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Sexual Precocity in a 16-Month-Old
. B1 Z( ~( V8 o( {Boy Induced by Indirect Topical
3 b% f: ~' W; kExposure to Testosterone
8 d  @% {6 U0 u# g: NSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2& x; I" ~" X* a6 \# ^( |# x
and Kenneth R. Rettig, MD1
2 p6 ]4 C' @$ `$ w# y, A% y6 rClinical Pediatrics2 F' H( @( D3 |/ ]# a: |
Volume 46 Number 6
% O2 ]: V8 t; n* F" o6 nJuly 2007 540-543
$ B8 s: Z" K! d4 z1 R© 2007 Sage Publications
3 }! o6 @  M2 \! w2 d10.1177/0009922806296651
3 `; Q5 v5 j, m0 zhttp://clp.sagepub.com8 D5 z- C+ R2 [  {
hosted at
4 N/ \5 ], k5 [2 N9 chttp://online.sagepub.com
7 ]& v# g+ C5 _5 Q  ~# xPrecocious puberty in boys, central or peripheral,9 I7 q6 ^! w! y8 x8 V
is a significant concern for physicians. Central
4 C' V# V, e$ B* m* q  K6 x" Eprecocious puberty (CPP), which is mediated
) e) e; j5 j# a: Z9 uthrough the hypothalamic pituitary gonadal axis, has" r% |* ]6 U' U5 E
a higher incidence of organic central nervous system
4 b# O2 M1 X' ?( U8 a2 Jlesions in boys.1,2 Virilization in boys, as manifested
/ J( U( U: m' j8 d5 Eby enlargement of the penis, development of pubic
' j  K" B; a0 A% c1 _& |5 F$ `; F: vhair, and facial acne without enlargement of testi-
8 x# v$ ?7 o$ z7 c$ V, S. d) s+ F0 S- _cles, suggests peripheral or pseudopuberty.1-3 We
, s: T8 H) {* l8 O* W  |: Creport a 16-month-old boy who presented with the0 w' F8 C* e. e  ?8 F/ k9 U
enlargement of the phallus and pubic hair develop-
5 \. Q# d6 u6 t, j3 J/ Fment without testicular enlargement, which was due9 k6 D8 ?1 p6 m$ m  Y
to the unintentional exposure to androgen gel used by
* y3 Y3 d0 s& v9 uthe father. The family initially concealed this infor-
7 d' h5 y& h9 }( Xmation, resulting in an extensive work-up for this
7 O: [  F* Y, q& H% I! g, gchild. Given the widespread and easy availability of
( S6 a1 \* `5 p0 ^9 y! A6 Atestosterone gel and cream, we believe this is proba-
$ [+ |4 |# w* W9 B/ ?: N7 ^: sbly more common than the rare case report in the) M' v$ d/ p3 s5 j
literature.4
1 p& v* B1 j8 t: V+ N7 \& T+ fPatient Report
+ W) U& Y5 K1 P/ `3 z( J: EA 16-month-old white child was referred to the: z; m8 c9 W) Q' k% p. @4 A/ S$ |; a
endocrine clinic by his pediatrician with the concern1 [! [% S' o% c" ?9 R9 R
of early sexual development. His mother noticed
3 m3 ]3 n# H0 E' b8 R; r  alight colored pubic hair development when he was
( q1 ~6 T7 C8 t& R5 ^. m" BFrom the 1Division of Pediatric Endocrinology, 2University of9 D' `) N0 r' O4 N+ s7 s* q8 v1 D& k
South Alabama Medical Center, Mobile, Alabama.
: |6 F" F' p$ F# Q0 C+ W8 \" NAddress correspondence to: Samar K. Bhowmick, MD, FACE,: X) U3 h$ r& D/ t
Professor of Pediatrics, University of South Alabama, College of
  E2 e" E4 X; x8 u* I6 J) L. ?$ [Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;) \5 P& D5 v- F  z
e-mail: [email protected].( i* D) [. b, P! K5 l
about 6 to 7 months old, which progressively became$ _. {' b; J* \; s5 t
darker. She was also concerned about the enlarge-, M! I( d' U$ E8 B
ment of his penis and frequent erections. The child" X3 d5 f# s# C1 o0 x+ N
was the product of a full-term normal delivery, with
# _" R. A: e  X' J3 Ha birth weight of 7 lb 14 oz, and birth length of+ f9 j- m& E* `' ^. z& _6 [. Y
20 inches. He was breast-fed throughout the first year  m# \6 x5 I  y8 A9 d2 y2 r8 S% {1 n
of life and was still receiving breast milk along with  @9 U2 P, U( T7 A
solid food. He had no hospitalizations or surgery,: T# }5 \4 C! q
and his psychosocial and psychomotor development6 ^. N9 I/ m+ y0 {0 `
was age appropriate.1 n! W4 @/ X+ A
The family history was remarkable for the father,
& L$ d. G# X5 P" m: bwho was diagnosed with hypothyroidism at age 16,
' I7 D' t2 l/ }& Ywhich was treated with thyroxine. The father’s! A' }" j2 S  @6 p# B; N& ~
height was 6 feet, and he went through a somewhat, k% F: `* J! P7 c( r$ |
early puberty and had stopped growing by age 14.9 A* c# Y0 P$ P1 N
The father denied taking any other medication. The/ x- B+ t( [- W) p2 g
child’s mother was in good health. Her menarche
2 ?) `3 y. d9 \" I# d+ G7 i9 X- Mwas at 11 years of age, and her height was at 5 feet
! ^, s: c" T* @* u8 C/ t/ i5 inches. There was no other family history of pre-
# Z- t8 `; n' C4 mcocious sexual development in the first-degree rela-
- K) M# Y- i! ]% o2 ptives. There were no siblings./ A7 N+ O( m( v! a" A6 ?
Physical Examination
/ z0 z3 \& o$ r6 }The physical examination revealed a very active,1 Z) v0 p  p- b; D1 v' C
playful, and healthy boy. The vital signs documented: o9 A! N" @( ]+ f4 b' @1 O
a blood pressure of 85/50 mm Hg, his length was) R5 p; S( ^) ^) p
90 cm (>97th percentile), and his weight was 14.4 kg
' \7 A/ }( y; L, k9 \# t& E(also >97th percentile). The observed yearly growth
5 y5 y9 v& J3 y7 Qvelocity was 30 cm (12 inches). The examination of
% t( @9 A" k9 Wthe neck revealed no thyroid enlargement.( M' ]& }4 K1 L. N) @9 J
The genitourinary examination was remarkable for
5 c' c, ]' R( q# Q6 nenlargement of the penis, with a stretched length of
2 p5 @1 z" c4 x' a& ?- M# h2 S3 S8 }8 cm and a width of 2 cm. The glans penis was very well) m: @: s6 u' o$ P8 B  Q& s% a
developed. The pubic hair was Tanner II, mostly around% G2 ?+ D1 q" q4 D; E6 j- `
540
) ^1 y1 t3 f4 a- z$ f+ `at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 _+ A9 O7 r% F* n! m% U% Ythe base of the phallus and was dark and curled. The
9 A9 @- c$ f! [# T$ L: h8 K  vtesticular volume was prepubertal at 2 mL each.- `* H! N+ @- Z2 d0 `- W
The skin was moist and smooth and somewhat
# m5 B9 u' y: V) g+ D( Uoily. No axillary hair was noted. There were no1 B6 {/ |/ `& G- \. K4 P  E" Y+ j6 A
abnormal skin pigmentations or café-au-lait spots.
. m7 n8 W% @1 KNeurologic evaluation showed deep tendon reflex 2+
4 s; f, h8 u' i: Y' T* i  kbilateral and symmetrical. There was no suggestion, r$ z* t& b- V/ |4 T' ?
of papilledema.* K0 k5 \5 n# W/ Z# o
Laboratory Evaluation; a( @0 q$ X1 w& V) X" w
The bone age was consistent with 28 months by
) d) {8 b5 L+ iusing the standard of Greulich and Pyle at a chrono-
6 u/ v7 r% [8 O+ Nlogic age of 16 months (advanced).5 Chromosomal
) C% E4 E0 q- j) ]1 F  L8 Fkaryotype was 46XY. The thyroid function test6 \$ V' }, J) A5 k+ F
showed a free T4 of 1.69 ng/dL, and thyroid stimu-, f# p! Z/ p0 J, i7 l
lating hormone level was 1.3 µIU/mL (both normal).. M9 k4 Y! I- G+ Q+ q& R3 W/ B0 i
The concentrations of serum electrolytes, blood7 S+ ~+ R# a( D( A
urea nitrogen, creatinine, and calcium all were
; g3 i: y- ?% J' U8 h1 u4 }, y/ Uwithin normal range for his age. The concentration
& `# K$ t$ E, b$ n) }of serum 17-hydroxyprogesterone was 16 ng/dL
! K1 G" a" W. M' q(normal, 3 to 90 ng/dL), androstenedione was 20
8 q& Z4 j8 M7 G6 {) wng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
$ T8 ]' E- s2 a4 O" \5 tterone was 38 ng/dL (normal, 50 to 760 ng/dL),
' U; T( [5 w6 n* Zdesoxycorticosterone was 4.3 ng/dL (normal, 7 to' V, v$ d8 t; a1 b$ O$ z! w
49ng/dL), 11-desoxycortisol (specific compound S)$ j1 W" g9 L+ G
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-0 T6 R- k9 D* m$ y
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
! s  w& i, s, T3 }& \4 {testosterone was 60 ng/dL (normal <3 to 10 ng/dL),, h3 _& L' s3 q! u
and β-human chorionic gonadotropin was less than( x- @* @% c& y; E8 Q% i: P% E
5 mIU/mL (normal <5 mIU/mL). Serum follicular
. [6 ^, \- b8 X4 kstimulating hormone and leuteinizing hormone
& l3 S) e5 @3 O9 F6 v" vconcentrations were less than 0.05 mIU/mL1 M, N& W  Z8 I2 E; I
(prepubertal).
/ T& F/ M$ h1 h9 xThe parents were notified about the laboratory0 ~& ~4 s# Y8 ^# B  W* O: r
results and were informed that all of the tests were; [9 X* b: S# P
normal except the testosterone level was high. The
8 `  ~) h0 x. O: l" E$ Bfollow-up visit was arranged within a few weeks to
$ \: D8 p$ E. Q: [. l4 fobtain testicular and abdominal sonograms; how-
$ m0 w. ]" V+ a) `ever, the family did not return for 4 months.
6 b. I  M: @# ]5 Z" [; T+ uPhysical examination at this time revealed that the* L$ m9 N. D8 `' K
child had grown 2.5 cm in 4 months and had gained3 O" Y/ V+ g' ~( M# u0 \
2 kg of weight. Physical examination remained+ P3 |) v* n7 C4 _& l" Q) t* k" U* F
unchanged. Surprisingly, the pubic hair almost com-
) \* b2 U2 w0 s, u) r1 {1 R- P; e% ~7 cpletely disappeared except for a few vellous hairs at+ c- e  X. z, p2 |6 F8 U( Q  }. D
the base of the phallus. Testicular volume was still 2" G; {6 V" k1 q' {
mL, and the size of the penis remained unchanged.
+ o! i2 ?' Q; z7 i# @: SThe mother also said that the boy was no longer hav-
1 n! a8 G# j/ K2 M+ s1 I/ |ing frequent erections.: @& C7 o1 N9 J3 a0 w
Both parents were again questioned about use of7 w$ Q' D; V/ Y2 |+ T
any ointment/creams that they may have applied to
5 d1 K) Z: p" W& j' |+ Ethe child’s skin. This time the father admitted the
8 h$ _( `" n+ o* B5 g$ L% `0 QTopical Testosterone Exposure / Bhowmick et al 541% `3 C8 a' q# N# J% p3 l3 b  {
use of testosterone gel twice daily that he was apply-
4 ]+ L: _# U* R# g9 Jing over his own shoulders, chest, and back area for
7 R8 o2 ~! t) B! ]" U  ma year. The father also revealed he was embarrassed7 r0 ~/ v, E' J( ^2 t- w3 f4 o
to disclose that he was using a testosterone gel pre-& |* T3 J$ H( N' I( S3 I7 i/ r
scribed by his family physician for decreased libido
, ]( F. ?9 A# Z9 u3 Z4 N7 l* Osecondary to depression.1 x0 W5 U, z$ t; W
The child slept in the same bed with parents.  @9 C' s9 W3 Y* M% q( A0 L. j$ M
The father would hug the baby and hold him on his
8 p6 f1 s: `6 x% j' ]! O' Jchest for a considerable period of time, causing sig-
+ T" d) g- [% j/ Z9 s/ qnificant bare skin contact between baby and father.
& C/ M" A7 s# u+ XThe father also admitted that after the phone call,
' |7 D, U* V" g: l6 A; q. P! Swhen he learned the testosterone level in the baby/ X/ F2 ]. d: L
was high, he then read the product information
! y: U4 k8 b4 a/ k- g3 K( Qpacket and concluded that it was most likely the rea-- w  d! u  P* C5 p1 r
son for the child’s virilization. At that time, they/ q5 q1 F3 X* }' O
decided to put the baby in a separate bed, and the
2 [# R( e) X* Q, R$ Y! j0 kfather was not hugging him with bare skin and had5 Z$ ]. g$ g7 L/ j2 ~; H
been using protective clothing. A repeat testosterone
( b% s' T0 y# r* A# Z2 Btest was ordered, but the family did not go to the2 L% P* Q$ P8 b3 t
laboratory to obtain the test.4 k  M8 M" a8 k* l9 y, z
Discussion) W. V; q9 v6 d; ]* z
Precocious puberty in boys is defined as secondary
  c9 M' Z* Z/ U+ f, N- Usexual development before 9 years of age.1,4* q1 A2 P1 [" i1 G
Precocious puberty is termed as central (true) when
; N- f/ s; {0 D0 m, _' H( Uit is caused by the premature activation of hypo-
4 t  s2 Q. D' H/ D7 u, W9 ]thalamic pituitary gonadal axis. CPP is more com-
9 F4 c; w: M/ F% a5 [* o2 P1 H' B+ umon in girls than in boys.1,3 Most boys with CPP- Y4 e- q! R) a0 Z; K! m
may have a central nervous system lesion that is
' e4 q. ~$ K3 _2 S4 P7 g/ Eresponsible for the early activation of the hypothal-2 n1 }4 A8 x% c+ \$ m: P" n( }
amic pituitary gonadal axis.1-3 Thus, greater empha-
4 R7 w1 R& i$ E+ X* {9 Usis has been given to neuroradiologic imaging in
7 h! q( @6 O3 Q/ z& b. _& r  Jboys with precocious puberty. In addition to viril-" ]+ j7 h4 ?& z. V* c
ization, the clinical hallmark of CPP is the symmet-, P, D& T' d3 S; r! \4 n
rical testicular growth secondary to stimulation by' u. ]% w3 a" y4 i% J
gonadotropins.1,3+ r% k8 U$ @8 [2 N
Gonadotropin-independent peripheral preco-
6 H+ _  {2 L/ Q' z* W; d( Y, ucious puberty in boys also results from inappropriate0 q" D$ L  l' P7 ~' Q
androgenic stimulation from either endogenous or, n4 v* Z: b' V
exogenous sources, nonpituitary gonadotropin stim-% G' S0 X9 x# C, }2 ~+ z
ulation, and rare activating mutations.3 Virilizing
% l0 U2 H9 x- B. z# ^2 t* ^( scongenital adrenal hyperplasia producing excessive/ u$ w6 Y: |% l
adrenal androgens is a common cause of precocious
+ I4 x# }# W& V+ D7 Xpuberty in boys.3,4
0 W- r2 _2 l% }$ M  dThe most common form of congenital adrenal) H- q% B, y7 W+ z
hyperplasia is the 21-hydroxylase enzyme deficiency.' i6 C" J- f- x$ U
The 11-β hydroxylase deficiency may also result in
" @  h* Y# s+ P  v, Sexcessive adrenal androgen production, and rarely,
) }% Z: ]4 p1 i6 \8 y1 ian adrenal tumor may also cause adrenal androgen
0 i# Y/ ^& v4 Q$ l; w2 [# Nexcess.1,39 x) _& `5 Q+ j2 O& l4 J- B
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* T' A: l8 Q/ k9 Y0 Y542 Clinical Pediatrics / Vol. 46, No. 6, July 20074 _$ S9 H) B* W- M" y: |
A unique entity of male-limited gonadotropin-
+ {+ E* z4 k2 s; ^4 p# Gindependent precocious puberty, which is also known# o+ O. A% u/ h9 E
as testotoxicosis, may cause precocious puberty at a1 M% A/ i& T0 ^
very young age. The physical findings in these boys
5 j) {+ W' `8 v9 e* D6 Owith this disorder are full pubertal development,; z) x- D0 ^- _8 D! z
including bilateral testicular growth, similar to boys
1 |2 W  q  W! y) m- {0 F0 A, u: C8 wwith CPP. The gonadotropin levels in this disorder: E; r" o( g! i# D3 U* a. \
are suppressed to prepubertal levels and do not show
2 d7 x6 f% a% g5 x7 U* wpubertal response of gonadotropin after gonadotropin-$ r( e; A: F. H4 q6 b3 U4 i
releasing hormone stimulation. This is a sex-linked! d# \+ u) ~" O1 ]& p8 U  k/ ]
autosomal dominant disorder that affects only
! [+ d' }% T# {  l# }+ ~4 dmales; therefore, other male members of the family. a: Y" ]! ], N' y; N; @
may have similar precocious puberty.3( m' ?5 W3 z$ b( v* \! e7 B( e
In our patient, physical examination was incon-6 a  C; O  |* L: v5 C
sistent with true precocious puberty since his testi-3 n! ^/ N) k: @) {
cles were prepubertal in size. However, testotoxicosis$ g5 _! W; z. Y+ u1 ?: o
was in the differential diagnosis because his father
/ K2 B/ A, Z- D9 jstarted puberty somewhat early, and occasionally,
$ m3 H  Q1 t6 `; e3 `) U; k) jtesticular enlargement is not that evident in the
0 H5 c: j$ @. d( _8 p& J" Nbeginning of this process.1 In the absence of a neg-
7 A9 Y5 N! k$ A4 m) y) e6 `ative initial history of androgen exposure, our
5 q6 c; @0 G& Hbiggest concern was virilizing adrenal hyperplasia,
- K% F* P- H4 [: {5 Ceither 21-hydroxylase deficiency or 11-β hydroxylase2 S7 `0 R# d) L! m
deficiency. Those diagnoses were excluded by find-
) y9 V4 P; J/ }  V6 S2 hing the normal level of adrenal steroids.
: }2 [$ T4 X3 w$ zThe diagnosis of exogenous androgens was strongly
8 m  j; W' M+ v  ?3 u" ksuspected in a follow-up visit after 4 months because: D' i6 ~6 C( ^! o3 d
the physical examination revealed the complete disap-! i' G: c4 K% M& K
pearance of pubic hair, normal growth velocity, and
. K8 S" |0 V4 T  I3 W+ \decreased erections. The father admitted using a testos-' F- `# ?: L0 I% N* g6 w) {
terone gel, which he concealed at first visit. He was
% C- w4 j6 T% y' }! ]- ausing it rather frequently, twice a day. The Physicians’3 k6 {, d3 W* `9 y9 X4 p
Desk Reference, or package insert of this product, gel or
' G3 _- j' ~  M0 n: V3 Xcream, cautions about dermal testosterone transfer to  q* `% M5 b$ D
unprotected females through direct skin exposure.
1 f. D. l1 A1 A1 [, q* h# M  lSerum testosterone level was found to be 2 times the
& y- e7 F6 ^) ^2 X* ~baseline value in those females who were exposed to
- h7 u' H, z; R2 ], z# [even 15 minutes of direct skin contact with their male
6 h1 c7 d7 r" `& |" v$ Lpartners.6 However, when a shirt covered the applica-
6 e+ Y, t9 m# e! btion site, this testosterone transfer was prevented.
9 i( V& r. g' U: h+ d0 ^8 i1 HOur patient’s testosterone level was 60 ng/mL,. q  b3 m' j8 X
which was clearly high. Some studies suggest that
6 a1 ?; p% V; I, rdermal conversion of testosterone to dihydrotestos-, M& l1 p+ y6 T  K- [/ O
terone, which is a more potent metabolite, is more3 O7 C; g" R" g; }+ t
active in young children exposed to testosterone7 C8 r$ j! u( [+ z# d
exogenously7; however, we did not measure a dihy-
% W  _4 a; `% c" odrotestosterone level in our patient. In addition to
7 M5 D9 e5 t1 H$ G% Y! ~9 Gvirilization, exposure to exogenous testosterone in
+ W( \6 u* i0 ochildren results in an increase in growth velocity and
8 f: B8 ?  m0 R7 W# ~advanced bone age, as seen in our patient.
$ w4 ^3 \* C6 Y" W7 WThe long-term effect of androgen exposure during# a- g& O' X. T; b3 @
early childhood on pubertal development and final
; @* q2 E2 e- t( fadult height are not fully known and always remain
; R! j2 w; m% x# Oa concern. Children treated with short-term testos-
  _2 u0 i: i6 ?6 m" d3 c$ bterone injection or topical androgen may exhibit some1 `/ |& D" y& {, l* K  A
acceleration of the skeletal maturation; however, after/ N7 l! }3 V- |. J1 e2 g
cessation of treatment, the rate of bone maturation3 v! U( x+ t# D
decelerates and gradually returns to normal.8,9# S" {9 g+ B: a, r" e
There are conflicting reports and controversy
3 M1 i  d+ T5 Y2 Jover the effect of early androgen exposure on adult9 w5 ~# v5 p& U9 {+ S& E
penile length.10,11 Some reports suggest subnormal
  A' w3 y! S8 madult penile length, apparently because of downreg-* B' A. t4 \' I. Q
ulation of androgen receptor number.10,12 However,( D6 B3 X3 t2 M5 v2 r. z9 `
Sutherland et al13 did not find a correlation between
1 I7 l5 N- ~3 f; E7 g0 M2 mchildhood testosterone exposure and reduced adult
, q8 H% j  L0 R6 P2 l6 F- ]penile length in clinical studies.
& u, r1 `$ v3 T' V  vNonetheless, we do not believe our patient is+ e0 u) X4 }( w
going to experience any of the untoward effects from
7 J* ]$ }5 a+ o# w8 ]6 w# btestosterone exposure as mentioned earlier because+ ^* \6 p$ z+ X5 C$ r6 H
the exposure was not for a prolonged period of time.
+ w. n7 b. I( F5 S* {. J$ jAlthough the bone age was advanced at the time of
- ?- ]# D# v9 R+ a7 O# F/ U+ `diagnosis, the child had a normal growth velocity at0 l3 A. E7 {3 R/ U2 p8 ^  W$ S
the follow-up visit. It is hoped that his final adult5 ^4 O0 ?& n0 f# n1 T
height will not be affected.# k3 a3 B" F; _9 T8 k1 D" i
Although rarely reported, the widespread avail-
' w: E' A, U# M' R; fability of androgen products in our society may6 f8 e4 {9 r$ R! C7 ^& e
indeed cause more virilization in male or female' f% z- n: b- @' n9 v" f4 b- Y$ R; t0 _& H
children than one would realize. Exposure to andro-0 O6 h* h5 C+ v) j6 t. m
gen products must be considered and specific ques-/ B9 k  p. S/ A) O) _
tioning about the use of a testosterone product or' _+ k; d/ @& m* O; _8 t! b% E0 d
gel should be asked of the family members during
! o! U# [* A0 l$ f4 ^6 n: S! _! |the evaluation of any children who present with vir-8 a, Z, ^. z7 X9 G" F
ilization or peripheral precocious puberty. The diag-% Q9 z/ I* N- V  t4 c# M- a3 `# ]6 b
nosis can be established by just a few tests and by$ ]% \5 M9 }0 U8 |6 A4 H$ f8 N* n6 V
appropriate history. The inability to obtain such a- z/ j% ]; ]+ x# p! O
history, or failure to ask the specific questions, may2 P! m" ?" Y7 F% |0 l- [4 s
result in extensive, unnecessary, and expensive6 b5 \; X7 p  W. U, ?; t
investigation. The primary care physician should be
) \6 h; @8 A* Q$ p  Vaware of this fact, because most of these children/ P* a! P3 Z- G6 M6 z
may initially present in their practice. The Physicians’8 B( B+ A- m. v* R# \
Desk Reference and package insert should also put a9 A5 b$ k& _4 o. K
warning about the virilizing effect on a male or; [5 o6 F6 B* k6 z, B% ^6 j& @
female child who might come in contact with some-
+ [  l# u+ Q7 \8 K3 o9 z! T( ^. Yone using any of these products.- B4 c8 u1 M  Q9 }$ S- e
References
8 n/ {8 [1 o- {0 {6 q1. Styne DM. The testes: disorder of sexual differentiation* H& b! v* F1 e# ~
and puberty in the male. In: Sperling MA, ed. Pediatric  a# I, k) s; B8 v& C) N' T
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
  `+ U: k5 t; \) r! \+ E( _  P% X2002: 565-628.+ [1 s, u( o- \. y" W! h
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious( ?7 B! d$ J% Y7 Q0 C$ D" X! i
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old  Z9 O% d: l9 a8 G! i4 k
Boy Induced by Indirect Topical# h; Z: _- I( r1 Y' u
Exposure to Testosterone% r, h" O  h; S0 i+ E# K& E- _
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
0 W) z$ p! R$ e8 pand Kenneth R. Rettig, MD1
( `$ n2 g3 t4 }& x  M! fClinical Pediatrics
! h% C' a3 v6 p  ^Volume 46 Number 6
, W/ u7 G3 }  |, @July 2007 540-543
) S! u% M# `( m" m& R© 2007 Sage Publications
# ?% }- A8 M0 F. Y10.1177/0009922806296651+ m1 i0 q% ~' j. U) Z
http://clp.sagepub.com& D0 h4 a+ `5 d7 T& I. P8 f
hosted at
# Q# j: ^* f. m; lhttp://online.sagepub.com0 x1 P% [" T0 g( C# z
Precocious puberty in boys, central or peripheral,
! B* ]# V( _. l. J$ W/ N6 b2 Dis a significant concern for physicians. Central
3 h' c8 f' F( s9 o4 rprecocious puberty (CPP), which is mediated
" x6 t6 o7 _' C5 Y3 qthrough the hypothalamic pituitary gonadal axis, has
8 [) X3 k. o; Y6 {" _) ga higher incidence of organic central nervous system
8 G3 i! `0 ~" N, D, olesions in boys.1,2 Virilization in boys, as manifested: G9 [/ [9 b3 b9 ]2 w
by enlargement of the penis, development of pubic
1 Y/ P% S/ g$ U! R9 ^0 y$ Ihair, and facial acne without enlargement of testi-
+ [* R# }4 N( K# f/ A+ g% E6 n( Qcles, suggests peripheral or pseudopuberty.1-3 We. _( ?  i/ U+ r( w7 q6 O; f7 N
report a 16-month-old boy who presented with the
2 I* P( ?+ P5 \9 e( u2 l4 g% kenlargement of the phallus and pubic hair develop-0 w" H% C" f3 w. B+ d% P1 |
ment without testicular enlargement, which was due1 Y) \" W' P5 V% F/ k
to the unintentional exposure to androgen gel used by# Z! R8 p, f7 ?$ u
the father. The family initially concealed this infor-
# t* q  A2 l3 m% C, p& tmation, resulting in an extensive work-up for this
# C* X' V7 D* S' g6 }child. Given the widespread and easy availability of7 g: U$ J/ W1 ~0 i" r- `: }
testosterone gel and cream, we believe this is proba-
# I" O: K* f& H7 e7 qbly more common than the rare case report in the
8 A/ s- R5 C3 j/ u. yliterature.4
+ o/ D$ A$ v# a* N6 e$ H; YPatient Report
' ?8 s& ?2 Q: H# F; cA 16-month-old white child was referred to the8 |- y" p9 e7 d9 F) |# O
endocrine clinic by his pediatrician with the concern% d7 o5 @1 r& q  N/ j/ B& b. g  [
of early sexual development. His mother noticed2 q( A7 P- H3 v
light colored pubic hair development when he was+ F4 I5 e: F( O: \( k) }; B- e
From the 1Division of Pediatric Endocrinology, 2University of+ {7 \/ A$ R) t6 E, D* R- z5 l
South Alabama Medical Center, Mobile, Alabama.! D4 X0 ]; a- I# j( t( R  [
Address correspondence to: Samar K. Bhowmick, MD, FACE,3 G8 l$ H& P9 F4 C
Professor of Pediatrics, University of South Alabama, College of
$ _% R' _) s' Y' u% {% GMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;! h" D" [# Z* }- ]5 N% a7 s
e-mail: [email protected].$ y$ r8 u3 I5 m
about 6 to 7 months old, which progressively became4 H' h, U* v! l. b+ @
darker. She was also concerned about the enlarge-
+ X2 F& F2 ?7 A% x+ L! R, ^, V! }ment of his penis and frequent erections. The child
. x7 v) m" u9 w  Q/ L! R4 dwas the product of a full-term normal delivery, with
( y# q$ |% k5 Xa birth weight of 7 lb 14 oz, and birth length of
$ c+ r4 N6 x" g; U* A20 inches. He was breast-fed throughout the first year
( a5 v* f$ [, T% o9 N0 m$ E" N( Eof life and was still receiving breast milk along with
/ N% A! W9 i$ k5 y( jsolid food. He had no hospitalizations or surgery," H8 y9 Y. p3 s/ i. g
and his psychosocial and psychomotor development
6 e; C/ V& ~# Z9 u, x# ~' \was age appropriate.* v  D; P# O+ P1 T
The family history was remarkable for the father,
0 u& x' A7 F1 B3 Iwho was diagnosed with hypothyroidism at age 16,- M' v( X# N# v: ^2 _) ?! A
which was treated with thyroxine. The father’s/ a  M1 T4 N4 Z8 W7 L4 b
height was 6 feet, and he went through a somewhat0 O2 K# u  G' M# z
early puberty and had stopped growing by age 14.
- {0 C& T( T6 iThe father denied taking any other medication. The3 v1 b  `9 c5 n, R: t6 V; P5 }, }
child’s mother was in good health. Her menarche: t4 o7 i$ x3 c/ ?* M
was at 11 years of age, and her height was at 5 feet2 F( E% q- @& ^/ i% w4 S$ O: E
5 inches. There was no other family history of pre-
6 \! w$ N4 e; s6 ^8 k  Wcocious sexual development in the first-degree rela-
* P' Y1 s" m8 n- Atives. There were no siblings.) R# n, g9 J9 e* M- f7 m: l* O
Physical Examination
, H1 H# B" c0 @. _% XThe physical examination revealed a very active,
' e6 Y) G$ r9 p: q# w% aplayful, and healthy boy. The vital signs documented( c5 N( `( N: Y- f1 G- e
a blood pressure of 85/50 mm Hg, his length was
6 n$ G- m8 ]2 T, N1 B6 m8 ]9 H( s90 cm (>97th percentile), and his weight was 14.4 kg9 U9 ?2 V( Q# K- h& }& P
(also >97th percentile). The observed yearly growth$ j! m0 z6 i6 K" e5 w8 l8 n4 s; U0 [
velocity was 30 cm (12 inches). The examination of, F' ~6 m* J$ E% n4 r  u% _1 i4 W
the neck revealed no thyroid enlargement.
6 o: n! ?6 q0 o' v3 L  ?1 E0 _+ yThe genitourinary examination was remarkable for
5 u0 i- k* J3 \1 a4 J4 a" Xenlargement of the penis, with a stretched length of0 K. B8 _+ ]( G! [: K
8 cm and a width of 2 cm. The glans penis was very well
1 y5 U% v- Z. t9 ~0 Ndeveloped. The pubic hair was Tanner II, mostly around
  N  Y! T5 N' Y" f) q, y. r540$ ^7 j" e$ v9 t$ O0 T; v- }
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: `3 k/ @& f% e9 `$ J* N, `9 athe base of the phallus and was dark and curled. The& D. G8 v* f& [9 r6 C6 Y
testicular volume was prepubertal at 2 mL each.. R4 i' m% m, n& t! B' H
The skin was moist and smooth and somewhat
7 f2 @7 k/ r& A' K! E4 M- ~/ Soily. No axillary hair was noted. There were no
$ y2 |; X/ w0 N  g! z! {abnormal skin pigmentations or café-au-lait spots.
7 ~# e+ Q$ U, v( N* TNeurologic evaluation showed deep tendon reflex 2+
" R, o& c$ F; Mbilateral and symmetrical. There was no suggestion2 B& T& d. e: A  c; r+ P- A) C! U
of papilledema.
% c1 t- j6 t* [/ f8 eLaboratory Evaluation
, N, X7 ^- q% aThe bone age was consistent with 28 months by7 x" Z; F3 M% m( y6 A0 c* n. U
using the standard of Greulich and Pyle at a chrono-8 P' k- H2 H7 U
logic age of 16 months (advanced).5 Chromosomal" g  _. N' m1 G# L8 G
karyotype was 46XY. The thyroid function test
* C  q: |, e+ ?3 jshowed a free T4 of 1.69 ng/dL, and thyroid stimu-( W( u+ D2 ?. }" l- N
lating hormone level was 1.3 µIU/mL (both normal).! U1 h* h5 v1 N; E
The concentrations of serum electrolytes, blood
  ~2 t1 ^  Y3 X) a7 Jurea nitrogen, creatinine, and calcium all were, y- r, q" `- _2 _, d( h6 @0 c5 p. x/ a
within normal range for his age. The concentration
. n4 ^* q9 E/ w1 i( G  zof serum 17-hydroxyprogesterone was 16 ng/dL
% _# _  p# c. b# i9 L/ T(normal, 3 to 90 ng/dL), androstenedione was 203 H3 \% m8 ]& i/ a
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-8 t& ?/ V2 X! O! F
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
7 c6 ]9 H! Z( K* [- udesoxycorticosterone was 4.3 ng/dL (normal, 7 to
$ I0 t$ f( a- D, a% E49ng/dL), 11-desoxycortisol (specific compound S)
% J- E0 q" h" X: Pwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
2 B$ f9 P* }& [! s( \: `tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total; D# q) }8 {" ~3 z! b4 J0 s. \
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
+ c* F  ~9 n, \! m- D4 Hand β-human chorionic gonadotropin was less than0 e- s! n6 v1 [& l
5 mIU/mL (normal <5 mIU/mL). Serum follicular7 M, S' o: t  y9 T0 n
stimulating hormone and leuteinizing hormone/ E- e* f' v' L. a5 f8 v' E' P
concentrations were less than 0.05 mIU/mL
: {" r0 {% b$ d(prepubertal).
4 V$ U( Y9 H/ TThe parents were notified about the laboratory
5 b7 g: H5 e- f9 X7 q4 S3 |results and were informed that all of the tests were
8 ], X4 t* n  |; W% I) K0 U/ j" tnormal except the testosterone level was high. The
% z: L+ f1 }2 r( Cfollow-up visit was arranged within a few weeks to
( r0 _* s* j' N! ?  x  B0 m6 N/ Robtain testicular and abdominal sonograms; how-- o1 S  ?1 F, n0 d; `( ~3 [
ever, the family did not return for 4 months.
; T8 B8 o4 E$ M1 c- n, BPhysical examination at this time revealed that the
9 X9 p3 h+ d/ g9 e0 Tchild had grown 2.5 cm in 4 months and had gained
( U8 Y8 E; U- y! G. A) z" g, S1 k2 kg of weight. Physical examination remained
) G" W0 ]* g( |+ X8 t3 ^unchanged. Surprisingly, the pubic hair almost com-( j5 M6 \, R3 P+ F9 `: R
pletely disappeared except for a few vellous hairs at
; j2 p3 a6 {) G, E+ I$ ]# lthe base of the phallus. Testicular volume was still 2
) K5 @5 q( V! u& hmL, and the size of the penis remained unchanged.' y. L# ~* X  o+ Q. v1 x
The mother also said that the boy was no longer hav-2 d# {6 ^- n' X8 _' {
ing frequent erections.& w" J1 Z/ S- E& Z& e% o5 r
Both parents were again questioned about use of
5 A2 _2 j# N+ @1 X7 w  A6 J# oany ointment/creams that they may have applied to
. H" g5 g: ]( u+ L- ythe child’s skin. This time the father admitted the  K2 I8 m" G7 Y7 Z& O: K8 i& P0 z' f
Topical Testosterone Exposure / Bhowmick et al 541
( G5 [: w/ H* u* h& J' p% juse of testosterone gel twice daily that he was apply-
% n4 Z0 S6 a6 f! t0 J2 w7 xing over his own shoulders, chest, and back area for
% w) x9 l7 G" P. |# k; ca year. The father also revealed he was embarrassed
$ O+ F0 I- T. K0 P" S! Y: Xto disclose that he was using a testosterone gel pre-8 G7 w$ Y" L5 u3 o) {7 o
scribed by his family physician for decreased libido
5 `; {9 g: |( }4 fsecondary to depression.# G) M! a6 ?: Y& v
The child slept in the same bed with parents.' S; U( X, ?# |% _( Z
The father would hug the baby and hold him on his" R2 R6 J7 M; ^# v
chest for a considerable period of time, causing sig-
7 Y, `/ u( Y" a4 G! Cnificant bare skin contact between baby and father.4 |1 p+ ^2 O0 E3 r  i$ m" j
The father also admitted that after the phone call,
& P3 o! b; G, Z) G( p, j) Ywhen he learned the testosterone level in the baby% J  V- I& s* q. T
was high, he then read the product information
* s6 y3 a0 A9 b# ~& k% V8 [  upacket and concluded that it was most likely the rea-5 P2 Y/ m% y1 \6 e6 d
son for the child’s virilization. At that time, they
, `" s( Z& w% }1 A( Udecided to put the baby in a separate bed, and the
- a; i0 z7 o9 f( t. N* ?father was not hugging him with bare skin and had8 ^# g8 s- N$ N$ m
been using protective clothing. A repeat testosterone! |0 g& g' X, @9 Y
test was ordered, but the family did not go to the$ r# E. w( e% U- d7 s% T% C+ ?/ K
laboratory to obtain the test.1 e0 c7 {; I8 v4 a' C
Discussion4 Y. f: n. o7 x$ j
Precocious puberty in boys is defined as secondary' M4 h! L& E# h- s' i# A
sexual development before 9 years of age.1,4
: y* o6 m) T4 f0 OPrecocious puberty is termed as central (true) when
: P& l% @& p' k4 u& Mit is caused by the premature activation of hypo-
  K$ `5 Q  G& l% o. O4 dthalamic pituitary gonadal axis. CPP is more com-
4 _- Q* M  |& V9 q' q. n- `mon in girls than in boys.1,3 Most boys with CPP
8 K" @+ d3 \8 }/ tmay have a central nervous system lesion that is" K, i) z/ O7 j! s
responsible for the early activation of the hypothal-1 H9 I+ v6 R2 L2 M
amic pituitary gonadal axis.1-3 Thus, greater empha-
6 g( ^2 n( k- `7 r  ]sis has been given to neuroradiologic imaging in
' P& e7 K: p' b, Z6 ]boys with precocious puberty. In addition to viril-
% h9 M" ]2 m7 Z0 c/ oization, the clinical hallmark of CPP is the symmet-6 b" m9 d% E& m* s5 D- @
rical testicular growth secondary to stimulation by
/ L7 |5 B/ j" {, X+ mgonadotropins.1,3
9 k7 F$ D5 c# S8 R1 o& @1 GGonadotropin-independent peripheral preco-
5 c7 x" D5 y8 }! K% j' x+ y' _cious puberty in boys also results from inappropriate* F$ P: u# {; _" w7 o/ [
androgenic stimulation from either endogenous or
; V8 B7 F2 X( I, k0 U; H8 L- Fexogenous sources, nonpituitary gonadotropin stim-. ^8 |. J, O: H6 q* _% Q
ulation, and rare activating mutations.3 Virilizing
( {% s9 p4 i3 I: Acongenital adrenal hyperplasia producing excessive0 m* k2 k; [$ }. y% {  D- A6 V- `+ w
adrenal androgens is a common cause of precocious
5 Z8 [4 {, x( A4 @puberty in boys.3,4
/ `1 P. M9 Q5 p! m1 _' w0 fThe most common form of congenital adrenal
# I- y& g/ V0 t+ j" n! \2 f" mhyperplasia is the 21-hydroxylase enzyme deficiency.9 J1 o$ }9 y6 E* T/ \
The 11-β hydroxylase deficiency may also result in2 s: ]% ]! `' Y  [
excessive adrenal androgen production, and rarely,
: c. [. Y! s3 Y6 n# pan adrenal tumor may also cause adrenal androgen
3 E" \) i( c0 B6 T4 _+ v: m1 Lexcess.1,3) G" o& A/ [2 _. ]2 f7 S: d7 v5 r
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# x: L$ t* I- [7 J; o; p; j4 T
542 Clinical Pediatrics / Vol. 46, No. 6, July 20075 U/ B: e) x; g7 m3 H
A unique entity of male-limited gonadotropin-/ E8 G0 T! J0 p, k2 v, o" K% w
independent precocious puberty, which is also known# i& N- k0 y- ~. B/ `  S
as testotoxicosis, may cause precocious puberty at a9 S! K/ q6 J+ t+ U
very young age. The physical findings in these boys
  _4 ~9 U' G" A2 kwith this disorder are full pubertal development,
! k" c0 D8 u- ?& ]8 R; h9 V6 l' uincluding bilateral testicular growth, similar to boys% m) Q8 G. c( |2 Z
with CPP. The gonadotropin levels in this disorder$ O  P0 E% v; J" W. w) |* \; |, j9 a
are suppressed to prepubertal levels and do not show7 ~2 f( g) u: h& w# _4 d
pubertal response of gonadotropin after gonadotropin-
% {' m) C' X0 creleasing hormone stimulation. This is a sex-linked
: w0 |* W  S# m8 uautosomal dominant disorder that affects only9 a4 j, k$ [0 V$ f3 B2 s% r
males; therefore, other male members of the family
" O1 k' X/ w8 omay have similar precocious puberty.3% ]- {- D/ @8 E+ s6 L, {
In our patient, physical examination was incon-
% O* p7 f5 w4 O2 b8 o) Qsistent with true precocious puberty since his testi-
# i& b  g4 U; E2 N  Rcles were prepubertal in size. However, testotoxicosis" {0 }8 r  M9 C$ }
was in the differential diagnosis because his father$ B7 L- p' X; I+ y: S$ e6 R! I0 D
started puberty somewhat early, and occasionally,
: ?7 z% R* I' a, F# W, ktesticular enlargement is not that evident in the
5 Q. [3 D. c0 @. qbeginning of this process.1 In the absence of a neg-
* R& D% o: B- lative initial history of androgen exposure, our
8 X6 K, D# }" t+ rbiggest concern was virilizing adrenal hyperplasia,
, _. W1 ~/ M$ r( ^2 R% [either 21-hydroxylase deficiency or 11-β hydroxylase* D( [6 n9 O! r. h
deficiency. Those diagnoses were excluded by find-
; t) g) `! `. [7 b' qing the normal level of adrenal steroids.& W! n* l" n1 ~6 f
The diagnosis of exogenous androgens was strongly4 Y7 b0 f% ]7 [, K9 V
suspected in a follow-up visit after 4 months because
, k- V2 A9 C' u7 jthe physical examination revealed the complete disap-' l2 p' Q8 d0 s0 R* o
pearance of pubic hair, normal growth velocity, and
$ N- F' V3 ~4 C0 E5 K( [6 Fdecreased erections. The father admitted using a testos-( ?8 U# p1 D# M
terone gel, which he concealed at first visit. He was
& v+ I0 ^8 ~& t6 @4 |using it rather frequently, twice a day. The Physicians’) _, x( v) w6 b4 ]: w- \; h
Desk Reference, or package insert of this product, gel or
& ]0 V- @' w$ o$ A1 l, H' d0 _cream, cautions about dermal testosterone transfer to& U3 X8 o) }6 V3 {( i  a5 p9 M, i
unprotected females through direct skin exposure., v: R! V' l; E' j
Serum testosterone level was found to be 2 times the! a4 {5 r" c9 d! Z6 y: i+ ?
baseline value in those females who were exposed to
6 J7 @5 v8 G$ N& f' Qeven 15 minutes of direct skin contact with their male
; Z6 G$ @) o# @( w3 q7 rpartners.6 However, when a shirt covered the applica-& k0 Z3 v5 m6 Y; ]6 t* q; N
tion site, this testosterone transfer was prevented.
; f! ~( U: B' n- z9 TOur patient’s testosterone level was 60 ng/mL,# \) B, F6 [( S3 ~9 W0 l
which was clearly high. Some studies suggest that
( ?) e- _  y3 w4 ^) ?dermal conversion of testosterone to dihydrotestos-
; P' r9 S, F: B+ l* R( iterone, which is a more potent metabolite, is more/ |0 J* {- p$ [. {
active in young children exposed to testosterone/ |. B3 F4 ?3 |% O2 j) p
exogenously7; however, we did not measure a dihy-% Y/ u1 p) _2 @/ h( ^+ C# y
drotestosterone level in our patient. In addition to1 L, \( m# p$ I2 V0 q
virilization, exposure to exogenous testosterone in# R/ y- M6 }8 u4 G
children results in an increase in growth velocity and' g2 e, E% h* X7 Y0 e) }
advanced bone age, as seen in our patient.
- @  O. t; B' `) AThe long-term effect of androgen exposure during
, M5 z+ P# A* |! Q5 @- }early childhood on pubertal development and final
% S* C; {4 O7 cadult height are not fully known and always remain
0 G2 [- Y3 o, G1 y, a# W2 T/ s% Qa concern. Children treated with short-term testos-* T9 ^8 w/ f4 o% q* T: o
terone injection or topical androgen may exhibit some
& i# c# X- ]8 F: l; A+ Uacceleration of the skeletal maturation; however, after! v+ x4 A& L( E
cessation of treatment, the rate of bone maturation
) F. q1 ^" h5 I  @( X( `/ O) Kdecelerates and gradually returns to normal.8,9
( g0 [( C: h' a* O( VThere are conflicting reports and controversy: s7 c/ V2 C, T9 ]
over the effect of early androgen exposure on adult) H- Z& n: e4 d  l" x
penile length.10,11 Some reports suggest subnormal- x! N* T7 ~. d, ^2 c
adult penile length, apparently because of downreg-
8 f) c1 h! t) e2 Y8 j$ Q7 Sulation of androgen receptor number.10,12 However,
$ F) J) d5 c3 Q, E( }) xSutherland et al13 did not find a correlation between, k& \& d0 o5 c$ T
childhood testosterone exposure and reduced adult
. G6 |/ k1 q  b5 \7 A/ b7 y! @8 xpenile length in clinical studies.* K  N, Y& r3 m- [9 N7 p
Nonetheless, we do not believe our patient is; C6 D* s3 w2 r. C; T: {
going to experience any of the untoward effects from
# r& Z3 P' [4 w2 T( G: qtestosterone exposure as mentioned earlier because. G* l8 n7 H& c
the exposure was not for a prolonged period of time.
& y) C5 p# D, J9 h; W8 YAlthough the bone age was advanced at the time of- n* g- q0 ]$ k/ M2 E
diagnosis, the child had a normal growth velocity at
9 M& R+ h5 c$ e# ]the follow-up visit. It is hoped that his final adult
* g0 b/ W2 r" M2 Oheight will not be affected.
& |( \0 u1 ^4 y& ^, t4 Z) fAlthough rarely reported, the widespread avail-& m, e. @; P! l" y5 o* Z5 G. n
ability of androgen products in our society may
/ l1 \  y* h# f" o( X8 |+ Rindeed cause more virilization in male or female
; l+ _2 C, {  j  C7 D  gchildren than one would realize. Exposure to andro-
3 P2 ~7 ~9 _. a7 t: Dgen products must be considered and specific ques-; R( A5 ]% q% `
tioning about the use of a testosterone product or
, w% H7 O2 [% {, |, Ygel should be asked of the family members during
. t9 m( U9 w5 d) G: `the evaluation of any children who present with vir-: J9 W7 g; y" Z$ I" M
ilization or peripheral precocious puberty. The diag-
! F- w2 r1 G) b5 Q9 `9 Snosis can be established by just a few tests and by
; F3 R0 S4 ~$ ^  I' {appropriate history. The inability to obtain such a
3 h, c" z8 q# z0 P7 ^. [history, or failure to ask the specific questions, may, `. o6 ?9 M/ U- Q/ ?
result in extensive, unnecessary, and expensive( R' W0 f$ N% i" p( C
investigation. The primary care physician should be
! [4 D0 J; u2 Y- H, u7 u& o& g( Maware of this fact, because most of these children
  j! s0 a* e, t0 p! H$ r1 Cmay initially present in their practice. The Physicians’
' U, [) L0 @+ {$ \$ G" k( E4 n3 @Desk Reference and package insert should also put a1 V! F3 T! ^# V. i% J
warning about the virilizing effect on a male or
+ A7 D6 d0 i+ |# Cfemale child who might come in contact with some-$ g$ i9 v( Q0 e# E0 n
one using any of these products.  ^- G! o5 n5 F7 d
References6 }% P% L3 J6 C3 r) S+ v
1. Styne DM. The testes: disorder of sexual differentiation3 a3 V9 p# F/ w  k
and puberty in the male. In: Sperling MA, ed. Pediatric
) z5 N$ `0 N/ G* c' o3 i8 PEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
. c( j* |# p+ P, Z2002: 565-628.
+ O- f: z# X1 ~9 u2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
! \$ ?, o! r6 y0 D1 W5 hpuberty in children with tumours of the suprasellar pineal
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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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
& H3 ~! {8 m+ o! ]
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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