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Sexual Precocity in a 16-Month-Old, f5 T8 U4 `/ T( i
Boy Induced by Indirect Topical0 b0 M3 e. d" p8 A) M: i; l" ]
Exposure to Testosterone
8 I' l* \! |, q% v/ U) wSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2' D; ^2 F- y- P4 V! G
and Kenneth R. Rettig, MD1) g; W6 h3 g, l. F9 ]0 o
Clinical Pediatrics
$ ~) d+ q. Q9 f" m+ AVolume 46 Number 6
" _2 v( x  E3 PJuly 2007 540-5437 c; T& G1 L" k, s" U
© 2007 Sage Publications0 M& j. S1 r, c5 C% G
10.1177/0009922806296651
. ^8 J, L" o: E9 ~- phttp://clp.sagepub.com& }* k% J8 W5 b- k
hosted at
! ?6 m8 R$ G3 C. Ihttp://online.sagepub.com# j1 {4 @8 J" T8 |' a) p
Precocious puberty in boys, central or peripheral,/ \# c9 I, o( b# |0 L  ^& V
is a significant concern for physicians. Central, X2 J  k/ c$ G! g+ w
precocious puberty (CPP), which is mediated! N; r, a: v* @5 w3 a
through the hypothalamic pituitary gonadal axis, has
3 k/ r0 q$ y9 N$ ?a higher incidence of organic central nervous system  s+ n6 z3 K0 w% l" J8 X
lesions in boys.1,2 Virilization in boys, as manifested: N4 e8 i+ o6 s( r& H* M
by enlargement of the penis, development of pubic
" b$ r" k+ n' X9 k; m/ T; @hair, and facial acne without enlargement of testi-
( ]! f: k0 e' x8 Zcles, suggests peripheral or pseudopuberty.1-3 We% a: i. D$ I. u! F& X9 L
report a 16-month-old boy who presented with the
, D$ c, l3 h" T  @2 b9 c; \5 E, x2 ]" fenlargement of the phallus and pubic hair develop-3 L; n  a. L8 \" s3 Z% I( a* p5 p
ment without testicular enlargement, which was due
+ h# j. r) s' v4 O, dto the unintentional exposure to androgen gel used by
4 Z5 n* N9 A& N. j. |, I+ z( \the father. The family initially concealed this infor-
3 o& X0 L/ B  w, h$ vmation, resulting in an extensive work-up for this/ J$ M# k7 j1 g: M) a
child. Given the widespread and easy availability of& Z3 q, n+ K9 z6 G
testosterone gel and cream, we believe this is proba-, h( g' j. Q) U# \6 `: t
bly more common than the rare case report in the
* J% E1 w: @) Y8 E5 u$ S8 X* Aliterature.4. F0 Q, G4 o$ {# I
Patient Report2 Y8 o! \* M+ i1 R
A 16-month-old white child was referred to the4 }/ i$ o7 J. [: L2 }
endocrine clinic by his pediatrician with the concern2 G* S2 m  b1 y4 x3 G
of early sexual development. His mother noticed
" f+ Z! E" N7 }; P- \light colored pubic hair development when he was
0 k7 h) Q8 f; L1 V" J- HFrom the 1Division of Pediatric Endocrinology, 2University of* `$ O1 z4 a" c6 C# P, w; }
South Alabama Medical Center, Mobile, Alabama.4 h$ ^1 ?0 k4 w7 |' T* X: a; j
Address correspondence to: Samar K. Bhowmick, MD, FACE,9 r+ \4 F9 I, g. R( _, e) w) Z
Professor of Pediatrics, University of South Alabama, College of
6 v' p, F- ]* x# f5 W$ VMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;2 g: S) H7 ^: i
e-mail: [email protected].
0 Y5 _7 X* B' f% x2 y/ c- }& B" Uabout 6 to 7 months old, which progressively became+ g9 o( s$ m+ ^5 v* v" J2 g7 |
darker. She was also concerned about the enlarge-
8 e( F" E0 @+ D" C# c2 fment of his penis and frequent erections. The child
$ w' L, ?6 u2 B. C" `- Jwas the product of a full-term normal delivery, with
# E  K2 \% z. W0 l' |8 s" b2 ^a birth weight of 7 lb 14 oz, and birth length of6 x% s, c* P2 W9 a) l5 E
20 inches. He was breast-fed throughout the first year
& o7 F- X1 b' E  T* Wof life and was still receiving breast milk along with
6 M1 {2 F: r; {solid food. He had no hospitalizations or surgery,# n; p! P7 q- z' a. ?3 P! k( M! f* e/ ~% H
and his psychosocial and psychomotor development/ o6 _; E, t; D2 R+ b
was age appropriate.5 |2 O# ~7 J' V& }4 a3 |
The family history was remarkable for the father,
0 h+ J2 T# U" l( J/ |# I8 @9 B% D9 Lwho was diagnosed with hypothyroidism at age 16,
/ \' ]9 c: M" v7 }" ^0 {which was treated with thyroxine. The father’s5 D/ F+ W. L( X8 A
height was 6 feet, and he went through a somewhat5 X3 z0 ]; y6 W. A7 }% ~9 C9 p( ^6 H2 Q
early puberty and had stopped growing by age 14.
5 \4 Z5 t! A8 W2 A2 A* }* l9 e. ?  kThe father denied taking any other medication. The; J. J! j7 T  o% y8 J7 |  H/ B
child’s mother was in good health. Her menarche
$ V3 k. s2 X5 w9 G* rwas at 11 years of age, and her height was at 5 feet" h: P6 C) ]2 |4 H; ]
5 inches. There was no other family history of pre-) V9 P8 K1 f' F8 R, I
cocious sexual development in the first-degree rela-
1 R  v2 O! a# n+ jtives. There were no siblings.- f) K2 K  C2 s! t2 x
Physical Examination6 E5 `3 w! f0 }5 K
The physical examination revealed a very active," m( R" P% `3 T- M  ~& @2 Y
playful, and healthy boy. The vital signs documented
3 O+ ?  B0 C2 U# Xa blood pressure of 85/50 mm Hg, his length was8 j5 n" ~, R5 c! ?
90 cm (>97th percentile), and his weight was 14.4 kg: S% V, d4 B! T4 W( e5 n
(also >97th percentile). The observed yearly growth
' Q/ [) Y, Y- D1 J9 ~9 Y7 w+ wvelocity was 30 cm (12 inches). The examination of
, M: m5 D) a; uthe neck revealed no thyroid enlargement.
8 S+ m- K9 p4 J7 u% q# s& KThe genitourinary examination was remarkable for4 r% @8 @: I* t- p* f" Z2 o2 i2 n8 o
enlargement of the penis, with a stretched length of
7 v) ]! ^2 @2 w: T# T) l# P8 K9 t8 cm and a width of 2 cm. The glans penis was very well
/ s# P- V% ^9 \4 {$ c& q$ Xdeveloped. The pubic hair was Tanner II, mostly around
! X% y; V, t6 g3 B" @540
# [3 @" K3 h1 s' m* p5 vat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 x: |( a2 f! }/ K2 ^/ l' s
the base of the phallus and was dark and curled. The
( _9 B' p! r: z2 ]testicular volume was prepubertal at 2 mL each.) c* V) P& a" p5 N! _9 R
The skin was moist and smooth and somewhat+ q  o6 O: U# B9 d2 L; I( ?9 g
oily. No axillary hair was noted. There were no4 R3 U8 E6 \( C* K8 a
abnormal skin pigmentations or café-au-lait spots.
% S+ P7 e* k' G+ }+ {Neurologic evaluation showed deep tendon reflex 2+, T! j( e5 ?$ L2 R# M0 u
bilateral and symmetrical. There was no suggestion
4 K, [2 p, C& ^. lof papilledema.6 P( H/ k# Q% l0 b  C$ f2 E, q( ^" w
Laboratory Evaluation) [1 S, D" H+ R
The bone age was consistent with 28 months by9 M$ z% K7 ]( X6 f$ Z
using the standard of Greulich and Pyle at a chrono-$ E5 l% c" c: K0 C' L. B& m: y
logic age of 16 months (advanced).5 Chromosomal# [+ R* y; R& \- y9 A+ u3 t' P
karyotype was 46XY. The thyroid function test
  z5 _  D9 v" v" p& z* Xshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
0 _, P, T" _4 M( ylating hormone level was 1.3 µIU/mL (both normal).
1 [3 u+ e: W6 B+ JThe concentrations of serum electrolytes, blood' s! l! `+ \+ g4 F
urea nitrogen, creatinine, and calcium all were6 c6 s+ B, z2 c' j) I5 I; g
within normal range for his age. The concentration
; g1 c, e( `  u% K; N- S9 [* Gof serum 17-hydroxyprogesterone was 16 ng/dL9 w& l4 a6 n% t7 V4 b0 I5 a
(normal, 3 to 90 ng/dL), androstenedione was 20
6 U4 C* O) d( yng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
6 K( j4 g6 D' Jterone was 38 ng/dL (normal, 50 to 760 ng/dL),8 K% ~) |0 R- O  W' Q
desoxycorticosterone was 4.3 ng/dL (normal, 7 to0 |7 ^2 ]  c! S# d. R  Q0 Y
49ng/dL), 11-desoxycortisol (specific compound S)+ w, k& Z1 {8 e: c+ h) T
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-% I6 |" W+ n, V" o7 e- k
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total5 ]5 `# c* b8 ^( t/ n, {8 o
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),2 h$ r- }) G. ^/ O2 S9 Z
and β-human chorionic gonadotropin was less than
0 q1 S+ S+ ~  f+ p$ g5 mIU/mL (normal <5 mIU/mL). Serum follicular7 E. R" S- _; W
stimulating hormone and leuteinizing hormone
' a: x3 J1 Q# g+ J  x& s# |& _concentrations were less than 0.05 mIU/mL
- ~8 H2 B6 x9 ?* H* N+ |5 r( R5 X9 [(prepubertal).+ J; ]8 S/ _8 ]! i8 @  I
The parents were notified about the laboratory
- [: n* z, ]" [  cresults and were informed that all of the tests were
$ M* ~" w1 P3 C0 c6 \3 qnormal except the testosterone level was high. The
* z; N! Z  \  q5 I! f/ M' Sfollow-up visit was arranged within a few weeks to+ |/ J% h+ E9 ^4 `0 t2 r) k, R
obtain testicular and abdominal sonograms; how-  z' w2 |9 P$ t9 {, s
ever, the family did not return for 4 months.
4 y  l% I' c" H8 G; UPhysical examination at this time revealed that the% W1 Z9 g' v& l8 _* j' v
child had grown 2.5 cm in 4 months and had gained
* C% w4 Y' d8 @2 kg of weight. Physical examination remained' p5 b& a  ]4 U/ i
unchanged. Surprisingly, the pubic hair almost com-4 f4 P" ?( A5 x. a0 B% W8 a6 F
pletely disappeared except for a few vellous hairs at; k; \* `" M* U+ `$ i
the base of the phallus. Testicular volume was still 25 Z5 {7 [: _/ T
mL, and the size of the penis remained unchanged.2 x, i3 J1 [& R
The mother also said that the boy was no longer hav-
6 e; |0 A- b4 M' Uing frequent erections.+ p7 ?* |- E2 Q
Both parents were again questioned about use of0 v! q+ @; w# b3 Z, a1 w6 Z. W
any ointment/creams that they may have applied to" T! B. A. J; {. }, q9 U7 h5 j
the child’s skin. This time the father admitted the
' q7 m* C3 p' b; S$ }/ B7 aTopical Testosterone Exposure / Bhowmick et al 541: s6 v) D  r  [4 l1 m2 n
use of testosterone gel twice daily that he was apply-
) o# E+ ]+ q# v5 ?' O! Ning over his own shoulders, chest, and back area for
5 b6 e+ K3 L' y6 ^a year. The father also revealed he was embarrassed/ H( L) y# I1 S# H4 }  e. R
to disclose that he was using a testosterone gel pre-8 W; W4 o- R' [* P
scribed by his family physician for decreased libido
; D/ _! }3 V+ }  o4 }+ S2 qsecondary to depression.
1 H' `& w* g  M6 A) J* RThe child slept in the same bed with parents.
! Z5 n( i! F) J# u) SThe father would hug the baby and hold him on his
. N. N2 r2 ^3 [' _2 A$ x' }chest for a considerable period of time, causing sig-. d1 x/ s* n* \9 J# B) c6 m) P
nificant bare skin contact between baby and father.
9 x" O( U& }4 c5 `3 \- n7 ZThe father also admitted that after the phone call,3 h1 \# N% I$ d- ]6 D
when he learned the testosterone level in the baby
+ u8 Y9 o8 _7 v5 y2 D2 Zwas high, he then read the product information2 S: B$ }  Y" b6 n
packet and concluded that it was most likely the rea-& f. H; t/ O  ~
son for the child’s virilization. At that time, they' {% w, s8 F! s0 _; g' C5 m: _1 Z- C
decided to put the baby in a separate bed, and the# W' F& U. c/ E$ `
father was not hugging him with bare skin and had
. H) s$ }7 b; rbeen using protective clothing. A repeat testosterone
* a6 f$ m1 _5 P0 o% j# V! v  R  |test was ordered, but the family did not go to the
7 ~$ X* P2 }- @' S1 N' v; ~laboratory to obtain the test.
% L: Z& e5 n. Q$ }8 w- \3 D8 vDiscussion
% K- D3 I9 Q) Q' n3 V$ IPrecocious puberty in boys is defined as secondary
9 a( H. p: z0 n- v' o* U$ s2 Gsexual development before 9 years of age.1,4
1 z- L6 g! N! ?Precocious puberty is termed as central (true) when5 q, j; d5 e4 [6 p- a
it is caused by the premature activation of hypo-
1 U. V4 P" Z. K+ jthalamic pituitary gonadal axis. CPP is more com-3 f# _; X# B9 ~3 p( F
mon in girls than in boys.1,3 Most boys with CPP
# ?% a. D3 V1 a6 ]1 j+ amay have a central nervous system lesion that is7 n5 ~" d& d- j# @/ k
responsible for the early activation of the hypothal-: s0 S5 F+ ~8 [
amic pituitary gonadal axis.1-3 Thus, greater empha-
, C4 B1 g7 g5 g3 }: J4 G9 ^% M* l* jsis has been given to neuroradiologic imaging in$ c4 R8 x) W9 A% [' _* K
boys with precocious puberty. In addition to viril-
  Z/ K# `6 {# ~) o# uization, the clinical hallmark of CPP is the symmet-
9 o% O; q! ?, i8 P4 H6 Srical testicular growth secondary to stimulation by: _% R% N, q  t# H
gonadotropins.1,3  k& m: V) F! I$ X
Gonadotropin-independent peripheral preco-" L5 S: l5 P. e+ c7 W2 k
cious puberty in boys also results from inappropriate
3 @2 x+ x$ {; |8 V* t' zandrogenic stimulation from either endogenous or
+ P! n% Q1 v& J4 Y& v5 i& Dexogenous sources, nonpituitary gonadotropin stim-9 |; K. Z' }$ m3 B7 r; R& }, o
ulation, and rare activating mutations.3 Virilizing
. e. }& [4 R, w' Hcongenital adrenal hyperplasia producing excessive
2 ]" {2 Y, m" Q9 v) yadrenal androgens is a common cause of precocious
  X; I* W0 Q) D3 Hpuberty in boys.3,4, `8 k1 g7 l6 u: L4 w: B% v+ _
The most common form of congenital adrenal/ D: ~% C6 S5 ^0 y0 q, U$ m
hyperplasia is the 21-hydroxylase enzyme deficiency.1 `% o+ t6 w  A: I
The 11-β hydroxylase deficiency may also result in$ o8 d" s6 X! u0 S' H: J* F* {
excessive adrenal androgen production, and rarely,9 L! B) J. H( [$ e% C5 g- h8 Q: T
an adrenal tumor may also cause adrenal androgen
6 C; U4 t8 o$ U- Xexcess.1,3
( Z' K6 P6 ^. e* h( hat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ Z% z, s. G# G' t6 g) S& J6 z) S542 Clinical Pediatrics / Vol. 46, No. 6, July 2007' I2 C: I5 J/ P/ }8 _* V
A unique entity of male-limited gonadotropin-) j8 A: n, @/ n5 }
independent precocious puberty, which is also known% G, U$ e) t  t4 |# e
as testotoxicosis, may cause precocious puberty at a
+ z2 Z9 o$ J2 V. ]$ g$ X7 _/ Bvery young age. The physical findings in these boys- r- i3 h1 I0 r& L0 n8 c
with this disorder are full pubertal development,) [# ^2 a7 V4 y$ h% g
including bilateral testicular growth, similar to boys
) r+ I- w2 T* H5 }8 Kwith CPP. The gonadotropin levels in this disorder( @0 R3 h; Q3 Z- t) j
are suppressed to prepubertal levels and do not show
1 p/ H# C( ?: Z- Kpubertal response of gonadotropin after gonadotropin-
7 _- S% x" k) e/ q5 |5 z7 i8 T" Wreleasing hormone stimulation. This is a sex-linked
" G3 G/ o6 ]. @3 X  ^( W; [1 T. @1 aautosomal dominant disorder that affects only: e; {  P0 }' u8 |7 b
males; therefore, other male members of the family
- x# h0 v+ Z7 ?& y! w( R0 \may have similar precocious puberty.3$ \8 B9 O. ^# C+ P
In our patient, physical examination was incon-
! E) V  [/ g8 X7 c3 V2 |% vsistent with true precocious puberty since his testi-; e' y: P- P$ X# C* l: o
cles were prepubertal in size. However, testotoxicosis/ }3 l( v: ?- X6 z& i) G: a5 {" _
was in the differential diagnosis because his father
" e/ Z" D) d  o" ~; y( g+ Xstarted puberty somewhat early, and occasionally,2 b1 D) v/ E8 |: d6 G
testicular enlargement is not that evident in the
! ^3 T8 d( Y& i% p2 i7 |5 G5 qbeginning of this process.1 In the absence of a neg-& q! K6 Y( j" P4 n- F5 q( w9 g
ative initial history of androgen exposure, our
; o3 `3 n9 E- m2 P( L8 E5 K! P8 mbiggest concern was virilizing adrenal hyperplasia,
6 e. k  K4 \$ P. O% veither 21-hydroxylase deficiency or 11-β hydroxylase
" i' t: E4 ^& t: ~( z3 C; Tdeficiency. Those diagnoses were excluded by find-+ G. O1 r( \) Q! k5 ]
ing the normal level of adrenal steroids.3 D0 e" R" u) z; X" e
The diagnosis of exogenous androgens was strongly
. \% t  l6 ~* X" Csuspected in a follow-up visit after 4 months because
: Z; \# j9 A1 k; T2 kthe physical examination revealed the complete disap-
. R* Z+ k, u* d2 B) v4 t) l* t. Wpearance of pubic hair, normal growth velocity, and. N! a: \; d/ D) E
decreased erections. The father admitted using a testos-
( _7 y( [8 O6 Cterone gel, which he concealed at first visit. He was( j) z7 |% j8 y% b/ _8 g* u
using it rather frequently, twice a day. The Physicians’
/ @9 T8 k* ]0 |2 _. q5 I6 v% Z8 ]Desk Reference, or package insert of this product, gel or# v. R2 x$ L) |4 g# l$ Z- h
cream, cautions about dermal testosterone transfer to
% W3 S& j& h3 q( v& M( |0 `& z$ dunprotected females through direct skin exposure.$ }3 `7 P2 Z6 j! Y" U
Serum testosterone level was found to be 2 times the
/ B5 o7 @- r8 H- bbaseline value in those females who were exposed to
. e1 Q, H: }* y0 Z; Peven 15 minutes of direct skin contact with their male; d) q6 k5 E$ q9 Z
partners.6 However, when a shirt covered the applica-' ^) ?* k$ }7 ]$ k
tion site, this testosterone transfer was prevented.$ i/ @7 v& j$ B, ^5 y
Our patient’s testosterone level was 60 ng/mL,8 R  P9 l5 M5 ^0 V
which was clearly high. Some studies suggest that/ C8 n* k6 \1 C
dermal conversion of testosterone to dihydrotestos-: p+ E' R! p  w1 R! y
terone, which is a more potent metabolite, is more& g. Y# @$ R% ?! K* A
active in young children exposed to testosterone
' \8 r7 {% B. ^exogenously7; however, we did not measure a dihy-- `8 \, k( u& }, p6 l& p
drotestosterone level in our patient. In addition to2 q9 a; d' e9 v0 r# n
virilization, exposure to exogenous testosterone in  }( n! C7 p( i: l5 p) N
children results in an increase in growth velocity and
# G* ]/ |- U* ]1 W+ tadvanced bone age, as seen in our patient.
* T' z- W2 N6 c# }8 f" `* LThe long-term effect of androgen exposure during4 k" u1 v2 w: d5 L' |3 X4 z+ r2 R
early childhood on pubertal development and final# {9 x9 D7 l: _. s
adult height are not fully known and always remain' N  i. L) g. \/ Y( b% s; S9 G
a concern. Children treated with short-term testos-, y0 |+ a$ F  @
terone injection or topical androgen may exhibit some
4 G- h1 T6 Z2 c) h7 }acceleration of the skeletal maturation; however, after9 @% o3 j5 H; U+ p) V
cessation of treatment, the rate of bone maturation
, \- k  [; F7 u9 w3 V- odecelerates and gradually returns to normal.8,9
; l& z5 A4 i( NThere are conflicting reports and controversy0 T4 b2 ?4 ^. P# h
over the effect of early androgen exposure on adult
$ v. A4 G' u7 T  i2 y" _$ Openile length.10,11 Some reports suggest subnormal( u- [) m, c1 D
adult penile length, apparently because of downreg-
$ ?# F0 J5 c) x; [6 Gulation of androgen receptor number.10,12 However,$ W% I& h7 l) m8 O' Q$ P
Sutherland et al13 did not find a correlation between# v- W  a  v+ }% [/ z2 C
childhood testosterone exposure and reduced adult
& N9 \" _# W. U0 i# Xpenile length in clinical studies.4 Z* o6 t+ W, y- b$ u
Nonetheless, we do not believe our patient is! I3 k' l4 i8 ^' c
going to experience any of the untoward effects from/ {" l- ^/ F) ?
testosterone exposure as mentioned earlier because6 A$ N, j5 b- s0 B- J
the exposure was not for a prolonged period of time.
" x" T! O3 \2 q6 B) VAlthough the bone age was advanced at the time of
0 r0 N7 x$ F) F* G/ @. k" `; z0 q* c- ^diagnosis, the child had a normal growth velocity at* Z% I# c  g& @4 C$ C! j
the follow-up visit. It is hoped that his final adult
' W9 t" k- h! ]: e4 P6 Oheight will not be affected.: R1 r9 n' F0 \+ g. D* U% z
Although rarely reported, the widespread avail-* B- q  i" b; \/ |. F1 @
ability of androgen products in our society may  Q) Y0 x. g7 t! o) g
indeed cause more virilization in male or female5 P* |9 X  D0 V( z
children than one would realize. Exposure to andro-. s6 l1 r4 E: h( ]7 [# @$ D3 U! I
gen products must be considered and specific ques-9 e+ H# d2 ?" ?7 f5 F3 x
tioning about the use of a testosterone product or
& [; U. @# f+ c( a6 ygel should be asked of the family members during$ S' }2 o3 J2 k
the evaluation of any children who present with vir-
4 {  n1 A$ q" t+ {) e. }ilization or peripheral precocious puberty. The diag-6 [* r  S9 C. ^3 o$ E
nosis can be established by just a few tests and by) T( D: L+ a1 H
appropriate history. The inability to obtain such a
9 X$ D4 A. ]- w' S) l7 _  _history, or failure to ask the specific questions, may9 p! x3 j# n$ \; |  J# ]
result in extensive, unnecessary, and expensive! J  @/ G( t' i$ B
investigation. The primary care physician should be
/ D1 P. X* t0 S! v5 p1 qaware of this fact, because most of these children3 Z6 ?- l2 W7 @* U  ]
may initially present in their practice. The Physicians’
. ^0 r% w0 S! w- t8 v. F$ ~3 c: P7 zDesk Reference and package insert should also put a
! g5 c; V: S0 ^2 A8 Z$ i, Mwarning about the virilizing effect on a male or+ J6 Z$ Q6 m  m+ L# a) ~" l4 \
female child who might come in contact with some-
7 w6 U" Q% N0 G# c' @& T; Cone using any of these products.
) _/ ~( x% o2 E6 g$ j3 J7 i0 qReferences
: J+ G" t& m7 `: w8 F' D1. Styne DM. The testes: disorder of sexual differentiation$ z1 A/ x+ f3 e3 t3 ]
and puberty in the male. In: Sperling MA, ed. Pediatric
1 E  n: _' E) T* K& u, s+ Y/ SEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
& i) c( E: B# W3 `0 i2002: 565-628.2 @& d- s2 Y  ?* d  A
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
. B3 _! X% G+ D& w! s/ K* r( N+ Fpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
; Q, O% Y  L  ~' ?* kBoy Induced by Indirect Topical
; z( Z* S% K, b" T) c6 `  C( }Exposure to Testosterone
/ j* E2 I! S* Q4 n8 q/ W- W3 ]" ~Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
0 K" u; t0 ^$ [7 b% \% Nand Kenneth R. Rettig, MD1- y0 Q9 V% D$ B( m8 P8 E; d
Clinical Pediatrics
# f2 O; h0 _* a+ e; G! aVolume 46 Number 6
+ K8 L% N3 E/ C; u9 kJuly 2007 540-543
" O; \% p# y1 \5 u* h3 x© 2007 Sage Publications
! w" G# d2 I+ A( e2 Z10.1177/0009922806296651
$ f  D3 i8 a; h+ `$ g2 q4 \5 `http://clp.sagepub.com3 ?9 i6 I. a' _* j2 q0 W
hosted at7 P- j1 T9 J9 Q9 b( `1 t2 M
http://online.sagepub.com
! e, r4 C, x! w8 ~4 Y' B4 r5 BPrecocious puberty in boys, central or peripheral,. y/ W! R. J6 X2 V2 @& T2 ^
is a significant concern for physicians. Central) R9 p1 X/ Y6 [
precocious puberty (CPP), which is mediated
( w. l: `6 |+ F$ a- G3 @, Athrough the hypothalamic pituitary gonadal axis, has! ]; m) ~0 X# V
a higher incidence of organic central nervous system0 a) k% k, {" f: W5 R* \
lesions in boys.1,2 Virilization in boys, as manifested
1 v6 {  [& h( f3 b; ?by enlargement of the penis, development of pubic, |: S- @* i2 {5 Z8 f$ ~
hair, and facial acne without enlargement of testi-
7 P2 d2 B2 b0 {1 ccles, suggests peripheral or pseudopuberty.1-3 We
+ ?$ B9 r1 J' ~; `  V! w; {( k, Creport a 16-month-old boy who presented with the3 ?; {" P" j4 D$ b
enlargement of the phallus and pubic hair develop-0 r4 O2 t4 g- b) W1 c
ment without testicular enlargement, which was due5 O2 _& }' h  O1 d* e3 x8 v. Q
to the unintentional exposure to androgen gel used by2 t& U" q+ }$ h; O( b: h7 M$ a7 K
the father. The family initially concealed this infor-- f  d. h4 N' a' _( k& `
mation, resulting in an extensive work-up for this2 Y5 ~' S0 K- O# W$ S- [  U0 |
child. Given the widespread and easy availability of
4 A+ v; A! b) ]3 J5 btestosterone gel and cream, we believe this is proba-
. e) z: T. @7 F' e. [bly more common than the rare case report in the
$ ^3 ?/ l& i5 d$ F) T; sliterature.4
# {2 J, X9 k9 J. a" DPatient Report2 x6 j8 ^  l( ~3 s6 ~
A 16-month-old white child was referred to the
; o# {  Z3 K  Q& p' G0 `1 t& Oendocrine clinic by his pediatrician with the concern
. Q, R9 W+ q; o& g3 V& B% S7 aof early sexual development. His mother noticed
1 `  ^) g8 u9 ?* z  {2 vlight colored pubic hair development when he was
# @: N6 s+ ]8 q7 D/ |3 iFrom the 1Division of Pediatric Endocrinology, 2University of
' p# [) B: z% p3 D% ASouth Alabama Medical Center, Mobile, Alabama.  b, N; }6 q: ^4 F
Address correspondence to: Samar K. Bhowmick, MD, FACE,
. X0 }8 J* I; m1 e; MProfessor of Pediatrics, University of South Alabama, College of
) {5 Q8 x* {. S* ]; ^% FMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
3 c* J5 j% z7 j9 F7 Ie-mail: [email protected].  a* d& c: j1 F1 p6 O
about 6 to 7 months old, which progressively became) I( o2 @0 p3 {, X+ E! I( g6 q! w
darker. She was also concerned about the enlarge-* G- I) u+ s: o8 V
ment of his penis and frequent erections. The child* n: Y0 ?- D! d; O$ ~
was the product of a full-term normal delivery, with* L3 b% R1 T2 ~$ [  a
a birth weight of 7 lb 14 oz, and birth length of
# @+ p- a! D+ H" c& T, Z' s20 inches. He was breast-fed throughout the first year
2 Z/ B# F' v% i' Z: qof life and was still receiving breast milk along with
, D  H5 ^+ c1 osolid food. He had no hospitalizations or surgery,
7 e* k4 y% `9 A7 aand his psychosocial and psychomotor development
/ o$ m% S: W$ Y3 l. [was age appropriate.
/ t. U, `5 _. K# U1 ?0 _# F: M3 O5 IThe family history was remarkable for the father,
7 E4 Y! p: K9 e& L$ kwho was diagnosed with hypothyroidism at age 16,
. F9 _- O, x% y8 T+ G% wwhich was treated with thyroxine. The father’s
/ @2 c& S3 P: d7 l0 yheight was 6 feet, and he went through a somewhat/ v( a# f" e2 j3 I
early puberty and had stopped growing by age 14.5 H8 h) s. y# c, b- F
The father denied taking any other medication. The
9 B" V) _4 H. C7 m1 o; P8 Kchild’s mother was in good health. Her menarche( q! b% @. r/ o* U: o6 o( L
was at 11 years of age, and her height was at 5 feet
1 q5 Z* G! H: t6 h4 j5 inches. There was no other family history of pre-( y" _/ b/ f( i) k# G% J
cocious sexual development in the first-degree rela-) y' h1 R- y. D% d
tives. There were no siblings.7 {' _3 h4 P7 P- H/ R
Physical Examination& \+ F/ N  M+ y+ g3 r
The physical examination revealed a very active,
% |# f/ Z: h( K! X7 Eplayful, and healthy boy. The vital signs documented
1 e* p5 f/ s1 c% sa blood pressure of 85/50 mm Hg, his length was
' Y2 m- d" ^& B# G  x90 cm (>97th percentile), and his weight was 14.4 kg, d; Q/ T. G1 `% r5 W0 f# S  E' ?9 a
(also >97th percentile). The observed yearly growth* {+ g  Q9 O0 O. C8 T
velocity was 30 cm (12 inches). The examination of
6 m; l+ j/ J1 xthe neck revealed no thyroid enlargement.
, z1 Z  C. L5 j% B# j% _- q7 BThe genitourinary examination was remarkable for
! {$ ?. g6 S' z! }" Wenlargement of the penis, with a stretched length of( |& Z0 b/ Y- o) }" c  d
8 cm and a width of 2 cm. The glans penis was very well
7 J# I" n4 Y$ T3 G" Jdeveloped. The pubic hair was Tanner II, mostly around
. u* _- N' Y6 @) e1 {$ D540
; T. C4 H( l. e, o9 H0 q  \1 ^at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 a+ w; i- N$ J1 o- q" F3 H4 ^the base of the phallus and was dark and curled. The
: V, L; X7 R4 f! U# Wtesticular volume was prepubertal at 2 mL each.9 M; k2 ?0 X6 g" d" }
The skin was moist and smooth and somewhat
; U/ d, N2 l6 c$ ^oily. No axillary hair was noted. There were no! L/ i9 u; j2 k8 H/ M
abnormal skin pigmentations or café-au-lait spots.
1 x- h* ]2 S) U. S. c0 u& ANeurologic evaluation showed deep tendon reflex 2+
- s- V5 l2 |2 E6 V/ xbilateral and symmetrical. There was no suggestion
& Q- w# F& K" }/ V* W# k! U1 B( lof papilledema.
- _1 @/ W  y/ P$ t  [, c( c5 L. lLaboratory Evaluation
0 R" V4 B& j0 P  {% D" UThe bone age was consistent with 28 months by# s: R& M6 a7 T8 @! w+ ?% `4 b  z8 b
using the standard of Greulich and Pyle at a chrono-  k; P5 E+ I* V: `4 F  s" Q0 h
logic age of 16 months (advanced).5 Chromosomal+ _# V1 n) ?: T* m: G7 [, Y5 ^5 L
karyotype was 46XY. The thyroid function test! Z$ N) W, j4 V
showed a free T4 of 1.69 ng/dL, and thyroid stimu-  U# \- s+ f2 j7 P% q% j
lating hormone level was 1.3 µIU/mL (both normal).
( W/ L2 E5 b. C. P/ }1 h" MThe concentrations of serum electrolytes, blood" P* {% O  Z3 V. `# C( Q
urea nitrogen, creatinine, and calcium all were
8 |- I) G0 U6 Rwithin normal range for his age. The concentration' ?  t0 ?$ Q6 k3 J+ W$ z$ t
of serum 17-hydroxyprogesterone was 16 ng/dL6 x( T5 x6 U+ n& l0 z& ]
(normal, 3 to 90 ng/dL), androstenedione was 20: m( Y: ~4 g* f; n0 x
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-( ^! ?. {6 {. W' J% \; U
terone was 38 ng/dL (normal, 50 to 760 ng/dL),6 n$ w# _  _* @/ W0 f, Q
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
2 `/ v& _! F) g7 h# s49ng/dL), 11-desoxycortisol (specific compound S)! w% N% G; Z# h9 x! [1 a0 v
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
2 M- M% s: L1 a/ Otisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
$ G' p4 \+ Q2 Dtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),; J& B* O" [5 s8 A5 i, d9 \
and β-human chorionic gonadotropin was less than" G+ w3 n2 [) O6 z: G
5 mIU/mL (normal <5 mIU/mL). Serum follicular
7 f+ K3 g$ Z; ~3 \stimulating hormone and leuteinizing hormone
0 Z1 ^, f) ~  g! Gconcentrations were less than 0.05 mIU/mL9 f; ^7 U/ Y1 M$ r
(prepubertal).
# X! z  b% I/ c. g! r: jThe parents were notified about the laboratory
2 q+ G9 a( b/ z/ }% K, H% j' Wresults and were informed that all of the tests were
& s$ s6 h7 M* x/ z' enormal except the testosterone level was high. The
9 d. E4 z4 V3 h6 E0 E$ p- |follow-up visit was arranged within a few weeks to  [' Z) R5 P- w' ~* N) V0 A  o8 Q! L
obtain testicular and abdominal sonograms; how-0 e$ \/ j- n$ r
ever, the family did not return for 4 months.
. L( d( ?/ a3 @Physical examination at this time revealed that the- f5 Z7 K, X5 G- l! |
child had grown 2.5 cm in 4 months and had gained# j* z; }- g% h" `' u
2 kg of weight. Physical examination remained
; t: o/ }8 S  l! Lunchanged. Surprisingly, the pubic hair almost com-
5 b) ?# s* Q" h* X# i$ p  vpletely disappeared except for a few vellous hairs at7 }; M2 h5 a! x
the base of the phallus. Testicular volume was still 2! G  c; f& p+ {" e* X
mL, and the size of the penis remained unchanged.
; E" e/ M: Q0 P' ?The mother also said that the boy was no longer hav-2 S2 _% t. h% u: D% ?( m! q
ing frequent erections.
% B, t) A$ Y" V; g6 yBoth parents were again questioned about use of
: a7 ~, q  }3 p5 V+ C: kany ointment/creams that they may have applied to# J  @" _0 n( z/ @- T5 @% g
the child’s skin. This time the father admitted the5 q$ {) j8 S4 @6 X1 \3 X! g6 O" [
Topical Testosterone Exposure / Bhowmick et al 541
; F! ~3 Y; u/ T4 Iuse of testosterone gel twice daily that he was apply-$ f' D  g0 z- t! _& k# T
ing over his own shoulders, chest, and back area for
  }1 g' u& [0 M; h0 H) ga year. The father also revealed he was embarrassed; y. G1 f) N; ?2 D0 ~" G
to disclose that he was using a testosterone gel pre-% p- T0 H( Y2 b4 K+ e8 F
scribed by his family physician for decreased libido
+ j. B/ H% B7 L. M; c4 @1 wsecondary to depression.5 M. N' ~( h" B  F  q  {
The child slept in the same bed with parents./ X  c7 L) Z) w3 F3 o1 f- ^
The father would hug the baby and hold him on his8 l' f! |8 f' A& h: S5 ]  j
chest for a considerable period of time, causing sig-' o1 q& B3 i; ~& d& |7 x) W8 h; \. m
nificant bare skin contact between baby and father.
( ?8 }7 r/ ]: l! YThe father also admitted that after the phone call,7 c$ }2 R% R" ^. \2 P- o, t
when he learned the testosterone level in the baby
; Q5 L5 p( m3 [was high, he then read the product information
4 r- O2 D; W/ e/ B# bpacket and concluded that it was most likely the rea-8 |7 m2 d* d+ C; m, a
son for the child’s virilization. At that time, they
5 F+ Z% ?0 O2 S& b- Q9 N8 W% |decided to put the baby in a separate bed, and the$ f4 B* W. }7 |" E& L0 W# |
father was not hugging him with bare skin and had% w; u1 w0 [  r
been using protective clothing. A repeat testosterone) O+ e' c4 _1 v1 |
test was ordered, but the family did not go to the
, S. f  T" k- x3 H. Olaboratory to obtain the test.# |1 B9 s, j9 ^( C' d( J
Discussion1 g" t, e1 @6 Y( z- @* L
Precocious puberty in boys is defined as secondary: }! p' q" N$ ?/ y) v* Z' j
sexual development before 9 years of age.1,4
& d5 o+ }+ N- aPrecocious puberty is termed as central (true) when7 d1 e% o5 f$ K5 K6 c
it is caused by the premature activation of hypo-
  a5 D  H) t+ N! wthalamic pituitary gonadal axis. CPP is more com-
; `; |5 }, V& S& ]) C( T/ o' dmon in girls than in boys.1,3 Most boys with CPP
1 l0 V7 q; W/ M) D* umay have a central nervous system lesion that is1 s: [$ N/ E! j/ D( U
responsible for the early activation of the hypothal-7 s. T" R+ A& C% \2 ~/ d
amic pituitary gonadal axis.1-3 Thus, greater empha-
( f+ M9 o1 H2 o. D6 f6 c7 K& `sis has been given to neuroradiologic imaging in+ W! Y1 [" v& o6 j
boys with precocious puberty. In addition to viril-
9 W  X9 t% k' ]3 V( x1 Zization, the clinical hallmark of CPP is the symmet-
) J$ ^# l* P" E" Xrical testicular growth secondary to stimulation by3 @$ v# F# Q- x5 h
gonadotropins.1,3+ M8 K9 B" @+ j  B
Gonadotropin-independent peripheral preco-
/ _$ _" D) C, T7 [. d, h# ^cious puberty in boys also results from inappropriate0 K" h% j3 L0 o' k
androgenic stimulation from either endogenous or  ]1 k2 k  u. t* V% Z$ x5 O1 p, p
exogenous sources, nonpituitary gonadotropin stim-: D, x4 @; F/ s7 R. ]' @6 |- |, a
ulation, and rare activating mutations.3 Virilizing
: l) X4 ~* ~) Dcongenital adrenal hyperplasia producing excessive
% e! s% n& O* yadrenal androgens is a common cause of precocious$ I7 |/ T- W2 P" X5 ]; l' I
puberty in boys.3,4  Q3 ?5 R/ |7 m  E
The most common form of congenital adrenal
% T0 i: ?) C" ?( xhyperplasia is the 21-hydroxylase enzyme deficiency.
1 B3 C- K( K# B8 W: v8 j; BThe 11-β hydroxylase deficiency may also result in6 O0 ]% ?/ I7 p( `
excessive adrenal androgen production, and rarely,* c* ]' d7 r: z5 l4 J
an adrenal tumor may also cause adrenal androgen- ~; h- \# l* M) ?- z5 O
excess.1,3" |- n* D! H9 i
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' P0 s, q& q( y
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
" n  D6 i" b; u4 V% |/ TA unique entity of male-limited gonadotropin-6 ~2 H0 O1 U5 O0 b1 {# d
independent precocious puberty, which is also known
$ p6 F  U0 U7 W4 D% Tas testotoxicosis, may cause precocious puberty at a
- P6 B$ x- D# ]- d. w- every young age. The physical findings in these boys
' ~* L0 r( L. R3 Q8 Nwith this disorder are full pubertal development,% a' ~: B7 V" x( ?
including bilateral testicular growth, similar to boys
; O) S5 }( G1 g6 E  v# s9 Xwith CPP. The gonadotropin levels in this disorder
9 w  {# P+ A$ M$ l$ @/ x: Tare suppressed to prepubertal levels and do not show8 O  _3 P. d4 q$ K3 Y$ F) _
pubertal response of gonadotropin after gonadotropin-' t- l* ^" x% D
releasing hormone stimulation. This is a sex-linked
( t4 l" [6 m7 |, W9 wautosomal dominant disorder that affects only
5 C; \3 ^2 Y0 w; J8 D6 emales; therefore, other male members of the family7 i" D7 \7 T$ T( P+ s; d( z- ]
may have similar precocious puberty.3
$ d% d% r( d2 J: pIn our patient, physical examination was incon-0 ]6 q0 |' b% y3 F  j# Z' ~
sistent with true precocious puberty since his testi-, K9 O5 i" l7 N! H! X  p  S
cles were prepubertal in size. However, testotoxicosis
1 K1 J, D. `, z/ Dwas in the differential diagnosis because his father
7 P8 T, h9 F8 U2 J! j+ A7 C9 Astarted puberty somewhat early, and occasionally,
7 d4 r9 O# Q' f. rtesticular enlargement is not that evident in the; l' v& d* h. h" S
beginning of this process.1 In the absence of a neg-
- f0 R. y; u8 j5 h, |: h& c* P. d* x/ Tative initial history of androgen exposure, our1 e$ |& R; n/ g7 Q$ N
biggest concern was virilizing adrenal hyperplasia,
! X5 |- I) F+ H3 u1 Y8 weither 21-hydroxylase deficiency or 11-β hydroxylase+ m& Z/ Z. t! t; ^3 D
deficiency. Those diagnoses were excluded by find-
6 X6 H. s4 K) v( S: i5 Y2 h* Ning the normal level of adrenal steroids.- f4 N4 d! }1 E; h- E
The diagnosis of exogenous androgens was strongly
6 q, Q3 x( a3 W( fsuspected in a follow-up visit after 4 months because8 P+ M* t# N% }$ x& d
the physical examination revealed the complete disap-
# Y5 n6 Z. @& D! S; o' E* dpearance of pubic hair, normal growth velocity, and6 M% F& `, q8 Z3 V) k& h- T
decreased erections. The father admitted using a testos-
9 m* Q  u0 n9 q6 i6 r3 c9 j& Tterone gel, which he concealed at first visit. He was
0 r4 K0 ?, k2 ~" U- jusing it rather frequently, twice a day. The Physicians’
1 O8 O" n' ]) D! ~7 L8 `Desk Reference, or package insert of this product, gel or
! M, c# |: r; J9 f6 q( `cream, cautions about dermal testosterone transfer to
3 u0 g. |/ u" o0 sunprotected females through direct skin exposure.- a& g! v; I/ e; y" x& h* N
Serum testosterone level was found to be 2 times the# w6 f6 z. t; _% }+ @+ o5 T
baseline value in those females who were exposed to
3 M5 W! M# ^7 N1 D0 s" ?even 15 minutes of direct skin contact with their male
$ y# X$ E$ k5 O( g  lpartners.6 However, when a shirt covered the applica-9 ?/ J/ [- M( R/ R
tion site, this testosterone transfer was prevented.8 B2 y# F2 r4 i, O8 M
Our patient’s testosterone level was 60 ng/mL,+ M1 m) E  E- Y' R  X
which was clearly high. Some studies suggest that& d) m3 H! h5 D7 N% q) X
dermal conversion of testosterone to dihydrotestos-
, o5 _$ l& R; j; J. l6 P0 wterone, which is a more potent metabolite, is more
2 f! X% u% D# w. Z3 O& L. Aactive in young children exposed to testosterone1 G6 ]* b& w+ P- @! y/ e1 A! }
exogenously7; however, we did not measure a dihy-
8 P5 t; C; \, ?drotestosterone level in our patient. In addition to4 o) |8 L# j; {1 d
virilization, exposure to exogenous testosterone in
5 b% m2 |, |% I0 T; ^2 p/ I$ @children results in an increase in growth velocity and
& H* M1 ?1 x8 Gadvanced bone age, as seen in our patient.6 h2 K# x% J; ?% e$ J
The long-term effect of androgen exposure during
1 W$ C8 D, h. u2 x) w6 z; m1 a9 a- R+ @early childhood on pubertal development and final
8 v0 H! V4 }& ]1 D/ o  fadult height are not fully known and always remain1 P* r0 D0 `: n# e( L$ H
a concern. Children treated with short-term testos-
0 K6 Z3 x. o- ^% Sterone injection or topical androgen may exhibit some. {6 o! q; [7 i! t
acceleration of the skeletal maturation; however, after
3 w3 Z3 v0 h5 C) ^3 y/ t7 }* ncessation of treatment, the rate of bone maturation1 k, ~; W3 q9 C8 u% e! y( z
decelerates and gradually returns to normal.8,98 |1 o* g, |/ R/ U/ N/ A- _
There are conflicting reports and controversy( [1 I% ?  c4 q* G! {6 ?
over the effect of early androgen exposure on adult
% {2 M& d$ D. Rpenile length.10,11 Some reports suggest subnormal3 P: E- |0 P" l& \+ B+ u, c( X- c6 g
adult penile length, apparently because of downreg-
' X0 T: n) R# m# \0 B7 [ulation of androgen receptor number.10,12 However,
9 |" o- v& t" Y! [; {Sutherland et al13 did not find a correlation between
$ }* D& w% Q* y0 ^( Tchildhood testosterone exposure and reduced adult0 M8 e4 Q: V# `; S' {
penile length in clinical studies.3 w( ?+ C; n- w) X
Nonetheless, we do not believe our patient is
/ K2 i7 Y  n' o9 w3 ^; egoing to experience any of the untoward effects from
+ |$ @! [0 y% i0 w% L8 ]% Ptestosterone exposure as mentioned earlier because
0 k& s. W: a6 kthe exposure was not for a prolonged period of time.9 M: H  P$ M9 F" Z" ^- M
Although the bone age was advanced at the time of" b/ b. U2 a  n8 @& t# Z3 e% o: U
diagnosis, the child had a normal growth velocity at
- p1 ~4 m* f& I4 F8 \9 R9 }9 fthe follow-up visit. It is hoped that his final adult8 l6 Q9 Y8 C/ C; T
height will not be affected.& ~9 J9 J* z! n9 J4 i
Although rarely reported, the widespread avail-: f6 d2 a) f$ C# U4 W! N2 |) N
ability of androgen products in our society may
4 S* ?9 n& i- T) |indeed cause more virilization in male or female4 x: N$ Y5 K# I) d* G
children than one would realize. Exposure to andro-
3 \) |# n" n9 V4 Rgen products must be considered and specific ques-
; b, j1 G0 B8 `4 ^tioning about the use of a testosterone product or
+ f  |  j% |4 _4 y* Fgel should be asked of the family members during3 V1 ^4 U9 z* n$ Y' N
the evaluation of any children who present with vir-
$ o! G/ _. \* Q) q7 d+ Nilization or peripheral precocious puberty. The diag-
) l+ d+ Q! b+ C2 Y, g/ ?- vnosis can be established by just a few tests and by' Y; d5 M' n' q
appropriate history. The inability to obtain such a0 B) O" y- t$ P- b
history, or failure to ask the specific questions, may, P7 P5 L) J, Y- \+ z1 o( i: w6 p* r
result in extensive, unnecessary, and expensive
# D( l0 c/ I  [1 ]8 N* Zinvestigation. The primary care physician should be& j1 ?' C. g* r2 }2 F3 {
aware of this fact, because most of these children  a' @0 U" ?; s
may initially present in their practice. The Physicians’
  w) r' s& ]' W2 U# i# P9 K/ eDesk Reference and package insert should also put a
' f* N; o( o- P4 M7 C+ m1 {( vwarning about the virilizing effect on a male or; \7 }4 g) l* @5 @$ J
female child who might come in contact with some-+ l4 h. t1 [0 v" C  V; e( [$ s
one using any of these products.
% I% a$ Y# I  _/ L* fReferences$ ~; J' L( L/ P% _
1. Styne DM. The testes: disorder of sexual differentiation3 l* E# u8 R/ T3 _- `1 Q. Z# g
and puberty in the male. In: Sperling MA, ed. Pediatric: e  T1 ~1 c2 S& x: h7 q
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
( t; w2 S: n* [* R* A# o; G9 W6 B* U2002: 565-628.
- c5 Z6 S- U( v3 G) ?8 o- D2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
$ R4 l2 W  n& x2 zpuberty in children with tumours of the suprasellar pineal
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這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
# W9 T# R; ^8 g6 r" T0 l
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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