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Sexual Precocity in a 16-Month-Old1 g5 M4 j8 ^3 d: q. x9 P
Boy Induced by Indirect Topical
' o3 ]/ _, S, \) \8 ?1 v/ e' k' V% gExposure to Testosterone
; W5 }$ U  Q* Y, R, XSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. G" {- Q' Z& ]2 i4 h
and Kenneth R. Rettig, MD13 Z; v9 ~! Y1 i& t; }
Clinical Pediatrics
- ~' \; M9 u! ?Volume 46 Number 61 W& Z* h/ ]( w9 D  _' ~( ~; q9 w
July 2007 540-543/ l9 l) |$ I# l! ]3 {" x9 g4 Y# D! x% `
© 2007 Sage Publications
! l) p# R9 I3 T! o; ?- x! ?10.1177/0009922806296651! K8 f' _: z7 x$ O! e
http://clp.sagepub.com9 |/ J+ L) i8 r8 i6 F
hosted at% b8 L, ]- Q9 i7 |! w$ h$ L
http://online.sagepub.com8 I5 b7 g: m4 \+ H* S+ N4 I4 ~
Precocious puberty in boys, central or peripheral,8 T4 {* S/ @0 l
is a significant concern for physicians. Central
; A3 G( o) u1 f& y, H6 @precocious puberty (CPP), which is mediated. a7 A2 E7 c  ~( ?" [. h9 F
through the hypothalamic pituitary gonadal axis, has. z+ x& z: a/ n8 [
a higher incidence of organic central nervous system, G4 U! F4 y7 `. j  d
lesions in boys.1,2 Virilization in boys, as manifested( q; T8 y% h0 t3 |: \
by enlargement of the penis, development of pubic& D- l$ G) N, |5 f
hair, and facial acne without enlargement of testi-
& Z, [4 w3 `1 ^  J7 C* c# F; Mcles, suggests peripheral or pseudopuberty.1-3 We
* m6 P9 z7 i) a; greport a 16-month-old boy who presented with the; b4 o- Y( S. N) \# d# [2 d" I
enlargement of the phallus and pubic hair develop-
- G! F- K. l& Zment without testicular enlargement, which was due
: J1 }/ Y8 B$ `, p4 gto the unintentional exposure to androgen gel used by
& o/ R& t" }2 Z6 R8 m- Sthe father. The family initially concealed this infor-
' _0 C  F! S! _# c: Nmation, resulting in an extensive work-up for this3 s5 _0 r, Z6 R+ |% F$ d* X6 Z
child. Given the widespread and easy availability of3 l5 [2 y( S. h' G% G8 o- L
testosterone gel and cream, we believe this is proba-
$ T+ n2 K8 C5 P7 v+ nbly more common than the rare case report in the
  K+ Y# e4 U0 M' O  @. ?literature.4
  Z1 ?4 _8 o- ]/ M# o; N6 jPatient Report, ^8 W  R# Q) f0 q
A 16-month-old white child was referred to the# {' G" E0 F# b6 L1 P
endocrine clinic by his pediatrician with the concern; ~, l; @' _, s  W, R6 H$ x8 m3 w
of early sexual development. His mother noticed! p, J2 Z4 k! v5 G) `) _
light colored pubic hair development when he was
/ n  {7 D- b# H( L' v, H$ Y  B% a) OFrom the 1Division of Pediatric Endocrinology, 2University of
; ^/ M2 E2 X. v/ ESouth Alabama Medical Center, Mobile, Alabama.# L/ ]2 J, x2 R- H: ~- I2 P- D
Address correspondence to: Samar K. Bhowmick, MD, FACE,
$ T% G! _, ^* U- ]8 a% i; yProfessor of Pediatrics, University of South Alabama, College of7 U$ z  w# q/ l) q+ N
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;. _% I* T7 G4 p6 N+ @
e-mail: [email protected].2 u" ^: o* q7 a! e5 d
about 6 to 7 months old, which progressively became  T4 w+ z. H* i& n) Q  [
darker. She was also concerned about the enlarge-" V& y  U4 C5 H6 C7 @
ment of his penis and frequent erections. The child
9 @6 T, J! k, A- n" lwas the product of a full-term normal delivery, with
0 r# o. U8 X8 i0 a5 ]$ W; Y: _% ba birth weight of 7 lb 14 oz, and birth length of
% q/ S: K! Z) h+ _20 inches. He was breast-fed throughout the first year/ t, d" }5 b8 r( ^
of life and was still receiving breast milk along with
( G; F( M$ c# asolid food. He had no hospitalizations or surgery,; Z1 p4 ~7 ]! o# K
and his psychosocial and psychomotor development
! y3 z4 h2 V% j4 H9 Xwas age appropriate.
' q7 w( T- h3 JThe family history was remarkable for the father,9 L+ r3 B8 l" K7 O% [. M
who was diagnosed with hypothyroidism at age 16,9 v+ m9 q2 x4 W. d/ T4 ~
which was treated with thyroxine. The father’s: a' h+ W" ]6 A
height was 6 feet, and he went through a somewhat$ f4 K4 a8 ~& H) A/ g8 \( u9 z  c9 z6 [
early puberty and had stopped growing by age 14.# }) ~6 E* t/ f  c+ [
The father denied taking any other medication. The8 q" V/ G2 {4 m2 X, l
child’s mother was in good health. Her menarche
& @" o- Q2 y5 h; vwas at 11 years of age, and her height was at 5 feet5 J! ^) H$ G+ v0 T
5 inches. There was no other family history of pre-4 s2 q. K, I2 P0 _+ S/ H
cocious sexual development in the first-degree rela-0 S( P; Q4 F2 b
tives. There were no siblings.; P& Q  r5 T+ i; [
Physical Examination; i) j7 {) v5 Z& }  h# \, Q" b6 O
The physical examination revealed a very active,
) A: a% ^  J- d! R6 F, Zplayful, and healthy boy. The vital signs documented. q# ]5 B$ R5 n
a blood pressure of 85/50 mm Hg, his length was
3 {, k$ r, y6 r4 V90 cm (>97th percentile), and his weight was 14.4 kg/ }1 }# q0 ]+ g3 w$ l/ L  P
(also >97th percentile). The observed yearly growth& r4 _5 H. f9 a4 Y5 m
velocity was 30 cm (12 inches). The examination of# W* E% @' k3 Z. D1 w1 Q
the neck revealed no thyroid enlargement.( \2 n3 R6 s% Z  Z$ ^! P
The genitourinary examination was remarkable for4 Q0 }) O) K/ f8 F- @/ q, V
enlargement of the penis, with a stretched length of
) n2 j" F" N1 j4 H4 m8 cm and a width of 2 cm. The glans penis was very well( `1 k2 @# k: y
developed. The pubic hair was Tanner II, mostly around
$ f2 `% \( e9 }" ]8 ~  f: N3 l540
: w8 b, k4 \0 ?& \at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) j; U0 C* y5 R4 C9 _' l9 l
the base of the phallus and was dark and curled. The
& B# P% G+ F, W$ j: A* G8 Htesticular volume was prepubertal at 2 mL each.3 U4 W4 I' ~- |& W6 G# D" G
The skin was moist and smooth and somewhat
# b# I- W# {- s3 s# |  \oily. No axillary hair was noted. There were no4 [1 N  i$ P2 _3 b: T, b' w
abnormal skin pigmentations or café-au-lait spots.8 \7 ^7 [% |: U9 P
Neurologic evaluation showed deep tendon reflex 2+
0 @3 s' E9 M. j1 z6 fbilateral and symmetrical. There was no suggestion4 u' g$ k( _- h( }5 D6 P# _
of papilledema.4 ~( w" Z. O3 c3 U' H4 I) _
Laboratory Evaluation
/ I$ g: c6 {# O" J1 z7 ]The bone age was consistent with 28 months by
9 A: T4 T- o( U+ O4 G1 u$ Z7 Gusing the standard of Greulich and Pyle at a chrono-7 J' [: w5 Y$ E! `, |
logic age of 16 months (advanced).5 Chromosomal, M- W$ D7 |7 h4 V
karyotype was 46XY. The thyroid function test
  b! X5 a/ p$ f/ U" \9 _' E) qshowed a free T4 of 1.69 ng/dL, and thyroid stimu-! ]2 W7 ~' E& i9 ~
lating hormone level was 1.3 µIU/mL (both normal).
% r" I2 _4 l1 h' J, [6 v# qThe concentrations of serum electrolytes, blood6 \1 |( j0 S- h, e- m" z. r# y
urea nitrogen, creatinine, and calcium all were/ W5 [) q+ W  x+ p- X
within normal range for his age. The concentration
  z/ z+ o" Q; o) \3 K( j2 Uof serum 17-hydroxyprogesterone was 16 ng/dL
) C. p5 e: ]7 l(normal, 3 to 90 ng/dL), androstenedione was 20- o1 y5 h- w0 c3 Z
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-" f. J2 K+ C- A! o4 w  e6 w# v
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
2 ]$ w) |  O+ O0 Zdesoxycorticosterone was 4.3 ng/dL (normal, 7 to& g0 R+ p9 j* ~: K/ d
49ng/dL), 11-desoxycortisol (specific compound S)4 B9 u+ n9 D/ X! L/ P% Q( _
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
' \/ s7 q1 B7 X! s, `) s2 ltisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total: M- a: X2 U' M7 t& [
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
& E( L' V9 G+ I0 o8 e& f+ Tand β-human chorionic gonadotropin was less than
( W- C8 ?% [; {# X- `: ]5 mIU/mL (normal <5 mIU/mL). Serum follicular
" W! n4 C, Q# H  V( Mstimulating hormone and leuteinizing hormone& M  b& ]" X+ c
concentrations were less than 0.05 mIU/mL
1 `, z' c  l9 f6 q2 X( R' K& x(prepubertal).2 G4 {  M" Q: S$ ]# F# H# G
The parents were notified about the laboratory# Q: O. s2 _$ y- G
results and were informed that all of the tests were
4 g! b- B1 ^) F: dnormal except the testosterone level was high. The
5 U  {$ B5 }9 G( X7 g0 K1 [follow-up visit was arranged within a few weeks to
# U( x- \( `) |4 g! o3 nobtain testicular and abdominal sonograms; how-( V( L* D# H. V7 a0 A, O. f
ever, the family did not return for 4 months.
3 M0 p( K9 T  X! Z" W+ e- z! q1 e! zPhysical examination at this time revealed that the
. e7 D' M5 x& Q. f3 Lchild had grown 2.5 cm in 4 months and had gained# M$ q4 S1 j. f+ i+ A
2 kg of weight. Physical examination remained4 B0 p7 g# A' a: p7 k
unchanged. Surprisingly, the pubic hair almost com-
1 Y- G: C" B, j2 f' ?: F- v7 c3 Qpletely disappeared except for a few vellous hairs at6 R9 \) l9 j1 c# h% D5 N
the base of the phallus. Testicular volume was still 27 h' L9 A" \: l) g% H. a1 F
mL, and the size of the penis remained unchanged.
3 }; ?7 `' j4 ~" ?! V; PThe mother also said that the boy was no longer hav-! [. X0 j% ~2 [# H$ y+ m8 T
ing frequent erections.
2 r. [& q4 \% N4 @0 a! b2 I5 u# v. `Both parents were again questioned about use of
4 a) u: _  w5 [& `" J5 `$ rany ointment/creams that they may have applied to
2 _5 y* H7 R" q' M( tthe child’s skin. This time the father admitted the
* i/ ~( _$ _! k$ @4 S: ~$ e% {Topical Testosterone Exposure / Bhowmick et al 541. I# F; t4 `1 t+ |  N3 V
use of testosterone gel twice daily that he was apply-2 X4 G$ e) i* P! g8 K
ing over his own shoulders, chest, and back area for' m+ \% p; N7 \3 u+ G! n
a year. The father also revealed he was embarrassed
6 O& v9 s3 V5 \. ^2 Q% \to disclose that he was using a testosterone gel pre-
9 h* f/ |3 r4 lscribed by his family physician for decreased libido- C$ S  Z: N: ?) W8 s
secondary to depression.
( Z5 `+ K- h) T% G3 F% r! l! q: DThe child slept in the same bed with parents.
7 _% g4 S: a: G% s3 W5 sThe father would hug the baby and hold him on his$ d- N# E+ c" G+ Z' S! d
chest for a considerable period of time, causing sig-
; C$ p+ q, V* Z$ [0 B# znificant bare skin contact between baby and father.
+ S: n3 B1 [5 J: FThe father also admitted that after the phone call,7 N7 f8 {9 f' k& k) L
when he learned the testosterone level in the baby; \  t9 \0 c3 S1 P0 d- y
was high, he then read the product information
4 V  |0 Q9 _1 P  j$ z  r( y7 y) K  bpacket and concluded that it was most likely the rea-4 V( r3 `/ i  V/ o* F
son for the child’s virilization. At that time, they- _* F$ \. H3 I0 ^0 g
decided to put the baby in a separate bed, and the$ |' `8 g: b/ y) t  ]- h
father was not hugging him with bare skin and had
! Q' j! n" o, G' Q" obeen using protective clothing. A repeat testosterone) C( Q/ D( j* W4 f; t* B0 o* }
test was ordered, but the family did not go to the
2 L' f7 a. s& f. }laboratory to obtain the test.% J/ Q' H* z4 s3 M$ }9 v
Discussion
* J0 s! J* u& U! E% Q$ GPrecocious puberty in boys is defined as secondary( h( `2 r2 g5 I( E2 r7 W
sexual development before 9 years of age.1,45 l- [+ p3 o# B1 I- \. U
Precocious puberty is termed as central (true) when
8 c; K6 U  e: Mit is caused by the premature activation of hypo-
& R) t/ n4 _' {7 Vthalamic pituitary gonadal axis. CPP is more com-  _3 }! B& j/ h. I( ]' d5 j- A3 d( @
mon in girls than in boys.1,3 Most boys with CPP( Z3 g' [. M0 F& ]* N4 v
may have a central nervous system lesion that is
+ l. X( j, C. I6 Xresponsible for the early activation of the hypothal-
2 L8 o* C5 {3 u; Y& z0 [0 D/ yamic pituitary gonadal axis.1-3 Thus, greater empha-
; O  J) i% m: G* V# r# B' F- Qsis has been given to neuroradiologic imaging in
' b2 M4 p2 {. m5 x6 ]- hboys with precocious puberty. In addition to viril-
/ Y6 H* Z' B# e8 sization, the clinical hallmark of CPP is the symmet-
: D0 p# n: e3 ]5 Drical testicular growth secondary to stimulation by- b- w! |* o2 H9 g! w3 f
gonadotropins.1,3. ^5 P( z+ @: I  n! m0 D6 c* g3 \
Gonadotropin-independent peripheral preco-  o4 R# H9 T6 }  Q  E4 p- ?( V
cious puberty in boys also results from inappropriate
. J! w1 |& [/ d0 [4 l  P! D6 uandrogenic stimulation from either endogenous or( x* H; c$ X) o8 f* G6 h
exogenous sources, nonpituitary gonadotropin stim-0 T9 l# P: S4 a% r# I( j/ `& i# \
ulation, and rare activating mutations.3 Virilizing6 R  O" }) P5 }* r1 w
congenital adrenal hyperplasia producing excessive6 j! ~) ^$ {) D: a
adrenal androgens is a common cause of precocious
2 \7 R( O  {% b; |0 `puberty in boys.3,42 w0 ~, v' T/ H+ a0 C% W
The most common form of congenital adrenal$ q: ?9 a7 Z/ Q6 W. m  x' n! X/ b
hyperplasia is the 21-hydroxylase enzyme deficiency.
- [& w& e% h) }$ s3 W4 PThe 11-β hydroxylase deficiency may also result in
4 w" s. W+ S! v  Nexcessive adrenal androgen production, and rarely,
: E% Z3 w; F7 d% ?, B# Aan adrenal tumor may also cause adrenal androgen' Z8 j. x5 G0 I
excess.1,3
1 b5 t! V+ H+ a+ Z! f) Wat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 T) F7 _2 ^1 X: K2 k4 r* E: A
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007; o# U: o. l5 [  L" _- X) f: F. B
A unique entity of male-limited gonadotropin-
2 N1 f3 K6 N7 b( V6 v3 ]% h. Mindependent precocious puberty, which is also known0 [* H# Y1 ]) j2 I3 [9 R
as testotoxicosis, may cause precocious puberty at a, S" I6 P* g' B0 Q8 ^" [
very young age. The physical findings in these boys
1 r, d+ h4 o4 c5 Zwith this disorder are full pubertal development,) i( G- Y& `, |
including bilateral testicular growth, similar to boys
1 h$ \8 N! g! t; ?  Rwith CPP. The gonadotropin levels in this disorder% E# T" v) k( R1 V0 y
are suppressed to prepubertal levels and do not show
0 w! C5 q/ F$ t$ ^pubertal response of gonadotropin after gonadotropin-' B  R0 y" }" O, E+ F
releasing hormone stimulation. This is a sex-linked2 K- [2 `0 l3 _, M2 w5 v& h
autosomal dominant disorder that affects only: e3 N' c7 F2 W/ d4 J8 o
males; therefore, other male members of the family
" X, @& F; C: }1 k: L4 {9 }7 wmay have similar precocious puberty.3
, E+ Y  e- |4 z( o  y" e- n* k3 S/ bIn our patient, physical examination was incon-
) Q. y; @3 j8 p+ b4 ?" ~) j( Csistent with true precocious puberty since his testi-' r+ W6 f2 n/ o! J
cles were prepubertal in size. However, testotoxicosis
# E- C; s% c6 n* Rwas in the differential diagnosis because his father
6 V8 D/ m7 ]" o. b9 a/ j3 z& o. Cstarted puberty somewhat early, and occasionally,
. Z  n4 H. K8 Ttesticular enlargement is not that evident in the
7 y# I2 q7 u, Wbeginning of this process.1 In the absence of a neg-
( V0 }* o8 Y" r+ b0 l7 Hative initial history of androgen exposure, our0 V/ V2 z4 W: w8 Q
biggest concern was virilizing adrenal hyperplasia,, q4 G' @# R# Q! v7 x7 v8 w
either 21-hydroxylase deficiency or 11-β hydroxylase/ @- u* f8 E7 @
deficiency. Those diagnoses were excluded by find-& ~* w9 K8 e: C; `2 ^  @: F% t
ing the normal level of adrenal steroids.
. W) ~1 ~  l0 bThe diagnosis of exogenous androgens was strongly
+ C9 L! p3 A$ |! s" Vsuspected in a follow-up visit after 4 months because" {7 a( e3 S- _9 C2 p
the physical examination revealed the complete disap-+ s# m7 v% K* y; E" p  [
pearance of pubic hair, normal growth velocity, and# B( O  n0 h( Y4 Y2 `7 c
decreased erections. The father admitted using a testos-
; h8 Z1 a( M( U  H- J# \terone gel, which he concealed at first visit. He was
( ?" p! }1 D5 o  I' Y: b, Q( x4 B6 Uusing it rather frequently, twice a day. The Physicians’  `+ ^" {% M" j/ m1 K
Desk Reference, or package insert of this product, gel or
" J1 t0 ]5 [9 a) S3 g$ Hcream, cautions about dermal testosterone transfer to' `4 |, L% s. _; ^+ m
unprotected females through direct skin exposure.$ v8 ^. V9 P- y* u9 y  t
Serum testosterone level was found to be 2 times the0 f0 w$ q, w6 m
baseline value in those females who were exposed to2 j$ o/ M" n3 o$ d
even 15 minutes of direct skin contact with their male& P4 T+ s4 r4 }  G
partners.6 However, when a shirt covered the applica-
9 I$ }# c% o, v. ~, A% b; B8 C' Stion site, this testosterone transfer was prevented.
" \) ~9 l. L8 E( g4 ^/ NOur patient’s testosterone level was 60 ng/mL,
. q- n: e% E# p9 {0 Lwhich was clearly high. Some studies suggest that
. I9 @1 G9 R  ^dermal conversion of testosterone to dihydrotestos-- k- M# H" Z. @# J/ v
terone, which is a more potent metabolite, is more" H5 a# ~' f" }8 v
active in young children exposed to testosterone
& i3 S  ]( S' \! I4 y! {' uexogenously7; however, we did not measure a dihy-4 x. s# C  @, Z) {
drotestosterone level in our patient. In addition to. X2 a( h& N# S5 I3 P
virilization, exposure to exogenous testosterone in& L$ x3 s' I6 L% G
children results in an increase in growth velocity and
, R7 Q$ c9 Z! O$ p, hadvanced bone age, as seen in our patient.
8 t1 P2 @2 ]: U1 rThe long-term effect of androgen exposure during
, W  h+ |" |8 K3 M4 O% ]& Jearly childhood on pubertal development and final2 |9 v% D; ]/ q5 Z; J) M- G
adult height are not fully known and always remain* D( z! Y, L3 X+ P& S+ A2 g
a concern. Children treated with short-term testos-2 o5 i0 k" d3 M" a5 _7 b
terone injection or topical androgen may exhibit some
& u- C/ @& f# z6 facceleration of the skeletal maturation; however, after
: Y/ i8 B# d8 b& Mcessation of treatment, the rate of bone maturation5 d" g0 ?$ S# A/ v8 Q
decelerates and gradually returns to normal.8,9
! ?) n; y4 R! j- Q+ UThere are conflicting reports and controversy
7 c2 B* {, L# G  D( Yover the effect of early androgen exposure on adult
/ Q( |& s1 ^  ^/ h, I0 O" a6 Mpenile length.10,11 Some reports suggest subnormal. L9 K: |9 g2 |4 L5 M+ `0 g
adult penile length, apparently because of downreg-
; Z3 t. L" L0 M0 n+ bulation of androgen receptor number.10,12 However,
. o# r5 D7 K9 `6 s0 GSutherland et al13 did not find a correlation between! c& R1 J0 _4 G& t
childhood testosterone exposure and reduced adult
# r; V' o% p- A$ M. o9 ?* ~: lpenile length in clinical studies.# U) u8 d# O5 S6 V7 n; T! U" l
Nonetheless, we do not believe our patient is
: u! W! L  K# X# D; Ggoing to experience any of the untoward effects from
% p7 U! F& E4 d9 [7 ~testosterone exposure as mentioned earlier because) M! g- V$ e" d* R2 ^; ^
the exposure was not for a prolonged period of time.
( c/ _( G) O; E: h. }( c  V/ v( tAlthough the bone age was advanced at the time of
1 ~1 G& E, z+ o1 o. h5 ]diagnosis, the child had a normal growth velocity at, r, L* ]# M( t6 ?8 |6 B
the follow-up visit. It is hoped that his final adult
$ b4 r2 A7 o3 J/ g+ Mheight will not be affected.
- K6 z5 T- T; @. m0 s' [Although rarely reported, the widespread avail-
3 u% T9 v% y) ]" t0 S7 ^( _5 Dability of androgen products in our society may
8 k" _! \- y! Z- f- P  Xindeed cause more virilization in male or female" {9 p# N, P. l1 c) B+ X
children than one would realize. Exposure to andro-1 @1 P1 E# k$ c/ T6 \3 g
gen products must be considered and specific ques-3 ?- g! O. E5 L# U1 L* ~
tioning about the use of a testosterone product or6 `% J. P6 H( o! N' B3 Z' a9 S
gel should be asked of the family members during% C( W* k; N9 k) M/ V$ w8 m
the evaluation of any children who present with vir-
1 n( Z7 {' \8 G  Q4 X% s  Lilization or peripheral precocious puberty. The diag-7 h1 c  Q% p6 b/ q5 k. Z2 P
nosis can be established by just a few tests and by1 l$ J5 J' d" S9 ?; G* i+ t
appropriate history. The inability to obtain such a
" u0 W9 s7 J# n' e9 M# mhistory, or failure to ask the specific questions, may$ ^( z. X. f: Q. v/ `0 V. j1 `; P7 l
result in extensive, unnecessary, and expensive3 N& D% g6 a9 G0 S& S
investigation. The primary care physician should be
# N1 _! f( w' N  q9 E# caware of this fact, because most of these children
2 u" n- w6 M$ R, D! U( `8 Gmay initially present in their practice. The Physicians’
0 a1 p" d% u/ D% u* i  x9 yDesk Reference and package insert should also put a; M: g* T7 t  N2 V3 m5 g* p
warning about the virilizing effect on a male or
+ c4 A* o" ~2 [& z8 a# }% Bfemale child who might come in contact with some-  x! `, a3 b/ ~) x/ t
one using any of these products.% Q' w4 r2 S" b% _1 v4 K
References
% x( g8 g8 z2 h6 g! d1 r2 y1. Styne DM. The testes: disorder of sexual differentiation% X, P7 G) B1 d1 k& F
and puberty in the male. In: Sperling MA, ed. Pediatric
  ~( |, N+ l! a5 t% ]Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
" B: l$ C3 c& I: ]8 L2002: 565-628.' L* w7 u6 v; v- I: o: X* B* A0 t
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious% r; J7 R! `$ A: x# b9 S/ i/ C
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
5 n  R% L; R- [) B4 D6 P( nBoy Induced by Indirect Topical
* @1 v3 k# q$ v5 eExposure to Testosterone
/ O; z" u1 ?3 d0 W) C. _Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
* Q- z; h  ~1 Oand Kenneth R. Rettig, MD1
3 o/ G, c4 }# I! V+ LClinical Pediatrics, j0 G$ {0 Q+ T9 r0 h
Volume 46 Number 63 I; S  J0 j% v. W/ e  V
July 2007 540-543
5 i$ X+ [" \* l  F  Y# `  E© 2007 Sage Publications* m# j: u2 ~/ S1 X+ O" Z; ?* X9 N
10.1177/00099228062966516 Q9 ^5 r, Q+ t8 q5 \: I! w
http://clp.sagepub.com; g5 I1 s$ |5 ~; G. x' S
hosted at
( E( X5 `% z, O5 shttp://online.sagepub.com
; Z) O/ g6 l6 D  R1 Y" gPrecocious puberty in boys, central or peripheral,: z& {/ @, ?$ N- D) B4 q8 F  P1 X
is a significant concern for physicians. Central( [2 p! J0 {9 ~! B2 y
precocious puberty (CPP), which is mediated
3 H1 e' c( E' h5 U6 sthrough the hypothalamic pituitary gonadal axis, has3 ^$ n- C5 S. O7 @
a higher incidence of organic central nervous system
2 u6 u- O' `/ n+ j, _. Klesions in boys.1,2 Virilization in boys, as manifested
% x$ X- w% a0 u1 Dby enlargement of the penis, development of pubic/ z4 ^8 y2 q! G4 d1 P* E
hair, and facial acne without enlargement of testi-+ n& p/ o. ^: C2 h9 F
cles, suggests peripheral or pseudopuberty.1-3 We2 E2 ]( T  V: e! c" `3 }; V: M* r
report a 16-month-old boy who presented with the9 ?+ k0 `$ c% `. n* s' x1 Y
enlargement of the phallus and pubic hair develop-8 a1 J  i; \+ o6 W1 B
ment without testicular enlargement, which was due
* O1 m/ q$ U9 W* N/ g" Fto the unintentional exposure to androgen gel used by9 q+ J; ^( Y  v7 h& }
the father. The family initially concealed this infor-
& R% w; _$ g' Z6 ?$ S* t. I2 i3 Lmation, resulting in an extensive work-up for this" ?1 k2 Z1 r0 h, B2 w$ C6 t6 a( L0 d
child. Given the widespread and easy availability of
) V. O* V5 I4 z6 L- C- ntestosterone gel and cream, we believe this is proba-
" q% ]5 {4 W, _( g2 j& S0 `bly more common than the rare case report in the
1 J, }8 c6 b, a* g; d; n/ ^literature.43 v1 R0 \' }& Z- K  V5 D' }8 d  S
Patient Report
4 K+ @, y8 V+ p# G2 i3 a. ^; CA 16-month-old white child was referred to the# ?3 M" |- c) e4 Y& M
endocrine clinic by his pediatrician with the concern
- R3 v$ h9 j5 [& h, _# Vof early sexual development. His mother noticed
8 p: R& g: `3 K# R7 ~" [light colored pubic hair development when he was
3 |" C. A( d0 Q6 r( }- Y. R$ u# g/ qFrom the 1Division of Pediatric Endocrinology, 2University of: Z  v4 d" P4 @6 z8 @) Q
South Alabama Medical Center, Mobile, Alabama.
0 F" x1 Y, P. y5 o, VAddress correspondence to: Samar K. Bhowmick, MD, FACE,1 _9 Y3 T4 \9 c1 A( f2 z/ M' |
Professor of Pediatrics, University of South Alabama, College of
1 h( I8 }$ @; B7 Z, _9 P# q6 @Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;9 B, r0 n% G/ M- p& j  R2 p( L
e-mail: [email protected].$ o) d( p& S( y8 q! X
about 6 to 7 months old, which progressively became
/ G/ b  a+ k+ |/ L/ ?5 mdarker. She was also concerned about the enlarge-( I3 |& f5 f* j5 [+ p* x( G* U
ment of his penis and frequent erections. The child. S/ q$ A) X( l
was the product of a full-term normal delivery, with
% O" {, O0 x3 H- @a birth weight of 7 lb 14 oz, and birth length of2 ?4 A; ^  Z( g9 O6 _
20 inches. He was breast-fed throughout the first year
2 x$ @) r  ?: W2 Q9 wof life and was still receiving breast milk along with0 ]- I  z- y, _9 T" I, u
solid food. He had no hospitalizations or surgery,3 s9 ]1 }6 ~9 ?, W/ x
and his psychosocial and psychomotor development2 _  m  F  I7 d6 C* I' B2 A( p
was age appropriate.
! X% d! }- E: @! I4 x0 MThe family history was remarkable for the father,
* `. L' o( [. twho was diagnosed with hypothyroidism at age 16,  d) Y0 y( u: b9 H5 \
which was treated with thyroxine. The father’s( M2 L# @+ B  t  D9 O0 r  Y9 [
height was 6 feet, and he went through a somewhat3 J  k/ y5 `( e2 c, R% Q4 G  W* ?! X
early puberty and had stopped growing by age 14.  T5 R1 A; A% L) [( ^
The father denied taking any other medication. The
* b7 x% f* J& J/ s# B+ Z! _+ Wchild’s mother was in good health. Her menarche
, H: H" A. u: Z- C) Z5 Kwas at 11 years of age, and her height was at 5 feet7 y, u+ f' s( f" D$ W
5 inches. There was no other family history of pre-
" X( @* n2 c$ E/ }' H" f2 ~cocious sexual development in the first-degree rela-
% `% i: W, y% htives. There were no siblings.- G0 q9 I: J$ y8 l$ V
Physical Examination, \7 A5 ?, Z' q: [: w( M$ G
The physical examination revealed a very active,) n& @  r/ s7 B' X2 ?
playful, and healthy boy. The vital signs documented
  O; q$ R. s$ Z) ?3 Ca blood pressure of 85/50 mm Hg, his length was
( p9 I; [+ d8 j1 l0 t; }5 Y  h+ ^90 cm (>97th percentile), and his weight was 14.4 kg
! i% E6 c- f0 e; J- p; a(also >97th percentile). The observed yearly growth3 ]% u2 u2 c1 q9 g* f$ A
velocity was 30 cm (12 inches). The examination of
& h1 t& g  L8 Rthe neck revealed no thyroid enlargement.# q$ K& E0 w# S, T: R" U0 c
The genitourinary examination was remarkable for
+ J) M7 _7 C/ _1 G) E! menlargement of the penis, with a stretched length of" W, J* K/ k+ S. A( H
8 cm and a width of 2 cm. The glans penis was very well  l5 x4 ~' e% x' J" t
developed. The pubic hair was Tanner II, mostly around
, j# i: S; i) [8 A  m540
' P: L- l, N8 \/ Sat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) k* p+ P3 g) E* V: p/ ]& I* d
the base of the phallus and was dark and curled. The
( C8 n4 ^# F& n3 W! t- Atesticular volume was prepubertal at 2 mL each.5 Q' @) p2 T+ K, ~5 X& g2 N
The skin was moist and smooth and somewhat
5 L4 z0 `- {* W3 ?oily. No axillary hair was noted. There were no/ ?3 w+ `) e! A9 `: }" n% P) ]0 c
abnormal skin pigmentations or café-au-lait spots.6 C' p5 j$ v5 o
Neurologic evaluation showed deep tendon reflex 2+3 c8 w4 D. m+ y& w! C
bilateral and symmetrical. There was no suggestion, J- n' K& G  w$ @$ F  f9 L* F. N
of papilledema.
3 s6 n- A5 y( GLaboratory Evaluation
, _' j' `) S6 |The bone age was consistent with 28 months by# I5 \1 C0 x9 I% M3 H# m
using the standard of Greulich and Pyle at a chrono-
  M0 ^/ Q# A& @+ T9 h6 ], o, elogic age of 16 months (advanced).5 Chromosomal
9 H5 q6 F1 F. p6 d( ~4 X, m. Mkaryotype was 46XY. The thyroid function test
7 Z& c+ c+ }# Z! d/ T, Wshowed a free T4 of 1.69 ng/dL, and thyroid stimu-* \; E# l& Y  V! G
lating hormone level was 1.3 µIU/mL (both normal).
9 Y8 k" G# ]. d( M* \5 `9 jThe concentrations of serum electrolytes, blood
' H) V8 D! G; {6 ]4 |. z; @0 ?, `urea nitrogen, creatinine, and calcium all were5 _' l. @" m1 Q* W
within normal range for his age. The concentration
: n) D4 j2 z# c) F, O1 a3 Gof serum 17-hydroxyprogesterone was 16 ng/dL4 g+ G  F+ p, X  Z! i! w1 [, F
(normal, 3 to 90 ng/dL), androstenedione was 20  Z7 A6 X& u& R' x5 I
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-' ^+ W* o1 H! q  ~. V' }6 u
terone was 38 ng/dL (normal, 50 to 760 ng/dL),8 J# A# d% m$ w
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
* U+ D; d! ~7 S) _( {49ng/dL), 11-desoxycortisol (specific compound S)
0 _7 R* b& u3 ~was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
3 z+ a# n' s* ?- q( |. X0 dtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
. p. Y# |5 M! f, rtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
/ g; v) b; _+ q8 y3 Pand β-human chorionic gonadotropin was less than
4 _  n, Z# e" X/ y8 l6 X& x5 mIU/mL (normal <5 mIU/mL). Serum follicular- H0 v; E% Z* j$ p
stimulating hormone and leuteinizing hormone* C' S2 X$ }& L& U) v7 G
concentrations were less than 0.05 mIU/mL
) w, D6 W0 _9 J1 @: W/ m! |(prepubertal).1 ]( c+ w$ Z/ J7 _0 |: `
The parents were notified about the laboratory
, ~- D" w4 e, }" }4 B3 T$ {results and were informed that all of the tests were
- P" Y( B8 z" t% d. e3 o8 e1 u8 k) Inormal except the testosterone level was high. The+ W& _6 H- U4 u  U8 y3 a$ V+ A. U
follow-up visit was arranged within a few weeks to, n  C5 s& {' i" B# V, S
obtain testicular and abdominal sonograms; how-
' L& C7 {* h" n1 Dever, the family did not return for 4 months.; C( [0 z5 b9 T! b& ~1 i+ L
Physical examination at this time revealed that the
0 q2 c& }. o& T$ k' W$ _child had grown 2.5 cm in 4 months and had gained9 z' l8 `3 w. h& W; w0 a9 J
2 kg of weight. Physical examination remained
: C) U& L% ~3 Z3 x, p; `unchanged. Surprisingly, the pubic hair almost com-
8 d5 d# M" F- B7 a. @+ D# a# z! Gpletely disappeared except for a few vellous hairs at5 s7 a) {, e1 T1 j5 Q7 V+ M1 j
the base of the phallus. Testicular volume was still 2# }& x3 m5 I$ d; }- b8 z6 L
mL, and the size of the penis remained unchanged.
+ K$ e7 B! y; V, [2 RThe mother also said that the boy was no longer hav-% G' _* B; @; A7 y& p
ing frequent erections.
% x5 g9 `5 a6 A4 D8 DBoth parents were again questioned about use of; m/ h2 A. V% Y0 J( t1 `  n3 k
any ointment/creams that they may have applied to8 S0 W9 w' c9 V& D
the child’s skin. This time the father admitted the
9 P' j6 ?  Y: M; W& v, F6 ~Topical Testosterone Exposure / Bhowmick et al 541" k3 R" t( T0 o5 U" I# I
use of testosterone gel twice daily that he was apply-+ G$ u% y* [, D. i
ing over his own shoulders, chest, and back area for3 [; j1 {; L% f. i; ]
a year. The father also revealed he was embarrassed8 l$ P) S" p  z" P  E( U1 f
to disclose that he was using a testosterone gel pre-
" |& u% {. H! F  T. b2 oscribed by his family physician for decreased libido
% I. C$ [0 n" Psecondary to depression.
- W* Q. g! g0 P$ h+ u7 W- DThe child slept in the same bed with parents.* E( v' S% H. l6 U5 a
The father would hug the baby and hold him on his' S& ?+ R0 S2 H2 e7 B) Q/ r- X
chest for a considerable period of time, causing sig-
* t7 B! r! t4 Nnificant bare skin contact between baby and father.+ v7 `$ P* L9 f1 X
The father also admitted that after the phone call,( g8 l( }7 \  p, d! M
when he learned the testosterone level in the baby* ^: t9 }0 c$ ^1 K" k
was high, he then read the product information
1 N, S* p% y% n. n" c1 c* X, apacket and concluded that it was most likely the rea-* M) g* D! _* X, n0 k
son for the child’s virilization. At that time, they
* _6 O2 H. E# V  j6 e7 O/ f/ [decided to put the baby in a separate bed, and the3 [. [3 D( ]% d! Y# f& V
father was not hugging him with bare skin and had
$ s. o' A+ `# E4 nbeen using protective clothing. A repeat testosterone
3 L; L* g" r/ Q! _# y& m( Itest was ordered, but the family did not go to the
, d& z; d0 i3 Ilaboratory to obtain the test.
. g/ W2 ?9 n8 L9 i4 q$ UDiscussion
" \, {4 T# I; s  r1 q4 KPrecocious puberty in boys is defined as secondary$ l. ~6 _$ [" X2 @. A
sexual development before 9 years of age.1,4  M+ w2 J0 U9 w# R
Precocious puberty is termed as central (true) when7 l% p+ G! O4 F# A+ S& M  O
it is caused by the premature activation of hypo-
1 `; M: E8 g" @) z, f6 dthalamic pituitary gonadal axis. CPP is more com-
+ m8 @7 h- V" t) U; i% L7 ]3 \) Zmon in girls than in boys.1,3 Most boys with CPP
3 l1 {. Y7 P( wmay have a central nervous system lesion that is5 p; T3 i3 W0 V
responsible for the early activation of the hypothal-
! N1 ~4 q6 M1 |4 t6 Zamic pituitary gonadal axis.1-3 Thus, greater empha-+ l8 ^" {5 t& h( M" e& }
sis has been given to neuroradiologic imaging in
6 v. ]1 C. P/ j! y1 y$ K4 `boys with precocious puberty. In addition to viril-
. x  m5 q  p3 R( q0 Z3 {7 `ization, the clinical hallmark of CPP is the symmet-
1 }. U- I; N; n% Crical testicular growth secondary to stimulation by
2 {0 f4 [8 c% _( u4 C  Rgonadotropins.1,3
- }+ I: g( i2 K& VGonadotropin-independent peripheral preco-8 X! F+ s$ ~2 }
cious puberty in boys also results from inappropriate, D* q  A3 E! B- }) b& j) E2 G
androgenic stimulation from either endogenous or
% Q2 Q. o7 Z: s# ]* Texogenous sources, nonpituitary gonadotropin stim-
1 M/ V5 m" Z0 Q  ]) Nulation, and rare activating mutations.3 Virilizing
- F+ [& v" b" D" j  `* P6 w6 pcongenital adrenal hyperplasia producing excessive7 z9 [+ O" l, y* u( I7 ^
adrenal androgens is a common cause of precocious3 A0 E: `* _, f' b$ }1 B' X6 B3 N
puberty in boys.3,4
1 a, ]9 q# p% ZThe most common form of congenital adrenal
/ E% ~/ |2 r3 @0 i. ^6 ahyperplasia is the 21-hydroxylase enzyme deficiency.& M- c/ ^7 `8 _/ L- u: j
The 11-β hydroxylase deficiency may also result in
6 S3 y2 o- [3 s9 xexcessive adrenal androgen production, and rarely,1 s* x. O$ h% J$ E
an adrenal tumor may also cause adrenal androgen
# J, X, R9 ^9 Nexcess.1,3: T  n* g7 D. j4 j! B. i
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" L3 n6 L5 w+ E6 v) J542 Clinical Pediatrics / Vol. 46, No. 6, July 20076 `4 N8 m2 N2 g  T
A unique entity of male-limited gonadotropin-
- d0 N5 x/ E: O# v& p- Findependent precocious puberty, which is also known
+ M0 I" R/ ?/ b/ u5 Y* Sas testotoxicosis, may cause precocious puberty at a# c- M5 U; ]% k4 E
very young age. The physical findings in these boys
( q6 R9 T- f  E5 X9 h0 jwith this disorder are full pubertal development,
1 ]2 u; D+ ]- g/ z1 Q8 Q/ Gincluding bilateral testicular growth, similar to boys" Z4 ~* v% y5 b/ f
with CPP. The gonadotropin levels in this disorder% y" a# H9 Q9 d3 T" I( {% z
are suppressed to prepubertal levels and do not show
0 M( i6 m9 Z: D: F+ T9 p& _pubertal response of gonadotropin after gonadotropin-; D, `# P& B& b+ H+ }5 q
releasing hormone stimulation. This is a sex-linked
) F- G3 b) g( h# X# yautosomal dominant disorder that affects only
, l$ _8 z' j6 k, [males; therefore, other male members of the family
, s0 R" o  v4 o6 P" ~# U/ omay have similar precocious puberty.3
9 c8 i, T4 {0 u; U% ^! D- X/ qIn our patient, physical examination was incon-1 {0 o, H5 c3 F9 ^
sistent with true precocious puberty since his testi-
/ |$ B) v: V; \" |- Ecles were prepubertal in size. However, testotoxicosis" D4 s, `) f5 ]7 _# }
was in the differential diagnosis because his father
8 O7 \4 Y% u2 x1 m; u/ u+ cstarted puberty somewhat early, and occasionally,
% Q- ~' n* r/ z8 b3 Ptesticular enlargement is not that evident in the
' j' H& Y, A: E# \beginning of this process.1 In the absence of a neg-. `. b7 C; l1 R
ative initial history of androgen exposure, our3 b: S8 Y" H" Z7 s. {1 u
biggest concern was virilizing adrenal hyperplasia,$ P' V  h8 f9 f( Q
either 21-hydroxylase deficiency or 11-β hydroxylase
3 K$ Q0 ^3 W* A* G1 bdeficiency. Those diagnoses were excluded by find-
" [. W4 I  E+ @# I/ A1 z' Ying the normal level of adrenal steroids.
; g+ [; ~  L: H% b- ?( B- kThe diagnosis of exogenous androgens was strongly
2 C, S' [8 r) i1 ]9 z, _0 K) \5 Rsuspected in a follow-up visit after 4 months because
  a, r, |9 ^6 I* E* c# zthe physical examination revealed the complete disap-4 Q: d) l$ q5 ]1 i
pearance of pubic hair, normal growth velocity, and' ]) z. l) A& M
decreased erections. The father admitted using a testos-# g) _8 y8 L7 \# ~7 ~$ J" J
terone gel, which he concealed at first visit. He was; C+ m' z$ ]$ o" v/ s* n2 k
using it rather frequently, twice a day. The Physicians’
" O* O9 r! s( D7 T9 GDesk Reference, or package insert of this product, gel or' q6 |- y. S, h) P# R
cream, cautions about dermal testosterone transfer to
/ g. b' j7 @- y+ j9 |) ?unprotected females through direct skin exposure.4 o, G! v) n; }- Q  c
Serum testosterone level was found to be 2 times the$ y' s! \9 q, u0 n
baseline value in those females who were exposed to
. P, y7 e* o0 |9 u+ w: s$ \even 15 minutes of direct skin contact with their male
7 h3 R: J, D0 S9 [- ypartners.6 However, when a shirt covered the applica-- T9 n+ t% a, D" L) o* f
tion site, this testosterone transfer was prevented.
9 g, s& k% b3 U2 K, A  IOur patient’s testosterone level was 60 ng/mL,
5 b  e$ _+ v7 q8 K9 d5 pwhich was clearly high. Some studies suggest that
' }9 R) G5 }6 q; p; j! Odermal conversion of testosterone to dihydrotestos-+ t8 D- v6 n2 i5 _; f
terone, which is a more potent metabolite, is more
0 k0 m3 C, p1 v; Z0 B5 h  |active in young children exposed to testosterone
0 f( E: y4 c4 f+ @exogenously7; however, we did not measure a dihy-
, g: j4 y: v- R# ^8 V; Adrotestosterone level in our patient. In addition to2 Q) {( y( z  A, b. j. }5 i0 z
virilization, exposure to exogenous testosterone in
" y, l1 |1 f2 A  d) ~children results in an increase in growth velocity and
. U* q) \# O( B+ j2 N5 v9 v8 ?advanced bone age, as seen in our patient.
( [7 ~, v, q1 S' t! L. [2 |The long-term effect of androgen exposure during# G( K  Q% T0 A- _4 j+ I
early childhood on pubertal development and final1 i9 o0 P( y) ]+ \: i6 [9 K6 r
adult height are not fully known and always remain# ~- N& ~& F& ^
a concern. Children treated with short-term testos-/ r- ^+ ]" r. E! l* f
terone injection or topical androgen may exhibit some2 }, V5 l$ ~' T: p
acceleration of the skeletal maturation; however, after
0 q& A/ w8 W9 ~( Lcessation of treatment, the rate of bone maturation
$ J& Q6 X! A( E/ N7 x% n% Xdecelerates and gradually returns to normal.8,9* [" L, v. I7 x! J
There are conflicting reports and controversy
, C7 e1 r4 w) |7 s1 c7 l; ~' vover the effect of early androgen exposure on adult
/ |9 b% C5 N  gpenile length.10,11 Some reports suggest subnormal
* I0 z) O" T7 Y9 m: Z9 d  tadult penile length, apparently because of downreg-) p# h. B2 I# a1 k7 h% g" M
ulation of androgen receptor number.10,12 However," a$ s& f/ [  b4 g
Sutherland et al13 did not find a correlation between% p+ V/ ~  T: t8 y
childhood testosterone exposure and reduced adult6 G- C2 h# H) a! z+ T- q
penile length in clinical studies.. W6 O) G, H* a5 {  A
Nonetheless, we do not believe our patient is1 [+ P) m) ^9 @
going to experience any of the untoward effects from( d4 ]- d. \% D3 y2 O& Q5 t
testosterone exposure as mentioned earlier because( }# `% R8 q) f; B1 r: @$ i' f
the exposure was not for a prolonged period of time.
, Z, ?% {. a3 l- J9 y" ]Although the bone age was advanced at the time of# L5 c0 y- d# U/ c6 X. w" n9 `
diagnosis, the child had a normal growth velocity at6 _7 _+ s6 Y; C$ S/ C
the follow-up visit. It is hoped that his final adult" Z$ x7 N: M$ I
height will not be affected.# r4 n4 }0 }' j) r; B7 x, V
Although rarely reported, the widespread avail-1 c2 j3 d$ R- W6 M, L; w
ability of androgen products in our society may0 j4 Q2 O2 C! ^$ ]
indeed cause more virilization in male or female% }1 t: f& l, d) [" J1 O, a
children than one would realize. Exposure to andro-7 B9 Q9 [, B7 P: f
gen products must be considered and specific ques-: k/ \: b; G9 p
tioning about the use of a testosterone product or( o# d( _8 n% }& N
gel should be asked of the family members during
: Z6 b" d% U0 H9 h$ U" p3 uthe evaluation of any children who present with vir-
* u) h6 v$ X/ vilization or peripheral precocious puberty. The diag-8 w0 g. y9 P; C9 f  I0 u
nosis can be established by just a few tests and by
5 M; I1 u$ N9 h0 i3 s% aappropriate history. The inability to obtain such a: B/ l5 C4 a& I2 u# K
history, or failure to ask the specific questions, may
1 ~$ m& y/ a' hresult in extensive, unnecessary, and expensive/ i$ ?! b4 {/ x* }/ X
investigation. The primary care physician should be
# H( o* }* p1 w6 @/ T$ p" ~aware of this fact, because most of these children
( I$ Z& N7 M/ j9 smay initially present in their practice. The Physicians’) W7 e' ?) c  p$ i: D
Desk Reference and package insert should also put a
/ l9 C2 J; _& e, |% |4 Iwarning about the virilizing effect on a male or& S4 g. T0 D7 K! `& m) K( G- w: H
female child who might come in contact with some-
- N# S# S+ s  `- `' L4 Xone using any of these products.1 q% B% h9 o/ H
References
* a+ ^% R: c2 {0 y( Y1. Styne DM. The testes: disorder of sexual differentiation
7 e( l3 `7 w& K$ C. P6 e) Dand puberty in the male. In: Sperling MA, ed. Pediatric: V# S5 Z0 S1 X8 F# ]  k8 h/ X. s9 |
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;! Z3 @& v  _& J7 x; h/ ]
2002: 565-628.
6 s* q  o$ i* K% w. {2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
" V. o( N7 d$ S: H+ vpuberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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
8 k( a- T8 y0 B$ a! J
精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!
發表於 2025-3-8 22:04:50 | 顯示全部樓層
絕對的好貼!謝謝啊!逐字逐圖地看完這個帖子以後,我的心久久不能平靜,感恩啊!
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