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Sexual Precocity in a 16-Month-Old( p' v! s! s: @( E5 j; V  {
Boy Induced by Indirect Topical
2 [1 G' S5 ^4 G5 g0 V" z! ~Exposure to Testosterone& h8 [& g& R5 K6 [8 c  [! T
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,28 `/ c! C/ {1 v) k1 B/ s
and Kenneth R. Rettig, MD1
9 E3 E  u3 M2 e/ j) fClinical Pediatrics2 k1 f: j9 F( J* k4 A
Volume 46 Number 6" w$ s( t; A, m% {* i
July 2007 540-543
( A8 o( ^7 \% V$ _© 2007 Sage Publications' ?) I. y; B2 {( J
10.1177/0009922806296651; t* n! p& S& i
http://clp.sagepub.com
& S( y, a0 v) O- M% s& N, ]hosted at
7 ^: N. O" T. x. t6 U. S( dhttp://online.sagepub.com
# }- X6 ~" F; V) T4 o2 d4 M! nPrecocious puberty in boys, central or peripheral,1 S, b% e0 s& s0 |) V6 B1 |: {
is a significant concern for physicians. Central. M  O/ F3 r4 i5 _
precocious puberty (CPP), which is mediated" m5 C. |) ?% @$ |
through the hypothalamic pituitary gonadal axis, has* e/ ]- `2 ]" E
a higher incidence of organic central nervous system
; Q+ I" s5 {% w9 w$ ^7 ]8 ?/ k* L, Mlesions in boys.1,2 Virilization in boys, as manifested
; L9 \7 R+ |9 L8 K6 Y' }6 E; H$ }by enlargement of the penis, development of pubic
" k8 f: \2 s4 l( d& fhair, and facial acne without enlargement of testi-
0 e; R0 @, Z' [( ucles, suggests peripheral or pseudopuberty.1-3 We6 a# l4 O7 O- t# `' t# k% {: l
report a 16-month-old boy who presented with the& z% C3 r  ]' `1 A& S. W4 }
enlargement of the phallus and pubic hair develop-
- q+ ^  E$ N0 q- v+ B; [ment without testicular enlargement, which was due
7 d: d, g3 I# f9 \1 h; Kto the unintentional exposure to androgen gel used by7 N& o  V' f: L3 x
the father. The family initially concealed this infor-
/ d+ T, q- E, L. M3 c  vmation, resulting in an extensive work-up for this
0 ?4 w0 n2 Y1 U+ N( |3 [" mchild. Given the widespread and easy availability of
0 y8 _8 h: v4 u: M: P4 {& \testosterone gel and cream, we believe this is proba-  K4 W8 A4 T2 _  s/ J( U5 n
bly more common than the rare case report in the7 n$ |! S% E* ^# ~6 t5 `, {
literature.4
: B, @/ C) j: K; t! Y7 e' C6 }) VPatient Report
0 J; a5 Y5 r% G$ d0 MA 16-month-old white child was referred to the0 w0 F, _2 K: j( P$ l
endocrine clinic by his pediatrician with the concern
( y& @& O5 ^6 _  v  N- ^! ]- Kof early sexual development. His mother noticed4 p8 G$ z5 q. [5 w5 w
light colored pubic hair development when he was  ^# P; V/ x* K7 B2 C5 \
From the 1Division of Pediatric Endocrinology, 2University of" z. P! p8 N( v8 M0 p8 M9 ^
South Alabama Medical Center, Mobile, Alabama.
' U% M; O  N! f9 G, ]  m: \" S7 _) vAddress correspondence to: Samar K. Bhowmick, MD, FACE,2 s0 |; E) c2 M4 \( Q& t
Professor of Pediatrics, University of South Alabama, College of* Z- C5 M- ^. Z0 L' E% f; b
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;/ j. G) V1 \$ G, K+ ^
e-mail: [email protected].
9 k4 w: a  W. x. Xabout 6 to 7 months old, which progressively became7 N) _) M6 H7 b6 R  O; y7 x# W
darker. She was also concerned about the enlarge-; Q4 j5 X1 r6 p
ment of his penis and frequent erections. The child
1 Z% w6 v+ z; s/ `was the product of a full-term normal delivery, with
: q, ]/ D7 Y" f$ p! U, T9 D$ F1 Da birth weight of 7 lb 14 oz, and birth length of" @: l9 w! W% ^" g0 D
20 inches. He was breast-fed throughout the first year
  Q7 i/ M$ r$ Q8 y4 f0 Cof life and was still receiving breast milk along with8 I6 N( l& ~4 O, V" Z
solid food. He had no hospitalizations or surgery,& \7 V5 M( ~: M3 V! a( b0 r
and his psychosocial and psychomotor development
) X7 ^8 ?: r5 D6 H5 ?# |was age appropriate.
6 J8 x: P5 ^6 f& [& g) vThe family history was remarkable for the father,( Q. S2 t' v" A, V) Y( y9 Z
who was diagnosed with hypothyroidism at age 16,$ ?" V! R) \4 t
which was treated with thyroxine. The father’s
3 t( A6 Q6 K5 J0 Jheight was 6 feet, and he went through a somewhat: @8 v+ x' n8 i& M: w, V, t
early puberty and had stopped growing by age 14.
4 S! t4 W( s; `9 M/ `5 L% QThe father denied taking any other medication. The
5 i. j; Z' ~( Z- }* \child’s mother was in good health. Her menarche
0 [0 n% l: M) K  xwas at 11 years of age, and her height was at 5 feet1 {4 r) y; P- V& w+ c0 g
5 inches. There was no other family history of pre-
) a9 \1 ?9 G/ K1 X+ J6 `) P9 ^- Ococious sexual development in the first-degree rela-
; Q5 Z& }9 e: wtives. There were no siblings.
& p# f6 Q; y5 ePhysical Examination! n: ?1 l7 y$ }. }
The physical examination revealed a very active,
/ X4 w5 c/ L# D3 m( a. Eplayful, and healthy boy. The vital signs documented! Y! T* v8 A, T4 |. z: n
a blood pressure of 85/50 mm Hg, his length was
2 u& X. L- ^) |7 M$ y3 @8 ~90 cm (>97th percentile), and his weight was 14.4 kg& h7 H. Q! T6 s. L0 r
(also >97th percentile). The observed yearly growth" N7 O& V$ x" j& v% n. U% D1 ~$ d
velocity was 30 cm (12 inches). The examination of/ o# q2 I6 a" E7 S, V0 `
the neck revealed no thyroid enlargement.
( c( [+ p3 J( F3 U$ g% K( M: H5 TThe genitourinary examination was remarkable for
- @" ~% y1 x  K& Q7 o& Q+ G. henlargement of the penis, with a stretched length of
. V" O5 L9 J/ A. U* f) Z: s8 cm and a width of 2 cm. The glans penis was very well
% P4 I4 O) _: ^3 s) p" qdeveloped. The pubic hair was Tanner II, mostly around0 _2 D  p! C5 P  t
540
7 I+ M# Q) R% e/ \7 F* Y: q' V' \at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& r0 k$ z9 W& T! p- b7 ethe base of the phallus and was dark and curled. The4 M" g8 P# W7 G  [/ J3 p9 t
testicular volume was prepubertal at 2 mL each.
- p0 g1 q7 B3 J1 P1 E& p9 KThe skin was moist and smooth and somewhat! l2 S' P' ?: \* [6 m
oily. No axillary hair was noted. There were no
% K6 h- r+ Q5 q3 habnormal skin pigmentations or café-au-lait spots.5 g+ M/ Q" `& W3 x4 |8 ^, L
Neurologic evaluation showed deep tendon reflex 2+
/ |( `% c1 N/ b" ?: hbilateral and symmetrical. There was no suggestion
, d. r% Y# v0 B/ R. M* I  Wof papilledema.$ D2 D9 R1 _, ^. \
Laboratory Evaluation
- ^& }: V: M( R3 e! W8 c4 g5 R/ xThe bone age was consistent with 28 months by* o5 t. N- ~8 ^0 F" r( U
using the standard of Greulich and Pyle at a chrono-, E) S' w0 I  G' @0 o3 @3 k: U* p
logic age of 16 months (advanced).5 Chromosomal  w6 T6 S2 e9 B1 q9 o  \
karyotype was 46XY. The thyroid function test
( R+ @0 F- u1 b% s+ G( D3 _2 ^+ Sshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
) w4 F2 m  y8 l* Y/ n6 t+ |lating hormone level was 1.3 µIU/mL (both normal).! `1 x+ g4 Z7 D. w. O. I
The concentrations of serum electrolytes, blood! V: A7 G: j& m* _4 ?/ P/ l) r
urea nitrogen, creatinine, and calcium all were
. K5 P: h1 M; L# y7 nwithin normal range for his age. The concentration
; Z; z  h: G5 ?# W' o1 v2 vof serum 17-hydroxyprogesterone was 16 ng/dL
; F0 B& y# f  p. }(normal, 3 to 90 ng/dL), androstenedione was 20* Y* B& o) H0 A1 s6 o0 G
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
, }: Y" ~! e. k& Q- {terone was 38 ng/dL (normal, 50 to 760 ng/dL),; ?# {: U) e6 M; }8 ?% b: h
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
& }4 u1 ]1 P  u5 X0 X49ng/dL), 11-desoxycortisol (specific compound S)
  u( A0 L. ~4 ^# O8 Y. Q- h& Nwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-: T/ R5 L6 f4 X. z) D
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
& x0 @( z" r" m' d! E( btestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
+ s+ V& i3 E7 g$ Y% tand β-human chorionic gonadotropin was less than
# t2 s/ }6 V" Z: H9 @1 d6 ~5 mIU/mL (normal <5 mIU/mL). Serum follicular1 k2 v" ]- U9 e3 }  G$ f
stimulating hormone and leuteinizing hormone, S: K% q/ H$ Q2 A! M
concentrations were less than 0.05 mIU/mL
# ?; {. ?9 S$ I8 |  @(prepubertal).9 n- F& j+ Z; c5 g+ i; ]7 N
The parents were notified about the laboratory4 ^3 w0 ~, Y' _% a* c$ i
results and were informed that all of the tests were
/ x+ I9 U* f2 d% Z9 gnormal except the testosterone level was high. The
' Q  r+ R8 ]/ \! {# ?+ b3 Q" w( Tfollow-up visit was arranged within a few weeks to1 D* P8 p5 g8 R5 W$ C
obtain testicular and abdominal sonograms; how-" }' s* O/ p5 e; i$ H8 P- k! F
ever, the family did not return for 4 months.
5 e$ o- z0 g+ Z" pPhysical examination at this time revealed that the
  p" t. `9 I( [/ ?% x" ?child had grown 2.5 cm in 4 months and had gained
, F6 b) v9 ?* d$ y2 kg of weight. Physical examination remained. i7 }: H2 F! ~" V" X9 d$ J# q
unchanged. Surprisingly, the pubic hair almost com-
/ K" |+ u, e9 o& i5 q) f4 kpletely disappeared except for a few vellous hairs at' W! R- O/ @; \
the base of the phallus. Testicular volume was still 2% Z) |9 f# D# S( d0 }3 j0 e% a
mL, and the size of the penis remained unchanged.
  E  Y7 S9 q& O9 N( ]) _4 |$ u& EThe mother also said that the boy was no longer hav-
; L3 V' b% `5 Y: Hing frequent erections.! b1 G, b0 g6 |' _$ Q6 B
Both parents were again questioned about use of
+ P% d  ?; \, zany ointment/creams that they may have applied to' e& z; N, y  L! k3 m4 W) \5 @
the child’s skin. This time the father admitted the& L/ l0 ~1 N( B% J- [6 x% }
Topical Testosterone Exposure / Bhowmick et al 541
+ u7 m9 C1 L8 P) q2 [5 nuse of testosterone gel twice daily that he was apply-
$ ]4 Q* x) V8 C" D( }ing over his own shoulders, chest, and back area for
) _: f6 Q- m1 w! ~, q0 Ka year. The father also revealed he was embarrassed3 [4 g+ F6 O, n. _" k
to disclose that he was using a testosterone gel pre-
. m) o, X3 o. S$ _7 oscribed by his family physician for decreased libido% w6 Z2 c/ c. P) T. U- Y8 l1 t/ Z
secondary to depression.& c5 L$ Y, B& Q' }* m& `
The child slept in the same bed with parents.
% c% H* {. Y$ m% i* pThe father would hug the baby and hold him on his/ R. Q- h3 s% j. Z
chest for a considerable period of time, causing sig-
5 h7 h9 a8 h+ V. X9 g- F3 r" _. inificant bare skin contact between baby and father.
+ G0 Z3 x9 G; M: Q- OThe father also admitted that after the phone call,
8 b+ N& {: D* X6 v' I0 H) L( twhen he learned the testosterone level in the baby0 {# Z( ~# V) @& c- N6 {* m* e
was high, he then read the product information
0 T, I7 s: r9 i! o* Apacket and concluded that it was most likely the rea-
- D# d, K$ ~' ?  Zson for the child’s virilization. At that time, they9 r) i+ a0 Y4 p& F1 }5 Q" z
decided to put the baby in a separate bed, and the* M2 D1 H8 h4 a+ D1 `
father was not hugging him with bare skin and had8 }6 t: Z7 E8 }2 T
been using protective clothing. A repeat testosterone
- x6 B  @# v( w. _- m9 b2 W* xtest was ordered, but the family did not go to the' A, C- r. s0 \: U
laboratory to obtain the test.
% j1 X% l9 }* l* o. p" g1 u" t, g3 yDiscussion* a! m3 d# ^# Y6 f# I' z- M
Precocious puberty in boys is defined as secondary- B; Z( i( d: [7 ~
sexual development before 9 years of age.1,4
6 y* q7 `+ U1 e( h# ?$ z: `+ zPrecocious puberty is termed as central (true) when  V) U7 H' r1 l  m# A
it is caused by the premature activation of hypo-" s# @0 R  o* j/ H" M$ l# O! Z
thalamic pituitary gonadal axis. CPP is more com-
: ~& G; u) ]9 r! m  n* o$ hmon in girls than in boys.1,3 Most boys with CPP
$ w6 t- d8 b: Z" F/ r- O& Imay have a central nervous system lesion that is  r- r* Q9 j  y2 M0 t
responsible for the early activation of the hypothal-* ^. E, a& }' E1 E2 r5 `* [
amic pituitary gonadal axis.1-3 Thus, greater empha-( j) V; q) {7 e; ~
sis has been given to neuroradiologic imaging in
' n: }" i- [( `7 Y3 G) Zboys with precocious puberty. In addition to viril-
1 M2 n# R; |. p+ a$ K  n" }" dization, the clinical hallmark of CPP is the symmet-
& g/ Y" I7 W; qrical testicular growth secondary to stimulation by% e7 N. i3 H9 |4 f& m7 j
gonadotropins.1,32 x: d9 h+ v+ m  E( a$ j$ `
Gonadotropin-independent peripheral preco-
9 f8 Q% t! m$ X& C5 ~: }cious puberty in boys also results from inappropriate
3 C' [8 n% C) T& Fandrogenic stimulation from either endogenous or' g# u' |. U# {5 t/ y5 b: w/ ~1 P
exogenous sources, nonpituitary gonadotropin stim-& W; Y6 @' N% E- T; ^/ Q
ulation, and rare activating mutations.3 Virilizing3 g& K+ x+ D9 \# |. _& [1 E
congenital adrenal hyperplasia producing excessive
, ^/ g$ Q+ t3 }  |2 I1 dadrenal androgens is a common cause of precocious. t' k5 B. w5 {" u9 G
puberty in boys.3,44 U* i& ?& B0 \3 a* G  n
The most common form of congenital adrenal5 H' y3 O- u+ W+ N3 i! c
hyperplasia is the 21-hydroxylase enzyme deficiency.+ |+ G* n( A% q% P& d2 c$ a
The 11-β hydroxylase deficiency may also result in
" P" v0 i8 t$ p* Y1 R& ?/ m9 k, `. d# _2 Vexcessive adrenal androgen production, and rarely,. t) ?) Q& a8 M1 P7 U
an adrenal tumor may also cause adrenal androgen, b' e7 W4 P. }; Z, b
excess.1,3" w9 _  ^: F) Q% U
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! R. X2 z% L: L8 _, S0 E542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
2 y; g# I" r  JA unique entity of male-limited gonadotropin-8 z2 x" Y/ s! Z7 ?0 b8 p
independent precocious puberty, which is also known$ d% J! t; v5 c) B( _$ I2 V
as testotoxicosis, may cause precocious puberty at a- _9 R* j3 m$ u) ^
very young age. The physical findings in these boys; l, K; i  P3 D& D6 I' I6 R
with this disorder are full pubertal development,2 v( o5 t3 X2 g5 i; u
including bilateral testicular growth, similar to boys
. H5 G1 L: ]9 }+ ~1 [8 o$ v' gwith CPP. The gonadotropin levels in this disorder" T7 u5 D2 ?, |
are suppressed to prepubertal levels and do not show
! l( d1 v1 S( U/ m. Rpubertal response of gonadotropin after gonadotropin-
9 ?- ~% L, G: Y& \releasing hormone stimulation. This is a sex-linked3 x7 s: [/ T2 w4 _: q" K: M
autosomal dominant disorder that affects only' Q( X0 t7 g: |0 ]2 b: _
males; therefore, other male members of the family
# S- \7 [3 w, A1 s  U" @. ?may have similar precocious puberty.3  K4 n% |, m( `, n1 F$ q
In our patient, physical examination was incon-- h+ u, G3 g: U" d% K1 p: `
sistent with true precocious puberty since his testi-! ^3 o; g$ ~1 c2 N7 \
cles were prepubertal in size. However, testotoxicosis, p) H& U8 ]7 ~# Q  [
was in the differential diagnosis because his father8 S$ P+ A5 D+ g; z3 J+ `5 `
started puberty somewhat early, and occasionally,6 g( u7 Z" f) T6 ~6 U! z9 q& l+ w' }5 |
testicular enlargement is not that evident in the3 f* `6 \+ p7 e! n/ M! t
beginning of this process.1 In the absence of a neg-5 Z0 Y& U" {( Z0 f, b! V  _
ative initial history of androgen exposure, our
0 u! S% n$ G: U9 G, Sbiggest concern was virilizing adrenal hyperplasia,+ {+ R; l* ?! Z7 `8 K
either 21-hydroxylase deficiency or 11-β hydroxylase& k$ ]( B" l7 |3 k7 x$ f
deficiency. Those diagnoses were excluded by find-" P( I4 V7 f5 C$ F
ing the normal level of adrenal steroids.+ B) s& E! k- O' u! {
The diagnosis of exogenous androgens was strongly. }8 y. K: e2 Y- c" u* u
suspected in a follow-up visit after 4 months because1 M# a1 ?/ S9 a- `6 h+ x; u
the physical examination revealed the complete disap-
) e3 x% i# Y& U& _- p; Ipearance of pubic hair, normal growth velocity, and
; p) b8 f1 c5 x# j7 T) p$ `+ [decreased erections. The father admitted using a testos-4 _- C7 v0 d  T7 {) D
terone gel, which he concealed at first visit. He was" P) @' a! V4 p" e- s, N" u. N
using it rather frequently, twice a day. The Physicians’, z+ G1 N0 y/ Z' J  F  D
Desk Reference, or package insert of this product, gel or
# \: b0 @  S9 m5 Y: acream, cautions about dermal testosterone transfer to2 g* `9 P" Q) `% h8 K
unprotected females through direct skin exposure.
6 k$ }0 V, C) i3 ?" I; kSerum testosterone level was found to be 2 times the0 v3 R0 z) b' X; I3 @4 P
baseline value in those females who were exposed to2 r" m# u: U5 G% R2 D5 G
even 15 minutes of direct skin contact with their male
! c( k# v  B7 n. S0 s# Bpartners.6 However, when a shirt covered the applica-
  a& t& U: f5 x# ftion site, this testosterone transfer was prevented.
* y6 t1 m0 V8 w) \( w* UOur patient’s testosterone level was 60 ng/mL,
( F" i2 @+ F$ S  _; b6 R- r. Jwhich was clearly high. Some studies suggest that
/ y" E) p$ A2 x; ]: K' qdermal conversion of testosterone to dihydrotestos-- B- `8 b9 c/ i6 L9 b: g/ M8 |
terone, which is a more potent metabolite, is more
, W- S& V; V& q* d4 ]; P4 Gactive in young children exposed to testosterone
' Z6 I, E# \4 y: ?+ qexogenously7; however, we did not measure a dihy-- |, ]5 f& q6 k: U+ M8 V
drotestosterone level in our patient. In addition to
% Q; K% {( Q9 V) Q7 c3 O( svirilization, exposure to exogenous testosterone in  r& J1 K: D6 G# _4 o; \
children results in an increase in growth velocity and
7 P; f' g9 I/ i/ |) nadvanced bone age, as seen in our patient.7 v( J& G9 J1 m" g3 r+ |
The long-term effect of androgen exposure during) r, _. E) \- [5 Q1 B
early childhood on pubertal development and final
! p2 z+ Q3 }1 _7 C# W- Fadult height are not fully known and always remain8 M5 y7 L4 \) G9 g& j# E
a concern. Children treated with short-term testos-
0 X) }7 D4 `5 @( z- mterone injection or topical androgen may exhibit some" T' v0 c( i/ k4 s1 T+ h4 s; t
acceleration of the skeletal maturation; however, after
' J6 E' ~* r/ Q, h  r8 ?1 ?cessation of treatment, the rate of bone maturation# a& |$ K. I! p
decelerates and gradually returns to normal.8,9# Q  j' m( f' z$ m) e
There are conflicting reports and controversy0 V& Y" F8 ^+ A; J# i! `
over the effect of early androgen exposure on adult+ e3 d. i4 a7 v" k
penile length.10,11 Some reports suggest subnormal$ m6 U7 B6 o, v, v( G+ ~! R
adult penile length, apparently because of downreg-0 b) u0 y4 x  Y* {, b
ulation of androgen receptor number.10,12 However,- p+ d" O8 m7 v) }1 U2 v* ]
Sutherland et al13 did not find a correlation between
. l; M6 A& A6 D2 K0 {% F+ H* }childhood testosterone exposure and reduced adult
" M: t: c  Z  S7 r/ c5 bpenile length in clinical studies.
# U4 ]1 o0 O2 N/ nNonetheless, we do not believe our patient is
) Z9 a) e# A. b! W" x! qgoing to experience any of the untoward effects from
" _/ ~1 g$ u8 ytestosterone exposure as mentioned earlier because' u7 t9 M$ U' b1 n2 |& f# c
the exposure was not for a prolonged period of time.7 T, D& k8 z! h6 `* x& v& a
Although the bone age was advanced at the time of/ d* W" O9 }8 S
diagnosis, the child had a normal growth velocity at. k/ J5 }5 Z) k! W. S
the follow-up visit. It is hoped that his final adult6 Y& r! W  G4 Q  O1 `" P2 \% p
height will not be affected.
/ p" Z$ r. ^* t# RAlthough rarely reported, the widespread avail-+ }% l; e( M7 r2 G
ability of androgen products in our society may3 r8 g- D2 g% i7 E+ ]9 M6 b. R3 l
indeed cause more virilization in male or female
; Y6 f5 K1 @8 X7 \; ]children than one would realize. Exposure to andro-
+ L3 k( E( f( q3 f5 agen products must be considered and specific ques-1 X; s2 L' b, M7 [9 P9 b2 `8 ~
tioning about the use of a testosterone product or7 H2 _# L9 @/ Z6 z+ P8 h0 d- ~
gel should be asked of the family members during
% O% Z1 D/ Y6 m7 P% Z0 f4 u7 ithe evaluation of any children who present with vir-* _3 x) v+ G7 \; [  H
ilization or peripheral precocious puberty. The diag-9 @+ w; Z5 }1 k
nosis can be established by just a few tests and by
$ S9 A$ F5 {* Wappropriate history. The inability to obtain such a
, P5 p% s8 T3 V9 ^( ?. {history, or failure to ask the specific questions, may
; x1 l* z) \! A1 K8 [) wresult in extensive, unnecessary, and expensive5 x' s- F! Z" \3 H$ m
investigation. The primary care physician should be
3 f: {; Z! l# Q+ E/ K% U; y; iaware of this fact, because most of these children8 X" X+ D- g, {+ O
may initially present in their practice. The Physicians’
3 V5 |+ v$ r0 f4 Q" t+ @' DDesk Reference and package insert should also put a1 O7 k1 Z6 k( S( [* y6 ^
warning about the virilizing effect on a male or4 `! h& H) B' y+ J
female child who might come in contact with some-" l/ B4 G* ^2 c! h5 e* m; t7 |; M
one using any of these products.
5 J. O" k: L9 w5 L/ DReferences1 y4 p# p& c% v: m- `* z; p, ]
1. Styne DM. The testes: disorder of sexual differentiation: @2 v* v" _% a
and puberty in the male. In: Sperling MA, ed. Pediatric
9 Z- P/ }3 ^0 SEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
; x0 t1 X/ ^" D0 d7 Y2002: 565-628., d$ [# R" v0 @
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
/ B; k% O! o" g  F2 ]# \+ Lpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old; D. D, D3 }9 {9 {8 L" j
Boy Induced by Indirect Topical
+ g2 I( ^- W" t4 ?2 G0 p7 E5 E, DExposure to Testosterone
9 o' O9 Q( w9 LSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 s7 O& `9 u1 c) sand Kenneth R. Rettig, MD1
$ O- [( f  F' j4 R) Z- @Clinical Pediatrics* ~6 ~, |- b# ~
Volume 46 Number 6& E* i* I- r4 [' T
July 2007 540-543
" Y6 Q: j# i( a3 ]© 2007 Sage Publications
2 Y7 T/ f0 \, C$ {1 {; P10.1177/00099228062966511 z) u: K8 [) l' x" F
http://clp.sagepub.com, k; @$ c) S3 s0 q+ E- _$ e
hosted at7 C* `6 g1 Q1 \" k, p1 h5 F6 S
http://online.sagepub.com  L* y. x  u# n( A& S# V7 T
Precocious puberty in boys, central or peripheral,+ W& Q0 n2 |1 g7 r; |  n
is a significant concern for physicians. Central# d5 S; v5 M4 _0 R6 r  n: M
precocious puberty (CPP), which is mediated
+ c- K( r% V: c! k4 z  |3 s, Q( U) ithrough the hypothalamic pituitary gonadal axis, has
5 s1 ]" H5 P# ha higher incidence of organic central nervous system
. N' c6 t3 J! h& A8 klesions in boys.1,2 Virilization in boys, as manifested$ O$ _- _: @9 e, J6 ^- v. d0 ~
by enlargement of the penis, development of pubic, }2 y' e& u  U
hair, and facial acne without enlargement of testi-/ m1 b; Q8 f0 g. l$ ~
cles, suggests peripheral or pseudopuberty.1-3 We+ p5 s2 {1 |! c
report a 16-month-old boy who presented with the$ |  K, p$ m' W# @4 ]/ {
enlargement of the phallus and pubic hair develop-
4 S" h- A# K9 S9 `2 R9 h0 Cment without testicular enlargement, which was due
3 E- A+ t7 N0 S2 jto the unintentional exposure to androgen gel used by
  x5 N, |$ F1 r5 b$ jthe father. The family initially concealed this infor-
) f. c8 W+ r. D; w; W" |9 \0 Qmation, resulting in an extensive work-up for this
9 J0 r% {# B5 b, cchild. Given the widespread and easy availability of
/ |, S: M& U" e( Rtestosterone gel and cream, we believe this is proba-6 i) t, B5 @: K
bly more common than the rare case report in the( L: T8 H0 B1 P2 w, r8 b0 I
literature.4
$ N2 F$ l) `6 `, q7 YPatient Report
1 z! Q  r5 \( Y  O) e- n3 AA 16-month-old white child was referred to the
* s* i, i& Q3 Y# I/ `: W- G7 z2 Wendocrine clinic by his pediatrician with the concern& ?' X9 ^3 {# Q7 s2 T
of early sexual development. His mother noticed
% a4 w' j/ _3 D" P, Ulight colored pubic hair development when he was
4 N( W) r  |. R: w# \From the 1Division of Pediatric Endocrinology, 2University of; m6 m5 G: g* l( I& x" D
South Alabama Medical Center, Mobile, Alabama., r' R" `  s4 _( P* h3 ?& i7 S6 Q
Address correspondence to: Samar K. Bhowmick, MD, FACE,$ k; I3 b7 t+ {2 T' O+ D
Professor of Pediatrics, University of South Alabama, College of
2 F+ ^! N1 z* f6 `1 S5 E" BMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
7 `, {5 S- K- o" ne-mail: [email protected].
) g  V$ H$ P( x2 w3 B# \. K+ Iabout 6 to 7 months old, which progressively became2 z7 Y- y- _  m) G) {3 N: z8 I
darker. She was also concerned about the enlarge-% u- G- h& ~: F+ t0 k6 ~
ment of his penis and frequent erections. The child& ~  ?& v! p! P
was the product of a full-term normal delivery, with8 e% g0 Q5 q: X
a birth weight of 7 lb 14 oz, and birth length of, H3 C& i& i! L' I$ q6 I, Y
20 inches. He was breast-fed throughout the first year; g3 J6 Q8 G4 V4 P* G
of life and was still receiving breast milk along with
0 Y+ R) Y5 M, L) S# l% Ysolid food. He had no hospitalizations or surgery,- ~# `+ z3 F0 C$ R- {* X
and his psychosocial and psychomotor development6 s0 e, [4 E- L8 U4 y: [8 d0 |
was age appropriate.
, Q, X1 g6 _" e1 _0 t  K7 M: vThe family history was remarkable for the father,5 H7 Q2 k6 i0 I# t- `( O8 X9 x+ d
who was diagnosed with hypothyroidism at age 16,
9 s0 A$ Q- E( S: O1 o4 cwhich was treated with thyroxine. The father’s0 ]6 D$ A! L2 z. i( a9 `0 [
height was 6 feet, and he went through a somewhat
* O9 X' O$ ^" Bearly puberty and had stopped growing by age 14.! M9 T" o6 J2 ?$ Y9 ?. r8 t
The father denied taking any other medication. The5 L- L7 a3 x2 E( w; }9 [% b! ~
child’s mother was in good health. Her menarche
5 U' J" {4 z  F1 qwas at 11 years of age, and her height was at 5 feet
! w! M- V& H3 R6 C, q3 H6 {8 N5 inches. There was no other family history of pre-) F1 W0 P0 Z- d
cocious sexual development in the first-degree rela-
1 o4 v6 O# l0 d9 L- ?; q! Ytives. There were no siblings.
- M; B$ D9 I1 ?" n5 lPhysical Examination
. H# ^# E  W9 w0 X/ Z2 RThe physical examination revealed a very active,! b+ I: R# C+ T3 s6 b" b) D9 I& o# [
playful, and healthy boy. The vital signs documented
* X- w: G# j4 v. [# }5 ?7 Pa blood pressure of 85/50 mm Hg, his length was
* A& @/ I1 ^* d0 z' j2 U2 K( v90 cm (>97th percentile), and his weight was 14.4 kg- v5 R+ W7 E! K: c
(also >97th percentile). The observed yearly growth
% x+ _0 {7 ^+ ?' W5 m0 L. ~* p  bvelocity was 30 cm (12 inches). The examination of
$ j" p8 ~5 l% z8 ]the neck revealed no thyroid enlargement.
6 Q% r8 e! l4 r- ]4 ]: b+ m7 XThe genitourinary examination was remarkable for
% D! C" V* {! s0 Z6 [! C# M% K- Kenlargement of the penis, with a stretched length of1 ^4 a; P2 y" L5 ]
8 cm and a width of 2 cm. The glans penis was very well
" T' b( \2 q7 Wdeveloped. The pubic hair was Tanner II, mostly around
8 u! i3 j, i* c. I, D5404 p9 J8 y( Q& M6 I7 b# n& b$ g
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 D  \+ n3 Q, U+ s) g7 I+ \4 wthe base of the phallus and was dark and curled. The
6 c0 i/ }1 Z6 |testicular volume was prepubertal at 2 mL each.
: ~2 I! i* c+ ?' NThe skin was moist and smooth and somewhat
. [1 t# H6 V" C* moily. No axillary hair was noted. There were no  S1 ~  C6 H' Z8 J5 c
abnormal skin pigmentations or café-au-lait spots.+ T3 h& K3 ^( w1 F! O; c& u" A
Neurologic evaluation showed deep tendon reflex 2+
8 v' y2 d5 o9 L% k5 Nbilateral and symmetrical. There was no suggestion
9 S7 T4 M  u" L6 _9 A7 n% e: \7 iof papilledema.
' ?! D( ?4 I1 J- g! T. dLaboratory Evaluation4 e: C2 u" Y4 j; `% ?% N% I9 V
The bone age was consistent with 28 months by' c& R1 j$ A0 N7 Z
using the standard of Greulich and Pyle at a chrono-
1 H5 i) u7 ?+ N# ?) z( Dlogic age of 16 months (advanced).5 Chromosomal
/ ^* O( {4 g# }0 Jkaryotype was 46XY. The thyroid function test
  D! L3 c( ~; h+ Vshowed a free T4 of 1.69 ng/dL, and thyroid stimu-! Z8 \0 u$ B/ x# n) V
lating hormone level was 1.3 µIU/mL (both normal).% l: Q  l& L8 a; t! A+ t1 H3 o
The concentrations of serum electrolytes, blood/ j; E& u% E" a  Q; r6 Z
urea nitrogen, creatinine, and calcium all were) [3 o# k9 O' ]( _" c, v" b6 Z
within normal range for his age. The concentration
( k( V5 I6 {) A0 hof serum 17-hydroxyprogesterone was 16 ng/dL
/ C1 Y. D2 ^$ s  d* Q8 X! K(normal, 3 to 90 ng/dL), androstenedione was 20% y/ [7 [' T; M+ t. f+ a
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
5 i0 `( X1 d1 g4 Z/ Zterone was 38 ng/dL (normal, 50 to 760 ng/dL),
" b" B3 h& ]& r# ~4 |desoxycorticosterone was 4.3 ng/dL (normal, 7 to
( m* N8 Z1 M( d- V49ng/dL), 11-desoxycortisol (specific compound S)) h( o$ |. n9 c( F- N! X# ?. u
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-; C! {7 s  S( G( L: \/ `+ G
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
8 C) W& b4 x! g! K% A0 ztestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
8 R4 x1 J0 l/ x: I( g; r7 fand β-human chorionic gonadotropin was less than
& b9 F$ r! G' k) ]7 b1 E5 mIU/mL (normal <5 mIU/mL). Serum follicular9 _) v( C$ O! J5 [; a
stimulating hormone and leuteinizing hormone) e* G5 j7 ^% B) D
concentrations were less than 0.05 mIU/mL
1 V2 U  e8 B0 }: c(prepubertal).
8 C* @( L' `3 m( LThe parents were notified about the laboratory
: ~" a5 }6 U) f. Hresults and were informed that all of the tests were) @5 x6 S2 p, u" E2 V$ c& @
normal except the testosterone level was high. The3 J  m# z% f# A% P9 R' a
follow-up visit was arranged within a few weeks to
3 v( }) U8 a  }1 B/ xobtain testicular and abdominal sonograms; how-
. [# L" V0 L5 y; S! Jever, the family did not return for 4 months.. c+ u) r9 @! H
Physical examination at this time revealed that the
2 O* L2 K: O$ |1 u- Dchild had grown 2.5 cm in 4 months and had gained
( e/ ]5 w: J1 A8 ]: b' f2 k2 kg of weight. Physical examination remained
; R* S) y5 m7 j: Tunchanged. Surprisingly, the pubic hair almost com-( {2 j6 H8 a. N( {2 M: ]
pletely disappeared except for a few vellous hairs at0 m0 J: x" ]8 d
the base of the phallus. Testicular volume was still 2
' c" q- r: d& E6 I3 }8 ]; smL, and the size of the penis remained unchanged.
, [" R, k5 N+ B, jThe mother also said that the boy was no longer hav-
- ]9 I/ A' j9 c" _, Oing frequent erections.
& D# U9 A( |9 E7 a6 hBoth parents were again questioned about use of9 O; L" v! n1 w3 j
any ointment/creams that they may have applied to
, r. R: K, v! O( F1 e$ O! I& H. b4 Zthe child’s skin. This time the father admitted the. y# b) t' l0 e- H9 n
Topical Testosterone Exposure / Bhowmick et al 541
( o  X; }/ v& G3 o# vuse of testosterone gel twice daily that he was apply-! D3 X3 i# i# d0 r) W
ing over his own shoulders, chest, and back area for! L' q9 ?, A& D( Z5 p
a year. The father also revealed he was embarrassed
, U7 i3 l; J% W/ Pto disclose that he was using a testosterone gel pre-
, d+ p, d5 z/ r. K8 Q0 Nscribed by his family physician for decreased libido: B) F8 K# @5 l- |; r  x" n1 K& r
secondary to depression.: d+ d( d+ I/ O' [: L* p
The child slept in the same bed with parents.
5 F' c" A2 X( W8 l$ @* O- vThe father would hug the baby and hold him on his/ S  z* r4 M1 R3 P4 R
chest for a considerable period of time, causing sig-6 i, r: K+ W, _4 v8 \
nificant bare skin contact between baby and father.  F7 l7 U+ l- k- l/ q, k
The father also admitted that after the phone call,
; c: k+ x% A# b' m" ]" s9 S) iwhen he learned the testosterone level in the baby
4 V* Y" @$ j- L) }0 Zwas high, he then read the product information
5 \+ V/ l, ?2 y5 N" y( a$ spacket and concluded that it was most likely the rea-
/ I6 E8 \$ ]6 Uson for the child’s virilization. At that time, they
. a! _, G0 G' P0 k$ Ndecided to put the baby in a separate bed, and the, O) _6 ]# w- |& x6 e
father was not hugging him with bare skin and had2 i2 v0 J# r0 [2 ]" \
been using protective clothing. A repeat testosterone
$ P4 i; t( s, |# {+ Q) Z8 jtest was ordered, but the family did not go to the
- R7 W# A& D* `# k- e4 N; x$ klaboratory to obtain the test.
& N* w; \% x2 J1 J2 CDiscussion
" d# ~4 E+ O! x8 ZPrecocious puberty in boys is defined as secondary. X8 n/ H5 G6 T
sexual development before 9 years of age.1,4+ g- F- V) w1 [3 \
Precocious puberty is termed as central (true) when- o& P( L; v9 n# P6 t
it is caused by the premature activation of hypo-& V7 r' H# n6 W: g. R' }
thalamic pituitary gonadal axis. CPP is more com-6 K  X" Z# x- p/ l
mon in girls than in boys.1,3 Most boys with CPP
! a/ x6 y# k+ b' Gmay have a central nervous system lesion that is! _% m. _& _* E4 X$ w! h0 w& J
responsible for the early activation of the hypothal-+ j" `- e7 R5 B
amic pituitary gonadal axis.1-3 Thus, greater empha-
8 B) ^$ D4 [  d+ o! Zsis has been given to neuroradiologic imaging in2 ~6 J4 i3 N% z) A% |4 `
boys with precocious puberty. In addition to viril-$ ^9 f: B. {# i* c% l$ b
ization, the clinical hallmark of CPP is the symmet-
8 T! M5 ~. G& X4 j/ m3 Urical testicular growth secondary to stimulation by
) b4 N' _9 P! B+ `  |% {gonadotropins.1,3
- m& h2 b& A; X9 X1 J# ^Gonadotropin-independent peripheral preco-* e* H- s6 }  |6 H2 N
cious puberty in boys also results from inappropriate
1 P" ~( }: j' o4 p! n9 xandrogenic stimulation from either endogenous or
) l+ m/ @2 p$ K. s1 Yexogenous sources, nonpituitary gonadotropin stim-; P! U1 {' S8 @( f+ M8 j
ulation, and rare activating mutations.3 Virilizing
7 |1 k8 v& e6 m8 y! {: v: }( z2 Acongenital adrenal hyperplasia producing excessive
4 T, s2 m. Z. Z+ k+ Kadrenal androgens is a common cause of precocious3 `1 P! l; m9 Y4 Y! S
puberty in boys.3,4" ^$ \! H  {$ s, f0 ?! K
The most common form of congenital adrenal
# G3 z; C4 s  v; ohyperplasia is the 21-hydroxylase enzyme deficiency.
6 X) _) n9 G5 L9 b* AThe 11-β hydroxylase deficiency may also result in
0 ]' c, w; b' e4 Xexcessive adrenal androgen production, and rarely,
/ k: T) U& ^. K" x. A* X& T, }an adrenal tumor may also cause adrenal androgen6 b" R3 I* g4 _3 ^, F& r7 ^
excess.1,30 j7 U9 R% m: d, t+ a" m$ I4 P  e
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 Y, p) C+ ^' F7 L542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
7 Y  ]" E- r$ p$ FA unique entity of male-limited gonadotropin-% ~1 e- P1 y0 K8 M* {/ e& X' p
independent precocious puberty, which is also known
' P8 J) ~( T# E/ o/ ^as testotoxicosis, may cause precocious puberty at a% U, `/ ~' j0 B
very young age. The physical findings in these boys
7 x; U. C- Q5 C0 n$ Owith this disorder are full pubertal development,0 F) q  P7 t' }  o) n
including bilateral testicular growth, similar to boys
) h+ p7 V0 x: @, @with CPP. The gonadotropin levels in this disorder* _, y) X' Z6 A  ?) l! H9 f
are suppressed to prepubertal levels and do not show! |+ ^) x- C/ U# f! T8 c
pubertal response of gonadotropin after gonadotropin-* t0 g2 \% p1 K  i
releasing hormone stimulation. This is a sex-linked, l( G% D' e8 i# k- r
autosomal dominant disorder that affects only; D5 l1 R  F9 j* w
males; therefore, other male members of the family& O' b% e$ ]* y2 E
may have similar precocious puberty.39 s; D% W1 `5 E! f2 ^
In our patient, physical examination was incon-) f) a: d7 }) v& e' [
sistent with true precocious puberty since his testi-# _  x) |* B0 |
cles were prepubertal in size. However, testotoxicosis- X  G" j  O' s2 }) j. A
was in the differential diagnosis because his father% P0 j3 k& S% C
started puberty somewhat early, and occasionally,
$ S6 v6 {# K% G& u8 t8 z' e3 jtesticular enlargement is not that evident in the1 }' q* o" G4 U9 v
beginning of this process.1 In the absence of a neg-8 v7 K7 H* R; e' m+ }- U1 e; e
ative initial history of androgen exposure, our# V' V7 W; f' k8 W1 c+ G+ U9 ]; ?
biggest concern was virilizing adrenal hyperplasia,
. K9 U8 E. S8 b0 d/ Qeither 21-hydroxylase deficiency or 11-β hydroxylase
! k% c5 E4 o. ?* H6 Edeficiency. Those diagnoses were excluded by find-# ?" L0 N- n3 K4 e
ing the normal level of adrenal steroids.3 F5 \5 j5 Y8 D
The diagnosis of exogenous androgens was strongly! u5 V" S2 y" M; m& L: b  x
suspected in a follow-up visit after 4 months because0 X, K% n* j8 m
the physical examination revealed the complete disap-
% n' H5 C4 i5 \* ?pearance of pubic hair, normal growth velocity, and
7 Y7 \" @+ y3 Y1 ldecreased erections. The father admitted using a testos-; d) Y$ a9 k+ H+ u+ m
terone gel, which he concealed at first visit. He was7 w; w; P: `, H! Z$ r
using it rather frequently, twice a day. The Physicians’
: E& K& X; ]6 nDesk Reference, or package insert of this product, gel or) z9 @1 ~" p: z# l
cream, cautions about dermal testosterone transfer to1 E/ ~6 D2 P/ ?. \8 I0 T! j
unprotected females through direct skin exposure.2 i. s( M4 Q  e9 A% n1 D. J9 P
Serum testosterone level was found to be 2 times the
2 g+ Y+ U7 l/ p9 H; M/ nbaseline value in those females who were exposed to9 i; p! b# s, {& E  G: S) I* [( J
even 15 minutes of direct skin contact with their male* @0 a: n2 }6 `4 o; y1 T- s& U
partners.6 However, when a shirt covered the applica-
# k' E3 k9 m) d  j8 R3 L# Stion site, this testosterone transfer was prevented.: Z4 i% A' p2 v7 y
Our patient’s testosterone level was 60 ng/mL,) }4 u/ t& U% \4 S2 t$ p
which was clearly high. Some studies suggest that
" t' O* Z( q9 K% w# m$ ?0 tdermal conversion of testosterone to dihydrotestos-  @8 w4 Q& c4 {7 X( W* s# g
terone, which is a more potent metabolite, is more5 r: w8 E( @+ ?7 `8 m# E6 a
active in young children exposed to testosterone& k9 l" p- t7 T0 e( W" x# g7 [4 ^9 F
exogenously7; however, we did not measure a dihy-" Y2 a& h% z+ T* V$ D, c/ Y0 Y3 L
drotestosterone level in our patient. In addition to
2 X$ R5 ~% ?5 A! qvirilization, exposure to exogenous testosterone in
4 S+ A0 P# s+ T* o5 Nchildren results in an increase in growth velocity and% j9 r$ a: ?3 W- h- ^
advanced bone age, as seen in our patient.
/ u/ W+ n% d0 {5 [' W" ]8 lThe long-term effect of androgen exposure during0 }% a" H5 I; L- c( C* C# R8 E
early childhood on pubertal development and final
# R2 V' d- _0 }+ {) K+ Y0 y( Madult height are not fully known and always remain
6 e% @3 y3 Y0 @) N: Ca concern. Children treated with short-term testos-
/ u9 T9 e; E8 z5 l* h+ B  A6 Xterone injection or topical androgen may exhibit some
. w7 d. |0 b% f1 Y9 Q2 O! nacceleration of the skeletal maturation; however, after2 R/ B2 ?5 V( T
cessation of treatment, the rate of bone maturation
8 X8 {3 ~- c& k6 h# ydecelerates and gradually returns to normal.8,96 j( q+ N4 b  _6 F( ^
There are conflicting reports and controversy& x9 ]6 d; F5 o/ H) C6 m
over the effect of early androgen exposure on adult, ]% h: T* \5 N2 J9 n9 U5 {
penile length.10,11 Some reports suggest subnormal' z& |: B, B5 W0 p
adult penile length, apparently because of downreg-
7 a& K/ U# ^4 d6 _3 Uulation of androgen receptor number.10,12 However,) m7 Y2 m' G. w# m" r
Sutherland et al13 did not find a correlation between
: W; n: W) ~3 D" w) Schildhood testosterone exposure and reduced adult
% t5 k; e# x; ^, }' U) Lpenile length in clinical studies.
5 Z7 k  `0 V4 V. E% B. rNonetheless, we do not believe our patient is+ D( N9 g% f$ I. N0 `
going to experience any of the untoward effects from
1 f- u* d9 Q1 \: J# i% `1 wtestosterone exposure as mentioned earlier because
% `2 K# e8 j3 a& x+ M( R" t2 Vthe exposure was not for a prolonged period of time.
9 {* V: W! u6 ^( ]" ZAlthough the bone age was advanced at the time of
$ `" s  W  b) xdiagnosis, the child had a normal growth velocity at
& H, |" ^0 u, \4 L. b& ?; j5 _the follow-up visit. It is hoped that his final adult9 A: w9 ?/ ~) R7 |. d
height will not be affected.$ a% F* F* N# T* w
Although rarely reported, the widespread avail-  U6 y4 D% A9 ~. E* e: s
ability of androgen products in our society may
& p2 _8 v& V7 x# [$ i; bindeed cause more virilization in male or female2 `& w/ z; [/ b* c7 D3 {0 `
children than one would realize. Exposure to andro-0 _! Q" F2 |/ c4 G( y9 E
gen products must be considered and specific ques-1 P$ ?' ]7 Y+ R4 |/ @5 T9 A, g# H' H' c
tioning about the use of a testosterone product or
  q6 Z  n7 a% u1 L% [* d1 T+ O7 }- pgel should be asked of the family members during
! Z: P  w8 t& H+ G8 vthe evaluation of any children who present with vir-5 D$ G" ^- P/ s/ C1 C
ilization or peripheral precocious puberty. The diag-; o7 p1 Y$ m+ @. P
nosis can be established by just a few tests and by+ \) G- G3 x' w  `' r0 G8 N
appropriate history. The inability to obtain such a: S! f4 g+ F2 Z8 R
history, or failure to ask the specific questions, may
0 X0 w6 D3 c" D7 D3 x0 t4 x4 [result in extensive, unnecessary, and expensive
" b' u3 m0 v/ G0 V7 `" r  u$ iinvestigation. The primary care physician should be3 Z: e) G$ B. c! t$ f8 s
aware of this fact, because most of these children
0 z; e) m8 A; N; y- c+ vmay initially present in their practice. The Physicians’
  a+ l3 y) R% ^! {# W+ d" e% V5 u4 mDesk Reference and package insert should also put a
6 c* i5 w. W% [: m, A7 [8 {4 fwarning about the virilizing effect on a male or
( H7 [  m! ?* H" j, o" Ofemale child who might come in contact with some-
6 S+ F9 U8 \4 z8 oone using any of these products.! g1 V0 t" X5 g9 n  y* x
References: M& M1 u4 r, J
1. Styne DM. The testes: disorder of sexual differentiation
' N3 R3 }& R  g5 O  {2 A8 iand puberty in the male. In: Sperling MA, ed. Pediatric
- J/ U) \; L7 X7 s1 s( `Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
' d) |! G3 U( B4 T& _/ }2002: 565-628.
7 X1 L' T: V- p7 s2 M. n) H2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
+ N" t* x" i6 L9 ]( _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

9 V/ X- M" f% g& {  I; T2 x4 u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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