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Sexual Precocity in a 16-Month-Old
7 H1 T) P; r  D: |% xBoy Induced by Indirect Topical3 U! w4 H8 t. f+ R3 s
Exposure to Testosterone1 O& y2 Y  S4 b$ i' n
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 Z5 |9 ]4 A! y5 v% ~6 [and Kenneth R. Rettig, MD1
* k( V  B5 G& I! A8 u/ nClinical Pediatrics( ~6 h% i8 Y3 c9 G
Volume 46 Number 6
: L9 H% t2 V+ ~July 2007 540-543: f0 f: M! p8 s) l( N
© 2007 Sage Publications
; i% Q3 |0 G1 B7 g; c* q; q/ N  r10.1177/0009922806296651
/ t. B3 \, F5 x  ^http://clp.sagepub.com
% |" I; x! ]6 s/ k- nhosted at  J6 `* V/ o& ~- e% f
http://online.sagepub.com. C! u8 l7 n. P9 j* S; g* `
Precocious puberty in boys, central or peripheral,4 P, a- @3 h1 z! |8 {
is a significant concern for physicians. Central
, z' B9 w% \" f' `  S# kprecocious puberty (CPP), which is mediated
) f( \' G& i1 W3 _! k* G" e* F6 ythrough the hypothalamic pituitary gonadal axis, has" W: S$ |; s1 {0 C
a higher incidence of organic central nervous system' L* I* Y4 k3 K% |% S3 F. T  W" N
lesions in boys.1,2 Virilization in boys, as manifested
2 m) s; V- U/ b  G; Z: v0 Fby enlargement of the penis, development of pubic* U$ P; C. j) O, C8 I$ a4 Z/ c0 D
hair, and facial acne without enlargement of testi-! n1 i3 Q+ v4 l( m( v3 l
cles, suggests peripheral or pseudopuberty.1-3 We# L% ]. K2 Y. m( A; w+ }. E
report a 16-month-old boy who presented with the
4 e4 G$ Z# ~3 ~0 E* Y7 @enlargement of the phallus and pubic hair develop-2 D7 u* U: Z+ g) c/ j5 z
ment without testicular enlargement, which was due! _, C5 v6 G2 m" h+ U- i$ z7 B) {
to the unintentional exposure to androgen gel used by0 \  W) Z  P( O$ c4 O, p8 L
the father. The family initially concealed this infor-( O7 _/ a: P9 }. K
mation, resulting in an extensive work-up for this7 ]0 ]; I4 `0 ~/ I: N2 o  s# D
child. Given the widespread and easy availability of0 o) I' I  E4 \
testosterone gel and cream, we believe this is proba-9 L8 t8 H! T1 G) A5 A* k8 r3 F
bly more common than the rare case report in the
- a. v. I1 p! K6 A! p- Bliterature.4
1 s% f2 I6 |* H" k& ePatient Report6 L! Z% G" [8 e6 G1 B5 E1 s( A
A 16-month-old white child was referred to the
; u9 f4 s. |! U8 }) B1 [endocrine clinic by his pediatrician with the concern
! d9 `$ o) r2 D& Tof early sexual development. His mother noticed1 Z' \+ t. l: w: S7 Q) c. s
light colored pubic hair development when he was$ [* J- N5 `% x% v( W/ K- s1 h7 R. m. W
From the 1Division of Pediatric Endocrinology, 2University of
$ Q$ k. z. \3 K& O* `8 ESouth Alabama Medical Center, Mobile, Alabama.+ `0 H0 A) Z0 f5 ?4 Y3 s& Y
Address correspondence to: Samar K. Bhowmick, MD, FACE,
( \5 |7 Z$ A  A1 }! t/ A+ CProfessor of Pediatrics, University of South Alabama, College of
; X, b1 _0 B" W; GMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
' e: O& i: [9 \1 N: U! Z# ie-mail: [email protected].
; H0 M2 r  @3 B) z& w) c5 Gabout 6 to 7 months old, which progressively became4 ]; e5 \; A" |  d( S4 \3 y# y) y
darker. She was also concerned about the enlarge-
; J! S/ k- G* c0 J7 D& ?+ B$ pment of his penis and frequent erections. The child6 A8 B, ~, P  L# |
was the product of a full-term normal delivery, with3 k6 N- S, U& W$ o2 X6 x! x; d
a birth weight of 7 lb 14 oz, and birth length of
# ^0 j5 t! V8 L# ?5 h- s6 o20 inches. He was breast-fed throughout the first year  S/ V9 A( D. r4 n8 n
of life and was still receiving breast milk along with: W% F' r0 [) ~+ O1 `
solid food. He had no hospitalizations or surgery,
# i  O% S  S5 O" W# oand his psychosocial and psychomotor development9 p+ r8 u$ X3 V. _6 \+ o; J
was age appropriate.
2 }" X# b- _! n4 OThe family history was remarkable for the father,: @  x( J8 W: a( M
who was diagnosed with hypothyroidism at age 16,
% b7 l( [9 T! [. \6 U: L9 c- Zwhich was treated with thyroxine. The father’s# }. e4 o9 D( y, j* o6 \; d# A4 N
height was 6 feet, and he went through a somewhat
( {: l# o1 }8 ^1 Eearly puberty and had stopped growing by age 14.. E$ p! V: Y7 g1 J, y. h; G+ H
The father denied taking any other medication. The  j  F6 L' v  U1 y/ B( I7 _* T
child’s mother was in good health. Her menarche+ {6 O; N  i9 b. u
was at 11 years of age, and her height was at 5 feet
# b2 Z7 n6 T9 a0 M5 inches. There was no other family history of pre-  `; T5 _% _4 F* e
cocious sexual development in the first-degree rela-, Z2 C$ ^9 k" C: m7 W
tives. There were no siblings.# i. l; b+ c4 n: v( [0 ~) C# E% a
Physical Examination- U4 ?0 f  I" C) l  S* `2 ^) s) V
The physical examination revealed a very active,  e* b. ~! S5 l5 F+ }2 U& w
playful, and healthy boy. The vital signs documented
5 b1 c& {$ n! R& ga blood pressure of 85/50 mm Hg, his length was
% K" c& X+ y" l' m90 cm (>97th percentile), and his weight was 14.4 kg
& l/ z4 G/ ?  n+ ?! @(also >97th percentile). The observed yearly growth/ ~2 b: m! b3 [% e: _3 Y$ `
velocity was 30 cm (12 inches). The examination of% P; n, v* }" c9 ~+ U
the neck revealed no thyroid enlargement.
! U+ a, e. G- J# f% x1 E! |The genitourinary examination was remarkable for
; n2 }  A. _+ s' G# xenlargement of the penis, with a stretched length of+ _% f$ |( j# N: j
8 cm and a width of 2 cm. The glans penis was very well
' P1 j" o! s: B! m( |( L  ideveloped. The pubic hair was Tanner II, mostly around
" t4 X( w: `/ b- g, j# _* ^2 m8 g+ o540! F' d0 C2 T7 t( e8 t1 [$ s- s
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) h( f2 k/ ]/ B3 e6 {1 F) Qthe base of the phallus and was dark and curled. The, u1 L, e2 k: C
testicular volume was prepubertal at 2 mL each.
; r. e$ ~2 Y# |! W; ~0 OThe skin was moist and smooth and somewhat
% I$ W7 e/ a: z* r9 }oily. No axillary hair was noted. There were no6 J6 `9 w3 ~/ U+ B! u
abnormal skin pigmentations or café-au-lait spots.
" J3 |3 j- g+ x3 r  L3 BNeurologic evaluation showed deep tendon reflex 2+* x% Y- q0 j- z$ Y# B6 y
bilateral and symmetrical. There was no suggestion
! [) u) Y! z2 G) n, Uof papilledema.) Q, k( v; ]7 G' Q. t: ^, \
Laboratory Evaluation
3 c: [: k/ z: w: O' y* A8 K3 pThe bone age was consistent with 28 months by' u4 F8 a; O0 B9 z9 I. \5 r3 X- j
using the standard of Greulich and Pyle at a chrono-
: ?! B' e' y4 Xlogic age of 16 months (advanced).5 Chromosomal
; B" t4 o7 P" Y7 x9 U# c8 A$ kkaryotype was 46XY. The thyroid function test3 q4 P$ t& N' c
showed a free T4 of 1.69 ng/dL, and thyroid stimu-2 n# G1 ]3 x' e2 p5 B# T4 Y4 j
lating hormone level was 1.3 µIU/mL (both normal).
, ?8 m# |8 o# ?The concentrations of serum electrolytes, blood
$ M$ z2 X) ~1 C4 Y! u% rurea nitrogen, creatinine, and calcium all were5 X" H* M" o0 |. J, b0 V
within normal range for his age. The concentration
5 x2 g2 V7 {) tof serum 17-hydroxyprogesterone was 16 ng/dL+ w1 C1 f6 u9 i
(normal, 3 to 90 ng/dL), androstenedione was 20
9 }7 c0 c( ~) \6 z) p5 \ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
1 c: q7 H7 j8 {; aterone was 38 ng/dL (normal, 50 to 760 ng/dL),# a, ^  m1 C% s; p5 x% o5 u3 L" t
desoxycorticosterone was 4.3 ng/dL (normal, 7 to3 k/ |6 A8 O/ L- X2 @' S( f
49ng/dL), 11-desoxycortisol (specific compound S)
, m1 K6 Q% c+ G6 e  u; ^was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-  s6 v2 x' s1 D* Q( {+ N8 ~5 v& ~0 L
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
) i% P) p( S& z% q" G3 Rtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
! I+ j5 }3 |; I6 e: c, Wand β-human chorionic gonadotropin was less than
( ?0 L# [0 g0 y/ Q+ U- O7 ?5 c5 mIU/mL (normal <5 mIU/mL). Serum follicular
! A0 ?3 f' z4 c3 |stimulating hormone and leuteinizing hormone, _1 Y$ \/ d# T
concentrations were less than 0.05 mIU/mL: o% p+ ~" `! a1 X$ v% T
(prepubertal).0 V+ s* O( ]1 G* P9 O; c$ F
The parents were notified about the laboratory! P0 H/ }; ~; e' ?- k& S- D
results and were informed that all of the tests were
7 @+ ]2 c7 G. ~4 y3 unormal except the testosterone level was high. The
2 F; e1 p; C! L# \' `( z& hfollow-up visit was arranged within a few weeks to4 q( P0 g- x7 {& V8 d" p) C' \+ U
obtain testicular and abdominal sonograms; how-
/ S2 h3 H& j* Qever, the family did not return for 4 months." _4 l2 x( T9 Q8 x$ G& j
Physical examination at this time revealed that the- {$ ]1 ^- D1 W+ C% V' X$ g
child had grown 2.5 cm in 4 months and had gained
" z' [- V( ?# r+ V( O6 q2 kg of weight. Physical examination remained: \; w! T) |6 I; s& y
unchanged. Surprisingly, the pubic hair almost com-5 L8 l8 W+ N6 Q# K8 G( N, O4 x
pletely disappeared except for a few vellous hairs at
; I+ O1 ?" V' o( U! S5 q& Nthe base of the phallus. Testicular volume was still 2
, f1 m; K& [8 M3 ~9 Z: ?mL, and the size of the penis remained unchanged.
1 Y5 f7 L1 I7 S& _7 aThe mother also said that the boy was no longer hav-
; Y- i" n6 `& {; U0 S5 ]& ning frequent erections.
! }4 i; [( X- T# a1 w* KBoth parents were again questioned about use of
' z3 \1 y; i; X/ g- y, Vany ointment/creams that they may have applied to
( `8 D3 P* @6 p  t5 E! @the child’s skin. This time the father admitted the
" p0 u6 S, U3 O2 y7 jTopical Testosterone Exposure / Bhowmick et al 541
2 P  \2 A: Y  n7 ^use of testosterone gel twice daily that he was apply-
8 ?+ d/ F0 I8 J8 N. O, S2 x- fing over his own shoulders, chest, and back area for
( l/ }- Y2 U" ^- }. Z7 j! T! Za year. The father also revealed he was embarrassed
3 w0 l# n& R5 G1 Y3 m. Bto disclose that he was using a testosterone gel pre-, v( q0 S7 L) _( g2 c
scribed by his family physician for decreased libido
( Z! a1 U% i" z0 N4 g. csecondary to depression.9 ^! y8 b9 M( ~5 U$ \
The child slept in the same bed with parents.
# N9 \4 v& {# Q4 _6 Q; VThe father would hug the baby and hold him on his. j# J* o7 b6 n! Y3 T% s! w
chest for a considerable period of time, causing sig-5 e/ v" m. x& K- W% ]9 O
nificant bare skin contact between baby and father.+ _0 @6 U- j9 y
The father also admitted that after the phone call,
9 v. p: Q& S* e$ s; c4 @( Z& T1 nwhen he learned the testosterone level in the baby
* m  j0 L" }" s. z) Qwas high, he then read the product information
- I+ Y' s+ A( m% A3 j9 _: jpacket and concluded that it was most likely the rea-
0 I- S# \( d7 Z. Fson for the child’s virilization. At that time, they, a. Q, k$ ~) ^: f8 P5 z( N: e
decided to put the baby in a separate bed, and the5 @5 T6 P" A# T
father was not hugging him with bare skin and had
0 e/ q$ R! n6 w9 V6 R$ pbeen using protective clothing. A repeat testosterone
) _0 H9 ?2 Y7 atest was ordered, but the family did not go to the2 L% q* U5 J. |- E+ F9 Z, U
laboratory to obtain the test.
" ?. I# J0 a, IDiscussion
. S& I2 e* `) L( EPrecocious puberty in boys is defined as secondary
* E% X' P' p7 E- S1 asexual development before 9 years of age.1,4' g3 |$ `+ u- W3 y' h& l
Precocious puberty is termed as central (true) when
# c8 W7 g. U7 g$ nit is caused by the premature activation of hypo-1 f: W. \7 |) ?& A
thalamic pituitary gonadal axis. CPP is more com-
" b! I6 T& o/ Pmon in girls than in boys.1,3 Most boys with CPP. s+ c& N& S8 [; ?0 b
may have a central nervous system lesion that is
+ D, F+ x. Q! v. Tresponsible for the early activation of the hypothal-
; _5 ~  c: v7 N$ H1 Oamic pituitary gonadal axis.1-3 Thus, greater empha-9 P/ H5 W- V" L% g8 ~- n) E6 m# M2 r
sis has been given to neuroradiologic imaging in
/ Z5 P7 k) E* ?: q, Y2 ~4 bboys with precocious puberty. In addition to viril-
" v% j" d+ t& `- K% A4 J' eization, the clinical hallmark of CPP is the symmet-8 I5 n' U/ G4 U( ?
rical testicular growth secondary to stimulation by! `% B- E' W% `9 S8 \4 ^
gonadotropins.1,3
' t5 t% `0 E1 _4 e& L, \) {Gonadotropin-independent peripheral preco-
) r! K3 d. k/ y1 d4 s, Wcious puberty in boys also results from inappropriate4 x; _6 n4 v% M9 Q7 M/ H, o
androgenic stimulation from either endogenous or
6 Y, P3 O7 K1 ~- h, G/ q, F( kexogenous sources, nonpituitary gonadotropin stim-
6 n. Z9 K9 q$ Y- }ulation, and rare activating mutations.3 Virilizing
+ ~4 I3 k7 J4 U. w; mcongenital adrenal hyperplasia producing excessive
! @* Q+ F* t; q$ i7 k( Ladrenal androgens is a common cause of precocious
4 W5 {# A; G: D- x" Jpuberty in boys.3,4
5 a8 y$ l# B! J  ^" o6 GThe most common form of congenital adrenal0 o9 ]" Y" u- y* ]# K* p/ }( H
hyperplasia is the 21-hydroxylase enzyme deficiency.
5 e+ Y* o+ b! S: F. u  DThe 11-β hydroxylase deficiency may also result in! \$ `6 l9 h2 j8 k. l1 i
excessive adrenal androgen production, and rarely,' }' u% r- S" j( J$ s/ x' r
an adrenal tumor may also cause adrenal androgen& S3 f5 Y/ Y9 c5 N' O
excess.1,3
5 ?& U8 S+ B* a. B0 f6 C) v) Mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' ]3 S" i4 \; L: T
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007+ j* P8 Z# ]1 r5 t
A unique entity of male-limited gonadotropin-
+ R$ Z  x4 ~/ c5 }8 aindependent precocious puberty, which is also known
/ ?5 G1 ~. s+ X4 k* y# D4 e7 Q5 Mas testotoxicosis, may cause precocious puberty at a2 |0 Z* k* Y4 i  F
very young age. The physical findings in these boys
" J" U% R; l9 K6 @: swith this disorder are full pubertal development,: B3 Y7 T5 N4 x4 ~2 r0 S
including bilateral testicular growth, similar to boys
, i! D$ L4 u$ \. p/ e% |1 Cwith CPP. The gonadotropin levels in this disorder
1 Q4 W0 f" u" j7 z- K7 Iare suppressed to prepubertal levels and do not show
) c- u# J  y; Upubertal response of gonadotropin after gonadotropin-, s/ v% k  t, U/ r. z
releasing hormone stimulation. This is a sex-linked6 g/ z* f" A' @
autosomal dominant disorder that affects only
3 ~  _' a) j4 v6 t) j3 l5 umales; therefore, other male members of the family
% L$ s% [' y" Q' gmay have similar precocious puberty.3; X) c/ c3 i: ?, b9 G
In our patient, physical examination was incon-8 `2 I. i/ \; J0 U+ V! r
sistent with true precocious puberty since his testi-5 z# o' r; j" {9 E6 C, d& J
cles were prepubertal in size. However, testotoxicosis
+ p1 d9 m2 m. k2 ^- kwas in the differential diagnosis because his father" `9 R2 W  j7 q- [! k: `: D  V1 E' T
started puberty somewhat early, and occasionally,
* K* n5 X- h6 }& i8 d7 R! J8 p  Otesticular enlargement is not that evident in the2 ^0 w' f4 Z0 C9 S2 L, J: |) k
beginning of this process.1 In the absence of a neg-
, r- w( ~* ^$ x4 V. _* D/ d3 sative initial history of androgen exposure, our
. F) u# G: O; ]+ L" ?" obiggest concern was virilizing adrenal hyperplasia,4 }( K- m7 A* a8 z
either 21-hydroxylase deficiency or 11-β hydroxylase* e" h1 P% h0 P* c
deficiency. Those diagnoses were excluded by find-% e: Y! W7 d+ L* V% k
ing the normal level of adrenal steroids.  ^" T. w0 H/ w0 I+ i' {( |/ d
The diagnosis of exogenous androgens was strongly
9 |* k8 ]* ^$ k' i7 Csuspected in a follow-up visit after 4 months because
( s# r; B4 w6 }% @- T$ U) m2 ?% Q- othe physical examination revealed the complete disap-1 w- K; K0 b, ~9 M5 Q; R4 t2 A
pearance of pubic hair, normal growth velocity, and
3 Z; H; H1 {( C% ?2 P& ddecreased erections. The father admitted using a testos-! A( f5 ]* w8 d
terone gel, which he concealed at first visit. He was
& S# [+ w' O& f% yusing it rather frequently, twice a day. The Physicians’! x' ^5 O2 ?( O  ~0 K- z1 w
Desk Reference, or package insert of this product, gel or
, _# B: Q6 ~- T% y" O  q; ~& Acream, cautions about dermal testosterone transfer to
& I5 g& P5 ~- B- r- O5 [" F# C( ^unprotected females through direct skin exposure.
5 V. R. N3 l2 r: a) XSerum testosterone level was found to be 2 times the
: R$ N8 R1 [6 l# b9 l1 S) b8 Mbaseline value in those females who were exposed to
& J+ R$ v  B- H4 Q, ]& ^5 xeven 15 minutes of direct skin contact with their male1 s- a  N  ^7 C- ^, Z
partners.6 However, when a shirt covered the applica-0 F1 i  x9 c" x
tion site, this testosterone transfer was prevented.9 k' p) H/ C. G/ `
Our patient’s testosterone level was 60 ng/mL,) f6 j/ J7 q# t5 G" t' `
which was clearly high. Some studies suggest that4 z+ i# j# M+ D" w! Z
dermal conversion of testosterone to dihydrotestos-9 O+ C' f( [: U& r; C7 N5 F
terone, which is a more potent metabolite, is more
  n2 l  i9 t  H" _6 S5 u& uactive in young children exposed to testosterone
6 j; g1 B+ P8 C* J  l6 sexogenously7; however, we did not measure a dihy-" @( Q. a. p. x* w
drotestosterone level in our patient. In addition to
5 J4 y/ y# z- `& ]* t" |virilization, exposure to exogenous testosterone in
" P% O  l% P; |% G& x( D) wchildren results in an increase in growth velocity and
/ c3 ^9 ]) {; R  P3 z5 l" Qadvanced bone age, as seen in our patient.$ G8 H; H+ k# F0 _5 |, {
The long-term effect of androgen exposure during
% f- ]: ?& x) Aearly childhood on pubertal development and final% G; O- O0 Y6 T' F6 R) T
adult height are not fully known and always remain. U4 z. Y6 K) @( }
a concern. Children treated with short-term testos-0 x4 U4 X8 O. d0 z$ k# \9 E
terone injection or topical androgen may exhibit some
6 X! z0 z/ `% \; cacceleration of the skeletal maturation; however, after
8 U8 J; ~& q1 K8 ycessation of treatment, the rate of bone maturation" T1 }+ F2 z2 `3 o
decelerates and gradually returns to normal.8,9
! r9 Y! ~2 J1 j3 |$ Z3 ?There are conflicting reports and controversy
' F' ?, A% m+ {5 r2 `* ~over the effect of early androgen exposure on adult
; I7 l  P" A: K: R( ypenile length.10,11 Some reports suggest subnormal
4 z  m5 J! q8 M, E3 `adult penile length, apparently because of downreg-
9 z" x4 [3 R3 S, fulation of androgen receptor number.10,12 However,
6 O/ H5 k2 S* |" \Sutherland et al13 did not find a correlation between
  Q) Z+ h: _" n6 t. bchildhood testosterone exposure and reduced adult
3 D* E6 x0 D4 Y' h4 M) x) `9 ~2 apenile length in clinical studies.0 ]" R5 |; K+ D6 r4 i, C4 f! H
Nonetheless, we do not believe our patient is" c9 M! o1 |+ Z  S9 J3 e+ l
going to experience any of the untoward effects from% x/ L$ K" |5 q: n" J# S) V
testosterone exposure as mentioned earlier because5 g! t8 b7 j% H" i- ^
the exposure was not for a prolonged period of time.5 @  x( j0 z$ b: X4 B3 A
Although the bone age was advanced at the time of5 C9 t8 n/ g, D
diagnosis, the child had a normal growth velocity at
7 t' ]$ R0 D# \8 U5 M. Ythe follow-up visit. It is hoped that his final adult
* T6 _( ^7 k9 L2 c/ \& m' K0 Eheight will not be affected.% V) u' R! n- }
Although rarely reported, the widespread avail-
7 Z+ f, H( U8 v' v/ a& j% xability of androgen products in our society may
& Y1 F7 F4 f% G' a; M1 \indeed cause more virilization in male or female
7 N+ N3 p, y. w4 b: \children than one would realize. Exposure to andro-
0 j/ k  A; r7 y0 C# m1 _3 \gen products must be considered and specific ques-, A* m  R( o1 d9 I4 ~
tioning about the use of a testosterone product or
' S0 `8 a& M( c2 Vgel should be asked of the family members during2 j* \! V1 Q0 Y( I/ ]  _
the evaluation of any children who present with vir-) D4 x1 k) e  {2 m
ilization or peripheral precocious puberty. The diag-
; n+ ]9 W  g  knosis can be established by just a few tests and by) D# x4 I# F* N( m2 V# i& _. s
appropriate history. The inability to obtain such a
" E7 k9 Y+ \+ o, K; ~3 vhistory, or failure to ask the specific questions, may
, {, |2 A+ g5 {/ sresult in extensive, unnecessary, and expensive
: `0 l8 d1 k5 [3 j) einvestigation. The primary care physician should be
4 S( k' w# I7 c% f% }$ paware of this fact, because most of these children4 K9 ?8 z/ H8 J: I* M' ?
may initially present in their practice. The Physicians’
9 r" M' a2 X' B8 B; R$ gDesk Reference and package insert should also put a$ o+ T; n+ w! i9 ^1 y
warning about the virilizing effect on a male or2 {/ @8 e9 t8 u" Q( G( y2 C+ i
female child who might come in contact with some-
7 `1 \( z  ]1 ]. g4 tone using any of these products.
0 f- d! J& ]( ]+ @9 p. JReferences+ i6 X/ c# E3 D
1. Styne DM. The testes: disorder of sexual differentiation3 [" `5 v0 d0 `7 O2 Z' Y
and puberty in the male. In: Sperling MA, ed. Pediatric
! Z! N! b+ S# \8 ?% q, SEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;4 r& s1 T4 \" |) S; M
2002: 565-628.
. f1 w6 i7 i! t2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
7 Y. X; \0 H& r' e# [2 mpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
" ?1 n( S" g) NBoy Induced by Indirect Topical: }0 ~6 x' j2 l5 B2 L% `# g& ?
Exposure to Testosterone, y% t6 [/ I$ F
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,29 _/ J5 p% b1 g5 U5 b
and Kenneth R. Rettig, MD10 z. k1 H: i  ^- ]1 m
Clinical Pediatrics
2 a8 V' N# o! i, L6 r6 TVolume 46 Number 6$ f" g  g" b) h3 M! q5 F5 C
July 2007 540-543
+ a* D4 T2 I; l9 @8 o+ B" q/ j© 2007 Sage Publications% M2 ]. y0 q' C% g
10.1177/0009922806296651& y+ g  q$ D* d! g0 X
http://clp.sagepub.com
7 A) T; @! [" L; v* Yhosted at
2 F( N6 Y2 @+ K$ g: t( z, x3 yhttp://online.sagepub.com
7 @5 ?7 D' g% ]0 F8 Z+ [! iPrecocious puberty in boys, central or peripheral,8 ?% X1 A+ q$ m, Q7 P1 X
is a significant concern for physicians. Central
; X# H. r3 {5 Z- v% r5 iprecocious puberty (CPP), which is mediated6 ~6 [  r, W. d) K
through the hypothalamic pituitary gonadal axis, has
. E3 G6 j  N2 W8 G0 Ya higher incidence of organic central nervous system) D" D8 ~/ M+ L6 G: E
lesions in boys.1,2 Virilization in boys, as manifested
( M7 p/ m3 e/ xby enlargement of the penis, development of pubic
$ h) e0 d/ d; X' Z' U; D, Uhair, and facial acne without enlargement of testi-
9 c! E8 S& Y; @  n+ s, L: ocles, suggests peripheral or pseudopuberty.1-3 We5 |' {) c/ d8 ^+ }+ [
report a 16-month-old boy who presented with the
- r7 ?8 t2 J9 M7 e  J- venlargement of the phallus and pubic hair develop-
3 i: u) l# p! p1 X' Z9 F1 i, kment without testicular enlargement, which was due9 R1 Y3 K" S) }8 s  }, B
to the unintentional exposure to androgen gel used by
, I  Y& b" C. X: q  F# ], @the father. The family initially concealed this infor-! n- G* B" l4 `# s* P
mation, resulting in an extensive work-up for this2 ?& m9 _: {; _7 v. T- ]7 G- u2 a
child. Given the widespread and easy availability of
/ [7 ?8 G8 [2 ^6 xtestosterone gel and cream, we believe this is proba-. B/ t3 u$ x6 F1 Z3 B
bly more common than the rare case report in the$ r$ F, d! r& j; U6 H
literature.4# x0 o& G7 d. x( A1 \
Patient Report
4 \8 o! c: u% R3 r2 ?2 K! b' x( WA 16-month-old white child was referred to the( c( K# ^' b, g# x7 E. T- s, M. W
endocrine clinic by his pediatrician with the concern- P3 G8 Y7 u3 n2 p! f: Q
of early sexual development. His mother noticed; ]" T% l3 e6 V" m! t/ }6 ^8 J1 g+ e
light colored pubic hair development when he was
5 Z/ C8 T" ^  LFrom the 1Division of Pediatric Endocrinology, 2University of: l& G9 c+ M& f9 C4 U" ?4 a
South Alabama Medical Center, Mobile, Alabama.  c5 T- d2 l0 G- s* q! T' k3 n
Address correspondence to: Samar K. Bhowmick, MD, FACE,
% @) u8 c2 t( M! r+ NProfessor of Pediatrics, University of South Alabama, College of. W4 s4 P  \( ^
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
" r( x5 |) h/ _$ G3 g$ Q6 ee-mail: [email protected].# j) @4 p, A" a  m' C1 q7 i
about 6 to 7 months old, which progressively became, _9 Q/ _- \) ]+ f1 h& W) a
darker. She was also concerned about the enlarge-! U. e; Q' J, Z% q, T) k
ment of his penis and frequent erections. The child3 D/ o, r  N* E# @4 q
was the product of a full-term normal delivery, with$ o) V& V3 @- B8 ~; Z
a birth weight of 7 lb 14 oz, and birth length of
6 L' D, ?, ~" q: P20 inches. He was breast-fed throughout the first year
3 @0 k3 W4 d" Tof life and was still receiving breast milk along with
; T# L1 k7 t# I, D! |$ Y4 h1 Z: w. C- osolid food. He had no hospitalizations or surgery,& L) }$ R0 Z3 i  Z9 A
and his psychosocial and psychomotor development
" |1 m8 z- Y" V2 awas age appropriate.
( _) x% @- L1 MThe family history was remarkable for the father,3 l/ r+ ?! Z  d0 r
who was diagnosed with hypothyroidism at age 16,  u0 H# G& Z; I& c5 a1 N% v/ ]
which was treated with thyroxine. The father’s
: L) \3 \; z4 C, ?6 o& x. R3 sheight was 6 feet, and he went through a somewhat2 F; H2 a1 |9 s* a
early puberty and had stopped growing by age 14.
# }* z1 f3 g" j3 RThe father denied taking any other medication. The6 `( ?5 u8 n- ]7 T! S8 v9 Z
child’s mother was in good health. Her menarche
: N2 Y0 T" F& ewas at 11 years of age, and her height was at 5 feet
6 k( a$ o, b1 V! z6 T1 c6 F5 inches. There was no other family history of pre-
' S1 h- U' B2 u: Y* d; H6 s4 hcocious sexual development in the first-degree rela-8 B3 K6 y# v: N, c  ^3 ?
tives. There were no siblings.
" d/ v/ _: x8 j1 \6 yPhysical Examination5 b0 M0 n; E' ~; g
The physical examination revealed a very active,  H7 E4 k! W$ R! `
playful, and healthy boy. The vital signs documented- @5 q5 b* Z- M# a7 L
a blood pressure of 85/50 mm Hg, his length was. h) U# h. D5 n$ X! C, B
90 cm (>97th percentile), and his weight was 14.4 kg
- p; k& N7 x( |& v) _, `4 D7 U(also >97th percentile). The observed yearly growth
' P2 Y( r& ]" T* n& ~velocity was 30 cm (12 inches). The examination of
7 l; Z4 |3 W0 _  a0 A; `5 gthe neck revealed no thyroid enlargement.2 t; u$ O  w5 M7 d- e1 l
The genitourinary examination was remarkable for
0 @* P8 C- T, d: Q& h4 }enlargement of the penis, with a stretched length of
  ~/ i5 }+ r0 v6 p) q0 J% R9 g  ]8 cm and a width of 2 cm. The glans penis was very well
( m) t% c6 h/ I( n# \0 ]developed. The pubic hair was Tanner II, mostly around
6 @9 E( E8 P) x" A/ B5409 k  p+ x3 k- S8 C
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
7 D( ~0 U2 J' x2 A9 i, l* Tthe base of the phallus and was dark and curled. The- w! Z3 T8 w: Y$ w8 O+ R
testicular volume was prepubertal at 2 mL each.
" P* u5 r8 P: |7 B! i4 R% oThe skin was moist and smooth and somewhat. Y  I3 \7 r' @  J
oily. No axillary hair was noted. There were no
7 ^8 P7 K# Z: r# S: o8 Zabnormal skin pigmentations or café-au-lait spots.. c/ R1 L4 b4 x3 y! M
Neurologic evaluation showed deep tendon reflex 2+- Z5 D; A/ A+ @4 @8 g" h- j4 z# F# M" V; q
bilateral and symmetrical. There was no suggestion/ M- ]1 R9 Y' Q+ \: y
of papilledema.
  u6 u* V  y  C$ YLaboratory Evaluation
% c* E2 }6 r% [/ P' i( v- hThe bone age was consistent with 28 months by
- L# m6 `: x4 f" H8 R, g% m( \7 x* Xusing the standard of Greulich and Pyle at a chrono-
9 U2 Q: y% f6 [: {. `  `logic age of 16 months (advanced).5 Chromosomal
7 o  d+ Y# m6 ]& z; H4 Ikaryotype was 46XY. The thyroid function test8 r& C7 M. N4 G
showed a free T4 of 1.69 ng/dL, and thyroid stimu-5 E- I# T! @# Q- Y+ j2 s: ?! a
lating hormone level was 1.3 µIU/mL (both normal)./ m# i" J5 d; I0 m% W
The concentrations of serum electrolytes, blood) o4 S7 N* f  k' o+ ~/ i
urea nitrogen, creatinine, and calcium all were
0 y4 `5 d# s, t( I4 X0 ?7 [: ]within normal range for his age. The concentration
/ A9 Q, }) A7 A, {) |- B9 ~: l! hof serum 17-hydroxyprogesterone was 16 ng/dL* T2 e; L$ ~1 x' J! n) N
(normal, 3 to 90 ng/dL), androstenedione was 209 W/ B/ J) Z$ c& ?# U% Y$ T9 Z
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-2 J/ s0 I: B1 f6 S
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
6 Z2 V' A! p/ \/ edesoxycorticosterone was 4.3 ng/dL (normal, 7 to
$ V. L0 f9 N5 W$ Y/ G7 b49ng/dL), 11-desoxycortisol (specific compound S)' q5 O# B& d$ U7 b
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-, i" I, c8 W4 L4 u/ G" j
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total) B% Y% j- J$ d, ~
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),1 x" U, y5 R4 U( B: N
and β-human chorionic gonadotropin was less than" j* g! k( w. ~' L3 t
5 mIU/mL (normal <5 mIU/mL). Serum follicular4 u. y/ G0 S) w, E2 w3 K# U
stimulating hormone and leuteinizing hormone: }8 j2 j) l+ O5 s
concentrations were less than 0.05 mIU/mL0 b# `9 K" }4 T! V- k
(prepubertal).
9 j4 w+ K# `0 |8 t  \9 o- gThe parents were notified about the laboratory
6 r: i. y) U% g" @- H9 {. M: Gresults and were informed that all of the tests were0 ?& F/ b9 P& e
normal except the testosterone level was high. The
$ C* }& l" R6 u  X. a" Ufollow-up visit was arranged within a few weeks to
$ n, H1 q1 M; x5 Zobtain testicular and abdominal sonograms; how-5 N; P7 G3 P2 j& I, |: [
ever, the family did not return for 4 months.
; K- M& _* T2 B% n% t! {' m+ lPhysical examination at this time revealed that the- l, p1 r% H2 G# e6 t
child had grown 2.5 cm in 4 months and had gained
3 S; s6 l6 I5 O( t: j$ J+ T$ l2 a2 kg of weight. Physical examination remained  X$ j9 v" y) e  A/ U( h
unchanged. Surprisingly, the pubic hair almost com-& ~' V$ `2 W8 x  w. A3 M
pletely disappeared except for a few vellous hairs at
* ]+ N  X% {7 I: K2 [3 k" qthe base of the phallus. Testicular volume was still 2# H! v5 d  ?- B' v$ G2 t: z: u
mL, and the size of the penis remained unchanged.' O& E' ?  l, p; i
The mother also said that the boy was no longer hav-/ D' _2 T- ]! ?. [9 c# }7 h6 Y+ x
ing frequent erections.# A1 i! v, i# x
Both parents were again questioned about use of
4 v, N! P7 i& r1 i1 S# Rany ointment/creams that they may have applied to9 q$ l, H' T- n3 r
the child’s skin. This time the father admitted the' J# r! R/ J, e! Z5 i
Topical Testosterone Exposure / Bhowmick et al 541
& F3 x/ A9 c  R" i! `use of testosterone gel twice daily that he was apply-7 y+ {8 b* m; h( \5 I
ing over his own shoulders, chest, and back area for3 L. f" r4 e; _& k( q  A, G1 M
a year. The father also revealed he was embarrassed
' @* h. {& n1 n: z/ M# Sto disclose that he was using a testosterone gel pre-1 ?- q! F2 H" i7 {0 X# N) d
scribed by his family physician for decreased libido
  l5 a, n6 J0 y: G4 t% h; C3 @secondary to depression.$ h# d% K$ E0 @$ r
The child slept in the same bed with parents.0 X, y. \8 r# v# z- H# K( ?
The father would hug the baby and hold him on his
: s/ |5 k0 a$ z/ s7 N3 P1 |9 Qchest for a considerable period of time, causing sig-9 ^  d( |$ U8 G/ W1 V( h0 K
nificant bare skin contact between baby and father.4 z& M/ p7 w5 X8 p% d0 ^* G1 n; l5 o
The father also admitted that after the phone call,
: A# K& w& p9 N, E2 Cwhen he learned the testosterone level in the baby
% r  e- \( O% {+ ^: h$ Dwas high, he then read the product information
$ a, O+ z/ [! o2 @3 [1 _packet and concluded that it was most likely the rea-+ O9 p0 z8 Y% Z3 B/ t$ j! d; m
son for the child’s virilization. At that time, they
0 Z  ?* ?1 Z2 Udecided to put the baby in a separate bed, and the3 {! r; }" I- f
father was not hugging him with bare skin and had
0 Z# y$ p+ X( J# U; T3 |been using protective clothing. A repeat testosterone
( k5 V- W- {+ Q: Btest was ordered, but the family did not go to the
4 u4 r$ x; @" |/ e) ulaboratory to obtain the test./ v3 T  X" ~  G% q( A
Discussion
& t8 s: f. m+ iPrecocious puberty in boys is defined as secondary
: b& F# E- F$ x8 \: l" H' wsexual development before 9 years of age.1,4
. f8 n6 i2 g) g5 F; V' S  D$ fPrecocious puberty is termed as central (true) when  I- Z' V' e% t9 n  T  }  y
it is caused by the premature activation of hypo-
- ~8 ?, J9 s' e, g& G! [( qthalamic pituitary gonadal axis. CPP is more com-) s2 C- n4 I4 H4 `6 n4 a
mon in girls than in boys.1,3 Most boys with CPP# C3 P: o- K5 _7 d0 M) z* }: q
may have a central nervous system lesion that is; h7 K/ M9 }7 s- \  {
responsible for the early activation of the hypothal-
' [- J- _, y4 z. t* hamic pituitary gonadal axis.1-3 Thus, greater empha-9 l5 I1 q. G+ M, L4 e8 u+ Z7 w
sis has been given to neuroradiologic imaging in
. _+ o6 P5 z7 j9 ~( qboys with precocious puberty. In addition to viril-
+ x* |3 g/ @/ x: y& n4 w& Tization, the clinical hallmark of CPP is the symmet-6 L, k! s( e! O: c+ k* c- R4 ^" B2 X, ~
rical testicular growth secondary to stimulation by
7 p4 K* O9 g; {* Kgonadotropins.1,31 |3 r8 X+ }5 h; M/ w; W
Gonadotropin-independent peripheral preco-- G, T9 o  p0 S( h" i, E0 e: z
cious puberty in boys also results from inappropriate! h4 L1 m! e3 S0 c+ H/ [
androgenic stimulation from either endogenous or
% B1 _  t8 {& S( Iexogenous sources, nonpituitary gonadotropin stim-8 h& d  F- X" ^) b+ h$ t
ulation, and rare activating mutations.3 Virilizing. f; }; V9 r6 e2 F% l; t* @
congenital adrenal hyperplasia producing excessive9 ?) k4 U* m3 x/ B! e, G
adrenal androgens is a common cause of precocious
* X( G6 F9 ^" f: k. J$ L7 w, J! Ppuberty in boys.3,44 E' e' j2 ]. A- I, ]
The most common form of congenital adrenal
2 {) N. o" t' z: U& a. n+ c# J2 uhyperplasia is the 21-hydroxylase enzyme deficiency.
$ q+ H/ H/ j0 ?The 11-β hydroxylase deficiency may also result in) S$ |  Q1 Q7 l; P/ C! Q3 d
excessive adrenal androgen production, and rarely,
% ~- u* D5 ?1 q$ p  I; Y3 u) Z! San adrenal tumor may also cause adrenal androgen
5 n5 L# N; x6 s& aexcess.1,34 t; ^& b/ z1 X! J2 s! r
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ K9 B( ^8 d+ a2 B/ H/ x3 {* ~( c542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
7 e. o' d4 r5 r& _+ L3 n% r( ~A unique entity of male-limited gonadotropin-5 S4 y$ O! a6 o# ?; Q
independent precocious puberty, which is also known; B& F" }  Z% R/ l. B* q
as testotoxicosis, may cause precocious puberty at a
: }0 r* d$ {7 b; Vvery young age. The physical findings in these boys
2 j! @0 c3 g6 S# P6 j; y- g! ^with this disorder are full pubertal development,
9 w; C: ~: r8 |# J% yincluding bilateral testicular growth, similar to boys8 z% a8 _3 g. P! E( U  Q
with CPP. The gonadotropin levels in this disorder# O9 V+ I( F5 J/ g( k% u) ^
are suppressed to prepubertal levels and do not show
# v/ R8 [" _" q' cpubertal response of gonadotropin after gonadotropin-; n+ ^' _! ^" A8 K" Z% x
releasing hormone stimulation. This is a sex-linked8 m9 ]# K% k2 o; S
autosomal dominant disorder that affects only5 Q: y( ~  \# k* V' T' @: B: a" N8 t
males; therefore, other male members of the family
, g: G: v2 Z! D0 Ymay have similar precocious puberty.3
2 G) o# y; s6 N) B* G, w! hIn our patient, physical examination was incon-6 \# a" p, }- n6 z& ~0 k3 U; R
sistent with true precocious puberty since his testi-
3 p! J3 S4 A1 T. D8 L  Wcles were prepubertal in size. However, testotoxicosis7 h" y1 N0 ^- r, \
was in the differential diagnosis because his father
& i5 u2 b! H, |% E( R+ d; x% Jstarted puberty somewhat early, and occasionally,
9 [  b3 n2 K% y+ L8 Otesticular enlargement is not that evident in the
" `: I; u2 T4 l7 i% e" Ubeginning of this process.1 In the absence of a neg-6 r6 T- D" [; h# ]
ative initial history of androgen exposure, our
. l2 N; m" I! R. C: O% l( |0 [biggest concern was virilizing adrenal hyperplasia,' C- V' @6 K1 n" {/ [
either 21-hydroxylase deficiency or 11-β hydroxylase
/ V6 H0 }/ B. r- N6 ^% L4 Ndeficiency. Those diagnoses were excluded by find-
7 N# D& s, _( X/ O' Jing the normal level of adrenal steroids.8 T  ?+ M- P. N3 D
The diagnosis of exogenous androgens was strongly) m% Y6 b9 h& O; R9 M
suspected in a follow-up visit after 4 months because
! y- ^! }! `6 Q6 d, ?& E: C+ ithe physical examination revealed the complete disap-
* z1 @, ], n1 v+ apearance of pubic hair, normal growth velocity, and
! D$ J, X+ \; ^2 s# ?" n/ x: @decreased erections. The father admitted using a testos-- H! ]% P6 Y0 r' b7 Z6 f) r
terone gel, which he concealed at first visit. He was9 n4 v7 m) N+ J; Q! k2 c
using it rather frequently, twice a day. The Physicians’2 G, _. K+ f% \! v; A0 {0 X7 f
Desk Reference, or package insert of this product, gel or" P2 J3 R* n6 F3 l3 K9 H6 o4 R: B# _
cream, cautions about dermal testosterone transfer to( @; t( p1 A2 M( j# a
unprotected females through direct skin exposure.
5 A0 T8 b% [' ]* vSerum testosterone level was found to be 2 times the8 z: W% b% \  B- `0 A$ r  j
baseline value in those females who were exposed to
0 [/ ]& A( a; p9 l# Keven 15 minutes of direct skin contact with their male! @/ P. D( H; T: W! _
partners.6 However, when a shirt covered the applica-
* X2 k" P; z! M. p& e7 Mtion site, this testosterone transfer was prevented.
- V# x+ ]/ j4 q! ~8 f; MOur patient’s testosterone level was 60 ng/mL,$ f, u5 s) h7 a5 _7 w
which was clearly high. Some studies suggest that
' E; _" J: `- d9 q/ `dermal conversion of testosterone to dihydrotestos-4 l5 q; a2 b% Y5 ^) p8 T/ J
terone, which is a more potent metabolite, is more
6 _- k3 K% _! _8 Sactive in young children exposed to testosterone
9 R/ T7 `0 C1 G6 _3 Vexogenously7; however, we did not measure a dihy-6 d" {; ^8 r* N3 s' M; j
drotestosterone level in our patient. In addition to7 u% R" ]6 a) P6 H) [+ V
virilization, exposure to exogenous testosterone in# o& M! `! R/ L
children results in an increase in growth velocity and4 E" D" i: F+ L0 i5 k7 S( t" t! y
advanced bone age, as seen in our patient.
" F6 a! n& G  C3 }7 x2 L& `* n* gThe long-term effect of androgen exposure during
- d2 x/ f) D8 oearly childhood on pubertal development and final2 D1 o! ]" G; T0 e: u
adult height are not fully known and always remain+ R& j0 Y2 u$ r2 `
a concern. Children treated with short-term testos-
' V: ]3 F$ [1 V$ [" I2 X% a0 Vterone injection or topical androgen may exhibit some2 e$ G; Y: [- H) \" G
acceleration of the skeletal maturation; however, after
2 v2 F6 I7 k' a6 l2 p: kcessation of treatment, the rate of bone maturation
0 ^: t- v, z! d2 p  rdecelerates and gradually returns to normal.8,9
# I1 q# H. m. T7 k! m* oThere are conflicting reports and controversy
6 i0 o: q2 |! Y% R; k0 xover the effect of early androgen exposure on adult3 E  p% ]/ \8 R" L: m% q0 n3 p9 g
penile length.10,11 Some reports suggest subnormal' X, q6 a, ]. Q" H
adult penile length, apparently because of downreg-
+ Q  i: V6 y/ [+ iulation of androgen receptor number.10,12 However,4 ~! c/ Z. j7 T$ I9 o
Sutherland et al13 did not find a correlation between
, i6 F+ B' @& h2 H: v, Xchildhood testosterone exposure and reduced adult; c" a  \$ t/ ?; i% J- A4 q
penile length in clinical studies.5 n# a& B2 d" I) ?6 i
Nonetheless, we do not believe our patient is; n, f- A! X! ~0 C7 f  w
going to experience any of the untoward effects from
0 [0 {# ^; W* u" g' |1 W; ftestosterone exposure as mentioned earlier because5 U$ `, `4 T, j; Z
the exposure was not for a prolonged period of time.
* i" g5 |: c3 y) N% G6 X5 aAlthough the bone age was advanced at the time of# O7 X# e+ x: O) m* H! {) q" s& o7 O
diagnosis, the child had a normal growth velocity at
  c1 H) q; N8 w2 |/ ~/ @( u7 R6 ~the follow-up visit. It is hoped that his final adult3 [0 `& F6 P* Q
height will not be affected.
' U+ I/ C& f6 d2 u( z; a5 L; Q6 h; JAlthough rarely reported, the widespread avail-
/ z8 `2 o+ t8 jability of androgen products in our society may
4 l2 [  t/ I4 r% tindeed cause more virilization in male or female2 G6 S. f. K' }5 F; A) }
children than one would realize. Exposure to andro-
3 \. k6 l/ X+ A* G# W: ugen products must be considered and specific ques-
/ `; l/ ]' a1 [tioning about the use of a testosterone product or
" m0 R. Z( L( h8 m+ cgel should be asked of the family members during
- _! F) ^0 S* ^, s' ythe evaluation of any children who present with vir-
$ H: y( M; h6 B) E+ cilization or peripheral precocious puberty. The diag-" F; {% R' o  D3 G
nosis can be established by just a few tests and by
# i4 p  h; j+ R: F- I% Fappropriate history. The inability to obtain such a
$ L" J0 j! A. N  H: @& Ohistory, or failure to ask the specific questions, may  w/ O2 s7 W% M) W9 ^
result in extensive, unnecessary, and expensive
; \+ j; k4 {) F$ j1 |investigation. The primary care physician should be1 _  Y5 ]" h5 s7 h& s
aware of this fact, because most of these children
  W9 g9 G1 x1 W: |, U2 Cmay initially present in their practice. The Physicians’
0 [2 n3 S2 |7 `% B7 J- F$ j4 EDesk Reference and package insert should also put a
3 b6 w0 [. G3 e( Z# ^4 Gwarning about the virilizing effect on a male or
* J: Z) [# }) u4 _- k0 q, A0 Pfemale child who might come in contact with some-5 }7 t7 k# h+ `  S$ C' D
one using any of these products.* x5 b. p# J2 [6 _% I
References
: U5 U. O3 h3 a  s1. Styne DM. The testes: disorder of sexual differentiation
# Z# M; ]  f# aand puberty in the male. In: Sperling MA, ed. Pediatric8 ~7 e& C5 E1 i
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;( P4 D( L- g/ t; i, x" p* }
2002: 565-628.; o# J6 s: L+ ?3 H3 b
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious4 d2 m5 W$ @7 S3 t. D) _) A# Q
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

% m1 U, O* K5 T" Z精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!
發表於 2025-3-8 22:04:50 | 顯示全部樓層
絕對的好貼!謝謝啊!逐字逐圖地看完這個帖子以後,我的心久久不能平靜,感恩啊!
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