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Sexual Precocity in a 16-Month-Old, I/ Q0 y7 ?- O2 r# l& u
Boy Induced by Indirect Topical# z2 J4 C+ t& [! r& ^
Exposure to Testosterone
" O8 E" p$ |/ KSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2/ Y/ h+ w6 w3 ?; E1 p6 r0 Q( Q/ O
and Kenneth R. Rettig, MD17 F/ k/ }$ h- p: l7 W) U+ r) ]
Clinical Pediatrics
3 w/ T8 ^. K' J! {, Z! vVolume 46 Number 6
+ m" g3 a3 f( E* m) SJuly 2007 540-5430 V# K0 B* O4 x
© 2007 Sage Publications
' v1 T: [  S: F% s( t; B2 g8 N10.1177/0009922806296651# N) l! v5 W# H% _% f8 @
http://clp.sagepub.com: Z+ T1 F7 i+ y: d; H
hosted at
$ A2 z" v9 {/ F6 q4 [9 e  Khttp://online.sagepub.com
! L; @+ V& z& ~2 j3 KPrecocious puberty in boys, central or peripheral,
% H5 N* X& P7 j5 K* uis a significant concern for physicians. Central
8 S9 R( D  S% |) \: W8 dprecocious puberty (CPP), which is mediated
) H2 s4 l# x8 k- d. p; c1 h. uthrough the hypothalamic pituitary gonadal axis, has5 h& m  n- |4 e. ^$ Q
a higher incidence of organic central nervous system1 Y% C) e+ L$ x3 W+ y
lesions in boys.1,2 Virilization in boys, as manifested
# w+ v* [3 p9 k4 o+ Xby enlargement of the penis, development of pubic
" @  K8 F* K0 A  A+ l& U9 chair, and facial acne without enlargement of testi-
* u) X- Q( u/ a- tcles, suggests peripheral or pseudopuberty.1-3 We7 \- }0 I4 o( h4 U1 ]( l" H
report a 16-month-old boy who presented with the- X+ y+ J% y4 |4 n; [0 o/ o9 ?' @
enlargement of the phallus and pubic hair develop-' |) S6 }* j& s5 F3 U
ment without testicular enlargement, which was due& I* b) a/ d5 x8 J' a! r9 Z
to the unintentional exposure to androgen gel used by
% C" ]5 s) H: Q  Athe father. The family initially concealed this infor-
+ p; _* i$ @# J. Wmation, resulting in an extensive work-up for this
4 G4 Y8 i. h& r8 Wchild. Given the widespread and easy availability of
9 F) d9 ?- G* v2 c8 b. q2 P) dtestosterone gel and cream, we believe this is proba-
, ^2 `3 F9 W+ Jbly more common than the rare case report in the, Z6 X8 _- K( g! \! G1 f0 [
literature.48 Z' ^9 `4 L: n( ]# U4 |* c/ z
Patient Report
9 Z9 p2 d" f5 U1 L0 ZA 16-month-old white child was referred to the" H( O+ V+ O7 b3 {
endocrine clinic by his pediatrician with the concern6 s; G7 |: X# n3 L
of early sexual development. His mother noticed
# }* J0 E: p" Hlight colored pubic hair development when he was
! |5 B. h! q6 W" t: HFrom the 1Division of Pediatric Endocrinology, 2University of8 N- U# J0 r/ a7 {2 Z7 ?) W2 T0 @
South Alabama Medical Center, Mobile, Alabama.8 `% Q3 H  g0 \* R) x" n$ ~* o
Address correspondence to: Samar K. Bhowmick, MD, FACE,% s7 _! N+ v' V9 @7 a4 v
Professor of Pediatrics, University of South Alabama, College of
& h% `9 I5 s, oMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;. m2 [* q$ s) P, x6 |8 B8 T
e-mail: [email protected].8 Q" O( ~% ?1 ^0 N# _
about 6 to 7 months old, which progressively became
" G& ]+ @0 E8 b1 Y$ Adarker. She was also concerned about the enlarge-
. o  T  z$ t6 ~4 u( |ment of his penis and frequent erections. The child
" k) c  b* r" n5 m: z" b9 Gwas the product of a full-term normal delivery, with
$ H. R0 I& m9 |9 a( [; ea birth weight of 7 lb 14 oz, and birth length of
9 ?, E# p( l+ Y/ [3 J3 A20 inches. He was breast-fed throughout the first year3 a$ W. s# q* `$ U, ?3 q' n
of life and was still receiving breast milk along with
! r9 z- |  e1 Wsolid food. He had no hospitalizations or surgery,
2 J+ \1 G( l* y! @7 u7 l5 d7 _5 Fand his psychosocial and psychomotor development
0 y) b4 b. B+ j4 lwas age appropriate.
  t& |. t$ [- d0 N. uThe family history was remarkable for the father,0 @, o) X: u8 c! k/ b6 n1 v
who was diagnosed with hypothyroidism at age 16,
, e8 T  Q5 i! q$ \9 |3 Wwhich was treated with thyroxine. The father’s
# {8 Z! }  z/ u9 O5 S% {/ Z3 cheight was 6 feet, and he went through a somewhat
, @. O% f  y- ]- |+ Kearly puberty and had stopped growing by age 14.
+ A) p; J$ g. t- V  r; OThe father denied taking any other medication. The
& i7 s- S" t) }& M. Q! ochild’s mother was in good health. Her menarche
6 e8 O0 T1 \# B! S' Gwas at 11 years of age, and her height was at 5 feet2 z% h9 q* I  O
5 inches. There was no other family history of pre-8 A6 F* b0 v, k) {
cocious sexual development in the first-degree rela-
, H( c" X3 _9 a- mtives. There were no siblings.
2 l- a% I5 u; Y+ j, Z9 q; iPhysical Examination
+ r6 ~0 Y# @' BThe physical examination revealed a very active,
, T: C  W) {% H* Pplayful, and healthy boy. The vital signs documented* y% [9 F: ~, u7 J& o
a blood pressure of 85/50 mm Hg, his length was6 x* H) r9 G( c% n
90 cm (>97th percentile), and his weight was 14.4 kg
$ j, l0 c6 y) g5 P(also >97th percentile). The observed yearly growth
$ i4 [! k9 {, Xvelocity was 30 cm (12 inches). The examination of
3 H7 A* S3 h& h8 i. ?9 ^" D7 ithe neck revealed no thyroid enlargement.& C4 M7 ?9 I  S4 D. x& z
The genitourinary examination was remarkable for
' w, p% U: ]3 G$ w* qenlargement of the penis, with a stretched length of. t  k2 a( g; G  ?. N1 z
8 cm and a width of 2 cm. The glans penis was very well# m; O: |( J& j& i, j2 I! G
developed. The pubic hair was Tanner II, mostly around. C% X6 `( V0 c% _9 C0 |" s' D; x9 `4 U
540" S; C5 D+ [2 V2 ~% {8 _0 D+ R* T
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# m0 L& p. T* g0 Fthe base of the phallus and was dark and curled. The- ]8 j+ O6 _: O* u+ ~4 x0 o  u
testicular volume was prepubertal at 2 mL each., u7 Y9 Z! Y! n- ]
The skin was moist and smooth and somewhat" ^( Y7 g7 X$ k$ I9 K! n! Q
oily. No axillary hair was noted. There were no5 Y0 _7 _) ~' ~- C$ I+ A
abnormal skin pigmentations or café-au-lait spots.
+ r. `( y6 o2 j* |( oNeurologic evaluation showed deep tendon reflex 2+2 l0 |( M' X/ z2 j, a; ]
bilateral and symmetrical. There was no suggestion
& P/ w" a* l7 r3 \$ lof papilledema.
9 L6 `+ ~$ s9 c* y# m4 B% yLaboratory Evaluation$ N* l, R% o* ]# @% }' w
The bone age was consistent with 28 months by1 z% k8 C* V5 Y
using the standard of Greulich and Pyle at a chrono-
5 w- G3 G+ {9 A! [" Wlogic age of 16 months (advanced).5 Chromosomal6 g( w# L1 f9 E2 l& ?. Z6 N
karyotype was 46XY. The thyroid function test
5 i- [( x5 [, R, @showed a free T4 of 1.69 ng/dL, and thyroid stimu-  J9 }6 G+ `9 l- T0 O' ^) J
lating hormone level was 1.3 µIU/mL (both normal).8 E5 e+ \- C( r5 ]9 J7 a
The concentrations of serum electrolytes, blood
6 O: E; e2 N$ L0 g/ l& x+ t  L/ purea nitrogen, creatinine, and calcium all were* Q1 f, m4 V; A
within normal range for his age. The concentration, V( V% K# n/ q: t* C
of serum 17-hydroxyprogesterone was 16 ng/dL- c1 X- C1 E' {5 u4 Y1 d
(normal, 3 to 90 ng/dL), androstenedione was 20) q% Y7 q! Z) E0 g. N  @6 ~! U3 R
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-( f5 t: s5 w: ~; |5 @
terone was 38 ng/dL (normal, 50 to 760 ng/dL),9 y& w$ b/ o2 |( U9 s+ b+ z, w
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
1 z) }& z1 s% p49ng/dL), 11-desoxycortisol (specific compound S)" e: I* X8 F+ \
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-( W; y( A2 C4 h, U2 A# a$ m3 {- X
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# e; r* B- C, M
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
& l+ M5 n$ J' Q% R9 l4 W9 Uand β-human chorionic gonadotropin was less than
1 E! d; _% m8 S4 A4 A# G5 mIU/mL (normal <5 mIU/mL). Serum follicular8 H% c7 c% V) _
stimulating hormone and leuteinizing hormone
, B, n, a% r  o' t0 ]( f) p  ^concentrations were less than 0.05 mIU/mL/ m% b( G; }5 ~4 ], I
(prepubertal).) |2 Q: q3 O/ O: i/ B1 X" U
The parents were notified about the laboratory
2 |/ e- W+ b' x6 U6 R" W9 P$ ?results and were informed that all of the tests were
* |' ~. y$ F9 T7 ?' K* Ynormal except the testosterone level was high. The5 E2 w9 g  r- G! T
follow-up visit was arranged within a few weeks to
' l! v5 W1 E1 c7 T" C* l  j( K0 ]4 }5 qobtain testicular and abdominal sonograms; how-( ~* e, y" P: r
ever, the family did not return for 4 months.5 Q0 P  [5 t6 j) x9 N2 v8 o" W
Physical examination at this time revealed that the' O! T3 D6 d9 d+ o
child had grown 2.5 cm in 4 months and had gained+ Z4 y3 B5 b/ Q* ?+ p
2 kg of weight. Physical examination remained# A! z% ^# @0 O% Y$ I5 L
unchanged. Surprisingly, the pubic hair almost com-2 ^' q7 C' z4 E( u6 U# t
pletely disappeared except for a few vellous hairs at5 p$ d4 `/ J, Y* W) p
the base of the phallus. Testicular volume was still 2* q' I( A9 n& R- N7 t
mL, and the size of the penis remained unchanged.; }& M* e8 E# M) p
The mother also said that the boy was no longer hav-
' P; z/ s" P0 H0 h  Ding frequent erections.
. Q; c- v: Q/ M5 `Both parents were again questioned about use of9 ]0 s4 T' m/ D, c( y' V% T1 A) @  n8 K! I
any ointment/creams that they may have applied to0 `2 F: H# k) m
the child’s skin. This time the father admitted the
1 y7 {; G% |2 m$ S9 ~; G- RTopical Testosterone Exposure / Bhowmick et al 541) \. d: O7 M1 q6 I
use of testosterone gel twice daily that he was apply-) x9 A6 L; d! {! O& S  H* b% l9 @' w; o
ing over his own shoulders, chest, and back area for
- H( Q0 v' O6 N  `, i* @: s. La year. The father also revealed he was embarrassed4 B7 W; w0 ~6 ~+ {( h- E2 k/ n. X
to disclose that he was using a testosterone gel pre-* A* i  ]2 z6 J8 c/ ?1 j
scribed by his family physician for decreased libido
( e7 c% P: R$ Y; D: i" `/ ksecondary to depression.
: R( v9 H/ c( Y* GThe child slept in the same bed with parents.
$ j) T' k- i# XThe father would hug the baby and hold him on his
. s+ z  Z; Y/ B8 S. f. B2 ^4 Uchest for a considerable period of time, causing sig-
: u+ M$ Q1 f6 S9 j! V4 ynificant bare skin contact between baby and father.( F4 _# N  ~4 _8 ~
The father also admitted that after the phone call,! A( J$ P- ~$ X3 f  z
when he learned the testosterone level in the baby
' k/ b9 r& {/ D9 J1 ywas high, he then read the product information1 O( P2 J! A8 V' w# H) c+ ]  Z. [, Y
packet and concluded that it was most likely the rea-; I# H: h4 a: O7 K0 q0 o
son for the child’s virilization. At that time, they
. r' v0 l0 E$ U& j8 mdecided to put the baby in a separate bed, and the; Y$ P- W& N: c. s0 w* J
father was not hugging him with bare skin and had
/ V8 m/ v4 D+ A- |3 h* `been using protective clothing. A repeat testosterone
" z+ h: h4 i5 t; ~% F( ytest was ordered, but the family did not go to the7 t5 `% T# \$ g& ^3 }3 D
laboratory to obtain the test.
5 h  e; O$ }' C: Q5 o( m! {( mDiscussion, P1 {7 a8 z4 v5 h
Precocious puberty in boys is defined as secondary
) |8 x8 z7 l4 b! gsexual development before 9 years of age.1,4
- k5 r) U2 o4 G. SPrecocious puberty is termed as central (true) when7 v: S. r9 L' f; s2 d  A
it is caused by the premature activation of hypo-6 e! g  N3 M) G- f
thalamic pituitary gonadal axis. CPP is more com-
" M  \8 I2 ^* N& M/ jmon in girls than in boys.1,3 Most boys with CPP
# ]+ l% }* \5 S, C; smay have a central nervous system lesion that is& i, F' r7 `# m' q
responsible for the early activation of the hypothal-
5 _  a9 k; ^: b6 |) D7 Mamic pituitary gonadal axis.1-3 Thus, greater empha-: \4 k% [) v. M: m; P4 `
sis has been given to neuroradiologic imaging in
# q7 J, y+ \, q8 Mboys with precocious puberty. In addition to viril-
. K& V& w2 J: r! p* \5 ^" rization, the clinical hallmark of CPP is the symmet-, `/ G6 |% `. f$ t4 _- T) @# `
rical testicular growth secondary to stimulation by
4 y6 K& s- h* _  L0 agonadotropins.1,3+ z6 z* y: `' q* R* B
Gonadotropin-independent peripheral preco-$ \  t, @' m! G0 v( }6 j
cious puberty in boys also results from inappropriate
2 \. n" W1 w+ _0 `androgenic stimulation from either endogenous or
& d, `/ }% o4 a' q9 ~% Z+ B8 j1 oexogenous sources, nonpituitary gonadotropin stim-
! R) p* J4 n( f; p+ f/ {ulation, and rare activating mutations.3 Virilizing/ N3 b6 n$ f" k& V
congenital adrenal hyperplasia producing excessive0 T" V% J+ D/ M7 r
adrenal androgens is a common cause of precocious# i( J4 T) j5 b" h/ o5 S  P; O
puberty in boys.3,4
! Y7 r% E7 W5 v/ ^4 M" mThe most common form of congenital adrenal3 x' F, s+ |! y, G9 a1 O# i6 ]! a
hyperplasia is the 21-hydroxylase enzyme deficiency.
: Z* h% R# D; d1 eThe 11-β hydroxylase deficiency may also result in0 n' y% j0 w& E$ p) V1 v
excessive adrenal androgen production, and rarely,
( C0 A- I7 _# [; D% ]an adrenal tumor may also cause adrenal androgen
0 u  `5 }" c" N+ j& g+ @# s2 xexcess.1,3
! ]6 v  g8 _: H: @. mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) |- T  m; |6 ?( G542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
- m- B  i& m" q9 \7 W+ F' fA unique entity of male-limited gonadotropin-) V# C" G9 `5 i  w/ o
independent precocious puberty, which is also known
0 t0 R/ Q  x6 x5 S9 o+ [4 yas testotoxicosis, may cause precocious puberty at a; i2 L' |; I& b) H8 \5 @' A' M
very young age. The physical findings in these boys
$ J: C$ O! n9 y" J" F6 `. t9 z, Ewith this disorder are full pubertal development,
$ s: i" ]: k6 v8 `! g" s; Qincluding bilateral testicular growth, similar to boys
( t+ j9 k2 ?! {; s" Q4 T0 Dwith CPP. The gonadotropin levels in this disorder( i9 X7 K5 i/ V
are suppressed to prepubertal levels and do not show
2 H( g$ u- ^! W! w" x4 Hpubertal response of gonadotropin after gonadotropin-
7 e2 p( E3 ], v7 Wreleasing hormone stimulation. This is a sex-linked: @. O& f# e) K5 f- e: H" I# L& ?
autosomal dominant disorder that affects only6 {6 \& j9 G6 g+ q
males; therefore, other male members of the family
6 p% s, v) X. o- q9 @, }8 I& P$ cmay have similar precocious puberty.3
, e" m4 Y* g/ Q/ @: a( qIn our patient, physical examination was incon-
4 P3 e7 Y4 [, H4 v: ~sistent with true precocious puberty since his testi-
; ]5 D# Y0 [# Y/ icles were prepubertal in size. However, testotoxicosis
0 U; Z; ?- s, k! {was in the differential diagnosis because his father. A- H# d6 k4 x5 ]9 p
started puberty somewhat early, and occasionally,1 v% b2 c) l/ b* C
testicular enlargement is not that evident in the
: {& n% J6 W7 x6 G! `, @( e$ }" qbeginning of this process.1 In the absence of a neg-% A8 t, N( e. P/ r; ]! f
ative initial history of androgen exposure, our
3 ]* e1 G* k* I( f" \: ^biggest concern was virilizing adrenal hyperplasia,# {8 m. H! {: b$ \8 L5 [
either 21-hydroxylase deficiency or 11-β hydroxylase
8 G2 S$ s4 B: \! S8 y9 zdeficiency. Those diagnoses were excluded by find-+ Y6 C& T* I9 H# r$ U! m2 A
ing the normal level of adrenal steroids.& L5 d7 }* Y3 B. e; L- n
The diagnosis of exogenous androgens was strongly& n3 S* S3 X# q4 o; P- `
suspected in a follow-up visit after 4 months because* A7 `& X. A0 H+ v$ p2 s
the physical examination revealed the complete disap-
6 X& g: B1 J. M4 }pearance of pubic hair, normal growth velocity, and
8 {1 L) x/ g3 u& @' D( K, p5 |2 ?' Udecreased erections. The father admitted using a testos-
: E. C* N+ c9 Z" W' Gterone gel, which he concealed at first visit. He was& g3 t- D6 S& p2 E' d
using it rather frequently, twice a day. The Physicians’7 w2 C8 X4 n2 x1 h1 n5 @* j
Desk Reference, or package insert of this product, gel or
+ x8 t# A& u/ J8 W+ V/ g  ucream, cautions about dermal testosterone transfer to
5 m2 ^" l7 Z4 g9 Yunprotected females through direct skin exposure.
. E$ ^7 o8 t) a9 c8 g0 R( P8 |Serum testosterone level was found to be 2 times the
. f0 [3 s8 s, ~( @; W1 i6 y1 e2 i. Kbaseline value in those females who were exposed to
0 A$ b9 E( ^, w+ y+ \0 deven 15 minutes of direct skin contact with their male/ l' r$ ?. a* t: k' Y
partners.6 However, when a shirt covered the applica-. X3 {+ {' |, W8 b
tion site, this testosterone transfer was prevented." i0 @5 r$ N  Q) ^2 a
Our patient’s testosterone level was 60 ng/mL,
8 Z6 n8 `) T7 k% iwhich was clearly high. Some studies suggest that2 L1 W8 ~- C* c5 p/ p
dermal conversion of testosterone to dihydrotestos-9 F3 `% o! E3 ^( g$ b+ n8 s
terone, which is a more potent metabolite, is more
2 ~, V) F) z# X( Z$ uactive in young children exposed to testosterone
' V& k# W4 R+ f8 u# U: T) eexogenously7; however, we did not measure a dihy-( T; I7 j( @. t# ]4 q$ i$ j
drotestosterone level in our patient. In addition to$ o! o. w6 v6 z! I2 i
virilization, exposure to exogenous testosterone in
( H) J1 s) F) E- i7 w- Y2 ^/ \children results in an increase in growth velocity and
  H9 M+ u! |& ]* Yadvanced bone age, as seen in our patient.; x8 |9 ~" G9 h. H) R( a2 t
The long-term effect of androgen exposure during+ [: e4 _1 F# S5 V; B/ J% N
early childhood on pubertal development and final
; c- @- r% t+ Z- f" B1 ]adult height are not fully known and always remain$ V2 S8 Z2 a. ~; X" m
a concern. Children treated with short-term testos-
1 e5 `7 S6 ^6 Z0 \$ aterone injection or topical androgen may exhibit some
# J2 u8 \2 d4 B9 B0 g2 Hacceleration of the skeletal maturation; however, after
' ~2 S6 S2 S8 a3 g* z- @& Dcessation of treatment, the rate of bone maturation/ t! |4 m$ Z" e  @3 w9 p/ M+ j
decelerates and gradually returns to normal.8,9
1 ?" `2 `9 p4 b8 B5 _There are conflicting reports and controversy  H+ _8 H4 K& N5 A# V
over the effect of early androgen exposure on adult* m+ I7 ^2 Y/ u& \; X: y  m
penile length.10,11 Some reports suggest subnormal
6 s" F. D5 k" o7 o4 Uadult penile length, apparently because of downreg-6 f# m. k" l- y- i
ulation of androgen receptor number.10,12 However,
# f! d  j1 d; }Sutherland et al13 did not find a correlation between5 |! r* V, m5 N% @' w, h9 u) m* e0 w
childhood testosterone exposure and reduced adult/ M; V0 T! O, X  n' {
penile length in clinical studies.' i9 j: z% G  y; m
Nonetheless, we do not believe our patient is' d% n, m$ D5 g/ L3 R3 y# X5 M
going to experience any of the untoward effects from' u' x# J6 o- A/ T$ J3 t. B
testosterone exposure as mentioned earlier because
# J7 M! G" A& L* K$ w& g$ ^7 wthe exposure was not for a prolonged period of time.% L: f. X5 x3 k! _
Although the bone age was advanced at the time of
+ x- x& p! F' j+ Idiagnosis, the child had a normal growth velocity at7 t: X. {9 b; j5 i0 y1 B4 J
the follow-up visit. It is hoped that his final adult
0 H% A9 ~7 s' }6 Eheight will not be affected.
- d7 M9 P$ v, W; ?, t* o# YAlthough rarely reported, the widespread avail-
' c# a- d' U5 N* X1 kability of androgen products in our society may
' O. R$ Y# y6 ~2 D  Y# mindeed cause more virilization in male or female5 O6 S7 ]3 R8 O8 J9 H
children than one would realize. Exposure to andro-
% }. V4 `' U6 @* ]gen products must be considered and specific ques-, e# C7 i- V! T/ M7 F- m* N
tioning about the use of a testosterone product or3 v, M; Q( w! c& f
gel should be asked of the family members during
8 O6 X4 R! x$ U. dthe evaluation of any children who present with vir-
  }6 _. S4 w! E/ w: ~+ Dilization or peripheral precocious puberty. The diag-2 x5 y6 ~6 r: \8 X
nosis can be established by just a few tests and by
/ F( p. e& N2 t. rappropriate history. The inability to obtain such a
$ Z. e' p1 y6 G% S# A1 ghistory, or failure to ask the specific questions, may
6 C9 K! o, v6 Kresult in extensive, unnecessary, and expensive
" Q! H- r3 H4 k5 ^5 G0 R. J3 @2 h- g' X, ?investigation. The primary care physician should be2 D( h  q6 S1 T6 S
aware of this fact, because most of these children- e# U, @4 |* _- Q2 v2 y/ q' x9 k
may initially present in their practice. The Physicians’7 ^8 y. l+ q. W) @/ Y! q
Desk Reference and package insert should also put a* G' {7 N5 ^- k8 M9 |6 |
warning about the virilizing effect on a male or
7 [1 W3 G4 A0 o$ e. mfemale child who might come in contact with some-, X$ W# F7 ^; ]& D  f0 I1 u( I4 l
one using any of these products.
2 Q* d4 N5 j! n* n2 y9 R& d) ]( JReferences2 W% R: E) R; y2 T+ m8 ~( o
1. Styne DM. The testes: disorder of sexual differentiation
2 w/ k+ n0 A' Q; F- W! C' Band puberty in the male. In: Sperling MA, ed. Pediatric
* U' ~3 G7 R. d+ ^4 A# bEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
# \- I$ E0 Q; I2002: 565-628.
: B( j4 z, V$ G( r& N( ?; k2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
) o! k# Z3 B% _* Lpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
( K5 R) _3 V9 |. u+ \2 n$ BBoy Induced by Indirect Topical+ X7 j3 E# r- r* |
Exposure to Testosterone9 d: C" n( c" L/ r0 Q2 j8 y5 J
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
/ S& `2 t% J% G3 Z0 Eand Kenneth R. Rettig, MD1# i2 s" k7 e; L& ]
Clinical Pediatrics8 G! }' x8 O3 y5 N  E; f
Volume 46 Number 6
9 X9 \5 u! d8 H9 N1 qJuly 2007 540-543& B0 V4 U, D+ N, v: w
© 2007 Sage Publications& T  C2 {7 n1 x
10.1177/0009922806296651
# Z" F# ]7 {, @9 o3 V; Y8 chttp://clp.sagepub.com, \7 ~  i1 s4 k
hosted at
! m( K6 n' p- o' y0 Vhttp://online.sagepub.com  \- ?2 p& d% V; P8 S- f; J; I
Precocious puberty in boys, central or peripheral,2 j( z9 c* E; U5 A/ I  T
is a significant concern for physicians. Central
! m2 z" Z1 f" T; z4 Q' Yprecocious puberty (CPP), which is mediated
0 f, A. u% P! Q: S5 C7 o7 Z3 tthrough the hypothalamic pituitary gonadal axis, has
3 A$ t4 u# D( v  q+ _& qa higher incidence of organic central nervous system3 k5 L" I& k7 B7 H5 P8 [
lesions in boys.1,2 Virilization in boys, as manifested0 w! Z1 s# q/ N( g9 g7 O
by enlargement of the penis, development of pubic
1 P8 W2 A) h& M+ M1 khair, and facial acne without enlargement of testi-8 `! N( g! t2 ^
cles, suggests peripheral or pseudopuberty.1-3 We
, m- n5 H; ~/ A9 lreport a 16-month-old boy who presented with the
/ u9 l3 }1 H8 ]2 P8 z/ A; E8 Renlargement of the phallus and pubic hair develop-
$ v6 |5 p* H8 O9 ^8 ]ment without testicular enlargement, which was due2 l' s. i8 s5 Y; t2 R# `
to the unintentional exposure to androgen gel used by* c; a6 E6 X& B1 ]) D4 t
the father. The family initially concealed this infor-
. r$ U+ b  D( N1 p8 Cmation, resulting in an extensive work-up for this* ?! S8 \" _: A% K. b8 b) N
child. Given the widespread and easy availability of
" ~- y) P" q. C5 G, i+ ^. {testosterone gel and cream, we believe this is proba-
' N2 @8 C& w8 Rbly more common than the rare case report in the
& U( f7 h. L9 y! dliterature.4
6 f+ ~& W) @1 {1 E! T7 z* bPatient Report: X3 O, Q5 D+ b0 h3 e( f& x
A 16-month-old white child was referred to the
  f5 ]; t4 m& q# O' Z/ k0 E. p7 Aendocrine clinic by his pediatrician with the concern
4 ?6 Y6 W6 c1 ^% U( h: sof early sexual development. His mother noticed* z! L  q- k8 p: N) L% B- k
light colored pubic hair development when he was6 N1 R$ Q' d- D6 ^: a; X
From the 1Division of Pediatric Endocrinology, 2University of1 H! L# X  a; W0 B' a; `7 Y  j+ g3 n
South Alabama Medical Center, Mobile, Alabama.9 y1 c7 B& v* b7 x
Address correspondence to: Samar K. Bhowmick, MD, FACE,! d$ L  M% n3 S- W' w" F
Professor of Pediatrics, University of South Alabama, College of
/ Q  A! T) j+ o% d, E" KMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;+ X) g( q: ~$ c0 k% t
e-mail: [email protected].$ [( i9 M5 ^9 }9 W
about 6 to 7 months old, which progressively became
$ {( u8 F/ X% ?  a, vdarker. She was also concerned about the enlarge-9 {% s, u. O6 N! }  m5 b
ment of his penis and frequent erections. The child
* ^4 e' [& s1 qwas the product of a full-term normal delivery, with! r! F3 v1 {$ |8 b# D* `
a birth weight of 7 lb 14 oz, and birth length of- z- I$ I+ a. p: j- g. F/ u
20 inches. He was breast-fed throughout the first year$ Y7 T; {$ o1 n0 V) U
of life and was still receiving breast milk along with0 O% o0 P5 |; E. c. h
solid food. He had no hospitalizations or surgery,
" Y8 [  Y. I8 G. Wand his psychosocial and psychomotor development0 U6 d8 _% Q( X5 v& D1 m4 `
was age appropriate.
* q/ C; g6 q, {* ~The family history was remarkable for the father,
+ p4 h* S; D* Z: W% J. Uwho was diagnosed with hypothyroidism at age 16,' K. f& ]3 Z- K: q
which was treated with thyroxine. The father’s
& t/ e5 [" H% P" C. b! Cheight was 6 feet, and he went through a somewhat
$ w. U$ c" ?0 F6 ]early puberty and had stopped growing by age 14.
9 R+ V9 A8 t6 t7 d8 E: `The father denied taking any other medication. The
! L) X# C2 n* Nchild’s mother was in good health. Her menarche
& B& [* |, h' T! r( [was at 11 years of age, and her height was at 5 feet" [9 b2 w' d8 S" k
5 inches. There was no other family history of pre-
( Y/ n0 h" n* K6 ?- @8 ]8 }cocious sexual development in the first-degree rela-% |: ]4 A; I3 H( Z
tives. There were no siblings.
: g# J, B$ E7 X# }% yPhysical Examination
" [5 Z# T3 S3 G; ZThe physical examination revealed a very active,
5 i: M* K% y* P2 k/ \9 |playful, and healthy boy. The vital signs documented
$ b3 Q" ?  T* |9 ?% f6 j3 N" ]a blood pressure of 85/50 mm Hg, his length was
" o: |3 s# U) Y3 R0 j90 cm (>97th percentile), and his weight was 14.4 kg
( l/ Z5 e4 X. K+ e7 L! I6 b; O5 K(also >97th percentile). The observed yearly growth
, K  T, }/ ]$ k" n  M& g7 }velocity was 30 cm (12 inches). The examination of* K# z9 N# V) p2 ?, `( F2 t5 j
the neck revealed no thyroid enlargement.: O# }3 A  v. {' U- N, I
The genitourinary examination was remarkable for
2 L2 |. I, H* Z7 [enlargement of the penis, with a stretched length of% K8 W0 q1 k% ^0 V
8 cm and a width of 2 cm. The glans penis was very well
$ b: b" l- N( d7 ddeveloped. The pubic hair was Tanner II, mostly around$ l3 b' g0 o0 b/ y6 U5 u
540
  n: h9 ], f7 [  H, l; dat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, B) O" N9 ~6 q( E- Cthe base of the phallus and was dark and curled. The* S8 B3 Q  J5 u1 b, N
testicular volume was prepubertal at 2 mL each.
; B$ C( q8 b! ^) S9 O( qThe skin was moist and smooth and somewhat
& ]0 x% Z* U& Z! U4 a+ w; [oily. No axillary hair was noted. There were no  \2 i2 N7 D4 K+ \4 `% A4 U. |
abnormal skin pigmentations or café-au-lait spots.9 |" q* t6 i9 R1 F: P; v# e7 D/ A
Neurologic evaluation showed deep tendon reflex 2+
" `8 t1 i; Q& A4 W1 }1 {& Cbilateral and symmetrical. There was no suggestion
4 Y$ B+ V+ n* P' p) |, O7 dof papilledema.8 {7 j) q; E3 x. \
Laboratory Evaluation! t6 L! [' ^! ^# C  D
The bone age was consistent with 28 months by* D) g' ^; a; R8 ?- i5 \
using the standard of Greulich and Pyle at a chrono-4 h; l6 W* k/ {( X
logic age of 16 months (advanced).5 Chromosomal
9 y* ?: Y( x7 r3 o4 }karyotype was 46XY. The thyroid function test
; V. L  R$ V8 h/ b$ \showed a free T4 of 1.69 ng/dL, and thyroid stimu-
- K% c) `! |# l4 e. `lating hormone level was 1.3 µIU/mL (both normal).' \0 s: t; I: h4 @" S
The concentrations of serum electrolytes, blood
' a1 F' }+ X: k9 I- Purea nitrogen, creatinine, and calcium all were$ u( V/ _! ~5 R4 l# t! t
within normal range for his age. The concentration# |0 h; e, X1 [% V+ `0 a; ]1 `* H
of serum 17-hydroxyprogesterone was 16 ng/dL" l5 F0 G0 Q4 v
(normal, 3 to 90 ng/dL), androstenedione was 20
% F+ L, }" L& a; j  fng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-' O7 X# N  w4 ]8 R. `* n' l
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
" O0 p& `- [- O4 c9 k, t8 n/ ldesoxycorticosterone was 4.3 ng/dL (normal, 7 to% l; d& e/ B! f8 M( A( \6 R% [
49ng/dL), 11-desoxycortisol (specific compound S): y8 L1 o6 k) D) }, d# s
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-, F, v4 ], m6 b5 Q. a( @) x
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
5 K/ A4 P7 D' ?- A6 }testosterone was 60 ng/dL (normal <3 to 10 ng/dL),% F/ H' g5 E8 F2 W5 d
and β-human chorionic gonadotropin was less than1 O% }! C6 v3 q; @
5 mIU/mL (normal <5 mIU/mL). Serum follicular
2 k' v" P+ d! i( U5 b4 Ystimulating hormone and leuteinizing hormone4 \0 ?+ b3 ~/ R
concentrations were less than 0.05 mIU/mL/ y+ P, F) P6 I3 j& O
(prepubertal).
5 i8 I+ j* a/ y  U1 k8 l' j3 M7 FThe parents were notified about the laboratory
3 r) G% d4 R# ?9 V: e) jresults and were informed that all of the tests were: N! z, ?& q5 B$ q3 ^
normal except the testosterone level was high. The
9 g, ~% B- ~; D2 j1 kfollow-up visit was arranged within a few weeks to( b  L* i" A$ ?7 _2 w
obtain testicular and abdominal sonograms; how-
6 n( d( t# R4 Z8 z/ Q  H- never, the family did not return for 4 months.: Z! C% @/ u' C& l/ t
Physical examination at this time revealed that the
% A+ C& ?0 @/ k& B1 J- A; t! x) Echild had grown 2.5 cm in 4 months and had gained; K9 w! s6 v5 _3 e) m8 C6 B
2 kg of weight. Physical examination remained
* r$ c( L" ^' `7 Yunchanged. Surprisingly, the pubic hair almost com-7 p% y0 A+ u- {5 |/ n$ @
pletely disappeared except for a few vellous hairs at7 X8 n& l( Q6 }
the base of the phallus. Testicular volume was still 2
- \" @  d, X3 w9 r3 j& umL, and the size of the penis remained unchanged.8 D" q( k' U3 q
The mother also said that the boy was no longer hav-: l% d* b. _( U% e( c& n; Y/ y
ing frequent erections." _! M. n! m0 o! D9 l+ F" ?
Both parents were again questioned about use of9 ?2 \# c  G& v' Z
any ointment/creams that they may have applied to" X1 C5 Z% \! Q7 s' i
the child’s skin. This time the father admitted the( Y& s9 w- J" q) g/ g2 @+ @; d
Topical Testosterone Exposure / Bhowmick et al 541
& g. b7 b0 }' |, S% K$ h1 x  Kuse of testosterone gel twice daily that he was apply-
2 I7 N& ]6 K9 n' R2 o1 t* b; Z6 Xing over his own shoulders, chest, and back area for
* m$ w$ M  H9 f& L: U4 d& Oa year. The father also revealed he was embarrassed
# y& ?4 h+ u) ato disclose that he was using a testosterone gel pre-
, p0 X% X1 u4 x$ Gscribed by his family physician for decreased libido$ |  j/ J6 I# S9 j, W/ S$ d
secondary to depression.
+ @" e( a; K; w2 x# KThe child slept in the same bed with parents.' v8 [. n9 l0 }# N: O1 c( |' ^
The father would hug the baby and hold him on his
& h. X- j4 |  L7 l4 cchest for a considerable period of time, causing sig-
0 X7 f2 @" v' Gnificant bare skin contact between baby and father.2 r, j. P/ o$ j7 A
The father also admitted that after the phone call,
/ I; f) t' \, {: z% {. hwhen he learned the testosterone level in the baby
; F/ N% X, ~* z7 U% W" A+ rwas high, he then read the product information
$ h* v9 B; Z! b& |; Npacket and concluded that it was most likely the rea-+ V  X3 \9 S5 _- ?) z6 O8 Y
son for the child’s virilization. At that time, they
# s  ^- i- a3 [  \9 M7 |decided to put the baby in a separate bed, and the7 y; u: G5 }+ z
father was not hugging him with bare skin and had$ s/ v4 y$ l; O
been using protective clothing. A repeat testosterone/ G# h& N- u( U6 q/ |$ W
test was ordered, but the family did not go to the+ n7 [2 M% V8 g7 ]
laboratory to obtain the test.
8 B( F" E1 l1 ~( O3 w) `  SDiscussion1 Q7 t3 Q* j% h) p# p' Q
Precocious puberty in boys is defined as secondary+ k8 {8 K; J8 q; _2 z. f# q2 E# k
sexual development before 9 years of age.1,48 ^! s+ J: D; @7 E$ T6 P  B
Precocious puberty is termed as central (true) when4 q' o( k8 E% ?# E% ^: J7 H, U
it is caused by the premature activation of hypo-
8 k; F+ }0 y; o( f  V" O8 Lthalamic pituitary gonadal axis. CPP is more com-
( P& U: n% g3 s3 z" u8 Smon in girls than in boys.1,3 Most boys with CPP
. ]' I" K, a6 \0 U2 w+ \0 J# ?1 Imay have a central nervous system lesion that is
1 o! q- ]% g" Q4 Y- tresponsible for the early activation of the hypothal-. o9 i( C# x4 S- D
amic pituitary gonadal axis.1-3 Thus, greater empha-: k8 N- ^+ V- q' x, \# n) b& {; A
sis has been given to neuroradiologic imaging in8 v5 Q& C( \* [
boys with precocious puberty. In addition to viril-
& H- J0 j" |9 A; I- }9 Eization, the clinical hallmark of CPP is the symmet-
4 C) B! p" Z, B! ^/ Orical testicular growth secondary to stimulation by# i: P# B7 U$ j  m$ C) u. j
gonadotropins.1,3: l( t+ d0 E  S: I0 Y( z* H
Gonadotropin-independent peripheral preco-8 f$ b) V* h0 k/ k3 e
cious puberty in boys also results from inappropriate
2 R: C7 T. ^% G! Fandrogenic stimulation from either endogenous or/ g" e1 M( v7 ?! b6 G' Y- A% H3 l# _
exogenous sources, nonpituitary gonadotropin stim-
9 A7 N9 z* ?4 r# d# M) C% ~ulation, and rare activating mutations.3 Virilizing
3 ~. L0 s1 \& J5 ?: q8 A& q2 H7 u) ~congenital adrenal hyperplasia producing excessive  d' _8 B0 b! O) U/ ?# O& _0 U
adrenal androgens is a common cause of precocious
, ]7 x7 y2 K# y7 Npuberty in boys.3,4
! V9 H3 k; U! A9 c1 y9 E7 W, T6 LThe most common form of congenital adrenal
. ?; f4 B3 y2 R" _. a- @hyperplasia is the 21-hydroxylase enzyme deficiency.
' a3 H1 h+ P- ]# @( \0 P6 eThe 11-β hydroxylase deficiency may also result in, B& l) X& L  V  j5 o& T7 B; \) O) t
excessive adrenal androgen production, and rarely,
. B% j! [- `# M* ran adrenal tumor may also cause adrenal androgen
1 Q  r! h. m0 [& C6 N- i; Lexcess.1,3) P( W3 I  k6 A, ]! N$ J
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' |% q% a2 r! |. N+ @* |542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
0 U8 [* ^" [; e. ]1 F4 l% l9 jA unique entity of male-limited gonadotropin-. n! z2 x& i$ e# F' g1 N; f
independent precocious puberty, which is also known9 D( u$ `4 Y; H) K3 }; X
as testotoxicosis, may cause precocious puberty at a) F- t7 [5 h) }. S, j8 A' M" ^! T
very young age. The physical findings in these boys
1 u' T) k% o% Z4 c6 c+ k9 Pwith this disorder are full pubertal development,% J$ \$ ^7 k2 h+ K% H9 M5 \
including bilateral testicular growth, similar to boys. q# r/ C, ^& A
with CPP. The gonadotropin levels in this disorder
. M& B; H# N8 O+ J* b1 ^5 Eare suppressed to prepubertal levels and do not show0 i4 o: z7 M. t1 V+ u8 d( x
pubertal response of gonadotropin after gonadotropin-
5 M2 i7 B4 |# l6 areleasing hormone stimulation. This is a sex-linked/ s; G, }" r: m/ J* k" |
autosomal dominant disorder that affects only( g3 N' a/ I( n3 [- V8 f
males; therefore, other male members of the family, ]) v3 D& `% u4 ^7 u/ A( T& t, O! T
may have similar precocious puberty.3
! q, U* [0 O* F$ k: h: A/ nIn our patient, physical examination was incon-
7 g2 R/ O6 w" o& b" p' lsistent with true precocious puberty since his testi-' {- A/ L8 K6 {8 W, Z
cles were prepubertal in size. However, testotoxicosis
, _( T6 W: F* P' m# Y+ [5 Bwas in the differential diagnosis because his father
; L: V* f4 Y- X9 u" bstarted puberty somewhat early, and occasionally,
8 v1 E+ y9 D1 J& V. Atesticular enlargement is not that evident in the
; o) e2 v% V& P; G) J- cbeginning of this process.1 In the absence of a neg-3 ?& l, @+ c8 K- t! J! {' Q. q
ative initial history of androgen exposure, our9 l& n9 x' T" F
biggest concern was virilizing adrenal hyperplasia,
6 I; ?0 ?$ H  G4 t" m$ Teither 21-hydroxylase deficiency or 11-β hydroxylase& a9 ^2 }5 ^- `) z2 F$ [
deficiency. Those diagnoses were excluded by find-
" T+ }6 Y+ M' J; C! W+ bing the normal level of adrenal steroids.* @# v0 ]$ M2 }& @5 `
The diagnosis of exogenous androgens was strongly
6 k& K; V% n) m2 C3 bsuspected in a follow-up visit after 4 months because3 F8 m; z( |/ g0 I" ~8 l- ]
the physical examination revealed the complete disap-1 T! b3 `& l& W+ i$ k3 `
pearance of pubic hair, normal growth velocity, and
- G8 @7 q  Y  K  Pdecreased erections. The father admitted using a testos-
4 `3 M) w) F2 T7 i$ Uterone gel, which he concealed at first visit. He was- x  b: Z$ H- ?2 |# h
using it rather frequently, twice a day. The Physicians’
0 r* `( r5 A$ D( e7 _* k& I) ~$ H! ]Desk Reference, or package insert of this product, gel or! R( x( h0 X  b0 K
cream, cautions about dermal testosterone transfer to5 |6 z8 K1 {5 A; Q8 G
unprotected females through direct skin exposure.' X0 q7 s- s$ a8 Y
Serum testosterone level was found to be 2 times the
+ M9 w2 z# ^! `7 pbaseline value in those females who were exposed to
" h- f# M' f$ N2 h& S1 X8 D! Zeven 15 minutes of direct skin contact with their male, t% x4 M6 |) s
partners.6 However, when a shirt covered the applica-. i2 D" z+ @1 Z9 b: W( S: }
tion site, this testosterone transfer was prevented.( {, z# c, E! H* t) r9 ?, x. V  `/ l
Our patient’s testosterone level was 60 ng/mL,
; C% c: E2 o+ P: q2 M; V9 Owhich was clearly high. Some studies suggest that
/ ]7 |* G" S% Y- n/ S5 x4 c: adermal conversion of testosterone to dihydrotestos-
- {! N( W$ w7 _' i1 k0 X; cterone, which is a more potent metabolite, is more
, Z' g  }8 p" C* t# Pactive in young children exposed to testosterone
2 e3 m* b' W9 h0 F5 D: Nexogenously7; however, we did not measure a dihy-( [- C" Z. v- \1 b5 ?
drotestosterone level in our patient. In addition to6 y7 J/ U. l: c; A
virilization, exposure to exogenous testosterone in
+ r$ T1 r' t: y  `9 i' A6 {children results in an increase in growth velocity and! @4 u$ X) ]8 Y* h
advanced bone age, as seen in our patient.
( Y4 h4 A6 W; O- k1 F5 Z8 O" OThe long-term effect of androgen exposure during: A. e# Z- m- [+ Y( ?
early childhood on pubertal development and final
; R4 L" u4 O+ e0 H% p; `1 vadult height are not fully known and always remain; P( W# t) d& O6 @; f9 S
a concern. Children treated with short-term testos-( g, Y/ O5 I3 A
terone injection or topical androgen may exhibit some) S  M' p# d8 F4 T
acceleration of the skeletal maturation; however, after
/ x( {* H6 G  X( dcessation of treatment, the rate of bone maturation
- f- v$ y. C2 M& Y' ydecelerates and gradually returns to normal.8,9! J8 I4 G: N+ x4 H% s" i
There are conflicting reports and controversy7 x" i$ M$ c! U# J
over the effect of early androgen exposure on adult; e+ V8 A9 i+ m0 d, v, F2 N
penile length.10,11 Some reports suggest subnormal
# ^) x# C3 d; G+ i3 q+ K7 padult penile length, apparently because of downreg-
! v5 j# p, ^3 f* ]# B6 Gulation of androgen receptor number.10,12 However,
1 n* N) m8 B4 r3 {Sutherland et al13 did not find a correlation between6 x1 j7 x( O2 h9 y
childhood testosterone exposure and reduced adult
/ s6 W$ T2 s: f: a+ Wpenile length in clinical studies.
3 u4 W( m4 h  w4 c& U' `$ lNonetheless, we do not believe our patient is$ H% C6 G  F7 I& J8 m
going to experience any of the untoward effects from
2 Q7 X" w( Y& A3 _4 Vtestosterone exposure as mentioned earlier because
, N8 f# x& W  I% cthe exposure was not for a prolonged period of time.
: \: \3 A; {" f- }Although the bone age was advanced at the time of6 t2 o, O$ p" O% E  W
diagnosis, the child had a normal growth velocity at+ X% G* k' ]+ b. y8 m
the follow-up visit. It is hoped that his final adult
! P# S5 r. ^& d0 L+ H( G. aheight will not be affected.
9 @1 [, v$ M1 ^$ Z% }, wAlthough rarely reported, the widespread avail-9 c( g) q. x& j6 z
ability of androgen products in our society may5 v# j6 `0 p" [& ^' |
indeed cause more virilization in male or female! V+ s( b7 _1 i: R" M. Q
children than one would realize. Exposure to andro-' B# C0 F# [; o' }
gen products must be considered and specific ques-
* q# ^( |: H" W6 C; Ctioning about the use of a testosterone product or
- r( P+ L$ w# n# F* i0 {gel should be asked of the family members during2 x% F' _- S% c  V  [
the evaluation of any children who present with vir-4 b: K& u3 ^& U; U- @1 g4 l' ]
ilization or peripheral precocious puberty. The diag-- U( d* [$ N& B. h6 B- ]1 Z
nosis can be established by just a few tests and by3 m* i; n+ I# {# g' M% ~/ T
appropriate history. The inability to obtain such a& C3 `# j. u( u6 G
history, or failure to ask the specific questions, may. M* z1 C% ]% W% R, b/ l$ l/ t, [
result in extensive, unnecessary, and expensive
# @! m( |' o5 C* [investigation. The primary care physician should be
6 Y' V9 e$ m$ g+ F6 r3 {$ @aware of this fact, because most of these children3 j. O  O$ h0 N# A: y7 B# U
may initially present in their practice. The Physicians’
. B" f# u3 Z2 v: [  q% DDesk Reference and package insert should also put a
% X$ O: Y* h# W! B% v& h# x4 hwarning about the virilizing effect on a male or
/ q0 J0 f" k  I8 v9 S8 Lfemale child who might come in contact with some-. }/ H3 O9 ?; r, t( i& M
one using any of these products.4 y) m& [- C* f; Q
References( B! |/ o5 Z+ a+ C2 o" k
1. Styne DM. The testes: disorder of sexual differentiation3 H4 K0 E! {7 q: k, Q
and puberty in the male. In: Sperling MA, ed. Pediatric
* c5 g! j5 H1 LEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;# f0 C  A  W# h! R* p% \: u
2002: 565-628.
( P" Z+ W% d( V0 j( i2 i' j2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 c5 y6 _. e5 l5 r+ X
puberty 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

& u" W# e& t" M0 v3 W3 d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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