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Sexual Precocity in a 16-Month-Old- w+ C( u, E) G: Q; S2 F
Boy Induced by Indirect Topical( i5 i5 q9 R- o8 z
Exposure to Testosterone
2 f- u' J( b( G8 n( J8 T( uSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2) x; X! G7 I7 Q. K
and Kenneth R. Rettig, MD1
! N; O. V1 i$ \+ {5 @& _+ w1 \! I4 \Clinical Pediatrics. p+ {+ ]3 f3 n: `
Volume 46 Number 6) Q( ]2 y, o9 f* V
July 2007 540-543$ f# E. C# I8 @, |0 l) |0 Y
© 2007 Sage Publications" Q8 y. f/ V' z) Y1 E) F0 `
10.1177/0009922806296651
# Z; B0 H) a+ t7 Rhttp://clp.sagepub.com
1 P, U; }: |2 l* q. w/ n0 Qhosted at
$ ?2 }' [/ G% J3 Q0 a% _http://online.sagepub.com4 k* }0 I2 v, n9 W$ X/ w7 l
Precocious puberty in boys, central or peripheral,
# ~; f' M1 O5 z$ W5 I2 [) Dis a significant concern for physicians. Central
( l- x* L7 n+ Uprecocious puberty (CPP), which is mediated% o! j. t9 m" n2 O9 a
through the hypothalamic pituitary gonadal axis, has
3 f  m+ v! K) {, ?" w" I$ aa higher incidence of organic central nervous system
' X8 \  y! x- Z$ k7 U  h7 ?# k  klesions in boys.1,2 Virilization in boys, as manifested
$ d( m$ ?, z" {  |+ fby enlargement of the penis, development of pubic
+ P! x9 L, F. C7 ^. I5 ~- khair, and facial acne without enlargement of testi-
; ?: b% E9 Q# G; M* r; @cles, suggests peripheral or pseudopuberty.1-3 We9 s: }* {+ n) v9 @- I% }
report a 16-month-old boy who presented with the
; _# p7 n% r; q. S1 W& [enlargement of the phallus and pubic hair develop-
; z9 g; t; X2 a$ w- w& O+ }2 `% Oment without testicular enlargement, which was due
6 c6 d3 Y* n' Tto the unintentional exposure to androgen gel used by2 A7 h4 s' W) c* t
the father. The family initially concealed this infor-: f" I9 m& z9 Z6 o* `
mation, resulting in an extensive work-up for this' l9 L! p6 @2 S* ]) \! M: i
child. Given the widespread and easy availability of( A( N( `# w2 T0 v# s  r# i. C
testosterone gel and cream, we believe this is proba-
$ s+ q4 K3 D7 B9 i( ?' Zbly more common than the rare case report in the# ]( Q4 z6 q/ B9 m/ A" `+ l
literature.49 K" }1 [) [1 {) J
Patient Report+ u5 k+ U- {/ R3 h4 P1 e& ?
A 16-month-old white child was referred to the1 S! i- H9 Q7 ]+ E
endocrine clinic by his pediatrician with the concern5 t$ g4 k& a+ U2 G# E/ O+ i2 i0 C- ?
of early sexual development. His mother noticed3 n2 ~& S- ~6 z# s: f
light colored pubic hair development when he was
* m1 ]6 o1 v- P! H4 fFrom the 1Division of Pediatric Endocrinology, 2University of
8 I, J/ a5 b3 U2 v, ]% Y; }0 pSouth Alabama Medical Center, Mobile, Alabama.
) ^5 T4 i6 C1 g6 RAddress correspondence to: Samar K. Bhowmick, MD, FACE,
4 ]& W5 T: u; J9 }8 g" N* ]Professor of Pediatrics, University of South Alabama, College of: n- \/ [& d; x: x/ N8 V- ?
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
; w3 \) Y. e5 g% `5 y4 ^e-mail: [email protected]." `* J) w1 A$ F0 v3 ~
about 6 to 7 months old, which progressively became
) [) D! T: q8 u$ o% Ydarker. She was also concerned about the enlarge-, \) N& H# e1 F6 N8 n
ment of his penis and frequent erections. The child; b) I, p+ y  z9 m! ~
was the product of a full-term normal delivery, with* t2 S# E* _; u
a birth weight of 7 lb 14 oz, and birth length of
6 c: i1 s  Y3 Y: e$ m8 {20 inches. He was breast-fed throughout the first year
9 Z! }- h4 v+ E- G* F' x" sof life and was still receiving breast milk along with
; |$ F/ F( K; i8 p! r: [! n& Ysolid food. He had no hospitalizations or surgery,+ k: x6 b. O- F3 N2 I# B) R
and his psychosocial and psychomotor development
1 n% l. W1 r% B6 i0 lwas age appropriate.
6 \2 u  Z  K" k* C) VThe family history was remarkable for the father,
9 I2 H* {; J. K  B/ \who was diagnosed with hypothyroidism at age 16,
# s- `; D( f! [' U! N# v- iwhich was treated with thyroxine. The father’s2 P- ?6 S: n+ I6 Z
height was 6 feet, and he went through a somewhat
) ^9 u! N/ U7 Y( H, O, l  d$ uearly puberty and had stopped growing by age 14." ]& i# a$ D. r+ ], f: Y
The father denied taking any other medication. The9 }8 v9 ^+ l& R3 D( w
child’s mother was in good health. Her menarche
9 `' z2 T: K* owas at 11 years of age, and her height was at 5 feet
" M, E% P+ T; X0 b5 inches. There was no other family history of pre-$ o. I+ y$ R7 X+ m! t
cocious sexual development in the first-degree rela-3 @0 E. t; A- b4 @; B4 F& H2 A
tives. There were no siblings.
8 b* Y) [5 r2 T5 jPhysical Examination% h9 u% b) s, _$ N+ {0 u
The physical examination revealed a very active,
) C* ]$ ]! P" L) B) `, `3 `- [playful, and healthy boy. The vital signs documented+ w  |+ ]8 _# a) N6 h. K
a blood pressure of 85/50 mm Hg, his length was
* j3 Q  y' @% O90 cm (>97th percentile), and his weight was 14.4 kg, H0 H1 f7 S# ^$ e8 r
(also >97th percentile). The observed yearly growth: s# ]( q/ \9 @
velocity was 30 cm (12 inches). The examination of
) Z7 ]/ {3 i$ c4 d1 c, uthe neck revealed no thyroid enlargement." z4 Q6 N5 s0 o9 ]* T, p0 V
The genitourinary examination was remarkable for( V% W. V9 A" v* U
enlargement of the penis, with a stretched length of
, R+ }% w! J# f- Z; |2 z0 z. q8 cm and a width of 2 cm. The glans penis was very well7 a. B- `6 f. ^: ~5 C; @
developed. The pubic hair was Tanner II, mostly around3 T( _8 o! V. f( C- ^3 c0 W
540  {3 ~) I% d& G. Q& K- l5 J, f
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 ~4 ?* }6 P* K( q
the base of the phallus and was dark and curled. The) i2 D& P2 ^! x/ f+ ?+ C* O. x  p  K; @
testicular volume was prepubertal at 2 mL each.4 T! Z1 G3 o- M; m. p- V; R
The skin was moist and smooth and somewhat
0 O- w9 i* ^+ ]! koily. No axillary hair was noted. There were no
4 Y$ @- F5 c* w/ d3 Uabnormal skin pigmentations or café-au-lait spots.8 i2 M1 d. |" n$ ?, @
Neurologic evaluation showed deep tendon reflex 2+
) w9 C+ j* R; s9 j) R+ H3 n* Y7 Sbilateral and symmetrical. There was no suggestion
/ U( S9 e! H/ ~$ U# M3 ]of papilledema.
/ c( X2 e; K& U8 {0 SLaboratory Evaluation
3 E7 U/ _1 Q# @The bone age was consistent with 28 months by+ X: Y1 K/ l3 m' ?' u7 g
using the standard of Greulich and Pyle at a chrono-3 J$ |8 E' P/ D) k1 B) w5 f
logic age of 16 months (advanced).5 Chromosomal
, e% [+ x; k. r* D7 ]# akaryotype was 46XY. The thyroid function test
# v2 U9 _  v7 B6 I5 Fshowed a free T4 of 1.69 ng/dL, and thyroid stimu-7 m& C7 B# j; W9 u- J  _. {+ l
lating hormone level was 1.3 µIU/mL (both normal).
, p! D* W" h% d* lThe concentrations of serum electrolytes, blood
7 C$ [1 i& i9 w. I2 Qurea nitrogen, creatinine, and calcium all were
4 N) ^* P( W8 ?, i) |( j+ o# Xwithin normal range for his age. The concentration# s" I/ s5 R* w8 z5 R
of serum 17-hydroxyprogesterone was 16 ng/dL
  _2 m( X- t" J0 U4 Y(normal, 3 to 90 ng/dL), androstenedione was 20
. z* n( _) X7 w- y5 I0 c$ ]. I# Nng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-1 P- n& k2 G2 P  _- }
terone was 38 ng/dL (normal, 50 to 760 ng/dL),; K' n! r2 c1 c! q, P' e( W
desoxycorticosterone was 4.3 ng/dL (normal, 7 to3 t: Q$ R, R' O2 |0 G
49ng/dL), 11-desoxycortisol (specific compound S)
+ {5 C" A8 y- A% e0 i& ?was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
6 b4 k: r$ F/ t& qtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total( @; O9 |/ M! [* k
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),5 I8 D$ x6 @! v# O& \# {# }( O
and β-human chorionic gonadotropin was less than  g9 Z7 X* @/ }, }9 J
5 mIU/mL (normal <5 mIU/mL). Serum follicular: K+ x& U  U, |/ d1 T/ m
stimulating hormone and leuteinizing hormone2 f  W# ]0 N% }2 }" j4 `; P
concentrations were less than 0.05 mIU/mL
& n1 Z+ D. ?) f8 n1 ?(prepubertal)./ F& A* [$ `1 F1 E
The parents were notified about the laboratory
- s9 G4 a( Z1 j, d7 l3 l0 }8 F' z6 u. qresults and were informed that all of the tests were! z) M6 F) T3 s7 [1 ]
normal except the testosterone level was high. The/ T5 [: E$ M" K* u0 C# e! F+ v
follow-up visit was arranged within a few weeks to' k0 e" P- c( Q- U3 J$ a6 t
obtain testicular and abdominal sonograms; how-
& g  V- G2 n$ I2 z0 `" Oever, the family did not return for 4 months.
  }6 p' \- t! E0 q9 oPhysical examination at this time revealed that the
/ \# e" H; |5 X% o: ]$ hchild had grown 2.5 cm in 4 months and had gained% T+ s% M9 U5 N% n, o
2 kg of weight. Physical examination remained) V: O' S4 [, N% x4 e, ?
unchanged. Surprisingly, the pubic hair almost com-
4 |* Y0 D  f" a  @' \8 U$ wpletely disappeared except for a few vellous hairs at- m3 E1 m/ z! @( i1 }! E; u' ^! `
the base of the phallus. Testicular volume was still 2* p; }  u7 J/ G- T" t
mL, and the size of the penis remained unchanged.* t% w/ d$ x- K, c
The mother also said that the boy was no longer hav-8 B3 L+ {6 \( g
ing frequent erections.; n; z: N$ p$ D' @0 f1 p
Both parents were again questioned about use of$ J7 c% i! [5 j: Y" ?0 z
any ointment/creams that they may have applied to, l. \0 R3 ^% H4 L2 P' H6 T  q
the child’s skin. This time the father admitted the8 ]9 P  ^! C! S
Topical Testosterone Exposure / Bhowmick et al 541
* n6 r+ ?2 U) s) Uuse of testosterone gel twice daily that he was apply-
& p7 G3 }1 U, ?1 Uing over his own shoulders, chest, and back area for
. G2 C- C: a2 }9 ^3 qa year. The father also revealed he was embarrassed
8 u; Z0 g0 M9 Y8 _4 kto disclose that he was using a testosterone gel pre-
8 i( f; ~; P. c" K* N9 Z2 m( [5 t/ Escribed by his family physician for decreased libido
4 M: V0 c: Z2 `3 M, O" D' \secondary to depression.
" w  Z; r) B9 F( r3 SThe child slept in the same bed with parents.4 @& x: N. h8 G
The father would hug the baby and hold him on his; _4 V7 y; }4 `9 U9 l/ I' T' F
chest for a considerable period of time, causing sig-" k3 c2 W" b. X& i) K" c5 z
nificant bare skin contact between baby and father.- x; [8 i  X, m. S0 [; D" z, T
The father also admitted that after the phone call,
' @4 P! y3 d. c: qwhen he learned the testosterone level in the baby
/ u. S' t  @1 {# [was high, he then read the product information
/ O  \( E6 `0 A# v6 G; [6 T: rpacket and concluded that it was most likely the rea-/ N2 S+ c7 }4 J+ ~( U
son for the child’s virilization. At that time, they
) a) k' ~8 ?& Udecided to put the baby in a separate bed, and the4 {$ J+ V" I8 b8 H
father was not hugging him with bare skin and had' G. Y6 g* i  t7 ^. n
been using protective clothing. A repeat testosterone) ^# H& ~: T9 j
test was ordered, but the family did not go to the
9 P# c: f& M1 x; Ulaboratory to obtain the test.+ P/ O( c4 @& B9 f
Discussion
) {3 t6 m$ B4 P4 l9 H7 X2 gPrecocious puberty in boys is defined as secondary
3 u* r" X( H5 [; h1 z4 Tsexual development before 9 years of age.1,4, K. \# \; @, f
Precocious puberty is termed as central (true) when  i. S, w: ~+ @' f5 p: r' }, U
it is caused by the premature activation of hypo-
. g2 {8 q: m8 u* K/ ~% vthalamic pituitary gonadal axis. CPP is more com-
5 {3 X, j+ [8 q  _) Xmon in girls than in boys.1,3 Most boys with CPP$ `) q. U4 C8 b% e$ Q
may have a central nervous system lesion that is4 |% Y& J! [) w" [* a3 f6 z$ h) X
responsible for the early activation of the hypothal-
5 c5 Q4 _: `1 G* N% `+ }+ Yamic pituitary gonadal axis.1-3 Thus, greater empha-7 z' T8 x/ |6 o7 k- }+ T. D2 w
sis has been given to neuroradiologic imaging in( r) m# B& R7 A' O$ D) {# U
boys with precocious puberty. In addition to viril-/ h6 z! r- U. Z! q1 x
ization, the clinical hallmark of CPP is the symmet-" N7 `- `( r, y8 C* N' ?
rical testicular growth secondary to stimulation by# O8 r7 {5 s+ L. x2 z  p: u) I
gonadotropins.1,3
$ D$ @. k9 F5 I8 pGonadotropin-independent peripheral preco-. P' N, l# \' I* a( [8 \/ h
cious puberty in boys also results from inappropriate% `/ h8 i5 C3 M- ]' ?; ?3 j
androgenic stimulation from either endogenous or
) i! j" U/ r1 T. Hexogenous sources, nonpituitary gonadotropin stim-
1 p6 A3 ?, R9 Gulation, and rare activating mutations.3 Virilizing/ W6 |* m9 R2 A- F
congenital adrenal hyperplasia producing excessive
- T9 H0 w6 \9 [) Padrenal androgens is a common cause of precocious. c9 c1 A" Y) \1 K. \. s
puberty in boys.3,4
" F2 Y* n# V1 k" S5 _$ {0 TThe most common form of congenital adrenal
% e1 o* g8 C, zhyperplasia is the 21-hydroxylase enzyme deficiency.
. r  R6 Q# K0 I/ p9 t$ `The 11-β hydroxylase deficiency may also result in
! g3 f0 @, P3 u8 wexcessive adrenal androgen production, and rarely,7 f) P* w( [  j+ {& Z
an adrenal tumor may also cause adrenal androgen
6 C' p6 ~7 M; f" R5 a, pexcess.1,3
9 ^, h; f6 C+ h, ]8 [at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 A$ i% \8 g3 W, [+ _
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
5 j& K* N2 h8 {2 n+ FA unique entity of male-limited gonadotropin-
. h" s4 X( P# }; R- h" ~independent precocious puberty, which is also known! [3 p, T2 j/ l! }7 e" T8 O
as testotoxicosis, may cause precocious puberty at a
! u! V# L' f- z% Y3 L) o- H4 Every young age. The physical findings in these boys* U- l0 o6 j- @* V& z
with this disorder are full pubertal development,
  m# r* V+ O, e# M7 y+ G8 f) aincluding bilateral testicular growth, similar to boys. X2 V# S/ o2 G1 O
with CPP. The gonadotropin levels in this disorder
7 e* ]+ H0 U9 W3 g2 C, @are suppressed to prepubertal levels and do not show, t6 O# _+ P2 C: G
pubertal response of gonadotropin after gonadotropin-$ @7 _! v6 L4 w
releasing hormone stimulation. This is a sex-linked
: X5 c! _' I0 z8 p+ W: D- P- pautosomal dominant disorder that affects only
* [# z4 e' z  y+ Smales; therefore, other male members of the family
6 c/ ^" P3 ?$ s/ R+ k' \9 b' Cmay have similar precocious puberty.3
0 @/ `" V; y6 VIn our patient, physical examination was incon-
  }, a- y  p3 dsistent with true precocious puberty since his testi-1 e8 O* m; ?4 b, U( I9 Q6 g
cles were prepubertal in size. However, testotoxicosis
* ?" N6 P* R9 r) |4 @$ ]- Lwas in the differential diagnosis because his father
$ ]$ E) g3 `0 B8 m' r0 nstarted puberty somewhat early, and occasionally,
5 \9 L$ ^, {( _+ e3 Otesticular enlargement is not that evident in the
, a* _! o- \6 D8 Ebeginning of this process.1 In the absence of a neg-
5 \$ L, J9 _0 R8 F6 B  N* O7 f1 m: Vative initial history of androgen exposure, our+ i6 ^+ w& M7 h* H
biggest concern was virilizing adrenal hyperplasia,
) Y' `) z% q' Q! X. aeither 21-hydroxylase deficiency or 11-β hydroxylase% c& [  G' N% ~& J
deficiency. Those diagnoses were excluded by find-
5 f% W# l; `8 l, w  K* T; P6 Zing the normal level of adrenal steroids.
( D% m* a! ?+ H( |The diagnosis of exogenous androgens was strongly
3 R* F8 ?5 n3 P1 zsuspected in a follow-up visit after 4 months because0 O. R# o$ N* A/ H1 {
the physical examination revealed the complete disap-. Q! u* F+ X' x: v! ?2 k9 X/ N
pearance of pubic hair, normal growth velocity, and% V# d- }8 y3 Z" q  L' A4 I
decreased erections. The father admitted using a testos-  v/ H: p* G* }* Z1 S' l* M
terone gel, which he concealed at first visit. He was
, S! P( M' P0 W5 f& A; |3 Z$ zusing it rather frequently, twice a day. The Physicians’
. E$ ?4 j2 O7 w6 MDesk Reference, or package insert of this product, gel or
2 I' ~7 }% ~( l! G$ D. Ocream, cautions about dermal testosterone transfer to
+ e4 d! I* W3 o7 runprotected females through direct skin exposure.
# ~& w" S) W1 R9 N5 G8 hSerum testosterone level was found to be 2 times the
, [* h3 A* Y- G7 h- Y! U+ {baseline value in those females who were exposed to' f1 \# O4 m; W# ]7 z- L5 r
even 15 minutes of direct skin contact with their male& U4 W* J8 ?. N5 j  D: l9 h2 F! E
partners.6 However, when a shirt covered the applica-
3 X6 f8 |( ?- ^! k6 V5 x9 ltion site, this testosterone transfer was prevented.
' }6 h8 J0 }- c9 v# f0 s% DOur patient’s testosterone level was 60 ng/mL,' Y5 W3 H& X" e8 }
which was clearly high. Some studies suggest that0 }# X' Q. [1 s: X6 Y
dermal conversion of testosterone to dihydrotestos-
4 o$ x) T+ ?# I' L2 U- p2 O. w% Wterone, which is a more potent metabolite, is more
4 A: T- H2 E8 q! g4 f. m% \active in young children exposed to testosterone& }' U. m! S) J
exogenously7; however, we did not measure a dihy-
) U# i7 c& f  ~7 O" Wdrotestosterone level in our patient. In addition to
' W$ |; o1 L& G5 Fvirilization, exposure to exogenous testosterone in
) |" y, `% n$ Jchildren results in an increase in growth velocity and: V0 f% q  u" v
advanced bone age, as seen in our patient.
* {  ~2 U3 P8 QThe long-term effect of androgen exposure during2 w0 c" d) l" k$ ^5 e; U) E
early childhood on pubertal development and final
9 V. c  H: y6 D6 r5 Iadult height are not fully known and always remain
. L$ ~: l# H$ q; R# a, aa concern. Children treated with short-term testos-' Q$ J9 U5 z' ?& A. g8 s! C
terone injection or topical androgen may exhibit some1 [8 i6 G, j" a( w9 F8 X- H
acceleration of the skeletal maturation; however, after
3 J! y- I! t6 `# f$ q0 P0 \# tcessation of treatment, the rate of bone maturation! h" N" s5 O- c( P( F9 u
decelerates and gradually returns to normal.8,9
1 D; N. l, C8 v6 ~% ~! XThere are conflicting reports and controversy
" U9 ^2 r( H4 h: F% Cover the effect of early androgen exposure on adult
% h, u7 U4 c7 S6 Gpenile length.10,11 Some reports suggest subnormal& U# m& N+ R) \) Z5 ^
adult penile length, apparently because of downreg-( S- g' j  B3 C8 T8 {
ulation of androgen receptor number.10,12 However,
; j9 _% R7 X' V8 K/ YSutherland et al13 did not find a correlation between
" |" c) t  w8 N: H( S6 i# r: e2 s8 Tchildhood testosterone exposure and reduced adult- s$ y" o* h6 L0 L1 I; o2 B# Z
penile length in clinical studies.
5 h2 }4 _$ o; pNonetheless, we do not believe our patient is' t7 @1 T/ N! w+ W% S; ?! \
going to experience any of the untoward effects from
" N! B0 \+ C/ `8 t0 d, q. Itestosterone exposure as mentioned earlier because
" s5 E) U" H, W4 Qthe exposure was not for a prolonged period of time.6 L3 S" }' M" N* T
Although the bone age was advanced at the time of0 u  E& k/ |" ?% Q
diagnosis, the child had a normal growth velocity at
" M( R& ^" v, [) W! zthe follow-up visit. It is hoped that his final adult  c; `* m3 S$ n# b
height will not be affected.0 y( {" {2 A- ^( w5 ~: P" V1 ?
Although rarely reported, the widespread avail-1 c. M5 F' p0 ^  H1 }6 b
ability of androgen products in our society may
5 A. r; z# Q% U2 }( |0 Vindeed cause more virilization in male or female2 m! t# h/ F% K5 |
children than one would realize. Exposure to andro-' Q% ?( k" B& v# s8 \( v# y1 D
gen products must be considered and specific ques-, E* D0 j; O/ Q
tioning about the use of a testosterone product or
) H7 K7 M* C0 r  l- |! i" [gel should be asked of the family members during
7 [5 r) X' b4 L: x) J; a+ L  Xthe evaluation of any children who present with vir-
4 x3 ^* _) I5 }) i$ V5 qilization or peripheral precocious puberty. The diag-; Y- h+ U" r8 n3 m5 y: q& [0 j. u8 K
nosis can be established by just a few tests and by6 T0 f- K( b! y! `5 d  Q
appropriate history. The inability to obtain such a" u' F, r7 q1 q$ k
history, or failure to ask the specific questions, may1 H: t" U' w5 h. q7 o& Z6 M) C
result in extensive, unnecessary, and expensive
0 Z5 m1 ^& a  R4 t1 e$ ^5 Ninvestigation. The primary care physician should be4 f) @9 ?! G: X5 s4 b6 ^
aware of this fact, because most of these children; l1 g* {, [' [6 M. j6 E+ ^9 I
may initially present in their practice. The Physicians’3 D4 ]) H* Y- a% q
Desk Reference and package insert should also put a
+ b) i* F8 v* I! Owarning about the virilizing effect on a male or
* t6 Y+ M# N. z& d# m8 R4 Mfemale child who might come in contact with some-( h& K7 y: j$ X. _! a, F( D" S4 P
one using any of these products.6 o$ Z  }0 R* T9 u
References! H- m, a. `1 a& ], ^, V
1. Styne DM. The testes: disorder of sexual differentiation" L# E+ g! `  |  H/ ~
and puberty in the male. In: Sperling MA, ed. Pediatric  v2 z; {, y9 T3 w
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
3 q+ \2 e" [0 t2 |, i2 l2002: 565-628.
& ]. N0 ?, ?% d" c% O0 x2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
& h3 p; k' ~/ m5 E( h: Cpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old. i& X/ l1 r  |7 z
Boy Induced by Indirect Topical
9 |" Q% e8 v3 ]: ~Exposure to Testosterone9 t  F# g$ x8 [" X
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
5 K- M0 p1 z. N; v7 s! jand Kenneth R. Rettig, MD1
: S, w$ k1 z( n* nClinical Pediatrics
# M; D: m: I) R+ Q. t2 KVolume 46 Number 6' e7 @1 p9 K+ c0 p4 ~3 E# q2 W8 l5 u
July 2007 540-543
( l# U& v3 V5 ~- y0 s© 2007 Sage Publications8 C0 a+ h. D1 P5 w* f- U- t
10.1177/0009922806296651
# {0 T3 O2 r5 uhttp://clp.sagepub.com
1 W3 T& k' {$ `hosted at$ i# _( I0 Z  B" {' D% `1 `1 L
http://online.sagepub.com
! J; S( y' ]; z' o; ^Precocious puberty in boys, central or peripheral,6 s- s, P0 t4 M2 c
is a significant concern for physicians. Central
8 \3 [6 r. r" P$ N1 \+ Wprecocious puberty (CPP), which is mediated& I0 R+ n, l$ ?
through the hypothalamic pituitary gonadal axis, has5 J" \! [, i  I. f  A8 y
a higher incidence of organic central nervous system2 \$ B& p/ ~& _3 K- x. X; k+ A
lesions in boys.1,2 Virilization in boys, as manifested1 D8 ^3 B7 H7 r0 [1 |. |
by enlargement of the penis, development of pubic
: u% G4 J5 f0 F' @- Xhair, and facial acne without enlargement of testi-1 P) v+ L' P# l2 c: N
cles, suggests peripheral or pseudopuberty.1-3 We
7 Q' O; b3 U- a1 s' k. ?report a 16-month-old boy who presented with the- u3 r  y$ [1 ^9 t3 E! l- g
enlargement of the phallus and pubic hair develop-9 w* }, S& p" f& c+ b& u2 _
ment without testicular enlargement, which was due  Y6 D0 E! U4 n* w( }- D
to the unintentional exposure to androgen gel used by, R- P* F/ g/ f' d
the father. The family initially concealed this infor-+ [' g9 s0 E, [* A" P6 F  n0 d8 X
mation, resulting in an extensive work-up for this
; t% ~) U8 u1 K, O/ c2 @$ K8 A$ Vchild. Given the widespread and easy availability of: b5 h' m5 E; F5 l% z& c
testosterone gel and cream, we believe this is proba-
5 J+ S/ _6 `- {/ l3 Q5 b  Zbly more common than the rare case report in the2 W; j! ]; g8 c$ ]+ @) B6 r
literature.4  Z  }( i8 c3 z+ W
Patient Report
  u; r5 s, }% G$ E3 z6 x5 nA 16-month-old white child was referred to the2 h/ R( n9 Z* w- h3 f& w& A$ e
endocrine clinic by his pediatrician with the concern7 c( p  ?3 P3 `( @! X6 b. L
of early sexual development. His mother noticed
* q/ ^( C- G/ ?" ylight colored pubic hair development when he was6 V& g' G, C' J1 r1 L- L
From the 1Division of Pediatric Endocrinology, 2University of
, ^1 N5 K9 u" ]/ G) {8 qSouth Alabama Medical Center, Mobile, Alabama.
; }2 x; ]  ~* ^8 @, F. @Address correspondence to: Samar K. Bhowmick, MD, FACE,7 W" |2 I0 y' {# ^! J# ?
Professor of Pediatrics, University of South Alabama, College of/ i7 H- k5 j. I" ]
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;& Q( f# c7 k0 N3 _% W2 L+ j' I1 e
e-mail: [email protected].
/ H" v- k: o& Wabout 6 to 7 months old, which progressively became
$ F. K! U; q$ o4 X/ D- D3 o, {, Sdarker. She was also concerned about the enlarge-! T# R3 y9 x. }, t* d" ^
ment of his penis and frequent erections. The child
- e9 a9 b& f: |0 p# x: }# ~was the product of a full-term normal delivery, with
6 u2 e1 D. ^' r' }7 a8 K  e$ |( w- Ga birth weight of 7 lb 14 oz, and birth length of
7 w" H; d0 u* ]6 w) Z4 y20 inches. He was breast-fed throughout the first year  p& X) B/ H) V- G
of life and was still receiving breast milk along with
# C1 `$ q; {" j" o- ]solid food. He had no hospitalizations or surgery,
6 @" V' B0 e. @4 C9 A& n5 k. p4 Tand his psychosocial and psychomotor development
! c" t. a2 X+ X" f' u  kwas age appropriate.) b! V0 i3 U% c
The family history was remarkable for the father,
2 ], ~0 Q8 x9 Z. s" M1 Qwho was diagnosed with hypothyroidism at age 16,
6 C$ G2 L& N- F& Ywhich was treated with thyroxine. The father’s
" ~4 t% V7 ?+ T. u( ~) b$ `height was 6 feet, and he went through a somewhat
5 y% i. ?) A/ aearly puberty and had stopped growing by age 14.
( P. s' |# u( e. r6 O9 BThe father denied taking any other medication. The
- ?) X" Y0 H+ w- i! bchild’s mother was in good health. Her menarche
. u/ {" L/ V4 H$ Z: }was at 11 years of age, and her height was at 5 feet' a- A# Z0 T2 A5 D7 i8 U6 L
5 inches. There was no other family history of pre-$ X2 L0 O6 ?3 X# X7 ^2 T$ B
cocious sexual development in the first-degree rela-
  g$ ^9 k9 H# V6 ltives. There were no siblings.+ J2 V( l  T* N3 E
Physical Examination
  q. I) |) d" R% C% LThe physical examination revealed a very active,- x& @4 [# ]* F8 I$ U. c3 o% d
playful, and healthy boy. The vital signs documented
2 V$ P/ D% q* l6 j4 _, u8 ea blood pressure of 85/50 mm Hg, his length was( G7 {5 f# h. w" v3 k5 }9 \! x5 Y
90 cm (>97th percentile), and his weight was 14.4 kg+ _: T/ A+ R6 U6 R) V& r' p
(also >97th percentile). The observed yearly growth$ n7 R! g& H% j: g% C6 G( }
velocity was 30 cm (12 inches). The examination of, f; C6 w2 p' ]7 p9 a0 z+ s
the neck revealed no thyroid enlargement.
# k: a/ I6 K+ f: D7 a0 v; R4 _# qThe genitourinary examination was remarkable for4 \4 z9 Y# S" s8 X4 B0 E: u
enlargement of the penis, with a stretched length of+ T/ I( ]1 D5 s- m  j
8 cm and a width of 2 cm. The glans penis was very well' b) O5 X2 ]  z% l/ @) W( b  p) \
developed. The pubic hair was Tanner II, mostly around
" U$ _0 w: E. f2 q540, v% ~# v0 a0 z) x3 d
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 L- j# R, p4 Y7 L
the base of the phallus and was dark and curled. The
; a7 p& \) u5 M# Q% u4 x7 O& vtesticular volume was prepubertal at 2 mL each.
7 ^: U/ V  t- J( X9 h4 p- o; YThe skin was moist and smooth and somewhat7 F* u' o& b+ o7 S7 e
oily. No axillary hair was noted. There were no/ K/ A: ?. ?: ?( |5 }6 X8 @& I0 r8 g
abnormal skin pigmentations or café-au-lait spots.
$ a' _5 B- F8 ^! V7 n. y8 Q+ RNeurologic evaluation showed deep tendon reflex 2+, {7 k) r! U$ f$ P3 P, @4 L; Z/ c
bilateral and symmetrical. There was no suggestion
1 a) R7 J  i" s; y+ O: Wof papilledema.
1 c. b8 _. s( }7 D+ J; QLaboratory Evaluation# M9 d, D# E* r# O7 k7 q! p$ T
The bone age was consistent with 28 months by2 F: _6 i5 R  y; r4 d8 Q4 \# f
using the standard of Greulich and Pyle at a chrono-
1 E6 Y- m: r$ ^( L# {logic age of 16 months (advanced).5 Chromosomal
4 _9 o0 J& \* {& ekaryotype was 46XY. The thyroid function test0 N2 D% k/ T4 P+ J6 N6 F0 }: E+ t
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ \) t! y% W" K4 K0 Y2 y$ A; ~! blating hormone level was 1.3 µIU/mL (both normal).* c, V  d5 v( C+ |
The concentrations of serum electrolytes, blood
# W, L1 _7 n5 h  jurea nitrogen, creatinine, and calcium all were
8 k0 D5 m/ J" r! G' Jwithin normal range for his age. The concentration) a5 V* [) x  w) v- ]+ {
of serum 17-hydroxyprogesterone was 16 ng/dL. G9 T) f* v# h1 c% c/ C( D
(normal, 3 to 90 ng/dL), androstenedione was 20
0 f8 U1 U  l  H6 r1 `ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-( r, M7 l8 F+ l. r( V4 N
terone was 38 ng/dL (normal, 50 to 760 ng/dL),  G) R4 Z. j0 Y6 K6 s1 n8 |
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
6 s9 P) y* M  k  B49ng/dL), 11-desoxycortisol (specific compound S)2 u2 U! @# u, W; z% o, d
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
, q) h9 h; q6 j  u: ?; G' Btisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
2 \( b: R( X" \( w7 _% ~  Ktestosterone was 60 ng/dL (normal <3 to 10 ng/dL),( {# X1 s; G) ], }5 |3 [
and β-human chorionic gonadotropin was less than/ {; g# D# [- _- o* L  v% ^5 I/ |- f
5 mIU/mL (normal <5 mIU/mL). Serum follicular: i* C1 w$ m4 U1 s- a( V
stimulating hormone and leuteinizing hormone" ]' K' a, w: P" U* X
concentrations were less than 0.05 mIU/mL5 q* g2 `, k' R( q4 g* X  u7 N% Q, g
(prepubertal).
2 Q1 S" r5 M' u5 v( B) _The parents were notified about the laboratory
( x. a/ l$ x4 e, ^, Nresults and were informed that all of the tests were4 T6 h1 g. E0 i5 G, X
normal except the testosterone level was high. The
, v% I  ~: S' w( Y) vfollow-up visit was arranged within a few weeks to2 i$ d! B  W9 E7 o4 ?
obtain testicular and abdominal sonograms; how-
" ~7 Q4 l. e5 {; o6 qever, the family did not return for 4 months.' T/ T# S9 e; t: ]* U
Physical examination at this time revealed that the
" U6 ~5 g7 q* m) |child had grown 2.5 cm in 4 months and had gained7 Q1 R' J9 |# P: S
2 kg of weight. Physical examination remained! ~8 J8 }$ w' F1 C" C
unchanged. Surprisingly, the pubic hair almost com-6 X* b: ]" R9 ^, h# R
pletely disappeared except for a few vellous hairs at
5 }3 T+ J0 t0 o  o' n  wthe base of the phallus. Testicular volume was still 2. m5 Q# P1 s6 \- Z
mL, and the size of the penis remained unchanged.0 ]; w* f" u* f$ B4 f% u, R+ o
The mother also said that the boy was no longer hav-
7 j$ G2 |0 s$ Z7 X# Hing frequent erections.& e5 J8 c  G8 G9 ~
Both parents were again questioned about use of
4 Y* W5 V1 ?1 t% ~- V3 cany ointment/creams that they may have applied to( F- q4 S2 B% P: O. S8 ^- \, A* j" F
the child’s skin. This time the father admitted the
0 y- _% G3 L% W& g! gTopical Testosterone Exposure / Bhowmick et al 541
4 x4 b3 x* d* `  y5 T: a. Yuse of testosterone gel twice daily that he was apply-
8 q, p9 @& x4 S' A  e; n2 Jing over his own shoulders, chest, and back area for  Q* b' e/ {) Y5 k7 ?, l+ S
a year. The father also revealed he was embarrassed
6 V% Z4 ]) N1 t; ^% Q2 ~to disclose that he was using a testosterone gel pre-/ g! x8 a. `8 K8 K1 ?! Z
scribed by his family physician for decreased libido
* I, K" X3 c7 ~secondary to depression.% M& [2 X) J' O+ ]; o
The child slept in the same bed with parents.
- N8 r# N: R% A. H  SThe father would hug the baby and hold him on his
) Y& ]! N# N  a4 |, wchest for a considerable period of time, causing sig-3 S* C) }- _, F6 z5 n3 n. ~
nificant bare skin contact between baby and father.3 F% I$ ^2 R: D3 ^3 j  ^
The father also admitted that after the phone call,8 C3 m* m8 x' u4 z
when he learned the testosterone level in the baby. z/ e9 K2 N* W1 h/ Q
was high, he then read the product information$ w% R. }. ^. B7 v
packet and concluded that it was most likely the rea-* D, g. k7 B' B3 m1 \+ @" s
son for the child’s virilization. At that time, they3 N# d/ q$ \; q3 V3 t. i$ o
decided to put the baby in a separate bed, and the
# g; Y5 H' K9 Xfather was not hugging him with bare skin and had
  J# V8 T- s; q3 Ybeen using protective clothing. A repeat testosterone
$ r5 }3 Y! w( ^  Z0 g' ]test was ordered, but the family did not go to the: M/ ^+ j! u3 C  V8 z- s
laboratory to obtain the test.+ C7 I: X% V) C% _; d8 p$ X
Discussion9 r/ C8 z+ x1 Y+ Q' v0 A$ f
Precocious puberty in boys is defined as secondary
, E- b1 z8 ^/ c) F1 y: p1 s3 r6 Tsexual development before 9 years of age.1,43 g3 |! ]6 h& f: ~" F( B
Precocious puberty is termed as central (true) when1 i3 ?4 N" p  v* ]* A' r
it is caused by the premature activation of hypo-
% V3 o3 D; w3 q& Mthalamic pituitary gonadal axis. CPP is more com-5 z1 n6 ?8 |" m4 Q9 ^; r
mon in girls than in boys.1,3 Most boys with CPP+ c' e* X3 T9 z% r+ X
may have a central nervous system lesion that is! \7 ^+ ~) A" u: x# v% `
responsible for the early activation of the hypothal-
5 V3 Y1 M% ]- V) h& \! _$ yamic pituitary gonadal axis.1-3 Thus, greater empha-7 G7 v# Y3 W) S$ g# ]
sis has been given to neuroradiologic imaging in
9 h& y. K- M- u& b& c( }% ~7 fboys with precocious puberty. In addition to viril-
: r1 n$ B9 h$ j' Xization, the clinical hallmark of CPP is the symmet-
, Y, F, g# ]6 \  \+ P* {! T3 F3 `8 m3 orical testicular growth secondary to stimulation by
, N" y7 L1 d3 S. |gonadotropins.1,3* L6 _1 g/ E5 c- y
Gonadotropin-independent peripheral preco-
5 T) E& q% w1 v* }/ scious puberty in boys also results from inappropriate
3 t2 l# ]0 d% q$ @0 K- vandrogenic stimulation from either endogenous or
2 b- H- M" I( G2 I2 r4 B( Wexogenous sources, nonpituitary gonadotropin stim-
+ x! A% W8 k* m: pulation, and rare activating mutations.3 Virilizing5 F2 K# f0 S. J" O9 {( V5 z
congenital adrenal hyperplasia producing excessive, @0 E8 }  u1 {: m0 E; }1 r
adrenal androgens is a common cause of precocious) X8 V# ?: C" m& B" F
puberty in boys.3,4
# u- g- b3 T6 ~The most common form of congenital adrenal5 O4 X2 `3 }2 k. j
hyperplasia is the 21-hydroxylase enzyme deficiency.
( V8 q) z' M7 S8 ?The 11-β hydroxylase deficiency may also result in( c' F" j0 ]2 K
excessive adrenal androgen production, and rarely,% Z9 ^1 G" K& Y
an adrenal tumor may also cause adrenal androgen8 d6 A  l/ L: y1 G  A, J- d: Z
excess.1,3# [6 l( [0 _5 R1 g
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! k" h: R- t  w( B' B9 T/ q542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
6 j$ P7 Y0 \. \A unique entity of male-limited gonadotropin-8 A8 j1 h7 q; ?# l
independent precocious puberty, which is also known& N( @9 L: p) @0 c; @0 X: C
as testotoxicosis, may cause precocious puberty at a
+ s% M! |6 d$ q7 @  S& \  overy young age. The physical findings in these boys
/ n: v) Q, j7 _2 G( U; ewith this disorder are full pubertal development,$ H7 u* U% s/ z* D
including bilateral testicular growth, similar to boys
( g* |) e" X2 z! }: t# ?with CPP. The gonadotropin levels in this disorder
. H4 U) u3 e% y: I3 Bare suppressed to prepubertal levels and do not show
$ K; _4 n/ m, U8 P9 dpubertal response of gonadotropin after gonadotropin-7 P) Z; G" a3 R' U
releasing hormone stimulation. This is a sex-linked3 U3 v* N. [" t8 H0 K3 \9 N2 l1 E
autosomal dominant disorder that affects only& c% t  K' T8 {! ~% u
males; therefore, other male members of the family% O! r9 o$ ~' R" G* J* l! Z
may have similar precocious puberty.3/ G* o$ N4 C7 @0 e
In our patient, physical examination was incon-
* |8 L# G1 r% c7 u$ x. `" rsistent with true precocious puberty since his testi-
$ a1 ]% e$ N# c- n4 g" `: ~4 z8 ~* Dcles were prepubertal in size. However, testotoxicosis
; @2 X: r7 U8 f+ j( t; P" Rwas in the differential diagnosis because his father
1 C1 u+ T% f" A% W9 hstarted puberty somewhat early, and occasionally,
+ f$ H  X. Z" E) v6 h0 w4 Ytesticular enlargement is not that evident in the
7 v5 |' x& U) `" R  ~% J" Ibeginning of this process.1 In the absence of a neg-
8 v7 F4 l( o. M9 n" @% Fative initial history of androgen exposure, our3 E# v1 w/ E4 o
biggest concern was virilizing adrenal hyperplasia,6 a3 j" {* X/ S
either 21-hydroxylase deficiency or 11-β hydroxylase1 ^# z; E+ v* ^5 ^$ c4 H
deficiency. Those diagnoses were excluded by find-
9 Q( w9 t7 F. Q0 u# C5 Ting the normal level of adrenal steroids.
# k9 D" ^) B$ \* nThe diagnosis of exogenous androgens was strongly
& q. V: |* H, A9 I8 qsuspected in a follow-up visit after 4 months because4 ^+ u; L5 M' p- T& ]: ]4 B6 L  j, `
the physical examination revealed the complete disap-
! z9 D( ~* l2 A+ N. g" epearance of pubic hair, normal growth velocity, and& \8 ~6 g' `, o1 T0 ]: R3 o
decreased erections. The father admitted using a testos-! X4 b) p2 L( z
terone gel, which he concealed at first visit. He was
5 k, b6 @* @7 p# t( D9 r- Zusing it rather frequently, twice a day. The Physicians’/ ?2 r( d+ D# s4 c- w6 V3 s
Desk Reference, or package insert of this product, gel or
$ D3 W) V6 e& \  r1 y' kcream, cautions about dermal testosterone transfer to
3 j0 ?$ E/ F5 c' _( }6 o0 Aunprotected females through direct skin exposure.8 l7 V8 ?, A% A7 f! I5 c
Serum testosterone level was found to be 2 times the
: `+ X3 z2 {) h. A5 `: x$ h" C$ Qbaseline value in those females who were exposed to- J2 n7 B/ x$ a0 L+ y7 K( ]
even 15 minutes of direct skin contact with their male
+ A5 O9 m5 ?7 W; H, H. cpartners.6 However, when a shirt covered the applica-. C2 V9 X$ w" d3 f( ]9 F: M6 ?- r: K
tion site, this testosterone transfer was prevented.
& J( t! F3 @+ a" ]Our patient’s testosterone level was 60 ng/mL,; }3 x3 I# u3 J( |6 H, k" u6 B$ w
which was clearly high. Some studies suggest that' G- V# D/ z* G: {) X
dermal conversion of testosterone to dihydrotestos-5 a. {  v. F- H+ a5 g( v5 g8 z
terone, which is a more potent metabolite, is more
; ~0 ]6 X" s6 Y. T) i9 w; Oactive in young children exposed to testosterone  y8 a/ q/ b$ Z- l7 a! K( |
exogenously7; however, we did not measure a dihy-
# K; ^1 h  J  y, l! Pdrotestosterone level in our patient. In addition to
+ v$ U; [( G. u! ?virilization, exposure to exogenous testosterone in9 j6 Q8 C# A* x& [- E1 L8 M3 B- f
children results in an increase in growth velocity and
% |& L" {2 X5 U& Hadvanced bone age, as seen in our patient.. e5 \# }! q) X, o2 c
The long-term effect of androgen exposure during
1 ?4 {+ z) q* B' J9 c: R/ {early childhood on pubertal development and final* [# X: T) P+ v7 S2 @- O
adult height are not fully known and always remain3 D+ ]: G/ J1 Q6 Z' h
a concern. Children treated with short-term testos-7 b# ~: `2 r+ `) H' I3 E
terone injection or topical androgen may exhibit some6 \. E; X2 @) o9 j! N3 C& M
acceleration of the skeletal maturation; however, after
) I( ~$ s, ~# Q2 w0 Dcessation of treatment, the rate of bone maturation2 K' }# x0 w6 m5 t
decelerates and gradually returns to normal.8,9/ F( c: A3 w- S* _$ @* v
There are conflicting reports and controversy7 ^! t3 r: L0 i
over the effect of early androgen exposure on adult
% m! G; i; m, l  d3 V9 w! V: lpenile length.10,11 Some reports suggest subnormal
, h- _7 D) j: j) ^1 Cadult penile length, apparently because of downreg-
- ^8 K9 ?! s$ z. G! z8 ?ulation of androgen receptor number.10,12 However," v3 U) Y5 J3 a" B- F! [
Sutherland et al13 did not find a correlation between
6 x$ h7 O' H5 Jchildhood testosterone exposure and reduced adult8 g3 ^/ Z! t* j/ X( g
penile length in clinical studies.4 y  J5 f" I9 }+ i+ l8 S
Nonetheless, we do not believe our patient is
" C& F9 x! a7 _1 H$ k# @) ?/ Jgoing to experience any of the untoward effects from
5 z  c& f- V& K' `9 Ntestosterone exposure as mentioned earlier because
1 T% z9 d3 D8 tthe exposure was not for a prolonged period of time.; {# @2 I* k* t. ^
Although the bone age was advanced at the time of
. \. c/ O+ A8 h* ]$ odiagnosis, the child had a normal growth velocity at
2 @1 D; M3 I9 Xthe follow-up visit. It is hoped that his final adult) }/ ]8 B: e$ _) n! A
height will not be affected.
$ F! |" p! D9 ~8 @Although rarely reported, the widespread avail-
; V0 g4 o0 g! g9 oability of androgen products in our society may* B& f. _7 h3 H% H
indeed cause more virilization in male or female( k, B* y9 _  u/ u! V" @/ M/ W1 L; Z, @
children than one would realize. Exposure to andro-
6 m% P4 |  R8 C- ]  K1 Dgen products must be considered and specific ques-
+ O3 x, ]6 N5 |! e% p+ F0 c# etioning about the use of a testosterone product or
+ M7 s6 B- z- o+ ~  J! P0 Z& kgel should be asked of the family members during6 A: Z; D, G! ~& W4 d, W
the evaluation of any children who present with vir-
) v! g- N8 `3 {2 v& y! U9 {ilization or peripheral precocious puberty. The diag-! w- K# _' h8 c0 x# I6 t
nosis can be established by just a few tests and by; a  l, v/ [. d
appropriate history. The inability to obtain such a' t) k& K0 |5 K5 l
history, or failure to ask the specific questions, may9 U$ h1 {. V% \0 H
result in extensive, unnecessary, and expensive
# r. t; M# q6 v/ S$ L; einvestigation. The primary care physician should be
6 s6 R" c: [. G) t# a; B+ f9 Eaware of this fact, because most of these children& b9 v: H6 N" V; c6 U
may initially present in their practice. The Physicians’
! |1 K$ P5 {# p: VDesk Reference and package insert should also put a
, J% U: d2 d9 ]  a6 twarning about the virilizing effect on a male or! @% L" _* p( Z( k7 R
female child who might come in contact with some-
3 m0 M% J3 i: t2 E. T+ \) Aone using any of these products.
/ q0 z5 n. c7 J! [* r+ t1 SReferences: g& X' c" x5 |5 r
1. Styne DM. The testes: disorder of sexual differentiation' {1 K) c% h/ X
and puberty in the male. In: Sperling MA, ed. Pediatric2 f9 }- q" ]" S& Q
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
5 w) e/ M% M, m. r" M8 K# l* A& u+ ~5 o2002: 565-628.8 M0 l/ V2 t. l, M
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
0 G9 c, q5 s! F2 V- w+ npuberty 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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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

3 |# [& i2 e$ n4 O( E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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