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Sexual Precocity in a 16-Month-Old0 i. m' Y% G0 r+ B2 N( r9 K- j+ ^
Boy Induced by Indirect Topical; d1 A$ A. h# [/ Z# Q& W( a+ k7 X
Exposure to Testosterone  H- }' E$ t5 p
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,26 p8 V9 y& k9 e& A' \, j; d3 y
and Kenneth R. Rettig, MD1" n! T. R5 z! @1 a+ |
Clinical Pediatrics; V( C" k2 u. g2 }: y
Volume 46 Number 62 x  h3 E2 H% |$ @! D- l  t
July 2007 540-543: ]- t: _( e! V! ^* H: r
© 2007 Sage Publications& A2 q: s  D" G& T( X2 h
10.1177/0009922806296651
  O/ s$ n1 [. }  I+ p1 C  ?http://clp.sagepub.com
; ^; ^1 U+ O6 L2 I3 V4 ahosted at
9 l7 R' f' o) k- `4 ], [http://online.sagepub.com# b% [. ]/ R* d% w0 L  Y+ C
Precocious puberty in boys, central or peripheral,
! a* S  p9 ^. d  p  L* u" W, h$ ]+ fis a significant concern for physicians. Central
1 E) d2 z) X3 V5 u! Z, d/ _( F/ nprecocious puberty (CPP), which is mediated
( `: `& H, p, athrough the hypothalamic pituitary gonadal axis, has6 _# R/ k4 X9 j0 Z) N0 a9 T/ U
a higher incidence of organic central nervous system
# m  `" P5 l4 Y1 X) v: \lesions in boys.1,2 Virilization in boys, as manifested* k- J: Y& E  ^* ]9 j3 @
by enlargement of the penis, development of pubic7 N: P3 o9 U7 g3 e0 Z
hair, and facial acne without enlargement of testi-
3 [( A0 E" G% L: y3 R0 ycles, suggests peripheral or pseudopuberty.1-3 We
9 |/ \' D4 M7 N) a9 yreport a 16-month-old boy who presented with the5 t& t. z, G: `# C
enlargement of the phallus and pubic hair develop-
+ f! n+ g: P9 V* ement without testicular enlargement, which was due
& }$ k( |% J: R, ^# e2 fto the unintentional exposure to androgen gel used by, l+ @( r* B" j# u$ {
the father. The family initially concealed this infor-. w0 c9 I% y! s- Y* R
mation, resulting in an extensive work-up for this
5 a6 S1 _# {# g! s7 Wchild. Given the widespread and easy availability of# M4 Y. S6 @' }% ^
testosterone gel and cream, we believe this is proba-% Z, F% K+ j4 h- ]; S
bly more common than the rare case report in the
2 Z( T$ [. Q: E7 Y0 i% |% cliterature.4
# b& a, m6 \1 bPatient Report
* H' v, A; w3 _7 q! z7 Y% w+ BA 16-month-old white child was referred to the4 ?5 t2 m+ t! d
endocrine clinic by his pediatrician with the concern% F4 O: z# g: R( j! P  `
of early sexual development. His mother noticed
( Z& T/ }" ]3 I9 k* O  j8 hlight colored pubic hair development when he was1 u8 T5 T% x& [; ?0 w% v* A
From the 1Division of Pediatric Endocrinology, 2University of
0 D6 C/ E% O8 ]  }" w8 ZSouth Alabama Medical Center, Mobile, Alabama.' i% n* A/ \5 q9 x
Address correspondence to: Samar K. Bhowmick, MD, FACE,
8 H+ N2 u, H" E6 Z0 XProfessor of Pediatrics, University of South Alabama, College of0 D2 ^- K' f# Y$ D% X
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;. @7 K* e. D" V9 }$ n8 w. g! K
e-mail: [email protected].
7 y4 P1 a/ v# P( K4 Uabout 6 to 7 months old, which progressively became
% X/ [8 D& g8 l3 w  fdarker. She was also concerned about the enlarge-
0 j% g4 I3 I& |9 h! ement of his penis and frequent erections. The child+ x4 e0 g: m/ j' M: \4 w" C
was the product of a full-term normal delivery, with
( V3 ]/ s( e, L* m: d/ U& ?% da birth weight of 7 lb 14 oz, and birth length of! K/ M# j6 v# k8 H: H
20 inches. He was breast-fed throughout the first year: T9 `! x+ C. m& j
of life and was still receiving breast milk along with
/ x& ^3 l/ K. D5 s! c2 Psolid food. He had no hospitalizations or surgery,% e3 I( b0 H( \" z
and his psychosocial and psychomotor development' {! d3 y6 G- t, d6 A
was age appropriate.+ ]- Y+ L0 X  r8 M. i/ Y1 S
The family history was remarkable for the father,+ P& ?4 Q- a, a& j1 \
who was diagnosed with hypothyroidism at age 16," L0 S' J. q$ A/ d7 H, x# d
which was treated with thyroxine. The father’s
$ g2 g$ n0 v0 }( a5 mheight was 6 feet, and he went through a somewhat3 ?5 f. L4 k( a0 L/ N+ c7 |. t% Z
early puberty and had stopped growing by age 14.+ W. e$ Y+ l( v, g7 M* |7 U/ L9 M
The father denied taking any other medication. The. O  I) ]6 u9 r: [7 u
child’s mother was in good health. Her menarche6 e3 _' |* I0 ^4 f& B% d
was at 11 years of age, and her height was at 5 feet
. N) Z; j# Y! K, w' I0 n5 inches. There was no other family history of pre-3 V+ z' c7 E3 B
cocious sexual development in the first-degree rela-
/ J: d6 \  h5 Htives. There were no siblings.
& o3 H5 x* K. A  ?* xPhysical Examination* F8 w/ Y( s, J4 }8 N& T. Q
The physical examination revealed a very active,* K& A: E- @1 _9 P5 a4 H. G( E! S+ l' j
playful, and healthy boy. The vital signs documented: I5 J% I0 w% b
a blood pressure of 85/50 mm Hg, his length was
3 ^3 `- r* e4 S6 [1 ?6 H! T( U# e90 cm (>97th percentile), and his weight was 14.4 kg' D  j$ ^) e6 [; e7 Y. P- H! M
(also >97th percentile). The observed yearly growth
! t2 l& U" ]# i) q8 C1 {5 fvelocity was 30 cm (12 inches). The examination of1 v( O. k( }5 c" m$ u6 E7 m6 @4 g# {
the neck revealed no thyroid enlargement.
1 r6 c% A3 S2 Q. ^2 B# p/ cThe genitourinary examination was remarkable for" h0 ?8 q! G5 ~+ S. s& b
enlargement of the penis, with a stretched length of$ s  `7 V  C1 i, n
8 cm and a width of 2 cm. The glans penis was very well
$ X3 J# |" X$ z4 _developed. The pubic hair was Tanner II, mostly around) s! r+ c0 T& _' }: Z* X5 H' _7 |0 H3 x
540" C. v0 v( P% P4 y& f2 C+ l
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 t$ d7 D5 h3 Q3 F0 d- n2 f; Hthe base of the phallus and was dark and curled. The
9 k" M& b1 \/ c) ~0 u, N! T8 Ytesticular volume was prepubertal at 2 mL each.0 Z3 `, C* {7 m
The skin was moist and smooth and somewhat9 P. V- R9 ~- n' l
oily. No axillary hair was noted. There were no! e) p3 v. E" ~9 M9 D7 ]: ?2 {6 D
abnormal skin pigmentations or café-au-lait spots.' C7 p' C% Q) m9 R; R) a
Neurologic evaluation showed deep tendon reflex 2+
! ^) m. A& [& y! `7 J! \bilateral and symmetrical. There was no suggestion
9 {, r* o, L7 X+ s/ Eof papilledema.
) c: u" [2 R6 ~7 a$ P' [% yLaboratory Evaluation+ l' W" |, p2 [% d$ G6 ?
The bone age was consistent with 28 months by! R' {, T2 }; j1 r
using the standard of Greulich and Pyle at a chrono-9 V2 N7 T( p+ k  k5 m% p; U- J
logic age of 16 months (advanced).5 Chromosomal2 j7 t+ m; S$ |$ Q  a
karyotype was 46XY. The thyroid function test- }2 ]) l0 Q$ d" H3 }
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
- w  R: E8 B+ h  M( P( hlating hormone level was 1.3 µIU/mL (both normal).
+ `9 w; u1 K- U/ ?0 _1 IThe concentrations of serum electrolytes, blood. C9 ]: l; f  K- G  J
urea nitrogen, creatinine, and calcium all were, i* R( L; a; k, L
within normal range for his age. The concentration
; t& C, w  {, Z3 Pof serum 17-hydroxyprogesterone was 16 ng/dL+ t" D* [0 A1 A- J
(normal, 3 to 90 ng/dL), androstenedione was 20
* X, }5 W$ X( T7 m5 jng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 Z* R, s7 x, B: uterone was 38 ng/dL (normal, 50 to 760 ng/dL),+ [' h/ ]; I2 c- c: N- Y9 L5 `
desoxycorticosterone was 4.3 ng/dL (normal, 7 to0 F1 V/ s7 e! {: z' C0 [
49ng/dL), 11-desoxycortisol (specific compound S)
( i" m6 d8 @) N. mwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
- b" t* A) ~* q( h% Otisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
  z, G  K+ U, B4 W* T, j2 vtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
8 T1 T) x4 u2 V) o, h' m. `$ Iand β-human chorionic gonadotropin was less than
: T* v  \+ H/ ~% i6 P3 Q: b5 mIU/mL (normal <5 mIU/mL). Serum follicular' j" }8 O, T, j3 c5 T7 e1 a, }4 |
stimulating hormone and leuteinizing hormone0 P# Z7 F: m! U
concentrations were less than 0.05 mIU/mL
) D6 h4 r5 Z  O! C- P2 Y- I. r1 ~(prepubertal).2 q6 ]+ H2 l# X2 [" q  G5 N, N
The parents were notified about the laboratory$ T4 c" T  F4 d. G
results and were informed that all of the tests were
5 f" M/ P# q5 d3 _3 ?: e  bnormal except the testosterone level was high. The
. N" _$ a/ S1 y' {/ S4 b# `follow-up visit was arranged within a few weeks to
4 H6 o+ c; C! {obtain testicular and abdominal sonograms; how-! a) t" p) O  o% n
ever, the family did not return for 4 months.! k  S' h( Q6 _/ U) @; r, Y
Physical examination at this time revealed that the, V& j- k! ]) z( e/ G0 E
child had grown 2.5 cm in 4 months and had gained
  Z6 ^$ Q- `9 y. D2 kg of weight. Physical examination remained
: x2 L! i' b& nunchanged. Surprisingly, the pubic hair almost com-( C& x# ?9 m8 p6 m& c8 `# Y
pletely disappeared except for a few vellous hairs at
' g" C  B; i6 p6 [& o* K, u' jthe base of the phallus. Testicular volume was still 21 U& {7 K9 m& j+ z" X$ P- t( V
mL, and the size of the penis remained unchanged.
' f1 p) X1 x3 JThe mother also said that the boy was no longer hav-
" Y% W3 v: [6 t& }3 L1 eing frequent erections.
% B: `  p% F* H6 E8 n3 pBoth parents were again questioned about use of# z: y; u" }/ T. [1 \: W1 ^/ n  e
any ointment/creams that they may have applied to& K( L$ W8 J/ C; k: h$ a
the child’s skin. This time the father admitted the
8 Y' U9 \- e3 `; f/ _6 nTopical Testosterone Exposure / Bhowmick et al 541- y6 I5 V$ B  y- y& I
use of testosterone gel twice daily that he was apply-* p& f( X# @# B& B  o3 z
ing over his own shoulders, chest, and back area for* \4 Q$ y# G) x/ f9 p. ~
a year. The father also revealed he was embarrassed
& s2 K/ r6 c, ~) S1 _5 A% Pto disclose that he was using a testosterone gel pre-
) u: B2 _4 l% }' _2 c: fscribed by his family physician for decreased libido
3 Z; H! L! [6 Nsecondary to depression.3 \7 ]) g: s# d1 L- l/ T2 D
The child slept in the same bed with parents.
4 V/ h; k- ~, oThe father would hug the baby and hold him on his
$ y; k5 r5 P5 P/ d: Q9 xchest for a considerable period of time, causing sig-
2 d1 I  o! s$ _3 Rnificant bare skin contact between baby and father.+ _, o4 w1 c1 ]2 r9 p. k8 M* @
The father also admitted that after the phone call,
0 ?' S4 q1 m9 f' j8 owhen he learned the testosterone level in the baby9 y, d& z, m$ L0 c2 b+ [
was high, he then read the product information
: L8 \# [0 a3 M" e0 Ipacket and concluded that it was most likely the rea-7 y$ m, B& c8 C6 \: X
son for the child’s virilization. At that time, they3 P! i$ U3 ~6 m6 u$ C
decided to put the baby in a separate bed, and the* J  G8 B; R* E3 a2 T# y0 u& p9 ]
father was not hugging him with bare skin and had& G; ]% M5 x' Q- r8 w
been using protective clothing. A repeat testosterone3 Q$ \* l2 Q. }, [0 Z  j% U
test was ordered, but the family did not go to the+ {" @1 y4 S) r. ]8 ^) ^/ r+ H7 @
laboratory to obtain the test." k" o9 M. ]" i6 m5 T  W
Discussion
  y5 i+ u% [7 Z& B9 @0 j2 ?Precocious puberty in boys is defined as secondary  c+ S7 y. V5 M9 }7 D; @7 H
sexual development before 9 years of age.1,4
0 L6 [- N0 U/ u$ g% CPrecocious puberty is termed as central (true) when$ ~6 }0 _2 l# V% m
it is caused by the premature activation of hypo-
7 A1 R! n/ l  U, E& _thalamic pituitary gonadal axis. CPP is more com-
/ g7 n7 i. y5 s! Jmon in girls than in boys.1,3 Most boys with CPP
0 n- \8 z" {! \3 q3 D9 Smay have a central nervous system lesion that is
7 W7 {/ N/ P5 H# vresponsible for the early activation of the hypothal-
: W3 y6 _5 j+ x( B3 Ramic pituitary gonadal axis.1-3 Thus, greater empha-
! Q) M) o$ E# M4 ^3 vsis has been given to neuroradiologic imaging in
- E% q  W/ R: a/ a/ |+ N/ q/ [( _boys with precocious puberty. In addition to viril-$ m0 S& r& l5 _: C1 j; s
ization, the clinical hallmark of CPP is the symmet-1 u& x( D$ j0 G1 O
rical testicular growth secondary to stimulation by7 e$ k. Y1 |, M7 a' N: g) c
gonadotropins.1,3
/ ^: f- b9 ]7 M; n6 {Gonadotropin-independent peripheral preco-1 A0 o. Y$ w0 {+ |
cious puberty in boys also results from inappropriate7 A5 T1 Z: R1 C7 Y
androgenic stimulation from either endogenous or
! ]$ M9 [( |5 W& L# [! }2 a! s2 \exogenous sources, nonpituitary gonadotropin stim-
& F3 L4 l1 ?3 Uulation, and rare activating mutations.3 Virilizing
7 X( S- Y+ x8 x5 L) Pcongenital adrenal hyperplasia producing excessive! v* I3 @& T  F5 o3 j8 A' r, A4 y
adrenal androgens is a common cause of precocious( x/ f2 I0 X' \" `: [4 g/ T% b
puberty in boys.3,46 b2 o, H' v) D5 a6 V* u
The most common form of congenital adrenal
/ y. n4 o0 g8 Bhyperplasia is the 21-hydroxylase enzyme deficiency.+ b  d, ?/ m3 ?
The 11-β hydroxylase deficiency may also result in" }* l/ N* r; T& ~$ P
excessive adrenal androgen production, and rarely,
5 o! Q6 |; G! C/ X7 g7 G. \an adrenal tumor may also cause adrenal androgen
) S9 W$ _. t2 C2 w! y3 C, Pexcess.1,30 g& J6 v$ M5 R  M$ L$ a9 y0 s" N
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" q! V# }- h' `542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
- y* a. I7 J# ?; h( nA unique entity of male-limited gonadotropin-
; i/ M# I9 M5 R% D3 a: g" cindependent precocious puberty, which is also known
/ [6 L2 t  u# R$ b4 Eas testotoxicosis, may cause precocious puberty at a
2 p! m- Z) n0 ]7 Fvery young age. The physical findings in these boys
. P; ]& B8 b0 _with this disorder are full pubertal development,
8 b% I+ n( s9 ?- J& M6 C* \0 {( B7 L$ }2 eincluding bilateral testicular growth, similar to boys& x% {% Y3 |9 i# h
with CPP. The gonadotropin levels in this disorder
" R7 ^' P8 g" U% Y# r* O/ |are suppressed to prepubertal levels and do not show
: H9 A) o* J( m% J1 ?9 f) Ipubertal response of gonadotropin after gonadotropin-
' i: K( x. A; ]% l% ureleasing hormone stimulation. This is a sex-linked
( x6 a0 |4 U4 [autosomal dominant disorder that affects only1 n4 ]4 k. I6 M; ^) x& O
males; therefore, other male members of the family
& b5 Z7 Q! F4 G% ^9 x* |may have similar precocious puberty.3/ _5 z) ?0 a% L8 G
In our patient, physical examination was incon-$ _4 e& f* ?$ o" r
sistent with true precocious puberty since his testi-
8 c7 P/ T/ q# [$ y: _# w! Qcles were prepubertal in size. However, testotoxicosis0 |! Z' Z+ X3 g2 A+ o+ j2 D
was in the differential diagnosis because his father
! Z* B* N" Y) A: o. j  S+ ]started puberty somewhat early, and occasionally,
  \% ^8 d1 G+ ptesticular enlargement is not that evident in the' B- M" |" V# f0 e' G( o
beginning of this process.1 In the absence of a neg-
2 v; O. W* H# Y2 iative initial history of androgen exposure, our$ c8 k6 V  j% p2 n8 t
biggest concern was virilizing adrenal hyperplasia,& N, e8 X5 n" G+ F! D
either 21-hydroxylase deficiency or 11-β hydroxylase
1 j' y4 J2 r* u2 }deficiency. Those diagnoses were excluded by find-7 b) e2 h8 X( e) b
ing the normal level of adrenal steroids.2 |- L7 e& J5 l1 J6 ?
The diagnosis of exogenous androgens was strongly
% Q' Q+ o+ |9 a3 xsuspected in a follow-up visit after 4 months because4 Z! ?  v* Y0 m8 H6 ?
the physical examination revealed the complete disap-
8 ~  D7 D/ G/ Y) s. i8 Jpearance of pubic hair, normal growth velocity, and% k; y+ _; J/ o2 w3 u1 Q, D; o9 g
decreased erections. The father admitted using a testos-# A7 P3 j- X' q/ p6 f$ p; Y
terone gel, which he concealed at first visit. He was
5 |# g- a# k. A9 ]6 n% zusing it rather frequently, twice a day. The Physicians’
$ S; ]8 g7 t) {2 P3 D# ODesk Reference, or package insert of this product, gel or( B$ Z! ?* d7 A+ N+ z) m
cream, cautions about dermal testosterone transfer to: o  q$ U; X, K+ z) b$ `
unprotected females through direct skin exposure.
6 v  J: L2 B7 Z7 W& y  tSerum testosterone level was found to be 2 times the
9 R. J  [+ K7 g# ~3 w# w5 E9 l& qbaseline value in those females who were exposed to2 B/ b5 H: h1 K, E% H: T- l8 B
even 15 minutes of direct skin contact with their male, q( M- ?" _( f7 s" d9 P$ w
partners.6 However, when a shirt covered the applica-( \5 _( v& }6 [9 F& l, O
tion site, this testosterone transfer was prevented.
2 c; I9 j5 _- T& P6 v* Q+ k8 {" q$ BOur patient’s testosterone level was 60 ng/mL,
7 l6 n8 Q8 e% l  b8 {1 R8 Gwhich was clearly high. Some studies suggest that
# a; A' K7 v! A3 J" U. u, gdermal conversion of testosterone to dihydrotestos-0 E5 y, b- w  ^" }
terone, which is a more potent metabolite, is more. e- K6 X( ~* n' q9 J4 J
active in young children exposed to testosterone; ~  p/ h! _/ V- t5 H
exogenously7; however, we did not measure a dihy-; T. [* F: x" y( e4 ~+ c
drotestosterone level in our patient. In addition to% j- U0 B/ T+ }
virilization, exposure to exogenous testosterone in: X3 e7 n( _* A7 W! C
children results in an increase in growth velocity and
  p. Z3 Y& Z  A* B8 oadvanced bone age, as seen in our patient.0 Q7 p; Y  Y# {  n) p0 q: w
The long-term effect of androgen exposure during; K9 U5 r+ T# [9 |
early childhood on pubertal development and final
) a" M  N) C$ T' t( qadult height are not fully known and always remain
$ \+ I' d: W% X( o# P8 z0 ya concern. Children treated with short-term testos-
1 z3 ?: `5 F5 y% ^# sterone injection or topical androgen may exhibit some
, ?% t3 \$ c. Z7 ?, J0 y4 nacceleration of the skeletal maturation; however, after* v3 w# c, D1 I( o
cessation of treatment, the rate of bone maturation
9 d' P4 d" W# _7 ]" x* t8 wdecelerates and gradually returns to normal.8,9! f* a8 y3 |7 ]+ T
There are conflicting reports and controversy. R& O3 ~3 X; w4 y% p& L, l' {
over the effect of early androgen exposure on adult0 j2 F2 v, g' `* j
penile length.10,11 Some reports suggest subnormal
/ m7 p& N( k9 Uadult penile length, apparently because of downreg-
; _  `- b  ]% v0 Z; \1 H' N0 Yulation of androgen receptor number.10,12 However,
9 O  u/ [7 h7 {9 ESutherland et al13 did not find a correlation between
3 q" \" O5 E+ v' kchildhood testosterone exposure and reduced adult" Q& p' ^4 o( j! A; j
penile length in clinical studies.- t! n  [5 C. M1 B
Nonetheless, we do not believe our patient is4 D' t$ U( m  U* c* F# `
going to experience any of the untoward effects from, a& P7 N8 i1 o- o$ V
testosterone exposure as mentioned earlier because
0 O' Q& s/ M3 hthe exposure was not for a prolonged period of time.! p! t9 {+ A  n8 z4 I" I6 x$ f
Although the bone age was advanced at the time of; j5 f' ?. i  c; K& l
diagnosis, the child had a normal growth velocity at* y1 Q' W+ h; ^) L$ o; I
the follow-up visit. It is hoped that his final adult
: K" H. [% T7 [height will not be affected.
& b: D- j. `# U0 L  tAlthough rarely reported, the widespread avail-* U: O; @9 _, U& N* P$ }/ ]1 w; G
ability of androgen products in our society may1 s0 B, p, z/ l
indeed cause more virilization in male or female
% F4 `' v  M5 |9 ^children than one would realize. Exposure to andro-
2 v5 ~% p/ Y$ `. j7 g& _# ygen products must be considered and specific ques-. ]" G" ^  g$ F  I
tioning about the use of a testosterone product or
! _9 Q9 K% q9 _5 r/ l! ?gel should be asked of the family members during1 z: ]9 C" m+ M. S8 E, ^) @. |+ u
the evaluation of any children who present with vir-
- J; }* s7 \4 l8 p2 f% dilization or peripheral precocious puberty. The diag-" q' z# n/ Y7 f3 W$ A
nosis can be established by just a few tests and by
) p- m9 y: K) |1 k; `appropriate history. The inability to obtain such a
2 G6 \: L) Z' |3 [; h# }history, or failure to ask the specific questions, may
0 N# F6 r1 ~! S& zresult in extensive, unnecessary, and expensive
! O2 P; h; @6 B8 }investigation. The primary care physician should be
  E% V" o( r6 b  @& laware of this fact, because most of these children3 d, i0 Y2 @9 n  K5 m
may initially present in their practice. The Physicians’( c& }( F" }* T- @- b) i- _
Desk Reference and package insert should also put a
; j. P$ ^- a( J& N/ h4 ]# hwarning about the virilizing effect on a male or
* {9 f  a+ s% h1 p6 l8 g  Mfemale child who might come in contact with some-+ ]1 S. }7 w  t! _, _
one using any of these products.
) e- j+ B; N4 p# w4 AReferences* V: q+ O5 J- Z) Z  x: G& b7 w
1. Styne DM. The testes: disorder of sexual differentiation: _4 a( _8 @3 d; @5 N- `
and puberty in the male. In: Sperling MA, ed. Pediatric
- x( M+ U" v  d* ^3 e" oEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- o! E% H9 k) F$ S( L, F2002: 565-628.; v) Y; w) T! j+ Z( U
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; T6 a1 Q! ~2 r* _" a* K; e
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old6 l  }; r) F9 B0 q% T
Boy Induced by Indirect Topical/ d4 A' ^1 V6 b, R( g
Exposure to Testosterone3 W6 Y( y2 V8 ^& S% P) N2 l+ ]
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
' \8 ~* R+ A- w$ J2 uand Kenneth R. Rettig, MD1
1 k* K7 M( L1 ~" |; XClinical Pediatrics9 ^5 B' [3 _* B" K
Volume 46 Number 6, \' d2 Z. n5 J, r
July 2007 540-543
7 I( E/ V8 a, C$ O4 `1 ]. ^% p/ \: s. b© 2007 Sage Publications
/ e# R! Q7 j+ \( G10.1177/0009922806296651
7 I4 \" K% C& Mhttp://clp.sagepub.com
! c* s" |2 j& M+ E  y. t& B( e- }- yhosted at! l9 c5 K1 q" `: f7 X5 i
http://online.sagepub.com, z5 m% T. c6 Z' z  l
Precocious puberty in boys, central or peripheral,
& ?- B+ N9 k" R1 Sis a significant concern for physicians. Central
! V2 w5 N% t! R9 a# P% y+ l6 ]. ~) fprecocious puberty (CPP), which is mediated5 F% O( V; y; U5 c1 l& K
through the hypothalamic pituitary gonadal axis, has
# V$ j1 T0 ^8 Aa higher incidence of organic central nervous system; n- e/ x4 |7 J4 q
lesions in boys.1,2 Virilization in boys, as manifested) y4 A+ z5 Q! S$ K
by enlargement of the penis, development of pubic
  n2 _  X$ ?4 w: A6 S  |, x4 ahair, and facial acne without enlargement of testi-
6 N# ]  L7 q7 r, G5 ucles, suggests peripheral or pseudopuberty.1-3 We0 c- h2 H' R# e% f
report a 16-month-old boy who presented with the
. ]2 z! g0 Z# T5 \6 p) venlargement of the phallus and pubic hair develop-9 G+ N6 c0 \9 Y1 f$ V9 F) `
ment without testicular enlargement, which was due
# J# B" Z0 [6 ?) s$ Q8 cto the unintentional exposure to androgen gel used by* o& D8 w" j$ [; f3 R
the father. The family initially concealed this infor-* J7 O# Q! i7 ]% U% M5 d& `
mation, resulting in an extensive work-up for this% H" g! y1 _. L2 Y6 f; Q4 L
child. Given the widespread and easy availability of
2 ]& ^' W9 B; Ntestosterone gel and cream, we believe this is proba-
$ }7 ~+ ~( h" C, a4 R% lbly more common than the rare case report in the1 Y2 X$ ~7 L* o+ L7 S
literature.4
! f  ^1 U1 A1 U& m$ q, F4 dPatient Report
% Y: a5 W2 u2 P  K+ I. TA 16-month-old white child was referred to the
3 a6 o, ?$ ^2 h0 `+ wendocrine clinic by his pediatrician with the concern
* L7 n) a; ~; ^. A  C4 [of early sexual development. His mother noticed
" V* F, F3 j* I9 s. ]4 {+ E8 p4 nlight colored pubic hair development when he was
3 @! u# l) \, O+ X/ Q& HFrom the 1Division of Pediatric Endocrinology, 2University of
9 M: d* g. p7 ^) v+ eSouth Alabama Medical Center, Mobile, Alabama.* s, Z+ g; G: o- O
Address correspondence to: Samar K. Bhowmick, MD, FACE,
( M8 |" E- ]+ A# YProfessor of Pediatrics, University of South Alabama, College of
" D( z4 d5 R  \2 y% |+ r2 RMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;8 v6 G+ f+ `3 ]
e-mail: [email protected].# h4 T& P* D, W4 V4 G2 b: c
about 6 to 7 months old, which progressively became
8 ]. t& u, y8 N- N2 odarker. She was also concerned about the enlarge-
4 m( R( G" V' c& x* m* R6 y. Nment of his penis and frequent erections. The child) s; R* S0 p- a; C8 }* ?
was the product of a full-term normal delivery, with0 F9 k, M9 H" R+ i
a birth weight of 7 lb 14 oz, and birth length of% @6 ]2 s$ r' m. J4 j
20 inches. He was breast-fed throughout the first year& p) q5 Y4 i! i. Y
of life and was still receiving breast milk along with4 n7 z" [  B! [
solid food. He had no hospitalizations or surgery,3 L( J7 k& U( i( \6 H! w
and his psychosocial and psychomotor development7 a: s/ n3 w4 C1 M. t4 a5 h5 s3 R
was age appropriate.
& e+ T% ?8 r& H& S/ c8 w$ v* UThe family history was remarkable for the father,% g2 Z( v# i0 |7 [  A& r; T6 K
who was diagnosed with hypothyroidism at age 16,
  E# ]6 o* O2 Z! u, M/ S& kwhich was treated with thyroxine. The father’s
6 [7 a, v) X' x& P3 {6 D% ^. eheight was 6 feet, and he went through a somewhat
: C- g9 R. @+ {early puberty and had stopped growing by age 14.2 ^# k# k5 O; S0 C& n
The father denied taking any other medication. The
+ U: f. b/ |+ _/ X% @# ichild’s mother was in good health. Her menarche
4 e9 Q' n4 X2 q+ Bwas at 11 years of age, and her height was at 5 feet
9 [) V* H: U( {/ \; X5 Y5 inches. There was no other family history of pre-; s' ~' N1 c: V
cocious sexual development in the first-degree rela-" P& S! g' h- k( D' X) K) t! [
tives. There were no siblings.& Q1 V* F$ |. b9 D; h
Physical Examination6 M  }$ i. U6 E) {) O% F
The physical examination revealed a very active,2 {( U6 @! H2 I8 e. T: h7 v( d
playful, and healthy boy. The vital signs documented
$ [6 C+ |) u; ra blood pressure of 85/50 mm Hg, his length was
0 c. \/ ?% l2 t/ @90 cm (>97th percentile), and his weight was 14.4 kg9 L- _. g1 x7 [5 v5 Z7 [
(also >97th percentile). The observed yearly growth
+ k% |  l' l$ O8 q5 {velocity was 30 cm (12 inches). The examination of* j$ i/ i( s. \. J3 N
the neck revealed no thyroid enlargement.; R* p8 j5 Z/ A) @5 P% E0 P
The genitourinary examination was remarkable for9 v! B4 P& o) J; A
enlargement of the penis, with a stretched length of
) L0 i. U- s# O2 u! u8 cm and a width of 2 cm. The glans penis was very well: q6 P. @# v) C
developed. The pubic hair was Tanner II, mostly around
7 O5 ^# c: m3 b8 G' p7 O( w540; R" [! f/ w, ^! |% p
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 u7 [. r* R9 o0 m1 B
the base of the phallus and was dark and curled. The
% o2 u! j5 \; Y/ C+ U3 G* stesticular volume was prepubertal at 2 mL each.3 o! V" a6 g8 [: l
The skin was moist and smooth and somewhat- N; M! D2 q, \) J, r! S9 c
oily. No axillary hair was noted. There were no) y: S) C; n4 i9 X: f4 y
abnormal skin pigmentations or café-au-lait spots.) X) H# d' u1 a
Neurologic evaluation showed deep tendon reflex 2+
: S) O1 t! D6 U3 l1 f7 u4 }bilateral and symmetrical. There was no suggestion
) i8 M( |7 m* C& @; n2 ?7 Vof papilledema.
3 U3 l' }  K' m2 `Laboratory Evaluation
2 W% x# k3 B/ D6 ?6 @; |The bone age was consistent with 28 months by7 z* g1 q5 u0 Y; m5 ^; g
using the standard of Greulich and Pyle at a chrono-& |+ o6 ]: s1 c8 a6 N
logic age of 16 months (advanced).5 Chromosomal8 Z) c  U8 m" V% X
karyotype was 46XY. The thyroid function test. E, ?) C- L7 O, z' x, [
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
& R/ f. S  Y: @6 T' ulating hormone level was 1.3 µIU/mL (both normal).
: c  S3 o" p# n2 O  K0 HThe concentrations of serum electrolytes, blood
+ z7 ], ?4 A- }% p( zurea nitrogen, creatinine, and calcium all were* ]2 ~2 d! N# V0 Y  i# {( D( N
within normal range for his age. The concentration
# E& U' n* I! c: Aof serum 17-hydroxyprogesterone was 16 ng/dL1 h! X' C; n9 p8 q
(normal, 3 to 90 ng/dL), androstenedione was 20
3 N( N* d0 e9 B0 y8 B+ nng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-- {) X! ?4 I+ c3 L# b
terone was 38 ng/dL (normal, 50 to 760 ng/dL),- R; c- E! ]* v+ }& S6 Q+ }$ s* ~
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
( J/ L& e- s' O6 E! y49ng/dL), 11-desoxycortisol (specific compound S)
" Q6 K: N$ O$ \was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-) W! r2 P3 j; e" O9 R
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total( Z7 j& F, \! R( }) G
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
2 k7 g- z: c. Z3 ~* {7 L  s0 d4 uand β-human chorionic gonadotropin was less than
6 \7 n+ a1 d* W; ?* g* Y  ^5 mIU/mL (normal <5 mIU/mL). Serum follicular
! ?/ g' O2 L7 b! lstimulating hormone and leuteinizing hormone
. C  @" j4 G8 v* u, z* aconcentrations were less than 0.05 mIU/mL, l; D! x8 \7 B
(prepubertal).  p% s  s" E& [# w" Z$ k
The parents were notified about the laboratory
6 L8 I/ s  X, @$ presults and were informed that all of the tests were
8 `6 ?* y% z$ n( O2 Y! Vnormal except the testosterone level was high. The
8 p) p$ e* I/ U9 U  nfollow-up visit was arranged within a few weeks to' \' I1 {0 }, J3 H0 k
obtain testicular and abdominal sonograms; how-
0 G/ I9 J4 p& j, Zever, the family did not return for 4 months.
3 N2 {8 T% F  M1 ?2 gPhysical examination at this time revealed that the
0 t( h2 \( ?  W% J* Jchild had grown 2.5 cm in 4 months and had gained9 A) ?9 M( c2 i: I9 \
2 kg of weight. Physical examination remained3 e, [- _2 ~6 u" j8 a& `
unchanged. Surprisingly, the pubic hair almost com-; x- G* Z: i5 b4 X8 ]; h9 ~
pletely disappeared except for a few vellous hairs at
" \* M. o% Q$ d. W4 Dthe base of the phallus. Testicular volume was still 2
2 K+ P; W% K/ s; m0 TmL, and the size of the penis remained unchanged.
- z. H9 f+ ~7 b, Z7 eThe mother also said that the boy was no longer hav-
0 G+ A' [! r) B- x6 ~- Fing frequent erections.0 b; Q+ F$ k: w! F% W9 X5 n
Both parents were again questioned about use of
, @5 Y' H5 w: r# K" Gany ointment/creams that they may have applied to# S: Y* |3 }- A. r8 Q* Z
the child’s skin. This time the father admitted the
1 P, |! q$ R* v) E; CTopical Testosterone Exposure / Bhowmick et al 541& k, Z% C; @# |4 q' g4 O, x
use of testosterone gel twice daily that he was apply-
$ E5 S  Z3 P( }ing over his own shoulders, chest, and back area for+ K1 a( y; ]" D- q2 B
a year. The father also revealed he was embarrassed
0 i9 H' F. o5 R  W' t0 O' Lto disclose that he was using a testosterone gel pre-
# ?/ h9 Z3 h* r# K" ~/ |3 Vscribed by his family physician for decreased libido
3 L* R; A. K) W. H2 n( g: Lsecondary to depression.8 f; k) G- V! A
The child slept in the same bed with parents.
1 i5 U0 p  f6 T+ `The father would hug the baby and hold him on his
# g" P6 z2 f, X1 tchest for a considerable period of time, causing sig-
# \& Z* m" v# I" A: k. Onificant bare skin contact between baby and father.
# d9 N0 j' C. H1 J% e- ]The father also admitted that after the phone call,+ h$ t4 h  q9 j6 G6 |1 U# G
when he learned the testosterone level in the baby
2 _9 f; h  H8 i' ]4 W/ Uwas high, he then read the product information. c' G! K0 r  P5 s
packet and concluded that it was most likely the rea-
& ^4 k# ^+ t& I6 y$ Zson for the child’s virilization. At that time, they+ [) J+ d/ V+ p; r; d: `. U; S8 X
decided to put the baby in a separate bed, and the% P, v0 V0 _, P
father was not hugging him with bare skin and had
/ O' h7 q9 K. s! ^been using protective clothing. A repeat testosterone
7 g. o$ b+ s% S8 j7 H7 Ytest was ordered, but the family did not go to the5 f# ?3 [  W1 m: }3 Y/ L" L
laboratory to obtain the test.  o. z4 M: g- Z  I; s6 B% @; x, I: F
Discussion
/ V/ q/ A1 k7 }. lPrecocious puberty in boys is defined as secondary5 u( r6 n0 H3 J
sexual development before 9 years of age.1,4
5 C2 B: U. T- s: b1 MPrecocious puberty is termed as central (true) when( D" H- y4 f" O% d
it is caused by the premature activation of hypo-
$ [% G% i$ u9 }) u' w( ~thalamic pituitary gonadal axis. CPP is more com-% E' s) x$ z; b+ c% n) P& j
mon in girls than in boys.1,3 Most boys with CPP
1 |0 i. b" P) X" M8 q# }may have a central nervous system lesion that is
1 @  O1 z; B1 [; P9 i' \* Oresponsible for the early activation of the hypothal-2 j. V% T( n- v0 ?, K$ X
amic pituitary gonadal axis.1-3 Thus, greater empha-
" Y" N" i  Y% K  y* U% @* Ssis has been given to neuroradiologic imaging in
# x3 @4 {! L/ I  g& ]boys with precocious puberty. In addition to viril-' j8 T( y/ e5 ~# {# A2 n2 Q
ization, the clinical hallmark of CPP is the symmet-9 d  f4 s; a+ C
rical testicular growth secondary to stimulation by
, G* x6 f5 J* k: x, lgonadotropins.1,3
$ _% a& Q8 R" p7 o" P1 Y$ n7 cGonadotropin-independent peripheral preco-7 x! U3 w! Z& Y4 V' F8 P  J
cious puberty in boys also results from inappropriate( O( a7 U5 R6 e
androgenic stimulation from either endogenous or
. M' d8 ?: ~" I9 D( f$ jexogenous sources, nonpituitary gonadotropin stim-
9 U# f1 f+ w: B9 o$ r' h2 \. bulation, and rare activating mutations.3 Virilizing
. A: Y. ~" a' S' dcongenital adrenal hyperplasia producing excessive/ @+ M3 t/ H9 `) x  Q9 V
adrenal androgens is a common cause of precocious: Y6 `4 J" R: v' o6 |
puberty in boys.3,4) m$ j# s' j4 j$ O$ e
The most common form of congenital adrenal& e, h- k7 G' q8 ?
hyperplasia is the 21-hydroxylase enzyme deficiency.+ C! X1 y' L7 M
The 11-β hydroxylase deficiency may also result in8 t( T' ]8 i7 A  X/ y/ p) C
excessive adrenal androgen production, and rarely,, [1 G2 n7 l3 g
an adrenal tumor may also cause adrenal androgen, j! n* x' S8 w6 A) @9 J* G
excess.1,39 e0 x$ X) t. P' q4 [
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 ^9 ]' d; s0 `542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
2 n( A9 n- K/ }8 {5 m! V; LA unique entity of male-limited gonadotropin-# N1 b5 L; E7 h& T0 s
independent precocious puberty, which is also known
) e) T+ }. t7 C/ A' fas testotoxicosis, may cause precocious puberty at a
5 W9 N1 w* b% W0 o) b/ |0 Vvery young age. The physical findings in these boys
+ I2 i" A& n& p' S9 Q! g/ ?3 uwith this disorder are full pubertal development,
2 O% e5 T( A$ n$ W2 G' Uincluding bilateral testicular growth, similar to boys
1 B3 O; T  L5 s. Q' @! Z2 l3 x% J( xwith CPP. The gonadotropin levels in this disorder" S& U, ?1 X2 a8 o+ v% Z- ]6 B
are suppressed to prepubertal levels and do not show8 i5 h: ~" H  E4 F& W9 [/ ^- Y- N
pubertal response of gonadotropin after gonadotropin-2 H3 o+ Q" a% h+ w" E+ c. K# `
releasing hormone stimulation. This is a sex-linked
: ^; f# r( M) e) G  C& tautosomal dominant disorder that affects only
9 U3 t/ m# L3 D6 B* M7 F! k$ Vmales; therefore, other male members of the family
, ~* C# u, w9 G  P6 Hmay have similar precocious puberty.3, a) J$ c0 u7 t  L+ [
In our patient, physical examination was incon-' K: G- L2 ?4 x5 n
sistent with true precocious puberty since his testi-
$ V, D- q2 a  F: J0 E; acles were prepubertal in size. However, testotoxicosis
+ ^  ~0 _( ]- g2 V, X7 |was in the differential diagnosis because his father
5 i7 j; C1 w1 {' w9 T( @/ zstarted puberty somewhat early, and occasionally,
/ `; `& h# x* }testicular enlargement is not that evident in the; F: ^3 Q4 k0 o4 [
beginning of this process.1 In the absence of a neg-8 _) L2 x  M, q! \4 k
ative initial history of androgen exposure, our3 L, g% @1 N! c- W2 `+ }- u- E
biggest concern was virilizing adrenal hyperplasia,
% H. e* A) ?% h3 W  Xeither 21-hydroxylase deficiency or 11-β hydroxylase
4 h6 A/ r2 e' X( y- vdeficiency. Those diagnoses were excluded by find-
. [* {/ `8 y  {$ [5 v" \% {ing the normal level of adrenal steroids.
1 q6 ?" I9 u$ Q0 kThe diagnosis of exogenous androgens was strongly6 F, M& d  @  Z
suspected in a follow-up visit after 4 months because0 _# c8 r1 i: n+ o( X$ w
the physical examination revealed the complete disap-
3 i; \* i; D0 k; J; H2 lpearance of pubic hair, normal growth velocity, and
( k% H* m$ V8 f8 Ndecreased erections. The father admitted using a testos-
# E7 v# l# d6 C4 bterone gel, which he concealed at first visit. He was
6 L& k% [, r! w: pusing it rather frequently, twice a day. The Physicians’" \; l$ g4 {* V- T6 L9 Y
Desk Reference, or package insert of this product, gel or
% d& s, y2 r6 M, @cream, cautions about dermal testosterone transfer to
1 E" ^9 |# G0 ]$ U% N7 Y0 h2 L9 Uunprotected females through direct skin exposure.
7 K5 e6 y* x$ z, b" ]6 {Serum testosterone level was found to be 2 times the
0 U- M1 r) U5 w+ b2 {& cbaseline value in those females who were exposed to+ M; B- K: I, ]/ O; J
even 15 minutes of direct skin contact with their male4 N1 a- n, R9 w& P4 r- y+ m
partners.6 However, when a shirt covered the applica-; @7 o0 M( v' b1 z6 D, b
tion site, this testosterone transfer was prevented.# x2 M' ?7 B8 S! Y9 c6 v
Our patient’s testosterone level was 60 ng/mL,
: L) r8 J6 z3 Z$ o: K6 @2 z8 T0 Swhich was clearly high. Some studies suggest that
+ j! b7 j8 O6 A: s5 adermal conversion of testosterone to dihydrotestos-
' N/ Y& s; x9 h& l% s2 d$ a7 u" Oterone, which is a more potent metabolite, is more
6 s$ N1 x. U8 G4 _* F- i$ [active in young children exposed to testosterone
# z" v2 \+ d1 A/ N: Jexogenously7; however, we did not measure a dihy-
! v: @5 x/ E! P' c8 h" `9 odrotestosterone level in our patient. In addition to
! w0 a6 @5 E* uvirilization, exposure to exogenous testosterone in: c( M8 j  [: E7 K9 @0 S
children results in an increase in growth velocity and7 G9 B7 Q2 K3 e
advanced bone age, as seen in our patient.: @8 |, w3 M9 Y
The long-term effect of androgen exposure during3 o7 l& H) r, c- Y! h/ A
early childhood on pubertal development and final! o* C4 t$ F, j1 `+ q3 w! o
adult height are not fully known and always remain
) J% _! ^: y) la concern. Children treated with short-term testos-
0 a1 Q* x, u, K% Z- v9 Jterone injection or topical androgen may exhibit some* ~) {  e7 z5 o
acceleration of the skeletal maturation; however, after) i, ]$ B7 C  m( f
cessation of treatment, the rate of bone maturation
! a" `3 Q1 u8 @/ tdecelerates and gradually returns to normal.8,92 u: X  e- r; Z- @* d6 D- m2 a
There are conflicting reports and controversy, U5 I0 Z. `( q3 G8 `5 I: X
over the effect of early androgen exposure on adult
! s# j; B! w" C7 M+ T5 j( Bpenile length.10,11 Some reports suggest subnormal
( A( [! t7 j3 ?adult penile length, apparently because of downreg-' X- Y9 A1 `1 }$ h3 p
ulation of androgen receptor number.10,12 However,
3 w" z; t0 j8 G- d% X6 I, HSutherland et al13 did not find a correlation between
4 l- W: X7 v6 l5 y2 hchildhood testosterone exposure and reduced adult
1 O/ `$ Q! p5 qpenile length in clinical studies.; \9 O8 N4 X; n  r8 y4 B5 l2 z& t6 E
Nonetheless, we do not believe our patient is: @$ A/ @5 d+ R# B3 p( y0 S
going to experience any of the untoward effects from
: K" @3 t5 A' o# Y2 a4 ?testosterone exposure as mentioned earlier because
9 F& v4 @: n( Ithe exposure was not for a prolonged period of time.
4 f6 i; A2 q: J1 EAlthough the bone age was advanced at the time of
1 r$ Z' w" A: b" H6 x& Ydiagnosis, the child had a normal growth velocity at
/ @* g8 u% _! V+ Y' P8 K0 a  `$ Vthe follow-up visit. It is hoped that his final adult' u- @1 I) i! I* v3 I6 y; E* ^2 {5 M& ^
height will not be affected.! @* ~& B. j+ Y+ l
Although rarely reported, the widespread avail-& g0 n. U" U" W
ability of androgen products in our society may
; h" C& B( h% h  Nindeed cause more virilization in male or female
  X( H; z0 K" j6 [. Ochildren than one would realize. Exposure to andro-
/ _0 c8 @' z0 tgen products must be considered and specific ques-
% j  n' D/ Z. b. R( g" Mtioning about the use of a testosterone product or
' P! y& U& a( \; X6 k, b, M$ vgel should be asked of the family members during
( o- `8 f- a' n- kthe evaluation of any children who present with vir-" E/ W# O9 j9 M1 b" H2 r' v
ilization or peripheral precocious puberty. The diag-
9 o" F! s- K; N2 y0 [) F/ Anosis can be established by just a few tests and by6 H6 a; C1 v$ Y% P; U  o& A
appropriate history. The inability to obtain such a
" o5 ]# T* b& W- ~# L0 V. N: r2 n  mhistory, or failure to ask the specific questions, may$ O3 D- \. k! v( i0 A/ o. \
result in extensive, unnecessary, and expensive& C, T' S/ E5 ^4 R+ V
investigation. The primary care physician should be
# D6 z8 ^3 O; Y! X$ xaware of this fact, because most of these children3 j) i: ~  @0 C5 _4 S9 G: y
may initially present in their practice. The Physicians’8 U" M/ N+ x) R( s8 [# M1 A
Desk Reference and package insert should also put a. U8 ~2 A5 j# L: L+ P/ j% G, o
warning about the virilizing effect on a male or
  M+ _% o3 x8 c) s/ dfemale child who might come in contact with some-
% y# [/ T4 X1 r: }# q0 G/ ~one using any of these products.
1 e3 m" H% Q5 ]0 ?5 l4 v# t9 XReferences9 K* |! Z  ~) K1 o9 I
1. Styne DM. The testes: disorder of sexual differentiation
& G$ n! @5 g8 Sand puberty in the male. In: Sperling MA, ed. Pediatric0 I5 G. @7 R. s1 D
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
( ?/ t. s) u& M+ c2002: 565-628.
; \: t; W( w8 a, B: R2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
. e. `6 r- Q: Q* `puberty in children with tumours of the suprasellar pineal
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
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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

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發表於 2025-3-8 22:04:50 | 顯示全部樓層
絕對的好貼!謝謝啊!逐字逐圖地看完這個帖子以後,我的心久久不能平靜,感恩啊!
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