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Sexual Precocity in a 16-Month-Old
8 I' k  Z2 M  `Boy Induced by Indirect Topical- ]2 U" e+ F+ p2 I, A# c  a8 O
Exposure to Testosterone2 v- s& r% a& z9 m6 j$ G! n
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2/ ?- E! @! z( c9 e7 Y
and Kenneth R. Rettig, MD1
3 U& e( h! |, h( a6 n+ }6 VClinical Pediatrics5 k* R1 i6 g3 y5 o, u
Volume 46 Number 6
( g9 I5 l: ~, p. cJuly 2007 540-543
6 ]; c) t- B, U© 2007 Sage Publications
% ^4 M$ e$ B/ Q8 w2 i. O% S! C10.1177/0009922806296651
- d% S4 Y7 a; Yhttp://clp.sagepub.com
& x2 n: v) k% I! s: |# G1 Lhosted at: i! u8 s3 W+ e5 c+ R9 r
http://online.sagepub.com
+ N1 f1 U3 `# Z( u4 P1 C+ Q7 ^- k2 TPrecocious puberty in boys, central or peripheral,
, G6 m9 B6 j: vis a significant concern for physicians. Central
% {; @4 M) b) e" D, z5 Dprecocious puberty (CPP), which is mediated. @- J% ?) w, F1 Z5 }* p0 d; Q
through the hypothalamic pituitary gonadal axis, has
# k1 \1 F5 Z) J+ \  F3 r/ Aa higher incidence of organic central nervous system
9 R: o7 V/ a- Zlesions in boys.1,2 Virilization in boys, as manifested
) F& J! a. J& `" j- ^by enlargement of the penis, development of pubic
: Z3 ~: L' H( Y& J% o/ lhair, and facial acne without enlargement of testi-
1 i* V2 J# g5 g: X& @cles, suggests peripheral or pseudopuberty.1-3 We
+ |6 g6 Y& B3 t0 d) }report a 16-month-old boy who presented with the4 y& B5 j5 K% i2 F1 M1 U( u
enlargement of the phallus and pubic hair develop-
6 U1 R- m+ m/ n; Qment without testicular enlargement, which was due: Y0 Q' k; g& E. W
to the unintentional exposure to androgen gel used by
: C0 H5 g5 |# X% t; i; cthe father. The family initially concealed this infor-
2 g4 i* ]  h3 C. k, L9 A( ?mation, resulting in an extensive work-up for this
8 X# K1 T  |, F: Xchild. Given the widespread and easy availability of# N, O- ?# k1 u
testosterone gel and cream, we believe this is proba-) E. Q4 C2 Q/ \( G
bly more common than the rare case report in the
0 Z/ E) x# i. q# O7 vliterature.4! V8 A7 W8 D& {
Patient Report+ F, s  v1 U: g% S5 T2 F" y
A 16-month-old white child was referred to the
. I) B. S! Z( b2 h+ j( {0 c$ P) @9 wendocrine clinic by his pediatrician with the concern7 r  V( z+ e  c  X1 x/ Z7 V
of early sexual development. His mother noticed' x3 n6 t: x: J/ S" G3 n
light colored pubic hair development when he was2 ~! o+ T0 X6 A6 {$ [
From the 1Division of Pediatric Endocrinology, 2University of8 {$ [; Y. P5 b5 q: ]
South Alabama Medical Center, Mobile, Alabama.. z6 S6 u# o& Q# g$ Z) L
Address correspondence to: Samar K. Bhowmick, MD, FACE,
. w- d0 L8 v( y8 P# q: q) xProfessor of Pediatrics, University of South Alabama, College of0 l5 d+ M, j  N% W  c2 @2 K
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;/ i3 l$ ~( S. c; q" T6 K4 V3 O- S
e-mail: [email protected].
3 x. f: \; @8 n8 ?$ e3 Nabout 6 to 7 months old, which progressively became2 u* }- {, S6 i: F
darker. She was also concerned about the enlarge-
3 n7 |6 e2 g/ i1 fment of his penis and frequent erections. The child
8 {1 j( U  Z$ u& V: lwas the product of a full-term normal delivery, with
9 u% l% ]' z7 `/ Y. |/ |9 Ra birth weight of 7 lb 14 oz, and birth length of
) D* _1 K0 z0 z' t20 inches. He was breast-fed throughout the first year: l2 J" E8 z0 S
of life and was still receiving breast milk along with; ^  K/ E/ h- g3 W7 \3 O, A4 e
solid food. He had no hospitalizations or surgery,' }, x& `& }: j' W
and his psychosocial and psychomotor development  Z0 X# h& R6 J0 F- J1 C+ k
was age appropriate.
$ X' i. L- {  E7 t. L& i4 qThe family history was remarkable for the father,
2 e4 H3 X$ j' @" b. {7 @) Vwho was diagnosed with hypothyroidism at age 16,
: s$ n+ h- @. |" {which was treated with thyroxine. The father’s
# T+ @2 v1 `; Qheight was 6 feet, and he went through a somewhat
8 X  s. J4 i' l. ^: N5 Fearly puberty and had stopped growing by age 14.
: I0 H. m% n9 [  t. ^4 e2 P* ^3 UThe father denied taking any other medication. The% i. R  s; m& M
child’s mother was in good health. Her menarche
, L# ]$ [5 \/ V5 E( E( U) mwas at 11 years of age, and her height was at 5 feet+ Z2 E4 l4 }/ R: }, X
5 inches. There was no other family history of pre-6 Z6 \( H* ?# L3 R
cocious sexual development in the first-degree rela-; x% i  v6 j6 k; ~/ n; |- V
tives. There were no siblings.
$ `" D7 }' I; q1 v( t2 N+ [* ]( wPhysical Examination: n8 e& H& R) L3 |
The physical examination revealed a very active,( P( I& u/ R* D2 R
playful, and healthy boy. The vital signs documented3 X' x0 F4 _  i) ?0 V9 J/ a; S: w
a blood pressure of 85/50 mm Hg, his length was
4 u2 p2 H5 q& x, y& u" R" H  {90 cm (>97th percentile), and his weight was 14.4 kg! @) E# d( k9 p; H+ ]/ E
(also >97th percentile). The observed yearly growth5 \: R4 A# }# C& I- L+ i9 L+ _
velocity was 30 cm (12 inches). The examination of5 {: Y2 C* K& d+ Z( v9 M7 M  P% K, j
the neck revealed no thyroid enlargement.
" c+ |$ p% j' o/ A, wThe genitourinary examination was remarkable for5 F% i% A( S- O( t0 F; Y8 v# N
enlargement of the penis, with a stretched length of) E% U. y9 U, w- M) R* B
8 cm and a width of 2 cm. The glans penis was very well4 S  a9 h2 z1 b1 M; E1 W
developed. The pubic hair was Tanner II, mostly around# p  t( W$ \0 }) t% n
540
) n* T( T- o% _* T& y4 {at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 b: m  u4 b, P
the base of the phallus and was dark and curled. The
0 p$ I  U, I. G" J0 Ptesticular volume was prepubertal at 2 mL each.; R+ A- B% y0 n5 V* B4 Y( V6 {! |
The skin was moist and smooth and somewhat
/ a! |% M/ l7 X8 K( ~1 M, voily. No axillary hair was noted. There were no
$ k$ }9 R- i' @; x/ A# n; tabnormal skin pigmentations or café-au-lait spots.0 _! f, W, U  K9 a: s# ]
Neurologic evaluation showed deep tendon reflex 2+
' ?; V) K* {7 p/ }% E+ zbilateral and symmetrical. There was no suggestion' j* x: ]) f! [5 T, g. c% O* c
of papilledema.1 B& c6 Y2 `3 j7 @$ x. ]% u
Laboratory Evaluation3 R  H, p! C. B: a, O
The bone age was consistent with 28 months by
% h- I/ y. X3 R# u1 r7 U- c/ T9 Ousing the standard of Greulich and Pyle at a chrono-& c8 e: x" ]$ O$ u
logic age of 16 months (advanced).5 Chromosomal  ~) }1 ^: J/ |% H; J1 ~
karyotype was 46XY. The thyroid function test, ?4 V5 I& q4 u' m1 t2 ]
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
8 i& @  o/ F+ slating hormone level was 1.3 µIU/mL (both normal)., B) \  f# H( x
The concentrations of serum electrolytes, blood" D9 D, H1 j! b; X5 \
urea nitrogen, creatinine, and calcium all were) i3 `9 g; F1 z) `( _+ J3 M; ]; _2 U  b
within normal range for his age. The concentration
1 s0 ?( _; e9 F- rof serum 17-hydroxyprogesterone was 16 ng/dL
4 Z, A8 M& H! m% W3 V1 q, H4 k; L(normal, 3 to 90 ng/dL), androstenedione was 20
# J$ P% h/ B1 c& u. cng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-  P! H" j# }" ]; Q4 q8 b) T+ v' z
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
1 e/ [: x8 H$ }4 I  n1 tdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
. l" h" O. o7 j49ng/dL), 11-desoxycortisol (specific compound S)) O1 i; @" A6 Q$ b0 \, d1 K
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
6 N& F9 Y. l* B6 J& i% L6 Jtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total/ _3 _3 Y2 k- d) D$ r' }- `
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
1 s2 F$ }6 D2 Y9 o) q; r' {and β-human chorionic gonadotropin was less than( ^/ Z  q& i' n% T; Q
5 mIU/mL (normal <5 mIU/mL). Serum follicular
) t# Q/ ^% q4 ]* y- zstimulating hormone and leuteinizing hormone" [) V+ e9 n4 }  r6 L. E
concentrations were less than 0.05 mIU/mL* @4 d5 ]( ~: |1 @) s8 H$ z2 N
(prepubertal).
* T2 S5 N# s# X/ ?& [: pThe parents were notified about the laboratory/ y- v: X0 N. n1 u1 D9 U5 R
results and were informed that all of the tests were0 L* Q2 _9 F0 C% a: b4 Q, `
normal except the testosterone level was high. The0 a. l7 F! C' x; K/ Z
follow-up visit was arranged within a few weeks to
0 e1 }4 K; X* T% R' y3 |obtain testicular and abdominal sonograms; how-1 R! ?. G+ E# H3 s; c8 `
ever, the family did not return for 4 months.4 [' r4 x' n! r
Physical examination at this time revealed that the2 @: d6 m) {+ b6 V& E
child had grown 2.5 cm in 4 months and had gained
/ ]: e1 l9 g& [& C2 kg of weight. Physical examination remained
7 x$ s2 J6 {' K2 iunchanged. Surprisingly, the pubic hair almost com-6 s% Y3 _% U: ^! q; Z
pletely disappeared except for a few vellous hairs at
% [' e3 O( o( w1 `" N: h7 cthe base of the phallus. Testicular volume was still 2
* J2 q) b8 H: H) U9 BmL, and the size of the penis remained unchanged." c& b4 F+ R% |2 u7 x+ ?
The mother also said that the boy was no longer hav-
- t" y% g; s7 z9 cing frequent erections., K/ }6 E$ O) m- B& h0 A, ~
Both parents were again questioned about use of& }+ K1 f: z  I" y  ?1 v. H: ]
any ointment/creams that they may have applied to
% p, d2 w2 L0 Y8 N! \7 Lthe child’s skin. This time the father admitted the1 Q9 T9 V, x3 g5 i: L/ |" _
Topical Testosterone Exposure / Bhowmick et al 541
; f. ?* A$ j3 Y- A! F* `3 y% Iuse of testosterone gel twice daily that he was apply-7 b* H7 G8 i8 M# [
ing over his own shoulders, chest, and back area for
+ n0 g1 M6 w7 t2 r& h, xa year. The father also revealed he was embarrassed
7 n' p2 f3 S' L# ~7 r% u! \( y6 Mto disclose that he was using a testosterone gel pre-( h9 d0 H+ ]  \1 p2 w  w. U
scribed by his family physician for decreased libido  ]5 n9 U1 v* L  W( _
secondary to depression.
6 @  p& ^" ~' a6 x) lThe child slept in the same bed with parents.
: ^$ F0 q0 Z6 M. C+ bThe father would hug the baby and hold him on his. }1 Y. X1 x7 g( U$ z% H8 A
chest for a considerable period of time, causing sig-
( b8 y5 u! {2 l$ l4 |nificant bare skin contact between baby and father.
# a0 f8 ]: [$ r/ p$ jThe father also admitted that after the phone call,
& J4 Q8 P' K) A2 Mwhen he learned the testosterone level in the baby
# z! G9 a, y: ]% ]7 y3 M7 A6 N& t. _was high, he then read the product information- [8 @, c/ p& Z
packet and concluded that it was most likely the rea-6 v% x! G/ S& o8 J+ a" \( `; J
son for the child’s virilization. At that time, they" X7 }. V' v0 B
decided to put the baby in a separate bed, and the% i* m+ x3 f5 m& z; k! T  w* @0 t
father was not hugging him with bare skin and had5 G9 u6 K. w( C9 k) e: i
been using protective clothing. A repeat testosterone. h+ X7 C# R3 J# T" x* ?0 \3 A
test was ordered, but the family did not go to the
+ S  J( N, }& T4 f5 N5 glaboratory to obtain the test.4 y- k, M  e/ V. t. d5 q6 S
Discussion5 h) Z; W: S2 {$ R0 G/ J" [# q, A
Precocious puberty in boys is defined as secondary2 l4 S+ Q% ?' |& C  N2 Q& p; n/ w7 @
sexual development before 9 years of age.1,4
0 g# V% P( N' y4 W  ~( t2 @2 ]Precocious puberty is termed as central (true) when
, s* f7 W1 J+ I  U: A/ p' E: l3 g4 cit is caused by the premature activation of hypo-
0 Y  f4 m: Z. @/ Y# R- Kthalamic pituitary gonadal axis. CPP is more com-
- r$ I! ]2 ]% y2 C; ]mon in girls than in boys.1,3 Most boys with CPP
7 ~, m+ V5 k8 D7 Y) [may have a central nervous system lesion that is9 V8 w: U% w$ g
responsible for the early activation of the hypothal-
1 y$ e* v! y' W/ Zamic pituitary gonadal axis.1-3 Thus, greater empha-3 \+ \8 o+ k4 L) e  I& C
sis has been given to neuroradiologic imaging in8 X7 ^5 u1 o; n
boys with precocious puberty. In addition to viril-* c' x( }1 e' ?
ization, the clinical hallmark of CPP is the symmet-: F! U' \1 x. F2 _9 E9 [
rical testicular growth secondary to stimulation by
8 C$ Q' e0 g$ P* |9 Xgonadotropins.1,31 F5 @1 |/ `* i- W- @
Gonadotropin-independent peripheral preco-9 ^' U" B" U8 n, C$ l! b7 L
cious puberty in boys also results from inappropriate
; g+ J/ M9 `; n9 z. I% c7 O! fandrogenic stimulation from either endogenous or2 W, u& g+ O- a/ [
exogenous sources, nonpituitary gonadotropin stim-
9 S# P4 h4 Q6 c5 R  Culation, and rare activating mutations.3 Virilizing
+ q! @4 |- l4 V5 ^congenital adrenal hyperplasia producing excessive
5 u" i* Q0 h: F: g& S1 {( B3 nadrenal androgens is a common cause of precocious, D! G/ X& M, [! @/ h5 p
puberty in boys.3,4
$ `8 r1 j3 Z5 H  DThe most common form of congenital adrenal
* Q" ?" k, |# m. Lhyperplasia is the 21-hydroxylase enzyme deficiency.
7 G7 q; n+ H) t$ \  |7 g1 Z; q4 Z9 bThe 11-β hydroxylase deficiency may also result in
- y* u. ~/ v$ C3 Xexcessive adrenal androgen production, and rarely,
0 ~: i% Y0 X8 U1 K3 can adrenal tumor may also cause adrenal androgen
1 }( G) p  l2 i% j/ E9 I1 _3 yexcess.1,32 L, h) W" h3 ~# R2 i: k+ \
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from8 V7 O& y. F# p! F. o( k/ ^( m; V
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& j# x8 n/ N% X1 I$ c2 P! h# nA unique entity of male-limited gonadotropin-
( W/ |. ?& x8 v5 W+ R' i' z3 mindependent precocious puberty, which is also known' B6 i5 J: Y3 F' f( c
as testotoxicosis, may cause precocious puberty at a5 S  v* R3 w; Y) o7 x8 i' Z
very young age. The physical findings in these boys: r: O: b* @9 c8 C. n  \
with this disorder are full pubertal development,5 a  p0 Z7 t& O( a% n+ f$ R. H
including bilateral testicular growth, similar to boys0 N6 G  E6 |# T7 p& d% Z
with CPP. The gonadotropin levels in this disorder
( X0 I6 P' p, h6 u; Fare suppressed to prepubertal levels and do not show
2 Z- u, W  D) \& U1 S' m; Gpubertal response of gonadotropin after gonadotropin-( s0 ?- G  R& V- o9 T
releasing hormone stimulation. This is a sex-linked
/ a% Q- f; C0 x6 ~1 f, b6 v' Oautosomal dominant disorder that affects only
/ U$ |" U5 x% d, Amales; therefore, other male members of the family
; H. R/ i& ]5 ~1 t2 V. Q8 Lmay have similar precocious puberty.3
$ z0 D: c' {- T& N/ e4 ~8 jIn our patient, physical examination was incon-
+ o, q* r. P& ^0 b5 B3 o5 hsistent with true precocious puberty since his testi-- t8 U; F5 l! H1 `3 d: A( d
cles were prepubertal in size. However, testotoxicosis
' r! n3 }3 j8 a/ d! A. uwas in the differential diagnosis because his father
4 o/ b8 v; K0 k2 F. lstarted puberty somewhat early, and occasionally,
7 }! T1 a$ F, g' [$ t" ~testicular enlargement is not that evident in the
" \7 ?& H+ ^$ X) `# t% y' Zbeginning of this process.1 In the absence of a neg-
/ {5 D$ r  |% j, }+ ~- I9 ]ative initial history of androgen exposure, our
6 u9 m8 d. i! f) W; [biggest concern was virilizing adrenal hyperplasia,
/ p/ B3 ^5 V+ @8 n; g7 F1 s0 Ieither 21-hydroxylase deficiency or 11-β hydroxylase+ K6 W& [/ A7 j# q5 o' U$ S! S
deficiency. Those diagnoses were excluded by find-
& G( G- B- H- ning the normal level of adrenal steroids.% d# \4 I, v9 b
The diagnosis of exogenous androgens was strongly
+ `; v0 y* ?4 ]% q; _suspected in a follow-up visit after 4 months because
' N8 I" q8 y2 p  V7 U  A3 Nthe physical examination revealed the complete disap-
4 K2 S: W3 V& a* @pearance of pubic hair, normal growth velocity, and6 `" C8 m; q6 F& K6 `) y0 i
decreased erections. The father admitted using a testos-
* [9 z9 Q3 G  C7 L7 d! sterone gel, which he concealed at first visit. He was
; A/ I& C- Y, |. kusing it rather frequently, twice a day. The Physicians’
& K9 t) }) e2 p) a. H8 aDesk Reference, or package insert of this product, gel or/ [# w) H, K, S  R- v- g( G, e5 p
cream, cautions about dermal testosterone transfer to$ K% C, ]+ o5 {2 \  w9 U& O# [
unprotected females through direct skin exposure.
& ~& j1 V# i# n9 jSerum testosterone level was found to be 2 times the
2 z* }- D9 r9 ~% a1 dbaseline value in those females who were exposed to) @4 Y8 s  q4 u, J  o
even 15 minutes of direct skin contact with their male
3 d% S9 C9 P7 |) j( T) R! t3 lpartners.6 However, when a shirt covered the applica-
" r) \8 {* Y! x( r' H% Ytion site, this testosterone transfer was prevented.' N; H/ o& P0 Q3 F
Our patient’s testosterone level was 60 ng/mL,/ J2 o3 S. ]2 u" z0 k% R  T
which was clearly high. Some studies suggest that
9 n3 g, a5 G- v* `dermal conversion of testosterone to dihydrotestos-# p/ W2 `  k% T: r6 Y& F
terone, which is a more potent metabolite, is more% y9 G) ^! j, @0 T- U
active in young children exposed to testosterone
9 P5 w# ]. M. ^* Mexogenously7; however, we did not measure a dihy-
6 Z" s$ b+ j* u7 h3 ~2 pdrotestosterone level in our patient. In addition to5 A8 \; Z; R* r7 E. c* s. }/ X- D
virilization, exposure to exogenous testosterone in8 n0 b. ~6 o! u6 R" b4 [
children results in an increase in growth velocity and% s! r0 ~# B) p0 c0 J& U; K
advanced bone age, as seen in our patient.. n) o; ^  f) Q2 x! J/ k5 }
The long-term effect of androgen exposure during) z+ q+ U# \* P3 |+ V% p: s
early childhood on pubertal development and final0 K( N, h) R; X! s, P) U4 Y
adult height are not fully known and always remain
; H! b. S1 L/ `a concern. Children treated with short-term testos-7 C1 U2 s; I. j$ E
terone injection or topical androgen may exhibit some+ U- ?2 ]4 J+ b* f
acceleration of the skeletal maturation; however, after
; P* S& N! Z2 f! wcessation of treatment, the rate of bone maturation
$ ?; Z* r5 |) f4 mdecelerates and gradually returns to normal.8,9+ O, J: R( x3 X( c! |  R
There are conflicting reports and controversy% B7 H% ~9 [" r8 P8 c
over the effect of early androgen exposure on adult
4 W; m! Z# r2 m0 r/ k& _8 Spenile length.10,11 Some reports suggest subnormal
2 V4 v, ^! a$ g! [8 T$ d. sadult penile length, apparently because of downreg-! X  a- ^) Z7 L- Y
ulation of androgen receptor number.10,12 However,
# t* j* B0 a' o3 _: ?Sutherland et al13 did not find a correlation between7 r* D" S3 o3 R: G. ~
childhood testosterone exposure and reduced adult
( }' Q7 R; v  q4 Z$ E% vpenile length in clinical studies.
8 m/ a' ^& w* |Nonetheless, we do not believe our patient is
& {8 N, I7 V9 w+ f3 v' U) v: U+ igoing to experience any of the untoward effects from8 W! x. j3 B3 J0 }  Y/ d; j' \
testosterone exposure as mentioned earlier because
3 f$ a, f3 P; k! p8 pthe exposure was not for a prolonged period of time.3 B' W9 U) B* R
Although the bone age was advanced at the time of, q" H2 j, N$ w' y6 }
diagnosis, the child had a normal growth velocity at, ]0 f* Q; Z4 L8 S- |
the follow-up visit. It is hoped that his final adult, u0 V' h+ r' _1 h- K$ a
height will not be affected.
: x) _) t  F/ V5 F, CAlthough rarely reported, the widespread avail-
3 B+ t- Q& Y$ d" {& |# _ability of androgen products in our society may
) ~- y% r/ M0 ?. h6 P( @% y$ y( sindeed cause more virilization in male or female
. R2 z: z% N; s6 ichildren than one would realize. Exposure to andro-$ g) V; `, z% S: L
gen products must be considered and specific ques-/ E/ {" L) }; {+ k4 o
tioning about the use of a testosterone product or
8 x0 C1 M0 k6 \, Ogel should be asked of the family members during/ Q( Q2 ^) `; z7 X
the evaluation of any children who present with vir-: x. u1 L, H' y, R: d
ilization or peripheral precocious puberty. The diag-# `( q* o, W/ u6 @9 `
nosis can be established by just a few tests and by
1 Q$ K; |% V8 z0 C4 qappropriate history. The inability to obtain such a. A8 b9 t2 n( ]% r: V. L) z. k
history, or failure to ask the specific questions, may
- P. N) s- @8 V8 A; Hresult in extensive, unnecessary, and expensive+ p2 [  T+ I+ x% N8 `; m
investigation. The primary care physician should be
1 b8 z) P/ J! faware of this fact, because most of these children
- F! F+ ]9 |" A- P& }* Mmay initially present in their practice. The Physicians’5 Q- z- b. Z1 d+ Q7 C$ m* a
Desk Reference and package insert should also put a" w5 b8 b$ V  q3 H4 Y
warning about the virilizing effect on a male or  @8 R5 X8 a* J/ m5 c; G: j- M  Z
female child who might come in contact with some-3 i' E* o; Z! C% d
one using any of these products.8 _* V( R/ x* d0 @
References
  I: X" d4 [2 O# [1 ]1. Styne DM. The testes: disorder of sexual differentiation
$ y" ]. ~/ W$ ^$ hand puberty in the male. In: Sperling MA, ed. Pediatric1 t! u' E3 t* p
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;1 J) v$ J& p3 I
2002: 565-628.9 T$ n- S0 E2 E( ~" C( x
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
' \, z" s# G! k2 Wpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old  ^. {" }: ?) p. X
Boy Induced by Indirect Topical
0 l5 ^8 E% `% UExposure to Testosterone
! l  k, {$ t8 u! {8 `, [' }$ P* gSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,26 j5 h; S0 G4 `) F& o2 c
and Kenneth R. Rettig, MD12 n- P# o8 [0 ?/ H: z
Clinical Pediatrics
2 n+ K8 D; {! W  e( }+ R3 _8 LVolume 46 Number 63 R8 \% A- _, x2 d" t3 \
July 2007 540-543
  G, Q4 r4 Y# k© 2007 Sage Publications' G* q: p9 m  O4 l
10.1177/0009922806296651
1 `& L# |5 E; |; F1 M) j0 [* N# uhttp://clp.sagepub.com% l5 @# N) P$ @& E1 n/ J( K
hosted at
  F/ H1 K4 o" [2 ehttp://online.sagepub.com3 Q' H" p% t: y  F
Precocious puberty in boys, central or peripheral,
. u  i/ G& k$ r8 ]  |! z7 xis a significant concern for physicians. Central4 \$ u. w6 D9 V+ v1 w: G# B% i; F
precocious puberty (CPP), which is mediated3 x6 u  \1 K& w+ h2 L. j
through the hypothalamic pituitary gonadal axis, has1 H* p0 K' ~! S, Z# s4 o* [" H0 j
a higher incidence of organic central nervous system
4 h/ c& C. o7 }. L2 }8 \lesions in boys.1,2 Virilization in boys, as manifested+ o; y/ B& d( K
by enlargement of the penis, development of pubic  k/ a/ \0 _4 S& N5 L! B' z
hair, and facial acne without enlargement of testi-
* T+ ^! H! e$ ?" G0 Xcles, suggests peripheral or pseudopuberty.1-3 We
" h* ]! _+ ]( v& e& Jreport a 16-month-old boy who presented with the- f8 w4 Z. Z6 \  W! h
enlargement of the phallus and pubic hair develop-
9 ~: m% a7 f1 Z& V# oment without testicular enlargement, which was due
# ~* s9 j- E, n( L' S2 |to the unintentional exposure to androgen gel used by# ]% z' \' n+ H7 ~
the father. The family initially concealed this infor-
3 n5 _0 Z) y- D; H8 ~0 `# rmation, resulting in an extensive work-up for this. V8 g5 R* K' I. H- W. h7 U
child. Given the widespread and easy availability of- X# J. O) p$ y$ h8 |6 r! G+ R
testosterone gel and cream, we believe this is proba-
! `7 V; z) R( q1 zbly more common than the rare case report in the, C( d; [! U6 X/ y, s0 Z0 i2 A6 f
literature.4- K8 G) W# n# S% _
Patient Report. t+ L: Q+ ]# ]7 `8 j
A 16-month-old white child was referred to the
+ O: z( y, h+ |: [6 fendocrine clinic by his pediatrician with the concern( W: H" P0 [. A+ N. F: y  D# R
of early sexual development. His mother noticed
1 y. O4 ~* L0 ?4 \2 Q0 D3 Q$ {light colored pubic hair development when he was
# c  V/ ^' b. ?From the 1Division of Pediatric Endocrinology, 2University of+ P* h: r" k7 ]( }/ `
South Alabama Medical Center, Mobile, Alabama.
% y+ {* G% K3 a$ ~- }# s# l! xAddress correspondence to: Samar K. Bhowmick, MD, FACE,
+ K9 I, \5 m9 g$ h) K- @) A: SProfessor of Pediatrics, University of South Alabama, College of
1 q+ J/ j9 j4 yMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;1 c7 T0 L1 L4 g1 f. R/ V
e-mail: [email protected].
) M; ]! @& T0 V/ R% ^+ ?about 6 to 7 months old, which progressively became5 K7 m1 n" {+ t( M. [! r
darker. She was also concerned about the enlarge-$ O9 y/ Y5 M# }6 d
ment of his penis and frequent erections. The child# Q# q+ G7 R  \& H+ o% C* f
was the product of a full-term normal delivery, with# D  E( ^6 X: [/ x" _! F9 K
a birth weight of 7 lb 14 oz, and birth length of1 y- c4 C5 I" N0 }8 e: W
20 inches. He was breast-fed throughout the first year: j4 d' T7 N0 f
of life and was still receiving breast milk along with
# O5 \" K) ^/ Q- osolid food. He had no hospitalizations or surgery,  L/ a' N' o* ]! \2 w/ }9 h; l
and his psychosocial and psychomotor development
& q4 @. y9 D% ~; ]: b6 w4 H+ J5 zwas age appropriate.
# M1 u5 @) ~& y; C3 cThe family history was remarkable for the father,# _- v( \8 p" i( b3 ^0 N/ V
who was diagnosed with hypothyroidism at age 16,
7 j- J6 I3 ?: kwhich was treated with thyroxine. The father’s  b$ z# o. I. x! j! u- D' H- [: @
height was 6 feet, and he went through a somewhat
! o- C: z! `, \early puberty and had stopped growing by age 14.
# z( f  Z! Z, x8 u8 gThe father denied taking any other medication. The+ Z7 Q! \6 C4 S% c4 q. ]
child’s mother was in good health. Her menarche8 R' o6 Q) X$ P& c
was at 11 years of age, and her height was at 5 feet
) B1 T1 x8 h+ G2 y. v9 h0 I5 inches. There was no other family history of pre-
% y: x  z: _; {# P. v6 x! gcocious sexual development in the first-degree rela-2 ~  K2 `/ C3 I2 `( t# i
tives. There were no siblings.4 _+ B5 X9 w4 k# H
Physical Examination
: j! h, q& I" W4 v  g. ~- J/ NThe physical examination revealed a very active,
& K! a5 ?  b& r, Q3 r" s! e  Q' X6 C$ Pplayful, and healthy boy. The vital signs documented
, g$ t8 W" k3 Ca blood pressure of 85/50 mm Hg, his length was/ B2 i% e' q' X9 `4 u' j. ]8 M
90 cm (>97th percentile), and his weight was 14.4 kg9 J+ B& v, h7 F0 }
(also >97th percentile). The observed yearly growth% S; U8 ~5 N. M  \1 B  N$ \
velocity was 30 cm (12 inches). The examination of
) w: N+ i" e9 S$ R* O) Ithe neck revealed no thyroid enlargement.
) \1 s2 ?2 c! f- rThe genitourinary examination was remarkable for
- Z/ ]1 ]% A2 c9 M; ~7 lenlargement of the penis, with a stretched length of* l6 T: R: q2 z* U. r" b$ `) z
8 cm and a width of 2 cm. The glans penis was very well( M8 R$ L1 V# Q3 w- B
developed. The pubic hair was Tanner II, mostly around( X5 R  g, S2 }% e" C. R. ^
5408 `4 D  p0 M" t' B
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) W7 b' Z6 T) Othe base of the phallus and was dark and curled. The* k" g+ y3 z) {$ o0 b- H
testicular volume was prepubertal at 2 mL each., q' F* b  s$ J
The skin was moist and smooth and somewhat
- {3 M4 B0 O0 _7 |8 Loily. No axillary hair was noted. There were no
! V6 f: x( j. k) a! {; U: b  }abnormal skin pigmentations or café-au-lait spots.) f0 k/ x$ Y5 M- C+ Z% u- s2 `
Neurologic evaluation showed deep tendon reflex 2+/ r" t. L5 e+ \  J" w% \+ K9 {5 K. A
bilateral and symmetrical. There was no suggestion) \8 n6 o' a6 G3 Z: u! p
of papilledema.9 D1 d* \, {3 {6 M: W5 [6 `
Laboratory Evaluation
2 m) w1 y( r: p" l) y1 [The bone age was consistent with 28 months by; b+ g7 l9 l9 I) T
using the standard of Greulich and Pyle at a chrono-- @: {2 m, B; F+ L9 a; c4 K  E; i
logic age of 16 months (advanced).5 Chromosomal
7 v1 J  ^. y  X# pkaryotype was 46XY. The thyroid function test9 b/ [8 i+ _4 }% ~  G
showed a free T4 of 1.69 ng/dL, and thyroid stimu-5 V' N; a4 `9 ]/ A/ ^2 [
lating hormone level was 1.3 µIU/mL (both normal).
  s, }4 L. c% [4 cThe concentrations of serum electrolytes, blood$ O) D; k9 o! ]6 M5 a
urea nitrogen, creatinine, and calcium all were
4 j5 D' J, j/ c& M0 Q& bwithin normal range for his age. The concentration2 ~) d! F$ w7 Q
of serum 17-hydroxyprogesterone was 16 ng/dL" T$ [, I, I0 A) |% h' T: F6 A  c; |
(normal, 3 to 90 ng/dL), androstenedione was 20
5 f' g; v% a" D  K' F9 @# a2 i7 Eng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
' V2 w7 [7 c* E, Aterone was 38 ng/dL (normal, 50 to 760 ng/dL),1 G+ F& s8 o9 Y% C8 X
desoxycorticosterone was 4.3 ng/dL (normal, 7 to8 p! v! W5 s% a* m+ T
49ng/dL), 11-desoxycortisol (specific compound S): p( j; ^9 P: q& a( e0 L/ b
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
+ ]+ g: V  |6 U& mtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total2 T7 d$ U; Y# Z% `5 V
testosterone was 60 ng/dL (normal <3 to 10 ng/dL)," r* B6 l3 E3 k$ V2 w
and β-human chorionic gonadotropin was less than
3 f: w; |  g# d8 m  e5 mIU/mL (normal <5 mIU/mL). Serum follicular  |- p0 g& ?. S( P  v
stimulating hormone and leuteinizing hormone" v4 j/ s9 G# x, Q5 a- ^- J
concentrations were less than 0.05 mIU/mL
( x' ~# D/ N* @9 s  d(prepubertal).0 e4 L6 v. S+ o% j
The parents were notified about the laboratory. n6 h! O. l/ k, i' r4 x
results and were informed that all of the tests were
, J1 _3 o! H7 i  ?5 R3 jnormal except the testosterone level was high. The& l: J' Y4 f. u6 s* e
follow-up visit was arranged within a few weeks to
2 D* n  P8 C4 |% ~% V: nobtain testicular and abdominal sonograms; how-
1 j4 c% F5 e8 Y0 P7 {ever, the family did not return for 4 months.0 x- g4 q4 c, T/ W
Physical examination at this time revealed that the# q1 C$ D! G' a3 k
child had grown 2.5 cm in 4 months and had gained
' C) D' K2 N$ ?4 f( e2 kg of weight. Physical examination remained9 O' `4 A8 u. q+ c: C. N% Q
unchanged. Surprisingly, the pubic hair almost com-
/ O! R1 h, `2 G) @% E9 `8 o2 Y3 Q6 kpletely disappeared except for a few vellous hairs at7 l" F) m5 f$ b' b& _/ e" B+ L
the base of the phallus. Testicular volume was still 2
$ _" \4 G' H6 N/ M) d% e5 AmL, and the size of the penis remained unchanged.
/ p+ K, N5 n) @( t0 P7 P1 [( VThe mother also said that the boy was no longer hav-
$ c& m2 R8 e" z7 ~. Ring frequent erections.
( b9 G! I  N6 f# Z' Y6 |  }! [Both parents were again questioned about use of7 a+ O" M4 U. ?& h# _
any ointment/creams that they may have applied to
+ Z0 Q7 u  G: U( W1 V3 |: Y5 p' Athe child’s skin. This time the father admitted the! ~: h7 n. Q# b
Topical Testosterone Exposure / Bhowmick et al 541
/ G& ], x! w! Y4 Iuse of testosterone gel twice daily that he was apply-  |0 Q6 s0 t  y5 S5 i* I' G
ing over his own shoulders, chest, and back area for  z$ i  z4 R: W, c/ W2 j
a year. The father also revealed he was embarrassed  G% l9 |$ Z% C8 F7 x$ j" [
to disclose that he was using a testosterone gel pre-
6 o/ P5 |9 c; W2 Y. N4 h* b8 S- Xscribed by his family physician for decreased libido
8 I+ C6 _$ m7 j/ y/ A* n+ J8 {0 F/ Fsecondary to depression.$ `4 p8 h, [) F+ A1 y. W* C0 }
The child slept in the same bed with parents.! s, V0 ?9 S3 v% U( p, C( Z/ q9 w
The father would hug the baby and hold him on his* |3 F4 @/ V  t+ o* ^2 w
chest for a considerable period of time, causing sig-- O: u( h- g5 C3 R$ E
nificant bare skin contact between baby and father.
, F8 D  \) b- k3 b# i7 `The father also admitted that after the phone call,
) b4 U! h9 F5 s4 @6 b& qwhen he learned the testosterone level in the baby
9 w$ Z# n# \2 T2 |, S9 ywas high, he then read the product information/ D  o2 i4 X1 Z1 [
packet and concluded that it was most likely the rea-
, j; v! G' g% V0 qson for the child’s virilization. At that time, they
! |6 e# e# y7 C+ O9 _0 Ldecided to put the baby in a separate bed, and the
' e" S0 }& x& R' ~7 \2 Q& ]/ \father was not hugging him with bare skin and had2 `' P+ g# {) u/ j, Z
been using protective clothing. A repeat testosterone2 p8 M7 @% o4 N. Q
test was ordered, but the family did not go to the7 D; l2 q  U# J8 f% r5 n
laboratory to obtain the test.
0 _# b+ A+ g$ k: x; g$ ~8 ~1 d4 \Discussion. D8 Z# g" y" c8 T, I
Precocious puberty in boys is defined as secondary" _  P  Y: ^. P5 [& k7 c% n( n
sexual development before 9 years of age.1,45 z, E+ B) O2 n% |" V0 J' n
Precocious puberty is termed as central (true) when! q/ h* U! s4 _4 ^3 I3 J' K
it is caused by the premature activation of hypo-
5 X2 G& G0 X1 V9 L( v1 h' Hthalamic pituitary gonadal axis. CPP is more com-
# e- g2 C7 @( V. E% b+ G* J% Dmon in girls than in boys.1,3 Most boys with CPP
* N" m5 ~& r) ?+ `- ?5 @; Nmay have a central nervous system lesion that is
9 e/ _! C. @7 q4 n$ yresponsible for the early activation of the hypothal-
& I: {# A. @* hamic pituitary gonadal axis.1-3 Thus, greater empha-
+ q1 x9 x( H& E8 i  t" msis has been given to neuroradiologic imaging in- {( [  S. P( k. h$ D
boys with precocious puberty. In addition to viril-
8 W$ U( v( L  T4 U2 z- U* W& |ization, the clinical hallmark of CPP is the symmet-
* K7 X1 o) M3 x# k/ irical testicular growth secondary to stimulation by
$ L1 F3 N* D$ V# f6 f* Q, y4 pgonadotropins.1,3% j, A8 b4 \# F/ K$ Z) M
Gonadotropin-independent peripheral preco-
% I: [, [, S1 A( jcious puberty in boys also results from inappropriate4 s' |1 b* A6 Y/ Q4 N5 x
androgenic stimulation from either endogenous or) |/ r0 o& |/ W* @1 G: F1 P- z8 T8 K
exogenous sources, nonpituitary gonadotropin stim-( N' S. r! h" |% n5 x0 B) O
ulation, and rare activating mutations.3 Virilizing
. j: r+ C' X+ \5 ^  ^congenital adrenal hyperplasia producing excessive
# I) e7 F! n$ V" [: Q, G! ?* Padrenal androgens is a common cause of precocious
/ p. T& e3 C; ]puberty in boys.3,4
5 T0 @& l( T* A" nThe most common form of congenital adrenal- v1 ^( |5 [& K2 p! B% E2 v
hyperplasia is the 21-hydroxylase enzyme deficiency.
& ~2 d- G2 W+ r  M) D" JThe 11-β hydroxylase deficiency may also result in- S0 v; ~* I, i- l. @
excessive adrenal androgen production, and rarely,! }5 O/ Z% J$ ^3 ?& e. n6 |
an adrenal tumor may also cause adrenal androgen
9 s( \5 S' ?0 k: S/ l+ Jexcess.1,3
$ }, Q! B: |3 kat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ j7 E# M6 V; q5 E& ?: x
542 Clinical Pediatrics / Vol. 46, No. 6, July 20072 ^- b  u% x8 z8 }5 t' z- `, S: z
A unique entity of male-limited gonadotropin-& G- p% o. w: K1 T( u3 R+ C
independent precocious puberty, which is also known" S* I& }; g; ^. ]9 t8 a1 c" C
as testotoxicosis, may cause precocious puberty at a
. p/ e0 z* T: ]# `4 a5 Z6 m( Dvery young age. The physical findings in these boys3 {! b, r2 J, u, E- T
with this disorder are full pubertal development,
" y& Z  B& o1 u+ W+ Gincluding bilateral testicular growth, similar to boys2 W" J* m% Y) |" O
with CPP. The gonadotropin levels in this disorder/ T! K+ T8 L0 N$ A2 L, I
are suppressed to prepubertal levels and do not show( `1 X! w# _+ I' t0 ?. f
pubertal response of gonadotropin after gonadotropin-
8 ]& z$ H$ s8 v; }9 j: f, _+ \releasing hormone stimulation. This is a sex-linked
& z3 y( B" l/ i' ]9 n4 V# `+ yautosomal dominant disorder that affects only
* }6 Q* E8 }, ^9 g/ J1 }males; therefore, other male members of the family
0 K2 o8 N4 B* @9 c' T6 _7 i% ^1 qmay have similar precocious puberty.3
- T! y7 {$ K) M/ V& QIn our patient, physical examination was incon-3 c" a4 c/ m# i& v: c4 Q7 O/ D
sistent with true precocious puberty since his testi-6 X( C+ i/ h& v- c6 U
cles were prepubertal in size. However, testotoxicosis1 r4 y! G. d7 G
was in the differential diagnosis because his father! h. q+ \. `6 _7 r# ?2 _* z
started puberty somewhat early, and occasionally,0 w$ y1 {" w3 ~
testicular enlargement is not that evident in the
! J" \: @' L# W1 g8 `& z8 ebeginning of this process.1 In the absence of a neg-% Z2 p/ H3 Z# t4 w
ative initial history of androgen exposure, our
7 q& C( p# e2 P2 X* o+ L5 Mbiggest concern was virilizing adrenal hyperplasia,
8 z& r( \( i! qeither 21-hydroxylase deficiency or 11-β hydroxylase
6 s' C* e, p/ _! [& J. H# b  H/ M2 fdeficiency. Those diagnoses were excluded by find-
. E/ O) R8 s4 \3 `ing the normal level of adrenal steroids.
7 ^; F  W. O9 ?The diagnosis of exogenous androgens was strongly
& w$ d- L% S- T: o0 Fsuspected in a follow-up visit after 4 months because
4 s. `! B( s. {6 Dthe physical examination revealed the complete disap-1 W. i) ~) c. s9 ^" i
pearance of pubic hair, normal growth velocity, and
4 r; ~- C; M0 B; D( [8 Ddecreased erections. The father admitted using a testos-' J; T+ D" k2 v- ~+ G: H8 w$ L
terone gel, which he concealed at first visit. He was
5 n4 p  K8 w6 Z& b, @  Musing it rather frequently, twice a day. The Physicians’- W5 r8 Z" }1 Z9 I
Desk Reference, or package insert of this product, gel or4 m4 i; Y& a& D" k! K
cream, cautions about dermal testosterone transfer to  Q9 D' G; L9 t  v
unprotected females through direct skin exposure.
5 K% g7 W/ S/ b4 P& c9 \) gSerum testosterone level was found to be 2 times the/ N6 a2 Z1 B( E3 P) e/ `; O0 e$ }
baseline value in those females who were exposed to( H- |3 [/ N9 w- S9 b$ z
even 15 minutes of direct skin contact with their male2 z, @  D, `% Q6 z
partners.6 However, when a shirt covered the applica-9 @8 h4 A+ v* m1 U& N
tion site, this testosterone transfer was prevented.6 x0 S+ E8 q2 D3 [* V* i( S
Our patient’s testosterone level was 60 ng/mL,
7 q9 L7 h( H' @8 ?) o9 c* w: kwhich was clearly high. Some studies suggest that
# r" N% m7 H* Jdermal conversion of testosterone to dihydrotestos-2 P) u* F* [4 u& _0 \7 a- L
terone, which is a more potent metabolite, is more* e' L8 c% ^7 f! s5 r  u
active in young children exposed to testosterone+ ~/ \, u* x# G% f4 P+ f
exogenously7; however, we did not measure a dihy-9 F: f  b7 {+ {* f. w8 G* m* b- t& D
drotestosterone level in our patient. In addition to
+ q. y# p/ @; ?  A8 k/ Ivirilization, exposure to exogenous testosterone in! g/ v3 d2 ?: Y0 h' M; d) s+ A
children results in an increase in growth velocity and1 q6 ?5 C' C, E' [& G" }6 d
advanced bone age, as seen in our patient.5 P* K% p5 ~" ^+ O; p0 b' X
The long-term effect of androgen exposure during& X3 k5 c# y6 I% j. f0 p
early childhood on pubertal development and final& Y. u- u5 a0 c% H& O  f0 Q: Q
adult height are not fully known and always remain, f7 J" O& P0 d- k) C5 X7 D
a concern. Children treated with short-term testos-
! N5 H- z- i1 b* [8 ]! cterone injection or topical androgen may exhibit some
0 f/ }: d) a1 n0 X1 iacceleration of the skeletal maturation; however, after. K8 y3 I5 ^! I. }$ M0 g. x
cessation of treatment, the rate of bone maturation& Z0 j8 Z. V: f2 O# O
decelerates and gradually returns to normal.8,9  a) }' |, N0 O3 f" e6 W5 M" m
There are conflicting reports and controversy5 W% S+ k3 z5 O1 G. \4 Z& ?
over the effect of early androgen exposure on adult+ J5 G, x3 B7 n5 M& a5 V2 t0 N6 Y
penile length.10,11 Some reports suggest subnormal
* m& n$ m* a8 F2 l% Uadult penile length, apparently because of downreg-
7 E8 O6 M6 m# u) W+ N. G& D  `ulation of androgen receptor number.10,12 However,1 z, m! H' A+ a% s% r8 }0 `
Sutherland et al13 did not find a correlation between
1 \5 F$ S" h/ r4 _. Q/ [childhood testosterone exposure and reduced adult2 H& M* X7 \' W, t  ]7 g$ b
penile length in clinical studies.
% E$ C# ]" J, S6 c9 KNonetheless, we do not believe our patient is% e/ {' I& u$ x" ~- i2 F' F
going to experience any of the untoward effects from1 b, w* d  A1 b& K- p
testosterone exposure as mentioned earlier because
/ e- e7 v+ C3 A1 ~6 T, Wthe exposure was not for a prolonged period of time.
3 N0 U! g' N+ l: |Although the bone age was advanced at the time of2 B# g6 |' o* j- k" _+ ~) j
diagnosis, the child had a normal growth velocity at
% e" U: \7 F  I4 sthe follow-up visit. It is hoped that his final adult+ q4 q2 l0 X3 [$ T
height will not be affected.- r0 \+ G  Q8 ]
Although rarely reported, the widespread avail-; e; |  R3 e! v, C+ q
ability of androgen products in our society may' y7 y9 g* V+ Z6 x8 j+ w5 g5 X
indeed cause more virilization in male or female
2 e9 h% k# H6 a7 E: ichildren than one would realize. Exposure to andro-( x: s; B5 i2 @- p! y8 J
gen products must be considered and specific ques-1 [1 _) t1 f$ v4 B6 l/ I, v6 {9 v
tioning about the use of a testosterone product or
4 Y; _4 l- J( ?: V  E! |8 s) A4 Mgel should be asked of the family members during7 e+ o! Z; ?) w" b+ H+ B! w
the evaluation of any children who present with vir-
! j" _; z+ m5 O9 [ilization or peripheral precocious puberty. The diag-
% L( g) N' @6 A5 z( Inosis can be established by just a few tests and by4 \+ K6 o1 d6 {$ s& z
appropriate history. The inability to obtain such a+ f6 Y: x7 Y! ~' {$ `7 K2 u& _
history, or failure to ask the specific questions, may) n6 D) [4 a3 S& f5 S9 v  L: x
result in extensive, unnecessary, and expensive! g* U7 _9 e9 \5 U" l
investigation. The primary care physician should be$ v; f5 w* E& G$ P5 _# |. G
aware of this fact, because most of these children: l9 w' Z$ F5 ^2 {: z7 |
may initially present in their practice. The Physicians’) h; a& ?8 N" f1 h. l: q
Desk Reference and package insert should also put a
$ E6 g" J* \# ~: ]0 t) w) Xwarning about the virilizing effect on a male or
& p3 Y; S: F% l- I( o; mfemale child who might come in contact with some-+ i6 A: ?. |1 Z$ n
one using any of these products.
6 ]0 |8 k  w0 O. U. j7 AReferences
" G  y: S, x. r# z4 V1 q( @1. Styne DM. The testes: disorder of sexual differentiation1 N) f) L; d3 B% q# k* C6 ]& [
and puberty in the male. In: Sperling MA, ed. Pediatric
6 I; H% M- {. M& }. v: Q- U$ iEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;$ A+ {( V# s' q3 j5 J/ \, ?
2002: 565-628.5 z7 H* y1 {; v# D* Z3 ~
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious! m) e0 P2 f4 \8 n" A/ d3 n
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
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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

& y: o8 j: s! ?0 ]5 R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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