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Sexual Precocity in a 16-Month-Old! }9 C9 X  U$ E
Boy Induced by Indirect Topical1 ~- @: C& P! J8 R* s  y. Z2 p
Exposure to Testosterone
& \% h" E7 V. t( F9 zSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 i# ^- M  [( g' y; C# z; hand Kenneth R. Rettig, MD1
/ q( L2 w7 ?5 u8 @# P2 O; oClinical Pediatrics/ }* Y; M/ A6 D7 C- R0 T" W! t
Volume 46 Number 6
  Q# c5 T" G1 x2 xJuly 2007 540-543
$ z; t' m3 i8 C) K1 z© 2007 Sage Publications
- }3 W# G- A: A# o10.1177/0009922806296651! w7 p, U3 K1 T& {& O- X
http://clp.sagepub.com
, X- q% W$ X( D: X# D, N$ lhosted at
( v# Q: ]! k: F+ shttp://online.sagepub.com% c4 y3 v0 W; {) i
Precocious puberty in boys, central or peripheral,
! }0 A' u# _: x/ D3 l' ^is a significant concern for physicians. Central
. W, B3 y# ?( k! q7 I; Gprecocious puberty (CPP), which is mediated
. |; p- i& N8 |/ l0 \3 ~' _3 j: {through the hypothalamic pituitary gonadal axis, has
  D% t$ G5 \; X' q  t5 Va higher incidence of organic central nervous system2 m$ \! `4 v% t# g- m
lesions in boys.1,2 Virilization in boys, as manifested
; V9 E  W& ^% Gby enlargement of the penis, development of pubic! s+ ^- o2 a7 ^
hair, and facial acne without enlargement of testi-
0 Q, l% u# E; y% O9 s" }cles, suggests peripheral or pseudopuberty.1-3 We: ?/ n. z2 Q* K: j  _2 b. u
report a 16-month-old boy who presented with the. K9 T- Q  R8 k' [# ~
enlargement of the phallus and pubic hair develop-
; @8 {+ ]. e; n+ h  i( \ment without testicular enlargement, which was due
( k) J9 b/ X! Y3 c* Lto the unintentional exposure to androgen gel used by2 k2 `) |2 M1 }
the father. The family initially concealed this infor-
; k+ x$ `( @7 u2 f9 M( T& _; _mation, resulting in an extensive work-up for this
3 P9 x3 E# {' b* echild. Given the widespread and easy availability of
" Q! k2 _) e  J# X# o6 w9 ntestosterone gel and cream, we believe this is proba-. M1 I3 B3 c7 S9 _2 v5 @
bly more common than the rare case report in the
( o* P& \! i5 y; X6 ?7 l$ Iliterature.4
! @! D2 Q5 c& u+ |Patient Report
4 C. {7 x8 {# g" z# h: `& H1 c- B& {A 16-month-old white child was referred to the
3 ?8 Y8 P- U0 Oendocrine clinic by his pediatrician with the concern
- ~$ S, ~  T3 l6 s0 O4 Q0 Bof early sexual development. His mother noticed
8 _) w& j! ~8 V* Q* [light colored pubic hair development when he was
6 w/ Q9 A8 B7 F3 [+ ^From the 1Division of Pediatric Endocrinology, 2University of2 o* }+ w) X" M7 l# J4 O  G" I
South Alabama Medical Center, Mobile, Alabama.$ \1 Q& w! v6 O2 l! g5 T
Address correspondence to: Samar K. Bhowmick, MD, FACE,$ E. [2 w0 k* x, a4 o% m
Professor of Pediatrics, University of South Alabama, College of
6 v, p$ H" Q2 U0 C/ vMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
$ m- ]7 E; O+ V+ O" {  Z: fe-mail: [email protected].3 t# W) z; }: A# H0 v* t" T& Z& _
about 6 to 7 months old, which progressively became# c) ~! p& G  ?; j$ \# m
darker. She was also concerned about the enlarge-% v/ x; @3 P1 x4 `  r& e. _, x
ment of his penis and frequent erections. The child) _" v$ I$ I& X1 s
was the product of a full-term normal delivery, with
9 |! I8 ?& H  k& va birth weight of 7 lb 14 oz, and birth length of
7 s. b6 @9 z2 t% ^( X20 inches. He was breast-fed throughout the first year
. Q8 u- m) W! E4 C5 e  \/ H; kof life and was still receiving breast milk along with
& I$ L4 `" |+ j7 u" j9 B7 f5 Y/ _% o; Usolid food. He had no hospitalizations or surgery,  I- @/ N# C$ p6 ~. Z) h5 R) K' p! v
and his psychosocial and psychomotor development
7 p4 B+ R) x! a( N% Z" _* vwas age appropriate.# M1 z7 L: h0 s6 ?
The family history was remarkable for the father,/ e- J8 ]4 C5 S
who was diagnosed with hypothyroidism at age 16,
0 I6 i+ I: {! M/ Jwhich was treated with thyroxine. The father’s& C( Z  p; F! D( X' e& B0 k; a
height was 6 feet, and he went through a somewhat
- e. O: H5 \* learly puberty and had stopped growing by age 14.2 ]- G7 p. D9 G2 f
The father denied taking any other medication. The
5 D: ^5 r9 s7 X9 ~  U. Hchild’s mother was in good health. Her menarche6 N2 F4 t& \6 j3 b! Z
was at 11 years of age, and her height was at 5 feet
) A% z- y2 p' P& K$ v) d8 K5 inches. There was no other family history of pre-
5 \/ A3 D# t- u) scocious sexual development in the first-degree rela-2 a: a- G+ C: a
tives. There were no siblings.2 D( {& s& v; M  X5 |6 I
Physical Examination
3 q* U5 C& }( P5 RThe physical examination revealed a very active,
" u2 c8 g" q+ h/ A8 ]playful, and healthy boy. The vital signs documented
/ W5 U" y# {) f. M) r& x2 R" \2 Ia blood pressure of 85/50 mm Hg, his length was7 i# I' `7 i) G, R* q( @
90 cm (>97th percentile), and his weight was 14.4 kg
1 U0 f5 i! p- B(also >97th percentile). The observed yearly growth% k4 G$ B# v" R- C7 ~
velocity was 30 cm (12 inches). The examination of
+ B6 r. d8 u2 H# U2 U/ b) `the neck revealed no thyroid enlargement.2 j  R* W' M4 h  p& z# C- M% J
The genitourinary examination was remarkable for
" Q/ a) s4 ?# ~enlargement of the penis, with a stretched length of$ ], L  M" |9 i. Z" A( U% m6 H2 i6 q
8 cm and a width of 2 cm. The glans penis was very well
/ b. D+ R! v% g+ Ndeveloped. The pubic hair was Tanner II, mostly around
+ {9 W" l& |8 m" C5 b540
6 t! A) S! O& F  \; Dat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: B& [, E; w0 ?; d) l
the base of the phallus and was dark and curled. The% m! p4 H0 W6 A5 g
testicular volume was prepubertal at 2 mL each.0 k; U) g1 {& y
The skin was moist and smooth and somewhat. P- H" D( Z. L- D: o
oily. No axillary hair was noted. There were no9 m: j& g1 [8 T1 l) I  Y4 V: n. r2 G
abnormal skin pigmentations or café-au-lait spots.
% h) w4 T# L2 \8 \2 mNeurologic evaluation showed deep tendon reflex 2+' ~6 V# E. b3 W( l
bilateral and symmetrical. There was no suggestion+ O7 d1 F9 ]: C6 l/ i# h9 H1 R
of papilledema.# W6 i7 g6 {- p" e. E' e& I0 W
Laboratory Evaluation
) a# ^, ^7 L. a0 |/ d5 lThe bone age was consistent with 28 months by- P: V, J( d* K; S) X+ k8 ^  c
using the standard of Greulich and Pyle at a chrono-
) r6 ]5 n0 W% \" A1 `9 k3 o; _* @1 Flogic age of 16 months (advanced).5 Chromosomal
2 c! H* m0 _, m  gkaryotype was 46XY. The thyroid function test8 c2 W  o6 e  B% d% J8 i, [
showed a free T4 of 1.69 ng/dL, and thyroid stimu-6 d$ m% C3 V  C$ o& ~
lating hormone level was 1.3 µIU/mL (both normal).$ B9 b3 A( N4 A2 s
The concentrations of serum electrolytes, blood
4 a* L+ @0 K& s8 f8 v5 |& C6 Aurea nitrogen, creatinine, and calcium all were) O* i% S" m$ @, p8 k
within normal range for his age. The concentration
! A2 G/ M+ b: c. W! n( v6 j6 _of serum 17-hydroxyprogesterone was 16 ng/dL
( m2 |1 h+ @9 c" }(normal, 3 to 90 ng/dL), androstenedione was 20
% ]8 n7 |; q: yng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
0 V) B  Y5 A3 O9 E9 s6 jterone was 38 ng/dL (normal, 50 to 760 ng/dL),7 B# {9 M& w8 Z% w5 ]* D
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
5 T4 N. `8 h. [, Z: q49ng/dL), 11-desoxycortisol (specific compound S)
- j+ e* B6 y' ]2 j: gwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-0 d$ z4 G2 s+ l  [
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
1 p' P- K3 h1 |7 |testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
* \- r5 H$ w% E, Dand β-human chorionic gonadotropin was less than
$ b. y: v$ x' C( u5 mIU/mL (normal <5 mIU/mL). Serum follicular
. q( Q! ?- q3 d+ Hstimulating hormone and leuteinizing hormone9 g" Q; ?! d+ G0 o6 Q( P: C
concentrations were less than 0.05 mIU/mL
9 J" h+ ^' v. V. N2 c(prepubertal).
8 W; m1 P9 u: X; r: |& SThe parents were notified about the laboratory2 T5 p; M+ i  {6 g# k( y* N3 }- Q
results and were informed that all of the tests were- C8 h1 b$ a* A" e& T1 X. X* \1 k
normal except the testosterone level was high. The
. c3 t) y& i* v$ c& yfollow-up visit was arranged within a few weeks to* `2 \; c3 L* V' D7 _- l
obtain testicular and abdominal sonograms; how-& b) H7 Z0 L9 l; q
ever, the family did not return for 4 months.
6 h% o1 f8 h) i7 PPhysical examination at this time revealed that the0 W/ i) h* z( ^- j; W( E% K6 ~8 Q/ I
child had grown 2.5 cm in 4 months and had gained
2 V3 W0 F! r  P: N( M+ N8 V2 kg of weight. Physical examination remained
+ Q. |! E- B) yunchanged. Surprisingly, the pubic hair almost com-
% s5 l3 Q* C$ H2 lpletely disappeared except for a few vellous hairs at
% |( c( \- ]4 d, Dthe base of the phallus. Testicular volume was still 2
2 q5 }! j9 j6 o! `4 @mL, and the size of the penis remained unchanged.: W2 C* l& ~) E
The mother also said that the boy was no longer hav-( d, R4 ?* j# V" R* k9 Y
ing frequent erections.* I1 s' r4 E: P1 d, }
Both parents were again questioned about use of3 g9 P( k) @* c& T. g9 A9 o
any ointment/creams that they may have applied to
" H5 S! P, V9 |8 [the child’s skin. This time the father admitted the
  ]6 f% A9 T& s& k# C" L2 E& XTopical Testosterone Exposure / Bhowmick et al 541
6 ?2 h' i" @: X6 m( ?use of testosterone gel twice daily that he was apply-. d1 b$ a- y! f
ing over his own shoulders, chest, and back area for
: c! B' y! h; za year. The father also revealed he was embarrassed
- p% e3 D- @5 H: k$ Sto disclose that he was using a testosterone gel pre-
/ t) c& [! n) |$ |( k- f5 gscribed by his family physician for decreased libido8 W0 h6 D) m4 |" P% d2 k
secondary to depression.6 \5 v6 s( t3 e  ]3 A
The child slept in the same bed with parents.. f% b5 z2 W$ S9 D/ e
The father would hug the baby and hold him on his
- G( a+ B/ k  c+ f7 x/ e3 Schest for a considerable period of time, causing sig-
  c- j1 g# g, ?8 a# Vnificant bare skin contact between baby and father.4 j4 m. L6 w6 e, y6 G
The father also admitted that after the phone call,
: a* y6 `7 |3 ywhen he learned the testosterone level in the baby' f+ y- g9 z, [, w$ ?2 q2 [( p6 [$ F
was high, he then read the product information& v. z3 c7 \$ P& V% [: b4 S" Q
packet and concluded that it was most likely the rea-
: q4 r/ M2 S  Ison for the child’s virilization. At that time, they
) c  X1 Q9 o, G7 X) D4 }0 tdecided to put the baby in a separate bed, and the  U! j1 q5 I3 f" Z
father was not hugging him with bare skin and had
) f2 r) L. w$ E/ gbeen using protective clothing. A repeat testosterone* a$ F+ _% `7 Y" e; Z
test was ordered, but the family did not go to the
& y+ j& S" A& o9 m& ?laboratory to obtain the test.+ Y2 J& V9 _% L5 p8 j! q, d
Discussion+ x! g2 N' @9 u: k- m8 g
Precocious puberty in boys is defined as secondary- D9 L- A- I3 \' ^
sexual development before 9 years of age.1,4
$ a" M/ U) M7 APrecocious puberty is termed as central (true) when. `9 C. h) {1 |. ~1 D6 A0 ?, o1 ?: q
it is caused by the premature activation of hypo-
4 a: T2 l8 t, Y5 W7 E4 Xthalamic pituitary gonadal axis. CPP is more com-
5 j  O6 Y# W- Y& mmon in girls than in boys.1,3 Most boys with CPP7 P- S' i4 {) C% |$ L# ~: \: ^
may have a central nervous system lesion that is7 m5 g) t% Y9 c! b& p
responsible for the early activation of the hypothal-
% c" E2 ^7 P$ z$ O' ?7 Yamic pituitary gonadal axis.1-3 Thus, greater empha-- N7 {8 u& x2 r
sis has been given to neuroradiologic imaging in
7 T# J% O% [5 Z' X' x% e; C+ {" Bboys with precocious puberty. In addition to viril-  w- [; k( c% r4 K( B
ization, the clinical hallmark of CPP is the symmet-/ E  l' @3 s# `
rical testicular growth secondary to stimulation by
/ C; i9 O; J5 ~2 ygonadotropins.1,36 h+ j+ q" y$ S
Gonadotropin-independent peripheral preco-
+ ^  X2 m( m) L2 c( G# Vcious puberty in boys also results from inappropriate
6 m- G8 H7 z  j# j9 Q* fandrogenic stimulation from either endogenous or
; H, x: `" q: R  t. nexogenous sources, nonpituitary gonadotropin stim-) @- g' b# L6 _( f6 y# {( m
ulation, and rare activating mutations.3 Virilizing. `  m8 f* V- m+ Q3 l: B, ^1 C$ d
congenital adrenal hyperplasia producing excessive
) a( o+ X* @8 M2 _adrenal androgens is a common cause of precocious
0 v6 d: z" w6 {: y2 P0 Epuberty in boys.3,4
5 H+ i4 q7 y0 [! MThe most common form of congenital adrenal8 l- F1 y2 {: [8 Z( R$ D, i
hyperplasia is the 21-hydroxylase enzyme deficiency.
4 ^- M. X, d  S) V- HThe 11-β hydroxylase deficiency may also result in
; ?5 _6 K6 q* R& o# M: S- ^( uexcessive adrenal androgen production, and rarely,- M# _, Q) i4 T5 i5 m8 H- `
an adrenal tumor may also cause adrenal androgen3 d# \3 u% S! j- Z6 r; @
excess.1,3$ o* R, \2 V  S9 W: N
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- `/ y! _$ d) |, w5 {8 u' N" C9 P
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
4 ^- H6 N) m; Q, }3 m$ b% j5 BA unique entity of male-limited gonadotropin-0 I3 @1 n/ a( a- c5 r$ T+ V6 ~0 c
independent precocious puberty, which is also known
$ Y7 k: E9 ^* w: U: A5 w5 Has testotoxicosis, may cause precocious puberty at a
' h% N$ _& {8 t  q+ B* T/ @' Q7 I. F6 m* vvery young age. The physical findings in these boys
5 m5 o& u! V. N" G& n: Pwith this disorder are full pubertal development,
" Y2 \3 q: m: V8 W8 Y4 S$ uincluding bilateral testicular growth, similar to boys
8 L( q) d( |/ n- u- ywith CPP. The gonadotropin levels in this disorder8 ]+ b( q/ C6 o
are suppressed to prepubertal levels and do not show
+ L" X# b1 N# t; J) h3 z" Kpubertal response of gonadotropin after gonadotropin-
; J3 q; e% u7 \! P7 F) b" ~! Sreleasing hormone stimulation. This is a sex-linked
1 }; S  h7 Y  i' G& ?autosomal dominant disorder that affects only7 Y7 h0 a, P( a  G
males; therefore, other male members of the family
) p1 s) @% {  T- ]: {2 lmay have similar precocious puberty.3
6 l) w. `* a8 l% WIn our patient, physical examination was incon-
- Z: P4 s: u# K. hsistent with true precocious puberty since his testi-- q/ j& M4 P; U
cles were prepubertal in size. However, testotoxicosis9 j3 M, A: Z# G" t7 n: R
was in the differential diagnosis because his father
5 Y2 A, d) `8 x1 [# i( v5 Y6 m* i/ e: rstarted puberty somewhat early, and occasionally,6 l, C5 z: ^- a7 u& O' l9 @3 }
testicular enlargement is not that evident in the
. }' U& M$ Z+ |2 A. Dbeginning of this process.1 In the absence of a neg-, O2 Z# U/ a! Z& Z- A5 Q6 t
ative initial history of androgen exposure, our4 w* F- h+ n- l' r0 R! \8 X
biggest concern was virilizing adrenal hyperplasia,
3 p. d) {. a# ^: O, A/ V, weither 21-hydroxylase deficiency or 11-β hydroxylase
. L( [3 @% L+ ^- y! w. W- ndeficiency. Those diagnoses were excluded by find-
# ?: k  U) |3 k% ~+ ~ing the normal level of adrenal steroids.1 A/ y: v. J: f" _: f! S
The diagnosis of exogenous androgens was strongly9 [7 [8 m* v8 v
suspected in a follow-up visit after 4 months because& V# d8 q5 j1 H# [- `6 {3 X
the physical examination revealed the complete disap-. e' i% P) x+ h9 c- W% ~
pearance of pubic hair, normal growth velocity, and+ }& j1 @0 z  z( o( Z  ?. T
decreased erections. The father admitted using a testos-
8 ]5 G5 ~7 O% |3 K/ kterone gel, which he concealed at first visit. He was
& S. G4 J' g% uusing it rather frequently, twice a day. The Physicians’6 I# U# i9 Y/ E$ u7 L# M
Desk Reference, or package insert of this product, gel or) |6 U* B6 w" h) ~1 T
cream, cautions about dermal testosterone transfer to! N# `5 W2 l7 |" S1 K. \: s
unprotected females through direct skin exposure.% K3 ]2 s" t2 d
Serum testosterone level was found to be 2 times the
$ H) e! x! B  f, ]1 Bbaseline value in those females who were exposed to
3 O  e0 L# a; J* l" Zeven 15 minutes of direct skin contact with their male, J% s! v- S# V
partners.6 However, when a shirt covered the applica-
! ^% F( c! o3 @0 g: y3 ~tion site, this testosterone transfer was prevented.
! x' B, E; M3 FOur patient’s testosterone level was 60 ng/mL,
1 \4 ^8 m! t0 M4 _5 {8 owhich was clearly high. Some studies suggest that
0 m7 @6 l+ C1 ]3 Y% u. vdermal conversion of testosterone to dihydrotestos-: q" W9 V8 \2 _
terone, which is a more potent metabolite, is more
8 p6 V) x5 @+ G3 h" c8 xactive in young children exposed to testosterone# L; m' t  L5 `- m
exogenously7; however, we did not measure a dihy-3 L  [8 X7 J8 p- Z; }
drotestosterone level in our patient. In addition to
! K% [( [5 {* Gvirilization, exposure to exogenous testosterone in5 b( i4 w! I% z# J. _" H
children results in an increase in growth velocity and" F- @4 }( ^, a
advanced bone age, as seen in our patient.
2 e, |7 l; U( ]( |The long-term effect of androgen exposure during# r$ ]+ |( ^3 y9 H, |" Q- U  F* i
early childhood on pubertal development and final! k9 }: O  F* D) D6 d2 S
adult height are not fully known and always remain+ p, l) l0 H- g# O; |6 D( R
a concern. Children treated with short-term testos-$ x; g3 r/ G2 I
terone injection or topical androgen may exhibit some
# z7 H+ T/ @/ Kacceleration of the skeletal maturation; however, after* f5 W" z2 h6 o) S
cessation of treatment, the rate of bone maturation* }3 j, y6 V9 z* e/ u
decelerates and gradually returns to normal.8,9' R" O# m& {0 m) f1 m: G
There are conflicting reports and controversy) X8 I, N( w2 ~4 Z8 {$ c
over the effect of early androgen exposure on adult
1 j! [  K' W& Z0 S) Dpenile length.10,11 Some reports suggest subnormal! r# j; j+ ^. u5 P2 B4 F, u
adult penile length, apparently because of downreg-
/ V7 n' n; W$ W( p7 f+ }" Pulation of androgen receptor number.10,12 However,
7 Y0 z0 l. v& ?9 z& Q$ ?Sutherland et al13 did not find a correlation between
% U( Y, i2 A! h; u9 `. ~! Y8 `childhood testosterone exposure and reduced adult& Z7 r$ u5 q2 W8 A7 b0 l+ Y
penile length in clinical studies.$ {; ?, E" F3 V# E
Nonetheless, we do not believe our patient is
" |1 g/ z7 l# ?) ^3 u7 @7 C9 rgoing to experience any of the untoward effects from
- h5 L7 F) n3 Stestosterone exposure as mentioned earlier because
/ l* F) b! v  s' R- c( uthe exposure was not for a prolonged period of time.+ V9 v, k' e3 O
Although the bone age was advanced at the time of: x/ y$ I( e) H. }- C% R; N( O! F
diagnosis, the child had a normal growth velocity at2 h! F- |/ A$ E% @1 P
the follow-up visit. It is hoped that his final adult; o# a& [! z3 z& {# n: Q) N4 q
height will not be affected.
0 S- M2 @7 W% `) UAlthough rarely reported, the widespread avail-
. m- V$ s/ W' [0 E. Y. l2 sability of androgen products in our society may
8 ]6 _% v$ ?' e1 t6 S8 kindeed cause more virilization in male or female* P: e4 u2 f$ {7 ~1 d4 q+ ]" r' O
children than one would realize. Exposure to andro-5 Y; x% [$ P9 i0 C% ^7 g
gen products must be considered and specific ques-5 z2 k2 W  V$ S9 t$ g" G+ c1 g
tioning about the use of a testosterone product or; W! e0 [/ B5 f6 ~" ?* |# Y+ r, s
gel should be asked of the family members during
' \8 K2 B0 e" I7 l% Ithe evaluation of any children who present with vir-8 W' h0 D9 ?8 C8 v2 _7 F
ilization or peripheral precocious puberty. The diag-
6 }8 _2 d& J- P* |& m/ Dnosis can be established by just a few tests and by
6 f* w) J3 ~) Rappropriate history. The inability to obtain such a
) E+ W7 q; V0 ]6 _; f0 ~8 Mhistory, or failure to ask the specific questions, may
3 q6 D& `0 ^/ c6 c3 Aresult in extensive, unnecessary, and expensive9 b+ g# G+ E( M8 Y
investigation. The primary care physician should be8 E3 I( `* j/ u) Y2 ?. X* R+ M
aware of this fact, because most of these children7 Q/ W5 x; C, w' P, h2 \% A
may initially present in their practice. The Physicians’
" H" ]6 s+ V5 E) [+ Y/ k! _7 xDesk Reference and package insert should also put a
0 V& I! A( Z% X8 \warning about the virilizing effect on a male or
" z* J* N+ m4 X/ ]. gfemale child who might come in contact with some-
( i: u+ K4 C2 c1 Pone using any of these products.9 T; I$ {; x. _7 f
References
" L7 I$ j2 ]) d1. Styne DM. The testes: disorder of sexual differentiation
' ]: E: V1 V) Y* j  hand puberty in the male. In: Sperling MA, ed. Pediatric& c4 E8 h4 O1 @3 I+ a
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;$ e* b* h2 T5 y- @8 R* p
2002: 565-628.! b6 l2 U. G8 e9 h3 z5 }
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
5 o0 e* S& U! ^2 y/ P5 D8 {5 Opuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
- v* _2 H: Z( H% N" K' ]2 O) b% vBoy Induced by Indirect Topical/ S$ l: _* B8 `( @1 j
Exposure to Testosterone7 T, J" R+ K3 C7 Q1 l
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2- m) ^: U4 x. y! H1 E1 X
and Kenneth R. Rettig, MD11 K9 d# t: ^( J6 A! \* l
Clinical Pediatrics! p/ `, B# A0 S7 x8 u1 L
Volume 46 Number 6
0 T1 v+ j) ?, v4 g' YJuly 2007 540-543
4 q  ~/ e' \% f' {6 `© 2007 Sage Publications
, ~. @0 J( Y0 c1 r0 `8 T10.1177/0009922806296651  e4 L- F; E4 h8 [" |$ M, F
http://clp.sagepub.com- Q* h( b! p/ Z$ e+ z; B! s
hosted at
: @( m+ R( d( _http://online.sagepub.com7 F/ P6 E. y( U2 _% C9 X! `8 E0 E; w
Precocious puberty in boys, central or peripheral,4 t! O( [6 k" N4 ^& c% q: b# a
is a significant concern for physicians. Central  P" ~  N1 ~% H/ ], a
precocious puberty (CPP), which is mediated
  q- u8 V4 Y5 J1 j& Fthrough the hypothalamic pituitary gonadal axis, has
, ]. ~+ [; j, l0 M& W7 Ga higher incidence of organic central nervous system
& y6 H# Q& P5 {9 {lesions in boys.1,2 Virilization in boys, as manifested
. C! W8 ^! P* A9 xby enlargement of the penis, development of pubic
' K- ^) S5 k/ V: rhair, and facial acne without enlargement of testi-$ e3 }- F* ]6 l+ }) f1 }6 e1 l
cles, suggests peripheral or pseudopuberty.1-3 We/ P% u$ G/ {% y& \. l9 C
report a 16-month-old boy who presented with the
$ W, z1 C* Q5 E  f4 ^6 Senlargement of the phallus and pubic hair develop-
) K; Q: z- u4 b8 N+ {ment without testicular enlargement, which was due
3 S5 R8 V  W' \5 T8 \- c- F$ b+ U/ a1 h- ?to the unintentional exposure to androgen gel used by3 w9 ^. V- a( w, Q
the father. The family initially concealed this infor-. |( t: Y0 K* L
mation, resulting in an extensive work-up for this- }. }9 n: c& I4 p+ x# n% n' _
child. Given the widespread and easy availability of% ^; J  x, q+ S  Y0 V5 i4 Q
testosterone gel and cream, we believe this is proba-
" p6 S: A5 R. M# |6 L# l9 Qbly more common than the rare case report in the- T' I' [7 A! K& |: S
literature.4
6 ?) h$ D3 \) T9 C3 WPatient Report4 m" C7 y# ~/ Y0 a: }
A 16-month-old white child was referred to the2 a; A. g- Z2 r- I4 R8 e
endocrine clinic by his pediatrician with the concern) z3 g2 ?, D" T; z. X% f
of early sexual development. His mother noticed
) ^" Z; X4 [% plight colored pubic hair development when he was
& v4 F/ M& Z, jFrom the 1Division of Pediatric Endocrinology, 2University of) H& P5 v9 L: a+ _7 w3 ?6 {1 g
South Alabama Medical Center, Mobile, Alabama.% [  N: J9 m" r
Address correspondence to: Samar K. Bhowmick, MD, FACE,
6 X2 X4 Y. z( b. h# J$ tProfessor of Pediatrics, University of South Alabama, College of
* g+ T% Q( ^9 T  s& }Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;# Y, w. g$ \7 z) ?
e-mail: [email protected].8 f- t+ Q6 b3 T! i# a
about 6 to 7 months old, which progressively became! @/ g. j9 M" y
darker. She was also concerned about the enlarge-
: q/ W8 o- G* _% M& pment of his penis and frequent erections. The child. |: M. B# x2 ^( o1 B. ]1 n: w
was the product of a full-term normal delivery, with- \7 m3 |9 G" M0 r7 N1 S! _
a birth weight of 7 lb 14 oz, and birth length of
) u: f/ w! C5 w9 T' V20 inches. He was breast-fed throughout the first year
2 |! t# D/ k8 V1 C* J8 E3 bof life and was still receiving breast milk along with. Z5 M/ W' B4 i, |
solid food. He had no hospitalizations or surgery,+ n9 \8 s; W) P# t& c: W: v
and his psychosocial and psychomotor development1 \& E- T1 }6 E# K
was age appropriate.$ }1 d. s4 D$ ^2 S+ T
The family history was remarkable for the father,' `0 |! ^0 F. }% S
who was diagnosed with hypothyroidism at age 16,0 u3 i  J/ y3 M2 T- z
which was treated with thyroxine. The father’s
7 F2 ?$ m. }# t9 t. _  s) W/ Hheight was 6 feet, and he went through a somewhat! n& p( n* W: w  J4 ~
early puberty and had stopped growing by age 14.0 h: U0 f; M# E- L0 ?
The father denied taking any other medication. The  A1 O. B6 \0 Q  @' |
child’s mother was in good health. Her menarche
- B' j: W3 {/ g+ uwas at 11 years of age, and her height was at 5 feet
; _/ s" D! R/ K) {0 h5 inches. There was no other family history of pre-  |: j; j/ ~: u6 S/ l7 `
cocious sexual development in the first-degree rela-
9 V, S$ v8 T4 U- ?7 Ytives. There were no siblings., {3 h' S: Q* m' O, m
Physical Examination' S, s/ F8 B) \( \
The physical examination revealed a very active,
  B' R9 q4 G, Q6 G" jplayful, and healthy boy. The vital signs documented
* {( h9 j5 U/ ?a blood pressure of 85/50 mm Hg, his length was
& S# |; R; r  q& P3 W6 B% q90 cm (>97th percentile), and his weight was 14.4 kg7 h% ~$ |( c- V( I) e; o
(also >97th percentile). The observed yearly growth& q  ?) |$ x& J* o
velocity was 30 cm (12 inches). The examination of
/ Y7 T- w) ?1 L0 R4 W: D8 X4 _3 {the neck revealed no thyroid enlargement.  M) }6 h. x  e" |" i- r
The genitourinary examination was remarkable for4 t3 K+ X5 l# C& g$ y8 y
enlargement of the penis, with a stretched length of& I. F! F( v& g
8 cm and a width of 2 cm. The glans penis was very well) s- \% [# t  R) o0 z6 z
developed. The pubic hair was Tanner II, mostly around& T$ k+ R7 v8 W
540/ L, J; p) [$ G, |7 Q2 l" O
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the base of the phallus and was dark and curled. The
4 g- K: L6 E7 s: T* e& d6 utesticular volume was prepubertal at 2 mL each.6 K: v' ^- ~" z# Y7 T; `
The skin was moist and smooth and somewhat/ Z5 K- }, V4 O$ Q; p, g! C
oily. No axillary hair was noted. There were no
6 g9 N0 ~0 C7 _# X7 Iabnormal skin pigmentations or café-au-lait spots., b8 O1 f! }1 g1 h; w
Neurologic evaluation showed deep tendon reflex 2+; w. x( o$ |6 C& d
bilateral and symmetrical. There was no suggestion; i2 @! t& W+ x9 ^% M( o
of papilledema.+ y  p% c' x4 @1 `6 @
Laboratory Evaluation
0 v* {4 Q2 P, d: qThe bone age was consistent with 28 months by% g1 Z2 e" n  g1 w: P
using the standard of Greulich and Pyle at a chrono-  [( B7 I" i# L+ K
logic age of 16 months (advanced).5 Chromosomal6 ?( h7 r7 T; u, {
karyotype was 46XY. The thyroid function test
  F/ P: w( O  e: N) F! m9 dshowed a free T4 of 1.69 ng/dL, and thyroid stimu-# k5 n, O, x7 m; D) E
lating hormone level was 1.3 µIU/mL (both normal).: [9 M: h0 ], J/ ?* ^0 V
The concentrations of serum electrolytes, blood
2 Y" x; p) ^6 R2 iurea nitrogen, creatinine, and calcium all were
+ G' k+ h5 O) N. h) ~( X& A% X5 s' Mwithin normal range for his age. The concentration
: Y. h0 j6 ?( t+ \: xof serum 17-hydroxyprogesterone was 16 ng/dL! M* `4 G% u' Y
(normal, 3 to 90 ng/dL), androstenedione was 20, F- j" M/ q0 `# R
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
* T/ W' e4 v; l2 b' i( G+ ^terone was 38 ng/dL (normal, 50 to 760 ng/dL),9 S* a9 U8 u' K/ r
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
6 o9 t+ t5 A) W$ B6 y% |49ng/dL), 11-desoxycortisol (specific compound S)
5 T& [) D4 Y; v' fwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-1 R0 `9 M  s, {( c
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total/ p6 J; S! t; f' C5 d
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),! H/ b! E7 T  `1 \. d; H
and β-human chorionic gonadotropin was less than" `" m4 ]: s7 X% D7 `( J
5 mIU/mL (normal <5 mIU/mL). Serum follicular
& G" u3 s; H2 L  d7 @, ~stimulating hormone and leuteinizing hormone
7 N1 n7 \8 f, _7 r# |concentrations were less than 0.05 mIU/mL2 i# `8 G4 Z6 x4 Q
(prepubertal).% C4 o3 q% U7 z: z7 _
The parents were notified about the laboratory
1 |" V1 X" F& Q- Sresults and were informed that all of the tests were
# n7 ]3 B8 s+ w& }4 Nnormal except the testosterone level was high. The9 i% b/ `5 L7 w# b3 ?1 q
follow-up visit was arranged within a few weeks to! F* b/ j0 M4 E2 ]! {; Q
obtain testicular and abdominal sonograms; how-
# Z, H& L: ], _ever, the family did not return for 4 months.) i; l7 b5 `" |. F) _* A
Physical examination at this time revealed that the* L& Y' _- u  m: }1 g; n' m
child had grown 2.5 cm in 4 months and had gained
9 S$ m0 H4 x* K* h2 kg of weight. Physical examination remained
8 B% H# R, s  d3 A/ L! q4 Runchanged. Surprisingly, the pubic hair almost com-1 T. n& a- `) s6 M
pletely disappeared except for a few vellous hairs at
+ Y! u8 e" K1 \" g4 f1 I+ jthe base of the phallus. Testicular volume was still 2
: h' ^2 T/ m; UmL, and the size of the penis remained unchanged.
8 a& e1 f1 B& D) L, f4 [The mother also said that the boy was no longer hav-: ?0 `" c& ~8 c: x; j$ l7 H
ing frequent erections.
- S8 u, S6 N) x$ ?Both parents were again questioned about use of
0 m" t% k  [. d& f0 L" O+ z5 |any ointment/creams that they may have applied to
! f9 l% U- F2 n( s; h+ _the child’s skin. This time the father admitted the
. t- M# _( v: U! N/ oTopical Testosterone Exposure / Bhowmick et al 541
; w- O# a; n, N8 quse of testosterone gel twice daily that he was apply-! S/ N2 F9 u2 p- b2 ^9 C
ing over his own shoulders, chest, and back area for/ w$ u; u2 J0 ]2 |7 V
a year. The father also revealed he was embarrassed% ^* g; b" I9 Q- q$ }
to disclose that he was using a testosterone gel pre-# C: d  V0 K, z% u9 p7 Q
scribed by his family physician for decreased libido
! t! `) S* u1 R1 |secondary to depression.. n) O& |) s. U( s4 L; ?( q
The child slept in the same bed with parents.7 n5 m( A; T4 O8 g
The father would hug the baby and hold him on his
9 \% ^% Q0 Q6 q3 m- `chest for a considerable period of time, causing sig-
& z+ E' g' I$ g- A3 K# {nificant bare skin contact between baby and father.
5 ]& k3 j6 \  L* w1 tThe father also admitted that after the phone call,
- t  H  ]$ {& x: Ywhen he learned the testosterone level in the baby! b7 A! i0 ?2 f7 {4 A* O$ _6 L5 O
was high, he then read the product information/ r- H' W3 O% J1 w8 {0 w+ j5 v
packet and concluded that it was most likely the rea-
) s. }0 s8 H% b8 n/ _son for the child’s virilization. At that time, they3 [$ s% T( ~$ f6 \$ ^' t6 H  ^
decided to put the baby in a separate bed, and the
$ D' i$ S( z+ P+ gfather was not hugging him with bare skin and had
& f) Q0 d' b; `/ D4 y1 Rbeen using protective clothing. A repeat testosterone
1 Z2 q: @# W2 E/ _% X- k8 ]test was ordered, but the family did not go to the
; d6 h2 k) Y' U/ o8 W3 ~laboratory to obtain the test.
( L+ G: X9 r9 o5 f- u; vDiscussion  p& }0 G) F& H$ o/ H6 g  J
Precocious puberty in boys is defined as secondary
: F6 O+ B& e+ G+ _7 [sexual development before 9 years of age.1,4+ }7 B0 K$ A5 r# |9 {
Precocious puberty is termed as central (true) when
6 \9 g2 A  S& B" ^it is caused by the premature activation of hypo-' S( E) t/ J- n2 g! O( x4 J
thalamic pituitary gonadal axis. CPP is more com-
. \3 ^: g/ X0 f2 g, M0 k) @/ Ymon in girls than in boys.1,3 Most boys with CPP
( E; e( N2 Z" }may have a central nervous system lesion that is
3 \/ W4 t/ v* v2 tresponsible for the early activation of the hypothal-% p" r& L4 T6 ?6 @* L
amic pituitary gonadal axis.1-3 Thus, greater empha-; O1 y3 G' q5 _& ~
sis has been given to neuroradiologic imaging in+ Y2 i& q( e" W% H% r
boys with precocious puberty. In addition to viril-
$ A  Q1 f  _  p8 t- O. @ization, the clinical hallmark of CPP is the symmet-
5 M3 d; f2 R8 O7 orical testicular growth secondary to stimulation by) C6 ~) X- p: v  e- }& a, F1 Q
gonadotropins.1,3  D& l8 `/ m  E
Gonadotropin-independent peripheral preco-
9 _( f: A* E* {9 V1 w5 a  \cious puberty in boys also results from inappropriate
0 m+ p! v) T; f$ R$ E' x/ v% {androgenic stimulation from either endogenous or
6 Q9 x! D+ r" r% W! t) p8 J" @exogenous sources, nonpituitary gonadotropin stim-6 {9 W3 \, I- p+ [0 n
ulation, and rare activating mutations.3 Virilizing
" }" m) t* L; J9 T! t9 A' rcongenital adrenal hyperplasia producing excessive
; d* s4 N& }* m+ y/ P" r1 o4 Hadrenal androgens is a common cause of precocious
# U3 N& n/ r9 Y: x7 C& d8 G: \$ npuberty in boys.3,4+ ~2 P6 a3 x7 A# s
The most common form of congenital adrenal
' q: w4 I* J; L5 h5 E6 y% ]; V1 y+ Jhyperplasia is the 21-hydroxylase enzyme deficiency.
" A* H8 o4 e" {- tThe 11-β hydroxylase deficiency may also result in
6 o; g- S1 ~7 Dexcessive adrenal androgen production, and rarely,9 X7 x1 J% ~/ k  k9 f( P# O
an adrenal tumor may also cause adrenal androgen) o! h# g" o3 M- g! |# N- h$ T/ r
excess.1,3
% Z8 W" [! G: x: ^at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% N8 }# j, D0 k, D' Y3 n: `
542 Clinical Pediatrics / Vol. 46, No. 6, July 20071 k  e4 y( L8 s/ u  e1 t* r; W
A unique entity of male-limited gonadotropin-
, S1 b4 Y9 E5 T  Eindependent precocious puberty, which is also known# ?2 I/ b" n& T
as testotoxicosis, may cause precocious puberty at a: h0 n# q( c8 a
very young age. The physical findings in these boys
2 |5 {  C: J/ S1 _with this disorder are full pubertal development,
' e+ D) F* T& c9 _8 C8 A# B# aincluding bilateral testicular growth, similar to boys
" [. j0 d, I( m) I* i: |with CPP. The gonadotropin levels in this disorder
- Y/ q" Z$ V2 M: h  Iare suppressed to prepubertal levels and do not show6 g2 l; ?: ?/ }5 e; }; S, ?) \
pubertal response of gonadotropin after gonadotropin-  T8 I5 h/ c# ?' o: k: l+ r, Q
releasing hormone stimulation. This is a sex-linked7 C6 T! o3 y% B. j0 O
autosomal dominant disorder that affects only0 E& y0 E9 K5 @$ |* G
males; therefore, other male members of the family
' @% H+ |* R, _. O0 O8 t$ K  fmay have similar precocious puberty.3
6 w6 u0 T% Z5 F6 {5 N' bIn our patient, physical examination was incon-( s, ?" [+ O  S4 P4 [  y# C
sistent with true precocious puberty since his testi-! O# ^  p: O# Y3 g. j
cles were prepubertal in size. However, testotoxicosis7 e0 Z0 l) M' |( l" }" X3 H8 [
was in the differential diagnosis because his father
! [# |. \' ~4 ostarted puberty somewhat early, and occasionally,
- M0 K, ~3 _! F- v5 w( d: O6 L) Mtesticular enlargement is not that evident in the
- Z, B3 c( {6 rbeginning of this process.1 In the absence of a neg-: O0 s/ w% n  h8 u
ative initial history of androgen exposure, our
8 y' N6 ~% Q4 `. T) w7 Y$ _biggest concern was virilizing adrenal hyperplasia,7 p, I% K, l& B0 L' u0 u) i/ _( A' E
either 21-hydroxylase deficiency or 11-β hydroxylase, l2 c9 @. _$ |: \# f) P' v' S: [9 b9 V
deficiency. Those diagnoses were excluded by find-8 _4 r+ `2 M6 x1 i1 t5 ^- T  n9 B
ing the normal level of adrenal steroids.
/ v2 n5 `: ]4 F0 G/ [$ X& R$ VThe diagnosis of exogenous androgens was strongly& T" U3 O: m' s8 s
suspected in a follow-up visit after 4 months because5 U2 L7 d4 l3 [2 Q$ s
the physical examination revealed the complete disap-% D! H6 j% e( [/ h
pearance of pubic hair, normal growth velocity, and
( j$ q( n' N% f4 p6 c" r! Qdecreased erections. The father admitted using a testos-) h* ~# `  Q% }& C6 W0 R3 Y- A
terone gel, which he concealed at first visit. He was5 @5 X. w% b$ j) K( v2 E8 |; [
using it rather frequently, twice a day. The Physicians’1 z) e9 E, t( g* b! q% X
Desk Reference, or package insert of this product, gel or- t8 U) `0 y4 S" N/ ?! ]
cream, cautions about dermal testosterone transfer to; Z- Q: K. v6 k
unprotected females through direct skin exposure.+ X- g8 Z! n# ]- _( P
Serum testosterone level was found to be 2 times the
# b1 _. c6 A9 i& |baseline value in those females who were exposed to( W" M; M" e( r+ d  w! m5 T, o
even 15 minutes of direct skin contact with their male4 @9 j- P) O2 I+ V! K  m% n: R5 h# W
partners.6 However, when a shirt covered the applica-
$ T: F2 v6 ?# a5 Z- a$ ztion site, this testosterone transfer was prevented.* _. }# I. W. _! h  A
Our patient’s testosterone level was 60 ng/mL,
( T' ]% F( a- E+ q: Q. L1 ewhich was clearly high. Some studies suggest that2 Q& v6 m# {  p! b' u
dermal conversion of testosterone to dihydrotestos-  c: O3 S- B8 G. M+ i9 E: J5 Y. l
terone, which is a more potent metabolite, is more
- ~" T6 g- R. q. `* i) D. c( Cactive in young children exposed to testosterone5 t# V+ `$ ]! l: P6 d5 O
exogenously7; however, we did not measure a dihy-2 K2 o! }4 j" z( G
drotestosterone level in our patient. In addition to
  _7 S4 _; n0 ]$ svirilization, exposure to exogenous testosterone in' N6 Z+ J# g, Y- Y" H
children results in an increase in growth velocity and
6 n; z7 g6 U" v( p/ {, jadvanced bone age, as seen in our patient.
7 A; g/ K+ V! Q! r; z% i/ I6 h- @0 jThe long-term effect of androgen exposure during/ |; E! {4 u7 x
early childhood on pubertal development and final# l+ v+ x& }; ?; v2 {: ]
adult height are not fully known and always remain1 w4 `; n  H* p) ~0 X) E
a concern. Children treated with short-term testos-3 Q- E2 x3 N* g$ W
terone injection or topical androgen may exhibit some
$ g- g% @$ V' V1 D6 h% }acceleration of the skeletal maturation; however, after
6 H) L) `/ U5 [cessation of treatment, the rate of bone maturation
0 A& W( O6 J. adecelerates and gradually returns to normal.8,9
1 `. w% [- s& h) o, T3 i  }There are conflicting reports and controversy4 `6 M( ^- Y: c' c: e; t
over the effect of early androgen exposure on adult8 W9 j: l$ n4 ?: e2 Y7 M
penile length.10,11 Some reports suggest subnormal
  M; n9 W: c3 a5 j  l' ]! {0 Xadult penile length, apparently because of downreg-0 ^. `. ~1 O2 \( T
ulation of androgen receptor number.10,12 However,6 \, L, I8 B; |* _0 g/ z3 t. B7 C
Sutherland et al13 did not find a correlation between6 g3 X, _; |+ G- b( a( X/ q
childhood testosterone exposure and reduced adult# [* L2 ~* ~  ?* c* _, [
penile length in clinical studies.( q  U: C% h. S3 P0 J0 J0 }
Nonetheless, we do not believe our patient is
5 X+ [( Q0 K' k  v  Kgoing to experience any of the untoward effects from
" S5 g6 U/ Y8 I# q- E" ctestosterone exposure as mentioned earlier because, E; g, s. A0 y$ B. l4 q
the exposure was not for a prolonged period of time.
7 @2 H. ]  O; A) F8 A$ ~4 C# |Although the bone age was advanced at the time of3 c9 o# v+ L3 Q8 _5 k7 R' H) W
diagnosis, the child had a normal growth velocity at) x3 g3 Y- e: f
the follow-up visit. It is hoped that his final adult
4 y/ D$ T0 M" U( _) D% [2 p+ |+ dheight will not be affected.6 Z' u; E9 g$ }$ ]
Although rarely reported, the widespread avail-) h0 z2 ^* T0 o% R
ability of androgen products in our society may
1 {; V  O1 S; [* r# v; Jindeed cause more virilization in male or female/ p0 @3 j) T. m% V6 d8 l
children than one would realize. Exposure to andro-2 H8 @  k% Y9 H. \2 G7 R$ P
gen products must be considered and specific ques-; X  k# a6 `+ ~
tioning about the use of a testosterone product or: v! j9 ]7 k2 ]+ j+ N: Q1 s
gel should be asked of the family members during
) ]" a1 w* u, V& e" Vthe evaluation of any children who present with vir-
3 U. v; i& d- |5 h: p/ z2 H- |8 Qilization or peripheral precocious puberty. The diag-! N) T& j! O2 n! C9 w2 O
nosis can be established by just a few tests and by
' u% R+ v; X* cappropriate history. The inability to obtain such a
: o- L# L) L( G  V. P* C2 |6 Fhistory, or failure to ask the specific questions, may
- j. |+ k! W& O, cresult in extensive, unnecessary, and expensive( u6 W' q+ m- q. o
investigation. The primary care physician should be
' g4 h/ f7 e% _' P" L% f! ]6 Raware of this fact, because most of these children/ e: Q6 u8 A) B: ~" B  Z% T1 h: V1 ^
may initially present in their practice. The Physicians’
1 W) C% l6 ?  d+ TDesk Reference and package insert should also put a+ q- C6 W4 D* z# [
warning about the virilizing effect on a male or9 J" y% k! H' v) X; q/ a3 ]) b/ D
female child who might come in contact with some-
4 B- V  O5 a5 E2 Lone using any of these products.
! H2 x$ n+ r: X( ?0 e7 dReferences- T/ C( i* A, T. s2 U3 U
1. Styne DM. The testes: disorder of sexual differentiation
0 K9 k. ^+ O; ]" p6 e0 S* Y5 a- Fand puberty in the male. In: Sperling MA, ed. Pediatric
' F6 u6 ?/ `/ K& r, l: @7 w( [* ?' cEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;1 P" {8 q" D: U) i7 }$ d& n
2002: 565-628.' m% ]( x& g$ B5 M0 I: A+ c
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
& A! W$ Z5 G& c' Z& V+ [) b( Tpuberty 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!
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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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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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