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Sexual Precocity in a 16-Month-Old9 {/ p2 s+ K8 Z9 [/ S+ v3 ?) L
Boy Induced by Indirect Topical
2 ~7 d, r% S. m- mExposure to Testosterone2 \$ A1 E9 i0 h4 B& y0 M2 S
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
5 t5 a3 _1 u' P1 Q) Xand Kenneth R. Rettig, MD1
4 B( M1 f' S* l3 g9 B4 }Clinical Pediatrics
! _: L" @) D1 J- D* J) RVolume 46 Number 6
% L" r6 O9 I4 W4 ]- y& g9 Y3 HJuly 2007 540-543
0 V- g0 ~4 z( f. M/ @8 N© 2007 Sage Publications
$ k9 v2 p% c! b' c10.1177/0009922806296651
4 e" n# ?5 P5 w  Z$ Q' b6 Vhttp://clp.sagepub.com: Q/ m# o/ }1 o- I1 D; P
hosted at
+ \1 h' M! }/ e- lhttp://online.sagepub.com
6 b" ?  Z9 b0 ~; ]4 `! dPrecocious puberty in boys, central or peripheral,: y5 ]7 S! g4 i# d5 l5 X2 R
is a significant concern for physicians. Central/ I$ J' U! _4 |1 d0 X2 M
precocious puberty (CPP), which is mediated
& h; F# x+ P# w/ r% Gthrough the hypothalamic pituitary gonadal axis, has! Z. G* ~# q3 Y
a higher incidence of organic central nervous system- y+ C! e# u" s9 u3 b  e) B
lesions in boys.1,2 Virilization in boys, as manifested
6 c8 y7 i9 R# A3 k: qby enlargement of the penis, development of pubic, V! [& Q5 Z2 C! K7 c' r" K
hair, and facial acne without enlargement of testi-
* x- u3 p) U! D3 a( s* }cles, suggests peripheral or pseudopuberty.1-3 We
" L  T  I8 @: B6 @: O9 yreport a 16-month-old boy who presented with the
7 @. ~( t% Z+ Z0 o& I, Penlargement of the phallus and pubic hair develop-& G8 `. o4 a3 Y! j" l& p" C
ment without testicular enlargement, which was due7 A# [. i: r- ^7 O% `$ ]( V
to the unintentional exposure to androgen gel used by( a4 g5 x, Y: b
the father. The family initially concealed this infor-
, a% F8 Y7 L  b4 o% {mation, resulting in an extensive work-up for this& r, {3 ]! ]2 @" O
child. Given the widespread and easy availability of5 B+ q1 s% E: ^% F( B! i9 ~6 B
testosterone gel and cream, we believe this is proba-# I' C  @/ i! ~7 {$ _) x
bly more common than the rare case report in the1 q! t2 V4 b% I& ?; ^
literature.4
+ U( }9 ~$ V! pPatient Report
5 s5 ^& v4 E7 U9 K+ f4 x" @A 16-month-old white child was referred to the9 b2 k6 D  s4 K
endocrine clinic by his pediatrician with the concern9 }0 W% a$ @  v) R: d: b' q
of early sexual development. His mother noticed
0 }% A; W; I1 {: y- F1 U" ]* B6 Elight colored pubic hair development when he was
& B0 Z1 \9 D+ F" i/ p) `  m' QFrom the 1Division of Pediatric Endocrinology, 2University of
" G1 W9 B& `+ ?& s! \South Alabama Medical Center, Mobile, Alabama.- e1 u3 X+ N. b' t; D
Address correspondence to: Samar K. Bhowmick, MD, FACE,
* _" S' Q1 ?+ D+ v& N( PProfessor of Pediatrics, University of South Alabama, College of3 O* J7 {# L; p
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;# ~; H- z9 @& u4 ^
e-mail: [email protected].
& r; t  @: a/ jabout 6 to 7 months old, which progressively became
# q0 p3 _$ |4 q) Y& h! Bdarker. She was also concerned about the enlarge-
4 ^8 a7 j, p9 tment of his penis and frequent erections. The child- p7 K3 n# f* l
was the product of a full-term normal delivery, with5 u8 X% q  w; f6 f* }) @3 h1 M
a birth weight of 7 lb 14 oz, and birth length of2 l+ x( ?2 x; t7 M
20 inches. He was breast-fed throughout the first year
: P. H7 y$ Y  n* l" x$ l& ?% Wof life and was still receiving breast milk along with
: v$ P6 e/ O3 O5 qsolid food. He had no hospitalizations or surgery,4 S$ A2 r7 V! a
and his psychosocial and psychomotor development8 o  F- q  {/ R3 f. A: ~
was age appropriate.8 d' o/ e: {2 Q% Y4 F, o# Y
The family history was remarkable for the father,' i3 i! t. M% i
who was diagnosed with hypothyroidism at age 16,$ I2 c! J) o( |
which was treated with thyroxine. The father’s: K" v( t. x" G7 ?
height was 6 feet, and he went through a somewhat+ O7 r8 i- _# i4 O$ H* `
early puberty and had stopped growing by age 14.8 m5 @7 h1 a& F" N* r; `0 a# K9 L
The father denied taking any other medication. The) D" P8 l/ j. c  u5 i
child’s mother was in good health. Her menarche
; U; s! Y! W* a, A5 m$ W6 kwas at 11 years of age, and her height was at 5 feet
% K. e7 K8 z! K3 n% ?5 inches. There was no other family history of pre-8 x9 \/ M& _, i; c
cocious sexual development in the first-degree rela-. c5 L& h5 U% n+ a* T
tives. There were no siblings.
4 s8 M- k: j4 JPhysical Examination
9 P0 U& X6 F) D6 QThe physical examination revealed a very active," a& f7 V4 v% @7 p* X5 q+ r/ N
playful, and healthy boy. The vital signs documented8 k/ G  m1 J' a
a blood pressure of 85/50 mm Hg, his length was  f/ r! o0 T, o- ?+ U; o
90 cm (>97th percentile), and his weight was 14.4 kg
; f5 |, r6 G' d% p2 O(also >97th percentile). The observed yearly growth
: Z' `2 A# `4 J" g5 l! V$ Pvelocity was 30 cm (12 inches). The examination of
2 Z( \8 ]" ^) {. V& l3 hthe neck revealed no thyroid enlargement.
5 O$ P2 c9 D5 y5 L+ Y% c5 w5 H( D5 P3 MThe genitourinary examination was remarkable for
7 {) w5 c# l2 l' c0 G% E1 denlargement of the penis, with a stretched length of
) r4 U( K5 b' H3 }, s! @% ?8 v- Z  V8 cm and a width of 2 cm. The glans penis was very well
0 B  ?; I! U5 t: {, X! I5 ]developed. The pubic hair was Tanner II, mostly around8 L. U" \' x6 U# `
5404 m" j2 L+ `3 o1 P- x
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' W; l, y1 N& w# Q
the base of the phallus and was dark and curled. The& T3 c/ k: e) ^4 \
testicular volume was prepubertal at 2 mL each.
# o; `  b. [2 s0 lThe skin was moist and smooth and somewhat2 z8 H% f: |# Y* L3 m7 h0 C
oily. No axillary hair was noted. There were no' R) F; W+ w6 K6 S3 m
abnormal skin pigmentations or café-au-lait spots.4 M! _2 f8 E  I' H
Neurologic evaluation showed deep tendon reflex 2+
' p  Y; L/ S  P) t) ^0 O+ r' [bilateral and symmetrical. There was no suggestion# S) u! |% b- v  C" B, h
of papilledema.( H/ S8 |2 q* W! a7 R
Laboratory Evaluation
% l: ~) J6 T9 ]% a4 |( A  E* WThe bone age was consistent with 28 months by
' Q, |( U8 j6 e4 d( |using the standard of Greulich and Pyle at a chrono-  N5 \. U. a0 Z) R- ]
logic age of 16 months (advanced).5 Chromosomal5 K; P, q! l, B" T# F
karyotype was 46XY. The thyroid function test  w' c7 N4 k( ~- ?
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
- w4 J1 C5 P* O) @7 `lating hormone level was 1.3 µIU/mL (both normal).
/ J/ r) ]2 i6 e% |. t$ ^/ i: uThe concentrations of serum electrolytes, blood8 i7 s: H+ _+ [! e7 p
urea nitrogen, creatinine, and calcium all were" V" \( W6 l. P3 {8 J) a
within normal range for his age. The concentration' m9 Z8 m" h5 q) a) R
of serum 17-hydroxyprogesterone was 16 ng/dL
. g) J$ G' w) \(normal, 3 to 90 ng/dL), androstenedione was 20
# z- z7 t6 M7 s6 s' }ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
  N0 _% a/ A' }; Aterone was 38 ng/dL (normal, 50 to 760 ng/dL),
2 Z1 t$ ^, J% zdesoxycorticosterone was 4.3 ng/dL (normal, 7 to6 w2 U3 Z6 J' k, n5 \- l
49ng/dL), 11-desoxycortisol (specific compound S)
3 q. W8 x* B4 q% U6 owas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
' \0 _+ S3 D* N2 Z, ]" H# e; p+ M" Rtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
5 Z- F  [3 v+ s) {6 m- ntestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
5 L9 z1 m5 h% m; q, k/ oand β-human chorionic gonadotropin was less than/ ~  z$ S3 s! |, X
5 mIU/mL (normal <5 mIU/mL). Serum follicular' D: ]( I5 K  ~
stimulating hormone and leuteinizing hormone
+ Y  c3 o. Y, `- N3 Q9 econcentrations were less than 0.05 mIU/mL
+ M% V7 Y2 z1 D0 a& u4 z, J(prepubertal).
$ Y9 h4 V; g3 c: u# m2 M3 l& GThe parents were notified about the laboratory
0 y7 K2 O  ^: @1 Tresults and were informed that all of the tests were
( Y- g5 O' U" T& knormal except the testosterone level was high. The
4 K) M0 f, u7 R  Z. Wfollow-up visit was arranged within a few weeks to
6 b9 G# ~" v6 }( K/ gobtain testicular and abdominal sonograms; how-
* \1 F  \# @, |+ R4 y6 S0 c% I+ Rever, the family did not return for 4 months.
; J/ t" H8 n* C( q$ k9 ?) n. s% @Physical examination at this time revealed that the& L; S6 X7 c& V, e2 ]0 [; {$ r
child had grown 2.5 cm in 4 months and had gained
8 h$ g6 K0 J% I5 @( e# H4 Z4 ^2 |; v2 kg of weight. Physical examination remained
$ n: P" |" Z$ c) C; W  d. o6 f; m8 G4 dunchanged. Surprisingly, the pubic hair almost com-
, s! G7 X: g# O* _0 R( A3 v* r% qpletely disappeared except for a few vellous hairs at
0 d: y6 O: S8 w* I- k* f3 S. |the base of the phallus. Testicular volume was still 21 G5 M5 j: M2 J: Y& d1 n6 o
mL, and the size of the penis remained unchanged.2 g1 j4 {; ?! Y$ g
The mother also said that the boy was no longer hav-
  p$ q# B1 s! [* @0 Ring frequent erections.) G" W' x% d8 Y/ x1 q" L2 ^
Both parents were again questioned about use of* t6 |7 h- I) y$ @) z
any ointment/creams that they may have applied to
6 T0 O: |" z7 W1 Nthe child’s skin. This time the father admitted the& A! p" H# [' ]& p& r* p: j
Topical Testosterone Exposure / Bhowmick et al 541
6 t. ~- B& a. b0 `2 q) f$ N" ~; Buse of testosterone gel twice daily that he was apply-
5 N* F+ K2 b0 cing over his own shoulders, chest, and back area for
8 }8 ]# K! A* va year. The father also revealed he was embarrassed) j& ]% b$ f$ m8 d" p
to disclose that he was using a testosterone gel pre-
. q6 t1 U; s" v- g- p. I% g/ d3 \scribed by his family physician for decreased libido* X# d2 R% L7 U7 ~( L9 M- t
secondary to depression.
1 C4 O# K. H8 s7 C/ r& [* `9 C1 KThe child slept in the same bed with parents.3 M" V* R# Q4 m% Q" E# w
The father would hug the baby and hold him on his3 q& ?3 \9 Q4 r! G0 C
chest for a considerable period of time, causing sig-
. F0 t1 \' b% x; {* Q0 `& Rnificant bare skin contact between baby and father.3 Q! E* t: o' y# k) x
The father also admitted that after the phone call,
! K  B1 B# E8 E5 X7 w( kwhen he learned the testosterone level in the baby
) P9 x) b  j! I2 c# }8 Lwas high, he then read the product information
5 m; ?  H4 H- k( V: l" K( j% fpacket and concluded that it was most likely the rea-
* C3 x" L3 s, y( B% N! T' qson for the child’s virilization. At that time, they
! [& F& w( R1 [: p) v* l% Gdecided to put the baby in a separate bed, and the5 {  F  c+ U4 v- m2 t" Y" [( _
father was not hugging him with bare skin and had
7 y' F  q5 |) L  M# A) ?% t  qbeen using protective clothing. A repeat testosterone- g' H9 s( y6 l! c! U* |9 D3 k5 `
test was ordered, but the family did not go to the, p# c0 T. z# K2 h
laboratory to obtain the test.3 W7 J/ Z' o8 y  {- z  r# W6 o
Discussion. h: }2 S/ l+ l: p$ H- `
Precocious puberty in boys is defined as secondary
- s+ L' k6 q0 j0 v' E& c4 e; ^sexual development before 9 years of age.1,46 R7 a) L0 m  s! f+ d1 r( [
Precocious puberty is termed as central (true) when
7 J+ E+ P( f3 b+ z6 V& Ait is caused by the premature activation of hypo-2 ^# k6 ~5 l. a$ l
thalamic pituitary gonadal axis. CPP is more com-
5 ~  j! S4 a) P7 ^1 z9 Dmon in girls than in boys.1,3 Most boys with CPP( J; @: h1 T. p7 L* ]. M6 {
may have a central nervous system lesion that is
5 V6 z+ m; ~/ F; o' Jresponsible for the early activation of the hypothal-
- d' A! R/ M+ }3 tamic pituitary gonadal axis.1-3 Thus, greater empha-( q( e8 \8 M9 G1 w: C0 ^# y1 F. e! H
sis has been given to neuroradiologic imaging in
: c& m/ x4 F/ Y0 \boys with precocious puberty. In addition to viril-: f; t7 Z7 n+ Q6 f4 m+ C# f6 y* f8 Y
ization, the clinical hallmark of CPP is the symmet-
5 c0 b, s" n, `1 `+ frical testicular growth secondary to stimulation by4 y& L" c$ z5 w* s, g0 s
gonadotropins.1,3$ _2 r8 c8 x2 J6 a6 C
Gonadotropin-independent peripheral preco-. a% @$ }6 ]5 k5 t/ E
cious puberty in boys also results from inappropriate; H, h3 g5 i! O! I  L
androgenic stimulation from either endogenous or
0 |8 z& Z, R! f. O0 B' ?exogenous sources, nonpituitary gonadotropin stim-
$ l. m% Q. ]3 bulation, and rare activating mutations.3 Virilizing5 ?; l6 K: g3 Y3 v
congenital adrenal hyperplasia producing excessive/ S$ T! A4 y3 H; s  A
adrenal androgens is a common cause of precocious- N' m+ D: l' w* e9 Q$ s- s
puberty in boys.3,4( \( R; v/ Z$ e( u0 }9 s0 Q# a: C
The most common form of congenital adrenal' M& j, b" K! N
hyperplasia is the 21-hydroxylase enzyme deficiency.* N3 |8 M! ], C
The 11-β hydroxylase deficiency may also result in
$ A0 o) `% u  [9 {excessive adrenal androgen production, and rarely,
6 C: }* [8 u& t& N6 Ban adrenal tumor may also cause adrenal androgen  s; ^7 B, E1 h' e- Z2 \4 L+ [
excess.1,3( c* [9 }" d1 q6 S0 }& a7 r) @' |+ ?. h
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ F8 [% ~3 }8 u$ ^, r8 E' l! J542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
3 v+ W' t- T) f& T7 ]1 ~7 ZA unique entity of male-limited gonadotropin-) h' l+ w+ {9 c
independent precocious puberty, which is also known
: W1 b8 ?# z& ~2 e. u, ~as testotoxicosis, may cause precocious puberty at a0 U! B2 g( n+ V& e. K
very young age. The physical findings in these boys
1 d% X. [1 X' ^! J% k0 y! wwith this disorder are full pubertal development,% H. K, U! c) j; Z( x$ @
including bilateral testicular growth, similar to boys
. E. W' X# z8 N3 Ywith CPP. The gonadotropin levels in this disorder' S. n" @: w! T& j  y
are suppressed to prepubertal levels and do not show
7 I- z2 w; T. hpubertal response of gonadotropin after gonadotropin-
/ T4 N6 F7 g8 s3 jreleasing hormone stimulation. This is a sex-linked
3 i6 V0 e5 |5 V' v2 K6 g/ J4 uautosomal dominant disorder that affects only+ M6 J+ i2 \6 c0 y
males; therefore, other male members of the family7 U: |" j, R& J( l- |% S# R
may have similar precocious puberty.3
/ q& s. ]1 P) M0 AIn our patient, physical examination was incon-' b# ?: J# T( E  z" n) [3 v1 D
sistent with true precocious puberty since his testi-9 a+ s* A  o1 i, m- g0 v
cles were prepubertal in size. However, testotoxicosis
0 L6 v1 B; x0 s  n0 m) }/ Ewas in the differential diagnosis because his father' x, ?+ B) C; Y. F" \
started puberty somewhat early, and occasionally,+ q, d$ F6 R4 Q2 j
testicular enlargement is not that evident in the! u0 Y0 K: l' _2 O# g  e1 p, m) w
beginning of this process.1 In the absence of a neg-( o' ?0 W, P- Z5 V
ative initial history of androgen exposure, our3 r3 Z& e' A  }1 d
biggest concern was virilizing adrenal hyperplasia,. r4 @: D" V1 @8 K& }0 @. s
either 21-hydroxylase deficiency or 11-β hydroxylase
* }$ J$ ]; f7 K% s3 K1 B& @% jdeficiency. Those diagnoses were excluded by find-
; G. F* V' |: A& K! Iing the normal level of adrenal steroids.
) `+ d8 O) e5 r/ g2 qThe diagnosis of exogenous androgens was strongly1 v7 s" u! Q: S2 v. l5 a9 R
suspected in a follow-up visit after 4 months because0 i. {7 ?) T# O' d$ v" x
the physical examination revealed the complete disap-
9 t' L$ U$ s! o9 v& f0 h' i1 |; Apearance of pubic hair, normal growth velocity, and) M) E" M2 A9 ^$ I& {& {" n
decreased erections. The father admitted using a testos-; W5 L) C0 H+ I% n: x7 q
terone gel, which he concealed at first visit. He was
+ a  @3 f# v" e7 X' ousing it rather frequently, twice a day. The Physicians’8 L8 }7 l" u& R2 I7 x* O
Desk Reference, or package insert of this product, gel or
& D7 k  F; Q1 m7 x9 Kcream, cautions about dermal testosterone transfer to
/ y% C3 F! D0 G$ }. j4 \& m' nunprotected females through direct skin exposure.
( H6 D- `; k# U, TSerum testosterone level was found to be 2 times the
5 b+ Z$ |* v1 X8 \/ A, hbaseline value in those females who were exposed to
. u' B4 _! p% \! @4 v* Meven 15 minutes of direct skin contact with their male
2 E( u5 ^* [) B2 d; ?partners.6 However, when a shirt covered the applica-1 e5 @3 [1 W+ B5 J! c1 z1 [
tion site, this testosterone transfer was prevented.
$ l9 J+ `5 r$ y6 O( Y3 M% \Our patient’s testosterone level was 60 ng/mL,
! u, B" z* G1 X. z9 n9 ewhich was clearly high. Some studies suggest that0 M) C5 K# ?3 G
dermal conversion of testosterone to dihydrotestos-
$ q7 F) C5 z) c6 Q, {terone, which is a more potent metabolite, is more
: H- w1 f- C2 z, L9 C: W+ m) N- z. Wactive in young children exposed to testosterone2 c: ]0 i0 V2 w
exogenously7; however, we did not measure a dihy-2 F- K& C: E7 F/ F
drotestosterone level in our patient. In addition to1 L# ^. t; G, Z& L5 {
virilization, exposure to exogenous testosterone in0 L5 N& ^8 _) X# P6 X
children results in an increase in growth velocity and. k! @! ]* {5 f# r9 T5 N
advanced bone age, as seen in our patient.
; P. b2 }2 Z  Z2 ~& k% XThe long-term effect of androgen exposure during
- Z! B) s' ~8 I! o" X; r3 E3 Pearly childhood on pubertal development and final
1 S! }. }% }- Yadult height are not fully known and always remain+ h1 P7 T$ a- F; E4 R5 F. ?
a concern. Children treated with short-term testos-
9 e1 v$ k, Y0 y5 E% Aterone injection or topical androgen may exhibit some
" M5 L( V8 n8 R: w# b. r3 w+ Lacceleration of the skeletal maturation; however, after* e  m, I# S* U6 w) |
cessation of treatment, the rate of bone maturation9 p8 l' R, x) C8 `
decelerates and gradually returns to normal.8,9. _5 F- U* o2 Z% q8 k% }5 X, @, X" t
There are conflicting reports and controversy* f2 |, Y; j  _
over the effect of early androgen exposure on adult
$ \/ _+ C3 w/ Tpenile length.10,11 Some reports suggest subnormal% g# {) u  }& C5 B: y4 I- ~( A
adult penile length, apparently because of downreg-
, G' F" Y6 v/ O. x6 ~& T* pulation of androgen receptor number.10,12 However,
, |. h! a7 `9 a1 r: o6 v! OSutherland et al13 did not find a correlation between, T. ~, q# U( N2 p
childhood testosterone exposure and reduced adult
1 ~$ A" {3 A# T0 w4 o; T* l" r2 Jpenile length in clinical studies.
) r) C2 U8 t) e1 Y+ yNonetheless, we do not believe our patient is9 |7 ~8 j% F/ i  e/ l" C) V* ~+ x) v
going to experience any of the untoward effects from
- j( D3 I* C1 w& U3 Xtestosterone exposure as mentioned earlier because
' W% X5 Y* S, W$ qthe exposure was not for a prolonged period of time.! n3 W6 Y2 E  X( T) G) m6 D
Although the bone age was advanced at the time of7 G: [: ~* U, J3 D1 D" P
diagnosis, the child had a normal growth velocity at  X# S* J# p- r' K# ?
the follow-up visit. It is hoped that his final adult
/ y4 f1 W7 ]$ kheight will not be affected.+ R& W8 ?. j- w
Although rarely reported, the widespread avail-
& @0 T' \, N( I" L, W5 xability of androgen products in our society may
" |, W9 C. Z& i( s$ p& ?7 eindeed cause more virilization in male or female
5 e7 g- L; K9 z0 xchildren than one would realize. Exposure to andro-
5 U* V/ T/ @4 c( K8 M! dgen products must be considered and specific ques-- u% J6 \9 Y% h9 l% N
tioning about the use of a testosterone product or# S( \' R7 @8 u& p" y4 B- x8 |' h
gel should be asked of the family members during
! `( O1 l7 [9 @the evaluation of any children who present with vir-
$ r6 |- k. E5 T4 O5 ?1 rilization or peripheral precocious puberty. The diag-0 Q+ U8 c/ }' T* {3 c5 s
nosis can be established by just a few tests and by
# a% j: l% D- v: Jappropriate history. The inability to obtain such a
% O2 `5 x" K$ s9 w+ u  C) P5 ghistory, or failure to ask the specific questions, may9 K# @, E, F0 v0 I- ^
result in extensive, unnecessary, and expensive) V4 d6 {7 z' [+ U- d
investigation. The primary care physician should be$ i4 t% Z( k7 L! n* A' {) h) t
aware of this fact, because most of these children
$ C7 b1 \, m- qmay initially present in their practice. The Physicians’
8 w1 Z2 p4 s) \  {Desk Reference and package insert should also put a
8 z+ ?4 Y4 Z+ J6 R# E0 jwarning about the virilizing effect on a male or
  j& V$ ]: |) m- X, s1 }; a2 N, q: A( Cfemale child who might come in contact with some-
3 F% C/ V) h# P' |* bone using any of these products.
. E( ]. V( X! b( j* KReferences* m, G$ P! J: k5 D  s
1. Styne DM. The testes: disorder of sexual differentiation7 y3 }7 a. h  R, R+ u
and puberty in the male. In: Sperling MA, ed. Pediatric! ~3 H( Y) L2 ^
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;5 _; |' [8 x$ h- ]9 E' C
2002: 565-628.; t- \# B, T& ^/ A' K$ J
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
2 f4 Q2 h8 a# w7 S$ V* i) }* f& Epuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old  i3 q" V- J9 L, b7 p- Z, @
Boy Induced by Indirect Topical
- j8 P6 S. }8 z4 k5 N5 Z  I$ jExposure to Testosterone
2 J' T7 s( {. n& P& i0 F# ESamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
& {4 ~) F+ `# m; Z  W4 [/ cand Kenneth R. Rettig, MD1
7 G) T! T& V( X! x1 uClinical Pediatrics8 U7 N6 Y% n: @: q
Volume 46 Number 6
4 f- k1 Z- b: ~" m# a! gJuly 2007 540-543
* z+ w, R  O* w3 e© 2007 Sage Publications
" \$ ]$ F7 B0 Y2 r2 c10.1177/0009922806296651+ q5 N- ^9 E: J" P9 X5 V
http://clp.sagepub.com9 P  }2 C5 Z1 a& d6 ~- T5 o2 t
hosted at
; w" n" S% [) A0 mhttp://online.sagepub.com
5 D1 o/ x3 k; t- X. T7 X6 \: APrecocious puberty in boys, central or peripheral,* f( U" Z% u6 S: O  v) K" ]
is a significant concern for physicians. Central
- |2 \/ J" i, ?+ {0 S6 a9 oprecocious puberty (CPP), which is mediated% I' |. b& }# B4 d0 c3 ?) g
through the hypothalamic pituitary gonadal axis, has
: e0 P  K* }6 ra higher incidence of organic central nervous system9 h6 q* d; c+ s( n' ]5 D! z
lesions in boys.1,2 Virilization in boys, as manifested
9 g4 G0 j# h6 d: Vby enlargement of the penis, development of pubic
4 ~+ |) f! ^5 O* khair, and facial acne without enlargement of testi-
! c7 W. }1 t: Q9 n' U# }1 f) Ncles, suggests peripheral or pseudopuberty.1-3 We
/ c* r" b; |' h3 treport a 16-month-old boy who presented with the( \% {7 A' [, m8 x; d# Z  k
enlargement of the phallus and pubic hair develop-
8 S1 A1 g) F; y/ S* ?/ Mment without testicular enlargement, which was due# W- M7 C5 n8 w3 [" h9 B+ W# x3 k/ j
to the unintentional exposure to androgen gel used by
) i/ p- O. R7 W6 w: p. tthe father. The family initially concealed this infor-0 K0 ]% D( J8 ?
mation, resulting in an extensive work-up for this
! M$ }) }% g3 L* s: `( z( Fchild. Given the widespread and easy availability of
0 U9 Y6 |; e. U* N/ U* P) Stestosterone gel and cream, we believe this is proba-
% W- `1 j* ~" ?bly more common than the rare case report in the1 [4 Q7 Q6 s  v
literature.4  E- h2 S1 v& z9 O$ w2 @; ^
Patient Report
& L2 Y8 }1 O- e5 T) R, {/ B- vA 16-month-old white child was referred to the$ d2 `2 b2 T3 p0 M( o
endocrine clinic by his pediatrician with the concern
/ _: ?/ a# y8 jof early sexual development. His mother noticed. l, T, w* a2 o, I
light colored pubic hair development when he was
* A2 h" s+ K1 P$ P1 Y6 K8 `5 V, k/ E9 a8 }From the 1Division of Pediatric Endocrinology, 2University of' N4 M# @. o, r2 c$ K1 |6 L/ P% q
South Alabama Medical Center, Mobile, Alabama.
8 g2 ^$ _8 T: q  {' Y) q, YAddress correspondence to: Samar K. Bhowmick, MD, FACE,
- j$ w# z; e! I5 n9 x- u- `' DProfessor of Pediatrics, University of South Alabama, College of: T8 O9 m/ G: T9 d8 W
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
7 [4 {) h& q5 a& K. M/ a- A6 v" ce-mail: [email protected].9 i0 p; n( M; S  s# Z+ S$ H
about 6 to 7 months old, which progressively became# f* z. U0 S0 T, G' n( `
darker. She was also concerned about the enlarge-$ s5 B2 w8 W7 R, Y
ment of his penis and frequent erections. The child
/ J- F" F8 b0 G* p- Nwas the product of a full-term normal delivery, with
1 [% {9 E. W) wa birth weight of 7 lb 14 oz, and birth length of
/ Q# Q8 v2 k) ]( L4 R5 P20 inches. He was breast-fed throughout the first year$ e/ b4 E5 O7 L+ j: L1 c8 i' N% o
of life and was still receiving breast milk along with; Z# z1 T( |* _8 i$ k
solid food. He had no hospitalizations or surgery,- ?" B* z; ?6 D
and his psychosocial and psychomotor development
2 Y( H, O! o8 D; h. b# P% awas age appropriate.
: Q  n5 V" y8 U/ I, OThe family history was remarkable for the father,
) G2 c( s% p! M' J( h; R" x5 {) jwho was diagnosed with hypothyroidism at age 16,
  `! T7 f( \, M* \! M8 @which was treated with thyroxine. The father’s9 X' i2 Y" R4 M! W
height was 6 feet, and he went through a somewhat
8 e/ i* D) w1 ^3 j* pearly puberty and had stopped growing by age 14.
3 M7 G( _, |* V8 T% S4 \! dThe father denied taking any other medication. The
$ A9 s! s' n0 c' qchild’s mother was in good health. Her menarche* c5 l8 n' q2 F5 ?, u
was at 11 years of age, and her height was at 5 feet
. c' R* U4 a% N% F6 q+ b8 ~( Z5 inches. There was no other family history of pre-/ t1 i1 c9 I0 K3 @* i: S
cocious sexual development in the first-degree rela-
2 Z. u" a! R' \  V, Ytives. There were no siblings.. s" S3 x& c" R2 Q
Physical Examination
  P% q" t" I- j# y  PThe physical examination revealed a very active,
1 i/ @. R7 k& K! R( Lplayful, and healthy boy. The vital signs documented/ F) U5 g/ h, D8 L) w/ v( }
a blood pressure of 85/50 mm Hg, his length was* B% K% P# ~+ {0 A! n- r/ F
90 cm (>97th percentile), and his weight was 14.4 kg! V8 Y& S$ i3 U& A
(also >97th percentile). The observed yearly growth9 a- a; U# f# e+ @6 s" j$ l) s
velocity was 30 cm (12 inches). The examination of- N* f- d7 X( j, q& L$ j
the neck revealed no thyroid enlargement.( x, A1 }  w' W$ A# D; c
The genitourinary examination was remarkable for
5 r/ P) L7 S2 s6 G1 F$ Venlargement of the penis, with a stretched length of! S8 U& o1 ^$ |7 s3 _5 Z1 Q3 Q
8 cm and a width of 2 cm. The glans penis was very well, R) _. i) w1 j
developed. The pubic hair was Tanner II, mostly around
" l- E' r% a- C5 Y  p# E540( m. Q  r& s# B" D8 z! w, I# R0 `" H) {
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
7 d0 M# |/ J6 y, H7 Gthe base of the phallus and was dark and curled. The
- M& \5 Q* _- k/ Q% Btesticular volume was prepubertal at 2 mL each.
' X- X5 z5 c! n' gThe skin was moist and smooth and somewhat
+ _. }% O. e' u  B* s7 H, t6 |oily. No axillary hair was noted. There were no; q# [/ I. T1 v' b
abnormal skin pigmentations or café-au-lait spots.5 s0 y+ U+ p, W1 j* O
Neurologic evaluation showed deep tendon reflex 2+
! I3 I5 {8 G: ^3 m$ q! `* sbilateral and symmetrical. There was no suggestion/ V( E# C3 _8 }( Y) ^* U/ ?  y! X
of papilledema.; P4 e  v$ i, p% S
Laboratory Evaluation
5 U1 R+ g# E7 x  O, XThe bone age was consistent with 28 months by
$ O% k$ q$ n* L3 i8 H! T# l+ I3 @using the standard of Greulich and Pyle at a chrono-
- `( [; i% G8 [1 t* Glogic age of 16 months (advanced).5 Chromosomal
" D& N/ c, g1 [5 ikaryotype was 46XY. The thyroid function test6 p! m. O' J, W5 z% d7 k6 D
showed a free T4 of 1.69 ng/dL, and thyroid stimu-+ d& a" U# \7 O# r2 W
lating hormone level was 1.3 µIU/mL (both normal).. Y8 V7 I* ^2 Z: G
The concentrations of serum electrolytes, blood% W. f+ f9 a$ R  ^
urea nitrogen, creatinine, and calcium all were
( D$ F! r$ }+ u! V. R1 B+ Jwithin normal range for his age. The concentration
; W; z+ G4 [9 ~% bof serum 17-hydroxyprogesterone was 16 ng/dL) D/ ~9 b0 v  I1 ^! t* D! ]7 K! V+ q+ z
(normal, 3 to 90 ng/dL), androstenedione was 20& ]& B  i# E! l& B
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-1 g( J& o/ J$ X3 Z" k% i% y+ T% Y2 _
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
  {3 S$ a; p& N- y: [" rdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
4 {0 w) m$ L/ M+ M' c  C8 M- A/ O49ng/dL), 11-desoxycortisol (specific compound S)
5 D) x; l& U. u# n; d, Cwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-0 ^7 w3 t1 L% R6 P  Q) ^
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
* G# r( H2 }4 M' {7 i& y* B. Wtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),9 q$ u% _  a: g) n  l
and β-human chorionic gonadotropin was less than* }9 S$ V/ ]1 B( R
5 mIU/mL (normal <5 mIU/mL). Serum follicular" m; W4 \+ {1 B+ @2 i$ A7 X2 t2 S
stimulating hormone and leuteinizing hormone
; C" Y6 Y( ^  x1 ^3 X7 p$ pconcentrations were less than 0.05 mIU/mL
- C3 r. e  u4 i5 e2 z8 Q, h(prepubertal).+ g: W* Z3 N, P' g( q1 L; U
The parents were notified about the laboratory" H) G% \- j! p1 x
results and were informed that all of the tests were
* v0 ]: M$ `4 N) ^- z( o" c8 m3 }normal except the testosterone level was high. The
: v* u- u/ Q) H; [/ x: dfollow-up visit was arranged within a few weeks to
  S4 A9 V' X  o0 A/ Wobtain testicular and abdominal sonograms; how-
4 j& z6 H( n" `( x5 Z* R& x- mever, the family did not return for 4 months.
) S; }' D5 h! K& N" c7 y+ MPhysical examination at this time revealed that the
' p/ w& _& T" Ochild had grown 2.5 cm in 4 months and had gained
( @- V8 `& |+ \/ K" |: X& `7 q$ f* d2 kg of weight. Physical examination remained
" X9 U' E% K, sunchanged. Surprisingly, the pubic hair almost com-( ^& _$ o0 ]5 X5 j# Z/ r/ r2 `$ ?
pletely disappeared except for a few vellous hairs at. @7 _' v/ B. V/ i- l% S7 l
the base of the phallus. Testicular volume was still 2
! G: L. o( P1 M6 n) [2 Q- LmL, and the size of the penis remained unchanged.$ O/ F4 Y+ M7 T: e
The mother also said that the boy was no longer hav-- d: ]# K0 e( C
ing frequent erections.- M" b% M: C! G# f/ o
Both parents were again questioned about use of) k2 }1 x" G. E! X
any ointment/creams that they may have applied to9 Q* ~: E! `  l' w# Y( @/ `2 h
the child’s skin. This time the father admitted the
% j: W; x) R( V0 \2 a) TTopical Testosterone Exposure / Bhowmick et al 541
8 o& z7 \7 ~# |% m8 e, D+ h7 Iuse of testosterone gel twice daily that he was apply-2 B. P2 v1 w1 D# u4 [% [3 v9 n
ing over his own shoulders, chest, and back area for9 A. h% p  R/ U' T+ r+ m/ ^
a year. The father also revealed he was embarrassed& c6 g3 _' Y4 L' d$ Y
to disclose that he was using a testosterone gel pre-
2 b4 T3 l" B7 R5 nscribed by his family physician for decreased libido
+ b0 @- U/ ]3 C9 W: d* {8 ?! F4 Ssecondary to depression.9 K3 `& J8 L) M7 V
The child slept in the same bed with parents., @4 a) n" {/ b3 r" a
The father would hug the baby and hold him on his
+ r; g0 F% D5 {# f2 pchest for a considerable period of time, causing sig-# p3 d( W6 k! h1 i
nificant bare skin contact between baby and father.
- l* ?2 N1 c- z8 vThe father also admitted that after the phone call,
- n5 [3 g. j& z$ Zwhen he learned the testosterone level in the baby
5 ]3 q3 G/ k* v2 B) Bwas high, he then read the product information
5 M" T5 B& j/ H- f' lpacket and concluded that it was most likely the rea-
) c( y& d$ c& W, u; {& `6 vson for the child’s virilization. At that time, they
) l7 `; _; ]% hdecided to put the baby in a separate bed, and the2 r5 O( j3 j( q; _& ?
father was not hugging him with bare skin and had7 q+ z, Y+ O- J" C) P2 m2 z/ D* k3 }
been using protective clothing. A repeat testosterone
0 j! w# w. C/ W$ C  ftest was ordered, but the family did not go to the
2 V) y4 ^( [4 |4 X9 h0 i/ Mlaboratory to obtain the test.$ w# q0 ]8 l7 f% }) y) K
Discussion
3 E- d1 X: P( ~* ]  EPrecocious puberty in boys is defined as secondary
2 l- A* S5 n6 ksexual development before 9 years of age.1,4
; W) k0 y  m# r6 T" lPrecocious puberty is termed as central (true) when9 B0 n  a- z- t& h, B" C
it is caused by the premature activation of hypo-5 i* J; n- j7 P: c6 h/ }& |4 F6 D
thalamic pituitary gonadal axis. CPP is more com-) Z: z/ Q- \4 m* O$ C5 q  j' w
mon in girls than in boys.1,3 Most boys with CPP
4 V2 N5 ~+ C4 z/ d. Pmay have a central nervous system lesion that is6 Q: v# [' R7 G2 [% P
responsible for the early activation of the hypothal-
4 O1 W/ {8 e4 m/ v5 d' T' Camic pituitary gonadal axis.1-3 Thus, greater empha-
# v- ]  P& w( \) [sis has been given to neuroradiologic imaging in' H+ O) t1 X1 }) I( H
boys with precocious puberty. In addition to viril-7 p' k( N9 s5 r
ization, the clinical hallmark of CPP is the symmet-
$ K! F( }; Q3 a2 q& s; V. T/ h2 z4 B1 yrical testicular growth secondary to stimulation by
1 P# [4 a5 t- K5 I  ogonadotropins.1,3
3 l7 `4 a3 P6 y. dGonadotropin-independent peripheral preco-4 \2 _2 }: Z% J. {- J2 X
cious puberty in boys also results from inappropriate
8 b; J" P) R: }$ a. R) _androgenic stimulation from either endogenous or
- W3 m1 v; p. V& lexogenous sources, nonpituitary gonadotropin stim-2 R' z% ]& ]7 `0 \* g* \0 y
ulation, and rare activating mutations.3 Virilizing
, D+ P& j6 W* [# k% ?2 ]9 Ccongenital adrenal hyperplasia producing excessive
% T9 N+ C1 b# G- x8 oadrenal androgens is a common cause of precocious7 R+ C& k3 `0 R' [
puberty in boys.3,4
, ~; W. z6 v# \" W/ yThe most common form of congenital adrenal
2 I' @% M( E% s0 `2 m$ k4 whyperplasia is the 21-hydroxylase enzyme deficiency.2 f4 U3 {+ `$ u- L+ U6 r0 m
The 11-β hydroxylase deficiency may also result in- b: @% q1 k7 u9 S) h% c
excessive adrenal androgen production, and rarely,
8 Y4 l& k+ B" u6 {# Van adrenal tumor may also cause adrenal androgen
8 h/ j' B7 e. b8 L* E7 R0 T5 e$ {; B( bexcess.1,3) T3 E  N- @5 g: L; G" V: Q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* G' b" ?- E; B- ^  [542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
. z1 r# G# {! IA unique entity of male-limited gonadotropin-0 R$ V5 w: ^2 {
independent precocious puberty, which is also known
2 D- W; `  `4 Z. Oas testotoxicosis, may cause precocious puberty at a8 P; F4 n9 C( d! w! y5 e
very young age. The physical findings in these boys
7 a$ J) T% y! F5 T8 I/ ~$ [with this disorder are full pubertal development,; T1 `* z- p1 s! ]2 [/ b
including bilateral testicular growth, similar to boys
& k5 _8 m6 v; L, Swith CPP. The gonadotropin levels in this disorder
0 g  _5 M: W' g9 {3 j5 qare suppressed to prepubertal levels and do not show6 E: \- |# C: m4 P
pubertal response of gonadotropin after gonadotropin-
6 F# b3 S. m* s0 D; k3 ^releasing hormone stimulation. This is a sex-linked  |* U: R0 d8 f  q3 K- j
autosomal dominant disorder that affects only" N5 t, A' J( q! U3 a) E( V9 w
males; therefore, other male members of the family" L8 {8 X3 W/ c
may have similar precocious puberty.31 q( y  I5 A6 S- q. |
In our patient, physical examination was incon-
( l6 c( \+ y/ Asistent with true precocious puberty since his testi-% I9 n% C+ h: D$ x: y* Y
cles were prepubertal in size. However, testotoxicosis; u4 R6 P8 _/ _
was in the differential diagnosis because his father
& m7 z' I7 J! Xstarted puberty somewhat early, and occasionally,
7 T: Q  s, F- I- Rtesticular enlargement is not that evident in the
, g: q' t5 k9 O9 Y; b+ Bbeginning of this process.1 In the absence of a neg-
' t; q- q+ x4 W, Z3 g* Jative initial history of androgen exposure, our9 K; V/ B) Z/ h- E* p
biggest concern was virilizing adrenal hyperplasia,
2 t( [' M$ R$ ^2 i& Ceither 21-hydroxylase deficiency or 11-β hydroxylase
1 z3 T4 M' z$ p- r* bdeficiency. Those diagnoses were excluded by find-: G7 }" l2 D/ @
ing the normal level of adrenal steroids.
3 ~5 m2 Z: h+ x4 e* K" TThe diagnosis of exogenous androgens was strongly
5 c. W  b% V1 b8 H7 }suspected in a follow-up visit after 4 months because; a2 F+ _: G; s3 P- w- K* b# Q
the physical examination revealed the complete disap-
! t. a* Z, B. O! d) [& V- upearance of pubic hair, normal growth velocity, and% }9 u9 `9 t) F# ?, }# U  j
decreased erections. The father admitted using a testos-1 w6 t& m! }1 f1 w' `
terone gel, which he concealed at first visit. He was  K* G( p9 J9 l/ W6 W; W6 i
using it rather frequently, twice a day. The Physicians’* ~0 K( |! ?# M) U& w
Desk Reference, or package insert of this product, gel or: g2 F8 t5 Y6 h& B+ m6 O
cream, cautions about dermal testosterone transfer to4 w' [$ `. J8 u* W: D
unprotected females through direct skin exposure.6 O( q3 O2 h+ j8 D$ w9 d
Serum testosterone level was found to be 2 times the3 j( Q9 d1 I/ U4 m1 x8 {
baseline value in those females who were exposed to
$ m' H  h% _6 N' a4 @4 Z2 Seven 15 minutes of direct skin contact with their male$ X4 F; \: h! Y. u( X% ?8 |
partners.6 However, when a shirt covered the applica-/ J: C2 q% p1 W; W
tion site, this testosterone transfer was prevented.0 R& ]- w. w* q! f- ~
Our patient’s testosterone level was 60 ng/mL,+ U* D1 a& J. |
which was clearly high. Some studies suggest that
% x1 |8 X4 y6 V2 `# zdermal conversion of testosterone to dihydrotestos-
9 v9 Z7 ?! j1 u, s. qterone, which is a more potent metabolite, is more
# O; j7 w4 e+ C8 y* P- s1 yactive in young children exposed to testosterone, _6 _& R0 v' y; x) `
exogenously7; however, we did not measure a dihy-
- T! ]% m2 H' S9 }' m5 w8 xdrotestosterone level in our patient. In addition to- z; R6 o# [. k' C" u6 }
virilization, exposure to exogenous testosterone in" R) \" o! }7 N# g/ @& |" p
children results in an increase in growth velocity and
% O6 r3 o# x) _1 F5 k2 nadvanced bone age, as seen in our patient.& X" h* W; s9 M6 C5 p5 C7 x
The long-term effect of androgen exposure during# s# V, D( v6 ~( X& }; M0 U; q
early childhood on pubertal development and final
) B/ t" k1 u/ A0 ]; l, L  C/ iadult height are not fully known and always remain* {: x/ ~4 Y8 n
a concern. Children treated with short-term testos-
) _: S" j! ~* ]* K+ fterone injection or topical androgen may exhibit some' _# E" S8 S+ E  ^5 Q! T$ i0 u; T
acceleration of the skeletal maturation; however, after
' m& x8 J0 V- |) Y' G6 Icessation of treatment, the rate of bone maturation: `# H- D8 h1 s9 c) ]
decelerates and gradually returns to normal.8,9
8 _6 H7 f/ G4 e: C, wThere are conflicting reports and controversy. p. z8 }, E. Q( i3 Z5 f0 M
over the effect of early androgen exposure on adult* W$ K4 q, ~7 e5 b
penile length.10,11 Some reports suggest subnormal
* ]; f; W+ G( y' N; padult penile length, apparently because of downreg-
  T% ?$ x1 m: z0 \ulation of androgen receptor number.10,12 However,$ f5 x+ r5 S. v+ O8 i& w- M
Sutherland et al13 did not find a correlation between# [, e5 p  D0 }5 I! W- d$ c
childhood testosterone exposure and reduced adult# h& N9 O+ y/ {! b, Q. a
penile length in clinical studies.
* L/ W6 c6 |+ S4 B! w, kNonetheless, we do not believe our patient is
- A- _2 w4 b- q5 n& [0 _3 Kgoing to experience any of the untoward effects from
0 o3 v# D8 G, E# ]" u3 ?/ U- W2 gtestosterone exposure as mentioned earlier because
8 O/ t9 g  o2 T0 a) @the exposure was not for a prolonged period of time.% P2 C0 ]" C1 g: B( U6 S
Although the bone age was advanced at the time of' b. d4 U( {, ]0 D, w( h
diagnosis, the child had a normal growth velocity at
; t0 g9 k6 ?: L' k9 _! ythe follow-up visit. It is hoped that his final adult2 F; K0 q: E% U/ _, Q: N
height will not be affected.$ U! V* D' _* c, N+ U  h* S
Although rarely reported, the widespread avail-
" ^- x7 O1 D9 }' n" t2 Tability of androgen products in our society may5 y/ D: v2 W+ h. q# G+ ^8 e7 \  B
indeed cause more virilization in male or female
- _" S8 F% I! Schildren than one would realize. Exposure to andro-
2 T# q, b. X& p; Z3 v2 t& V  rgen products must be considered and specific ques-
; ^/ \7 ?+ N9 [9 M7 z- jtioning about the use of a testosterone product or
+ \% d; \2 O( `0 Ngel should be asked of the family members during
" y! M, s! `" ^: |1 O+ Lthe evaluation of any children who present with vir-
3 P) e! P; }( Jilization or peripheral precocious puberty. The diag-' g9 F4 ^7 n" q* e2 m6 E- z
nosis can be established by just a few tests and by9 @) g- Y( L1 y. F8 T) e- O
appropriate history. The inability to obtain such a
! M( w+ M8 ~- V& x  j) hhistory, or failure to ask the specific questions, may3 R) Z/ U" l" c( ~: o
result in extensive, unnecessary, and expensive9 o( ]6 c5 c; y4 ~
investigation. The primary care physician should be! N  S5 V0 v0 r8 ]3 N
aware of this fact, because most of these children+ l1 X0 x* P) Y# \' M+ M! ?
may initially present in their practice. The Physicians’
3 H! Y' c* m! [# S4 S1 bDesk Reference and package insert should also put a/ s8 w, {, W8 o  A; }
warning about the virilizing effect on a male or
+ `3 [  i% V7 e( h$ Ifemale child who might come in contact with some-" Q- K; t  b4 d$ B7 ?2 `7 N
one using any of these products.. R2 W8 z0 P3 g+ r7 D) v
References
8 |8 A! Y( s$ s- ^1. Styne DM. The testes: disorder of sexual differentiation  x# x- i4 u7 Y5 d4 o
and puberty in the male. In: Sperling MA, ed. Pediatric
8 J8 _0 o3 w* M) l$ oEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
* i4 I0 _' \% \: J8 {: X8 r& i7 n2002: 565-628.$ M" C, b  V6 ]- S* ?4 s3 z
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious, v1 j, f# V) e# d# V
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
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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
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

& {8 U- }! l6 ?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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