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Sexual Precocity in a 16-Month-Old  [  z* M$ F( Y
Boy Induced by Indirect Topical2 B4 k8 _+ S* s
Exposure to Testosterone. W3 E# T. |, Y. P. Y5 ]5 C6 s
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,23 X, }% x# q* w' Y. i0 w) D
and Kenneth R. Rettig, MD1
: @' r: u9 W* H9 K# aClinical Pediatrics; k6 E; N8 X& q) X9 e! s
Volume 46 Number 6
' f2 z! h( |3 g( J/ [9 r# @July 2007 540-543
* f% f" J9 }  E© 2007 Sage Publications
8 }* u& t# N# G+ C' x+ k10.1177/0009922806296651
- V; ]" T* i  i- T; f9 f& Ahttp://clp.sagepub.com5 {' F7 S9 B. P7 a- d- |
hosted at! j  }$ k$ U. ?
http://online.sagepub.com! b2 |- P2 Y! E& N! e7 h' ~1 P/ J3 e
Precocious puberty in boys, central or peripheral,7 f1 m# K( G! s+ o) @7 o
is a significant concern for physicians. Central# i/ A  z  y' G$ p; M
precocious puberty (CPP), which is mediated
0 J# |0 t' m0 e. |+ gthrough the hypothalamic pituitary gonadal axis, has
& f$ _# N1 @0 p4 ua higher incidence of organic central nervous system6 ~' r' N+ g/ G0 f2 @$ b
lesions in boys.1,2 Virilization in boys, as manifested
; u- Y) ]7 T, _* Y+ f" N" Q' ^by enlargement of the penis, development of pubic; X7 j3 W- C4 I: U6 {! a( S
hair, and facial acne without enlargement of testi-
! n7 z7 B; [7 ^3 Wcles, suggests peripheral or pseudopuberty.1-3 We
5 x5 f4 |; O' P7 O% x# greport a 16-month-old boy who presented with the
5 x, |3 O' M' \. Z4 T# i1 Venlargement of the phallus and pubic hair develop-! U4 F0 X! a, A6 l* [( O
ment without testicular enlargement, which was due
. s7 x! s9 E- _to the unintentional exposure to androgen gel used by, U, X, m# ~; l, Z3 \1 M7 y
the father. The family initially concealed this infor-
7 G& f: P' \9 o5 v* @5 bmation, resulting in an extensive work-up for this
4 Z' i$ J4 O, l/ u# Cchild. Given the widespread and easy availability of& y* q* d# d$ F3 O7 i* K
testosterone gel and cream, we believe this is proba-$ c' j3 G$ \- J; J
bly more common than the rare case report in the! L0 t) E9 p3 f; c' C0 S
literature.4
5 j# Z7 W0 X! s0 O/ u! dPatient Report
# @/ z! s& @9 b: F4 v. W. LA 16-month-old white child was referred to the# {9 ]7 K4 ^/ O( u
endocrine clinic by his pediatrician with the concern
" F  z* H" A3 |) |4 @7 Gof early sexual development. His mother noticed
" X' i; u1 n+ d6 w' [light colored pubic hair development when he was
" _& p9 M* w( Z& WFrom the 1Division of Pediatric Endocrinology, 2University of+ _6 g* J5 Q$ G0 J! `
South Alabama Medical Center, Mobile, Alabama.
0 O' e. \( `2 [% vAddress correspondence to: Samar K. Bhowmick, MD, FACE,
) X4 C* W7 M2 D  _  fProfessor of Pediatrics, University of South Alabama, College of6 ]* N0 S9 R# V" A8 _; ]7 G3 g( {
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;# T# r6 I: l4 ~& J( @! p( P3 d7 e" n  c/ X
e-mail: [email protected].6 s* ^$ M( }* I, W8 X( i. k
about 6 to 7 months old, which progressively became  ]9 l. p- p3 ^* W4 h: i
darker. She was also concerned about the enlarge-
0 Z, d& Q9 m# A, d  @ment of his penis and frequent erections. The child
# J3 V4 h) `" J7 ?was the product of a full-term normal delivery, with
' w  w* j# ?( }' }6 F# oa birth weight of 7 lb 14 oz, and birth length of7 p. Z+ @5 @0 C3 y9 X
20 inches. He was breast-fed throughout the first year3 I9 g8 R( F% A4 I9 X- ?
of life and was still receiving breast milk along with$ I2 l9 j9 F0 ^, |
solid food. He had no hospitalizations or surgery,* o! Q- v" H' }9 Y
and his psychosocial and psychomotor development0 L3 g- V9 ]$ @- d
was age appropriate.0 w, P# U* ]0 \' R. X* C
The family history was remarkable for the father,
. I7 d* A- o, \. v% |, F- _who was diagnosed with hypothyroidism at age 16,
) k- N5 K, ~' b' F. n* Zwhich was treated with thyroxine. The father’s9 G2 L9 Q. ^+ C
height was 6 feet, and he went through a somewhat3 m6 X6 \3 g3 N, [5 C4 C1 R
early puberty and had stopped growing by age 14.
# b4 u6 T$ ^0 A& d6 XThe father denied taking any other medication. The
; p+ m" x1 U3 |! j# |! ~child’s mother was in good health. Her menarche
! _# I) L' z8 ~was at 11 years of age, and her height was at 5 feet
! j5 V+ t1 U$ d; L/ r- k5 inches. There was no other family history of pre-4 R* D% N1 I7 A% Z) L4 U
cocious sexual development in the first-degree rela-
) n3 n" r2 X. @) R% ttives. There were no siblings.
1 `% Q3 h4 A: n( y) r1 ~' _Physical Examination, U( X) A& }! @- l* W
The physical examination revealed a very active,
% a. a9 W3 Q% ~) F/ e0 @playful, and healthy boy. The vital signs documented
5 J7 m! t& [& `0 }- ta blood pressure of 85/50 mm Hg, his length was
# d& A. w5 |7 O90 cm (>97th percentile), and his weight was 14.4 kg
$ a2 [  d' e7 T: X# }6 S" h(also >97th percentile). The observed yearly growth
5 A" }' j) J/ e9 k. lvelocity was 30 cm (12 inches). The examination of
* e: R; f' s2 _) R$ t. Sthe neck revealed no thyroid enlargement.! M* v$ x' z$ G8 X9 C8 J. O# ]8 }; x
The genitourinary examination was remarkable for7 ?2 ~$ f- U& E  J0 U5 q
enlargement of the penis, with a stretched length of
8 ]4 g! A; K4 ?7 R" g8 L8 [8 cm and a width of 2 cm. The glans penis was very well7 C3 ~9 Z6 `/ m" K) G6 j
developed. The pubic hair was Tanner II, mostly around* M& U2 b% M4 \1 L
540# |; J- M1 h$ G* G& R
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 R7 G& s* v, d# w' q0 P
the base of the phallus and was dark and curled. The
/ D0 v: z( M9 I) m8 jtesticular volume was prepubertal at 2 mL each.
% Z) t, h1 ~4 l+ QThe skin was moist and smooth and somewhat
) c4 l" d* q& s( `$ T% y$ e$ u( h6 uoily. No axillary hair was noted. There were no: l3 g# I* O% e  s1 n$ @
abnormal skin pigmentations or café-au-lait spots.8 x& S, Y) E2 W; q4 i
Neurologic evaluation showed deep tendon reflex 2+
; F7 F8 q! r  R/ rbilateral and symmetrical. There was no suggestion  C" G& M: h6 H
of papilledema.
1 @. K8 _: T) U1 P7 P  G2 }( LLaboratory Evaluation
. `! C, L( K8 eThe bone age was consistent with 28 months by& Y/ J) Q9 q) a9 M4 D
using the standard of Greulich and Pyle at a chrono-$ T# s5 f* G/ Z
logic age of 16 months (advanced).5 Chromosomal3 r3 S/ F7 M1 g5 k7 q
karyotype was 46XY. The thyroid function test6 N# p5 U; y! }/ }+ ]; F7 N
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
6 O( x' [4 z* Z7 T4 nlating hormone level was 1.3 µIU/mL (both normal).
# U6 O0 K; p, V/ i6 J2 p- RThe concentrations of serum electrolytes, blood) f) \( D& G% o: r- ]
urea nitrogen, creatinine, and calcium all were/ j& I8 d0 c3 R2 }2 I
within normal range for his age. The concentration
, A8 K7 x* G& g; o+ ]7 vof serum 17-hydroxyprogesterone was 16 ng/dL
% M7 H! ~7 ]* [(normal, 3 to 90 ng/dL), androstenedione was 202 M  K4 Z4 ?3 a% x3 \! r+ x
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
# e  @3 `5 S) ?! N  m  nterone was 38 ng/dL (normal, 50 to 760 ng/dL),
- V7 s6 z  H) R9 A/ sdesoxycorticosterone was 4.3 ng/dL (normal, 7 to: W7 j  o+ w* ~
49ng/dL), 11-desoxycortisol (specific compound S)1 U3 M, X: s- Q; E! J/ P. g
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-" S1 U4 a8 m5 I/ ]
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total/ U" A$ W" a4 B- a6 K; [4 V4 }! P
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
6 k: i5 _) A9 i/ k. |' Yand β-human chorionic gonadotropin was less than
+ J# o" M+ q& I: G5 mIU/mL (normal <5 mIU/mL). Serum follicular. e- z! D# {' k4 b/ ^
stimulating hormone and leuteinizing hormone
7 k+ f) k8 Y, _' s8 z; R5 {$ Nconcentrations were less than 0.05 mIU/mL" t7 G0 I4 \& {8 e6 C+ f1 ~
(prepubertal).0 A5 g5 G" f: |& D' q! N
The parents were notified about the laboratory
/ z  p9 V1 u' A9 z3 q: aresults and were informed that all of the tests were. n$ @3 @; D8 t: }0 J  ?
normal except the testosterone level was high. The
$ m* S  ?' N# \7 Rfollow-up visit was arranged within a few weeks to
. r) i: z5 |6 H8 gobtain testicular and abdominal sonograms; how-
& L6 V# x, E9 C, @. y, Yever, the family did not return for 4 months.; A% D1 Q  m- B
Physical examination at this time revealed that the  N0 q6 R; v, r4 k% t: h9 l; A. k
child had grown 2.5 cm in 4 months and had gained" ]* W$ c4 _# \8 V1 D7 G7 U: u& s7 e% N
2 kg of weight. Physical examination remained
" m+ o. N, Y( ?0 M, U# r1 H, T- lunchanged. Surprisingly, the pubic hair almost com-
# m% @/ K; l; p9 i8 }  apletely disappeared except for a few vellous hairs at$ R; e* X) q. b- s1 W' `7 p
the base of the phallus. Testicular volume was still 2
# h( w6 K+ p' W) ^# qmL, and the size of the penis remained unchanged.# h% F: P. W1 @' v% l
The mother also said that the boy was no longer hav-; v! ^' ]8 U& `+ x) T5 x
ing frequent erections.) C$ S  X5 K% f. n
Both parents were again questioned about use of
6 s0 m" n+ M, ?' Y3 hany ointment/creams that they may have applied to  J- Y, B" s% V. V; p1 |+ _
the child’s skin. This time the father admitted the
3 t" r7 L/ ~0 O& G& w; bTopical Testosterone Exposure / Bhowmick et al 541
7 D$ a( {4 k, k* d; f/ D1 K0 _use of testosterone gel twice daily that he was apply-
8 s& y* b. q' _2 N* x& {0 Iing over his own shoulders, chest, and back area for( y% ]7 T, A3 ~( `! K) x4 o5 r
a year. The father also revealed he was embarrassed3 [$ L: T, R: `
to disclose that he was using a testosterone gel pre-( N- |- G; w7 c* P& p
scribed by his family physician for decreased libido+ m6 M' Y3 H+ e& s/ m1 |( n
secondary to depression.
; `) W6 @& [$ w  x- d& E0 N. xThe child slept in the same bed with parents.
; k$ N' j' Q- [, b! q& k, A* n1 }The father would hug the baby and hold him on his
1 B6 \+ ^2 D1 n4 N* M9 Qchest for a considerable period of time, causing sig-5 e% O' l9 }. g7 Q* n  j
nificant bare skin contact between baby and father.5 e1 n5 ?2 |0 g% f3 g
The father also admitted that after the phone call,4 y! s- n5 s' {% i$ |0 H, ]- b
when he learned the testosterone level in the baby
$ r5 L2 }6 F+ |0 Q8 Z  Ywas high, he then read the product information
* L( A% K+ l2 j7 V) ~packet and concluded that it was most likely the rea-
& e# Y9 M/ v! `son for the child’s virilization. At that time, they+ J  F' C# {( _- y
decided to put the baby in a separate bed, and the0 ~; e3 o% @( V0 Q! P# q7 o! A
father was not hugging him with bare skin and had
: g. P' j- Z: _( U: V& w. Mbeen using protective clothing. A repeat testosterone2 O- L5 r4 U0 h% x! L3 N$ C( n, S
test was ordered, but the family did not go to the
. m/ o5 t$ l% }laboratory to obtain the test.
/ Y; s* h4 f! I( z, n% XDiscussion
8 j/ x! }% i9 u; Z2 f; DPrecocious puberty in boys is defined as secondary" Y& d0 ?& u0 q8 w
sexual development before 9 years of age.1,4, B5 P  R" D* N' f
Precocious puberty is termed as central (true) when
0 W! P7 a3 n% z' x; ?. n9 E: Cit is caused by the premature activation of hypo-7 W1 t8 }3 Z( R+ ?
thalamic pituitary gonadal axis. CPP is more com-
2 w/ x: e; ]4 k- ?/ Nmon in girls than in boys.1,3 Most boys with CPP
  Q: h) a" }1 r4 W( _8 N! Wmay have a central nervous system lesion that is3 T4 v9 o& D, V4 X' s
responsible for the early activation of the hypothal-
5 L. j7 y7 m* E/ R5 S/ j% c8 pamic pituitary gonadal axis.1-3 Thus, greater empha-) Z4 m7 V8 y/ T/ g3 x+ X! W: [$ V
sis has been given to neuroradiologic imaging in
- L6 u  [6 G, d( \/ eboys with precocious puberty. In addition to viril-
* R4 J' B# t* Z! F4 B' Bization, the clinical hallmark of CPP is the symmet-3 W$ F! A* r5 D* y+ ]5 F
rical testicular growth secondary to stimulation by
. `# t5 ^  C- J5 g; Y- _4 D9 Dgonadotropins.1,3
$ j  S* N8 G, j* n" G) JGonadotropin-independent peripheral preco-
  {8 E* i6 U! |! ]cious puberty in boys also results from inappropriate
# V1 F7 M. ~6 M* q1 z! qandrogenic stimulation from either endogenous or
! g* d& j  P. G" j* y% L9 Kexogenous sources, nonpituitary gonadotropin stim-, c) y8 O9 r: K
ulation, and rare activating mutations.3 Virilizing' D8 J( _* l2 L( K0 q4 [/ c2 \
congenital adrenal hyperplasia producing excessive
* h4 x2 @, g, V* fadrenal androgens is a common cause of precocious: `1 F6 W" R" C2 w" y( z) ~) c* |4 p' i
puberty in boys.3,4& Y5 n+ |  F* x( V
The most common form of congenital adrenal
& U, k+ |) L: }% ^, Shyperplasia is the 21-hydroxylase enzyme deficiency.
4 M' a& [: F+ y$ q. @The 11-β hydroxylase deficiency may also result in
- [) J: \  ]/ E3 s: sexcessive adrenal androgen production, and rarely,' C. c# N6 v( l7 K0 z  E
an adrenal tumor may also cause adrenal androgen+ s0 {$ @# A" g* h. G" h( {: @" R2 O
excess.1,3
1 }. I0 a7 {$ C0 Q+ I4 mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 Y: V  \- n/ _
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007. ?0 J3 f& l* W6 T4 B
A unique entity of male-limited gonadotropin-* d. B8 P7 q, Y4 |4 y% ~% q$ {+ ?
independent precocious puberty, which is also known
% `/ y+ M3 F2 {2 p9 `4 ras testotoxicosis, may cause precocious puberty at a) `5 ~( ~$ ~4 T' a6 _  e# w
very young age. The physical findings in these boys) I, K5 J2 {- h; O9 Q( p
with this disorder are full pubertal development,6 [7 I- F8 w: {" y- m
including bilateral testicular growth, similar to boys* K+ E- c& r2 \3 c. r5 v
with CPP. The gonadotropin levels in this disorder" V, X# i* I/ j5 i
are suppressed to prepubertal levels and do not show
/ @2 \/ O) `$ m2 N) T1 Gpubertal response of gonadotropin after gonadotropin-  K, h& i1 o, B) b+ F
releasing hormone stimulation. This is a sex-linked3 W, C3 i; |% ^# v; [9 w+ M$ F
autosomal dominant disorder that affects only
' y( P1 X7 K% |4 Y, Fmales; therefore, other male members of the family
+ d* U3 ]! J1 W2 g; I. X6 Mmay have similar precocious puberty.3
2 M: @4 _- j* u$ E2 k7 J+ I! |& n/ ^In our patient, physical examination was incon-
% ^$ N) p1 O( R  k* q- X- t6 Usistent with true precocious puberty since his testi-
6 C- r# y) W1 P. y& Ccles were prepubertal in size. However, testotoxicosis6 ^5 u; a' `+ k8 }; i1 e
was in the differential diagnosis because his father
' f6 e" s! b8 h& ustarted puberty somewhat early, and occasionally,
8 J' _+ A3 i5 _* Ttesticular enlargement is not that evident in the
/ K! }9 ^$ D* ^) x9 n% Cbeginning of this process.1 In the absence of a neg-4 V  [" k2 }) T) `4 g
ative initial history of androgen exposure, our. k# c/ v* R- b! n6 W- \
biggest concern was virilizing adrenal hyperplasia,# d' d/ [- Y* |  ~  Q( ^. U
either 21-hydroxylase deficiency or 11-β hydroxylase
6 F  t" s4 x8 n9 o5 m. A( I0 |* Cdeficiency. Those diagnoses were excluded by find-
8 q9 U2 A. |  l; Ding the normal level of adrenal steroids.
) g" X0 z0 M, OThe diagnosis of exogenous androgens was strongly
& A' ~( l+ [8 ]7 L3 Dsuspected in a follow-up visit after 4 months because" X: x$ b2 D; j% k8 ]  Q/ a; r+ D
the physical examination revealed the complete disap-
* L! z5 Y% Q, Q& \5 ~6 F- c% vpearance of pubic hair, normal growth velocity, and
; Y9 q( j0 i% j0 ~8 J) I3 Z2 q7 }- Ddecreased erections. The father admitted using a testos-
1 M8 A/ f5 i/ E8 D) }: ^terone gel, which he concealed at first visit. He was- m* ~* @6 @  k6 T
using it rather frequently, twice a day. The Physicians’
/ }' m/ M, I8 T! O/ \7 CDesk Reference, or package insert of this product, gel or2 x  e/ z- W' J! v- z+ q
cream, cautions about dermal testosterone transfer to
& ]9 |( A3 d6 K- E, r: I6 P4 Aunprotected females through direct skin exposure.
3 C' O" L% N" A  u0 O# ASerum testosterone level was found to be 2 times the
% w3 E+ F3 O- B: T0 Sbaseline value in those females who were exposed to
9 \2 Q8 P% i; O/ z4 e7 veven 15 minutes of direct skin contact with their male2 @) R6 n6 I" ?4 ^& U6 m
partners.6 However, when a shirt covered the applica-/ t8 |" @' F7 j: p
tion site, this testosterone transfer was prevented.+ d' w) K/ e1 R! e* b+ G- _
Our patient’s testosterone level was 60 ng/mL,
/ \% }/ q4 ?# Fwhich was clearly high. Some studies suggest that* V6 e: ?% o4 }: B! B/ |
dermal conversion of testosterone to dihydrotestos-: [8 \5 f' @7 ~  Z% }) v/ @2 d, _: V
terone, which is a more potent metabolite, is more/ s5 K$ |1 D$ L" f+ B/ Z3 I# E
active in young children exposed to testosterone
' H( D+ V+ S7 v! L/ n( Fexogenously7; however, we did not measure a dihy-
& r5 J# W3 j4 c* R7 [+ ~drotestosterone level in our patient. In addition to
- a% T7 M& l; H- D0 Z- dvirilization, exposure to exogenous testosterone in' Y& [+ y; j! z: W; F( R
children results in an increase in growth velocity and0 G9 m% `% O1 n+ H% m
advanced bone age, as seen in our patient.. O4 G. ]' ?/ k6 j% z
The long-term effect of androgen exposure during% V+ @$ e+ `3 i& l' t3 f7 A
early childhood on pubertal development and final1 M- c  k" Z; _, l2 o2 G9 ^2 ~+ @5 q
adult height are not fully known and always remain  D9 p7 q+ q7 [$ E4 P% N9 i& O
a concern. Children treated with short-term testos-
' f  k  r. T3 C: c8 hterone injection or topical androgen may exhibit some  q7 u9 R; P6 x% A# E
acceleration of the skeletal maturation; however, after
0 C1 W0 j; ~" vcessation of treatment, the rate of bone maturation9 P; ]. E2 ~2 ^* b/ q* Q- j
decelerates and gradually returns to normal.8,9
% K: N/ ~% n0 u; a# {+ wThere are conflicting reports and controversy, H5 K' q3 ^, \) Z: f# N
over the effect of early androgen exposure on adult3 u) L2 m1 a1 t- a4 E& c  W! }. m' \
penile length.10,11 Some reports suggest subnormal
( ], h  [( e5 wadult penile length, apparently because of downreg-+ ]/ }+ Q/ V2 C7 ~! P3 G
ulation of androgen receptor number.10,12 However,! }9 S' V+ h" ?; x) S
Sutherland et al13 did not find a correlation between( ]3 v  |" N, E4 a
childhood testosterone exposure and reduced adult
( r% C& M/ w$ ^" F& h1 `penile length in clinical studies.
# u% C0 S) M0 r8 k- U# Q! mNonetheless, we do not believe our patient is
7 }3 x) E5 U6 w. {  tgoing to experience any of the untoward effects from
1 a4 i8 m7 u# n! {) @testosterone exposure as mentioned earlier because& d0 D1 H; |8 I6 K  k) N" t; n$ V) l
the exposure was not for a prolonged period of time.
! E4 C( U4 u! v/ A0 l" Q6 W- _/ ^+ `8 RAlthough the bone age was advanced at the time of, C4 Q, i9 M3 f3 `+ e
diagnosis, the child had a normal growth velocity at( ?% M" {% [4 _6 b8 X7 l9 q
the follow-up visit. It is hoped that his final adult! [- t5 A3 E* f+ F6 E
height will not be affected.
" Y3 |  h' S9 S5 i5 I" x% WAlthough rarely reported, the widespread avail-( l2 R9 f; a! e5 g% z9 K) n! H+ {" h
ability of androgen products in our society may
- k) h, ~" \3 ]. h1 Y) a1 N  h9 yindeed cause more virilization in male or female
$ q: w5 R, j/ V1 ]children than one would realize. Exposure to andro-
* F) r* w0 n" Agen products must be considered and specific ques-) f4 g3 F8 {$ d5 w
tioning about the use of a testosterone product or. \4 s% m6 ^# D4 G+ l$ q1 }
gel should be asked of the family members during
6 p* A/ F: n+ I) t- I/ ?the evaluation of any children who present with vir-
  v9 G" ~. b- c: Xilization or peripheral precocious puberty. The diag-
8 \. n8 w: [7 \; Rnosis can be established by just a few tests and by
. H5 `0 D: _- G' R! S1 Pappropriate history. The inability to obtain such a
6 d, ]8 k2 C: A. Phistory, or failure to ask the specific questions, may4 J7 l( i3 D0 N" ^
result in extensive, unnecessary, and expensive
" O4 K* G5 {9 Y9 D! ninvestigation. The primary care physician should be
, ?* d2 S) o' i$ K1 `% i5 X: B# p7 Gaware of this fact, because most of these children& e  V6 x7 U$ J  A; F" d
may initially present in their practice. The Physicians’
* A3 H0 s/ b) T7 @/ SDesk Reference and package insert should also put a# M* n( r* i) w6 P
warning about the virilizing effect on a male or
% l) Q+ v& w5 k. S: ~: V; ^; `5 N8 h- Qfemale child who might come in contact with some-; Y8 Y2 h2 s3 t% h
one using any of these products.
) I0 R/ W# L; Q* q( c2 zReferences7 D6 m- T# \# [
1. Styne DM. The testes: disorder of sexual differentiation. ^1 Z9 K. A" o& e, z* D
and puberty in the male. In: Sperling MA, ed. Pediatric
& J4 c6 n; D0 D  z8 BEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;" z; U2 [1 @4 C8 v
2002: 565-628.
+ L: |$ t- v' Y: c" j2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious. p, X& w4 ?1 h2 J: X
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
3 p, j* S& H$ ABoy Induced by Indirect Topical
% D2 Q4 @$ Z- wExposure to Testosterone
# I5 }0 E1 k1 C8 E  JSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
1 P9 d1 @4 o8 V, aand Kenneth R. Rettig, MD1
3 w1 ]% ^9 ~* h6 a$ yClinical Pediatrics
% b) Z% h# \3 P8 C: I1 [6 [Volume 46 Number 66 Z- @- q( ~. m0 J: s6 w
July 2007 540-543; }) B3 Q. M- g- ~
© 2007 Sage Publications
5 b% |# l- q: O: k: {% I& F10.1177/0009922806296651
: o& V% v# }- whttp://clp.sagepub.com1 ^' x4 a6 d8 t9 U. r: r
hosted at
+ z5 ~* I- Y# Z2 S: Y# ehttp://online.sagepub.com: o) U9 h; Q4 t. V% \) Q
Precocious puberty in boys, central or peripheral,9 z, r, w0 O# f* w/ L
is a significant concern for physicians. Central( }6 q4 Y9 H8 p- M) B( S
precocious puberty (CPP), which is mediated
# f3 y: E8 l4 ]7 A! ]; Zthrough the hypothalamic pituitary gonadal axis, has
6 n6 V. u6 e9 B: ^1 e1 B& N4 ma higher incidence of organic central nervous system
) O) P  P; W- t) L2 [& Dlesions in boys.1,2 Virilization in boys, as manifested
; F3 w2 l" d+ i+ {4 {" Z- Q9 Iby enlargement of the penis, development of pubic
. v* @4 S  r7 ^hair, and facial acne without enlargement of testi-  ]- t" T% F( C2 m& M8 b) ]
cles, suggests peripheral or pseudopuberty.1-3 We+ v* i0 r! ]1 O' L2 g+ o0 T
report a 16-month-old boy who presented with the
2 K% N9 a7 D* @2 g7 @+ Z$ Menlargement of the phallus and pubic hair develop-# t. W- ]# r0 h8 m) G/ ~+ }9 I
ment without testicular enlargement, which was due7 b& L+ H! L' X3 Q6 o# P! E
to the unintentional exposure to androgen gel used by
# F0 I6 H4 ^! I3 ?- [- }the father. The family initially concealed this infor-6 x9 I& W0 I1 V
mation, resulting in an extensive work-up for this
  V# E( k8 M4 X% N) Mchild. Given the widespread and easy availability of
) P3 `$ T( m9 E5 V0 ^2 ]( _- k. Ktestosterone gel and cream, we believe this is proba-
$ r% B7 v& C0 M7 Lbly more common than the rare case report in the7 n8 C0 n6 U4 h8 w4 h+ h0 W1 @
literature.4) j9 r, q7 W# p% K
Patient Report1 `8 b) o+ U7 j2 G1 v. a
A 16-month-old white child was referred to the7 }2 d! k  b0 n, K; ], m
endocrine clinic by his pediatrician with the concern1 G) Q' n. u0 f4 J  g9 L
of early sexual development. His mother noticed
9 p/ b2 I/ E# |6 l: S6 Q$ Alight colored pubic hair development when he was
# I: X1 H* D1 |( gFrom the 1Division of Pediatric Endocrinology, 2University of
& R9 r& _1 {! E7 S8 ESouth Alabama Medical Center, Mobile, Alabama.
3 [  W; O" C3 A+ X. A) CAddress correspondence to: Samar K. Bhowmick, MD, FACE,2 @: X% |- H3 E0 B4 i/ I
Professor of Pediatrics, University of South Alabama, College of
3 w( N, S' p. p% L0 bMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;, A: @& P& l) a+ N  H7 N5 u
e-mail: [email protected].
+ D0 o8 d4 y# \' ~7 Pabout 6 to 7 months old, which progressively became% G# h+ i' l0 C" R* C5 W
darker. She was also concerned about the enlarge-' {8 b! S# v$ O! r( g: e
ment of his penis and frequent erections. The child
- b. h2 N- Q- f* [2 W3 Cwas the product of a full-term normal delivery, with
- P% |+ P; D' Ia birth weight of 7 lb 14 oz, and birth length of
9 ~& U! f, A2 `8 T) f" v( w+ T. z" a20 inches. He was breast-fed throughout the first year
# ?1 a& g, w/ R0 lof life and was still receiving breast milk along with
+ a  K- E5 [! E' z5 ?solid food. He had no hospitalizations or surgery,
1 K, q4 q6 c$ D1 _% b6 oand his psychosocial and psychomotor development
5 S, l. U# B3 f; ]was age appropriate.
! {' I" B& H8 ~' u- z  S! M" rThe family history was remarkable for the father,
  h3 b  ?! W; Y9 Qwho was diagnosed with hypothyroidism at age 16,7 A5 M- f8 t& s" Z2 a3 v$ z1 S
which was treated with thyroxine. The father’s6 Y5 u, G: f7 o" `. w( V
height was 6 feet, and he went through a somewhat
+ [3 P6 X# p7 m. S& x: V  l7 Wearly puberty and had stopped growing by age 14.
$ i& b: t5 w4 C! F! J' F/ KThe father denied taking any other medication. The2 E" {. \: f1 h( i8 I
child’s mother was in good health. Her menarche
. t( h# t/ y- B" U; H7 hwas at 11 years of age, and her height was at 5 feet% p2 L* b6 a2 v) x
5 inches. There was no other family history of pre-& g$ D2 J8 }3 w3 I
cocious sexual development in the first-degree rela-6 J/ I1 ~# K6 b: y( w
tives. There were no siblings.
( U1 P# G9 y) H9 F7 s! f, @# MPhysical Examination4 Z* f3 P( m& Y# Q
The physical examination revealed a very active,
, k# w# q! K- Eplayful, and healthy boy. The vital signs documented
# S  d$ E; J; C! A0 \, ^6 s  Ka blood pressure of 85/50 mm Hg, his length was
, _  ?# ^" z2 E90 cm (>97th percentile), and his weight was 14.4 kg# d3 C4 d1 L% Q+ I! ~8 P
(also >97th percentile). The observed yearly growth
7 v8 V5 V% }7 E1 ], H0 S; w% Uvelocity was 30 cm (12 inches). The examination of
" U! {; {4 z- Ithe neck revealed no thyroid enlargement.6 A* u) n' I! u1 Y9 _1 }3 Q
The genitourinary examination was remarkable for
' i6 f6 Z( i7 N) aenlargement of the penis, with a stretched length of6 n5 ~, n6 R  u' ?3 k% W
8 cm and a width of 2 cm. The glans penis was very well% P% Z" \3 f2 H+ o, P8 P+ N- u9 F
developed. The pubic hair was Tanner II, mostly around
1 j% u, ]) z/ y; Q7 _540
2 ?  N( U  d( _. ~! @3 Rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' X( u+ F9 K& y& d
the base of the phallus and was dark and curled. The" x8 v% R. u8 e3 o3 V* _- f
testicular volume was prepubertal at 2 mL each.  y' ?9 r+ h" z$ F3 t& Y% ]
The skin was moist and smooth and somewhat
% L1 G/ C5 l/ U; z7 N# k" `+ \0 Foily. No axillary hair was noted. There were no
: [" |/ A% d; |% T3 N: T0 rabnormal skin pigmentations or café-au-lait spots.
& \' R; v$ f) m  h- LNeurologic evaluation showed deep tendon reflex 2+! U8 d. A% x- b% n- A* ]4 m& V
bilateral and symmetrical. There was no suggestion
5 {2 |+ T% ?1 Rof papilledema./ D# f3 P: u2 j7 {+ |
Laboratory Evaluation2 v: ^. J! h& d
The bone age was consistent with 28 months by9 ?. B0 H  _8 E# W% O' L2 V
using the standard of Greulich and Pyle at a chrono-# X) E" |) f$ S8 [& q; N9 k+ ]5 V/ u
logic age of 16 months (advanced).5 Chromosomal
0 O  J8 e1 s- t, v9 B9 Rkaryotype was 46XY. The thyroid function test% m7 v% v$ y& E- e! L. v0 H. w, ^
showed a free T4 of 1.69 ng/dL, and thyroid stimu-, X6 w5 v$ R; x
lating hormone level was 1.3 µIU/mL (both normal).8 _+ v$ o" P0 v1 B
The concentrations of serum electrolytes, blood  _) U9 W1 ~' W( g7 U
urea nitrogen, creatinine, and calcium all were; i/ ^! g( H9 _* j. I5 j3 |
within normal range for his age. The concentration
& H) V9 S+ h" E+ g  I' iof serum 17-hydroxyprogesterone was 16 ng/dL
, }+ ]7 G- a" s6 H7 y(normal, 3 to 90 ng/dL), androstenedione was 20- r6 e+ p( S4 v  W
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
1 \+ N6 Q$ y8 l: h9 p  kterone was 38 ng/dL (normal, 50 to 760 ng/dL),3 e7 i/ w8 E/ k: k
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
3 w8 s' p+ Q- O, j9 e. B49ng/dL), 11-desoxycortisol (specific compound S)6 o: p5 N' ?0 t' `
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
* N5 h; M- u( o+ ytisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total! B# a% m( f1 M. B
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
) S- V2 `' z; n# Nand β-human chorionic gonadotropin was less than
& R/ [4 ~! d0 O! c9 J5 mIU/mL (normal <5 mIU/mL). Serum follicular! M; w8 A6 {1 R* I9 Y
stimulating hormone and leuteinizing hormone
1 h# q" i8 B* B& L0 ]* r# Z( c# R) K, rconcentrations were less than 0.05 mIU/mL
7 t$ _2 i1 E2 a# o$ w( U) e9 B(prepubertal).
7 j- L5 M( X4 @7 dThe parents were notified about the laboratory" j* j5 v0 ^6 ?: H4 x! p
results and were informed that all of the tests were6 u0 n9 `' V0 }$ O( v3 E8 a
normal except the testosterone level was high. The% k( t0 V9 N3 Q9 A
follow-up visit was arranged within a few weeks to
; t4 M, S& i3 pobtain testicular and abdominal sonograms; how-0 \4 J7 P" d' ~4 ]
ever, the family did not return for 4 months.
% m0 \, m# t, }( c5 @9 KPhysical examination at this time revealed that the
5 G+ S  A- {) g% i  E. ]child had grown 2.5 cm in 4 months and had gained
, K9 E0 k/ Q9 h. B2 kg of weight. Physical examination remained
. b' E5 |& ?1 X  w# ounchanged. Surprisingly, the pubic hair almost com-3 ~3 T! Y" H, S5 x' u6 b! r
pletely disappeared except for a few vellous hairs at6 R9 x; }& F# M7 F2 }  r0 G
the base of the phallus. Testicular volume was still 2
4 T7 R3 c3 R/ r. umL, and the size of the penis remained unchanged.! I) h" o( P" Q& E
The mother also said that the boy was no longer hav-
, Z- @% t6 c. king frequent erections.' m7 U! @/ J5 x0 W4 X; Z8 l
Both parents were again questioned about use of% d  g8 p6 [8 h9 v" j
any ointment/creams that they may have applied to
( O% A& o( N) n! W: r6 ithe child’s skin. This time the father admitted the( g. z: t. s, ^" o
Topical Testosterone Exposure / Bhowmick et al 541" F( D$ Z3 o! z& r  N2 K- U
use of testosterone gel twice daily that he was apply-
) m3 W$ d! {( Y; B7 Ping over his own shoulders, chest, and back area for3 f$ }. B% z- M: T
a year. The father also revealed he was embarrassed
5 D- P  C, V- G& B- Lto disclose that he was using a testosterone gel pre-2 {: z9 @: `/ c3 ?9 \
scribed by his family physician for decreased libido" |* w. e& z* _0 J9 {1 e
secondary to depression.
9 c4 ^8 a" u  o" x* ]( AThe child slept in the same bed with parents.; z! U- q  j- v: k1 p! Z* D0 g5 K
The father would hug the baby and hold him on his
( L6 G* X7 z$ k* Bchest for a considerable period of time, causing sig-
: T) M! r$ g$ x9 a! V6 i6 ]$ g" \# hnificant bare skin contact between baby and father.
& q, |$ F) Z% r$ Q: d. ^8 fThe father also admitted that after the phone call,
; w7 r* i) m0 |( g, wwhen he learned the testosterone level in the baby0 H9 o1 ^# A  }) N  V. e! U3 G
was high, he then read the product information
2 v# V" {+ W. }* H7 W% `+ |packet and concluded that it was most likely the rea-- \, G$ Z* K- A* ~2 w  H3 W7 D
son for the child’s virilization. At that time, they) P4 C# B4 ^% e2 i, _/ m
decided to put the baby in a separate bed, and the% `* `' R6 D3 `9 s: r2 ]4 R% b
father was not hugging him with bare skin and had$ E2 Z9 ?% k# \+ v
been using protective clothing. A repeat testosterone
! ~3 q$ _5 j/ N6 ]5 U$ L- U8 Rtest was ordered, but the family did not go to the
- G. ^7 b9 h! b" b- K& ?& f% H7 N4 Elaboratory to obtain the test.
6 w$ b! W2 a/ W1 h$ d# ?Discussion, a3 w" _! C- b/ ~0 e
Precocious puberty in boys is defined as secondary
. A( A) L  _) E' D0 s( [; Ksexual development before 9 years of age.1,4: b* j" ]8 `0 v, }, x! y
Precocious puberty is termed as central (true) when0 `* a. r* [, N
it is caused by the premature activation of hypo-0 a% n1 J  y; ^: m0 m, }  }% G
thalamic pituitary gonadal axis. CPP is more com-& v: u2 p9 R8 ?2 _6 d$ Z7 p
mon in girls than in boys.1,3 Most boys with CPP
. j- L. j. @+ wmay have a central nervous system lesion that is
. }9 e3 e, J5 Yresponsible for the early activation of the hypothal-2 ]' a, F) z! E2 N# L5 I
amic pituitary gonadal axis.1-3 Thus, greater empha-
3 O  N+ w  F$ Isis has been given to neuroradiologic imaging in2 `/ s) I0 h1 y- H
boys with precocious puberty. In addition to viril-
) f) P. y# V/ l: n0 g( Lization, the clinical hallmark of CPP is the symmet-
, [# H& w9 D* B9 t+ v* vrical testicular growth secondary to stimulation by1 N- x) Z$ D- q& ?' R
gonadotropins.1,3
( t1 ^3 z# P+ \5 i. {+ I0 a/ tGonadotropin-independent peripheral preco-
' m* e4 O! I4 ~- zcious puberty in boys also results from inappropriate. g" P) B5 r+ Y0 {7 X
androgenic stimulation from either endogenous or; u; B- j# _  q/ v& ^+ f, m
exogenous sources, nonpituitary gonadotropin stim-) j$ H1 b7 w6 x/ [% S7 S
ulation, and rare activating mutations.3 Virilizing
- x/ k3 ?  e' A* s! G7 wcongenital adrenal hyperplasia producing excessive
0 |$ M5 d! [; j( g+ D6 Kadrenal androgens is a common cause of precocious2 z$ ]5 O& z/ f' Y2 w# B) x
puberty in boys.3,4* L6 b. {- M6 B: t" b2 I6 l
The most common form of congenital adrenal& K7 ~1 b' w7 ^6 z5 I+ n6 e
hyperplasia is the 21-hydroxylase enzyme deficiency.
! t, i& ^0 T+ Z) J8 }* CThe 11-β hydroxylase deficiency may also result in5 g. q/ m# u# C! o) A
excessive adrenal androgen production, and rarely," P3 V/ N1 k8 v& ]% _3 D
an adrenal tumor may also cause adrenal androgen! ^1 B  E( `& c  b' @
excess.1,3
; y& `" h6 _$ U/ M8 t8 eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. B) x9 P( H6 b& J0 G
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007; B# v( K( F; t, k( m
A unique entity of male-limited gonadotropin-
3 {/ ~; ^% \7 C. ]! gindependent precocious puberty, which is also known' w% O8 t9 U# a7 u
as testotoxicosis, may cause precocious puberty at a6 [; [+ }# D1 q3 Y2 @  ]7 \
very young age. The physical findings in these boys2 q- `7 s# j1 W) }4 v# b
with this disorder are full pubertal development,
6 P- K9 l, V1 Sincluding bilateral testicular growth, similar to boys
5 r) n* v9 h/ f2 K9 M( H- Ewith CPP. The gonadotropin levels in this disorder
4 e8 C/ L0 F5 k7 |6 X7 N+ T& X+ zare suppressed to prepubertal levels and do not show
) H" z7 L! C* c0 f+ T' j/ t1 rpubertal response of gonadotropin after gonadotropin-9 b6 y  s: u2 B# T, y
releasing hormone stimulation. This is a sex-linked
8 g+ R  w  ^% u* E5 m& \' tautosomal dominant disorder that affects only
+ M! S1 |; T3 K* k+ @+ Mmales; therefore, other male members of the family
  @0 y' N4 z4 ?may have similar precocious puberty.3
- }: O, M& U5 \* dIn our patient, physical examination was incon-* H0 n+ C! a2 C; R, \
sistent with true precocious puberty since his testi-0 r0 H* @1 p4 l9 H! U/ F, }0 D5 ^4 x
cles were prepubertal in size. However, testotoxicosis
' s: q# m0 Z! ~5 _& rwas in the differential diagnosis because his father
( B0 c! S! [0 W+ s1 d6 estarted puberty somewhat early, and occasionally,) b" V. }) c# c% t) \) d
testicular enlargement is not that evident in the
' e# F( G' M. e( l& N: D6 X1 T. Ybeginning of this process.1 In the absence of a neg-
/ I8 O9 r6 E6 w4 D3 |+ b- l. {ative initial history of androgen exposure, our& D7 z' w3 [* E4 I
biggest concern was virilizing adrenal hyperplasia,
. Q! ^4 g- c+ {: Veither 21-hydroxylase deficiency or 11-β hydroxylase
2 Q0 Y$ C" ]1 w+ R& a2 E& ]deficiency. Those diagnoses were excluded by find-
/ ~8 K# N! @3 C0 i5 q. Ging the normal level of adrenal steroids.
8 h3 c, \7 i8 R% J/ e7 L# }( x+ sThe diagnosis of exogenous androgens was strongly
% b6 [( _! p% I# ~; ^, _suspected in a follow-up visit after 4 months because
% v1 X+ ^" x5 p# }. P: \the physical examination revealed the complete disap-
7 i! u6 @( i, Y2 Wpearance of pubic hair, normal growth velocity, and/ n! q) \% U$ |7 D$ ^1 i9 i% u8 M
decreased erections. The father admitted using a testos-
& o( U0 L9 h* ~terone gel, which he concealed at first visit. He was
" z' d7 {3 B$ ~+ B, y1 s, O1 gusing it rather frequently, twice a day. The Physicians’
1 m( r! D) z# _. V, f' n" D: _Desk Reference, or package insert of this product, gel or( [# m( X4 U. I) G4 e1 d. H' u: H
cream, cautions about dermal testosterone transfer to# n+ ?' i/ O. p. V9 L& V/ _
unprotected females through direct skin exposure.( G5 [: C+ H4 J
Serum testosterone level was found to be 2 times the
+ U7 J0 G5 e! s" L& a4 ~! [! abaseline value in those females who were exposed to5 f: f( ^0 D$ z
even 15 minutes of direct skin contact with their male
; n* \) b) x7 [, wpartners.6 However, when a shirt covered the applica-
; a# C0 _5 T6 i% ]tion site, this testosterone transfer was prevented.; w, l# B9 I. \: f
Our patient’s testosterone level was 60 ng/mL,4 e5 P( K' ?# N, n$ I  _/ C5 b
which was clearly high. Some studies suggest that( h' e' W4 F( K: f( n& }
dermal conversion of testosterone to dihydrotestos-# q1 }. m; L! |* F' E( @8 K
terone, which is a more potent metabolite, is more
; H/ |2 \" q) i- F3 D, Iactive in young children exposed to testosterone
6 p2 ]8 V: x9 \  L8 D! A$ \# Iexogenously7; however, we did not measure a dihy-' M) l  V% u4 y6 }" Z7 ]2 X
drotestosterone level in our patient. In addition to
' ^4 i; E5 W# G, r8 {, I: b5 {virilization, exposure to exogenous testosterone in
2 Z0 w$ v8 G  Dchildren results in an increase in growth velocity and
  T! U" ~/ w# V+ x4 L& k7 W: M# r+ iadvanced bone age, as seen in our patient.) z5 v0 V# q- T
The long-term effect of androgen exposure during
% _- u) q+ ?4 s$ y1 yearly childhood on pubertal development and final+ Z  x; `' Y  J, p
adult height are not fully known and always remain
8 v9 ]4 h: B) g$ i6 \a concern. Children treated with short-term testos-
/ k% O" _1 |( L2 R0 F6 L$ bterone injection or topical androgen may exhibit some
# w7 m- p& v6 C6 _9 M, Z2 P& ^acceleration of the skeletal maturation; however, after
* ~+ I# n5 b4 u9 mcessation of treatment, the rate of bone maturation- \4 M2 K: T7 V- Y  ~
decelerates and gradually returns to normal.8,9
9 y$ p1 `- K  A, S$ a5 e0 SThere are conflicting reports and controversy
% S/ q  W2 r/ |( G. T0 a% aover the effect of early androgen exposure on adult
- h5 x( m; n4 y9 a7 T6 upenile length.10,11 Some reports suggest subnormal$ h: i0 E4 T  p, W
adult penile length, apparently because of downreg-" u- X0 E; ]* w, z: L6 p9 M
ulation of androgen receptor number.10,12 However,
4 S9 `1 e) Z( ?1 a5 PSutherland et al13 did not find a correlation between+ F2 L' \( K7 R4 a
childhood testosterone exposure and reduced adult; ?/ B2 m/ c& N
penile length in clinical studies.: s! x% J, c% W9 z) Q
Nonetheless, we do not believe our patient is
9 a- v, E2 R; r) r: J: \, bgoing to experience any of the untoward effects from3 c  h0 U, S- j6 \' [  z
testosterone exposure as mentioned earlier because
5 ]9 f6 N- X: z' mthe exposure was not for a prolonged period of time.# G/ i3 a* d, T% h
Although the bone age was advanced at the time of5 D  S8 Y. @  S' E1 y) P) ?8 h0 A. Z6 @
diagnosis, the child had a normal growth velocity at
* V* L/ h6 E2 _  z$ E' vthe follow-up visit. It is hoped that his final adult
8 V8 X& E. [5 |' O! ?height will not be affected.
! Z0 Q; G4 s+ A2 QAlthough rarely reported, the widespread avail-4 b) a3 |# x  U' t: b9 ?
ability of androgen products in our society may! f# v# F  N) [- I" N4 m4 R
indeed cause more virilization in male or female
& f1 T, ?' _  |4 K; q+ [: w0 wchildren than one would realize. Exposure to andro-0 f- z; h) {4 d" e1 \0 J/ O; L
gen products must be considered and specific ques-
" \5 a1 q5 G+ p4 N. \5 qtioning about the use of a testosterone product or$ X3 e; G, k- }; [, r% \& X
gel should be asked of the family members during
4 l( P3 b- n  o7 ~2 Z# @4 Ethe evaluation of any children who present with vir-
5 Z" k0 x/ T- j8 W% ?# e( A, ~ilization or peripheral precocious puberty. The diag-. R& j) J+ o, J; e+ \! p; u9 J
nosis can be established by just a few tests and by
; k- S2 \# t+ Z' _2 M5 z- Xappropriate history. The inability to obtain such a' O  H3 G; E- A( a( r
history, or failure to ask the specific questions, may" Q2 b: h) k# Q8 j! F+ n9 n5 q
result in extensive, unnecessary, and expensive' _. g. }) H+ V3 K, i( ?+ l
investigation. The primary care physician should be7 e( _, a" l0 N4 W% S* ?' M3 y+ C
aware of this fact, because most of these children5 f9 Q+ s3 w6 [
may initially present in their practice. The Physicians’
! c: r6 I- X. X" x: A" NDesk Reference and package insert should also put a- W7 R: K" N1 t  |
warning about the virilizing effect on a male or
2 b) e; h. T4 A8 o6 T$ I0 K% Lfemale child who might come in contact with some-
& r! o7 f' |: A* ?" Oone using any of these products.
$ x  y. e+ R! O8 s; `" p8 ^References6 g6 T+ Q6 a7 {
1. Styne DM. The testes: disorder of sexual differentiation$ L$ A4 `0 f' i  p/ i3 p4 Y* Q: M
and puberty in the male. In: Sperling MA, ed. Pediatric
  }/ {3 ?/ |. D0 U' dEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;$ D5 Z3 u0 p  c. r; F) z
2002: 565-628./ G5 C/ Q9 n! ?$ Y
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
, k7 l1 N3 w( E& V. X6 _5 @puberty in children with tumours of the suprasellar pineal
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這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 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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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
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

6 Q; L/ o. m8 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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