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Sexual Precocity in a 16-Month-Old9 f: ?  j3 g; ~4 J9 @
Boy Induced by Indirect Topical1 w+ G1 B' k9 |, A/ U; T/ Y) m1 P
Exposure to Testosterone/ h8 c0 k4 M, {. Q' ~
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
' I+ V% ^# Q' `4 G$ @- Y* T' ]. Band Kenneth R. Rettig, MD1
7 A+ G/ \; ^0 X! ^, s+ EClinical Pediatrics
1 a0 B, z6 H# ZVolume 46 Number 6, z! H9 N2 `$ b4 G6 o+ o  Y& d% q
July 2007 540-543
" \  O1 @7 o5 N1 u" N+ \5 E( o' j© 2007 Sage Publications% t# R7 K; q! f# Z
10.1177/00099228062966514 T, u) S6 l- Z# J
http://clp.sagepub.com2 V1 [# ]- n$ N" R/ f6 [+ Q6 |
hosted at
: \9 w+ \5 F4 j+ ]3 a* \http://online.sagepub.com
- m+ c' N) X, j' P2 Z3 ePrecocious puberty in boys, central or peripheral,
8 A% s& i* W3 ?- t; x3 f  x1 ~; Wis a significant concern for physicians. Central. `$ w0 ^9 o( l/ u/ M$ h9 y4 V
precocious puberty (CPP), which is mediated9 M2 U3 D) C/ N0 A5 C. ]$ A
through the hypothalamic pituitary gonadal axis, has
9 W0 H) T7 Z. [, m; \0 h& Sa higher incidence of organic central nervous system
6 h. v. r$ C/ N* [+ ?8 dlesions in boys.1,2 Virilization in boys, as manifested( \! {+ H, z& c8 E& I
by enlargement of the penis, development of pubic
: l# Y: A- R! y2 K+ @hair, and facial acne without enlargement of testi-9 e/ g0 \& f1 |& X3 @" ^+ Z% c4 x
cles, suggests peripheral or pseudopuberty.1-3 We. I6 r) }7 o7 o& |  W& L9 N& i  N3 G& z7 c
report a 16-month-old boy who presented with the
! g7 g$ S2 ?' \2 f# Zenlargement of the phallus and pubic hair develop-- J* k& z/ R! H( H! o
ment without testicular enlargement, which was due
3 @  D6 l9 {* K; Sto the unintentional exposure to androgen gel used by5 \% y& t7 r- Y$ s
the father. The family initially concealed this infor-
! x, K  p4 Z$ xmation, resulting in an extensive work-up for this
# v: f. I; [- `child. Given the widespread and easy availability of3 A$ [# `# P' q* Z
testosterone gel and cream, we believe this is proba-
5 H7 L; {0 T# Tbly more common than the rare case report in the2 o3 b2 |: g# _6 h2 e
literature.43 i* a% J& v9 u, R/ L
Patient Report
  Y: W, s$ }, q: ZA 16-month-old white child was referred to the! D) k- m$ d% m" X& J
endocrine clinic by his pediatrician with the concern
# O# J: G4 F0 U" }of early sexual development. His mother noticed4 ~- x& y, i2 R# i
light colored pubic hair development when he was5 L$ p: ~7 Z3 f4 t+ b/ w/ q  s4 O
From the 1Division of Pediatric Endocrinology, 2University of# B7 Q6 U; D7 N! B- W+ A0 w
South Alabama Medical Center, Mobile, Alabama.4 j4 T" P5 G  r3 T$ l7 |
Address correspondence to: Samar K. Bhowmick, MD, FACE,
* p: `$ Q- l6 C+ _8 Q2 HProfessor of Pediatrics, University of South Alabama, College of! a# X' ^/ z3 J
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;" a; b8 S1 C$ B' b' I. N; Y
e-mail: [email protected].
4 Y% S7 `1 |: }2 B( Yabout 6 to 7 months old, which progressively became
8 @  i1 p" }  D# T% xdarker. She was also concerned about the enlarge-
  ]- p8 N% @4 z- E! K5 O' Pment of his penis and frequent erections. The child
% f0 C# j( Q% L- ~& |! ?was the product of a full-term normal delivery, with3 b4 _* K0 c, ?6 Q) s
a birth weight of 7 lb 14 oz, and birth length of
1 Y, q9 X- y9 ?  ?2 z8 v4 _4 e20 inches. He was breast-fed throughout the first year2 j+ u4 |/ D$ ?! D* o
of life and was still receiving breast milk along with
. R! F, m( Z, D3 N0 {solid food. He had no hospitalizations or surgery,
: o0 [$ S$ S2 F' t+ W5 j" iand his psychosocial and psychomotor development
' T/ i& X4 e% ~" J0 Wwas age appropriate.
0 y3 W+ y/ h: T' k9 w  ZThe family history was remarkable for the father,$ A" m9 ]( W+ y( k( j
who was diagnosed with hypothyroidism at age 16," ]+ `3 k9 ^% ^4 O: b# ?
which was treated with thyroxine. The father’s4 G0 m/ r; P6 y
height was 6 feet, and he went through a somewhat0 h- r: k; F4 E6 R$ k5 A
early puberty and had stopped growing by age 14.
# P/ b' R7 P5 j# QThe father denied taking any other medication. The3 a( l6 C& C! o' y
child’s mother was in good health. Her menarche
+ W8 p+ T8 ]" l8 g3 s* Iwas at 11 years of age, and her height was at 5 feet6 [, S, ~) D9 a1 M$ z
5 inches. There was no other family history of pre-7 z9 ?  b) H) S) o* v/ I
cocious sexual development in the first-degree rela-
1 t8 S2 W. L% U: Atives. There were no siblings.
6 k7 y0 l5 ]8 O* t+ a5 B/ {2 PPhysical Examination2 `4 L7 y- }4 ?  M* L- t" U, X7 P/ D
The physical examination revealed a very active,: O8 l  ~: G' I- p
playful, and healthy boy. The vital signs documented
) Z. A: l- _4 k; \. [; _$ Z4 O* Pa blood pressure of 85/50 mm Hg, his length was
2 D& ]+ y  D9 I0 D8 @: `: m90 cm (>97th percentile), and his weight was 14.4 kg
1 A+ P, v" T9 R9 a(also >97th percentile). The observed yearly growth6 j( G, r4 Y/ f1 K8 i6 D: A
velocity was 30 cm (12 inches). The examination of
2 _4 E7 P# Q8 Gthe neck revealed no thyroid enlargement., D/ R( X' h/ |9 V5 q
The genitourinary examination was remarkable for
# g5 q8 ~# e) Menlargement of the penis, with a stretched length of1 v! R, E( J1 [  N  U
8 cm and a width of 2 cm. The glans penis was very well$ e' m% X" A. G( b8 y2 J( B
developed. The pubic hair was Tanner II, mostly around8 G) o. R: t+ D( h' u
5400 E+ U$ Q9 i$ l: [
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the base of the phallus and was dark and curled. The
$ q) f- d# n, g- c5 Etesticular volume was prepubertal at 2 mL each.6 d# S* f3 j$ z2 q0 d/ G
The skin was moist and smooth and somewhat  S$ }, L" N1 [6 i- w
oily. No axillary hair was noted. There were no
6 ^# n1 Z  g- ~2 C  pabnormal skin pigmentations or café-au-lait spots.  e( Z5 b! C; m
Neurologic evaluation showed deep tendon reflex 2+) k  W) x) b8 q
bilateral and symmetrical. There was no suggestion
) z- q( `0 G6 _& g" yof papilledema., x" V/ w; M$ l3 b. E
Laboratory Evaluation
+ H& u  z9 a. j$ xThe bone age was consistent with 28 months by. i3 U) V% x$ M& H! {/ [
using the standard of Greulich and Pyle at a chrono-
4 |3 w- D  M3 f2 B7 }logic age of 16 months (advanced).5 Chromosomal& |' R1 Z7 J: I/ L' S$ Z+ l9 W
karyotype was 46XY. The thyroid function test* ^0 H$ \; k% f
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
- Y- r5 R. D9 F* c( {8 ]7 _- }lating hormone level was 1.3 µIU/mL (both normal).1 c+ o8 E6 d, ?8 b$ y! H
The concentrations of serum electrolytes, blood
* l7 G4 Q% ]2 w1 p" Uurea nitrogen, creatinine, and calcium all were. A1 m; D6 b7 n8 Y% x! Y+ s
within normal range for his age. The concentration! f7 @- d5 r$ }5 \, @9 f* o
of serum 17-hydroxyprogesterone was 16 ng/dL6 B0 d8 O4 `$ L
(normal, 3 to 90 ng/dL), androstenedione was 20
% s# V7 l; V" L2 b2 z/ F; y6 {( U9 e7 sng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
6 C- C* Z" l! M0 a# M# uterone was 38 ng/dL (normal, 50 to 760 ng/dL),! ~! |4 n' P( E+ ]: ?& c) s' _
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
: i# h% l+ H- V9 a49ng/dL), 11-desoxycortisol (specific compound S), _5 b3 b: H% m7 _4 b; w
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
" [7 Y9 x" G* E! _1 Ztisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total: e$ r5 I+ J( s
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),; t& s6 i$ @* ~- l9 M; H3 h
and β-human chorionic gonadotropin was less than
8 t# Z! i0 g1 R$ y. B% f5 L( {4 M# w5 mIU/mL (normal <5 mIU/mL). Serum follicular- ^, H- V$ d3 D# B" }$ p% O2 x
stimulating hormone and leuteinizing hormone4 }5 ^/ n8 V. V: H; M$ p1 }; T$ Q* H
concentrations were less than 0.05 mIU/mL+ [/ e4 B9 C; t9 A+ x  ?. g
(prepubertal).: N5 r9 \6 R/ j* P* G
The parents were notified about the laboratory
4 }# z" V$ h1 R: E: }, ~$ D) Kresults and were informed that all of the tests were8 n) D$ m& l% m+ e; ~4 V2 v
normal except the testosterone level was high. The. l1 a/ o3 x* `7 i
follow-up visit was arranged within a few weeks to
$ {0 C+ c5 e5 q9 k% R' g7 O( |) C* dobtain testicular and abdominal sonograms; how-: Q* t5 G: m; H/ Y, w
ever, the family did not return for 4 months.; e2 ~2 q$ Q: m1 {3 K
Physical examination at this time revealed that the
2 [, f  Q$ S9 T8 Lchild had grown 2.5 cm in 4 months and had gained
# u( W. p# L) t) f, ]! j2 kg of weight. Physical examination remained
2 b  g8 H. `/ ^( V! Hunchanged. Surprisingly, the pubic hair almost com-
7 e1 B$ v# }+ b) ~+ z3 ^9 u$ upletely disappeared except for a few vellous hairs at
" y4 c: L! K# R1 U: u0 y6 Xthe base of the phallus. Testicular volume was still 2
- E& F, {2 n! \mL, and the size of the penis remained unchanged.2 s2 {8 M  M8 d: ]0 @! K( U( l
The mother also said that the boy was no longer hav-
4 N$ U. z/ |7 S& a  Iing frequent erections.
  \' L( _6 r5 R+ SBoth parents were again questioned about use of# Y: Q! |' t1 D2 f7 Q# l0 A0 P
any ointment/creams that they may have applied to
! J' n! r" }" q: v! Q5 s; {the child’s skin. This time the father admitted the5 j7 J/ T; y$ j1 X! a6 f
Topical Testosterone Exposure / Bhowmick et al 541  {& V& Y1 r. W1 W; `
use of testosterone gel twice daily that he was apply-' U+ O0 }. @; x* ~* o5 s2 W9 w
ing over his own shoulders, chest, and back area for
3 O6 f1 v, r1 L& [a year. The father also revealed he was embarrassed4 H' Q1 H# P% D4 d+ K
to disclose that he was using a testosterone gel pre-
4 \7 u- B! v3 k; Z8 R& k3 Dscribed by his family physician for decreased libido- }0 Z* c- T6 {' b" i
secondary to depression.& N2 G) e- S( N4 W. z
The child slept in the same bed with parents.
9 p/ q, I, f: ]1 _: yThe father would hug the baby and hold him on his
4 E! s" Z* e; o! b! Z/ ]  kchest for a considerable period of time, causing sig-) v( @& r0 N6 R4 l
nificant bare skin contact between baby and father.* B% T1 l2 f; h6 b+ \" J. V% {4 G
The father also admitted that after the phone call,
6 F2 l* Q2 }- Q) qwhen he learned the testosterone level in the baby3 i9 D! @; A2 Z+ Y0 K9 }
was high, he then read the product information
5 _5 l; J+ y1 ^. m* N5 V: z9 U% Jpacket and concluded that it was most likely the rea-8 r( [, y; N% c2 f- D
son for the child’s virilization. At that time, they0 U% x6 [* ^2 ]1 j5 u0 R" u
decided to put the baby in a separate bed, and the& t4 d1 X0 E; E9 C5 d  A3 D
father was not hugging him with bare skin and had
3 K5 Y/ m: i# ^- {been using protective clothing. A repeat testosterone6 v5 a# y# h6 B2 B
test was ordered, but the family did not go to the
6 q& h& ~5 I7 @) G# blaboratory to obtain the test.$ f/ q; V3 z( U1 U* L- ^
Discussion( d+ l$ u2 `! y7 C
Precocious puberty in boys is defined as secondary
$ c  o& P& h) a  j: Ssexual development before 9 years of age.1,4
) z+ I9 T% L! U6 Z2 }3 WPrecocious puberty is termed as central (true) when
, t3 `9 Y- Y9 y9 n" \it is caused by the premature activation of hypo-
- L1 V' |5 @8 vthalamic pituitary gonadal axis. CPP is more com-
! Q9 g7 A( Z) y3 U/ h7 y: Fmon in girls than in boys.1,3 Most boys with CPP
, Q) v: ]. s! }5 {. Vmay have a central nervous system lesion that is* @3 }% r. a  u# h9 |
responsible for the early activation of the hypothal-
+ A! u9 r2 ]( c$ ^amic pituitary gonadal axis.1-3 Thus, greater empha-6 R8 Y/ j0 n, S4 u, N* g
sis has been given to neuroradiologic imaging in
( w3 q! i* M$ T" t, eboys with precocious puberty. In addition to viril-/ e% q2 n% w6 O9 F" L; o9 [
ization, the clinical hallmark of CPP is the symmet-, j5 X' A4 v: U; F& O3 i
rical testicular growth secondary to stimulation by
5 w1 W1 I4 R# A* Ugonadotropins.1,3
9 X8 f1 a# B0 L1 `- i! YGonadotropin-independent peripheral preco-6 Q3 G  w. _; l
cious puberty in boys also results from inappropriate! x2 T" v7 u9 N$ w
androgenic stimulation from either endogenous or
8 N7 ]! z1 Z0 ~0 `) Y3 {+ C4 ]: Bexogenous sources, nonpituitary gonadotropin stim-: @) Q/ B& [0 S1 ?
ulation, and rare activating mutations.3 Virilizing' c- v, g  M) x9 n
congenital adrenal hyperplasia producing excessive; m* a# A4 F9 C5 t" T% Z/ B" V
adrenal androgens is a common cause of precocious' c# E$ B/ |. v
puberty in boys.3,4
& h9 R, F# C- Z$ o( V! EThe most common form of congenital adrenal
6 A1 e9 Y* V; o! Phyperplasia is the 21-hydroxylase enzyme deficiency.0 k. J" W6 l5 i2 Q3 P1 _
The 11-β hydroxylase deficiency may also result in
: c! s( y: }5 `+ }: x" Bexcessive adrenal androgen production, and rarely,
7 H4 B+ Q% s# nan adrenal tumor may also cause adrenal androgen& K5 Q) l  F) ?2 E6 V- }
excess.1,3! x4 r& \6 Z5 @2 D1 L# b/ G
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 y, s1 Q2 Q" f9 `7 ?% |542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
% v) o" d7 ^" y" ZA unique entity of male-limited gonadotropin-
" Z5 _! o! u4 J4 S" windependent precocious puberty, which is also known6 Z& g+ T+ R9 L5 i( o5 z5 @+ C6 D1 u
as testotoxicosis, may cause precocious puberty at a6 _/ j0 n! t9 |0 i, ?* S
very young age. The physical findings in these boys
$ n0 w3 o+ A, Swith this disorder are full pubertal development,1 z3 L9 D+ ~/ p( ?  z  e
including bilateral testicular growth, similar to boys
; H( A" _* H! s1 [( X9 T: lwith CPP. The gonadotropin levels in this disorder. p3 e/ m# _. ?7 v
are suppressed to prepubertal levels and do not show" z$ U$ ?' Q3 d
pubertal response of gonadotropin after gonadotropin-
2 m5 [$ j& `7 a/ A* W+ lreleasing hormone stimulation. This is a sex-linked
1 x+ C# \# ]" q! Dautosomal dominant disorder that affects only) h" i, @- Y* c4 {% g$ h1 Y) R: M
males; therefore, other male members of the family
0 g5 D4 ]( R6 [+ W# z* |may have similar precocious puberty.3# V8 k0 X0 x9 k# S- m4 a) [
In our patient, physical examination was incon-: v* P) ^- d6 a+ @5 x4 C
sistent with true precocious puberty since his testi-! ]* t( ~; [" V: Z
cles were prepubertal in size. However, testotoxicosis
# N  ~8 y1 v/ h  l# H: J( w% }was in the differential diagnosis because his father4 Y- Y0 j: r0 C, N8 ~- V1 \
started puberty somewhat early, and occasionally,
9 c3 f% R1 I0 k) etesticular enlargement is not that evident in the
4 B. H) l' }6 X8 i& @6 dbeginning of this process.1 In the absence of a neg-1 I0 g+ t8 [9 m- C6 R+ r: A5 L
ative initial history of androgen exposure, our& N; H' R7 A' M& F, H5 H
biggest concern was virilizing adrenal hyperplasia,: u+ n* m0 p8 |% q. _0 B
either 21-hydroxylase deficiency or 11-β hydroxylase' d9 O/ n. Z( j( p. _: E  g
deficiency. Those diagnoses were excluded by find-
* e$ Q7 d8 b( g# jing the normal level of adrenal steroids.
- X4 q; e( |3 I4 S9 v$ T  zThe diagnosis of exogenous androgens was strongly
2 f: n; P% i" ususpected in a follow-up visit after 4 months because
/ \+ {' E' p9 c& h2 @5 g$ L3 j5 W/ W( \the physical examination revealed the complete disap-
7 _/ p, V) }" R" t" j. n# Gpearance of pubic hair, normal growth velocity, and
+ R- V  P: N. y/ B* _$ e% ~; wdecreased erections. The father admitted using a testos-5 p1 s/ I2 m9 A* y$ f- d' @+ Q! ]8 c
terone gel, which he concealed at first visit. He was) c" M5 v! L! K- R# F. V0 Z5 ^
using it rather frequently, twice a day. The Physicians’& Y' y% K1 V3 m
Desk Reference, or package insert of this product, gel or
' W# g  d/ I* ?/ J3 R4 w+ xcream, cautions about dermal testosterone transfer to' R8 @$ T* C/ Q  o8 A$ {
unprotected females through direct skin exposure.) m, T5 }4 H/ h6 E9 q+ L4 m  t
Serum testosterone level was found to be 2 times the
# K3 {/ y  s7 B, i6 K9 ?baseline value in those females who were exposed to
$ A- v3 f1 @- L* Zeven 15 minutes of direct skin contact with their male
6 X$ J+ ]- w6 fpartners.6 However, when a shirt covered the applica-4 C+ O, c: z) d& f  E* Z* [# k7 n
tion site, this testosterone transfer was prevented.! h2 I9 S+ l) m; o
Our patient’s testosterone level was 60 ng/mL,
$ }# V0 W* @9 C* C6 @which was clearly high. Some studies suggest that
8 ~5 j& W' ], a  ddermal conversion of testosterone to dihydrotestos-
) N  q, ^% Y" s3 w6 b/ r" cterone, which is a more potent metabolite, is more
/ ]& U# f9 ?: v: p5 f/ h  F  Factive in young children exposed to testosterone4 z) y/ p* ~! _) L  Y% H2 F7 v
exogenously7; however, we did not measure a dihy-
$ P# R% H9 G( L! {) \9 n2 t, N# cdrotestosterone level in our patient. In addition to% [1 [: B# e9 h9 k
virilization, exposure to exogenous testosterone in5 T  N0 }$ j4 S( s% e
children results in an increase in growth velocity and
1 F$ i4 ^% R2 zadvanced bone age, as seen in our patient.4 n" V+ ^7 ]$ o5 q
The long-term effect of androgen exposure during* r8 y$ ]& `0 m1 e0 y" p
early childhood on pubertal development and final
3 f% U$ j0 `* H2 A/ a* v" eadult height are not fully known and always remain
9 u3 a5 x7 z% {" i, Q' N) Y: |a concern. Children treated with short-term testos-6 M8 r! Z! Q  x/ C, F
terone injection or topical androgen may exhibit some" p( P$ n& W" z1 ~0 F
acceleration of the skeletal maturation; however, after; l* e" w- ~- X
cessation of treatment, the rate of bone maturation
* _( {! c+ k2 f: C- ndecelerates and gradually returns to normal.8,92 T: H. H6 S+ U7 L8 i# i% H
There are conflicting reports and controversy
- D+ B6 U9 d3 {# c( l3 C# Vover the effect of early androgen exposure on adult' Q& N4 }6 h; J- G; i' F1 `
penile length.10,11 Some reports suggest subnormal$ |) K5 i6 f7 S/ l9 l; k
adult penile length, apparently because of downreg-$ J' {* V* g% m5 R% C
ulation of androgen receptor number.10,12 However,
3 o  u1 t$ j1 _* _1 p) F: p8 fSutherland et al13 did not find a correlation between7 N8 u) F( d/ l# W% P
childhood testosterone exposure and reduced adult
+ R/ S4 q' _3 Q# ]3 d- y' jpenile length in clinical studies.) q, j0 b. j0 Z4 l
Nonetheless, we do not believe our patient is
+ s- e- M- s9 f; |7 J, D& k3 Q5 @4 \" ugoing to experience any of the untoward effects from& B7 [( y. S4 j: E" c
testosterone exposure as mentioned earlier because: c0 P" p4 a- Z% {' N2 E2 c/ \' W
the exposure was not for a prolonged period of time.
7 G4 }3 k: ~# Z" L2 m/ C5 cAlthough the bone age was advanced at the time of
; p1 s. I1 C% ^diagnosis, the child had a normal growth velocity at5 o% t7 r5 z: n8 S: P7 _! ^3 E  s
the follow-up visit. It is hoped that his final adult! z1 q( `0 ~: ]
height will not be affected.% O6 D- }2 [9 s3 |* v4 a1 p  \1 t
Although rarely reported, the widespread avail-
2 J- k- s  ]# Dability of androgen products in our society may
; D1 }9 P! o3 d9 h# ~* f( @6 Eindeed cause more virilization in male or female9 r. \9 Y+ ~5 K( G" U
children than one would realize. Exposure to andro-
! A! ?3 T7 M, `4 e  M2 o4 Sgen products must be considered and specific ques-! v+ ]4 q! w. u7 P
tioning about the use of a testosterone product or
0 }8 h/ ^) F- X4 Q0 M) qgel should be asked of the family members during# G4 ]. C+ D& K  p4 i, [0 @
the evaluation of any children who present with vir-; r1 Z; ^  ^1 Y! e2 p1 `
ilization or peripheral precocious puberty. The diag-3 f# d$ f8 p" U" S6 u* r
nosis can be established by just a few tests and by
' m+ T' t% S6 r' ]' A2 `3 uappropriate history. The inability to obtain such a9 Q/ G2 I9 X8 x% n8 o) X
history, or failure to ask the specific questions, may# x6 b: R; g8 n
result in extensive, unnecessary, and expensive! A* Z6 _" f0 y7 j6 J, a! V8 N/ c
investigation. The primary care physician should be8 [  u. I& A' a  ^: K
aware of this fact, because most of these children1 Q8 b/ j4 ^7 c# J9 e( e
may initially present in their practice. The Physicians’
8 e6 n8 ]% @" }, l' G, lDesk Reference and package insert should also put a0 `- B1 Z9 [: J7 c5 J% O" ]: H
warning about the virilizing effect on a male or
7 D: b8 D) f/ G4 E  \4 Wfemale child who might come in contact with some-, m7 [* w# J5 s( N0 b
one using any of these products.
  s% k# R2 ^; n4 A6 N# e7 |References" }6 P8 o; Y2 k% g9 @# K5 ~6 c- C
1. Styne DM. The testes: disorder of sexual differentiation* ^3 v3 m3 n' K' ^' M
and puberty in the male. In: Sperling MA, ed. Pediatric
; E! _8 A# W: N6 O9 i8 HEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;4 q$ x+ O7 D( t% V/ b: c+ X
2002: 565-628.9 H7 Y2 V+ n+ z& c* ]
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious% ?8 \1 f3 x4 P* ~- c6 P: y! E6 h
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
2 v. C/ X* E5 _4 j9 y2 Z8 aBoy Induced by Indirect Topical
) _8 {8 H$ I; U% x+ [' S8 x' ~% SExposure to Testosterone
' d8 q7 \0 A6 z" Z! K% ?Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
; Z3 r: O) Z/ H% k( |and Kenneth R. Rettig, MD1
6 v8 t/ A% A/ f; @$ ?) z( |Clinical Pediatrics- v0 ?5 |! v1 k
Volume 46 Number 6
. w3 E* n9 Y* c: c  Z. E5 W5 ^July 2007 540-543* u. F0 G7 u9 g! l. a& u, d
© 2007 Sage Publications, l, |9 a! n4 u; F
10.1177/0009922806296651; T8 f. V, |2 J9 m! ~4 a
http://clp.sagepub.com& b9 S2 F: C' o5 e: l' o
hosted at2 U& y3 C9 S: {5 @4 j+ u% N
http://online.sagepub.com6 C6 I( A, \- d+ B& V& }' Z# x
Precocious puberty in boys, central or peripheral,! t5 o. m, U( K1 K* B$ _
is a significant concern for physicians. Central9 _# D2 i! ]3 U- T( e- i  N
precocious puberty (CPP), which is mediated- P. X, F4 s2 Q# b
through the hypothalamic pituitary gonadal axis, has4 ^" R; z: i+ q& X% I
a higher incidence of organic central nervous system! b" w; D- @9 V5 T6 i2 |
lesions in boys.1,2 Virilization in boys, as manifested7 U9 A% b) b9 u+ l
by enlargement of the penis, development of pubic
3 E2 u! A- n9 n* v, u" yhair, and facial acne without enlargement of testi-$ h" {1 Z+ d. h" T1 O: m
cles, suggests peripheral or pseudopuberty.1-3 We
/ f! `% M: }7 Q% t+ o$ u9 Freport a 16-month-old boy who presented with the
3 K8 |4 l, a6 B  F, b1 U/ a$ ?; Nenlargement of the phallus and pubic hair develop-
4 `- e* W. H+ J% Oment without testicular enlargement, which was due; j: a% m  B% y3 y+ g
to the unintentional exposure to androgen gel used by; q7 v2 S; I! x# M7 \2 ]1 N
the father. The family initially concealed this infor-8 p; A7 R4 [4 t4 j" K6 Q. R* n2 L2 A
mation, resulting in an extensive work-up for this
: f" d1 J3 R& x% z8 ~child. Given the widespread and easy availability of
+ h. ~7 @2 O9 f- \/ s. ^3 Dtestosterone gel and cream, we believe this is proba-. l# a$ J; ^/ ?9 G2 t4 J
bly more common than the rare case report in the3 X) P9 n5 j# n5 t/ H" }
literature.4, E* g* Y& `: M* ]" g
Patient Report8 Y! S* D# T. k6 c" o
A 16-month-old white child was referred to the/ G6 d9 X+ @, w. O
endocrine clinic by his pediatrician with the concern4 k; q& l& \% D8 z3 [
of early sexual development. His mother noticed& r5 |' C7 U' I+ Y+ w3 \8 x& B
light colored pubic hair development when he was
7 Y5 @6 l' @6 P7 LFrom the 1Division of Pediatric Endocrinology, 2University of! |0 c9 Y4 c- c3 ^
South Alabama Medical Center, Mobile, Alabama.
" V: K" N" y1 s$ j/ ]  ]Address correspondence to: Samar K. Bhowmick, MD, FACE,6 [. R' g+ l+ |4 q. ]: ?& e
Professor of Pediatrics, University of South Alabama, College of
/ v9 n5 C& J: k5 g1 VMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;7 B; v& g* B) l4 ~# ]! d3 d9 [0 u
e-mail: [email protected].
0 Z$ o; L" p6 h# I( x( J  Z$ ]about 6 to 7 months old, which progressively became: Z& G# m3 t8 x
darker. She was also concerned about the enlarge-
, I" z5 Z0 B$ H8 I- D! Bment of his penis and frequent erections. The child
( i7 }2 o+ b( \1 x9 D/ ]was the product of a full-term normal delivery, with! I8 T9 k6 Q4 P8 D1 ~
a birth weight of 7 lb 14 oz, and birth length of( r: H+ h6 L% M! ?# H2 y1 ^/ E1 C
20 inches. He was breast-fed throughout the first year
( a8 Y/ ]/ P7 R' Aof life and was still receiving breast milk along with$ D1 c. w+ F3 E. n1 u! a
solid food. He had no hospitalizations or surgery,9 \4 D4 L# c* D4 j0 Z, f
and his psychosocial and psychomotor development6 i$ o9 r4 X( h
was age appropriate.) E* ~* ?* \  u/ I  Q( W8 U
The family history was remarkable for the father,
6 v! E4 y) h3 ~/ z$ y$ ~# \who was diagnosed with hypothyroidism at age 16,5 W  O- @/ H& |! m7 C7 H' W
which was treated with thyroxine. The father’s" i2 E% x2 t" w! J: V* G
height was 6 feet, and he went through a somewhat! {4 M9 B+ D& _3 h
early puberty and had stopped growing by age 14.$ g: a1 Q# A: j. T1 e0 ?% y
The father denied taking any other medication. The3 x. `5 M/ Z3 I9 d
child’s mother was in good health. Her menarche' U2 M. D' V1 N! f- I) u
was at 11 years of age, and her height was at 5 feet
3 h) _6 ^; Z* k3 o- C5 inches. There was no other family history of pre-, m# k7 E( `% Q4 v3 }
cocious sexual development in the first-degree rela-. Z1 J3 L; Q; a, p/ r9 u
tives. There were no siblings.
* j  `3 P! H" `8 ^* p3 D  {2 ^Physical Examination
/ T1 E, E" X- }& h5 pThe physical examination revealed a very active,
8 Q2 w" m, u0 V+ D4 D6 M) ?playful, and healthy boy. The vital signs documented$ r- p8 ~( ?  u; [3 x$ M0 Q- X; O
a blood pressure of 85/50 mm Hg, his length was; r$ g" A' V/ o5 L
90 cm (>97th percentile), and his weight was 14.4 kg* z2 m' E9 l8 c& [
(also >97th percentile). The observed yearly growth
/ @" I- w1 B  vvelocity was 30 cm (12 inches). The examination of
) [/ m: i* N2 U4 ^( Xthe neck revealed no thyroid enlargement.8 W$ W1 r, _' O* B4 T' g2 R, W
The genitourinary examination was remarkable for
; T- m& M; ~) E9 x8 j1 Venlargement of the penis, with a stretched length of1 |+ d' s5 }0 q" V% J* _
8 cm and a width of 2 cm. The glans penis was very well2 D% w. o5 T8 I. Q
developed. The pubic hair was Tanner II, mostly around
1 d/ s% k& w- j% \5 M5404 |- k: ^' i. s* R
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: t  q6 n+ z! A8 N2 Q# g5 I! W  }the base of the phallus and was dark and curled. The
. C- w; }/ W% {  h# `9 Ytesticular volume was prepubertal at 2 mL each.
: ]% [' j+ A& C7 aThe skin was moist and smooth and somewhat9 y& p! t# s  |1 S  B. l
oily. No axillary hair was noted. There were no
( C: G4 F1 W7 ?5 Yabnormal skin pigmentations or café-au-lait spots.! V+ M' @; v  {$ a" ~5 k) m
Neurologic evaluation showed deep tendon reflex 2+
5 Z" N8 _# @# dbilateral and symmetrical. There was no suggestion8 I: O4 ?) F' i
of papilledema." I) z1 q+ k5 n3 F7 g6 N, i7 e: Z3 d" U
Laboratory Evaluation- O5 ~2 c& F/ m5 V  `! T
The bone age was consistent with 28 months by+ ^! x( H" d* |0 \
using the standard of Greulich and Pyle at a chrono-) D5 X% O, A, q0 A7 }! O" R
logic age of 16 months (advanced).5 Chromosomal
: Q6 g% `! d, ~0 r) x) J; m( vkaryotype was 46XY. The thyroid function test9 i# n) q6 m! {0 ]4 P( c& O
showed a free T4 of 1.69 ng/dL, and thyroid stimu-# l6 g! U* q7 N8 T( D
lating hormone level was 1.3 µIU/mL (both normal).5 B1 B/ S/ Y# J6 l$ n8 K/ v
The concentrations of serum electrolytes, blood
% |" \& f  ~3 _; s4 O4 Z8 Qurea nitrogen, creatinine, and calcium all were
9 L/ A) A& P6 j5 X# Z; A  M* Hwithin normal range for his age. The concentration* d; F* k, u# n4 Z$ R4 [
of serum 17-hydroxyprogesterone was 16 ng/dL
* |! Q) l: V& t- J3 t6 [  g, `(normal, 3 to 90 ng/dL), androstenedione was 20* T" [" K- \: }+ r5 ~# T5 }
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
. p. O( H" q/ _- Nterone was 38 ng/dL (normal, 50 to 760 ng/dL)," Z! I' f6 W7 v
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
: o8 m; U. t! z% l' {0 J  _1 q49ng/dL), 11-desoxycortisol (specific compound S)
1 P  T6 \& G. `6 \  J! X( Hwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
# v  C  j4 A1 @/ u/ w* ntisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total! G# t3 a. C; J: c
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
* R& N0 L5 r2 c. D# Fand β-human chorionic gonadotropin was less than
* y. ?4 F* _/ `* K1 r" g5 mIU/mL (normal <5 mIU/mL). Serum follicular
- F9 ^/ _" a4 ~stimulating hormone and leuteinizing hormone1 ?' v4 q% c: P  q: t" W% \
concentrations were less than 0.05 mIU/mL9 B- g( L9 \3 w% _8 M* w
(prepubertal).; T6 Q( @# ^9 p) b! `
The parents were notified about the laboratory
2 Z5 q- f/ H+ qresults and were informed that all of the tests were5 O" V5 J4 w& i! l
normal except the testosterone level was high. The( P5 w  a  h2 L4 ?2 Q: [6 r- c7 |
follow-up visit was arranged within a few weeks to
' L5 @  @& ]( z1 Yobtain testicular and abdominal sonograms; how-: H( \& N; Z6 K! ]; |/ ]
ever, the family did not return for 4 months.1 ]8 x1 D0 I( F& B/ u2 [2 o& A) F
Physical examination at this time revealed that the
. G# [5 o% E' q; Schild had grown 2.5 cm in 4 months and had gained
1 g& P& t, R7 x! Z+ a) e! O2 kg of weight. Physical examination remained
2 a) H7 R1 D% r  O) ?unchanged. Surprisingly, the pubic hair almost com-9 q6 i, h6 y5 Q
pletely disappeared except for a few vellous hairs at
; M% N0 P/ Y9 G6 W+ E- ythe base of the phallus. Testicular volume was still 2
1 G1 c1 Z' z, G, z5 e9 c3 omL, and the size of the penis remained unchanged.: |+ _6 V/ N* T8 ?2 h5 X/ c  P
The mother also said that the boy was no longer hav-
" p0 c, D" y1 E: T  A) iing frequent erections.; f8 A+ k5 o# s, y" E) W# F+ \% U
Both parents were again questioned about use of8 |% ^7 C2 e% X7 \2 N  C1 N: Z
any ointment/creams that they may have applied to
' |6 I2 s* Y6 Y0 P, S1 ~  o* Hthe child’s skin. This time the father admitted the: P* `+ H) j# [" b2 C- [1 o; z
Topical Testosterone Exposure / Bhowmick et al 541
% Q4 j4 B6 ~5 s8 D" _5 N/ @use of testosterone gel twice daily that he was apply-% x5 w& {( W7 M! F
ing over his own shoulders, chest, and back area for+ P' J& ~8 Z, B( m0 X% z0 X
a year. The father also revealed he was embarrassed0 }! j4 ?3 o6 V% O
to disclose that he was using a testosterone gel pre-
0 R% }) |* ^. C; hscribed by his family physician for decreased libido
, J3 P; U; Y7 S/ |9 jsecondary to depression.
; M1 h& i7 f0 z2 jThe child slept in the same bed with parents., v- s5 N; E0 E% w2 Y, Y; C3 N
The father would hug the baby and hold him on his
3 s2 u4 I5 A3 V/ Schest for a considerable period of time, causing sig-2 @5 q& z7 Y; ?+ Y3 R) q* q
nificant bare skin contact between baby and father.! T& K" p' O  o
The father also admitted that after the phone call,
4 F- {+ }2 G6 s8 lwhen he learned the testosterone level in the baby
. ?/ d4 F# u/ L" b. [was high, he then read the product information
; Y. C9 N; x$ u6 t9 kpacket and concluded that it was most likely the rea-
: A9 f2 I+ |3 }0 X: s# M# P7 H4 y& Fson for the child’s virilization. At that time, they3 _6 H0 \" h% W9 Y, O0 k; @
decided to put the baby in a separate bed, and the
' v. \; F+ k2 tfather was not hugging him with bare skin and had; {' K1 k$ V3 E5 u: e6 A
been using protective clothing. A repeat testosterone
( o* I% z% R% F1 A* Etest was ordered, but the family did not go to the
0 M; `0 }. z. B( n, m: j' T% jlaboratory to obtain the test.
1 b; R) I' ]. v9 m: V9 N4 i9 [8 ZDiscussion6 i1 a$ D  U3 {1 R! T' }1 K
Precocious puberty in boys is defined as secondary% K; H* X) c5 ]1 q1 B/ E
sexual development before 9 years of age.1,4) i' D8 k# d7 i5 R) e! \
Precocious puberty is termed as central (true) when8 y3 U6 H$ ~0 E  j
it is caused by the premature activation of hypo-6 x* a0 v% p/ S4 H. \/ E
thalamic pituitary gonadal axis. CPP is more com-
; W5 S4 ~" K& x5 x! @. Qmon in girls than in boys.1,3 Most boys with CPP, D2 A8 W* _8 U9 e
may have a central nervous system lesion that is
8 m9 A1 y; S4 k! x9 x1 iresponsible for the early activation of the hypothal-" S8 M5 ]3 s+ M. Z+ ^( @' q6 g6 x
amic pituitary gonadal axis.1-3 Thus, greater empha-7 o" J8 @: a7 E
sis has been given to neuroradiologic imaging in
, ]$ v7 Q4 y% \' eboys with precocious puberty. In addition to viril-
1 [# U! K0 f& Sization, the clinical hallmark of CPP is the symmet-
; l& @0 G- u) ~4 x8 nrical testicular growth secondary to stimulation by# W3 ~8 h/ Z0 |5 \0 F3 H8 M4 U
gonadotropins.1,39 V8 F8 Y: X5 J+ e* j
Gonadotropin-independent peripheral preco-
6 o6 C/ H6 X' L5 h) |2 N% ^1 `cious puberty in boys also results from inappropriate( J3 ~& U' I: r0 X- @' D$ e
androgenic stimulation from either endogenous or
4 y- R; j3 z3 i7 ?$ O% Dexogenous sources, nonpituitary gonadotropin stim-
$ q0 d! ?, O% o& R; A/ `0 ^7 @ulation, and rare activating mutations.3 Virilizing6 d& G) S. n& P3 z. q7 O( W
congenital adrenal hyperplasia producing excessive
# F$ [; F; m/ Z8 L9 e5 sadrenal androgens is a common cause of precocious' B5 @& X% H- V/ S; q3 m) X' k% H
puberty in boys.3,4) T. q) T, d# v! m2 T
The most common form of congenital adrenal( n- P5 J# N$ O. j* B
hyperplasia is the 21-hydroxylase enzyme deficiency.
# j6 k9 t& J* s, AThe 11-β hydroxylase deficiency may also result in
6 Y6 ~) x0 h3 L; Z0 c  Q: Mexcessive adrenal androgen production, and rarely,+ t* O& k+ A  x4 M, W/ {; j
an adrenal tumor may also cause adrenal androgen7 W$ H4 p1 d8 B. c7 U+ [5 R
excess.1,3
4 l9 J2 V4 W) {, l5 ^  W+ Y/ rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 W  q: k/ j% }& J$ b4 f
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007) N* X  e' i. ^2 v
A unique entity of male-limited gonadotropin-
- t7 b  x* U, J  qindependent precocious puberty, which is also known0 Y- {9 Q6 r; f9 O$ K( E" o! R* D
as testotoxicosis, may cause precocious puberty at a
  b  b, K" R- ]9 N. vvery young age. The physical findings in these boys3 i2 E) k2 R, E& y
with this disorder are full pubertal development,2 ?8 G! D' E- s, v: ]' P
including bilateral testicular growth, similar to boys1 V& |6 i7 w+ |' @2 P
with CPP. The gonadotropin levels in this disorder
6 A/ G0 Q$ U% Dare suppressed to prepubertal levels and do not show
. A6 b' H! Q5 Q1 bpubertal response of gonadotropin after gonadotropin-
5 R: p/ G3 a' n, n- s/ @/ {  Rreleasing hormone stimulation. This is a sex-linked8 `8 @6 m, ~' @- T
autosomal dominant disorder that affects only
9 v+ P0 z5 K2 z* ^: B# @$ Imales; therefore, other male members of the family. X! [4 n. i7 X- J, S
may have similar precocious puberty.3
: }) ^* }2 D# Z6 H7 D! O- k) eIn our patient, physical examination was incon-
3 h# v* H$ X/ U7 F' X( Csistent with true precocious puberty since his testi-
2 [& h& {8 E8 Y1 f2 q$ ccles were prepubertal in size. However, testotoxicosis
; l9 v; K7 D" M  ~( j' Bwas in the differential diagnosis because his father
% S# M: S8 ~9 i6 mstarted puberty somewhat early, and occasionally,
; {+ ^7 g3 k5 V7 p  P; Z$ xtesticular enlargement is not that evident in the( h. x; D4 C" i+ v/ n3 K
beginning of this process.1 In the absence of a neg-; g. d) @( G7 q; ^+ h9 X5 C/ o
ative initial history of androgen exposure, our9 S% ]& s( v8 Q( ]; c) v1 }
biggest concern was virilizing adrenal hyperplasia,' c8 f* s8 M: F" w4 a9 C# f* H( c
either 21-hydroxylase deficiency or 11-β hydroxylase
2 F( j0 V) I/ a  I/ l/ ?deficiency. Those diagnoses were excluded by find-+ Y% d, ]9 ?8 g9 G) G* F& Q# {
ing the normal level of adrenal steroids.
' q% q! W% H6 ^  z- S( eThe diagnosis of exogenous androgens was strongly! V5 n+ y) h5 x, d- ^
suspected in a follow-up visit after 4 months because
3 h: E3 C; m: {; |" o. ethe physical examination revealed the complete disap-$ r: C8 o% o* j* s$ j; a
pearance of pubic hair, normal growth velocity, and& e9 V. u4 Q, _) V6 F1 c9 O
decreased erections. The father admitted using a testos-, M5 y& H  K9 B) X" j( Y) w8 j1 f
terone gel, which he concealed at first visit. He was
/ u# s% M: v4 _& `, o& _using it rather frequently, twice a day. The Physicians’
+ g3 W* ^( t1 x  g* qDesk Reference, or package insert of this product, gel or
( O# y# n' N* r6 B9 m) vcream, cautions about dermal testosterone transfer to
; d( X/ n: ~$ j# S7 p' kunprotected females through direct skin exposure.
+ v! G. m+ _+ w, M/ O" G% U- \9 `Serum testosterone level was found to be 2 times the1 _, z# B( P- R
baseline value in those females who were exposed to$ z+ E( k/ X) ~4 f$ u
even 15 minutes of direct skin contact with their male. A, N* Q! [, S! Z
partners.6 However, when a shirt covered the applica-. P% g& J  I4 n3 j  |
tion site, this testosterone transfer was prevented.
# ~/ n4 A0 Q: }7 V. c( f- d& m2 @Our patient’s testosterone level was 60 ng/mL," ?1 l8 p6 }4 a5 d( a# o
which was clearly high. Some studies suggest that
9 v4 m% U) z2 F5 ^+ Udermal conversion of testosterone to dihydrotestos-
/ s4 H, ^, `4 E+ P$ _# e4 gterone, which is a more potent metabolite, is more
' }2 p* x. a& g- C( `! }active in young children exposed to testosterone
7 A* n4 o1 v- [exogenously7; however, we did not measure a dihy-
' W" }4 _( N/ ]0 ^: pdrotestosterone level in our patient. In addition to0 h7 L, n+ b- f: J6 N% L  f. `$ q
virilization, exposure to exogenous testosterone in
2 o) \- ?. v  n) bchildren results in an increase in growth velocity and
0 P+ }4 D9 C6 M/ W9 radvanced bone age, as seen in our patient.( v0 ?" o  O  {- ^
The long-term effect of androgen exposure during
. r0 ~; A% P( g5 qearly childhood on pubertal development and final
+ U4 `4 h( u& P5 Sadult height are not fully known and always remain6 u# J4 ]4 {) s. w
a concern. Children treated with short-term testos-1 }" ?  u! h6 ?& R4 c+ k
terone injection or topical androgen may exhibit some- n! G( y) F* v& G; H) m
acceleration of the skeletal maturation; however, after
7 l0 c1 h+ y3 Wcessation of treatment, the rate of bone maturation
9 R% y' X! o, N. ~9 Jdecelerates and gradually returns to normal.8,9- I1 l& D7 ]+ P8 p' d. F% E
There are conflicting reports and controversy
2 I; I. O7 ^- j9 ~# lover the effect of early androgen exposure on adult
- N' M/ ]: H& g" S' E2 v. p! h$ hpenile length.10,11 Some reports suggest subnormal( o9 U5 x2 w- f* `" `( F, U! b
adult penile length, apparently because of downreg-
  u5 T9 k+ h' C) |; @ulation of androgen receptor number.10,12 However,
6 R- a0 H: [& m) O: ?; vSutherland et al13 did not find a correlation between2 o% ^! ]5 b  `! }1 D
childhood testosterone exposure and reduced adult5 S9 u% ^, b  |. t" V
penile length in clinical studies.1 P  E. W$ q/ T1 a/ \
Nonetheless, we do not believe our patient is
6 t: H* G% I# Fgoing to experience any of the untoward effects from9 Z; R( y) ]- V+ \# s" x) x9 i
testosterone exposure as mentioned earlier because
8 C6 o% u# L8 v( wthe exposure was not for a prolonged period of time.
: k+ x, H* k5 S2 pAlthough the bone age was advanced at the time of
. z- ?$ Z$ ]3 _9 o! _5 n2 t' d& zdiagnosis, the child had a normal growth velocity at
. I* J2 b$ W" P7 _: O* O4 Pthe follow-up visit. It is hoped that his final adult
6 j" q" A. I( a. f+ pheight will not be affected.4 a+ R& H5 K; R% r1 X- a( e
Although rarely reported, the widespread avail-- y  g" I6 k$ W
ability of androgen products in our society may
1 S0 l2 G; g* ?  Mindeed cause more virilization in male or female4 V) v1 O; Z7 u* i- G
children than one would realize. Exposure to andro-+ L7 m- O+ y# C
gen products must be considered and specific ques-
+ {( k5 }3 j4 M5 M8 D8 n2 {tioning about the use of a testosterone product or
7 W& k. B7 N+ {  @" g( Ngel should be asked of the family members during' _5 I: ]. w5 T% |6 \* V& l
the evaluation of any children who present with vir-
5 x8 L! ^3 X( \& Y4 ^% }+ t3 s( ?- _ilization or peripheral precocious puberty. The diag-
3 j' s( |# y- e) n! Z8 j' Anosis can be established by just a few tests and by% J% ?0 T7 K# A! V/ ~
appropriate history. The inability to obtain such a
9 `/ L& `3 D2 a- ^8 o+ O- vhistory, or failure to ask the specific questions, may) q2 o* X$ ~* k% {) U$ C& y: h9 P
result in extensive, unnecessary, and expensive
2 j' J0 c  H  G+ a9 u7 e* A: linvestigation. The primary care physician should be$ v3 U4 _$ `. q: K- T- r  h3 q% [
aware of this fact, because most of these children
$ D- d0 z0 A; q% b: M; `& omay initially present in their practice. The Physicians’5 ~! B+ l) A+ H6 J; e
Desk Reference and package insert should also put a/ h% O3 ~8 }2 |8 |/ o
warning about the virilizing effect on a male or/ b9 Y+ r% }$ f: \! X9 X) l% q" i
female child who might come in contact with some-6 N/ n2 L7 f( `. ~3 P6 w
one using any of these products.
. A2 l" r, A+ e3 O& p% v7 vReferences+ D$ i5 y( F1 [2 ~4 s$ z
1. Styne DM. The testes: disorder of sexual differentiation
" q* u/ \$ B2 B2 M$ v  @and puberty in the male. In: Sperling MA, ed. Pediatric9 r! S( Q/ y) H# c0 A/ J) |' t
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;" C/ q: w% p3 l  X; @- O  G
2002: 565-628.7 d* }. `* |' q4 M$ o" o
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious1 {4 D5 E+ V. v7 s' o, w
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
8 O, L. `( L9 y/ y
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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