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Sexual Precocity in a 16-Month-Old+ `; I5 x0 h8 n1 }0 \
Boy Induced by Indirect Topical
8 K# s7 z& z1 g3 N# k: RExposure to Testosterone
- Q7 R5 d: Y2 W1 E$ R4 BSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
4 u* n: P1 M" I5 S5 \and Kenneth R. Rettig, MD11 `1 a/ ^  N3 B" e" u
Clinical Pediatrics& h7 Z4 o7 E$ W: U: [; _' V
Volume 46 Number 6
: F! i) c* m0 oJuly 2007 540-543% m7 O4 ?4 j" k6 z2 h
© 2007 Sage Publications: p% B2 C2 d" X+ J
10.1177/00099228062966510 @* `" m% [+ q) R8 V
http://clp.sagepub.com
$ f7 q3 l) @! Whosted at
( K( F/ @# x0 d3 m! F% Nhttp://online.sagepub.com$ Z: A& _0 S$ |3 h+ A6 T
Precocious puberty in boys, central or peripheral,
/ a/ g) H; x* bis a significant concern for physicians. Central
- i0 u- B6 j- C! P" i# [$ k4 `' xprecocious puberty (CPP), which is mediated( F' F; V% r$ E7 f; @
through the hypothalamic pituitary gonadal axis, has" v# u2 f7 e% a/ {
a higher incidence of organic central nervous system( l' d6 H0 v+ f
lesions in boys.1,2 Virilization in boys, as manifested
/ s2 M" @- r6 g+ \2 g# w& n8 Gby enlargement of the penis, development of pubic
  a; M2 o0 l, `6 l) Fhair, and facial acne without enlargement of testi-6 @6 I( O8 y% b
cles, suggests peripheral or pseudopuberty.1-3 We
' w: z; N. J6 r4 ?( g0 [, greport a 16-month-old boy who presented with the: j: \+ Y; f/ v5 \' m
enlargement of the phallus and pubic hair develop-
& o0 o) C8 H& M' {( m6 Pment without testicular enlargement, which was due
/ Y4 J' o4 z2 N  O6 r4 {9 nto the unintentional exposure to androgen gel used by: W, h! r& h7 C, {/ J  q# O$ T
the father. The family initially concealed this infor-
& N" @+ L' x6 t1 f# Gmation, resulting in an extensive work-up for this7 Q; _( U1 a6 ?5 u
child. Given the widespread and easy availability of: r! L6 d" f- D/ @1 V* `( |
testosterone gel and cream, we believe this is proba-+ K) x8 a% o" r3 L* _3 t
bly more common than the rare case report in the
7 j9 L/ {' T3 ^* O1 a3 a+ @literature.4! m4 P7 z. o( k' A/ a
Patient Report! b; X! @! g5 D# u& J
A 16-month-old white child was referred to the3 E8 q' _+ Y7 }/ z: n* n. R1 k
endocrine clinic by his pediatrician with the concern5 w; O) e* @) ^0 g( A& |% \7 e
of early sexual development. His mother noticed
7 S! `8 J$ o& m* W9 J# ~& S: n/ nlight colored pubic hair development when he was
! G3 K! P3 r: G' R1 R9 nFrom the 1Division of Pediatric Endocrinology, 2University of( u; l( B1 V& J+ Q& b4 N
South Alabama Medical Center, Mobile, Alabama.
  ~9 s" P0 \" ]Address correspondence to: Samar K. Bhowmick, MD, FACE,
$ D7 _$ i! K) [Professor of Pediatrics, University of South Alabama, College of9 @/ L2 O/ |* A/ V$ c+ O6 w4 s* O" K
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
& q  S: ?( V) x" E3 s* j3 [2 h( `6 Le-mail: [email protected].
( M9 Z& K/ D$ h! @about 6 to 7 months old, which progressively became
' E/ X1 J+ y/ f  d/ ]2 ~3 }% c& Bdarker. She was also concerned about the enlarge-( i, U  Y2 _5 V5 e0 A6 h
ment of his penis and frequent erections. The child
3 Y4 A- q( v/ P- k9 T0 N. [- `was the product of a full-term normal delivery, with
" S3 [0 a1 F  \* v; C6 P2 ~0 O+ \a birth weight of 7 lb 14 oz, and birth length of
5 @; l) s" Z1 Z, [8 |20 inches. He was breast-fed throughout the first year
# c$ a$ q8 a! U8 I( Qof life and was still receiving breast milk along with
( ]% v! M0 u. O7 nsolid food. He had no hospitalizations or surgery,
9 F- p1 m7 V# Y4 ^2 b( d, E! G& Tand his psychosocial and psychomotor development9 P& e" Q0 x- E! F) t1 W
was age appropriate.
9 D* D* B8 G% ^The family history was remarkable for the father,
% n* Z% ^  ]% Z" L! }5 ywho was diagnosed with hypothyroidism at age 16,
- J% V# u2 J9 X4 e6 O' r4 @which was treated with thyroxine. The father’s
! S4 k8 B: p, F/ nheight was 6 feet, and he went through a somewhat
2 T' k- t# u' c- u) m& e+ Qearly puberty and had stopped growing by age 14.
4 W" e2 O4 P( I6 i8 u+ zThe father denied taking any other medication. The" {& K$ {) @$ x: y8 |% D0 k1 D' c
child’s mother was in good health. Her menarche( J' i5 m; Y. h. U( c2 x) l
was at 11 years of age, and her height was at 5 feet
0 c( o2 q# P" p. z. y+ ]5 inches. There was no other family history of pre-
& o' m$ r" f: I- D: u# l0 tcocious sexual development in the first-degree rela-5 G6 H  Q5 W% L$ \6 P8 j  W
tives. There were no siblings.( a& b/ C$ u) |, m% b8 P& u
Physical Examination, z+ V2 v" C$ Z) V4 [
The physical examination revealed a very active,2 ?4 b' j) e3 c: t
playful, and healthy boy. The vital signs documented
6 x4 q$ f2 K  w* k7 _- L$ Ma blood pressure of 85/50 mm Hg, his length was
# R! C( m% w: @. Y7 |/ s90 cm (>97th percentile), and his weight was 14.4 kg
; {) O7 H7 M1 V) @(also >97th percentile). The observed yearly growth
" R, M  {) Z3 E' _velocity was 30 cm (12 inches). The examination of" N8 B( H. ~+ d
the neck revealed no thyroid enlargement., n9 \6 n4 y# @% k: }
The genitourinary examination was remarkable for4 {* H5 J3 O7 t
enlargement of the penis, with a stretched length of
$ e  C# [& p0 g; o; x0 [/ [5 ?+ H8 cm and a width of 2 cm. The glans penis was very well
& M) a+ Q1 I6 W+ Z5 S' p0 zdeveloped. The pubic hair was Tanner II, mostly around
) H! U0 J0 u' j540) Q% ]1 Q: i/ `  L4 W
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 o: F& P- E7 o. H' v4 V& z( `. m
the base of the phallus and was dark and curled. The
# d5 K3 C6 x1 C7 W) ktesticular volume was prepubertal at 2 mL each.9 W5 D3 ?9 E& g# a* F) c/ X: j
The skin was moist and smooth and somewhat
  |$ K9 q: L4 A4 p. h) y  R% woily. No axillary hair was noted. There were no0 @& f2 S4 c6 v8 X8 b2 ~0 t1 u
abnormal skin pigmentations or café-au-lait spots.
, h4 s  t& G( oNeurologic evaluation showed deep tendon reflex 2+1 q0 Y0 O( @0 D) h) z
bilateral and symmetrical. There was no suggestion
' [) {# Y9 r0 `" v( I0 s) Iof papilledema.; j; S2 K' D- Z' S) O* E
Laboratory Evaluation
* p, ?/ C1 p9 |, O" fThe bone age was consistent with 28 months by
+ e( I% B$ [; n5 }/ S4 b& E0 ~using the standard of Greulich and Pyle at a chrono-
/ [2 v+ H3 M% u* B4 U: X: t  llogic age of 16 months (advanced).5 Chromosomal4 E8 q4 ~0 Y4 U7 ^  F6 G- `
karyotype was 46XY. The thyroid function test
& L' k8 w  X/ X3 v6 y) }showed a free T4 of 1.69 ng/dL, and thyroid stimu-8 E6 ?, h" k4 A9 O
lating hormone level was 1.3 µIU/mL (both normal).
! y6 b5 s" ~  r* {% |, x7 i6 `. wThe concentrations of serum electrolytes, blood
0 E3 V0 s; [) l! z7 \4 Xurea nitrogen, creatinine, and calcium all were& r8 F' T. w7 _  J9 I
within normal range for his age. The concentration& M" Q6 h6 s/ s4 S$ b
of serum 17-hydroxyprogesterone was 16 ng/dL; Z2 ~) G0 g! B4 _/ P, x$ {) S
(normal, 3 to 90 ng/dL), androstenedione was 20
+ \+ S, l- p! j, X- T- N& m0 i' ~ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-! Q5 a2 @# M2 R3 R3 o: T7 ]
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
2 n% b$ O; d! z; G: rdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
. n9 g6 `7 d7 m, E49ng/dL), 11-desoxycortisol (specific compound S)
2 r" w# H( C! {; R) Z5 Mwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-$ O$ R7 G, Y# `7 g# @
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
) I' r2 h' M8 F* t: G1 g  jtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
+ p6 K: ]' ?) zand β-human chorionic gonadotropin was less than
7 Q: M3 T- P6 R8 f$ ^- F% F# i5 mIU/mL (normal <5 mIU/mL). Serum follicular
$ V4 C" v- v9 t' t2 vstimulating hormone and leuteinizing hormone
1 P  w/ d* i% I$ M7 Gconcentrations were less than 0.05 mIU/mL' s& @* ~  u, Z* U! t
(prepubertal).
8 A! J& B9 y3 H8 {The parents were notified about the laboratory
0 e3 p: u6 g2 W' dresults and were informed that all of the tests were6 z. E% n8 k) B
normal except the testosterone level was high. The
+ C- c+ w- D! l, Hfollow-up visit was arranged within a few weeks to
8 r. B+ x' o  ?* u7 Y6 f8 f6 ~: l0 cobtain testicular and abdominal sonograms; how-- ?. Q/ G5 w2 N4 q- L
ever, the family did not return for 4 months.
! S, `. ?5 P* k+ E' q, sPhysical examination at this time revealed that the  x$ Q6 E/ R  F, T! C/ r4 g
child had grown 2.5 cm in 4 months and had gained
' G4 ?6 F; \- _) ~( G2 kg of weight. Physical examination remained
" b( u  K" o6 J, q) m. ^6 Xunchanged. Surprisingly, the pubic hair almost com-
- |0 x' s# b8 p2 m' [; kpletely disappeared except for a few vellous hairs at$ D6 ^& `3 G3 r9 z% B+ m
the base of the phallus. Testicular volume was still 2  D  ?% U- q: Q* I6 g3 z; @
mL, and the size of the penis remained unchanged.
* \: e6 r' m) Y0 r( ^7 R- N" PThe mother also said that the boy was no longer hav-. P1 X- m/ a# N0 C: b
ing frequent erections.- P" Q6 h% ^0 o) ]+ |0 R
Both parents were again questioned about use of: c/ e9 w0 ^( E$ v% u7 Y- v0 ~
any ointment/creams that they may have applied to
8 @. I) n! i- T! {1 N& D$ Fthe child’s skin. This time the father admitted the& L" j1 \) d$ R0 N+ h$ f" Y/ P
Topical Testosterone Exposure / Bhowmick et al 541& B# S1 r, J5 d" X1 s6 X& u
use of testosterone gel twice daily that he was apply-
' c2 `, @8 S1 u; n/ Y8 w# b1 [ing over his own shoulders, chest, and back area for8 e9 S- R+ _( m$ g
a year. The father also revealed he was embarrassed; h, L4 }2 G) k) Z
to disclose that he was using a testosterone gel pre-! z1 G9 L  y$ {8 y/ S
scribed by his family physician for decreased libido# J- }' s1 E! A: _! ]4 J
secondary to depression.+ x, w1 F; c' K1 k
The child slept in the same bed with parents.
2 ~8 ~# k' h) i  Z- ]0 ]+ MThe father would hug the baby and hold him on his
) ]. a! |% K. o) p( x' N6 I5 [chest for a considerable period of time, causing sig-/ a& T& l9 v1 |$ W0 I# C
nificant bare skin contact between baby and father.5 w+ @2 c, R( g; h" h0 \
The father also admitted that after the phone call,
6 q) }6 X* C- v$ B, hwhen he learned the testosterone level in the baby
$ c. O! c4 N2 Q* y1 J8 Z! Rwas high, he then read the product information  G. E8 }5 ?0 d* j( c5 x7 M% R
packet and concluded that it was most likely the rea-
1 K1 [, a' |% ]2 M4 M4 gson for the child’s virilization. At that time, they
% n/ d' u/ X% T- y4 _) |, F6 M# }decided to put the baby in a separate bed, and the
( W( m1 ?* d5 ^5 p) tfather was not hugging him with bare skin and had8 j5 s0 a' m7 z0 p  b' Z, |  D
been using protective clothing. A repeat testosterone* I& o! k  h0 m0 l0 L& j
test was ordered, but the family did not go to the
( O" g& p2 G/ G+ d* ?1 \& @4 M' Hlaboratory to obtain the test.8 e1 b8 q. E( }
Discussion
- C1 V! y$ l, }0 V1 h4 |Precocious puberty in boys is defined as secondary
! H7 E6 k9 V& N  y& S( ^& `/ @sexual development before 9 years of age.1,4; l+ x  G0 P7 C1 a! q1 e: O
Precocious puberty is termed as central (true) when6 P0 {7 ~, |7 e, K5 w0 c+ Y, _
it is caused by the premature activation of hypo-3 o3 K( U$ u( X7 {8 J; Y
thalamic pituitary gonadal axis. CPP is more com-8 [+ f; l4 |! R( {% q
mon in girls than in boys.1,3 Most boys with CPP
1 P5 ~4 S7 b) y& l$ r, a6 M3 I6 Vmay have a central nervous system lesion that is- Z5 d5 a' i. Z3 Q/ D
responsible for the early activation of the hypothal-
! i" X. S; c4 t2 A0 ~/ oamic pituitary gonadal axis.1-3 Thus, greater empha-6 R" s7 ~2 G, A! U' A. \! `  T7 B
sis has been given to neuroradiologic imaging in( E9 g  I* x7 G) V2 d# `) m  o' Z
boys with precocious puberty. In addition to viril-4 ?7 U  u  a& D! }# b( T# w
ization, the clinical hallmark of CPP is the symmet-1 a" x9 ^8 U0 h/ w8 Y
rical testicular growth secondary to stimulation by# I% s  ?2 ?: _% ^
gonadotropins.1,3: o2 h0 l! V1 _" Z  w: I
Gonadotropin-independent peripheral preco-7 }; w. A8 ~8 d- s& k
cious puberty in boys also results from inappropriate* r! Q* `& a3 t' |+ t
androgenic stimulation from either endogenous or9 A" r4 e* N6 r4 Z" I$ {
exogenous sources, nonpituitary gonadotropin stim-
* {3 J2 _+ J9 D) R5 g  L# Gulation, and rare activating mutations.3 Virilizing6 o5 D$ ~; r5 |+ l1 @' R
congenital adrenal hyperplasia producing excessive, }1 x; E  V' ]$ \# |
adrenal androgens is a common cause of precocious; B* o' l7 @3 \) F& G
puberty in boys.3,4
/ m4 ]' R" i( w  U* wThe most common form of congenital adrenal
1 K$ G$ ~8 }$ b) H7 Khyperplasia is the 21-hydroxylase enzyme deficiency.9 y9 c9 r1 G, k/ d
The 11-β hydroxylase deficiency may also result in
( r+ O& _/ C* D- i& _' t2 r2 vexcessive adrenal androgen production, and rarely,; ]) g1 ~0 m" y0 b$ @, ~
an adrenal tumor may also cause adrenal androgen
. _+ r$ `/ V4 \+ Wexcess.1,3
$ _, z1 _, |0 ?8 t  ^7 q' cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, ?' x& H( Z+ Z% Y1 J' a
542 Clinical Pediatrics / Vol. 46, No. 6, July 20079 I5 V, L3 c# P  Y! f+ f+ k
A unique entity of male-limited gonadotropin-! _1 ~4 u) S# \
independent precocious puberty, which is also known
( Y4 h4 {* q5 D' F: r4 q! _as testotoxicosis, may cause precocious puberty at a
( B* J. P  q, v3 j* j6 S5 Q2 s4 k! Qvery young age. The physical findings in these boys
, z2 s/ B! y& D4 Y& s$ i9 W; y1 S# Fwith this disorder are full pubertal development,
* {/ Z) X/ q6 n6 |3 P* A4 \including bilateral testicular growth, similar to boys; e4 ?( I2 v5 H" d6 y0 s) O! L
with CPP. The gonadotropin levels in this disorder/ o# S% ?. W" J, M8 a
are suppressed to prepubertal levels and do not show
" f0 I& [( C9 R- J4 X% g1 }pubertal response of gonadotropin after gonadotropin-
: @* D+ w' x8 U4 t& a9 F5 Sreleasing hormone stimulation. This is a sex-linked
0 a% D0 d' D: k, X3 Z" [* yautosomal dominant disorder that affects only' h8 t& Q* R" A
males; therefore, other male members of the family
0 O. \1 |& g2 Y; T2 Rmay have similar precocious puberty.3
4 J8 P% u* v2 f' ?* X! O% S, sIn our patient, physical examination was incon-
4 C3 g" n0 J6 V. p6 M: X  P2 vsistent with true precocious puberty since his testi-
% V% H. x' L9 U4 rcles were prepubertal in size. However, testotoxicosis. F/ G3 u% ~( N; B1 V
was in the differential diagnosis because his father
' V: e  v- N" G" I1 E- ostarted puberty somewhat early, and occasionally,
" ]6 H# k- W- Z3 }2 M1 o% {testicular enlargement is not that evident in the
7 c9 x$ B# L" o! G. Tbeginning of this process.1 In the absence of a neg-! j6 k. o6 ?# L0 b2 [2 r  `
ative initial history of androgen exposure, our
+ R1 }% d$ b& ^( F4 k% r; ebiggest concern was virilizing adrenal hyperplasia,
$ c. W1 H, U) J) V$ Teither 21-hydroxylase deficiency or 11-β hydroxylase2 `+ c+ @; ?2 _' \* E$ X" v  q
deficiency. Those diagnoses were excluded by find-
& x  x& i0 c& }6 Ving the normal level of adrenal steroids." C6 \, a. j7 d/ t7 Q, z% Z0 F9 B
The diagnosis of exogenous androgens was strongly' |$ N0 O& ]# q- {( V5 \) n
suspected in a follow-up visit after 4 months because
( H5 a1 s( c6 H+ q! jthe physical examination revealed the complete disap-
  j% c3 W1 F2 e& j  Zpearance of pubic hair, normal growth velocity, and! h& o( h; |' Z$ l
decreased erections. The father admitted using a testos-+ X' i7 d4 [( x* H2 X
terone gel, which he concealed at first visit. He was! q  A6 q+ _+ e- V5 x8 G
using it rather frequently, twice a day. The Physicians’
8 y4 l( t( g+ j' B# ~( R( KDesk Reference, or package insert of this product, gel or) e3 ?' ?/ I4 z, K+ e5 m
cream, cautions about dermal testosterone transfer to
; ]  N3 L1 M! V  ]! C# uunprotected females through direct skin exposure.
: r7 Z  Y( ^# ?! I& bSerum testosterone level was found to be 2 times the" X% g& W. h* T6 J* S5 x
baseline value in those females who were exposed to
3 ?1 ?7 y2 Q% Q. K' @1 v* Deven 15 minutes of direct skin contact with their male( Q) d4 D0 [  c/ a3 G
partners.6 However, when a shirt covered the applica-' i5 t  L( Q! O/ T
tion site, this testosterone transfer was prevented.6 ~( p0 Q1 G4 w  k! t! `4 q  F
Our patient’s testosterone level was 60 ng/mL,9 Y3 j6 R9 i- Q) e: O
which was clearly high. Some studies suggest that
- |9 c8 r1 F$ W4 L) c/ s$ Rdermal conversion of testosterone to dihydrotestos-, i2 r8 \! v7 G6 |
terone, which is a more potent metabolite, is more1 b& O1 [7 D7 L
active in young children exposed to testosterone
+ b4 T' c; ?  ]1 o- C/ Xexogenously7; however, we did not measure a dihy-7 U! ]! q  v8 g, d- T( @
drotestosterone level in our patient. In addition to
$ Y/ J. Z/ n0 g5 Ivirilization, exposure to exogenous testosterone in  y6 q% Q+ U0 D) H
children results in an increase in growth velocity and
& C# s( C" o: c6 nadvanced bone age, as seen in our patient.' h, y0 m7 a. c, Y3 X
The long-term effect of androgen exposure during2 G( P+ K) j7 {7 m4 I- R
early childhood on pubertal development and final% i( ^6 F4 ~5 d. Q9 j1 {
adult height are not fully known and always remain8 m! U5 P9 Y6 s
a concern. Children treated with short-term testos-: p2 D. T+ l. d
terone injection or topical androgen may exhibit some1 o3 A: ^* L1 x" P8 g0 J
acceleration of the skeletal maturation; however, after: u( Y4 c% u- ?) [* m+ E
cessation of treatment, the rate of bone maturation
, L" S- U  u' E3 k1 k- ^. `( O0 idecelerates and gradually returns to normal.8,9
" g( o$ e; `/ |# S8 F2 u" O# E+ xThere are conflicting reports and controversy
  G# w, X/ @' L* x4 L8 ?over the effect of early androgen exposure on adult
6 ^4 v1 R" @& Q7 ]% T7 ~" l0 Ypenile length.10,11 Some reports suggest subnormal( W7 L0 x& x7 a, m
adult penile length, apparently because of downreg-
0 \! v0 R" b' L. Bulation of androgen receptor number.10,12 However,. Z; d6 P# [% V! f' M
Sutherland et al13 did not find a correlation between" @( s9 B5 @0 F5 C4 j: A' O
childhood testosterone exposure and reduced adult
& w" o5 L% \' I( cpenile length in clinical studies.
7 x; l0 X. V0 g6 \Nonetheless, we do not believe our patient is" |: f, m. W! `1 Q0 P+ P
going to experience any of the untoward effects from
* U6 w3 f+ `+ atestosterone exposure as mentioned earlier because
' [" [1 K0 w7 G) a( G, q! r. t! Uthe exposure was not for a prolonged period of time.) O2 z3 F. y9 t, o0 r6 r
Although the bone age was advanced at the time of% h9 ^& l1 I# J4 X
diagnosis, the child had a normal growth velocity at' P' t. @$ F3 ~7 |- V) s$ q
the follow-up visit. It is hoped that his final adult: N0 c3 B& t7 F/ ]$ c0 ?' R, q% g
height will not be affected.  d8 s0 A# F+ ]5 k* n# }) `
Although rarely reported, the widespread avail-7 e; M, l3 ^. O
ability of androgen products in our society may  @. ^, [' Y0 I) ~* c( o
indeed cause more virilization in male or female
8 Q2 N. k) V7 s, K* O6 zchildren than one would realize. Exposure to andro-+ M$ e6 X% R5 @; c+ T& x
gen products must be considered and specific ques-4 y) @9 ]! a/ Q. Q
tioning about the use of a testosterone product or
! C9 a0 K+ G& U" f1 [* ygel should be asked of the family members during
9 n* U7 j- c+ g& D% h8 V) bthe evaluation of any children who present with vir-
! D5 A0 X" r, \ilization or peripheral precocious puberty. The diag-. g# j2 V6 t: u- v. d$ \3 S% \
nosis can be established by just a few tests and by
1 K) n+ l0 h5 u6 Q7 ?3 mappropriate history. The inability to obtain such a
* b+ C& d6 S: e& L- [4 f. K& Hhistory, or failure to ask the specific questions, may
5 X. s3 L! H) uresult in extensive, unnecessary, and expensive: U6 ]/ A$ m. m* u
investigation. The primary care physician should be
- Z/ d2 r8 F' h- faware of this fact, because most of these children( O6 X$ z: s( d3 Y' ?1 O  }
may initially present in their practice. The Physicians’
! A9 v0 Q' M! |$ [% LDesk Reference and package insert should also put a
: {& e7 {4 C5 c% e1 }warning about the virilizing effect on a male or/ m+ O( D, F+ Q
female child who might come in contact with some-' K  h- O# Z1 \" w
one using any of these products.
( w& h, }( W; @! C- C, zReferences* @% P+ [6 E6 G9 Q, x6 k  D6 P% E
1. Styne DM. The testes: disorder of sexual differentiation+ ~# z- O' Z" N2 s0 }% V; D$ U
and puberty in the male. In: Sperling MA, ed. Pediatric0 U) b( E, M! G2 n+ E$ t/ l
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
8 j1 @- X  i$ C$ S3 Z# i# C2 D2002: 565-628.; E. E/ r- S' s" }3 F0 d# B) O
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious( Q6 m# o, _. p5 I9 J& X: ]& ?  x
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old2 X* `5 D0 J  R  O
Boy Induced by Indirect Topical
+ p9 E1 T1 G" ~- AExposure to Testosterone
( u7 J! L5 Y0 k3 m  M* ?* CSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2: O: X0 y" B; @; n/ I! v9 l, r
and Kenneth R. Rettig, MD1
9 u% ]3 w# X  @. ?Clinical Pediatrics+ ]: R  [" t- l1 A. y
Volume 46 Number 6
7 _, g2 d7 O: `9 W4 IJuly 2007 540-543) W+ o8 q3 e' r" h( U8 z/ C9 }. d
© 2007 Sage Publications
% k0 A) K3 ^$ I/ W2 O9 c10.1177/0009922806296651
8 J. w) W& {6 ^http://clp.sagepub.com
6 h0 f# c2 K! Qhosted at/ k$ H8 E  V- x% a% o. g: W9 V
http://online.sagepub.com
3 z4 d0 B4 f! X6 B& I8 ePrecocious puberty in boys, central or peripheral,& K8 f3 a2 x; H/ n' r$ v
is a significant concern for physicians. Central
0 Y$ p7 q7 p6 Z1 G# Fprecocious puberty (CPP), which is mediated
, ^) ~! s4 i! k) ~5 f4 V5 nthrough the hypothalamic pituitary gonadal axis, has' a" O7 J/ O( U4 |- R* s
a higher incidence of organic central nervous system: x, l" V% w5 C! ^: S/ F$ I0 U; X6 H
lesions in boys.1,2 Virilization in boys, as manifested
8 h+ v4 i/ T2 s- H- @3 _$ tby enlargement of the penis, development of pubic* M3 W3 S3 w# _. A
hair, and facial acne without enlargement of testi-* N% `# e7 y) g3 y
cles, suggests peripheral or pseudopuberty.1-3 We
5 X+ j5 K' E* V; p4 h2 y7 L0 Greport a 16-month-old boy who presented with the* \' p% p8 ]5 U- A: _- a7 h' b
enlargement of the phallus and pubic hair develop-3 M! D: `" e. N; E0 c
ment without testicular enlargement, which was due3 y) c1 t; v) a2 p5 E4 W
to the unintentional exposure to androgen gel used by
$ b- V; k( G, ^. ]5 {; uthe father. The family initially concealed this infor-. V9 z0 K* s: D9 n! p+ n
mation, resulting in an extensive work-up for this! T+ \8 k3 C" a- D  N
child. Given the widespread and easy availability of7 h6 v: \9 m/ c! n3 S- |1 |
testosterone gel and cream, we believe this is proba-0 K, n1 _4 J2 S5 V/ v+ B
bly more common than the rare case report in the
' V3 x0 q# x" s5 B" z0 Q4 {% oliterature.4, h* g% y+ D% \  p" I8 k
Patient Report
* T8 f- w& m5 {/ pA 16-month-old white child was referred to the
5 _, t/ C9 N: T, oendocrine clinic by his pediatrician with the concern
& o3 p6 A6 B1 \. o% Gof early sexual development. His mother noticed7 N9 ^+ z/ u/ C7 ?+ F# w
light colored pubic hair development when he was
. w: H# w+ G) c' e: b4 mFrom the 1Division of Pediatric Endocrinology, 2University of
! C6 P4 O, W5 q% o: e8 ySouth Alabama Medical Center, Mobile, Alabama.
" \% C: n1 ?9 K& T' }Address correspondence to: Samar K. Bhowmick, MD, FACE,/ H9 E+ g+ i+ i2 s  W
Professor of Pediatrics, University of South Alabama, College of
' Y3 H* }$ [, C$ V6 dMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;% y& {. X) Q. V: i, Y8 |' g
e-mail: [email protected].  a3 I, N- s$ ^7 _1 s* V' d
about 6 to 7 months old, which progressively became: K& v- M- o, T  @$ d7 G
darker. She was also concerned about the enlarge-
0 u: s! A0 p5 M. O. [" b3 Jment of his penis and frequent erections. The child' e) r2 k# x# v1 }3 X# y
was the product of a full-term normal delivery, with
3 m& J+ \; w* x) W1 h+ S- G& {a birth weight of 7 lb 14 oz, and birth length of8 \  E% `+ ?! P5 e1 P2 \
20 inches. He was breast-fed throughout the first year
) N7 T* k- l) y: e- Nof life and was still receiving breast milk along with
; H; m8 X+ {0 x' s% q' N6 ]solid food. He had no hospitalizations or surgery,4 z$ G: W. Y3 j- A' l5 S- B
and his psychosocial and psychomotor development
4 x; q' a! T. e7 q$ z" P& A! `was age appropriate.
0 r7 A( ]: l& ^. aThe family history was remarkable for the father,/ g' O& }- L7 b# ]0 _% G
who was diagnosed with hypothyroidism at age 16,
3 q! n  t; u" a3 _3 twhich was treated with thyroxine. The father’s
9 m+ p* T9 i% C& `height was 6 feet, and he went through a somewhat8 y8 o7 y1 {" h+ X. j+ G
early puberty and had stopped growing by age 14.
7 G# i" G( F+ C( n  U$ y. TThe father denied taking any other medication. The
6 m* s6 p! B" Y4 Achild’s mother was in good health. Her menarche+ A9 j% d+ X1 u$ W2 `( X3 l3 K
was at 11 years of age, and her height was at 5 feet' \0 o, r7 A/ R/ M! i
5 inches. There was no other family history of pre-- Q6 n5 Q6 }4 q5 C% C3 i
cocious sexual development in the first-degree rela-
7 i0 }3 Z5 G7 Z: b  |% N6 xtives. There were no siblings./ d% T6 S7 ]9 O; q; Q4 r
Physical Examination2 |  I0 x; R+ w; _- m- z( U
The physical examination revealed a very active,
% O- H! ^7 C8 J, }6 J9 Vplayful, and healthy boy. The vital signs documented
5 u7 ]; r, M. K' Z3 @5 za blood pressure of 85/50 mm Hg, his length was
) z* T# d" {# b9 I90 cm (>97th percentile), and his weight was 14.4 kg& G9 f" C8 M  P) k8 {
(also >97th percentile). The observed yearly growth. J. [$ L* t7 \5 y7 m0 D
velocity was 30 cm (12 inches). The examination of
$ J4 }$ f* P- `: c, Jthe neck revealed no thyroid enlargement.4 S( S/ W9 P( Q
The genitourinary examination was remarkable for
) i: M4 K' Q# t: x% M4 Eenlargement of the penis, with a stretched length of4 F9 q  v+ v/ ~0 V" f
8 cm and a width of 2 cm. The glans penis was very well& Q5 ?3 q: ^+ |9 h. x
developed. The pubic hair was Tanner II, mostly around: m, b! @3 m) H
540( s# m1 k/ e! }3 U, R
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! U$ O: N2 [7 |; y5 x3 `, N6 Q
the base of the phallus and was dark and curled. The# d9 |& ?' L5 `# S3 f) ~7 k! C
testicular volume was prepubertal at 2 mL each.
  O+ H* y% h: j0 @The skin was moist and smooth and somewhat  d" q8 u  @7 |$ W
oily. No axillary hair was noted. There were no) p& Q8 h  ]& n. i1 s0 F' n
abnormal skin pigmentations or café-au-lait spots.0 E0 u6 i! ?2 o+ h  _
Neurologic evaluation showed deep tendon reflex 2+( C  K' |9 ~; F
bilateral and symmetrical. There was no suggestion4 R5 }3 `: l) `# n
of papilledema.* o& d& P' K1 X, U' b
Laboratory Evaluation1 m/ Y  h  h& Y$ H- u& Q& H2 K
The bone age was consistent with 28 months by* u; b8 {/ W; [+ }3 j( ?- e
using the standard of Greulich and Pyle at a chrono-
; Y( r3 t1 g3 D! `$ M- ulogic age of 16 months (advanced).5 Chromosomal
! Y, P- t, y4 y6 k6 W2 ?karyotype was 46XY. The thyroid function test
- a( v! b4 j( I# fshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
: S1 K! N0 ~% E' tlating hormone level was 1.3 µIU/mL (both normal).
5 e* E) N( }3 ]- h1 Q8 }( RThe concentrations of serum electrolytes, blood
  K  X; X' C0 U" ]1 T, Nurea nitrogen, creatinine, and calcium all were" r& P. z1 T/ @+ F  e& n0 s
within normal range for his age. The concentration
# V( Y+ d5 w. eof serum 17-hydroxyprogesterone was 16 ng/dL
7 y& G5 p. |3 |; I0 s. e(normal, 3 to 90 ng/dL), androstenedione was 20$ D" L+ {/ D8 J" X) I3 Z
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-" O; ]5 ?' L* g" v2 e: T9 e
terone was 38 ng/dL (normal, 50 to 760 ng/dL),- Z2 a" `# s0 a2 ^1 W, x( v6 c2 B
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
5 T' f' I/ C$ J2 |1 I$ X: F8 q49ng/dL), 11-desoxycortisol (specific compound S)
7 T7 C3 r. J0 I, uwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-. d- e1 T' ?, b5 Z
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total/ G2 K2 J1 X0 u+ F  S. A0 M5 a6 a
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),+ \, m) B& J. E" `0 \$ Q/ O+ _3 T
and β-human chorionic gonadotropin was less than! Q# P5 m) d7 H0 T4 z
5 mIU/mL (normal <5 mIU/mL). Serum follicular
/ N" Q+ m% x3 W0 V% Mstimulating hormone and leuteinizing hormone
( Z! E& ]' @  b# \concentrations were less than 0.05 mIU/mL5 C8 y  M8 Q& ~
(prepubertal).; f* w! u2 d9 i" W
The parents were notified about the laboratory
# [+ v. K( _; w6 W! bresults and were informed that all of the tests were- P" ~1 a* d( }# b1 G4 o& Y, B
normal except the testosterone level was high. The
$ ^: a- _) q0 Z* y3 f2 |3 yfollow-up visit was arranged within a few weeks to1 }! G$ [0 Y/ b) [
obtain testicular and abdominal sonograms; how-
( r1 M9 u& n( J3 u# lever, the family did not return for 4 months.
4 J9 u0 z, ?1 U4 E6 K2 V! B0 xPhysical examination at this time revealed that the
# _4 @/ A1 e9 l7 ~/ X* |9 gchild had grown 2.5 cm in 4 months and had gained
6 ?8 D3 j, L+ T/ M8 ^: R2 kg of weight. Physical examination remained1 {! v9 P& G4 x1 T
unchanged. Surprisingly, the pubic hair almost com-2 N9 F7 _/ i4 w! ^. k7 V
pletely disappeared except for a few vellous hairs at7 g0 L$ ]6 o# w: u" t( }
the base of the phallus. Testicular volume was still 2' W( d9 M" q- f( k$ c9 x
mL, and the size of the penis remained unchanged.- b# h4 |# o( a( q3 `
The mother also said that the boy was no longer hav-
0 P% b; R' k/ s6 fing frequent erections.: Q% j( U( r7 {
Both parents were again questioned about use of( o( X. e: c" Z( p' d
any ointment/creams that they may have applied to
: v+ X+ r. R+ O* M5 i, \3 v: dthe child’s skin. This time the father admitted the8 l, m$ C" s! Y8 M  ^
Topical Testosterone Exposure / Bhowmick et al 541
; X* Y& U( t! vuse of testosterone gel twice daily that he was apply-
9 G# g6 ]2 a! zing over his own shoulders, chest, and back area for
" p7 V) ^% n$ x4 ka year. The father also revealed he was embarrassed: Q! d- @1 a# c# r' O( p
to disclose that he was using a testosterone gel pre-- u% G# n8 a( Z1 P
scribed by his family physician for decreased libido' p3 n6 a; c( H& m* j  B6 G- P
secondary to depression./ w1 M; c: C! s7 E
The child slept in the same bed with parents.
# g7 @4 p$ S+ t. p4 k: ZThe father would hug the baby and hold him on his/ F+ V$ p. a- \( q6 ~
chest for a considerable period of time, causing sig-# F! ]( T& Z1 ]9 y; c
nificant bare skin contact between baby and father.6 U2 S1 x3 e) E1 O: f+ {
The father also admitted that after the phone call,
6 ]9 r4 v7 w% m9 [0 V0 y7 [' Lwhen he learned the testosterone level in the baby
% H% A; V) k4 c7 Iwas high, he then read the product information
1 Z# \. m, I6 @8 Rpacket and concluded that it was most likely the rea-; P+ x; g% @7 }9 c! t4 {- U- u4 U
son for the child’s virilization. At that time, they
/ F  R2 {! _. ?6 edecided to put the baby in a separate bed, and the7 t0 v1 f( o. r. h7 I4 r: _
father was not hugging him with bare skin and had) w( }. z+ z" l# |, i4 y+ D
been using protective clothing. A repeat testosterone/ R- S8 H, }0 {9 e& x* Q) w
test was ordered, but the family did not go to the
7 T1 d6 |" E0 ]6 P# U6 klaboratory to obtain the test.# ?* G% {+ S4 _
Discussion
8 G! R: v% k, K' p1 `/ S' \Precocious puberty in boys is defined as secondary4 J( \) r8 E3 N; B' M. @& X
sexual development before 9 years of age.1,4
6 b+ {3 [/ y. U* x$ e" U/ }Precocious puberty is termed as central (true) when
; [  J' R9 T4 J( C- ^+ b9 \" s8 w4 ?it is caused by the premature activation of hypo-
9 e9 S  ^( y5 ithalamic pituitary gonadal axis. CPP is more com-, R4 o2 ]9 t5 V) n/ X/ u
mon in girls than in boys.1,3 Most boys with CPP6 k9 g# g- W+ s4 w5 G& o1 E
may have a central nervous system lesion that is/ d; `+ b3 J  \! N' E7 H
responsible for the early activation of the hypothal-3 m# Y8 u5 g" B; z
amic pituitary gonadal axis.1-3 Thus, greater empha-( w$ a" h+ V: O6 k9 W
sis has been given to neuroradiologic imaging in
% o% P/ X4 i: O5 n( G- Xboys with precocious puberty. In addition to viril-
9 p" y: i; g1 E) ]+ Q8 d) t. Z! `ization, the clinical hallmark of CPP is the symmet-: O* V3 d3 _. a- }  P
rical testicular growth secondary to stimulation by9 b: l% ~' S! h4 {) k1 l& j
gonadotropins.1,3! L* G; m" ~0 I5 `$ _
Gonadotropin-independent peripheral preco-
, l6 d+ F/ \' J/ _6 n! Kcious puberty in boys also results from inappropriate
' x# D% X8 r9 E: Sandrogenic stimulation from either endogenous or
- }3 a! _$ O! J6 {* kexogenous sources, nonpituitary gonadotropin stim-
/ {/ }7 c0 x' ]3 I3 @& aulation, and rare activating mutations.3 Virilizing7 ?2 k$ P; L' G# ?# o
congenital adrenal hyperplasia producing excessive
. x! o6 B: F5 k. R' Zadrenal androgens is a common cause of precocious
' e2 m9 I7 f& J# Opuberty in boys.3,49 \' [! W! ^) P8 \% D$ C' |3 N9 N
The most common form of congenital adrenal% M" w" ?1 T1 N2 |! \9 ~  B+ I
hyperplasia is the 21-hydroxylase enzyme deficiency.4 }4 f- Y) q5 b4 Q
The 11-β hydroxylase deficiency may also result in
  U0 e4 F0 F+ u( Y8 _5 Kexcessive adrenal androgen production, and rarely,
8 H5 b2 \. V8 ]7 A% G( V  m9 Can adrenal tumor may also cause adrenal androgen4 _4 j7 D4 H9 C' I2 s9 [8 x5 n2 O
excess.1,3
* T! b9 G/ B; N% b9 cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' Z5 }4 f$ }" L1 p542 Clinical Pediatrics / Vol. 46, No. 6, July 20073 L: s  O) G8 R& Y
A unique entity of male-limited gonadotropin-
3 p# [" s3 q  t8 Sindependent precocious puberty, which is also known
& i& M& i7 d4 Z& Sas testotoxicosis, may cause precocious puberty at a3 l( F1 K, H3 {0 Y7 @/ A( t
very young age. The physical findings in these boys( p+ I6 S& b. Y% P
with this disorder are full pubertal development,, t9 ]* p; g7 G5 R, I/ ^: N
including bilateral testicular growth, similar to boys" Q& {$ j% W+ L
with CPP. The gonadotropin levels in this disorder
( N4 n) {: A5 ?$ U/ P/ v$ lare suppressed to prepubertal levels and do not show
. W' T8 U% S+ ^7 x+ K$ ?+ Tpubertal response of gonadotropin after gonadotropin-) B$ s# |4 U$ T3 M/ S
releasing hormone stimulation. This is a sex-linked
, J$ D: E5 Q- z! ~4 }! G( g* f$ |autosomal dominant disorder that affects only# ^+ H; _3 A8 p7 H
males; therefore, other male members of the family
5 b. B0 I2 ~6 amay have similar precocious puberty.3
: Q& y. a" K" s+ ZIn our patient, physical examination was incon-
2 L0 b" v/ z: K8 wsistent with true precocious puberty since his testi-
; Q8 R! i7 N0 rcles were prepubertal in size. However, testotoxicosis
; q1 L8 q5 n" Y  a1 Ewas in the differential diagnosis because his father8 W8 o5 L4 o# j& V
started puberty somewhat early, and occasionally,$ m: B$ X  C3 H6 T. T! i- S
testicular enlargement is not that evident in the
% C* ^/ S3 B$ a& a+ j! M5 ]beginning of this process.1 In the absence of a neg-7 r. b  D- x% k9 Q
ative initial history of androgen exposure, our
% O* N) @6 x2 T. G4 U# @. ~: Zbiggest concern was virilizing adrenal hyperplasia,
- w# C- W, Y* {3 I! ^/ C- O0 O, Seither 21-hydroxylase deficiency or 11-β hydroxylase
  b! @& l- S3 m- n$ {. @deficiency. Those diagnoses were excluded by find-+ \* ^; \4 S8 p' s4 P
ing the normal level of adrenal steroids.& E7 M7 u0 x/ E3 v, k
The diagnosis of exogenous androgens was strongly
* X: q: V( g0 r' ^* u, S8 Ysuspected in a follow-up visit after 4 months because% \0 N# K& N3 G( w4 n' h) Y
the physical examination revealed the complete disap-
6 d, L5 A3 {& E' l4 c: opearance of pubic hair, normal growth velocity, and
; l1 j6 ]3 [& E+ o" ~decreased erections. The father admitted using a testos-( U5 Z& H" y9 \* F% u% n
terone gel, which he concealed at first visit. He was' ]& C7 q( q9 S% T6 o
using it rather frequently, twice a day. The Physicians’
8 M9 v5 a- \, f% dDesk Reference, or package insert of this product, gel or1 `5 }- A8 H+ k. d
cream, cautions about dermal testosterone transfer to( k/ \2 `( b2 j% x# g
unprotected females through direct skin exposure.
$ L; G6 g4 T! e- _" iSerum testosterone level was found to be 2 times the
% |: N" Z) m4 s5 pbaseline value in those females who were exposed to5 Y) `% N) M8 F$ s
even 15 minutes of direct skin contact with their male
/ q  m* M. ]8 b" G; Z# Hpartners.6 However, when a shirt covered the applica-
% a/ }! L" Y& H4 k$ ~tion site, this testosterone transfer was prevented.
7 k2 E3 q9 c' R9 `- POur patient’s testosterone level was 60 ng/mL,1 }0 t8 Q% y& ]' t" u2 n
which was clearly high. Some studies suggest that
7 J3 X+ w% x4 k0 ]0 e- t( m" o6 vdermal conversion of testosterone to dihydrotestos-  E  S4 H: y* i/ P% Z; H+ M# `  A
terone, which is a more potent metabolite, is more; W7 i$ p; Q- p  ?
active in young children exposed to testosterone' N& F1 p- w1 z2 [% T
exogenously7; however, we did not measure a dihy-$ ~. M3 X6 B6 `. J* h5 w
drotestosterone level in our patient. In addition to
- M, z7 p# i4 F' B# O0 z' Mvirilization, exposure to exogenous testosterone in% H- L% Y' `. y0 C2 {+ e( f
children results in an increase in growth velocity and" ^  M& e& w: W. B4 o! a; w. u9 f
advanced bone age, as seen in our patient.
2 s. m% U7 i- C- o% IThe long-term effect of androgen exposure during
! K6 ~' m  m. _/ l  jearly childhood on pubertal development and final, Y1 L6 J7 ?6 B! v" U
adult height are not fully known and always remain
# l2 z$ `# n8 F- m- E& V' v& c( }a concern. Children treated with short-term testos-
8 f8 Q5 m% o% I# Y1 T% I- yterone injection or topical androgen may exhibit some! p8 h) k9 @) c0 }
acceleration of the skeletal maturation; however, after% `& [" Z1 \" U% N6 s. }
cessation of treatment, the rate of bone maturation
3 {- S2 l. V0 d. X! m# v1 c9 |decelerates and gradually returns to normal.8,9
& ?) U8 H% E& J4 a% a" xThere are conflicting reports and controversy
! Q) E" X+ C* A8 c5 d4 D; W+ Qover the effect of early androgen exposure on adult# J# y3 ]+ N: U! R
penile length.10,11 Some reports suggest subnormal" {# u6 S2 z. b# z$ g$ t6 F& H, F$ ^
adult penile length, apparently because of downreg-
1 ^; U) Q! C. J$ Julation of androgen receptor number.10,12 However,
  R0 s' s* E4 `* F) nSutherland et al13 did not find a correlation between3 H5 @9 [; a) U  ?& i: s  M
childhood testosterone exposure and reduced adult
0 a& Q3 g8 H/ Spenile length in clinical studies.
8 i( t( F. U. \. v# L2 ~. ONonetheless, we do not believe our patient is
: D7 O0 k! @4 S; E, U8 }1 |% x5 qgoing to experience any of the untoward effects from
# ?- @% c/ ?/ o6 x) C# d  Ztestosterone exposure as mentioned earlier because- Y; ^# b/ N& J( ^5 _2 a
the exposure was not for a prolonged period of time.+ i" Z  U; R9 \
Although the bone age was advanced at the time of
" f* i& N, @  a* D! [$ Cdiagnosis, the child had a normal growth velocity at2 z& g' @$ u' ~, t3 Y5 w
the follow-up visit. It is hoped that his final adult9 [/ d/ U* p# i
height will not be affected.: F0 f# l, d# V9 C
Although rarely reported, the widespread avail-8 e" r2 K9 G& ]3 S, n4 t
ability of androgen products in our society may
- |7 n" [( {. R% I6 [9 |4 \indeed cause more virilization in male or female( |' M8 B: [; S+ R5 N
children than one would realize. Exposure to andro-2 F# n) ~2 y8 n* s( o* \
gen products must be considered and specific ques-- ?6 ?" |" o" c6 ~2 J9 N5 B6 Z& e
tioning about the use of a testosterone product or
% h9 Z! v) C& \; i! _# K, ^  N6 ngel should be asked of the family members during
( X0 i, l/ e5 O# ]& cthe evaluation of any children who present with vir-
8 R. H  b& A7 }7 Oilization or peripheral precocious puberty. The diag-: |+ O' D) ?$ U
nosis can be established by just a few tests and by( _- v4 k; V0 B( s0 U  J/ ?9 T
appropriate history. The inability to obtain such a. i: u; Q% o4 p# [
history, or failure to ask the specific questions, may
! V# {. Z; l" tresult in extensive, unnecessary, and expensive
( T9 d# B) @: l9 v$ `* p' `; hinvestigation. The primary care physician should be3 e6 {( J% I" ]+ h8 U; z1 p+ [
aware of this fact, because most of these children# U0 d! Y, c  t0 K
may initially present in their practice. The Physicians’
7 x7 c4 S9 M6 j9 Y# y. e7 {Desk Reference and package insert should also put a
1 H$ L6 i* z8 uwarning about the virilizing effect on a male or
' b6 [$ A, K( z* }* X2 bfemale child who might come in contact with some-8 l  K! `' t2 ^! X) b. Z* W3 R
one using any of these products.
* O0 \& s- g6 W4 hReferences
/ x4 u) @" e9 a; h1. Styne DM. The testes: disorder of sexual differentiation% J! Y! [" W- H0 L8 N8 u) `
and puberty in the male. In: Sperling MA, ed. Pediatric
6 w: t0 s! L: r9 ^# o, T$ C0 [; HEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;% ?% P: Z, u* e+ v+ B6 R+ H
2002: 565-628.% ?8 B) s. Q$ {
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
8 f8 ]& E+ W" v" Apuberty 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
* [7 n8 o+ |+ i1 S; @9 H
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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