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Sexual Precocity in a 16-Month-Old" `& R5 |2 w6 s' N! \3 t
Boy Induced by Indirect Topical
8 Y0 J4 Y1 Q: Y4 ^) W) Z/ uExposure to Testosterone
  p. N9 Y3 J% K' F8 X- mSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2% u6 l5 b& `( X; M3 P# i- ?& ]
and Kenneth R. Rettig, MD1
6 n$ @5 E  ~& H% V) u2 FClinical Pediatrics. L5 S# X3 R- r; `- o3 z
Volume 46 Number 6
6 M. F8 A" j- @9 W  aJuly 2007 540-543( d! b2 c+ ?) f$ C! B0 u: a' E
© 2007 Sage Publications0 A3 \+ {0 O# W9 I5 s1 D
10.1177/0009922806296651
  r$ E) U2 K% N: @; X) e5 S! q% @http://clp.sagepub.com% i; G/ f$ o1 C" s' V1 ^  O1 B1 ]
hosted at
; z. p0 K+ E$ B1 A4 Ghttp://online.sagepub.com
6 {5 K3 e$ e+ D: nPrecocious puberty in boys, central or peripheral,2 S9 a' P; j6 h4 h
is a significant concern for physicians. Central) |. Y' ^/ I% A- [8 J' }( U& C6 L& w
precocious puberty (CPP), which is mediated
6 Q' A* ?) D; ~+ ?7 pthrough the hypothalamic pituitary gonadal axis, has! u# X" D2 ^. t# i+ Q( }* I# S2 U
a higher incidence of organic central nervous system
0 u% N) J( f0 w! r* Elesions in boys.1,2 Virilization in boys, as manifested* |' y: `( |& i; o# b# M
by enlargement of the penis, development of pubic2 M5 l5 b2 S1 Q7 P1 b0 T( r
hair, and facial acne without enlargement of testi-; n- \+ y& q9 s/ M- N# P6 ?
cles, suggests peripheral or pseudopuberty.1-3 We
& h/ |  L' B& I+ ]/ E4 `report a 16-month-old boy who presented with the0 {" J. l- l  i9 q. q& j# {
enlargement of the phallus and pubic hair develop-
* p2 k0 ]8 n  _) C: y; p" g+ Wment without testicular enlargement, which was due
6 s( W; L" Z3 ~0 Zto the unintentional exposure to androgen gel used by4 M. c: S9 S+ K" w  K! x3 r. ~5 v
the father. The family initially concealed this infor-+ ?4 M( f$ d: D  H+ g. n
mation, resulting in an extensive work-up for this
) r  S* A/ Y& F, q( Q5 ?& |* s; Cchild. Given the widespread and easy availability of: d! z. W; X9 @
testosterone gel and cream, we believe this is proba-8 \1 E9 N$ X# Z- K, z
bly more common than the rare case report in the
& H/ R6 A* U: E% v+ q7 ^9 bliterature.4! b# T% v# n& [) p
Patient Report4 L5 Z$ Y: E- O% f
A 16-month-old white child was referred to the
3 w; S4 a2 K+ h- s3 {' t2 [7 B5 Zendocrine clinic by his pediatrician with the concern! j  \4 m- E0 h& j
of early sexual development. His mother noticed
& i+ D( o$ c5 `5 M6 I& P9 P$ tlight colored pubic hair development when he was
& z$ w. c2 |( F) l+ m" q( ~+ [From the 1Division of Pediatric Endocrinology, 2University of
, x; J% E/ |* V, M4 CSouth Alabama Medical Center, Mobile, Alabama.
& }1 I& r6 i: ]5 M1 CAddress correspondence to: Samar K. Bhowmick, MD, FACE,
# \& y; m9 `( H9 I" |" MProfessor of Pediatrics, University of South Alabama, College of6 D. m4 H: U, B' E
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;) F; R( h# z+ T+ {; j$ W
e-mail: [email protected].
- E' ~9 ^5 }. q- `/ T' gabout 6 to 7 months old, which progressively became
, L7 r4 B6 V% p7 e1 L! U9 w+ odarker. She was also concerned about the enlarge-
. e, D# j+ S: F8 w8 u( ^ment of his penis and frequent erections. The child
8 \0 v' o# I. Z2 L5 [7 bwas the product of a full-term normal delivery, with
+ x# i: k" R* I& ]: na birth weight of 7 lb 14 oz, and birth length of
" {0 h1 f* M0 [! l+ s, r20 inches. He was breast-fed throughout the first year' J# Z5 m, V' D
of life and was still receiving breast milk along with; ]2 c4 v3 {) O2 i! O; @5 d  g
solid food. He had no hospitalizations or surgery,
2 g. V8 K  R/ n3 Wand his psychosocial and psychomotor development
2 N; w; `# f" c% T. w, ]was age appropriate.
$ `# x! o% P& M% N0 KThe family history was remarkable for the father,. S; l1 T' L6 Q, |$ D0 y; r" c0 X& x
who was diagnosed with hypothyroidism at age 16,
0 S$ F/ I9 ~" ?' t1 T; K& Lwhich was treated with thyroxine. The father’s
0 S3 V& _+ n3 H9 \* hheight was 6 feet, and he went through a somewhat
6 Y- s7 ^: b. J7 S7 searly puberty and had stopped growing by age 14.
. u2 ^9 G* f4 q5 ~6 v2 GThe father denied taking any other medication. The1 A- s; {$ O5 J3 R6 U
child’s mother was in good health. Her menarche7 r- W+ y* ]' [) d& H6 I
was at 11 years of age, and her height was at 5 feet
0 W& T: l) C0 k6 S5 inches. There was no other family history of pre-
( x; t* f: k  G6 A+ \* [: y7 |7 @' Vcocious sexual development in the first-degree rela-
3 G8 J' m' r2 e/ y" J9 N5 ttives. There were no siblings.
, |9 @' x7 d+ E6 HPhysical Examination/ I4 j- {4 P& K1 u9 ^- z
The physical examination revealed a very active,
: y; i% N. A( Y- r/ u/ j* Rplayful, and healthy boy. The vital signs documented- A" P7 E1 q1 k& j1 ?; Z7 u
a blood pressure of 85/50 mm Hg, his length was
' t2 h' h3 _4 o% P0 O90 cm (>97th percentile), and his weight was 14.4 kg
$ Z, ^4 _9 x1 f7 q+ b9 `(also >97th percentile). The observed yearly growth
; O8 b/ `& W0 K- o* j* ]velocity was 30 cm (12 inches). The examination of. {; p3 M  S, R& s: R. c' l$ ?# M
the neck revealed no thyroid enlargement.) ]5 g1 k1 J% s+ v: [
The genitourinary examination was remarkable for7 j) @$ K- M1 Z  L- J8 A
enlargement of the penis, with a stretched length of
5 x  J! k# V2 B5 n7 v8 cm and a width of 2 cm. The glans penis was very well6 `9 a+ _) s! Z( k% v
developed. The pubic hair was Tanner II, mostly around
) w0 J' V3 j4 M" [% n( c6 ]540% B$ t0 J! r, ~) M. @( B2 a
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 `$ \! g5 a) F1 w2 ~
the base of the phallus and was dark and curled. The
: C8 }2 |- D, Z; m  E6 {1 rtesticular volume was prepubertal at 2 mL each.
8 _1 Y4 {/ n, G# x5 `The skin was moist and smooth and somewhat
5 Y, |) q* L. S1 k+ s4 k4 b8 ^oily. No axillary hair was noted. There were no
$ l0 d4 r% u3 M+ @4 rabnormal skin pigmentations or café-au-lait spots.
* ~. |: N+ x) Z* Y, gNeurologic evaluation showed deep tendon reflex 2+
- N2 w' Z- X1 A% h/ C) ?  r9 A9 ibilateral and symmetrical. There was no suggestion
/ C8 a6 c3 X/ D' Nof papilledema.
4 i: b; I& f% A  l* `4 iLaboratory Evaluation
2 @0 J) \0 }* z2 z. XThe bone age was consistent with 28 months by7 S% i) x8 I- K: ]8 h6 x4 z
using the standard of Greulich and Pyle at a chrono-
# I% S  z1 t" O$ s/ @, P# llogic age of 16 months (advanced).5 Chromosomal+ X4 E7 }* V! \& S, g9 s( |6 t" d
karyotype was 46XY. The thyroid function test
' L' u: S' I' Q) E+ C% G6 G0 Wshowed a free T4 of 1.69 ng/dL, and thyroid stimu-8 \( q8 E! m- H
lating hormone level was 1.3 µIU/mL (both normal).
2 T4 L* p! m! U7 R  t, ~2 T; uThe concentrations of serum electrolytes, blood
$ u9 h: e: V1 h3 R5 r  nurea nitrogen, creatinine, and calcium all were8 S7 G! h; a; E" s
within normal range for his age. The concentration" e# B8 p7 o) Y/ P: s
of serum 17-hydroxyprogesterone was 16 ng/dL
& m$ c3 i4 w1 B) h- v(normal, 3 to 90 ng/dL), androstenedione was 206 Z8 o+ |( N* I* ]
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 z% `2 _# m( A6 c  q( }- K: kterone was 38 ng/dL (normal, 50 to 760 ng/dL),
; d& o! d* ?7 A- G* X. P; S  Kdesoxycorticosterone was 4.3 ng/dL (normal, 7 to* R. F0 X: e2 d+ ]
49ng/dL), 11-desoxycortisol (specific compound S); U6 j6 {. }4 m/ J% X  c
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-" y! D" T- Q7 y
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total) U& f6 n, l8 u- T- Q2 h
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
; J: {4 Z+ S  g& Fand β-human chorionic gonadotropin was less than
; S6 f& s6 l5 T5 mIU/mL (normal <5 mIU/mL). Serum follicular
, o  I0 M, T8 y! l! Fstimulating hormone and leuteinizing hormone
! @$ o6 Y+ d! v9 c) u0 a6 M+ P. Dconcentrations were less than 0.05 mIU/mL
& {5 I2 p4 y4 C- D8 H7 v(prepubertal).' }; U# i6 a; F3 o, e- Z) R5 b
The parents were notified about the laboratory1 D' K! p  t# w1 C0 o7 d; M# U$ [
results and were informed that all of the tests were6 L1 ?4 w; p- Z5 t  Q& Z' \$ m$ F7 R
normal except the testosterone level was high. The
' f) T; T: D! J' X+ o8 R. Bfollow-up visit was arranged within a few weeks to
+ R7 `/ P- |) {* eobtain testicular and abdominal sonograms; how-
( H* N; s# N8 Uever, the family did not return for 4 months.0 y$ p$ u) Y) x2 q) {" P
Physical examination at this time revealed that the
. {8 t/ Q5 S, g/ H' X" d7 q! {8 \3 Jchild had grown 2.5 cm in 4 months and had gained2 k0 y4 ?( ^7 K) D9 r
2 kg of weight. Physical examination remained7 j3 D1 W9 R# ^  f4 C' U0 M
unchanged. Surprisingly, the pubic hair almost com-
6 H# ]$ N) {8 H+ m+ D* fpletely disappeared except for a few vellous hairs at
* [% i5 Z  o7 ^6 B* b8 x' Fthe base of the phallus. Testicular volume was still 20 D" a+ g/ z% _1 h5 W! F
mL, and the size of the penis remained unchanged.
0 ]5 M3 ~9 r3 s! r. \, X" d- fThe mother also said that the boy was no longer hav-8 T( }5 O0 J/ m2 M9 d4 M
ing frequent erections.: J, I& d% M7 \9 o
Both parents were again questioned about use of/ B+ `7 y/ `0 _) F
any ointment/creams that they may have applied to" ~8 l9 x! o4 U+ ?; ]5 b* Y, q
the child’s skin. This time the father admitted the; B- e/ B5 f! y
Topical Testosterone Exposure / Bhowmick et al 541
. O" `7 h5 A; a9 u1 o  Xuse of testosterone gel twice daily that he was apply-# [0 A0 U8 l+ v- s
ing over his own shoulders, chest, and back area for* i, k' Z( _9 o5 }* _# [
a year. The father also revealed he was embarrassed
$ O6 F3 b. x3 T& A3 l2 Q. D; D& O9 ^to disclose that he was using a testosterone gel pre-" z: U9 @% H5 Z* H3 G7 _
scribed by his family physician for decreased libido1 G" _3 \) @3 s4 ]- ~/ d: Q
secondary to depression.
5 ~" y2 W0 }. f5 ?6 _# d# I/ I% MThe child slept in the same bed with parents.( ^8 L4 R0 E) l/ {) Y$ l
The father would hug the baby and hold him on his" J" m" w7 A& H  k0 u( I
chest for a considerable period of time, causing sig-
0 b4 {: w/ P, D9 enificant bare skin contact between baby and father.
; k! E. O2 z# g* a7 z$ g7 XThe father also admitted that after the phone call,4 J6 _7 S/ D7 T- C* D
when he learned the testosterone level in the baby
2 _  @. J6 K, X2 b0 R! owas high, he then read the product information& j' ]' |3 U+ G" d8 v, T* q% c
packet and concluded that it was most likely the rea-  ~3 _( E3 L, o( s( a
son for the child’s virilization. At that time, they
  m5 z% t; q) Z. D. G/ j* H7 Hdecided to put the baby in a separate bed, and the0 E' p; E* _. r& B3 z* b( A, f
father was not hugging him with bare skin and had1 G* j  V8 x2 T+ a3 h3 H
been using protective clothing. A repeat testosterone
" Q- @' j& {9 Vtest was ordered, but the family did not go to the
7 A$ j$ z. D: Q9 V7 g2 e6 A( hlaboratory to obtain the test.
! ^+ N3 \1 g# Y- _Discussion* h6 g) {. f! y
Precocious puberty in boys is defined as secondary
7 v& H  m- V4 L4 isexual development before 9 years of age.1,4) M) b7 f( _0 R' Z9 p, V
Precocious puberty is termed as central (true) when
" M5 C# X( F1 D' ^$ D' G6 {it is caused by the premature activation of hypo-
! I+ R" Y3 t1 g3 R  athalamic pituitary gonadal axis. CPP is more com-
, V  G! U5 U3 W* c. omon in girls than in boys.1,3 Most boys with CPP
% H6 u5 |, @5 _  ?0 {1 ]) Vmay have a central nervous system lesion that is8 w/ X9 `; ~7 y. s9 Y' i+ X2 i; H
responsible for the early activation of the hypothal-! L/ j' o- ~+ K& {  S
amic pituitary gonadal axis.1-3 Thus, greater empha-
, C$ y3 R  |" X: n0 vsis has been given to neuroradiologic imaging in
# O# `5 o8 z( O3 M% nboys with precocious puberty. In addition to viril-
8 E' Q% {7 ^4 Z8 t- Y" gization, the clinical hallmark of CPP is the symmet-+ y, _/ C7 U- i# K9 f6 ]: M
rical testicular growth secondary to stimulation by: X! b5 G! y( }5 i+ L. {( l7 R9 D
gonadotropins.1,3
0 K- ~2 @& J2 }1 v$ fGonadotropin-independent peripheral preco-$ u/ V! x6 l" M/ D9 i+ W
cious puberty in boys also results from inappropriate
1 F# ~+ \4 J1 L) I! [1 r9 Gandrogenic stimulation from either endogenous or
/ ?/ `, E# ^2 l/ l, K. eexogenous sources, nonpituitary gonadotropin stim-
5 C! @! a& d2 ?3 @+ c) J3 {" }ulation, and rare activating mutations.3 Virilizing, l! g" ^) [6 s. G- Y! e0 F
congenital adrenal hyperplasia producing excessive4 K. M2 N* Z6 ^2 e! r% N) k9 E
adrenal androgens is a common cause of precocious
5 g7 W  }/ L5 p3 B9 M1 F( jpuberty in boys.3,4
  S6 x: t% c3 d% g4 QThe most common form of congenital adrenal
7 H7 F1 D1 W# p! R4 Nhyperplasia is the 21-hydroxylase enzyme deficiency.
+ |7 `: n- x* q" UThe 11-β hydroxylase deficiency may also result in! K" O6 i! N4 M) {
excessive adrenal androgen production, and rarely,8 d% X# V" ^; t
an adrenal tumor may also cause adrenal androgen* p0 d+ E- K' F* T- v7 h
excess.1,3
+ g/ B4 A7 e: G/ B" xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 Z/ z4 H  \  d/ L+ r9 W
542 Clinical Pediatrics / Vol. 46, No. 6, July 20073 i( g4 w+ y$ ?& \
A unique entity of male-limited gonadotropin-
4 H5 U$ ~1 Y9 M' k/ @; z" mindependent precocious puberty, which is also known
0 f* H1 p) B* ~5 M1 M% j7 cas testotoxicosis, may cause precocious puberty at a
0 D& p! H1 M% Pvery young age. The physical findings in these boys- u) @2 m2 q4 a1 V9 a' H5 X# m$ Y" J6 v
with this disorder are full pubertal development,
) P) U0 Y8 ]0 d- g8 a0 R0 P( f. j: yincluding bilateral testicular growth, similar to boys) a& j; O( B) i5 K# F2 Q, q, Z" d
with CPP. The gonadotropin levels in this disorder
' o  M1 ?5 C9 F3 b" H1 q: Lare suppressed to prepubertal levels and do not show6 n( K: w, S  A. P
pubertal response of gonadotropin after gonadotropin-( E& Y8 |/ J8 l% y( I# S0 j/ g: j
releasing hormone stimulation. This is a sex-linked
- h* @. o7 F: t5 c: |# u- G) Mautosomal dominant disorder that affects only
0 l+ s6 K& v! r% H- ]7 a( `4 ?1 Jmales; therefore, other male members of the family
* A5 N, X4 ]  I- |/ x$ m6 t! qmay have similar precocious puberty.3
7 p$ ]9 R9 P; Y( C3 K; `: O; |! uIn our patient, physical examination was incon-% ]: v; Y! \7 [! m: i
sistent with true precocious puberty since his testi-
2 Q) {9 G$ c2 l& |2 H  }cles were prepubertal in size. However, testotoxicosis
* E, y+ J5 @* b. t: I3 o' nwas in the differential diagnosis because his father
( z% t0 S: Q8 S- jstarted puberty somewhat early, and occasionally,7 ]  Y; {  d8 ?# F. K( E6 N2 }" G
testicular enlargement is not that evident in the
# V' J7 K6 |9 m. B6 a/ }beginning of this process.1 In the absence of a neg-
1 ?7 v2 @6 q5 X- I& @& E1 m- x+ Sative initial history of androgen exposure, our
5 q5 s) |) G$ X; a8 L5 Fbiggest concern was virilizing adrenal hyperplasia,! H, _* U5 {6 n& [0 J+ ?$ O: Y9 B4 Z
either 21-hydroxylase deficiency or 11-β hydroxylase
/ u. R  o7 t: U, f1 r2 y) adeficiency. Those diagnoses were excluded by find-$ Y( U9 @; y& [( y: f8 m' ^
ing the normal level of adrenal steroids.; Y3 {+ p- A; [
The diagnosis of exogenous androgens was strongly$ [1 ]" l# H$ w/ g8 H
suspected in a follow-up visit after 4 months because% {2 g7 v( n: d8 n
the physical examination revealed the complete disap-" B# P/ e  w4 S, \" u( j4 w
pearance of pubic hair, normal growth velocity, and7 `: Q9 H2 P6 d
decreased erections. The father admitted using a testos-+ t7 ^5 p+ h+ N: H
terone gel, which he concealed at first visit. He was
. y- r! z1 @( C3 W% \using it rather frequently, twice a day. The Physicians’
- v; T4 Q2 H0 B$ a* SDesk Reference, or package insert of this product, gel or  H: L! ?4 Q, Y3 I4 O
cream, cautions about dermal testosterone transfer to3 x$ }- T- F, q1 l' k
unprotected females through direct skin exposure.4 L* W9 Q, u. i( R" s8 A& \
Serum testosterone level was found to be 2 times the- s* ]! Q$ N( }+ U  B& f
baseline value in those females who were exposed to% n0 b& r: l% t: F0 J$ s
even 15 minutes of direct skin contact with their male! \+ H' a! X5 X0 i" s4 n- n
partners.6 However, when a shirt covered the applica-
& h. K' X7 u0 S& }tion site, this testosterone transfer was prevented.9 ^6 u; _- G" f6 a2 C6 [- H; s. y
Our patient’s testosterone level was 60 ng/mL,
+ `9 b2 `# u  ]8 {1 fwhich was clearly high. Some studies suggest that
% O, H& A, a: x% mdermal conversion of testosterone to dihydrotestos-
$ v0 K" @7 D: y0 B6 X' b2 Jterone, which is a more potent metabolite, is more; }5 n; T% O6 X% H" L
active in young children exposed to testosterone  m( b  Q  w: t4 [+ m
exogenously7; however, we did not measure a dihy-1 `/ X* J) y5 F9 T
drotestosterone level in our patient. In addition to
0 z( _. X: J- H/ @virilization, exposure to exogenous testosterone in  c/ C6 h! H- U9 p& q8 _
children results in an increase in growth velocity and
9 N5 J0 L4 C1 s6 Ladvanced bone age, as seen in our patient.( P: Q! ]: `4 r7 [+ a1 L
The long-term effect of androgen exposure during
9 d9 f! D: U: @! u, searly childhood on pubertal development and final2 `5 F5 Z7 o+ e5 p/ i; g
adult height are not fully known and always remain
9 y# m1 n6 {" ^! h/ ?a concern. Children treated with short-term testos-
- p# ~* R" {( E* a1 N5 Xterone injection or topical androgen may exhibit some
& ~' V4 y: W4 H% dacceleration of the skeletal maturation; however, after
; G0 O2 H8 b4 p! c) wcessation of treatment, the rate of bone maturation
, [) K+ O# {! a/ [0 X6 Mdecelerates and gradually returns to normal.8,9. {; x$ K) @8 T- [
There are conflicting reports and controversy+ \! t3 d" g" ~2 K+ z6 [3 [( F. g
over the effect of early androgen exposure on adult
! }# f, h9 l  q  t% j9 Fpenile length.10,11 Some reports suggest subnormal
; l' Z( C' m  y+ _adult penile length, apparently because of downreg-# {0 N& i; ?3 g% s1 V
ulation of androgen receptor number.10,12 However,
' J0 h  ?7 Z8 s6 H) USutherland et al13 did not find a correlation between, S0 L+ ^" ?0 K! Q0 x
childhood testosterone exposure and reduced adult7 O. L* z7 X" T
penile length in clinical studies.
( W( x% V2 W+ u) L6 YNonetheless, we do not believe our patient is1 W, c" A/ F8 \! m3 i# u
going to experience any of the untoward effects from8 V; h4 u9 M* S6 ^6 v) J
testosterone exposure as mentioned earlier because
) S1 O$ \+ K' e  a+ ~+ a7 l  |the exposure was not for a prolonged period of time.) M& m5 W( y# d' {' \  c
Although the bone age was advanced at the time of
8 t. Y9 I- Z' H( V2 Ndiagnosis, the child had a normal growth velocity at/ p( ]1 P( C+ Q; r) a# ^; y" q. \
the follow-up visit. It is hoped that his final adult
; f4 ]7 x% c4 O- Z5 _height will not be affected.
. X3 c3 G0 s5 Q6 P( I* ~Although rarely reported, the widespread avail-
. A# U" p3 N. w* y# zability of androgen products in our society may
3 d# W. C0 [$ x+ ^indeed cause more virilization in male or female
3 @+ i7 |( t# U/ v4 L5 x( nchildren than one would realize. Exposure to andro-) K8 h4 `# \2 O6 |( X3 S! v5 }% M
gen products must be considered and specific ques-/ L6 ^7 i8 C8 L  |$ m3 ^/ e* N8 x5 c
tioning about the use of a testosterone product or
. D4 L* ^+ ^9 d0 ?; J0 Ygel should be asked of the family members during) n0 N  h- W7 q6 m1 j
the evaluation of any children who present with vir-
  o  w1 Q$ \7 g# J0 p' qilization or peripheral precocious puberty. The diag-
6 B; X9 [3 f5 A, D7 ?nosis can be established by just a few tests and by. Q) [* j/ Q/ N% i/ Y
appropriate history. The inability to obtain such a3 q7 u$ Q( O$ Q  j! g' n/ ~/ W( ^' h
history, or failure to ask the specific questions, may) m2 `. `& g5 z; Y8 a/ T  y; [3 F  o
result in extensive, unnecessary, and expensive, f  X5 _4 t7 y/ o! j  ]
investigation. The primary care physician should be+ c& z2 B' e  w% f6 D& X2 b
aware of this fact, because most of these children
4 D* S* T8 P* o0 t9 cmay initially present in their practice. The Physicians’
4 c9 L. b, ^) W2 q4 f# ADesk Reference and package insert should also put a
$ o5 I$ @$ a  j0 C! h; T- [warning about the virilizing effect on a male or
' D7 B; S* i! l- T2 Kfemale child who might come in contact with some-7 r% S, _. s6 Y( ~6 I
one using any of these products.
  @9 F7 B- r. p; |: k) F6 GReferences
6 i# c5 }3 E/ `2 s$ }; r1. Styne DM. The testes: disorder of sexual differentiation- T- e  L3 `( a: f
and puberty in the male. In: Sperling MA, ed. Pediatric
' X& n6 D7 h' E9 X; _) ~/ yEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
( M7 U& R+ }3 o; _3 [% \2002: 565-628.7 z2 F( H  `3 O- B; \
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious% @# @" Z5 R6 ]6 }
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
% }( J& @) ^8 o4 P* aBoy Induced by Indirect Topical
  m" `1 }6 T, U0 QExposure to Testosterone
8 ]# ^4 R7 N( |. ?Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2; r" j7 C2 Q0 ~% M8 d: s! F5 l
and Kenneth R. Rettig, MD1# W9 V0 z' ^8 J$ @3 O: q' Q! _
Clinical Pediatrics+ p8 J2 L% s  l3 C" ]# J3 ]
Volume 46 Number 62 @% H7 d/ c/ L
July 2007 540-543- ?; Q  M) M# K5 y6 j
© 2007 Sage Publications
& @) n  T. _; I* f! M; H% T10.1177/0009922806296651$ k" T% Y; l7 n# e( G
http://clp.sagepub.com
+ z$ i1 r/ ~/ x! Ahosted at
8 F+ }0 m/ u- Qhttp://online.sagepub.com
; D/ q% S' l% D1 q5 v2 H7 gPrecocious puberty in boys, central or peripheral,$ z/ Z& Z! ?! p/ f% h
is a significant concern for physicians. Central
2 x) H( V: X5 j6 P- C5 e* X  vprecocious puberty (CPP), which is mediated
) E& P" d# O3 ?. X1 x  Cthrough the hypothalamic pituitary gonadal axis, has  U6 V  L* i( X
a higher incidence of organic central nervous system
. r8 o# g& w  H4 q9 r- Flesions in boys.1,2 Virilization in boys, as manifested
! t! ~6 ^, V+ v' ]5 k, \  p; q% U) hby enlargement of the penis, development of pubic+ j; _( s8 f- Y! Q! m; }
hair, and facial acne without enlargement of testi-
$ P2 ], s; ~# K1 @% acles, suggests peripheral or pseudopuberty.1-3 We! T3 X: _1 @6 C5 h5 ?; N
report a 16-month-old boy who presented with the; @- p- _# S4 B, ?: K+ s$ Z: G
enlargement of the phallus and pubic hair develop-
' I) o% G0 Q$ ]4 vment without testicular enlargement, which was due4 H5 N: ^. B+ A5 p/ z
to the unintentional exposure to androgen gel used by% i. W1 w* d) W4 n" z
the father. The family initially concealed this infor-
' ?& |3 ]& p% C2 [* y% T: @mation, resulting in an extensive work-up for this/ R- q9 K# H, W; v( ~. u
child. Given the widespread and easy availability of8 ~. z: Y3 b# r& F. ]$ S# b$ z
testosterone gel and cream, we believe this is proba-
( x4 s) F9 }4 A4 }% Nbly more common than the rare case report in the  l* i# [2 k0 B8 U4 K  m- }
literature.4
; O3 X1 Z: Q" u; H# W' G3 pPatient Report8 g. S1 T. D! `# N0 _' n: G3 G" p/ g
A 16-month-old white child was referred to the
0 u; e, g- J* L5 |: Pendocrine clinic by his pediatrician with the concern
; m7 f  v' D0 Uof early sexual development. His mother noticed
$ j8 a6 c7 Q" L+ M% p* A% {light colored pubic hair development when he was
' K( J3 ^, p/ _3 {) q* dFrom the 1Division of Pediatric Endocrinology, 2University of% ?- k; q% g: y( y6 k
South Alabama Medical Center, Mobile, Alabama.7 o4 u: U0 U+ v+ N5 g
Address correspondence to: Samar K. Bhowmick, MD, FACE,( K3 z2 v; h+ ~
Professor of Pediatrics, University of South Alabama, College of
% C; l9 z0 Q" l; mMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
# ^+ {( k8 E! b- M/ u3 @e-mail: [email protected].* D6 J  ?! h. Z5 t0 u2 d
about 6 to 7 months old, which progressively became. ]+ s' w. f2 |4 h5 ~! I2 O) q
darker. She was also concerned about the enlarge-
' k2 \5 o( U; x* i/ w" X5 q9 ~: Nment of his penis and frequent erections. The child
4 {) C! X5 t, a, Y- owas the product of a full-term normal delivery, with
" H, U4 y5 \5 Ea birth weight of 7 lb 14 oz, and birth length of
" r. H- k- F, ]20 inches. He was breast-fed throughout the first year
( C/ G/ J' s& U8 dof life and was still receiving breast milk along with
# m( o" H$ d" a! Dsolid food. He had no hospitalizations or surgery,
4 ?8 w; {' d* ^& d  eand his psychosocial and psychomotor development
4 R/ ^* s6 @3 E; W7 |) Zwas age appropriate.5 P' N- i. p( Q- {/ \, D
The family history was remarkable for the father,
1 k4 O  u0 f  t0 Twho was diagnosed with hypothyroidism at age 16,
7 B. S$ }# a4 X7 \( pwhich was treated with thyroxine. The father’s, q, z  x" m( X/ A3 q# b  x0 i+ ~
height was 6 feet, and he went through a somewhat
! d3 ~# D" m+ O5 N/ qearly puberty and had stopped growing by age 14.
$ h: ^) U. x( H8 `$ f7 ^The father denied taking any other medication. The3 J/ a0 B! n) }% u" v
child’s mother was in good health. Her menarche
4 ?8 D8 W" z7 [7 ]1 o2 y4 k5 s8 Lwas at 11 years of age, and her height was at 5 feet3 E6 ]% a1 y+ r2 `+ Q
5 inches. There was no other family history of pre-
+ `3 ^" K4 q1 acocious sexual development in the first-degree rela-# s0 S' t) a% n  K: b$ N9 c
tives. There were no siblings.
& X- H# S/ v. N" ZPhysical Examination
4 B! H6 z" x+ g6 FThe physical examination revealed a very active,
6 u3 c# Z6 C, ]1 C7 i' @, h" S+ M8 xplayful, and healthy boy. The vital signs documented! @: z+ C1 E! l+ D% ^' R  r5 K
a blood pressure of 85/50 mm Hg, his length was
7 K* W( H3 {2 G  _( M4 O: @) Y90 cm (>97th percentile), and his weight was 14.4 kg
: P+ o) ?- m+ D' s/ w" W(also >97th percentile). The observed yearly growth
5 z4 A! |9 M1 k. Q% C: Pvelocity was 30 cm (12 inches). The examination of, X- L1 S' }6 G" ^. V/ ?9 }
the neck revealed no thyroid enlargement.! @) ?8 G6 L# t+ P3 g" U$ h
The genitourinary examination was remarkable for
- o4 ^0 q- w4 L3 z' [$ E. i. d' d2 zenlargement of the penis, with a stretched length of
/ z, Y; o5 }* C8 cm and a width of 2 cm. The glans penis was very well
* Z5 ?, y4 [- {9 ldeveloped. The pubic hair was Tanner II, mostly around
1 x+ g+ k4 o0 R! k" Y6 ~, j540! [1 Z# j$ D9 Q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ ]- s+ F& g+ r) D( d8 Ythe base of the phallus and was dark and curled. The: h$ a" r- I! {6 W% w. L
testicular volume was prepubertal at 2 mL each.
, j* A/ \8 w, n! cThe skin was moist and smooth and somewhat
4 f: w6 F( h! [6 Ooily. No axillary hair was noted. There were no
0 |6 L# v: n: a! t$ mabnormal skin pigmentations or café-au-lait spots.  Y& P' d6 H  g1 w$ ]0 D
Neurologic evaluation showed deep tendon reflex 2+
/ t4 }3 N: Q* Ubilateral and symmetrical. There was no suggestion6 p& l. Q( Z* T7 z/ p: I% {
of papilledema.7 L7 _+ t: x/ A+ P( q, H
Laboratory Evaluation/ x5 C4 c" u8 e6 E
The bone age was consistent with 28 months by# E5 `4 M5 ~" V2 R
using the standard of Greulich and Pyle at a chrono-$ {* u2 u) ?) a5 l  w" l' ~9 a/ B4 F. v
logic age of 16 months (advanced).5 Chromosomal, h3 t2 u+ f% X* x$ S7 J
karyotype was 46XY. The thyroid function test
# s6 L! \  [: a) jshowed a free T4 of 1.69 ng/dL, and thyroid stimu-! }6 V9 K& G; P( X7 N2 i+ X
lating hormone level was 1.3 µIU/mL (both normal).
2 f/ s- y2 M* {The concentrations of serum electrolytes, blood
. K$ N' n( g5 Y  u1 nurea nitrogen, creatinine, and calcium all were
/ |( }; C9 N; M6 h$ p2 b& ]/ u% }within normal range for his age. The concentration
( F* B- ^7 ?6 C4 Z6 S! m0 E! Z+ P& M- _9 Vof serum 17-hydroxyprogesterone was 16 ng/dL
! W. u9 y  Q' K* s7 G2 j+ ?(normal, 3 to 90 ng/dL), androstenedione was 209 x5 r' J5 K1 Q4 V2 W) N, ~/ s# d/ _2 @
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-' n* O3 x( l5 J- v' v; I
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
4 I/ Q% v5 }- s' wdesoxycorticosterone was 4.3 ng/dL (normal, 7 to) c- g$ }) o$ T& h8 M7 c: e
49ng/dL), 11-desoxycortisol (specific compound S)& ^* h9 V' P, P: ~' `
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# u# G" N7 [+ u- ?. p
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
! ?  |6 T/ O9 g* o9 d, ftestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
" C+ C/ }7 e+ T' qand β-human chorionic gonadotropin was less than- @+ K" o' ^: C9 S
5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 S& N0 S6 m0 P* O9 Mstimulating hormone and leuteinizing hormone, _# W+ Y/ K0 d( s5 c2 V
concentrations were less than 0.05 mIU/mL+ D6 u7 U0 L7 a0 y/ i' R2 f
(prepubertal).1 @8 A3 @% c  ^
The parents were notified about the laboratory$ ]9 B8 y( H: u& L0 G7 J- k% B
results and were informed that all of the tests were
( ]7 `* k7 ?$ m8 D2 enormal except the testosterone level was high. The  g* ]1 }2 r3 k# [2 q6 f4 ^
follow-up visit was arranged within a few weeks to! n: X0 k( }* Y9 f- y. {
obtain testicular and abdominal sonograms; how-, Z* N( t. Q* {2 g
ever, the family did not return for 4 months.; e% @7 [$ v) }
Physical examination at this time revealed that the
3 N* K6 m5 u' z( N7 Pchild had grown 2.5 cm in 4 months and had gained8 z; t, t- J- N- z7 K; W3 D3 p
2 kg of weight. Physical examination remained
1 V5 {& O6 J5 L5 k0 n9 runchanged. Surprisingly, the pubic hair almost com-  C: j$ L$ _; V  d
pletely disappeared except for a few vellous hairs at, f. I3 V1 P: H) n0 |- t" d6 Z
the base of the phallus. Testicular volume was still 2
) w* r# ?7 s% U% u0 KmL, and the size of the penis remained unchanged.
/ w) e* q# e! ~1 RThe mother also said that the boy was no longer hav-
! f  ?) d& e; D. g+ e; Y& z) @: c0 king frequent erections.
2 E$ e+ a! K$ ~1 jBoth parents were again questioned about use of8 g, P+ [8 y- ?/ I$ n/ M0 b( n
any ointment/creams that they may have applied to
+ z; [/ k  |1 Ethe child’s skin. This time the father admitted the' O0 m, ]' I8 J3 D) S
Topical Testosterone Exposure / Bhowmick et al 541
+ C8 ~3 q6 E- s& D& n" duse of testosterone gel twice daily that he was apply-
# |1 L1 |" |& N  X+ l! o" x4 F: Ning over his own shoulders, chest, and back area for
6 u  ]0 F5 w+ v7 z% z4 Pa year. The father also revealed he was embarrassed
: m) n' I8 ~: F" V! a4 qto disclose that he was using a testosterone gel pre-
! @3 R$ `( S* @$ ?scribed by his family physician for decreased libido4 x  r8 B, S  V9 R! {4 i( z( T* x1 @
secondary to depression.5 o3 A) U8 F8 r: K; ~" ?
The child slept in the same bed with parents.' J0 i2 ?3 ^9 C4 |) P# X
The father would hug the baby and hold him on his
. o' T; j) n1 @0 bchest for a considerable period of time, causing sig-' w6 D! I. f, a; D! R# k
nificant bare skin contact between baby and father.7 q. x6 R+ @' `1 X+ Z% B' I
The father also admitted that after the phone call,' \4 g" J& h. U& B
when he learned the testosterone level in the baby
8 W' L) e3 j5 X& P& ~0 ~was high, he then read the product information2 x5 m7 o% W0 V# t; ^
packet and concluded that it was most likely the rea-6 S# P3 S+ q0 ^1 M0 X
son for the child’s virilization. At that time, they9 U% x0 O5 g, S4 _8 }; g
decided to put the baby in a separate bed, and the; X" u& h2 m. z4 n2 ?# F
father was not hugging him with bare skin and had
* }3 S' @2 O7 W, w  G4 w; Vbeen using protective clothing. A repeat testosterone
& D3 m$ w  Y% Q$ D6 e4 e( A' Htest was ordered, but the family did not go to the
5 ^. t, j7 O, V* F. xlaboratory to obtain the test.# W% R7 p% m  @# I$ @. P( x
Discussion' e3 o! i- I5 V4 S% ], v
Precocious puberty in boys is defined as secondary9 B+ V/ e8 {1 b# p7 h
sexual development before 9 years of age.1,4
8 X; I5 D9 T8 ?0 p7 j6 FPrecocious puberty is termed as central (true) when
& T0 g( u( T4 ^2 O& D! yit is caused by the premature activation of hypo-3 b0 I& L4 k9 n3 {. C4 z6 N) @
thalamic pituitary gonadal axis. CPP is more com-
: E4 E8 O, N; Z) ?0 ~2 Y$ d0 @mon in girls than in boys.1,3 Most boys with CPP. U! N# O; c  J+ }0 q) F
may have a central nervous system lesion that is% o5 F% R& R7 l! v" Y
responsible for the early activation of the hypothal-
0 m. h  Z& G$ M7 _2 D) m6 R7 g) i7 Samic pituitary gonadal axis.1-3 Thus, greater empha-! ]3 [0 ]4 C' q
sis has been given to neuroradiologic imaging in9 C2 b, d9 A/ @  U
boys with precocious puberty. In addition to viril-) i: U5 R. A# I; n" I5 J
ization, the clinical hallmark of CPP is the symmet-
* m9 E, ]' J: f+ }+ Krical testicular growth secondary to stimulation by
& V3 p+ @$ e. {: e5 agonadotropins.1,35 u) g( z: D- V8 a# M& r+ y
Gonadotropin-independent peripheral preco-
% T; n5 d  W6 L5 pcious puberty in boys also results from inappropriate
0 S. M; V1 U/ u# d, Vandrogenic stimulation from either endogenous or
% v6 c$ q  n' z# j0 aexogenous sources, nonpituitary gonadotropin stim-
1 K( Q3 H% z  K" P! x- Bulation, and rare activating mutations.3 Virilizing) X8 H0 V) o2 j( `8 }6 Z
congenital adrenal hyperplasia producing excessive8 A' t. f$ Z' I7 W0 S, j- }  c
adrenal androgens is a common cause of precocious
/ y/ }6 `4 [; h! @8 n: Xpuberty in boys.3,4
" o4 f3 f( ?  F9 u5 {, c% T9 l# ~$ nThe most common form of congenital adrenal0 l! u$ ~0 [/ C' k( s  I
hyperplasia is the 21-hydroxylase enzyme deficiency.
4 r! f8 _! Z. Q6 }) h5 KThe 11-β hydroxylase deficiency may also result in# G" @1 Y2 d( s4 z
excessive adrenal androgen production, and rarely,
5 ?9 ]& E) G4 h2 J# ^0 E, q4 t' h+ dan adrenal tumor may also cause adrenal androgen: z+ M3 T/ M4 V- ~2 n
excess.1,3% L2 x* [( B! R8 o" u
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 G! ^* Q- a  _4 u1 E2 E542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
9 \4 p) i$ }3 c* F" ~- \5 B. FA unique entity of male-limited gonadotropin-/ t# Z( p) }$ Y6 I0 J3 W
independent precocious puberty, which is also known
% O- e; M0 n. tas testotoxicosis, may cause precocious puberty at a7 x+ v" z8 K# a
very young age. The physical findings in these boys* E1 o+ j, ~5 k# R5 k4 @! o5 y
with this disorder are full pubertal development,
: Q* i# n. u1 p. [3 F' ^including bilateral testicular growth, similar to boys1 O1 k& B: @* P8 }( Z' s
with CPP. The gonadotropin levels in this disorder* v& a% O: C" ]7 \+ u+ r3 G  M& u
are suppressed to prepubertal levels and do not show, e/ a7 k/ y* H$ }- f
pubertal response of gonadotropin after gonadotropin-' R7 k) C" Y1 k# f$ {/ s
releasing hormone stimulation. This is a sex-linked
2 ~( N0 x: e2 v! w2 v' G. fautosomal dominant disorder that affects only( [6 e& K- D1 K' v8 u' c
males; therefore, other male members of the family
# T! u' Q$ c4 I+ _7 b2 ]may have similar precocious puberty.3
7 h2 p0 u- I, @In our patient, physical examination was incon-
( g* k2 q  P+ X% C2 a: C% X  psistent with true precocious puberty since his testi-
& X; z7 s+ C7 Kcles were prepubertal in size. However, testotoxicosis5 x4 E- F' T% P, D9 A
was in the differential diagnosis because his father
% e4 u" {- f& P# D+ X( Z: K- [& `started puberty somewhat early, and occasionally,
7 k3 J* x. k+ V/ X' B7 A1 k& dtesticular enlargement is not that evident in the
) Q, G9 E7 f7 k2 y9 R7 A) s; o2 v3 V- Vbeginning of this process.1 In the absence of a neg-0 P/ |! ^: r9 m: r
ative initial history of androgen exposure, our
2 Q# K5 K7 |$ ~1 H2 `biggest concern was virilizing adrenal hyperplasia,
  e" v7 y5 @2 l1 `! `either 21-hydroxylase deficiency or 11-β hydroxylase7 n0 e: o5 W( H* {- D5 j- y
deficiency. Those diagnoses were excluded by find-- }/ ?) f3 s7 R" V- P2 v
ing the normal level of adrenal steroids., e$ c5 c, C. N0 V6 H
The diagnosis of exogenous androgens was strongly9 P2 [1 E6 L2 }7 X3 n2 F
suspected in a follow-up visit after 4 months because) B# p  j6 _& H2 ^
the physical examination revealed the complete disap-. t' E7 p$ R8 Q+ S: m- v$ V
pearance of pubic hair, normal growth velocity, and# _8 r" c, @4 O) n$ ^' J
decreased erections. The father admitted using a testos-
- m1 T( O& E* K4 Qterone gel, which he concealed at first visit. He was
; U4 `! z7 C$ b! M2 N" M* uusing it rather frequently, twice a day. The Physicians’" z  ?% R! P# E
Desk Reference, or package insert of this product, gel or3 ]% t$ S- u) b! @5 z! r9 C
cream, cautions about dermal testosterone transfer to; R* p5 F& G1 z6 [
unprotected females through direct skin exposure.
. x% z; `& V2 D- }. S" c8 H) OSerum testosterone level was found to be 2 times the# l  N" q- Q1 n8 _* P
baseline value in those females who were exposed to
; a$ n, X4 F; V3 B* j; a4 m% Ieven 15 minutes of direct skin contact with their male, S+ q8 J; A$ C. A7 b8 Z0 v; Z- N8 w
partners.6 However, when a shirt covered the applica-
/ p$ }1 U4 C* ]# z/ }7 Xtion site, this testosterone transfer was prevented.1 _7 }% v* a4 A1 |5 ?8 t
Our patient’s testosterone level was 60 ng/mL,
5 }  h, e. i% M, z5 X' \which was clearly high. Some studies suggest that. y$ |; j  _2 m: z' g* Y
dermal conversion of testosterone to dihydrotestos-4 m& G/ Y* Z8 n$ U: O! Q
terone, which is a more potent metabolite, is more
+ Y4 n9 e6 z$ X7 k# |- E3 Y" ?active in young children exposed to testosterone
/ X" u+ s0 ^  @/ `$ U0 `exogenously7; however, we did not measure a dihy-
; [) y9 e! G! {' F. d% }1 ldrotestosterone level in our patient. In addition to/ h+ t  j. S( {% Z# n
virilization, exposure to exogenous testosterone in
2 u! @8 C$ Y$ W' ^children results in an increase in growth velocity and
3 ]1 P" A9 P, v$ Nadvanced bone age, as seen in our patient.
: K& e, V7 Y4 w$ G- M8 BThe long-term effect of androgen exposure during( L0 h& K2 v/ f5 P! w  g& _9 u
early childhood on pubertal development and final% U8 F  z# K' H
adult height are not fully known and always remain
0 P- s9 h6 @4 f' w+ X& d$ a# \a concern. Children treated with short-term testos-
8 e7 q5 \' _* s1 A& K( l% }( h7 ^- zterone injection or topical androgen may exhibit some
1 `9 G* v. z4 ~* w% J3 cacceleration of the skeletal maturation; however, after) e( `3 ~: Y& H& Z) W
cessation of treatment, the rate of bone maturation
  B0 v6 }* o( edecelerates and gradually returns to normal.8,9) k2 m1 F# j  h2 K3 l/ o
There are conflicting reports and controversy7 J3 l' S' h5 O9 Q8 ^
over the effect of early androgen exposure on adult
# ~8 y- e0 v* e% t: j# P1 Npenile length.10,11 Some reports suggest subnormal
; c; e  [: c5 \" A( _. C0 m% fadult penile length, apparently because of downreg-0 D+ ]8 _, M4 Z5 z
ulation of androgen receptor number.10,12 However,) E* N- a6 e7 o6 C- `& o
Sutherland et al13 did not find a correlation between
9 x; }( X8 z1 H! Z, |childhood testosterone exposure and reduced adult" Y+ {. t/ r) }
penile length in clinical studies.  _/ v* A9 f0 B& j
Nonetheless, we do not believe our patient is$ Y, ~- H' e8 N
going to experience any of the untoward effects from
& N+ l% P: L( E% gtestosterone exposure as mentioned earlier because
, m- @5 W0 m5 q! n) O" |7 Dthe exposure was not for a prolonged period of time.
7 n7 C% a- o7 Q. `Although the bone age was advanced at the time of
( X! s" T3 X, v9 [diagnosis, the child had a normal growth velocity at9 d: ~' f' p6 S! l) G' P
the follow-up visit. It is hoped that his final adult/ j, m- U1 A; R; v. a9 x
height will not be affected.
) P$ T' I3 }$ z# {0 f. A3 XAlthough rarely reported, the widespread avail-& o: T2 X( v+ O$ R, T  w
ability of androgen products in our society may
$ ~) v2 L% f/ H: tindeed cause more virilization in male or female4 p- n5 _1 M9 q* m
children than one would realize. Exposure to andro-/ m, t; x& e" U: d5 i: ?, p
gen products must be considered and specific ques-+ J4 W+ W* c2 Q6 X- w1 \& o) F
tioning about the use of a testosterone product or
( d( D4 B' b  h$ t' }; |2 _gel should be asked of the family members during
/ W# K5 ?8 m4 w9 {the evaluation of any children who present with vir-6 p& c0 L: W' s3 N( m: O4 n' f+ ]8 J* t; x
ilization or peripheral precocious puberty. The diag-
* \4 U/ T' g  H1 D& ^; N8 Hnosis can be established by just a few tests and by9 M8 s+ V! m- y. b1 P. V
appropriate history. The inability to obtain such a( E, |% z0 P: C1 E; n7 ~6 I
history, or failure to ask the specific questions, may* t$ n: t8 P5 I) a  G
result in extensive, unnecessary, and expensive! A, P* ?* y, f5 ~9 }( |, [+ n# [3 ~
investigation. The primary care physician should be
/ X+ @7 r2 a( m) _' L% naware of this fact, because most of these children* ~% O" v2 A4 j( }' D6 I( ~
may initially present in their practice. The Physicians’6 J# i- r6 x3 p4 U2 a" Q$ J# S/ y
Desk Reference and package insert should also put a& Q( [; P8 O9 f% H" Z
warning about the virilizing effect on a male or
: d: B. q3 c+ y8 z  |8 J3 y0 vfemale child who might come in contact with some-4 U  v2 j( t6 n4 g$ k
one using any of these products.
% f# |& k8 E! Y' P. XReferences% I! ]( @8 B: ?4 [
1. Styne DM. The testes: disorder of sexual differentiation
; o$ p( l8 C! B) |" H& E' P/ Qand puberty in the male. In: Sperling MA, ed. Pediatric
; I) l$ s/ v$ g& F6 \% wEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
& w/ d& E; _/ M$ M. q  p2002: 565-628., R: r3 x& a3 [5 U0 k
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
+ m+ y+ v6 _) g* `" j- M% V7 W! opuberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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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

. D# o& r  F9 M/ p% e9 k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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