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Sexual Precocity in a 16-Month-Old
0 I$ R7 W/ o' w' GBoy Induced by Indirect Topical  |6 k; B! ^9 P  q
Exposure to Testosterone
2 O( L5 h% ?3 l6 z6 `Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2$ T; U: k/ R" j- d0 K
and Kenneth R. Rettig, MD1
& t) M* @( O/ `! i& qClinical Pediatrics
/ G1 v$ b6 n" h& Z& vVolume 46 Number 6) }: m% \  L5 w# n" t7 b6 f
July 2007 540-543
% {. F! R5 o3 q% ?9 F# H0 @; S$ P. q© 2007 Sage Publications  q  ~  x( p: k6 `" C$ A$ ~" J
10.1177/00099228062966519 ^. d) a. O" [8 G1 u" g
http://clp.sagepub.com
# V+ N4 j( r1 G( Xhosted at
8 @% o# j* q6 S1 w6 }) chttp://online.sagepub.com
6 P/ Q) F8 I; _& e  T" @0 O/ QPrecocious puberty in boys, central or peripheral,7 x* g9 R% F9 O- s- o, }, e' L! ^
is a significant concern for physicians. Central1 [5 {* H$ ^2 ]& @
precocious puberty (CPP), which is mediated
3 F; C' p4 W& ?* H6 Nthrough the hypothalamic pituitary gonadal axis, has" U1 O8 ^$ p3 s, g
a higher incidence of organic central nervous system
* T' X; y1 ^: llesions in boys.1,2 Virilization in boys, as manifested* U" l% o$ D# V0 X0 @! c" N) L
by enlargement of the penis, development of pubic; T1 p3 q* w+ u# l
hair, and facial acne without enlargement of testi-% w2 J0 N4 l6 r5 Z8 S) d2 G
cles, suggests peripheral or pseudopuberty.1-3 We9 U8 v/ ^  r0 a7 w
report a 16-month-old boy who presented with the
; W* x0 _, g2 L9 A5 K0 Ienlargement of the phallus and pubic hair develop-
) B; b6 D4 \/ Z7 \ment without testicular enlargement, which was due
  u8 N) i' B3 R1 w  `( \$ Rto the unintentional exposure to androgen gel used by, N% H1 W) k% M/ \  v
the father. The family initially concealed this infor-
+ ~6 K2 T2 z3 B2 N2 s# ~4 T+ kmation, resulting in an extensive work-up for this& l/ n" `1 y) D; P! O# W
child. Given the widespread and easy availability of* |& l+ B# p% ]" k
testosterone gel and cream, we believe this is proba-
& r1 h3 i) k5 x/ Bbly more common than the rare case report in the
& d5 ^  b0 h+ X9 M5 c6 k7 [literature.4
3 N" l# `# e( `! ^* APatient Report- v2 U& a5 @% f
A 16-month-old white child was referred to the
/ x# V$ c. J7 U$ Q/ j4 ]endocrine clinic by his pediatrician with the concern3 k1 F- @. {# M! Z& `+ c
of early sexual development. His mother noticed
- z9 C3 N/ i# ~5 L. A$ R" q' ]light colored pubic hair development when he was; n. U/ r5 P: s. r7 u, ?
From the 1Division of Pediatric Endocrinology, 2University of
- }# b9 b/ f. o: Z& y/ [3 J% p5 dSouth Alabama Medical Center, Mobile, Alabama." z# z* U" E' v' a0 N3 y! i) K
Address correspondence to: Samar K. Bhowmick, MD, FACE,
: i  y1 Z9 t2 w# e$ d1 kProfessor of Pediatrics, University of South Alabama, College of
+ e, u, M$ S# q4 `) }% aMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;" a3 Q% a/ @4 X9 L- g
e-mail: [email protected].
; @- T1 [3 A9 I4 X% @0 W  y* Labout 6 to 7 months old, which progressively became
* ^$ k; x4 n* s5 Ydarker. She was also concerned about the enlarge-# j7 n5 [; J9 I9 A1 r  D7 h
ment of his penis and frequent erections. The child/ P% B# s, m+ V, y
was the product of a full-term normal delivery, with
) B( L, P: b; G4 Sa birth weight of 7 lb 14 oz, and birth length of- i! @" E! M# n6 L. B; z& ^
20 inches. He was breast-fed throughout the first year
" x0 t# n1 e8 p) ]$ p/ q/ xof life and was still receiving breast milk along with# c/ p5 o$ P; E% @% z& \) c5 J1 w
solid food. He had no hospitalizations or surgery,
- z" l( t+ X& f: Z7 d: U; rand his psychosocial and psychomotor development
$ g! ~7 o& j) M, @was age appropriate.0 F4 j* A  f5 G; Q( ]: ~
The family history was remarkable for the father," z& E$ v2 m. P" b0 s3 w5 J
who was diagnosed with hypothyroidism at age 16,
4 ]" P5 \& e* Jwhich was treated with thyroxine. The father’s
4 z2 ?' c/ _) w2 `" mheight was 6 feet, and he went through a somewhat
6 i7 S+ i& h/ e; Oearly puberty and had stopped growing by age 14.% k0 V5 y" a9 v
The father denied taking any other medication. The/ R7 c  X3 [* \5 O; j; U+ ]
child’s mother was in good health. Her menarche
% Y& c& _0 ^, D6 ?was at 11 years of age, and her height was at 5 feet8 y0 y8 Q5 P! m6 C( L4 q5 p
5 inches. There was no other family history of pre-
& E$ j: Z. m' k, tcocious sexual development in the first-degree rela-+ E( m& P1 |* O0 _+ z1 s6 y
tives. There were no siblings.  {4 g: Q: W% `4 k" B
Physical Examination4 @$ i9 C% q" E% Y) i- h6 C! z
The physical examination revealed a very active,
( Q0 C& ?) W) D  A4 R; u+ M- |playful, and healthy boy. The vital signs documented2 t4 i* ]& T5 P5 [: L# J, C
a blood pressure of 85/50 mm Hg, his length was
/ {+ P2 B$ p; n  u90 cm (>97th percentile), and his weight was 14.4 kg
( T: k5 S: |# ], R: d% m1 d(also >97th percentile). The observed yearly growth
+ L& K' v6 @/ r# [5 M' X5 ^velocity was 30 cm (12 inches). The examination of
* @0 Q! T7 {/ P2 f: _" W. ~4 Athe neck revealed no thyroid enlargement., J: f" F& u) i" R6 i2 |
The genitourinary examination was remarkable for
3 S0 G9 m* F, S, m& Venlargement of the penis, with a stretched length of
& z5 {/ I, k  b4 e# N( U$ l. U, [* c8 cm and a width of 2 cm. The glans penis was very well/ @( t! C- q  \$ F
developed. The pubic hair was Tanner II, mostly around
6 x  D. D' b# Z3 J2 }) z& ?8 t540; f7 T. ^) n2 t: V0 u& n
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, B; A% O. i% c/ p% k3 F: S, o
the base of the phallus and was dark and curled. The
: H# m+ Q$ S+ B9 `. N9 ?testicular volume was prepubertal at 2 mL each.! U. k- n0 {' z& `
The skin was moist and smooth and somewhat3 n+ P" }5 T4 G+ e- k
oily. No axillary hair was noted. There were no5 Q% E6 m, N% M3 p% S% ~
abnormal skin pigmentations or café-au-lait spots.
; G" _2 i+ r8 L% ^9 cNeurologic evaluation showed deep tendon reflex 2+6 e+ U! A  F: _$ D
bilateral and symmetrical. There was no suggestion. {/ _# I" d0 _" l
of papilledema.2 }% T& T1 L4 o6 T' _  S
Laboratory Evaluation
' @2 _) M9 F. ?. R, N- Y2 e) \The bone age was consistent with 28 months by% x. h2 {- J5 Y' F8 [
using the standard of Greulich and Pyle at a chrono-! u3 s+ b) P- t8 z' v2 v
logic age of 16 months (advanced).5 Chromosomal
! B7 V; O1 t+ r/ d$ E/ akaryotype was 46XY. The thyroid function test
( A4 v) i" F! [# h& S3 k6 Zshowed a free T4 of 1.69 ng/dL, and thyroid stimu-+ R9 V' u  x0 u. i* J
lating hormone level was 1.3 µIU/mL (both normal).
" H) L6 j  M3 z' x3 ~! `. fThe concentrations of serum electrolytes, blood& L, G; h! Q9 s- _4 ?* @% u
urea nitrogen, creatinine, and calcium all were
+ R# Q4 L8 s! x" Mwithin normal range for his age. The concentration
" Q" b7 G0 u' ]5 w$ j% K9 Lof serum 17-hydroxyprogesterone was 16 ng/dL
% p* _8 W# q( H. }(normal, 3 to 90 ng/dL), androstenedione was 20; O  E9 i& V9 U
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
3 B9 e8 e9 f/ [3 b2 [5 Rterone was 38 ng/dL (normal, 50 to 760 ng/dL),9 X  ^: U2 I: S: D, @+ Z6 [0 U3 O
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
4 s. M# P( @) x' H( n1 J49ng/dL), 11-desoxycortisol (specific compound S)- \% Y( {6 l1 m1 e& E8 Q
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
) u, Q; K: M* m3 \tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total- k2 d% c: U/ N
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),! j1 E$ l9 h' M: f6 ]" f
and β-human chorionic gonadotropin was less than
6 o, E8 A: A/ @# B5 mIU/mL (normal <5 mIU/mL). Serum follicular$ M) J/ L9 p+ G$ b' k7 X
stimulating hormone and leuteinizing hormone- B+ N: c" l; ?5 w* o0 X
concentrations were less than 0.05 mIU/mL
. E* r+ L) Q& a" K1 H. [0 J(prepubertal).: a; c7 a" W* ~( q2 b0 O( T3 X) }
The parents were notified about the laboratory
3 C' m  K- p# U- u7 P% }results and were informed that all of the tests were
  a$ L: n0 ^4 d! @normal except the testosterone level was high. The1 i" q) ?% \3 n2 |3 A0 D
follow-up visit was arranged within a few weeks to. e0 K- o6 U; U
obtain testicular and abdominal sonograms; how-
* N- V* m- K; U4 r; Iever, the family did not return for 4 months.
5 k) }" I& x3 YPhysical examination at this time revealed that the
8 T, Y& A- L2 G, j% T* k* |: m# Wchild had grown 2.5 cm in 4 months and had gained6 x# z" L" J# N8 E( L2 Y- i: D/ P( i
2 kg of weight. Physical examination remained, Q/ S! S. _9 C  o
unchanged. Surprisingly, the pubic hair almost com-* m3 C  G3 D, @% y  q
pletely disappeared except for a few vellous hairs at
3 ~# @9 ^7 F# U6 u6 n( [1 R& Lthe base of the phallus. Testicular volume was still 22 E: z0 M8 \' y1 z: _6 q1 {
mL, and the size of the penis remained unchanged.9 z- ?$ z3 `; ^8 d5 k: [3 W
The mother also said that the boy was no longer hav-' [9 |1 A! i( T" @5 t
ing frequent erections.
4 i2 x- |* m! |6 j2 b  FBoth parents were again questioned about use of
' q2 {3 a- ^* f% U0 I7 Gany ointment/creams that they may have applied to
/ g4 n; `3 B4 N* Nthe child’s skin. This time the father admitted the( R% q: L& V" \$ t! v4 @+ c4 A6 u
Topical Testosterone Exposure / Bhowmick et al 541- H) Y3 S5 _/ y* t
use of testosterone gel twice daily that he was apply-; O& f* `% ?: p) R$ E7 Q# G
ing over his own shoulders, chest, and back area for
; {" j( D+ w) p& j: la year. The father also revealed he was embarrassed2 ~  N9 g" ^% p2 `4 J7 i* V
to disclose that he was using a testosterone gel pre-, o3 ^2 `/ k  _. ~
scribed by his family physician for decreased libido
- Z, f2 j# K& z' X6 j- I8 _secondary to depression.
5 u# Z5 o; {; G) fThe child slept in the same bed with parents.
2 t6 H! T) j$ N+ j5 l, WThe father would hug the baby and hold him on his
% w1 ^# H( ^: h8 z! nchest for a considerable period of time, causing sig-/ a( E$ h, E; b: R- C7 }
nificant bare skin contact between baby and father.+ v+ E# S- f* y5 V6 U' n
The father also admitted that after the phone call,: f  ~* c0 W; T3 z3 k
when he learned the testosterone level in the baby- i& V9 j" b8 t2 J  B2 H$ A
was high, he then read the product information
9 a/ q$ F6 d; D7 d0 I6 K0 epacket and concluded that it was most likely the rea-2 X- M5 ~: l4 V  U- ]' l6 m
son for the child’s virilization. At that time, they
: m; [, u2 J& h- Rdecided to put the baby in a separate bed, and the
' s- A: K* Y1 Xfather was not hugging him with bare skin and had$ g, F: y5 O6 k0 Y: j3 ~% c- ~) r8 R
been using protective clothing. A repeat testosterone
- O* r2 O% T8 htest was ordered, but the family did not go to the
  k, P2 l1 V  U5 |: hlaboratory to obtain the test.3 w1 g7 e7 q: M( }
Discussion9 F" ], N: O& A* Z( R
Precocious puberty in boys is defined as secondary
% |5 B/ n+ \+ w( |% j; K( V( qsexual development before 9 years of age.1,4
9 N4 [7 z/ \3 p  wPrecocious puberty is termed as central (true) when
- P7 _4 t  q# A, Lit is caused by the premature activation of hypo-
! A8 I, b# s$ p0 Y6 kthalamic pituitary gonadal axis. CPP is more com-, |  h- h8 n' T! t/ N
mon in girls than in boys.1,3 Most boys with CPP
4 ]" H* t0 i. R, j/ @) gmay have a central nervous system lesion that is8 S' L, u2 N+ U/ I; F- n
responsible for the early activation of the hypothal-2 U$ f) [% g* d6 I8 j% O
amic pituitary gonadal axis.1-3 Thus, greater empha-* U) h3 O" E7 m8 k& k# [
sis has been given to neuroradiologic imaging in
) J/ |* L4 t  H2 p' Z- \- sboys with precocious puberty. In addition to viril-
( y8 n& {/ J) ^6 ?: z$ O5 uization, the clinical hallmark of CPP is the symmet-* Y6 F5 J% C0 \8 l+ U
rical testicular growth secondary to stimulation by
/ k3 B" \- l- R% [2 X" h9 Y# J# `: O4 |gonadotropins.1,3& M+ F- L. V7 d& ]- U, Q( l+ l4 o8 v: l
Gonadotropin-independent peripheral preco-
  N5 B, w8 m- i; C8 |; Icious puberty in boys also results from inappropriate
9 y7 w) g1 ]+ ~* [androgenic stimulation from either endogenous or: e/ n1 c: z: O# Q/ M6 r
exogenous sources, nonpituitary gonadotropin stim-* b4 Z9 x7 ~. N8 R7 u! ~; ~
ulation, and rare activating mutations.3 Virilizing9 p4 m$ C) J1 {% N, k/ ^
congenital adrenal hyperplasia producing excessive
) e, {( x! s" k6 s: U) V$ o2 K% Oadrenal androgens is a common cause of precocious9 u2 ]% W) z! h  Q- e6 Q
puberty in boys.3,4
) L( [6 x, ^6 V. F, t2 j4 eThe most common form of congenital adrenal6 B4 |0 V6 [# T; v
hyperplasia is the 21-hydroxylase enzyme deficiency.
# I% V5 [  \; _( U1 M/ V9 m) rThe 11-β hydroxylase deficiency may also result in
+ S2 P1 j9 n* j$ Xexcessive adrenal androgen production, and rarely,
. J0 Q7 i( g! q( W) Ran adrenal tumor may also cause adrenal androgen' k9 U- w, f  b
excess.1,37 k; \/ V, C# ]6 D) f
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 |  ]$ o6 A4 w( m1 M542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
% X1 P: ?9 C* h+ ]$ A1 IA unique entity of male-limited gonadotropin-
# p# w# F3 m$ G% d9 i% Rindependent precocious puberty, which is also known9 v  U# @1 W5 k0 T- `
as testotoxicosis, may cause precocious puberty at a' l# U4 |1 l& g" u: w; a3 n  V
very young age. The physical findings in these boys1 |9 c0 r, t' J/ [( t
with this disorder are full pubertal development,
3 b7 K6 @/ s" C' Gincluding bilateral testicular growth, similar to boys; f+ l/ m4 q* y( A- i
with CPP. The gonadotropin levels in this disorder7 `' q. N0 B4 v1 l) g
are suppressed to prepubertal levels and do not show
5 ^1 j) @( J# T" ]1 j+ A9 Ypubertal response of gonadotropin after gonadotropin-
- ?/ m/ n, r+ zreleasing hormone stimulation. This is a sex-linked$ r7 s4 E4 A9 J4 B' T* e7 z$ A
autosomal dominant disorder that affects only5 f% \4 o3 e8 b. H3 Q4 k& m6 q
males; therefore, other male members of the family4 ^; X; G$ ~# i3 K
may have similar precocious puberty.32 u( q' o4 _" r+ k1 H) r! H
In our patient, physical examination was incon-3 v: F3 c7 h7 G2 F, t" z9 W( G4 N
sistent with true precocious puberty since his testi-$ m! S' X; D# B1 C7 ~* K% }
cles were prepubertal in size. However, testotoxicosis+ F1 @& L- w6 g
was in the differential diagnosis because his father
2 P" L; l5 M- h  E; Vstarted puberty somewhat early, and occasionally,3 x1 x/ _  n* R4 ^
testicular enlargement is not that evident in the$ y; B* ^) `! v& A
beginning of this process.1 In the absence of a neg-% w0 n% _7 v8 G3 w- t( o3 {
ative initial history of androgen exposure, our
& S0 K" @7 c2 `$ ?4 Y! U: s8 G& w8 Tbiggest concern was virilizing adrenal hyperplasia,
! C0 A# d% M/ @either 21-hydroxylase deficiency or 11-β hydroxylase
. A! ^, ^3 r( }deficiency. Those diagnoses were excluded by find-
: P) p/ |: l2 G1 G. Ming the normal level of adrenal steroids.! P/ \! I) y  b8 T; z
The diagnosis of exogenous androgens was strongly
  P3 y5 m4 L" J4 u' R2 Fsuspected in a follow-up visit after 4 months because
3 w6 z0 ^2 m; i+ I. W& b# gthe physical examination revealed the complete disap-
. I" \( k6 u9 X; c# y! wpearance of pubic hair, normal growth velocity, and
  ]+ e/ h7 F% a- U4 Ydecreased erections. The father admitted using a testos-; F4 c( z9 a4 c; G
terone gel, which he concealed at first visit. He was$ Q- P: c: J" c# z! X
using it rather frequently, twice a day. The Physicians’% B. y) e( C4 v* f. O
Desk Reference, or package insert of this product, gel or5 |, ^4 j4 g% E' t! L( u. d
cream, cautions about dermal testosterone transfer to
4 w  `# ^* v# _2 r- cunprotected females through direct skin exposure.6 B2 Q1 M& l8 I: e; L
Serum testosterone level was found to be 2 times the7 W2 i5 ^& v; |' h
baseline value in those females who were exposed to$ L% F: G% M& x6 }! X* A- @
even 15 minutes of direct skin contact with their male5 h" ]4 q6 G4 m0 c- x$ Q& B
partners.6 However, when a shirt covered the applica-. Z2 u  Y" |* I) M) [
tion site, this testosterone transfer was prevented.
! j7 L0 T4 x+ a' P; POur patient’s testosterone level was 60 ng/mL,
) [6 {% Y9 C" b! r3 {which was clearly high. Some studies suggest that9 s" X( z! m8 @+ _: I
dermal conversion of testosterone to dihydrotestos-3 ?" r2 c6 q7 l3 f) g# _
terone, which is a more potent metabolite, is more
- g/ K! u( ]/ _5 a2 Uactive in young children exposed to testosterone4 I, g, y. h& M$ h6 K: O* ?
exogenously7; however, we did not measure a dihy-: {0 i) W% U1 B4 s* e7 V# n9 O* f; W; Y
drotestosterone level in our patient. In addition to
* d" s' a) N- {2 Z# \virilization, exposure to exogenous testosterone in* X# g; D, ~1 w' p' j
children results in an increase in growth velocity and- c: S4 X- @6 u! L& l: u5 v
advanced bone age, as seen in our patient." u1 c' \+ G( A! K' v' N
The long-term effect of androgen exposure during
0 }# F" {' V( \( {# `% J! Mearly childhood on pubertal development and final: s' v0 V/ O8 u! N
adult height are not fully known and always remain7 G, F% t* m  O) i: B
a concern. Children treated with short-term testos-
2 c% K! e7 I3 i, O, e& v$ L1 Vterone injection or topical androgen may exhibit some; A% P& f7 S3 e! P/ u
acceleration of the skeletal maturation; however, after  {5 ]: f9 u9 z4 x: m% n0 ?6 y
cessation of treatment, the rate of bone maturation
8 J. v# p3 n' w' V7 [1 qdecelerates and gradually returns to normal.8,9
" @8 D" c2 u% y2 Y3 iThere are conflicting reports and controversy5 K; N  u; |3 `; Y9 M
over the effect of early androgen exposure on adult* U, b3 o, u/ U2 c& U! v/ i0 |. E4 ]
penile length.10,11 Some reports suggest subnormal3 {0 @% P% {, f# w& a0 v
adult penile length, apparently because of downreg-! s  G, B2 H* ^* p! p: H( c- |
ulation of androgen receptor number.10,12 However,
7 Y% ]) U; f1 y0 ~+ eSutherland et al13 did not find a correlation between% }7 K+ }$ X4 O. ^- @7 L% ~
childhood testosterone exposure and reduced adult
9 A& S+ U2 h* C( q( g5 hpenile length in clinical studies.
, w% A2 k; \; A( H' t2 F+ `Nonetheless, we do not believe our patient is7 u. k- ]$ O! B+ _+ _
going to experience any of the untoward effects from- s1 t# v3 F/ H) [
testosterone exposure as mentioned earlier because
' q4 Q( [6 g3 Ethe exposure was not for a prolonged period of time.
7 G: z3 ~( K( u% I* pAlthough the bone age was advanced at the time of, M. c( g2 q" \# L, o6 q4 T: ~
diagnosis, the child had a normal growth velocity at2 Q# ?# W3 q4 G5 h3 B
the follow-up visit. It is hoped that his final adult1 N1 T5 Y0 B: j- @- n: B
height will not be affected., D( L' I: t8 D+ T# ~7 i# s
Although rarely reported, the widespread avail-
1 ?6 m+ K5 O; \ability of androgen products in our society may2 d$ e5 D5 Q1 X+ f9 S4 }
indeed cause more virilization in male or female# y) u& F7 D  X: U7 A
children than one would realize. Exposure to andro-1 _. D& u' ^4 u6 S2 i
gen products must be considered and specific ques-
$ C  d% ~: W- _tioning about the use of a testosterone product or' r4 Q0 |& e; S; T; @! q
gel should be asked of the family members during( }* D7 u1 c: L$ n% k
the evaluation of any children who present with vir-5 c! {: _9 @( i1 s
ilization or peripheral precocious puberty. The diag-
0 j) c. y* X% anosis can be established by just a few tests and by
6 R( W  }( Y7 Rappropriate history. The inability to obtain such a
8 B2 d; g+ p  ]8 Phistory, or failure to ask the specific questions, may6 s: b0 u2 s; H/ L
result in extensive, unnecessary, and expensive
9 ], Y$ S- S% d! Z* U5 b5 Einvestigation. The primary care physician should be
, s' ~9 k  M1 N/ qaware of this fact, because most of these children
9 D# X4 B* ?+ I& s  ]9 x3 G. Y: @may initially present in their practice. The Physicians’
6 O- G1 p' D* Q) q! F1 PDesk Reference and package insert should also put a  g6 `9 S- j% y
warning about the virilizing effect on a male or
( V5 }3 @, Y! xfemale child who might come in contact with some-
7 X0 H2 |, Y9 oone using any of these products.
, y2 M7 z! [4 E$ ^2 ?References* z$ S# w0 J, q+ G$ Y
1. Styne DM. The testes: disorder of sexual differentiation( I1 ]: u& R  y
and puberty in the male. In: Sperling MA, ed. Pediatric& M. _5 }& E/ H5 Z3 p8 B( V
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;8 P- a" R" g% M* y* p8 X5 Y
2002: 565-628.$ a, p& m: A  i* {$ R
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
8 M/ v& Z  ?4 d# Ipuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old, K5 E- m6 ?" g1 N2 _; i) L
Boy Induced by Indirect Topical
1 |  H9 N% H6 ~  w9 I# XExposure to Testosterone
' ~8 p8 b, ^# a6 P2 @0 ESamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
5 N4 J/ X2 U( G/ z& g7 `and Kenneth R. Rettig, MD1. Z$ i( H- P7 G
Clinical Pediatrics
& C8 b7 B, \- \9 ZVolume 46 Number 6+ B' B$ a0 Z( \: `1 L
July 2007 540-543
- ]8 h" t+ I0 y0 P6 B7 L* z© 2007 Sage Publications
# u. J% y+ H5 Q  j/ c, B; s7 x10.1177/00099228062966518 Y  [  F; W4 g+ l6 S7 l
http://clp.sagepub.com: k# G. W( b/ k- f. s
hosted at' M* D8 b9 [, h1 e
http://online.sagepub.com
7 i) R5 @3 `. U2 s1 _7 y1 OPrecocious puberty in boys, central or peripheral,
/ E: q5 K# |9 S/ R- q4 Ois a significant concern for physicians. Central7 ^9 ?: X+ K* H" W
precocious puberty (CPP), which is mediated
% g) X# y! O+ g0 D( d* X* ?; Lthrough the hypothalamic pituitary gonadal axis, has, z2 X; S+ w9 a1 |0 u
a higher incidence of organic central nervous system
, m9 d9 J( a  A' Y2 klesions in boys.1,2 Virilization in boys, as manifested
8 u% }& h7 E" R" `2 v/ @! x: rby enlargement of the penis, development of pubic, _) n$ K* x, p: j" R8 t
hair, and facial acne without enlargement of testi-8 h$ I" v% F( ]( L2 M% w3 V7 v
cles, suggests peripheral or pseudopuberty.1-3 We
: {3 |1 [/ ~# G) T# lreport a 16-month-old boy who presented with the( [/ w" Y) M3 J$ V
enlargement of the phallus and pubic hair develop-
1 v; G. J/ U$ N; p: tment without testicular enlargement, which was due
- z% e6 G2 ^; xto the unintentional exposure to androgen gel used by
! H- Q. I; E, L( C* _2 x' Ythe father. The family initially concealed this infor-" X4 Z. T% c' D5 u1 p/ [5 ?
mation, resulting in an extensive work-up for this
. x# d3 `' ~; X0 C7 ~child. Given the widespread and easy availability of
  P1 U. v- L# G# ]) y+ I7 h% Y9 ltestosterone gel and cream, we believe this is proba-" y& L4 i, X! s! Z
bly more common than the rare case report in the
! G4 E: @; e8 }8 yliterature.4' k0 f- i4 q+ O
Patient Report
9 L  i7 d; j* q4 W* C# qA 16-month-old white child was referred to the
! }0 x& W4 J2 Bendocrine clinic by his pediatrician with the concern
! y+ Y! c& T! f# l, dof early sexual development. His mother noticed( E" j; p$ F. ?' ]: n' ?4 w
light colored pubic hair development when he was% z( L4 C  ]7 W3 E- N# ?& R, r
From the 1Division of Pediatric Endocrinology, 2University of
7 Y8 n* N; L2 A# Q# {. }3 ]4 x) MSouth Alabama Medical Center, Mobile, Alabama., s$ K  n# B- R- u
Address correspondence to: Samar K. Bhowmick, MD, FACE,9 v; N8 z! T& U( ?
Professor of Pediatrics, University of South Alabama, College of
7 G4 V2 S' ?7 T" z3 Q* `Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
+ d3 q. I: S" E& w' }e-mail: [email protected].
5 @# x  g8 C# Y2 uabout 6 to 7 months old, which progressively became
7 i  h' X- i1 R' mdarker. She was also concerned about the enlarge-
, R" x+ {! p7 `' Qment of his penis and frequent erections. The child
, `/ {6 W) w" v$ @) Zwas the product of a full-term normal delivery, with
; d/ N7 ^" ]9 Za birth weight of 7 lb 14 oz, and birth length of
$ N  G  K! r: b; E, |7 A, U* u20 inches. He was breast-fed throughout the first year" i4 }3 e( c# E" m$ y% }
of life and was still receiving breast milk along with
" M+ g) ~1 i! z  @solid food. He had no hospitalizations or surgery,5 h6 Q0 l$ }% l. c
and his psychosocial and psychomotor development
( c: z8 w7 Z: E& F- v  Ywas age appropriate.
. }) t; Y# _' p- G4 H5 `The family history was remarkable for the father,9 ^% f& r+ n( X: f
who was diagnosed with hypothyroidism at age 16,! H/ ^$ z& i. q& X4 Q
which was treated with thyroxine. The father’s
* a# L7 s& o- t5 K. ]height was 6 feet, and he went through a somewhat
5 O0 o/ o5 M. learly puberty and had stopped growing by age 14.1 u2 A. T" o7 _0 t
The father denied taking any other medication. The
$ s9 ?( A  y' S) Z( E2 N4 f2 Ochild’s mother was in good health. Her menarche
1 W4 p& v* I! S8 f, nwas at 11 years of age, and her height was at 5 feet$ ]6 y; I: H! A2 j
5 inches. There was no other family history of pre-
( ?# X0 g$ a. j2 Gcocious sexual development in the first-degree rela-
7 _- x, [* z4 i% L/ V  Atives. There were no siblings.
# ]) ~! C' O9 K, V) r$ l  BPhysical Examination
* t3 c# x/ C: @' hThe physical examination revealed a very active,4 a4 i# n) ^+ b& S
playful, and healthy boy. The vital signs documented
  r! G' g2 t" L, x6 @, i+ a% ]7 {a blood pressure of 85/50 mm Hg, his length was4 u8 t& K6 A8 G  G% `
90 cm (>97th percentile), and his weight was 14.4 kg
9 A. S1 H0 h  D3 b(also >97th percentile). The observed yearly growth8 Y( C  B5 U- }* h" m9 a
velocity was 30 cm (12 inches). The examination of
. I! _! f( s/ @5 nthe neck revealed no thyroid enlargement.- Y/ i' a1 V6 y
The genitourinary examination was remarkable for
6 q& v+ U& ?. E' s) i- ienlargement of the penis, with a stretched length of$ {& `" |0 T# ^# R+ C9 M2 {# C2 L
8 cm and a width of 2 cm. The glans penis was very well
8 e* J7 c* U; u& H& ]  K$ Z8 Q" y3 J# Edeveloped. The pubic hair was Tanner II, mostly around
- u' N# @5 b/ X5 `/ I540
7 C9 T/ E) c5 X  z8 y4 ?at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; d/ V+ f( ]+ l* s& y; Y$ y
the base of the phallus and was dark and curled. The
$ }$ X9 G5 Q! M& `4 Y" o0 Gtesticular volume was prepubertal at 2 mL each.
$ ?7 u: r% l: s6 _The skin was moist and smooth and somewhat' L7 H& ?7 w, A8 Y7 z( q4 ?
oily. No axillary hair was noted. There were no
  `% x2 d6 L7 t0 |* rabnormal skin pigmentations or café-au-lait spots.
7 a4 d- N+ w" t6 f+ BNeurologic evaluation showed deep tendon reflex 2+
! y) T7 [; K' cbilateral and symmetrical. There was no suggestion
4 w1 ?+ H' c" P' l2 e1 V" a  D1 @of papilledema.+ x- r, M3 ?  I
Laboratory Evaluation
  I9 c9 E  N( d  ]8 WThe bone age was consistent with 28 months by+ @) y% I& R7 e7 S5 m
using the standard of Greulich and Pyle at a chrono-5 x! `' ^4 @+ G% X) b- K' e3 V: k
logic age of 16 months (advanced).5 Chromosomal& b/ R3 ~2 i! ~' k: b$ f3 ]
karyotype was 46XY. The thyroid function test
1 _4 y$ u$ o9 M# Xshowed a free T4 of 1.69 ng/dL, and thyroid stimu-5 ?$ X* v7 L6 H1 P' H0 F: V0 j
lating hormone level was 1.3 µIU/mL (both normal).  E8 P$ v2 R) f" z3 z" C, c. p
The concentrations of serum electrolytes, blood# W2 h  ?4 n) q0 U9 i* v
urea nitrogen, creatinine, and calcium all were
' t" I% Z9 ?* h9 Y1 s7 W# y; Wwithin normal range for his age. The concentration( }+ }) _, e4 ?9 k: z
of serum 17-hydroxyprogesterone was 16 ng/dL# x7 U) a: R6 e. G3 a) e: m/ R
(normal, 3 to 90 ng/dL), androstenedione was 204 ^/ J, Q3 [* i; f' c% A8 N- C0 q
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
5 i% g& q) [  m" T2 V- uterone was 38 ng/dL (normal, 50 to 760 ng/dL),
- Y% U! v8 W$ Y5 w8 C5 I: t9 ?desoxycorticosterone was 4.3 ng/dL (normal, 7 to; Y2 U- y* ~$ L  f% K' U
49ng/dL), 11-desoxycortisol (specific compound S)* F: r9 o- h. r" [* [# A' v, J7 X
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-, I# X# f" H4 B
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
( w) _4 \, D1 e/ ^  i9 l1 I, Ptestosterone was 60 ng/dL (normal <3 to 10 ng/dL),- i2 [* m0 s- d1 B7 j! R% w9 E' I
and β-human chorionic gonadotropin was less than+ g  c2 L& U6 ^) N" d9 B0 ^
5 mIU/mL (normal <5 mIU/mL). Serum follicular
) C' p% S2 I: U! |+ t% |stimulating hormone and leuteinizing hormone
, A7 z: u# E: Cconcentrations were less than 0.05 mIU/mL
9 y- P0 d5 o- E(prepubertal).  A) V1 N" f3 A' w  N  t' s
The parents were notified about the laboratory# y8 }$ g! D! f3 g& F& e; K
results and were informed that all of the tests were
) D/ j; p; R% {7 e4 b% b& Tnormal except the testosterone level was high. The
" }- s8 M0 F, S2 Tfollow-up visit was arranged within a few weeks to
9 x& \3 I; q% o# Q3 c' w2 pobtain testicular and abdominal sonograms; how-; q( H' s0 N4 O% |4 K1 ~
ever, the family did not return for 4 months.
& y, j% N" H" \7 FPhysical examination at this time revealed that the$ c& m5 V- O+ K! [2 j4 v
child had grown 2.5 cm in 4 months and had gained
5 A9 D4 p) X% G2 X4 K( c3 Q% M2 kg of weight. Physical examination remained+ x$ ~# _* p- @
unchanged. Surprisingly, the pubic hair almost com-. Q1 I; p# p' u
pletely disappeared except for a few vellous hairs at
" w1 p2 U0 p7 ^( F7 }' Qthe base of the phallus. Testicular volume was still 2
) c: \* m. c2 w% U  D, GmL, and the size of the penis remained unchanged.; o+ {. V: i& a& \' f; u' P
The mother also said that the boy was no longer hav-
. T5 e3 R3 H6 g0 K$ zing frequent erections.# f3 K' @/ H. Z6 t" P& i# @
Both parents were again questioned about use of
+ Z1 w2 a6 [6 t- R7 Jany ointment/creams that they may have applied to+ u3 w/ P$ J$ R9 g3 u) {! E6 E
the child’s skin. This time the father admitted the* r( e* o0 a  w9 [  c
Topical Testosterone Exposure / Bhowmick et al 541
6 A6 ^, f- n9 ]* j9 buse of testosterone gel twice daily that he was apply-; U" R% ]5 h8 ]8 S
ing over his own shoulders, chest, and back area for. q2 z* {/ c' N4 q
a year. The father also revealed he was embarrassed6 n% x( i1 u% B, n
to disclose that he was using a testosterone gel pre-) I' e, o' Z# l& y. s
scribed by his family physician for decreased libido) Z( I1 T6 b& g5 `8 b/ H. Z
secondary to depression.
6 w3 Q% ]9 i' U) e. e6 h1 AThe child slept in the same bed with parents.6 k* ?! V3 e2 ~5 H. E$ S1 W
The father would hug the baby and hold him on his! l/ k+ u8 I- u. `4 t5 p6 ^. ?
chest for a considerable period of time, causing sig-9 D1 L4 ^8 D: K5 @
nificant bare skin contact between baby and father.
) q6 D+ O& H; e: [2 ~/ bThe father also admitted that after the phone call,
3 s$ e# [2 |* }4 a2 L- k; \8 Rwhen he learned the testosterone level in the baby* S% p, g% G! u! }* u0 w8 ]/ ~8 R+ X
was high, he then read the product information
7 ]+ p# j( \' h  d5 M4 _6 _8 \packet and concluded that it was most likely the rea-
8 J+ B7 F$ |( |% Z, Vson for the child’s virilization. At that time, they9 n: u5 P0 x+ [/ |, k
decided to put the baby in a separate bed, and the. }! Z/ O  G% p7 H/ P- Q
father was not hugging him with bare skin and had( |( t8 Y9 R3 [4 _$ S$ j/ A
been using protective clothing. A repeat testosterone
/ Q2 j3 M, G0 d  @# Y% Atest was ordered, but the family did not go to the6 I- H8 o% f. {( Y9 V: A+ b* x, y
laboratory to obtain the test.1 h. B# z$ C3 N# @  p* N' f6 E
Discussion! m  U# R/ n9 t1 f( h# }
Precocious puberty in boys is defined as secondary
" v# z; h/ F; E) J1 v6 Y& u# E% m6 \sexual development before 9 years of age.1,40 {( M" P; [6 d6 B* p
Precocious puberty is termed as central (true) when3 a3 J4 C" U6 {
it is caused by the premature activation of hypo-" n( [; l3 r& i: u# ^
thalamic pituitary gonadal axis. CPP is more com-+ d6 r- }! f& U. e& P- A1 J6 A' u
mon in girls than in boys.1,3 Most boys with CPP4 e6 B3 f" z3 L8 S- r/ f( |  i
may have a central nervous system lesion that is
; `2 I0 G4 O+ a9 \& \responsible for the early activation of the hypothal-
! }2 v" ^0 o+ I. V$ D4 N  Tamic pituitary gonadal axis.1-3 Thus, greater empha-* D, u' i1 k: B1 v. o5 ]# Q6 O
sis has been given to neuroradiologic imaging in
! m; i& i" I8 f: U/ [boys with precocious puberty. In addition to viril-
, G4 e( M) q' A% H$ [. v: dization, the clinical hallmark of CPP is the symmet-( p" T9 w1 J1 e- a. K0 V6 n
rical testicular growth secondary to stimulation by6 e& D$ ?- q3 N8 A/ E1 m
gonadotropins.1,3
- ^5 W% f% c3 w4 T( BGonadotropin-independent peripheral preco-8 {9 [. Y8 d: f) _% E$ b5 X- S
cious puberty in boys also results from inappropriate" S! e5 |* Q  f
androgenic stimulation from either endogenous or; _! h! R/ \& P, `* l
exogenous sources, nonpituitary gonadotropin stim-  b: {4 F/ p; p2 O( @
ulation, and rare activating mutations.3 Virilizing
& F$ w& c9 w& ?! Vcongenital adrenal hyperplasia producing excessive
9 e7 c1 ]8 |% i* q7 n( h/ w0 B/ Eadrenal androgens is a common cause of precocious) N# D$ F) l' \& t  |# ]# d0 o
puberty in boys.3,4) {; k# w. E: P* G" o8 R
The most common form of congenital adrenal
7 r& L8 N4 Y" x. n" \hyperplasia is the 21-hydroxylase enzyme deficiency., b* ]" P% T8 D
The 11-β hydroxylase deficiency may also result in0 G) y4 W: U8 m8 b" n$ B
excessive adrenal androgen production, and rarely,& b( ^$ d5 X. L% D* o9 E
an adrenal tumor may also cause adrenal androgen! \: i; J. ]1 I/ {
excess.1,3
+ [& @1 |- s9 l, I, h, Qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
% x' g9 }& h: w& H- e0 C542 Clinical Pediatrics / Vol. 46, No. 6, July 2007; ?6 ^) |4 v. w3 ]3 D. T  ^0 t
A unique entity of male-limited gonadotropin-
6 N) o; E/ f+ U; Rindependent precocious puberty, which is also known  Z9 |  o/ z! a% b5 ?
as testotoxicosis, may cause precocious puberty at a) o% U7 L  n! S2 [
very young age. The physical findings in these boys  W6 J1 Y3 n7 B7 K7 `/ Z; H4 A
with this disorder are full pubertal development,
% r3 `2 d5 v- Y+ \including bilateral testicular growth, similar to boys
; B5 X4 A" ?. M) `5 L- E2 \with CPP. The gonadotropin levels in this disorder. {- U; n9 h5 Q- Q  e; t2 r5 |
are suppressed to prepubertal levels and do not show, w8 A" w4 w/ b9 S! {3 F
pubertal response of gonadotropin after gonadotropin-% W" Q3 }8 X, u0 u$ C
releasing hormone stimulation. This is a sex-linked
& w  }) q1 q8 i) ]' g) hautosomal dominant disorder that affects only) H# s+ ^' Z1 }( ~! B2 v
males; therefore, other male members of the family3 S  R- u$ n. i3 y
may have similar precocious puberty.3
4 g% P" L0 c9 S7 o/ ]! ^In our patient, physical examination was incon-
$ i# X3 A4 P' B0 esistent with true precocious puberty since his testi-
* o- \( @- |' k, I( Lcles were prepubertal in size. However, testotoxicosis, L. ]1 B7 Y: R8 C: `, Y
was in the differential diagnosis because his father' m) X% e" w; B4 N# M. K
started puberty somewhat early, and occasionally,
8 K. J( c7 x1 Q$ j: Btesticular enlargement is not that evident in the
7 B7 R0 g$ ~! U: Z1 Zbeginning of this process.1 In the absence of a neg-+ T6 q9 P, T" @2 R. g7 x, ?' @0 X
ative initial history of androgen exposure, our" m/ L& J& d- o; [: @) F
biggest concern was virilizing adrenal hyperplasia,
& n: O2 ~4 P# B$ reither 21-hydroxylase deficiency or 11-β hydroxylase
' U! H& `& S5 H# _0 G2 }deficiency. Those diagnoses were excluded by find-
, P$ b+ I) }0 N& |/ M4 g0 e4 D- ving the normal level of adrenal steroids.
1 U$ o+ {$ l* H% {& ]0 s- o7 Q- _The diagnosis of exogenous androgens was strongly) n4 @6 ?# L: R# N9 Y3 c
suspected in a follow-up visit after 4 months because) x; A; W$ _  |7 `; s% e* z
the physical examination revealed the complete disap-
- P6 x( f1 j$ v0 ]! bpearance of pubic hair, normal growth velocity, and
3 E; c7 c1 Y9 W( R, `, ~decreased erections. The father admitted using a testos-1 X3 p5 t8 R8 t% o( W
terone gel, which he concealed at first visit. He was: |' ]; ]$ B8 _+ P5 z7 _6 S
using it rather frequently, twice a day. The Physicians’
' k) l3 I7 c* A) L  cDesk Reference, or package insert of this product, gel or
: J: |$ m9 C0 }3 K7 gcream, cautions about dermal testosterone transfer to' Y5 i! e& d( h
unprotected females through direct skin exposure.; E9 |' @2 A! u, D9 A# T# ^
Serum testosterone level was found to be 2 times the3 B2 ~) B7 Q( b  \+ J# D3 v+ W; Q
baseline value in those females who were exposed to
; g, D6 {; P: l: J. jeven 15 minutes of direct skin contact with their male
: g8 p+ W6 |+ r5 T* U! r* y3 \partners.6 However, when a shirt covered the applica-0 g3 o9 T8 r4 p0 m* x3 h3 K
tion site, this testosterone transfer was prevented.  e* n: @( s8 C& |
Our patient’s testosterone level was 60 ng/mL,) W+ n* B& p* ]9 ?
which was clearly high. Some studies suggest that
; |; w4 f& t7 b8 b4 \4 Rdermal conversion of testosterone to dihydrotestos-0 Y$ m+ h8 d% v8 o
terone, which is a more potent metabolite, is more, t) V+ q; ~# E
active in young children exposed to testosterone% |& u! f  b* C5 u9 u" ~0 ?' I
exogenously7; however, we did not measure a dihy-  S: K  |; y+ m/ T5 M
drotestosterone level in our patient. In addition to+ C) t! `, o. e/ L; T# a
virilization, exposure to exogenous testosterone in
9 `/ j8 l9 {+ ]$ G: g! ?, P2 Y" dchildren results in an increase in growth velocity and* M% w7 u: @+ [" K1 c- P
advanced bone age, as seen in our patient.
8 n- n7 \! ?" N1 T% M2 y6 C0 J4 MThe long-term effect of androgen exposure during
1 N' H% b2 ^/ y1 c; |+ ]4 Wearly childhood on pubertal development and final) i# q4 @' ]' M4 B- {
adult height are not fully known and always remain
( }6 L* S/ c/ Z" t* K" R( z! ]; x8 Ca concern. Children treated with short-term testos-$ \+ ]9 `/ M+ B! B- t+ z( k) H) `3 W
terone injection or topical androgen may exhibit some
$ F; k* D+ C% ?1 racceleration of the skeletal maturation; however, after
! Q" ~0 D; y3 A+ Y* bcessation of treatment, the rate of bone maturation
5 S0 K0 F  r+ k/ Q# ~3 [3 J1 ?decelerates and gradually returns to normal.8,9
& \+ ]5 c4 z( ?, f) m+ mThere are conflicting reports and controversy1 x) G+ f7 V9 F, [
over the effect of early androgen exposure on adult5 T/ i3 B' h5 F/ B  e. E6 Q) r+ l$ g
penile length.10,11 Some reports suggest subnormal* g* K# R( L% M, H
adult penile length, apparently because of downreg-
8 T: `" H! s. M5 Oulation of androgen receptor number.10,12 However,
. @: e( m9 ^0 \: f" X- ySutherland et al13 did not find a correlation between# j* K. v2 k* }- Z& I0 I) o
childhood testosterone exposure and reduced adult
! n$ {5 F) t7 ~& U" D- [. Cpenile length in clinical studies.
# G! f) F/ W. K5 t  G6 y) PNonetheless, we do not believe our patient is
9 P5 [9 T  k% B5 K7 `& _going to experience any of the untoward effects from9 h; |  F! ]+ ^$ p3 U1 `
testosterone exposure as mentioned earlier because0 P1 v5 @1 [9 o: V  ]' @, {9 r' c
the exposure was not for a prolonged period of time.: [$ N' R% \! Z
Although the bone age was advanced at the time of# k) F0 y2 l" q
diagnosis, the child had a normal growth velocity at
* B: G7 \6 P, U7 _# q7 Rthe follow-up visit. It is hoped that his final adult
) S! a: j' u/ S: A. k: q0 Pheight will not be affected.
3 r8 X2 h" u  p% ~, R- DAlthough rarely reported, the widespread avail-
9 p8 t. a) }. P0 ?+ i, c& gability of androgen products in our society may
( C# s. @+ T: N& iindeed cause more virilization in male or female
1 {$ B' Y  V6 N. Xchildren than one would realize. Exposure to andro-
. V1 M5 t2 U9 z' p/ b# f9 Ugen products must be considered and specific ques-
) P" U; U3 L1 L2 ~9 U" Dtioning about the use of a testosterone product or; W: p) Q' C( I
gel should be asked of the family members during9 p/ ?; T, s- |0 m
the evaluation of any children who present with vir-
# ^2 x: Y& [2 `8 F% D: Bilization or peripheral precocious puberty. The diag-
6 M4 K3 p+ Z& [. Bnosis can be established by just a few tests and by
% a! `  i' h9 M, k$ ^; `- Zappropriate history. The inability to obtain such a
3 N* s3 H: R$ ~$ Zhistory, or failure to ask the specific questions, may
. d- p& R3 u( yresult in extensive, unnecessary, and expensive
( u  z: N# c' M! d5 H( P$ I$ `investigation. The primary care physician should be4 \* q' |) ?  O
aware of this fact, because most of these children# u3 M+ Y) b6 U
may initially present in their practice. The Physicians’7 L3 a; |% v1 L. C. S) a$ U0 D2 p
Desk Reference and package insert should also put a1 Q, Z! Q9 [( @' v
warning about the virilizing effect on a male or
- X0 Y: i5 c  qfemale child who might come in contact with some-: b# E; H  H4 q
one using any of these products.
+ r8 L+ N7 H3 J6 x' S+ rReferences
  P, R9 u2 R: S  M1. Styne DM. The testes: disorder of sexual differentiation; k( u6 \7 j- z  J- L
and puberty in the male. In: Sperling MA, ed. Pediatric
! Y5 [  c$ I. R; XEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;" I0 j6 i# ]3 C) w( k: @0 O# B. W, |
2002: 565-628.
$ W8 e7 C8 V! i" `+ t) [- k; g2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious* i4 \( T7 l% ~, ^
puberty in children with tumours of the suprasellar pineal
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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

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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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