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Sexual Precocity in a 16-Month-Old
# l8 q% d  H# }; _! b: A6 KBoy Induced by Indirect Topical! Q7 a& j4 Z2 s9 i! B1 i# h8 J0 q3 B& F
Exposure to Testosterone
1 i: S$ c6 s0 r7 YSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
, Y+ P7 i$ f$ a. v$ X% o& f6 G% {and Kenneth R. Rettig, MD1& ]. {% `+ A4 d( K* a
Clinical Pediatrics
4 }( |. U7 {+ v! T! w9 U1 ]Volume 46 Number 6
3 ~$ Y2 E5 m$ E! A4 GJuly 2007 540-5438 c6 L2 A6 ^, R9 O# E
© 2007 Sage Publications
9 B) L; Z8 g0 K( H: c10.1177/00099228062966515 I9 C  z. j# M9 D6 V1 M8 p4 i. d
http://clp.sagepub.com
3 m7 A4 |; K- q' t8 [( E( j9 `hosted at
7 S- \) R8 k# b- I: Bhttp://online.sagepub.com  W. S9 M, J' M5 ?: I
Precocious puberty in boys, central or peripheral,6 v) @6 Y# Y& N; e' z
is a significant concern for physicians. Central( v4 ^: S3 Q, F8 y* M9 t
precocious puberty (CPP), which is mediated
9 @, C$ a% s4 V- f2 G: `through the hypothalamic pituitary gonadal axis, has
- _/ |1 Q- J4 V5 X' c+ |& [# S9 ga higher incidence of organic central nervous system
' T. E! [& X! P0 Blesions in boys.1,2 Virilization in boys, as manifested
2 f$ t. u' C9 C# xby enlargement of the penis, development of pubic% I! |9 D) b. c# d7 n9 E5 ^
hair, and facial acne without enlargement of testi-8 P0 |! u( [5 A' l& f' F$ [1 ^$ [
cles, suggests peripheral or pseudopuberty.1-3 We) V/ H3 j2 ]9 u
report a 16-month-old boy who presented with the
! `* U2 h. V2 t6 u8 D2 oenlargement of the phallus and pubic hair develop-
. n/ r9 @8 x. k) M& mment without testicular enlargement, which was due# X8 k& X8 z+ F9 f3 n5 _, k5 E
to the unintentional exposure to androgen gel used by4 s& X( m( X# w" ~# t) Y5 `: q
the father. The family initially concealed this infor-/ N/ l0 q  p0 @- T* g* Y! l- l
mation, resulting in an extensive work-up for this
) ^7 m( z& ?2 y5 X1 s/ Z' l! {child. Given the widespread and easy availability of
/ c4 S; v1 |7 c+ w) }testosterone gel and cream, we believe this is proba-
7 Q$ i0 I5 ^' q/ u5 @0 q7 Gbly more common than the rare case report in the" C5 n% j5 D+ u' O3 z* g! Y
literature.4& ?. I( }) L. y8 j! y" Q
Patient Report7 p! m0 |7 U4 I! q& K
A 16-month-old white child was referred to the7 U4 t, U, a( \: f' w( f
endocrine clinic by his pediatrician with the concern
" n: v2 d: z# n# Aof early sexual development. His mother noticed
5 B3 L1 L: q6 F% n/ H5 R6 Llight colored pubic hair development when he was
/ ~  J) w) ?! ?From the 1Division of Pediatric Endocrinology, 2University of+ s; K% I$ \2 E. t0 s
South Alabama Medical Center, Mobile, Alabama.( X) J" d( [6 Y( B0 Q3 y2 l
Address correspondence to: Samar K. Bhowmick, MD, FACE,' ]  ?( u7 {6 O- l1 Y) x
Professor of Pediatrics, University of South Alabama, College of/ k6 F5 E0 l* X5 d
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 @- p/ K' w2 n. f) s
e-mail: [email protected].
& M. B5 d, s- \$ L) r% [& m1 uabout 6 to 7 months old, which progressively became, M0 l5 a, ]( h. L8 n3 o1 G
darker. She was also concerned about the enlarge-; g3 E' Q6 ?) Q3 J3 c/ _
ment of his penis and frequent erections. The child
1 W  a7 Q, ~" Qwas the product of a full-term normal delivery, with
3 U5 a0 b% z# E0 u4 N5 Ja birth weight of 7 lb 14 oz, and birth length of7 s) A) j! o  ?: B7 M, t
20 inches. He was breast-fed throughout the first year; i+ Q4 Y( q" l7 X, A
of life and was still receiving breast milk along with) K: a& j* f0 b% W* j" H5 t
solid food. He had no hospitalizations or surgery,) _7 b7 E+ y( d: [2 g" b  E' X
and his psychosocial and psychomotor development% a& d2 l1 u8 J+ J' E5 R: T
was age appropriate.' i7 ~6 E6 x. ^- ]( Q3 ~# K+ ^5 Q
The family history was remarkable for the father,( }8 w: \. D/ L2 B( T9 G, N5 t5 }
who was diagnosed with hypothyroidism at age 16,* `$ ^0 X- K3 x5 V' o
which was treated with thyroxine. The father’s1 Z& z  D2 e3 r! T( L
height was 6 feet, and he went through a somewhat
7 l, R; k+ K3 a" }early puberty and had stopped growing by age 14.) i; s1 K0 b: l. a3 e
The father denied taking any other medication. The
8 Z) h3 W' P$ X! D  Bchild’s mother was in good health. Her menarche5 K* ?. Z  f) a: j6 _# n$ x1 A
was at 11 years of age, and her height was at 5 feet
4 m9 N0 A! u/ ?8 T: p3 \, }5 inches. There was no other family history of pre-* H0 O) W. R0 q  a1 i  P
cocious sexual development in the first-degree rela-
, K$ r: l6 H& ]3 J  z  b+ p6 etives. There were no siblings.5 ~3 Z$ K3 H- x2 B, R: c
Physical Examination
% C& m* [. z: {0 A6 d7 cThe physical examination revealed a very active,
1 ?5 U7 s- \" M2 j7 i; t. j+ ?playful, and healthy boy. The vital signs documented0 M" B, X" W& `- ?6 K% {; R
a blood pressure of 85/50 mm Hg, his length was
! q+ ?, V& R/ J0 U8 [90 cm (>97th percentile), and his weight was 14.4 kg
5 l7 @3 T4 y6 D/ |, E(also >97th percentile). The observed yearly growth+ A- T& n; f% e' G
velocity was 30 cm (12 inches). The examination of/ S) ?/ b0 P5 ]; z: t
the neck revealed no thyroid enlargement.
- C% h! O% M" J0 _( Z' g( [The genitourinary examination was remarkable for5 Q( q+ q% Q; u4 _: _. {
enlargement of the penis, with a stretched length of
( r+ L3 Z: f0 s! ~0 @8 cm and a width of 2 cm. The glans penis was very well/ m5 n0 S# K! B0 l/ r5 ^/ n3 s
developed. The pubic hair was Tanner II, mostly around" l2 {% Y2 {4 e/ R1 h4 Y* x% J. t
5401 x/ w& o6 G- `1 J
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 Z, d; @$ b3 h$ jthe base of the phallus and was dark and curled. The6 ?0 K* F& i% q5 Y  R2 Q
testicular volume was prepubertal at 2 mL each.( _+ M1 R' E" {3 K( |+ I, n
The skin was moist and smooth and somewhat  k! b9 |7 n! A& f' `- `
oily. No axillary hair was noted. There were no: A' J  A" r- b0 _" C9 W
abnormal skin pigmentations or café-au-lait spots.
5 M- v+ Z; N1 K; d: u; Z$ _0 d1 mNeurologic evaluation showed deep tendon reflex 2+
7 G% ]# f9 K7 M% M( tbilateral and symmetrical. There was no suggestion, u8 ?. v  i, u" l3 R6 i
of papilledema.
2 q  P3 |* p$ ^% Z+ q: @Laboratory Evaluation6 c) n( V# k; R" @+ j; @9 Q4 i2 c
The bone age was consistent with 28 months by: r+ u6 z) B& h
using the standard of Greulich and Pyle at a chrono-5 w( n2 O8 j( n$ w9 j
logic age of 16 months (advanced).5 Chromosomal
' m+ o0 `  T8 y6 ]( e, }* T7 o: ~# M" Mkaryotype was 46XY. The thyroid function test
: P: s  R, F/ ?showed a free T4 of 1.69 ng/dL, and thyroid stimu-
  t% ?- U' Y' k7 H) ~; u0 t" flating hormone level was 1.3 µIU/mL (both normal).
$ @/ Q7 p8 `) G# ~The concentrations of serum electrolytes, blood, |- {" y0 m1 u& s+ Y$ t  P
urea nitrogen, creatinine, and calcium all were
2 g. H1 H4 D: T. Q2 Z" B1 M4 wwithin normal range for his age. The concentration( g1 z1 t  s* z6 ^/ R( d0 o
of serum 17-hydroxyprogesterone was 16 ng/dL( p, K2 l3 f9 w8 f
(normal, 3 to 90 ng/dL), androstenedione was 20
- b, h$ M5 t* r% dng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
0 k1 a/ |, i# B! D, m6 Dterone was 38 ng/dL (normal, 50 to 760 ng/dL),; i- S5 R* ~8 Q+ i' a9 E: }1 e: `
desoxycorticosterone was 4.3 ng/dL (normal, 7 to- ?7 _* u1 _& M. v4 `$ {
49ng/dL), 11-desoxycortisol (specific compound S)6 |- @5 t( V, V3 Q% }4 u
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-6 H7 [$ w0 y4 L% x4 ?* ~# _
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
5 g# i" |+ E, ~$ atestosterone was 60 ng/dL (normal <3 to 10 ng/dL),. A( r1 M( j- ^& G& Z
and β-human chorionic gonadotropin was less than
# g5 C$ ]" J* m& Q8 Q+ n0 W5 mIU/mL (normal <5 mIU/mL). Serum follicular
, u/ a0 z- u! T" B- astimulating hormone and leuteinizing hormone
5 h8 z7 D' @  w0 O; Z9 ~( Dconcentrations were less than 0.05 mIU/mL- n! I! ~- v7 a2 i# K
(prepubertal).6 k) Z2 [) K5 j1 s4 n- V
The parents were notified about the laboratory
) ~5 @0 g/ l- dresults and were informed that all of the tests were
1 i- `6 ?7 @2 I* ?. n4 G, P+ N! ?) }normal except the testosterone level was high. The+ d! A' E4 x0 M! V7 ?
follow-up visit was arranged within a few weeks to0 O7 ~; b: s; ?( d9 E6 `0 A
obtain testicular and abdominal sonograms; how-
  L1 O$ `  F. D! N( W. n) `ever, the family did not return for 4 months." k% a, a$ w9 e4 A4 B
Physical examination at this time revealed that the
0 S. u/ z2 k, {2 Vchild had grown 2.5 cm in 4 months and had gained
$ ~$ V6 L: T) l3 z) P. w2 kg of weight. Physical examination remained& T( L' v/ F- |8 M# T1 P
unchanged. Surprisingly, the pubic hair almost com-/ J5 T  U- [4 T
pletely disappeared except for a few vellous hairs at4 U; U% C; R0 p1 a; Y
the base of the phallus. Testicular volume was still 29 Y  [3 v% O, m5 D* _( |/ t- `& `
mL, and the size of the penis remained unchanged.3 ?* H; P0 \# W2 O6 U9 r
The mother also said that the boy was no longer hav-% M: D% L, ]" L- L: d
ing frequent erections.7 n/ D0 |2 ?7 F
Both parents were again questioned about use of9 L7 b1 i# I1 s9 U
any ointment/creams that they may have applied to4 F: u' ~* B/ ]- A4 _
the child’s skin. This time the father admitted the2 }! Y$ ~. j7 J' y
Topical Testosterone Exposure / Bhowmick et al 541
  i. {) x0 D7 U9 Fuse of testosterone gel twice daily that he was apply-  D, U* t0 f+ a9 D( h
ing over his own shoulders, chest, and back area for
' e1 a% G2 f3 u( h- ^/ Ra year. The father also revealed he was embarrassed
4 m# b. h2 h/ Fto disclose that he was using a testosterone gel pre-7 ~2 g6 m8 {: K
scribed by his family physician for decreased libido' n+ N9 J0 \6 u' h3 g/ m# r/ ^
secondary to depression.
. ]2 T. R% A( c1 @" p4 WThe child slept in the same bed with parents.
* r6 k3 n& n5 iThe father would hug the baby and hold him on his% Z) ]& h! h; J* H1 {, z
chest for a considerable period of time, causing sig-
# H& ~% i, A/ ?+ o" Lnificant bare skin contact between baby and father.* k" ~. n8 G& A1 j7 R6 D
The father also admitted that after the phone call,
0 R6 N( N0 a- h% P; ?. H, rwhen he learned the testosterone level in the baby
  h5 g' M  N! w1 w6 p$ X( Lwas high, he then read the product information
" \% O. H9 Z, k8 \packet and concluded that it was most likely the rea-
4 B( N. ?$ s8 k! sson for the child’s virilization. At that time, they
0 M; y( p% D9 M" r7 pdecided to put the baby in a separate bed, and the8 Y' V& }6 W2 L  a8 n( n
father was not hugging him with bare skin and had
7 U+ S7 e/ C- K7 V% lbeen using protective clothing. A repeat testosterone
4 R. X7 _; B6 G7 M' Q2 m- xtest was ordered, but the family did not go to the
) a0 z& G/ m1 }7 V; `laboratory to obtain the test.9 {1 a  J' m% h/ ~% O5 U# d  C
Discussion4 t, S8 U& `& @7 d$ t
Precocious puberty in boys is defined as secondary
( S9 |& M( Y2 c) osexual development before 9 years of age.1,4
3 I3 f( M, W9 N1 ^Precocious puberty is termed as central (true) when
  c: u+ \% P" t6 yit is caused by the premature activation of hypo-) r( z1 E$ Y' }6 J8 _( u5 [
thalamic pituitary gonadal axis. CPP is more com-
4 f& ~+ [, B2 a3 E! L# K, gmon in girls than in boys.1,3 Most boys with CPP
# l3 |# h/ Z4 S: gmay have a central nervous system lesion that is% W9 \, P" m3 L. R( B
responsible for the early activation of the hypothal-- {6 X- y, j/ g& G' |  X
amic pituitary gonadal axis.1-3 Thus, greater empha-7 W7 n$ s2 u. r; q0 V! ^( }
sis has been given to neuroradiologic imaging in
1 D; T5 o+ b2 g$ s! xboys with precocious puberty. In addition to viril-6 {6 a: ?* q  H/ h1 R% t+ ]
ization, the clinical hallmark of CPP is the symmet-8 A: l) Z" l) K2 c( S+ v1 |0 N
rical testicular growth secondary to stimulation by
( w: |4 [9 W" h1 r& Q& L0 \( igonadotropins.1,3
. v$ {9 t9 _* fGonadotropin-independent peripheral preco-
( h7 A4 m; a2 ]  E3 _cious puberty in boys also results from inappropriate2 l2 m. N' ?/ e8 y6 M
androgenic stimulation from either endogenous or2 r+ K  R! X. s1 f5 [
exogenous sources, nonpituitary gonadotropin stim-
3 M/ R; x& R3 s& mulation, and rare activating mutations.3 Virilizing
: {4 Q4 T7 O# Mcongenital adrenal hyperplasia producing excessive' @6 c( z) N% Q
adrenal androgens is a common cause of precocious
: K- A4 [- E0 x' Spuberty in boys.3,44 }' s. W& s7 a/ V9 S- o( s" {  s
The most common form of congenital adrenal' @% c! y  W6 _- c* ~! u  R% I
hyperplasia is the 21-hydroxylase enzyme deficiency.
6 y( k( W3 d$ P& }/ ?- K4 }The 11-β hydroxylase deficiency may also result in! Q" P" c. C/ N2 ~0 k1 D
excessive adrenal androgen production, and rarely,
& y  o2 L+ L( e9 Oan adrenal tumor may also cause adrenal androgen9 M/ @+ x2 A1 c& E5 A5 {
excess.1,3
# `* C! J, l" d# r; f0 z2 cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from8 I# D, W9 S3 H, O& S: ]
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
8 X, `' T6 N2 i! p" Y5 tA unique entity of male-limited gonadotropin-
, {- V3 O7 c) N5 E2 ]7 G( L0 W* @: Oindependent precocious puberty, which is also known
# z1 ~0 g" T3 g: w2 c( I9 X$ @8 b: ?as testotoxicosis, may cause precocious puberty at a0 N" u, R- \1 [' z' Z
very young age. The physical findings in these boys
  ^5 g# u& t% [( j+ M" i3 @with this disorder are full pubertal development,
; H8 y- d4 J0 \  D1 d8 ?% }including bilateral testicular growth, similar to boys+ _+ C* ]& `; @4 Q
with CPP. The gonadotropin levels in this disorder
6 `0 z# _9 n0 N3 e/ P/ nare suppressed to prepubertal levels and do not show
# y5 m# ~+ S- G% e- B: U! k+ upubertal response of gonadotropin after gonadotropin-
0 ~1 v3 N& d% l- J4 w0 k7 xreleasing hormone stimulation. This is a sex-linked7 A0 s8 s8 `1 C  X1 Q& f
autosomal dominant disorder that affects only
$ D: G% L( ?: f8 m% c( zmales; therefore, other male members of the family
( s4 {, g7 S2 X! K+ z+ Q/ B: R( F# ~may have similar precocious puberty.3
, R7 N5 l, ^) W; [8 z) m) I2 qIn our patient, physical examination was incon-- x) Y( Q" |1 Q4 _
sistent with true precocious puberty since his testi-2 T# k4 \) z5 w& C7 u9 I
cles were prepubertal in size. However, testotoxicosis
% ]+ \, U1 X& L4 rwas in the differential diagnosis because his father, K, Y2 L8 L- p* E+ e6 l6 p5 z
started puberty somewhat early, and occasionally,& b! ]1 |3 O0 l( ~5 l7 H/ r
testicular enlargement is not that evident in the
* u, k$ O- u& p- L3 v$ abeginning of this process.1 In the absence of a neg-/ h  a9 I/ F( B& O# e
ative initial history of androgen exposure, our3 N7 K( e9 r0 P2 Y" |6 i5 I/ x* j( C
biggest concern was virilizing adrenal hyperplasia,
* N, P" f' Q" f% z+ Ieither 21-hydroxylase deficiency or 11-β hydroxylase1 w4 S2 F$ K: A- d6 E, `
deficiency. Those diagnoses were excluded by find-" V: H2 B6 f  ~' J: Z! Y
ing the normal level of adrenal steroids.
4 ^: g- K9 K% \1 Y! AThe diagnosis of exogenous androgens was strongly
5 M! o" S  Y4 p+ psuspected in a follow-up visit after 4 months because* y: h" Y0 g0 ]/ x! {) x2 ?
the physical examination revealed the complete disap-
% r1 U9 D% w/ J1 U) D, W1 ~, ?pearance of pubic hair, normal growth velocity, and8 P+ L% N0 e3 E3 _- V
decreased erections. The father admitted using a testos-
; j  ?7 ]- u8 I; ~terone gel, which he concealed at first visit. He was
3 b. [( r- @, Wusing it rather frequently, twice a day. The Physicians’3 I# u. J5 k( w; P7 m3 Z; ^
Desk Reference, or package insert of this product, gel or
- n* s! a' U# J7 acream, cautions about dermal testosterone transfer to* a, e3 v0 E5 ?! h" V. I9 L) k2 y. ?2 a
unprotected females through direct skin exposure.+ m: G9 e, Y- v* I2 X: {
Serum testosterone level was found to be 2 times the( E) y. V* f# p; x+ d3 P
baseline value in those females who were exposed to
( t8 K$ p2 _, }, Z6 Weven 15 minutes of direct skin contact with their male5 i& V/ c1 o1 u# T
partners.6 However, when a shirt covered the applica-
- b7 w( T! p6 J9 k  R. O$ ition site, this testosterone transfer was prevented.. P2 i9 E+ |* `: V3 m$ w6 r
Our patient’s testosterone level was 60 ng/mL,( }) b; z$ m$ i; ?# q' T, s7 ]
which was clearly high. Some studies suggest that
. I4 @3 e8 d% ^# x2 V% xdermal conversion of testosterone to dihydrotestos-
" g9 ?: F5 V; X. w( t( w- xterone, which is a more potent metabolite, is more
) U. i! x$ `  @2 ]* `active in young children exposed to testosterone0 M3 J$ r) K# j! J
exogenously7; however, we did not measure a dihy-
: Q1 i: k* F3 n3 p% hdrotestosterone level in our patient. In addition to
9 q/ Q& @) s8 r9 qvirilization, exposure to exogenous testosterone in
0 s3 N2 \; M! v5 v  l9 |# N. G6 n0 {children results in an increase in growth velocity and, L: q/ @8 s3 y! M" K3 i
advanced bone age, as seen in our patient.
; [8 h% |/ |. kThe long-term effect of androgen exposure during/ x- h* a1 _4 l6 Y! [& E$ o
early childhood on pubertal development and final
5 G5 A& `: T( sadult height are not fully known and always remain
# ^3 _& P1 V6 A7 }+ w0 U; K' ta concern. Children treated with short-term testos-: o1 q4 ~. e. _
terone injection or topical androgen may exhibit some
( X* b7 A5 ~! J7 O, jacceleration of the skeletal maturation; however, after7 G/ Y1 y7 ]% C1 ?! p! {6 J
cessation of treatment, the rate of bone maturation  N# ]6 S: h  u# M5 x/ v5 b2 l8 N. s
decelerates and gradually returns to normal.8,9+ {2 x- O1 w0 ], Q
There are conflicting reports and controversy
$ A0 R' N& h& F6 i" Y4 vover the effect of early androgen exposure on adult
, [# Z/ P( Z* X0 z& ^) ~: wpenile length.10,11 Some reports suggest subnormal
5 v- }/ k( Z* |7 }2 S8 ?adult penile length, apparently because of downreg-
9 g( s9 v: y4 h3 \8 Z8 b' tulation of androgen receptor number.10,12 However,  v' l: k  U. A# W7 D
Sutherland et al13 did not find a correlation between
* f. J4 ~! g" f2 {- `) Jchildhood testosterone exposure and reduced adult
. a8 E2 t' U5 A2 `. t* }8 v# dpenile length in clinical studies., c9 B& ~9 i  N5 M, `
Nonetheless, we do not believe our patient is- m+ ?/ O$ o: ^( {
going to experience any of the untoward effects from2 T9 `# P$ S7 E) h; {
testosterone exposure as mentioned earlier because' }/ ^* g2 _2 m/ T: e
the exposure was not for a prolonged period of time.% S4 l& ?  ?$ r2 ?5 @
Although the bone age was advanced at the time of
6 P( H4 T& i& o* a7 G, f9 Ndiagnosis, the child had a normal growth velocity at
( T# g( K, P8 v9 H: D7 f; k$ O9 O5 Mthe follow-up visit. It is hoped that his final adult
, |  [7 B4 S. V4 s, M. kheight will not be affected.
# }0 `$ n4 P) I; lAlthough rarely reported, the widespread avail-/ Q$ u/ t8 x: L8 n# H/ @/ Q
ability of androgen products in our society may
" h' \$ [" i: ]( \. Windeed cause more virilization in male or female
: L) H2 m  Z& dchildren than one would realize. Exposure to andro-6 K$ ?/ i8 P& x. J1 I' x
gen products must be considered and specific ques-
5 k" P# b. m- G; ?9 L' Y" Utioning about the use of a testosterone product or
& A$ G' `! s. ^3 j2 E" ]( ogel should be asked of the family members during3 e8 e% |, H. }- `; I
the evaluation of any children who present with vir-
8 x5 X7 M/ v3 `+ l9 x# r9 nilization or peripheral precocious puberty. The diag-
, Q: C! n$ }* o( `nosis can be established by just a few tests and by
) J" L. b7 I. ]3 E8 x3 r2 Pappropriate history. The inability to obtain such a2 \8 Y1 h  {: [2 @( ^% e! Q
history, or failure to ask the specific questions, may
5 Z8 j1 n( }+ H1 N" W  k( Kresult in extensive, unnecessary, and expensive
" v: ^: b2 H1 l, ]" [0 finvestigation. The primary care physician should be6 K- ]5 ~$ P4 D
aware of this fact, because most of these children/ J3 j( `6 }* g" n( h
may initially present in their practice. The Physicians’, V& a- {' T! x/ f( v: i
Desk Reference and package insert should also put a
- J# v+ Z; F! L; S4 Ywarning about the virilizing effect on a male or
& }3 F( e; k" H, I& X( O6 Y" }- ffemale child who might come in contact with some-, D  x% s; U# D1 P
one using any of these products.5 R  a0 p/ |, Y! Z
References! Q1 F/ v  d5 c$ X" S4 Z9 K
1. Styne DM. The testes: disorder of sexual differentiation# Z0 q- L2 ^1 |( c( F
and puberty in the male. In: Sperling MA, ed. Pediatric
: c6 c+ {) T% d# C4 A* wEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;/ U: Y& I  o/ q& P4 t5 n
2002: 565-628.
2 v+ _' u0 J% U$ I" q2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious) r* O% R7 t% w$ k1 R9 d1 p; y! e( v
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
. l3 I. l3 E( {3 L3 p9 V9 A  \. x& KBoy Induced by Indirect Topical0 h6 d+ F: ~* z% W$ J7 Z6 |
Exposure to Testosterone! D# `1 N* ]/ g0 b# Z, v
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2' ?$ l* ~% _! E
and Kenneth R. Rettig, MD1
/ ~7 I6 O+ d) \$ ~' \: mClinical Pediatrics
" V0 `6 ?* N# ]Volume 46 Number 6
! [" g$ f7 ~! e$ y2 {July 2007 540-543; r% ]2 Y. x4 V. E' ?& d
© 2007 Sage Publications
. ^; Y% r- C- C1 r" q+ K10.1177/0009922806296651# i  M& d1 r: [; P) W; {) V9 M
http://clp.sagepub.com
" @. x  @" ]% p5 z8 |( P7 Nhosted at
4 |7 P2 G* S/ p* b, I" Y9 Nhttp://online.sagepub.com% _5 `" N" s' o  t
Precocious puberty in boys, central or peripheral,3 J! y/ b* ?1 d/ h  I- X
is a significant concern for physicians. Central
1 A5 G* E6 T4 q/ f* Vprecocious puberty (CPP), which is mediated7 D5 `2 R9 L6 d4 `0 R
through the hypothalamic pituitary gonadal axis, has# I2 O: u0 N3 Q, ~6 I. e- \
a higher incidence of organic central nervous system
6 _9 r% j  n1 r. glesions in boys.1,2 Virilization in boys, as manifested8 a! M* V, N  u
by enlargement of the penis, development of pubic7 K: N* H7 V! q. I( v
hair, and facial acne without enlargement of testi-) I8 E$ y( L* M( z! G
cles, suggests peripheral or pseudopuberty.1-3 We5 k4 o+ w! e0 ?% O
report a 16-month-old boy who presented with the8 ?$ ^0 ~3 V5 O1 |
enlargement of the phallus and pubic hair develop-# K3 p( y% Y  N) v" ]: _
ment without testicular enlargement, which was due0 c4 n6 k( j3 N
to the unintentional exposure to androgen gel used by
6 ?4 n4 N1 o* G; G: Y# ^the father. The family initially concealed this infor-$ Z8 y. `, Q- a* N; R0 G2 c
mation, resulting in an extensive work-up for this0 z* F! U* _6 Y
child. Given the widespread and easy availability of, v+ [5 o9 l$ W
testosterone gel and cream, we believe this is proba-
9 A9 s% A/ Y" |7 Cbly more common than the rare case report in the! ]3 n8 i0 V7 {3 |  X
literature.4
+ M0 n1 r8 L! W5 x7 l! HPatient Report1 L( K' [3 i% l1 [2 ?. p8 Q/ X
A 16-month-old white child was referred to the$ F) `! Y2 K! ~, q0 D* e
endocrine clinic by his pediatrician with the concern
4 X0 ?9 O- @& Kof early sexual development. His mother noticed2 A$ m. O8 b4 c
light colored pubic hair development when he was) O+ ~! D7 L3 P% R
From the 1Division of Pediatric Endocrinology, 2University of- H, d1 o: B- V8 _, W/ {
South Alabama Medical Center, Mobile, Alabama.
: \/ z9 f+ B9 z$ v8 K1 |Address correspondence to: Samar K. Bhowmick, MD, FACE,$ ~( J( c' `8 Y& C
Professor of Pediatrics, University of South Alabama, College of0 t0 _/ p# p0 S" e& E
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
7 o- {8 Z" o0 f4 s1 K0 pe-mail: [email protected].
  l( d- o; p6 E3 H/ ]6 M+ Labout 6 to 7 months old, which progressively became
6 d5 Y! l6 X# A9 p6 n/ o- _* tdarker. She was also concerned about the enlarge-. e8 I4 d  O  B3 _& g
ment of his penis and frequent erections. The child9 u2 k% E; o( p( }9 ^
was the product of a full-term normal delivery, with/ u# u+ g% f3 R8 O" F0 l
a birth weight of 7 lb 14 oz, and birth length of& I/ h+ x2 k8 l4 I# }3 v& j
20 inches. He was breast-fed throughout the first year( _9 u+ ^0 S( j
of life and was still receiving breast milk along with
! h* F; s- k) J8 S5 a# vsolid food. He had no hospitalizations or surgery,8 c, D$ }- K+ X
and his psychosocial and psychomotor development
6 r% M8 I7 `8 Rwas age appropriate.  A$ R# z+ i2 `. Z) }0 p! V% G. Y
The family history was remarkable for the father,8 Q& v5 B7 a' ?' c3 ?0 ?1 o& {8 ]
who was diagnosed with hypothyroidism at age 16,: D6 }$ x2 ]4 F* F" ]  a7 i
which was treated with thyroxine. The father’s( M% d- Z' _( k6 g2 l
height was 6 feet, and he went through a somewhat
1 w6 C& u$ j/ D3 {/ aearly puberty and had stopped growing by age 14.+ [( P; G0 J" B; l: P
The father denied taking any other medication. The: {0 ]9 l9 j" `: e) S
child’s mother was in good health. Her menarche
) f& P) I9 |* U0 s9 p/ L+ m, Fwas at 11 years of age, and her height was at 5 feet$ i1 W1 Q% Q% W" P
5 inches. There was no other family history of pre-
2 {# p1 ^2 [" n/ d" ?" ococious sexual development in the first-degree rela-) L2 [" X. f3 D: x: m
tives. There were no siblings.
# B  Y- f0 z* T( |Physical Examination4 U' `% x* |/ T& J
The physical examination revealed a very active,
" S& U" u" {$ k- H. N" ~; r+ X! m. [playful, and healthy boy. The vital signs documented
" s" ]8 U+ U# B. J1 m8 sa blood pressure of 85/50 mm Hg, his length was
, o0 K1 b3 o% Q0 j90 cm (>97th percentile), and his weight was 14.4 kg5 F7 D1 x) i8 E* O
(also >97th percentile). The observed yearly growth
$ H. w; [- m. r# [velocity was 30 cm (12 inches). The examination of  Q' C6 ~! h5 ]1 t9 {- F
the neck revealed no thyroid enlargement.9 z8 @7 _% B) Z3 ^  O
The genitourinary examination was remarkable for
0 \, B1 |- @6 E- i; J9 F- Ienlargement of the penis, with a stretched length of; ?! r' }0 Y4 D% S. D& z
8 cm and a width of 2 cm. The glans penis was very well
2 T' `( c  F# z! D0 sdeveloped. The pubic hair was Tanner II, mostly around# o8 K: z$ [6 Z' M8 Q
540
; E1 r+ G) p1 N7 F- S% hat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, ?+ z8 m6 ]- @5 S
the base of the phallus and was dark and curled. The
6 r* k9 z8 F# F1 k" a! {testicular volume was prepubertal at 2 mL each.
1 b: g! U& x7 ?6 r- S$ TThe skin was moist and smooth and somewhat
" Q2 a5 K4 ]7 _1 goily. No axillary hair was noted. There were no! ^9 m6 \. E' @/ V7 @4 `  Y
abnormal skin pigmentations or café-au-lait spots.
5 R7 v7 {( I2 U& d& p1 w0 DNeurologic evaluation showed deep tendon reflex 2+$ q/ O% u" |+ U; p$ Q7 m
bilateral and symmetrical. There was no suggestion  y) k5 p7 m3 A- n% ?* a: S/ H8 \
of papilledema.
$ o# k5 _4 y/ m* h! g5 J% o4 B8 fLaboratory Evaluation
: N) J" B+ h5 A% d% ^8 v# SThe bone age was consistent with 28 months by" I, }8 J  B6 w7 `( ^
using the standard of Greulich and Pyle at a chrono-9 L7 `; l0 z8 C% \0 K
logic age of 16 months (advanced).5 Chromosomal
; |6 v0 n, \. c' `- Bkaryotype was 46XY. The thyroid function test
  w0 N, l( o9 h2 `) B4 sshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
2 K# E) z* u+ Qlating hormone level was 1.3 µIU/mL (both normal).% L  }) }+ g& f# ?2 A; y
The concentrations of serum electrolytes, blood
( N+ o( D' \" o6 U0 O) }  @urea nitrogen, creatinine, and calcium all were# e: |& z% E. k3 K" H
within normal range for his age. The concentration  K4 S( S+ y- x& [
of serum 17-hydroxyprogesterone was 16 ng/dL4 A3 U: V( s" }" _* q
(normal, 3 to 90 ng/dL), androstenedione was 207 _: F4 x3 [& V  n& V& m
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
; ~/ f/ m0 p# jterone was 38 ng/dL (normal, 50 to 760 ng/dL),
; c! |9 ?5 L* K$ ]+ Qdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
' u. ?  p; H6 ^( x# x2 |49ng/dL), 11-desoxycortisol (specific compound S)& D# E. W6 m" L
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
& N. `- ?0 }4 p& I2 L: u* W8 ~8 q- Htisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
) V! Z5 o" y& ~3 Dtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
2 V% u, l4 m  L( Z0 ~* r* Rand β-human chorionic gonadotropin was less than4 d( c/ C/ b/ _
5 mIU/mL (normal <5 mIU/mL). Serum follicular, D$ L3 z8 f2 L5 g7 I& }9 d& n
stimulating hormone and leuteinizing hormone
8 s# x4 T7 b% ?& L! ]" |2 Lconcentrations were less than 0.05 mIU/mL
" G1 R4 J2 i$ w+ f' d(prepubertal).
( [( W  l6 L) g+ M9 G& zThe parents were notified about the laboratory, }, _+ q: z& S" D2 L
results and were informed that all of the tests were2 e. }; q# P6 D  k8 {
normal except the testosterone level was high. The
0 u* {. @1 @9 w' A9 p- p+ B7 k8 M" Yfollow-up visit was arranged within a few weeks to1 }" q8 i* p& i4 u2 i- r' h
obtain testicular and abdominal sonograms; how-
9 {8 P0 `# W* _8 b+ u5 gever, the family did not return for 4 months.% r1 }0 H, H3 L4 N; H; v' x) t/ ]
Physical examination at this time revealed that the
6 |4 o& l5 L1 Y' g) l5 ?# z% Pchild had grown 2.5 cm in 4 months and had gained5 D8 e! u3 r3 B5 n0 |  \
2 kg of weight. Physical examination remained, J. W& E: A8 \5 f! s
unchanged. Surprisingly, the pubic hair almost com-9 ^, K4 ]7 r) K5 X
pletely disappeared except for a few vellous hairs at
# {: ?4 c+ |" G  \3 \the base of the phallus. Testicular volume was still 2+ T* q* C1 W$ L# p1 x; n  D
mL, and the size of the penis remained unchanged.0 R5 z$ R0 b* T' b0 y% v
The mother also said that the boy was no longer hav-$ a& i5 Z# n0 V+ E0 r; m+ n9 t) e% l
ing frequent erections.
* s; a- n3 ^# J  F, c! gBoth parents were again questioned about use of9 ~) F  |& @& `2 B0 z5 a+ ^" e
any ointment/creams that they may have applied to
7 z$ g% ~0 g  l+ r6 A% Bthe child’s skin. This time the father admitted the: \1 }7 B( \6 p: P7 Q6 t; u
Topical Testosterone Exposure / Bhowmick et al 541! s! @( |* @& w& F7 d0 g( K
use of testosterone gel twice daily that he was apply-
1 I' e- s' v( f0 z# Iing over his own shoulders, chest, and back area for
# w; u' j3 u! a, N( G, k  u  a2 va year. The father also revealed he was embarrassed- ^* S! S- G9 O: a( p4 g
to disclose that he was using a testosterone gel pre-
( M) `, J8 ?. `: V2 B- e; uscribed by his family physician for decreased libido; L, h+ K. {$ V0 G8 o
secondary to depression.
) l7 L7 s" i# Q  ~  XThe child slept in the same bed with parents.$ m3 A. n+ t4 R/ _3 }9 c
The father would hug the baby and hold him on his
: O) P0 Q% x- v9 Mchest for a considerable period of time, causing sig-
" n( z9 P" E4 C9 Rnificant bare skin contact between baby and father.
' m, O$ }' U& WThe father also admitted that after the phone call,
5 I6 d* {* g, t8 pwhen he learned the testosterone level in the baby, \' z4 Y( D* W& T/ E3 ?
was high, he then read the product information- i/ g+ S: Z! C# m( p& P# P
packet and concluded that it was most likely the rea-( A! @2 i% _) g
son for the child’s virilization. At that time, they* K" q2 x3 q  f9 r+ D6 n
decided to put the baby in a separate bed, and the) }% B2 B- F/ j' K! E' [
father was not hugging him with bare skin and had2 \+ A& U$ X; e1 R2 ~
been using protective clothing. A repeat testosterone
: \; X$ \3 O& I( ~- }test was ordered, but the family did not go to the' ?6 g1 P' y) B4 i  p4 t' S' K
laboratory to obtain the test." K0 v) N/ k% e3 S
Discussion! m3 R6 \2 A. s7 K
Precocious puberty in boys is defined as secondary
, R! N- Z! _6 Z: G  \sexual development before 9 years of age.1,41 V  l; u4 y4 M1 B
Precocious puberty is termed as central (true) when
  o$ \1 w4 M; `+ O) W) ait is caused by the premature activation of hypo-7 s9 U5 A7 v: c2 o% Z$ |0 \
thalamic pituitary gonadal axis. CPP is more com-' N% F9 i" J8 L5 X- Q
mon in girls than in boys.1,3 Most boys with CPP2 q, C" u9 ]. \9 L: l
may have a central nervous system lesion that is' L/ T- I2 P; X2 V
responsible for the early activation of the hypothal-3 V% L+ N. `/ c' Y8 F0 a
amic pituitary gonadal axis.1-3 Thus, greater empha-6 X" e0 Y  K7 m; W& E& \! c
sis has been given to neuroradiologic imaging in
, r4 h" U5 |4 d/ n* Fboys with precocious puberty. In addition to viril-. {$ s1 P' W; T! w$ H( o
ization, the clinical hallmark of CPP is the symmet-; [5 Y! r1 I3 N+ k( X, ?/ l) \
rical testicular growth secondary to stimulation by! h, r: H0 I. n5 A
gonadotropins.1,3
& e1 }: F5 `6 [- M. P3 D- w) PGonadotropin-independent peripheral preco-
# u2 I/ H  I- J5 qcious puberty in boys also results from inappropriate
. g+ a- g( D4 S8 g1 \. w) mandrogenic stimulation from either endogenous or9 o. Q! d! u' r+ c( h
exogenous sources, nonpituitary gonadotropin stim-6 X5 g4 q& U! h+ E9 j/ l
ulation, and rare activating mutations.3 Virilizing
; [$ F1 @- C/ Xcongenital adrenal hyperplasia producing excessive
* n% A* i# r. e! W( ]1 s0 dadrenal androgens is a common cause of precocious3 x. L4 V0 B! v- ^- y- }9 @
puberty in boys.3,47 [. Y" p2 ~; W
The most common form of congenital adrenal* t; G6 W0 ]& v% X# O9 y
hyperplasia is the 21-hydroxylase enzyme deficiency.6 a2 S% p$ L. C8 I
The 11-β hydroxylase deficiency may also result in
, q0 G& ]' j: F9 a8 T& }excessive adrenal androgen production, and rarely,! z6 \& d7 ?6 y7 M2 Q0 p+ e; a
an adrenal tumor may also cause adrenal androgen! {6 q; j) K$ n. B
excess.1,3- P7 K# _0 h1 e. j+ w
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 V4 k7 }, r9 g( Q
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
- S' d1 C" d- V* H' pA unique entity of male-limited gonadotropin-
8 P/ |) G% q" c5 windependent precocious puberty, which is also known
  I. H/ u& \$ M5 _4 s) ~9 kas testotoxicosis, may cause precocious puberty at a/ R8 U! T7 [" `6 v. o
very young age. The physical findings in these boys
  h9 {$ _) y# d/ o" bwith this disorder are full pubertal development,8 G' F1 }  Q- a0 q# V1 `
including bilateral testicular growth, similar to boys+ _3 u5 d! N2 }3 X9 |0 b; D
with CPP. The gonadotropin levels in this disorder  l  C: r) S6 v/ l% @
are suppressed to prepubertal levels and do not show
4 A6 F1 o# }/ w# \( Y* apubertal response of gonadotropin after gonadotropin-$ i+ J4 c9 [1 L% g7 X) @
releasing hormone stimulation. This is a sex-linked
3 d5 y+ f/ A& \% L; aautosomal dominant disorder that affects only
6 _4 J/ w' u0 U. _$ H/ K/ Wmales; therefore, other male members of the family" H4 |% U* {6 U0 }* Z
may have similar precocious puberty.3
0 z6 l4 b6 [0 c! _In our patient, physical examination was incon-0 j8 ^7 Z+ @" u2 ^+ o
sistent with true precocious puberty since his testi-& N* i9 X4 Q3 t! O3 `9 y( m! Q
cles were prepubertal in size. However, testotoxicosis  p: K& L$ }$ j0 s1 E* ?( }4 f# u
was in the differential diagnosis because his father1 j$ Z2 Y# |; ^
started puberty somewhat early, and occasionally,
" j; ?# _8 D% n% N6 v3 j3 q$ ztesticular enlargement is not that evident in the
1 R" m1 H0 K  Jbeginning of this process.1 In the absence of a neg-
- E1 O3 f1 l3 l* _8 n  u7 Jative initial history of androgen exposure, our1 j) N9 ]) Z  g3 o
biggest concern was virilizing adrenal hyperplasia,
, M: c6 K. W7 F# Aeither 21-hydroxylase deficiency or 11-β hydroxylase
9 L' t, [) _5 T; Hdeficiency. Those diagnoses were excluded by find-* o0 T: U8 b: @& g
ing the normal level of adrenal steroids.
- k! Z4 k+ w+ r; ~$ x  E) R% ?3 t+ }2 bThe diagnosis of exogenous androgens was strongly
+ w% o3 f% o5 V# ususpected in a follow-up visit after 4 months because& A: z$ K$ C/ G( o
the physical examination revealed the complete disap-8 m$ H0 t- W7 N, b& k3 S
pearance of pubic hair, normal growth velocity, and! b  Q5 u, E3 d+ ~
decreased erections. The father admitted using a testos-( d/ \" c% [9 j! r& z( E
terone gel, which he concealed at first visit. He was( }% }% p. H0 T$ y; ?! s
using it rather frequently, twice a day. The Physicians’
( T9 F  ~7 @( j7 oDesk Reference, or package insert of this product, gel or6 {0 r9 [  b. |5 c7 N2 Y: p
cream, cautions about dermal testosterone transfer to8 R3 ^! {: j3 W0 H, l
unprotected females through direct skin exposure." C4 P- y: B& P( v; l# Q
Serum testosterone level was found to be 2 times the  R. j( q; E; v; N' E
baseline value in those females who were exposed to
9 v2 c5 r7 x. F* s- O' seven 15 minutes of direct skin contact with their male
8 V1 V# V7 \# h2 s0 F% Qpartners.6 However, when a shirt covered the applica-
! Q3 t- a  W# Ztion site, this testosterone transfer was prevented.
1 [0 E# `1 n* SOur patient’s testosterone level was 60 ng/mL,' X' d6 w! {# @9 ]8 A
which was clearly high. Some studies suggest that
' \7 Q# J; G& rdermal conversion of testosterone to dihydrotestos-
" e/ h, Y" f+ ]3 j  q( N  vterone, which is a more potent metabolite, is more
. s9 R% {$ e- c% X" J3 jactive in young children exposed to testosterone
6 D4 t) o8 I+ h/ U7 b$ aexogenously7; however, we did not measure a dihy-# X1 X! Z3 |+ H" [; g' s
drotestosterone level in our patient. In addition to
+ E, l, W# K: m. Evirilization, exposure to exogenous testosterone in
) V  {4 R" \" E) _- Achildren results in an increase in growth velocity and
! P  l' }5 \4 }3 j' i: F$ o& Kadvanced bone age, as seen in our patient.* T3 j" l2 ^5 U/ h
The long-term effect of androgen exposure during6 l2 p! Q  O: B; P" k
early childhood on pubertal development and final
4 P, v; n5 q# o! s9 v" }. T! h0 }adult height are not fully known and always remain
, @$ Y7 H0 V' J6 X; d* U7 aa concern. Children treated with short-term testos-
/ q7 S/ k: }0 F$ Z- W# I( X: t' wterone injection or topical androgen may exhibit some3 y! X) S0 U, A6 k; K7 m$ m
acceleration of the skeletal maturation; however, after6 n# J( p* t9 T: |& x' X- g
cessation of treatment, the rate of bone maturation
- s" \  S9 d4 a8 vdecelerates and gradually returns to normal.8,9
# e3 O' ]+ p3 K0 D' A0 r$ TThere are conflicting reports and controversy
) @; I4 ~( s5 b6 f6 B% G1 ^over the effect of early androgen exposure on adult  {, ?; a1 @; M0 R
penile length.10,11 Some reports suggest subnormal$ u1 J: _! F. }  Y7 b! e4 ]
adult penile length, apparently because of downreg-0 {; `& Y1 ~9 p1 S' c& m, R% I
ulation of androgen receptor number.10,12 However,& j. P/ r/ L3 }- w
Sutherland et al13 did not find a correlation between
8 v" c/ @5 H) D' ]7 gchildhood testosterone exposure and reduced adult; V/ i6 [3 m( v$ y1 N' N
penile length in clinical studies.) ?4 e0 A! c) l' Q, d. F2 ^" O: E
Nonetheless, we do not believe our patient is% _# [1 b7 i, ?2 d( y
going to experience any of the untoward effects from
/ J. A; a9 ^. {3 t$ _testosterone exposure as mentioned earlier because
4 a5 m9 Z5 }. O# R! T4 cthe exposure was not for a prolonged period of time.( D8 l( f7 }3 v, Z/ ~& z4 e
Although the bone age was advanced at the time of6 o3 h7 X; R" c1 |7 _2 o/ S$ X# L
diagnosis, the child had a normal growth velocity at
7 O/ b' O$ L& }- t+ F+ Mthe follow-up visit. It is hoped that his final adult: m  b' C6 L4 B4 f
height will not be affected.  X; z- ], p4 f4 T
Although rarely reported, the widespread avail-/ v( K9 a+ V, W
ability of androgen products in our society may
+ h! \# d/ j8 }. S9 gindeed cause more virilization in male or female) p, l' m2 g' r9 @  ?5 O
children than one would realize. Exposure to andro-
+ `! g/ D( c0 }4 N& Q3 B3 Mgen products must be considered and specific ques-
( R: l2 k3 }3 \2 Utioning about the use of a testosterone product or
1 H" q! W, Y) }6 ~7 ~gel should be asked of the family members during
* H- x" e, M; j% w8 h- o1 kthe evaluation of any children who present with vir-
& C8 x; M" A+ m1 a8 @ilization or peripheral precocious puberty. The diag-( y$ d: R1 f8 |2 x
nosis can be established by just a few tests and by
+ W& x( N: J) t  N/ f6 K+ eappropriate history. The inability to obtain such a
9 k- ]( `. u# a! Z6 K! Dhistory, or failure to ask the specific questions, may
# Q7 `8 N9 @2 Iresult in extensive, unnecessary, and expensive
; ~& M$ I, ?/ r3 ]: I, `5 f- ninvestigation. The primary care physician should be- a* |5 }$ x. ]0 h0 z6 w/ D! R0 l
aware of this fact, because most of these children
5 S. H& U$ _- k7 t5 v4 I/ c& X% dmay initially present in their practice. The Physicians’
/ z6 g9 ~1 |; q* o* Q8 |Desk Reference and package insert should also put a
. z0 T6 M% a$ b" C8 T5 z7 R& h' @1 Wwarning about the virilizing effect on a male or
7 _9 Q% \2 [& t- A. q& A+ cfemale child who might come in contact with some-4 x' K0 K  \- O' d
one using any of these products.% N3 }* ~" p, [  i; v
References9 D4 u1 v/ W8 x' z/ |) Q% [
1. Styne DM. The testes: disorder of sexual differentiation' }6 X( i4 E, {5 t5 p- y
and puberty in the male. In: Sperling MA, ed. Pediatric& [. R* F* s# \, {
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
! n( e- o) x( w  D9 Q2002: 565-628./ s8 i, E- s5 t6 N
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious8 i- {( n' }3 w) n/ E( ?
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

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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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