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Sexual Precocity in a 16-Month-Old
' B' F5 r# \# d1 G5 \0 nBoy Induced by Indirect Topical
3 }- r+ B$ o; CExposure to Testosterone- \# h, E; h5 H
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2$ j4 F" ]3 W; U4 u. h
and Kenneth R. Rettig, MD1$ W( P# K6 L2 l* A0 t
Clinical Pediatrics5 {5 A# M7 K! q2 {0 `
Volume 46 Number 66 B3 B  T, l5 }7 k# B
July 2007 540-543
. W7 l! e, ]% }' [© 2007 Sage Publications4 a$ w( i7 p8 n. }! J* R" ?9 H
10.1177/0009922806296651% D/ }( S1 c1 d) R1 v6 t& }- p
http://clp.sagepub.com' M- ?& j5 e5 H; I4 r, @. P
hosted at
' i; l1 \* }: f* shttp://online.sagepub.com
2 m+ T& w$ q2 p# t7 ~8 yPrecocious puberty in boys, central or peripheral,
) [" l# O  d, P$ h! ais a significant concern for physicians. Central
3 b4 U# w# o. R) D) F9 Nprecocious puberty (CPP), which is mediated
* y8 e4 o6 J& Lthrough the hypothalamic pituitary gonadal axis, has
7 _& ]" H! Y) M- a; Fa higher incidence of organic central nervous system
5 T7 q, `2 {0 c3 B% l6 j, k# Rlesions in boys.1,2 Virilization in boys, as manifested$ O: O0 u' P8 a
by enlargement of the penis, development of pubic
$ A( `5 ?7 Z0 B6 y3 fhair, and facial acne without enlargement of testi-
0 h9 V4 X" z" }6 Z% Qcles, suggests peripheral or pseudopuberty.1-3 We
# ?& W6 B& |2 F7 l9 N4 _report a 16-month-old boy who presented with the
  M, P; t  a2 g! h- X2 i4 U4 h# Senlargement of the phallus and pubic hair develop-; {4 @% l/ r# X& ?% q, D; d2 N2 w
ment without testicular enlargement, which was due$ d! h$ v  r! u8 n6 v- A
to the unintentional exposure to androgen gel used by
  P. e) r" ]$ F0 l1 g2 p$ wthe father. The family initially concealed this infor-
( g! Q& j7 V5 N" N9 Gmation, resulting in an extensive work-up for this
+ @$ V  R. b' n" I% z5 j2 O* ]child. Given the widespread and easy availability of
, c/ [$ o# }4 O& }, Z& h6 M  Ztestosterone gel and cream, we believe this is proba-' c9 M, r) ?: k$ @, L' i) U
bly more common than the rare case report in the- ~8 ~3 v/ `3 E3 `+ G0 ]' R6 a
literature.4
9 V7 u& S" Y4 W+ HPatient Report' T$ T# W" G9 ~. I
A 16-month-old white child was referred to the
. P1 H. R' w5 d! {endocrine clinic by his pediatrician with the concern
' b1 h1 b$ U6 Q/ x0 z: hof early sexual development. His mother noticed
0 x- N& H+ E' b) X7 r8 Qlight colored pubic hair development when he was2 y# Q6 l7 H" ]' A$ w6 j
From the 1Division of Pediatric Endocrinology, 2University of
( @3 ~1 k- x! R" Q0 cSouth Alabama Medical Center, Mobile, Alabama., A0 D  M7 }. O* q7 G% R
Address correspondence to: Samar K. Bhowmick, MD, FACE,
3 w6 C' O5 q; {9 \; n' Y& `Professor of Pediatrics, University of South Alabama, College of6 D9 |0 Y' W  y% g: e, ]
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
4 M, _4 a5 u. }6 pe-mail: [email protected].
2 A0 R! X4 X3 pabout 6 to 7 months old, which progressively became
* \2 n6 X3 M9 M- e* hdarker. She was also concerned about the enlarge-6 N2 S, a; a4 ]8 n1 b  p
ment of his penis and frequent erections. The child
2 R+ Q5 c4 y) ?: Twas the product of a full-term normal delivery, with7 Z$ q" ], o* F* y: `7 O- ]1 W
a birth weight of 7 lb 14 oz, and birth length of
5 c3 j9 S; f5 v% c20 inches. He was breast-fed throughout the first year
: b% c, C( I+ c$ f( ]- hof life and was still receiving breast milk along with- W8 B* v$ s% W# B
solid food. He had no hospitalizations or surgery,
" G3 x' s1 y$ C  ?) S' Hand his psychosocial and psychomotor development$ U( H5 X. w) f7 Q; W
was age appropriate.6 |% u( _4 \$ L! }  l
The family history was remarkable for the father,
0 V1 s  Z7 [1 R) T" N& w9 lwho was diagnosed with hypothyroidism at age 16,/ `$ x* {/ c6 m$ X* U
which was treated with thyroxine. The father’s/ |5 L( o5 [4 N; H
height was 6 feet, and he went through a somewhat9 c& c+ v1 }8 J# N; o: i; g
early puberty and had stopped growing by age 14.
+ H5 |8 _: C( {0 O; y$ r4 dThe father denied taking any other medication. The
3 I/ i5 ~% R# x5 s% p, Echild’s mother was in good health. Her menarche1 Q9 s; w. \8 i% O
was at 11 years of age, and her height was at 5 feet
! l  C  c. h% k5 inches. There was no other family history of pre-
: W' m' y$ P( l" ^3 V  O  n! `cocious sexual development in the first-degree rela-9 G: h  O& a) p# p0 i4 }
tives. There were no siblings." D2 c& a* d( \4 y1 e
Physical Examination
1 {. M& C/ U2 V# s; }! S4 IThe physical examination revealed a very active,- f+ F; C! d0 |6 ]0 q3 a( I+ X
playful, and healthy boy. The vital signs documented+ d! z6 p! i8 j# k  P& H, h0 L% k0 a
a blood pressure of 85/50 mm Hg, his length was
2 O! |# j. x  ?- a- n  n# I90 cm (>97th percentile), and his weight was 14.4 kg: M( k* K7 u" X6 L. h, T# g
(also >97th percentile). The observed yearly growth% @/ a4 a- [# b: R; I
velocity was 30 cm (12 inches). The examination of
5 X7 @/ h! N. Y% e1 a% k/ ?; Y* k& Gthe neck revealed no thyroid enlargement.
0 c' j! i: |9 E9 R, M& NThe genitourinary examination was remarkable for
9 h6 k: c/ J* genlargement of the penis, with a stretched length of8 f) j% I8 p( k# ^3 e( G' s
8 cm and a width of 2 cm. The glans penis was very well4 V4 }6 l; K% i8 O$ r& l6 Z
developed. The pubic hair was Tanner II, mostly around
7 l- z5 m. c; e' ?6 Y540
8 S7 p) F! ]4 K0 o: p5 K& qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ h" m( e# ~; y" j1 r( p) L
the base of the phallus and was dark and curled. The/ W3 @9 Q$ g2 F4 H! q$ w# V" }* A
testicular volume was prepubertal at 2 mL each.
) o: k4 o% Q6 p) \. U- ?The skin was moist and smooth and somewhat
1 p( r7 \. I# F0 Y& V* U; I* m( aoily. No axillary hair was noted. There were no
, R( x" s1 n# c  _abnormal skin pigmentations or café-au-lait spots.
8 V1 d5 L  m- H6 r0 uNeurologic evaluation showed deep tendon reflex 2+  w5 S; x* W$ x5 G* a( u+ J7 x2 A, P
bilateral and symmetrical. There was no suggestion# z3 H1 Z- T. _9 z
of papilledema.' c+ p  R$ Y$ ^* P+ g. g
Laboratory Evaluation
3 A; p8 d# Q; ~' mThe bone age was consistent with 28 months by4 i( U9 \5 x0 s$ E$ R- A. d
using the standard of Greulich and Pyle at a chrono-
% j# W4 E' W4 W0 ~0 Klogic age of 16 months (advanced).5 Chromosomal
" e( x. }& t, ?! Skaryotype was 46XY. The thyroid function test
$ G, J3 z4 x* ~' Mshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
& K1 S. u' U9 ]7 alating hormone level was 1.3 µIU/mL (both normal).
% |& Y( P: p$ {" rThe concentrations of serum electrolytes, blood
2 [1 D6 j: L5 }# iurea nitrogen, creatinine, and calcium all were
7 d% x! x) i) bwithin normal range for his age. The concentration
) ^# K0 @3 \7 O  zof serum 17-hydroxyprogesterone was 16 ng/dL
- W1 P! `. {4 O- P(normal, 3 to 90 ng/dL), androstenedione was 20
/ v9 H: C/ k' b7 ^8 Yng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-( Y2 m& C/ ]& D$ d% `
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
: D5 j. ?) X9 {5 A, p% Sdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
( ?! R3 _) l- f' J- Y; {' J8 M49ng/dL), 11-desoxycortisol (specific compound S)
- e- \  O( W) c9 \4 Rwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
0 m" h/ a0 A# ctisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' R$ |, p' V; K! o
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
# I! J( P% i8 H' }" G/ D% Mand β-human chorionic gonadotropin was less than
: `3 _& |7 e' |& Q, @5 mIU/mL (normal <5 mIU/mL). Serum follicular
2 l8 e" E( A) q2 c) ]1 x% A  n7 jstimulating hormone and leuteinizing hormone. O! q) {2 Z, C. m6 o* ?5 A; u, z  N3 f4 o
concentrations were less than 0.05 mIU/mL8 R) X0 l9 A8 g: F
(prepubertal).
- o+ w' A; x5 J; L# J! gThe parents were notified about the laboratory- @; }5 M& U4 {& h
results and were informed that all of the tests were$ [5 Q0 a$ C4 h9 Q5 c
normal except the testosterone level was high. The8 d. D1 Y: K  ?% C
follow-up visit was arranged within a few weeks to
7 L0 ^6 i+ m! ^0 a* ?6 g- `obtain testicular and abdominal sonograms; how-
4 H& k) }6 l$ Y9 H5 m$ |3 y# Iever, the family did not return for 4 months.6 p. y+ r: E5 M; d+ _
Physical examination at this time revealed that the5 O. Y1 `: X# d8 q. E) ^4 \- f
child had grown 2.5 cm in 4 months and had gained
* i2 G( P2 L" U4 X* |' W# X2 kg of weight. Physical examination remained, y/ k; {1 _1 L; Z* x, ^9 l" G
unchanged. Surprisingly, the pubic hair almost com-
( p3 G) o& Z3 ^pletely disappeared except for a few vellous hairs at0 p( t/ A# ?4 u8 I
the base of the phallus. Testicular volume was still 2: x9 u9 F6 L  @1 @
mL, and the size of the penis remained unchanged.
6 @  T. P4 g* B, L4 j- {) ?The mother also said that the boy was no longer hav-
! l. c8 g( D) F: \ing frequent erections./ i3 ?; v6 _. p' I' h: D
Both parents were again questioned about use of
' U5 l7 ?  y6 k# q( v# O" Y( ~any ointment/creams that they may have applied to
  D' X. B8 G" }2 d8 o0 Othe child’s skin. This time the father admitted the
+ a" P5 z0 x$ A/ {Topical Testosterone Exposure / Bhowmick et al 541  T- N3 b7 @0 L; y3 x
use of testosterone gel twice daily that he was apply-) |& s# s7 v- |+ {% x+ B( B3 h7 }
ing over his own shoulders, chest, and back area for
9 Z& ?% x4 P  ^) I4 S1 V# r$ u1 _a year. The father also revealed he was embarrassed: d7 n, e! M9 r7 m9 P
to disclose that he was using a testosterone gel pre-
5 _( Y  T' C% R3 L  t! @scribed by his family physician for decreased libido
  f4 k  R4 |( p6 Csecondary to depression.
7 u8 D, }% ~" qThe child slept in the same bed with parents.
3 _, z# U. |% W: K8 ]. ]The father would hug the baby and hold him on his
7 ?( Y3 H& S0 [7 s! O/ [6 Uchest for a considerable period of time, causing sig-
/ @; h" L- b( L# j# jnificant bare skin contact between baby and father.
1 t5 C6 ^8 o7 f& sThe father also admitted that after the phone call,
$ Y7 Z6 h. [" s% qwhen he learned the testosterone level in the baby
& L8 X' }0 A/ @/ c0 ?+ dwas high, he then read the product information) M8 o' u: E( n+ i
packet and concluded that it was most likely the rea-3 x9 Y- ?" k- `! J2 I
son for the child’s virilization. At that time, they
  P' X6 v- b/ x2 c- F: `decided to put the baby in a separate bed, and the. X  c7 [: m3 d5 k
father was not hugging him with bare skin and had
$ @5 h: G! ~" Dbeen using protective clothing. A repeat testosterone- d( }5 E7 o4 l0 I
test was ordered, but the family did not go to the' V. H# D) M) Z+ ]* x; U+ ~2 j
laboratory to obtain the test.
2 U; E2 Y9 Z0 n' [% z9 wDiscussion
9 B! A8 X" t! p  E% B3 r1 SPrecocious puberty in boys is defined as secondary1 Q6 L# c% O/ O! _! g) p( `5 y
sexual development before 9 years of age.1,4
  h: Z. J# T. ^Precocious puberty is termed as central (true) when3 R3 H# d0 S, G2 o& {( P
it is caused by the premature activation of hypo-. Z8 b6 e6 M$ }& r5 E. b# X, Y
thalamic pituitary gonadal axis. CPP is more com-3 v4 r  H5 w3 S
mon in girls than in boys.1,3 Most boys with CPP
0 b8 s8 g! M  amay have a central nervous system lesion that is/ o6 M- V/ f% V/ B3 A) u
responsible for the early activation of the hypothal-' V: x8 i& H( A
amic pituitary gonadal axis.1-3 Thus, greater empha-8 a0 S5 v( A8 g" w+ `, Z  t
sis has been given to neuroradiologic imaging in) w& O* z, A8 b; N' h
boys with precocious puberty. In addition to viril-" w* l8 n: E$ Z2 ~' x4 u( C
ization, the clinical hallmark of CPP is the symmet-
& R, r2 F: ?3 j0 drical testicular growth secondary to stimulation by
/ b) M* m, k) }9 T$ dgonadotropins.1,3
  E8 K  {' e+ MGonadotropin-independent peripheral preco-& R  H- `# x" `9 Q( x! Z
cious puberty in boys also results from inappropriate, z7 Z0 w  X, D3 v+ K8 K2 b( L% g
androgenic stimulation from either endogenous or
$ @8 S  K( y0 O, I9 Hexogenous sources, nonpituitary gonadotropin stim-; N9 r6 c4 Y1 k, e, K* O& d
ulation, and rare activating mutations.3 Virilizing" ?. K& `  Y8 R! c9 w  ]8 @8 G1 L8 q
congenital adrenal hyperplasia producing excessive
% V9 E+ i! U5 P1 f  E. u, dadrenal androgens is a common cause of precocious! A* g* u6 F4 ~
puberty in boys.3,4: Y- ~, a% n0 u: w( _& `
The most common form of congenital adrenal
6 k3 ?" x+ f0 @8 Bhyperplasia is the 21-hydroxylase enzyme deficiency.$ K4 F$ g/ w5 ^( B) e7 A" Z
The 11-β hydroxylase deficiency may also result in. d2 g/ `( _! ~( b  Y2 l
excessive adrenal androgen production, and rarely,
: q1 a8 d6 J" g9 P+ Xan adrenal tumor may also cause adrenal androgen: L8 d# y- W8 G5 x' h7 }( t
excess.1,3
8 ~/ x5 E. J3 m) Z, C+ U% gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* M8 Q" L/ u' x8 c# R
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007( x7 ]' G1 g2 W/ x6 ~% N
A unique entity of male-limited gonadotropin-
& r  P4 _% T0 d$ Tindependent precocious puberty, which is also known
1 H5 y7 N) W. u6 G! W# B3 K+ k+ @as testotoxicosis, may cause precocious puberty at a
- q3 X* T3 ~+ |, q2 \very young age. The physical findings in these boys$ g/ ]/ ^2 F' }: z0 y- _
with this disorder are full pubertal development,
2 T4 Q) Z7 {5 G# z% C8 rincluding bilateral testicular growth, similar to boys
. Q( _7 Y2 n, F: xwith CPP. The gonadotropin levels in this disorder
" q; b+ V2 \  ?; Vare suppressed to prepubertal levels and do not show
0 r$ Y: e6 g8 ~$ jpubertal response of gonadotropin after gonadotropin-  E. X! I  {5 e( d
releasing hormone stimulation. This is a sex-linked
+ k+ v9 a" Z& Y  ?+ Uautosomal dominant disorder that affects only
  |% w6 b. z" f0 L; Omales; therefore, other male members of the family# X# _2 ^( z' c& w
may have similar precocious puberty.3
5 F+ ], X  J" h  g# GIn our patient, physical examination was incon-
$ g# E- G6 |/ i! s- s0 `sistent with true precocious puberty since his testi-4 g0 W8 e  z3 G7 K: w% w* `
cles were prepubertal in size. However, testotoxicosis2 E& `, d; ~3 `* G" A/ g. z
was in the differential diagnosis because his father
( I" Q9 g+ r# N8 s; a. n: xstarted puberty somewhat early, and occasionally,* R+ V2 p2 B" `2 M  J( T0 \1 R. i
testicular enlargement is not that evident in the  A! `9 v$ d. U
beginning of this process.1 In the absence of a neg-' O: E2 g' u$ R( N
ative initial history of androgen exposure, our
3 b: r3 E& D; u* f& N7 Bbiggest concern was virilizing adrenal hyperplasia,* t" o. a. b/ z' `+ Q
either 21-hydroxylase deficiency or 11-β hydroxylase3 ~: M4 ?$ O  V4 f; }3 U1 [7 n6 h
deficiency. Those diagnoses were excluded by find-
2 n, j: [/ W/ G; [2 o/ W' Ting the normal level of adrenal steroids.1 x$ b' K$ O8 E
The diagnosis of exogenous androgens was strongly' i% q8 Y0 o# b
suspected in a follow-up visit after 4 months because
- o: C8 g# U( W  Z; V: Ithe physical examination revealed the complete disap-
+ Y9 M% L( C+ ~5 {, R9 f) x' }pearance of pubic hair, normal growth velocity, and
+ v7 c! d% u. @* S- g$ }  Q$ rdecreased erections. The father admitted using a testos-, K( q0 I9 y6 j$ c& R% i% E
terone gel, which he concealed at first visit. He was
5 u4 E9 K9 I/ U! h1 N+ _! c0 \using it rather frequently, twice a day. The Physicians’" h0 E( T3 ~0 b% ?- r/ j
Desk Reference, or package insert of this product, gel or
- Y8 b/ `5 o" T$ l. \6 wcream, cautions about dermal testosterone transfer to& V2 b' Y, D$ `" U: J
unprotected females through direct skin exposure.
& s6 ^$ S' Q' Z( f: E$ bSerum testosterone level was found to be 2 times the5 s" n4 @  c  v
baseline value in those females who were exposed to' f( t2 c$ z0 c8 q# T
even 15 minutes of direct skin contact with their male
1 x- I4 M- d; X) c4 ~partners.6 However, when a shirt covered the applica-6 C: J3 \3 ?, U$ b4 g9 }  G# T
tion site, this testosterone transfer was prevented.
2 R% a$ K6 A1 i8 C% r4 ~: d' BOur patient’s testosterone level was 60 ng/mL,7 w) G# n. S( g8 n# F. b' M- ?1 A
which was clearly high. Some studies suggest that% |7 Q1 p* E: B* X! w% @+ p, d
dermal conversion of testosterone to dihydrotestos-
' d. X+ a4 b$ g- X4 L; dterone, which is a more potent metabolite, is more
- c9 N+ F- ?) G% ?active in young children exposed to testosterone
' c* F3 b" b3 l2 ~0 kexogenously7; however, we did not measure a dihy-5 i! l& T  X% l) j  j5 w
drotestosterone level in our patient. In addition to
$ V. \7 ?: b& f$ T( @virilization, exposure to exogenous testosterone in
7 f: X" b. s3 nchildren results in an increase in growth velocity and6 I/ Y9 _$ \3 S- f( g$ b
advanced bone age, as seen in our patient.  W* I* [$ s/ h& e: o% S  n, s
The long-term effect of androgen exposure during
# r5 L/ a3 j) A  u/ N4 k) Kearly childhood on pubertal development and final+ Z0 n( ~  L$ K/ T% G
adult height are not fully known and always remain7 y: {* i1 n. R3 ~/ _+ z/ `& m2 q
a concern. Children treated with short-term testos-3 }$ p+ ?6 O7 c+ `+ E
terone injection or topical androgen may exhibit some# o+ }% W% G: F# F
acceleration of the skeletal maturation; however, after
+ h. i- N( \+ D4 P! R2 ucessation of treatment, the rate of bone maturation
3 l7 X  ^* m$ {5 [# ^decelerates and gradually returns to normal.8,9- L3 W( d/ A% P4 y2 [
There are conflicting reports and controversy$ h* ]& m3 P8 a1 b
over the effect of early androgen exposure on adult
9 Z  G# ]" u6 r$ `( xpenile length.10,11 Some reports suggest subnormal
2 _$ c5 Y# v; j4 h6 X* B: Iadult penile length, apparently because of downreg-+ `) X5 F& {* {+ m( E/ Y
ulation of androgen receptor number.10,12 However,. t9 K0 j2 L& A4 q
Sutherland et al13 did not find a correlation between
5 _+ l7 W- F" E" _" P: u: Dchildhood testosterone exposure and reduced adult9 Z# e1 s# ]0 V* f
penile length in clinical studies.6 q! X2 p) x- P
Nonetheless, we do not believe our patient is
2 A1 y+ Y) n6 U. @" v/ O, o* r) rgoing to experience any of the untoward effects from
. X$ g1 y  m( ?; B" m$ stestosterone exposure as mentioned earlier because
- \1 V& L% U( A: t2 T3 A. L% C  |the exposure was not for a prolonged period of time.
. R5 e# T8 f3 [3 z% D% ~Although the bone age was advanced at the time of
2 V+ }# {1 C" l9 adiagnosis, the child had a normal growth velocity at, D5 Z6 N; _* @: n5 K
the follow-up visit. It is hoped that his final adult
3 u5 W, p, D) }1 S9 H. k5 {: {height will not be affected.
8 L6 k4 j6 y: i0 WAlthough rarely reported, the widespread avail-
9 S. b( G! d8 a5 _, a0 Wability of androgen products in our society may, ^& J* X, M- i0 S* o
indeed cause more virilization in male or female6 f8 S6 e; i+ l
children than one would realize. Exposure to andro-1 r5 f3 M: ~' L
gen products must be considered and specific ques-
' c9 d+ V6 v1 J3 }tioning about the use of a testosterone product or7 O$ X2 N  i# a4 c3 r; F
gel should be asked of the family members during  a2 o9 {# G& \
the evaluation of any children who present with vir-
7 P1 R) L, ^" J0 @, W8 Tilization or peripheral precocious puberty. The diag-
% O" T; h1 ^& z- Inosis can be established by just a few tests and by
' g+ }: Y: ?3 k# d' R$ K, q% Mappropriate history. The inability to obtain such a
, G4 c( {8 ^# thistory, or failure to ask the specific questions, may
9 i3 J; X5 X1 v  r  \result in extensive, unnecessary, and expensive
: Q: Z% Q6 j! [+ Qinvestigation. The primary care physician should be$ @  D5 f# A7 [( `! H
aware of this fact, because most of these children1 U2 T# m, i! N/ ]5 m5 H
may initially present in their practice. The Physicians’
& \& q/ F5 J7 mDesk Reference and package insert should also put a
2 D1 m* T6 K, Bwarning about the virilizing effect on a male or
! z- o  v: Y* o, B5 ^! b! Qfemale child who might come in contact with some-
( D' U; N( d( eone using any of these products.
4 c1 }( F5 |# {% ?( oReferences/ x1 I9 L8 Q* }! [: p  P
1. Styne DM. The testes: disorder of sexual differentiation2 ?* f9 h2 S. l$ W* d
and puberty in the male. In: Sperling MA, ed. Pediatric: _, x& M# S9 r% b" z, h6 n9 B
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;# ~# E) y9 Z+ w! {& c: v1 r
2002: 565-628.* W) ?) o1 @& V- G# x
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious9 A% Y3 b% X4 t- q$ e
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
3 C3 B# d* V9 KBoy Induced by Indirect Topical$ y. J2 F5 g2 m5 w- @
Exposure to Testosterone+ Z0 H3 f8 M' V4 w7 q$ ~6 G9 B
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. ^5 d+ ?* b. |' F1 c% [
and Kenneth R. Rettig, MD1
& o+ O( j/ N* l* `Clinical Pediatrics
7 p1 k& v% D- a) v. TVolume 46 Number 6* ^9 \, ?9 B, r/ m, K, R* L
July 2007 540-543
8 z* m- B, r. O! W2 ?" ~© 2007 Sage Publications7 @  k# }) u0 G. \4 f- h
10.1177/0009922806296651" F1 ~. Q. f% K8 h' N
http://clp.sagepub.com8 ~. S: y+ K  r1 S$ V+ A- B
hosted at
# ?. {: Y( k* q/ Chttp://online.sagepub.com
# e: b3 K1 s' n( ePrecocious puberty in boys, central or peripheral,
! U4 q' V6 Q8 l, K$ g- ^- |, A2 Tis a significant concern for physicians. Central& A! w( _9 o. Q* l6 @, \3 \
precocious puberty (CPP), which is mediated
) r+ e& I- E7 A; U! m; Y5 |through the hypothalamic pituitary gonadal axis, has
7 p+ G4 w  }& z+ s) K8 aa higher incidence of organic central nervous system
! t8 w3 k3 K8 ^1 o# V8 ilesions in boys.1,2 Virilization in boys, as manifested( h0 D9 F" X9 @5 f
by enlargement of the penis, development of pubic) C) h( n  ?" H( Q1 S
hair, and facial acne without enlargement of testi-
; ^" \, R: b  d8 k8 a2 xcles, suggests peripheral or pseudopuberty.1-3 We
  t6 F; Y3 k+ m% n5 r% Breport a 16-month-old boy who presented with the
* p% v3 K( s8 Z8 I: menlargement of the phallus and pubic hair develop-) F: W6 q+ Z: q/ H
ment without testicular enlargement, which was due
, O- i7 |) ]9 {: s$ O' K3 `to the unintentional exposure to androgen gel used by
0 y! G2 {8 B+ N- w5 s. {the father. The family initially concealed this infor-1 o5 @0 @$ P) z* E/ F" B
mation, resulting in an extensive work-up for this$ V3 ?' L8 C  o/ G9 q  D
child. Given the widespread and easy availability of+ x* ]5 `( N) b3 K
testosterone gel and cream, we believe this is proba-
; N, g7 d+ Y( F% K0 G" ^  |% gbly more common than the rare case report in the
1 f; x6 ]: K, z8 _  ~literature.4  j% P! U. W8 `2 E! H
Patient Report
: [) H7 H" b7 C3 h) W: Z5 L' p+ dA 16-month-old white child was referred to the
' A# w" p% ]0 s  X3 {+ Pendocrine clinic by his pediatrician with the concern
4 y. ?+ |$ X. C7 z7 @of early sexual development. His mother noticed( _+ H; ^5 P0 P1 _
light colored pubic hair development when he was: \* f% ?; p" B. r
From the 1Division of Pediatric Endocrinology, 2University of( ?% h+ D  X+ g2 H& w
South Alabama Medical Center, Mobile, Alabama.8 ?$ R3 c! f% k  E
Address correspondence to: Samar K. Bhowmick, MD, FACE,8 H) U3 f+ ?3 _) Y' [. p
Professor of Pediatrics, University of South Alabama, College of3 Z2 e  F! `/ T/ R1 i3 E
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
7 Q: r( N8 W! \e-mail: [email protected].
+ {+ ?& K/ Y+ C* e* B0 c$ r/ ^# }( I2 V) babout 6 to 7 months old, which progressively became( K& p* s) U& z
darker. She was also concerned about the enlarge-6 U5 R- S+ @/ s  ^4 t9 b% L3 l  p/ ?
ment of his penis and frequent erections. The child
- N3 n, A' g+ @9 Iwas the product of a full-term normal delivery, with
: @2 {9 A' N: h1 ^6 s+ ka birth weight of 7 lb 14 oz, and birth length of
, m9 m" y$ B& |# Y* z/ J8 Y( u# @8 G20 inches. He was breast-fed throughout the first year
: ?  b+ P- e9 u( P' Y# Mof life and was still receiving breast milk along with
, ]1 Z7 q: G; u0 V! Y. @solid food. He had no hospitalizations or surgery,- r" I: z8 O  R% |- V
and his psychosocial and psychomotor development5 R. [; d. f2 O! x
was age appropriate.) [3 h% Z$ s2 l- {5 i/ _0 }- r
The family history was remarkable for the father,
. t* V4 @! V- X5 p8 M5 S& |who was diagnosed with hypothyroidism at age 16,
( ?3 Z. K" O- j9 a8 d# kwhich was treated with thyroxine. The father’s
3 \! h: E" T3 R% b$ \$ Eheight was 6 feet, and he went through a somewhat
* F% _# r9 w$ M, \early puberty and had stopped growing by age 14.
" a6 R' _* f" t% p7 J+ j: zThe father denied taking any other medication. The
2 b4 f9 a0 U; q& o1 `child’s mother was in good health. Her menarche
1 Y$ ~( C& k3 e9 xwas at 11 years of age, and her height was at 5 feet8 C. x% {6 |8 D( v# D
5 inches. There was no other family history of pre-
" O$ C; a- J$ D& |) ycocious sexual development in the first-degree rela-! y1 w% V) j4 \3 B  u* ]
tives. There were no siblings.
/ h, V# L5 P2 E& \: m9 oPhysical Examination
0 i, s: F; L# ^' qThe physical examination revealed a very active,7 x/ G8 k# \' N7 W. _- K" v1 B
playful, and healthy boy. The vital signs documented
2 \7 p2 R" y! g1 s* P4 b4 l9 Ka blood pressure of 85/50 mm Hg, his length was9 h0 T( `# B; A+ D
90 cm (>97th percentile), and his weight was 14.4 kg
" l7 w* z! T" W, p% f# ?(also >97th percentile). The observed yearly growth  c5 A9 o8 d( w# A1 v- \8 B
velocity was 30 cm (12 inches). The examination of
* P* Y8 U) X& ^+ ^8 L7 ~6 p; ethe neck revealed no thyroid enlargement.
$ n$ L0 x' q+ j" S+ Z1 f: PThe genitourinary examination was remarkable for
& C/ V0 q* x  R3 ^enlargement of the penis, with a stretched length of
0 J9 P" @4 \' ~! f3 b/ t5 Q8 cm and a width of 2 cm. The glans penis was very well( E4 j0 \, U4 o$ q
developed. The pubic hair was Tanner II, mostly around
; ~6 l/ k! ~  g' l0 s2 b8 o540- b+ k6 ?$ W) y4 L! ?+ \
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: ]2 |! n/ a5 w# O* ]4 c& x
the base of the phallus and was dark and curled. The2 `# B$ u6 }& }  T; o
testicular volume was prepubertal at 2 mL each.
4 V0 ~% O0 u0 dThe skin was moist and smooth and somewhat
, ?7 j' M5 l: M7 P8 M: C" woily. No axillary hair was noted. There were no
5 p  B  ^1 h: J6 ?abnormal skin pigmentations or café-au-lait spots.
% {: {# l7 M$ m' g2 GNeurologic evaluation showed deep tendon reflex 2+$ K" |$ I( m- o/ b
bilateral and symmetrical. There was no suggestion
+ a1 T7 N5 `1 g2 sof papilledema.% n3 s/ O1 G1 ]% H  L6 p& U/ j
Laboratory Evaluation5 ~9 ?1 r6 M& _/ r
The bone age was consistent with 28 months by
4 z7 ~, e1 u4 S1 gusing the standard of Greulich and Pyle at a chrono-
7 b0 `. q% `' O+ B; Q4 k; ?9 ylogic age of 16 months (advanced).5 Chromosomal
. n: H0 n% L5 z# Z" ], ]karyotype was 46XY. The thyroid function test
# m7 B8 N8 E+ a. O" b4 [$ xshowed a free T4 of 1.69 ng/dL, and thyroid stimu-" J, _6 ]6 U- E3 c# q4 k& }
lating hormone level was 1.3 µIU/mL (both normal).
% v) ^. n% K' {+ r6 X- wThe concentrations of serum electrolytes, blood% \3 x( Y# u' s! ~6 _# a, l
urea nitrogen, creatinine, and calcium all were
+ g# x' k/ L1 w, R* p( V# p! qwithin normal range for his age. The concentration0 Q* Y; ^) I9 u# d% u
of serum 17-hydroxyprogesterone was 16 ng/dL. s" L' z" H, S0 b& Q5 x- U5 ]
(normal, 3 to 90 ng/dL), androstenedione was 200 I5 z- K/ {9 r% n1 f; ~" o) V
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-* ]2 K; r) E) {, C, ?
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
- Z9 [% Y" K7 w6 A4 cdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
( ~9 k- O: |- o3 B49ng/dL), 11-desoxycortisol (specific compound S)' @. S! G$ f; a, E9 A% S+ l6 I
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
0 x% G, U! ^% Qtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total. x. p/ }& a1 Y; z. K# W
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
; c/ N. c: y- B$ ~6 b1 ~and β-human chorionic gonadotropin was less than
! f8 v! h0 O0 q2 [6 j5 mIU/mL (normal <5 mIU/mL). Serum follicular
% h" o; O* l& Z" J' ]8 Hstimulating hormone and leuteinizing hormone
+ r- ]* C$ I: |$ h- econcentrations were less than 0.05 mIU/mL. C, i, i: g+ H& ~
(prepubertal).
# }* u7 s* Q0 WThe parents were notified about the laboratory# u4 F" Z% ^' b, j8 [  C( |9 k# ~
results and were informed that all of the tests were
6 M$ R- \# C: e7 n4 k# snormal except the testosterone level was high. The! a9 S8 R0 v! j+ H8 c6 q0 U
follow-up visit was arranged within a few weeks to
2 {7 ?2 o8 {& g& E/ V& xobtain testicular and abdominal sonograms; how-# v  _$ @. E% `. F
ever, the family did not return for 4 months.( S' ~9 H7 T- h5 _+ D/ j6 t
Physical examination at this time revealed that the
4 ?( i& N5 Y. u( H9 M% C7 U; hchild had grown 2.5 cm in 4 months and had gained2 m( N1 h& |* `% \) q3 B
2 kg of weight. Physical examination remained# D6 K; t* v- O$ i' v
unchanged. Surprisingly, the pubic hair almost com-
9 y. B$ `' j& i* y& \pletely disappeared except for a few vellous hairs at! S& i/ H4 G7 M2 e/ J' ^$ C) [
the base of the phallus. Testicular volume was still 2& l% C% u% S6 o# M' o& q* E
mL, and the size of the penis remained unchanged.
( E4 `+ ^1 H& BThe mother also said that the boy was no longer hav-
# ~) ^4 Z- o8 n: k7 ving frequent erections.
0 t  l+ h6 r7 h) I/ R  YBoth parents were again questioned about use of; g. ]8 q0 q2 c
any ointment/creams that they may have applied to
- A% _: h4 W1 l$ K6 p3 d6 t6 tthe child’s skin. This time the father admitted the
# m% A* \1 r7 ?9 u8 k; bTopical Testosterone Exposure / Bhowmick et al 541
9 u- V% L  `3 v7 Huse of testosterone gel twice daily that he was apply-
4 g% }! ]: `/ k( i" i1 Uing over his own shoulders, chest, and back area for; C6 K) r% p8 K# [6 _* j
a year. The father also revealed he was embarrassed" Z6 n4 L8 {# ?% s5 t7 q! ~
to disclose that he was using a testosterone gel pre-
9 j" c4 q( E+ F' |2 l' z4 ~scribed by his family physician for decreased libido$ `5 C1 f( W6 [% Q& S2 }" Y& H
secondary to depression.
+ ~4 [1 i; I1 z/ u1 k) cThe child slept in the same bed with parents.
) O3 S: ]: G1 wThe father would hug the baby and hold him on his" C. @* b0 j+ e  }* [8 B' z
chest for a considerable period of time, causing sig-
2 H6 E6 F, R( m( M% Snificant bare skin contact between baby and father.9 g( _7 ?) M5 F
The father also admitted that after the phone call,: T2 G: n9 J3 o1 C6 @3 r
when he learned the testosterone level in the baby' f/ U3 s- j& l+ O/ x( a$ M$ W$ h
was high, he then read the product information
9 w, T1 q0 t) H& J9 Z% zpacket and concluded that it was most likely the rea-$ W; \8 C2 t! @. T% q4 {2 v5 s
son for the child’s virilization. At that time, they
* J6 a2 A" c* y2 Pdecided to put the baby in a separate bed, and the
) E9 v3 ?, \3 m6 C" J6 j* pfather was not hugging him with bare skin and had
' o" p3 L9 G( X9 y( {" B4 a( Bbeen using protective clothing. A repeat testosterone  y% V% \% q5 ?! G" @
test was ordered, but the family did not go to the& p+ R3 D4 V6 Q% s2 W8 }* z5 S
laboratory to obtain the test.+ E% V- d8 Z& k7 ?1 @
Discussion$ v9 j2 ?4 V8 t9 {. T7 k' m
Precocious puberty in boys is defined as secondary
) c1 E. @7 H! q+ B  rsexual development before 9 years of age.1,4
$ i2 N7 M2 h* z9 NPrecocious puberty is termed as central (true) when
& D- `3 ]+ j" m! Lit is caused by the premature activation of hypo-  w5 h" o5 |; E: ]" ~* H0 F* ~
thalamic pituitary gonadal axis. CPP is more com-
' \1 w" W% X7 k) [( Umon in girls than in boys.1,3 Most boys with CPP
6 B' A: Y5 _1 h  A3 F: n$ rmay have a central nervous system lesion that is, W0 E3 w( E' c' [& K
responsible for the early activation of the hypothal-
$ [8 d) n+ `! P/ T# a/ h9 ]amic pituitary gonadal axis.1-3 Thus, greater empha-; O5 h7 Q/ Q) ]+ m% f
sis has been given to neuroradiologic imaging in
' y$ Q# S, x# f" J& eboys with precocious puberty. In addition to viril-. A- p  n: Q0 C. e" s( F" ]
ization, the clinical hallmark of CPP is the symmet-5 q+ f0 F2 H/ q
rical testicular growth secondary to stimulation by* b- R: W9 {, C9 _% g( _2 G+ R' v
gonadotropins.1,3
; t2 p- v* K% x! E+ o' y: i1 r+ G1 mGonadotropin-independent peripheral preco-. A4 ]+ ^' P  h; j" ], A
cious puberty in boys also results from inappropriate6 v: ^# w9 o6 \0 U( @$ D
androgenic stimulation from either endogenous or, Z4 e) ^8 e( }8 b* k! f
exogenous sources, nonpituitary gonadotropin stim-
, I3 W& H( g, L* M4 E! julation, and rare activating mutations.3 Virilizing4 S. b, U3 I+ F! ]# ]
congenital adrenal hyperplasia producing excessive" Z; G8 u# g  ?6 ?! }0 G
adrenal androgens is a common cause of precocious
' K$ Z1 P+ D- \8 t0 {puberty in boys.3,4
$ |: M7 s2 z( a: }. f2 ^, S0 rThe most common form of congenital adrenal
- Z$ u7 E3 Y3 l' O6 c! whyperplasia is the 21-hydroxylase enzyme deficiency.0 K; g. q: f" @* `! l( p- X# x
The 11-β hydroxylase deficiency may also result in
) ]( z5 E7 ^' E5 l6 Yexcessive adrenal androgen production, and rarely,' ?4 i, `3 I" r, W: R
an adrenal tumor may also cause adrenal androgen1 H$ u0 x; U6 P& B
excess.1,3% S  I% x/ z4 ]) f. e) X/ M
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& L  b, e& \  ]  M3 `9 l542 Clinical Pediatrics / Vol. 46, No. 6, July 2007+ k! ]* c4 O) c) ^
A unique entity of male-limited gonadotropin-
# R  K3 p: y" t# v, Sindependent precocious puberty, which is also known9 A+ N5 O1 H" c0 u
as testotoxicosis, may cause precocious puberty at a
5 b, g! {' T2 U& c/ w6 }0 d, g; y0 Nvery young age. The physical findings in these boys
9 t& j% |: A7 A* _with this disorder are full pubertal development,. d5 Q7 R9 }9 p, E3 U. o
including bilateral testicular growth, similar to boys. z3 D: l6 e- K  ^
with CPP. The gonadotropin levels in this disorder
/ k" o. C9 s$ I1 z3 y+ o" l- Eare suppressed to prepubertal levels and do not show  n( U1 t, X& w0 D
pubertal response of gonadotropin after gonadotropin-1 @! U4 Z- ?7 w: E7 a, v
releasing hormone stimulation. This is a sex-linked" }* R/ w! @" |. d0 X8 F
autosomal dominant disorder that affects only
8 L" H+ f. _" L  \+ X+ nmales; therefore, other male members of the family* b) n& n, y5 P8 w- P3 j
may have similar precocious puberty.3
* n- m- S# [( Q6 A9 GIn our patient, physical examination was incon-
. O5 a: D! C3 e; b. P( k! n" Hsistent with true precocious puberty since his testi-: K3 {2 B8 O# z
cles were prepubertal in size. However, testotoxicosis  ~- b/ X% f8 m* U# O
was in the differential diagnosis because his father. B6 ?3 @  G/ m- I
started puberty somewhat early, and occasionally,
/ d8 X1 v+ K, ^/ i, Ptesticular enlargement is not that evident in the
5 h3 M2 @( @( {beginning of this process.1 In the absence of a neg-" T. t1 k/ M7 A# S+ u9 J
ative initial history of androgen exposure, our* o5 o+ @, M+ j! F. i
biggest concern was virilizing adrenal hyperplasia,
# w& Q3 J# l! Z) p; Q# ~. _either 21-hydroxylase deficiency or 11-β hydroxylase
8 @7 ~$ M0 s2 }8 Tdeficiency. Those diagnoses were excluded by find-( f* p7 D6 h* v/ ?( j% p
ing the normal level of adrenal steroids.; c" B1 t* N- T+ e  q  `2 l
The diagnosis of exogenous androgens was strongly
% a. e5 U! X$ x* xsuspected in a follow-up visit after 4 months because) I, b/ T5 W( j6 m
the physical examination revealed the complete disap-
: V4 D. t2 s) h5 `pearance of pubic hair, normal growth velocity, and
( i, \6 c. p( D! O, ldecreased erections. The father admitted using a testos-, X5 O: W0 E5 P' w
terone gel, which he concealed at first visit. He was: ]3 N! q, r: O. h, E+ [# k: ]
using it rather frequently, twice a day. The Physicians’
  }. F" B4 ^6 [  }& t: K% f1 xDesk Reference, or package insert of this product, gel or: ]: L4 t: M  E: R  |
cream, cautions about dermal testosterone transfer to
' X5 y$ {& P) U  ]( b7 ^& |unprotected females through direct skin exposure.8 O6 A5 G( F/ f. X6 P7 d
Serum testosterone level was found to be 2 times the
4 [$ w7 y2 n" W7 A* J1 J- u, dbaseline value in those females who were exposed to
) J8 L( u$ X* @* Peven 15 minutes of direct skin contact with their male
$ p  u) Q7 F! l2 `( ?partners.6 However, when a shirt covered the applica-9 X: s' u4 `0 u% r, B0 l
tion site, this testosterone transfer was prevented.+ R8 C$ G: h0 j
Our patient’s testosterone level was 60 ng/mL,$ f+ [2 T7 N) ^' E( e" {
which was clearly high. Some studies suggest that; J- X! D5 g+ B8 l" ]) f7 A9 o5 H; s
dermal conversion of testosterone to dihydrotestos-
4 c9 e: |& n3 c, I% d+ {: p* Zterone, which is a more potent metabolite, is more# g" S/ k) B( {
active in young children exposed to testosterone$ V7 c! J1 a) [
exogenously7; however, we did not measure a dihy-( [6 F4 ^2 J1 w8 W& {% k
drotestosterone level in our patient. In addition to
6 O2 A7 C6 ~( ?9 Pvirilization, exposure to exogenous testosterone in
$ E9 q; z5 D3 v6 V! c* ~' S+ ochildren results in an increase in growth velocity and* ?8 A! o2 b) e2 E; q
advanced bone age, as seen in our patient.% s! P1 Y- l( E' X2 o
The long-term effect of androgen exposure during
9 b3 E4 Q  I4 z8 Q) K! ?# Vearly childhood on pubertal development and final4 p8 ^7 C" Z; n+ E7 C" n
adult height are not fully known and always remain
. V+ o+ n6 ^2 wa concern. Children treated with short-term testos-
2 k) k6 x" T. f/ ^, x0 c  wterone injection or topical androgen may exhibit some
& N7 t/ E3 l. i$ K7 ]3 iacceleration of the skeletal maturation; however, after
; G0 R" I" `- R( _cessation of treatment, the rate of bone maturation4 ~" d( I' Y4 }. z
decelerates and gradually returns to normal.8,9/ U$ x! p( e+ F6 m) M
There are conflicting reports and controversy2 a- t0 f' f$ ]; X2 N  p: B
over the effect of early androgen exposure on adult9 _, `# ~- c9 O1 P1 \$ b: }/ m
penile length.10,11 Some reports suggest subnormal& K( ~- o4 p: t/ [9 a0 b8 `
adult penile length, apparently because of downreg-; ~0 d8 A( r$ p+ n  \/ x
ulation of androgen receptor number.10,12 However,0 s0 ^( s+ R* M" J0 e) E, v
Sutherland et al13 did not find a correlation between  C' T- C  i. `
childhood testosterone exposure and reduced adult- b) }( k  o, z2 Z
penile length in clinical studies.4 b1 e7 {8 j8 D9 b. i
Nonetheless, we do not believe our patient is: T6 ^8 I4 |3 t2 U2 d
going to experience any of the untoward effects from+ ~" {! u$ b5 O
testosterone exposure as mentioned earlier because- ?8 ~8 z: J/ P/ e& G2 m2 M! A+ ^
the exposure was not for a prolonged period of time.- k" a# A3 b0 v9 |
Although the bone age was advanced at the time of
; p$ o( k4 O2 S& i6 Fdiagnosis, the child had a normal growth velocity at$ v0 n$ Z; a0 q" q8 ~5 m1 N# m
the follow-up visit. It is hoped that his final adult
% {9 e, G8 }# ~8 k5 {, Y, T9 lheight will not be affected., a7 o% q  `4 j" @, R
Although rarely reported, the widespread avail-
/ Y8 T: O2 ^4 Pability of androgen products in our society may' ~/ T& A: ?- A# C. e* j& N8 x' i
indeed cause more virilization in male or female* `9 o2 I8 Q+ ~- N; C
children than one would realize. Exposure to andro-8 j% `$ j& K9 F' H4 x
gen products must be considered and specific ques-
9 F/ }9 A3 x1 D/ Ptioning about the use of a testosterone product or1 |5 R6 P+ Q: t' J" U% X
gel should be asked of the family members during
, z* ~$ n) T: c: C8 ?! s  }the evaluation of any children who present with vir-; H* Z  L' l- }5 |6 Y% d
ilization or peripheral precocious puberty. The diag-5 v# s. c* Y1 L7 y' X' G
nosis can be established by just a few tests and by, Z: ~% Z* A! x) K4 g5 r7 f  j- R
appropriate history. The inability to obtain such a1 a* u+ B) m7 [6 C- N' g. H$ ]
history, or failure to ask the specific questions, may
+ L4 I/ W6 q3 r. J* ~result in extensive, unnecessary, and expensive2 c/ k# u9 a9 r. w
investigation. The primary care physician should be2 e8 j" o- }& E# i* r! q7 n; I( O
aware of this fact, because most of these children) s; J4 o9 \8 G4 u6 L$ {: W
may initially present in their practice. The Physicians’
* n* f) d6 X! r8 ?( s0 ]! H& O- ?Desk Reference and package insert should also put a7 H8 Z! W2 k3 E1 o8 R
warning about the virilizing effect on a male or
8 M# v% l/ e, N: h% \! S+ Tfemale child who might come in contact with some-
5 @6 X: L: o$ ?4 r! Z) Lone using any of these products.  Y7 L2 y5 |& b3 n. T: W
References
% [. s' y- s8 s. P0 y, _% ]1. Styne DM. The testes: disorder of sexual differentiation
6 b+ J/ U/ R; ]9 k2 o$ tand puberty in the male. In: Sperling MA, ed. Pediatric" _) H+ H7 }7 b* p) ^
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
9 \- K8 w9 p, t2002: 565-628.- x& ~& t- w& g! A) {
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious6 @6 ]  c" G$ U" \$ R# s
puberty in children with tumours of the suprasellar pineal
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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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