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Sexual Precocity in a 16-Month-Old
7 v1 T8 |1 k, c( a  `Boy Induced by Indirect Topical8 K0 i' ^: q7 W4 A( J  p& H2 i% W
Exposure to Testosterone
& S8 {+ g  w" G  s+ j. t4 hSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
) R5 b& `& h& \/ H# O4 |$ nand Kenneth R. Rettig, MD1
& b( c7 [2 D( \! D+ D: x; x  DClinical Pediatrics
) \6 k/ ]" U! W, W5 c9 vVolume 46 Number 6
4 C  y4 T# K& n9 d0 I* lJuly 2007 540-5439 n: E! `' e+ I! }
© 2007 Sage Publications
1 O9 [, p% _$ n4 h; u10.1177/00099228062966513 C% Y' V5 H% c; K- ]5 Q- j
http://clp.sagepub.com
% U4 ~5 ^3 b0 c* g3 e, Nhosted at( t' a( m" x- O, l3 T
http://online.sagepub.com: [, \! ?1 N5 @
Precocious puberty in boys, central or peripheral,! p; @4 A6 [+ P$ E/ [6 `, j) Y6 r2 O
is a significant concern for physicians. Central2 i6 `( P' ?/ i0 n6 O' g' O
precocious puberty (CPP), which is mediated
( K4 o9 c$ X2 X) F- D' ^through the hypothalamic pituitary gonadal axis, has4 A7 n9 E+ K7 U0 v; |! l1 g5 O
a higher incidence of organic central nervous system. P/ E6 `, d2 c: S& w6 p- e/ @
lesions in boys.1,2 Virilization in boys, as manifested8 Y( d# r9 y& Z
by enlargement of the penis, development of pubic
- k$ C/ |7 o/ b- w. [" ^- |  khair, and facial acne without enlargement of testi-7 E' ~. ^) {+ ^* t
cles, suggests peripheral or pseudopuberty.1-3 We9 R5 V# O9 N# m7 H+ l4 v# l3 W
report a 16-month-old boy who presented with the
$ Z! I+ v' P; c; l  `  H# J5 `enlargement of the phallus and pubic hair develop-, H6 F; n2 u( h4 J6 H3 J3 k
ment without testicular enlargement, which was due" n; m" \) D% n& h% Z! h2 ^. c
to the unintentional exposure to androgen gel used by
9 G# n/ d6 o* q; V  d: [the father. The family initially concealed this infor-& V8 N) t  V; |. t
mation, resulting in an extensive work-up for this4 M& I, C/ n7 F# _* S
child. Given the widespread and easy availability of. ^; K1 D- Y0 _  M1 B8 _% l
testosterone gel and cream, we believe this is proba-
2 ~, {8 @2 C$ e& \  A# m0 @bly more common than the rare case report in the! b1 d4 q. r2 d( Z: L% N9 v' o
literature.4
$ `0 \; d4 ^  v4 vPatient Report
. [+ Z# Q6 O, c3 ]! qA 16-month-old white child was referred to the
8 @* d4 R, u) j: v+ i/ Y. _8 hendocrine clinic by his pediatrician with the concern
6 Y+ G4 U7 M7 }( jof early sexual development. His mother noticed
2 l$ B$ t: ^, U! w5 c) \1 N( W: H- [* llight colored pubic hair development when he was
& @1 [& r0 L" ?! {/ w/ D8 l+ c3 k, PFrom the 1Division of Pediatric Endocrinology, 2University of: O5 ^9 p1 K! Y
South Alabama Medical Center, Mobile, Alabama.6 S1 _3 N+ }. w! D
Address correspondence to: Samar K. Bhowmick, MD, FACE,7 [7 v+ T& k, J) U, h: ~
Professor of Pediatrics, University of South Alabama, College of
. m7 P& m9 r5 z7 k- L6 ^; ?Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;9 B5 n! s4 Z- q
e-mail: [email protected].8 R8 [# |3 T5 }# k. V
about 6 to 7 months old, which progressively became% G0 l- E# B9 v/ d4 Z
darker. She was also concerned about the enlarge-
6 }5 h4 P: H$ }ment of his penis and frequent erections. The child9 U3 z% m/ V$ @" `
was the product of a full-term normal delivery, with
5 F  S# P( q) D& h4 b) }  ^a birth weight of 7 lb 14 oz, and birth length of5 }0 {& ?  R( ?6 l/ [, l) G
20 inches. He was breast-fed throughout the first year0 z3 A  [9 Z% d, f
of life and was still receiving breast milk along with
7 k: }( m9 Z  z. M& B7 ]4 Ksolid food. He had no hospitalizations or surgery,* \) v! o- x2 H5 i+ W2 |
and his psychosocial and psychomotor development
4 F1 T6 I. M  _: d2 }was age appropriate.
  X3 ]8 b4 H2 MThe family history was remarkable for the father,
$ F0 \% ~; f9 h' g6 D9 Ewho was diagnosed with hypothyroidism at age 16,
- ~8 E  I$ S& y( ]which was treated with thyroxine. The father’s0 j. ^; u$ _6 o4 X* w0 r) {0 ^! L
height was 6 feet, and he went through a somewhat8 `! b+ x5 }5 U- E' L
early puberty and had stopped growing by age 14.  y$ j% k' e0 m; `1 j
The father denied taking any other medication. The7 g8 ~, }. M" b8 @
child’s mother was in good health. Her menarche& g# y/ B2 d/ ?; M8 z+ U
was at 11 years of age, and her height was at 5 feet6 U, m- M' E& g- p- _( k9 w5 n/ C5 v
5 inches. There was no other family history of pre-$ z8 L, ^! g, Y
cocious sexual development in the first-degree rela-( @1 |* r9 Q2 u( U# ]- D8 P
tives. There were no siblings.) F; y6 @9 q  c+ a0 J1 j2 p# i- }
Physical Examination
( N2 m. o, [8 PThe physical examination revealed a very active,. n. P# P- I) N/ g
playful, and healthy boy. The vital signs documented
/ l( l+ E. Y7 S8 _& Ma blood pressure of 85/50 mm Hg, his length was
2 D( |+ b' @4 p90 cm (>97th percentile), and his weight was 14.4 kg! `6 Y/ E" I. D+ i( z% n4 u4 x
(also >97th percentile). The observed yearly growth
) g3 K6 K2 k% s& A1 j: \2 I2 k0 Fvelocity was 30 cm (12 inches). The examination of
) x2 t2 m# y5 ~  W# T2 j) T% Fthe neck revealed no thyroid enlargement.! e* {$ j0 D1 P% X( d: _2 b* ^6 Q
The genitourinary examination was remarkable for* N0 Z) U) l. d
enlargement of the penis, with a stretched length of
# e% z% C) |9 T; v  U4 ?8 cm and a width of 2 cm. The glans penis was very well4 H1 j. f; A: w, E( P8 X
developed. The pubic hair was Tanner II, mostly around
7 U3 K. s5 x6 C540
& n7 y3 Q6 W! s' P# H. H3 J$ |at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 i  |2 e. Y7 Y2 @* w7 t. Ethe base of the phallus and was dark and curled. The
% R/ c! ^5 q+ A& t$ ^6 q8 Wtesticular volume was prepubertal at 2 mL each.2 a4 p/ b& x) K1 R
The skin was moist and smooth and somewhat
5 H5 _! k4 U- t0 xoily. No axillary hair was noted. There were no
4 O" |; j$ G& {, U% s# n/ |abnormal skin pigmentations or café-au-lait spots.
0 e& ^6 U  H. P$ FNeurologic evaluation showed deep tendon reflex 2+
3 s& l" T: h# k) T9 w5 M: Gbilateral and symmetrical. There was no suggestion
5 L& G6 l" K. C* f& @2 A- T3 `of papilledema.
5 s( }( [- f+ J- t  hLaboratory Evaluation
; c: k3 ^# o: y  O: {The bone age was consistent with 28 months by
4 q" c# B: a9 g+ f, @; z0 E8 Musing the standard of Greulich and Pyle at a chrono-
+ B1 n$ Z" t& @3 u9 J; ~! c7 n! xlogic age of 16 months (advanced).5 Chromosomal
6 }+ e9 [" K4 W3 U* @karyotype was 46XY. The thyroid function test
$ d7 B; G/ I. v* Y& z) |) l# qshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
1 _+ R) ~; e) Y/ g+ q" h6 q$ Nlating hormone level was 1.3 µIU/mL (both normal).
; \% z9 [- j. t- g/ H( ]" Y# L# ZThe concentrations of serum electrolytes, blood
5 M1 g4 @7 |( ?5 n1 Furea nitrogen, creatinine, and calcium all were7 c7 C1 M% [; Q+ `
within normal range for his age. The concentration) I/ o0 y1 Q& ~8 C( Y/ @' p1 C) H
of serum 17-hydroxyprogesterone was 16 ng/dL
; Z) l8 w6 j! v  E2 ~(normal, 3 to 90 ng/dL), androstenedione was 20: O9 n. t/ B, z& W
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
: ]) p# n9 S1 W7 oterone was 38 ng/dL (normal, 50 to 760 ng/dL),
. n$ q4 R1 ]0 G! f: Ldesoxycorticosterone was 4.3 ng/dL (normal, 7 to
0 ?6 q7 S6 L/ m; j0 F0 N3 P/ ?/ [49ng/dL), 11-desoxycortisol (specific compound S)1 j# B& w% Q9 \
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
) R6 [, y5 x- H- r& L, ^1 i/ L! Rtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total2 ^+ U& o) h( r! n0 p6 n$ b& \8 E
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),. \, K7 }# z+ a0 l& @
and β-human chorionic gonadotropin was less than
) O* ^0 k. m0 w: i: ^% D; b; ]5 mIU/mL (normal <5 mIU/mL). Serum follicular' C9 z/ S0 O3 Q" X
stimulating hormone and leuteinizing hormone% _  k7 B9 ]" H- e3 f
concentrations were less than 0.05 mIU/mL: ^6 G9 d: O! s* ~8 R
(prepubertal).. B3 A: O1 X) Z: ^
The parents were notified about the laboratory: A. R' _% l8 z
results and were informed that all of the tests were) `  d4 W2 X* ^% b5 q$ Q
normal except the testosterone level was high. The
0 u1 Y7 M: l$ U) X3 d4 W& @follow-up visit was arranged within a few weeks to
( [# U! D8 q6 ~" q3 @; q3 Kobtain testicular and abdominal sonograms; how-
1 H5 X. t6 M: A3 jever, the family did not return for 4 months.
# A+ t3 k# L. \$ _: X, yPhysical examination at this time revealed that the  G) ^  d8 E7 I) I" w2 t' w
child had grown 2.5 cm in 4 months and had gained
1 [% i( h+ P) o2 kg of weight. Physical examination remained
' e: }1 b0 p: F* S0 A  I' E- \# \) uunchanged. Surprisingly, the pubic hair almost com-
* d; P: T+ J1 D) |pletely disappeared except for a few vellous hairs at0 I7 U" i- z- E+ d4 E' S+ P( ^3 S
the base of the phallus. Testicular volume was still 2
% {  q6 f/ ^0 P: X3 \6 M) K& JmL, and the size of the penis remained unchanged.
3 M  V& X7 z1 o% G' [! m: b! X  P5 xThe mother also said that the boy was no longer hav-- K, C4 r" {% W3 f+ Q5 ~- b5 l4 d
ing frequent erections.: ^0 v8 l& n6 I
Both parents were again questioned about use of
/ ^6 J  G9 e5 e. X2 u# X" E8 oany ointment/creams that they may have applied to
8 g: ?4 E- j2 J3 zthe child’s skin. This time the father admitted the% o5 v& n7 [1 ?
Topical Testosterone Exposure / Bhowmick et al 541$ l6 {! V4 L+ V- U. D
use of testosterone gel twice daily that he was apply-+ ?: q1 X8 A. y" a- x/ ~* C
ing over his own shoulders, chest, and back area for( y* g' B# i  ~' `# ^0 L* J
a year. The father also revealed he was embarrassed5 o: J  n3 K8 ?9 `1 y2 i- `3 H5 b
to disclose that he was using a testosterone gel pre-2 s1 X& R7 k0 q" t) M/ M1 \
scribed by his family physician for decreased libido
3 j2 L% i" d6 ^  S" D# xsecondary to depression.
! N, G( W0 a( a5 ~! f" K# [2 z0 IThe child slept in the same bed with parents.
2 x0 j- J: N5 h# b( T/ GThe father would hug the baby and hold him on his- _% i3 Q( G" z$ ]
chest for a considerable period of time, causing sig-
  P: r7 M7 L* P2 _/ snificant bare skin contact between baby and father.. H  j4 S3 z6 g7 M
The father also admitted that after the phone call,
3 u2 v2 {# X4 ]& {when he learned the testosterone level in the baby
0 H# n+ n8 ~0 k! o9 }* M# J5 O( Xwas high, he then read the product information
/ I4 H+ S* [' r( f6 Ppacket and concluded that it was most likely the rea-
. p& F9 U! \" g9 V, B: a( Y- _son for the child’s virilization. At that time, they, h9 X$ ]* w) N: C* m) u( x+ v! J
decided to put the baby in a separate bed, and the3 x3 d* T) T$ D3 r
father was not hugging him with bare skin and had3 t4 ?- X/ B) ?7 z" U5 I
been using protective clothing. A repeat testosterone
2 N* N, R- O( J) i: Q, [; v( |test was ordered, but the family did not go to the. L6 ?9 A  j- l+ E0 E/ W, L
laboratory to obtain the test.
$ r' a4 f! _& Q+ d7 |8 F8 U" GDiscussion+ w7 V# D/ B2 O( |9 w: _/ x/ x
Precocious puberty in boys is defined as secondary
2 c! ~2 t( U4 k. x5 p" Zsexual development before 9 years of age.1,4
1 z. X6 g8 L% b! NPrecocious puberty is termed as central (true) when
4 S' u* b+ h0 f  c" Sit is caused by the premature activation of hypo-$ O' `) g5 j, h# n/ s0 Z
thalamic pituitary gonadal axis. CPP is more com-- _5 |5 R9 x5 B2 A$ d& g
mon in girls than in boys.1,3 Most boys with CPP
  B' r% z9 J& K+ M. |may have a central nervous system lesion that is4 v* z2 h2 S! X" a2 j
responsible for the early activation of the hypothal-, d  J( R* i7 z- V/ j! {. o1 h2 A7 ]
amic pituitary gonadal axis.1-3 Thus, greater empha-( f, C; A3 j4 k
sis has been given to neuroradiologic imaging in
  n6 t; a: N) a" v2 xboys with precocious puberty. In addition to viril-. O3 u/ v  N9 n3 |8 N, W. a& \  A
ization, the clinical hallmark of CPP is the symmet-, K2 z7 w1 T  R8 @. \; j
rical testicular growth secondary to stimulation by
+ O& M8 u5 c9 F& egonadotropins.1,3% X0 {* s" Y6 k0 c
Gonadotropin-independent peripheral preco-
" S: `$ l+ c1 F, ^cious puberty in boys also results from inappropriate
; o/ G% z) [! J6 D- i1 c' Eandrogenic stimulation from either endogenous or
1 e% \% l  Q% I: X/ v, yexogenous sources, nonpituitary gonadotropin stim-
/ _4 o$ M$ l" Nulation, and rare activating mutations.3 Virilizing
5 I4 |* A; ]5 x2 ^congenital adrenal hyperplasia producing excessive
- q6 X1 d& ~; i, Y/ Q9 a9 D0 Wadrenal androgens is a common cause of precocious+ x, Y- T9 N6 ]. H& |* k
puberty in boys.3,41 N& }- h' W1 [6 J, u' ~3 x. x
The most common form of congenital adrenal
- j  }5 D5 A1 q2 P" d- b: f) {hyperplasia is the 21-hydroxylase enzyme deficiency.
' z) @( i) x1 e: r2 n$ Q2 FThe 11-β hydroxylase deficiency may also result in
" g- E( y& g) qexcessive adrenal androgen production, and rarely,
: s; @% {  H  ]! t: l4 Jan adrenal tumor may also cause adrenal androgen
& ^9 M- q+ Q) D/ H; `- ]" sexcess.1,3
8 c2 u9 s7 b5 ?/ gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* j  T3 ~' Z6 K/ q6 [
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& [2 c. j% y; q. ]1 F2 DA unique entity of male-limited gonadotropin-
9 w7 w$ R7 r- @  `4 Rindependent precocious puberty, which is also known; Z9 y+ d% A4 A' R) D  M
as testotoxicosis, may cause precocious puberty at a
3 R! A# R+ r3 c" n8 Qvery young age. The physical findings in these boys) U* R+ r/ {/ J) |
with this disorder are full pubertal development,
: X5 o; @  y5 \9 i( a6 ~. fincluding bilateral testicular growth, similar to boys
0 q# a: p" B; W. k0 }with CPP. The gonadotropin levels in this disorder
( Y  L5 X4 x" P) x) R) xare suppressed to prepubertal levels and do not show2 t3 }' s# @0 C( k
pubertal response of gonadotropin after gonadotropin-6 a' p8 u. u0 S1 K
releasing hormone stimulation. This is a sex-linked+ d8 D/ {1 H1 z& X3 d( r
autosomal dominant disorder that affects only" _% R1 Y+ g0 x4 a) a
males; therefore, other male members of the family& v' o2 F5 E& s& J/ I/ ^8 m3 C
may have similar precocious puberty.3% C* W: j8 _) |) h) J
In our patient, physical examination was incon-
: a& u( L2 h" ]# Q" ~! Wsistent with true precocious puberty since his testi-
( f3 L# ]% L& e  Tcles were prepubertal in size. However, testotoxicosis1 Z& k$ j2 V1 `4 ^$ Z
was in the differential diagnosis because his father2 J4 v. g7 m% Q( E* a
started puberty somewhat early, and occasionally,) N! @0 [$ B( y0 V# ^6 d
testicular enlargement is not that evident in the. E- l! @) r( s& W0 f; d- Y  g3 i
beginning of this process.1 In the absence of a neg-6 j$ y4 J) X: L5 j1 ]2 \
ative initial history of androgen exposure, our
$ m$ z5 ?0 e7 o6 a7 C9 w' Y/ }9 cbiggest concern was virilizing adrenal hyperplasia,
# ]6 i: ]9 r4 N" p$ p: y# i( Meither 21-hydroxylase deficiency or 11-β hydroxylase
$ G4 R7 M7 i1 k0 D+ f3 Pdeficiency. Those diagnoses were excluded by find-
6 P% C- F: S, Sing the normal level of adrenal steroids.
' d6 c7 A1 z6 @) M8 ]+ P) A+ QThe diagnosis of exogenous androgens was strongly4 m- t4 ~9 p+ V9 C
suspected in a follow-up visit after 4 months because/ T( j( q6 X' J1 @" q8 ?8 s
the physical examination revealed the complete disap-
" ^! b/ o! x1 i0 ]8 Q. zpearance of pubic hair, normal growth velocity, and
8 N% f3 I2 Z9 h" N# Pdecreased erections. The father admitted using a testos-, `% Z1 }9 ~& t) ?7 B9 d
terone gel, which he concealed at first visit. He was
- c% W2 F# g# K- b& P+ fusing it rather frequently, twice a day. The Physicians’' w5 R9 n* X1 A6 ^' U# p) n1 c
Desk Reference, or package insert of this product, gel or
4 d6 s2 C6 Q7 ]' k/ [7 Fcream, cautions about dermal testosterone transfer to" C! u1 j$ _1 ?
unprotected females through direct skin exposure.
" T7 S  K' N/ o/ |0 l$ B! E) dSerum testosterone level was found to be 2 times the, ]' H. g, W! m$ M" g! a; B% I# Z
baseline value in those females who were exposed to
& R- q5 _( h: k$ @6 N! Reven 15 minutes of direct skin contact with their male; ]. B) n( w( ~
partners.6 However, when a shirt covered the applica-
3 d7 f' }4 ~7 L0 I; Etion site, this testosterone transfer was prevented.: T$ ~4 I0 @( E5 G' L& y1 p
Our patient’s testosterone level was 60 ng/mL,: K; |8 u/ L4 G$ A& v
which was clearly high. Some studies suggest that$ f8 x& w: Z- X* G# J% u
dermal conversion of testosterone to dihydrotestos-- d* L# W4 W0 {% T# h+ L  g# X
terone, which is a more potent metabolite, is more4 ?8 [/ B! d- B. r; q  `( m- ]4 f
active in young children exposed to testosterone4 c/ [( v1 D, \3 r
exogenously7; however, we did not measure a dihy-
0 R* E$ A2 w1 k4 [5 C" Mdrotestosterone level in our patient. In addition to
5 t7 q: f2 B: h2 d4 Z6 B9 S1 _virilization, exposure to exogenous testosterone in/ P! ]  N) D! f, Z
children results in an increase in growth velocity and7 I/ f6 ?) N0 N$ j5 m# @  I0 |9 d
advanced bone age, as seen in our patient.
8 c# D% f+ @/ {* IThe long-term effect of androgen exposure during
  F  E% e4 h8 M$ Q  x- y: [early childhood on pubertal development and final- m% l5 K$ ~) \/ ^4 e$ y, e$ _
adult height are not fully known and always remain/ n3 E( C7 ^. f4 _: W. i/ X
a concern. Children treated with short-term testos-+ p/ Q- n+ |! X
terone injection or topical androgen may exhibit some
$ q3 ]2 X5 C* }, w6 d+ bacceleration of the skeletal maturation; however, after+ \; k; @4 L% F" n3 [6 g% E! J" @
cessation of treatment, the rate of bone maturation0 C4 |9 w. Q+ F* h# \+ r
decelerates and gradually returns to normal.8,9
5 u' k0 P4 A5 x' _There are conflicting reports and controversy% G* Y9 ~8 y5 o* m& Y) c
over the effect of early androgen exposure on adult
! F# H. R, _; p0 v: Tpenile length.10,11 Some reports suggest subnormal+ A* k1 U0 d: M$ u
adult penile length, apparently because of downreg-
" x5 w" h8 M6 W6 Z, lulation of androgen receptor number.10,12 However,4 m, V% n9 [3 \! g6 ?" z" p
Sutherland et al13 did not find a correlation between5 ~' n! P' X& Y5 V  G. W3 M" `
childhood testosterone exposure and reduced adult) {# b4 r8 x, Y9 f
penile length in clinical studies.# O% Z0 X* s4 f/ q1 K
Nonetheless, we do not believe our patient is
. E, G. ?# P: p4 l& s4 }1 t9 l5 Wgoing to experience any of the untoward effects from
  H6 ?, D! D# u# wtestosterone exposure as mentioned earlier because
  L# a+ H9 O1 u, L8 B+ K$ f$ \9 Zthe exposure was not for a prolonged period of time.
  ~( _5 x; M8 c6 sAlthough the bone age was advanced at the time of
8 i& y' A$ }$ k! {! Tdiagnosis, the child had a normal growth velocity at. }( H! J1 ^0 d0 c  ?
the follow-up visit. It is hoped that his final adult
  C) a4 s, L, v" Y! B2 gheight will not be affected.+ D7 Z" W# x+ E( ]
Although rarely reported, the widespread avail-7 o  z. P0 i. E1 Y9 O/ I
ability of androgen products in our society may$ q# ?  b+ C9 l$ {
indeed cause more virilization in male or female
! A& I4 Z& a: Y" Mchildren than one would realize. Exposure to andro-4 S7 w% ~5 M% L' |% I; n
gen products must be considered and specific ques-
: k, i" X) D  ~tioning about the use of a testosterone product or
; `9 p( x) G: o; a" l) \- Ggel should be asked of the family members during
8 r: y- U0 T: W* |* jthe evaluation of any children who present with vir-' z! J9 ?8 m0 ]: H, ~& C
ilization or peripheral precocious puberty. The diag-# N. E0 K3 e% q+ n3 D! i+ V
nosis can be established by just a few tests and by! |% C: {7 r% {/ x3 M# `
appropriate history. The inability to obtain such a
& q2 g5 p3 ^% a  w* h# Lhistory, or failure to ask the specific questions, may
& u1 ~6 n$ _7 ?; Q/ P) r' Bresult in extensive, unnecessary, and expensive
% W* }) u3 a+ S: zinvestigation. The primary care physician should be
, I8 e2 d# o( _$ y( Z7 _- oaware of this fact, because most of these children1 V0 }7 ?* L2 h* m' I! f
may initially present in their practice. The Physicians’
) P9 g9 G7 E# cDesk Reference and package insert should also put a( }  T& u/ C& A; Z' C, b
warning about the virilizing effect on a male or6 g- o# m9 a- o& n: u, f; A: a- N
female child who might come in contact with some-, v& a6 Z9 ^5 k# s3 t
one using any of these products.
5 [! u: [% s1 I/ n, T; XReferences
1 E/ F5 u- \' p- b/ b1. Styne DM. The testes: disorder of sexual differentiation: E! S$ G6 g5 o: d# u& g6 o
and puberty in the male. In: Sperling MA, ed. Pediatric8 N9 |1 D0 U7 P  U+ y
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;& X5 e* m$ i( t3 y$ {6 S
2002: 565-628.# n& M" f. v# a0 u
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious+ i5 H# ]) U7 o7 E- V! w3 ]
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old! X* Q! y- _% b# f
Boy Induced by Indirect Topical
0 N, p" Q- ^( Y0 H7 `; ?: `Exposure to Testosterone
# ~3 U' j9 D1 b$ R3 f" W. ~0 s% JSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
6 ^5 o* Y0 r: m9 t+ ~2 d8 u; Nand Kenneth R. Rettig, MD1
, w: |9 G: r7 V/ K( Q0 V& JClinical Pediatrics
! D' p! n+ Q. _9 \5 |. tVolume 46 Number 6
" F  v3 Z- C4 A( x2 MJuly 2007 540-543
9 d/ D6 Q, @# _/ y/ g! x2 D© 2007 Sage Publications
' w/ @4 @' f1 X" I- O10.1177/0009922806296651$ J7 [3 {8 J; _& U' m0 X; m" S2 U
http://clp.sagepub.com  a- Q% R( @5 B# c" ^
hosted at. e: i1 p2 B* n  W! R
http://online.sagepub.com) P. b) G7 {; v
Precocious puberty in boys, central or peripheral,
$ Q: K0 H8 t# Z* d. b. w+ c# F0 His a significant concern for physicians. Central7 o9 d- v+ t1 C# y# n
precocious puberty (CPP), which is mediated( f5 f* b/ f/ ]: u9 P: s
through the hypothalamic pituitary gonadal axis, has  e" v5 j# g2 v: S# I3 N
a higher incidence of organic central nervous system7 \+ a8 b/ O4 ^
lesions in boys.1,2 Virilization in boys, as manifested2 I8 N: }! x: R* X3 f7 j
by enlargement of the penis, development of pubic% v. U! o5 I) e9 g! u
hair, and facial acne without enlargement of testi-! Y5 K% [# q. P2 Q
cles, suggests peripheral or pseudopuberty.1-3 We
# c( i  t! O7 k: t, d4 zreport a 16-month-old boy who presented with the: n% e( `2 m, `1 G5 O+ ]/ E6 x. w
enlargement of the phallus and pubic hair develop-. e# X( g+ W- ~$ q, j) ^$ V$ L9 l
ment without testicular enlargement, which was due' y0 G- E$ X' }+ y
to the unintentional exposure to androgen gel used by
& i8 I: P6 x' p5 ^: p3 ]the father. The family initially concealed this infor-
/ _+ p: e5 R9 T, F; Wmation, resulting in an extensive work-up for this  X7 q$ x6 v. L
child. Given the widespread and easy availability of
( f+ ]. ]! p( @% _( gtestosterone gel and cream, we believe this is proba-
8 ^5 E% S& s4 |9 U+ K; [3 xbly more common than the rare case report in the
7 ]' J+ o6 G6 Z) n- {! Wliterature.4' Y& r! i/ u& W/ s5 `, b
Patient Report
+ ~4 S2 R! l+ E: y+ I1 {- j3 bA 16-month-old white child was referred to the
% E; ]" \# s6 r$ |) Z9 |endocrine clinic by his pediatrician with the concern
0 c1 ?6 @2 F1 x) q0 X7 |of early sexual development. His mother noticed  g- V4 G9 n* W. C' P% X2 t/ P
light colored pubic hair development when he was4 {) @& g/ O6 X9 g5 U' L  S- D
From the 1Division of Pediatric Endocrinology, 2University of
4 Q. Z& I) m4 Y: h3 I9 ?South Alabama Medical Center, Mobile, Alabama.! V6 c* |# N2 I4 B5 @. m; n
Address correspondence to: Samar K. Bhowmick, MD, FACE,9 n, E+ t+ h9 Y! J5 ]& g+ Q2 Z1 ^1 G
Professor of Pediatrics, University of South Alabama, College of
, N! N, e9 ?) X$ _+ u# @, u- p9 YMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;5 ^) f8 G( P" L$ ]! s' Z/ p+ T  V
e-mail: [email protected]." Y2 [7 g; U( v5 u  E
about 6 to 7 months old, which progressively became0 i4 g9 C/ ?, K' l
darker. She was also concerned about the enlarge-
! H7 v( A4 i$ k4 t. e# X9 mment of his penis and frequent erections. The child8 G( ]- H( B! i" R* Z' V8 M3 [3 V
was the product of a full-term normal delivery, with, w+ W% n' g4 P! A6 o& K6 ?
a birth weight of 7 lb 14 oz, and birth length of' x( {) i1 s; Z2 U1 t  R: Z$ J
20 inches. He was breast-fed throughout the first year) l2 w: }( g1 N- ~% P: w7 c
of life and was still receiving breast milk along with2 b9 ~. D8 w% z+ }4 i9 |  {+ Q0 B
solid food. He had no hospitalizations or surgery,
9 W  l6 `! b$ k3 N5 jand his psychosocial and psychomotor development
2 l% n* @) M$ w5 jwas age appropriate.. M" B! x4 Q. ~9 }1 R1 H& |
The family history was remarkable for the father,
+ p- [( P, T5 j, H* m& J5 C+ s1 }5 L7 Gwho was diagnosed with hypothyroidism at age 16,
7 [5 }5 z8 O3 ]' ywhich was treated with thyroxine. The father’s1 [, B- s6 d9 @; d- g
height was 6 feet, and he went through a somewhat) g% H. i5 B& ?9 F- K
early puberty and had stopped growing by age 14.
/ H- C: u1 l6 g* }* w4 ~. M4 Z( yThe father denied taking any other medication. The2 j- Z3 B  K+ @: k
child’s mother was in good health. Her menarche
- j* G9 a* c5 s$ Lwas at 11 years of age, and her height was at 5 feet- I- ?* h: ?( s. a+ G
5 inches. There was no other family history of pre-" [5 t: ]- c- J4 B) X3 L
cocious sexual development in the first-degree rela-" @9 y# }4 B2 c* m* [+ s4 ~2 w
tives. There were no siblings.
5 U. S1 `% }6 NPhysical Examination
5 n( g1 P! g$ H: _; k- w8 `  t8 CThe physical examination revealed a very active,+ x9 ~7 z' o0 C
playful, and healthy boy. The vital signs documented
) S6 g, V3 o! h6 @# |a blood pressure of 85/50 mm Hg, his length was
: v6 N6 N8 N1 @  C9 P90 cm (>97th percentile), and his weight was 14.4 kg5 ]- a0 o# C5 P8 d
(also >97th percentile). The observed yearly growth8 D+ k% t6 d( Q6 H2 O: {
velocity was 30 cm (12 inches). The examination of
1 `. L- J+ n5 j3 A' Wthe neck revealed no thyroid enlargement.
; f4 H. o! l, I9 Q0 o6 aThe genitourinary examination was remarkable for' _+ l9 g' e+ l' U
enlargement of the penis, with a stretched length of
) r6 ^. M7 d* `- e3 M8 cm and a width of 2 cm. The glans penis was very well
( ]6 h' b  c$ Y1 M. Ddeveloped. The pubic hair was Tanner II, mostly around5 M& Z7 H8 y* P6 r
540
& L. j7 ]' O3 ~9 ~# Kat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ N0 @8 u! d) w; P
the base of the phallus and was dark and curled. The
( @5 X2 ?" E" r* h9 ^* H) ttesticular volume was prepubertal at 2 mL each.
8 d8 |; y& k  L) O2 DThe skin was moist and smooth and somewhat
$ p& U3 p$ K# |2 `oily. No axillary hair was noted. There were no* o  \/ w- n; G7 e' {3 T
abnormal skin pigmentations or café-au-lait spots.; v$ s6 V: \3 C# {- r0 g- e7 Q
Neurologic evaluation showed deep tendon reflex 2+1 J& y  ^$ H8 I/ C+ E
bilateral and symmetrical. There was no suggestion
. ~. Q. [9 K7 Q! E9 F" g+ Q; d, cof papilledema.' A9 L* S% o2 F3 i: t6 u3 [
Laboratory Evaluation8 O4 X  z- a6 e9 V" Y0 k* Z6 ~
The bone age was consistent with 28 months by* i& [, G; C* u
using the standard of Greulich and Pyle at a chrono-* Q" Q- X7 F$ d; K4 M- m
logic age of 16 months (advanced).5 Chromosomal
/ J* `* r# t1 e* i+ Y7 kkaryotype was 46XY. The thyroid function test- e. f0 @2 o4 N: U, p0 @1 {5 I: f  ]
showed a free T4 of 1.69 ng/dL, and thyroid stimu-7 w. o! W7 B5 H0 t% [* R
lating hormone level was 1.3 µIU/mL (both normal).
; D' Y9 J' J8 ~; kThe concentrations of serum electrolytes, blood
( k0 X* i  c/ ?- u  ~6 uurea nitrogen, creatinine, and calcium all were. H) A1 [" D+ h9 v+ y& R* x
within normal range for his age. The concentration/ w. i* y: l' i6 z6 j: L- Q
of serum 17-hydroxyprogesterone was 16 ng/dL
6 M) L" V; H5 E8 z! [% F2 W0 T(normal, 3 to 90 ng/dL), androstenedione was 20
/ f6 c: X/ j/ u2 o/ Y3 h( P( q4 v2 ~! gng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-/ u1 Y4 E% y0 s: d
terone was 38 ng/dL (normal, 50 to 760 ng/dL),  {8 T- R* f0 s9 x$ v
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
+ p, }3 k: B- G8 }  c: X7 R5 a49ng/dL), 11-desoxycortisol (specific compound S)
. n: }: i! D& X9 Vwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
% Q- j! f: x  utisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
$ V/ s- H2 P) Z6 e- C- Jtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
0 p& o/ o, z7 P  ]3 Uand β-human chorionic gonadotropin was less than
  F- P0 q3 o  {5 mIU/mL (normal <5 mIU/mL). Serum follicular
9 W( y% T! k$ vstimulating hormone and leuteinizing hormone% M. G5 N8 D% c( \" Y( y
concentrations were less than 0.05 mIU/mL
) N, u0 H6 ?6 O6 \- k; }, Q  d6 G(prepubertal).# e5 S' O& [/ v0 M6 s3 D
The parents were notified about the laboratory
& z9 ?$ @: {( q" Oresults and were informed that all of the tests were/ b& p4 V/ Q: V5 ]" W6 ~  t
normal except the testosterone level was high. The, |! e. n0 c- e/ p5 J5 H& l4 _
follow-up visit was arranged within a few weeks to
: _- X" A* r( k! O, K$ Fobtain testicular and abdominal sonograms; how-. m8 b  Z& l% ~6 v: n
ever, the family did not return for 4 months.
/ w+ s1 w9 |3 L/ i) q. P$ I- MPhysical examination at this time revealed that the
! k/ |4 Y6 K' V/ qchild had grown 2.5 cm in 4 months and had gained% _& W) b* R% L) `* c1 H! d( C/ D4 K
2 kg of weight. Physical examination remained
6 O: H& X" I' q9 _unchanged. Surprisingly, the pubic hair almost com-
0 Y( b9 `. d2 V9 F' qpletely disappeared except for a few vellous hairs at2 W7 e- [8 D' E3 u& l' ]
the base of the phallus. Testicular volume was still 2
  p# U$ b5 F2 a( B. [, imL, and the size of the penis remained unchanged.2 i' _$ b! O3 x! P, C
The mother also said that the boy was no longer hav-% @# u+ a. _; P, a0 Z9 |" |
ing frequent erections.' F$ a& h5 _7 h6 N  C( W/ H
Both parents were again questioned about use of5 D: M" g1 A$ J  @1 h. O
any ointment/creams that they may have applied to
7 E6 O# }1 j2 ^6 y3 B6 v1 u1 wthe child’s skin. This time the father admitted the$ r* h, f$ z" P9 T& j# L- A- @. Z' P4 r
Topical Testosterone Exposure / Bhowmick et al 541
6 b7 Z7 C' g% Q3 c% k1 }use of testosterone gel twice daily that he was apply-
4 v8 l0 C3 H8 {7 C0 S. N9 Cing over his own shoulders, chest, and back area for  X; r% n! _3 |7 F2 y
a year. The father also revealed he was embarrassed& t6 W/ Q2 M# T) g9 a& w% _
to disclose that he was using a testosterone gel pre-
5 v: V* G! p6 B; A3 o2 d8 Xscribed by his family physician for decreased libido$ J& ~* t. [: ?, S& ^
secondary to depression.! Z/ C& Z; s5 H9 N% w
The child slept in the same bed with parents.( H) i& W4 F' m8 f
The father would hug the baby and hold him on his1 w7 T: y. C9 ]7 [% I
chest for a considerable period of time, causing sig-& _, c& {, H; Q3 P5 Q
nificant bare skin contact between baby and father.
4 `$ |. V  e7 V7 i1 nThe father also admitted that after the phone call,
: D9 A% V4 h; m; r5 D7 kwhen he learned the testosterone level in the baby' m2 h+ J! p& {
was high, he then read the product information
' ]  M/ m6 u6 @2 y$ c  Opacket and concluded that it was most likely the rea-" J( }& j. s% j) Y
son for the child’s virilization. At that time, they
! a# \& f4 Z( e* P: n. C' Xdecided to put the baby in a separate bed, and the; O/ l6 O% G1 \/ k+ ?0 {5 J% Q4 O4 s
father was not hugging him with bare skin and had+ ^' Q# @0 f) [2 p  j0 G
been using protective clothing. A repeat testosterone
, F9 k: k& R5 b  D/ k& v, K; jtest was ordered, but the family did not go to the
, G5 f7 x& l! p+ |laboratory to obtain the test.7 r- d" r+ |; J! @3 F, B5 A) E
Discussion
7 V: f: V8 k1 \0 M  @4 `' I# S1 `  rPrecocious puberty in boys is defined as secondary+ A' B4 q! E- G! K+ ]0 s+ A( S$ L2 y
sexual development before 9 years of age.1,4- N& _: l. G# V9 K. A
Precocious puberty is termed as central (true) when0 s+ ^9 e) z% Y. n" s
it is caused by the premature activation of hypo-  y) I1 W) t. {4 u6 E1 R
thalamic pituitary gonadal axis. CPP is more com-
4 c! n  `  x4 k* b$ l- W2 cmon in girls than in boys.1,3 Most boys with CPP; x" L: V, @6 b; s+ m' x2 e% P. z
may have a central nervous system lesion that is
* D& Z+ R, Q7 O3 b$ p0 Yresponsible for the early activation of the hypothal-3 b0 E" D! b8 B5 N% a
amic pituitary gonadal axis.1-3 Thus, greater empha-
. h  ?% a' X( Z) E: dsis has been given to neuroradiologic imaging in1 d8 `3 @! x5 ]
boys with precocious puberty. In addition to viril-6 j  f$ R( ]: B0 r
ization, the clinical hallmark of CPP is the symmet-
8 X# _+ Q/ H7 \rical testicular growth secondary to stimulation by
0 d' L* s$ O$ t* x0 k, G7 Cgonadotropins.1,3( d5 l& O! @5 f% t! v) B% _# K
Gonadotropin-independent peripheral preco-
, v% z3 F5 C% v# k8 vcious puberty in boys also results from inappropriate
: [1 ]" x6 b! randrogenic stimulation from either endogenous or2 C- p. U) k* ~% [7 U. v7 M! l3 I
exogenous sources, nonpituitary gonadotropin stim-) d. U1 O. k) [7 v
ulation, and rare activating mutations.3 Virilizing
+ C' v/ w+ F8 S+ m4 C- ~: lcongenital adrenal hyperplasia producing excessive
( }" h4 E; b. o$ ?adrenal androgens is a common cause of precocious
/ O# p3 i3 K7 }% P9 U: Y8 M# xpuberty in boys.3,45 U0 Z) f0 g( S9 ~
The most common form of congenital adrenal5 K3 N- D  i' ~: S
hyperplasia is the 21-hydroxylase enzyme deficiency.# w% r% O; _9 R
The 11-β hydroxylase deficiency may also result in# }2 L3 J% w  Z7 p! \# q( B  v
excessive adrenal androgen production, and rarely,3 \* r4 x1 y( J8 _* H3 A1 z! a# x- E
an adrenal tumor may also cause adrenal androgen
' b2 r$ _: |6 e- s  I/ Hexcess.1,3
: K3 ^* t! |0 Q6 I  Iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 W4 T# j' i; Z2 k8 s0 Z6 \542 Clinical Pediatrics / Vol. 46, No. 6, July 2007  b- g# |# c( U4 A& w# J. |
A unique entity of male-limited gonadotropin-- w) b4 Q) `8 m1 c8 f
independent precocious puberty, which is also known
9 W6 G0 K4 Y/ M8 Jas testotoxicosis, may cause precocious puberty at a% F3 k, C( M! `7 d4 d
very young age. The physical findings in these boys$ r7 K: \( W$ {7 u5 T. l- L- ~3 c
with this disorder are full pubertal development,
9 E- z% ?7 T$ E8 Q6 j( X: Xincluding bilateral testicular growth, similar to boys* O" z4 z, h! `- ]9 C" |% `  S7 R
with CPP. The gonadotropin levels in this disorder3 m/ k6 Y1 g* l9 L7 l+ ^* ^
are suppressed to prepubertal levels and do not show+ ~) z4 S# O, d( j. X3 `
pubertal response of gonadotropin after gonadotropin-" Z* d' g/ R) [6 `, }& |, q
releasing hormone stimulation. This is a sex-linked
& B3 q3 {7 ?! w2 Tautosomal dominant disorder that affects only
* d, n3 ?& B* f6 }% L, m! b' L: imales; therefore, other male members of the family( D0 U* ^4 u% u! i$ G5 l1 g/ g+ J
may have similar precocious puberty.3( ?) j2 @2 F9 K, j% S
In our patient, physical examination was incon-9 k4 @8 g0 y$ T7 q& m
sistent with true precocious puberty since his testi-8 M  y8 c  f9 j4 E& W: |5 ^
cles were prepubertal in size. However, testotoxicosis! L. ]/ e3 Y0 `# m7 h) Z" \! T
was in the differential diagnosis because his father' y& F% }+ p, \8 Q- {% ]% R+ f
started puberty somewhat early, and occasionally,2 H  L2 S: V% V" i) h- ?
testicular enlargement is not that evident in the
; o& Q+ M5 }2 P& V" k6 t; u" Ibeginning of this process.1 In the absence of a neg-
) \" E6 T5 z! F1 L* a  {ative initial history of androgen exposure, our1 w, \, Y5 V$ v8 W
biggest concern was virilizing adrenal hyperplasia,
2 w6 D% A; {! e% W* E5 deither 21-hydroxylase deficiency or 11-β hydroxylase
, l( \* d5 J5 a  o' D& j- Sdeficiency. Those diagnoses were excluded by find-
& S- l1 x% K- O) A; ?. y  ~& Xing the normal level of adrenal steroids.
$ L! z# M* _% f9 H% ^9 jThe diagnosis of exogenous androgens was strongly0 h/ O+ H: k0 I
suspected in a follow-up visit after 4 months because
/ G8 g1 d& B: w2 o. y! Vthe physical examination revealed the complete disap-
4 z1 }' C- ^; I/ i" W) |pearance of pubic hair, normal growth velocity, and
. z( v+ K7 R' bdecreased erections. The father admitted using a testos-4 r- j) }8 M7 z- c' W
terone gel, which he concealed at first visit. He was
. m! u4 t' y! ^4 X3 \using it rather frequently, twice a day. The Physicians’6 O! \8 _, M8 K7 ]+ g$ f2 |
Desk Reference, or package insert of this product, gel or
, j! `/ ]: M, h- o3 i- Wcream, cautions about dermal testosterone transfer to
7 k& w( Z# N0 P. q  R3 zunprotected females through direct skin exposure.
7 ?  R3 s7 r  B+ W: J* zSerum testosterone level was found to be 2 times the
* H2 w7 R( }/ jbaseline value in those females who were exposed to
# K$ ~' t. p) s$ `even 15 minutes of direct skin contact with their male2 s) ?) r- ?8 U$ a6 z8 R/ T$ i
partners.6 However, when a shirt covered the applica-% @0 z& j% ^3 O( `( M' ?4 x6 D
tion site, this testosterone transfer was prevented.  i( K* \# Y# }/ v" u
Our patient’s testosterone level was 60 ng/mL,( Z' C9 B8 q9 b3 k
which was clearly high. Some studies suggest that7 G6 }" a# c; f$ p) c  x/ B
dermal conversion of testosterone to dihydrotestos-
% q+ ]3 [) V6 z, y# Uterone, which is a more potent metabolite, is more. ~) h5 k1 `& ]! S
active in young children exposed to testosterone
  j# d+ c# u( u- J/ C0 P/ U; Jexogenously7; however, we did not measure a dihy-, Q; v8 C! W: C  f% A; _1 M
drotestosterone level in our patient. In addition to( ~0 M9 b: j4 z+ t7 A
virilization, exposure to exogenous testosterone in% M$ Q9 K$ P$ Z& L; |6 e& m. u
children results in an increase in growth velocity and. G" H9 t$ ~, k! e: Z  P2 B
advanced bone age, as seen in our patient.
* R* C! f1 k+ A* f2 CThe long-term effect of androgen exposure during  y  g4 A0 l! ~# x: i+ g
early childhood on pubertal development and final8 Z: g# \: l8 f- q" Y. M
adult height are not fully known and always remain
# L6 w/ m, I2 p# C# k) ]0 G" Ma concern. Children treated with short-term testos-: G) B. v. F: ^% I1 T2 o. d
terone injection or topical androgen may exhibit some
4 s( }. ^" ?& jacceleration of the skeletal maturation; however, after: l, f; H* e7 z! ?# p1 A# N5 H
cessation of treatment, the rate of bone maturation" g, M8 u& ?  r7 C, h  A4 R
decelerates and gradually returns to normal.8,9$ M' P; o4 w+ l, M* P% A, [% U
There are conflicting reports and controversy
$ S% e# D, @! E8 Gover the effect of early androgen exposure on adult
) y$ ?7 L  q5 A% dpenile length.10,11 Some reports suggest subnormal
% t+ D" w& ^$ B' q9 E) u% R6 cadult penile length, apparently because of downreg-4 A2 \$ D% D. f
ulation of androgen receptor number.10,12 However,) D6 J" J' D, a+ V
Sutherland et al13 did not find a correlation between) K0 n. F, Q: X/ _
childhood testosterone exposure and reduced adult+ w9 z/ U. W3 z* U: R5 x
penile length in clinical studies.
( U  e* [" l! a3 @& bNonetheless, we do not believe our patient is
  g2 y% Q" x0 m- ?( mgoing to experience any of the untoward effects from
5 u  f( T7 x* k4 B" ytestosterone exposure as mentioned earlier because' h' f) @: m( K, h# O( U1 O
the exposure was not for a prolonged period of time.
6 Q& |9 G6 |! j9 u* zAlthough the bone age was advanced at the time of
& M, V( F6 O$ {diagnosis, the child had a normal growth velocity at
6 f& j; F8 i, rthe follow-up visit. It is hoped that his final adult# m' F+ ~* _& M: S
height will not be affected.+ o( y9 ?/ y6 p: j
Although rarely reported, the widespread avail-
  x* _* L) ^8 }  ]" j' M5 m. r6 Hability of androgen products in our society may
0 z2 T: ?% M% F& f2 h) g2 a2 [indeed cause more virilization in male or female
( f6 M4 U. m4 X+ {4 ?9 R! O; ?children than one would realize. Exposure to andro-
% A' I% G$ B: m8 T2 c- `gen products must be considered and specific ques-
7 ~7 r& E( a1 U! I3 w( w0 Itioning about the use of a testosterone product or- i- ]2 a  y0 z6 B3 f) R
gel should be asked of the family members during6 q  o) G3 o9 [& F; X
the evaluation of any children who present with vir-
% c5 j& O; n7 N4 k. oilization or peripheral precocious puberty. The diag-
& M% C5 p% S+ J" C6 W1 Snosis can be established by just a few tests and by
/ S- W) z$ \% s1 P+ H1 lappropriate history. The inability to obtain such a
( s+ {- C! `6 B7 f* Chistory, or failure to ask the specific questions, may
" q; L( C! q9 n6 \4 _result in extensive, unnecessary, and expensive8 D! T# t0 `' R( H1 o3 i
investigation. The primary care physician should be
/ G7 ?* @: Q4 p( f9 saware of this fact, because most of these children
4 N4 F! b$ |) hmay initially present in their practice. The Physicians’
2 F; K- ~; }. U2 U9 YDesk Reference and package insert should also put a# m# |8 H1 n6 w5 R( l0 v  H
warning about the virilizing effect on a male or
% c' v: a" H3 G' e( hfemale child who might come in contact with some-9 A: O  ~4 q% ?0 n% c  T
one using any of these products." ^! I8 D2 t) n7 z0 |
References# q. c2 P2 m: v# Q9 S
1. Styne DM. The testes: disorder of sexual differentiation
8 [* O& V' R1 [5 i( ^and puberty in the male. In: Sperling MA, ed. Pediatric
4 q5 F6 i! V0 u- v/ u/ O, UEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;* q2 m, M5 n8 o, N2 {0 d3 O+ k. _
2002: 565-628.
( |5 `: D4 S1 L2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
3 @- o  Z" n$ d- F; l( lpuberty 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

& P% }! R. D" Q5 @5 g( V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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