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Sexual Precocity in a 16-Month-Old
8 V' y& _9 H6 e3 d# [Boy Induced by Indirect Topical
2 h+ q7 B2 L, T% Y, OExposure to Testosterone
4 I& ~; N/ I6 @' n3 e* i4 `' mSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
5 w6 V. ^2 v5 `1 Vand Kenneth R. Rettig, MD18 d6 {. r; K# G$ {: T
Clinical Pediatrics: }6 ^3 r  X( Y! i8 M1 b
Volume 46 Number 6
0 G* s7 L3 a) m% b! }& }7 QJuly 2007 540-5435 T% y" C4 V/ O
© 2007 Sage Publications: g% C5 q0 o' J$ ~) I4 Z
10.1177/0009922806296651
1 s6 Q* t* @6 [3 y2 mhttp://clp.sagepub.com
/ m. Z' k3 _- O# k7 Rhosted at/ \- J7 F. N" T
http://online.sagepub.com3 x% w. }( q* N. `/ r# a# y
Precocious puberty in boys, central or peripheral,( N- }7 Y5 q2 ~/ B6 |& s1 j6 D8 E
is a significant concern for physicians. Central
$ r7 g/ @: }% T  T) \precocious puberty (CPP), which is mediated
* N& a# m4 i" c/ d7 t" tthrough the hypothalamic pituitary gonadal axis, has: t4 i& D$ I% A3 }2 q- o- T: F+ ?
a higher incidence of organic central nervous system  l1 \" Q+ l$ U+ P3 G  q
lesions in boys.1,2 Virilization in boys, as manifested
  a" m" H7 p' u3 p; yby enlargement of the penis, development of pubic* M) D: a7 a# `, }: C. F
hair, and facial acne without enlargement of testi-
% G3 K! B; ~2 n( rcles, suggests peripheral or pseudopuberty.1-3 We  l$ Y" z4 y- ~' h2 n7 K: `6 ]# g
report a 16-month-old boy who presented with the
- z1 M5 Y" l  U1 f3 senlargement of the phallus and pubic hair develop-: Q/ s: E+ L+ |% H( K, Z
ment without testicular enlargement, which was due9 O" v2 u8 ~6 K- I* p
to the unintentional exposure to androgen gel used by, Y3 ]% l1 D/ v7 I9 p3 w
the father. The family initially concealed this infor-) G) A5 g/ H2 P; a
mation, resulting in an extensive work-up for this
# Q4 f2 g8 A, u. P- Jchild. Given the widespread and easy availability of! d2 a! _9 X6 @
testosterone gel and cream, we believe this is proba-4 K; y" k  I/ {" y- `4 ]
bly more common than the rare case report in the
6 D8 S/ x4 W; _) `: E+ Aliterature.4
9 B3 Y! b. F3 J3 D( Q, \. A& [$ }Patient Report0 i7 m- J. d! R5 ?% K, ]4 M
A 16-month-old white child was referred to the
9 |0 o  D$ _5 i8 Q$ k6 H) Z" [endocrine clinic by his pediatrician with the concern4 K, \$ K5 k+ }% `" c: _* ~
of early sexual development. His mother noticed
9 ~/ q* e& G0 a: I- `  Blight colored pubic hair development when he was2 P+ y4 p4 d, D/ l
From the 1Division of Pediatric Endocrinology, 2University of, \! r8 @+ [9 b" b
South Alabama Medical Center, Mobile, Alabama.) g5 i" v* f5 U$ P' Y; n
Address correspondence to: Samar K. Bhowmick, MD, FACE,
) }2 U3 u  g" c7 |$ b+ {Professor of Pediatrics, University of South Alabama, College of  B4 |2 f0 U# s  [
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;; F/ R3 w8 K, n" V0 G
e-mail: [email protected].4 ~+ w3 s. t) O8 g4 s4 k+ h6 w  X6 R
about 6 to 7 months old, which progressively became
4 c1 L* M5 V; L* @* C+ q: D. tdarker. She was also concerned about the enlarge-9 [. {5 j! b4 X3 b% T2 e3 u
ment of his penis and frequent erections. The child* {5 A# t* I4 @7 m5 G
was the product of a full-term normal delivery, with9 n" L0 q4 l' T
a birth weight of 7 lb 14 oz, and birth length of* r7 K$ Y4 V: d3 I
20 inches. He was breast-fed throughout the first year9 j) V7 d, C/ A: h
of life and was still receiving breast milk along with* L9 v" h$ i1 E, g
solid food. He had no hospitalizations or surgery,
, }4 ], L, e( J" v4 Nand his psychosocial and psychomotor development
( D6 B# Q3 {2 nwas age appropriate.
( V7 d$ M( H* V+ VThe family history was remarkable for the father,
5 S) |3 a; O; ~. [, @" cwho was diagnosed with hypothyroidism at age 16,) }3 k$ d8 }# x* [# r5 B
which was treated with thyroxine. The father’s
5 G3 X8 V  Z0 m  z# n( u4 c: Y5 zheight was 6 feet, and he went through a somewhat( Y' O6 \" Y2 A: o
early puberty and had stopped growing by age 14.' Z0 C* g) O% h- B; a: ]6 r( z
The father denied taking any other medication. The, [& V( L. A3 K# c
child’s mother was in good health. Her menarche
5 b- ^% U' d; T- f: v  Lwas at 11 years of age, and her height was at 5 feet
- ]' ~+ Y+ s+ A& H" D5 inches. There was no other family history of pre-
$ [% c9 g$ s4 X2 ^cocious sexual development in the first-degree rela-( |4 ^# o6 f# r8 V, M  i( f! C
tives. There were no siblings.( c9 v1 ]1 j! C' h- Z3 E  ?! Q0 w
Physical Examination% @& J7 a& G9 i4 B( u% F
The physical examination revealed a very active," L1 i! `' {7 \  c8 W
playful, and healthy boy. The vital signs documented
* J! N, S5 x& ?* \& c/ [4 Da blood pressure of 85/50 mm Hg, his length was
: X1 h5 c/ }( \90 cm (>97th percentile), and his weight was 14.4 kg8 c% j4 s) Z& I% w9 C
(also >97th percentile). The observed yearly growth6 m/ @7 r' J; z" s
velocity was 30 cm (12 inches). The examination of* v# w9 ^3 y: j  @* j7 O
the neck revealed no thyroid enlargement.- ?4 E" B' L: H6 z$ m- Q
The genitourinary examination was remarkable for6 Q1 l! z* Q! ]8 a" c' J
enlargement of the penis, with a stretched length of# [' l) x5 D* @" ]
8 cm and a width of 2 cm. The glans penis was very well
. z$ _# O5 J4 ~0 {developed. The pubic hair was Tanner II, mostly around1 A6 A; u. D) q; M+ O8 ^, @: |
540/ Z1 N0 t# ]1 V
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" H2 G- V( ~- f. @1 l1 Jthe base of the phallus and was dark and curled. The
2 d6 b' w5 ~5 j1 E) M' @; J- S0 {testicular volume was prepubertal at 2 mL each.- z! ]+ P0 Y6 O& P6 ^! E
The skin was moist and smooth and somewhat
; _4 v$ M" n/ \4 n9 N% boily. No axillary hair was noted. There were no
" O7 G5 _1 \1 B8 aabnormal skin pigmentations or café-au-lait spots.% r1 K% E8 w) W8 y0 {& U* s
Neurologic evaluation showed deep tendon reflex 2+
* c2 ]3 m" r7 M& @; I5 \9 @bilateral and symmetrical. There was no suggestion
# b) C5 `' W! }& b: f* a* vof papilledema.
5 w! N' b; k8 U# j' I: ZLaboratory Evaluation
# |% E/ @" T" P' n) w5 d# D9 f  Y/ [The bone age was consistent with 28 months by6 Q* ]: |9 p' G8 P2 C
using the standard of Greulich and Pyle at a chrono-. {: j/ I9 D- D7 c; n/ k
logic age of 16 months (advanced).5 Chromosomal
* N% o* i5 I# o+ z+ c. ^9 H  \" ?karyotype was 46XY. The thyroid function test
9 f" I5 `! z* X7 Hshowed a free T4 of 1.69 ng/dL, and thyroid stimu-5 _, U& U9 T* f6 n- `
lating hormone level was 1.3 µIU/mL (both normal).
5 u( ~! H$ G$ R, nThe concentrations of serum electrolytes, blood+ G: t! |, c: M4 X( l
urea nitrogen, creatinine, and calcium all were
, u6 `2 g0 o' M/ d, swithin normal range for his age. The concentration& \( W9 B; o3 v9 n5 ^! {
of serum 17-hydroxyprogesterone was 16 ng/dL# W. Y) n; w" Z# E  M% O
(normal, 3 to 90 ng/dL), androstenedione was 207 b7 d, u+ ?5 l; T5 Z
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-9 v  o! q. D! J
terone was 38 ng/dL (normal, 50 to 760 ng/dL),# U" ]( h0 T3 K2 o# f8 L+ j
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
* h9 b2 G& }6 w# N: h49ng/dL), 11-desoxycortisol (specific compound S), L  p- L) R: a+ f2 i( k. J
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-& }, V, B1 |" Q/ v$ h, K3 c
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total9 U% b6 u/ U  V3 [
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
, b5 J, }+ n) w% }+ zand β-human chorionic gonadotropin was less than: _) V5 `- f2 p* i) P- @  G9 Q
5 mIU/mL (normal <5 mIU/mL). Serum follicular
  K6 d  P3 l5 v; B) k4 e/ xstimulating hormone and leuteinizing hormone
9 k2 @( h3 {; oconcentrations were less than 0.05 mIU/mL' l& v( `4 @8 D8 r1 ^
(prepubertal).
7 t4 a" I. t. Y" @9 TThe parents were notified about the laboratory" e; P. @- j% o  S
results and were informed that all of the tests were& U  D1 {0 C# w" r; P- z
normal except the testosterone level was high. The
6 [7 {. E5 r  R  |  Dfollow-up visit was arranged within a few weeks to
2 T# t, \! ]* r' V; E9 A4 h5 F+ P; K0 ]obtain testicular and abdominal sonograms; how-0 X2 ]2 u2 H& K% j- f& s1 [
ever, the family did not return for 4 months.
* Q/ [: `( G% O+ k: K/ Q, qPhysical examination at this time revealed that the) F& a* p, s9 V; T* x
child had grown 2.5 cm in 4 months and had gained5 r# m  e. q! x* t3 h3 G  l' w
2 kg of weight. Physical examination remained
5 ~) h& B! H& L' Gunchanged. Surprisingly, the pubic hair almost com-
( t6 _+ [# C% K/ n# Q1 s$ vpletely disappeared except for a few vellous hairs at
. S& E% n6 _- r& i; S! S+ _the base of the phallus. Testicular volume was still 2
- ]; L* e( c# z) N2 p7 VmL, and the size of the penis remained unchanged.: t" @; K! V) W" D) F5 E/ t
The mother also said that the boy was no longer hav-) v" o  W2 t; A1 z2 \- a
ing frequent erections.6 B: F# g: U' \8 F" O3 y3 \
Both parents were again questioned about use of3 A7 F! \6 p4 T- T! C
any ointment/creams that they may have applied to
) V8 U. P$ R! K6 w$ Jthe child’s skin. This time the father admitted the
7 B, ^6 y; v7 y- c+ F3 k0 |Topical Testosterone Exposure / Bhowmick et al 5410 R1 V0 y' N! {$ B- e
use of testosterone gel twice daily that he was apply-
2 S7 \1 q. u+ l* ~! c5 m" King over his own shoulders, chest, and back area for
. A' j% y. J3 Ja year. The father also revealed he was embarrassed
$ z  j7 r$ e* t* n& x8 |to disclose that he was using a testosterone gel pre-" t, K. ?( j5 L( ~) u: p1 J+ T
scribed by his family physician for decreased libido
7 w: U& r' s, _+ l9 T% r. Ysecondary to depression.+ g# T5 M: m4 b" A3 n' v. K
The child slept in the same bed with parents.! u+ @* |5 ~% H& T% p7 q
The father would hug the baby and hold him on his
- z4 u' k  E* E! c( Tchest for a considerable period of time, causing sig-% g3 {0 t- [5 i( c0 J- {
nificant bare skin contact between baby and father.0 o, A3 s. ^1 g
The father also admitted that after the phone call,/ |+ U2 P# Y; W5 K0 T! b
when he learned the testosterone level in the baby' O* `; t. W' a. L
was high, he then read the product information
+ E- ^7 t( m. a) O  A+ e  Lpacket and concluded that it was most likely the rea-
9 W/ I; A6 @6 g, o! ?; t8 json for the child’s virilization. At that time, they
( x9 E7 K0 g8 }8 G9 B. idecided to put the baby in a separate bed, and the
0 _' x  |7 U# N) g# i2 l% M$ mfather was not hugging him with bare skin and had$ J4 V% y) O0 c' T6 ]% L
been using protective clothing. A repeat testosterone
( k2 J4 L5 }. i2 v% B" x6 j: N, utest was ordered, but the family did not go to the
1 h( b% N0 O9 m- i9 z& _+ Xlaboratory to obtain the test.
. G, p2 d7 ?! A, [' EDiscussion/ j  E! e/ D- @, o
Precocious puberty in boys is defined as secondary7 N: a, Q# d4 z: g
sexual development before 9 years of age.1,4
2 q* n# H: A2 m* ^6 x6 MPrecocious puberty is termed as central (true) when
, @* d$ H0 Z6 v- xit is caused by the premature activation of hypo-
) N+ T. t5 ~7 l4 s( [) C6 p) Wthalamic pituitary gonadal axis. CPP is more com-
' |; w. F' X! t5 v" dmon in girls than in boys.1,3 Most boys with CPP. Z! h% l. Y1 i9 z& t% c8 J# t
may have a central nervous system lesion that is5 r* @7 |$ x5 s$ m
responsible for the early activation of the hypothal-
; `0 u+ C& O, o5 T. {8 H) `+ m1 Oamic pituitary gonadal axis.1-3 Thus, greater empha-$ C& k6 o1 g; c% t5 o% L2 q" W) v
sis has been given to neuroradiologic imaging in
" o9 S  m  j* `, ~boys with precocious puberty. In addition to viril-
4 p, G; E7 n4 X/ S" Cization, the clinical hallmark of CPP is the symmet-, J5 Y* g+ p: C% a# X
rical testicular growth secondary to stimulation by
8 P7 n) l( j4 z; G- ]% lgonadotropins.1,3
3 u' d) e. A: F% E3 H2 V" M' fGonadotropin-independent peripheral preco-
" R+ D( }) V. Z9 {6 p' f! Qcious puberty in boys also results from inappropriate
9 v- F: n# e, F) F$ Candrogenic stimulation from either endogenous or
5 q0 i  v% M& W2 eexogenous sources, nonpituitary gonadotropin stim-
6 C9 x1 J! H6 n3 b& c) mulation, and rare activating mutations.3 Virilizing" G5 |' x* }) x  y* V
congenital adrenal hyperplasia producing excessive
/ C* B3 S( |' W! q$ I, _0 J% E; s% n' [2 @adrenal androgens is a common cause of precocious
5 V2 x% b" f4 o# mpuberty in boys.3,4( s: m, u+ [, w. K3 W' y' u! L
The most common form of congenital adrenal4 `+ _0 D. \2 H# W0 a& e( a
hyperplasia is the 21-hydroxylase enzyme deficiency.4 I! }- |2 q" A* s9 }
The 11-β hydroxylase deficiency may also result in, h% X; D( H+ S0 n
excessive adrenal androgen production, and rarely,
: g# x4 c+ U8 `" Z* Kan adrenal tumor may also cause adrenal androgen2 Y& E4 e( ], v% ?5 l, B0 @
excess.1,3- U# r" C6 t7 ?( I1 \8 m) Q& f0 y6 \+ v
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 F$ I6 g# e1 q0 v. K, `
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007! ^/ E0 I6 ~7 F1 u5 ^8 G4 t) f. \
A unique entity of male-limited gonadotropin-# Y* ~' a+ I) o0 [5 `
independent precocious puberty, which is also known. {+ o! f" e: T& i7 p9 ~5 l: `
as testotoxicosis, may cause precocious puberty at a3 n6 z* L2 ?0 a/ _2 B9 }: ^
very young age. The physical findings in these boys4 P! b3 ]7 V9 {& G  s. `2 g1 p( @
with this disorder are full pubertal development,$ v$ u; E* E; K7 k8 i  c: ^' `! N  g
including bilateral testicular growth, similar to boys
3 v. r, T% H. _8 Xwith CPP. The gonadotropin levels in this disorder
! {! _" M) v' ?; b+ Kare suppressed to prepubertal levels and do not show
: C" [4 v. }; U8 c6 apubertal response of gonadotropin after gonadotropin-
5 Q. ~* h8 R) R5 N- ireleasing hormone stimulation. This is a sex-linked
" q8 I+ D( V4 e/ E2 O0 `autosomal dominant disorder that affects only# Q9 S; ^. e! `# ^0 k; _
males; therefore, other male members of the family; i* }/ [1 Y2 E- ~& g4 n2 [4 T
may have similar precocious puberty.3: p+ Y$ f: a( ]2 G
In our patient, physical examination was incon-  |8 n6 c- m; S+ Q# v
sistent with true precocious puberty since his testi-
: x9 V$ Z- C" T7 J4 ccles were prepubertal in size. However, testotoxicosis
0 W3 [* v! J4 r! Uwas in the differential diagnosis because his father
. M% ]; b. O5 g: z. V+ zstarted puberty somewhat early, and occasionally,
3 L0 X. e! _. f2 m# M0 x7 a! t1 S. Itesticular enlargement is not that evident in the2 h/ _3 F8 U) Q+ ]  O
beginning of this process.1 In the absence of a neg-& X# C" g# o! X2 b3 ^
ative initial history of androgen exposure, our2 @- S+ g- f9 \; h0 o$ z. f" b6 K
biggest concern was virilizing adrenal hyperplasia,2 z2 h5 _. m# x) H7 C1 ]) P" M# I
either 21-hydroxylase deficiency or 11-β hydroxylase
0 X3 P) X5 t- b! Y) x7 E' R& }0 sdeficiency. Those diagnoses were excluded by find-
2 m+ u& }  p3 p" _& t  O4 _9 Ping the normal level of adrenal steroids.
6 I/ l$ t  z$ G! gThe diagnosis of exogenous androgens was strongly
& _# I4 N* o' c/ R. osuspected in a follow-up visit after 4 months because1 l6 q3 l3 e* g$ s6 A  B) |: ~. H7 j
the physical examination revealed the complete disap-
" \6 Z. V& `- V! Z2 g  X$ epearance of pubic hair, normal growth velocity, and6 w+ A% s" x: l
decreased erections. The father admitted using a testos-
  \4 M& v7 n) I. T  T/ Iterone gel, which he concealed at first visit. He was
( q4 d% t' i2 ~& Ousing it rather frequently, twice a day. The Physicians’* Z' C5 v) A' M+ `. P3 X" ?
Desk Reference, or package insert of this product, gel or7 r/ @. K1 O$ o/ ^4 p
cream, cautions about dermal testosterone transfer to8 M2 L: R$ M5 j1 x# B) Q
unprotected females through direct skin exposure.
  C% |# V$ J# N% |# \* @/ }Serum testosterone level was found to be 2 times the
4 p3 y, L: e9 r3 F+ ~2 u2 Fbaseline value in those females who were exposed to
) S( u4 B, G6 o2 U, J, `& o& _even 15 minutes of direct skin contact with their male
" j$ P  h  B' ^" D% f, E; rpartners.6 However, when a shirt covered the applica-8 J' F& S  C* D# J
tion site, this testosterone transfer was prevented.
# Z0 `" C3 G+ f: {$ s, UOur patient’s testosterone level was 60 ng/mL,# A, j. L6 X7 J$ I% Z6 M7 M
which was clearly high. Some studies suggest that8 E* l) b- j! Z  W  [
dermal conversion of testosterone to dihydrotestos-
) K& a; d' y( Xterone, which is a more potent metabolite, is more8 F7 R* \: Z1 P7 l3 `
active in young children exposed to testosterone
1 A3 L# I- {! n# aexogenously7; however, we did not measure a dihy-4 Q! p0 T! b1 g" A: G' o0 E
drotestosterone level in our patient. In addition to/ W/ A- G5 u8 e0 X1 }
virilization, exposure to exogenous testosterone in0 I' ~4 |4 S  Q. o, n
children results in an increase in growth velocity and5 V8 Q8 h; D6 y4 l7 w7 C1 z5 Z
advanced bone age, as seen in our patient.
. V* z7 _5 S% I0 r9 n( O: i; uThe long-term effect of androgen exposure during, P( l. p: d* w) G: L
early childhood on pubertal development and final
% G. r) w9 [0 j. _9 V7 P* R) X8 P1 u# @7 dadult height are not fully known and always remain8 j' a& b1 v6 S" J0 i& L4 |# Q, ^% Y
a concern. Children treated with short-term testos-5 D+ s" I3 C7 x1 ^! K3 j
terone injection or topical androgen may exhibit some6 K9 u" i0 i5 v: O2 K
acceleration of the skeletal maturation; however, after
$ q: s0 Y* q1 X" D, X" ycessation of treatment, the rate of bone maturation8 Q. @2 q9 _+ u5 N! |- `- K! Y+ o
decelerates and gradually returns to normal.8,9+ k- c/ i" ~3 \9 {# P4 o. S# m
There are conflicting reports and controversy) v* M8 ?5 ]2 W& ~9 k
over the effect of early androgen exposure on adult
, c. u! y* j9 K. m# L2 n* mpenile length.10,11 Some reports suggest subnormal
8 `9 s- w9 u4 o4 ~8 aadult penile length, apparently because of downreg-; c* o$ ^. B/ e, b4 C
ulation of androgen receptor number.10,12 However,. W- S9 G/ N, j* \+ R4 U
Sutherland et al13 did not find a correlation between
) n7 y+ q8 H  ychildhood testosterone exposure and reduced adult
/ y9 i6 T# j9 I! E: |' {6 t4 _  h6 Hpenile length in clinical studies.
' ^, H4 C2 J% H3 ], W5 ?2 zNonetheless, we do not believe our patient is
* {1 z( Y1 U% W& y5 @% o$ x/ cgoing to experience any of the untoward effects from7 I9 C+ g/ ^3 p- W& W1 r- l; j
testosterone exposure as mentioned earlier because: O; U, i; \3 f
the exposure was not for a prolonged period of time.
; G" P3 V5 [( ]Although the bone age was advanced at the time of
7 a% h2 m+ P+ t8 Y& h3 @diagnosis, the child had a normal growth velocity at/ f$ Z$ j, l$ b# P1 ^% G
the follow-up visit. It is hoped that his final adult) H+ `& b5 Z; z, Y/ s3 X, _# p
height will not be affected.* w5 Y! z2 W8 F( Q, I/ G8 a
Although rarely reported, the widespread avail-
! T3 T# e$ f- H& ?- I: sability of androgen products in our society may
7 m/ K% O4 Q# U; {1 G5 }indeed cause more virilization in male or female) o+ C6 @6 [0 k( `3 W/ D$ Y
children than one would realize. Exposure to andro-) l( C* ]% M) y$ }
gen products must be considered and specific ques-1 H6 G0 @; D+ q3 E* r( f% h2 f* ~+ f
tioning about the use of a testosterone product or
: v: N" F, ~# u+ {. d1 \gel should be asked of the family members during
; Y/ p% n4 f8 T8 A2 u7 z9 \- Cthe evaluation of any children who present with vir-
0 @6 w8 D6 I/ V/ rilization or peripheral precocious puberty. The diag-
& J5 d$ N  D& {) P4 O# }nosis can be established by just a few tests and by
, f3 H2 n& a. t! u4 e1 k5 O" Lappropriate history. The inability to obtain such a
4 Q" O. p* Z! k7 k" |history, or failure to ask the specific questions, may
; Z* P: @  @; p* rresult in extensive, unnecessary, and expensive# \( N# H' H3 d6 }
investigation. The primary care physician should be
9 f- Q- T2 S6 s9 Q; `aware of this fact, because most of these children1 o; O# U1 Y" C  j0 E
may initially present in their practice. The Physicians’
# g& w) P5 `3 j/ ZDesk Reference and package insert should also put a
! C9 `# @- J6 {2 x8 Z% Nwarning about the virilizing effect on a male or
6 p3 ~. I  k- y3 q8 Hfemale child who might come in contact with some-0 W  F7 {5 }- n7 w
one using any of these products.+ `- Q( F$ x0 ]
References4 |) P8 j# U9 x
1. Styne DM. The testes: disorder of sexual differentiation2 w, K. [8 |& i! C& D8 A+ G/ P: I
and puberty in the male. In: Sperling MA, ed. Pediatric7 U' ?4 W( ?+ e: q5 C, h& d
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
0 ]4 L* _, E2 w; f2002: 565-628.
/ s9 I0 q: U9 ^( ^+ D2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious( E8 c7 j- Z; Y' a
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old( M) f) X0 q1 R! ^5 R
Boy Induced by Indirect Topical% {2 o, Q8 a" }2 w; x
Exposure to Testosterone
) |; P  |# ?! U/ i* nSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2/ Y  u- c5 Q. ^- h; }6 y; M3 O
and Kenneth R. Rettig, MD1; t/ n  v2 |+ g. z# X. b7 C0 W2 F' j
Clinical Pediatrics! N* U5 L0 G" R  k$ t1 g/ ]- z1 q
Volume 46 Number 6
: x+ p7 A8 S1 g( Y3 aJuly 2007 540-543& @9 I2 R5 s# J/ S
© 2007 Sage Publications
' R3 ]% c; `4 u6 T8 c0 Q10.1177/0009922806296651
6 ^# j* B+ ^/ O  Ghttp://clp.sagepub.com, ]7 ]. K; L/ m6 j3 P1 Z& m0 X
hosted at
: k7 _8 X- Q. ^) [2 M" vhttp://online.sagepub.com
, |; |) q0 S" x: SPrecocious puberty in boys, central or peripheral,
% r2 n) Q: _" M8 S$ fis a significant concern for physicians. Central
9 R* X# Q$ J3 X# b9 K, ?: ?! Y' bprecocious puberty (CPP), which is mediated7 p/ i' k+ P' \* a+ ^. O7 P
through the hypothalamic pituitary gonadal axis, has
+ G6 G' x8 o% v3 [) ^6 h; ta higher incidence of organic central nervous system
! F, t  Z+ l, Llesions in boys.1,2 Virilization in boys, as manifested
; ~! @; z( r; q0 _; D9 |' O( ~by enlargement of the penis, development of pubic
+ r5 [% D( A/ Y# ?% Xhair, and facial acne without enlargement of testi-2 i/ w9 A  g% P7 y
cles, suggests peripheral or pseudopuberty.1-3 We3 h: T1 e. i# q4 i. S
report a 16-month-old boy who presented with the3 Q; m3 _9 ?+ S
enlargement of the phallus and pubic hair develop-4 ~5 {1 L0 W( |0 D" A
ment without testicular enlargement, which was due
: d7 e- \" W! y& g0 V" \to the unintentional exposure to androgen gel used by3 T6 w( n( n5 E3 k
the father. The family initially concealed this infor-) h# e# t2 R# M% E5 z/ K, k1 N, E
mation, resulting in an extensive work-up for this
& i6 Q- {6 `9 ~5 R; Z+ cchild. Given the widespread and easy availability of0 B% y# q0 I# t
testosterone gel and cream, we believe this is proba-
$ ]! n# G, D  ]7 j# ?- I) T' ^bly more common than the rare case report in the/ F& W; R  ^  p
literature.4
7 ^- M/ i1 I4 xPatient Report
3 _. Y3 H9 v) [* W( \1 JA 16-month-old white child was referred to the
2 g! I% [) m8 yendocrine clinic by his pediatrician with the concern! h( M8 h* Q6 R4 i1 T" ?7 }! C
of early sexual development. His mother noticed! \( Z. [5 |0 C' t) X
light colored pubic hair development when he was
* _9 S$ {8 z, G, W0 t+ d/ uFrom the 1Division of Pediatric Endocrinology, 2University of
0 w1 W/ `$ `* i2 |1 CSouth Alabama Medical Center, Mobile, Alabama.
6 t: b# Y# C( QAddress correspondence to: Samar K. Bhowmick, MD, FACE,
6 @8 ^* A9 \0 `. Y) ~Professor of Pediatrics, University of South Alabama, College of
+ E0 _" F; j7 D" S4 AMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
. M/ Z. i" f2 D3 M9 [; o$ `6 l, ye-mail: [email protected].) V6 V1 f2 X& ?
about 6 to 7 months old, which progressively became
. ^7 c7 X3 {% K. F- s) vdarker. She was also concerned about the enlarge-# M6 k8 i3 n6 V) C
ment of his penis and frequent erections. The child8 e# f3 H5 Q! b2 v
was the product of a full-term normal delivery, with
& z+ ?9 H) {# V" {a birth weight of 7 lb 14 oz, and birth length of$ T5 r( J7 l# M
20 inches. He was breast-fed throughout the first year
- y2 [* |( U$ vof life and was still receiving breast milk along with: f. A! \% k+ F4 ?8 r
solid food. He had no hospitalizations or surgery,7 F) m/ E) m$ G$ m9 X. ^" ]
and his psychosocial and psychomotor development# u: m8 C% D5 B* O, R6 R. h# Q2 m
was age appropriate.
# Q9 ~' y3 M# A* NThe family history was remarkable for the father,
) G/ v& Q, K9 d# }8 @3 V; ~who was diagnosed with hypothyroidism at age 16,
3 G/ T9 @3 y# n  R  fwhich was treated with thyroxine. The father’s
' u8 n+ h0 r7 E$ U6 w: Z* Hheight was 6 feet, and he went through a somewhat9 q5 H% C( d6 }4 T* Q
early puberty and had stopped growing by age 14.
/ K, Z! s; P; n; ~The father denied taking any other medication. The# p. r) G1 [  H2 Q% V
child’s mother was in good health. Her menarche
1 ^+ f. ]7 p4 Zwas at 11 years of age, and her height was at 5 feet
" [/ K! k6 m% D5 P) C# R5 inches. There was no other family history of pre-# D7 ^1 d  w  W$ u% M6 R, B
cocious sexual development in the first-degree rela-8 p7 f( a4 ?7 X# {
tives. There were no siblings." g2 M; C6 @7 G1 n& a2 X
Physical Examination4 [' t( q* S& p" x
The physical examination revealed a very active,
* Q; N5 a2 L5 S, Rplayful, and healthy boy. The vital signs documented. {- l3 S1 v" L3 M: x7 q1 h8 e) z' @& R
a blood pressure of 85/50 mm Hg, his length was& f/ R9 G  d( K/ X0 e
90 cm (>97th percentile), and his weight was 14.4 kg
# X) {' Y5 W6 w9 g0 h8 v) o1 x+ }1 w(also >97th percentile). The observed yearly growth
$ q0 z1 T# q& N* Mvelocity was 30 cm (12 inches). The examination of6 c; L' }! X! S
the neck revealed no thyroid enlargement.
: m* C" @+ P, Q5 V* H: fThe genitourinary examination was remarkable for
$ I6 L% W1 B0 O6 ]$ Senlargement of the penis, with a stretched length of# S1 b+ n. l, ^
8 cm and a width of 2 cm. The glans penis was very well9 L! R0 ]# G" Q" q' t
developed. The pubic hair was Tanner II, mostly around
# {+ J$ A! X. K3 f540
( X  K* G" G, e- Aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 k/ M$ V5 d" q2 o% s: S
the base of the phallus and was dark and curled. The
1 S# a, P% q9 W# n' \3 R7 k5 B" Vtesticular volume was prepubertal at 2 mL each.2 D/ }4 n) h0 P2 k9 I9 i
The skin was moist and smooth and somewhat# K2 G" b8 O0 `" i. O$ s1 C7 j: \
oily. No axillary hair was noted. There were no* e' N1 I* o6 Q* l: y
abnormal skin pigmentations or café-au-lait spots.
! X) Q/ I$ K/ T. J# W# ^: g1 ?. ONeurologic evaluation showed deep tendon reflex 2+1 x. g; k" y, y, X9 O2 m. d6 B
bilateral and symmetrical. There was no suggestion' z# ^! o0 h2 N* E
of papilledema.
+ ?$ u1 W5 ~& \2 N2 ?2 a$ J, p' nLaboratory Evaluation& e$ X, P1 @+ U: ]  ]9 E
The bone age was consistent with 28 months by
2 J9 i+ \- x7 U/ uusing the standard of Greulich and Pyle at a chrono-
! r' D+ A; q& `logic age of 16 months (advanced).5 Chromosomal% Q* R$ L  p; x7 w/ ?1 e* ?
karyotype was 46XY. The thyroid function test
9 ^# g  J+ Y6 c2 h. P& ^6 Q- a5 _+ C/ qshowed a free T4 of 1.69 ng/dL, and thyroid stimu-$ O4 [7 w2 T" x
lating hormone level was 1.3 µIU/mL (both normal).0 _$ K# C: _. O* e: s9 r# B
The concentrations of serum electrolytes, blood  H  f0 V$ D/ S$ N! @
urea nitrogen, creatinine, and calcium all were( |* w* j. R2 F! \
within normal range for his age. The concentration
6 L0 R9 B  ]! p" a1 sof serum 17-hydroxyprogesterone was 16 ng/dL
$ P6 y5 n1 A5 d, q& _5 Q5 g(normal, 3 to 90 ng/dL), androstenedione was 20
! G; @/ O' k3 O' l1 Cng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
/ X6 j6 D3 d2 j8 W3 Uterone was 38 ng/dL (normal, 50 to 760 ng/dL),; }5 ^1 ~5 L4 s0 D2 n) E
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
% `8 b8 z$ J/ n  d! l& n% W; j49ng/dL), 11-desoxycortisol (specific compound S)
) C* w1 e3 X2 Z2 F8 e- Q" U; V2 k0 bwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-* v' r& ?% ?7 q  G
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
- P7 h, M" u5 V) itestosterone was 60 ng/dL (normal <3 to 10 ng/dL),1 z9 K7 T( {9 `9 i5 h
and β-human chorionic gonadotropin was less than% G" q; F) I" _, m* u6 N: W; {
5 mIU/mL (normal <5 mIU/mL). Serum follicular
5 V- r7 R7 Z1 E$ l* qstimulating hormone and leuteinizing hormone$ `# y9 O2 f8 [% Z, y6 l$ g
concentrations were less than 0.05 mIU/mL7 J; b* D7 k- i7 @4 M+ v1 u
(prepubertal).
( a& H& S9 Q9 d# ZThe parents were notified about the laboratory
) m+ }( Q9 ^! y. X# ?- |0 }- lresults and were informed that all of the tests were, R) K% k0 g% j% k; Z+ _
normal except the testosterone level was high. The. K: j7 [# Z( n' l
follow-up visit was arranged within a few weeks to0 {# ~/ ?, z6 e9 ^
obtain testicular and abdominal sonograms; how-( o8 i0 p' [% ?/ E: ?5 |
ever, the family did not return for 4 months.3 E7 |2 {# `  a! X8 ]
Physical examination at this time revealed that the
: S4 Z7 f- q% I; w0 b9 _) fchild had grown 2.5 cm in 4 months and had gained1 j2 s  s$ q; j0 A* ^
2 kg of weight. Physical examination remained. }+ J8 U# l; \7 R
unchanged. Surprisingly, the pubic hair almost com-
) W, k% M9 r& `: {pletely disappeared except for a few vellous hairs at! t( e5 K9 A& O; U& q
the base of the phallus. Testicular volume was still 26 m7 _  U. }' @( W5 @
mL, and the size of the penis remained unchanged.) |- ?' W, A$ Q  }- s
The mother also said that the boy was no longer hav-
7 R3 A; n; z9 G6 [ing frequent erections.8 R+ z2 u( G" |* c1 n
Both parents were again questioned about use of
4 x! x; b# e( g2 r7 pany ointment/creams that they may have applied to
) S: W- n# I" T+ }! ~( G  |" W9 o" Nthe child’s skin. This time the father admitted the/ c# ~; x( z" w, r. A3 j
Topical Testosterone Exposure / Bhowmick et al 541. K9 C' [8 n  }. X4 E4 l3 @9 g6 f
use of testosterone gel twice daily that he was apply-
  C7 ]5 B" w; e7 W4 Y% c; N& k) x/ ring over his own shoulders, chest, and back area for" i5 q2 L3 ]! C5 }
a year. The father also revealed he was embarrassed& n) }) Q0 b& M& T+ O
to disclose that he was using a testosterone gel pre-
9 F# P5 S$ `( g! D# E4 K: Jscribed by his family physician for decreased libido
( h/ d1 Y1 a( }+ B4 P7 ksecondary to depression.& Y8 y; k$ {' w. r
The child slept in the same bed with parents.6 T9 N' p: J. W0 i- v5 Y
The father would hug the baby and hold him on his
9 ]5 Q  s' w. R1 D/ ?chest for a considerable period of time, causing sig-$ U4 Q: `- t5 l9 X$ _( R3 }" j
nificant bare skin contact between baby and father.
5 z3 b3 W4 Z2 D" YThe father also admitted that after the phone call,
# @/ o( ~# U" D' O: ]# b" h6 t. Twhen he learned the testosterone level in the baby
1 }- ^5 z3 a2 |9 T: Qwas high, he then read the product information
* Z! q. a# ^* p' m2 V0 Rpacket and concluded that it was most likely the rea-
, ~- u; C+ r8 o( C  p1 n6 s, @+ Wson for the child’s virilization. At that time, they) Q3 ^$ l  g* {# X
decided to put the baby in a separate bed, and the
8 ?: Z  S5 a, n" z% afather was not hugging him with bare skin and had3 s7 l' U5 t$ J, k
been using protective clothing. A repeat testosterone$ C- D4 P) _+ Q* A% D) D
test was ordered, but the family did not go to the
) E( o/ y! u2 ^8 _& Elaboratory to obtain the test.
' h, I( \  U7 N. p( q* BDiscussion
! I( O% h1 t( I- u) iPrecocious puberty in boys is defined as secondary
& s5 A4 j3 r* Ysexual development before 9 years of age.1,4
* X8 W7 O- I' d& X4 G8 G8 z. B+ ^, ^Precocious puberty is termed as central (true) when9 x8 T) R* M4 R( i. X3 n$ }
it is caused by the premature activation of hypo-& o% q- `1 b7 D  H9 \
thalamic pituitary gonadal axis. CPP is more com-
" g9 s7 t6 D* u( e% M( V- fmon in girls than in boys.1,3 Most boys with CPP
: H' d, a8 ?$ d, y7 Emay have a central nervous system lesion that is
) o1 w3 O$ _/ O, a; U8 t. xresponsible for the early activation of the hypothal-0 y9 c  K% ~2 a6 ?# }4 c7 j
amic pituitary gonadal axis.1-3 Thus, greater empha-
5 f: y# x& n; Rsis has been given to neuroradiologic imaging in/ K6 d+ ~4 d" _& n3 J# n
boys with precocious puberty. In addition to viril-1 F+ I! B1 D3 ]. |1 i
ization, the clinical hallmark of CPP is the symmet-
; P7 w: J5 G7 Y( ^2 erical testicular growth secondary to stimulation by- N& G! H1 G, _4 s2 ~
gonadotropins.1,31 e! E  Z6 [( E+ u# E+ ?
Gonadotropin-independent peripheral preco-2 I" f$ U8 t/ Q  D9 F# }
cious puberty in boys also results from inappropriate
1 v, \; r, J7 o- @5 ]# Aandrogenic stimulation from either endogenous or
$ [5 g9 l6 L. u) ^% k7 Y' U- Texogenous sources, nonpituitary gonadotropin stim-+ K* I& O* \( \; N# ^- R, i
ulation, and rare activating mutations.3 Virilizing
; S* L" z; N& W- e& @) N& q" Gcongenital adrenal hyperplasia producing excessive+ h+ I) a2 \+ d( V
adrenal androgens is a common cause of precocious1 `% T8 J, Z. p$ p4 ~# D
puberty in boys.3,4
" @! i( W! `0 ]2 I* j6 @7 |The most common form of congenital adrenal
/ N/ F+ X% ?: a$ H) `hyperplasia is the 21-hydroxylase enzyme deficiency.9 H; q5 W% a. h7 F7 X
The 11-β hydroxylase deficiency may also result in
2 c  M( Z7 H# U7 G& ?) g  fexcessive adrenal androgen production, and rarely,- O( P0 ]' u9 c1 ?
an adrenal tumor may also cause adrenal androgen
& W' M: a0 G8 o8 texcess.1,3
, d( @0 ]1 T( o: zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 W% H& v" D. W: L- t$ x
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
; t. H. m5 t6 i4 `3 T4 ^2 @; h9 UA unique entity of male-limited gonadotropin-
$ G3 N& \2 q2 H: I  p4 vindependent precocious puberty, which is also known' P3 X7 ^5 O9 ?* \8 W
as testotoxicosis, may cause precocious puberty at a
- I9 d: @" y6 d- Xvery young age. The physical findings in these boys
! K7 ?! J* x- p+ K5 _1 U* w$ \" T* ^6 }with this disorder are full pubertal development,
3 t7 e$ V6 ^3 _8 R- [7 {# b& {( xincluding bilateral testicular growth, similar to boys
! y3 l" ]; q# j! a7 f; Y0 r/ h. wwith CPP. The gonadotropin levels in this disorder; v4 w5 ]6 h% G
are suppressed to prepubertal levels and do not show4 X- Q- w& y, p% x
pubertal response of gonadotropin after gonadotropin-7 W% N1 Q) s' a  }& m# ]
releasing hormone stimulation. This is a sex-linked% Z% p( x' S# x
autosomal dominant disorder that affects only0 v- i5 |, \. n8 V. X, G! C
males; therefore, other male members of the family: t& Y/ B! ~. r' s
may have similar precocious puberty.3
, |5 P& n+ L$ E/ d2 Z" m$ mIn our patient, physical examination was incon-8 v+ M* ]0 u5 u& s4 N& `
sistent with true precocious puberty since his testi-
# Z# W" ^% G( Z. [2 G2 B1 acles were prepubertal in size. However, testotoxicosis
: e/ |( q$ h: j2 {* a% z) w# Jwas in the differential diagnosis because his father
2 C2 R$ v+ [3 `, astarted puberty somewhat early, and occasionally,& e# j) V/ R: I/ k+ j
testicular enlargement is not that evident in the
+ x8 R& @3 w* k. }1 l/ H+ Xbeginning of this process.1 In the absence of a neg-
6 ]; }% J3 y: E" ?* `ative initial history of androgen exposure, our# X5 ]: R+ m% ~0 o- J  p/ y
biggest concern was virilizing adrenal hyperplasia,' q  [1 P1 f' M$ F7 y/ ?
either 21-hydroxylase deficiency or 11-β hydroxylase
7 f) ?$ u  ~# T3 qdeficiency. Those diagnoses were excluded by find-0 J% }+ R3 u/ m* P/ O1 [
ing the normal level of adrenal steroids.
* i7 k2 k  |1 o1 r" `The diagnosis of exogenous androgens was strongly- Y) ^2 L4 P! u% h
suspected in a follow-up visit after 4 months because9 l0 F6 R' B! T) \% y$ ~
the physical examination revealed the complete disap-9 f" M7 _5 T: T$ ~# D( h- k+ k
pearance of pubic hair, normal growth velocity, and1 n3 M- `: j' ~# E4 O
decreased erections. The father admitted using a testos-
% c6 W, J2 U/ o! J5 l, u2 ]/ Jterone gel, which he concealed at first visit. He was
% V, R4 R1 Q" q+ zusing it rather frequently, twice a day. The Physicians’
9 R$ W, j% p; F  ]8 _Desk Reference, or package insert of this product, gel or
& t/ V8 L. R: P; dcream, cautions about dermal testosterone transfer to
- j4 c4 d) V& w/ ^9 ?: j( D1 junprotected females through direct skin exposure.
/ ?8 V  Y/ v* B' U' [% S0 ]Serum testosterone level was found to be 2 times the) E; t- n: T0 ?0 `
baseline value in those females who were exposed to/ U# V+ e; M) c+ r* k! d* p
even 15 minutes of direct skin contact with their male
& q0 S: ^9 d; E: [partners.6 However, when a shirt covered the applica-7 d1 R" \7 d7 g# q+ x$ b  y: E
tion site, this testosterone transfer was prevented.
: C. @2 X% H+ y0 |! y! h9 ROur patient’s testosterone level was 60 ng/mL,
$ b8 Q2 n6 f9 ~' c% {which was clearly high. Some studies suggest that
4 n2 v( q$ a; K7 i# fdermal conversion of testosterone to dihydrotestos-& z9 S! ?& J& F5 S
terone, which is a more potent metabolite, is more7 X/ Q, U& K2 W$ Q
active in young children exposed to testosterone6 Y4 `% w& a4 Q! R
exogenously7; however, we did not measure a dihy-
# b4 L% e) G: k* q8 edrotestosterone level in our patient. In addition to) U$ M& g# A, A4 Y5 @& Q
virilization, exposure to exogenous testosterone in8 s3 X4 g$ B9 b- W& k& L
children results in an increase in growth velocity and
* L% s, v$ B% N' K+ V! qadvanced bone age, as seen in our patient.$ R  E& t. A8 q5 d
The long-term effect of androgen exposure during
( C* T; ~9 k2 q* C: S- z% {) C/ k3 Pearly childhood on pubertal development and final
8 n- C- H! m6 p( D! f0 v; Z, C' uadult height are not fully known and always remain, I4 r% ^1 e& @! T
a concern. Children treated with short-term testos-) X  Y( S/ ?$ K9 `* y' k
terone injection or topical androgen may exhibit some
0 v$ ]8 p, Z' A. ?* v; s! w: dacceleration of the skeletal maturation; however, after, k9 |% z6 V. e/ F
cessation of treatment, the rate of bone maturation
# |9 p* M. Z! }; I3 x+ M' i/ j. A- }decelerates and gradually returns to normal.8,9* j" V- j& ?: J3 r+ v! X5 C8 g. p6 Y
There are conflicting reports and controversy$ F( z3 z4 p6 B0 x- H# P& `0 _
over the effect of early androgen exposure on adult
, u3 `1 E3 T5 p# Mpenile length.10,11 Some reports suggest subnormal
1 M! i3 D- h- R" G. w; Tadult penile length, apparently because of downreg-
0 q. L& l9 L6 B# iulation of androgen receptor number.10,12 However,
. `) W/ }7 w! C7 z0 j  O+ gSutherland et al13 did not find a correlation between
6 L) P( p) x: J: [childhood testosterone exposure and reduced adult
+ E1 T+ V2 V1 K' g/ y% Lpenile length in clinical studies.
) t, @+ X8 w- ^# j8 Z2 j2 j/ ANonetheless, we do not believe our patient is
1 v* A5 U7 F8 x/ [$ s- N: r4 ggoing to experience any of the untoward effects from5 ^! ~: \; @! Z* l7 _+ H
testosterone exposure as mentioned earlier because1 j! C) e" X1 }$ |) p! u
the exposure was not for a prolonged period of time.
8 r& C1 E" s5 q# R/ v  PAlthough the bone age was advanced at the time of6 P  r! m4 S; p* G% U$ {
diagnosis, the child had a normal growth velocity at
) Z  s( l% L6 ?$ _3 Y8 I5 E( f* Mthe follow-up visit. It is hoped that his final adult7 t4 X$ B2 y7 J$ Q
height will not be affected.
* o+ T0 c) S! M" \; ]4 `  SAlthough rarely reported, the widespread avail-
: G% ?  P- i' B1 m- \- Gability of androgen products in our society may- t" S  U, h8 R' k
indeed cause more virilization in male or female) ~  W, s% e: g# x, i' W
children than one would realize. Exposure to andro-
$ h4 c$ T; H% k0 Ogen products must be considered and specific ques-  y' N/ [5 _- G3 R2 G
tioning about the use of a testosterone product or9 g) F/ b4 B- n* a! ^) v' T
gel should be asked of the family members during4 u7 O. d' V7 K& L4 K
the evaluation of any children who present with vir-
$ C1 ~7 A& ^9 b" b) `ilization or peripheral precocious puberty. The diag-1 w  Z, \' H! e* W5 x$ q+ R
nosis can be established by just a few tests and by" g4 l7 I" R& F/ E
appropriate history. The inability to obtain such a& q* |0 e" B  {# Y& p. f0 e! n
history, or failure to ask the specific questions, may
7 g& M( A. ?( p  wresult in extensive, unnecessary, and expensive
' j9 B' D3 K* ainvestigation. The primary care physician should be
" ]7 d" H/ c0 f# caware of this fact, because most of these children
7 S; Q- j7 ?3 p$ ?) @may initially present in their practice. The Physicians’
' i) {  c4 C# U2 eDesk Reference and package insert should also put a* i, {4 N' H- Y4 u# ^  r
warning about the virilizing effect on a male or# X& s* Y3 I; H4 v- X8 p/ ~
female child who might come in contact with some-" N  ^. n8 x5 q" X7 F- ]
one using any of these products.5 S# S9 F7 @  b) w
References, C9 |3 b/ r# K$ E6 d. n
1. Styne DM. The testes: disorder of sexual differentiation
& Z6 e* ~% V* A3 d) v) uand puberty in the male. In: Sperling MA, ed. Pediatric3 Q- P. i$ z- J" ]
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;  h- `( I! \; J1 {
2002: 565-628.
& U+ `$ p& _, r5 d( K. h: b2 A2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious! I5 i+ B+ @5 j# e% r& p
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
加入VIP,享受高級特權宣傳賺金又升級,超級棒
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
- P  R* t7 J( u
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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