( R) wearly childhood on pubertal development and final
9 N$ U2 A* Z; Z: t( }9 ladult height are not fully known and always remain
! [8 I8 B2 G8 U6 o; ?, ?/ m8 k3 \a concern. Children treated with short-term testos-) }6 F$ X. P$ t# N7 N9 ~6 B. w
terone injection or topical androgen may exhibit some, X3 b9 h- {* t
acceleration of the skeletal maturation; however, after% y/ I: @) y, K  Q2 b
cessation of treatment, the rate of bone maturation
0 m3 ~. {" |# g1 U' T7 ^+ k; A$ sdecelerates and gradually returns to normal.8,9
! L) b7 G8 p1 k' z- v6 r" Q3 qThere are conflicting reports and controversy
5 W; I2 D' Z# xover the effect of early androgen exposure on adult
' [' V% C$ \5 K3 I7 B# `penile length.10,11 Some reports suggest subnormal* a3 n' j/ o, k5 `+ X& U! n8 f
adult penile length, apparently because of downreg-$ x: ]3 Q$ }& J; A
ulation of androgen receptor number.10,12 However,& O6 B# h& {- z, ~7 P( j8 j3 b
Sutherland et al13 did not find a correlation between3 f0 f7 Z, m; B' s7 K! N
childhood testosterone exposure and reduced adult4 y. `( V- l4 g/ m9 ~
penile length in clinical studies.3 H( ~' |9 L, A2 p1 P
Nonetheless, we do not believe our patient is8 t1 t$ r, W" z
going to experience any of the untoward effects from. a/ M8 u* B6 e% K6 X
testosterone exposure as mentioned earlier because
% a9 X2 D8 e9 w  k  I) dthe exposure was not for a prolonged period of time.4 x$ `$ z1 d% K+ M
Although the bone age was advanced at the time of
" P2 G& |: y7 R, y5 c- Gdiagnosis, the child had a normal growth velocity at
7 l$ p' Z: r! W) U# S! A( _the follow-up visit. It is hoped that his final adult
  x) J; ^6 L( X, A+ ^$ v0 z0 sheight will not be affected.& R# k0 }5 j6 U9 h# M) o
Although rarely reported, the widespread avail-% |% F+ I% F7 D. ^% S
ability of androgen products in our society may. Z; s9 n0 F2 f" L! }0 i
indeed cause more virilization in male or female+ N; w. P& J4 @! Q! b$ J0 h( V) w
children than one would realize. Exposure to andro-
$ L/ |5 I$ l# {! x+ o! mgen products must be considered and specific ques-' @3 b- F2 q$ d$ Y
tioning about the use of a testosterone product or1 y0 T$ F5 K" |( a# j
gel should be asked of the family members during
) ~0 X! C0 C6 J0 |the evaluation of any children who present with vir-
& D9 k+ ]& z8 q1 iilization or peripheral precocious puberty. The diag-. Q8 g; P; A0 d$ K' ^) E0 h
nosis can be established by just a few tests and by
1 L7 n- D' X9 }8 `" Xappropriate history. The inability to obtain such a: b9 Y* q# y# Q1 u2 D) t# Z6 {9 q  e
history, or failure to ask the specific questions, may
3 c+ G# N/ X5 i* t& a1 {4 }5 j2 z/ U* T5 Oresult in extensive, unnecessary, and expensive
& \4 q: A' k1 q  k% e5 O4 m0 Winvestigation. The primary care physician should be
6 l! t3 {" H6 Q9 f. caware of this fact, because most of these children
+ i# w! i0 T2 J4 K2 imay initially present in their practice. The Physicians’9 K1 h' W* L) w( D- g; x$ o
Desk Reference and package insert should also put a
! p+ s1 H' w$ l. ~" rwarning about the virilizing effect on a male or0 Z2 ]1 i! f9 C* k0 v
female child who might come in contact with some-+ ?8 S; E- ~( B( w$ A! p
one using any of these products./ n. z  Y9 d; t: }
References# d8 e8 B; a, h: d4 A
1. Styne DM. The testes: disorder of sexual differentiation  }4 a' y+ L. X% ^
and puberty in the male. In: Sperling MA, ed. Pediatric5 _4 k$ D' j4 H5 F. k
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
( i9 N. M5 }2 R* {0 L$ i# d) m2002: 565-628.
7 f- E4 O* q1 g. q0 W4 [2 A! Q2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious7 O8 b/ [1 H3 |6 k
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
( m- \9 {. r- y- |Boy Induced by Indirect Topical
( \7 z& s) l2 `$ G! bExposure to Testosterone
0 B' E1 x9 I  X: v8 N$ YSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2  M! C/ ?( }- B( V- H. e
and Kenneth R. Rettig, MD1
: `9 @" n6 z9 I% e( p( wClinical Pediatrics* E- ~# R  s' R, _
Volume 46 Number 6
! J: O! ]  \  v! I2 a" SJuly 2007 540-543
& T6 a+ r$ Q" R8 ?8 ^© 2007 Sage Publications
% a5 q+ r& }9 |/ \: Z. v4 C10.1177/0009922806296651( A  t' L9 n# X# b2 w
http://clp.sagepub.com
) F$ m' ^2 v. p' w/ _- h5 ahosted at
% L6 r$ h5 G* l2 |http://online.sagepub.com5 b/ C" E& }* L
Precocious puberty in boys, central or peripheral,
% V0 q/ c- ^: ]4 T, x0 u$ i; Bis a significant concern for physicians. Central: E9 X6 U8 P. u' h9 R
precocious puberty (CPP), which is mediated
  l" x4 a- e$ j$ w0 ~! ]% s# ]! E% qthrough the hypothalamic pituitary gonadal axis, has: @% a& b' L$ ]/ A
a higher incidence of organic central nervous system. j7 H0 x5 \9 L6 ~& c
lesions in boys.1,2 Virilization in boys, as manifested
& P' ]* y! N% H9 ~by enlargement of the penis, development of pubic
2 S4 k2 g$ `+ e( I- c8 khair, and facial acne without enlargement of testi-1 r9 ^5 y4 E+ r( Z+ ]
cles, suggests peripheral or pseudopuberty.1-3 We
5 a- x8 j6 H  T3 ?  m" y; ereport a 16-month-old boy who presented with the
5 m% W/ o( K8 H& s  [enlargement of the phallus and pubic hair develop-
3 C0 p( ]/ z3 P- P/ \" w  s5 _2 rment without testicular enlargement, which was due" D8 x% W- b$ j' w% H, e
to the unintentional exposure to androgen gel used by' H2 D( @8 R, `. x  V4 F& }
the father. The family initially concealed this infor-! U8 m' S/ ^! J" p. \
mation, resulting in an extensive work-up for this
9 R$ ?: Y2 h; ]+ x4 c* W) Ichild. Given the widespread and easy availability of
* n! {6 O) f/ mtestosterone gel and cream, we believe this is proba-8 q- _) E( O$ U" ^, ^) @8 }
bly more common than the rare case report in the
- z8 K/ w' b: ]$ g/ F; I$ G* m. v7 cliterature.4/ b0 o% B) a/ ~6 h6 j$ `
Patient Report% e0 R7 W1 |9 ^+ q8 l. ?! D( l
A 16-month-old white child was referred to the$ i( L0 j$ s3 a4 P+ Y+ i! w
endocrine clinic by his pediatrician with the concern
$ U2 z; L" p' Kof early sexual development. His mother noticed
  l% B" Q: t9 p2 tlight colored pubic hair development when he was# {2 V$ Y6 [! [" y! ?9 M
From the 1Division of Pediatric Endocrinology, 2University of; }% P! v5 ?' E" r! o) c6 p) `0 q
South Alabama Medical Center, Mobile, Alabama.; Y+ a* i9 f; ]# O/ I
Address correspondence to: Samar K. Bhowmick, MD, FACE,$ V; R' |+ A: k* F* a3 @
Professor of Pediatrics, University of South Alabama, College of
+ O/ f* F$ }$ R8 [7 ?$ p% {Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
2 R( D+ y' U2 U4 a: O! m2 je-mail: [email protected].
, V$ X$ Z8 X/ `# K  V6 B# @about 6 to 7 months old, which progressively became$ c- b5 C& M% i3 V1 s
darker. She was also concerned about the enlarge-4 A2 k+ T, h. l& G
ment of his penis and frequent erections. The child! T6 R8 d: a0 K* L( L1 z
was the product of a full-term normal delivery, with+ c7 g3 \# g! {7 t& a
a birth weight of 7 lb 14 oz, and birth length of
- }( j0 T( e2 w+ w) V& \20 inches. He was breast-fed throughout the first year
4 j1 d4 g1 o8 ?; aof life and was still receiving breast milk along with+ v0 U0 }3 _7 w% M' E% o! ~
solid food. He had no hospitalizations or surgery,
3 r% n3 G! b; O6 S5 B% ]- Tand his psychosocial and psychomotor development
- n, g0 |; E* f# v: F( R+ @/ jwas age appropriate.
0 B# W7 H4 l5 Q: r/ VThe family history was remarkable for the father,
6 s3 [6 a" b' C# f+ ?; ?who was diagnosed with hypothyroidism at age 16,( B5 a: Z% o" ^" L: h
which was treated with thyroxine. The father’s, j% L% h- d5 r0 J$ L# z
height was 6 feet, and he went through a somewhat
% e6 a2 E% B0 E  ^early puberty and had stopped growing by age 14.% Z. f9 F7 f3 f+ O  I
The father denied taking any other medication. The& A+ H% {" V$ N/ h1 G, T$ C7 A, d; b
child’s mother was in good health. Her menarche6 G  ^0 h: V) X9 V
was at 11 years of age, and her height was at 5 feet2 r" y  p% b  a0 W8 K: y  G
5 inches. There was no other family history of pre-
9 Q6 L# \* l- x4 c! o2 pcocious sexual development in the first-degree rela-* @8 W$ e; w5 o: d. a" u
tives. There were no siblings.
: Y  |, x! M7 L& l1 gPhysical Examination1 u4 n  I" J: I3 B: `
The physical examination revealed a very active,$ s2 _7 B0 W, ^& A; k& Q  m8 o
playful, and healthy boy. The vital signs documented! p- H3 a8 |4 ~; L- k
a blood pressure of 85/50 mm Hg, his length was7 v" x$ J" N) Q2 |9 C: b/ L6 \
90 cm (>97th percentile), and his weight was 14.4 kg
( h. U* C$ S: _; H1 F# p  u(also >97th percentile). The observed yearly growth
6 A. G7 a7 g$ B6 v8 U$ T/ Yvelocity was 30 cm (12 inches). The examination of, H6 C: Q6 G5 P1 z4 w7 z* {
the neck revealed no thyroid enlargement.
1 W) i  K4 W: R, K/ s- d7 i- F6 gThe genitourinary examination was remarkable for
4 P% W# e; Y* r9 z$ kenlargement of the penis, with a stretched length of3 G  ?! G5 c+ L: ]& D( M) o/ f( \( S
8 cm and a width of 2 cm. The glans penis was very well
/ x; o% a# L; X- \6 h0 Cdeveloped. The pubic hair was Tanner II, mostly around5 ^* G; {3 p! S8 v
540
% ?' o% n: k) h# J, Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 V+ }4 E  ~; p% Y( [( |+ v  J, Uthe base of the phallus and was dark and curled. The/ f' G, x: @6 X3 c; k' {" ~: ^
testicular volume was prepubertal at 2 mL each./ c( w- ?; Q* n4 c; Z
The skin was moist and smooth and somewhat
: E( M- a( \, Aoily. No axillary hair was noted. There were no; i! Q( Y2 X, y) z- b) O- \7 g
abnormal skin pigmentations or café-au-lait spots.
& o, v$ u. [, i# J0 j. DNeurologic evaluation showed deep tendon reflex 2+: l+ W! i9 {! ~) ^% M' F; S
bilateral and symmetrical. There was no suggestion1 D. S/ ~2 \8 N# [3 b
of papilledema.2 B8 j, n+ F" ]; i: I: ]2 ?
Laboratory Evaluation
/ |! v( L- W+ n/ UThe bone age was consistent with 28 months by6 @: _3 n# V$ \& }
using the standard of Greulich and Pyle at a chrono-
, I" `. j: U6 E' G& h" Jlogic age of 16 months (advanced).5 Chromosomal
9 E, V, ?) P& N- h) ]( Kkaryotype was 46XY. The thyroid function test0 \& I* t. }  d, N* o
showed a free T4 of 1.69 ng/dL, and thyroid stimu-8 B4 L+ O2 F" |9 d1 w: c, S
lating hormone level was 1.3 µIU/mL (both normal).
5 a2 z- }( X2 J8 B8 D2 E( f7 _The concentrations of serum electrolytes, blood
* d8 G7 n1 n6 M+ H6 }urea nitrogen, creatinine, and calcium all were
/ ^/ ~! C0 O. @within normal range for his age. The concentration
. W! R' _! b. V4 q# D, ~of serum 17-hydroxyprogesterone was 16 ng/dL/ e! V8 s( f2 W, L3 q3 `
(normal, 3 to 90 ng/dL), androstenedione was 208 I; x1 b" o  K- `8 F# C
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-; Q  z; g- @" E! ^+ e
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
8 |+ n, ^' _- _0 B9 x9 bdesoxycorticosterone was 4.3 ng/dL (normal, 7 to3 J' v- a8 K: @+ j1 Z0 U& g. T+ ^
49ng/dL), 11-desoxycortisol (specific compound S)
) h. U& S; f3 \7 p% Hwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
9 Y! d. d! w" x+ q; c3 u( l  |tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total$ C; U) R/ H2 F$ Y! X6 n6 ?9 H' b
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),- ~/ E$ _9 y/ C) i
and β-human chorionic gonadotropin was less than
/ Z! e6 a- m6 i5 G5 mIU/mL (normal <5 mIU/mL). Serum follicular5 }! s4 v/ v$ C+ D+ W& P8 b$ [+ W
stimulating hormone and leuteinizing hormone& a" d3 R, m, @7 x2 B4 {+ l  {
concentrations were less than 0.05 mIU/mL) [5 w' ~4 r2 h' I. {$ G
(prepubertal).
5 b& y+ q+ ^; I* n! ]4 g$ B6 b9 mThe parents were notified about the laboratory5 S! `2 Z8 T# z7 o" R! d
results and were informed that all of the tests were
2 U6 q( u9 H5 k2 A3 w: bnormal except the testosterone level was high. The
2 Z: X8 [. I: A' o1 Bfollow-up visit was arranged within a few weeks to
# t9 O0 ?# ?$ K9 bobtain testicular and abdominal sonograms; how-  r7 E9 C, a' F: C) a- a& ^: v. L
ever, the family did not return for 4 months.& T' _: `% ?/ z0 {7 |6 t
Physical examination at this time revealed that the
5 T4 u6 {) c0 r6 i, Fchild had grown 2.5 cm in 4 months and had gained# [8 k/ p6 Z( ^
2 kg of weight. Physical examination remained7 l  f4 |4 ^) z6 d3 G
unchanged. Surprisingly, the pubic hair almost com-! R9 e0 o7 w* S  J* P' R
pletely disappeared except for a few vellous hairs at
2 }& N, R4 Z- Q+ N  Bthe base of the phallus. Testicular volume was still 2
5 A' f. c* z) D9 k7 bmL, and the size of the penis remained unchanged.: Q. G7 s# l% u
The mother also said that the boy was no longer hav-
% o  v  y# D  I. @0 }ing frequent erections.
, D3 m2 m, X1 L7 n9 nBoth parents were again questioned about use of7 x4 d# d4 W. l. G" Y
any ointment/creams that they may have applied to
. E: K, B; z/ u2 D, Cthe child’s skin. This time the father admitted the
5 z) k/ a3 g2 E+ V* |Topical Testosterone Exposure / Bhowmick et al 541* A8 Z: S3 D& h! r6 L
use of testosterone gel twice daily that he was apply-: ?8 d, X! P) `
ing over his own shoulders, chest, and back area for
2 l1 z+ [: d& L$ ?* K1 p* La year. The father also revealed he was embarrassed
- U- i( e5 M" z1 M/ qto disclose that he was using a testosterone gel pre-: Y4 _  l6 L) A' j* R
scribed by his family physician for decreased libido) y' _! j; Z. p6 a: D; e! Q
secondary to depression.
9 m( H$ }% `- v0 K, GThe child slept in the same bed with parents.% E" t4 [8 ]. z1 F
The father would hug the baby and hold him on his
* M4 \8 o( N/ c, @! B; nchest for a considerable period of time, causing sig-
1 r# @9 h' f2 L2 K* Q) X; n) U8 [5 gnificant bare skin contact between baby and father.
7 X. M2 j+ D- w5 j/ H, mThe father also admitted that after the phone call,# b: Z& ^+ ~1 _( K" F9 @
when he learned the testosterone level in the baby
) z# N- ^: e, z2 B4 x, ?was high, he then read the product information
8 q5 x* f, e7 u, k% ?( Tpacket and concluded that it was most likely the rea-
2 K$ C2 R! j8 Y1 e: @3 O& Mson for the child’s virilization. At that time, they6 K- M2 n3 g: e, \
decided to put the baby in a separate bed, and the" C* j4 \7 m* g' x/ p, v% G# v6 ?% k
father was not hugging him with bare skin and had) Z4 w+ V& ?- Z/ \2 U9 S- S
been using protective clothing. A repeat testosterone
( T: U. A1 G$ ]+ {$ B1 ctest was ordered, but the family did not go to the
4 G1 C- I7 R0 ilaboratory to obtain the test.; N5 W2 \& Q5 Q# d9 X" _8 q4 }2 s
Discussion2 V" h4 m$ Q- S
Precocious puberty in boys is defined as secondary
3 C* _: P# n5 g. I& csexual development before 9 years of age.1,41 \! X$ v; w! ]! r/ v
Precocious puberty is termed as central (true) when6 q+ {5 a6 H* G) H
it is caused by the premature activation of hypo-
: L( {9 c' e7 Ethalamic pituitary gonadal axis. CPP is more com-3 d8 P: Y7 J1 R
mon in girls than in boys.1,3 Most boys with CPP! |, [) b" @0 O) D9 W3 X
may have a central nervous system lesion that is
1 A2 I" v0 Y) U) V$ {" qresponsible for the early activation of the hypothal-
1 Z1 o/ n* n! V0 B9 |1 `2 T+ G1 e% l, Xamic pituitary gonadal axis.1-3 Thus, greater empha-
- C% [, C" [& M1 Q' ]& U9 osis has been given to neuroradiologic imaging in
  F$ p2 L- c5 y( @+ O5 hboys with precocious puberty. In addition to viril-
$ ^: p) o7 }1 O9 x/ U4 Uization, the clinical hallmark of CPP is the symmet-
( R. {, I  ^* ]3 g2 H5 yrical testicular growth secondary to stimulation by
  O7 w1 {- \1 b5 ogonadotropins.1,3
  P# E+ L: {/ m+ {1 k9 q) d9 OGonadotropin-independent peripheral preco-
1 m7 {- p, H' H; Q6 tcious puberty in boys also results from inappropriate
4 D# |4 i% c3 u0 e" k1 yandrogenic stimulation from either endogenous or3 @5 `% i, t4 N# R" u4 s& b7 A, `8 L
exogenous sources, nonpituitary gonadotropin stim-: w* `/ {0 Y- |9 B2 a
ulation, and rare activating mutations.3 Virilizing
7 `6 q$ m5 q% v* D& ^congenital adrenal hyperplasia producing excessive
; V( q- w! A9 g1 k/ `9 Oadrenal androgens is a common cause of precocious' t: Y: k% p+ R0 n& J
puberty in boys.3,4& k% s6 M& i& v( w
The most common form of congenital adrenal
+ O+ w7 k" O- W( z, d3 j$ lhyperplasia is the 21-hydroxylase enzyme deficiency.' h# W7 u/ ?6 j0 J, h# _# [* N
The 11-β hydroxylase deficiency may also result in
" x1 Z& V5 Q$ Z" [5 r9 vexcessive adrenal androgen production, and rarely,: c' v% H. A+ c6 a+ W6 S: Y
an adrenal tumor may also cause adrenal androgen5 i! }5 f( _% r0 e" c3 n
excess.1,3$ y3 f; d1 V( R, V) S5 Z$ D
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) f3 J2 I( ~2 o( d) w  F542 Clinical Pediatrics / Vol. 46, No. 6, July 2007) x$ i% {2 K$ H/ ^
A unique entity of male-limited gonadotropin-- g, h1 }" q6 n0 w; R/ Y- t6 g
independent precocious puberty, which is also known5 z+ S  [- H' j
as testotoxicosis, may cause precocious puberty at a* v7 s. l) _8 M
very young age. The physical findings in these boys
3 I' b( P* s6 r* O# lwith this disorder are full pubertal development,$ F! C) g" V  Z" x+ E& W
including bilateral testicular growth, similar to boys1 e, k# f0 L- c' n9 ^7 L1 ~
with CPP. The gonadotropin levels in this disorder8 x0 _: I8 Z$ I( ~" m+ ]9 i
are suppressed to prepubertal levels and do not show
( j0 t( ]8 Y9 T1 m% v( u! P; p% Q6 tpubertal response of gonadotropin after gonadotropin-
. Z0 {- ~+ g0 m2 g0 C* [! Ureleasing hormone stimulation. This is a sex-linked
8 e- L$ ?8 c- pautosomal dominant disorder that affects only3 Q: c2 N* n% \3 k/ f( c
males; therefore, other male members of the family
: Z2 m( e" P' Lmay have similar precocious puberty.3
" r0 {' A. m9 r6 M3 s6 ?' B; F, j/ FIn our patient, physical examination was incon-- m/ c3 y# W' W% c9 c
sistent with true precocious puberty since his testi-
; |+ [/ \- F% \/ d: M) Acles were prepubertal in size. However, testotoxicosis
; S. T5 T/ s# f$ o7 X9 S. M6 [" lwas in the differential diagnosis because his father
: n) H) I% g9 R% Ostarted puberty somewhat early, and occasionally,
! Z6 E/ d9 q8 p- v9 Xtesticular enlargement is not that evident in the5 P1 {" p+ i" ^% ?- ^( f, @! m
beginning of this process.1 In the absence of a neg-
' i/ u- p: H$ Q6 X9 u  |ative initial history of androgen exposure, our
% ?8 v; j9 z( I2 l4 o% q8 ~biggest concern was virilizing adrenal hyperplasia,
; y$ }  h1 E5 u% V4 O. weither 21-hydroxylase deficiency or 11-β hydroxylase
6 `7 M1 X: e! Pdeficiency. Those diagnoses were excluded by find-
. R# z$ ]0 f# c3 Bing the normal level of adrenal steroids.. w/ Q+ j/ o) S
The diagnosis of exogenous androgens was strongly
! v0 W5 r  ^; {& Q& m: q! {suspected in a follow-up visit after 4 months because
. k$ T& p( I$ {- B4 C( y" bthe physical examination revealed the complete disap-( V" j' S9 g* ]
pearance of pubic hair, normal growth velocity, and# i" P" C3 _8 }* J
decreased erections. The father admitted using a testos-% a& v9 z" V& Y
terone gel, which he concealed at first visit. He was$ D/ o$ A& ?: o6 w; G
using it rather frequently, twice a day. The Physicians’. p& r# z  E  C% A3 s& v
Desk Reference, or package insert of this product, gel or1 w# O5 S) B0 Y! V2 D
cream, cautions about dermal testosterone transfer to
9 |! j, k7 q; e% g9 J+ I& Punprotected females through direct skin exposure.
6 y: S2 b5 d: [2 |9 L& N* d5 uSerum testosterone level was found to be 2 times the
7 O& \/ q+ D; o9 I9 o6 ?1 Cbaseline value in those females who were exposed to
. _" U) X' \1 i& C; ieven 15 minutes of direct skin contact with their male
2 `( x% B) X2 Hpartners.6 However, when a shirt covered the applica-1 h) U0 x  P( v6 _9 I# R4 M( e
tion site, this testosterone transfer was prevented.
' K$ b0 t4 q3 a% Q# n& cOur patient’s testosterone level was 60 ng/mL,* [# \9 y; w2 m  k" W) t
which was clearly high. Some studies suggest that
4 \, b! z8 d( `6 b! P& Mdermal conversion of testosterone to dihydrotestos-& _2 N0 l$ x0 ^7 n+ z! Q
terone, which is a more potent metabolite, is more
2 q+ w) O7 K7 c' v8 m6 w% }  L" Factive in young children exposed to testosterone
0 M5 _( y# a* i) X, n0 ?exogenously7; however, we did not measure a dihy-- u- @5 {: k+ N& B2 W
drotestosterone level in our patient. In addition to
2 w/ y9 `- T8 b" @* Mvirilization, exposure to exogenous testosterone in
9 p3 m& t$ Y; o7 Ichildren results in an increase in growth velocity and% _* ^0 P2 W! B! s+ n, o3 `/ N6 F8 b
advanced bone age, as seen in our patient.
+ b9 r$ z. y  c9 A7 y; dThe long-term effect of androgen exposure during' a$ M9 U# U9 e; C3 |- \! W+ Q
early childhood on pubertal development and final5 x4 j+ }" q2 a$ C  l. q
adult height are not fully known and always remain3 F- [# H8 C3 `2 v2 o
a concern. Children treated with short-term testos-7 t- S# a$ w  `
terone injection or topical androgen may exhibit some
0 c- t0 K1 N! v0 \! ]0 ?4 Hacceleration of the skeletal maturation; however, after
: _* {9 q. g- l+ rcessation of treatment, the rate of bone maturation
3 [7 ~6 k. V. Q/ n# r2 vdecelerates and gradually returns to normal.8,9
% h5 k+ E9 L. pThere are conflicting reports and controversy2 l3 a9 R4 q# b' D' r: [  |" Z, L6 O
over the effect of early androgen exposure on adult
# N/ i  u) O2 V; w1 w- [penile length.10,11 Some reports suggest subnormal# I# j# l* i6 \
adult penile length, apparently because of downreg-# O$ ?; B8 o4 |' p" Z# t4 ]: ]+ O; }
ulation of androgen receptor number.10,12 However,: {7 `8 Q7 Y% q8 u
Sutherland et al13 did not find a correlation between  Y! X8 \* U, c& N+ l' f
childhood testosterone exposure and reduced adult
+ Z" M6 B: R% N2 [2 H  J4 _penile length in clinical studies.
; j5 Z0 _6 q/ _7 U9 QNonetheless, we do not believe our patient is! ?" L  P  W' t# H/ H
going to experience any of the untoward effects from
8 U1 ~. T' i) i0 H3 }testosterone exposure as mentioned earlier because
+ b8 h7 h& ?8 b% Q( {- b. Ithe exposure was not for a prolonged period of time.
7 v/ E0 N  l6 E+ v( o5 PAlthough the bone age was advanced at the time of
6 V* i- s1 `) R2 E; M3 d1 tdiagnosis, the child had a normal growth velocity at! x- b1 @  H* h: {' V
the follow-up visit. It is hoped that his final adult
3 E* J3 k: I' \" o, O/ _: {- c" Dheight will not be affected.
  s' L# t6 F7 x; E5 f. WAlthough rarely reported, the widespread avail-# y- e# z4 Z" {3 m
ability of androgen products in our society may1 `  i0 Y$ i4 t; L8 Z+ P0 N9 `
indeed cause more virilization in male or female. E+ E  L( _  I; a% P8 o$ E- B
children than one would realize. Exposure to andro-
7 O; X9 [5 `6 V+ Mgen products must be considered and specific ques-9 R1 _) |$ [* a7 q- v6 A
tioning about the use of a testosterone product or
8 b+ H) N9 S! q0 {& U; ^8 `gel should be asked of the family members during6 H! U  b, x+ l" n9 f
the evaluation of any children who present with vir-
  d& C- M% p2 d1 J0 v, T$ c* w3 jilization or peripheral precocious puberty. The diag-* t; U' E* `; D+ V/ K
nosis can be established by just a few tests and by3 F# f4 W; b7 w# S, L% Q# c
appropriate history. The inability to obtain such a
4 \( @% i+ T/ s5 |. R4 f/ yhistory, or failure to ask the specific questions, may2 J* E# A3 |+ G
result in extensive, unnecessary, and expensive  b6 H& I) _! E& I
investigation. The primary care physician should be
2 g; _5 J* A: {* T: T6 i4 oaware of this fact, because most of these children
& Y. }0 k/ n& c! A# z: u1 qmay initially present in their practice. The Physicians’: `" m# k# g$ j! O' r/ R
Desk Reference and package insert should also put a+ t- e8 R1 b  {4 I3 R0 r
warning about the virilizing effect on a male or/ V# L: ~: B, }+ _
female child who might come in contact with some-
, @+ X- }2 w0 V9 a& h- qone using any of these products.
5 n3 z5 ^. y, n# ?9 ?References+ j5 a0 i5 u! B& q2 @- S
1. Styne DM. The testes: disorder of sexual differentiation) V. |- m, h- z
and puberty in the male. In: Sperling MA, ed. Pediatric: @( A% k3 W: U/ @$ [( Z! V7 H
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;. \! B2 P& J3 i* @/ K. [
2002: 565-628.
1 o, A3 G& p9 Y! A/ ^2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious' I8 t) k# [3 u2 @
puberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
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

' F. n9 }2 ?& {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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