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Sexual Precocity in a 16-Month-Old
7 R7 W. V- I8 M( D6 ?6 \Boy Induced by Indirect Topical/ A! L5 ?6 r3 x- g' k( d6 A8 f# o
Exposure to Testosterone1 a" p( ?  \& J$ |- M
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
+ z2 U. C2 T- u) R, kand Kenneth R. Rettig, MD1
5 E4 X5 ^! B! _+ y4 o( YClinical Pediatrics* @0 v0 m2 d3 ^3 Q6 k9 S
Volume 46 Number 6+ Q; y, `, t: S7 r7 p
July 2007 540-543" {  N' I9 g% R! h
© 2007 Sage Publications
9 c8 i0 Z6 o) A4 D* z" G10.1177/0009922806296651! K' v2 }8 Y, z( G+ I
http://clp.sagepub.com
- Q9 H3 Y) Q0 _hosted at
6 U2 Z' H% b* Khttp://online.sagepub.com
$ ^+ b  B3 Z& C6 J( S- ]Precocious puberty in boys, central or peripheral,
2 H" i% k6 A- P( @7 k7 \! qis a significant concern for physicians. Central5 S( O+ Q$ U7 u' p2 b: c! }
precocious puberty (CPP), which is mediated3 m9 B8 Z- M+ q9 n' l
through the hypothalamic pituitary gonadal axis, has
: A: v, ?4 S& R6 L0 ua higher incidence of organic central nervous system
1 F1 Q9 s+ i9 s% ^lesions in boys.1,2 Virilization in boys, as manifested
- q3 m/ O& N5 n. o: w( o% ~by enlargement of the penis, development of pubic+ X! S! \0 Q0 G9 G( o
hair, and facial acne without enlargement of testi-
/ i" Q# d  G2 R1 Gcles, suggests peripheral or pseudopuberty.1-3 We
! I$ _  F, i9 |7 \. G6 ureport a 16-month-old boy who presented with the
$ H! |3 O( o6 e; benlargement of the phallus and pubic hair develop-
$ f7 {) o$ g& n7 r5 U2 Qment without testicular enlargement, which was due
$ W6 h" s7 i/ B% ~: ~to the unintentional exposure to androgen gel used by
. [( @8 |5 `8 L7 _- n& B( zthe father. The family initially concealed this infor-
, J% \. {2 ~0 i8 t: emation, resulting in an extensive work-up for this' z4 C7 {8 a& G( Q
child. Given the widespread and easy availability of1 d$ e% G) k1 ]4 i/ [
testosterone gel and cream, we believe this is proba-: [1 G/ n; k5 }9 l1 b
bly more common than the rare case report in the5 k5 h6 z8 K0 L& @% O+ u
literature.43 ^* H( `# v9 e# S1 b7 Z* O
Patient Report
: Y( U+ S1 }& z, {! e; {A 16-month-old white child was referred to the4 V. C) _  P  q. S2 j: x9 h
endocrine clinic by his pediatrician with the concern8 G1 ]& z2 H$ {, Z; G, K* ]
of early sexual development. His mother noticed
. s8 [! S5 [4 Tlight colored pubic hair development when he was6 }, n9 a% p/ S5 I# ?+ u/ A) F/ {
From the 1Division of Pediatric Endocrinology, 2University of. l8 i1 V8 n+ }5 ?' Y! y- e
South Alabama Medical Center, Mobile, Alabama.
& L/ Z1 c6 C& I, `8 U' g- l) qAddress correspondence to: Samar K. Bhowmick, MD, FACE,
2 n- m- z' q5 @" B* ~Professor of Pediatrics, University of South Alabama, College of
+ G1 ]& q* g) M9 N2 N: bMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
' C2 c) L8 l% T2 |e-mail: [email protected].- J+ K" h0 _; ?+ `& J0 l; Q9 u5 y
about 6 to 7 months old, which progressively became7 I; C3 _5 J) w/ l% J- _# r
darker. She was also concerned about the enlarge-
2 f, ~5 X) f0 O% D  y8 Zment of his penis and frequent erections. The child$ l$ q: Q' J2 S4 l$ v+ H/ p" a) N
was the product of a full-term normal delivery, with" c8 n, ?# J( K( S; j
a birth weight of 7 lb 14 oz, and birth length of9 f$ r8 X3 N# H. U' x* x2 W
20 inches. He was breast-fed throughout the first year$ |( P) c, B1 f, k1 M7 N4 D
of life and was still receiving breast milk along with
, s0 {) b9 x3 n1 a$ T' C! ~0 esolid food. He had no hospitalizations or surgery,7 C; Z  L, V6 ~! R  a5 Q
and his psychosocial and psychomotor development
+ l: t, T$ p! V* P$ u; J/ `2 }. Iwas age appropriate.6 f: e; ~3 v( J. b
The family history was remarkable for the father,: t3 v7 o) i' X4 ?
who was diagnosed with hypothyroidism at age 16,
% ?' q3 m7 J) t7 L8 u  {6 q  vwhich was treated with thyroxine. The father’s
# Y/ `! C# E9 ~+ Mheight was 6 feet, and he went through a somewhat. n/ ]: B5 f2 O1 A# T
early puberty and had stopped growing by age 14.+ @% ], C2 A3 f" P9 j) b9 v
The father denied taking any other medication. The
6 s, |9 P2 ~3 m+ rchild’s mother was in good health. Her menarche
, W/ k& R. a, ~was at 11 years of age, and her height was at 5 feet3 X" {5 j4 U4 z, z
5 inches. There was no other family history of pre-( i) P1 v7 E, ^9 s1 E, S
cocious sexual development in the first-degree rela-
- d" K! u$ y$ H' b0 N; T% E% k3 otives. There were no siblings.
' L2 m3 ^* _& v: u. M8 EPhysical Examination
- S) E5 U3 N) _- y$ zThe physical examination revealed a very active,/ m* W6 r; {7 Y: a
playful, and healthy boy. The vital signs documented
( p, q' K, Z" u- ^4 Fa blood pressure of 85/50 mm Hg, his length was
$ W; `5 t! s" q- |/ \90 cm (>97th percentile), and his weight was 14.4 kg
. d/ \4 b: k% _* V, Q: i  B(also >97th percentile). The observed yearly growth
* o' M, s+ b, Vvelocity was 30 cm (12 inches). The examination of3 @9 T$ l, M2 P" `6 m; c8 A
the neck revealed no thyroid enlargement.4 z) R# s% ^; Z
The genitourinary examination was remarkable for& M+ f  o2 o+ X" Z" G3 j0 x
enlargement of the penis, with a stretched length of, W# c7 x/ j' w- [+ ~
8 cm and a width of 2 cm. The glans penis was very well
" s; U! f# [4 F% h# n. `  \developed. The pubic hair was Tanner II, mostly around
$ y# k6 \$ ~3 C: S1 i+ ]540
" {/ a1 P+ J; D9 H& i3 rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! _5 g+ f; y) W3 A+ `) A0 i8 ?the base of the phallus and was dark and curled. The
) u9 c4 x; G. p- R* y! ]0 @; ltesticular volume was prepubertal at 2 mL each.! P- R, h: E, D- i6 S; Q; ~9 Y
The skin was moist and smooth and somewhat
( H5 N  V) J4 ~; s9 Y8 \oily. No axillary hair was noted. There were no
! Z* R; R' D2 R8 V/ Q/ \5 @abnormal skin pigmentations or café-au-lait spots.( I5 X. |$ G9 ^  {
Neurologic evaluation showed deep tendon reflex 2+
4 i2 V4 W! [& v0 m3 h' U+ K& vbilateral and symmetrical. There was no suggestion8 k# z* R* a. ]: P! E% I* q7 f- W
of papilledema.
. Z# B5 w0 s' u  R6 W9 }Laboratory Evaluation
& a- l) ~: d* }& i- Y% {2 n1 WThe bone age was consistent with 28 months by; s4 P1 m1 w, n! H( V- L9 s1 w
using the standard of Greulich and Pyle at a chrono-
/ c, U* x6 B+ x4 Blogic age of 16 months (advanced).5 Chromosomal& g! w$ H: T( k+ d& d. f" i
karyotype was 46XY. The thyroid function test2 N& z! u+ B5 p5 Z+ q7 f- D
showed a free T4 of 1.69 ng/dL, and thyroid stimu-( |; |) g4 d: L- N
lating hormone level was 1.3 µIU/mL (both normal).
' Y, Q$ @" B% A5 k$ I  q5 FThe concentrations of serum electrolytes, blood
" ]0 U3 X  M) D: @urea nitrogen, creatinine, and calcium all were
4 F/ k- [; ?6 J! a2 |within normal range for his age. The concentration
' |- c" Q: U0 J4 z& R1 z* bof serum 17-hydroxyprogesterone was 16 ng/dL
: w* S$ J( m4 N" ?. ~(normal, 3 to 90 ng/dL), androstenedione was 200 ^" A- L% E' s% V' B$ q! Z
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
1 s; {) F# a7 L: Bterone was 38 ng/dL (normal, 50 to 760 ng/dL),7 X3 x: p* {8 t: v  ]+ ~8 i4 Q1 n4 E% \
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
; W" o( Z: k# s49ng/dL), 11-desoxycortisol (specific compound S)
( t' A- _: i6 h2 [3 Iwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-3 X0 S, `8 ~' W
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
) ], ]) Y7 n/ c5 c2 m9 M6 jtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),( s% G  S& B! I$ G9 W
and β-human chorionic gonadotropin was less than7 N& _" V; U' T# c
5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 H2 @( d4 E4 P  B& W" `, {9 w3 s- {stimulating hormone and leuteinizing hormone  g0 B% z0 [) S( k7 f! J
concentrations were less than 0.05 mIU/mL- A4 G! L' h) l7 \# L: ^
(prepubertal).0 Q, x7 o5 {5 U9 v, X( _1 G
The parents were notified about the laboratory
  Q$ T6 m/ j, y/ [results and were informed that all of the tests were
9 A( }1 @- N! A3 L4 c, mnormal except the testosterone level was high. The
/ D1 d0 m& _* x3 D9 ?, bfollow-up visit was arranged within a few weeks to
5 ?1 F6 A: ]$ x% u; zobtain testicular and abdominal sonograms; how-1 r4 E4 @" w! I2 D% d$ z
ever, the family did not return for 4 months.) [" _. Y: e- T0 L1 g
Physical examination at this time revealed that the# J* z* p1 o6 K) [# o2 E" n0 d# f1 R
child had grown 2.5 cm in 4 months and had gained
$ X" N( ~. D" k$ G9 t# G) X. A2 kg of weight. Physical examination remained
" e/ o6 l! u0 M; n1 kunchanged. Surprisingly, the pubic hair almost com-6 P/ f- l. n. B7 O+ X
pletely disappeared except for a few vellous hairs at
( c: f/ i/ Y# y! l. j. f( x8 p4 othe base of the phallus. Testicular volume was still 2  L) G: ?$ N6 e/ \/ ]' _5 p; J
mL, and the size of the penis remained unchanged.
) H' m6 G9 s! N) \3 M7 LThe mother also said that the boy was no longer hav-$ ^' h: S( v; U, C
ing frequent erections.
8 A* |# A# }  k' H( eBoth parents were again questioned about use of
( G8 c' N1 h! b; `, Xany ointment/creams that they may have applied to
) O* \$ C: V1 S% b. z5 n( ?9 Cthe child’s skin. This time the father admitted the; j# d2 ?& f7 F
Topical Testosterone Exposure / Bhowmick et al 541% ~$ U/ o3 [4 d6 m4 u& a  \( X
use of testosterone gel twice daily that he was apply-
! S# g2 I8 s" d9 P: bing over his own shoulders, chest, and back area for
6 u9 i8 n# K! ga year. The father also revealed he was embarrassed
# f2 f; m; f/ J! L4 d1 Uto disclose that he was using a testosterone gel pre-! v; u2 |! V. E5 Q; x; v- L; E
scribed by his family physician for decreased libido* X) f+ K$ o1 w$ O2 r
secondary to depression.
0 F% w  v/ F, r; z: dThe child slept in the same bed with parents.
$ h3 ?9 i) D9 @) f* q% iThe father would hug the baby and hold him on his6 |2 C/ j. E) U  j! T* D) V4 G
chest for a considerable period of time, causing sig-+ u( C3 J9 d0 f6 C, e) j
nificant bare skin contact between baby and father.0 Z2 J% z1 q" R3 C' h' a, c3 x! N
The father also admitted that after the phone call,. [( |9 Y8 r  C" \
when he learned the testosterone level in the baby
5 V1 ^6 ?" C1 j4 Z# ewas high, he then read the product information
  u" Y4 i; z4 l# Dpacket and concluded that it was most likely the rea-
) L* t) z$ j6 v. x7 o0 {% Dson for the child’s virilization. At that time, they
/ Y, X9 Q% j' j1 n7 e! F* [9 \decided to put the baby in a separate bed, and the/ U4 v# w. \) U: T
father was not hugging him with bare skin and had
; Q/ j; j* t  ]3 [, Y# P" \! abeen using protective clothing. A repeat testosterone2 D: b$ K1 @) Q8 E! G4 t
test was ordered, but the family did not go to the: {- A& k+ C. H
laboratory to obtain the test.
: X) A2 j0 D  S) ODiscussion! t# t, v! h: C
Precocious puberty in boys is defined as secondary
7 d/ c3 M: X& ]+ @8 v8 csexual development before 9 years of age.1,4; V: {5 U/ l4 a" W
Precocious puberty is termed as central (true) when
. }- S$ }9 q, P7 mit is caused by the premature activation of hypo-
$ t" S* i% A) e+ V4 Xthalamic pituitary gonadal axis. CPP is more com-/ W( L, K4 `6 \1 U. E' p% H
mon in girls than in boys.1,3 Most boys with CPP
: G7 f  j6 n: L6 ?  w2 i2 K4 Zmay have a central nervous system lesion that is# J) [3 S& S. i# Q
responsible for the early activation of the hypothal-
5 v, K0 M9 e8 G1 ]amic pituitary gonadal axis.1-3 Thus, greater empha-; I, i0 v! O- d1 b0 ^! Q5 j$ S
sis has been given to neuroradiologic imaging in
9 X5 K' W$ q- {2 b& ?: T  gboys with precocious puberty. In addition to viril-
9 k# z: H! m6 U2 v2 z" vization, the clinical hallmark of CPP is the symmet-
7 P, `  h! ~, [8 ^: ]0 u8 mrical testicular growth secondary to stimulation by
1 j% z+ j: N4 c$ N! t3 Mgonadotropins.1,3
9 u" R7 x7 ^, g2 A) A: L% uGonadotropin-independent peripheral preco-
+ M% @8 `/ {7 u% @% L" o2 ?cious puberty in boys also results from inappropriate
' d; g( m* B" ?5 |3 ^. N: aandrogenic stimulation from either endogenous or
; S/ K* ^/ l# d7 H3 ?; Mexogenous sources, nonpituitary gonadotropin stim-* [7 K9 a  m, h. y5 R
ulation, and rare activating mutations.3 Virilizing' r8 f0 u( Q! H# H
congenital adrenal hyperplasia producing excessive6 x$ R7 ^# U5 k4 J; W; P9 I6 R
adrenal androgens is a common cause of precocious
8 f: m' m: E0 ]3 `" qpuberty in boys.3,4
- ]6 d' o) ~$ E" ZThe most common form of congenital adrenal7 r( k9 j8 d" I. ~! `" I5 t! G
hyperplasia is the 21-hydroxylase enzyme deficiency.* S5 X5 i" p2 d! _1 }
The 11-β hydroxylase deficiency may also result in4 {8 A* f( @3 o9 @/ Y
excessive adrenal androgen production, and rarely,
5 A. U: I% f, V+ x. B0 a' \9 uan adrenal tumor may also cause adrenal androgen
1 |) _. A& g1 V: E* R5 Q# ?: Yexcess.1,3
2 \" T" u* H. i+ P3 L: H/ Q* m' tat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 h9 l) @, h# z! ^* ]0 f- Y' d7 ?542 Clinical Pediatrics / Vol. 46, No. 6, July 2007& F$ X! x( ?  @7 e5 @
A unique entity of male-limited gonadotropin-: [+ c4 k" w; a. s" L5 `
independent precocious puberty, which is also known
6 M- S; l+ D2 |9 [9 j( N/ H6 i4 uas testotoxicosis, may cause precocious puberty at a
+ ^' G1 Z. I6 [: ^very young age. The physical findings in these boys
. \- y4 P8 h2 Ywith this disorder are full pubertal development,( T3 i& p8 z5 p; J0 [2 ]9 R" i
including bilateral testicular growth, similar to boys
, C% |) u( z. u: b8 C& S3 F' r% c8 ywith CPP. The gonadotropin levels in this disorder/ V, X2 s# D! k
are suppressed to prepubertal levels and do not show
8 c, r) `; @# hpubertal response of gonadotropin after gonadotropin-
+ e7 @# e) D  `3 }2 v5 K# Sreleasing hormone stimulation. This is a sex-linked5 c' L5 q" J) [: N" w# |: C* ^
autosomal dominant disorder that affects only; K9 O3 C# }; U! O4 H3 u" V+ q
males; therefore, other male members of the family
. B& S- V9 h' zmay have similar precocious puberty.3
# t- a1 p. b: I# ?+ t* J, N2 AIn our patient, physical examination was incon-
3 z$ ~% B4 b2 D) ]8 Esistent with true precocious puberty since his testi-0 s3 Q! Y# p# D- D0 B  l
cles were prepubertal in size. However, testotoxicosis
& j4 A1 S( }0 H* `( pwas in the differential diagnosis because his father
+ u9 [+ d9 u3 m4 j/ p/ Kstarted puberty somewhat early, and occasionally,
  P+ q  ?- W: A  Y3 ptesticular enlargement is not that evident in the
$ R+ d. z+ f* I6 A8 P  \( j# fbeginning of this process.1 In the absence of a neg-
8 [. o% D4 b8 I; f- ~1 T; Aative initial history of androgen exposure, our
3 I' J& b% @( E; L- x4 ybiggest concern was virilizing adrenal hyperplasia,
" v+ e" f. Q% _  o, c& I3 yeither 21-hydroxylase deficiency or 11-β hydroxylase
4 C0 V4 p. a) u. b$ Pdeficiency. Those diagnoses were excluded by find-7 }: P  J! Q$ _7 @. E- C
ing the normal level of adrenal steroids.$ O9 Y! p& H" c  J% a
The diagnosis of exogenous androgens was strongly
0 D1 ~. `- F- U, Ssuspected in a follow-up visit after 4 months because
; [8 r' L. P, [# d* U& R4 athe physical examination revealed the complete disap-
; M% M- _3 _' o, R2 b+ `. N7 j& opearance of pubic hair, normal growth velocity, and
  f" i, o) {$ e& F- Sdecreased erections. The father admitted using a testos-
# s7 v1 K0 `4 U+ n/ Lterone gel, which he concealed at first visit. He was
, q" d! Q% e2 [1 v' k, ^using it rather frequently, twice a day. The Physicians’
! U' Q+ B7 v0 M, ~2 U3 V' E/ F& oDesk Reference, or package insert of this product, gel or
3 c) y' K* y4 u/ i& g  r& W" ^1 Bcream, cautions about dermal testosterone transfer to0 c4 r$ ^* G( V& @+ b$ v! |8 r
unprotected females through direct skin exposure.
) `% c/ C' j$ @/ JSerum testosterone level was found to be 2 times the8 @/ N# j- Z0 f+ e% B( }
baseline value in those females who were exposed to
- F9 S9 Q6 n! peven 15 minutes of direct skin contact with their male8 @' X" V0 h* c& J4 @& v: ~
partners.6 However, when a shirt covered the applica-, |' y& B  @& q" H. O
tion site, this testosterone transfer was prevented.( l2 U8 R$ m/ B% z7 i) g
Our patient’s testosterone level was 60 ng/mL,6 G/ W" K& g* ~" `( k
which was clearly high. Some studies suggest that
/ Z5 D+ ]% a0 [4 h- R2 A& tdermal conversion of testosterone to dihydrotestos-
0 ]% @" F, X- j: M% S/ L: uterone, which is a more potent metabolite, is more
4 v' I& K# x! ~% ~1 V) F7 N" ractive in young children exposed to testosterone. U- c( K  a0 C
exogenously7; however, we did not measure a dihy-4 ?$ e" C3 [( ~8 Q4 F
drotestosterone level in our patient. In addition to+ v0 E" V2 k, @# X; Q4 W+ G1 T
virilization, exposure to exogenous testosterone in; S% E: L. B; V  G; }
children results in an increase in growth velocity and
- N# O, E" p9 n% zadvanced bone age, as seen in our patient.) W, M% H) G( H; k
The long-term effect of androgen exposure during0 E! K$ `7 p/ x( c
early childhood on pubertal development and final" I5 X2 }" s# ]4 {: }% z3 D6 W
adult height are not fully known and always remain
( s" q8 {+ Y! W- t5 a, K( Za concern. Children treated with short-term testos-
, I1 j3 `. l' V( d! ^2 o3 _4 cterone injection or topical androgen may exhibit some- v, ?% e( @0 h  ~1 k, R5 d
acceleration of the skeletal maturation; however, after; M. p+ A2 y2 A* d% x
cessation of treatment, the rate of bone maturation
2 w- j  A  c6 T& l3 v  ]1 T- u* xdecelerates and gradually returns to normal.8,9
0 H3 L4 ]" J1 j) _6 eThere are conflicting reports and controversy% q) E6 `0 {. [
over the effect of early androgen exposure on adult5 p! F1 ]& }, I# R- [
penile length.10,11 Some reports suggest subnormal
( d. w! n0 c6 p: o/ \adult penile length, apparently because of downreg-
  ]7 z( G+ U4 k3 e# m, ~2 X: xulation of androgen receptor number.10,12 However,
  }  r# e4 t+ G7 k: H0 BSutherland et al13 did not find a correlation between' Q0 l" x, x; I3 T% U! Y) o: _
childhood testosterone exposure and reduced adult" d9 o# M  B& B7 O. d; Y1 I/ A) I
penile length in clinical studies." E; S2 x1 P0 t& P
Nonetheless, we do not believe our patient is
" j- |! b6 Z  r6 wgoing to experience any of the untoward effects from
% d9 s' |% I$ y: }" w  K- Ntestosterone exposure as mentioned earlier because) k* B* v2 a8 m9 J# H; z& T
the exposure was not for a prolonged period of time.3 @0 r6 R0 L- o1 Q& o; T
Although the bone age was advanced at the time of
# i* r8 M* i! tdiagnosis, the child had a normal growth velocity at$ H& A9 I+ |8 f( g5 e1 V" s
the follow-up visit. It is hoped that his final adult
  w& O; U+ s. {2 `7 u# L: rheight will not be affected.5 R" a! V5 L  C( E7 y  x: c
Although rarely reported, the widespread avail-
% _$ g2 l3 f/ Q& K& lability of androgen products in our society may
$ A- N% E; @# c( \! Hindeed cause more virilization in male or female, \# o# i$ `" a7 c
children than one would realize. Exposure to andro-/ I7 O1 H& S- n7 h6 k7 l2 g
gen products must be considered and specific ques-
) U9 B" _4 R7 r9 ltioning about the use of a testosterone product or/ T) Z- T' J) ^
gel should be asked of the family members during
5 g: M) E' K2 M1 A* Qthe evaluation of any children who present with vir-0 Y3 ?3 W7 U" T
ilization or peripheral precocious puberty. The diag-
9 l6 K7 A) ~- `; A/ Vnosis can be established by just a few tests and by; y$ M# n9 d0 E
appropriate history. The inability to obtain such a
6 O8 p0 x% L/ Uhistory, or failure to ask the specific questions, may
6 K+ t% K8 W2 {; ?& f8 a( o- j2 zresult in extensive, unnecessary, and expensive
& v8 J) V; Q8 B3 R  C5 `investigation. The primary care physician should be6 m+ G6 y1 r$ {+ M8 ?  w; D, X7 R6 ^" R
aware of this fact, because most of these children
% M# Y- b+ ~, u9 E6 bmay initially present in their practice. The Physicians’, B8 ]- P! O5 {5 Y4 E: {
Desk Reference and package insert should also put a0 E7 S: m, r* h3 N5 y  y
warning about the virilizing effect on a male or. `# ^" w( u, ~
female child who might come in contact with some-
0 _" [/ t# t$ K4 }& d8 Rone using any of these products." w. z$ l0 i# J% E$ P* d
References
$ o, D; ?) Y6 n* q1. Styne DM. The testes: disorder of sexual differentiation
. s  }" _, E; \4 X' c' q8 ^" ?; _1 Mand puberty in the male. In: Sperling MA, ed. Pediatric/ E8 v5 e, Y( s
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
. E9 Z7 J( {4 }, S0 B2002: 565-628.5 B0 l7 n  u/ Q. Y0 _: }7 S& I
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious  k+ r1 s& Z* D4 q  n
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old- i% f# c- q# l4 u3 z- n
Boy Induced by Indirect Topical
. {: I4 \5 i! {% gExposure to Testosterone! f  h" S7 b8 X3 ?* w* d" a/ U
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
1 W# Y" Q8 B+ U+ Z" n6 hand Kenneth R. Rettig, MD1
& s* M1 A" F. M/ t# ~Clinical Pediatrics
4 E, o) }$ A2 m( UVolume 46 Number 6
1 s# y8 d: ]5 U+ jJuly 2007 540-5432 e+ ]1 J( J+ m+ D/ |" @( f
© 2007 Sage Publications, r9 x$ Y9 F$ J- t. ~) M- f
10.1177/0009922806296651
8 T( h6 p2 \' ohttp://clp.sagepub.com% e! i: t" Q/ r3 i
hosted at
4 G3 c# C. d) Uhttp://online.sagepub.com
0 H5 @3 }$ A3 {Precocious puberty in boys, central or peripheral,
  W$ {( |( \- Q: `* fis a significant concern for physicians. Central% l& H; p9 V( w# A( H( Y
precocious puberty (CPP), which is mediated$ l2 q9 s9 C' O; P" Z; [7 r
through the hypothalamic pituitary gonadal axis, has
+ n4 L3 Y* R5 H2 X. i3 [a higher incidence of organic central nervous system% ]7 n. Y5 G" e7 Y& i/ }& E2 e
lesions in boys.1,2 Virilization in boys, as manifested
0 M; N; z! _; }by enlargement of the penis, development of pubic# P' Q6 I& r; \/ {) W! }1 `
hair, and facial acne without enlargement of testi-! e+ t7 x3 A/ [5 k
cles, suggests peripheral or pseudopuberty.1-3 We
8 E3 T! {1 T' U% }; Greport a 16-month-old boy who presented with the
9 g8 U" ^. W. n* q; ?2 r% cenlargement of the phallus and pubic hair develop-
! R: U1 g4 s& S, f0 L: `ment without testicular enlargement, which was due
% F9 y1 o+ G( G8 Sto the unintentional exposure to androgen gel used by
: A% p: p. C8 O) ?the father. The family initially concealed this infor-
2 S( a. }+ O) q2 ?  K' Rmation, resulting in an extensive work-up for this( e& j) D8 x2 Q. o6 x) ^; J" p
child. Given the widespread and easy availability of
1 _9 R& O9 X, w6 o/ @testosterone gel and cream, we believe this is proba-
8 A% U: D# m8 X  `bly more common than the rare case report in the
7 `1 a% G9 [( o1 @. Bliterature.4
) t9 R) x8 d% s9 X2 L4 p- H1 M% Z" rPatient Report2 q- ~! c+ ^5 O( x) m, d, v
A 16-month-old white child was referred to the
/ [0 K0 U, m6 ~, U  A  xendocrine clinic by his pediatrician with the concern% G$ a9 [8 M) a+ Q
of early sexual development. His mother noticed1 t' H  c+ E! g0 {! @; _3 j/ {
light colored pubic hair development when he was, K2 n7 `, c& o# o- D: c
From the 1Division of Pediatric Endocrinology, 2University of6 H7 ~' [& E' u0 ^  p4 |  s
South Alabama Medical Center, Mobile, Alabama.* c$ h8 G- e) K: T; `- r6 Q7 @
Address correspondence to: Samar K. Bhowmick, MD, FACE,
/ t5 I4 F0 d0 O' B1 F- [Professor of Pediatrics, University of South Alabama, College of+ G- v9 x0 L. w9 t4 x
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;5 k. K& j9 h+ k- h. ~
e-mail: [email protected].9 X) e! a, ?9 ^' g7 ^" C! ?
about 6 to 7 months old, which progressively became
! M. v* `* C  i2 ^, Pdarker. She was also concerned about the enlarge-
  Q' x  g2 G; q! Gment of his penis and frequent erections. The child
, ?3 o% B$ C5 O9 i4 Pwas the product of a full-term normal delivery, with( _* r, _" t5 J" L/ \
a birth weight of 7 lb 14 oz, and birth length of
2 B8 K; w1 a% V9 k# k20 inches. He was breast-fed throughout the first year
3 J" `! \# z7 q4 M  N9 Uof life and was still receiving breast milk along with- I+ s, x" y- O0 T- N3 S9 Z
solid food. He had no hospitalizations or surgery,2 T- n3 V! }9 F
and his psychosocial and psychomotor development1 {8 v2 L) ]9 v, f. A6 x# T
was age appropriate.
" X$ z" w/ U( c# q. S/ d* _The family history was remarkable for the father,# G4 C1 \4 j6 ?6 |
who was diagnosed with hypothyroidism at age 16,
2 y$ J: m+ R5 \) F: }  a% R- a% Swhich was treated with thyroxine. The father’s
! p1 m( Z+ K- {+ Y: yheight was 6 feet, and he went through a somewhat0 A& x& L; I( H8 K2 i, Y4 a" a( b
early puberty and had stopped growing by age 14.# i) L/ Y# J9 n2 c
The father denied taking any other medication. The
/ ~7 b5 W/ D8 S+ Qchild’s mother was in good health. Her menarche9 P7 d3 y& P$ G6 \' A2 |3 i5 l
was at 11 years of age, and her height was at 5 feet* s  Z% r5 ^. O; H
5 inches. There was no other family history of pre-
9 f# @3 ]) n$ ?cocious sexual development in the first-degree rela-
7 H* o2 L0 G+ U4 m/ u4 v7 i* Atives. There were no siblings.
1 K2 w- l' y% E! }. L4 @Physical Examination5 k5 U6 E' F2 ]. R
The physical examination revealed a very active,
  r  b9 q6 K% f" ^9 Hplayful, and healthy boy. The vital signs documented
1 L+ u) p$ `, y5 [4 S5 pa blood pressure of 85/50 mm Hg, his length was
! S) F/ l, u1 @! D90 cm (>97th percentile), and his weight was 14.4 kg
+ D. `( O  q  T8 s& f(also >97th percentile). The observed yearly growth
( w9 Y' b8 D4 Q* ]velocity was 30 cm (12 inches). The examination of- Y  ^. i2 h  m0 L( O' I* K
the neck revealed no thyroid enlargement.
! l( h. ^9 T4 cThe genitourinary examination was remarkable for
4 z8 f$ z# y9 N* Qenlargement of the penis, with a stretched length of: r. W# e+ D9 m: g0 s4 a
8 cm and a width of 2 cm. The glans penis was very well# @: ^% I* N8 s% u- x, w! a
developed. The pubic hair was Tanner II, mostly around
9 x: H( Z# i  }. C) H5408 ]; w0 ~. O! I( q" V9 b/ o
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" O  G! j' R9 e9 q, z5 sthe base of the phallus and was dark and curled. The
2 ^! T8 j& q, Ztesticular volume was prepubertal at 2 mL each.
* c: \$ l' R* x  [' D5 x* {The skin was moist and smooth and somewhat7 [2 `. D: i. B" K- _* L
oily. No axillary hair was noted. There were no
2 j' F; H5 e4 C% a6 Labnormal skin pigmentations or café-au-lait spots.
& l8 ]3 v! T( sNeurologic evaluation showed deep tendon reflex 2+6 A0 j# a$ {5 ^! A6 E" s
bilateral and symmetrical. There was no suggestion1 k4 n; i, ]& G0 _$ @- p3 r
of papilledema.
0 G, K# n$ b- t8 [1 _: xLaboratory Evaluation) t# ?' g! E: F3 o0 {4 o
The bone age was consistent with 28 months by
& ?# H- v! r3 musing the standard of Greulich and Pyle at a chrono-+ z$ ~/ Y( o8 r9 b# ?
logic age of 16 months (advanced).5 Chromosomal
/ b0 n; K9 V  w! r9 g. Z8 lkaryotype was 46XY. The thyroid function test) n4 S+ Y' Z% D8 o7 X3 f
showed a free T4 of 1.69 ng/dL, and thyroid stimu-  f+ d- ]- T. o4 r
lating hormone level was 1.3 µIU/mL (both normal).
% O, F. T" o( w; g  h6 F' NThe concentrations of serum electrolytes, blood: q- R: s$ l, H6 y6 v" l
urea nitrogen, creatinine, and calcium all were8 h  D' Z' m+ A$ C% _' U2 H
within normal range for his age. The concentration9 C( K# ?9 K. {' k
of serum 17-hydroxyprogesterone was 16 ng/dL" R$ w: v2 K8 B1 V# E) ~( k. b# b; b1 _
(normal, 3 to 90 ng/dL), androstenedione was 202 F5 g; Q4 }  O9 S  N
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
4 f8 c5 O! A$ p& Y' c1 dterone was 38 ng/dL (normal, 50 to 760 ng/dL),9 i# S& z3 w; P* a! F8 b$ G- |2 I3 C
desoxycorticosterone was 4.3 ng/dL (normal, 7 to3 `1 c) O& l& Z6 I: O* T: V( C
49ng/dL), 11-desoxycortisol (specific compound S): K) K, l! U- T; k
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# h" _" O' G" w  h2 R- V3 G3 E3 Z
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# U: W: O5 W4 w- O' v2 ^0 c0 B5 ~
testosterone was 60 ng/dL (normal <3 to 10 ng/dL)," r$ p, M0 x: J2 m, n
and β-human chorionic gonadotropin was less than/ {# t" o* A, ^) ], E; P' \( d
5 mIU/mL (normal <5 mIU/mL). Serum follicular+ y$ q! K7 N! {7 `9 G& n
stimulating hormone and leuteinizing hormone
  s. I* i0 j0 d2 yconcentrations were less than 0.05 mIU/mL: l- ~! V  `& ?7 h3 |  G
(prepubertal).
7 n  j  r9 e1 i; I  Q: S' |The parents were notified about the laboratory5 d# i/ N3 N. c) ]
results and were informed that all of the tests were
# }$ R. R6 x) \. Znormal except the testosterone level was high. The5 u9 P& e" y; Q7 p) A( E2 X' s
follow-up visit was arranged within a few weeks to
5 `$ Q- U) `0 `- X& A1 s/ }) iobtain testicular and abdominal sonograms; how-
  w2 P% d3 k2 M" ^8 zever, the family did not return for 4 months.9 |% ~$ _6 r' \
Physical examination at this time revealed that the
, I+ |1 u9 S/ f5 c/ h6 T( S# _4 Dchild had grown 2.5 cm in 4 months and had gained
: Y; z6 ?0 M% Q! Z$ D2 kg of weight. Physical examination remained5 k- V5 U+ V3 x. d3 d0 q) J
unchanged. Surprisingly, the pubic hair almost com-
& K5 p9 [, X$ z% B7 e9 Wpletely disappeared except for a few vellous hairs at  M  q: u5 Q" }/ l; N6 H! T/ r
the base of the phallus. Testicular volume was still 2! Z6 `# g4 m, B" o
mL, and the size of the penis remained unchanged.
  D/ d$ w! }4 C" u2 @The mother also said that the boy was no longer hav-
  u: I* ?! y+ t2 s$ ding frequent erections.3 r$ v/ Y& Y$ x. B# G
Both parents were again questioned about use of
# h, `6 }+ {; P$ J: S) I) tany ointment/creams that they may have applied to3 Y& N7 y9 [3 ~+ p
the child’s skin. This time the father admitted the; r' S$ {/ Z- Y# G/ Z
Topical Testosterone Exposure / Bhowmick et al 541: ]# B2 t% T8 L. f/ b
use of testosterone gel twice daily that he was apply-3 P8 Q, k9 f" L, Y% `) f* _5 ^0 R% V6 O1 z
ing over his own shoulders, chest, and back area for
' A: N5 o: z& x, \a year. The father also revealed he was embarrassed' o7 R+ n2 t' `  L6 X$ g6 H8 z4 x
to disclose that he was using a testosterone gel pre-- z9 _, p4 \3 J/ o# l$ r- T
scribed by his family physician for decreased libido( G: u& M6 R5 q4 h3 Q% X
secondary to depression.
* E/ F$ t) j: O7 ]The child slept in the same bed with parents.' i3 i: J; A0 i' E5 T
The father would hug the baby and hold him on his
9 ^! ]' H7 V. lchest for a considerable period of time, causing sig-8 @) X- ~9 {! T; B
nificant bare skin contact between baby and father.( w+ G# N; [, I2 D  t% h
The father also admitted that after the phone call,
$ k7 k& ]( @2 v$ L+ v) M- h- Cwhen he learned the testosterone level in the baby
  }7 y2 q0 L3 v) E) jwas high, he then read the product information
6 k4 w" R& T/ k0 o# `* opacket and concluded that it was most likely the rea-( s) z3 g4 t2 ]& c1 [
son for the child’s virilization. At that time, they
/ Q  V  L- a1 P- Y  M' G) w& q! Adecided to put the baby in a separate bed, and the$ f* H2 ~: p8 B9 \/ b; M
father was not hugging him with bare skin and had
0 M2 x# ?* m( P+ h  M% Tbeen using protective clothing. A repeat testosterone
6 @' s( N! c, W& t  g4 z! ptest was ordered, but the family did not go to the0 A) ^  o3 s8 P# b2 g& `
laboratory to obtain the test.( b1 K& ^  `4 j1 g4 u4 O0 V  b
Discussion: j; N- z3 P3 G- X
Precocious puberty in boys is defined as secondary
" u7 b* _+ J* M: I1 p/ msexual development before 9 years of age.1,40 q; e! F! y/ W1 y  Z, @, _+ K2 i
Precocious puberty is termed as central (true) when/ _5 g5 T+ t% d0 G$ S0 \
it is caused by the premature activation of hypo-
9 a$ I0 |# R+ H9 Ethalamic pituitary gonadal axis. CPP is more com-
- \. F- @5 h6 T+ f: Qmon in girls than in boys.1,3 Most boys with CPP
; M% S& ~( Q" O8 ^5 N/ N; Zmay have a central nervous system lesion that is' B- H( a+ s7 D; m- s; x& G; Q
responsible for the early activation of the hypothal-
: G2 p! z: u$ C% Z2 L9 ?amic pituitary gonadal axis.1-3 Thus, greater empha-
% m& t* Q: Y: vsis has been given to neuroradiologic imaging in7 X7 h( U9 ^( p4 L% {
boys with precocious puberty. In addition to viril-( C! L0 G' K! f
ization, the clinical hallmark of CPP is the symmet-( S3 `. F3 o9 R; T
rical testicular growth secondary to stimulation by
5 K4 S: s3 ~0 S' p3 [4 Ygonadotropins.1,3
3 X) x' o4 ^. h; FGonadotropin-independent peripheral preco-' q5 a- r6 {% Q' a
cious puberty in boys also results from inappropriate
/ a6 R+ z/ U, b9 }0 c7 k: ~1 \" mandrogenic stimulation from either endogenous or
4 w& j9 ?' c; [7 f; o5 A! e  ^exogenous sources, nonpituitary gonadotropin stim-
/ ?8 z1 P$ d3 n6 f6 eulation, and rare activating mutations.3 Virilizing: K5 B9 I& z; l* Z8 X
congenital adrenal hyperplasia producing excessive' t6 ]! b- R; S/ J7 x' }- S
adrenal androgens is a common cause of precocious
  @0 j0 |" i9 ^! Upuberty in boys.3,4- W0 @! i% S+ G1 W7 W
The most common form of congenital adrenal- C& X% `! D% N! Z
hyperplasia is the 21-hydroxylase enzyme deficiency.
& S6 R7 z" o. l! Y: ]5 eThe 11-β hydroxylase deficiency may also result in( Q$ y' |4 ^2 w- B- G+ R
excessive adrenal androgen production, and rarely,
& F7 {1 M6 }% Ban adrenal tumor may also cause adrenal androgen' @; X7 I+ Q- }
excess.1,3/ J- B7 i6 B% Y
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 w8 T1 _1 h% x542 Clinical Pediatrics / Vol. 46, No. 6, July 2007: c, l0 {1 t  C: G' Z9 ]
A unique entity of male-limited gonadotropin-* P, g" @( |  E
independent precocious puberty, which is also known2 }' N+ M; L8 F3 W$ e2 Y, F
as testotoxicosis, may cause precocious puberty at a
+ p2 q! V7 |) p; S- w. U' S; Rvery young age. The physical findings in these boys* i$ {, H4 _" _4 a# y3 E
with this disorder are full pubertal development,& a. S8 M% Z9 n: M& d7 L
including bilateral testicular growth, similar to boys
; c  J' z0 n6 d+ |/ ~: }8 t5 Jwith CPP. The gonadotropin levels in this disorder
4 W2 ^# Q8 w3 ]& [" X+ M. p# ~are suppressed to prepubertal levels and do not show7 L: p$ g7 D8 o% _1 s0 R
pubertal response of gonadotropin after gonadotropin-
) K" _) b# L. Z% x# c2 Nreleasing hormone stimulation. This is a sex-linked9 |1 I# ]$ u" \/ Z2 N4 i! o
autosomal dominant disorder that affects only" N* a  B6 z2 I2 Y
males; therefore, other male members of the family
6 l; I' x% w  F, U) Tmay have similar precocious puberty.3) l" j7 \& C1 ]) I
In our patient, physical examination was incon-
0 ~2 N+ M3 D2 D; dsistent with true precocious puberty since his testi-
/ M! K: w: j# k" E0 O" ^2 Qcles were prepubertal in size. However, testotoxicosis
# t$ W6 G9 Q% w5 Kwas in the differential diagnosis because his father
+ d, i0 }  X! t# v7 r: `started puberty somewhat early, and occasionally,0 x4 g. R2 x3 A2 r# V7 d' }
testicular enlargement is not that evident in the
8 E7 Y9 J7 Z! T8 Dbeginning of this process.1 In the absence of a neg-& |' e, R. [) I1 u: B5 B7 P) _
ative initial history of androgen exposure, our
$ ~  ?8 H6 Y1 E9 X3 Rbiggest concern was virilizing adrenal hyperplasia,
  L  l+ C- `4 W9 [- K2 Q9 feither 21-hydroxylase deficiency or 11-β hydroxylase
/ [* I9 r  O1 C( p$ w6 i9 mdeficiency. Those diagnoses were excluded by find-
8 x- x. \" f8 d* U+ H  ning the normal level of adrenal steroids.
% i% D) B8 ~5 B% c3 E& z# @The diagnosis of exogenous androgens was strongly
2 v+ \1 ?! S8 x6 ^- tsuspected in a follow-up visit after 4 months because
: c8 i- ~! G/ {the physical examination revealed the complete disap-: q( P4 u% I& X  D+ |/ q  l
pearance of pubic hair, normal growth velocity, and
: V5 h& @* A. c+ Z) S7 Zdecreased erections. The father admitted using a testos-
2 l( [/ X, }; z( d( ]( Dterone gel, which he concealed at first visit. He was  R1 @  n: Y+ Z9 l7 t& D2 o
using it rather frequently, twice a day. The Physicians’
7 d4 j4 \0 X% W6 iDesk Reference, or package insert of this product, gel or
  G/ D' N: U- C( \8 Y) hcream, cautions about dermal testosterone transfer to
; z; n, ?) Y5 {* Q) }* Punprotected females through direct skin exposure.
4 h# f4 K2 h' i8 X) }Serum testosterone level was found to be 2 times the
9 r: `$ I0 J- @# L: ]( U' Lbaseline value in those females who were exposed to  W: u& h, d/ ?7 ^& J/ ^! d! T
even 15 minutes of direct skin contact with their male
, k; y5 n9 R+ a& M. ipartners.6 However, when a shirt covered the applica-
# j7 ^  w- C9 g  T2 \$ jtion site, this testosterone transfer was prevented.2 B& D+ V& ]- n
Our patient’s testosterone level was 60 ng/mL,; A2 z4 o/ b+ S; b' e) W
which was clearly high. Some studies suggest that* |  @4 ~4 A2 b$ [; K! J
dermal conversion of testosterone to dihydrotestos-
0 [( E: \6 `+ }4 {# h4 n( Rterone, which is a more potent metabolite, is more
$ @3 W; t5 U- z. G* dactive in young children exposed to testosterone
( T4 f* Q# _4 z- |2 ]exogenously7; however, we did not measure a dihy-
# P1 I4 K- Z4 u6 ]drotestosterone level in our patient. In addition to, h( b6 U) ^6 A4 X
virilization, exposure to exogenous testosterone in" h# G' m9 d8 i9 R. r
children results in an increase in growth velocity and
* }' L, v& c0 e7 }, Z, W5 Tadvanced bone age, as seen in our patient.' J/ }% F1 B( Z% P0 i1 C: C5 B7 ?9 Y
The long-term effect of androgen exposure during
: i- \# Q# |) U- kearly childhood on pubertal development and final
( M- u+ j+ \- q5 ~: aadult height are not fully known and always remain  u. V# ], k& C: V) B
a concern. Children treated with short-term testos-' |: U$ B4 U7 |/ v; I1 E
terone injection or topical androgen may exhibit some
, P- H# P' ]9 f8 Y, Z" Vacceleration of the skeletal maturation; however, after
" E  \( `! S  Y$ u" N% u7 hcessation of treatment, the rate of bone maturation$ F. t7 o; T3 T+ G$ Q# t
decelerates and gradually returns to normal.8,9: ?7 I/ C9 k/ j- O6 ~: N; y
There are conflicting reports and controversy6 ~- n! F7 |* \5 y5 s/ z1 u
over the effect of early androgen exposure on adult
! h5 a' j. N) Q% _  ^( Zpenile length.10,11 Some reports suggest subnormal+ ^1 H& x& {  a
adult penile length, apparently because of downreg-- y# ~, |. F5 d0 u
ulation of androgen receptor number.10,12 However,
! S! ~/ ~) J3 x# ZSutherland et al13 did not find a correlation between
( k) B- i+ M/ I/ [: f: r: |, ochildhood testosterone exposure and reduced adult; P! r" i$ ]! ~
penile length in clinical studies.
2 {8 w- `4 j' Q/ {Nonetheless, we do not believe our patient is
1 p$ ^5 B, g8 v7 V1 j3 }8 bgoing to experience any of the untoward effects from
9 q! a/ D. ], F' D" Jtestosterone exposure as mentioned earlier because
# D. ?8 a" m" K; c+ ^the exposure was not for a prolonged period of time.
6 z2 O1 [8 V: m) Q$ E8 ?Although the bone age was advanced at the time of/ [* s3 i8 \9 W6 M: u
diagnosis, the child had a normal growth velocity at
- l) P% j5 O8 h) Sthe follow-up visit. It is hoped that his final adult& H/ {) j$ ~) y$ N  a
height will not be affected.* j! Q& N1 K+ l8 V2 _. N- s
Although rarely reported, the widespread avail-
. B  _, ?) P; h: Qability of androgen products in our society may
# _# i: ^& R1 o- Jindeed cause more virilization in male or female: Y1 Z. U) b7 H) ?; F- @
children than one would realize. Exposure to andro-$ a8 `" h/ Y6 V+ b& g9 Z0 u; R
gen products must be considered and specific ques-( j0 X/ ~& H9 j: j: ?& Y% F
tioning about the use of a testosterone product or
  i' w% Y: X. s. x9 bgel should be asked of the family members during
! T" K0 `0 d  o' p: i5 h8 N" fthe evaluation of any children who present with vir-6 G8 i6 L7 @! P
ilization or peripheral precocious puberty. The diag-
1 ~' {5 F% q+ n& ynosis can be established by just a few tests and by
, k, t/ a0 `. k& P  v9 @! Oappropriate history. The inability to obtain such a7 \, ]8 Q: a6 K1 B) q
history, or failure to ask the specific questions, may
- t( T' @5 g8 M) z+ K2 [3 A, f8 Eresult in extensive, unnecessary, and expensive
% S! j7 E! |1 j9 O3 {investigation. The primary care physician should be. I% c7 w8 z. U
aware of this fact, because most of these children" s8 `- F# c  E  y
may initially present in their practice. The Physicians’! H- _' G/ W& o% l9 o
Desk Reference and package insert should also put a7 F0 ]8 n0 E, u' ~  i7 x1 Y( c
warning about the virilizing effect on a male or
% G, p$ c- L3 L" V8 zfemale child who might come in contact with some-
, c& T$ z) O* @9 O0 Z" G( I3 Tone using any of these products./ l4 z9 U! @8 o, ]% I1 C( \
References
4 J8 C, s' f# A' G: M5 m! R8 k1. Styne DM. The testes: disorder of sexual differentiation
* z% m$ S" l( ^( M- I) o# Oand puberty in the male. In: Sperling MA, ed. Pediatric! M. r7 m  K6 ~- P8 o8 q8 v+ o7 ~
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
' ~1 S1 P! W, ~8 l( |/ y. J. D$ d2 \2002: 565-628.
3 S+ ?( C6 o$ v; H: Q3 a/ Q4 u2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
& }3 R* _3 q* |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

% e9 s5 c! V3 p  _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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