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Sexual Precocity in a 16-Month-Old
( U% L+ C' |$ s: kBoy Induced by Indirect Topical+ o+ Z8 g" k; |, I! K$ v9 {# \
Exposure to Testosterone
1 L2 m  C! |: `! @Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
; F( O* b) H7 X6 t5 c" i# z, sand Kenneth R. Rettig, MD1
# N; p7 J2 }$ Y% W* k9 ~4 ~Clinical Pediatrics$ }7 b- U9 j- Z; y' v
Volume 46 Number 61 \; m) |0 Q0 ?. ]9 S! c+ p3 g
July 2007 540-543
% q8 @  z% z! H& q+ x' r3 W, B© 2007 Sage Publications
! _- A: E9 d0 `4 I8 X1 P0 q10.1177/0009922806296651
% s0 N' b3 p. m  c" u- Z! Chttp://clp.sagepub.com
4 L3 a! b: l4 D/ B2 T* uhosted at5 S5 `6 O! t- b! ?! u) b
http://online.sagepub.com
2 i1 _. A* O$ k6 a" C1 sPrecocious puberty in boys, central or peripheral,+ F) g- q9 K2 c8 E
is a significant concern for physicians. Central
2 O* B) }# q% P( k+ f  M7 _precocious puberty (CPP), which is mediated
. `" ~$ {: z- @$ Uthrough the hypothalamic pituitary gonadal axis, has
9 J" r+ I' \, s6 @+ D- _3 Ja higher incidence of organic central nervous system
, b1 K" f% C6 F' m/ e( ~! @- jlesions in boys.1,2 Virilization in boys, as manifested
8 n; M% |! z. w! Jby enlargement of the penis, development of pubic
4 r% |) n8 {( l# Khair, and facial acne without enlargement of testi-/ O2 C4 u, z! F! O
cles, suggests peripheral or pseudopuberty.1-3 We
' S" j" u0 T0 C3 k! ~8 p5 u4 Sreport a 16-month-old boy who presented with the
  n; w/ h7 F# h6 v2 Fenlargement of the phallus and pubic hair develop-
# \' v9 T1 k1 g% I) @, F2 I. S1 Hment without testicular enlargement, which was due
( x# |, Z  A; ~to the unintentional exposure to androgen gel used by5 |2 f8 r4 s! m. z) a3 L$ \
the father. The family initially concealed this infor-
: [! j0 @" r4 z& s5 n4 A& ^9 Lmation, resulting in an extensive work-up for this
! F& e) ]; [; }# X4 w. _( ^7 Ichild. Given the widespread and easy availability of) V3 w) N/ l2 T" N8 y' k1 Z
testosterone gel and cream, we believe this is proba-  H8 [. z9 W; k( P/ F  V' c3 p" d
bly more common than the rare case report in the. i, U8 ]4 V) y4 _. W  `
literature.4
& j$ _: s$ \: t2 F  X0 BPatient Report, h: M+ q0 v" F8 W! [; N
A 16-month-old white child was referred to the+ _: Y" _3 U3 t: X, |
endocrine clinic by his pediatrician with the concern! g3 M3 I: F# ]$ ^
of early sexual development. His mother noticed
& |% b" B* B4 Nlight colored pubic hair development when he was  i/ C' q8 t$ V  N
From the 1Division of Pediatric Endocrinology, 2University of
, }! `# [9 q" N! q: w* f. jSouth Alabama Medical Center, Mobile, Alabama.) k/ T' P# L' {. K6 `
Address correspondence to: Samar K. Bhowmick, MD, FACE,
, M! S: @/ J1 Z+ I) b9 X$ _2 {Professor of Pediatrics, University of South Alabama, College of
: S& p2 C4 k9 F' m9 A, E! u) oMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;5 Q  d% S8 f) Q& O7 ?6 |
e-mail: [email protected].
" w+ \% P' E; w- Y% ~about 6 to 7 months old, which progressively became
5 ^/ k- Z. Q' [  rdarker. She was also concerned about the enlarge-+ ?0 N) \' ~; J+ K% F+ I
ment of his penis and frequent erections. The child
7 r5 m% l! x  P3 Q8 h' C& ewas the product of a full-term normal delivery, with3 U* Y7 V( C! |* f& J8 b9 @
a birth weight of 7 lb 14 oz, and birth length of! ^2 x9 M3 e2 |; r" V& r/ W9 ~: ~
20 inches. He was breast-fed throughout the first year
7 o$ Q; k; M2 P; Mof life and was still receiving breast milk along with
3 c/ l4 M1 l0 L9 J) Y2 x8 w, j# nsolid food. He had no hospitalizations or surgery,
6 w9 ^' e# P7 d; B0 `$ J5 }and his psychosocial and psychomotor development
$ n! C" V4 L# Twas age appropriate.
) K5 I0 u2 L4 y: O+ YThe family history was remarkable for the father,8 S$ e# V: w' f
who was diagnosed with hypothyroidism at age 16,
) [% E: |: d7 |; u1 t8 _* ewhich was treated with thyroxine. The father’s+ l' N% s! N  ]2 N- F, M
height was 6 feet, and he went through a somewhat
  L8 z$ p  ^9 O$ W. Wearly puberty and had stopped growing by age 14.
4 l% |: W" |. J. j* a: n* U: b# c/ WThe father denied taking any other medication. The8 R+ J, Q8 V1 |# j- g
child’s mother was in good health. Her menarche
2 z  y" ^+ P( a  Qwas at 11 years of age, and her height was at 5 feet% @7 T( ]4 s$ }; W. L9 ?5 y, w
5 inches. There was no other family history of pre-
3 W/ J9 F3 I6 H& L" i5 lcocious sexual development in the first-degree rela-
8 ~6 ^7 z: ~$ z! d: stives. There were no siblings.
+ {& A9 u+ w5 TPhysical Examination
8 D  F0 ?( D* ]& I& A9 FThe physical examination revealed a very active,, i" W0 b0 e- [1 [% g. ~* [3 b* f) V% |
playful, and healthy boy. The vital signs documented5 m% [( K9 I5 G9 K% y
a blood pressure of 85/50 mm Hg, his length was4 `1 K! o3 _# j' ?& |
90 cm (>97th percentile), and his weight was 14.4 kg0 q; V( t$ {( i# J' t- O% m* s- Z3 S
(also >97th percentile). The observed yearly growth' n# b  i- u& M7 j: l
velocity was 30 cm (12 inches). The examination of
' Y7 f: g$ f, Y& Q; o9 s5 ]2 Othe neck revealed no thyroid enlargement.
; j) `! a8 t8 w9 XThe genitourinary examination was remarkable for
' G$ B, L, F5 P6 c: M) tenlargement of the penis, with a stretched length of3 ]. `2 s2 p3 [! Z' r
8 cm and a width of 2 cm. The glans penis was very well. V: L5 r# T9 @
developed. The pubic hair was Tanner II, mostly around
9 w: h" S6 M2 G, W7 R. Y& y# v540% E, V$ P" D+ \/ z5 h- N* ~3 y2 J  s
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) W& K  L8 B) U( {
the base of the phallus and was dark and curled. The
5 e% Q4 e5 x" }% Vtesticular volume was prepubertal at 2 mL each.
  n, A7 y( l5 J8 [The skin was moist and smooth and somewhat* L: y0 K  O: G7 H
oily. No axillary hair was noted. There were no
( O: g3 n, w- L( ?* J- o( k/ Babnormal skin pigmentations or café-au-lait spots.
7 h2 o+ x) d, x/ j, z, {Neurologic evaluation showed deep tendon reflex 2+
) u# \" [8 _) F# m- O$ y/ Jbilateral and symmetrical. There was no suggestion
0 ]: q! E  G3 ]$ K* S" e* lof papilledema.! |+ j! }3 ]: b8 k8 \, U/ L
Laboratory Evaluation
/ \% z  s. A3 q$ e* [( [The bone age was consistent with 28 months by+ E' ]$ B' F8 d; p* g  I  Y
using the standard of Greulich and Pyle at a chrono-9 b- R& J  W# F4 x
logic age of 16 months (advanced).5 Chromosomal% r6 l+ {/ H" ?$ _6 E
karyotype was 46XY. The thyroid function test: b$ y) j& I5 c* O# d8 V5 n
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
# z* V% `+ F$ ~1 L1 }lating hormone level was 1.3 µIU/mL (both normal).+ }' Z% r/ j/ |0 \2 `1 t9 u
The concentrations of serum electrolytes, blood- E. e- Z2 e! p- n5 K; D
urea nitrogen, creatinine, and calcium all were% t7 j4 i- j* H' ?2 U3 B6 h) _9 |
within normal range for his age. The concentration
9 e! L/ {$ |$ ?of serum 17-hydroxyprogesterone was 16 ng/dL* {: C3 z: S$ E+ A
(normal, 3 to 90 ng/dL), androstenedione was 203 i0 x+ i9 s0 X! G4 v3 U( E
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-: z' w: s% L$ [% p, H2 C$ G4 o5 d
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
/ ?) g1 J, Z7 S$ S3 \1 b  I  adesoxycorticosterone was 4.3 ng/dL (normal, 7 to
2 ]; n7 s5 ?2 y8 X5 N( ]( v49ng/dL), 11-desoxycortisol (specific compound S)
# Z; C0 x5 \. y3 Swas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-" T5 ^- j4 u( C, t  Z. Z4 V
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total+ c3 y2 I/ ~8 e$ v& }
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
, T% m7 h" D' xand β-human chorionic gonadotropin was less than; W) U% P4 p1 n2 P6 e) d
5 mIU/mL (normal <5 mIU/mL). Serum follicular
3 A4 M6 a, G  j5 n. Mstimulating hormone and leuteinizing hormone- v( v8 ?. W2 `: F7 r+ p3 W- f
concentrations were less than 0.05 mIU/mL
: J" Y; l8 ~$ q& }+ z; s: W: d(prepubertal).
" w. I9 n' e1 J1 l2 a+ R0 yThe parents were notified about the laboratory/ c; l$ n4 u6 k6 r4 G: X
results and were informed that all of the tests were
8 `; s. v# H9 L& b( F' xnormal except the testosterone level was high. The
5 a8 _( Z2 p* Z; \. n! W/ [! Sfollow-up visit was arranged within a few weeks to
- o, B# I8 \  J, Z" V" \, iobtain testicular and abdominal sonograms; how-. ?0 I/ ^7 C0 y2 E  I% t9 }
ever, the family did not return for 4 months.
; I6 u0 N; K6 l* C5 nPhysical examination at this time revealed that the
0 ~# O. g  V5 [. M, ^child had grown 2.5 cm in 4 months and had gained
* N# c+ j4 |% d6 w( K2 kg of weight. Physical examination remained6 Y# F" \7 R  O4 W
unchanged. Surprisingly, the pubic hair almost com-
: Y% h) L2 c6 }! R+ s! N5 `. @pletely disappeared except for a few vellous hairs at
2 H% D1 L8 y* j* ^6 x3 ~4 xthe base of the phallus. Testicular volume was still 2* ^. R5 L- T: T4 z& u5 v
mL, and the size of the penis remained unchanged.( n) W$ Z% E. a$ l% l
The mother also said that the boy was no longer hav-6 j7 G% k8 V) g4 p% u: X/ H
ing frequent erections.
" v) K7 B6 |) `" PBoth parents were again questioned about use of" W# s4 |9 _! g8 ^8 H
any ointment/creams that they may have applied to
1 J/ Y" c' @) G) nthe child’s skin. This time the father admitted the1 _8 t- B8 v( W6 y
Topical Testosterone Exposure / Bhowmick et al 541, j) B, D. P! s5 F( Z
use of testosterone gel twice daily that he was apply-
9 w& i, u$ \# @0 `3 _) w$ a1 Ving over his own shoulders, chest, and back area for; o5 T9 j* n* S4 Q! Z! W6 V% D
a year. The father also revealed he was embarrassed) G% [: B2 Y0 _7 S/ ]  P. M; n
to disclose that he was using a testosterone gel pre-" ?5 Z7 z3 J! e9 |9 M5 X
scribed by his family physician for decreased libido
# O; U; T' ?( _1 u; Ksecondary to depression.& e6 m3 \2 }7 @! ~6 c
The child slept in the same bed with parents.2 v+ S, S2 @: F$ F5 d. o
The father would hug the baby and hold him on his6 [, Y$ Q4 H/ A# E+ M
chest for a considerable period of time, causing sig-+ \; t2 K( d9 g9 M4 y! I
nificant bare skin contact between baby and father.* O$ k/ H' ?3 ^. P
The father also admitted that after the phone call,/ w% z8 h9 q# F% b; \
when he learned the testosterone level in the baby' Z6 d: O1 A6 H2 |
was high, he then read the product information
) O+ w3 U* I% O" A/ kpacket and concluded that it was most likely the rea-" g* y6 N6 o2 _8 B
son for the child’s virilization. At that time, they
- ]4 ?/ @3 v* ~* Hdecided to put the baby in a separate bed, and the
" @" u7 |9 `0 `& i+ j# G) vfather was not hugging him with bare skin and had2 W0 @0 E$ Z8 T9 J( K! Z4 _
been using protective clothing. A repeat testosterone5 v# o% y, D. I6 Q2 b
test was ordered, but the family did not go to the
8 Z& t! Y! H9 Y( X& g$ r! Q4 Zlaboratory to obtain the test.
- X; D7 Z  g9 I4 n7 }9 b8 }Discussion9 G6 p/ n+ F8 F8 `8 x+ w
Precocious puberty in boys is defined as secondary4 V5 f, T5 Z0 n8 H# i- C' I
sexual development before 9 years of age.1,4; `; |0 v8 J0 L( h' t- S
Precocious puberty is termed as central (true) when
# N+ Y! z" y3 d; N% l0 Cit is caused by the premature activation of hypo-: ~) C$ a3 e0 u+ z8 c' g
thalamic pituitary gonadal axis. CPP is more com-
/ l/ O- b$ x5 L/ u, L0 L4 f9 x& d- Omon in girls than in boys.1,3 Most boys with CPP
7 n7 l( o% G+ t1 mmay have a central nervous system lesion that is
1 [& P9 o! g) e) p- f1 C7 q# Fresponsible for the early activation of the hypothal-
* i) z# t4 P2 Y% @. Lamic pituitary gonadal axis.1-3 Thus, greater empha-
0 f: X5 [& t$ B1 @% Wsis has been given to neuroradiologic imaging in
* Y/ ~- Z- [4 h1 Z, Gboys with precocious puberty. In addition to viril-
9 B  ~% |2 ?! M* e" Vization, the clinical hallmark of CPP is the symmet-3 t6 J- q( [0 p4 F) U
rical testicular growth secondary to stimulation by) Z/ ?! ~& W7 y( A3 W; ]
gonadotropins.1,3* Q: A% e6 a$ W  Y, V0 X# c. J" o
Gonadotropin-independent peripheral preco-0 n2 K2 {! o  g; X7 F+ v
cious puberty in boys also results from inappropriate. `& f: L$ R9 P) O9 _9 z) o- D
androgenic stimulation from either endogenous or! q, f5 \- A+ W% W3 u+ w+ m: s
exogenous sources, nonpituitary gonadotropin stim-$ M* Z( Q8 P, j( y* z. c- A! @
ulation, and rare activating mutations.3 Virilizing
) y3 }+ [7 h! S4 H2 X9 Scongenital adrenal hyperplasia producing excessive
; b, b% A5 [* }1 d+ Ladrenal androgens is a common cause of precocious
( \9 p) {" t  G$ W3 cpuberty in boys.3,4
" s1 r, L, }: S% O9 v$ @/ sThe most common form of congenital adrenal* B; z4 I. ]0 ]4 I- c5 j
hyperplasia is the 21-hydroxylase enzyme deficiency.
7 w2 j; W9 I, e7 k+ KThe 11-β hydroxylase deficiency may also result in7 H% B3 K) S, P
excessive adrenal androgen production, and rarely,
$ L% E3 Z3 h5 ean adrenal tumor may also cause adrenal androgen0 ~! j! D6 }3 b& \. v( N: {! H2 [2 V
excess.1,3- g5 V7 I/ w5 W1 M5 d' @
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from" j, y6 s4 A6 @0 B7 B' m! T- t6 P+ J
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
% R2 L: p+ M  wA unique entity of male-limited gonadotropin-9 j2 w9 y2 P9 u0 r$ p# |
independent precocious puberty, which is also known. k1 L, k' ]5 d) H( l) B
as testotoxicosis, may cause precocious puberty at a7 z( F! I6 A4 X4 [% d$ D  u
very young age. The physical findings in these boys1 s6 ^& ^. c! _" W
with this disorder are full pubertal development,6 l% R# a0 ]9 x" D- o
including bilateral testicular growth, similar to boys. Q) w/ `, ]* x$ \) [) |
with CPP. The gonadotropin levels in this disorder9 |+ R! D9 b" n4 }4 ?- E  a
are suppressed to prepubertal levels and do not show# w3 P1 X! T& h, h* Q! N
pubertal response of gonadotropin after gonadotropin-
' p* p6 {; ?% ^releasing hormone stimulation. This is a sex-linked3 N, }7 B1 Z" l! P  z; x2 m
autosomal dominant disorder that affects only& m! o/ D+ N$ G6 A. c$ M
males; therefore, other male members of the family
, t" V$ E$ }2 n9 X) g* b1 o4 {7 I3 h5 hmay have similar precocious puberty.3
- R- r( A5 S  M4 bIn our patient, physical examination was incon-' T* \* [7 c4 O' b
sistent with true precocious puberty since his testi-( ~8 V2 _4 Y; _+ X
cles were prepubertal in size. However, testotoxicosis
& s/ G& f- ?/ y) u8 U6 kwas in the differential diagnosis because his father& g& _8 n+ t. i8 Z
started puberty somewhat early, and occasionally,
# ?: ?+ l  r$ S# B( vtesticular enlargement is not that evident in the
: Z/ _) x0 L' R5 ibeginning of this process.1 In the absence of a neg-
% t9 o/ a4 M8 l/ @9 zative initial history of androgen exposure, our
- N" Z7 ^. h) {0 r; }/ y6 [biggest concern was virilizing adrenal hyperplasia,+ P% q6 h9 S( c- n" q  f" L% Y/ l
either 21-hydroxylase deficiency or 11-β hydroxylase
9 E$ i& B1 L& |% [% _* sdeficiency. Those diagnoses were excluded by find-% M6 h3 y1 {1 ?+ x' \% {
ing the normal level of adrenal steroids., d$ z( `' a6 r/ g6 Z
The diagnosis of exogenous androgens was strongly
. C; e& X9 [. w5 K( msuspected in a follow-up visit after 4 months because: M, [7 d0 t) }( ^5 }
the physical examination revealed the complete disap-
8 e3 O' ]$ G5 n1 B0 Tpearance of pubic hair, normal growth velocity, and
3 ]/ I- A" i6 u3 S/ \0 vdecreased erections. The father admitted using a testos-
( u. i& M5 z  M. @. _2 V+ A+ k6 ~terone gel, which he concealed at first visit. He was; [: V0 W7 i2 ~& v; r
using it rather frequently, twice a day. The Physicians’
/ k' q4 }8 p# E+ x5 |' Y; U8 Q6 Q3 sDesk Reference, or package insert of this product, gel or
1 S0 H9 z3 l4 l+ k* Acream, cautions about dermal testosterone transfer to
1 w! i) b/ ]3 E# [unprotected females through direct skin exposure.
# l/ O. R& `4 X: ]+ q1 a2 [- gSerum testosterone level was found to be 2 times the
. L4 u' F7 a4 bbaseline value in those females who were exposed to
, E' C- }0 W% \even 15 minutes of direct skin contact with their male
4 K* h* F# H4 M% j8 I- F# bpartners.6 However, when a shirt covered the applica-6 B  O% D, b! @3 A
tion site, this testosterone transfer was prevented.
# }4 b/ i( |; HOur patient’s testosterone level was 60 ng/mL,. X' w' u: I& Z; ^" \1 n- s; O2 V% j
which was clearly high. Some studies suggest that
) f8 T1 ?& p6 C% y' C; ddermal conversion of testosterone to dihydrotestos-
( i. T# n0 f) k# B; \! X4 K5 ^4 q7 Wterone, which is a more potent metabolite, is more
- n+ p( Q( u4 s, W9 H6 q# C- bactive in young children exposed to testosterone
, F4 q3 I* |- _' \' m$ rexogenously7; however, we did not measure a dihy-
# d% w7 K. y8 t  Wdrotestosterone level in our patient. In addition to
0 l1 a) a! h0 w3 Evirilization, exposure to exogenous testosterone in: u) E" d0 O0 G# N9 o' U
children results in an increase in growth velocity and0 ]6 N( |, e- a6 c2 _$ y" U4 i3 L
advanced bone age, as seen in our patient.! x$ a2 n% _3 A+ x$ F. r
The long-term effect of androgen exposure during
% j' D/ @" N8 r( u9 K9 q% a9 Dearly childhood on pubertal development and final3 L4 l% y  l3 z8 |. _  [' _
adult height are not fully known and always remain, L5 [  G- N& Y) v/ d# I
a concern. Children treated with short-term testos-
# t" z0 r! E+ V' Bterone injection or topical androgen may exhibit some  l: \/ }3 E% U5 H
acceleration of the skeletal maturation; however, after# I- @" U# X; o
cessation of treatment, the rate of bone maturation% g/ ?+ K7 y# N1 w' P7 `
decelerates and gradually returns to normal.8,9+ D1 M* Y% u5 t! n
There are conflicting reports and controversy
1 J4 Y/ s2 \5 _/ ~over the effect of early androgen exposure on adult! T8 D9 ~% |* i% ~, M) o* v3 [
penile length.10,11 Some reports suggest subnormal
& t% y0 y6 Q8 d% dadult penile length, apparently because of downreg-8 O$ V8 @0 Z9 C' S7 Y) l
ulation of androgen receptor number.10,12 However,; L0 h/ }+ ^! b. Q  z
Sutherland et al13 did not find a correlation between1 x2 M2 R+ z% R! }
childhood testosterone exposure and reduced adult: G/ r+ v2 z2 O) }8 D. M; v: c
penile length in clinical studies." S, N+ K  x0 G# V
Nonetheless, we do not believe our patient is# d" q- j+ L, Y# |6 [
going to experience any of the untoward effects from9 Z4 I  ^1 |. f( q5 b
testosterone exposure as mentioned earlier because) v; R3 x* m" p6 ]& ]3 h' N
the exposure was not for a prolonged period of time.3 C9 Y& z! |, i. A3 ]* Y8 v* o
Although the bone age was advanced at the time of
" k" ^* h  \- f8 E  Ndiagnosis, the child had a normal growth velocity at9 ~% I. I) t5 e" o5 J4 R0 \
the follow-up visit. It is hoped that his final adult
% |( o3 N9 Y' N) pheight will not be affected.
3 j2 X" B, ^+ V7 nAlthough rarely reported, the widespread avail-
# C. V, w- E8 r: b; _: s9 iability of androgen products in our society may5 t' W- F% l( ]4 @: s  q
indeed cause more virilization in male or female1 _! s- a0 x% J6 @: N" ~
children than one would realize. Exposure to andro-9 B# w2 L+ \9 f/ i, R! b6 v9 J
gen products must be considered and specific ques-
+ o1 @, i  ~/ W- Gtioning about the use of a testosterone product or' C) l0 B. A( S/ G8 {! m7 x3 s
gel should be asked of the family members during
* ]6 \1 b( x. b9 a7 g; H% O+ e) I& ]the evaluation of any children who present with vir-
7 F5 Y! e  i2 [* D7 Silization or peripheral precocious puberty. The diag-
( Z) e0 H$ K: }$ H; Qnosis can be established by just a few tests and by, b3 o* i# s9 i
appropriate history. The inability to obtain such a
, T& ?; ?* q* s+ s7 @history, or failure to ask the specific questions, may
2 J$ l- c/ J, w$ m& I7 Xresult in extensive, unnecessary, and expensive- h! \8 k! t+ p6 i
investigation. The primary care physician should be
9 i$ H, d" C* y# \7 @* n: ?aware of this fact, because most of these children
6 `2 ?. i. Z/ a# |" p: gmay initially present in their practice. The Physicians’& }( \" Y2 k: U" I  v# O$ P
Desk Reference and package insert should also put a
0 G, x( J% X$ J& k; u/ `7 Ewarning about the virilizing effect on a male or
+ u0 L& W* H( }$ R+ hfemale child who might come in contact with some-* I  U1 h& ]2 F: m1 S% o
one using any of these products.
  v& }3 d6 H# l, o4 ]References
5 d, z: A! w: c3 a( B1. Styne DM. The testes: disorder of sexual differentiation$ F; ], c5 z+ j. S
and puberty in the male. In: Sperling MA, ed. Pediatric
' d- V, `! a; q9 cEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
: A* f. i8 L2 T  S9 ?2 l$ ^. K2002: 565-628.$ X0 ]0 y1 d+ ]  h# q7 b9 S
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious( G& H  O4 `: ]5 X1 ]. w6 \/ Q# S
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old* D7 o* v9 R+ e  @
Boy Induced by Indirect Topical
$ @0 s  q9 B+ ~$ ^) Y8 x+ DExposure to Testosterone/ W+ c2 P; L9 Z6 o, p
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2% W8 d* f+ ~! o. y
and Kenneth R. Rettig, MD1$ t  Q% d5 X. Q% o$ y
Clinical Pediatrics
& {3 o$ d8 P) X2 `Volume 46 Number 68 b& @5 w5 O$ {
July 2007 540-543: r: r3 P3 I" k' h* y% f3 _; _5 n% D2 o
© 2007 Sage Publications
* z/ u" I' w) s' F6 U0 ]10.1177/00099228062966514 I" G+ f8 R( ~, ^
http://clp.sagepub.com  {; w! t  ]- T8 T6 ]. N  P: e3 m
hosted at
8 P2 b: ~5 Q4 R! K+ B3 yhttp://online.sagepub.com
' _% L* |9 Y2 U& ~6 x6 y+ x( S& ePrecocious puberty in boys, central or peripheral,' ~' q- ?9 p! H
is a significant concern for physicians. Central2 s6 P& l# Q! A3 F# m4 v3 P
precocious puberty (CPP), which is mediated; d6 Q6 w" A. b: J7 e5 C" u% B
through the hypothalamic pituitary gonadal axis, has
0 |6 X, F' p# _, b. u+ ja higher incidence of organic central nervous system
+ n& G- z5 y3 Slesions in boys.1,2 Virilization in boys, as manifested
/ O2 G; |: F2 q2 x& t* S& Rby enlargement of the penis, development of pubic
! l* d0 N0 K9 dhair, and facial acne without enlargement of testi-
6 t9 I( H( |4 s8 V9 J5 V) Ccles, suggests peripheral or pseudopuberty.1-3 We
7 D3 h5 s  `+ Q" Qreport a 16-month-old boy who presented with the! T( s2 J% }% @. J
enlargement of the phallus and pubic hair develop-
. V9 N' {+ F% {1 A, l' A; cment without testicular enlargement, which was due6 `8 Q8 f$ ^3 F) ?% F9 z* Q
to the unintentional exposure to androgen gel used by
3 z% S# c8 n6 V$ N+ pthe father. The family initially concealed this infor-
2 b% g% @; a2 C# \" }0 o1 Pmation, resulting in an extensive work-up for this
4 t/ }3 P9 z& Y2 @& [; Ychild. Given the widespread and easy availability of
$ ~, ]" N" b) y( r; n! z0 a* ktestosterone gel and cream, we believe this is proba-
8 e( a! m, W5 L" L# c" T! qbly more common than the rare case report in the
( ?; I4 k8 J8 |7 t1 U+ Y- b4 y( S8 Uliterature.41 i  f( @; J5 S" U5 r
Patient Report
5 G' a' E0 E, [$ KA 16-month-old white child was referred to the
) ]3 N: a3 U. E4 O# }. Gendocrine clinic by his pediatrician with the concern7 v. F; w5 H' y0 K' z7 y* D
of early sexual development. His mother noticed
) c- T0 L2 R- ~+ B# W0 m$ Mlight colored pubic hair development when he was3 O8 ]; n& Q2 F  u" e: z
From the 1Division of Pediatric Endocrinology, 2University of
& g  W+ O8 T& r0 M+ v+ i/ ^South Alabama Medical Center, Mobile, Alabama./ K7 H* L1 a: l
Address correspondence to: Samar K. Bhowmick, MD, FACE,' _! ^, Q  ^( l; h  @$ p) d
Professor of Pediatrics, University of South Alabama, College of
9 k9 R3 T" |0 m5 b! _8 r( N9 _% TMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;& ~, p" b9 I! D% u0 G
e-mail: [email protected].
; Z0 M$ @& ]: W0 f4 o7 yabout 6 to 7 months old, which progressively became# x( E+ x7 e+ J0 C. I$ t- p
darker. She was also concerned about the enlarge-
5 ^+ M* ^2 d, Q/ D+ U7 K$ Tment of his penis and frequent erections. The child
, w5 u# X) o; [* Ywas the product of a full-term normal delivery, with
! X( z: e4 J3 @9 f& q# j5 ]6 ~a birth weight of 7 lb 14 oz, and birth length of* j2 `) \# d1 Q. t' j
20 inches. He was breast-fed throughout the first year/ k+ L# w7 V8 H- A1 |# I
of life and was still receiving breast milk along with
1 Z; O) L$ `, E- v  p# c8 ^5 dsolid food. He had no hospitalizations or surgery,1 n+ l0 s$ v/ X/ A, V2 _# J8 ]; k
and his psychosocial and psychomotor development
- q1 M* u: Q# K8 d2 ]was age appropriate.
* a/ f% U2 K2 a6 f+ E8 tThe family history was remarkable for the father,
4 _% O) u. k: h, B! l8 _4 iwho was diagnosed with hypothyroidism at age 16,& ], \4 Q) n% J, @1 f! E
which was treated with thyroxine. The father’s! N5 Z. f" Z& k
height was 6 feet, and he went through a somewhat9 n5 E8 K8 s% {7 M) o$ n# ]6 ?
early puberty and had stopped growing by age 14., }  N  C2 w3 J' p6 r
The father denied taking any other medication. The& X  c9 u& N! p. z
child’s mother was in good health. Her menarche7 R9 T" d1 w# t; V  d( ?6 H
was at 11 years of age, and her height was at 5 feet
8 ~9 B# y1 ~4 U; d5 inches. There was no other family history of pre-
4 n/ P* p  L+ dcocious sexual development in the first-degree rela-4 B$ q% Q" p8 ~9 C, H; z: [
tives. There were no siblings.3 [# H  m! W! Y( ]
Physical Examination* O4 m' A1 X  K1 t
The physical examination revealed a very active,' w6 c+ c4 i. O1 a" m
playful, and healthy boy. The vital signs documented8 T: l) J* C5 l2 d( C8 D& V
a blood pressure of 85/50 mm Hg, his length was" l& u5 N' C1 U& e) K% c6 _: F1 t/ z
90 cm (>97th percentile), and his weight was 14.4 kg7 f( j# d  L- V, N
(also >97th percentile). The observed yearly growth# q! k+ ^% L0 S  i
velocity was 30 cm (12 inches). The examination of
# |0 ?; O  _6 x& [2 Ythe neck revealed no thyroid enlargement.  `* h4 P' `" b+ Z6 v
The genitourinary examination was remarkable for
$ ?6 A& n" H/ O6 z3 I) Fenlargement of the penis, with a stretched length of
( j& T% K# y; f" A  ?8 cm and a width of 2 cm. The glans penis was very well
- m( H% ], V6 @: odeveloped. The pubic hair was Tanner II, mostly around
3 K) Y* U' B7 H" a: p4 u' l540
, y+ f6 `$ O8 z5 `4 c: Sat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) b( P4 k2 {: |
the base of the phallus and was dark and curled. The
  L+ g  S7 f: K$ Y3 `/ J5 f# Y4 d$ \testicular volume was prepubertal at 2 mL each.
7 o/ C, P6 p7 y/ h+ gThe skin was moist and smooth and somewhat9 t$ P, a/ V) P! S/ W! T2 `' o
oily. No axillary hair was noted. There were no
: l7 k$ E* ]6 d: A- E- [1 b6 y& i; Xabnormal skin pigmentations or café-au-lait spots.  e4 c' H  U/ f) X
Neurologic evaluation showed deep tendon reflex 2+
% I2 p- y+ Q( w; Z/ ]bilateral and symmetrical. There was no suggestion
1 _" {7 G3 A% ]7 y& d1 Lof papilledema.' @+ p; D% G# N. r9 f6 n! C
Laboratory Evaluation
" e' K) a# ^9 q) v3 RThe bone age was consistent with 28 months by
! L+ x: d# @: Q5 M: P0 z: {using the standard of Greulich and Pyle at a chrono-, |' X; J- n8 u9 s
logic age of 16 months (advanced).5 Chromosomal
$ g; s& D$ c1 C$ t& Xkaryotype was 46XY. The thyroid function test( f& l$ [1 \. S0 @2 h# r8 M( s
showed a free T4 of 1.69 ng/dL, and thyroid stimu-. T3 s6 `, o  y) a1 \" f1 B1 k" {
lating hormone level was 1.3 µIU/mL (both normal).6 \  r. s6 ^2 D: R. f" Y) ^' R
The concentrations of serum electrolytes, blood
  T7 t" R/ ?+ F( @* `0 Jurea nitrogen, creatinine, and calcium all were; x3 [7 T+ ?4 h$ V# }" g; j
within normal range for his age. The concentration
. C3 w# {6 W# y- y. j6 n/ i' Rof serum 17-hydroxyprogesterone was 16 ng/dL
  l$ X4 y* p% ]% H, @5 q" Q(normal, 3 to 90 ng/dL), androstenedione was 20
( F% {5 K9 S' i3 Q5 I) }ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
/ A- Q, g5 {2 F- T# X' \1 mterone was 38 ng/dL (normal, 50 to 760 ng/dL),
- h! W9 f6 u' [7 m7 c3 a# ~% ]8 Sdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
8 K9 o8 i, K" \' M1 @% i) H" @, p49ng/dL), 11-desoxycortisol (specific compound S)" w! B% r4 K0 a! I( f( J
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-3 B, m( T% z, w. D% t, @( {: t6 e
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total5 ]& ?7 h" E: A, @
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),. U, h- ^% \& w
and β-human chorionic gonadotropin was less than; y0 w* V& k! D9 b0 Y: C
5 mIU/mL (normal <5 mIU/mL). Serum follicular
' l- }- Y- S5 {stimulating hormone and leuteinizing hormone% k. ?- Q* }  O, i5 m
concentrations were less than 0.05 mIU/mL
8 O2 |4 q6 F% f; @" I: ^(prepubertal).- ^8 _. X% t  |# @/ F2 l6 t) f
The parents were notified about the laboratory
( O) u6 V% F7 `5 a( Mresults and were informed that all of the tests were$ I: g. C6 ]) f  N5 T; k, P
normal except the testosterone level was high. The
6 s, w; |9 j! v& V+ Hfollow-up visit was arranged within a few weeks to
" K3 R# j! x% r  B: B3 ?obtain testicular and abdominal sonograms; how-
- Z2 _* a+ V0 dever, the family did not return for 4 months.
3 ~/ `  Q" {! m# KPhysical examination at this time revealed that the% N1 J! [4 A0 o& h6 X# ^9 @* v$ E
child had grown 2.5 cm in 4 months and had gained
) p! G6 `. `0 H" v: E1 R/ O2 kg of weight. Physical examination remained5 T; v4 \4 X2 U/ F8 r# B
unchanged. Surprisingly, the pubic hair almost com-" {) d. I, W9 `0 V+ J+ N9 s+ h
pletely disappeared except for a few vellous hairs at
7 C# ], z' y5 O: A+ N4 sthe base of the phallus. Testicular volume was still 2
' {- l. o- W# g% omL, and the size of the penis remained unchanged.
) \; o1 U* Y- }The mother also said that the boy was no longer hav-# Q( E3 m% |4 m5 d
ing frequent erections.
% U8 ?8 n% Q8 b, O  f. {( P& tBoth parents were again questioned about use of* s- g: T: b: x9 n; p
any ointment/creams that they may have applied to
3 D. i: _( }% c7 J8 S+ f6 Mthe child’s skin. This time the father admitted the
/ K: \5 W7 Q, G! Y5 lTopical Testosterone Exposure / Bhowmick et al 5412 M* ?+ M0 V. z$ u
use of testosterone gel twice daily that he was apply-0 l; J7 h: E' d% z! O7 A  b1 A- a$ g/ b
ing over his own shoulders, chest, and back area for
9 ?$ M6 K2 ^* i% s" V3 @a year. The father also revealed he was embarrassed. f& H$ n/ o6 F& S( L
to disclose that he was using a testosterone gel pre-
) B* Q+ p5 P. N! k% e$ |6 Cscribed by his family physician for decreased libido
& I+ h$ w* v! ?- lsecondary to depression.
3 ~4 S# Y* p, F' Q6 QThe child slept in the same bed with parents.9 C2 x; U% W# v7 W: H3 r. ~1 ~, j
The father would hug the baby and hold him on his& F& j3 w: J3 v% o
chest for a considerable period of time, causing sig-
; L6 |/ D& M  c. bnificant bare skin contact between baby and father.9 C9 `1 @; o  ]/ T1 G2 G
The father also admitted that after the phone call,
  W8 ^- q) t2 ]3 T/ a1 xwhen he learned the testosterone level in the baby; C2 j+ `, x' Z  @; c) h- E8 V
was high, he then read the product information# v* M. t" J5 v& I/ a
packet and concluded that it was most likely the rea-( X5 S/ N- \9 ^) [* v! h+ _
son for the child’s virilization. At that time, they
: c+ T; d  t% xdecided to put the baby in a separate bed, and the% l6 L6 e+ ~+ y& N2 v
father was not hugging him with bare skin and had5 v9 @2 z5 n. ^: g/ P( r8 m5 Y! l
been using protective clothing. A repeat testosterone; p8 }  {& K. t
test was ordered, but the family did not go to the
% W" q3 I8 V6 [: d  t  x, Z" X% O" klaboratory to obtain the test.
$ W9 t4 R4 ~% B/ ^1 CDiscussion
' m# `: U5 K% F' NPrecocious puberty in boys is defined as secondary9 t( F* L" f% m& q" n! Q+ `
sexual development before 9 years of age.1,47 ?! @8 K- ]" F1 J4 B
Precocious puberty is termed as central (true) when% h: Z& Q7 h8 ^  q
it is caused by the premature activation of hypo-
- g) I5 j1 `, {* `thalamic pituitary gonadal axis. CPP is more com-% r4 ~( G( K7 U% F
mon in girls than in boys.1,3 Most boys with CPP
/ o) j* c6 v  U% C/ jmay have a central nervous system lesion that is( g$ T  V; T- X* a! R( W
responsible for the early activation of the hypothal-, J" D" t5 [+ G: N( C
amic pituitary gonadal axis.1-3 Thus, greater empha-- K! |  T7 r, g7 K3 g
sis has been given to neuroradiologic imaging in& Q8 [% x/ r! e, d- f% d) R
boys with precocious puberty. In addition to viril-# ], e& l& v% c% V
ization, the clinical hallmark of CPP is the symmet-6 m( p% D$ \) c+ I
rical testicular growth secondary to stimulation by4 [( H8 X) e; D- |9 f. Q# X/ v
gonadotropins.1,37 K0 [0 L: T: O3 U5 X$ L2 y1 y
Gonadotropin-independent peripheral preco-4 R" m( y1 e, {& g/ X. G, s4 ~8 ]+ L
cious puberty in boys also results from inappropriate
' R4 \9 U/ l# J3 |" c, m" aandrogenic stimulation from either endogenous or
8 T+ Q1 j5 w7 ~# X0 L! A3 ^exogenous sources, nonpituitary gonadotropin stim-
- u( M8 V4 H1 k) @$ ?ulation, and rare activating mutations.3 Virilizing
$ a- u/ K5 O1 H4 r4 Y2 X5 j9 }congenital adrenal hyperplasia producing excessive
) T0 T, A, R% A# N' e" Aadrenal androgens is a common cause of precocious
, W6 v' V1 V, @$ y; E$ ]# R8 Lpuberty in boys.3,4/ E2 q5 l; l, c2 F
The most common form of congenital adrenal
2 f( w. |5 |3 ]7 V( o/ ?: `9 @1 Mhyperplasia is the 21-hydroxylase enzyme deficiency.
! x8 F3 p2 e. z/ v5 W4 L7 {4 NThe 11-β hydroxylase deficiency may also result in% K4 V5 A8 B4 N& |6 F
excessive adrenal androgen production, and rarely,
- M- p. ]4 F; v7 n6 yan adrenal tumor may also cause adrenal androgen( d& H4 k& L1 p5 Z
excess.1,39 H7 m/ h6 `) j
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# O( W9 h  K0 z! t4 b
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007' E5 L$ |' I5 B2 ?9 d
A unique entity of male-limited gonadotropin-2 k. Z4 C( b% l
independent precocious puberty, which is also known# r8 D" ]3 m' v5 E7 O# v9 I0 n
as testotoxicosis, may cause precocious puberty at a* p7 f2 l. x, ?' k0 q# Q5 ]/ [" V! A
very young age. The physical findings in these boys/ d$ k/ v8 a- V3 q' }: z
with this disorder are full pubertal development,! A- B; }" ~$ y# p8 w
including bilateral testicular growth, similar to boys
8 a% |8 g3 `3 mwith CPP. The gonadotropin levels in this disorder
; J6 V1 ^5 C, d, vare suppressed to prepubertal levels and do not show
7 k5 E7 M+ C1 z8 @) |pubertal response of gonadotropin after gonadotropin-
) E( N; ?" T1 ?8 oreleasing hormone stimulation. This is a sex-linked
' s! u( r# v! I# l% D1 bautosomal dominant disorder that affects only
# ?0 {+ I( k5 C8 i: c/ B$ I& Bmales; therefore, other male members of the family0 L% \) E- w( f' k+ q3 {/ A
may have similar precocious puberty.3
$ n5 W! q( \) C) H  H; j4 }In our patient, physical examination was incon-
6 A* u2 k* {6 E! |8 Y) J- hsistent with true precocious puberty since his testi-
5 \. {5 D: k8 }' T& R- ]; Qcles were prepubertal in size. However, testotoxicosis7 f% t5 h* k$ R$ X8 W4 }
was in the differential diagnosis because his father
- d3 K! |. |2 O+ S3 D8 `0 zstarted puberty somewhat early, and occasionally,
$ _. G6 ?1 [; ctesticular enlargement is not that evident in the
# M: z+ f' F0 w+ b. Q; sbeginning of this process.1 In the absence of a neg-; t  w2 f# D9 p- P8 z1 _0 m' m
ative initial history of androgen exposure, our8 o( g, P" @7 C7 c3 H; _7 T
biggest concern was virilizing adrenal hyperplasia,
$ p# V- [! n4 W2 q5 Peither 21-hydroxylase deficiency or 11-β hydroxylase
, \; R. _; @/ \/ ?deficiency. Those diagnoses were excluded by find-
1 J8 u8 {# \: e1 Y6 hing the normal level of adrenal steroids.' C, ]0 ?* a1 u- H
The diagnosis of exogenous androgens was strongly! |/ D: C, m$ a8 Q
suspected in a follow-up visit after 4 months because
4 S+ a+ X& |* j6 A5 f& ?8 A4 [; g0 Sthe physical examination revealed the complete disap-
8 F3 g9 N" x  v0 T% Q0 ^& k* ]pearance of pubic hair, normal growth velocity, and4 N) P# N2 l; U; C
decreased erections. The father admitted using a testos-
6 a7 W; U/ y& H- {* l& I4 y6 d6 mterone gel, which he concealed at first visit. He was! ?# H" m% D6 i1 z$ w1 c
using it rather frequently, twice a day. The Physicians’: D0 X+ S' ~8 z1 I7 R/ |  m
Desk Reference, or package insert of this product, gel or, D3 D* k; y  C
cream, cautions about dermal testosterone transfer to) Y. b+ n4 X* ^6 J, I& Z" r# n: O6 @5 w
unprotected females through direct skin exposure.7 l# Y# _8 f3 M7 g
Serum testosterone level was found to be 2 times the8 V* m# g/ D& [( s
baseline value in those females who were exposed to
8 m; {+ v# a5 E( f; r; d+ Oeven 15 minutes of direct skin contact with their male; U2 k  f" _1 p  N/ R
partners.6 However, when a shirt covered the applica-9 E# y; [7 X+ q7 e, ^& w9 E$ c, |
tion site, this testosterone transfer was prevented.
7 A6 R9 o4 U7 O6 `6 f! MOur patient’s testosterone level was 60 ng/mL,/ n% O; l0 k& m( l- q8 U& u
which was clearly high. Some studies suggest that1 _% n& L. J  X, O
dermal conversion of testosterone to dihydrotestos-
" u2 u0 i; k  a4 I( ]9 m" J0 U5 Gterone, which is a more potent metabolite, is more
: @8 d% U' s+ m' E7 gactive in young children exposed to testosterone
' S* A1 R. l: l5 C- i' l/ H" iexogenously7; however, we did not measure a dihy-
9 k1 {% w/ ?* h9 N9 [! Z- Mdrotestosterone level in our patient. In addition to) F) c' D% [& I6 z  i
virilization, exposure to exogenous testosterone in& L) \% H) O; G( X0 E8 X) P2 c
children results in an increase in growth velocity and$ d% W: L9 |: p& _  ?" Y2 a/ Y
advanced bone age, as seen in our patient.5 S: P2 \/ c7 V. m/ A: v. [
The long-term effect of androgen exposure during
7 E* ?4 Z3 I# s+ Hearly childhood on pubertal development and final
1 w. X% t% l4 i9 k3 F6 i/ Padult height are not fully known and always remain( w! m0 S! F1 j
a concern. Children treated with short-term testos-
" R) G. u& f, B' iterone injection or topical androgen may exhibit some+ x9 Y; ^, h3 O
acceleration of the skeletal maturation; however, after7 J: s9 Z& `. b) h5 w4 {, p' M$ U
cessation of treatment, the rate of bone maturation
- R5 b% `& _- \6 ~decelerates and gradually returns to normal.8,9
: U" t/ h" h7 KThere are conflicting reports and controversy
. t: Y( J- r% e, eover the effect of early androgen exposure on adult
0 ?+ }9 P; T# [penile length.10,11 Some reports suggest subnormal9 T" l9 Z: T6 S! ~+ i# y( x- x
adult penile length, apparently because of downreg-
& D, V# P3 B) Tulation of androgen receptor number.10,12 However,; O- s, h8 e* a3 b3 x. B
Sutherland et al13 did not find a correlation between5 E; @2 ]0 N4 p2 k
childhood testosterone exposure and reduced adult
& q; E3 P* d% u  S) ?3 ]2 Ypenile length in clinical studies.
4 a' k& I5 x4 H" s7 YNonetheless, we do not believe our patient is
- t& X/ e) B# X! u9 p8 s. P, ?" }) Y1 mgoing to experience any of the untoward effects from; K7 V% J) O8 N0 V8 V5 B
testosterone exposure as mentioned earlier because
. w  t  J3 b$ S; E& }5 b' Rthe exposure was not for a prolonged period of time.+ _. H: B7 s: R; l: p! K
Although the bone age was advanced at the time of$ ?0 @4 m0 ^" k; G" ]
diagnosis, the child had a normal growth velocity at
0 }# p, z2 Q7 W, U! Ithe follow-up visit. It is hoped that his final adult4 w# [3 \5 I% P( {: U! b1 i
height will not be affected.( c8 o; F. S+ A( T
Although rarely reported, the widespread avail-
) W# w6 V# Q& n6 A4 pability of androgen products in our society may
7 d) w2 B' J# `) I# P2 Z0 `! c* pindeed cause more virilization in male or female
  Q( P9 ^2 V/ @( h+ g" Nchildren than one would realize. Exposure to andro-9 {: ]; P( m/ ?2 d
gen products must be considered and specific ques-0 k+ t3 e( Y* s4 L3 l$ |
tioning about the use of a testosterone product or0 h% F4 P% h, b3 u  @+ o6 S
gel should be asked of the family members during9 c( o/ r7 m$ A' A
the evaluation of any children who present with vir-
# X7 T6 Y. N8 |" C* l3 |, c$ vilization or peripheral precocious puberty. The diag-
0 t9 J5 L; f6 w& @  ^. \nosis can be established by just a few tests and by
; P: c: X; l+ N8 {+ u) J- J" Dappropriate history. The inability to obtain such a& z( [* P8 Z3 W6 W- x% L" h
history, or failure to ask the specific questions, may
+ u! y% H: P) C5 ]result in extensive, unnecessary, and expensive
) q9 }5 P& k# H0 g- u! minvestigation. The primary care physician should be
# G8 y) B& ]0 v0 E+ Maware of this fact, because most of these children
: h! c- H9 T+ `may initially present in their practice. The Physicians’
+ C; G% H1 K* o1 k0 }Desk Reference and package insert should also put a* j5 u  B6 k) D: j' E7 `
warning about the virilizing effect on a male or
8 h6 i  ^& H! L# wfemale child who might come in contact with some-
+ B4 F# {1 M& Rone using any of these products.8 F8 ^" t# j! c, l% }
References
1 u0 F4 v+ i. z( O8 u8 N1. Styne DM. The testes: disorder of sexual differentiation% L# z& f* v! ?: p2 [; p
and puberty in the male. In: Sperling MA, ed. Pediatric
, M  U1 \+ U2 H7 _( J, nEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;% H# ]! n+ h: B& R- ]/ d. o
2002: 565-628.
" a9 @# F) i4 G$ E0 N2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
: c8 ~5 s% b4 Z3 ?6 qpuberty 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

$ U' x# g0 b+ \4 U* J3 s: b; X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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