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Sexual Precocity in a 16-Month-Old6 ?6 ?, s/ U- s, S( r
Boy Induced by Indirect Topical) \$ Q$ D1 o6 @, |" I1 ^$ W& c
Exposure to Testosterone3 P/ K' v+ U( k, D
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2! s9 e/ c- |4 g% O+ u' E* s
and Kenneth R. Rettig, MD1
+ }. `8 Z1 D% }$ q8 ZClinical Pediatrics
3 s& y/ D2 Q8 c  m# ~, tVolume 46 Number 6
4 v% K: \3 m5 oJuly 2007 540-543
+ o3 R3 R3 u9 T& H( b© 2007 Sage Publications8 \0 ^! l  a! v, ]; l; {  z  T( I
10.1177/00099228062966510 J8 c' d+ H+ N7 \
http://clp.sagepub.com" ?# l, y/ d( n% x6 s; {6 U% |" e: F
hosted at/ k4 T. n  w# m$ P# ^6 h- J
http://online.sagepub.com3 R  Q4 g: P# {- c0 s3 S7 d7 V
Precocious puberty in boys, central or peripheral,0 N6 ?' A/ ]5 Y% K
is a significant concern for physicians. Central3 a2 T# a: _4 \! ^" P
precocious puberty (CPP), which is mediated6 w9 s8 ?. ]2 Q+ Q
through the hypothalamic pituitary gonadal axis, has
% g, _$ ~/ [3 B: za higher incidence of organic central nervous system8 U; ~  u, u- M1 _3 M; Q
lesions in boys.1,2 Virilization in boys, as manifested
0 _0 ], ]2 G- I; qby enlargement of the penis, development of pubic
0 ]' T) g  t0 M$ k; x, A2 q5 L8 Yhair, and facial acne without enlargement of testi-; P3 k; Q) m2 s9 o3 n$ g
cles, suggests peripheral or pseudopuberty.1-3 We$ C6 y- g+ J& C
report a 16-month-old boy who presented with the" \! B6 K# x% A
enlargement of the phallus and pubic hair develop-* n; m6 W9 R+ `4 N* T  G  g
ment without testicular enlargement, which was due$ H* I' b& q, p
to the unintentional exposure to androgen gel used by
; v3 p9 ]7 e9 `) z! P$ Q( n& Tthe father. The family initially concealed this infor-
  b# |7 y$ J. e6 nmation, resulting in an extensive work-up for this1 J- i, |" r) W/ L
child. Given the widespread and easy availability of
: o, C2 I9 n: g6 V0 H) c% ktestosterone gel and cream, we believe this is proba-: r# C; S  u0 W8 s
bly more common than the rare case report in the1 I4 K2 ~- s! N- k
literature.4; J1 [* W! j* i: R- |7 D2 ~# m
Patient Report; `" D7 o" E1 j  B  u! B
A 16-month-old white child was referred to the
2 [& Y9 N' m6 @4 |7 c- Eendocrine clinic by his pediatrician with the concern
% A+ ~# X; f6 ?0 y3 Iof early sexual development. His mother noticed4 O2 ?* j3 A% E. x# {1 M* R
light colored pubic hair development when he was
! }# G2 N2 J3 a7 E* E6 tFrom the 1Division of Pediatric Endocrinology, 2University of
) W; V/ }4 E0 f1 q6 i2 SSouth Alabama Medical Center, Mobile, Alabama.6 b$ ~% y+ f! D
Address correspondence to: Samar K. Bhowmick, MD, FACE," i" }( p8 @% i# p
Professor of Pediatrics, University of South Alabama, College of8 }' c" j* T% g- ~1 P
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
' p1 }9 {" {9 }e-mail: [email protected].
0 q/ ~; x5 a( P; ]. A  babout 6 to 7 months old, which progressively became6 D( Y' u. s: |
darker. She was also concerned about the enlarge-8 R0 j1 Y0 `$ W8 Z. C
ment of his penis and frequent erections. The child
) ^6 H# @$ G0 P9 g" Cwas the product of a full-term normal delivery, with) F' ^$ S" V0 Q
a birth weight of 7 lb 14 oz, and birth length of
" v+ \* }2 s# J4 ~+ s* h20 inches. He was breast-fed throughout the first year0 H% Z, h4 g; s" ^1 Z7 v
of life and was still receiving breast milk along with) j, p9 Q  [  z, n
solid food. He had no hospitalizations or surgery,
; U9 [- U7 g( yand his psychosocial and psychomotor development8 Q: ~' n$ c' e
was age appropriate.; I8 A, _) Z$ o( `0 [9 g; T
The family history was remarkable for the father,' Z+ Q/ ^3 K) s" Q9 d
who was diagnosed with hypothyroidism at age 16,
1 o+ a# D" o+ I3 ]) W9 P; Dwhich was treated with thyroxine. The father’s
. u6 Q' c" ]0 `& cheight was 6 feet, and he went through a somewhat
. w/ C6 h9 E$ U% v) J6 Z/ Yearly puberty and had stopped growing by age 14.
/ {7 H+ f1 }8 x, r5 o: HThe father denied taking any other medication. The; q1 {- d/ {$ P2 A5 G2 C
child’s mother was in good health. Her menarche* n% r: ?4 Z4 u- n
was at 11 years of age, and her height was at 5 feet/ q6 u8 z4 M+ A5 o0 Q! `
5 inches. There was no other family history of pre-6 h- b2 G4 _8 m7 R2 h
cocious sexual development in the first-degree rela-
/ F6 T6 c% }( E: {- otives. There were no siblings.! y5 Y% m$ j0 N  R
Physical Examination% v. {. P9 E9 q3 |2 v! s
The physical examination revealed a very active,
- B$ V# S& C+ e+ Wplayful, and healthy boy. The vital signs documented! z8 |0 f$ ?( Y6 I  q6 l9 W
a blood pressure of 85/50 mm Hg, his length was
# z8 {' {5 a& F0 \; s" U4 L90 cm (>97th percentile), and his weight was 14.4 kg' u# a; h) x0 d" [2 A
(also >97th percentile). The observed yearly growth
3 Z) i% G6 I4 l0 X+ o0 avelocity was 30 cm (12 inches). The examination of/ X! f/ a. G% p  u: E
the neck revealed no thyroid enlargement.
& }0 c8 _) H. V4 c" f, [The genitourinary examination was remarkable for
( P1 p; ?- ~; R7 `0 Z5 w; n6 qenlargement of the penis, with a stretched length of
% X% W7 W7 k" g6 i; r8 cm and a width of 2 cm. The glans penis was very well
0 e. Y3 e; |& Z$ h$ adeveloped. The pubic hair was Tanner II, mostly around( G# @; J+ A1 |/ t1 c* A
540
3 m, }' X' V' y" F: I+ u, Pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 j& ]* C* y) U& H/ a! U
the base of the phallus and was dark and curled. The( N0 F7 I( _% f2 z- r
testicular volume was prepubertal at 2 mL each.: l* l/ B. I/ t  ?0 p, W0 i, l$ j
The skin was moist and smooth and somewhat1 Z  k' s; o* }$ z, y- Y
oily. No axillary hair was noted. There were no% P. k5 q: D( [  B; H8 a# g
abnormal skin pigmentations or café-au-lait spots.
; @5 `% V7 Q2 [  V! ]Neurologic evaluation showed deep tendon reflex 2+, Y9 \1 z  R& i, t( l4 Q8 z1 n
bilateral and symmetrical. There was no suggestion
/ _- g" a# G6 R0 cof papilledema.
# p% E' y0 ]0 R7 vLaboratory Evaluation/ J: }- `; X9 Y* B5 J3 s) }
The bone age was consistent with 28 months by' L1 V. l9 ~% @& P, L. ~1 C- j
using the standard of Greulich and Pyle at a chrono-. ]+ y( U+ }; t0 m! L' y: A
logic age of 16 months (advanced).5 Chromosomal/ q$ a6 [( N* _7 S4 ]1 h
karyotype was 46XY. The thyroid function test
: ]% x+ ?% k0 ~showed a free T4 of 1.69 ng/dL, and thyroid stimu-- v  f3 L& C9 ^7 \* f
lating hormone level was 1.3 µIU/mL (both normal).; J  p  l+ l' C% k- K5 B  @/ D7 i
The concentrations of serum electrolytes, blood* f$ g/ r7 U! t7 G# X
urea nitrogen, creatinine, and calcium all were+ u% X; Q& i8 D; ]5 s
within normal range for his age. The concentration
: W7 Q, k2 S8 w  uof serum 17-hydroxyprogesterone was 16 ng/dL
5 _( ^" ]3 c% T(normal, 3 to 90 ng/dL), androstenedione was 20
' Q6 B/ f) f: I4 lng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
9 _  r; T$ {. [2 T! h1 aterone was 38 ng/dL (normal, 50 to 760 ng/dL),
& t1 P: i6 `4 @* o8 u! d& u1 Udesoxycorticosterone was 4.3 ng/dL (normal, 7 to
9 `% N5 Z% p. F2 d2 g3 \49ng/dL), 11-desoxycortisol (specific compound S)6 ~' w7 `7 I1 m# [4 t
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-% u7 A9 j; |8 W) \1 k6 T) b" M
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
) w2 A: Q) G7 c; V+ ]testosterone was 60 ng/dL (normal <3 to 10 ng/dL),* }4 I( c* z- `1 k
and β-human chorionic gonadotropin was less than& e& w1 a" n3 D% I5 r" H$ d
5 mIU/mL (normal <5 mIU/mL). Serum follicular6 p1 e& J6 H! y
stimulating hormone and leuteinizing hormone/ O; j) p7 N) x5 a) R: O7 R
concentrations were less than 0.05 mIU/mL3 b5 Y% ^2 U5 ?" e# Q
(prepubertal).
: _. F3 t" D8 u& A% c+ a/ ^The parents were notified about the laboratory
" {' S7 L  Y3 r0 J! z7 e9 cresults and were informed that all of the tests were
* ?9 n, a" u, j$ V+ r. k" a; k( Lnormal except the testosterone level was high. The  s; L% ~; P* P4 U1 s- ?9 Y
follow-up visit was arranged within a few weeks to
/ d4 N6 g. e( P. {- ^. Aobtain testicular and abdominal sonograms; how-' e( [7 ]. L9 Q: q2 _
ever, the family did not return for 4 months.
* T/ J5 I- S+ ]' I! lPhysical examination at this time revealed that the9 ?4 f' M6 H2 x. n8 a
child had grown 2.5 cm in 4 months and had gained
, i# x) n  E+ i  O7 e2 kg of weight. Physical examination remained7 i8 [( v9 N1 l  [, X2 H& b
unchanged. Surprisingly, the pubic hair almost com-
7 G7 F# j% R4 o$ }& w7 Upletely disappeared except for a few vellous hairs at2 Y! z7 B! k# a6 q( g
the base of the phallus. Testicular volume was still 2
4 k" A# p9 `0 l2 M7 o% Z6 k3 P% kmL, and the size of the penis remained unchanged.
* o! J0 z2 r# h+ ^8 {The mother also said that the boy was no longer hav-  z) ~) c* O- h2 F1 Z- d, {6 }
ing frequent erections.6 F( x. [6 N% M: O  n& K
Both parents were again questioned about use of
! a1 j, x& A" ~) ~any ointment/creams that they may have applied to2 o- N; b- v7 P2 }6 F2 c  a; H, R
the child’s skin. This time the father admitted the
, Z  p5 _4 C- S: y6 ^6 R# Y; E0 }Topical Testosterone Exposure / Bhowmick et al 541
2 p1 B  ?) ^' ~$ L/ ~% {, m$ Luse of testosterone gel twice daily that he was apply-
& ^1 m- \9 Y0 n* zing over his own shoulders, chest, and back area for/ x0 _' c3 t2 ~$ C, n( t7 K
a year. The father also revealed he was embarrassed( ^- U8 O* ^/ `6 |# O9 p: x# ]
to disclose that he was using a testosterone gel pre-* R! l2 W! q9 a* g
scribed by his family physician for decreased libido
; z" b6 y) Q1 B$ y! u( Msecondary to depression.
% N- W0 o/ ?: L7 Y: F. ]The child slept in the same bed with parents.
1 ^9 i$ A+ d) W, S( [: w2 [* G. UThe father would hug the baby and hold him on his6 l7 J' b0 ~) n
chest for a considerable period of time, causing sig-
) L+ o% r7 m8 {4 Anificant bare skin contact between baby and father.
( M4 S/ `" s8 |/ x$ U  W( {The father also admitted that after the phone call,+ G' r9 d: C8 S4 |6 n/ M: N) y) n
when he learned the testosterone level in the baby
. s! @% C6 \" D1 x0 ~: B0 f8 }& u6 qwas high, he then read the product information+ Z! b% j% k8 _6 h5 r8 c! h  T! P, t
packet and concluded that it was most likely the rea-1 c2 Y7 p6 o- T7 w8 K$ P: u; f! M
son for the child’s virilization. At that time, they) x/ z2 M, k: \% k. J! A( w
decided to put the baby in a separate bed, and the
" }! ~/ G( _" U0 tfather was not hugging him with bare skin and had
* l& ~6 |* ]  Q: kbeen using protective clothing. A repeat testosterone1 y- s# X5 \8 c4 a
test was ordered, but the family did not go to the
% R" L; u1 Z" `! v5 m& Olaboratory to obtain the test.
3 Q, e; U& B+ _4 p/ W* `# GDiscussion) F  J2 |* b+ B
Precocious puberty in boys is defined as secondary: `: ?# u7 @) ]
sexual development before 9 years of age.1,4; N5 ?0 j$ z' \: r" z
Precocious puberty is termed as central (true) when
, S3 v) i  S+ a6 q6 S! h* rit is caused by the premature activation of hypo-: ]- u: c: n& x% m4 t
thalamic pituitary gonadal axis. CPP is more com-
. Y! j+ N2 P  w% D1 M/ y% `mon in girls than in boys.1,3 Most boys with CPP/ y4 r. b  i3 T# |4 E8 q5 p+ i
may have a central nervous system lesion that is4 \2 Z! T3 _6 z! x1 j
responsible for the early activation of the hypothal-% K7 w% |2 R% r- k( Q# v5 q2 l
amic pituitary gonadal axis.1-3 Thus, greater empha-/ Z" _$ N* Y1 Y9 W4 Z6 a% D: ^
sis has been given to neuroradiologic imaging in# [# f) {+ c; k: p+ G8 M) y
boys with precocious puberty. In addition to viril-5 v& E5 q- Z$ O$ c6 U3 y
ization, the clinical hallmark of CPP is the symmet-
/ V; t5 D" _/ m/ Xrical testicular growth secondary to stimulation by
9 q! W. M5 G8 `; wgonadotropins.1,32 D5 n, z" b2 n
Gonadotropin-independent peripheral preco-
3 o  x# G. k7 kcious puberty in boys also results from inappropriate
' K% u9 v% Z$ P/ ]" v; `, Candrogenic stimulation from either endogenous or. M+ z* z* v( O/ a
exogenous sources, nonpituitary gonadotropin stim-3 r7 `# q$ ~& D) r4 i; t4 W
ulation, and rare activating mutations.3 Virilizing
0 \7 K5 C# o5 G2 O0 ocongenital adrenal hyperplasia producing excessive- e* M, Z! t% z# F1 F2 g3 Q) m
adrenal androgens is a common cause of precocious# y, G2 G' D2 C
puberty in boys.3,4/ r5 H& `1 k7 ~
The most common form of congenital adrenal& h: x' i' w3 L7 L8 _
hyperplasia is the 21-hydroxylase enzyme deficiency.: p3 k9 O; M, R
The 11-β hydroxylase deficiency may also result in9 w' {3 a+ c0 O" s8 }5 h
excessive adrenal androgen production, and rarely,
5 S& P' |5 i) c8 _$ Lan adrenal tumor may also cause adrenal androgen7 `9 L" q0 Y+ ~) a2 Q8 m
excess.1,3- t5 C  y1 N+ k9 w6 b, n' L" x
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& K: x* d. W7 A& b, U6 T) P. g* z
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
' k* N0 A9 M5 X) JA unique entity of male-limited gonadotropin-
7 F$ z& n: ?% ~/ F" T+ }- mindependent precocious puberty, which is also known
  {$ b9 w5 ~- l5 u1 Z3 Sas testotoxicosis, may cause precocious puberty at a
- H9 j6 P& ~& x+ F8 d5 Overy young age. The physical findings in these boys; V4 }+ w% O6 M$ U
with this disorder are full pubertal development,) ?/ k2 I% u$ O: C& J- o
including bilateral testicular growth, similar to boys1 l# f% R! \; `/ C- T- p
with CPP. The gonadotropin levels in this disorder
+ }" e& o5 d6 T% r( n: v9 Iare suppressed to prepubertal levels and do not show
) g) G4 F8 m- _3 b, o6 c' x& |% B! Upubertal response of gonadotropin after gonadotropin-3 L8 c* V6 ?9 Z
releasing hormone stimulation. This is a sex-linked9 L; c! ~  ]) e
autosomal dominant disorder that affects only
5 D! v# y4 b) e/ C9 Q  |males; therefore, other male members of the family
9 b& G4 x" E/ F% a; r  _2 omay have similar precocious puberty.3( {3 F8 o8 n1 g" d$ j  g- E: L
In our patient, physical examination was incon-
0 ^5 |8 [, k5 rsistent with true precocious puberty since his testi-- ^6 ^. V9 i# j. \" H) d1 w2 F
cles were prepubertal in size. However, testotoxicosis7 z0 n/ I' m# `! v
was in the differential diagnosis because his father% o0 ?+ i) ]  X( A9 E
started puberty somewhat early, and occasionally,7 H2 f2 R) V; ^7 l
testicular enlargement is not that evident in the. e( a" L5 q, t( n' [2 F. E
beginning of this process.1 In the absence of a neg-/ _4 c* {- O7 r4 s9 s
ative initial history of androgen exposure, our
) s: f7 p1 W3 y' [9 F4 {biggest concern was virilizing adrenal hyperplasia,
/ P5 O3 O7 M$ k" ?0 t- A0 o3 A7 m7 ~0 Leither 21-hydroxylase deficiency or 11-β hydroxylase
- Y7 r- t1 M2 x& I1 zdeficiency. Those diagnoses were excluded by find-: r, F$ T1 j  J6 q* M
ing the normal level of adrenal steroids.* J/ ]. K2 T2 m7 n, t4 o
The diagnosis of exogenous androgens was strongly# U6 C/ i/ |+ B9 b! G+ K3 F. u
suspected in a follow-up visit after 4 months because
6 J6 P, X  f$ K1 S5 {the physical examination revealed the complete disap-
( `5 ?* e- p/ j5 s) k& K2 opearance of pubic hair, normal growth velocity, and6 U4 j7 X* d! O, P  T
decreased erections. The father admitted using a testos-
" s- a# P. o5 l0 F0 \  O  G) dterone gel, which he concealed at first visit. He was3 U# a& u& q- u+ `' Z5 e
using it rather frequently, twice a day. The Physicians’
. |" }& _1 A( B! p, bDesk Reference, or package insert of this product, gel or
0 a( l% a3 g/ W  [. s  @7 q/ }cream, cautions about dermal testosterone transfer to6 S( W5 h8 {5 c% Q
unprotected females through direct skin exposure.
$ ]+ q. O) x0 X; v# }  A& @Serum testosterone level was found to be 2 times the
: A* Z7 J6 ~8 H* R: D1 ubaseline value in those females who were exposed to) ?2 ~2 O/ d9 ~' @. `  U
even 15 minutes of direct skin contact with their male# f9 Z! b6 Y4 Z! l3 x! Z
partners.6 However, when a shirt covered the applica-) b- r7 Q' \! s/ l2 Q- d# @
tion site, this testosterone transfer was prevented.
) O$ x  }0 A9 u! oOur patient’s testosterone level was 60 ng/mL,
  q" |' Z) \, b# Qwhich was clearly high. Some studies suggest that5 M, T9 S5 i& z7 a
dermal conversion of testosterone to dihydrotestos-) ^  p7 V& F; M3 [. e0 X. k
terone, which is a more potent metabolite, is more' r3 ^6 a- y6 R) f3 B
active in young children exposed to testosterone
9 E- _9 e/ _, x6 v6 zexogenously7; however, we did not measure a dihy-
. k& R7 N' A/ S: Qdrotestosterone level in our patient. In addition to2 V" @2 D) I' H0 ?
virilization, exposure to exogenous testosterone in
* k9 q& h* _& }0 t# x* uchildren results in an increase in growth velocity and% |$ e1 g6 m; X) j* h& z
advanced bone age, as seen in our patient./ ~+ C* k% h* `$ r" E8 j
The long-term effect of androgen exposure during
4 U- O: D: W1 K0 Q  N- Gearly childhood on pubertal development and final+ S3 C+ h. K+ S  Y. N/ b
adult height are not fully known and always remain
9 c/ N5 Q$ ~* o6 }5 E0 w+ l1 j- ~a concern. Children treated with short-term testos-
5 L/ M' ~- @' D* O5 [terone injection or topical androgen may exhibit some4 P1 Y. h2 _% k
acceleration of the skeletal maturation; however, after. L' l& k, G  `1 L
cessation of treatment, the rate of bone maturation
$ p# ]" [% p+ Tdecelerates and gradually returns to normal.8,9' {  N. S$ L/ _' K8 \- `, v
There are conflicting reports and controversy  D! s7 U# ]3 W6 B# T' K: w1 w
over the effect of early androgen exposure on adult
: F8 v1 v5 Y! D# A3 Hpenile length.10,11 Some reports suggest subnormal
4 b$ `* T- u9 D- U( N9 Badult penile length, apparently because of downreg-
& h+ i6 ?# v- r* [1 @ulation of androgen receptor number.10,12 However,. t* {7 g# P, c# p
Sutherland et al13 did not find a correlation between5 u4 d9 c- N1 u* T
childhood testosterone exposure and reduced adult
$ d! E$ U/ V8 s4 j( openile length in clinical studies.
! q2 i4 Y, u" f( ?; ZNonetheless, we do not believe our patient is
4 A( F9 t/ M9 n  q% P* Qgoing to experience any of the untoward effects from
' k4 L8 }) s$ F/ w$ i! G+ Htestosterone exposure as mentioned earlier because% s" d# b* U; U1 f' k
the exposure was not for a prolonged period of time.6 x- f, s; C# B3 q7 X2 N
Although the bone age was advanced at the time of
; E, R& X+ [  ~' Pdiagnosis, the child had a normal growth velocity at! L  C1 F% _* `5 L: C
the follow-up visit. It is hoped that his final adult
$ r% q9 f2 [; \$ t9 vheight will not be affected.
0 g  \, `1 j2 `% j! |5 K0 y+ q. dAlthough rarely reported, the widespread avail-
$ `1 i' R. }/ Kability of androgen products in our society may
  W* q. C& |8 g# d3 Tindeed cause more virilization in male or female
' @2 q7 m+ {. P* u$ J: A# F" Vchildren than one would realize. Exposure to andro-
' T& ^- N1 A" n7 i8 R; Ugen products must be considered and specific ques-
  L  s$ M  u& Z* O# vtioning about the use of a testosterone product or& z; J2 H. o0 a8 y" W/ m, n
gel should be asked of the family members during/ C# Z7 [. }# w; x
the evaluation of any children who present with vir-5 S; I* @% G( L: ~( S7 u
ilization or peripheral precocious puberty. The diag-; u) U9 Z! F9 P% d0 x7 x: u
nosis can be established by just a few tests and by; n4 U) b7 R. z+ o
appropriate history. The inability to obtain such a  _% e# L6 j( \
history, or failure to ask the specific questions, may* |4 `7 `3 S. P; B. w5 ~# B4 U  p
result in extensive, unnecessary, and expensive/ i, X% ?% b/ `0 i) y
investigation. The primary care physician should be& {' C: _! k8 z; z& w6 ]' d* ?, g
aware of this fact, because most of these children, K9 ?4 P1 a% ?& I5 o! \
may initially present in their practice. The Physicians’
. x/ }0 s( k# Q4 p2 |  v. y2 c- |Desk Reference and package insert should also put a# a' ~6 Y' P- M: N% _
warning about the virilizing effect on a male or3 t8 M) z2 Q+ \; ~# C
female child who might come in contact with some-, X$ U$ d2 w2 g+ m% ~
one using any of these products.8 R0 ?# s; V& e
References7 ]" S. [% I. z  ]
1. Styne DM. The testes: disorder of sexual differentiation( p1 S! w! u. \% i
and puberty in the male. In: Sperling MA, ed. Pediatric4 Y* a  h* [% j( ^
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
) x/ w) q; I# b7 x- i6 S2002: 565-628., O) h/ o  w* ]
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious4 o# U' W/ a" T' z3 V! F- g( {
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old. u; e9 q" a, K4 K( u3 [
Boy Induced by Indirect Topical& Y+ h' w  X9 ^- r4 n0 ^; n; l
Exposure to Testosterone. [" Q0 ~: v8 [
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2$ @/ F: w  z5 c; ^- g6 Q: }! p# Z8 x
and Kenneth R. Rettig, MD1
, e' g2 |% ?( YClinical Pediatrics" g. O: K4 O+ y# Q: S  ^: ~
Volume 46 Number 6; I* ^4 \; i# l3 J! N- t" q
July 2007 540-543# S# d% _4 ]* A3 J8 u) x) G
© 2007 Sage Publications
, l6 C/ X6 Y4 U; t9 }  q10.1177/0009922806296651  q# p  L- j' F
http://clp.sagepub.com8 ]4 u8 `9 A& M( z3 w
hosted at
' A7 i* c) Q" S4 c& F7 K6 `; J# yhttp://online.sagepub.com; U9 x2 i  R! i2 g& J) B
Precocious puberty in boys, central or peripheral,
1 e) e, a1 o% l+ a, J* G* Bis a significant concern for physicians. Central3 m5 S5 p2 G$ R
precocious puberty (CPP), which is mediated8 u/ `6 g$ a6 D* }( O
through the hypothalamic pituitary gonadal axis, has3 w/ E8 _* \1 u8 C
a higher incidence of organic central nervous system
( l8 k) X& q: f" \0 {lesions in boys.1,2 Virilization in boys, as manifested
' {1 J# _3 h2 |by enlargement of the penis, development of pubic% Q8 M. n0 x# |
hair, and facial acne without enlargement of testi-# C# w: K7 H4 {) g! t: {
cles, suggests peripheral or pseudopuberty.1-3 We
/ J$ L* g: i& ?4 `! treport a 16-month-old boy who presented with the
: I$ Q- M0 a8 G6 r0 ?enlargement of the phallus and pubic hair develop-, Q3 z, ?6 b( X& L. y/ U- D
ment without testicular enlargement, which was due$ u$ i2 L' k% h+ ~+ L6 e2 W) K/ m
to the unintentional exposure to androgen gel used by& [) G" f# U! Z1 i
the father. The family initially concealed this infor-
% J4 J1 H% ?7 _: f) Tmation, resulting in an extensive work-up for this
: Y- H9 X5 J! k. O+ |child. Given the widespread and easy availability of: g1 s% e3 @# ~' v9 S
testosterone gel and cream, we believe this is proba-' }6 y% l: i& h
bly more common than the rare case report in the
, i3 ^* G% K( X. Aliterature.4
' c* x) s* y" x7 c$ ?! GPatient Report3 z. F9 e; O# H, {+ y
A 16-month-old white child was referred to the
4 x) v9 z! i; I( ?& k7 r3 L! v4 Cendocrine clinic by his pediatrician with the concern
4 d7 G- _2 d5 d9 f4 aof early sexual development. His mother noticed* L3 G) {3 E7 K! U9 i
light colored pubic hair development when he was
% T9 g1 A( g+ q) u2 ~7 YFrom the 1Division of Pediatric Endocrinology, 2University of( h, R: K$ W$ C1 |. ]0 ^
South Alabama Medical Center, Mobile, Alabama.
# D; Y4 c/ I3 f! HAddress correspondence to: Samar K. Bhowmick, MD, FACE,
6 I" [' F1 E" W8 G( HProfessor of Pediatrics, University of South Alabama, College of% T( h8 b. k7 S
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;7 d+ U$ |/ z  U4 d4 u( ^
e-mail: [email protected]." Y/ d, H4 v/ r
about 6 to 7 months old, which progressively became
& Z; `$ |9 f, b/ edarker. She was also concerned about the enlarge-
* g- G9 g# h3 {! Sment of his penis and frequent erections. The child8 d3 P# V5 I3 t0 ]4 T
was the product of a full-term normal delivery, with2 m0 }2 n0 u9 c8 o* L1 M
a birth weight of 7 lb 14 oz, and birth length of
, Q" Q9 A5 h! [6 p5 X+ |1 O! J1 [, _% o20 inches. He was breast-fed throughout the first year
& W+ p+ d6 L$ u% K* Dof life and was still receiving breast milk along with
' |0 a8 c& J! m) Tsolid food. He had no hospitalizations or surgery,
/ f' {$ L1 M! Z* r6 S6 @and his psychosocial and psychomotor development
) O, ]) Z; D5 O6 ?* ?+ K# cwas age appropriate.
0 y' m) V/ _- m5 a0 {The family history was remarkable for the father,( q5 r. d; e/ y  M+ ]
who was diagnosed with hypothyroidism at age 16,6 w1 k6 s. I" j, z
which was treated with thyroxine. The father’s
" i) Q; l/ y8 J% n& c. sheight was 6 feet, and he went through a somewhat! Z. ^* n8 f- t% a# L5 t" P
early puberty and had stopped growing by age 14.
8 M4 a1 T) K- k" p5 SThe father denied taking any other medication. The( B0 r1 o$ n1 _
child’s mother was in good health. Her menarche
0 A+ r+ N1 h6 b: F2 i" P, a/ Fwas at 11 years of age, and her height was at 5 feet
6 E1 }. d, n1 m5 inches. There was no other family history of pre-7 f. Z5 }, u/ K. r! ~" k
cocious sexual development in the first-degree rela-1 t* l6 i& q  v3 ?: F2 q" o! _8 d4 B
tives. There were no siblings.4 n$ p/ L: p  ^4 \5 t
Physical Examination
8 y6 \& k9 L6 T8 n% \The physical examination revealed a very active,
+ S2 k8 C9 C! x4 z3 a, ^+ Jplayful, and healthy boy. The vital signs documented: L$ L+ t4 Q" J" j& K
a blood pressure of 85/50 mm Hg, his length was
$ i. X5 ]1 y5 Q1 [' I( Z  o$ F" f90 cm (>97th percentile), and his weight was 14.4 kg
3 L7 M# ~7 `! c% Z/ _$ x(also >97th percentile). The observed yearly growth
0 b" W0 E6 c! i- z  i8 Lvelocity was 30 cm (12 inches). The examination of
8 f' ]: e  g6 R, {! h, `7 n+ {9 Wthe neck revealed no thyroid enlargement., v( H  o+ O7 B4 P, s% g- M
The genitourinary examination was remarkable for
& b6 K4 F8 F& _% O0 w/ Lenlargement of the penis, with a stretched length of. P& z( n  P. A. {* l3 s5 w" d% X
8 cm and a width of 2 cm. The glans penis was very well
5 G8 F% E4 n3 ]( X. Ndeveloped. The pubic hair was Tanner II, mostly around
* X" Y( M; Y& Z( p# M540
- g" q( t, q# O. H) ]at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from" q; t- @) _8 A5 K: ~. _" r
the base of the phallus and was dark and curled. The" T. ]9 B5 o' t
testicular volume was prepubertal at 2 mL each.& }! N& z* c8 L
The skin was moist and smooth and somewhat* q, q1 [" }6 r3 m: ~* h
oily. No axillary hair was noted. There were no' K/ [, W& G% \6 _: F0 k
abnormal skin pigmentations or café-au-lait spots." Z. E9 U4 _, X& r1 b: H# E) v
Neurologic evaluation showed deep tendon reflex 2+" H& G8 [1 D/ G7 a6 X- v
bilateral and symmetrical. There was no suggestion
$ d- Z- |& z4 d2 ^; k. j3 v& A, C, o* uof papilledema.! V" ^- w3 b/ B7 Y3 M3 g" n
Laboratory Evaluation6 x* f4 a* E$ P6 S5 s. s
The bone age was consistent with 28 months by
! m7 h% o6 T* f) F* s! j' susing the standard of Greulich and Pyle at a chrono-" v2 q) x- X. k: c' m
logic age of 16 months (advanced).5 Chromosomal
0 p$ F) m9 ?* `karyotype was 46XY. The thyroid function test* A8 l) K/ R. X& C( D
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
* U' s" {# @- Z3 k3 E- wlating hormone level was 1.3 µIU/mL (both normal).6 u7 ]. H( p% ^. L# @* z# b8 u* W9 N
The concentrations of serum electrolytes, blood
& z6 [9 C% f& P5 C8 n2 Lurea nitrogen, creatinine, and calcium all were
+ g) A- o) z9 Xwithin normal range for his age. The concentration
" I) N7 g2 `- w1 A8 l( \, Iof serum 17-hydroxyprogesterone was 16 ng/dL
6 Z) f3 }* ]$ d9 H(normal, 3 to 90 ng/dL), androstenedione was 20* ]. a" ]5 B; w& ]
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
& X+ W" V7 h# Pterone was 38 ng/dL (normal, 50 to 760 ng/dL),
3 W9 t  o5 a8 _5 m/ ldesoxycorticosterone was 4.3 ng/dL (normal, 7 to
$ }. I8 f- W2 q1 k49ng/dL), 11-desoxycortisol (specific compound S)0 o% J# q; m% D- d4 p: b
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
' z7 ]) u  e  L2 L( @tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
4 I8 _& a" ~4 _% E4 q& dtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
/ b9 t! H+ `8 Gand β-human chorionic gonadotropin was less than; V( h* ], w+ |. ]% B& E6 K' r, E
5 mIU/mL (normal <5 mIU/mL). Serum follicular
# W5 D* V) F( V/ S$ l1 Z4 \$ c( pstimulating hormone and leuteinizing hormone
9 q% ~, g8 U* c5 I9 t1 F# S' E4 econcentrations were less than 0.05 mIU/mL
& s5 ]" u2 ^( \" x8 }& t: [5 A! z(prepubertal).
" j+ R: l$ Z2 Q+ ?' o3 P- W% c& R9 NThe parents were notified about the laboratory- t6 \. \- k5 T' S  [
results and were informed that all of the tests were
* Z) K3 k6 v- h* vnormal except the testosterone level was high. The- A+ o# s0 u* T
follow-up visit was arranged within a few weeks to
$ g- }* d8 D5 |, P5 ~1 I4 e. \: eobtain testicular and abdominal sonograms; how-
; h/ z7 Z8 d% wever, the family did not return for 4 months.
" @/ J( k6 g" D; \/ p8 e6 pPhysical examination at this time revealed that the) D* D. F6 V5 T+ `7 Z: D
child had grown 2.5 cm in 4 months and had gained
* ^# B, P) T: {+ k2 kg of weight. Physical examination remained7 J5 ^1 u4 Q: h8 t
unchanged. Surprisingly, the pubic hair almost com-
6 X1 w+ m( [8 k" a* @8 X4 Q1 rpletely disappeared except for a few vellous hairs at
5 q- c- D" ]6 N5 W; Q( Hthe base of the phallus. Testicular volume was still 2+ k: y) ^2 r6 n  K9 Y; w
mL, and the size of the penis remained unchanged.
  Y% Z) K  J5 d8 L* J! x  {The mother also said that the boy was no longer hav-
9 Y! [; [  {: t6 v2 t5 King frequent erections.; \$ K6 b" D4 y# W6 [+ ]  b
Both parents were again questioned about use of' N6 m5 W0 s3 E9 p9 o' j
any ointment/creams that they may have applied to) F, `5 t9 P' e) F6 M& d
the child’s skin. This time the father admitted the
. {5 R. N$ H4 T. v' d5 CTopical Testosterone Exposure / Bhowmick et al 541" o! E+ ]  o. W6 w
use of testosterone gel twice daily that he was apply-/ z2 Z9 U' Q0 L7 Z: [! |/ _- H
ing over his own shoulders, chest, and back area for
/ J, [8 T' V- I9 \5 d) C' J( ga year. The father also revealed he was embarrassed$ Y" C  l+ f! t7 ^/ n; B+ a* {/ \
to disclose that he was using a testosterone gel pre-4 w3 ^! `$ l  T$ A+ ^# _
scribed by his family physician for decreased libido
* G9 u8 [& J7 t6 i- e- d4 X' {( a! k) Psecondary to depression.. }: g2 R! X  \7 j* M) v( ~
The child slept in the same bed with parents.4 ]* ?( |% a, R
The father would hug the baby and hold him on his
7 L# f* y3 p) q- j' J0 a6 m! Dchest for a considerable period of time, causing sig-
" u/ x2 h. F. Cnificant bare skin contact between baby and father.
* m2 @! b5 _3 G! ~' w# kThe father also admitted that after the phone call,% f9 D, s$ P/ t( P) f
when he learned the testosterone level in the baby% e( X# j" s( ?
was high, he then read the product information
1 S  [7 D, L4 `6 Zpacket and concluded that it was most likely the rea-$ t4 Z3 c( x; g( v3 q+ Q
son for the child’s virilization. At that time, they
7 E. U& p/ N! w0 N+ `7 W9 x. V) }* Kdecided to put the baby in a separate bed, and the( J! b2 ]$ W+ T2 U( m- K! X; V% Q9 i
father was not hugging him with bare skin and had3 \5 Y: M/ h& m
been using protective clothing. A repeat testosterone1 T! h& i) W5 V% l+ z
test was ordered, but the family did not go to the
1 o; p; S: G9 E. alaboratory to obtain the test.
# c! q- Y! T: o( P( y0 W0 U: k$ TDiscussion
# p, ?4 o! u" \% t3 W% hPrecocious puberty in boys is defined as secondary
  Q. G3 c2 x: ?2 g& N. esexual development before 9 years of age.1,4% Y0 P9 s4 k/ J/ H% o* `7 D; o
Precocious puberty is termed as central (true) when5 i5 [4 K5 d* F" m( c& [
it is caused by the premature activation of hypo-
1 B5 U5 @9 ?8 s6 ethalamic pituitary gonadal axis. CPP is more com-  C* S( {* C" W9 j; x" c' a( i$ \
mon in girls than in boys.1,3 Most boys with CPP% T8 k8 R2 D# o7 \
may have a central nervous system lesion that is. L2 Y- A, v' G+ ?* G; ~6 r7 o: p: W
responsible for the early activation of the hypothal-
9 a2 P5 v% Z: ~, damic pituitary gonadal axis.1-3 Thus, greater empha-8 _( U- `2 Z+ }; j4 l& i
sis has been given to neuroradiologic imaging in3 N+ L6 L  p( x6 {1 B8 l( n3 J
boys with precocious puberty. In addition to viril-
. E/ d. P( T9 ~ization, the clinical hallmark of CPP is the symmet-
3 [+ V% a* i9 Xrical testicular growth secondary to stimulation by
/ p: a8 C) L" H  {8 ]' n! Dgonadotropins.1,3, K6 \4 b- y0 W* w  S
Gonadotropin-independent peripheral preco-
$ W7 `5 V; o5 _cious puberty in boys also results from inappropriate' W+ d6 I4 Z. P, B, P& Q
androgenic stimulation from either endogenous or$ {0 @% l7 @% w
exogenous sources, nonpituitary gonadotropin stim-
0 f" T1 n. L( j  X8 Aulation, and rare activating mutations.3 Virilizing
  c) D, b1 E: S% `. J  tcongenital adrenal hyperplasia producing excessive* D# ^( F  ]* t. s0 o1 I
adrenal androgens is a common cause of precocious
2 q3 L0 K8 P, o. cpuberty in boys.3,4' u8 L& g& ?  h# C
The most common form of congenital adrenal" h* o0 Z+ a, u0 a7 l! {
hyperplasia is the 21-hydroxylase enzyme deficiency., N' e1 F+ b+ B+ w# F* ^
The 11-β hydroxylase deficiency may also result in
( O9 e. o. j' ^7 Q; W; }- pexcessive adrenal androgen production, and rarely,
) U0 O  b3 i& O6 z0 b6 m) r, Q/ Dan adrenal tumor may also cause adrenal androgen
. G  u$ J, {% I: _4 @excess.1,3! Y1 p' `; t6 O' m
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) j- {5 |$ Q0 s( ^3 k! E2 {542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
4 n& L6 ]. F8 D. sA unique entity of male-limited gonadotropin-* l* U% U$ L1 g' T& O# s
independent precocious puberty, which is also known
0 f- @. b( g7 x' q0 t2 _as testotoxicosis, may cause precocious puberty at a  o- [) n7 k/ u% q  C  n8 [0 {
very young age. The physical findings in these boys# w7 m  q& s& N2 O+ n4 Y$ Q
with this disorder are full pubertal development,
! c8 x" ^+ x& [9 {' g* i: K. ?4 ]including bilateral testicular growth, similar to boys, h; c4 l; F) i1 C' a
with CPP. The gonadotropin levels in this disorder
2 I; d. w; v# u0 u/ A+ u0 }are suppressed to prepubertal levels and do not show; \  O; Y- }' P( r
pubertal response of gonadotropin after gonadotropin-
. o$ J$ X# }: J/ k* ]releasing hormone stimulation. This is a sex-linked# w6 J& ~' T  `" U
autosomal dominant disorder that affects only$ j3 ^) Z" L% Z$ S
males; therefore, other male members of the family
; l) n. z( v% |may have similar precocious puberty.3
3 `( a& Y6 b6 M, S+ E9 FIn our patient, physical examination was incon-
7 S$ i( k' M; Y& g& Qsistent with true precocious puberty since his testi-% m, o! c7 R. c  C0 U" {8 ?
cles were prepubertal in size. However, testotoxicosis
& b$ |; u8 a7 H2 n' o! Q! j. Uwas in the differential diagnosis because his father
  D8 Q5 b5 Y& ostarted puberty somewhat early, and occasionally,4 c- ~, U& r9 U/ k
testicular enlargement is not that evident in the
2 u9 O4 X; R2 h; r1 fbeginning of this process.1 In the absence of a neg-
# C$ Z' h! Q8 I' Z6 {ative initial history of androgen exposure, our7 u0 \1 a: Z- R) P# z1 \" w
biggest concern was virilizing adrenal hyperplasia,) v+ N2 u! O* Z
either 21-hydroxylase deficiency or 11-β hydroxylase1 H8 Y: M5 t2 Z1 W: k0 Z
deficiency. Those diagnoses were excluded by find-& i+ I1 j6 \' C/ R% U
ing the normal level of adrenal steroids.
( k& U0 Q, t- v8 p1 ~The diagnosis of exogenous androgens was strongly5 P5 J  ?6 s6 _2 |  |& y
suspected in a follow-up visit after 4 months because
* d" R% G1 l8 F2 o2 Pthe physical examination revealed the complete disap-
/ `4 q: F9 T" z6 N- ]pearance of pubic hair, normal growth velocity, and
( K( @8 A6 B8 i% hdecreased erections. The father admitted using a testos-3 l5 |+ w+ O6 C' P
terone gel, which he concealed at first visit. He was
! z" }& w. f( @8 i. [using it rather frequently, twice a day. The Physicians’
8 ~3 Z8 E( E1 U* d. r2 J6 n, \1 NDesk Reference, or package insert of this product, gel or- D$ @& P: T7 M0 O0 i( h! e
cream, cautions about dermal testosterone transfer to
; H/ h: g8 X! z1 H3 @unprotected females through direct skin exposure., {" G# {, V1 V3 ^
Serum testosterone level was found to be 2 times the
$ r1 o; t3 M) g' H. X4 N2 jbaseline value in those females who were exposed to
7 O  ^: u0 W" a2 I- t  ?5 F' v7 {even 15 minutes of direct skin contact with their male3 e3 G' b( y7 Q3 V" V; p  @0 E
partners.6 However, when a shirt covered the applica-4 u/ A0 P0 G$ W4 T$ @/ `; T5 |" c
tion site, this testosterone transfer was prevented.2 b3 V$ L2 P3 n6 n
Our patient’s testosterone level was 60 ng/mL,; W; u* |- _/ Y! X- y* Q
which was clearly high. Some studies suggest that" Y8 k7 P* S0 a6 ?1 |  H
dermal conversion of testosterone to dihydrotestos-; y7 K7 }7 q' C( ]
terone, which is a more potent metabolite, is more* W* Y8 _) o% U
active in young children exposed to testosterone* c" N! u( J8 ~, M0 y* K; v+ F" I
exogenously7; however, we did not measure a dihy-
  z# E1 q4 {: A( W. h, ?. n$ K: A6 ]drotestosterone level in our patient. In addition to
$ i1 i/ `* ~( m7 ?) Cvirilization, exposure to exogenous testosterone in, a3 K- x* C( y0 z
children results in an increase in growth velocity and4 p8 _  P/ S' O1 A
advanced bone age, as seen in our patient.! y1 q; V1 }& T  [: q
The long-term effect of androgen exposure during( X: C9 h, U3 A7 U2 S/ U
early childhood on pubertal development and final
  F' \# k! [4 f4 @3 w2 M* {+ e$ H! Yadult height are not fully known and always remain3 a% j' [; L! \  r/ F* n
a concern. Children treated with short-term testos-7 j5 [* K( s/ Z' C3 c0 B5 U
terone injection or topical androgen may exhibit some, y6 t# u! ?$ c
acceleration of the skeletal maturation; however, after- _- D' y% n6 `- X, x
cessation of treatment, the rate of bone maturation
2 {3 m7 I, K" z4 i! O5 C7 qdecelerates and gradually returns to normal.8,9. v, K2 Z& M0 I% x+ o
There are conflicting reports and controversy
2 o  s# r6 W# ^! S! rover the effect of early androgen exposure on adult8 n* R' C5 a" M* W7 u1 X
penile length.10,11 Some reports suggest subnormal
, f" ^+ m( N& G: cadult penile length, apparently because of downreg-- k. n+ G" X7 h9 _/ @5 H9 P: K
ulation of androgen receptor number.10,12 However,. |: x% g/ |% ^
Sutherland et al13 did not find a correlation between
, L! ^1 x- w: W9 g1 tchildhood testosterone exposure and reduced adult& _' Z( M. J& ?) h5 A" \
penile length in clinical studies.
4 ^* R, Q$ P( ZNonetheless, we do not believe our patient is* L& J: J" _: l6 W2 _; J
going to experience any of the untoward effects from
$ Y/ H% T2 t: q/ ltestosterone exposure as mentioned earlier because
2 W5 m; {, L% S* `0 s, {* wthe exposure was not for a prolonged period of time.
) D. s6 ~% ]. LAlthough the bone age was advanced at the time of4 Z, U/ b- K% J7 j& |" u& N
diagnosis, the child had a normal growth velocity at& {5 C( V3 k! _& Y
the follow-up visit. It is hoped that his final adult, S# E) C3 T4 N) D( W7 p
height will not be affected., T& t( e4 k5 p
Although rarely reported, the widespread avail-
$ f5 W, Y0 [' c, J. F0 Lability of androgen products in our society may# k1 q/ l( I* f- t/ ^" T
indeed cause more virilization in male or female
1 t; s9 F. F# m% echildren than one would realize. Exposure to andro-
3 V- ~% q: P* Hgen products must be considered and specific ques-
' {3 V, |7 j' `2 V$ Q, xtioning about the use of a testosterone product or+ c$ z# C3 e% A8 u7 _# G/ }
gel should be asked of the family members during
% h2 V0 h3 t: ^& @the evaluation of any children who present with vir-
& k; ]  Y3 z0 Q, g( h+ v3 }ilization or peripheral precocious puberty. The diag-' d+ z# D# Y  t$ Q
nosis can be established by just a few tests and by
" Y! E( W$ R1 L  Z2 l) T+ |! ?( qappropriate history. The inability to obtain such a. h3 {+ ~% s) }2 K, l
history, or failure to ask the specific questions, may
5 f, ~( W( L  `result in extensive, unnecessary, and expensive
2 H. Z( e6 n5 T2 @  yinvestigation. The primary care physician should be
; ^% O( R" k, o: Oaware of this fact, because most of these children5 G, n* i0 q- m) B  n! J' t
may initially present in their practice. The Physicians’2 `% g. {7 Z/ J* u
Desk Reference and package insert should also put a
8 c2 m/ Z0 g6 z$ Ywarning about the virilizing effect on a male or
' z; X# z7 J: mfemale child who might come in contact with some-
- F( i$ ]4 Q! u! ^3 l" gone using any of these products.
) l5 h" [  m* u. e+ qReferences+ H7 z- I) \8 S
1. Styne DM. The testes: disorder of sexual differentiation4 U# u" z' H( l: i7 a% `6 d1 A
and puberty in the male. In: Sperling MA, ed. Pediatric9 {9 Q" f; n4 P0 G& D0 x
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
% T( X8 I$ K: }6 v6 S7 k! N2002: 565-628.
  f; @' u  A$ q2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious# Z7 N1 D8 P/ m
puberty in children with tumours of the suprasellar pineal
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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
4 D" U* x. n# f) ^& h. ~
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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