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Sexual Precocity in a 16-Month-Old
) m; A7 k0 e- XBoy Induced by Indirect Topical
' c6 B7 O2 Q* I$ K/ |- X+ PExposure to Testosterone1 c$ J2 O1 b8 D0 ~# Q& n& i
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2% y6 }6 L. ~/ T& V; R
and Kenneth R. Rettig, MD17 O& ]8 n2 Y) v' J& z# V
Clinical Pediatrics
4 i8 _* \: ^3 j. D8 q2 d) f9 s( mVolume 46 Number 6
: o# p( ?* L+ D3 L4 k$ rJuly 2007 540-5435 V$ ]& C! A7 q6 g; \5 n2 T" D
© 2007 Sage Publications
4 R1 P2 c9 \: o5 Y& {; ?3 Y10.1177/0009922806296651' L# r  e! m$ R5 D9 Z) s
http://clp.sagepub.com. ^8 _2 z" m" H% h/ \
hosted at
6 A  g4 a5 R; N/ E- ]http://online.sagepub.com
6 u/ _) i2 \0 s, S7 \8 SPrecocious puberty in boys, central or peripheral,! R6 y6 v! g9 s. K
is a significant concern for physicians. Central
2 o1 b0 G" R4 v9 H* Mprecocious puberty (CPP), which is mediated' m6 B; w1 C+ ~! E/ w' t
through the hypothalamic pituitary gonadal axis, has
5 b5 y/ z: z8 s+ c3 Ya higher incidence of organic central nervous system
+ f9 P# S, Q: i/ c# @, W7 nlesions in boys.1,2 Virilization in boys, as manifested6 O/ S" e% \" E* N  B6 m
by enlargement of the penis, development of pubic
) B4 o1 `! x% J# F3 I- E( rhair, and facial acne without enlargement of testi-
+ `( ~7 W) Q. h3 ]. x) o- i# H& Ycles, suggests peripheral or pseudopuberty.1-3 We) \2 e6 ^$ l3 e7 K6 w+ r0 s" o
report a 16-month-old boy who presented with the
& G4 n# Q) F3 W5 @3 z- denlargement of the phallus and pubic hair develop-
: B7 q& J( k$ r  ^  _ment without testicular enlargement, which was due
" I9 k* z" E% P  L0 N  tto the unintentional exposure to androgen gel used by
$ {7 `) w" U  r0 v; l5 [( kthe father. The family initially concealed this infor-0 c% r; l/ Z  ]8 w( i4 U2 j  X
mation, resulting in an extensive work-up for this% X0 \2 d; Y( z( @- }9 N" _
child. Given the widespread and easy availability of
9 i# u9 D- p5 _) f  B4 [testosterone gel and cream, we believe this is proba-$ H8 t( M! `( ?" i5 t# C
bly more common than the rare case report in the. h! r! y1 ]  c  b9 @$ z) j/ L
literature.4
2 [4 `8 [; g+ s2 VPatient Report
* |$ C8 r+ T$ s4 Y* mA 16-month-old white child was referred to the  l5 h1 v* y5 w8 r; q- _
endocrine clinic by his pediatrician with the concern9 T5 A& b% {% Z) m( W" M
of early sexual development. His mother noticed
- C/ n: u. b# n, d' t! `9 {light colored pubic hair development when he was! O) [0 M8 {1 b3 Y2 Y
From the 1Division of Pediatric Endocrinology, 2University of  K% P0 P; Z$ n
South Alabama Medical Center, Mobile, Alabama.
, A/ `6 P. q" B% hAddress correspondence to: Samar K. Bhowmick, MD, FACE,6 H: ~+ t1 U4 z% ~5 g+ h5 h
Professor of Pediatrics, University of South Alabama, College of
8 `$ v, W( |" s# }1 Z8 N2 [2 [) [Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
1 x9 G2 v0 x" H0 Y3 ue-mail: [email protected].2 w1 B' W  p& o# B6 d
about 6 to 7 months old, which progressively became
7 \; c6 a1 T; l% s, T: E! kdarker. She was also concerned about the enlarge-8 p. c; Q. {) @& p1 t, {
ment of his penis and frequent erections. The child
) C: S( d8 q# ^2 T. S1 K( Kwas the product of a full-term normal delivery, with
! L3 F& c' U, G: M1 N1 la birth weight of 7 lb 14 oz, and birth length of/ ^% M; W: @8 _# p
20 inches. He was breast-fed throughout the first year' K" n% P, e. k7 B# ~! v& V
of life and was still receiving breast milk along with  J0 c% s3 {, S
solid food. He had no hospitalizations or surgery,
  h; ]9 f% g+ Tand his psychosocial and psychomotor development$ a! U/ E0 F! W1 e! @
was age appropriate.
( ?% Q( B' k) o  cThe family history was remarkable for the father,
2 E4 L7 K, m. U" [  X' dwho was diagnosed with hypothyroidism at age 16,
1 B% S% k1 G5 \/ mwhich was treated with thyroxine. The father’s
" K# ~1 ~& ]# M# G8 T* |height was 6 feet, and he went through a somewhat' |: k8 @, A& }# c
early puberty and had stopped growing by age 14.
5 `( y" e) ?$ @The father denied taking any other medication. The
: O5 P: v6 E9 Y2 {+ e! ]5 T3 F3 Hchild’s mother was in good health. Her menarche
& f; C9 V! {& ^3 ?' Iwas at 11 years of age, and her height was at 5 feet
% O7 F- ]7 f9 g1 B) \/ H, m5 inches. There was no other family history of pre-
: \" {" R0 i" h# y4 ucocious sexual development in the first-degree rela-  F9 ^% T& Q& G
tives. There were no siblings.
+ H0 S+ i6 o9 I* }7 \; h3 FPhysical Examination8 A4 h+ Z9 \  b* G0 D& Z8 W* L
The physical examination revealed a very active,* f3 F4 S& `, s/ H; G$ [
playful, and healthy boy. The vital signs documented
4 e7 w4 w6 X% Y# {2 Ra blood pressure of 85/50 mm Hg, his length was' G+ ~) n) J- P
90 cm (>97th percentile), and his weight was 14.4 kg
8 S! ~; o% ]( i) s( Y6 C5 q(also >97th percentile). The observed yearly growth9 A3 h- a4 R  j) _' [* R0 ~  z
velocity was 30 cm (12 inches). The examination of
3 B: i, O* @/ Q8 q: Pthe neck revealed no thyroid enlargement.
9 p8 n8 K3 K3 u. `The genitourinary examination was remarkable for
8 d0 g5 R& t2 x4 r# _enlargement of the penis, with a stretched length of
8 C1 _8 T4 c8 L8 ~8 cm and a width of 2 cm. The glans penis was very well! g& ^7 y0 q( s7 C' g; k* Z
developed. The pubic hair was Tanner II, mostly around/ |$ ~8 ?0 J6 x6 Y" U  }& X
540
2 `  s) B4 J/ s3 A; xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 U$ p; M4 C  X0 H7 O' f! L0 i
the base of the phallus and was dark and curled. The
% {5 c1 y' e: \1 btesticular volume was prepubertal at 2 mL each.
3 T% m$ S/ \4 o  _The skin was moist and smooth and somewhat
! F: g0 {' f  [/ f3 ]0 Toily. No axillary hair was noted. There were no
. E6 N+ I0 y5 `% Z+ Tabnormal skin pigmentations or café-au-lait spots.
5 _& h# |: g$ r6 I/ _* h- WNeurologic evaluation showed deep tendon reflex 2+
5 r, b% P2 r7 ?bilateral and symmetrical. There was no suggestion9 j! ^1 h0 X# L# ]0 j5 m0 c- t9 k" y
of papilledema.
: B. Q, ~: i1 ]# f1 FLaboratory Evaluation3 s  _& k+ |/ G8 q& c6 M+ U
The bone age was consistent with 28 months by
+ B% o: y7 E- Y! g9 s% Tusing the standard of Greulich and Pyle at a chrono-; U5 u3 s$ g  }
logic age of 16 months (advanced).5 Chromosomal: i4 y$ p) t3 Z$ I( O4 s; ^; b
karyotype was 46XY. The thyroid function test3 K! Q3 L1 B/ N) S9 t+ z, p
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
) \' K4 M2 y2 S% J) Alating hormone level was 1.3 µIU/mL (both normal).: K3 P, G) }. b' Y
The concentrations of serum electrolytes, blood
: H4 w2 M  D( i7 F, k6 |urea nitrogen, creatinine, and calcium all were6 [6 x) R' A7 \* Y& y9 J
within normal range for his age. The concentration* }! _' e: `* s$ U" p7 @  T
of serum 17-hydroxyprogesterone was 16 ng/dL: n" d/ R; {' @% A1 j
(normal, 3 to 90 ng/dL), androstenedione was 204 [$ A* R: i" {2 A# r$ L* `; k5 K
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
% U/ i* Z% x# o+ _, C2 nterone was 38 ng/dL (normal, 50 to 760 ng/dL),: u9 o0 }! l' w7 }7 z1 t% |( ~
desoxycorticosterone was 4.3 ng/dL (normal, 7 to. Z, _, P& c/ j7 Z4 `0 D
49ng/dL), 11-desoxycortisol (specific compound S)
5 p- Y9 B; d6 G6 v. M' Twas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-  R1 }1 {/ l( N- f
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
+ H4 B8 T0 C9 i: Qtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),5 Q* N6 l  h. `5 }" k
and β-human chorionic gonadotropin was less than% s8 {8 U: G4 k. C% z+ F
5 mIU/mL (normal <5 mIU/mL). Serum follicular3 X  v9 r9 _4 M. s8 v9 k
stimulating hormone and leuteinizing hormone" o$ r/ r1 T0 U0 ]% b  e, y
concentrations were less than 0.05 mIU/mL
+ @. S0 R! v1 {) r& A1 N. u(prepubertal).
+ `9 e% k+ }) h& l8 S7 ^  F4 ZThe parents were notified about the laboratory0 ~) W$ C6 }; i2 q% ]; Q
results and were informed that all of the tests were8 Z- J' X$ b: r) F) z2 L
normal except the testosterone level was high. The- e; F- l/ I& l
follow-up visit was arranged within a few weeks to
; z* n/ `+ v& B5 b0 a7 h# Uobtain testicular and abdominal sonograms; how-
9 S/ p$ v; q6 \+ m- jever, the family did not return for 4 months.) j; a& \" ^  j1 k3 u6 ?1 K, C
Physical examination at this time revealed that the
& H. ^( e0 L' I. Ichild had grown 2.5 cm in 4 months and had gained( a* v$ ~/ |3 o- }
2 kg of weight. Physical examination remained  C5 r0 G! ^' l9 }) l; e) u0 m
unchanged. Surprisingly, the pubic hair almost com-
! e9 y8 \8 _; T% D$ Y! ~pletely disappeared except for a few vellous hairs at6 j3 @+ R3 E# w! Y
the base of the phallus. Testicular volume was still 2
+ W8 M: ~) L' [" T$ a' {$ g1 l7 ^: PmL, and the size of the penis remained unchanged.
+ l; `; X6 R6 x% d  WThe mother also said that the boy was no longer hav-) M8 \% [; W6 m3 d  e* a+ _6 \2 q
ing frequent erections.9 B! m! W" V3 V' L- ?1 D3 k: a
Both parents were again questioned about use of- }$ P$ a: m: b
any ointment/creams that they may have applied to
3 C, W0 Q6 C1 ~; }3 Ythe child’s skin. This time the father admitted the/ a& T! I% \* V+ @
Topical Testosterone Exposure / Bhowmick et al 541
: b; A, H# n3 e7 N2 t3 ?% g6 `use of testosterone gel twice daily that he was apply-! F( h1 E. u, N  a1 M5 c
ing over his own shoulders, chest, and back area for/ P. r9 N( i+ g# W7 X, @
a year. The father also revealed he was embarrassed
9 E/ j" k- {9 ?  T: z6 gto disclose that he was using a testosterone gel pre-! m( {; s6 a8 P3 ^6 X" [
scribed by his family physician for decreased libido
6 z# x( @7 U! A7 Vsecondary to depression.* z0 c1 L+ q) K/ {7 |0 s
The child slept in the same bed with parents.
5 R" V" J7 k/ X2 e2 c# y, G7 `The father would hug the baby and hold him on his4 o7 U& p0 @0 \, p- J/ N
chest for a considerable period of time, causing sig-2 y6 t8 P+ A1 C1 f' |, K" q
nificant bare skin contact between baby and father.) _' A7 l. n! p
The father also admitted that after the phone call,
+ K4 n$ H' a5 [# Y7 U! W9 ?7 }when he learned the testosterone level in the baby
8 \7 J, n2 p) `3 m# V: f1 a0 Lwas high, he then read the product information
& f7 u$ W- e: Z6 \5 i) dpacket and concluded that it was most likely the rea-
5 _. ?# y8 h+ j" \$ mson for the child’s virilization. At that time, they
# ^+ W5 K8 |7 M" ~+ o) cdecided to put the baby in a separate bed, and the
# N7 X3 d( o% A. J& X" _father was not hugging him with bare skin and had
* m7 \- G( W' \; m; _# {been using protective clothing. A repeat testosterone
' }6 d) L* v' U. \" atest was ordered, but the family did not go to the. @5 {  D0 y- [/ _. D# o
laboratory to obtain the test.- L% N8 J# z6 ~; ~' F$ v; i
Discussion7 }& ^; w" e, P. W7 N2 y  D, j& j
Precocious puberty in boys is defined as secondary, A  E+ k  i- e) F; T; P
sexual development before 9 years of age.1,4
/ ~, I  Y$ C. b6 k. L+ b0 X: xPrecocious puberty is termed as central (true) when1 V, g# n+ s0 S0 @, s
it is caused by the premature activation of hypo-
( w* s1 S& o+ Fthalamic pituitary gonadal axis. CPP is more com-
. `! `* T' [8 n/ o9 s7 Xmon in girls than in boys.1,3 Most boys with CPP
% p! K2 _2 M5 p, K* ~% Bmay have a central nervous system lesion that is4 _- ^" Z$ Q( o/ V- n& w
responsible for the early activation of the hypothal-0 i, `9 ^. v$ T( k, F# J) \5 J5 q& I
amic pituitary gonadal axis.1-3 Thus, greater empha-7 D+ l/ q- s: e
sis has been given to neuroradiologic imaging in0 R- C$ j' F. K! J9 l# D' b1 S4 d0 a
boys with precocious puberty. In addition to viril-  \# P+ b0 W2 ?( h: m6 ]5 z) Q
ization, the clinical hallmark of CPP is the symmet-3 U4 \3 I. r9 s" g
rical testicular growth secondary to stimulation by
* E1 `6 Z) K" B) i8 p9 E! O/ ?8 ~gonadotropins.1,3
  u5 _( l3 D5 n9 q/ m- W0 jGonadotropin-independent peripheral preco-( X! X& i+ p& c. `4 I
cious puberty in boys also results from inappropriate- O, s6 M! `5 G
androgenic stimulation from either endogenous or
/ g% _  O' W6 C% x, z1 e& c5 Kexogenous sources, nonpituitary gonadotropin stim-4 C6 M  m6 V) G0 w. P
ulation, and rare activating mutations.3 Virilizing
) h9 {$ X4 T! N) H& [congenital adrenal hyperplasia producing excessive
& |' u: |/ t. O6 j8 s: Z, `adrenal androgens is a common cause of precocious( ^6 @' g% R1 e0 C0 \1 B) |# S
puberty in boys.3,4
6 }" Q, o7 F: lThe most common form of congenital adrenal
- [$ @+ p7 f3 B+ N7 h. K# \- S: Bhyperplasia is the 21-hydroxylase enzyme deficiency.- _" V+ T0 b' T3 _: ]! \) O
The 11-β hydroxylase deficiency may also result in
( g% x9 }* @9 n0 qexcessive adrenal androgen production, and rarely,
2 {# U2 v- G2 V0 Q2 Z+ lan adrenal tumor may also cause adrenal androgen- x# t4 l; H# F7 D+ d2 i# E( |
excess.1,3+ M: v' Y7 P- W( l* k. T' G
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 _  `0 K' p: z542 Clinical Pediatrics / Vol. 46, No. 6, July 2007# m) x. _) h" |% h! r  z' B  z
A unique entity of male-limited gonadotropin-+ A3 N6 X! ]: Y$ y
independent precocious puberty, which is also known
- c3 b0 e- N3 x+ has testotoxicosis, may cause precocious puberty at a
8 n* L% z( l$ A+ V" ?very young age. The physical findings in these boys9 Y7 o$ G% A  T9 p. _% N  k
with this disorder are full pubertal development,. p4 S, r2 q' A8 B( ~  |6 [
including bilateral testicular growth, similar to boys  g( [; N& w. h& S6 |
with CPP. The gonadotropin levels in this disorder7 b, |8 y: D7 y7 P9 A
are suppressed to prepubertal levels and do not show( [: k8 C6 w$ h* g5 E. ^; l5 V
pubertal response of gonadotropin after gonadotropin-/ `+ h4 e% `6 T+ b, {' M
releasing hormone stimulation. This is a sex-linked# V0 |( y4 f  y  V3 j, H" X( N
autosomal dominant disorder that affects only
: v& |/ |) F1 d: X/ Emales; therefore, other male members of the family
' L/ z% H. E$ n% g/ V1 ~may have similar precocious puberty.3
/ ]  V) B. p+ g6 q: P! \In our patient, physical examination was incon-: e9 u/ ^- S2 D& h% s5 X& F& `
sistent with true precocious puberty since his testi-
: z; i$ z" N7 I/ tcles were prepubertal in size. However, testotoxicosis# z# T% s/ i$ {: M8 k/ i1 C
was in the differential diagnosis because his father
3 G3 C0 C, {: b- Y& qstarted puberty somewhat early, and occasionally,( O, |. R& l) ?) w. C3 `9 |
testicular enlargement is not that evident in the8 E3 k  u3 d& T+ l
beginning of this process.1 In the absence of a neg-* E- }, k( O) Y7 |  o; p
ative initial history of androgen exposure, our
3 y2 C/ C1 w! m- bbiggest concern was virilizing adrenal hyperplasia,+ V; {$ z( \# ^+ z' \' v7 a9 P. k
either 21-hydroxylase deficiency or 11-β hydroxylase: `5 f- V: E4 q* r4 z9 B2 K' B" r% p
deficiency. Those diagnoses were excluded by find-
8 c9 z5 U) y: Q7 Fing the normal level of adrenal steroids.
9 o: T% x1 U& {! _The diagnosis of exogenous androgens was strongly
! [" k3 J1 i# n5 F; e0 A* Zsuspected in a follow-up visit after 4 months because7 C9 o1 G. c  M# H& q- g7 C
the physical examination revealed the complete disap-
/ F7 k8 _8 U0 X/ e5 M. _pearance of pubic hair, normal growth velocity, and: q2 `% w( k+ ?2 X% s) G
decreased erections. The father admitted using a testos-/ D" O# ?; V0 G
terone gel, which he concealed at first visit. He was
1 Z. o) c+ `8 ^4 j/ n4 Xusing it rather frequently, twice a day. The Physicians’3 K( l/ t- y+ _& ^+ Q; q$ I8 ^* q: `$ r) e
Desk Reference, or package insert of this product, gel or0 S1 Q$ _+ N9 ]% W" Z
cream, cautions about dermal testosterone transfer to' ]; S0 {; E4 e* |: E2 ?* C' h
unprotected females through direct skin exposure.
0 o+ {9 v! n( X& cSerum testosterone level was found to be 2 times the
9 i) @% L5 o& v3 f4 ?8 E; |baseline value in those females who were exposed to
- s2 ]$ k) _8 b/ M' xeven 15 minutes of direct skin contact with their male- l" B9 Y4 Y) e7 Z$ R$ _
partners.6 However, when a shirt covered the applica-6 Z7 H' R" ?) ^: a' s7 a/ Z
tion site, this testosterone transfer was prevented.
. Z. n: N' F" S& {! i8 j+ e3 qOur patient’s testosterone level was 60 ng/mL,9 J- I8 @" F7 m' ~1 o# N
which was clearly high. Some studies suggest that
( a0 v1 t' \0 _# bdermal conversion of testosterone to dihydrotestos-! e# I: d. s4 O5 r
terone, which is a more potent metabolite, is more- g+ {# M( h5 ~) b- X! ~
active in young children exposed to testosterone- q9 V: m) Q1 y# r  R  R
exogenously7; however, we did not measure a dihy-! m, l: q+ f# q3 j, m. p8 L. q
drotestosterone level in our patient. In addition to: G; ?8 O& j$ y3 {$ j3 k' C
virilization, exposure to exogenous testosterone in4 K/ h$ q6 y4 |' Q
children results in an increase in growth velocity and- E2 N+ r0 d0 y! c$ X) |3 t
advanced bone age, as seen in our patient.
: D9 z! ~% u$ F- z8 X& s+ \0 [The long-term effect of androgen exposure during
! Q; ^0 }0 {& k/ P8 F1 Q/ Q$ vearly childhood on pubertal development and final9 Y- [. l1 Y* A' ~9 M0 @
adult height are not fully known and always remain4 I( ~0 z$ }" b: J- L; X
a concern. Children treated with short-term testos-3 h% c& B- @9 L7 H
terone injection or topical androgen may exhibit some5 F4 e+ S, p  m5 S5 l5 T3 c
acceleration of the skeletal maturation; however, after
4 c6 l+ Y* j8 _' r; U- F( tcessation of treatment, the rate of bone maturation9 a; H* V! d0 ?2 E; R, V' [+ x) k
decelerates and gradually returns to normal.8,9
' F/ Y& a( D9 Q  H7 I$ {There are conflicting reports and controversy
2 f9 E" _( ^7 i1 }0 ~# Aover the effect of early androgen exposure on adult
0 K3 B0 y- b9 F' Kpenile length.10,11 Some reports suggest subnormal+ T0 A$ i% {4 G& d6 v
adult penile length, apparently because of downreg-
! X2 e: X; E& ^. Fulation of androgen receptor number.10,12 However,
* F" y2 r  v' g% }0 @/ j4 O" xSutherland et al13 did not find a correlation between
% \6 G; h0 z8 W, B! a6 f2 Hchildhood testosterone exposure and reduced adult) u, f2 w1 b4 x& s
penile length in clinical studies.
. Z0 T7 J; s& W# ^- ]Nonetheless, we do not believe our patient is
7 \8 x6 n+ ^8 _1 W- k3 V' |going to experience any of the untoward effects from
5 p/ @+ n: t# _/ Ktestosterone exposure as mentioned earlier because0 Y4 M) I+ `, U7 J3 g- x
the exposure was not for a prolonged period of time.2 \; ^" J- B' k( G
Although the bone age was advanced at the time of
6 Q' n1 m+ J* j+ g# }diagnosis, the child had a normal growth velocity at% I3 u& r5 i+ X3 P1 w
the follow-up visit. It is hoped that his final adult
$ ~* T. O9 X% t+ ?9 Rheight will not be affected.
8 F, h/ F9 L# i; u. A5 P/ [Although rarely reported, the widespread avail-
9 g1 h( B, ~& s( k4 dability of androgen products in our society may: P* O7 }6 j( x0 n# B+ Q
indeed cause more virilization in male or female" b; Z# F- a4 b( X" }; N% r9 z
children than one would realize. Exposure to andro-# x+ \5 N0 Q$ j/ h; v
gen products must be considered and specific ques-
# V( ]. G9 f1 ~* K5 V% f+ Qtioning about the use of a testosterone product or3 N2 i* L$ J2 H5 |* d& ?( _
gel should be asked of the family members during: N1 f* P: y8 w# x3 P. O, M
the evaluation of any children who present with vir-3 U$ R) f( y  ^4 _+ P
ilization or peripheral precocious puberty. The diag-
0 @3 J! Z: X! D6 G- e1 qnosis can be established by just a few tests and by- {* n' I! O1 [( E
appropriate history. The inability to obtain such a
) q! }; o$ k- ~0 O! S/ z0 ihistory, or failure to ask the specific questions, may
/ S# ]+ v+ d" a/ e/ t1 _result in extensive, unnecessary, and expensive9 h) j9 m- [+ R8 ]% G# d
investigation. The primary care physician should be
( N( L$ S# h+ u# F4 haware of this fact, because most of these children
6 @$ {! E3 `0 n/ M9 {0 ymay initially present in their practice. The Physicians’* ?2 T3 ]7 y& @( X
Desk Reference and package insert should also put a  Z6 Y6 c9 n6 @2 T* {- i$ I" A
warning about the virilizing effect on a male or
, I9 i! m1 h0 z0 Pfemale child who might come in contact with some-- _: Q( n1 t9 G9 ?8 B
one using any of these products.7 ^0 q, l  J5 E0 q
References$ t9 L9 N9 ?+ f/ r6 U
1. Styne DM. The testes: disorder of sexual differentiation
! \$ u" c/ q& _% n) i5 [and puberty in the male. In: Sperling MA, ed. Pediatric) F& Z! V) Z& P" m# H% J) x
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
$ ~. D, A- D7 s, Y/ M2002: 565-628.
) I$ l$ L. v/ ^* F( O& T2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
2 E4 u/ V$ S5 opuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
6 f; @% a9 O% `$ z) @7 L/ F2 NBoy Induced by Indirect Topical
: _* H; U! |) t& j0 C% S6 mExposure to Testosterone
- B' k" P2 `1 z; R: o# ~Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,26 c1 r+ U6 X5 j5 @* h
and Kenneth R. Rettig, MD1
* K, E& t  y6 A1 t% OClinical Pediatrics/ C% k: h. K" b0 J" E6 W2 Q/ v  W
Volume 46 Number 6
! j( c. @% D8 _6 C( FJuly 2007 540-543+ h( ^! j2 w9 g+ q  |  P
© 2007 Sage Publications+ a+ w# C+ j, [& t  O/ w
10.1177/00099228062966514 L# b; j; P3 {* ~7 Z  a# f) t1 q
http://clp.sagepub.com+ q* P. K4 F9 p/ H
hosted at1 X9 Q9 }' Q; X4 o9 B* m" ]" G/ k
http://online.sagepub.com
% f8 b1 M/ r1 K: V, Z4 s2 j8 |Precocious puberty in boys, central or peripheral,; n. M; y: y2 u4 U0 w
is a significant concern for physicians. Central4 l( c: g( L  w9 @) ?4 ~
precocious puberty (CPP), which is mediated
9 f7 h6 A: v+ i: ^- T8 kthrough the hypothalamic pituitary gonadal axis, has- G0 `  q8 \' H6 l) B
a higher incidence of organic central nervous system/ q7 J5 C6 {; T% y" r
lesions in boys.1,2 Virilization in boys, as manifested. a7 j( w; k; f% ?$ P# n. B
by enlargement of the penis, development of pubic
! T1 m* n% S7 F: dhair, and facial acne without enlargement of testi-
$ b0 M2 B6 ~  W. e! r% s; zcles, suggests peripheral or pseudopuberty.1-3 We
: H0 K' c- X' l: I8 q1 @report a 16-month-old boy who presented with the
% [" y- p$ A5 x; U/ g" W* t' `. renlargement of the phallus and pubic hair develop-+ N) E# L# E0 G+ @, l6 J+ L" g- Q
ment without testicular enlargement, which was due
7 c) i: Q. \/ k5 \' g7 S- i& pto the unintentional exposure to androgen gel used by  U! Y  X# A5 B$ W8 }2 m9 p/ p
the father. The family initially concealed this infor-
9 N0 c0 ~$ N/ b4 F% \5 b5 Omation, resulting in an extensive work-up for this* e3 ^/ z! ^! }3 D& ^
child. Given the widespread and easy availability of
& B# i; Q6 ^, D& n. Dtestosterone gel and cream, we believe this is proba-
1 ^0 @: O1 T* F$ s8 h' |bly more common than the rare case report in the+ J( q! p7 F) b% |5 W' z
literature.4
) r" {+ G; s/ D7 E. MPatient Report- Y/ W6 N% G: |4 Q4 Y. p0 N
A 16-month-old white child was referred to the
7 r5 z2 M" b2 a' r* N1 v3 `endocrine clinic by his pediatrician with the concern
* E9 M; w5 y* a6 mof early sexual development. His mother noticed
6 M. Z; Q0 P5 Z' E6 qlight colored pubic hair development when he was
% T0 H$ d2 e  T9 a; OFrom the 1Division of Pediatric Endocrinology, 2University of
0 W0 y" P3 D; c( p& d0 \) U! W2 oSouth Alabama Medical Center, Mobile, Alabama.
! |3 Z" E& d2 t: e+ T9 U5 pAddress correspondence to: Samar K. Bhowmick, MD, FACE,1 H* V5 i( M0 B3 s# z+ b* [" X& v
Professor of Pediatrics, University of South Alabama, College of, ?7 A: D: f- o9 w/ o& \/ A* O
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
% p" g4 C" N9 m1 G* o. U8 @  ]e-mail: [email protected].
2 [4 U0 ~( b3 c& cabout 6 to 7 months old, which progressively became
" N. v! o. q, h' {darker. She was also concerned about the enlarge-
: R9 [7 [' A+ \- l% c% ~* Pment of his penis and frequent erections. The child3 ?( c$ \7 p/ o0 b: K7 v" o! Q: q$ I
was the product of a full-term normal delivery, with
& f. I1 g: H- [a birth weight of 7 lb 14 oz, and birth length of1 S, _" Y1 u4 _0 x
20 inches. He was breast-fed throughout the first year2 z5 g# p# F- w1 h! Z
of life and was still receiving breast milk along with2 |$ J/ V# V* a. o* e2 a4 l' @) ]
solid food. He had no hospitalizations or surgery,0 O  s2 X! C1 ]5 C' K1 r5 g; v
and his psychosocial and psychomotor development; {/ d" v0 \# b( Q. g+ `( f" l
was age appropriate.
$ A  y( P. m. Y- }" MThe family history was remarkable for the father,
7 y" N- A( d+ Z# Q7 `/ c5 `4 wwho was diagnosed with hypothyroidism at age 16,
4 Y- @" ?* `& @) ~# Jwhich was treated with thyroxine. The father’s5 a% m9 f$ }% F8 f7 x- M, m" [  W
height was 6 feet, and he went through a somewhat
  _. B; r' @1 n  _8 L" kearly puberty and had stopped growing by age 14.& V0 E) v7 p, j/ @
The father denied taking any other medication. The
4 X1 v/ c$ t/ Q% \! Y6 \child’s mother was in good health. Her menarche) c" e7 j; B' G& _
was at 11 years of age, and her height was at 5 feet/ H8 }7 }- {* l( ^+ F$ i
5 inches. There was no other family history of pre-
: u5 {0 ]+ i# z$ I: ococious sexual development in the first-degree rela-
/ m8 z: `: \$ K& r5 Z; ntives. There were no siblings.
0 x: }! \1 I: N. DPhysical Examination$ m1 X5 Z0 p; i9 I! u
The physical examination revealed a very active,, B  g' i7 j7 s3 [3 H
playful, and healthy boy. The vital signs documented
4 l/ ^8 c: V; k/ \* B1 Da blood pressure of 85/50 mm Hg, his length was! T2 m: H# k3 O
90 cm (>97th percentile), and his weight was 14.4 kg
- R- E0 t6 m# X. W(also >97th percentile). The observed yearly growth$ K0 N/ {4 B4 M8 A3 V/ ^- o6 E0 P
velocity was 30 cm (12 inches). The examination of& S: |& @! c# A2 s4 p# A  u
the neck revealed no thyroid enlargement.
4 v8 [! B' h) P" z/ Q, u) yThe genitourinary examination was remarkable for8 |0 L0 |7 D% Z' M  Q
enlargement of the penis, with a stretched length of
+ d1 b' O& @  l7 a& e: }8 J8 cm and a width of 2 cm. The glans penis was very well4 M+ S$ }, m( l
developed. The pubic hair was Tanner II, mostly around
! S8 W1 G. ]. K" k1 ?6 o540
& I! Y) D4 }  gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 [6 R0 x/ d! S, Wthe base of the phallus and was dark and curled. The
4 J% [2 G" G8 c0 X/ x( ], E( z, Qtesticular volume was prepubertal at 2 mL each.
& r- u/ a% }" H- C, `9 bThe skin was moist and smooth and somewhat
5 E7 a8 h: [7 {) z: {& \oily. No axillary hair was noted. There were no# f" f! M' Y+ \; n
abnormal skin pigmentations or café-au-lait spots.
# @3 l! ^7 M4 j' gNeurologic evaluation showed deep tendon reflex 2+
* f; U0 _1 n' e3 z% R9 Qbilateral and symmetrical. There was no suggestion
3 H/ q8 I4 x# B3 W3 Bof papilledema.
8 T4 y& C  j2 ^3 m+ y- ~1 C9 ^; L! l7 ?Laboratory Evaluation! J: R% t/ K3 x# f
The bone age was consistent with 28 months by% Z9 [+ {% ?! q1 I
using the standard of Greulich and Pyle at a chrono-9 `0 j2 `2 l! P, V
logic age of 16 months (advanced).5 Chromosomal9 Y' |0 L8 D4 ]. V  a2 b* I
karyotype was 46XY. The thyroid function test
- D, q0 F' S1 X$ A- q- x, V  Hshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
' O$ @( {, x; h, a( r! O# x& ]' rlating hormone level was 1.3 µIU/mL (both normal).1 f2 K' J# U" P
The concentrations of serum electrolytes, blood4 L0 n( j! [, L4 v! K* ]0 z- ?5 v
urea nitrogen, creatinine, and calcium all were" a5 r7 l- {1 t- q% h1 e
within normal range for his age. The concentration
6 H8 r+ g3 M- iof serum 17-hydroxyprogesterone was 16 ng/dL
9 j* [/ }- ~$ Z- e" |" e  m(normal, 3 to 90 ng/dL), androstenedione was 207 @* \8 f: u$ S0 G/ o
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-4 o) d1 Z. \5 H0 U! u
terone was 38 ng/dL (normal, 50 to 760 ng/dL),# B6 @+ m9 q# P6 x! B7 U1 V$ v
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
3 }& `% i, v. O' y49ng/dL), 11-desoxycortisol (specific compound S)
* l9 i. C2 E' F, c% nwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
+ w2 l% q/ e6 Stisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
: F/ \3 T! C, [% Ntestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
! z2 G: H% Z* _and β-human chorionic gonadotropin was less than7 D5 `" X* J& Q; @/ Y
5 mIU/mL (normal <5 mIU/mL). Serum follicular" u9 _! y% J  ~/ ~0 o
stimulating hormone and leuteinizing hormone
& p8 b* Y# @0 w+ A2 ]concentrations were less than 0.05 mIU/mL
2 w* c0 {4 p+ Y(prepubertal).
7 V! N6 ~- D, y; d6 SThe parents were notified about the laboratory. d2 e& d4 R1 a3 x& n6 X
results and were informed that all of the tests were0 Y; ]# f0 P- O9 M6 ^0 r6 t) D) l3 f) J
normal except the testosterone level was high. The
% A8 J- D# ^4 V% P; M% b6 h- Tfollow-up visit was arranged within a few weeks to8 Y; V6 s/ w5 S* A
obtain testicular and abdominal sonograms; how-, V0 r6 A  Z- O& z: O2 S
ever, the family did not return for 4 months.
+ M1 s4 A" \2 Q8 }( J4 V1 jPhysical examination at this time revealed that the
  o) o1 i) s7 Q' P, N' Cchild had grown 2.5 cm in 4 months and had gained- r% ?: `. \* g; @$ h- U6 C9 ?
2 kg of weight. Physical examination remained8 X% e1 _9 s) p0 d6 V! a1 f
unchanged. Surprisingly, the pubic hair almost com-+ P& ^3 q% j5 J' a: ~: k8 f; G2 E
pletely disappeared except for a few vellous hairs at
, P* w' t! R' X5 [% r2 Q* f  Gthe base of the phallus. Testicular volume was still 2
/ N* Y  m6 b" q" ]) }# j& R2 T2 P- FmL, and the size of the penis remained unchanged.
3 ^2 u/ ^3 P& u3 |% w+ ~+ Y0 a2 HThe mother also said that the boy was no longer hav-
$ w8 t1 K8 k( h3 ~5 g# H4 P; }ing frequent erections.8 k; U1 T( ?  W0 r, C; R7 I
Both parents were again questioned about use of
/ X: g: h5 i2 e. z4 b& ]any ointment/creams that they may have applied to6 f' X8 _. j; s" ~
the child’s skin. This time the father admitted the
" }8 m" e$ `" KTopical Testosterone Exposure / Bhowmick et al 541+ z+ r! _$ \+ t8 E
use of testosterone gel twice daily that he was apply-
- A9 ^& @2 J! p$ E, B$ r. o& i+ |ing over his own shoulders, chest, and back area for+ D% W% ^1 X. V2 W5 C- N2 j
a year. The father also revealed he was embarrassed9 b( t8 A8 M$ b( z" f1 z
to disclose that he was using a testosterone gel pre-0 @& D5 ]# K+ b
scribed by his family physician for decreased libido
; }; e+ X! _  Z# Y0 V, usecondary to depression.
' B8 a. e1 u/ W7 Z* Y. \The child slept in the same bed with parents.
  q4 A( v# @; Q  x1 j+ _$ QThe father would hug the baby and hold him on his4 _8 A) Q% l  I% U. n: i) z$ M: K  g
chest for a considerable period of time, causing sig-
) i6 ]6 |# m$ fnificant bare skin contact between baby and father.
$ M6 G/ d2 w9 ~9 k% ?The father also admitted that after the phone call,
" m6 ^* ^4 w) j* A$ nwhen he learned the testosterone level in the baby
5 {+ S6 F3 s  t3 |was high, he then read the product information$ y6 D% K: B8 \3 I0 p
packet and concluded that it was most likely the rea-9 |) H$ X0 M. T$ j  ~* s1 o
son for the child’s virilization. At that time, they1 j) Q- m+ m' G8 x" Q
decided to put the baby in a separate bed, and the' i4 l7 e5 W* L# r& e. k
father was not hugging him with bare skin and had! z. V8 N! D. h0 D. c
been using protective clothing. A repeat testosterone
2 B) a% }& Q: y" g- J5 Y2 otest was ordered, but the family did not go to the
0 l! U% q( b# `% X  f# i! vlaboratory to obtain the test.; Y, T5 J9 e$ a: C  r
Discussion& |, B9 F) n& i* P, e7 P9 y0 |
Precocious puberty in boys is defined as secondary. r+ R$ j. u7 h# C
sexual development before 9 years of age.1,4
2 Y3 |- k- q' o8 M3 Y4 v7 X( H4 Y4 qPrecocious puberty is termed as central (true) when# |1 Q: T+ m! O* w5 V
it is caused by the premature activation of hypo-4 Z, Q5 `9 y7 U& [& L
thalamic pituitary gonadal axis. CPP is more com-6 ]5 B! ~2 z# q; }
mon in girls than in boys.1,3 Most boys with CPP
$ F) O0 C  \$ r3 A! y$ q% amay have a central nervous system lesion that is# a* A' B0 M( A9 P8 k) H& ^
responsible for the early activation of the hypothal-8 K& n9 ~0 P1 U" e, k
amic pituitary gonadal axis.1-3 Thus, greater empha-
7 r0 M1 M9 f0 W$ F4 Csis has been given to neuroradiologic imaging in
9 L. t/ v* _- q$ m+ T- R9 g( Dboys with precocious puberty. In addition to viril-
, j3 o) T4 U+ y: g$ \0 L& ?ization, the clinical hallmark of CPP is the symmet-" n7 n8 I8 g& E7 {2 G- e
rical testicular growth secondary to stimulation by
4 {; t) d6 }6 Q$ o* H0 Tgonadotropins.1,34 x: C, Z# V) o- {3 \
Gonadotropin-independent peripheral preco-
0 c6 u9 o9 ~- s  r7 _' |- wcious puberty in boys also results from inappropriate# j! F6 c7 M# e! `4 l4 }# H# h
androgenic stimulation from either endogenous or; `6 s, r. {; i8 x/ _4 p0 \2 J
exogenous sources, nonpituitary gonadotropin stim-
) {* E( S& O! o6 K& n/ [/ ~ulation, and rare activating mutations.3 Virilizing
" k/ q, R! W! {: K1 U0 s; l" wcongenital adrenal hyperplasia producing excessive
$ Q. O# H, {( |/ B, I& [adrenal androgens is a common cause of precocious3 y1 y  }2 x# w
puberty in boys.3,4
5 ~: {* c2 i/ x: p- }The most common form of congenital adrenal. k" {0 I0 V8 ^% P  }
hyperplasia is the 21-hydroxylase enzyme deficiency.. N4 i% N* O: f$ H4 F
The 11-β hydroxylase deficiency may also result in
' B  Y8 L8 m, V* u. z0 L8 Vexcessive adrenal androgen production, and rarely,; S% ?, x/ v- d5 G2 e. ^6 r
an adrenal tumor may also cause adrenal androgen
0 v/ m0 ?! J) f: q+ y3 A8 Gexcess.1,3
, ?( Q! R" X# q# {. ^+ e8 Rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, O) u* k9 _8 C3 N! |542 Clinical Pediatrics / Vol. 46, No. 6, July 2007- @: V; [5 Y  n' }4 w% V- M+ C
A unique entity of male-limited gonadotropin-
  V% e- A+ U8 y9 i3 V) }independent precocious puberty, which is also known$ B$ G+ z+ ]7 g
as testotoxicosis, may cause precocious puberty at a
+ i3 Q/ @& P& E  U% q( pvery young age. The physical findings in these boys
7 f- d: \1 H( \0 H; swith this disorder are full pubertal development,
* P# F( d8 E( M  K+ \* i- ?including bilateral testicular growth, similar to boys0 |8 O; a2 }( @" e# G0 e: u
with CPP. The gonadotropin levels in this disorder
/ n  z" |8 e/ P" o  h, s  G  Iare suppressed to prepubertal levels and do not show
) L5 w9 `" z7 R6 w  q, Epubertal response of gonadotropin after gonadotropin-
6 f5 _3 {; N0 S6 c+ v6 areleasing hormone stimulation. This is a sex-linked) R  M& e9 N/ X' s1 J: ?
autosomal dominant disorder that affects only1 u# |- }9 c  f7 }4 m  Z% A
males; therefore, other male members of the family3 \# \8 {6 u# j, K3 f
may have similar precocious puberty.3/ _; r2 J- I* ^# n
In our patient, physical examination was incon-
1 j4 P- k. [, K1 A# Rsistent with true precocious puberty since his testi-
: k0 F. t/ ~& J8 Rcles were prepubertal in size. However, testotoxicosis
! |" C1 ~  J% m8 D7 X6 d$ nwas in the differential diagnosis because his father
8 b' E9 F, [5 n; N$ o$ vstarted puberty somewhat early, and occasionally,
4 B: {- j2 t/ r, j1 Gtesticular enlargement is not that evident in the/ i* E1 A- \2 I
beginning of this process.1 In the absence of a neg-
1 s* l' y1 T& N' Z9 n" |ative initial history of androgen exposure, our
0 t2 E5 `" z6 \) gbiggest concern was virilizing adrenal hyperplasia,
7 w. J2 r9 ~' y5 ueither 21-hydroxylase deficiency or 11-β hydroxylase
6 T  i& w, v+ |: c: G) P: Y) cdeficiency. Those diagnoses were excluded by find-
" d& H. z6 ~6 m0 Jing the normal level of adrenal steroids.
. D- h; s5 }( GThe diagnosis of exogenous androgens was strongly  j$ _9 a4 J7 t! B  W9 |$ `% b
suspected in a follow-up visit after 4 months because
7 F4 \' X% A) j4 [1 I2 K: Wthe physical examination revealed the complete disap-
0 G; I4 @+ E/ Q, f& ~0 g/ upearance of pubic hair, normal growth velocity, and9 [4 O* D9 j: Y/ C9 R' r
decreased erections. The father admitted using a testos-" T0 ~2 @9 g( _; I3 j
terone gel, which he concealed at first visit. He was2 L+ z- O) M; p. F' }; m
using it rather frequently, twice a day. The Physicians’( ~$ z1 A& [! F+ }. r8 ^
Desk Reference, or package insert of this product, gel or8 v4 T; ]3 b( S! z$ F* O/ o
cream, cautions about dermal testosterone transfer to
! H- B- y0 w3 h' Y, F' vunprotected females through direct skin exposure.
$ |' r9 T/ \2 f! K+ `1 {Serum testosterone level was found to be 2 times the
% S. c! h  ^( g% k4 bbaseline value in those females who were exposed to
6 _, c% p! L9 _2 P* beven 15 minutes of direct skin contact with their male8 M- y3 R4 u) P, o) h  C
partners.6 However, when a shirt covered the applica-0 f! k& I. _7 [3 V. E
tion site, this testosterone transfer was prevented.5 |" I/ M( p: d0 M9 P( p/ Q' f; R$ `
Our patient’s testosterone level was 60 ng/mL,7 b" W  `' K5 Z/ A& a
which was clearly high. Some studies suggest that; |, J6 o9 z  z: d, l
dermal conversion of testosterone to dihydrotestos-
! p# e, j: a4 Q( [9 m; ^. q6 xterone, which is a more potent metabolite, is more1 j; U2 P( @, Z: S& Y
active in young children exposed to testosterone
* [; j. w+ M: z- u: q1 j8 Vexogenously7; however, we did not measure a dihy-
, P. i2 ^. W& ]/ H$ C- Rdrotestosterone level in our patient. In addition to0 ]1 ?8 j5 m  C) }0 _! s+ @' \
virilization, exposure to exogenous testosterone in( q1 ^8 n: m+ B" V$ K% [& ]) W2 M
children results in an increase in growth velocity and
! E* r9 c0 Y1 L% n0 q3 V' Kadvanced bone age, as seen in our patient.; ?3 l! M' }. t0 Y# g% y
The long-term effect of androgen exposure during
( f3 p' c. c' s4 q" M/ c$ T2 Kearly childhood on pubertal development and final
( s1 ^& [1 R$ d; ~5 _5 yadult height are not fully known and always remain0 B% B0 w) k7 H1 D0 S7 E
a concern. Children treated with short-term testos-
/ `; h: L& c: [- p( U; t& Mterone injection or topical androgen may exhibit some# F8 o( k1 I+ l/ R5 R
acceleration of the skeletal maturation; however, after" o* Q+ h, E  N1 M3 O% z/ c
cessation of treatment, the rate of bone maturation
+ Z3 D" f& M9 P* v, Fdecelerates and gradually returns to normal.8,9  }: V$ K% w, c- W$ D# N
There are conflicting reports and controversy! F% R! C2 H4 f# i' e
over the effect of early androgen exposure on adult
# S/ J( D! |" J! v& mpenile length.10,11 Some reports suggest subnormal. _5 v; M8 b6 q" C4 C3 t/ f
adult penile length, apparently because of downreg-( `  v8 D+ _2 l6 |9 W
ulation of androgen receptor number.10,12 However,
1 A' f: D% n& L# _4 b, [" {0 P6 [Sutherland et al13 did not find a correlation between# k' P, C& ~" W+ B8 K6 Z
childhood testosterone exposure and reduced adult& q& o" i" t, \
penile length in clinical studies.
. O* q( ?: z# @" P8 l* vNonetheless, we do not believe our patient is
. H9 X% U( R7 ^) l9 Vgoing to experience any of the untoward effects from3 N9 f0 A5 T7 L+ v3 I" ?  |
testosterone exposure as mentioned earlier because5 \7 a4 g: K' v, G9 r  y
the exposure was not for a prolonged period of time.
/ I$ j; V1 i' C2 ]4 K$ c( xAlthough the bone age was advanced at the time of
/ l2 b- B  ]2 S3 K% I2 E$ Vdiagnosis, the child had a normal growth velocity at6 x; |' \3 J2 [1 ]4 u- X& b
the follow-up visit. It is hoped that his final adult
& D: ?) V8 j7 s# |& Xheight will not be affected.
: k4 ~2 W) E7 y3 h' |5 D- o& ?) [Although rarely reported, the widespread avail-: r2 }0 l. O) |# A- e6 P
ability of androgen products in our society may
; a/ e: _9 i! C2 P* f% m- R' h  ~indeed cause more virilization in male or female# {$ I& U/ h$ I. W/ Q; x
children than one would realize. Exposure to andro-
$ p- A$ R4 p& D3 s9 ngen products must be considered and specific ques-
$ U+ H! T' X! u* j5 X+ E1 Ytioning about the use of a testosterone product or
4 `  H# D9 @1 d2 u# M$ ?gel should be asked of the family members during* n+ X- N8 E; n2 G
the evaluation of any children who present with vir-% y& q7 H* N2 h
ilization or peripheral precocious puberty. The diag-- y0 h. w; K' K9 T/ Q
nosis can be established by just a few tests and by! i  Q) y) B, f0 @- n5 P
appropriate history. The inability to obtain such a8 B1 C  i; G' N& Y0 z! \/ D% v
history, or failure to ask the specific questions, may$ V% Q7 s5 E- @; Y
result in extensive, unnecessary, and expensive8 T* k4 O. @: t& A; r* w3 j7 ~
investigation. The primary care physician should be, C' f6 ^- e" C0 e9 K
aware of this fact, because most of these children
5 g1 K  Z1 s: {5 lmay initially present in their practice. The Physicians’
5 n2 V, t& f, V: j0 b3 @Desk Reference and package insert should also put a
( J, Z3 ]+ K! G' g. gwarning about the virilizing effect on a male or( U# H& S. y% M0 l& d" n
female child who might come in contact with some-; Y  }" F3 C8 k+ n3 c
one using any of these products.  w8 H) u& P3 }. a- K& i
References
, z$ }0 V7 I& c3 ~, H% L1. Styne DM. The testes: disorder of sexual differentiation& V3 f2 O* P3 g# y$ _5 |
and puberty in the male. In: Sperling MA, ed. Pediatric
8 p* S) Z3 ?! H1 EEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;! F. E3 q( H  j
2002: 565-628.2 S' q" X  |0 J' w) w9 L* i: T2 K4 O
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
% d! q) V! H, q, {6 l8 c# Upuberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
* n3 ^7 a1 M. S
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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