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Sexual Precocity in a 16-Month-Old' y) C6 s  U& v% @- o  I+ c
Boy Induced by Indirect Topical
2 g6 A+ ?5 @( H: O( h3 U* s7 cExposure to Testosterone1 I. C8 V( S: h6 Q
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2# g" w4 N7 _! ^3 \! R, a( }) T
and Kenneth R. Rettig, MD1
4 l4 g6 b2 R9 f7 h9 y7 {Clinical Pediatrics& I0 O4 J4 O( M0 _$ E
Volume 46 Number 6
. |  d4 h' q/ g- T2 Y6 |' S8 CJuly 2007 540-543, l6 J6 W+ a7 O! f% e
© 2007 Sage Publications
  V& l& G$ a* Y# a, k' K10.1177/00099228062966512 o5 S( l* C, I5 c! K
http://clp.sagepub.com
( s2 I+ r, ?5 F2 fhosted at
  }7 W, l% _6 l6 v3 Uhttp://online.sagepub.com  k1 L- B$ x! }5 q9 n1 s
Precocious puberty in boys, central or peripheral,
- N% v# I% D  z( bis a significant concern for physicians. Central3 H' Y5 v: o, S7 H1 o% }
precocious puberty (CPP), which is mediated
$ \& B+ Q1 u7 X! F: ^through the hypothalamic pituitary gonadal axis, has
( I, l/ ~9 |" da higher incidence of organic central nervous system
8 F# a" t2 q+ l( Clesions in boys.1,2 Virilization in boys, as manifested
* R) A( ]: ^. @; ~by enlargement of the penis, development of pubic0 E( B+ e% K5 x. N
hair, and facial acne without enlargement of testi-3 u5 m: O) c. Q9 r/ W
cles, suggests peripheral or pseudopuberty.1-3 We
0 Z% }0 ], j5 A4 g% b: q7 Areport a 16-month-old boy who presented with the% {6 o* i; T4 L7 |& R2 q+ E
enlargement of the phallus and pubic hair develop-6 m% y  `% ?% G
ment without testicular enlargement, which was due+ h+ @+ [9 L) e0 g7 r; u* X
to the unintentional exposure to androgen gel used by! x' h. k4 x3 n2 N% v# ^$ G
the father. The family initially concealed this infor-
' ^2 ^& F0 C% Q4 w( L; Emation, resulting in an extensive work-up for this7 l% U' P( a2 V! b, R+ s" I! Q
child. Given the widespread and easy availability of" P) E: d9 @$ c; G
testosterone gel and cream, we believe this is proba-
" r' [/ l/ X5 H  X, Y4 P. u5 y$ Zbly more common than the rare case report in the
: C! s9 Y0 Z) O2 Aliterature.4  q0 |* l- _& G$ ~; R. w# g- L
Patient Report3 f6 ?6 w1 @8 P/ p
A 16-month-old white child was referred to the1 j+ Q# O" y! n& T0 C8 y5 t
endocrine clinic by his pediatrician with the concern  O$ ?5 r( p* F& N- _4 V/ v; w
of early sexual development. His mother noticed' Z. m  d) ]% V2 H! w
light colored pubic hair development when he was" [" N9 E4 ?8 A4 |/ y  w
From the 1Division of Pediatric Endocrinology, 2University of
% l' [+ D5 f  y  A/ f" GSouth Alabama Medical Center, Mobile, Alabama.
4 u9 t8 I$ B5 J( o( Y# \4 d! a8 YAddress correspondence to: Samar K. Bhowmick, MD, FACE,* u7 Z3 i- Q- j  @2 N3 E
Professor of Pediatrics, University of South Alabama, College of1 l  d6 }: A7 N$ a
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;# z4 [2 x# q+ \, R; \
e-mail: [email protected].6 Q* a* _9 n8 y8 F) b& q
about 6 to 7 months old, which progressively became
# U* Y' V- M  [; S& Zdarker. She was also concerned about the enlarge-
& u, p& [- W- O9 }( oment of his penis and frequent erections. The child( Y) z1 H# a5 n, G9 I
was the product of a full-term normal delivery, with
! [' m  A: p! L* e0 P3 t  L' ba birth weight of 7 lb 14 oz, and birth length of1 Y% C$ P: B; A
20 inches. He was breast-fed throughout the first year* F, R7 H, {3 e* G, @
of life and was still receiving breast milk along with% ^$ ~: z  R6 g& w: F* `9 r
solid food. He had no hospitalizations or surgery,
1 R! N, L: R0 Sand his psychosocial and psychomotor development
6 r$ H# ]# A$ ^& L2 Hwas age appropriate./ n; |- Q) e8 Q1 P) T6 P
The family history was remarkable for the father,( S% v9 ^7 n! [! ]5 m
who was diagnosed with hypothyroidism at age 16,
5 [  r4 y( t9 _; ^which was treated with thyroxine. The father’s* Z8 [# s1 y* k8 K$ Z$ R
height was 6 feet, and he went through a somewhat
' \& M& E9 J7 N# N) Oearly puberty and had stopped growing by age 14.( w: T& W6 x$ Z. i$ f) h$ k2 l+ ^  L- ?) Q
The father denied taking any other medication. The! F' N& ~& }; M. I% J9 ~- U5 {
child’s mother was in good health. Her menarche4 J5 n. B" C$ Q' Y5 m
was at 11 years of age, and her height was at 5 feet* ]6 y1 e! r# V& A2 ^, {# z
5 inches. There was no other family history of pre-4 G8 F8 {0 H  k4 Z- K
cocious sexual development in the first-degree rela-
3 Z  f2 C* W* T' s' _# ^tives. There were no siblings.( W8 V8 V- L- H6 M# A% m- b6 U; a
Physical Examination* ]; R3 J& p6 x: L. E( b) l1 B
The physical examination revealed a very active,# \  A5 t) V- y
playful, and healthy boy. The vital signs documented+ C& _( E, B, j
a blood pressure of 85/50 mm Hg, his length was: Q& B$ W2 e2 R- E4 K' L( Y( I9 g# |
90 cm (>97th percentile), and his weight was 14.4 kg% q% R  m4 D8 p$ K* h9 I  y' r
(also >97th percentile). The observed yearly growth! T& I, h( s# I4 l  ]7 P7 A6 k
velocity was 30 cm (12 inches). The examination of
& t. I" A7 k. F6 h  n3 vthe neck revealed no thyroid enlargement.
  \/ X- v/ p3 g) ?# jThe genitourinary examination was remarkable for9 j( A$ q, P: u5 l
enlargement of the penis, with a stretched length of+ g) I8 b9 o) t1 {6 E
8 cm and a width of 2 cm. The glans penis was very well
9 S7 r! T1 j# F( {# [/ E. V3 i" b7 h6 cdeveloped. The pubic hair was Tanner II, mostly around
  }$ d: }4 E5 w: U2 V540
. o% |  i( z+ N4 ?/ Hat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 P7 p! P: s6 u, Wthe base of the phallus and was dark and curled. The0 @* e/ F7 Y9 @& C' Y
testicular volume was prepubertal at 2 mL each.' T6 P, H# p" |  G' ^% Q
The skin was moist and smooth and somewhat9 Y, q# D, x: r( `' v: s2 z
oily. No axillary hair was noted. There were no1 o- Y# X8 e9 \# @1 V3 [
abnormal skin pigmentations or café-au-lait spots.
- f% `' j9 ~4 P2 e% \Neurologic evaluation showed deep tendon reflex 2+
  ?7 L2 j9 I! `/ M& [6 zbilateral and symmetrical. There was no suggestion
; S' q. `- `9 T' e0 ?6 Cof papilledema.7 z, [; M' ]! s( V! o
Laboratory Evaluation
% [) k# C8 L- p$ Z0 IThe bone age was consistent with 28 months by, S$ C  j: [+ R7 f. S
using the standard of Greulich and Pyle at a chrono-5 }/ A% u& u5 s8 V( @  l8 ?0 O) l
logic age of 16 months (advanced).5 Chromosomal1 L# V/ Y0 R; y
karyotype was 46XY. The thyroid function test6 y) n. P! `# x$ r) w9 l3 j) I
showed a free T4 of 1.69 ng/dL, and thyroid stimu-+ ?; T8 v' c" `5 b" a, D- L: e% t0 i
lating hormone level was 1.3 µIU/mL (both normal).
  h" A: ~4 A3 r) F6 N2 n4 N4 tThe concentrations of serum electrolytes, blood
7 f; j' w/ z9 k- u7 v: o$ ^urea nitrogen, creatinine, and calcium all were
: H& H6 V( c- A7 w$ y! Twithin normal range for his age. The concentration1 S( `. F+ c5 V$ `/ F. Z3 }. O/ q
of serum 17-hydroxyprogesterone was 16 ng/dL" l! \& m% @2 M9 q' _
(normal, 3 to 90 ng/dL), androstenedione was 208 }/ ?5 K; I! `% S% Y$ t
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
  z8 {6 y2 W/ j- P9 Dterone was 38 ng/dL (normal, 50 to 760 ng/dL),9 v$ s3 j- A- L/ F: ~3 \/ I
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
9 k( o/ o6 {3 |5 U$ c. q. B49ng/dL), 11-desoxycortisol (specific compound S)$ n! A* W/ W* n7 ~2 I* \0 }! R( F
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
7 ?8 w% B& w/ v" U' ptisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total; Q/ }8 R' u0 Y, L
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
5 A1 F% |) g4 D( Fand β-human chorionic gonadotropin was less than! R1 Y# X! |! c) ~' H0 u9 S! |
5 mIU/mL (normal <5 mIU/mL). Serum follicular4 d$ J& O9 P- j& h
stimulating hormone and leuteinizing hormone# u" O/ {8 V2 K0 |" @
concentrations were less than 0.05 mIU/mL
" l0 N" P6 _' r8 X8 B# X* e/ ?(prepubertal).7 n' F3 L1 R' I% W5 {# w
The parents were notified about the laboratory
* G" E" G" E) g; tresults and were informed that all of the tests were4 t$ M1 D) d1 Z, u
normal except the testosterone level was high. The8 S! j5 V) ~, M4 ?& Z
follow-up visit was arranged within a few weeks to! U8 l* G3 t0 G6 G
obtain testicular and abdominal sonograms; how-" Z/ j' u- h& Q% A# D& J
ever, the family did not return for 4 months.
' ?- d) y. }7 b& Z/ dPhysical examination at this time revealed that the
) j* M$ a' {8 }- ~, J$ pchild had grown 2.5 cm in 4 months and had gained# e$ K9 `( }5 m6 X+ |3 O0 q
2 kg of weight. Physical examination remained. e  h/ h8 a( J) ]9 l' A2 P) d
unchanged. Surprisingly, the pubic hair almost com-' u6 U( A! D9 \" l( q& h) Q! M2 J0 i9 q
pletely disappeared except for a few vellous hairs at
0 [! v8 S$ k6 uthe base of the phallus. Testicular volume was still 2
3 q5 j9 C+ O0 K- R3 cmL, and the size of the penis remained unchanged.
3 d1 ?* ^6 O& v+ ]% q  s6 L, SThe mother also said that the boy was no longer hav-# L" V! ~' A' F  f9 p! C/ f6 U
ing frequent erections.
! e2 a# n) C; r' U% p" JBoth parents were again questioned about use of
, T9 J/ P3 H: ~8 g3 b. ~6 zany ointment/creams that they may have applied to$ Q* M3 l) g" e, N
the child’s skin. This time the father admitted the9 H( Q- X; q5 i+ K2 q1 A. L. E
Topical Testosterone Exposure / Bhowmick et al 541
' i. O, v- T* h1 d: xuse of testosterone gel twice daily that he was apply-5 u) N7 z$ j' Z
ing over his own shoulders, chest, and back area for
# ~5 \' g  r1 m1 G! U+ ya year. The father also revealed he was embarrassed
6 R: T" Z3 l' c6 i+ r  `" n8 e& wto disclose that he was using a testosterone gel pre-
, P0 b% M. F& I5 qscribed by his family physician for decreased libido4 a$ }" I9 X" h) }; E7 T
secondary to depression.4 ~, I" L( O- E) @$ n9 E4 ^
The child slept in the same bed with parents.. A% X0 u& Q3 @5 p2 Y
The father would hug the baby and hold him on his$ M0 z5 s  Z5 R: v3 T
chest for a considerable period of time, causing sig-
1 J9 s. U+ i. ?& ~+ t3 ?nificant bare skin contact between baby and father.
7 ^6 ^4 q6 o# k  a2 J9 Z; e: PThe father also admitted that after the phone call,
, t5 P0 a0 @% X9 M8 twhen he learned the testosterone level in the baby; }' q  w" P0 R/ a! U
was high, he then read the product information% T) I5 R" P- s; }; x+ v- Y' w9 {) R# \
packet and concluded that it was most likely the rea-/ o0 r: A  Q1 U! W; e/ f7 G* ]5 m& ?
son for the child’s virilization. At that time, they  g+ w5 ]/ ~/ A; Y5 C, V
decided to put the baby in a separate bed, and the
# u8 {0 Q  I, W3 g5 {! n/ Gfather was not hugging him with bare skin and had
9 N5 ~+ d) W  [" X, x3 ]been using protective clothing. A repeat testosterone" ?! |+ `- L" p* k4 @. a# a
test was ordered, but the family did not go to the
& t: [  e9 {3 p6 U) g% n2 tlaboratory to obtain the test.6 g% x/ Y! B# q5 b: D
Discussion
" p5 E. U) F: pPrecocious puberty in boys is defined as secondary
3 A- l8 m( T2 B) B3 e. I4 s) G! w6 `( H' wsexual development before 9 years of age.1,4
% a- S+ M4 i9 e% J4 kPrecocious puberty is termed as central (true) when
  i& ^8 f' W# r2 W" X( ]it is caused by the premature activation of hypo-: q! m, b7 P& X* n0 E+ X
thalamic pituitary gonadal axis. CPP is more com-
/ o6 M3 G1 B4 o3 Qmon in girls than in boys.1,3 Most boys with CPP0 E# n5 D% g3 S
may have a central nervous system lesion that is
' o4 D5 z- k' B# y4 V' jresponsible for the early activation of the hypothal-5 F0 s# F. h1 Z* n
amic pituitary gonadal axis.1-3 Thus, greater empha-" X: W8 N& I# x: p. v' G8 O$ c9 {& }
sis has been given to neuroradiologic imaging in4 C7 _! w3 X2 f* D" f4 T. ^4 m
boys with precocious puberty. In addition to viril-
9 U9 L0 C6 d9 a* _+ U0 |  Jization, the clinical hallmark of CPP is the symmet-3 p$ i& x; r. H
rical testicular growth secondary to stimulation by0 ~/ t5 ?4 c6 U% P2 j
gonadotropins.1,3
, h8 s8 N9 l4 M  Z* h! xGonadotropin-independent peripheral preco-
$ M( H6 e  M- d+ i. vcious puberty in boys also results from inappropriate4 Q8 b0 s, |+ h3 Z) T- Q# p
androgenic stimulation from either endogenous or
- E9 }  x2 ^4 e- u9 uexogenous sources, nonpituitary gonadotropin stim-
- H5 J# q+ y3 d2 e3 r* Bulation, and rare activating mutations.3 Virilizing& C0 M3 R1 v4 W5 h
congenital adrenal hyperplasia producing excessive  f* A. I1 P4 U+ w
adrenal androgens is a common cause of precocious3 [1 o/ a+ A% J) w
puberty in boys.3,4
. l5 _3 C" _1 |/ eThe most common form of congenital adrenal- V- b8 A& a+ c5 E& I
hyperplasia is the 21-hydroxylase enzyme deficiency.
1 K- J2 K) r6 {: w4 ]8 Y0 R7 e! D1 [The 11-β hydroxylase deficiency may also result in
4 B8 E: ?3 u* l6 _3 O( |excessive adrenal androgen production, and rarely,
6 e5 l; u1 b- k1 L7 z$ Wan adrenal tumor may also cause adrenal androgen
( [6 W  m! W7 r) [7 j4 Vexcess.1,32 F( N, u7 `& `6 j7 c
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( Q; o8 T/ {3 K9 d. D' Y/ _$ F542 Clinical Pediatrics / Vol. 46, No. 6, July 2007* X" ]( _, U$ q
A unique entity of male-limited gonadotropin-
# Z! e2 ]# l4 }; m' z- S# Oindependent precocious puberty, which is also known
* Z5 Y" E: n* Q8 F# q5 tas testotoxicosis, may cause precocious puberty at a  ?+ V5 m) X* G+ n1 ^5 r& b7 ]8 y% v+ e
very young age. The physical findings in these boys
( f3 |* s! f. s: pwith this disorder are full pubertal development,8 W) }* L! D5 |6 _3 b7 P, x
including bilateral testicular growth, similar to boys( J+ R: z0 O$ Y( J7 X
with CPP. The gonadotropin levels in this disorder
) ~, B* @1 a$ t7 F! U  Oare suppressed to prepubertal levels and do not show5 M4 g3 k3 c2 R
pubertal response of gonadotropin after gonadotropin-
7 x; O# i0 T) m. Kreleasing hormone stimulation. This is a sex-linked0 w# s$ y. ~. p
autosomal dominant disorder that affects only# u  G3 R  X4 [3 L5 q' i
males; therefore, other male members of the family- s; \, A9 }3 d/ {- Z( O6 g3 N7 f
may have similar precocious puberty.3
& w5 l6 M3 N; l2 [* ~, pIn our patient, physical examination was incon-0 H$ W7 b$ w& ]5 _  [
sistent with true precocious puberty since his testi-
+ W, w5 y9 ]8 k  ]* `( Zcles were prepubertal in size. However, testotoxicosis! _" \8 e, I5 {
was in the differential diagnosis because his father
& l2 c8 n$ T! Y$ n) g: K2 Bstarted puberty somewhat early, and occasionally,
) I2 Y; \' M4 j3 ~testicular enlargement is not that evident in the/ B; f7 {  s$ n) L, P
beginning of this process.1 In the absence of a neg-
# K" U! h$ c: C2 ^% ~! mative initial history of androgen exposure, our5 ?0 W7 S+ k4 _3 z6 ]2 A5 H$ Y, C* a
biggest concern was virilizing adrenal hyperplasia,
5 d) N  b2 D8 I# F+ b  teither 21-hydroxylase deficiency or 11-β hydroxylase3 _; z' |! R3 A, H$ O: Y- h
deficiency. Those diagnoses were excluded by find-
, a& F1 Q2 B) X) n% Ping the normal level of adrenal steroids.
/ S3 {+ t2 j% D# g* \+ ?( n- r3 IThe diagnosis of exogenous androgens was strongly
! Q7 F: [$ i* osuspected in a follow-up visit after 4 months because: [, {3 D: o2 B3 s
the physical examination revealed the complete disap-
7 T( p' X/ [) I# Q6 D) Lpearance of pubic hair, normal growth velocity, and
8 P& y; ~0 C  C+ ]" N; G3 V9 Bdecreased erections. The father admitted using a testos-
' k+ Y: x/ h+ v" Yterone gel, which he concealed at first visit. He was
0 O& S+ U- x, yusing it rather frequently, twice a day. The Physicians’
- H4 c# Q0 j7 }% e9 e: q/ }/ D, @) uDesk Reference, or package insert of this product, gel or
; q- N) j5 n3 M" hcream, cautions about dermal testosterone transfer to
$ R' b# l# J1 kunprotected females through direct skin exposure.
5 C( z4 T- ~. n! j$ TSerum testosterone level was found to be 2 times the
" F/ Q7 ^6 }* ?  h" h2 N& R8 o/ m+ jbaseline value in those females who were exposed to; d' q8 h6 \  R  {  }
even 15 minutes of direct skin contact with their male
) N2 D5 Z) X3 Q0 m3 z% qpartners.6 However, when a shirt covered the applica-
1 e7 ^5 u) N7 W; z# u1 ntion site, this testosterone transfer was prevented.. L) n$ S6 j2 g
Our patient’s testosterone level was 60 ng/mL,2 [! p4 E0 H7 O4 ]2 C
which was clearly high. Some studies suggest that
# L' [0 H& M# r% d. S4 ndermal conversion of testosterone to dihydrotestos-
% }5 T" ]  Z( q. f+ I: {, bterone, which is a more potent metabolite, is more
$ k  A2 E9 I1 R# nactive in young children exposed to testosterone9 n3 z- |' C" ~7 r9 ?7 Q
exogenously7; however, we did not measure a dihy-
' S/ ~6 n+ ~0 I& ndrotestosterone level in our patient. In addition to
0 @) X9 a" M% p! Zvirilization, exposure to exogenous testosterone in+ }" z2 `+ i& ]6 y
children results in an increase in growth velocity and) s; r1 L8 J% @1 f
advanced bone age, as seen in our patient.
; ?; N$ ?  e9 y2 J2 ?The long-term effect of androgen exposure during' e( k% d0 X8 ~, w# Z  l
early childhood on pubertal development and final6 r! Z' C. \0 i& u) h; D
adult height are not fully known and always remain: o% w) j) H) e! t2 d% C" l% v
a concern. Children treated with short-term testos-
6 j4 u, [5 r+ ]8 Fterone injection or topical androgen may exhibit some
8 E# F9 e0 ~. w/ ?  gacceleration of the skeletal maturation; however, after
7 B' n6 |5 B4 j: ]* hcessation of treatment, the rate of bone maturation! S9 R7 S) q. s4 R  ~( t  i7 ~/ D) S& g
decelerates and gradually returns to normal.8,9
3 B' {& r6 ?" o$ Z. mThere are conflicting reports and controversy
/ d! S0 P6 Q7 k# N9 J/ Jover the effect of early androgen exposure on adult- Q& K; ]3 p" X/ X0 m4 U
penile length.10,11 Some reports suggest subnormal
, U" y0 i% a' l2 wadult penile length, apparently because of downreg-
$ `2 k5 r) E9 a8 o! g& _" W  Zulation of androgen receptor number.10,12 However,
* ~" t7 G5 D8 ^3 D" p9 q& sSutherland et al13 did not find a correlation between
- b' {( D) w$ G5 k1 d' Q6 v* O) y9 Kchildhood testosterone exposure and reduced adult
2 l- I# G( _4 p2 {# Kpenile length in clinical studies.
3 Y2 y5 ^, d+ W" `Nonetheless, we do not believe our patient is
6 x6 v1 g7 T$ M6 S* R9 Agoing to experience any of the untoward effects from- `5 W  F; P* O% K
testosterone exposure as mentioned earlier because
$ B1 E* X1 {; p9 B% kthe exposure was not for a prolonged period of time.
/ W% O1 k+ {2 c8 Q. aAlthough the bone age was advanced at the time of
8 `3 \" \# y$ R, Pdiagnosis, the child had a normal growth velocity at% D0 u4 V  B4 ^7 k- d
the follow-up visit. It is hoped that his final adult- m& Z+ `7 S! R+ F9 M, f
height will not be affected.
+ |7 h& g0 a% k' Q4 M. OAlthough rarely reported, the widespread avail-
6 k! X1 H# Y1 X' B+ x, ~' C$ jability of androgen products in our society may0 A" W) r: I  k6 S# {, O
indeed cause more virilization in male or female
( L; U2 l0 y& D$ dchildren than one would realize. Exposure to andro-
; ~5 X6 `. U. p) K* Igen products must be considered and specific ques-' ^5 v1 C: I. o8 E" Q' B
tioning about the use of a testosterone product or
* }3 Z! C7 J8 R& H  C) |gel should be asked of the family members during
7 L0 Z  m& h: k, k7 X0 u" l6 ^1 Hthe evaluation of any children who present with vir-# H, V0 O+ J( \6 \
ilization or peripheral precocious puberty. The diag-! t6 s: j$ |3 p* s* A
nosis can be established by just a few tests and by$ P7 C% b1 n" u
appropriate history. The inability to obtain such a) C8 I5 ^" r+ q$ r8 J- }3 Z
history, or failure to ask the specific questions, may
6 ~* ~8 L$ u% U9 f4 B+ m8 _result in extensive, unnecessary, and expensive
" m2 H; i/ Q0 I; Y# S. U; G( linvestigation. The primary care physician should be! H' g" v- r, Y
aware of this fact, because most of these children
' h+ D- S9 `4 c# i( f6 Jmay initially present in their practice. The Physicians’  S0 r% w5 I( T: s  G  Q. E
Desk Reference and package insert should also put a& F7 V; f" k7 r& D& `0 P
warning about the virilizing effect on a male or2 [  q% [4 W" l  Z
female child who might come in contact with some-$ y# w7 v8 D, r& e. s& A
one using any of these products.5 [8 n7 V" h, H. C/ S0 y' v  d
References
: l- m7 {: x% {1. Styne DM. The testes: disorder of sexual differentiation
  k5 q( G) E4 ^) nand puberty in the male. In: Sperling MA, ed. Pediatric6 Q) y7 a! H; d) Z' S* P/ u+ e
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;$ r; Y2 |. Q  Z: j
2002: 565-628.
. P" l/ K# _8 H2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
1 k. m( c( ^& g" h$ Jpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
( G! E5 k1 ~. g. D' I6 H4 h1 B& o- rBoy Induced by Indirect Topical
/ b; P. c& E$ a% _# r; I8 TExposure to Testosterone
+ B" D* f6 Y6 i8 v4 {Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 q- T' f1 l4 _0 S: t/ J" oand Kenneth R. Rettig, MD1! ?" ?# _. w# U5 B
Clinical Pediatrics
; i' Y3 f. E# `- E0 Y* H& dVolume 46 Number 6* Y8 P* }+ r2 V: n6 i# N  C: a
July 2007 540-543
5 F: L- c4 h5 N) V; F© 2007 Sage Publications
/ o  @& k3 x( V- D2 R% i/ K! Y7 s10.1177/0009922806296651
; N. P+ W$ H* K8 t2 P& fhttp://clp.sagepub.com
7 J0 v: w2 M8 H" P7 }* T; Z. Khosted at5 i* t2 @4 Y. b: s" Q
http://online.sagepub.com0 v- o; v" N# @; K
Precocious puberty in boys, central or peripheral,' p7 R# L4 Q8 G2 Q; {  I+ Q: L
is a significant concern for physicians. Central
$ y& B* Q; Q0 e5 J: R6 Jprecocious puberty (CPP), which is mediated
$ g1 w8 Y& @- U1 N$ i6 ythrough the hypothalamic pituitary gonadal axis, has) c1 }* f' i" B( a
a higher incidence of organic central nervous system
# P# I* r" w! ]$ _8 z/ M- Dlesions in boys.1,2 Virilization in boys, as manifested4 ^8 f0 a( f4 w4 E
by enlargement of the penis, development of pubic
% b& F  j6 N- `3 S+ Phair, and facial acne without enlargement of testi-
1 V: A4 f" B3 E& hcles, suggests peripheral or pseudopuberty.1-3 We
0 b: P7 I( t0 I) S$ Z' G( P& {, Mreport a 16-month-old boy who presented with the% a/ d* t4 O+ z
enlargement of the phallus and pubic hair develop-
% N: E. {0 Y+ U2 Q- b9 z/ r7 Zment without testicular enlargement, which was due/ l6 c3 t$ K; e8 c' x
to the unintentional exposure to androgen gel used by+ h. t& Z! O) \: n+ f0 ~
the father. The family initially concealed this infor-1 W/ e& X$ C. i5 q/ D
mation, resulting in an extensive work-up for this! X1 R; ?5 C3 q0 Q' K4 N
child. Given the widespread and easy availability of
+ D6 K) y) o& {4 W  _testosterone gel and cream, we believe this is proba-+ ?! U  i/ O- C9 g; w
bly more common than the rare case report in the5 B" R2 I. a% j
literature.4
5 _3 D3 R7 j$ f& c' aPatient Report9 O) s0 w9 r4 `: E& i) A$ e
A 16-month-old white child was referred to the7 a0 I& H8 Q, l! r6 _
endocrine clinic by his pediatrician with the concern
" J3 O% M2 O& Y* ]of early sexual development. His mother noticed
8 k% M. e3 z) T2 _. z" mlight colored pubic hair development when he was
7 k) z3 J: E, B, s; LFrom the 1Division of Pediatric Endocrinology, 2University of
$ n. f' f& G- q+ _+ u4 JSouth Alabama Medical Center, Mobile, Alabama.
: R% ~& N9 n6 M2 }# Q$ JAddress correspondence to: Samar K. Bhowmick, MD, FACE,9 z* `& g2 K/ T4 H
Professor of Pediatrics, University of South Alabama, College of" @4 A- ?' k, E# ]  @% A; V
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;4 c6 b; y6 O3 U, q
e-mail: [email protected].
" ]9 N$ @# v. U3 Habout 6 to 7 months old, which progressively became
- r( f8 I, @  Y& hdarker. She was also concerned about the enlarge-9 _$ o, j* p3 S: k0 O
ment of his penis and frequent erections. The child
  B0 S& H, O# owas the product of a full-term normal delivery, with$ m, z$ X7 z/ G) L# J& t
a birth weight of 7 lb 14 oz, and birth length of3 _$ y* V) |  p/ T# F% R7 |
20 inches. He was breast-fed throughout the first year! a+ }0 V1 \6 a4 I
of life and was still receiving breast milk along with
$ q, e/ N0 q- R# V4 dsolid food. He had no hospitalizations or surgery,
- z% a! E, H5 z; }and his psychosocial and psychomotor development
+ V  G0 [8 M* J- b' vwas age appropriate.
7 g6 s4 X+ E( e. g6 U; AThe family history was remarkable for the father,! f5 @  ^7 j  F5 a
who was diagnosed with hypothyroidism at age 16,6 p8 R- v6 v. d2 F6 v
which was treated with thyroxine. The father’s' q. s4 v& y6 S" N8 w1 v
height was 6 feet, and he went through a somewhat
, I+ D+ b5 t0 Oearly puberty and had stopped growing by age 14.9 t, y! ]- f6 \
The father denied taking any other medication. The
: T% h, [' I. e# fchild’s mother was in good health. Her menarche. T% b& X8 s( x1 O- r7 B$ Z0 `; s
was at 11 years of age, and her height was at 5 feet# c) }+ l0 m  J1 S2 o
5 inches. There was no other family history of pre-
8 j, L) A/ e- jcocious sexual development in the first-degree rela-
7 S! k8 K  l& k- G& U* itives. There were no siblings.. X: [+ h- ^" B9 d8 O3 i
Physical Examination
6 h1 ?, x. L% ]) @8 v1 DThe physical examination revealed a very active,, O7 \5 K3 o6 k' z
playful, and healthy boy. The vital signs documented" m/ I, ~( m# F' L$ s- H
a blood pressure of 85/50 mm Hg, his length was, E/ r0 Z) \8 S, ~( {6 Q: A7 @- V3 i% j
90 cm (>97th percentile), and his weight was 14.4 kg
7 [" S# ]7 a4 l/ ?' e& i; N+ f(also >97th percentile). The observed yearly growth# b' t% t; g! s0 M: H  t2 M
velocity was 30 cm (12 inches). The examination of
4 N; B2 {! X( S& Sthe neck revealed no thyroid enlargement.
, v5 j0 ~: Z! K) aThe genitourinary examination was remarkable for
% P4 s& H& n: Y, T1 p3 K0 I8 x  Senlargement of the penis, with a stretched length of- R" T& X/ o. s% H8 _4 e
8 cm and a width of 2 cm. The glans penis was very well; f7 ?0 V$ ]8 @: K; Y* _+ |# Q
developed. The pubic hair was Tanner II, mostly around( s& B8 k1 q& Y" Q7 t/ p( o- z
540
& u$ {/ n2 p" B. r. R' ]at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 S5 C! T" j0 M4 X8 H  E6 r
the base of the phallus and was dark and curled. The+ R4 S. A5 X( o: R% L9 d2 F
testicular volume was prepubertal at 2 mL each.
. d. l+ `$ [5 _4 v1 V: j* mThe skin was moist and smooth and somewhat
6 t: D" ^+ @% v$ n, I- j5 Uoily. No axillary hair was noted. There were no- w/ L( z! h- y
abnormal skin pigmentations or café-au-lait spots.5 P. h7 ]. k8 Q$ M, w3 ^  C: h
Neurologic evaluation showed deep tendon reflex 2+; t: Z" i$ [1 F8 [* O8 ^) J% @
bilateral and symmetrical. There was no suggestion
0 _: I& P9 N& y3 x4 Z# uof papilledema.( I) q! ?1 M5 |5 M
Laboratory Evaluation
& z' G8 ~6 k# X; k6 CThe bone age was consistent with 28 months by4 Y# |# b% b8 d0 |" j
using the standard of Greulich and Pyle at a chrono-
) x% c5 |( z0 ]: _6 n' Slogic age of 16 months (advanced).5 Chromosomal% Q. L, B8 `9 {4 T. A
karyotype was 46XY. The thyroid function test( ~. b. M9 X4 f+ b; x
showed a free T4 of 1.69 ng/dL, and thyroid stimu-; b7 A3 R5 h- k, U+ u4 m
lating hormone level was 1.3 µIU/mL (both normal).
1 ^# _. |+ W% p5 dThe concentrations of serum electrolytes, blood6 S* G9 H! ?  e- N8 ^4 E
urea nitrogen, creatinine, and calcium all were
7 v' F* @. `; q; ~7 q6 n3 i0 O% j- wwithin normal range for his age. The concentration
# H; M0 R5 R, L) c0 Tof serum 17-hydroxyprogesterone was 16 ng/dL4 L: v4 v8 V2 k; x
(normal, 3 to 90 ng/dL), androstenedione was 20! Y' `# a) W3 z% x2 m5 D% N+ K1 }' m
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-/ `4 s1 i" w; b
terone was 38 ng/dL (normal, 50 to 760 ng/dL),: n" w! |3 H* `. H; ^7 Y
desoxycorticosterone was 4.3 ng/dL (normal, 7 to9 J: T" T; }( X1 U! N
49ng/dL), 11-desoxycortisol (specific compound S)$ e; B- p9 X& P/ D2 J
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-4 N* e( R4 }# y  y: Y7 y
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total! j- y4 i( p( p5 ]
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
; R% d  q7 l! D# u; o# gand β-human chorionic gonadotropin was less than
, @$ j" \1 K3 \8 B' E5 mIU/mL (normal <5 mIU/mL). Serum follicular
4 j# z2 A5 |" W+ [4 f" y* ^stimulating hormone and leuteinizing hormone
8 h) F/ C$ t# z1 aconcentrations were less than 0.05 mIU/mL
: m7 q+ T5 {+ R+ |( z( l5 |(prepubertal).5 D, I% R( J) ?% w' U! g0 q
The parents were notified about the laboratory
' ^$ Y: o. J& a8 H) Lresults and were informed that all of the tests were
# h' ^% x- V& l) anormal except the testosterone level was high. The
& L( m$ S+ j- L  K- rfollow-up visit was arranged within a few weeks to$ ?6 W4 y) Q7 T6 ]  h
obtain testicular and abdominal sonograms; how-
/ Z; l* ~- b. s$ k/ `ever, the family did not return for 4 months.0 x4 v7 t% v2 I2 Q# z6 W% S
Physical examination at this time revealed that the
7 \, w) j4 l3 ]/ K6 `" t3 Kchild had grown 2.5 cm in 4 months and had gained
% U6 \* a8 ]! e* X4 A8 |2 kg of weight. Physical examination remained
* O9 J3 k8 |3 J( l/ }1 u: f8 qunchanged. Surprisingly, the pubic hair almost com-# ?' K7 U* C7 k* B
pletely disappeared except for a few vellous hairs at! U/ d/ M" r) I! s/ A7 C( l
the base of the phallus. Testicular volume was still 2
6 z& \  p# o7 ymL, and the size of the penis remained unchanged.7 ~/ _/ b& ]6 c7 F( G9 A
The mother also said that the boy was no longer hav-, X/ d6 q) K5 i4 o# Q
ing frequent erections.! {& O8 ]& ?) i& W  V+ z
Both parents were again questioned about use of
. @  f* }+ A0 wany ointment/creams that they may have applied to2 Y0 k, u  @8 d& H0 q
the child’s skin. This time the father admitted the
9 x& I( O: D) j" M/ J- g) w- n. ETopical Testosterone Exposure / Bhowmick et al 541
! p6 n0 D2 B: [# t& F! Ruse of testosterone gel twice daily that he was apply-
# b0 W9 q, b/ ]( G* B& o" B7 w5 f9 Fing over his own shoulders, chest, and back area for
9 R6 W" e/ @& S; U5 la year. The father also revealed he was embarrassed
. Z8 D- |. ?- m" B7 pto disclose that he was using a testosterone gel pre-
! G( s6 F0 j) Y" V9 Gscribed by his family physician for decreased libido
4 R' q9 d2 V) ]2 Ysecondary to depression.
( B9 K: R( D  r1 L" C( iThe child slept in the same bed with parents.
9 ]6 L( H* G$ e, SThe father would hug the baby and hold him on his6 L) c% e5 i- k# m7 s
chest for a considerable period of time, causing sig-6 V8 f$ N$ Q& n. x2 ~) b
nificant bare skin contact between baby and father.9 h' V" |. g( u- r
The father also admitted that after the phone call,. K$ T% [; C- j- @! n6 ]9 T
when he learned the testosterone level in the baby3 t9 ~: n3 t& M1 n! x1 l
was high, he then read the product information
; Z1 Y0 a9 X7 C6 W8 l, xpacket and concluded that it was most likely the rea-. x3 |( _0 N7 P" C# m8 J1 u
son for the child’s virilization. At that time, they
0 c& h. o1 c7 |7 Y* J% O! Kdecided to put the baby in a separate bed, and the9 H7 W  i' ?$ A, W/ `
father was not hugging him with bare skin and had7 d% N  T5 G6 p& c
been using protective clothing. A repeat testosterone7 E0 |' E+ H9 n$ i: L9 M
test was ordered, but the family did not go to the
* P6 s0 v$ A3 }+ X% a7 d3 ~laboratory to obtain the test., y: x: y$ [/ s! U8 Y
Discussion
+ d& I, f# m0 `% C1 R# Z! ]( XPrecocious puberty in boys is defined as secondary, ~$ N2 l$ i* c$ ^* ^9 j- }: b3 v
sexual development before 9 years of age.1,4
% \" v+ h* Y" q4 u. b0 U) V6 rPrecocious puberty is termed as central (true) when2 V! q/ ^1 T& ?4 o6 I: h
it is caused by the premature activation of hypo-' l2 \9 t! y! K: Y4 s$ Y
thalamic pituitary gonadal axis. CPP is more com-
/ n( r) l# r( O+ v9 y: G8 jmon in girls than in boys.1,3 Most boys with CPP
; T& `% b2 `0 i4 {% tmay have a central nervous system lesion that is, O! P# g+ p1 F+ u$ Y( A" }6 v
responsible for the early activation of the hypothal-
- L- Z  o+ w8 R9 famic pituitary gonadal axis.1-3 Thus, greater empha-
. ^* `9 s! F7 `7 I& s) Msis has been given to neuroradiologic imaging in
3 ]& W" x* q* t% e+ Jboys with precocious puberty. In addition to viril-- c+ v! A! i7 P! Z: M7 e6 b
ization, the clinical hallmark of CPP is the symmet-* y3 u+ m/ k3 b7 C% W$ v
rical testicular growth secondary to stimulation by
4 w5 i: `, h( ~# T& A" o3 r1 l+ }gonadotropins.1,39 Q' r! S2 H: Z5 d9 ^
Gonadotropin-independent peripheral preco-: j/ o4 C0 S1 Q, E
cious puberty in boys also results from inappropriate
: R! j' X9 `& R  t/ |, vandrogenic stimulation from either endogenous or! r- d& U* o3 O- O4 b
exogenous sources, nonpituitary gonadotropin stim-( F/ \& j/ [  }
ulation, and rare activating mutations.3 Virilizing
6 h! i! V3 _, v! b" r' Gcongenital adrenal hyperplasia producing excessive
( ~- U( k) q% N0 }. _3 Yadrenal androgens is a common cause of precocious) b' d+ O: t& |- {! n
puberty in boys.3,4
/ Q: _& ?3 B3 b  _. {6 [, x! L- UThe most common form of congenital adrenal0 Z! z( s9 [4 z( f0 {
hyperplasia is the 21-hydroxylase enzyme deficiency.
! D, L3 ^6 l8 M) HThe 11-β hydroxylase deficiency may also result in
' f1 c+ @3 m6 @; n4 v  y% gexcessive adrenal androgen production, and rarely,$ e/ p0 L1 N5 e- U; |6 ?
an adrenal tumor may also cause adrenal androgen
2 E! P: m0 E7 h2 K8 H# Gexcess.1,38 V0 l  W  D: J. u/ ~- X- P
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
. Q  B: u7 d. _5 D( U542 Clinical Pediatrics / Vol. 46, No. 6, July 2007* ]! [8 W$ R, N, T1 h
A unique entity of male-limited gonadotropin-# N+ B. F; u$ [$ H$ W0 P
independent precocious puberty, which is also known# j2 u& V2 N$ V' @4 Q' N
as testotoxicosis, may cause precocious puberty at a
; }9 F4 U' W0 o7 f! P* Q1 rvery young age. The physical findings in these boys
2 m9 J+ ?3 w! Y4 C6 mwith this disorder are full pubertal development,# N; d: g1 j* O4 R7 c, M0 z" Q
including bilateral testicular growth, similar to boys/ j" A' b! O: P0 D
with CPP. The gonadotropin levels in this disorder
0 n. Y! v$ [$ [) xare suppressed to prepubertal levels and do not show0 X/ U& Z+ h# [- v& ^
pubertal response of gonadotropin after gonadotropin-" C; w  j; ~% F% I; s7 X+ T
releasing hormone stimulation. This is a sex-linked$ L! Y, E3 i9 A& F2 ]
autosomal dominant disorder that affects only0 e+ r9 x: t: r( c/ |; k- ?& k2 n4 h
males; therefore, other male members of the family2 a8 K5 C: h2 _/ e+ N4 R! u
may have similar precocious puberty.3
3 {1 a6 E" ?! M$ [In our patient, physical examination was incon-
9 ^: C) \+ U, y! o: _3 rsistent with true precocious puberty since his testi-
! q( {; V  s# N2 X- s; Ecles were prepubertal in size. However, testotoxicosis9 n6 y9 }% E" \9 ^
was in the differential diagnosis because his father4 V7 t; R( e8 g9 w
started puberty somewhat early, and occasionally,$ {. ]& W* W  l. ]1 V9 w" _
testicular enlargement is not that evident in the
5 O/ S7 F3 \# u1 \" P/ Qbeginning of this process.1 In the absence of a neg-* i) z9 N& \6 J# d
ative initial history of androgen exposure, our/ j, ]! a1 |9 N
biggest concern was virilizing adrenal hyperplasia,) u; B* r: U8 X- |
either 21-hydroxylase deficiency or 11-β hydroxylase
9 P( Z. L% R6 p' p% T" e( @) u/ k6 Rdeficiency. Those diagnoses were excluded by find-
/ b- r4 c) v' l$ N; @ing the normal level of adrenal steroids.% A" c' P; }8 A6 u- U/ S' {
The diagnosis of exogenous androgens was strongly; [# t; q. l: y/ }: @7 t0 m
suspected in a follow-up visit after 4 months because( k3 E8 m, e- i& j
the physical examination revealed the complete disap-
4 _2 k: z& |+ apearance of pubic hair, normal growth velocity, and
( `6 b+ h* T) `9 d. ?decreased erections. The father admitted using a testos-
& `( G/ h, b+ i+ C# [2 a. dterone gel, which he concealed at first visit. He was
) x! V2 v+ O( H( Pusing it rather frequently, twice a day. The Physicians’8 W# S* D4 T# {7 n
Desk Reference, or package insert of this product, gel or% l5 {! H) C# q1 {, R% `, E
cream, cautions about dermal testosterone transfer to3 |+ i. r4 V1 u/ Q. X+ r6 Y  F' X
unprotected females through direct skin exposure.
6 C1 J0 W7 M8 R9 V6 P# s7 i: rSerum testosterone level was found to be 2 times the
& B  F0 e6 N$ r: q6 W4 ^baseline value in those females who were exposed to, x: a+ ?, \3 P3 g; _+ i  _* u
even 15 minutes of direct skin contact with their male
% T2 _% C) X. g& {& Q' e9 ipartners.6 However, when a shirt covered the applica-8 ?2 R6 m* t& e$ ~9 p6 h1 R9 v
tion site, this testosterone transfer was prevented.
4 `$ |1 k/ ?0 _/ Q! F: ~Our patient’s testosterone level was 60 ng/mL,7 o" a" t5 Y' v8 W3 f
which was clearly high. Some studies suggest that
7 i+ E( M* j5 L8 t6 q% r! w" odermal conversion of testosterone to dihydrotestos-: s; p8 L% e& M% @
terone, which is a more potent metabolite, is more
' H$ o6 z# b) \active in young children exposed to testosterone0 A' C1 C# U" ~  p% S7 k
exogenously7; however, we did not measure a dihy-/ f( \0 U" ~* r. l. `  O2 {- f
drotestosterone level in our patient. In addition to+ j8 A. D* o7 w( v* q) E
virilization, exposure to exogenous testosterone in
6 n. D7 v" m* `0 U( bchildren results in an increase in growth velocity and
% B, K& w3 j/ R2 Y$ \  w3 U4 eadvanced bone age, as seen in our patient.0 o$ o( q$ O  k/ o: {
The long-term effect of androgen exposure during* U4 z4 I' U' a
early childhood on pubertal development and final
  |7 i" `& n& J- ]% B' tadult height are not fully known and always remain
$ S) b8 }! v' [a concern. Children treated with short-term testos-
/ @; l$ h' Z) m$ e' W+ u) r: nterone injection or topical androgen may exhibit some
8 f0 B8 p% C0 o# c0 ^: {0 K% G( f/ D8 qacceleration of the skeletal maturation; however, after4 d- D3 m: J$ O' X9 @) I
cessation of treatment, the rate of bone maturation
3 a7 F, |1 ]1 x! P/ p# z3 q/ l1 e( Idecelerates and gradually returns to normal.8,9
/ X4 Y( |7 n* e# N2 \% DThere are conflicting reports and controversy
; ^( Z, F' X# V- [over the effect of early androgen exposure on adult, U  x$ ^% Y1 G3 B) i$ U( n
penile length.10,11 Some reports suggest subnormal; g% H+ p+ w: j% a3 k5 ~7 \* _
adult penile length, apparently because of downreg-6 m$ k) `2 ^( w0 B: b
ulation of androgen receptor number.10,12 However,
( C$ _" g3 V- b$ C. J$ v: eSutherland et al13 did not find a correlation between
& s0 T. ~: a) O* \" \  M; Z& ychildhood testosterone exposure and reduced adult
" [" W7 A0 B" j$ B) u5 L: rpenile length in clinical studies.9 J1 b' c+ Q( b! A1 n& P7 ?
Nonetheless, we do not believe our patient is5 B2 [1 r. R1 ~2 g' M2 ~: D; E
going to experience any of the untoward effects from
/ c0 ~5 O1 H2 o7 K- ]  Vtestosterone exposure as mentioned earlier because
% v4 v2 R6 s1 \+ Lthe exposure was not for a prolonged period of time.- f/ g' n5 _! S
Although the bone age was advanced at the time of/ U" W$ V3 y" l+ u5 _
diagnosis, the child had a normal growth velocity at
. v7 i# c& F9 F9 s& Bthe follow-up visit. It is hoped that his final adult3 Q: R( q! u4 p6 L) @( D
height will not be affected.1 ]3 g8 r/ i+ D' Y  z2 M  F
Although rarely reported, the widespread avail-
9 n2 K- O( \2 B# G' c4 r% lability of androgen products in our society may
( D& ^# B; }* s; uindeed cause more virilization in male or female( u, D7 s+ J; u2 U
children than one would realize. Exposure to andro-
6 ~7 t$ w: d6 _! cgen products must be considered and specific ques-+ w0 w' m6 w" w+ L) M  T3 P
tioning about the use of a testosterone product or
! z7 Y, l& K6 `gel should be asked of the family members during; u" Y9 |+ D0 S! C: C0 n1 w$ q
the evaluation of any children who present with vir-
0 ]- ^" Y2 v, R- b0 Wilization or peripheral precocious puberty. The diag-
1 F& T( j. x7 h+ l' Vnosis can be established by just a few tests and by$ A, R" T7 u5 l* e+ d* X
appropriate history. The inability to obtain such a* N2 ], M6 g1 `
history, or failure to ask the specific questions, may1 e% p5 x) V: {+ A5 i' x! Y& k
result in extensive, unnecessary, and expensive- @8 j. ]9 f  I& w; E( {
investigation. The primary care physician should be
: K- K' w, `) F/ G1 ~' R9 h* Uaware of this fact, because most of these children* t$ I2 y4 G1 C! d0 M* k% s
may initially present in their practice. The Physicians’; a/ M4 F$ u$ F
Desk Reference and package insert should also put a
+ ?2 S8 j) c$ Z5 N8 swarning about the virilizing effect on a male or
. q8 f4 p  Q6 `9 Dfemale child who might come in contact with some-
: r0 T+ `% _. O* q, W5 ~. Pone using any of these products.
# _" G3 x% C/ L0 dReferences. v9 Y; j5 @0 \- X' {
1. Styne DM. The testes: disorder of sexual differentiation% V, n- @, j& o6 P1 R  |
and puberty in the male. In: Sperling MA, ed. Pediatric
& l! k: y+ J/ pEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
# W: ?) P9 ]( F2 {, A2002: 565-628.7 _2 U' M) v5 z3 Y$ c! @( n1 p
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
1 j/ c) U& e9 C! x: ^( |! l  t& {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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

4 w; s2 H: b) v' t4 `2 i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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