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Sexual Precocity in a 16-Month-Old
- p' T& Q% l4 _) j) f( y' S! aBoy Induced by Indirect Topical
  s% ~, M2 w9 E( \Exposure to Testosterone' h# [: j3 d7 a, X. k# C7 c2 N
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
: Y3 D  g7 l+ N- Z5 m  fand Kenneth R. Rettig, MD1
% E0 B' p1 q6 J% w7 j* Z4 k& e: GClinical Pediatrics5 ]% S% e: S4 \( o# v# q1 B5 p- o- m* _
Volume 46 Number 6
8 J& |, i/ g& s, R% w) c. }) _July 2007 540-543, |, b7 F2 S3 @' `7 l
© 2007 Sage Publications3 Q& t! c+ P; J/ M  u
10.1177/0009922806296651
* {& R* _7 p" Z$ s, Y) c5 phttp://clp.sagepub.com
+ T9 n* X2 L% c! {( yhosted at" p" [3 b) E" }0 ^5 ?$ X* _: `" W
http://online.sagepub.com
1 I7 ~/ u  Y+ z0 d$ y, fPrecocious puberty in boys, central or peripheral,
. Y: }+ Y, q+ n1 {& Ois a significant concern for physicians. Central+ n6 B! Q# u* ]7 C+ t4 e5 K' i
precocious puberty (CPP), which is mediated
4 C3 S6 C7 y6 ?1 Wthrough the hypothalamic pituitary gonadal axis, has
( j' L% t! ~! ]a higher incidence of organic central nervous system
( H) h' t7 u% Z7 ^1 ~3 D) mlesions in boys.1,2 Virilization in boys, as manifested
7 t; n% l- `, w: Kby enlargement of the penis, development of pubic
! m8 l5 |5 A( I& bhair, and facial acne without enlargement of testi-
; O' Q0 X/ D8 q# kcles, suggests peripheral or pseudopuberty.1-3 We; l/ G6 O' z' \! R+ R( k1 n
report a 16-month-old boy who presented with the9 |' S- ]0 q) \* P* p
enlargement of the phallus and pubic hair develop-
* S! P- [6 ]. _) X  n2 |+ iment without testicular enlargement, which was due: N3 d& }% u$ F9 b  r+ O
to the unintentional exposure to androgen gel used by
0 E' [2 O# Y7 f+ l* i6 ythe father. The family initially concealed this infor-
: {4 u" j( x9 amation, resulting in an extensive work-up for this% Q; {& @- W$ h# ^- E7 l
child. Given the widespread and easy availability of
1 i4 j! s$ ?  ~( }3 ]testosterone gel and cream, we believe this is proba-4 b8 A# \7 ]! N# S2 `
bly more common than the rare case report in the
& f7 _9 Q: K$ I1 i: \" aliterature.4
( f  F" g* T' e4 o5 D3 }& }Patient Report8 k9 C5 i4 }0 ]7 y
A 16-month-old white child was referred to the2 l3 A/ R7 ^& C/ k5 C2 ?
endocrine clinic by his pediatrician with the concern# L; X; }/ y; ?8 F. [/ v
of early sexual development. His mother noticed
5 V9 e* D4 A* S) t+ klight colored pubic hair development when he was
# A) G$ z3 s1 M9 KFrom the 1Division of Pediatric Endocrinology, 2University of
& z# _, Q# g) x. {" GSouth Alabama Medical Center, Mobile, Alabama." J; H8 [7 B+ p! Z8 h2 X4 f
Address correspondence to: Samar K. Bhowmick, MD, FACE,4 T$ k- a' R7 O3 R" q) M
Professor of Pediatrics, University of South Alabama, College of( d$ }' P/ P6 L/ G
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
/ H8 M7 g. R& v' H0 N' d, U' ^5 |8 ce-mail: [email protected].# n: f  x* ~: F9 x3 M& V
about 6 to 7 months old, which progressively became3 q1 }. p, o% F/ E0 @" ?$ ]
darker. She was also concerned about the enlarge-
1 I' N( j' H  B5 b- K* qment of his penis and frequent erections. The child+ B4 O- X% d9 m0 z' N9 P+ k
was the product of a full-term normal delivery, with# t! Z% a  U* o, Z1 l8 m
a birth weight of 7 lb 14 oz, and birth length of5 j: y* ]5 O" e* Q& ?
20 inches. He was breast-fed throughout the first year% x5 b* q! t3 {3 S  W
of life and was still receiving breast milk along with# n; S) v9 g+ X
solid food. He had no hospitalizations or surgery,. T$ i" @  ]: X; T" ]
and his psychosocial and psychomotor development( {2 }( w* {; v) a5 K* p* N
was age appropriate.5 f* F; g/ w  E1 _/ [1 S
The family history was remarkable for the father,
' v; \; ~$ p$ F! g0 h1 f# S# Hwho was diagnosed with hypothyroidism at age 16,4 Y8 m0 V. ~' _& z! b- _
which was treated with thyroxine. The father’s1 m( ]9 k# a) f
height was 6 feet, and he went through a somewhat* C6 \' }  T8 p' |3 k" u' x
early puberty and had stopped growing by age 14.$ W7 @; e: D( Q5 [% g; G, D  H
The father denied taking any other medication. The1 Z2 I2 }. p/ D8 |- E. D
child’s mother was in good health. Her menarche
. o! W+ f, I0 o3 `was at 11 years of age, and her height was at 5 feet3 E" j9 s+ v; |6 K  U2 C
5 inches. There was no other family history of pre-3 K4 S2 _! ~. V5 H8 \
cocious sexual development in the first-degree rela-8 Q! g4 R. H# p* ?- A! L
tives. There were no siblings.5 b" I1 h) }% |4 X* T" c0 m
Physical Examination
# }! X* ^+ l  {5 oThe physical examination revealed a very active,+ O" a# E$ m9 k( _/ ^9 D
playful, and healthy boy. The vital signs documented
* {* H% B& E9 y4 ?4 L( na blood pressure of 85/50 mm Hg, his length was
2 X6 ?% Q7 h' [90 cm (>97th percentile), and his weight was 14.4 kg
7 w) ]# U8 C* j3 p2 e(also >97th percentile). The observed yearly growth
% [5 ~9 ~) A, ?0 }velocity was 30 cm (12 inches). The examination of
" O0 X5 A$ C8 O9 H; pthe neck revealed no thyroid enlargement.$ ^- c1 @- V9 K5 V" b0 a
The genitourinary examination was remarkable for9 H  u, g/ W# ]! V
enlargement of the penis, with a stretched length of, n  d1 Y8 n& ?) L' g  v' w
8 cm and a width of 2 cm. The glans penis was very well
( \; I7 f7 ]/ {( Mdeveloped. The pubic hair was Tanner II, mostly around
5 W! [: Z# {* U1 |540* M4 ~& _9 E$ W0 w$ N
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 x% Q6 f) H3 z% `
the base of the phallus and was dark and curled. The% N- C% _0 d* ?  k& L
testicular volume was prepubertal at 2 mL each.) s9 Q9 B: P5 x) K9 s. t( t
The skin was moist and smooth and somewhat8 ~  j# `' M$ B- F# U  b4 |' l
oily. No axillary hair was noted. There were no0 g2 ~. ]( \3 n/ f
abnormal skin pigmentations or café-au-lait spots.# K9 k- e1 V7 z! q) G
Neurologic evaluation showed deep tendon reflex 2+2 U! J3 x# s0 q0 h& w* c
bilateral and symmetrical. There was no suggestion- q( ?! }* W) \
of papilledema.* u. L& L5 h' \4 q% Q9 F
Laboratory Evaluation
7 I1 a- l9 Q; s/ x& RThe bone age was consistent with 28 months by4 T0 m) X% T7 a/ g8 E
using the standard of Greulich and Pyle at a chrono-
* Q4 c+ ~" r$ _1 i7 _) Flogic age of 16 months (advanced).5 Chromosomal% I/ L, R- a( ?: r3 V
karyotype was 46XY. The thyroid function test/ Z0 U9 C9 L; y. R( o
showed a free T4 of 1.69 ng/dL, and thyroid stimu-' ~  [+ Q$ G4 |8 {& }5 \
lating hormone level was 1.3 µIU/mL (both normal)." O/ _' d4 H. g, ^  S* {1 K- x: B: o
The concentrations of serum electrolytes, blood- N' U. f4 z' h* N  y% H
urea nitrogen, creatinine, and calcium all were6 `& w1 h; {7 W  g( k
within normal range for his age. The concentration
: m5 Q/ |3 N/ M( }of serum 17-hydroxyprogesterone was 16 ng/dL7 b- _8 b; G7 R$ q( g0 x
(normal, 3 to 90 ng/dL), androstenedione was 20! r- p% A. N+ _, B5 |' K' ~! g( E
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-) K9 M4 F1 Z3 P" y, ?5 R: \
terone was 38 ng/dL (normal, 50 to 760 ng/dL),6 v* l/ E; t$ Q
desoxycorticosterone was 4.3 ng/dL (normal, 7 to4 K5 t% S+ y* K$ ]9 n" H: f
49ng/dL), 11-desoxycortisol (specific compound S)
. A( w0 @9 T1 P0 F2 cwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-4 t: w1 ~7 N5 F* j3 S$ @
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total4 k. m% `  W9 r6 r# {
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),0 R4 e7 `9 [9 W' q2 ?$ q
and β-human chorionic gonadotropin was less than
% y* y5 U+ x5 F7 |5 mIU/mL (normal <5 mIU/mL). Serum follicular5 L9 F* E# b. P% i
stimulating hormone and leuteinizing hormone2 s! x/ i, @3 O( ~* e
concentrations were less than 0.05 mIU/mL
! G0 h# m- ^0 P: R) _- I9 Y! g(prepubertal).
7 ]: o  s1 J' h0 |8 g2 K: cThe parents were notified about the laboratory
3 @4 }2 s2 Z; G. aresults and were informed that all of the tests were- ]- r5 |6 r  Z3 s. i& x% V
normal except the testosterone level was high. The+ G8 n5 D% @; D; M  T
follow-up visit was arranged within a few weeks to9 `. s0 R$ z) T* M  V4 y
obtain testicular and abdominal sonograms; how-
& U5 {3 S' e0 }9 ^8 j# z/ q: `" `ever, the family did not return for 4 months., w! f( v. x. a( M
Physical examination at this time revealed that the* t7 J  D0 G. r& v
child had grown 2.5 cm in 4 months and had gained6 j) x! W9 b% b) l6 @- s
2 kg of weight. Physical examination remained
; Q1 y6 S  u# D* j( D0 x1 y6 Dunchanged. Surprisingly, the pubic hair almost com-
% |# q$ u! z# T' k% h1 s3 B0 npletely disappeared except for a few vellous hairs at" M3 r* b5 l* j; E4 ]
the base of the phallus. Testicular volume was still 2' W8 ~$ I7 U) M7 Y6 i7 G' n
mL, and the size of the penis remained unchanged.
( S! i2 ]2 j# X6 i4 e( p- IThe mother also said that the boy was no longer hav-
) @) [" K* C( Q: W. X: Oing frequent erections., J) S$ d$ l$ a  P6 o5 u
Both parents were again questioned about use of: g( i8 D7 ]7 R: s0 s. Q
any ointment/creams that they may have applied to
7 r9 |% C( Q5 E! M# V* R4 zthe child’s skin. This time the father admitted the
2 J" M: e- s2 u1 z% p3 |  L% VTopical Testosterone Exposure / Bhowmick et al 541
3 B+ c/ \5 u2 j/ juse of testosterone gel twice daily that he was apply-( z% o" K4 w. s3 k$ _
ing over his own shoulders, chest, and back area for
2 t2 e6 Q  E: f! ia year. The father also revealed he was embarrassed
( A" J7 o8 Y  l# kto disclose that he was using a testosterone gel pre-
+ V: v0 q0 [  ^" t1 @7 M8 O0 {  @scribed by his family physician for decreased libido
2 F( |. H3 P! D( h. I' ^secondary to depression.
( b. f7 C  X8 l& v* T& ~, y+ HThe child slept in the same bed with parents.
% m& W8 o+ D# P$ v0 @The father would hug the baby and hold him on his
2 m2 s% t2 ], i) @, O" Q! K8 fchest for a considerable period of time, causing sig-) m( r" n: @* q0 n$ P
nificant bare skin contact between baby and father.
% I! A: i+ h! e! aThe father also admitted that after the phone call,
/ S# ^# C' u" U% P8 _6 vwhen he learned the testosterone level in the baby
$ i" B$ t( I: @9 n  }was high, he then read the product information. J4 R3 W4 H' g
packet and concluded that it was most likely the rea-$ T2 v& s9 w! Q# X& Z
son for the child’s virilization. At that time, they
' m4 t2 E7 \( c4 A. ddecided to put the baby in a separate bed, and the" m- b( A' T& W/ g% e
father was not hugging him with bare skin and had/ ~# y) z) a" ?3 P
been using protective clothing. A repeat testosterone; G5 S& F$ D" n9 d6 t5 J4 d
test was ordered, but the family did not go to the, d, q: a/ m( W5 s
laboratory to obtain the test.
& a3 i! |& g( n7 V# v2 Z4 ODiscussion
2 l$ v# Q2 V. e% j# P/ S, t: g2 DPrecocious puberty in boys is defined as secondary$ @7 b# V& T: F( I) t% k3 J
sexual development before 9 years of age.1,42 ]8 a6 I, U" l8 D2 h
Precocious puberty is termed as central (true) when
2 G. [2 }+ n1 U) c; P8 mit is caused by the premature activation of hypo-
* O5 y3 C! M+ b, a3 q6 B4 }thalamic pituitary gonadal axis. CPP is more com-
, l( p  a2 o6 o- H$ K4 \7 Jmon in girls than in boys.1,3 Most boys with CPP
5 T) h+ x! J7 W$ Bmay have a central nervous system lesion that is) ?: l7 `+ W, e7 B
responsible for the early activation of the hypothal-
2 |& W6 |0 U0 O1 ^: Hamic pituitary gonadal axis.1-3 Thus, greater empha-
8 p# M: R, z" ^( P" }. \sis has been given to neuroradiologic imaging in# ], y8 S& J% Y, _5 J6 O7 d
boys with precocious puberty. In addition to viril-
1 i: w% x- ~% z& M' xization, the clinical hallmark of CPP is the symmet-
% g' k- I7 C9 \7 d, [rical testicular growth secondary to stimulation by. \, M" J2 w7 w) G5 g2 X
gonadotropins.1,3
  O+ t) x: z% s+ S/ p. E' K9 PGonadotropin-independent peripheral preco-
( w# U4 k# Z/ P8 }1 c( D& D8 tcious puberty in boys also results from inappropriate) ^1 L6 v! ?( Q) `# F
androgenic stimulation from either endogenous or. |  _2 ]* _8 K! t, l
exogenous sources, nonpituitary gonadotropin stim-
2 `0 E0 K3 ?0 ]) Kulation, and rare activating mutations.3 Virilizing
' q4 g% L- Z# g8 [congenital adrenal hyperplasia producing excessive# A# l) y0 {, U' ~
adrenal androgens is a common cause of precocious5 {$ g' F5 ]# O5 L4 ~2 a
puberty in boys.3,4
& o9 u& U4 N( o8 B9 w% |The most common form of congenital adrenal
8 U, X8 {6 Q6 l  Z" L2 s0 N* h6 Z% Ghyperplasia is the 21-hydroxylase enzyme deficiency." g5 D1 k9 s: l" `" V6 \  C9 q
The 11-β hydroxylase deficiency may also result in
0 r) t1 {% W! a5 aexcessive adrenal androgen production, and rarely,, i, b" `$ `# \( K4 Q4 E+ s# T
an adrenal tumor may also cause adrenal androgen' o3 t6 ~% r9 a5 [/ |! M. l
excess.1,31 W, Z2 {3 O1 J6 ?& J5 z6 O
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 w9 D4 R/ ^( f5 [542 Clinical Pediatrics / Vol. 46, No. 6, July 2007$ x4 g; y% y) z* g+ g
A unique entity of male-limited gonadotropin-
- x4 h0 y$ ?" I& M) F+ mindependent precocious puberty, which is also known2 ?: h% P) }1 G' C& h% D
as testotoxicosis, may cause precocious puberty at a
- W# J6 ]* }. l- i. h) H2 M% rvery young age. The physical findings in these boys
. |$ l5 }* |+ F. Cwith this disorder are full pubertal development,2 C3 K0 R6 g; ]7 `  |& N+ m
including bilateral testicular growth, similar to boys
1 T( G8 a: s+ Z+ i+ j$ e8 u7 Gwith CPP. The gonadotropin levels in this disorder" i0 T; k6 n$ j' l: c
are suppressed to prepubertal levels and do not show
/ e% q. |, Y  E/ |9 m5 e' p' ipubertal response of gonadotropin after gonadotropin-; q. ~: t( s8 K% m' Z
releasing hormone stimulation. This is a sex-linked* {/ [& ^- R9 ^5 Y. B) A5 X1 b
autosomal dominant disorder that affects only3 Y& G+ j5 c! _" r2 r2 g
males; therefore, other male members of the family+ V$ W. K0 D* |( w: I  P; x
may have similar precocious puberty.3* T, V2 P% r7 `& r% `5 n  }
In our patient, physical examination was incon-
- _% k' [# T1 P* w1 ^sistent with true precocious puberty since his testi-
- N0 X/ w4 W! T5 Y; \cles were prepubertal in size. However, testotoxicosis, l% h9 f9 E& t
was in the differential diagnosis because his father
6 `6 `, Q7 W* m  dstarted puberty somewhat early, and occasionally,+ n5 E+ i' F4 _- J( r; Q  h
testicular enlargement is not that evident in the# B# @" o) d6 B- j/ X3 Q
beginning of this process.1 In the absence of a neg-0 I+ I/ k1 `1 Q6 w* a( M2 m
ative initial history of androgen exposure, our. o8 J/ u9 `5 H! s3 l( z
biggest concern was virilizing adrenal hyperplasia,- P1 l/ y4 I3 k. i" X! [8 \/ h; O
either 21-hydroxylase deficiency or 11-β hydroxylase- Z0 |9 e; y4 l8 N
deficiency. Those diagnoses were excluded by find-. w4 @3 k4 |+ t+ E+ c- r( B: t
ing the normal level of adrenal steroids.& b7 U, D, @! h! C- C2 p+ k( `& _0 O
The diagnosis of exogenous androgens was strongly
9 |8 A8 l1 h; s+ rsuspected in a follow-up visit after 4 months because
5 H4 |! p, X  x7 t8 Xthe physical examination revealed the complete disap-9 T* K9 F! N0 ]" ?1 w9 O* v4 H
pearance of pubic hair, normal growth velocity, and; C: x$ b2 A+ l. V. O( X- T
decreased erections. The father admitted using a testos-
) B# A- ~8 \) N. Z/ U2 P- {% p- lterone gel, which he concealed at first visit. He was5 ]0 z# B0 X: j1 h# J% ~) |5 O
using it rather frequently, twice a day. The Physicians’; l0 E0 b3 e2 d
Desk Reference, or package insert of this product, gel or
( c8 X  ~. M1 x$ o# @. E6 u, J) Icream, cautions about dermal testosterone transfer to
$ Z. o$ w) `: `1 K9 K& m1 Z6 \unprotected females through direct skin exposure.% ?( k; r8 R+ J  q& ?+ @* X
Serum testosterone level was found to be 2 times the! l* q4 D% G8 o- W$ ~
baseline value in those females who were exposed to6 F3 e. D+ m8 _' ?: x5 j
even 15 minutes of direct skin contact with their male
/ z1 |9 N, k% X4 b1 n9 m5 [+ |partners.6 However, when a shirt covered the applica-
- t6 F- B! j( @, w" Q0 jtion site, this testosterone transfer was prevented.; R# @( A4 {) \4 O* x' M/ a$ T
Our patient’s testosterone level was 60 ng/mL,6 p# O4 z% }  V& X* p  k
which was clearly high. Some studies suggest that+ t$ B' `+ q; N% r$ q# _
dermal conversion of testosterone to dihydrotestos-
( |0 m( Y, J' N2 j8 [- o3 Tterone, which is a more potent metabolite, is more5 W) T0 U* v. I! I
active in young children exposed to testosterone
5 Q: Y: L2 u9 ^  _- n; qexogenously7; however, we did not measure a dihy-
! @8 g' V' F) V. Z9 n/ _) j0 b$ gdrotestosterone level in our patient. In addition to
6 C8 |$ o) s0 k8 s( r" jvirilization, exposure to exogenous testosterone in
6 Y6 L/ V) s! L* g4 Uchildren results in an increase in growth velocity and  d/ m. e, }5 ^# S
advanced bone age, as seen in our patient.
# z8 j3 v8 n0 l4 WThe long-term effect of androgen exposure during
1 }9 c. T7 a3 u/ R' Wearly childhood on pubertal development and final
' V5 v& x  ~* P9 C. `2 x; Padult height are not fully known and always remain2 x7 n, H! p. u8 C8 _
a concern. Children treated with short-term testos-6 o" p7 P+ G* L3 h4 U
terone injection or topical androgen may exhibit some7 H- |4 D3 _" {4 V
acceleration of the skeletal maturation; however, after& ?0 X( Q$ N7 C7 @) b) M7 N
cessation of treatment, the rate of bone maturation8 k: c: ^4 x; w# a
decelerates and gradually returns to normal.8,9( D2 \3 e3 H1 \5 m
There are conflicting reports and controversy
9 |+ A# T+ I0 Z8 qover the effect of early androgen exposure on adult
- k( W. b* D! v' s2 w; z5 R( zpenile length.10,11 Some reports suggest subnormal
8 x9 K+ p' A' N! q% p. ?0 O$ Aadult penile length, apparently because of downreg-
: \/ u6 i4 p  E* A3 yulation of androgen receptor number.10,12 However,
, \4 m$ e* g4 k9 ~Sutherland et al13 did not find a correlation between
+ N6 H1 j, _) G. l& _+ z- l1 J, ?7 Ychildhood testosterone exposure and reduced adult
; ?; G4 B# }' s0 d$ C# n; Wpenile length in clinical studies.
( K" G) \( t' v0 H, ]Nonetheless, we do not believe our patient is
+ E( H4 Y# {) B$ [4 U! [, V0 A& ygoing to experience any of the untoward effects from  U6 d* H+ _0 _( a/ p
testosterone exposure as mentioned earlier because
. e- r' D9 A& c& l/ V- R* G. Ethe exposure was not for a prolonged period of time.
: ?& [8 v6 D" U( S$ eAlthough the bone age was advanced at the time of
8 a3 S9 l+ b- X4 I$ Q; \diagnosis, the child had a normal growth velocity at; K+ @: o8 }' W# r
the follow-up visit. It is hoped that his final adult5 Y8 `0 ]: G$ ^( L2 d% q( Q: p0 l
height will not be affected.. N! c! ^7 s% M) t5 f
Although rarely reported, the widespread avail-" W& w- N  J1 _  p$ t: v; ]1 y
ability of androgen products in our society may2 W# _) b3 y4 ]" I
indeed cause more virilization in male or female5 I% ^( ^8 b" i" o
children than one would realize. Exposure to andro-
! w' R- R$ t3 mgen products must be considered and specific ques-/ B2 Y! H) d" j! m
tioning about the use of a testosterone product or
+ \( m% c' @4 Rgel should be asked of the family members during
- {; X$ T2 S: N( H# A. pthe evaluation of any children who present with vir-. M+ S  l0 b# m
ilization or peripheral precocious puberty. The diag-- Q$ z6 h. L1 q% ]0 i
nosis can be established by just a few tests and by' s4 R. p6 J# h3 B7 w6 X* B. w. j
appropriate history. The inability to obtain such a
- k1 D; X9 }$ y# ]$ @! uhistory, or failure to ask the specific questions, may
5 l: y& H0 v8 f. w. oresult in extensive, unnecessary, and expensive0 n: `. S( d- D. u+ _& u, M
investigation. The primary care physician should be/ A; ]/ c2 l3 s7 E
aware of this fact, because most of these children
# g$ n! q# p: v+ ~6 H  b4 [. Ymay initially present in their practice. The Physicians’
5 U* ~7 Y2 J/ Q5 CDesk Reference and package insert should also put a
" N8 Q5 `7 N5 G- q' ?$ W" Z" e3 s3 Ywarning about the virilizing effect on a male or
& x* G; ^; G9 h, c4 V% ifemale child who might come in contact with some-" K9 p) }- p. l' L  ]0 p9 M: x8 }
one using any of these products.9 S6 _# ?! I2 f' o
References
( v& Y' d: S5 n6 y; n0 Z1. Styne DM. The testes: disorder of sexual differentiation
5 C1 [( P! z' a, ~; l3 g- p- _9 Aand puberty in the male. In: Sperling MA, ed. Pediatric
+ l0 `5 P! ]8 H- l  E$ Y" IEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;& d2 {7 I& ]; R; z. e. {  J
2002: 565-628.+ \$ a4 e9 N& ]7 ^5 Y. _4 N& g
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious% @1 `& f$ l( J. s
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
5 [/ j. R/ ^1 k! z) m" |Boy Induced by Indirect Topical! }5 Q# Q3 Y, r3 D
Exposure to Testosterone
, w) m+ P% P4 E! O6 ?, s! T2 `, lSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,21 [- u, M# \3 O# L8 X7 `
and Kenneth R. Rettig, MD1
( A8 U; b+ y! K% {, i% aClinical Pediatrics
/ t4 `5 ~+ t, w) n8 T) vVolume 46 Number 6
$ L) V: }* c9 l+ _$ r6 ~July 2007 540-543
* B/ \: M/ W- M" @& e+ g/ r; D© 2007 Sage Publications/ c- y4 k4 U2 S
10.1177/00099228062966515 @* l5 n. W: g$ _8 w
http://clp.sagepub.com% v! C0 Z# F$ I. u$ D4 L- q5 Y
hosted at  k, r0 a* ?. \5 b8 g! s4 d
http://online.sagepub.com' |# k1 A6 I" W' n% A" k- F
Precocious puberty in boys, central or peripheral,9 f2 `4 h  S. p  V+ z
is a significant concern for physicians. Central
/ |8 ?  B; ^3 k# \5 @3 B6 o& b: A4 Mprecocious puberty (CPP), which is mediated
0 K3 t# h" G! V* I. h9 Ethrough the hypothalamic pituitary gonadal axis, has
' y# y/ w: }) @: qa higher incidence of organic central nervous system: m3 u! s* n6 p- j
lesions in boys.1,2 Virilization in boys, as manifested
, J* F; }2 I+ J- C# u3 Nby enlargement of the penis, development of pubic6 y' F/ g1 G" V+ J
hair, and facial acne without enlargement of testi-
9 l2 \+ v0 b0 I( Wcles, suggests peripheral or pseudopuberty.1-3 We
0 u; C- @+ ?, zreport a 16-month-old boy who presented with the5 ?, G- y7 |. h7 [  N+ N
enlargement of the phallus and pubic hair develop-; T6 R: A" t, `- A; x- z! O. j
ment without testicular enlargement, which was due5 b1 L4 }, P( E' ?# B
to the unintentional exposure to androgen gel used by
  [2 t5 s% e, F# rthe father. The family initially concealed this infor-! O9 i! l6 V) Q6 E. K( V
mation, resulting in an extensive work-up for this" V0 Q0 H$ z; q4 ~/ o
child. Given the widespread and easy availability of
$ Q( p; B7 N( a$ c3 ]5 ?testosterone gel and cream, we believe this is proba-2 L  @# M5 Y/ p3 x5 B; [
bly more common than the rare case report in the9 g8 X+ u: |2 w% r# z7 D, h
literature.4
# O$ F( W6 T" d8 nPatient Report
& N: s; z* I: a( ?7 e+ pA 16-month-old white child was referred to the
9 B3 _) |  f# Aendocrine clinic by his pediatrician with the concern3 r' N2 s5 g! ^3 u* N% y9 w3 e
of early sexual development. His mother noticed
* B* B8 O, I6 Olight colored pubic hair development when he was/ @% a; a" I' |& |
From the 1Division of Pediatric Endocrinology, 2University of
: \+ r" w9 U" ]6 \. o7 f& n/ gSouth Alabama Medical Center, Mobile, Alabama.
0 @! r# @2 f" G! C, ]; j( TAddress correspondence to: Samar K. Bhowmick, MD, FACE,
8 `5 z/ n# `( f1 ~$ W/ M! f+ L! @) {Professor of Pediatrics, University of South Alabama, College of
# c  F& b9 l4 m1 D! BMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;! S( T6 {! t  f; Q
e-mail: [email protected].6 ~& W7 @5 g9 `% c
about 6 to 7 months old, which progressively became
9 ^8 I! N) ]" x* Hdarker. She was also concerned about the enlarge-$ s0 Z2 k: e) |  l
ment of his penis and frequent erections. The child
9 y! o  m: A4 `+ [- e- X& i4 ]was the product of a full-term normal delivery, with4 C' M6 x1 o, `& |. J1 H, j
a birth weight of 7 lb 14 oz, and birth length of4 K- p/ m% _& [% F
20 inches. He was breast-fed throughout the first year
8 a( P1 l$ i. M( Tof life and was still receiving breast milk along with( {- L- X2 O5 @- S3 S, B$ c
solid food. He had no hospitalizations or surgery,4 t2 C6 ~( @  H* |
and his psychosocial and psychomotor development
1 p! Y# y5 L+ c3 j. P8 o' Bwas age appropriate.
& [) _7 E" _, X( l) |/ K" r# dThe family history was remarkable for the father,; E& |0 c2 c. l" I( l
who was diagnosed with hypothyroidism at age 16,) X$ S  j. d6 V4 b3 d' ~  K# Y
which was treated with thyroxine. The father’s; a1 _* ^/ B( k0 h$ h
height was 6 feet, and he went through a somewhat9 ]2 ^) O. D) r) j. T0 F' Y4 Q7 t
early puberty and had stopped growing by age 14.  K1 c/ G; `* Q( }
The father denied taking any other medication. The
( D- x, C$ |4 }child’s mother was in good health. Her menarche
2 {+ u! I0 Z8 N  t7 x: {+ kwas at 11 years of age, and her height was at 5 feet
8 g& G7 K5 C5 G* H4 G7 w5 inches. There was no other family history of pre-
2 S$ q. d% ~* C* V1 C/ X5 d8 D# Qcocious sexual development in the first-degree rela-  j$ n% C& R9 U. v. u. L
tives. There were no siblings.
+ X' L- Q# i) p9 y9 kPhysical Examination  O% K8 U) Z, u
The physical examination revealed a very active,
8 D0 @+ A- N7 {4 P5 S; R7 hplayful, and healthy boy. The vital signs documented
5 ?. l" W9 G+ ?& [! D# ka blood pressure of 85/50 mm Hg, his length was
, K2 k7 ]6 J; U0 Q) a0 G0 l/ x90 cm (>97th percentile), and his weight was 14.4 kg
. Z4 x; V8 x' s9 A" f4 d& m(also >97th percentile). The observed yearly growth
. h+ y& k1 D5 l& a) u! t* t6 y  nvelocity was 30 cm (12 inches). The examination of- R! {& p$ ^% o6 t$ L
the neck revealed no thyroid enlargement.
/ I3 v; D" N1 y8 i3 q* |The genitourinary examination was remarkable for
" U% H) ]3 n4 D0 `4 i+ }3 zenlargement of the penis, with a stretched length of5 [! B2 M1 J+ Q0 V0 I- |
8 cm and a width of 2 cm. The glans penis was very well. N6 ]- k6 D2 K
developed. The pubic hair was Tanner II, mostly around6 |% `2 M; N% p
540
3 c$ l" d/ b) V2 ]$ Vat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
7 z, \1 E1 T, O( |3 Y: y! k$ W/ Ythe base of the phallus and was dark and curled. The
6 Y+ D# }0 s, O5 T% Etesticular volume was prepubertal at 2 mL each.
( ~( K6 y8 g0 p- t" VThe skin was moist and smooth and somewhat
. P$ r* K" ?5 t- y# G* toily. No axillary hair was noted. There were no
; t) M8 b/ Y8 n! V5 Xabnormal skin pigmentations or café-au-lait spots.0 l$ b5 j8 W$ ^
Neurologic evaluation showed deep tendon reflex 2+
8 M3 L' t: n" z+ |bilateral and symmetrical. There was no suggestion
8 D: F) E7 K% s$ zof papilledema.; z# I: K) Z8 j/ B2 R
Laboratory Evaluation
& C4 Y/ [: ~3 C  R- dThe bone age was consistent with 28 months by
% B3 ]: B# {# ^, n, f. P" ?! Lusing the standard of Greulich and Pyle at a chrono-! ]( X6 R- B/ r) Q! ?, w+ `
logic age of 16 months (advanced).5 Chromosomal# i2 C! W6 a( ?/ ~2 b
karyotype was 46XY. The thyroid function test
) Z( {; g4 r4 V4 ?showed a free T4 of 1.69 ng/dL, and thyroid stimu-
2 y) u' k0 P: ?; C# q( blating hormone level was 1.3 µIU/mL (both normal).
: M% m1 U/ J+ {! i2 RThe concentrations of serum electrolytes, blood
( p. H$ f2 M, Kurea nitrogen, creatinine, and calcium all were
) K9 z, b+ s- Xwithin normal range for his age. The concentration
# G4 u! X$ o5 g0 z. E3 [' H) bof serum 17-hydroxyprogesterone was 16 ng/dL; F. D! a9 p9 Z. g
(normal, 3 to 90 ng/dL), androstenedione was 205 ^( d3 W/ b, o3 W+ b2 g
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
9 y4 Q9 G# j  ^( }4 Nterone was 38 ng/dL (normal, 50 to 760 ng/dL),1 b  k2 j8 I$ n" e5 v
desoxycorticosterone was 4.3 ng/dL (normal, 7 to, G& L0 D2 ]/ c% s+ m" V7 k7 P
49ng/dL), 11-desoxycortisol (specific compound S)
* W' u9 ^, F7 O0 A7 Zwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-; f2 K: t8 w/ u
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
) R! C8 Q; O7 Z: Y/ s) U  Ztestosterone was 60 ng/dL (normal <3 to 10 ng/dL),  y. U% f, A/ [: g) t6 X0 i( U
and β-human chorionic gonadotropin was less than
" l7 i8 o4 q% r. O8 U) J& ?8 O5 mIU/mL (normal <5 mIU/mL). Serum follicular
5 x; @+ J# N- V) d0 A% @stimulating hormone and leuteinizing hormone
+ q8 Y# ?7 ~2 y/ s  |- U) Rconcentrations were less than 0.05 mIU/mL# _6 A; C. j, i  U. j0 i
(prepubertal)., w: \* ^/ a) y: Z/ w$ v
The parents were notified about the laboratory
* F1 Q2 l2 w! t/ O0 s! oresults and were informed that all of the tests were
5 ]: l$ P4 O: ~1 x* T5 K% Onormal except the testosterone level was high. The
4 @2 F& Z5 J3 n" Ufollow-up visit was arranged within a few weeks to; ?8 i2 U0 h# }" E8 H% U; N
obtain testicular and abdominal sonograms; how-
; I) E$ n+ t9 b* Aever, the family did not return for 4 months.+ T1 D- Y+ o/ P
Physical examination at this time revealed that the* M$ r6 n, n8 h0 W/ M
child had grown 2.5 cm in 4 months and had gained* h4 F6 P0 L& a5 l2 }2 S+ m
2 kg of weight. Physical examination remained5 G2 |/ Z0 _7 T' r( ~8 |
unchanged. Surprisingly, the pubic hair almost com-; t: Y; G9 Y2 z3 L, z% u# S
pletely disappeared except for a few vellous hairs at
0 A. e; V9 ~. D5 J2 y- u  b- |4 `the base of the phallus. Testicular volume was still 28 Y; v7 |$ T% E4 G- n" v
mL, and the size of the penis remained unchanged.
- Z! @- L4 s/ }The mother also said that the boy was no longer hav-1 E5 n* B7 C6 l
ing frequent erections.  a# T& C" r- z
Both parents were again questioned about use of
5 D, Q$ v$ Y8 Rany ointment/creams that they may have applied to# w8 E* l' h' m
the child’s skin. This time the father admitted the: m' U) ~  Y1 h) E
Topical Testosterone Exposure / Bhowmick et al 541
& j/ P  X/ w0 ~" |3 Fuse of testosterone gel twice daily that he was apply-: J. N- j/ {6 I$ S& C. g
ing over his own shoulders, chest, and back area for! b$ M" W; G2 E- x4 b2 Y* i
a year. The father also revealed he was embarrassed
. }/ e: p0 l1 ?* ^3 |8 N9 Bto disclose that he was using a testosterone gel pre-0 e/ r5 {% N$ l
scribed by his family physician for decreased libido& \% A, I$ C' @% ]4 L9 A& q
secondary to depression.
' E  m* ~, a1 Y/ ]) H3 B8 R, J# eThe child slept in the same bed with parents.
* ?0 N  ^' L% v$ O2 rThe father would hug the baby and hold him on his
) N0 e7 G! L1 {+ R  D7 y, {chest for a considerable period of time, causing sig-
5 S1 c' w8 y/ _nificant bare skin contact between baby and father.
4 `8 S; \! |& l( I5 ^) j2 aThe father also admitted that after the phone call,
. M/ e- i2 d8 ~5 e3 swhen he learned the testosterone level in the baby
: Z; o! J8 ^  G0 B8 _- E* Kwas high, he then read the product information7 J# O; V9 t  b5 p, R
packet and concluded that it was most likely the rea-
( N" t# }% U6 G3 W& nson for the child’s virilization. At that time, they3 c6 a1 `* u( u  k& _
decided to put the baby in a separate bed, and the4 ^% p2 ^9 C0 `3 a( I8 i
father was not hugging him with bare skin and had
& w4 x. f8 I5 A$ c; M% abeen using protective clothing. A repeat testosterone
# P& e5 K+ R1 D/ j4 w' ]4 Ytest was ordered, but the family did not go to the
6 v3 N$ f8 b5 V) klaboratory to obtain the test.
+ ~  G# A4 z  b' ^, v2 P) TDiscussion
- G, w" |2 \- n% h& G% C* [( PPrecocious puberty in boys is defined as secondary
0 b1 o$ L2 I  G0 {3 E$ s! bsexual development before 9 years of age.1,47 T6 n  V+ y1 ~; G& K
Precocious puberty is termed as central (true) when1 S" {- m5 d" W: R6 O
it is caused by the premature activation of hypo-/ _6 p; P: @$ w) e
thalamic pituitary gonadal axis. CPP is more com-  \2 o; k; K, H* d0 S, q, d
mon in girls than in boys.1,3 Most boys with CPP/ R7 e) C  ^$ ?( U
may have a central nervous system lesion that is; [* h) I" ]! [
responsible for the early activation of the hypothal-
& E9 y* z, c" y* `' Samic pituitary gonadal axis.1-3 Thus, greater empha-/ t2 c9 p& e, s+ G1 Y! i
sis has been given to neuroradiologic imaging in9 f8 S3 H2 N/ l# x- T
boys with precocious puberty. In addition to viril-
- [" \6 j. [' x' i; H6 G4 E6 Jization, the clinical hallmark of CPP is the symmet-
9 b3 z, U; U* T) x/ e+ r- Srical testicular growth secondary to stimulation by/ u+ I$ Y  A* V8 e0 z* \5 U
gonadotropins.1,37 i9 P7 q* z, t3 k5 F: ^
Gonadotropin-independent peripheral preco-
4 J7 ~* r0 G) T& F. bcious puberty in boys also results from inappropriate
9 {5 k5 x0 K3 ]; J' ^4 [0 f* Landrogenic stimulation from either endogenous or
7 j2 e* U' b1 c8 S; Wexogenous sources, nonpituitary gonadotropin stim-' X5 D- R8 f8 J- j) K1 s
ulation, and rare activating mutations.3 Virilizing2 t! G8 P# {5 z6 C% V
congenital adrenal hyperplasia producing excessive& g6 g) x2 S8 ^# s" a- I
adrenal androgens is a common cause of precocious: k4 o. D4 x/ B0 `! ?6 c& a
puberty in boys.3,4
; }, H5 k4 x) W1 N4 X3 Z! PThe most common form of congenital adrenal
* e0 c! t9 ]* {& V/ rhyperplasia is the 21-hydroxylase enzyme deficiency.
0 z4 P9 C+ `* d7 aThe 11-β hydroxylase deficiency may also result in+ U' M0 s2 t: q: s% `
excessive adrenal androgen production, and rarely,
& t/ o  I- p, U. f8 o% yan adrenal tumor may also cause adrenal androgen
+ ]: f: p) S. nexcess.1,3- f% m2 B( p7 z( x- J9 D
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# R' m8 }/ @' g: W" T6 S# L542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
, o+ m" D/ |( a: i$ Y6 v0 WA unique entity of male-limited gonadotropin-4 Q( x& m4 k% M7 n/ u/ Z
independent precocious puberty, which is also known
& h* v4 z2 [! C" gas testotoxicosis, may cause precocious puberty at a
! g% {/ y- Y7 I4 Yvery young age. The physical findings in these boys9 U- o+ u5 e( J: R& w8 P% J
with this disorder are full pubertal development,
. z; e, L; |3 Xincluding bilateral testicular growth, similar to boys% D0 n& G! m7 f4 W7 p' v3 |4 F
with CPP. The gonadotropin levels in this disorder' E6 p1 i; `- t$ ^4 N
are suppressed to prepubertal levels and do not show
: Q5 g9 k1 C' R: _2 ypubertal response of gonadotropin after gonadotropin-  x9 e; d* @* |
releasing hormone stimulation. This is a sex-linked5 |$ k, F" @3 N7 M7 G. ?
autosomal dominant disorder that affects only/ H  E) x8 y# C
males; therefore, other male members of the family9 N) m  l$ @' _, u2 Q+ D
may have similar precocious puberty.3
. a9 o2 j) e8 D1 h$ O9 xIn our patient, physical examination was incon-
  p9 S& _8 _1 Z1 {; hsistent with true precocious puberty since his testi-
5 f- w: }1 v2 g  h* m% m! `* n6 D7 Ncles were prepubertal in size. However, testotoxicosis
' Y0 d: H; `3 Owas in the differential diagnosis because his father
. P7 k+ O" G2 B  o5 g! estarted puberty somewhat early, and occasionally,
" o$ B$ D4 U7 k# k1 ^0 K1 ptesticular enlargement is not that evident in the
! A- O7 U& C+ q  q/ Q" |6 rbeginning of this process.1 In the absence of a neg-% {! ^; J2 Z# n  _
ative initial history of androgen exposure, our* D+ p; W9 A5 i5 H6 E  Q
biggest concern was virilizing adrenal hyperplasia,$ F6 v6 o- [7 p7 j$ v
either 21-hydroxylase deficiency or 11-β hydroxylase7 m3 e; ^3 O, a5 D! C/ w
deficiency. Those diagnoses were excluded by find-7 I; u) A3 x9 m& }9 h* ^
ing the normal level of adrenal steroids.2 w! ?8 [( Q( b. w% V! O
The diagnosis of exogenous androgens was strongly
. M5 I, e( c% T/ N' bsuspected in a follow-up visit after 4 months because# Q$ c* S) f; R' ~/ i+ @
the physical examination revealed the complete disap-
4 M  {& \9 H7 }2 H5 e6 K9 \- z4 jpearance of pubic hair, normal growth velocity, and
7 C) t9 `& {; ndecreased erections. The father admitted using a testos-/ {% S/ n( G9 M( W' M  e
terone gel, which he concealed at first visit. He was; e3 s+ m" Q" f
using it rather frequently, twice a day. The Physicians’
. E' \# ?" E0 n1 @: H# PDesk Reference, or package insert of this product, gel or2 k- W, @2 a: K
cream, cautions about dermal testosterone transfer to
3 M) P/ T0 F- T' ?unprotected females through direct skin exposure.! g4 m9 U% W& Y5 I
Serum testosterone level was found to be 2 times the
$ H7 e" O3 B  g, {7 Hbaseline value in those females who were exposed to- I% i7 x/ ]4 ]# k# Y
even 15 minutes of direct skin contact with their male- E4 ]6 v. t$ Q& d  e
partners.6 However, when a shirt covered the applica-
5 {1 e% n" \; I& R9 {8 f' Btion site, this testosterone transfer was prevented.+ L- y' T8 D( |
Our patient’s testosterone level was 60 ng/mL,! S- I& I' _! s  M8 O/ u3 D' Z# m8 t
which was clearly high. Some studies suggest that
, |! \# N4 K& M: R. `7 Ldermal conversion of testosterone to dihydrotestos-
  J9 M3 O7 y4 I7 Z* k/ pterone, which is a more potent metabolite, is more1 ]8 Q, N5 C( j# M; |- ]
active in young children exposed to testosterone$ d9 J" g5 P$ _8 d" }
exogenously7; however, we did not measure a dihy-. F8 P5 S; _$ v# v: l6 S
drotestosterone level in our patient. In addition to
7 w) _" A/ N- Zvirilization, exposure to exogenous testosterone in
+ F+ M6 {. r- @1 O+ Echildren results in an increase in growth velocity and
1 y) }7 }3 F1 S, wadvanced bone age, as seen in our patient.
) c9 f* m7 [( B. ^The long-term effect of androgen exposure during, j* m! R& T' c7 c; M
early childhood on pubertal development and final
  [% w4 ?8 ]. i: zadult height are not fully known and always remain
4 s( f$ Q& n: \( g  }( b0 ra concern. Children treated with short-term testos-
$ \: W  A) [: _terone injection or topical androgen may exhibit some3 I7 Y/ j4 R( l2 L7 z+ N& [* V
acceleration of the skeletal maturation; however, after& J% C: Z& \4 d0 x7 \4 q6 w
cessation of treatment, the rate of bone maturation
3 \/ r! B- t( `1 A  |decelerates and gradually returns to normal.8,9
/ \3 q6 H6 o, h0 {$ ]1 _9 i, H1 JThere are conflicting reports and controversy
$ l( ^* i5 E# E/ ]over the effect of early androgen exposure on adult
  I0 @7 N; v6 }' ]penile length.10,11 Some reports suggest subnormal7 r/ s: @- T. _1 G" c
adult penile length, apparently because of downreg-
. w4 e1 m+ E6 Y3 S' Eulation of androgen receptor number.10,12 However,4 ?- I, a4 \5 J
Sutherland et al13 did not find a correlation between) j( n# B7 l! A" F
childhood testosterone exposure and reduced adult
4 I. Y7 m# }- h# i4 {4 I% vpenile length in clinical studies.: V5 D1 t: [. H: s
Nonetheless, we do not believe our patient is
- Q5 [5 h& C7 U/ M6 g( pgoing to experience any of the untoward effects from9 k, w& B4 c. ?, u. U* t7 h
testosterone exposure as mentioned earlier because+ b# e6 P% @) m  s1 U% J9 C
the exposure was not for a prolonged period of time.5 C; s0 Y7 y0 Q  V4 M: _4 u" B
Although the bone age was advanced at the time of
4 i! r& Z# D' Q8 Ydiagnosis, the child had a normal growth velocity at8 e6 b. N9 O/ {& {* _) `; J$ A) v
the follow-up visit. It is hoped that his final adult
$ ]! v, h; \4 T; G- F2 N: Uheight will not be affected.$ P: S/ j; w4 `9 o
Although rarely reported, the widespread avail-+ X% N' f8 m( H4 N) a% A$ @
ability of androgen products in our society may
" _) A$ H0 U  U  V1 qindeed cause more virilization in male or female+ M* R% U3 t; x: `/ j
children than one would realize. Exposure to andro-; y3 G1 |" A+ `: c9 k1 |9 j1 }
gen products must be considered and specific ques-" x0 \- e4 ^, F1 Z! Y% c' p
tioning about the use of a testosterone product or
' N" G' L( f3 G4 a; [$ ugel should be asked of the family members during
; K3 O' ^) g6 x, _5 u9 n9 \  x5 Wthe evaluation of any children who present with vir-
7 ^* @4 J2 N; S% H. Dilization or peripheral precocious puberty. The diag-  U. u5 o2 ?2 D! l- S& f
nosis can be established by just a few tests and by2 b1 H$ E  P% v: h* a3 O
appropriate history. The inability to obtain such a
) d5 W# w; g4 Lhistory, or failure to ask the specific questions, may
3 w) D+ O) R4 V1 @# v; s% aresult in extensive, unnecessary, and expensive) N1 t- {% B$ Y6 f5 U" \
investigation. The primary care physician should be
( y1 J/ u7 L% n& M8 _aware of this fact, because most of these children
  X# P6 f; x/ y$ C8 ^& \may initially present in their practice. The Physicians’0 C9 m. D% z1 B- M, n- ~: G) t) j
Desk Reference and package insert should also put a; `! `1 N0 i* q6 S- O+ f
warning about the virilizing effect on a male or
8 S8 m+ @* `# L0 Ofemale child who might come in contact with some-. M5 @+ d: C, W5 v
one using any of these products.
( _7 e1 ~! Z0 V0 k7 T8 UReferences' N  {& e# X% g. O# I
1. Styne DM. The testes: disorder of sexual differentiation
  K& g) @4 E2 g8 c5 i& eand puberty in the male. In: Sperling MA, ed. Pediatric% I+ m% Q; D# O" e
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
5 R8 b! I( Z; u1 @* v7 X2002: 565-628.' C. r" X& V9 U+ ^! v
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
, b& `: a: e1 B* w8 k! u. Spuberty in children with tumours of the suprasellar pineal
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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!
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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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發表於 2025-1-19 02:41:05 | 顯示全部樓層

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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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