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Sexual Precocity in a 16-Month-Old
* i: l2 u8 M# HBoy Induced by Indirect Topical
' \  I! {+ J9 O4 {/ \Exposure to Testosterone
1 R; |: g" Q" k/ T4 I# hSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
. f& a/ s4 c  z+ W5 p) I/ G4 b8 eand Kenneth R. Rettig, MD1
/ g+ U7 ~+ L+ o, E9 VClinical Pediatrics' M9 n4 q$ a1 f8 {, e$ [
Volume 46 Number 6/ l" Q9 W, w- k  ~) }' |' `
July 2007 540-543
4 X9 f0 U( ~( C& @! h© 2007 Sage Publications, g' ]# H" a- E
10.1177/0009922806296651
8 ]1 W* g) U8 n: v2 f0 W6 Ohttp://clp.sagepub.com* {6 H5 ?( N9 N; `' g- `
hosted at3 _* b4 F: T; F1 k
http://online.sagepub.com7 n  ~2 q6 i1 E. W4 z+ z
Precocious puberty in boys, central or peripheral,* p6 a/ L) |" b2 N% o; L$ ?
is a significant concern for physicians. Central8 |- Y, O' t& o4 e& z& F" [) c
precocious puberty (CPP), which is mediated
" L- |- Z1 P6 y3 b6 p+ n; a) Wthrough the hypothalamic pituitary gonadal axis, has
  E) J, k* m! s/ e+ la higher incidence of organic central nervous system: Y, |& f/ z) K) m  e5 v! O8 f
lesions in boys.1,2 Virilization in boys, as manifested
: H- }% \, M% V5 [! t! Xby enlargement of the penis, development of pubic- J) T" H) Y: U3 r
hair, and facial acne without enlargement of testi-
+ p8 v8 J% f: ]! D, n5 `cles, suggests peripheral or pseudopuberty.1-3 We
  P% Z8 J& F& R9 ]2 M0 f$ Qreport a 16-month-old boy who presented with the8 q9 h4 f6 T- i+ q  J$ L, c
enlargement of the phallus and pubic hair develop-
* f8 B8 t, x& w( `* U2 h+ k) P, Mment without testicular enlargement, which was due  ^# N8 A" D5 I6 F% O5 {
to the unintentional exposure to androgen gel used by
( p% `; B5 t5 c* \the father. The family initially concealed this infor-
+ O6 x! ^2 f# n9 q" |mation, resulting in an extensive work-up for this
8 `! G' S3 p4 Q0 u) {child. Given the widespread and easy availability of/ h' v. }$ @) A) C, [" X: t* f$ X
testosterone gel and cream, we believe this is proba-. k+ p1 L8 X& W8 O: O
bly more common than the rare case report in the
/ O; a$ v8 \  l/ I9 f* {literature.41 ?; a& ]$ O* B& O
Patient Report
+ z! \8 Z5 d0 ^, |9 rA 16-month-old white child was referred to the
. h( y9 r# D) H/ j5 d9 D8 d3 mendocrine clinic by his pediatrician with the concern
, d! Q/ ?0 E% m! @of early sexual development. His mother noticed
6 O9 E4 Z& _& h: f& }" i6 nlight colored pubic hair development when he was
8 D4 I  c, h- j" P) SFrom the 1Division of Pediatric Endocrinology, 2University of
3 @. }/ \! ^* @; c9 R" t/ }South Alabama Medical Center, Mobile, Alabama.# k+ g, L/ g0 P, F
Address correspondence to: Samar K. Bhowmick, MD, FACE,( F, D/ C2 t1 l4 @3 M
Professor of Pediatrics, University of South Alabama, College of% {  u& T5 r$ x( |1 h0 c
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;# x. F( y3 [1 l
e-mail: [email protected].
3 ]. w3 w" [/ cabout 6 to 7 months old, which progressively became' ?+ k% ^$ @: \8 f& ?$ q+ A3 A  g, D
darker. She was also concerned about the enlarge-
* |) o  D+ [3 ]' j& o9 x5 i. l5 l) Pment of his penis and frequent erections. The child3 W& p+ y( R% m% o- ?2 `
was the product of a full-term normal delivery, with
7 j3 j" J' _) |5 l% ca birth weight of 7 lb 14 oz, and birth length of1 b; y* d8 _. x/ j; w
20 inches. He was breast-fed throughout the first year
! F( b2 k. `# v/ k5 hof life and was still receiving breast milk along with( [" ]& m+ x5 f$ s4 X
solid food. He had no hospitalizations or surgery,' H& {. \( B2 v' t8 N0 D  U8 \
and his psychosocial and psychomotor development
( E5 A- {+ d2 Y6 m4 ewas age appropriate.
" ]5 x- k; q9 @The family history was remarkable for the father,( d  K4 p  x+ _. j
who was diagnosed with hypothyroidism at age 16,
% p0 a* K. i! T$ c$ Y% Cwhich was treated with thyroxine. The father’s, W6 D. X# b- A. c6 g& T
height was 6 feet, and he went through a somewhat. L- B$ J! |# {' }& G
early puberty and had stopped growing by age 14.
0 j/ R5 ^- Z2 q0 u. VThe father denied taking any other medication. The8 {2 J0 B0 c7 ]: f' d8 F
child’s mother was in good health. Her menarche
% O# ?* q$ g3 g0 |5 V4 }2 N) Vwas at 11 years of age, and her height was at 5 feet& E1 r- E  p" ^! a/ n% n* L
5 inches. There was no other family history of pre-
  r2 Q* ^6 H  b* W. Xcocious sexual development in the first-degree rela-
8 [; M* i; d  Q& i2 u+ ], O( ptives. There were no siblings.$ e' F  _" z6 W/ L$ n, T- E
Physical Examination
9 e( |. `- x. X8 YThe physical examination revealed a very active,0 Z* F  Z( A' M6 P
playful, and healthy boy. The vital signs documented' d! ?5 |) x6 @$ z0 A2 ~) j3 F
a blood pressure of 85/50 mm Hg, his length was& c+ ]2 f, y5 N: s0 N* I6 E- Z! X
90 cm (>97th percentile), and his weight was 14.4 kg% }" n3 \8 k4 y
(also >97th percentile). The observed yearly growth* o* u: H: T8 M# a9 w+ I. }( ~
velocity was 30 cm (12 inches). The examination of& F, n. W1 d5 z* P. H; N/ k0 {" C
the neck revealed no thyroid enlargement.
6 @( N6 c: i$ q) f/ UThe genitourinary examination was remarkable for! b8 |5 c, L0 y4 X2 I0 F' o1 {+ H
enlargement of the penis, with a stretched length of
( O1 g: K3 b# h8 cm and a width of 2 cm. The glans penis was very well# S$ X$ U% d5 s8 ]2 c* y! W
developed. The pubic hair was Tanner II, mostly around
/ ~7 D  U- @# R% E5 D* m540
8 C& Q$ J6 ]+ u% b7 xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* I; I0 O4 h9 X8 Q! u0 o/ r
the base of the phallus and was dark and curled. The; Z; y/ Z/ V; f2 s
testicular volume was prepubertal at 2 mL each.
5 c0 }4 a5 }% o8 |# EThe skin was moist and smooth and somewhat
& M! j/ ]! M7 Woily. No axillary hair was noted. There were no
% b- u& [$ l( x3 \3 a" n2 {  xabnormal skin pigmentations or café-au-lait spots.
" `( m( Z3 Z* I8 U! D/ v$ XNeurologic evaluation showed deep tendon reflex 2+$ a5 \! h! c# q* x- _4 U$ G
bilateral and symmetrical. There was no suggestion
# p# ^2 M5 {/ y# v) }/ f" ~% Lof papilledema.
! U" s/ a9 P  x7 ^; O! jLaboratory Evaluation
: U* T! k. m0 i' U$ ~1 [5 W# v# JThe bone age was consistent with 28 months by
% ]4 w" x+ `9 Yusing the standard of Greulich and Pyle at a chrono-
7 X9 E- J8 X1 @$ a; R( Vlogic age of 16 months (advanced).5 Chromosomal4 k: Y, C  M* j5 q# z# `
karyotype was 46XY. The thyroid function test" z! l! j- h) z: M$ B3 |2 O
showed a free T4 of 1.69 ng/dL, and thyroid stimu-0 t0 x8 G. }& x  S2 t- a
lating hormone level was 1.3 µIU/mL (both normal).( o% c: ~: w1 H6 U0 E' J5 L
The concentrations of serum electrolytes, blood
6 e5 ~6 n0 B. `urea nitrogen, creatinine, and calcium all were
5 ?0 S# q7 @+ M4 ?* kwithin normal range for his age. The concentration4 H( C- ~/ Z5 u. \* T3 y
of serum 17-hydroxyprogesterone was 16 ng/dL: e5 Y. f" V$ P+ {+ s4 L, B
(normal, 3 to 90 ng/dL), androstenedione was 20+ O7 _. f' \1 p' X; G. g+ U  S
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-8 y, a) k8 l  T; }0 e
terone was 38 ng/dL (normal, 50 to 760 ng/dL),1 E+ X5 ?& c! {6 G
desoxycorticosterone was 4.3 ng/dL (normal, 7 to* O% ?. I7 |9 |/ s! `
49ng/dL), 11-desoxycortisol (specific compound S)
/ ?3 s5 T6 D# S. i6 W) v1 \8 L: D" nwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
- p1 ^/ N$ {$ W# s8 X6 Wtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total8 ?+ t  w8 x7 D* L( ~& c7 s# b4 E
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),/ v& t5 I$ k9 g! t
and β-human chorionic gonadotropin was less than
, Y* f2 G6 ~. N6 H# E) p5 mIU/mL (normal <5 mIU/mL). Serum follicular2 O1 u* }' H* ^1 y# X
stimulating hormone and leuteinizing hormone+ \. f- ^+ c! ^( X+ g
concentrations were less than 0.05 mIU/mL. l" C% Q- O; s& ]7 `3 E
(prepubertal).
' l( d6 d2 n/ j; [The parents were notified about the laboratory+ E6 I- x& Z9 U% [! f; `
results and were informed that all of the tests were
! W3 V# V5 Q* q. G4 Lnormal except the testosterone level was high. The
" O: q+ j3 O; @7 xfollow-up visit was arranged within a few weeks to, S" z5 W' w( j' q  f2 [) {" n
obtain testicular and abdominal sonograms; how-$ h1 ?( E- \+ R2 {/ Q
ever, the family did not return for 4 months.
. l! ~! G1 t1 i% Z. bPhysical examination at this time revealed that the
) t! o6 T: x- V& P  W3 J! R# B" Wchild had grown 2.5 cm in 4 months and had gained
8 c; l! K/ i% X( V2 kg of weight. Physical examination remained
0 m0 t  s9 I: v1 u( o6 M0 |4 Kunchanged. Surprisingly, the pubic hair almost com-
. l5 ?* m- g$ S, j% L: p6 ppletely disappeared except for a few vellous hairs at1 T1 l5 P/ H& m8 b$ W
the base of the phallus. Testicular volume was still 2* H3 A* o# b$ [* H" {" Z% ~7 c* m
mL, and the size of the penis remained unchanged.$ B7 x# o5 s; u3 x7 P
The mother also said that the boy was no longer hav-, i# V2 j: |" I9 W( A
ing frequent erections.
) B0 K6 a8 ~3 J; e9 Q0 Y% a: sBoth parents were again questioned about use of
& ^/ a* J! b4 Q* Zany ointment/creams that they may have applied to
; M2 y, {+ k: D5 l. nthe child’s skin. This time the father admitted the
3 w1 J/ Z, e0 E; }4 bTopical Testosterone Exposure / Bhowmick et al 5418 T# ]8 i6 e8 h; ?
use of testosterone gel twice daily that he was apply-
/ h/ _: D* N' T; @% A9 w6 U0 Ting over his own shoulders, chest, and back area for
  J* C, c$ h( z) qa year. The father also revealed he was embarrassed2 K+ f" i7 ~: ~
to disclose that he was using a testosterone gel pre-
- N5 k* u" i4 U8 g. T4 R+ Vscribed by his family physician for decreased libido
8 u2 m6 D) J4 v9 Vsecondary to depression.
2 `5 ^$ a- {+ s- G/ s. ?5 N% aThe child slept in the same bed with parents.
2 S) E) a7 |) i  h' QThe father would hug the baby and hold him on his
, v: q) g. R, q+ E2 q! e1 ]chest for a considerable period of time, causing sig-
. G4 r# ^9 m) J( g+ G7 Z1 }nificant bare skin contact between baby and father.
, |. k* x6 v2 o; p$ `& ~The father also admitted that after the phone call,
, _" A' H* H- x* R6 fwhen he learned the testosterone level in the baby
; r8 g' V/ ~  g  _6 H' Y9 @- lwas high, he then read the product information7 {, Q- e2 _  D' X0 L/ p. L
packet and concluded that it was most likely the rea-, L) ^8 Q2 U3 S4 c
son for the child’s virilization. At that time, they
0 A1 P* D; M5 Y+ j9 q' R# fdecided to put the baby in a separate bed, and the
/ P0 ^; `9 |: @- `. l) ]father was not hugging him with bare skin and had8 ]9 h. x  U; n% \0 ]. Q1 Q+ R5 e7 y
been using protective clothing. A repeat testosterone
5 _* M* {0 I$ ~% Q1 o: mtest was ordered, but the family did not go to the
8 v- O1 m0 `3 h: S6 o; Y2 ^9 }1 Q  qlaboratory to obtain the test.
- P7 `3 t* j2 D& HDiscussion
( H, F! o3 U# rPrecocious puberty in boys is defined as secondary& z9 c+ O# @- v' D3 s, p* m  V
sexual development before 9 years of age.1,47 Q8 s; s$ _: G! X4 H* o& u; \% s
Precocious puberty is termed as central (true) when* f, [" x% u9 b. Q: C
it is caused by the premature activation of hypo-
# N. J' d0 N" {. @  R( a# Othalamic pituitary gonadal axis. CPP is more com-! ?  f' G6 ~4 d2 g3 ]  J
mon in girls than in boys.1,3 Most boys with CPP
: t5 d* a7 H; J2 Dmay have a central nervous system lesion that is
: h2 ?4 S  G3 S7 _7 J2 iresponsible for the early activation of the hypothal-
9 s9 A3 l0 g9 i4 s0 T8 P0 ~4 Mamic pituitary gonadal axis.1-3 Thus, greater empha-4 v6 `  m" u& b7 i
sis has been given to neuroradiologic imaging in
, e/ V( l+ T" o5 ~2 Nboys with precocious puberty. In addition to viril-# O3 w1 h# s9 x
ization, the clinical hallmark of CPP is the symmet-, X2 B. S7 k/ B  S
rical testicular growth secondary to stimulation by0 d& @$ I* N; E; V! [% l0 E7 i9 l
gonadotropins.1,31 P0 p6 f0 p; A! k4 `4 f/ W
Gonadotropin-independent peripheral preco-6 G3 [5 I8 A3 N, f2 x+ C- }. f
cious puberty in boys also results from inappropriate
1 |4 T' s. e$ F$ h- Zandrogenic stimulation from either endogenous or
/ M6 B1 C* m/ y' Pexogenous sources, nonpituitary gonadotropin stim-
6 c3 O* C- r) r" Fulation, and rare activating mutations.3 Virilizing
$ _; H, |; l4 W8 V" qcongenital adrenal hyperplasia producing excessive
9 i+ ?& F& {- R; r% Uadrenal androgens is a common cause of precocious
+ u, _# h0 C; g0 N4 {2 H' z- |: x" \puberty in boys.3,4) O) `1 G# p( z9 [& J
The most common form of congenital adrenal3 m, q( W0 N4 Q$ M$ r
hyperplasia is the 21-hydroxylase enzyme deficiency.
2 X: ]# |: ]9 bThe 11-β hydroxylase deficiency may also result in
! E+ \3 X' v: w: @excessive adrenal androgen production, and rarely,/ B0 @# }+ [, a& q
an adrenal tumor may also cause adrenal androgen4 ~. n7 n" k$ x% k, N- O
excess.1,3! e% o; c3 q9 o& A$ C
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 @/ W# b" n. b1 S) R3 T
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
! z# m, q% V- s8 c. e' yA unique entity of male-limited gonadotropin-
, K& Z$ A" Y2 zindependent precocious puberty, which is also known5 R6 O/ g, I2 ^% q$ b  _
as testotoxicosis, may cause precocious puberty at a2 |4 ~8 o  ~* i/ {
very young age. The physical findings in these boys/ t7 Z0 E/ H7 e4 L; @- R8 `
with this disorder are full pubertal development,1 A* `; ]) Y0 s- L' B
including bilateral testicular growth, similar to boys6 B  P2 j6 z  v% Z* n6 ?. l
with CPP. The gonadotropin levels in this disorder8 Q/ S/ ^/ `$ W! d, Z( o, U
are suppressed to prepubertal levels and do not show0 g: G& P5 K; B+ x- M
pubertal response of gonadotropin after gonadotropin-
: v; w  I- ?% ^! c2 freleasing hormone stimulation. This is a sex-linked. v  T, b! ~& ~4 r
autosomal dominant disorder that affects only; q) W9 T- w4 q
males; therefore, other male members of the family$ U3 {' P4 x* B" Y; F! A
may have similar precocious puberty.37 V2 I1 e+ o% G
In our patient, physical examination was incon-* M# D! j+ c; S3 o$ Y1 z
sistent with true precocious puberty since his testi-
6 P, ], s2 i& @3 s5 G; C, acles were prepubertal in size. However, testotoxicosis
$ E0 H% {( f0 uwas in the differential diagnosis because his father2 ?2 d6 S& y* k, A& P
started puberty somewhat early, and occasionally,
5 b( F, s' q8 X' E' utesticular enlargement is not that evident in the
9 e" Y6 v; o, T$ h/ `$ `4 hbeginning of this process.1 In the absence of a neg-* |0 t$ i+ a8 ?/ A" o  l+ F
ative initial history of androgen exposure, our0 E. W* d: Z' ?, f! Q6 ?
biggest concern was virilizing adrenal hyperplasia,  D) b" I8 [2 R! V! b
either 21-hydroxylase deficiency or 11-β hydroxylase) X: G) D0 H5 I# i& I0 ]- Y2 B; G
deficiency. Those diagnoses were excluded by find-
& v1 A- ]( i8 @- C. Ying the normal level of adrenal steroids.9 i- X5 w$ U, Y3 L0 _* W' x4 ^2 z" P- I: A
The diagnosis of exogenous androgens was strongly
- `0 b0 g% Z0 |; X8 gsuspected in a follow-up visit after 4 months because$ l$ j- K: j% {( w
the physical examination revealed the complete disap-
3 g, W' c% L1 i( gpearance of pubic hair, normal growth velocity, and
* Q0 }6 k; x% c. t0 {( hdecreased erections. The father admitted using a testos-
7 {7 _; h6 L# g7 {terone gel, which he concealed at first visit. He was
, y$ [- _) _9 @4 Musing it rather frequently, twice a day. The Physicians’
1 M" w2 _9 e3 @/ S0 qDesk Reference, or package insert of this product, gel or# o+ i# o0 x' M# Q% ~  y$ W
cream, cautions about dermal testosterone transfer to
% Z0 {( X/ I& h6 I: m7 v7 gunprotected females through direct skin exposure.
3 C. u; C0 Z& D5 R$ V+ j4 PSerum testosterone level was found to be 2 times the! A! v3 b+ z$ u
baseline value in those females who were exposed to1 C8 n0 Z, N# y
even 15 minutes of direct skin contact with their male. ?( X0 D5 k' `' ]
partners.6 However, when a shirt covered the applica-' O/ A2 B9 s  _) p8 F" o1 W
tion site, this testosterone transfer was prevented.
' K* D2 W: c7 ]2 AOur patient’s testosterone level was 60 ng/mL," f" f4 q) N; c. H. q% f
which was clearly high. Some studies suggest that4 ]* N1 h6 o2 x+ M4 C2 u
dermal conversion of testosterone to dihydrotestos-9 _% z8 o# B" I  P. ?$ X' P5 ?8 ^
terone, which is a more potent metabolite, is more
1 T$ |2 L; C6 P) Mactive in young children exposed to testosterone
9 L  i) J, Y* h1 [; ]exogenously7; however, we did not measure a dihy-8 J' n4 H3 }- f# X# v
drotestosterone level in our patient. In addition to
) h: T( s$ W2 ?9 R, Hvirilization, exposure to exogenous testosterone in4 T' I. y$ E* G5 y( w& @
children results in an increase in growth velocity and
$ h$ l# v. C2 ^4 a4 O$ `  D+ \* H3 Aadvanced bone age, as seen in our patient.
" c: r, f. I' t: c3 HThe long-term effect of androgen exposure during
2 E: L) }! g8 c( Bearly childhood on pubertal development and final& h- x, A) h5 U9 m( M
adult height are not fully known and always remain
$ }; O6 X6 }. ^# n" N' @! Z" ^a concern. Children treated with short-term testos-) m/ a: G. S5 L1 [4 N5 Y% U$ t
terone injection or topical androgen may exhibit some
  g0 C0 O6 Z3 @* [, o( A# a' Lacceleration of the skeletal maturation; however, after( [7 o2 J6 I6 h2 z8 @
cessation of treatment, the rate of bone maturation+ J& f0 M, y$ D  B6 w  \
decelerates and gradually returns to normal.8,96 E0 l( s2 Z/ y( u( T; z$ Y. ]  q) E
There are conflicting reports and controversy6 Y% C5 {1 O. I
over the effect of early androgen exposure on adult
) v5 Q4 i8 d3 K% lpenile length.10,11 Some reports suggest subnormal
7 L1 Y. v# _* X2 ?9 J& J& y) a2 D' Zadult penile length, apparently because of downreg-
/ G( x7 ^( a/ q8 I5 L$ fulation of androgen receptor number.10,12 However,
: d* R: ]& C  _5 H9 f6 P" rSutherland et al13 did not find a correlation between+ \* A8 b2 X; c, }& Y. k# p/ [
childhood testosterone exposure and reduced adult
; O$ c' ^  s/ h% r" @  npenile length in clinical studies.
5 B% f, m/ H7 L7 p9 o1 }; C4 ANonetheless, we do not believe our patient is) h8 {; u( F- J: D' G4 d
going to experience any of the untoward effects from1 d' T3 \! q( z) ^" e: y
testosterone exposure as mentioned earlier because
/ q) A8 n2 A- fthe exposure was not for a prolonged period of time.. U" c& x& l: _* K  P9 n& o. c6 f% P
Although the bone age was advanced at the time of
* O& }& O) O% ~" h, N# o1 w2 ddiagnosis, the child had a normal growth velocity at3 H! Y1 |6 @% B4 o3 R0 Q7 P
the follow-up visit. It is hoped that his final adult
. U: f/ g1 i4 w/ O; H8 j- v. o/ f. Pheight will not be affected.
" Y$ P. p: A. f1 Z! Q  @2 ]7 B; dAlthough rarely reported, the widespread avail-# @' ^; q! `- K) F" y) `' R4 E
ability of androgen products in our society may
* R0 e5 h! c1 @" q" Mindeed cause more virilization in male or female9 y8 o/ w, S' y
children than one would realize. Exposure to andro-! k" y9 m$ P5 y6 W. h
gen products must be considered and specific ques-. O1 R' i$ ~& {. e8 U
tioning about the use of a testosterone product or
" I$ g1 s( y$ vgel should be asked of the family members during. [! ]/ e* O2 ]7 t' C6 x
the evaluation of any children who present with vir-6 k' X- A" Y* Y2 t9 y% M+ v
ilization or peripheral precocious puberty. The diag-
. R0 a$ x- C, ]$ }2 L0 y- K0 ]nosis can be established by just a few tests and by5 \+ ~" P+ P, A. i0 h
appropriate history. The inability to obtain such a
! @$ z' \( y& p  T- r! J2 ^history, or failure to ask the specific questions, may
5 i1 u" I7 ]" u* E% e: }result in extensive, unnecessary, and expensive$ F1 @4 J  ~* b
investigation. The primary care physician should be
; S7 S% `! f$ h5 e. P: faware of this fact, because most of these children2 v2 G3 @* f, k% G+ F
may initially present in their practice. The Physicians’$ a9 z+ j. Q' ]" ^$ {  \
Desk Reference and package insert should also put a9 D; Z" F& s! W$ s' F& N; T, n
warning about the virilizing effect on a male or
. a9 t* y# V# o8 m- c. x0 gfemale child who might come in contact with some-6 o$ x4 _; b2 [" s4 y
one using any of these products." s+ @/ i5 @% d1 X: z1 G
References
: X1 E' J2 a' f! Y7 a1 q1. Styne DM. The testes: disorder of sexual differentiation
) u! B: L! r; Z; {and puberty in the male. In: Sperling MA, ed. Pediatric) D. K% D4 U7 k; U
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
1 S, Y$ }6 _- I  ~6 _' b  T1 E0 Q2002: 565-628.5 a  a; O5 z) M% q9 J( U: [. T8 |, T8 a
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious' ]6 h$ P- M/ `7 ^1 z; T! ?
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old" w' \& L; w/ a& m0 x5 O! T8 r
Boy Induced by Indirect Topical
+ N* z8 I. J8 cExposure to Testosterone. P* \6 G7 ?( R, d
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2) P  ?' r" ^; ], r3 i  |: ^
and Kenneth R. Rettig, MD1
* N5 q9 d/ B0 n$ {Clinical Pediatrics
+ k' T1 @) Z7 F, JVolume 46 Number 6" u& X! U2 W, U
July 2007 540-543
& T  R' Z3 g+ Q/ Z7 N+ I© 2007 Sage Publications
+ f4 g7 V" `% h  R4 e0 x10.1177/0009922806296651
" N1 R- r: z4 Shttp://clp.sagepub.com
% n- d5 b) V2 s; @* {hosted at
- R9 v* _1 q0 ~# v( Ohttp://online.sagepub.com+ ~5 @, H8 ?/ o  {' E2 g+ g
Precocious puberty in boys, central or peripheral,
4 O5 t. W: [+ j4 ]  yis a significant concern for physicians. Central
0 H% d& U; Z, s/ e! g; _, pprecocious puberty (CPP), which is mediated
% ]; H; c$ l. X8 uthrough the hypothalamic pituitary gonadal axis, has: F! X/ m) L; {; c  I& a# \4 f; M
a higher incidence of organic central nervous system5 ~" p. W9 ~" U. o
lesions in boys.1,2 Virilization in boys, as manifested0 s9 o' i. s; \& {* P  W2 }5 R
by enlargement of the penis, development of pubic: r9 [; J8 k( Y* @+ \
hair, and facial acne without enlargement of testi-% x* B- N9 B# W" F( N/ G  e* L
cles, suggests peripheral or pseudopuberty.1-3 We+ _( D+ i9 W+ |7 B7 s
report a 16-month-old boy who presented with the
( _! w) l1 p3 ?0 m# f& f6 {* qenlargement of the phallus and pubic hair develop-
4 H: q% o# Q$ p9 B. c3 ?ment without testicular enlargement, which was due) _3 B1 Z$ H4 a: p+ t+ s) s
to the unintentional exposure to androgen gel used by
. p( c  `! V0 C" H2 @6 m4 Hthe father. The family initially concealed this infor-
- [% _, N3 B! |' nmation, resulting in an extensive work-up for this  i# w$ Z% ]* U9 f
child. Given the widespread and easy availability of
; e' A2 Q; y! ^' _. n- ktestosterone gel and cream, we believe this is proba-
/ o* _% _0 a9 z6 g( s! K9 Zbly more common than the rare case report in the2 d) o) V( p* i( b
literature.4
0 i) W; z! H* R  M7 y. n# }- tPatient Report3 w  u4 a" E$ ~6 I" [. o  q
A 16-month-old white child was referred to the. N+ H, x  c* ^- C, A
endocrine clinic by his pediatrician with the concern
& e% Z( r7 ~6 ]! `1 L) Jof early sexual development. His mother noticed
  s" }) Y! |# u/ b+ M/ Llight colored pubic hair development when he was
: r" J& A4 d: }From the 1Division of Pediatric Endocrinology, 2University of# W# T1 T6 G( `, S! L. W2 c& T
South Alabama Medical Center, Mobile, Alabama.
, N. B6 b8 K4 G5 ~! u* gAddress correspondence to: Samar K. Bhowmick, MD, FACE,# U) ?6 _' r+ r8 Y! H3 t
Professor of Pediatrics, University of South Alabama, College of# T) r5 r4 U% ]4 [# ?4 J( Y
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;9 [/ a5 L* @* R5 }) w- k+ {
e-mail: [email protected].
9 h0 x! `2 L% B' L( X  iabout 6 to 7 months old, which progressively became
: V- x; L3 E9 ~1 @" qdarker. She was also concerned about the enlarge-2 {' H0 v6 q3 m6 |, D/ f0 ]
ment of his penis and frequent erections. The child
( t9 A2 b- ?* H2 p9 jwas the product of a full-term normal delivery, with+ Y$ G  ?0 z) x
a birth weight of 7 lb 14 oz, and birth length of
' k" M; C" b6 b) ~20 inches. He was breast-fed throughout the first year
$ |$ g) v$ W7 c& e( D. K" \of life and was still receiving breast milk along with
$ y0 ^8 v2 D3 h7 xsolid food. He had no hospitalizations or surgery,
+ s5 W' d8 p, F( m' \and his psychosocial and psychomotor development7 {( n# Q, n0 ~9 v, M+ t" c
was age appropriate.
( z5 y& x+ J8 g) q+ g4 D* T5 WThe family history was remarkable for the father,4 z7 G+ d% x) S+ s) Y
who was diagnosed with hypothyroidism at age 16,3 G6 c4 Z  b3 ?. G6 b
which was treated with thyroxine. The father’s8 w7 L. j! Z+ r; r/ e$ a" v  }
height was 6 feet, and he went through a somewhat* D. X& `$ @3 Y' U+ Y' l7 l
early puberty and had stopped growing by age 14.
9 Y3 e# x9 F, }+ I  {The father denied taking any other medication. The
0 m) v8 L$ ^; x4 g/ D7 q9 r. E" Ichild’s mother was in good health. Her menarche* |7 O; ^7 g& K; }# ?- R3 J
was at 11 years of age, and her height was at 5 feet* {. p# a- I1 v9 G4 M" G
5 inches. There was no other family history of pre-# t6 s7 ?5 V) x8 g) }0 y; V
cocious sexual development in the first-degree rela-7 n& S" J- R6 x# \( R
tives. There were no siblings.
7 Q: j- [3 u9 U0 GPhysical Examination
5 G! C4 ], o( ?6 [( LThe physical examination revealed a very active,
! [$ V" g' h& p! y0 N3 Mplayful, and healthy boy. The vital signs documented$ M$ S8 Y) f: ]1 B% Z
a blood pressure of 85/50 mm Hg, his length was
% Z9 z# j! \1 ?# K5 f1 X90 cm (>97th percentile), and his weight was 14.4 kg
% a) ]' ^, G. R% r$ s(also >97th percentile). The observed yearly growth
4 V; L1 ?$ z" T* M- c' {- C7 `velocity was 30 cm (12 inches). The examination of* s/ @' p4 l- n: O7 {
the neck revealed no thyroid enlargement.
2 S) o4 ~( c5 ?+ C: _, g, o4 oThe genitourinary examination was remarkable for$ |+ C/ k1 g$ a3 E
enlargement of the penis, with a stretched length of/ H) y6 u4 l6 h. r; E
8 cm and a width of 2 cm. The glans penis was very well
1 ?. e3 B. e/ Y' @8 l9 _/ w" Qdeveloped. The pubic hair was Tanner II, mostly around
% J* {% X6 L3 g' {( u! C540
3 d- w5 K  E0 t3 Q% b$ K( }8 mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ @7 |5 l0 f$ f" G+ sthe base of the phallus and was dark and curled. The& u% g0 N+ ?* d1 z
testicular volume was prepubertal at 2 mL each.6 O) P  s' c" B
The skin was moist and smooth and somewhat; v4 D# H* F. h/ z# b* m" S
oily. No axillary hair was noted. There were no
4 P' Z  L/ U+ _; r; Fabnormal skin pigmentations or café-au-lait spots.
. f( [  j$ s$ aNeurologic evaluation showed deep tendon reflex 2+9 A: S* `1 w; W6 O( I
bilateral and symmetrical. There was no suggestion- N$ ]; K7 J. h$ J) c
of papilledema.0 Z1 n6 v0 C5 s4 s) |
Laboratory Evaluation
! ~2 H6 \. S/ f- SThe bone age was consistent with 28 months by
: Z4 d9 ^' ]# X: vusing the standard of Greulich and Pyle at a chrono-
5 f1 y( I  a* |) Z1 Elogic age of 16 months (advanced).5 Chromosomal% h! L; |( v8 G& \1 j
karyotype was 46XY. The thyroid function test, U1 z& H1 y4 m% [7 f: a
showed a free T4 of 1.69 ng/dL, and thyroid stimu-- Q5 X# m' w* ^( t$ y% i7 Q
lating hormone level was 1.3 µIU/mL (both normal).; J( l: c. G, O$ w
The concentrations of serum electrolytes, blood( U6 T* R+ S4 Z* E
urea nitrogen, creatinine, and calcium all were1 d1 \0 ^0 i' ]  S. w# Y
within normal range for his age. The concentration2 d7 z5 `7 P# n( s
of serum 17-hydroxyprogesterone was 16 ng/dL
* |- p( U% s9 w( D) I(normal, 3 to 90 ng/dL), androstenedione was 20
6 [+ V' M: `- X; D0 z) |ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
& z6 ~0 J- m! M* o2 A/ I$ kterone was 38 ng/dL (normal, 50 to 760 ng/dL),
) l4 ]- Y) c. A% \desoxycorticosterone was 4.3 ng/dL (normal, 7 to
- G. y, _& y- D1 m/ f& L49ng/dL), 11-desoxycortisol (specific compound S)
" C6 u; c7 }0 T% X$ X, Xwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-/ i. [  j2 t- I$ ]+ R2 j
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
  y* k) i' `# r2 @3 B' gtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),$ X& Z0 \" c8 E
and β-human chorionic gonadotropin was less than9 |6 V& u1 _! ?7 w7 S
5 mIU/mL (normal <5 mIU/mL). Serum follicular
3 K" P4 L- v8 b) ^& o) }! Z7 G7 Zstimulating hormone and leuteinizing hormone
6 L- ~* G1 {) ]. p" `3 Kconcentrations were less than 0.05 mIU/mL
7 A8 P# J; W! F  x' e/ x& ^(prepubertal).
3 ~0 Q8 t- I3 N# HThe parents were notified about the laboratory# O$ @& }( y. I8 H% J1 H; g
results and were informed that all of the tests were" i8 r, }6 y6 T- D
normal except the testosterone level was high. The. u8 X9 D7 `# J/ ]
follow-up visit was arranged within a few weeks to* s; `/ ?4 o( j% G
obtain testicular and abdominal sonograms; how-
. o- b  s6 t7 g3 C' n* Iever, the family did not return for 4 months.
9 ~2 `& Q' \  zPhysical examination at this time revealed that the. z+ l/ _, @3 s% j. k
child had grown 2.5 cm in 4 months and had gained
5 }7 V& \4 W+ k+ e2 kg of weight. Physical examination remained7 n$ b+ n& O+ z4 G" K" B3 S
unchanged. Surprisingly, the pubic hair almost com-
) W8 ^5 {7 L7 Z& ?pletely disappeared except for a few vellous hairs at
) P7 |. T! B( b; I8 S  g* B( Wthe base of the phallus. Testicular volume was still 2
$ k, _  o1 [+ R& D4 }3 Y/ r) ymL, and the size of the penis remained unchanged.; g2 \5 m1 [) {2 A) n% @4 Q" L2 n
The mother also said that the boy was no longer hav-
5 V. x: z4 h" u9 N$ C# g  S% E. |ing frequent erections.8 V$ E8 ^5 R2 F" G' ]1 e
Both parents were again questioned about use of% d' ~& I" s, I9 v% s; v
any ointment/creams that they may have applied to
& A; w. a) x. Nthe child’s skin. This time the father admitted the% b+ A& k; c- i, {! _, h
Topical Testosterone Exposure / Bhowmick et al 5419 ?( O9 V" E# e6 t. w) ]
use of testosterone gel twice daily that he was apply-
$ s: \4 w4 S" S/ ding over his own shoulders, chest, and back area for1 ]  |7 t2 S5 E! x# K
a year. The father also revealed he was embarrassed
  R9 l# u, Q% Vto disclose that he was using a testosterone gel pre-
( b) m; K( B# }$ l9 o) Q5 s) {$ }scribed by his family physician for decreased libido$ b' G* r: t/ ]' ^
secondary to depression./ g. m: u6 }# i3 N" m. u
The child slept in the same bed with parents.7 J4 h0 R% C! C& |4 d; N
The father would hug the baby and hold him on his$ V; M  z+ E. r; @- R. ^$ o
chest for a considerable period of time, causing sig-9 H! v" D3 W" D( e) ?& V
nificant bare skin contact between baby and father.
$ [7 R) k9 i4 Y( A0 ?The father also admitted that after the phone call,
1 Y) E2 |" s+ N7 K3 Jwhen he learned the testosterone level in the baby% n( V% ?% n3 @. S$ g% t
was high, he then read the product information* }2 {2 ~) r* Y% v! L
packet and concluded that it was most likely the rea-7 S  e5 @- n2 f' G! m
son for the child’s virilization. At that time, they
" `0 n/ x! V3 e. A- F9 vdecided to put the baby in a separate bed, and the* q8 o/ x0 `) g0 w4 e
father was not hugging him with bare skin and had
# d7 n1 l8 [+ Zbeen using protective clothing. A repeat testosterone
: x/ m; e* E* O' i$ ^7 Ttest was ordered, but the family did not go to the! O0 S7 O9 s  }! e' o
laboratory to obtain the test.
4 D9 E7 m6 U% u' U1 jDiscussion
+ B( `4 Z+ T/ l, k7 zPrecocious puberty in boys is defined as secondary& @# n  z2 x2 M; S8 B7 [
sexual development before 9 years of age.1,4
1 e( T) d3 K2 x6 Z8 UPrecocious puberty is termed as central (true) when, m3 h4 ~2 {6 e1 ]( V# d
it is caused by the premature activation of hypo-
- ?) `3 W+ G- `% E) I/ y3 A) ~thalamic pituitary gonadal axis. CPP is more com-
: c1 M8 W# h$ Q  @' [mon in girls than in boys.1,3 Most boys with CPP
# O' F3 G7 ]# a; e! umay have a central nervous system lesion that is4 ^- f; K9 {8 k  V
responsible for the early activation of the hypothal-- L$ o) F& c0 Y( k3 f4 s: m. i% r
amic pituitary gonadal axis.1-3 Thus, greater empha-9 G3 p, `" _! L, b
sis has been given to neuroradiologic imaging in
2 U5 Y* ]8 y& y1 Sboys with precocious puberty. In addition to viril-# J7 d6 J  p9 R1 m  u) o
ization, the clinical hallmark of CPP is the symmet-
6 z) `- k9 z  V' Q3 b$ u+ x- y7 Arical testicular growth secondary to stimulation by. ?/ h  ?; p2 }( o! i7 m8 s5 C
gonadotropins.1,3( v8 X5 ]8 s7 ~4 ~7 r6 }7 E
Gonadotropin-independent peripheral preco-& H* `" a9 g! H& {' f8 F
cious puberty in boys also results from inappropriate( ]+ n: S* J/ V# _# @, t% Q
androgenic stimulation from either endogenous or) Y: F+ g* c$ U
exogenous sources, nonpituitary gonadotropin stim-5 T. Y) t1 P0 g+ P* i# f$ G5 v
ulation, and rare activating mutations.3 Virilizing' ~# S( @; [2 ?4 Q! v
congenital adrenal hyperplasia producing excessive
9 A: A* V6 L) l; _' r6 a& a& Tadrenal androgens is a common cause of precocious
. ^5 k$ K( q6 q* ]! D9 ipuberty in boys.3,47 f# Z8 Z, _  x7 t. P, u& x7 N
The most common form of congenital adrenal* A2 h; \4 _& a& b
hyperplasia is the 21-hydroxylase enzyme deficiency.8 R' X! ^3 _" z' L
The 11-β hydroxylase deficiency may also result in# M! q1 {, \! f/ i8 W  T
excessive adrenal androgen production, and rarely,
; f" k+ G+ e( j0 }an adrenal tumor may also cause adrenal androgen0 n/ q' H# D5 V; i+ P
excess.1,3& W+ ~' x) l- Z3 Z5 \
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: T' `" C% P' }4 G. i542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
# S+ j" N' ^. o0 X9 y/ @$ XA unique entity of male-limited gonadotropin-
- h- ]7 o+ I( `1 _- Lindependent precocious puberty, which is also known0 w+ v3 B) ?6 e
as testotoxicosis, may cause precocious puberty at a9 m+ ^3 c' \/ Q/ v) l
very young age. The physical findings in these boys; k$ q0 F# d! h
with this disorder are full pubertal development,
4 a. {7 N# [* T- ?3 Y: w) Jincluding bilateral testicular growth, similar to boys9 E- G' w# t4 p4 M) R8 {
with CPP. The gonadotropin levels in this disorder* o9 _4 r' Z: X! d3 ~2 m
are suppressed to prepubertal levels and do not show
2 B$ k8 Z. Z3 d3 V- d  Y8 Lpubertal response of gonadotropin after gonadotropin-$ r/ A* [. R' D" z! r
releasing hormone stimulation. This is a sex-linked0 b2 I: n% `9 N$ K
autosomal dominant disorder that affects only
0 I( {$ I# _" G+ X3 f1 E. Wmales; therefore, other male members of the family, m0 g  m" R% z9 q
may have similar precocious puberty.3
5 z4 V/ S3 Q" h/ q. zIn our patient, physical examination was incon-$ [" i! k: @: V/ Z& H! d
sistent with true precocious puberty since his testi-
8 z7 ?: P6 k' h* M5 \6 L/ d; G; Hcles were prepubertal in size. However, testotoxicosis
! r$ V9 l% t% w3 zwas in the differential diagnosis because his father
) F5 d- y' P+ x& j3 h$ Q- d, E8 tstarted puberty somewhat early, and occasionally,
+ }. d  h. L2 x7 X+ Q" V% K! x9 \( btesticular enlargement is not that evident in the
! R1 a3 c8 V4 J) q6 xbeginning of this process.1 In the absence of a neg-( n* v; Q$ B% ~/ V+ O. ?& a' O
ative initial history of androgen exposure, our. x7 _' h6 x3 Z+ P$ f
biggest concern was virilizing adrenal hyperplasia,
9 g" F  _; D( s0 ^! weither 21-hydroxylase deficiency or 11-β hydroxylase
5 b5 z9 S2 B% F! B2 w% N0 Qdeficiency. Those diagnoses were excluded by find-+ V' V& W+ ~& v: b8 W1 h
ing the normal level of adrenal steroids.
0 x4 O1 h4 G& K+ T* xThe diagnosis of exogenous androgens was strongly
1 i0 }6 D7 a8 B$ H2 C( ksuspected in a follow-up visit after 4 months because) A2 p6 u. F/ v
the physical examination revealed the complete disap-. c  h0 ~$ T5 Y- D% B& P) h5 C
pearance of pubic hair, normal growth velocity, and% N: Y! I( G& d- x' a* {
decreased erections. The father admitted using a testos-
; M- X- ]9 a5 o  Hterone gel, which he concealed at first visit. He was
7 w( W( _) A! A* C; R7 l3 busing it rather frequently, twice a day. The Physicians’: }9 W; s2 e" y5 l2 O8 d
Desk Reference, or package insert of this product, gel or; L, s# Y) A0 p% r/ I" _
cream, cautions about dermal testosterone transfer to
' B; s( T2 i# E* I7 _; x( n. `unprotected females through direct skin exposure.
7 i9 s' ?7 k7 k8 v+ mSerum testosterone level was found to be 2 times the
9 D7 J& e/ l* z; O. h; Cbaseline value in those females who were exposed to1 B: ^2 g" Z& P; _7 Y$ F
even 15 minutes of direct skin contact with their male
0 {- k0 v& x7 @  N: l/ Z  ]$ Bpartners.6 However, when a shirt covered the applica-
' S2 g; C. [) ?: {/ ation site, this testosterone transfer was prevented.
1 t' ^! \& j6 ]  }Our patient’s testosterone level was 60 ng/mL,
, p8 z. ~5 y1 p0 ^# Zwhich was clearly high. Some studies suggest that% J& V8 w' E# f) o  d5 }
dermal conversion of testosterone to dihydrotestos-
4 ]6 w4 I. n( c2 gterone, which is a more potent metabolite, is more
- v9 l0 t$ s* Bactive in young children exposed to testosterone
3 O: W5 m  w1 Z1 [6 ^exogenously7; however, we did not measure a dihy-( K* c6 Z0 A% y) }# t9 U
drotestosterone level in our patient. In addition to
1 u) Q7 W6 N5 n6 h1 tvirilization, exposure to exogenous testosterone in
3 o0 o4 f" y' I( N; P6 M0 n7 hchildren results in an increase in growth velocity and
/ O' m) y4 T' _! t4 iadvanced bone age, as seen in our patient.
( z/ t* O8 W% X* LThe long-term effect of androgen exposure during+ g) D* j1 m5 L5 `+ O1 N& k* Y) e
early childhood on pubertal development and final  |2 K1 z( i- `5 R- s4 _; I4 ]; R
adult height are not fully known and always remain
8 S1 n* p- @, r5 Qa concern. Children treated with short-term testos-
3 E2 D* ^# o0 Q" j  b4 pterone injection or topical androgen may exhibit some+ e* J* x- T) Y" P0 M/ m; B! Y
acceleration of the skeletal maturation; however, after
& x+ y+ U! S6 B7 J: ccessation of treatment, the rate of bone maturation$ y1 n  [7 a; c  |  c- l
decelerates and gradually returns to normal.8,9. @# q, n3 S" }1 b0 C
There are conflicting reports and controversy' ?+ ?; `1 p: L/ ?  w! A% F+ C
over the effect of early androgen exposure on adult
- I5 `. G9 M2 cpenile length.10,11 Some reports suggest subnormal
; @3 p! x3 R+ p: Y- Zadult penile length, apparently because of downreg-
# L+ B, e8 S" V# a# _ulation of androgen receptor number.10,12 However,
: }7 j* s, ^. \- LSutherland et al13 did not find a correlation between  M- w2 x: N- G- k9 g" V
childhood testosterone exposure and reduced adult$ X" \/ @+ y% _: ?  p1 N7 f) x/ t
penile length in clinical studies.
+ }. U& C+ k1 r. H/ FNonetheless, we do not believe our patient is
4 g' r" E0 D* }* i  Kgoing to experience any of the untoward effects from
8 @$ \! U/ i; n; X. ftestosterone exposure as mentioned earlier because+ ?4 t& s6 v6 r0 g
the exposure was not for a prolonged period of time.& f4 g! W. t2 Z8 n& X) I1 `9 Q' Q
Although the bone age was advanced at the time of5 R5 F2 _/ o8 W& F  z
diagnosis, the child had a normal growth velocity at. }8 u$ H) ^! I) y# \
the follow-up visit. It is hoped that his final adult
/ A; X4 ?; ]# c6 pheight will not be affected.4 V) z: z* ~$ N: _1 I
Although rarely reported, the widespread avail-
, v) v% c- j$ B# x2 vability of androgen products in our society may. L- t: O9 A4 P
indeed cause more virilization in male or female9 F) D$ u" |, M. o) V
children than one would realize. Exposure to andro-$ `2 b! e+ B' }
gen products must be considered and specific ques-# B( }$ w5 D; Y" U3 _
tioning about the use of a testosterone product or+ o7 i+ M5 ^% K- @9 J0 G' x& S
gel should be asked of the family members during& L1 l6 Q& ~- T1 V9 B8 i7 f
the evaluation of any children who present with vir-
' T, l8 {& m8 ^% Milization or peripheral precocious puberty. The diag-* F+ o! E/ _: r, R2 v. r8 |. E4 v3 O
nosis can be established by just a few tests and by
0 G$ r3 n) p, r/ E3 u2 H5 _' A1 jappropriate history. The inability to obtain such a9 V9 j4 O7 c5 \
history, or failure to ask the specific questions, may% o/ n  @( Z) t' h2 [
result in extensive, unnecessary, and expensive
% [( q* L& v7 ^* Iinvestigation. The primary care physician should be
  y% L& k# p7 }" J3 Naware of this fact, because most of these children
/ Z( W( x# C2 ]may initially present in their practice. The Physicians’
0 g+ y" [! \$ L" C7 eDesk Reference and package insert should also put a
- k) _+ N1 b; A- |6 X% Twarning about the virilizing effect on a male or. f* k, L' h  ^' w
female child who might come in contact with some-
0 S, V, d4 B+ z% B' A; Eone using any of these products.
6 B# s) ]- k) ^/ D: U$ n" b# jReferences
) D( b  ^4 E+ S7 m$ L- E1. Styne DM. The testes: disorder of sexual differentiation6 s& X8 q6 Z, `7 v- Y% b1 }
and puberty in the male. In: Sperling MA, ed. Pediatric# w8 Y4 L. \4 h1 b
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
  T9 d2 U6 j0 U' S; `0 c3 f2002: 565-628.6 ?3 T  w7 N, |2 _3 l2 ]5 K
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
7 I; v7 y) F. e) T2 ipuberty in children with tumours of the suprasellar pineal
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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
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
8 Q% ?$ b( A( K* ]! d
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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