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Sexual Precocity in a 16-Month-Old2 E0 o: Y* w0 J5 k
Boy Induced by Indirect Topical5 J, n0 K0 c# S8 P8 `0 {
Exposure to Testosterone. k0 J1 |8 ?2 x, K0 o1 E  Y: c
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
+ U; q  |% q' ?8 k& Uand Kenneth R. Rettig, MD1
8 @' Y- h9 m. C9 M/ X- ^, b# pClinical Pediatrics+ i7 k" t3 `3 n: {' \
Volume 46 Number 6
$ t) N1 l6 j' S- @July 2007 540-543
9 _/ B) _2 _* i& A8 ?© 2007 Sage Publications+ ?5 G( z& [, q  A
10.1177/00099228062966512 ^! l% a3 m8 F. ~, o; s
http://clp.sagepub.com
- v* ?$ S( E2 U; q. ahosted at
! V6 k# r1 N# l  J, E3 ]' y$ @http://online.sagepub.com: C& S' Z0 \( i7 r+ O/ @) V7 t) K
Precocious puberty in boys, central or peripheral," E! v9 M7 I- l4 K% r& m6 T* `
is a significant concern for physicians. Central
8 z8 w& j4 g  ~) t" wprecocious puberty (CPP), which is mediated* u% U! r4 b* U2 y$ P1 S* ~: ?
through the hypothalamic pituitary gonadal axis, has
6 ?8 G; ?! N0 ^& ya higher incidence of organic central nervous system; G8 v' Q7 \8 @% P! }
lesions in boys.1,2 Virilization in boys, as manifested
* l) _: j% s/ c4 m4 O3 q* ?by enlargement of the penis, development of pubic: S' ?( o: c1 g: q9 a$ }9 |
hair, and facial acne without enlargement of testi-& s/ B8 Z# `+ J, z9 O9 W* a  F
cles, suggests peripheral or pseudopuberty.1-3 We# V4 f( Z1 V% r
report a 16-month-old boy who presented with the
: U5 x* m8 }5 p8 a6 `1 u2 zenlargement of the phallus and pubic hair develop-; k* g# O4 H& _0 b$ Q
ment without testicular enlargement, which was due
; T% e! B1 `; P! ?" U5 P8 p( }to the unintentional exposure to androgen gel used by
8 `& ?) \$ v! V& k/ b: ?- xthe father. The family initially concealed this infor-) p: D" u& H2 M) p$ p& [
mation, resulting in an extensive work-up for this
* G3 c% B1 {# ychild. Given the widespread and easy availability of. G& ^$ j: |, w, T
testosterone gel and cream, we believe this is proba-
2 W; n9 |" d+ w+ |" Z5 ably more common than the rare case report in the
; D5 i9 S! B  ?+ y7 L: }literature.4
4 H+ ^) A) X. E5 Y  APatient Report
' {% }+ g% y' y9 ?6 gA 16-month-old white child was referred to the
& A% z& m  T0 ]2 l: c3 mendocrine clinic by his pediatrician with the concern
8 F/ F8 X* a5 ^of early sexual development. His mother noticed8 J+ X3 n" V8 i0 W1 F0 i
light colored pubic hair development when he was
' i% E& H) T( U( lFrom the 1Division of Pediatric Endocrinology, 2University of
. r2 y5 l. P, L! _/ w% y& T7 LSouth Alabama Medical Center, Mobile, Alabama.
; D3 d% i2 F9 lAddress correspondence to: Samar K. Bhowmick, MD, FACE,
. a4 J6 V' p4 K8 L/ A1 L$ XProfessor of Pediatrics, University of South Alabama, College of
9 P6 }# p- j9 M% Q4 d; J4 ?1 j" zMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;1 ]: o! j) y5 x4 x9 K
e-mail: [email protected].
. `7 n( s0 |/ w: C2 z& e8 u$ Kabout 6 to 7 months old, which progressively became
& [% S  y& e2 a$ q; z3 w) hdarker. She was also concerned about the enlarge-
# I1 T3 [+ B- r  J5 |" \2 ]; a$ `+ pment of his penis and frequent erections. The child
5 C0 O7 ^! G% M6 j  X2 ~/ Iwas the product of a full-term normal delivery, with& z( e$ p% v) U
a birth weight of 7 lb 14 oz, and birth length of/ e+ _3 y4 F/ {9 C
20 inches. He was breast-fed throughout the first year
- T/ T$ W: A/ l# y0 Sof life and was still receiving breast milk along with
) W3 M( `, f0 Bsolid food. He had no hospitalizations or surgery,
7 X' w; K6 ?& B3 a. O# {and his psychosocial and psychomotor development
% H3 C- F# B: ]1 O* W' Dwas age appropriate.( O( `% z% [8 L; P8 V
The family history was remarkable for the father,
! E9 \' d' c8 z# h2 ^2 [$ Z1 h7 xwho was diagnosed with hypothyroidism at age 16,: H7 p/ d9 l+ w- a* ~
which was treated with thyroxine. The father’s4 R4 k5 I7 K0 a2 p0 N' g
height was 6 feet, and he went through a somewhat
, o8 l7 o0 j8 m5 ^4 a- C( _1 Dearly puberty and had stopped growing by age 14.
# q' n' ]7 d; wThe father denied taking any other medication. The# l' {( k8 I5 b2 q* t9 O3 L! B
child’s mother was in good health. Her menarche5 O: v  X0 z' R9 K' ^
was at 11 years of age, and her height was at 5 feet
7 m; l9 t) P; ~0 X' t* `5 S5 inches. There was no other family history of pre-8 _& H# K: {) T, q* I0 Y
cocious sexual development in the first-degree rela-. n; X3 I6 A+ E: s& u* m! M: c. x
tives. There were no siblings.
1 _/ @) n0 X+ ^4 F; l. jPhysical Examination/ e2 z7 G2 J$ a: p
The physical examination revealed a very active,
+ i& g. j2 h, V0 V' [playful, and healthy boy. The vital signs documented3 L( r% ]. i6 j" ^$ h
a blood pressure of 85/50 mm Hg, his length was) K- e6 k) F' q, V
90 cm (>97th percentile), and his weight was 14.4 kg
" M" o: ^2 d& p, S" D7 b/ }(also >97th percentile). The observed yearly growth
" h; ~6 w( [) z* Q5 q( x3 Ivelocity was 30 cm (12 inches). The examination of# x* _4 i7 p* l- K3 U9 b" m
the neck revealed no thyroid enlargement.6 ~3 z! U' W; `
The genitourinary examination was remarkable for
; M5 D# o+ l) G, s" Penlargement of the penis, with a stretched length of
" `3 b# f1 B( c5 O; Z# _6 `! V2 r8 cm and a width of 2 cm. The glans penis was very well; J/ F2 F+ t+ ^% N7 i
developed. The pubic hair was Tanner II, mostly around; y. b( z% O1 U
540
: {. b' \: n3 w: I# u4 zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# e; c" \% M  Y: q8 K: d; |the base of the phallus and was dark and curled. The
% p2 F: ]0 c, i; Rtesticular volume was prepubertal at 2 mL each.$ c# a: V9 y! T* w; a+ p/ @) w& o
The skin was moist and smooth and somewhat- S5 t* s$ X8 ?7 u5 N* X' y
oily. No axillary hair was noted. There were no! b7 k6 v% r, z( o' M
abnormal skin pigmentations or café-au-lait spots.) D. C9 \& [6 o9 t& {
Neurologic evaluation showed deep tendon reflex 2+) s0 H& A1 ]0 Y% Q( I
bilateral and symmetrical. There was no suggestion
  Y3 Z( P; J) a1 uof papilledema.
0 a; |$ U. F- H% M' g1 q; MLaboratory Evaluation+ |3 K1 V3 R, p. `1 b' g9 h3 o
The bone age was consistent with 28 months by
) F, `3 K. w9 Q8 H* {8 q/ yusing the standard of Greulich and Pyle at a chrono-' M* `8 R  M8 U. x
logic age of 16 months (advanced).5 Chromosomal
/ h( t- n% N7 F  ckaryotype was 46XY. The thyroid function test
% B. [) q+ i. m& y3 D1 J0 s% X" ?: Sshowed a free T4 of 1.69 ng/dL, and thyroid stimu-# o& x+ m: u9 D( p1 v; g9 G
lating hormone level was 1.3 µIU/mL (both normal).  h1 X# q7 k$ h6 R  \2 A3 ~0 E3 K0 `
The concentrations of serum electrolytes, blood
3 p9 Q+ u# Q$ ]1 B! D" _( @9 U6 Purea nitrogen, creatinine, and calcium all were* m8 M1 F& c! |% T, Q2 q  ?
within normal range for his age. The concentration
$ o0 [3 I5 [$ a4 Mof serum 17-hydroxyprogesterone was 16 ng/dL
+ T# K" p2 N4 O1 x9 V8 H: Y* m, U(normal, 3 to 90 ng/dL), androstenedione was 20' F3 K' Q+ D7 }9 B0 M
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
: n# f' D, I9 j* l6 Q# h7 cterone was 38 ng/dL (normal, 50 to 760 ng/dL),
7 b  C2 e( G2 b+ M: rdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
  Z2 v2 \1 V6 U) i, d/ `8 @0 b49ng/dL), 11-desoxycortisol (specific compound S)& u  t  j. Q+ E
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- C3 I6 B- n0 ~4 o
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
, J/ q3 L" H) o+ c6 S( qtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
8 }. [, n; b" s4 l  O; I3 pand β-human chorionic gonadotropin was less than
( O/ j9 y& k+ J1 O5 mIU/mL (normal <5 mIU/mL). Serum follicular
9 Z8 u; X& O, j8 T6 zstimulating hormone and leuteinizing hormone) Z( ]! M" P# \; O4 @" L' @
concentrations were less than 0.05 mIU/mL7 x# M- h3 i% u8 x- R$ M
(prepubertal).3 F0 ^3 t5 @4 k) i) @0 _
The parents were notified about the laboratory# m( J7 R3 j0 o2 H1 D! ^/ a1 y
results and were informed that all of the tests were
! ^5 J8 u( S- t! Ynormal except the testosterone level was high. The
/ ~- q+ h' i9 b0 g  t3 Qfollow-up visit was arranged within a few weeks to
6 k  m% W- E$ _* Y4 Fobtain testicular and abdominal sonograms; how-
2 G3 ~( {. L  u$ F4 {ever, the family did not return for 4 months.
" R2 d/ N, K9 a& r2 M' m( U8 TPhysical examination at this time revealed that the% L2 `8 n/ Q; h, a/ x' I
child had grown 2.5 cm in 4 months and had gained. k' f& N& k" m4 W
2 kg of weight. Physical examination remained
5 \4 A" N0 [& _unchanged. Surprisingly, the pubic hair almost com-9 Y/ Z5 N/ b$ f) @
pletely disappeared except for a few vellous hairs at
+ O% H8 l7 B8 A' N- ithe base of the phallus. Testicular volume was still 2& U3 x# M6 M% W; H
mL, and the size of the penis remained unchanged.
4 o4 z4 j8 E+ C' Z4 j5 K2 Y% {! ^4 Y) uThe mother also said that the boy was no longer hav-9 P9 z2 I7 f7 P3 q% M7 G
ing frequent erections.9 X9 q+ J+ F# u. x- _! D
Both parents were again questioned about use of
. I0 W$ k, }: sany ointment/creams that they may have applied to" `7 D& A6 g5 Y/ j
the child’s skin. This time the father admitted the
0 C: w, O7 g1 T. _* l7 qTopical Testosterone Exposure / Bhowmick et al 541( t: Z+ A( z3 S  V8 V8 o
use of testosterone gel twice daily that he was apply-) [0 U, |" {" H2 ^: z
ing over his own shoulders, chest, and back area for' y( |2 k+ e/ X
a year. The father also revealed he was embarrassed
$ K8 N2 v7 }" m5 f) r- y0 wto disclose that he was using a testosterone gel pre-
0 S5 \/ H' K  b# r' J4 @- W3 g/ c) Tscribed by his family physician for decreased libido/ h2 y$ @0 n9 R2 v# E: S0 X
secondary to depression.5 k0 B7 `- w, u
The child slept in the same bed with parents.* d$ M9 d! w; |7 {( J  F! L
The father would hug the baby and hold him on his  N+ D4 d" C6 o; U5 {; a
chest for a considerable period of time, causing sig-
0 I( H% q, y. jnificant bare skin contact between baby and father.
6 e! q& K/ R* y- r! zThe father also admitted that after the phone call,' z# O; b' r/ K; h
when he learned the testosterone level in the baby
" ]- l) k" c  ?/ {: iwas high, he then read the product information
2 D' o: v2 W2 v/ s! opacket and concluded that it was most likely the rea-! n1 O. [9 [. g/ W+ [
son for the child’s virilization. At that time, they
+ i' ]  g& ^2 x; ], a8 _decided to put the baby in a separate bed, and the
; @9 T8 F' p# {9 V2 J% kfather was not hugging him with bare skin and had
' n; j6 s- w% kbeen using protective clothing. A repeat testosterone5 ]* f5 c. k0 I7 Z; ^$ z  g0 _% k
test was ordered, but the family did not go to the
9 g3 V( l0 D& f; k+ [# Klaboratory to obtain the test.9 y4 f5 ]% W; i& f$ ]
Discussion8 F0 }3 B+ X5 S" D  D2 q5 o6 n
Precocious puberty in boys is defined as secondary
9 J3 N0 n  E+ p, M. G9 i  d4 |' @sexual development before 9 years of age.1,4
7 i$ T3 k9 M1 @' M2 `6 `8 U3 lPrecocious puberty is termed as central (true) when& A; t4 H$ g* s& R
it is caused by the premature activation of hypo-
' I8 A3 X& O& {thalamic pituitary gonadal axis. CPP is more com-% l6 |3 D  f8 o- n0 v5 |8 b# e0 \
mon in girls than in boys.1,3 Most boys with CPP$ e: u% ]- O7 |2 D& C& J  M
may have a central nervous system lesion that is
2 y# `' _, N9 }3 Z, l' v. P, {responsible for the early activation of the hypothal-# f2 D6 X3 B6 P+ }, T# x- g
amic pituitary gonadal axis.1-3 Thus, greater empha-3 u* c. R( r6 p5 Z6 {% ?! G
sis has been given to neuroradiologic imaging in
9 r: l- g) {  S0 {/ lboys with precocious puberty. In addition to viril-0 V2 q2 d4 d3 S  J
ization, the clinical hallmark of CPP is the symmet-
) P+ B! @. T6 R4 {# l; B) Mrical testicular growth secondary to stimulation by
6 x4 W- @: l9 Zgonadotropins.1,3
  K/ l* O0 Z5 X4 q# k1 W7 R& lGonadotropin-independent peripheral preco-. D  P8 x, b$ Z1 n. G
cious puberty in boys also results from inappropriate
6 ?" L$ M8 h& V8 f$ L  Oandrogenic stimulation from either endogenous or8 A  r& Y  g' G
exogenous sources, nonpituitary gonadotropin stim-+ ]5 w& _9 U1 C% ~8 E3 d5 S
ulation, and rare activating mutations.3 Virilizing/ k) S+ m3 c$ U8 S
congenital adrenal hyperplasia producing excessive
- B2 I8 Y  T9 `& Q1 \; ]adrenal androgens is a common cause of precocious
2 U1 t* K  ?0 l8 \- k. Gpuberty in boys.3,4
' M: x+ M8 b" t. v" dThe most common form of congenital adrenal
6 G) p" r0 ~" n: s2 nhyperplasia is the 21-hydroxylase enzyme deficiency.
! e( n/ t. W' F% e8 d2 s' eThe 11-β hydroxylase deficiency may also result in1 T* @7 k3 R5 E& e, x3 R
excessive adrenal androgen production, and rarely,
) b, \% {" S0 T+ f6 l# jan adrenal tumor may also cause adrenal androgen
2 [# d7 \/ j* |: h' C4 J# zexcess.1,3
4 K5 S! J4 h+ m- H' o0 v' `at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. e& V0 `; H# }0 C3 S6 C
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
. T' @3 Y/ T& z) [4 M7 AA unique entity of male-limited gonadotropin-
  E) ^4 o; Z; \0 u9 d% C9 Pindependent precocious puberty, which is also known4 U+ U$ l* R* Q
as testotoxicosis, may cause precocious puberty at a
& D- U& I0 u( ?1 n! l7 m" C- _very young age. The physical findings in these boys  K# x9 j) G6 W5 z9 V
with this disorder are full pubertal development,
) b0 \7 A( P) T" Sincluding bilateral testicular growth, similar to boys
, h# H) L9 S. s( Nwith CPP. The gonadotropin levels in this disorder
( i% P! o+ j# I  w' ware suppressed to prepubertal levels and do not show# D* C6 I( n2 m  J% z
pubertal response of gonadotropin after gonadotropin-1 [0 M* J0 w3 \7 e: q0 {
releasing hormone stimulation. This is a sex-linked
( D2 E! }+ H, a2 ?  E  uautosomal dominant disorder that affects only3 J( k) X5 y$ z3 f$ P4 j
males; therefore, other male members of the family
# s+ t8 S, g/ A, c; ?may have similar precocious puberty.3" V' J4 A, _% q! ?, L
In our patient, physical examination was incon-- w3 h) V; i; \7 \. C4 c) F
sistent with true precocious puberty since his testi-9 h3 ^$ H8 r) T7 F+ P+ @
cles were prepubertal in size. However, testotoxicosis
, G: C2 ]! @8 i( Dwas in the differential diagnosis because his father
( \2 y) K( I+ l  qstarted puberty somewhat early, and occasionally,
1 m7 S% M) ]1 y) Wtesticular enlargement is not that evident in the/ g, D' u+ q! U2 w2 e
beginning of this process.1 In the absence of a neg-
& w' G6 b, D+ K3 r  x- D) m' pative initial history of androgen exposure, our) @, [7 `. Y5 F3 ]9 v
biggest concern was virilizing adrenal hyperplasia,$ e% p: u& ]4 D- t
either 21-hydroxylase deficiency or 11-β hydroxylase
4 B' k; B- [5 s# w4 K- c. G! rdeficiency. Those diagnoses were excluded by find-9 o1 ~0 w% C8 L' q' A$ _+ b
ing the normal level of adrenal steroids.
/ e. Y) Q% T; U6 yThe diagnosis of exogenous androgens was strongly
% p1 N2 Y. d# y+ Y3 j  |( Rsuspected in a follow-up visit after 4 months because
8 d3 P$ x) K: \  I; ethe physical examination revealed the complete disap-
( K$ [# W6 u3 r$ h0 fpearance of pubic hair, normal growth velocity, and
  n5 A; |: V9 L9 _decreased erections. The father admitted using a testos-6 y3 p2 d. w2 s  w# g$ U' g
terone gel, which he concealed at first visit. He was
+ b6 r: q& \1 _( \8 k' ~using it rather frequently, twice a day. The Physicians’
( ^! E! r! ^- P3 KDesk Reference, or package insert of this product, gel or
' \; a! E# {$ Dcream, cautions about dermal testosterone transfer to
" f$ C- ^% [" i7 W1 O* k6 }% F" _, Lunprotected females through direct skin exposure.( D4 O; }3 m% _( M6 q
Serum testosterone level was found to be 2 times the
5 r. g8 k' ~, n0 a+ f  Ybaseline value in those females who were exposed to8 J8 @# w$ ?3 H4 y" s6 [
even 15 minutes of direct skin contact with their male
4 j1 C0 _# h: ^" ]partners.6 However, when a shirt covered the applica-
: Z; g* u2 K/ Q- Ction site, this testosterone transfer was prevented.
! |0 x8 R. S2 V5 NOur patient’s testosterone level was 60 ng/mL,% v, M+ e& e( X6 D7 y
which was clearly high. Some studies suggest that! f4 h# Y: a, j! @% O( `" T- Z
dermal conversion of testosterone to dihydrotestos-' i0 b3 ]# f$ Y! M- c7 l3 D
terone, which is a more potent metabolite, is more- F2 T, s! U! {9 Z* N6 @
active in young children exposed to testosterone+ ^, f' `+ {$ `( E5 h
exogenously7; however, we did not measure a dihy-
! B( s$ m$ H# M! Rdrotestosterone level in our patient. In addition to
$ S) W# I, g* w0 c7 qvirilization, exposure to exogenous testosterone in
6 u9 P/ ]) [  ?. c  H% Ichildren results in an increase in growth velocity and
$ f7 P$ t5 m+ `- fadvanced bone age, as seen in our patient.
1 W. l. h( N3 C* X( E7 A/ WThe long-term effect of androgen exposure during% c# L$ f$ @1 O+ m' v
early childhood on pubertal development and final( x( ^! R- f, x: ]3 M2 w! Z  d
adult height are not fully known and always remain9 C9 p$ H. d* Z! e7 O3 F  B% [3 \" f
a concern. Children treated with short-term testos-
; F2 d2 M6 t9 Bterone injection or topical androgen may exhibit some; T# S( |+ S% p8 z. o
acceleration of the skeletal maturation; however, after
: `: Y2 h" `* K# T1 |cessation of treatment, the rate of bone maturation
" N% N( F- \/ g% zdecelerates and gradually returns to normal.8,95 Z/ {! _5 i! H% t. |* f
There are conflicting reports and controversy
7 H, g5 ]/ W- ?$ X, C& xover the effect of early androgen exposure on adult0 H9 ^  q  p+ B( Y& M; x9 e% G
penile length.10,11 Some reports suggest subnormal
- w  v8 C: X7 c1 H# kadult penile length, apparently because of downreg-
. d) o) v0 Y" p' julation of androgen receptor number.10,12 However,& L' M3 d% _& \7 D+ Q( u  g! a
Sutherland et al13 did not find a correlation between) l% B5 U9 r. O, P8 ~
childhood testosterone exposure and reduced adult/ o8 k$ q& @7 r2 ]
penile length in clinical studies.6 X) C, g6 q8 B& A! L9 ]! g/ N& Z
Nonetheless, we do not believe our patient is( K* j2 n3 i; e( P4 n! X& L
going to experience any of the untoward effects from
' R% ]% \+ G( x  l9 [5 \testosterone exposure as mentioned earlier because
" i& l1 ]3 M; @" lthe exposure was not for a prolonged period of time.
: c# ?+ s+ [) g& O/ ?7 }  eAlthough the bone age was advanced at the time of9 g. b  S# }7 n
diagnosis, the child had a normal growth velocity at
$ H* f* n. [$ E+ Hthe follow-up visit. It is hoped that his final adult$ J: t1 K% f9 p3 \$ o* M
height will not be affected.
$ w4 a( D" z9 G% \( j1 C( ZAlthough rarely reported, the widespread avail-
  i8 X0 w- F5 h: o9 c: K4 T5 rability of androgen products in our society may
% m  V* B0 M+ N7 Q/ A, O) E$ tindeed cause more virilization in male or female, t0 i$ G/ q) Q3 r( r( n3 ]. l: J
children than one would realize. Exposure to andro-
& f6 g. M* @' C: igen products must be considered and specific ques-1 ~4 m4 z% j0 u
tioning about the use of a testosterone product or
2 y  O: Q$ a) hgel should be asked of the family members during  O/ R8 T( S: \9 P/ }
the evaluation of any children who present with vir-
! c' _5 D/ l3 w% K& S, milization or peripheral precocious puberty. The diag-
  |$ T, Z) e) l0 j4 T1 o" vnosis can be established by just a few tests and by6 U7 I, I5 r% F+ O$ q! h
appropriate history. The inability to obtain such a! K# c% B/ Z& B- O' [/ f
history, or failure to ask the specific questions, may
% d9 W9 H$ X% k$ t. _* F' Q5 R5 Uresult in extensive, unnecessary, and expensive3 Y$ r4 K$ A6 p, Y$ E( f
investigation. The primary care physician should be; I' l3 w" y5 s. f: ^- G. _0 B- _4 U9 [
aware of this fact, because most of these children
6 e4 `1 s* ^$ J! k  V! umay initially present in their practice. The Physicians’
0 U  T3 x! J% l* ~Desk Reference and package insert should also put a
/ g9 \( p" j* @) F1 G9 f$ P( ^warning about the virilizing effect on a male or( [' x# U* h4 J
female child who might come in contact with some-; Q* q0 @2 I5 s
one using any of these products.
* u1 `& J8 c* A1 H  H+ r5 fReferences
+ r6 ^4 z6 m1 R% [1. Styne DM. The testes: disorder of sexual differentiation
. o& {* |/ t* \5 s1 Wand puberty in the male. In: Sperling MA, ed. Pediatric# c$ ?7 X6 L1 l- m% P! M6 E
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
' p0 D& |6 }. H, f  A# Z: Z' x2002: 565-628.
7 C9 g. ?* L# J/ X2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious& c. K5 v$ _) q9 j( K3 i8 q7 S
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
7 w6 I! C7 l, J; ^+ M& @* ?* t$ hBoy Induced by Indirect Topical
+ D% s- [1 P# a' h0 ]Exposure to Testosterone, V: P8 d' g2 O: S
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
& s; g/ s8 y& b6 S; O' D) Jand Kenneth R. Rettig, MD1
/ c& W4 y; g8 c, x0 pClinical Pediatrics; X/ ~! v3 m4 k" X! R7 }
Volume 46 Number 6
1 }: j6 U5 [' S- L% jJuly 2007 540-543
- i' t8 H1 [) Z/ q# w' s© 2007 Sage Publications
) R" n& X: T1 t1 D10.1177/00099228062966516 _( ]) c- W# B
http://clp.sagepub.com) y4 i2 K$ q" V2 u" D3 h7 l
hosted at$ n! S' b) {) ]# y: E- P1 ^
http://online.sagepub.com
  v, ^; _4 ^* b- y. mPrecocious puberty in boys, central or peripheral,
0 E' h9 y# n+ U3 ^+ iis a significant concern for physicians. Central3 j8 ]: i9 O6 y+ c# M% y: E+ R
precocious puberty (CPP), which is mediated% D7 d  l; ?- v+ P8 Y* h" v
through the hypothalamic pituitary gonadal axis, has" I8 p; b" }0 O  T6 n
a higher incidence of organic central nervous system5 v9 [( ~9 Y5 _9 R7 e! \% b, Y" H4 p
lesions in boys.1,2 Virilization in boys, as manifested
6 x( z# `5 ]: a" Xby enlargement of the penis, development of pubic( i8 S; _; H) k, d* ~' m$ d2 k
hair, and facial acne without enlargement of testi-
, o2 H( i1 \/ l, Ccles, suggests peripheral or pseudopuberty.1-3 We3 v0 p/ \" q) r5 d# N4 r
report a 16-month-old boy who presented with the! S. X* ^- P2 L, y! l7 s# a: y
enlargement of the phallus and pubic hair develop-+ Y3 ~* l3 M- ~3 ~5 x7 g9 w$ o+ E
ment without testicular enlargement, which was due6 l6 H7 H6 ]# _1 d7 t( k7 N( C
to the unintentional exposure to androgen gel used by
& u- _: h$ O, y% f: |the father. The family initially concealed this infor-
& x% T- z8 b1 X  @mation, resulting in an extensive work-up for this: a5 m: m4 E1 e. S1 t* S
child. Given the widespread and easy availability of
3 p- M5 j% S7 O. m+ ntestosterone gel and cream, we believe this is proba-' j5 \; |2 n  x
bly more common than the rare case report in the% _: C# S3 x/ |, i
literature.40 v  A' R5 l2 m
Patient Report
: {0 b6 _+ X! L7 n: _A 16-month-old white child was referred to the
* F% t1 q$ \( y' l. M) Xendocrine clinic by his pediatrician with the concern0 E1 L8 {! N& f# F5 H# a
of early sexual development. His mother noticed. ~; n; f7 I" k2 W
light colored pubic hair development when he was7 T  O6 C+ C, m6 T$ i
From the 1Division of Pediatric Endocrinology, 2University of9 y) v- \; ]: E$ G- v& c
South Alabama Medical Center, Mobile, Alabama., K/ N  g( N1 `& Q# q+ Q
Address correspondence to: Samar K. Bhowmick, MD, FACE,
* Q" u( A  @' ]) }; WProfessor of Pediatrics, University of South Alabama, College of
) P/ k  F" o5 P) h+ @Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ z* F: q# |5 {: ?
e-mail: [email protected].5 j# ^) l5 z5 b9 p* z
about 6 to 7 months old, which progressively became: M/ @  E3 Y: K" ]: p& t
darker. She was also concerned about the enlarge-) ]' O9 T8 E0 z: i5 Z3 S
ment of his penis and frequent erections. The child
/ m, b% u% L" z" x% awas the product of a full-term normal delivery, with
) u  P: a. G" N3 d4 Y" }- [a birth weight of 7 lb 14 oz, and birth length of
" Z0 ~" \& t# a" E* ~: p2 M2 \7 D20 inches. He was breast-fed throughout the first year( G9 c/ l# X+ ], z( Z
of life and was still receiving breast milk along with9 \+ _. i1 s8 X( K
solid food. He had no hospitalizations or surgery,% _8 T1 X, Z! \' x' x
and his psychosocial and psychomotor development: a1 S1 N- I0 Z3 z8 i+ j
was age appropriate.
7 @# O' B: k4 c6 G$ M8 v- @( [The family history was remarkable for the father,
, L) u: `7 l& x% m% C( ewho was diagnosed with hypothyroidism at age 16,
+ C- J  [" j( ^) m; P; uwhich was treated with thyroxine. The father’s
( G' i4 {8 J! G9 O0 w7 \height was 6 feet, and he went through a somewhat8 o: r( b- @# r, ]; h
early puberty and had stopped growing by age 14.7 o. T8 t  t  e% h6 [! ?# E
The father denied taking any other medication. The
. O$ N6 M8 h( z% ~5 R: `child’s mother was in good health. Her menarche
/ g& z3 q+ P  C2 G& S0 r1 q- J. rwas at 11 years of age, and her height was at 5 feet
" e" l2 {5 t/ L% Q! G5 inches. There was no other family history of pre-+ B# {3 f3 V/ u0 I+ g3 V& c
cocious sexual development in the first-degree rela-
/ q  F! a2 A& T, ^$ o' f. h( ftives. There were no siblings.
" O1 |0 q  `% FPhysical Examination; P; Q7 |! a' u7 C# z
The physical examination revealed a very active,
+ V' J2 E' x# }# ?0 H! F0 eplayful, and healthy boy. The vital signs documented
! _- c; L5 m, R2 s7 la blood pressure of 85/50 mm Hg, his length was
5 h6 f3 \* F* @7 A4 f90 cm (>97th percentile), and his weight was 14.4 kg7 [3 Q! a2 Y' u1 `
(also >97th percentile). The observed yearly growth1 J9 M& f9 o" y% x1 }! H4 L% \
velocity was 30 cm (12 inches). The examination of: e" g0 t3 M" K1 J" p
the neck revealed no thyroid enlargement.$ V! R, `1 a; B' P  a
The genitourinary examination was remarkable for% I' H( p: n' u) d: n
enlargement of the penis, with a stretched length of& x% B6 ~3 K5 H/ P2 P
8 cm and a width of 2 cm. The glans penis was very well
) H; C% ?; d& |8 L1 @" tdeveloped. The pubic hair was Tanner II, mostly around
  d6 \+ H9 e$ s; y2 z4 n' K% G540: H  R* v$ s+ o" O% b
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 N5 g% m% ]+ l; p- o9 |7 n
the base of the phallus and was dark and curled. The
* T* Y+ X9 v) A$ R; ?testicular volume was prepubertal at 2 mL each.) h# x5 ?" d+ l
The skin was moist and smooth and somewhat
( a' F7 B. p5 Y/ ]$ Roily. No axillary hair was noted. There were no) ^1 w) t$ W+ P5 M6 d. F
abnormal skin pigmentations or café-au-lait spots./ H1 `- {$ q+ C" z2 Q3 U4 u
Neurologic evaluation showed deep tendon reflex 2+4 I$ @# N8 a3 j6 V. d, A8 F
bilateral and symmetrical. There was no suggestion, O( J3 {. ^8 n6 K1 g; B
of papilledema.9 _# r; l6 E5 O" v1 v0 F  |
Laboratory Evaluation
' `3 |9 Q3 z2 M- B2 lThe bone age was consistent with 28 months by+ M8 ~: p0 ?' {2 h
using the standard of Greulich and Pyle at a chrono-" X% }: o, ^& P! m
logic age of 16 months (advanced).5 Chromosomal- C# b  N# e1 a5 }  v- |
karyotype was 46XY. The thyroid function test
8 ^' Z  ], M/ l6 Q6 Ushowed a free T4 of 1.69 ng/dL, and thyroid stimu-1 A8 X2 z1 ^- ^- `4 W
lating hormone level was 1.3 µIU/mL (both normal).
4 P3 l7 Q! z" e4 \5 }The concentrations of serum electrolytes, blood
6 g4 ]) R$ D4 \urea nitrogen, creatinine, and calcium all were" c; I6 V4 J2 _- B1 i4 e, w
within normal range for his age. The concentration/ k" M; }9 o1 t
of serum 17-hydroxyprogesterone was 16 ng/dL: x' z' ~8 ~3 L1 N" i
(normal, 3 to 90 ng/dL), androstenedione was 20
; B5 h) c; y! ~5 e9 G2 Gng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-; E7 W$ J1 w$ f6 ~8 F2 u
terone was 38 ng/dL (normal, 50 to 760 ng/dL),# P' X# G+ N, t  C
desoxycorticosterone was 4.3 ng/dL (normal, 7 to: f' H# ^1 g6 B
49ng/dL), 11-desoxycortisol (specific compound S)7 i' h& g8 N0 x7 v5 G9 H8 B1 M
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-4 M* V, i5 X% |- k/ A' v# l1 Y1 M
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
8 @) H" h. J7 w" `testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
0 O5 _( t/ U# o2 tand β-human chorionic gonadotropin was less than
. D4 L/ O: F6 {5 ^; B# N5 mIU/mL (normal <5 mIU/mL). Serum follicular  q$ e8 B  B' ~1 N
stimulating hormone and leuteinizing hormone
$ E! T# |) [, U6 ], xconcentrations were less than 0.05 mIU/mL( R. ^( a/ J0 o
(prepubertal).
4 Q: [. M& H; M- G1 f+ i% I6 T' ?, ^! `The parents were notified about the laboratory
. y2 ~$ E* F7 Uresults and were informed that all of the tests were
- ]' D' g3 s; g* \3 L+ qnormal except the testosterone level was high. The% y) u" P! w% j  [* t- w) \( M2 [
follow-up visit was arranged within a few weeks to1 M8 X" `6 R6 l( H' i7 U' j; X! G
obtain testicular and abdominal sonograms; how-" O( s: \& ^  g& h
ever, the family did not return for 4 months.% m' Q+ r* ?( J- A3 z5 v9 @2 b
Physical examination at this time revealed that the; _2 r: T$ q8 ~# ?' X) J
child had grown 2.5 cm in 4 months and had gained
, [2 `' ]. z: ]. R! i3 f3 O2 kg of weight. Physical examination remained% Y" l! c3 U& U; v: l
unchanged. Surprisingly, the pubic hair almost com-% _* R' W" k% k
pletely disappeared except for a few vellous hairs at
/ p% p+ T" E# G: ^$ Othe base of the phallus. Testicular volume was still 2* o& F. ~" F1 I1 H2 |* {$ U. U8 o2 x0 d; _
mL, and the size of the penis remained unchanged.# b+ t  n2 v/ B1 @
The mother also said that the boy was no longer hav-
* H% c' R7 T6 [6 n; ying frequent erections.. o- h7 r! l, n
Both parents were again questioned about use of
- q. U, S$ K1 T# H/ d' R4 @9 vany ointment/creams that they may have applied to
( K' Z  `& V2 ?3 Othe child’s skin. This time the father admitted the
+ j% P" D) U. |1 M( z- L* ~$ ATopical Testosterone Exposure / Bhowmick et al 541* C# u9 W. @/ f% \$ ~
use of testosterone gel twice daily that he was apply-
% ]( r6 y4 h  y: V$ \3 u# {! ling over his own shoulders, chest, and back area for6 ~+ K6 w/ d6 [* u$ t7 x' X9 n
a year. The father also revealed he was embarrassed3 c" s0 P+ ]; U9 l; k4 h1 l3 d/ z
to disclose that he was using a testosterone gel pre-& r0 P2 l; E6 d, l) j. g  D
scribed by his family physician for decreased libido, C% ^$ d4 {" I+ e# `% ~" `
secondary to depression., h# o5 K$ [5 Z, ~& o
The child slept in the same bed with parents.4 ~7 d# m, l: y0 ?+ L; |
The father would hug the baby and hold him on his7 g* M: g% O5 {3 P: V! P
chest for a considerable period of time, causing sig-" o. U* i& s; c2 F
nificant bare skin contact between baby and father.
$ s2 A( W  y: Z- kThe father also admitted that after the phone call,( O1 v$ D/ n8 @7 f3 t
when he learned the testosterone level in the baby
5 r  _% U  J: w) F& p1 q0 Ewas high, he then read the product information
( w; I5 P/ Y9 U4 W- S5 Q* v8 _packet and concluded that it was most likely the rea-
3 S8 c1 {5 ]- d2 f0 T: s7 eson for the child’s virilization. At that time, they# I9 B+ k, `6 H8 P9 l/ ]
decided to put the baby in a separate bed, and the
4 l7 c- c" B! \- k% M& tfather was not hugging him with bare skin and had' v' b3 ~( g* n. N3 A  y
been using protective clothing. A repeat testosterone
) B) G8 B) J7 p- e* ttest was ordered, but the family did not go to the
) D, k2 c1 r/ s& llaboratory to obtain the test.+ s- `- W# O2 Y3 g6 V
Discussion8 T, D- z5 y8 r
Precocious puberty in boys is defined as secondary- o5 E  o( ~) L2 L
sexual development before 9 years of age.1,4  p# \( C) h$ z: K# j3 A
Precocious puberty is termed as central (true) when; [% j7 t, ?) r8 }8 M5 i
it is caused by the premature activation of hypo-
; |. U: ]4 w7 p; D4 Xthalamic pituitary gonadal axis. CPP is more com-
* g: p4 ~1 D$ H; R, ~9 F- x" gmon in girls than in boys.1,3 Most boys with CPP
$ m2 g& B, Z4 h0 z# N+ tmay have a central nervous system lesion that is
$ ?4 W5 A  B$ q, I2 o% x4 y5 z$ |  mresponsible for the early activation of the hypothal-' l' J) x4 M# t# H0 h+ F$ [9 |
amic pituitary gonadal axis.1-3 Thus, greater empha-
+ L8 G8 ?  ~( w- n' `sis has been given to neuroradiologic imaging in
! O0 M$ [: }+ S3 ]boys with precocious puberty. In addition to viril-0 q8 o8 v5 A7 X5 H6 Q# H
ization, the clinical hallmark of CPP is the symmet-
5 Q/ c  D3 o+ a1 ^( f, brical testicular growth secondary to stimulation by
  M$ ~2 X1 v7 ygonadotropins.1,3( ]/ D( p& l  \& j7 {4 E6 ^
Gonadotropin-independent peripheral preco-
; M6 t9 q! z) J, I$ A% U  Hcious puberty in boys also results from inappropriate0 n8 @- g* K* }# Z' E
androgenic stimulation from either endogenous or/ q. r$ H  Z6 m6 ^) x4 d
exogenous sources, nonpituitary gonadotropin stim-
3 ]+ T) Q5 N; rulation, and rare activating mutations.3 Virilizing8 s3 S+ @! a7 |& I0 k
congenital adrenal hyperplasia producing excessive$ e+ I1 p+ L' A, {6 L
adrenal androgens is a common cause of precocious& J0 O4 e' K* T) w7 x% {$ \, m2 q
puberty in boys.3,4* L! X; n2 V0 ^% P
The most common form of congenital adrenal4 @. L8 W7 g( x( |6 m1 Z& ]
hyperplasia is the 21-hydroxylase enzyme deficiency." @- K, s, h0 O# W1 B
The 11-β hydroxylase deficiency may also result in
4 y9 L* W2 b5 ?excessive adrenal androgen production, and rarely,) |& Z- h. E; k
an adrenal tumor may also cause adrenal androgen, @' W9 _& N  u1 g& o8 g
excess.1,3- P5 s, p- W+ t5 g& b# C
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
  |3 u% e9 Q0 [' E) j5 L542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
7 A$ [6 m6 L/ v0 _3 i) ^& z3 y: `0 a5 ZA unique entity of male-limited gonadotropin-/ m/ y% i$ t8 W  D& r, A+ C
independent precocious puberty, which is also known
5 x0 p0 F" n, @+ \" {# B4 ?as testotoxicosis, may cause precocious puberty at a$ v! }! o0 r9 c5 H
very young age. The physical findings in these boys
% |& c5 e$ |0 e% v4 v3 Y8 v& ^with this disorder are full pubertal development,3 A8 ?% [7 {% g& u2 b
including bilateral testicular growth, similar to boys' l- j6 F. U6 V8 X
with CPP. The gonadotropin levels in this disorder
8 Q0 c$ A" p3 q, W  b! m: \8 S1 hare suppressed to prepubertal levels and do not show$ @2 P* j" Z$ q! o9 p8 D+ G2 w) m
pubertal response of gonadotropin after gonadotropin-; }2 }9 Z' I/ w
releasing hormone stimulation. This is a sex-linked
- X  p" V  [: H' i6 L9 V% aautosomal dominant disorder that affects only
9 P+ j) F4 ]$ W/ S8 {' g( q) D" L9 G8 imales; therefore, other male members of the family0 s. U0 i5 f+ I5 L; z: N
may have similar precocious puberty.33 }  u, k% K+ O$ q! {1 @
In our patient, physical examination was incon-
; _" S/ E" g" T- m9 |sistent with true precocious puberty since his testi-* y4 t7 Q, N# ~0 V
cles were prepubertal in size. However, testotoxicosis) {  [% p3 }5 d( K
was in the differential diagnosis because his father
  Y) T; O# d& [) ~started puberty somewhat early, and occasionally,7 Q. S: u+ Y& b8 z4 F
testicular enlargement is not that evident in the
2 G1 q0 o1 L2 X" f+ t: o' j. kbeginning of this process.1 In the absence of a neg-; K" ?9 A( o' L" X5 v- m
ative initial history of androgen exposure, our; y( w- d# t7 X( R3 P5 |% |( ~
biggest concern was virilizing adrenal hyperplasia,+ c- Y) h7 E7 ?5 K/ L7 y2 P
either 21-hydroxylase deficiency or 11-β hydroxylase
7 U0 T, t: N. L- W4 `  xdeficiency. Those diagnoses were excluded by find-$ {' s8 E. o; |6 c- N
ing the normal level of adrenal steroids.
2 y. ^5 `6 b* S3 ?The diagnosis of exogenous androgens was strongly
5 k2 R, L/ q& g, X7 a) Q6 u5 z- Lsuspected in a follow-up visit after 4 months because
  C+ o$ V  R/ g/ C& x. M6 R9 ?the physical examination revealed the complete disap-
: l' [0 c; [2 ~! vpearance of pubic hair, normal growth velocity, and; P' T  n, I  E- h$ _
decreased erections. The father admitted using a testos-
& Q0 i7 c/ F) {terone gel, which he concealed at first visit. He was
" B: B# N5 I/ R2 l2 Xusing it rather frequently, twice a day. The Physicians’6 q8 d' u0 `! E- E
Desk Reference, or package insert of this product, gel or& |1 ^2 P% y3 \3 W7 B# Q
cream, cautions about dermal testosterone transfer to2 G* B9 A. G$ j5 Z! O3 Y# e$ W+ m
unprotected females through direct skin exposure.& A. v& g8 `! L. v6 Y% @+ }2 p
Serum testosterone level was found to be 2 times the
; _, @% e, h1 {" M- Pbaseline value in those females who were exposed to+ _4 A% F& G' x' `1 n$ i
even 15 minutes of direct skin contact with their male
5 A3 L- q; ^/ X6 dpartners.6 However, when a shirt covered the applica-
/ i0 j* ]) N  }, btion site, this testosterone transfer was prevented.
6 m# i7 Z  B, s- OOur patient’s testosterone level was 60 ng/mL,
. l! ?5 L% T; e4 \which was clearly high. Some studies suggest that5 `* f) g0 b: }* n8 Z
dermal conversion of testosterone to dihydrotestos-
# W& \3 R( T6 h& u6 sterone, which is a more potent metabolite, is more
( _* W0 w9 o- `% X1 Vactive in young children exposed to testosterone
& u, R, H! Q( m' O3 {( @exogenously7; however, we did not measure a dihy-5 v) {" l) r4 l% ?+ b
drotestosterone level in our patient. In addition to
  W3 O+ M! r6 b6 Avirilization, exposure to exogenous testosterone in
, Y7 C; ~) s8 l6 {children results in an increase in growth velocity and
1 p8 d# j! b+ {3 d3 }) e2 padvanced bone age, as seen in our patient.6 S: Y( d- r( W( m+ U
The long-term effect of androgen exposure during
  [$ s0 J$ G; @# e% m/ ~' wearly childhood on pubertal development and final( a; O+ [. A& @& K7 Q# A) O
adult height are not fully known and always remain& K; e$ q1 Y% _" V
a concern. Children treated with short-term testos-- [6 \/ ]7 ?0 f! s0 [
terone injection or topical androgen may exhibit some! I! i, b) g6 a+ s/ w5 @
acceleration of the skeletal maturation; however, after/ G5 S+ M5 t" \3 H$ X1 U) U
cessation of treatment, the rate of bone maturation1 }; W& V6 ?* }& B+ G5 o  @9 D! N
decelerates and gradually returns to normal.8,9- k/ k; |5 K0 p8 }. C
There are conflicting reports and controversy
  p: p3 W9 w# b- C: \: V( W5 lover the effect of early androgen exposure on adult
6 g* D$ A8 X6 p0 L' xpenile length.10,11 Some reports suggest subnormal* X, l8 J' }; |0 B" z. Q
adult penile length, apparently because of downreg-
" Q9 I9 E8 Z( E+ Culation of androgen receptor number.10,12 However,
" |2 j& c8 d% k% s7 d8 }Sutherland et al13 did not find a correlation between% L. k. G  v  o& h. s1 D  Z. D
childhood testosterone exposure and reduced adult
( I7 Y$ n8 I; ~9 _$ N" \penile length in clinical studies.
& \8 z3 e" D% n- K; d% YNonetheless, we do not believe our patient is" l3 j" c: E; ?6 r! w+ G0 D
going to experience any of the untoward effects from
$ c4 p5 J; \! C1 n! S& ntestosterone exposure as mentioned earlier because
/ U2 a7 Q4 u% }$ {" N& P) athe exposure was not for a prolonged period of time.5 y- X" ]5 ^7 \0 t9 c% v; a
Although the bone age was advanced at the time of
6 v+ Z! l3 C  W3 Bdiagnosis, the child had a normal growth velocity at5 H8 F/ z! X6 y: V% p7 s3 ^
the follow-up visit. It is hoped that his final adult
- f( d/ ~; u5 X9 `4 q0 B/ v* Gheight will not be affected.) i9 j  Z6 z/ g' o' V
Although rarely reported, the widespread avail-8 N' C8 ?0 V2 w: h% L
ability of androgen products in our society may  E/ p% n8 [! C8 k8 I( l+ _
indeed cause more virilization in male or female8 R/ B+ k& G( u
children than one would realize. Exposure to andro-
# h% w! g9 w9 T7 F: Qgen products must be considered and specific ques-
6 Y7 _& i9 g4 h6 w' R* [! etioning about the use of a testosterone product or+ }& ?1 r9 ~8 q) u8 I
gel should be asked of the family members during" k: B9 D3 t. l8 h( \
the evaluation of any children who present with vir-
7 i# a1 U1 _$ L# M5 n9 W8 `' }ilization or peripheral precocious puberty. The diag-" I4 `+ G# Q! x8 P; @
nosis can be established by just a few tests and by
- o0 f; L% z( X' ]$ E, i3 iappropriate history. The inability to obtain such a' T2 R9 P% g# W# p  v& J
history, or failure to ask the specific questions, may
; N- h" S, v) {9 F. I5 Q0 a( \  [$ \result in extensive, unnecessary, and expensive/ Y9 A1 T6 [) y% ^$ z9 p5 k, |. A
investigation. The primary care physician should be. v/ Z( H9 u0 M
aware of this fact, because most of these children+ [& M- h- N, x8 V, L8 N7 L* W
may initially present in their practice. The Physicians’
0 d5 b% `: E- p" X; C9 ?Desk Reference and package insert should also put a+ A7 g# u2 z. n9 j3 @
warning about the virilizing effect on a male or
- O0 n4 q+ `6 a! O# q+ P0 V( Wfemale child who might come in contact with some-
: N6 B- @/ u' g4 e, P- W8 |: l9 a  Mone using any of these products.
* x  u! @3 K) [$ ^References1 z# J; B0 N+ g% ?+ _
1. Styne DM. The testes: disorder of sexual differentiation
( U9 i- H8 _+ e  d5 wand puberty in the male. In: Sperling MA, ed. Pediatric
, w; k4 x1 R& f3 a# N) K/ s# yEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;" H& B9 Y9 c6 @8 D; k
2002: 565-628.
7 o. n2 Y( t( o7 @! L0 {: a" x3 V2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
: ]' ?' @5 C1 L' `) Y) ]5 Apuberty in children with tumours of the suprasellar pineal
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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
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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
% l# _* Z: W0 j
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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