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Sexual Precocity in a 16-Month-Old! b. a) r6 p% R; ]* f
Boy Induced by Indirect Topical2 [" w( \; x$ ?. V- t1 c
Exposure to Testosterone
) |4 q  S$ C* U5 Q9 \Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,25 @: ]/ `. \, X7 {7 x; M3 f/ B
and Kenneth R. Rettig, MD1
. l9 i% M  N* J3 y. Y3 _2 k% EClinical Pediatrics
" m# i! m5 ?. T2 ~Volume 46 Number 6
; X! n0 g- A; h5 T% d! mJuly 2007 540-543
- N! c2 `9 S  r3 W$ S+ ~6 A- ~© 2007 Sage Publications+ ^+ O3 `4 ~0 W; w
10.1177/00099228062966514 ~1 i9 B9 m) P$ Y6 q* d, C& _
http://clp.sagepub.com
  j2 U8 z& D: Whosted at
2 w: ^  x/ Z1 {" q- v" Qhttp://online.sagepub.com
: v8 `" y+ C* R" |7 ~, W  nPrecocious puberty in boys, central or peripheral,, c* p7 A+ O/ O7 X+ f; D- i8 _
is a significant concern for physicians. Central7 b3 i4 N4 W' l, P, n2 A! G" g6 W
precocious puberty (CPP), which is mediated
/ T. x# @1 H7 i9 dthrough the hypothalamic pituitary gonadal axis, has* t# T2 P7 V4 Y3 K+ Y  v; s. b! e* F
a higher incidence of organic central nervous system% M$ G9 ~7 L, |4 @5 I# ]2 R
lesions in boys.1,2 Virilization in boys, as manifested$ E' u, M1 l) o8 {6 l! ], ?. u
by enlargement of the penis, development of pubic7 Y; O$ G; a7 z8 q, |+ e" A* b1 [( J
hair, and facial acne without enlargement of testi-+ A/ [) V2 g1 V/ e" y. E
cles, suggests peripheral or pseudopuberty.1-3 We5 k: ?# s4 D: h  s$ b0 t
report a 16-month-old boy who presented with the3 O7 K7 K  D  Z% }6 x, f
enlargement of the phallus and pubic hair develop-! `+ e' D- [0 s( Q5 |# @* m
ment without testicular enlargement, which was due3 O5 g6 x3 l$ Y
to the unintentional exposure to androgen gel used by
& W8 Y7 u! V: ?5 }/ [, k) d; L7 Nthe father. The family initially concealed this infor-! D- u- q! _( X8 Y7 `$ o
mation, resulting in an extensive work-up for this
) s; m$ E" J+ t2 zchild. Given the widespread and easy availability of8 S9 o3 G4 z2 f9 j
testosterone gel and cream, we believe this is proba-
: T, G+ p1 ?! X* ~2 {6 Z, C0 }bly more common than the rare case report in the0 p( ?$ T, @- d
literature.42 n/ @3 v2 L: Q  o0 s
Patient Report" r6 f2 F9 t: U- i8 o7 F6 |
A 16-month-old white child was referred to the* V! B( `) b* O0 q! r, M( R
endocrine clinic by his pediatrician with the concern1 k% Q+ h! M# q3 b4 J6 I
of early sexual development. His mother noticed8 e- v: h8 |% x; n
light colored pubic hair development when he was
  h8 l1 e1 c6 F6 }' q$ WFrom the 1Division of Pediatric Endocrinology, 2University of
, c$ j. m, b/ ]& e9 t- O' w+ @: `South Alabama Medical Center, Mobile, Alabama.
! |. r. x2 j6 d  Y! G' X7 OAddress correspondence to: Samar K. Bhowmick, MD, FACE,$ R2 k) e  ?& ?$ D! p, y- w0 I
Professor of Pediatrics, University of South Alabama, College of; U6 x; |% ?4 k; h8 i  _" o
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;( t! L0 p( m3 D0 R; t
e-mail: [email protected].6 i+ y  ^) O, a6 ^7 k% e8 D
about 6 to 7 months old, which progressively became
  g! w0 M  o/ }) Ldarker. She was also concerned about the enlarge-
; S! J3 W- _1 f& W2 w( Pment of his penis and frequent erections. The child8 M4 A4 D+ E# B! F3 V
was the product of a full-term normal delivery, with4 E& `4 x: L/ f$ m. ]
a birth weight of 7 lb 14 oz, and birth length of5 B2 @6 Y1 [, y1 D2 \% Q
20 inches. He was breast-fed throughout the first year
8 Q/ a2 I4 B( G- U* [" `) B  q& t$ L, oof life and was still receiving breast milk along with1 d* z3 z& k+ ]; T
solid food. He had no hospitalizations or surgery,
, Z5 U* f8 [1 U& A5 Nand his psychosocial and psychomotor development9 \. j0 c' G, m
was age appropriate.
- G! e, }# ?7 Y( A. x/ z5 aThe family history was remarkable for the father,
5 B1 \/ ]+ Z% _who was diagnosed with hypothyroidism at age 16,3 {# s( o! c4 S) @) s' p4 B
which was treated with thyroxine. The father’s
, e% u6 N. d4 ~3 J) b0 D* iheight was 6 feet, and he went through a somewhat
7 w6 V! c$ C/ t4 m4 bearly puberty and had stopped growing by age 14.
$ F) ~) Y, F- L  U# [" YThe father denied taking any other medication. The
+ k$ t. [- K: d  [( ~9 t  J" P- u2 xchild’s mother was in good health. Her menarche9 D4 Q  P2 p0 C5 s
was at 11 years of age, and her height was at 5 feet
3 p0 g6 Q( \9 E' ~7 q5 inches. There was no other family history of pre-9 j: z5 c; u1 H9 c, T$ K
cocious sexual development in the first-degree rela-
* P, P" ~8 ~/ \. A! q6 Ytives. There were no siblings.. D! K" y+ K# }& `5 D5 Z
Physical Examination
& _2 H5 N4 W9 L1 U% rThe physical examination revealed a very active,
  o2 o+ a1 Y6 N- \# z5 K& Vplayful, and healthy boy. The vital signs documented; s& @. E; o5 o$ A/ [2 }) V* l
a blood pressure of 85/50 mm Hg, his length was
0 t1 L8 d8 e! C5 a: {( V% t" d90 cm (>97th percentile), and his weight was 14.4 kg1 T1 Y. x4 B0 p- {. F" x
(also >97th percentile). The observed yearly growth& w+ v, ~$ T0 @
velocity was 30 cm (12 inches). The examination of( y/ O  u4 o9 V; N3 d
the neck revealed no thyroid enlargement.
( e$ C7 L* P, [( gThe genitourinary examination was remarkable for
$ g6 Q, f$ s* _: t3 G) Qenlargement of the penis, with a stretched length of
$ v: V, V0 O1 K3 I% a( q( \8 cm and a width of 2 cm. The glans penis was very well) x6 s2 x0 p$ v) E1 [- Y8 J
developed. The pubic hair was Tanner II, mostly around
- {8 ~, b0 n! ^' M! Y9 _5402 Q# M. s: q8 F2 b3 q5 [
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& M9 |: G1 j2 _+ ~5 A1 y
the base of the phallus and was dark and curled. The
% C+ f& w1 V2 x' Etesticular volume was prepubertal at 2 mL each.
3 R# u8 n9 E  l$ kThe skin was moist and smooth and somewhat# h4 M& T2 K8 }' u8 a) h; {: d& t& A
oily. No axillary hair was noted. There were no
6 I/ R- l2 M- ]; K* I3 pabnormal skin pigmentations or café-au-lait spots.6 A8 O6 F% v( I& P/ o/ z
Neurologic evaluation showed deep tendon reflex 2+
& v( H' Q* {/ n5 @2 i" q6 Dbilateral and symmetrical. There was no suggestion! g( l+ `8 Z- S/ L8 y+ [# h8 w
of papilledema.
5 _$ C% [6 i/ cLaboratory Evaluation
  J; |. m$ o) U% P/ u5 U% h3 `The bone age was consistent with 28 months by4 ]7 u7 M& W0 \/ H% I0 Y2 e! N
using the standard of Greulich and Pyle at a chrono-
0 Y5 e( A- R' m; L5 Mlogic age of 16 months (advanced).5 Chromosomal
7 M" ^" P6 \  r: ~7 h/ B: hkaryotype was 46XY. The thyroid function test
; m8 D+ L. g2 K6 F' U& Mshowed a free T4 of 1.69 ng/dL, and thyroid stimu-; ~: E- u- C2 u! T0 L
lating hormone level was 1.3 µIU/mL (both normal).
. d! y4 r, F! i) z" z7 x3 E+ lThe concentrations of serum electrolytes, blood' t/ D7 H4 Y2 e3 ?3 `% {
urea nitrogen, creatinine, and calcium all were' t. x, K8 u6 S# J2 j! v
within normal range for his age. The concentration
& i' T: e% |( b$ ?+ h. Nof serum 17-hydroxyprogesterone was 16 ng/dL
. @; W9 h1 X( u. ]6 a  F- Z(normal, 3 to 90 ng/dL), androstenedione was 20; t/ g( n0 K* F1 R
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
2 M  y9 S  {1 P7 U% U  E% I4 gterone was 38 ng/dL (normal, 50 to 760 ng/dL),# L* O! }  K& w  i! c
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
1 y* z8 ?* ^5 \49ng/dL), 11-desoxycortisol (specific compound S)
! h- F7 f2 S( f  {% uwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-% g% s+ f( y3 j# U: ^
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
7 q& k" O6 k  ?# C; P. Q1 Y( Wtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
9 j& m: l  n. R* ^and β-human chorionic gonadotropin was less than/ A1 H9 Q  i0 E2 k! n9 |8 [0 ^
5 mIU/mL (normal <5 mIU/mL). Serum follicular3 |+ q$ O9 t; ]6 f3 O
stimulating hormone and leuteinizing hormone
' `7 E8 b& X- G; ~0 H% S/ ?: ]+ Y7 xconcentrations were less than 0.05 mIU/mL& q. j+ e, y! e. H) Q# f# ?
(prepubertal).  N2 j* X6 _, e6 [1 K' i
The parents were notified about the laboratory. ]) |' ]' Q* t/ L; m& j
results and were informed that all of the tests were! }( L) Y( j( i0 e. m
normal except the testosterone level was high. The
) `9 o% b, e2 A. I: m$ Ofollow-up visit was arranged within a few weeks to
# ]6 f; Q9 X6 T* [9 Q- U( Z' Cobtain testicular and abdominal sonograms; how-5 [  T$ s: S# J/ `9 Z  G
ever, the family did not return for 4 months.% C& J. m: h- B! m
Physical examination at this time revealed that the: S4 g( r: p' G" M0 H
child had grown 2.5 cm in 4 months and had gained
" Q" H& O( z0 x2 y: }+ x2 kg of weight. Physical examination remained
7 \% H& n- d* munchanged. Surprisingly, the pubic hair almost com-( F! j. m) p/ K, [
pletely disappeared except for a few vellous hairs at8 K% }$ C7 d, |2 ^5 D( H6 g
the base of the phallus. Testicular volume was still 2
0 c+ L9 w+ b* m4 a# Z: r; EmL, and the size of the penis remained unchanged.
$ U' H) ~& p, E1 t/ lThe mother also said that the boy was no longer hav-3 X2 R8 `1 O5 b" j
ing frequent erections.
* w" P5 f8 r" K5 ~( T1 lBoth parents were again questioned about use of
+ K' q5 A( \. F2 S- Q# ~: Zany ointment/creams that they may have applied to- ?0 T8 A5 H0 P6 r
the child’s skin. This time the father admitted the
# d8 F( Q% I0 }$ a# {5 PTopical Testosterone Exposure / Bhowmick et al 541
/ r8 J9 l4 f# Q: z, \use of testosterone gel twice daily that he was apply-+ w' u2 n4 [# `  X& O2 }- B
ing over his own shoulders, chest, and back area for
4 u) O6 I) V) c, E* Za year. The father also revealed he was embarrassed
+ h- B! Z3 C6 l* G- k2 `to disclose that he was using a testosterone gel pre-
  u1 z. \( c! cscribed by his family physician for decreased libido  l1 _" q7 C* a; d* f
secondary to depression.4 N+ L0 M1 ?  s! n* ^9 P7 y
The child slept in the same bed with parents.6 r8 u% ]1 Y7 T  n# j
The father would hug the baby and hold him on his
. ^8 _. v! \1 B7 Cchest for a considerable period of time, causing sig-. J5 ~0 b' b: P! C6 U" W6 _2 J: y1 g
nificant bare skin contact between baby and father.
, O  m+ |6 k2 I. F* MThe father also admitted that after the phone call,1 U- e! d) B& I. ]  E- X4 q
when he learned the testosterone level in the baby
! c7 m2 e$ y  I  xwas high, he then read the product information4 a2 ]% n. l; m! H1 s9 y) s1 A% Y
packet and concluded that it was most likely the rea-
' a( Y+ E( s9 N) bson for the child’s virilization. At that time, they
7 T/ z. a* t9 |, ^& m6 \! o& ndecided to put the baby in a separate bed, and the
2 p8 J# y: l- X& yfather was not hugging him with bare skin and had) C: g8 T- Q, g/ ~8 Y6 M! X
been using protective clothing. A repeat testosterone8 j9 z6 M; g! w. M( |
test was ordered, but the family did not go to the4 S0 C- D" [# C7 }
laboratory to obtain the test., J) [4 V/ C% W" `0 @; O
Discussion  l4 j: F, p0 C- i0 h
Precocious puberty in boys is defined as secondary9 h8 N& S7 U4 ~  }% N( L2 z8 q
sexual development before 9 years of age.1,4* W* l8 h% o. P/ c3 u" ?7 G
Precocious puberty is termed as central (true) when
8 R' S$ G5 n# A4 @* r( wit is caused by the premature activation of hypo-4 r) P6 Z$ K: V
thalamic pituitary gonadal axis. CPP is more com-* i" ^" f2 y' k- Q0 D( V+ L  p
mon in girls than in boys.1,3 Most boys with CPP
4 Q* O0 Z5 t$ Dmay have a central nervous system lesion that is
# g; \+ D. |( p+ z- J0 presponsible for the early activation of the hypothal-# [( Z( {1 E8 m; T7 F8 @  y+ |
amic pituitary gonadal axis.1-3 Thus, greater empha-
  b( j. V- f. f2 rsis has been given to neuroradiologic imaging in. [6 o; B% X/ ]" A: I, g- V. W
boys with precocious puberty. In addition to viril-
6 l. I5 }( {7 ]( T0 ?) y' eization, the clinical hallmark of CPP is the symmet-8 _" P: q, B, l7 N: J8 L: `
rical testicular growth secondary to stimulation by8 I# I! F3 v1 ^# m
gonadotropins.1,31 ]5 j% R9 U" M7 @! r* S
Gonadotropin-independent peripheral preco-. H% F6 ^, H! s" x
cious puberty in boys also results from inappropriate
) Z: v: H9 s6 o1 L3 Uandrogenic stimulation from either endogenous or3 F& j4 M6 }6 j4 A8 f
exogenous sources, nonpituitary gonadotropin stim-
7 K5 q& k: w6 H7 A( lulation, and rare activating mutations.3 Virilizing
& L5 r# S5 ^# V  S+ Kcongenital adrenal hyperplasia producing excessive8 L2 {% U0 h' \, W7 l
adrenal androgens is a common cause of precocious
( ^1 r3 J  I: @( Spuberty in boys.3,47 A" {4 v3 B9 K( z1 z! m) k* a
The most common form of congenital adrenal+ ^9 F4 o: |0 ]* F  u, r
hyperplasia is the 21-hydroxylase enzyme deficiency., x9 d* O8 p' X- H) S" g' F5 J
The 11-β hydroxylase deficiency may also result in
7 |/ y) L  b" a1 f5 w* jexcessive adrenal androgen production, and rarely,7 V. w' j  e3 u0 P% d" O; ?7 h
an adrenal tumor may also cause adrenal androgen
4 r+ ], h( O0 o% q; g/ E3 B/ C4 wexcess.1,3# K8 M! W: S( D# `' A  g" J
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( x2 N1 g, p$ ]7 q542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
  F+ G) h! S! C3 XA unique entity of male-limited gonadotropin-. ^  Z6 I$ ]* J+ B
independent precocious puberty, which is also known
# l7 r: r8 }3 |9 q" X4 Eas testotoxicosis, may cause precocious puberty at a
, m, A! ~' f3 G* L" s7 [very young age. The physical findings in these boys
8 [) ?7 b2 a. @$ Bwith this disorder are full pubertal development,  E# ?( t! T3 `/ O( O" }
including bilateral testicular growth, similar to boys
: O) G7 P2 q2 K( Z# r" C( v3 iwith CPP. The gonadotropin levels in this disorder
( j8 g, ^5 i8 a$ W- }% P8 iare suppressed to prepubertal levels and do not show
$ Z- M; u/ B$ E; @6 m, G2 n/ X: ?, ~+ ~pubertal response of gonadotropin after gonadotropin-4 j7 s. A2 }7 X- r
releasing hormone stimulation. This is a sex-linked, F( s6 d* g: M; O9 ]# E2 K6 ~
autosomal dominant disorder that affects only+ q* f6 x3 c$ @4 T( p) b3 P; K
males; therefore, other male members of the family
( h# Z# x' Y; q+ |: L, rmay have similar precocious puberty.3% x2 O" [2 ~9 ?6 S
In our patient, physical examination was incon-: t9 ^6 d- o8 D9 Y
sistent with true precocious puberty since his testi-# ]. E7 B$ y) u$ C6 q% e- E  C* i
cles were prepubertal in size. However, testotoxicosis
( s7 [9 ^; u$ W% e% F$ _% |was in the differential diagnosis because his father( d. o  j- s7 E
started puberty somewhat early, and occasionally,
/ p# {0 p: `7 ~3 @testicular enlargement is not that evident in the' {4 @" M( M! `( `! _
beginning of this process.1 In the absence of a neg-+ M6 Q, E! d" z1 ~& a6 S  S: L- l4 t% K
ative initial history of androgen exposure, our; _1 L1 ~+ `8 o: H5 @$ n
biggest concern was virilizing adrenal hyperplasia,
: C& o' }% x' x8 Aeither 21-hydroxylase deficiency or 11-β hydroxylase
& F; x6 e4 X1 [9 X2 ~; U. xdeficiency. Those diagnoses were excluded by find-
3 f, k' a, S! E0 q8 {- c: M! W" Q4 uing the normal level of adrenal steroids.7 l! ?3 I3 \& P
The diagnosis of exogenous androgens was strongly$ T% G5 [: ]3 `5 s6 Z: ]
suspected in a follow-up visit after 4 months because. v) e2 ?7 e7 v" c0 }7 X! E. D
the physical examination revealed the complete disap-
" ^$ Z$ s. ]! gpearance of pubic hair, normal growth velocity, and
$ e! @/ d6 A; Qdecreased erections. The father admitted using a testos-
. @& w1 g6 ?: J% H" v% rterone gel, which he concealed at first visit. He was
3 d& H, z; _7 d4 x1 k; T# pusing it rather frequently, twice a day. The Physicians’
$ E, S9 v" `" o3 H: [+ GDesk Reference, or package insert of this product, gel or9 ?4 X) U, ^3 k9 o5 Y% |
cream, cautions about dermal testosterone transfer to
# Y6 P0 C" C  h& ^unprotected females through direct skin exposure.0 H4 |7 f  s4 O0 H6 L
Serum testosterone level was found to be 2 times the
8 [; v. r  c# @) }' t6 lbaseline value in those females who were exposed to+ F3 K) n( E3 a& L. J
even 15 minutes of direct skin contact with their male
' D5 r: ]- ?$ a; \1 z8 @# u8 rpartners.6 However, when a shirt covered the applica-
0 a+ D" T7 I, {9 l# Q0 \. ution site, this testosterone transfer was prevented.
* J* c! T4 y: |5 L6 \3 W0 k; MOur patient’s testosterone level was 60 ng/mL,
7 g0 f" A9 N: g; {6 Kwhich was clearly high. Some studies suggest that
  F8 L3 {% |0 g5 G0 ]dermal conversion of testosterone to dihydrotestos-) o/ d  e9 \) _$ P" z
terone, which is a more potent metabolite, is more
" Z0 E8 y9 l+ wactive in young children exposed to testosterone
4 d4 ?/ _+ e& I8 e# Z$ }( U: [' mexogenously7; however, we did not measure a dihy-
& U$ m: a4 ^( \drotestosterone level in our patient. In addition to
& j3 g! G5 r* V5 C  ?: D- H% m9 @virilization, exposure to exogenous testosterone in+ G/ V2 t) G/ f' i! F7 x; G5 J9 h! v
children results in an increase in growth velocity and" s. m! d" y& ^4 C0 Y
advanced bone age, as seen in our patient.
, Q! F' p) F" l2 r' o! VThe long-term effect of androgen exposure during
% \* A. f4 B4 u$ Y8 }* A- I2 Mearly childhood on pubertal development and final( @, q& {6 e  k2 E$ V9 I( Y* m
adult height are not fully known and always remain
* x% O+ W! Y6 ]a concern. Children treated with short-term testos-% ?+ P! D, F9 h8 W( M9 g5 C% \
terone injection or topical androgen may exhibit some
5 m) w* M3 G4 c, F9 {) j5 lacceleration of the skeletal maturation; however, after
1 _. `& v5 W6 B+ X' wcessation of treatment, the rate of bone maturation
% u  I/ I8 p0 [& Q/ Cdecelerates and gradually returns to normal.8,9; m* W8 x  p' N3 \4 i3 _9 s
There are conflicting reports and controversy9 F- g1 t) }, M  Q
over the effect of early androgen exposure on adult9 r) \- I% o% s1 P3 W  W" J
penile length.10,11 Some reports suggest subnormal1 J9 Q, X8 ^$ ]( J6 S# N
adult penile length, apparently because of downreg-  s- k/ D& v7 {$ `; l$ p
ulation of androgen receptor number.10,12 However,
" [5 s& A, i. OSutherland et al13 did not find a correlation between+ c# U6 N' x& c4 ~
childhood testosterone exposure and reduced adult
; |" x6 y2 d4 V) d" }3 M) Vpenile length in clinical studies.
" ]8 L% I" v4 \Nonetheless, we do not believe our patient is
* n3 X* ]5 M- d6 V2 ~going to experience any of the untoward effects from" y; B2 z' A. W2 Q0 e
testosterone exposure as mentioned earlier because
* S6 p, y" m  s- Q, u! Hthe exposure was not for a prolonged period of time.
" L8 z; Q% E4 Z! Z( E% h9 iAlthough the bone age was advanced at the time of
) G9 V( h+ H: q6 y0 Idiagnosis, the child had a normal growth velocity at
7 y+ G' T8 x6 n0 j/ b% Ythe follow-up visit. It is hoped that his final adult+ R: R  x0 C" a) V8 {/ j
height will not be affected.' X5 I$ Z, y" m" `0 b4 z" `
Although rarely reported, the widespread avail-  n0 K" K* \4 }7 W4 _
ability of androgen products in our society may! f2 [% h7 V+ I; ~
indeed cause more virilization in male or female. c' z7 N  g2 j/ A( ]  I8 Y
children than one would realize. Exposure to andro-* }9 \8 ~4 ]% z2 f* Z0 u4 b# q
gen products must be considered and specific ques-
' U- `( ?; j$ o( a9 s  jtioning about the use of a testosterone product or. _3 W$ y6 ~) i0 j. N- D
gel should be asked of the family members during+ f2 ~+ k+ H8 a. l& i, o
the evaluation of any children who present with vir-
8 q, A' F/ a4 ?( N( `ilization or peripheral precocious puberty. The diag-* a, }9 W- P- Z5 W8 d( n+ C! M. ~1 \( m
nosis can be established by just a few tests and by! P$ w0 w3 B! m4 z' z
appropriate history. The inability to obtain such a" V; X3 o6 D* o
history, or failure to ask the specific questions, may
* I. n! v' C: @1 b# Jresult in extensive, unnecessary, and expensive
: G6 A5 j: {5 ^* P* ^investigation. The primary care physician should be
5 C$ a- G' N( Q5 J* N' C: waware of this fact, because most of these children
" w5 b" C( @3 f4 x* M) Umay initially present in their practice. The Physicians’
: y0 U- \' C5 G* R, [9 r$ c. f) `Desk Reference and package insert should also put a- q) {# t( L7 u5 f" C; e2 @
warning about the virilizing effect on a male or
. @, b* H5 w8 T6 dfemale child who might come in contact with some-
6 }$ V' m& Z  f; Pone using any of these products." E6 V" P+ @) `
References6 X. j  Z4 I) t5 J- W
1. Styne DM. The testes: disorder of sexual differentiation+ H! N* P4 q9 \2 N6 t9 D
and puberty in the male. In: Sperling MA, ed. Pediatric
1 r# j% C+ n# nEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;) Q1 G: n1 }( N) W- F
2002: 565-628.
4 ~% I8 y  n! f% i3 {2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
2 n8 d0 e- b  L1 D9 O# [puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old( e1 C3 L" }$ W0 ?' j7 U7 [, P
Boy Induced by Indirect Topical$ X7 E9 Q9 X0 \2 F' Z1 F  x. Z
Exposure to Testosterone
2 O3 w) |( {5 E1 u. ASamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
( T" J% z4 F6 ?2 O4 O* w+ band Kenneth R. Rettig, MD1
! |3 i; _& u8 S/ `4 K. R& M+ kClinical Pediatrics
! b1 i: ]+ ?% u& U* g* G# NVolume 46 Number 66 J6 G8 n6 [! \% K& I$ B
July 2007 540-543# H# n/ i' b% J! P+ x4 v6 m
© 2007 Sage Publications
: w5 K2 z( k9 B3 V" r10.1177/0009922806296651
* p, I1 z( r3 Q8 ]; L. S# \http://clp.sagepub.com  ^( ~% ?3 A& W; v  k
hosted at
% ?: R5 T+ F+ g& A. \6 k! P4 Whttp://online.sagepub.com
- P; R9 X" x! Q4 _Precocious puberty in boys, central or peripheral,
' N$ F; ]& e: e  @is a significant concern for physicians. Central
. {) A: \2 m1 S; @% y' A9 `. qprecocious puberty (CPP), which is mediated
# ?$ L$ ^& T! X" Uthrough the hypothalamic pituitary gonadal axis, has; ?# h5 @3 U; `: n) y2 f2 F4 D* e+ d
a higher incidence of organic central nervous system
) a' a; p) |$ e, d; h9 Q! H0 O$ Nlesions in boys.1,2 Virilization in boys, as manifested  ]8 B1 [2 R' [4 z: L) v! Y1 ?
by enlargement of the penis, development of pubic1 J/ e9 A; h+ I$ v: B  k& \) _
hair, and facial acne without enlargement of testi-: w: q$ k; B3 z( z7 N+ y
cles, suggests peripheral or pseudopuberty.1-3 We
" P0 M* g! b) X7 Q. yreport a 16-month-old boy who presented with the1 h! C7 e0 B" O1 H( U' M: h
enlargement of the phallus and pubic hair develop-
0 d+ o3 C* O: K( P; X% [4 ]ment without testicular enlargement, which was due
: I" B4 `% B# R% ^6 z! u- i* sto the unintentional exposure to androgen gel used by
# f6 \+ I6 ?5 y7 {0 J: u6 Pthe father. The family initially concealed this infor-
: R! r* X7 d  X' b7 a1 Rmation, resulting in an extensive work-up for this' O7 |0 f2 G$ E) e0 X! U
child. Given the widespread and easy availability of, I7 S/ X. K$ J
testosterone gel and cream, we believe this is proba-
5 e% _: Q" _, T2 d6 d9 O! ~bly more common than the rare case report in the3 a, }0 j  V5 U3 G, _5 V
literature.4
2 K1 i( x% \, pPatient Report
' X0 D# J3 s& B& B* r7 f: ]; ]A 16-month-old white child was referred to the
  i) t- d; p5 v+ |endocrine clinic by his pediatrician with the concern( \2 @! E5 r4 d) q, P
of early sexual development. His mother noticed
1 ^- x* c0 O6 I3 }8 ?0 {6 J: Ylight colored pubic hair development when he was7 T5 y% r. A& D3 [4 f
From the 1Division of Pediatric Endocrinology, 2University of& G& J* s# k* x- j
South Alabama Medical Center, Mobile, Alabama.
8 F9 f* f5 o, F8 \: fAddress correspondence to: Samar K. Bhowmick, MD, FACE,8 a% i( L4 l2 ]- {
Professor of Pediatrics, University of South Alabama, College of
; a& j" @4 R# _1 E: ?Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
4 `6 r% P: X9 S1 X5 i$ Ge-mail: [email protected].
3 B- J, T3 W+ i3 r/ k, V6 Fabout 6 to 7 months old, which progressively became
8 w, p+ N2 A2 N1 m% k! W1 rdarker. She was also concerned about the enlarge-, |8 P* r. _1 A% k+ \! t5 {, h
ment of his penis and frequent erections. The child: m4 L' P, t9 c8 Z; p, M
was the product of a full-term normal delivery, with0 G5 Z: H* D; g7 T! L
a birth weight of 7 lb 14 oz, and birth length of
3 T: ~* |( G, a0 n20 inches. He was breast-fed throughout the first year
" ~( K4 a% b" V0 t/ {of life and was still receiving breast milk along with
0 ?( B, V( n9 R. W- V9 T0 w; i' Vsolid food. He had no hospitalizations or surgery,9 L" E) D# J. V
and his psychosocial and psychomotor development( J3 s! r; l% k/ u. X, r9 b
was age appropriate.
$ j4 S/ {5 f! B9 C1 b4 ZThe family history was remarkable for the father,
4 E0 i; R9 C- f* D2 L1 Dwho was diagnosed with hypothyroidism at age 16,9 _& Y* O% L+ q5 H' f* d0 `  G2 V
which was treated with thyroxine. The father’s
2 V3 }+ T9 U8 uheight was 6 feet, and he went through a somewhat
' T* [1 E) c8 gearly puberty and had stopped growing by age 14.; U$ V% W$ F8 i. r% g
The father denied taking any other medication. The3 o* X  I% K7 |* h) G6 e' x
child’s mother was in good health. Her menarche5 [" w, a6 R( e6 V
was at 11 years of age, and her height was at 5 feet! F; T. t1 N& ^2 |! P( P7 k
5 inches. There was no other family history of pre-
4 Y1 N- G& V( e4 P  Qcocious sexual development in the first-degree rela-; P; }2 @) ^6 ]; {
tives. There were no siblings.( F* x- }- K5 a( G4 b+ ^
Physical Examination
+ W$ F$ g' W1 a+ C) N4 ]7 [The physical examination revealed a very active,) D" H3 Q& j0 n4 B
playful, and healthy boy. The vital signs documented
5 E( M- z" a3 U8 a4 n6 ^6 r4 T! qa blood pressure of 85/50 mm Hg, his length was1 A, t4 K$ d5 Q
90 cm (>97th percentile), and his weight was 14.4 kg' }6 }& L- [9 S. t
(also >97th percentile). The observed yearly growth
/ R. G7 z- y" D# Ivelocity was 30 cm (12 inches). The examination of% @6 h$ K: k9 f2 m5 m  R: L  B' t
the neck revealed no thyroid enlargement.7 `7 N5 {2 l$ c6 `0 U* j
The genitourinary examination was remarkable for5 |+ y, H7 K* e, L
enlargement of the penis, with a stretched length of! r/ \; a: H. o1 j9 d
8 cm and a width of 2 cm. The glans penis was very well
5 _! _; Y; d! ^7 n* F% adeveloped. The pubic hair was Tanner II, mostly around  z2 j$ g7 {% S8 A0 m8 i' q
540$ o: ~3 d* N5 ]' j; I
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 {6 ~0 E6 X) L3 m8 W- `the base of the phallus and was dark and curled. The1 i0 \+ h- L: o" `
testicular volume was prepubertal at 2 mL each.0 Z  r+ Q# z6 _  c# e* n0 X1 J* T
The skin was moist and smooth and somewhat2 x0 K7 E4 [/ e. \
oily. No axillary hair was noted. There were no3 F+ E: e; P7 F0 G" h, m
abnormal skin pigmentations or café-au-lait spots.' E: G8 k* I2 L" m* f: H- \- X) k5 }
Neurologic evaluation showed deep tendon reflex 2+
7 {0 x7 n  W% W3 bbilateral and symmetrical. There was no suggestion
8 d  x" [+ W+ q: N# z9 [of papilledema.
% b! E# Y/ Q* ~" ALaboratory Evaluation
6 L7 h& F6 h& y) n* S$ j# \7 TThe bone age was consistent with 28 months by2 R$ z' d& l' q1 s+ U) T
using the standard of Greulich and Pyle at a chrono-
) r6 o. a2 D) J6 k1 ?- Y7 vlogic age of 16 months (advanced).5 Chromosomal
, _. l1 K# o) E+ dkaryotype was 46XY. The thyroid function test
5 B, g7 y5 ]6 w) ?$ g3 N3 rshowed a free T4 of 1.69 ng/dL, and thyroid stimu-* r, K# ~; `: q0 i1 k/ M
lating hormone level was 1.3 µIU/mL (both normal).
8 k1 K  R8 O  i$ \The concentrations of serum electrolytes, blood9 _6 y; L( i1 m: Q+ o) A8 }$ D4 D
urea nitrogen, creatinine, and calcium all were4 }/ ]9 Y3 {. S* ^
within normal range for his age. The concentration8 s; ], C; T( n9 i4 {
of serum 17-hydroxyprogesterone was 16 ng/dL
: K4 \$ S) g8 [(normal, 3 to 90 ng/dL), androstenedione was 208 Q: w/ N2 U( N; i5 z3 z3 V
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
" u0 I! [3 r  V2 e% K; uterone was 38 ng/dL (normal, 50 to 760 ng/dL),% t% x+ J4 i; i! j, b' U# X1 X0 H
desoxycorticosterone was 4.3 ng/dL (normal, 7 to3 ]* K2 P; j3 ]3 ^
49ng/dL), 11-desoxycortisol (specific compound S)' @8 s% Y+ ?" s' U
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
, J1 k) O/ @/ r# E% w) n% P$ Ftisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total; G/ k. x) o9 A6 j% B
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),& b. |3 |2 Y$ k) n. i" Q2 W
and β-human chorionic gonadotropin was less than
9 ^# ]3 j6 g9 S' \# x( T5 mIU/mL (normal <5 mIU/mL). Serum follicular0 A3 ^9 t" [% X2 ?
stimulating hormone and leuteinizing hormone: }0 {) e- d% G
concentrations were less than 0.05 mIU/mL
6 h8 o0 \0 z" s( I4 d(prepubertal).
) |1 Q% a$ y# Q2 Z7 wThe parents were notified about the laboratory# \; k' [' J* `# `9 J
results and were informed that all of the tests were! d1 o% I* f6 ^: G
normal except the testosterone level was high. The
. c" `0 {/ U; C: S( ^  Zfollow-up visit was arranged within a few weeks to5 P6 d$ M/ ]( x$ a9 K
obtain testicular and abdominal sonograms; how-% w; d, p: [/ v) m! _; i
ever, the family did not return for 4 months.
9 H% h2 e' X( @' ~- yPhysical examination at this time revealed that the3 L. g/ j2 x- Z6 [
child had grown 2.5 cm in 4 months and had gained8 y9 f( j" y2 m7 Q
2 kg of weight. Physical examination remained, X" u, `8 j5 u" g
unchanged. Surprisingly, the pubic hair almost com-
4 D$ U' _- |/ Q, Z; G6 spletely disappeared except for a few vellous hairs at
5 a4 I9 v  W9 h9 v$ S! Mthe base of the phallus. Testicular volume was still 24 X" \& |6 n9 q% I% a) ?
mL, and the size of the penis remained unchanged.* e1 {# b% x/ s9 c  `  |4 q
The mother also said that the boy was no longer hav-! q& S4 j0 I/ z& o/ o4 R: }: G
ing frequent erections.
) r; ~: k/ D, w+ ]9 `* L, S8 nBoth parents were again questioned about use of1 o6 B, E' O1 h5 {4 V  y& p) C  O2 A
any ointment/creams that they may have applied to6 G$ p# e+ d' P3 d
the child’s skin. This time the father admitted the
; K. U* U+ \5 d% `Topical Testosterone Exposure / Bhowmick et al 541
3 U: h! S1 W7 huse of testosterone gel twice daily that he was apply-0 N/ T6 W4 r* l: j3 r# L
ing over his own shoulders, chest, and back area for! ^4 x9 _7 J2 U2 _
a year. The father also revealed he was embarrassed
- g8 P$ R- O& K9 v) Nto disclose that he was using a testosterone gel pre-/ V: O) m# g/ u
scribed by his family physician for decreased libido0 T6 `: z$ ~  V' c- R' Q0 z
secondary to depression.
  W' V+ W9 ~  h. t. X0 V  EThe child slept in the same bed with parents.# H* p+ f3 H3 y* }8 z
The father would hug the baby and hold him on his# U, m" \3 J, `% U* {
chest for a considerable period of time, causing sig-- e2 B( E7 J: U! w+ i) D3 \# S) Y
nificant bare skin contact between baby and father.
1 b* ]5 A8 [8 G) P/ a+ C7 QThe father also admitted that after the phone call,
1 L  }% J: n; a: l& o8 Kwhen he learned the testosterone level in the baby
4 i: u' b, b- |0 x2 E7 B! Mwas high, he then read the product information3 H' r8 E8 X( c0 N. l9 f/ W) u
packet and concluded that it was most likely the rea-
' ^3 r, Z+ H4 U+ j4 ]& x; Wson for the child’s virilization. At that time, they9 g5 I" {- i; u9 \6 C1 S
decided to put the baby in a separate bed, and the
' p2 q0 O" y* }5 Ffather was not hugging him with bare skin and had
3 N* {5 R% A- Z8 l, ?/ r+ x( {been using protective clothing. A repeat testosterone! t8 v+ g& @7 E: V( |2 C& Y
test was ordered, but the family did not go to the+ ?2 l4 c/ e6 {* |. P, {
laboratory to obtain the test.
; w9 p8 Q3 F& @( m% Z; GDiscussion2 H* q; S+ K$ X% U
Precocious puberty in boys is defined as secondary% m, Y7 ~0 d: n5 Z4 ~2 [
sexual development before 9 years of age.1,4
. c% j0 I5 ^2 UPrecocious puberty is termed as central (true) when
( L& g9 k! w' A8 Qit is caused by the premature activation of hypo-8 \4 ?9 s$ r7 R
thalamic pituitary gonadal axis. CPP is more com-5 N2 Z/ {! K6 }0 |
mon in girls than in boys.1,3 Most boys with CPP6 u5 G% t) s  l) x9 @9 L
may have a central nervous system lesion that is
& X2 N$ C" v+ Q# W: |responsible for the early activation of the hypothal-- I' P- E" B! V- z( u
amic pituitary gonadal axis.1-3 Thus, greater empha-+ z3 _; x! |8 J7 ^9 X
sis has been given to neuroradiologic imaging in% y3 _1 a& b4 A& H
boys with precocious puberty. In addition to viril-9 T) X/ @: m. S* x; H5 S
ization, the clinical hallmark of CPP is the symmet-
, |4 W$ g; L: J; H" @- Y1 Jrical testicular growth secondary to stimulation by5 O8 `! w' i3 ]) W
gonadotropins.1,3/ _5 p/ l7 ?6 \. B6 Y
Gonadotropin-independent peripheral preco-
; q) }# @* n0 u, L' y& q$ `7 xcious puberty in boys also results from inappropriate
( J) N( ?6 P; y3 k7 pandrogenic stimulation from either endogenous or. e4 i1 r/ t) a4 ?
exogenous sources, nonpituitary gonadotropin stim-# s$ O7 I' V& e) V: m: n0 o+ V
ulation, and rare activating mutations.3 Virilizing1 w: Q8 L7 c: q
congenital adrenal hyperplasia producing excessive
+ z; E/ t1 X( A! h; H+ ~# a  Xadrenal androgens is a common cause of precocious* Y. Q2 I& T5 J4 E2 g$ F
puberty in boys.3,44 t, `8 S* b8 y" ~( l
The most common form of congenital adrenal
2 T, O) m6 b7 F# m" E! S2 e2 Lhyperplasia is the 21-hydroxylase enzyme deficiency.
' D5 K, T( T9 Y. W& _% m% XThe 11-β hydroxylase deficiency may also result in1 M2 f- F5 H# \6 @
excessive adrenal androgen production, and rarely,
2 D+ R4 z/ m) [. [# [: ?. t+ ran adrenal tumor may also cause adrenal androgen6 b7 S. L- J) j
excess.1,3
/ m3 v/ ?7 s0 q% y* b( eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 }" K- o5 s5 _$ N% h  S+ g# ]
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007* s; a# T2 ], \
A unique entity of male-limited gonadotropin-% \+ p7 s  g2 t' }2 \4 N! p/ C
independent precocious puberty, which is also known$ P4 M' S1 b$ ^7 \6 }" c: F
as testotoxicosis, may cause precocious puberty at a3 u- Q- t7 X' ~4 c0 j/ H: N/ V, Z
very young age. The physical findings in these boys
6 Y, H% t2 }5 c9 H" J1 uwith this disorder are full pubertal development,+ o/ h; y8 Z( Q# C: Z) m
including bilateral testicular growth, similar to boys
9 T- l6 j; Q, \with CPP. The gonadotropin levels in this disorder% x4 r: {8 Z: P8 X5 p
are suppressed to prepubertal levels and do not show
( \9 p, h5 O5 p- j, a& q  x. u0 Upubertal response of gonadotropin after gonadotropin-
/ E) y) ^( N: ?1 t$ L4 y6 zreleasing hormone stimulation. This is a sex-linked
& z( Z4 _1 e! }& Wautosomal dominant disorder that affects only: _# X2 ?5 \- b& n+ F0 H
males; therefore, other male members of the family
0 [0 T) l/ j7 N* g% N2 I, dmay have similar precocious puberty.3
  Y9 Y7 f! ~# s$ v+ v" ]In our patient, physical examination was incon-
) Y+ o5 G. @" n8 _$ `, }sistent with true precocious puberty since his testi-
6 ]9 b; u8 V' e! d* E0 scles were prepubertal in size. However, testotoxicosis
7 a& v; D+ C% p% Z  Vwas in the differential diagnosis because his father
8 t; d+ e1 ?! o  Estarted puberty somewhat early, and occasionally,* R4 ?6 |% s6 ?' h# E/ t
testicular enlargement is not that evident in the
8 E1 V6 W9 ^; v  ?0 U% W, _beginning of this process.1 In the absence of a neg-2 m0 S5 n$ O& F* H, H
ative initial history of androgen exposure, our+ [- @, q- |" X8 E2 @7 Z# S
biggest concern was virilizing adrenal hyperplasia,
, k, D0 I2 J6 leither 21-hydroxylase deficiency or 11-β hydroxylase* _. j/ a1 e! i4 i; Q; T2 r! |
deficiency. Those diagnoses were excluded by find-* _, H0 r  }; v0 f' X0 q' b; a/ U
ing the normal level of adrenal steroids.
! q( D1 q! D9 T1 X, I1 [+ BThe diagnosis of exogenous androgens was strongly8 n6 T  B( G% I2 q! z
suspected in a follow-up visit after 4 months because
; J$ l6 p8 l* a/ U9 O1 D" w7 Sthe physical examination revealed the complete disap-
( |$ A& b3 _7 [0 s( W. J  upearance of pubic hair, normal growth velocity, and
. i0 p7 E: q9 L7 C4 t' qdecreased erections. The father admitted using a testos-
1 H7 d7 ?' Q+ {( ~# B8 ^terone gel, which he concealed at first visit. He was
2 v" M. M& O+ i5 ?using it rather frequently, twice a day. The Physicians’3 Q" ]5 h( y7 j4 Z
Desk Reference, or package insert of this product, gel or
& N5 u5 i- e" m1 W: mcream, cautions about dermal testosterone transfer to
, [+ Y) g7 u- f1 S& tunprotected females through direct skin exposure.& j: D8 B  `4 K4 t; J' A
Serum testosterone level was found to be 2 times the
5 U( S, T( Y+ r% F  o! M; o& qbaseline value in those females who were exposed to
5 G5 c9 A3 G+ L; j* ieven 15 minutes of direct skin contact with their male7 J) E" u8 ^9 v: h: x
partners.6 However, when a shirt covered the applica-
: b* e1 z2 [$ t* B$ G) k) i( }tion site, this testosterone transfer was prevented.; R1 O, B7 z9 V$ _& P7 |" n" \( M, b) _
Our patient’s testosterone level was 60 ng/mL,
& S, ]9 E; p5 A/ |% dwhich was clearly high. Some studies suggest that
9 i  n1 W1 j: U/ y; }; ?7 Ldermal conversion of testosterone to dihydrotestos-/ N8 I3 i* v8 G: c5 W! w
terone, which is a more potent metabolite, is more
) ^" n, A: T! aactive in young children exposed to testosterone+ o( E6 R8 O2 ~4 P4 O, C
exogenously7; however, we did not measure a dihy-# E5 Y9 q  P" E! `' I1 }" G  K
drotestosterone level in our patient. In addition to
/ A6 h6 s4 J8 G2 S/ o+ R) F4 Jvirilization, exposure to exogenous testosterone in
1 c6 x) L* }* Dchildren results in an increase in growth velocity and
% t( c. e) \/ U$ e8 eadvanced bone age, as seen in our patient.6 p# @! Z$ ?2 F9 a1 }3 k, d0 m
The long-term effect of androgen exposure during4 n; h/ N5 l' }+ C9 I+ V7 u% a
early childhood on pubertal development and final/ A, P3 r5 G0 o- B0 \: E
adult height are not fully known and always remain
( o5 Z0 m' l; z  S+ aa concern. Children treated with short-term testos-" l9 M6 J  |) ?9 M, k. q# \
terone injection or topical androgen may exhibit some
; R% C# g  P- F4 N- w! a7 xacceleration of the skeletal maturation; however, after: [6 T3 V* d! ^' N
cessation of treatment, the rate of bone maturation
% c! m" f' \! Ldecelerates and gradually returns to normal.8,9. ^0 Q, ~, P$ P1 C- K" W
There are conflicting reports and controversy
1 \9 ]0 {) t( b1 x( F$ `* v# Yover the effect of early androgen exposure on adult
: H. `& x$ Q* f" j  mpenile length.10,11 Some reports suggest subnormal
* m* _2 o/ {& u* p' f2 A6 J7 Tadult penile length, apparently because of downreg-+ B: A$ v2 v1 u* G3 d
ulation of androgen receptor number.10,12 However,
" _$ r- j1 f5 V7 E* |+ J# |Sutherland et al13 did not find a correlation between
5 h% O, ?( j) H6 B. g3 xchildhood testosterone exposure and reduced adult
5 d$ P* D  c. M+ X0 D+ A9 Xpenile length in clinical studies.7 j. k& v7 |+ C( b
Nonetheless, we do not believe our patient is& c: |1 j/ T, `' }5 ?+ L
going to experience any of the untoward effects from
3 q' _' S8 o8 `testosterone exposure as mentioned earlier because
" G/ }" k" q, K5 S7 P+ Rthe exposure was not for a prolonged period of time.3 `; D) ?+ f  d9 T
Although the bone age was advanced at the time of
/ y0 C5 @, y+ gdiagnosis, the child had a normal growth velocity at6 b# `! Z1 f5 E* y8 {% t+ V
the follow-up visit. It is hoped that his final adult. `- q! i7 X# @% S! L5 }
height will not be affected.7 S9 \. S0 a6 |- \. g: z
Although rarely reported, the widespread avail-' ^/ V) u9 W) ~7 F. V3 }  J5 {
ability of androgen products in our society may# p  [( O) g7 M! t
indeed cause more virilization in male or female, ?! Y+ L+ `5 c
children than one would realize. Exposure to andro-& c' W% L* F& y+ b' J( _
gen products must be considered and specific ques-
: u1 p5 j( T: ?/ N6 E1 A7 Qtioning about the use of a testosterone product or
) K8 s3 I' I9 A; U9 c  Ngel should be asked of the family members during
8 l3 J  y9 R8 s& l+ M9 A7 mthe evaluation of any children who present with vir-
3 h# }- c- \- v. silization or peripheral precocious puberty. The diag-
+ B, V6 T# o% {1 V3 Anosis can be established by just a few tests and by4 R% V- z; K6 I$ z5 z4 `
appropriate history. The inability to obtain such a6 r8 K  \/ n. W
history, or failure to ask the specific questions, may! @$ R# ?# `5 ?. i( \1 x+ f
result in extensive, unnecessary, and expensive! m% I" C* ]' J2 l* W0 S+ L- x, }
investigation. The primary care physician should be
' x! l6 y- z) R- vaware of this fact, because most of these children
9 o% J7 F' \; W) ~+ g7 A5 Qmay initially present in their practice. The Physicians’
9 g; A1 H! a5 r# W" v; x+ Z3 KDesk Reference and package insert should also put a% ~' S$ ~2 {  Y, H
warning about the virilizing effect on a male or" [- l: m3 q: O: |
female child who might come in contact with some-5 R; D" T9 i" P( V* L$ o
one using any of these products.
* s6 N, W' X* Z# M) c5 gReferences
4 z1 @% F' H  f3 x1. Styne DM. The testes: disorder of sexual differentiation$ M- }! V' n) L# D) K
and puberty in the male. In: Sperling MA, ed. Pediatric* l" T$ V) G$ W7 W
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
: _$ e$ s% r  G$ z" i/ M! X" m2002: 565-628.
7 I0 u, m/ w% [2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious. v, [, C6 Z/ r; x
puberty 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

" w; B* y. [0 L' m6 X$ j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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