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Sexual Precocity in a 16-Month-Old
% @- D0 M- ~: n( S# P+ b; U' uBoy Induced by Indirect Topical3 ]- C$ T- ?- N3 f2 F; Z
Exposure to Testosterone* V# C- }1 ^- M( S- g& t8 N
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
$ D, w8 [0 r* H7 tand Kenneth R. Rettig, MD1. |) A/ }* {8 e" ?
Clinical Pediatrics6 l9 }6 S5 U4 s1 |# v, v3 z, s7 k: `0 E
Volume 46 Number 6- n* J  E2 C  }& i  }5 O
July 2007 540-543
* f" d  o$ z; J: f* J' s9 N© 2007 Sage Publications# ]9 B+ B, G2 g& W
10.1177/0009922806296651& Y+ f7 x0 U1 Y$ a) n' Y3 E
http://clp.sagepub.com
. S7 g% A2 V1 M+ zhosted at3 `! u3 j/ Q& Q( e
http://online.sagepub.com  Z% X+ l" y0 E. k2 o4 T* i: h, g! I
Precocious puberty in boys, central or peripheral,; r1 n/ A: \% E: a- R( [* S
is a significant concern for physicians. Central" t! |: ?# J1 e& ?% V; P1 c4 Z
precocious puberty (CPP), which is mediated
2 W4 a' j! O8 X' k& Dthrough the hypothalamic pituitary gonadal axis, has. A, X/ C* H; _4 c4 B+ t$ x
a higher incidence of organic central nervous system
0 z+ H, m" f' Nlesions in boys.1,2 Virilization in boys, as manifested6 ~8 T3 M& k. S0 v+ t, u" b6 c8 k
by enlargement of the penis, development of pubic
! g% Y7 n3 w1 {6 ?( Z/ e2 _hair, and facial acne without enlargement of testi-
  R8 H8 _* s  _  Z! p0 @1 L/ ?, Icles, suggests peripheral or pseudopuberty.1-3 We
% z" |5 D2 \' Q* }1 V3 |! ~report a 16-month-old boy who presented with the
1 E& |$ o( v* G, oenlargement of the phallus and pubic hair develop-2 U: V2 t: I/ i+ |# R, N5 `
ment without testicular enlargement, which was due
/ i$ X, |  _7 k* i9 x% ato the unintentional exposure to androgen gel used by
7 I# Q! i) k9 z2 fthe father. The family initially concealed this infor-
4 R1 E  w( W- b5 G# Y" p' {mation, resulting in an extensive work-up for this7 J1 J# S# V8 h! M& ~, A
child. Given the widespread and easy availability of
7 Z5 T2 o% e7 Q$ ]7 n! S6 mtestosterone gel and cream, we believe this is proba-
1 l  {4 M* ~$ U: X/ S* kbly more common than the rare case report in the
+ [1 o& V- B0 F2 P, U9 Fliterature.47 R) o) H  N' W
Patient Report' }# B$ P& ]7 U4 d8 H. d7 h# e
A 16-month-old white child was referred to the
  A1 z+ u* D# n  \1 u0 M+ b3 R' iendocrine clinic by his pediatrician with the concern
( y# U0 g- _: A4 B/ Pof early sexual development. His mother noticed
8 S. r. ?. s( N3 ?9 g0 C( I' ~light colored pubic hair development when he was
+ _5 G$ H- W4 O' w( n9 sFrom the 1Division of Pediatric Endocrinology, 2University of% U' u  d! m3 A% F# H+ y+ y
South Alabama Medical Center, Mobile, Alabama.- }2 V7 L! }$ ]+ Z4 \0 m" T5 c
Address correspondence to: Samar K. Bhowmick, MD, FACE,% c6 L3 o* k0 w& @$ m0 Y! n
Professor of Pediatrics, University of South Alabama, College of# t. E- r7 _7 A( ]7 C# X% I
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
; E, M- D* u, g  v# ~+ Je-mail: [email protected].' [1 H& c2 l1 p2 |# A& E! w+ l
about 6 to 7 months old, which progressively became6 g: |  s, K4 o! y  ~: k( K
darker. She was also concerned about the enlarge-: u* s' X7 @  r% m. c
ment of his penis and frequent erections. The child
4 S. e( A3 C* Q; E& m- \6 \: awas the product of a full-term normal delivery, with) t7 b" r. l$ n
a birth weight of 7 lb 14 oz, and birth length of2 @1 g& H& b; V' k
20 inches. He was breast-fed throughout the first year
$ M- g. P: g# I. wof life and was still receiving breast milk along with
- M$ u* ?5 E3 R7 t$ G8 nsolid food. He had no hospitalizations or surgery,
/ D5 Z( S; ^5 p5 kand his psychosocial and psychomotor development
$ J, `0 k! p5 Uwas age appropriate.$ b, d* O" N/ X/ J% W7 d# |- ^
The family history was remarkable for the father,
7 @8 N8 p( m( H1 K& I' s. Fwho was diagnosed with hypothyroidism at age 16,- c7 Z5 B) J- E; M, L( g
which was treated with thyroxine. The father’s; Y2 O  \0 r. D3 j( k
height was 6 feet, and he went through a somewhat
6 R7 G) ?7 N9 O" T( x. }' d  Learly puberty and had stopped growing by age 14.1 z% t' t9 G0 J0 o8 f
The father denied taking any other medication. The
4 K+ G+ ]! G% m9 s8 B5 K4 hchild’s mother was in good health. Her menarche
8 P5 Z! \' s$ S$ b$ \1 w9 s9 Iwas at 11 years of age, and her height was at 5 feet
/ f3 r& {4 c& x# S( e8 S9 \5 inches. There was no other family history of pre-6 [; C- L) e6 ~. i/ Z  P2 o' w1 u' ^/ w
cocious sexual development in the first-degree rela-
0 Q; a) \! e4 V9 x3 Otives. There were no siblings.( @! B; w( G6 V/ G8 r
Physical Examination
$ F; d9 s/ ]' P, xThe physical examination revealed a very active,
" d. J. T- y/ v# _playful, and healthy boy. The vital signs documented
8 w7 R3 ^+ }5 c" U, ^a blood pressure of 85/50 mm Hg, his length was
; z) J+ w1 M; m8 j% z6 t90 cm (>97th percentile), and his weight was 14.4 kg
! d& i/ l, Q' k* C. s(also >97th percentile). The observed yearly growth
# N9 ]7 P' }6 w1 S3 u- R- A" g9 fvelocity was 30 cm (12 inches). The examination of; j% _% [2 S" N4 U
the neck revealed no thyroid enlargement.
6 n$ ~5 e( W- B5 k5 t4 C1 {The genitourinary examination was remarkable for
! c# C: b9 t: p0 C9 Kenlargement of the penis, with a stretched length of/ n0 }+ z6 R/ K$ d7 J
8 cm and a width of 2 cm. The glans penis was very well. z- j7 ?  }8 R7 x) ?
developed. The pubic hair was Tanner II, mostly around1 F4 a$ o8 C8 u- o0 i$ M
540
9 e' o4 M$ V. |' \at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% w8 X2 S6 @) F1 l1 W
the base of the phallus and was dark and curled. The
- `# ]8 W5 p2 N7 ~; \testicular volume was prepubertal at 2 mL each.- T' H  x' X; ^6 W$ }
The skin was moist and smooth and somewhat
: }7 _: ]0 r$ v, A4 Aoily. No axillary hair was noted. There were no$ v1 V0 d* s' p9 y8 X( `
abnormal skin pigmentations or café-au-lait spots.  H) F5 q3 _- T& o7 x$ D4 O8 v
Neurologic evaluation showed deep tendon reflex 2+
) _5 M; k8 ?- U, i' a' y/ Dbilateral and symmetrical. There was no suggestion: l  s" E4 c3 c- x; [$ j# Z
of papilledema.1 F& y1 B' V8 n4 u, N, e
Laboratory Evaluation
' S' L/ x6 Z7 m6 E, Z; a& W" F+ EThe bone age was consistent with 28 months by
' P8 f! G4 ~7 i5 J1 t# T/ e% q/ {6 m! nusing the standard of Greulich and Pyle at a chrono-8 N3 |6 D* o* M& b' j
logic age of 16 months (advanced).5 Chromosomal+ B2 U, I* i2 P$ M1 ~+ C" a# @( w
karyotype was 46XY. The thyroid function test
& z. E% g# W4 W% G: y# [  i6 {# vshowed a free T4 of 1.69 ng/dL, and thyroid stimu-3 ^- D/ x# y7 @" o! T
lating hormone level was 1.3 µIU/mL (both normal).
+ v( g2 k" X  D$ ]5 u  K6 Z, q: n9 cThe concentrations of serum electrolytes, blood
* D+ M4 @7 j0 B4 M' O$ Nurea nitrogen, creatinine, and calcium all were
4 ~8 B1 ?% \' o5 h" S. k  b- mwithin normal range for his age. The concentration
; a) S# k3 h& R0 z; ?* B1 p9 A; kof serum 17-hydroxyprogesterone was 16 ng/dL7 z% U+ w4 Z" X! v' H
(normal, 3 to 90 ng/dL), androstenedione was 203 E8 L6 g! z' J* f3 U' Z! a& |, D
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-: Q/ i1 P0 r+ z& y. B
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
( [* l3 h4 @& z  a) H: rdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
( g! d) P2 J6 ?* Q1 t$ E% U49ng/dL), 11-desoxycortisol (specific compound S)
" R* o, Y5 x  }8 I0 w0 h/ wwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
  E8 H8 W; ^" c% z% U" _& rtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' r# r, F$ C. T0 B
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),8 m8 _- @; t3 j4 I; O" w
and β-human chorionic gonadotropin was less than
" v5 F! R1 i- y+ e" C- O. a5 mIU/mL (normal <5 mIU/mL). Serum follicular; s% X5 M- p/ B, M
stimulating hormone and leuteinizing hormone5 J, i) O8 T7 H  {1 ~! l8 H/ X4 Z
concentrations were less than 0.05 mIU/mL
0 c- y9 s) s/ V" a. k3 e) h(prepubertal).
, R" {$ w) i! f. }+ hThe parents were notified about the laboratory
  D! C6 z3 }5 z: W  x: M: lresults and were informed that all of the tests were
& p- j/ f3 _  D- o, o& {normal except the testosterone level was high. The. q6 G3 [  I  z, \; n( J3 Q
follow-up visit was arranged within a few weeks to% f1 i9 F& x' Z0 ?% l
obtain testicular and abdominal sonograms; how-
* X$ m# g/ x' N0 ~3 \0 U* W  P; E4 @ever, the family did not return for 4 months.
. F" b- o, J5 [6 s3 @Physical examination at this time revealed that the
" j! N+ ^. u4 P* a7 Fchild had grown 2.5 cm in 4 months and had gained1 S+ b6 R$ ?9 E' V5 A8 P; A
2 kg of weight. Physical examination remained
6 f$ s  |' a* l8 j$ S+ l5 Zunchanged. Surprisingly, the pubic hair almost com-3 a7 f' A- S$ W: T- ?& D$ E
pletely disappeared except for a few vellous hairs at6 y5 p! T6 Q. {# _2 N: A
the base of the phallus. Testicular volume was still 2
% m' K0 ], \3 ]mL, and the size of the penis remained unchanged.
; w( J, j4 Q9 z3 VThe mother also said that the boy was no longer hav-+ }3 x. Q+ x3 [4 [! g( t( Q* [0 M
ing frequent erections.7 N/ K" Y# y6 z  t0 e& n
Both parents were again questioned about use of
& H! Y  ~$ z1 I$ _1 Hany ointment/creams that they may have applied to
: o% y0 z  Y8 ?( y; m8 ~$ O$ Gthe child’s skin. This time the father admitted the' N: m2 T' A$ u5 C6 Y
Topical Testosterone Exposure / Bhowmick et al 541* y2 R( x* L6 [% K
use of testosterone gel twice daily that he was apply-
; s4 C6 }- N/ v0 N9 y% }$ g* Ping over his own shoulders, chest, and back area for, L! d5 N% }5 q4 h. a/ X1 ~; _
a year. The father also revealed he was embarrassed
) U' U$ z& C9 h% nto disclose that he was using a testosterone gel pre-
, [  l/ }/ O% Fscribed by his family physician for decreased libido( C. z9 U1 l- N" j
secondary to depression.
& Q& ?  F$ S! G& ]6 E# T' vThe child slept in the same bed with parents.
; b7 P3 L% f9 h, W2 N" P+ e; @The father would hug the baby and hold him on his1 P. ~' k& N: k5 L. b# }8 a8 L; C2 e
chest for a considerable period of time, causing sig-
& s9 ]4 M/ C# d" Lnificant bare skin contact between baby and father.
6 a& t6 }0 l4 }/ v; \The father also admitted that after the phone call,: x: i3 ]4 S2 l* Z" Z- k% w
when he learned the testosterone level in the baby* q1 u& m, A  I. g
was high, he then read the product information, w2 o8 E5 E8 L# N+ o! \( _
packet and concluded that it was most likely the rea-! u: @3 u$ j1 H1 V$ h  `% |9 e5 ]. d
son for the child’s virilization. At that time, they
2 Y! \) z6 S) l* idecided to put the baby in a separate bed, and the2 |6 g- i9 f  Q8 x& F
father was not hugging him with bare skin and had" Y9 O8 A8 Z& W. ~
been using protective clothing. A repeat testosterone
* D# ^# Q% R- K* t. z1 s' I  P4 A  |test was ordered, but the family did not go to the
8 T8 e% k2 H# e& Y) v+ u9 X7 ]3 L7 Xlaboratory to obtain the test.3 U) I$ f2 n& r$ ?& d' c
Discussion
4 E1 x' O5 e. ]) [  G5 jPrecocious puberty in boys is defined as secondary
7 Z+ L# a3 I4 a' q6 l3 i/ {+ osexual development before 9 years of age.1,4
% Y! K9 A4 x/ b7 Z& ?: sPrecocious puberty is termed as central (true) when
. u) y# A5 ^9 `6 E$ s+ ?; n0 Jit is caused by the premature activation of hypo-. E6 b' f! s; z/ a5 h( T
thalamic pituitary gonadal axis. CPP is more com-2 p5 }* Y0 j3 m/ b, f% y$ L) \
mon in girls than in boys.1,3 Most boys with CPP3 U* W  k  F" Q) Z
may have a central nervous system lesion that is' u7 `1 ]7 `2 J- S) F- `0 o2 q( [
responsible for the early activation of the hypothal-
% Z' E% M8 l: x9 E- c$ k  namic pituitary gonadal axis.1-3 Thus, greater empha-
7 \$ _2 @' i# Zsis has been given to neuroradiologic imaging in& c+ \/ D" N' ^. Z$ Z$ v
boys with precocious puberty. In addition to viril-$ r  q7 K. }2 n& Q: _: W
ization, the clinical hallmark of CPP is the symmet-
4 o% h, n5 N( L+ srical testicular growth secondary to stimulation by, i. r, v9 S9 a6 I' V
gonadotropins.1,3
) X* c5 _* G0 G- PGonadotropin-independent peripheral preco-
" Y# v% x0 R7 G4 \$ \cious puberty in boys also results from inappropriate1 W; D9 \0 {; ]% S! f7 J  {/ A
androgenic stimulation from either endogenous or# V% _9 K& c) F* W" w
exogenous sources, nonpituitary gonadotropin stim-
9 |! W, s& l; `. N& a7 D: D/ T, F6 hulation, and rare activating mutations.3 Virilizing' L/ i* h4 h- [& u/ Y8 t
congenital adrenal hyperplasia producing excessive
0 q8 j7 ]7 k, S' b& Aadrenal androgens is a common cause of precocious3 p; s8 H7 G( `; z% Y6 \3 r
puberty in boys.3,4
6 @/ f5 f9 B9 d" HThe most common form of congenital adrenal
7 W3 m! e4 b  e/ a/ i! m1 l) Khyperplasia is the 21-hydroxylase enzyme deficiency.% f, m0 u8 J6 O# z, ?4 W7 T
The 11-β hydroxylase deficiency may also result in: N' G1 \6 h# x3 ~4 O
excessive adrenal androgen production, and rarely,  W+ V; F: r) x8 t/ u9 j
an adrenal tumor may also cause adrenal androgen7 Q# I" h3 i8 q: `& w) H4 f
excess.1,3
) ?) Q: C2 W, f# aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 t: K2 |; O3 G" X
542 Clinical Pediatrics / Vol. 46, No. 6, July 20074 [' p& o  F# m1 p
A unique entity of male-limited gonadotropin-2 Q6 Z6 U) `. e& M2 a$ Z5 N# o
independent precocious puberty, which is also known* h) S" V4 z: v5 S) g, F# D
as testotoxicosis, may cause precocious puberty at a# B$ G" y2 [: s& o( k' m" x
very young age. The physical findings in these boys
: \" j" E& P3 z2 i3 v& k0 j; dwith this disorder are full pubertal development,& }% b( K3 J" _6 }# z
including bilateral testicular growth, similar to boys5 L' H8 b8 j1 @$ a8 p
with CPP. The gonadotropin levels in this disorder; U, b/ l2 \$ F) H" E
are suppressed to prepubertal levels and do not show8 O# s8 |4 S0 i  N
pubertal response of gonadotropin after gonadotropin-4 P6 @( A3 F1 V8 I
releasing hormone stimulation. This is a sex-linked
5 x9 [6 @% p- j2 k; w" S/ A' G5 yautosomal dominant disorder that affects only- ?* f( n  W1 K& [& A; H# x
males; therefore, other male members of the family5 P! W/ G# ~0 Z  }8 U/ _8 u
may have similar precocious puberty.31 ?+ @7 o" _7 R9 h6 Z4 `: q
In our patient, physical examination was incon-5 b# f2 x* M) D+ ^- x
sistent with true precocious puberty since his testi-
+ z- {) Z, g6 m) ~cles were prepubertal in size. However, testotoxicosis% m6 i" P' Q5 ~8 b3 J3 q
was in the differential diagnosis because his father! P3 X) G) y# D2 t' L
started puberty somewhat early, and occasionally,+ f3 w' z$ \" V! j" E8 J
testicular enlargement is not that evident in the* y  t6 W: l/ x* c/ _, y
beginning of this process.1 In the absence of a neg-% P" [8 j5 X8 M
ative initial history of androgen exposure, our2 p/ V3 _) c- \9 x8 N; _- t# l7 {' W- ]3 s
biggest concern was virilizing adrenal hyperplasia,
. q5 R* Y, ^' heither 21-hydroxylase deficiency or 11-β hydroxylase
1 }) D7 P- ^( a+ Tdeficiency. Those diagnoses were excluded by find-
& f/ o/ x* W5 |% n6 Jing the normal level of adrenal steroids.
1 _) C5 {; w# D. f( I' f% F) wThe diagnosis of exogenous androgens was strongly
8 Q2 w. U$ s( {8 g% osuspected in a follow-up visit after 4 months because) N3 k; p' s5 g/ x/ c: k7 r( m' g
the physical examination revealed the complete disap-( T2 `3 m4 V) C5 ?* p
pearance of pubic hair, normal growth velocity, and
% J- h6 f8 a9 q# hdecreased erections. The father admitted using a testos-7 S1 V' j- t, B3 S: Q, E% h, M
terone gel, which he concealed at first visit. He was
2 T" O  m  W$ a8 ^* X. h, |using it rather frequently, twice a day. The Physicians’
& `9 z7 W* s4 S" Z; L# wDesk Reference, or package insert of this product, gel or
: k2 s( Y0 d1 vcream, cautions about dermal testosterone transfer to5 Q! C- t0 L1 Q: r  Y4 Z% T2 k1 U
unprotected females through direct skin exposure.; N( \. M9 r" d) c7 C: j
Serum testosterone level was found to be 2 times the1 a8 A! h4 b. K" w& ^) U" G0 E! R
baseline value in those females who were exposed to
  s% t; B1 U- _4 geven 15 minutes of direct skin contact with their male
8 C, J' n6 [4 }) U- Zpartners.6 However, when a shirt covered the applica-
. c5 n4 u% B# L  x# l  ttion site, this testosterone transfer was prevented.
& N3 v9 }! b( S% w+ |6 c4 t  XOur patient’s testosterone level was 60 ng/mL,
  @8 P4 @. x, Q, i% S" Nwhich was clearly high. Some studies suggest that
/ q% ]8 L' C! N/ N: Tdermal conversion of testosterone to dihydrotestos-
) D6 }5 D  W6 M8 x% zterone, which is a more potent metabolite, is more
. h) h, J: B) o$ n6 u: Dactive in young children exposed to testosterone
6 v7 E! v7 _& K+ H0 zexogenously7; however, we did not measure a dihy-, j! n# h$ O0 ^$ c4 f
drotestosterone level in our patient. In addition to
; Z& }- N, }9 v  e7 \virilization, exposure to exogenous testosterone in
/ P6 i; S  a+ X$ @7 @, Dchildren results in an increase in growth velocity and  u- z( L% O: D; K4 o! |$ c
advanced bone age, as seen in our patient.2 }- i) c; D3 R$ f
The long-term effect of androgen exposure during: c  r! O, x3 u- w+ ^' M% f2 I1 |) l
early childhood on pubertal development and final
6 q, }0 o+ b) kadult height are not fully known and always remain3 T2 l6 z" H, s" R6 S
a concern. Children treated with short-term testos-+ E1 ?5 r6 v- u' b" }- s
terone injection or topical androgen may exhibit some) N; P8 x4 _$ p
acceleration of the skeletal maturation; however, after
, K3 f4 s8 N/ ]! Ocessation of treatment, the rate of bone maturation1 P9 N$ t# x# u3 d0 b
decelerates and gradually returns to normal.8,9
- G  f1 E' G3 ~$ Z1 t6 s5 ~1 R/ aThere are conflicting reports and controversy
% m- U8 ~: x0 W" i" ~' x' q8 Eover the effect of early androgen exposure on adult3 o( h; C, k: V/ i5 \% [
penile length.10,11 Some reports suggest subnormal
) [/ C- Z. p3 t$ Vadult penile length, apparently because of downreg-0 r7 ~6 i8 ]3 e( l+ `
ulation of androgen receptor number.10,12 However,: P* Y! {0 j& D. [/ H$ \! N
Sutherland et al13 did not find a correlation between
6 ~$ C/ s/ u3 s8 N: k  `childhood testosterone exposure and reduced adult/ o1 \- o- S( n+ s/ R/ w
penile length in clinical studies.: L/ x5 |) C, K
Nonetheless, we do not believe our patient is. a1 [- M' t) m3 g" W* J( j9 G  \
going to experience any of the untoward effects from
  u. z" R1 ]5 x; r4 w& Otestosterone exposure as mentioned earlier because
( x' Y. c$ m, f& f+ T1 q  X) w9 U) nthe exposure was not for a prolonged period of time.0 q, |% ~: v2 X- v3 A! \( u3 p
Although the bone age was advanced at the time of4 R. M/ ]6 z5 s& z- i& H3 x) g9 [
diagnosis, the child had a normal growth velocity at
' s: N: D; W) s; z/ ythe follow-up visit. It is hoped that his final adult0 V3 T0 O+ a% n& M* c/ T
height will not be affected.
$ R, }6 r' j' HAlthough rarely reported, the widespread avail-! C( T2 K: S5 B) b' f4 L
ability of androgen products in our society may3 i  Y4 F  z1 R0 C: t' @
indeed cause more virilization in male or female
4 N' W% G6 a+ w- S) [' rchildren than one would realize. Exposure to andro-9 l# @) g6 l3 G! g7 [
gen products must be considered and specific ques-, B: a( Z* ^" C5 f1 W. I- A
tioning about the use of a testosterone product or! p& B) s0 R& E0 J  `3 t
gel should be asked of the family members during: g* o1 s( G1 v8 [- M; {. n& G
the evaluation of any children who present with vir-
  S: o# a7 I2 ?+ B2 y- X$ cilization or peripheral precocious puberty. The diag-& w& K8 [. @8 _9 w2 U
nosis can be established by just a few tests and by( s/ g! w/ U7 f" J6 l' p% r
appropriate history. The inability to obtain such a& z2 h" e; A# F
history, or failure to ask the specific questions, may
1 Z. i: P. v/ x1 b; dresult in extensive, unnecessary, and expensive
% u; i9 D+ _0 ~- Ainvestigation. The primary care physician should be
2 n3 B4 H/ m/ h( Z2 v+ A, eaware of this fact, because most of these children
1 Y! c, K- Y2 @& k. Hmay initially present in their practice. The Physicians’
  h$ V- v  c) _; BDesk Reference and package insert should also put a
/ f/ y  G5 A6 hwarning about the virilizing effect on a male or- L( Z, ~. R5 u' Y7 N: i" C/ ]- C$ J
female child who might come in contact with some-
6 }2 E0 n6 X; T! g2 T) p, k: R4 w2 ione using any of these products.
0 g9 \- ^' V' P0 O4 V  c3 R: AReferences
) h! ~, N& q" O! Q! q# l1. Styne DM. The testes: disorder of sexual differentiation1 b9 f8 F2 L: G; r! D* P  V
and puberty in the male. In: Sperling MA, ed. Pediatric
/ x- n" d1 J! [( N8 u0 D2 z/ W- j9 I% IEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;7 h9 T4 X1 Q7 C
2002: 565-628.9 E& N# Y. O2 T2 z( _. D
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious+ O/ W3 q" C! r
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
5 e) S9 c7 H3 |5 k5 \% pBoy Induced by Indirect Topical
0 n+ T. g; o0 h9 JExposure to Testosterone
+ [) v1 n4 w. oSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
1 V& Z/ Z" e( K3 Rand Kenneth R. Rettig, MD1
: y( ~5 Q- [9 i  IClinical Pediatrics) i5 n7 i, _* ?' ^
Volume 46 Number 6) ^) m6 j% w9 m5 P
July 2007 540-543
1 F: T$ t/ E" ]© 2007 Sage Publications
. f) m1 t# K  c* b6 F10.1177/0009922806296651
9 x+ C# D8 I& Z7 r. g# E% m9 n! \http://clp.sagepub.com- g. G) F! J0 w! c
hosted at/ b$ q3 }6 m4 i" |$ Z- H
http://online.sagepub.com8 s' `  u& _( u: K$ s7 u0 \
Precocious puberty in boys, central or peripheral,. p# A5 P% X- }% `
is a significant concern for physicians. Central
6 P1 U8 O, f9 mprecocious puberty (CPP), which is mediated2 ?& h! p6 I# Y+ m8 f0 d
through the hypothalamic pituitary gonadal axis, has
9 L% _: }7 I3 ^7 a4 l( W* Ma higher incidence of organic central nervous system5 U, R! q+ D) w8 D: b$ w
lesions in boys.1,2 Virilization in boys, as manifested: Z! ~2 @% e0 h5 d+ c
by enlargement of the penis, development of pubic# [+ f' R# t1 i* U, ?% r3 s/ R( e: [
hair, and facial acne without enlargement of testi-
' y( d" z3 J3 p2 b% Lcles, suggests peripheral or pseudopuberty.1-3 We
" D9 b  x8 b+ v5 A% Ireport a 16-month-old boy who presented with the
2 n/ G( P5 |8 F# y! D/ @% z9 q3 wenlargement of the phallus and pubic hair develop-8 M8 i2 f1 m3 h0 k
ment without testicular enlargement, which was due
  p# r2 P/ }- d1 ^to the unintentional exposure to androgen gel used by
  R/ h+ x+ }' q3 Pthe father. The family initially concealed this infor-% Q) L2 U/ Q; L* Z; I5 _
mation, resulting in an extensive work-up for this* A! ]; c9 K3 l5 R, x" B  K
child. Given the widespread and easy availability of
7 E3 u" _8 N4 L& htestosterone gel and cream, we believe this is proba-, Y2 J, u% C. |. b( u
bly more common than the rare case report in the
; {6 o! I; b8 r" Q. tliterature.4
4 l& I+ U' T5 J& T* L4 H& yPatient Report7 ^6 C2 a4 E; ^0 e  d
A 16-month-old white child was referred to the
# ^! ~3 E( Q" |& u! B; uendocrine clinic by his pediatrician with the concern/ Y7 A* J6 b5 p, Z
of early sexual development. His mother noticed  V- j8 E' p$ L5 \: B/ b0 ?# x
light colored pubic hair development when he was" a: I3 @( J) m3 i
From the 1Division of Pediatric Endocrinology, 2University of+ a( p' G/ M& g
South Alabama Medical Center, Mobile, Alabama.
4 Q; {) p# ?. i; J0 |8 K. V, ZAddress correspondence to: Samar K. Bhowmick, MD, FACE,
4 f- {. {, y; d; L2 uProfessor of Pediatrics, University of South Alabama, College of
( k) {9 m1 B, j6 M* @8 L# GMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;0 q7 t8 D" \) `% b4 s
e-mail: [email protected].; g# s0 [/ k1 }( |1 j3 x
about 6 to 7 months old, which progressively became
* f8 s3 r. n9 Q* r, h, odarker. She was also concerned about the enlarge-
7 [! n/ Z& X8 ]( m- Ament of his penis and frequent erections. The child
( `( V: X+ G1 d# f6 ~. u2 V, Owas the product of a full-term normal delivery, with/ d( u. p1 U- |7 V
a birth weight of 7 lb 14 oz, and birth length of
6 \- V& w( c( h8 f20 inches. He was breast-fed throughout the first year  l* y& H4 _; x
of life and was still receiving breast milk along with6 w- @: m9 Y; x6 X" G  O- m+ H
solid food. He had no hospitalizations or surgery,% g3 U# }3 p2 g7 o
and his psychosocial and psychomotor development
+ G. ^/ W1 b2 q0 iwas age appropriate.
  L- k' L3 e9 G4 p- j5 X2 oThe family history was remarkable for the father,! q9 i8 L8 Z$ c! ^* u7 w6 v) Q
who was diagnosed with hypothyroidism at age 16,
5 @% b( \. S% L0 d/ [which was treated with thyroxine. The father’s
2 Z5 J* |+ J% G- j1 B& E, zheight was 6 feet, and he went through a somewhat
5 ^1 s$ h/ O9 xearly puberty and had stopped growing by age 14., H" P* V0 o  O8 S* S* {1 b; I
The father denied taking any other medication. The, E2 F1 p# y9 v. u
child’s mother was in good health. Her menarche
8 u. m, u5 Y- {0 ]6 i4 H* Rwas at 11 years of age, and her height was at 5 feet
1 H. L* W: z+ p0 w* T7 g5 inches. There was no other family history of pre-
3 }, @$ P% n; C; a$ i; Ccocious sexual development in the first-degree rela-
  `$ o8 M# A! ~* Qtives. There were no siblings.- }. d3 T. E8 y8 b
Physical Examination6 H7 r1 p% ?5 D( N9 }5 H- a1 ?7 B
The physical examination revealed a very active,
0 Z: \" }9 C5 Zplayful, and healthy boy. The vital signs documented4 i0 k  k7 R/ F, i4 c( s
a blood pressure of 85/50 mm Hg, his length was
& @! H! _1 T7 K* F% X, ~: a* c90 cm (>97th percentile), and his weight was 14.4 kg
% V! @! y( @9 s, h) Y4 _6 d/ o(also >97th percentile). The observed yearly growth
1 j7 g8 N' n% Q4 ]; M9 d* f. |  y$ xvelocity was 30 cm (12 inches). The examination of
+ L5 ~5 u9 d" y+ m+ u$ H; Ythe neck revealed no thyroid enlargement.; {  `; K/ y6 p3 J0 v8 J
The genitourinary examination was remarkable for( W6 B. F7 }( x6 }$ {1 _
enlargement of the penis, with a stretched length of" F3 `9 l4 q/ d2 v" K9 L" P
8 cm and a width of 2 cm. The glans penis was very well
- t7 |* _  U6 v, Ndeveloped. The pubic hair was Tanner II, mostly around
4 u5 x0 V. J/ D  w* I8 h4 P540& K( U' Z8 e, D6 d
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! _* S9 c9 m' Athe base of the phallus and was dark and curled. The4 G( F0 [4 p4 u: e
testicular volume was prepubertal at 2 mL each.5 V8 o  Z. M! I2 Y, I# i& I
The skin was moist and smooth and somewhat1 V; I" Y2 K6 ~4 z7 o
oily. No axillary hair was noted. There were no
- ~) L7 g) C) b7 ^abnormal skin pigmentations or café-au-lait spots.
$ v( E4 ]: o6 c6 \0 y" xNeurologic evaluation showed deep tendon reflex 2+
5 D2 z5 B: l; h* _. V2 l$ vbilateral and symmetrical. There was no suggestion
9 U7 S+ ~) D! \) t$ K* s) Jof papilledema.
2 [* U* N, K5 jLaboratory Evaluation
  y/ \5 C: Y  }$ x6 v, cThe bone age was consistent with 28 months by
; n" e0 e8 a* @& |4 o" l! [using the standard of Greulich and Pyle at a chrono-
) v$ O. y2 @$ n( |$ C% S0 w0 Q' Mlogic age of 16 months (advanced).5 Chromosomal$ t0 F9 S9 O6 J; m& P5 E1 q
karyotype was 46XY. The thyroid function test
8 B3 ^- b; e% E% Lshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ V/ ]. B/ K& J( H8 X3 Plating hormone level was 1.3 µIU/mL (both normal).
8 W2 D1 e9 F. j* t8 N4 m4 vThe concentrations of serum electrolytes, blood& w0 A+ D/ Q! C( M  _* T4 e/ Q2 y
urea nitrogen, creatinine, and calcium all were
3 Y, C! O. X9 _1 X& R1 owithin normal range for his age. The concentration6 ^  U7 z; `2 m6 R% w* y
of serum 17-hydroxyprogesterone was 16 ng/dL
7 ]' o9 a6 v8 i7 Q(normal, 3 to 90 ng/dL), androstenedione was 20
' i2 x5 o: X- H' r+ sng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
! a4 M+ M4 q4 y  O) jterone was 38 ng/dL (normal, 50 to 760 ng/dL),
/ x# l6 j8 C. U, V4 k' U8 Cdesoxycorticosterone was 4.3 ng/dL (normal, 7 to, R4 i5 _5 _7 D1 Y4 B7 E" ~  `
49ng/dL), 11-desoxycortisol (specific compound S)
$ p6 z; R% y! y! j' V8 ^( D- Dwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
% T' _( Y* ?. Ntisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total! G1 \  |5 C2 N8 |+ d2 c' e0 s$ Y; v
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
* D, a7 B9 T" M: \! p. t$ g: Aand β-human chorionic gonadotropin was less than
  F: _+ ]' z" ?) w5 mIU/mL (normal <5 mIU/mL). Serum follicular
* A, n3 s* q2 q8 Jstimulating hormone and leuteinizing hormone6 {0 ]& k2 O( ?- h2 K; A4 u" `
concentrations were less than 0.05 mIU/mL
" K3 {3 [9 o$ U' l: N; h(prepubertal).
0 y0 z0 C5 V% FThe parents were notified about the laboratory
  \  V9 z  y& @  g" h4 q) fresults and were informed that all of the tests were
: |! }/ _% e2 H2 J  dnormal except the testosterone level was high. The
' j3 [. a2 L- K  ]5 u) K; kfollow-up visit was arranged within a few weeks to
$ E' [+ s9 r+ {9 K$ q& {obtain testicular and abdominal sonograms; how-2 W- Q. ~8 i- ^3 e, S0 C
ever, the family did not return for 4 months.
' C8 H" |# M" YPhysical examination at this time revealed that the5 Q, D  a) Z! Z* R8 B& b( n9 p
child had grown 2.5 cm in 4 months and had gained
- G6 f* \7 G2 J0 x  O: Z9 m5 }2 kg of weight. Physical examination remained
1 w+ I7 n: q. e' ^% W: Funchanged. Surprisingly, the pubic hair almost com-
7 v# H  |% K. ^7 V( r+ T' Npletely disappeared except for a few vellous hairs at6 W/ r' E! s) K. [
the base of the phallus. Testicular volume was still 2
" J) y7 c8 o9 i8 ymL, and the size of the penis remained unchanged.
5 B5 o( M8 \1 KThe mother also said that the boy was no longer hav-
5 F0 ]& f5 W. ^( Z  C( ning frequent erections.
& P: g( r8 d( ?! W) R' ?2 bBoth parents were again questioned about use of
7 e' l( _7 t2 S2 I; `any ointment/creams that they may have applied to
% e  p  L) B) V: |* e% e+ ^2 |the child’s skin. This time the father admitted the
8 J& ^2 @( F, K2 M! ]! [Topical Testosterone Exposure / Bhowmick et al 541. i9 @( W" i" _' L) H9 x
use of testosterone gel twice daily that he was apply-$ t, V( f) u" \1 a$ I- }
ing over his own shoulders, chest, and back area for* }" l" z1 p  p. P1 v$ F
a year. The father also revealed he was embarrassed
' r4 l+ g/ j% xto disclose that he was using a testosterone gel pre-" h! x4 m/ X: y
scribed by his family physician for decreased libido
7 I$ n" K$ n7 b; {' [; ysecondary to depression./ J3 X% \7 H0 \5 z+ k
The child slept in the same bed with parents.
- a/ l" N2 m$ L% W# CThe father would hug the baby and hold him on his
3 T+ n: _! j( I1 xchest for a considerable period of time, causing sig-/ x1 a  o3 `) O% i5 r8 j. P9 g
nificant bare skin contact between baby and father.
- {5 u" y6 ?1 X' l5 d$ P7 P( LThe father also admitted that after the phone call,5 M8 r( {" X! f: z* G- G. K
when he learned the testosterone level in the baby; h# _& @, H, G# j
was high, he then read the product information( C' X: I& W; y( Z% F
packet and concluded that it was most likely the rea-
$ I% s" v3 @5 f. v" Q5 Z. pson for the child’s virilization. At that time, they* O9 A  e0 T, G& d' b: Q
decided to put the baby in a separate bed, and the
: E6 @8 q- B$ wfather was not hugging him with bare skin and had: ?# E/ j. G2 j. P
been using protective clothing. A repeat testosterone
+ z% C# p! [: c4 _test was ordered, but the family did not go to the4 h+ |! \% z; u* y7 q: \
laboratory to obtain the test.
/ e2 N) V$ Z: m) bDiscussion7 [& Z7 E2 g. x; J4 }# ~! A: J5 q
Precocious puberty in boys is defined as secondary0 Z& R* d( h/ V+ J+ }# h3 C1 \
sexual development before 9 years of age.1,4, X( f7 u9 o5 X% i# ~* X
Precocious puberty is termed as central (true) when
1 Y3 Q: ]3 c. E$ u' ]0 q" P8 e3 mit is caused by the premature activation of hypo-
1 x5 w! I7 m. v$ {4 K9 Wthalamic pituitary gonadal axis. CPP is more com-; W- L) b2 [# e( T) v" x6 K* k( k
mon in girls than in boys.1,3 Most boys with CPP
3 Z' f+ N6 c+ o6 }; Imay have a central nervous system lesion that is- V  n/ q; v0 h" o
responsible for the early activation of the hypothal-
& N' q! S+ [5 hamic pituitary gonadal axis.1-3 Thus, greater empha-1 V; E, U% J; [( e4 \* X
sis has been given to neuroradiologic imaging in2 z% B4 X3 s; K
boys with precocious puberty. In addition to viril-( |( V/ T/ A) a* e9 o4 R
ization, the clinical hallmark of CPP is the symmet-; \+ S' S" m, s/ E; i8 u
rical testicular growth secondary to stimulation by
) o4 O' Z$ S  N( |0 vgonadotropins.1,3
- r1 r8 |0 m' V$ p  w" z5 mGonadotropin-independent peripheral preco-( @$ Q% i, C/ z1 W) V( ]
cious puberty in boys also results from inappropriate. S3 T& i% i4 u, H
androgenic stimulation from either endogenous or, X. c& v1 `4 F! A) `
exogenous sources, nonpituitary gonadotropin stim-
8 e7 Q# V" B  R1 E6 Rulation, and rare activating mutations.3 Virilizing
1 V* ^: ?7 P6 U) C9 scongenital adrenal hyperplasia producing excessive% r0 K$ |. T' L, I
adrenal androgens is a common cause of precocious1 z$ `8 G) }4 ], `, {
puberty in boys.3,45 `$ y0 j6 U* x& D4 ?3 ]
The most common form of congenital adrenal, L2 R: |" j! r1 G& a) j$ g
hyperplasia is the 21-hydroxylase enzyme deficiency.6 F- ~. b8 a5 f$ D6 }
The 11-β hydroxylase deficiency may also result in" Y* b4 k' G, D3 S; W9 S/ b0 ]
excessive adrenal androgen production, and rarely,3 e  p1 `- R, ~3 h6 h
an adrenal tumor may also cause adrenal androgen7 m5 \0 m/ S. u+ r
excess.1,3( j$ V/ j( `: V" Z9 U. w9 O. p7 |
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 P. ]% N$ x4 i  a& g
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
) B6 R; T4 |$ U& L' Y* l7 {) |  FA unique entity of male-limited gonadotropin-
& h8 O8 Q0 x+ q; \. Findependent precocious puberty, which is also known
" ^$ D1 C, c- [; ~9 _as testotoxicosis, may cause precocious puberty at a+ h  h6 Y7 ]6 `4 x
very young age. The physical findings in these boys
% E; N4 p5 O& Z( [with this disorder are full pubertal development,$ W) F: G! V# F
including bilateral testicular growth, similar to boys
" C1 Z  Y- {: d4 L& {% Mwith CPP. The gonadotropin levels in this disorder5 h% G0 A/ o6 A% M! M8 s7 }
are suppressed to prepubertal levels and do not show
& r: c% W9 V2 K- @  Spubertal response of gonadotropin after gonadotropin-
# o% H8 a# g6 J  {! Kreleasing hormone stimulation. This is a sex-linked
; E/ B+ X- T7 Y; o5 `- g) Fautosomal dominant disorder that affects only9 c! ^" r' Y9 p7 b. g- I
males; therefore, other male members of the family7 }) R+ ~6 M1 V  y  x
may have similar precocious puberty.3
) [! J* g) r+ ~% }8 U+ P# i- CIn our patient, physical examination was incon-1 }: `! b# m% P6 t. D  f, {6 {
sistent with true precocious puberty since his testi-( z% y1 [& `. k8 d3 O
cles were prepubertal in size. However, testotoxicosis9 L9 F8 [- ?% j8 |* ^
was in the differential diagnosis because his father
) C2 q# I6 R( G) x9 o+ g* c3 X+ wstarted puberty somewhat early, and occasionally,+ _6 v, D7 y# c- V
testicular enlargement is not that evident in the
2 [" U7 X/ C2 }7 k  Pbeginning of this process.1 In the absence of a neg-
: n. |5 q3 S4 c: F. o4 e( Sative initial history of androgen exposure, our' d6 {0 A8 d, D  W4 ~' D: V' O
biggest concern was virilizing adrenal hyperplasia,! ?% c. o! o  a. Z
either 21-hydroxylase deficiency or 11-β hydroxylase# R' Q) i1 W3 s- q
deficiency. Those diagnoses were excluded by find-9 P+ g% B- u7 Y
ing the normal level of adrenal steroids.# i& {5 c- K; y- K* i0 @( \% g
The diagnosis of exogenous androgens was strongly! K- F8 A0 {9 @
suspected in a follow-up visit after 4 months because0 }/ N! U9 A2 V7 s* ^
the physical examination revealed the complete disap-
# H9 @/ k, ^6 g. A7 K4 o5 Epearance of pubic hair, normal growth velocity, and
+ w) u# ]5 _) Y$ a; K2 t9 hdecreased erections. The father admitted using a testos-4 _- E: K0 A9 ]4 v" E/ g9 m% w$ ^
terone gel, which he concealed at first visit. He was' [7 [' Y. w) @1 t- p
using it rather frequently, twice a day. The Physicians’
4 D# p. F' @0 ^. R" T+ t; m! xDesk Reference, or package insert of this product, gel or
/ J. C8 s1 o( Acream, cautions about dermal testosterone transfer to
+ q0 R, M6 K6 }9 [unprotected females through direct skin exposure.
! @) t# O; `0 B& }Serum testosterone level was found to be 2 times the
3 K# N0 Q% A5 z$ y7 Q1 |' G  Ubaseline value in those females who were exposed to5 j  D1 L, e, ?+ a; C/ g
even 15 minutes of direct skin contact with their male) [2 V% S2 P/ `$ i
partners.6 However, when a shirt covered the applica-
* W( I7 P" x7 jtion site, this testosterone transfer was prevented.- X; U' @" d8 c
Our patient’s testosterone level was 60 ng/mL,6 F: @5 |7 \9 R
which was clearly high. Some studies suggest that, y% W; p+ N& K& ?) p
dermal conversion of testosterone to dihydrotestos-6 h3 h  f: X. _7 N' G
terone, which is a more potent metabolite, is more' P8 X$ E# q- ]' M
active in young children exposed to testosterone4 u7 x* M- C% B/ j% |  B) u
exogenously7; however, we did not measure a dihy-
2 `1 A- N2 i- g  Ydrotestosterone level in our patient. In addition to
% Y# K& d: c6 @* s9 Xvirilization, exposure to exogenous testosterone in0 \+ e$ ^& p4 m' `9 u
children results in an increase in growth velocity and" K3 ^3 ~( a9 a# F  I9 Q( u
advanced bone age, as seen in our patient.  k" l. ]5 i$ ^6 \' H0 z% _
The long-term effect of androgen exposure during: }/ r/ u4 A# Q
early childhood on pubertal development and final: }- b& r' N' Q
adult height are not fully known and always remain4 N4 z7 s3 w9 N( w/ R- a5 F: S
a concern. Children treated with short-term testos-
3 l; K+ w. a9 v  @0 pterone injection or topical androgen may exhibit some
5 E) B6 _) T9 F# e, U1 Dacceleration of the skeletal maturation; however, after
4 R, g  {( \/ C& I/ \cessation of treatment, the rate of bone maturation$ B1 c- T9 P( M. e% W9 C
decelerates and gradually returns to normal.8,9- e3 G7 M, y+ o- Q3 Z
There are conflicting reports and controversy% C. E. }4 X' Y: t  D. j
over the effect of early androgen exposure on adult
6 ~; V' f) F/ O- Hpenile length.10,11 Some reports suggest subnormal
4 b% e' n) d3 d9 b8 ]+ I, uadult penile length, apparently because of downreg-
& i6 ^1 ~7 @5 C9 V+ _: aulation of androgen receptor number.10,12 However,
# w) C3 ~! A( HSutherland et al13 did not find a correlation between" W) L' g0 r7 M" W6 v' ^
childhood testosterone exposure and reduced adult. w) g$ k0 l& D+ u9 c+ ]
penile length in clinical studies.
7 ^+ _% S& j$ n& R0 R1 W6 ]Nonetheless, we do not believe our patient is3 v: u1 l- t! g/ ^  ^8 o8 U0 G* D
going to experience any of the untoward effects from  Z& h4 _4 y( _" b
testosterone exposure as mentioned earlier because
1 C9 |, N, j$ X( n8 Y  Fthe exposure was not for a prolonged period of time.9 w2 {9 M$ H3 v0 n/ Q+ S
Although the bone age was advanced at the time of
: u, ~- N0 g4 T: Z9 V& I/ `diagnosis, the child had a normal growth velocity at
. N" v) J+ i8 v1 i: V4 I8 ^) nthe follow-up visit. It is hoped that his final adult. m6 ^. Q; ?2 P7 c& n4 D4 g
height will not be affected.# o5 ^- {! ~, n! T' Y" `* p
Although rarely reported, the widespread avail-( J! a" ~0 V# B# _/ r
ability of androgen products in our society may. G% m% Y  [$ Z$ W  ~+ _
indeed cause more virilization in male or female+ H* |! r. y% i% k) y* m
children than one would realize. Exposure to andro-2 _, ~/ O9 G* w/ z
gen products must be considered and specific ques-- u6 d5 r+ Z3 i; y* G
tioning about the use of a testosterone product or
9 c: p* v! @& X' B7 y& h8 A% Zgel should be asked of the family members during# e! g+ S8 y& j6 S$ @% b
the evaluation of any children who present with vir-
5 q6 ?# H. k* o! dilization or peripheral precocious puberty. The diag-
; e9 I5 |  [9 Wnosis can be established by just a few tests and by
& R1 W# E$ c- v9 [7 J" F4 zappropriate history. The inability to obtain such a
( C+ @1 s) O7 P6 phistory, or failure to ask the specific questions, may
) _/ X; T5 J! zresult in extensive, unnecessary, and expensive; U9 Q# \& H' A2 j* I" L' e
investigation. The primary care physician should be. e0 S- Y9 i1 s* E
aware of this fact, because most of these children8 U) C4 N7 A. m# S- Q
may initially present in their practice. The Physicians’9 m: T2 F: ]7 v0 Z) Q8 c4 G
Desk Reference and package insert should also put a
$ F; c( T: |6 ?- U9 e! ^warning about the virilizing effect on a male or
  y3 }6 C! A6 i* H5 Q8 w" }female child who might come in contact with some-
$ G, F$ M7 {: h6 @7 E. Qone using any of these products.0 ^( l8 m: B3 u" j0 }
References6 p. w9 r$ v9 `2 C) F
1. Styne DM. The testes: disorder of sexual differentiation
! S0 d' ~/ o" s+ H3 |/ Sand puberty in the male. In: Sperling MA, ed. Pediatric5 c3 O+ c: W- G, ?! R
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;2 x# }! @! |: _9 F9 P' o
2002: 565-628.
& d! q- r* j# @! b" y2 ~2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
7 q3 ]5 y! p4 [4 h. N: m9 s3 Apuberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

6 j  D* X, Z' d$ ~5 V: X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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