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Sexual Precocity in a 16-Month-Old
6 {+ m- W5 h/ W4 n8 cBoy Induced by Indirect Topical
+ H# @! [3 a* w( f7 G/ h1 TExposure to Testosterone. r2 \( p$ Q4 {- i* x( n
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2( L/ z, e  ~8 W8 m) y/ U( ]
and Kenneth R. Rettig, MD16 `- L1 Q) s/ z: ?% Y- @& m# @
Clinical Pediatrics
2 O8 g4 b; ]/ w9 X) W3 g" WVolume 46 Number 6
2 b) v* C- E: B3 _- TJuly 2007 540-5433 x# S$ U7 K$ m( h/ [- r
© 2007 Sage Publications
4 Z! m. ]) C* U: K0 H) T10.1177/0009922806296651. j7 p- Q( h; n  Z7 U+ y  Y. [9 q
http://clp.sagepub.com
( ~5 g+ Z- F, rhosted at/ I/ W: ^" u+ z+ O7 B
http://online.sagepub.com( b0 ?; |9 c7 b6 \8 G" n
Precocious puberty in boys, central or peripheral,
# C9 a0 S9 K0 K+ I* Y9 T2 pis a significant concern for physicians. Central
1 q( G, F7 o& r6 |4 c; Sprecocious puberty (CPP), which is mediated# `7 o8 s6 `$ j% X9 C: R( a# f
through the hypothalamic pituitary gonadal axis, has) }% b  s- n+ V, Z9 R5 W0 R- Q2 F
a higher incidence of organic central nervous system! W/ ?, N" D( C8 R0 [2 Q9 W
lesions in boys.1,2 Virilization in boys, as manifested
* z; o7 r" r( H3 s% P& z! zby enlargement of the penis, development of pubic  Z/ c) \$ V) _( f; v) L
hair, and facial acne without enlargement of testi-
, V3 u3 A; [0 O: ?5 O- Hcles, suggests peripheral or pseudopuberty.1-3 We0 n5 T7 @( p3 }: ~% Q; j' n
report a 16-month-old boy who presented with the
; \/ C+ r; [& a! w' x% x9 Zenlargement of the phallus and pubic hair develop-0 p5 }7 \7 H$ J% I# M5 a# E: F+ t. }
ment without testicular enlargement, which was due
' H3 t+ h- \7 \, eto the unintentional exposure to androgen gel used by  o& v1 [& x$ _& {# B4 }
the father. The family initially concealed this infor-
0 V9 G7 g/ s5 dmation, resulting in an extensive work-up for this
& X5 x8 E; b0 C, K- ychild. Given the widespread and easy availability of
# u: H' j- j- J7 g0 Otestosterone gel and cream, we believe this is proba-
0 W3 ^$ X8 X7 v, mbly more common than the rare case report in the
) W1 j6 F( ]% e# V5 j! c" @& x  ]4 w, qliterature.4% [0 X, q+ w8 \6 ^. O' O. W
Patient Report4 \! |/ c  i$ v" ]* N, p0 Z
A 16-month-old white child was referred to the7 {) W% @- x0 ?: N
endocrine clinic by his pediatrician with the concern
' ~# Z' W- u6 Fof early sexual development. His mother noticed: i1 k7 }! n2 ?  l$ k% K
light colored pubic hair development when he was
9 _* b& x% o  q; r) j/ a) DFrom the 1Division of Pediatric Endocrinology, 2University of
  ~6 C. Y  S2 P* D9 {6 i' NSouth Alabama Medical Center, Mobile, Alabama." d& K  Z2 d. Y" I& {
Address correspondence to: Samar K. Bhowmick, MD, FACE,
8 F  {! z: i0 \# w. j0 yProfessor of Pediatrics, University of South Alabama, College of
* n" L1 `. j0 t7 ~; ?. gMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;1 ^! o! E' `% v  l) Q' C
e-mail: [email protected].8 U0 T+ z) O  S% S( C; _7 b% l5 t
about 6 to 7 months old, which progressively became
3 m& X8 o6 K4 T' k. d. |darker. She was also concerned about the enlarge-
, }; O! {1 v) I' g% `7 C1 r1 Ement of his penis and frequent erections. The child2 s4 O' l# @# s" N3 Q
was the product of a full-term normal delivery, with
3 C! {  d3 y. w% `- t2 {$ na birth weight of 7 lb 14 oz, and birth length of
( Z9 e, y& x2 Z: S/ l20 inches. He was breast-fed throughout the first year8 T$ W' g4 P2 r0 P7 ?& z% c
of life and was still receiving breast milk along with" e9 T; j" J+ v! x
solid food. He had no hospitalizations or surgery,5 c- M7 J: r& _8 @
and his psychosocial and psychomotor development  x: ~4 j/ j% k+ A' l! d! y! ]! p
was age appropriate.5 F* U5 y$ I  i* }. K5 O. O' B
The family history was remarkable for the father,& B& |3 `. m. R9 h0 h4 U
who was diagnosed with hypothyroidism at age 16,
2 f+ C5 H8 K: ^" I% q$ [" Hwhich was treated with thyroxine. The father’s
) I, [+ O+ C8 b' oheight was 6 feet, and he went through a somewhat
# @1 E! B" B  pearly puberty and had stopped growing by age 14.2 J* I, j6 W2 Q: _, d# T& X
The father denied taking any other medication. The! a1 {* J; f  p
child’s mother was in good health. Her menarche$ p) A, p! j* W( k
was at 11 years of age, and her height was at 5 feet
4 j2 F) J& u# R/ g+ e; F( Z0 M: d$ Q5 inches. There was no other family history of pre-
& `+ M7 z" \3 M4 Xcocious sexual development in the first-degree rela-1 `  Y. m0 c, x! ~# S
tives. There were no siblings.
# N6 c9 q9 l& e6 n0 M9 QPhysical Examination2 {# ~7 I! }0 m7 C( m3 M" |
The physical examination revealed a very active,( m$ d. ?: E3 e* {( x
playful, and healthy boy. The vital signs documented1 M, X5 x& ~: l, }- d
a blood pressure of 85/50 mm Hg, his length was
$ Y4 t2 T7 g. G& h90 cm (>97th percentile), and his weight was 14.4 kg, b& Z3 @$ ], F( c% x
(also >97th percentile). The observed yearly growth' G* f, h4 V' f$ Z+ Q0 ]- j
velocity was 30 cm (12 inches). The examination of5 F$ U7 c/ I1 x" E% i
the neck revealed no thyroid enlargement.6 Z! U. }4 \5 F
The genitourinary examination was remarkable for
, [& b6 ^; V) Jenlargement of the penis, with a stretched length of3 r0 i  f+ m  v& l1 {7 F; X" P% z
8 cm and a width of 2 cm. The glans penis was very well1 Q+ L+ ?. V( Q- j( Z5 a; [
developed. The pubic hair was Tanner II, mostly around. _# ?7 ^+ [5 `' P
540$ z, ], l1 \% n3 {
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( B# I8 p( _$ F; b) h- sthe base of the phallus and was dark and curled. The' r5 j9 ~* Z% s) E
testicular volume was prepubertal at 2 mL each.4 G- \5 W0 U( O' a
The skin was moist and smooth and somewhat0 s& o7 b8 i$ M' T. D* _
oily. No axillary hair was noted. There were no
! q2 i% H1 S0 l( Y& gabnormal skin pigmentations or café-au-lait spots.- B7 F! {7 _$ i9 C  [$ J
Neurologic evaluation showed deep tendon reflex 2+
- J6 f+ v" h5 o- S1 ^) ibilateral and symmetrical. There was no suggestion
, I6 O1 K! Q  O( m* D# u1 pof papilledema.$ l6 G* G, S) A$ s. f2 f: n
Laboratory Evaluation& B1 y% u# z  z9 z' x; `% Q9 g
The bone age was consistent with 28 months by4 x2 T0 B2 F) Y0 P3 U- _0 R: J( z5 r
using the standard of Greulich and Pyle at a chrono-
. p4 q5 f; z9 d, k- S5 v/ Nlogic age of 16 months (advanced).5 Chromosomal/ p) f: q4 ^& @; O2 @, N  s
karyotype was 46XY. The thyroid function test& u+ K& a5 j9 g+ I( }6 M+ f! B4 P3 B
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
! d& l3 k! u' Ulating hormone level was 1.3 µIU/mL (both normal).6 i$ [0 g2 `, Y1 q9 Z
The concentrations of serum electrolytes, blood  z  j5 O7 U8 [) i9 _8 P% E
urea nitrogen, creatinine, and calcium all were$ V$ G" X$ U, B- v+ q* Y
within normal range for his age. The concentration
) R- E, p$ F9 f  S7 F) N% Vof serum 17-hydroxyprogesterone was 16 ng/dL
2 ?5 d5 i- f; L! q3 M5 n  J$ s(normal, 3 to 90 ng/dL), androstenedione was 20
8 M1 U' ~2 z/ Rng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
7 [% C8 @  w, O  }7 B2 hterone was 38 ng/dL (normal, 50 to 760 ng/dL),( o4 d6 y8 t. `! k9 w5 L* A: m5 f
desoxycorticosterone was 4.3 ng/dL (normal, 7 to+ M$ x4 B7 u  F3 c" b$ ^
49ng/dL), 11-desoxycortisol (specific compound S)) ~3 y3 ^$ k) Z5 K8 M
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
1 G  I9 I+ O8 E6 w9 r7 A0 ]5 T0 ^  Dtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
2 A+ k' a+ @/ T- y% _9 g  V+ ]testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
0 {" H2 ^" u0 ~- ~- |5 C3 ~and β-human chorionic gonadotropin was less than: }0 b+ q0 r0 v+ m9 `+ x( b+ g0 C
5 mIU/mL (normal <5 mIU/mL). Serum follicular
6 O( X7 {* Y; P) j7 O) x1 w! wstimulating hormone and leuteinizing hormone
1 @9 y' w7 |1 iconcentrations were less than 0.05 mIU/mL
! b7 m! F7 l2 X0 y- n(prepubertal).* r  w; `' F% x$ E' s
The parents were notified about the laboratory: d! J# e+ x) Z  T
results and were informed that all of the tests were
1 V: i  d5 b- h! d7 R7 A- E$ cnormal except the testosterone level was high. The
: Y+ g; v& z2 xfollow-up visit was arranged within a few weeks to% o  G$ _' m4 q
obtain testicular and abdominal sonograms; how-
$ F" l9 F7 M4 V6 G# ?# g" kever, the family did not return for 4 months.
# w6 t* I8 W* d( e) ^" a' l' FPhysical examination at this time revealed that the
7 e3 P7 u4 \+ {+ dchild had grown 2.5 cm in 4 months and had gained
  m/ @1 [' D: Y2 x2 kg of weight. Physical examination remained' w- C) r6 l; y: B- T$ h* F8 \- p$ U
unchanged. Surprisingly, the pubic hair almost com-, C* i& C' U4 K( `) N2 Z7 `
pletely disappeared except for a few vellous hairs at% @! `# B2 r) v; S, A' U2 H7 q4 w
the base of the phallus. Testicular volume was still 2( _) I: H2 Q5 o) A: F4 c* I
mL, and the size of the penis remained unchanged.
  V- {3 P9 K7 Y  c% W; |The mother also said that the boy was no longer hav-/ B& @  E: H* @8 H. ]/ Z
ing frequent erections.' ~& N, [8 u9 b' k/ w" o% y  N
Both parents were again questioned about use of
6 K- e# q% X( t' xany ointment/creams that they may have applied to
- R- A6 [  T" H; `5 s. N$ `the child’s skin. This time the father admitted the
- U# o, _& e. q. pTopical Testosterone Exposure / Bhowmick et al 541# a/ N/ N3 @2 |& \. {& O/ \
use of testosterone gel twice daily that he was apply-% `- |6 ^4 Z. }- Y! b1 W% H- V
ing over his own shoulders, chest, and back area for
2 z1 k) ]3 F9 S, K, o/ sa year. The father also revealed he was embarrassed
# _4 a1 U- x( h4 }% u( Nto disclose that he was using a testosterone gel pre-
# G5 \' Z# }3 p9 r+ q8 ~' sscribed by his family physician for decreased libido
  H$ f3 e( t! r5 Z% A8 y+ o" s, f5 ~secondary to depression.! U0 L. N6 V' e) ^! a; E, D. W' B
The child slept in the same bed with parents.
# q7 Z7 Y, E- S! C* |$ n9 L' wThe father would hug the baby and hold him on his& O" ?% S* a. y' j8 |
chest for a considerable period of time, causing sig-
* O- d+ O& s: p! f; tnificant bare skin contact between baby and father.6 D+ ^1 Q$ `1 w. x! }- f0 g! @: C% Z
The father also admitted that after the phone call,* }2 \; l  O, V% f: K
when he learned the testosterone level in the baby
/ _6 F; G3 V' |& I$ G/ ?was high, he then read the product information2 M( S# l. K( {, p* g) b
packet and concluded that it was most likely the rea-
1 \. Y  T3 ?+ R+ A$ o+ t2 ?son for the child’s virilization. At that time, they
& K2 Z! p$ u, P* h$ v$ B2 h# ydecided to put the baby in a separate bed, and the
; _$ m' i1 J8 dfather was not hugging him with bare skin and had3 A, ]2 D0 Q& ^& ~
been using protective clothing. A repeat testosterone/ l( f- J: S3 l) p
test was ordered, but the family did not go to the8 K) a) k; a5 l0 E4 G3 U) ]0 H
laboratory to obtain the test.
" Y% B2 s. [6 l" cDiscussion# S4 f. [; u5 @8 d9 y9 M7 s* o
Precocious puberty in boys is defined as secondary( z3 y8 O7 J& t' |, j( i9 ?
sexual development before 9 years of age.1,4
! {  S9 K1 N6 ]3 X- M9 x0 F2 ^Precocious puberty is termed as central (true) when
* q% W" Y' l! a' R8 Sit is caused by the premature activation of hypo-
7 S- X+ D' D  ?& o$ s% Q7 ~- _thalamic pituitary gonadal axis. CPP is more com-
3 @: F$ y* y  v% B" Pmon in girls than in boys.1,3 Most boys with CPP
* H$ F+ B4 J; _- v2 ?' n5 kmay have a central nervous system lesion that is
* k% a2 O; H2 sresponsible for the early activation of the hypothal-, ^# ?5 o0 |- ?! F0 R/ B
amic pituitary gonadal axis.1-3 Thus, greater empha-
0 C4 {2 D  p% D$ }" O' Wsis has been given to neuroradiologic imaging in
- h+ r; V* Y1 X+ y- J, sboys with precocious puberty. In addition to viril-
% L( |$ N" n7 \6 `( `ization, the clinical hallmark of CPP is the symmet-
- D: a8 j  s. F: Zrical testicular growth secondary to stimulation by
( |0 o% }3 K7 H. K/ [+ Dgonadotropins.1,3) T% T! h9 F. Q7 A, `1 W) @' a
Gonadotropin-independent peripheral preco-+ q! x  d6 F1 q0 U
cious puberty in boys also results from inappropriate
, d* l# j$ c* V" X) Tandrogenic stimulation from either endogenous or% V4 n3 J+ H7 \
exogenous sources, nonpituitary gonadotropin stim-0 m2 |1 k5 s; {, }. I: d0 ?# \& U
ulation, and rare activating mutations.3 Virilizing
3 [- ~) P' d/ R6 U* v. k+ O3 ^4 ccongenital adrenal hyperplasia producing excessive- Y4 I8 ?( B- H5 A7 M% _9 R, H$ C
adrenal androgens is a common cause of precocious8 R% S( q, u/ b/ [
puberty in boys.3,4
# [% F, R! ]9 `: v5 q+ d3 xThe most common form of congenital adrenal- y/ s6 H) B5 E7 E: r- g, d
hyperplasia is the 21-hydroxylase enzyme deficiency.3 ]3 ^, P- q/ o
The 11-β hydroxylase deficiency may also result in$ P! c. |) X$ T  A+ F, N
excessive adrenal androgen production, and rarely,+ V7 m5 W' w7 d1 l7 j$ f
an adrenal tumor may also cause adrenal androgen' T1 R5 a- ~5 A- y1 t
excess.1,3
8 w( u' I, ]! t& W* d0 j* hat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: Q. T) R9 S, N0 ^542 Clinical Pediatrics / Vol. 46, No. 6, July 2007. O; Q1 @* i  Z" ~& q
A unique entity of male-limited gonadotropin-
8 U* z- I- |1 M, i0 kindependent precocious puberty, which is also known: f% v( L. m- S6 A; H
as testotoxicosis, may cause precocious puberty at a+ C/ G$ w* }. O+ A. d! o0 v: e
very young age. The physical findings in these boys
# g) j/ u* D6 Q# D) g$ K+ G" _with this disorder are full pubertal development,
" S+ B+ l: k8 {9 p% Z0 p+ hincluding bilateral testicular growth, similar to boys7 Y! v# E7 S+ g+ }% Y2 S& \
with CPP. The gonadotropin levels in this disorder
9 h  R9 n' E& I9 n8 {8 S1 zare suppressed to prepubertal levels and do not show
) X; C: S0 ~! A% vpubertal response of gonadotropin after gonadotropin-
5 a0 s( n/ y. o* r& b, X2 _releasing hormone stimulation. This is a sex-linked
. W3 w% O" D' a) B6 X+ D  gautosomal dominant disorder that affects only
* K0 L9 G9 l7 A4 Q) C% Zmales; therefore, other male members of the family
* M& q9 i1 X$ k% H" z) \& ?may have similar precocious puberty.3
3 i) U% m/ V% c: S6 z$ X2 KIn our patient, physical examination was incon-
8 l1 B' ?4 f' g/ \9 Ysistent with true precocious puberty since his testi-
+ r/ x% @. N1 z( M. W. x! M. f$ pcles were prepubertal in size. However, testotoxicosis$ A* A* @5 D' {! Z+ G4 Q  A
was in the differential diagnosis because his father
/ [3 \! s2 m. O1 \! q0 pstarted puberty somewhat early, and occasionally,  d; g) C# u5 A4 e) D+ M
testicular enlargement is not that evident in the& C, k7 _- k+ Y
beginning of this process.1 In the absence of a neg-  P& M" N8 @: [8 _& |
ative initial history of androgen exposure, our
; u5 i, [( e; Wbiggest concern was virilizing adrenal hyperplasia,8 [5 z0 [3 A! |6 L0 i6 P
either 21-hydroxylase deficiency or 11-β hydroxylase
4 _0 h5 S# _& J' p! x9 i4 wdeficiency. Those diagnoses were excluded by find-5 p0 G8 h; U4 b% c. \8 F' K
ing the normal level of adrenal steroids.9 M1 v2 i" r, J' d- D1 a
The diagnosis of exogenous androgens was strongly
; G& q6 r% w) Z2 C& Dsuspected in a follow-up visit after 4 months because% [6 b2 S. E; J5 c" {' o. J
the physical examination revealed the complete disap-" c9 D- \8 ~8 X+ k# W. |! M
pearance of pubic hair, normal growth velocity, and
# h  o  T, L& S% n4 h; ^/ o6 h$ adecreased erections. The father admitted using a testos-
, v7 U/ k% q" cterone gel, which he concealed at first visit. He was2 i! k# Q+ o8 {$ m
using it rather frequently, twice a day. The Physicians’* Y/ w: W2 y7 h* V% Y+ A1 U
Desk Reference, or package insert of this product, gel or
  h! M. S+ s7 Xcream, cautions about dermal testosterone transfer to$ B; ?$ z+ ]8 e. x' s1 ]" x
unprotected females through direct skin exposure.
3 L0 T5 p5 W8 jSerum testosterone level was found to be 2 times the9 u0 H, h% t1 t. N4 Q% Y1 I: D7 Z
baseline value in those females who were exposed to" j" N$ C9 t* ]+ P" R5 u
even 15 minutes of direct skin contact with their male- W5 q( {- M0 e/ m6 f6 N' A; J
partners.6 However, when a shirt covered the applica-
) k) X5 b: S: V& {tion site, this testosterone transfer was prevented.
9 M: \* b2 U0 c7 F* J( W- i! {# eOur patient’s testosterone level was 60 ng/mL,
8 u% ?5 T5 m8 I9 d) P! w: d6 y& N! s; [which was clearly high. Some studies suggest that* h+ |; W* q  D. q, a1 n6 z6 H9 g7 R, g
dermal conversion of testosterone to dihydrotestos-
4 E( q+ Q" G0 k* i3 B/ _terone, which is a more potent metabolite, is more* {$ s5 V. H1 b6 T4 i/ t
active in young children exposed to testosterone
5 K' R. p8 k1 ~1 f0 T! K) S2 wexogenously7; however, we did not measure a dihy-" C5 {" \/ ]9 x8 i' j) l: f
drotestosterone level in our patient. In addition to5 C- ]" W7 j3 C7 \* q
virilization, exposure to exogenous testosterone in% p% w& Y, b; R# t# e- {: B
children results in an increase in growth velocity and
+ r/ I" y% r3 A9 [3 Iadvanced bone age, as seen in our patient.6 x( ~$ ]7 b) z  E2 P' R" i5 ~
The long-term effect of androgen exposure during
5 T9 }  [6 \+ I; y0 b2 w8 V6 e; uearly childhood on pubertal development and final
& T9 c, y' B# D. T9 L; O5 A% Y1 i' radult height are not fully known and always remain
: T. g6 a, b, V$ B3 \5 f8 s; ja concern. Children treated with short-term testos-
+ `5 g7 b7 K& [4 S! n5 vterone injection or topical androgen may exhibit some
$ d4 g- h' P0 d1 a& ~/ Nacceleration of the skeletal maturation; however, after% C5 U1 x3 w, E4 ]
cessation of treatment, the rate of bone maturation: V0 S8 |* w% \; W' z- s0 g
decelerates and gradually returns to normal.8,9
% ?* }0 V. H. E* W% @) h/ LThere are conflicting reports and controversy& R2 c% l* h* C8 y0 q
over the effect of early androgen exposure on adult
9 a( G0 h+ V  apenile length.10,11 Some reports suggest subnormal
) K& P* `6 Y  Y- C1 kadult penile length, apparently because of downreg-
) S6 ]. Z. i3 ~0 bulation of androgen receptor number.10,12 However,
1 }" A+ w( \6 M- TSutherland et al13 did not find a correlation between
+ x5 Y# R  i2 h0 \$ o. ^# K/ Mchildhood testosterone exposure and reduced adult5 r: D& K; K- V# t2 E
penile length in clinical studies.
$ P* e4 a- ^+ p* g, I# j! u9 ONonetheless, we do not believe our patient is9 M! n# U0 o3 I- L
going to experience any of the untoward effects from1 D8 Q: T8 M: I  E: ]) P
testosterone exposure as mentioned earlier because
3 ?0 H2 P0 Y1 g' m: l/ n- N4 ]$ `" @the exposure was not for a prolonged period of time.
) \5 \7 C' G4 y9 a$ w( z5 B! P7 H1 k6 F" ZAlthough the bone age was advanced at the time of
/ Z7 l, l" y, S7 a+ M( Mdiagnosis, the child had a normal growth velocity at
1 H9 F6 t# r, X2 }, O6 I0 s& `) Rthe follow-up visit. It is hoped that his final adult
; ]& H; z# R0 Nheight will not be affected.5 t9 D4 e  u& K: ?+ R  ^
Although rarely reported, the widespread avail-
8 f1 ?$ a/ o! Aability of androgen products in our society may
9 N" F* h0 D# T& [! ?indeed cause more virilization in male or female
9 {# H! Z/ I: R+ mchildren than one would realize. Exposure to andro-
" f( H' d. p, q2 _% qgen products must be considered and specific ques-% E' _) x% ^- c5 c* D4 h$ p
tioning about the use of a testosterone product or
2 s% e0 q3 ^( e3 \  v* ogel should be asked of the family members during
) f4 e- M! @0 G# v7 a; Q9 bthe evaluation of any children who present with vir-
2 W9 N$ {) S+ L& nilization or peripheral precocious puberty. The diag-( N7 g' _2 }6 l, z$ N( e' n" T/ x
nosis can be established by just a few tests and by0 k& u7 e9 l& U' U0 _% w
appropriate history. The inability to obtain such a9 `5 f2 E; r4 Z3 t; S" w
history, or failure to ask the specific questions, may4 m' e1 Z% ]9 t) A+ }. ^& y$ L
result in extensive, unnecessary, and expensive7 r( B  n  Y( l; q  z' l& l. ]
investigation. The primary care physician should be
' ^9 @/ ?# d- c/ X" N( A2 D  Z* i8 qaware of this fact, because most of these children
6 }3 K2 B+ a* M( n) Nmay initially present in their practice. The Physicians’8 R6 q8 r7 X5 I, r' H: x
Desk Reference and package insert should also put a, O# U# E% ^4 P  ~5 r! r
warning about the virilizing effect on a male or
% u* _1 D& [% W" Q( `8 @female child who might come in contact with some-
3 \- Z6 ]# w# D9 Z, Aone using any of these products.
$ q1 M1 B8 v: Q3 Z* NReferences% j: C  X( ~* o' m+ y1 g* j
1. Styne DM. The testes: disorder of sexual differentiation4 h  r' F- h4 q) S3 E4 {7 W1 t
and puberty in the male. In: Sperling MA, ed. Pediatric( Q, ?# h2 B0 {2 G7 h* E' `% }( o
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;0 S  M$ A0 f! |" D
2002: 565-628.
, a' Y+ t+ u7 U% I2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious2 V: @2 e0 B/ e) k- U0 [4 d+ F
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old0 U; J. X! ~+ d
Boy Induced by Indirect Topical0 ?! c4 F" I- L/ A" P2 Q+ N8 J
Exposure to Testosterone
; l1 T1 F( h7 Q# ~: ^( qSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
* q- _0 a4 O7 E4 f: ^: _: N3 Rand Kenneth R. Rettig, MD1+ k2 V% F8 A3 {4 a" `* `
Clinical Pediatrics
: o( k1 D& _8 IVolume 46 Number 6
; g9 c# _7 s9 x. T; O. W+ KJuly 2007 540-543' y$ J$ a. [2 Q4 Q( k
© 2007 Sage Publications, H! f0 l. }# k  |
10.1177/0009922806296651
, _. D: P% d9 G- q- rhttp://clp.sagepub.com+ I# O3 Y! ~2 b' Y. {
hosted at4 Z. J! b  ]; }  p
http://online.sagepub.com
1 n3 |1 @0 R: d) L0 u0 X' rPrecocious puberty in boys, central or peripheral,+ x7 H# L9 B! d/ a/ s$ g) ^
is a significant concern for physicians. Central
- r5 J9 d+ h4 S* nprecocious puberty (CPP), which is mediated
4 S& ?$ A3 b6 I  Ethrough the hypothalamic pituitary gonadal axis, has
& O! l: B  e  Ka higher incidence of organic central nervous system7 K2 A7 s$ N) K1 @
lesions in boys.1,2 Virilization in boys, as manifested7 l* V7 |/ h  J
by enlargement of the penis, development of pubic
/ C9 n% w( l% qhair, and facial acne without enlargement of testi-
* Z7 o: I5 Q' Y+ b+ n: \cles, suggests peripheral or pseudopuberty.1-3 We
; g/ c3 o" c* Freport a 16-month-old boy who presented with the
: k# ~6 [/ |& l1 Y0 S% ]enlargement of the phallus and pubic hair develop-5 H: m) u: T( n; `4 w
ment without testicular enlargement, which was due) ~, N8 K) X& _. ~# {% q
to the unintentional exposure to androgen gel used by
6 `: z( N. F6 t4 l$ Qthe father. The family initially concealed this infor-
% ?5 d* W/ f: _. B+ v5 p% Cmation, resulting in an extensive work-up for this
5 a- Q( Y: B% C' Uchild. Given the widespread and easy availability of$ e1 F6 `# |5 W  j  c" g3 `! a
testosterone gel and cream, we believe this is proba-
+ v' o! Z$ }- P) `: T8 Lbly more common than the rare case report in the! w! o8 X3 f0 {, N
literature.4
" m8 I0 F7 ]+ O& F7 `( VPatient Report
: H8 G6 C: J8 W& r7 iA 16-month-old white child was referred to the
: g/ G/ p9 Q% L' `+ X( K- lendocrine clinic by his pediatrician with the concern. }! e, n  j/ l% b, Q' h
of early sexual development. His mother noticed
4 p5 R4 j1 d4 I( K$ l. z0 Rlight colored pubic hair development when he was
0 x9 c& ~+ V- W4 x' i( a9 n' i: _From the 1Division of Pediatric Endocrinology, 2University of; S) v/ r( o9 ]
South Alabama Medical Center, Mobile, Alabama.( R( z6 U6 Q% P2 c$ f( A. J  d' B
Address correspondence to: Samar K. Bhowmick, MD, FACE,$ ]- `# `# v1 X7 x. C& @0 N0 v
Professor of Pediatrics, University of South Alabama, College of
; A( x; d+ p; f8 K0 i# P& b3 oMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;, m3 Q; _2 z6 _' P
e-mail: [email protected].. ]8 k: X6 G; Q9 a' Q5 j
about 6 to 7 months old, which progressively became
3 s- w& }8 }! D7 K( udarker. She was also concerned about the enlarge-
3 L( p' v5 Z* p% t; L; wment of his penis and frequent erections. The child
. l/ m; R; O$ Owas the product of a full-term normal delivery, with" U' w& @3 H( N- ~3 u: E
a birth weight of 7 lb 14 oz, and birth length of
) Y( C9 N6 n9 Q" U3 o7 _20 inches. He was breast-fed throughout the first year) @: @+ @2 W5 o/ h) m$ b  y
of life and was still receiving breast milk along with
: r/ {  F& G" ^solid food. He had no hospitalizations or surgery,7 h1 g" y1 L& e/ A7 ^7 G" [4 h
and his psychosocial and psychomotor development& S/ v" [+ o" N# }3 U  |
was age appropriate.
6 W( a$ g! ~4 b1 `# d- m' TThe family history was remarkable for the father,5 v4 ]1 T, q# k& f2 o, `. M
who was diagnosed with hypothyroidism at age 16,
. y0 u, P7 v5 K6 p/ \1 |6 x& _which was treated with thyroxine. The father’s6 X' x: l& A+ J$ |  J
height was 6 feet, and he went through a somewhat
. K+ O+ I7 q" G0 R0 A5 M& A1 D, P! yearly puberty and had stopped growing by age 14.
4 M, q6 }! b$ m: E: I, _1 Q& ZThe father denied taking any other medication. The$ s6 O9 `. W( p5 X; |8 V
child’s mother was in good health. Her menarche% g3 u/ ^+ E& A( S1 h
was at 11 years of age, and her height was at 5 feet
4 a4 ^6 a; ^* i  h, v0 S5 inches. There was no other family history of pre-
1 h" V4 r3 ]  d+ h2 gcocious sexual development in the first-degree rela-1 D- e* b# I+ v& p4 L6 f
tives. There were no siblings.
+ m2 k3 @: {2 s5 S( APhysical Examination
4 a4 v  w4 D. s/ JThe physical examination revealed a very active,* `: j3 e. m/ t& ?8 ^0 e
playful, and healthy boy. The vital signs documented
; Q# L4 I+ T4 `! S( Na blood pressure of 85/50 mm Hg, his length was
8 p% J5 G7 b: P3 o90 cm (>97th percentile), and his weight was 14.4 kg" j1 h" [  s( Q$ T5 u" @
(also >97th percentile). The observed yearly growth
" U# ?! Y; o2 v6 P* v0 |9 F/ a6 xvelocity was 30 cm (12 inches). The examination of
" S/ I" C, F4 h: ~4 nthe neck revealed no thyroid enlargement.6 |) A+ g& u+ ^
The genitourinary examination was remarkable for
, p  A1 X* t6 C' J7 b  Lenlargement of the penis, with a stretched length of
9 @( X& E$ q1 V1 \9 [7 q8 cm and a width of 2 cm. The glans penis was very well
0 I6 e# K, X" W- x' Kdeveloped. The pubic hair was Tanner II, mostly around* Z8 N0 u) P6 @6 h, r
540
  ^5 u$ ^4 H* ?, Y7 Y" ^at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ U6 u, j# T9 h; o& ythe base of the phallus and was dark and curled. The# u* Q8 w; t1 O
testicular volume was prepubertal at 2 mL each.
" e) J- w2 M' I& \5 DThe skin was moist and smooth and somewhat- Y4 {8 s/ Z- y" \3 k. t
oily. No axillary hair was noted. There were no+ u4 G  X! m  o7 b+ u# ]/ a+ v. O
abnormal skin pigmentations or café-au-lait spots.
+ T* d" p& `1 W4 Q! i- ~Neurologic evaluation showed deep tendon reflex 2++ p7 Q4 S5 k, I
bilateral and symmetrical. There was no suggestion
9 D# ~1 R' C  e  x# ?of papilledema.' G& t& d% ?0 f  n' p+ m  O  l1 R
Laboratory Evaluation
: E; B, F& X% ^5 U  m3 AThe bone age was consistent with 28 months by7 I/ A- j' Q; N/ }  S
using the standard of Greulich and Pyle at a chrono-
1 u9 e8 ^/ x& o' `/ ulogic age of 16 months (advanced).5 Chromosomal
! t" N3 C. Y$ i/ ^# A& i2 Ukaryotype was 46XY. The thyroid function test. q' t: v) {4 |
showed a free T4 of 1.69 ng/dL, and thyroid stimu-5 n% o9 h6 I2 h# [+ g- x
lating hormone level was 1.3 µIU/mL (both normal).  a; Y! q" W* i
The concentrations of serum electrolytes, blood" K! O! y( o/ q. r5 W& e# s- ~  i+ M
urea nitrogen, creatinine, and calcium all were
8 S* @# N+ \8 p) V2 N$ [; Mwithin normal range for his age. The concentration% J' P# x  g* v, \. F4 c: d
of serum 17-hydroxyprogesterone was 16 ng/dL$ _) f7 e; s. y# J, _8 L  l3 F
(normal, 3 to 90 ng/dL), androstenedione was 20' _0 _% n6 Q8 m9 r# N" b+ H
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-5 V9 v- N6 G+ s9 b! c* x
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
( N& {2 V3 [/ v0 l5 b. `desoxycorticosterone was 4.3 ng/dL (normal, 7 to7 E7 ~) J0 r8 S$ l- A
49ng/dL), 11-desoxycortisol (specific compound S)7 D5 B  {' Z( u; j5 h6 Q0 }/ q
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-; q# L; p8 w, \% ?# `
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
2 l" h1 b' r: ^* i7 ^- ntestosterone was 60 ng/dL (normal <3 to 10 ng/dL),/ C% b  E& c$ x& d2 d. y! K$ H
and β-human chorionic gonadotropin was less than
7 I# s. x% d% V& e4 U' ~5 mIU/mL (normal <5 mIU/mL). Serum follicular
1 S9 P' U+ ~- a# Z# ~stimulating hormone and leuteinizing hormone! d  O2 ?4 {( w9 D/ j4 Z- o5 p
concentrations were less than 0.05 mIU/mL+ Y% a" c; r+ @: t# p+ o5 K1 |7 V
(prepubertal).
3 l8 m/ Q+ \. k# _/ tThe parents were notified about the laboratory
9 ]! \  j% c1 d# [4 Q  Iresults and were informed that all of the tests were- C' `4 ^1 W5 y9 K
normal except the testosterone level was high. The2 r* n  d* W# f8 [5 F
follow-up visit was arranged within a few weeks to
  N- K6 u/ O. s; Oobtain testicular and abdominal sonograms; how-; I; D- T. P4 @4 K
ever, the family did not return for 4 months.9 V0 ]: c$ Y7 k7 T6 y* m
Physical examination at this time revealed that the  x% B, u9 G7 I
child had grown 2.5 cm in 4 months and had gained  F4 O  X, F/ s' m  ^; B0 E
2 kg of weight. Physical examination remained
' |, @, I2 @, qunchanged. Surprisingly, the pubic hair almost com-
( c  G5 \* R( ^  upletely disappeared except for a few vellous hairs at# V4 W0 w  V1 u, s* P1 q  d% A
the base of the phallus. Testicular volume was still 2
6 a% t+ y+ k# U1 a, s8 n4 \mL, and the size of the penis remained unchanged.8 v! ^% s- I1 b1 R
The mother also said that the boy was no longer hav-
' N& n' @% ?2 b, [. {: w# Wing frequent erections., `- j: r/ F* w) c
Both parents were again questioned about use of5 [+ I5 d) X# D( v' `6 ~
any ointment/creams that they may have applied to2 I: l/ ~4 ]% j4 H
the child’s skin. This time the father admitted the, W" i3 A% W3 P& u* F& g8 G, M
Topical Testosterone Exposure / Bhowmick et al 541
5 @. P6 N2 \! X3 E9 j% ause of testosterone gel twice daily that he was apply-
! Z: }5 Q. U. C6 }- ving over his own shoulders, chest, and back area for
; M# G$ D, f$ L0 ba year. The father also revealed he was embarrassed* j+ E( g! J9 \6 t
to disclose that he was using a testosterone gel pre-
5 Y: J  V% J) f4 H& zscribed by his family physician for decreased libido
8 v5 i7 A* T; J) Q" a6 \secondary to depression.2 [4 x' A. l* }
The child slept in the same bed with parents." M. y6 ?1 q9 H( i
The father would hug the baby and hold him on his' k# _% u% C7 f& b/ t0 a! r) U
chest for a considerable period of time, causing sig-8 s- X, _" S# l' r
nificant bare skin contact between baby and father.
1 b! w, E* v1 w7 H7 Q! m+ FThe father also admitted that after the phone call,0 V- Q: ^+ _) y0 M$ c2 c( e
when he learned the testosterone level in the baby# X$ I$ T2 |( f' Q5 M9 Q
was high, he then read the product information
+ O: S2 E' [6 T. hpacket and concluded that it was most likely the rea-. p! B" M5 h* P- M; }! P( P4 Q; }
son for the child’s virilization. At that time, they9 u! a, a" K0 a2 d. x) w& l
decided to put the baby in a separate bed, and the
4 n8 i* s0 I( r: g5 cfather was not hugging him with bare skin and had  o# X3 _4 o. h/ @# N/ R7 i6 {% Z
been using protective clothing. A repeat testosterone4 I# @! i% Y0 ?# e+ R  D# R- S) J
test was ordered, but the family did not go to the( K# C; A4 }% g8 e1 x: ]
laboratory to obtain the test.: b3 O3 V+ ?, v6 ^
Discussion6 a/ a' @8 P% Y; d% ~$ g, A
Precocious puberty in boys is defined as secondary& w  D: l6 v% N
sexual development before 9 years of age.1,4
9 c7 A" I. I' d  E$ sPrecocious puberty is termed as central (true) when6 u9 c8 I3 `9 y5 `! _2 k
it is caused by the premature activation of hypo-
) ?( r( w) D: \: |* G; Athalamic pituitary gonadal axis. CPP is more com-3 f5 O, G- e# o
mon in girls than in boys.1,3 Most boys with CPP
8 |8 A% r' C# a+ {may have a central nervous system lesion that is$ }' B/ p. Z3 V; P
responsible for the early activation of the hypothal-
, I/ s* f3 k: |. Qamic pituitary gonadal axis.1-3 Thus, greater empha-
; W7 e0 B; q" P( Osis has been given to neuroradiologic imaging in2 J% W" ~* S$ f& S4 S6 s1 @
boys with precocious puberty. In addition to viril-) Z: m: k3 x6 r# f
ization, the clinical hallmark of CPP is the symmet-
4 u7 [- S- a. U3 r, `: urical testicular growth secondary to stimulation by
# y5 J' A/ d+ @6 U" O/ g5 bgonadotropins.1,3
# \) A& a& g# C$ l/ t- S6 MGonadotropin-independent peripheral preco-
( _: s$ W" W9 O" Ucious puberty in boys also results from inappropriate
1 c# T5 _* W0 {( U0 z3 G9 Mandrogenic stimulation from either endogenous or/ S% ~) Q2 f2 |
exogenous sources, nonpituitary gonadotropin stim-4 M# B1 Y: N" l, T/ L
ulation, and rare activating mutations.3 Virilizing3 Z  f! g4 y# k$ x" O$ ]
congenital adrenal hyperplasia producing excessive
6 r2 X5 m0 ~" q. qadrenal androgens is a common cause of precocious5 F* Y4 K# h2 F$ m
puberty in boys.3,4$ i$ @& g- E4 @: q1 {. Y6 g
The most common form of congenital adrenal( A2 J: L; q- D0 g5 E
hyperplasia is the 21-hydroxylase enzyme deficiency.
; B8 V5 F0 V" p4 \The 11-β hydroxylase deficiency may also result in5 i' d# d/ d5 h) V9 m: E
excessive adrenal androgen production, and rarely,7 X2 F% O$ q% x  u  `
an adrenal tumor may also cause adrenal androgen
2 d8 F( p+ Q! d, w9 Dexcess.1,3* W4 Q8 x- T6 M* |
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 X$ `' S8 G1 w
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
7 ~/ C4 h( y9 V( J$ g9 G+ yA unique entity of male-limited gonadotropin-
1 Q$ S8 P1 C6 M9 N6 _independent precocious puberty, which is also known
9 g( S9 J/ w+ I  v- F8 \5 ras testotoxicosis, may cause precocious puberty at a  T2 t- A, C) [% O& q; L
very young age. The physical findings in these boys
0 ?1 r0 m+ y1 w' Cwith this disorder are full pubertal development,+ M: c8 p8 {0 M' b# N9 x% B
including bilateral testicular growth, similar to boys7 H5 q% D6 `! L7 n9 m. j
with CPP. The gonadotropin levels in this disorder
6 q% H8 H+ X: u: y0 Hare suppressed to prepubertal levels and do not show8 G) L' A+ E% O& w
pubertal response of gonadotropin after gonadotropin-
  B1 ^. P# X1 I& R6 m, a3 K( Ireleasing hormone stimulation. This is a sex-linked
+ o9 u- o" ?/ W6 E1 cautosomal dominant disorder that affects only$ ?% |( J4 j, y' t
males; therefore, other male members of the family
  E. X; z- |* |" _may have similar precocious puberty.3" v! `3 u% i+ i% ^
In our patient, physical examination was incon-& `% m# {# G# g5 ?; I9 P. E
sistent with true precocious puberty since his testi-2 u  C3 m7 m. Y# O# [
cles were prepubertal in size. However, testotoxicosis2 ^: K- U4 B0 U# r
was in the differential diagnosis because his father  n: k. I( `7 k4 y# |% O5 Q7 G
started puberty somewhat early, and occasionally,$ f* I% Q% S; ^/ z
testicular enlargement is not that evident in the
3 Q4 x- q/ F& G3 Dbeginning of this process.1 In the absence of a neg-. ?6 p7 b& \+ M
ative initial history of androgen exposure, our  D/ h' D6 u- H1 {5 q5 g
biggest concern was virilizing adrenal hyperplasia,
* z4 Y9 y; R: C# Veither 21-hydroxylase deficiency or 11-β hydroxylase
& o" O4 U, I2 D* [deficiency. Those diagnoses were excluded by find-' l* ~! }0 F0 m" Z, }6 N" a
ing the normal level of adrenal steroids.
/ n% |5 q, S0 d4 hThe diagnosis of exogenous androgens was strongly6 U/ i4 z/ J$ B  [
suspected in a follow-up visit after 4 months because
; T$ u; ^9 x9 A* z/ Gthe physical examination revealed the complete disap-
% y- U2 D) q9 P( |4 X& }" ipearance of pubic hair, normal growth velocity, and2 N& S+ N& s- T3 S9 b* a
decreased erections. The father admitted using a testos-
& ?4 `: g8 U$ X6 f$ e  y9 V5 R; _% F9 vterone gel, which he concealed at first visit. He was
- H+ o5 s) w4 k" W# j( busing it rather frequently, twice a day. The Physicians’& j( C3 L; n! y- G/ _0 k. y
Desk Reference, or package insert of this product, gel or
8 C' Q0 D! r/ T0 u1 i9 P- pcream, cautions about dermal testosterone transfer to
5 S+ c: ^& |% ?unprotected females through direct skin exposure.0 I- w1 o/ ]1 E/ Q
Serum testosterone level was found to be 2 times the. P8 c2 ~5 C- {+ w4 ]( O- ^5 x" N6 h# Z  L
baseline value in those females who were exposed to4 Y; J) R: }% O9 e, q/ t; ~# t
even 15 minutes of direct skin contact with their male
. o8 e0 ~: |. j! ^% I1 d9 b% Lpartners.6 However, when a shirt covered the applica-% {' U, N! f: {* x
tion site, this testosterone transfer was prevented./ D( {4 {- c) T( R4 Y
Our patient’s testosterone level was 60 ng/mL,* k" b* L* O% ^3 b% {0 ?. I$ ^. R
which was clearly high. Some studies suggest that- b# o4 |3 l8 p: t/ T
dermal conversion of testosterone to dihydrotestos-, v" I' U: g* ?' V4 J! O% J$ n% R% I9 M
terone, which is a more potent metabolite, is more" i( v7 z2 M) @$ Q  k
active in young children exposed to testosterone8 v  w& o: c* V! c7 I
exogenously7; however, we did not measure a dihy-, _+ q% s6 V" R. r  |
drotestosterone level in our patient. In addition to8 \: ]0 O& z' W
virilization, exposure to exogenous testosterone in
5 W) t9 i/ \3 D+ y( lchildren results in an increase in growth velocity and
  v5 I4 s0 h  N+ u' Nadvanced bone age, as seen in our patient.
- B4 b2 j4 v* K8 E* a% gThe long-term effect of androgen exposure during
0 I% W% J4 N/ r- m0 e: g7 aearly childhood on pubertal development and final8 x" {8 s8 ]; {4 X6 W
adult height are not fully known and always remain6 K; X9 q' |! W% k2 e) }( `0 M
a concern. Children treated with short-term testos-" k* \6 p0 |0 ?4 ~' Z+ `" i
terone injection or topical androgen may exhibit some
, t9 Y- ^: ?8 l6 cacceleration of the skeletal maturation; however, after5 H% F2 o8 Z1 K) O
cessation of treatment, the rate of bone maturation
$ t& P. h% Z& ^decelerates and gradually returns to normal.8,9
# k# |! m1 V) o- U! g1 M3 K% p' RThere are conflicting reports and controversy
% r0 q7 G5 O' k6 B" e9 Jover the effect of early androgen exposure on adult% x' K0 j2 a0 U# e, i7 x
penile length.10,11 Some reports suggest subnormal
; k% x- y. P0 Jadult penile length, apparently because of downreg-
5 K0 o! ]/ A8 Sulation of androgen receptor number.10,12 However,: v8 @( O9 \+ |* e1 C% W, k. e( ]
Sutherland et al13 did not find a correlation between
/ i2 \" i+ n, ^6 J) z8 b$ Lchildhood testosterone exposure and reduced adult
1 j0 M6 K7 A( j; @' F7 Vpenile length in clinical studies.
; f8 s/ G+ P: T& _1 k, m' @! x. TNonetheless, we do not believe our patient is
3 f" r3 i/ M$ S  [# A; v% V* rgoing to experience any of the untoward effects from0 s) Y! y. m) a5 P' m+ u
testosterone exposure as mentioned earlier because0 T9 f* I0 T0 r  I# d
the exposure was not for a prolonged period of time.
' S) Z/ j5 x& p1 d. ?' O. m: W/ W2 U; VAlthough the bone age was advanced at the time of
5 F7 `  M7 w" I  ?. D3 Kdiagnosis, the child had a normal growth velocity at
8 X- l- e/ h0 p# I9 Y7 y# jthe follow-up visit. It is hoped that his final adult5 ^. ~5 p! H2 f% y
height will not be affected.
$ l; }$ X  t) f& lAlthough rarely reported, the widespread avail-
9 z5 L% e! x" y% v/ A: a" a* gability of androgen products in our society may
; e) a$ O- s# r' n/ N& y7 C' C5 L8 [indeed cause more virilization in male or female8 I+ g% I$ c! t
children than one would realize. Exposure to andro-! ?5 K( X9 Z" f& Q
gen products must be considered and specific ques-9 ~* e! j# |& i2 Q6 D3 H# h
tioning about the use of a testosterone product or: E. L/ V5 L! W/ q2 w& a
gel should be asked of the family members during( \. _9 Q& N+ `+ u
the evaluation of any children who present with vir-
- \. }9 W& D/ q6 T! f5 {ilization or peripheral precocious puberty. The diag-0 t/ l* o& o3 n$ f- t3 f/ a
nosis can be established by just a few tests and by
5 Q) F  [1 p" c9 c; D9 @appropriate history. The inability to obtain such a
- F$ i1 B  M$ N1 {: ]history, or failure to ask the specific questions, may; I& G! L" f0 b. `, j
result in extensive, unnecessary, and expensive
& b7 F' a! F- oinvestigation. The primary care physician should be
% B; e' K0 K0 _aware of this fact, because most of these children0 d* R+ ]. n& ?5 t
may initially present in their practice. The Physicians’
2 u  p! h! c: l  `$ N6 {$ P: WDesk Reference and package insert should also put a
8 T% j$ B, K8 ^warning about the virilizing effect on a male or
/ E. `# Z& Q; L# h: N4 }female child who might come in contact with some-
8 s" e3 R* }) E, C7 s5 Pone using any of these products.
' N  J# y% u- J: L9 bReferences
1 T1 X: s7 ~( X# C1 k1. Styne DM. The testes: disorder of sexual differentiation3 Z7 \( Z8 U( o. _3 B
and puberty in the male. In: Sperling MA, ed. Pediatric
# Z+ Q( u3 j* R! K# y$ |" k7 oEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
9 O( Z" Z3 n6 j* ^( W' E+ G  [3 z2002: 565-628.
' W. R' e! X3 u3 D9 n0 ?- L2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
$ a/ s1 i: `; k5 E) 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
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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
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
# M8 _& k0 |4 f) n) K
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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