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Sexual Precocity in a 16-Month-Old8 q. u) A; ?: g3 f" k
Boy Induced by Indirect Topical8 u" Y% K( x5 |- P6 \
Exposure to Testosterone3 Y  Z4 P/ O1 X+ e7 z
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
2 ~9 Z5 T7 B& o6 j5 }& ^: V1 b) band Kenneth R. Rettig, MD1, M; J5 I" W3 n! N
Clinical Pediatrics! R8 A: R& w8 y9 y: Z- E1 e
Volume 46 Number 6' s4 u/ Z6 L7 k+ @+ k
July 2007 540-543
0 v1 `! {& g- i/ j0 c% R© 2007 Sage Publications
  t) P3 L, u8 E- n10.1177/0009922806296651
; C, a# A) A: ?# [9 `+ A2 ?7 ehttp://clp.sagepub.com8 \/ d( Q% o& s% U% i
hosted at
# j" d- T: c" n+ U# I- _http://online.sagepub.com
& Y) Q4 r0 P+ p. \+ }- fPrecocious puberty in boys, central or peripheral,
, w+ h. N* Y* r- w( tis a significant concern for physicians. Central) h8 L% D+ n2 [, {
precocious puberty (CPP), which is mediated
8 o5 n# T3 W$ E3 ~through the hypothalamic pituitary gonadal axis, has9 g2 l/ W0 V8 I* A& ?
a higher incidence of organic central nervous system% u/ X: I2 @9 P+ n4 i
lesions in boys.1,2 Virilization in boys, as manifested
; h0 K6 L0 F: S' M+ {( eby enlargement of the penis, development of pubic3 R1 S* _# p. {+ R/ v, Z
hair, and facial acne without enlargement of testi-3 a* r' C, N9 s
cles, suggests peripheral or pseudopuberty.1-3 We
5 b1 @4 y& I$ H5 f; t3 c9 [report a 16-month-old boy who presented with the
5 `4 t( S/ f+ kenlargement of the phallus and pubic hair develop-$ L! i2 D  {8 ?1 h
ment without testicular enlargement, which was due/ Z: D% d3 W8 `8 J% w
to the unintentional exposure to androgen gel used by4 A' ?* m( I% K, ~  D3 P  @
the father. The family initially concealed this infor-1 ~8 L% Z- N, W" d  F+ R
mation, resulting in an extensive work-up for this
& o& I1 t' |0 i& ^+ Qchild. Given the widespread and easy availability of
" T  t6 N: W" X  y) b; htestosterone gel and cream, we believe this is proba-% h/ E. r3 o- [- }  x7 S3 i* s/ R  b
bly more common than the rare case report in the1 w% d! o* X% n1 a
literature.4% Q. y7 n& S1 U1 W6 |$ D' ~3 R
Patient Report* a3 g2 g0 Q7 ]8 p7 i' c% D) P
A 16-month-old white child was referred to the# }: a. f4 W! |+ c  B4 U
endocrine clinic by his pediatrician with the concern
. x3 D- _: [' R9 e/ Gof early sexual development. His mother noticed: l: }# @. m; n, @1 ?
light colored pubic hair development when he was0 y- b5 g7 f  H! }! z2 e; P* Z
From the 1Division of Pediatric Endocrinology, 2University of% l$ a$ U: G! k0 t( w2 Y8 g- C$ H
South Alabama Medical Center, Mobile, Alabama.2 N" V% ^  X1 ?6 R  `1 @
Address correspondence to: Samar K. Bhowmick, MD, FACE,
, _" H+ W& p1 s& F# AProfessor of Pediatrics, University of South Alabama, College of! ~7 i6 _$ T  c) g' m
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ }/ y4 @5 j% m) K
e-mail: [email protected].2 s6 ]3 I- [2 @4 l: t* Z
about 6 to 7 months old, which progressively became
8 ^, n, {" j5 H/ l1 |2 p8 X: ^darker. She was also concerned about the enlarge-5 B8 D6 P! ~$ \3 A4 B
ment of his penis and frequent erections. The child
7 u( H! S+ V8 A: E/ w3 ewas the product of a full-term normal delivery, with4 m. {2 D6 u6 |, ^8 R- b
a birth weight of 7 lb 14 oz, and birth length of
, ?% ~: c6 U( [/ H20 inches. He was breast-fed throughout the first year) w2 L& O/ D  _9 u1 Z) C
of life and was still receiving breast milk along with$ u1 u; j; J5 v# Y/ \
solid food. He had no hospitalizations or surgery,
8 G/ x* R7 e5 E  Z9 X3 ?and his psychosocial and psychomotor development5 g. F) k6 Y0 a- `8 f( F5 p
was age appropriate.5 O7 [  F, _3 O
The family history was remarkable for the father,
, f9 m' q9 q' H8 ^# f9 Kwho was diagnosed with hypothyroidism at age 16,
( o- p  ?' s8 I0 `5 g$ l8 swhich was treated with thyroxine. The father’s
( V8 m8 L; n7 lheight was 6 feet, and he went through a somewhat
7 R, h- H& J- F, Nearly puberty and had stopped growing by age 14.! X' Q7 x6 T, Y7 p5 J- ?
The father denied taking any other medication. The
; D5 q1 E* E* M0 P  f0 Cchild’s mother was in good health. Her menarche7 V, T0 O, w  n3 e1 b9 q) h5 I
was at 11 years of age, and her height was at 5 feet
4 B  p$ j& Y" {4 K& P2 v* O5 inches. There was no other family history of pre-
* A$ l6 q7 V- icocious sexual development in the first-degree rela-9 X. X: e2 P, o) m& g7 F! W" @
tives. There were no siblings.
  k9 a/ }& ^4 k" l6 PPhysical Examination
0 S4 v& C6 |! @The physical examination revealed a very active,  Q# r; F. \) u& w* _; N4 }* w+ @' R
playful, and healthy boy. The vital signs documented
  t) A$ m+ Y0 L" y2 y. L* P1 @" ma blood pressure of 85/50 mm Hg, his length was+ f- e- q) r* p& u! ]( w
90 cm (>97th percentile), and his weight was 14.4 kg0 k- R: X& u6 I
(also >97th percentile). The observed yearly growth1 s9 Y+ X* v" B- c# ^7 f$ d8 I7 K
velocity was 30 cm (12 inches). The examination of! B; c' R% O5 ?8 X
the neck revealed no thyroid enlargement.
' K8 j# C! D: U" AThe genitourinary examination was remarkable for
4 V  W- o- ^, K8 X; j& G* benlargement of the penis, with a stretched length of
! [$ P& `8 f. ]! d3 a9 M6 e" e+ N8 cm and a width of 2 cm. The glans penis was very well6 j, _0 p% `% D0 g6 N
developed. The pubic hair was Tanner II, mostly around
+ f% e* y: `4 u3 Q540
) C4 X5 S2 q- ^1 h& g# ~& ~! Dat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ [5 R. D! ~# c% {5 V4 t, `: ~  S
the base of the phallus and was dark and curled. The8 T% a& A* [# I- z* o4 j
testicular volume was prepubertal at 2 mL each.
; m. l8 `$ I  Z. t* S; BThe skin was moist and smooth and somewhat
9 ^" j# z6 ]5 \0 m+ h% }oily. No axillary hair was noted. There were no: Y+ W! Z  d1 K  Q
abnormal skin pigmentations or café-au-lait spots.* H1 ^* _; V' j$ o2 P4 U
Neurologic evaluation showed deep tendon reflex 2+
5 v8 p5 y* e/ L; c  i  Gbilateral and symmetrical. There was no suggestion
! I3 S1 c/ o9 w6 k9 R, ?' wof papilledema.
' d; p# B' T# Y4 Y$ bLaboratory Evaluation2 v; Q1 ^  s/ U9 z  l) K2 l
The bone age was consistent with 28 months by. V& R2 a( U& H) I4 t
using the standard of Greulich and Pyle at a chrono-  b. ]& }0 ]% ~8 s! L. W4 h
logic age of 16 months (advanced).5 Chromosomal
+ Y, V- c, R5 N. Z& M  B; qkaryotype was 46XY. The thyroid function test$ u  G9 q8 _7 a) l6 O
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
, v, \" x- c7 U5 ^0 |, V' Y8 j& Plating hormone level was 1.3 µIU/mL (both normal).
: r2 r0 K- J' r+ L' fThe concentrations of serum electrolytes, blood: t: Y* a5 w+ N  I/ z$ [$ d. r) _
urea nitrogen, creatinine, and calcium all were% \7 z" z( v8 M; G* {
within normal range for his age. The concentration6 y0 f+ m8 ^; X% f" f- a
of serum 17-hydroxyprogesterone was 16 ng/dL- k8 f' d9 [" E( }# L/ K
(normal, 3 to 90 ng/dL), androstenedione was 204 x/ X6 V9 J2 T# A- x
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
1 L, I9 D/ l$ z( q, Wterone was 38 ng/dL (normal, 50 to 760 ng/dL),* L# x) ^$ o3 q+ P8 ?! x
desoxycorticosterone was 4.3 ng/dL (normal, 7 to8 |$ \/ p. b$ P# g) g" c( {
49ng/dL), 11-desoxycortisol (specific compound S)  ~  H( U) k6 C+ d: ]' N
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# c* d7 {6 B0 L  k: s8 a% M
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' H/ l% ]6 W: D1 M% u
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
4 }+ p7 Z( R* k- s2 _8 m, c: f, mand β-human chorionic gonadotropin was less than* c. i8 C, _  }, L7 J. f
5 mIU/mL (normal <5 mIU/mL). Serum follicular
* m# {" G  S3 [stimulating hormone and leuteinizing hormone) ^8 n, B; }4 q; t" ~: U6 c! d
concentrations were less than 0.05 mIU/mL* q, E$ f9 ~, p# o% N$ v0 R/ p
(prepubertal)./ P0 l2 S) J; Z- ?; D
The parents were notified about the laboratory
7 ~+ H/ O; D* h- a) |# [3 j0 eresults and were informed that all of the tests were
. L9 u8 E1 n( Inormal except the testosterone level was high. The) E$ Z+ W- z  F0 U/ h- h
follow-up visit was arranged within a few weeks to0 B) i& p$ a, t* [8 r7 P6 p
obtain testicular and abdominal sonograms; how-
6 E( X4 A0 [6 G' c# b/ bever, the family did not return for 4 months.+ f8 o; q) ?" ~7 X! y$ o' {% _
Physical examination at this time revealed that the8 e# @: Z  t0 D
child had grown 2.5 cm in 4 months and had gained7 R" o: A5 M, y6 s- S- M
2 kg of weight. Physical examination remained
0 H: s0 v+ h, `  Junchanged. Surprisingly, the pubic hair almost com-3 P% ~/ U* x, O# Z- i# y( O3 i
pletely disappeared except for a few vellous hairs at
6 f9 M' |- A% x9 |* L6 Xthe base of the phallus. Testicular volume was still 2
! ]. [* |! \* Z7 I$ KmL, and the size of the penis remained unchanged., o; \0 n. t& P" v7 t" B
The mother also said that the boy was no longer hav-' }. x5 r' Q. L  I+ e% s! i
ing frequent erections.6 x. g) D2 E# q# F& C0 s+ O
Both parents were again questioned about use of8 b3 ]! z& S4 T2 k- g/ @, [
any ointment/creams that they may have applied to
6 z- s% S/ @+ z2 `the child’s skin. This time the father admitted the+ s! A% m! T" I# q$ d
Topical Testosterone Exposure / Bhowmick et al 541& d7 B( Q5 w8 w3 a9 a' D$ f
use of testosterone gel twice daily that he was apply-
0 [5 }/ Q; O9 ]& f& }" y* [ing over his own shoulders, chest, and back area for% C" o. n# x4 m0 b; p( k0 T  Q
a year. The father also revealed he was embarrassed
$ H0 C1 Z8 Z" bto disclose that he was using a testosterone gel pre-. J  l; b" T7 W" Z: y
scribed by his family physician for decreased libido5 J' e7 u: h9 ?3 t0 J0 e
secondary to depression.
& s" @' c, B7 D! r9 y! u: F' u: GThe child slept in the same bed with parents.$ n; t# y' {& i6 R) W4 x0 A( K
The father would hug the baby and hold him on his! {+ ]3 r/ t. |/ j9 z
chest for a considerable period of time, causing sig-, I0 O. |. g/ ~7 A5 d0 v
nificant bare skin contact between baby and father.
) C4 ]5 ]/ _, K' u7 a$ {. r0 YThe father also admitted that after the phone call,
- D. y4 X! R1 i& N! y4 bwhen he learned the testosterone level in the baby
. N5 g6 w+ P/ z7 H$ R  z9 Wwas high, he then read the product information  |. X' O# _0 |: c* l+ z  L
packet and concluded that it was most likely the rea-( p7 X; h" S0 [& M
son for the child’s virilization. At that time, they' W- Y' W7 t, u/ d' l0 X& g
decided to put the baby in a separate bed, and the7 J$ t8 y. f+ y- p+ z
father was not hugging him with bare skin and had; `0 [7 f  e1 x. K+ o( n- m
been using protective clothing. A repeat testosterone- o& X; [6 e0 Q/ J; [
test was ordered, but the family did not go to the
% u/ W* X" Z# q8 I& f7 slaboratory to obtain the test.$ i& F- s3 L2 o: l2 N- D& T0 a' b
Discussion5 F- G; z% M/ ^3 `8 c0 L2 N4 |
Precocious puberty in boys is defined as secondary
/ Y6 j0 Y1 I; b3 m+ Usexual development before 9 years of age.1,4  m8 \: b, X9 m! u
Precocious puberty is termed as central (true) when  t% _& g% f: r$ P# V4 ~* R
it is caused by the premature activation of hypo-
9 F% h+ ?. C& {; G. [7 G3 Ythalamic pituitary gonadal axis. CPP is more com-( ~1 O! @1 f+ I* m" c( A
mon in girls than in boys.1,3 Most boys with CPP
& m& n% |0 i# Y) U. v" m- Hmay have a central nervous system lesion that is( k) N2 r0 [2 M$ ?" x0 h& h
responsible for the early activation of the hypothal-: r( M3 @" o4 D- y3 O* h5 K) m. ^
amic pituitary gonadal axis.1-3 Thus, greater empha-
3 b+ J1 K$ D8 I* i  t6 k% Q$ ^sis has been given to neuroradiologic imaging in
9 A. ^+ K* ]8 hboys with precocious puberty. In addition to viril-
3 o! }5 P* y, m* pization, the clinical hallmark of CPP is the symmet-
/ \* G4 j  C6 l* o0 e$ Zrical testicular growth secondary to stimulation by3 N$ s6 F9 P/ x! z) v; p
gonadotropins.1,3
& a( H8 B" b2 u: B" YGonadotropin-independent peripheral preco-
% }0 P9 v# |5 O4 Acious puberty in boys also results from inappropriate- R. `6 B! m6 [0 J& p6 {" T' f
androgenic stimulation from either endogenous or. |5 S4 [! @* D) R% W# L( c. k
exogenous sources, nonpituitary gonadotropin stim-* O- z1 F' Z8 v. Y6 v
ulation, and rare activating mutations.3 Virilizing$ q- s. L' t/ E: t$ k& ~
congenital adrenal hyperplasia producing excessive
0 |# a9 W4 V9 K! m" V% Tadrenal androgens is a common cause of precocious
( U  t- Y  }) _# P2 C- Fpuberty in boys.3,4
' H/ G/ N- K2 i; k5 N" V) F, TThe most common form of congenital adrenal
0 M5 ^2 r  d  f8 `1 ehyperplasia is the 21-hydroxylase enzyme deficiency.
/ o3 z, j! B/ Y, qThe 11-β hydroxylase deficiency may also result in! `' m/ l& Y) V0 G3 q  M
excessive adrenal androgen production, and rarely,
% S) P8 {! ]% ?& z, S* ean adrenal tumor may also cause adrenal androgen% \( |( R+ p% Y3 M- J: f' |
excess.1,3
9 z  }% E" V8 k* {  F' t5 I: K! mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 y- n4 ]# F/ t& p2 O542 Clinical Pediatrics / Vol. 46, No. 6, July 2007# p4 S- R8 q0 `  X& _7 Q7 p
A unique entity of male-limited gonadotropin-4 j0 ^, k* I1 P$ W( i& w
independent precocious puberty, which is also known
# N( z! e) C6 H+ z. Mas testotoxicosis, may cause precocious puberty at a$ k( ~5 s9 Y. q. ^7 q
very young age. The physical findings in these boys
. m5 i. I/ r/ K, Q, C6 Qwith this disorder are full pubertal development,( E4 e  p7 g3 P  m
including bilateral testicular growth, similar to boys) r+ M7 Q( V* T8 B# G- X. ~
with CPP. The gonadotropin levels in this disorder6 Y: U2 {7 d# \% D; K" r" E
are suppressed to prepubertal levels and do not show
5 H* G; [2 u7 K8 G8 spubertal response of gonadotropin after gonadotropin-
4 {. T% t1 \# o2 {releasing hormone stimulation. This is a sex-linked
8 r2 p; y4 x: K  v4 \3 q& f# Oautosomal dominant disorder that affects only
" W+ D. [$ p( v# Emales; therefore, other male members of the family
, G# Y. B1 i0 g! H! X, B# H6 m+ ~may have similar precocious puberty.3
( c  _, c. Y: U4 X' b) ^3 J! CIn our patient, physical examination was incon-$ h4 D' t& v- g" f# Z  ^1 f# k
sistent with true precocious puberty since his testi-
' `& D5 @: i9 G9 `* I; Acles were prepubertal in size. However, testotoxicosis, @4 G8 o* g4 o. o- f, y
was in the differential diagnosis because his father% v2 s6 p, ^; T4 L6 v2 r
started puberty somewhat early, and occasionally,4 l; z) Y* r$ T' d) u3 q! T) E
testicular enlargement is not that evident in the  m' e* r" ^$ i) B9 u8 l( j2 R
beginning of this process.1 In the absence of a neg-( o2 ~7 x& z! R, h6 ?
ative initial history of androgen exposure, our" d7 T  T. T1 R: E
biggest concern was virilizing adrenal hyperplasia,8 ?4 ^4 N& ~0 X
either 21-hydroxylase deficiency or 11-β hydroxylase
! V3 U0 s5 D9 E+ J$ C6 ndeficiency. Those diagnoses were excluded by find-0 m) G* b9 Z/ I, c; n# w0 ~# y/ n
ing the normal level of adrenal steroids.
; }, ~' O1 [( [' y2 P( IThe diagnosis of exogenous androgens was strongly( z1 n, {- h, L9 C' x& |' B' q
suspected in a follow-up visit after 4 months because3 j; |4 J: W1 X$ _+ z
the physical examination revealed the complete disap-
% c6 y7 N1 Q3 V& i2 Gpearance of pubic hair, normal growth velocity, and# g; M) ?8 r4 H0 n, n- p* {0 c
decreased erections. The father admitted using a testos-, k$ a' }/ D- }  ]7 m) J
terone gel, which he concealed at first visit. He was
3 p+ t6 @# x6 W. M# {) i" \: @% ?using it rather frequently, twice a day. The Physicians’
. e' N& \5 y8 ]! @; ~% nDesk Reference, or package insert of this product, gel or
3 i+ h6 V2 ~. ~& f# A4 G7 Q- u2 `8 Tcream, cautions about dermal testosterone transfer to) L! J& D& u8 [9 B( Y% t8 T
unprotected females through direct skin exposure./ D1 @, S6 r5 L
Serum testosterone level was found to be 2 times the
7 T0 V7 F; f3 X2 Nbaseline value in those females who were exposed to6 f; b; a) Q$ i) `1 ]
even 15 minutes of direct skin contact with their male4 @- [/ V1 q, Z/ D, J
partners.6 However, when a shirt covered the applica-  p7 g% k6 i% G* M( k
tion site, this testosterone transfer was prevented.9 A' y5 g" ]" u' k
Our patient’s testosterone level was 60 ng/mL,
# V7 Q2 d. q6 D' K0 s& Uwhich was clearly high. Some studies suggest that# D# f5 M# ?. W+ \- z! L9 P+ H
dermal conversion of testosterone to dihydrotestos-' M$ E: }; V8 X0 j* w8 {
terone, which is a more potent metabolite, is more
: c* p% Y. a7 e9 F/ r4 w/ Factive in young children exposed to testosterone
/ E' J9 J+ X# E! uexogenously7; however, we did not measure a dihy-
8 P( F2 r* D, A$ E8 q3 _drotestosterone level in our patient. In addition to, |" s4 z7 E5 m8 a5 |8 L, I
virilization, exposure to exogenous testosterone in* e# Q/ M1 D2 P4 b9 ?
children results in an increase in growth velocity and
- a" S; u* t9 M+ {' f. Xadvanced bone age, as seen in our patient.
8 j/ p9 V, y* ?" G1 IThe long-term effect of androgen exposure during
) e; L& F7 o  L& Bearly childhood on pubertal development and final1 f  i$ q, k/ S8 h* ]" N
adult height are not fully known and always remain3 X& i1 |% n- K4 S4 U3 ^, e1 u$ e
a concern. Children treated with short-term testos-
9 T/ T9 b  J/ n# y; e0 _terone injection or topical androgen may exhibit some) n& d9 V* `9 W( [4 [3 T; g
acceleration of the skeletal maturation; however, after& d0 [, A! U) s% f' K; ?
cessation of treatment, the rate of bone maturation
4 b. ^( N7 Q# k3 W/ c( O$ j. ~  i: \( cdecelerates and gradually returns to normal.8,9$ z, Y5 x( m8 e8 j. @
There are conflicting reports and controversy
* S& F2 r# G8 ]- O6 N2 zover the effect of early androgen exposure on adult) V5 B. p- f; [, M% ]
penile length.10,11 Some reports suggest subnormal
+ l) r/ U0 R$ L: @adult penile length, apparently because of downreg-
$ [1 [' t  B9 w$ hulation of androgen receptor number.10,12 However,
; H8 y+ l7 j5 H& lSutherland et al13 did not find a correlation between
! M/ N0 U( I9 W& V! kchildhood testosterone exposure and reduced adult  g% ~/ Y8 [  j
penile length in clinical studies.
# o& z# f' b9 E- ^2 @6 VNonetheless, we do not believe our patient is
; N/ a. J& a7 h  [$ Wgoing to experience any of the untoward effects from+ d3 w& f' i7 P& I. e
testosterone exposure as mentioned earlier because1 V( D6 o& H" B8 ~4 x
the exposure was not for a prolonged period of time.
9 Q, C+ k2 @- t6 I5 r* {/ }. iAlthough the bone age was advanced at the time of
, R& @! N$ M' e! y( A% W/ odiagnosis, the child had a normal growth velocity at
3 i7 V* A6 ~, O( E9 W" Hthe follow-up visit. It is hoped that his final adult
* d; T. G/ r$ I! Z3 mheight will not be affected.2 d5 C" [# f, X( d, Q, f7 X
Although rarely reported, the widespread avail-
, e: L  |1 I* \- eability of androgen products in our society may
8 O! l1 d( D4 h) A6 [+ ~indeed cause more virilization in male or female
7 N5 \. R) M/ G. Y  q: Q" j- Zchildren than one would realize. Exposure to andro-* K: G7 Q( p4 j- g% I
gen products must be considered and specific ques-7 W& S8 a8 N' a: d& P% K% ^
tioning about the use of a testosterone product or
" c8 F; J/ L" ^/ c3 M5 ^* ggel should be asked of the family members during
" H. j0 Q0 c' e) H7 I! l* R4 k+ m' Kthe evaluation of any children who present with vir-  c) l2 f& q5 x4 m/ K3 ?6 z) W. ]
ilization or peripheral precocious puberty. The diag-
4 z+ A: V8 b' q+ l( O( Knosis can be established by just a few tests and by
$ n1 X/ C) `; J1 M# Fappropriate history. The inability to obtain such a
; v* k4 e7 o. N$ U/ C7 s1 p* mhistory, or failure to ask the specific questions, may) w  i; z$ h1 m( i* Z" Y' I
result in extensive, unnecessary, and expensive
& x9 I, v: P' W- D) Ginvestigation. The primary care physician should be$ L2 G, F% W2 L  _# ~3 r3 L) Y% @
aware of this fact, because most of these children% |  m6 k; n0 K; c( x
may initially present in their practice. The Physicians’
' G( Q% C8 z( R5 @' RDesk Reference and package insert should also put a2 q4 S, u' }' v* M7 y7 e
warning about the virilizing effect on a male or
- z. T2 T8 c6 U& r! `female child who might come in contact with some-
, `- A# W6 R$ }9 ]one using any of these products.6 a. K0 y+ {8 A6 v' K, M% _% l
References
/ ~1 z0 U- a1 ~. l/ a: b- h) D1. Styne DM. The testes: disorder of sexual differentiation' r0 P( J. S" n/ A# I; K
and puberty in the male. In: Sperling MA, ed. Pediatric4 ^! R, S( `+ Z- P- K4 P: x
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, }% ?& z: |5 p! a4 l
2002: 565-628.- t: k+ }3 H! g: V
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious- y% G; V- ]1 V
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
) z( @: r  R7 J! A8 {! l! wBoy Induced by Indirect Topical  o" I8 {' X+ w6 Q
Exposure to Testosterone9 a) ^. X8 P% d1 B" ^4 X+ Y
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2$ T5 P5 r+ Y4 s
and Kenneth R. Rettig, MD1
- R) k" Q. E* uClinical Pediatrics, l) O/ e2 D, `/ G0 d
Volume 46 Number 6
4 Z9 H# P6 {) B1 }July 2007 540-543
8 j  n0 U# U, f© 2007 Sage Publications
# Z; W. g! [+ z2 [2 J& C0 B10.1177/00099228062966512 m: j# q5 p) y# e
http://clp.sagepub.com
9 r- {7 T4 D6 @% P  Y; Y, R9 Lhosted at
7 K& E/ L3 S* p- Zhttp://online.sagepub.com7 b# ^5 J" |, v7 D( Y" a
Precocious puberty in boys, central or peripheral,+ ]  `) r. n" y4 A, i
is a significant concern for physicians. Central4 l6 P) e' a2 G" t- [
precocious puberty (CPP), which is mediated
3 V  \2 e7 \; x/ p) Y9 y$ E+ Ithrough the hypothalamic pituitary gonadal axis, has  I4 e5 Z  [  o* Z2 N. f' q$ H
a higher incidence of organic central nervous system! r$ h' a3 N9 o$ j2 Z" i
lesions in boys.1,2 Virilization in boys, as manifested
3 O' _8 q- o) i+ g7 Kby enlargement of the penis, development of pubic
* M$ ^  u0 S, s/ bhair, and facial acne without enlargement of testi-
, z$ m+ C! t/ R, `- f8 G# Y3 Mcles, suggests peripheral or pseudopuberty.1-3 We
1 O; x- m# D0 v! @: y4 I% s0 Ireport a 16-month-old boy who presented with the
- ~1 P: j0 ?$ T3 renlargement of the phallus and pubic hair develop-
' v0 }, O0 W3 x& U' ^7 F0 O  qment without testicular enlargement, which was due. v  ?+ ^# l) p  F& K
to the unintentional exposure to androgen gel used by
( I6 z, `3 S; X* sthe father. The family initially concealed this infor-5 X( M* b& k3 [* I
mation, resulting in an extensive work-up for this
0 {# I1 X6 l4 T2 Ichild. Given the widespread and easy availability of
4 Z+ L) ?& X, X9 ttestosterone gel and cream, we believe this is proba-3 R  g5 F1 }7 [, h6 O% \7 V. ?  u
bly more common than the rare case report in the5 T* |( x5 @/ O' j% Z8 X
literature.4
% q. J" s) h5 V6 b: y; `7 mPatient Report
! X, j8 z( @( l7 h; q1 OA 16-month-old white child was referred to the" ^1 r( S7 ~+ d" v7 J$ s
endocrine clinic by his pediatrician with the concern0 [  w$ j# T0 ^& `* I
of early sexual development. His mother noticed9 L8 {. d% {. Y% j5 V
light colored pubic hair development when he was
4 G( H) W) ~9 y5 v. RFrom the 1Division of Pediatric Endocrinology, 2University of
  Q/ N& }; F( QSouth Alabama Medical Center, Mobile, Alabama.
$ X! B! Y- Y9 D5 J4 U; i5 D" PAddress correspondence to: Samar K. Bhowmick, MD, FACE,& t, ~) K2 ^) R2 _
Professor of Pediatrics, University of South Alabama, College of, Y; D* t5 G( c: N* S
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;1 v4 p: L, \# q- E) X
e-mail: [email protected].
. S) a. A' n' U! t# i2 yabout 6 to 7 months old, which progressively became
' X0 R2 F0 v( ?% C1 s; o, h( Sdarker. She was also concerned about the enlarge-
, g$ [% p6 [; T' Y7 ]( b, Bment of his penis and frequent erections. The child7 R+ `- Q& p- u$ s; P
was the product of a full-term normal delivery, with
3 F. [- n( n5 Z/ U: G0 _a birth weight of 7 lb 14 oz, and birth length of; b" D+ b' }( X8 r1 a
20 inches. He was breast-fed throughout the first year; {& `. l- ]* [/ M% q" w5 l3 `! w
of life and was still receiving breast milk along with8 l2 e- A( L: {$ F( [/ b3 @; i1 k$ \
solid food. He had no hospitalizations or surgery,+ A5 T3 K5 Y8 C8 h, {, n' B/ u
and his psychosocial and psychomotor development
8 y; P6 q& R# @7 ]) I4 c4 \was age appropriate.
. N! |9 D5 P& \5 k0 m+ |The family history was remarkable for the father,. g# [0 }; u0 G+ j
who was diagnosed with hypothyroidism at age 16,. h& Y2 `9 Z$ Q. ]8 ~
which was treated with thyroxine. The father’s
" Q1 a- D2 [& k7 P7 a/ Qheight was 6 feet, and he went through a somewhat
6 ^/ m" \) c+ F& o  L' e  qearly puberty and had stopped growing by age 14.; W) m# O; b+ }9 G% o: e
The father denied taking any other medication. The& Q% _9 \% l- M& I
child’s mother was in good health. Her menarche
% t3 f- s, u. Z0 pwas at 11 years of age, and her height was at 5 feet
. ]: h0 V0 Z! d. t5 inches. There was no other family history of pre-
* X. E" ?; l8 v2 ]cocious sexual development in the first-degree rela-, b! ~* b% a- m# m0 W9 n
tives. There were no siblings.
# L5 ]% g4 j# ?0 y( SPhysical Examination
, n3 o4 [- X3 m9 A2 SThe physical examination revealed a very active,# m" `8 k" H6 N! z
playful, and healthy boy. The vital signs documented
- J+ m4 Z& R6 d& Q  ya blood pressure of 85/50 mm Hg, his length was
9 M% h7 n1 ^3 N/ `" \5 b90 cm (>97th percentile), and his weight was 14.4 kg
8 w- i* Y" a0 \' R0 ^3 N6 }9 h* C(also >97th percentile). The observed yearly growth
/ R+ p) B5 a0 }9 @0 x! ^; Lvelocity was 30 cm (12 inches). The examination of
) P- q( n1 U8 |3 ithe neck revealed no thyroid enlargement.. x1 O) Z3 h+ T* L
The genitourinary examination was remarkable for
' a- w4 b# c; d' ~" \: K* f- K! Zenlargement of the penis, with a stretched length of
3 }) @! k4 L0 I8 Z& d6 S8 cm and a width of 2 cm. The glans penis was very well& {- F. `! [% u" W
developed. The pubic hair was Tanner II, mostly around
1 x9 {6 e& s" `  @7 Q540
7 q. i  p7 N5 ^. gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 d0 o$ K' L2 gthe base of the phallus and was dark and curled. The6 D. ~. j9 m6 U
testicular volume was prepubertal at 2 mL each.
- Q8 L( W' i3 r/ O, jThe skin was moist and smooth and somewhat
* F  l" [; q( n- d& p$ hoily. No axillary hair was noted. There were no/ D: P7 ~/ {# _0 a7 F( @
abnormal skin pigmentations or café-au-lait spots.
8 G3 Q3 t! e, c( \: V; z1 hNeurologic evaluation showed deep tendon reflex 2+
+ w+ v- A+ a) Z+ dbilateral and symmetrical. There was no suggestion
0 i+ x, `9 H! l# h* Kof papilledema.
& o5 G& q/ e4 x3 M' |Laboratory Evaluation
) S+ h3 Q9 s) N; N; Z- K1 i' EThe bone age was consistent with 28 months by
+ n) c0 C  F' G; ~) u: E, k2 N  vusing the standard of Greulich and Pyle at a chrono-
, C9 {- F* ~; R! s/ B: ~logic age of 16 months (advanced).5 Chromosomal4 T2 M) |! W" ~! @; {( r
karyotype was 46XY. The thyroid function test! ^! v1 Z# g+ T* p0 }* ?# o
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
7 k4 |5 f- B4 b6 O/ x9 q9 olating hormone level was 1.3 µIU/mL (both normal).
$ M3 z$ ?8 O) h9 @% M: R- ~6 ^The concentrations of serum electrolytes, blood
3 ]# e  e7 @3 G! b: N1 X8 ?urea nitrogen, creatinine, and calcium all were7 p% _( \6 V8 h. v3 @
within normal range for his age. The concentration4 F1 [2 ~$ R$ U. N$ [
of serum 17-hydroxyprogesterone was 16 ng/dL
! c+ C- Y) `, W; _(normal, 3 to 90 ng/dL), androstenedione was 20$ Y* K  [2 k+ t. f" S
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
: r5 V+ S: I4 Q8 K) v) I, G2 v$ G% hterone was 38 ng/dL (normal, 50 to 760 ng/dL),
# O: a. f2 s4 Z( C( }( m( Ddesoxycorticosterone was 4.3 ng/dL (normal, 7 to
, u. n. J- w- d1 v/ d+ K! S49ng/dL), 11-desoxycortisol (specific compound S)
% u6 q, g- w9 K$ y( f! }was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# T- Y; Q$ i" R" I
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total1 p9 G( y0 j9 \' _: ~: U6 v! u
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),5 z* \6 Z9 n  \9 \! U( Q" V
and β-human chorionic gonadotropin was less than7 O$ g* @: {9 \
5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 `1 O* L3 J# `$ V  o( z  V5 K. fstimulating hormone and leuteinizing hormone0 I( U" o* t% H6 P3 C. ?) @6 G
concentrations were less than 0.05 mIU/mL
# T3 t0 q& `% B/ q(prepubertal)., g7 U1 j$ r2 M( J" B% [5 g% [
The parents were notified about the laboratory
0 k1 F: O  e* l4 N9 N, w; J' R# l/ fresults and were informed that all of the tests were2 i8 o1 k/ U% S9 l# A6 S+ `
normal except the testosterone level was high. The$ Z3 E4 d% q, a3 D
follow-up visit was arranged within a few weeks to* G  O! M1 S: n9 q- \
obtain testicular and abdominal sonograms; how-
; k( x% j0 C' D( |/ M6 d' Cever, the family did not return for 4 months.
! f1 H$ B7 p2 \& c0 B, v' a% a' ZPhysical examination at this time revealed that the! X  M' r% f$ k: v& r
child had grown 2.5 cm in 4 months and had gained1 q; d7 |; k* K5 U: L, e
2 kg of weight. Physical examination remained( o8 \. W* K! T( j7 ]
unchanged. Surprisingly, the pubic hair almost com-0 C8 _3 `2 O4 \( a: A  B' m# D# g2 f
pletely disappeared except for a few vellous hairs at
2 y9 ]5 p; M+ s, x2 G# \' X5 `/ _, x3 qthe base of the phallus. Testicular volume was still 2
9 c" p. G0 R# D% U, _. z6 UmL, and the size of the penis remained unchanged.
8 ?( J, n& q1 H3 y% RThe mother also said that the boy was no longer hav-+ |4 M1 l) X7 H# o  o  ~8 i% s
ing frequent erections.
% @0 \- T0 v" e" \' @Both parents were again questioned about use of9 m' y9 m/ c) u( m' u# _
any ointment/creams that they may have applied to8 K: ?0 c$ e; N
the child’s skin. This time the father admitted the% d* p: e' d3 [' N: L3 Q+ @+ E
Topical Testosterone Exposure / Bhowmick et al 541+ M% h0 V- }' Q& R- R5 z* y  u& k
use of testosterone gel twice daily that he was apply-
9 m1 z2 G) n* ]ing over his own shoulders, chest, and back area for
! H( Q& a8 i; M4 ta year. The father also revealed he was embarrassed
2 T, W3 P# C; k7 M8 Qto disclose that he was using a testosterone gel pre-; U/ S5 j3 L- d$ m
scribed by his family physician for decreased libido. U8 \  v% B9 M$ ^
secondary to depression.
* S, y- K$ G) }  o6 h  F; _; iThe child slept in the same bed with parents.
4 B: B' Z" `$ \, c' w9 jThe father would hug the baby and hold him on his. h$ M8 M- u5 f/ I$ Y/ d+ V
chest for a considerable period of time, causing sig-
$ P8 |! M( w1 Q$ T/ H) l  W9 ]nificant bare skin contact between baby and father.
/ X; w3 t# X0 F: p( w/ ?  VThe father also admitted that after the phone call,
: E" ^9 }$ N: cwhen he learned the testosterone level in the baby, E7 Q, W1 r8 T2 B) Z1 Y: N1 R/ Q
was high, he then read the product information6 l4 i, P0 `8 e; U- D* b3 Q% y
packet and concluded that it was most likely the rea-7 M9 }  o% v! [( C0 j1 _5 f
son for the child’s virilization. At that time, they
# n3 E0 E7 W8 S4 [decided to put the baby in a separate bed, and the
1 g8 K! h" j! Q* ^7 u4 L# _father was not hugging him with bare skin and had* c3 j" e6 f& k, h6 k2 X
been using protective clothing. A repeat testosterone/ [! _* P" u4 m3 u9 e/ `- \, c
test was ordered, but the family did not go to the
7 G( c% o  V6 C4 r! llaboratory to obtain the test.
. w" G$ I4 Y5 Y7 T5 ]- B" B! ~Discussion
; E9 M+ n- Q, N# A2 l  J1 L$ [Precocious puberty in boys is defined as secondary% r4 u  K7 p8 S5 J+ G2 W
sexual development before 9 years of age.1,4. Q! I# F! S9 w3 p& r4 w9 v
Precocious puberty is termed as central (true) when  [) p" o' b( i  b/ T8 j4 f
it is caused by the premature activation of hypo-& @8 s8 D" s1 P
thalamic pituitary gonadal axis. CPP is more com-
  V* I& ?) p* l- ?/ Y/ |9 wmon in girls than in boys.1,3 Most boys with CPP
: U- `1 U$ E; y: P- p8 [; c3 Pmay have a central nervous system lesion that is/ o  p! `2 b% k4 F9 W  n
responsible for the early activation of the hypothal-* q( D8 {" S' ?$ Y- ?/ j2 Y0 T
amic pituitary gonadal axis.1-3 Thus, greater empha-
) ?7 m1 m! a0 C% m. s6 Jsis has been given to neuroradiologic imaging in
# L6 A4 }# i9 q7 ^- @! C& O8 ]boys with precocious puberty. In addition to viril-
/ `" P& w9 p# x0 iization, the clinical hallmark of CPP is the symmet-$ P( N7 Q7 j+ o+ Y3 O  y
rical testicular growth secondary to stimulation by
. B: k* k) r0 p# `' ogonadotropins.1,3
8 [/ |+ q. ]) ]" g- `; w9 `) y0 MGonadotropin-independent peripheral preco-' s1 q9 q% e- F( e0 K
cious puberty in boys also results from inappropriate
1 V( A  q# s9 Z0 t; \androgenic stimulation from either endogenous or
: w6 `% W" h0 |0 Y. ?+ ~/ O  uexogenous sources, nonpituitary gonadotropin stim-
5 Y% T3 ~) k+ i8 M) B; i) D/ {ulation, and rare activating mutations.3 Virilizing
+ ^' T; v* O2 M4 Z3 `" s9 xcongenital adrenal hyperplasia producing excessive
1 Y- T/ A  N0 N( z9 Fadrenal androgens is a common cause of precocious
- K" D2 O8 F7 T, K! L# K& Ypuberty in boys.3,40 S3 U& q% n1 R; s' P3 b+ ]$ c
The most common form of congenital adrenal  r* i/ C" P0 v' e
hyperplasia is the 21-hydroxylase enzyme deficiency.
; V. I+ b5 @" |1 _The 11-β hydroxylase deficiency may also result in- x' v& O  K4 ]- F, L5 n
excessive adrenal androgen production, and rarely,
' e# O5 f' `1 [, wan adrenal tumor may also cause adrenal androgen
% K+ }1 E6 p2 t, s; Gexcess.1,3, j" q8 P" I  l9 `- t
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' T  |* M" M' W9 F7 `
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& \/ h- T' N* R+ m! rA unique entity of male-limited gonadotropin-/ R$ i/ g6 X5 x" j# R8 X( L
independent precocious puberty, which is also known
8 I# `# G0 F, n* t1 t' V) j. q8 das testotoxicosis, may cause precocious puberty at a3 l  }, h! a) q
very young age. The physical findings in these boys
8 w$ A1 T2 @9 o, V# f. [with this disorder are full pubertal development,
. d# n: ^& G) K2 g) R( Mincluding bilateral testicular growth, similar to boys
, M$ J6 W/ m9 W8 k: M% i% vwith CPP. The gonadotropin levels in this disorder: h0 I2 E# U9 w( t1 c# y: O
are suppressed to prepubertal levels and do not show
/ C0 o: V0 ~7 \! R9 h+ k9 E' ]pubertal response of gonadotropin after gonadotropin-
. x. `- r! i! D7 o4 }0 zreleasing hormone stimulation. This is a sex-linked) i& O+ T8 o8 D) r- K+ |- k
autosomal dominant disorder that affects only
. O  D% D6 ]: Bmales; therefore, other male members of the family
$ V8 P( K" V! C: u5 emay have similar precocious puberty.3
( F6 T0 X5 w7 o- n) yIn our patient, physical examination was incon-
1 T% Q2 ]% ?2 {* C4 Hsistent with true precocious puberty since his testi-
/ j! G, i& P, F* w4 {cles were prepubertal in size. However, testotoxicosis
$ a2 o* l) t" q" U9 k  Q0 Lwas in the differential diagnosis because his father) @1 a5 l5 k# l, f, E
started puberty somewhat early, and occasionally,
$ H. d7 G1 W$ D4 U/ ltesticular enlargement is not that evident in the. i' H8 S4 T' B( X, L; i" F. ]6 `6 q
beginning of this process.1 In the absence of a neg-; c% x1 `; e* a6 C9 @
ative initial history of androgen exposure, our
' U: O4 E  n. B5 j) C/ t3 y4 Mbiggest concern was virilizing adrenal hyperplasia,/ H4 D2 l3 O" K$ a4 o3 b
either 21-hydroxylase deficiency or 11-β hydroxylase
* t. A3 I& V$ z5 o2 pdeficiency. Those diagnoses were excluded by find-. n! X; j7 O1 L$ _
ing the normal level of adrenal steroids.
1 N4 L: g! q8 ~6 _3 ?' J, W$ ZThe diagnosis of exogenous androgens was strongly
2 I! `7 @/ B1 X# H$ I4 _; Qsuspected in a follow-up visit after 4 months because' s: b/ x4 a# k1 @, ?' q3 r3 Q
the physical examination revealed the complete disap-
! `' m0 D: D3 }: Zpearance of pubic hair, normal growth velocity, and
. u& N% g; W( u1 _decreased erections. The father admitted using a testos-
% f: t& P( \7 z# o8 H( E1 Qterone gel, which he concealed at first visit. He was
% b' `8 P4 a! C8 d+ f6 t! Jusing it rather frequently, twice a day. The Physicians’
2 O8 M! @4 I) GDesk Reference, or package insert of this product, gel or
" a% j* P; v# h$ R2 ocream, cautions about dermal testosterone transfer to
1 u) ^* w9 {& l5 @$ `# Funprotected females through direct skin exposure.
: P: ]% S8 U# P( S2 ISerum testosterone level was found to be 2 times the& X; O. N  K1 y. c- @2 X
baseline value in those females who were exposed to/ p% N' N$ i2 G1 i$ E, Y
even 15 minutes of direct skin contact with their male+ U7 f3 O6 x* P& a* L4 T
partners.6 However, when a shirt covered the applica-
! v6 P9 k9 x0 L! Q  y) b* O7 Etion site, this testosterone transfer was prevented.2 ]! C- G' _( u% y. k
Our patient’s testosterone level was 60 ng/mL,
! S1 ?  V; l+ qwhich was clearly high. Some studies suggest that
0 o- H6 |+ h2 a* S! ?dermal conversion of testosterone to dihydrotestos-6 \+ W  y. q9 x' M# b) g9 n
terone, which is a more potent metabolite, is more+ ?6 w* L; ^, C) @8 |
active in young children exposed to testosterone0 P3 Y8 v5 }& k/ Q& `/ H- e( ?8 W$ K. z
exogenously7; however, we did not measure a dihy-( y; B* l" m& w1 w6 i
drotestosterone level in our patient. In addition to4 {/ X. g& k+ A1 d* D" u+ D
virilization, exposure to exogenous testosterone in- {+ J5 i; B0 ?5 d2 _
children results in an increase in growth velocity and
: D3 }. s/ S; b! Dadvanced bone age, as seen in our patient.
8 _4 e9 P- P. b; ?# [" s$ aThe long-term effect of androgen exposure during
9 W, S# E+ Q2 g4 Bearly childhood on pubertal development and final  k1 m0 n: ?' @: R8 `( R
adult height are not fully known and always remain
3 ?; Z. W! E2 x$ B) y3 @5 Ma concern. Children treated with short-term testos-
# a5 m" B7 R3 n. a: X. Yterone injection or topical androgen may exhibit some; t9 V, a$ Y+ l0 H& v1 Q. K
acceleration of the skeletal maturation; however, after
; [5 I! y# F) }- t8 ocessation of treatment, the rate of bone maturation; [3 [2 @8 `* P$ t" B* J: M" [; L, _
decelerates and gradually returns to normal.8,9
. g! [8 T+ r( p% U+ A+ lThere are conflicting reports and controversy8 }+ K1 u5 e9 Z/ n4 [! C
over the effect of early androgen exposure on adult% F5 Q( R9 H7 @# X: I
penile length.10,11 Some reports suggest subnormal
& F1 N& |  c, U) k: Nadult penile length, apparently because of downreg-
4 R  @: E$ z$ W. p+ Kulation of androgen receptor number.10,12 However,
$ [' H4 o' x# ^6 `# M2 b3 R- DSutherland et al13 did not find a correlation between
( N* ^( P8 ^$ N  x: T3 S! ^5 q/ `childhood testosterone exposure and reduced adult3 w7 F1 O; [, I% R  ^
penile length in clinical studies.( `& B0 A4 j9 u% t) D
Nonetheless, we do not believe our patient is
0 x0 j3 s( T5 M) Sgoing to experience any of the untoward effects from& T/ D: a6 l5 _$ J3 G; v. C
testosterone exposure as mentioned earlier because
$ s0 s2 q& P( R3 p/ w) H& a' w/ fthe exposure was not for a prolonged period of time.' g5 ]: S" ]* ^  V
Although the bone age was advanced at the time of
/ i1 \' X4 V3 m4 y" x% B5 p! M' k$ udiagnosis, the child had a normal growth velocity at2 k9 j' d* F4 D# E2 r3 z: E, R; n
the follow-up visit. It is hoped that his final adult8 b$ B# ^* Z: Q' _" \
height will not be affected.
- ^7 y$ o8 t: z: f+ YAlthough rarely reported, the widespread avail-; r- p( O! B8 S7 R  M
ability of androgen products in our society may
( t4 V9 Y5 W, S4 {6 ~0 q0 v$ `indeed cause more virilization in male or female, a6 x4 U( b* i+ Q9 F2 ~
children than one would realize. Exposure to andro-: p( c& {3 {5 B! a) n- U! R
gen products must be considered and specific ques-
9 z4 d+ G% Y6 k9 R+ O/ Ntioning about the use of a testosterone product or* M4 t1 X. g6 U' P4 D- U( [
gel should be asked of the family members during) s& Q. x% D' t2 c4 X
the evaluation of any children who present with vir-( [; t7 z! k% r4 ]
ilization or peripheral precocious puberty. The diag-
. J2 N% X1 I! f8 L0 xnosis can be established by just a few tests and by7 K9 M7 v" j5 V! q2 C
appropriate history. The inability to obtain such a
) ~7 H! B( Q. Q& h. }" V( whistory, or failure to ask the specific questions, may$ }  x/ ]7 z8 H' C5 J& S# w
result in extensive, unnecessary, and expensive
. B% O: ?% M$ P5 X1 H# J8 m  ?investigation. The primary care physician should be
% ~1 e7 {; c7 H1 Caware of this fact, because most of these children9 p2 B9 p9 M7 c4 d# _; P2 m
may initially present in their practice. The Physicians’& W8 j, ]1 z0 Z5 o- M/ H
Desk Reference and package insert should also put a
2 _- M; L" Z1 B3 }# \: vwarning about the virilizing effect on a male or
7 g- T7 U* P# `female child who might come in contact with some-0 I! |5 H% \2 \& ?% p
one using any of these products., \6 a& h+ x5 W" u3 ^8 Q7 ]
References
& f& |4 ?: o7 |8 R1. Styne DM. The testes: disorder of sexual differentiation
2 Q/ o6 z. S7 k- c. [and puberty in the male. In: Sperling MA, ed. Pediatric
) ~9 g7 F8 t/ J) MEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;7 m* j. c7 n# J+ c; e+ E9 Q
2002: 565-628.
$ s7 Z6 r! p# x+ n% S# K# @: l1 U2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
9 m5 U  K: b: ^- w" a. Spuberty 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

6 O% w; o) O0 ^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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