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Sexual Precocity in a 16-Month-Old4 y' R% b- M3 T
Boy Induced by Indirect Topical  O( q9 X+ k3 h) p7 n9 `2 E
Exposure to Testosterone
  G6 R" E1 }' K! x; rSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,29 o; q# V7 T, P! L8 }6 D
and Kenneth R. Rettig, MD1, d8 d( V% ~- d* a* r" K. ^( j/ U/ I
Clinical Pediatrics; r, s7 t8 g, z# k) m4 [3 H
Volume 46 Number 6
- j& ]* \" M" z' r  b. AJuly 2007 540-543( j' X$ }6 W( K
© 2007 Sage Publications. Q' |$ J/ M. [
10.1177/00099228062966511 d+ X6 O" S2 M" W; Z! \
http://clp.sagepub.com
8 a$ Q& k: j5 q4 h- v: vhosted at9 G* R1 x; M! S# |/ `
http://online.sagepub.com3 m+ Q. k2 X1 b3 E6 @
Precocious puberty in boys, central or peripheral,
% i5 o8 ]4 Q: c+ T6 [  z: ois a significant concern for physicians. Central
- k4 ^/ _8 \! t0 H) k' s' iprecocious puberty (CPP), which is mediated8 c) f2 q/ s  ^: B/ }) |
through the hypothalamic pituitary gonadal axis, has  k$ I) Q. E0 s! ?/ ^4 l
a higher incidence of organic central nervous system4 A+ E- P8 n7 W3 N  n, A7 [. R/ ^
lesions in boys.1,2 Virilization in boys, as manifested4 @& T* o' J% L0 U2 w4 b
by enlargement of the penis, development of pubic
8 J. L  e' t& J8 `hair, and facial acne without enlargement of testi-9 M! ?7 ^3 I7 Z; X: g7 B* c) y
cles, suggests peripheral or pseudopuberty.1-3 We2 M- Z! F  }0 |
report a 16-month-old boy who presented with the
+ h! g* B* N6 I5 {5 N6 s$ ~2 u, Qenlargement of the phallus and pubic hair develop-
8 ?5 O0 p7 v5 Fment without testicular enlargement, which was due
. C  N+ I* }9 }# f! Q8 d5 gto the unintentional exposure to androgen gel used by6 P. k! t4 Y! v/ M
the father. The family initially concealed this infor-
" u' S2 ?7 u# z3 k- q% cmation, resulting in an extensive work-up for this
; x0 g8 w; S3 Y( `, Dchild. Given the widespread and easy availability of5 `! j( p. N- S" R+ e! ~
testosterone gel and cream, we believe this is proba-* y% H5 U5 S4 o1 q; D& n# U
bly more common than the rare case report in the- s$ H" G' ~2 ~& q
literature.4
1 ^* k" W2 w+ }5 A# F: A# p  I- e% S% kPatient Report
( {; |9 q. b& z! [; yA 16-month-old white child was referred to the" E* E& w/ X5 n* H* `
endocrine clinic by his pediatrician with the concern4 n& d% W- ?1 }- i. c0 P  a9 {
of early sexual development. His mother noticed% }" ?0 h+ B4 V
light colored pubic hair development when he was
# p& a0 ?4 V  n1 k6 SFrom the 1Division of Pediatric Endocrinology, 2University of
6 e7 y  S& f- o% S  X; T2 u- G/ YSouth Alabama Medical Center, Mobile, Alabama.
2 K0 @: a$ o1 YAddress correspondence to: Samar K. Bhowmick, MD, FACE,
9 s* L! r! g4 {8 ?7 TProfessor of Pediatrics, University of South Alabama, College of3 Z% s1 V( q. f% L. K
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;( S( _# j0 B6 }5 S# O; ?
e-mail: [email protected].
. W0 w6 ]% J# i( X" w" c3 {5 [1 Jabout 6 to 7 months old, which progressively became8 Q: _, c% [* R# X- [# O
darker. She was also concerned about the enlarge-* x3 a8 W1 S4 l2 z
ment of his penis and frequent erections. The child
1 |8 e( e0 X0 \) `, j1 ?9 W/ u& Swas the product of a full-term normal delivery, with
, l* k: z/ V" P! l2 a9 ma birth weight of 7 lb 14 oz, and birth length of
( n2 `' S! h  K7 m4 H4 e. z20 inches. He was breast-fed throughout the first year. r  g# S  w' p  I4 D
of life and was still receiving breast milk along with
3 N/ T/ t! i# Wsolid food. He had no hospitalizations or surgery,! R0 M) i$ L7 c  b; G9 @
and his psychosocial and psychomotor development
6 J5 ~0 i2 V0 }! q8 X5 Pwas age appropriate.! [) m; r5 o; `' _% q2 {% [8 m
The family history was remarkable for the father,
0 d$ A' c5 S2 [4 K' {who was diagnosed with hypothyroidism at age 16,
( c; Z7 x5 |! N, u: |which was treated with thyroxine. The father’s
6 F! C  e% m4 @! h" F: Bheight was 6 feet, and he went through a somewhat
) @2 ]& f' ]. Z- [9 Gearly puberty and had stopped growing by age 14.6 g4 g8 c- c. l6 O2 i, E5 q
The father denied taking any other medication. The
7 |6 P/ m1 }/ a- E' k. j& l8 [child’s mother was in good health. Her menarche9 ?2 G- q+ a: v2 x. ?
was at 11 years of age, and her height was at 5 feet4 L/ c$ ~. C; f) n4 Y
5 inches. There was no other family history of pre-
7 L9 O( _9 J% N- D1 Jcocious sexual development in the first-degree rela-# z$ r0 c4 Y) e( [1 I* E* y" F
tives. There were no siblings.6 @, R) [" j6 e3 Q8 x: @; }
Physical Examination
/ w* [4 w6 |) O( H4 h- w  }The physical examination revealed a very active,- N- `. ~0 C7 f2 b/ \6 S
playful, and healthy boy. The vital signs documented3 j, w2 B& A) W3 Z
a blood pressure of 85/50 mm Hg, his length was
9 C9 P9 Z* j& C+ l90 cm (>97th percentile), and his weight was 14.4 kg
; g8 {+ z: s2 N6 e(also >97th percentile). The observed yearly growth
6 |- F1 J  b. u0 s- w) a8 a3 c" Lvelocity was 30 cm (12 inches). The examination of  ?; G. |1 ~2 @& W
the neck revealed no thyroid enlargement.- d; b& m7 e2 q' S! G5 W4 @
The genitourinary examination was remarkable for: T5 Q! G! v1 F
enlargement of the penis, with a stretched length of
) [3 f+ \% |9 g/ [/ p8 cm and a width of 2 cm. The glans penis was very well7 q9 J. q: i/ w- F4 b( B- p
developed. The pubic hair was Tanner II, mostly around! ?7 N* _% p! d6 c7 n
540# Y" _. \" m5 {1 A; `" w
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! t: X  x  D+ T* D7 lthe base of the phallus and was dark and curled. The4 m; r7 ?" Z* \4 r- O9 {
testicular volume was prepubertal at 2 mL each.& n9 K$ _; U7 a7 e
The skin was moist and smooth and somewhat' _7 i4 d* o. H$ F6 F
oily. No axillary hair was noted. There were no
$ n; g9 B# E: m. t6 q* t- ^5 Wabnormal skin pigmentations or café-au-lait spots.
0 t) \( j! T1 rNeurologic evaluation showed deep tendon reflex 2+
$ C. I( W( D1 h3 k( Q* t/ M! Q7 Ybilateral and symmetrical. There was no suggestion
% W1 |: h5 ~' |: oof papilledema.
- e( T- b9 u  m2 }9 A# E0 O0 ELaboratory Evaluation) Q/ H/ G8 K7 B; z# l3 a
The bone age was consistent with 28 months by: y  l* Z) P+ f4 _1 l+ z
using the standard of Greulich and Pyle at a chrono-
9 I0 W3 G5 ?0 O! J" K$ Y% ?0 rlogic age of 16 months (advanced).5 Chromosomal0 l2 P; M4 k! |" M3 [9 N3 `
karyotype was 46XY. The thyroid function test' T+ x8 z7 S. s7 P1 s' a. K! X
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
- B# [* ?( g2 B% u, \lating hormone level was 1.3 µIU/mL (both normal).
5 b6 A1 `. r$ Y( m# }3 d' ZThe concentrations of serum electrolytes, blood
8 }+ ?1 Q1 z" j4 e4 W8 E1 ]urea nitrogen, creatinine, and calcium all were) l( R& t6 ]1 I# L& |& N
within normal range for his age. The concentration1 c; P4 y' b2 O" L6 G
of serum 17-hydroxyprogesterone was 16 ng/dL
9 o- @! J  y6 o; d/ D(normal, 3 to 90 ng/dL), androstenedione was 202 y% w  M7 Y" T/ X0 J0 z
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-, E& P4 G# W/ H# O6 k
terone was 38 ng/dL (normal, 50 to 760 ng/dL),* S! n9 K. f/ R
desoxycorticosterone was 4.3 ng/dL (normal, 7 to) q8 h3 \1 T: b2 |5 I
49ng/dL), 11-desoxycortisol (specific compound S)
' G# b  u% s" ]was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
2 o" S* _: S. Ktisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
) ~# q  u( S# e! a7 I' p  ?6 ~4 m3 F  Ktestosterone was 60 ng/dL (normal <3 to 10 ng/dL),( d2 p4 n& h- o: w; ^* g8 i% V
and β-human chorionic gonadotropin was less than( t4 X& j, Q, d
5 mIU/mL (normal <5 mIU/mL). Serum follicular: ~1 X2 u7 _5 M  ~
stimulating hormone and leuteinizing hormone
3 h# {: T0 {, S3 y/ J# Wconcentrations were less than 0.05 mIU/mL
" u+ ]! W5 r7 T; Y0 [(prepubertal).
9 x9 T2 |7 R; c" z$ y* FThe parents were notified about the laboratory) s" R$ X- k1 h( i. M
results and were informed that all of the tests were# M! l( W4 k2 Q' P3 r
normal except the testosterone level was high. The
$ B" R+ C' z7 \follow-up visit was arranged within a few weeks to8 ^: X& ?5 p9 l1 ~9 h
obtain testicular and abdominal sonograms; how-5 T: b. K; ?- O3 _
ever, the family did not return for 4 months.  t5 H/ s. D" Z( j9 Z8 P- \+ k7 Y
Physical examination at this time revealed that the9 w# F/ ~+ M: z
child had grown 2.5 cm in 4 months and had gained
8 `) _/ p  p# K+ A- p5 }* p' J; I0 }2 kg of weight. Physical examination remained/ Q1 g$ y3 Y. h. P3 J) o" b
unchanged. Surprisingly, the pubic hair almost com-
; x) }; r, a6 g. G( ?+ ipletely disappeared except for a few vellous hairs at
+ Z2 J' o: K1 o" L* B- kthe base of the phallus. Testicular volume was still 2
. ^! q8 X5 W& |- gmL, and the size of the penis remained unchanged.0 c5 l, n; l& j3 X; }
The mother also said that the boy was no longer hav-. W0 [/ P! p$ o" |5 k! a
ing frequent erections.
- y4 J- k: V" t0 xBoth parents were again questioned about use of' F6 T3 a5 \7 k- |5 N
any ointment/creams that they may have applied to! `# n# D9 ~, \, ~: ?& J/ E+ _
the child’s skin. This time the father admitted the0 k0 R3 f  L; i# B- h$ k8 I
Topical Testosterone Exposure / Bhowmick et al 541
+ ?  a8 w2 x2 M. r" huse of testosterone gel twice daily that he was apply-; M# i! G  d5 j8 W
ing over his own shoulders, chest, and back area for8 x% W2 n$ [( U3 }- k1 d
a year. The father also revealed he was embarrassed
* P# D" x, F+ X# e1 u8 mto disclose that he was using a testosterone gel pre-
/ u+ _7 J% Y* p9 ~. Mscribed by his family physician for decreased libido
7 L2 U8 S0 D$ [2 M7 W; ssecondary to depression.6 ?! G, g- U/ m% l2 O0 \' H
The child slept in the same bed with parents.2 `: J; D3 V' H5 E# ?& `) d2 ]
The father would hug the baby and hold him on his& _3 ~9 o) ~; q  L0 t# i2 [
chest for a considerable period of time, causing sig-+ O% {8 U; P  r8 u! v
nificant bare skin contact between baby and father.1 U1 Z% ]1 t2 p1 \: t9 x5 [
The father also admitted that after the phone call,
/ L1 p& l8 G& K! Mwhen he learned the testosterone level in the baby9 o' x2 `0 I8 D$ H) ~; s8 M
was high, he then read the product information  }% G8 t# t3 s+ |! J. R/ q6 V' ~
packet and concluded that it was most likely the rea-. D* V2 N) g' @5 ^) g7 x
son for the child’s virilization. At that time, they
4 Y6 o) r+ {. D( {/ odecided to put the baby in a separate bed, and the
4 h1 Q  }1 g% d5 `; B" H+ T: X% ~father was not hugging him with bare skin and had! I0 l& k1 f( G8 m4 v8 }9 I* d8 q* b
been using protective clothing. A repeat testosterone- ^+ A. h' Y. M+ r- {( d' \% k& q
test was ordered, but the family did not go to the8 M2 a& V6 f. c
laboratory to obtain the test.
* `+ K1 W8 I' s# i' C+ w# aDiscussion
5 w5 {, n; H* I* HPrecocious puberty in boys is defined as secondary
  k# Y$ M  y' R; D% `! E, E/ Ssexual development before 9 years of age.1,4
5 k' ~. A: `# f2 W, _Precocious puberty is termed as central (true) when! B( x- t6 V& l# `
it is caused by the premature activation of hypo-2 |& D5 h/ x5 f
thalamic pituitary gonadal axis. CPP is more com-
5 O* K- f5 @0 R' C& Tmon in girls than in boys.1,3 Most boys with CPP' y+ O) V* L7 K3 V5 p& H
may have a central nervous system lesion that is
6 K2 S" T0 S; N! aresponsible for the early activation of the hypothal-
# Q$ s1 y/ ?# ]- G; V7 @* jamic pituitary gonadal axis.1-3 Thus, greater empha-2 b8 @2 T0 P9 o3 d- O5 t, D
sis has been given to neuroradiologic imaging in
) H2 j8 X* _2 A" fboys with precocious puberty. In addition to viril-
% N4 |9 x0 d9 w0 I0 Fization, the clinical hallmark of CPP is the symmet-" c; T: G5 H; v9 v& E
rical testicular growth secondary to stimulation by
# {4 I5 u- N- X  s( C0 xgonadotropins.1,3
; {& _) G- \, O! z1 RGonadotropin-independent peripheral preco-
6 x- s+ E- u% u6 Q" Y0 A5 _" gcious puberty in boys also results from inappropriate( L" l$ ]. M  [+ h
androgenic stimulation from either endogenous or
# h6 @1 c- p/ Y/ o, ^1 wexogenous sources, nonpituitary gonadotropin stim-
: B( ^# K7 a% _5 ^) g6 Fulation, and rare activating mutations.3 Virilizing  p9 @% a- c+ F* u6 @. F
congenital adrenal hyperplasia producing excessive7 V- A! R7 E! J1 Q, n- ?
adrenal androgens is a common cause of precocious8 J  S; }% y( z: c+ ^5 G
puberty in boys.3,4
/ ~% _0 ]/ g0 t! X. b. `  hThe most common form of congenital adrenal1 z" L/ \4 h, ]/ k+ E) f2 Z
hyperplasia is the 21-hydroxylase enzyme deficiency.9 K, m, y7 P8 {) F8 I/ B- ^
The 11-β hydroxylase deficiency may also result in5 C% D  H* l( i, o5 q3 C4 L
excessive adrenal androgen production, and rarely,
, K" V- _" T! \9 O" L( Gan adrenal tumor may also cause adrenal androgen, z+ R* F: E/ ]: n: Y
excess.1,3
; D# L  e0 i5 Bat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 S3 W7 ~  B# @6 w3 {' G542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
7 M2 O" Z2 i' ?A unique entity of male-limited gonadotropin-5 w- w/ S5 Y. w8 k, f, p
independent precocious puberty, which is also known  d- {- B  u9 V8 j% D# o6 J
as testotoxicosis, may cause precocious puberty at a
5 j2 n5 S/ f# u5 n; l; U0 uvery young age. The physical findings in these boys/ O) D/ ?+ L: [" z/ ^
with this disorder are full pubertal development,! z, p. A" O" N& Q$ S
including bilateral testicular growth, similar to boys7 L9 m6 @5 U; U: D+ h" z$ m# E
with CPP. The gonadotropin levels in this disorder
& Q8 Y$ T2 B0 t" _/ M- ?8 U( A% ?are suppressed to prepubertal levels and do not show
# q, k% q, B3 n& G* h# }pubertal response of gonadotropin after gonadotropin-
) u+ p3 A! D: |7 D0 creleasing hormone stimulation. This is a sex-linked
0 M8 m3 k0 y9 y4 k7 _5 _autosomal dominant disorder that affects only3 x4 ]: e4 @- \
males; therefore, other male members of the family
' {: z: I+ T& ?1 umay have similar precocious puberty.3; h) G. d9 r& h. [2 ^
In our patient, physical examination was incon-
& ]3 h1 N7 d1 `2 V) j+ m" qsistent with true precocious puberty since his testi-" y$ f6 Z7 h' k% F1 f' r# R  X) l
cles were prepubertal in size. However, testotoxicosis
5 M- s: h# s, Uwas in the differential diagnosis because his father3 o% {2 W8 X) U& n
started puberty somewhat early, and occasionally,
! w& D/ {: u& etesticular enlargement is not that evident in the; u4 h& ?) l7 j- S( j* I
beginning of this process.1 In the absence of a neg-" \1 `: O9 H( t; V, d: [
ative initial history of androgen exposure, our6 M' Z) O! p: Y$ d
biggest concern was virilizing adrenal hyperplasia,; G; t8 ?& Z8 }* {: D- W: \+ c
either 21-hydroxylase deficiency or 11-β hydroxylase
  k9 ~6 Y- D3 h( l' }) |deficiency. Those diagnoses were excluded by find-
( u7 C' k4 U% n. a$ L$ n8 sing the normal level of adrenal steroids.1 z( ]  u' u" x9 q6 }1 ~, ?
The diagnosis of exogenous androgens was strongly' c+ g( q: B: t2 r8 x9 j2 W
suspected in a follow-up visit after 4 months because4 L1 H2 h% c3 [8 i/ \/ [
the physical examination revealed the complete disap-1 E$ h6 b) U4 V; p) F1 B* T
pearance of pubic hair, normal growth velocity, and9 H+ O3 V& X  G/ W8 A9 U
decreased erections. The father admitted using a testos-
8 C3 p: B- a$ U9 v. v% Y$ T" }terone gel, which he concealed at first visit. He was
4 w- o4 B- g' u( F! W' q) Y! busing it rather frequently, twice a day. The Physicians’
7 x3 N3 O3 Z! G' Q/ D' HDesk Reference, or package insert of this product, gel or* O! [- L/ M3 f2 A5 ~0 [& d' @
cream, cautions about dermal testosterone transfer to
8 c: m  l2 A- Y7 R, c$ Ounprotected females through direct skin exposure.' K- {. |6 v) P9 Y1 i" e
Serum testosterone level was found to be 2 times the2 J3 ]/ S. t5 \( j
baseline value in those females who were exposed to
) J% U- |) o" h* U7 J! D6 Ceven 15 minutes of direct skin contact with their male
. X7 C" v0 H' l" }; {partners.6 However, when a shirt covered the applica-/ T6 k; r& A, i4 M2 O, O8 ]4 U
tion site, this testosterone transfer was prevented.
# y8 }/ \3 P: r- }3 VOur patient’s testosterone level was 60 ng/mL,
' Q6 h0 j: e6 w  }  Dwhich was clearly high. Some studies suggest that
) G' N" F3 u' U4 a+ ~! k$ S1 bdermal conversion of testosterone to dihydrotestos-8 s* U4 d1 t# K: b
terone, which is a more potent metabolite, is more
# x1 R- K6 Y  N; L0 W+ zactive in young children exposed to testosterone7 b5 g7 \; C4 L# w, X
exogenously7; however, we did not measure a dihy-
" Y- ?  G+ S* M. R& ?drotestosterone level in our patient. In addition to
8 N  t- Y& I- L3 I; Uvirilization, exposure to exogenous testosterone in
7 k. ?) b2 h+ h2 y* v. }% Echildren results in an increase in growth velocity and* l7 v$ Y$ \+ ~2 c) k* I9 U
advanced bone age, as seen in our patient.+ `% A2 z; q8 S* e$ ]; t8 J* Z
The long-term effect of androgen exposure during# {" @3 p2 J9 D6 e# f- u+ A' \
early childhood on pubertal development and final
0 T4 ~0 g1 }. e/ N, Q8 [( \# J! vadult height are not fully known and always remain2 b' W, o" `# [7 L$ H" }* N$ C
a concern. Children treated with short-term testos-/ }  o9 ?( [  P- F$ {/ r. A
terone injection or topical androgen may exhibit some5 G* j! q! `/ y( O/ t) Y8 G/ ?9 H
acceleration of the skeletal maturation; however, after
( p8 v2 v6 N5 E' y/ r$ U9 pcessation of treatment, the rate of bone maturation, p$ r( X" {# y. q6 o8 r8 U
decelerates and gradually returns to normal.8,9
, X. S5 }7 h, g8 n+ VThere are conflicting reports and controversy
+ [# P( n5 z5 X0 `over the effect of early androgen exposure on adult
# n" ]' |+ u, w7 w2 [* epenile length.10,11 Some reports suggest subnormal+ ?) \' x& n$ `# B6 O3 j5 O) O; S
adult penile length, apparently because of downreg-
; g8 U. I+ p8 {: D3 `ulation of androgen receptor number.10,12 However,
4 f/ a% [9 N! B' D2 l* g. ~9 W* FSutherland et al13 did not find a correlation between
5 D5 D) s! ]. i/ wchildhood testosterone exposure and reduced adult% B: n* a: j" k% K5 s
penile length in clinical studies.; {% j  ?: y; F' _! ]' u
Nonetheless, we do not believe our patient is
6 F+ D+ {/ `+ U" O' w$ q) A$ w7 igoing to experience any of the untoward effects from. m  f8 }0 |. r, g
testosterone exposure as mentioned earlier because4 N# ?7 L% S( C+ K
the exposure was not for a prolonged period of time.3 p% m. C( f, P' H* m2 Q* S% F" E
Although the bone age was advanced at the time of
0 c6 Y* @1 |: s$ gdiagnosis, the child had a normal growth velocity at! p9 A5 ~5 W' ~$ Y  F
the follow-up visit. It is hoped that his final adult# S1 b9 B- F. `! J, j- j
height will not be affected.
: J& }- \9 h. `! j" G9 s4 gAlthough rarely reported, the widespread avail-& R2 w4 H# \  W) ^2 H
ability of androgen products in our society may8 B5 Q6 i) o$ A& K& ~4 f, j
indeed cause more virilization in male or female3 d6 |( W9 y( S
children than one would realize. Exposure to andro-
, x# {) n2 Z# p, B, H/ Hgen products must be considered and specific ques-' i/ `# {( A% W# x# n
tioning about the use of a testosterone product or! Y5 _# Z& e* @$ C! G2 V5 H3 v
gel should be asked of the family members during" v) }( v: A. V/ `1 F
the evaluation of any children who present with vir-
- s6 ~9 O( X! p; pilization or peripheral precocious puberty. The diag-
6 q; J/ o* ]' M7 d- M9 {nosis can be established by just a few tests and by! f7 Q. A: @1 h" u
appropriate history. The inability to obtain such a, u6 p! Y8 O6 [5 l
history, or failure to ask the specific questions, may
$ O* [2 C' r4 `% L: I& }: D5 yresult in extensive, unnecessary, and expensive9 q/ D  @% Y# ]( Z. c& t  C) J# @
investigation. The primary care physician should be$ i/ a" ]! }; w* G
aware of this fact, because most of these children! G, `. m. [" G& O
may initially present in their practice. The Physicians’
( n. w% m( {: U$ GDesk Reference and package insert should also put a; U# n6 O4 i* R4 b9 t  V+ Y
warning about the virilizing effect on a male or
$ h2 }: u2 Q# @female child who might come in contact with some-& A1 _7 \6 Q/ E/ a5 A- t9 [
one using any of these products." c9 J7 H: S7 G
References& c  |( c% a1 t3 U0 E4 c: }0 D+ w
1. Styne DM. The testes: disorder of sexual differentiation
7 a- z8 \4 T% b% Dand puberty in the male. In: Sperling MA, ed. Pediatric
5 }- K- I$ b+ B" @2 S/ Y5 L+ t+ [Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;5 [5 o, D( Y% R, h( u; C" V
2002: 565-628.
1 q5 O3 x. r2 K$ N" o- {3 ?' L2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious. _; g9 y3 ]% K  I& k4 T7 u
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old$ A$ k) e" S" @# N- @' F: s) W
Boy Induced by Indirect Topical: G( _! Y! J( V# S  t) z
Exposure to Testosterone
+ B3 [/ b: X: ISamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
: @9 H* M$ _5 U$ c: sand Kenneth R. Rettig, MD1
9 W9 B9 J: U1 Z& G/ I6 ^( dClinical Pediatrics! C1 P) g% ]' B- e0 d; P2 I
Volume 46 Number 63 I) h! [7 T9 @9 |) H. U
July 2007 540-5437 |1 g% T& M; j, z, e; n
© 2007 Sage Publications
5 ?3 Z8 d8 y; J4 v6 J; X; R* _10.1177/0009922806296651! s: E8 n, E$ _  c" j# ?" k5 O/ u/ X
http://clp.sagepub.com
- U0 T% N' F+ T" ]3 fhosted at* L7 ]" S- W5 }3 @- [- [
http://online.sagepub.com
) H: B# ~6 i1 l; ?  ePrecocious puberty in boys, central or peripheral,
% S5 Q0 K+ d) A* U3 J% ]+ [is a significant concern for physicians. Central/ K' H% J' g3 u" h) n
precocious puberty (CPP), which is mediated9 }8 M4 P& _4 t# {& j1 E" g9 w
through the hypothalamic pituitary gonadal axis, has) r$ a, Z. n" u1 j! W
a higher incidence of organic central nervous system  q) K' z! d2 w
lesions in boys.1,2 Virilization in boys, as manifested7 k. a. m# o6 }; m9 U2 j
by enlargement of the penis, development of pubic
  M* R; `+ X" j4 a% a6 [hair, and facial acne without enlargement of testi-
9 U  d# O" D' l) W4 P3 }cles, suggests peripheral or pseudopuberty.1-3 We
9 b( w0 T, [) y  areport a 16-month-old boy who presented with the) w7 D% Y/ \2 ~* ?
enlargement of the phallus and pubic hair develop-
. T5 ]( d% Z7 r* _( zment without testicular enlargement, which was due# }4 X3 ^# E' h) n  y
to the unintentional exposure to androgen gel used by/ y% T0 R8 r! \7 h% l  }
the father. The family initially concealed this infor-) u' U  {" q/ E4 s2 K" o! U
mation, resulting in an extensive work-up for this9 |$ a: d, C: @+ Y
child. Given the widespread and easy availability of
0 g# e9 H: e) Y$ gtestosterone gel and cream, we believe this is proba-+ z/ A2 _! M# P; @0 m
bly more common than the rare case report in the
! ^5 t% s( t! q2 ~9 \4 _' }; rliterature.4' ~: U' Q. u5 E6 l
Patient Report
. m/ y1 i! ~& @8 s' Y2 Y, XA 16-month-old white child was referred to the0 q% `0 o5 Q1 f/ X+ Z$ ]% q
endocrine clinic by his pediatrician with the concern
9 M- z1 F9 `$ Gof early sexual development. His mother noticed
: g  |( O) e1 U. N. i/ clight colored pubic hair development when he was
5 |% t2 ^6 Y- g0 }" AFrom the 1Division of Pediatric Endocrinology, 2University of7 a7 W) i1 X6 {8 I- d8 m& V
South Alabama Medical Center, Mobile, Alabama.
( X& I& ]/ N1 b8 H  V% {% CAddress correspondence to: Samar K. Bhowmick, MD, FACE,
) _5 c; ]6 ?6 y8 c, ~Professor of Pediatrics, University of South Alabama, College of
( v( r& S. ~& S# [/ ]Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;# |8 N0 `6 G; v0 x! K) V, ^" H7 z
e-mail: [email protected].
& d; v; A1 E# {; S1 D0 K9 @about 6 to 7 months old, which progressively became0 @& C5 {4 Q2 \% H
darker. She was also concerned about the enlarge-% X3 _: n) q& n+ b, y
ment of his penis and frequent erections. The child
- m8 j6 V5 s6 z7 X- F* I# xwas the product of a full-term normal delivery, with
: m5 q( Y3 {' b5 R- u$ ]a birth weight of 7 lb 14 oz, and birth length of
% ~) G. r  V: ^. V3 ^20 inches. He was breast-fed throughout the first year: m8 H2 r" Y3 r6 X! X4 y& q( |1 ]
of life and was still receiving breast milk along with
. e1 m+ r- z# d6 P# ]solid food. He had no hospitalizations or surgery,3 L( a4 G/ u) ~5 D. S
and his psychosocial and psychomotor development
! \! ^- |- J: M: jwas age appropriate.
. ^) X4 o: A; P. Q: b1 lThe family history was remarkable for the father,
6 _. a( p) f* q+ p& swho was diagnosed with hypothyroidism at age 16,
+ n5 r2 M/ F5 J! J  f; mwhich was treated with thyroxine. The father’s
+ h+ v  j- |9 P4 b+ J$ H9 Jheight was 6 feet, and he went through a somewhat
$ w) }0 g7 |& m' F" Qearly puberty and had stopped growing by age 14.
# ]0 n9 x9 U( d# YThe father denied taking any other medication. The3 F% T- O8 x8 ^# G3 M
child’s mother was in good health. Her menarche  ]( E3 E  T6 K
was at 11 years of age, and her height was at 5 feet
$ p9 Q9 T, T7 J' W* j4 L5 inches. There was no other family history of pre-
- P9 B: s# j# ~* H1 N3 C+ F  Gcocious sexual development in the first-degree rela-
# I& h& n5 n: ntives. There were no siblings.
6 n6 i* W; H7 P# W* z+ V( gPhysical Examination
: t7 U# s+ i. E- S7 F/ r; o9 nThe physical examination revealed a very active,
! H0 B6 ?! B! `) E) }% S/ iplayful, and healthy boy. The vital signs documented) L5 z& D8 v! S% m
a blood pressure of 85/50 mm Hg, his length was! c' W! B! S2 Z3 c- O, y
90 cm (>97th percentile), and his weight was 14.4 kg
$ c+ l7 z8 A; o" P3 K1 [7 U( M; x- Z(also >97th percentile). The observed yearly growth
& D' Y% z8 m' O- }' H- Nvelocity was 30 cm (12 inches). The examination of% e+ e& F: r' H* R
the neck revealed no thyroid enlargement.
: O- g6 Z+ N5 A6 g- }) z1 h4 P" |9 J- A9 |The genitourinary examination was remarkable for
- P/ h# @4 v8 f$ Oenlargement of the penis, with a stretched length of$ @( |8 x4 b$ I& Z" e1 M. H
8 cm and a width of 2 cm. The glans penis was very well
$ V0 O6 S6 i- ^' M0 i9 j" Wdeveloped. The pubic hair was Tanner II, mostly around
* n3 ^1 z' q; s( A( U540
) l) r4 Y% {0 `( K* yat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- k' S3 j% s! s" Sthe base of the phallus and was dark and curled. The/ f! i( R; @0 d
testicular volume was prepubertal at 2 mL each.
) c: T0 b) Q  q$ n: _. ]  D6 ZThe skin was moist and smooth and somewhat0 n9 ]( `- `9 t7 }& r; ]
oily. No axillary hair was noted. There were no
7 c& G* e5 h3 _/ c& Gabnormal skin pigmentations or café-au-lait spots.+ \( x# Q0 F; ?* z
Neurologic evaluation showed deep tendon reflex 2+8 s( [, k' ^, k- J/ K7 H! ]% J
bilateral and symmetrical. There was no suggestion. b' [$ R, q( j! c1 |
of papilledema.6 u# y- V3 O4 [4 C: S5 B
Laboratory Evaluation5 x$ m7 ^# I  t
The bone age was consistent with 28 months by
0 f: c: `5 t! pusing the standard of Greulich and Pyle at a chrono-4 z+ p- F0 M6 Z& t; X) o
logic age of 16 months (advanced).5 Chromosomal
) _8 V, y: Z) O( r& i; t  Zkaryotype was 46XY. The thyroid function test0 v5 v6 X4 G  G
showed a free T4 of 1.69 ng/dL, and thyroid stimu-5 y: x4 z1 a9 }% L& g+ K
lating hormone level was 1.3 µIU/mL (both normal).
8 J/ G) x) }; L! Y1 ^' ]5 l& R: |The concentrations of serum electrolytes, blood) t; _0 l) Q9 S4 L0 L2 q2 e- W
urea nitrogen, creatinine, and calcium all were$ h/ ]' X" U0 K4 _
within normal range for his age. The concentration
$ U/ C: e; ~* p1 n+ u) Yof serum 17-hydroxyprogesterone was 16 ng/dL, P1 t  R  O4 ~3 O( R8 F
(normal, 3 to 90 ng/dL), androstenedione was 20/ ^( |( z/ j5 c; D% l5 @
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
, [  f  {; n0 U( E7 oterone was 38 ng/dL (normal, 50 to 760 ng/dL),; A- X! V; i8 O3 a! q% k
desoxycorticosterone was 4.3 ng/dL (normal, 7 to+ b8 P8 ]- I, o
49ng/dL), 11-desoxycortisol (specific compound S)' W/ o2 S, W3 z# ?
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-" `& U7 m3 W5 G/ z
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total7 W7 i6 n$ R( z- H
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
/ D9 k/ {4 O+ [8 L) A$ ~% ?, s& p6 iand β-human chorionic gonadotropin was less than: V9 t' k1 ~8 V( _6 H& }7 j
5 mIU/mL (normal <5 mIU/mL). Serum follicular
: S; ~* M/ ]: Kstimulating hormone and leuteinizing hormone; u0 K; R5 \: H+ N5 l
concentrations were less than 0.05 mIU/mL& z2 \$ A7 L& J, Z# T2 F5 m
(prepubertal).
9 k( r* V+ C) ~4 l% j, BThe parents were notified about the laboratory
3 Y7 r( B& a' n. X& Bresults and were informed that all of the tests were+ s% A4 G+ j4 Q7 U# ^
normal except the testosterone level was high. The
2 y) y1 _( T+ o! C9 t# n5 Ffollow-up visit was arranged within a few weeks to7 a  K5 D* k* [0 |
obtain testicular and abdominal sonograms; how-$ y6 w% Y" y7 l3 U( f1 l. k
ever, the family did not return for 4 months.! z0 K# b! t/ h* Q; ~
Physical examination at this time revealed that the
& ]4 X! w  F9 f  a( o# q4 qchild had grown 2.5 cm in 4 months and had gained+ a( k9 H% l0 `8 {: B2 T: Z
2 kg of weight. Physical examination remained
# z/ F. c6 A1 l+ funchanged. Surprisingly, the pubic hair almost com-
: c7 y9 T0 @, s* b  S# T- i* V4 npletely disappeared except for a few vellous hairs at
! T0 y0 R- B6 I2 uthe base of the phallus. Testicular volume was still 2
  d9 k. ~* k; [* g; @) ~6 zmL, and the size of the penis remained unchanged.
8 z# n$ l. O4 b! F% ^( ^  [The mother also said that the boy was no longer hav-
7 X+ Q- l( g, O$ l. ?# Ming frequent erections.+ h0 v/ U* _8 \7 U- Y
Both parents were again questioned about use of" C; E$ g, U7 |# S- v9 |& z
any ointment/creams that they may have applied to
: w) q4 J$ z7 `* I' Hthe child’s skin. This time the father admitted the6 [1 o3 c7 r$ J2 f: N& K
Topical Testosterone Exposure / Bhowmick et al 5417 k" _6 P! \% G  I
use of testosterone gel twice daily that he was apply-
3 P1 P  d7 G. R; F1 [& O& Jing over his own shoulders, chest, and back area for1 _8 A4 T$ d5 `, f% c% h
a year. The father also revealed he was embarrassed
; k; _- b7 S4 `- {6 rto disclose that he was using a testosterone gel pre-
3 p8 s! T5 j  j( G2 Q8 W: cscribed by his family physician for decreased libido
/ p& P, c* u5 B% |! ksecondary to depression." U9 I( l& J# {( }" S
The child slept in the same bed with parents.+ {- ^$ T5 B; B& U) h0 |& G7 z% X
The father would hug the baby and hold him on his- }! {# n! Q1 T, i# J6 ]; x
chest for a considerable period of time, causing sig-
# {. s$ p* e0 i1 D8 z1 Ynificant bare skin contact between baby and father.
7 K) W! t1 H" @. T  D8 ]2 LThe father also admitted that after the phone call,
3 E2 X9 Y) j; R$ z) uwhen he learned the testosterone level in the baby8 I& Q# e/ c. H
was high, he then read the product information
% H8 A/ f6 J$ J& V: Zpacket and concluded that it was most likely the rea-
% w3 L. v: W1 u2 H8 |; Nson for the child’s virilization. At that time, they; q, t9 w$ l" g. @- @! s) C
decided to put the baby in a separate bed, and the
" {6 S+ A4 q7 P% m# hfather was not hugging him with bare skin and had8 I8 I3 K: a8 q
been using protective clothing. A repeat testosterone
; y& c( w; [  {- X7 J' Xtest was ordered, but the family did not go to the
& \+ _% B. }9 `$ d- a! B5 Dlaboratory to obtain the test.0 U; j7 e- \+ N) D4 _
Discussion3 ]& }" ]3 e' o7 L
Precocious puberty in boys is defined as secondary
! f2 j0 j, q& }. P& N9 ysexual development before 9 years of age.1,4
- E2 b/ i' a+ L  [Precocious puberty is termed as central (true) when
+ f( x8 k" s; \) oit is caused by the premature activation of hypo-
# o) f4 H7 `6 ]$ B: g, i7 tthalamic pituitary gonadal axis. CPP is more com-
4 `0 C: p+ R( L# {* Smon in girls than in boys.1,3 Most boys with CPP$ k* G+ N. b0 p
may have a central nervous system lesion that is
0 o) y' i% q9 c; Y+ ?# v6 \responsible for the early activation of the hypothal-
6 T5 g  `; P. `) s0 Z9 Ramic pituitary gonadal axis.1-3 Thus, greater empha-
: C  d4 A$ Z# ?4 |+ `, ksis has been given to neuroradiologic imaging in2 d1 D6 K) ]( g" U9 _
boys with precocious puberty. In addition to viril-5 p7 X9 \7 i4 G6 K2 f7 ?" f
ization, the clinical hallmark of CPP is the symmet-; p4 V( k! X; o3 n! M
rical testicular growth secondary to stimulation by! {% }& V5 u; @, m
gonadotropins.1,3
% \, Q$ j, B$ o, |Gonadotropin-independent peripheral preco-2 s% F0 r2 g7 b9 |, x
cious puberty in boys also results from inappropriate
$ b  c& r$ }4 y$ o; [2 Bandrogenic stimulation from either endogenous or
1 V8 A7 g, k. a' O/ K" O. z2 Cexogenous sources, nonpituitary gonadotropin stim-- _" W/ ?9 b  e4 g
ulation, and rare activating mutations.3 Virilizing
4 p  a2 S& G4 F, G3 |  q$ b. s3 ?9 o# icongenital adrenal hyperplasia producing excessive
, I# v. h6 H) H* \0 |7 b( A  Jadrenal androgens is a common cause of precocious: i# n8 i% |3 r- D0 |- S
puberty in boys.3,4
8 y2 p5 k9 Z5 ^! L  VThe most common form of congenital adrenal
, M9 c2 {) Y& A( d9 T4 x- q" C: {hyperplasia is the 21-hydroxylase enzyme deficiency.
0 k! K2 }3 d+ `- nThe 11-β hydroxylase deficiency may also result in- K9 z5 p. F; e) b0 a& O" H
excessive adrenal androgen production, and rarely,
' L0 L" b- n$ M  h/ y8 Ean adrenal tumor may also cause adrenal androgen+ f; I0 A  p) J
excess.1,3
0 b3 o% n1 k: d) X% cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# m- @6 [' s- U( \542 Clinical Pediatrics / Vol. 46, No. 6, July 2007" x5 }! `! f7 H: R
A unique entity of male-limited gonadotropin-
; H5 S6 x6 [: a9 K9 K+ Windependent precocious puberty, which is also known
! d" H, J1 R$ l4 t: p& \* o) A- Ras testotoxicosis, may cause precocious puberty at a) ~" S' z+ ^* W- m* L
very young age. The physical findings in these boys
) B- H8 G. e- c. g/ G5 Lwith this disorder are full pubertal development,
2 Q8 n" E) f( E# @8 W+ dincluding bilateral testicular growth, similar to boys- Y1 V4 \  z3 m6 `" O
with CPP. The gonadotropin levels in this disorder0 P, r% H. h6 S" o; @% z# F2 Z
are suppressed to prepubertal levels and do not show
6 Y, F- a/ B! y& \6 W; {" Opubertal response of gonadotropin after gonadotropin-- n+ ?" i/ q1 ~5 G
releasing hormone stimulation. This is a sex-linked, m- G* |# M& _
autosomal dominant disorder that affects only% |9 N; {9 u: {7 d! {& [
males; therefore, other male members of the family
- X, W1 L) @2 @; \9 t* Z0 D4 v( Fmay have similar precocious puberty.3
/ ~1 A+ _: j2 l! qIn our patient, physical examination was incon-  D1 H& `  b0 J* \# r" I
sistent with true precocious puberty since his testi-  O5 a9 K& K, S  I7 i- V! s  Q
cles were prepubertal in size. However, testotoxicosis
+ ?7 `* f# W: u. G" lwas in the differential diagnosis because his father
' {& m' ]7 q$ H6 |! f( U9 V4 g+ Kstarted puberty somewhat early, and occasionally,
  J2 G+ P$ u3 C( v3 v# btesticular enlargement is not that evident in the
) [- Y' a$ i- d1 h( E; [beginning of this process.1 In the absence of a neg-
4 A- v9 k& E8 ?1 I. Rative initial history of androgen exposure, our2 u4 l3 t; Q- U  C! V8 h/ \
biggest concern was virilizing adrenal hyperplasia,8 ?# I+ s% b/ o8 K4 ]. G
either 21-hydroxylase deficiency or 11-β hydroxylase; j4 ^1 R* \+ m3 E
deficiency. Those diagnoses were excluded by find-
  d* f* \5 W* ^  q. I+ w0 Eing the normal level of adrenal steroids.. b1 }, n$ s2 C
The diagnosis of exogenous androgens was strongly& @8 @! J7 a! l, D
suspected in a follow-up visit after 4 months because$ O  @3 p5 D- r% e7 M# P
the physical examination revealed the complete disap-
# ^& C% O. h, F# Apearance of pubic hair, normal growth velocity, and0 P6 x: {7 [1 `2 T/ g. h2 u
decreased erections. The father admitted using a testos-" M7 _; f8 N! Q5 ?  b
terone gel, which he concealed at first visit. He was
. Q+ T1 |4 e5 o2 ^  o; fusing it rather frequently, twice a day. The Physicians’
7 N7 K" g# }  p% G% Y2 M( b4 cDesk Reference, or package insert of this product, gel or
5 u( ~4 f- Q  [  K7 s: Mcream, cautions about dermal testosterone transfer to
; ^* t; ?5 j5 P# n) Bunprotected females through direct skin exposure.
% O0 `' {: |1 xSerum testosterone level was found to be 2 times the
" ]# ^$ u  P* y1 n7 M6 T, Sbaseline value in those females who were exposed to
" g8 ?6 d) K) ]even 15 minutes of direct skin contact with their male
% t9 h+ ]4 v  E9 d6 B  r4 Jpartners.6 However, when a shirt covered the applica-9 [# V' H+ ?0 Z/ w
tion site, this testosterone transfer was prevented.$ I+ e& D4 u( z! c- r9 F4 R+ t
Our patient’s testosterone level was 60 ng/mL,
* E" w% t, m1 n+ r4 f; bwhich was clearly high. Some studies suggest that
5 a( e; h# f5 R0 `: A$ y0 `dermal conversion of testosterone to dihydrotestos-: c+ r) [- z$ h
terone, which is a more potent metabolite, is more' T, l& i8 E4 I0 ~: D7 H
active in young children exposed to testosterone7 |7 l$ T7 ~5 K9 i
exogenously7; however, we did not measure a dihy-
9 s$ Z3 y# h/ B1 t. E! ^% Adrotestosterone level in our patient. In addition to
/ X7 S5 J+ x7 o2 a, k: G" O9 j' evirilization, exposure to exogenous testosterone in; B6 [) d1 b) m/ a
children results in an increase in growth velocity and/ ~# q! S# H$ K) a: Q1 J- b
advanced bone age, as seen in our patient.5 J; n* }% I: c7 m: w" t) A
The long-term effect of androgen exposure during; n6 ^4 J7 |+ d0 |7 C# h, A
early childhood on pubertal development and final
( K: a2 S  P; oadult height are not fully known and always remain! k: n* T1 }' P
a concern. Children treated with short-term testos-
# ^# |4 |/ d  [terone injection or topical androgen may exhibit some% R1 [  l1 z2 j+ p/ M
acceleration of the skeletal maturation; however, after( `9 H8 ?; \) C
cessation of treatment, the rate of bone maturation
4 L- d- P  I. d3 P* |0 l1 ydecelerates and gradually returns to normal.8,9* B2 d3 t4 t% D# U
There are conflicting reports and controversy
- ]; l/ C. ?! r+ k& ^over the effect of early androgen exposure on adult7 t/ v+ w, O7 w/ s* C6 T0 g
penile length.10,11 Some reports suggest subnormal
3 d/ u2 D* j2 h) a0 A/ ?adult penile length, apparently because of downreg-
9 `$ K# d6 r: H6 i7 Y: x2 U$ zulation of androgen receptor number.10,12 However,) `0 P& Q) ~1 n8 m7 d; r3 B" b
Sutherland et al13 did not find a correlation between
" m7 K+ E' c/ g0 p/ uchildhood testosterone exposure and reduced adult; X( ]' O& v( `. V
penile length in clinical studies." O/ e0 f& R. a; S4 Z
Nonetheless, we do not believe our patient is
# |, u+ R9 ^+ ]/ G* G/ R' I  F0 [5 Qgoing to experience any of the untoward effects from6 b3 c' a4 n2 s+ J
testosterone exposure as mentioned earlier because
* D) j* n4 T1 i; u3 q) Gthe exposure was not for a prolonged period of time.  C# w! O0 K& h; Q* Z4 T
Although the bone age was advanced at the time of
3 `" |4 T3 K. e( K7 s% n" Idiagnosis, the child had a normal growth velocity at
8 D$ ?! q# N# G# _7 ^1 N' S" jthe follow-up visit. It is hoped that his final adult% t% Y! N9 l' @
height will not be affected.4 I' O1 B2 N6 a' E6 G8 D
Although rarely reported, the widespread avail-9 m8 ^* \# l0 ~, f! f! H. d3 q
ability of androgen products in our society may
# h- E0 b7 c% {7 H$ m% {indeed cause more virilization in male or female+ e& g5 X0 a/ d9 A9 o
children than one would realize. Exposure to andro-
0 ?8 B# r/ E- J' c0 Zgen products must be considered and specific ques-; C$ }& v+ C  l7 ^; s7 w9 i
tioning about the use of a testosterone product or# B- E; o4 l) {
gel should be asked of the family members during9 m; e1 }1 z+ ^/ S3 E2 S9 |
the evaluation of any children who present with vir-
9 L' v4 w( ?2 Y4 Qilization or peripheral precocious puberty. The diag-; B4 |) M* B: I& i& s: ?5 U0 ~
nosis can be established by just a few tests and by8 x- k4 j! I; c  L2 v& i
appropriate history. The inability to obtain such a6 k+ W2 A" v( W! b
history, or failure to ask the specific questions, may
# C6 A) }6 f; P  [result in extensive, unnecessary, and expensive
" L" z% m8 l  Z- iinvestigation. The primary care physician should be; n/ ]# l1 i' F7 ~2 R
aware of this fact, because most of these children* h  ]. o/ R. ]/ s4 J8 ^/ X
may initially present in their practice. The Physicians’2 s  n. k& t& \9 k" c
Desk Reference and package insert should also put a
" t" r& _: @4 f" ewarning about the virilizing effect on a male or, x3 C& b3 x; Y: L8 e/ o2 {
female child who might come in contact with some-
" s1 |& C/ G+ [! d9 Aone using any of these products.
, T3 B3 e4 t$ Y( ~/ ~) V8 vReferences
2 E7 T# W& ~9 H# U3 m5 D2 }1. Styne DM. The testes: disorder of sexual differentiation3 k, Q) U; {5 ?) l
and puberty in the male. In: Sperling MA, ed. Pediatric
. Y9 Z' M0 |1 iEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
  f# _: d+ Y# A& F, a2002: 565-628.
& X6 n6 g9 X* v3 b# O2 ?) P2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious8 ~! E* t2 R' |0 `4 w. D' v. d2 A( w* k
puberty 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

' Y. P/ e' f$ G7 {/ P0 t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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