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Sexual Precocity in a 16-Month-Old/ O8 g- |/ W* s
Boy Induced by Indirect Topical) p$ N3 M- H! [& K
Exposure to Testosterone
6 n5 O4 R# i9 v2 `0 _1 tSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
5 v" m$ Q8 x0 b* K! ^7 fand Kenneth R. Rettig, MD1
; s) N  Y5 C' G9 U7 o- S6 AClinical Pediatrics
- F- [/ I- x' q# {5 jVolume 46 Number 6& H0 J2 p9 r. M, Y% E9 Q5 o
July 2007 540-543' v, m8 m; }* K+ }& h
© 2007 Sage Publications
1 ~% v' {# k( u) i) a# f7 c10.1177/0009922806296651
" y1 K  E: @2 N7 _* B. Ahttp://clp.sagepub.com
$ }# Y2 [  G2 u" xhosted at+ N  y, `0 j" f
http://online.sagepub.com' j- }1 D, L  ^
Precocious puberty in boys, central or peripheral,
; j' V: M/ D4 m7 X8 n0 ~/ uis a significant concern for physicians. Central
6 D1 Q. G! k6 S& u$ W, p- r+ [precocious puberty (CPP), which is mediated
2 |  H# `1 i+ Cthrough the hypothalamic pituitary gonadal axis, has
! @6 ]0 c& v) ^+ va higher incidence of organic central nervous system0 f' C" N1 Q0 z, @' M: _, ?0 k* a: a
lesions in boys.1,2 Virilization in boys, as manifested' z1 T- ~, }" X) e
by enlargement of the penis, development of pubic
. @1 G* {' b8 v0 G8 Xhair, and facial acne without enlargement of testi-8 b0 I7 u- z- S
cles, suggests peripheral or pseudopuberty.1-3 We) i2 W$ k5 f: X8 H5 v
report a 16-month-old boy who presented with the
1 y, l& @7 z5 N. m6 B+ Benlargement of the phallus and pubic hair develop-
: j) m5 F1 H! w2 s  a. mment without testicular enlargement, which was due3 z$ \/ A- Z* i' E! s
to the unintentional exposure to androgen gel used by6 n. Y" S' g3 i6 X
the father. The family initially concealed this infor-
0 l% F9 ~0 q, H- }" i6 U* w$ imation, resulting in an extensive work-up for this/ A; z1 u, Z% ?) ^& ?3 D
child. Given the widespread and easy availability of" o4 p5 N% ?0 i# ^- R2 n
testosterone gel and cream, we believe this is proba-
5 v1 J# l1 \9 M# Y/ N1 jbly more common than the rare case report in the8 d- k. |! _' v2 x8 _) U$ X( N
literature.45 m) }& L  ?; c% B) E+ d& O
Patient Report; V) k0 |3 _3 b
A 16-month-old white child was referred to the
6 X) n5 j5 K  ?endocrine clinic by his pediatrician with the concern
- d/ G% Y$ ?* |of early sexual development. His mother noticed
5 P/ y9 S( j, x6 L3 S* [1 r* ?8 Glight colored pubic hair development when he was7 q1 b) A  o- E8 L/ \6 N# Y" @# w
From the 1Division of Pediatric Endocrinology, 2University of8 x# ]/ g$ T) z' ?" e% b; F
South Alabama Medical Center, Mobile, Alabama.
# b. d9 b, M% {$ v8 s1 o7 Y" z! cAddress correspondence to: Samar K. Bhowmick, MD, FACE,
1 A/ v+ d3 E6 S1 V" S$ G" MProfessor of Pediatrics, University of South Alabama, College of
( l7 o0 D. q, P: K" EMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;( ~* i; [, s7 [
e-mail: [email protected].5 q$ m& l2 @# i' s
about 6 to 7 months old, which progressively became9 r4 A7 k) |7 Z0 j. J2 l8 n1 }
darker. She was also concerned about the enlarge-
; R% @+ ?0 ]; z; r- n8 w0 r% c  t. k7 ument of his penis and frequent erections. The child
6 R4 T/ n6 Z( d" l, vwas the product of a full-term normal delivery, with2 T* ~/ O! {  |8 l6 p, L- q
a birth weight of 7 lb 14 oz, and birth length of7 s- d: M' z6 ^' ~4 C! i8 f
20 inches. He was breast-fed throughout the first year2 Q: H% H( c5 G8 ]9 N2 x) r
of life and was still receiving breast milk along with
7 |( d( E+ U& R: E; ?solid food. He had no hospitalizations or surgery,
" {: d) ]8 l+ V0 H2 k6 fand his psychosocial and psychomotor development6 s1 q( U+ `# S
was age appropriate.
7 T) i% z! `3 k9 E2 |  O: t- iThe family history was remarkable for the father,
7 w, P% R+ D% x$ V& p# pwho was diagnosed with hypothyroidism at age 16,& S- l3 ~$ z$ B, C9 U
which was treated with thyroxine. The father’s
1 H  a8 o7 T3 Hheight was 6 feet, and he went through a somewhat
& l! `) Z1 e' c+ G1 I2 W; e1 tearly puberty and had stopped growing by age 14.
0 i. V# q8 g- n" j8 dThe father denied taking any other medication. The
( b: F6 C' D6 _# v& R, j% mchild’s mother was in good health. Her menarche' B: O: u9 `' l
was at 11 years of age, and her height was at 5 feet
0 n1 a' T3 F' y, S$ _+ J0 k5 inches. There was no other family history of pre-; z$ W2 z. g9 ?) G0 P
cocious sexual development in the first-degree rela-
1 |+ T. E: Y# R# ltives. There were no siblings.9 a# N$ s) Y* k4 U, n  c; @
Physical Examination
3 X9 W5 X5 t/ h) G- BThe physical examination revealed a very active,! W- t+ o) r( k" j; Y
playful, and healthy boy. The vital signs documented9 I1 h" U& ~" X* _
a blood pressure of 85/50 mm Hg, his length was
' A4 x% i# j* K: i/ a" {% X90 cm (>97th percentile), and his weight was 14.4 kg8 ]) u( {( `) _( V4 F9 t' A
(also >97th percentile). The observed yearly growth
: P3 N/ O' v6 P  o: mvelocity was 30 cm (12 inches). The examination of
( h4 Z0 c' }3 jthe neck revealed no thyroid enlargement., ]& c* e" n' R" k3 p
The genitourinary examination was remarkable for
8 w& p% N" M8 |! K  ^9 ienlargement of the penis, with a stretched length of8 K. P6 S& k3 r# M) [( D6 Q7 R8 @
8 cm and a width of 2 cm. The glans penis was very well1 E2 U2 v. S0 P- D5 w& W
developed. The pubic hair was Tanner II, mostly around' d, m5 x( c" S* t$ B, j" r
540
4 O9 }. R& x/ @2 E% F' {at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# z: X3 L$ A+ b, k4 u0 F4 B6 x' Dthe base of the phallus and was dark and curled. The
9 ^) t. J9 n  a8 utesticular volume was prepubertal at 2 mL each.0 f0 A7 T# Z! g' G5 t( I
The skin was moist and smooth and somewhat; y  s! t7 @4 |6 U0 c
oily. No axillary hair was noted. There were no
0 D, V9 A% j) T/ \abnormal skin pigmentations or café-au-lait spots.+ n* C6 w1 o: V( m" \- y+ @
Neurologic evaluation showed deep tendon reflex 2+! v- x' q+ v) s0 m2 |) a4 P3 o
bilateral and symmetrical. There was no suggestion" M3 y- X9 ^4 B( h, ^$ h
of papilledema.: _. \( x4 L2 c$ Y7 v1 ^3 t3 C* Y6 d
Laboratory Evaluation
# y( z- M2 B. [) XThe bone age was consistent with 28 months by, t8 c- \! u( d" }6 Z. S' `! E
using the standard of Greulich and Pyle at a chrono-5 T& m1 v! {  R; P) e
logic age of 16 months (advanced).5 Chromosomal
2 M. c& \* H: P2 a: Xkaryotype was 46XY. The thyroid function test
( ?3 T8 r: y0 Q/ z. D; o2 C$ U) fshowed a free T4 of 1.69 ng/dL, and thyroid stimu-' j& v8 J) O% o; P0 G( i
lating hormone level was 1.3 µIU/mL (both normal).
3 Y  h" v8 t* W  OThe concentrations of serum electrolytes, blood# |4 b, g. O* `* h- t% [
urea nitrogen, creatinine, and calcium all were
9 `" ?# U( u5 _5 d- G7 g$ ?within normal range for his age. The concentration# P1 p- `" c8 S# d# A* A3 W/ L
of serum 17-hydroxyprogesterone was 16 ng/dL6 u! ^3 {; O( N1 N! l# y( @+ @* e2 C
(normal, 3 to 90 ng/dL), androstenedione was 20
+ x( G) F! G# |! J* X0 K( xng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-1 w) I# p+ E) y8 c. l, ^
terone was 38 ng/dL (normal, 50 to 760 ng/dL),; z3 V& ^! O& k0 c2 Z
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
) [2 p# [" z; N0 C! f  A+ X9 m( e/ W49ng/dL), 11-desoxycortisol (specific compound S)7 u2 F# r( _2 {& u7 N- n: t
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# D$ H4 {2 o1 Z4 c2 _4 B: M& \
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total! ]6 i, h" d  @: d8 U
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
% F4 e) \+ ^$ D8 F5 `and β-human chorionic gonadotropin was less than
0 n- |& q9 k% B+ r* |) z: a6 f5 mIU/mL (normal <5 mIU/mL). Serum follicular
( @: O6 v1 h: v, A- h! {stimulating hormone and leuteinizing hormone
4 K8 W5 i* a8 }& m9 O# Vconcentrations were less than 0.05 mIU/mL3 T! J5 q- V. R2 `! h/ R
(prepubertal).  f* i% X9 |3 y9 \% R
The parents were notified about the laboratory
% @; b4 F  P% g4 ^% l# r6 A  gresults and were informed that all of the tests were6 r+ v1 O* N+ P9 b7 Q2 h& g3 o) A6 w& `
normal except the testosterone level was high. The
0 i1 o0 F5 }& D2 W  P4 l, i8 a& yfollow-up visit was arranged within a few weeks to% y( ]- t  O* g) H! `) ?3 @
obtain testicular and abdominal sonograms; how-
6 e2 `9 }0 D2 ~+ J8 x7 P1 K* fever, the family did not return for 4 months.3 @9 z5 R2 F6 N6 Z: P
Physical examination at this time revealed that the
2 ^9 |* n1 W; z1 ?0 ~8 t) g$ Qchild had grown 2.5 cm in 4 months and had gained
) \1 R' D$ [) ~% T! Y  ^; F2 kg of weight. Physical examination remained
" f1 A% x8 N* [1 U% zunchanged. Surprisingly, the pubic hair almost com-
$ Q! l6 {/ ?% v8 Fpletely disappeared except for a few vellous hairs at
$ }) X: i8 K( L: \8 f8 c- Pthe base of the phallus. Testicular volume was still 2
; [4 C: c' E+ Y* V" V0 g2 CmL, and the size of the penis remained unchanged.3 V! T, K8 C7 Y  {% i+ c4 ?
The mother also said that the boy was no longer hav-
3 N0 r, G0 ^1 C, C, c/ z7 Ving frequent erections.$ y1 Z/ a* G* c  X$ G6 W3 E
Both parents were again questioned about use of
* S/ H) b0 Q* qany ointment/creams that they may have applied to
( r2 j( @( v* j: ]$ ]- othe child’s skin. This time the father admitted the1 k' H7 s) p- F" S  t) g
Topical Testosterone Exposure / Bhowmick et al 541
& F" w, P3 Q6 U2 s6 I2 ause of testosterone gel twice daily that he was apply-
0 E  {9 N3 ]. L- z' a( ping over his own shoulders, chest, and back area for
1 w/ T4 g( `2 T) I* ]( Ca year. The father also revealed he was embarrassed: o) o9 p% Y5 K; W
to disclose that he was using a testosterone gel pre-
% e2 Y$ y) K: m8 d+ w# }7 T( hscribed by his family physician for decreased libido
3 ^+ R5 Q" }1 U* r* y. V: `& Rsecondary to depression./ v& o# o+ I9 t) w7 X
The child slept in the same bed with parents.& O* I+ J- b: w" p- F
The father would hug the baby and hold him on his. l' W- M" W7 h1 t, ^3 U. l
chest for a considerable period of time, causing sig-
) H9 ?+ m$ Y9 ynificant bare skin contact between baby and father.8 b  m; N6 ?. D% s2 o5 _4 ?
The father also admitted that after the phone call,7 `/ t/ x) w6 E( R4 ]
when he learned the testosterone level in the baby
) L3 _9 y  L- i! T/ d& k+ zwas high, he then read the product information
% ], {/ j7 X" X: _/ N/ i) U3 rpacket and concluded that it was most likely the rea-
8 p6 Q4 M" m4 w6 b& @- ^son for the child’s virilization. At that time, they
( F( f# }! Z5 L; Q# J5 c& Kdecided to put the baby in a separate bed, and the6 {& q. B' k! X+ w1 q2 k1 t4 S$ ~0 j
father was not hugging him with bare skin and had
8 ]4 P, v/ l. q  W4 Ubeen using protective clothing. A repeat testosterone) g# l2 V$ G1 J3 W: p* h7 P
test was ordered, but the family did not go to the- q. W$ o' R9 b7 m" d; u
laboratory to obtain the test.. P4 z  k/ N- n/ w/ s- |  Z
Discussion* v0 L) K, O) d
Precocious puberty in boys is defined as secondary( o9 W2 t9 B" A5 W/ o
sexual development before 9 years of age.1,4' c1 d9 N3 a6 H
Precocious puberty is termed as central (true) when
' ?/ j. o. N8 D% Cit is caused by the premature activation of hypo-
7 K4 [4 q9 U1 t9 Y" c, @5 Rthalamic pituitary gonadal axis. CPP is more com-* U& E  s  f8 a" E
mon in girls than in boys.1,3 Most boys with CPP
& M' e" h: O& ?  b% Gmay have a central nervous system lesion that is
) n2 t0 ?/ q, s2 A$ M: j( Cresponsible for the early activation of the hypothal-; m# ^. K. k* o, g+ c
amic pituitary gonadal axis.1-3 Thus, greater empha-
; T8 V6 u  U. L" a3 Tsis has been given to neuroradiologic imaging in3 @3 m9 t3 J# c4 w
boys with precocious puberty. In addition to viril-
4 Z1 ~! i" T  ^2 A: x3 e6 Wization, the clinical hallmark of CPP is the symmet-
  s. F; @" i; U5 crical testicular growth secondary to stimulation by
- W3 \6 I+ `- I3 @  Y$ Egonadotropins.1,3! S3 J& {5 f7 j
Gonadotropin-independent peripheral preco-% D# _/ w! Y. M3 R6 V' C5 w7 s* N* g
cious puberty in boys also results from inappropriate
+ h. T" ^. y( |; h- V7 r( pandrogenic stimulation from either endogenous or5 B9 f/ B4 b/ V9 l
exogenous sources, nonpituitary gonadotropin stim-  T% a! c+ D( `. k' u: I
ulation, and rare activating mutations.3 Virilizing; Y  @4 ]4 H! N2 A; @' [. ]
congenital adrenal hyperplasia producing excessive( X5 b5 Y# Y' n! I# W" @
adrenal androgens is a common cause of precocious, G/ j7 e8 h" X7 b2 ?9 I" f* e/ l* e
puberty in boys.3,4& s  u# `5 x# p1 I. b" f5 L
The most common form of congenital adrenal. M( A8 D" G# ~+ n3 z
hyperplasia is the 21-hydroxylase enzyme deficiency.8 w# l4 X2 s+ W7 L
The 11-β hydroxylase deficiency may also result in  F# F) P4 G, W; q% {' m
excessive adrenal androgen production, and rarely,3 v- X- g- n6 e9 X, u% h
an adrenal tumor may also cause adrenal androgen+ x) n  y% W1 v/ ^. @* a
excess.1,3
7 [: U8 P# y8 C2 j0 P: Rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 N0 N: \7 P! V' O9 F# K5 a
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007& H( P3 n( u, }
A unique entity of male-limited gonadotropin-
1 Y2 i; B: j& X6 ]! w, n, }: Rindependent precocious puberty, which is also known4 i$ G% O: \) I% @9 Q
as testotoxicosis, may cause precocious puberty at a
4 c6 y# P$ C& `very young age. The physical findings in these boys/ D0 }3 g# J; j, m: [" L; p
with this disorder are full pubertal development,
) }3 j! p" W) Z1 y1 K0 Kincluding bilateral testicular growth, similar to boys7 m3 f) S' C" B1 L/ @9 q  p
with CPP. The gonadotropin levels in this disorder
) c1 r/ E0 Y, ~0 B# |are suppressed to prepubertal levels and do not show
( P. y( G" F0 Y/ ]pubertal response of gonadotropin after gonadotropin-/ E" V+ U* A+ o4 r) j
releasing hormone stimulation. This is a sex-linked1 J0 {2 e% V3 o9 ?* e
autosomal dominant disorder that affects only
! O& _) Q1 h! T: dmales; therefore, other male members of the family
, n- u  a" @$ K2 Q$ H# s5 _may have similar precocious puberty.3# `/ M; C9 B* d0 F# h
In our patient, physical examination was incon-& ^9 ~* T0 d+ J8 D+ ^' ^* a
sistent with true precocious puberty since his testi-
0 N9 H- A; D. H" `7 e+ _cles were prepubertal in size. However, testotoxicosis* x* z& U# j  a7 `3 W- T
was in the differential diagnosis because his father
' w/ E1 Z, c, A) ?started puberty somewhat early, and occasionally,
+ h8 z- S3 ?0 r7 itesticular enlargement is not that evident in the4 s& a5 d- c( B& c( X- j
beginning of this process.1 In the absence of a neg-
+ R- Q3 j- Z* S! X* z6 yative initial history of androgen exposure, our
8 L$ o* L, \- T+ ~biggest concern was virilizing adrenal hyperplasia,1 {. Y9 u- M9 V( {
either 21-hydroxylase deficiency or 11-β hydroxylase5 e  F, |2 Q  _; @4 A1 B: r
deficiency. Those diagnoses were excluded by find-
- N) M) r, T+ j* Ting the normal level of adrenal steroids.
% L! h# C, m4 s* t4 c9 VThe diagnosis of exogenous androgens was strongly; c% C/ M; y! y9 R: C
suspected in a follow-up visit after 4 months because
2 o4 n4 W4 z4 m8 m- lthe physical examination revealed the complete disap-! F  J3 E5 z+ v* F2 z9 L) \3 X
pearance of pubic hair, normal growth velocity, and
6 y9 x& Z/ G" m( ^2 H" wdecreased erections. The father admitted using a testos-
1 i4 V  L" M7 C" M  vterone gel, which he concealed at first visit. He was
& f" }( O1 r0 h$ k1 ^& Ausing it rather frequently, twice a day. The Physicians’% ^' H, W1 f0 v( [. L5 T: q7 X
Desk Reference, or package insert of this product, gel or, A2 J9 p, ^( ^
cream, cautions about dermal testosterone transfer to
3 b, {2 ~6 P, l: punprotected females through direct skin exposure.
; J4 ^2 p4 R$ [" v: H3 |Serum testosterone level was found to be 2 times the  J, M( p+ R7 y" D
baseline value in those females who were exposed to1 Z/ P% M9 U1 F" m
even 15 minutes of direct skin contact with their male2 q* m4 n' x6 H5 F
partners.6 However, when a shirt covered the applica-
/ S- C. K& v2 y# o6 stion site, this testosterone transfer was prevented.
! q7 m5 b# t. S( c0 B" Q: dOur patient’s testosterone level was 60 ng/mL,1 I/ i1 Q) @- a0 w% _( h" r
which was clearly high. Some studies suggest that+ J$ g8 f; G( T7 `
dermal conversion of testosterone to dihydrotestos-
- r' _# B+ L1 J5 Pterone, which is a more potent metabolite, is more
# }4 Q1 W! S1 n' _5 cactive in young children exposed to testosterone
- b2 u, e7 y5 [6 s( r9 H5 I1 ?exogenously7; however, we did not measure a dihy-3 R/ ]( g& K9 J; B  A
drotestosterone level in our patient. In addition to5 E' e0 a% X9 Z. G) p2 B
virilization, exposure to exogenous testosterone in7 J2 C! k( [3 ^" l
children results in an increase in growth velocity and
" H  c, Z% _+ Z# ?3 l5 f& I  _6 L* l% Uadvanced bone age, as seen in our patient.
7 \5 J4 N+ O4 X! I2 cThe long-term effect of androgen exposure during
, M# Y! h+ {9 d* f' v% Y# T5 d. C; _early childhood on pubertal development and final& |5 _5 k7 ~& ~
adult height are not fully known and always remain
8 t8 Z; r6 f- }a concern. Children treated with short-term testos-
. x3 n1 ?1 G2 zterone injection or topical androgen may exhibit some: B( x5 n  a. ]3 _$ V8 L3 z
acceleration of the skeletal maturation; however, after& C2 F$ ]5 k# y9 _; v$ p
cessation of treatment, the rate of bone maturation/ A: [: f: f3 H% j4 T
decelerates and gradually returns to normal.8,94 z  J7 R% E' P; T
There are conflicting reports and controversy
  r1 u' X- D. T+ B7 J+ ?/ H3 Sover the effect of early androgen exposure on adult
! o: f" O: r' D: `penile length.10,11 Some reports suggest subnormal# l0 f1 l0 ~" Q( v! _4 Y
adult penile length, apparently because of downreg-
! `/ P+ p$ R' s. B2 c1 Qulation of androgen receptor number.10,12 However,2 e3 k1 E# Y& m3 `9 B/ I
Sutherland et al13 did not find a correlation between
  c9 D" Z0 p2 t" l7 k& C. G' k* {childhood testosterone exposure and reduced adult& I# C* B" B  v/ M8 Q. ~, K" e
penile length in clinical studies.5 }. G/ U; f" i9 k6 Z9 ?
Nonetheless, we do not believe our patient is5 @4 e) D8 @+ P. z3 |: g# c! G# s5 G
going to experience any of the untoward effects from! N' q& C* k" u6 j  A
testosterone exposure as mentioned earlier because0 s7 l  C( [' T- B8 F, g5 t% G
the exposure was not for a prolonged period of time.
- ^" }. B  J9 z; z$ uAlthough the bone age was advanced at the time of! X+ I  M! [$ t" `: _% p
diagnosis, the child had a normal growth velocity at
( g, F1 t8 X  C. @the follow-up visit. It is hoped that his final adult
! M! N$ A* j& m( y8 |# D  T" rheight will not be affected.
; d. A8 X2 E* a; JAlthough rarely reported, the widespread avail-. y# X5 c, V; F6 ^" z" U- z, I
ability of androgen products in our society may
& r) d6 I& c0 r, d, X9 C6 u  U5 r( |! Zindeed cause more virilization in male or female) m) ]% m6 X7 {4 J+ b$ ?8 I
children than one would realize. Exposure to andro-4 B: Y/ R$ L, U0 f
gen products must be considered and specific ques-
9 B) e6 \" w' c3 Z. z' \" ntioning about the use of a testosterone product or. q! J2 X$ ?8 s: d: G6 a
gel should be asked of the family members during
; U+ i0 z' [1 z- g8 jthe evaluation of any children who present with vir-2 V! A+ m: ^7 f' l4 i
ilization or peripheral precocious puberty. The diag-
8 N9 X0 E/ N& x* U4 Anosis can be established by just a few tests and by
/ I( U. G: U7 M$ z+ eappropriate history. The inability to obtain such a
' O4 q2 x8 m& w* Q- V6 ^+ [  t7 ^6 P; Whistory, or failure to ask the specific questions, may
% }; m; i+ n6 Iresult in extensive, unnecessary, and expensive
$ r8 Z- C( t3 hinvestigation. The primary care physician should be
0 L: _& k8 n! i# ^* j4 x5 zaware of this fact, because most of these children
& o$ C" T3 Q: s4 Z& h: o+ w: Gmay initially present in their practice. The Physicians’2 a' r* i/ K* A/ h
Desk Reference and package insert should also put a0 R" d. \' O  i
warning about the virilizing effect on a male or
' P  [, E4 a& t$ _! Lfemale child who might come in contact with some-
6 @* g& U. H7 s6 o  u+ Lone using any of these products.) q  l" Y& @% r9 c  X; M6 A
References6 Y) V& Q* Q' ]( o1 p" A
1. Styne DM. The testes: disorder of sexual differentiation, f3 w3 o7 u, h' T! j
and puberty in the male. In: Sperling MA, ed. Pediatric
8 k0 Y; X" u0 n% W) W; }Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
! G3 x! W1 J  c8 E8 g2002: 565-628.
/ u( o! H. j/ A8 a4 u2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious2 ^; Y' g$ ^" n) c7 G
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
, V" y+ v8 }9 B, JBoy Induced by Indirect Topical
7 ~% x' U8 r" v/ A9 A- x& |3 f) [Exposure to Testosterone
/ ^( r' `5 v1 }Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,27 N  N& P( N- |* L3 e8 ~
and Kenneth R. Rettig, MD1- ?* j( O4 s. n
Clinical Pediatrics
+ \6 q1 a6 R( K3 t. [( vVolume 46 Number 66 I  L+ O/ o0 g) Q
July 2007 540-543& T' k0 r  C8 F$ |$ m+ [
© 2007 Sage Publications) h6 O4 x0 ^6 e, S% \
10.1177/0009922806296651
+ d7 {( @  s" D; a& C% mhttp://clp.sagepub.com' I0 g( U3 `- V
hosted at2 M, k3 k; L! a5 L1 y; @
http://online.sagepub.com
! A- b( h% I% v/ q7 `Precocious puberty in boys, central or peripheral,) Y5 s0 E2 Y& g$ r; d0 ?
is a significant concern for physicians. Central% e4 j! B1 j. w- e) [
precocious puberty (CPP), which is mediated
# m, q9 Y) v* Q; Q8 w* Y# jthrough the hypothalamic pituitary gonadal axis, has
4 I+ H7 B0 F  Ma higher incidence of organic central nervous system
0 \; E' V* W& M3 ?8 B" D2 i) Zlesions in boys.1,2 Virilization in boys, as manifested. j* k( K% P& l* C
by enlargement of the penis, development of pubic
# V$ ]7 f1 ~/ Q* f: |hair, and facial acne without enlargement of testi-
" u) g6 B5 M( X0 mcles, suggests peripheral or pseudopuberty.1-3 We5 o/ h; [4 k, x8 _( H8 B; d' X) l
report a 16-month-old boy who presented with the: R6 J' X/ K7 i( I/ \
enlargement of the phallus and pubic hair develop-1 q7 A" V, }7 h; I7 V! O  K
ment without testicular enlargement, which was due. @8 V# J: J5 t- ?* K5 h
to the unintentional exposure to androgen gel used by! _7 U( G  V. L' A8 u* z. y
the father. The family initially concealed this infor-
2 m. b4 r$ j; G7 F# @, Fmation, resulting in an extensive work-up for this
" y7 T% @( A# _% Tchild. Given the widespread and easy availability of
' ]( Z4 [* M! F: j3 `' \testosterone gel and cream, we believe this is proba-
- ?3 C$ [' |( ?* Dbly more common than the rare case report in the! Q: l3 {- U. A, F+ ]" F( i
literature.4( L# T* P& p/ N5 v
Patient Report
& j7 ]; E! M/ N( o3 D" ?: pA 16-month-old white child was referred to the
$ o/ r) r- w5 r1 w2 }! |endocrine clinic by his pediatrician with the concern
" k7 Q; P0 S: u( F3 {: u8 ~of early sexual development. His mother noticed
7 k! H6 k- \" U! e- R+ Nlight colored pubic hair development when he was
5 Q- p7 }6 ~' nFrom the 1Division of Pediatric Endocrinology, 2University of  p9 f9 s. I; w/ I) P7 K7 O
South Alabama Medical Center, Mobile, Alabama.' ^; k1 F1 ~5 @) Y: D9 Y, Q
Address correspondence to: Samar K. Bhowmick, MD, FACE,
9 W) r5 E+ P: K2 V5 A6 D9 r! |! jProfessor of Pediatrics, University of South Alabama, College of6 o# H+ ]2 j- Q5 R& y
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
+ B1 ~+ l/ ?! w+ {5 P( ]* {e-mail: [email protected].
4 @, a. V3 U$ [1 ^1 Labout 6 to 7 months old, which progressively became: X" o9 U( P; T5 F% H0 B" [
darker. She was also concerned about the enlarge-1 v/ e( z, `9 y  ]
ment of his penis and frequent erections. The child' S; ?9 w4 F4 t
was the product of a full-term normal delivery, with/ v, K2 E4 c/ o/ w$ Q; g3 l
a birth weight of 7 lb 14 oz, and birth length of
" c9 `! O' f% ^' i, A20 inches. He was breast-fed throughout the first year9 J2 ^7 X4 E  L5 I, h/ h
of life and was still receiving breast milk along with
& H2 V% S9 l$ `3 y* ?solid food. He had no hospitalizations or surgery,! u, M) K0 i! I( k( q% `2 P
and his psychosocial and psychomotor development4 z4 a3 F1 M5 C
was age appropriate.
$ [* E4 r/ T) Y' @" q' |The family history was remarkable for the father,
" X" ^8 }; H+ Xwho was diagnosed with hypothyroidism at age 16,3 W) a+ A4 y' g7 z8 F
which was treated with thyroxine. The father’s( u5 j& F- _4 e; h1 V
height was 6 feet, and he went through a somewhat
: I* A- \0 t! ^; Q1 e: Mearly puberty and had stopped growing by age 14.& ?" o: @+ u7 V/ K8 R
The father denied taking any other medication. The( ?  S0 t, W3 l" {+ V. R+ l
child’s mother was in good health. Her menarche
9 \9 w, `5 ~9 m" l. p8 lwas at 11 years of age, and her height was at 5 feet
3 ^2 W/ a; r; B- V$ r5 inches. There was no other family history of pre-
% C  c- G6 ?1 V1 q1 [* x; Ccocious sexual development in the first-degree rela-" s9 X9 c# r( x2 ?( d* `1 V( q: e
tives. There were no siblings.. t, V( ?8 V+ N$ R7 h" q
Physical Examination( `, p3 I9 G/ N
The physical examination revealed a very active,
3 e7 H5 z! J* _1 wplayful, and healthy boy. The vital signs documented
% N# l% F5 }' R9 g, |. T( R* Va blood pressure of 85/50 mm Hg, his length was) k! ]; q: `- m. d
90 cm (>97th percentile), and his weight was 14.4 kg
4 Y& S) _5 _& c/ l& b( l! p# x8 B& i1 ~(also >97th percentile). The observed yearly growth6 z) p% Y0 I0 {' ]# d4 a
velocity was 30 cm (12 inches). The examination of
# [( K( z$ S+ K7 X8 G2 y7 Ythe neck revealed no thyroid enlargement.+ Z5 P8 X3 `: V$ i
The genitourinary examination was remarkable for
' s' B  h! K! t* f$ Z9 D) h3 Henlargement of the penis, with a stretched length of7 P( ^/ d, A& c2 j% X0 r) w
8 cm and a width of 2 cm. The glans penis was very well
% k: V# [; o" @& o1 \developed. The pubic hair was Tanner II, mostly around
2 Z$ K$ i6 C% L  j! Y' ]6 Q540
, M+ j) C4 j" e5 e  cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: E! H) f( B( Q, s: i0 p4 p9 x
the base of the phallus and was dark and curled. The; N7 t. v, W8 L! T; m
testicular volume was prepubertal at 2 mL each.* O! L3 j* P& D& k
The skin was moist and smooth and somewhat9 J' |( o. w3 q, g
oily. No axillary hair was noted. There were no$ m1 s* r6 ?$ [1 _
abnormal skin pigmentations or café-au-lait spots.& ^5 b, f" f/ T$ ^
Neurologic evaluation showed deep tendon reflex 2+8 f( K" t% `# c1 {/ ]# K4 R
bilateral and symmetrical. There was no suggestion* w2 O* V$ P# H+ s: b+ s& V
of papilledema.
, R# `' h3 l' F0 v) RLaboratory Evaluation
  }; E4 z: F/ n2 X8 d" x9 A9 z% qThe bone age was consistent with 28 months by9 E5 @3 ?3 K7 G- U7 b# L
using the standard of Greulich and Pyle at a chrono-' g" u: i( G/ u4 P$ C( `
logic age of 16 months (advanced).5 Chromosomal5 G+ i( `1 I! d, H. q0 R
karyotype was 46XY. The thyroid function test6 B( E- M: W: u( r: ]0 f
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
9 [2 r$ v( J7 b1 e9 @) ]# elating hormone level was 1.3 µIU/mL (both normal).; C7 B  P& V& m0 Y7 j
The concentrations of serum electrolytes, blood
: k- u) A: P, m) K: W; Jurea nitrogen, creatinine, and calcium all were
' a( F2 `  E' ywithin normal range for his age. The concentration
! [/ T/ J8 J4 x6 w  b: X5 z$ Rof serum 17-hydroxyprogesterone was 16 ng/dL
" B0 f: e7 G3 @4 h) D: O/ y(normal, 3 to 90 ng/dL), androstenedione was 20- v' Q1 d8 ~, u& m% Q
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-* z6 _# o- C* |  ]) p% ]6 o  S
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
- \1 b9 L  n+ U! I( d9 k5 |6 Hdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
$ i, L( j3 K) y49ng/dL), 11-desoxycortisol (specific compound S)
* g$ |# g. F7 b' m/ t% cwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
9 v# V+ w! E6 ^0 R3 ttisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
) T9 C; X1 E+ y" R$ Htestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
. q) ^% p, r# x) I' F+ Pand β-human chorionic gonadotropin was less than2 b8 |8 C7 Z$ L* `" E4 I/ X- @
5 mIU/mL (normal <5 mIU/mL). Serum follicular* `* D, h. z5 |; u; F# ]% z% D! y$ p
stimulating hormone and leuteinizing hormone
6 H+ A# r; A1 l" ]! f- mconcentrations were less than 0.05 mIU/mL
) N- g. W: ]- L, G(prepubertal).
- r8 k1 q/ P9 ~The parents were notified about the laboratory5 k3 K: d4 t4 d
results and were informed that all of the tests were
. C: b& h8 L% l* w* b8 _! `7 a3 Unormal except the testosterone level was high. The
  c7 Q7 M  [$ E9 E1 ~: n- s  Y; u: yfollow-up visit was arranged within a few weeks to3 N# e9 q, O/ V& q
obtain testicular and abdominal sonograms; how-
* _' p1 H. n+ r$ o; W7 Hever, the family did not return for 4 months.. e2 W) }" q/ l/ Y) X# q" g0 c6 l
Physical examination at this time revealed that the
. U! ]$ T- }2 ~& _& _4 O& qchild had grown 2.5 cm in 4 months and had gained
1 j) l  R! H; D3 n# K1 b3 D9 {: a2 kg of weight. Physical examination remained
7 w4 F+ x/ [' f+ L, \) p& p+ `unchanged. Surprisingly, the pubic hair almost com-0 {, W5 A: X6 P' L
pletely disappeared except for a few vellous hairs at& F) t5 H/ T0 J2 q
the base of the phallus. Testicular volume was still 2; _% J& K) x" w: K* L9 F1 X* h% v
mL, and the size of the penis remained unchanged.4 M0 y. R7 ]: Y8 N& ^+ {
The mother also said that the boy was no longer hav-' Y& ?( N6 c$ n6 ~
ing frequent erections.% y' X/ z* S# j4 M1 y7 T  \( _
Both parents were again questioned about use of, I+ y& r# K2 l0 v+ v
any ointment/creams that they may have applied to
. f( M8 q  A) ]the child’s skin. This time the father admitted the
5 h* D0 n5 j2 u2 U1 r& H; |Topical Testosterone Exposure / Bhowmick et al 541
6 v9 r* y7 ]. J/ Z. Juse of testosterone gel twice daily that he was apply-) \* w! P4 C4 d! j% s3 r
ing over his own shoulders, chest, and back area for7 a) N0 b# w/ j' t* H
a year. The father also revealed he was embarrassed
  I# N/ ~# B. yto disclose that he was using a testosterone gel pre-0 @. I8 H5 l+ w% I% W1 {8 ~
scribed by his family physician for decreased libido
& `/ F; }5 r. ?4 z, Qsecondary to depression.2 y% G5 k, L! A: Y
The child slept in the same bed with parents.
4 C. o+ Z* e: R! P7 JThe father would hug the baby and hold him on his, g% b$ H6 k5 u2 f7 @
chest for a considerable period of time, causing sig-
5 `* {% {! ?: W; T" o0 J6 cnificant bare skin contact between baby and father./ [  `6 E0 [3 u4 B# I
The father also admitted that after the phone call,
9 D. r8 f$ H5 V  q: l* Awhen he learned the testosterone level in the baby8 i# b7 Q; D+ `
was high, he then read the product information0 y, ^5 |. E; `/ l/ W& r  C" _* c: s
packet and concluded that it was most likely the rea-
( [+ T; ^! T* C  k) p6 r$ Eson for the child’s virilization. At that time, they
! @+ R4 e; n% A, Pdecided to put the baby in a separate bed, and the0 w! s" o0 h$ ], F7 M5 u3 ^
father was not hugging him with bare skin and had& O2 O: ~4 |! L; \
been using protective clothing. A repeat testosterone
! K7 \! p* l7 z6 ctest was ordered, but the family did not go to the. k/ g) Z& G- V1 b1 _7 m0 x
laboratory to obtain the test.
7 A$ Y4 ]0 z& T! w/ D+ f8 qDiscussion. d5 ^. V4 _8 z! E. }3 q+ E/ X
Precocious puberty in boys is defined as secondary
& ?  h$ l: E& u: Z/ ]1 ?sexual development before 9 years of age.1,4+ r2 C$ s4 W$ z$ W
Precocious puberty is termed as central (true) when1 s0 i- Z2 T8 U7 M% A: g
it is caused by the premature activation of hypo-
, k4 ^5 m( j/ U2 z% L8 Y- g  q& I/ Mthalamic pituitary gonadal axis. CPP is more com-
! L: i0 R5 }# e! Wmon in girls than in boys.1,3 Most boys with CPP% K' }2 f- E. t/ ^( U' W1 g9 D
may have a central nervous system lesion that is
+ a# @  I, C% j2 Mresponsible for the early activation of the hypothal-- W* a2 g  Q% U2 Q
amic pituitary gonadal axis.1-3 Thus, greater empha-
7 c2 I9 ~# G6 R( m$ y+ ?& I; Osis has been given to neuroradiologic imaging in9 T. A* B5 B! K- c1 r
boys with precocious puberty. In addition to viril-3 l; _9 s' }2 |) @
ization, the clinical hallmark of CPP is the symmet-
6 y: n, E/ D$ _8 N$ u- V6 Drical testicular growth secondary to stimulation by' U7 c( U3 _( r* o
gonadotropins.1,3
; {$ E% ^3 e0 l- @2 _Gonadotropin-independent peripheral preco-1 W1 y& L, I* N9 m) J  i2 R9 w
cious puberty in boys also results from inappropriate
$ B7 ]9 ~" Q7 c2 @; {# N5 {androgenic stimulation from either endogenous or" L& X7 }! z. N' U  ?* r5 t
exogenous sources, nonpituitary gonadotropin stim-
- p- ~; K' k/ j# n% s/ G( Zulation, and rare activating mutations.3 Virilizing
+ C0 T5 c. Z5 o9 n& ~congenital adrenal hyperplasia producing excessive- B- U( {* R4 i
adrenal androgens is a common cause of precocious* g# K3 ?9 C3 ^. H/ F& R" E4 E; s7 E
puberty in boys.3,4
9 T" q+ m) u" F$ `5 ~# PThe most common form of congenital adrenal7 H; k4 T5 C6 m  \" n
hyperplasia is the 21-hydroxylase enzyme deficiency.* b0 W8 m- w; b% V
The 11-β hydroxylase deficiency may also result in
& i: b' n+ W: a7 ^' B. @excessive adrenal androgen production, and rarely,
4 r5 L6 s) Z( C7 ^& `4 qan adrenal tumor may also cause adrenal androgen$ l1 D" p3 c  v" K
excess.1,35 {- z" k# L* h% i' S& l
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 j  f6 U! p7 s: R  z/ Y
542 Clinical Pediatrics / Vol. 46, No. 6, July 20077 G% }, n& A: c6 ], H& t5 |  d
A unique entity of male-limited gonadotropin-+ w' E( u9 ?9 \2 I
independent precocious puberty, which is also known3 Q4 ^% I4 W' u" Z
as testotoxicosis, may cause precocious puberty at a8 B& N1 u2 A4 @
very young age. The physical findings in these boys, K* `2 w: k* |  j3 h
with this disorder are full pubertal development,
0 g$ I% g* c1 T, _, D9 bincluding bilateral testicular growth, similar to boys* j) M! v" A% l# S
with CPP. The gonadotropin levels in this disorder
. \% V& r7 }1 {0 c% s0 i0 W6 Sare suppressed to prepubertal levels and do not show- ~- o& q, C! P. S
pubertal response of gonadotropin after gonadotropin-. ]" m* Z+ R! g- G. b
releasing hormone stimulation. This is a sex-linked* P) O! @" c( m; [0 h$ y
autosomal dominant disorder that affects only6 z/ ], P% R$ w: k2 Y1 X+ s
males; therefore, other male members of the family
: U  u5 h3 F' v3 omay have similar precocious puberty.3
% M& u8 ]8 C! Y5 ]In our patient, physical examination was incon-  S% D& }$ E6 b! S. ?
sistent with true precocious puberty since his testi-! }# y: |: z" D6 T7 N$ N6 w
cles were prepubertal in size. However, testotoxicosis
  ]+ N& h# k/ ?, Y0 ^+ l5 Kwas in the differential diagnosis because his father  F  Y- x$ u& b& w- [
started puberty somewhat early, and occasionally,: ~' b5 F9 E3 n# W: R8 J/ ~3 m2 f( `
testicular enlargement is not that evident in the4 Q, I. j$ m: H* l6 Z' R& N. n
beginning of this process.1 In the absence of a neg-7 [/ ~* v, q. v) I2 g4 X- a
ative initial history of androgen exposure, our
! s0 S; h% D9 j! f. e: T; |biggest concern was virilizing adrenal hyperplasia,
; }4 h( X- t. x9 Weither 21-hydroxylase deficiency or 11-β hydroxylase
7 a3 `1 h" `* C' t" f0 Mdeficiency. Those diagnoses were excluded by find-
! y" B( E' {1 s: B3 c- w: Ving the normal level of adrenal steroids.
; P& b* N& M3 E1 bThe diagnosis of exogenous androgens was strongly
3 l7 [: G& L, {) msuspected in a follow-up visit after 4 months because
7 W7 b" v! Z; ]1 e  D3 [the physical examination revealed the complete disap-1 q6 d. v& {& A. x
pearance of pubic hair, normal growth velocity, and" D2 P& Y, @) g* v
decreased erections. The father admitted using a testos-9 M- t  q* J" x' V8 _' @. ?
terone gel, which he concealed at first visit. He was1 E! P: ?" ?( P- m) U" |; M
using it rather frequently, twice a day. The Physicians’
, f2 a7 w9 k# ^2 p0 M3 NDesk Reference, or package insert of this product, gel or
, s) y1 p+ ~3 p# P1 d" ~cream, cautions about dermal testosterone transfer to- ]8 t4 N' Q# C3 X  u! s8 d. {2 D
unprotected females through direct skin exposure.
) C+ t  H  B  g7 h# l! }Serum testosterone level was found to be 2 times the
( C1 C+ g% [) O9 j, O/ ^baseline value in those females who were exposed to
. e( }3 ]- \0 r$ Feven 15 minutes of direct skin contact with their male
& [1 r2 N0 `. O; u, N- }* w1 s. ppartners.6 However, when a shirt covered the applica-
' U3 h$ m4 X% G. C6 Ntion site, this testosterone transfer was prevented.
1 j' {8 p# C3 A! U: WOur patient’s testosterone level was 60 ng/mL,0 M5 y6 Z0 [4 {8 N) r+ f& k3 s
which was clearly high. Some studies suggest that
6 g$ F% N6 ^; e' }9 A; r" l8 Udermal conversion of testosterone to dihydrotestos-
! O8 Q5 |4 J" L$ }terone, which is a more potent metabolite, is more
# X# ~& U' U1 l( Q7 cactive in young children exposed to testosterone
$ s( b8 z. s: M- u$ f0 X9 uexogenously7; however, we did not measure a dihy-8 B! @, X7 C8 M  S; R$ o
drotestosterone level in our patient. In addition to
% d3 ]' X5 s; U! m' `virilization, exposure to exogenous testosterone in# {3 X6 {- Q$ _: r9 S
children results in an increase in growth velocity and
; l! k8 e2 n1 H& M0 K3 Cadvanced bone age, as seen in our patient.8 _& n: S& D. R% W# X9 J
The long-term effect of androgen exposure during
6 H) d; U' f& P6 a4 bearly childhood on pubertal development and final+ P+ J: w% [& y$ _
adult height are not fully known and always remain8 p9 q4 @  s: _9 ~! |
a concern. Children treated with short-term testos-
8 z2 o$ D6 F7 E) |# n2 D# R9 B9 G% mterone injection or topical androgen may exhibit some6 e0 @/ M0 j3 q4 K% X
acceleration of the skeletal maturation; however, after+ O2 R, ]5 N7 j; P) P
cessation of treatment, the rate of bone maturation
( c0 u( P) ^& H- I" t* u4 vdecelerates and gradually returns to normal.8,9) }: `6 t0 G+ w
There are conflicting reports and controversy- c- v$ O3 {7 w
over the effect of early androgen exposure on adult% |& F4 u5 B8 ]! N
penile length.10,11 Some reports suggest subnormal
2 _" Z; W( F7 vadult penile length, apparently because of downreg-
! m# u8 ~# o) e; Qulation of androgen receptor number.10,12 However,
( J0 b, |" ?+ K7 M6 V2 Q) B8 kSutherland et al13 did not find a correlation between8 z  s5 P' @- U3 P  i$ }
childhood testosterone exposure and reduced adult
3 y& d; Q; e# H) v% G4 ~6 apenile length in clinical studies./ E- U1 ~& S; w5 @+ B
Nonetheless, we do not believe our patient is
9 e+ v4 R/ j2 h$ g. N  e5 ~, U1 K! Mgoing to experience any of the untoward effects from
% c! A# w* C% z% z% Y2 w  atestosterone exposure as mentioned earlier because
3 l+ i0 B* B# F, x5 jthe exposure was not for a prolonged period of time.8 y' a. s; S0 R8 L$ `) v# n
Although the bone age was advanced at the time of/ W. K( j1 J/ T# J7 k5 ?/ w3 _8 F
diagnosis, the child had a normal growth velocity at
, {  u9 v, f/ i: L$ z* v+ athe follow-up visit. It is hoped that his final adult
) C2 H  y+ x9 ]2 ^+ vheight will not be affected.
) K; H8 o  n1 K- V0 WAlthough rarely reported, the widespread avail-$ u4 `1 g, k  S+ t* W
ability of androgen products in our society may
5 c% H! y4 b4 oindeed cause more virilization in male or female; x; s/ n0 W4 A( l8 V( l4 E4 E
children than one would realize. Exposure to andro-8 @5 R7 i/ k' ^% ?, n& H$ P% q' w
gen products must be considered and specific ques-
& [0 v0 Y# Q  Ztioning about the use of a testosterone product or
+ E. u- [5 [1 G" V5 }& ~2 ?: Hgel should be asked of the family members during
0 }9 j+ L/ K& G8 b9 V1 wthe evaluation of any children who present with vir-
3 `4 V( a( w/ U+ n0 Oilization or peripheral precocious puberty. The diag-4 F0 b: N/ k4 h  G: e5 T1 o
nosis can be established by just a few tests and by4 ]) ~$ l0 U7 W) z
appropriate history. The inability to obtain such a
0 m: V( A& {; vhistory, or failure to ask the specific questions, may9 k; n$ g+ `+ i  Z' Z
result in extensive, unnecessary, and expensive/ Z/ R. |4 w9 v
investigation. The primary care physician should be
6 L  g5 n" f; W( ^* Uaware of this fact, because most of these children' c6 X/ ^, V' ?) J( Z1 S
may initially present in their practice. The Physicians’
2 E/ X2 @( m- g; s& s4 l$ o( HDesk Reference and package insert should also put a
, a1 r7 [1 O* E5 `1 ]7 f: pwarning about the virilizing effect on a male or; T. W' R, ?; |3 u
female child who might come in contact with some-
7 p- p% {  A. a* p# N/ sone using any of these products.4 Z& q* ^! Y0 Z- _
References
( ?2 q( S  k7 u5 C6 J. B1. Styne DM. The testes: disorder of sexual differentiation5 \6 E. j1 L% i$ p/ L# B
and puberty in the male. In: Sperling MA, ed. Pediatric
6 h& J: m0 Y- a" `3 \Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
& f9 k; D' ^$ S$ V2002: 565-628.) [0 a) ]1 H" r% x1 J0 o+ y  l! i7 @
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
% |  E* w" G  ~$ ?' z2 [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
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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

  g# g4 _9 h( G2 ?8 v3 f8 ?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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