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Sexual Precocity in a 16-Month-Old9 Q2 a3 `: W( V7 \9 F
Boy Induced by Indirect Topical
4 F# O* c9 s) Q0 Y2 mExposure to Testosterone( |7 u8 Q9 Z; o% N! Z. ~
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
1 B$ E' M; {/ B3 vand Kenneth R. Rettig, MD12 I+ _1 j+ O. u: h
Clinical Pediatrics' F0 D! r0 d, g! Z4 H
Volume 46 Number 60 h# ?0 D! n: y3 j! S
July 2007 540-543, H4 Z- ~% I. s( z* B
© 2007 Sage Publications
0 }( N  a; v  \; q9 z. x  v10.1177/0009922806296651
7 I7 [5 _* H1 M2 Uhttp://clp.sagepub.com, G$ w8 _2 b* ^3 H1 X$ @% j
hosted at/ D% v. g6 o9 W# K( f2 c& T
http://online.sagepub.com; M. Z: o% s) ?- `7 I9 _4 y# E) Z
Precocious puberty in boys, central or peripheral,
4 [1 Y& ]6 n) H" C/ Kis a significant concern for physicians. Central
; f/ H" ^' p, n# `: v4 hprecocious puberty (CPP), which is mediated
# v; m7 K0 \8 D" ~1 E% @( C& Jthrough the hypothalamic pituitary gonadal axis, has' H2 |; W5 y+ l- }
a higher incidence of organic central nervous system
3 j  l6 I- u, B1 k! W3 clesions in boys.1,2 Virilization in boys, as manifested
8 c$ x+ D. v0 J* [by enlargement of the penis, development of pubic
4 a! Z( o; y; ^( d; ^hair, and facial acne without enlargement of testi-" L& Z; K; S/ c7 ^9 b; }! d
cles, suggests peripheral or pseudopuberty.1-3 We
9 X4 \9 _8 t* d) sreport a 16-month-old boy who presented with the$ V. W  i$ T+ U, C$ ?
enlargement of the phallus and pubic hair develop-# ]- g9 F9 S' X  {: h
ment without testicular enlargement, which was due4 h, m1 x& H/ @/ G" R
to the unintentional exposure to androgen gel used by3 I2 u1 F; |; z+ t- Z1 P8 N
the father. The family initially concealed this infor-
: _0 D$ m: ]2 q) {) W/ Imation, resulting in an extensive work-up for this
9 f& X" V" r6 k  g1 [" r4 dchild. Given the widespread and easy availability of
* b# K' ?+ p% k" R9 E/ ~) H& vtestosterone gel and cream, we believe this is proba-" o  z7 S7 q3 w9 x7 `
bly more common than the rare case report in the7 f  l9 O+ R8 m8 b' v5 ]9 n, n0 o
literature.4
- r- p4 i+ \. ^' ?$ W! h% nPatient Report$ g; E: }9 c: y0 g1 z
A 16-month-old white child was referred to the- u- |) S- U: i4 c  m1 {& k+ K
endocrine clinic by his pediatrician with the concern
, y+ v; a* }1 u( l5 oof early sexual development. His mother noticed- _$ H& g% Z. z
light colored pubic hair development when he was. _5 M, }& n# ~+ C, v( [5 ]8 [
From the 1Division of Pediatric Endocrinology, 2University of
+ c* ?1 U. y: [+ XSouth Alabama Medical Center, Mobile, Alabama.! x$ K4 W2 {- ?* n. h7 q
Address correspondence to: Samar K. Bhowmick, MD, FACE,
7 A& N9 f3 Y/ z1 m' oProfessor of Pediatrics, University of South Alabama, College of
9 Y) M1 T& b) j7 P9 N8 ?2 VMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;8 h- ^: t$ J3 h  S5 S
e-mail: [email protected].
2 J+ \) u2 ?' ?- M- |about 6 to 7 months old, which progressively became
1 V+ o( w! I3 E6 Sdarker. She was also concerned about the enlarge-( K. m  \# W# i) }/ v" ?  ^' w
ment of his penis and frequent erections. The child
: D5 R3 Z  \2 z6 x* F/ _- vwas the product of a full-term normal delivery, with
  G& S7 O3 J" v# a+ N5 @  ma birth weight of 7 lb 14 oz, and birth length of
; X' ]/ U1 t* _' @* }6 p+ H( G2 X. P20 inches. He was breast-fed throughout the first year
8 N( F& n$ l1 r" {of life and was still receiving breast milk along with- u( z% |  C$ J& Z3 ?% ^# r5 G
solid food. He had no hospitalizations or surgery,8 T7 M& N1 E) H/ ]
and his psychosocial and psychomotor development+ G: I0 h" w- Q  [7 B
was age appropriate.0 y' A2 B/ V4 ^4 u8 P4 q( d. `
The family history was remarkable for the father,
) ~4 W. ?' s# r) a! Y  D" ewho was diagnosed with hypothyroidism at age 16,
2 W' O$ ?& \; y# w! |& Kwhich was treated with thyroxine. The father’s
. L: f" M. T: o; ?height was 6 feet, and he went through a somewhat
, J6 V% y7 ~' Dearly puberty and had stopped growing by age 14.
2 S5 ~* k; \: k3 h; j5 f2 y) s% PThe father denied taking any other medication. The* x5 }& O  {$ J% g$ L8 H' g: i
child’s mother was in good health. Her menarche! {7 l' _2 \' {$ ^+ d
was at 11 years of age, and her height was at 5 feet8 y# A7 W4 c6 w, K0 n, H
5 inches. There was no other family history of pre-5 ]; s4 h" o4 h  U  M3 T% F' X0 g
cocious sexual development in the first-degree rela-! `5 h# L6 R4 }& V; O
tives. There were no siblings.
0 A9 g$ n7 s( E2 TPhysical Examination" C+ X- |$ r: d" L
The physical examination revealed a very active,
. n9 m1 i& E: m9 o$ S  H# y7 tplayful, and healthy boy. The vital signs documented
( i& ~' z5 z4 W, G- xa blood pressure of 85/50 mm Hg, his length was- X5 F! I% K6 j# N  Y1 |6 }: v
90 cm (>97th percentile), and his weight was 14.4 kg( i' A7 D: E* J& J2 f
(also >97th percentile). The observed yearly growth
8 {, y' p0 p2 S( t3 B& _9 tvelocity was 30 cm (12 inches). The examination of
' k) `5 K; }, N8 Dthe neck revealed no thyroid enlargement.0 G0 |; s  h  ^8 F4 _& ^  m
The genitourinary examination was remarkable for
% a* w3 ~. x/ C( F8 x% Tenlargement of the penis, with a stretched length of
6 J0 @( B) z' s8 cm and a width of 2 cm. The glans penis was very well' Z3 G; T# Q7 L9 W1 w5 `  {+ e
developed. The pubic hair was Tanner II, mostly around, Z* p2 I5 h, M1 ^2 F+ C; F
540
0 R  l. k3 t2 p1 L; G7 n2 e9 gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) @' A8 k# `" J$ [1 a4 O( F' _3 i' e3 J& ?the base of the phallus and was dark and curled. The0 i9 j4 Y& U/ }# Z
testicular volume was prepubertal at 2 mL each.
# x0 c  |4 W! k' [The skin was moist and smooth and somewhat
* C0 r, n# j9 M+ \3 [6 }# K* Y# w; goily. No axillary hair was noted. There were no
8 R! {$ E. p, m0 H# T+ ]abnormal skin pigmentations or café-au-lait spots.
3 l6 r3 d7 e: @: c, _- j5 R4 W3 pNeurologic evaluation showed deep tendon reflex 2+8 C1 f9 A# b- o) j
bilateral and symmetrical. There was no suggestion+ u8 D+ L8 T+ H/ Z1 J2 @# K* k
of papilledema.
* d) k3 {" J' L1 j0 x/ A, j$ u  ULaboratory Evaluation
% x( M% H# q$ _5 _- RThe bone age was consistent with 28 months by% F2 l+ i" |6 Y, w
using the standard of Greulich and Pyle at a chrono-
3 W- }) s, h8 I" [logic age of 16 months (advanced).5 Chromosomal) P, }+ ?8 J$ n! f5 S
karyotype was 46XY. The thyroid function test
- ^7 ]/ i- i& @  xshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
6 U# H- ^3 y' i1 s5 Tlating hormone level was 1.3 µIU/mL (both normal).; q3 b/ D7 ]% [
The concentrations of serum electrolytes, blood
8 J2 U/ }& C, Z' d6 turea nitrogen, creatinine, and calcium all were. n; j: }' S( P( b
within normal range for his age. The concentration
  r6 J+ S! X- R+ V9 q, ^/ Aof serum 17-hydroxyprogesterone was 16 ng/dL
# c% J# Q% p. U(normal, 3 to 90 ng/dL), androstenedione was 20; e. W: B; M4 M5 I
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
  `# O9 ]9 U0 W, S/ r6 Aterone was 38 ng/dL (normal, 50 to 760 ng/dL),
* O" d; l" T5 n" l0 C6 Ldesoxycorticosterone was 4.3 ng/dL (normal, 7 to
3 A2 m% A, o, @! M0 y49ng/dL), 11-desoxycortisol (specific compound S)
! E) {2 M& y8 s* X& l+ _5 Y$ Zwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-% |+ T" Q: z: C4 Z$ h
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total. v  Z5 ?% O3 h* H  z2 T
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),& I1 g. M; E! w7 z' }7 [0 `
and β-human chorionic gonadotropin was less than
: M8 A  t# Y: d$ M' |7 r5 mIU/mL (normal <5 mIU/mL). Serum follicular% S  `& ]2 W/ N1 X1 D  {2 o4 r# w5 Z
stimulating hormone and leuteinizing hormone
, K& j% G6 o, Qconcentrations were less than 0.05 mIU/mL  y! d" l) h5 Y
(prepubertal).
! `5 z; o! `+ E3 q4 ^3 @The parents were notified about the laboratory
9 ~  L) a, G4 f% q/ o2 x- _, {4 Vresults and were informed that all of the tests were
$ {3 T" j. g! L! d1 M. |normal except the testosterone level was high. The  d, z: F, c3 |
follow-up visit was arranged within a few weeks to+ B$ _  o9 Z- r
obtain testicular and abdominal sonograms; how-, L0 b/ Q5 w; N; v
ever, the family did not return for 4 months.: u6 C% J8 y# L! |, R( V4 g  X. N
Physical examination at this time revealed that the
" d, y) t4 u7 @child had grown 2.5 cm in 4 months and had gained
. ]6 m- }9 o: O2 p- j) z2 kg of weight. Physical examination remained
9 K5 k9 S5 k' \$ z( nunchanged. Surprisingly, the pubic hair almost com-
4 A2 e0 m) d4 F% Ppletely disappeared except for a few vellous hairs at/ f7 Y) |/ z& p2 A: g4 C$ Z
the base of the phallus. Testicular volume was still 2
; G& a0 y3 r4 \mL, and the size of the penis remained unchanged." c0 B8 ^3 X: A) P
The mother also said that the boy was no longer hav-
* H; R& m3 a/ H3 \$ x, Jing frequent erections.
" M: X+ C: H- J9 m; F6 @3 pBoth parents were again questioned about use of
5 U; a% m) C, {3 ^- gany ointment/creams that they may have applied to
7 N# ]# r* g' T3 b: Vthe child’s skin. This time the father admitted the
$ w6 }$ s' u5 l  K% h& pTopical Testosterone Exposure / Bhowmick et al 541
0 c5 w8 ]' s1 U# V* b, i- euse of testosterone gel twice daily that he was apply-
! O- [) z  L4 oing over his own shoulders, chest, and back area for. l1 Y+ K. l2 V1 T' S8 e$ i6 z
a year. The father also revealed he was embarrassed7 K0 x' ^" y+ _, m
to disclose that he was using a testosterone gel pre-
4 B/ t3 x9 j/ \# E# fscribed by his family physician for decreased libido2 s9 S& X& p8 c, C2 i) I6 ~6 L
secondary to depression.
, b+ Y& J! o  L! mThe child slept in the same bed with parents.
4 a: d. K" }' D# t6 TThe father would hug the baby and hold him on his
! s1 k7 E0 H9 T  O( N6 F/ }2 |# _chest for a considerable period of time, causing sig-
  P6 X( |; n, O# b; k9 r! V8 D5 knificant bare skin contact between baby and father.
' S2 f' M) I5 U2 m- S+ t4 pThe father also admitted that after the phone call,. c* H  E* T9 i& _! f. F, D2 c
when he learned the testosterone level in the baby( F4 Z: P4 j) T9 d$ J# }
was high, he then read the product information
" s5 Z: g; R. Xpacket and concluded that it was most likely the rea-
/ F! f# {( R  J; N/ ^son for the child’s virilization. At that time, they9 U& [% G8 C6 [$ @+ O, L. m
decided to put the baby in a separate bed, and the
5 d  C9 q$ ^9 v% E2 ofather was not hugging him with bare skin and had" B  ^3 I# I* O+ A
been using protective clothing. A repeat testosterone
. h& B# T7 v& s+ v  |2 d2 l2 Stest was ordered, but the family did not go to the: w5 \9 {$ i# W! g- X% Q+ d
laboratory to obtain the test.
5 m) i6 L6 @1 i. R; a( F, zDiscussion
1 m( _$ w+ E5 t" I( a8 x1 vPrecocious puberty in boys is defined as secondary( U" y& S0 ?7 Z" ?) I# k, p
sexual development before 9 years of age.1,4
, G( E; [' Y. Q) ~0 p9 z. h" y9 X( DPrecocious puberty is termed as central (true) when) w$ b+ N0 H1 ^! _  Y9 O$ y
it is caused by the premature activation of hypo-! A5 `% _! Z  \$ Z. X
thalamic pituitary gonadal axis. CPP is more com-; _% y; x; U& _+ T& I. n' x5 M( X
mon in girls than in boys.1,3 Most boys with CPP2 t. B/ K4 ]4 S! k. c3 t7 @5 s
may have a central nervous system lesion that is
; l* ~  h: Y( w8 yresponsible for the early activation of the hypothal-& B3 j1 M* w( B1 c( c: z
amic pituitary gonadal axis.1-3 Thus, greater empha-. h9 V' t7 i; w  m" n
sis has been given to neuroradiologic imaging in
& s5 \" W4 u7 [7 Gboys with precocious puberty. In addition to viril-
# T6 f7 l9 W- X4 Z4 I$ D) i  |ization, the clinical hallmark of CPP is the symmet-
7 W9 X/ ~( d4 Y( b8 rrical testicular growth secondary to stimulation by; J5 v' m2 I2 B0 I$ _
gonadotropins.1,3
& e# O+ L# W3 j2 Q+ [8 g+ ~4 B  YGonadotropin-independent peripheral preco-
9 _: L4 j: g! G! lcious puberty in boys also results from inappropriate+ r6 e5 c0 S; Z" u8 C' p
androgenic stimulation from either endogenous or0 e# r7 I" C0 y5 c0 E( O
exogenous sources, nonpituitary gonadotropin stim-
% ^3 D: {& |9 x  G, Z  z7 ^ulation, and rare activating mutations.3 Virilizing
: P# I; l9 ^. A6 K' \- G' J' jcongenital adrenal hyperplasia producing excessive4 U6 J7 g1 \0 h/ ]' b
adrenal androgens is a common cause of precocious9 Y, ]0 n5 p. d1 |6 U: h9 m. o/ A
puberty in boys.3,4
3 j+ Z9 H5 [: F7 H  DThe most common form of congenital adrenal# R+ X0 c  W! {" }& H! a
hyperplasia is the 21-hydroxylase enzyme deficiency.' ], ?9 K1 ?5 M
The 11-β hydroxylase deficiency may also result in) }  t6 I$ e6 s6 ]# f: R  c
excessive adrenal androgen production, and rarely,
! F: J6 W. E7 U% x' d/ _an adrenal tumor may also cause adrenal androgen+ I; h/ b# Q" t
excess.1,39 z$ i( x# H% @  k0 H) G: T% H
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 I% p; r. s7 V8 z* s
542 Clinical Pediatrics / Vol. 46, No. 6, July 20076 j% b* W3 u4 ]$ b$ y. T
A unique entity of male-limited gonadotropin-; ^- `& h$ v' J/ G1 m' Y
independent precocious puberty, which is also known
# P; I5 L; H! O' }as testotoxicosis, may cause precocious puberty at a1 P+ q! z& w* p( b: Q' N" W. }
very young age. The physical findings in these boys4 {6 Z' e* p3 G  i0 ^' b' [0 q
with this disorder are full pubertal development,$ z* [8 ]+ {1 w3 N: E5 @
including bilateral testicular growth, similar to boys% s1 x) g2 ]2 e
with CPP. The gonadotropin levels in this disorder- B% h$ W, J& H! L( A2 _9 j
are suppressed to prepubertal levels and do not show' P0 }3 |: \9 C% W' h3 Y- Y7 z
pubertal response of gonadotropin after gonadotropin-9 ]; f* Y8 ]( n! D6 f3 v7 I& S
releasing hormone stimulation. This is a sex-linked
& f: b4 i* ?/ A) L. I' m2 k, dautosomal dominant disorder that affects only
: q) y' ^0 T; I( Nmales; therefore, other male members of the family' u9 ^- D( `/ d7 r
may have similar precocious puberty.3" o, }& ^9 r9 ]9 z" d2 ?
In our patient, physical examination was incon-2 V; g) D# w6 f* z- z9 q
sistent with true precocious puberty since his testi-/ f6 }" U+ O2 e2 U% F
cles were prepubertal in size. However, testotoxicosis/ D) k4 X; u+ ?5 N/ x* [2 o
was in the differential diagnosis because his father
- w: d4 C% [; \& [/ m9 jstarted puberty somewhat early, and occasionally,5 J3 k' Y8 c3 w# X( h6 m
testicular enlargement is not that evident in the& R# H$ ?( w0 _8 l
beginning of this process.1 In the absence of a neg-
9 y" U' W, p# U7 X3 ]. @" U+ W8 Jative initial history of androgen exposure, our
, s! {* ^: j+ Jbiggest concern was virilizing adrenal hyperplasia,
' g( l+ ~6 e' U  S' Deither 21-hydroxylase deficiency or 11-β hydroxylase
" O: `  ?" @! M1 V: c$ Q$ fdeficiency. Those diagnoses were excluded by find-
& t7 s, A) `/ C& ]3 V" b/ Sing the normal level of adrenal steroids.
9 C5 W8 n) k. BThe diagnosis of exogenous androgens was strongly7 S( @. ]/ K  A" s9 A% f
suspected in a follow-up visit after 4 months because/ L5 d: C% `, H% R) m. X
the physical examination revealed the complete disap-
8 @7 W  R0 w+ ~' s. `pearance of pubic hair, normal growth velocity, and
0 G. |& t% l. B2 Hdecreased erections. The father admitted using a testos-
$ o5 u+ O: {5 Q( j3 ?7 H$ rterone gel, which he concealed at first visit. He was$ O* `  b; Q8 r2 }/ q
using it rather frequently, twice a day. The Physicians’3 ?  K& x# l" Y4 O  h6 }+ N
Desk Reference, or package insert of this product, gel or+ v0 q; \( y# C& x* Z2 r0 C
cream, cautions about dermal testosterone transfer to3 a9 E; Y8 d* A. d9 E5 p6 }
unprotected females through direct skin exposure.
* s! U- Y. n/ m; d  P7 b; Y4 C( I; p1 uSerum testosterone level was found to be 2 times the) O- \; K" m+ Z! O; E% H" u
baseline value in those females who were exposed to$ N) F( J1 S0 I1 t7 I. S+ U
even 15 minutes of direct skin contact with their male7 N) m. Q& s; p7 g- ?1 h
partners.6 However, when a shirt covered the applica-
- M; ~5 d  b! y- ?7 p" Ztion site, this testosterone transfer was prevented.
2 R# H3 a1 ~/ a. r' TOur patient’s testosterone level was 60 ng/mL,
! K# y! m( i' A6 R& k5 b: }- {9 J2 Swhich was clearly high. Some studies suggest that
4 Y* I3 n7 L6 y: ^8 S0 ldermal conversion of testosterone to dihydrotestos-! E$ A4 b8 V* C% f! f
terone, which is a more potent metabolite, is more- p0 J0 j) q# \
active in young children exposed to testosterone
: _) D& T3 V( U, ]2 gexogenously7; however, we did not measure a dihy-
* I, l+ n0 H" q& }; h0 jdrotestosterone level in our patient. In addition to
3 r7 S3 h) f  lvirilization, exposure to exogenous testosterone in
  \' {3 N& k+ F5 H! U, Jchildren results in an increase in growth velocity and
& O5 |# Z+ i1 Q4 ~- vadvanced bone age, as seen in our patient.
, I7 n7 J- L+ m9 N& G& \7 [) p. l1 ^The long-term effect of androgen exposure during
, c7 n4 U7 Q1 @$ A: r( h; rearly childhood on pubertal development and final6 M# r% b( B3 U
adult height are not fully known and always remain
1 y/ v- K" b7 ta concern. Children treated with short-term testos-9 S6 B) _% }( \& {
terone injection or topical androgen may exhibit some
. Z) }) v6 c2 V. P/ p/ K1 zacceleration of the skeletal maturation; however, after
9 N9 g/ g! C; ]) ^; jcessation of treatment, the rate of bone maturation
& l; @. k% L. _8 r4 p! Jdecelerates and gradually returns to normal.8,9
% ?/ N7 U: u& e& h' Q/ IThere are conflicting reports and controversy8 v2 O, @' @) ?3 x# q
over the effect of early androgen exposure on adult0 ], o7 o" Q# T% z5 B/ _9 E8 ~
penile length.10,11 Some reports suggest subnormal
) {/ |3 `% ~: Qadult penile length, apparently because of downreg-' S6 _$ P8 g& _- M3 w% e" @$ K2 w
ulation of androgen receptor number.10,12 However,
, B) T$ H7 x2 _* [/ j+ }8 GSutherland et al13 did not find a correlation between
, T3 {$ G7 d! n! `$ ]: Vchildhood testosterone exposure and reduced adult$ w) ~2 X6 m5 F0 @# I; b6 i0 Y; C, ?! i
penile length in clinical studies.
8 r& V# q! z. sNonetheless, we do not believe our patient is
2 L' j6 \' @* A( R# \6 Ygoing to experience any of the untoward effects from
. C5 x( ]- i# I6 m7 Stestosterone exposure as mentioned earlier because2 a  m5 Q" n- J* _# {2 p
the exposure was not for a prolonged period of time.
0 I, i3 ^2 R5 j  e9 }Although the bone age was advanced at the time of3 \7 Y3 U9 I/ J* q/ l( y
diagnosis, the child had a normal growth velocity at0 }/ l; k0 P% }" O  T
the follow-up visit. It is hoped that his final adult7 p& W6 R) B; I2 j& b! o
height will not be affected.
' J1 ~% c. B) {" Y6 lAlthough rarely reported, the widespread avail-5 a  W( n. w; B+ B& b
ability of androgen products in our society may: o3 E5 D3 u' ^% H9 Z3 o
indeed cause more virilization in male or female( {) t) f7 U6 G9 b' e
children than one would realize. Exposure to andro-
/ R; N; ]; |" C: x% T  }9 dgen products must be considered and specific ques-9 B% ~+ ~" L) j$ f, V- E
tioning about the use of a testosterone product or
3 L) `! R) d: w! }2 _gel should be asked of the family members during
$ s2 E% G+ Z1 ethe evaluation of any children who present with vir-
' N* n7 p% |/ V- U' bilization or peripheral precocious puberty. The diag-
" m) L2 w: v  Z1 S, fnosis can be established by just a few tests and by
2 }7 j3 Y( p$ X; C( |appropriate history. The inability to obtain such a
) X1 g  e3 Q% I+ ^/ dhistory, or failure to ask the specific questions, may! ]$ f* I: b! l9 ^
result in extensive, unnecessary, and expensive+ b6 f2 U0 o6 x2 u) Z
investigation. The primary care physician should be
" e/ T& q/ D1 ^" P% ^aware of this fact, because most of these children5 r6 @" b/ ]- S# h
may initially present in their practice. The Physicians’8 u  i; z# R" q: t6 ?" v; K
Desk Reference and package insert should also put a7 h/ \/ B! ^  C5 q/ E5 O8 b9 C
warning about the virilizing effect on a male or
* t5 b* H4 I3 m$ K6 I- z9 rfemale child who might come in contact with some-% ^% C2 d9 x0 N8 Q" p7 G) N( |
one using any of these products.
/ J3 F. Y. F) k% i8 ~References& L/ D) g  ?. u# ~8 V, K3 F  u& }8 E
1. Styne DM. The testes: disorder of sexual differentiation- N% s  Y: {* P- p
and puberty in the male. In: Sperling MA, ed. Pediatric
6 r( I& j" w# a+ ^Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;4 F( E6 ?. v' H8 T9 `# v3 ^+ z) Q
2002: 565-628.
0 w4 F( `; \1 }6 Z* B1 J2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious+ R, C8 v; Q" ~' \
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
4 a) r# {" q/ ~& d  YBoy Induced by Indirect Topical4 _# d: W# X8 Z/ }$ v+ E' q
Exposure to Testosterone3 r3 C- ?9 v1 \
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
' I. r1 B$ }5 Z3 [0 f) fand Kenneth R. Rettig, MD1) f' z3 W( X3 B
Clinical Pediatrics0 l( A3 E. N3 f' `# S* L( d4 Y# g, U
Volume 46 Number 6
1 p% a$ T  e: T6 ?2 [. _/ x4 jJuly 2007 540-543
2 _- N! J* m6 h" l1 q© 2007 Sage Publications
6 h8 Y6 t' n' `9 c7 I% i2 Q/ r10.1177/0009922806296651
8 t$ ]% D5 A# s( p5 |http://clp.sagepub.com! n& s  a: }" K
hosted at  p! ^$ B% q& b% T; j
http://online.sagepub.com" q. H; X- M" ^, m7 d
Precocious puberty in boys, central or peripheral,
' H; f8 c; p+ qis a significant concern for physicians. Central
8 `& W4 S: F0 Q, R+ `precocious puberty (CPP), which is mediated
4 e& I$ X, Z% s) m1 @through the hypothalamic pituitary gonadal axis, has
% w3 D0 ]2 h( Z$ U* Q& ya higher incidence of organic central nervous system
' O, D3 a; i! R6 ~! S! G% elesions in boys.1,2 Virilization in boys, as manifested
+ s! }( S! T1 E( @9 x% u" \by enlargement of the penis, development of pubic
, N, t- o& O# i5 Chair, and facial acne without enlargement of testi-9 [6 j1 l) K2 c# B! f
cles, suggests peripheral or pseudopuberty.1-3 We
# T- A8 W( s5 N" vreport a 16-month-old boy who presented with the
9 M* e! N: I2 t* S- W  venlargement of the phallus and pubic hair develop-6 U$ J2 _; `/ R6 d0 s! W/ g
ment without testicular enlargement, which was due8 `# K) g6 F9 a# o/ f
to the unintentional exposure to androgen gel used by' {* o6 e2 Z/ [6 @" D
the father. The family initially concealed this infor-
6 A+ l5 |" Q) T0 a  u! bmation, resulting in an extensive work-up for this
1 c% }- N; m; v, E- v$ j% B; u* j( zchild. Given the widespread and easy availability of$ Y& i; ~1 V  S" F
testosterone gel and cream, we believe this is proba-
, x" c0 O& c' U4 X% nbly more common than the rare case report in the/ @8 n4 [- |6 F+ X# r0 P; G
literature.4, O( M5 U7 b+ p# e5 Y& g6 O
Patient Report
' }$ J* U) p. V2 D, tA 16-month-old white child was referred to the
+ D- y( T8 U1 V& D$ D) Yendocrine clinic by his pediatrician with the concern6 V1 G6 {# H0 g6 V' X/ [
of early sexual development. His mother noticed
& i1 Q$ J7 l" k- N- D1 \light colored pubic hair development when he was5 s& K+ n% V! L, U$ R! V3 o
From the 1Division of Pediatric Endocrinology, 2University of2 b4 H4 i) V; S. K
South Alabama Medical Center, Mobile, Alabama.
4 U0 {' U  B9 e2 M9 @% `Address correspondence to: Samar K. Bhowmick, MD, FACE,
% b1 |7 X) X/ Y/ QProfessor of Pediatrics, University of South Alabama, College of4 s# W) {" R6 o
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
" B% a/ T  D+ B: h1 oe-mail: [email protected].
" L3 K& J% ?' `: t5 y4 a" xabout 6 to 7 months old, which progressively became
5 m* o0 d( F$ e: pdarker. She was also concerned about the enlarge-3 ]: ^7 V  C- E% |& x
ment of his penis and frequent erections. The child
1 u; T8 @2 P/ Dwas the product of a full-term normal delivery, with# W2 {! ]3 o9 ^3 \
a birth weight of 7 lb 14 oz, and birth length of
# d, j/ {3 |: [, J* A20 inches. He was breast-fed throughout the first year$ H7 E# u9 g4 h* C& a5 c! X
of life and was still receiving breast milk along with
6 X: p+ K# V4 F) Csolid food. He had no hospitalizations or surgery,0 m8 U) ^$ H  m; ~  F9 {8 M
and his psychosocial and psychomotor development
: G6 Q6 A- E( Q$ }4 q) s( y( [' {, owas age appropriate.+ D) i$ s' {9 d8 C0 p
The family history was remarkable for the father,
- P: w9 p0 [8 p& v7 ~- h" w8 Lwho was diagnosed with hypothyroidism at age 16,) P6 |0 F: D' `) Z" Y0 x; ^$ r! a
which was treated with thyroxine. The father’s
# |' Q, ?8 |1 S; l. V0 Iheight was 6 feet, and he went through a somewhat( d, d& j% ~( }$ g1 @
early puberty and had stopped growing by age 14.
( ?  y8 i! j' pThe father denied taking any other medication. The
7 D# s4 K# T: E3 u. gchild’s mother was in good health. Her menarche
: ?. Q- N3 M2 O0 Q* w  K+ }$ k2 Zwas at 11 years of age, and her height was at 5 feet+ g4 w) [6 W  V9 S+ x
5 inches. There was no other family history of pre-
% k- Q7 v$ a2 T: zcocious sexual development in the first-degree rela-
' U# Y/ W1 F9 N3 z3 Etives. There were no siblings.
0 B) O" z4 \3 z/ E. X* jPhysical Examination
$ U) h) |2 P2 u" G' D/ EThe physical examination revealed a very active,
3 s& G# v( T7 F5 B- E  S' ]playful, and healthy boy. The vital signs documented
/ a; n! f+ s- Oa blood pressure of 85/50 mm Hg, his length was, R) e4 k. P6 D' `
90 cm (>97th percentile), and his weight was 14.4 kg# P7 o+ ]/ b. ~
(also >97th percentile). The observed yearly growth: e* I7 s# M5 v' r& g3 _
velocity was 30 cm (12 inches). The examination of
* T7 Q$ J8 Z. K! g9 sthe neck revealed no thyroid enlargement.! q2 r6 ~" Z# O, X: Y
The genitourinary examination was remarkable for
! G0 g' z% V- t" P7 oenlargement of the penis, with a stretched length of+ X# {8 k' H" p% P
8 cm and a width of 2 cm. The glans penis was very well
5 }4 S* y+ l' O6 q& B4 vdeveloped. The pubic hair was Tanner II, mostly around" B9 Z6 k9 n- U* N) T5 L
540: M2 y" V# z5 u; {& P, A) B1 X, r
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from( V# D" G2 \6 L3 D
the base of the phallus and was dark and curled. The0 h% M# q4 p; _9 Z" o
testicular volume was prepubertal at 2 mL each./ R2 q: ~, [* y4 ?+ y" x
The skin was moist and smooth and somewhat3 s  T+ V) t- |: r9 C
oily. No axillary hair was noted. There were no
3 z- y5 c+ t% m9 v3 t4 s3 i- ^abnormal skin pigmentations or café-au-lait spots., [+ j/ s4 j# h. |  b8 A5 G
Neurologic evaluation showed deep tendon reflex 2+
. U# j9 S0 d3 gbilateral and symmetrical. There was no suggestion
- W! c/ p, C8 C$ O6 [1 [% E4 |of papilledema.
5 [* U3 R3 m+ Q1 m( LLaboratory Evaluation
, ?6 h/ O# H, J, g2 y0 cThe bone age was consistent with 28 months by4 ?" u3 |! z: K- \0 `& a1 |( m
using the standard of Greulich and Pyle at a chrono-
+ [2 j. E; k( h  E: d" Klogic age of 16 months (advanced).5 Chromosomal$ N1 S0 D1 f. E$ a) G+ A% Z
karyotype was 46XY. The thyroid function test1 T+ m; r* a8 q& P* H& |
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
  Y. ]7 B" l6 x5 c0 n/ ~lating hormone level was 1.3 µIU/mL (both normal).
) I% n0 e9 e" O0 n/ g6 GThe concentrations of serum electrolytes, blood. ^. w& |1 \, {/ t
urea nitrogen, creatinine, and calcium all were
+ f4 l) ^8 S, F- b0 U& q2 k* Rwithin normal range for his age. The concentration4 W1 P/ a# p- J6 v5 l2 U" T
of serum 17-hydroxyprogesterone was 16 ng/dL- u% T  d; y# t1 J3 @
(normal, 3 to 90 ng/dL), androstenedione was 20
9 j% P: ~1 T" N6 ]! [6 z/ O  tng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
' z5 ]/ l5 u* O( N5 z2 Qterone was 38 ng/dL (normal, 50 to 760 ng/dL),
6 h0 \) ~" s, K9 hdesoxycorticosterone was 4.3 ng/dL (normal, 7 to# z! ]! ^0 B& _# u0 v- j+ b
49ng/dL), 11-desoxycortisol (specific compound S)
4 U0 H& [' _! d3 g6 Swas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
4 Y$ E4 Z- w! d/ Q+ U* ktisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
1 B/ O" a( z# H( e) Jtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),5 {/ I* K: f0 @, P8 E/ b" N1 M
and β-human chorionic gonadotropin was less than! C9 D0 l- b* ~, y4 A; o! U
5 mIU/mL (normal <5 mIU/mL). Serum follicular
0 g' `2 S& k' k/ b) m  {: Astimulating hormone and leuteinizing hormone. X. V* q- J6 ~1 y" X6 M
concentrations were less than 0.05 mIU/mL  z1 Z7 |0 [* u1 {1 h  ]+ M
(prepubertal)., ]& Q: N, q& p" R/ Z( @
The parents were notified about the laboratory4 T8 b5 _6 C% A: B
results and were informed that all of the tests were% U9 n( P' Y: m3 K# l6 k
normal except the testosterone level was high. The5 t( G/ l+ S/ ^$ {+ a
follow-up visit was arranged within a few weeks to
" V5 X8 _5 o; j' N3 X) lobtain testicular and abdominal sonograms; how-( G- O) h) v) T7 E
ever, the family did not return for 4 months.2 i' }" O- q: g! B* C
Physical examination at this time revealed that the
  B4 O& I- v1 K% k$ v; X; ~child had grown 2.5 cm in 4 months and had gained" J1 M" ]' q1 A
2 kg of weight. Physical examination remained2 H0 v# X9 x4 v7 G
unchanged. Surprisingly, the pubic hair almost com-" y/ j( h$ @8 ~4 D0 p
pletely disappeared except for a few vellous hairs at" e/ _: X/ w4 j8 l
the base of the phallus. Testicular volume was still 2
" ?4 r! }: B! F* A7 a: `' H# QmL, and the size of the penis remained unchanged.
9 i; v1 h( v! RThe mother also said that the boy was no longer hav-
) @% H/ L0 H* b( j5 \0 ying frequent erections.
" y8 s+ a2 [. p4 p. \7 \$ \Both parents were again questioned about use of
  @3 Y& `( W0 k" t9 eany ointment/creams that they may have applied to; Z' q- z' N" Y8 ]
the child’s skin. This time the father admitted the/ p; N5 K2 A, @5 Z. A2 K1 b
Topical Testosterone Exposure / Bhowmick et al 541
9 L/ S5 m  d; m; |  muse of testosterone gel twice daily that he was apply-
% U7 G" m( O- S; T0 C3 k0 ?' jing over his own shoulders, chest, and back area for
( q' ~" B& u; O9 ?2 Ra year. The father also revealed he was embarrassed
" z& s3 l5 _9 Q! }' mto disclose that he was using a testosterone gel pre-& a. I( P7 Y0 G# {# B2 F. V
scribed by his family physician for decreased libido8 S2 |' |$ [. |
secondary to depression.# s2 m- Y' a; U# R$ s4 W( H! I
The child slept in the same bed with parents.
/ |$ G0 L5 {3 D' N7 p% BThe father would hug the baby and hold him on his
$ n! x: u* N" J/ V9 E1 wchest for a considerable period of time, causing sig-
& }' d3 C+ J. N) Fnificant bare skin contact between baby and father.
2 L- E8 Z4 K& C6 T+ b: L8 `The father also admitted that after the phone call,
" W2 n) F& m7 L5 z. S; Swhen he learned the testosterone level in the baby: I8 l# S) v6 e8 q
was high, he then read the product information! t; q. P0 {' m& u  ~/ }* I
packet and concluded that it was most likely the rea-( {- i! x: ]0 ~9 @# `
son for the child’s virilization. At that time, they7 j/ b6 S, S( y' H
decided to put the baby in a separate bed, and the4 n0 ], W/ J2 o1 s9 t; _, E0 h
father was not hugging him with bare skin and had* \. G: v6 ~2 w  [$ ?- Q
been using protective clothing. A repeat testosterone7 N, I! R/ P+ w: J" O/ M8 h
test was ordered, but the family did not go to the
$ L% a  k( v. ?6 s$ e7 c9 Ulaboratory to obtain the test.4 D3 m3 Z5 N" O) W. h% r
Discussion2 L* {/ e/ `) k5 |9 k' t! Z; s
Precocious puberty in boys is defined as secondary
" C8 b% T' T9 P8 z; fsexual development before 9 years of age.1,4) F4 E- k3 C& g; d" o4 R
Precocious puberty is termed as central (true) when7 a4 x. U. N% K& G9 f5 t
it is caused by the premature activation of hypo-. W+ m) L% s) f# K2 N  v7 A/ s6 G
thalamic pituitary gonadal axis. CPP is more com-
$ d8 G. ^! N& ]5 _) [5 P5 Y/ C/ \mon in girls than in boys.1,3 Most boys with CPP6 w- E5 o! g/ y9 Z6 j* k
may have a central nervous system lesion that is
. {2 e; I3 V$ }6 k' Jresponsible for the early activation of the hypothal-' l; _4 _8 q- A0 H8 z6 q2 ?4 ]
amic pituitary gonadal axis.1-3 Thus, greater empha-0 T6 F( I$ w5 J: s
sis has been given to neuroradiologic imaging in! z& \: b: k3 ^
boys with precocious puberty. In addition to viril-
2 n' ~, R& i4 q9 N# e3 B6 jization, the clinical hallmark of CPP is the symmet-
- F( ?" [! C& Q4 x  k& o4 Krical testicular growth secondary to stimulation by
! ?# Z  R& s, J7 H- z: s7 vgonadotropins.1,3
* q/ F: ^0 A* `' g0 b  \Gonadotropin-independent peripheral preco-1 g" \; [. `0 l: a( L: }( a! ^
cious puberty in boys also results from inappropriate: S7 w5 N( d8 [2 }4 A- ~
androgenic stimulation from either endogenous or# x; n1 x4 E; ~. p* h# t
exogenous sources, nonpituitary gonadotropin stim-
: s1 K# I7 F+ Tulation, and rare activating mutations.3 Virilizing2 }8 @* Y% {; c- t5 a
congenital adrenal hyperplasia producing excessive. V) n# W) f) X5 Q
adrenal androgens is a common cause of precocious
0 y+ ~' \8 R# Z6 ^8 fpuberty in boys.3,41 R: s4 A' v" @: b3 p6 {2 O
The most common form of congenital adrenal
# N, }! h% h0 P% s5 t7 j% b. rhyperplasia is the 21-hydroxylase enzyme deficiency.
$ t2 J9 i8 `7 ]( C! ~5 tThe 11-β hydroxylase deficiency may also result in
( K/ d' t3 R. o' C( oexcessive adrenal androgen production, and rarely,
, B2 O  |+ u8 f* e2 tan adrenal tumor may also cause adrenal androgen
! g9 e1 l  t9 H- cexcess.1,3  W: M, L- V' C& Y2 O# f
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. X) d3 t) i. `  s! L$ j
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
* H1 I) f; H; E" SA unique entity of male-limited gonadotropin-
: M1 Y9 K, U! ]# H* V$ L% ~. Z  |independent precocious puberty, which is also known
- e9 ~& Z% T  V$ F9 F2 k8 Ras testotoxicosis, may cause precocious puberty at a
+ D5 G% e2 Y1 P6 \3 Kvery young age. The physical findings in these boys
* m/ Y) a! _& b1 n4 Swith this disorder are full pubertal development,
6 M3 Y9 B- E& i  M+ a) Hincluding bilateral testicular growth, similar to boys/ I7 {3 `) _( s4 g! I: _0 q
with CPP. The gonadotropin levels in this disorder
# f( j# |6 E% j3 Gare suppressed to prepubertal levels and do not show
; |  C- r! k7 U1 x. W( ?' Z# epubertal response of gonadotropin after gonadotropin-" o( o0 n  Y; T3 y6 g3 m$ p) M
releasing hormone stimulation. This is a sex-linked, f& p" v9 G4 H+ R0 p$ q
autosomal dominant disorder that affects only; L. ?. M: @( M9 \6 Y. ?
males; therefore, other male members of the family) w! |6 u. F2 |! f1 o
may have similar precocious puberty.3( N2 e; \7 [2 t- P1 Q" K
In our patient, physical examination was incon-
' I( ~$ U0 \- _1 usistent with true precocious puberty since his testi-! U6 k# {; Y& J' C  O6 W% x4 t
cles were prepubertal in size. However, testotoxicosis
" r" g/ j5 N% P5 i6 A: @was in the differential diagnosis because his father* j' `' {: K0 L) g: R# P! w+ C$ @
started puberty somewhat early, and occasionally,
  p) }$ O+ t3 O/ i4 ?# Wtesticular enlargement is not that evident in the
0 E, \# b: z! d- X1 P8 Jbeginning of this process.1 In the absence of a neg-4 `% W$ }5 W, S. X! x+ g
ative initial history of androgen exposure, our
: ~$ r$ ^3 s1 w5 r  dbiggest concern was virilizing adrenal hyperplasia,
! z* m4 S- Q& V1 h9 ^( p; b4 Geither 21-hydroxylase deficiency or 11-β hydroxylase
  C3 T1 F) U; T! j! z4 F9 Odeficiency. Those diagnoses were excluded by find-
% Y  R* i7 ~- w5 Ning the normal level of adrenal steroids.* {% o: Z* D9 }
The diagnosis of exogenous androgens was strongly
4 y0 G6 [, t0 w5 W" Rsuspected in a follow-up visit after 4 months because
+ \7 ~( O4 @4 P, w" Othe physical examination revealed the complete disap-  @; h( B6 T+ J
pearance of pubic hair, normal growth velocity, and
, {3 L! a+ m6 mdecreased erections. The father admitted using a testos-2 S4 \& D  J: w# Y+ M) ?
terone gel, which he concealed at first visit. He was
  `" l6 r0 w8 k7 j. q$ P9 ]3 v' v! e4 Kusing it rather frequently, twice a day. The Physicians’
' b" W9 b' X* h. b  FDesk Reference, or package insert of this product, gel or
1 J! |9 W" }; }4 J3 K  ~cream, cautions about dermal testosterone transfer to6 T" P+ }" I6 X
unprotected females through direct skin exposure.- C; m& {7 W& L% ^
Serum testosterone level was found to be 2 times the% D  U2 l& ~  \4 _
baseline value in those females who were exposed to
; f& f  {0 _  yeven 15 minutes of direct skin contact with their male- C7 {0 S0 n3 V5 [3 c" q1 X* `0 s
partners.6 However, when a shirt covered the applica-3 {+ K# p7 k$ M/ X1 p9 j6 u2 u
tion site, this testosterone transfer was prevented.
3 Y# B+ Z: K6 v' c! q  ~Our patient’s testosterone level was 60 ng/mL,
0 f, z9 V, |5 Y8 Qwhich was clearly high. Some studies suggest that3 k8 a+ d& t4 m: N1 u
dermal conversion of testosterone to dihydrotestos-
) ?2 Z( u3 M* v: qterone, which is a more potent metabolite, is more
! S. g( E7 K, C7 U# F8 Gactive in young children exposed to testosterone( }# F2 i$ K2 o( e
exogenously7; however, we did not measure a dihy-
- M$ k7 S# r$ j8 H4 ~drotestosterone level in our patient. In addition to
, Y9 }3 N4 M" s+ V% P$ j/ z+ C0 Dvirilization, exposure to exogenous testosterone in, S8 M( f! {% q# C/ C; \6 y/ d4 D/ r
children results in an increase in growth velocity and
: o5 M6 t: N; p. gadvanced bone age, as seen in our patient.
& X+ v, f: y1 k  P3 i7 XThe long-term effect of androgen exposure during
/ S! W% J7 D$ s0 w1 N; D+ k9 eearly childhood on pubertal development and final8 t  q: U2 |( x8 X0 c+ c' L4 E8 ~
adult height are not fully known and always remain3 M. r: a2 q% D" F' u% r0 Y
a concern. Children treated with short-term testos-
* J) L7 }6 }6 L% c$ i0 Nterone injection or topical androgen may exhibit some1 {, R4 b! w/ M2 x( s
acceleration of the skeletal maturation; however, after
4 `% k4 {- }8 E3 G4 E7 p* Jcessation of treatment, the rate of bone maturation1 P+ `7 Z. r5 c' Q. H5 B, Y5 V" X
decelerates and gradually returns to normal.8,9
5 B  p+ Q! S* p4 B! U! f' Q, i; p6 yThere are conflicting reports and controversy
( O0 N  L' r; T$ U( ]over the effect of early androgen exposure on adult
7 C; d4 o4 `. P# ?+ \7 o0 `5 b( H) tpenile length.10,11 Some reports suggest subnormal9 m: e& A" }: `" ^: H" _
adult penile length, apparently because of downreg-3 |; W, o7 I. V- G: d# u) D. \
ulation of androgen receptor number.10,12 However,6 K. ~$ S2 _8 o' t& p* g0 t" v
Sutherland et al13 did not find a correlation between
0 g6 @9 f  E1 p% I! N+ Uchildhood testosterone exposure and reduced adult
! y$ i5 M" Y4 v9 [penile length in clinical studies." O& w! i2 X# s5 P
Nonetheless, we do not believe our patient is7 B; a; p% A8 |% U7 q9 x; y
going to experience any of the untoward effects from
1 c* r. W' J, M7 ?testosterone exposure as mentioned earlier because( Z6 E# t. V2 ?7 L$ u
the exposure was not for a prolonged period of time.4 g  M  i2 G- I0 h5 U% k
Although the bone age was advanced at the time of# W: X- z3 J3 g+ k5 b; \
diagnosis, the child had a normal growth velocity at# g/ U) M5 A& X! Y3 l1 ^
the follow-up visit. It is hoped that his final adult# A( u1 `$ J! t6 p) G
height will not be affected.
# ]9 |, ]# c; C) V4 UAlthough rarely reported, the widespread avail-( t0 f. x9 [" @. _! v% O
ability of androgen products in our society may
" A9 N& t3 L6 l: _indeed cause more virilization in male or female
$ D$ E$ K0 }; ?& a0 w" z) c2 Ichildren than one would realize. Exposure to andro-3 S$ d$ B) k/ Y' V2 D7 r7 p
gen products must be considered and specific ques-
% j: P- Y2 \3 r) Htioning about the use of a testosterone product or# Y: \0 U- }2 q& j, W
gel should be asked of the family members during
* m% @/ a; Q1 m+ v. e2 x. {6 t1 I  G6 Athe evaluation of any children who present with vir-% |/ N" M) O  m! O: i3 q* ]
ilization or peripheral precocious puberty. The diag-) y( F2 @! M7 b$ \9 b
nosis can be established by just a few tests and by
1 r5 q# F+ E& w) Z" I$ Pappropriate history. The inability to obtain such a) o1 Y& B5 A) Y- q6 w, o+ v
history, or failure to ask the specific questions, may
- c1 E# ^; x' I* `* P. Mresult in extensive, unnecessary, and expensive1 M4 c  e9 _0 D0 I9 A0 V
investigation. The primary care physician should be1 N$ S1 @$ D8 a" ~
aware of this fact, because most of these children- Q2 J  h6 O9 j& U
may initially present in their practice. The Physicians’6 r$ u: w7 B; _" M- i
Desk Reference and package insert should also put a8 M9 h2 i. j1 A
warning about the virilizing effect on a male or# ~' Y* u! U/ T( [& b1 ]
female child who might come in contact with some-- w/ j, J) j9 K& K
one using any of these products.( a8 H% o, T. J5 }6 s, r- `% K- G
References+ H+ E0 d8 y! Z
1. Styne DM. The testes: disorder of sexual differentiation
0 n! e  O- V" b2 e& Hand puberty in the male. In: Sperling MA, ed. Pediatric
# y0 i; J5 ~) v0 v/ hEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- P( Y8 x* f+ w2002: 565-628.! }/ Q. g* V0 |+ }5 I" L
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious# F; i3 Q1 W9 @% e1 {2 p
puberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

3 }" e& O& i1 v' F4 C8 B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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