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Sexual Precocity in a 16-Month-Old
" _5 x+ P, }7 W. {( [Boy Induced by Indirect Topical6 T5 n; ], l% W# [, h  p3 G$ E; t
Exposure to Testosterone
8 t' `; \1 u; J1 eSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,25 Q6 |: |7 D  `( E% j1 _
and Kenneth R. Rettig, MD15 Y0 A. q& H0 p7 r0 x
Clinical Pediatrics
# E% t6 T9 _6 h8 a6 wVolume 46 Number 6
7 {0 M7 h5 A: C2 y# `July 2007 540-543* j$ T6 x( R2 B
© 2007 Sage Publications6 m0 R4 q& {3 c9 V
10.1177/0009922806296651
! s, K" }$ M# T, f  P: L4 _5 `) vhttp://clp.sagepub.com
+ a) K6 b5 I" X* m3 i9 E8 Ehosted at* I: ~$ Y+ {: q% C: c( G  A
http://online.sagepub.com! m. v$ r& S" t
Precocious puberty in boys, central or peripheral,
2 @9 U) B& \% L% \  ]7 xis a significant concern for physicians. Central
4 w% X2 X$ y2 ~" C' F5 M0 eprecocious puberty (CPP), which is mediated+ a6 P: h( _' J2 D  z
through the hypothalamic pituitary gonadal axis, has# [/ ]6 a( Q( A9 v0 o8 |" Y" q
a higher incidence of organic central nervous system
0 d: N7 U8 b$ qlesions in boys.1,2 Virilization in boys, as manifested; P( |  G, E! M
by enlargement of the penis, development of pubic) e- V) W6 K3 c3 R' t* X
hair, and facial acne without enlargement of testi-
  [4 A* m; _" K+ ucles, suggests peripheral or pseudopuberty.1-3 We$ T8 k5 R/ z) b% E5 |0 _2 g
report a 16-month-old boy who presented with the
: ?, N8 p9 t+ `+ \- ~enlargement of the phallus and pubic hair develop-
+ y3 m3 \3 E1 {1 Q; h/ |ment without testicular enlargement, which was due
: T' L* x- I3 V& D: pto the unintentional exposure to androgen gel used by* `/ s' w* V) s) {& j
the father. The family initially concealed this infor-
8 k0 K( B- Q# m7 q( G8 t, zmation, resulting in an extensive work-up for this. `: X: g; _5 y' t5 ?7 g# R& ], Y9 t
child. Given the widespread and easy availability of
0 K* N4 E' Q" T, L/ \% mtestosterone gel and cream, we believe this is proba-
& v. |! X- B7 H2 b+ Y: }bly more common than the rare case report in the2 \/ O; `. Y4 t4 y. Q% |  n- _
literature.4
0 c3 F5 Z8 o( s2 ~# A: GPatient Report" S% E) E* p# w( a- C) w* D$ w
A 16-month-old white child was referred to the
6 L" q" l; p& t; ^5 Iendocrine clinic by his pediatrician with the concern
, i5 Q, ~8 t7 J0 F( Lof early sexual development. His mother noticed
2 u" f; ^3 I9 V7 z: Hlight colored pubic hair development when he was- e; o6 K, b8 N
From the 1Division of Pediatric Endocrinology, 2University of& S- D; b8 L# _5 a
South Alabama Medical Center, Mobile, Alabama.- X2 H7 X  g. }7 c/ p
Address correspondence to: Samar K. Bhowmick, MD, FACE,
, V7 R  t& m0 O" kProfessor of Pediatrics, University of South Alabama, College of# y* _- N! v+ ^
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
# m8 F0 U/ d) m: e  o. P" Qe-mail: [email protected].' R# s  h/ m0 x# W5 f% X
about 6 to 7 months old, which progressively became
9 q# ]1 }8 n; P7 |' i* Vdarker. She was also concerned about the enlarge-+ v7 g9 }+ @, i7 \) W: I7 `
ment of his penis and frequent erections. The child' Y8 V8 u7 Q, e5 h% t
was the product of a full-term normal delivery, with
8 k( q/ w5 ?. W* Ba birth weight of 7 lb 14 oz, and birth length of. {: D0 m: o& ]8 p; f2 ?7 \
20 inches. He was breast-fed throughout the first year( W9 C1 t5 h) l" v% h
of life and was still receiving breast milk along with' w% ^; V) B1 e' x1 p( a
solid food. He had no hospitalizations or surgery,) d' d7 g! W  j! @
and his psychosocial and psychomotor development
' `) T$ \4 V8 w/ `, Nwas age appropriate.$ r& _  I& e* x9 y" ?" t- C
The family history was remarkable for the father,2 Q* D( W/ P$ d. h
who was diagnosed with hypothyroidism at age 16,
- p7 r' u: Y% b3 x' V) hwhich was treated with thyroxine. The father’s2 ~0 s' X, R- C# ]
height was 6 feet, and he went through a somewhat
2 P1 A  d7 A/ a$ C+ Q0 E# nearly puberty and had stopped growing by age 14.$ A- K. L# W" X" Z+ \9 U
The father denied taking any other medication. The
0 A8 a* A3 f- q, P' E; ]5 O5 ?7 _child’s mother was in good health. Her menarche" P* e$ X4 s$ _7 D+ f8 X
was at 11 years of age, and her height was at 5 feet" f3 H) \* [- o- Q' r
5 inches. There was no other family history of pre-
, A% N. e+ K% }# W+ Ecocious sexual development in the first-degree rela-7 e& J. \6 a- D- x9 I
tives. There were no siblings.
% V7 I) V% q5 F$ aPhysical Examination) C7 F& i6 z  y* X, F. J: T7 [
The physical examination revealed a very active,
' M4 e  t9 k: q5 E4 f2 O. Tplayful, and healthy boy. The vital signs documented
4 d/ h% T  \1 _4 E& i4 k, m( A& S. \) L. Aa blood pressure of 85/50 mm Hg, his length was6 @" C, n0 `8 p/ m7 c
90 cm (>97th percentile), and his weight was 14.4 kg  h0 f3 ]' L" w0 s1 z
(also >97th percentile). The observed yearly growth
/ x8 N1 ~: D  J; Vvelocity was 30 cm (12 inches). The examination of
5 D3 D# g; k5 r1 U" e0 kthe neck revealed no thyroid enlargement.
: x; t8 P. ?  w0 A& @) XThe genitourinary examination was remarkable for+ p4 `; E# E) P! J/ f& F
enlargement of the penis, with a stretched length of8 M! J. ?/ V$ R( d3 J* P
8 cm and a width of 2 cm. The glans penis was very well5 ~; v9 L$ o9 R/ ~' Y5 }7 ^
developed. The pubic hair was Tanner II, mostly around- C  W+ z: l. A1 b0 T) d9 D# ]! s
5409 J  n' T# R8 s: N  e1 K6 g
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 |$ J3 o$ {2 S# q8 k, I) ythe base of the phallus and was dark and curled. The
+ d" e% C6 K. m# Otesticular volume was prepubertal at 2 mL each.4 P! B. _, [0 F9 Q
The skin was moist and smooth and somewhat, f& F3 @; J* `9 p7 n: w% u0 n1 i
oily. No axillary hair was noted. There were no
6 J& h+ p' q+ y5 n- mabnormal skin pigmentations or café-au-lait spots.9 q' y6 J$ l' e, {) z! t+ J, Q
Neurologic evaluation showed deep tendon reflex 2+& q- D* n' S; i, S# O5 J9 A" ^( _& t
bilateral and symmetrical. There was no suggestion& P7 ?0 v! ~% K8 c. ~, u% A
of papilledema.
) A! S: {9 |0 B, j! @4 j1 {Laboratory Evaluation  c0 `0 Q8 N, {  D) n
The bone age was consistent with 28 months by
+ a( G, i8 I9 ausing the standard of Greulich and Pyle at a chrono-# ^0 Z2 V# x( u
logic age of 16 months (advanced).5 Chromosomal
4 p5 I( o& C( vkaryotype was 46XY. The thyroid function test
8 m- n! [& K0 c1 {; k8 A) t# v" R, _showed a free T4 of 1.69 ng/dL, and thyroid stimu-2 U6 ]) V* W' u; h
lating hormone level was 1.3 µIU/mL (both normal).
, E: a% i5 ?/ jThe concentrations of serum electrolytes, blood
: i/ X& e& O2 O* a1 k) B( gurea nitrogen, creatinine, and calcium all were8 n' R8 \$ v; }1 d2 c
within normal range for his age. The concentration( p8 U7 y; T0 v2 X8 o
of serum 17-hydroxyprogesterone was 16 ng/dL3 @1 G7 c6 c) J. k# Q# U
(normal, 3 to 90 ng/dL), androstenedione was 200 Z* a* a+ f- x9 ?% W
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-/ Y" E/ E* k& Q3 t% F( W1 z$ e
terone was 38 ng/dL (normal, 50 to 760 ng/dL),7 y; y& a$ h7 x- S3 }
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
+ ~6 a4 T4 x4 W9 f3 @" z, Z% z49ng/dL), 11-desoxycortisol (specific compound S)7 P7 q: R5 b* s" o
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-" H- j" I5 B* ~3 M
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
9 H0 r  u  ]6 z  X6 T7 @& ptestosterone was 60 ng/dL (normal <3 to 10 ng/dL),$ d& e# K. e% L/ z& l
and β-human chorionic gonadotropin was less than
+ n( _5 y1 k+ s6 J( I5 mIU/mL (normal <5 mIU/mL). Serum follicular1 c7 U9 W  t- {( X- M$ e5 x( J
stimulating hormone and leuteinizing hormone
# e. Z- d, P+ o, ]7 Rconcentrations were less than 0.05 mIU/mL% l0 P& I3 w  d6 @
(prepubertal).
7 P& v! ]( e' g% |+ I' NThe parents were notified about the laboratory+ F: ^' o+ K+ d
results and were informed that all of the tests were
/ h3 e4 D, q* l+ Z3 N8 m  pnormal except the testosterone level was high. The9 k- t0 R! j8 x* R: J2 G
follow-up visit was arranged within a few weeks to
* ~+ z* ^2 M0 _6 F8 _, n2 i, Robtain testicular and abdominal sonograms; how-5 Y4 N  E6 j6 c, w: ^# O/ D0 D
ever, the family did not return for 4 months.
  h0 W+ |- m8 L- ^- y4 X1 bPhysical examination at this time revealed that the
$ H! H; K+ _( \2 x- ]child had grown 2.5 cm in 4 months and had gained
* i% H* _: C9 `7 T2 kg of weight. Physical examination remained: ~6 J9 q. O1 B& J6 F) E& @' C
unchanged. Surprisingly, the pubic hair almost com-7 S5 Y3 n0 Q- E3 h/ l* y$ A
pletely disappeared except for a few vellous hairs at7 h  w* h& L* K) ]3 C5 g. ?
the base of the phallus. Testicular volume was still 2
& |5 X% w- H, y  r! E5 H8 @% kmL, and the size of the penis remained unchanged.
  v  t+ w) g8 M% [8 b) XThe mother also said that the boy was no longer hav-1 b( U" B% M* c6 b% V0 w! _- E
ing frequent erections.
" T" J( W+ S% \: p" C! zBoth parents were again questioned about use of( O5 f6 U  W( l% `$ i
any ointment/creams that they may have applied to
! H& |+ x" k; W' ~% R4 nthe child’s skin. This time the father admitted the
. o* \5 G8 p- b* E$ z& ?Topical Testosterone Exposure / Bhowmick et al 541! D9 z  l2 s. H% P* e( A
use of testosterone gel twice daily that he was apply-
+ ~. ]. D( n2 m( A) b% Qing over his own shoulders, chest, and back area for2 n$ p0 R( l+ ^3 H( W
a year. The father also revealed he was embarrassed; k; d6 k( J. j$ c" X8 g! H  ]
to disclose that he was using a testosterone gel pre-
1 U  j- m6 a+ P! |, i; zscribed by his family physician for decreased libido: m, R+ m( H+ [, g
secondary to depression.5 i" p- q  [* }0 f
The child slept in the same bed with parents.( S/ q4 A* F9 Z0 g; u# K0 I  I
The father would hug the baby and hold him on his  R8 X, y4 o/ v. U
chest for a considerable period of time, causing sig-
/ I( D; Q3 [  j; M" p$ o$ N( cnificant bare skin contact between baby and father.
! h7 u5 `/ u; G) T  r# z9 TThe father also admitted that after the phone call,, A' P6 w+ d+ x$ _: B0 g
when he learned the testosterone level in the baby
7 S* V: L$ X$ Owas high, he then read the product information
: n6 ^8 J+ m) q2 J9 Rpacket and concluded that it was most likely the rea-
- c" I7 p& F6 \! y* Y9 ~# ?+ bson for the child’s virilization. At that time, they/ e& h' U. a# K( s7 {8 {4 ?, _
decided to put the baby in a separate bed, and the
5 q, d7 A1 b4 R. A" Qfather was not hugging him with bare skin and had  K9 k9 U- @: ?# e# G7 N" S
been using protective clothing. A repeat testosterone+ ]3 b% w" A) E* `( S$ T5 ^
test was ordered, but the family did not go to the$ a" H' y9 Y/ p8 V
laboratory to obtain the test.5 Q* i! @1 e4 G
Discussion3 W* b4 m' G/ I, s% p
Precocious puberty in boys is defined as secondary5 d% \3 v, l8 U9 K8 u
sexual development before 9 years of age.1,4* v- B* R6 }1 K5 Q9 u6 w8 R
Precocious puberty is termed as central (true) when
6 P# R1 }$ _) B+ v1 X8 ait is caused by the premature activation of hypo-% r/ F0 Z$ I4 x
thalamic pituitary gonadal axis. CPP is more com-" j' v# R! f7 O+ M4 e1 D7 w
mon in girls than in boys.1,3 Most boys with CPP
6 o. i2 v8 d7 G3 Hmay have a central nervous system lesion that is. S2 B6 Y7 k3 C! S; \- S0 Y
responsible for the early activation of the hypothal-) V, c; v6 Z/ o
amic pituitary gonadal axis.1-3 Thus, greater empha-
! v. [$ _9 j0 t" |sis has been given to neuroradiologic imaging in/ C' {, A! z% N6 r0 c
boys with precocious puberty. In addition to viril-
6 I8 [, o7 I" F, ]; Y& Sization, the clinical hallmark of CPP is the symmet-9 ^  G7 U6 j) ]) I) \
rical testicular growth secondary to stimulation by& Y$ j3 K  P+ ^+ B, W
gonadotropins.1,3- q+ g' a2 O$ E3 b" f0 Q
Gonadotropin-independent peripheral preco-: e. N  ?  j  H* ~5 h
cious puberty in boys also results from inappropriate( h  u& C1 ^! r: i) F
androgenic stimulation from either endogenous or
) M- ?/ b# D9 ~3 ]$ L5 u. f, Mexogenous sources, nonpituitary gonadotropin stim-# ]! ]7 ~8 m! c  O% W& K
ulation, and rare activating mutations.3 Virilizing7 N; `/ D% i9 ?. T2 B: v; a
congenital adrenal hyperplasia producing excessive
( k% k$ b' D' z/ ^adrenal androgens is a common cause of precocious9 m7 O6 c3 i! }5 x. T
puberty in boys.3,4
1 M, K( J$ K, B, H9 |/ [9 q" [$ JThe most common form of congenital adrenal
! _# r7 |! O/ A. G( S) z8 o; Mhyperplasia is the 21-hydroxylase enzyme deficiency.+ ~' ~7 `$ A  p/ x, e0 |
The 11-β hydroxylase deficiency may also result in
8 C+ Z+ B9 x6 Y( _excessive adrenal androgen production, and rarely,
9 z: V( r2 }. i' g  }3 _an adrenal tumor may also cause adrenal androgen
' @1 T) D/ r8 G# I: [; Sexcess.1,3( a8 y' O- @+ M1 I' G) ]
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: C! X  ]; {* i+ f2 L
542 Clinical Pediatrics / Vol. 46, No. 6, July 20079 l0 M+ o4 ]7 a* r, ?2 J& z
A unique entity of male-limited gonadotropin-
7 X( U; x7 ?; P& T7 ~+ J( k, x) W) Oindependent precocious puberty, which is also known: Z  o7 L8 K  U, y& z* s
as testotoxicosis, may cause precocious puberty at a$ t8 \3 J2 I; t7 q0 a0 t
very young age. The physical findings in these boys, G3 \5 [0 n5 c2 ^( L. F
with this disorder are full pubertal development,
7 t% D4 H9 V3 ~  u( K( Yincluding bilateral testicular growth, similar to boys
, W" j) @% A  I1 U1 lwith CPP. The gonadotropin levels in this disorder
" D3 d6 J0 V. q2 u. C! @are suppressed to prepubertal levels and do not show7 O( p2 [; k1 ]' I4 `# W  E( @
pubertal response of gonadotropin after gonadotropin-) C; }7 g6 x! Q- f8 l2 x
releasing hormone stimulation. This is a sex-linked
$ A5 z& D# u! Y7 tautosomal dominant disorder that affects only) v. i3 n# E. j  J; Q6 U0 L+ r
males; therefore, other male members of the family
3 o) S) e7 |; Omay have similar precocious puberty.3
% Q$ F6 Z7 a' R& a8 eIn our patient, physical examination was incon-
1 a, a. f' g& X* j( usistent with true precocious puberty since his testi-
$ b$ ^' G4 J" {2 N- u! X7 icles were prepubertal in size. However, testotoxicosis6 F. h. }5 }& n/ r: i# F; P1 [
was in the differential diagnosis because his father
0 l" N; R4 ]. |1 s! X  l* wstarted puberty somewhat early, and occasionally,
$ o4 T5 Z$ n9 ~- c9 m( Ctesticular enlargement is not that evident in the
: Y8 g; l7 t/ U/ ^beginning of this process.1 In the absence of a neg-7 k8 Z* N6 r; O- t3 E9 ]
ative initial history of androgen exposure, our
1 I2 z- h6 F; A1 D7 \3 K! D$ obiggest concern was virilizing adrenal hyperplasia,
; O0 o6 _% o# k  b% T: p1 s* reither 21-hydroxylase deficiency or 11-β hydroxylase
8 J3 ?% m! T; r* X' Cdeficiency. Those diagnoses were excluded by find-
$ m- g; [- q. U& }/ ^! N) king the normal level of adrenal steroids.6 K. Q4 G8 N# K8 ?, H
The diagnosis of exogenous androgens was strongly
# d9 y& B$ h  R5 g" v( I8 Bsuspected in a follow-up visit after 4 months because9 b3 T0 b0 l4 ^
the physical examination revealed the complete disap-
: S: Q" o2 D# `. ~1 spearance of pubic hair, normal growth velocity, and
  p$ p2 o* O* U: ~, p+ o7 S1 Ldecreased erections. The father admitted using a testos-6 B3 f- _3 G) P* M
terone gel, which he concealed at first visit. He was
( m0 h/ x8 D0 g( c+ H! Eusing it rather frequently, twice a day. The Physicians’
' `4 P4 O( }  L8 q+ ]Desk Reference, or package insert of this product, gel or
6 p5 O" r; R0 p0 V- gcream, cautions about dermal testosterone transfer to
3 t- p) K& X0 p. o8 I) i/ p) yunprotected females through direct skin exposure." g2 k% E/ E  t3 S) x
Serum testosterone level was found to be 2 times the
+ G& I/ ~+ f+ p1 }3 a! Dbaseline value in those females who were exposed to- `. W* Q1 i6 K' S! S6 e: g
even 15 minutes of direct skin contact with their male' c( d& C: _4 A
partners.6 However, when a shirt covered the applica-
: X5 z7 a( R) C) `+ gtion site, this testosterone transfer was prevented.* `+ Z. u  w( Y) N3 O
Our patient’s testosterone level was 60 ng/mL,( a  k* @2 _4 d5 |0 c0 |
which was clearly high. Some studies suggest that
2 ^0 z0 S  ?6 z: k( tdermal conversion of testosterone to dihydrotestos-
" t- i* l5 `# K: b" j8 tterone, which is a more potent metabolite, is more6 Y  U2 C/ t2 I/ i2 U! K/ C/ q2 B% U
active in young children exposed to testosterone6 ^: N3 c/ y4 y8 ]% e, b
exogenously7; however, we did not measure a dihy-: y2 j7 D& _8 Q6 L* x( f
drotestosterone level in our patient. In addition to
! ?1 O4 U/ R$ X0 Y* ^virilization, exposure to exogenous testosterone in3 X  }7 ?& }! r1 N. C
children results in an increase in growth velocity and
: n1 U  Z6 R6 n* zadvanced bone age, as seen in our patient.
8 r) p  e) a- X3 ], VThe long-term effect of androgen exposure during
+ C. M% e' J# v$ ?5 pearly childhood on pubertal development and final
& D; @7 S( M; q: Gadult height are not fully known and always remain
) H, c6 ~) U5 r( a* Pa concern. Children treated with short-term testos-. |6 W' Y/ ]+ S
terone injection or topical androgen may exhibit some& J# V4 R  P  d1 \1 y
acceleration of the skeletal maturation; however, after
2 ]7 l! T; |: Q$ f" Qcessation of treatment, the rate of bone maturation& [- s1 U% y" r8 z% `% {* |  M
decelerates and gradually returns to normal.8,9$ p2 m. I, G' \* i3 z" e
There are conflicting reports and controversy
2 |5 n( O  U* ]+ ~: ~+ nover the effect of early androgen exposure on adult
9 e! H" g) n6 U  d% upenile length.10,11 Some reports suggest subnormal
5 D6 N5 e& k# y( Tadult penile length, apparently because of downreg-
9 I( W7 n3 @: ^& z5 @ulation of androgen receptor number.10,12 However,
, v9 B- p( \5 |) c+ mSutherland et al13 did not find a correlation between; {& T" V! i) M5 ?6 ?4 x
childhood testosterone exposure and reduced adult7 |! t9 R5 U, O0 G) w# u
penile length in clinical studies.8 Q% x' ?  s% c1 v
Nonetheless, we do not believe our patient is
; ?# a5 g4 y+ s& B" g/ N- E. X  zgoing to experience any of the untoward effects from6 d" c& x+ L5 k, i! [2 j
testosterone exposure as mentioned earlier because, O$ z( \3 m6 k! b4 T: @& j
the exposure was not for a prolonged period of time.( h* ^' Q7 x5 }; O0 f3 \+ J- D! X/ J
Although the bone age was advanced at the time of% p8 |& e9 A+ h& |! U
diagnosis, the child had a normal growth velocity at7 h; n' I/ \- ?$ k
the follow-up visit. It is hoped that his final adult
+ v" k: F  o& n6 J) sheight will not be affected.+ d0 u" k9 ?" t# A  v- X/ P
Although rarely reported, the widespread avail-  b4 i% M/ U4 Z, X; p" K; o- `
ability of androgen products in our society may
6 w+ Q3 d1 b% F2 N+ M. d  Zindeed cause more virilization in male or female' Q2 R6 M# f2 m$ [# b  a! e
children than one would realize. Exposure to andro-
0 Q6 U: S1 c+ s4 y! C# ^& Zgen products must be considered and specific ques-
- J4 x, q  {+ _+ d$ K$ ^9 rtioning about the use of a testosterone product or
5 ~5 a* l/ j: s- v' ~# _" @gel should be asked of the family members during% l  C1 h0 \% i' {, h. `
the evaluation of any children who present with vir-
3 v  `! k" D& E0 f  ^( y# Eilization or peripheral precocious puberty. The diag-
# \5 ^$ \- X: Ynosis can be established by just a few tests and by
3 }% s4 W; f7 Nappropriate history. The inability to obtain such a
1 O+ ]/ C& ^) Z3 N' K8 X* |history, or failure to ask the specific questions, may
+ V) w9 q1 t! h, [- _' ^result in extensive, unnecessary, and expensive
' L8 h) Z2 L& Iinvestigation. The primary care physician should be' n3 H! ?! r& ~1 l0 E$ T
aware of this fact, because most of these children
5 B! F. S/ `# a1 ^3 }* Nmay initially present in their practice. The Physicians’
' r2 E2 G0 s2 E' J$ kDesk Reference and package insert should also put a
8 m5 V& W& G6 @5 G) W9 fwarning about the virilizing effect on a male or
$ L- q) [# s, @5 l- n# v7 q' ]) Ofemale child who might come in contact with some-
( \, f* }, J3 k% I8 f- cone using any of these products.8 e5 S* M- N9 Y: }
References
- A' S% i3 S  z/ s8 x  l8 M& A  G1. Styne DM. The testes: disorder of sexual differentiation7 L( E6 q6 D- V9 z; Y8 e
and puberty in the male. In: Sperling MA, ed. Pediatric5 K2 r0 W! P3 e* b1 K1 L
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
; S/ `; f& D1 t" N" n2 p; p2002: 565-628.2 r, v; a8 C2 S
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
* r/ e: K  }0 d& j5 mpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
- R& X9 s8 S% y  oBoy Induced by Indirect Topical: R% [% U" u# M/ e/ \, F
Exposure to Testosterone) o# o; n& A) J$ i8 F
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
4 q8 h4 Y& w8 y" X0 v  yand Kenneth R. Rettig, MD1
  u0 G$ L% D) d- ~1 e; R' uClinical Pediatrics! S/ n7 V: Y( w8 v1 ^, N  Q# s2 ~
Volume 46 Number 6" T! [9 v  C: r' V3 i$ H- y5 V
July 2007 540-543
4 a' }* J' n* W6 e$ o# d© 2007 Sage Publications$ m' y( W+ O, d( h. C! B
10.1177/0009922806296651& c1 w9 A0 v: a
http://clp.sagepub.com* X1 N- p% y! G/ B: N
hosted at  v. h% [: X. w% e2 D
http://online.sagepub.com
. D* v1 ~# C3 c7 T" j! MPrecocious puberty in boys, central or peripheral,
* Y: A' E/ b& O, d# ^4 X+ vis a significant concern for physicians. Central
. s3 G9 o" m7 d. ^2 Z( V' {precocious puberty (CPP), which is mediated
' n& {" n4 @- N7 U$ h4 hthrough the hypothalamic pituitary gonadal axis, has
2 F5 Y& y7 F( t$ T% t( F+ I) G3 fa higher incidence of organic central nervous system5 @  q7 ?* L# j; C" }2 C
lesions in boys.1,2 Virilization in boys, as manifested  R+ @; B' V8 o- g
by enlargement of the penis, development of pubic, ^" t' \) G+ W# z" i  j
hair, and facial acne without enlargement of testi-
" J& a8 }( k5 `, Jcles, suggests peripheral or pseudopuberty.1-3 We# |8 b- G3 i/ q5 S! e
report a 16-month-old boy who presented with the
+ ]9 j7 ?/ o, l7 U, henlargement of the phallus and pubic hair develop-
+ M% `4 ^: W+ J0 e5 _% d1 k. n+ |ment without testicular enlargement, which was due
: K0 B' q9 J  k8 y7 c6 Z7 K1 Sto the unintentional exposure to androgen gel used by  c4 [7 C! i" J7 H, ?4 A# @' g
the father. The family initially concealed this infor-
( h" E: E: U' ^) i5 z. N6 emation, resulting in an extensive work-up for this
% G4 t9 R0 g5 |: u; achild. Given the widespread and easy availability of
  [2 L4 T/ z+ Y( u& z: C5 O* ]testosterone gel and cream, we believe this is proba-
; T7 B2 l) r9 N. L8 Fbly more common than the rare case report in the
- l- T2 |; x' s- O& sliterature.4
& E0 r$ F7 K1 t/ h# V9 E+ g% Y( iPatient Report9 Q; C9 @, Y4 |9 E
A 16-month-old white child was referred to the( |0 L: |5 y3 M4 h, b8 i5 e
endocrine clinic by his pediatrician with the concern
" i# z7 n* r" ?3 Cof early sexual development. His mother noticed3 M% d$ ^$ L8 C/ |# b
light colored pubic hair development when he was
9 W* F: J) L/ o( E( ^7 a7 tFrom the 1Division of Pediatric Endocrinology, 2University of* n2 U8 A# d( K3 A$ t, h4 ]
South Alabama Medical Center, Mobile, Alabama.5 Y6 K+ h5 R# o2 ]0 d. G4 v% ^+ G% P. ]7 m
Address correspondence to: Samar K. Bhowmick, MD, FACE,
( J& }3 x# C/ l0 a" J9 X8 W+ bProfessor of Pediatrics, University of South Alabama, College of8 i( [$ s$ t: x4 f7 O4 ?- f
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;# V  n$ c; r, v( z5 y+ ], n1 Y6 M
e-mail: [email protected].7 K% n. X1 O7 M. Z/ u+ l  r& S/ t
about 6 to 7 months old, which progressively became8 |- |! r$ m8 K6 D. ]
darker. She was also concerned about the enlarge-. e# k7 C- O4 C! N; D1 Z
ment of his penis and frequent erections. The child& N$ |$ d9 i8 z3 l: }+ m
was the product of a full-term normal delivery, with3 a/ k2 u3 ~+ s& B/ j0 z0 z
a birth weight of 7 lb 14 oz, and birth length of; H4 D; ?" u+ V0 X) E& V
20 inches. He was breast-fed throughout the first year
+ d$ ~- g4 m) i1 T- C: l. Sof life and was still receiving breast milk along with
' o# z* a( B, w2 t% n5 A% isolid food. He had no hospitalizations or surgery,. e! K- I% i/ n+ U& r
and his psychosocial and psychomotor development" N) c. [8 N  z# H& t" h
was age appropriate.
" |" L9 q$ A- i6 O0 ]3 N& T" Y0 ]& QThe family history was remarkable for the father,$ s; l( \! O1 H
who was diagnosed with hypothyroidism at age 16,
  K. L% \: v5 w5 ?. K  P+ ~which was treated with thyroxine. The father’s- E* V* y6 w$ J4 A
height was 6 feet, and he went through a somewhat
% ?3 h# |) G/ t  t8 Q# w& Yearly puberty and had stopped growing by age 14.
# g5 j  u/ i; V. F1 R& d6 T8 aThe father denied taking any other medication. The  l9 y/ g: z( h$ |" v. _
child’s mother was in good health. Her menarche
0 w7 w; R( ~' W7 n. x, [& f% i4 Ewas at 11 years of age, and her height was at 5 feet% u* I$ `. w# ^8 T% Q
5 inches. There was no other family history of pre-
, g2 n* D7 v" }1 o1 icocious sexual development in the first-degree rela-
% h6 c) K1 v& h' Y2 V$ e! dtives. There were no siblings.
# o$ g6 |; {: a7 f/ L. \Physical Examination' a8 I% [) H) @+ t9 R
The physical examination revealed a very active,
8 W+ p4 Q' e& n6 K6 ?( `playful, and healthy boy. The vital signs documented8 N& x2 J- H% T8 U3 r9 N$ u
a blood pressure of 85/50 mm Hg, his length was
$ {/ @/ f( ?9 f5 T& \6 t  V90 cm (>97th percentile), and his weight was 14.4 kg' b$ a! l  S' T( V) ~* N; H2 a
(also >97th percentile). The observed yearly growth; \1 h/ g( {1 D. c/ x
velocity was 30 cm (12 inches). The examination of: P% L5 p: ?# \/ Y2 l/ j" C
the neck revealed no thyroid enlargement.# R0 g( m8 I$ o, g- Y
The genitourinary examination was remarkable for
; S; r7 O6 V, T: ~enlargement of the penis, with a stretched length of; p1 l; z; f/ X1 N4 C
8 cm and a width of 2 cm. The glans penis was very well: L- \* V5 s/ [- F, N
developed. The pubic hair was Tanner II, mostly around
6 l0 K  H, [. r& y. P/ K4 V5402 |7 L9 t! F* e5 v7 f; [
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) C+ A  e  ~: Z! v+ L8 Z
the base of the phallus and was dark and curled. The
* t8 ]8 V) X; \7 Htesticular volume was prepubertal at 2 mL each., K- z# T- e! Q- v1 {
The skin was moist and smooth and somewhat
, u0 u; j1 \. C# y! ~oily. No axillary hair was noted. There were no, e8 m$ G& Q( E# D3 C! J
abnormal skin pigmentations or café-au-lait spots.
, H: U$ R* `7 D& P# b+ fNeurologic evaluation showed deep tendon reflex 2+
  i! e: I6 S# \4 n3 z$ M  [! L) Mbilateral and symmetrical. There was no suggestion
* D" ?0 Q) Y( z" N& R3 \9 y  Bof papilledema.
4 g' X: g( A! [' _" J& J+ c! GLaboratory Evaluation
8 v' z7 f) D6 L. M& k: L) UThe bone age was consistent with 28 months by
+ z" z  ]  z4 |; y. n' Q6 W% u% Cusing the standard of Greulich and Pyle at a chrono-( v2 w3 V- s' O. ]
logic age of 16 months (advanced).5 Chromosomal
& }( R* a' i3 ^, ykaryotype was 46XY. The thyroid function test
0 Q4 M' E  y" sshowed a free T4 of 1.69 ng/dL, and thyroid stimu-/ z" j9 j5 j) n" l$ G6 S
lating hormone level was 1.3 µIU/mL (both normal).
  p" L+ h, v; J" jThe concentrations of serum electrolytes, blood( U6 ?4 j; B1 k( m
urea nitrogen, creatinine, and calcium all were- \% @: e" S/ l* t
within normal range for his age. The concentration; j7 i: i- O: l7 A  y
of serum 17-hydroxyprogesterone was 16 ng/dL, C: o6 @0 x5 w' i
(normal, 3 to 90 ng/dL), androstenedione was 204 T5 Z" k5 v9 o& W7 ~
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-- N4 L5 F; U1 V* k
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
0 D% H3 b: y2 S; y; Udesoxycorticosterone was 4.3 ng/dL (normal, 7 to0 G( G4 n, j/ |( D' W
49ng/dL), 11-desoxycortisol (specific compound S)
9 b) z2 x: O! b/ K, i( U# Xwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- y3 z+ O0 q: Q' X* T  [- h' j
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# z% V3 b1 r' p+ T& `
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
9 c6 X4 O/ B: J) qand β-human chorionic gonadotropin was less than- E7 t1 O8 H, N3 ^
5 mIU/mL (normal <5 mIU/mL). Serum follicular
6 J' J7 w: h/ P' k6 z; I# C% Hstimulating hormone and leuteinizing hormone
8 p$ g# t# j: I; c4 Gconcentrations were less than 0.05 mIU/mL: V( g  E! T: X$ L% @; ^. h
(prepubertal).: Z- x6 _- W6 @
The parents were notified about the laboratory
# O1 B7 v4 q, Y2 presults and were informed that all of the tests were6 t, U, u" `5 t6 Y7 c# Z' a$ L
normal except the testosterone level was high. The
" [: \; a- d1 M/ l, F8 `+ bfollow-up visit was arranged within a few weeks to2 o5 [* g8 e) D! ?) j6 |7 N
obtain testicular and abdominal sonograms; how-
  H& ~2 p! g5 L+ w# f, P6 S4 Iever, the family did not return for 4 months.
  H; m: C" M6 v- r0 N# ^# y/ |6 tPhysical examination at this time revealed that the
# Y( y- q$ m; A) J* z) I+ `1 mchild had grown 2.5 cm in 4 months and had gained
/ n4 X3 z# V- B' @& u8 Z- n1 ^$ d2 kg of weight. Physical examination remained; ]5 X  q6 P. F: V# r
unchanged. Surprisingly, the pubic hair almost com-
4 r/ f$ k2 u5 f. q8 P/ a! Wpletely disappeared except for a few vellous hairs at. L2 S$ p& U3 m+ a; `
the base of the phallus. Testicular volume was still 2
4 b+ K+ I1 j; l3 C* smL, and the size of the penis remained unchanged.
9 ]: z. a! l* B. i8 p+ c; UThe mother also said that the boy was no longer hav-
* @0 p- f" T6 D$ g$ Sing frequent erections.
9 z3 S3 K8 y( e+ {9 z" f" M$ `Both parents were again questioned about use of1 m2 I4 r3 i1 A* P- v  S
any ointment/creams that they may have applied to" C- F( U( {  m6 h, N8 |
the child’s skin. This time the father admitted the
* ~- v( O0 v1 V+ PTopical Testosterone Exposure / Bhowmick et al 541
, ~, W$ ~" Z, Tuse of testosterone gel twice daily that he was apply-
! A& J; W8 C( _ing over his own shoulders, chest, and back area for
$ X1 U5 d$ T1 O) i% B. Ha year. The father also revealed he was embarrassed
6 N" b5 K  B8 @to disclose that he was using a testosterone gel pre-
4 d. ]+ p7 s( v& p- Rscribed by his family physician for decreased libido
9 v) Z7 g* `* l8 [0 \) g4 a% Ssecondary to depression.
  a4 T% w5 U! ?9 ^+ cThe child slept in the same bed with parents.
5 L& n& c) V) k  ~- F- U4 I7 bThe father would hug the baby and hold him on his
0 i2 v+ d' l  R6 gchest for a considerable period of time, causing sig-
4 _, {+ I) i  n7 S' s4 [2 |7 Qnificant bare skin contact between baby and father.. F) A  B  v, X
The father also admitted that after the phone call,7 T8 e5 T% T" T% \, x
when he learned the testosterone level in the baby
- \" y  `9 d$ |6 Q& Jwas high, he then read the product information% `/ b/ s8 a6 Z) O3 b6 e4 C
packet and concluded that it was most likely the rea-) C( ]) @. C) `  t  F5 G& P0 o# j
son for the child’s virilization. At that time, they7 t; |" Y) a3 ^
decided to put the baby in a separate bed, and the
) G  L* m5 o0 H: k8 }- dfather was not hugging him with bare skin and had# F/ J6 o% A" l! ~+ f0 j0 ?* `
been using protective clothing. A repeat testosterone& D2 r- H: d9 d
test was ordered, but the family did not go to the
& ?$ G" ^9 h7 dlaboratory to obtain the test.
4 Y; {5 H) w  t. sDiscussion
7 A; r$ U% B+ a3 R$ a7 F/ Y0 lPrecocious puberty in boys is defined as secondary1 D* Q3 R) R: O$ Q9 _+ }( \, S
sexual development before 9 years of age.1,4
5 j: K' P9 G; @% ]: `Precocious puberty is termed as central (true) when# z& A9 `* L5 Z% w- u
it is caused by the premature activation of hypo-
$ Q+ |) l- x2 Kthalamic pituitary gonadal axis. CPP is more com-
. p( e- l1 i$ q$ }mon in girls than in boys.1,3 Most boys with CPP6 c" F# d& F5 D( s+ M/ A
may have a central nervous system lesion that is9 J9 H" @# c& d
responsible for the early activation of the hypothal-, M) x3 O4 H$ M2 y8 K, J! i
amic pituitary gonadal axis.1-3 Thus, greater empha-) x+ r, b! j7 t2 H8 n
sis has been given to neuroradiologic imaging in
" A1 q6 }  l  ]& T2 ]# dboys with precocious puberty. In addition to viril-
; _% K' a, u4 v9 M, ]: {ization, the clinical hallmark of CPP is the symmet-* P4 g% \: P$ |7 x" U& f( x" J0 P
rical testicular growth secondary to stimulation by
* B5 s& g, [) W- A5 e/ [9 o4 hgonadotropins.1,3
2 \4 k% @( E; P. t- YGonadotropin-independent peripheral preco-
8 v$ L8 i$ _2 s1 Q$ [3 Qcious puberty in boys also results from inappropriate
* ~. k4 `( k. Q8 T# K3 Eandrogenic stimulation from either endogenous or' C: a% s& o. L& P
exogenous sources, nonpituitary gonadotropin stim-
8 R. z6 @- }( V0 f$ wulation, and rare activating mutations.3 Virilizing, F6 e! X0 s4 |6 o% z0 o
congenital adrenal hyperplasia producing excessive$ ^4 l# `0 D  }1 \
adrenal androgens is a common cause of precocious
  b! ~1 l* b) q$ N- S/ y/ N' u6 qpuberty in boys.3,4
  M+ T! u: y7 q4 JThe most common form of congenital adrenal
+ E: T# I1 z- ]) G1 U- f- {9 Ghyperplasia is the 21-hydroxylase enzyme deficiency./ z) N& H4 J  v- N- t
The 11-β hydroxylase deficiency may also result in$ k, B" r4 T# {
excessive adrenal androgen production, and rarely,
% }: K0 L& ?; A" {8 e9 gan adrenal tumor may also cause adrenal androgen. N9 j8 p. S% w
excess.1,33 B% ^+ f# O, x( a* w1 C; g6 ?. g, O
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 w% T5 u1 u" ~4 u; o) z
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007' q. Y* B* n: q% g0 Q; T! O
A unique entity of male-limited gonadotropin-, B; F" M* X' N: ?2 E
independent precocious puberty, which is also known
: f' c1 u+ m7 _% G/ c! pas testotoxicosis, may cause precocious puberty at a9 q% r' [3 r; O0 a! e4 n: n
very young age. The physical findings in these boys
) m( X7 u) v" c% w$ g- Q3 \: Y, Iwith this disorder are full pubertal development,* \0 ^0 I3 O% L# ^) Q# m
including bilateral testicular growth, similar to boys- ?5 B& ]% ?- ^9 ~/ V! Y3 {
with CPP. The gonadotropin levels in this disorder
9 b/ j5 ~5 n4 W* yare suppressed to prepubertal levels and do not show
0 p6 V6 G( T" P) Upubertal response of gonadotropin after gonadotropin-
1 p8 Q2 L8 q8 O  d6 o7 preleasing hormone stimulation. This is a sex-linked6 d& S; q" i1 W5 g" r: F
autosomal dominant disorder that affects only, |; |: v3 y- Q% z8 m8 L* w7 a0 A4 q
males; therefore, other male members of the family
/ Q$ ]6 V- k8 L& }7 Bmay have similar precocious puberty.37 G* z# i+ Q$ ]4 u# j
In our patient, physical examination was incon-0 b; e$ n4 a# @/ n+ b0 W9 B2 o
sistent with true precocious puberty since his testi-
7 b& A) N" |* n5 n5 B5 \0 ^cles were prepubertal in size. However, testotoxicosis6 l% p1 }6 T2 W6 t. V! z) \* @
was in the differential diagnosis because his father2 [5 d: l) `5 N8 U9 ?. n" i
started puberty somewhat early, and occasionally,
2 ?/ l$ z* N( O0 [testicular enlargement is not that evident in the1 K5 v7 y. }  M8 Z( x" O
beginning of this process.1 In the absence of a neg-3 r8 E0 P' V& Y+ L
ative initial history of androgen exposure, our9 S7 ^4 {  F( ]9 H) b( b
biggest concern was virilizing adrenal hyperplasia,$ c; r7 `% ]$ Z' I: i8 a
either 21-hydroxylase deficiency or 11-β hydroxylase
4 J  C$ n8 z  O, ?8 z3 kdeficiency. Those diagnoses were excluded by find-
+ y' t! a- ]' g6 s* eing the normal level of adrenal steroids.
  |- X% U) n: y( ~0 dThe diagnosis of exogenous androgens was strongly
% h% h. b/ O, [1 W9 Isuspected in a follow-up visit after 4 months because0 k) s/ _1 h5 i/ ~
the physical examination revealed the complete disap-1 m4 S& c9 `  H1 m4 I( K2 ^2 ?
pearance of pubic hair, normal growth velocity, and
4 N3 y1 T9 w. A1 F: kdecreased erections. The father admitted using a testos-- z, @: B9 K- d9 J- y2 ?
terone gel, which he concealed at first visit. He was/ C4 H8 f/ }6 i/ M
using it rather frequently, twice a day. The Physicians’
7 ~' m5 M* ^" t% G& e5 W9 ODesk Reference, or package insert of this product, gel or" \1 p' y! [0 \9 D  p* |' Y
cream, cautions about dermal testosterone transfer to, ?: ?6 N( Z/ j) E' G
unprotected females through direct skin exposure.$ e* M7 |! N; m, b- N6 P0 p
Serum testosterone level was found to be 2 times the
+ |4 N4 a, q( Ubaseline value in those females who were exposed to: q9 A: h" ~; D& V6 _, Z7 S
even 15 minutes of direct skin contact with their male
5 k9 r; Z4 ~* u/ V" M9 mpartners.6 However, when a shirt covered the applica-, W' A* X1 X8 n
tion site, this testosterone transfer was prevented.
0 q. A* m! f% o; JOur patient’s testosterone level was 60 ng/mL,5 n$ x4 j$ [5 T; R
which was clearly high. Some studies suggest that
0 J% n, U( r) ~* J( A2 z) K* l% Xdermal conversion of testosterone to dihydrotestos-
% C* ?0 D4 C+ ?+ Z  U2 u  R5 c5 _terone, which is a more potent metabolite, is more
* [2 F; m1 F1 c- @. |7 Iactive in young children exposed to testosterone
* o$ D# X5 k. u* ^! `exogenously7; however, we did not measure a dihy-
, F5 E/ O  a6 \5 E7 @2 Ldrotestosterone level in our patient. In addition to
  G3 {7 S4 s0 Z; y; N" {, I2 Rvirilization, exposure to exogenous testosterone in6 ?* a, d: o9 z3 U4 w
children results in an increase in growth velocity and! I+ Z0 |/ b& v5 q2 O5 S1 ~) R
advanced bone age, as seen in our patient.1 L" V) _" l; f9 k' {3 ^  s
The long-term effect of androgen exposure during* M( I: v- J3 k# \, N
early childhood on pubertal development and final8 H  ?% v; n! V2 s; }1 _
adult height are not fully known and always remain: T/ @% C, ]& O/ y
a concern. Children treated with short-term testos-) S4 J3 P5 @7 `" k
terone injection or topical androgen may exhibit some- g# r/ X) h) ~+ ^
acceleration of the skeletal maturation; however, after
, c) s6 m- o5 E( v. bcessation of treatment, the rate of bone maturation: m+ ~5 q$ {- k; ^1 `  i
decelerates and gradually returns to normal.8,92 ^0 C, R& M6 u1 v8 g
There are conflicting reports and controversy8 x& i7 v9 O# @+ E  X: c; U
over the effect of early androgen exposure on adult; \4 B: O9 T# Q8 M' A. ^
penile length.10,11 Some reports suggest subnormal
, U% P) U" b7 k& Dadult penile length, apparently because of downreg-" Y0 q$ ^4 W- m  @, O2 P
ulation of androgen receptor number.10,12 However,2 I2 `# S; ]# t. Z5 n. v+ s3 v+ Q* l
Sutherland et al13 did not find a correlation between
: `& u0 Y$ Y; {, Echildhood testosterone exposure and reduced adult0 I+ t! ^) t2 f% V& U/ U( a
penile length in clinical studies.5 B2 ?5 V+ P8 f9 e
Nonetheless, we do not believe our patient is2 G5 U( S$ T! e! C* W6 y
going to experience any of the untoward effects from3 J# H$ X+ k' k! M# g+ R
testosterone exposure as mentioned earlier because
# Y# H( J$ C- f* e7 ~the exposure was not for a prolonged period of time.: c% J2 R% j' ?  R0 A" l
Although the bone age was advanced at the time of
0 U7 s+ a$ A; m! i5 v) M3 \diagnosis, the child had a normal growth velocity at3 k& ^+ z$ C+ q9 i; o
the follow-up visit. It is hoped that his final adult
3 f/ [$ s8 }% m6 ^# ~6 Eheight will not be affected.
8 h7 v5 E" {& H0 `Although rarely reported, the widespread avail-  P. q+ Z6 t1 N
ability of androgen products in our society may
- g6 K* L4 y7 U( o; mindeed cause more virilization in male or female
) n' `- P  j& {$ d' }4 J  O, ]. ^children than one would realize. Exposure to andro-
  _9 e5 Q5 {( N( [gen products must be considered and specific ques-2 r( p! f; G2 X6 H0 U/ F( n2 V
tioning about the use of a testosterone product or; s/ h1 f7 r, g# w
gel should be asked of the family members during
! N6 @3 B2 E6 a0 sthe evaluation of any children who present with vir-# I6 B9 Y/ j3 W" O9 t% r
ilization or peripheral precocious puberty. The diag-: ?* y4 @, n! P: H5 B
nosis can be established by just a few tests and by# K. n! J3 r% n/ v- @' d; t
appropriate history. The inability to obtain such a
2 ]- J7 K: s# bhistory, or failure to ask the specific questions, may
/ k, }: K4 ?3 F3 ~result in extensive, unnecessary, and expensive/ \9 p& v8 r  J8 z+ P
investigation. The primary care physician should be
5 E" Q- ^  D& ~aware of this fact, because most of these children, X( f; r" j2 q% |1 j  y
may initially present in their practice. The Physicians’; j2 _) e( W1 f* W; L. Y
Desk Reference and package insert should also put a# w% f1 Y, M' D
warning about the virilizing effect on a male or. F& V, h9 m/ b1 _
female child who might come in contact with some-8 H3 E8 b- W$ o5 s
one using any of these products.. O: ^. a3 j0 H8 g
References" m6 T" d: U$ A4 K2 t+ L' g" H
1. Styne DM. The testes: disorder of sexual differentiation
% e" l9 e" [* uand puberty in the male. In: Sperling MA, ed. Pediatric
, _( c/ b; n( m! |  X$ W( k2 uEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;$ B1 s. u# [5 K
2002: 565-628.9 J# T9 V% W, r: V% H! Z  n
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
/ u) K7 n! \9 Y' n3 bpuberty 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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
6 _8 w/ ?* L- V' T
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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