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Sexual Precocity in a 16-Month-Old
2 i6 Y+ |( B: v# x. \3 n4 ]6 O' rBoy Induced by Indirect Topical1 m$ [) H. e# u# r
Exposure to Testosterone2 e$ S- H3 {9 o2 F+ g' Y1 P
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2/ E! y% K% k. B# Y7 v
and Kenneth R. Rettig, MD1. X$ S& U3 k" I
Clinical Pediatrics* V4 H4 k, `; ~: ^, P- j
Volume 46 Number 6
( E. e( c. M6 O5 xJuly 2007 540-543, K$ x8 G& i% g: p$ j* j
© 2007 Sage Publications
3 V) b8 Y+ ~, u5 P10.1177/0009922806296651
+ f2 I7 f! E' W  @/ xhttp://clp.sagepub.com
; J( P# O5 f' ~6 {. W4 whosted at
/ W& C1 U. c, }7 k  ?/ S0 uhttp://online.sagepub.com! p5 a: p+ `6 ^2 G
Precocious puberty in boys, central or peripheral,
; `$ A. F* ?, m7 y" D8 }is a significant concern for physicians. Central
; w% i  }# u3 D8 C: s; Bprecocious puberty (CPP), which is mediated3 X5 O# d" h/ h
through the hypothalamic pituitary gonadal axis, has! B8 u# O+ p& Y& h* U, _# S& J
a higher incidence of organic central nervous system* e; d; Y) T/ B1 U3 q' j0 c! u1 [
lesions in boys.1,2 Virilization in boys, as manifested
* c1 T; f8 S& L4 k9 q) `- T: ]by enlargement of the penis, development of pubic
( t7 Q$ z3 y" K" g7 I- Uhair, and facial acne without enlargement of testi-
5 H) N& h& s6 ~, W; o% T$ `, Ocles, suggests peripheral or pseudopuberty.1-3 We9 B; R! @1 J: F  W6 d5 Y
report a 16-month-old boy who presented with the
$ r  U$ y1 w. q8 m1 C1 w# c8 Nenlargement of the phallus and pubic hair develop-3 R! d# W( Y! N& Y) r. \
ment without testicular enlargement, which was due* k* l# w+ {- h- e3 O
to the unintentional exposure to androgen gel used by: D% O+ A/ }! s
the father. The family initially concealed this infor-
# D( B) h) p1 {* H; amation, resulting in an extensive work-up for this
0 p: x4 n; d* p/ P1 `child. Given the widespread and easy availability of
( T$ t; ?9 Q! h1 z8 j5 V' Dtestosterone gel and cream, we believe this is proba-/ T9 S% o+ P' b% [$ @
bly more common than the rare case report in the) w: Y# Z( Q! r8 }8 _5 g  t
literature.4
8 r2 A. K9 X5 i! l% IPatient Report
+ K# W$ V9 p5 C% s/ q$ cA 16-month-old white child was referred to the
1 I( _" E; z% ~endocrine clinic by his pediatrician with the concern
) u/ H' X9 i) Xof early sexual development. His mother noticed; I# T1 c9 H+ \1 ?$ }/ `
light colored pubic hair development when he was
; K! u, z" {8 F3 t: r. }From the 1Division of Pediatric Endocrinology, 2University of" r0 |8 m0 @' O- j: i
South Alabama Medical Center, Mobile, Alabama.
& p2 E  Y& Q9 P9 r* \Address correspondence to: Samar K. Bhowmick, MD, FACE,
. U9 D# @. N% D3 J5 FProfessor of Pediatrics, University of South Alabama, College of& `9 _1 ]5 P. ]0 W8 s8 B1 X
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
0 A1 |3 f* W1 Ce-mail: [email protected].$ P' E# ?3 {2 p
about 6 to 7 months old, which progressively became+ k# p" r. k4 V" A7 }
darker. She was also concerned about the enlarge-
' v' @7 U; E' ~* W6 P; W& u& T  bment of his penis and frequent erections. The child0 \3 \+ w0 C4 T- w1 |
was the product of a full-term normal delivery, with
3 i* t# @3 E5 b0 R9 g+ J- }$ Sa birth weight of 7 lb 14 oz, and birth length of
5 s$ c5 R3 y, x) ~' k20 inches. He was breast-fed throughout the first year
* W6 X1 r8 l4 M& |& Fof life and was still receiving breast milk along with+ a" r$ ?. U2 v* q
solid food. He had no hospitalizations or surgery,! k. i$ M9 z; [) S8 x3 V
and his psychosocial and psychomotor development! U7 y1 F! t- P' @5 b" C! u
was age appropriate.
# m; Y. @) x- W4 C# \% ?The family history was remarkable for the father,
/ \4 {" }1 i& N# ^! l' _# owho was diagnosed with hypothyroidism at age 16,0 f7 w# U% y) X) t
which was treated with thyroxine. The father’s
9 m/ r) V" e6 i& t, iheight was 6 feet, and he went through a somewhat
0 T1 f  ?& ^# f  _early puberty and had stopped growing by age 14.
3 ?& e2 i" a* x- U  pThe father denied taking any other medication. The
) P1 T) k2 [, r+ L6 tchild’s mother was in good health. Her menarche
$ L; K) _* s# P; j7 s+ rwas at 11 years of age, and her height was at 5 feet
0 a+ ?. C' P8 y5 inches. There was no other family history of pre-
, ~" }4 L3 z; g& [: p# Vcocious sexual development in the first-degree rela-# d. m1 q$ N4 F5 m4 h
tives. There were no siblings.% s" V' x% s" b( n+ X, r
Physical Examination
* }$ e6 |& ?' k. |The physical examination revealed a very active,  V' h# R  d5 g+ o, [# B
playful, and healthy boy. The vital signs documented! Z9 y- @# l+ v; h/ d
a blood pressure of 85/50 mm Hg, his length was5 H' O3 }% w! R" W
90 cm (>97th percentile), and his weight was 14.4 kg
! y( V- C' _. Z+ \* d3 q0 y# T* H(also >97th percentile). The observed yearly growth/ ]- f! z$ I+ m+ \- V9 G5 c, @
velocity was 30 cm (12 inches). The examination of/ k, K* f" n; L0 B
the neck revealed no thyroid enlargement.3 y3 m+ z( m5 L" s# D7 X
The genitourinary examination was remarkable for% n  O8 W. D. C7 L
enlargement of the penis, with a stretched length of
$ F  d% ?0 T4 w) e# _$ E) A/ y4 l1 x8 cm and a width of 2 cm. The glans penis was very well. O  N+ o& x7 V, I5 e
developed. The pubic hair was Tanner II, mostly around
! r1 L: J5 E$ ^3 a  ?; M540
! o9 n( q2 f: L6 }at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 j- Q  j2 x  I6 \, A! V1 w! athe base of the phallus and was dark and curled. The
& W! e- ~; g) d2 Z1 p5 c+ stesticular volume was prepubertal at 2 mL each.
3 O9 m1 f, J! Z) c6 H5 D# c" B7 MThe skin was moist and smooth and somewhat- o$ A. s9 G6 l' L( [
oily. No axillary hair was noted. There were no# D7 l& T/ c! }9 [% a' x
abnormal skin pigmentations or café-au-lait spots.
  F( r7 a1 P; F  }) R( ]# |8 vNeurologic evaluation showed deep tendon reflex 2+
# H1 K' X. |/ Y  n# l! sbilateral and symmetrical. There was no suggestion
1 w; a! ]8 }- w7 B! a& bof papilledema.! ^* J( _" m4 k  j) S- W
Laboratory Evaluation
) U: O* v; \0 _# x' z* pThe bone age was consistent with 28 months by2 u6 z; Z" T' p5 }- o: K7 i6 T
using the standard of Greulich and Pyle at a chrono-0 t5 y! {' y% M$ q7 H
logic age of 16 months (advanced).5 Chromosomal+ e0 i% z) R; \' {+ @% f6 h6 p' P9 }
karyotype was 46XY. The thyroid function test+ `$ u  t/ j6 |$ _3 E
showed a free T4 of 1.69 ng/dL, and thyroid stimu-6 t) b1 U/ r  N) G6 |! y+ y
lating hormone level was 1.3 µIU/mL (both normal).0 v4 V4 U' _( D$ ~5 o! j3 F
The concentrations of serum electrolytes, blood
% f. O  z- p* q5 P# e  ]urea nitrogen, creatinine, and calcium all were
! M+ Q$ _9 U2 X; v' f, Rwithin normal range for his age. The concentration
, t$ c$ o) o$ `8 _) H) C( gof serum 17-hydroxyprogesterone was 16 ng/dL3 i) R) x2 I+ z% D3 Y1 F
(normal, 3 to 90 ng/dL), androstenedione was 20
5 \9 I3 R: l5 j4 [6 T0 h, Yng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-1 g9 b+ A" R7 U, s. `$ ~
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
5 _* y5 x0 R) P! i1 @desoxycorticosterone was 4.3 ng/dL (normal, 7 to
8 Y/ [; s7 y! S- L# v* s49ng/dL), 11-desoxycortisol (specific compound S)4 [; X, R5 U' u8 V2 L% |4 P6 N: `
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
) f0 K3 v% ]$ W& Etisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' V* P) S- b3 Q5 {- w
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),+ s% j4 A* [9 h* `
and β-human chorionic gonadotropin was less than
# A" I/ U7 M; Z# c5 mIU/mL (normal <5 mIU/mL). Serum follicular5 M, i$ T: D4 ~+ G: v6 I1 k" ?
stimulating hormone and leuteinizing hormone9 |% k7 h, \7 A" P2 v
concentrations were less than 0.05 mIU/mL5 W8 N7 I3 K. f+ e; n! ^$ j) r9 ~& n
(prepubertal)." N0 {$ E5 n! @! D; q' Q! d) n! s
The parents were notified about the laboratory. b* E2 v. e% }/ i7 b* {; b
results and were informed that all of the tests were
% @* k( w$ N. @) h- S/ N2 J. onormal except the testosterone level was high. The
; B& Z* V9 v- |  W- J$ cfollow-up visit was arranged within a few weeks to: O/ z# S2 F- w' F+ k7 T2 j
obtain testicular and abdominal sonograms; how-
- {; K1 F( J" t2 X5 X7 @ever, the family did not return for 4 months.
. ^6 F7 S: V7 p* G# N8 @, UPhysical examination at this time revealed that the
% J8 G, R4 a# G* {# g/ Pchild had grown 2.5 cm in 4 months and had gained( ^! V$ f1 _3 ?! D; W. c9 I* s) x2 Z" J
2 kg of weight. Physical examination remained6 C# N, O" a- n9 I- e3 z
unchanged. Surprisingly, the pubic hair almost com-8 i2 O$ C0 j% N6 W7 t" Z3 N3 f
pletely disappeared except for a few vellous hairs at/ z  R( D  \! p) m
the base of the phallus. Testicular volume was still 2
; ?8 V) L! |; F6 ~, j! X/ j2 ymL, and the size of the penis remained unchanged.
; c+ _! ]9 T& U0 GThe mother also said that the boy was no longer hav-
' Z5 Q% E3 x* z& ging frequent erections.
/ i8 Z! t4 e3 _, y* Z/ pBoth parents were again questioned about use of
& I! h- p7 `% v* vany ointment/creams that they may have applied to0 H$ |* D( _6 X" y" s
the child’s skin. This time the father admitted the( m# E: ^5 D" J' \/ g0 x+ ~
Topical Testosterone Exposure / Bhowmick et al 5416 k* z& e" J5 ]
use of testosterone gel twice daily that he was apply-
% D  F% g% F& d  Ting over his own shoulders, chest, and back area for! P0 I( {: m0 v$ G0 _: x) v
a year. The father also revealed he was embarrassed
& g! I* r2 D) O- K. m7 `3 e6 Pto disclose that he was using a testosterone gel pre-
+ _8 d+ H) i! @* i1 w# _scribed by his family physician for decreased libido: Q9 h, P* \# `/ r
secondary to depression.
* @) g6 X9 s$ }2 ?9 p( t2 L3 f5 RThe child slept in the same bed with parents.
( q/ U! c1 ?: y) t) A$ [, eThe father would hug the baby and hold him on his( v- ^1 g. w$ L3 W+ x/ ?' v1 j
chest for a considerable period of time, causing sig-7 z3 p: Q; T1 U7 P5 q. C
nificant bare skin contact between baby and father.
" c7 b$ J2 K, r: P( U# k& V5 X" iThe father also admitted that after the phone call,
  K5 n- v5 L; R: i# `' B; Qwhen he learned the testosterone level in the baby
# m% `- n) u' I" M4 E$ |5 [was high, he then read the product information& q& ^3 j. b+ O9 Q- D
packet and concluded that it was most likely the rea-
9 n4 t9 y8 O% x# B2 @" M- S; Kson for the child’s virilization. At that time, they, g) ~( m; [2 e! i1 Q9 P
decided to put the baby in a separate bed, and the; |# w. [2 Y, k7 D4 P
father was not hugging him with bare skin and had
/ D: D% Y  j- g. k( d5 n* sbeen using protective clothing. A repeat testosterone
* Z: i. v' o" t# v, p. Jtest was ordered, but the family did not go to the+ p7 N/ F' d8 y9 W, B' ^" Z5 ?
laboratory to obtain the test.0 N# x* O5 ]* B
Discussion7 Z6 I% z& K# n" O1 S' e4 D
Precocious puberty in boys is defined as secondary1 |0 h5 k4 C. I/ r
sexual development before 9 years of age.1,4
+ t/ e9 T5 t1 @; ?6 i, l3 ^/ p$ e6 YPrecocious puberty is termed as central (true) when" t" |0 M5 D2 U) |; K% a
it is caused by the premature activation of hypo-
' z( j8 y3 E8 zthalamic pituitary gonadal axis. CPP is more com-
/ K( I, _" g7 `9 v7 j& C2 A1 V8 smon in girls than in boys.1,3 Most boys with CPP3 o. n& b; z3 k4 P/ p" U
may have a central nervous system lesion that is# K- T$ k- Y! j! h3 c" ^+ D) U
responsible for the early activation of the hypothal-1 b! n- x  k4 `( _9 S
amic pituitary gonadal axis.1-3 Thus, greater empha-
/ l! U- D( F: s0 i/ hsis has been given to neuroradiologic imaging in
. H1 |8 Q" N) l4 W. g9 u2 b# ^boys with precocious puberty. In addition to viril-" L9 [- W1 K# i; ^8 P
ization, the clinical hallmark of CPP is the symmet-+ @# h! m- J9 @5 @" ]
rical testicular growth secondary to stimulation by$ {% x: e$ y5 }* i. i. @& a- f# A9 V
gonadotropins.1,32 z6 Q! W* j; `% ~2 m& J
Gonadotropin-independent peripheral preco-( K$ V& g6 }3 U
cious puberty in boys also results from inappropriate
$ e; G0 v- [1 Iandrogenic stimulation from either endogenous or9 n1 a" v+ {5 U0 D; M! i+ w; a
exogenous sources, nonpituitary gonadotropin stim-$ \! L  k3 A; n+ _
ulation, and rare activating mutations.3 Virilizing8 T( [. u& _& T0 B" x/ _0 F. U
congenital adrenal hyperplasia producing excessive! n: _$ Y- N8 m. W& T0 N5 N% f4 j
adrenal androgens is a common cause of precocious
% K( f* A5 z) J% w5 W/ J/ ypuberty in boys.3,4
- m! T4 n; l! m7 Z5 W. _( pThe most common form of congenital adrenal
& @3 Y7 y: h$ n+ l1 Y7 Ahyperplasia is the 21-hydroxylase enzyme deficiency.
# v0 @( s; y& z+ U3 \3 O+ X) DThe 11-β hydroxylase deficiency may also result in( F9 x2 v, c/ l# }$ i. I
excessive adrenal androgen production, and rarely,
2 `7 R' J; T$ Y6 oan adrenal tumor may also cause adrenal androgen' T5 E# f5 X% v: R" w& y* h" W
excess.1,3
2 l% T+ D" D, t0 Dat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% Z5 O, C, S' @9 k% @. N
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007" f+ o; D4 H0 b# {, i9 _5 E8 o
A unique entity of male-limited gonadotropin-% r1 x9 {2 [- I5 G4 i3 M0 f% ^
independent precocious puberty, which is also known
& K0 F; f) s  c1 \- T4 j; i7 ?# das testotoxicosis, may cause precocious puberty at a( I) L( z. h4 L8 F
very young age. The physical findings in these boys: G7 `( \+ m0 ^& C  t
with this disorder are full pubertal development,
% H+ M5 P* C4 Z. O7 [" Q; mincluding bilateral testicular growth, similar to boys
' z: o; z" R/ iwith CPP. The gonadotropin levels in this disorder& Z$ B; b6 X' `+ x- Y
are suppressed to prepubertal levels and do not show
" ?0 z' P; a  K+ b# z+ bpubertal response of gonadotropin after gonadotropin-
/ v7 I$ d# B3 `releasing hormone stimulation. This is a sex-linked
* i4 t& F7 i) A/ P" J1 V' qautosomal dominant disorder that affects only1 M1 l2 Q/ @/ d! O: q% B! v3 r
males; therefore, other male members of the family) D& `9 C" r, f9 m; X
may have similar precocious puberty.3
3 W* R: o$ n8 [9 w; r' X6 R0 iIn our patient, physical examination was incon-
- I+ H; y" M5 h1 J: {sistent with true precocious puberty since his testi-
2 J! h/ B. l2 _, H6 ^4 Y! pcles were prepubertal in size. However, testotoxicosis
. z, p# n0 w% [9 {2 zwas in the differential diagnosis because his father: w) x* V0 W2 E5 z4 P
started puberty somewhat early, and occasionally,# G/ _7 p1 i+ W
testicular enlargement is not that evident in the5 [; Q: o- h/ G
beginning of this process.1 In the absence of a neg-/ O% r2 l" P2 ~/ s4 E) L  l
ative initial history of androgen exposure, our
2 `" y: n) m% V# tbiggest concern was virilizing adrenal hyperplasia,
: i+ J+ _( M) }! O3 a9 `+ ceither 21-hydroxylase deficiency or 11-β hydroxylase# C# {! l; q0 d2 t4 F" o, K
deficiency. Those diagnoses were excluded by find-
! d8 d  o6 s# Q6 E, v1 }8 Eing the normal level of adrenal steroids.
- i* H; `) v' h7 z& pThe diagnosis of exogenous androgens was strongly
; B  u9 U- d0 ?" S) y+ p9 wsuspected in a follow-up visit after 4 months because
  X" b) x' V5 ~' |: _0 pthe physical examination revealed the complete disap-6 p7 _& o2 \' U2 T; W
pearance of pubic hair, normal growth velocity, and- b% k0 U# x; ~- @7 [2 c
decreased erections. The father admitted using a testos-
/ L* S5 G# k- `5 j5 _' P7 B5 p& Rterone gel, which he concealed at first visit. He was
! l; a  u& K0 U$ R$ `( `  Iusing it rather frequently, twice a day. The Physicians’
  Y3 J6 G9 _) B; D! P% A6 pDesk Reference, or package insert of this product, gel or
/ U3 Q. |7 F% j: U) I2 gcream, cautions about dermal testosterone transfer to
6 |) B' f- s5 S# j. y9 Wunprotected females through direct skin exposure.8 l/ K- L4 L6 e5 T: f
Serum testosterone level was found to be 2 times the& y9 b2 {" x* s& B( z) T( O7 e: ]
baseline value in those females who were exposed to, y3 ~& ~$ H5 \
even 15 minutes of direct skin contact with their male
3 U- W9 e' L( r) J/ ^. s7 p  tpartners.6 However, when a shirt covered the applica-
7 p8 B+ O& z8 T; K" Z0 X3 x3 x: o1 C. }tion site, this testosterone transfer was prevented.
6 w8 j6 }2 S1 ^1 v+ S' u* E1 ]Our patient’s testosterone level was 60 ng/mL,$ h( r- c. j/ U% N- m
which was clearly high. Some studies suggest that' ]8 f# ~. R' x4 f7 l- k9 h4 G) |* T
dermal conversion of testosterone to dihydrotestos-: K0 N- H$ W' Q6 d1 q3 }% r5 w
terone, which is a more potent metabolite, is more  F/ p! D0 Q/ L1 R% x- F8 ^
active in young children exposed to testosterone7 x$ J8 M" g, t
exogenously7; however, we did not measure a dihy-
+ u! b1 {1 v, p8 Idrotestosterone level in our patient. In addition to) s' w4 `$ j9 M5 d" g8 l
virilization, exposure to exogenous testosterone in
5 ~# r; N  u4 K: ^children results in an increase in growth velocity and
0 J: ?" H+ X1 L# |. radvanced bone age, as seen in our patient.
8 ~) v5 M2 J4 y& [& y1 dThe long-term effect of androgen exposure during7 ~* f) s" _" c/ K
early childhood on pubertal development and final
: z; {! J5 |& `5 nadult height are not fully known and always remain
7 e. a+ J2 y( Z% [a concern. Children treated with short-term testos-
( k2 f1 w1 E0 p* ~# L: j7 \& tterone injection or topical androgen may exhibit some
; c9 }  l6 D- d1 r1 A- macceleration of the skeletal maturation; however, after1 d4 n& m' G! d% J9 s8 g
cessation of treatment, the rate of bone maturation0 T; e8 x3 q+ l8 N9 ]! o
decelerates and gradually returns to normal.8,9
- S* @. }5 X7 C, VThere are conflicting reports and controversy
( W* }  V& I7 @0 Nover the effect of early androgen exposure on adult4 J: R6 ^/ v( y9 U4 h: ~8 S5 A8 H
penile length.10,11 Some reports suggest subnormal
. i* b9 w6 [7 ]" N1 S, q7 {adult penile length, apparently because of downreg-
$ X1 d" U( }' s* H: l0 U) T  C( Mulation of androgen receptor number.10,12 However,
0 W7 E- L& F$ g+ nSutherland et al13 did not find a correlation between
9 |9 V$ k5 P9 B  T- T/ y' y* k2 Gchildhood testosterone exposure and reduced adult- U! q- ]( d! [2 X  Z. m
penile length in clinical studies.
& r% n/ V1 B) b$ FNonetheless, we do not believe our patient is
7 m1 P# ]" W9 a! m1 @- q$ y  ~* Cgoing to experience any of the untoward effects from+ `% D0 A9 Q( {) U0 v
testosterone exposure as mentioned earlier because
/ ?7 ^$ `2 x% j8 u: ]( I/ rthe exposure was not for a prolonged period of time.* b  s; _/ f2 Q4 r( S
Although the bone age was advanced at the time of
, R; n; p( S$ k- [* D) r  Q6 ldiagnosis, the child had a normal growth velocity at
4 C6 J+ A7 s( lthe follow-up visit. It is hoped that his final adult  E4 W* C& Z) M5 t( T6 g5 k
height will not be affected.
6 ]/ q5 l5 \5 d: E- \Although rarely reported, the widespread avail-
* n4 R# M6 p. A" h' F* y% [ability of androgen products in our society may5 f! K7 }+ S  L$ g2 L+ P4 D1 }. _
indeed cause more virilization in male or female
/ K$ J" I+ W; o2 Ichildren than one would realize. Exposure to andro-5 U6 ^5 n4 }7 c& N0 e
gen products must be considered and specific ques-
& M! ]. O% |: X0 f0 Gtioning about the use of a testosterone product or* @5 l4 X- l/ A
gel should be asked of the family members during
3 K$ m3 f4 t  ethe evaluation of any children who present with vir-
# }# y7 S& l# R- ~ilization or peripheral precocious puberty. The diag-. E& L8 L" p1 Z: I9 C; F
nosis can be established by just a few tests and by0 p# w( }3 G; v: M( K
appropriate history. The inability to obtain such a
: c6 w. A% d4 [5 B6 b( Xhistory, or failure to ask the specific questions, may
3 ^" q& n0 H  I/ F7 U: vresult in extensive, unnecessary, and expensive
( x5 E* p, Z/ N4 C  Tinvestigation. The primary care physician should be
3 d9 `  m* }$ L' Caware of this fact, because most of these children  b- W# f: |4 P$ O4 l* G. D
may initially present in their practice. The Physicians’2 l# ~/ O: I$ J0 j: [
Desk Reference and package insert should also put a
" Q) c# d, f, Y1 ]warning about the virilizing effect on a male or
: Q8 w0 i& [' m4 @4 ~; r2 Bfemale child who might come in contact with some-
: N1 t+ q% e/ u+ X6 [" kone using any of these products.
7 w& Q  U& C. I( zReferences
8 p2 X% e+ C  L+ {* c1. Styne DM. The testes: disorder of sexual differentiation; k7 E9 j& a" k6 Q( X& L
and puberty in the male. In: Sperling MA, ed. Pediatric) _+ c6 R- I, v; s
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;+ @1 m- {9 X7 X  G) M
2002: 565-628.
6 o$ e7 P, R+ s* i2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious2 V9 Q5 I/ s' b- J% O$ e
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old7 l& w5 p7 d- T# R5 @
Boy Induced by Indirect Topical3 \! O: O* ?% i6 y. D
Exposure to Testosterone6 n0 g3 ^1 A3 O$ w" w0 B3 I4 s  F1 j
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
5 w; q7 u* a: {6 ~and Kenneth R. Rettig, MD1
9 X4 r) |: D9 w9 {3 U8 u# B) _1 `' |Clinical Pediatrics' i/ Z$ o1 w9 W9 M- y' x, H! u
Volume 46 Number 6
' I) C- Z9 [* b1 \8 V5 x  JJuly 2007 540-543
# `. V1 g- F: M- {© 2007 Sage Publications
' h% w, l) g7 A) q3 ]: N3 x+ [10.1177/0009922806296651
6 y% }; t: \  s6 Q; x! M- C1 [http://clp.sagepub.com( w: E8 V/ f" w
hosted at
/ E3 p$ y$ \; t% }# Ehttp://online.sagepub.com3 B& H9 h0 b! R6 A% D: C$ n
Precocious puberty in boys, central or peripheral,
% E9 v& j' s# ?0 C# ?2 R) Lis a significant concern for physicians. Central
/ o( z, y# n+ {3 @2 o- G2 Qprecocious puberty (CPP), which is mediated- ]( l6 }! X- R- v" j
through the hypothalamic pituitary gonadal axis, has
! H9 [' P9 X1 n# D4 ca higher incidence of organic central nervous system
/ q7 A2 @7 j0 g0 Y- d, q6 Alesions in boys.1,2 Virilization in boys, as manifested
) j/ m7 G) O7 }& P6 A% _by enlargement of the penis, development of pubic
" Z' M2 i/ H$ O$ A( @  \hair, and facial acne without enlargement of testi-
! R/ t3 R/ i* dcles, suggests peripheral or pseudopuberty.1-3 We
0 v0 A8 I" Q- t. |5 L1 ireport a 16-month-old boy who presented with the. a8 D, R8 {0 N( t
enlargement of the phallus and pubic hair develop-
7 ?% ]! K' E+ w7 `  h' Ument without testicular enlargement, which was due; x- Q+ W4 r# `7 S+ F
to the unintentional exposure to androgen gel used by
6 D7 N# h, F1 o1 r9 f+ Tthe father. The family initially concealed this infor-
5 f8 q; h# ~' c- z  O2 u5 W) ^mation, resulting in an extensive work-up for this9 S( E4 q% B9 \+ p, S' b. }! V* Q
child. Given the widespread and easy availability of
. ]/ f; O) N' _* H3 L+ {4 {testosterone gel and cream, we believe this is proba-# x4 Y7 J2 \: `  l( g8 k- w
bly more common than the rare case report in the
2 W- y6 J" p! ^3 wliterature.40 M) W& g: |: [7 A  Z+ i! v8 ~
Patient Report
; _2 \) x/ w2 D8 T7 X" D% b6 U8 AA 16-month-old white child was referred to the& @7 k3 z/ n8 g" c
endocrine clinic by his pediatrician with the concern
' c3 E  V4 s- ^of early sexual development. His mother noticed" u" w$ f( N$ y
light colored pubic hair development when he was
/ n# }5 N1 h  c7 AFrom the 1Division of Pediatric Endocrinology, 2University of; G3 x& s5 l$ @$ x$ U' l3 l
South Alabama Medical Center, Mobile, Alabama.% p" g) U' L: W, H( c) n" n
Address correspondence to: Samar K. Bhowmick, MD, FACE,
4 L3 O1 x1 O1 o) K; ?& J, g; ^Professor of Pediatrics, University of South Alabama, College of. f, f. m" I! V1 j# x% `, v
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;8 S4 p; @5 r4 @8 x$ _5 a% l  z$ g8 I! O
e-mail: [email protected].
  x  j4 P" R0 u& f0 H; Nabout 6 to 7 months old, which progressively became& J$ s( e- |' Z" ~' H# Y
darker. She was also concerned about the enlarge-/ R, I: [' K8 s; R: x* M
ment of his penis and frequent erections. The child
1 G' [( L) A0 g" Awas the product of a full-term normal delivery, with
. V7 x4 ?3 p& X4 U# F" |$ Ba birth weight of 7 lb 14 oz, and birth length of
' j+ k' l$ P8 u* X3 R5 ^" x4 R20 inches. He was breast-fed throughout the first year- `. s1 R" W4 R' Y7 F5 |
of life and was still receiving breast milk along with2 `2 l. T, H+ k, S6 r. C" g6 Z
solid food. He had no hospitalizations or surgery,2 X: w" T% y1 Y7 V
and his psychosocial and psychomotor development
/ }8 {$ }+ u& S, v8 c7 I9 k" Qwas age appropriate.
" X; ^) l8 A- Z3 r4 _4 g0 m& nThe family history was remarkable for the father,* |* }4 z4 L" [9 k/ t
who was diagnosed with hypothyroidism at age 16,0 u, F. e4 t" @. L' t/ E5 ?
which was treated with thyroxine. The father’s9 B0 |* |% f; V3 E& z
height was 6 feet, and he went through a somewhat3 n. s% t& u. A
early puberty and had stopped growing by age 14.5 c6 V' Q" d) z( A
The father denied taking any other medication. The+ A  \+ M5 h. @- R9 {- E
child’s mother was in good health. Her menarche7 l4 }$ k9 @3 X
was at 11 years of age, and her height was at 5 feet
5 N4 ~2 U7 k& a1 _5 inches. There was no other family history of pre-
, {+ `& s4 m8 D! l. M) Zcocious sexual development in the first-degree rela-
7 i4 h% r3 f( k% W9 _  G7 rtives. There were no siblings.
  ]$ O2 |' [6 ^! o) R6 pPhysical Examination
* L& E; e6 R4 u& ^0 g6 u, v  E( {The physical examination revealed a very active,$ X4 q+ n8 E" e0 o0 Z$ y* U2 u
playful, and healthy boy. The vital signs documented) a: @: M# F+ J% s
a blood pressure of 85/50 mm Hg, his length was
0 r$ C5 a: J: a" O0 H90 cm (>97th percentile), and his weight was 14.4 kg! F1 `& J  y0 N# i, q  b& X6 }. i
(also >97th percentile). The observed yearly growth$ a: N" {8 e8 o  W9 A
velocity was 30 cm (12 inches). The examination of& w4 p% W/ ]9 F& C3 N8 q6 n8 M
the neck revealed no thyroid enlargement.. j; @5 M& x, U) e; `+ c
The genitourinary examination was remarkable for
$ L/ f5 Q; e+ eenlargement of the penis, with a stretched length of; `6 S7 v& S# f
8 cm and a width of 2 cm. The glans penis was very well8 L% \8 w3 h' H* ]7 w) p& [) e* A
developed. The pubic hair was Tanner II, mostly around
) {8 c9 U) Z& |, H4 ?& B& S540
0 n- g% @7 ]  Jat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 t' s  J$ b/ o6 b' tthe base of the phallus and was dark and curled. The, `9 ~6 U* P8 j- l' m/ g. @' o
testicular volume was prepubertal at 2 mL each./ Q( Z8 u7 ~1 U( }7 M
The skin was moist and smooth and somewhat2 ?0 I* K% Z1 y0 _% X
oily. No axillary hair was noted. There were no4 V: L5 q# R6 f  v! {2 V& w7 ^! A" {
abnormal skin pigmentations or café-au-lait spots.
8 d5 x7 X. l3 Q. y% T5 N) [. y1 q' lNeurologic evaluation showed deep tendon reflex 2+
; A# O, K& a% w/ Qbilateral and symmetrical. There was no suggestion% J( K& }( R1 R) r& p
of papilledema.
/ j* j- P; A9 Q4 Z1 ^- FLaboratory Evaluation6 \# V* [) \! y5 [
The bone age was consistent with 28 months by
1 w6 ?) I( X- X( w/ Kusing the standard of Greulich and Pyle at a chrono-
% D2 e8 u! s* ?: r. Vlogic age of 16 months (advanced).5 Chromosomal$ A" b8 ?! Y5 _& h) O' Y
karyotype was 46XY. The thyroid function test
% q7 c' n2 I% \$ kshowed a free T4 of 1.69 ng/dL, and thyroid stimu-7 i) ^0 g  G7 \& t5 }
lating hormone level was 1.3 µIU/mL (both normal).0 |( m. c+ F  V8 V9 a
The concentrations of serum electrolytes, blood
+ X5 l3 i. _" b. e, Z3 k9 b& w+ S. yurea nitrogen, creatinine, and calcium all were
4 j! ]) V% Z( o: i4 Nwithin normal range for his age. The concentration, r. V3 i) X# G
of serum 17-hydroxyprogesterone was 16 ng/dL. e3 Q3 l3 B- c& M
(normal, 3 to 90 ng/dL), androstenedione was 20; Y/ r2 U4 `  k" k
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
" v$ M6 B- @* R8 B* dterone was 38 ng/dL (normal, 50 to 760 ng/dL),5 `6 I7 @4 q# s5 V+ v3 A
desoxycorticosterone was 4.3 ng/dL (normal, 7 to2 `! E1 ?6 r$ i8 }1 B
49ng/dL), 11-desoxycortisol (specific compound S)' U: V* X0 o( ~3 R: s
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-! P: q( i+ r; O/ n
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total5 m6 ~  D- l  w$ m) |9 ]5 R2 |4 k
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
" k1 H9 L2 a5 q- p4 c7 cand β-human chorionic gonadotropin was less than8 H+ @6 H+ ~- t
5 mIU/mL (normal <5 mIU/mL). Serum follicular6 B0 q2 Q9 m& O4 C6 f
stimulating hormone and leuteinizing hormone7 q+ e% ^' A; f' j8 L8 B& l# K1 ~
concentrations were less than 0.05 mIU/mL
& @3 M% \3 R' A) \- d, V9 a, k(prepubertal).- E4 y* `; ]8 i- f) l% L/ A
The parents were notified about the laboratory
; e% z* r. O$ sresults and were informed that all of the tests were  ]6 w: p3 k+ Y
normal except the testosterone level was high. The; o# l# m" v# @; p7 J; o- }: V
follow-up visit was arranged within a few weeks to2 Y: o7 P! Y8 a
obtain testicular and abdominal sonograms; how-, K1 T2 k: F* J% ]8 a8 [: q! f
ever, the family did not return for 4 months.
+ X4 }6 F# U  jPhysical examination at this time revealed that the
; H; j( n- c- X5 Qchild had grown 2.5 cm in 4 months and had gained9 x0 ~( _: d8 X; y$ n
2 kg of weight. Physical examination remained6 H5 L  P0 m; t8 K4 p' p
unchanged. Surprisingly, the pubic hair almost com-* [8 K' d" R$ u9 e+ y( P
pletely disappeared except for a few vellous hairs at
* f7 ]9 H" C) K$ E( P, ~# N* [the base of the phallus. Testicular volume was still 2
. s# ~" S7 I# c1 R% m* J/ amL, and the size of the penis remained unchanged.0 d! D4 n3 x# W; N9 m5 {9 g
The mother also said that the boy was no longer hav-2 e( g8 {) T3 \. M; v; u
ing frequent erections.
& H8 B( n. y$ `, V6 SBoth parents were again questioned about use of# z* c4 p. s; Q, B5 L
any ointment/creams that they may have applied to
- k- _7 S7 d( }1 zthe child’s skin. This time the father admitted the
: L0 }5 K! D/ l/ eTopical Testosterone Exposure / Bhowmick et al 541" q2 V6 R$ q1 ?7 z  F" y
use of testosterone gel twice daily that he was apply-+ b$ ^; Q, c* x
ing over his own shoulders, chest, and back area for
  Q$ n2 L) ~/ E/ W8 Ha year. The father also revealed he was embarrassed
# S/ C. \! N: R9 K/ a- s/ P% K% rto disclose that he was using a testosterone gel pre-
0 _& l8 z7 B5 X" G: A3 d+ iscribed by his family physician for decreased libido  G: a: P6 @# G2 u) m8 ^
secondary to depression.2 V+ s/ q4 S, F# p; M! z
The child slept in the same bed with parents.
8 e* t5 N! _* ]! QThe father would hug the baby and hold him on his( j, c0 K% L0 I- o9 X( a
chest for a considerable period of time, causing sig-5 S; c1 m, W$ @1 V- m+ B$ e
nificant bare skin contact between baby and father.. ^+ L* N4 `+ h* l
The father also admitted that after the phone call,
$ T' q4 U  D$ v# ~when he learned the testosterone level in the baby
9 @" m4 ^' E6 c& k" Rwas high, he then read the product information# a7 f6 W/ U, V0 o* `7 z% }
packet and concluded that it was most likely the rea-
( Q( l' `, I# m4 v9 t( K, Ison for the child’s virilization. At that time, they
  ?( o9 g- p3 s0 Z* B3 A$ Qdecided to put the baby in a separate bed, and the7 M) s3 |7 e5 S
father was not hugging him with bare skin and had
6 I! x4 b- x' {( Pbeen using protective clothing. A repeat testosterone
4 h) ?& }& h; htest was ordered, but the family did not go to the
& [1 v( o% }/ N: Alaboratory to obtain the test.8 k5 m2 C7 u+ D  i  t
Discussion5 o3 R4 x1 ~% H8 x; B4 X1 ]% w! p
Precocious puberty in boys is defined as secondary
4 G) X6 e/ M) o9 o, @0 l- L9 Tsexual development before 9 years of age.1,4& l1 x6 F0 L6 v
Precocious puberty is termed as central (true) when8 b8 ~8 z. B" X6 i- J# J
it is caused by the premature activation of hypo-
) t2 B0 O1 }7 Q  U& {5 P- Y' mthalamic pituitary gonadal axis. CPP is more com-
3 P2 n0 N8 L. Nmon in girls than in boys.1,3 Most boys with CPP0 S" m. m7 B5 I4 U- ]" Y
may have a central nervous system lesion that is4 r. ~4 M/ |; O
responsible for the early activation of the hypothal-2 Y  \4 w/ j3 c8 K5 k0 F
amic pituitary gonadal axis.1-3 Thus, greater empha-0 W3 ^3 O& u& H1 F) Q5 e4 B
sis has been given to neuroradiologic imaging in
) G$ O+ B  o, ?) ^5 gboys with precocious puberty. In addition to viril-
% |  B, T7 }  n) c& \% lization, the clinical hallmark of CPP is the symmet-
7 E* S! [; J7 k* l! R( ^rical testicular growth secondary to stimulation by) y& r0 P% s% h
gonadotropins.1,33 {/ c9 I$ x# N9 R
Gonadotropin-independent peripheral preco-
8 k( k& I% G4 A# Lcious puberty in boys also results from inappropriate- ?+ _6 \/ [" }
androgenic stimulation from either endogenous or; w" q+ N7 ]3 z4 K
exogenous sources, nonpituitary gonadotropin stim-
) }: B! A% d9 f/ Wulation, and rare activating mutations.3 Virilizing8 G1 C  U1 e  y8 K& m' N
congenital adrenal hyperplasia producing excessive
& g; T+ `. F, O+ k5 O6 c4 u! jadrenal androgens is a common cause of precocious
' C4 u( Q8 B( C( ?puberty in boys.3,46 f( M4 i! _) B* P( N9 g
The most common form of congenital adrenal
$ g# ?( |5 O: mhyperplasia is the 21-hydroxylase enzyme deficiency.
" W$ h* j2 A* M; EThe 11-β hydroxylase deficiency may also result in
  S- s1 ~' e# s% m+ w* Eexcessive adrenal androgen production, and rarely,
2 @$ L6 j' O' d4 T/ k$ Gan adrenal tumor may also cause adrenal androgen! @: z- ]+ w# q2 p
excess.1,37 H! h9 N# p0 z4 [
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 Z2 E6 G* R% X8 d% h. m: R
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
; Y0 {, n- @9 f& |5 j3 u$ n+ k; hA unique entity of male-limited gonadotropin-
  K$ o# }- G" M& _: N$ @# Rindependent precocious puberty, which is also known; }$ M1 o& s4 ^* `
as testotoxicosis, may cause precocious puberty at a. E2 m- _' H6 T) T, ^- H( M7 f
very young age. The physical findings in these boys' U9 i  e; N  N8 C/ O) ]
with this disorder are full pubertal development,
1 H) I" U3 R, r  kincluding bilateral testicular growth, similar to boys
6 G( `0 N: S0 }( J7 \with CPP. The gonadotropin levels in this disorder
) u" c, k, \- B* p0 E5 g5 Dare suppressed to prepubertal levels and do not show7 ~+ S0 U' [6 h; T+ f) \
pubertal response of gonadotropin after gonadotropin-# U9 K0 z) Z$ g! K
releasing hormone stimulation. This is a sex-linked
1 A! D' {3 b6 Z3 Lautosomal dominant disorder that affects only) U1 V) l7 |* I  n, Y+ p. K8 S
males; therefore, other male members of the family
: J1 y" M* w3 M1 umay have similar precocious puberty.3
+ N* x: }9 A4 k3 T8 @In our patient, physical examination was incon-- S- o- s! }4 w) W6 M2 n
sistent with true precocious puberty since his testi-+ ~, ]6 O1 i: B1 A1 J2 B6 ]
cles were prepubertal in size. However, testotoxicosis
3 o! a  f. t3 A$ Awas in the differential diagnosis because his father8 }4 J* F9 ^+ z3 C
started puberty somewhat early, and occasionally,4 F) O1 m8 e# f& R9 m; D
testicular enlargement is not that evident in the
0 F1 t% @, t$ m5 W8 K% wbeginning of this process.1 In the absence of a neg-$ Y: o. n" W' v; I) |3 N: e4 ]
ative initial history of androgen exposure, our& ]; q: k! a" Z( w* n4 x* D  D
biggest concern was virilizing adrenal hyperplasia,: R. z) l$ I1 p9 m4 O$ x
either 21-hydroxylase deficiency or 11-β hydroxylase; Y% f! T' P3 w$ s9 l; b' T* @, P
deficiency. Those diagnoses were excluded by find-& y8 |0 g- S! r1 @. v
ing the normal level of adrenal steroids.
( p- \% |/ u# bThe diagnosis of exogenous androgens was strongly0 E/ c# A, A2 @
suspected in a follow-up visit after 4 months because& \+ z, X; W* k
the physical examination revealed the complete disap-
5 g. A5 s8 B; Y! upearance of pubic hair, normal growth velocity, and
. v  h! U4 p4 g2 K- qdecreased erections. The father admitted using a testos-( C) c- B: l; c2 P
terone gel, which he concealed at first visit. He was8 |% O4 K& A  n5 o* [. ~) a/ |
using it rather frequently, twice a day. The Physicians’0 K! I! T7 i& S/ C( I! ]
Desk Reference, or package insert of this product, gel or! f: `. R/ ~. ?
cream, cautions about dermal testosterone transfer to
/ v9 A' O' R1 d1 B7 {- Vunprotected females through direct skin exposure.
# \! E8 v- r" F# `6 L! z5 MSerum testosterone level was found to be 2 times the
$ }! e, v& H: O+ Y6 F0 J3 i5 V3 ]baseline value in those females who were exposed to; |, `% J: p+ x, O# o; S; ^
even 15 minutes of direct skin contact with their male
' ]; W1 t8 K  {, ~partners.6 However, when a shirt covered the applica-0 p: r& y9 v/ h8 h1 ?7 v7 a
tion site, this testosterone transfer was prevented.3 g8 c1 }( j9 z: n4 S# `# r% N
Our patient’s testosterone level was 60 ng/mL,+ Q- c  |9 l4 o9 h8 g# S
which was clearly high. Some studies suggest that
$ S! V+ W+ P+ i5 z. T6 bdermal conversion of testosterone to dihydrotestos-, ]6 H) U* e7 a! P; O
terone, which is a more potent metabolite, is more& _' T- C0 U* J; u
active in young children exposed to testosterone) W; q7 h1 k0 x* a5 o% Y5 ]
exogenously7; however, we did not measure a dihy-6 z3 k: \; n/ e0 u% T$ Z
drotestosterone level in our patient. In addition to. P0 c( t: Z: Y0 E2 u: W" N5 n. N9 K5 I& k
virilization, exposure to exogenous testosterone in
) g- {% Q6 |7 xchildren results in an increase in growth velocity and
' Q- A$ `* J0 B+ R. Radvanced bone age, as seen in our patient.6 Y+ ~8 Q8 }$ k' }! w% e
The long-term effect of androgen exposure during2 _8 C& |$ T  b, o) z8 R
early childhood on pubertal development and final
1 Q& N$ S$ a" q4 ^9 N$ G6 Xadult height are not fully known and always remain5 l/ Y7 O6 `) t: B+ n, `& O* e
a concern. Children treated with short-term testos-' n3 K  l; V* e- O
terone injection or topical androgen may exhibit some* G- m0 @% N0 r  A
acceleration of the skeletal maturation; however, after
5 B; c6 Y2 j' h4 \3 kcessation of treatment, the rate of bone maturation
* W# F0 f) [6 [0 ]# w1 edecelerates and gradually returns to normal.8,98 A  s; C3 g: G+ C4 [$ y
There are conflicting reports and controversy- q: |; d# [% D0 A; w/ |5 q
over the effect of early androgen exposure on adult
% L* R6 ~2 x7 }( O) ]penile length.10,11 Some reports suggest subnormal
# U$ W# k4 r9 i3 v0 |8 `adult penile length, apparently because of downreg-
1 ]8 d6 T- x1 g& x& [ulation of androgen receptor number.10,12 However,. S5 g( `# W7 z3 X# ?
Sutherland et al13 did not find a correlation between- u, U) [  j3 {- }1 ~6 p
childhood testosterone exposure and reduced adult3 g# v# V3 m. y7 _! W% g) p
penile length in clinical studies.6 m2 b) |" w0 \, R
Nonetheless, we do not believe our patient is( y, Y7 Y4 f" L% R) s/ f' i
going to experience any of the untoward effects from
& M4 R8 A& k. D! X+ Atestosterone exposure as mentioned earlier because0 J8 c6 P, _- n7 a+ O/ k! [9 R9 f- B
the exposure was not for a prolonged period of time.2 V! L2 ^, c4 Q1 s
Although the bone age was advanced at the time of
4 o/ g# r. B) vdiagnosis, the child had a normal growth velocity at
- |9 Q, m4 W1 ]  Fthe follow-up visit. It is hoped that his final adult
: L& g9 z" a' j2 Z* ]5 j4 vheight will not be affected.# u9 X- r) H% t0 D- H0 d3 Y
Although rarely reported, the widespread avail-; m4 ?! |$ h# j6 B4 w/ |7 x) E* x
ability of androgen products in our society may" @! z4 B) s0 A& \
indeed cause more virilization in male or female7 f, [9 [" m! i
children than one would realize. Exposure to andro-" X! c7 G  x0 R" h) b" ?
gen products must be considered and specific ques-. [+ p) a# _, q' K8 n" B
tioning about the use of a testosterone product or
+ K* y1 h1 L, S, r9 S* Tgel should be asked of the family members during. [* S( P  Z! e6 n
the evaluation of any children who present with vir-
1 X6 Q' ?* M  f& Ailization or peripheral precocious puberty. The diag-
6 u! [. U6 J8 w; F2 ]' ^2 T' Xnosis can be established by just a few tests and by7 E+ t  v3 B! |$ ]0 D
appropriate history. The inability to obtain such a+ x  `, t0 ~1 s
history, or failure to ask the specific questions, may
5 E9 @7 X% p0 ^! u. N5 }- dresult in extensive, unnecessary, and expensive
( N+ B/ S, T2 L' U1 z/ v2 Vinvestigation. The primary care physician should be; |- u0 s  f- s8 Y1 I& B
aware of this fact, because most of these children1 l2 x* U6 z( u4 ]' d
may initially present in their practice. The Physicians’9 @  g9 o. Z0 Y
Desk Reference and package insert should also put a
5 E8 F; p# @+ j0 lwarning about the virilizing effect on a male or/ v# }+ k. ]2 ?1 O% x
female child who might come in contact with some-: t) }) p" B0 _7 A, u
one using any of these products.  \* Z, \3 F- A$ @
References
. L0 I' N- t& f, c0 d. R. t1. Styne DM. The testes: disorder of sexual differentiation; j3 C6 Q! s8 `. _7 {
and puberty in the male. In: Sperling MA, ed. Pediatric: }( p1 ?% J: V& C( n7 Q' J
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
* p( o6 n3 _: W* c4 W. L2002: 565-628.
4 A" r' e) ~+ c1 j. E1 i' b. L2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious* l% s6 ~1 q& w0 c" q8 P1 Y. ]
puberty in children with tumours of the suprasellar pineal
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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
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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

" s& R, z, j0 l" f; T" R/ m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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