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Sexual Precocity in a 16-Month-Old. ^$ k7 d" V1 c% R( O
Boy Induced by Indirect Topical
7 y- J- W, o) K- g) P+ e3 }2 [Exposure to Testosterone  P/ a7 i, g; j% @; I
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
- v" [5 p$ S" t6 f3 cand Kenneth R. Rettig, MD1
3 n8 s4 U7 h* i8 c0 jClinical Pediatrics
; S+ o/ ]' l: T" V/ w5 vVolume 46 Number 6
5 D" c% v$ T- ~7 n* r( X& S( g  J' hJuly 2007 540-5435 D; E+ t- n/ P( c0 a# h
© 2007 Sage Publications
/ G7 e, W; ]% ^, A! M10.1177/0009922806296651" {& m7 p: a5 g. A1 G6 k, r9 q& ~  j
http://clp.sagepub.com
1 m0 `+ ?( R/ J$ _3 ?( Whosted at
& e% q+ q* z8 G1 @/ d( `- \http://online.sagepub.com) [6 _" ]# r  L+ U' w! [0 y' ~
Precocious puberty in boys, central or peripheral,
0 @5 K& ?5 O# B  cis a significant concern for physicians. Central
9 [# B, q& r9 l3 Fprecocious puberty (CPP), which is mediated. l& m9 a! U: y2 z
through the hypothalamic pituitary gonadal axis, has
5 v0 P7 ^' _" H% y% @a higher incidence of organic central nervous system9 O% V7 a4 Q7 O
lesions in boys.1,2 Virilization in boys, as manifested: v- J( c! J, J& _
by enlargement of the penis, development of pubic
3 w- \4 u4 ]9 C1 E) whair, and facial acne without enlargement of testi-& K/ y2 Q$ q9 j* H
cles, suggests peripheral or pseudopuberty.1-3 We- P1 i8 r4 k1 f) ~0 _
report a 16-month-old boy who presented with the; Y6 p! A/ E/ w" }  z
enlargement of the phallus and pubic hair develop-7 k4 [  R& \* L+ x; i. J  Z
ment without testicular enlargement, which was due
- L. C0 ?' g4 Q1 n" o# E# D/ _to the unintentional exposure to androgen gel used by
1 ?/ v2 b0 |3 D7 B! y  r' Tthe father. The family initially concealed this infor-: v; d  F: i  {5 t6 a/ a; T
mation, resulting in an extensive work-up for this
6 _4 `$ r. I: Y+ S# Uchild. Given the widespread and easy availability of2 ?' g6 G# m$ ]3 o
testosterone gel and cream, we believe this is proba-; V/ |/ Q# B$ ]8 Q8 n! S2 p
bly more common than the rare case report in the& T6 p6 D' F/ t1 k% a
literature.4
2 m( W/ W* E# k) N% x3 H; Y3 FPatient Report0 Z2 V' o" C6 {1 g$ Q& ?9 |1 j
A 16-month-old white child was referred to the
- i" M6 l8 V, eendocrine clinic by his pediatrician with the concern5 L/ k$ X5 h# V: F, s# {
of early sexual development. His mother noticed
: Z  ]2 o$ B* j4 y6 i2 s! Elight colored pubic hair development when he was. t' Z! f% L/ z2 Z0 k1 `1 t% H% _
From the 1Division of Pediatric Endocrinology, 2University of
, U" w$ n2 G# USouth Alabama Medical Center, Mobile, Alabama.
( D& j5 X8 h( x5 D( S7 _+ ZAddress correspondence to: Samar K. Bhowmick, MD, FACE,
; D: @: I+ p' m/ Q8 e) l+ TProfessor of Pediatrics, University of South Alabama, College of, ~9 M. z( P: [/ f
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;0 Q2 t, j0 R: w0 s
e-mail: [email protected].
9 G# g+ u& ]% P, F# yabout 6 to 7 months old, which progressively became& [+ B! x" W; X  S" ?, [
darker. She was also concerned about the enlarge-
8 ~, i" |' D5 H% v) Jment of his penis and frequent erections. The child
1 u6 `: n' q* U2 U/ i" {+ p4 Nwas the product of a full-term normal delivery, with% @  W4 i3 G6 z9 z0 \
a birth weight of 7 lb 14 oz, and birth length of
! y, G; K8 F+ `! z20 inches. He was breast-fed throughout the first year- y8 J3 n; B& Q2 m; ~; B
of life and was still receiving breast milk along with
: ]: j: U6 P& z* N9 n, M9 Esolid food. He had no hospitalizations or surgery,' v# [" `* g4 Q6 j( p- y' m3 \
and his psychosocial and psychomotor development3 ~* e. ^4 i, o* e
was age appropriate.
2 R% T; p8 S: d. Z1 t9 S( KThe family history was remarkable for the father,
: N+ y( {' \/ h" s6 \/ c# N& X) D" kwho was diagnosed with hypothyroidism at age 16,. L  D2 n# p& u) V
which was treated with thyroxine. The father’s
# h5 V' ~0 [# J* s9 ?* iheight was 6 feet, and he went through a somewhat. f- M9 k8 }3 _
early puberty and had stopped growing by age 14.
7 M  @, i* `* K$ V& S" ^The father denied taking any other medication. The
, U0 v6 N7 v9 n/ Y1 \child’s mother was in good health. Her menarche
. M7 K+ p: }3 f7 M( q8 ?8 ewas at 11 years of age, and her height was at 5 feet- J6 U& Q5 }/ g
5 inches. There was no other family history of pre-3 N8 W3 R# c0 c. }& b3 q2 l  g
cocious sexual development in the first-degree rela-
; c! b3 I) R$ z3 ftives. There were no siblings., g0 S! q0 D5 ~
Physical Examination% z) V7 E( e% B
The physical examination revealed a very active,
. S# H% y- a9 g+ z4 Jplayful, and healthy boy. The vital signs documented; K+ e) @3 t+ _# `
a blood pressure of 85/50 mm Hg, his length was4 I6 v8 z2 o5 J  l+ K" Y5 N
90 cm (>97th percentile), and his weight was 14.4 kg$ b" c( i( s- P1 C
(also >97th percentile). The observed yearly growth
1 ], g' F8 ~0 m% T9 evelocity was 30 cm (12 inches). The examination of
6 j0 k2 A8 o# \' jthe neck revealed no thyroid enlargement." v+ f- ?0 _( l4 A6 L, X
The genitourinary examination was remarkable for
  ?5 S8 f1 h3 ]  J' r; n. fenlargement of the penis, with a stretched length of
" |4 p4 m4 K4 F& {8 cm and a width of 2 cm. The glans penis was very well
6 N1 V, Q: A3 J1 c! ~developed. The pubic hair was Tanner II, mostly around
% B% G8 X  J6 e7 i- K540
* y+ _  s5 l' b3 r+ U1 vat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 F$ [7 ?, e; k- _& Pthe base of the phallus and was dark and curled. The
4 x: K- C5 [0 U! l6 p7 Atesticular volume was prepubertal at 2 mL each.+ s$ u! D  M  e; A( Y5 s% i
The skin was moist and smooth and somewhat! i0 w9 R) @+ h8 [: U7 m; z- c
oily. No axillary hair was noted. There were no9 q1 ^5 S" {' L, ^  T
abnormal skin pigmentations or café-au-lait spots.5 {* E+ d0 N! {% n. E1 l
Neurologic evaluation showed deep tendon reflex 2+
' l: W* \- R7 U. _( Ebilateral and symmetrical. There was no suggestion! x. I5 m: G- g$ _: ~. P! D; v
of papilledema.
: e7 V4 G9 m$ v! G8 z  B( ULaboratory Evaluation
4 K7 ]" w- w# u+ l# gThe bone age was consistent with 28 months by. ^! R" h- ^8 |' l1 G; v
using the standard of Greulich and Pyle at a chrono-
7 a# ^0 [  V8 Z: E4 R* \" G, jlogic age of 16 months (advanced).5 Chromosomal" r8 H6 Q0 d1 Z8 S3 p# i# a9 u+ W
karyotype was 46XY. The thyroid function test) k3 W/ J4 Y+ i3 d6 N1 R1 L* {
showed a free T4 of 1.69 ng/dL, and thyroid stimu-7 u" W' i( o; e. {. u' q+ q& R
lating hormone level was 1.3 µIU/mL (both normal)., h3 R6 y2 o4 m; G3 L
The concentrations of serum electrolytes, blood
) m# b) ?0 V" w1 I3 R7 p  Aurea nitrogen, creatinine, and calcium all were' X7 f4 F" S! ?  a- G# x
within normal range for his age. The concentration
3 u0 N& V0 @8 H! Hof serum 17-hydroxyprogesterone was 16 ng/dL
8 d; \5 I, E# Q9 F$ p1 h(normal, 3 to 90 ng/dL), androstenedione was 20+ e* {9 x+ g7 E  C# |7 b7 h
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
3 _- D! _; W  d3 c; Aterone was 38 ng/dL (normal, 50 to 760 ng/dL),
, r6 A8 y8 H# m1 f2 W0 ddesoxycorticosterone was 4.3 ng/dL (normal, 7 to8 N; N5 ~: l; ]& q* A
49ng/dL), 11-desoxycortisol (specific compound S)
7 ^# f- f- g! Z4 Y0 twas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-' h4 O/ F( f, L* y4 z1 `
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
/ f& _1 w& N$ a* B3 itestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
% d) u. r# q6 b% d6 e/ D8 oand β-human chorionic gonadotropin was less than. G9 ?9 s! t% a( w
5 mIU/mL (normal <5 mIU/mL). Serum follicular/ _( H1 F# D' U# i" C6 M, k6 J
stimulating hormone and leuteinizing hormone+ W" E5 Y- X4 T8 m
concentrations were less than 0.05 mIU/mL, n8 k1 I* u* s7 X7 l
(prepubertal).
- W6 }7 l! u& U+ q! {( N2 _7 Y3 \The parents were notified about the laboratory9 B- ]) L& y+ o. t( q
results and were informed that all of the tests were3 k$ F( l9 {2 r& r
normal except the testosterone level was high. The
! x- F6 J( W9 ufollow-up visit was arranged within a few weeks to
( p3 I* R# E$ C) `1 Cobtain testicular and abdominal sonograms; how-7 L+ w( x- \! e- p; j* I" n
ever, the family did not return for 4 months.
9 j0 L+ W$ V- x  d/ M5 N0 QPhysical examination at this time revealed that the( I- h/ P+ b, [! E. R/ f4 o* z
child had grown 2.5 cm in 4 months and had gained
9 I9 b$ s  b* j# ^# O8 m2 kg of weight. Physical examination remained0 J: G" A* B9 k# z# ~2 }2 _! Y
unchanged. Surprisingly, the pubic hair almost com-
7 l2 w7 @$ o9 J: V, Wpletely disappeared except for a few vellous hairs at
$ y6 F3 R" |+ C+ [; p" e5 |3 k9 Gthe base of the phallus. Testicular volume was still 2
& m) C& ~, C& B2 g3 s0 ~4 C7 j) S& hmL, and the size of the penis remained unchanged.2 A5 ~! ^( m& F8 h: {6 e9 p
The mother also said that the boy was no longer hav-
' B) Y0 s  O- H6 ~7 q5 Z% Qing frequent erections.7 X+ i3 V1 z6 f9 F# d+ N' J% j+ M
Both parents were again questioned about use of
% \2 j: ^2 _2 s& \0 s; ^* H3 [* N- b7 aany ointment/creams that they may have applied to
# z: w. u% Q3 C! n9 @( ]4 Qthe child’s skin. This time the father admitted the
' g, p/ O- b! f! K! ~% d4 sTopical Testosterone Exposure / Bhowmick et al 5410 k/ l4 `3 ~" N" Y
use of testosterone gel twice daily that he was apply-2 S9 n  t( |; z6 `" s" g
ing over his own shoulders, chest, and back area for
' X! @* M  z- Y' r4 ya year. The father also revealed he was embarrassed
# b: d. V  B" x  Qto disclose that he was using a testosterone gel pre-
+ C& }3 u) F) K! ?scribed by his family physician for decreased libido( \) s2 z: Z; @$ ^" U3 u) P
secondary to depression.
3 P; S# p/ _; q& A" ~3 ^! W, `! fThe child slept in the same bed with parents.
* x! g' a6 G! N. ~- p% P* T3 lThe father would hug the baby and hold him on his& Y$ E( X, ]% G- B
chest for a considerable period of time, causing sig-8 Q6 v; W) d  o
nificant bare skin contact between baby and father.9 E7 x0 U8 l* q8 N2 U9 U
The father also admitted that after the phone call,+ J2 ?# d7 }# ~
when he learned the testosterone level in the baby
, i# `8 ~2 P7 c1 }) o  kwas high, he then read the product information; P6 U; n# U1 t
packet and concluded that it was most likely the rea-% a1 e+ J8 M# U. N) s! `4 I% [
son for the child’s virilization. At that time, they& j$ Z' Q7 A4 a4 E
decided to put the baby in a separate bed, and the
" M" ^9 {2 N3 _8 V7 p0 Kfather was not hugging him with bare skin and had, ^8 h7 n1 n5 i) d4 Y
been using protective clothing. A repeat testosterone9 x$ O. V# I9 v6 k3 X' b5 t
test was ordered, but the family did not go to the
6 J% X2 J" g/ Xlaboratory to obtain the test.
% s3 f/ L% m: W+ lDiscussion. |1 n& p5 j# J
Precocious puberty in boys is defined as secondary
( G9 c6 ~; Q3 E( s$ P4 x5 E! Ysexual development before 9 years of age.1,4' \/ S: Y5 j  M) G2 k2 I9 u- b
Precocious puberty is termed as central (true) when
) Q( Z8 S0 `2 W% A. z0 h9 q. H) o7 mit is caused by the premature activation of hypo-
& y/ u1 l0 ^: K) [( K% g) Mthalamic pituitary gonadal axis. CPP is more com-+ h, V2 Y8 q+ V5 p. z
mon in girls than in boys.1,3 Most boys with CPP
  |3 x2 [4 P5 Z7 c4 ?& jmay have a central nervous system lesion that is! k  k5 |' F* V/ K1 {! @
responsible for the early activation of the hypothal-0 ?* P) K. t$ S* H
amic pituitary gonadal axis.1-3 Thus, greater empha-- R8 I) O* ^/ C+ i* a
sis has been given to neuroradiologic imaging in
) P, q& [4 q+ N  }7 b& b6 r% aboys with precocious puberty. In addition to viril-
) h0 |+ K! w' V' Cization, the clinical hallmark of CPP is the symmet-
+ H- }8 l* t* Z; h. z4 Yrical testicular growth secondary to stimulation by
* A7 D& x5 h" h' j' y( Z$ [0 p% Cgonadotropins.1,3
8 S) [$ ~& b& x% D. eGonadotropin-independent peripheral preco-
) x# q( S3 z6 f5 l. ycious puberty in boys also results from inappropriate  f; [+ m' e! `) E! X% k
androgenic stimulation from either endogenous or. G4 k* \% _# M/ ~' h
exogenous sources, nonpituitary gonadotropin stim-
7 O2 ]+ v- [4 e' Kulation, and rare activating mutations.3 Virilizing3 {- y; F5 u" M9 {1 `) O% y% A9 I
congenital adrenal hyperplasia producing excessive7 X- [% s! {& N8 U3 d3 ?
adrenal androgens is a common cause of precocious' Q! P6 a' U- j' t1 A
puberty in boys.3,4
, X4 d: T" e; H( f3 dThe most common form of congenital adrenal' R/ [9 ~3 K/ P* E
hyperplasia is the 21-hydroxylase enzyme deficiency.# U8 D5 L9 c* E4 k- Z% m3 n  j- }
The 11-β hydroxylase deficiency may also result in5 ^2 q8 s& i  @* N4 t
excessive adrenal androgen production, and rarely,
1 ^, z. K; R" f( E) @; A3 C' dan adrenal tumor may also cause adrenal androgen9 ~8 H3 ^( B- K' d% V9 Y0 ^1 O
excess.1,35 o# E. L/ _. I
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
7 J: b) o* F7 @  y) @542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
# {, |8 B+ m& ~: B6 _9 f8 o8 A1 K- aA unique entity of male-limited gonadotropin-
. I, z  N) l; G* k+ Rindependent precocious puberty, which is also known
  F; j: }# c: `; ias testotoxicosis, may cause precocious puberty at a, T' N: r$ r$ H2 y
very young age. The physical findings in these boys& a5 k! i! k" a# D2 X  u
with this disorder are full pubertal development,
8 [5 C) \0 E8 C5 g7 F: wincluding bilateral testicular growth, similar to boys6 `6 V  D3 H% ]& A6 l2 k5 \& [
with CPP. The gonadotropin levels in this disorder
$ {0 G; Z& l  M" [, xare suppressed to prepubertal levels and do not show
' q. \, @* V; Z% E4 w/ }6 L  spubertal response of gonadotropin after gonadotropin-8 X6 L" g% N, i/ }6 T# C# V
releasing hormone stimulation. This is a sex-linked+ I9 O6 H; }5 Y; W7 ^% i
autosomal dominant disorder that affects only" F2 H$ G3 r( g' Q9 L% ^8 j% |
males; therefore, other male members of the family  o5 d4 \" N! m0 }% n/ {+ D4 |) W
may have similar precocious puberty.3
6 L% J6 n$ G2 |/ g  YIn our patient, physical examination was incon-/ T: v' n4 G5 v
sistent with true precocious puberty since his testi-# B/ I5 Q" C  I6 X1 Q
cles were prepubertal in size. However, testotoxicosis
1 p1 z, z! M6 l8 h; D4 `was in the differential diagnosis because his father
% M; W- x( n: h# R+ Estarted puberty somewhat early, and occasionally,- G5 B. C+ [5 q' m# b4 a+ \
testicular enlargement is not that evident in the& g% c! Y- s5 f/ G) b! P
beginning of this process.1 In the absence of a neg-# [. F1 c# z+ w$ [
ative initial history of androgen exposure, our8 _6 U6 [2 u% E+ C+ s4 h
biggest concern was virilizing adrenal hyperplasia,
5 T/ C# ^8 p2 a3 F& `either 21-hydroxylase deficiency or 11-β hydroxylase
' t" T: h( P' W- F3 \deficiency. Those diagnoses were excluded by find-6 L! j! {7 M7 j; R
ing the normal level of adrenal steroids.
: I$ c% C8 D* _The diagnosis of exogenous androgens was strongly
9 X& V3 K4 P  W1 D/ Q% tsuspected in a follow-up visit after 4 months because
  v- {8 Q. ~5 K+ W" D% lthe physical examination revealed the complete disap-
! g! C5 _8 V5 K2 Tpearance of pubic hair, normal growth velocity, and
8 k7 j( y9 ]. ?; ydecreased erections. The father admitted using a testos-5 Y0 K& x- p0 e
terone gel, which he concealed at first visit. He was
) O+ b0 z; S! ?5 A$ ^using it rather frequently, twice a day. The Physicians’
4 h0 m2 Y. }# f: v  `3 ?1 FDesk Reference, or package insert of this product, gel or
2 G& }" @1 w2 C+ f6 \  W6 ucream, cautions about dermal testosterone transfer to
) y$ z7 S* S1 U# x" yunprotected females through direct skin exposure.
& Y& B( p) {& y/ `6 z9 GSerum testosterone level was found to be 2 times the
" c' i3 X  p: q5 {, K' Ybaseline value in those females who were exposed to
. h4 S+ r- H2 ]1 m. R1 aeven 15 minutes of direct skin contact with their male
2 Y$ z) V- c; Vpartners.6 However, when a shirt covered the applica-5 C' z; F* j3 [& H& \
tion site, this testosterone transfer was prevented./ i4 Q$ u3 d- K! W; @
Our patient’s testosterone level was 60 ng/mL,
$ {/ e% L$ \  c' p$ E' wwhich was clearly high. Some studies suggest that; x/ k2 u* r* w( z& s) Q
dermal conversion of testosterone to dihydrotestos-7 r- _: Q* R+ N: g
terone, which is a more potent metabolite, is more
( L1 _& s# I8 L& S9 Z1 Sactive in young children exposed to testosterone
- d9 b  n- Y- X6 |' g5 eexogenously7; however, we did not measure a dihy-
: z, O# d! t: a: |/ e0 Udrotestosterone level in our patient. In addition to8 X% d. m" y$ N# c+ Q
virilization, exposure to exogenous testosterone in
; Q; l( o0 ]; M: d. J$ _7 }children results in an increase in growth velocity and
, ]" N( c9 D- i. O6 C# ?advanced bone age, as seen in our patient.
9 T# r! B# m$ [3 T9 {' a7 I7 jThe long-term effect of androgen exposure during6 r: }: K7 D9 F8 k, E9 O& N' V
early childhood on pubertal development and final) e! s: H, l1 H9 C
adult height are not fully known and always remain
" _* K$ t! K& e7 ~1 Ia concern. Children treated with short-term testos-* t5 y  n. \$ ], z% |/ z+ T
terone injection or topical androgen may exhibit some
& V/ q1 a1 Y/ b* I7 _$ R% }acceleration of the skeletal maturation; however, after
4 ^/ b9 G  P* b9 B8 V2 ]cessation of treatment, the rate of bone maturation+ k3 `% [" K" ~3 k3 N
decelerates and gradually returns to normal.8,9
+ H) Y& o, l8 ?* a5 v  g( d, v7 rThere are conflicting reports and controversy
* N9 p7 w  u: |* A1 wover the effect of early androgen exposure on adult: t$ x9 O  Z8 L# ^: P2 P
penile length.10,11 Some reports suggest subnormal
  K, S0 v9 ~+ w! F9 @8 C2 ~8 Badult penile length, apparently because of downreg-6 A- ]1 U; s$ t/ |
ulation of androgen receptor number.10,12 However,9 p; _9 z% ~) [+ _0 ~" `1 I5 b
Sutherland et al13 did not find a correlation between
! d8 ^" d+ w3 j; cchildhood testosterone exposure and reduced adult9 e9 l) S- w7 H6 j3 ?: q
penile length in clinical studies.
- S3 L+ z9 I6 q" @1 B0 }4 qNonetheless, we do not believe our patient is
! a5 g) Q9 r" w, w6 |$ {! q+ {1 ^going to experience any of the untoward effects from
) T! i6 |+ o  f3 n3 ~8 O6 J' Wtestosterone exposure as mentioned earlier because9 P' Y' `$ {; F0 o
the exposure was not for a prolonged period of time.
& M) R2 W& x* k" \3 t2 D% r/ dAlthough the bone age was advanced at the time of/ K+ |1 P% \4 P- D6 n( [- a
diagnosis, the child had a normal growth velocity at4 Q0 R3 b- b: Y5 x6 x
the follow-up visit. It is hoped that his final adult, f6 _& L' Q% @: i6 H6 t! Z
height will not be affected., o1 w" l. \9 A' l6 w. m- V
Although rarely reported, the widespread avail-
6 b6 e5 ?! Z  P. T, r! @$ J$ i5 zability of androgen products in our society may4 z/ j! C. U$ r- N, Q
indeed cause more virilization in male or female
2 @; L; S, y! j" u5 x0 schildren than one would realize. Exposure to andro-/ l, ^7 x& D" h0 K$ ]/ z
gen products must be considered and specific ques-+ S0 u  m4 y0 e% U: [6 ~% M
tioning about the use of a testosterone product or
9 |! u9 d# _; A9 @7 Ggel should be asked of the family members during& b& t2 i# X* s9 \, h
the evaluation of any children who present with vir-" v, A4 O8 h% @6 ?3 N
ilization or peripheral precocious puberty. The diag-
, ?9 F' L; Y2 M0 v. O: B! Knosis can be established by just a few tests and by
$ Z" w! k6 T0 A( L# a; m) Oappropriate history. The inability to obtain such a
4 A  `; k/ i$ ~# u2 fhistory, or failure to ask the specific questions, may: L! x6 d+ g: L1 v, \0 {. D; y: a
result in extensive, unnecessary, and expensive
$ o  ?6 {4 f' d0 Z% _5 ninvestigation. The primary care physician should be$ L/ \& @+ w8 q2 U4 ^/ a
aware of this fact, because most of these children9 l  Z& w) n3 [8 m( ~
may initially present in their practice. The Physicians’
+ B! G+ o: s- ~& o. Q6 ^9 f4 FDesk Reference and package insert should also put a. G6 g, [7 m# n" K; P3 I4 b1 m4 D2 s
warning about the virilizing effect on a male or
8 Z. g( v9 s9 wfemale child who might come in contact with some-
2 g8 b1 e# D3 R7 Yone using any of these products.
, g% f( V5 ]7 l& g' zReferences
5 K+ b* h+ o7 {0 W1. Styne DM. The testes: disorder of sexual differentiation
. @) c0 x$ d' H& a7 b$ Oand puberty in the male. In: Sperling MA, ed. Pediatric; E5 G3 n1 q  J& q: {
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;* k' H6 z7 T; K1 l8 {' @
2002: 565-628.
- s/ K2 [" x! D, S0 z- n, \2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious. {+ T: q- z' ^# L' }# V$ \- q
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
7 ?9 b* p( M1 u# h6 tBoy Induced by Indirect Topical
; e) P- o; A5 ?; E% S! s4 l2 xExposure to Testosterone; k/ U1 }+ m4 c5 m6 S" d
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
: w/ [& ^" E+ |6 g+ R, ~0 ^: Pand Kenneth R. Rettig, MD1
# I/ C1 p) N0 @' g, Z: XClinical Pediatrics
  P) r  w7 @. [9 k; m% DVolume 46 Number 6
/ N9 ~( ~, F( Z( E* U$ jJuly 2007 540-543$ s5 O8 j( p- c% R
© 2007 Sage Publications
) g! o5 U) b' m& t* U. o10.1177/0009922806296651: R7 t3 k- h; k5 \6 Q
http://clp.sagepub.com# u9 |- l# E2 r  i8 a* E
hosted at
7 R1 x; ?  @* J, ~. K6 uhttp://online.sagepub.com( V% s( A1 N3 [0 X% X6 G4 a
Precocious puberty in boys, central or peripheral,
$ r6 `/ r6 g7 e9 C; |5 K; Y8 D$ Y  iis a significant concern for physicians. Central
  b7 k* x0 J0 N8 Z- vprecocious puberty (CPP), which is mediated, `7 V2 K2 V: s. ?
through the hypothalamic pituitary gonadal axis, has4 m; A& x9 L! Q0 k) K
a higher incidence of organic central nervous system; G/ c; U% V8 H) a7 Y* Q2 `
lesions in boys.1,2 Virilization in boys, as manifested* m* U2 t* t6 w. f8 ?
by enlargement of the penis, development of pubic
" [" H( V$ B5 Z. @; M  {! A# W! f$ Thair, and facial acne without enlargement of testi-) M0 z' u( D8 \6 W& [
cles, suggests peripheral or pseudopuberty.1-3 We3 a2 S: Y( E' `) c
report a 16-month-old boy who presented with the; N% Z1 {* B2 Z% B$ P* A! r
enlargement of the phallus and pubic hair develop-. E' }1 U4 ^) t# x% s0 }, @- I8 V( V
ment without testicular enlargement, which was due
' Y7 a% o+ |  \! ?: ~& wto the unintentional exposure to androgen gel used by& B7 r4 I% j$ P6 {( ^: |% ~8 I
the father. The family initially concealed this infor-
' T$ z! L) t9 x' D4 imation, resulting in an extensive work-up for this+ E; F* Z+ F# b1 u, `
child. Given the widespread and easy availability of7 |' y# c/ r7 s$ i* _' ?
testosterone gel and cream, we believe this is proba-
# ?; ]8 y+ y/ D, v0 Z0 j# Jbly more common than the rare case report in the
$ F6 _8 [6 }+ v+ Xliterature.4+ i$ I$ w2 l# C
Patient Report* T7 H5 y$ C7 z  s3 W& i( k
A 16-month-old white child was referred to the
' e) V8 w, c, T1 e) O- Q" pendocrine clinic by his pediatrician with the concern
* E" ]. r% J( ?) X# aof early sexual development. His mother noticed1 k" `' y# w+ p4 h0 Y
light colored pubic hair development when he was
5 p" S5 n/ X9 H$ e8 gFrom the 1Division of Pediatric Endocrinology, 2University of% }4 E, `& V+ c5 R
South Alabama Medical Center, Mobile, Alabama.
9 {6 D/ e9 w6 |3 d$ u. Q/ p$ ~Address correspondence to: Samar K. Bhowmick, MD, FACE,3 e2 k$ X7 a8 f
Professor of Pediatrics, University of South Alabama, College of
! Y( `; S: m2 ?9 a9 G5 uMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
/ l# c2 E+ {+ C$ M6 o+ Ze-mail: [email protected].
5 f* w8 U8 t. ?about 6 to 7 months old, which progressively became
3 v  {3 s0 a* P  x  x# Jdarker. She was also concerned about the enlarge-
' T+ B1 J4 E: X* bment of his penis and frequent erections. The child
0 |: F- O2 ^, \: G* cwas the product of a full-term normal delivery, with& J; y3 {- p3 F6 {6 f
a birth weight of 7 lb 14 oz, and birth length of3 g. s) h. s6 k0 t4 `1 V* L. V
20 inches. He was breast-fed throughout the first year
+ C/ D- d+ X8 c* m0 L. Mof life and was still receiving breast milk along with
* _$ w" x8 `8 c% Ssolid food. He had no hospitalizations or surgery,
) L3 A8 l# U( j2 x4 d0 W0 Hand his psychosocial and psychomotor development
/ M+ L  g1 x+ `0 _was age appropriate.
& x7 r$ `3 L6 k/ [: TThe family history was remarkable for the father,
9 i* Q: O: e% m1 p* m( @& Hwho was diagnosed with hypothyroidism at age 16,  Y$ X9 c% D3 ^2 s$ e  f
which was treated with thyroxine. The father’s4 L0 X8 r7 s" m
height was 6 feet, and he went through a somewhat- p0 N$ T2 E1 e( o5 a# ?
early puberty and had stopped growing by age 14.
7 }# P( i4 E) _7 M0 {9 |3 ?The father denied taking any other medication. The
  ]7 N" W! R0 h5 `6 m: E1 lchild’s mother was in good health. Her menarche
' \2 e: Y( F0 R* h) z+ n" r) Xwas at 11 years of age, and her height was at 5 feet
4 @4 G$ S' ^5 D- u) R5 inches. There was no other family history of pre-, D( h8 ~& F# F9 V- ~5 n
cocious sexual development in the first-degree rela-
2 `2 c0 I9 e: F% K( `tives. There were no siblings.
  d: \2 C5 O) h0 [5 Y# HPhysical Examination
0 E: m" v) O9 V/ qThe physical examination revealed a very active,3 [' ?* `4 O: j& U# l* x* A/ `
playful, and healthy boy. The vital signs documented/ m7 I3 a7 {. q
a blood pressure of 85/50 mm Hg, his length was
- ]) y9 C2 ?1 {0 w90 cm (>97th percentile), and his weight was 14.4 kg
2 k# n7 ~3 V1 Z. P6 g5 J; d- {(also >97th percentile). The observed yearly growth
" d7 ^9 A* g/ k% e0 V0 d' j3 X2 ovelocity was 30 cm (12 inches). The examination of
% ]3 a9 p4 g2 T$ ^. V9 B; cthe neck revealed no thyroid enlargement." B2 I; }* \* C8 |# Z- G3 `
The genitourinary examination was remarkable for
4 g- s$ j. `6 J3 H' ~  K" e6 Uenlargement of the penis, with a stretched length of) ^5 u2 |* ]+ |% n2 J
8 cm and a width of 2 cm. The glans penis was very well
" `* F5 b4 `7 y& _: H) C! p2 [developed. The pubic hair was Tanner II, mostly around7 d7 j5 `! ~$ M& `) n
540" ^) p" Z& _  N
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# s! G" L5 }/ w3 Sthe base of the phallus and was dark and curled. The* J' \/ `% [* S/ P
testicular volume was prepubertal at 2 mL each.( g/ A! {3 {+ C# A1 S& C1 A+ L
The skin was moist and smooth and somewhat0 J7 z2 e2 a* N# @1 F
oily. No axillary hair was noted. There were no8 I8 {/ R5 j5 S+ X, [$ d8 J4 m
abnormal skin pigmentations or café-au-lait spots.9 k( ]9 @* v) @! u/ W
Neurologic evaluation showed deep tendon reflex 2+7 G9 i: y  M& S4 V: W
bilateral and symmetrical. There was no suggestion5 \; q5 f  v6 F! c0 _' V" H$ E
of papilledema.
& ?& M# `. A: U- @# M* YLaboratory Evaluation
1 b7 m3 T+ @+ t5 z0 T7 w2 i5 JThe bone age was consistent with 28 months by
2 _4 W: m! i+ \8 n3 Dusing the standard of Greulich and Pyle at a chrono-  F3 \0 t' z, n9 W' j
logic age of 16 months (advanced).5 Chromosomal
+ D7 q; L; c' X3 k# H% a* L1 nkaryotype was 46XY. The thyroid function test- c$ @& J# x2 V) A; G3 T
showed a free T4 of 1.69 ng/dL, and thyroid stimu-  V, y4 F! \5 g! @/ S7 [2 m8 m8 h
lating hormone level was 1.3 µIU/mL (both normal).' C- a6 W, y" i5 V$ q' u( n2 P
The concentrations of serum electrolytes, blood' R9 Z+ s) m  M, ?6 E! y
urea nitrogen, creatinine, and calcium all were
' I$ O# j$ N- n9 d8 Y* m3 ~7 ywithin normal range for his age. The concentration
% o3 Y4 b4 k* r5 W0 _0 }5 Yof serum 17-hydroxyprogesterone was 16 ng/dL% y2 l2 E  A  c: w8 k3 {
(normal, 3 to 90 ng/dL), androstenedione was 20
! ~, K! L8 e6 M4 g) u5 vng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
1 m; Z1 U$ Y1 X( kterone was 38 ng/dL (normal, 50 to 760 ng/dL),
3 L2 K5 r9 D9 q( u8 U, N4 X& e1 ydesoxycorticosterone was 4.3 ng/dL (normal, 7 to) E+ _! ]1 Z. c" r" J0 _! q
49ng/dL), 11-desoxycortisol (specific compound S)
( ~5 N( s% g" n: g7 i: Nwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- c7 i0 I5 q) ]
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
% Y# ?2 E* K6 K  Z: Rtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),/ P  [3 Q( H% y- E3 L3 ?! h! ~) x
and β-human chorionic gonadotropin was less than
6 s$ U0 k! s& u3 M' G5 mIU/mL (normal <5 mIU/mL). Serum follicular
) v6 u- y% j( M! K) \, V( u! e- g( Estimulating hormone and leuteinizing hormone4 `3 l+ c; E/ m9 [$ C7 u6 R9 L
concentrations were less than 0.05 mIU/mL9 y7 q8 P6 x, [4 L  ?2 f- t
(prepubertal).' {3 l4 a5 D/ K: q- j
The parents were notified about the laboratory
% r# v9 A+ g2 D' _* c6 F7 i9 L4 [2 Qresults and were informed that all of the tests were" s! e# U% q% Y1 y! F
normal except the testosterone level was high. The
" _# R, [8 \3 e1 Z; I" C$ Xfollow-up visit was arranged within a few weeks to7 X6 w9 R1 c+ f2 M- O# R% H" r+ J
obtain testicular and abdominal sonograms; how-
; H8 s" C& Q/ v  J- f5 [" W" R. r5 _* Tever, the family did not return for 4 months.  N+ s- _6 T/ k  h, ?& p3 R' X
Physical examination at this time revealed that the
: T& t% w; X) [0 Schild had grown 2.5 cm in 4 months and had gained
7 _8 L/ O( n) S+ f3 b: h" ]( F2 kg of weight. Physical examination remained* e4 `; p) _9 B* }2 B" O
unchanged. Surprisingly, the pubic hair almost com-
, k6 \) V# m$ N& W3 t  n. G0 M8 Q$ Epletely disappeared except for a few vellous hairs at; E7 {. {7 G& k% K
the base of the phallus. Testicular volume was still 2
1 [+ t% R0 B5 W! G/ {1 ]- u0 F2 fmL, and the size of the penis remained unchanged.
* G1 y4 Z% a! {The mother also said that the boy was no longer hav-' _/ t$ V+ B1 }! r0 S4 w
ing frequent erections.
/ ~, f; S3 ]4 s. W) y  {0 k$ h. {Both parents were again questioned about use of% P/ {. Q+ `* S% |7 h+ ~
any ointment/creams that they may have applied to
# r" m+ e4 W% ethe child’s skin. This time the father admitted the8 k4 N5 ^) f6 N9 n# E3 x2 H$ K
Topical Testosterone Exposure / Bhowmick et al 541
+ Y) ?6 [# R: q, b0 z/ Zuse of testosterone gel twice daily that he was apply-
6 H3 R# Q; w; x, X% King over his own shoulders, chest, and back area for
( ^) G6 }2 w/ R2 j: l; W- U6 pa year. The father also revealed he was embarrassed
4 |9 Q$ K$ G* U9 Uto disclose that he was using a testosterone gel pre-
2 r6 y' ?0 |4 p" y3 d& Q2 u+ p$ fscribed by his family physician for decreased libido
! U/ Z& P( ?1 \6 Ssecondary to depression.
  f2 a/ [  ?6 WThe child slept in the same bed with parents." N9 |8 ]3 Z; o' ^" s- |/ N
The father would hug the baby and hold him on his
8 |  ^7 `+ ~) n% ^chest for a considerable period of time, causing sig-
6 m, ]+ L  P* b8 s( lnificant bare skin contact between baby and father./ N' g6 K: I6 [, b) L! n
The father also admitted that after the phone call,
- N2 g4 x7 F* }$ F; Owhen he learned the testosterone level in the baby' t* m8 B  w' B5 c/ N
was high, he then read the product information
/ W* k8 n* i3 B( Spacket and concluded that it was most likely the rea-2 ^/ T% s8 M- a- F# \- m9 h( T4 V
son for the child’s virilization. At that time, they
+ k2 N! ~" @0 Y- b$ C7 e/ udecided to put the baby in a separate bed, and the$ ~! ~) v3 f9 l: U/ h! K( s
father was not hugging him with bare skin and had# b. x# o  P+ W; n% g' L
been using protective clothing. A repeat testosterone
8 H6 f2 Z/ O2 p4 F/ U* ]test was ordered, but the family did not go to the
+ x5 k4 ^1 R" W6 plaboratory to obtain the test.0 T3 Q* @/ J" G# R: @
Discussion
; t" V$ ]1 s0 Y5 D' pPrecocious puberty in boys is defined as secondary
2 T3 V) R- U3 U* R7 m/ l+ [# }sexual development before 9 years of age.1,4
! J$ F1 F0 |$ Q. Y1 S" H  \Precocious puberty is termed as central (true) when8 N$ V  M( k4 D6 V
it is caused by the premature activation of hypo-& F+ _! |% e, p' w4 c1 O; E( Q: y
thalamic pituitary gonadal axis. CPP is more com-
3 J7 r+ s! n; _( f) B6 N0 V% gmon in girls than in boys.1,3 Most boys with CPP
) n& l! ?- N7 amay have a central nervous system lesion that is
% p' k2 y1 J: l" D' B) P( d6 G, T( uresponsible for the early activation of the hypothal-
- {% r4 Z* r4 [  oamic pituitary gonadal axis.1-3 Thus, greater empha-5 [) }* Y6 K& _6 l
sis has been given to neuroradiologic imaging in5 z; h0 D; W0 u1 q) h
boys with precocious puberty. In addition to viril-
! f7 @5 K. I& z! l% t) t) x. pization, the clinical hallmark of CPP is the symmet-
& G" O( S) S( Xrical testicular growth secondary to stimulation by; c: L: |" A. f3 e; ]& ]
gonadotropins.1,39 p7 r5 x! b1 b( j: {! P" Z
Gonadotropin-independent peripheral preco-' {& N1 _& a" S; n/ T* E
cious puberty in boys also results from inappropriate8 a: X) N! R2 f# U; t, F
androgenic stimulation from either endogenous or7 r8 v* G" O: x6 Q6 B7 I' V& ~! j
exogenous sources, nonpituitary gonadotropin stim-% l& y! [( k" p% I8 R
ulation, and rare activating mutations.3 Virilizing* R8 j8 Y2 j$ i9 ]+ M
congenital adrenal hyperplasia producing excessive
/ e& i1 G$ O3 radrenal androgens is a common cause of precocious/ G* \' g7 q7 I- D" o
puberty in boys.3,46 z5 y5 D- ?' T
The most common form of congenital adrenal
. n. ?1 N7 U# H& M" L5 ]3 ihyperplasia is the 21-hydroxylase enzyme deficiency.1 D4 v6 B- S% X3 t$ R% n
The 11-β hydroxylase deficiency may also result in) `: y% U- W9 _
excessive adrenal androgen production, and rarely,
2 P$ D& @( d4 N, f) Wan adrenal tumor may also cause adrenal androgen
4 n+ x, V( y, m2 Q9 g. bexcess.1,3* @5 e9 ^  ?6 b, l# x) y
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 b: C/ F1 \: T( Q' p8 r
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007: _' C/ Y6 x2 a
A unique entity of male-limited gonadotropin-
% j$ D- U5 T2 bindependent precocious puberty, which is also known6 b7 [4 E- k. J3 Y# s
as testotoxicosis, may cause precocious puberty at a
+ A+ v* f4 K; B. r( v0 Bvery young age. The physical findings in these boys
( k6 Y  D, J* U! a( B/ Iwith this disorder are full pubertal development,
1 U2 c, M! {& ~. Y6 ]; tincluding bilateral testicular growth, similar to boys
+ j. o' m( D  Q5 G" w" rwith CPP. The gonadotropin levels in this disorder
6 m# l9 _5 U* V* J5 R. \( k9 Gare suppressed to prepubertal levels and do not show3 P7 S$ V& n" d7 O
pubertal response of gonadotropin after gonadotropin-8 Z) q; O, b2 G+ M
releasing hormone stimulation. This is a sex-linked
0 E5 D" X4 \4 Z! uautosomal dominant disorder that affects only9 {+ m7 W& Q/ e
males; therefore, other male members of the family
4 {' v6 z0 a  q" B5 lmay have similar precocious puberty.3
# h' K) I1 d9 q8 v1 A3 S1 h! U9 r) lIn our patient, physical examination was incon-
$ T- Q# W) r7 r3 Jsistent with true precocious puberty since his testi-
9 f7 c+ x- Z2 \# ?1 ecles were prepubertal in size. However, testotoxicosis) ^7 r0 l8 H2 s
was in the differential diagnosis because his father
4 L6 _1 t+ W& L3 h% qstarted puberty somewhat early, and occasionally," U: Z" l; l' i  W
testicular enlargement is not that evident in the+ ?2 K5 d0 f; l+ a3 t3 S/ A/ Z
beginning of this process.1 In the absence of a neg-
+ H$ J6 g! w- P; d6 v: L4 V+ Z" ?ative initial history of androgen exposure, our
2 C" T' Y3 U& H- R) Cbiggest concern was virilizing adrenal hyperplasia,- N: N- e6 Z* r* J& M
either 21-hydroxylase deficiency or 11-β hydroxylase& r/ x' e" R9 G
deficiency. Those diagnoses were excluded by find-
: M% u& K" n* e" Sing the normal level of adrenal steroids.4 L  I& _: t3 O
The diagnosis of exogenous androgens was strongly* f1 }& A' v8 K3 s& ~
suspected in a follow-up visit after 4 months because
8 |! [  G" D$ p/ o  `+ [( E$ ~the physical examination revealed the complete disap-# @& a% G  j/ w8 s% w4 }
pearance of pubic hair, normal growth velocity, and* D; K+ t/ K# s- ]2 a  e
decreased erections. The father admitted using a testos-
9 ~0 |2 Z, n1 K% zterone gel, which he concealed at first visit. He was4 T- ~% K1 H# W& Y' k( r( D/ u" L
using it rather frequently, twice a day. The Physicians’
* J: R5 F: n* j+ t) h9 vDesk Reference, or package insert of this product, gel or
  h" z) l; x0 y# r# L5 T, icream, cautions about dermal testosterone transfer to* s( o7 N- h/ R: Z- ?& T. T9 s
unprotected females through direct skin exposure.
& B& w+ e) U  X$ eSerum testosterone level was found to be 2 times the
0 |! }% _& O9 ?# p7 Jbaseline value in those females who were exposed to
* x. t' \/ m6 A# M0 {3 m% Q5 eeven 15 minutes of direct skin contact with their male
; P& e* O+ i7 Qpartners.6 However, when a shirt covered the applica-
6 q5 k, `& N3 r4 Ntion site, this testosterone transfer was prevented.7 ]9 j7 y. d4 l) K) A( g* B
Our patient’s testosterone level was 60 ng/mL,& n1 A% ]; V$ V
which was clearly high. Some studies suggest that2 @& N' i, z7 ]5 q4 [* I9 G- u
dermal conversion of testosterone to dihydrotestos-
9 }' d# P5 {  B* ^terone, which is a more potent metabolite, is more" s9 R0 n7 n+ z* L
active in young children exposed to testosterone
; A1 \+ |$ ^" q6 o. @% k5 Yexogenously7; however, we did not measure a dihy-: Z7 P9 X7 A$ f  b4 K
drotestosterone level in our patient. In addition to
( k1 u5 a0 r5 _virilization, exposure to exogenous testosterone in
! D$ e4 V: [( g& }) A0 I, V6 X' fchildren results in an increase in growth velocity and
  p# m, b4 J8 s, E# L4 ~" Tadvanced bone age, as seen in our patient." K1 a  X% M+ m; `
The long-term effect of androgen exposure during  d9 K1 T; ]8 ?% [& o
early childhood on pubertal development and final6 M; J: @3 M& P7 U# e2 C
adult height are not fully known and always remain
. Z5 @8 H* n# t3 |a concern. Children treated with short-term testos-1 ]  A4 W" V/ ]7 J% Y. W/ f
terone injection or topical androgen may exhibit some# I* S' q3 h9 K0 z3 ~
acceleration of the skeletal maturation; however, after
- o8 M8 A" @& W! \cessation of treatment, the rate of bone maturation0 h- n7 i- V: U5 F; k
decelerates and gradually returns to normal.8,9/ f- P6 p: ]% ]8 K- j  b
There are conflicting reports and controversy
* M' l; V: f0 E- U" e1 G5 I, cover the effect of early androgen exposure on adult1 X3 @$ i" V& x; R( ?7 ^
penile length.10,11 Some reports suggest subnormal% ^# @$ i! z" W
adult penile length, apparently because of downreg-
( g; C4 U# ?# e2 \0 yulation of androgen receptor number.10,12 However,) x1 R5 [: d* F3 D
Sutherland et al13 did not find a correlation between' z" B. b) O; Q
childhood testosterone exposure and reduced adult
) D0 Y2 Q* k" z$ wpenile length in clinical studies.
* h: l) W# s6 ]0 Y. K2 tNonetheless, we do not believe our patient is: ^# x- }+ a8 j% V9 D
going to experience any of the untoward effects from
3 m, i; V+ T, h$ ~2 M1 w& z7 w2 V# jtestosterone exposure as mentioned earlier because
6 u: j3 X- G) _5 {6 j# ~; kthe exposure was not for a prolonged period of time.
; y+ q/ k. i" t; P, ~8 k$ W4 i! AAlthough the bone age was advanced at the time of
, s9 D5 N# M7 [' `6 l  \7 pdiagnosis, the child had a normal growth velocity at
$ f0 D6 _9 I' Uthe follow-up visit. It is hoped that his final adult
& f5 Q9 Z* s4 R" C% z8 Qheight will not be affected.6 {1 z% _1 j! p( g- O
Although rarely reported, the widespread avail-0 N9 }% m6 m6 f& `& @
ability of androgen products in our society may. D0 S# D: e9 j! t8 I4 ]- Q, g
indeed cause more virilization in male or female7 y0 O; b9 {6 H" C5 d
children than one would realize. Exposure to andro-
# p- a- U4 q$ T" P0 K1 E5 ?% n: I1 Ygen products must be considered and specific ques-; i4 d& X* N$ d0 D
tioning about the use of a testosterone product or! j/ Z+ {# {/ T$ ?. y. [
gel should be asked of the family members during2 t) w( i5 A& X$ }  ?0 ?
the evaluation of any children who present with vir-2 u6 k- ~% p) v0 m
ilization or peripheral precocious puberty. The diag-
5 H7 Z2 P; }/ o8 V# L7 Cnosis can be established by just a few tests and by
" N9 {+ ^$ H0 _8 w1 D: F+ zappropriate history. The inability to obtain such a% m7 o, `' b- a8 }( M- C' n' o
history, or failure to ask the specific questions, may
/ y7 I' C" E, Q# x8 e- q4 iresult in extensive, unnecessary, and expensive
4 E7 B2 {: }! Y9 minvestigation. The primary care physician should be; |8 A7 C6 i. P) l3 z( N- o
aware of this fact, because most of these children
% F  d9 U  c) \# pmay initially present in their practice. The Physicians’
, N" x2 p$ q: X5 Q7 `; C6 O" {Desk Reference and package insert should also put a5 K' y- B7 m4 U  t8 _. V/ j2 z% k
warning about the virilizing effect on a male or+ \! S( F% P2 z! V; Z9 N8 e
female child who might come in contact with some-
( g5 h3 W$ B+ rone using any of these products.% Y# w: G+ p% t+ j* l
References
. [! [% K, f% A+ S4 D0 a  W& [5 D  X1. Styne DM. The testes: disorder of sexual differentiation+ k4 x# K# J. A
and puberty in the male. In: Sperling MA, ed. Pediatric4 k- b7 D/ c  p- O# b
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;0 Q& ?" O3 l) x1 A6 {0 p0 ~
2002: 565-628.
& s; [: T- Z# U' q! Z) O0 X& ?: C2 s2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious+ N8 c% Z: S% p4 n6 E" Y
puberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

5 c: m' s0 {! Q" N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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