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Sexual Precocity in a 16-Month-Old- F+ k* {8 J. P5 f) D
Boy Induced by Indirect Topical
. c9 g& }8 D& K! N: a* @! MExposure to Testosterone
9 P' m% u1 x! l! [Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 M& G/ k: g0 E, E# U* pand Kenneth R. Rettig, MD1
# ~# X6 g: ]2 `4 I( J5 S, w4 PClinical Pediatrics( ^1 D; Y* D6 S. V4 ]2 Z
Volume 46 Number 6% S% A* r% x& |6 u, N- q- ^
July 2007 540-543
5 k4 Z  S7 X# n- t3 l2 l* Z7 S9 A& O- Q0 k© 2007 Sage Publications
2 [5 O3 r" w4 N3 V10.1177/0009922806296651$ v& j9 J8 a; Q- I- c7 O8 V, _/ l! m
http://clp.sagepub.com
2 r9 B( ]4 M" J# F$ U4 X& j$ U( F1 Mhosted at
: p  J1 I' Z& ?) H2 t9 p, j: Hhttp://online.sagepub.com  \% f6 o  p/ O8 e3 c0 C9 e/ O
Precocious puberty in boys, central or peripheral,5 ?$ @# j3 t. B4 m4 K1 c
is a significant concern for physicians. Central
# p2 t. c% R  n6 T1 d( Pprecocious puberty (CPP), which is mediated  D/ U3 V& W3 q6 ^
through the hypothalamic pituitary gonadal axis, has4 @0 j2 l/ D& N, y, d; b# C: k
a higher incidence of organic central nervous system
, H+ f. i% m9 t' v) qlesions in boys.1,2 Virilization in boys, as manifested
' ]* y8 _( B8 n8 P# Hby enlargement of the penis, development of pubic! C2 M/ J' E: M! ^/ y. {8 d
hair, and facial acne without enlargement of testi-
2 Z. N( |! Y/ A) J, H' x$ q# {cles, suggests peripheral or pseudopuberty.1-3 We* w7 ~) W0 h8 H6 {( y: O( |
report a 16-month-old boy who presented with the
& z/ B( c# `3 F9 tenlargement of the phallus and pubic hair develop-  y4 ~! c! {! f2 w
ment without testicular enlargement, which was due
4 s# l. o! c$ J2 Nto the unintentional exposure to androgen gel used by8 L$ }8 K' K# h+ c9 v; U# j+ {  M
the father. The family initially concealed this infor-
+ t, Y" a* ]% Z) n3 u" amation, resulting in an extensive work-up for this
- ~. N+ J/ U& Q! ]1 u; F! A2 u6 vchild. Given the widespread and easy availability of
. a2 L5 f% m  u. j6 Vtestosterone gel and cream, we believe this is proba-, z, }$ t5 o3 m$ v: L9 k" a
bly more common than the rare case report in the
6 P  L7 ?( Q# S2 j9 }4 Qliterature.4
3 G: ^) s4 a, F' K( k& hPatient Report" `: I8 R7 |2 R; V' k; n) M& E
A 16-month-old white child was referred to the1 }# o$ r. h( _$ W, r
endocrine clinic by his pediatrician with the concern
8 q2 l6 H8 t$ X4 G9 Jof early sexual development. His mother noticed7 N/ K9 x3 z- a1 L7 q( N
light colored pubic hair development when he was
) U# A4 a1 R* Z6 m. Z% zFrom the 1Division of Pediatric Endocrinology, 2University of" _3 c1 t7 m+ B+ B! ?, w. D
South Alabama Medical Center, Mobile, Alabama.
( y* \6 `9 L4 _# m) _  WAddress correspondence to: Samar K. Bhowmick, MD, FACE,! ?2 c* ?( D0 w% o( R5 q! ^- J& l, Y
Professor of Pediatrics, University of South Alabama, College of
0 ~8 \/ z1 o1 M* e  w8 p( D) @Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;9 j5 @5 e# X" f+ E- `" f
e-mail: [email protected].
1 r5 N0 e/ p) \# J0 z' I5 n2 ?4 Qabout 6 to 7 months old, which progressively became4 s+ e' [" ^3 q# W0 J! J) C/ f) y0 x
darker. She was also concerned about the enlarge-
+ g. j% ~( B* j6 |# wment of his penis and frequent erections. The child
/ f* U7 x( |% v1 O* mwas the product of a full-term normal delivery, with6 ?7 {- T6 c) j" [) r; {2 k
a birth weight of 7 lb 14 oz, and birth length of
/ F% @3 ^5 Y7 K1 b$ C20 inches. He was breast-fed throughout the first year
7 x! F4 _$ |! ~! g: ]of life and was still receiving breast milk along with1 w, B7 ?8 V+ j  e
solid food. He had no hospitalizations or surgery,8 K% e: ]0 G% }( G% D
and his psychosocial and psychomotor development
- E* Z7 h, i; y' a* mwas age appropriate.
! W; h$ d6 g" g0 [The family history was remarkable for the father,
; r3 u$ t% Q+ m  m4 owho was diagnosed with hypothyroidism at age 16,
2 `' N. P3 \5 |8 \- Swhich was treated with thyroxine. The father’s
0 k: U; Y% l& K/ n) ~/ L, [height was 6 feet, and he went through a somewhat) C; n3 B" d% Q  ^/ b5 [: v2 f- s
early puberty and had stopped growing by age 14.
" O, g- ]! |8 J6 q; V; \/ \& e3 |& p/ WThe father denied taking any other medication. The
2 }: c+ ]4 y! l: gchild’s mother was in good health. Her menarche1 W: u# R7 \7 U' U5 P
was at 11 years of age, and her height was at 5 feet
/ n2 ]2 ?& r+ C$ r4 v; F% Y5 inches. There was no other family history of pre-% ]& t( Q+ I, D
cocious sexual development in the first-degree rela-
! H4 s5 }0 w) Xtives. There were no siblings.% K; j' n) W% ^5 r4 A
Physical Examination
3 W  a& R6 u# S; D  a3 OThe physical examination revealed a very active,3 i5 X, N9 X; ~- R
playful, and healthy boy. The vital signs documented
* k7 T5 d% u9 D; [: ca blood pressure of 85/50 mm Hg, his length was
2 b. ?8 N3 S) Q: Q: R3 v! ^' F8 v90 cm (>97th percentile), and his weight was 14.4 kg8 v; {# r( l, Z# l# r9 F
(also >97th percentile). The observed yearly growth( R' y/ }4 M8 i9 E) |+ \
velocity was 30 cm (12 inches). The examination of: i6 D3 |6 z( J$ M2 ]+ @# F0 v  {
the neck revealed no thyroid enlargement.
( ^  D; z  B; a, o" M' JThe genitourinary examination was remarkable for9 }8 @* [% t% N- f; G
enlargement of the penis, with a stretched length of) z0 R  m! {, X# w: n9 {* R
8 cm and a width of 2 cm. The glans penis was very well3 v, O: K& I6 I  `
developed. The pubic hair was Tanner II, mostly around
+ z8 {5 a0 t0 [0 r! D" [540' k, ~! G, G+ N5 c; G
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 R0 d: _5 b' G1 `/ R
the base of the phallus and was dark and curled. The
0 W- c, c; F5 A  i* Q3 B1 Atesticular volume was prepubertal at 2 mL each.
: ?4 S& M. T+ g) a( g7 q6 ]4 q4 FThe skin was moist and smooth and somewhat7 g8 z4 x) @5 U( n8 o0 C; n0 K
oily. No axillary hair was noted. There were no: y1 f8 T# f& S5 I, I' m. k  K
abnormal skin pigmentations or café-au-lait spots.7 F" L) S! J+ v: A7 r% i
Neurologic evaluation showed deep tendon reflex 2+4 N* ~  v& n' O) N0 w3 ]
bilateral and symmetrical. There was no suggestion
* s: |2 W* N  n- h+ V! Vof papilledema.0 a: j7 R% o* f# }8 r' M: s" [
Laboratory Evaluation
: `  l# ~0 ?( ]5 T! E$ u. B  PThe bone age was consistent with 28 months by
9 n9 R' |5 h# k0 ~% eusing the standard of Greulich and Pyle at a chrono-( z- I: h, ?& z" H0 F
logic age of 16 months (advanced).5 Chromosomal  o, y- a, y* O# @4 K9 u! [, o1 H6 X
karyotype was 46XY. The thyroid function test8 R9 K- V' ~# `9 P3 t
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
9 _, P# w8 E* L* W9 _8 B. Z) Flating hormone level was 1.3 µIU/mL (both normal).4 {9 M# u* n, b- A" m# i. d
The concentrations of serum electrolytes, blood
( M* q: N6 b5 i) q0 g/ iurea nitrogen, creatinine, and calcium all were6 B& @3 g+ `& ~
within normal range for his age. The concentration
8 I0 ]' z0 s- U0 p" {# Fof serum 17-hydroxyprogesterone was 16 ng/dL* {! j  w* s' T3 ]3 q" K6 y- {
(normal, 3 to 90 ng/dL), androstenedione was 20
  A; ?8 A  ~  ^: hng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-6 Y2 S6 f% |8 {- w
terone was 38 ng/dL (normal, 50 to 760 ng/dL),; G3 l% K0 N' U8 C9 L( b
desoxycorticosterone was 4.3 ng/dL (normal, 7 to" D: b. D- i1 j# \. |4 d
49ng/dL), 11-desoxycortisol (specific compound S)
/ F6 `4 V% }, P9 N; Z! p" ~1 Awas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-% i& i. t* S3 x# s- h
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total% R4 O1 y+ V2 j6 {; d# G
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
( r* V# h' p' R2 }and β-human chorionic gonadotropin was less than
7 c4 t/ K1 V! t: C: E  b5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 K/ r* Z4 C& z- o0 |stimulating hormone and leuteinizing hormone$ P3 b* R6 y0 U1 K+ L8 Q( I" F
concentrations were less than 0.05 mIU/mL
* P) _" C8 Q+ D* O(prepubertal).* l2 y' E$ R  p+ A
The parents were notified about the laboratory/ [- I, B6 O& X8 a' s
results and were informed that all of the tests were
6 w% h: ~9 `0 `- d' D, y1 n& rnormal except the testosterone level was high. The2 J& }9 l/ a  V4 o/ E
follow-up visit was arranged within a few weeks to0 M) A0 C* R* m2 `( s4 i: V  L( m
obtain testicular and abdominal sonograms; how-
* {* [; y" E8 e) b  {+ qever, the family did not return for 4 months.
; {4 U8 m( g! ?7 f- `* K$ sPhysical examination at this time revealed that the; ?9 E3 ^4 r9 t% t+ p; m  d
child had grown 2.5 cm in 4 months and had gained
3 C, e" P* ?$ u0 U1 N2 kg of weight. Physical examination remained7 B2 [  s# g- W, k
unchanged. Surprisingly, the pubic hair almost com-
! t. t* d5 K7 W5 C- q6 Upletely disappeared except for a few vellous hairs at
( j8 Q1 s6 X( ~- N& X) F5 F! Kthe base of the phallus. Testicular volume was still 2
  g+ l' g; S" _3 HmL, and the size of the penis remained unchanged.' O" X( I5 H' j' m! w
The mother also said that the boy was no longer hav-! K! x8 q4 {: e) N; U. b) Y- e9 L
ing frequent erections.
" e7 h. O. v6 n7 HBoth parents were again questioned about use of
  ?3 p/ l2 O- r0 P% [any ointment/creams that they may have applied to
) e0 O. \6 ^+ q! W4 Z- O) B+ [6 T' |, Ithe child’s skin. This time the father admitted the1 g  G2 X5 h$ \; S& `0 A4 G
Topical Testosterone Exposure / Bhowmick et al 541
2 u2 @' J0 Z7 N: Cuse of testosterone gel twice daily that he was apply-
2 K3 s& R% ~& J( c+ Cing over his own shoulders, chest, and back area for8 Y0 B8 T" f+ q
a year. The father also revealed he was embarrassed
! U6 ]( m; {* I5 w$ Ito disclose that he was using a testosterone gel pre-1 A' m+ R* Q2 d2 ^" F( K
scribed by his family physician for decreased libido
2 ?$ x5 ?- ?: a! Z: T9 C# qsecondary to depression." v* Y: {) {! r, S% o" K% B  t6 @) e
The child slept in the same bed with parents.
* e& S% K- c) m# U9 W# `# r' ZThe father would hug the baby and hold him on his
# M+ S5 s6 G8 d; C8 Cchest for a considerable period of time, causing sig-
. O, w" ^. ]9 Z  w, C, C* Ynificant bare skin contact between baby and father." W# B- y* k, H% L: N
The father also admitted that after the phone call,
8 A5 K* o3 X0 B1 [9 [( k, u* X1 Rwhen he learned the testosterone level in the baby
7 ?7 Q( C/ q. n) Kwas high, he then read the product information
6 a, [9 a( e8 ?% r8 ]packet and concluded that it was most likely the rea-8 D) u* t# ?! b  M
son for the child’s virilization. At that time, they
: _0 k9 R! _' ]2 J$ H7 r( edecided to put the baby in a separate bed, and the
# y! S! N, [- Rfather was not hugging him with bare skin and had
5 V- Z) d0 {5 b1 d1 ubeen using protective clothing. A repeat testosterone
2 t1 m& p4 y* i( c9 n+ P  P; Mtest was ordered, but the family did not go to the* v; ^* j1 @4 d
laboratory to obtain the test.
5 X; g+ T; w, i) H" Y! P0 mDiscussion8 A  x' ]* z5 `: k& i
Precocious puberty in boys is defined as secondary# H# I* L' e4 t( x& l* I
sexual development before 9 years of age.1,4
0 _# b1 i* d' `: z" _Precocious puberty is termed as central (true) when
% \; {* \- Z6 K* {6 lit is caused by the premature activation of hypo-4 Y5 A2 s3 k3 q8 B, ]
thalamic pituitary gonadal axis. CPP is more com-1 k/ [4 s9 z- R# P* c
mon in girls than in boys.1,3 Most boys with CPP
* N  p: h: U7 w* Bmay have a central nervous system lesion that is) I- O! y2 X! h$ l
responsible for the early activation of the hypothal-
! v0 I6 w# _( ~5 D( o2 {7 Z7 |$ O: o5 t- Vamic pituitary gonadal axis.1-3 Thus, greater empha-
, j' s% Z5 r- _/ s! S1 @' Jsis has been given to neuroradiologic imaging in
) M( K5 Q" \2 G# `. c' o' R6 eboys with precocious puberty. In addition to viril-
. `5 t3 A/ U+ v; m3 X5 {9 |. Z: L8 zization, the clinical hallmark of CPP is the symmet-) a) t  ?9 i* }9 t* r6 U
rical testicular growth secondary to stimulation by
/ P" ~& `9 B7 G$ `3 j( Z+ e! m% D5 j' pgonadotropins.1,3
- Z) y9 W3 a/ X3 AGonadotropin-independent peripheral preco-
1 m# o7 n$ V# Rcious puberty in boys also results from inappropriate
$ n3 z" `8 C* C* ^$ Randrogenic stimulation from either endogenous or
( v' w3 B- {- w4 Z# c' ~* W" \exogenous sources, nonpituitary gonadotropin stim-$ }. K' L7 g! e/ |: S+ a- H) L
ulation, and rare activating mutations.3 Virilizing1 Z0 u+ Z$ I2 \/ Q
congenital adrenal hyperplasia producing excessive3 B) J/ l& _0 I: `- h$ S
adrenal androgens is a common cause of precocious
* [& f  F) Q2 W' Tpuberty in boys.3,40 a2 i) D( i- |
The most common form of congenital adrenal
( T+ x/ ~. @% }) K4 a# u! n8 shyperplasia is the 21-hydroxylase enzyme deficiency.
8 u9 N5 \  H, C6 _; X2 VThe 11-β hydroxylase deficiency may also result in* s2 h! ~5 p! d% ?. D- z+ B( ~
excessive adrenal androgen production, and rarely,
, y9 `% o7 S3 Y4 O7 n* y7 \an adrenal tumor may also cause adrenal androgen4 [; B. R3 j- N0 U" r; r: @  V6 o# u
excess.1,3
, b% D5 N8 M) S- U, }- P# @/ Vat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, u) k* C6 }+ U& C4 M542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
. q8 `" O2 k+ H  |# [A unique entity of male-limited gonadotropin-
6 S- U* j; N; x8 c" sindependent precocious puberty, which is also known
' v# }) k0 ^; ?- F" b' U/ U8 Has testotoxicosis, may cause precocious puberty at a
7 g. u$ V! i8 w! ]; @4 }3 bvery young age. The physical findings in these boys
3 v6 w$ z6 m( ~- L+ \/ e1 B4 jwith this disorder are full pubertal development,4 q  a5 ^7 n6 I. G9 J8 ~- t
including bilateral testicular growth, similar to boys* o/ v* F- ^1 Q0 K3 G) X! {
with CPP. The gonadotropin levels in this disorder
# w6 Y3 Y, x( P2 Z: B; _" ~) ]  care suppressed to prepubertal levels and do not show& Y0 p1 p) l- A$ J' c0 U: u
pubertal response of gonadotropin after gonadotropin-& R6 c; p9 D6 h0 ]! f) y# a" S
releasing hormone stimulation. This is a sex-linked/ G* B# g4 H5 u: l5 S( a6 E
autosomal dominant disorder that affects only
) E% D+ u, v4 G7 ]males; therefore, other male members of the family
9 l3 I/ Z6 K: }may have similar precocious puberty.3
) |2 J' h, }! o+ t* }: C- AIn our patient, physical examination was incon-; U; ?  L' L7 z0 n7 g/ \
sistent with true precocious puberty since his testi-
& e2 |' V  S; ^, b  w& Q: S' w9 ~cles were prepubertal in size. However, testotoxicosis, i7 z/ p9 H- J4 r4 H
was in the differential diagnosis because his father' w& ]' X9 `' Y1 h5 R
started puberty somewhat early, and occasionally,
( R7 f) ?3 K3 S7 ntesticular enlargement is not that evident in the
: S+ [6 p" `' f2 a( N9 I  v, Gbeginning of this process.1 In the absence of a neg-% k( Z; U) t/ @" Q6 O8 [
ative initial history of androgen exposure, our4 d9 H* B! k8 Q# G6 U- G
biggest concern was virilizing adrenal hyperplasia,
2 i# V" _+ [4 Z& k5 Geither 21-hydroxylase deficiency or 11-β hydroxylase
& [: P7 k$ ]! s9 K2 g+ adeficiency. Those diagnoses were excluded by find-
; ^3 Z. d8 ~% Cing the normal level of adrenal steroids.
# u1 \! `( b6 j* \& NThe diagnosis of exogenous androgens was strongly
; \7 g5 d' R: x5 rsuspected in a follow-up visit after 4 months because
7 [% ]# N8 ~. c* Z! N" wthe physical examination revealed the complete disap-* C7 G7 l: m4 ~& f
pearance of pubic hair, normal growth velocity, and9 k9 Y7 v) u0 b5 x5 p- @
decreased erections. The father admitted using a testos-
1 h2 i5 x- \/ f1 Fterone gel, which he concealed at first visit. He was% v3 j' O" N1 {3 P+ x
using it rather frequently, twice a day. The Physicians’
) P4 f/ X/ U. V# BDesk Reference, or package insert of this product, gel or
2 N2 u; c. w, c* R% c) Jcream, cautions about dermal testosterone transfer to2 L' H* @4 V/ @' U/ M  U5 ]
unprotected females through direct skin exposure.9 p0 }4 I( q4 z: D- g, A: k% v
Serum testosterone level was found to be 2 times the& X& n( b* k9 b+ I2 k- F
baseline value in those females who were exposed to
9 |) s* h4 h7 h) {" b, ?* yeven 15 minutes of direct skin contact with their male
8 [# _9 i% g* [& H; Hpartners.6 However, when a shirt covered the applica-  l$ c$ p7 ]6 i( x
tion site, this testosterone transfer was prevented.
5 \0 U, i% {: b& n6 j; D5 L$ mOur patient’s testosterone level was 60 ng/mL,
# e/ }  [& z3 g# H( t' y5 s1 @0 i- Jwhich was clearly high. Some studies suggest that
+ k5 ~! t; j1 n( a% _dermal conversion of testosterone to dihydrotestos-
# n; P: I9 `& b, r8 oterone, which is a more potent metabolite, is more( ~' U9 \7 R  Q: \, ^
active in young children exposed to testosterone4 `2 [, Z  z. U% t* m
exogenously7; however, we did not measure a dihy-" Z% \. ^' E5 }, ^& s
drotestosterone level in our patient. In addition to
: z7 q) w: X' Svirilization, exposure to exogenous testosterone in
6 N: f9 a8 T' uchildren results in an increase in growth velocity and8 |( g3 |5 A1 p5 j
advanced bone age, as seen in our patient.
, Q& d# L4 _" o; w8 W. [8 gThe long-term effect of androgen exposure during% ?8 J) q1 Y) l  u5 i$ z
early childhood on pubertal development and final
5 [* T1 j/ G' {9 D) Eadult height are not fully known and always remain, X1 ^, u# U6 a% x
a concern. Children treated with short-term testos-
2 t5 x3 B5 `. f$ g9 a; `( h7 B( S& cterone injection or topical androgen may exhibit some5 t: {& s1 N( L4 n! d
acceleration of the skeletal maturation; however, after/ ~$ J% y; q% a2 j$ o- C
cessation of treatment, the rate of bone maturation( ?$ u5 ~/ |9 O( W8 z( l# ?: x9 b
decelerates and gradually returns to normal.8,9" D( z1 l8 d6 `6 @5 L- a* \
There are conflicting reports and controversy
- d: O6 i3 i  Y( e7 q# ?0 Iover the effect of early androgen exposure on adult0 p7 s* u: C3 `2 w/ D4 U8 _% z
penile length.10,11 Some reports suggest subnormal
: }1 ?$ J) R! [6 F% a% I: sadult penile length, apparently because of downreg-! P* L* c; }) k
ulation of androgen receptor number.10,12 However,
2 B% O( W8 h( ]% c3 R  b& q. aSutherland et al13 did not find a correlation between
- F( u) C' I& B4 Gchildhood testosterone exposure and reduced adult
7 x2 B: d" h5 a! v' G5 x; p, g' V6 Rpenile length in clinical studies.
" ?2 T. N+ [, NNonetheless, we do not believe our patient is# h) W% _3 n* P: ]5 z
going to experience any of the untoward effects from; w- t% i5 U  E+ h
testosterone exposure as mentioned earlier because: u3 B: y  A' ~) r9 y
the exposure was not for a prolonged period of time.
! B" Q, c: Y$ M1 J9 S' n# rAlthough the bone age was advanced at the time of
" \( ~* \" Q. Y) \1 n) ]9 ]diagnosis, the child had a normal growth velocity at
: _, X0 F5 m8 e! e  }" Z, Rthe follow-up visit. It is hoped that his final adult6 Y: t$ G# q+ h5 W$ F, R
height will not be affected.
: f/ m( J. Q! I) l' ?Although rarely reported, the widespread avail-
5 S% q) T2 ^$ @8 a0 Wability of androgen products in our society may$ W! o+ \/ \& p% Z9 j
indeed cause more virilization in male or female4 F' p/ S8 M8 m
children than one would realize. Exposure to andro-
1 f3 V) u; c; K6 l& H$ l7 T1 j6 [gen products must be considered and specific ques-
0 f$ e+ t" ]& q: N- {tioning about the use of a testosterone product or% a5 I2 N! v' P- y9 b
gel should be asked of the family members during5 [3 r0 _4 q# h! H( Y( d% E; L8 {
the evaluation of any children who present with vir-9 ~5 o9 A5 ?2 f& L
ilization or peripheral precocious puberty. The diag-
; z' Y; W# ~) w* l6 znosis can be established by just a few tests and by0 W% x  S; }5 n( y
appropriate history. The inability to obtain such a5 d1 ?, a( l2 q+ l& i$ e7 b3 G. v) s3 f1 p
history, or failure to ask the specific questions, may
7 F1 A- `" W+ T& u9 E1 q8 sresult in extensive, unnecessary, and expensive  Z9 I1 y) t4 c" D1 `3 [' `$ F$ @
investigation. The primary care physician should be- d2 s9 `' i% V; P  D
aware of this fact, because most of these children
; G0 {; N! I4 T* i2 Gmay initially present in their practice. The Physicians’
' w6 V% E6 ]; F5 x# h) zDesk Reference and package insert should also put a
3 W5 F& b2 z7 cwarning about the virilizing effect on a male or
- y3 }1 p& h  V) j/ p' X8 ?female child who might come in contact with some-
# l* ]& m7 [6 S6 H6 U0 R1 Ione using any of these products.
7 ~1 b) E3 g( C" x- aReferences
5 T8 N- _) N/ }  w2 c1. Styne DM. The testes: disorder of sexual differentiation
( |( ^$ h3 [: oand puberty in the male. In: Sperling MA, ed. Pediatric
" ^) t" ~4 o- d* @( ZEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
* h0 @  f1 t# k  |8 J2002: 565-628.
9 @8 Y6 X  r. m; E; j5 W( N2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious  f2 M/ R) i! g* A/ D/ }  k6 q
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old1 N2 s( u* \, P
Boy Induced by Indirect Topical
' D+ I7 a, G3 f3 N! r, N# vExposure to Testosterone
0 P% r6 [6 @# }4 \  cSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
  i9 m' A3 V* a8 A% w$ e. C# ?3 Wand Kenneth R. Rettig, MD1# k* i, S5 k% O" E+ ]
Clinical Pediatrics
9 b5 ~  n  b, h& ~Volume 46 Number 6
3 ]3 ]: U; I8 ?: B/ V. M, C2 EJuly 2007 540-543
: \3 b) z  @+ o6 O© 2007 Sage Publications% n0 M: d' k" r( V$ ]; f5 c6 [
10.1177/00099228062966519 r- T- f; {" x+ U* Z
http://clp.sagepub.com3 b% z; k* `9 ]' Z/ Q. l
hosted at+ F+ o/ L2 Q4 w/ p1 W9 O4 ^
http://online.sagepub.com
" k' {, J% O. L/ ^& _' A' w6 `Precocious puberty in boys, central or peripheral,; ^8 G' ]! v7 G
is a significant concern for physicians. Central- Q+ J! k0 f: N$ j+ ?8 z& I9 N
precocious puberty (CPP), which is mediated4 k: ~  b) @- D. O* _
through the hypothalamic pituitary gonadal axis, has- P3 g! E9 x& s& @
a higher incidence of organic central nervous system
0 S3 W1 x& W8 C' Q/ M& A  Qlesions in boys.1,2 Virilization in boys, as manifested
: y, E# R$ v1 t  {6 O& L) `by enlargement of the penis, development of pubic, Q7 ~) r: |/ C$ P7 y7 n
hair, and facial acne without enlargement of testi-
% W' S* Z3 i$ _$ G# [# Rcles, suggests peripheral or pseudopuberty.1-3 We' t2 c# v) U* ?* U
report a 16-month-old boy who presented with the
3 m. e7 }9 A8 U; F. b, G1 genlargement of the phallus and pubic hair develop-0 j6 j4 `' x- z, V# i  G% W3 E7 G% K
ment without testicular enlargement, which was due: V8 [' ~4 w' q2 u& G3 r% b; m: K8 {
to the unintentional exposure to androgen gel used by! l3 @+ ?& B7 ?; ]& y' E# s' u. |. b
the father. The family initially concealed this infor-6 Y) o4 u: }6 ~6 ~0 U8 l
mation, resulting in an extensive work-up for this) b5 b" x+ N3 S
child. Given the widespread and easy availability of
9 }' ~4 d+ Q4 \0 F" S$ b0 v2 |testosterone gel and cream, we believe this is proba-
& p3 ^* u$ j, p8 \! S! Z2 `bly more common than the rare case report in the
$ j7 Y; z- e0 C& \# fliterature.4
. y& c* ]4 h) Z3 I- DPatient Report+ ^8 ?1 L7 W; ?
A 16-month-old white child was referred to the7 G- v4 m. j0 d% n
endocrine clinic by his pediatrician with the concern; H# a" P: x: [/ f3 L, l
of early sexual development. His mother noticed5 n; m1 j. Y; b, C+ a1 M6 `
light colored pubic hair development when he was' g2 O) g# k" Q
From the 1Division of Pediatric Endocrinology, 2University of
3 C& a& B$ M4 c$ F" b4 OSouth Alabama Medical Center, Mobile, Alabama.
" \4 k: t# B' w$ y8 T9 ^- HAddress correspondence to: Samar K. Bhowmick, MD, FACE,
; s- Y, O/ o1 A1 w+ ZProfessor of Pediatrics, University of South Alabama, College of0 s1 z# h! s7 n. H$ |6 v' @7 p- H9 C
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
1 W3 \9 o& ^+ S; ge-mail: [email protected].
6 K1 o2 O$ w$ W5 ~3 _about 6 to 7 months old, which progressively became! u3 O+ O) z0 s5 D- E
darker. She was also concerned about the enlarge-8 l$ E  J. Z1 g) d
ment of his penis and frequent erections. The child
8 F8 J. o2 f" S* L# [$ W- J! uwas the product of a full-term normal delivery, with
7 ^7 E+ a( v1 m1 U3 A7 l& b" Za birth weight of 7 lb 14 oz, and birth length of
* m3 w! A. I4 q$ V20 inches. He was breast-fed throughout the first year
# z, m9 K) P9 f# Qof life and was still receiving breast milk along with2 ^% o8 r3 Q& c- G. F; }
solid food. He had no hospitalizations or surgery,
7 X' Z' H/ \% F& J& b3 Cand his psychosocial and psychomotor development0 [3 ^2 t& D% C& |
was age appropriate.
  {" ^: I5 W& M4 kThe family history was remarkable for the father,7 K# a9 _, P# n) r
who was diagnosed with hypothyroidism at age 16," ]/ N# j# z- m% {; \
which was treated with thyroxine. The father’s( N" d  o$ A4 Q+ D: E6 W" b+ M
height was 6 feet, and he went through a somewhat; E9 P+ C5 P" J# _3 w: B
early puberty and had stopped growing by age 14.
: b+ t% f: L  v  l( K% C) ?The father denied taking any other medication. The  m' N: w% K' ^- Z, t; ?: y) X, q
child’s mother was in good health. Her menarche" l  K3 ~* ^! j0 w4 N
was at 11 years of age, and her height was at 5 feet* n+ Y* b, K+ a8 @6 r7 v# G
5 inches. There was no other family history of pre-' V+ d" F( W7 i" |5 {* Z# y
cocious sexual development in the first-degree rela-
# Z1 z$ }4 \7 Y+ s' btives. There were no siblings.
  y6 Q; Z/ e! a) P! RPhysical Examination
4 o2 d4 j6 A9 d" I3 |, h8 e2 kThe physical examination revealed a very active,9 v5 Y0 r9 l; @
playful, and healthy boy. The vital signs documented
1 m$ K- D$ Y) B2 O7 a) N% @a blood pressure of 85/50 mm Hg, his length was
. b! P( W0 i) b90 cm (>97th percentile), and his weight was 14.4 kg1 }* V# [, `- z
(also >97th percentile). The observed yearly growth
3 m! @2 T, S! R% [6 d' g* Ivelocity was 30 cm (12 inches). The examination of' \% [- ^3 F3 c! b$ [1 ?+ \% B
the neck revealed no thyroid enlargement.
8 {5 }0 z8 G# k5 n" v. @/ M, u4 e0 gThe genitourinary examination was remarkable for
9 J, |+ U  f3 D& y3 y' Senlargement of the penis, with a stretched length of3 k& @$ F* ~3 D
8 cm and a width of 2 cm. The glans penis was very well; [! F9 S! a1 Y9 M2 B
developed. The pubic hair was Tanner II, mostly around# o4 N' H' Y' R! O: M
540
5 u6 i) ^2 b, |% nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: @) G- k4 X) ?: h, q6 qthe base of the phallus and was dark and curled. The) R- |8 C- [3 J& T
testicular volume was prepubertal at 2 mL each.
, v" {1 a) `" x; qThe skin was moist and smooth and somewhat! U/ [% p+ M) c' n3 Z
oily. No axillary hair was noted. There were no
" y: S- m" u% V; h: Q0 e( G% e& cabnormal skin pigmentations or café-au-lait spots.
' y1 c! q$ E) K( I! q7 W4 b% [Neurologic evaluation showed deep tendon reflex 2+8 A0 t! Y! U7 }! f
bilateral and symmetrical. There was no suggestion
9 ^- U# [5 i  M- Q7 V2 Sof papilledema.
4 u! H2 |  d* l. c0 @Laboratory Evaluation
/ o' [4 o. [  I2 t% |The bone age was consistent with 28 months by
& o& |, d0 V4 t1 ^1 ~! P! Gusing the standard of Greulich and Pyle at a chrono-/ [. \# C) t( e1 n& U
logic age of 16 months (advanced).5 Chromosomal
8 f" E0 B; q( U; i- n5 }/ ekaryotype was 46XY. The thyroid function test3 H. N( H+ Q* g5 r3 h+ v% D
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
  _- K' l% D! P% n( i' F, j0 flating hormone level was 1.3 µIU/mL (both normal).
  A$ ?. X* A+ r2 y9 tThe concentrations of serum electrolytes, blood$ X/ o: t: b. V4 p% z
urea nitrogen, creatinine, and calcium all were
( O& e: M5 P- _' x; uwithin normal range for his age. The concentration# }# P- ]7 _8 S+ Y
of serum 17-hydroxyprogesterone was 16 ng/dL
/ i' }0 v4 e+ y& o, H(normal, 3 to 90 ng/dL), androstenedione was 20
; V) {5 y$ g# U5 }2 Dng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
- q1 f: c' a, |$ l& Z3 x/ Q8 L! p% qterone was 38 ng/dL (normal, 50 to 760 ng/dL),1 L, z5 v* _+ }6 k# X
desoxycorticosterone was 4.3 ng/dL (normal, 7 to9 t$ u. ~* q0 G' p3 ]
49ng/dL), 11-desoxycortisol (specific compound S)
6 ?/ ]% }6 n: Y# x9 jwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
. n; B, t: ]4 D4 s0 a( C1 Qtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
3 \5 B) X$ Q+ e- `3 Htestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
( J! ]; @2 b$ _. K  Gand β-human chorionic gonadotropin was less than
. [  O; \! Y# R. ?& f' t2 t5 L5 mIU/mL (normal <5 mIU/mL). Serum follicular9 q/ c( A4 ?; z
stimulating hormone and leuteinizing hormone
3 `) T7 o7 ~' Tconcentrations were less than 0.05 mIU/mL
9 Q0 u; i2 a2 Q' n(prepubertal).0 x9 m5 q1 y$ \: j
The parents were notified about the laboratory
6 J, w1 C2 @0 Jresults and were informed that all of the tests were' j& _6 Q+ M# |8 B4 x
normal except the testosterone level was high. The' e/ n. M& K. K( X
follow-up visit was arranged within a few weeks to, G/ H7 X3 N4 v; ?4 u
obtain testicular and abdominal sonograms; how-
/ F' w3 |7 w2 K8 r% p7 q, }ever, the family did not return for 4 months.
, R- p) a* j0 l8 S! m& t8 ePhysical examination at this time revealed that the9 t) S4 L, h% d+ Z, n+ h- m
child had grown 2.5 cm in 4 months and had gained
; @4 Q+ z. Y+ B% L" d& A3 `) M, E2 kg of weight. Physical examination remained. O! p  s* @- k$ q% k; A) a3 E& _( P8 n
unchanged. Surprisingly, the pubic hair almost com-. ]7 c  i) T3 L4 _% l8 b2 u! i
pletely disappeared except for a few vellous hairs at; W5 K2 Y- k" z8 m8 \9 h
the base of the phallus. Testicular volume was still 2
2 V: _8 o: m- Q; F4 ?* imL, and the size of the penis remained unchanged.
- M1 y3 K8 _  _3 {) V8 d# K% EThe mother also said that the boy was no longer hav-8 P! T! y2 I8 x
ing frequent erections.- W/ t: R4 E( N$ o* s) u
Both parents were again questioned about use of4 M8 q4 p" F$ ?7 ~) ?" Y8 u. @
any ointment/creams that they may have applied to7 b; D8 @2 {) `# B# R6 n' q- q
the child’s skin. This time the father admitted the
! U! C5 a$ @7 @3 BTopical Testosterone Exposure / Bhowmick et al 541
7 E- E+ Z( F+ o  y& y4 duse of testosterone gel twice daily that he was apply-
+ j3 @, t/ \( Ding over his own shoulders, chest, and back area for
+ @# |# h4 D+ Ia year. The father also revealed he was embarrassed
+ F# c/ ^  K( l' |+ t4 h5 w! mto disclose that he was using a testosterone gel pre-
6 F' ]2 _5 ], ^6 n. tscribed by his family physician for decreased libido
7 ^0 a* k7 F- e3 ^. q$ Asecondary to depression.
: l( W, ?4 H9 oThe child slept in the same bed with parents.
3 z) ]5 D0 q9 l  x1 [. w: D9 S9 O: CThe father would hug the baby and hold him on his4 i6 ?6 ?" g) z
chest for a considerable period of time, causing sig-
2 ]& M! @! q1 a/ G; X$ Fnificant bare skin contact between baby and father.5 H. A4 b, i; @+ F. m
The father also admitted that after the phone call,. c. Y. g. _/ U1 m/ L* [2 P
when he learned the testosterone level in the baby
8 o8 `7 G# H/ N% H/ M$ ]1 ~8 n3 Twas high, he then read the product information
% `; e7 T$ J, N. f4 v9 vpacket and concluded that it was most likely the rea-* T& {! E! t# ]( P) {/ ?' }$ Q
son for the child’s virilization. At that time, they
3 {$ U- @  M9 Pdecided to put the baby in a separate bed, and the
7 ]) M: p  d' F/ ?0 B' _& n" xfather was not hugging him with bare skin and had
1 R6 [) U: l) U, ^( Nbeen using protective clothing. A repeat testosterone
" a: z: W" N8 ~: @% p7 jtest was ordered, but the family did not go to the
/ l- u7 o3 `% |( llaboratory to obtain the test.
+ B7 `7 e8 y. p% j5 eDiscussion; G" ?5 k5 ~# y7 i+ ]' j9 Q" t% d
Precocious puberty in boys is defined as secondary
, b* v. S9 X3 ?" f1 isexual development before 9 years of age.1,4
# R1 w" h* ~: O: r. rPrecocious puberty is termed as central (true) when5 l7 l" }/ @6 d) y) [% T  i& `
it is caused by the premature activation of hypo-/ ^% x/ l; K7 y6 }% ?
thalamic pituitary gonadal axis. CPP is more com-/ M& M5 `9 q- A' x2 R$ D# @6 F% n
mon in girls than in boys.1,3 Most boys with CPP
3 h* i/ N; ^8 s  K5 N2 k0 u& imay have a central nervous system lesion that is* s9 v6 U0 ?( R; f7 t" R  w1 W: ]
responsible for the early activation of the hypothal-0 L9 f0 T1 J" Y9 H% B$ b* C
amic pituitary gonadal axis.1-3 Thus, greater empha-
. _/ B  q2 {3 R$ ]; Usis has been given to neuroradiologic imaging in
, j0 ]% U- c; G& x0 \7 u( q( Rboys with precocious puberty. In addition to viril-) I: ]) o' I" ~, \3 m# z
ization, the clinical hallmark of CPP is the symmet-: G8 R! I' b3 S4 A; X
rical testicular growth secondary to stimulation by0 i* l9 d) ?% Y( ]# e, P
gonadotropins.1,3' b& Z# H8 i: y
Gonadotropin-independent peripheral preco-0 i, O& h1 {; |7 r
cious puberty in boys also results from inappropriate
# o" Q5 y1 K7 e! a- i6 {6 A! D0 j& ]androgenic stimulation from either endogenous or: X# F2 x0 o5 p) |* Y
exogenous sources, nonpituitary gonadotropin stim-5 Z1 v, |1 K6 W7 l& d/ B; `3 P! O8 ~; E
ulation, and rare activating mutations.3 Virilizing! f1 K/ x8 U' j# @! v+ |* W
congenital adrenal hyperplasia producing excessive
- E& p( G9 p2 w& T. {0 X+ Y8 ?adrenal androgens is a common cause of precocious' P% ~% p0 t5 t6 X# I
puberty in boys.3,4; X& A  D6 R1 e  @. ]
The most common form of congenital adrenal
1 u# s2 i% G  s) }6 [hyperplasia is the 21-hydroxylase enzyme deficiency.
5 s" N! q( z) l) K' n' LThe 11-β hydroxylase deficiency may also result in
; @; _  X7 ^0 g5 s# j! Zexcessive adrenal androgen production, and rarely,4 k" ]* M8 n* P3 P9 E) m
an adrenal tumor may also cause adrenal androgen0 w* A( ?4 }$ G% _6 y
excess.1,3! \0 _7 m! j! e# E- M
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! x2 s: O  o; Z4 _' a& a
542 Clinical Pediatrics / Vol. 46, No. 6, July 20070 G! }( S! ^+ P3 G
A unique entity of male-limited gonadotropin-
8 @- E7 c+ K8 H: ^* U1 ~. Windependent precocious puberty, which is also known
$ J' N* P. ]! Cas testotoxicosis, may cause precocious puberty at a3 p! T0 S  ^+ c* F% s/ z
very young age. The physical findings in these boys
7 J4 a, E' y9 @* |6 @/ E! b- j/ pwith this disorder are full pubertal development,
; L8 g: ], C. f& a' [$ K- ?( zincluding bilateral testicular growth, similar to boys/ Z, |, `( _. F2 S: ]) F  T% @" M
with CPP. The gonadotropin levels in this disorder. k" t1 z$ n, u& w$ R4 `
are suppressed to prepubertal levels and do not show: @) J# \- F* @! D+ p
pubertal response of gonadotropin after gonadotropin-
$ z; ~$ {7 Z9 p' d4 mreleasing hormone stimulation. This is a sex-linked5 {0 P2 \3 Z* k, L0 N# A
autosomal dominant disorder that affects only( q' \3 A0 z, M' j) G( e
males; therefore, other male members of the family2 a' ^/ J( ?( s2 j6 \. E' g
may have similar precocious puberty.35 H0 p, b8 n$ N8 @' Y, I- O1 w
In our patient, physical examination was incon-8 d1 f, l5 M1 |9 a1 c
sistent with true precocious puberty since his testi-
2 R, d0 I) H1 t& E& @0 Ncles were prepubertal in size. However, testotoxicosis: j9 l0 e6 x9 \
was in the differential diagnosis because his father
3 a5 G+ j' T/ M+ Z  V. w- O' Ystarted puberty somewhat early, and occasionally,/ l. {& n  o& d' j# V& t
testicular enlargement is not that evident in the
. }! }; B4 W  @* a. kbeginning of this process.1 In the absence of a neg-
  {# m1 v# U& b' O/ B: O" s* bative initial history of androgen exposure, our
* e0 i# X6 Z% M: @% r! `1 ?6 Ubiggest concern was virilizing adrenal hyperplasia,
6 a& K5 r8 n' B6 j  s- Ceither 21-hydroxylase deficiency or 11-β hydroxylase2 Q0 a% ?  C. h! N
deficiency. Those diagnoses were excluded by find-9 _% r; o( G$ H0 G
ing the normal level of adrenal steroids.0 a  T: D3 ^/ ]) G
The diagnosis of exogenous androgens was strongly8 g; y7 A( B$ g6 v( g
suspected in a follow-up visit after 4 months because* l7 N8 g  \7 ]* |/ J5 L
the physical examination revealed the complete disap-
6 E6 K7 x0 Q5 t0 ~6 e3 [0 g( v' R+ _pearance of pubic hair, normal growth velocity, and% b4 c% d* z) W' P5 ]- t* ?
decreased erections. The father admitted using a testos-
2 ]9 g: q7 q  l6 uterone gel, which he concealed at first visit. He was8 Q, P7 X. v  j! D; `- Y8 x% _5 k& V
using it rather frequently, twice a day. The Physicians’
  s8 t* ?6 k$ A# ^% v1 t9 [Desk Reference, or package insert of this product, gel or
; j7 Q9 w: l  X& b$ w) g- Ncream, cautions about dermal testosterone transfer to/ N" i& X, ?5 i2 H" k
unprotected females through direct skin exposure.
* I2 I+ O6 V3 M- A7 X- n9 ^Serum testosterone level was found to be 2 times the
( a( N: g+ D7 L2 z  Pbaseline value in those females who were exposed to
  G2 k' o$ W% heven 15 minutes of direct skin contact with their male+ n, n# T6 P7 @( h
partners.6 However, when a shirt covered the applica-0 N- l) U/ X- p# h
tion site, this testosterone transfer was prevented.
+ l7 u  x# g: g5 U  ^1 n$ `Our patient’s testosterone level was 60 ng/mL,. ~2 e4 o7 O8 [+ x$ h% W( F0 C
which was clearly high. Some studies suggest that. @5 Z9 X: j$ j5 Z& Z
dermal conversion of testosterone to dihydrotestos-
! @3 `8 q8 y1 l. b' C2 h' \terone, which is a more potent metabolite, is more) V$ R3 h3 Q: a0 x" I' b6 G% |
active in young children exposed to testosterone
0 _7 l+ b+ D+ wexogenously7; however, we did not measure a dihy-
/ l+ J# X2 A7 Kdrotestosterone level in our patient. In addition to
# F: g9 K8 C8 d) A% Wvirilization, exposure to exogenous testosterone in
6 @1 g- Q( m5 n" y/ Rchildren results in an increase in growth velocity and
' H1 K8 I! q- v, a9 Q* l9 Wadvanced bone age, as seen in our patient.
- b+ Z3 m. S% ?8 aThe long-term effect of androgen exposure during
7 E0 b* j  a& z5 ~3 ]early childhood on pubertal development and final
6 }1 I. l% r4 j  {adult height are not fully known and always remain& q4 W& x7 T, E
a concern. Children treated with short-term testos-+ q$ b. Z  ?4 K
terone injection or topical androgen may exhibit some
% w+ a) `; c. i1 Sacceleration of the skeletal maturation; however, after
+ p& z5 E, i6 o2 e3 v7 D: R0 B( |cessation of treatment, the rate of bone maturation
/ v7 L! e3 P  _- B2 e* T+ fdecelerates and gradually returns to normal.8,9
# E9 g% t3 ]$ n0 PThere are conflicting reports and controversy
1 ?% e: \. @' A5 v6 x4 U& Dover the effect of early androgen exposure on adult/ V, n. n4 @; b' V+ j9 ]
penile length.10,11 Some reports suggest subnormal
$ |' i# D" F: F' X, I* v* iadult penile length, apparently because of downreg-! y, e" k: t/ M, [& y" [. @
ulation of androgen receptor number.10,12 However,
- |# d  o1 R6 SSutherland et al13 did not find a correlation between* T7 s, Q8 v, e- \0 y( K
childhood testosterone exposure and reduced adult. k+ ?) r4 D% B( e- O' ~
penile length in clinical studies.( \* X3 ~) ~  s: V& t( b
Nonetheless, we do not believe our patient is
& D& b2 V% j. U9 |' ^& sgoing to experience any of the untoward effects from
  L0 I' }) t7 B- [  G' Q: Etestosterone exposure as mentioned earlier because! m1 b$ M0 k% V: o4 W7 e. {
the exposure was not for a prolonged period of time.
5 T* \' _$ \& c& RAlthough the bone age was advanced at the time of
3 M1 x: W% `4 V# h1 |diagnosis, the child had a normal growth velocity at& P9 ^; w* R' J$ A( x
the follow-up visit. It is hoped that his final adult
$ n4 w3 e% M5 Y7 g7 Iheight will not be affected." }* c: I' T5 _/ H3 v. w- z
Although rarely reported, the widespread avail-
( t! `$ }$ j% E2 ^ability of androgen products in our society may
+ a& O& p! [  m3 v: o; x1 D% Bindeed cause more virilization in male or female
) }# @& b! E0 B3 ]& X5 a; l6 Rchildren than one would realize. Exposure to andro-2 T' V( ^4 X. }1 G1 p( r; o- a; l
gen products must be considered and specific ques-
4 J, H3 v( O. Otioning about the use of a testosterone product or. ~+ f4 k- f, p: w% Y. H1 u) r, V
gel should be asked of the family members during% J, M+ o0 E. U' K' g! E: j# m8 m- ^( Z
the evaluation of any children who present with vir-. a8 k. M! ^( ]* `2 H5 e+ s4 }
ilization or peripheral precocious puberty. The diag-- W) A0 I6 _! o3 ~8 C0 }' k
nosis can be established by just a few tests and by% ^/ `$ R$ ], l7 Z! r* O
appropriate history. The inability to obtain such a
: h! p7 Z; h, U0 ?history, or failure to ask the specific questions, may
! j1 H' W- Z" S0 y- ~result in extensive, unnecessary, and expensive& i" s  Z1 H8 f/ z' @  {
investigation. The primary care physician should be  I- B) ^2 a1 |, A$ W) m  B
aware of this fact, because most of these children1 ~' ~) r& |: A3 N
may initially present in their practice. The Physicians’
' s$ s* g6 e4 l" G" xDesk Reference and package insert should also put a
* K4 Y9 C( N  Q+ P. a4 E/ `' lwarning about the virilizing effect on a male or& `; G  T" \3 ?# v
female child who might come in contact with some-
3 p& \4 f& m; p4 a! {. Yone using any of these products.
/ u  e" Z3 q* o! `References
) \  Z- `  G2 F) R! J1. Styne DM. The testes: disorder of sexual differentiation5 |$ ]; A6 N9 f$ Y' R3 W
and puberty in the male. In: Sperling MA, ed. Pediatric
6 b- l3 E0 _7 z* NEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
3 B' f7 T. \7 [  r; b6 u; b, h- t2002: 565-628.
. q, v2 z0 k) l8 b/ Z3 B2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; t' S# M- X" C9 O  y( a. g0 N
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

/ O9 F$ H, F2 D7 W3 J( a5 }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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