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Sexual Precocity in a 16-Month-Old& z$ ]6 x7 G5 b7 Q: X- v2 W
Boy Induced by Indirect Topical, v8 i$ Q" _" b6 g% O  {8 R' s
Exposure to Testosterone
: q1 w0 @; O* i* Q4 b! s) d. FSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,21 [/ k8 c1 \( q1 M4 E' b  H
and Kenneth R. Rettig, MD1
$ o- R" A8 y: Y& ~* T9 [Clinical Pediatrics! \  `  B# f7 P+ k& P! u& e9 J( P
Volume 46 Number 69 Z( N/ v0 I$ c0 d1 t: N# T: Z
July 2007 540-543
: Y3 T# R* d7 Z+ A© 2007 Sage Publications
7 E+ J, x. F& f7 N1 d4 d9 K' ?10.1177/0009922806296651/ U* T% U- p( P  J3 o& v$ [% i
http://clp.sagepub.com
. O# w* Z+ Z0 D8 a/ C, ~/ x6 b0 yhosted at
  K7 F4 Y7 T/ C/ M& Ihttp://online.sagepub.com5 J- S; A& N3 P
Precocious puberty in boys, central or peripheral,9 _/ D! ^9 J# d' _( r; t
is a significant concern for physicians. Central! S" |$ |' ]2 j$ s9 q2 l3 Y
precocious puberty (CPP), which is mediated+ m" Z+ A7 z" G4 T
through the hypothalamic pituitary gonadal axis, has
7 c$ f" J  x- B9 R9 @" |. R: v+ W8 _a higher incidence of organic central nervous system
7 r0 Q$ c) r/ i6 ?+ C5 m. Rlesions in boys.1,2 Virilization in boys, as manifested
" ]7 \! l8 h) R; m' U. Hby enlargement of the penis, development of pubic
$ \. H6 w9 u4 h; `% Yhair, and facial acne without enlargement of testi-
* Z9 z6 u. u$ lcles, suggests peripheral or pseudopuberty.1-3 We5 h4 x' e# Z- {
report a 16-month-old boy who presented with the
  n, Q, c$ \# Z  w( yenlargement of the phallus and pubic hair develop-  r$ @; ^% z; Y% _; z
ment without testicular enlargement, which was due2 w6 |1 C; S1 @9 m5 o  e3 D
to the unintentional exposure to androgen gel used by& A' i8 V" p: c
the father. The family initially concealed this infor-
$ j) F" O, i( K$ s0 M% _. u! hmation, resulting in an extensive work-up for this
0 V. Z* X7 ^' J$ A3 e  _child. Given the widespread and easy availability of! J( }" y2 f' z% O
testosterone gel and cream, we believe this is proba-6 D( L; j: Z+ b" T- L5 U, K' I  x5 [
bly more common than the rare case report in the
1 A4 v2 A, Z: _" aliterature.4( z/ |0 `: d* Z  s" V9 E
Patient Report
" Q, P' C& Z+ O" M( LA 16-month-old white child was referred to the/ a0 {4 @7 x/ n( K0 V" c
endocrine clinic by his pediatrician with the concern
3 h9 L8 |; a; H/ |' rof early sexual development. His mother noticed
# N8 W9 T4 Z: _3 k, D$ ]light colored pubic hair development when he was3 p* C( P! H5 N' e) r; j/ ?9 c: c
From the 1Division of Pediatric Endocrinology, 2University of: |7 ^: n; @. E9 l# d# C- i; m
South Alabama Medical Center, Mobile, Alabama.
4 x( z1 D+ Y; e$ \& P0 w( NAddress correspondence to: Samar K. Bhowmick, MD, FACE,7 T5 E% Y# s1 l! }+ Q' Q% A
Professor of Pediatrics, University of South Alabama, College of. N; y8 Q7 K8 F5 g7 ]2 p) X
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
8 ?+ c% E9 _* d9 q' S( ^" Ce-mail: [email protected].& }! @% S3 R- j# U" F
about 6 to 7 months old, which progressively became
( B1 W- f) O5 bdarker. She was also concerned about the enlarge-9 l. K/ h% w3 I9 E7 J
ment of his penis and frequent erections. The child& a( D- [! |9 ]+ v" t" p
was the product of a full-term normal delivery, with
  L' c3 Y/ _. D6 G4 ka birth weight of 7 lb 14 oz, and birth length of( _3 e$ F/ R: G* T1 G- ^+ K
20 inches. He was breast-fed throughout the first year
& j$ F+ r7 m* f' c5 ~of life and was still receiving breast milk along with0 k& a. O" W, z) ^: g
solid food. He had no hospitalizations or surgery,0 G* a) Q/ E* t9 h! D( f& \" [
and his psychosocial and psychomotor development' r6 D3 t) z1 P
was age appropriate.
( |2 G* s/ g& e! t) ], EThe family history was remarkable for the father,
9 S% `: d! \$ c. C1 {% ewho was diagnosed with hypothyroidism at age 16,8 f" W7 @% D; B* T% h3 b: z
which was treated with thyroxine. The father’s
- e" Y$ Q* m3 c* Q5 g( I" Z. \height was 6 feet, and he went through a somewhat6 {  |9 {1 y/ ^  y/ C; l
early puberty and had stopped growing by age 14.
" V8 R0 ?; ~- q" O) g  O7 ]The father denied taking any other medication. The5 S) h5 @. {5 o8 V- d  b
child’s mother was in good health. Her menarche
1 \4 v* v; {  p: F5 Ewas at 11 years of age, and her height was at 5 feet0 z8 X) p: Q* ~
5 inches. There was no other family history of pre-
8 o. B& U% O7 V) f* r+ ecocious sexual development in the first-degree rela-0 |) X* L. S# i  t: V, l
tives. There were no siblings.  @1 G1 L8 F& i; w4 S" d
Physical Examination
& }+ R7 n2 Q/ c( J3 S' A8 `) M2 @, sThe physical examination revealed a very active,0 @% i, a0 q3 \' u
playful, and healthy boy. The vital signs documented
( z9 f3 r( Z! I9 l" {5 ga blood pressure of 85/50 mm Hg, his length was
& T1 D7 M# [1 i5 E4 y% }6 G90 cm (>97th percentile), and his weight was 14.4 kg9 E! t& N, O/ l# ?. b
(also >97th percentile). The observed yearly growth
  m5 Z* I+ \1 b! c# ~velocity was 30 cm (12 inches). The examination of- }' Z9 |4 C& V: N
the neck revealed no thyroid enlargement.3 X1 N5 a. G% Z2 B7 M. l9 @
The genitourinary examination was remarkable for# C/ Y. e4 k; l: l
enlargement of the penis, with a stretched length of: A' H9 ]: ^% c3 }5 W
8 cm and a width of 2 cm. The glans penis was very well6 b% p9 c1 ]5 m1 ?) d: {
developed. The pubic hair was Tanner II, mostly around
* `% @  Q( d2 I  u% U* _* k% b5409 m$ V3 a9 M" r# O
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- _" u% g9 d) y0 D, `+ H8 {# {1 g
the base of the phallus and was dark and curled. The
# G" {- C1 U4 \2 i4 rtesticular volume was prepubertal at 2 mL each.$ r/ x1 I; D" t, b7 c! I
The skin was moist and smooth and somewhat
: ]$ J* ?9 L/ P5 E2 F# ^oily. No axillary hair was noted. There were no
) `3 N) W% i# x+ L- h" Rabnormal skin pigmentations or café-au-lait spots.! p) D9 R( C' p- @
Neurologic evaluation showed deep tendon reflex 2+) H7 U& Y7 p* Z: n$ g0 r* F
bilateral and symmetrical. There was no suggestion
7 O- }* ^- G7 k2 d7 d# D. i, |0 mof papilledema.7 n# F0 c- e& y+ [: F  N4 u
Laboratory Evaluation' i6 W. |+ e, P1 t/ u
The bone age was consistent with 28 months by6 A) y' e0 W+ M% E
using the standard of Greulich and Pyle at a chrono-3 q. U7 U& w3 I1 l1 Z
logic age of 16 months (advanced).5 Chromosomal- |( l: F6 I# _- c5 J
karyotype was 46XY. The thyroid function test. V' c: S  d- \) T: n+ s
showed a free T4 of 1.69 ng/dL, and thyroid stimu-7 o# p0 \0 A" a& D6 p
lating hormone level was 1.3 µIU/mL (both normal).
  B, m! x! U" MThe concentrations of serum electrolytes, blood  Z4 `+ Z3 [3 S5 l3 g' Y$ O
urea nitrogen, creatinine, and calcium all were
3 a" c7 t9 [' y: [# twithin normal range for his age. The concentration4 B% _8 x" d2 Z6 y- F
of serum 17-hydroxyprogesterone was 16 ng/dL; P" J$ W  a* x
(normal, 3 to 90 ng/dL), androstenedione was 203 d4 u. z  A4 w5 y: F. i# A
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-% {0 z  {; j! c
terone was 38 ng/dL (normal, 50 to 760 ng/dL),4 ~( o) x8 w/ S$ R1 B' J
desoxycorticosterone was 4.3 ng/dL (normal, 7 to& w8 e. X# X3 [, \/ H; X
49ng/dL), 11-desoxycortisol (specific compound S)( J+ H' Y$ W  |. Y* \) T
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
7 [. R4 j0 L: @' Y/ i+ z- @tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
* C! ?0 Z1 p3 C) |$ Dtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),& N( W" v5 E& k, D1 ?
and β-human chorionic gonadotropin was less than: t& q! {3 @" X6 q, I  `
5 mIU/mL (normal <5 mIU/mL). Serum follicular
) B4 C3 a5 ]0 I6 _# G4 W1 B' tstimulating hormone and leuteinizing hormone
' k/ g+ T; j4 Q" Y2 }! Tconcentrations were less than 0.05 mIU/mL' ?- m, r7 j7 k+ K7 x1 i0 I! q
(prepubertal).
; M- b8 l& E& K+ R; t- A3 e& ]The parents were notified about the laboratory
5 m, f$ z' y3 j% x( n: dresults and were informed that all of the tests were6 Z% H4 z* f2 C5 |0 s7 g# u
normal except the testosterone level was high. The' X, t; y/ N/ o2 z7 `" g
follow-up visit was arranged within a few weeks to8 S! J" G3 j2 |% g6 ~
obtain testicular and abdominal sonograms; how-9 X& Z3 {# K% |- H4 l
ever, the family did not return for 4 months.
  Y9 _% }0 V: Q8 w; f% Z7 P& O- m$ l. iPhysical examination at this time revealed that the
, N0 K: @) n6 e* \, nchild had grown 2.5 cm in 4 months and had gained/ z$ p+ c% z) L( W1 s1 X& m2 Z, l6 A
2 kg of weight. Physical examination remained
, i3 t$ B# c1 H2 k! j$ Gunchanged. Surprisingly, the pubic hair almost com-( B6 J* s8 t9 T& U1 |" @
pletely disappeared except for a few vellous hairs at: v6 w- W% C. H3 v
the base of the phallus. Testicular volume was still 2
8 {$ ^/ h7 [7 v/ h; D* u: r! BmL, and the size of the penis remained unchanged.$ L' B. E5 E! l* s2 X, `
The mother also said that the boy was no longer hav-, n. @6 i, Z+ O: c. n0 X+ g1 k9 d
ing frequent erections.7 Q( H, K5 D) n& P( S& T/ n( F: z" h
Both parents were again questioned about use of9 P% h4 D6 P+ `" e
any ointment/creams that they may have applied to
4 w& r' @  y" n2 q4 Z- wthe child’s skin. This time the father admitted the
% X8 D/ W9 i2 `$ k) h0 ITopical Testosterone Exposure / Bhowmick et al 5415 z  P  g; T5 \7 C
use of testosterone gel twice daily that he was apply-, R3 h5 O% W" ?9 @" O3 ^
ing over his own shoulders, chest, and back area for
0 M3 Y# \0 R; ?( xa year. The father also revealed he was embarrassed
% ^! l# c6 P" ?! Qto disclose that he was using a testosterone gel pre-
! u- y8 u8 f8 z' mscribed by his family physician for decreased libido
/ ?$ @6 @5 J7 asecondary to depression.
8 E6 u8 K! S0 i9 G( YThe child slept in the same bed with parents.5 d: Z% g/ c$ d2 A  w( j
The father would hug the baby and hold him on his) n$ w' e1 c- [6 h
chest for a considerable period of time, causing sig-; p6 `1 u4 b  X3 d% A
nificant bare skin contact between baby and father.
$ T" w* u$ y" n7 M" p9 `The father also admitted that after the phone call,
# s, S, Q" o) z0 S8 Awhen he learned the testosterone level in the baby7 f) U0 ~, v; _! D2 d* q" h; i
was high, he then read the product information3 e' Y6 e; J0 D) Y0 V
packet and concluded that it was most likely the rea-
4 p8 o3 R6 Q& {2 @son for the child’s virilization. At that time, they
/ ^, F' ]# ^  u) O2 Z2 ]2 @7 F- ydecided to put the baby in a separate bed, and the  j% ], \1 \6 z# V" ]! ]( c& d
father was not hugging him with bare skin and had
& l) p$ L3 I& {* b# W  Kbeen using protective clothing. A repeat testosterone& {: f, f2 {- r- D9 `9 [* [& u
test was ordered, but the family did not go to the
. }' b  w, \2 \9 |. Z/ ^8 K6 Slaboratory to obtain the test.% \4 Y( t# ]6 ]  ?; g
Discussion! Q! F/ o4 H" t% u
Precocious puberty in boys is defined as secondary
; ]) ?& K) ^# {, E( asexual development before 9 years of age.1,4
' b* D! R/ p8 w' `+ }- NPrecocious puberty is termed as central (true) when
/ M( q2 z+ L: j; a* vit is caused by the premature activation of hypo-
; E: I$ p& o' ^! cthalamic pituitary gonadal axis. CPP is more com-- H6 ^) u% Z. y% U  L3 z
mon in girls than in boys.1,3 Most boys with CPP
. |  g' q5 }) e  `may have a central nervous system lesion that is  z4 v! |1 Y, w! i) H
responsible for the early activation of the hypothal-
% q) F8 H5 w! ~2 gamic pituitary gonadal axis.1-3 Thus, greater empha-
! M" v3 [) T: [( F+ \sis has been given to neuroradiologic imaging in% r5 u4 L/ U  C: N. J- K8 d
boys with precocious puberty. In addition to viril-
6 F, k/ J  H2 Q. `6 x$ jization, the clinical hallmark of CPP is the symmet-& `' N- V2 e6 U% ]( O% k" Z+ `+ {8 j
rical testicular growth secondary to stimulation by
8 T. r4 j' k' T5 y( `! B1 m% zgonadotropins.1,3" ~, ]7 r9 o6 y1 e2 N
Gonadotropin-independent peripheral preco-
) H! c5 o4 A& T+ zcious puberty in boys also results from inappropriate
+ m$ o0 p9 w. ^androgenic stimulation from either endogenous or
9 {1 r/ ?. ~6 T: H9 f/ @4 [2 Qexogenous sources, nonpituitary gonadotropin stim-
' |9 |) E6 k* ^$ culation, and rare activating mutations.3 Virilizing/ w. o) Q. x0 M2 N9 I. i5 G9 \. T
congenital adrenal hyperplasia producing excessive5 B" d9 s. L5 J, B( ^
adrenal androgens is a common cause of precocious
8 d/ a5 t8 Q, S1 Fpuberty in boys.3,42 |  D/ q8 U3 e3 S- H9 y3 o& @
The most common form of congenital adrenal
/ k! M/ f  z( P, O2 c4 V5 Yhyperplasia is the 21-hydroxylase enzyme deficiency.
; m% i# t) N2 aThe 11-β hydroxylase deficiency may also result in2 G% m# w* D# L3 @/ T
excessive adrenal androgen production, and rarely,
* c$ ~: F+ p( E+ J- @, Yan adrenal tumor may also cause adrenal androgen' _* U! z$ D! y; ]
excess.1,3  {" {$ E: z$ v
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
% E2 Y0 M9 t- U% J& w: C% ~542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
9 r: {& @, a% r6 |2 sA unique entity of male-limited gonadotropin-
& |3 J0 u: v: a" |3 Pindependent precocious puberty, which is also known
3 \- I9 D$ L. Das testotoxicosis, may cause precocious puberty at a
4 @0 I' R+ J( r3 T3 Every young age. The physical findings in these boys
! `) ?) l7 z  y1 g7 E  zwith this disorder are full pubertal development,
5 c. L0 L/ {* g+ Iincluding bilateral testicular growth, similar to boys* u/ v: J, h% m
with CPP. The gonadotropin levels in this disorder
* z6 Q! M; Q3 d. S, m. C$ g" xare suppressed to prepubertal levels and do not show1 P1 B' T) G5 {7 O6 O# ~5 O1 J
pubertal response of gonadotropin after gonadotropin-8 O* B$ e4 ^# y( o- y, \& x7 P
releasing hormone stimulation. This is a sex-linked
) q7 S$ l9 t2 Q4 @autosomal dominant disorder that affects only
. x  ~* A4 e, Hmales; therefore, other male members of the family
! n* t# \, v7 qmay have similar precocious puberty.3
" f/ g1 b( u/ E, LIn our patient, physical examination was incon-
4 w1 t3 k/ c" Z' a! x0 t* Jsistent with true precocious puberty since his testi-; c' U, A4 j4 p
cles were prepubertal in size. However, testotoxicosis
  g" Y' u+ I0 F; `was in the differential diagnosis because his father) b  @% J( C1 r/ E) G1 u: ^
started puberty somewhat early, and occasionally,3 k7 u7 R0 F7 G4 p8 X* W/ p/ o0 d
testicular enlargement is not that evident in the
! k: S9 a- W! C  n- V7 L8 Gbeginning of this process.1 In the absence of a neg-
( O0 h& x5 L5 r6 E# t; D5 jative initial history of androgen exposure, our2 A: ~" k; k3 q5 e2 r9 L3 {
biggest concern was virilizing adrenal hyperplasia,
1 ^. z7 g0 [0 a6 G4 {either 21-hydroxylase deficiency or 11-β hydroxylase
1 ^6 X5 g0 ~3 [- B* o' D$ |2 ~% ~deficiency. Those diagnoses were excluded by find-1 K7 Z9 q  v; _& l
ing the normal level of adrenal steroids.
. y0 H$ b; F# q% o% P- EThe diagnosis of exogenous androgens was strongly
9 h' a. D& E. _7 Y* C" r% R: w1 nsuspected in a follow-up visit after 4 months because; B4 K% g/ |4 n  b! \( j
the physical examination revealed the complete disap-
* w8 Z: K! `& fpearance of pubic hair, normal growth velocity, and( B# ^" R& `- T: U
decreased erections. The father admitted using a testos-6 X# j% _: e& x+ b4 U  x
terone gel, which he concealed at first visit. He was! Y  H0 w) X8 E) x7 ?
using it rather frequently, twice a day. The Physicians’
& q" P8 I# }8 G8 @8 B" P& o# m# |# MDesk Reference, or package insert of this product, gel or& [/ v5 `3 X2 \* x5 A! ?
cream, cautions about dermal testosterone transfer to
7 h* p% E- J( V5 {, eunprotected females through direct skin exposure.7 {0 a5 D, @6 X+ L
Serum testosterone level was found to be 2 times the
2 `( w- [7 C3 F5 R2 l) T/ lbaseline value in those females who were exposed to( m& c/ y) K5 T
even 15 minutes of direct skin contact with their male
2 v: [5 m. U  J+ m! t- Spartners.6 However, when a shirt covered the applica-  H; G! W4 f- O* q5 W3 W# x% k3 N
tion site, this testosterone transfer was prevented.
3 q% X+ w5 |0 e* n; G4 _+ }6 WOur patient’s testosterone level was 60 ng/mL,
7 b! _; ]. f  H! {which was clearly high. Some studies suggest that
/ P" R$ N! ^1 Y3 g' v) h2 Hdermal conversion of testosterone to dihydrotestos-! z$ }- d! l& L* r7 ]
terone, which is a more potent metabolite, is more/ K+ t& E1 s) N% q  Z& J* X6 q8 i6 ]
active in young children exposed to testosterone, T5 t: Q8 f) z3 @
exogenously7; however, we did not measure a dihy-
" g) m7 \3 o+ t% b  @9 Z5 ddrotestosterone level in our patient. In addition to$ z! C9 F" }2 p2 V0 m/ x
virilization, exposure to exogenous testosterone in
: Y2 Z/ F4 J8 Kchildren results in an increase in growth velocity and
* C$ {! M6 ?* y, iadvanced bone age, as seen in our patient./ v( k$ {9 o" b; S
The long-term effect of androgen exposure during
$ @' X  k; c+ B, vearly childhood on pubertal development and final# z3 [3 R8 w; K$ g/ E, J# p' j
adult height are not fully known and always remain2 K6 O. ^, H9 L' S: c0 ~1 _- T
a concern. Children treated with short-term testos-
$ D# r7 f; P! F# jterone injection or topical androgen may exhibit some$ n$ t& _  Q/ H; r' [# G+ U/ W; P
acceleration of the skeletal maturation; however, after
2 y1 }, N/ N& x4 N. Scessation of treatment, the rate of bone maturation
2 D: T$ {+ h1 L  {5 Mdecelerates and gradually returns to normal.8,9& k' d: a9 R' H. V: p1 ]
There are conflicting reports and controversy
" f6 a) d9 U; J& r/ U! A! Tover the effect of early androgen exposure on adult9 w8 Q& O5 \: \" F, |7 ^2 }
penile length.10,11 Some reports suggest subnormal
8 f6 Z4 H; f* T* @, }adult penile length, apparently because of downreg-6 _1 L9 f2 R8 v0 e% U6 @
ulation of androgen receptor number.10,12 However,. |: o4 W. B6 i' h/ l
Sutherland et al13 did not find a correlation between: H. e# T3 Q) K5 c6 K* u
childhood testosterone exposure and reduced adult. d. m  C1 ]6 g# f2 d: o) p3 E
penile length in clinical studies.
1 }: I: ^( F- Z; INonetheless, we do not believe our patient is
! Z4 N3 V7 j) W9 |9 xgoing to experience any of the untoward effects from
6 R) k0 Z! n" btestosterone exposure as mentioned earlier because
; X- q0 o9 {; W& rthe exposure was not for a prolonged period of time.0 ~. @0 h; `  h  f& h
Although the bone age was advanced at the time of! V" i; L& j$ T1 X3 M
diagnosis, the child had a normal growth velocity at
0 P' G$ f& {- i+ j; P6 S' Cthe follow-up visit. It is hoped that his final adult
+ T  d* R# B7 x  v0 c3 N' Aheight will not be affected.
" A# N" Y8 `1 A) u0 G1 V8 iAlthough rarely reported, the widespread avail-
# C' E8 U7 X1 W0 O2 D' _% \ability of androgen products in our society may/ s3 S0 Z4 X  z
indeed cause more virilization in male or female! O9 N# I: o. H) Z
children than one would realize. Exposure to andro-' J$ H# {0 P5 v" x3 ^
gen products must be considered and specific ques-
' L- [7 f: n# ]8 l0 H% K( vtioning about the use of a testosterone product or
, }; D. s- U' q7 _0 sgel should be asked of the family members during
# ?* g& d& O- p) A* m3 J  Bthe evaluation of any children who present with vir-1 {8 l0 M3 w+ M# \- Y  ^$ z/ B
ilization or peripheral precocious puberty. The diag-3 Z/ ?$ ]  N# b7 ?+ X8 C. R
nosis can be established by just a few tests and by
6 Y7 Y+ ~# d2 Z6 w. K2 \8 Bappropriate history. The inability to obtain such a9 A0 o4 d" M7 s% E
history, or failure to ask the specific questions, may
, Z! F) r2 [. o$ T1 x. A. q0 nresult in extensive, unnecessary, and expensive
. r4 F. y. C, o' L: Q2 j" hinvestigation. The primary care physician should be0 ?' T( J4 [: j2 C+ j" g
aware of this fact, because most of these children
, E& m$ w8 G$ w* \1 N% p. wmay initially present in their practice. The Physicians’$ X% b1 e& p0 y1 `( @
Desk Reference and package insert should also put a$ i' u+ s5 m$ r* r8 z+ ]8 u
warning about the virilizing effect on a male or2 p) }5 n# R* \8 a. q
female child who might come in contact with some-( W7 x2 L1 R% R' I4 l
one using any of these products.
5 K( N  q8 W6 V! PReferences
$ ^* r2 f1 b7 q1. Styne DM. The testes: disorder of sexual differentiation
3 E2 R) Q0 X/ Y9 n, X( p7 n; o; X$ band puberty in the male. In: Sperling MA, ed. Pediatric& A: s6 I- N& Q
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;  k, V) J9 J; m+ ?5 b. ~
2002: 565-628.
- s' A6 h* z5 m4 q2 E, ^2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
2 r8 G& H1 Q! n) y/ J% Ipuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
+ E1 j- O" w. c" j# {  RBoy Induced by Indirect Topical# |6 b9 k" ^' t. A& @9 I
Exposure to Testosterone: H3 I. K* L& {2 ]
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2% S' \, x& P1 n! g
and Kenneth R. Rettig, MD1
- U: I: F9 S# w* R  L* Z+ YClinical Pediatrics
7 Z. X2 ~1 B; YVolume 46 Number 6
" j. F5 ~/ ]9 P5 |, cJuly 2007 540-543. b4 R( y  Z/ I/ m0 _: S$ N- ]
© 2007 Sage Publications( ~; N$ p. V* r- g( c
10.1177/0009922806296651
- e7 g, _5 j# H1 `- U, w0 x* q5 Mhttp://clp.sagepub.com4 V: b9 c5 a' M. s/ A1 Y
hosted at) n; y* T2 q; o% c7 m' s
http://online.sagepub.com
+ O/ l; b% l% t$ p; B! VPrecocious puberty in boys, central or peripheral,
3 s" p0 o. u  ^% m3 W* H0 T. His a significant concern for physicians. Central
, Q4 ]; @  O. Oprecocious puberty (CPP), which is mediated$ F( q5 [5 m+ O& z) X" l2 Z, M
through the hypothalamic pituitary gonadal axis, has: G5 k- f! }$ ^  Q
a higher incidence of organic central nervous system
8 d& p( k/ n; p* xlesions in boys.1,2 Virilization in boys, as manifested7 w* J* r( e) w5 i: z
by enlargement of the penis, development of pubic
% J, s/ O$ ?( z* B. R& e, vhair, and facial acne without enlargement of testi-
' _! I. C7 q% z) x' Ccles, suggests peripheral or pseudopuberty.1-3 We
' E, d9 @; f* M/ M( B+ xreport a 16-month-old boy who presented with the' y( H7 a, \* j8 }3 n; ~2 F3 b7 d
enlargement of the phallus and pubic hair develop-
2 R0 w' i# F9 g& D' a/ S+ Ement without testicular enlargement, which was due$ m4 \- i9 C. I3 O  \; J+ e* c
to the unintentional exposure to androgen gel used by
6 ~; ^: V- S+ A2 F: `9 Ithe father. The family initially concealed this infor-
8 E7 W# [- h: P/ ^5 x& k  amation, resulting in an extensive work-up for this  P& b  M1 V* C2 W' A8 Z
child. Given the widespread and easy availability of
* n5 u$ K2 y0 u0 ]  Stestosterone gel and cream, we believe this is proba-4 @1 r* ]7 {: w) y8 Z
bly more common than the rare case report in the9 g7 j/ h0 N) K  c
literature.4
9 Z5 X: C( u+ r& K% H3 K. cPatient Report( A2 k" I% k. D7 A7 b
A 16-month-old white child was referred to the
7 m6 \1 l( p6 T) k# g8 Gendocrine clinic by his pediatrician with the concern7 Y8 P* Q2 M3 Q. E+ v2 g) _
of early sexual development. His mother noticed
& X# @' c8 Z1 \, k3 Z/ _2 Plight colored pubic hair development when he was& k% q; I3 m7 D* f7 E. u
From the 1Division of Pediatric Endocrinology, 2University of( c: G5 T, C- p& B4 ~
South Alabama Medical Center, Mobile, Alabama." h) ]& a3 q3 S- C( A4 M/ g+ e4 Y
Address correspondence to: Samar K. Bhowmick, MD, FACE,
6 D% d0 f( k  D0 B3 pProfessor of Pediatrics, University of South Alabama, College of& w) U9 V% d) ], l7 s) F- [. U
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
9 P4 C& \" s$ y" de-mail: [email protected].
5 S  ~. M( T1 _+ @( i7 Habout 6 to 7 months old, which progressively became
- |- R' A" ~" [1 r+ G. F: Y7 v! Sdarker. She was also concerned about the enlarge-
6 [4 k' m3 `. J& \* ?. wment of his penis and frequent erections. The child/ Y8 p$ l3 Q- e2 f4 i2 ^
was the product of a full-term normal delivery, with
; j' i( ?, b. e4 @: Va birth weight of 7 lb 14 oz, and birth length of4 i1 M3 u. C: q% y6 f2 V
20 inches. He was breast-fed throughout the first year' {( y4 O8 @0 h. a  t& H3 o  f
of life and was still receiving breast milk along with
' \! y4 r8 @% e. xsolid food. He had no hospitalizations or surgery,
- V# k4 [1 @) e0 \; Nand his psychosocial and psychomotor development6 ~" c: t8 p; @. ^0 y" V9 G5 u9 a
was age appropriate.
& T' z4 ^5 N. x# \. AThe family history was remarkable for the father,* B. N( I! K6 c5 V" T
who was diagnosed with hypothyroidism at age 16,
& r9 ]; D  ^! P- Gwhich was treated with thyroxine. The father’s
! b/ [9 ^5 Q" z2 Z1 t+ \height was 6 feet, and he went through a somewhat
+ V* ^/ c/ o, Zearly puberty and had stopped growing by age 14.4 B: E) M$ n/ l5 d
The father denied taking any other medication. The% U" y: p  J5 }( r) i: ~% }( b
child’s mother was in good health. Her menarche, B; U  o0 w0 m
was at 11 years of age, and her height was at 5 feet
& v, a0 V* i. M4 h( I5 inches. There was no other family history of pre-
- }" Z, Y5 `$ k. b9 ?& M4 X0 Jcocious sexual development in the first-degree rela-2 F3 r; Q8 i/ Q+ X
tives. There were no siblings.
7 C: a4 g; C8 Z! U- zPhysical Examination
3 F0 H/ L) }/ z' dThe physical examination revealed a very active,2 H' M6 M4 O' l
playful, and healthy boy. The vital signs documented# N9 e2 B6 W3 H8 i
a blood pressure of 85/50 mm Hg, his length was
1 u; i% g1 T8 y! |9 Q90 cm (>97th percentile), and his weight was 14.4 kg
* g) k) e6 n0 h(also >97th percentile). The observed yearly growth
+ e1 i8 w# r; t& @' S5 uvelocity was 30 cm (12 inches). The examination of
  h+ n8 H% W, n6 nthe neck revealed no thyroid enlargement.
* x& l7 }7 a# b2 ?$ I5 R( B! @The genitourinary examination was remarkable for$ I  K5 l. Y0 f9 k* y% X& @
enlargement of the penis, with a stretched length of
. e% a, K- |7 W1 V. b4 z8 cm and a width of 2 cm. The glans penis was very well
3 w& Y" t. s& O% P/ Z- I- Jdeveloped. The pubic hair was Tanner II, mostly around. m* ]# ]' Q: b3 n6 j/ k
540
6 n/ J8 |# {4 j8 vat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 D; d$ e: }7 C4 qthe base of the phallus and was dark and curled. The# K7 ?7 o, O  K, Z6 L7 S% p2 x
testicular volume was prepubertal at 2 mL each.* ~: @# E& q* k2 E' {. G2 }
The skin was moist and smooth and somewhat$ O3 R" j9 h$ @( ^- Z. Q- k) p# Y* l# D$ c
oily. No axillary hair was noted. There were no
2 O# h, W$ b: ?8 d& p5 j0 R! habnormal skin pigmentations or café-au-lait spots.! ~* s- O( |* e+ i: y! ~
Neurologic evaluation showed deep tendon reflex 2+
5 c- A  m6 m( Xbilateral and symmetrical. There was no suggestion, O* B( I8 Q* [$ l  X; {! w
of papilledema.5 u) b* `( @1 Y3 Q: n5 Y2 i" O
Laboratory Evaluation
( X3 X$ W9 J9 @+ y9 Y3 rThe bone age was consistent with 28 months by" O# z& Q# w& h6 Q& c+ V/ B8 N; O
using the standard of Greulich and Pyle at a chrono-
- J1 i, M# _; M6 J' [& Zlogic age of 16 months (advanced).5 Chromosomal
, M6 s8 s  H$ Z/ Kkaryotype was 46XY. The thyroid function test
! a; Q/ Y7 O+ s9 D+ A; xshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
9 Y, J0 Y1 j" J! G( v5 `! [lating hormone level was 1.3 µIU/mL (both normal).4 J+ H6 P4 ^4 F. c8 u
The concentrations of serum electrolytes, blood
$ Y# G8 _+ b7 P& ?6 v! vurea nitrogen, creatinine, and calcium all were( N& g$ u$ C/ V  N9 _: D/ H9 R
within normal range for his age. The concentration! A+ _7 Q% g% o0 {
of serum 17-hydroxyprogesterone was 16 ng/dL+ Y0 _/ x: l0 x' m, Q% y( l
(normal, 3 to 90 ng/dL), androstenedione was 20/ o" e) E' n; Y2 C# f
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
7 P  P% `/ U! z' bterone was 38 ng/dL (normal, 50 to 760 ng/dL),
% |2 E! F) c& h9 B3 T; ~desoxycorticosterone was 4.3 ng/dL (normal, 7 to! v0 O) I! g2 ?0 d$ a/ j$ \
49ng/dL), 11-desoxycortisol (specific compound S)
: c) S( |+ S2 n* n) qwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
) s! h; u& I7 D9 Utisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
- U4 z8 z* |) Wtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),% ^. O# T) M- l" j3 T# x' Q
and β-human chorionic gonadotropin was less than; u# X9 e: q" ~6 ~: U6 s
5 mIU/mL (normal <5 mIU/mL). Serum follicular
  e$ v$ \% R8 |( z8 N1 Hstimulating hormone and leuteinizing hormone' b8 r! ~+ J$ k3 N, Z$ c0 t/ L$ ]
concentrations were less than 0.05 mIU/mL& n' b5 I  ?, P+ O2 }8 h9 }3 y
(prepubertal).
0 n' A6 {7 F4 W1 Q$ @! M) m) hThe parents were notified about the laboratory( A! H) j# ^: N: L. L1 v
results and were informed that all of the tests were
8 ]! a6 G( y6 D* M5 I2 snormal except the testosterone level was high. The
9 @. Y1 _& P5 E  [7 l  Nfollow-up visit was arranged within a few weeks to
* W/ }% O' L- Y" K) x( }obtain testicular and abdominal sonograms; how-1 `8 X- k9 ?5 r' E
ever, the family did not return for 4 months.) t+ |$ _& z" e' E4 J, L  V
Physical examination at this time revealed that the( t( r2 o2 u: A+ H+ n
child had grown 2.5 cm in 4 months and had gained3 U) a# U6 T3 p
2 kg of weight. Physical examination remained/ c$ F, R9 v( F0 [( i( C) m
unchanged. Surprisingly, the pubic hair almost com-
6 j# T- e& @9 Y, Kpletely disappeared except for a few vellous hairs at, S, X; v$ @. H$ i) ^% Y6 x' _4 i
the base of the phallus. Testicular volume was still 2: X+ \) M  M8 w
mL, and the size of the penis remained unchanged.( N. T' p: o" W7 G* M* }3 b4 D
The mother also said that the boy was no longer hav-/ a) _: M$ M7 p( b
ing frequent erections.! Y. {- o; T& X. c3 u  T5 I8 J& P/ L" w
Both parents were again questioned about use of
* I; ^2 x+ X) X% tany ointment/creams that they may have applied to: x1 G2 e& b$ E9 ]4 c: R/ I
the child’s skin. This time the father admitted the# w1 o4 V- r2 A) R7 ^
Topical Testosterone Exposure / Bhowmick et al 541
- M9 M% c0 T; B3 b1 @use of testosterone gel twice daily that he was apply-3 C2 U/ S1 y: o1 J/ u- j
ing over his own shoulders, chest, and back area for
( E0 [' r) j/ P+ }, d% Ba year. The father also revealed he was embarrassed
2 a6 f7 O. x) n# Q+ @& Wto disclose that he was using a testosterone gel pre-( A+ I6 ?% s! Q
scribed by his family physician for decreased libido
0 i7 e% W4 T4 Usecondary to depression./ F& g( N/ O) s( z' o& Z& d9 u$ J
The child slept in the same bed with parents.6 `$ I. X' j; \) x: R
The father would hug the baby and hold him on his5 F( H$ E: h; A  i, o! R
chest for a considerable period of time, causing sig-* a- T1 l+ l8 U' ?0 b4 ~
nificant bare skin contact between baby and father.
5 k3 U/ @3 G& r( w3 WThe father also admitted that after the phone call,4 Q* U9 [! ], u! d8 X- A$ a8 N" o. u
when he learned the testosterone level in the baby( V5 |2 _( j  Q6 U9 W. y
was high, he then read the product information
5 y; m1 [5 z: O7 o; x; Y/ q0 epacket and concluded that it was most likely the rea-' q1 u: ?) F, I; v$ Z
son for the child’s virilization. At that time, they
/ _! D/ U# T# mdecided to put the baby in a separate bed, and the
7 ~( P2 h' j, ?6 m* Zfather was not hugging him with bare skin and had
* K/ [" i/ P* R4 h- i6 R& Qbeen using protective clothing. A repeat testosterone
, M# q; U8 p1 N! c& t0 A. Mtest was ordered, but the family did not go to the( E- D! k6 ?# Y5 c9 w: Z: u
laboratory to obtain the test.
% p! k2 C4 ~7 L* b- C; VDiscussion
3 G, j; T$ w) g! C8 \* ]" ]Precocious puberty in boys is defined as secondary0 o1 A9 n* _/ }
sexual development before 9 years of age.1,4& v9 t  e1 }0 t2 f  p* G( D
Precocious puberty is termed as central (true) when
% B2 J' x5 p: Q* K7 E& j1 Wit is caused by the premature activation of hypo-! K1 e, U( k" Y3 {. L- h
thalamic pituitary gonadal axis. CPP is more com-. D) T) p$ {: k0 }) K8 l$ f
mon in girls than in boys.1,3 Most boys with CPP
) @/ G; I' K! \, J$ O0 W& umay have a central nervous system lesion that is0 g2 d8 l7 Q) H  I& H6 Q
responsible for the early activation of the hypothal-% b( f' }8 V; s5 B3 Y; p/ @
amic pituitary gonadal axis.1-3 Thus, greater empha-
! R2 v" S5 R/ {% k: J6 osis has been given to neuroradiologic imaging in
  W# @' K1 d3 h4 g7 X2 ~8 X: ~boys with precocious puberty. In addition to viril-0 S3 q1 t. F$ l, I3 r7 g  p
ization, the clinical hallmark of CPP is the symmet-
+ Q" p! F, p# ?# t8 B# X' i% {rical testicular growth secondary to stimulation by
3 i. e' [; d8 D0 o8 m2 wgonadotropins.1,3: o, D+ q$ z2 C- D
Gonadotropin-independent peripheral preco-8 z$ q: [2 h4 Y* e
cious puberty in boys also results from inappropriate
9 B' ]" t6 t9 f! P9 `' |/ tandrogenic stimulation from either endogenous or
5 W2 z, X2 Q  U8 u$ V2 N8 x, rexogenous sources, nonpituitary gonadotropin stim-6 p2 v/ n4 f1 L
ulation, and rare activating mutations.3 Virilizing
# X9 r: F3 D6 k7 Z0 e, i+ Gcongenital adrenal hyperplasia producing excessive& @: g! N6 C& Y' a, x4 d9 ^' h8 i
adrenal androgens is a common cause of precocious
; s1 e/ Z: t' u6 ]) s; Z( Hpuberty in boys.3,49 Q1 J& X1 p  p& o- D7 R2 N
The most common form of congenital adrenal
; ]% @9 }" Y8 [2 b( Fhyperplasia is the 21-hydroxylase enzyme deficiency.) _5 w) y2 r0 T2 ]* W) |% H" b
The 11-β hydroxylase deficiency may also result in
4 q; p0 q9 }! S5 T; z( y- `excessive adrenal androgen production, and rarely,* @7 v1 f! D0 h7 q! z$ T
an adrenal tumor may also cause adrenal androgen0 a9 H) M9 [" Q5 r! A; A- y
excess.1,31 b; e; Y2 L% B8 z  r' T
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ k. R% M4 n- A1 _4 f4 C
542 Clinical Pediatrics / Vol. 46, No. 6, July 20074 L" |% }% H1 G1 p+ J
A unique entity of male-limited gonadotropin-
) T& D( B6 [- Z1 H; B& ]independent precocious puberty, which is also known5 ^; H3 @: @3 O$ d1 b, S7 q
as testotoxicosis, may cause precocious puberty at a9 n  P; S! P0 _  [2 K( F
very young age. The physical findings in these boys$ _5 z! a% Y4 i" g7 M, S0 Q* O9 w; Z
with this disorder are full pubertal development,
$ K; y7 K% b& Y! _: \2 Rincluding bilateral testicular growth, similar to boys
/ u6 y/ V  h" e" Uwith CPP. The gonadotropin levels in this disorder) s! M6 \  C- `3 N
are suppressed to prepubertal levels and do not show( J8 l- h9 r# w0 a
pubertal response of gonadotropin after gonadotropin-5 c) I0 I6 Y5 Y0 u# q" _
releasing hormone stimulation. This is a sex-linked1 B: N- x' O7 W6 x  f4 `+ e
autosomal dominant disorder that affects only, X( Z. S! t7 Y& j6 C3 f. X
males; therefore, other male members of the family# j/ y9 x2 _; G$ d- h# a& C
may have similar precocious puberty.3
- i9 l  a2 C1 a2 k) Q) PIn our patient, physical examination was incon-/ d4 t) l2 r/ G# n) N
sistent with true precocious puberty since his testi-
+ C; Z: V. x" W8 p  C0 p* Tcles were prepubertal in size. However, testotoxicosis. F1 n9 S" O" r. @% h- n; r
was in the differential diagnosis because his father1 T. q4 m$ Y9 G( l+ W
started puberty somewhat early, and occasionally,+ ^1 f# ]4 A9 u
testicular enlargement is not that evident in the
' w  D' F6 K7 X1 t& L, tbeginning of this process.1 In the absence of a neg-) l* R" q6 j9 N% T
ative initial history of androgen exposure, our
( g  k$ Y- g2 b3 @- V- c0 lbiggest concern was virilizing adrenal hyperplasia,
# |/ V9 |" v' f( reither 21-hydroxylase deficiency or 11-β hydroxylase3 L. g3 n9 V$ y4 s. F( r
deficiency. Those diagnoses were excluded by find-
; m) Q& o5 W2 V5 H/ u9 K& X6 Xing the normal level of adrenal steroids.0 x) h$ e2 v: ~: ^
The diagnosis of exogenous androgens was strongly1 t5 s* ]% D; g  r
suspected in a follow-up visit after 4 months because9 c0 o- _& V" G0 z3 F
the physical examination revealed the complete disap-* I: S; l. e3 P' Q* O8 `
pearance of pubic hair, normal growth velocity, and
, c, Z' u# B  n4 |# K* Tdecreased erections. The father admitted using a testos-
8 T* f" x0 Y5 x# }2 `terone gel, which he concealed at first visit. He was9 i+ I' V& }6 ~& }# w! X1 l
using it rather frequently, twice a day. The Physicians’/ H0 @& {- z- K# ?  p# g- f
Desk Reference, or package insert of this product, gel or
: Q( e" n+ x3 x: S( ^cream, cautions about dermal testosterone transfer to
# n# w+ j! L' r* o8 P# R2 t+ d! Ounprotected females through direct skin exposure.5 w9 T9 O) \! g7 K& {+ t
Serum testosterone level was found to be 2 times the
7 W6 z# s" a: {- Sbaseline value in those females who were exposed to
2 W2 L  D. ?6 ~: o. k7 keven 15 minutes of direct skin contact with their male
" T+ Z) [9 q1 w: \: vpartners.6 However, when a shirt covered the applica-8 ?2 E6 p% Z6 J
tion site, this testosterone transfer was prevented.8 b4 d2 J+ C2 V6 E+ g% U5 Z8 \) L
Our patient’s testosterone level was 60 ng/mL,$ S  F$ E. d  \" c) d
which was clearly high. Some studies suggest that1 G; k1 z; n. B% j  X& E
dermal conversion of testosterone to dihydrotestos-
. }0 u8 x- U+ L& O% i. l; `terone, which is a more potent metabolite, is more! K0 M! X2 L% N% l; _1 w9 Y0 v/ t+ N
active in young children exposed to testosterone
2 t. Q/ p- O) `, T, lexogenously7; however, we did not measure a dihy-
- E" K$ k+ h: s. m" y0 Udrotestosterone level in our patient. In addition to6 O! Y$ |4 c( U: F7 @
virilization, exposure to exogenous testosterone in
& [3 \+ C6 p; F4 ]children results in an increase in growth velocity and
; g6 ?9 r% C' q6 x9 Wadvanced bone age, as seen in our patient.
9 x3 t* G6 A7 t# f3 U' Y% HThe long-term effect of androgen exposure during" Q/ z- r4 f1 q& x" f0 S4 N- M, G
early childhood on pubertal development and final3 `8 p9 O2 F. t6 N) I* _3 K
adult height are not fully known and always remain7 I9 y7 x7 x. c) H! \2 \
a concern. Children treated with short-term testos-
- ?  \+ C* |1 @. cterone injection or topical androgen may exhibit some. Z' R! C$ m+ _8 p* h# r9 p
acceleration of the skeletal maturation; however, after
5 j1 t4 Y$ Y1 O1 d/ ?cessation of treatment, the rate of bone maturation
3 c% c& G2 g# @decelerates and gradually returns to normal.8,9
. t/ a7 [7 G" T/ o$ nThere are conflicting reports and controversy' N8 b' W  e& N7 u/ F+ ]
over the effect of early androgen exposure on adult
( L5 d2 T5 _3 G9 k) Openile length.10,11 Some reports suggest subnormal7 q7 P: C2 G5 o& q7 j; h
adult penile length, apparently because of downreg-
( @4 {0 C# C% ?8 w- C$ Q$ Yulation of androgen receptor number.10,12 However,+ A7 b6 J( X$ t0 ]+ x& l
Sutherland et al13 did not find a correlation between
" v3 ]1 ]/ Z" l9 wchildhood testosterone exposure and reduced adult4 [, p$ _- k0 y( V
penile length in clinical studies.
4 L! a5 m3 d. F0 c+ q2 cNonetheless, we do not believe our patient is
( I3 l# _: _6 ogoing to experience any of the untoward effects from3 M* S4 `7 s. ?& C% q- M
testosterone exposure as mentioned earlier because
. p( C: p$ k2 G/ x% f( `the exposure was not for a prolonged period of time.
- \; a! }+ \( v0 NAlthough the bone age was advanced at the time of
' U, e/ P- p. c. J) W$ g- k0 z2 x% A/ g- bdiagnosis, the child had a normal growth velocity at
0 Q2 o( \  q% Q$ {. W! zthe follow-up visit. It is hoped that his final adult7 x' {! ?, o! B8 d: Y8 J
height will not be affected.6 s% E6 o& Y& V& Z# w# o
Although rarely reported, the widespread avail-
) O  U  s  ^0 o( H; `: h6 sability of androgen products in our society may
) e! z1 @# i5 [3 I0 Dindeed cause more virilization in male or female
1 \# ?4 ^& j2 d# W9 O! X1 Dchildren than one would realize. Exposure to andro-- x7 b, z1 M: O
gen products must be considered and specific ques-
5 i) H9 _: q1 p* H, g; e. Otioning about the use of a testosterone product or
1 v" @: S: [' f8 N. a6 ?2 B- pgel should be asked of the family members during
: x; H/ g: c- p( cthe evaluation of any children who present with vir-* L( d2 F, J8 b% b: u
ilization or peripheral precocious puberty. The diag-; @9 v$ E+ T+ O9 t% N2 X
nosis can be established by just a few tests and by( c2 u/ Y$ Z8 O/ C! p  j- [
appropriate history. The inability to obtain such a
, |8 S+ b/ j- `: B5 h& Yhistory, or failure to ask the specific questions, may- r: e8 c! i/ O6 r' X
result in extensive, unnecessary, and expensive# h- F  v! V; o3 B; D2 w
investigation. The primary care physician should be
, q) \1 O; g: K8 D9 g' P/ d6 aaware of this fact, because most of these children# m0 B! |1 g  t) r; S  k, d
may initially present in their practice. The Physicians’
  w! \' r/ x4 N8 xDesk Reference and package insert should also put a
% h, @3 o8 u4 g) L4 ]warning about the virilizing effect on a male or
0 D4 ?  R! b, w1 f( \3 l0 K2 jfemale child who might come in contact with some-- I( w3 z7 ?- r% B
one using any of these products.
  r/ W' a' b/ a5 b+ eReferences
: M0 D; W9 ^- r4 u6 W+ {1. Styne DM. The testes: disorder of sexual differentiation
. b' b0 M! P9 I: D  _& |" Tand puberty in the male. In: Sperling MA, ed. Pediatric) P7 b+ N6 D' W  E
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
. R! `: X4 y7 {0 Q' ?% y9 x- m2002: 565-628.
, _: s  O; t0 z" b  W2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
5 P% l/ A+ [. p: [( e) s9 ]6 ppuberty 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

6 n# g) P8 h2 X% j, v: d# R/ S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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