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Sexual Precocity in a 16-Month-Old) ?" k8 R8 ]6 _% k! v* ]9 G1 o
Boy Induced by Indirect Topical
. b* S5 k9 u* [2 ?# @5 B( l/ bExposure to Testosterone% e" x! l" f6 ?* Q8 l6 I# J
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. }; n& O1 ?$ l8 {" a+ A* F% F
and Kenneth R. Rettig, MD1* \+ }" q  |% L' z) I
Clinical Pediatrics
% K% X, g' D/ h3 m, \1 m  ]- x; @Volume 46 Number 6
6 y) x8 O0 t8 ~! L: Q1 Q4 O6 K' tJuly 2007 540-543* g6 _- A$ [+ d: L# @, @
© 2007 Sage Publications! A! I3 A# _7 V% Z; w6 l+ [
10.1177/0009922806296651
& _- K' t1 W# M7 e/ ~http://clp.sagepub.com# P' h% \* ?* [, w3 j
hosted at1 c6 L- n4 T5 F( ]% ?9 ~
http://online.sagepub.com6 O) c0 o5 ?# G5 Q/ B
Precocious puberty in boys, central or peripheral,; a! J  O2 M; j1 @. f
is a significant concern for physicians. Central
6 v9 J+ c3 \; ?: tprecocious puberty (CPP), which is mediated
6 ?* P" q0 O% Athrough the hypothalamic pituitary gonadal axis, has: a; S. L3 A. O
a higher incidence of organic central nervous system* B% J! E; z3 w: H$ O+ h: M# k1 F+ O
lesions in boys.1,2 Virilization in boys, as manifested! c( i; w5 E0 k& a
by enlargement of the penis, development of pubic
  r, l9 S, ~* M3 E; ^hair, and facial acne without enlargement of testi-4 p! \6 s8 N" c
cles, suggests peripheral or pseudopuberty.1-3 We
8 i8 H; m  W) e& F% breport a 16-month-old boy who presented with the( j2 k" q; f1 {, k5 z: e
enlargement of the phallus and pubic hair develop-' @4 ~4 L/ G+ I1 O0 [
ment without testicular enlargement, which was due
7 k: X: I) S  j2 rto the unintentional exposure to androgen gel used by
, m# ]( z7 F) j3 h& a4 L& Tthe father. The family initially concealed this infor-) @. R) r- j) {( P% O& a3 u/ O% m
mation, resulting in an extensive work-up for this  y$ ~; n/ d' G' X) c
child. Given the widespread and easy availability of
( h$ z+ n6 Q# ?* D8 M0 rtestosterone gel and cream, we believe this is proba-
5 P4 S* |! A6 M% k# V7 @0 qbly more common than the rare case report in the
, \! q: f. P* B+ ^" G) Dliterature.4
4 }9 Q: N% I+ p3 yPatient Report: J4 t# \# D+ v' S; |
A 16-month-old white child was referred to the
+ R' ^" N# d. |  V9 Qendocrine clinic by his pediatrician with the concern
, A% W( A# N0 W- i  {of early sexual development. His mother noticed. n- A  }7 \& U  Z& h' b" ~
light colored pubic hair development when he was
/ t1 T0 `4 i: S/ wFrom the 1Division of Pediatric Endocrinology, 2University of
) c( x/ @* s; o- O. LSouth Alabama Medical Center, Mobile, Alabama.
% A$ h$ {- i) pAddress correspondence to: Samar K. Bhowmick, MD, FACE,
% @$ z+ v$ Z: XProfessor of Pediatrics, University of South Alabama, College of6 a0 v; f; \" k  I
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
, A2 q. A. c. w" p7 K# O7 ]7 P- ce-mail: [email protected].$ [" Y1 `" u6 S1 \, p+ M5 R
about 6 to 7 months old, which progressively became
0 t8 d7 y8 m) T  \: Sdarker. She was also concerned about the enlarge-5 B% h. e% A8 p% J, M' _
ment of his penis and frequent erections. The child+ M6 P, ~) ~; M" S3 m% F; X/ j
was the product of a full-term normal delivery, with
5 R; B: G$ ^* E3 s* W' s+ d5 Ra birth weight of 7 lb 14 oz, and birth length of: r( G& V" o( _, c. h) k; K9 q
20 inches. He was breast-fed throughout the first year
2 ]) {4 ~- k9 ?( V2 Qof life and was still receiving breast milk along with  l6 {2 ?: Z: B
solid food. He had no hospitalizations or surgery," K/ o  q- u3 O
and his psychosocial and psychomotor development9 ]: P1 v+ M  N  ~( V
was age appropriate.
/ R1 T+ X) D8 N3 E) KThe family history was remarkable for the father,/ {& ^0 w3 H! @% g+ v9 q4 U+ U
who was diagnosed with hypothyroidism at age 16,2 g; w( T7 }$ B( t
which was treated with thyroxine. The father’s" a/ Y7 P* C/ q6 F2 s2 Y- j+ g; M
height was 6 feet, and he went through a somewhat
- r2 {+ W2 ~; _early puberty and had stopped growing by age 14.$ k$ b/ m8 z3 S  D# c
The father denied taking any other medication. The
3 Z5 }4 f: o0 D1 j4 K  S3 gchild’s mother was in good health. Her menarche
3 a# J; s8 q# R: H. lwas at 11 years of age, and her height was at 5 feet
2 n8 V1 n( I  a: n5 inches. There was no other family history of pre-! S8 s/ k, `2 J  _5 t
cocious sexual development in the first-degree rela-
, }( W* v, M- ~& Q4 |; [) \tives. There were no siblings.
0 g" J. }8 Y1 d5 P& z% p. [Physical Examination
$ S6 B, q; i& A% }* {) I' K4 `The physical examination revealed a very active,9 |( A, }8 v. ^: l3 p# y
playful, and healthy boy. The vital signs documented
0 j; J( A5 k# d' P  V* R2 Na blood pressure of 85/50 mm Hg, his length was6 ^7 G% t8 f* O6 `  I2 Q, Y
90 cm (>97th percentile), and his weight was 14.4 kg
8 k, d2 n; m6 S7 I% e  v" m8 G(also >97th percentile). The observed yearly growth
, k& l4 r+ n# }9 [5 qvelocity was 30 cm (12 inches). The examination of
' o/ B8 b1 j+ qthe neck revealed no thyroid enlargement.
% Z) s( z7 d4 v, b4 y. I, F' tThe genitourinary examination was remarkable for
' K2 g) g3 ~' H3 x5 e0 ?) renlargement of the penis, with a stretched length of5 S' P- x* f4 g& v8 y% L
8 cm and a width of 2 cm. The glans penis was very well) Y0 u* j5 B/ h& c0 U
developed. The pubic hair was Tanner II, mostly around; B3 b- ^. z9 H
540
; x; H' x6 P. k. A4 U- G9 A, p7 ?at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  G8 S7 |; [% v5 X
the base of the phallus and was dark and curled. The. i( F# ]. K' Q4 T, Q- V* G
testicular volume was prepubertal at 2 mL each.
' n' V- u; U& U# VThe skin was moist and smooth and somewhat! W2 }! S( U9 _
oily. No axillary hair was noted. There were no' l! @6 L8 @& o* j) T# i
abnormal skin pigmentations or café-au-lait spots.
0 q+ j( y0 ]' p5 x  c# C; ^Neurologic evaluation showed deep tendon reflex 2+4 X0 r7 d( I6 h; a
bilateral and symmetrical. There was no suggestion
3 m; {+ @' p5 k2 yof papilledema.
; \  `2 f# {& Y9 C& ILaboratory Evaluation5 M1 _& l& s8 L+ N0 r& p2 I* X
The bone age was consistent with 28 months by
+ h5 I- N& h5 E" L7 P1 Husing the standard of Greulich and Pyle at a chrono-( u9 U( C" W& b. }' m' i* I4 A
logic age of 16 months (advanced).5 Chromosomal% O# m3 N/ s0 I  x. b
karyotype was 46XY. The thyroid function test! s; l/ ?% Q+ A  s) j
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
; J6 s$ [, _8 |: s+ j; Q" I/ i' Tlating hormone level was 1.3 µIU/mL (both normal).
1 {5 I4 C6 l7 ?( s( zThe concentrations of serum electrolytes, blood
6 I- t: T  C5 z) H; I0 A# p0 x" curea nitrogen, creatinine, and calcium all were
2 h* [4 V6 N; k! c  bwithin normal range for his age. The concentration
9 N& L6 T: y  X6 Wof serum 17-hydroxyprogesterone was 16 ng/dL
% b. [# }1 D$ f1 V5 R+ n(normal, 3 to 90 ng/dL), androstenedione was 201 Y0 v% p, |$ a( f, O
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-# ?$ o4 f) i% u4 P( n
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
9 m" D4 l4 J8 U9 ^, Z+ Mdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
: P- \9 S. @9 Z8 T1 O* o49ng/dL), 11-desoxycortisol (specific compound S)
' Z/ z- _* n" ~: x. }- e! ^; g+ @was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
1 G/ i' k4 N* E6 Q% S- Itisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
) \6 O- O2 T' N9 ^2 ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL),2 n. r! o7 g% ]
and β-human chorionic gonadotropin was less than' [+ i* {3 `0 @) D
5 mIU/mL (normal <5 mIU/mL). Serum follicular4 _' u7 _' A& _" b* U4 \. q3 F( ^
stimulating hormone and leuteinizing hormone
" @, ]. a+ o# d  R' l9 |concentrations were less than 0.05 mIU/mL1 d- A( ~- W/ K) k, N$ b( H- @# H
(prepubertal).1 j1 E, `- e$ n+ ~
The parents were notified about the laboratory" r; y0 {9 {, w
results and were informed that all of the tests were
( i) r. Q# a- P( G* S- ]! Anormal except the testosterone level was high. The- n5 V9 H/ A6 m1 l% w
follow-up visit was arranged within a few weeks to
8 n2 X$ w# g1 q/ r% ~obtain testicular and abdominal sonograms; how-
8 E* V0 t2 f. o0 U+ f7 i8 eever, the family did not return for 4 months.
# {* l, x4 U. d6 ]0 a1 [5 Z9 ~5 J6 uPhysical examination at this time revealed that the
, n5 N/ Z% X* o$ U  q+ k2 ychild had grown 2.5 cm in 4 months and had gained" T( Q6 J4 ~, b$ k! H9 h  Y( U+ K
2 kg of weight. Physical examination remained
9 k4 p4 g+ q! Eunchanged. Surprisingly, the pubic hair almost com-; p% X1 h# Q, W- C( d3 r) |3 [
pletely disappeared except for a few vellous hairs at
; b3 S6 u) `' o) {the base of the phallus. Testicular volume was still 27 _! T2 a8 X  \3 n  ^1 N. `
mL, and the size of the penis remained unchanged.$ ]# R2 L# b" j& o5 r. z  J
The mother also said that the boy was no longer hav-
& @5 c3 Z7 U1 a8 {3 ging frequent erections.
2 k* e/ b; m8 L9 y0 ?+ a9 ]4 T* ]Both parents were again questioned about use of4 E3 T. c8 b3 Z- S7 O
any ointment/creams that they may have applied to" ]2 ]" q# G& a( X6 n# n( G
the child’s skin. This time the father admitted the# Q4 v: E- W) L, Z2 A6 X
Topical Testosterone Exposure / Bhowmick et al 541
% ]9 m" ]* t4 ]* ^use of testosterone gel twice daily that he was apply-
  j% A/ X) `# t: J) N; fing over his own shoulders, chest, and back area for2 D1 M9 l* z8 y% S3 z# T0 W1 d
a year. The father also revealed he was embarrassed
8 o9 h( O% c. E9 `3 q( n% M" _to disclose that he was using a testosterone gel pre-) ]1 M, O! k3 f& n9 ]! T3 @4 u
scribed by his family physician for decreased libido/ L% a4 K+ {* D% u0 O. l+ f8 r
secondary to depression.
2 N" o& |, n4 b8 Q2 U' _( NThe child slept in the same bed with parents.
. ?7 }7 x' w- j/ e1 H: jThe father would hug the baby and hold him on his1 y! \  s7 z* M6 V0 [/ V4 F
chest for a considerable period of time, causing sig-. n7 R' t0 n6 |' _8 g. ~
nificant bare skin contact between baby and father.
/ {- N9 [8 O. m. F1 `6 bThe father also admitted that after the phone call,
8 A$ j0 E! b8 j& Y  j5 w7 @* Swhen he learned the testosterone level in the baby
# b3 Z/ s# u; p( x/ y; Nwas high, he then read the product information
/ G! N( l- `1 B3 u' r. c7 bpacket and concluded that it was most likely the rea-' `+ X3 ]3 ^- w7 X) L" k
son for the child’s virilization. At that time, they. e( h+ S8 K" T7 h- Q: p0 s4 c
decided to put the baby in a separate bed, and the5 {6 b$ I! R# k8 b9 d, p
father was not hugging him with bare skin and had% A& S( \2 L2 ]
been using protective clothing. A repeat testosterone9 [/ a$ ]: O9 ]1 M! X$ y
test was ordered, but the family did not go to the% Y1 i/ e1 C+ f  k2 r. @" f8 s3 h- ~
laboratory to obtain the test.5 E# M  R3 H. p9 l$ S& z
Discussion9 U' y& p, }& _3 H6 n6 `
Precocious puberty in boys is defined as secondary' v+ O& U. y! h
sexual development before 9 years of age.1,4! \+ k! N1 k& }- w$ N
Precocious puberty is termed as central (true) when
/ Q8 e+ C$ Q3 E5 i* D( C( ^it is caused by the premature activation of hypo-
- R; V8 r) C/ H& vthalamic pituitary gonadal axis. CPP is more com-
+ Y6 F( l- A2 }4 P% nmon in girls than in boys.1,3 Most boys with CPP
, U2 ?" X" H0 ^& I0 Y& Vmay have a central nervous system lesion that is' D9 H, _+ q! |: {, f( U
responsible for the early activation of the hypothal-6 W5 f5 {# v  T( D" u7 y
amic pituitary gonadal axis.1-3 Thus, greater empha-
+ c, f7 l. b  W! i1 _( L$ f. msis has been given to neuroradiologic imaging in$ ^6 r" o0 W. M+ u
boys with precocious puberty. In addition to viril-% Z9 y1 A, w# ]$ O. g% k# X
ization, the clinical hallmark of CPP is the symmet-, k* _% H! d7 I
rical testicular growth secondary to stimulation by
3 v7 B& C) y# f! a* ngonadotropins.1,3
; k% F) q9 K1 F  s2 w7 @7 ^. f7 WGonadotropin-independent peripheral preco-" k% E3 D) t4 _- C  N7 Z' j4 Z
cious puberty in boys also results from inappropriate
. o" u! z, K/ Eandrogenic stimulation from either endogenous or+ p! g8 r- W: T: v* H- b2 J& H7 `
exogenous sources, nonpituitary gonadotropin stim-
( L! l( E" n1 Gulation, and rare activating mutations.3 Virilizing
' n1 D: C8 ?- i4 h0 p# Dcongenital adrenal hyperplasia producing excessive% P' N. r9 e- ^, u& s1 B- T
adrenal androgens is a common cause of precocious
3 I2 r( ~7 J2 `# n4 @! D$ O2 X( cpuberty in boys.3,4% N1 M+ {. Y0 w6 y6 R* d
The most common form of congenital adrenal
/ V, C9 P3 }  T" P2 @  zhyperplasia is the 21-hydroxylase enzyme deficiency.& a+ f! s3 F6 Z# `) {7 F+ K
The 11-β hydroxylase deficiency may also result in# U% Q9 c% S0 e$ D0 \& b4 c1 x. R1 Y9 d
excessive adrenal androgen production, and rarely,* R- O: Z8 {9 T0 a& K
an adrenal tumor may also cause adrenal androgen
, j# o3 C% h: h/ b6 Y" lexcess.1,3
1 t2 o; y& f: v5 U$ m, i6 oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 s6 z% k5 a" ]. n5 `4 t8 }542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
- s) U1 M, d  F- t0 E8 }* Z8 NA unique entity of male-limited gonadotropin-3 B: d* Z4 |. R" m, d
independent precocious puberty, which is also known9 U7 i4 K, g$ j( i6 |
as testotoxicosis, may cause precocious puberty at a
+ l: Q, D$ l8 x8 b. s2 Q5 ]) L: x$ E$ mvery young age. The physical findings in these boys7 I$ M# Y! b# o1 a2 ~! @# Z" S* G
with this disorder are full pubertal development,8 Z! z+ J5 n2 J2 k
including bilateral testicular growth, similar to boys
6 c) [! T0 m2 Awith CPP. The gonadotropin levels in this disorder$ t* [7 w( N* `8 S
are suppressed to prepubertal levels and do not show9 s- m& V( V3 S$ T- P- t0 {; y
pubertal response of gonadotropin after gonadotropin-3 ^' Z& k9 L* s, h8 h; n
releasing hormone stimulation. This is a sex-linked) K  j( {+ @5 m" `2 ?1 L
autosomal dominant disorder that affects only
+ e7 y1 I, O2 V% U+ Kmales; therefore, other male members of the family
' g# X! `% a8 c0 R8 w  r  q" mmay have similar precocious puberty.3
. c4 u, k! N8 Q: i. J1 {In our patient, physical examination was incon-3 p' u* i, C3 m# D- |
sistent with true precocious puberty since his testi-
: m: K0 [" v6 ucles were prepubertal in size. However, testotoxicosis
; E9 R: U8 h# v8 N4 kwas in the differential diagnosis because his father
0 [3 K5 T1 Z8 |1 v) rstarted puberty somewhat early, and occasionally,6 _+ z/ x9 V$ k6 i4 w+ I
testicular enlargement is not that evident in the6 P2 d# ?% I; S- w$ q6 m5 ]
beginning of this process.1 In the absence of a neg-8 F& {1 g+ w8 |, w, ^& ?
ative initial history of androgen exposure, our3 r- J$ C! i: u- E2 Q% p
biggest concern was virilizing adrenal hyperplasia,5 L' l/ `( Q0 P5 s
either 21-hydroxylase deficiency or 11-β hydroxylase/ [% x# [8 f* Q
deficiency. Those diagnoses were excluded by find-
8 v; E0 i5 E" A+ X2 F: l- w9 ping the normal level of adrenal steroids.( |3 x8 }8 {! I* i4 R& J) X
The diagnosis of exogenous androgens was strongly/ Q8 z4 ?) X- `2 T; A
suspected in a follow-up visit after 4 months because9 S& w8 Q6 n6 v2 l& L% y
the physical examination revealed the complete disap-
, s# |. o+ @9 dpearance of pubic hair, normal growth velocity, and& X: ]; n* c/ I7 t
decreased erections. The father admitted using a testos-; O; h. _: I3 r
terone gel, which he concealed at first visit. He was) m+ q: R1 \/ X9 z6 W
using it rather frequently, twice a day. The Physicians’
' y, }( n, y0 p9 u0 D/ U: wDesk Reference, or package insert of this product, gel or
' J5 S% A  s# Z" M: ?* u0 Zcream, cautions about dermal testosterone transfer to6 f+ r# Y& }- b; O
unprotected females through direct skin exposure.
1 m( {7 T# [9 F1 J5 DSerum testosterone level was found to be 2 times the
3 ]8 h9 U: F. c: m4 R, m; Mbaseline value in those females who were exposed to/ n. z( D: N( l1 S2 G% a
even 15 minutes of direct skin contact with their male  E* U* k; m6 j: R# |
partners.6 However, when a shirt covered the applica-+ {& A- s: {4 |0 N- A9 e
tion site, this testosterone transfer was prevented.3 n, C6 K0 r$ X$ N; S, w2 l
Our patient’s testosterone level was 60 ng/mL,
2 T  M+ p* e& y2 T( nwhich was clearly high. Some studies suggest that
6 j8 M# e+ j! l4 [1 m% }dermal conversion of testosterone to dihydrotestos-3 p+ k5 G# L+ }4 ]) `% ^0 B
terone, which is a more potent metabolite, is more3 M7 d6 M) F  }4 G; M, s+ B2 i
active in young children exposed to testosterone, O& I7 p( _* [, j# m) e7 R
exogenously7; however, we did not measure a dihy-: C& {7 S  k$ a$ V$ u
drotestosterone level in our patient. In addition to9 q2 A3 }6 T  c) F: t/ A
virilization, exposure to exogenous testosterone in: R- P5 A. a* w  i0 g2 l; `9 E% d
children results in an increase in growth velocity and& b( P! H- M/ r( w5 `" [
advanced bone age, as seen in our patient.
& ~6 E% I" O# o5 V( i& T& mThe long-term effect of androgen exposure during: S; F9 Q5 ]; n$ s
early childhood on pubertal development and final
  \# H4 N/ N4 F+ B) R5 xadult height are not fully known and always remain
. k1 P# f# ^9 g6 a$ g0 t! N* Ta concern. Children treated with short-term testos-
( l9 i  p8 G/ s+ [+ w. jterone injection or topical androgen may exhibit some9 V+ V" T$ M( _9 o  L
acceleration of the skeletal maturation; however, after
3 U8 T" A( g) zcessation of treatment, the rate of bone maturation8 `: P9 U' f; e/ O& p
decelerates and gradually returns to normal.8,9
* ?' Z; K( Z0 J# k1 bThere are conflicting reports and controversy  h" i+ X8 u. u1 a6 h6 \
over the effect of early androgen exposure on adult
5 t& b3 Q) S' ?0 q& T% f% M; \( Npenile length.10,11 Some reports suggest subnormal, k, m! b" t# |1 U6 P! u: D
adult penile length, apparently because of downreg-
* R( L/ F2 h9 u# {$ }  c3 `ulation of androgen receptor number.10,12 However,
, O5 x+ S2 ?$ R% l: wSutherland et al13 did not find a correlation between6 O* O) n3 i) Y. M: p
childhood testosterone exposure and reduced adult" C; m  Y! Y& h* S9 t" s
penile length in clinical studies.2 S. k0 L2 r/ S& S
Nonetheless, we do not believe our patient is' H, n" x* _6 H3 [" \5 {
going to experience any of the untoward effects from
/ G( i' i! Q: h7 ^7 t- O! M9 H2 vtestosterone exposure as mentioned earlier because
% r  x4 {2 C2 A5 ~) ^the exposure was not for a prolonged period of time./ }; j1 R  E- r/ }; q1 [7 y: e5 Q
Although the bone age was advanced at the time of
) ^4 m, T1 a' f0 G0 Fdiagnosis, the child had a normal growth velocity at6 C, ]) I0 O1 y  n  e/ w
the follow-up visit. It is hoped that his final adult- [* z0 ]) f) |) x- _  p
height will not be affected.
5 F3 ~% |- N- A% h3 ?' [Although rarely reported, the widespread avail-
  P8 u1 S+ K4 T9 jability of androgen products in our society may: a2 `* y- f( r  h; \, C) h" X
indeed cause more virilization in male or female( T; M" \" s. t' |. ^7 j; {; ?
children than one would realize. Exposure to andro-
& \2 d7 n5 H9 n$ Cgen products must be considered and specific ques-
# E; [4 V3 _! g5 u* itioning about the use of a testosterone product or
: J8 a% ^9 e3 L7 n9 W/ r, zgel should be asked of the family members during0 w, ?6 T0 r/ w
the evaluation of any children who present with vir-
. Z' g% T! A- z( q' i  i) m5 w5 zilization or peripheral precocious puberty. The diag-" Z3 a. K8 m" s+ C
nosis can be established by just a few tests and by5 b5 O  }$ [; ~! Z
appropriate history. The inability to obtain such a
& C% K- ?: M. k4 L$ _history, or failure to ask the specific questions, may
. B9 v9 c0 i" _3 l7 R) rresult in extensive, unnecessary, and expensive
0 [# j6 s! b" t& G7 O8 [investigation. The primary care physician should be
0 G. {- I; V) _; j$ N  V/ z; S  Y* zaware of this fact, because most of these children1 T6 y( ^3 p. O7 K/ ?% h
may initially present in their practice. The Physicians’
+ ^' \$ }( D) [& h) i) f! H* HDesk Reference and package insert should also put a# k% {* k- l! h! K4 S7 b& c  m' F
warning about the virilizing effect on a male or
; G1 ^+ ]* c5 Y  wfemale child who might come in contact with some-
6 H; l8 H2 N% m( E# Aone using any of these products.
. Z0 |: p* G* p, P) j$ A; y( sReferences
$ a* T1 g( Y: V( E1. Styne DM. The testes: disorder of sexual differentiation
: ?6 `4 R* q4 Hand puberty in the male. In: Sperling MA, ed. Pediatric" ^" o1 ~! |- v' s& B9 B( v$ h
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
6 @( ~9 O5 w/ X4 d& m2 p& t2002: 565-628.
7 M. X( l- z8 n2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
, U- @1 k" Q8 `  ^9 upuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old$ u  t) z6 j6 p' u% t
Boy Induced by Indirect Topical
+ B3 ^8 ~! \! JExposure to Testosterone/ J4 m; J$ `! f- u0 I$ N
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
4 ?$ t/ S) J1 d' A6 J6 m+ G9 wand Kenneth R. Rettig, MD1/ z; I6 Y3 d- E% ]5 X9 c/ \
Clinical Pediatrics
: v4 f$ \2 z0 [/ J! UVolume 46 Number 68 M5 P  L( f/ M+ Z. |
July 2007 540-543, I0 a7 L4 E- z
© 2007 Sage Publications
% P& E3 x: K4 k) P3 x3 p2 w8 D10.1177/0009922806296651
$ _) r: F$ R. p: B2 f* V+ uhttp://clp.sagepub.com! g: z9 w; m0 H5 U$ l" P* |, s7 t& M
hosted at) w9 O' {$ X# L
http://online.sagepub.com7 n5 R" b4 p4 ^6 w4 Q
Precocious puberty in boys, central or peripheral,4 Q% }, ^. B3 H0 M4 M
is a significant concern for physicians. Central
- {+ k% A/ k- o! {6 iprecocious puberty (CPP), which is mediated
% L1 R6 }1 ]2 p# w) ]2 a" m  ~! fthrough the hypothalamic pituitary gonadal axis, has5 q$ B# A% T# G  L" H/ F
a higher incidence of organic central nervous system
* S1 h# C% F  q# r# P5 J0 Elesions in boys.1,2 Virilization in boys, as manifested1 l# ~0 i0 d7 l9 k: l
by enlargement of the penis, development of pubic8 w$ P6 g& F( U& c* y9 q/ g. D
hair, and facial acne without enlargement of testi-2 {1 m9 v7 s) ]$ ^& T/ v- y
cles, suggests peripheral or pseudopuberty.1-3 We. w: ^7 O: h5 {3 y
report a 16-month-old boy who presented with the) E" t- d. @; q2 I; N
enlargement of the phallus and pubic hair develop-
4 x" A- z3 t. t% mment without testicular enlargement, which was due3 p3 w4 N% a% E9 _  G* C9 c2 O
to the unintentional exposure to androgen gel used by
; m; C$ ?8 V+ \% G7 zthe father. The family initially concealed this infor-8 o5 }  F+ p% X6 H7 m4 b% I
mation, resulting in an extensive work-up for this
; {( e! Z" p  W5 gchild. Given the widespread and easy availability of" e* X, r1 \3 |7 i# a$ J# f
testosterone gel and cream, we believe this is proba-  k* G4 {% Z! h! R$ H1 W
bly more common than the rare case report in the
4 ]- N6 G$ r, W. Gliterature.42 R  X( f0 i- Z# V/ F( V" Z) _
Patient Report
- u% j; U3 q$ s8 ]  AA 16-month-old white child was referred to the
6 O% e/ A9 q' P5 Fendocrine clinic by his pediatrician with the concern
: n! g8 {9 y8 J5 W" Q- T5 }5 D6 }of early sexual development. His mother noticed
( _1 z; ]6 g$ h: Y" Xlight colored pubic hair development when he was
2 N, V+ Y2 W) w6 q$ zFrom the 1Division of Pediatric Endocrinology, 2University of
7 x- m8 Z* ]; n8 |/ G+ D) XSouth Alabama Medical Center, Mobile, Alabama.0 I4 ~/ i4 j6 G5 ]; \1 m
Address correspondence to: Samar K. Bhowmick, MD, FACE,
5 E: O6 Z7 T( D4 Z2 \Professor of Pediatrics, University of South Alabama, College of
8 P  [& _2 U: U+ }Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 C5 a* v# j4 o: n
e-mail: [email protected].8 M9 {; e6 }+ {" A' ^- f5 {
about 6 to 7 months old, which progressively became" y/ [4 L5 {  D, D; u$ ^6 G
darker. She was also concerned about the enlarge-
# ~7 N% Z) X  l5 lment of his penis and frequent erections. The child
' @8 @7 |5 k3 y, }1 Q! {3 f" swas the product of a full-term normal delivery, with
' [0 V9 y5 D( ]: j9 da birth weight of 7 lb 14 oz, and birth length of5 h) u4 V& W. P4 @
20 inches. He was breast-fed throughout the first year
  q4 ^8 a8 |/ v9 E; o: Zof life and was still receiving breast milk along with
  c- i8 F/ ?4 s- P, B" J7 b( Asolid food. He had no hospitalizations or surgery,
8 ]/ |2 j% Y  J7 i# E; L' q7 P4 aand his psychosocial and psychomotor development
. T' N4 {! ], B: l4 xwas age appropriate.3 `' g1 ]0 l1 I
The family history was remarkable for the father,
- T5 ~/ H0 q7 v6 C$ C( Lwho was diagnosed with hypothyroidism at age 16,
4 g  N! V  q$ Y' R0 X8 C) J3 E0 ^1 f: `which was treated with thyroxine. The father’s3 m4 M! \9 U7 `
height was 6 feet, and he went through a somewhat
3 x- U! k& q8 Mearly puberty and had stopped growing by age 14.
" g' y7 d) K8 W/ L' C4 e& [; {The father denied taking any other medication. The2 p3 v4 [! R% |$ u, q7 ^! ^
child’s mother was in good health. Her menarche
& x3 y! c. O8 Bwas at 11 years of age, and her height was at 5 feet4 d! H8 N& }5 y: Y. d- k% D
5 inches. There was no other family history of pre-
0 c8 Y9 `0 u  O' ~# y: i5 I3 bcocious sexual development in the first-degree rela-
6 r0 v1 O! N, ?) _% D* g" f- ntives. There were no siblings.
) m2 `, ~6 ?6 {9 s' H& O  O" C) TPhysical Examination
; b) [. L' v# E4 SThe physical examination revealed a very active,
6 a7 F+ l6 ]$ J# X' w. K1 Pplayful, and healthy boy. The vital signs documented9 i) k% n' {2 g6 m. {
a blood pressure of 85/50 mm Hg, his length was
, \9 k: Q8 i' G90 cm (>97th percentile), and his weight was 14.4 kg
' Q* Z9 L1 M9 L7 a2 A/ P(also >97th percentile). The observed yearly growth  D7 D. ]$ e6 r9 p
velocity was 30 cm (12 inches). The examination of) P9 V4 u. ^# H4 k. G; u- Z( e
the neck revealed no thyroid enlargement.' v) n2 `' k8 @) X/ }
The genitourinary examination was remarkable for& D2 r& D: O7 y: b, D! Y
enlargement of the penis, with a stretched length of" ^# E( X" ]. D, x# J
8 cm and a width of 2 cm. The glans penis was very well. a$ n/ a8 a; }% ?% ?# J
developed. The pubic hair was Tanner II, mostly around# }# `0 o3 L, x# t# |
540; A3 u" ~/ N* ^) \1 ~+ T
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 S- x9 z) o+ N1 S8 dthe base of the phallus and was dark and curled. The3 V& a" f$ }8 _6 ^6 D0 b
testicular volume was prepubertal at 2 mL each.
) i  ^: N# R2 a* O  m+ Q6 t" X. f8 SThe skin was moist and smooth and somewhat
. K  F8 Q; V% h6 D; O+ c$ Boily. No axillary hair was noted. There were no
) E: c; d/ b" L* q. yabnormal skin pigmentations or café-au-lait spots.
' K5 L5 p2 u5 V; Z* ^  {0 Q8 ^Neurologic evaluation showed deep tendon reflex 2+
  O+ g* J, _0 |' r, \" H/ abilateral and symmetrical. There was no suggestion
  C4 ~5 L! y: M& Dof papilledema.( I, v0 w* U1 m: O2 e: u
Laboratory Evaluation; w( `. ^. L" ?: ~2 z& T  v
The bone age was consistent with 28 months by: K3 ]" z- w: q3 V( h! i
using the standard of Greulich and Pyle at a chrono-
7 Z/ i6 H3 l* J! ]0 T/ _: N' Z. Q* Z! mlogic age of 16 months (advanced).5 Chromosomal. a) j: E$ g9 M8 p3 J( j
karyotype was 46XY. The thyroid function test
' |4 N5 U* f6 |) [/ Sshowed a free T4 of 1.69 ng/dL, and thyroid stimu-. o, i, C4 s5 Y3 b7 k7 h# U  o
lating hormone level was 1.3 µIU/mL (both normal).% w3 X, D- s- d2 C
The concentrations of serum electrolytes, blood, d" N0 F3 X& P
urea nitrogen, creatinine, and calcium all were
, [! S  u+ r3 l3 b3 C1 Lwithin normal range for his age. The concentration* ~$ {; I9 b! B0 l
of serum 17-hydroxyprogesterone was 16 ng/dL
* P; I, {0 {/ c6 x# d5 N! W# t(normal, 3 to 90 ng/dL), androstenedione was 20" I5 m) W  V/ E. i, i! J
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-3 k5 ]8 R; p" m
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
. y7 g/ d* a( j" }1 A: ~desoxycorticosterone was 4.3 ng/dL (normal, 7 to
2 j# C  G" k2 ?0 i49ng/dL), 11-desoxycortisol (specific compound S)
1 y6 L7 g. g8 ^0 awas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-4 `5 F& [* \/ _+ L; ^$ O
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total* [' M9 E4 I4 F5 i  c
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),6 V+ ?# }  m- }& @4 n& Q' |9 ~
and β-human chorionic gonadotropin was less than
6 O" f2 N; S1 o7 s& |) Y' U3 U, |5 mIU/mL (normal <5 mIU/mL). Serum follicular. E) J/ ?' X# Y  N: M, U& x6 E  G
stimulating hormone and leuteinizing hormone/ ~" {# x" `& s* k' ^
concentrations were less than 0.05 mIU/mL
' R/ K6 w. c( x0 a: f% O: ^0 Y2 k(prepubertal).2 d, J  }! v& ~& M
The parents were notified about the laboratory
0 Z" P( s6 }* Q# wresults and were informed that all of the tests were
$ |6 {* R, g4 jnormal except the testosterone level was high. The
& ?, E1 j# E9 c+ B) P4 `follow-up visit was arranged within a few weeks to8 S4 M. Q/ q- U
obtain testicular and abdominal sonograms; how-
& J, b- R7 V6 @ever, the family did not return for 4 months.
+ {; L) O) S8 J; v$ ~Physical examination at this time revealed that the& A( Q/ F9 ^: Z. a' i4 {
child had grown 2.5 cm in 4 months and had gained% a+ |4 b4 d  r& q6 B6 }
2 kg of weight. Physical examination remained  ?: ^2 q9 r- _. a) a
unchanged. Surprisingly, the pubic hair almost com-! Z: R7 ]  T; s0 f
pletely disappeared except for a few vellous hairs at/ B; {+ m) A0 g; B# d+ \( d' v
the base of the phallus. Testicular volume was still 20 d- [- c; Z$ S/ R
mL, and the size of the penis remained unchanged.
& k+ D) K7 m! m; i4 g" PThe mother also said that the boy was no longer hav-8 a* n6 f: ?, q) U, s) R! m
ing frequent erections.) l9 W( z/ V3 ^. b; U
Both parents were again questioned about use of
: I: g9 U: \% T/ c8 o! {any ointment/creams that they may have applied to
0 F1 }* X; M. Tthe child’s skin. This time the father admitted the1 Y9 K3 A7 J, O4 l; y8 P% ~
Topical Testosterone Exposure / Bhowmick et al 541
" z% S. ?, A4 w* j" c& A. y4 z3 ?5 @8 [/ {use of testosterone gel twice daily that he was apply-7 |) C0 E+ a. _7 g" i5 o- S
ing over his own shoulders, chest, and back area for! J( j  u! p* G& v7 ?' R" G
a year. The father also revealed he was embarrassed
- y1 P: ^- b& I; e1 s' bto disclose that he was using a testosterone gel pre-5 L5 x0 C9 g$ a
scribed by his family physician for decreased libido0 J, v" ~% X( X! t; o6 {
secondary to depression.; Q4 y. N, X6 Q# q- ^8 [# A
The child slept in the same bed with parents.# y# x* W& o  J7 l  A  ^8 W
The father would hug the baby and hold him on his
! p1 T+ G- s, z' t3 c$ cchest for a considerable period of time, causing sig-
# G4 b+ G  f; U# Dnificant bare skin contact between baby and father.  F( z2 _1 H+ J* ?/ z: ^
The father also admitted that after the phone call,
2 g9 C! e& V  T) Jwhen he learned the testosterone level in the baby2 \, t9 o6 @+ @, [; X
was high, he then read the product information- |( i5 U7 P1 V1 I
packet and concluded that it was most likely the rea-
1 j6 _' e7 h; B# gson for the child’s virilization. At that time, they, r) {. N9 X9 ^5 g3 ^
decided to put the baby in a separate bed, and the
% n+ {, l3 q! `7 Sfather was not hugging him with bare skin and had- U$ f3 A1 V2 I5 _! m- v
been using protective clothing. A repeat testosterone
3 V6 Z/ b0 a, d" J* k4 Qtest was ordered, but the family did not go to the. |( t+ t+ `8 g
laboratory to obtain the test.5 Q- r# C" r7 ~
Discussion+ d( t3 d/ h0 k  H
Precocious puberty in boys is defined as secondary
: ?* @' u* d8 E3 hsexual development before 9 years of age.1,4
- d5 \1 K  t7 ^! x  S/ l6 o& mPrecocious puberty is termed as central (true) when
* R" n8 P. @  r! [" T  Bit is caused by the premature activation of hypo-6 _9 H$ U7 i) U4 R. o% g
thalamic pituitary gonadal axis. CPP is more com-
8 q5 f; j, ^6 ]; e- J. M* e3 cmon in girls than in boys.1,3 Most boys with CPP3 L. ?( V: f8 k2 h
may have a central nervous system lesion that is
' ~/ p% I5 v: c8 r  O* [* Tresponsible for the early activation of the hypothal-' [- K' {0 {3 a- c; u% V+ O
amic pituitary gonadal axis.1-3 Thus, greater empha-. q8 i" C3 L. N; |( ~4 E5 Q
sis has been given to neuroradiologic imaging in
* ^8 D, Q( ~( n, V1 cboys with precocious puberty. In addition to viril-: \4 G8 w7 o$ R8 k& w; {
ization, the clinical hallmark of CPP is the symmet-! O5 Q; X) y7 f' \
rical testicular growth secondary to stimulation by! u2 x$ P' S3 F0 i" g: w
gonadotropins.1,3
: [. ]9 L5 i, s2 z: kGonadotropin-independent peripheral preco-6 M7 \' w# T/ R5 b; z
cious puberty in boys also results from inappropriate
: D. v4 l5 m" y; `# g  Jandrogenic stimulation from either endogenous or& W. A4 y3 t0 x1 z- ~* C. e2 j8 k6 L
exogenous sources, nonpituitary gonadotropin stim-7 u" G8 n3 O3 Y) d
ulation, and rare activating mutations.3 Virilizing. P) o! v; M1 e( O
congenital adrenal hyperplasia producing excessive
  Y0 ~$ U; Z& H& fadrenal androgens is a common cause of precocious, b- T2 h& B, V5 w* ~+ V$ _
puberty in boys.3,48 i6 c$ p3 j# B& Q/ i( Q+ P7 k
The most common form of congenital adrenal+ w! I2 F, \1 B2 v  I) Z  b
hyperplasia is the 21-hydroxylase enzyme deficiency.! M# b3 ]3 ^0 y4 }3 J) L7 \
The 11-β hydroxylase deficiency may also result in1 x4 {+ q' G& k9 d
excessive adrenal androgen production, and rarely,. f$ r/ m3 E8 B4 Y0 q6 j% H" X' f
an adrenal tumor may also cause adrenal androgen5 I& H( T5 l) `6 m2 W9 J
excess.1,3
) U, h  F# X! Z" C! m! hat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 f3 V* J! O$ P& |+ P8 r542 Clinical Pediatrics / Vol. 46, No. 6, July 2007- U& A1 p+ P3 M7 x1 b7 D
A unique entity of male-limited gonadotropin-3 ?. c5 u$ E" l2 O
independent precocious puberty, which is also known
* [1 f0 A2 d0 }& i! Q+ k9 o" gas testotoxicosis, may cause precocious puberty at a
) p) P# V. x; v& U0 p7 i" B- V" Gvery young age. The physical findings in these boys
- Q2 U# R3 q  \; U; Z( Bwith this disorder are full pubertal development,
# R9 N' J/ L  T; B  a/ d- Bincluding bilateral testicular growth, similar to boys
) y" u2 }0 ]+ R1 H& iwith CPP. The gonadotropin levels in this disorder
$ d5 r6 j5 l- I' D, Oare suppressed to prepubertal levels and do not show+ o2 P& @( q6 p4 [/ ^
pubertal response of gonadotropin after gonadotropin-$ o. F6 c, {8 c& u! V* k
releasing hormone stimulation. This is a sex-linked
0 r# a- ?& n- }2 n2 W0 O* ^autosomal dominant disorder that affects only
% k8 b. J8 w: [1 f* z# smales; therefore, other male members of the family  S8 W1 S# _& R' _
may have similar precocious puberty.3
8 R# k" u" s* ]& M3 E. jIn our patient, physical examination was incon-
) d+ E+ G: g8 z( h# l7 Esistent with true precocious puberty since his testi-
! u. K5 ^0 O4 D7 [cles were prepubertal in size. However, testotoxicosis8 E3 o% _& I; f; G4 k% W; e
was in the differential diagnosis because his father
- ?% `) A* M( Fstarted puberty somewhat early, and occasionally,# U0 f& q& E1 v7 p
testicular enlargement is not that evident in the
  L: K  B# R. e8 w* s* z* Gbeginning of this process.1 In the absence of a neg-- K# J- Y2 v( ~! J6 V
ative initial history of androgen exposure, our
: D" T+ P$ q- s" Obiggest concern was virilizing adrenal hyperplasia,* }- ~6 ^& Y% M4 c
either 21-hydroxylase deficiency or 11-β hydroxylase
7 y; |* `& I! I) wdeficiency. Those diagnoses were excluded by find-
, R( j  J/ j1 R8 ting the normal level of adrenal steroids.5 F. ^4 y; h0 b/ n
The diagnosis of exogenous androgens was strongly5 v( A3 ?4 N+ E: W- |4 x: t
suspected in a follow-up visit after 4 months because! S& i) v; s: n
the physical examination revealed the complete disap-
- _% k- E: n& K4 _/ F+ p8 opearance of pubic hair, normal growth velocity, and, A# w, w9 ?# Q, c4 o
decreased erections. The father admitted using a testos-
* e* ]4 k& s& Y: r! uterone gel, which he concealed at first visit. He was9 l. o3 O% K. R- [' e* z& [
using it rather frequently, twice a day. The Physicians’  P. o% W! v8 v& c+ y* D% ~
Desk Reference, or package insert of this product, gel or
  U: d/ x  [; ]- S" Z. L: }0 Mcream, cautions about dermal testosterone transfer to
" W  D3 F* e! `2 h4 H$ Yunprotected females through direct skin exposure./ K# j; p) ~, X+ N2 X0 p# W7 W4 b
Serum testosterone level was found to be 2 times the/ `& U2 _* g1 c) q; ?+ \9 a1 T
baseline value in those females who were exposed to
. l& {  z+ i! J7 u% S- keven 15 minutes of direct skin contact with their male
9 Q1 q) k# S5 E2 j  D) a- y, kpartners.6 However, when a shirt covered the applica-
- ?2 i* g" x) W7 \1 U( h6 ]tion site, this testosterone transfer was prevented.
) D3 M. d& c7 a1 ]) |; s' z1 Z. GOur patient’s testosterone level was 60 ng/mL,2 `2 d1 C9 m2 K  Y4 j1 j$ h
which was clearly high. Some studies suggest that& K8 M0 k8 {4 c; ?
dermal conversion of testosterone to dihydrotestos-1 k8 B8 C5 Y1 a. N  R& P
terone, which is a more potent metabolite, is more
! h! V' m# B6 e7 k* z/ }active in young children exposed to testosterone( X/ P4 o' f5 v, c( {8 `7 U$ R
exogenously7; however, we did not measure a dihy-9 m8 s) s! F' V0 ?* e5 |  q
drotestosterone level in our patient. In addition to
7 G; s- N; o1 t  H9 n1 E7 pvirilization, exposure to exogenous testosterone in, E# M, `* ]9 f( n2 C8 t+ X
children results in an increase in growth velocity and5 X8 ~9 ^1 o2 X: Q9 a, E# v
advanced bone age, as seen in our patient.9 r% y# d! N7 Y0 m3 U
The long-term effect of androgen exposure during
: B+ Q) P2 Z: N& c$ Xearly childhood on pubertal development and final( P/ [7 V" o% u6 a2 c; }
adult height are not fully known and always remain& J& l( e  \5 v
a concern. Children treated with short-term testos-
; P" L9 j% L! n" ~terone injection or topical androgen may exhibit some
# h/ h6 t6 }* e9 U) n* \. o# L4 kacceleration of the skeletal maturation; however, after  ^+ [+ A' |/ a2 R5 H/ O, q
cessation of treatment, the rate of bone maturation
- X6 g4 v  y7 p8 O2 U/ ldecelerates and gradually returns to normal.8,9! j! Y7 r0 V( A% N
There are conflicting reports and controversy$ r: M' `' C3 c& g
over the effect of early androgen exposure on adult
/ @4 w4 E( I2 {penile length.10,11 Some reports suggest subnormal
% a4 G  q7 u0 j0 J! ^! U! qadult penile length, apparently because of downreg-7 b1 h% D$ c6 E) c
ulation of androgen receptor number.10,12 However,
: Z) q2 I0 U' q( `Sutherland et al13 did not find a correlation between" D, Y) {7 m2 @$ _5 R& b8 G
childhood testosterone exposure and reduced adult8 q4 E3 n8 y2 P4 k+ D3 l2 z
penile length in clinical studies.4 q) ]6 l2 z4 [2 |6 m% T
Nonetheless, we do not believe our patient is
3 Y. n, R1 }1 I0 Y7 t  t- ~% Ygoing to experience any of the untoward effects from# H8 r- R3 u- H+ s% k
testosterone exposure as mentioned earlier because
' ]3 u& s. H& G8 `2 t# ?the exposure was not for a prolonged period of time.
; d$ q* I- s3 r' X3 O5 B: s+ qAlthough the bone age was advanced at the time of
" l5 r0 Z, w" f: G+ n6 D, idiagnosis, the child had a normal growth velocity at
( e0 `$ I. Q) t; h) Pthe follow-up visit. It is hoped that his final adult
' W* b1 D, }, S; M* o& p) |6 }( Mheight will not be affected.
* A. t" G" Y( EAlthough rarely reported, the widespread avail-# L4 u9 Z3 i  E( b: L
ability of androgen products in our society may
! F/ N5 G# A0 }: x8 hindeed cause more virilization in male or female! [, s$ l" k/ I' |- Z* T2 T
children than one would realize. Exposure to andro-
  z9 z1 A( ?6 u, H+ Dgen products must be considered and specific ques-' W' l: C' f5 m$ E6 T5 u
tioning about the use of a testosterone product or. e' t6 }, c* F% b
gel should be asked of the family members during
1 @+ Y3 D( V# A4 V& C7 Ithe evaluation of any children who present with vir-
# W/ i2 g5 B4 N. M3 w2 d$ |( d* J9 wilization or peripheral precocious puberty. The diag-* m; i: C8 `% Z6 q
nosis can be established by just a few tests and by( k5 B6 b! R+ V- |4 I4 I
appropriate history. The inability to obtain such a8 a; Y# v* W$ Z( a" K: ~' z
history, or failure to ask the specific questions, may
5 E6 p/ P7 |" G' }' Q. q* X: U( r6 ]result in extensive, unnecessary, and expensive
# M  J8 ?/ F" Z0 Z* zinvestigation. The primary care physician should be
* E- Z# r" V; B# yaware of this fact, because most of these children
+ D1 J0 e1 v' N& m& Y# |4 ?may initially present in their practice. The Physicians’
3 K9 I. e- ]0 }$ V# }- QDesk Reference and package insert should also put a2 l. [/ p/ z; G, _4 E$ g  _1 Q& ]
warning about the virilizing effect on a male or, c3 Q- L& a+ n8 q
female child who might come in contact with some-
" H& v7 D9 W: r: X7 {one using any of these products.
! a- L; V% X7 B( E4 W, v) k  GReferences7 F6 C+ }) x0 G2 c1 z, d. l3 G
1. Styne DM. The testes: disorder of sexual differentiation; q! ]* [! o& W2 f" l: Q6 Z* Y
and puberty in the male. In: Sperling MA, ed. Pediatric
; C3 B4 C7 C1 q( _6 ZEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;. ]" ~- H# ?6 c$ u: C5 z; R# e
2002: 565-628.
0 i, B" e7 i, L2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
; L6 B; D7 L! I5 P" ]puberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
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
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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
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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
. X' ]) P$ g" K
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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