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Sexual Precocity in a 16-Month-Old
. m0 ?6 j, r( |: vBoy Induced by Indirect Topical) l6 [" l( D+ F  V& Z
Exposure to Testosterone
) c$ z) U% F) b* _7 G5 E0 V1 fSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
" a# j; O) ^/ z5 R6 T( i- u5 }8 ^and Kenneth R. Rettig, MD1; I8 g4 p) L, t1 P+ L- X+ e
Clinical Pediatrics
0 M/ N4 X/ j3 _3 h7 LVolume 46 Number 6; d6 T# c& |! D6 S4 a, c/ o! i" l
July 2007 540-543
0 p- b( t. D& g! \( q, V© 2007 Sage Publications
9 p" q( i8 v7 \" x3 C7 x10.1177/0009922806296651
9 N" v- e: J. Y% }# Y8 Dhttp://clp.sagepub.com
) h7 `9 k# B' j1 P; rhosted at9 S. [! [! @5 j' |
http://online.sagepub.com6 L$ x/ ]; x4 q
Precocious puberty in boys, central or peripheral,
7 u( S+ Q$ ~3 e3 Y3 t" I# Cis a significant concern for physicians. Central
; _; n. I# B9 Nprecocious puberty (CPP), which is mediated
2 L" S8 c$ u6 n% K6 F. rthrough the hypothalamic pituitary gonadal axis, has
) A: i. c9 G. s1 ~1 qa higher incidence of organic central nervous system
, O" W: q, n+ @! g# {$ J0 N/ ?7 @lesions in boys.1,2 Virilization in boys, as manifested1 o1 j) x& T6 o' ~0 p8 i
by enlargement of the penis, development of pubic
: Y1 i  ^& A' ~! T: [hair, and facial acne without enlargement of testi-
+ E0 \  x5 k3 S; F7 q0 }; Wcles, suggests peripheral or pseudopuberty.1-3 We
( M5 _  Y6 V  @2 k& Z+ K# J" zreport a 16-month-old boy who presented with the
+ k3 G% r# P# T. q) V( genlargement of the phallus and pubic hair develop-
  j% S$ H& R- u: x8 W, R6 gment without testicular enlargement, which was due
+ `! V2 S! Z5 H& \8 b" D# e7 n- G% ?to the unintentional exposure to androgen gel used by
2 Z3 I: Z: R+ Pthe father. The family initially concealed this infor-2 {5 i) B6 R$ c: ~9 [' w0 B. c
mation, resulting in an extensive work-up for this3 S7 x9 F  ~: \+ I7 Y
child. Given the widespread and easy availability of
+ b( D0 O6 p% q  M6 Etestosterone gel and cream, we believe this is proba-
2 e* C& I- B4 M8 n  tbly more common than the rare case report in the
+ D/ e3 e+ c- o+ O; x# Y% ~literature.4
  B/ }, v0 \- D# g& ^2 H6 qPatient Report: [1 u9 w; @7 @  w' ]1 s+ T9 [1 @
A 16-month-old white child was referred to the1 L# B, h, v* T: d
endocrine clinic by his pediatrician with the concern" ]+ \- ]+ L0 g# I) r/ m4 [
of early sexual development. His mother noticed
  Y) E  O& G/ C! {" @2 X; Tlight colored pubic hair development when he was
) z" |5 ]9 A* e4 g. {" X5 [" GFrom the 1Division of Pediatric Endocrinology, 2University of7 Z  n/ N3 r2 }7 y( V/ y  W
South Alabama Medical Center, Mobile, Alabama.
9 ~$ M- u& M/ s4 X! hAddress correspondence to: Samar K. Bhowmick, MD, FACE,
: \4 k/ e- ], m2 K: DProfessor of Pediatrics, University of South Alabama, College of
( ?% v- K; [. I3 Q0 B4 eMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
; q7 @, i* X  s0 L' Q5 ]e-mail: [email protected].& B* p! l- _! l$ X- v" O
about 6 to 7 months old, which progressively became
! {9 Z: O0 k# A% W% odarker. She was also concerned about the enlarge-
2 ~9 K  X4 D. }. Q* Xment of his penis and frequent erections. The child
% o, V2 D. B3 {2 p% q" ewas the product of a full-term normal delivery, with
9 Z% {0 z1 ?" G/ W5 a# Q! ta birth weight of 7 lb 14 oz, and birth length of0 {  J" t6 X2 r* X/ E
20 inches. He was breast-fed throughout the first year
7 x8 I* G  c% [" h$ zof life and was still receiving breast milk along with
9 ?* x% g4 c) Dsolid food. He had no hospitalizations or surgery,
# W( U1 m  c' t) \and his psychosocial and psychomotor development
2 _4 S4 ^2 K* U. _9 f6 ~was age appropriate.9 m% o, k$ ]: H  ]& ~: }
The family history was remarkable for the father,: j0 f% Y7 [8 f/ l  a
who was diagnosed with hypothyroidism at age 16,% J$ ]9 V, s+ B7 a
which was treated with thyroxine. The father’s
7 I1 z1 A# r  b2 s% |6 J! Lheight was 6 feet, and he went through a somewhat
  S- k+ P: M) _" [early puberty and had stopped growing by age 14.
3 K5 u, O$ _( W) A) F4 F% t% q  @The father denied taking any other medication. The0 S: Q4 D& o2 ]
child’s mother was in good health. Her menarche
3 n! ~; R9 u9 T9 N  p) w9 D6 y  ]( Awas at 11 years of age, and her height was at 5 feet
' Q6 |& {! R8 c+ ]% }7 h5 inches. There was no other family history of pre-
, C$ w7 f' G5 A& q3 p$ ~cocious sexual development in the first-degree rela-
% F& v# B/ s$ n& \tives. There were no siblings.% @& E- k' J% t2 V+ I: a+ _
Physical Examination
) y" A/ m. a- t9 U7 vThe physical examination revealed a very active,
) a% C& ~( i; V% }1 K, ~2 pplayful, and healthy boy. The vital signs documented' s: s% w4 t- Z* ^0 z/ K* j
a blood pressure of 85/50 mm Hg, his length was
. Y, N  {9 a9 Z+ @+ I( @) B  S9 N90 cm (>97th percentile), and his weight was 14.4 kg
. D0 ^+ J1 j: @/ a- P& m(also >97th percentile). The observed yearly growth
- [0 ?# f# q  B3 A( Fvelocity was 30 cm (12 inches). The examination of6 G* f! @$ l+ e. b8 f: D
the neck revealed no thyroid enlargement.
! \7 n  O: B: ?! NThe genitourinary examination was remarkable for
9 X4 N9 ?7 n6 ^. b' b3 U) Eenlargement of the penis, with a stretched length of
( }+ c3 m  I' ^) ?8 n5 A. H: c( o8 cm and a width of 2 cm. The glans penis was very well( Y* A. I. C" n& B! {6 S5 _; [
developed. The pubic hair was Tanner II, mostly around  C3 ]. r# @. e7 T
540
  |8 T4 Z: a- c& u' xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 V$ U3 x* F* W# ]" h+ B3 S" i
the base of the phallus and was dark and curled. The; \5 i$ v' h$ a5 T$ x" Q" ~
testicular volume was prepubertal at 2 mL each.
# a/ n" a; x3 J, L6 m6 S4 Q- c9 uThe skin was moist and smooth and somewhat
; R0 x% A2 i7 y8 g  ]/ Coily. No axillary hair was noted. There were no; j" N" R' T3 G. u
abnormal skin pigmentations or café-au-lait spots.
% h" H2 V6 l0 L- _) cNeurologic evaluation showed deep tendon reflex 2+
1 {2 F! P$ v  v9 {7 c; |( n5 Dbilateral and symmetrical. There was no suggestion2 m, m7 y3 z  d' s. U8 ^# |, x
of papilledema.
" A5 w% R$ q: Z" W6 C! z+ `Laboratory Evaluation" h2 u5 m& h, \3 |
The bone age was consistent with 28 months by
4 y, q& C8 a- d. b5 s- ]using the standard of Greulich and Pyle at a chrono-
5 I: X6 J! S3 @: }6 o. hlogic age of 16 months (advanced).5 Chromosomal7 u  H6 @  Y9 z6 r: Y# m; ^
karyotype was 46XY. The thyroid function test
2 M& L; p( x# x5 U1 Oshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
8 r; B: u7 m! ?' \lating hormone level was 1.3 µIU/mL (both normal).  M1 z* n2 ~# f2 c6 ?
The concentrations of serum electrolytes, blood
5 E; ], x) T! @6 burea nitrogen, creatinine, and calcium all were
+ X2 Q& a4 j2 o9 J( @' ?$ Dwithin normal range for his age. The concentration$ F4 F3 i6 D* [# o/ J7 I6 P
of serum 17-hydroxyprogesterone was 16 ng/dL
- \" D/ c- \3 _0 K* W* y: a(normal, 3 to 90 ng/dL), androstenedione was 20
8 O$ `0 C, R. J+ m4 w1 u/ Jng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
( B( |" `" K4 W. v6 k1 V7 T' Iterone was 38 ng/dL (normal, 50 to 760 ng/dL)," N- C& N  }8 {! J! G8 X
desoxycorticosterone was 4.3 ng/dL (normal, 7 to" T3 H; ?( [4 F7 z. P+ P2 z
49ng/dL), 11-desoxycortisol (specific compound S)
- K" G3 E) u" S% u6 N$ J. @was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-9 V( o* X! m6 j6 u+ b/ X7 N% j
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
: x; N& D  A2 J( m! n3 x1 Y& ntestosterone was 60 ng/dL (normal <3 to 10 ng/dL),; V/ N" b. E1 b6 }9 F
and β-human chorionic gonadotropin was less than  H, Z. H$ k! G
5 mIU/mL (normal <5 mIU/mL). Serum follicular
0 V+ O$ R& C4 q& @! @$ Dstimulating hormone and leuteinizing hormone6 V% ]1 ~6 X/ l7 R' Y
concentrations were less than 0.05 mIU/mL7 X4 u0 S9 p% m& }. \5 R/ Q1 U
(prepubertal).% b5 F! ]  c+ k" t5 I1 Y3 Q7 M
The parents were notified about the laboratory" i; Z6 b! T3 Y; T
results and were informed that all of the tests were
6 q/ Z7 D, A& g) u8 v( c- xnormal except the testosterone level was high. The
7 @% J9 \/ A0 pfollow-up visit was arranged within a few weeks to0 D! `" h& ?% t9 O. I
obtain testicular and abdominal sonograms; how-3 O9 @0 S/ p, y# R
ever, the family did not return for 4 months.
+ [5 p* o1 S2 @Physical examination at this time revealed that the6 o1 H9 e2 q* a6 c# v% `4 [: L
child had grown 2.5 cm in 4 months and had gained6 R, q) D% Y8 ^5 |) P+ W0 A9 k
2 kg of weight. Physical examination remained' @2 @) |3 X1 ]- w0 |) ?0 O; ]' X& e
unchanged. Surprisingly, the pubic hair almost com-
& p7 `' q% D5 t2 N+ e/ w  x3 f/ dpletely disappeared except for a few vellous hairs at! T3 i  J) B( {2 ]3 b0 s& |% i& {7 q
the base of the phallus. Testicular volume was still 2: \% s" _- R9 f4 w' F: E! ]
mL, and the size of the penis remained unchanged.1 Z: ?" E$ }# d, ~2 \+ s% B
The mother also said that the boy was no longer hav-, }3 q3 I$ ~5 B3 t6 w
ing frequent erections.# a* E; V3 W" r$ b1 b
Both parents were again questioned about use of& F% M3 g. `( g( Q4 K! ]
any ointment/creams that they may have applied to" v6 k! s! n6 P" T
the child’s skin. This time the father admitted the
# @5 ]: Z/ A3 O0 D5 zTopical Testosterone Exposure / Bhowmick et al 541
$ [  c8 @" U) |* huse of testosterone gel twice daily that he was apply-6 M% N3 ?+ x+ x% W9 e- e
ing over his own shoulders, chest, and back area for
% t8 H1 _  Z" b0 ha year. The father also revealed he was embarrassed
- j) l) s. k( G6 bto disclose that he was using a testosterone gel pre-# g" J( p! _' E. ]/ o! s/ C
scribed by his family physician for decreased libido
1 @. [0 x% g+ |8 usecondary to depression.8 o' Z0 q4 O3 K/ m2 d3 d2 C
The child slept in the same bed with parents.
8 |* H# e8 z1 V. d. M, J' e/ E% NThe father would hug the baby and hold him on his" l% g# ?7 c: E8 v, ^
chest for a considerable period of time, causing sig-, A6 B+ F  W/ c0 H0 Q- @
nificant bare skin contact between baby and father.8 }+ q& o/ F7 K; C, r1 ?
The father also admitted that after the phone call,
0 T, J4 |; E) O2 o! Dwhen he learned the testosterone level in the baby
' J& s; K/ w8 o4 ?' nwas high, he then read the product information; v1 Q2 _' r) [: E9 ^) I
packet and concluded that it was most likely the rea-2 e4 R" {6 g6 C! F0 G; _
son for the child’s virilization. At that time, they/ J0 x  r" i1 D& I
decided to put the baby in a separate bed, and the
8 }' k" c& o1 O  S! Kfather was not hugging him with bare skin and had
5 H/ c' V' h( D" M  J# s5 n0 j: vbeen using protective clothing. A repeat testosterone
: r9 L9 F2 U& }test was ordered, but the family did not go to the# O2 c" |; i' _, B7 j5 v
laboratory to obtain the test.
! B2 [! n7 D+ T$ |Discussion
0 ^: m  a& z9 ^9 {. `7 YPrecocious puberty in boys is defined as secondary9 d1 \5 J( z0 c- H% d8 h
sexual development before 9 years of age.1,4
* j# h3 z% |# a* m) f5 YPrecocious puberty is termed as central (true) when/ H7 `. D9 J) \9 Y1 D
it is caused by the premature activation of hypo-# c, s' g/ u1 K  N3 H/ J
thalamic pituitary gonadal axis. CPP is more com-6 r" u! i/ G) G3 `
mon in girls than in boys.1,3 Most boys with CPP
5 B5 L+ ]: G, Kmay have a central nervous system lesion that is+ B4 \- }3 R; {# {$ j5 x  q6 O  |  \
responsible for the early activation of the hypothal-
: \# U* S  V" Q( Lamic pituitary gonadal axis.1-3 Thus, greater empha-- H8 c: [/ h/ \/ y) L
sis has been given to neuroradiologic imaging in
9 e1 I5 X2 r/ e0 G* Xboys with precocious puberty. In addition to viril-
# U7 q5 A7 Y" _+ cization, the clinical hallmark of CPP is the symmet-: T; n( H& o& w! C
rical testicular growth secondary to stimulation by* }% F2 s9 F7 H) F# C
gonadotropins.1,3
  G2 [: [0 O' M3 mGonadotropin-independent peripheral preco-
7 S$ N: h9 D" F, u6 Q: q& [cious puberty in boys also results from inappropriate% [6 q3 L2 f" J0 g0 {
androgenic stimulation from either endogenous or4 g7 \; ~$ P- {. Q) U
exogenous sources, nonpituitary gonadotropin stim-# j9 q7 z7 w, f
ulation, and rare activating mutations.3 Virilizing
! X' e4 i6 P4 O' D) A, Xcongenital adrenal hyperplasia producing excessive! ^4 d, ]# |/ \9 e/ y3 h
adrenal androgens is a common cause of precocious+ k* x# |8 [5 _) O: h5 ?; k
puberty in boys.3,4& F( l& `# `3 u: Z# R
The most common form of congenital adrenal7 ^- Q/ L5 v, p* |" n
hyperplasia is the 21-hydroxylase enzyme deficiency.
5 A: e" v# T% r. mThe 11-β hydroxylase deficiency may also result in
2 \  J/ i2 b5 z6 c# C8 G5 X5 B. {excessive adrenal androgen production, and rarely,; r( l; v% G, z0 V) s. g5 v
an adrenal tumor may also cause adrenal androgen% ?5 j  R, f2 G4 m4 X2 x" m
excess.1,3
7 f7 t% l) W! x- p* eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 \3 {: b! v* Y; B8 s' p
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
$ m, d; i4 K  n6 E1 \. XA unique entity of male-limited gonadotropin-
* E0 E9 q; H% Z' U# Zindependent precocious puberty, which is also known
0 z: R( {1 H  F$ |- v: r+ H3 bas testotoxicosis, may cause precocious puberty at a
4 j9 {5 ~4 h0 Y8 `* Pvery young age. The physical findings in these boys# K6 `! ]' g* g+ J# \7 T1 @3 R& ]
with this disorder are full pubertal development,
+ G, Z( @. G5 Yincluding bilateral testicular growth, similar to boys8 d' w$ O- g2 i2 F
with CPP. The gonadotropin levels in this disorder1 \1 I9 J" @- x' W2 j
are suppressed to prepubertal levels and do not show  y& j+ W$ H! C5 m! D" p7 Y; o+ K
pubertal response of gonadotropin after gonadotropin-
$ Z+ A' [' v/ B6 t1 H% Breleasing hormone stimulation. This is a sex-linked" _6 Q6 A. Q( a, c) L: j1 G
autosomal dominant disorder that affects only
$ Y9 \1 |0 A* ^8 ~  \- ?males; therefore, other male members of the family
1 m% u1 a+ B6 B% w' ?0 Gmay have similar precocious puberty.3
6 b& x- `8 T% F$ zIn our patient, physical examination was incon-5 M! |" g9 v" \. I4 A; z$ W
sistent with true precocious puberty since his testi-4 H' f5 ^* z/ D# ?: S
cles were prepubertal in size. However, testotoxicosis, k& W1 w8 q5 e- k: v& s
was in the differential diagnosis because his father5 o: W! O3 T/ q8 `/ z
started puberty somewhat early, and occasionally,
- p- E1 x% ]4 b. o4 ^2 Qtesticular enlargement is not that evident in the
2 ?0 H% [) e/ W" o& \beginning of this process.1 In the absence of a neg-
0 x: X! y: m: P7 \" m2 Y# ^7 Wative initial history of androgen exposure, our+ ]+ M. }0 L3 E( ^! R
biggest concern was virilizing adrenal hyperplasia,
- F6 o  j& B1 A. meither 21-hydroxylase deficiency or 11-β hydroxylase% m' F& l3 D! D0 L0 Q! _9 D
deficiency. Those diagnoses were excluded by find-/ e" f! k7 k/ K, H( L3 G- |
ing the normal level of adrenal steroids., c3 ^; {- D3 ?1 Q, v+ |* I" `3 R& k
The diagnosis of exogenous androgens was strongly& t4 b! O) u. i/ J
suspected in a follow-up visit after 4 months because
% K6 @2 X' A4 I1 r, {the physical examination revealed the complete disap-0 N# K% ^2 d) |  t+ i1 c; r
pearance of pubic hair, normal growth velocity, and! |# \4 j0 b, W9 M5 H9 P
decreased erections. The father admitted using a testos-
" S, D( h/ x  Q- m. \terone gel, which he concealed at first visit. He was
9 g  Z7 j4 I7 ^) m; |/ Iusing it rather frequently, twice a day. The Physicians’  C5 x2 E  I3 Y- j' n
Desk Reference, or package insert of this product, gel or
' R# g' ~) z* Q+ @cream, cautions about dermal testosterone transfer to
$ {6 y% `$ B& x% o0 r4 r4 I. `" runprotected females through direct skin exposure.: g# w0 w) M5 t* O
Serum testosterone level was found to be 2 times the
. P6 Z( J- x0 vbaseline value in those females who were exposed to
5 q4 u, b0 ]' X, P/ ~' `4 S- keven 15 minutes of direct skin contact with their male; ?  ]- A' e* [# ]" G: N( ^. M
partners.6 However, when a shirt covered the applica-# o/ {$ B# K, t) V% {( M3 u3 D
tion site, this testosterone transfer was prevented.
; C  p) p2 `( f" P, U7 G9 H# sOur patient’s testosterone level was 60 ng/mL,
: Z& A6 C4 c! j3 S1 nwhich was clearly high. Some studies suggest that
1 C! M. X0 O' b: ~" }8 [0 c, z) Odermal conversion of testosterone to dihydrotestos-
+ B' {3 J; {  ?/ D/ q7 Eterone, which is a more potent metabolite, is more# |7 d$ n( h$ \  H3 u0 ~, L
active in young children exposed to testosterone; \- ^, p. p3 a  n& j3 F' E
exogenously7; however, we did not measure a dihy-
" v% F/ R* A- ~: Pdrotestosterone level in our patient. In addition to
0 q+ `  D6 U; q% y8 d$ U% Gvirilization, exposure to exogenous testosterone in/ O9 c. V& a3 a% f" q2 b% x% l
children results in an increase in growth velocity and: P9 Y, e9 T, E, r
advanced bone age, as seen in our patient.% B& T$ D  [/ K
The long-term effect of androgen exposure during
$ x1 y( b! `# B# u( q8 @# Z8 fearly childhood on pubertal development and final5 e3 J4 m' U$ M5 O& O5 B) y/ T) T0 w
adult height are not fully known and always remain
& ~$ M1 \5 V2 J! @/ y2 |a concern. Children treated with short-term testos-
6 g- M  R$ Z6 }  Z, Z/ G$ Qterone injection or topical androgen may exhibit some
9 U5 k) B- J4 m; _& m0 V. kacceleration of the skeletal maturation; however, after
5 C4 R8 X* t' m/ q# t& a8 xcessation of treatment, the rate of bone maturation$ z  B9 B$ a: ~8 }9 o% [
decelerates and gradually returns to normal.8,98 o1 h' w0 O' U& z
There are conflicting reports and controversy
! p9 t% D8 o' C  r* S( c# _: xover the effect of early androgen exposure on adult/ G7 P/ a( a5 C  A* ?* h( e7 @
penile length.10,11 Some reports suggest subnormal
- z& f4 c& N, h& g- Z! \adult penile length, apparently because of downreg-
! i3 B: Q% q$ a$ C  \/ T5 P1 Culation of androgen receptor number.10,12 However,
' {1 v# Y$ t$ Y1 k" ~Sutherland et al13 did not find a correlation between
( ]9 S6 H) B  r& n4 B) Y- z  bchildhood testosterone exposure and reduced adult
, o8 d( M3 Z7 z" Ypenile length in clinical studies.
- W, F' M; i7 W9 YNonetheless, we do not believe our patient is& j( k+ a. u/ y, U( [' n2 H5 U
going to experience any of the untoward effects from
5 g0 {+ L& q6 v9 _testosterone exposure as mentioned earlier because) W/ o4 b7 `/ D7 k' ~7 V
the exposure was not for a prolonged period of time.$ z5 L% t7 e/ k& [
Although the bone age was advanced at the time of
+ A3 i" p; Y, `% Sdiagnosis, the child had a normal growth velocity at
) m1 a7 v" w$ Jthe follow-up visit. It is hoped that his final adult
$ Z% k+ s, J) e7 a1 kheight will not be affected.
. f" n; d, l) w9 gAlthough rarely reported, the widespread avail-
9 N. l1 v) g: _4 K1 s3 o! Fability of androgen products in our society may
8 {# [( F- e# oindeed cause more virilization in male or female5 V: V; `2 w7 r9 E5 t
children than one would realize. Exposure to andro-
! s( c7 f# t6 A6 \gen products must be considered and specific ques-1 t* X5 I/ d# u0 P9 ?9 O
tioning about the use of a testosterone product or" Y3 j: h  i4 A$ w( D5 r4 K1 s7 g
gel should be asked of the family members during# X* C3 m" v, A; x: V  A  F
the evaluation of any children who present with vir-0 H1 r* S+ _) C) l
ilization or peripheral precocious puberty. The diag-. r5 g6 s6 b4 H- ?, _
nosis can be established by just a few tests and by
7 B. D) M1 ~( }9 u: t& jappropriate history. The inability to obtain such a
9 S! f: D. q! K  ~( Hhistory, or failure to ask the specific questions, may, M/ ?1 m% f; ]$ _( E! m# g
result in extensive, unnecessary, and expensive
( L$ e0 {+ @2 s2 j7 einvestigation. The primary care physician should be! v" n1 D: A8 p3 P; W
aware of this fact, because most of these children( D9 U: d* Q6 v2 b
may initially present in their practice. The Physicians’$ A* ^- d  I+ N( {$ ~% M
Desk Reference and package insert should also put a
" J+ u# k; n- w' ^( q- wwarning about the virilizing effect on a male or, `4 Q* @, y" X9 i
female child who might come in contact with some-% O6 Z6 P/ ~4 _) y: S! F; G
one using any of these products.
* O5 |3 k3 ?$ d0 lReferences3 R: s0 X( ]: P5 g( |
1. Styne DM. The testes: disorder of sexual differentiation
) }+ \" a: j$ s# Eand puberty in the male. In: Sperling MA, ed. Pediatric
/ b, I" B) L$ p: a0 KEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
* q& F# o, h) u' W5 t4 r2002: 565-628.( p# h2 x6 |, Z4 S7 Q! c4 [/ U
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
2 k+ s  t3 \$ H" Z: g8 F2 Kpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old& [4 n& x4 {! ]- k1 H7 p
Boy Induced by Indirect Topical8 ?1 ]9 j3 u5 M) n1 o. ^
Exposure to Testosterone
* c' X* o1 u+ d3 a6 p) D; \% O. YSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2- E! L0 U' ~3 G8 U: t: m
and Kenneth R. Rettig, MD1
/ C# Q" o$ ]4 a9 S# e8 h+ H; k2 YClinical Pediatrics( i: v* J: K2 J/ U
Volume 46 Number 6
& q$ F) J* j9 l3 ^. rJuly 2007 540-543( Q$ C& N6 V: l1 N- U2 o* ^8 Z' ?
© 2007 Sage Publications9 d+ P- R2 Z1 m
10.1177/0009922806296651. n: H; Z' m8 d% O- O, G: W# x& V
http://clp.sagepub.com
, t2 x  i( {" r( Ghosted at: y2 Q  |3 x& O3 Y7 W: d
http://online.sagepub.com
' u; [' H: Q$ h% p3 t% c9 z* X6 |% vPrecocious puberty in boys, central or peripheral,3 N( ?7 `8 z* c7 K
is a significant concern for physicians. Central
4 n& ^+ m" B2 V+ R$ Vprecocious puberty (CPP), which is mediated) f* W4 k. q  }1 i9 A: N
through the hypothalamic pituitary gonadal axis, has) A' }/ f# R& K8 p& q5 O
a higher incidence of organic central nervous system9 `0 J+ K: h0 x6 w  q, X
lesions in boys.1,2 Virilization in boys, as manifested
' u8 M- e$ e& f" ?" Y/ \# O; |/ qby enlargement of the penis, development of pubic
- C' u3 n- W$ J4 f! P  rhair, and facial acne without enlargement of testi-8 R! b7 f) B/ E, C. I7 V
cles, suggests peripheral or pseudopuberty.1-3 We
0 p& m8 U) c5 P5 \, l6 ?; Greport a 16-month-old boy who presented with the2 o- S, u; T8 g7 d
enlargement of the phallus and pubic hair develop-' F$ d1 ^2 \/ z8 y$ H
ment without testicular enlargement, which was due  q4 `# v/ _: }, w
to the unintentional exposure to androgen gel used by
" E" c' [, v- J/ G9 H' Lthe father. The family initially concealed this infor-
/ W' g* i! M- |" b; ]mation, resulting in an extensive work-up for this
) Z% ^9 P7 t+ U9 e% j" tchild. Given the widespread and easy availability of
0 F9 V: G- l" h+ |* j; J, h8 Ytestosterone gel and cream, we believe this is proba-; j0 U3 u! B4 i, `* a8 y. h' b0 I- [
bly more common than the rare case report in the3 J- N8 }, q% ?$ J( p  q
literature.42 G1 @6 ]+ q4 }6 x2 g
Patient Report
/ q0 r) l3 R, U7 g9 G7 AA 16-month-old white child was referred to the" X" ]# }: y2 [  [) k' P
endocrine clinic by his pediatrician with the concern
# y  X6 A" {8 ]9 q$ Rof early sexual development. His mother noticed
* g. {: S0 i4 }light colored pubic hair development when he was/ j: U0 z) P$ U) o3 {: _
From the 1Division of Pediatric Endocrinology, 2University of+ U* V  h4 l6 m+ |7 n8 k
South Alabama Medical Center, Mobile, Alabama.
6 C4 y; ]9 M8 h! P8 tAddress correspondence to: Samar K. Bhowmick, MD, FACE,
( T6 m6 f! u4 ~5 {Professor of Pediatrics, University of South Alabama, College of9 _8 K8 I2 K- j3 L2 X6 z  I
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 Q) g& P% T# N: y
e-mail: [email protected].# }5 w  p. |/ u1 c/ H: W( z
about 6 to 7 months old, which progressively became
. w( Q; `* i+ R) tdarker. She was also concerned about the enlarge-7 T+ Q4 [3 a2 y0 x1 t
ment of his penis and frequent erections. The child
6 {3 X7 x: [* ?; V5 D! fwas the product of a full-term normal delivery, with% [' Z: X, B0 [& d6 Y2 `! z' p
a birth weight of 7 lb 14 oz, and birth length of- ~. W* |6 ~" B- v$ d7 f; q" I
20 inches. He was breast-fed throughout the first year
5 ?0 k. q7 G& b3 f1 s7 i3 tof life and was still receiving breast milk along with# X( \6 d0 i! J
solid food. He had no hospitalizations or surgery,
0 l: ~# W; j6 M0 w. x3 t% Kand his psychosocial and psychomotor development0 G4 }# K9 b: C
was age appropriate.5 x. D& G7 R% x' e- |6 {. ^
The family history was remarkable for the father,
# {& E& e5 Y& f7 O) I( D& ^6 I' Nwho was diagnosed with hypothyroidism at age 16,6 y  _5 U/ J+ {, \; o2 Z" w
which was treated with thyroxine. The father’s4 _; C$ m( C2 x$ ~# {# o5 o
height was 6 feet, and he went through a somewhat+ j2 n7 L; u0 X* u2 r
early puberty and had stopped growing by age 14." N7 n  p& t9 E' P; C; i
The father denied taking any other medication. The: C; Q5 ^' o4 H( P& K0 B2 F* w
child’s mother was in good health. Her menarche
# U* @. S, ?5 G0 V  p( f, ~: swas at 11 years of age, and her height was at 5 feet* _2 c  G1 p3 B* K: f' a! L" \
5 inches. There was no other family history of pre-
  L) M7 f  ~3 l1 f, ~cocious sexual development in the first-degree rela-" p) w& b& |% a  w5 p5 `) D
tives. There were no siblings.) X+ _2 |. [5 Q6 V# Q
Physical Examination9 g  }" |8 y% ]/ \5 I& i# h* c
The physical examination revealed a very active,
  ^, c7 L9 ^/ F0 dplayful, and healthy boy. The vital signs documented
5 \1 }6 K2 b3 H6 @a blood pressure of 85/50 mm Hg, his length was+ @- c2 Y% Q0 ~( z
90 cm (>97th percentile), and his weight was 14.4 kg' o4 e) b% A1 H3 t
(also >97th percentile). The observed yearly growth( }7 Y& T2 L$ V; Y/ H$ K$ s( D) I
velocity was 30 cm (12 inches). The examination of
6 y+ c4 @9 k& k2 @& wthe neck revealed no thyroid enlargement.
3 N# b6 B. s* F+ |7 A# }5 TThe genitourinary examination was remarkable for
8 B' N- X# S. y1 i( T5 S( ienlargement of the penis, with a stretched length of2 h4 R& L& j) c% e  Q4 ?
8 cm and a width of 2 cm. The glans penis was very well% H% K- w- H. A5 a: l
developed. The pubic hair was Tanner II, mostly around
# V8 X2 D& \% C( D" p( |540
$ [0 Y+ B0 Q: [1 zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 |% l2 Y6 G0 E8 i- k5 {" rthe base of the phallus and was dark and curled. The
. L& ^$ e( {0 {5 Ctesticular volume was prepubertal at 2 mL each.
0 a/ x# p2 O2 r" u& T5 aThe skin was moist and smooth and somewhat- _/ m/ }3 u- w+ G3 ~
oily. No axillary hair was noted. There were no8 Q- x' I3 X6 K+ r, o1 l
abnormal skin pigmentations or café-au-lait spots.- F6 \& {- i; K: L7 F% h
Neurologic evaluation showed deep tendon reflex 2+$ L: @2 R- c# J  e* p$ b
bilateral and symmetrical. There was no suggestion
- J7 \+ Z* h( `! E. pof papilledema.& ^- G' O- U' Y
Laboratory Evaluation
' i: O  n! p  N1 u  V7 S' cThe bone age was consistent with 28 months by
. b& U! Q* b, d  Yusing the standard of Greulich and Pyle at a chrono-- ?' C5 s' L7 G7 {0 z7 @
logic age of 16 months (advanced).5 Chromosomal" z' Y/ C) M, _$ e9 F
karyotype was 46XY. The thyroid function test
& S0 R' E$ d% Kshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
! j" ~: m6 [$ r: S9 flating hormone level was 1.3 µIU/mL (both normal).) A" V" y  T% z( o- G  @
The concentrations of serum electrolytes, blood
/ ]# ?+ M! O& {. V& J  uurea nitrogen, creatinine, and calcium all were
; v6 _4 X# l/ y3 i5 hwithin normal range for his age. The concentration
( i6 k. ]; s8 g$ eof serum 17-hydroxyprogesterone was 16 ng/dL1 }# K* h, k; q, y$ e, W5 N
(normal, 3 to 90 ng/dL), androstenedione was 20
. j$ L( Q3 D( D# f- t1 C$ Ing/dL (normal, 18 to 80 ng/dL), dehydroepiandros-5 p1 I* v3 V8 o0 l" x0 E
terone was 38 ng/dL (normal, 50 to 760 ng/dL),/ [$ `9 l1 N+ T  ]0 t3 }+ u+ N
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
. |" w5 ?) F7 e4 {0 W& ^1 n49ng/dL), 11-desoxycortisol (specific compound S)
+ }9 Z, k3 [8 j9 v9 i) U3 ~was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-7 H- C1 H1 G) `) ?
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total3 r( Y+ `% X# }
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
) w* W# V7 O; f2 E5 T8 Sand β-human chorionic gonadotropin was less than9 u4 J/ n* |- t# [/ L
5 mIU/mL (normal <5 mIU/mL). Serum follicular% @! m  F% M9 v
stimulating hormone and leuteinizing hormone& E" F+ X1 O: ~
concentrations were less than 0.05 mIU/mL1 A, }+ P" ?) Q1 a( i* O$ i
(prepubertal).
9 p0 T3 ?" D& k# z% nThe parents were notified about the laboratory
6 \8 B* Y* s3 Y" K' D/ }results and were informed that all of the tests were1 l, N: W/ d5 X' X9 d& y
normal except the testosterone level was high. The& f6 S% m- [8 G6 ^
follow-up visit was arranged within a few weeks to
; t1 [$ n! x) |/ wobtain testicular and abdominal sonograms; how-
! U3 ?3 U; u" I" v0 u- _- l) dever, the family did not return for 4 months.
" b( B' M) z! U4 i) |Physical examination at this time revealed that the; T+ P4 v/ j& L$ A8 F
child had grown 2.5 cm in 4 months and had gained  c6 ^2 w$ k" y) _6 o
2 kg of weight. Physical examination remained
/ T* x5 b2 c9 K6 p  bunchanged. Surprisingly, the pubic hair almost com-* h% S; K; _2 i2 M7 o- @5 z
pletely disappeared except for a few vellous hairs at( h) o, i( h* m+ L2 U! N
the base of the phallus. Testicular volume was still 2& y& C- q2 l8 Z; N
mL, and the size of the penis remained unchanged.7 y+ N' \2 T: }
The mother also said that the boy was no longer hav-4 y2 m+ B/ v( f# c2 v1 h1 Y
ing frequent erections.. O' `! I1 e# _
Both parents were again questioned about use of
. q( C1 ^: B. Dany ointment/creams that they may have applied to6 F, T" Y7 m  |' n
the child’s skin. This time the father admitted the
( K/ A$ v6 u1 V. Q. c, I5 sTopical Testosterone Exposure / Bhowmick et al 5414 w' T' D2 X: r' I1 {' F
use of testosterone gel twice daily that he was apply-; D7 ]! t0 _5 J. D4 |' [
ing over his own shoulders, chest, and back area for
9 s# q" e) [( Z/ }, W7 @a year. The father also revealed he was embarrassed4 Q% x+ F& s, ?; x/ w
to disclose that he was using a testosterone gel pre-1 H7 e6 D. S' x* ^, u/ i% _3 |6 k
scribed by his family physician for decreased libido
. c8 Y5 M+ s0 b0 r7 `. Asecondary to depression.
6 `/ b( e- C8 s. ]. sThe child slept in the same bed with parents.
9 {, t- q* U6 `( kThe father would hug the baby and hold him on his( ]( O0 J* b: f4 v: F; d5 G
chest for a considerable period of time, causing sig-
5 Q. H& {! b4 _" R9 N1 jnificant bare skin contact between baby and father.2 l& Q- K6 |; f5 w. K& Z
The father also admitted that after the phone call,
5 C2 ]% H: T8 o( vwhen he learned the testosterone level in the baby
8 B: A: g- y" H( g7 P4 kwas high, he then read the product information  D$ ?6 @) Z# Y
packet and concluded that it was most likely the rea-
# b+ s! I3 M1 D% N* |- s6 [' sson for the child’s virilization. At that time, they( k/ k4 C0 W" g2 y: M
decided to put the baby in a separate bed, and the6 e! q# _* ?5 O2 y# X  s
father was not hugging him with bare skin and had
- U* [5 D  Q' r1 \+ cbeen using protective clothing. A repeat testosterone
9 T  {. x8 S' w* S2 ktest was ordered, but the family did not go to the
! b5 p; }$ y9 d, F, I8 Klaboratory to obtain the test.
2 L% V7 m8 Q: Z! \, J# _Discussion
/ ^% e( r5 l$ ?3 BPrecocious puberty in boys is defined as secondary
# a5 F# D( y$ L4 Xsexual development before 9 years of age.1,4
2 f& s% x- \5 _/ l& M& wPrecocious puberty is termed as central (true) when
- P) B' e) Q( c8 @it is caused by the premature activation of hypo-  |$ t4 t) \$ K/ @
thalamic pituitary gonadal axis. CPP is more com-" `( A% G$ Y& g0 z2 ?% k
mon in girls than in boys.1,3 Most boys with CPP0 f8 J/ H# j" M4 i5 {
may have a central nervous system lesion that is
6 S' x0 K% s7 _7 E0 F9 g) ^responsible for the early activation of the hypothal-2 [& P# N/ t, U* Q; S
amic pituitary gonadal axis.1-3 Thus, greater empha-
1 r: n3 @7 ^: ~sis has been given to neuroradiologic imaging in' j( U. q* A0 R8 C
boys with precocious puberty. In addition to viril-
2 \' q3 m6 h4 z, a; rization, the clinical hallmark of CPP is the symmet-* M3 |# x' m# F" o+ F
rical testicular growth secondary to stimulation by; @% C: N, T. \( I- Q6 B( g! L: l
gonadotropins.1,3% r" J- c# l# M- K$ u  u7 \
Gonadotropin-independent peripheral preco-
# a* ]. E' ~( @7 }. ?8 ccious puberty in boys also results from inappropriate
% d! R+ H; R4 Q, d9 oandrogenic stimulation from either endogenous or& u2 ~/ J9 E- M# F& g  G
exogenous sources, nonpituitary gonadotropin stim-/ A# J+ p, b! w( l" n8 T, x0 X4 u1 O; T
ulation, and rare activating mutations.3 Virilizing0 ~) ^" c! l, t3 \# d
congenital adrenal hyperplasia producing excessive
# i2 [' a# p* b  ?" g8 aadrenal androgens is a common cause of precocious' P! {0 ~6 Y0 Z# {: M" a. m0 k/ ^
puberty in boys.3,4
! ^5 Y, v9 I4 PThe most common form of congenital adrenal
) j7 y$ d4 j0 s% S  }, U9 Chyperplasia is the 21-hydroxylase enzyme deficiency.
6 |5 z& _8 q# \1 f. P: h# x  |# m# `The 11-β hydroxylase deficiency may also result in  J  V0 r# ~# z7 {
excessive adrenal androgen production, and rarely,
9 o6 P3 U2 u; t* man adrenal tumor may also cause adrenal androgen
# m# u2 T" V, I- G" kexcess.1,30 k: R, v& S$ Z8 T" N' @
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% \( [: m2 s* o4 c8 K7 j
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007! K: r: e0 ]6 T8 Q& [5 S( n
A unique entity of male-limited gonadotropin-4 T9 l; R+ L/ A, g' Q; ]% f
independent precocious puberty, which is also known8 {" N, s8 E5 z" t) V  g9 l3 D
as testotoxicosis, may cause precocious puberty at a
1 A1 a' z& F% ^! U6 \7 cvery young age. The physical findings in these boys1 |  }4 r4 p9 c( s
with this disorder are full pubertal development,. r" o& F3 V. j. y4 V5 s: c
including bilateral testicular growth, similar to boys& Q  z9 D# T0 M/ W* `3 X6 B
with CPP. The gonadotropin levels in this disorder
6 k0 y4 W7 |" S' xare suppressed to prepubertal levels and do not show
! a9 r6 e) B' ^9 [! Ypubertal response of gonadotropin after gonadotropin-- n6 P  b+ ^! b+ _
releasing hormone stimulation. This is a sex-linked
* p1 m( ]# I, T# w" g5 O! Xautosomal dominant disorder that affects only9 b2 q, }, T) a* ~( X3 H% B: w
males; therefore, other male members of the family
1 b, y& e' j" C5 [may have similar precocious puberty.3
2 R) d' E8 ?1 P9 I: {3 YIn our patient, physical examination was incon-
( Z3 e  ^0 M* w2 Wsistent with true precocious puberty since his testi-
( T0 e6 {$ ^7 q3 p6 F, Q" }( Y8 ycles were prepubertal in size. However, testotoxicosis
) X1 R! D, W5 ~) ?) _& Nwas in the differential diagnosis because his father
: ~/ w; D1 k5 N! W5 M* |8 Xstarted puberty somewhat early, and occasionally,
# P5 A6 m3 D* q! v/ E4 V6 ?testicular enlargement is not that evident in the! H. J& g0 J' ^
beginning of this process.1 In the absence of a neg-3 h3 D' O  s1 C, g9 N6 C
ative initial history of androgen exposure, our
" t% C+ H) P# t  W0 Xbiggest concern was virilizing adrenal hyperplasia,4 Y' g% A  x! e+ j: A  ]% N
either 21-hydroxylase deficiency or 11-β hydroxylase; \& t5 k" w* l
deficiency. Those diagnoses were excluded by find-% W  P! P' U2 z
ing the normal level of adrenal steroids.
4 o6 @/ u/ a3 i4 v: lThe diagnosis of exogenous androgens was strongly# U! o/ @1 x2 W) R. y
suspected in a follow-up visit after 4 months because) j2 R( e5 Y' _8 Y" s- q
the physical examination revealed the complete disap-
5 c- }4 R2 [# z6 _pearance of pubic hair, normal growth velocity, and: ^* `) _. c& A, ?5 P
decreased erections. The father admitted using a testos-
  _8 f: t6 I6 v. l1 g9 ]: tterone gel, which he concealed at first visit. He was
  o' i6 ?- Y5 ]' qusing it rather frequently, twice a day. The Physicians’" N8 P- _7 `2 i; ]# ?( g. w' \# g
Desk Reference, or package insert of this product, gel or* _6 l: f/ [5 N0 J
cream, cautions about dermal testosterone transfer to
" L3 P- n7 I- [4 nunprotected females through direct skin exposure.# K# `3 @3 d- X
Serum testosterone level was found to be 2 times the
& U9 R: y! a% Q# a, [baseline value in those females who were exposed to# E7 ]2 M9 P& z9 _3 s
even 15 minutes of direct skin contact with their male
; |0 i) T& g# |4 a+ I3 f" \: B( Spartners.6 However, when a shirt covered the applica-
# h) d( h% k4 rtion site, this testosterone transfer was prevented.# h. \- @, v, F9 D( `/ j8 Y
Our patient’s testosterone level was 60 ng/mL,! g& Y6 A, Z/ W4 z: ]
which was clearly high. Some studies suggest that! P$ S. M$ L! B2 L
dermal conversion of testosterone to dihydrotestos-
0 b/ L" u  d' \% sterone, which is a more potent metabolite, is more: H) Q; r1 l& v7 c
active in young children exposed to testosterone
* s1 f! h$ R5 v6 s' Z; sexogenously7; however, we did not measure a dihy-6 T8 k8 B$ y' V1 ?0 L, e+ ~
drotestosterone level in our patient. In addition to' e4 N+ T& N; C
virilization, exposure to exogenous testosterone in/ F: w: Z+ M1 {* ~* |
children results in an increase in growth velocity and8 H; z* d  ]2 G+ t8 H! R( V  @
advanced bone age, as seen in our patient.
7 @) Y( B2 d8 OThe long-term effect of androgen exposure during) \4 `) \2 m- o% t+ S7 {
early childhood on pubertal development and final6 B; g" {2 X( T9 w# R) ?- i' \
adult height are not fully known and always remain# A1 Y+ C0 l' o+ J' j
a concern. Children treated with short-term testos-
4 A  N% G4 j  @% F5 e# Q7 iterone injection or topical androgen may exhibit some8 H# H, ~+ f* D8 _! e" n6 ?
acceleration of the skeletal maturation; however, after6 `$ f5 @& W# {
cessation of treatment, the rate of bone maturation
/ B* y$ s: [, K; @1 R+ a8 ?decelerates and gradually returns to normal.8,9; u& ~) G! Y4 s
There are conflicting reports and controversy
: f- W( Y* e+ R+ g! {& c; |  h; n+ aover the effect of early androgen exposure on adult+ p1 U, \# D2 D) t
penile length.10,11 Some reports suggest subnormal; o% W! N4 j, |# P& Q! I/ ]$ n
adult penile length, apparently because of downreg-
, u4 T7 N: \* r8 ]2 [& P) Fulation of androgen receptor number.10,12 However,
  [1 `, T' h. m2 k6 y4 f, @, j. LSutherland et al13 did not find a correlation between8 ?( f  X4 b: Z3 V9 A4 i, L
childhood testosterone exposure and reduced adult
% E8 G$ F2 r" ~. @- h; tpenile length in clinical studies.# E1 Q. D* P5 e/ c
Nonetheless, we do not believe our patient is/ T8 N% ]$ o" `( u
going to experience any of the untoward effects from( F8 e# ~& _- V) g3 l5 P+ H
testosterone exposure as mentioned earlier because
# E0 K3 m# e) O% Y- Y9 d6 n/ Ythe exposure was not for a prolonged period of time.$ J& i' E* z$ I! R/ e
Although the bone age was advanced at the time of
9 @6 {3 j, ?) _diagnosis, the child had a normal growth velocity at
; ]( _5 t8 O* {the follow-up visit. It is hoped that his final adult  c# s: s* d. w3 M$ g% J7 v
height will not be affected.% ~4 V8 P3 E' r: V8 z$ w! I. g" t
Although rarely reported, the widespread avail-
( V' f8 `4 w5 R: e3 hability of androgen products in our society may. p  J$ g7 ]3 p( B( j0 B4 f
indeed cause more virilization in male or female
3 T2 {4 q0 ]3 |" a: g, Pchildren than one would realize. Exposure to andro-% {3 \, S( t2 G1 ]/ P4 {- @
gen products must be considered and specific ques-$ I# ?$ a$ }7 W0 i) O6 f
tioning about the use of a testosterone product or6 I* C; b& w* V
gel should be asked of the family members during% ^) v, O' |; z6 _, v" \0 J4 s
the evaluation of any children who present with vir-7 H. `1 [$ f( h. r; P
ilization or peripheral precocious puberty. The diag-& K! N) F3 H. b
nosis can be established by just a few tests and by% `3 Y# u  f$ ^- V9 o% T( E* }
appropriate history. The inability to obtain such a. M8 R9 b; l' d# E" G0 M& F- P
history, or failure to ask the specific questions, may
/ K, [8 P+ h. Presult in extensive, unnecessary, and expensive+ j2 o% _4 Q! e* \* k% p
investigation. The primary care physician should be
# i/ n/ L9 W. p- E' Caware of this fact, because most of these children" A4 [% Y4 n: j7 i8 u& u) h9 }: @( `1 A
may initially present in their practice. The Physicians’# X2 ?7 q% K/ d+ m( U" ]
Desk Reference and package insert should also put a: _, S2 P$ Z6 R( _% P- ^
warning about the virilizing effect on a male or
3 g: z: B# E, H) h% m( m% wfemale child who might come in contact with some-( i+ K3 M& }/ c( q$ K: e! w7 B2 u- [
one using any of these products.
& x, @4 W0 Q, i# Q) ~References
' b' }9 W5 Q0 L  m- L' s% ~" u1. Styne DM. The testes: disorder of sexual differentiation
( D5 m: s/ w% _: [( ]and puberty in the male. In: Sperling MA, ed. Pediatric
' r7 q0 K  {7 \. n! N+ K: j8 O& KEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
4 A; l0 h* A- V* L$ ?  B2002: 565-628.
, T. A4 `/ Z# h; [7 [7 B7 K2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious( O* N' k$ o) h$ z
puberty in children with tumours of the suprasellar pineal
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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
  B/ O+ v" \* K/ _& n% t8 T
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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