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Sexual Precocity in a 16-Month-Old
4 c( R1 D& y6 g) zBoy Induced by Indirect Topical: @& o. o, v- |2 p& {
Exposure to Testosterone
, z7 s+ v9 [/ R& z( \Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2! ~4 ?1 b0 F+ h2 K
and Kenneth R. Rettig, MD1$ u4 [7 k% Z& o) Y$ Z
Clinical Pediatrics# _6 K0 d/ q  a+ ~8 |# B" S6 C
Volume 46 Number 6
, I' ?0 o, z! v( M& qJuly 2007 540-543
3 X0 [1 v7 B4 m# V, R2 w* Y  ~; z© 2007 Sage Publications
7 Z2 G5 _$ w7 {( b& q10.1177/0009922806296651
/ `# z* r6 L4 }" M4 d# Whttp://clp.sagepub.com
' |; V8 U( b! ~3 S4 K5 t; T. ?9 Chosted at7 r5 I$ L% E% O2 k" L0 e
http://online.sagepub.com$ N6 c( E& r* C& K
Precocious puberty in boys, central or peripheral,( R" h' n" S& O0 n1 S5 b9 O) ^2 X
is a significant concern for physicians. Central
. K. s3 ]9 l+ ~3 g: eprecocious puberty (CPP), which is mediated7 Z( w8 D- k2 G1 s/ n
through the hypothalamic pituitary gonadal axis, has7 L1 }" ?9 ]$ D) r3 p: [& \* Q7 H: v
a higher incidence of organic central nervous system
1 U# f$ e: L$ y/ \( M3 r$ g2 j  [lesions in boys.1,2 Virilization in boys, as manifested& W7 X$ s6 b! R  K, y$ k
by enlargement of the penis, development of pubic
% ]- e6 T: S3 U0 n" R0 u) [- ^hair, and facial acne without enlargement of testi-2 }5 b1 d, N9 G3 L+ ?
cles, suggests peripheral or pseudopuberty.1-3 We
6 G& X7 ^7 S3 y2 @  Ereport a 16-month-old boy who presented with the
& c+ v# Q, B8 t% J) O, Nenlargement of the phallus and pubic hair develop-
1 T5 }% u4 }5 q7 \4 Hment without testicular enlargement, which was due) I7 h' P. J8 Q, X8 b( g
to the unintentional exposure to androgen gel used by
2 E3 T2 E2 l. b6 pthe father. The family initially concealed this infor-
. I: I& v& c3 r5 z" X# ymation, resulting in an extensive work-up for this
9 w& W' n% K- `child. Given the widespread and easy availability of
8 \5 t- C* W8 G' d$ ^testosterone gel and cream, we believe this is proba-
7 S# t3 b1 q" y; ?& L" x% I' x" M3 z, vbly more common than the rare case report in the
2 |. u. G) R/ I6 r/ ^6 _literature.41 W# j9 N) ]* {8 c
Patient Report: j& J% q- p% @: \7 c/ M
A 16-month-old white child was referred to the  X0 c( n- x+ ^; d0 b
endocrine clinic by his pediatrician with the concern
& w# c5 X! N" a# G& rof early sexual development. His mother noticed
% D! A* K# M8 ^: llight colored pubic hair development when he was
" U, p- n- |8 ?: q* m/ OFrom the 1Division of Pediatric Endocrinology, 2University of% d4 ~2 D) h* G; n% |! ~8 s
South Alabama Medical Center, Mobile, Alabama.
* H3 R8 F: G; Z% R) n6 DAddress correspondence to: Samar K. Bhowmick, MD, FACE,2 n5 y! {2 E2 m) Z5 M* ]) E; i! W: T
Professor of Pediatrics, University of South Alabama, College of6 z7 C' N0 L* t; a; m* V
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
8 V6 e3 x+ |1 g7 N! {e-mail: [email protected].
+ _5 h5 N8 n2 s& V- E" pabout 6 to 7 months old, which progressively became5 ^8 U5 d6 K7 q. p9 o
darker. She was also concerned about the enlarge-1 w; c( N  W' X9 T: Y, Z
ment of his penis and frequent erections. The child
5 B- F0 ^! C+ s7 o/ z' k3 g6 Iwas the product of a full-term normal delivery, with
4 X5 V4 Y7 }' ha birth weight of 7 lb 14 oz, and birth length of
* K0 K6 n) o3 y3 n) k. W20 inches. He was breast-fed throughout the first year% U' J4 `- w; K6 A4 L6 i% g! P
of life and was still receiving breast milk along with
' X# E$ w% Z/ q5 R- Z0 U& S' @5 `solid food. He had no hospitalizations or surgery,
, e' ?3 G2 i* I. b- ]and his psychosocial and psychomotor development
- H$ f/ M- R( {$ Owas age appropriate.
% g: D2 w3 z  `( s% M: dThe family history was remarkable for the father," P; s' x& v" T9 _
who was diagnosed with hypothyroidism at age 16,
$ G; \6 l9 ]* V; x& U+ Gwhich was treated with thyroxine. The father’s
, N9 c/ ]/ n, [' K' K) K5 ~/ N( B6 Oheight was 6 feet, and he went through a somewhat$ t: f% Q8 W& p0 ]
early puberty and had stopped growing by age 14.1 y* w* p' y3 ~
The father denied taking any other medication. The
3 N) g$ |0 h( d1 ?9 ^child’s mother was in good health. Her menarche
4 _% K% W9 A6 _0 l5 kwas at 11 years of age, and her height was at 5 feet
/ C5 U! t) X; v( ~  s! v: {5 inches. There was no other family history of pre-
6 S* ?) \( w/ a) A  M2 Lcocious sexual development in the first-degree rela-2 x* s. x9 f6 Z9 C- k  y
tives. There were no siblings.. U5 t: G. l* _- r3 P. L
Physical Examination4 |9 V/ a( z9 s6 c
The physical examination revealed a very active,5 t# F+ j' y) ?6 I
playful, and healthy boy. The vital signs documented
+ L* _4 [3 c. _$ oa blood pressure of 85/50 mm Hg, his length was
& [0 r' D4 W/ _6 z7 s1 K, u6 u9 |2 x7 z90 cm (>97th percentile), and his weight was 14.4 kg
& \% q  C% v. {* J: `+ c2 h(also >97th percentile). The observed yearly growth
& b$ L1 _( E6 u0 B$ Rvelocity was 30 cm (12 inches). The examination of
  |9 A% _8 j7 ^! Zthe neck revealed no thyroid enlargement.
8 ?/ c" T( E/ S/ }1 CThe genitourinary examination was remarkable for1 ^( O! s2 @; u! e
enlargement of the penis, with a stretched length of6 F1 X0 ^3 Z, E2 |: Y& E
8 cm and a width of 2 cm. The glans penis was very well
7 U: P: x5 u" Y. Rdeveloped. The pubic hair was Tanner II, mostly around) j# f9 X! Q; J4 y& i% `
540. ?+ I. C9 q4 H
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* Z) w) B$ \! \1 K0 l' S% |the base of the phallus and was dark and curled. The, {) D4 ?- B5 R+ S5 L9 R
testicular volume was prepubertal at 2 mL each.
$ `  c. M1 S( a' ^0 ZThe skin was moist and smooth and somewhat
9 e# R, g/ t. ]" I+ K2 h# Roily. No axillary hair was noted. There were no- _$ h' F. H$ `; m& ]( x: q( ?9 n
abnormal skin pigmentations or café-au-lait spots." m9 \6 @; R# [( `
Neurologic evaluation showed deep tendon reflex 2+' b" }3 M4 h+ }2 t9 I1 g
bilateral and symmetrical. There was no suggestion* J$ U+ C& j2 \$ N! c8 w
of papilledema.; ]0 R0 j4 S' D; W& }* V' Q% @
Laboratory Evaluation. z- h9 ?! r8 |6 S8 A
The bone age was consistent with 28 months by
/ h# F1 r2 y1 |8 h% }/ k0 kusing the standard of Greulich and Pyle at a chrono-* v& o8 k; m* D9 r
logic age of 16 months (advanced).5 Chromosomal5 q+ i  U; j; y3 [8 N- G
karyotype was 46XY. The thyroid function test% P# C4 |# `, S7 L
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
! e: c- q% k8 Z& f. I+ flating hormone level was 1.3 µIU/mL (both normal).
. S4 y6 ^" h, d/ L1 z* VThe concentrations of serum electrolytes, blood; ~, e8 N! `- v* {2 |6 Y
urea nitrogen, creatinine, and calcium all were; j3 {, ]$ ^. S8 h  j9 A
within normal range for his age. The concentration
- s$ U. B( V! [3 V- r0 e, Dof serum 17-hydroxyprogesterone was 16 ng/dL
2 F1 S9 g2 {9 |(normal, 3 to 90 ng/dL), androstenedione was 201 C) u  a1 m; M5 [6 M$ J4 K
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-7 h' K4 B+ @) v9 B6 h# S0 g4 x7 _
terone was 38 ng/dL (normal, 50 to 760 ng/dL),& I4 j/ o' G" t* g
desoxycorticosterone was 4.3 ng/dL (normal, 7 to0 m! ?, g) r! m
49ng/dL), 11-desoxycortisol (specific compound S)
2 U0 h1 b* C8 v, {, {& Cwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
" ^1 i0 y1 _5 }( J7 K: Ctisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total, s1 y: F+ U, i1 I2 ?
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),9 }) T2 m6 M6 i" \+ `  W
and β-human chorionic gonadotropin was less than
. K0 j9 d, ?) z4 G: f# D5 mIU/mL (normal <5 mIU/mL). Serum follicular& C% f) o. D5 q- [6 u: I
stimulating hormone and leuteinizing hormone# w6 Q7 i# A% a, [. A, [1 I1 _
concentrations were less than 0.05 mIU/mL9 e! G* Z9 ], F; B
(prepubertal).
( Q7 \7 k/ T( R" J; L- XThe parents were notified about the laboratory
$ ?/ G$ T- v! |8 v/ u3 G1 Y' Nresults and were informed that all of the tests were1 b* N7 K3 d9 g; ~/ E% V# d+ C
normal except the testosterone level was high. The" E2 j1 i+ |! J4 M7 \
follow-up visit was arranged within a few weeks to
- E) s3 P, F& c5 s5 {. T! R2 Robtain testicular and abdominal sonograms; how-
. {' f6 B! d1 @; u( _ever, the family did not return for 4 months.+ @, z! _% ]* j' Z0 u3 r+ m
Physical examination at this time revealed that the
* R5 b! Q0 b' t% p8 Q7 Ichild had grown 2.5 cm in 4 months and had gained$ }( K2 N  x, C: V. Z$ p# u# P( E) Y  x2 ]
2 kg of weight. Physical examination remained. h% K, T, a9 s+ f+ H
unchanged. Surprisingly, the pubic hair almost com-! H0 q1 Q/ e, T6 C! ?5 T. u
pletely disappeared except for a few vellous hairs at
9 O. ?+ v$ Z* \' k' Y" \0 Jthe base of the phallus. Testicular volume was still 2
" B% _! K1 j7 _1 N8 W3 k% b! hmL, and the size of the penis remained unchanged.2 A) b( }! ^; s
The mother also said that the boy was no longer hav-
4 \! _3 h/ s7 a9 t" m( j: `' F6 |( @3 \: eing frequent erections.
( s' f# d& u" T. u6 l, Q3 q1 Z* FBoth parents were again questioned about use of
! j& n0 J# f3 J3 x: I/ {any ointment/creams that they may have applied to! V3 i  G" O) W* N2 \
the child’s skin. This time the father admitted the
& B' v) \2 H3 o, @" D9 d& tTopical Testosterone Exposure / Bhowmick et al 541
* A3 P5 M1 b9 juse of testosterone gel twice daily that he was apply-5 y& Q. w6 W5 s) b) w
ing over his own shoulders, chest, and back area for* Q+ L( W* P/ \$ @, q) \
a year. The father also revealed he was embarrassed
7 I- @8 \& j: y- f3 M( h9 lto disclose that he was using a testosterone gel pre-
; r& A; ?% ~& N, h+ W8 F/ T) z( O- F" Lscribed by his family physician for decreased libido
% d  G$ L4 \9 tsecondary to depression.8 g0 ^" I- Z1 Q& o- @8 n
The child slept in the same bed with parents.4 y2 a1 v8 J9 s
The father would hug the baby and hold him on his
+ A. h/ B% J0 |( k7 U4 i9 [chest for a considerable period of time, causing sig-
! Y: x9 \4 s. k% Z) B0 Xnificant bare skin contact between baby and father.8 ?* d7 g: c9 x
The father also admitted that after the phone call,
, ~/ x) e+ t, j# {' o& `8 xwhen he learned the testosterone level in the baby0 D: {7 k* @$ i$ ~
was high, he then read the product information
1 t; c. l' U% @9 r9 V3 E' |6 Spacket and concluded that it was most likely the rea-
5 L! \4 q4 |$ N5 T! ]2 }) L# F( {son for the child’s virilization. At that time, they
; Q1 M. v- n% x. R$ Mdecided to put the baby in a separate bed, and the
0 {* \3 {& i# y5 e; G" v0 t5 Vfather was not hugging him with bare skin and had/ |2 A/ B4 h# I9 B# O
been using protective clothing. A repeat testosterone
7 g% n. l' N# M  Z% r+ Jtest was ordered, but the family did not go to the
$ E0 ^! C, C; ^: X2 J: ~laboratory to obtain the test.  j5 f+ \1 B) {1 {0 d4 k( [
Discussion' U  o+ b5 z5 h$ J6 d
Precocious puberty in boys is defined as secondary5 Q% O$ ?) [' ]0 N
sexual development before 9 years of age.1,4: h& l, E1 [: T  V# |/ F4 l+ r
Precocious puberty is termed as central (true) when0 J+ o) I/ \  r# Q! J1 A, K
it is caused by the premature activation of hypo-
4 U9 T- w8 r* k9 cthalamic pituitary gonadal axis. CPP is more com-
7 B, y! n' G$ zmon in girls than in boys.1,3 Most boys with CPP; y+ q( E: d0 O
may have a central nervous system lesion that is. R7 z& j. ~. y" @) t
responsible for the early activation of the hypothal-
8 b% M, m8 M& lamic pituitary gonadal axis.1-3 Thus, greater empha-- G! Z  x. o& L. Y; E2 I. q
sis has been given to neuroradiologic imaging in0 Y8 A; r2 B/ Y
boys with precocious puberty. In addition to viril-, f2 K5 s  j, U, y
ization, the clinical hallmark of CPP is the symmet-) p/ Y% {; t0 j+ ~5 [
rical testicular growth secondary to stimulation by
" |) F$ B5 K- V& Q; `/ `# r& J7 Wgonadotropins.1,32 v3 k5 D1 D& c% U& o5 T1 x  J
Gonadotropin-independent peripheral preco-
/ G3 K. I7 q) H- l8 b" n  vcious puberty in boys also results from inappropriate; z2 I! N6 ~% `6 \; |1 b% p
androgenic stimulation from either endogenous or* O0 R' Q7 J1 d8 h
exogenous sources, nonpituitary gonadotropin stim-& U* r4 t. @& g9 l' o6 D
ulation, and rare activating mutations.3 Virilizing( }: W3 m1 Q) D3 o( V7 F- R" l
congenital adrenal hyperplasia producing excessive
* h9 g. u9 Q4 O( p4 o0 Y5 A# Nadrenal androgens is a common cause of precocious
" A3 E7 h" C! p) a* b9 Mpuberty in boys.3,4
, Q/ t1 T8 f% _* FThe most common form of congenital adrenal
+ n  y& V+ H' B; I" I3 dhyperplasia is the 21-hydroxylase enzyme deficiency.9 [' u" J% V3 H" ?1 x
The 11-β hydroxylase deficiency may also result in
7 u5 E5 \# h& m2 t4 Wexcessive adrenal androgen production, and rarely,' t2 s- f. _. w% J9 }! ^; s! L% D
an adrenal tumor may also cause adrenal androgen
; d( g& B5 W! Y$ i: {' R; v3 Sexcess.1,3
; y& t# ]6 a% Gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ V) v9 @0 L) b9 f# `542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
2 v1 f7 f, \! jA unique entity of male-limited gonadotropin-
* F7 K( P4 T: ^independent precocious puberty, which is also known( O2 t, ~& @: h9 G# Y
as testotoxicosis, may cause precocious puberty at a& c# F% ^$ n$ F5 C
very young age. The physical findings in these boys
0 G4 R( z7 d. E  X1 bwith this disorder are full pubertal development,& v1 L/ Q, o, p4 ]. m6 B
including bilateral testicular growth, similar to boys
- v# f+ z- F  f* b+ e# Z" Qwith CPP. The gonadotropin levels in this disorder
: K7 C1 i& m' X  Uare suppressed to prepubertal levels and do not show# E. V% e. a% r  {, j
pubertal response of gonadotropin after gonadotropin-
( p# Z1 L) S# `$ ?9 s. Creleasing hormone stimulation. This is a sex-linked8 ]& K, f, I& |' W) i* L
autosomal dominant disorder that affects only7 {3 Z7 R' d4 z9 Y' B
males; therefore, other male members of the family
0 W. I( l" @! N- y6 dmay have similar precocious puberty.38 x4 D: F, O2 c! i4 u$ Z
In our patient, physical examination was incon-% h% u# `% \$ f, J! q8 B* F- r
sistent with true precocious puberty since his testi-8 {) u8 _( z; U" L" O
cles were prepubertal in size. However, testotoxicosis) p: o' l& i1 B( q. t
was in the differential diagnosis because his father) h# B8 `$ b) E+ Z8 G: b
started puberty somewhat early, and occasionally,  @; g4 G+ d( c/ g
testicular enlargement is not that evident in the+ ~# L6 p3 P% F$ _% s
beginning of this process.1 In the absence of a neg-' _9 r* A! q3 r- V0 P
ative initial history of androgen exposure, our
' K' A1 L' c6 l+ D# vbiggest concern was virilizing adrenal hyperplasia,
* O1 M1 I9 V' }/ t& ieither 21-hydroxylase deficiency or 11-β hydroxylase
/ T0 H; M: k* u* udeficiency. Those diagnoses were excluded by find-0 ]! ?* r0 v! I5 m" q
ing the normal level of adrenal steroids.
3 s# c8 L2 K0 m1 oThe diagnosis of exogenous androgens was strongly
& N( Y9 m- |5 H. A, C, u& U0 v, ususpected in a follow-up visit after 4 months because
& Y5 \5 ?9 o+ x0 Cthe physical examination revealed the complete disap-
5 {( b! `5 O1 B; \( @pearance of pubic hair, normal growth velocity, and
: [5 a& ~# _, U& B- edecreased erections. The father admitted using a testos-  X, n/ }3 ]9 S8 E" I" T. h6 S5 e: \
terone gel, which he concealed at first visit. He was6 \1 P, F( Y  |
using it rather frequently, twice a day. The Physicians’% ]+ F: ~4 ^# s; R: @6 O5 G  k
Desk Reference, or package insert of this product, gel or
8 P: w2 U0 C* |$ V& jcream, cautions about dermal testosterone transfer to
9 g5 K; v9 G0 l/ junprotected females through direct skin exposure.+ `$ t, L( \# W8 Z/ T+ K
Serum testosterone level was found to be 2 times the
; B$ T% ^) ]$ G  y) obaseline value in those females who were exposed to4 R1 `  r$ ~1 P' k% J; p& ^, V
even 15 minutes of direct skin contact with their male. }" f+ ]* B5 g0 w- K1 ^4 ^0 D
partners.6 However, when a shirt covered the applica-
6 `6 G& K" D: l  Y8 Mtion site, this testosterone transfer was prevented./ _' z- v4 b; e! P& Y1 H
Our patient’s testosterone level was 60 ng/mL,. s3 |8 Y4 h7 I$ w9 u, e: e
which was clearly high. Some studies suggest that
; G8 L# ]6 C: S. [+ J3 _: U& Adermal conversion of testosterone to dihydrotestos-+ G7 l: _+ r! C& L! U6 m
terone, which is a more potent metabolite, is more
; c4 _& q- b+ X3 [" q7 m5 vactive in young children exposed to testosterone
9 x% o- H+ V' |/ W% \2 pexogenously7; however, we did not measure a dihy-) w  {% |7 L" G7 P3 A3 [
drotestosterone level in our patient. In addition to
5 T; M4 F# b5 y. Qvirilization, exposure to exogenous testosterone in8 _, Z$ ^# I  ~* t
children results in an increase in growth velocity and
. U$ g5 M0 C& u) E! D  c; U+ _advanced bone age, as seen in our patient.
1 }) h" F# c3 Y! N5 A6 SThe long-term effect of androgen exposure during
( S  m% M9 w* g( s) W3 dearly childhood on pubertal development and final3 S6 D& c6 c  `3 q- Y9 F3 R  a
adult height are not fully known and always remain
: L7 c) p1 T# {2 }1 wa concern. Children treated with short-term testos-. j& L( K1 K9 I# m$ k5 C6 @/ {
terone injection or topical androgen may exhibit some
2 Y  z$ W; X# e( H' f6 vacceleration of the skeletal maturation; however, after; o0 {& Y8 S4 o- F
cessation of treatment, the rate of bone maturation; S( M4 b3 f1 ~
decelerates and gradually returns to normal.8,9" t7 c- F3 C$ O. C
There are conflicting reports and controversy8 R* V, ]* V# k$ o
over the effect of early androgen exposure on adult5 E% I. P( T2 s6 q$ l4 Z
penile length.10,11 Some reports suggest subnormal
" G+ w* i3 N- [adult penile length, apparently because of downreg-5 @# o2 L8 R% C; z3 ]
ulation of androgen receptor number.10,12 However,' N" }. {, {$ `# Z8 z- Z, H
Sutherland et al13 did not find a correlation between. S+ F$ l& V  X" w2 t* P$ D
childhood testosterone exposure and reduced adult
9 u8 V$ E) g) _1 T! Tpenile length in clinical studies.
" [/ y- D2 k; y5 qNonetheless, we do not believe our patient is4 k- P# V& b% m4 Z+ K3 ?1 {/ k
going to experience any of the untoward effects from5 l) d  x1 R, d3 A) S2 V* d
testosterone exposure as mentioned earlier because# J6 l/ J4 o( F6 v' z
the exposure was not for a prolonged period of time.( ~( b. j, ]8 t& x5 I" Y! C
Although the bone age was advanced at the time of
. R6 \6 O: \0 z' r! q3 @0 I% mdiagnosis, the child had a normal growth velocity at* K) K. ^; R. c7 G/ z4 z8 w9 j
the follow-up visit. It is hoped that his final adult
+ l$ D. ?/ \% z" {: P( s  Q: F* hheight will not be affected.
0 \# `; \" k4 h. C2 N5 w. f- wAlthough rarely reported, the widespread avail-/ b& R" o! j  U- x" J% _  \
ability of androgen products in our society may4 s! b  [" T7 l1 C6 q' R8 G: m
indeed cause more virilization in male or female1 Z" A+ d( r0 u
children than one would realize. Exposure to andro-
4 @% V: t& r# t8 |* ^" F% N: Zgen products must be considered and specific ques-9 S, w, T3 M* f3 d0 h) P
tioning about the use of a testosterone product or4 W3 A  B$ ^8 ^  H
gel should be asked of the family members during
  u/ [3 ~( |/ A$ S  M- ythe evaluation of any children who present with vir-6 Q+ C  ]. p, G$ s
ilization or peripheral precocious puberty. The diag-
! B2 S9 P. H1 `0 ^/ A; \$ `nosis can be established by just a few tests and by
( r* O) ?) r- {- q8 V; j: Rappropriate history. The inability to obtain such a3 ]; w% x, Z9 ?. A7 a1 _
history, or failure to ask the specific questions, may' R0 h8 L6 E% w1 c. [) {: W/ `7 ?
result in extensive, unnecessary, and expensive# h. I0 a8 s) b; ^  Q1 u
investigation. The primary care physician should be
0 l& Y' V+ [3 E, ~7 w8 eaware of this fact, because most of these children3 u, W8 j1 M- h. Y
may initially present in their practice. The Physicians’- O3 J3 _) b( w2 l  p1 o
Desk Reference and package insert should also put a0 A+ W# {! B7 O% |$ F2 r5 i9 x
warning about the virilizing effect on a male or
" g- ~4 ~" r. y" W; N. x: D) `/ ?female child who might come in contact with some-4 L& j3 ~+ B$ s9 G
one using any of these products.
3 P+ Y0 K9 j! m# f8 SReferences
" i( L8 j: y/ g# r1. Styne DM. The testes: disorder of sexual differentiation& j' K7 R) Q# X( H% M3 v  j
and puberty in the male. In: Sperling MA, ed. Pediatric
" ]/ P& H) Q2 {$ n$ m7 _, u& HEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;! O( Z1 t" C0 ?  S  g7 h( L+ S: q/ G; _
2002: 565-628.
1 E% F- ?( S9 F% B3 |/ {& V2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious& v& H; f: W+ l  _/ u) j
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old# C! s" l) f2 e
Boy Induced by Indirect Topical
; @7 K+ U) Y: g4 C- R0 lExposure to Testosterone
# v9 D( p* q# ?! _Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
* I7 P# d7 x5 @2 [and Kenneth R. Rettig, MD1
+ Q' @' O+ R- \2 D. @9 _/ J1 SClinical Pediatrics. D5 q8 W. m7 \& p& H
Volume 46 Number 6
1 @+ G' \8 ~! R4 x0 TJuly 2007 540-543" w+ M# F& L6 S
© 2007 Sage Publications9 }) r* y+ r& {: d. C
10.1177/0009922806296651& K* [1 B% H, U0 M8 Y. n
http://clp.sagepub.com
- L2 T& I( k6 W: P+ J/ q% {hosted at
: o0 b: J  [. \. M  d$ phttp://online.sagepub.com
6 E4 O% t9 ?7 G2 s4 C& MPrecocious puberty in boys, central or peripheral,/ _- J/ O" h' G4 R! k  U7 v
is a significant concern for physicians. Central% _) A2 F& b' C
precocious puberty (CPP), which is mediated: S$ A, H: j( c) ^
through the hypothalamic pituitary gonadal axis, has
  U7 s, D, \& g7 ta higher incidence of organic central nervous system
# x% F1 A- q7 a" m0 V5 slesions in boys.1,2 Virilization in boys, as manifested
" o0 H9 l! E' G% i% N) a' j! h0 g5 kby enlargement of the penis, development of pubic  _, H6 h  B8 D  g2 M" {+ J
hair, and facial acne without enlargement of testi-. ?: p5 I& C7 j  u5 M+ d
cles, suggests peripheral or pseudopuberty.1-3 We
. @2 J% M4 v: W2 p; m! `  Nreport a 16-month-old boy who presented with the; ?- ^* W0 z7 F# F. y
enlargement of the phallus and pubic hair develop-
0 h1 M' R+ B( S; x; U3 Z7 o9 Qment without testicular enlargement, which was due# `1 k) h" ^5 Q- T9 `
to the unintentional exposure to androgen gel used by
' q' w, `& ^5 p0 u5 p+ V% D8 @/ Y  Xthe father. The family initially concealed this infor-# i6 g: E8 E% W- j. B& B
mation, resulting in an extensive work-up for this1 k! U6 g( M# d& m; r, p
child. Given the widespread and easy availability of
6 ^: I7 B) j0 [testosterone gel and cream, we believe this is proba-
. V. B$ Z$ O# @" @6 F$ Gbly more common than the rare case report in the7 o. Z' z- [* I1 t* x
literature.4
+ s7 E# @5 S! W, s/ YPatient Report  Z& R2 ^" k# |+ g! \* n0 y
A 16-month-old white child was referred to the& O+ b3 x" T3 o3 p7 I
endocrine clinic by his pediatrician with the concern
4 ~: }9 v7 l9 \/ D; Dof early sexual development. His mother noticed
0 Z2 {5 ]: Y2 w4 |light colored pubic hair development when he was2 f) ~# @. A1 G+ j9 A& X# V
From the 1Division of Pediatric Endocrinology, 2University of+ _3 x# ^- r1 F; E2 Y$ V+ F
South Alabama Medical Center, Mobile, Alabama.
2 Q: b, ^$ S0 V9 q; b) rAddress correspondence to: Samar K. Bhowmick, MD, FACE,' j( Q4 w( X# ]
Professor of Pediatrics, University of South Alabama, College of
4 D) z/ R( ?8 }( C% SMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
2 G: F( q! d' `, Re-mail: [email protected].5 j% W( d& U4 o) I+ d
about 6 to 7 months old, which progressively became
! B+ M, ]0 S# adarker. She was also concerned about the enlarge-
; B) e, K: ^  {- j) ament of his penis and frequent erections. The child/ O' G5 u+ s4 t5 i! A5 J0 n0 _1 k
was the product of a full-term normal delivery, with: s# b  h% Y0 v4 C7 @; G
a birth weight of 7 lb 14 oz, and birth length of* e4 t; g7 @, d( a
20 inches. He was breast-fed throughout the first year2 C7 W  i% g  I5 j
of life and was still receiving breast milk along with. S4 L" z, k1 m
solid food. He had no hospitalizations or surgery,
# l! ~: Y$ J( O3 pand his psychosocial and psychomotor development# ?# m4 j9 b' V8 i' {  i# z) N
was age appropriate.6 Z- C& R' E' g' l
The family history was remarkable for the father,
3 O8 M/ \. r( f- t9 c/ u0 Wwho was diagnosed with hypothyroidism at age 16,
7 f6 R+ N( t* S/ m' ~, F& t4 gwhich was treated with thyroxine. The father’s6 v' x6 B# Y# x  T+ ]$ h/ @6 Z
height was 6 feet, and he went through a somewhat
; I4 `5 U- u0 L0 l" j' Cearly puberty and had stopped growing by age 14.
' {+ S* c9 `  Z% G. J0 A+ GThe father denied taking any other medication. The
* @' C* |. `( e/ u; K$ x6 Nchild’s mother was in good health. Her menarche
6 e( L8 G6 U1 \. Wwas at 11 years of age, and her height was at 5 feet
' V5 f% ]5 T/ i  W3 M5 inches. There was no other family history of pre-9 `* w2 |% [% w1 b3 z! _' Z/ m' a
cocious sexual development in the first-degree rela-  g9 l( \; }3 A3 O5 j1 A/ R% @' F* H
tives. There were no siblings.
# C/ V. D1 G$ d1 G' K$ sPhysical Examination
* ?2 ~3 C+ h* A; D3 lThe physical examination revealed a very active,
, S; v8 ^! i/ P$ d9 W8 ?2 b( Uplayful, and healthy boy. The vital signs documented
) g5 [+ M8 ~+ ja blood pressure of 85/50 mm Hg, his length was' g1 d7 |0 h" {* Z* U
90 cm (>97th percentile), and his weight was 14.4 kg; s# i' x  B2 p
(also >97th percentile). The observed yearly growth) x5 ~6 \1 j/ x
velocity was 30 cm (12 inches). The examination of
8 c- Q0 f4 c! t1 athe neck revealed no thyroid enlargement.
0 u3 |- P" ]$ E3 d! U* Q, DThe genitourinary examination was remarkable for8 `) I+ c8 t' c& ~3 D
enlargement of the penis, with a stretched length of
3 q1 x# @( u( y( ~3 v8 cm and a width of 2 cm. The glans penis was very well
2 D. @2 N) b4 sdeveloped. The pubic hair was Tanner II, mostly around
& V/ |9 E3 G1 o, S5 l  y540
  I( M1 E! ~8 h2 y5 I1 Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' S) L% U' \2 S' @the base of the phallus and was dark and curled. The6 v! ^. p" @$ J( s3 X- o( j0 v: _5 g
testicular volume was prepubertal at 2 mL each.
4 ?1 i* d. f( y* a: n( y3 ZThe skin was moist and smooth and somewhat
3 \+ u' a7 n" T( F/ {+ Zoily. No axillary hair was noted. There were no
4 A/ A$ `0 M0 @abnormal skin pigmentations or café-au-lait spots.
/ f0 L; N+ T) i" b/ @Neurologic evaluation showed deep tendon reflex 2+
! B/ t5 w+ s7 hbilateral and symmetrical. There was no suggestion0 `6 s) Q3 |* h4 c
of papilledema.5 q! N9 F7 b- ]9 ^
Laboratory Evaluation7 I! e2 R6 `1 g
The bone age was consistent with 28 months by2 s0 g" m2 n0 ?# z+ I
using the standard of Greulich and Pyle at a chrono-
: ?6 }0 U- a1 m4 T0 n- _8 alogic age of 16 months (advanced).5 Chromosomal" ]7 k6 A! }. M1 R9 B
karyotype was 46XY. The thyroid function test
9 ^+ [( z1 |4 c( P/ ?, l* l& U2 Wshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
0 i* y/ I2 P3 [+ ulating hormone level was 1.3 µIU/mL (both normal).
; C% X- ?" R$ @; h0 LThe concentrations of serum electrolytes, blood7 U, k/ D9 {( O% r
urea nitrogen, creatinine, and calcium all were& w2 ?8 u4 n, Z
within normal range for his age. The concentration$ ^3 u7 H3 f& h  l+ V
of serum 17-hydroxyprogesterone was 16 ng/dL: J, P5 u" H& P/ }% F
(normal, 3 to 90 ng/dL), androstenedione was 20
3 p8 E; r! N: L1 p/ }ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-# U4 }& @& x2 T( w
terone was 38 ng/dL (normal, 50 to 760 ng/dL),* r/ q3 h, {* U  {/ z8 ^+ X7 {" W
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
( V) u+ `4 k* o" v5 n49ng/dL), 11-desoxycortisol (specific compound S)+ V% \# \* g, h3 ~9 P. [
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-; l- ~3 t' B7 u1 x; t# ]3 U7 O
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
4 R: {: F! X8 n- ?# m" Ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
# @2 J) q, K7 q/ g0 C4 tand β-human chorionic gonadotropin was less than* K+ F) s+ z9 r2 h
5 mIU/mL (normal <5 mIU/mL). Serum follicular
" o1 s/ U+ {) L& {9 Vstimulating hormone and leuteinizing hormone
* S; m* |8 M$ B0 oconcentrations were less than 0.05 mIU/mL7 W4 _" k8 W# S, _$ H
(prepubertal).7 \3 j. |/ c- X2 l$ S  D! d  D
The parents were notified about the laboratory
5 W6 U- [" f& e6 [results and were informed that all of the tests were
4 m1 n1 d' M5 [normal except the testosterone level was high. The
' B9 X, q3 a' V) {8 ]follow-up visit was arranged within a few weeks to
8 I9 \4 a; z0 ?3 `. g0 jobtain testicular and abdominal sonograms; how-0 n, B0 V, k, t( X$ u
ever, the family did not return for 4 months.7 Y6 P2 E# B3 I( K3 n
Physical examination at this time revealed that the
3 ?8 F0 ]9 Q* q0 Y# U8 B! S  echild had grown 2.5 cm in 4 months and had gained3 @/ `0 ], K# Z/ A8 l1 Q
2 kg of weight. Physical examination remained
! o7 Z9 K4 V) \( f& Munchanged. Surprisingly, the pubic hair almost com-
2 t1 {3 {4 R( t7 U( m4 R' s! Jpletely disappeared except for a few vellous hairs at: w& L- c$ Y% r8 {0 B3 N1 \+ ?
the base of the phallus. Testicular volume was still 24 G- V, B5 a& L; z9 }
mL, and the size of the penis remained unchanged.
8 A- \0 N; F2 d8 f4 ^5 v% EThe mother also said that the boy was no longer hav-8 v- ~1 |; c5 A5 c6 R& s- m
ing frequent erections.! Y' `# C+ N3 U
Both parents were again questioned about use of, t. [2 ^: U: [7 J4 h, u' E" [
any ointment/creams that they may have applied to
+ S$ ]5 e+ Y2 _/ D; J6 S0 @the child’s skin. This time the father admitted the' l8 ?: K( R+ ^/ w' V7 _6 Q3 ?
Topical Testosterone Exposure / Bhowmick et al 541( k: `( l; ^/ ?- C
use of testosterone gel twice daily that he was apply-- C. `& I* R0 u9 `1 f% K7 L
ing over his own shoulders, chest, and back area for' H: v& [$ I( k) v0 ~
a year. The father also revealed he was embarrassed# J' n. V7 h( i% t+ Z
to disclose that he was using a testosterone gel pre-
5 c: T* \" }2 \' q: f2 Fscribed by his family physician for decreased libido& F8 R/ s) P7 u
secondary to depression.
, S! q0 B' f: V; e( @The child slept in the same bed with parents.; ~: ~7 t* S8 n/ m4 m& z
The father would hug the baby and hold him on his/ j2 C$ d3 c! E6 w: J0 c9 r
chest for a considerable period of time, causing sig-2 m9 I/ U9 b. \. y
nificant bare skin contact between baby and father., a* x& e5 k; `6 {& w" D% ^9 }
The father also admitted that after the phone call,
, {+ _  J: l5 Owhen he learned the testosterone level in the baby
- d$ {# O8 U4 X- \5 iwas high, he then read the product information
  ]+ ]7 b3 `- I6 x3 p) o% x; Ipacket and concluded that it was most likely the rea-
. ?% @  j/ O( J% kson for the child’s virilization. At that time, they
' Z. R  k% L9 Q: Fdecided to put the baby in a separate bed, and the- Y! {8 d/ U; G$ w! T
father was not hugging him with bare skin and had
. _: V* r) y+ b% Q5 [+ |  Ybeen using protective clothing. A repeat testosterone
1 c2 }, o7 u4 h. ^5 dtest was ordered, but the family did not go to the
" x# L: D4 V7 Hlaboratory to obtain the test.1 @  w* j- h. ?* y& P2 k, ^
Discussion
7 u0 }1 \7 t5 n+ g- @Precocious puberty in boys is defined as secondary
! |2 {8 O7 B/ Y6 u- a8 tsexual development before 9 years of age.1,4) v3 @* q7 s' C3 p' b
Precocious puberty is termed as central (true) when! M7 v+ n7 I& u/ V6 n
it is caused by the premature activation of hypo-
3 i2 [# u8 }5 D) |: s. J# ^7 F! D$ Tthalamic pituitary gonadal axis. CPP is more com-# Y# v% t* C7 A
mon in girls than in boys.1,3 Most boys with CPP
* @$ |. I3 c; `% @% o# X% smay have a central nervous system lesion that is
( v) l: O6 ]3 g- u- O1 n) ~responsible for the early activation of the hypothal-
# ]8 |7 P7 l# w, ^- V* [# m) Camic pituitary gonadal axis.1-3 Thus, greater empha-
5 I& |3 P# r' xsis has been given to neuroradiologic imaging in) C" [# F5 W: _3 I% t- G9 {/ ?# A
boys with precocious puberty. In addition to viril-0 \) u( _- Y' L& y& ~2 \2 T
ization, the clinical hallmark of CPP is the symmet-
; T& w% A; c2 K# Orical testicular growth secondary to stimulation by
" p6 W6 L1 `. Jgonadotropins.1,3+ k1 E( A' J% p8 a( x6 H' q! U- c  w
Gonadotropin-independent peripheral preco-
3 t8 |- ]+ Z/ h+ u! W6 Y* |9 Y5 C- Fcious puberty in boys also results from inappropriate9 s6 ^1 m5 h7 Y9 J- H8 ~# a2 U* k
androgenic stimulation from either endogenous or
7 X( J% P' B5 |* j% v* ^exogenous sources, nonpituitary gonadotropin stim-' t" {# G# ^# ?& y. q" d
ulation, and rare activating mutations.3 Virilizing
0 ?" [* O! E. Q" D& Pcongenital adrenal hyperplasia producing excessive/ t- I  J7 N4 K
adrenal androgens is a common cause of precocious
/ ^" w) @+ H7 {- ^puberty in boys.3,4+ O2 Y5 C7 L& S3 O4 v+ f  |( H7 E
The most common form of congenital adrenal
7 O2 [, M% E4 y* phyperplasia is the 21-hydroxylase enzyme deficiency.
! X) t, J! |% U( ~! T! i& X- C4 UThe 11-β hydroxylase deficiency may also result in
/ Q7 o5 ^# _, ^' ~excessive adrenal androgen production, and rarely,
; X8 V" h7 g0 Y% H. k0 i& Can adrenal tumor may also cause adrenal androgen5 R# {; i7 b. r2 Z5 ^/ W
excess.1,30 ?$ W" L6 Q6 s% z( T
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: P. E8 J3 Y5 m; I/ e
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007  T; k4 m5 h! e/ [2 Q9 N) L' L8 T
A unique entity of male-limited gonadotropin-
( q' O; r# m, e2 x& |4 }independent precocious puberty, which is also known* E* j6 d6 n5 Y7 k! K( d
as testotoxicosis, may cause precocious puberty at a3 T" a5 j% O& \; ^/ @3 X) t
very young age. The physical findings in these boys( a: q4 ^$ I% F/ |
with this disorder are full pubertal development,* W3 c" h( q$ b/ r  f, L3 ^
including bilateral testicular growth, similar to boys: i5 c* }  j* V+ W$ j' Q
with CPP. The gonadotropin levels in this disorder
) Z! Z  w) j$ T6 A- e3 }6 Nare suppressed to prepubertal levels and do not show
7 C! k3 D0 U+ s) ^5 L3 C4 O/ |pubertal response of gonadotropin after gonadotropin-9 W( l! N$ T  m# g
releasing hormone stimulation. This is a sex-linked
7 H4 p: U. q! m9 Sautosomal dominant disorder that affects only/ N' O4 }) `+ K# p* b
males; therefore, other male members of the family$ X' }. U0 w+ ^
may have similar precocious puberty.3
% M8 @2 t3 }! }* |* K: mIn our patient, physical examination was incon-1 {1 X/ ~' s0 M8 V; i& D3 N+ R- M
sistent with true precocious puberty since his testi-
# o5 z, ~5 _3 y8 Kcles were prepubertal in size. However, testotoxicosis, z2 @! {; c5 Q) y6 L% o7 r
was in the differential diagnosis because his father
: `: f2 T5 Q$ A& \4 Fstarted puberty somewhat early, and occasionally,
( @5 [3 X" H; z# U) h, Qtesticular enlargement is not that evident in the
2 s) S3 B5 e  s& l! ibeginning of this process.1 In the absence of a neg-; z/ k; O% g7 c% U% m) r
ative initial history of androgen exposure, our
4 \& w( z' @) i* Wbiggest concern was virilizing adrenal hyperplasia,# ~  j5 ^- J9 U, E7 S
either 21-hydroxylase deficiency or 11-β hydroxylase. C9 t( O0 e6 t$ d% f
deficiency. Those diagnoses were excluded by find-- m" N4 h& c) Y4 [! D3 r# v( ~
ing the normal level of adrenal steroids.
7 {2 P+ W3 S6 F4 {+ G0 F+ B: SThe diagnosis of exogenous androgens was strongly7 `% c% f' A4 a( h
suspected in a follow-up visit after 4 months because
3 `4 g) I. P8 L2 _the physical examination revealed the complete disap-
4 ^1 Q; }! x( s1 O, Q  Bpearance of pubic hair, normal growth velocity, and' X/ a2 |/ e  g5 g, I  U9 [" v" i& E
decreased erections. The father admitted using a testos-% Z; X+ c7 d( ]* r& _0 p) s
terone gel, which he concealed at first visit. He was* [% O1 ~2 H* F
using it rather frequently, twice a day. The Physicians’
' H% g$ g' ~: ?Desk Reference, or package insert of this product, gel or0 A8 s. i2 R6 j( r+ M/ ?* }
cream, cautions about dermal testosterone transfer to
1 J" |2 j7 \4 |1 q/ D* ^+ Aunprotected females through direct skin exposure.8 [+ w) X0 I: H) Y2 M
Serum testosterone level was found to be 2 times the
) M3 G0 u/ M; f3 z- p- Sbaseline value in those females who were exposed to
* P+ R4 a# k$ ]/ Peven 15 minutes of direct skin contact with their male
3 }5 A& w/ y$ t+ i3 Z- ^  Mpartners.6 However, when a shirt covered the applica-
' P6 X; c2 b* d! Ltion site, this testosterone transfer was prevented.
5 P8 A; s2 Q( X2 h, [4 AOur patient’s testosterone level was 60 ng/mL,
8 y: m; H. z! }4 _3 u- Xwhich was clearly high. Some studies suggest that0 @8 R, O0 O; v( Q
dermal conversion of testosterone to dihydrotestos-! S5 y& D0 B0 f0 q6 V
terone, which is a more potent metabolite, is more) N, L% h5 d* }* d% f( B- O" d
active in young children exposed to testosterone: C1 o5 ]4 b- L! v* `
exogenously7; however, we did not measure a dihy-
1 H9 e  Q9 T9 k2 Vdrotestosterone level in our patient. In addition to* i6 Z( C8 Y3 j* G7 p4 h
virilization, exposure to exogenous testosterone in
+ k5 c5 t+ I. Nchildren results in an increase in growth velocity and
, o, \( V3 u. q' Hadvanced bone age, as seen in our patient.% o" O3 L! M6 [* ?- A. q; n' c
The long-term effect of androgen exposure during
! Y& @- y6 D6 E5 B4 ^4 Mearly childhood on pubertal development and final
& P3 A2 Q2 v2 |) \8 ]; L! W" Nadult height are not fully known and always remain
6 e# I; Q. x- j) z+ la concern. Children treated with short-term testos-
8 h1 C3 f, a8 R  pterone injection or topical androgen may exhibit some
8 d1 O# O, [0 i) eacceleration of the skeletal maturation; however, after
/ p$ w/ h/ B7 Icessation of treatment, the rate of bone maturation
: _5 ?0 P1 I  z, K) cdecelerates and gradually returns to normal.8,9% G9 k) G3 h, r3 z
There are conflicting reports and controversy6 @! D' l! {$ B$ ?" Q
over the effect of early androgen exposure on adult
% O: X2 W' |2 k" d! Epenile length.10,11 Some reports suggest subnormal
  T0 N' V+ y. z3 madult penile length, apparently because of downreg-6 v# Y/ O9 e* x$ c' j# R+ A+ ?
ulation of androgen receptor number.10,12 However,
/ b, k1 [+ ^6 p/ o/ t' h' ?7 LSutherland et al13 did not find a correlation between0 ~6 I8 S, p3 |( O% x
childhood testosterone exposure and reduced adult; P/ O2 A6 m* @; X5 i0 X
penile length in clinical studies.
* H1 C* p  P5 c3 MNonetheless, we do not believe our patient is
' u) T$ D; q' j. e+ Z/ D; ~: ggoing to experience any of the untoward effects from
% J) O/ P3 c/ z7 |testosterone exposure as mentioned earlier because5 f* ?8 x! K2 ]/ J
the exposure was not for a prolonged period of time.# T" u. _9 n) k% l
Although the bone age was advanced at the time of8 I* x5 U8 E7 q& X: r
diagnosis, the child had a normal growth velocity at
1 Z/ W$ H% T% ?& i4 _the follow-up visit. It is hoped that his final adult
: G( W% H- i' F) vheight will not be affected.
9 s# e7 D. a8 M: G0 |7 T/ l, d2 ~Although rarely reported, the widespread avail-* c+ n& Y: ^: L. M2 T& ^. C
ability of androgen products in our society may; e" p3 s7 ]; h
indeed cause more virilization in male or female
+ I7 @0 Q; |) T0 d5 r5 tchildren than one would realize. Exposure to andro-& m, u  y6 w$ h' K) L
gen products must be considered and specific ques-
1 W) ~. A: ]/ v; X  R9 X* Mtioning about the use of a testosterone product or3 J1 l% T. x# F) S- b# ]2 p/ b; _/ X+ W
gel should be asked of the family members during/ p  A' ?5 u+ t5 t3 y2 f4 A- v
the evaluation of any children who present with vir-( \/ j4 {4 N# s# M5 k+ u- y
ilization or peripheral precocious puberty. The diag-
! k7 q- J4 G. y) Bnosis can be established by just a few tests and by
# o! \/ x3 ^7 }( c2 C8 [( _! ^appropriate history. The inability to obtain such a
0 B* P3 F3 E6 \' ]0 A7 h; f( ^, Ohistory, or failure to ask the specific questions, may7 ~; S* [9 u: E; Z9 U
result in extensive, unnecessary, and expensive7 x* ~: |3 O% |5 e* Q
investigation. The primary care physician should be! s& R& w5 ?* ~! w% p! Z6 p, a/ f; V
aware of this fact, because most of these children/ W9 s. m+ |0 \0 w- g" B' j
may initially present in their practice. The Physicians’
- j6 T5 `' V) Z+ E. BDesk Reference and package insert should also put a- A( t4 J1 J& @- z3 o' e
warning about the virilizing effect on a male or* A/ _- ?6 ]3 e+ r: _
female child who might come in contact with some-! x6 B# R, p8 k+ U4 |
one using any of these products.6 _$ B* a2 a4 d. q
References& q7 g3 h" S; J5 d
1. Styne DM. The testes: disorder of sexual differentiation- G  @1 i' W3 I5 D
and puberty in the male. In: Sperling MA, ed. Pediatric
  o7 O' z9 T: H$ D2 d% ZEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;& V2 V/ R8 [% e
2002: 565-628.
, }( h% _! d1 ?  |0 U, n, a5 t2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious* Q7 J7 S8 P! }
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!
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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

' k) J+ P# O/ u  ?$ U3 o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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