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Sexual Precocity in a 16-Month-Old7 e  m8 q5 V. Y" {2 c
Boy Induced by Indirect Topical, p+ ?1 f- I& z' x3 v7 |
Exposure to Testosterone
" t/ \5 b8 `7 a7 Z8 ?0 PSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
% }" G' ]8 h* F) t, `- B, jand Kenneth R. Rettig, MD1
3 F5 j2 O( O3 K6 T) I7 m; H. UClinical Pediatrics
% x4 N* @, J& u% H6 Z0 p. u, X  tVolume 46 Number 69 O! k* ^4 p' N( L" q# {. v
July 2007 540-543
- y- H6 |  ]- x+ {5 a& Q/ g© 2007 Sage Publications6 Q7 V+ F6 w# `) L
10.1177/0009922806296651, i2 \% d7 N, q6 Y
http://clp.sagepub.com
: O6 C$ B% W2 }2 z7 K, }hosted at. w( e8 Q5 Z. O3 B. D3 A
http://online.sagepub.com
& W, r, N. k) P& vPrecocious puberty in boys, central or peripheral,' Q2 j6 }" w: T1 N, x" l6 W
is a significant concern for physicians. Central
# ]- ]" |, M8 O5 `precocious puberty (CPP), which is mediated
! N: b& V3 j' K4 D$ ithrough the hypothalamic pituitary gonadal axis, has" z4 d" ~/ |+ ^* D1 v+ d
a higher incidence of organic central nervous system; d) w$ t9 m: i, g1 l! |5 S
lesions in boys.1,2 Virilization in boys, as manifested# k& l9 p7 `8 L
by enlargement of the penis, development of pubic
. Y+ |! x9 D- Q3 @hair, and facial acne without enlargement of testi-
1 i! U6 q6 h5 tcles, suggests peripheral or pseudopuberty.1-3 We
" C* J/ _) E& ~9 G+ d2 t7 t) {report a 16-month-old boy who presented with the
, U# A* _% {* `& senlargement of the phallus and pubic hair develop-
+ W+ v8 K) \# Z- b2 N3 q5 Pment without testicular enlargement, which was due
+ A4 ?# S4 \2 y5 |to the unintentional exposure to androgen gel used by
& h3 o8 ]$ Z/ t7 E. W; e  Fthe father. The family initially concealed this infor-
4 C- I, v. w# J, Z4 vmation, resulting in an extensive work-up for this( ^. i; ]0 u9 B/ a9 W+ c2 t. P
child. Given the widespread and easy availability of
  [; M. ^8 v- y$ p1 Gtestosterone gel and cream, we believe this is proba-
* m/ G7 M6 G3 c* Z3 p$ Obly more common than the rare case report in the, f! z6 E& v# W7 j
literature.4) O7 u  M5 r8 f" T! O. E
Patient Report1 f* K9 `9 N/ Z: W1 C, }- ^
A 16-month-old white child was referred to the4 f5 }* p6 |1 v
endocrine clinic by his pediatrician with the concern" |" S6 S. ^# N4 ^( P
of early sexual development. His mother noticed7 W) k: O( @8 _- w- k+ j( e' \8 z" s! [9 H
light colored pubic hair development when he was' F* |6 V+ ^2 x6 L. Z. l% ^( y
From the 1Division of Pediatric Endocrinology, 2University of
& f1 E  ~7 V7 g3 j4 XSouth Alabama Medical Center, Mobile, Alabama.
. T3 y" A' {; J2 E  G" ^Address correspondence to: Samar K. Bhowmick, MD, FACE," `/ N* x8 m& R. |/ O8 Q% F$ w
Professor of Pediatrics, University of South Alabama, College of5 ?* I9 ~5 Z2 H/ v- S
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;2 z* H* X# I& T8 Z# [# F
e-mail: [email protected].
. L% `( n: s* e9 h6 S+ w! Eabout 6 to 7 months old, which progressively became
( \9 \# Q/ g8 j0 @/ h# Z* ]) Xdarker. She was also concerned about the enlarge-  i" C" l& x# i9 n( x% a9 W
ment of his penis and frequent erections. The child3 k/ @7 M8 _/ S9 p. A
was the product of a full-term normal delivery, with5 r1 U5 l% F" ~/ w5 H. Z; R& O
a birth weight of 7 lb 14 oz, and birth length of! z6 L* u. q7 Q6 x$ g* V4 a) b) M
20 inches. He was breast-fed throughout the first year9 w8 A6 R) Y/ U$ x* M  X1 G# g
of life and was still receiving breast milk along with
: P( s3 o9 T: F$ l- Bsolid food. He had no hospitalizations or surgery,3 A9 C% U/ f: _* L+ Y
and his psychosocial and psychomotor development% f: h5 U' ]3 ^; l8 V6 c8 V& V
was age appropriate.
7 s7 U# H0 o5 f! nThe family history was remarkable for the father,
% m# h/ [% b2 L1 }5 f5 Q8 l5 ]who was diagnosed with hypothyroidism at age 16,
( T' x2 A8 T& ]# C) ]9 G) U, e2 Fwhich was treated with thyroxine. The father’s+ [7 D- ^9 u4 h
height was 6 feet, and he went through a somewhat8 ]8 Q1 H& g, l% X" @
early puberty and had stopped growing by age 14.
" P! E2 y9 H. r( U* K% ?  uThe father denied taking any other medication. The, C9 }5 o: U6 T/ I
child’s mother was in good health. Her menarche2 K* B7 g  p' H; J2 {, A# f
was at 11 years of age, and her height was at 5 feet! J  B; C1 s7 [
5 inches. There was no other family history of pre-+ E8 p1 p4 O0 J* c* h0 c
cocious sexual development in the first-degree rela-
) {9 c  ^' t  Wtives. There were no siblings., \+ P" a+ k, Z0 L. O; ^
Physical Examination6 a1 \/ p" S; B& l, Z# V# o: P0 T
The physical examination revealed a very active,7 I* W. u1 ~  \! l! b1 T0 W
playful, and healthy boy. The vital signs documented
% b7 d  H, s, z; b0 T+ L6 na blood pressure of 85/50 mm Hg, his length was
1 N; Y. `# K( h: T+ U$ Y90 cm (>97th percentile), and his weight was 14.4 kg
, O3 U# ^0 A( y. ]) g# y+ u3 L(also >97th percentile). The observed yearly growth6 x* ^/ M! n9 ]  e: }3 K& v: E
velocity was 30 cm (12 inches). The examination of: ?9 }, @0 k3 \% ^% M+ |
the neck revealed no thyroid enlargement.
; J1 I; r/ e0 K+ S# ^- l9 nThe genitourinary examination was remarkable for
7 ^( a8 {6 b4 |8 K% h# Zenlargement of the penis, with a stretched length of
: R3 r1 ]- I+ W7 ?  t& g8 cm and a width of 2 cm. The glans penis was very well: @9 O9 `9 L/ r) M
developed. The pubic hair was Tanner II, mostly around
) e  }! J! t+ v5404 r; z1 }8 ^; a- s0 [6 `6 Z( ?( }
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, W  u& ?; x( u9 N( g+ Hthe base of the phallus and was dark and curled. The
& R4 J" ?) L& O/ Atesticular volume was prepubertal at 2 mL each.
5 P" e) Z. a7 E3 CThe skin was moist and smooth and somewhat' E$ Y* s- d- C4 k' ?
oily. No axillary hair was noted. There were no
& [  \4 L4 i( b1 w/ Gabnormal skin pigmentations or café-au-lait spots.- N4 H5 B. {% q4 e" G* E& Q+ Q
Neurologic evaluation showed deep tendon reflex 2+
: e; a+ r' s+ j5 |5 l8 b5 k5 Mbilateral and symmetrical. There was no suggestion
% L+ R8 x& G' h/ U  H( u3 \of papilledema.
1 Z5 W8 w5 M; C& l) {" MLaboratory Evaluation
2 P1 |( o. H* S, ~2 x, uThe bone age was consistent with 28 months by
; q/ J+ h( d& A, @% l: @using the standard of Greulich and Pyle at a chrono-
, r3 h9 ?4 C) [( n& Glogic age of 16 months (advanced).5 Chromosomal
- U3 a* U) \' H, pkaryotype was 46XY. The thyroid function test! M6 @( G/ A0 t  h7 g, p, Y. y8 J
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
5 z: [0 n% R8 `( b8 Q/ f1 A8 ?lating hormone level was 1.3 µIU/mL (both normal).# U5 g  p9 v! t0 Z" J
The concentrations of serum electrolytes, blood
' ^; U1 _7 l. D; ]( murea nitrogen, creatinine, and calcium all were
6 o7 h5 A! X5 A! C& jwithin normal range for his age. The concentration& n! _+ p! G+ ^0 S* v! d( @
of serum 17-hydroxyprogesterone was 16 ng/dL  U0 G" j1 q) h* P' @. b- ]9 x% {3 M
(normal, 3 to 90 ng/dL), androstenedione was 20, ^$ b# X7 T( V
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
/ J; H1 S% B/ r' e) u1 Z1 zterone was 38 ng/dL (normal, 50 to 760 ng/dL),9 r; Y5 X0 Z) d4 J  Z  W
desoxycorticosterone was 4.3 ng/dL (normal, 7 to- F" R' A$ t4 g7 b9 C; Q
49ng/dL), 11-desoxycortisol (specific compound S)
0 d  f. }* @" f7 O, N# v$ u% ~was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
4 R1 g* t5 T  ftisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total" r5 c  E) c, W5 {: P: l
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),/ _' S3 A% b: c- u
and β-human chorionic gonadotropin was less than4 W3 O3 S( r1 V8 C- f* h. Z
5 mIU/mL (normal <5 mIU/mL). Serum follicular3 M. k0 K3 X$ k" d) t  f( e5 ?; _
stimulating hormone and leuteinizing hormone
* f& f$ f/ p* o  u: u. Cconcentrations were less than 0.05 mIU/mL
1 r9 K3 J, y+ e(prepubertal).
1 \9 V# \3 _, u3 AThe parents were notified about the laboratory7 q9 g; n& ^) \8 i
results and were informed that all of the tests were. S& k  \2 c4 k8 v7 w2 X
normal except the testosterone level was high. The# }3 w, Q4 U9 J+ v, z0 E
follow-up visit was arranged within a few weeks to
. z3 L; W* I5 `8 O+ Oobtain testicular and abdominal sonograms; how-
- [2 _( E2 A- x2 e, P+ tever, the family did not return for 4 months.
# \, Q3 }/ ?, D4 u# sPhysical examination at this time revealed that the
$ j, R( t& e4 ^) Z2 Achild had grown 2.5 cm in 4 months and had gained
# }* E4 y$ ?, b9 A# W1 L5 P2 kg of weight. Physical examination remained
( d% e0 A  ]. O8 {3 z8 F+ |unchanged. Surprisingly, the pubic hair almost com-* K9 ~6 M( E( V5 ]9 _( l: g
pletely disappeared except for a few vellous hairs at
! L* ~! p4 ^; a5 Q4 Qthe base of the phallus. Testicular volume was still 2' P- Y* U4 a# \7 a; T! ~# q, d
mL, and the size of the penis remained unchanged.! }. J/ X3 x- n4 p
The mother also said that the boy was no longer hav-$ z9 |% k0 M1 b5 a
ing frequent erections.
& S& S' F; d; P+ Y2 f' Z- o. rBoth parents were again questioned about use of' p7 V% I/ o2 K/ ^+ @3 F1 Y
any ointment/creams that they may have applied to
9 H( G: i8 J! J" j+ l2 rthe child’s skin. This time the father admitted the9 Q, F2 G* ^" @8 w2 l) F7 R- d
Topical Testosterone Exposure / Bhowmick et al 5418 @8 @2 C, ]  y2 H0 @0 b( z
use of testosterone gel twice daily that he was apply-+ b. F; p4 M: d
ing over his own shoulders, chest, and back area for
/ _1 u! l$ V* I7 W  wa year. The father also revealed he was embarrassed
& _% F+ E) S2 q# ]5 [) R3 W, Nto disclose that he was using a testosterone gel pre-+ x" V9 p3 l- h3 Q
scribed by his family physician for decreased libido6 k! I5 K2 _5 p  Z# R; n% R2 x
secondary to depression.2 Z/ U( f0 H7 S" n+ K
The child slept in the same bed with parents.+ Q5 u- C) {8 \0 k; `, [
The father would hug the baby and hold him on his; W. |4 Y- @/ w, k6 K
chest for a considerable period of time, causing sig-+ r. J1 ^  V- _) D9 y, w
nificant bare skin contact between baby and father.9 V1 U2 \% l* ]0 ^' u  h. @
The father also admitted that after the phone call,
0 e* _; s# Z6 H, rwhen he learned the testosterone level in the baby5 D5 L" r9 ]: x8 @
was high, he then read the product information
0 c4 E+ ^& b" }. n/ L5 u) U' B' G: _" mpacket and concluded that it was most likely the rea-
( m) L+ G4 I8 D+ b3 K- d9 xson for the child’s virilization. At that time, they( N( `* M8 ~  f" j: J/ T
decided to put the baby in a separate bed, and the
8 ]6 w. B. n& X! q6 r6 [father was not hugging him with bare skin and had! Y$ j( R. j( |% g
been using protective clothing. A repeat testosterone% i" I; \9 C2 h) I9 U! P8 _
test was ordered, but the family did not go to the0 ?% m8 z8 x. f/ o
laboratory to obtain the test.; B' z/ @$ O1 I+ f# i& F
Discussion
* i. R, E! Y& }( c% m- B: n: QPrecocious puberty in boys is defined as secondary
3 g0 e9 ?, k# H+ W3 }sexual development before 9 years of age.1,4
+ k! ^" M$ ^& s1 u$ dPrecocious puberty is termed as central (true) when
# U3 a6 L* f5 hit is caused by the premature activation of hypo-$ K9 W$ N$ U6 X" B5 a/ b3 \% c% K
thalamic pituitary gonadal axis. CPP is more com-& M4 v" o- i* e& L( K( U/ I% a; y$ P
mon in girls than in boys.1,3 Most boys with CPP9 o7 X+ f! ^3 f+ d, M7 D# i1 @$ o
may have a central nervous system lesion that is
' s+ V6 u0 S: d, q# D4 N* Kresponsible for the early activation of the hypothal-
, t1 A$ n7 O# E: R  Y. f4 Vamic pituitary gonadal axis.1-3 Thus, greater empha-
8 D5 N0 V" @- J( m4 y/ Csis has been given to neuroradiologic imaging in4 D. h4 {. |" A9 [
boys with precocious puberty. In addition to viril-
/ Q, i7 N/ m) Q4 v  Rization, the clinical hallmark of CPP is the symmet-. p/ N" V& {6 ~
rical testicular growth secondary to stimulation by
' B. B/ ?0 k( t5 u$ x( g* Q0 G% Ggonadotropins.1,3- |  E& g& s) \3 d5 N/ m7 X' ?
Gonadotropin-independent peripheral preco-
% p* y! p; _1 fcious puberty in boys also results from inappropriate
  h5 f" U: U5 dandrogenic stimulation from either endogenous or
) Z# X6 J) p" |; rexogenous sources, nonpituitary gonadotropin stim-
5 h& a8 z$ M1 O( M0 ~( O' aulation, and rare activating mutations.3 Virilizing
# }8 u7 K# J6 n) ~2 icongenital adrenal hyperplasia producing excessive% a( D8 x9 y) a; z; R& `, k, |/ ?* u7 T
adrenal androgens is a common cause of precocious
+ g. b3 y6 m0 u% A8 C8 Xpuberty in boys.3,4
; L- Q6 B% f. s7 \, ~# ]$ B9 ^6 xThe most common form of congenital adrenal
5 j: }- ?1 A' L7 ^+ X+ i/ thyperplasia is the 21-hydroxylase enzyme deficiency.; u  F/ F! F; x! ]% Z- S. j2 m
The 11-β hydroxylase deficiency may also result in
" c) {2 _* V9 z# Z) F/ V, pexcessive adrenal androgen production, and rarely,) ^2 f; w: C+ K  E
an adrenal tumor may also cause adrenal androgen, X( m) W0 o9 |. ]
excess.1,3
7 |" F/ [8 u( q/ W3 b* z7 E  v( Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 A( h( ^+ k& O5 U/ r
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
3 {5 j) E9 ~! b7 q3 S' I: N7 iA unique entity of male-limited gonadotropin-6 {0 @- V  C" ?# h- V
independent precocious puberty, which is also known: ^2 V1 c) l0 T! x$ b
as testotoxicosis, may cause precocious puberty at a
6 ^2 j& x) Y; q% o( r5 X% O( Q& d" Svery young age. The physical findings in these boys2 A& R" }; L) ~+ x6 n7 T9 S
with this disorder are full pubertal development,
5 w1 g5 M( Q% @. f1 h% x, S7 nincluding bilateral testicular growth, similar to boys
& ]" K6 V3 P- S. v" `with CPP. The gonadotropin levels in this disorder1 _( p0 h8 Y' |
are suppressed to prepubertal levels and do not show) T9 w7 v* i5 ]6 C0 i+ _6 n
pubertal response of gonadotropin after gonadotropin-
) Z2 Q3 A# o6 q* `# u. |4 nreleasing hormone stimulation. This is a sex-linked9 D! K) J* u* S
autosomal dominant disorder that affects only" Z) I; p! H! _8 K. Z" v+ ^' b& K! `
males; therefore, other male members of the family3 ]8 i8 ?& y/ R7 L
may have similar precocious puberty.3
+ Y8 K0 e6 n4 r& OIn our patient, physical examination was incon-$ p) o5 q7 p8 H! R- m1 ^9 b
sistent with true precocious puberty since his testi-
( ^( }5 G" G/ Z- o  U9 mcles were prepubertal in size. However, testotoxicosis8 i9 ]3 M3 z3 W! o
was in the differential diagnosis because his father
3 a# F. F! k$ N3 H" H9 M! `started puberty somewhat early, and occasionally,
9 y6 \( _2 e0 ~4 c0 h% L) j' V/ U9 _testicular enlargement is not that evident in the" K7 K5 `5 ?1 s! u6 _. d# r, O
beginning of this process.1 In the absence of a neg-, K8 T' d. p; t) A
ative initial history of androgen exposure, our; C9 ]" h# u& d1 K$ E# J( @6 k
biggest concern was virilizing adrenal hyperplasia,. d/ k9 Q( ?( q) V
either 21-hydroxylase deficiency or 11-β hydroxylase
& f  a+ K; y* odeficiency. Those diagnoses were excluded by find-6 _) S- p+ C9 `  L
ing the normal level of adrenal steroids.. a5 R/ f6 G# C# a
The diagnosis of exogenous androgens was strongly/ y: y* ^! |1 Z6 n+ x
suspected in a follow-up visit after 4 months because
* ~3 j7 V" p  D! f9 Uthe physical examination revealed the complete disap-! q6 h! F1 v8 ]1 \& @+ F9 K
pearance of pubic hair, normal growth velocity, and) a, p8 V1 |8 v0 f0 J8 W
decreased erections. The father admitted using a testos-7 y! c; o9 a0 l& K$ \: [1 Z8 j
terone gel, which he concealed at first visit. He was" r. t: b6 y: M- h. v
using it rather frequently, twice a day. The Physicians’
6 ~9 z' J% E( eDesk Reference, or package insert of this product, gel or
+ |! {" K( j+ Icream, cautions about dermal testosterone transfer to* B; g$ p( i. C8 w0 j5 K1 E
unprotected females through direct skin exposure.
, v6 `  u- w# z5 v1 pSerum testosterone level was found to be 2 times the
7 S  ^( _/ O7 P0 g& kbaseline value in those females who were exposed to8 y2 t# A0 ]# |$ C/ V1 z
even 15 minutes of direct skin contact with their male2 d8 n% G6 n6 r- \
partners.6 However, when a shirt covered the applica-
) Q8 {% G. c1 Wtion site, this testosterone transfer was prevented.
6 @  ~( f& }' ^4 z1 IOur patient’s testosterone level was 60 ng/mL,
* K3 N: u6 V  twhich was clearly high. Some studies suggest that
& A6 I( V9 a5 B: {, N3 b$ M) k; ndermal conversion of testosterone to dihydrotestos-7 [& E$ Z+ g8 r5 d/ I
terone, which is a more potent metabolite, is more
# T: e4 n/ c! ?# k0 L- l7 Y1 Pactive in young children exposed to testosterone
8 H. M  K% X8 N6 l* E' qexogenously7; however, we did not measure a dihy-
  g$ [; ^, W3 L9 [2 M9 F1 Cdrotestosterone level in our patient. In addition to
" Q0 i9 j, L" z  ?: `3 I* N9 lvirilization, exposure to exogenous testosterone in
/ |4 [* \; W; P' n* [) d  T; u6 S: schildren results in an increase in growth velocity and( R. V6 G6 z* x' x7 c* q
advanced bone age, as seen in our patient.$ ]# n# x, y& `2 I9 h
The long-term effect of androgen exposure during* L; [3 U9 f" \1 ^
early childhood on pubertal development and final
7 u6 J" Y2 u) d- _# C% Zadult height are not fully known and always remain
5 J' l5 k/ P. y& ya concern. Children treated with short-term testos-% X/ d) G3 T3 y4 U0 b+ Q! l
terone injection or topical androgen may exhibit some
9 ]- z- \- h# s6 macceleration of the skeletal maturation; however, after
1 s4 H# y8 V- g; T$ g4 Ocessation of treatment, the rate of bone maturation  _. _/ l. Q! X+ C+ U1 C
decelerates and gradually returns to normal.8,9
7 Q% m3 n7 n6 ~2 NThere are conflicting reports and controversy
/ o, u+ Q9 _7 X+ Oover the effect of early androgen exposure on adult1 y8 s% g2 g' T% [) S
penile length.10,11 Some reports suggest subnormal
1 r3 S8 l0 H1 A4 i& R0 B" J$ ?adult penile length, apparently because of downreg-" u  f! Z: _; r9 v9 Z* H0 z
ulation of androgen receptor number.10,12 However,5 r5 ]# ]4 ^0 ?# f% \
Sutherland et al13 did not find a correlation between
( H% c; p' n! ^5 p* Cchildhood testosterone exposure and reduced adult6 ?- n" k$ c; F- `- G
penile length in clinical studies.
& i' W$ w" q, o8 [0 ~3 ?& ]Nonetheless, we do not believe our patient is; v. N' H8 E! ]8 T8 c
going to experience any of the untoward effects from
3 w- T) n! a: E4 {5 Ltestosterone exposure as mentioned earlier because
" M' B" C/ W  L5 Z# Pthe exposure was not for a prolonged period of time.
0 z4 Z& b# x2 T6 |, zAlthough the bone age was advanced at the time of  v; O0 S$ p: j- o' ~& z; k
diagnosis, the child had a normal growth velocity at0 @# x* ]$ D& p( v: q  D
the follow-up visit. It is hoped that his final adult5 Y: v/ t" _- Z1 @
height will not be affected.) D9 l* c0 ^6 Z; y9 ?9 ^) F
Although rarely reported, the widespread avail-
: N$ @8 c( e, j8 N: jability of androgen products in our society may% Y4 ]+ W7 S9 W1 k: I
indeed cause more virilization in male or female" k; @8 `$ F; f; s$ {
children than one would realize. Exposure to andro-, R( O7 p4 s# Z! n/ L1 r
gen products must be considered and specific ques-3 u; C, T9 z' Z- f
tioning about the use of a testosterone product or
8 H% G8 |( r9 C" v) [: e# S! U* `gel should be asked of the family members during/ f9 h( L3 o% T
the evaluation of any children who present with vir-
. G3 e" h  F7 h4 cilization or peripheral precocious puberty. The diag-
+ q, T3 l# Z( {8 d+ X# h; P/ fnosis can be established by just a few tests and by5 ^7 r( U* J3 z, L9 R0 O# Y
appropriate history. The inability to obtain such a
* b' d2 J, e9 x: m$ ihistory, or failure to ask the specific questions, may
( x1 K& D. m9 t7 `- Fresult in extensive, unnecessary, and expensive& C! L, f8 p1 H& Y5 a
investigation. The primary care physician should be+ F! o9 `7 }- P# b& j. ^
aware of this fact, because most of these children
, H$ D1 W5 D' P3 b4 f' n; hmay initially present in their practice. The Physicians’! ~  Y$ `. E" q1 d1 w7 @1 k# [
Desk Reference and package insert should also put a
0 j7 V2 K3 V4 n4 @' dwarning about the virilizing effect on a male or
0 O5 W; u! [' L. F6 J6 ~( Gfemale child who might come in contact with some-
* }2 A, ^# k: Lone using any of these products.
4 ~) S3 J4 i& j: y7 i! tReferences* O- F7 L( ]: x( }( n
1. Styne DM. The testes: disorder of sexual differentiation
3 c* e7 c2 }( R; L. S0 tand puberty in the male. In: Sperling MA, ed. Pediatric  q2 a0 _4 R  T5 r, k
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;+ C0 m& R; r! m! v, E2 \; ~: z
2002: 565-628.
# Q$ }2 g2 i7 ?: n2 H2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
9 k1 M3 M% c6 u4 S; C$ E. lpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
- n8 g* e/ e# i, g4 C; M+ IBoy Induced by Indirect Topical
1 L. _4 ?  p8 |Exposure to Testosterone- {5 m+ e, y5 G% c2 t5 ?0 ~/ y
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
# i. t2 v+ o8 Tand Kenneth R. Rettig, MD1
! o8 Y" E5 T5 D2 |3 J0 _' GClinical Pediatrics, F1 b* X, o% D* g
Volume 46 Number 6
# @' [& R" `7 N" |7 l. h! T2 rJuly 2007 540-5433 ]! t2 j4 y/ y7 U1 g9 n* I
© 2007 Sage Publications
/ _$ {& I& B+ H8 x% `$ U) [10.1177/0009922806296651. E$ k5 e& o: E
http://clp.sagepub.com
2 B* `0 I- X9 Y. Xhosted at
; Z" ?: L; `- n1 K6 D  ~http://online.sagepub.com
. \/ n: n& i5 f/ K* m  x! pPrecocious puberty in boys, central or peripheral,; D9 N+ ]- C# ?
is a significant concern for physicians. Central- B1 j3 F8 T! m, m# U" C9 g
precocious puberty (CPP), which is mediated
, \" D3 ?% X& C/ V; g$ Ythrough the hypothalamic pituitary gonadal axis, has
- z; M# w. Q" \" A9 va higher incidence of organic central nervous system2 N* c: Y0 D' ~
lesions in boys.1,2 Virilization in boys, as manifested
. M: u+ W9 f& C7 _; yby enlargement of the penis, development of pubic. Y" m+ g# @$ G; W: c
hair, and facial acne without enlargement of testi-* f" f) f* @7 W- L6 w
cles, suggests peripheral or pseudopuberty.1-3 We" o4 Z- P) M/ m6 e' A
report a 16-month-old boy who presented with the
+ d- u/ t$ @! Menlargement of the phallus and pubic hair develop-
1 S  x# n- Y# jment without testicular enlargement, which was due) H+ ]2 H1 ^9 g1 w. F1 N
to the unintentional exposure to androgen gel used by6 Q$ n3 i7 Z# ?" P# ~* M6 k3 x
the father. The family initially concealed this infor-
( u5 S. T& W% _7 e3 bmation, resulting in an extensive work-up for this
" g; t: \, o, a( }child. Given the widespread and easy availability of
/ v- @. S7 R9 i$ u% u* w$ L0 ]' Utestosterone gel and cream, we believe this is proba-
0 Z6 b1 `. ]7 B* lbly more common than the rare case report in the
) r, x9 u! u' o6 h; J) G: f7 pliterature.4
% j2 x1 M3 P# {; a6 K, r8 x2 pPatient Report; O' S( H8 ^! b
A 16-month-old white child was referred to the
. \+ B* ]( u, P0 {3 t! qendocrine clinic by his pediatrician with the concern
* W3 i0 _9 a; p2 B8 |of early sexual development. His mother noticed$ q' R) ^9 K8 t6 z& y6 L
light colored pubic hair development when he was
+ A# Q! Z$ o& c5 eFrom the 1Division of Pediatric Endocrinology, 2University of% Q4 F' E( N& T6 ~& z2 ?" c
South Alabama Medical Center, Mobile, Alabama.3 g: p% F% N" B' W( d
Address correspondence to: Samar K. Bhowmick, MD, FACE,! U, `8 E! |  {! H  x
Professor of Pediatrics, University of South Alabama, College of
8 ~( U; U+ H; a+ O& B) qMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
& m0 f. M' j0 O& |e-mail: [email protected]., p$ _) e8 O$ E
about 6 to 7 months old, which progressively became2 v. C8 \( _" ~# h
darker. She was also concerned about the enlarge-. ^, r3 o; V# H2 d. q
ment of his penis and frequent erections. The child2 [$ x! T. ~+ }% F+ I) G( d7 p& M- I
was the product of a full-term normal delivery, with
0 {5 J- ?: D/ a. B+ w& Z) R" W; k; ga birth weight of 7 lb 14 oz, and birth length of; E5 Q3 O( B; b' _1 r
20 inches. He was breast-fed throughout the first year
1 ]/ c  Z7 z% [- h$ _  P" h6 jof life and was still receiving breast milk along with& v1 w4 X6 q; E# o4 q; `
solid food. He had no hospitalizations or surgery,9 R& z* O& }6 v7 M, t
and his psychosocial and psychomotor development0 k! C$ h) h2 M, _
was age appropriate.) z2 O. s4 p5 c8 [. M9 b" f  M
The family history was remarkable for the father,- R; f4 i! O4 ^& @1 p9 a: k( P% ~* Q7 V
who was diagnosed with hypothyroidism at age 16,6 w4 p) m0 {& `/ B
which was treated with thyroxine. The father’s( f9 ~8 x4 l9 l9 I/ u5 S: k
height was 6 feet, and he went through a somewhat
* W$ `! H# Q- E2 |8 h1 c/ L' K9 c2 Tearly puberty and had stopped growing by age 14.+ ^7 L# p/ K6 i0 G0 y
The father denied taking any other medication. The' t0 P  r" X1 L0 F  `; h
child’s mother was in good health. Her menarche5 [3 N) _: p' Q4 K/ q3 l  K
was at 11 years of age, and her height was at 5 feet; x+ O. t) G9 A7 C
5 inches. There was no other family history of pre-
6 q( X; ~. N  m$ l* q3 t3 b/ L; G- W) o- O, Icocious sexual development in the first-degree rela-
% t! }2 p% T7 b) h. B/ utives. There were no siblings.$ T8 f9 B7 Y4 L7 E- K
Physical Examination" z6 \8 J; _$ ^! N$ c
The physical examination revealed a very active,
+ }$ g& W6 S2 S3 @playful, and healthy boy. The vital signs documented
" B: M/ x0 j5 j+ ]a blood pressure of 85/50 mm Hg, his length was! a3 v$ D2 L! U: {% Z* Y. ^$ m
90 cm (>97th percentile), and his weight was 14.4 kg8 s9 P; b/ \2 m, I
(also >97th percentile). The observed yearly growth) E% J! H, [: L/ J/ Q( W, y
velocity was 30 cm (12 inches). The examination of
( @5 K8 }! Y, @0 Jthe neck revealed no thyroid enlargement.
2 Y5 E: g% B* Y% H2 LThe genitourinary examination was remarkable for! T9 q1 n! j: _! c' J+ ~& }
enlargement of the penis, with a stretched length of  m7 {" g9 c$ Q$ I, g: i
8 cm and a width of 2 cm. The glans penis was very well
; b3 ?: C' W2 r- A0 L' s. G3 Ydeveloped. The pubic hair was Tanner II, mostly around
4 K' E, Z8 Q* E5 r* x5400 \( z  K! C0 {; Q* e$ d+ ?1 @
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from" |4 v: @! r& A1 }1 g/ {0 N
the base of the phallus and was dark and curled. The; M9 h; U1 P+ J& ?1 v9 x+ R9 K
testicular volume was prepubertal at 2 mL each.
0 F: P# S1 s2 g- g2 v7 x% `The skin was moist and smooth and somewhat
( Y: Q# [' \* o& Doily. No axillary hair was noted. There were no
: E& ~3 m0 y& Y! X' }% _6 Vabnormal skin pigmentations or café-au-lait spots.
" r' m) f+ O( l. e2 f: `' qNeurologic evaluation showed deep tendon reflex 2+# }6 E( j4 z8 ?1 N
bilateral and symmetrical. There was no suggestion
. U% p# F& a/ |; a7 Pof papilledema.
% l. }9 H; _% I8 R/ f- Z$ n' D* ZLaboratory Evaluation
% @  p6 s  @: c* c! c5 NThe bone age was consistent with 28 months by+ c7 c) I/ z, H1 U" C7 X
using the standard of Greulich and Pyle at a chrono-
5 x" l# O' ^) w2 e6 Tlogic age of 16 months (advanced).5 Chromosomal, p3 K) O5 y( _& `) F
karyotype was 46XY. The thyroid function test
& h/ `% @7 p' [8 e9 ~showed a free T4 of 1.69 ng/dL, and thyroid stimu-1 ?% {8 h# i4 ]1 q9 H4 S; Z
lating hormone level was 1.3 µIU/mL (both normal).  [: h- U$ j6 Q5 w; e5 R4 X$ I" l
The concentrations of serum electrolytes, blood  B8 \; ^8 |7 _# g3 P- y
urea nitrogen, creatinine, and calcium all were
) }" [& e% ^; I( D1 H' L9 wwithin normal range for his age. The concentration! Z+ I- g& y, w0 h' h# t
of serum 17-hydroxyprogesterone was 16 ng/dL
1 C$ V! m5 ]' I5 N+ ~(normal, 3 to 90 ng/dL), androstenedione was 203 G6 O& g- u* J7 k
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-% A: A7 x0 S  e9 N' w. m
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
0 K( V" L7 S$ [! |7 xdesoxycorticosterone was 4.3 ng/dL (normal, 7 to6 ?5 f( e4 C% {4 }( x. o% U% ?; P
49ng/dL), 11-desoxycortisol (specific compound S)( y# w6 Z0 S% c: d
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-4 w" ?% ^( x2 _% S. R) _% N
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total) `: O5 B4 k; z4 J, B1 b  G
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
* j0 u. k5 j+ ^and β-human chorionic gonadotropin was less than
3 X0 N& o$ H* j. V7 S; O, d3 u5 mIU/mL (normal <5 mIU/mL). Serum follicular/ G9 y3 z7 ]0 z
stimulating hormone and leuteinizing hormone
& N( c" k2 y4 S1 B( h3 q- o+ t7 tconcentrations were less than 0.05 mIU/mL" c4 p# I4 U  X. }7 m' H1 j2 f1 f
(prepubertal).
( o' P6 S5 S7 ], S6 a0 S3 {The parents were notified about the laboratory
4 e3 `/ C5 D$ U0 g' iresults and were informed that all of the tests were
% ~0 f& r% o) b9 b% d; ~normal except the testosterone level was high. The
7 F4 U0 Q, k6 |$ [follow-up visit was arranged within a few weeks to
# B" ^9 ?- A3 C! }  _& ?% c& W  vobtain testicular and abdominal sonograms; how-& ^* w) o# B* D1 D5 ]
ever, the family did not return for 4 months.) Y5 r5 R$ z3 s6 \! x
Physical examination at this time revealed that the2 ^- D" @8 `( o9 z8 v1 q
child had grown 2.5 cm in 4 months and had gained
: Y3 Y: M4 M3 o+ r* y2 I" N1 p2 kg of weight. Physical examination remained$ ?3 i, K+ Q3 g! B: ]3 v
unchanged. Surprisingly, the pubic hair almost com-
3 F8 X0 N2 [5 q! ]8 Ipletely disappeared except for a few vellous hairs at
% I6 f6 V# O: h2 M1 Cthe base of the phallus. Testicular volume was still 2$ v, [& F0 J/ N/ {
mL, and the size of the penis remained unchanged.
  j& I7 R% S% T/ s8 dThe mother also said that the boy was no longer hav-
3 e* ?8 |  e; V, J- T) ?! Bing frequent erections.8 ?- d8 l& q3 }- ~# h5 T2 o
Both parents were again questioned about use of* d/ `( f) T1 ~9 r9 s6 P
any ointment/creams that they may have applied to. N# g& J1 }2 q- e  @
the child’s skin. This time the father admitted the
: q  [" P5 c' u' BTopical Testosterone Exposure / Bhowmick et al 5412 d0 B0 T. ^' C* M4 B/ D/ s
use of testosterone gel twice daily that he was apply-( w2 }" I  V: @: S3 ^
ing over his own shoulders, chest, and back area for2 ?& [# C( L' v. c: ]
a year. The father also revealed he was embarrassed" N: ]: p( k! Q1 z$ f
to disclose that he was using a testosterone gel pre-
. h0 ~/ H/ Q' q; d  Rscribed by his family physician for decreased libido
8 q$ B/ \+ |+ s4 ^8 B4 ^) nsecondary to depression.% S4 V$ v$ n% @! O, A' v$ g4 o6 c3 a
The child slept in the same bed with parents.$ D" e% b- Y5 l" {, @* t
The father would hug the baby and hold him on his9 y* m3 e. Z9 m% l
chest for a considerable period of time, causing sig-
8 c  Q8 E* H* ?( t: }nificant bare skin contact between baby and father.
( b; P9 O1 A4 v3 HThe father also admitted that after the phone call,5 X9 G; i9 X$ g4 R: k
when he learned the testosterone level in the baby. ^% ?) H+ C2 I, F1 w/ A
was high, he then read the product information
; v" s1 E) P! U: w5 K& bpacket and concluded that it was most likely the rea-/ s' O) x. h$ x
son for the child’s virilization. At that time, they0 f) G6 p3 u7 p1 ]$ D! M2 |
decided to put the baby in a separate bed, and the, u* n2 r4 t6 Y& A  d' b$ }% j
father was not hugging him with bare skin and had
( p$ m4 F' H: f# cbeen using protective clothing. A repeat testosterone
8 [. I9 ?6 B1 z" vtest was ordered, but the family did not go to the0 X/ ^! l2 w* x' f
laboratory to obtain the test.
. G" }( l. @; W* MDiscussion
( T# U; K7 r- P- fPrecocious puberty in boys is defined as secondary
. T" U' ~. U! |+ ~7 gsexual development before 9 years of age.1,4
: Z1 S0 m" l. z4 dPrecocious puberty is termed as central (true) when
. e1 i  p% @! \& H, kit is caused by the premature activation of hypo-
7 L# U- _. Y% q4 x' C  U, O% P: [thalamic pituitary gonadal axis. CPP is more com-7 D. E) R9 p5 J7 g
mon in girls than in boys.1,3 Most boys with CPP
) T+ \3 T! g1 s1 W7 j% |may have a central nervous system lesion that is0 B8 p& F' u- r: g$ H3 G4 O! w
responsible for the early activation of the hypothal-
5 L5 A4 D" Y/ O% Q9 Q$ c: B* C) a2 mamic pituitary gonadal axis.1-3 Thus, greater empha-$ q: n% `) m. j* P1 s. R
sis has been given to neuroradiologic imaging in- I! X9 f9 O3 E3 d' j2 F2 T+ d4 ?
boys with precocious puberty. In addition to viril-
8 {1 U) y' I7 K: M/ w" w( A) Pization, the clinical hallmark of CPP is the symmet-
- L3 V; ]3 P. }* z9 {. Arical testicular growth secondary to stimulation by
, h9 `: L; i9 J6 v% t  wgonadotropins.1,39 h1 Q5 ?+ [. s% a: F# z
Gonadotropin-independent peripheral preco-9 g3 u. G' F( P, D- _
cious puberty in boys also results from inappropriate
3 ?- I7 V& d, O# D+ }) Vandrogenic stimulation from either endogenous or
1 w3 a% ]" w6 f! xexogenous sources, nonpituitary gonadotropin stim-
$ b" S, Y8 A* Zulation, and rare activating mutations.3 Virilizing* D) z/ ^/ c7 X& ?3 H
congenital adrenal hyperplasia producing excessive. W) _' r: m$ H- p, F$ V- d
adrenal androgens is a common cause of precocious1 S* O& ], m' z! D
puberty in boys.3,41 {. h: S4 M* F3 c8 N
The most common form of congenital adrenal
; v2 a& l4 u  Z- p% uhyperplasia is the 21-hydroxylase enzyme deficiency.
$ @' O! _$ I, O3 O. X1 uThe 11-β hydroxylase deficiency may also result in
( o7 `7 {' o* b' p5 R7 U7 J" Y+ dexcessive adrenal androgen production, and rarely,- w- `) Z7 J9 A$ k" @$ A+ d
an adrenal tumor may also cause adrenal androgen( M' b" I% O' K0 Z1 L9 D
excess.1,3/ p  G5 D5 P& v4 F# m5 d/ t: ?
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 h0 o( c5 [. f2 v: t# O0 d
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007+ S9 O% \) y: U% e4 _; ]9 ^+ l, A# d
A unique entity of male-limited gonadotropin-! p  f$ w7 a8 y" b
independent precocious puberty, which is also known
8 U" O, H- _* e, aas testotoxicosis, may cause precocious puberty at a
3 _) T. U! f8 ?, p* c/ P6 lvery young age. The physical findings in these boys
- B" z) j, @( V, Z" v& p" swith this disorder are full pubertal development,3 D6 F- p/ ?# p1 ~+ p
including bilateral testicular growth, similar to boys8 s; r) t2 M) F$ d# `7 ^/ G
with CPP. The gonadotropin levels in this disorder
; ~7 K5 J; G, Dare suppressed to prepubertal levels and do not show8 I. ?6 I$ M7 j# G8 A# }+ s9 l9 i
pubertal response of gonadotropin after gonadotropin-
+ j* F  h. {8 f& L0 q) freleasing hormone stimulation. This is a sex-linked
! \1 j' J1 m' T7 R4 f* Iautosomal dominant disorder that affects only6 J6 ]' j) }, F
males; therefore, other male members of the family- C" t* c2 H# i3 o
may have similar precocious puberty.3
3 D; q7 z* W, P& qIn our patient, physical examination was incon-
- L: ?  B2 [% c/ D, F4 ksistent with true precocious puberty since his testi-9 X8 Y9 U4 a) c1 Z
cles were prepubertal in size. However, testotoxicosis
( B3 v  e. q9 R, owas in the differential diagnosis because his father  O: Z7 \8 y5 [: o% R
started puberty somewhat early, and occasionally,
& \- z- I2 y6 s( }% i9 Mtesticular enlargement is not that evident in the
9 N3 j' a- P6 I3 i& i3 X0 kbeginning of this process.1 In the absence of a neg-
/ K0 i7 D+ p* `. m8 J* native initial history of androgen exposure, our: p  s+ l" [- y( Y2 j- S# Z. p+ G" D
biggest concern was virilizing adrenal hyperplasia,
* d) J% j% K5 A9 qeither 21-hydroxylase deficiency or 11-β hydroxylase9 t+ h. B1 n4 I
deficiency. Those diagnoses were excluded by find-+ d  F$ T6 e! P# k- n
ing the normal level of adrenal steroids.
; C/ [. C7 G+ |3 oThe diagnosis of exogenous androgens was strongly
( ^5 ^# _. N# [! }3 jsuspected in a follow-up visit after 4 months because" H2 S7 w6 j6 J  `' @
the physical examination revealed the complete disap-% n- t# x) M4 ^+ A3 y4 s7 O/ u
pearance of pubic hair, normal growth velocity, and
5 }+ s& o- v( r. m" edecreased erections. The father admitted using a testos-
. n8 m  |- N8 v! ?9 `- ?terone gel, which he concealed at first visit. He was
; {  B  s% C: E1 F- b& gusing it rather frequently, twice a day. The Physicians’
2 d- O# b& s/ S; r, _( s! C* R% F) LDesk Reference, or package insert of this product, gel or# D: y6 V* Y0 a) \; b" i4 j
cream, cautions about dermal testosterone transfer to  l  E! k& R: ?
unprotected females through direct skin exposure.
9 v% H9 B5 M0 ~- m4 ZSerum testosterone level was found to be 2 times the
7 d) o" [1 H9 Z& p0 `baseline value in those females who were exposed to
! O' D4 X' G: aeven 15 minutes of direct skin contact with their male
- x( i/ z0 U% P4 C  i" y) zpartners.6 However, when a shirt covered the applica-! R" v3 u/ l; k
tion site, this testosterone transfer was prevented.% u, @+ R3 O& q
Our patient’s testosterone level was 60 ng/mL,& V- ]" Y7 w0 i. L) {" M
which was clearly high. Some studies suggest that
5 V+ m0 L' w# W+ Ddermal conversion of testosterone to dihydrotestos-
/ b' T  {0 J8 I! ^& Bterone, which is a more potent metabolite, is more3 ?3 P" `9 X" z) D( [
active in young children exposed to testosterone
7 t: N8 S9 u* X# G' w- C( R1 x  aexogenously7; however, we did not measure a dihy-6 |2 a  E# T+ B/ Q
drotestosterone level in our patient. In addition to
# h5 @3 f5 l: T1 Rvirilization, exposure to exogenous testosterone in
$ V' J/ U! }7 K  |9 s, g0 s6 pchildren results in an increase in growth velocity and
8 V. G; X7 ]7 c# j2 v' Y5 Q) nadvanced bone age, as seen in our patient./ l( d7 A3 W+ A+ c6 K# h% \7 r
The long-term effect of androgen exposure during# i: M% p8 j9 _0 d% \7 m
early childhood on pubertal development and final
5 p% |/ i& m) A- sadult height are not fully known and always remain+ c$ a. S% J) n! o: |9 D
a concern. Children treated with short-term testos-, G0 p. f+ X1 [. ~
terone injection or topical androgen may exhibit some/ R- K! a) A  `( z* q
acceleration of the skeletal maturation; however, after( ^% O9 Z  W. E# f- y; f, X
cessation of treatment, the rate of bone maturation5 a, W2 B' }" R, J  \1 `
decelerates and gradually returns to normal.8,9/ D. C* f  ^# ]. ^
There are conflicting reports and controversy$ H/ F( b6 P+ y. s* F& x
over the effect of early androgen exposure on adult
% \8 X+ ~) E1 l6 I, @* R$ O  v# ~, mpenile length.10,11 Some reports suggest subnormal
! D- m$ R" H$ [adult penile length, apparently because of downreg-, H, f8 ~0 m% Z' i  S2 [
ulation of androgen receptor number.10,12 However,+ i. S3 R6 g8 _2 p. R
Sutherland et al13 did not find a correlation between) E# q- |0 q0 k6 `* U( ?, v
childhood testosterone exposure and reduced adult. A8 h5 R9 u6 c1 h
penile length in clinical studies.
6 \8 ~. x0 q/ O* A. F4 g2 bNonetheless, we do not believe our patient is5 |4 O! y' Z% G1 s$ ^+ T/ y
going to experience any of the untoward effects from
( j5 o* S5 C2 b6 @' Mtestosterone exposure as mentioned earlier because
/ T  M; r7 Z1 tthe exposure was not for a prolonged period of time.& v6 L0 K$ {% N% i9 m  N! Z7 p
Although the bone age was advanced at the time of$ K; V* p* A7 g7 T+ n5 i- N' V' _9 c
diagnosis, the child had a normal growth velocity at, g0 V; ^& b# _
the follow-up visit. It is hoped that his final adult  E9 V9 \7 [; Z. |- V
height will not be affected.
$ U$ h5 N; o3 v/ l2 j8 g* {Although rarely reported, the widespread avail-0 u. x# Y3 `, U; D+ b' a8 a
ability of androgen products in our society may* Y3 d, I  ~) W6 X/ J- C$ |
indeed cause more virilization in male or female4 V, K$ h* k" B  k
children than one would realize. Exposure to andro-' l" \$ n9 ^" T. Z+ P0 z
gen products must be considered and specific ques-. c; [' L- T- }! w
tioning about the use of a testosterone product or$ y" `( z# O; o9 d3 o' G
gel should be asked of the family members during
& x0 [( }% z  ?& a! xthe evaluation of any children who present with vir-
! K2 i0 U$ A' O& c! Oilization or peripheral precocious puberty. The diag-2 A- g( N8 w1 K$ E$ I9 N. `
nosis can be established by just a few tests and by
9 c, X1 Y' l/ i: }% [2 {4 V: R8 T3 Xappropriate history. The inability to obtain such a$ J/ u0 E. z* m% Q% c2 M
history, or failure to ask the specific questions, may
1 a7 k* f6 t2 O9 M5 c# X+ }( r& Nresult in extensive, unnecessary, and expensive8 K% i$ P& t# t9 v* H" A
investigation. The primary care physician should be
4 h; |/ T7 g$ q) h8 s' Uaware of this fact, because most of these children
' h: W! m0 x* Q; \  r5 M% H. Wmay initially present in their practice. The Physicians’# }6 X: G  F1 E; o
Desk Reference and package insert should also put a
4 ^* }$ J3 i6 V( P) J( gwarning about the virilizing effect on a male or
  {. ?; ^9 s. `female child who might come in contact with some-
. N( {+ q. a. S0 ^2 cone using any of these products.
1 q! e2 s5 u% Q% _References# t' A- m: V* }- `9 H) E
1. Styne DM. The testes: disorder of sexual differentiation
$ H7 a8 k$ W; c- ?$ ]" ~- k2 d7 cand puberty in the male. In: Sperling MA, ed. Pediatric) z5 I" y, r$ f- x! h
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;  K0 ^) ~% E! N& o
2002: 565-628.4 I) ^! H! a2 d) |2 q4 ~9 w
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
6 m: G  b+ c' S+ Ppuberty 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
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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
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

+ U( `" X( E' i; f5 Z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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