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Sexual Precocity in a 16-Month-Old
  x. ^  s* z- B5 ^9 DBoy Induced by Indirect Topical* {: n- v" {1 e6 a# c3 U& }+ X
Exposure to Testosterone/ W3 ?2 r9 t2 z* h1 j
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
4 S; n% G7 D  G: Q" C  X4 land Kenneth R. Rettig, MD1: Q. v% E0 H0 B* M& U
Clinical Pediatrics6 `; J  Z. ^$ n
Volume 46 Number 6
1 C6 c! G+ q8 WJuly 2007 540-543, H( p" o8 J' T5 j
© 2007 Sage Publications
1 m- |4 [5 d* w1 n10.1177/0009922806296651$ i/ `/ W7 p- R& i8 W8 Z% K" w
http://clp.sagepub.com2 Z0 ?+ S" w* Y8 d
hosted at3 [7 i, N3 z" o& z! X% g
http://online.sagepub.com
; u' L* h7 M4 V0 d& y! K' SPrecocious puberty in boys, central or peripheral,2 G+ o% E! Q, ?+ c0 _+ q
is a significant concern for physicians. Central
& H6 x) |8 F( v0 qprecocious puberty (CPP), which is mediated
6 h" E6 ~8 B! d2 l$ C. h- n* m& gthrough the hypothalamic pituitary gonadal axis, has( @  e, }/ X% F
a higher incidence of organic central nervous system# F  ^, G0 E! C1 e/ a, k: R
lesions in boys.1,2 Virilization in boys, as manifested; O8 b& |# T5 [) j5 Q
by enlargement of the penis, development of pubic
/ h, _/ b0 `! Lhair, and facial acne without enlargement of testi-0 {- I0 Z, y/ ^1 L1 U% H5 h
cles, suggests peripheral or pseudopuberty.1-3 We7 h$ k( B3 I+ W4 ^0 A2 U
report a 16-month-old boy who presented with the1 k4 |1 X: X  H; S4 E% n
enlargement of the phallus and pubic hair develop-4 h: H1 u' @# a8 E9 |
ment without testicular enlargement, which was due
& w2 c5 Q% Z5 x& J# n9 A" fto the unintentional exposure to androgen gel used by
  r7 b2 c, @4 `+ Hthe father. The family initially concealed this infor-  |/ x% Y  @4 x
mation, resulting in an extensive work-up for this
; B' ^2 _. E+ Z  ochild. Given the widespread and easy availability of! [) D2 S/ O. m
testosterone gel and cream, we believe this is proba-
! l) x# G9 @/ {( Ibly more common than the rare case report in the0 ?3 W; e" j) j" L/ M9 Z
literature.4, U1 q" R2 Z* A2 A/ [
Patient Report# B& ~' }/ @' x  V
A 16-month-old white child was referred to the' L+ \. q( T+ |9 d2 @. E9 e( N  L
endocrine clinic by his pediatrician with the concern
/ m% m- v/ e/ U1 ~3 b& wof early sexual development. His mother noticed0 w  Z& R6 D! I+ \) g6 [  {) i0 }
light colored pubic hair development when he was
% u; z: N/ N  B: LFrom the 1Division of Pediatric Endocrinology, 2University of
3 q# r. t3 D+ c9 c5 d1 Y$ hSouth Alabama Medical Center, Mobile, Alabama.6 d$ f' @+ A+ Z
Address correspondence to: Samar K. Bhowmick, MD, FACE,
7 y% m9 B* x; R, zProfessor of Pediatrics, University of South Alabama, College of
4 B6 q7 C% \+ G! m) [5 kMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
4 e; W% c. r- T: P. ue-mail: [email protected].
7 a$ x6 I4 }; w! Vabout 6 to 7 months old, which progressively became
1 r. o! l5 g$ ]/ Z- U( a4 a! @darker. She was also concerned about the enlarge-# s5 q- R4 D0 a3 H# M2 G
ment of his penis and frequent erections. The child
/ P+ O5 Z9 F0 C9 twas the product of a full-term normal delivery, with% S+ a4 \6 h: G7 S% V
a birth weight of 7 lb 14 oz, and birth length of0 T6 A3 E) s$ U2 F1 d' K0 T+ I# Y
20 inches. He was breast-fed throughout the first year
$ N/ i& N7 k+ x  k  G8 {of life and was still receiving breast milk along with$ h: Z$ y" i% L* b
solid food. He had no hospitalizations or surgery,
. |/ i( B: H2 {1 c  w8 r2 sand his psychosocial and psychomotor development
1 M2 j* P; p6 C0 f6 ~was age appropriate.3 u( I7 T. k, ~+ t& C/ `
The family history was remarkable for the father,% g& @4 n4 n( Y) n1 s, f0 W
who was diagnosed with hypothyroidism at age 16,9 ]3 o* U4 P( s: \% `+ h6 r# [6 o. U
which was treated with thyroxine. The father’s
  `9 p; m; l$ f7 e  Q4 |height was 6 feet, and he went through a somewhat
- g& F5 V7 D8 q) O0 S$ I0 G- ?  V2 jearly puberty and had stopped growing by age 14.
( y- N  P" S' `The father denied taking any other medication. The; ^8 ^; U( [. {+ |/ P
child’s mother was in good health. Her menarche0 }% i1 P. a9 T
was at 11 years of age, and her height was at 5 feet
- o. j" A! c0 l/ |: _5 inches. There was no other family history of pre-! {8 Q$ N: f! l4 q) T7 b
cocious sexual development in the first-degree rela-
- V! V- A! O- q4 ztives. There were no siblings.
9 O1 |0 T; R3 _: R5 YPhysical Examination7 p6 A! K3 J7 W) e5 Y8 w5 B7 C
The physical examination revealed a very active,
9 K, a0 Q9 X2 e1 m/ f: v" @playful, and healthy boy. The vital signs documented5 w$ Z$ E3 K+ C
a blood pressure of 85/50 mm Hg, his length was
. k+ v% r9 ~  T5 e$ z9 I90 cm (>97th percentile), and his weight was 14.4 kg
/ q& Q0 @2 H1 z, \% ?, w(also >97th percentile). The observed yearly growth
4 i& x& R  v, j. C  c4 P, C9 G+ pvelocity was 30 cm (12 inches). The examination of- ]! l9 X7 I7 |, v+ R
the neck revealed no thyroid enlargement.
6 w' L: l* v( E) N" U: \The genitourinary examination was remarkable for
( b& ^( T3 b# F: \9 ]enlargement of the penis, with a stretched length of
7 u- k% W* ^) Y8 cm and a width of 2 cm. The glans penis was very well( `$ p# r5 X& e! [& U/ j5 [1 ^
developed. The pubic hair was Tanner II, mostly around
8 T: \9 E/ |" x% Q3 I  W1 E0 k- V: |. k540: ^. }* T$ X+ Z* h4 n, O' u- E
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 R* t2 X  M1 L4 K# ythe base of the phallus and was dark and curled. The5 r& Q. Z9 b  \- Z! ~7 g& Y3 o# d
testicular volume was prepubertal at 2 mL each.
# D7 z; e& q6 @3 @. GThe skin was moist and smooth and somewhat
2 T! l7 A% m: Qoily. No axillary hair was noted. There were no; p: N% e% {  ^2 w
abnormal skin pigmentations or café-au-lait spots.9 U* n9 l- @9 H6 W
Neurologic evaluation showed deep tendon reflex 2+
( x5 B& ~. h9 F. G# K; x) Obilateral and symmetrical. There was no suggestion
; r5 ~" L* }( h4 F' p4 H  t9 Dof papilledema.& Y8 l" h3 j+ o4 N  F+ E
Laboratory Evaluation3 P  ~& ]4 U* @6 P/ t
The bone age was consistent with 28 months by
1 q" u% R- F6 p, Busing the standard of Greulich and Pyle at a chrono-, i' M3 F4 n& a1 v. h: F
logic age of 16 months (advanced).5 Chromosomal
7 s% Q- k0 s# F! p7 Q' b3 k6 |- tkaryotype was 46XY. The thyroid function test- b  v  e/ O2 `9 s8 F% b# O( Q
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
" I2 _+ {, B+ Y# r! C# glating hormone level was 1.3 µIU/mL (both normal).( ^. k& }0 w6 G# s  M8 s
The concentrations of serum electrolytes, blood  }: R' G6 Z( v
urea nitrogen, creatinine, and calcium all were
/ a% z* Y+ T8 O3 _( vwithin normal range for his age. The concentration" v& c5 o0 [- H
of serum 17-hydroxyprogesterone was 16 ng/dL
* V* n' g) Z# n( Z) i9 X0 J(normal, 3 to 90 ng/dL), androstenedione was 20) n5 \' V6 h' ~0 t3 o
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
% m) |- ~9 ^, S3 M" Xterone was 38 ng/dL (normal, 50 to 760 ng/dL),# W2 _' y& {8 d3 y8 V# s
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
) |, E8 g6 y1 ?49ng/dL), 11-desoxycortisol (specific compound S)) x  _: p( J' q
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-  E2 @$ N% U2 R8 i& t" y* I  K
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
6 y3 z& |! w7 ~( Vtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),) A/ E) V3 s: `# m8 m; V
and β-human chorionic gonadotropin was less than
6 B3 g2 Q5 H+ N( t5 y4 E5 mIU/mL (normal <5 mIU/mL). Serum follicular3 r# W5 ~9 I1 u! Y* P
stimulating hormone and leuteinizing hormone
* k5 t) i! I$ \" Fconcentrations were less than 0.05 mIU/mL( ~) B) A' ~" i! r" {3 o! J
(prepubertal).% L% [* _' h4 z- ~  @
The parents were notified about the laboratory, k- D5 B# L7 q8 J( q, o# e  ]2 |
results and were informed that all of the tests were
- b$ E; {3 }9 ^3 j! E0 d0 }normal except the testosterone level was high. The4 y( {, M% |' \# I+ r
follow-up visit was arranged within a few weeks to
% z. o: c) y) _3 _: Zobtain testicular and abdominal sonograms; how-
7 M* s! O8 O2 cever, the family did not return for 4 months.
) L% m- K, T: |" M; J" ?7 t5 bPhysical examination at this time revealed that the
5 v: @/ u0 p7 y7 \! u1 jchild had grown 2.5 cm in 4 months and had gained
. Y" ~& w$ `2 `2 Y2 kg of weight. Physical examination remained
2 g* e; x# P8 Ounchanged. Surprisingly, the pubic hair almost com-
; f/ h  N# o6 Hpletely disappeared except for a few vellous hairs at4 i& [+ X7 n9 U) _
the base of the phallus. Testicular volume was still 2
0 m3 f1 C5 K4 A2 HmL, and the size of the penis remained unchanged.
1 S+ k& I) C& J# r  sThe mother also said that the boy was no longer hav-
' z+ d* U, g2 q/ _- j; z) H3 ying frequent erections.: `8 y, }& e3 O9 a
Both parents were again questioned about use of
2 n% a7 _6 e  `any ointment/creams that they may have applied to
) e# G: g( H  w3 p: {+ y  h1 Xthe child’s skin. This time the father admitted the
, U- s7 C- q/ g  H$ ~/ eTopical Testosterone Exposure / Bhowmick et al 541
* v5 t4 Q- J! x" l* Yuse of testosterone gel twice daily that he was apply-8 J! A2 |. d7 G+ C8 b
ing over his own shoulders, chest, and back area for/ Z1 l3 A/ j" X$ f" h- d) c
a year. The father also revealed he was embarrassed
9 A0 h7 M, A: I3 E5 Bto disclose that he was using a testosterone gel pre-( c( `, L$ w/ p7 U8 a
scribed by his family physician for decreased libido
; l9 ?1 l9 j9 R8 r& b6 d) c9 Ksecondary to depression.
; m; e% n: a) s, D) s$ ]; bThe child slept in the same bed with parents.4 d' B* X( N% B" a7 ]# l. E6 ]
The father would hug the baby and hold him on his
0 O  A7 P2 y' p- F) Y( rchest for a considerable period of time, causing sig-
: Z  n( S! ?9 j0 s4 ~% P3 E9 Rnificant bare skin contact between baby and father.; \* ~& B( f0 ]0 {0 C' J
The father also admitted that after the phone call,
& p2 S4 _6 r1 J% B6 Cwhen he learned the testosterone level in the baby8 ?  v2 l: ?7 w
was high, he then read the product information2 Z# }( w) o& e- [% g8 H- S; `
packet and concluded that it was most likely the rea-
* P9 K. h6 Z; Z) R3 t( T/ E2 |son for the child’s virilization. At that time, they- {9 Y, x6 x5 `% L" n
decided to put the baby in a separate bed, and the1 N* M6 t' K- B
father was not hugging him with bare skin and had
1 C0 R, B3 N; N$ qbeen using protective clothing. A repeat testosterone0 J3 q5 k/ Y1 c- _. k& k( v$ B, S* T6 t' [
test was ordered, but the family did not go to the
8 \0 F5 A4 P3 nlaboratory to obtain the test.
: L% |3 X$ t5 M6 zDiscussion( ~! Z* o! c* W1 h& _* N3 p
Precocious puberty in boys is defined as secondary
  E$ i; p, p5 l- Ksexual development before 9 years of age.1,4& x+ Q# X& [6 N/ ~
Precocious puberty is termed as central (true) when3 A# U( |6 P2 W3 x
it is caused by the premature activation of hypo-
+ v& I' w3 H9 h: S5 P8 Cthalamic pituitary gonadal axis. CPP is more com-
2 Y9 s6 G, r6 Y4 |8 d7 J7 o" bmon in girls than in boys.1,3 Most boys with CPP4 L/ W9 @2 [/ g
may have a central nervous system lesion that is; \4 K# D. v+ U2 a& Y9 q
responsible for the early activation of the hypothal-8 u/ \4 N/ h* y; J" h2 ?
amic pituitary gonadal axis.1-3 Thus, greater empha-
3 ^6 X$ X/ f& ?1 E& c: usis has been given to neuroradiologic imaging in
$ d6 U& ^/ B2 @) ]boys with precocious puberty. In addition to viril-0 k6 W& V( H/ a! k! p+ Q
ization, the clinical hallmark of CPP is the symmet-" n; o5 T9 G- q) r$ Y# ?( Z) `
rical testicular growth secondary to stimulation by
8 Z& _% V, D  J) m9 ggonadotropins.1,3
  @$ I2 Z2 h3 r: ?5 k3 C1 ]" cGonadotropin-independent peripheral preco-
5 l& H1 ~2 {) f; Vcious puberty in boys also results from inappropriate
8 y8 S# R3 T: L* [# fandrogenic stimulation from either endogenous or
) Y0 c1 L- s% k1 q! i, \, A' Mexogenous sources, nonpituitary gonadotropin stim-
7 }: z6 N. E1 X' V; ?ulation, and rare activating mutations.3 Virilizing
7 J9 i  Y. Q# ^" C2 c& {9 pcongenital adrenal hyperplasia producing excessive
! N: r+ n" b' k% E3 u/ }- Qadrenal androgens is a common cause of precocious
% w0 a: ?1 o# b1 c4 n! R$ `puberty in boys.3,4' c: P+ m2 P$ H1 `* y4 C
The most common form of congenital adrenal
+ S# A+ j* T# O# Z  b/ R+ Lhyperplasia is the 21-hydroxylase enzyme deficiency.
7 x: i& D' L- o5 J) k5 QThe 11-β hydroxylase deficiency may also result in
0 s0 d9 v+ i/ \/ P' f. X! X1 @" Yexcessive adrenal androgen production, and rarely,7 O6 Q+ v$ O6 L& s* h, T, h
an adrenal tumor may also cause adrenal androgen
1 L5 \9 K- R  i. Q& v1 A% C% i6 Bexcess.1,3
0 E# v- E8 }; M% e& A( k* Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' m/ L1 u  Z; N9 k
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
. A4 K  v/ l4 }; x+ m! p8 F( _) GA unique entity of male-limited gonadotropin-" o2 S; d4 n+ x$ u
independent precocious puberty, which is also known& u8 S# J; f1 T& y
as testotoxicosis, may cause precocious puberty at a7 N/ i& l/ z4 A" ]
very young age. The physical findings in these boys, v1 s2 N: P; p8 i3 J. R' {% i
with this disorder are full pubertal development,
- W& G8 ?" e6 Qincluding bilateral testicular growth, similar to boys5 b: S/ E$ p" M0 }$ y/ @
with CPP. The gonadotropin levels in this disorder
( f& S7 E" L! V5 f1 S5 f. Qare suppressed to prepubertal levels and do not show
: {2 |/ e9 N" Y5 K7 m+ a- Bpubertal response of gonadotropin after gonadotropin-! @+ B, i: r4 l+ V+ ?
releasing hormone stimulation. This is a sex-linked: J' Z' B1 E$ d$ H/ a
autosomal dominant disorder that affects only7 B& K0 G: n0 @% |& U  w
males; therefore, other male members of the family& t/ M' X( c  V* H# B) W
may have similar precocious puberty.3
6 X. R* J) n$ S; a6 w0 m* RIn our patient, physical examination was incon-
8 W- o( k; ~$ y$ U6 ssistent with true precocious puberty since his testi-  J3 q, h4 }9 X1 o
cles were prepubertal in size. However, testotoxicosis
) k  p: n* Q  I- O$ r% i( s7 x0 Nwas in the differential diagnosis because his father
1 X6 Y4 B% t# t5 G; ]6 p0 \& ]4 Ystarted puberty somewhat early, and occasionally,0 S: O3 K1 I: D+ V) F' @
testicular enlargement is not that evident in the* V" P5 a/ E! }7 F6 r
beginning of this process.1 In the absence of a neg-( n/ r3 g* }' k1 i9 p
ative initial history of androgen exposure, our# H9 k; S# w5 p
biggest concern was virilizing adrenal hyperplasia,) l) l4 J* L/ k4 t+ j* I
either 21-hydroxylase deficiency or 11-β hydroxylase- U' [2 O6 c% J, h
deficiency. Those diagnoses were excluded by find-
! M2 ?2 V# S% k" |7 ?4 `, ping the normal level of adrenal steroids.! G- [* a9 `/ r" ?7 L7 q3 Z% j
The diagnosis of exogenous androgens was strongly
6 x+ Y# e* S/ f5 b. ^) ususpected in a follow-up visit after 4 months because6 b- v; N; ^# e6 [! B" h: V/ c* `+ Q
the physical examination revealed the complete disap-4 ^# {: Q2 \" s% d0 T9 C5 b
pearance of pubic hair, normal growth velocity, and
8 r0 q/ a* F: B: }decreased erections. The father admitted using a testos-% |- S0 E' a- R1 Z; X
terone gel, which he concealed at first visit. He was
9 C- s  ^5 ?3 s( v5 Dusing it rather frequently, twice a day. The Physicians’$ ?: Z) O/ M* q8 ^4 L' d& {: J) M3 j
Desk Reference, or package insert of this product, gel or" d1 f4 W& U6 y7 \: L; G
cream, cautions about dermal testosterone transfer to
* B7 q; s) C. j5 xunprotected females through direct skin exposure.+ L  z$ _- O6 _' w& m- O( m
Serum testosterone level was found to be 2 times the
% s3 S- |) }; J; H( n1 e9 pbaseline value in those females who were exposed to
' Z- j% V7 B% Ceven 15 minutes of direct skin contact with their male0 k' W. G( d  G$ G2 y, ~# X
partners.6 However, when a shirt covered the applica-
7 t+ r& u0 ^. W" |8 @* Btion site, this testosterone transfer was prevented.  R* i" G; |. X' ^
Our patient’s testosterone level was 60 ng/mL,$ ]9 R& o- E- Q; D
which was clearly high. Some studies suggest that* Y4 \: K' A6 p9 U# X3 y: G
dermal conversion of testosterone to dihydrotestos-
7 A- L! K+ m/ Q( ^5 t) o( w5 U2 E$ @terone, which is a more potent metabolite, is more0 Z  A& c# m7 s( o$ x+ j) X  T
active in young children exposed to testosterone, W+ ^* {/ `# ?$ z
exogenously7; however, we did not measure a dihy-: G1 `; `. `  s: Q8 L" F
drotestosterone level in our patient. In addition to
6 d3 S- Z6 F0 d% rvirilization, exposure to exogenous testosterone in8 n; v5 W4 s: C# K
children results in an increase in growth velocity and
) B6 @) X1 H. u! B# ladvanced bone age, as seen in our patient.# _0 h9 n; L+ u! [0 i1 O/ Z
The long-term effect of androgen exposure during
. g3 L# x% S4 w8 W6 zearly childhood on pubertal development and final1 ~6 Q& Y4 L. f: F7 ?! W
adult height are not fully known and always remain
  w. {% U3 Q9 ]% k! k7 M* Oa concern. Children treated with short-term testos-2 u1 x5 i6 ]( P. i' r; f
terone injection or topical androgen may exhibit some
" U. [  z/ v3 @acceleration of the skeletal maturation; however, after
: C4 V" w1 M! ucessation of treatment, the rate of bone maturation
8 ?8 `. p# N# r8 o% S( Hdecelerates and gradually returns to normal.8,9( T& i3 w" g% |
There are conflicting reports and controversy% j/ s* E1 q+ ]& I  ^6 B: F& Y
over the effect of early androgen exposure on adult. l& g6 ]4 j6 Y4 z' M8 a8 }) @: X/ _
penile length.10,11 Some reports suggest subnormal
; l& |8 N0 _8 h; v1 _: E% _adult penile length, apparently because of downreg-. r2 {+ y1 v, U  j
ulation of androgen receptor number.10,12 However,
8 Q3 D! d' l- l) }" C2 eSutherland et al13 did not find a correlation between3 |3 D/ h. ~  d% d  D. [1 D2 h
childhood testosterone exposure and reduced adult
$ y( d$ o* {# xpenile length in clinical studies.
5 H; B3 Q$ ]3 u1 y/ ]6 ?  aNonetheless, we do not believe our patient is
: C" K% A$ Z% {going to experience any of the untoward effects from$ v) V3 E* M3 ]- ~' N7 O$ k
testosterone exposure as mentioned earlier because! h" [" r7 I/ N0 r/ n1 }
the exposure was not for a prolonged period of time.
, r% \5 P' c  \$ R! QAlthough the bone age was advanced at the time of2 R# `6 g$ ^7 W+ O5 ?7 A! ^
diagnosis, the child had a normal growth velocity at0 {' z, N' A& p/ e& |) |# F  B
the follow-up visit. It is hoped that his final adult, Y/ Z: U' y& C  v& z
height will not be affected.- @5 P" f! X1 `. V9 I% ]8 ~
Although rarely reported, the widespread avail-
6 n; R. R8 d' Q' Bability of androgen products in our society may% J1 a. D: Q# C& e  ^
indeed cause more virilization in male or female
, t1 {2 e  j# A, `. L5 O5 hchildren than one would realize. Exposure to andro-) k8 ~: g, o7 L/ U* C
gen products must be considered and specific ques-
) S: O0 \4 h7 P/ [! H: jtioning about the use of a testosterone product or6 n. }/ X7 O( ]5 r" r# F
gel should be asked of the family members during0 r( h: \) v% C5 v% ~- v, I
the evaluation of any children who present with vir-
( a7 W$ g7 z" x2 o$ b" yilization or peripheral precocious puberty. The diag-
. _! X9 {5 ^7 c& U2 x9 ^+ h8 Jnosis can be established by just a few tests and by" ]5 F5 U# ]/ w" W/ o+ j/ q4 h
appropriate history. The inability to obtain such a
" K& ^5 d" V! o1 |+ khistory, or failure to ask the specific questions, may" h3 X3 h3 h6 {# p* b- v; ?( ]( T
result in extensive, unnecessary, and expensive
) l5 @+ ]+ j' {6 Zinvestigation. The primary care physician should be- F3 ?1 w8 e) i: W  t$ l% J' p6 t
aware of this fact, because most of these children2 L; C- D# W; q$ }# U7 o" ~
may initially present in their practice. The Physicians’" o1 |  e4 S& y/ }5 S4 X4 d- @
Desk Reference and package insert should also put a
! t3 ^1 L! T$ P) V' u; `3 o7 swarning about the virilizing effect on a male or
  p. H7 w3 f" ~- ?" T0 lfemale child who might come in contact with some-1 x- V, P, q' K/ H3 v
one using any of these products.
+ U% x4 `8 X# `  D" z: _- sReferences* `# |4 G" v6 f8 H' R, A( F4 C
1. Styne DM. The testes: disorder of sexual differentiation6 P2 n& _' B8 P, H
and puberty in the male. In: Sperling MA, ed. Pediatric
- J/ Q5 y2 `( M, S, xEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;8 Z* {) |. D3 A' G! K" n9 f% w" [
2002: 565-628.4 B7 O9 W2 U. x: u' ~+ M* ^
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
* [! c+ l1 X/ g5 n2 Q2 j6 N2 tpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
/ [( {) {, E/ z+ x$ R& a9 mBoy Induced by Indirect Topical/ i" ~( n; q! _8 U4 R0 v, t8 M5 G
Exposure to Testosterone5 C7 f0 C- I( F1 I9 @
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 V3 q4 y7 S; n8 s8 n) U2 Land Kenneth R. Rettig, MD13 e1 }4 R# I  \" X$ F" S
Clinical Pediatrics
3 S" w+ c* n# W( p5 v4 AVolume 46 Number 6
; g# \8 ^& M% Z% b* q0 sJuly 2007 540-543
6 P5 _6 H6 V; U- |/ U© 2007 Sage Publications
4 y3 t" o2 L* A7 K& F) x10.1177/00099228062966511 w" d, d) ?9 K  p- E
http://clp.sagepub.com
& v3 V$ N0 J' [hosted at) q( \' c. `8 V2 a1 K( E* N
http://online.sagepub.com
. w! a- p: m9 H, [" ePrecocious puberty in boys, central or peripheral,
2 x  g- b# ~( ~1 O) ^is a significant concern for physicians. Central) p! @  E( W1 G) x6 h
precocious puberty (CPP), which is mediated
. g6 _9 i7 s( q. N& k% Gthrough the hypothalamic pituitary gonadal axis, has, N3 l& E0 b) ^- f& U
a higher incidence of organic central nervous system
' e7 j9 f" H) m4 F& Clesions in boys.1,2 Virilization in boys, as manifested3 o& n) M1 W. L
by enlargement of the penis, development of pubic1 T' Q$ _& C; ~5 g
hair, and facial acne without enlargement of testi-2 o9 k$ G% {7 ~6 f# Z$ i( H
cles, suggests peripheral or pseudopuberty.1-3 We+ J8 ]3 |/ s# g
report a 16-month-old boy who presented with the
% Z* n5 }" D/ Fenlargement of the phallus and pubic hair develop-& n9 g$ e2 y# H. R( i' O
ment without testicular enlargement, which was due! v8 h3 i7 I9 m; B. K, H
to the unintentional exposure to androgen gel used by5 J. p7 z( i2 C* N/ D7 _9 T
the father. The family initially concealed this infor-) d7 W' Q* I- l( l% G$ ?/ }6 ~
mation, resulting in an extensive work-up for this
9 ?& u% J2 ]' p* x: G5 r. a! L. Pchild. Given the widespread and easy availability of3 f/ d3 k: `# o$ ]; Q: W- s
testosterone gel and cream, we believe this is proba-
- S4 J6 W( p/ [bly more common than the rare case report in the
, b0 [4 V4 x5 P( e, J/ y3 _literature.4: }' w2 Z$ \- ~" I' X
Patient Report+ n0 s) @6 {5 C! X
A 16-month-old white child was referred to the0 J& N1 g1 `( N$ Z
endocrine clinic by his pediatrician with the concern
8 j% T+ y4 G. ?( r! Fof early sexual development. His mother noticed! V" ]) L1 K0 n% o1 k2 i3 B+ w
light colored pubic hair development when he was
& O" L) d: C; o4 bFrom the 1Division of Pediatric Endocrinology, 2University of
# U' J% _1 l6 |5 CSouth Alabama Medical Center, Mobile, Alabama.
. W) R& U; J, e' g/ v. A9 tAddress correspondence to: Samar K. Bhowmick, MD, FACE,
, z! f, {* j3 b8 Z, Z( }8 [Professor of Pediatrics, University of South Alabama, College of& H2 g2 P% |" {3 v. Z1 S& \5 Q9 f
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
& }% E5 r/ h& G2 r7 l* ?e-mail: [email protected].
4 M6 ?, e9 ~" @( ~: Z$ Jabout 6 to 7 months old, which progressively became4 x& v  i6 F& k% X/ g( m$ i
darker. She was also concerned about the enlarge-
- K" ^) F2 C$ z2 }ment of his penis and frequent erections. The child
3 M$ k/ o& W! Q+ Jwas the product of a full-term normal delivery, with6 C: F1 P9 j6 q* Q+ P# d
a birth weight of 7 lb 14 oz, and birth length of
" f# P" q( G, m& y2 O6 {; t20 inches. He was breast-fed throughout the first year
+ q! d% d8 ~3 ]  y/ Gof life and was still receiving breast milk along with
; k9 {* w) d6 e0 i# ssolid food. He had no hospitalizations or surgery,
! |6 c2 f5 c' @7 p! Dand his psychosocial and psychomotor development4 @) f6 ]# Z3 U' P
was age appropriate.* @- K2 G" n) p4 J0 o' D# E
The family history was remarkable for the father,) V, J  `8 A# |: A  b( T) ]
who was diagnosed with hypothyroidism at age 16,- e# ^- T/ R/ V! f4 T
which was treated with thyroxine. The father’s
9 x8 _, L$ G, R  ^height was 6 feet, and he went through a somewhat
- |$ p6 M2 Z6 U5 l0 H0 C5 hearly puberty and had stopped growing by age 14., f5 o+ [+ i' M
The father denied taking any other medication. The
6 e# _3 Z6 B& a$ `3 s. B' Bchild’s mother was in good health. Her menarche9 }  x( v2 _4 ~: W; q3 c2 d2 i
was at 11 years of age, and her height was at 5 feet
6 N* v6 J; B% S7 I3 Z0 `) S2 z5 inches. There was no other family history of pre-
5 O- |' q  m5 N; Scocious sexual development in the first-degree rela-3 {- u6 ^! X  Z/ P+ K. t7 |# o1 n
tives. There were no siblings.
9 R9 L7 l# L' n! ePhysical Examination
4 D3 S/ w8 p) L/ _The physical examination revealed a very active,
+ q( S$ x% @; H, B. {- K8 ~playful, and healthy boy. The vital signs documented# d2 g& G% R- c1 ]) n
a blood pressure of 85/50 mm Hg, his length was
, [3 W! ?' t- x+ B1 O90 cm (>97th percentile), and his weight was 14.4 kg
7 e# m. }1 t+ z  ?  [(also >97th percentile). The observed yearly growth
  \. `$ u( g/ Mvelocity was 30 cm (12 inches). The examination of% l6 z8 b% W* h, t7 g# D3 ^  h5 o
the neck revealed no thyroid enlargement.$ [' u* }1 o0 M. e; S3 X
The genitourinary examination was remarkable for% ~  }2 F% D8 ~' {1 j$ a9 [, Q& D) ?
enlargement of the penis, with a stretched length of; N6 t6 a+ u# f) b
8 cm and a width of 2 cm. The glans penis was very well
. I6 Z  \* S. Ideveloped. The pubic hair was Tanner II, mostly around
3 k4 x* A8 ?: G5 \. R, D( g540
( h/ ^) ^6 x' }) C+ P8 Pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% g; [2 u2 A3 [' D  C' c
the base of the phallus and was dark and curled. The
( {  t# `( t7 }testicular volume was prepubertal at 2 mL each.
- u$ c5 b( c& d, g0 QThe skin was moist and smooth and somewhat$ U# v5 [7 ~2 d% C) p, X0 `4 [4 J; u
oily. No axillary hair was noted. There were no
) t! [  ]0 J" Z( wabnormal skin pigmentations or café-au-lait spots.
4 _$ _+ g% M5 f% l* KNeurologic evaluation showed deep tendon reflex 2+" C. @2 V$ @* _: z/ X
bilateral and symmetrical. There was no suggestion
7 |- h3 d6 f% ?( l+ {6 D# Dof papilledema.2 ~% I3 b) E4 l
Laboratory Evaluation
; u7 Z2 O# S" o- LThe bone age was consistent with 28 months by
; ]3 |3 A: t7 h1 n/ p. dusing the standard of Greulich and Pyle at a chrono-" [& r1 _: Y" {* o6 H" o
logic age of 16 months (advanced).5 Chromosomal
; T3 C9 ~# ]/ Rkaryotype was 46XY. The thyroid function test
/ Q$ P# m0 V" ?- p: u8 Y7 fshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
8 p( [- H3 m0 R, a- D$ U! Jlating hormone level was 1.3 µIU/mL (both normal).
7 u: Y; L1 U. t" w3 gThe concentrations of serum electrolytes, blood
4 J; K5 Z5 B, a6 B, Rurea nitrogen, creatinine, and calcium all were# o7 D' V7 {# B( w$ U5 d
within normal range for his age. The concentration
* W( ~) s3 F6 T2 q: y1 I' ?of serum 17-hydroxyprogesterone was 16 ng/dL" j# m4 {/ q' X0 M% Y
(normal, 3 to 90 ng/dL), androstenedione was 20* O/ P% Z, F7 X) P) o, a
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-3 }% I9 v+ K0 f! M
terone was 38 ng/dL (normal, 50 to 760 ng/dL),% T& G% X: T' Z2 f7 a0 f
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
0 q: t4 |# {1 e  j. r3 w; ?/ M49ng/dL), 11-desoxycortisol (specific compound S)
, w6 |/ y+ V1 E. l; ewas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-6 Q5 w6 Q; J( Q! T- |$ P7 a2 r
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
  X$ C" U' @! h7 F' r' c# S% gtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
  n/ ]4 L, `) r* E5 m" sand β-human chorionic gonadotropin was less than
# g$ ]" `5 I. f, c" q5 `5 A) n( J5 mIU/mL (normal <5 mIU/mL). Serum follicular6 l+ I% i6 K" L0 F3 h
stimulating hormone and leuteinizing hormone% d$ R( c5 e" o. N
concentrations were less than 0.05 mIU/mL7 D8 |/ q+ Z9 g% {7 a8 P$ j
(prepubertal).# D- G' ~' b+ ^/ K4 r
The parents were notified about the laboratory$ q* c0 N& p9 G5 j: s8 k
results and were informed that all of the tests were( p3 W+ O/ j7 o
normal except the testosterone level was high. The
. F5 J$ {5 k+ r; D% Hfollow-up visit was arranged within a few weeks to. y! _3 a+ s4 i/ l- k
obtain testicular and abdominal sonograms; how-
: K& M& y# U6 t+ y7 l/ ?5 Never, the family did not return for 4 months.; O* m+ {. t0 Y4 K2 d, K4 K$ p3 E3 S
Physical examination at this time revealed that the+ p% l9 T, W4 V' s
child had grown 2.5 cm in 4 months and had gained
5 F) w3 d, H" C$ ^% \* `- t2 kg of weight. Physical examination remained; `* b& I" s+ i" o! }1 L
unchanged. Surprisingly, the pubic hair almost com-
: N/ d/ B3 X6 ?% J4 c! p3 apletely disappeared except for a few vellous hairs at8 f$ Y% K4 W( }. Z- Z
the base of the phallus. Testicular volume was still 2
; r6 S- A% x# f. }mL, and the size of the penis remained unchanged.# X1 x3 i; P- ~
The mother also said that the boy was no longer hav-
& X! F2 |; [2 K. k$ c6 oing frequent erections.
; z1 _) T, Q) r: U5 GBoth parents were again questioned about use of1 G- U6 L, F+ Q1 p. f6 p% x0 S
any ointment/creams that they may have applied to
: z' ]- O' i0 G2 i. t, M) Q. ?2 Qthe child’s skin. This time the father admitted the% t1 L3 V: ]3 k2 L8 N+ a2 N
Topical Testosterone Exposure / Bhowmick et al 541
! g2 B6 l. f" J: I9 W5 B3 D1 yuse of testosterone gel twice daily that he was apply-
" m5 J0 j/ z# q% j2 {0 v- King over his own shoulders, chest, and back area for
* A. e) \" q' xa year. The father also revealed he was embarrassed9 o& `! w. b5 E$ Q, \
to disclose that he was using a testosterone gel pre-
* m1 q" `0 M$ |scribed by his family physician for decreased libido
& t5 P( w/ H' U. Nsecondary to depression.
0 c- i% Z2 L( W, rThe child slept in the same bed with parents.
5 {. V& d; c5 {  tThe father would hug the baby and hold him on his( X" L+ |8 a! S* ]
chest for a considerable period of time, causing sig-- d% e/ B: {8 s" f/ a8 c4 c
nificant bare skin contact between baby and father.
7 k; x2 @4 J9 F8 r9 h. _8 d; u5 ?The father also admitted that after the phone call,8 y4 y& e9 g9 S# Q- {
when he learned the testosterone level in the baby
7 d- Q$ Y8 z* h9 P# \was high, he then read the product information% e/ a2 A7 d( R* @4 @
packet and concluded that it was most likely the rea-
, `% T, D# Y4 ^. ?2 Gson for the child’s virilization. At that time, they
' L2 |; @+ G9 b* w; p$ H& c- s6 edecided to put the baby in a separate bed, and the4 o  |1 [" e$ a. G2 |6 E4 y" E
father was not hugging him with bare skin and had. |8 F3 Y/ X, Z; U" V  t
been using protective clothing. A repeat testosterone1 s* ~& x3 D( q6 n
test was ordered, but the family did not go to the5 o- X$ g0 u; `
laboratory to obtain the test.
  q  ^0 |7 X- o  F) j8 ^Discussion- y9 q0 L+ Z# ?
Precocious puberty in boys is defined as secondary. o1 X; z# B0 u7 h8 s2 n
sexual development before 9 years of age.1,49 q. W. J1 Z: [
Precocious puberty is termed as central (true) when! o3 _# M# y8 @& [) U
it is caused by the premature activation of hypo-& o- V" g4 x, S- k* v
thalamic pituitary gonadal axis. CPP is more com-
  M8 @. k" q1 ^& D1 {; E% X% R6 pmon in girls than in boys.1,3 Most boys with CPP
, G0 n/ o( N/ T; g# jmay have a central nervous system lesion that is( I: t* I6 ~( r' h: L" z
responsible for the early activation of the hypothal-
! a  a3 g% {  M/ q# V3 e& T8 Mamic pituitary gonadal axis.1-3 Thus, greater empha-
% ?, v+ K1 V# ]2 R3 Z2 A6 Msis has been given to neuroradiologic imaging in  q" C2 r  d+ z5 i* m/ [
boys with precocious puberty. In addition to viril-9 h' L- f3 s" @7 u0 q- R
ization, the clinical hallmark of CPP is the symmet-0 H* K1 l! |6 M. p
rical testicular growth secondary to stimulation by/ F7 i2 R& s- m! H
gonadotropins.1,3
. \# X7 O: r& @/ d. jGonadotropin-independent peripheral preco-
( s3 ~3 g: t1 x: m8 F6 bcious puberty in boys also results from inappropriate
' N( C) D1 n1 n% D* A5 m9 vandrogenic stimulation from either endogenous or+ ?# U5 S1 |& n' T
exogenous sources, nonpituitary gonadotropin stim-8 _7 {2 a5 G3 d) Z3 n. h& G0 e
ulation, and rare activating mutations.3 Virilizing
: J2 M# g$ y( `0 j  Wcongenital adrenal hyperplasia producing excessive  ^; S! s+ V& [6 W, p- n9 J9 W
adrenal androgens is a common cause of precocious
. m0 Y* \' @' S. F# M6 ^3 q1 Ppuberty in boys.3,4
, n" d' y( a" SThe most common form of congenital adrenal9 E) P' D0 r: y
hyperplasia is the 21-hydroxylase enzyme deficiency.) C# A5 g  c0 ^" B1 p: x
The 11-β hydroxylase deficiency may also result in- Y7 t6 w& r5 `0 J' f( H. s
excessive adrenal androgen production, and rarely,
7 s/ [7 j3 K0 ^* K9 J  a% W5 Nan adrenal tumor may also cause adrenal androgen
  ?7 L& I0 R, ~* ]: x+ jexcess.1,3
" F  {; w2 Z$ g8 i' J% {4 j# Cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' A8 u$ T& G: {2 |2 G  {
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
- w! v- P1 I3 b) b2 pA unique entity of male-limited gonadotropin-; P1 s* b( X  v% L# U0 o
independent precocious puberty, which is also known) X' ^: M% T7 j1 x: l
as testotoxicosis, may cause precocious puberty at a
+ [5 q# W" a6 ^4 ~+ }* r) Lvery young age. The physical findings in these boys4 l$ Y) W0 w' z- O* z6 n& ?1 G) F
with this disorder are full pubertal development,
2 j# f# M" w) E5 M4 G) C6 j! ]. vincluding bilateral testicular growth, similar to boys; }+ s8 Q& p' @" X
with CPP. The gonadotropin levels in this disorder
4 Q4 k$ z. \0 l: @are suppressed to prepubertal levels and do not show
6 _" C- U8 X1 f/ ?9 _- O+ Jpubertal response of gonadotropin after gonadotropin-' I( W( N$ B" x- ?  `
releasing hormone stimulation. This is a sex-linked7 Y$ i- B: F% G5 ?! s) ]
autosomal dominant disorder that affects only' w7 v9 X% {8 e& X! A9 V
males; therefore, other male members of the family8 d# r( }% c7 P! Z3 E) f1 m
may have similar precocious puberty.3
; j3 t) c/ W4 B. F# G) jIn our patient, physical examination was incon-
( Z  R' b7 ~, U3 P. vsistent with true precocious puberty since his testi-
8 N# v2 ]; T  z8 B& p: D8 ]- H, V/ _+ ]cles were prepubertal in size. However, testotoxicosis
- i/ d( s4 V# e' D0 ~' `was in the differential diagnosis because his father
, @  |  j( L1 Z0 U. Z5 Zstarted puberty somewhat early, and occasionally,
% V  ^& q2 q- A+ ]* }/ P1 xtesticular enlargement is not that evident in the
, I5 D9 c; n5 z4 ^$ _: Ubeginning of this process.1 In the absence of a neg-( k2 P, h, b) Q7 ~% N: l
ative initial history of androgen exposure, our/ K) A9 n9 B1 F( s
biggest concern was virilizing adrenal hyperplasia,7 G  I- r6 B: n! V
either 21-hydroxylase deficiency or 11-β hydroxylase
# a  `; F4 X4 L' ]deficiency. Those diagnoses were excluded by find-
9 s1 [, Q3 `# x$ ring the normal level of adrenal steroids.
' p' f; {/ G/ xThe diagnosis of exogenous androgens was strongly
+ R$ @3 G! `" T8 p) r- ssuspected in a follow-up visit after 4 months because/ K# y/ d3 Y+ x5 K1 F2 a
the physical examination revealed the complete disap-
+ c2 E: I8 z' Q1 d( Epearance of pubic hair, normal growth velocity, and
2 w1 B) A& t: D# gdecreased erections. The father admitted using a testos-( f5 k+ q6 A2 o3 M) m$ [( [
terone gel, which he concealed at first visit. He was
2 q2 l" C, ~# |/ ?using it rather frequently, twice a day. The Physicians’
! a5 I1 d, T! t0 d; w6 p3 Y* oDesk Reference, or package insert of this product, gel or
/ ]: q7 I) B4 j, P2 |- Ecream, cautions about dermal testosterone transfer to
+ n' r& C7 S' D1 ^unprotected females through direct skin exposure.' [' Q- Y" k# Z" W7 ~! T
Serum testosterone level was found to be 2 times the8 h( k* V; w+ K" M# Z7 f
baseline value in those females who were exposed to
( i" q- z1 u, O5 a& }9 v5 b2 x/ O/ eeven 15 minutes of direct skin contact with their male
5 r& a! A* e" @$ f2 Y; Xpartners.6 However, when a shirt covered the applica-
, z: N1 ~, x) Ztion site, this testosterone transfer was prevented.
* E8 S, w! y9 b/ q  aOur patient’s testosterone level was 60 ng/mL,
+ M, A! I# O4 {/ _! m" iwhich was clearly high. Some studies suggest that, b# R5 g& S+ g. z4 L9 v
dermal conversion of testosterone to dihydrotestos-2 }& L0 q( h" t; x. Y7 P
terone, which is a more potent metabolite, is more( n( I  _$ R- v. Q5 J
active in young children exposed to testosterone
& ?% a1 o/ V% q* R' O: E( uexogenously7; however, we did not measure a dihy-4 }  f$ |1 G  u2 d* c  F
drotestosterone level in our patient. In addition to% O( @! b& d, W! @9 E
virilization, exposure to exogenous testosterone in
. p  {0 x) x) Q& j2 a( ]1 K- Fchildren results in an increase in growth velocity and
- Q$ x# \  H0 \* D5 tadvanced bone age, as seen in our patient.
  g6 U+ p- @& ?" R. T# R) TThe long-term effect of androgen exposure during& I: M8 b, D0 _
early childhood on pubertal development and final
# a" E  Q1 n6 p" V0 H8 iadult height are not fully known and always remain
1 `0 |+ Q/ H2 n0 C  m; h* ja concern. Children treated with short-term testos-
; e; |( |. Z4 _terone injection or topical androgen may exhibit some8 M0 S* Z9 \! m- F( z# M; E
acceleration of the skeletal maturation; however, after
, u: n" |8 Q. ucessation of treatment, the rate of bone maturation6 M. |& e# V) ~; t  E3 p" |( l
decelerates and gradually returns to normal.8,9$ T* w. |+ q* t4 `/ O) B
There are conflicting reports and controversy2 \5 F: X: t' ~
over the effect of early androgen exposure on adult
" Q8 o& @9 z+ ?' i8 zpenile length.10,11 Some reports suggest subnormal  D# I& S9 P# [* [; S* M
adult penile length, apparently because of downreg-
8 U: q- }: J1 U+ X* q: Vulation of androgen receptor number.10,12 However,
, B( V0 ^; b9 tSutherland et al13 did not find a correlation between* k' k6 s: t% k% z8 Y7 G  c5 i
childhood testosterone exposure and reduced adult
8 U& z) [! m! ~  ^3 z' _3 Dpenile length in clinical studies.
" ~  B  n, w# V  ?# }Nonetheless, we do not believe our patient is
% \! E1 C6 R; D& B$ kgoing to experience any of the untoward effects from
6 g2 t3 \( q" y5 g/ C% Ztestosterone exposure as mentioned earlier because
4 Z- @! s/ t2 @3 r5 F  Z! _the exposure was not for a prolonged period of time.0 q( J' ^# m" S% }, C
Although the bone age was advanced at the time of
8 d7 V$ u3 j8 Y  U) {1 U2 @  v) Pdiagnosis, the child had a normal growth velocity at
1 K% b$ z1 G, S- c" cthe follow-up visit. It is hoped that his final adult
* u$ R; t* y- Y8 w: P3 u' G/ uheight will not be affected.- J* Q. Z7 S$ L' c# t' P
Although rarely reported, the widespread avail-3 q6 j) K9 K9 g
ability of androgen products in our society may3 k: {6 S$ r* a* K1 j2 q# k, F
indeed cause more virilization in male or female
% A. n' I# n$ o0 w' f2 u, t, Zchildren than one would realize. Exposure to andro-2 [' a, M8 l: z  h. O# N
gen products must be considered and specific ques-
+ U8 r/ w2 \/ h% btioning about the use of a testosterone product or$ |3 Z6 J, C' x+ V9 L* w6 T
gel should be asked of the family members during1 f4 G+ P5 M8 o$ ~/ @9 W
the evaluation of any children who present with vir-' g; n, k- z% K5 }/ y# Y' t& g! O
ilization or peripheral precocious puberty. The diag-( r) i% A2 D# z9 e6 U3 c2 x
nosis can be established by just a few tests and by; o: I1 g% e# N, y3 T
appropriate history. The inability to obtain such a
9 Y5 B& j6 z# |history, or failure to ask the specific questions, may
1 n8 z. J; M7 T. I7 B: ~9 R. cresult in extensive, unnecessary, and expensive$ n' E( H- x4 X! v+ `3 B
investigation. The primary care physician should be
1 t; {+ t6 S' s# f# Yaware of this fact, because most of these children' f. _2 X$ T" U- B; I
may initially present in their practice. The Physicians’5 `) A1 b3 c- V* p1 o5 A
Desk Reference and package insert should also put a( E" T& [% u& i1 `3 j
warning about the virilizing effect on a male or
# O, Q& |$ R2 s1 ]; K% D! c9 @female child who might come in contact with some-; U( i7 ]  ?3 r  \: k; x. `3 c
one using any of these products.* g+ y8 s( R9 b
References% H% H3 b9 F& q4 H8 d8 `- r
1. Styne DM. The testes: disorder of sexual differentiation
' p$ q) F0 C. {' Oand puberty in the male. In: Sperling MA, ed. Pediatric
+ @$ `& ?7 K) C+ g" @% oEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;- u# E. }+ A6 J8 w0 r4 h
2002: 565-628.
4 J4 C3 ~2 X' ^2 a' v2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious5 N# W1 h' d2 b( \
puberty in children with tumours of the suprasellar pineal
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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
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

9 F8 t" `* L: V9 B) e2 Y% H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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