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Sexual Precocity in a 16-Month-Old! Z3 x* B' Q. C- `+ T# _
Boy Induced by Indirect Topical
$ y0 K1 q) a5 v0 t# dExposure to Testosterone/ t- W+ h4 j* `2 |* A
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
8 P( F( ]5 E" Z% Wand Kenneth R. Rettig, MD1
+ }% e1 `2 v6 o4 wClinical Pediatrics/ b4 C: E" j5 Y5 z8 L, B
Volume 46 Number 6
/ S0 [" d: j  i" ~& }: vJuly 2007 540-543
+ o1 P' @. d9 [& ^" y4 C© 2007 Sage Publications+ I. F9 |! h  Z" `, u& F+ H
10.1177/0009922806296651  [3 {  Z8 X% a
http://clp.sagepub.com, u) O& ?3 D3 m0 ~0 J; e: W
hosted at
  u9 _0 g; ^# o% a: U0 `http://online.sagepub.com
8 \  T, T# W! |3 o  e6 _Precocious puberty in boys, central or peripheral,% c6 u' s$ y4 I, `; k/ q
is a significant concern for physicians. Central
: a+ k, n0 H( u( j* t4 qprecocious puberty (CPP), which is mediated
( u; R2 r; b, q5 R$ ]" R; Z: B) i$ f5 sthrough the hypothalamic pituitary gonadal axis, has
8 o$ x9 n% [6 j. w: Ka higher incidence of organic central nervous system
* I# B% @+ ~, Wlesions in boys.1,2 Virilization in boys, as manifested. q, b' s2 I: f
by enlargement of the penis, development of pubic/ D8 q7 T% s4 F8 P& i, C
hair, and facial acne without enlargement of testi-4 W* J* z5 s  o7 _( U) m$ z5 p- I
cles, suggests peripheral or pseudopuberty.1-3 We, R5 U* W1 ?. u2 g0 p
report a 16-month-old boy who presented with the
1 o  b) f4 [  g+ henlargement of the phallus and pubic hair develop-; d! z8 X; c8 C  T( _/ |
ment without testicular enlargement, which was due* P. k+ Q+ Z5 t( o* }- V
to the unintentional exposure to androgen gel used by2 M  L! s( L" |& l) @
the father. The family initially concealed this infor-7 W3 o+ l* w% @! W# ~: }5 X+ z
mation, resulting in an extensive work-up for this
+ V% S3 A4 K* achild. Given the widespread and easy availability of
+ I( N0 v, T  c, R4 {testosterone gel and cream, we believe this is proba-
, W' }# _& m8 k: m4 p. wbly more common than the rare case report in the
1 k- Z1 ~/ D5 i' _2 z$ q) cliterature.4
8 l& I! _2 r- `Patient Report
  ~' ]* F4 k: h! HA 16-month-old white child was referred to the5 x% V7 U2 @$ t
endocrine clinic by his pediatrician with the concern
$ q% d$ J; \- U% X: y: Qof early sexual development. His mother noticed
, B4 s- M% \2 ]light colored pubic hair development when he was
) }/ N: j; M7 `4 v: A/ c8 Z) N: YFrom the 1Division of Pediatric Endocrinology, 2University of
: R7 ]+ U, K5 d8 h7 N% J: CSouth Alabama Medical Center, Mobile, Alabama.
0 {) d3 m. U3 O6 |. X) d6 `1 IAddress correspondence to: Samar K. Bhowmick, MD, FACE,5 d5 V1 ~" [! X6 h1 R6 J( Z
Professor of Pediatrics, University of South Alabama, College of
* u( ]' t8 C; A" q3 b# ]Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ @9 G* v6 H" s2 K5 @, d
e-mail: [email protected].2 w* q5 L$ R' R& L' c. t% u7 }
about 6 to 7 months old, which progressively became
; ?- O8 ^! m  B! _darker. She was also concerned about the enlarge-
+ c) Y! b- |$ S6 O5 Pment of his penis and frequent erections. The child2 T- o, i# i4 Q& w( a& c- w: u" w& ~
was the product of a full-term normal delivery, with
2 r$ V- k& ]' W9 z! Y: o. Na birth weight of 7 lb 14 oz, and birth length of
& O$ T7 G' ~8 m' r7 ]$ n( ?9 D! Z20 inches. He was breast-fed throughout the first year* O& j! W( e' |7 b8 T$ ~7 t
of life and was still receiving breast milk along with7 w# W! [- ~! G; _4 s7 q6 c" M3 e0 u2 m
solid food. He had no hospitalizations or surgery,
8 `/ n. `0 ~- T% T. zand his psychosocial and psychomotor development
3 J, o& k$ E- ^7 ]0 E1 @0 C; f3 Qwas age appropriate.
% w% J6 c9 c4 ?The family history was remarkable for the father,
1 D; k5 J  a4 g6 X; vwho was diagnosed with hypothyroidism at age 16,, G) k" _, r/ [: Z5 U6 Q
which was treated with thyroxine. The father’s
( T* L7 ^2 T* Y7 A1 h0 A; O( ]0 n6 ?height was 6 feet, and he went through a somewhat
2 k& o7 _& y9 s- gearly puberty and had stopped growing by age 14.2 N% X. H% T7 y2 j  f' z# P
The father denied taking any other medication. The
$ n  W0 m% {3 n3 `child’s mother was in good health. Her menarche0 q  x. M. S2 Q) a8 [- O# X+ i
was at 11 years of age, and her height was at 5 feet) \+ q  P. D7 ]
5 inches. There was no other family history of pre-
" D5 Y  [5 A+ Y, @# ecocious sexual development in the first-degree rela-! O3 T( T; k- X
tives. There were no siblings.
, H# J# a& K- `- c7 DPhysical Examination
" S8 i& G- `2 Q5 M9 f4 X8 fThe physical examination revealed a very active,- ^  U/ \+ \$ f8 J9 y
playful, and healthy boy. The vital signs documented5 C% p9 ~& r4 X
a blood pressure of 85/50 mm Hg, his length was: s, }* E! p& V; R. F4 {4 Y
90 cm (>97th percentile), and his weight was 14.4 kg  w% @& @8 E" V7 y9 c2 W* r1 n) A
(also >97th percentile). The observed yearly growth# B3 M1 P% J! N0 H7 s
velocity was 30 cm (12 inches). The examination of. [+ f0 X2 B: {$ w7 P. j8 w8 [7 P
the neck revealed no thyroid enlargement.4 I" [6 A) f8 f8 H
The genitourinary examination was remarkable for
' d+ d+ R8 A, ^1 |& ?' P8 G% j- [enlargement of the penis, with a stretched length of
8 f. U/ f; F) I9 T8 cm and a width of 2 cm. The glans penis was very well
* M/ D1 y  j2 J6 Y) edeveloped. The pubic hair was Tanner II, mostly around+ R3 e2 _2 i* B% W& y& I
5408 T/ E7 k5 w  q5 s- t3 [! Z  K
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
% U9 Y9 _# t  S& T0 w4 B2 Ithe base of the phallus and was dark and curled. The
* A7 g6 x, Z# P1 J0 \+ R: Itesticular volume was prepubertal at 2 mL each.
7 b$ i5 r8 E& g0 q2 nThe skin was moist and smooth and somewhat$ ?$ j: f& U7 w3 f: @
oily. No axillary hair was noted. There were no
/ R8 K) D  E& c0 I9 sabnormal skin pigmentations or café-au-lait spots.
9 t' o  _1 @8 m, ^% p: hNeurologic evaluation showed deep tendon reflex 2+$ D8 Z' u8 P  w2 I5 k7 C- k
bilateral and symmetrical. There was no suggestion
6 V. @1 M0 m/ I- a+ Kof papilledema./ s9 e7 ^4 ~5 _5 L% O; H: e
Laboratory Evaluation9 m6 X( N& f% D3 Z: I$ m1 i( X0 b
The bone age was consistent with 28 months by0 J8 a2 R' o+ q0 [5 [
using the standard of Greulich and Pyle at a chrono-
" F* l  h2 k! H4 k( I  Tlogic age of 16 months (advanced).5 Chromosomal+ M( D+ F" a0 A; N& r
karyotype was 46XY. The thyroid function test
# Z0 i2 {( Y/ }+ I$ t, yshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
9 g0 \/ d  ?% L/ w- Nlating hormone level was 1.3 µIU/mL (both normal).
( R! D2 d9 r8 P! Q$ E: TThe concentrations of serum electrolytes, blood: e. p" F; G4 R, {' m- c( l4 W& L
urea nitrogen, creatinine, and calcium all were
4 ^  z9 \$ z0 L- l' a' J1 c$ Gwithin normal range for his age. The concentration
  j$ l% M" g- [7 i7 u' t8 ~  }of serum 17-hydroxyprogesterone was 16 ng/dL
$ Q$ E4 e+ [, {2 D1 Z. V(normal, 3 to 90 ng/dL), androstenedione was 20
  Y* K" Q& j8 jng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-4 N  E) T( L, L) C2 h; T
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
, D) q. Y; U) q" H  g) K- F1 ~" ndesoxycorticosterone was 4.3 ng/dL (normal, 7 to  Y* K. Z- q9 P! C4 d0 l
49ng/dL), 11-desoxycortisol (specific compound S)6 D9 K; o% F" y- j6 e0 z0 p, S- L
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-; G- u. ^# |# H" }, d* }
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# Y! G$ T- Q5 C, K/ W
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),* z; d8 E  ~- k4 w7 D
and β-human chorionic gonadotropin was less than. P5 j/ e8 }& @5 z+ L9 d- l' s+ @
5 mIU/mL (normal <5 mIU/mL). Serum follicular
* f- Y( `) [/ O9 Ostimulating hormone and leuteinizing hormone# j" J5 j6 c: U. ?; x
concentrations were less than 0.05 mIU/mL' Y0 |3 `0 S) q* T4 |6 T* k
(prepubertal).
$ V+ d" o# I9 W, K  ]0 V5 n) G9 bThe parents were notified about the laboratory
' J' |* o6 j4 E7 r* mresults and were informed that all of the tests were
! `" I0 B* C% n' ^normal except the testosterone level was high. The' [3 t0 M+ v" M0 R$ q" Q- S3 f) \7 t
follow-up visit was arranged within a few weeks to
2 C+ |$ g+ B: z9 X# h5 w) E2 `( lobtain testicular and abdominal sonograms; how-  N/ B: q; K9 \6 ]
ever, the family did not return for 4 months.
& i  X7 H9 F1 w& n+ O* C# H& [Physical examination at this time revealed that the
( d( p0 N+ x3 Xchild had grown 2.5 cm in 4 months and had gained5 l# n9 S5 \0 f+ _0 @4 z
2 kg of weight. Physical examination remained
# L8 t. w8 p& n( D1 v8 `, P$ Yunchanged. Surprisingly, the pubic hair almost com-
/ T6 m5 A( i! T9 u, ]pletely disappeared except for a few vellous hairs at' O0 N" K7 o2 Z2 o! S+ A
the base of the phallus. Testicular volume was still 2
. i3 C& X! W9 a, d: @mL, and the size of the penis remained unchanged.
3 z' t. E" T* B1 B; _The mother also said that the boy was no longer hav-
, g* z' k* G. G* C3 Fing frequent erections.
, d5 }7 M' y7 m" D  H( tBoth parents were again questioned about use of
% p! X+ s" P# Z$ J3 w* Many ointment/creams that they may have applied to
6 ?9 Z2 I/ {' m0 s1 Z9 `! Xthe child’s skin. This time the father admitted the- B6 ?' u, i. ^- Z' Y* v2 O* h' s4 ?
Topical Testosterone Exposure / Bhowmick et al 541( u+ o7 b6 W- L
use of testosterone gel twice daily that he was apply-
; n" e/ b; U) E" n3 o8 B# ?ing over his own shoulders, chest, and back area for
- P+ R$ x9 ?2 M' M+ va year. The father also revealed he was embarrassed- ?, x5 s4 {& r4 c! y, h
to disclose that he was using a testosterone gel pre-8 i; F2 r$ C, z. U9 l
scribed by his family physician for decreased libido
( Y* l1 d+ e: o. \/ V( a, Hsecondary to depression.
' Q3 x' S1 E' H' r5 M4 K! Q' AThe child slept in the same bed with parents.
& l6 |" h0 n7 q/ X, W$ UThe father would hug the baby and hold him on his
6 y/ U" Q. i  w6 u1 m, r/ ~chest for a considerable period of time, causing sig-
) C! @$ Q) h7 Y, K# k( Z6 Rnificant bare skin contact between baby and father.: D$ |  T. E4 }4 \& J/ ]/ Y& J
The father also admitted that after the phone call,+ V# Z* f0 G5 ~2 j% }" i$ f
when he learned the testosterone level in the baby: D% f. f8 q( ]4 W7 q8 w3 J! d
was high, he then read the product information- y7 _. L2 K3 S2 b
packet and concluded that it was most likely the rea-2 H6 Z% ?7 S! \/ q- m# E
son for the child’s virilization. At that time, they
/ }2 \5 a6 F+ ?! {decided to put the baby in a separate bed, and the4 t* Q- T! D* J" t; e$ q
father was not hugging him with bare skin and had; F3 g0 C2 P% C# d- d) i+ Q& w
been using protective clothing. A repeat testosterone
& q5 ^9 o1 e2 a9 X2 Jtest was ordered, but the family did not go to the
- Z4 p1 b0 |# B) A2 p+ Alaboratory to obtain the test.
, r3 J! R# F! o! T4 Z. A8 }. _- fDiscussion
8 I% u" A% a3 b: n. s- rPrecocious puberty in boys is defined as secondary
$ h. L% h' ?  Z! x0 ^( J6 tsexual development before 9 years of age.1,4
5 f) _2 G  Q/ V5 y; z# dPrecocious puberty is termed as central (true) when+ |  C" u$ o6 l, u' W) B8 {) G
it is caused by the premature activation of hypo-; X+ z9 l3 p. }6 M% ^- j. D
thalamic pituitary gonadal axis. CPP is more com-
! {8 [* J! y1 Q+ Bmon in girls than in boys.1,3 Most boys with CPP
5 L& O& M5 q" ^4 Bmay have a central nervous system lesion that is
! g4 U( J& o5 C) v; i, M0 A8 r9 cresponsible for the early activation of the hypothal-) O% S* @/ M! w
amic pituitary gonadal axis.1-3 Thus, greater empha-" u' g% a! ?7 {) c) w4 X+ T- N5 w
sis has been given to neuroradiologic imaging in
8 `0 [2 D) t7 \4 G7 w9 g2 |; {boys with precocious puberty. In addition to viril-
% A' V% [1 X$ F, ~1 Zization, the clinical hallmark of CPP is the symmet-
4 ~0 z% B8 S9 Y! Orical testicular growth secondary to stimulation by' t1 s: r, K, }; m. m+ z
gonadotropins.1,3
& b! C0 f$ p9 {2 F. e4 C2 b7 gGonadotropin-independent peripheral preco-
  n0 \  F7 ?* qcious puberty in boys also results from inappropriate9 F, r& ~, m; a$ ]( y" X! ?
androgenic stimulation from either endogenous or
- ?/ j& b, q5 t  R0 F6 @exogenous sources, nonpituitary gonadotropin stim-
) g: r: {% H7 s! f( oulation, and rare activating mutations.3 Virilizing$ \$ s* J6 {2 {! G1 Z% Y2 A! ~; L
congenital adrenal hyperplasia producing excessive
: h2 B& ]$ M! N/ m3 Jadrenal androgens is a common cause of precocious
* U0 s$ X  G; Npuberty in boys.3,4( l6 |# h2 K0 U$ J- v& v" b
The most common form of congenital adrenal. y8 Y; \: K( J
hyperplasia is the 21-hydroxylase enzyme deficiency.4 h; f  K) t& I: `$ |7 S( _; O
The 11-β hydroxylase deficiency may also result in
, Q" Z" T3 W- `+ ~' M, qexcessive adrenal androgen production, and rarely," ?6 u" Z/ g/ y
an adrenal tumor may also cause adrenal androgen; s1 d* E1 S) J4 d
excess.1,3
* Z" C4 Y  N/ K5 j# o6 Fat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- V% W8 i( s+ C" T6 ]542 Clinical Pediatrics / Vol. 46, No. 6, July 2007# W- B% x% ~3 r
A unique entity of male-limited gonadotropin-
  [) Q: m- {6 ~8 |3 ?independent precocious puberty, which is also known* W& x, @- b( N1 Z2 _6 O
as testotoxicosis, may cause precocious puberty at a; n4 Z* L* h5 K4 e! Y
very young age. The physical findings in these boys
/ P  j# j6 g. Uwith this disorder are full pubertal development,
, u+ T' `# r9 a. ?, cincluding bilateral testicular growth, similar to boys
4 d; x3 d! X! r  c) h' @7 g9 L5 y# Q! y$ Twith CPP. The gonadotropin levels in this disorder
  v/ Q$ I$ w' L5 y" e- e; A2 \' `  ?are suppressed to prepubertal levels and do not show
6 ]2 l; {6 D4 K5 d9 L( ^pubertal response of gonadotropin after gonadotropin-
1 m2 u" f% I. v% ~" Q) E, v! Vreleasing hormone stimulation. This is a sex-linked2 T* T6 ^- X6 s' M5 a0 i9 u
autosomal dominant disorder that affects only- J  q2 ~8 y" Q5 M  B
males; therefore, other male members of the family# ^5 ^5 \$ A3 ?$ ]2 R. F
may have similar precocious puberty.3
, K# i( ]2 v; S; tIn our patient, physical examination was incon-8 w! n9 j5 G6 ]# e+ [5 M
sistent with true precocious puberty since his testi-
) i, _4 Q$ H' V7 p0 icles were prepubertal in size. However, testotoxicosis
3 S1 e" s. n" L  q2 O- xwas in the differential diagnosis because his father
8 n) T9 j3 b' u$ ^& {4 H. a" Ostarted puberty somewhat early, and occasionally,
2 b# I* }0 ?+ x4 }* o  h9 t9 itesticular enlargement is not that evident in the+ p! j9 g4 @$ ~4 K
beginning of this process.1 In the absence of a neg-
  x: e. Y8 I% f4 O9 {' ?# lative initial history of androgen exposure, our
9 W& u$ \. H* z+ i+ O; d' }& bbiggest concern was virilizing adrenal hyperplasia,8 V% ]! B  o$ l% C0 e1 [
either 21-hydroxylase deficiency or 11-β hydroxylase
0 {& W/ T7 K$ c6 v% e5 vdeficiency. Those diagnoses were excluded by find-- H2 S+ J  z7 J: Y* s
ing the normal level of adrenal steroids.
7 t: Q* I9 j. ^3 qThe diagnosis of exogenous androgens was strongly
# `& }( ?$ M$ ?suspected in a follow-up visit after 4 months because# C( p5 Z$ V% s6 g5 @* T
the physical examination revealed the complete disap-( G( z4 r8 v2 P: a6 {
pearance of pubic hair, normal growth velocity, and, u0 {# D. }. l5 M
decreased erections. The father admitted using a testos-
$ b0 b' P& w* [" |0 _terone gel, which he concealed at first visit. He was
& z$ j- N5 @6 p) g' Y: R" X; Nusing it rather frequently, twice a day. The Physicians’) o) [, o  h# u( y* t0 ]
Desk Reference, or package insert of this product, gel or
! I$ f4 N3 m2 }( V) G' T! m6 T% hcream, cautions about dermal testosterone transfer to
  v& e2 X5 O: ]unprotected females through direct skin exposure.
+ J0 v/ P1 ^1 M1 \0 B* ^Serum testosterone level was found to be 2 times the
# |2 O0 [+ a  n! U2 r. j/ kbaseline value in those females who were exposed to+ e2 v/ y! [6 ~9 X$ o- h2 _1 E
even 15 minutes of direct skin contact with their male/ `1 p6 h, G/ ]
partners.6 However, when a shirt covered the applica-& |( r6 k2 M: v
tion site, this testosterone transfer was prevented.( s; Z% w2 c1 R+ n" f
Our patient’s testosterone level was 60 ng/mL,
# L; T5 @' b4 _2 }which was clearly high. Some studies suggest that
5 E. ?/ Y3 J) F$ Fdermal conversion of testosterone to dihydrotestos-9 ~# G2 _: S) ]$ E6 E; D
terone, which is a more potent metabolite, is more; X) L% q1 I9 {+ d
active in young children exposed to testosterone7 L( |6 d! Z5 k8 g2 {
exogenously7; however, we did not measure a dihy-/ _5 `% e1 b. v% g( P) R7 ^% u
drotestosterone level in our patient. In addition to/ R1 T; H( \+ R$ u3 `; Z* n1 y
virilization, exposure to exogenous testosterone in
! a; y3 O: Y: X* S0 c1 E) e5 i& E' Dchildren results in an increase in growth velocity and2 g: _8 \9 {# _, \8 S- [! l
advanced bone age, as seen in our patient.7 B2 ]# |1 [1 c2 l8 i7 X& s- G0 `
The long-term effect of androgen exposure during4 W  C7 v& t0 D" q. t! C7 v. d
early childhood on pubertal development and final
8 X; Y/ w* k& p' y0 vadult height are not fully known and always remain
4 Y  @  F- Q) Z6 I3 v" d- N/ ua concern. Children treated with short-term testos-
7 |& x4 H5 Z  K; p, B3 b) q6 R: Q% j) @terone injection or topical androgen may exhibit some$ ~% w. d5 I9 z( {7 y6 y
acceleration of the skeletal maturation; however, after" O) r( U0 q6 O0 H
cessation of treatment, the rate of bone maturation
4 ^% k, l: E1 m. J/ Y( w9 vdecelerates and gradually returns to normal.8,9
- B- X* j9 c+ o( k. P+ N5 lThere are conflicting reports and controversy
; N5 X1 i4 _# I; r& d' U9 nover the effect of early androgen exposure on adult/ ~8 X% F4 S0 n; z! o' b& _
penile length.10,11 Some reports suggest subnormal
2 L: X3 z0 Q# q: oadult penile length, apparently because of downreg-
$ t  B) }4 ?$ l7 m0 kulation of androgen receptor number.10,12 However,
) p- ~- t: `8 k+ `1 |. d  e5 qSutherland et al13 did not find a correlation between# {  m5 |6 L$ e6 u0 r% y# M, h
childhood testosterone exposure and reduced adult" c% Y9 ?3 ~6 g. [0 J1 J
penile length in clinical studies.
/ q, c3 D2 |( I: j& n3 ZNonetheless, we do not believe our patient is1 A6 B  ]1 c" U1 q6 A) H, [
going to experience any of the untoward effects from
: {2 e/ v8 I1 htestosterone exposure as mentioned earlier because
; n5 p1 U# k& V  x! Z* m, kthe exposure was not for a prolonged period of time.
8 e2 j& W! Z# i( ^/ J3 n$ N+ p( k4 jAlthough the bone age was advanced at the time of3 s+ i- ?( e6 X! m' x/ a
diagnosis, the child had a normal growth velocity at
  D* d8 E7 l7 l; {+ W# {  wthe follow-up visit. It is hoped that his final adult
( B5 p: y- x& t$ [6 s  b. ~height will not be affected.
' t8 A# s( d8 P0 Q: rAlthough rarely reported, the widespread avail-- E: H6 d' i9 g4 L
ability of androgen products in our society may( [3 [: M$ N' ?: }/ h1 a
indeed cause more virilization in male or female
1 D: B  I# e: o, s# n8 echildren than one would realize. Exposure to andro-
) ?4 O: i/ Q4 r' y9 }9 O/ qgen products must be considered and specific ques-5 E( r2 `  `9 G4 p9 q2 K* ?3 y# w' F7 y- P. p
tioning about the use of a testosterone product or/ [/ \3 l# t9 E. A, D% J
gel should be asked of the family members during/ Y9 O0 P6 m  G7 V8 y2 G
the evaluation of any children who present with vir-
. k. a0 b0 E; ^, B: U$ iilization or peripheral precocious puberty. The diag-" D/ w3 s) [* Q, I
nosis can be established by just a few tests and by
& C3 z7 }8 `  a3 s- A& x. wappropriate history. The inability to obtain such a7 Z, i' A6 n* v9 s7 M* e" k
history, or failure to ask the specific questions, may+ S3 b7 ~, K/ k" x5 n; R* q
result in extensive, unnecessary, and expensive8 F7 b9 _  E( R3 Z+ C1 N
investigation. The primary care physician should be
. ^( `3 {& P( Z0 x  h0 j7 y, Laware of this fact, because most of these children
* O3 y7 J1 `$ W$ O# O, w" Emay initially present in their practice. The Physicians’
3 z" x5 e3 f& x5 `! Q; S" y1 ~" m4 JDesk Reference and package insert should also put a4 K2 n4 \' q# g$ v1 y
warning about the virilizing effect on a male or
! y4 b6 V& l1 c% a8 d2 Cfemale child who might come in contact with some-
: s7 y3 s9 ]1 N4 G2 Ione using any of these products.: _7 C& _5 |  u$ K9 }
References
( L8 ]' r! T$ R1. Styne DM. The testes: disorder of sexual differentiation" J, y( o8 Y( a, V2 x) `& y
and puberty in the male. In: Sperling MA, ed. Pediatric8 w4 q6 M/ i$ J4 Y6 [( E
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
( ~( c2 _6 u) ]; j* e% a& I. q2002: 565-628.! l7 n2 I' ?7 {% o( T! _
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
4 }" L( l& w2 w8 d. fpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
7 k9 G1 s9 K: L. a$ ^/ QBoy Induced by Indirect Topical9 e) B$ W. o, P0 f; K+ Y8 J* V# i
Exposure to Testosterone
" H' T3 o% i3 e2 E1 f; FSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2% h) K( Y2 O, j9 f! h5 P
and Kenneth R. Rettig, MD19 N- }# ^2 Q. g( J7 B5 ?, G
Clinical Pediatrics
; b+ f: G- X8 P9 F8 }: v& ]+ YVolume 46 Number 6/ X0 {$ ?9 A  t' @. C
July 2007 540-543
: H& V0 q( U4 `/ k+ j4 ^% |© 2007 Sage Publications
; E# \3 e+ z* M# m& F! }/ o10.1177/0009922806296651
- S' W5 h0 D0 S3 ]& w9 s( Vhttp://clp.sagepub.com; [0 d$ C7 P/ f, x( l: g" t9 x
hosted at0 q# y! I0 A( O8 q
http://online.sagepub.com
! J- ]! X/ w. x- }0 cPrecocious puberty in boys, central or peripheral,
9 Q  L& j8 C* u* j3 kis a significant concern for physicians. Central
. l. E' O# k# C0 F7 gprecocious puberty (CPP), which is mediated0 H# i+ a' _4 s, Q
through the hypothalamic pituitary gonadal axis, has
. H, H/ g, m) p2 U3 i5 d/ ^! H( r0 Aa higher incidence of organic central nervous system- u) A. z1 E$ q
lesions in boys.1,2 Virilization in boys, as manifested( W& O, I$ P% n
by enlargement of the penis, development of pubic
6 |1 N6 [! g# _5 ]+ P5 g  x3 ^1 qhair, and facial acne without enlargement of testi-" \8 h6 {8 V- Y% j; G0 a
cles, suggests peripheral or pseudopuberty.1-3 We1 m: ~8 M% e2 ?4 K  T2 |
report a 16-month-old boy who presented with the
  H: b0 k  p. q" L* oenlargement of the phallus and pubic hair develop-: C" N* _+ F3 ~& b# a
ment without testicular enlargement, which was due* r5 T5 }. b9 x- n" X- ]8 c
to the unintentional exposure to androgen gel used by
1 v6 ~, i( s! U5 u9 a3 v: ~the father. The family initially concealed this infor-
! \4 D- u; I  o& I# V$ W" ^5 N2 zmation, resulting in an extensive work-up for this
8 @0 y. X6 f: w" Kchild. Given the widespread and easy availability of
) j) N; Z' I; \0 wtestosterone gel and cream, we believe this is proba-8 `( k/ v3 B. ^2 {
bly more common than the rare case report in the2 p  F! z, q) r9 o/ y
literature.4
+ K/ E1 B0 c! w+ [Patient Report
! @0 J" B  P* W6 rA 16-month-old white child was referred to the$ \) N7 }5 o2 l/ \, X3 E+ r
endocrine clinic by his pediatrician with the concern
, |: p$ l& _- w4 r! gof early sexual development. His mother noticed
3 e- ]6 ~+ }' G- Mlight colored pubic hair development when he was& h: C/ Y% Z8 j8 m% R
From the 1Division of Pediatric Endocrinology, 2University of
" C" X- h! |' C0 A1 F7 v3 }' {1 KSouth Alabama Medical Center, Mobile, Alabama.
5 X5 }- ?' ]9 H) H1 ^Address correspondence to: Samar K. Bhowmick, MD, FACE,; B. @: r2 L  o3 U6 j0 \  T" S9 o
Professor of Pediatrics, University of South Alabama, College of
% `0 y# O3 @1 x1 HMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
7 k4 m: I- b( t% O/ R  C! \e-mail: [email protected].
5 w$ ~( B, [: _; _7 U- labout 6 to 7 months old, which progressively became# E" q4 ]) O4 H" y+ Q: w; s) }3 F
darker. She was also concerned about the enlarge-, T! g  ~1 ], s7 V* B2 X; i3 C
ment of his penis and frequent erections. The child
) ~- \/ n  q5 c5 w' Cwas the product of a full-term normal delivery, with
/ M+ ]' f" H& B8 D. }a birth weight of 7 lb 14 oz, and birth length of- B, {! X$ p7 g
20 inches. He was breast-fed throughout the first year4 s: Z) e% S9 }% x4 H) [
of life and was still receiving breast milk along with
% s2 O* U2 ~8 M( R% x9 e6 r- j6 M% rsolid food. He had no hospitalizations or surgery,* z4 K* i' A( B  n" d& h
and his psychosocial and psychomotor development& x  f% G% V) p/ ~5 v
was age appropriate.
* r, c# W; t8 N$ H- x1 eThe family history was remarkable for the father,9 L$ d3 I6 w1 O  N$ F
who was diagnosed with hypothyroidism at age 16,
" o0 K7 t4 n8 R$ o6 a; J' Iwhich was treated with thyroxine. The father’s
9 ^2 u* @* C8 R- C4 q* C2 ~- vheight was 6 feet, and he went through a somewhat
0 l3 k% g5 u1 g3 ?  ]early puberty and had stopped growing by age 14.
0 a! t; H4 p6 U% BThe father denied taking any other medication. The
' @7 x6 ^  ?5 schild’s mother was in good health. Her menarche
6 \+ N- |7 |; dwas at 11 years of age, and her height was at 5 feet
' P$ B; O& Z* D2 c& n5 inches. There was no other family history of pre-
( g; @- C, b6 r# i) h/ m7 D) Fcocious sexual development in the first-degree rela-
. a) ?% w4 V( R8 ?$ k6 gtives. There were no siblings.
) |) E# P& s! o; [Physical Examination
; m' J( e+ ^# c7 ?The physical examination revealed a very active,
$ c, W3 S& _6 f8 N; dplayful, and healthy boy. The vital signs documented- M( T8 @3 S  u7 L, {, g
a blood pressure of 85/50 mm Hg, his length was) ~  b( w, d) ^2 r5 x: }
90 cm (>97th percentile), and his weight was 14.4 kg
: r& k9 o* f4 x9 W6 P9 s6 B  @, X(also >97th percentile). The observed yearly growth0 G$ K9 G% D% `5 V% s# t* a( q
velocity was 30 cm (12 inches). The examination of$ F7 M) q, ?/ H' R- P4 V
the neck revealed no thyroid enlargement.8 P: U0 z& k, K9 \0 s) N# T( p& B
The genitourinary examination was remarkable for
8 L& i7 Z1 v$ z: @6 ]9 \enlargement of the penis, with a stretched length of* W& R& U! d* O. m3 M
8 cm and a width of 2 cm. The glans penis was very well, d% P( j3 i( c5 h: d. J" F
developed. The pubic hair was Tanner II, mostly around" l' d  H8 Z: F2 A1 A
540* N$ O1 ^2 m+ A# K
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& E% |5 V" V1 M- |2 V  c6 H! [7 vthe base of the phallus and was dark and curled. The
+ O& b+ w# _2 {2 ^testicular volume was prepubertal at 2 mL each.
+ J: B$ }. O! N7 ]5 MThe skin was moist and smooth and somewhat- G( Q8 e5 {7 _
oily. No axillary hair was noted. There were no
8 t1 k. m! t) Y  E+ `abnormal skin pigmentations or café-au-lait spots.
+ C/ f$ {! r/ C. UNeurologic evaluation showed deep tendon reflex 2+
8 t1 Q7 \8 N- t9 P  u: w2 w* }bilateral and symmetrical. There was no suggestion5 D7 o; M* v* K7 d( f$ `
of papilledema." h# B% r, j, w5 j
Laboratory Evaluation
# C: k2 p4 e% g1 M% xThe bone age was consistent with 28 months by' {# x+ e1 y2 w' |/ r: A0 i4 A
using the standard of Greulich and Pyle at a chrono-
) w* L2 n% I7 O' H, j8 s( ulogic age of 16 months (advanced).5 Chromosomal
" L8 L1 C5 S- X0 h1 H' y! o% Ykaryotype was 46XY. The thyroid function test' a) }2 [6 M) G: m& m& B/ d! {# l
showed a free T4 of 1.69 ng/dL, and thyroid stimu-% X* y3 O$ ?8 t7 C' S, h
lating hormone level was 1.3 µIU/mL (both normal).0 k4 B( e$ [8 F
The concentrations of serum electrolytes, blood+ \" [$ q( g9 N% }& K
urea nitrogen, creatinine, and calcium all were
, |" Q7 S) D' U4 Rwithin normal range for his age. The concentration( R# U8 I) }' Y* p( l# ?2 [8 N
of serum 17-hydroxyprogesterone was 16 ng/dL
$ c9 i. {& s$ I(normal, 3 to 90 ng/dL), androstenedione was 20
) [+ _6 `9 @- M' |. |ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
4 j7 n6 ]! G5 a9 `1 g9 g3 ?terone was 38 ng/dL (normal, 50 to 760 ng/dL),
- y$ w$ Q; w7 D! k0 tdesoxycorticosterone was 4.3 ng/dL (normal, 7 to5 k$ P1 {9 X; M2 f2 l( g
49ng/dL), 11-desoxycortisol (specific compound S)
- y% o+ J/ A0 W+ zwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-; V' u: u/ g6 {' a3 b
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total. z! X; c5 x1 f" L: \. t1 c5 {
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),1 s4 Y9 m0 ]$ ?, k2 Q) y: s6 G
and β-human chorionic gonadotropin was less than% R8 y% c8 g$ g6 D
5 mIU/mL (normal <5 mIU/mL). Serum follicular8 r$ e% l. L9 F4 d% Y8 J& d
stimulating hormone and leuteinizing hormone
. s/ u# C9 w( Y. s$ g5 X( wconcentrations were less than 0.05 mIU/mL
( z. j0 H9 J% I( `/ ^& i: p+ g1 `(prepubertal).
0 ~: M$ c# P8 H7 FThe parents were notified about the laboratory1 |, K- \# R( X& N& S5 J' N' [
results and were informed that all of the tests were3 `5 k& B5 t/ S& U: @  u, M. P
normal except the testosterone level was high. The* k; U8 g/ m# g) ^# x
follow-up visit was arranged within a few weeks to' a! S5 s4 K, a* h: X* `! t
obtain testicular and abdominal sonograms; how-
/ B. C* O% N& t* Y3 Dever, the family did not return for 4 months.
3 X) N7 J+ g- p3 @Physical examination at this time revealed that the
! C/ u& K# K+ J) ochild had grown 2.5 cm in 4 months and had gained1 c  n: Q2 [# Z, ~: |
2 kg of weight. Physical examination remained4 \. Y5 S1 r% X) G5 R3 J& C9 c
unchanged. Surprisingly, the pubic hair almost com-
9 ]" p9 i+ [; v3 f1 F/ hpletely disappeared except for a few vellous hairs at
# V& R9 K1 [' ^3 M2 m* M# |3 cthe base of the phallus. Testicular volume was still 2: W2 O; ]: \" o8 B- L5 S
mL, and the size of the penis remained unchanged.
  S) N$ C# j* V; o- y9 m1 wThe mother also said that the boy was no longer hav-
! E8 C8 a. d$ y) S" H4 ]$ n: ting frequent erections.4 A5 k7 K5 |7 {4 G  J( ?4 h0 x
Both parents were again questioned about use of
" a: ?0 r$ v0 u9 Many ointment/creams that they may have applied to
7 z  r2 V1 N! O' ~1 y! Athe child’s skin. This time the father admitted the! O, ?- o+ v4 a3 h# k8 V; ^
Topical Testosterone Exposure / Bhowmick et al 541
. R" Q9 h9 q4 {. I7 P4 euse of testosterone gel twice daily that he was apply-
9 {6 M$ A  _0 F! E( Oing over his own shoulders, chest, and back area for2 w- L5 `6 b: ~  w" p( q
a year. The father also revealed he was embarrassed! V, n- q; S3 \) @- Q& K
to disclose that he was using a testosterone gel pre-) ^3 B2 ~% {* p4 J( x" e# Q8 D0 G( W/ s
scribed by his family physician for decreased libido! z0 y$ F8 {1 u" E2 J& ?+ N
secondary to depression./ N$ t. b+ M8 H$ o6 W
The child slept in the same bed with parents.
3 E: N: E) L+ Z+ {The father would hug the baby and hold him on his
5 S5 ?) ?" J  M5 _0 h& dchest for a considerable period of time, causing sig-( s9 v% M9 g1 u4 |9 u& r
nificant bare skin contact between baby and father.% ]1 H& N' E0 h) J, X: u
The father also admitted that after the phone call,
& E1 D$ E+ q2 L. Q# l" awhen he learned the testosterone level in the baby7 @9 o9 p6 A9 Q6 D" }8 U
was high, he then read the product information! e2 ^0 Y& w+ `, y, {
packet and concluded that it was most likely the rea-3 Q, M  `0 @4 m! G7 Y1 c9 z
son for the child’s virilization. At that time, they. d! D2 U+ T) f9 u1 q4 O4 F
decided to put the baby in a separate bed, and the
3 g" K7 X* n6 k, B6 A6 U& {father was not hugging him with bare skin and had
& n5 l1 ]: S6 H  ?' ~, S) qbeen using protective clothing. A repeat testosterone
7 w1 f& @4 I! I2 ^. Etest was ordered, but the family did not go to the
$ R& Z& ?, h) Y) `# b: blaboratory to obtain the test.) ]1 a* X9 c8 N2 s: v
Discussion
/ i8 \# d" X# X: Q" ^6 i& j; fPrecocious puberty in boys is defined as secondary' C5 ^- w8 B0 g: \6 z
sexual development before 9 years of age.1,4
0 n7 @* F+ ?$ J' Z; J/ w4 k: oPrecocious puberty is termed as central (true) when1 y, g  |6 p- O+ y& t
it is caused by the premature activation of hypo-' C: t0 o' a9 e
thalamic pituitary gonadal axis. CPP is more com-2 Y$ d0 z! k: j% N2 h; q4 ~  `! l. j
mon in girls than in boys.1,3 Most boys with CPP4 p$ w4 Q* f# N
may have a central nervous system lesion that is  e$ v: E8 b9 T7 f6 X
responsible for the early activation of the hypothal-
6 A8 ~% W% Y5 y* K' gamic pituitary gonadal axis.1-3 Thus, greater empha-9 r& _" {: n& i1 G
sis has been given to neuroradiologic imaging in6 e/ N/ B% c9 Q& h" k  F4 x
boys with precocious puberty. In addition to viril-
5 Z9 @" u, H" f1 f# U( a2 ]0 Aization, the clinical hallmark of CPP is the symmet-
+ B" I/ A( [8 {/ Z0 ]' krical testicular growth secondary to stimulation by( Q* g. ^$ c/ O1 }0 `2 ?
gonadotropins.1,36 X1 I( @7 K/ R% I4 M, t
Gonadotropin-independent peripheral preco-
" \! m; M0 P; O5 p3 m( U! C# Vcious puberty in boys also results from inappropriate
7 Y+ x0 S1 j+ q% O- Wandrogenic stimulation from either endogenous or& b# C  A( H4 Y) w$ q
exogenous sources, nonpituitary gonadotropin stim-  I% K9 C' v! A% x
ulation, and rare activating mutations.3 Virilizing% @; t9 X/ W" E" I) w+ L
congenital adrenal hyperplasia producing excessive
+ u% e: S7 c2 c: W1 k! P; ~$ Yadrenal androgens is a common cause of precocious9 @9 {$ L7 D9 L% Y8 w
puberty in boys.3,4
8 i: S, t* i# Q5 yThe most common form of congenital adrenal/ {, M( H: t$ [) d3 g7 S7 b
hyperplasia is the 21-hydroxylase enzyme deficiency.
2 V9 U7 y, _9 @3 i& `) G$ g, r; I$ a$ `The 11-β hydroxylase deficiency may also result in
' L) ^/ o$ R4 J$ z1 S  @/ pexcessive adrenal androgen production, and rarely,+ `* ]: p% u7 o& e% o! U* V
an adrenal tumor may also cause adrenal androgen
9 m  H, ?6 F- O. D# f. cexcess.1,3
9 R. t; U% e4 [$ kat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, _4 E5 X# ^4 B: d542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
- L5 M4 |3 U& m4 w! I' rA unique entity of male-limited gonadotropin-
( W5 G% D1 e" z- s, S$ \independent precocious puberty, which is also known5 V2 `/ o7 v* O( `
as testotoxicosis, may cause precocious puberty at a; E- ^, Y9 B  t% i8 ]
very young age. The physical findings in these boys) T( c) n* _# y8 L
with this disorder are full pubertal development,5 \; U, K; m9 U2 y) G
including bilateral testicular growth, similar to boys
& w, @+ T9 ?0 r  F; q1 t7 Vwith CPP. The gonadotropin levels in this disorder
+ ]7 ^% X0 C; R5 ]: c, i2 Care suppressed to prepubertal levels and do not show9 \; T* h( `9 H' T1 o; d
pubertal response of gonadotropin after gonadotropin-% ]" @0 m( z9 P  Q- e
releasing hormone stimulation. This is a sex-linked% e9 B# V  m7 J
autosomal dominant disorder that affects only
- r0 p) `) q' r8 V+ A" Smales; therefore, other male members of the family! q6 j' j# j' l) i. e- a0 t8 j
may have similar precocious puberty.3
! X0 d; n' p  J9 `In our patient, physical examination was incon-
5 ?4 |( M& F$ G- P5 F, |/ N2 csistent with true precocious puberty since his testi-
( D6 W7 J8 |8 u  i' U3 N. vcles were prepubertal in size. However, testotoxicosis% j% z9 a0 Z& [1 R3 s: R0 |
was in the differential diagnosis because his father% X( [% Q# _0 Q/ d" e% o( h
started puberty somewhat early, and occasionally,0 M7 V0 S3 z- h. V3 `. l/ q
testicular enlargement is not that evident in the
' v% y6 y! a) d: g  qbeginning of this process.1 In the absence of a neg-- h) l/ ^$ [3 k! D
ative initial history of androgen exposure, our9 E8 P' G6 p7 D
biggest concern was virilizing adrenal hyperplasia,
3 e; G' q" r& m- seither 21-hydroxylase deficiency or 11-β hydroxylase5 d' w7 M- t* P5 u7 f; \
deficiency. Those diagnoses were excluded by find-$ u$ C. P, {2 b. C8 u! W( S* b
ing the normal level of adrenal steroids.; M/ \# u1 x% q# S, U" L6 E. F
The diagnosis of exogenous androgens was strongly
% f% D% d" W' n  c7 m4 csuspected in a follow-up visit after 4 months because4 r: s& w* r3 k; S) y" f9 Z- _, }
the physical examination revealed the complete disap-
0 N. y+ o  q: s! z, Hpearance of pubic hair, normal growth velocity, and
: {  v4 ?7 w. ddecreased erections. The father admitted using a testos-
& @/ f' ?  w, H/ R) l$ E: d5 ]terone gel, which he concealed at first visit. He was7 ^/ f2 O2 h( {3 b, |* @& n
using it rather frequently, twice a day. The Physicians’
) f7 i, K2 v9 vDesk Reference, or package insert of this product, gel or* [1 P8 c1 Q6 h  p' U/ n/ v  u
cream, cautions about dermal testosterone transfer to
* c! |* r# ^8 p2 e, ]unprotected females through direct skin exposure.3 H) U6 `9 ~" w
Serum testosterone level was found to be 2 times the4 H0 h" x7 b+ V# ?! i
baseline value in those females who were exposed to
8 [; S1 C/ `. M  Y: U% x( z+ M: qeven 15 minutes of direct skin contact with their male/ |5 x4 m& d, g4 C2 L; r
partners.6 However, when a shirt covered the applica-
) |/ c7 t  Q2 O" I& c/ ytion site, this testosterone transfer was prevented.# R8 u! O: y8 A% C/ ~; C
Our patient’s testosterone level was 60 ng/mL,
: v1 n: W$ x# }which was clearly high. Some studies suggest that8 c1 C8 H* c) Q' G
dermal conversion of testosterone to dihydrotestos-9 _- w5 @" q9 n; j
terone, which is a more potent metabolite, is more
% R; i+ {' \: uactive in young children exposed to testosterone
) l* |0 Z8 {% b' c. V: Aexogenously7; however, we did not measure a dihy-
4 J7 h) g7 y1 E- Qdrotestosterone level in our patient. In addition to# M& A. x/ S0 @1 m  Y! W6 m, o4 w
virilization, exposure to exogenous testosterone in
; H/ p6 q# Z6 _5 \. jchildren results in an increase in growth velocity and) M& |: m4 x5 x. C
advanced bone age, as seen in our patient.
' h1 y+ h6 {9 z4 d; QThe long-term effect of androgen exposure during* S  N+ B2 @' D
early childhood on pubertal development and final
9 G  c# @$ t0 G" X1 }  @* Qadult height are not fully known and always remain0 Z4 E+ n6 Q0 L/ B
a concern. Children treated with short-term testos-
7 j4 ?! i* N, z& s; N; e1 w8 Bterone injection or topical androgen may exhibit some7 Y* w* K2 d' q; e" u$ e
acceleration of the skeletal maturation; however, after
3 A& F0 k+ }! mcessation of treatment, the rate of bone maturation$ \1 b$ y: b  Y5 S7 z2 i2 r. ?6 d0 `
decelerates and gradually returns to normal.8,9& h' N" R# u' M0 t1 o
There are conflicting reports and controversy
- U4 V- i7 {9 d$ E- ]" aover the effect of early androgen exposure on adult
: }% Q: I9 O. m" npenile length.10,11 Some reports suggest subnormal& W" _2 }% P( c  ?' x
adult penile length, apparently because of downreg-7 M* Z9 \9 `1 @
ulation of androgen receptor number.10,12 However,, B$ h, b6 I$ Y8 K9 j
Sutherland et al13 did not find a correlation between9 g" `0 U" t4 d8 r) H# h
childhood testosterone exposure and reduced adult; p; V  s2 t1 a  `: m
penile length in clinical studies.3 P  v: Q: a5 @' Y
Nonetheless, we do not believe our patient is
  y/ h1 K2 M/ L6 c( V3 R7 n9 h! a( [going to experience any of the untoward effects from
& x" ?* g( l7 q0 P* ttestosterone exposure as mentioned earlier because# ?4 i- \' }6 w9 w6 `
the exposure was not for a prolonged period of time.4 O3 X  s5 e7 A" n( \4 }
Although the bone age was advanced at the time of( v+ X) ?% a& M# v
diagnosis, the child had a normal growth velocity at+ M, L4 F# A9 D' H# [( W! F
the follow-up visit. It is hoped that his final adult
6 y/ |. x! Y/ l6 N" aheight will not be affected.
; H' s6 ]% k" [  S8 z4 v: FAlthough rarely reported, the widespread avail-
* X; {% u8 c4 [ability of androgen products in our society may
: u8 |5 A  Y9 i" c% @indeed cause more virilization in male or female
2 S8 Y8 ]) T3 N2 W8 v9 {" E+ F9 hchildren than one would realize. Exposure to andro-& v  Y+ S% ?6 B, e7 I
gen products must be considered and specific ques-
1 [* R! e% @- j1 M2 S2 ytioning about the use of a testosterone product or- N( i4 l! p$ C- [6 N5 m% j' H% o1 T
gel should be asked of the family members during
; e9 y. f+ a' S3 p% T! a  ?6 Mthe evaluation of any children who present with vir-4 `, P4 g' g7 q+ G8 B- E; w
ilization or peripheral precocious puberty. The diag-9 {' F& G* c% q6 Y, l, i, ?. H6 O
nosis can be established by just a few tests and by
0 @/ i! W, M# Jappropriate history. The inability to obtain such a
1 [! P" x6 @" a( L+ T" K$ W( a' g" V1 Uhistory, or failure to ask the specific questions, may* q9 T. X' F1 C9 C* R
result in extensive, unnecessary, and expensive. S. A) d5 G9 O' C$ s
investigation. The primary care physician should be
6 M( [7 a2 s4 Taware of this fact, because most of these children8 l3 Y; K/ V9 W# K
may initially present in their practice. The Physicians’7 s  F7 t- o9 x6 }; Z' W
Desk Reference and package insert should also put a7 n! P4 W5 Z$ o5 S  J
warning about the virilizing effect on a male or2 v4 B* q6 W: W9 w
female child who might come in contact with some-8 e! @: I1 Z) }; e' N7 j; K
one using any of these products.  d+ M, d$ p& X1 e$ {  q& o
References
% S: H. P. U, D# z- N2 A6 y1. Styne DM. The testes: disorder of sexual differentiation
; G' E2 t$ k4 ~3 t% F5 e% _and puberty in the male. In: Sperling MA, ed. Pediatric
. `9 l3 @* Y/ UEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;& q5 V5 d0 N6 K6 P  N5 F5 s# ~
2002: 565-628.
. z2 Q0 u2 O7 ~% f2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious2 W- k, V5 @0 j7 P8 c
puberty 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
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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
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
& q* X+ C' x: _6 S2 ?+ V" i- s+ M
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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