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Sexual Precocity in a 16-Month-Old
( g8 s: p  t  Y/ V+ r5 F* pBoy Induced by Indirect Topical' i# M" `, C- K* O
Exposure to Testosterone
# M, X1 W% _* n; MSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,26 n, N( N4 x. y7 f4 ^) ]+ ~
and Kenneth R. Rettig, MD15 }7 d6 T- L- J5 t8 V
Clinical Pediatrics, w) k% C( }/ d# o- i- c/ e. Q
Volume 46 Number 6+ N* P" q; n2 N7 @9 s* l3 N
July 2007 540-543
* n1 i# }) K/ d9 X© 2007 Sage Publications
( n! U! i' m- d! y6 V5 i10.1177/0009922806296651
7 G, ~. |& K1 i# Z& x9 `4 I' \http://clp.sagepub.com3 ]8 F3 H: y+ _9 F2 i- P# t0 g( K
hosted at
/ z( x# D4 }- p5 z- bhttp://online.sagepub.com
$ V+ Q, Z7 r$ C; R. {1 {; B/ J0 P' _5 EPrecocious puberty in boys, central or peripheral,
# m% V' D; a  n( m6 b4 Xis a significant concern for physicians. Central
4 Q8 T0 M8 G0 C( S; xprecocious puberty (CPP), which is mediated
$ r9 b1 P5 |6 K, z6 A0 J1 w& Z2 b1 |. Hthrough the hypothalamic pituitary gonadal axis, has
$ [5 m0 r& I/ x4 Va higher incidence of organic central nervous system: @* W$ [$ z# n& z/ C
lesions in boys.1,2 Virilization in boys, as manifested; s/ }8 G/ U' H9 {1 H( U
by enlargement of the penis, development of pubic
5 a, l) A3 E  w" g$ |! ihair, and facial acne without enlargement of testi-5 f/ X8 F% E1 t; z3 z( [2 T
cles, suggests peripheral or pseudopuberty.1-3 We
  T( |7 @, W! Y% {( ^report a 16-month-old boy who presented with the% R# l8 f) C  H% X
enlargement of the phallus and pubic hair develop-/ Y1 j: ~2 O. p  v) r
ment without testicular enlargement, which was due
3 T; G& E  K' P4 T2 |+ q2 Tto the unintentional exposure to androgen gel used by+ u1 J+ d1 T+ A0 I$ x6 a* W
the father. The family initially concealed this infor-/ b1 c9 i3 `9 |' _
mation, resulting in an extensive work-up for this
$ h$ Z! [5 G; b% h+ @child. Given the widespread and easy availability of" T1 ~* w- ]3 u! M0 D8 p& E
testosterone gel and cream, we believe this is proba-, o" {) c  V6 b' H- i& S0 |8 R
bly more common than the rare case report in the# @( b# @3 f- Q, t% b! p
literature.4
$ i$ H5 X/ ]6 HPatient Report' w& x# ]$ g4 [5 M
A 16-month-old white child was referred to the8 M0 Y1 `$ i- y9 u  F* p3 Q6 j
endocrine clinic by his pediatrician with the concern5 q0 o6 a# w3 T
of early sexual development. His mother noticed
4 M' C" i% G2 ^: vlight colored pubic hair development when he was
) G: V/ d% @  JFrom the 1Division of Pediatric Endocrinology, 2University of' x, ~# E" [( J) A2 w
South Alabama Medical Center, Mobile, Alabama.- V2 n3 w; }/ p. m6 Z5 T
Address correspondence to: Samar K. Bhowmick, MD, FACE,
* R# z: _. Q9 E- }/ XProfessor of Pediatrics, University of South Alabama, College of! u6 `" z4 R: o
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;9 X9 @# d; V8 Z/ X. R) F7 C
e-mail: [email protected].
' ?# `; ^1 s: ?9 x  @about 6 to 7 months old, which progressively became5 [! I5 n9 M) `! y
darker. She was also concerned about the enlarge-( V7 [, R8 f2 B8 k& N& P) {3 t
ment of his penis and frequent erections. The child
* t5 t4 S* F3 `3 ^/ O/ C* C0 r* u/ Wwas the product of a full-term normal delivery, with
5 H) i6 G) ^! P5 j7 ia birth weight of 7 lb 14 oz, and birth length of- |( v5 }7 Y" f0 A2 @6 p& `4 \: u
20 inches. He was breast-fed throughout the first year9 |/ J  n' L" }3 o4 B7 y( b2 Z( G
of life and was still receiving breast milk along with. }7 p* q8 {  R: J1 ]0 K1 z' T
solid food. He had no hospitalizations or surgery,
7 X2 d) A$ A2 qand his psychosocial and psychomotor development
) q  h$ A' l, V2 A+ wwas age appropriate.  \6 M, Z: j+ L; x/ }" j
The family history was remarkable for the father,
: W) ^2 Y0 n1 ?6 o  c8 d; Fwho was diagnosed with hypothyroidism at age 16,
( y6 F+ }( X& Q" f+ Xwhich was treated with thyroxine. The father’s1 O% W. [. ]5 P1 L1 B9 d
height was 6 feet, and he went through a somewhat; q: O- _: V( P
early puberty and had stopped growing by age 14.; I/ L! l1 m( b* P1 ^- W9 b. V
The father denied taking any other medication. The: d! E+ S6 p8 s& t; s. w
child’s mother was in good health. Her menarche' m$ v" x0 Y' Z' j7 w- F5 {
was at 11 years of age, and her height was at 5 feet
, D4 ?& ^9 b! v9 n7 B; G) J5 inches. There was no other family history of pre-
' p( {8 T. F% D* h: i( v" qcocious sexual development in the first-degree rela-
0 [' L; _, B& F( Ntives. There were no siblings.
) I- M: z$ D; s: E* g" T8 sPhysical Examination) U* K% y; C, z9 B7 l
The physical examination revealed a very active,
! X2 L, R2 z# ^1 M' D- U+ K3 Fplayful, and healthy boy. The vital signs documented
, y) |2 n( H# ?% ^) V# J" H9 b! ra blood pressure of 85/50 mm Hg, his length was& B1 I' o4 |" N
90 cm (>97th percentile), and his weight was 14.4 kg& ~7 M/ P& r  P1 ^
(also >97th percentile). The observed yearly growth* j" M" O$ k! S, Y/ D+ I6 {) P
velocity was 30 cm (12 inches). The examination of
. H8 i+ |0 D8 k/ B1 lthe neck revealed no thyroid enlargement.
* o& I& j; _- }The genitourinary examination was remarkable for
$ J5 p6 t* h' i# N, e( O7 t& l! Oenlargement of the penis, with a stretched length of6 M+ g# ~4 W0 |$ i4 ]; R  u
8 cm and a width of 2 cm. The glans penis was very well
' Z) K3 a; O4 V; zdeveloped. The pubic hair was Tanner II, mostly around9 q3 K/ n! r" ?: A) I8 u5 @2 I1 j1 e  z) v
540
) B2 t7 K% k. C; Rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 g+ R& ~7 x8 L/ g+ T$ Vthe base of the phallus and was dark and curled. The  M$ G+ B- L- \0 E6 D3 Q  ~
testicular volume was prepubertal at 2 mL each.+ l# ^# A% e# ]6 @, y/ H. h
The skin was moist and smooth and somewhat% {' ?) u4 K8 z" f1 A3 e  i% G
oily. No axillary hair was noted. There were no6 w9 c! o1 L2 G7 \9 J1 T- ]
abnormal skin pigmentations or café-au-lait spots.* b$ m% e, E" [
Neurologic evaluation showed deep tendon reflex 2+
# m- L. }5 r9 P7 v. p9 i0 Pbilateral and symmetrical. There was no suggestion
8 v4 t8 ?* z7 Z1 I! m5 A% P3 `of papilledema.# Q  P$ J8 t  M1 M' ^9 q4 [
Laboratory Evaluation
$ L! N' b; M5 |; J! y$ u1 {The bone age was consistent with 28 months by
- L. S; }! W: n% Vusing the standard of Greulich and Pyle at a chrono-! e% ~3 U1 b' A
logic age of 16 months (advanced).5 Chromosomal+ v. E" T$ h8 V! L8 b6 v
karyotype was 46XY. The thyroid function test
  z! O# O4 i( q4 oshowed a free T4 of 1.69 ng/dL, and thyroid stimu-' F6 u2 c5 v: s* ]
lating hormone level was 1.3 µIU/mL (both normal).
4 f+ O, m. c0 P1 ZThe concentrations of serum electrolytes, blood
  |" i7 ?: e5 n" t  i/ G4 ?# @8 yurea nitrogen, creatinine, and calcium all were
( e- w6 c' C- `3 M. y. ywithin normal range for his age. The concentration" I; Q" H+ l: [2 B) v& @% [
of serum 17-hydroxyprogesterone was 16 ng/dL$ n" C! E* P. Q. ^  P; j5 a
(normal, 3 to 90 ng/dL), androstenedione was 209 H+ D2 D1 t& c' |5 e/ {+ m
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-4 r' I; a# Q3 W- |7 ^" D. ^* Q5 H
terone was 38 ng/dL (normal, 50 to 760 ng/dL),5 o& m7 m0 f% q- X3 z$ g9 B" D
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
  ~7 w9 @8 W% j" ]' s49ng/dL), 11-desoxycortisol (specific compound S)
0 `& V! J/ w& I% wwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-2 [* h5 m* l+ Q+ d( \' X
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
. Z  `! H: }6 Y8 S( Htestosterone was 60 ng/dL (normal <3 to 10 ng/dL),1 Z2 c* N& s( S7 g! k1 v
and β-human chorionic gonadotropin was less than% T: b& A9 j& `5 K/ J
5 mIU/mL (normal <5 mIU/mL). Serum follicular  I, u+ t/ F5 n2 e7 D* S1 m+ J5 k
stimulating hormone and leuteinizing hormone1 ]: U% S/ j# T8 K  c' |1 y: m
concentrations were less than 0.05 mIU/mL
( z& n  ?0 a& N. ^$ }(prepubertal).
1 X4 Q, k  ]6 TThe parents were notified about the laboratory4 V+ U1 L8 ?7 I& I) K& \
results and were informed that all of the tests were7 y" Z8 X. x2 f0 @" Q3 J
normal except the testosterone level was high. The' m; x: N7 o: I1 C
follow-up visit was arranged within a few weeks to/ u1 q0 c- h* q% s; B  m
obtain testicular and abdominal sonograms; how-
# l6 \) k2 g% e. P0 q+ o# A) C0 s& Vever, the family did not return for 4 months.: ^$ Y) t' p; Q' o4 @9 m6 D9 D7 A
Physical examination at this time revealed that the4 q4 J; A7 e8 q) W
child had grown 2.5 cm in 4 months and had gained) E; a; K5 [' P. u  {
2 kg of weight. Physical examination remained( q5 x9 P* e3 I+ Q: _$ U- I7 W
unchanged. Surprisingly, the pubic hair almost com-
  o/ j% F; B3 g; _pletely disappeared except for a few vellous hairs at
- n. A% [4 m7 i- @the base of the phallus. Testicular volume was still 2! j4 `. N' T" n2 l6 L* q/ l5 `
mL, and the size of the penis remained unchanged., T# u% n! m8 W
The mother also said that the boy was no longer hav-& W$ B% ?( {( C2 t* Q. n
ing frequent erections.# i. Y( L* U, ]! y
Both parents were again questioned about use of
; T, R* C/ w( v! p/ x& ~9 pany ointment/creams that they may have applied to( \9 l6 F2 C4 t) F& Z; k) ^" N
the child’s skin. This time the father admitted the0 f) {% {0 C, ~6 K
Topical Testosterone Exposure / Bhowmick et al 541
5 e$ C+ {1 D2 R8 uuse of testosterone gel twice daily that he was apply-
  d" u& z3 l+ G) A3 R# hing over his own shoulders, chest, and back area for
) ]; |/ v) n0 b8 x' B0 B2 C8 n+ Ca year. The father also revealed he was embarrassed
* g# V: W, C- t# Nto disclose that he was using a testosterone gel pre-
7 Z( w/ q9 |) w# N- x5 Dscribed by his family physician for decreased libido. C1 y6 N- k! m( E" W, ?
secondary to depression.; i9 {, w4 |9 @& U
The child slept in the same bed with parents.
+ ^0 p" D% A' G% @The father would hug the baby and hold him on his
4 s! G/ K8 a6 u' D- ]1 L0 p0 lchest for a considerable period of time, causing sig-
& |# V# Y. t1 ?nificant bare skin contact between baby and father.
2 H: {* v# S& p7 O; AThe father also admitted that after the phone call,
3 ~4 p" x, {9 {; p2 Twhen he learned the testosterone level in the baby
6 |, ?' K% J2 D8 H9 l& F& K4 Ywas high, he then read the product information
/ h! m6 N" p$ J$ ipacket and concluded that it was most likely the rea-
# `7 l* r) d0 |& C- qson for the child’s virilization. At that time, they; z6 K" O9 j, L7 `0 @
decided to put the baby in a separate bed, and the$ ?' P5 ~8 y  y& M
father was not hugging him with bare skin and had: j& ^. `6 d* ?/ b9 r$ K. l) B! F
been using protective clothing. A repeat testosterone1 M7 m, }- F! N( C: d! r% ?2 @
test was ordered, but the family did not go to the
7 e% L, E2 Y. {# g+ q3 D- jlaboratory to obtain the test.% h1 T0 s9 D# `
Discussion& D8 R: M( i) J
Precocious puberty in boys is defined as secondary% E4 s0 y( I8 E, A  {! |/ {
sexual development before 9 years of age.1,4+ s. P; O$ ?7 A6 `8 E3 d
Precocious puberty is termed as central (true) when
) W9 `$ S. H3 F) H+ {* M% f$ vit is caused by the premature activation of hypo-' v& f: D, W9 d- A6 S
thalamic pituitary gonadal axis. CPP is more com-+ V# f" p0 q* A6 c! v  V( H
mon in girls than in boys.1,3 Most boys with CPP
$ f* g, `0 L# Bmay have a central nervous system lesion that is/ E9 ~9 \4 G3 r' C# d$ `& |
responsible for the early activation of the hypothal-
$ J, i* i. h1 l; Z* B+ u( hamic pituitary gonadal axis.1-3 Thus, greater empha-
: \+ K! q' B' a5 I* `. f0 psis has been given to neuroradiologic imaging in! B  E; s: ?: q8 N# F/ e* H% l9 L+ v
boys with precocious puberty. In addition to viril-9 N# y. m  R2 C9 M4 v/ ^' |$ j) b) L
ization, the clinical hallmark of CPP is the symmet-$ n/ w/ J+ i& |& q: I7 I# p
rical testicular growth secondary to stimulation by
6 }9 v2 ^. |1 b) x0 i/ L& sgonadotropins.1,3
1 H) M/ I5 M2 B' K$ rGonadotropin-independent peripheral preco-5 X0 V5 g1 t+ w+ J
cious puberty in boys also results from inappropriate6 R% g( }3 Z! k
androgenic stimulation from either endogenous or) _: [6 k/ _, a) M/ a/ Q
exogenous sources, nonpituitary gonadotropin stim-( P, ~$ U+ M) D. T; @
ulation, and rare activating mutations.3 Virilizing2 A5 \  ^) ^% Q( x
congenital adrenal hyperplasia producing excessive7 t8 m$ a# T3 D4 B- m$ s" N
adrenal androgens is a common cause of precocious, D2 f: y. c/ h
puberty in boys.3,47 S8 b+ J6 Z& r
The most common form of congenital adrenal1 K! _) l: J/ ?4 }7 v( f
hyperplasia is the 21-hydroxylase enzyme deficiency.
7 h3 ]1 S) U2 ~) U. Q: L$ {The 11-β hydroxylase deficiency may also result in; @' `* [' C* l: A8 u/ R& w2 u
excessive adrenal androgen production, and rarely,7 S7 T' L5 }+ e; e. l
an adrenal tumor may also cause adrenal androgen: C2 J9 ]- O' d) z4 [1 B! K
excess.1,3
  }! C4 N4 x1 F4 ^8 ]3 lat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 {/ O! v( u) K2 _, T
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007. z6 b- j+ x* i* Y( R
A unique entity of male-limited gonadotropin-
/ J' J: E& n. Y6 t+ F+ X+ Kindependent precocious puberty, which is also known8 K- o" n( g4 s/ c+ u" P# Y
as testotoxicosis, may cause precocious puberty at a- h/ ~9 H+ c) n! u5 `
very young age. The physical findings in these boys
9 x) m' T; c# S0 m4 twith this disorder are full pubertal development,
! w. H4 m2 g$ D9 Y: l' r0 ^4 sincluding bilateral testicular growth, similar to boys# B; Y: r1 `+ k
with CPP. The gonadotropin levels in this disorder; J# i& Y) N$ e. f8 b& }
are suppressed to prepubertal levels and do not show
6 t; Q& ]0 G7 a- p& F4 B4 Cpubertal response of gonadotropin after gonadotropin-
4 n& x2 }  b1 }1 W& z4 N  }& Wreleasing hormone stimulation. This is a sex-linked
1 f8 n1 h5 w+ F/ a4 Y  q8 Q3 P, gautosomal dominant disorder that affects only6 ^! r8 g  ^4 ~: L( `8 r1 R7 T
males; therefore, other male members of the family
& O  R# ]( ]9 v; y! Omay have similar precocious puberty.3' w! w* ]1 f; i( i1 E
In our patient, physical examination was incon-
, l+ P; D9 o8 [, |2 }% Vsistent with true precocious puberty since his testi-5 E# e$ r3 _9 E4 y
cles were prepubertal in size. However, testotoxicosis6 t! ^- S5 b7 M# ]6 D) d+ g7 q
was in the differential diagnosis because his father
$ K" ^( E, W3 l! [started puberty somewhat early, and occasionally,9 S4 ]$ Z  H2 s
testicular enlargement is not that evident in the' }2 {7 U' @+ ]" n8 j+ U* w
beginning of this process.1 In the absence of a neg-
- D9 {9 f. B6 ]+ t# Qative initial history of androgen exposure, our. H4 A. K1 W, g9 ~
biggest concern was virilizing adrenal hyperplasia,
, z& G; f! l) z- f" N! x# Meither 21-hydroxylase deficiency or 11-β hydroxylase: l+ r+ B+ J* ]6 ?+ Y/ v# p
deficiency. Those diagnoses were excluded by find-
) E. ]; q4 ]1 oing the normal level of adrenal steroids.
1 O$ f. ?0 L. I6 lThe diagnosis of exogenous androgens was strongly6 _$ O0 r0 H! O: n# B' V
suspected in a follow-up visit after 4 months because
; |2 p) r2 Y" a, |  p6 j4 I- i  z2 ~the physical examination revealed the complete disap-
, s! ]7 }3 o% W# Xpearance of pubic hair, normal growth velocity, and3 @! z! ^2 ?6 s
decreased erections. The father admitted using a testos-) `1 |" R2 u$ R5 o. Y
terone gel, which he concealed at first visit. He was2 s* o: x- L& ], d! b
using it rather frequently, twice a day. The Physicians’9 z( f( m; b' c9 X) q
Desk Reference, or package insert of this product, gel or0 a% G& p5 A( X# I0 m
cream, cautions about dermal testosterone transfer to; A  D: w7 E( u: \; ]/ m
unprotected females through direct skin exposure.
9 q: H" s( a. m! w! t1 O( sSerum testosterone level was found to be 2 times the4 i  |9 R0 y6 W6 {5 t) d3 M( i
baseline value in those females who were exposed to5 X; o; h9 Q) {  x8 Q  F
even 15 minutes of direct skin contact with their male
+ }- |  r1 C$ J7 r& v* b, tpartners.6 However, when a shirt covered the applica-1 b  K! v: M: i# o
tion site, this testosterone transfer was prevented.# @  s. A8 G, B& r. v1 f; x
Our patient’s testosterone level was 60 ng/mL,
/ J" a* t# Y/ w: Vwhich was clearly high. Some studies suggest that& x: G4 D( s8 c) S8 ?
dermal conversion of testosterone to dihydrotestos-
1 ^. h) F' D& B; Z- Lterone, which is a more potent metabolite, is more7 I. f! F# V( Z. y4 l' t( v! ]4 M
active in young children exposed to testosterone& M9 R7 T* {# p: W" c& B
exogenously7; however, we did not measure a dihy-% O  V) n. Q% t/ f2 T% \
drotestosterone level in our patient. In addition to
5 F5 L; @, s) d$ p0 t* Pvirilization, exposure to exogenous testosterone in8 N, P) I$ }3 h3 F
children results in an increase in growth velocity and
  t- K/ o# }2 radvanced bone age, as seen in our patient.
  N6 m- A+ a% L; n6 SThe long-term effect of androgen exposure during! g; \& O# E$ {/ v  X
early childhood on pubertal development and final8 x$ z* _; _) a) |' G
adult height are not fully known and always remain  T3 G# h) _! B2 [/ {6 Y3 p
a concern. Children treated with short-term testos-
( P2 [' l. P( X4 p# gterone injection or topical androgen may exhibit some6 ?" ^! M- Q. Q. W# F9 t
acceleration of the skeletal maturation; however, after/ f  [! \1 T6 W! C, M
cessation of treatment, the rate of bone maturation% G3 W3 A( s# U- C5 ?4 T
decelerates and gradually returns to normal.8,9
2 _& Z! o/ ?! q) j5 a% @There are conflicting reports and controversy
* W! }2 E& c- V  z2 U* [$ V- O8 Iover the effect of early androgen exposure on adult
7 C) [1 s& ^, P6 o$ d; vpenile length.10,11 Some reports suggest subnormal6 m. X$ p9 D& K& v  ^2 w) t( g4 S# x
adult penile length, apparently because of downreg-
# h: c. G' P5 V5 D/ nulation of androgen receptor number.10,12 However,
4 A/ c, q. G# w' R- w  X) z: QSutherland et al13 did not find a correlation between0 o/ I) @0 g2 M2 q9 E
childhood testosterone exposure and reduced adult: a9 ]+ w% D/ [$ {' E- a
penile length in clinical studies.
; s8 K3 n7 b$ t1 K2 a% V0 wNonetheless, we do not believe our patient is2 u; r( o/ c+ K3 b2 y/ M/ l) P% G' a2 O
going to experience any of the untoward effects from
" ]' p& q% n$ btestosterone exposure as mentioned earlier because  a$ Q1 ~0 v4 `
the exposure was not for a prolonged period of time.
' X: q6 H2 S5 \Although the bone age was advanced at the time of" B) o% ]6 S3 K1 r' h; u( x
diagnosis, the child had a normal growth velocity at# J. A9 u6 j2 V+ W6 {
the follow-up visit. It is hoped that his final adult3 j$ X- z& ?# g$ h% \
height will not be affected.
3 f# L0 m  A/ m# t: a/ e5 ~Although rarely reported, the widespread avail-1 \% e. f# a  O
ability of androgen products in our society may
* \/ d" W7 ~  f! h+ }; {indeed cause more virilization in male or female
! K7 E" _- l  W+ z  `children than one would realize. Exposure to andro-
6 ?. U  P! b1 o5 }3 Ggen products must be considered and specific ques-
7 B6 J+ \. b" ?3 I; Stioning about the use of a testosterone product or" M. j8 J1 Y# H/ C
gel should be asked of the family members during8 r$ t' _( D" B3 l8 k1 h4 F
the evaluation of any children who present with vir-& ]9 b; V% u4 v# A  I& A* C
ilization or peripheral precocious puberty. The diag-
& I! [' O# @8 q0 @) qnosis can be established by just a few tests and by
1 y$ ~3 {( d" u, M% C) ?' ~appropriate history. The inability to obtain such a
! G; d1 E# t* t0 [. j3 J# n, ghistory, or failure to ask the specific questions, may
3 E1 q+ i& X. a0 l  rresult in extensive, unnecessary, and expensive
1 o4 |8 h% a9 i& Vinvestigation. The primary care physician should be% `# e: x3 X: S  [  \( ~
aware of this fact, because most of these children! [0 s* E5 f3 K5 q2 u
may initially present in their practice. The Physicians’
8 w! O5 O% M; m/ M4 }" Q, Z/ k' UDesk Reference and package insert should also put a
. _% h: `% h! L& F! o. Zwarning about the virilizing effect on a male or
0 Z( U' s. Q' u) N0 Afemale child who might come in contact with some-. a/ x9 L1 f" R' [. D- c' H+ ?
one using any of these products.
1 w% Y7 D) M$ {References& y  K0 ^4 O( D9 `& z3 l
1. Styne DM. The testes: disorder of sexual differentiation, z) k0 S% U: F2 }3 N8 R7 M1 g
and puberty in the male. In: Sperling MA, ed. Pediatric
, `. V; ?& s" m, E0 [, ]Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
: R# c$ o$ J: `6 W, J1 ?2002: 565-628.( x# I2 O2 P6 F, W6 \( Y3 w
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious2 |2 _% h& ^0 ]
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old, n' o, T, W1 T1 s
Boy Induced by Indirect Topical
1 P, l5 h: {# B# t" M. t; ?% OExposure to Testosterone, ]  U9 \+ m3 z7 ?$ s
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,23 H6 G! ]) U& _/ P' X
and Kenneth R. Rettig, MD1
% I, \+ V$ X/ f8 I7 aClinical Pediatrics' x; E# z* i1 e) S9 S* h" I/ i
Volume 46 Number 6
4 Y; d  {# v/ m% u; o/ oJuly 2007 540-543: u3 Q# c1 n8 X  H# \
© 2007 Sage Publications
. L) J* ?. ?& a( w- n10.1177/00099228062966515 [8 V" l/ V4 F& n( e3 V9 m2 K
http://clp.sagepub.com
7 C+ }$ _" c/ }& Z" }/ ehosted at& D7 [- z# g9 ~9 Y1 s7 o2 A
http://online.sagepub.com5 Q. Z7 U$ T/ u$ C. Y; e8 @
Precocious puberty in boys, central or peripheral,6 w  b( N1 o$ a( Q: T$ }9 G* d
is a significant concern for physicians. Central
# J: Q% g% R3 z% o/ w2 \precocious puberty (CPP), which is mediated
$ A9 |8 M* p  B; H6 [, B; ?  Vthrough the hypothalamic pituitary gonadal axis, has# ?5 T! X5 L) u' Y8 g8 h
a higher incidence of organic central nervous system
3 z) V/ W" s1 p. ~0 T7 G' S; glesions in boys.1,2 Virilization in boys, as manifested
! @& s$ t. t, V6 N9 Q3 Pby enlargement of the penis, development of pubic
$ D! ~8 ~4 [3 Vhair, and facial acne without enlargement of testi-; @0 [. M% K1 s# C
cles, suggests peripheral or pseudopuberty.1-3 We
* D$ U7 j  c; y* z4 ~" K' x1 }2 Lreport a 16-month-old boy who presented with the
9 U$ [" V5 \9 Eenlargement of the phallus and pubic hair develop-& }7 ]6 X7 N+ E' D6 R
ment without testicular enlargement, which was due
8 X7 K) K6 _) Y# }to the unintentional exposure to androgen gel used by
0 ?0 p: z4 q$ n6 }$ e) fthe father. The family initially concealed this infor-% |& q; E/ s* L* Z8 v
mation, resulting in an extensive work-up for this
, q. C! q, S1 b! y* Kchild. Given the widespread and easy availability of6 I9 D% O. v: u( e( B" }2 d
testosterone gel and cream, we believe this is proba-
3 O! N+ ~6 R1 f& g- lbly more common than the rare case report in the8 ]& K- T5 E$ c
literature.4
$ B3 G7 u- G' s7 \/ s- D. O4 EPatient Report! j8 u4 @# k- @7 u* w" R# k- o1 X
A 16-month-old white child was referred to the
, p! p# w0 `1 @) e$ A2 Nendocrine clinic by his pediatrician with the concern. z8 |1 A/ B# n( \1 X% P0 r
of early sexual development. His mother noticed; T- ^& Z& {) u2 {+ R, R$ U
light colored pubic hair development when he was
$ t! |9 x# y/ e' OFrom the 1Division of Pediatric Endocrinology, 2University of# U4 a* ]" @4 J' {& q# ?6 x+ q! `
South Alabama Medical Center, Mobile, Alabama.9 \8 \- |" e# g# K
Address correspondence to: Samar K. Bhowmick, MD, FACE,$ v3 z! Z% ?: f9 h
Professor of Pediatrics, University of South Alabama, College of
6 }# D3 p5 r- F& d+ @Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;+ s2 e- E4 B- @: p1 G
e-mail: [email protected].8 O- K1 W8 w  L$ Q# L3 z
about 6 to 7 months old, which progressively became
& r* `5 p5 D6 w1 i, R$ S0 jdarker. She was also concerned about the enlarge-
9 p& p+ t: `& m- T3 E! `$ N& wment of his penis and frequent erections. The child- I4 d2 p; t' m) R7 v# }
was the product of a full-term normal delivery, with
5 T6 i" O# q( b0 I' @. v. r: Ca birth weight of 7 lb 14 oz, and birth length of
/ z( V( J- w6 e$ Z20 inches. He was breast-fed throughout the first year  ]% A  j7 k- [3 l6 h- \! J
of life and was still receiving breast milk along with) {0 l; s0 C2 C7 C! C' F. ~8 f
solid food. He had no hospitalizations or surgery,# |$ f# t; n4 L
and his psychosocial and psychomotor development
9 W1 k3 ]$ _8 F2 v# a, ewas age appropriate.. L9 F- @1 b# Y6 |$ H* q
The family history was remarkable for the father,4 ]3 ~/ `3 g. H" ~
who was diagnosed with hypothyroidism at age 16,
' x; h1 b3 ?9 B: gwhich was treated with thyroxine. The father’s8 X- o1 M+ |% m5 i  p1 m! F
height was 6 feet, and he went through a somewhat, W9 @* h" [2 m6 T% h
early puberty and had stopped growing by age 14./ j5 T* B. X0 M! ~7 h1 M4 O# i# u
The father denied taking any other medication. The
  W5 {  R0 C) T8 k! i" }0 cchild’s mother was in good health. Her menarche& h9 C4 o. ?0 V& P
was at 11 years of age, and her height was at 5 feet
: i# j; W8 x+ m5 inches. There was no other family history of pre-
( \4 G5 h* i( t( `  V- Jcocious sexual development in the first-degree rela-2 D& Q* Z+ r& M1 x1 j
tives. There were no siblings.
( ^2 c" L3 }3 y" O' APhysical Examination' D$ U. X2 E& H# e  T  F1 d% r
The physical examination revealed a very active,5 E* s% H4 X. K" D  ~3 a
playful, and healthy boy. The vital signs documented) j+ h5 C0 @. ~; j9 Q
a blood pressure of 85/50 mm Hg, his length was
( q/ L+ A1 z5 X! L; _& S8 @0 t1 O: X90 cm (>97th percentile), and his weight was 14.4 kg
$ q! @/ S# u4 Q(also >97th percentile). The observed yearly growth% I. ~1 a* C; R" e: G
velocity was 30 cm (12 inches). The examination of
2 R+ Z% |- x' |% E# r" ~$ _( w3 A+ Nthe neck revealed no thyroid enlargement.
6 u, X) a8 c5 pThe genitourinary examination was remarkable for: o- C  b( W) {
enlargement of the penis, with a stretched length of
2 v" m1 a0 M$ b6 d8 cm and a width of 2 cm. The glans penis was very well4 O* Z' k! H0 Y5 t/ H8 E7 i
developed. The pubic hair was Tanner II, mostly around- C/ S& N" w0 p9 b1 f
540
3 D5 ]( X6 ?6 [0 O9 Oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" H. h! B$ C/ ]5 ?) U# C; ythe base of the phallus and was dark and curled. The
7 R! ^( k0 ^, q; h& dtesticular volume was prepubertal at 2 mL each.9 o; ]& T% M; O& e2 l1 Y
The skin was moist and smooth and somewhat- W6 [; y5 c4 ^6 K
oily. No axillary hair was noted. There were no
* _5 m& J+ t% Jabnormal skin pigmentations or café-au-lait spots.
0 j; l) o4 L5 `/ W+ c* p2 dNeurologic evaluation showed deep tendon reflex 2+2 M1 V$ y6 v6 `7 H! l
bilateral and symmetrical. There was no suggestion- f1 R) n0 P  n; W1 ~- a4 q$ T
of papilledema.6 L4 ?) J  \# V3 L3 F
Laboratory Evaluation5 f) J8 D8 m& |/ U& L" n
The bone age was consistent with 28 months by- _$ s* B' ^* O& ~' }& ]
using the standard of Greulich and Pyle at a chrono-+ l8 I8 \& _, U0 J5 \; @, o- I: B" w
logic age of 16 months (advanced).5 Chromosomal2 Q0 t7 T3 Z  H  b7 U' K2 v7 Q
karyotype was 46XY. The thyroid function test3 R5 s& o! r; b) ^8 u
showed a free T4 of 1.69 ng/dL, and thyroid stimu-9 N$ W" ^- w' z* c" h9 h. \, {
lating hormone level was 1.3 µIU/mL (both normal).
% d( g, t! P, b, [* h% c8 ?The concentrations of serum electrolytes, blood& Z7 f5 ]& H% H6 ?# c
urea nitrogen, creatinine, and calcium all were& e/ M) [/ k9 Y$ o
within normal range for his age. The concentration
. o/ P- W: m, J) H. yof serum 17-hydroxyprogesterone was 16 ng/dL' c' ?# x5 l# K3 R6 b- q( v
(normal, 3 to 90 ng/dL), androstenedione was 20
5 O- h2 ]) M! p5 t& ]ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
7 m% L8 J0 j# {( L$ s) u8 yterone was 38 ng/dL (normal, 50 to 760 ng/dL),
6 L: T8 C7 l* j. hdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
: y+ I% o5 l5 z. d6 H( ]3 i' v: q49ng/dL), 11-desoxycortisol (specific compound S)
1 O6 I; v* q% Q0 Z- k; kwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-( P% \7 o1 I( t" b) r
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total, |4 B$ t9 z4 g2 r% W6 v- [7 t  ~
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),% `1 e4 C. E1 Y
and β-human chorionic gonadotropin was less than6 ]: t4 Q& Z: ~' k( C
5 mIU/mL (normal <5 mIU/mL). Serum follicular
& D9 Z* z- \" m4 e( K; |stimulating hormone and leuteinizing hormone. M# r% r" k0 [& {2 w
concentrations were less than 0.05 mIU/mL# k+ K, J3 t# R# n
(prepubertal).6 ^- _9 v* c; [$ q
The parents were notified about the laboratory
$ H+ q0 p9 t: S) V+ I6 Wresults and were informed that all of the tests were- z7 ]- O9 F9 t& ^" N3 `& F
normal except the testosterone level was high. The
. H8 l$ @$ p) U+ v! b% n6 nfollow-up visit was arranged within a few weeks to: B/ C0 t4 C/ t+ I
obtain testicular and abdominal sonograms; how-
* ^2 k1 ~) x* I' O' G: Qever, the family did not return for 4 months.: g: B  ]" x! N+ C
Physical examination at this time revealed that the
1 N! ]9 [; r+ z! C: B  z3 Nchild had grown 2.5 cm in 4 months and had gained% D* b* Z& x5 Z* W! _
2 kg of weight. Physical examination remained. D% u6 r1 O$ P/ y
unchanged. Surprisingly, the pubic hair almost com-/ x$ b7 A! n. ?6 K
pletely disappeared except for a few vellous hairs at
& l  U% v1 {' L# C$ Kthe base of the phallus. Testicular volume was still 2
+ S- I1 m6 z4 P0 m4 L& PmL, and the size of the penis remained unchanged.
# D9 G; t& v4 F$ AThe mother also said that the boy was no longer hav-) v# H$ W2 y6 v9 o
ing frequent erections.
  d: U+ X2 B" x' B8 J! w. }Both parents were again questioned about use of; N3 b9 |, ^; U
any ointment/creams that they may have applied to
/ x* z) H# V; Sthe child’s skin. This time the father admitted the
2 x5 s5 Y! a& _7 W. t; f/ UTopical Testosterone Exposure / Bhowmick et al 541
) r1 D$ t: J7 [5 _$ Y$ P' ruse of testosterone gel twice daily that he was apply-  M3 E: N/ K$ a) i
ing over his own shoulders, chest, and back area for# i+ b. L9 h9 Q0 l) X, r, F4 l
a year. The father also revealed he was embarrassed
& R1 ]% a) h" K) rto disclose that he was using a testosterone gel pre-/ k% L) s! Y2 F0 @. n" h
scribed by his family physician for decreased libido
* ?. ^2 ?; T6 A7 D+ n# lsecondary to depression.
* V! s% v9 H5 b0 z6 L) UThe child slept in the same bed with parents.
5 {+ G7 R9 Z1 {4 LThe father would hug the baby and hold him on his. ]* G5 [) r3 o* S
chest for a considerable period of time, causing sig-
' T3 O* p) p* x# Y) x# c3 Unificant bare skin contact between baby and father.+ B- ]' e+ q$ O& I1 H6 x
The father also admitted that after the phone call,
) p1 \  b' r: y& {% |) K* a: J9 ~! zwhen he learned the testosterone level in the baby
9 w" m- w8 r/ y$ Wwas high, he then read the product information
# X6 r# Z$ p( `2 @, qpacket and concluded that it was most likely the rea-
; z4 d" L/ o# zson for the child’s virilization. At that time, they
  F( L0 v$ p1 \; Xdecided to put the baby in a separate bed, and the
. J- K9 @' H( d0 V$ t2 _) t5 rfather was not hugging him with bare skin and had: v. I' o2 m5 D
been using protective clothing. A repeat testosterone
6 v/ [# h- Z7 g" btest was ordered, but the family did not go to the
+ ?5 a1 M4 D/ C9 y- F1 Slaboratory to obtain the test.
5 X4 [6 r% U2 A( \8 zDiscussion9 G" W, ~3 ^" n, r3 U
Precocious puberty in boys is defined as secondary5 p3 y0 _7 ]+ [$ I& q1 u' j/ d1 E1 k' d
sexual development before 9 years of age.1,4+ H) J, \# h1 U# K
Precocious puberty is termed as central (true) when8 R* J4 D# S" ^% n& M  W, j+ r
it is caused by the premature activation of hypo-! e, f9 Z$ c& @4 {/ U1 L
thalamic pituitary gonadal axis. CPP is more com-
( Z% ^6 Y/ D9 g# M6 Q3 c9 t& Tmon in girls than in boys.1,3 Most boys with CPP
6 \' i" {! F; V0 Y9 {may have a central nervous system lesion that is5 C% X0 N" T7 n( [
responsible for the early activation of the hypothal-' K: q' u: C: W' S$ O
amic pituitary gonadal axis.1-3 Thus, greater empha-- W2 ]& A3 B9 O; ^
sis has been given to neuroradiologic imaging in
2 b1 `! l8 u7 a- U/ Cboys with precocious puberty. In addition to viril-
" Y$ q7 R' p3 _6 c+ o9 k6 fization, the clinical hallmark of CPP is the symmet-. T5 ]. ~/ [5 u: d  l, [
rical testicular growth secondary to stimulation by
9 n( ~1 g% G6 N) n2 q8 kgonadotropins.1,35 h, _4 P& V. q/ M2 k: ]
Gonadotropin-independent peripheral preco-8 h! f. \0 t7 x9 r
cious puberty in boys also results from inappropriate- p2 g( \2 ?( u4 G. P1 }
androgenic stimulation from either endogenous or
5 u% K- j- C& d) r2 h7 z; I2 [: nexogenous sources, nonpituitary gonadotropin stim-) a* w2 E" `  E0 L) H" f2 Y( v
ulation, and rare activating mutations.3 Virilizing& B7 p  h- h6 Z! |8 {# X
congenital adrenal hyperplasia producing excessive
7 a; ~, F. |( q; A# U1 Xadrenal androgens is a common cause of precocious
3 ^: ~) @# D5 z* t: G5 L0 z% l2 Wpuberty in boys.3,4
, ^) u& U/ `7 g# M1 v5 o1 dThe most common form of congenital adrenal1 k* T3 n( a% ?2 i$ `1 d
hyperplasia is the 21-hydroxylase enzyme deficiency.
7 c7 h/ S2 m( r+ fThe 11-β hydroxylase deficiency may also result in: |( V2 O+ m+ s3 y
excessive adrenal androgen production, and rarely,7 ^% ]# Q6 _* Q
an adrenal tumor may also cause adrenal androgen) ]+ z. ~7 l- q) U. ^
excess.1,36 b3 p9 ?1 D4 R; g" y
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ x( X, w# L6 E' D# ]" u0 a
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007, x: C  \. `, J, e
A unique entity of male-limited gonadotropin-, r9 j: E. {; Q" v/ }1 h
independent precocious puberty, which is also known$ [0 e4 a7 S9 E9 m! L6 ^) y
as testotoxicosis, may cause precocious puberty at a6 ~8 O3 F/ x3 ?  Y' v
very young age. The physical findings in these boys/ j0 a: y) X0 I& w, d9 k
with this disorder are full pubertal development,
' B, I' ]  W5 Sincluding bilateral testicular growth, similar to boys
$ p' P. v1 ~$ q0 P5 H& r; gwith CPP. The gonadotropin levels in this disorder
$ v- d; x' H8 oare suppressed to prepubertal levels and do not show' K* @" f( `( X9 o% z$ L
pubertal response of gonadotropin after gonadotropin-% @  n; o. q3 A$ z- X* r
releasing hormone stimulation. This is a sex-linked" g) f. |, B0 z1 T* s- r
autosomal dominant disorder that affects only3 P* B$ `* ?1 q) Q; Z
males; therefore, other male members of the family$ }: m4 i: F; }8 p
may have similar precocious puberty.3; \/ Y4 l$ p+ ?: ]3 N
In our patient, physical examination was incon-$ W% J" S" m3 P/ b' e3 s
sistent with true precocious puberty since his testi-
( K. J, I. z6 s( A  `  Dcles were prepubertal in size. However, testotoxicosis
3 f% R/ |: d% g" wwas in the differential diagnosis because his father/ a( m/ B- Q0 t/ g! S2 R+ c
started puberty somewhat early, and occasionally,
- u, J6 |/ _2 a. G5 B0 A/ i0 r. rtesticular enlargement is not that evident in the5 O% w3 V. N1 D. n! d
beginning of this process.1 In the absence of a neg-
% B( s" r6 B4 m4 ]) N, s3 k2 s- ]$ Sative initial history of androgen exposure, our0 @( y/ L" ?# c9 s/ X7 B, V
biggest concern was virilizing adrenal hyperplasia,, _+ a% Y$ V8 V& O5 R7 D
either 21-hydroxylase deficiency or 11-β hydroxylase+ m4 p2 A) ?7 F+ e: B$ N, n" z7 G& ?
deficiency. Those diagnoses were excluded by find-
) u$ p' T3 k4 l. B% I" Z2 ying the normal level of adrenal steroids.
# H2 j' c8 ]4 hThe diagnosis of exogenous androgens was strongly9 G0 i0 k+ M! w% k# H# P
suspected in a follow-up visit after 4 months because. _* C& T' ]2 I
the physical examination revealed the complete disap-
/ c1 u5 o; g$ L" s) Jpearance of pubic hair, normal growth velocity, and2 U! [5 M5 E, E# Z* c, w
decreased erections. The father admitted using a testos-
+ ?" N9 y0 u4 B; E! _terone gel, which he concealed at first visit. He was
+ x, C3 I1 ^" {, A; q! s6 T( fusing it rather frequently, twice a day. The Physicians’
+ U9 ?7 H; n6 X3 @5 }; o/ l4 s3 x9 q' bDesk Reference, or package insert of this product, gel or4 G4 N$ y$ A. y% U/ h% e3 U  e
cream, cautions about dermal testosterone transfer to
2 K" L: Y5 R7 L$ Y% w# y0 K: uunprotected females through direct skin exposure.
8 z) B" o/ z4 n1 E) CSerum testosterone level was found to be 2 times the
" O) w) s1 l- rbaseline value in those females who were exposed to
) A& Y/ y5 O! ^8 n) i: feven 15 minutes of direct skin contact with their male( A& a- H% Z* P- \' [" j8 A) _
partners.6 However, when a shirt covered the applica-/ i) i5 ?1 ?+ z5 @& v* i" V
tion site, this testosterone transfer was prevented.+ b" h- a( y* q2 Z6 f( D
Our patient’s testosterone level was 60 ng/mL,6 p4 s" e1 b" E5 N( k% ^- q$ X
which was clearly high. Some studies suggest that( f) B, k! x' q0 N6 C7 \8 H) W5 D2 m
dermal conversion of testosterone to dihydrotestos-2 \) R, k& J, Q
terone, which is a more potent metabolite, is more
- P  l5 e" M/ s% xactive in young children exposed to testosterone/ B9 X6 h! J7 p* ?6 o" z
exogenously7; however, we did not measure a dihy-! g' G1 v3 I& }+ H! o" \5 _9 X
drotestosterone level in our patient. In addition to
8 j0 ?, x7 C4 M, avirilization, exposure to exogenous testosterone in
& y2 Y/ V0 k% C; k" f6 S( _0 t! rchildren results in an increase in growth velocity and
2 b* ^" m, Q# Z/ I7 aadvanced bone age, as seen in our patient.( [0 _( @3 h5 |7 P
The long-term effect of androgen exposure during$ [3 h9 x, u) o+ i* ^- h
early childhood on pubertal development and final2 f  [. O( o6 o) L
adult height are not fully known and always remain8 U8 }+ \8 V0 j5 ^3 d0 \
a concern. Children treated with short-term testos-) @! T% f8 M0 y  t" r$ `  m
terone injection or topical androgen may exhibit some
4 h! H- ~. Q6 m0 Z$ N) dacceleration of the skeletal maturation; however, after
- k7 N9 Y/ f4 W6 t* K4 _cessation of treatment, the rate of bone maturation
& o" w9 k& W* h$ r$ u* y; ^decelerates and gradually returns to normal.8,9
7 i0 J- A9 B2 {- J' nThere are conflicting reports and controversy; _9 ^& P' H% X0 l9 P
over the effect of early androgen exposure on adult1 c  T( y/ b: U1 t, E( F- [, e
penile length.10,11 Some reports suggest subnormal# t$ Z+ V4 d1 _$ w/ x6 s- f9 u3 K
adult penile length, apparently because of downreg-. L0 J% b! r* x. m* H: v
ulation of androgen receptor number.10,12 However,
' |1 i/ o& @" z& R1 u4 W$ Z9 t+ CSutherland et al13 did not find a correlation between
1 f% ^) z% F9 u) U5 m( bchildhood testosterone exposure and reduced adult
5 z  V: F$ r5 I0 l3 Lpenile length in clinical studies.
5 C7 }+ O7 B& B1 @9 |Nonetheless, we do not believe our patient is
  F! V$ ?' {6 ~) Ggoing to experience any of the untoward effects from
( _3 M/ @4 e5 j: m0 Ztestosterone exposure as mentioned earlier because
) H  Q7 h& |' qthe exposure was not for a prolonged period of time.
. K* m, `0 s2 H+ i& y' HAlthough the bone age was advanced at the time of% E5 V. h2 E- e4 o1 H
diagnosis, the child had a normal growth velocity at
% w2 y/ o# C  H5 Y) k( H0 ethe follow-up visit. It is hoped that his final adult
# p# n, B+ V, s' \: ]height will not be affected.
, P- A% ]) t! H* o) Q8 mAlthough rarely reported, the widespread avail-
8 _) d; K& `+ U' c, g3 Gability of androgen products in our society may
' v- y. D% b& w( y5 Qindeed cause more virilization in male or female
4 N5 q1 w3 J4 L& ^9 A. `children than one would realize. Exposure to andro-0 ?  G  Q- r0 f
gen products must be considered and specific ques-
2 m' h* v8 f9 J* _' z' o8 ationing about the use of a testosterone product or
- h% C! s4 m7 R7 _2 K/ x" jgel should be asked of the family members during
% x0 v4 `2 ~2 ?! U! J# X9 i# ]  hthe evaluation of any children who present with vir-
" @& S+ i0 _. j4 p3 `ilization or peripheral precocious puberty. The diag-
) G9 `7 ^. F  M7 k9 n* p6 I8 {nosis can be established by just a few tests and by
7 y% t7 J& }% [/ Z7 Cappropriate history. The inability to obtain such a
: ?$ D! \, S" f5 _9 Phistory, or failure to ask the specific questions, may: M  ?  Z; @4 v: I: w
result in extensive, unnecessary, and expensive$ K/ R+ k7 _$ n, e  U3 K1 ~6 @# C) ^
investigation. The primary care physician should be9 ^7 U& N/ A, t0 Q
aware of this fact, because most of these children
* ?2 g( j) Q3 G8 A, |+ j3 {may initially present in their practice. The Physicians’: w: Z6 F0 [0 a: o
Desk Reference and package insert should also put a
& V. U. ~3 D9 Y6 ~- awarning about the virilizing effect on a male or" ^& ]4 b; ~  Y+ ^7 u: u
female child who might come in contact with some-# y7 v! j, T+ J4 t4 g
one using any of these products.6 \# v" o5 _) K% b
References, Q1 \+ y  r9 d8 I* q
1. Styne DM. The testes: disorder of sexual differentiation3 a! `) J/ |4 D7 Z+ v' h1 q
and puberty in the male. In: Sperling MA, ed. Pediatric
* b5 r8 X2 {" o% G9 F5 C4 X+ IEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
( h1 M. d* N6 g, _6 P2002: 565-628.
9 m* B. g# N7 o2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
( }- s5 ^& f8 l& G4 M) _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

. d8 \6 B8 M) @5 b8 Y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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