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Sexual Precocity in a 16-Month-Old
/ Z% p" ?. C( P4 V0 h3 N6 lBoy Induced by Indirect Topical
, d. e/ k5 g) f" r' I- u; S! aExposure to Testosterone
7 c' n* z, ]2 _" }0 MSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2% H  `5 D/ ]3 I+ B' S! B
and Kenneth R. Rettig, MD1
4 V6 Y. r4 `6 S0 VClinical Pediatrics5 U* d) |9 w( ^+ _" A
Volume 46 Number 6
, O; m/ X* D' P- ]0 y& h+ vJuly 2007 540-543
  w! S, h. {+ _© 2007 Sage Publications
* H7 r9 g( {( q: n0 I+ R: N# ^$ N10.1177/0009922806296651
0 Z. A. N2 c; M- J+ Qhttp://clp.sagepub.com
4 B' o+ _+ t9 @) j' }- q( l- E5 \: I* rhosted at
8 f1 V3 W7 s  B* O5 Q' Q2 x& hhttp://online.sagepub.com
8 U; Z9 a9 h7 z2 b1 ~Precocious puberty in boys, central or peripheral,& V6 ^6 P3 ^/ r1 w8 n, Y, n
is a significant concern for physicians. Central$ W1 |5 K, H+ o" v  j
precocious puberty (CPP), which is mediated, P3 ?6 G  s/ W! ?
through the hypothalamic pituitary gonadal axis, has6 ?3 ^' S* C: Z! K) `: W& m1 K, Z
a higher incidence of organic central nervous system
! N, O! m# J: T$ e( hlesions in boys.1,2 Virilization in boys, as manifested- R. [4 f0 T" s( U0 N7 `
by enlargement of the penis, development of pubic! H. Y6 W9 K8 X. t) [: K0 s
hair, and facial acne without enlargement of testi-
4 H$ B# S1 S# G- m' mcles, suggests peripheral or pseudopuberty.1-3 We: z3 \7 v" |  P9 y
report a 16-month-old boy who presented with the$ ~* s6 ]+ z  I: w* z6 f% o4 x  G1 ~
enlargement of the phallus and pubic hair develop-
/ a3 _& Z5 X. Y/ _3 r/ y4 yment without testicular enlargement, which was due
9 X) J  ]3 r+ Bto the unintentional exposure to androgen gel used by
1 K3 r9 Q2 `* Q+ d# [3 othe father. The family initially concealed this infor-
6 `( V8 A+ M3 e6 {) e; X* u0 Q, qmation, resulting in an extensive work-up for this5 ?7 }9 o/ p/ }! n0 ~8 j# W$ c
child. Given the widespread and easy availability of
# z9 A4 }$ N/ y3 b7 g; N/ Vtestosterone gel and cream, we believe this is proba-
% T7 [8 U' d, n  A3 m. A  Q3 Kbly more common than the rare case report in the# i- y4 U5 G2 o, Q9 d3 Y4 f, J
literature.4! [+ s2 B4 P% k' ]
Patient Report; z0 R+ |; ]5 F+ I" M0 j8 X" C( E9 ]
A 16-month-old white child was referred to the
5 a, W# V9 u% n$ c2 Nendocrine clinic by his pediatrician with the concern
  H2 k. N0 u* z. a8 _: R  Z- Kof early sexual development. His mother noticed
  P0 |. U$ ^+ glight colored pubic hair development when he was* T3 F2 ]9 I$ H( |1 D0 u! s
From the 1Division of Pediatric Endocrinology, 2University of
* k0 H) l- q+ a  I% s) }South Alabama Medical Center, Mobile, Alabama.
5 O. \  Z) W3 N+ a6 ?Address correspondence to: Samar K. Bhowmick, MD, FACE,
# q% ^8 m7 q5 I# O$ D8 q8 l4 R2 |6 ^Professor of Pediatrics, University of South Alabama, College of/ j2 ]6 }% C" u. P0 t2 ?( O
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;0 h) F0 J4 y6 G7 S8 p
e-mail: [email protected].( o6 ^* ?% x; o/ C' A
about 6 to 7 months old, which progressively became7 P$ O7 a9 V- E# ~
darker. She was also concerned about the enlarge-
' R5 B  r0 D2 M3 S! iment of his penis and frequent erections. The child
. V2 X& ]& x8 w; L, cwas the product of a full-term normal delivery, with
5 P* L1 i$ s' u( Y! m# aa birth weight of 7 lb 14 oz, and birth length of
( p& h1 z( |- j20 inches. He was breast-fed throughout the first year- g" p7 B, u# x/ w1 p" F" T( Y
of life and was still receiving breast milk along with
8 V( ]# h' N9 psolid food. He had no hospitalizations or surgery,6 y; K2 w! I6 h4 F4 ]* Z! X; {" ~* }4 C' H
and his psychosocial and psychomotor development$ r+ p+ p$ x. b# i* M
was age appropriate.
$ `+ X, s- e9 ~" _$ P5 jThe family history was remarkable for the father,
8 F  p7 M0 ]) b: A$ X2 b2 qwho was diagnosed with hypothyroidism at age 16,0 l5 n8 n) C# \+ j- ^
which was treated with thyroxine. The father’s
) N' f$ T, j3 A% o- ~' B' jheight was 6 feet, and he went through a somewhat
) K! J/ B- |$ F/ Learly puberty and had stopped growing by age 14.
/ Z7 M1 ]2 z. I/ l/ E4 {% N, VThe father denied taking any other medication. The/ g2 b# m. ]$ [& r' }6 h
child’s mother was in good health. Her menarche# z5 w/ x6 ^" b- b" Q
was at 11 years of age, and her height was at 5 feet
* `1 A! Z/ z: j- [8 c6 Y  c$ Z) ?5 inches. There was no other family history of pre-( f" e0 n; G2 \: N# m
cocious sexual development in the first-degree rela-. }  c/ a- y5 n' z1 d/ r
tives. There were no siblings.8 O# m9 T( q& k$ z; d; L7 C0 [
Physical Examination
; Q% ~/ j( [3 U5 aThe physical examination revealed a very active,; R) `4 V, `* P7 M" F% ]9 S1 Y  ]' @
playful, and healthy boy. The vital signs documented
+ Q7 y( h* S% p1 K& I; {1 j) ^a blood pressure of 85/50 mm Hg, his length was, V0 w  v: S# U* q. w
90 cm (>97th percentile), and his weight was 14.4 kg  X# A4 v/ \. N" b+ ]+ ]- w
(also >97th percentile). The observed yearly growth
7 _% f$ z: @* Mvelocity was 30 cm (12 inches). The examination of' Z5 ^8 j% `9 J/ T8 t/ \% s
the neck revealed no thyroid enlargement.
# T" b1 q! ^/ y1 DThe genitourinary examination was remarkable for
% d" U4 a/ ]  R" I4 [- c; E5 O" Genlargement of the penis, with a stretched length of
8 S1 S# C# b' S. S6 P7 G8 cm and a width of 2 cm. The glans penis was very well
( b/ I' q0 K. `4 _; y9 Cdeveloped. The pubic hair was Tanner II, mostly around! ~( x  _: D" \; q# x
540: F, N1 u$ s- D; O# d
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 K2 Z' W* o' Z; i- l, Y, pthe base of the phallus and was dark and curled. The; Y$ A' A( n) \# T1 K8 _
testicular volume was prepubertal at 2 mL each.
9 ~' t. T' m5 @1 ?( g- @. \The skin was moist and smooth and somewhat
  U6 V. S5 E1 h1 _, G7 V( Zoily. No axillary hair was noted. There were no; N/ `3 w8 p% P& O
abnormal skin pigmentations or café-au-lait spots.
# }' B  R, B7 x: zNeurologic evaluation showed deep tendon reflex 2+/ g- r$ Z: F; h
bilateral and symmetrical. There was no suggestion3 V- g" \, M9 E% d
of papilledema.9 }' c% I6 N* G' Q# c
Laboratory Evaluation
, J4 A4 }- M$ i' D/ j% oThe bone age was consistent with 28 months by& }( N+ \. c$ Z8 |7 [, O: B- G" |7 J
using the standard of Greulich and Pyle at a chrono-- g5 Y4 B2 h. k7 n1 {$ B: d3 Y
logic age of 16 months (advanced).5 Chromosomal) \" J: j) N# O. }5 B, f1 [& S1 v
karyotype was 46XY. The thyroid function test
" I, z% R8 R: L% r* oshowed a free T4 of 1.69 ng/dL, and thyroid stimu-$ H# i8 d% o: u0 s
lating hormone level was 1.3 µIU/mL (both normal).
2 h: w6 c. Q; }The concentrations of serum electrolytes, blood
% X1 ?% _' H4 f- [urea nitrogen, creatinine, and calcium all were+ p+ L* W5 o+ x
within normal range for his age. The concentration
" b6 q6 T. K1 H% ]9 @* ?of serum 17-hydroxyprogesterone was 16 ng/dL
1 {( r9 H5 g7 ~0 P(normal, 3 to 90 ng/dL), androstenedione was 20: Z8 C2 |1 e8 ~, Q$ ~, K% p# @
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-; E3 ~% ~- L% K
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
. y9 D! Y# v* _' G* g9 Cdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
6 j/ ]& i, L! Z% t1 r49ng/dL), 11-desoxycortisol (specific compound S)4 {& E6 K/ l7 P7 T5 q  c0 _
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-. ~0 g/ h3 S4 Y9 M+ S% i  v4 \- s
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
  t. F7 }3 e0 A8 Otestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
9 n( o% f& ]% f6 I, I( B( ?and β-human chorionic gonadotropin was less than2 l* E, U1 L9 o
5 mIU/mL (normal <5 mIU/mL). Serum follicular7 l. P2 U, O; e
stimulating hormone and leuteinizing hormone1 Q; @, T; [3 A+ f8 h/ c8 M/ r
concentrations were less than 0.05 mIU/mL' h9 _- b# O  s9 I* C+ M% t
(prepubertal).* Y; y1 \9 I) ?5 Y0 p- u9 q5 t
The parents were notified about the laboratory) M2 t/ ]! A! c1 H
results and were informed that all of the tests were5 H3 e8 `9 C# s  k
normal except the testosterone level was high. The
# m* F) U# E8 Rfollow-up visit was arranged within a few weeks to
- e3 Z- x( {5 m7 W5 Aobtain testicular and abdominal sonograms; how-0 U+ C+ X4 D2 P/ ~" C2 b
ever, the family did not return for 4 months.
; X! H1 K4 G  y  I# O2 G' \Physical examination at this time revealed that the
9 l: J/ U7 l: ~5 o( c% n0 Cchild had grown 2.5 cm in 4 months and had gained0 c' [3 l! p& D' b( i
2 kg of weight. Physical examination remained
' y3 O5 N0 K0 n0 Q2 R9 i* Zunchanged. Surprisingly, the pubic hair almost com-7 {; i) m) c# n% e1 q% K& L8 C
pletely disappeared except for a few vellous hairs at
  E. Z9 f7 ^7 W: A: _the base of the phallus. Testicular volume was still 2* M$ P& j7 c, A7 ^4 z0 j( ]
mL, and the size of the penis remained unchanged.: L3 L$ \# q! `% G
The mother also said that the boy was no longer hav-3 U5 T( J- k' ]2 [4 `  g4 v! l
ing frequent erections.
' V3 j" _6 B1 q$ sBoth parents were again questioned about use of
, |" v% T  {% S) H0 V; Nany ointment/creams that they may have applied to
6 |4 r, @! w8 L. \the child’s skin. This time the father admitted the
3 q7 e8 [* _8 r% o( e/ STopical Testosterone Exposure / Bhowmick et al 5410 [% A0 _; m7 @6 x( j
use of testosterone gel twice daily that he was apply-
; [9 m. q& _, e* R# ]$ f6 a# ming over his own shoulders, chest, and back area for, z) j  |6 B% @6 H* H/ z: I2 I  |
a year. The father also revealed he was embarrassed8 N7 F/ w/ \2 z) Y- p# A
to disclose that he was using a testosterone gel pre-
! F: p  ?/ S  M; `7 wscribed by his family physician for decreased libido
( l" h) K% j& ~( z6 v) J2 asecondary to depression.
1 [1 S& `. y5 r4 t" [. _The child slept in the same bed with parents.
% L8 a2 f2 f7 D# k! NThe father would hug the baby and hold him on his8 Z) }- j2 b! j: h7 H2 ?
chest for a considerable period of time, causing sig-
  K* ?! ?' u( i9 E  bnificant bare skin contact between baby and father.3 S+ J* a( Q% i. ?2 i
The father also admitted that after the phone call,; k  p1 O% {( m
when he learned the testosterone level in the baby' K$ P! ?$ a) M$ t' M7 e
was high, he then read the product information2 }. e/ \; G& z- e) k
packet and concluded that it was most likely the rea-
# F; ^% G2 V0 W: Y  Q; a8 vson for the child’s virilization. At that time, they
6 J3 L9 d! ?6 ]/ ^2 Qdecided to put the baby in a separate bed, and the1 R3 J0 |# ~; H1 T- \, m
father was not hugging him with bare skin and had
3 }. ?# `+ A3 e1 O1 R7 Bbeen using protective clothing. A repeat testosterone
* V7 z1 M( Q" I# k( l& O' q6 w& Rtest was ordered, but the family did not go to the
2 ]" f+ V6 R* r7 ^0 Y6 Q. E% n/ klaboratory to obtain the test.; {5 U: U/ D+ v
Discussion) }" }3 P) P1 K2 D8 Q+ @
Precocious puberty in boys is defined as secondary7 @* E; }8 q8 _1 u" K4 Y$ o7 T
sexual development before 9 years of age.1,4, h$ Z+ G: U- ^' W/ |- d
Precocious puberty is termed as central (true) when& K/ m, G) j. P& D% i: Y
it is caused by the premature activation of hypo-7 S4 T9 B. l. x
thalamic pituitary gonadal axis. CPP is more com-2 L2 @8 p0 ~6 `6 K% C3 i* k
mon in girls than in boys.1,3 Most boys with CPP8 S$ |4 W5 E0 N$ A' P7 U
may have a central nervous system lesion that is
( s- f2 L( C! ?  S) Iresponsible for the early activation of the hypothal-; ^4 D7 K" H/ o$ J& r
amic pituitary gonadal axis.1-3 Thus, greater empha-
- \$ r8 s# W5 ~6 [sis has been given to neuroradiologic imaging in
" v6 D$ q: I/ V( f7 _boys with precocious puberty. In addition to viril-
( b2 }" F" |  T. lization, the clinical hallmark of CPP is the symmet-+ d# @, N# J/ {8 m& a/ C5 S
rical testicular growth secondary to stimulation by# E. X, f, U7 V% h0 J, v& L
gonadotropins.1,3, o: f# g' b% w' |
Gonadotropin-independent peripheral preco-
' K  }- d# Y: L4 M( Xcious puberty in boys also results from inappropriate
& k: i% B3 R  T9 N' Wandrogenic stimulation from either endogenous or- i7 F* r1 b) c; z# m
exogenous sources, nonpituitary gonadotropin stim-  I) X# z& C, O  @
ulation, and rare activating mutations.3 Virilizing
! L: W# I; _/ v. g9 X  X3 hcongenital adrenal hyperplasia producing excessive8 V/ ^" w/ v  u5 J1 F
adrenal androgens is a common cause of precocious
0 N( {7 U! g, [9 V4 e$ e5 r( I' spuberty in boys.3,40 h1 F$ |! _. Y7 J% _
The most common form of congenital adrenal9 t& V6 C, G& {0 B/ I/ a' n/ y
hyperplasia is the 21-hydroxylase enzyme deficiency.
2 Z0 h; V  y& I' tThe 11-β hydroxylase deficiency may also result in( `; q0 k& d9 |! e* y1 N
excessive adrenal androgen production, and rarely,1 `3 _; u( S* Y' U, H
an adrenal tumor may also cause adrenal androgen0 e6 g& c- q* d- B8 f4 f
excess.1,3
7 b1 {; a7 ~1 s) X" Q! G9 m2 k" r1 Pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# n. n' T; z- x542 Clinical Pediatrics / Vol. 46, No. 6, July 2007, D% N4 h6 b5 J$ X, \% d$ D, g2 a
A unique entity of male-limited gonadotropin-9 x; I  b- V1 e$ T6 e( V* x
independent precocious puberty, which is also known, F! U+ ]* ]" b) n  }4 o5 }: r
as testotoxicosis, may cause precocious puberty at a( x5 A4 A. L8 {
very young age. The physical findings in these boys
3 C  q6 ?" [3 H0 E+ ]- Hwith this disorder are full pubertal development,
6 X" R; j+ G3 Y1 X) l7 {  Iincluding bilateral testicular growth, similar to boys
( J2 G. t2 _% e* N5 d/ _; ?* M4 {* {with CPP. The gonadotropin levels in this disorder
8 I& L1 w7 a! Y) E/ D4 m: w% zare suppressed to prepubertal levels and do not show
7 V) A! c6 F1 t% ?  N5 p3 i0 ^pubertal response of gonadotropin after gonadotropin-$ Y% z4 W7 y; R, o) t
releasing hormone stimulation. This is a sex-linked# N3 t# v. [! P; F* D( |3 |
autosomal dominant disorder that affects only
! J3 f1 s3 k+ h1 W/ @( O0 u) C7 zmales; therefore, other male members of the family
7 e/ X2 N% P8 `: m9 `6 u& mmay have similar precocious puberty.3
4 E+ a' t" M' r9 ?+ a! eIn our patient, physical examination was incon-
' j% _" l' a7 n$ Z/ Ksistent with true precocious puberty since his testi-2 [4 X2 Q3 b& o# H* A
cles were prepubertal in size. However, testotoxicosis) @/ I  A4 Z" \6 }
was in the differential diagnosis because his father
  S$ p* }: k* F4 E- astarted puberty somewhat early, and occasionally,
- E& O8 K. ^# t  Q; ?9 D) x9 jtesticular enlargement is not that evident in the" f% d! G/ q4 h% `; F; l1 ^
beginning of this process.1 In the absence of a neg-. n" l* `7 U: y/ y( M
ative initial history of androgen exposure, our
3 O# ]5 e+ f- o7 u* e6 D0 K4 dbiggest concern was virilizing adrenal hyperplasia,
! ]4 C. n+ N; c: J2 W, b! w1 Leither 21-hydroxylase deficiency or 11-β hydroxylase
/ G# ~( q5 M( l4 @; I: [deficiency. Those diagnoses were excluded by find-
. L1 T. @" C" a% P' E9 Iing the normal level of adrenal steroids.
: J" K) L9 ?2 n% B$ G) YThe diagnosis of exogenous androgens was strongly* c! ?& @$ S6 O7 K3 E: ]
suspected in a follow-up visit after 4 months because, J9 K6 ^9 F6 @5 X  ]
the physical examination revealed the complete disap-) `5 c3 B) F) c, p$ r7 m( p
pearance of pubic hair, normal growth velocity, and; W9 u" {& X; Y
decreased erections. The father admitted using a testos-- `# I7 c+ S: p( Y6 J0 \
terone gel, which he concealed at first visit. He was
) \( h/ H0 X0 `using it rather frequently, twice a day. The Physicians’
, u1 E# ^6 {. R" c* A# IDesk Reference, or package insert of this product, gel or' }$ K' H8 ?8 V4 {9 |) K
cream, cautions about dermal testosterone transfer to7 M7 X9 q% ~. m6 S
unprotected females through direct skin exposure.9 ]. |9 a; Y  w& k
Serum testosterone level was found to be 2 times the+ A7 b  v: z# j3 r/ C
baseline value in those females who were exposed to. L) s6 X. }. [1 e) u
even 15 minutes of direct skin contact with their male
* C7 K$ \# l. H6 k, S, S  h6 ?/ Vpartners.6 However, when a shirt covered the applica-4 l; C/ X$ \' _( z. n0 [7 Z; a: r
tion site, this testosterone transfer was prevented.# y1 i) [, }; d- K
Our patient’s testosterone level was 60 ng/mL,6 ~1 W) p+ U0 S$ _
which was clearly high. Some studies suggest that
) V1 ?) q9 |7 cdermal conversion of testosterone to dihydrotestos-
6 Y, m/ Y$ h$ C, ]5 Tterone, which is a more potent metabolite, is more5 J( Z. S* X/ U6 w
active in young children exposed to testosterone1 ~6 M8 w6 {, }
exogenously7; however, we did not measure a dihy-. P# X% E2 X9 b4 `/ M1 `+ ^
drotestosterone level in our patient. In addition to
: [" P( h2 }8 o& j: V& Y# Fvirilization, exposure to exogenous testosterone in
6 y" ?3 j/ [' i5 K5 a' J6 b1 tchildren results in an increase in growth velocity and/ }. h6 @, Q. q. p2 D
advanced bone age, as seen in our patient.3 N2 X( O5 ^  z+ B6 b. q
The long-term effect of androgen exposure during
- F! T4 M6 _/ k5 {' m$ @8 _- ?6 [early childhood on pubertal development and final8 Q: e% I; i: l7 f! d+ U
adult height are not fully known and always remain0 e! ]  ~0 X* @& w; e! d
a concern. Children treated with short-term testos-
3 B# K4 B. h$ ~, {$ e: C+ v' Mterone injection or topical androgen may exhibit some8 J. n7 Q% q' e, y  X, E1 A5 {6 {' Z/ ]
acceleration of the skeletal maturation; however, after, e$ V- h- z2 Q, N( C- `
cessation of treatment, the rate of bone maturation( ^# G4 k* n& U+ D8 D
decelerates and gradually returns to normal.8,94 h0 G4 a3 T( G/ ?; Y
There are conflicting reports and controversy
+ m2 c: s3 n* L% Y  bover the effect of early androgen exposure on adult
8 S* q) q' s) A7 f, t) M0 s; Lpenile length.10,11 Some reports suggest subnormal
! H5 O8 \, L+ [7 t2 i2 W8 aadult penile length, apparently because of downreg-; H! i& e' f( B4 \
ulation of androgen receptor number.10,12 However,
7 r: I) Q' P- YSutherland et al13 did not find a correlation between5 b( e, W' _# k$ {8 ^
childhood testosterone exposure and reduced adult
3 L- K' N" e) `' D- mpenile length in clinical studies." `  ?% v/ X) v1 q$ k+ p- R. @
Nonetheless, we do not believe our patient is
" [; s; {7 A$ s; agoing to experience any of the untoward effects from
8 D# d2 R; \$ R, Dtestosterone exposure as mentioned earlier because- m) e3 ?/ k6 A6 m0 a* R
the exposure was not for a prolonged period of time.3 j' \, r" x" P* S( h6 |9 `. e, o; [
Although the bone age was advanced at the time of
* h- n, F, M1 N% ~diagnosis, the child had a normal growth velocity at+ a. `, [0 x+ r
the follow-up visit. It is hoped that his final adult. V/ h4 X3 S5 Y8 N1 d
height will not be affected.
: Q/ B3 E+ b( y: A, I! ^Although rarely reported, the widespread avail-
+ }, Q" _5 k* ~& C6 c# aability of androgen products in our society may' M* V" q( {- C  P& u& Z: j5 U1 c
indeed cause more virilization in male or female0 H# I& i3 r" O- v% Z* Y
children than one would realize. Exposure to andro-( J& b4 H; F  z6 C$ }: ]" s
gen products must be considered and specific ques-7 K8 y5 O0 e' P
tioning about the use of a testosterone product or
7 J, w2 j$ S4 a9 Ngel should be asked of the family members during: R) v6 i& x  I# [; {
the evaluation of any children who present with vir-
2 }9 o/ i2 h, R0 i; k" N# Filization or peripheral precocious puberty. The diag-6 u3 M) v, D8 F3 [
nosis can be established by just a few tests and by+ S$ \6 _- G0 v8 A; ^
appropriate history. The inability to obtain such a. Y! g9 _0 q6 E% w7 J! n% F1 ?$ E
history, or failure to ask the specific questions, may
6 W9 n1 U6 B' G' [- qresult in extensive, unnecessary, and expensive. |' p4 t% r' R6 v5 ~7 ^6 }
investigation. The primary care physician should be: l- g$ [/ t1 q4 g$ X0 _: A% r
aware of this fact, because most of these children
0 ~8 F1 l) Z$ t3 |. v& }1 |' X6 qmay initially present in their practice. The Physicians’! P! c+ v/ a  B% x
Desk Reference and package insert should also put a6 |! P1 n9 {! f( u$ k+ E
warning about the virilizing effect on a male or
( V3 ]+ W& ~  a1 V4 sfemale child who might come in contact with some-
# `0 ]' X# X  sone using any of these products.
  m. m; c3 j# Q/ n' p0 M5 k5 BReferences
  `' p9 v7 {4 q$ N! |8 E1. Styne DM. The testes: disorder of sexual differentiation
  X' _& M0 ]9 P$ A- E& Q/ d* Hand puberty in the male. In: Sperling MA, ed. Pediatric" ?9 C* T/ `9 T; ~' L
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;  Q, N8 P- k# I6 s2 Y* Y
2002: 565-628.4 |! N% b: N/ ]/ |
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
: r+ V# n) M" U( [& hpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old# _" |9 N$ g0 C' A
Boy Induced by Indirect Topical
% N' i1 ]5 D" O. _$ tExposure to Testosterone6 W5 N5 f+ [1 E! q
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 u) [& E  w. T+ u& Uand Kenneth R. Rettig, MD1/ e  U- g& W* f% T: L5 f
Clinical Pediatrics
2 U2 D7 _( F" D7 q/ t3 `Volume 46 Number 6( d) ?) ^6 ~: y# r/ ?
July 2007 540-543; `; S7 a# ~2 g% {, C& ~0 ]
© 2007 Sage Publications0 A$ x9 |  g7 M- S7 Q; j; `; _
10.1177/0009922806296651. v& j2 ^$ \3 v4 U  Z9 \; t
http://clp.sagepub.com
0 U" V) v+ ]4 F  Chosted at
+ l' r7 q  ]2 Q3 B8 B  U$ dhttp://online.sagepub.com
" q# W. R6 g4 h# _$ H" uPrecocious puberty in boys, central or peripheral,* s3 N; E8 Q4 i0 Q) O# ^
is a significant concern for physicians. Central& t& Q; x; t' \7 [! s  W
precocious puberty (CPP), which is mediated2 H( T/ z/ i  o2 X/ E
through the hypothalamic pituitary gonadal axis, has
) d6 ?& Q" c; V7 Q& H  ea higher incidence of organic central nervous system
$ }( v$ `& H4 C6 J4 Glesions in boys.1,2 Virilization in boys, as manifested
% e) h  M5 `* B) Z8 N6 uby enlargement of the penis, development of pubic
6 n9 [# ]5 ?6 Z& O4 vhair, and facial acne without enlargement of testi-3 b1 G  s8 C% u4 k
cles, suggests peripheral or pseudopuberty.1-3 We
) u2 l$ T5 V) g. ~/ greport a 16-month-old boy who presented with the/ x8 U; z# H$ E' ~
enlargement of the phallus and pubic hair develop-
% p: z& F2 Y$ q1 Y( c0 P* qment without testicular enlargement, which was due
$ y4 W/ \, ]9 Q$ ato the unintentional exposure to androgen gel used by
) K) u" R* C9 G7 t7 W) G5 u" Tthe father. The family initially concealed this infor-
! R( K) {; r+ P" u6 w: x0 R" Qmation, resulting in an extensive work-up for this. E" H  F( n$ }1 i: W
child. Given the widespread and easy availability of$ {5 |5 x' Z$ t7 K2 S
testosterone gel and cream, we believe this is proba-
1 J4 _$ g6 D/ P6 n% C& A( o; |bly more common than the rare case report in the
" W  v* g% j- K# I0 Qliterature.4
8 ?- d! ^& O7 ~+ M" T. l2 v/ K0 @Patient Report( j8 I$ X0 \* M  ~' \
A 16-month-old white child was referred to the! f7 d$ x. _$ a, W0 Y
endocrine clinic by his pediatrician with the concern' v- V0 C2 y8 p; S
of early sexual development. His mother noticed
2 h& C! I. F7 u+ p1 }) L2 a5 }  l% Ulight colored pubic hair development when he was
7 X/ U& _  f) `; E! v- g6 fFrom the 1Division of Pediatric Endocrinology, 2University of
( Z3 W4 {' b5 _5 {South Alabama Medical Center, Mobile, Alabama.* b% t/ N- K5 p; g6 B7 x1 @
Address correspondence to: Samar K. Bhowmick, MD, FACE,9 G6 F( v5 z( ~0 h3 X' f
Professor of Pediatrics, University of South Alabama, College of
8 V/ c% L5 v1 Y% Z7 cMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
- z& k' P" ^# [3 ye-mail: [email protected].! K4 a. @9 G) i' e/ y
about 6 to 7 months old, which progressively became  P  c, K& u, z* w5 y6 ^. C+ V
darker. She was also concerned about the enlarge-% ~& N- r! @: e0 t: w
ment of his penis and frequent erections. The child
, L" s3 s/ i7 g0 vwas the product of a full-term normal delivery, with
( ~2 A; B/ ?! ia birth weight of 7 lb 14 oz, and birth length of6 I' s; I4 Q) H' Y" F
20 inches. He was breast-fed throughout the first year
, `/ c7 _1 p8 r& rof life and was still receiving breast milk along with& a9 Z5 E- ?/ i
solid food. He had no hospitalizations or surgery," a. a1 n0 d( f; j) B0 x* T2 F
and his psychosocial and psychomotor development, }1 L. z- q/ U3 ^  z! p1 K# O) ~
was age appropriate.1 I& ~: T) y. W9 E# V$ x( u! V2 U1 j
The family history was remarkable for the father,; `- L  ]* C. C0 ^9 h8 |
who was diagnosed with hypothyroidism at age 16,
/ E( ~7 ]; t9 j5 Twhich was treated with thyroxine. The father’s5 K$ C4 h( ~7 P& A" j6 H7 S" `
height was 6 feet, and he went through a somewhat
9 D( K/ P0 p$ v) a6 c  k  t, Gearly puberty and had stopped growing by age 14.4 B* m: O8 C! p9 T
The father denied taking any other medication. The7 |" K7 r4 U& ~+ q' }# Z" |+ c
child’s mother was in good health. Her menarche
: Y* o! b2 W, uwas at 11 years of age, and her height was at 5 feet) P+ k7 n# _$ m3 C
5 inches. There was no other family history of pre-
* G9 c* k; T! \/ _: S# e- {cocious sexual development in the first-degree rela-
/ e: F& I7 u' x+ E0 mtives. There were no siblings.
& ^% N$ k& I9 c) |* C3 F8 T5 VPhysical Examination' L5 P" Q; F3 H
The physical examination revealed a very active,: _$ a# p0 s5 B1 [
playful, and healthy boy. The vital signs documented: E+ Z# s9 {3 E; Z" f
a blood pressure of 85/50 mm Hg, his length was7 q- N% `$ u9 j: j
90 cm (>97th percentile), and his weight was 14.4 kg
! f: ]# [% `9 |6 x(also >97th percentile). The observed yearly growth3 ]1 a( {3 D2 M, v, [. \' C
velocity was 30 cm (12 inches). The examination of
+ @! r  u3 e  Z. s6 t9 o) G" e1 cthe neck revealed no thyroid enlargement.
$ |- t! r, [6 M/ N8 e& VThe genitourinary examination was remarkable for$ E0 j  W: I8 u3 u$ R
enlargement of the penis, with a stretched length of
" B8 U. P5 B& i! k3 n) P8 cm and a width of 2 cm. The glans penis was very well
: i4 |. L7 q3 W0 g% Odeveloped. The pubic hair was Tanner II, mostly around
4 \) O4 F5 x" l- H! L( k3 K540
5 e! C& B2 U! i- Fat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! G/ ]# o% Q& D6 O& b: hthe base of the phallus and was dark and curled. The- i! T) t8 I* Y
testicular volume was prepubertal at 2 mL each.
- @: E$ V% j( mThe skin was moist and smooth and somewhat
+ p1 L( R1 d$ K; G! Y) Loily. No axillary hair was noted. There were no* ?. x) {3 o5 {  M+ J. x
abnormal skin pigmentations or café-au-lait spots.; A4 A' b0 {& {
Neurologic evaluation showed deep tendon reflex 2+$ v1 Q9 c" C8 O9 X! q
bilateral and symmetrical. There was no suggestion8 W! _9 }: w+ v
of papilledema.
8 y: G8 T7 a; E/ OLaboratory Evaluation
5 f# Q  M. A+ [9 U" hThe bone age was consistent with 28 months by
2 T% n& d7 K8 o! L' u- S% |using the standard of Greulich and Pyle at a chrono-
# g' W& Q3 S/ j% t. V) qlogic age of 16 months (advanced).5 Chromosomal
) c( x( g# j8 B% S9 i; D4 fkaryotype was 46XY. The thyroid function test
% v8 [9 v1 a! y( [7 _showed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ B# ?9 X0 t5 a* ^4 z" Hlating hormone level was 1.3 µIU/mL (both normal).
% |: n* [! ?& |+ u" e6 u# ]The concentrations of serum electrolytes, blood
/ p6 A- x8 q/ Y5 Q! [/ ]urea nitrogen, creatinine, and calcium all were
7 h0 O; s! z: I' V. b' M8 h9 n& w9 ewithin normal range for his age. The concentration
& v; ]' J: h" o1 \3 v0 |3 vof serum 17-hydroxyprogesterone was 16 ng/dL
5 k/ Q; X  \# z# V: b(normal, 3 to 90 ng/dL), androstenedione was 20
" M" _0 O6 L% S! d' mng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-! _& \3 U2 q, v9 O. p, }; P
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
6 e- x* Q" ^+ ^4 kdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
/ C" z8 Q4 Q- M( P; q% ^2 b49ng/dL), 11-desoxycortisol (specific compound S)4 A$ s& z5 u/ D, Y# q  P
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
7 F* B/ [3 n: }, S, K" U& ytisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total8 [% h7 n4 w( I7 ^  |! B
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
& X8 x1 d3 x3 K# land β-human chorionic gonadotropin was less than
0 t* D7 L* V# Q! j$ Q3 _5 mIU/mL (normal <5 mIU/mL). Serum follicular
/ K9 b: h) @  H3 V* P2 dstimulating hormone and leuteinizing hormone
! [/ z, Q) u% ~5 t8 n8 Kconcentrations were less than 0.05 mIU/mL& W  r4 x, z- L* M* b( n/ a
(prepubertal).
. n* Z% M7 X) b6 Q. h2 XThe parents were notified about the laboratory
6 o* Y# n% f( e! K, O/ eresults and were informed that all of the tests were
$ l  \( N! o/ s! Knormal except the testosterone level was high. The% y0 l+ k* _& L% ?( ~
follow-up visit was arranged within a few weeks to- ?- p' W( ?4 S/ _3 {* d9 S0 j& n' l
obtain testicular and abdominal sonograms; how-  g9 z3 r4 C- |8 b5 k/ U4 P4 C
ever, the family did not return for 4 months.
# Q6 C1 e3 {& k" M' |8 YPhysical examination at this time revealed that the5 o& U: o2 E: J
child had grown 2.5 cm in 4 months and had gained9 r" x5 F( ~8 M2 q
2 kg of weight. Physical examination remained
6 ]8 O+ D9 w  H/ D0 K6 V/ C  ?unchanged. Surprisingly, the pubic hair almost com-
+ j3 o# V: W! }pletely disappeared except for a few vellous hairs at
' [  F/ u5 Q3 y# m" ?3 Ethe base of the phallus. Testicular volume was still 25 X3 u" c0 f5 V# J$ A" A
mL, and the size of the penis remained unchanged.  V" ?  N/ m+ W0 @/ [, C
The mother also said that the boy was no longer hav-! L: T$ v# ?7 Z' t, j$ e# c& q( [
ing frequent erections." D7 M' \( j0 }( Q
Both parents were again questioned about use of6 ^& @& ]2 l7 b, g/ M6 e3 L
any ointment/creams that they may have applied to
# [& i+ Y' L( }1 b- Athe child’s skin. This time the father admitted the3 p3 q& l! }0 y7 H; h7 m1 W  k+ l9 E
Topical Testosterone Exposure / Bhowmick et al 541
) V2 [5 |* t' x$ _4 kuse of testosterone gel twice daily that he was apply-
) q- `9 @. I4 r1 d) e: Y2 P: U: Iing over his own shoulders, chest, and back area for5 e# p% M' T6 C3 m4 b$ E9 t( h
a year. The father also revealed he was embarrassed
) ]* c, m1 U9 U: J* }( fto disclose that he was using a testosterone gel pre-
$ P( o5 h8 Y0 H. `scribed by his family physician for decreased libido
. C9 A1 M8 ^. r# c% t3 Asecondary to depression.. c7 _$ X) v( A* O& @
The child slept in the same bed with parents.0 H$ r1 y$ q, C4 ?
The father would hug the baby and hold him on his4 N6 ?% S, B  }" d
chest for a considerable period of time, causing sig-0 G8 J4 h/ B+ V9 S6 _( `7 M) s
nificant bare skin contact between baby and father.. Z) T" Y; c# V5 n
The father also admitted that after the phone call,4 K4 k# S. m) d1 y4 W
when he learned the testosterone level in the baby3 z6 @* @/ s' \' K# }, l4 ]( `9 P% t3 ]
was high, he then read the product information" |. S2 m+ }7 F% L8 U3 C
packet and concluded that it was most likely the rea-
# O- P* i3 N% J5 u6 ~2 R. |son for the child’s virilization. At that time, they
2 q; O! f: n3 }) g, Ydecided to put the baby in a separate bed, and the
6 s0 G2 s' Z5 sfather was not hugging him with bare skin and had; f3 W: B8 M. ^4 T  R
been using protective clothing. A repeat testosterone& `9 a0 ^% [1 b  ^
test was ordered, but the family did not go to the
2 V5 k$ G% M& a# _laboratory to obtain the test.3 I9 @: v! b6 ]) h" X% ]
Discussion6 d2 r8 c1 {2 t! _( b* l. R
Precocious puberty in boys is defined as secondary
$ X) e6 Z4 i* P! o0 d( ^$ p6 S! ]0 \sexual development before 9 years of age.1,4
0 v9 ~  I* h4 X! Z9 H4 t5 z, V: OPrecocious puberty is termed as central (true) when6 W, b) X  L0 B' j- c
it is caused by the premature activation of hypo-
1 @4 k" i% l- ~2 X! @) f+ {thalamic pituitary gonadal axis. CPP is more com-) w% ^; W$ O7 X# s( [* |' H/ @& I3 H
mon in girls than in boys.1,3 Most boys with CPP
: C: D  r( ~/ Y5 gmay have a central nervous system lesion that is
3 B  d8 K* `" E( O& Uresponsible for the early activation of the hypothal-9 O3 V* B1 B& `% g3 v% h6 t4 c
amic pituitary gonadal axis.1-3 Thus, greater empha-
# j/ b/ T0 n! a5 S$ ^sis has been given to neuroradiologic imaging in7 M2 ]$ t, ~0 v: \9 H; K, \" w
boys with precocious puberty. In addition to viril-+ T  P% r7 T- P, m8 P+ s
ization, the clinical hallmark of CPP is the symmet-
4 y( J+ c' ]! srical testicular growth secondary to stimulation by
& K) T6 t+ J8 \" E! E6 h" a4 _+ agonadotropins.1,3+ S3 s+ f0 v$ \5 d; [6 `+ F
Gonadotropin-independent peripheral preco-
" \5 o2 E3 R% u" S8 W, tcious puberty in boys also results from inappropriate
& ?* z5 M* B# D$ Yandrogenic stimulation from either endogenous or2 k& T8 n* X2 n
exogenous sources, nonpituitary gonadotropin stim-
. r! q9 o7 _/ Z$ g# X1 Yulation, and rare activating mutations.3 Virilizing% K/ X* Q& [" k% z( g6 k/ L0 t5 N
congenital adrenal hyperplasia producing excessive
. C# S  y0 p' Y5 Sadrenal androgens is a common cause of precocious
) C: Y6 s# @4 t- H* h* c# apuberty in boys.3,4
% i% F* ^" I4 s/ Q' SThe most common form of congenital adrenal1 X8 ?* }* M! B; T. _3 l8 d, i
hyperplasia is the 21-hydroxylase enzyme deficiency./ j0 }$ _/ E6 l3 O, D/ r4 B
The 11-β hydroxylase deficiency may also result in; y$ L- P$ S& u4 z$ j- c7 T  e2 e
excessive adrenal androgen production, and rarely,
: x: S- `& _; r. e, Xan adrenal tumor may also cause adrenal androgen( Q7 B. m8 u* K; h' `6 M+ f! C
excess.1,3! O6 x! H+ Z6 H" A3 E
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: B' i( A" o5 H, n6 H2 O, T542 Clinical Pediatrics / Vol. 46, No. 6, July 20071 O" s% ~+ y% \* F8 }3 i/ U
A unique entity of male-limited gonadotropin-0 W+ B" z! b& k2 ]! [
independent precocious puberty, which is also known
5 U* t  G  m6 ?- ras testotoxicosis, may cause precocious puberty at a
  W# m; y5 ]  F% qvery young age. The physical findings in these boys4 x, h3 J% X3 J- K$ s: \$ X
with this disorder are full pubertal development,
# f* F  A: q! O1 n3 ]% _1 }including bilateral testicular growth, similar to boys
! C6 H- @# D- m. t3 Nwith CPP. The gonadotropin levels in this disorder2 I1 q' F3 G! w$ |" j, \
are suppressed to prepubertal levels and do not show
9 j/ a' @- v. Y7 k# _pubertal response of gonadotropin after gonadotropin-
( u% d' S7 g: a2 U$ vreleasing hormone stimulation. This is a sex-linked. F  F4 q0 l4 q. q) e
autosomal dominant disorder that affects only
2 y8 ?0 I3 u0 K2 G7 \( {  K* M* G7 {males; therefore, other male members of the family
* {; m. X. q0 ^( e& E+ n. Imay have similar precocious puberty.3" n/ V  [5 F+ l' h$ T
In our patient, physical examination was incon-0 ~3 E6 C5 y: p* H. m" r6 c. l
sistent with true precocious puberty since his testi-* e7 z# `6 R) R4 B
cles were prepubertal in size. However, testotoxicosis6 |+ j0 H. m' P- N0 g
was in the differential diagnosis because his father8 }: [5 O' `% j+ D* J2 j" h7 \  d
started puberty somewhat early, and occasionally,
9 C1 d5 G/ L5 p/ O- k: ?8 \, Btesticular enlargement is not that evident in the  v4 x. X. {5 O/ u4 F0 E
beginning of this process.1 In the absence of a neg-' {( H+ e6 o7 j
ative initial history of androgen exposure, our
7 y1 H# S$ X0 s& v6 w9 U% gbiggest concern was virilizing adrenal hyperplasia,
4 Z# Z" r% `9 {' A4 reither 21-hydroxylase deficiency or 11-β hydroxylase
/ U2 t3 f+ T1 H  I$ Udeficiency. Those diagnoses were excluded by find-
+ V, k& V4 l: N0 L9 Ning the normal level of adrenal steroids.' W: ]1 Y, I( f3 ~( X+ O: ?
The diagnosis of exogenous androgens was strongly
) U' b! ?- [9 K8 i9 ?  w: M7 D. s  E: Bsuspected in a follow-up visit after 4 months because; s$ ]" K2 J4 |! K0 c: u3 z
the physical examination revealed the complete disap-
6 l: h+ W5 ~; D8 opearance of pubic hair, normal growth velocity, and
3 N) y% C" B. [- Wdecreased erections. The father admitted using a testos-! l$ b$ z' {: ]
terone gel, which he concealed at first visit. He was: U! z' d" G; V% v! d) Y  ]
using it rather frequently, twice a day. The Physicians’
+ |6 \' D4 K: ]- S% kDesk Reference, or package insert of this product, gel or) Y9 x, X' s  E; C
cream, cautions about dermal testosterone transfer to
% E% R" e/ p" J/ f$ H' Yunprotected females through direct skin exposure." ?, C8 I! d2 q4 U
Serum testosterone level was found to be 2 times the
7 r6 T' {+ }8 x1 Jbaseline value in those females who were exposed to1 k; x+ \6 Z9 \# D( S% t
even 15 minutes of direct skin contact with their male
- u" ?3 y8 a3 b& h- ~- \' zpartners.6 However, when a shirt covered the applica-2 w, z) e8 {3 u
tion site, this testosterone transfer was prevented.% y7 e' g7 R( V- g9 J/ w6 @( v1 _
Our patient’s testosterone level was 60 ng/mL,1 b$ h# B) C, {8 q& P
which was clearly high. Some studies suggest that" O) o* @2 z0 [$ B6 `1 d7 |) [
dermal conversion of testosterone to dihydrotestos-9 C5 i/ T  O% z. Y0 c; t
terone, which is a more potent metabolite, is more& }5 G9 w# {/ [7 y0 U3 s
active in young children exposed to testosterone
6 b" |6 m: Y, v; ^4 u" pexogenously7; however, we did not measure a dihy-( u  D, k, u' i- A2 J
drotestosterone level in our patient. In addition to. i2 L/ b- V: n# b( @6 T% p
virilization, exposure to exogenous testosterone in; E* g+ p( w: O5 s8 S
children results in an increase in growth velocity and
8 |; Y% Z: P5 Oadvanced bone age, as seen in our patient.! E$ q. q3 g, O2 d; _, G% T% ?
The long-term effect of androgen exposure during7 Y3 s2 F  d; p( L3 T! ]  a  g
early childhood on pubertal development and final
9 P5 X8 V1 y+ ]5 b4 Iadult height are not fully known and always remain
6 r( g% O1 _. \3 z: @a concern. Children treated with short-term testos-2 d. X5 V3 p4 D5 l+ S3 @
terone injection or topical androgen may exhibit some
1 M/ H0 Q* Q* y" Y$ E3 i* iacceleration of the skeletal maturation; however, after: i% n+ ^: n& |9 V
cessation of treatment, the rate of bone maturation
; O. y4 ]2 _  u: ~; s' B$ T! ldecelerates and gradually returns to normal.8,9- E/ e' r4 z, t
There are conflicting reports and controversy
0 g& X% \& X/ [. nover the effect of early androgen exposure on adult) H- d; k. G* C: ]. C2 `1 r
penile length.10,11 Some reports suggest subnormal" G; a$ J. \: G# Q6 x
adult penile length, apparently because of downreg-. y3 N, O' [' H: a$ \) t( G( m
ulation of androgen receptor number.10,12 However,/ c7 g2 T4 G( t
Sutherland et al13 did not find a correlation between6 a4 v- u7 t! t
childhood testosterone exposure and reduced adult
- O( o! t. w' @8 Spenile length in clinical studies.- D& ^6 p: b5 X- u  q+ z
Nonetheless, we do not believe our patient is3 D+ i9 ]8 w& a$ w! V
going to experience any of the untoward effects from3 W" ?6 O2 V( Z! M- a* q! f) G; K
testosterone exposure as mentioned earlier because9 u8 q9 v, Q+ a3 S7 v& n# s- c
the exposure was not for a prolonged period of time.
; O! Z' E7 c' ~Although the bone age was advanced at the time of# K$ z0 k/ N' Z7 y& R2 G
diagnosis, the child had a normal growth velocity at$ Z/ r* H5 W0 n7 G7 W) G
the follow-up visit. It is hoped that his final adult4 V$ @% p7 F; i, G
height will not be affected.
$ V0 {7 Q" E" {$ d8 t* bAlthough rarely reported, the widespread avail-) E" ^; Y; B8 U8 O  C# R
ability of androgen products in our society may+ j3 y* i5 i) j* M; P: B
indeed cause more virilization in male or female# ?( |; _; c" \5 o* J
children than one would realize. Exposure to andro-: z! `& `& S. |; j+ j; T, `
gen products must be considered and specific ques-
! E& ~' z7 H) _$ K  `- V' `5 B  z5 Mtioning about the use of a testosterone product or( G$ z$ {0 A# X( `1 G: N
gel should be asked of the family members during
( G  W( Q% R' S, L9 Y" i, u& Z7 mthe evaluation of any children who present with vir-
% i: F+ d, g0 T; ]- rilization or peripheral precocious puberty. The diag-
# ~0 z( _5 H+ I& N; ~! Hnosis can be established by just a few tests and by
1 k# C/ U  ^* ^4 Sappropriate history. The inability to obtain such a/ I' R* |0 {  O% r* y! D
history, or failure to ask the specific questions, may& i, w7 T. t) ?5 _
result in extensive, unnecessary, and expensive, a7 y* U6 P6 D& z
investigation. The primary care physician should be
- @1 H9 S- ~% o5 v8 S1 u: i, Saware of this fact, because most of these children3 [. d' o( f. O
may initially present in their practice. The Physicians’
1 z/ m' f$ |; D! aDesk Reference and package insert should also put a6 p/ R% j8 p# [) H2 F( {' K* o/ ~9 Z! C
warning about the virilizing effect on a male or
2 j  h' v' z' t, W/ tfemale child who might come in contact with some-2 W* }5 m9 f3 O/ c+ m: K
one using any of these products.
  N1 I$ K+ j% x( h) n% l. M" X" XReferences; m4 f% F0 ^7 F  ?1 w4 a; L
1. Styne DM. The testes: disorder of sexual differentiation- C( n& A+ v* r; u4 f
and puberty in the male. In: Sperling MA, ed. Pediatric, W- c  t* }4 C# O4 |  R
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;  x: g3 [& H  ~+ T
2002: 565-628.. u( j0 R4 V( [% x& J3 ^
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious- A% |( @+ P* P' s3 L: e
puberty in children with tumours of the suprasellar pineal
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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!

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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!
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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

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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?
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發表於 2025-1-19 02:41:05 | 顯示全部樓層

3 F2 Q9 L3 S& U5 m" ]- p0 P精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!

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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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