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Sexual Precocity in a 16-Month-Old
5 H  J; `! M; O- ^( X2 a: Y, ?' `6 c" tBoy Induced by Indirect Topical
5 `* }- w( r- G- I+ BExposure to Testosterone5 {8 Z9 N; [5 G3 Z. Y4 p0 \
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,27 ?( v  m& O6 }' M
and Kenneth R. Rettig, MD1
; H1 Q. t0 ~2 X; zClinical Pediatrics: d! v* F% t6 q. C% A$ p
Volume 46 Number 6
- x  k- ]7 n  V4 xJuly 2007 540-543
& T) K9 A. r1 z1 w3 A0 B© 2007 Sage Publications
9 M- f' q0 N' u6 L10.1177/0009922806296651
/ d6 l$ H( D. Shttp://clp.sagepub.com9 C0 ?/ X) u! r7 i4 y; T
hosted at( I8 t& G9 u/ s/ v
http://online.sagepub.com/ k# g' F) G7 e- r' x* [9 p
Precocious puberty in boys, central or peripheral,# B. I+ `, ^! {, m9 A" d- i
is a significant concern for physicians. Central) U# w2 S8 u3 z  a$ ?6 f+ ?3 m$ f
precocious puberty (CPP), which is mediated
# r1 ]3 g% ~; I. r/ G7 j; Lthrough the hypothalamic pituitary gonadal axis, has2 o; |5 J8 T; L3 y3 J6 ?
a higher incidence of organic central nervous system
' ^' A: h7 Z# xlesions in boys.1,2 Virilization in boys, as manifested
9 X/ |4 e9 B7 M9 v( S6 B9 M# k$ Qby enlargement of the penis, development of pubic- {. _0 X0 Q  z
hair, and facial acne without enlargement of testi-
; {! G& ^! [. ?/ P" K* Ucles, suggests peripheral or pseudopuberty.1-3 We
( v( v: G# s- }. Q, oreport a 16-month-old boy who presented with the/ k* e. N, R; a# p8 p) c
enlargement of the phallus and pubic hair develop-
! s; H4 X; Q  U" T0 h3 Nment without testicular enlargement, which was due1 ~7 L; N( N/ j; y: b! ~
to the unintentional exposure to androgen gel used by. H: n: T5 b! Z: P1 O
the father. The family initially concealed this infor-
7 j; h* \6 {6 n& D- N4 M- Fmation, resulting in an extensive work-up for this
$ u; \+ K. p- u/ F8 \# uchild. Given the widespread and easy availability of
6 v7 H+ {) k% b! k0 Ztestosterone gel and cream, we believe this is proba-
, A5 E- ]4 B- }( H8 z: u4 f3 P; ^6 A  [bly more common than the rare case report in the- t* ^- ^5 b% @. d1 ]
literature.4( b" G7 ?- p+ V
Patient Report- r0 \( |+ p+ z' X- i% M; ~
A 16-month-old white child was referred to the9 R$ P; h; b* D0 T9 Z( ~
endocrine clinic by his pediatrician with the concern9 E/ ]7 p8 Z) A4 W) ^1 F% B: N
of early sexual development. His mother noticed
# ]: I& k9 [% ~$ |5 m$ F* M6 u9 {light colored pubic hair development when he was0 }% Z1 c: U$ m8 m9 C7 i) o
From the 1Division of Pediatric Endocrinology, 2University of7 L6 W' ]7 ]% ~9 `0 v
South Alabama Medical Center, Mobile, Alabama.
! g% |. l; Y  G# K5 f) DAddress correspondence to: Samar K. Bhowmick, MD, FACE,
4 k) U; s, I8 pProfessor of Pediatrics, University of South Alabama, College of3 R& C! }% h) K0 _: l, t
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
* v5 B* J: d+ }) m) x" T; pe-mail: [email protected].- x( k6 N& M& M6 g* C7 e2 N
about 6 to 7 months old, which progressively became& f3 B  S/ ~/ P. L1 c* p3 n
darker. She was also concerned about the enlarge-
% \4 W4 z3 P) W( wment of his penis and frequent erections. The child; g/ L9 P! c0 ]# i5 r* r
was the product of a full-term normal delivery, with
' V% S- |5 g3 \: n4 y7 d# Q, Ca birth weight of 7 lb 14 oz, and birth length of2 [& P8 i9 L* w5 R& S% ~
20 inches. He was breast-fed throughout the first year2 B$ m  i' x$ v
of life and was still receiving breast milk along with9 p* s+ v, |/ L! R+ C! [7 W
solid food. He had no hospitalizations or surgery,& q3 }; f7 W6 G: N' z9 K
and his psychosocial and psychomotor development
# F! n) m: y% [' P, Mwas age appropriate.$ \8 t6 R9 _" m  x8 t
The family history was remarkable for the father,) L& x+ x6 w) V, u1 q4 r
who was diagnosed with hypothyroidism at age 16,; c5 T$ z! H; c0 o1 s
which was treated with thyroxine. The father’s! v3 D% R7 @' D; {- M5 P$ v  ]
height was 6 feet, and he went through a somewhat% s! F' o6 j" `# J) q+ r8 O+ R0 T
early puberty and had stopped growing by age 14.
5 K$ z: r  v( C2 {, b$ Z- zThe father denied taking any other medication. The6 z( j$ g6 ^: y1 q" K# i: ^. \
child’s mother was in good health. Her menarche
. S' j" l+ B! b. a- ^; Twas at 11 years of age, and her height was at 5 feet
& n5 G0 j9 v6 i% a5 inches. There was no other family history of pre-: H' T, Q6 C) M
cocious sexual development in the first-degree rela-5 i$ ?1 ~+ ?% X& k
tives. There were no siblings.+ h$ n0 E  z2 ]/ @
Physical Examination
" z* @) Z8 J* w3 m; O, j. n" b6 m; c6 ^The physical examination revealed a very active,
) d  [- l' {0 _0 O% N3 bplayful, and healthy boy. The vital signs documented- ]' z& [9 S7 Q1 a/ |
a blood pressure of 85/50 mm Hg, his length was
+ s( R6 i5 W3 R6 W: K4 J) `0 b90 cm (>97th percentile), and his weight was 14.4 kg
/ Q% s4 Y' @/ m/ k(also >97th percentile). The observed yearly growth
/ c7 \) R9 Y9 \) f: j3 Z0 v" ~velocity was 30 cm (12 inches). The examination of
1 P* I* o: ]% A7 E' ^# x+ gthe neck revealed no thyroid enlargement.
# [( l. J0 R! V  KThe genitourinary examination was remarkable for4 }+ _* p! P/ m& P* E. b& W
enlargement of the penis, with a stretched length of
* L4 M- N0 K5 H8 cm and a width of 2 cm. The glans penis was very well' A6 h$ k, ~. j  a: G5 f
developed. The pubic hair was Tanner II, mostly around
0 }- Z, r/ B3 z  R9 q7 V. d540
! ]3 l4 }  p" o0 F3 eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) s2 ~9 u+ u# R6 o2 y1 k. \3 gthe base of the phallus and was dark and curled. The' A; o% n9 T- E" q8 |8 W4 S, }
testicular volume was prepubertal at 2 mL each.5 ~; w) Z9 V. p0 B3 K
The skin was moist and smooth and somewhat$ q. W4 A: h" `2 v
oily. No axillary hair was noted. There were no
  p" P2 `3 m& H7 B* Kabnormal skin pigmentations or café-au-lait spots.
/ D* r' X- C# T4 h. `Neurologic evaluation showed deep tendon reflex 2+
9 T0 t' m! |6 ?( S- [bilateral and symmetrical. There was no suggestion5 A  W0 z5 M: o) C1 t4 }5 R
of papilledema.
2 ?4 s0 w. ~6 Q- H5 t: YLaboratory Evaluation
2 c( ^3 g4 ?) c# e7 w: L- `The bone age was consistent with 28 months by" R! B1 v3 e* ]5 q  Q
using the standard of Greulich and Pyle at a chrono-
1 f* o/ p# i: X0 }3 V' K/ _logic age of 16 months (advanced).5 Chromosomal5 |1 N: i7 P  G3 v/ U
karyotype was 46XY. The thyroid function test: ?3 N2 E$ U5 F$ N6 L
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
  k7 Q/ F$ f# c2 j( D$ j7 Rlating hormone level was 1.3 µIU/mL (both normal).8 Q5 K$ Y7 F3 L. k, M
The concentrations of serum electrolytes, blood
& Q  c+ J" c6 n$ o' Purea nitrogen, creatinine, and calcium all were
3 B' Y7 R2 k# o5 V' jwithin normal range for his age. The concentration
4 e+ O3 Z' Q0 w4 A1 D& q- ^; `of serum 17-hydroxyprogesterone was 16 ng/dL
: ~; R* X3 @* J  J: ^, ?3 w  ](normal, 3 to 90 ng/dL), androstenedione was 20& g) e* z9 T0 a, d7 [
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-" B* Z" k1 @3 b
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
; l- u5 r5 U& A' V5 c8 W. r$ {desoxycorticosterone was 4.3 ng/dL (normal, 7 to) F9 A' u7 r# k
49ng/dL), 11-desoxycortisol (specific compound S)
$ {- O. e# Z! \: N5 [8 y+ {was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-4 n; J. |! G) P: b
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total; g9 y2 Z7 K: Q8 V4 }- w) h3 q" r  K/ H
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),* A+ c6 S; ?& e" r' ]" W5 p
and β-human chorionic gonadotropin was less than5 N# W6 u( W- ~" n( u, C
5 mIU/mL (normal <5 mIU/mL). Serum follicular% b: v! T3 s1 H
stimulating hormone and leuteinizing hormone
  |4 r; e) ]! G9 O$ z" p7 z5 ^concentrations were less than 0.05 mIU/mL
! q# E* B3 t# x& {( B(prepubertal).6 Y- d$ G" w0 g* ?9 K8 T
The parents were notified about the laboratory
, U+ n9 h; l* f, ]6 ?) n: B8 k! o7 Dresults and were informed that all of the tests were# d7 n1 I) ~  ?% T
normal except the testosterone level was high. The
/ E8 h  C4 O3 O$ t. ]follow-up visit was arranged within a few weeks to# u( w* c1 E0 v6 `7 m& g, W' _" X
obtain testicular and abdominal sonograms; how-3 [/ K, n5 F, H- J# c3 d" l
ever, the family did not return for 4 months.1 V: q+ q" L+ |9 ~+ R: I4 J
Physical examination at this time revealed that the
! R/ H1 O8 |1 b0 Echild had grown 2.5 cm in 4 months and had gained
! i4 I, D( M5 \+ B* |) g2 kg of weight. Physical examination remained9 U: D7 R5 o- Q9 Q& o; q. _: A2 Q
unchanged. Surprisingly, the pubic hair almost com-" z7 A2 O- s8 H  }2 m5 d( q
pletely disappeared except for a few vellous hairs at
7 l' y) D/ y6 M4 u/ n0 Gthe base of the phallus. Testicular volume was still 2
% p( j- H; O3 f2 ?mL, and the size of the penis remained unchanged.
/ f8 G: |, x  v( ?2 u" kThe mother also said that the boy was no longer hav-4 Y& w. b1 v& ^; q* S3 a! J, S3 n1 Q
ing frequent erections.+ L; t2 j- R, J- P+ o% S
Both parents were again questioned about use of
: K" p( x; [" H9 J- fany ointment/creams that they may have applied to
0 Q: z# o. z2 ^4 F+ g# Ithe child’s skin. This time the father admitted the& ]+ [8 K* ?$ A' i; ]! @
Topical Testosterone Exposure / Bhowmick et al 541
, B# W0 ~$ }8 [+ X- }9 Ause of testosterone gel twice daily that he was apply-7 K( `! y7 i. B# y6 E% l9 J/ f
ing over his own shoulders, chest, and back area for# i' ?1 |7 ~+ v7 x* b0 f
a year. The father also revealed he was embarrassed
( c! T3 [, I: }; @9 [to disclose that he was using a testosterone gel pre-0 X9 F7 U1 o- ~$ W9 W/ x( r5 F, b! _
scribed by his family physician for decreased libido" G1 ?9 k3 y$ O& m+ v
secondary to depression.7 _( ~) i1 c% A. H0 _* [0 g
The child slept in the same bed with parents.
1 f# F2 P4 x$ q3 W7 z! hThe father would hug the baby and hold him on his) ]& Z1 U: j( u, \
chest for a considerable period of time, causing sig-
5 S/ e7 }( `9 t( M2 p8 [# znificant bare skin contact between baby and father.
" l5 w. v% m& V  A0 `The father also admitted that after the phone call,
( M$ T0 }& C. |1 i& c* awhen he learned the testosterone level in the baby/ O" N, ^2 }( z$ e" R
was high, he then read the product information
3 ^- t6 f+ M! `5 a; D; npacket and concluded that it was most likely the rea-5 W6 D4 s1 K5 R! B; k: M
son for the child’s virilization. At that time, they
* E2 y& Q7 B/ l: Cdecided to put the baby in a separate bed, and the5 e: G/ B  h; G0 h* z4 @* A
father was not hugging him with bare skin and had' B! S# w4 Z& c
been using protective clothing. A repeat testosterone" \8 F. V- X! P
test was ordered, but the family did not go to the8 m, G5 }  y; B2 ~# o' T
laboratory to obtain the test.1 @  \$ P. ?8 v/ Q" q5 v
Discussion0 z) j0 C( o3 P: u7 P
Precocious puberty in boys is defined as secondary+ a! K4 w& I5 ^4 T- H; V+ f9 S
sexual development before 9 years of age.1,41 X$ `2 Z" k. B' Q6 c
Precocious puberty is termed as central (true) when
) N# P: v8 ]# Cit is caused by the premature activation of hypo-
0 A) b2 A  F# sthalamic pituitary gonadal axis. CPP is more com-9 S- L2 h7 y8 ]8 O/ S& k% o9 }$ O
mon in girls than in boys.1,3 Most boys with CPP1 r: o  Q0 B& s6 r$ }, M3 F
may have a central nervous system lesion that is
; p8 r4 ~. W: s$ K9 j- v! Eresponsible for the early activation of the hypothal-, W. z  U$ d6 B
amic pituitary gonadal axis.1-3 Thus, greater empha-$ P( b) B5 d5 d: p6 G% `2 B
sis has been given to neuroradiologic imaging in
2 {' R4 {/ B& T5 q0 r+ ~0 Lboys with precocious puberty. In addition to viril-8 R$ U/ B# Z" Z% \+ f# P/ U
ization, the clinical hallmark of CPP is the symmet-
% K, B& I% _5 j2 e+ g* I/ k1 drical testicular growth secondary to stimulation by; I& c7 X  w! I" R3 \7 ^! T
gonadotropins.1,3
! |% ^6 }- G- p+ u2 }9 {* d6 BGonadotropin-independent peripheral preco-& n! I2 _9 o4 W% Y- j0 i7 |. n
cious puberty in boys also results from inappropriate7 X, L" t5 y- ^/ u/ B7 L
androgenic stimulation from either endogenous or1 a3 }% K( k$ w
exogenous sources, nonpituitary gonadotropin stim-
' ^3 X( i% `' a( |- qulation, and rare activating mutations.3 Virilizing
: y9 _+ H' ^1 |/ Rcongenital adrenal hyperplasia producing excessive5 F4 [2 A7 O( {; s7 O- G
adrenal androgens is a common cause of precocious
% J4 k5 K) h% t  s* Npuberty in boys.3,4$ r5 M7 t0 y' ^/ I+ Q
The most common form of congenital adrenal
; G% s. U8 R. P  j- B/ ohyperplasia is the 21-hydroxylase enzyme deficiency.; `6 P% ]0 ]" e7 ?1 z0 A+ h
The 11-β hydroxylase deficiency may also result in  m, i# f3 q3 w6 D! O; h$ ?
excessive adrenal androgen production, and rarely,
& j. |7 n. q1 E$ F' l; G" [an adrenal tumor may also cause adrenal androgen
$ y! z- p' H6 j+ O% O3 Uexcess.1,3
, I7 _0 R* H! y5 m7 B  [at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 ]+ S8 s) I1 \+ p
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007- J% |  _- d* j. V$ S: o
A unique entity of male-limited gonadotropin-8 |6 r+ ?8 I! i% O5 f( h
independent precocious puberty, which is also known
* a5 l8 s3 K, M$ Vas testotoxicosis, may cause precocious puberty at a" E5 A: ]3 A8 z4 r  Y& D
very young age. The physical findings in these boys
. q& G8 J$ ~( Q. w# _with this disorder are full pubertal development," q. \, |3 y: b% V
including bilateral testicular growth, similar to boys  Z3 d: i& W8 ?; T% Y
with CPP. The gonadotropin levels in this disorder! [. t( d4 t( z. Z3 {7 i% T" H
are suppressed to prepubertal levels and do not show$ S7 z5 t. x& S  i8 U1 ]8 H
pubertal response of gonadotropin after gonadotropin-3 n  ^/ |5 d; P5 |! i0 D2 `
releasing hormone stimulation. This is a sex-linked$ k( f# G: l# Q
autosomal dominant disorder that affects only
0 @/ o3 I  L+ L: ?males; therefore, other male members of the family
/ ]$ ^, f  k; `6 [may have similar precocious puberty.3
5 u: `+ u* h: m& ?: U: @! G- n# OIn our patient, physical examination was incon-
4 B5 T- J; s  s; \+ r: `' osistent with true precocious puberty since his testi-
$ y% J% h& B  v. x0 C& F5 jcles were prepubertal in size. However, testotoxicosis
. v  N3 l" q$ K5 [# Jwas in the differential diagnosis because his father
% L1 k! c' s+ s. U9 rstarted puberty somewhat early, and occasionally,  X5 X( _9 {& t& v# B& A& J
testicular enlargement is not that evident in the
; z; x7 l- d& D. Zbeginning of this process.1 In the absence of a neg-
% f! z9 @6 J. h. U2 ~ative initial history of androgen exposure, our
! L* z, K  M1 J0 d+ U- K" B/ q( zbiggest concern was virilizing adrenal hyperplasia,
8 Q. u* S& G. M& F) C; Y. ^either 21-hydroxylase deficiency or 11-β hydroxylase7 t  q- F& r1 P8 K- l
deficiency. Those diagnoses were excluded by find-. P8 W9 k+ l% P: _- e; x5 U+ j" y
ing the normal level of adrenal steroids.( a7 E1 X! `4 p- w4 d
The diagnosis of exogenous androgens was strongly
' H# [! f, P8 t/ ksuspected in a follow-up visit after 4 months because% Y/ \& _# K5 G: n  ?% n: [
the physical examination revealed the complete disap-
. F8 ^& {5 f# J+ [! n9 M& xpearance of pubic hair, normal growth velocity, and% i3 D0 r  N+ s5 q7 y
decreased erections. The father admitted using a testos-3 f% u& [1 j* ~: j2 u, @
terone gel, which he concealed at first visit. He was
3 o/ b# G5 q5 n1 q$ Zusing it rather frequently, twice a day. The Physicians’
4 G- m& }: l* ZDesk Reference, or package insert of this product, gel or
# v. _, |7 b8 S" gcream, cautions about dermal testosterone transfer to- y5 z* D/ H! d" j" p4 K# [
unprotected females through direct skin exposure.
  D3 J) w0 d- Z5 zSerum testosterone level was found to be 2 times the; c5 {$ S& o" v  h0 R
baseline value in those females who were exposed to" W8 l4 V! W( M* J8 Q1 W8 ~7 U, A
even 15 minutes of direct skin contact with their male
3 |/ B" |# S& k8 l# xpartners.6 However, when a shirt covered the applica-
' j2 D! K: P7 L5 {" V+ f7 D, j$ _tion site, this testosterone transfer was prevented.' V. S7 e% \* |8 b8 ?% b% u" L
Our patient’s testosterone level was 60 ng/mL,8 C9 O' x( p& v% g' [  a/ N3 F
which was clearly high. Some studies suggest that
; S4 T2 @+ n. {  K" S% Zdermal conversion of testosterone to dihydrotestos-$ D7 c: K5 a% y- U+ q6 @+ ]' a* ]* R* f
terone, which is a more potent metabolite, is more
. v: u3 r$ I4 M+ w6 ^5 ^6 W) ?active in young children exposed to testosterone
+ N4 t( n  }8 M0 n" [1 qexogenously7; however, we did not measure a dihy-
0 p/ R& h3 j8 [6 X1 q. tdrotestosterone level in our patient. In addition to* o1 v  F- p, Z2 j2 a6 N1 J
virilization, exposure to exogenous testosterone in1 U' X% ]& \( p* D
children results in an increase in growth velocity and
- c7 _; |! s1 iadvanced bone age, as seen in our patient.
* D$ u$ f  ~: V! ?' c- UThe long-term effect of androgen exposure during5 p1 s6 n( C1 c2 z9 `/ `
early childhood on pubertal development and final  E% S7 p; R. D
adult height are not fully known and always remain
8 f% r! d2 t. Na concern. Children treated with short-term testos-
7 q% \1 X9 A2 n$ B/ s9 pterone injection or topical androgen may exhibit some: P# w! d0 _# W$ W) n' @
acceleration of the skeletal maturation; however, after
3 i4 k- Q9 a* ]/ d1 bcessation of treatment, the rate of bone maturation
/ D5 W$ g7 R. U- mdecelerates and gradually returns to normal.8,9
+ z# I+ @  x! {0 d; ~8 z' O" |# zThere are conflicting reports and controversy
: S( v9 j: G0 q1 y( Y) @over the effect of early androgen exposure on adult9 q% [0 A, }9 _' P0 x
penile length.10,11 Some reports suggest subnormal- j4 L7 o: W" |' z
adult penile length, apparently because of downreg-
( j& `7 e' r) d  A/ l0 X: X" gulation of androgen receptor number.10,12 However,
$ b# z$ Z8 Y8 X1 dSutherland et al13 did not find a correlation between
% e' ^, E$ {* [, P  }+ Bchildhood testosterone exposure and reduced adult
) T3 \  P2 g3 L, u& J( P2 Jpenile length in clinical studies.0 R& A" J$ K3 V9 z
Nonetheless, we do not believe our patient is
9 `/ L* Q; s9 ~$ ]# l( k8 i( b9 z7 |going to experience any of the untoward effects from
! A- ]0 w3 x+ e% itestosterone exposure as mentioned earlier because/ ]- C1 Z2 k4 h! M3 `
the exposure was not for a prolonged period of time.
8 R, J% w7 I0 A4 wAlthough the bone age was advanced at the time of. v1 t8 ?9 T. P: x; \3 T
diagnosis, the child had a normal growth velocity at2 x) W+ ?4 H( E" y, P$ ^
the follow-up visit. It is hoped that his final adult7 s* L% d( v; ?9 N1 \8 |+ ~8 ?
height will not be affected.9 U) J* {9 |( k  X3 o( Q
Although rarely reported, the widespread avail-% Q9 _8 s" F1 P3 n+ k' }) c! O
ability of androgen products in our society may
% h& _5 Y3 _. {* E5 ~( V& B+ Windeed cause more virilization in male or female2 x; b* W6 x: H& Q! L7 D6 Z
children than one would realize. Exposure to andro-2 K! ]* R) w& _' R+ i
gen products must be considered and specific ques-1 X. y; C4 T1 a& K0 b4 e
tioning about the use of a testosterone product or' G4 h7 F% F8 |1 c* |
gel should be asked of the family members during
7 e' Z* s9 ^- G+ w* Gthe evaluation of any children who present with vir-# A+ m* H( }1 U* {
ilization or peripheral precocious puberty. The diag-
7 C# S% \+ A9 Lnosis can be established by just a few tests and by' F/ b5 ?! s" Q! Y/ e) w. R( q
appropriate history. The inability to obtain such a
6 n6 k$ c5 l" L1 {$ h7 @1 A- ]history, or failure to ask the specific questions, may
8 e3 s4 }; R7 U  nresult in extensive, unnecessary, and expensive" u6 B" r: I! ^: U( N. c, o
investigation. The primary care physician should be
! N% t( A9 ~4 O+ xaware of this fact, because most of these children" L* p+ U9 y% m5 N! X9 \7 r
may initially present in their practice. The Physicians’$ v/ I- e0 @/ h7 R2 S
Desk Reference and package insert should also put a
5 O9 [, O3 l4 b$ iwarning about the virilizing effect on a male or/ o! O& E3 l4 Q! L# h, W! }
female child who might come in contact with some-5 C) \' x3 H8 h* r6 A4 E* T
one using any of these products.- }- Q* A8 v0 s% \2 F  S, n- D( M
References& ^, p2 p/ ?# L$ I8 z2 c
1. Styne DM. The testes: disorder of sexual differentiation. j8 W6 R4 v+ o* A/ \
and puberty in the male. In: Sperling MA, ed. Pediatric
( @; R, j- h# p; ?3 C0 T- ~Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
; I5 n1 Q3 b. z; I$ w* @5 i2002: 565-628.0 }  Y  }- ~/ `9 _) e% T8 G9 D
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
, j, [* h# Q9 ^5 Xpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old: l7 j" l; e) f' z+ O
Boy Induced by Indirect Topical/ M* Q# _( _' z1 O2 n
Exposure to Testosterone
, ?* ~* ^6 D- j1 P& |- ~* |Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
+ e1 K1 N3 ^4 @, Zand Kenneth R. Rettig, MD1
1 _  q& }0 z- K3 _' z/ pClinical Pediatrics
, u$ g. D5 ?* L$ l* o1 ]  k' PVolume 46 Number 6# A! ^( `4 ^6 o8 h; v" v( s9 p
July 2007 540-543  q: s5 V$ z' I+ p
© 2007 Sage Publications* m7 U# q- G+ @9 C; Q' a# m1 C
10.1177/0009922806296651
. X: e: V2 P! M2 Lhttp://clp.sagepub.com
4 B5 I. {5 p: \! {4 A9 D" Shosted at
2 D. z" T* X" v' _- ?, `* Ghttp://online.sagepub.com
. I4 f& D1 p, J& D+ @Precocious puberty in boys, central or peripheral,+ b  ~3 C% v; z+ _9 F& [3 ?
is a significant concern for physicians. Central( t) M  y# q# g5 K1 a
precocious puberty (CPP), which is mediated9 R- _: c; N) ]9 u5 U" a
through the hypothalamic pituitary gonadal axis, has
4 D5 U9 Y/ x4 C" Qa higher incidence of organic central nervous system. W" E/ p0 T2 y; C" N9 ?
lesions in boys.1,2 Virilization in boys, as manifested! u7 B2 H- }/ x2 A1 }4 K* _9 `/ t
by enlargement of the penis, development of pubic
3 L! K) A3 {" w# F' B4 s  d- z0 Qhair, and facial acne without enlargement of testi-) i6 f. u& i- m; X4 ~5 t0 G
cles, suggests peripheral or pseudopuberty.1-3 We! m% R4 |# [$ F( k8 y
report a 16-month-old boy who presented with the
) F1 t* z( w8 |) z, Wenlargement of the phallus and pubic hair develop-. C/ }  O& P3 V$ d/ {. C) l. k+ ?
ment without testicular enlargement, which was due$ @: C* W& u- m) @# Q
to the unintentional exposure to androgen gel used by
! T3 a" k9 u4 g- l2 e. d% xthe father. The family initially concealed this infor-9 r0 M0 k" H7 }
mation, resulting in an extensive work-up for this
, C4 J( P6 Q! R. m$ B, Uchild. Given the widespread and easy availability of; X# i' g6 f8 l: R; W
testosterone gel and cream, we believe this is proba-
& m& E) Z. g! y3 V: s' ebly more common than the rare case report in the
" `# S* q' c% z, Y4 E( |literature.4
) b$ w: l4 m' o1 L" w5 i8 R2 mPatient Report8 T" U4 f3 Q; M4 b& P4 z  i" `- |% ]  d
A 16-month-old white child was referred to the- R& D  n6 i7 V! p
endocrine clinic by his pediatrician with the concern
# k  k4 [4 z# d' i7 }* P. Wof early sexual development. His mother noticed
# W4 U( O: g- V$ U( a% }light colored pubic hair development when he was- M6 q- Z+ p+ m
From the 1Division of Pediatric Endocrinology, 2University of
$ N( N! D: ~7 w! ?9 |1 `) XSouth Alabama Medical Center, Mobile, Alabama.
  p" b0 I1 W) t1 l+ [Address correspondence to: Samar K. Bhowmick, MD, FACE,
/ q2 r  V- n+ J( F, i' uProfessor of Pediatrics, University of South Alabama, College of
' Y& c/ F% L: N( o! @Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;, u1 Z+ D7 w; T
e-mail: [email protected].+ [( E- H. d# G$ e9 x: z  W2 T" u
about 6 to 7 months old, which progressively became6 a* k% X3 _7 I% f" a- M8 L
darker. She was also concerned about the enlarge-! ?' ?  k2 h! _9 h& f% J+ S
ment of his penis and frequent erections. The child
$ u0 O2 l) \" Zwas the product of a full-term normal delivery, with  y1 F/ V$ m" ^
a birth weight of 7 lb 14 oz, and birth length of) `% N( J$ |5 e5 Q+ U" M5 U, x/ }8 j
20 inches. He was breast-fed throughout the first year& n1 d' C; \( |* c8 M) S- c6 E4 _
of life and was still receiving breast milk along with
9 o& z3 y/ \/ Z8 Esolid food. He had no hospitalizations or surgery,; o  [$ t; l# ^0 @7 S+ }5 n
and his psychosocial and psychomotor development+ h7 p3 B4 u$ x* M
was age appropriate.' G; b5 w' h5 ?
The family history was remarkable for the father,! ]" Q, f- n& C7 A5 T& m3 x
who was diagnosed with hypothyroidism at age 16,' D' A) x+ L) i9 p
which was treated with thyroxine. The father’s; b, O* V8 v; S  ^: l
height was 6 feet, and he went through a somewhat+ B9 P% w4 b  _$ J% C
early puberty and had stopped growing by age 14./ z; f) e, \+ ]5 L  u0 U" ^5 @
The father denied taking any other medication. The
! Q5 j$ R- k; G+ t+ Y# ]child’s mother was in good health. Her menarche# N; G7 C0 F* }
was at 11 years of age, and her height was at 5 feet: H* u* P) w- a. [3 v
5 inches. There was no other family history of pre-& `( |2 c0 W* y% t; }3 W8 B
cocious sexual development in the first-degree rela-2 Y+ v; ]+ e  T9 x3 i& e- d% V( S
tives. There were no siblings.
( G+ h3 p9 J! j1 D9 TPhysical Examination
! k. X; \  T* Y& k  UThe physical examination revealed a very active,
+ N% t2 S, e. Y0 |! Q5 u# F5 O4 D; E9 |playful, and healthy boy. The vital signs documented: V  H3 T7 G- K$ n; g  L
a blood pressure of 85/50 mm Hg, his length was
) O1 s: e& X9 h; ?" d" a( _90 cm (>97th percentile), and his weight was 14.4 kg* ?- b' y  J/ u* C
(also >97th percentile). The observed yearly growth
' Y' a/ n6 B* e. V6 K3 [velocity was 30 cm (12 inches). The examination of* K. u1 i9 ?+ L! W1 S) {8 j
the neck revealed no thyroid enlargement.* f, S$ T& d3 S$ Q. l' I7 m0 U
The genitourinary examination was remarkable for4 ?/ |( J) C0 j+ W. w
enlargement of the penis, with a stretched length of
( e: u- @% p) }; T8 cm and a width of 2 cm. The glans penis was very well- `% w. G* p& J+ a% @/ M2 r% s" z
developed. The pubic hair was Tanner II, mostly around% T/ M( r* }* j" t3 T6 N+ e( U
540/ _% ~7 ]/ L, Q6 S8 d& j' T
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 k( w* T; \2 a0 y7 y# K1 ~the base of the phallus and was dark and curled. The
" M& D& p- p- [0 X$ o2 ktesticular volume was prepubertal at 2 mL each.+ |1 K. M+ W4 K! K( ?
The skin was moist and smooth and somewhat6 C! x% ]: u3 Y  ~2 n+ J0 ]7 R
oily. No axillary hair was noted. There were no( F4 d3 Z3 L; Q$ q) M% Y' \1 A& w" S
abnormal skin pigmentations or café-au-lait spots.3 F, O& c0 V& c0 b1 b
Neurologic evaluation showed deep tendon reflex 2+
, [3 L3 d& L  p! s4 }$ O5 Q0 Obilateral and symmetrical. There was no suggestion
& ]# B; N$ E3 e& S" U( G" Dof papilledema.3 V5 ?7 v3 C5 t8 r% C3 {+ e
Laboratory Evaluation7 U8 D) Z" Y( O1 @/ t' a
The bone age was consistent with 28 months by* p( s" E3 a+ X* b. t- a
using the standard of Greulich and Pyle at a chrono-
7 D1 o3 d6 e/ ilogic age of 16 months (advanced).5 Chromosomal
1 P8 K% }( q! l+ ?$ O3 g6 ~karyotype was 46XY. The thyroid function test
4 k& X# `& v4 p7 M! [showed a free T4 of 1.69 ng/dL, and thyroid stimu-
* [2 g& I3 \6 S: `; \$ F4 ?lating hormone level was 1.3 µIU/mL (both normal).  T$ W% ]: `3 u$ @/ v- t0 x; Z9 u$ ^
The concentrations of serum electrolytes, blood
% E) A. l1 j4 K* ^1 Murea nitrogen, creatinine, and calcium all were) i2 x/ _, J: h( o1 ^# z" I! e
within normal range for his age. The concentration  ?6 i& y9 s7 |: f0 u
of serum 17-hydroxyprogesterone was 16 ng/dL& y( a+ d+ e) q* C; R
(normal, 3 to 90 ng/dL), androstenedione was 20  B* p4 x) ?2 b4 a3 f
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
+ }8 `  f* j5 i: l+ S8 h) [, |terone was 38 ng/dL (normal, 50 to 760 ng/dL),
8 M# w( ^. j3 l( K2 E+ S/ \' ldesoxycorticosterone was 4.3 ng/dL (normal, 7 to
4 G1 p& p8 v" _: ]+ R  @# s49ng/dL), 11-desoxycortisol (specific compound S)3 {. U$ ~) [3 t* N$ i
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
& I2 i  r3 @& J/ w5 @$ R0 Dtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total  X* J# t) Q  [2 x8 I. L6 q
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
# Y* J; E; x3 k5 `" Cand β-human chorionic gonadotropin was less than' x' n7 l* e; |% F0 `: y% Z5 A7 @
5 mIU/mL (normal <5 mIU/mL). Serum follicular
6 G" Q0 c; {3 C5 ~stimulating hormone and leuteinizing hormone
3 t: v1 L3 y$ ~% nconcentrations were less than 0.05 mIU/mL
+ G& L: I) ^6 Y$ w9 f(prepubertal).  Z$ q4 O8 K  P8 c! A0 W
The parents were notified about the laboratory9 ^+ u& _9 h1 C( V2 D0 k
results and were informed that all of the tests were
* |! _8 d, Y3 D7 ^5 Y0 [1 |normal except the testosterone level was high. The
  }0 }# n; K' \( Z# l: b4 \follow-up visit was arranged within a few weeks to+ i/ m4 E9 B4 `! L, ?/ k7 U, y
obtain testicular and abdominal sonograms; how-
" V; k" m. n. Kever, the family did not return for 4 months.
$ H7 U. Y4 B* X5 _& t! ^7 i/ ^Physical examination at this time revealed that the
; \/ C( w2 Q" |: o& t% H; ^2 [child had grown 2.5 cm in 4 months and had gained- A4 B- ?% z) ?- w
2 kg of weight. Physical examination remained
# l  p/ ?4 h; w4 Punchanged. Surprisingly, the pubic hair almost com-
( n3 X/ f. r6 U* _pletely disappeared except for a few vellous hairs at
  U6 r  f& N) jthe base of the phallus. Testicular volume was still 2
4 w6 `* E3 W& P4 r" cmL, and the size of the penis remained unchanged.; d2 ?" i5 i2 f# m4 R
The mother also said that the boy was no longer hav-
) H7 S, X, p. M( q* W6 Qing frequent erections.+ [- W' q) P. c
Both parents were again questioned about use of2 Y9 ^, P0 W, L: {# Z. a
any ointment/creams that they may have applied to; D3 x6 u2 `6 |: @: H" L
the child’s skin. This time the father admitted the$ f: j' Y! N# n' _3 V4 ?. Q
Topical Testosterone Exposure / Bhowmick et al 541% M9 o- ?; e) M  {3 x$ C. U! _; V
use of testosterone gel twice daily that he was apply-* i' W$ O) n2 T. E) a$ x4 @
ing over his own shoulders, chest, and back area for5 r3 ?9 |, W: |# o
a year. The father also revealed he was embarrassed
* n. y) S* [& R+ W. _to disclose that he was using a testosterone gel pre-+ l/ s' r. u6 S+ o7 P" n6 ~
scribed by his family physician for decreased libido* E3 ]9 M, c9 v) @  @# N
secondary to depression.
. u7 \) x  v, F6 w  ZThe child slept in the same bed with parents.
/ ^- @0 T  a- d8 Z8 uThe father would hug the baby and hold him on his
5 F* I9 R$ c; b+ V1 M5 achest for a considerable period of time, causing sig-7 y: S5 o8 E& O) ^* X
nificant bare skin contact between baby and father.8 x  M$ w) Y  {+ Q0 m! ?
The father also admitted that after the phone call,5 @" J/ ]! y' L; ^
when he learned the testosterone level in the baby
5 Z. i+ Q' E0 t- F8 ewas high, he then read the product information
" s. X- a* K6 q! Bpacket and concluded that it was most likely the rea-" g' u8 s) @+ v2 T" r
son for the child’s virilization. At that time, they; `1 d6 @. U3 C3 [9 E7 g# y
decided to put the baby in a separate bed, and the
/ i; r$ `6 C. ^, s9 B8 X0 E: `father was not hugging him with bare skin and had
; f( O+ h5 \% O- |! ]been using protective clothing. A repeat testosterone
9 V9 {+ E0 B2 f1 Ztest was ordered, but the family did not go to the3 ~+ I% O* S& \) t, A4 x6 w2 U; K
laboratory to obtain the test.
, O! [  m5 D* T4 y- BDiscussion
7 e5 _# n4 U! R7 e5 uPrecocious puberty in boys is defined as secondary) L! |, k: u! }+ m& Q  B: Z! m; R/ K
sexual development before 9 years of age.1,4# ~+ u4 a/ ^' m/ w# u# |; ?
Precocious puberty is termed as central (true) when
  L( V; D! z0 i8 X, a; _$ Z. mit is caused by the premature activation of hypo-6 {+ b  |- S  j) d- w
thalamic pituitary gonadal axis. CPP is more com-' Y+ A# ?$ u0 ]4 o9 w0 N
mon in girls than in boys.1,3 Most boys with CPP
, G3 A$ }% i+ C2 U+ i6 amay have a central nervous system lesion that is+ F& @) |" {9 Q1 U
responsible for the early activation of the hypothal-
( E2 ]' [8 L+ `$ [amic pituitary gonadal axis.1-3 Thus, greater empha-! z6 @) v4 I/ A6 i5 P( I
sis has been given to neuroradiologic imaging in
8 @3 g: F% Q" d1 fboys with precocious puberty. In addition to viril-
& t1 k  `6 P9 lization, the clinical hallmark of CPP is the symmet-" A& \6 \" ]' b( U8 Q0 Y
rical testicular growth secondary to stimulation by
4 C* W( A, z7 K) h. ?; ygonadotropins.1,3) B6 ?4 ^" T; ]1 V( n; |
Gonadotropin-independent peripheral preco-' A  \0 \6 J$ T. a9 c
cious puberty in boys also results from inappropriate
$ k5 K( f3 G) i4 Aandrogenic stimulation from either endogenous or" @) s5 `6 O( b( x
exogenous sources, nonpituitary gonadotropin stim-1 @$ G* n% r# P% Y2 C
ulation, and rare activating mutations.3 Virilizing
* b5 q0 V1 e0 @5 T+ S, s$ e/ w4 j: xcongenital adrenal hyperplasia producing excessive- j- a8 y8 F2 b- h: R/ D- k
adrenal androgens is a common cause of precocious
  C" R, r/ F4 B) Ppuberty in boys.3,4# a& I' ^& @6 X, D
The most common form of congenital adrenal
* }+ E0 k2 k6 o& w9 a9 B5 Fhyperplasia is the 21-hydroxylase enzyme deficiency.
6 q& `0 A/ X2 e$ T4 A9 c$ S" h5 V4 GThe 11-β hydroxylase deficiency may also result in
; J3 d! b; o8 Fexcessive adrenal androgen production, and rarely,
0 a6 p7 E5 T; M3 ~- ~3 b% U/ z6 Uan adrenal tumor may also cause adrenal androgen4 j/ {+ Q) r. M2 f1 Y0 a
excess.1,3  b" B% ~/ w# p' ]( I- ?
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
. Z% N; e% k! c( u" ?1 B" m% d' V" v542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
. \* m( Y+ d; P3 iA unique entity of male-limited gonadotropin-' \* F7 J) r# {, z% `! b- b, O
independent precocious puberty, which is also known0 W7 D9 O8 }% O% ^: s
as testotoxicosis, may cause precocious puberty at a
/ n. i+ h! ^  Xvery young age. The physical findings in these boys: r3 ?- G" f6 ?, p/ b8 R5 m9 }: L
with this disorder are full pubertal development,6 s3 U) ~2 G, S3 G+ H" }. |
including bilateral testicular growth, similar to boys6 M* ^8 F3 G- Y3 F' l# M
with CPP. The gonadotropin levels in this disorder/ G7 Q, R! c) t2 q& u
are suppressed to prepubertal levels and do not show
$ n  m9 [! i: p4 Z( {pubertal response of gonadotropin after gonadotropin-
3 [3 w  }1 _  `4 w* ]( lreleasing hormone stimulation. This is a sex-linked0 Y6 d( G; E$ d0 Q, A7 P% E* f
autosomal dominant disorder that affects only8 B! ?  o7 c* T  e
males; therefore, other male members of the family+ x0 }: \8 V5 C0 G4 O5 d
may have similar precocious puberty.3: i1 ~( Y2 N* G
In our patient, physical examination was incon-0 I: ]# h2 }; W' ?- O4 g
sistent with true precocious puberty since his testi-
. T/ m' A4 ]- c% B2 Lcles were prepubertal in size. However, testotoxicosis6 I. m4 ?+ h  ?: @
was in the differential diagnosis because his father4 E$ t0 ?+ m$ t, [; ?1 L
started puberty somewhat early, and occasionally,
* l" b9 _; d( n' Ntesticular enlargement is not that evident in the! m& i. u8 i; E! h, M3 ?
beginning of this process.1 In the absence of a neg-
5 {$ _- t6 v" g! I1 Rative initial history of androgen exposure, our4 A1 c- t6 i  F& g- d  p
biggest concern was virilizing adrenal hyperplasia,5 O+ }( e' }4 p% ~
either 21-hydroxylase deficiency or 11-β hydroxylase
6 P# k, g6 j( |1 t6 z- h9 Pdeficiency. Those diagnoses were excluded by find-
, U/ A1 x! y4 q2 T8 f( s( ring the normal level of adrenal steroids.
; f( q9 \! _/ b6 |The diagnosis of exogenous androgens was strongly  t2 s1 M- }& q$ N& Q+ @- O& d. R
suspected in a follow-up visit after 4 months because, [7 w, T3 ]8 J2 W" W0 F0 o7 h
the physical examination revealed the complete disap-
0 b, B% G$ i9 o2 P3 @1 Hpearance of pubic hair, normal growth velocity, and
# H# {* P% u/ z6 U+ V2 v( M2 wdecreased erections. The father admitted using a testos-
( J2 {1 q9 h5 ~& i- U$ A# r# V; hterone gel, which he concealed at first visit. He was% y4 p- H/ c, ^) P! L
using it rather frequently, twice a day. The Physicians’1 ?4 T$ `6 L- a6 ]3 }5 L# e' W" m3 T4 g
Desk Reference, or package insert of this product, gel or$ p; m1 U% b8 f6 e7 @/ Z  e
cream, cautions about dermal testosterone transfer to; T/ X2 N: s6 ~! ]
unprotected females through direct skin exposure.
& c# V9 B# O# d$ |7 o& `Serum testosterone level was found to be 2 times the
# f2 P' [- I/ Zbaseline value in those females who were exposed to
+ w! }. O& Y5 M* Peven 15 minutes of direct skin contact with their male
8 I1 B/ o8 W7 t! T4 E! Vpartners.6 However, when a shirt covered the applica-8 m* j$ }* u: g( x
tion site, this testosterone transfer was prevented.
1 Y5 C) Y0 q# G& v) o4 r( w7 Q5 JOur patient’s testosterone level was 60 ng/mL,
& H( T' w$ r5 O. l6 a0 z/ |which was clearly high. Some studies suggest that6 L  h& p- x3 F% K, s# e, y
dermal conversion of testosterone to dihydrotestos-
: Y5 K6 a$ ~3 a8 b% D& Dterone, which is a more potent metabolite, is more
$ f( S# J- X: j4 j; u9 Ractive in young children exposed to testosterone/ h  g; r6 W/ m- z0 X) Z7 \
exogenously7; however, we did not measure a dihy-
/ v* N: o4 M6 J) Mdrotestosterone level in our patient. In addition to3 A7 @8 D4 ~( l, l& c
virilization, exposure to exogenous testosterone in2 W1 x7 ]6 s0 Y5 r
children results in an increase in growth velocity and
$ r- y& ]8 ~* k7 `$ }  T) a) [advanced bone age, as seen in our patient.. L; A) K8 B9 f0 `
The long-term effect of androgen exposure during- }, z' A! U0 r
early childhood on pubertal development and final. Y! B: j7 i" }0 B
adult height are not fully known and always remain7 g# d$ g+ ^$ i) B6 Q
a concern. Children treated with short-term testos-
) ~& Q4 y& o$ {$ B- h6 oterone injection or topical androgen may exhibit some  O5 i5 Y0 q, j
acceleration of the skeletal maturation; however, after
& G' n  Z# q. I. q' K; qcessation of treatment, the rate of bone maturation
. E1 h5 n8 Z; P3 d6 Z& S6 D" tdecelerates and gradually returns to normal.8,9
* q0 {/ d/ o9 f. yThere are conflicting reports and controversy
5 \! d0 J/ k$ Vover the effect of early androgen exposure on adult
) T: U7 P4 f. e& ^# dpenile length.10,11 Some reports suggest subnormal8 J" o% H2 x! e+ X2 T% F
adult penile length, apparently because of downreg-1 d8 ]( z  W+ W3 g9 s  _
ulation of androgen receptor number.10,12 However,
1 D# o$ O0 k* I1 X0 V# WSutherland et al13 did not find a correlation between
' z$ U1 l5 j" p6 U- Q- k8 mchildhood testosterone exposure and reduced adult2 G  H1 o! P; D, E- e" k
penile length in clinical studies.$ I% Q4 {. W  q$ G; i. r. m
Nonetheless, we do not believe our patient is; E' ^/ d8 V8 v! d' q
going to experience any of the untoward effects from/ i" C" C* o. z8 G7 J: |* ^
testosterone exposure as mentioned earlier because* Q4 a2 `# Y, Z8 T1 o8 }$ y) X. B
the exposure was not for a prolonged period of time.
# i; P9 f; B' @" w9 |3 P& a* DAlthough the bone age was advanced at the time of
# T7 h( y* Y4 f4 ]3 [- kdiagnosis, the child had a normal growth velocity at5 c& s! e' Q" y5 f0 `2 W/ R$ W3 @2 e
the follow-up visit. It is hoped that his final adult
2 b" ^8 k  c0 @: Gheight will not be affected.; G  A% o( T# Z8 ~; I
Although rarely reported, the widespread avail-
8 v4 n& S/ c$ z* Q" ]+ v# oability of androgen products in our society may
+ j1 u( {7 l% y  ]/ ~indeed cause more virilization in male or female
; J" E0 n, m+ [* d0 ?- o2 W4 hchildren than one would realize. Exposure to andro-
* Q0 D- s, [  d; k7 k# f; tgen products must be considered and specific ques-3 T$ f/ U1 P" {, g% }8 D9 {
tioning about the use of a testosterone product or
6 e; w$ F, M0 {4 fgel should be asked of the family members during
# S, G) p( t+ Z0 A# v2 \7 sthe evaluation of any children who present with vir-3 Y' ^9 G8 D4 W, o8 E) |
ilization or peripheral precocious puberty. The diag-( [* R# F+ ^1 j" u/ n/ J  D
nosis can be established by just a few tests and by
( g' ~7 B/ T$ o: A& _6 n. ~appropriate history. The inability to obtain such a
! z# z9 h$ U  `history, or failure to ask the specific questions, may
* N4 x5 k' ]$ R4 K& q. Y$ u$ Tresult in extensive, unnecessary, and expensive
9 p: H3 s- l: m* N1 _' ?+ j, x( O% rinvestigation. The primary care physician should be
+ O( P. d3 m, \  u! E$ u0 aaware of this fact, because most of these children
% B# Y- _2 g# M. q9 ]. tmay initially present in their practice. The Physicians’
# g: D& B' A# j7 e( SDesk Reference and package insert should also put a: K1 u7 G6 ~4 u5 o: y5 ~
warning about the virilizing effect on a male or
5 H) s% {# N; o8 T" w; O6 C9 Kfemale child who might come in contact with some-8 L( n% t2 r1 M- R# \: Q& U2 Z
one using any of these products.
; M- {/ D3 }( o1 W) |, sReferences
' ^6 Y3 E* p5 c; m* ^+ \* n1. Styne DM. The testes: disorder of sexual differentiation
( h! w) n6 v1 }/ E! eand puberty in the male. In: Sperling MA, ed. Pediatric: L& W. S! U2 d# ?9 j( S. _
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
8 B4 ]3 {" ?1 c; d- ]% ~2002: 565-628.
; D! `0 h8 S# m0 V2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
9 q6 Z# D4 j! z$ z! w  b$ mpuberty 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
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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

! K9 K/ t# f4 k3 B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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