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Sexual Precocity in a 16-Month-Old7 o# M/ l* p) O/ a  D. _
Boy Induced by Indirect Topical
* K- \8 _8 e7 d4 P4 N( @Exposure to Testosterone' w0 u# [+ X' F  r1 G" o$ {
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,24 \" ~4 A  @0 z2 ^4 E
and Kenneth R. Rettig, MD1
$ z# ~# L! C8 ]1 ]3 `/ u5 AClinical Pediatrics+ u: B+ d; s, p  B
Volume 46 Number 6
6 b5 m) S  Q. o, iJuly 2007 540-543- c  t$ [  ^& D, [6 r, k. }) U
© 2007 Sage Publications9 S8 l9 C) F$ x6 g/ b" H
10.1177/0009922806296651
6 X6 s8 U2 P0 p+ r7 ]* G6 x8 I" _( ehttp://clp.sagepub.com$ j0 O7 P5 _  u  ~
hosted at
4 N2 M7 Q! Z# h5 j: y; a2 j9 m3 whttp://online.sagepub.com
5 z: @% S! |3 ?% v! \2 f% m* hPrecocious puberty in boys, central or peripheral,2 S, n0 e; v& ?) B" e
is a significant concern for physicians. Central
* F8 `* Z1 s6 _precocious puberty (CPP), which is mediated4 @& N- t7 I- c2 }. z/ L6 f1 d/ h
through the hypothalamic pituitary gonadal axis, has4 H1 a) V4 W; y4 G3 A
a higher incidence of organic central nervous system
3 o. P$ f$ r+ elesions in boys.1,2 Virilization in boys, as manifested4 s: G1 \& q+ |8 g( Q
by enlargement of the penis, development of pubic
3 I4 F+ l; \% E' k9 g+ _4 xhair, and facial acne without enlargement of testi-& c) x1 |) v0 W( W2 r- L
cles, suggests peripheral or pseudopuberty.1-3 We
  r% N6 D% D! a' zreport a 16-month-old boy who presented with the: f: D- Z4 F' g% i% A! T
enlargement of the phallus and pubic hair develop-
2 ^; C! m2 I/ P  R6 [ment without testicular enlargement, which was due/ f5 D% V$ N+ _) H6 m8 K
to the unintentional exposure to androgen gel used by
, O# R/ D! w5 z8 L: ]1 o0 a, E+ ~& J) sthe father. The family initially concealed this infor-$ r. f3 j# ~8 d! D8 ]2 c) X
mation, resulting in an extensive work-up for this
5 X, e. g* b( Ychild. Given the widespread and easy availability of/ [) `) l" O* i# d
testosterone gel and cream, we believe this is proba-9 o2 c2 L/ j: O4 s
bly more common than the rare case report in the" g+ m3 t" z# E0 m6 A
literature.4
7 h7 }: B* J/ k" W1 u$ QPatient Report
* ^5 e; y' ]6 O" V0 h- @/ y9 eA 16-month-old white child was referred to the2 I3 r5 M1 k& j, d5 J4 f2 z
endocrine clinic by his pediatrician with the concern
  K6 S6 [$ G# g7 z0 x. @( p7 d, dof early sexual development. His mother noticed+ T$ S' I" D; F
light colored pubic hair development when he was* z( _. D$ D1 s7 B& C; i# ~8 B
From the 1Division of Pediatric Endocrinology, 2University of
. _: M* Z7 H0 \( @6 S% {South Alabama Medical Center, Mobile, Alabama.
. `/ w% y6 e# m$ K: [Address correspondence to: Samar K. Bhowmick, MD, FACE," }. a: U  B8 Q) v
Professor of Pediatrics, University of South Alabama, College of
! r7 {0 b* `& Q# zMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;8 y/ h" ~3 n. S: f/ c
e-mail: [email protected].
; m; N* h+ E3 Y3 w( l4 b9 `about 6 to 7 months old, which progressively became
& V. X) F1 M0 b% L# ~6 B/ idarker. She was also concerned about the enlarge-, r1 I) R. e$ L4 ?
ment of his penis and frequent erections. The child
: P$ O' g, }" _0 h, Nwas the product of a full-term normal delivery, with
1 K6 G5 l# H% y% o, c3 v: Y# \; ]# W' k6 `a birth weight of 7 lb 14 oz, and birth length of
1 S6 w0 T- R; q1 f; y9 T. ^# @5 K20 inches. He was breast-fed throughout the first year
) p- _- ~* Z+ g4 N- {# A' nof life and was still receiving breast milk along with
' t3 B) `" A* ~* N0 Xsolid food. He had no hospitalizations or surgery,: c7 C) X7 r0 O2 ?! f, \
and his psychosocial and psychomotor development
3 E5 ~( a2 {, x& N! B& b9 {was age appropriate.
4 [5 ^/ J( L9 L. k/ ?9 EThe family history was remarkable for the father,
& l: Q% U/ U) }/ f& E+ Uwho was diagnosed with hypothyroidism at age 16,
+ s) ~, j1 l4 a9 R7 j2 mwhich was treated with thyroxine. The father’s1 n8 L1 P: ^( r+ r8 v2 D9 u
height was 6 feet, and he went through a somewhat
7 v8 E, V4 U4 u. Z9 _, t/ hearly puberty and had stopped growing by age 14.  X. S+ `! v! ^0 K/ ?2 p& x
The father denied taking any other medication. The: o/ p) S- z0 u. e
child’s mother was in good health. Her menarche, m. E6 }( Y$ X0 B3 m
was at 11 years of age, and her height was at 5 feet
  i8 j- L' a3 r5 h1 E8 ?( P; I& d2 R8 N5 inches. There was no other family history of pre-
6 p9 [9 [: q% q0 d, q8 Xcocious sexual development in the first-degree rela-
' X, E. n1 U3 M) r/ U: s* ^tives. There were no siblings.
" q) ^1 J3 U% p" U, y: q" W' dPhysical Examination
: f% f8 N( v) O; o* u- hThe physical examination revealed a very active,
# D4 G8 q: [2 _' q0 }, y+ dplayful, and healthy boy. The vital signs documented" g1 p5 ?2 V4 h& I
a blood pressure of 85/50 mm Hg, his length was3 z9 l  V1 W6 _: r4 M# y) ^/ Z6 |
90 cm (>97th percentile), and his weight was 14.4 kg) U! G; N0 i6 o' Q( R( u) ?
(also >97th percentile). The observed yearly growth. d8 t/ p# F4 s( o8 s0 M; d
velocity was 30 cm (12 inches). The examination of
4 Q7 \- |' s! v5 x) Vthe neck revealed no thyroid enlargement.7 P/ e: I/ X9 H+ k. i' X, D
The genitourinary examination was remarkable for3 C0 V, Z( K) u+ N% u
enlargement of the penis, with a stretched length of7 _- V- a2 u+ O. z2 v, X
8 cm and a width of 2 cm. The glans penis was very well% u8 R3 C6 @5 x! _0 U$ d8 R
developed. The pubic hair was Tanner II, mostly around
7 Q% z; Z2 ]) d- ?+ l' V* Z540
6 b0 h8 I; d6 E7 B; Y1 R5 d) Q% aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 M8 E! J) V# G; Cthe base of the phallus and was dark and curled. The
' E) [( L, U6 p7 Z+ Stesticular volume was prepubertal at 2 mL each.5 }9 C$ u* F6 Y5 L6 u
The skin was moist and smooth and somewhat0 d$ M3 y, F: W8 t7 ]" P/ e$ k- [
oily. No axillary hair was noted. There were no
3 m, F$ f& C) f7 ]abnormal skin pigmentations or café-au-lait spots.5 r5 v/ l) ~3 q
Neurologic evaluation showed deep tendon reflex 2+1 L0 {  Z% H8 s- d9 Y
bilateral and symmetrical. There was no suggestion4 m  K+ K/ P9 u6 J
of papilledema.
# s! _0 S* L% ~$ L0 LLaboratory Evaluation
4 F2 R+ C2 r" r! YThe bone age was consistent with 28 months by: D4 N+ K4 X, |" x7 s* U
using the standard of Greulich and Pyle at a chrono-
. r5 x9 R: ^4 Llogic age of 16 months (advanced).5 Chromosomal, ]# L- k+ n2 d! |3 \  ?. I7 B3 D1 e3 P
karyotype was 46XY. The thyroid function test: x: k% r* p6 w. n
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
  W% p9 J" N, B. h% z# Klating hormone level was 1.3 µIU/mL (both normal).
* t7 o& X0 G7 U% u7 l5 YThe concentrations of serum electrolytes, blood7 I# u9 X7 ?5 P2 ?
urea nitrogen, creatinine, and calcium all were
1 t  U  i. i3 ~! T% nwithin normal range for his age. The concentration
2 `/ @  e1 h2 Aof serum 17-hydroxyprogesterone was 16 ng/dL
3 w8 Q3 o8 f; M+ L(normal, 3 to 90 ng/dL), androstenedione was 20
5 R7 [9 U. o' `ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-) e0 X  P  d  F) h
terone was 38 ng/dL (normal, 50 to 760 ng/dL)," c' ?( N6 E4 T+ E
desoxycorticosterone was 4.3 ng/dL (normal, 7 to. z( T1 s9 \6 l0 Z' s6 S3 K4 w- ?
49ng/dL), 11-desoxycortisol (specific compound S)
3 r3 u2 I  z+ o+ h) a, `) dwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-: Z3 p- K" z, V9 S$ V, E% ], L
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
$ J1 F& |/ I! X( ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
0 d8 t$ T; ~1 m( Q! X' Kand β-human chorionic gonadotropin was less than
7 p7 I1 D' _; r( h8 V# m" e2 m6 @; `7 r5 mIU/mL (normal <5 mIU/mL). Serum follicular$ T( S: t1 H: J6 [+ d+ ^( q
stimulating hormone and leuteinizing hormone
6 `) q! L( r, i, S5 a8 |3 {concentrations were less than 0.05 mIU/mL  ^1 P5 v. T: ^7 ?
(prepubertal).: q4 S6 R+ x- s( u  b' [
The parents were notified about the laboratory1 A2 n  y/ j# ], Y8 ^6 H
results and were informed that all of the tests were
, E  s! N0 ]# Znormal except the testosterone level was high. The
# c* E  c/ Y5 Gfollow-up visit was arranged within a few weeks to
! I  J! v' L  C7 p. e" j) ]obtain testicular and abdominal sonograms; how-. M5 S6 e; D8 y# K9 F' c
ever, the family did not return for 4 months.
- w/ i  B( ^) K. u% Z- \Physical examination at this time revealed that the
# O- ?% f1 Z5 {. t, e2 S- xchild had grown 2.5 cm in 4 months and had gained
( A& z( i6 f4 ^2 kg of weight. Physical examination remained
2 s4 p! a* c4 ^: X( H  ~unchanged. Surprisingly, the pubic hair almost com-: `' |3 b" t4 U4 `6 s
pletely disappeared except for a few vellous hairs at
" A- I) b6 a4 [5 J  Ythe base of the phallus. Testicular volume was still 2
* m9 h! @- _, j  v) k* ZmL, and the size of the penis remained unchanged.. X6 ]: O9 _0 W# C  v
The mother also said that the boy was no longer hav-3 ]- O' G8 q) v. M6 b
ing frequent erections.# O$ I! \3 S5 F
Both parents were again questioned about use of5 e- v- ?2 ^1 [: c3 o: ~+ y2 u
any ointment/creams that they may have applied to
( z' G/ ]' L, c( Q1 ^the child’s skin. This time the father admitted the
% `% w" |5 Y$ h3 P" lTopical Testosterone Exposure / Bhowmick et al 541
& h$ V: c& ~4 T; I) i% Nuse of testosterone gel twice daily that he was apply-: n( h- t3 Q' j, x& y4 T- U$ s
ing over his own shoulders, chest, and back area for
' b% h7 t3 U7 qa year. The father also revealed he was embarrassed7 R& G% y$ R/ @9 K4 X
to disclose that he was using a testosterone gel pre-& t+ q& H1 z$ X0 z6 @4 }
scribed by his family physician for decreased libido- d9 p7 H4 _% h* z1 X
secondary to depression., L; Q5 V8 q5 G" e+ D) c
The child slept in the same bed with parents.# T: I5 u+ P. |% s# R
The father would hug the baby and hold him on his3 t% {; Y5 I4 h2 {7 c" }4 x/ H
chest for a considerable period of time, causing sig-+ }- G/ s/ V) H& x
nificant bare skin contact between baby and father.
, ?4 Y! O# H3 z6 k9 H' DThe father also admitted that after the phone call,9 h1 i4 u& U- z+ p/ B% I$ R
when he learned the testosterone level in the baby9 h% p1 |4 G& L
was high, he then read the product information5 _1 b/ ^$ P$ f
packet and concluded that it was most likely the rea-
. D$ @4 ^3 H' o8 \son for the child’s virilization. At that time, they
3 h+ H. P% [; D! wdecided to put the baby in a separate bed, and the
7 B; D: D) ?1 H) x; zfather was not hugging him with bare skin and had
0 r4 L* a# A$ [been using protective clothing. A repeat testosterone. h. _" l4 i1 `4 `6 W/ O4 h
test was ordered, but the family did not go to the
0 {6 l  f; W) @- Flaboratory to obtain the test.
9 f( h2 O/ Y9 h0 MDiscussion
/ [7 M& t- {4 M7 D4 CPrecocious puberty in boys is defined as secondary
( u) F5 B0 V* N! ~8 g1 m# Msexual development before 9 years of age.1,4
) ^6 W3 o: U( pPrecocious puberty is termed as central (true) when( U6 a$ F, ~: |& y/ o- P
it is caused by the premature activation of hypo-
3 y( u' L+ e0 v8 [0 Y3 [: a$ Athalamic pituitary gonadal axis. CPP is more com-
# S0 q3 }0 G5 x; n0 c: T* amon in girls than in boys.1,3 Most boys with CPP
+ M$ d# N: T3 [3 Tmay have a central nervous system lesion that is
( E9 T! i. ~% |9 f6 Y: Gresponsible for the early activation of the hypothal-
, S7 a7 P; L4 O9 z2 Pamic pituitary gonadal axis.1-3 Thus, greater empha-
& Y3 o  Y' L2 G' m+ T; i% W/ q5 zsis has been given to neuroradiologic imaging in
7 c5 v9 T' m3 b. c$ cboys with precocious puberty. In addition to viril-: h* z  z# O% C3 Q: Z
ization, the clinical hallmark of CPP is the symmet-5 `* m# B% }3 S' @  Z
rical testicular growth secondary to stimulation by
; \# f* Y9 g! M4 T4 L* S8 b8 k3 }gonadotropins.1,3
& z- n- r$ C4 r4 g3 ]Gonadotropin-independent peripheral preco-
# m# k; W4 d3 K4 n9 E, ?3 Acious puberty in boys also results from inappropriate- O/ ~* A/ q' H! ]1 F9 v4 w
androgenic stimulation from either endogenous or
: x7 m% Z, [  V8 x$ X6 Jexogenous sources, nonpituitary gonadotropin stim-4 }, c5 |, {# i8 t0 |( R& x+ M
ulation, and rare activating mutations.3 Virilizing0 Q1 s3 s% E9 {! B! V
congenital adrenal hyperplasia producing excessive; W* H& E, P8 y
adrenal androgens is a common cause of precocious
4 u2 i. ]; W& _" Y9 P& b. n* M# Ypuberty in boys.3,4$ [% k5 Q8 J1 X+ _$ U7 N# ?* c2 L
The most common form of congenital adrenal
4 e* f) x# A- S% ~hyperplasia is the 21-hydroxylase enzyme deficiency.
4 g2 e' \' {9 ~5 A5 nThe 11-β hydroxylase deficiency may also result in# c8 c3 l$ b2 t: S
excessive adrenal androgen production, and rarely,
& C- T1 B: g( Q; W  k8 Fan adrenal tumor may also cause adrenal androgen
. @# P# _1 l7 R2 F8 k5 Aexcess.1,3
/ T. s. q+ L) ^3 T% Lat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% Y3 J% g/ r* K
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
0 j, Y' R" d' Q2 pA unique entity of male-limited gonadotropin-
+ a& L% @2 S- `independent precocious puberty, which is also known: y, [$ i1 C' }+ v7 l( v7 m
as testotoxicosis, may cause precocious puberty at a
( L' K# [/ U; \7 jvery young age. The physical findings in these boys
4 a0 f2 _. T# U: |1 Mwith this disorder are full pubertal development,
1 Q6 U3 _8 L  Oincluding bilateral testicular growth, similar to boys
5 a- L' _; p% r+ vwith CPP. The gonadotropin levels in this disorder
) e/ c: a" h, W3 c7 n7 Pare suppressed to prepubertal levels and do not show
) ]3 g" l: J' S1 Y: W4 M8 u% wpubertal response of gonadotropin after gonadotropin-* i+ A; d) X( u5 X3 W
releasing hormone stimulation. This is a sex-linked) H# G( w/ C, Q7 }( U( ]8 k/ c* l
autosomal dominant disorder that affects only
/ l: H1 R8 C. N2 Qmales; therefore, other male members of the family
- u$ z# }6 c9 Z* I# [may have similar precocious puberty.3
4 `# O% V2 P( WIn our patient, physical examination was incon-
' u' n, d% E% @" T0 z. y% hsistent with true precocious puberty since his testi-' k  `8 F3 D% ~* Q4 I
cles were prepubertal in size. However, testotoxicosis
* @' b7 h# |9 h0 d  Y, R' p( ]was in the differential diagnosis because his father' f$ w  Z5 \: ?- p
started puberty somewhat early, and occasionally,
! ^2 P- B" C, F/ W8 [testicular enlargement is not that evident in the
8 L( k- q6 \/ `beginning of this process.1 In the absence of a neg-, S" j  U9 Y# W, `. |
ative initial history of androgen exposure, our9 f* N7 |, F; M5 c! I4 K
biggest concern was virilizing adrenal hyperplasia,7 T5 g) T; p& F; E- A
either 21-hydroxylase deficiency or 11-β hydroxylase
  s' _9 E! p& |. hdeficiency. Those diagnoses were excluded by find-' L* Z8 w4 X7 A; ^4 w
ing the normal level of adrenal steroids.5 |% R; H- }' f3 l0 E  N: A; A
The diagnosis of exogenous androgens was strongly
* ]" N, A0 M9 z: B' \- Hsuspected in a follow-up visit after 4 months because- d- i5 T7 v% ?; r) H% A3 ]
the physical examination revealed the complete disap-
/ g( A5 R3 X8 X( M9 I. Kpearance of pubic hair, normal growth velocity, and" R0 Q' f, {! o$ s9 ?( E* r
decreased erections. The father admitted using a testos-
% D; l0 w: |; u! ^4 P) G1 L" ~terone gel, which he concealed at first visit. He was% f2 T  I/ N& f; f" G, ~' t
using it rather frequently, twice a day. The Physicians’
! h3 {9 _* A9 p8 l* qDesk Reference, or package insert of this product, gel or' U& W& D, W  Z, A* I7 x) W, L  l
cream, cautions about dermal testosterone transfer to0 q. z! f! Y! P# E
unprotected females through direct skin exposure.0 W! U& s2 W. ?! j: N' e  H
Serum testosterone level was found to be 2 times the
$ W. r. Q' o, f( }8 {8 }$ ?7 G( Cbaseline value in those females who were exposed to
6 x" D$ ~1 @1 R; X( h& }4 aeven 15 minutes of direct skin contact with their male
* J  f: A, ], l& x2 ?partners.6 However, when a shirt covered the applica-* v! E$ o0 A' f. _$ C( B- M
tion site, this testosterone transfer was prevented.' T# c/ u; I7 p( k- w3 `) \) F
Our patient’s testosterone level was 60 ng/mL,/ o% ~9 G3 N2 n% v
which was clearly high. Some studies suggest that
. ^# O0 S+ b: y1 D1 J/ K3 Q) s) S  pdermal conversion of testosterone to dihydrotestos-3 f3 o2 X7 _& E* m
terone, which is a more potent metabolite, is more: f" M# X1 _( X; g* K) T
active in young children exposed to testosterone7 L) r9 n4 h) k
exogenously7; however, we did not measure a dihy-/ [# r. @$ @4 i6 \/ _
drotestosterone level in our patient. In addition to
1 p- n$ u( d# u* e4 v- Dvirilization, exposure to exogenous testosterone in: ^7 Q0 L3 `) o$ ]9 B/ V& {
children results in an increase in growth velocity and
2 Y$ L/ D: v- u" a" f1 Z+ \advanced bone age, as seen in our patient.: z; G1 S# R, E3 h/ l' c
The long-term effect of androgen exposure during
* p" n: S7 S9 O% e% F0 searly childhood on pubertal development and final
' |# k  b# x2 p( _adult height are not fully known and always remain
2 h3 r! C# j: Ha concern. Children treated with short-term testos-/ Z  t, {5 t' b( Q( n- H# G5 e9 Q
terone injection or topical androgen may exhibit some
0 i6 H+ k2 s- d3 T$ Facceleration of the skeletal maturation; however, after1 j- p# Z1 p5 o6 p$ s
cessation of treatment, the rate of bone maturation
4 R. m0 ?  t; M, `& @$ zdecelerates and gradually returns to normal.8,9* `! ?- M8 r1 s; w0 m
There are conflicting reports and controversy
- N, F) E6 \9 d, c4 sover the effect of early androgen exposure on adult6 `% x0 ~2 {& K" R( \/ U- a
penile length.10,11 Some reports suggest subnormal
. g6 n, r0 F2 w0 h4 N/ w$ }7 Kadult penile length, apparently because of downreg-
" M" L; ^1 I( B+ I4 eulation of androgen receptor number.10,12 However,6 ?+ l3 D3 i. ]( N4 ^7 @8 b# B1 e+ _* _
Sutherland et al13 did not find a correlation between
& X. F/ r: i" |2 l2 ~$ Fchildhood testosterone exposure and reduced adult5 x/ r  ~3 r( _! \% y4 T
penile length in clinical studies.: a( ~3 c* r8 Z! h( O  J4 E7 Z
Nonetheless, we do not believe our patient is, M8 |% V3 W) {$ ]. d* |
going to experience any of the untoward effects from
: u3 Q" `  o/ j" g& `, Jtestosterone exposure as mentioned earlier because
$ I2 ^  V4 D, B, [0 X; |8 Z' f. c& }the exposure was not for a prolonged period of time.
2 \% C1 w, d+ K: JAlthough the bone age was advanced at the time of# }+ N# |& M5 B9 r4 p/ R1 T7 N6 X
diagnosis, the child had a normal growth velocity at
, L% y. m  s+ c! e6 @the follow-up visit. It is hoped that his final adult+ y$ Q! P3 a3 x7 x' e2 P
height will not be affected.
3 t2 v5 J, [9 `  h4 ~+ E9 V: b0 tAlthough rarely reported, the widespread avail-
6 M  K. i- @+ ?2 F( Qability of androgen products in our society may# K: Z/ w* h9 {3 }% J3 ^( K
indeed cause more virilization in male or female$ |0 P0 t: v) F" Z
children than one would realize. Exposure to andro-
! `" C7 g3 M" `( F: s. n' rgen products must be considered and specific ques-4 j% c4 S, `' o/ G
tioning about the use of a testosterone product or! B2 M9 P  |6 m( B8 X% p- C
gel should be asked of the family members during7 b- X4 k9 _+ P2 V
the evaluation of any children who present with vir-6 Z3 R/ z: M  M# R& e
ilization or peripheral precocious puberty. The diag-
! [' S! U/ c( \! V5 o0 ]nosis can be established by just a few tests and by
9 k$ d* b0 G. `4 I$ G/ l4 x, cappropriate history. The inability to obtain such a2 f* \8 i5 x) a
history, or failure to ask the specific questions, may/ S/ G( M$ d9 G+ _$ D. ?2 w
result in extensive, unnecessary, and expensive/ T5 D! C6 Q8 \9 F1 P8 M; J
investigation. The primary care physician should be
2 c+ N. ^# O  S2 f% M" v. ?aware of this fact, because most of these children2 {& N# w! y" T, q" X/ m3 P1 t$ w+ B8 M
may initially present in their practice. The Physicians’) a+ y; Z0 |+ c* ]5 q7 P5 d
Desk Reference and package insert should also put a
( {2 E9 S3 E3 y) e1 twarning about the virilizing effect on a male or
$ b, ~5 f- @( E+ H1 {; {2 Hfemale child who might come in contact with some-
. I3 n4 y! G' [/ |7 ^5 X- J& bone using any of these products.
( ^0 k& Z& \: v- Y! D" M  rReferences
$ l& ~& T0 P+ [' _9 H& A1. Styne DM. The testes: disorder of sexual differentiation
! r* H1 r" f0 u/ d4 y! G, u  Hand puberty in the male. In: Sperling MA, ed. Pediatric- Z" b8 \  \: D" F8 f
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;. K$ ^) K4 M3 Y  \( a8 C: L
2002: 565-628.9 N! s* M1 d+ B
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious! G2 }- r5 D, o3 b# ?
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
2 B, U  ?& a: b& w9 N  i5 x7 oBoy Induced by Indirect Topical% @& Y7 F/ P5 s0 X$ t
Exposure to Testosterone4 e, f6 a+ y3 f; d
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
6 Y  i/ F; X  b0 W; Mand Kenneth R. Rettig, MD1
  Q; ^3 x3 ~) T) E5 \$ MClinical Pediatrics1 B% T, C4 f' b. ]9 N$ L
Volume 46 Number 68 H0 X% @: M: ]; J
July 2007 540-543
3 u/ B  A3 F( [3 D( Y; |© 2007 Sage Publications
4 w8 h" O: h1 X) u; i) E8 N, a# W10.1177/0009922806296651- z0 v$ B8 ^1 K4 u
http://clp.sagepub.com
) D# H% l; Q  ~6 i8 G: ghosted at
3 Y* I! t5 {2 M8 e; M# V- dhttp://online.sagepub.com0 K, H) p  B$ E" B0 [/ z
Precocious puberty in boys, central or peripheral,
4 r8 p2 I4 ?1 Z$ \3 e; X% u* `is a significant concern for physicians. Central% ]* w- E& p! C* J" W) M$ k
precocious puberty (CPP), which is mediated/ Q- X5 r& v) o2 p+ n* l, P5 N) J
through the hypothalamic pituitary gonadal axis, has: D1 V6 Y% r) g" o0 @
a higher incidence of organic central nervous system
# R  K4 u  Q1 E2 M' W/ ?" T, D" u; M' glesions in boys.1,2 Virilization in boys, as manifested+ M) g: a3 @; ~, e3 C* m* }
by enlargement of the penis, development of pubic# g( M$ t  Z) t3 t
hair, and facial acne without enlargement of testi-% L, K: c7 B' S1 Y1 ?  m
cles, suggests peripheral or pseudopuberty.1-3 We
  K3 M# m- U1 L  v' Treport a 16-month-old boy who presented with the$ R4 d/ Q, F7 H
enlargement of the phallus and pubic hair develop-" T) L* \! G' R
ment without testicular enlargement, which was due
7 c( ?% Z" i: f" x& @3 p* Dto the unintentional exposure to androgen gel used by
0 {3 H* }8 q( ]8 Bthe father. The family initially concealed this infor-! K0 m3 j5 a$ k* j+ z) P) J$ q
mation, resulting in an extensive work-up for this  e. e& i& F5 b# S2 x
child. Given the widespread and easy availability of
% e. G9 C4 X( E% btestosterone gel and cream, we believe this is proba-3 F) ?+ z1 C- g7 }/ S
bly more common than the rare case report in the
! X3 m, U* w1 Lliterature.4+ B; K& U! v4 e' S% ?, o7 Q4 p+ L
Patient Report
0 h! v6 E, L: y7 @A 16-month-old white child was referred to the
, f4 i3 l3 r5 k  m, @' ~/ A/ Jendocrine clinic by his pediatrician with the concern9 Q; i, e! S& c+ Y9 i' q
of early sexual development. His mother noticed
( v2 k' i% M4 r9 F, `) dlight colored pubic hair development when he was
& L  I. i5 P# P5 N5 l+ VFrom the 1Division of Pediatric Endocrinology, 2University of& l5 E1 _* q+ [, I
South Alabama Medical Center, Mobile, Alabama.
9 C$ x0 P* D" P! \# rAddress correspondence to: Samar K. Bhowmick, MD, FACE,
$ o3 n- V4 o: GProfessor of Pediatrics, University of South Alabama, College of
, P4 C4 z* k0 W$ GMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;& o5 S% r1 l0 e1 h9 J
e-mail: [email protected].
) h, i1 S8 \' q9 ?+ fabout 6 to 7 months old, which progressively became
( M# x/ N) V1 N% j" n2 ~darker. She was also concerned about the enlarge-
+ C9 Y; V5 S& _9 xment of his penis and frequent erections. The child3 x- E( ?4 |2 g2 m, y4 W
was the product of a full-term normal delivery, with  n9 J, x, s. ^4 [- h
a birth weight of 7 lb 14 oz, and birth length of
! w, D9 Z" U4 H; }20 inches. He was breast-fed throughout the first year
9 E( d$ N" k6 r' T. Nof life and was still receiving breast milk along with0 R# o0 `6 s. I6 X$ w
solid food. He had no hospitalizations or surgery,
) X0 I: ^: Y+ |" i* U7 Z. u, n  {- K, pand his psychosocial and psychomotor development
' I' q, [; t9 W6 ^* uwas age appropriate.1 G" b# P' U, B# M* N; y: H/ z
The family history was remarkable for the father,
, R" T/ v- _9 twho was diagnosed with hypothyroidism at age 16,
3 ^2 e- ]/ l3 r9 R$ B0 L$ O$ e2 Vwhich was treated with thyroxine. The father’s
! _3 _9 v# |; V; Dheight was 6 feet, and he went through a somewhat& c( G6 B, ^# g. s) V. q; H
early puberty and had stopped growing by age 14.1 s9 B: Z7 h" ~
The father denied taking any other medication. The
/ Y- N, h: n9 S1 E3 B2 Hchild’s mother was in good health. Her menarche5 d8 v; N; e4 t3 O/ o6 V3 _
was at 11 years of age, and her height was at 5 feet
1 G! \4 p5 _4 Y9 ~0 T) S" |5 inches. There was no other family history of pre-
$ l9 S2 @% x& }: lcocious sexual development in the first-degree rela-: t; m1 b* l7 L
tives. There were no siblings.- M6 o- X9 T2 [- H+ q) c
Physical Examination- V; G* N8 j- L& L: r
The physical examination revealed a very active,: n3 l2 f- P; `# [9 b, T9 H, W
playful, and healthy boy. The vital signs documented
2 ]* e5 A7 ]8 ~a blood pressure of 85/50 mm Hg, his length was
/ N0 m9 R4 _& J+ p( C# C1 V  V90 cm (>97th percentile), and his weight was 14.4 kg
  }: s# I8 ?. z+ ~- J(also >97th percentile). The observed yearly growth
) v- b! ?$ |* X0 Dvelocity was 30 cm (12 inches). The examination of: P7 A* g" [: r$ A' t
the neck revealed no thyroid enlargement.
3 m/ C. u. A3 l2 n( QThe genitourinary examination was remarkable for- m- `! B  o2 A) O9 I; Y" h
enlargement of the penis, with a stretched length of' v+ T$ Z+ q3 G; @/ N+ J9 h7 E
8 cm and a width of 2 cm. The glans penis was very well
' ?' y2 b- @6 e& ~developed. The pubic hair was Tanner II, mostly around
5 I1 w) I: J2 V. A0 }$ k5407 Z' ?: W% k9 G# v& K! @
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" D8 s4 ~/ n0 y1 ]% j9 B4 A: |% C/ |the base of the phallus and was dark and curled. The2 C( ]. W7 A' X
testicular volume was prepubertal at 2 mL each.
+ U$ n7 d9 C, I$ x5 wThe skin was moist and smooth and somewhat
* C- ]6 a1 _( s0 Qoily. No axillary hair was noted. There were no
% N0 [3 h" @' i, u* q$ h3 Rabnormal skin pigmentations or café-au-lait spots.6 g! \, @- h! Q, [% D& @/ d" P. F
Neurologic evaluation showed deep tendon reflex 2+
4 R/ O5 g) \7 ?% F) I. k0 Obilateral and symmetrical. There was no suggestion, D9 M8 [6 o, l7 Y" {7 x% t% H
of papilledema.3 ]- c7 k4 [6 e2 g& m9 q6 A
Laboratory Evaluation
' o7 v5 I! Y. |! g6 VThe bone age was consistent with 28 months by
$ P8 v; [, D7 Wusing the standard of Greulich and Pyle at a chrono-3 x% N9 c2 ]4 p( h; |
logic age of 16 months (advanced).5 Chromosomal
& C7 [  |. V1 g2 g8 Vkaryotype was 46XY. The thyroid function test3 n# n& a' D7 w4 f
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
5 O7 ]# v  o- alating hormone level was 1.3 µIU/mL (both normal).
& @. }" Q6 @9 e) w& m" i# o* ~The concentrations of serum electrolytes, blood3 K- {1 t' U. _
urea nitrogen, creatinine, and calcium all were+ e1 H' E8 z/ j. `9 q
within normal range for his age. The concentration
% G4 @# R+ Y: p, _8 vof serum 17-hydroxyprogesterone was 16 ng/dL3 J% |9 H7 ^) |
(normal, 3 to 90 ng/dL), androstenedione was 20
4 B) E; d, j) |9 S* @, v. }ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-- m' I( w" O2 @; W0 |+ x/ P5 ~) X
terone was 38 ng/dL (normal, 50 to 760 ng/dL),& W  n0 L# |5 ^  b7 J3 r# q$ C  g
desoxycorticosterone was 4.3 ng/dL (normal, 7 to. [1 B  z+ e2 T3 ^
49ng/dL), 11-desoxycortisol (specific compound S)3 v$ y8 j* L5 G9 Y" A
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-9 W8 C+ i0 _, T6 H( [- g0 I
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
' o2 m$ T) ?- [( z7 Z2 I; t3 [9 U7 ]testosterone was 60 ng/dL (normal <3 to 10 ng/dL),- m: e( M9 F  y8 L1 K
and β-human chorionic gonadotropin was less than
9 z9 u) `/ y9 _; j$ \# e* s5 mIU/mL (normal <5 mIU/mL). Serum follicular
3 H1 [* L& I4 L/ V. istimulating hormone and leuteinizing hormone
' v& k: B; i) G3 Pconcentrations were less than 0.05 mIU/mL
( R7 V4 B7 @# w% u0 k6 d6 M(prepubertal).+ M  a  i4 N( k" b, K
The parents were notified about the laboratory0 m: I! ~* Z$ m3 q
results and were informed that all of the tests were/ U% Z6 z- v+ {; q
normal except the testosterone level was high. The
8 y  x# @- I: w- ?5 F$ hfollow-up visit was arranged within a few weeks to% }. A# h" |6 Z! w/ \
obtain testicular and abdominal sonograms; how-
" `$ f3 c4 K) Q6 \ever, the family did not return for 4 months." Y. l; _. {$ I% l, m6 Z
Physical examination at this time revealed that the$ a' x. |4 i/ v# t! l
child had grown 2.5 cm in 4 months and had gained
/ N4 k2 ~5 M4 ?* i2 kg of weight. Physical examination remained
4 V" X5 ~! A( Z; I6 X% l+ Funchanged. Surprisingly, the pubic hair almost com-
+ `4 }2 m% \9 D' Y% F# |0 E' f. c3 Ppletely disappeared except for a few vellous hairs at
3 O) x: ]. u$ M5 X  T/ jthe base of the phallus. Testicular volume was still 2' W# O2 u9 v: A( X
mL, and the size of the penis remained unchanged.' `1 n/ M8 v, b  k. k" a* ^. [& P$ A
The mother also said that the boy was no longer hav-6 G+ U+ Y3 N8 t' B3 M" X, ^% P
ing frequent erections.
- i) d2 n' I4 NBoth parents were again questioned about use of
/ }5 h4 A/ g* n; [- p# Wany ointment/creams that they may have applied to
+ ]  ~5 X( J" Lthe child’s skin. This time the father admitted the
' \" D9 h5 ]4 A, U1 `Topical Testosterone Exposure / Bhowmick et al 541/ |8 f1 d8 C! _) d3 B
use of testosterone gel twice daily that he was apply-: L' L( o" A: U! G
ing over his own shoulders, chest, and back area for" N  u* m# D+ ]& M+ l. s
a year. The father also revealed he was embarrassed
: Z+ B( r( m0 ^5 Vto disclose that he was using a testosterone gel pre-$ Y$ B' J! {7 k$ W/ x( H
scribed by his family physician for decreased libido/ V4 Y8 q- R4 x1 H" E
secondary to depression.6 [: [2 M$ h% F8 I0 X, X; E9 a
The child slept in the same bed with parents.
. i& C# Y/ h0 i5 T/ `0 f8 p. @The father would hug the baby and hold him on his
3 e1 T, B$ w$ y' Uchest for a considerable period of time, causing sig-) n+ w7 d  r6 Y7 s
nificant bare skin contact between baby and father.
" f. z8 ~- ?, e+ lThe father also admitted that after the phone call,
6 N& c# J1 y- ]  G  }9 ]when he learned the testosterone level in the baby
: k: Z- V* t, h* C5 I' j9 n/ ^was high, he then read the product information  `$ F7 d% s# L/ S) }
packet and concluded that it was most likely the rea-
( j( n% Z- N8 B2 _' q& {son for the child’s virilization. At that time, they5 @) A& v6 G* }- @- u7 m4 b9 V+ `
decided to put the baby in a separate bed, and the
3 l7 S9 p2 }" j) S( ^father was not hugging him with bare skin and had3 k/ B* `3 b- j. ^0 z' C; g
been using protective clothing. A repeat testosterone
' h9 \( n9 o5 O/ C* x% ztest was ordered, but the family did not go to the* }+ C2 d3 W( z
laboratory to obtain the test.5 P. z+ @' T% Z/ S3 ]" h
Discussion( b6 [  Y% A# e% l4 j$ B8 I$ m! ~# @
Precocious puberty in boys is defined as secondary
# x6 p& {  S$ Psexual development before 9 years of age.1,4
8 y$ C! a* i" `- b. mPrecocious puberty is termed as central (true) when
+ d! K. ]) T4 H) @- Jit is caused by the premature activation of hypo-9 F' V$ Q: l/ y: i0 \! g2 T  [
thalamic pituitary gonadal axis. CPP is more com-
  r/ Z2 G0 \% Y& h" g  i6 Jmon in girls than in boys.1,3 Most boys with CPP3 v" k) Q8 v. |4 e, c8 @: N# c/ [
may have a central nervous system lesion that is
6 K% |) ~! O  s; V; u! ^0 kresponsible for the early activation of the hypothal-) n7 z: m- L1 K/ J5 m5 c( M; k- x
amic pituitary gonadal axis.1-3 Thus, greater empha-/ z5 B% K8 X; o+ Z8 I1 l: p  F
sis has been given to neuroradiologic imaging in
6 I- t- C3 R7 R* e. r6 c  D& kboys with precocious puberty. In addition to viril-- m9 E) G3 j8 ~" b3 K
ization, the clinical hallmark of CPP is the symmet-& r: q2 l- {. Y, ?
rical testicular growth secondary to stimulation by7 @7 M# v0 ^; {' a9 o5 Q9 Z) T
gonadotropins.1,3
1 g; O& @; N4 {' s0 ]$ cGonadotropin-independent peripheral preco-8 M: {& o6 n# U: L0 L; a
cious puberty in boys also results from inappropriate5 d& @- c4 h$ X
androgenic stimulation from either endogenous or
, \2 x, A. x+ P- c6 w' a, bexogenous sources, nonpituitary gonadotropin stim-6 x2 u5 {! ]7 F$ R' v7 [
ulation, and rare activating mutations.3 Virilizing
, v! ~7 ^5 ~+ V9 J( [congenital adrenal hyperplasia producing excessive& u) C# J5 ?7 R: r
adrenal androgens is a common cause of precocious
* |. N7 X, Q1 [& |( Z0 r+ bpuberty in boys.3,4
- P0 L3 e# Q# U. `9 M  uThe most common form of congenital adrenal
8 R9 e* e4 C: e  B: K& i4 ohyperplasia is the 21-hydroxylase enzyme deficiency.( |4 R+ J) U! S, p+ m2 c
The 11-β hydroxylase deficiency may also result in
" a8 e) K8 M% A! m) F2 y# fexcessive adrenal androgen production, and rarely,  L! l$ B2 o5 ^) N! N
an adrenal tumor may also cause adrenal androgen: U. B- X! t2 P3 ~8 O
excess.1,3
6 F4 k7 L( ?( F: R2 bat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 J: g# Z' `, t+ [+ X0 a
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
2 ]7 l; n8 U5 ^0 KA unique entity of male-limited gonadotropin-; M' d; I$ U4 ?
independent precocious puberty, which is also known
" \% x( A$ [; q3 sas testotoxicosis, may cause precocious puberty at a
3 d9 j' U' }! s; h7 B. Cvery young age. The physical findings in these boys; j8 y/ V+ [, }
with this disorder are full pubertal development,
5 j1 a4 O$ X4 B7 T% F  T3 S3 bincluding bilateral testicular growth, similar to boys: I% d2 C8 [; y! t
with CPP. The gonadotropin levels in this disorder
! G0 F" f6 K% v# m2 v2 |are suppressed to prepubertal levels and do not show
: G' r9 b8 ~$ ~( ]pubertal response of gonadotropin after gonadotropin-
2 b& o# e- w) c" h3 L+ H3 L9 ?releasing hormone stimulation. This is a sex-linked$ N& l& N) ]2 A, n  s' f0 h2 @
autosomal dominant disorder that affects only
; o$ p! Q) o  b7 K7 Nmales; therefore, other male members of the family2 c# O8 W3 M. C" J; l0 a+ W. V6 V
may have similar precocious puberty.3
* X  r. v' r. T& ]In our patient, physical examination was incon-* b$ `2 o0 n& f; Q2 ^
sistent with true precocious puberty since his testi-
; p4 `( R6 U* ]3 n( Rcles were prepubertal in size. However, testotoxicosis
/ i' T3 @  d4 K9 Iwas in the differential diagnosis because his father  I9 Y2 F  }9 W! i' D" d$ {! z
started puberty somewhat early, and occasionally,2 K; Z7 \% N" U
testicular enlargement is not that evident in the+ E+ n8 P) v9 j0 }9 Z
beginning of this process.1 In the absence of a neg-. c# j" e. p1 {2 ?* T
ative initial history of androgen exposure, our
/ P9 V5 i4 i# o( r& hbiggest concern was virilizing adrenal hyperplasia,, F# f1 M9 Q" o9 j+ v! y
either 21-hydroxylase deficiency or 11-β hydroxylase. f5 }; l3 ^+ j5 m$ C! f
deficiency. Those diagnoses were excluded by find-
8 }% u( ]: o8 Z/ @) ming the normal level of adrenal steroids.
6 E1 I& \4 B) h7 W7 O2 `2 E/ J6 @3 G4 oThe diagnosis of exogenous androgens was strongly* X& X' J7 J# }9 p/ X$ x% v' z
suspected in a follow-up visit after 4 months because! o% }. ?+ }# D& x, ?
the physical examination revealed the complete disap-% i9 }% P/ m% a% M$ H' i
pearance of pubic hair, normal growth velocity, and
- e- `) r, H0 s6 _decreased erections. The father admitted using a testos-
" i& z, D, e+ H) A7 jterone gel, which he concealed at first visit. He was
5 g: s" U. ^. ?( m  Fusing it rather frequently, twice a day. The Physicians’
1 b8 Q# |; ]. g3 \8 ^Desk Reference, or package insert of this product, gel or
* R0 [7 ]9 U, g, L$ tcream, cautions about dermal testosterone transfer to/ {, s. R# v/ ^$ k7 ~# j
unprotected females through direct skin exposure.( a4 D# N6 ?0 J. V- ~# Y5 r2 F
Serum testosterone level was found to be 2 times the
% U$ ~4 w! X4 f4 Q0 ~' ibaseline value in those females who were exposed to
. M5 q$ s. m0 ^& i; e. h9 c; B6 t, keven 15 minutes of direct skin contact with their male  `5 d9 ?& p1 y/ X& _: D
partners.6 However, when a shirt covered the applica-. V! n) i2 o8 B- o! E2 K6 G
tion site, this testosterone transfer was prevented.
+ I* D' e3 ?) K+ ROur patient’s testosterone level was 60 ng/mL,
, q" {8 U" B4 d- x( [which was clearly high. Some studies suggest that
1 I9 g/ F7 t0 U8 V% Odermal conversion of testosterone to dihydrotestos-
. c7 T; u6 I, q  W, Y- Bterone, which is a more potent metabolite, is more
9 {1 _4 u, f: i/ s) Jactive in young children exposed to testosterone+ q& H0 x0 r) o. T% q* Z3 N! b8 R) j' s
exogenously7; however, we did not measure a dihy-
( n4 K6 _( b$ M: i1 ldrotestosterone level in our patient. In addition to
$ N; v2 @- ]  p+ A& z5 p" I: Svirilization, exposure to exogenous testosterone in$ m: _. h0 o2 ]3 _1 M8 f0 L
children results in an increase in growth velocity and
7 X# B' g8 n: P3 |0 fadvanced bone age, as seen in our patient.! h# N0 H9 h8 ]% g1 G9 U
The long-term effect of androgen exposure during
4 j& m  L2 c' eearly childhood on pubertal development and final0 d& F# G6 y( w# ~# K  g
adult height are not fully known and always remain- Z8 S/ [6 p; l
a concern. Children treated with short-term testos-2 Y+ A7 i8 ^; [# W9 r
terone injection or topical androgen may exhibit some
4 U" [/ E3 P( _/ vacceleration of the skeletal maturation; however, after4 u9 @9 N+ g1 {" x' g/ \
cessation of treatment, the rate of bone maturation
- M- P( ~3 G- d% w7 n0 u8 fdecelerates and gradually returns to normal.8,9
( c, ?9 l7 n  n/ N, v! tThere are conflicting reports and controversy
7 I* ?: k! N4 e4 o/ w; Zover the effect of early androgen exposure on adult2 D# f% i, s$ k4 q' ~
penile length.10,11 Some reports suggest subnormal
. Z8 S4 H2 i4 o4 _3 Y0 Wadult penile length, apparently because of downreg-
! g' n) u4 B0 i# ~  {ulation of androgen receptor number.10,12 However,( m$ {/ m: u) |# f7 v
Sutherland et al13 did not find a correlation between1 `' i: D% w0 j* U* Z# |$ ^& a1 E  ~
childhood testosterone exposure and reduced adult5 w$ U. _$ N$ {; |7 F2 u, {; w
penile length in clinical studies.5 X6 p+ E; l/ _  W. f
Nonetheless, we do not believe our patient is
* Y1 q( }8 f2 V; k- @going to experience any of the untoward effects from' g& B) \3 \4 W
testosterone exposure as mentioned earlier because
; t3 p& G4 o9 P8 ]  `the exposure was not for a prolonged period of time.
, {( B/ H, o& U5 z* hAlthough the bone age was advanced at the time of$ Z: X  d( R: N) R
diagnosis, the child had a normal growth velocity at$ {' h$ F1 t  M% E8 o7 _. p
the follow-up visit. It is hoped that his final adult' B+ z: d# L. T1 M
height will not be affected.
) |: G8 t* Q* f7 g3 H1 D5 S7 f6 xAlthough rarely reported, the widespread avail-
& b+ N2 @7 B1 `- ^" oability of androgen products in our society may  z3 V7 W1 \; @7 p2 G% H: e
indeed cause more virilization in male or female
% V/ ?( X( l! z& k8 wchildren than one would realize. Exposure to andro-+ Y, R  L( {5 o. c. _8 ?
gen products must be considered and specific ques-
3 k+ v5 q1 y. }( Ytioning about the use of a testosterone product or5 d! H4 R- V# s
gel should be asked of the family members during
& W$ F' K$ G% j% pthe evaluation of any children who present with vir-
$ I( x$ e8 V% Oilization or peripheral precocious puberty. The diag-
& V8 m& B, K% e$ `5 _7 K. Pnosis can be established by just a few tests and by
! e6 E6 e: v; j" _/ _9 Y! |0 mappropriate history. The inability to obtain such a
  |3 t) h0 A7 w* S, o1 vhistory, or failure to ask the specific questions, may
; J$ b! Q, Z9 N2 presult in extensive, unnecessary, and expensive2 E) g. c! ^9 H3 b  o7 f
investigation. The primary care physician should be
3 b3 h% b! l0 kaware of this fact, because most of these children
, a$ n3 ]" m- f; D) m5 d9 i' ymay initially present in their practice. The Physicians’  I- C2 D8 _8 W" q! \' u" G
Desk Reference and package insert should also put a4 `! x$ f+ X( \& l
warning about the virilizing effect on a male or
+ E# k5 C$ L' _" tfemale child who might come in contact with some-* t) q: ^( Q# N
one using any of these products.* U7 W$ X  ~* o* B$ W. V/ M: `$ e
References* {. r3 Y2 A5 x6 K+ Y- |
1. Styne DM. The testes: disorder of sexual differentiation6 @- I2 W7 f9 f# U5 x
and puberty in the male. In: Sperling MA, ed. Pediatric& @" T# Q# V" e, ~3 z+ D
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;/ m! w7 R) {' t% d% @
2002: 565-628.3 W* C: o8 z7 ?
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious7 G% L3 {) q8 _1 O1 c
puberty in children with tumours of the suprasellar pineal
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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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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
5 V* ~( g' ]* z
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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