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Sexual Precocity in a 16-Month-Old
, ^+ A* j8 A' zBoy Induced by Indirect Topical8 W5 j) i- {, Y/ s& J
Exposure to Testosterone% v; B' d% [' B5 T& T1 D. A0 w. B
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
" O* n( Q- b2 k* Z3 f" f( Z' nand Kenneth R. Rettig, MD1
# l6 X$ A& I) D3 G1 pClinical Pediatrics' r, x. [# S  v) e0 p  n0 `
Volume 46 Number 6( i) V% L& W5 r; M' J  \
July 2007 540-5432 M5 |8 p* k5 |  u6 K4 ]
© 2007 Sage Publications* v- E" P2 M% k+ a
10.1177/0009922806296651
# q/ G0 ]% O  j1 t5 a/ Bhttp://clp.sagepub.com5 h1 `- q7 |3 M7 |! T5 u
hosted at
" Z. c6 E$ {+ U" C/ J! B! a; g4 @3 Chttp://online.sagepub.com
7 {4 k, Q" s* W& N& {5 v$ yPrecocious puberty in boys, central or peripheral,9 B) c/ r" e1 I3 Q
is a significant concern for physicians. Central
) w7 q4 Z6 Y% b* Z. k2 U# eprecocious puberty (CPP), which is mediated) s) x! v. \4 p# Y
through the hypothalamic pituitary gonadal axis, has
) c8 ~5 U+ R9 D0 da higher incidence of organic central nervous system
2 n* o# F. k+ R6 @6 Q3 elesions in boys.1,2 Virilization in boys, as manifested
5 U# E0 [* w$ m2 V* m& L, F0 y4 D& vby enlargement of the penis, development of pubic
( j+ ?; K, u" U1 g2 x; T  Z$ M+ [hair, and facial acne without enlargement of testi-6 g% r7 _) c" ]# o
cles, suggests peripheral or pseudopuberty.1-3 We
) |: x! f' Z9 z8 a0 Zreport a 16-month-old boy who presented with the
7 y$ o1 i; g  \: ienlargement of the phallus and pubic hair develop-2 b" H& ]4 c( U; W7 G; M4 h$ k
ment without testicular enlargement, which was due- u! O# Z" ?: r& N0 r9 X4 j8 s& h7 G
to the unintentional exposure to androgen gel used by
& x- V8 s! Z0 N! e" `/ _; b2 P1 Y1 U" Sthe father. The family initially concealed this infor-$ i3 B' y) l. N, @( `
mation, resulting in an extensive work-up for this
& U# l7 J8 @/ r. H0 Y& O: Hchild. Given the widespread and easy availability of5 I6 k# k' U% b# m6 q9 s& e) e% G
testosterone gel and cream, we believe this is proba-! w* _$ c! N& l( \
bly more common than the rare case report in the- @2 ~; v2 F$ Z$ q, L$ e
literature.4, x1 H8 A  f" D' m2 T
Patient Report0 n& @: `0 o2 K0 d1 G
A 16-month-old white child was referred to the
$ Y) L( i9 d3 C0 `; v6 @endocrine clinic by his pediatrician with the concern4 B2 \4 Q( L7 n  T( \3 L
of early sexual development. His mother noticed
; Q) ^. V' J$ e0 L% ^% Jlight colored pubic hair development when he was
: F/ e, z$ `) e1 S% `From the 1Division of Pediatric Endocrinology, 2University of9 ?4 m9 u' w* ?4 x  o
South Alabama Medical Center, Mobile, Alabama.
$ z4 i# h! T) p0 @/ E9 v+ x) Z( gAddress correspondence to: Samar K. Bhowmick, MD, FACE,
. j( E4 Y2 g4 T' x$ J# K3 rProfessor of Pediatrics, University of South Alabama, College of& L5 c8 P5 f- F; {% f1 V2 M
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;2 ~$ P4 o  n/ u7 z" w
e-mail: [email protected].
9 A' h  m" Z. `8 M: iabout 6 to 7 months old, which progressively became& l$ R4 t4 a. a% w" O
darker. She was also concerned about the enlarge-( b. S  \& z6 a, w
ment of his penis and frequent erections. The child
3 W8 e) j; \1 O# L4 B) y& G0 o- uwas the product of a full-term normal delivery, with, }9 i# R% d8 [) I& S2 W9 G: e8 @
a birth weight of 7 lb 14 oz, and birth length of
7 ~. D3 K1 U% T) s0 \7 b4 I: p* f20 inches. He was breast-fed throughout the first year4 n: X" d; m, X$ |* ?0 J( \
of life and was still receiving breast milk along with! W* U. V$ g2 @+ U  D+ L
solid food. He had no hospitalizations or surgery,& |& F. Z5 {/ h' z% }5 X
and his psychosocial and psychomotor development. d: \- B7 a- Y! w9 A" C
was age appropriate.
# ^$ M1 `" f8 Q0 M" x2 ]* FThe family history was remarkable for the father,
+ f( q  c2 e( q  Twho was diagnosed with hypothyroidism at age 16,
1 t6 S2 V8 m  t6 c( [$ twhich was treated with thyroxine. The father’s
$ F/ c/ u2 ?$ ^3 Q: y6 Nheight was 6 feet, and he went through a somewhat
4 M# d/ L7 R( h/ Eearly puberty and had stopped growing by age 14.
4 v% A  Q  C+ ZThe father denied taking any other medication. The. ~& r& `, |6 o: {  e, {
child’s mother was in good health. Her menarche. p( ~* z) N+ |6 J  L8 i* ^& t3 k
was at 11 years of age, and her height was at 5 feet
8 W9 z" I+ g* T! T! y$ W5 inches. There was no other family history of pre-; A- W2 o8 j. S1 r) x
cocious sexual development in the first-degree rela-
2 h! @4 `$ i2 B3 R9 b5 Ltives. There were no siblings.8 o% J# k' ~, F
Physical Examination; Y" n+ w6 H1 L. d
The physical examination revealed a very active,
8 h# }  q9 _: P- h& gplayful, and healthy boy. The vital signs documented7 ^* u2 S1 _5 f3 E9 w
a blood pressure of 85/50 mm Hg, his length was
- r0 g- M' b: O" d90 cm (>97th percentile), and his weight was 14.4 kg
% A* A: ?. k& C- S  W2 U: t% @(also >97th percentile). The observed yearly growth$ L. o6 [: w+ b
velocity was 30 cm (12 inches). The examination of; s( a" t3 c, l' X2 P
the neck revealed no thyroid enlargement., b+ i% e5 a4 U+ W, W
The genitourinary examination was remarkable for- O. `* ^8 z& `3 s- r7 _
enlargement of the penis, with a stretched length of
: I0 |* W$ ^# |8 cm and a width of 2 cm. The glans penis was very well7 f) F0 o! V% L2 u2 @! E7 O1 T( W
developed. The pubic hair was Tanner II, mostly around. I& l. P& o; R; \0 P& r& J& C( J2 k
540
" D( w% W9 ]* O7 @at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from" f$ l$ O3 z0 F6 ^
the base of the phallus and was dark and curled. The
( @# W# p, r$ D& J: H2 ttesticular volume was prepubertal at 2 mL each.% Q# W4 T. R' e, n8 F- k$ t
The skin was moist and smooth and somewhat
+ b% h) z$ Z: o7 k! q4 ooily. No axillary hair was noted. There were no* J; d# b( T7 o" p$ ]
abnormal skin pigmentations or café-au-lait spots.# E4 g5 }+ |- Z) _' I1 h
Neurologic evaluation showed deep tendon reflex 2+
2 t1 t* \0 m' rbilateral and symmetrical. There was no suggestion
! l; q1 F$ s3 J2 Qof papilledema.
1 l( A6 ]6 k: \! E0 i) _- c5 H1 ^Laboratory Evaluation
0 x7 p( C7 u) a  b! l& ~+ ?+ ^The bone age was consistent with 28 months by8 Q4 [1 r, R* o3 _# D+ V7 Z; n  F
using the standard of Greulich and Pyle at a chrono-/ g6 ?8 a5 d2 O0 ~
logic age of 16 months (advanced).5 Chromosomal5 O) w2 M, V; b: ?* X
karyotype was 46XY. The thyroid function test
4 C, [" F; J  ?$ C/ y6 x3 Zshowed a free T4 of 1.69 ng/dL, and thyroid stimu-5 l  s( H, x/ }" E7 v! m9 r2 B' t: V, |$ Y
lating hormone level was 1.3 µIU/mL (both normal).( \6 ~( z. m% ?$ ]4 n1 U
The concentrations of serum electrolytes, blood
. h2 g0 l+ B  r' _3 lurea nitrogen, creatinine, and calcium all were# y8 d& P3 P$ e* Y$ c
within normal range for his age. The concentration
) [6 k4 {/ m( s9 }of serum 17-hydroxyprogesterone was 16 ng/dL! e  _* C( n# O: ]) g
(normal, 3 to 90 ng/dL), androstenedione was 20
9 ?9 z; h- ~7 Kng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
/ o( E8 O/ a/ P8 `* O+ v/ j; Fterone was 38 ng/dL (normal, 50 to 760 ng/dL),
5 e9 s/ [! H* pdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
+ M* a1 f/ H3 I5 p) B49ng/dL), 11-desoxycortisol (specific compound S)7 K- t: H6 U- Q1 [5 o
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-) ?0 j0 K) r! ]6 v, f
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total4 t" f6 v" u) V* f2 @: }! d
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
2 Y$ C: S9 @, {and β-human chorionic gonadotropin was less than! h. U1 ^3 y- T- M1 f$ L/ v
5 mIU/mL (normal <5 mIU/mL). Serum follicular  G4 Q5 h) j$ y1 C7 i. O4 Q
stimulating hormone and leuteinizing hormone" ?/ C, G# e3 u) y9 U9 y
concentrations were less than 0.05 mIU/mL
  s, z) I9 K- z0 u9 a) v9 o/ e(prepubertal).0 s( d+ i0 e+ X0 D
The parents were notified about the laboratory2 I5 F+ K5 p2 n0 `! Y5 o
results and were informed that all of the tests were
. t2 J. G" D6 q8 d/ r, h' jnormal except the testosterone level was high. The) S# g) j- Y- h! Q+ N% J; l% T5 K
follow-up visit was arranged within a few weeks to9 b; l3 A2 }( x) `) H# j
obtain testicular and abdominal sonograms; how-& ~7 q/ _9 k9 m( }5 o. @
ever, the family did not return for 4 months.
1 P: H8 l6 j* n5 |) [Physical examination at this time revealed that the
- N3 W- M$ E7 G- cchild had grown 2.5 cm in 4 months and had gained4 h: O) p% ^% ?- X- H
2 kg of weight. Physical examination remained- E, n3 @' P3 L6 k: O% @+ l
unchanged. Surprisingly, the pubic hair almost com-
- ^/ N% \% Y0 L& q9 z1 q( w) rpletely disappeared except for a few vellous hairs at/ m0 ^9 k; P" U3 W
the base of the phallus. Testicular volume was still 2) N. M9 f0 n! L3 R# l* d
mL, and the size of the penis remained unchanged.
5 `) S' ?( \) s+ {- [The mother also said that the boy was no longer hav-6 K( z' z' }( ]7 h0 v( j
ing frequent erections.% s6 Y6 Z% R! y2 _& }; P8 E. {
Both parents were again questioned about use of
8 W+ ~& W( }4 z& {any ointment/creams that they may have applied to, H! k; v" E& z
the child’s skin. This time the father admitted the* J5 f4 t# Y8 @  ?9 T9 F
Topical Testosterone Exposure / Bhowmick et al 541
8 v3 b& l4 j: Duse of testosterone gel twice daily that he was apply-7 V' I5 v& ], }& {, l
ing over his own shoulders, chest, and back area for4 P, e5 K/ i6 r1 |
a year. The father also revealed he was embarrassed
+ x  H( V  {/ zto disclose that he was using a testosterone gel pre-
, t$ k0 A: G. ~! ~6 [& \( cscribed by his family physician for decreased libido% d. P* v" ]. S6 b, g
secondary to depression.
7 R5 g  b: x5 T, [4 n* kThe child slept in the same bed with parents." q9 L/ y8 i; X0 L$ d' ^
The father would hug the baby and hold him on his' J" }* M, M& X7 f, g7 Z
chest for a considerable period of time, causing sig-9 o( j7 B! b' p+ g# M
nificant bare skin contact between baby and father.
) G, @0 O6 L) ~* W3 V' U0 tThe father also admitted that after the phone call,
+ D; L. R) }7 B: Y" Q" L! \when he learned the testosterone level in the baby2 y) s2 H7 H8 ^( C7 u+ ?
was high, he then read the product information
8 Q- l- `# M2 L/ Npacket and concluded that it was most likely the rea-
6 m' C( p& F0 M9 r: J* J4 Fson for the child’s virilization. At that time, they( C( }  }3 }# n9 g2 G6 @, X+ n
decided to put the baby in a separate bed, and the
  K* ]5 L* w0 N& k3 rfather was not hugging him with bare skin and had
( g- N+ p- G- f- g7 Nbeen using protective clothing. A repeat testosterone+ y$ E# l. A3 h
test was ordered, but the family did not go to the
$ t- ?. \) K5 K. a( p5 H, O, Q( Vlaboratory to obtain the test.
0 g" h+ m% x; K9 e7 v) fDiscussion" R6 j& }0 L% \& F; l
Precocious puberty in boys is defined as secondary1 u- J# x- {4 L1 {8 e) N
sexual development before 9 years of age.1,45 z$ S9 g6 _# H0 e6 b
Precocious puberty is termed as central (true) when7 j# t0 W' o( s/ Z. ]
it is caused by the premature activation of hypo-# d" A1 W; @8 Z2 F2 p& O
thalamic pituitary gonadal axis. CPP is more com-& g7 p2 a! H: z
mon in girls than in boys.1,3 Most boys with CPP% O9 b! R  p/ J6 ~8 n6 s" C! @
may have a central nervous system lesion that is: r% h# ]- ^" N" D: g0 Y/ S4 y, c
responsible for the early activation of the hypothal-
3 a: w/ g+ y, n3 R5 q& Ramic pituitary gonadal axis.1-3 Thus, greater empha-
( q7 k) @% M  ksis has been given to neuroradiologic imaging in
" X8 w5 x1 [- mboys with precocious puberty. In addition to viril-
9 g2 e9 ]$ t' V" ]9 p, Bization, the clinical hallmark of CPP is the symmet-
4 |4 k$ w9 p' U* ]- }6 U+ B( \7 Trical testicular growth secondary to stimulation by5 a" @6 k6 v) X2 I
gonadotropins.1,3/ z! n0 \  V! k% F+ c6 Q
Gonadotropin-independent peripheral preco-( K  B! ?+ _) u" o  b
cious puberty in boys also results from inappropriate
5 r' A" U5 m/ ~4 M2 r' Nandrogenic stimulation from either endogenous or' J* u! Q' R' `( S
exogenous sources, nonpituitary gonadotropin stim-' D0 A/ t1 F: r) ^3 M; y
ulation, and rare activating mutations.3 Virilizing
5 R6 t$ b& [9 [$ S6 G& ycongenital adrenal hyperplasia producing excessive8 h# i8 ^/ J2 ^
adrenal androgens is a common cause of precocious
. N* h. m5 j' V7 V6 kpuberty in boys.3,4% T- s6 E5 U% o' B7 L: H5 E
The most common form of congenital adrenal
" A- g- _7 T) C6 c& n" dhyperplasia is the 21-hydroxylase enzyme deficiency.
' E: [' z& F) X7 ?7 g1 ~1 HThe 11-β hydroxylase deficiency may also result in0 |& B; e/ @- i8 e6 F. y
excessive adrenal androgen production, and rarely,$ r* [3 g: R& ^
an adrenal tumor may also cause adrenal androgen  d3 q, L$ O4 O2 L8 U
excess.1,3
% e  r* F& a' N7 Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 M" K0 l0 u# N' z7 }7 _6 K
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007, H9 T- o# W  T. j5 |
A unique entity of male-limited gonadotropin-& v0 Q5 G$ i: C) F4 H- [# K
independent precocious puberty, which is also known9 k! u4 _6 U6 z* }/ `3 R- H
as testotoxicosis, may cause precocious puberty at a
6 q6 X" P9 Z' W( h% d! d4 L* Vvery young age. The physical findings in these boys# h" A7 v% W0 p) c: A
with this disorder are full pubertal development,
+ H4 J, ^/ ~# R& D/ \. q1 oincluding bilateral testicular growth, similar to boys
" y7 M4 g7 M" U% I3 f1 _with CPP. The gonadotropin levels in this disorder3 L/ }5 }: t3 v+ `3 D! f
are suppressed to prepubertal levels and do not show, q) L4 s4 M  A& Q" i; {
pubertal response of gonadotropin after gonadotropin-
/ x0 L  V. x( c/ sreleasing hormone stimulation. This is a sex-linked
9 z7 x, ~3 |  qautosomal dominant disorder that affects only9 @9 q, J: k6 O0 f3 p! m( V8 m
males; therefore, other male members of the family
# U+ t1 o# \( \3 m! D  U; b* Jmay have similar precocious puberty.3- j) s9 v1 B$ y4 P' O0 ], a: o
In our patient, physical examination was incon-$ P9 x7 @  g4 a% b
sistent with true precocious puberty since his testi-1 B" d& I" I6 z8 c* O$ ^, d
cles were prepubertal in size. However, testotoxicosis/ m2 A4 [5 X: G! w$ r. o. Z# U: v
was in the differential diagnosis because his father
9 ?* f) v; a( d& ]# B; tstarted puberty somewhat early, and occasionally,
$ N5 Y0 E5 U% p" E6 K% ~testicular enlargement is not that evident in the
$ E% V! U' Z4 ~. k+ e8 H, Vbeginning of this process.1 In the absence of a neg-' D3 E7 p! \2 B2 _, h
ative initial history of androgen exposure, our
, \3 [. H% K- O" N$ o7 c, e3 o/ kbiggest concern was virilizing adrenal hyperplasia,! x, u, `& p0 ?& b3 I/ I; m" D
either 21-hydroxylase deficiency or 11-β hydroxylase
; Y6 q8 J' Y- J7 {0 S  \5 Cdeficiency. Those diagnoses were excluded by find-
- [( C0 b# F3 v  i+ \& ging the normal level of adrenal steroids.
$ s5 v" k4 d" G% R! X1 C: YThe diagnosis of exogenous androgens was strongly0 A& r; s: s9 z" V, t5 ~7 ?
suspected in a follow-up visit after 4 months because
$ i2 F; V2 q. @$ Y, u2 F1 Tthe physical examination revealed the complete disap-+ C  m! S9 F- S! J& ^
pearance of pubic hair, normal growth velocity, and; a$ N( L2 u( |% x' d& P% a* a7 ?
decreased erections. The father admitted using a testos-
( q, ~! \  a4 {$ S. @9 U7 o( l2 Vterone gel, which he concealed at first visit. He was
: a( E$ }) [# x+ i# A/ susing it rather frequently, twice a day. The Physicians’6 j4 O6 l3 a4 g# u! `- j3 c
Desk Reference, or package insert of this product, gel or
6 E6 ]+ s, N& a# w5 ~$ X4 ?& kcream, cautions about dermal testosterone transfer to8 Q- s7 q4 Y: j
unprotected females through direct skin exposure.- q/ s9 S7 P( X$ v) l" X) N
Serum testosterone level was found to be 2 times the
& @- R5 @. O' |; A2 g8 q) ebaseline value in those females who were exposed to
, T: d, [8 A3 N3 Ieven 15 minutes of direct skin contact with their male
' g$ y8 \( R% a) e" @partners.6 However, when a shirt covered the applica-
5 G, _6 w$ d  L' X8 S3 dtion site, this testosterone transfer was prevented.
6 r, e" W3 ^: Y9 dOur patient’s testosterone level was 60 ng/mL,- Z4 y6 `5 g; |! O4 `
which was clearly high. Some studies suggest that4 B$ P4 P1 ^- j* Z: Z" S
dermal conversion of testosterone to dihydrotestos-
% [- r, G4 s* f8 _3 {terone, which is a more potent metabolite, is more
4 b: R) ~. s6 Y1 T% factive in young children exposed to testosterone& O7 R& S" j3 }' e! ^: B6 P
exogenously7; however, we did not measure a dihy-
. L2 I; a8 y# ]5 L$ vdrotestosterone level in our patient. In addition to
$ q! f8 W) H) l/ r- p( H. k5 wvirilization, exposure to exogenous testosterone in: @) g* a5 f8 V3 S( s
children results in an increase in growth velocity and
7 x" \, O  @" q' a5 w* {advanced bone age, as seen in our patient.0 V! E9 i. U0 m' v  w6 o
The long-term effect of androgen exposure during
; G* |. t) L7 \  \! W$ E/ @early childhood on pubertal development and final4 K+ {! S2 r* k* |
adult height are not fully known and always remain7 R- b! e! `; a+ S9 R# U4 @' l! Z( T
a concern. Children treated with short-term testos-# l8 f' r: ]- w4 a# Q
terone injection or topical androgen may exhibit some
# R( F# I& ~" _& F9 H1 ~0 M( _acceleration of the skeletal maturation; however, after6 T( W+ A0 l. O; r: |
cessation of treatment, the rate of bone maturation0 y" k! t1 ^8 W& J' k6 t
decelerates and gradually returns to normal.8,9, f( x  R$ e7 g* G! C! f) Z' F
There are conflicting reports and controversy
! V' ]: a- N% w  l- Oover the effect of early androgen exposure on adult5 t) f) |3 o5 t: V  [: s
penile length.10,11 Some reports suggest subnormal" T: Q. K% N3 ^& v
adult penile length, apparently because of downreg-$ G  i0 b* S9 S# v. I# ?. U  s
ulation of androgen receptor number.10,12 However,0 ~" v% ?' r0 R$ [. M
Sutherland et al13 did not find a correlation between
7 Y6 w+ K* `% Q# y1 mchildhood testosterone exposure and reduced adult/ Y3 {. Y9 P1 T. Z
penile length in clinical studies.
* _* a! _8 m4 }2 i6 _: aNonetheless, we do not believe our patient is1 x# l; z6 U, C' Z/ k6 n: P
going to experience any of the untoward effects from; [7 V$ _+ g) x- X% Y9 Q
testosterone exposure as mentioned earlier because
! }6 c% U7 O, [4 ]2 ?the exposure was not for a prolonged period of time.1 H  X% `% K$ t7 c
Although the bone age was advanced at the time of
+ ~5 g9 O) ]7 `0 n0 kdiagnosis, the child had a normal growth velocity at) p) S, {/ r& U# d4 A1 ?
the follow-up visit. It is hoped that his final adult- i$ @7 t, f1 ]: r$ o2 c) I
height will not be affected.
( w& V( A6 w, _Although rarely reported, the widespread avail-" w: ~1 B' M6 c- ?% V6 c$ z! O
ability of androgen products in our society may- r' I- F' Z( @4 K, ]( p# v( K
indeed cause more virilization in male or female; b* |* @8 l3 j: F6 f9 f; X
children than one would realize. Exposure to andro-
" t! b/ F* j  q' k: J6 R6 y! G" E* igen products must be considered and specific ques-
( T2 t2 P) Y2 y+ E$ t. [4 _% ^tioning about the use of a testosterone product or7 m8 L# Q  y- w4 i: \5 }. m
gel should be asked of the family members during& w6 o" @" Q5 a" g8 m. \
the evaluation of any children who present with vir-
6 }! l% o6 v9 D( @. C% ?2 u& uilization or peripheral precocious puberty. The diag-9 w2 l$ k9 K- h  Z: K9 R
nosis can be established by just a few tests and by, A) r6 W8 h1 @7 i0 E
appropriate history. The inability to obtain such a
( e: X5 o4 O5 O! ]1 chistory, or failure to ask the specific questions, may
8 Y+ m  s: N3 D. |8 C) `- O# X6 Aresult in extensive, unnecessary, and expensive
. x7 O# V4 ?1 y. J9 G* Q* O6 ginvestigation. The primary care physician should be
( R1 Q; @2 v; g- y% z, haware of this fact, because most of these children* X; x+ q6 D5 K) Q# e" [! `
may initially present in their practice. The Physicians’$ Q1 K& [% B" w( C/ q+ W6 Z0 X
Desk Reference and package insert should also put a
( C- k. V; i9 ]( A5 Swarning about the virilizing effect on a male or
, b; Z* s: C* l& g+ `female child who might come in contact with some-
" |+ G# [! s" e/ L. [3 G8 E; H4 M: Eone using any of these products.6 }2 S% _  x9 O8 c6 r
References
' Z8 a+ A- B4 D7 `, {8 i1. Styne DM. The testes: disorder of sexual differentiation
' P; a# @: ^$ F% Zand puberty in the male. In: Sperling MA, ed. Pediatric* C# {& ]* T( [& ~2 `
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
" G0 ~* Y$ q, H# V2002: 565-628.
* s( C5 @* f2 ~% H1 h1 }2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
: c& h1 F9 L5 ]( Qpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
/ ]# |1 `! J) u1 dBoy Induced by Indirect Topical5 z9 g* g, E3 h+ y- U) O* H
Exposure to Testosterone
6 q( \' z# u7 y7 CSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2' t5 h; g; a1 w, W; C7 Q0 Q' r
and Kenneth R. Rettig, MD16 \6 o1 W6 z2 T8 ]) s! s" [
Clinical Pediatrics3 I( b! e4 A0 D' T- `& J
Volume 46 Number 61 }. N# j7 L: _# M# V
July 2007 540-543
$ W1 C3 w* a$ o5 M© 2007 Sage Publications
! `( S% V8 {* Z9 F" V10.1177/0009922806296651" K" S7 X3 `) L/ E
http://clp.sagepub.com- f. }2 J& c4 j  ~, C! W
hosted at
; J/ ?( Q. @( a: V+ d# u  Y/ T! shttp://online.sagepub.com
7 K9 f" a) e& [+ ~$ n; I7 _Precocious puberty in boys, central or peripheral,! d0 U" j2 Q( d! W  n' i
is a significant concern for physicians. Central0 [, k. t/ m8 u4 e+ ^
precocious puberty (CPP), which is mediated
4 [: x9 Q# O( F+ P8 Pthrough the hypothalamic pituitary gonadal axis, has
! o* m" {5 D3 Ha higher incidence of organic central nervous system
) e2 J. {0 H3 k3 Flesions in boys.1,2 Virilization in boys, as manifested  t8 \# _6 h8 p& R  d# D3 j" }
by enlargement of the penis, development of pubic6 y2 Z7 S4 B- D2 a3 W4 w
hair, and facial acne without enlargement of testi-& [9 ?7 B0 h1 P0 v7 m- R. s
cles, suggests peripheral or pseudopuberty.1-3 We
) n- n2 c; S/ r5 t9 ^report a 16-month-old boy who presented with the  H0 m, O( a! j
enlargement of the phallus and pubic hair develop-
8 m8 ]$ e0 w! f; J4 e9 a0 Mment without testicular enlargement, which was due; {, T  l* s& K- |& V# W
to the unintentional exposure to androgen gel used by
+ g, z, B% t% X! }the father. The family initially concealed this infor-0 O  m/ \( O7 s$ `  r' R
mation, resulting in an extensive work-up for this! q  S+ P! I* i+ p( i
child. Given the widespread and easy availability of
* y/ _4 x- Z* |' U1 Etestosterone gel and cream, we believe this is proba-
7 L  d/ Q0 K$ |) B% t' Vbly more common than the rare case report in the1 m* D- g* R4 v$ x3 [2 G. ^2 q
literature.4
* O- F7 v1 B( m4 h+ t. CPatient Report8 b8 P8 x8 q- ]% h! ^' E
A 16-month-old white child was referred to the& \; s- D! h: Q) \
endocrine clinic by his pediatrician with the concern
' u+ j6 Q8 s1 @' x, `' G9 ]7 ~0 Lof early sexual development. His mother noticed3 M+ W: }- r2 n( z" l
light colored pubic hair development when he was
2 B' ~% ]: N" A/ ]. T0 zFrom the 1Division of Pediatric Endocrinology, 2University of
$ v3 t- L, X/ o' ESouth Alabama Medical Center, Mobile, Alabama.
8 w" R2 [" Q4 p+ p  jAddress correspondence to: Samar K. Bhowmick, MD, FACE,
* Z7 r2 t- ~: g6 q/ W* V/ ]Professor of Pediatrics, University of South Alabama, College of
# ]! [! Y: E+ b0 o5 E# Z2 z. XMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
  c7 G" R& i: o' x- ]: ie-mail: [email protected]., b2 k0 A, B3 t/ i+ N+ P
about 6 to 7 months old, which progressively became
5 t/ ~5 \9 U9 o- [- O& Edarker. She was also concerned about the enlarge-& j0 l) I4 [& k% ?* F
ment of his penis and frequent erections. The child4 I" X$ O$ b$ G/ w  v
was the product of a full-term normal delivery, with% e2 _' P5 |+ _; \) w
a birth weight of 7 lb 14 oz, and birth length of% f6 P, R8 z3 x# X3 r
20 inches. He was breast-fed throughout the first year3 x; }* D  w: h$ Y1 i, v
of life and was still receiving breast milk along with
# z+ C! o: B* _# Xsolid food. He had no hospitalizations or surgery,
: O- T% ]! r) T" ~! dand his psychosocial and psychomotor development
1 y4 [+ J- K/ h# B4 W# p6 hwas age appropriate.( H' H; C5 X  M$ o: L  F/ L  D& w
The family history was remarkable for the father,
6 j: m$ M: B9 N0 j3 D* vwho was diagnosed with hypothyroidism at age 16,
; G  V$ C5 f. y9 W' J3 h6 d2 l1 Fwhich was treated with thyroxine. The father’s+ a# p( ^" y1 v+ o$ {$ W
height was 6 feet, and he went through a somewhat& |& P  G+ H3 w; V; n5 ^
early puberty and had stopped growing by age 14.2 z5 t+ P5 E, N8 i
The father denied taking any other medication. The
* N+ K# k- G1 m! O) z8 n7 cchild’s mother was in good health. Her menarche
4 T* |2 j4 l2 |  Lwas at 11 years of age, and her height was at 5 feet
9 q) V, e' D3 F0 ^) e5 inches. There was no other family history of pre-8 W; w8 p0 z* U. H* T) p& m
cocious sexual development in the first-degree rela-# H  K8 t5 P7 Y0 R! G+ z
tives. There were no siblings.
% E; l% O& b( D" B; SPhysical Examination
4 p- D5 B4 E6 m! B5 x, ?$ `The physical examination revealed a very active,2 E7 \8 _7 y: d/ U/ e
playful, and healthy boy. The vital signs documented
. h# u2 E# b( b2 a. H2 Aa blood pressure of 85/50 mm Hg, his length was0 }" E  g; I; U; T2 h% [4 c
90 cm (>97th percentile), and his weight was 14.4 kg
: Y# \3 X, ~' I4 P0 ?" U: X) Z(also >97th percentile). The observed yearly growth
! K! A, e$ I7 t2 {* @0 Lvelocity was 30 cm (12 inches). The examination of6 O4 Q0 R) U; K0 ^; ]# k
the neck revealed no thyroid enlargement.. w/ \# f* M; s! ^
The genitourinary examination was remarkable for2 Y8 H$ k3 |' s( B( J9 t" b
enlargement of the penis, with a stretched length of
# u* _# [4 k8 i% I3 M" L' A8 cm and a width of 2 cm. The glans penis was very well: n& s% y  D6 B6 L! @% k
developed. The pubic hair was Tanner II, mostly around
; `( }% a. q' M1 j1 z540
- i3 k5 K& P. N; W( D( O7 p7 Rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* S) s4 B- U" s7 ithe base of the phallus and was dark and curled. The. {4 V$ ^4 z. y( N9 y; z; Z
testicular volume was prepubertal at 2 mL each.1 Z, B5 i! u/ r$ u
The skin was moist and smooth and somewhat- z( r) L% T) e: U8 ?+ j# L  _
oily. No axillary hair was noted. There were no5 [. K, }6 h4 R9 p6 t
abnormal skin pigmentations or café-au-lait spots.5 i# e2 F9 h( a# d6 Z/ M
Neurologic evaluation showed deep tendon reflex 2+4 k  ?! R7 b: Z4 ~
bilateral and symmetrical. There was no suggestion+ Y# B% s' z$ T$ f
of papilledema./ R8 }( o; p/ U: x" G$ o- [
Laboratory Evaluation# G4 w0 O3 x; X
The bone age was consistent with 28 months by! M6 J/ r1 D& d) w! Z: F4 \; x
using the standard of Greulich and Pyle at a chrono-6 [7 I+ p' ]6 D# ?
logic age of 16 months (advanced).5 Chromosomal
2 J4 `2 H" J: h5 v) p# L- m8 Ukaryotype was 46XY. The thyroid function test' `: \  F# E0 ]  h5 G
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
) t- L5 `! U$ X$ s% G! b$ Vlating hormone level was 1.3 µIU/mL (both normal).
* y5 S" ?: A9 ^! [  b0 y3 ZThe concentrations of serum electrolytes, blood
% S) i$ I4 x; Iurea nitrogen, creatinine, and calcium all were
  x& m* Z! ^5 ^, l  j& Owithin normal range for his age. The concentration
" Y& q( L: |5 j, Dof serum 17-hydroxyprogesterone was 16 ng/dL
1 Q' `) w8 W7 m) H2 j(normal, 3 to 90 ng/dL), androstenedione was 20
$ M, Z1 \' M( K7 png/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
$ B9 f  s4 D; g7 @) ]2 _. F9 Cterone was 38 ng/dL (normal, 50 to 760 ng/dL),
; w; \+ I1 H* Idesoxycorticosterone was 4.3 ng/dL (normal, 7 to
+ P( \$ S* C3 h6 |. ~, g& B49ng/dL), 11-desoxycortisol (specific compound S)
+ {! k1 k' ~' xwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-. A. p7 U, {# u2 Z. L8 j
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
% N" W" V7 s* x9 Ytestosterone was 60 ng/dL (normal <3 to 10 ng/dL),/ e! B, F6 Y' u" s. S& h4 N; X& k
and β-human chorionic gonadotropin was less than2 T6 v( g3 P  K3 P# V- q' ?
5 mIU/mL (normal <5 mIU/mL). Serum follicular. W& d5 G" v" s  _. h$ J& }- ]
stimulating hormone and leuteinizing hormone, [+ e  F: G3 E; O  Z: g) a& u
concentrations were less than 0.05 mIU/mL
# n8 [2 h- T! A0 @# g(prepubertal).! i+ d8 h2 j" h9 Q, H9 a
The parents were notified about the laboratory4 r9 G+ x0 h+ k( D2 u
results and were informed that all of the tests were# p% j% J9 l# p# D" G. b1 c/ ^
normal except the testosterone level was high. The, H# l3 J9 s$ J$ U" k" ^
follow-up visit was arranged within a few weeks to
; ~+ I! M$ H' l: j0 S# |( `1 x: yobtain testicular and abdominal sonograms; how-8 u+ ]$ M8 z1 \; P+ W& e1 b
ever, the family did not return for 4 months.* R. }4 t- t: f( b0 L
Physical examination at this time revealed that the
# {3 Y9 j; x6 M# a7 x) V1 r& R" u8 Hchild had grown 2.5 cm in 4 months and had gained. B& t/ K& x& b9 o! v0 E0 B# s
2 kg of weight. Physical examination remained4 q2 n* h6 n: u+ A' g
unchanged. Surprisingly, the pubic hair almost com-
3 v6 S3 [' I$ ypletely disappeared except for a few vellous hairs at
7 W4 f0 [# M/ A& Gthe base of the phallus. Testicular volume was still 2
( g! s% @# }/ b+ U; }1 D' ^3 |mL, and the size of the penis remained unchanged.
7 {3 q1 Y5 w+ rThe mother also said that the boy was no longer hav-
( _$ _, n9 {; F# ?, f6 }$ B* Ping frequent erections.
7 f9 T5 A) Z) V5 b6 vBoth parents were again questioned about use of
9 l/ u% l; G' v# `/ e+ Xany ointment/creams that they may have applied to
! U7 d8 h5 [8 b4 h7 C8 a0 \* Pthe child’s skin. This time the father admitted the: M7 c+ ?) j7 \" E, ?% [% v
Topical Testosterone Exposure / Bhowmick et al 541
5 ^9 a; N/ W2 H( q6 ^* ouse of testosterone gel twice daily that he was apply-
) e4 V+ J  s. Z- y$ _* T. _4 ming over his own shoulders, chest, and back area for: u4 c; `% |# h: P0 s/ l
a year. The father also revealed he was embarrassed
- V7 k* l% o" q7 ]to disclose that he was using a testosterone gel pre-. l% I) S: W/ z# Q: I. }# A
scribed by his family physician for decreased libido* [- A! B* M/ p9 T! \8 [  Y
secondary to depression.
7 Y2 y, o1 e7 e2 M' `8 X" _4 \The child slept in the same bed with parents.
( P  j# q/ F# B; z3 Y' UThe father would hug the baby and hold him on his
: g5 J& |- j" t+ n8 y. j6 e& Lchest for a considerable period of time, causing sig-! H' d2 p3 c# q) f/ k8 H8 G
nificant bare skin contact between baby and father.
" L) m( ~3 N4 b+ ^3 G% p, pThe father also admitted that after the phone call," Z% O2 r4 l6 H2 \- V; t
when he learned the testosterone level in the baby
6 c' a* G9 e( f" ?6 ]& iwas high, he then read the product information1 E$ _6 X$ f/ z, U, u" G% s
packet and concluded that it was most likely the rea-
! i% C5 F% S7 B- ]: y$ O- Json for the child’s virilization. At that time, they
0 a' A. _9 g7 f' k8 t' O6 jdecided to put the baby in a separate bed, and the2 }* ]4 h! M" t4 C8 j, {1 c
father was not hugging him with bare skin and had: m9 u$ V% f" \, d& U: A
been using protective clothing. A repeat testosterone
: I% X) T/ F) ?+ |/ Etest was ordered, but the family did not go to the5 T, f, Q2 Z3 ?. v& J. J
laboratory to obtain the test.! u9 x1 |" R3 q( _
Discussion" U0 `) e0 [% I" M7 W0 Y$ o
Precocious puberty in boys is defined as secondary
( w  N$ t! u6 ~* O" Usexual development before 9 years of age.1,4
! Q2 [  t  n2 cPrecocious puberty is termed as central (true) when
4 k: k3 N0 L2 q3 yit is caused by the premature activation of hypo-
: O2 H+ a2 y5 c' P; k! C$ Vthalamic pituitary gonadal axis. CPP is more com-& d- f+ C. I8 |6 w' U6 C' c6 ]6 V2 m
mon in girls than in boys.1,3 Most boys with CPP
8 {! ]5 z; y) Q% zmay have a central nervous system lesion that is
% h- l1 Y( d$ R# |3 yresponsible for the early activation of the hypothal-+ c0 e) {2 v8 _* D, U6 ~( ~
amic pituitary gonadal axis.1-3 Thus, greater empha-/ }+ `- V* l, p+ Q( H$ ~# w
sis has been given to neuroradiologic imaging in" Y% V# ~' c6 N. C6 I9 a
boys with precocious puberty. In addition to viril-( o! g! e+ W8 T/ e4 }
ization, the clinical hallmark of CPP is the symmet-1 }0 i* y2 C3 I
rical testicular growth secondary to stimulation by% ]& k$ V6 w+ G" |' E3 E/ D" G
gonadotropins.1,3
' w7 N. z1 {; v4 t# b) [Gonadotropin-independent peripheral preco-$ r$ k3 l* r& L$ K
cious puberty in boys also results from inappropriate
* J" C5 W/ ?  n9 U# xandrogenic stimulation from either endogenous or$ b/ S" u- p8 e9 W9 D' ]
exogenous sources, nonpituitary gonadotropin stim-
+ x  j5 W3 p# i9 `, Vulation, and rare activating mutations.3 Virilizing/ G; F' J) o$ N  _
congenital adrenal hyperplasia producing excessive9 h1 y' b- E( Q* ?7 ~
adrenal androgens is a common cause of precocious+ D' N( R9 |# ^5 M
puberty in boys.3,41 T9 q. h2 V9 E$ J. O7 R3 {
The most common form of congenital adrenal% Z/ O% R& U: D: ]2 t, x- \3 {% A% |
hyperplasia is the 21-hydroxylase enzyme deficiency.' G. k4 T7 z2 r) S& V8 s7 r
The 11-β hydroxylase deficiency may also result in
- }6 H1 S9 t# _6 v8 Y. Texcessive adrenal androgen production, and rarely,
0 d  G% m, L: o' Nan adrenal tumor may also cause adrenal androgen
6 |0 P$ N0 ?3 yexcess.1,3
4 ]) ~9 ?+ c* R8 |at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
7 l2 ~( {& c& E# R# ?542 Clinical Pediatrics / Vol. 46, No. 6, July 20076 P7 e0 q' ^: G5 R) X! l- S
A unique entity of male-limited gonadotropin-4 D* b+ ]1 Q( U
independent precocious puberty, which is also known5 k$ y& }+ y4 i, g) b
as testotoxicosis, may cause precocious puberty at a
! M7 m2 Q- G% B" Zvery young age. The physical findings in these boys7 L* C; F* @9 [* [3 Q1 H
with this disorder are full pubertal development,
. [8 b8 y) M6 Eincluding bilateral testicular growth, similar to boys# n! @$ g, B: [$ l* ~
with CPP. The gonadotropin levels in this disorder9 l; t2 g! h8 k) j% K+ [% B
are suppressed to prepubertal levels and do not show
4 L3 q8 k. A1 W  E) a3 f* mpubertal response of gonadotropin after gonadotropin-% T: X$ h0 }3 K9 B  u
releasing hormone stimulation. This is a sex-linked% \- w* ^- w/ C* _$ n% m& ^5 H
autosomal dominant disorder that affects only
5 t4 @$ D0 J" {& @+ `males; therefore, other male members of the family+ _' a  V4 o( R$ R: {
may have similar precocious puberty.3
: C3 M1 ^3 @5 D: t9 yIn our patient, physical examination was incon-: i; E0 {! T$ z# c* P1 Q
sistent with true precocious puberty since his testi-' F& S2 Q. N  c8 X1 _
cles were prepubertal in size. However, testotoxicosis
$ r4 [& f, H7 P; m, Nwas in the differential diagnosis because his father& v: d# Q/ m2 D! E3 d# A& r" Z3 _
started puberty somewhat early, and occasionally,
2 s! f( q7 ]" ?, J1 V% \- ~; P8 C0 Xtesticular enlargement is not that evident in the* k/ n) M5 @4 p) k5 q# N
beginning of this process.1 In the absence of a neg-
/ M/ t) _4 I2 `, H7 F' I- D! a8 Q& Oative initial history of androgen exposure, our# E# t& V2 c- ~# y
biggest concern was virilizing adrenal hyperplasia,
4 ?( _9 B5 t& B$ J0 _% seither 21-hydroxylase deficiency or 11-β hydroxylase
6 W4 ?1 l: S/ |  o7 B. D+ qdeficiency. Those diagnoses were excluded by find-: j: ^, a# M2 Y) M0 E
ing the normal level of adrenal steroids.
9 k+ y& Y/ A) T$ I) a( Z+ ]8 E1 TThe diagnosis of exogenous androgens was strongly
( y+ r% b+ A4 N- r# }/ Nsuspected in a follow-up visit after 4 months because
% D2 N0 l  }6 N) E& \3 N8 B9 Q7 nthe physical examination revealed the complete disap-
: R1 w" B) ?: c7 O$ i' Apearance of pubic hair, normal growth velocity, and) a( I  F( A: l, O3 |, j
decreased erections. The father admitted using a testos-* E( @4 z1 p7 L8 L* m; w0 b
terone gel, which he concealed at first visit. He was
) M6 b: O  s' M6 ], l; v! w2 ousing it rather frequently, twice a day. The Physicians’
+ P/ k; |8 P1 R( DDesk Reference, or package insert of this product, gel or
' {$ u: f! g/ B; `4 vcream, cautions about dermal testosterone transfer to
' o3 a, K6 E' H' c! F8 z% E& Vunprotected females through direct skin exposure.4 K3 Z1 c. N) p" ?# ~3 B: Z6 Z1 M
Serum testosterone level was found to be 2 times the
( V4 O: Z% I3 F$ g  v8 dbaseline value in those females who were exposed to
) _* w% Y8 H6 i5 }( meven 15 minutes of direct skin contact with their male3 V8 s2 O' b* W8 r- t
partners.6 However, when a shirt covered the applica-
. e9 l! }" d/ p$ z6 P6 D& S9 Ption site, this testosterone transfer was prevented.4 u4 @5 f3 N( Q; a! _. W7 v
Our patient’s testosterone level was 60 ng/mL,0 t+ j* S4 x5 i  e$ M$ K
which was clearly high. Some studies suggest that4 j6 R+ U7 b! T1 L9 A4 h, F
dermal conversion of testosterone to dihydrotestos-
3 ~, {4 u) z( s2 Oterone, which is a more potent metabolite, is more& N9 u! W  Z1 V; E! [; f) c. g; P
active in young children exposed to testosterone6 R. d  ], @& g# J6 L. W
exogenously7; however, we did not measure a dihy-
$ K" Q2 N- L( rdrotestosterone level in our patient. In addition to
" [$ X/ {) \* T/ [  W0 rvirilization, exposure to exogenous testosterone in
, F$ ^+ J" S$ u4 E3 Tchildren results in an increase in growth velocity and
: n! ]$ Z) Z! Cadvanced bone age, as seen in our patient." T6 t( J+ h' X; T! }( @
The long-term effect of androgen exposure during+ ]4 D# P7 ^$ g4 q$ F
early childhood on pubertal development and final% Y% y" Z7 \8 T0 d7 l* b
adult height are not fully known and always remain
9 _' q* {' a4 o1 za concern. Children treated with short-term testos-
8 n3 h" O0 ?! Kterone injection or topical androgen may exhibit some$ `; y! n+ s8 k$ {5 W; f, u9 d- a
acceleration of the skeletal maturation; however, after. f* X2 Y4 Z* B8 q6 Y
cessation of treatment, the rate of bone maturation
+ [" N3 _  m. E3 b! \: hdecelerates and gradually returns to normal.8,9
9 b+ O. k0 v6 q2 x, s8 XThere are conflicting reports and controversy) O3 S& E8 l) J  ?/ ~0 R6 V0 P2 C5 B: X$ p
over the effect of early androgen exposure on adult; |) c  h1 X7 j6 r0 }. r
penile length.10,11 Some reports suggest subnormal
6 t  U5 w( Z! H4 T5 {. E- Xadult penile length, apparently because of downreg-7 p3 c" n6 D7 r6 y
ulation of androgen receptor number.10,12 However,9 P7 A" B! _% N
Sutherland et al13 did not find a correlation between
* z9 Q4 b" T  G: T% Cchildhood testosterone exposure and reduced adult
7 L' i4 t4 B( N  d) Apenile length in clinical studies.
" R/ N& g7 B  v. T. }% oNonetheless, we do not believe our patient is7 H' a2 ~) `* I" ]5 T1 ?4 R
going to experience any of the untoward effects from2 a! Q2 U3 l* |; U
testosterone exposure as mentioned earlier because* H' L9 J! f3 t$ Q5 V
the exposure was not for a prolonged period of time.
  n; i- |( d) k+ z& v6 v6 Z  G: ~Although the bone age was advanced at the time of
8 g% r% I1 g2 [( S' y8 i9 Xdiagnosis, the child had a normal growth velocity at
$ i4 F8 y& V6 Z% S$ J. othe follow-up visit. It is hoped that his final adult
2 {* B% ~: r6 ]8 @) z4 jheight will not be affected.  J% Y5 P6 b$ j  V% ^
Although rarely reported, the widespread avail-% Z5 j- H0 w; B- m+ W: k6 \' Z
ability of androgen products in our society may
2 _! T4 B2 A/ c, F2 tindeed cause more virilization in male or female0 h; y. Z7 H( }: {
children than one would realize. Exposure to andro-8 U0 t. v" _9 j# B4 ~* h
gen products must be considered and specific ques-' V! K$ y2 J! ]3 X# g  L4 Q9 ]/ A
tioning about the use of a testosterone product or! t: V, [4 X4 m$ G2 w7 o
gel should be asked of the family members during
2 Y; P: L2 J/ h6 [1 ythe evaluation of any children who present with vir-
# H0 k& F$ e1 i' T" B3 ~ilization or peripheral precocious puberty. The diag-
7 Q+ L4 I8 v2 e+ anosis can be established by just a few tests and by
1 G1 u% e8 K. C% y& Pappropriate history. The inability to obtain such a
! a6 c0 x# ]- J( V; ^& X/ chistory, or failure to ask the specific questions, may8 @7 i2 ]) F" c( Y9 w5 W1 c; U
result in extensive, unnecessary, and expensive
$ }2 }) J( B; n+ T! S% I9 j: Y. G' Yinvestigation. The primary care physician should be
( r5 Z) x8 A+ Qaware of this fact, because most of these children
- a' k8 V$ b$ u3 V9 ?% Y" g8 Pmay initially present in their practice. The Physicians’
8 x" y2 ^& ~8 UDesk Reference and package insert should also put a
* H, g( f! Z! V9 N  s, }3 F1 Awarning about the virilizing effect on a male or
  A6 o/ h6 {, U5 z6 efemale child who might come in contact with some-2 D: K2 e" m) n6 G7 Z
one using any of these products.3 D' I: [: ]: L' C
References5 F' o1 Z* Q7 E  Z4 Z, N. B
1. Styne DM. The testes: disorder of sexual differentiation
6 s; Z8 o3 Q' u6 D$ b. f1 Wand puberty in the male. In: Sperling MA, ed. Pediatric+ S0 E( J: m$ @. z6 }; ]$ I. [
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;" X$ V3 k: _4 M) h9 Q/ e# V
2002: 565-628.
2 H& O/ q( f) f- _0 R( g2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious$ t: G3 E0 X4 l& v0 Y$ z) [
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

( O5 ?$ g. n* G1 D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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