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Sexual Precocity in a 16-Month-Old
) v- U0 K. @) D8 P$ ]Boy Induced by Indirect Topical
3 U. ^- ~% j8 A8 b, m- OExposure to Testosterone
7 ]; Z5 k$ X& KSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
# I9 L" e9 T) K" M- f3 tand Kenneth R. Rettig, MD19 p. ^& g: D) U6 g- a! V! F
Clinical Pediatrics
( V1 |7 ]9 M& A8 QVolume 46 Number 64 U( a: n' D3 a
July 2007 540-543
; M, ]: h6 K2 r5 [+ ^" u1 Q© 2007 Sage Publications$ b; [$ W1 I3 h+ z
10.1177/0009922806296651
3 |9 C0 O4 t9 n. d3 qhttp://clp.sagepub.com
' x% m. H" ~3 _( P; ahosted at
1 t% E# t( O1 f4 v# G. Ehttp://online.sagepub.com
4 C8 y7 v4 ?6 v3 ^7 }Precocious puberty in boys, central or peripheral,2 R& K: h# P' U. n8 M
is a significant concern for physicians. Central
# m8 M1 u# Q4 w$ bprecocious puberty (CPP), which is mediated
+ c/ m' l; m$ U% s' B: wthrough the hypothalamic pituitary gonadal axis, has
2 {- @5 ^* \. p' o+ Da higher incidence of organic central nervous system
- Y5 o: ^( Q* K; e/ s" L! }lesions in boys.1,2 Virilization in boys, as manifested
+ D$ d; y7 g% A( j4 ?* f* M5 Qby enlargement of the penis, development of pubic1 ^! `8 Y' |0 O: g7 \
hair, and facial acne without enlargement of testi-
+ I- E1 r9 P) @cles, suggests peripheral or pseudopuberty.1-3 We
2 j+ a6 ^6 ]0 kreport a 16-month-old boy who presented with the
/ x  y) U6 w6 l  S2 Ienlargement of the phallus and pubic hair develop-
- l9 W$ g& B. M, ]& Hment without testicular enlargement, which was due+ O: U- k3 x' w' L5 e" @
to the unintentional exposure to androgen gel used by
; D) e. b: u5 R$ d9 _the father. The family initially concealed this infor-
/ i& L' q9 f! C7 r6 \" hmation, resulting in an extensive work-up for this  h5 E  l' q  Z$ W4 y# z
child. Given the widespread and easy availability of
6 X9 w3 i% b8 E- a: btestosterone gel and cream, we believe this is proba-0 T" t, Q5 u/ ?; Y
bly more common than the rare case report in the
  f" ], ~2 _' Vliterature.4
9 }! [8 I9 \7 p3 m! c- NPatient Report
8 E# J' T3 z6 m0 Z/ WA 16-month-old white child was referred to the
. _4 J0 r9 Y& f3 a4 I9 \endocrine clinic by his pediatrician with the concern) c: `$ j/ h% S3 q' f8 u$ g! L1 _
of early sexual development. His mother noticed' y9 h. Q) k$ b2 \+ g" r  h
light colored pubic hair development when he was
$ U9 `$ ]3 F( Q1 n7 B& V) iFrom the 1Division of Pediatric Endocrinology, 2University of
9 t- }. |5 ^/ d/ ISouth Alabama Medical Center, Mobile, Alabama.0 P% f: H& Z0 C& y/ d
Address correspondence to: Samar K. Bhowmick, MD, FACE,4 _3 V2 n+ \8 i: t
Professor of Pediatrics, University of South Alabama, College of
5 u8 Y( z; [3 |0 o+ K. g; O( ~Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;" Z4 i9 O5 f2 P9 p  |7 w4 S9 D
e-mail: [email protected].
, j( T5 }" J1 B3 Pabout 6 to 7 months old, which progressively became
/ O$ O: I* z4 adarker. She was also concerned about the enlarge-, p, O9 |$ B- N8 e. T+ M' d
ment of his penis and frequent erections. The child: t* H) y! g' z! |" n
was the product of a full-term normal delivery, with
2 I/ s( G7 }8 J# O$ H4 k% G! A  S" c( Va birth weight of 7 lb 14 oz, and birth length of
+ B; p1 l" U# I20 inches. He was breast-fed throughout the first year1 e, |" r+ G' M  b
of life and was still receiving breast milk along with
" U  z- i  u, Wsolid food. He had no hospitalizations or surgery,
- Q0 |( \6 k$ c9 b7 q; S; Wand his psychosocial and psychomotor development
) _* {( Z1 ]1 i2 Z: e6 A9 Twas age appropriate.
- {9 C" ]. d+ E1 ^  m; w5 nThe family history was remarkable for the father,
' n9 ]  y+ U& Q4 xwho was diagnosed with hypothyroidism at age 16,
  S) S3 b3 C/ e2 P7 R3 k$ A0 t; Rwhich was treated with thyroxine. The father’s
6 R, r& T# X) _! Z; y' a2 i# @height was 6 feet, and he went through a somewhat6 ?" H+ v  C5 n6 d* ]$ k% |. P/ V" D# N
early puberty and had stopped growing by age 14.
- p! N" }  t" I) C9 f% SThe father denied taking any other medication. The# ]1 O1 B9 q& K
child’s mother was in good health. Her menarche: s& {+ P, r9 H; M0 k; u' O. H4 S
was at 11 years of age, and her height was at 5 feet
5 Z( `$ W' U2 l  Z2 G* y5 X5 M5 inches. There was no other family history of pre-# }4 m) n( `) ^" A  x* ]# @
cocious sexual development in the first-degree rela-" m  N; u$ F2 v) P$ N. `
tives. There were no siblings.
; D5 p* _6 }# j" r0 rPhysical Examination! F: F" j4 y) P! F- o8 o
The physical examination revealed a very active,
4 d" X2 t. l: \( C! X+ |- O2 T( _* v/ Qplayful, and healthy boy. The vital signs documented
) H. y" ]+ R# g. K1 t; N" m+ G1 S2 `a blood pressure of 85/50 mm Hg, his length was# y! C' ~9 L3 L( k3 ^
90 cm (>97th percentile), and his weight was 14.4 kg
9 W* S# |& o% k, p0 O(also >97th percentile). The observed yearly growth2 x% O8 E6 b: O2 l& y
velocity was 30 cm (12 inches). The examination of
! m, y; N6 d9 Q1 x4 I4 Nthe neck revealed no thyroid enlargement.  A0 J9 x! z. }( E
The genitourinary examination was remarkable for5 q5 b% O3 V. V0 F* u
enlargement of the penis, with a stretched length of
3 P3 H1 K- Z6 X  J3 K* O8 cm and a width of 2 cm. The glans penis was very well  N, p4 m  O5 ~. d! m7 `# x7 k! k
developed. The pubic hair was Tanner II, mostly around% u+ V, N9 D) D- ?' D' T
540
' a# K0 r9 B$ b/ mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 b" h9 H" `; u; C: i; V$ zthe base of the phallus and was dark and curled. The! {. h1 {/ ?8 c
testicular volume was prepubertal at 2 mL each.! S5 h1 l. W/ N/ K5 M
The skin was moist and smooth and somewhat3 q6 w6 O# i# s: E' I8 c
oily. No axillary hair was noted. There were no
9 }3 Y' g+ s8 U) h  s% Q3 Xabnormal skin pigmentations or café-au-lait spots.& @$ h3 v+ Z7 Z
Neurologic evaluation showed deep tendon reflex 2+% k3 z0 M1 i/ i; o
bilateral and symmetrical. There was no suggestion2 b' i' x; n# U; [3 c' j
of papilledema.# W: R" j# H) f) V
Laboratory Evaluation
$ V4 _: P/ r( q0 V# }# sThe bone age was consistent with 28 months by. k$ k; V: {7 f. Y8 R
using the standard of Greulich and Pyle at a chrono-
, T& v( X. z8 f/ g; alogic age of 16 months (advanced).5 Chromosomal
1 ~$ s8 O7 q- j  x/ G9 E7 Bkaryotype was 46XY. The thyroid function test4 |) P; q, t# l/ U8 r" b
showed a free T4 of 1.69 ng/dL, and thyroid stimu-7 D* `& a3 K- k' N$ w$ w, l6 D
lating hormone level was 1.3 µIU/mL (both normal).# v+ T, I6 w4 E- g2 P  q- U2 @2 G
The concentrations of serum electrolytes, blood
  J9 d9 Q: _7 H% H% X9 ^# uurea nitrogen, creatinine, and calcium all were
5 p6 f) B3 F$ V2 F; |' G6 Twithin normal range for his age. The concentration, Q: y$ w7 }' h
of serum 17-hydroxyprogesterone was 16 ng/dL2 d, }, z4 ^  r) l+ x1 U
(normal, 3 to 90 ng/dL), androstenedione was 20+ e# ?6 F! o2 I  U8 E' [
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
# l, f7 Y) G/ hterone was 38 ng/dL (normal, 50 to 760 ng/dL),5 D6 Z+ z5 L$ h) ~5 F
desoxycorticosterone was 4.3 ng/dL (normal, 7 to$ G% I. Z# v  ?/ d4 F
49ng/dL), 11-desoxycortisol (specific compound S)
6 ~* T* b: Z% u0 R1 w% Ewas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
' G( S* g1 J4 w  ^( Stisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
( O7 K9 H  K" Dtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
5 o- [2 R3 m5 m" f" }8 kand β-human chorionic gonadotropin was less than
% I# h  C: ~  }1 R) c/ m* w( G& t$ X9 K5 mIU/mL (normal <5 mIU/mL). Serum follicular
! i5 h, g. X  A. r2 n, B; Wstimulating hormone and leuteinizing hormone* i0 b' h( V8 F) _) \8 C
concentrations were less than 0.05 mIU/mL/ F9 N+ T; W1 l1 j
(prepubertal).% u4 g2 _0 h( R8 ^& F6 o' R
The parents were notified about the laboratory1 L! K$ I0 ]6 ^* h
results and were informed that all of the tests were2 f8 f4 \$ j7 H
normal except the testosterone level was high. The7 s/ D$ S/ c& V0 b6 T
follow-up visit was arranged within a few weeks to" k4 G6 K! T+ O$ L
obtain testicular and abdominal sonograms; how-
6 _2 _- N/ B( S, Yever, the family did not return for 4 months.
' P$ `! ~0 \; J4 R) e; e# DPhysical examination at this time revealed that the
9 Q9 i8 c0 Q9 w& ychild had grown 2.5 cm in 4 months and had gained3 e: t1 E; ^3 x6 L
2 kg of weight. Physical examination remained
) o8 K4 U& G# |3 }# I8 punchanged. Surprisingly, the pubic hair almost com-
( S  s7 S5 H6 cpletely disappeared except for a few vellous hairs at
, T! n4 S4 \4 n* I0 T8 j8 e4 ithe base of the phallus. Testicular volume was still 2$ b& ~4 P9 j- y  A9 W0 e3 I; y
mL, and the size of the penis remained unchanged.
" ?$ L7 _, W% {The mother also said that the boy was no longer hav-
7 a8 O0 U: ?) i( a; L/ q5 King frequent erections.
4 a: e( u" w7 x& bBoth parents were again questioned about use of9 D0 y. S: H1 O
any ointment/creams that they may have applied to! i8 o: H2 _/ z2 z
the child’s skin. This time the father admitted the; Z5 q) N# O/ M* c  s
Topical Testosterone Exposure / Bhowmick et al 541
/ j5 X% y4 ^9 T/ F6 K2 puse of testosterone gel twice daily that he was apply-
6 e5 z8 o" ]3 L. Ning over his own shoulders, chest, and back area for' M! M+ k% M, E8 b
a year. The father also revealed he was embarrassed8 ]  d) g1 }* N# n& ^$ a7 T( e
to disclose that he was using a testosterone gel pre-
7 J5 a6 q7 B0 M3 Mscribed by his family physician for decreased libido8 o9 W- b, N! ^1 m$ g9 k
secondary to depression.3 g# _' }, b. A4 r' y$ T1 q8 ]( M% }
The child slept in the same bed with parents.6 n7 e7 K( h- W2 v. w) w+ P. g
The father would hug the baby and hold him on his6 R$ t  b$ r' u  d+ [! P
chest for a considerable period of time, causing sig-
" j+ l: p* d2 g1 Y6 _- ^+ n  T9 snificant bare skin contact between baby and father.
" G. @# o: W1 F- ^The father also admitted that after the phone call,& X. b# g# t8 v$ R& l7 ^& p' {7 E
when he learned the testosterone level in the baby6 }3 _4 c- n) k, g
was high, he then read the product information% P. I8 v% Z1 m0 e5 O5 e+ U6 n
packet and concluded that it was most likely the rea-
% ^( c& z2 c, ?son for the child’s virilization. At that time, they
- |0 Z4 F' s3 M8 vdecided to put the baby in a separate bed, and the+ ]9 ^! Y! p+ h- [+ e4 ~2 N
father was not hugging him with bare skin and had1 ^+ I6 [* w/ T6 j  X$ _: i
been using protective clothing. A repeat testosterone
5 O0 q. U* E/ C+ s4 [9 D/ s. Mtest was ordered, but the family did not go to the, H2 G9 M2 J- [8 M0 |' f* V
laboratory to obtain the test.+ T! c/ R3 h, ]' l; C) K, u
Discussion
% }/ s% [' H7 Z4 U& R3 D- t0 M, hPrecocious puberty in boys is defined as secondary+ f3 E, K0 T# g, D# Q! Z
sexual development before 9 years of age.1,4
7 O5 j& w& {. v& K5 XPrecocious puberty is termed as central (true) when1 T7 E6 z+ Z2 X. p. j# K) ?) j: N
it is caused by the premature activation of hypo-+ C1 w/ b: e: I- b, n/ P  S0 l
thalamic pituitary gonadal axis. CPP is more com-$ z2 L8 [' c) p$ U4 M, s- ^
mon in girls than in boys.1,3 Most boys with CPP
  H2 c- A2 i0 r  \* ~& qmay have a central nervous system lesion that is- ~6 B( m; n9 T) q1 `8 T# Z
responsible for the early activation of the hypothal-! \- `- n: n+ }/ u2 [' W1 B
amic pituitary gonadal axis.1-3 Thus, greater empha-( V6 ~. C8 U, [4 @
sis has been given to neuroradiologic imaging in
: ?" m8 L( \: }6 {# y8 X0 [boys with precocious puberty. In addition to viril-
( p% V6 [- J, r0 }# X" H9 Yization, the clinical hallmark of CPP is the symmet-
( @# s$ H3 q' r( Lrical testicular growth secondary to stimulation by# |1 K6 X, h' X! k- ^& ]
gonadotropins.1,39 a6 S( D( f; o6 g5 G' Y
Gonadotropin-independent peripheral preco-
0 I& `. C! a$ w" E: p+ hcious puberty in boys also results from inappropriate2 H  d$ p. f6 x: i6 d0 {
androgenic stimulation from either endogenous or: c: A: `) u9 ~2 C9 c4 B
exogenous sources, nonpituitary gonadotropin stim-
+ z% C8 T, \* E, N& n. Zulation, and rare activating mutations.3 Virilizing
; L0 h9 C" p8 j6 m0 _/ R: Icongenital adrenal hyperplasia producing excessive0 j6 `8 Q" Y' ]- y/ C# W
adrenal androgens is a common cause of precocious
5 P  {1 }5 N6 z. U6 ^- \3 Q1 fpuberty in boys.3,4
% G6 g' m1 s0 P! T( }  \6 Z" }The most common form of congenital adrenal* P# o1 e" P  J/ I! A6 p7 E3 J( |) V
hyperplasia is the 21-hydroxylase enzyme deficiency.
) I5 H) |% ~% k9 C- P. jThe 11-β hydroxylase deficiency may also result in: q  ~$ G! a' `* K$ v0 M
excessive adrenal androgen production, and rarely,
7 C9 D  k/ V- @  P0 ~* r+ `* Aan adrenal tumor may also cause adrenal androgen- H8 N$ t& N+ H! D! O# K
excess.1,3; B# A8 @9 I" A4 y+ V- E! T5 w1 Z# Y
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  N$ p7 ]7 ^" |4 z
542 Clinical Pediatrics / Vol. 46, No. 6, July 20078 E3 V2 g$ J) C( E
A unique entity of male-limited gonadotropin-3 j$ f6 D  Z& B$ `) J& r, l( j
independent precocious puberty, which is also known
' A# p0 E7 I7 x* x* f4 j0 Vas testotoxicosis, may cause precocious puberty at a8 R" K$ C  Y  M  b! ^9 \) m+ F) A
very young age. The physical findings in these boys
: ~* x6 b9 J0 b( W" v- U/ u1 \with this disorder are full pubertal development,
  h! k' s+ n" M6 i: u/ E4 `including bilateral testicular growth, similar to boys% J3 x7 Q: M& W( i- U" B
with CPP. The gonadotropin levels in this disorder
1 \% `, \3 p% [- r) b/ p- [& Oare suppressed to prepubertal levels and do not show" U. y% f9 Q# f0 q4 k7 Y$ q. D' n
pubertal response of gonadotropin after gonadotropin-
5 W: {0 G/ c1 F! L0 b  x, Lreleasing hormone stimulation. This is a sex-linked+ Z5 X# t8 L9 S
autosomal dominant disorder that affects only- P/ n( N* V$ O
males; therefore, other male members of the family
& x9 N) U; h3 {+ ?! b. g: I8 \may have similar precocious puberty.3
* x4 u0 \8 l* b  {In our patient, physical examination was incon-, V. P) P  C9 r" ]1 e- n& m6 k
sistent with true precocious puberty since his testi-
+ C9 W: u' `/ V$ N/ K8 hcles were prepubertal in size. However, testotoxicosis
) W: Y1 ]6 H' ]' iwas in the differential diagnosis because his father
' l& \5 \4 G) s/ c9 j. ?started puberty somewhat early, and occasionally,
% u/ k" X4 W) n$ m* ctesticular enlargement is not that evident in the3 L" }; s6 A+ j: Y- K& X8 I
beginning of this process.1 In the absence of a neg-- _& D2 Z4 v/ R' }; z9 ]3 L- N
ative initial history of androgen exposure, our) r" H+ z5 K% ]% S
biggest concern was virilizing adrenal hyperplasia,( B' x# f- b. A' M: {2 k7 [8 L, A
either 21-hydroxylase deficiency or 11-β hydroxylase, @' P9 W9 W" U3 U/ M0 E2 Z
deficiency. Those diagnoses were excluded by find-% c6 W% D: B, H5 c
ing the normal level of adrenal steroids.
7 t1 L9 U# g5 J; S! qThe diagnosis of exogenous androgens was strongly
5 m) m% ]9 q/ n; s; g( y5 E/ U/ m; l% w4 gsuspected in a follow-up visit after 4 months because* X- v! Y" U- \" P6 D. }
the physical examination revealed the complete disap-
3 U* d) w" W0 \! L. X- u1 V9 Bpearance of pubic hair, normal growth velocity, and
" N, X& M+ Y) j* X  ?' gdecreased erections. The father admitted using a testos-
/ j/ E7 w: _1 r$ M! Eterone gel, which he concealed at first visit. He was9 z7 @$ R% i. \7 s
using it rather frequently, twice a day. The Physicians’
. [- C7 ]) y, H9 E. \( KDesk Reference, or package insert of this product, gel or& |4 ~1 @/ q! m
cream, cautions about dermal testosterone transfer to
9 ~0 V7 ]! _$ z5 [* m4 wunprotected females through direct skin exposure.
5 C+ ^7 D4 [4 lSerum testosterone level was found to be 2 times the- x) c2 K3 r) Q( ]' d
baseline value in those females who were exposed to6 b! |( p( m1 S2 V" |
even 15 minutes of direct skin contact with their male- L; S) L9 J- i  n+ ~
partners.6 However, when a shirt covered the applica-  }: o" c# U" s
tion site, this testosterone transfer was prevented.0 N5 _9 D' H3 h# ^, E6 d
Our patient’s testosterone level was 60 ng/mL,6 O% y3 G& e4 D2 ?) f3 f0 K
which was clearly high. Some studies suggest that
) `; r1 j/ `. \% R6 ~% udermal conversion of testosterone to dihydrotestos-" s% i! Y6 ]+ s: J" h5 b4 i' t
terone, which is a more potent metabolite, is more; g% K9 P. k, X& Q4 D0 Q$ h
active in young children exposed to testosterone
5 g: y/ y+ O! z) nexogenously7; however, we did not measure a dihy-
8 c% |$ \, Z7 U, Bdrotestosterone level in our patient. In addition to
( y  ]: l8 Q. Q3 W& _' g0 U5 @5 e2 Zvirilization, exposure to exogenous testosterone in5 ^* Z7 {( Y# b- a" C
children results in an increase in growth velocity and
. W+ I  j8 F8 Q! q& zadvanced bone age, as seen in our patient.
6 O+ I- O5 G1 ~8 _; C, C; S5 @8 HThe long-term effect of androgen exposure during" S' {+ o# s% ?0 U0 S$ t
early childhood on pubertal development and final) r' U% i9 f4 J5 ?
adult height are not fully known and always remain
: @% |& b) a% L9 t+ _a concern. Children treated with short-term testos-
0 }9 t! q: \8 ^, j( ]6 jterone injection or topical androgen may exhibit some
3 K! W: Y3 `! e) e" t3 ?) p; {acceleration of the skeletal maturation; however, after
) W) I# p$ K, C0 q6 dcessation of treatment, the rate of bone maturation' k+ _4 M7 _: o3 y: v& V0 ?
decelerates and gradually returns to normal.8,9
) y* }: E  M8 Z0 @0 H9 N, d* DThere are conflicting reports and controversy
! O0 t; E2 u+ I, Vover the effect of early androgen exposure on adult
3 |; o. c4 o4 Ypenile length.10,11 Some reports suggest subnormal; n" P0 R) X3 B2 D( m+ v4 |
adult penile length, apparently because of downreg-6 ^' b, x2 A; N! @$ s5 j
ulation of androgen receptor number.10,12 However,
' `. B3 W! J) m- A% q( vSutherland et al13 did not find a correlation between
3 ]4 _# ~! f) u, d& l& I/ Cchildhood testosterone exposure and reduced adult
7 d: U/ v4 c& q5 M  Z: i( `0 A5 O/ openile length in clinical studies.
( ?/ g: x, u, w) {% D( A" w5 HNonetheless, we do not believe our patient is2 b; V4 \% W% f
going to experience any of the untoward effects from" @  ~* u$ v/ n* S" u2 W2 N
testosterone exposure as mentioned earlier because
7 d5 n+ B4 \0 _! q! `. Tthe exposure was not for a prolonged period of time.
+ B! y& o( _: x# h* k$ yAlthough the bone age was advanced at the time of
5 [- p  P2 W" ?6 L7 J% T3 s8 m& Fdiagnosis, the child had a normal growth velocity at
7 m& O& q1 r7 P# f  t- fthe follow-up visit. It is hoped that his final adult
6 o- B1 L% O9 gheight will not be affected.
! m# s* V; n# p, Y7 _7 ^5 dAlthough rarely reported, the widespread avail-
7 {0 w- R, |& F0 M; [# ^/ Fability of androgen products in our society may; u. O  z! e( ]- [* b
indeed cause more virilization in male or female/ F/ b& g1 @) `4 I3 k) T# N
children than one would realize. Exposure to andro-
) w! a5 m2 |( k- z0 |gen products must be considered and specific ques-4 v' M- ?$ B' v+ d6 t
tioning about the use of a testosterone product or8 S. J( C2 k  o9 Z
gel should be asked of the family members during
2 {/ V) ^  Y6 h  u# S& ythe evaluation of any children who present with vir-. D- H* \: y* ?6 w% j
ilization or peripheral precocious puberty. The diag-
9 i- \- U" ~1 n( c! h  Z4 Anosis can be established by just a few tests and by7 c: O8 ?) @0 o& a$ D. J' d$ w( @
appropriate history. The inability to obtain such a  ?* m- s2 `6 O9 X) `: y
history, or failure to ask the specific questions, may
* ]4 _5 x7 g! R8 {. eresult in extensive, unnecessary, and expensive
. Y! Z% T0 D. p$ b' {investigation. The primary care physician should be- t& V& U- d9 V+ v, o# ^  f; i
aware of this fact, because most of these children- h) A$ u/ c( g5 E9 }
may initially present in their practice. The Physicians’
/ X6 x3 c3 i; U* }2 z- l2 d& LDesk Reference and package insert should also put a1 _" o& t" A4 O5 Z
warning about the virilizing effect on a male or
6 j) [* f. \8 F- m8 {female child who might come in contact with some-% U) Y" \  U  r: \5 m* o( P0 B0 a1 u
one using any of these products.
. ?1 Y" l5 R2 L/ h% l- x5 ^References
$ o2 w1 d4 T2 H$ d! _: P2 e/ B! y% ^1. Styne DM. The testes: disorder of sexual differentiation8 r* c9 [2 f( E6 n# ~8 e7 j6 v
and puberty in the male. In: Sperling MA, ed. Pediatric
2 u% L# i! F+ z9 BEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
8 K+ }, i/ g" Q2002: 565-628.3 J4 z+ K4 T: K, G" X  r, Y
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
1 L5 K; b7 F+ Y$ i3 a2 Lpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old% ^8 |/ m8 c; y- {
Boy Induced by Indirect Topical7 X0 w! h" X# |
Exposure to Testosterone
4 S9 ^$ w+ R5 Y* L9 USamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 N; Z/ j/ n* ^5 ]and Kenneth R. Rettig, MD1) I) P: ]3 E8 z# P8 M
Clinical Pediatrics
3 H8 M6 q* F( Z- L6 d2 {! TVolume 46 Number 6
5 g0 u4 n- N% R- n& j$ u* ZJuly 2007 540-543
; C( R; o. k+ D4 W: Z& a+ \© 2007 Sage Publications8 k* i4 c0 o( `1 q+ M: }
10.1177/00099228062966514 R+ o( i- d" G8 [7 O
http://clp.sagepub.com; Y& W' a2 }$ d- Z. b) l& w
hosted at
: D/ Z; o$ O, W# t4 E8 a) k/ {http://online.sagepub.com
7 Z6 _8 E# a8 A3 W: A) w! a9 CPrecocious puberty in boys, central or peripheral,* R2 ^. s8 e, \, u2 n& i
is a significant concern for physicians. Central* c( y4 ~& P$ u/ t4 X2 S- o
precocious puberty (CPP), which is mediated
2 l5 x* ]* r4 w7 |0 C; Wthrough the hypothalamic pituitary gonadal axis, has0 K$ L6 ~4 D. z; N" Y2 p( e
a higher incidence of organic central nervous system. P  L" u8 O) Z0 T! V* g+ s
lesions in boys.1,2 Virilization in boys, as manifested
  }( \3 ?2 }2 D6 T( x7 d1 eby enlargement of the penis, development of pubic
( G& x# V* V+ d. s+ R4 whair, and facial acne without enlargement of testi-
# [2 v* q: J8 m! w0 Lcles, suggests peripheral or pseudopuberty.1-3 We+ v. t" x. h) `+ {% u) l
report a 16-month-old boy who presented with the7 n  r& t  z0 a. r% ^
enlargement of the phallus and pubic hair develop-) Y9 H6 r8 p. k# U' l+ x, Z% ^
ment without testicular enlargement, which was due7 B  m4 H8 a6 F$ D7 n( y
to the unintentional exposure to androgen gel used by
0 g5 J) M: ?8 f* l$ Fthe father. The family initially concealed this infor-3 e- L1 E+ u0 C/ J' @% x$ Y
mation, resulting in an extensive work-up for this
/ H9 W5 v! Z0 x) K. d8 F4 P$ Q( Jchild. Given the widespread and easy availability of% o( Y6 x/ j* c4 [8 G9 t
testosterone gel and cream, we believe this is proba-
. \4 J$ M3 r" cbly more common than the rare case report in the
/ A, q# o( ~% u) B3 Zliterature.4% [0 E. p  [4 W# I' r
Patient Report
0 b; V2 [( [/ L6 \A 16-month-old white child was referred to the' z1 V" N& ]0 }
endocrine clinic by his pediatrician with the concern
1 M* m5 X  k8 }4 v- o2 X5 _! ~of early sexual development. His mother noticed$ `' m# Y) ]5 Y4 ~# v/ S
light colored pubic hair development when he was  d1 _0 S1 o0 N! s8 p4 L" F8 _( K
From the 1Division of Pediatric Endocrinology, 2University of3 S0 f- `; o- w
South Alabama Medical Center, Mobile, Alabama.5 e3 f- A. ~; l- y7 f
Address correspondence to: Samar K. Bhowmick, MD, FACE,/ C% S9 a4 _' K  h: L4 U
Professor of Pediatrics, University of South Alabama, College of# y3 T3 {- \# L6 l2 j9 x) F+ ?
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
0 V) ^( k% ~4 M$ o5 Ee-mail: [email protected].! g& J* L$ v0 _' ]
about 6 to 7 months old, which progressively became
# e) f2 q2 o$ w! @9 [" C4 mdarker. She was also concerned about the enlarge-
# d1 y+ d* _! Y" o  H/ b% xment of his penis and frequent erections. The child3 u" W1 t% `  P( [- }
was the product of a full-term normal delivery, with
; b2 r) O& [4 F6 V" d4 Ba birth weight of 7 lb 14 oz, and birth length of4 T- u$ C5 u! y/ T$ v) i, r% p! X
20 inches. He was breast-fed throughout the first year  j: a) _, k8 d# L4 p: Y& D0 o
of life and was still receiving breast milk along with
1 @" G. n3 Q& gsolid food. He had no hospitalizations or surgery,
0 o' ^* l% W+ Dand his psychosocial and psychomotor development  h. i- ^; f" O; N- w' v! o
was age appropriate.
! U  N, r' }+ p3 y" q) }& ?- @The family history was remarkable for the father,
. P' T' \3 \* g! `who was diagnosed with hypothyroidism at age 16,. E: H+ t: ]' ^5 R3 q
which was treated with thyroxine. The father’s; P! D5 j( d' `* |
height was 6 feet, and he went through a somewhat" ~' x% [) D* e  W
early puberty and had stopped growing by age 14.3 d4 X# O! O: W7 }) c9 f
The father denied taking any other medication. The% ?1 [, q1 E5 M6 C
child’s mother was in good health. Her menarche0 m* o1 m* E" d6 R- K
was at 11 years of age, and her height was at 5 feet4 }- N/ X$ X+ E+ i6 V  A# S0 z  W+ z
5 inches. There was no other family history of pre-1 v0 l  `5 B3 V# C* M
cocious sexual development in the first-degree rela-0 v  [. E# b1 ^5 S! f2 A: g7 ]6 w
tives. There were no siblings.
' V+ y, t" S2 {# S+ s6 HPhysical Examination
& B* p: [$ H" @- a' W5 S" @# f( GThe physical examination revealed a very active,
( S! n. }$ E3 G0 p2 j2 A5 Z/ [playful, and healthy boy. The vital signs documented
8 a/ R5 C6 Q) e# u  za blood pressure of 85/50 mm Hg, his length was0 ?+ c8 }, h% M" S) H2 g
90 cm (>97th percentile), and his weight was 14.4 kg) x. I: I- x( H# D+ V6 h! D' d7 T
(also >97th percentile). The observed yearly growth
# M( E3 G$ o, d6 i; m- bvelocity was 30 cm (12 inches). The examination of
0 ?1 p2 v: T8 K0 P9 P# cthe neck revealed no thyroid enlargement.' }/ ]( v* D7 m# b/ m5 [
The genitourinary examination was remarkable for
* Y& e  U; Y% T% G9 ~3 Menlargement of the penis, with a stretched length of8 P( Z" [9 a" [' R3 w
8 cm and a width of 2 cm. The glans penis was very well
, \1 N4 ^4 s- K/ r; a+ Xdeveloped. The pubic hair was Tanner II, mostly around
9 m+ j" s1 U. A$ `. e540* e% c) ~: X3 L# Q# N
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
7 Z( ^% r8 U; ~: P9 athe base of the phallus and was dark and curled. The
5 X2 U6 r" u5 U0 e0 X- Htesticular volume was prepubertal at 2 mL each.
" J: O9 b/ [* S, R& Q4 aThe skin was moist and smooth and somewhat: x. Y  I' m( [8 v6 q! t
oily. No axillary hair was noted. There were no
) V& ]+ k( W6 \* j; Yabnormal skin pigmentations or café-au-lait spots.! c6 H3 e& |4 `  _) n
Neurologic evaluation showed deep tendon reflex 2+
$ D1 U4 b+ e8 A( k# pbilateral and symmetrical. There was no suggestion
3 \7 {' `- h: O$ Dof papilledema.) Z5 V7 a9 ?6 x8 I" _7 g
Laboratory Evaluation3 N- C$ m# a8 U) T* t, C
The bone age was consistent with 28 months by- ?: x0 \+ k% b- b* M* ?
using the standard of Greulich and Pyle at a chrono-7 z  S( d% Q. }8 E
logic age of 16 months (advanced).5 Chromosomal- F1 X2 p8 R: E; V  W4 |7 m* D
karyotype was 46XY. The thyroid function test
/ F6 Z2 [7 s8 E- Q2 E% Zshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
( \( o' I8 n  J; y# F8 hlating hormone level was 1.3 µIU/mL (both normal).
! M( i: ?+ _: V# @3 z3 A, b$ dThe concentrations of serum electrolytes, blood
9 T) G, q1 M6 F. X5 Burea nitrogen, creatinine, and calcium all were
5 q. L1 x6 J* \/ ]+ dwithin normal range for his age. The concentration
; d- b. m: w7 f3 G( uof serum 17-hydroxyprogesterone was 16 ng/dL" B& e& L; j3 @0 m) L
(normal, 3 to 90 ng/dL), androstenedione was 20+ e  t# E! j9 V, K& D* r: n
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-9 E2 A& I2 y' F4 }
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
3 F. o2 ^5 B* l# x' gdesoxycorticosterone was 4.3 ng/dL (normal, 7 to! w9 ?# F7 {, x* o. e7 @6 M% V5 L4 e
49ng/dL), 11-desoxycortisol (specific compound S)
! m0 m3 D0 r( w3 z% nwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
# z8 D  G* Y4 H- Xtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
7 y- w4 M8 V- M3 L' o8 ]( ztestosterone was 60 ng/dL (normal <3 to 10 ng/dL),* ]; ]' J% u9 u. W, C8 ]* g5 m
and β-human chorionic gonadotropin was less than: W3 i/ H. x1 J; }) [4 _3 A
5 mIU/mL (normal <5 mIU/mL). Serum follicular% x$ O  {$ q. N( a
stimulating hormone and leuteinizing hormone3 D  D. ^1 ?0 K
concentrations were less than 0.05 mIU/mL+ J3 w, r9 R. M; Y
(prepubertal).
' y. ?  z9 q: xThe parents were notified about the laboratory
/ a& r- R- h/ ~1 H$ Jresults and were informed that all of the tests were
- C$ O9 [, C* ^0 K" H& G' |normal except the testosterone level was high. The
0 [, \4 h. Q" V2 Q! v. l; n0 q- ofollow-up visit was arranged within a few weeks to
( G5 T+ n' ^5 vobtain testicular and abdominal sonograms; how-( |/ C, c. _3 c/ z# Z
ever, the family did not return for 4 months.# J5 Q: I1 i; I8 T1 b" U+ j
Physical examination at this time revealed that the. `, ~+ T2 W  [" }) E4 i. o
child had grown 2.5 cm in 4 months and had gained
$ d' i- s! k! T% ^4 H4 S2 Z) W. |; ^2 kg of weight. Physical examination remained
' {. C- D2 m  G8 w8 O) i# h, z6 W7 p# \3 iunchanged. Surprisingly, the pubic hair almost com-3 Z/ x' v/ ~- @8 A7 w+ A
pletely disappeared except for a few vellous hairs at4 j' y1 x. S; B8 b; f
the base of the phallus. Testicular volume was still 2. J3 ^! G7 [6 V' x) x% F
mL, and the size of the penis remained unchanged.5 I( @& U  q5 n7 A, j1 G
The mother also said that the boy was no longer hav-
& w) B( c6 a# C! C5 H- @, aing frequent erections.
1 u0 I. N* M8 RBoth parents were again questioned about use of. ]& g( |3 Y6 N5 \
any ointment/creams that they may have applied to% ?# W- r$ L) l! r0 j; V
the child’s skin. This time the father admitted the8 C7 g' e5 f! D8 q
Topical Testosterone Exposure / Bhowmick et al 541
$ ^- n. |+ |2 p8 A# ]use of testosterone gel twice daily that he was apply-
. n3 K2 a! n+ h# aing over his own shoulders, chest, and back area for- U! o8 _' d# V0 e: g! A
a year. The father also revealed he was embarrassed
; p) E) o2 C$ r, c7 g" Bto disclose that he was using a testosterone gel pre-2 o" L& Q) R8 W+ I
scribed by his family physician for decreased libido
9 m$ }2 X5 o5 g% i. v' ~secondary to depression.& I% f+ E" Z! z$ O9 F! Y  ~9 z
The child slept in the same bed with parents.4 C4 m7 ]/ c2 s9 ^8 S3 |! `4 S/ ?# ?
The father would hug the baby and hold him on his
  f' d$ v+ ?. Z/ {" T3 |chest for a considerable period of time, causing sig-# x" x4 I/ N' G  S& ^$ z
nificant bare skin contact between baby and father.
2 L5 O9 h7 |4 j( \7 ?6 f- U1 PThe father also admitted that after the phone call,
# h& P2 Q9 j9 y7 z- K  Swhen he learned the testosterone level in the baby
- M/ A4 K! G1 B+ D: w. Uwas high, he then read the product information
3 B/ ^2 g7 n: e2 Wpacket and concluded that it was most likely the rea-: R6 }1 P. z5 N( E( R9 Z
son for the child’s virilization. At that time, they! ^6 v5 P8 ^9 ^2 A( N% `8 q" M
decided to put the baby in a separate bed, and the
7 n3 }; s6 G+ y9 b& i" sfather was not hugging him with bare skin and had
1 c8 b$ r1 R* x# hbeen using protective clothing. A repeat testosterone
3 n# F; e; Q+ C* B6 C, w! |test was ordered, but the family did not go to the# y! e1 L% m9 v
laboratory to obtain the test.
1 H) y& B: N$ T4 v7 X" jDiscussion
; W7 V3 f% s+ n' }9 q- HPrecocious puberty in boys is defined as secondary/ p6 }% R7 K: w# i  m
sexual development before 9 years of age.1,4
7 M1 v: ]" T- g: [; x, OPrecocious puberty is termed as central (true) when' n/ q, e/ O3 D6 m  D- Q! `- k
it is caused by the premature activation of hypo-
  [6 |% U. k' W6 Z2 U% }thalamic pituitary gonadal axis. CPP is more com-1 c/ k8 U( l& k: A5 ?- j
mon in girls than in boys.1,3 Most boys with CPP- M7 K1 g# d3 ~# `: m9 K
may have a central nervous system lesion that is
% V. ]) B& \( e  e, v9 D5 ^responsible for the early activation of the hypothal-
8 v) ^9 A% u1 r6 J' b9 L/ _amic pituitary gonadal axis.1-3 Thus, greater empha-; R3 i2 d' j. p$ g- p4 C
sis has been given to neuroradiologic imaging in! ^9 m: e$ P" A2 y% Y
boys with precocious puberty. In addition to viril-
; p8 m5 n- O1 L7 q% tization, the clinical hallmark of CPP is the symmet-/ Q6 A+ x% z0 [- X
rical testicular growth secondary to stimulation by# f6 A0 E- r% s1 q6 V
gonadotropins.1,3
+ t. {: O9 `, {+ A  B. v3 JGonadotropin-independent peripheral preco-8 X" Q& \6 _) F% v4 m7 _
cious puberty in boys also results from inappropriate
- V9 T7 o. Y$ A" T% w( q9 J4 N4 J( Yandrogenic stimulation from either endogenous or
6 `7 x) M! b$ z$ o2 pexogenous sources, nonpituitary gonadotropin stim-
; c1 V1 g0 N6 {; V" vulation, and rare activating mutations.3 Virilizing
; G0 m  B0 z  q- M  l3 zcongenital adrenal hyperplasia producing excessive
. g; m/ J% e4 iadrenal androgens is a common cause of precocious" `  f. X0 P9 u4 Z, j, ~# l
puberty in boys.3,4- e- u8 s% E) l) f, x
The most common form of congenital adrenal
  s0 S, i( Y; ^) N1 L; Jhyperplasia is the 21-hydroxylase enzyme deficiency., x6 P2 s8 e! V% k6 P- S
The 11-β hydroxylase deficiency may also result in
% ~/ I7 }2 K- O& w: [excessive adrenal androgen production, and rarely,9 c, o& [) x+ ^+ |1 b
an adrenal tumor may also cause adrenal androgen/ O  q5 c3 N# D' t; T- G
excess.1,3
" d6 Q+ g0 d2 Yat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 j% @" r1 E' E! ]/ W8 v542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
4 `( g' p$ r$ c9 C/ L8 UA unique entity of male-limited gonadotropin-
4 E! J, L$ ~$ Q% y7 hindependent precocious puberty, which is also known. a( b0 f* d* d$ \
as testotoxicosis, may cause precocious puberty at a
& X9 k7 f0 i2 {: [9 F* Overy young age. The physical findings in these boys$ Y9 _: d* S8 X/ v( ?: n& @+ ], I
with this disorder are full pubertal development,
+ X7 \# r+ @4 x8 I" ^8 vincluding bilateral testicular growth, similar to boys- i5 e9 T' N# u7 X1 K
with CPP. The gonadotropin levels in this disorder
* O9 f- Z; r" vare suppressed to prepubertal levels and do not show
: `' C) n8 q! X- v. V' x$ Gpubertal response of gonadotropin after gonadotropin-
7 {; ^; \' M8 y* Lreleasing hormone stimulation. This is a sex-linked1 {! P  h9 f' X4 v6 e& C0 U
autosomal dominant disorder that affects only. S4 o4 K! Q' \. q, t
males; therefore, other male members of the family; k3 l1 J; k2 V
may have similar precocious puberty.36 c' r! Y7 _$ J( z' p
In our patient, physical examination was incon-& b$ s, L" I) j9 Y; n
sistent with true precocious puberty since his testi-0 K  D# u: g0 v
cles were prepubertal in size. However, testotoxicosis
" p8 N3 h3 Q; v# gwas in the differential diagnosis because his father+ Z) ]* O2 l1 T3 I$ u4 e
started puberty somewhat early, and occasionally,; M  X" X  W. Z
testicular enlargement is not that evident in the- }' ]& o/ Z3 ^$ ]2 {0 l( Q+ {
beginning of this process.1 In the absence of a neg-
5 w: r* m! p% P4 Y. Bative initial history of androgen exposure, our
& P4 L- H( P1 F( C! c+ y# Abiggest concern was virilizing adrenal hyperplasia,
9 o4 J2 T$ t3 t. L. Heither 21-hydroxylase deficiency or 11-β hydroxylase. |  S" I  p7 F
deficiency. Those diagnoses were excluded by find-, @5 C" ~& l* _' G0 q4 o( l
ing the normal level of adrenal steroids.% u7 N1 a3 J, y2 P# P
The diagnosis of exogenous androgens was strongly* h) i: A# E! o* A1 }/ Y% u) p) T
suspected in a follow-up visit after 4 months because; B# Z7 O% L; V: O1 ]4 E2 B
the physical examination revealed the complete disap-. @' z8 C2 K0 `
pearance of pubic hair, normal growth velocity, and, v( s5 ~5 m& q4 q5 _
decreased erections. The father admitted using a testos-( R* E5 b+ D. i* d
terone gel, which he concealed at first visit. He was# A) L7 u$ @) ~1 U( {9 B& M; T& z- D, ?
using it rather frequently, twice a day. The Physicians’
, z9 F# H$ K0 u' F# YDesk Reference, or package insert of this product, gel or
' o  C3 Z5 A0 c1 S: h* Ccream, cautions about dermal testosterone transfer to7 q, a# }% G% W& P1 M, }- W# c
unprotected females through direct skin exposure.
/ v* I8 I4 y5 J1 iSerum testosterone level was found to be 2 times the
, [9 e4 @& s9 Zbaseline value in those females who were exposed to2 ]7 k9 ~- n6 Z) @- U3 ?
even 15 minutes of direct skin contact with their male3 t- h  w+ n5 P0 d) G
partners.6 However, when a shirt covered the applica-! l; e+ p8 Z' q$ K! k/ |  e
tion site, this testosterone transfer was prevented.
. f: {9 y, M+ _! r% aOur patient’s testosterone level was 60 ng/mL,7 p7 u4 w  g: `1 a: }
which was clearly high. Some studies suggest that- Q# ?- z2 d& ~
dermal conversion of testosterone to dihydrotestos-
1 G7 ^; F& `! y0 e5 F6 uterone, which is a more potent metabolite, is more6 Q8 k' e1 a( q8 s1 B1 |
active in young children exposed to testosterone
' m0 k# c$ O& [: A: |5 B! g% jexogenously7; however, we did not measure a dihy-2 }) p6 a8 C! S; r) t
drotestosterone level in our patient. In addition to& Y7 S2 I; E* |( [
virilization, exposure to exogenous testosterone in( L$ h! ^: a0 I$ j  P" _, y+ _
children results in an increase in growth velocity and  l: _( R, P$ B. D* S$ C+ R8 [
advanced bone age, as seen in our patient.6 m: H, z1 U) b
The long-term effect of androgen exposure during+ v$ a6 h7 A; x% ?
early childhood on pubertal development and final
8 a8 ?/ x1 {$ i, V2 ladult height are not fully known and always remain
5 B5 b7 _* g6 X: N$ b/ R/ \4 h1 P, Ua concern. Children treated with short-term testos-
- A, T, s8 e' h* a9 fterone injection or topical androgen may exhibit some
' L, o% |% @7 V- [: s0 Z. o4 I* |acceleration of the skeletal maturation; however, after& o/ _; z$ P( n4 m
cessation of treatment, the rate of bone maturation
8 }- D9 J8 j& P& V! _decelerates and gradually returns to normal.8,9
5 z3 \$ u. \. |1 y3 |# ~( NThere are conflicting reports and controversy
% M7 G- N% c6 E& jover the effect of early androgen exposure on adult
& ~& h3 y+ k9 L$ ?4 W( p! Dpenile length.10,11 Some reports suggest subnormal, V. i" d4 h) R; [( b; L9 n, m
adult penile length, apparently because of downreg-
5 X: W5 L" k, j) F# s, \* {* W% E+ \ulation of androgen receptor number.10,12 However,
) Y& o" \" T! N2 m0 l, B4 ~Sutherland et al13 did not find a correlation between
  q0 ?8 F6 ^+ n5 O$ Schildhood testosterone exposure and reduced adult6 X0 i4 E$ C: g$ @
penile length in clinical studies.
% D4 E. i; w* f  j; v" K" INonetheless, we do not believe our patient is+ N) X1 v+ @) g* s0 l) d: z7 Q/ _
going to experience any of the untoward effects from
* k1 |2 S' J1 T# |2 e; h: U! Ktestosterone exposure as mentioned earlier because
) }% D5 R) \1 T8 tthe exposure was not for a prolonged period of time.* V; n: L: k4 b: d9 @. h: N0 z
Although the bone age was advanced at the time of
3 I8 u+ u/ K( V( o3 d& X1 Kdiagnosis, the child had a normal growth velocity at7 p6 c5 V5 x, e) K) D
the follow-up visit. It is hoped that his final adult
, F* |4 ~& F4 \! d- kheight will not be affected.
8 K1 B2 n5 B- H7 WAlthough rarely reported, the widespread avail-
$ |$ b" r: G1 a, o" S$ K/ r' fability of androgen products in our society may; k: e8 g- @4 I) `- x' b4 A
indeed cause more virilization in male or female
) n4 a, O2 b; }* Hchildren than one would realize. Exposure to andro-
1 R1 S8 i" @" {# ?! T1 lgen products must be considered and specific ques-
$ j7 w) t0 _( U; _' M& d; Vtioning about the use of a testosterone product or
3 Q# S0 n# K. X/ [gel should be asked of the family members during
, `# H) {1 \/ p% z3 pthe evaluation of any children who present with vir-- F" n( A/ b8 N: A4 Q8 U8 k2 U
ilization or peripheral precocious puberty. The diag-
! }5 L( F: o) h# O. xnosis can be established by just a few tests and by
. C; a( x6 A. }% Oappropriate history. The inability to obtain such a
, [* B! |: L& w7 f9 ~history, or failure to ask the specific questions, may
3 U& b2 B' F! z6 aresult in extensive, unnecessary, and expensive
2 Q6 c( K5 k3 n" X* ?investigation. The primary care physician should be
! p3 Q, B; P0 T' zaware of this fact, because most of these children* c7 o" E; \( D' v
may initially present in their practice. The Physicians’
0 M# c. T9 c8 S9 WDesk Reference and package insert should also put a. S" K8 }0 e8 Z& w5 `* @! m
warning about the virilizing effect on a male or$ t( b7 ^* s6 I! b% v# s1 b/ Q
female child who might come in contact with some-
6 q2 a2 @5 B- K. tone using any of these products.: T% P' L$ U$ w; w: M1 B
References; I$ S9 }1 K6 g4 a9 t
1. Styne DM. The testes: disorder of sexual differentiation
1 r: x5 K% s5 i* m2 fand puberty in the male. In: Sperling MA, ed. Pediatric
7 ]* X: O- p' `5 \7 _/ cEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;3 M: K" _9 ?, [4 j4 f
2002: 565-628.3 ]( j3 |. ?( C; q% L+ K
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious: X; S# c* q1 d& N- H
puberty 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
% Q) J9 G' G$ q- e6 v; }& n
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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