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Sexual Precocity in a 16-Month-Old9 X6 s, n# m% K) H+ x- K6 ?9 F
Boy Induced by Indirect Topical! `6 B3 n+ U4 `
Exposure to Testosterone
: Q. S9 E( }& O$ b' L5 N' O2 u9 DSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2# o. o( ^' j0 n
and Kenneth R. Rettig, MD1. K6 ]* f1 d0 Z. u0 L, l
Clinical Pediatrics
$ A& ?8 @. E# T) a; g- x2 j. eVolume 46 Number 6
2 {0 U: K/ e/ CJuly 2007 540-543
8 @. U0 q( u4 B© 2007 Sage Publications
4 M! M* o+ V; t3 N10.1177/00099228062966516 V4 b2 g9 e- x2 ~9 ]$ ?/ p$ a
http://clp.sagepub.com
  u6 d0 t# @5 }hosted at
# Q- K( H0 C5 H3 [http://online.sagepub.com6 H6 D: O4 [5 s
Precocious puberty in boys, central or peripheral,
. B8 C6 T0 z9 ~' ~5 n, P# I& Q- wis a significant concern for physicians. Central1 y6 [9 Z( @. i* T2 v1 ?- z
precocious puberty (CPP), which is mediated) f& c1 I2 }4 @5 t7 I9 [
through the hypothalamic pituitary gonadal axis, has- G" C9 m( G0 R3 C2 D
a higher incidence of organic central nervous system
  q$ A1 l5 J. }4 a/ Alesions in boys.1,2 Virilization in boys, as manifested8 Z) n! K7 h+ B1 Z2 a
by enlargement of the penis, development of pubic
% W/ R, W/ B+ }hair, and facial acne without enlargement of testi-
8 D8 z& C% a7 n! O& G+ n* o9 e, Ncles, suggests peripheral or pseudopuberty.1-3 We. r: X6 X; _( K* ?1 P
report a 16-month-old boy who presented with the
- H& Z4 F8 j+ Y+ m8 n# i9 Venlargement of the phallus and pubic hair develop-6 I2 G9 a4 {( Z; H2 b
ment without testicular enlargement, which was due
( Q+ S# P& I" A# \9 T& o' }- E! @( f6 zto the unintentional exposure to androgen gel used by
% M, K* W& b: S8 w# [" fthe father. The family initially concealed this infor-/ E5 g2 v7 p" Q' x# V8 u
mation, resulting in an extensive work-up for this
* K. P& v6 M* {child. Given the widespread and easy availability of- N% N& K3 v* U
testosterone gel and cream, we believe this is proba-% T8 Q- U6 z& l" @3 r. T; s
bly more common than the rare case report in the
" b, Q4 V& J# f6 {literature.4
$ m$ A& `6 h: ^7 P7 O' A+ g4 IPatient Report- x- @, d2 |- X5 Y. p# t/ w9 y
A 16-month-old white child was referred to the8 v$ l) `$ d- }! D; Z! @
endocrine clinic by his pediatrician with the concern) d/ w0 y" a: q% y6 f. p
of early sexual development. His mother noticed
4 E. o/ b* ?! Alight colored pubic hair development when he was. d3 W2 O, u: `
From the 1Division of Pediatric Endocrinology, 2University of& J3 A1 n. G* ~& F3 ^( [: l2 D4 j: ?6 b
South Alabama Medical Center, Mobile, Alabama.( A4 O7 O0 L8 \& D" n/ k
Address correspondence to: Samar K. Bhowmick, MD, FACE,
. i5 c) Y( s; K3 ?: OProfessor of Pediatrics, University of South Alabama, College of
: j6 }# b6 v3 d# W! ]Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;; A, h9 p8 S  b7 i. ?8 Q/ j8 P
e-mail: [email protected].
  }4 p# h) j+ i3 P) v, d! ?; ?. Zabout 6 to 7 months old, which progressively became
7 B4 U( u4 t( j/ o" Z) Y" u. J. Adarker. She was also concerned about the enlarge-. G, o7 d( a  |
ment of his penis and frequent erections. The child- W' y: Z8 A  M. n; T0 @, C2 t4 M9 e% a" C$ M
was the product of a full-term normal delivery, with+ S; ^7 I8 G$ Q4 T2 G* o" V) N) F
a birth weight of 7 lb 14 oz, and birth length of
7 D9 g: Z/ X1 o3 w2 r0 X20 inches. He was breast-fed throughout the first year  ^7 _/ f0 @( B  V( q4 y
of life and was still receiving breast milk along with
( R- p7 e) b/ N6 E" k+ xsolid food. He had no hospitalizations or surgery,
6 w) j3 o* J+ P: \7 rand his psychosocial and psychomotor development
5 I% k7 j! z* X* }7 k: W9 vwas age appropriate.
2 V7 Z) z' i* y9 p4 I' dThe family history was remarkable for the father,4 X! D. j: v% S' @
who was diagnosed with hypothyroidism at age 16,4 [* l3 ^, P* O0 R; c: K4 ^
which was treated with thyroxine. The father’s' F' R& u% c9 A, j3 }
height was 6 feet, and he went through a somewhat9 ?0 a# K) Y  }! n4 h5 m9 L. V
early puberty and had stopped growing by age 14.
! {4 U  @% j0 v& `2 jThe father denied taking any other medication. The" r, c+ x* v  }3 j0 \) ^$ w7 Y
child’s mother was in good health. Her menarche7 m( {) L* b" X
was at 11 years of age, and her height was at 5 feet
. w5 V) G/ s0 M8 A) F4 W5 inches. There was no other family history of pre-0 W: E  C" B6 l0 \
cocious sexual development in the first-degree rela-
4 O2 _8 C3 A$ }tives. There were no siblings.) @7 z) U! {& P, ?
Physical Examination
+ F! m% @/ k( p5 C! dThe physical examination revealed a very active,6 H6 H# {  y8 {$ U: w
playful, and healthy boy. The vital signs documented  `/ a8 w% E( k$ _7 a8 s
a blood pressure of 85/50 mm Hg, his length was
0 X' e, x3 J  f+ L90 cm (>97th percentile), and his weight was 14.4 kg
( z) P' m. w: {# S(also >97th percentile). The observed yearly growth9 G! t5 W2 h  C2 b: Q& t; o
velocity was 30 cm (12 inches). The examination of) ]; O5 L- t) a! ]& {2 L
the neck revealed no thyroid enlargement.
9 N0 `4 l* [% e; JThe genitourinary examination was remarkable for
9 Q+ L5 j+ l$ N1 a( F* L! M" x3 Qenlargement of the penis, with a stretched length of
4 r" y# h! H' S, h4 T8 cm and a width of 2 cm. The glans penis was very well; o6 \8 |: w5 [8 v, L! Q
developed. The pubic hair was Tanner II, mostly around& }, a3 i  b& X) s2 F& P& H4 |
5401 D" j! w) x! Y! {% A
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from8 ?' k. h9 Z' i( c5 p; b9 }+ H
the base of the phallus and was dark and curled. The1 _0 [5 R7 ]: T5 y! s5 f
testicular volume was prepubertal at 2 mL each.& A2 u6 X& f5 c" y6 j( q
The skin was moist and smooth and somewhat" G! O# k! L* E3 P
oily. No axillary hair was noted. There were no
7 j4 [+ O( Z" T- ]/ v7 p  Oabnormal skin pigmentations or café-au-lait spots.' }0 Z! q! T0 f8 {" V4 Y! V2 l; q
Neurologic evaluation showed deep tendon reflex 2+
0 g- O' o5 \; ?4 S  R2 V1 Abilateral and symmetrical. There was no suggestion
9 ]( q6 `9 E6 n$ k: l* @. Dof papilledema.
* |/ F% C/ _. K* TLaboratory Evaluation+ d3 A- {  e$ a
The bone age was consistent with 28 months by1 ]) v$ p; o4 M& S& f# `" J# S1 p
using the standard of Greulich and Pyle at a chrono-5 T: Y. @+ t, d9 T4 [: Y
logic age of 16 months (advanced).5 Chromosomal: ?% Z, o/ }# ^3 e% _0 s+ p9 x
karyotype was 46XY. The thyroid function test
" s9 W2 P* y! x% T, S! _showed a free T4 of 1.69 ng/dL, and thyroid stimu-8 ~. [' Q/ E2 h; W& P" k. B* g$ b( y
lating hormone level was 1.3 µIU/mL (both normal).
7 h1 ~, I5 H5 j& L, P( \- lThe concentrations of serum electrolytes, blood
" Z- m9 I5 B/ Qurea nitrogen, creatinine, and calcium all were
& h5 o, W9 G' T; {8 a# g0 twithin normal range for his age. The concentration
. d; V, v/ U) Q- N9 Fof serum 17-hydroxyprogesterone was 16 ng/dL
7 [$ w$ ]3 T, {0 n& S4 P(normal, 3 to 90 ng/dL), androstenedione was 201 H# ]8 ^, i7 ]( ~1 ?& O/ U
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
) T% Y& [* P( n. r) Pterone was 38 ng/dL (normal, 50 to 760 ng/dL),
( f) L- {6 l& ndesoxycorticosterone was 4.3 ng/dL (normal, 7 to. s8 {. N0 l1 E' a$ _
49ng/dL), 11-desoxycortisol (specific compound S)
1 |3 }" k/ u3 ?$ Jwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
. C" g& I& [9 B5 c# u* A) Utisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total; k7 G& t3 r2 g
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),7 G+ h2 K: J5 r3 k5 h9 s
and β-human chorionic gonadotropin was less than: p$ o' z* ?  h9 A
5 mIU/mL (normal <5 mIU/mL). Serum follicular
, O5 ^. a( y/ }/ l1 xstimulating hormone and leuteinizing hormone
( O- n3 `4 q( z! Z  D6 econcentrations were less than 0.05 mIU/mL3 m0 x0 B: E+ d4 W) j$ w
(prepubertal).. e9 r9 K' I/ e  i8 d
The parents were notified about the laboratory: f; A4 y2 [6 e% M; g. l
results and were informed that all of the tests were
* ]( ^+ x5 c) A9 e: T4 y2 ~) Nnormal except the testosterone level was high. The
0 X4 R3 _, `6 `9 S9 k" j. bfollow-up visit was arranged within a few weeks to9 ^" _5 y+ w3 W- r4 d
obtain testicular and abdominal sonograms; how-/ {6 A3 t! U+ {7 d
ever, the family did not return for 4 months.  F: \3 [! @2 q+ Y: V
Physical examination at this time revealed that the
% C2 C% F% I( [/ Y/ h3 W+ B+ `child had grown 2.5 cm in 4 months and had gained* M7 I$ Z* l" e
2 kg of weight. Physical examination remained
* d/ {6 w& ?: I" zunchanged. Surprisingly, the pubic hair almost com-- `, N7 I! ?% C6 L" j* y
pletely disappeared except for a few vellous hairs at
( q! ?: a6 ~6 N1 C/ \* Ethe base of the phallus. Testicular volume was still 2
( x! u/ j  k& z! b  g" CmL, and the size of the penis remained unchanged./ h0 S# p5 U) T1 s
The mother also said that the boy was no longer hav-
# C2 E# N: {" E, o; ting frequent erections.
5 ^! j' Q& o3 }! y7 k! J$ nBoth parents were again questioned about use of
; n2 D9 p" E8 N8 d, rany ointment/creams that they may have applied to. |7 j* {3 G& o" f. o* U
the child’s skin. This time the father admitted the! r2 G' O' E; Z6 k: j/ q
Topical Testosterone Exposure / Bhowmick et al 541
: d$ F- h$ C- g2 D* }use of testosterone gel twice daily that he was apply-, O, I, H  H" t4 i
ing over his own shoulders, chest, and back area for
2 `$ }& Y3 \! v2 Aa year. The father also revealed he was embarrassed
* N4 _% ?3 r; Q2 ?to disclose that he was using a testosterone gel pre-
$ q" _" |# K/ F5 ~, A3 z) tscribed by his family physician for decreased libido
* g8 {9 t- n7 a0 b) ssecondary to depression.
& s. D, B+ y' {# Z" y3 a+ R" L, }The child slept in the same bed with parents.
. b& L  a4 X, G0 m# X3 }4 U: ~The father would hug the baby and hold him on his
* @6 T& I( M# O- Zchest for a considerable period of time, causing sig-6 |1 }* h0 ^5 z! n
nificant bare skin contact between baby and father.
! a4 J  q9 j2 LThe father also admitted that after the phone call,
; H  @  \+ q: U% N; n$ @when he learned the testosterone level in the baby
, w$ H6 g  P) P2 ^  N! l& W4 owas high, he then read the product information
2 F+ o* z; K8 I% s( Qpacket and concluded that it was most likely the rea-" a! c  J" z- _* P
son for the child’s virilization. At that time, they4 {% a9 j, S% m3 S% C9 U0 n
decided to put the baby in a separate bed, and the
, t  F* o$ Z  a' }0 E! Z, M6 Xfather was not hugging him with bare skin and had
7 c" L1 c  O9 x4 b9 nbeen using protective clothing. A repeat testosterone
+ p7 c" m) b8 t) ctest was ordered, but the family did not go to the4 J5 I2 j2 r- K" ?+ D) `8 S
laboratory to obtain the test.
2 K4 @0 J0 L1 `; pDiscussion5 `5 b/ E9 K# n
Precocious puberty in boys is defined as secondary
  G1 O$ j: H/ ~- ]sexual development before 9 years of age.1,4% @% S& F# Y. o! ?3 l. m$ @7 f6 r" S1 z
Precocious puberty is termed as central (true) when
- D, ]4 ^( U  \9 a  {it is caused by the premature activation of hypo-
- c. G! i  m( u% |9 m) Ithalamic pituitary gonadal axis. CPP is more com-, l* j1 Z# X3 \+ M% x
mon in girls than in boys.1,3 Most boys with CPP
0 n$ L$ `3 U! e1 S% C$ _0 f6 @may have a central nervous system lesion that is) R: s/ F  t' ]7 ]4 z. G
responsible for the early activation of the hypothal-
4 c) {/ R4 N+ r3 vamic pituitary gonadal axis.1-3 Thus, greater empha-( t6 ^& C9 O  t" m0 S
sis has been given to neuroradiologic imaging in+ E: m$ \* C/ [: j
boys with precocious puberty. In addition to viril-8 `( M. `1 L% e- E
ization, the clinical hallmark of CPP is the symmet-) [# I+ [2 v2 h: n2 K
rical testicular growth secondary to stimulation by
' f8 Q% d/ @7 @' l- n0 {1 Tgonadotropins.1,3, v) P6 @0 h- a+ s
Gonadotropin-independent peripheral preco-
- Q* s  X: R: H' ]0 [/ T3 b) Jcious puberty in boys also results from inappropriate
% h0 _& j" m4 h' jandrogenic stimulation from either endogenous or
& Q. I# f/ ?  Y. n# iexogenous sources, nonpituitary gonadotropin stim-
0 B) y+ ^/ s9 d$ }ulation, and rare activating mutations.3 Virilizing7 ], u: W6 e9 d2 S8 x
congenital adrenal hyperplasia producing excessive/ x0 [) i% p) v' H) r2 r% u
adrenal androgens is a common cause of precocious9 U* z) L9 @2 T+ d& }' P$ F* s
puberty in boys.3,4* ?; r& T. C; p/ _( {0 l: V
The most common form of congenital adrenal
0 f" x* G; \0 N  K& Y1 R! @- {* @9 ehyperplasia is the 21-hydroxylase enzyme deficiency.
& E" m# a8 z( P0 _1 o$ J1 b# v- `The 11-β hydroxylase deficiency may also result in" n* C# ^" t# [# D! q1 k
excessive adrenal androgen production, and rarely,1 n# p" O# h) C. F% ?9 l
an adrenal tumor may also cause adrenal androgen! D: d$ b5 D( E( z( z3 x* y9 b9 a
excess.1,3
$ r$ K1 _- U, }1 ~3 [at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ ]6 T4 [: y$ p' ^5 F
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007( ?0 Q/ ?1 ^, K- t$ [' Q
A unique entity of male-limited gonadotropin-! S7 C& V( T" X) ]: @* R3 [
independent precocious puberty, which is also known
5 U( ~" d& T( e: w& Y8 s+ X$ t1 kas testotoxicosis, may cause precocious puberty at a
7 N, a# ~' h3 N- jvery young age. The physical findings in these boys
2 L4 d7 @. m3 t! \% Z0 y. e  t& b/ Mwith this disorder are full pubertal development,
" l; j* [: f8 D; F0 Dincluding bilateral testicular growth, similar to boys
* R8 d& W; @* a7 jwith CPP. The gonadotropin levels in this disorder
8 P# n; Q/ f3 j" b% E. vare suppressed to prepubertal levels and do not show5 S/ y+ G  y$ G5 k
pubertal response of gonadotropin after gonadotropin-
1 C9 ^5 b: W8 X* S0 t9 H+ q+ Nreleasing hormone stimulation. This is a sex-linked
$ p" g- K# U+ Z1 j! }0 Jautosomal dominant disorder that affects only7 t! r, e, H6 @4 n4 Z. b" K( x
males; therefore, other male members of the family
3 y: q+ q# W5 Q& S& Z0 p$ umay have similar precocious puberty.34 F% O6 D. C' b6 K) C$ S/ X
In our patient, physical examination was incon-
) z& |, {7 E) H+ lsistent with true precocious puberty since his testi-# }% e0 |' u2 s. P8 N& q
cles were prepubertal in size. However, testotoxicosis
0 |* R8 `' ?2 i. M2 {was in the differential diagnosis because his father% z0 g( H( R" P7 R
started puberty somewhat early, and occasionally,4 n# Y8 v# f: f! z# E8 ]) g1 f
testicular enlargement is not that evident in the$ M5 ?0 N) N; I9 f2 H: j
beginning of this process.1 In the absence of a neg-, f8 M9 s; M: r; Y: |2 V# @. k+ ]# ^
ative initial history of androgen exposure, our
4 o1 [4 @8 @4 _  W- tbiggest concern was virilizing adrenal hyperplasia,
' o4 s9 ]' F4 ~" p' Ieither 21-hydroxylase deficiency or 11-β hydroxylase7 j- g6 {" n1 K
deficiency. Those diagnoses were excluded by find-
# n' n/ h: {% K1 H; Q4 U& Cing the normal level of adrenal steroids.! f* h# }0 E$ T9 e
The diagnosis of exogenous androgens was strongly
1 A1 I  b6 H$ @) y, Jsuspected in a follow-up visit after 4 months because* g; ?3 V7 M+ g' P/ a
the physical examination revealed the complete disap-  T3 l8 Y1 h( x5 v$ ^4 ?" a% c
pearance of pubic hair, normal growth velocity, and8 v0 @/ U6 F0 @1 j9 I/ d9 ?
decreased erections. The father admitted using a testos-
, E! U/ ^% Z7 S% q: ^& {# }terone gel, which he concealed at first visit. He was1 G9 G, [! M$ {. _) [3 z; p
using it rather frequently, twice a day. The Physicians’
; h6 {5 d$ _7 c- MDesk Reference, or package insert of this product, gel or; N5 W' y$ t, b' C& C$ k4 r4 V8 _
cream, cautions about dermal testosterone transfer to# r$ [" c* g) V9 ~6 D0 f
unprotected females through direct skin exposure.( i! A4 ~' ~" Z# b- c, `% j
Serum testosterone level was found to be 2 times the; a# _0 K$ K: F) z/ i$ c/ j
baseline value in those females who were exposed to
! P1 b2 t. v4 b7 P; I# Ueven 15 minutes of direct skin contact with their male
% ^8 G  Q9 M/ e. Tpartners.6 However, when a shirt covered the applica-/ m, N+ y7 j5 m2 g+ R) C- x
tion site, this testosterone transfer was prevented.- ?3 F& ?2 n$ w* O. g
Our patient’s testosterone level was 60 ng/mL,
1 O$ g& D' _+ z5 swhich was clearly high. Some studies suggest that' H8 Q: A4 ?  s5 G* a# L
dermal conversion of testosterone to dihydrotestos-
9 {$ `9 I( A( t% j1 e( K$ yterone, which is a more potent metabolite, is more
% x2 V  {/ h5 {/ b* \& ?7 H9 Q' Nactive in young children exposed to testosterone5 Q- u3 ]! c; L* r! q3 w
exogenously7; however, we did not measure a dihy-+ q& P5 \3 B: f
drotestosterone level in our patient. In addition to
& j$ D# w3 \, O$ B, Z; _virilization, exposure to exogenous testosterone in
6 a% h( Z. P% Uchildren results in an increase in growth velocity and' F$ g+ v5 D. Y7 y7 p% R9 v
advanced bone age, as seen in our patient.; v& M6 t! y* X  s+ A- g3 P7 t' k
The long-term effect of androgen exposure during
7 I7 u$ v( I8 S3 l7 aearly childhood on pubertal development and final- M) x  T- p6 V/ o8 T6 A3 s
adult height are not fully known and always remain4 f1 U/ }; l( P2 }4 Z
a concern. Children treated with short-term testos-
% H- n% I- @  j* G: a7 iterone injection or topical androgen may exhibit some# p: h1 H. h, Y2 m% t0 @
acceleration of the skeletal maturation; however, after
: T; y: V  y/ D; F* T* L+ L, Qcessation of treatment, the rate of bone maturation
% ^& Q7 V% w4 }  z' }( H* l) wdecelerates and gradually returns to normal.8,9
  E2 |! T- e' `There are conflicting reports and controversy2 S. a: r0 u. F( M0 I
over the effect of early androgen exposure on adult# ~. M+ K# d4 _5 |3 r. B
penile length.10,11 Some reports suggest subnormal
3 K1 s0 J4 U3 E& S' Yadult penile length, apparently because of downreg-+ t. G- ~+ e+ G" Y
ulation of androgen receptor number.10,12 However,7 H- w" P0 ^7 R) b1 z: G
Sutherland et al13 did not find a correlation between7 K/ b: F* d0 C' U
childhood testosterone exposure and reduced adult3 L0 O+ a6 @6 T  U+ t* a
penile length in clinical studies.5 O4 V. |. l9 C
Nonetheless, we do not believe our patient is
' w, {8 H- O" @) ]1 Jgoing to experience any of the untoward effects from
# V4 t7 E' j; H0 Atestosterone exposure as mentioned earlier because! |2 D. H; j" L/ V7 m
the exposure was not for a prolonged period of time.2 d+ v7 j3 ]6 a6 O; n
Although the bone age was advanced at the time of
  N0 S  j6 U0 C7 E% [( jdiagnosis, the child had a normal growth velocity at0 m! N& `4 |7 c+ m
the follow-up visit. It is hoped that his final adult/ s$ ?9 |" W3 F( P& V" ?6 g
height will not be affected.- ^  f; U+ v# H* r1 P
Although rarely reported, the widespread avail-
. u7 d8 M) r+ U5 G4 F' Eability of androgen products in our society may
/ K, q7 t6 R1 P$ \9 u) W! Xindeed cause more virilization in male or female
5 I- E/ z$ A4 Tchildren than one would realize. Exposure to andro-
2 d0 G% r3 `$ o  u$ ogen products must be considered and specific ques-. O3 `8 e' U* S) E5 |: j- i
tioning about the use of a testosterone product or
; Z( L/ ~8 ?. H0 mgel should be asked of the family members during
' k6 N2 q( z( i) vthe evaluation of any children who present with vir-; c3 E; `: Z4 L) A' Y& \
ilization or peripheral precocious puberty. The diag-# r+ ^2 m/ Y/ H6 n% {  h
nosis can be established by just a few tests and by( E, p2 D% m. ]  g( }8 p$ V
appropriate history. The inability to obtain such a$ ]1 _% }- R6 x. `* t
history, or failure to ask the specific questions, may6 p) {+ ^4 s' P7 d( ~$ e/ X
result in extensive, unnecessary, and expensive
9 {; V( d& K' a  x6 K0 L8 Winvestigation. The primary care physician should be0 \& ?% l. l4 V( S1 E9 y
aware of this fact, because most of these children
) h9 I) `' J% i6 [may initially present in their practice. The Physicians’9 Y4 w1 ?/ O1 I7 N* o) s% P6 L
Desk Reference and package insert should also put a  B% j$ a4 Q) q$ ?' D4 c
warning about the virilizing effect on a male or
" ?& j6 ~& U6 @- r6 vfemale child who might come in contact with some-# Q+ r( T, _1 ~1 Q
one using any of these products.' W( i+ A0 |1 {- D3 x: X
References
! K( p7 x0 ]! q. S& H; ?1. Styne DM. The testes: disorder of sexual differentiation
! l( x. `6 {# A1 J/ w' Jand puberty in the male. In: Sperling MA, ed. Pediatric
2 W0 P9 ^; S8 ^1 d/ |% S$ u5 h: SEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;* I, x0 i3 p: }2 K
2002: 565-628.
  b/ w& @3 q6 W2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious) r) `3 b4 U8 G  h! y" j* v3 L
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
% F( E/ n, g3 ]! T8 @Boy Induced by Indirect Topical) g% ^9 D/ b) ]2 i+ w6 |2 Z
Exposure to Testosterone, J7 ]' A0 D) M" ~
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
1 R2 Q7 F& D, i: hand Kenneth R. Rettig, MD17 b. G' D  O4 U1 @7 C
Clinical Pediatrics3 \; c$ b6 ~; w7 `( n5 U
Volume 46 Number 6; p: ~1 v9 A9 m
July 2007 540-5436 V) x. M6 g- y# T2 s
© 2007 Sage Publications
& T2 {3 s! J5 W- C# n) s& I10.1177/0009922806296651
8 J! |' s* T$ H) Z/ ~http://clp.sagepub.com. [( x- `2 T  ~' R' _7 `: `) F# g
hosted at; q9 A8 ?3 n# R9 y
http://online.sagepub.com
5 x. ~2 b2 l$ j: e; }# gPrecocious puberty in boys, central or peripheral,
+ h9 n! @" B% X# e# G7 h$ uis a significant concern for physicians. Central- N$ Q3 e) @; ^5 q6 G6 Y: }! M2 f
precocious puberty (CPP), which is mediated1 g+ T% R* E0 _5 {/ `7 k" `) ?
through the hypothalamic pituitary gonadal axis, has) g% s) U$ S" X" \5 D5 Y+ ~
a higher incidence of organic central nervous system
! [# [) d. W$ W* hlesions in boys.1,2 Virilization in boys, as manifested2 @/ {' b9 |5 q5 F
by enlargement of the penis, development of pubic$ G; C; J$ P  j9 W
hair, and facial acne without enlargement of testi-& c% v: P: n( l
cles, suggests peripheral or pseudopuberty.1-3 We
; U; ~+ _9 W9 c. @4 c, O2 [" Kreport a 16-month-old boy who presented with the/ x/ l9 k9 S! {: ?; O7 e' A, L1 @
enlargement of the phallus and pubic hair develop-
, @3 A1 c" o. B' Nment without testicular enlargement, which was due
6 Z5 d1 E) f1 n. x/ ~& Oto the unintentional exposure to androgen gel used by
/ a/ U9 J% w4 b# T/ Lthe father. The family initially concealed this infor-/ C  [* n5 G+ K- e8 W! ?
mation, resulting in an extensive work-up for this$ C3 t: b/ @  O+ Z
child. Given the widespread and easy availability of
; G& I( M0 p9 d( ~- ?+ ltestosterone gel and cream, we believe this is proba-# Q! \$ A6 C6 g" e
bly more common than the rare case report in the3 l8 ~, S6 {8 j- U0 B$ M8 U+ U
literature.4/ H( C% ^* Z. u  m
Patient Report) T* X5 ~7 w1 u" ^% V; u
A 16-month-old white child was referred to the
0 }6 I; I3 t+ Qendocrine clinic by his pediatrician with the concern" @. k; q6 |( A& e3 e/ T2 H. A; c! K
of early sexual development. His mother noticed5 y7 g3 w6 x9 C, r% O2 g' w. E
light colored pubic hair development when he was( U9 t# a/ j1 k- m/ O3 e% I
From the 1Division of Pediatric Endocrinology, 2University of
# u+ ~  z6 k% @2 _2 |4 h+ a  zSouth Alabama Medical Center, Mobile, Alabama.
, z3 Z1 C* L1 {, ^! ]Address correspondence to: Samar K. Bhowmick, MD, FACE,  `4 h6 x- x$ ~( J! F' @
Professor of Pediatrics, University of South Alabama, College of" |+ b9 E/ V8 l
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;- h% i/ r1 N' o8 w4 [6 v
e-mail: [email protected].
# D6 t5 }3 g! }/ zabout 6 to 7 months old, which progressively became2 s& y* i1 a/ Y7 s
darker. She was also concerned about the enlarge-: M2 q- f# P% n( z4 |% S4 X1 }
ment of his penis and frequent erections. The child, l2 @3 a  s; k! K- N# _2 Q1 }
was the product of a full-term normal delivery, with/ {# X8 e* A$ b  a9 B+ S. b. `
a birth weight of 7 lb 14 oz, and birth length of
: _9 C9 E- G7 C! x2 G( u20 inches. He was breast-fed throughout the first year
) q7 {5 f/ W  l" K' w9 y# Jof life and was still receiving breast milk along with! F! c: m% q8 h
solid food. He had no hospitalizations or surgery,
/ r' c9 s1 q* j3 xand his psychosocial and psychomotor development
' e9 D1 M' q* W/ t& T$ gwas age appropriate.
  ^7 v3 W! C" ]: w! T$ L. cThe family history was remarkable for the father,
2 U  M: s8 E' b: R1 e7 z7 `who was diagnosed with hypothyroidism at age 16,! R# h3 i: M: H+ T' Y# a
which was treated with thyroxine. The father’s
% ^- X4 ?7 v- \* h9 ^. c/ |height was 6 feet, and he went through a somewhat+ s% r3 a( D7 U/ ^- l# S
early puberty and had stopped growing by age 14.9 N" p& I: e) i7 d+ S$ h
The father denied taking any other medication. The
( v& p+ }/ T) r5 Ychild’s mother was in good health. Her menarche  I- b; \* C0 w) J, X
was at 11 years of age, and her height was at 5 feet
  k$ e7 o- ^1 K8 \( `, v5 inches. There was no other family history of pre-
/ S3 S; H( T& d; Q) r' jcocious sexual development in the first-degree rela-* O2 A: Y( w4 D) U6 z1 E, H! W
tives. There were no siblings.+ t7 H/ i  l; \4 E
Physical Examination
, Z6 |: J# z, L& K, YThe physical examination revealed a very active,2 K5 K" F/ o5 k; \1 i6 V
playful, and healthy boy. The vital signs documented6 U" b+ ~+ [- R( L
a blood pressure of 85/50 mm Hg, his length was
; p4 i/ z& R" }5 x4 Z9 N90 cm (>97th percentile), and his weight was 14.4 kg7 o/ y8 ]# e8 C* F4 k/ m2 Y  G6 d' K5 c
(also >97th percentile). The observed yearly growth
1 B4 V& t" N  Z  H3 e& Y5 I% `* U6 avelocity was 30 cm (12 inches). The examination of: r- M8 K0 W# g8 X& @" a
the neck revealed no thyroid enlargement., B) J8 p7 p, A& z- Y/ N0 X" ?
The genitourinary examination was remarkable for
6 `9 l1 O& P, c( senlargement of the penis, with a stretched length of
! n! n& R8 }( _0 ?1 Q8 cm and a width of 2 cm. The glans penis was very well; w( o, k' [& N
developed. The pubic hair was Tanner II, mostly around
5 l9 }1 t5 I1 r2 S* _540( C" D+ W. D2 j( ?3 d$ Q& `; {
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; e( }) K: W* `/ r( l8 Y' O$ Tthe base of the phallus and was dark and curled. The
) n+ z0 F" g. o3 Jtesticular volume was prepubertal at 2 mL each.4 N1 L, K6 G7 ]/ p
The skin was moist and smooth and somewhat
1 j7 u9 U( r# d  @5 Koily. No axillary hair was noted. There were no  a% N5 h9 [" ^* L
abnormal skin pigmentations or café-au-lait spots.
3 q' ?. u0 J! o; ~  M3 QNeurologic evaluation showed deep tendon reflex 2+
4 c/ {) q* E- ]1 mbilateral and symmetrical. There was no suggestion( s/ v3 g2 K+ x  v
of papilledema.# ]8 L) f0 M$ Y1 V/ z$ S3 e! ~
Laboratory Evaluation
" T1 y+ ^7 ~  d6 @% m: SThe bone age was consistent with 28 months by3 [3 {% ]9 `: C( R; y3 @
using the standard of Greulich and Pyle at a chrono-# S' X; u2 l! ]1 A+ v
logic age of 16 months (advanced).5 Chromosomal
" k( B  f, X  c, Q: Akaryotype was 46XY. The thyroid function test
& a, y5 T5 L( J, D- K9 i. Mshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
3 E! u) u7 W: n' Q! D2 ?lating hormone level was 1.3 µIU/mL (both normal).2 v3 D( R5 I, ]( h& @3 v5 a
The concentrations of serum electrolytes, blood; ~* N& N6 O7 R7 i0 l, [
urea nitrogen, creatinine, and calcium all were
. U" X1 [% l, vwithin normal range for his age. The concentration
# ~2 A4 A( {* C' V5 Z0 k- Mof serum 17-hydroxyprogesterone was 16 ng/dL
& f4 F! r# M2 j! R# R# t' t" l(normal, 3 to 90 ng/dL), androstenedione was 20
4 O7 g! ^& I$ o2 y0 Jng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
  M+ ^3 p9 l8 iterone was 38 ng/dL (normal, 50 to 760 ng/dL),; R5 W- [3 X& B, b% C7 f
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
' b( m% t" p( ^- p0 W- b49ng/dL), 11-desoxycortisol (specific compound S)
- F9 L* F; X+ W4 q1 Zwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
. N% @2 N- T+ }+ H$ T* htisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total7 T0 R# x3 [$ ^
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),4 I; X. {+ H# A7 R6 B
and β-human chorionic gonadotropin was less than
! Y! @- f$ f. ^5 mIU/mL (normal <5 mIU/mL). Serum follicular/ W* v, Y& I& u# _8 x" N2 ]
stimulating hormone and leuteinizing hormone
5 @" p7 J& }7 W$ W' O( F7 K! Q- xconcentrations were less than 0.05 mIU/mL6 a- ^" p2 Z* Z. L; b, r
(prepubertal).# o  Q8 d7 a; C& O/ C/ `. X
The parents were notified about the laboratory/ ?0 L$ n  J; i; R8 |
results and were informed that all of the tests were
" B+ c% l; P2 u% \; h! t2 Ynormal except the testosterone level was high. The7 B# o5 A0 \# q* g
follow-up visit was arranged within a few weeks to, _1 U$ f. \4 O* H  X
obtain testicular and abdominal sonograms; how-7 N4 l$ I1 X; o8 {. M/ z
ever, the family did not return for 4 months.
. C* i/ b+ w* e1 D8 tPhysical examination at this time revealed that the
$ ^0 _/ @/ W" v  x; rchild had grown 2.5 cm in 4 months and had gained6 n: J: o& W9 K$ V
2 kg of weight. Physical examination remained: E: z  |0 b( |: L! i$ w
unchanged. Surprisingly, the pubic hair almost com-$ q, n. U* g! `3 o6 y
pletely disappeared except for a few vellous hairs at1 q7 A( }5 m8 A9 B" q0 H, d& h
the base of the phallus. Testicular volume was still 2
" Z+ l2 i& F; }( cmL, and the size of the penis remained unchanged.: d) w0 S7 c" n8 K) x. a! J# G0 @
The mother also said that the boy was no longer hav-" s+ S% A9 ~; {% W
ing frequent erections.
% p3 v6 p  H4 L) cBoth parents were again questioned about use of1 w/ \7 R/ {- R1 @3 e: B2 N( @
any ointment/creams that they may have applied to; @" r( @% M( J7 Z
the child’s skin. This time the father admitted the/ A- L  F4 q3 p3 i& O% V4 c
Topical Testosterone Exposure / Bhowmick et al 541% M( a, c, B7 k8 N' K; M3 ~- \
use of testosterone gel twice daily that he was apply-
8 T4 t4 q: x/ _ing over his own shoulders, chest, and back area for* G  l9 G& h$ {
a year. The father also revealed he was embarrassed5 i& E: l1 h& n0 q/ _/ x; N
to disclose that he was using a testosterone gel pre-/ w; H; l' |( L
scribed by his family physician for decreased libido
5 l+ N! u. `" i; Isecondary to depression.( B5 e8 M2 ^. ?( r% [
The child slept in the same bed with parents.
9 w% U$ l5 S% Z$ b* ^The father would hug the baby and hold him on his
" @8 W# X# u, ^2 v6 c% Qchest for a considerable period of time, causing sig-
+ a" \- J  Q9 b/ qnificant bare skin contact between baby and father.
& _6 Y! j! d  y+ P" s5 PThe father also admitted that after the phone call,6 h9 R% z9 y3 R# D8 i6 E$ l0 W
when he learned the testosterone level in the baby( h) W4 K/ a9 a: B4 G& z
was high, he then read the product information
. d% ^' b/ |" X) E0 Gpacket and concluded that it was most likely the rea-
4 b" {8 I1 \* l' f! T- s" Oson for the child’s virilization. At that time, they
. ?3 i& B! x2 D5 W* }5 L+ \# d/ bdecided to put the baby in a separate bed, and the
6 {! T) V5 n, ^# t; F: lfather was not hugging him with bare skin and had- i0 r- ~( F5 i9 o* R+ G
been using protective clothing. A repeat testosterone. i4 B( H# C; y8 n
test was ordered, but the family did not go to the
! Y4 ^" s5 i- {/ }$ X. O  Flaboratory to obtain the test.
! y, V  I0 p- b+ F) T) rDiscussion. d5 V8 S/ s% |. e6 [3 e6 O
Precocious puberty in boys is defined as secondary
2 o/ _) s& c! Q% H' ^* jsexual development before 9 years of age.1,4
( c' ~8 N+ }) i+ u' GPrecocious puberty is termed as central (true) when
' S3 H5 V( v9 D) C+ C6 J2 i9 Wit is caused by the premature activation of hypo-
2 `% ]: h! h' @- y! N# ethalamic pituitary gonadal axis. CPP is more com-8 U- p; _7 m  U, y
mon in girls than in boys.1,3 Most boys with CPP6 [: y+ f4 M0 Y1 ~
may have a central nervous system lesion that is
# J0 s. K4 N5 Y$ |, {9 a" Z2 y: ?responsible for the early activation of the hypothal-
( j% y9 {/ I/ n# U6 Qamic pituitary gonadal axis.1-3 Thus, greater empha-
" e; T% W0 ?4 [: j. [+ Ysis has been given to neuroradiologic imaging in
5 v5 d3 a5 S: g" Uboys with precocious puberty. In addition to viril-
5 K9 N) f% r9 o; Kization, the clinical hallmark of CPP is the symmet-
9 O' F+ V6 m1 Xrical testicular growth secondary to stimulation by& p6 U8 M& M) z3 D
gonadotropins.1,3
& {6 T+ s0 ~& D, nGonadotropin-independent peripheral preco-1 j6 L5 [- }* q- D& K5 [5 I  I
cious puberty in boys also results from inappropriate( ~, I" \5 x  V& P0 D
androgenic stimulation from either endogenous or9 H7 v) F, N' t5 {6 v/ [
exogenous sources, nonpituitary gonadotropin stim-3 b: \% e% w( u
ulation, and rare activating mutations.3 Virilizing, j0 N& t8 ^" I6 i
congenital adrenal hyperplasia producing excessive5 P9 c8 j0 `' n3 l1 ^: h6 P% d
adrenal androgens is a common cause of precocious' k3 `) i5 q! V! ~( \: n. R
puberty in boys.3,4' _' H. \/ V( \8 f$ Z
The most common form of congenital adrenal
+ }2 A# L$ E) N) ihyperplasia is the 21-hydroxylase enzyme deficiency.
; T4 q% @7 H* r; {The 11-β hydroxylase deficiency may also result in4 V8 Y5 P, S0 k  h1 M) W& N
excessive adrenal androgen production, and rarely,
( V; w% d' U3 z/ y) ?% o, P8 m6 D" Xan adrenal tumor may also cause adrenal androgen! l0 r$ g3 n1 Q6 i1 |
excess.1,3: Z& U' _0 d" s9 I
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 g; p+ X2 x# ~) U0 u
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
+ [" O8 Z- c1 _4 A" _: ?3 y! tA unique entity of male-limited gonadotropin-
7 I' L. a% P5 H& L5 j: j; M) bindependent precocious puberty, which is also known
/ d( F9 @" W9 ^* [as testotoxicosis, may cause precocious puberty at a4 N$ i* K1 \# `* t6 G. I! W( L
very young age. The physical findings in these boys
" i- {+ H" ]* J2 d  S* lwith this disorder are full pubertal development,/ a6 M! \# a$ E5 m2 i; }
including bilateral testicular growth, similar to boys
% w- n4 w1 _4 ~; @! T& i9 H" H2 fwith CPP. The gonadotropin levels in this disorder* u* j' J. {8 d6 O" g& Q7 K
are suppressed to prepubertal levels and do not show3 B; t9 q! c5 ?
pubertal response of gonadotropin after gonadotropin-: R& t' Z. n2 ^7 D& g2 c7 A# ^
releasing hormone stimulation. This is a sex-linked
8 l5 F" l6 G; [$ ~autosomal dominant disorder that affects only
3 ]1 w5 @% z' N. B! ?1 @- Cmales; therefore, other male members of the family. x+ X0 L) I. J8 f( p3 Q
may have similar precocious puberty.3
4 l) f+ s/ o0 q* t& M1 ^In our patient, physical examination was incon-3 N. d& u" G' ]1 g
sistent with true precocious puberty since his testi-
/ L- K8 r; p' j) D' _) E  \7 T) xcles were prepubertal in size. However, testotoxicosis: w0 n+ G0 m- j+ o3 T4 A
was in the differential diagnosis because his father% M' V6 a+ J8 p: ~
started puberty somewhat early, and occasionally,0 n- R+ t- r5 p# c! H' b0 \) T
testicular enlargement is not that evident in the
; _) f; m9 ]3 ~- gbeginning of this process.1 In the absence of a neg-3 H9 b- K6 o: s2 O4 Y0 D! V- L
ative initial history of androgen exposure, our4 x1 [1 [7 i2 s, N& Z9 O
biggest concern was virilizing adrenal hyperplasia,
- [! Q2 m6 G; |4 meither 21-hydroxylase deficiency or 11-β hydroxylase. i# k- ~6 }& ]$ }
deficiency. Those diagnoses were excluded by find-
% `7 d+ c8 H+ s  F: y& x+ X; hing the normal level of adrenal steroids.
3 S- Q8 J+ D  y# o7 |& ?The diagnosis of exogenous androgens was strongly! D1 t2 [( g! D0 |4 u- a
suspected in a follow-up visit after 4 months because
7 @8 N, b1 `8 c8 w$ V, \, h! sthe physical examination revealed the complete disap-
' p1 a/ n$ u# u, p7 bpearance of pubic hair, normal growth velocity, and
0 p' E: A2 B7 t2 f; Tdecreased erections. The father admitted using a testos-# T8 K. v+ g# ~: i
terone gel, which he concealed at first visit. He was
+ t7 c7 r8 M. L8 f  ?- u2 L. [using it rather frequently, twice a day. The Physicians’7 [; j# H, j% e
Desk Reference, or package insert of this product, gel or3 }& h: D  e5 B. V
cream, cautions about dermal testosterone transfer to
! z; \, i4 b4 ^! V7 v5 s  dunprotected females through direct skin exposure.
& K( J% ]3 G% o8 gSerum testosterone level was found to be 2 times the
8 ~+ L+ L3 z' P# X) P4 J4 pbaseline value in those females who were exposed to7 |2 y+ R1 M  v' d: W1 ?
even 15 minutes of direct skin contact with their male
6 l1 V& S& a0 \, Q3 f6 `8 zpartners.6 However, when a shirt covered the applica-0 ]3 x6 h$ m' i8 }1 t
tion site, this testosterone transfer was prevented., ~" b- d5 }  @, c
Our patient’s testosterone level was 60 ng/mL,( L$ S1 i, }2 b6 d. ?
which was clearly high. Some studies suggest that
$ G5 l1 W. V8 u" Y; mdermal conversion of testosterone to dihydrotestos-5 Q% c0 k) i+ Z3 v8 ^0 w$ m
terone, which is a more potent metabolite, is more- u$ t. x. ]4 a( L9 M5 ^5 _
active in young children exposed to testosterone
5 p4 L7 Z& e4 a1 X. \' b& gexogenously7; however, we did not measure a dihy-
) e, s4 v* L* \9 O6 F! w5 e+ Fdrotestosterone level in our patient. In addition to( x3 G1 P( c# U( y& c, s
virilization, exposure to exogenous testosterone in
  K4 ~3 f; }' Q4 P6 u9 bchildren results in an increase in growth velocity and
4 O0 j5 p* z6 j( O' e9 j& V, D* p; Gadvanced bone age, as seen in our patient.
2 H8 @# {" U$ iThe long-term effect of androgen exposure during
$ l* j% ?" \+ E$ gearly childhood on pubertal development and final; v9 u9 o2 F, s' o& h4 ~* ?6 P' C! V
adult height are not fully known and always remain, c, g% V+ n6 I% [. W
a concern. Children treated with short-term testos-% D- E! @8 [+ ~$ t
terone injection or topical androgen may exhibit some  n5 L) _# S- U- `( |% p
acceleration of the skeletal maturation; however, after
2 ]2 m) t* j1 d1 J2 L$ E' ?$ h( |( Ycessation of treatment, the rate of bone maturation
) i" Q: s" v1 `% g5 f+ {decelerates and gradually returns to normal.8,91 ~+ X* @* T+ ^
There are conflicting reports and controversy6 Z; e: t$ s) h2 ^: O
over the effect of early androgen exposure on adult
& C; G1 R( v* Q7 Hpenile length.10,11 Some reports suggest subnormal
/ I0 h" d5 i' O" H0 Wadult penile length, apparently because of downreg-
. o( W( w+ w/ T) Oulation of androgen receptor number.10,12 However,
8 X5 O6 C7 q, \+ x6 R: G$ hSutherland et al13 did not find a correlation between0 Z  [% I' T! S
childhood testosterone exposure and reduced adult
# e( n0 x. D0 X, s. J7 ipenile length in clinical studies.7 E  U" M( T/ r1 x* ?' C. A
Nonetheless, we do not believe our patient is- c2 B1 ~# Q6 q( ]
going to experience any of the untoward effects from* ~  E: m0 p7 K) c8 ^) [; K
testosterone exposure as mentioned earlier because& x) P9 p9 ?6 ^. K! ~5 p
the exposure was not for a prolonged period of time.
& b! G; _  p( ?- a% b* _Although the bone age was advanced at the time of, E3 x& c5 w- m+ }0 I
diagnosis, the child had a normal growth velocity at
- T2 W3 i. F) }0 hthe follow-up visit. It is hoped that his final adult
0 W- d: y3 m: t" lheight will not be affected.
7 j4 E3 x1 ~4 O- f) ~1 }Although rarely reported, the widespread avail-- e6 }1 m. g& F6 d
ability of androgen products in our society may
) Q& A6 {8 g  r" J5 Oindeed cause more virilization in male or female0 \+ i" w/ d8 r! K' r: o
children than one would realize. Exposure to andro-
8 M6 d5 v+ d, s' K5 H- c2 m) w% dgen products must be considered and specific ques-) o. i) @; J. g. V+ L
tioning about the use of a testosterone product or
% N# [) p9 }4 G) K) k2 ngel should be asked of the family members during
& u3 S1 }, r+ C3 k: U/ [" bthe evaluation of any children who present with vir-. f+ q* m# F/ g
ilization or peripheral precocious puberty. The diag-- M2 y+ z9 t) O, ^
nosis can be established by just a few tests and by3 i# r6 q4 u( J0 T
appropriate history. The inability to obtain such a
/ E# q& D9 s1 x) Z# Q# J5 Thistory, or failure to ask the specific questions, may1 T8 q6 Z! g* j3 g3 q9 ]
result in extensive, unnecessary, and expensive
) r1 [% U" H4 q: C$ R( Einvestigation. The primary care physician should be
% e. h9 @0 `4 q& uaware of this fact, because most of these children' \( N$ q2 q* j
may initially present in their practice. The Physicians’
# @% y( d3 z5 \8 d. p0 CDesk Reference and package insert should also put a
2 R2 Q( b5 O% N8 j; |( Z4 Rwarning about the virilizing effect on a male or. u) G0 n, S$ \8 w# T# @1 k( G+ p
female child who might come in contact with some-0 a  T% m, z7 [
one using any of these products.
8 [* M) J/ {+ X+ cReferences
8 J2 A) N1 k( x  ]8 f! w1 Z7 c1. Styne DM. The testes: disorder of sexual differentiation  g2 b/ t2 j- Q* Z+ c2 Y  U
and puberty in the male. In: Sperling MA, ed. Pediatric0 k5 e) n# e( o' P% e
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;' a% h: q  ]. i% H
2002: 565-628.' N3 F. D; E4 ~% N
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious8 {* B2 l0 K0 |# e* w  o
puberty in children with tumours of the suprasellar pineal
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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
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

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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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