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Sexual Precocity in a 16-Month-Old
- [4 B# L( X* x  a* nBoy Induced by Indirect Topical0 ?4 z9 E3 L- U0 l4 c0 }
Exposure to Testosterone
8 N$ ]: B# G+ J9 ~6 n, P# lSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2( X; `7 o3 S; S
and Kenneth R. Rettig, MD1
8 M5 g0 z! y8 d+ `3 ?8 V7 D- BClinical Pediatrics' I* m" I& c  W* z+ Y
Volume 46 Number 6
0 R/ f4 F8 G7 H; @, j/ P" ?July 2007 540-5431 w( S6 ~* M7 H- D+ B/ R+ C
© 2007 Sage Publications* N* j1 g! [: A" k, T/ k
10.1177/0009922806296651
1 p( n. f, H  Q, @7 w. ^http://clp.sagepub.com
! A4 N  C3 f6 {! ^& D9 d8 ghosted at
; @7 u5 s  _- B. Q1 ]0 zhttp://online.sagepub.com
8 \# c  X" P/ v7 LPrecocious puberty in boys, central or peripheral,
1 t" G( k5 e$ [! ois a significant concern for physicians. Central
% C3 H: i7 l0 r8 |precocious puberty (CPP), which is mediated& V1 F' e# t- v& }. Y
through the hypothalamic pituitary gonadal axis, has1 T5 I1 Q' x" O: i
a higher incidence of organic central nervous system5 a! j% A9 s3 h! F2 y
lesions in boys.1,2 Virilization in boys, as manifested) J0 A4 B0 u9 U4 E7 s9 H* t
by enlargement of the penis, development of pubic+ j2 @6 S& z0 M' G! v# i5 [
hair, and facial acne without enlargement of testi-- T; y" @! C' D2 X0 U  F
cles, suggests peripheral or pseudopuberty.1-3 We
+ r( \% n0 S3 m4 T9 Zreport a 16-month-old boy who presented with the% `% E" {! a% \3 N' y
enlargement of the phallus and pubic hair develop-7 C( ~5 F- H1 d5 K. H# Y* z3 _
ment without testicular enlargement, which was due1 }' `$ c- c, Y
to the unintentional exposure to androgen gel used by
% n" |, U* k; }9 G8 R' Pthe father. The family initially concealed this infor-
: S' M( t2 U' n% @& X( r6 ymation, resulting in an extensive work-up for this
) J" ?1 I' K' w8 B0 R* Zchild. Given the widespread and easy availability of
: D4 E, Y! f( C: ?9 ztestosterone gel and cream, we believe this is proba-
/ x# K  _- P/ p$ W- [bly more common than the rare case report in the
0 r- R7 o3 ?4 n. B2 pliterature.4
  I' n9 ^$ r/ W3 k$ A: Z- RPatient Report1 e5 J; K! d0 N4 s$ N) }
A 16-month-old white child was referred to the5 E* L! b( j0 K5 @
endocrine clinic by his pediatrician with the concern% m( A6 W: r. i
of early sexual development. His mother noticed
! S6 e. g& x- Y5 A9 klight colored pubic hair development when he was7 u- I5 i7 N2 V8 [
From the 1Division of Pediatric Endocrinology, 2University of
  C7 {! `6 D( u1 E2 b9 bSouth Alabama Medical Center, Mobile, Alabama.0 ~1 u, p: [/ Z. P
Address correspondence to: Samar K. Bhowmick, MD, FACE,
% i( K" E( P0 I5 j3 m/ T; O: r, XProfessor of Pediatrics, University of South Alabama, College of3 L7 l8 K0 w- e5 L% S' E
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;+ ]$ N% w; ^/ S7 i* m9 T! }
e-mail: [email protected].
% T$ S  S, {: @# Sabout 6 to 7 months old, which progressively became
, {9 G% Z  f' a- hdarker. She was also concerned about the enlarge-2 U, X+ ]7 V8 B* O% g, B3 f
ment of his penis and frequent erections. The child' K3 ^9 _4 Q7 x! B; }
was the product of a full-term normal delivery, with
0 a# b7 {4 I  f/ {  V9 aa birth weight of 7 lb 14 oz, and birth length of
8 R5 G2 n9 o8 U; c1 i1 g, j  R20 inches. He was breast-fed throughout the first year
7 Q. ?8 P$ _8 Lof life and was still receiving breast milk along with
, h! d9 S1 S, E. |solid food. He had no hospitalizations or surgery,% H& I8 v4 \4 T; J
and his psychosocial and psychomotor development
: F# U4 C" i" h7 r" s& ~was age appropriate., t5 m6 _" G# p) U
The family history was remarkable for the father,
4 G9 G3 E: v( B9 D; swho was diagnosed with hypothyroidism at age 16,& k  T/ \& P% Q5 `; u! O0 V
which was treated with thyroxine. The father’s/ g3 B( s4 S& H0 g
height was 6 feet, and he went through a somewhat1 N( F8 Y& F& r6 H2 D% j& M
early puberty and had stopped growing by age 14., i8 I) d0 ]8 G8 T
The father denied taking any other medication. The, r- ?! O# G" w7 Z
child’s mother was in good health. Her menarche
1 k) ?! O/ r$ ^( q/ `! vwas at 11 years of age, and her height was at 5 feet/ s) x# {% d3 h( v
5 inches. There was no other family history of pre-8 e. G, @2 E* C& u# g
cocious sexual development in the first-degree rela-4 B" @4 `9 ]' \% ?% U
tives. There were no siblings.( a: A- Z; F* [  T. l; f
Physical Examination" d, `/ F) n# i% C/ ?2 a9 D5 ]+ M* x
The physical examination revealed a very active,$ i: R7 w- z$ c
playful, and healthy boy. The vital signs documented
0 ^, I: m& S) N& L: e1 x, m! Ca blood pressure of 85/50 mm Hg, his length was
: w; o! N" J. m& K( p90 cm (>97th percentile), and his weight was 14.4 kg5 P% j8 i6 p  n2 y
(also >97th percentile). The observed yearly growth
" [+ H, G4 m* c* |( |velocity was 30 cm (12 inches). The examination of
! N) ^: l" S$ p$ \' Ythe neck revealed no thyroid enlargement.' y. l  S6 j) v6 C' ?
The genitourinary examination was remarkable for* j8 x6 Y. u% C: _/ X! j
enlargement of the penis, with a stretched length of
: t) l/ I0 [! `6 g; r) y4 Y8 cm and a width of 2 cm. The glans penis was very well( Y3 s1 N, C5 x
developed. The pubic hair was Tanner II, mostly around
) \; S1 b8 f8 |5 m540. J) R% L0 x/ J( l4 F2 u
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ b- v  p! o* d0 [2 D8 A
the base of the phallus and was dark and curled. The. C) ^# r0 B3 K9 a% x  d/ d
testicular volume was prepubertal at 2 mL each.& y1 ^6 M* }' X: ]) Q$ Y! J
The skin was moist and smooth and somewhat
- B! e1 O# D! U! |oily. No axillary hair was noted. There were no* B* r; S4 K, e5 w0 m
abnormal skin pigmentations or café-au-lait spots.% b& L. Q/ L. n* ]% }
Neurologic evaluation showed deep tendon reflex 2++ b% f2 q! ?" D8 M, i% _
bilateral and symmetrical. There was no suggestion- M8 W; f$ f/ r
of papilledema.% u( t* _. f1 p0 M/ Z( X" I  ^
Laboratory Evaluation
8 s) G7 t5 U5 Y8 t7 PThe bone age was consistent with 28 months by; H' i8 T  h4 F$ l5 n" V$ v& u
using the standard of Greulich and Pyle at a chrono-
  H, z' r5 ?. f: L0 F" {; wlogic age of 16 months (advanced).5 Chromosomal9 g  a1 i1 ~. I3 f) N3 g: h
karyotype was 46XY. The thyroid function test+ B9 h5 `2 @5 P
showed a free T4 of 1.69 ng/dL, and thyroid stimu-/ H' J6 I  _: m( P: b% h" b
lating hormone level was 1.3 µIU/mL (both normal).
3 J& R0 F/ b  @1 d7 |) ]The concentrations of serum electrolytes, blood
( c, P5 E* k8 u. v- curea nitrogen, creatinine, and calcium all were" a: K2 R* U$ j9 `1 a( |
within normal range for his age. The concentration: z8 Y) n1 e& X6 T% p1 X& A
of serum 17-hydroxyprogesterone was 16 ng/dL5 V* L; _' n" }
(normal, 3 to 90 ng/dL), androstenedione was 20# j! Q0 t* \) l0 G0 C- U2 f3 O. g
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-4 x7 p4 B' F' D' M0 G* k
terone was 38 ng/dL (normal, 50 to 760 ng/dL),, _* i8 C! v& U. w# ~' h
desoxycorticosterone was 4.3 ng/dL (normal, 7 to) h4 {) k4 l5 O; K
49ng/dL), 11-desoxycortisol (specific compound S)
% B) q8 ]- Z9 d' ~' F: k1 t9 o/ Jwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
8 t$ _' b% E" s2 p, _  btisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
( Y% T* H6 K3 k1 H0 {' l$ Jtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),% E3 V/ l& o; ]' A
and β-human chorionic gonadotropin was less than. e# S! e1 C" u- `6 @% D8 L
5 mIU/mL (normal <5 mIU/mL). Serum follicular  p7 |* }$ {+ b9 f
stimulating hormone and leuteinizing hormone
) O( h5 j: a% J& ]" s9 h, C7 Kconcentrations were less than 0.05 mIU/mL
$ ], M* @( j( @/ k5 }(prepubertal).
7 a4 ^0 @# ^. |3 b1 S! O& S. ~8 Z4 dThe parents were notified about the laboratory) P7 F7 Q6 l4 ]
results and were informed that all of the tests were
! O2 `, j* I8 T2 J2 Wnormal except the testosterone level was high. The
& `) S" p/ I7 Y" x/ E8 O* t: sfollow-up visit was arranged within a few weeks to
. _. K3 o1 ]/ p7 L2 S( N6 Y6 eobtain testicular and abdominal sonograms; how-
: M9 L1 k, e+ I5 X$ c! ~2 c4 zever, the family did not return for 4 months.
( G5 X5 t7 S: d, p+ ?Physical examination at this time revealed that the- p9 L: N( q+ d
child had grown 2.5 cm in 4 months and had gained
6 U2 [6 ^  c  P& c* O) ]' M) q2 kg of weight. Physical examination remained" G3 j% i* I& r
unchanged. Surprisingly, the pubic hair almost com-7 r7 C0 P3 e. C3 o9 G
pletely disappeared except for a few vellous hairs at: d9 }- y5 x5 X
the base of the phallus. Testicular volume was still 26 o5 k* [) u  p# |0 P, P- Z
mL, and the size of the penis remained unchanged.
, n+ b1 b9 I$ f4 X$ _$ s: Z4 |3 ZThe mother also said that the boy was no longer hav-% C) [9 x9 G5 e+ e
ing frequent erections.! }+ U" a1 O5 n0 {
Both parents were again questioned about use of
0 ~* R, ^4 f: z' i: N0 f0 K3 wany ointment/creams that they may have applied to9 t' f+ x: \4 }* ]
the child’s skin. This time the father admitted the
$ V4 b- c$ x" a) s/ |$ RTopical Testosterone Exposure / Bhowmick et al 541
  I1 j, Z5 c4 r" X( w- p$ i, Guse of testosterone gel twice daily that he was apply-
- Z+ t! M6 s3 j( [# T$ g. D7 xing over his own shoulders, chest, and back area for& w2 ~5 n" U6 I* L, T8 W
a year. The father also revealed he was embarrassed
. F# L- a4 n$ a9 N1 Ito disclose that he was using a testosterone gel pre-
" r5 W" Z; h, P: pscribed by his family physician for decreased libido
& l( I: a& V! l: V5 {) j. E) }secondary to depression.
1 F3 u8 n. o: K* \) LThe child slept in the same bed with parents., z7 w. L/ C3 e- Q" e+ i3 D$ C
The father would hug the baby and hold him on his
( K/ j0 j9 T' L* D0 I5 \+ d4 n+ u9 }chest for a considerable period of time, causing sig-- L! ], I! }; ?0 B. C
nificant bare skin contact between baby and father.; P1 D8 S) y0 x4 a
The father also admitted that after the phone call,3 ?; Y0 E" k4 v) l* t
when he learned the testosterone level in the baby
7 \) i  F  {( \4 s" ywas high, he then read the product information) {7 {" J3 g! }5 p0 z% \( j
packet and concluded that it was most likely the rea-7 I/ w' V3 C+ y8 {  G' H& S
son for the child’s virilization. At that time, they
9 k; h8 [  z" N+ Pdecided to put the baby in a separate bed, and the
* `4 Q. x4 X2 a3 {5 `0 Bfather was not hugging him with bare skin and had
% Q! V6 W- L- A7 D! i' z2 n7 }$ @been using protective clothing. A repeat testosterone4 j7 _8 F5 z9 ?8 U# z* `2 g5 b# d: |
test was ordered, but the family did not go to the! r5 m, G" c) v; ~
laboratory to obtain the test.
  p: k, u1 S2 j& }' n9 hDiscussion
1 {( p0 S8 ^# U6 G( l4 fPrecocious puberty in boys is defined as secondary
+ c  a1 z, K9 z6 _+ B* f8 X7 |/ }sexual development before 9 years of age.1,42 H2 E4 n0 q. g. ?
Precocious puberty is termed as central (true) when6 Y" V2 n$ H7 d' ^$ t
it is caused by the premature activation of hypo-
! b- b' L( \# E5 a1 A2 |thalamic pituitary gonadal axis. CPP is more com-
4 N& n5 w/ d$ b: z" H0 U8 Gmon in girls than in boys.1,3 Most boys with CPP  w4 U) T0 f8 X. o( o8 c* i
may have a central nervous system lesion that is
. A2 `/ P' ]1 \5 v# gresponsible for the early activation of the hypothal-5 q: \- v- `) K5 S
amic pituitary gonadal axis.1-3 Thus, greater empha-0 D2 d7 I$ j2 {0 e6 W% `5 m# K
sis has been given to neuroradiologic imaging in
- n  X. `4 W( c4 l* t. h5 O2 t: K( iboys with precocious puberty. In addition to viril-0 O; |" R6 u2 \/ X
ization, the clinical hallmark of CPP is the symmet-+ L4 A; ?3 ?/ T. C8 J1 B, g
rical testicular growth secondary to stimulation by
3 f6 _6 h9 S% H+ w: Ogonadotropins.1,3
& B. {% [' H/ I5 G% aGonadotropin-independent peripheral preco-9 ?7 c( l+ z* d! @( u" H& @6 B: W
cious puberty in boys also results from inappropriate, }+ v/ l, S9 a
androgenic stimulation from either endogenous or" a9 @+ y7 D* R8 q) u$ v
exogenous sources, nonpituitary gonadotropin stim-
) j8 M5 h1 A# I' wulation, and rare activating mutations.3 Virilizing
, F' t6 c+ m4 t) Econgenital adrenal hyperplasia producing excessive
/ h5 s' r6 A  r$ r7 S! _% y9 Y' uadrenal androgens is a common cause of precocious5 k6 V  l3 q8 N, I  d3 J8 m
puberty in boys.3,4+ o: i4 i: i" E% Q! R3 D$ _- z
The most common form of congenital adrenal7 B( g  a/ g0 A$ W) ?
hyperplasia is the 21-hydroxylase enzyme deficiency.
1 x8 ^: h& M* e! Y2 `The 11-β hydroxylase deficiency may also result in
' k. N( m9 V3 f7 N# P5 Z  nexcessive adrenal androgen production, and rarely,
3 \7 G  z: a2 S+ b) F, _an adrenal tumor may also cause adrenal androgen
& S& t; P- Z9 t2 J/ a9 n' `excess.1,3
) D: C& u$ V9 y5 v1 [( V- wat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" r* |  f& J. d0 G+ l  l: x" A542 Clinical Pediatrics / Vol. 46, No. 6, July 20078 }$ a4 Y9 s7 ?
A unique entity of male-limited gonadotropin-
( r; Y3 r9 T4 g& ?- yindependent precocious puberty, which is also known- t' Z% T. X  c! f
as testotoxicosis, may cause precocious puberty at a' Y0 n( }+ |9 ]
very young age. The physical findings in these boys
. h1 P. I& Z* ?* hwith this disorder are full pubertal development,
, B- L: ?6 f; u/ V7 @2 Wincluding bilateral testicular growth, similar to boys
. ]4 r7 I$ f# Pwith CPP. The gonadotropin levels in this disorder
5 }! x3 p( j3 J# L. Nare suppressed to prepubertal levels and do not show' `5 R. a4 X! F8 ^) h: C3 f3 H7 h
pubertal response of gonadotropin after gonadotropin-+ n0 a9 {$ x/ ?: c* v( r- T& H( r" H
releasing hormone stimulation. This is a sex-linked
4 }0 O) Q, {) i% n3 `9 z' r6 Tautosomal dominant disorder that affects only
; n) @0 n0 B: E: r$ amales; therefore, other male members of the family5 ~/ W$ _9 R, W- H: G0 W4 u6 u% n
may have similar precocious puberty.3
* j6 E/ a( ]# z; Z0 M9 PIn our patient, physical examination was incon-
4 K! @: o, A9 V& k1 I2 B+ m  v8 Rsistent with true precocious puberty since his testi-
/ p  f% _, W6 R$ f/ |cles were prepubertal in size. However, testotoxicosis
9 k3 @) G& A5 ~; Q! ]* K- Bwas in the differential diagnosis because his father
/ D5 }; V9 i' F3 @8 c0 C5 \" Nstarted puberty somewhat early, and occasionally,
# [: b) y6 @9 K. j) x) x4 H1 Ktesticular enlargement is not that evident in the
+ G; M! J! Z$ n$ mbeginning of this process.1 In the absence of a neg-# N; `: J5 F9 B3 X& b
ative initial history of androgen exposure, our& A$ r, J4 O6 M
biggest concern was virilizing adrenal hyperplasia,
/ @* i, o# o. @7 x, W. x8 Beither 21-hydroxylase deficiency or 11-β hydroxylase; g4 L8 }+ l5 ?8 O
deficiency. Those diagnoses were excluded by find-
  ]2 i- `# N" y, b* k. ?( F& x) Ping the normal level of adrenal steroids.3 F: w' m$ ?7 J, V4 C
The diagnosis of exogenous androgens was strongly
& t. A7 ]1 g7 @% a  T8 Ususpected in a follow-up visit after 4 months because
1 {9 G% H2 d3 j4 Fthe physical examination revealed the complete disap-" V9 R: `2 x6 }! ~; w
pearance of pubic hair, normal growth velocity, and- d0 X: K2 L1 ^) s1 x5 N4 ~% L8 k5 j
decreased erections. The father admitted using a testos-
5 {. @5 K$ Q: {/ u3 k# Jterone gel, which he concealed at first visit. He was
, @' B* p! n1 h1 ~- z, c$ Rusing it rather frequently, twice a day. The Physicians’: p) o" Y; \$ R2 E3 i/ G
Desk Reference, or package insert of this product, gel or1 `# x6 R+ r. o, `6 a
cream, cautions about dermal testosterone transfer to
* v. Q& C" N  r" B* L9 Tunprotected females through direct skin exposure.
: O$ W0 c! \' h0 k+ K5 f3 LSerum testosterone level was found to be 2 times the5 r- n6 Y' z+ b+ p, t  ?
baseline value in those females who were exposed to! c( H0 M- }- W2 A* _/ r5 w
even 15 minutes of direct skin contact with their male
8 Q5 o' L: L0 g& v% P( bpartners.6 However, when a shirt covered the applica-5 u; _7 v1 [" D* i; m- f7 X
tion site, this testosterone transfer was prevented.! y; ]* w. c+ T# @6 s! D7 Z* t
Our patient’s testosterone level was 60 ng/mL,0 E, @1 w1 P$ ?7 D; P9 ^4 W
which was clearly high. Some studies suggest that7 Z' V: G- N: N0 @0 _: z$ w* w
dermal conversion of testosterone to dihydrotestos-
3 ]8 Y5 m+ l! G$ D& aterone, which is a more potent metabolite, is more# E5 `3 H2 {# K. O7 C' t! f, |
active in young children exposed to testosterone& f, b: o2 T: f+ j- O+ K" M1 ^
exogenously7; however, we did not measure a dihy-
# t9 G+ O) p7 {& n4 u1 cdrotestosterone level in our patient. In addition to5 X* m4 d) r( f: U
virilization, exposure to exogenous testosterone in4 [2 ?. J* W& S: e- U
children results in an increase in growth velocity and1 x% h# T7 r) N+ O: b9 U, k" U
advanced bone age, as seen in our patient.
  Y. v* I" r1 m3 SThe long-term effect of androgen exposure during' a5 a; Y& K9 E! y3 Q
early childhood on pubertal development and final. w9 E. ]# @) G7 X" C" m
adult height are not fully known and always remain
7 j6 g1 T1 y! q( M$ A* D% t8 H- Xa concern. Children treated with short-term testos-& K: P# o2 c6 A/ |2 L
terone injection or topical androgen may exhibit some9 U0 `' \  n5 {$ ?
acceleration of the skeletal maturation; however, after( e" u) r8 T# \: V
cessation of treatment, the rate of bone maturation7 ]; I. e. a: H1 J2 Y' Y/ T: [
decelerates and gradually returns to normal.8,9  S- [8 _0 ^( \% j. O6 @. V- }
There are conflicting reports and controversy5 S* V* S# G/ C  G
over the effect of early androgen exposure on adult
. h6 i$ [) a6 Q% \+ j3 _* q1 Hpenile length.10,11 Some reports suggest subnormal
7 \0 o) X) D+ U- L8 `4 |* Qadult penile length, apparently because of downreg-3 z! r4 c, t% w8 N) U- k, K! a
ulation of androgen receptor number.10,12 However,
6 s5 c2 `+ B( l) USutherland et al13 did not find a correlation between0 ^  R; t. n" V* g& H( Q
childhood testosterone exposure and reduced adult- _% [2 u% \1 ~, d0 e$ J  j3 T
penile length in clinical studies.
+ u6 g8 z! I+ h7 M# u+ VNonetheless, we do not believe our patient is
6 m5 w# s) k& X6 k$ O: G' xgoing to experience any of the untoward effects from
2 u  F9 B$ ?: {  Ctestosterone exposure as mentioned earlier because
$ x( U1 b! f! }6 ^- q. u4 }9 \the exposure was not for a prolonged period of time.
9 H( e- A, j3 |) [: u& {+ TAlthough the bone age was advanced at the time of6 A- E4 D: M6 x7 o* G7 L* e7 M
diagnosis, the child had a normal growth velocity at& j2 s8 `; A; z" J( ]
the follow-up visit. It is hoped that his final adult; G7 i% Y' P8 U2 O. [& E. e
height will not be affected.
4 X( D3 g+ d. c, GAlthough rarely reported, the widespread avail-* [  g* g5 Y* ^" ?& D1 {
ability of androgen products in our society may( h7 ^1 S3 g+ a+ Y1 \0 ^
indeed cause more virilization in male or female4 G3 h9 ?7 {, q
children than one would realize. Exposure to andro-2 v+ w  m7 l) B3 e8 e# y3 n) e
gen products must be considered and specific ques-; j* I! G1 k' \# W: }8 W8 S9 _) [5 O
tioning about the use of a testosterone product or
! n5 H8 L" [! W6 V& B" {gel should be asked of the family members during
, o! j. ^: `2 @% othe evaluation of any children who present with vir-
  u# f+ I4 _7 D  Y# ailization or peripheral precocious puberty. The diag-
# o$ i/ X+ i0 D7 A+ Dnosis can be established by just a few tests and by
* X7 Z( q9 c$ b! x& Eappropriate history. The inability to obtain such a0 Y, ~9 o+ n/ H" y3 Z
history, or failure to ask the specific questions, may
  I$ p2 P: C! c1 q7 C) a% n, hresult in extensive, unnecessary, and expensive* Y7 w9 p. u- q% w
investigation. The primary care physician should be& F7 B$ @$ R( o
aware of this fact, because most of these children
7 G& P' e$ C% E4 rmay initially present in their practice. The Physicians’4 K2 b4 a+ C6 u( k$ x3 g, r
Desk Reference and package insert should also put a
' j' A1 f6 f' n( p$ _& x5 l& G. ?& u5 Vwarning about the virilizing effect on a male or
0 I0 i0 d7 [  J; q" y& f% S; ?" kfemale child who might come in contact with some-
% f3 E4 f# s7 d$ s' l, n  G$ Kone using any of these products." i9 x# T  o9 Z7 Z2 o6 G- Y, @
References7 C. G& @* k- b6 p' o) ]6 S
1. Styne DM. The testes: disorder of sexual differentiation
: X0 |( S' J6 u2 Mand puberty in the male. In: Sperling MA, ed. Pediatric# M$ a" j% X# h" C8 I; t7 G9 A
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
6 L  O8 b+ ?( C( }4 y2002: 565-628.
1 D+ Q9 b* x2 w' [2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
  I7 t: v, ^/ r- ipuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old9 Q# J: ~3 B8 v+ C$ ?3 a& Z
Boy Induced by Indirect Topical
) q- \; [: h+ e# y: a# CExposure to Testosterone* O5 V5 P8 f- Q( x  W% R! z
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,24 M0 v5 Y) U. \( T+ U
and Kenneth R. Rettig, MD1
. }( `/ {9 F, t2 \6 a2 s- l. i7 k" QClinical Pediatrics6 f, r7 H5 o( i! q) v
Volume 46 Number 6
5 e/ W9 J7 p! h+ BJuly 2007 540-543
3 Z) [( C1 }1 @8 H( A; |' z© 2007 Sage Publications) `0 c/ ?6 g1 w4 x2 h1 P
10.1177/0009922806296651
& G. L5 k2 W  Whttp://clp.sagepub.com
. e+ O" ?" e) n! U$ _3 Chosted at
: y7 s# d% Y5 S/ K& [* y/ ghttp://online.sagepub.com
! N! L  i4 d& r& w- l8 x  |Precocious puberty in boys, central or peripheral,
' U8 q8 T5 V0 ]. \is a significant concern for physicians. Central
& r% F. ]! |0 A! c) bprecocious puberty (CPP), which is mediated
; r0 s2 w* Y/ M" I( cthrough the hypothalamic pituitary gonadal axis, has9 {6 k  M' Y5 U+ W
a higher incidence of organic central nervous system
3 D) N! T  X+ C; N# S5 l/ e! I3 b% flesions in boys.1,2 Virilization in boys, as manifested
* |; |! x, n) q0 z" Fby enlargement of the penis, development of pubic
$ U2 b( i# `; ~: b( ?, a8 fhair, and facial acne without enlargement of testi-
9 B1 ?) l0 X3 w  \cles, suggests peripheral or pseudopuberty.1-3 We9 _  y8 i) {3 y. l0 i  O) T6 R
report a 16-month-old boy who presented with the) o8 ?+ y. T) _7 f: N
enlargement of the phallus and pubic hair develop-7 b" {( Z2 e  E1 w% }1 S, |
ment without testicular enlargement, which was due# O: J' X+ T5 E8 M) R
to the unintentional exposure to androgen gel used by) H1 p/ J) R, B* Q5 F: W6 {) R
the father. The family initially concealed this infor-' v! x  S- [! d3 y# m
mation, resulting in an extensive work-up for this
2 T( T  h# N1 T+ ^) [3 U* achild. Given the widespread and easy availability of1 ~* b0 Q5 ^1 Z0 |" e6 k
testosterone gel and cream, we believe this is proba-
" ^! \7 {# k9 |% T* |bly more common than the rare case report in the- v$ R0 x, R! s8 b+ H# c3 P; }
literature.4: ?8 j8 ~$ F+ k% C
Patient Report% W; Z. J) ^0 o( u) [
A 16-month-old white child was referred to the
# ]) m3 y& I. ~: B( }endocrine clinic by his pediatrician with the concern8 e( O7 j/ S3 x0 J
of early sexual development. His mother noticed" j6 e) e) P7 @  F7 x8 Q7 S
light colored pubic hair development when he was4 L1 i# [5 f  Q& r6 i6 F
From the 1Division of Pediatric Endocrinology, 2University of* A. z9 n1 `& `, b
South Alabama Medical Center, Mobile, Alabama.
3 t0 B/ t$ o7 l1 }% @# ~9 wAddress correspondence to: Samar K. Bhowmick, MD, FACE,7 G4 _9 L( w' V* ?; u
Professor of Pediatrics, University of South Alabama, College of
5 X# F! t6 p( O5 P6 {" J8 DMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
6 h: m% D) x/ a2 K4 oe-mail: [email protected].# T3 p  \: Z( ~5 ^: e' K
about 6 to 7 months old, which progressively became! {% [6 f9 E/ `! P. q
darker. She was also concerned about the enlarge-4 d; C* w1 t' Q" R/ j/ y
ment of his penis and frequent erections. The child
$ o# f: A) z2 s* k) Swas the product of a full-term normal delivery, with3 W- ~$ t: f3 J0 d8 \) O: C- H" U
a birth weight of 7 lb 14 oz, and birth length of  q5 k) C/ G+ l# F9 l
20 inches. He was breast-fed throughout the first year
2 n* \9 r# x2 n& Rof life and was still receiving breast milk along with6 r  `. G  Z3 [# M! c8 Q
solid food. He had no hospitalizations or surgery,  R; y+ Y8 \; w
and his psychosocial and psychomotor development5 e8 E4 ^+ s0 @2 O  S4 X5 E; K
was age appropriate.
. ^* l! v1 E; h  tThe family history was remarkable for the father,( h. [: u/ W/ W. Y4 o, ]" Y) [3 [7 u
who was diagnosed with hypothyroidism at age 16,- l7 ~" I# q* X# l- M9 d" H
which was treated with thyroxine. The father’s
5 P" e5 F5 C1 H  S& Pheight was 6 feet, and he went through a somewhat
2 k) ^" B. J. g4 `* w2 Yearly puberty and had stopped growing by age 14.
8 h9 e2 k6 u( D& u; ]The father denied taking any other medication. The
, ^( C$ f: D# E+ W! \! Bchild’s mother was in good health. Her menarche* {1 @; ^, J, H6 Z2 d; V$ i' q
was at 11 years of age, and her height was at 5 feet1 z" Y& {3 a$ k: ?. c+ X5 I
5 inches. There was no other family history of pre-
& }1 g# C! J( k; Rcocious sexual development in the first-degree rela-
! |5 `- N+ j0 Ktives. There were no siblings.2 t& |7 j7 i5 Q- S% b3 r
Physical Examination1 s) f5 E; V# o( v9 j
The physical examination revealed a very active,
8 Z- |' \/ p% n& t  n2 ]( J3 gplayful, and healthy boy. The vital signs documented0 o- @. h4 ?) Q: i9 \7 g+ ~
a blood pressure of 85/50 mm Hg, his length was' {1 D! _* b; \6 H- n- d
90 cm (>97th percentile), and his weight was 14.4 kg2 ?# F4 Q+ ]( _: g# f: o
(also >97th percentile). The observed yearly growth) Z( G: @. {2 z" q! d$ H' }
velocity was 30 cm (12 inches). The examination of
% ^  N+ N1 _. k( `' J# o6 _2 h( v5 ethe neck revealed no thyroid enlargement.
2 R3 a: }/ B8 s/ \, \6 g- dThe genitourinary examination was remarkable for; j) m5 b* x7 @4 A0 h2 l8 [
enlargement of the penis, with a stretched length of4 `. [7 W% j, B
8 cm and a width of 2 cm. The glans penis was very well* E# u' j$ u% E* q/ q2 N) ^; {! c5 O' a
developed. The pubic hair was Tanner II, mostly around
% c9 G& n% e6 `: h  Y6 E540! l5 a5 x2 L' \5 `$ z4 M$ [/ n
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 R. {  ]# U! L; [the base of the phallus and was dark and curled. The
% e8 A; D# n9 ^7 d# ltesticular volume was prepubertal at 2 mL each.) U3 o1 M4 p- Q
The skin was moist and smooth and somewhat# q) F* z# y4 b5 x- Y; U
oily. No axillary hair was noted. There were no/ L# z! V' ]3 s% A* D5 I
abnormal skin pigmentations or café-au-lait spots., b$ ~6 H) C- K; n
Neurologic evaluation showed deep tendon reflex 2+
" O9 s- s8 ^( S3 h( abilateral and symmetrical. There was no suggestion
0 ]" ?0 C6 K- \  X) ^  ~( uof papilledema.) _- B& }6 j+ O3 W) }
Laboratory Evaluation
* \6 @% Y( [8 i3 L  O( MThe bone age was consistent with 28 months by
  Z0 X' ^9 m7 ?8 _$ N( c1 i4 susing the standard of Greulich and Pyle at a chrono-$ `' \/ A+ ~( j: Y' W+ s
logic age of 16 months (advanced).5 Chromosomal
$ _/ P+ _, s$ ekaryotype was 46XY. The thyroid function test4 x' e7 z- L0 V
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
; G' D6 E' R9 ~* k! clating hormone level was 1.3 µIU/mL (both normal).
# a. r" l) i" b! E  w" F( i3 l: \The concentrations of serum electrolytes, blood
0 r1 a9 }5 o/ s$ m: N7 I  Furea nitrogen, creatinine, and calcium all were0 K/ J6 ?- C& L: S" @: [. ?! ?# }
within normal range for his age. The concentration
, _0 @% z) G6 f# h) r! qof serum 17-hydroxyprogesterone was 16 ng/dL' ^  ~$ r; y; K+ v% ?. B8 D& o
(normal, 3 to 90 ng/dL), androstenedione was 20
- B4 r- q) G% O( jng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-" q5 Q8 U& Z4 ^
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
: M2 R- r; H1 \desoxycorticosterone was 4.3 ng/dL (normal, 7 to9 D, x  s" l9 ]; X) s
49ng/dL), 11-desoxycortisol (specific compound S)* v$ l! {/ ]% n' [. J
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-3 ~- k$ Q# @" c# o5 c/ [
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total$ y9 X! l* U+ n9 @- w
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),! ]+ _& x& c! n) ]. n
and β-human chorionic gonadotropin was less than
( ^; |+ i8 Q" v& B5 mIU/mL (normal <5 mIU/mL). Serum follicular
6 Z* [+ M& W* i1 K, @stimulating hormone and leuteinizing hormone
, m& L2 C2 A4 @0 Vconcentrations were less than 0.05 mIU/mL! g7 K* C. G2 l7 N% h7 j
(prepubertal).
) v7 `5 O' m) ?0 `) K$ p+ }3 IThe parents were notified about the laboratory; X. f6 X, V$ O+ E# v
results and were informed that all of the tests were
+ M6 g' I8 G+ ~normal except the testosterone level was high. The# U3 ~( U2 }  F0 [2 a
follow-up visit was arranged within a few weeks to! B/ J! J1 L" `7 y' ]( E  D# i
obtain testicular and abdominal sonograms; how-( [2 C$ X' J2 d5 _0 Z) B
ever, the family did not return for 4 months.
1 p1 f; E1 b( K9 X2 aPhysical examination at this time revealed that the0 i+ R6 |/ y% ~6 M: L2 t
child had grown 2.5 cm in 4 months and had gained
( G) R, L2 Z+ Y; d, n. `" B2 kg of weight. Physical examination remained# b& P/ M2 \7 m8 F' K0 n2 j/ i
unchanged. Surprisingly, the pubic hair almost com-
# x6 z$ a6 q& P' [0 vpletely disappeared except for a few vellous hairs at6 C8 c7 X; Z5 ?) N& ~
the base of the phallus. Testicular volume was still 2; d; x, A+ c* W! s' p
mL, and the size of the penis remained unchanged.3 j! h" v, R. o2 I: l
The mother also said that the boy was no longer hav-* j- t0 Z6 w* C0 W( e! y
ing frequent erections., Z+ Q9 Z1 N3 c3 B9 L/ }4 @# `
Both parents were again questioned about use of
% d# `# h0 Q4 e2 |0 t/ Vany ointment/creams that they may have applied to
6 Q: W7 r( G% t& Jthe child’s skin. This time the father admitted the: e  L% r9 f5 z6 B. e
Topical Testosterone Exposure / Bhowmick et al 541
7 a0 f, l- V/ n; d) @use of testosterone gel twice daily that he was apply-
, P0 u" Z3 i. u) q  l8 U5 u$ l' c0 I) hing over his own shoulders, chest, and back area for
6 P: \, p+ O# ^2 e8 oa year. The father also revealed he was embarrassed, t% D" o) M; o2 q; g
to disclose that he was using a testosterone gel pre-6 C5 x! y1 l2 U, w3 i7 {
scribed by his family physician for decreased libido6 `' I/ B  R; i0 y9 r
secondary to depression.
+ ^. a- `* r. f  sThe child slept in the same bed with parents.
9 ?  h' s. ]# B2 T/ QThe father would hug the baby and hold him on his4 N8 U. A% K+ h4 k5 _; H
chest for a considerable period of time, causing sig-3 s- y1 _9 T6 L! @9 m) Q3 u% `
nificant bare skin contact between baby and father.- i) e) L1 s7 i4 p8 C. Y3 H) Z
The father also admitted that after the phone call,
* j! i7 f: \& pwhen he learned the testosterone level in the baby
; \0 s0 l* ?" o# m0 swas high, he then read the product information5 [1 {  C3 G4 e7 l* K
packet and concluded that it was most likely the rea-
2 {0 J- u2 p9 Z' wson for the child’s virilization. At that time, they. }3 `% e! h" N( ~% r2 Q
decided to put the baby in a separate bed, and the
4 c3 z3 n! v+ d9 Q# q* Yfather was not hugging him with bare skin and had
& J/ K1 @& X+ x% P$ H: i9 q! Hbeen using protective clothing. A repeat testosterone# F  d5 _/ x$ A
test was ordered, but the family did not go to the
- d, o9 n5 ~1 r$ D/ B+ E8 F# alaboratory to obtain the test.3 \8 D: D- y9 z* w
Discussion
* s( l1 Z9 `' y5 cPrecocious puberty in boys is defined as secondary
& O" V, {  C8 a" w: Dsexual development before 9 years of age.1,4
, P" }8 R& C& {* q7 w# @Precocious puberty is termed as central (true) when4 F! f: l4 i& b& i* g: W
it is caused by the premature activation of hypo-$ K- L  C! \, J3 `3 f
thalamic pituitary gonadal axis. CPP is more com-" A) t  T- Z9 @
mon in girls than in boys.1,3 Most boys with CPP
: w4 q$ y0 ?5 imay have a central nervous system lesion that is4 f9 [2 u4 H6 n# q
responsible for the early activation of the hypothal-$ G0 \6 |. Q. \9 [
amic pituitary gonadal axis.1-3 Thus, greater empha-
1 Y6 L) f6 r, \' K/ zsis has been given to neuroradiologic imaging in
, [/ K  A1 X) a# V- R" uboys with precocious puberty. In addition to viril-
/ b2 s4 A+ N1 cization, the clinical hallmark of CPP is the symmet-
6 b& Q1 W6 a$ F/ C1 frical testicular growth secondary to stimulation by
2 n4 j: R9 K; ?4 U0 J9 F5 q6 ygonadotropins.1,3& @/ F$ Q4 J; s% R1 Z
Gonadotropin-independent peripheral preco-- k  Q; Z- z6 h9 q; c7 n( ^" B
cious puberty in boys also results from inappropriate
+ v  D* ~, Z' M9 c/ ~  r9 \4 J$ E4 candrogenic stimulation from either endogenous or
, y. X7 o4 y, v' lexogenous sources, nonpituitary gonadotropin stim-+ v6 E% ~" f9 n1 d
ulation, and rare activating mutations.3 Virilizing1 o! K" x4 |" S
congenital adrenal hyperplasia producing excessive7 t% l2 S7 c  y, S# L: ~- {
adrenal androgens is a common cause of precocious$ o7 B' c+ K( ^! C; N
puberty in boys.3,4
# Y) ~" B$ G% k8 ~The most common form of congenital adrenal
) H8 |1 }+ E$ @( w( Jhyperplasia is the 21-hydroxylase enzyme deficiency.! ^+ G* I$ b/ z! }9 A
The 11-β hydroxylase deficiency may also result in
2 O8 b  ~1 I  C$ [) c, |" Q  texcessive adrenal androgen production, and rarely,
+ i# l0 _6 [. [- ~5 xan adrenal tumor may also cause adrenal androgen* Y' m0 C3 x/ ~( U) K  d; d
excess.1,3# H+ D- E- ]2 Y2 i$ ?! x+ `" g, @7 l' c
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! e  z) j0 [- Y& v1 R5 d
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007' i3 \7 V" r- G0 p% s  j4 }! c
A unique entity of male-limited gonadotropin-
! e4 q+ S) ~+ Gindependent precocious puberty, which is also known
, Z% M4 c7 D: d! Tas testotoxicosis, may cause precocious puberty at a7 R& e. ^. y( ]) n# M2 N
very young age. The physical findings in these boys
+ t4 \9 m+ s4 v6 Fwith this disorder are full pubertal development,
1 q3 s% V, u1 X7 }including bilateral testicular growth, similar to boys$ G6 K5 ~# z8 {8 `2 V# @
with CPP. The gonadotropin levels in this disorder
* ^! D7 `# R% C: n1 F  `1 nare suppressed to prepubertal levels and do not show+ R: n. v: X5 s& F5 L7 {# [
pubertal response of gonadotropin after gonadotropin-, L7 y6 U0 Z$ g  S9 J/ t+ c- I3 w/ ?
releasing hormone stimulation. This is a sex-linked
+ H7 ?5 ^! z& Q" M" jautosomal dominant disorder that affects only4 e% q  |9 K9 D  O3 j% O; q
males; therefore, other male members of the family5 Y8 X- ?5 R8 s% c
may have similar precocious puberty.3, }7 |! L7 f# o" K' K9 ~, _9 ^
In our patient, physical examination was incon-
; K- T! d2 c3 c9 ]; d+ Xsistent with true precocious puberty since his testi-6 q0 \5 N3 O0 Y* S7 F
cles were prepubertal in size. However, testotoxicosis
5 }8 v- s- \2 E* A; w' r2 ]1 l4 Gwas in the differential diagnosis because his father" `9 c! F* i4 J
started puberty somewhat early, and occasionally,
+ v% G& t: J: w( f: c. t0 l6 }' j; Vtesticular enlargement is not that evident in the
( \1 h4 ]; J5 l& w, hbeginning of this process.1 In the absence of a neg-
: k2 J9 F$ W0 A7 V" |$ o6 Aative initial history of androgen exposure, our* C7 G' j5 D9 U1 E% t& X, F8 q
biggest concern was virilizing adrenal hyperplasia,
+ U; m5 c6 p3 i& V% X/ G8 L+ N/ oeither 21-hydroxylase deficiency or 11-β hydroxylase
( S5 H8 t" w9 k. ydeficiency. Those diagnoses were excluded by find-
9 c1 C4 n! u. D- c+ L9 X; Y# V4 {ing the normal level of adrenal steroids.
9 y2 m9 k6 ?. LThe diagnosis of exogenous androgens was strongly
( v) d9 c, E0 C4 e! p, w0 Gsuspected in a follow-up visit after 4 months because. y' `/ A) s3 ^1 U
the physical examination revealed the complete disap-
" T6 s. L9 h3 S' ~+ u. spearance of pubic hair, normal growth velocity, and& J' B. S( t2 T$ |' q9 p' f
decreased erections. The father admitted using a testos-
% m* n; a( F" _3 n  s1 {% ~terone gel, which he concealed at first visit. He was* i, T$ D) }% U, X% f* w, u
using it rather frequently, twice a day. The Physicians’
2 w8 G9 e( D' D( t! |Desk Reference, or package insert of this product, gel or7 k; L9 O' k" w0 L8 h1 G: Q
cream, cautions about dermal testosterone transfer to  C% K+ A, U+ A7 U% n4 O8 P
unprotected females through direct skin exposure.
& C7 U) H0 C; J4 h# Q, |/ ^3 gSerum testosterone level was found to be 2 times the( |6 [7 n2 B7 l& A+ }& @; A8 H6 ^
baseline value in those females who were exposed to4 @: J0 J$ H% Y! ~5 z6 {
even 15 minutes of direct skin contact with their male
1 M2 y' N/ n# W7 tpartners.6 However, when a shirt covered the applica-
% R  W( t/ N* i/ Q! _& Ution site, this testosterone transfer was prevented.
2 i; h  L% {8 n8 H' o# W5 cOur patient’s testosterone level was 60 ng/mL,4 T  G2 f# n& K+ `
which was clearly high. Some studies suggest that/ ]$ m1 W7 h. w, m6 K% e
dermal conversion of testosterone to dihydrotestos-6 X2 z$ N- o. h3 R* B0 t  j  s, [
terone, which is a more potent metabolite, is more) T( i  l4 x, Z. y0 H) F4 b/ W
active in young children exposed to testosterone" F0 q* \" o% z. u$ P
exogenously7; however, we did not measure a dihy-
7 K- z: P) Z' S) C, l) s. W7 d2 ~: adrotestosterone level in our patient. In addition to
, w* ?% T" ^% f# U6 zvirilization, exposure to exogenous testosterone in1 t+ D, p% N2 |7 }9 q
children results in an increase in growth velocity and
3 T3 S0 i8 J) _! v, sadvanced bone age, as seen in our patient.
8 t& `. ~  L: WThe long-term effect of androgen exposure during0 V2 I7 C0 ?) {) j4 E4 s
early childhood on pubertal development and final) }3 K- c: K! u. \
adult height are not fully known and always remain
& g7 O5 d% X, A" |" f+ v; X; R) {a concern. Children treated with short-term testos-
$ P8 l" S+ p% m0 jterone injection or topical androgen may exhibit some; T* n0 u0 R: u4 ]
acceleration of the skeletal maturation; however, after' N7 p: K2 H9 q
cessation of treatment, the rate of bone maturation
5 D1 s; `; C# Fdecelerates and gradually returns to normal.8,9
: b7 w0 x/ d8 l, O) w* M0 E0 ~There are conflicting reports and controversy
, G# v! D* j3 k' T5 Q: Hover the effect of early androgen exposure on adult" b; u& F8 S7 ~' ^* `
penile length.10,11 Some reports suggest subnormal
0 z& k9 f: Z+ Y% w9 H- Eadult penile length, apparently because of downreg-
+ M9 \% k% f# T- nulation of androgen receptor number.10,12 However,
1 h2 ^7 ]( Y8 p/ NSutherland et al13 did not find a correlation between8 t' J! L, k; @
childhood testosterone exposure and reduced adult- U; H& `, M6 }  Y6 ^& k2 e! W
penile length in clinical studies.$ x6 V7 H9 Y# @( t
Nonetheless, we do not believe our patient is
% w, A' L) @6 s  M" K7 K; rgoing to experience any of the untoward effects from
. s4 w$ X- b) C* \) [testosterone exposure as mentioned earlier because
) ]6 w0 G7 \  P( Q) U6 H; _% Bthe exposure was not for a prolonged period of time.' r) ~+ z( }% A
Although the bone age was advanced at the time of
, s* l: V9 N( b& vdiagnosis, the child had a normal growth velocity at
# ]6 E8 [8 u$ `2 n  l( Athe follow-up visit. It is hoped that his final adult6 w" K0 g+ W) Y- D. x
height will not be affected.
9 c& A7 |, `, u8 {6 _3 }Although rarely reported, the widespread avail-
* o/ J7 F! A5 c  |9 G* ]& {ability of androgen products in our society may5 v; \: T& |+ s2 s) ~! }
indeed cause more virilization in male or female' J/ p' w2 j% t3 u
children than one would realize. Exposure to andro-$ P0 w: @9 V. j' i( |$ C$ d- N
gen products must be considered and specific ques-
# d; ]  Z( z" q- P+ R, J8 X% M( Y& ]tioning about the use of a testosterone product or! d+ O2 S6 B4 P3 d3 P5 I
gel should be asked of the family members during
; K7 _) t6 d0 e) vthe evaluation of any children who present with vir-
$ I2 F( \! B7 |2 `7 B  _ilization or peripheral precocious puberty. The diag-: Q% `; q! z1 w2 T/ f. Q
nosis can be established by just a few tests and by  t1 @0 l% Y- s0 y5 X3 D
appropriate history. The inability to obtain such a1 \; M; M: h' o
history, or failure to ask the specific questions, may
) u# Q% d; L( [1 cresult in extensive, unnecessary, and expensive
" w4 q6 Z% z% A& o' P( \* |investigation. The primary care physician should be
9 s% S9 W  p( q9 ]# paware of this fact, because most of these children( ?0 n5 M0 ?. y) U+ ^& t
may initially present in their practice. The Physicians’
, q) {1 l( v' B* LDesk Reference and package insert should also put a
! V9 M! T6 c" H  Y; k" l5 u. i; {warning about the virilizing effect on a male or9 d1 `) Q$ f# e) Q& A/ Q
female child who might come in contact with some-
- s( D* P  R) ]! Lone using any of these products.
" M: k9 p* G7 @6 n! BReferences
7 D1 A; g* E8 U% G& M1. Styne DM. The testes: disorder of sexual differentiation
  w4 o+ L. H/ \: Q5 _8 }! Land puberty in the male. In: Sperling MA, ed. Pediatric- K$ K$ `" W# W3 m9 K# H/ R' ^+ A1 C
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
: L, u0 T1 l& B- |" x% m2002: 565-628.
8 e4 M0 y9 W- u* |- H2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
' M0 `% N7 k) ^1 E% @& q) b& Epuberty 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
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

1 A! n+ c" y1 M5 f& l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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