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Sexual Precocity in a 16-Month-Old
  V, `  Y% ?, z- N4 y; o4 S3 k5 IBoy Induced by Indirect Topical
; P& z' x' d8 }- o# l% N% ~( UExposure to Testosterone9 c" {! j0 Z1 C) s
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
' W  V' |9 I& N! Z5 land Kenneth R. Rettig, MD17 s" L( D! v" D) D
Clinical Pediatrics* ?  p* c6 h9 l1 a0 H
Volume 46 Number 6
2 B9 Z( h2 K! Z; @July 2007 540-543/ l) \5 V) K4 _3 z" `
© 2007 Sage Publications2 {5 e, j. ~6 ]1 y1 a8 M
10.1177/0009922806296651
5 @+ N5 E% D$ ]http://clp.sagepub.com- @$ ?# h* e& G' v: \" K
hosted at
) q1 [1 r! [$ s( Z( ]+ i6 `- Nhttp://online.sagepub.com2 e( f0 U: q: ?, V. B
Precocious puberty in boys, central or peripheral,
8 ]9 E3 ]: ]/ ]1 y2 t: {is a significant concern for physicians. Central, P7 t0 X5 q0 L4 |
precocious puberty (CPP), which is mediated
2 h0 P+ g; V  {* S1 zthrough the hypothalamic pituitary gonadal axis, has
2 g. f5 [- A0 R- v$ v' ~5 Na higher incidence of organic central nervous system
! G/ S, i, s5 o. C% ilesions in boys.1,2 Virilization in boys, as manifested
6 B7 _- M0 B; g2 j* `3 e/ Aby enlargement of the penis, development of pubic
: E9 e& T/ f3 |7 o; z+ Chair, and facial acne without enlargement of testi-) b5 s) I" W, B3 Y
cles, suggests peripheral or pseudopuberty.1-3 We
5 b4 H; R& |/ [) Rreport a 16-month-old boy who presented with the1 ^/ j7 i4 H7 e
enlargement of the phallus and pubic hair develop-4 ?* N8 G, [8 X1 Z6 q, N* Z2 i
ment without testicular enlargement, which was due2 M9 I8 P4 K) S/ C- a& c8 N
to the unintentional exposure to androgen gel used by5 @8 @6 ?9 F, y2 F3 @
the father. The family initially concealed this infor-
4 w. a# L3 Q! p7 Q+ p1 Umation, resulting in an extensive work-up for this
9 ?8 Y& i& K, n! w2 mchild. Given the widespread and easy availability of8 w- Q  l  e( ~. I. i
testosterone gel and cream, we believe this is proba-
8 D9 ]; X9 P: ^" b; D  fbly more common than the rare case report in the
0 [* c0 n5 k& G0 f9 C" yliterature.4
( C% b! A5 X! @" J0 GPatient Report
9 R6 D1 Q0 y1 B" HA 16-month-old white child was referred to the- u% L5 T0 s4 n
endocrine clinic by his pediatrician with the concern
. X( Q/ |! g0 t; H$ N' X3 r4 ]of early sexual development. His mother noticed
( M% d$ r: R: W% Y  t( Llight colored pubic hair development when he was
2 Z; V) N5 p& Y% H7 o" x5 vFrom the 1Division of Pediatric Endocrinology, 2University of
- Q3 [2 F' K1 \  X/ F0 \8 v1 bSouth Alabama Medical Center, Mobile, Alabama.
: h' ?6 M, G; k& jAddress correspondence to: Samar K. Bhowmick, MD, FACE,
$ d/ ?/ W( N) {/ w) ~) kProfessor of Pediatrics, University of South Alabama, College of5 w  w5 ^" l3 m# h1 \
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
  E$ T( Y$ e8 N" x* o$ s" oe-mail: [email protected].
# G9 j3 e3 I- H) B, L, A2 j/ Xabout 6 to 7 months old, which progressively became  H% z- {7 r, S! i4 D, \3 ~- b) P% c  O
darker. She was also concerned about the enlarge-. `! L: F. f1 l. t7 `, R
ment of his penis and frequent erections. The child
! `9 C+ t( Q" \( \0 Ywas the product of a full-term normal delivery, with
$ Q$ [9 r. u0 s8 P# Y! I! {1 r9 `a birth weight of 7 lb 14 oz, and birth length of
) D9 @" l9 H' V2 ]20 inches. He was breast-fed throughout the first year6 G9 f9 V3 r5 S4 R  P
of life and was still receiving breast milk along with+ t+ w. V7 b  ]& v7 |* e9 `4 k
solid food. He had no hospitalizations or surgery,
) ^; D2 |  ~5 _) Q0 `4 ]and his psychosocial and psychomotor development
4 j( {! ]6 y: A7 b2 ~# E3 a- [was age appropriate.( w% O9 D0 D! v" a. |2 f
The family history was remarkable for the father,9 s# v/ g0 {$ w5 y/ U8 m
who was diagnosed with hypothyroidism at age 16,. C) Q# A  N5 U. L. |8 `( Q
which was treated with thyroxine. The father’s1 y7 E  D. x: ~9 ~0 T( X
height was 6 feet, and he went through a somewhat( k" ~1 R) D# P" Z5 u  o
early puberty and had stopped growing by age 14.
, t* g! Z* f6 S4 i$ a* qThe father denied taking any other medication. The" ^) z+ B: R8 _3 \7 Z" @
child’s mother was in good health. Her menarche
6 s, b! y- b# _9 a& S$ \was at 11 years of age, and her height was at 5 feet
+ c% ~' ~: m! x0 V% e$ ?5 inches. There was no other family history of pre-
6 b. p: V& \0 t; l$ ?$ g' D6 ycocious sexual development in the first-degree rela-
  H& ~) i! S$ R" Z$ u5 ^tives. There were no siblings.
3 w% {( d1 O- CPhysical Examination
- O( q* D- r  T; S; e. ?+ ]# ZThe physical examination revealed a very active,
% `- {# t9 ^% Tplayful, and healthy boy. The vital signs documented3 w3 t" ?/ I- }9 R- M! b0 [
a blood pressure of 85/50 mm Hg, his length was
# U! {' |! P- Q# r& r5 }90 cm (>97th percentile), and his weight was 14.4 kg
6 k8 a) i+ }  w6 z(also >97th percentile). The observed yearly growth& `/ |9 {% T. J" t: q
velocity was 30 cm (12 inches). The examination of
& w0 c5 j# J% N8 K& g8 _* Jthe neck revealed no thyroid enlargement.
2 h0 c; P7 s# r& ?The genitourinary examination was remarkable for
9 D4 O" m/ |$ [1 p% Y  Jenlargement of the penis, with a stretched length of
( {% w( }! {# Y8 cm and a width of 2 cm. The glans penis was very well
! N, ~! q, a2 q7 A4 ideveloped. The pubic hair was Tanner II, mostly around
, E7 c/ k# [$ J540  M& L# D7 `+ ]: J8 L& D  _) E0 K
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' O6 ?( z/ E% m8 H
the base of the phallus and was dark and curled. The
% G# j6 c2 q5 x1 M0 T* p: f, N) Btesticular volume was prepubertal at 2 mL each.
: W. Q: l2 p6 I# c' W: BThe skin was moist and smooth and somewhat, p, _2 A1 N/ L* r
oily. No axillary hair was noted. There were no
# @, n+ u. [/ f( Rabnormal skin pigmentations or café-au-lait spots.
1 I0 h& J2 N0 `7 }: |9 wNeurologic evaluation showed deep tendon reflex 2+& e- B3 h- w; ^
bilateral and symmetrical. There was no suggestion' Y, D7 w: y  }7 H( x# B" c
of papilledema.
# K9 s; G* P5 m1 FLaboratory Evaluation3 h* Q$ p5 y" N9 _6 u' @
The bone age was consistent with 28 months by+ n  I$ v  m/ y& f3 _3 j3 P
using the standard of Greulich and Pyle at a chrono-/ k1 D( c* |# Q$ L+ K7 c' B
logic age of 16 months (advanced).5 Chromosomal
3 g1 x* J: ?2 L/ ?0 v9 W1 Vkaryotype was 46XY. The thyroid function test3 s! R) u' O7 }7 Y9 }
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
5 W* E* K# r2 Z* \2 }+ ]lating hormone level was 1.3 µIU/mL (both normal).* Z0 P7 _( c& p9 x0 h- m4 y- u
The concentrations of serum electrolytes, blood3 M. l  V6 P( N4 O% d5 w# x
urea nitrogen, creatinine, and calcium all were
7 p  }( `3 f- s! v& @. y$ b% Owithin normal range for his age. The concentration
$ x6 M7 f8 t. U3 h/ c( }of serum 17-hydroxyprogesterone was 16 ng/dL; K8 S' X( f) Z6 g) W  ^
(normal, 3 to 90 ng/dL), androstenedione was 20
& O7 B8 ?# A9 K  o; @6 y# T% Zng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
; U" s* w- l) A4 Y' rterone was 38 ng/dL (normal, 50 to 760 ng/dL),, m) F' B+ M1 R3 ?; `
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
+ Q8 v: O* ]* t$ M3 M49ng/dL), 11-desoxycortisol (specific compound S)/ Z: m7 v. X% Y- S) I' d# |
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
7 G2 V! v/ Z; a7 ktisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
) ~' O& b* D; U7 b$ Atestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
/ i  B! w& Y' P& X6 m, ^and β-human chorionic gonadotropin was less than( I9 C0 h& a0 j: u* O3 W
5 mIU/mL (normal <5 mIU/mL). Serum follicular; U: `: w  F- I% `6 w3 ~
stimulating hormone and leuteinizing hormone
, O; d) u$ T/ Iconcentrations were less than 0.05 mIU/mL
- L' Z2 B( t; ]4 C(prepubertal).
* Z9 n  _+ L4 z& uThe parents were notified about the laboratory
2 U: _7 B% c! v& x# d) K0 L, f3 l/ Fresults and were informed that all of the tests were5 Q! g/ k( c5 R- M& v. V& T" Q2 V9 N
normal except the testosterone level was high. The
* b  v; O/ d1 d: L0 d, ~/ {follow-up visit was arranged within a few weeks to# v, I& z# B0 o* }" Q8 _5 k/ R1 Z
obtain testicular and abdominal sonograms; how-6 L* y' d) d0 V* v& X' q# }
ever, the family did not return for 4 months.# R/ l1 G( j9 O3 I; c
Physical examination at this time revealed that the
7 n: T8 O) ~8 `5 U* V4 j3 kchild had grown 2.5 cm in 4 months and had gained  m7 X- c* K9 L, ]% t% a$ D/ Z
2 kg of weight. Physical examination remained
/ P& y' s: ]" Y' S0 X" q! hunchanged. Surprisingly, the pubic hair almost com-
7 p& q: e' q/ spletely disappeared except for a few vellous hairs at9 p6 I% U& T, Z+ a8 V" V
the base of the phallus. Testicular volume was still 2
& j$ }+ u! K- [) e: E7 BmL, and the size of the penis remained unchanged.
* [* C1 j7 ?$ C2 }; ]The mother also said that the boy was no longer hav-
+ g9 D& y5 C+ Q2 j8 {ing frequent erections.
5 }* u  O! T' j1 Q3 T$ `4 P. QBoth parents were again questioned about use of
$ P- {( x, E! ?# S0 A" V: Rany ointment/creams that they may have applied to
3 a+ y: c+ k/ b9 [9 l- othe child’s skin. This time the father admitted the2 w0 O6 \1 X5 s! U2 l
Topical Testosterone Exposure / Bhowmick et al 541
8 X2 G  E% @. a1 W  o9 fuse of testosterone gel twice daily that he was apply-( ]+ o, O7 ]1 ?$ a4 U
ing over his own shoulders, chest, and back area for& b2 r7 K9 L* y; @
a year. The father also revealed he was embarrassed
- N( d4 g; D7 y6 \/ R5 h' T4 vto disclose that he was using a testosterone gel pre-6 L1 ~0 F. g/ t: u/ m( Z9 E) F* V: n
scribed by his family physician for decreased libido. L5 f' Z: i& O3 t/ a+ z2 r
secondary to depression.
2 w" w$ Q5 C; K  r4 |The child slept in the same bed with parents.
/ ^/ E3 S9 F2 x7 ?. R  jThe father would hug the baby and hold him on his
) V$ A9 ?. U* f$ y3 qchest for a considerable period of time, causing sig-7 Z$ T" b0 ?. B$ F9 R. z
nificant bare skin contact between baby and father.( w0 b: g$ q  M2 @# V0 u
The father also admitted that after the phone call,
9 Z2 B3 ^4 [  y: t- x9 o' Qwhen he learned the testosterone level in the baby5 m( L6 L; g! q2 U6 X
was high, he then read the product information
4 _( l3 |9 ], s4 M0 rpacket and concluded that it was most likely the rea-
3 G- i7 F# A0 z- s) uson for the child’s virilization. At that time, they) l, y: r" `! t- K$ ^
decided to put the baby in a separate bed, and the3 X' p: k, r9 f
father was not hugging him with bare skin and had7 ]5 O: g3 x! F( H4 e, n
been using protective clothing. A repeat testosterone
: r( o6 N' Y% s' n0 vtest was ordered, but the family did not go to the3 k( D, o. J" b3 r7 J0 }
laboratory to obtain the test.. z( e8 R# `% j# u+ K5 ^
Discussion8 g1 v9 h! n+ C7 \+ i& O. N
Precocious puberty in boys is defined as secondary
; c& j& c! L9 N( x" l7 `sexual development before 9 years of age.1,4# L6 k1 j+ L# z0 q- J( m4 {
Precocious puberty is termed as central (true) when
3 ?/ ?/ [* d7 R9 J) i- Hit is caused by the premature activation of hypo-8 i  O6 v! o" y
thalamic pituitary gonadal axis. CPP is more com-8 V, J0 X3 H! E4 _: A
mon in girls than in boys.1,3 Most boys with CPP
7 u: t/ i3 E% [. V2 lmay have a central nervous system lesion that is$ ]; n. z2 }+ \1 {/ {  b
responsible for the early activation of the hypothal-
: x4 o/ h7 U. [) ]amic pituitary gonadal axis.1-3 Thus, greater empha-
3 x; H( \5 N8 F+ r, Bsis has been given to neuroradiologic imaging in
$ P) ]- b7 L5 F1 g0 C9 X: Lboys with precocious puberty. In addition to viril-( A9 B9 }* l  y# w, ]
ization, the clinical hallmark of CPP is the symmet-
+ Q) ^5 E" ?+ P6 T6 o9 drical testicular growth secondary to stimulation by" v  g# l9 _! U
gonadotropins.1,3
2 x8 t( t3 t3 B- uGonadotropin-independent peripheral preco-" X" ~$ w0 P2 I5 s; w8 K
cious puberty in boys also results from inappropriate
& ]) A* p& F5 d4 Y$ S4 c* bandrogenic stimulation from either endogenous or
9 ?5 l0 s$ s& b+ w6 D' V0 qexogenous sources, nonpituitary gonadotropin stim-
. ?+ M* e% c/ c# h! d: Hulation, and rare activating mutations.3 Virilizing, Y" n3 `: D# I3 T3 O
congenital adrenal hyperplasia producing excessive
8 K2 C( g. I8 j+ x( Cadrenal androgens is a common cause of precocious
8 e( D6 f9 Y/ T# z/ m1 fpuberty in boys.3,4
5 z4 j4 O& w3 {' r7 d3 CThe most common form of congenital adrenal
3 g) C% d  F" E5 Hhyperplasia is the 21-hydroxylase enzyme deficiency.
) S6 W6 W- U  h* w( b- }+ xThe 11-β hydroxylase deficiency may also result in
1 a. _/ J' p8 N' F# S+ _( ^% b$ kexcessive adrenal androgen production, and rarely,; z. X, }# H% E8 \2 n
an adrenal tumor may also cause adrenal androgen
# x" ]" i! r- g0 Qexcess.1,3) Z$ @5 R( q& N( `3 P$ ]
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 f9 G$ }2 k5 g$ ^% X542 Clinical Pediatrics / Vol. 46, No. 6, July 2007) o; }7 \4 P* m
A unique entity of male-limited gonadotropin-1 \" }! w& Y! s
independent precocious puberty, which is also known
* Y! X8 A" P; n+ pas testotoxicosis, may cause precocious puberty at a5 t% |: e# J1 t# d  m0 s: Q
very young age. The physical findings in these boys
" W# l6 g/ W9 A* g2 N9 vwith this disorder are full pubertal development,! ~  ~7 w5 C: l+ o; r! `
including bilateral testicular growth, similar to boys
5 ?% r' K  A# G) t) F2 f9 Lwith CPP. The gonadotropin levels in this disorder
) `$ u; R/ o$ k& K! u0 bare suppressed to prepubertal levels and do not show
, O3 D1 X  D" H8 M, ?0 rpubertal response of gonadotropin after gonadotropin-
. J' ?2 n; L3 t0 c0 ^- n4 K% A6 g# Qreleasing hormone stimulation. This is a sex-linked2 O$ F" m/ L+ }: v% k( Q  D
autosomal dominant disorder that affects only" Y7 D$ X5 x! Y, g( C, |( j
males; therefore, other male members of the family
/ ]& a2 m% E' t8 G* {1 amay have similar precocious puberty.35 a$ Q6 A: Y# m; `
In our patient, physical examination was incon-/ t& \) p; J) @9 t9 Q
sistent with true precocious puberty since his testi-
8 T/ B. k  C& ?4 O9 \) fcles were prepubertal in size. However, testotoxicosis
: W; t# n: ^& ]was in the differential diagnosis because his father. i7 N- h, S2 _  f% |" t+ t
started puberty somewhat early, and occasionally,
8 p7 _; t7 t! L0 J0 Ntesticular enlargement is not that evident in the6 ?/ P3 s* G* Y0 a5 E9 O3 J) X" n8 [8 Z( ~; u
beginning of this process.1 In the absence of a neg-
% d; q1 L3 u0 _: w  {" ^7 x7 Qative initial history of androgen exposure, our
! J, A" j: G- J7 d$ Y0 s' Mbiggest concern was virilizing adrenal hyperplasia,! U3 ~7 F  n: N
either 21-hydroxylase deficiency or 11-β hydroxylase: K8 e) }1 N& p1 v. P
deficiency. Those diagnoses were excluded by find-& R& f7 O8 v- D$ ~$ N! v0 {
ing the normal level of adrenal steroids.
8 r. n, H8 W$ G4 l2 m0 jThe diagnosis of exogenous androgens was strongly
9 S/ V' G7 S2 K' osuspected in a follow-up visit after 4 months because
/ P0 D* N  l8 Y2 B% N9 ?the physical examination revealed the complete disap-+ `1 e1 M% g, `7 S3 }& L; r
pearance of pubic hair, normal growth velocity, and
% U$ f9 _& n5 O9 R# k% O, G% y! mdecreased erections. The father admitted using a testos-
2 e# O5 o; q6 Y# b; ]2 ]3 _terone gel, which he concealed at first visit. He was  j( n2 t- r3 q4 s
using it rather frequently, twice a day. The Physicians’
: o% H7 p1 g, V: v9 w+ sDesk Reference, or package insert of this product, gel or
5 c3 F. D6 }# \1 y) Lcream, cautions about dermal testosterone transfer to
3 Z7 T5 V4 E' ~; ~; i4 ?unprotected females through direct skin exposure.
8 q0 x, q9 n' ^3 P9 F3 QSerum testosterone level was found to be 2 times the
( J& i4 ~$ k# Y* t. G( Kbaseline value in those females who were exposed to
, Y( L; K& w9 ieven 15 minutes of direct skin contact with their male
8 R7 e/ s4 A8 G; t, O7 Bpartners.6 However, when a shirt covered the applica-
! w- L: P9 F6 Q" Q5 o% xtion site, this testosterone transfer was prevented.
' P; g/ W; K+ v  [Our patient’s testosterone level was 60 ng/mL,3 T( z/ [7 o& F$ z5 D' z7 e( O
which was clearly high. Some studies suggest that
" k7 ^2 L/ ]5 u  E; x. q. g4 @dermal conversion of testosterone to dihydrotestos-2 P6 @: v# Q! R8 I' H; V, m: X# g
terone, which is a more potent metabolite, is more
. d! t! |* p- k# \* V+ gactive in young children exposed to testosterone
. J( J9 w2 U/ r9 r- p9 jexogenously7; however, we did not measure a dihy-3 c' ~! Z9 w  {# h* k
drotestosterone level in our patient. In addition to' L. l* q- j4 V( r* F1 D
virilization, exposure to exogenous testosterone in
1 C+ j' ^* h2 ^; d8 ichildren results in an increase in growth velocity and
& N# E* Z' o- g. \/ }: padvanced bone age, as seen in our patient." c, }5 w5 _) W" {, e8 I% m
The long-term effect of androgen exposure during, _& g5 [! k3 K* c1 P, N
early childhood on pubertal development and final
. @' }' A! x1 Z* A  j1 |adult height are not fully known and always remain0 ?3 i( D+ w# u! O0 |0 L: M5 F
a concern. Children treated with short-term testos-
/ a, L/ I4 {7 D. Y# U1 @5 dterone injection or topical androgen may exhibit some
! i- P( X) b& B8 ^7 g( Vacceleration of the skeletal maturation; however, after0 N5 a6 B3 c0 m4 O8 S; R
cessation of treatment, the rate of bone maturation; [# v$ ~+ ?) f$ z1 U: l8 `) A
decelerates and gradually returns to normal.8,9
3 O8 T  u$ I9 F7 Q5 a0 eThere are conflicting reports and controversy
0 ]! n2 z4 D3 @0 E& l5 e1 Qover the effect of early androgen exposure on adult
  g" |0 Y0 f8 j6 lpenile length.10,11 Some reports suggest subnormal" \/ l% ^2 u1 p
adult penile length, apparently because of downreg-
7 q8 G+ V& G3 b# T" `ulation of androgen receptor number.10,12 However,- ^. m' p7 Z6 l- l) Z
Sutherland et al13 did not find a correlation between3 H; X- p; `4 O# E; ]0 X8 k
childhood testosterone exposure and reduced adult' B/ Q! R. W) _& K8 G; [4 W2 ?
penile length in clinical studies.
5 o( i' ^) {( h+ M( YNonetheless, we do not believe our patient is
: |5 @  n% l  L' zgoing to experience any of the untoward effects from4 [$ r6 L) G9 J/ D5 D# ~' u
testosterone exposure as mentioned earlier because( Y# P* g+ N* ?! z# f( A* T
the exposure was not for a prolonged period of time.
" o  t" b. |% e0 n' \Although the bone age was advanced at the time of
' j6 Z8 e: c  Adiagnosis, the child had a normal growth velocity at) d, \* O" |& h
the follow-up visit. It is hoped that his final adult
6 I7 a1 g0 o/ u5 L. m9 p1 Y! mheight will not be affected.- K9 R% q- P5 W+ W! H9 O& e) C( `
Although rarely reported, the widespread avail-9 u" `7 e8 a' ]5 a% {
ability of androgen products in our society may
( E( K  Z  S. P( cindeed cause more virilization in male or female' _) ^6 R. x. ?' Z
children than one would realize. Exposure to andro-
7 f( ?* P3 W0 l# J% ^gen products must be considered and specific ques-- A% T% Q7 A( R5 _1 k
tioning about the use of a testosterone product or+ j- |- k. Y" f+ u, ?; m4 T
gel should be asked of the family members during
; a' X0 M* o: |0 Vthe evaluation of any children who present with vir-) Q* ]5 b; y! k+ c1 ~4 \) K
ilization or peripheral precocious puberty. The diag-9 ^. p* C. K9 c9 q" ~7 z; s; V. Z
nosis can be established by just a few tests and by
1 `! ?+ c* a2 x3 |appropriate history. The inability to obtain such a* G! ]4 [  f. j
history, or failure to ask the specific questions, may
" k* c( C2 x+ s% t5 B. M4 [result in extensive, unnecessary, and expensive
- V* W2 n8 S8 v3 cinvestigation. The primary care physician should be
; v; P8 R: W: N8 m: G& Taware of this fact, because most of these children6 i  b1 h( }$ X$ z% e7 n, B
may initially present in their practice. The Physicians’
/ q' O' ]- `4 S# F" w0 [1 oDesk Reference and package insert should also put a
+ \" p6 @9 O. }5 r7 a4 K# |warning about the virilizing effect on a male or
4 |5 @* s6 f, L5 ~9 U; vfemale child who might come in contact with some-1 R3 X1 m5 `6 `% `. T& w, ~
one using any of these products.
5 L+ ~2 x2 E0 p& [References7 F# Y! f2 Q. Z" G% c3 P8 k& Z+ Y
1. Styne DM. The testes: disorder of sexual differentiation2 ]1 U, m/ @/ @! _) l9 g2 B0 Y
and puberty in the male. In: Sperling MA, ed. Pediatric
5 d# }* S9 J" X1 M& h4 [Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
. u2 }" J* p2 L2002: 565-628.
9 o) p9 _. U6 W- M9 l1 ?2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious' V) W5 h. x) E7 N% o* W- u
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
9 M6 _! {1 S2 e$ v( xBoy Induced by Indirect Topical
1 G6 U! F3 E/ E% [Exposure to Testosterone
8 a5 p+ ], h* M* H, x. C9 Y9 V. [Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
. H: b' a& U0 I' _6 o: a$ ?6 Fand Kenneth R. Rettig, MD1
: L5 U2 z8 L2 M& KClinical Pediatrics$ s. [/ s# `" H% T
Volume 46 Number 6
9 n) U! _4 ]- W; K" DJuly 2007 540-543  t; A3 L0 T: o1 m
© 2007 Sage Publications1 U- \$ p! T; }* Y3 V0 v1 J" ?) B
10.1177/0009922806296651
6 p0 S+ g6 ?. s; q  h: A! B" L/ i% C6 ehttp://clp.sagepub.com
# F: ]4 g$ A- f3 Shosted at
- `- j2 V9 S! m+ j, qhttp://online.sagepub.com
5 N; b9 d. S9 r% ?5 kPrecocious puberty in boys, central or peripheral,$ h6 ]# @8 ~& v
is a significant concern for physicians. Central" n8 s9 t& O6 n$ n& B
precocious puberty (CPP), which is mediated
- |% Y4 y  Y) k9 Ethrough the hypothalamic pituitary gonadal axis, has
7 V3 M4 P; ?* |1 X+ Va higher incidence of organic central nervous system, }/ ]( q0 |/ x, ^) c' i+ s
lesions in boys.1,2 Virilization in boys, as manifested
" \% S! C6 `0 n; X: {) [by enlargement of the penis, development of pubic
5 z3 p  V0 m- j8 whair, and facial acne without enlargement of testi-" K! q! s" |/ ~
cles, suggests peripheral or pseudopuberty.1-3 We, ~9 ?( U7 T; o5 J# `) w. s, l7 o
report a 16-month-old boy who presented with the
# Y' z: e6 |: R' j9 `8 Qenlargement of the phallus and pubic hair develop-
7 O7 \: p4 I2 |1 D# ]2 C/ F6 V# }+ Ament without testicular enlargement, which was due3 M, Y' ?1 H( q: c/ F
to the unintentional exposure to androgen gel used by" b; e! x5 k) f6 a
the father. The family initially concealed this infor-5 R# R6 r  L' P, J
mation, resulting in an extensive work-up for this& x. s; S2 ]4 Z' @; Q
child. Given the widespread and easy availability of
$ K" J0 N7 @7 {: Z  W6 P! Ptestosterone gel and cream, we believe this is proba-6 U  {( X0 n; H/ t+ P6 Z9 j
bly more common than the rare case report in the1 }1 e" [% ]' }% q) h" \
literature.4
+ M9 s- d4 h5 l. bPatient Report
  y$ ^3 W1 |0 y) ]4 L5 pA 16-month-old white child was referred to the
. m# N9 g  a) j: |5 `* dendocrine clinic by his pediatrician with the concern
2 t9 Z5 ?' f' e% \2 Dof early sexual development. His mother noticed. e5 B7 V& N5 E; @( {1 ?: }
light colored pubic hair development when he was
. p- ~7 n- J# F0 s4 H  EFrom the 1Division of Pediatric Endocrinology, 2University of
+ ?! m, ^" \2 K0 f- T6 n! ?% rSouth Alabama Medical Center, Mobile, Alabama.
& K0 Q5 d/ m4 ^: _* x. _$ IAddress correspondence to: Samar K. Bhowmick, MD, FACE,: S8 E6 n7 R2 e: [: Z
Professor of Pediatrics, University of South Alabama, College of' b' S. {3 [, d: D& g
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;. v+ q, M3 ~6 |6 V! u# }) C
e-mail: [email protected].# q/ x6 ?- x9 I. i# w0 E
about 6 to 7 months old, which progressively became
8 m! k( U4 c$ udarker. She was also concerned about the enlarge-' b/ O  g/ O+ z% Q: G3 m: h
ment of his penis and frequent erections. The child% A+ B9 v1 F: [
was the product of a full-term normal delivery, with
: y! |' x* g3 C3 @6 [* ia birth weight of 7 lb 14 oz, and birth length of
5 q1 P$ C; h& w( X20 inches. He was breast-fed throughout the first year4 Y+ F4 s- R+ H
of life and was still receiving breast milk along with
+ n) T6 x( O4 |. }% {8 U& a8 Tsolid food. He had no hospitalizations or surgery,
& o$ E% j3 e6 q3 }" B8 K1 i, x3 Dand his psychosocial and psychomotor development
+ {  k$ G+ B/ qwas age appropriate.1 D& a4 Z) s+ E/ ?0 }# Q2 J
The family history was remarkable for the father,, t/ C1 R2 R# `( n- M- u
who was diagnosed with hypothyroidism at age 16,
9 K' q" p2 g+ u# Ewhich was treated with thyroxine. The father’s
& @" k8 p+ l7 ^1 Bheight was 6 feet, and he went through a somewhat
& j+ P: ]% X2 s0 g) j2 Bearly puberty and had stopped growing by age 14.
2 d0 k4 A$ c2 b% N. f" p7 `0 j" iThe father denied taking any other medication. The
0 U# T- y1 t$ l/ [2 [child’s mother was in good health. Her menarche
# w: s) s% H! k2 x0 a: s0 Y$ kwas at 11 years of age, and her height was at 5 feet
/ F% V6 G+ N+ d! x$ V( j5 inches. There was no other family history of pre-$ L# U: y: P* x' ?( s
cocious sexual development in the first-degree rela-. w5 C* ?( D; E2 N! ^: u9 j
tives. There were no siblings.: @+ [  W8 g2 o; W
Physical Examination: ?1 [% Z- ^& Y% m+ ^" G3 Z8 R
The physical examination revealed a very active,/ Q& X5 a) j! H9 k4 f
playful, and healthy boy. The vital signs documented
- n1 _3 I. c+ N1 Aa blood pressure of 85/50 mm Hg, his length was2 {3 T3 v" {% f# T" F
90 cm (>97th percentile), and his weight was 14.4 kg
5 ]( _0 Q2 C. L; X& M(also >97th percentile). The observed yearly growth
) Q, W, a4 o) m0 w) T; Dvelocity was 30 cm (12 inches). The examination of% b$ c' e' B6 P3 W4 k+ r, W3 D
the neck revealed no thyroid enlargement." z5 D2 F1 j9 z) e4 E5 B7 |& f
The genitourinary examination was remarkable for
4 A% h3 L, z! \& kenlargement of the penis, with a stretched length of7 s9 d' m3 W: S) y( C8 y9 G
8 cm and a width of 2 cm. The glans penis was very well% B, ]$ F  b: R1 e
developed. The pubic hair was Tanner II, mostly around
1 R9 x9 J: p6 m, {/ y540$ W! i' ^1 H( W
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; s& D" \% V! S$ `/ Y2 ~the base of the phallus and was dark and curled. The" n/ B' L9 T0 G
testicular volume was prepubertal at 2 mL each.2 A; q1 n# G- y
The skin was moist and smooth and somewhat
2 B( e3 L1 q! Doily. No axillary hair was noted. There were no) d3 b: J+ G; I, W0 ?0 O
abnormal skin pigmentations or café-au-lait spots.
9 ]* T6 C# D1 _Neurologic evaluation showed deep tendon reflex 2+
1 e! b5 C. N4 D" C* g1 zbilateral and symmetrical. There was no suggestion
" l- m  M' X' s2 `3 Dof papilledema.8 U4 q/ E! i0 t/ P7 m5 X+ v5 l( k8 b
Laboratory Evaluation! Z4 I  y2 N) x0 W$ C1 [* P, D
The bone age was consistent with 28 months by
, O* b0 [* z! `5 T7 r3 Z4 uusing the standard of Greulich and Pyle at a chrono-
4 v. g0 p/ w  g5 z6 F& Slogic age of 16 months (advanced).5 Chromosomal
3 D: Z3 K3 ?/ {+ Xkaryotype was 46XY. The thyroid function test
$ \& h) V$ X9 ]+ F- V" L3 Lshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
  {  a/ [- \' Wlating hormone level was 1.3 µIU/mL (both normal).
9 I8 W: A: [; mThe concentrations of serum electrolytes, blood
' `; U! d% N4 A' ^urea nitrogen, creatinine, and calcium all were
" S( D, h" l) z4 e% iwithin normal range for his age. The concentration' f0 [3 M3 y$ m- \# ^& d
of serum 17-hydroxyprogesterone was 16 ng/dL. j8 Y" x* |0 W& m/ c
(normal, 3 to 90 ng/dL), androstenedione was 20
5 ~- o' ~6 Q; J$ [ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-8 c% U: K. o* x+ ^! m
terone was 38 ng/dL (normal, 50 to 760 ng/dL),& v0 n% D* P% q8 I0 w* C7 F
desoxycorticosterone was 4.3 ng/dL (normal, 7 to8 I' @' x% F5 `- @
49ng/dL), 11-desoxycortisol (specific compound S)
6 F$ u, F8 I, Jwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-$ ~$ n1 e9 a' |4 t( `( s# e
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
* ?* F+ O, z& v8 Z5 l' q( ~" w# Htestosterone was 60 ng/dL (normal <3 to 10 ng/dL),: Y1 t0 w9 c5 j2 P
and β-human chorionic gonadotropin was less than3 m( U$ D  _8 h4 V% p  d- Z
5 mIU/mL (normal <5 mIU/mL). Serum follicular: E. E6 t9 t- f, S$ e, g
stimulating hormone and leuteinizing hormone0 y% p' K9 p! \6 L3 l: u  p  E; A$ B; S
concentrations were less than 0.05 mIU/mL
& T, u- y2 W$ }4 ~8 Q4 a) {(prepubertal).
2 J' T1 e  w1 W' l. J$ E/ pThe parents were notified about the laboratory
/ ^1 h& Z  r  N: kresults and were informed that all of the tests were! m* y0 b8 x1 j+ Y
normal except the testosterone level was high. The
+ c  L3 f" ~; d% V6 V/ p# Gfollow-up visit was arranged within a few weeks to( S6 ^5 Q% }' e# m
obtain testicular and abdominal sonograms; how-
  j" e  l8 u& b, c& K$ U; Jever, the family did not return for 4 months.4 U& x# Q4 v8 `$ H
Physical examination at this time revealed that the* e/ J3 V8 @2 k  t" p# x
child had grown 2.5 cm in 4 months and had gained$ t/ n. k+ s" ]& \, N
2 kg of weight. Physical examination remained4 J/ Q, f- x8 Y4 _# u
unchanged. Surprisingly, the pubic hair almost com-$ p  g: z" c1 ~" B* P
pletely disappeared except for a few vellous hairs at
; E6 ]- a$ V2 J, l0 Ithe base of the phallus. Testicular volume was still 2. f+ j6 c, n% U( O: ^
mL, and the size of the penis remained unchanged.  C4 W3 `" u+ P4 K/ |# q
The mother also said that the boy was no longer hav-* S: x& {/ n; }. z# C; U
ing frequent erections.
# [; @6 V3 R6 sBoth parents were again questioned about use of' M3 J2 g  p0 G7 y2 q2 h' u. U/ e
any ointment/creams that they may have applied to
/ X4 O5 k2 I+ Kthe child’s skin. This time the father admitted the
7 m) Z2 s5 w; Z" n: FTopical Testosterone Exposure / Bhowmick et al 541' D9 }4 @4 c+ l7 C2 ?6 d% L4 x' v
use of testosterone gel twice daily that he was apply-- a& o7 O' \; T6 C, x
ing over his own shoulders, chest, and back area for
* {" Z- O( L% w5 {* ba year. The father also revealed he was embarrassed3 q1 S5 h0 R: d" W8 Z
to disclose that he was using a testosterone gel pre-
( \4 X- K: B; H) M1 Mscribed by his family physician for decreased libido7 `5 R* U' L. u- O# G9 t4 T9 q
secondary to depression.
( ]" `$ E" N  s) ~The child slept in the same bed with parents./ s* N- ?* B! u. Z- N( M
The father would hug the baby and hold him on his' e' K1 s) Z& [
chest for a considerable period of time, causing sig-
2 p$ W6 ~8 C3 T! W- z2 O# Nnificant bare skin contact between baby and father.7 O3 [% f6 b% J+ t. F! @& r. j* a
The father also admitted that after the phone call,) ^0 m1 T9 ^1 u; t. p2 U
when he learned the testosterone level in the baby
! {7 ?8 L2 J: q2 T9 iwas high, he then read the product information" O- J+ `% M9 i- A: F# ^
packet and concluded that it was most likely the rea-
" b! a, r/ n! V% q! vson for the child’s virilization. At that time, they
$ @, o& d$ M. P& Ddecided to put the baby in a separate bed, and the- N/ L+ r( _( P/ r7 |
father was not hugging him with bare skin and had* g$ A) H9 l  C- v# A8 U- I
been using protective clothing. A repeat testosterone) M) y. {- l. r( M& G0 {3 e
test was ordered, but the family did not go to the: ]. m& ]' @2 u6 n! M# b% J
laboratory to obtain the test.
) x4 J8 ?; n9 E8 IDiscussion
8 B9 R4 r2 a0 h1 DPrecocious puberty in boys is defined as secondary
& u0 Z# k# u! T7 Y7 b, N" Hsexual development before 9 years of age.1,4
$ V9 h+ p, R; Y- M. _Precocious puberty is termed as central (true) when
9 l, G5 \) D8 V! Z: X5 _it is caused by the premature activation of hypo-. f5 @: a* B% l2 o4 x
thalamic pituitary gonadal axis. CPP is more com-
9 ^: ]) E% g( nmon in girls than in boys.1,3 Most boys with CPP0 _% @( r6 X# i; s# \4 H
may have a central nervous system lesion that is& B& Z/ `: o0 E& r
responsible for the early activation of the hypothal-, C% d) Q* W2 K1 @9 v, g3 ]
amic pituitary gonadal axis.1-3 Thus, greater empha-/ ]$ p+ }5 y, M7 D$ x) w
sis has been given to neuroradiologic imaging in
, a& H5 z2 J% g! A" nboys with precocious puberty. In addition to viril-
% ^: w, }+ L, o6 dization, the clinical hallmark of CPP is the symmet-9 z& U9 H% [1 O2 G
rical testicular growth secondary to stimulation by
$ l3 K, d# W) o% j7 E( dgonadotropins.1,3
8 T/ K! K$ t9 k3 ~9 hGonadotropin-independent peripheral preco-7 r' D7 S# j, |
cious puberty in boys also results from inappropriate/ R3 M1 m- q; o& Z; D
androgenic stimulation from either endogenous or
, ?1 e/ G) o  e' nexogenous sources, nonpituitary gonadotropin stim-$ b) C, S: j( `( N" S- r" _; s7 v
ulation, and rare activating mutations.3 Virilizing! }" R% U) ?! U6 E: A
congenital adrenal hyperplasia producing excessive
% c6 {# P* i) J) vadrenal androgens is a common cause of precocious1 r% K) P. E2 l" g
puberty in boys.3,4
" c1 D7 o3 J" k0 L3 h" `The most common form of congenital adrenal" I7 v: S5 b% e: T8 l
hyperplasia is the 21-hydroxylase enzyme deficiency.0 z' M; O, f0 R: _- e( [" t7 \
The 11-β hydroxylase deficiency may also result in
/ G, q: u; [* q0 \5 K+ x8 kexcessive adrenal androgen production, and rarely,! q/ v" c: M- W* c4 r
an adrenal tumor may also cause adrenal androgen7 V1 m7 ?1 ~3 l7 S4 }6 v4 k7 V& I1 T
excess.1,3
- Y: ~/ s" q' Tat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& M3 A9 [. w% S542 Clinical Pediatrics / Vol. 46, No. 6, July 20071 o0 ?- r8 p" Y$ Q0 h: m8 F
A unique entity of male-limited gonadotropin-
+ b) c' _8 v9 I. Jindependent precocious puberty, which is also known& C# l- g( F. d( `2 i" Q; q
as testotoxicosis, may cause precocious puberty at a" q- g3 z% t1 e$ K, R
very young age. The physical findings in these boys4 n: y$ c# F+ Q% K& h# Q2 U9 B
with this disorder are full pubertal development,
! r" `0 ?: d1 S5 Aincluding bilateral testicular growth, similar to boys$ m/ _# X8 U4 s% g6 ~& d0 C& V
with CPP. The gonadotropin levels in this disorder
& ~! ^) u$ q0 @are suppressed to prepubertal levels and do not show
- f2 {" V; H( C; D2 T: K) B) k( fpubertal response of gonadotropin after gonadotropin-/ |! j1 ^2 T/ T- j, c! [" E
releasing hormone stimulation. This is a sex-linked7 Y/ |5 d; x7 ^8 _' J
autosomal dominant disorder that affects only6 V7 Q. A- k4 e
males; therefore, other male members of the family
: L9 L" }$ |  R# W1 W' A2 n3 gmay have similar precocious puberty.3
1 y& w( ~* C) u2 a5 @1 LIn our patient, physical examination was incon-
8 T! ^1 {4 s! R$ j8 K/ w; |sistent with true precocious puberty since his testi-2 y9 G% Z! M& x! @, s0 q2 ]0 ?1 @
cles were prepubertal in size. However, testotoxicosis
" D! H: }/ T0 d1 k8 N6 L: d1 A9 Jwas in the differential diagnosis because his father8 x: k  w; z" o6 z, |
started puberty somewhat early, and occasionally,9 _) D8 Z: q) `- o! M( V8 ]) o
testicular enlargement is not that evident in the
& y/ _0 E5 \! V& \8 Abeginning of this process.1 In the absence of a neg-
1 ?+ v) M8 \# {. h1 Jative initial history of androgen exposure, our
9 @+ n! [- d% b  O- q: nbiggest concern was virilizing adrenal hyperplasia,5 \: V9 d1 n; P) D6 O
either 21-hydroxylase deficiency or 11-β hydroxylase
# K: X9 [; |# f! w# D6 y) d5 Adeficiency. Those diagnoses were excluded by find-
1 K2 u8 w3 O  R6 N9 f' ~8 [ing the normal level of adrenal steroids.
* p4 Z! f( X" r# [4 x( GThe diagnosis of exogenous androgens was strongly' ?  c3 w/ W& T9 y5 D
suspected in a follow-up visit after 4 months because
, C( ^  V0 H4 v/ T7 ]4 {. Lthe physical examination revealed the complete disap-# H  S$ v9 c6 b: r. w
pearance of pubic hair, normal growth velocity, and- \  l% i, ]* b3 S/ @) ^6 g) v
decreased erections. The father admitted using a testos-
( u, \9 _! f, l9 U- V8 c& I/ A  f; w' Fterone gel, which he concealed at first visit. He was0 C1 |3 j2 ^2 y' L1 {
using it rather frequently, twice a day. The Physicians’# {$ G# X/ L5 F) K1 Q7 g2 V/ G# S- I
Desk Reference, or package insert of this product, gel or3 x0 s: ^: T* q1 J7 J
cream, cautions about dermal testosterone transfer to/ U3 J5 r4 S1 j' C& E; E( K
unprotected females through direct skin exposure.& i/ E& h; m4 f' D
Serum testosterone level was found to be 2 times the
0 h% g- k+ p- j/ q& H5 Qbaseline value in those females who were exposed to, ^2 J- L0 O$ r3 M8 K( H' s) k% Z
even 15 minutes of direct skin contact with their male
! y9 M2 C6 x) z* R) m# \( L9 V/ \partners.6 However, when a shirt covered the applica-7 f% k- U" l! I0 C- c( w4 S  ^2 r
tion site, this testosterone transfer was prevented./ h& j2 [* e8 V
Our patient’s testosterone level was 60 ng/mL,$ ^; F# {& Z7 v, \- V0 q
which was clearly high. Some studies suggest that% {: V; T( O# o! z5 P/ A; J
dermal conversion of testosterone to dihydrotestos-
% n; G# _3 Z8 Z& B3 {+ {* ~8 Gterone, which is a more potent metabolite, is more1 X1 M! ~; d# U1 @+ O  R
active in young children exposed to testosterone& {' P8 `/ `2 z) {
exogenously7; however, we did not measure a dihy-) \3 T8 f7 t1 x( F0 s# o
drotestosterone level in our patient. In addition to
: C7 \: S: i( w; b' H. m7 Hvirilization, exposure to exogenous testosterone in* ~& K& g  o9 s; Z, u
children results in an increase in growth velocity and( h! H$ Y+ H2 O
advanced bone age, as seen in our patient.
$ Y8 U6 Q9 f8 H" uThe long-term effect of androgen exposure during4 n8 R( w/ o0 T" ^! p5 ~
early childhood on pubertal development and final
3 j  C8 |5 Z. u! q! madult height are not fully known and always remain3 d  k  f9 M5 _) P) B: u1 s9 E; q, t4 d! u
a concern. Children treated with short-term testos-7 {2 g8 W4 @* [. @
terone injection or topical androgen may exhibit some
5 Y! j. U# [4 ~' x. O3 bacceleration of the skeletal maturation; however, after$ u/ X: j/ a( D+ e' X
cessation of treatment, the rate of bone maturation% L6 A- n& q& B) i0 |( j4 a" z
decelerates and gradually returns to normal.8,9" {! g- f! V( ]% C- y
There are conflicting reports and controversy
( s7 k) U/ {# a2 ^( i  Wover the effect of early androgen exposure on adult
/ T  b9 g5 @! i6 `penile length.10,11 Some reports suggest subnormal
, R* C! Z# K% H: p) aadult penile length, apparently because of downreg-
7 C+ h" B/ |* _; H+ |4 s2 N. Aulation of androgen receptor number.10,12 However,3 _9 x% \# l& x- q
Sutherland et al13 did not find a correlation between
6 W4 C1 O* n2 S0 o# Echildhood testosterone exposure and reduced adult4 i9 U5 b5 j( I  B) n  a9 u- Q
penile length in clinical studies.
' t% @! K& q# b2 lNonetheless, we do not believe our patient is3 P3 I. K/ l1 |. |" Q  U
going to experience any of the untoward effects from
8 e8 S6 ^4 J* ktestosterone exposure as mentioned earlier because( _% L3 W- O7 B+ o2 h% Z
the exposure was not for a prolonged period of time.8 K" ], D: F. K# ]! W( A; F
Although the bone age was advanced at the time of2 I  |. g! ~% ?: w) G0 E! m( [
diagnosis, the child had a normal growth velocity at" N( P4 k: i% {9 c8 R5 |( @
the follow-up visit. It is hoped that his final adult7 j9 d2 a& ~+ l. P+ Y; O
height will not be affected.0 Q( B/ G: Q0 _) q, e, w
Although rarely reported, the widespread avail-
1 j/ {, ?) u* vability of androgen products in our society may
+ n5 m$ a! _' N( nindeed cause more virilization in male or female1 ^; x4 P1 P) U; q7 w) E9 O/ J
children than one would realize. Exposure to andro-) T  Y$ X; W( Y3 Q
gen products must be considered and specific ques-3 G& ?+ Y: r9 Z- _- R; o
tioning about the use of a testosterone product or
; E! U3 D$ C' B* Xgel should be asked of the family members during* Q- z# r. l. }0 E5 G/ {
the evaluation of any children who present with vir-
$ I4 ]) i  K4 m7 cilization or peripheral precocious puberty. The diag-+ q! |" b# |; Y+ A; f
nosis can be established by just a few tests and by4 a1 Z( y2 w8 v5 q% |; ~
appropriate history. The inability to obtain such a9 G# }. F5 M, p0 A6 [' P, C
history, or failure to ask the specific questions, may; C- T  ^0 l8 F# v/ |% w
result in extensive, unnecessary, and expensive, e) R9 y+ {& `. \
investigation. The primary care physician should be
' C9 _4 y% |/ B# y3 v$ yaware of this fact, because most of these children4 p3 o0 ~- e, h/ f
may initially present in their practice. The Physicians’3 E; J/ l3 W9 S, A* s/ X: F
Desk Reference and package insert should also put a, j2 J$ z, P& w+ @
warning about the virilizing effect on a male or1 H5 B. i9 k- l8 U/ b4 _& e6 ]
female child who might come in contact with some-* T4 s9 `4 y) d4 B. K( \6 Q
one using any of these products.- E/ {* U& q- \# y$ P1 D/ H7 I
References
+ ~! x* D# U# O& N8 I  X" \, @1. Styne DM. The testes: disorder of sexual differentiation8 Z4 f8 M: m( j
and puberty in the male. In: Sperling MA, ed. Pediatric/ n1 F4 R" H8 Q7 z2 s
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;! ?' ]3 d! X3 Z$ I. I
2002: 565-628.
$ z  u' t" I* g8 Z4 y2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; g8 Q( }8 I! ?* Q: i9 ]
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
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

. O0 y+ W6 v" S/ M5 o% m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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