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Sexual Precocity in a 16-Month-Old
; E9 A0 R: L' l, |# M" b. z1 wBoy Induced by Indirect Topical
4 J$ {+ A( d2 ?" e7 x5 X/ dExposure to Testosterone4 Y; y9 v4 i; E7 {
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,22 M4 F2 P% B) |4 w4 [' d# R0 [
and Kenneth R. Rettig, MD1( \( J! _) R3 s6 |; O: O: G
Clinical Pediatrics4 T5 ]' Z6 c) `1 @3 W
Volume 46 Number 6
% C$ q" t- l1 k- N6 K. fJuly 2007 540-5436 Y9 Y5 M3 H8 V( M) H
© 2007 Sage Publications
8 y* x, @& X$ J) A7 ]- u- j10.1177/0009922806296651
) C6 N$ k9 R- B! j7 u9 W; n# Rhttp://clp.sagepub.com
5 O: F7 b$ b* t4 k8 _1 {7 `0 L8 vhosted at
0 [5 R( A1 @8 f  n9 ihttp://online.sagepub.com
5 U0 P! N- a* B! z+ @2 ^* j) uPrecocious puberty in boys, central or peripheral,' Z; [$ w% C2 ^' t3 N' P
is a significant concern for physicians. Central
2 x. D* @0 B1 v' P8 nprecocious puberty (CPP), which is mediated( Q' v% s8 L2 t+ {4 |3 o
through the hypothalamic pituitary gonadal axis, has" c% d' C4 G* `3 T# p4 o) B
a higher incidence of organic central nervous system" V) c8 t  v/ l: X! D
lesions in boys.1,2 Virilization in boys, as manifested/ q% ]6 C1 m5 B, U# C
by enlargement of the penis, development of pubic
! c5 _- ~1 j9 Q7 |6 Ohair, and facial acne without enlargement of testi-
8 |$ K3 u9 j' K! gcles, suggests peripheral or pseudopuberty.1-3 We
& \5 t7 ?" T1 E$ n  @2 T) ?4 u4 _! o* Zreport a 16-month-old boy who presented with the
9 c; M4 }0 r7 ]" J$ Yenlargement of the phallus and pubic hair develop-1 J  Q4 q6 c/ O  N" Z7 a
ment without testicular enlargement, which was due$ M8 {! E9 @" f8 S/ N' ]9 ~& ~* Q
to the unintentional exposure to androgen gel used by
8 j, h, ]2 N8 x" B! b' B: S0 w8 nthe father. The family initially concealed this infor-
/ v- y9 A8 O/ ]2 ~8 @mation, resulting in an extensive work-up for this0 ~; d4 d& [3 q+ U
child. Given the widespread and easy availability of1 \3 Z3 P- R% Q# `* F
testosterone gel and cream, we believe this is proba-  z& D8 R4 H& M, ~* @0 W0 K
bly more common than the rare case report in the
7 X: j0 i+ l  M- x5 Rliterature.4
$ l: _/ G: p: d( `Patient Report! o; M+ o7 h6 s$ C8 R# X7 `
A 16-month-old white child was referred to the; g. Y, Z, j. Q  m
endocrine clinic by his pediatrician with the concern
) z; m" N) D& {8 h8 O- {of early sexual development. His mother noticed& K+ i, m2 g1 m% n3 O) q! i
light colored pubic hair development when he was: M6 w7 [1 O* Y9 z
From the 1Division of Pediatric Endocrinology, 2University of
, t1 w& B  k+ B, J, K- OSouth Alabama Medical Center, Mobile, Alabama.
! h! @  _, Q) u, ?' d6 ZAddress correspondence to: Samar K. Bhowmick, MD, FACE,
$ e/ [( d) o7 h3 u0 J) v) p% aProfessor of Pediatrics, University of South Alabama, College of- A* B2 g7 h$ b! L& `3 z+ @: g
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;4 P. ]; p# R9 K
e-mail: [email protected].
6 n3 n+ B7 Y: {- f" Uabout 6 to 7 months old, which progressively became
* X, S0 Z/ I4 M. n. x2 ^darker. She was also concerned about the enlarge-
+ f: ?+ g) U( @  Z2 Y1 C$ \9 \ment of his penis and frequent erections. The child
; d: E( I2 ]; y" j1 s/ Y9 y6 [! I" nwas the product of a full-term normal delivery, with
4 T! L1 S9 m/ k7 A* Y) O6 S2 L6 xa birth weight of 7 lb 14 oz, and birth length of
/ Z  P% ?1 h% G20 inches. He was breast-fed throughout the first year( [8 J5 M* T' P* i" s# Q2 ~0 b" i
of life and was still receiving breast milk along with8 R- `" t* g8 Q# e% X5 d
solid food. He had no hospitalizations or surgery,
8 v+ r2 v! ?6 D1 }& Cand his psychosocial and psychomotor development8 m" Y& M6 ?2 c5 A5 ^
was age appropriate.6 f; S  J  d& u$ P7 v
The family history was remarkable for the father,
8 }% A1 D: p) h( lwho was diagnosed with hypothyroidism at age 16,
& R2 T7 d: X7 a) [+ n5 n1 a5 _, rwhich was treated with thyroxine. The father’s
4 o0 g0 b7 s) vheight was 6 feet, and he went through a somewhat
  C* x  Q6 s6 O) learly puberty and had stopped growing by age 14.& F5 e. P! N& x% p
The father denied taking any other medication. The+ E, v/ v& F3 D# b' B" C* T3 [
child’s mother was in good health. Her menarche3 d5 ^- T8 \' W; c" j4 D* R
was at 11 years of age, and her height was at 5 feet
: ?  h& D+ l" s! h. r2 j5 inches. There was no other family history of pre-
( X, m) Z, n: [$ j' |cocious sexual development in the first-degree rela-* f2 M5 X$ A# x: A- q
tives. There were no siblings.
! u! \- ]2 A' m- m6 t2 bPhysical Examination5 |1 C! k7 [/ D1 M
The physical examination revealed a very active,
  [5 p& B0 s, _  X) O  D6 Eplayful, and healthy boy. The vital signs documented0 l, m- A  x) N/ j7 n
a blood pressure of 85/50 mm Hg, his length was0 b4 ?+ D8 D& C. F# j" o- j  ]% {& M
90 cm (>97th percentile), and his weight was 14.4 kg
2 W6 u2 `; j  B1 k- @; l. \(also >97th percentile). The observed yearly growth# @0 F5 V9 c0 V9 }$ P, ~
velocity was 30 cm (12 inches). The examination of; x5 z6 _( F$ Q3 I2 _
the neck revealed no thyroid enlargement.+ d' k5 O6 x# X  Q' J* E# D
The genitourinary examination was remarkable for
" l" g/ f  R/ Y5 c# cenlargement of the penis, with a stretched length of
& T1 L+ Z7 P3 X3 U, _3 y2 k8 cm and a width of 2 cm. The glans penis was very well
  |. o$ \8 C$ Rdeveloped. The pubic hair was Tanner II, mostly around
" n0 f% x0 `+ g0 A4 s/ J5406 G( ^" l- p5 B) K6 a
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, m9 _( B) {9 H9 j# r4 i: Dthe base of the phallus and was dark and curled. The
# O3 i; @  a# s2 Y: Q% Dtesticular volume was prepubertal at 2 mL each.
( |' |& \3 }0 c. ]The skin was moist and smooth and somewhat$ e" f" ]/ s6 @! z$ h1 `& V
oily. No axillary hair was noted. There were no% N, u0 y: \' `, |% f3 T* y( i
abnormal skin pigmentations or café-au-lait spots.
, Q; ^) y. a$ z* e6 i7 E6 E  }Neurologic evaluation showed deep tendon reflex 2+
' s' S" ]2 k* B3 S3 ]$ u6 [( c+ f9 P+ fbilateral and symmetrical. There was no suggestion, E  N5 d: v+ U6 C! b
of papilledema.
; B+ c) y' _; t5 A- D# u& ?, BLaboratory Evaluation
- ?& a) V' ^8 E$ T" hThe bone age was consistent with 28 months by5 A" E) m1 \7 c, h% e
using the standard of Greulich and Pyle at a chrono-. b- A# c7 j1 x
logic age of 16 months (advanced).5 Chromosomal+ @2 h( f0 Z) N* E
karyotype was 46XY. The thyroid function test9 i; }  N1 K0 h( i5 p
showed a free T4 of 1.69 ng/dL, and thyroid stimu-, P2 M- A7 h) G1 M& y
lating hormone level was 1.3 µIU/mL (both normal).: Q' f1 {! k5 U/ n. o7 D' t
The concentrations of serum electrolytes, blood) C  f0 h) W7 f4 |5 Q
urea nitrogen, creatinine, and calcium all were
& Y% [  _: g# N5 e; m9 V5 `within normal range for his age. The concentration
( H& J" k( d" w; U0 O8 V$ fof serum 17-hydroxyprogesterone was 16 ng/dL
8 ~, [- h5 t# n. \  K& z) h, T(normal, 3 to 90 ng/dL), androstenedione was 20
9 L) Q# s: I$ ?' p6 c  w8 j% u" }ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-0 K- u* G8 @# i
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
/ `! d- j. a' _desoxycorticosterone was 4.3 ng/dL (normal, 7 to+ f" k1 U' a7 d; I8 D
49ng/dL), 11-desoxycortisol (specific compound S)% g. a& J. Q: Q7 K9 _
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-8 f; J5 b, r* K- Q
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total4 ?  n( p0 u6 u' p! I# [
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),4 p( t0 g, G& O" A. B8 W
and β-human chorionic gonadotropin was less than
9 l3 J+ S4 U$ k/ @6 [' ?. i5 mIU/mL (normal <5 mIU/mL). Serum follicular* y# ~& g. i) B' `' {
stimulating hormone and leuteinizing hormone
0 Z/ p, Z9 ]* e; Cconcentrations were less than 0.05 mIU/mL6 h5 W  m6 b: ?* j5 a* Q1 U, l
(prepubertal).# `, a0 H: F( j
The parents were notified about the laboratory
4 h6 T& l- I9 q# R  Presults and were informed that all of the tests were# k! c5 ^. F5 B5 F$ {- b& u
normal except the testosterone level was high. The6 M! X% C4 Y" y# n. c
follow-up visit was arranged within a few weeks to' n9 I! O- v9 F5 R4 _: o5 h
obtain testicular and abdominal sonograms; how-  H$ k1 w% x+ n' ^2 @
ever, the family did not return for 4 months.
# |6 b+ ]7 V* BPhysical examination at this time revealed that the3 D( n9 g- ^& S; @2 O  \
child had grown 2.5 cm in 4 months and had gained8 u# A  b7 C5 G) n+ u! [& {
2 kg of weight. Physical examination remained6 J1 {- c8 w5 n$ g) w: u3 q/ c; V) ]
unchanged. Surprisingly, the pubic hair almost com-
& E9 c( R8 ]; }2 F. xpletely disappeared except for a few vellous hairs at7 g7 {# z; a$ Y) }0 i, G' t5 _
the base of the phallus. Testicular volume was still 2/ O4 m$ Z/ ], z$ b. p+ C
mL, and the size of the penis remained unchanged.  _  r. T/ i. b8 p" |* k) X+ C
The mother also said that the boy was no longer hav-
- |) n. i* e; Q* king frequent erections.4 d& g& }1 l/ K2 L
Both parents were again questioned about use of( p0 O7 H, H, g  D' F; j$ r
any ointment/creams that they may have applied to  O# q/ F) k$ m* k# X- e
the child’s skin. This time the father admitted the
) ?  J9 K; Z% o% Y8 O* O/ CTopical Testosterone Exposure / Bhowmick et al 541
! L& f- l6 ^  f4 n7 H& buse of testosterone gel twice daily that he was apply-
1 ^+ a1 k/ D% x+ ging over his own shoulders, chest, and back area for6 Y* f+ M9 X8 a1 G
a year. The father also revealed he was embarrassed# Y5 o  w/ r1 l7 Z. ?9 x9 k. u
to disclose that he was using a testosterone gel pre-9 X' v$ R8 ?( c+ h% w6 y6 S5 c0 R
scribed by his family physician for decreased libido
! A- S5 I% E0 ~  qsecondary to depression.) Y. a9 X% U# ?5 W2 {, E) W; _
The child slept in the same bed with parents.
+ v2 A2 U6 q/ ZThe father would hug the baby and hold him on his
$ k$ S/ w8 p. d9 Zchest for a considerable period of time, causing sig-9 X9 }& f' k& H, }. J
nificant bare skin contact between baby and father.
. J$ ?* A+ K: T9 hThe father also admitted that after the phone call,
: P& {0 V3 Q% Lwhen he learned the testosterone level in the baby0 g$ j! P) w7 m+ K0 f
was high, he then read the product information3 g1 X7 F# n( m0 j1 H, U
packet and concluded that it was most likely the rea-5 u( {& g2 _$ C6 c
son for the child’s virilization. At that time, they
: n! U2 A  {& P, J2 Hdecided to put the baby in a separate bed, and the1 p) v1 J7 Y6 q! {/ z
father was not hugging him with bare skin and had" d. G( r1 Q4 \$ `# {& U/ X
been using protective clothing. A repeat testosterone
1 u& k3 |' d2 c4 r' h; T2 l7 Stest was ordered, but the family did not go to the
4 I# m# J& l5 o8 [  qlaboratory to obtain the test./ \# o1 b# z4 u: S/ t
Discussion/ b, h# z. o0 G1 A  m, u# j
Precocious puberty in boys is defined as secondary
8 k+ i2 H) D1 y2 J0 Vsexual development before 9 years of age.1,4/ z6 {% n7 A$ v: z0 j; j
Precocious puberty is termed as central (true) when0 d# b' [  h% C  _7 Y6 @/ l
it is caused by the premature activation of hypo-6 v, a7 E3 I! C& v! c) H
thalamic pituitary gonadal axis. CPP is more com-
0 I- e0 h6 b/ y% kmon in girls than in boys.1,3 Most boys with CPP# P9 B4 w6 z. {1 H4 B* D. r$ Q
may have a central nervous system lesion that is+ w, u: D/ `: H, ~. f# _* L& n
responsible for the early activation of the hypothal-/ m$ L& R& g* d
amic pituitary gonadal axis.1-3 Thus, greater empha-
% H# K$ @8 x- A( w8 C+ W. w0 ]sis has been given to neuroradiologic imaging in
3 T) D3 z0 Y0 ^! P7 Eboys with precocious puberty. In addition to viril-
% V. E3 X* a# g1 B* z  Wization, the clinical hallmark of CPP is the symmet-; i6 W  T! ]' A! q( m
rical testicular growth secondary to stimulation by
: l  T% N/ K" T+ @  f) Y+ H( ogonadotropins.1,3* Z3 p# _$ q' i. K- A
Gonadotropin-independent peripheral preco-! U% C# |, E  E% \
cious puberty in boys also results from inappropriate- k7 n" Y( ?- {; v5 b
androgenic stimulation from either endogenous or$ A9 ]) C, C1 s" b; C
exogenous sources, nonpituitary gonadotropin stim-: T$ O6 e& B0 n! s
ulation, and rare activating mutations.3 Virilizing
7 _$ u. O: \( j+ W; u+ r5 _congenital adrenal hyperplasia producing excessive
& O9 B* s" w+ d5 z' y& p# Iadrenal androgens is a common cause of precocious' Z0 N8 Z2 d. w
puberty in boys.3,4
6 f% ?8 ^4 s" Y9 ?/ dThe most common form of congenital adrenal
* r3 J- H& ]% Z$ T4 [hyperplasia is the 21-hydroxylase enzyme deficiency." K6 \0 q5 q( [6 u0 W
The 11-β hydroxylase deficiency may also result in
2 ]! R; K. |( ~4 yexcessive adrenal androgen production, and rarely,
  Z3 `1 _: [  Oan adrenal tumor may also cause adrenal androgen
2 V7 Q9 W* t- i: X! C) Kexcess.1,3
7 ^7 {" S! e' K. v& O7 Gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# X- \" h" ]+ m542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
* w: \+ ?" v& S  m/ A  f2 j" GA unique entity of male-limited gonadotropin-
: L' o. }& B! S( B* k1 Z  xindependent precocious puberty, which is also known& W5 {9 e3 e# w
as testotoxicosis, may cause precocious puberty at a' k' r4 U3 |- F( v' Z: z
very young age. The physical findings in these boys
' l% q2 X' T. h7 s' x& rwith this disorder are full pubertal development,
! m" z$ R& k: e0 Gincluding bilateral testicular growth, similar to boys, X+ v/ E. D- @5 p' b# Y
with CPP. The gonadotropin levels in this disorder5 o% D& j. z' y1 E4 E* g0 q
are suppressed to prepubertal levels and do not show
" D: K4 q" X6 u. |8 a0 F4 hpubertal response of gonadotropin after gonadotropin-, P) o) J3 q! p1 I7 D
releasing hormone stimulation. This is a sex-linked3 W$ |) [( X  n/ a' E" N" Z* ]
autosomal dominant disorder that affects only% Q/ P5 ~) E$ ^7 z7 {9 W
males; therefore, other male members of the family0 _" R& y8 ~4 n9 s& C9 @- o% Y
may have similar precocious puberty.3
% _7 ^- D9 V# A1 U4 S/ _# s  j, ~$ _In our patient, physical examination was incon-# K# L+ G/ f# o7 @* P- Z. I$ n* b
sistent with true precocious puberty since his testi-
& c& w% j; G* ^: O5 }1 X# r4 Tcles were prepubertal in size. However, testotoxicosis) s$ O- S: t4 D8 j& g
was in the differential diagnosis because his father
+ T! {. H. o! v! e& \; ]started puberty somewhat early, and occasionally,
8 i9 p: |0 R" [  @testicular enlargement is not that evident in the
# d( h9 t; g0 Y6 U* tbeginning of this process.1 In the absence of a neg-: s# K* {& c) H/ x" @
ative initial history of androgen exposure, our0 [; z3 W- d1 x/ m
biggest concern was virilizing adrenal hyperplasia,
5 D- j. i5 b6 Q# c3 `either 21-hydroxylase deficiency or 11-β hydroxylase. E( i6 m$ i' i+ q9 H! q+ }
deficiency. Those diagnoses were excluded by find-  U  P. R% T0 [
ing the normal level of adrenal steroids.( c- w& @5 e. u3 d
The diagnosis of exogenous androgens was strongly
; }- a9 e3 v4 D7 Psuspected in a follow-up visit after 4 months because
0 v+ z2 d# y3 {* X- r+ x& [the physical examination revealed the complete disap-. f3 n8 y8 e3 P  Z% }. {; T$ R9 [
pearance of pubic hair, normal growth velocity, and# C' E  {0 W9 T
decreased erections. The father admitted using a testos-
, {' P# ~6 [3 U% y6 D9 @" W. Eterone gel, which he concealed at first visit. He was; y5 n( p1 F1 A$ E' m
using it rather frequently, twice a day. The Physicians’% [5 @- s- h/ }. `6 |: O6 C
Desk Reference, or package insert of this product, gel or
" U' X& x( ]1 k- b) U: wcream, cautions about dermal testosterone transfer to+ g+ x" M0 B6 d
unprotected females through direct skin exposure.8 ?& P3 W+ b3 o- H3 g) R8 o) `
Serum testosterone level was found to be 2 times the
7 @8 [4 w0 Q( j5 R% vbaseline value in those females who were exposed to2 L1 z9 S8 v( V% T
even 15 minutes of direct skin contact with their male
( @1 w8 {# P9 C4 w' v2 M( j, |1 mpartners.6 However, when a shirt covered the applica-8 N- E& {: G7 s( u2 q
tion site, this testosterone transfer was prevented.
( @* F- K# J8 v$ Y* z" vOur patient’s testosterone level was 60 ng/mL,
8 T: w! P# W8 d0 l& s3 ~which was clearly high. Some studies suggest that
. j5 H8 B3 ?# X$ |dermal conversion of testosterone to dihydrotestos-
9 V% p4 w# A' Gterone, which is a more potent metabolite, is more0 C! I9 M0 V5 _5 T
active in young children exposed to testosterone9 R6 Y% I8 i: T; j3 \4 U
exogenously7; however, we did not measure a dihy-! }7 i' `9 o/ \+ U7 [
drotestosterone level in our patient. In addition to
" I+ W; w/ }& j/ R/ y. Y& H0 e# Dvirilization, exposure to exogenous testosterone in
" U) k3 C7 l/ c8 l+ c  t# ?0 |children results in an increase in growth velocity and
, H2 r# @0 Q' [* iadvanced bone age, as seen in our patient.. D% t+ y+ Y2 W
The long-term effect of androgen exposure during
2 k) ]3 i( `2 u$ b+ r9 ^early childhood on pubertal development and final
6 x" I" _# Z; @3 N  J2 k* radult height are not fully known and always remain
$ M3 U! [3 F( n! F% F9 b, i1 Ka concern. Children treated with short-term testos-% G; `! |4 |/ s2 d7 i' d
terone injection or topical androgen may exhibit some$ N  t* Y* W. k3 R
acceleration of the skeletal maturation; however, after# H) c8 n/ u' m4 z* H1 d
cessation of treatment, the rate of bone maturation6 M: @5 t' E4 Q" d" R8 c$ B
decelerates and gradually returns to normal.8,9
3 i+ t8 Y9 _# s$ j1 `There are conflicting reports and controversy
8 J7 i( j! |) H! r  X* hover the effect of early androgen exposure on adult
# c- C9 U4 }5 r0 v2 D( C7 Mpenile length.10,11 Some reports suggest subnormal
3 k( w6 o( q% m- d" a9 Gadult penile length, apparently because of downreg-5 i" O/ B( g8 A: E8 Z  t
ulation of androgen receptor number.10,12 However,( z2 J. j8 U% Y) ]. m
Sutherland et al13 did not find a correlation between8 `2 r1 R  P% s
childhood testosterone exposure and reduced adult
! T6 y! I$ }, a, r0 r  i$ L1 x4 Tpenile length in clinical studies.& G1 B' v1 a" u  k; V+ g/ @
Nonetheless, we do not believe our patient is
+ Z0 D* J( }" }going to experience any of the untoward effects from/ t) H- z- e2 @% }3 J- @0 ^5 ~
testosterone exposure as mentioned earlier because4 R( C0 f" ^" n4 q
the exposure was not for a prolonged period of time.
3 n* c) v- J- l5 D  K! MAlthough the bone age was advanced at the time of) J/ q& @+ x7 F4 U
diagnosis, the child had a normal growth velocity at
2 K* T, L- n, z2 a3 Mthe follow-up visit. It is hoped that his final adult2 c3 d. N0 H% D9 Q; p
height will not be affected.
, l. n- C8 j9 N) V+ dAlthough rarely reported, the widespread avail-
  o8 w# t* r" U5 eability of androgen products in our society may
6 d6 t( T' _6 M1 I* S6 o$ ~2 Pindeed cause more virilization in male or female
8 D4 V3 m' e) Q  {# ~children than one would realize. Exposure to andro-, M& ~' T4 g8 n& O2 t
gen products must be considered and specific ques-
' u6 h$ M/ d, N; W! f: W9 ]tioning about the use of a testosterone product or8 @- F- b( t6 F; I9 v; w  L$ `2 s
gel should be asked of the family members during
" c. @  B2 B* L% d# Lthe evaluation of any children who present with vir-7 T: w4 P7 ^- b4 U4 z' g
ilization or peripheral precocious puberty. The diag-5 |2 F6 l( o3 A
nosis can be established by just a few tests and by# {0 E! y/ }" }. g, B
appropriate history. The inability to obtain such a
0 L1 X( E2 b. ihistory, or failure to ask the specific questions, may6 Q2 L0 i1 {: h/ [0 E( W
result in extensive, unnecessary, and expensive1 h3 f; \1 X2 c) L0 C
investigation. The primary care physician should be6 j/ N. a5 H& F4 E8 |0 t/ `0 a
aware of this fact, because most of these children
5 h: w9 H! A& b' k+ ~, ~may initially present in their practice. The Physicians’( q9 H& u4 s6 Y+ [, I; i' m. E% y2 R
Desk Reference and package insert should also put a% c4 ~! b. J/ Q* d& ^
warning about the virilizing effect on a male or
3 y' E! S- W, r: H: tfemale child who might come in contact with some-
# o; I$ t5 }0 L( aone using any of these products.
+ v- q6 }' r# t. r- FReferences
: }2 [! q" S4 Q& |- z1. Styne DM. The testes: disorder of sexual differentiation* x9 I' u; l' z- H+ N
and puberty in the male. In: Sperling MA, ed. Pediatric
4 m2 q( Y" R8 E, s' R4 U7 CEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;+ I+ E& O; Z9 v. B6 Y% K+ ^
2002: 565-628.
2 p4 u- F* P) F3 a$ C% o- j' J% U4 f2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious+ h2 N2 u8 `0 Y" P
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old- c! B( G6 g: q, f. t- w8 S
Boy Induced by Indirect Topical
! z6 R( y5 h1 U5 y9 I, zExposure to Testosterone
# D4 U0 P5 y; q0 C% ~Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2) k" {/ d! B- ]+ e' x- V5 g4 {
and Kenneth R. Rettig, MD1
$ i2 ]  k. C+ _5 h& q0 f8 FClinical Pediatrics' D) N1 M9 |0 F9 D- K- Q
Volume 46 Number 6
# l& k; F$ b+ ]1 m& }3 F2 HJuly 2007 540-543$ O4 p' C9 b* p$ d1 I
© 2007 Sage Publications5 v* V2 {) a. i$ g
10.1177/00099228062966516 |3 @+ Y' {: _4 b6 y
http://clp.sagepub.com
" j$ f# E' U) l1 T( {! ~2 thosted at
% B" i" V" ~# F& e# Ihttp://online.sagepub.com
* G$ K$ m6 X5 P0 c; KPrecocious puberty in boys, central or peripheral,0 E7 ]5 O  P% |$ F, x& O( V$ ]
is a significant concern for physicians. Central9 w4 P+ c1 p8 h" t, ^  d
precocious puberty (CPP), which is mediated
0 ?  _0 Q, F% k8 S# B4 S0 x: Ethrough the hypothalamic pituitary gonadal axis, has, f+ I: _& P# g$ K
a higher incidence of organic central nervous system
) F9 A) P! J6 Tlesions in boys.1,2 Virilization in boys, as manifested: n: ~6 m* Z& ]/ d3 R+ S6 O( g
by enlargement of the penis, development of pubic
# I7 R- A4 l  ?8 z: _2 l  S1 l$ f) shair, and facial acne without enlargement of testi-( ~9 K+ O" X3 t, Y& _5 W
cles, suggests peripheral or pseudopuberty.1-3 We6 l  R7 n9 v3 A
report a 16-month-old boy who presented with the
! v3 ~) O* P; c3 E( L2 Menlargement of the phallus and pubic hair develop-
/ S. R% c8 O! t0 ?. Zment without testicular enlargement, which was due. m$ {5 P5 L  ^3 A. h" Y8 ^& l
to the unintentional exposure to androgen gel used by% s. o9 t/ s- n# K. o4 U
the father. The family initially concealed this infor-! W) _" K8 f' `5 ?7 v+ s7 L
mation, resulting in an extensive work-up for this
4 a- N& [% J& M. g$ n4 p% w  I7 K  Zchild. Given the widespread and easy availability of
- v4 e- u/ s5 B# R$ r) }1 M+ htestosterone gel and cream, we believe this is proba-" p5 v/ A$ D7 f& w3 O
bly more common than the rare case report in the5 z; C" i4 i$ n/ C" R; O- m
literature.4
- ]  x. j" f, I  u- uPatient Report
7 X( W7 |) J  gA 16-month-old white child was referred to the* O' X6 ^/ S5 C! _1 q
endocrine clinic by his pediatrician with the concern
! t+ U, y4 E: q3 W7 aof early sexual development. His mother noticed7 I" s4 \( r* y4 \: R6 `
light colored pubic hair development when he was
( p& a5 U! a  |4 O# b, |7 A( zFrom the 1Division of Pediatric Endocrinology, 2University of( _: l0 P1 u  G  L# J- e7 z% ]
South Alabama Medical Center, Mobile, Alabama.1 _" K. y$ f* R( o. Z' x7 `
Address correspondence to: Samar K. Bhowmick, MD, FACE,) n  P; }/ ]2 T6 |2 X7 H- z
Professor of Pediatrics, University of South Alabama, College of
7 ]% j5 F  P2 _4 M/ {& n; rMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
% l9 q( F1 C7 ^$ }; k' ye-mail: [email protected].$ O9 q: ^6 \# L- ?- V6 R- H9 Y
about 6 to 7 months old, which progressively became4 Q. N% j. E# R. g2 Y5 f# t
darker. She was also concerned about the enlarge-
6 D4 A* Y" k1 F3 C) Hment of his penis and frequent erections. The child
) X4 Q" c3 i( e- k. m. Z3 U( ~( ywas the product of a full-term normal delivery, with3 D1 U* b5 H  f" X1 c" Z1 e5 j- |$ ]
a birth weight of 7 lb 14 oz, and birth length of
+ V$ d4 X+ n. Q" K' q20 inches. He was breast-fed throughout the first year) r" }2 ?) n( [: R& a% E8 }
of life and was still receiving breast milk along with0 |) u: [) x5 [( }% ]
solid food. He had no hospitalizations or surgery,
) `0 W2 x# C; `5 [and his psychosocial and psychomotor development' I$ X4 W" x: f3 p+ p6 o
was age appropriate.
) S" @4 u6 D+ _8 n' FThe family history was remarkable for the father,
# U3 v# x( _0 v/ L2 {who was diagnosed with hypothyroidism at age 16,) U# M$ {+ i3 o: V
which was treated with thyroxine. The father’s
6 H, x- R- f: x4 uheight was 6 feet, and he went through a somewhat
) T8 m0 w' w0 K- Q/ yearly puberty and had stopped growing by age 14.+ p, ~: |; i6 a% {9 M: G% [
The father denied taking any other medication. The: ]! w2 c% G6 D+ ~! p
child’s mother was in good health. Her menarche8 P5 o3 w7 A& q& x4 C- v
was at 11 years of age, and her height was at 5 feet( w0 V+ |) s+ Z* y. k4 `
5 inches. There was no other family history of pre-: Y3 M$ n' R  H" W  ?! K
cocious sexual development in the first-degree rela-. o& L  n+ e& m' n+ @
tives. There were no siblings.
# k+ @! y% |: I) E% ^4 @Physical Examination9 r  u$ [* Q$ K( U# V4 [/ \
The physical examination revealed a very active,
8 b5 B+ z# E, {7 W. iplayful, and healthy boy. The vital signs documented
# ~( g( h; b) f( e+ Q0 \1 ha blood pressure of 85/50 mm Hg, his length was  q+ g; _2 I( H9 U) \/ H
90 cm (>97th percentile), and his weight was 14.4 kg: i6 |+ d& U6 P
(also >97th percentile). The observed yearly growth0 I' @5 Q8 r  f0 {& V1 T3 u
velocity was 30 cm (12 inches). The examination of
5 {) d/ K: y9 y9 z$ @. a: o  Ethe neck revealed no thyroid enlargement.9 t. D8 t9 b: J( s2 h* w
The genitourinary examination was remarkable for% B7 g0 O' v6 ~, [0 Q' @
enlargement of the penis, with a stretched length of- A3 v2 R3 S9 i4 F5 }' a
8 cm and a width of 2 cm. The glans penis was very well
- L. p( C! s& w0 [developed. The pubic hair was Tanner II, mostly around. J: B6 D( ^  L8 Y5 h) }: D
540
$ W' I3 O( _1 s, Q* S9 }9 Q: Sat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ ^2 Z. P( J* n! f0 C; P
the base of the phallus and was dark and curled. The
/ a2 R" G& {" Q* ~; M+ u+ Wtesticular volume was prepubertal at 2 mL each.
1 N% ]2 |" I/ sThe skin was moist and smooth and somewhat
6 Q0 q# [4 C2 \& Y2 k3 Zoily. No axillary hair was noted. There were no: m4 O5 D8 V7 T/ A  Z$ t
abnormal skin pigmentations or café-au-lait spots.0 R! H. v0 A! z' T( {0 X1 Q
Neurologic evaluation showed deep tendon reflex 2+' i4 C3 ^' j) M
bilateral and symmetrical. There was no suggestion* f# E" ^6 I& S9 ^4 t, |
of papilledema.3 p5 ?8 P, c7 d* X
Laboratory Evaluation
  A* C0 A0 s# v* v! X1 ]. sThe bone age was consistent with 28 months by, F- I; T6 K. K* v" x' b( j0 p
using the standard of Greulich and Pyle at a chrono-
/ j% d" u. K7 @logic age of 16 months (advanced).5 Chromosomal2 N  T: c: N5 s8 W1 }+ M
karyotype was 46XY. The thyroid function test
/ ?  ^: ~% s3 |9 Bshowed a free T4 of 1.69 ng/dL, and thyroid stimu-/ v& ?. Y: S3 u! g
lating hormone level was 1.3 µIU/mL (both normal).- r3 U! f# Q; D5 f
The concentrations of serum electrolytes, blood2 ^' K/ u# _" y7 n5 J& ~9 V% }
urea nitrogen, creatinine, and calcium all were8 Z7 V* v8 @) A8 m; V
within normal range for his age. The concentration, i" l2 O+ ?  U$ V5 f# o) P4 w( B
of serum 17-hydroxyprogesterone was 16 ng/dL& b# b) g$ ]9 n; d7 Y
(normal, 3 to 90 ng/dL), androstenedione was 200 D* e: s* @6 ~0 H
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
  R: l* d' f# L0 z9 F# i( n2 ~terone was 38 ng/dL (normal, 50 to 760 ng/dL),
7 D6 Z7 ^1 D# l( @* mdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
7 n8 ^5 I  u3 x0 X3 b+ ]49ng/dL), 11-desoxycortisol (specific compound S)# J  @' K; i8 D1 @; k/ m
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-4 D" `- \% g+ N
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
" s7 G/ U" ^) ^3 ttestosterone was 60 ng/dL (normal <3 to 10 ng/dL),5 E/ B' n7 r$ C
and β-human chorionic gonadotropin was less than
  ^/ P8 d' ~$ [/ F5 mIU/mL (normal <5 mIU/mL). Serum follicular
% s; \- t4 ?6 R: Y! ~stimulating hormone and leuteinizing hormone" o" @# f) e1 i
concentrations were less than 0.05 mIU/mL2 o8 c: R1 `, ~2 ^9 b
(prepubertal).
; D7 o5 F3 s# l4 B/ w& Y0 j0 s2 K& aThe parents were notified about the laboratory+ W+ N2 L3 e/ t' v( b
results and were informed that all of the tests were  f& g! K& E0 c
normal except the testosterone level was high. The, [: l7 k- ]+ h) w& Y8 I6 A9 R) ^
follow-up visit was arranged within a few weeks to
* q+ V) s& H, T3 i* A  r, xobtain testicular and abdominal sonograms; how-0 R% I2 O6 V& l" }0 g- S; a. ?
ever, the family did not return for 4 months.1 N: L! ]7 w- \) Y- m; Y9 @0 W
Physical examination at this time revealed that the( j; z& U( q0 ^; H
child had grown 2.5 cm in 4 months and had gained
+ c" O5 u& v1 s5 ?2 kg of weight. Physical examination remained9 J* F$ j- h# q; l8 f- u
unchanged. Surprisingly, the pubic hair almost com-& u) Y7 U  p$ S4 p. {
pletely disappeared except for a few vellous hairs at1 h( K1 \  x  t, {
the base of the phallus. Testicular volume was still 2' S9 R# o' g& j1 Z+ h' ^6 {( v
mL, and the size of the penis remained unchanged.
, t& x- k4 O' u) d  \* X; NThe mother also said that the boy was no longer hav-
4 _6 G. L7 U- aing frequent erections.! b9 m! D4 E. c( k, d; x6 B1 g- n* D
Both parents were again questioned about use of3 f" w3 M' P( {& L6 I
any ointment/creams that they may have applied to
$ Y; Z) }. l  H) r9 P. Ythe child’s skin. This time the father admitted the
) \1 B! f" S2 N- N( lTopical Testosterone Exposure / Bhowmick et al 5411 s9 y8 W" I% J& F# K& Y
use of testosterone gel twice daily that he was apply-
& S0 e9 i8 G# ]3 e5 f" uing over his own shoulders, chest, and back area for
2 l: E+ N& d9 j, F' d, La year. The father also revealed he was embarrassed
" r% o  r: t/ L) Hto disclose that he was using a testosterone gel pre-
9 U  ?+ o7 n& v3 T- v8 F/ I8 G$ Sscribed by his family physician for decreased libido
1 o6 x8 U( S' a) ~8 N$ tsecondary to depression.# n+ i& p- C' t  P, m3 @
The child slept in the same bed with parents.
6 e: F( B$ Y; {! w9 U; jThe father would hug the baby and hold him on his
1 {3 Y/ z2 O( j. R: Zchest for a considerable period of time, causing sig-
; a# ^0 C* I5 z8 fnificant bare skin contact between baby and father.( m- p" B4 q; S
The father also admitted that after the phone call,2 T, J& L9 @$ ^, Q
when he learned the testosterone level in the baby
+ x- x! Z( R. }, M; fwas high, he then read the product information
7 M  g' _* C/ j* z7 Wpacket and concluded that it was most likely the rea-
2 {% J8 ^6 k7 m5 M/ vson for the child’s virilization. At that time, they
# ~4 \# @- i5 {7 J9 x8 m4 Q6 m0 @decided to put the baby in a separate bed, and the5 v# J& O7 j! o* D4 E9 }
father was not hugging him with bare skin and had8 u: j7 c! u! A) S& O2 ^
been using protective clothing. A repeat testosterone* n; h5 D; b( g( Q7 F5 U+ N
test was ordered, but the family did not go to the" f; B9 J* i0 t0 a2 I9 H0 ~
laboratory to obtain the test.: |) M$ t0 V$ n" f' T. V
Discussion
8 S( Z$ h+ }9 C1 @( YPrecocious puberty in boys is defined as secondary
: W: P( L3 P" Ysexual development before 9 years of age.1,4
) }2 P" D5 j8 V0 L. EPrecocious puberty is termed as central (true) when5 V: X6 w$ o" L; d& Q
it is caused by the premature activation of hypo-
* G* s: a- J( s9 c+ X5 V8 Fthalamic pituitary gonadal axis. CPP is more com-* B$ n5 d3 n+ g4 M3 W9 f
mon in girls than in boys.1,3 Most boys with CPP
. I% a& C7 H& Q) c0 I7 H1 f5 smay have a central nervous system lesion that is) r7 x+ v: R. ]2 u9 m
responsible for the early activation of the hypothal-! t( h6 V, t& V$ H/ l1 N- Z: @
amic pituitary gonadal axis.1-3 Thus, greater empha-3 y* w7 Q0 E& y# w# J) i( u
sis has been given to neuroradiologic imaging in; U" w* j/ A  i5 ?* ~% r
boys with precocious puberty. In addition to viril-* Q" S; w% C- Q% x* [. u
ization, the clinical hallmark of CPP is the symmet-2 v* a! A7 h2 r9 j4 P% R
rical testicular growth secondary to stimulation by0 t% R* \  Z0 Z8 r7 J9 ~5 Z
gonadotropins.1,3) n9 H! g7 J/ S
Gonadotropin-independent peripheral preco-
# v1 N5 g7 G9 T, ycious puberty in boys also results from inappropriate1 V9 G7 R& e( s* r% z' O$ @
androgenic stimulation from either endogenous or
& a3 d- f! H- y# o7 W* Texogenous sources, nonpituitary gonadotropin stim-1 q: d* X% H$ W$ V
ulation, and rare activating mutations.3 Virilizing6 G' k) d( y; l0 }5 Z7 o0 s
congenital adrenal hyperplasia producing excessive1 C9 }( g) F: {' z
adrenal androgens is a common cause of precocious
: ~# j) ]) p) {% tpuberty in boys.3,4
$ f7 P2 ?5 V0 UThe most common form of congenital adrenal
, x/ f3 ~! O, K- \hyperplasia is the 21-hydroxylase enzyme deficiency.
" W) y3 a- A  U2 u! ]8 w, HThe 11-β hydroxylase deficiency may also result in' h! S/ Y+ U' c  v; y& B- o4 f
excessive adrenal androgen production, and rarely,) S! X) H& r+ M2 n7 n% o* I
an adrenal tumor may also cause adrenal androgen
2 d2 m! \! H( ]% M* ]* N- G: E5 `: \excess.1,38 Y- u7 e6 q+ Z- ~) M% O
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 Q' R+ B" X2 i! p542 Clinical Pediatrics / Vol. 46, No. 6, July 2007& g2 ]3 s8 ]# Y1 E) U6 h
A unique entity of male-limited gonadotropin-
  X) d: X( J- O6 \' E/ @; Dindependent precocious puberty, which is also known
: B: r6 z, f, T' z3 ^as testotoxicosis, may cause precocious puberty at a6 U, s8 e1 G2 P8 X8 |. X8 \- q8 g
very young age. The physical findings in these boys
0 @# z# b; h( P0 q# v/ lwith this disorder are full pubertal development,
; Z1 p- h3 h. n$ c+ T4 aincluding bilateral testicular growth, similar to boys2 J) Z# ~0 `! A/ K
with CPP. The gonadotropin levels in this disorder
1 `4 U- v; y9 o7 N0 Bare suppressed to prepubertal levels and do not show& w) L  h0 {1 v3 `+ `8 z, ~
pubertal response of gonadotropin after gonadotropin-5 |/ n1 k6 {' H4 J9 H5 r6 V. s
releasing hormone stimulation. This is a sex-linked
+ E% P  h* P: ?- L9 Qautosomal dominant disorder that affects only
# k  t" P3 }2 v; s' I0 W' a' s3 L/ b9 S5 Dmales; therefore, other male members of the family1 t4 u' x) @# b7 l" e
may have similar precocious puberty.32 S- N' S2 ?0 O/ O& F4 \9 s
In our patient, physical examination was incon-
0 H  i- J6 v; X) \" U5 Tsistent with true precocious puberty since his testi-
) \- H2 Z( H# `' Ccles were prepubertal in size. However, testotoxicosis
4 j  J& h  k1 T  o' T6 U" |was in the differential diagnosis because his father
" h4 I( J" k" N% M! l! h( y: Mstarted puberty somewhat early, and occasionally,0 P- O) \7 R+ _" ^, N
testicular enlargement is not that evident in the% _& G0 d1 B- k4 h) q, f
beginning of this process.1 In the absence of a neg-
. ^0 I+ d8 b4 V! z: `1 D; g" qative initial history of androgen exposure, our
" T; R8 i4 h- b6 Kbiggest concern was virilizing adrenal hyperplasia,
% e, e  i% _7 A3 G+ m3 n' xeither 21-hydroxylase deficiency or 11-β hydroxylase2 }% u% l' m! g, {5 S( L$ Z* Y
deficiency. Those diagnoses were excluded by find-8 H7 g, m9 @4 _% ^2 G
ing the normal level of adrenal steroids.
7 ]* D3 n% d# i# z) {! D. vThe diagnosis of exogenous androgens was strongly& u, e: i! u. O- f, T- ^. ~
suspected in a follow-up visit after 4 months because
! t3 y8 J% _6 ]the physical examination revealed the complete disap-$ R% Y/ e+ p# Q6 [, Y( V, C
pearance of pubic hair, normal growth velocity, and7 Y: ]9 T0 B2 l9 ?) w5 y, x
decreased erections. The father admitted using a testos-) O( {( V2 H+ {. k% H9 h
terone gel, which he concealed at first visit. He was
( U: L: g" J' P2 Jusing it rather frequently, twice a day. The Physicians’
( E3 q+ J+ f0 oDesk Reference, or package insert of this product, gel or
4 E4 w5 p7 j( t; C  j- Zcream, cautions about dermal testosterone transfer to
! }8 r' ], \& d7 `( Sunprotected females through direct skin exposure.2 J5 B% t9 R! i2 t
Serum testosterone level was found to be 2 times the
; Z9 z# }3 t3 _4 N+ G5 j" R7 }baseline value in those females who were exposed to4 q' P/ J8 q, |) B% ?- d
even 15 minutes of direct skin contact with their male
8 P# f# {$ E0 L% a/ U( q4 _partners.6 However, when a shirt covered the applica-# K6 V% b, g$ a3 H2 t/ [; B
tion site, this testosterone transfer was prevented.
5 s9 K/ m& P6 d8 d7 R! tOur patient’s testosterone level was 60 ng/mL,0 ^, V% }- G' f. v$ P3 p
which was clearly high. Some studies suggest that
0 K7 ~  y' X. Z6 E) f; ]; N% Vdermal conversion of testosterone to dihydrotestos-( a* V8 z' T, T0 ^! U6 l4 ]: h0 Q
terone, which is a more potent metabolite, is more
* [- ]; o- M  Hactive in young children exposed to testosterone  q) t  }5 M0 s+ Y/ l* D% F# x
exogenously7; however, we did not measure a dihy-2 e+ ]3 q+ T2 k0 @. @: h1 _( i+ d4 E
drotestosterone level in our patient. In addition to' K5 \/ X9 y, C& H
virilization, exposure to exogenous testosterone in6 a! Q3 H4 A6 R2 p# o& n
children results in an increase in growth velocity and
5 v, u( i8 k/ z4 `" Zadvanced bone age, as seen in our patient.; g( ^/ k- U- E" O
The long-term effect of androgen exposure during& |  s  @* j, l& h
early childhood on pubertal development and final
, W& w$ O4 [9 B6 s; r/ g; y# |adult height are not fully known and always remain
$ C; U6 r0 V( Da concern. Children treated with short-term testos-
% T* }; d7 ~2 B1 r' F* Z& V# Vterone injection or topical androgen may exhibit some) q( l6 V* R; S. T
acceleration of the skeletal maturation; however, after
% n- X% Q! X( p* Q# e/ dcessation of treatment, the rate of bone maturation7 v" X  `0 a8 h; ?* ^
decelerates and gradually returns to normal.8,90 e( A8 V0 p5 w5 R
There are conflicting reports and controversy
, p+ ?! H: I% z: e9 n/ c' Kover the effect of early androgen exposure on adult$ F& u+ Z) @8 l2 A+ J
penile length.10,11 Some reports suggest subnormal
) n# D1 U" `: {5 ladult penile length, apparently because of downreg-: D( H; W% p4 @; a4 L
ulation of androgen receptor number.10,12 However,1 E9 Z1 }; l4 h# M3 _, f( s
Sutherland et al13 did not find a correlation between& P( g! t5 K6 U( L
childhood testosterone exposure and reduced adult
/ Z, P7 K: @0 d; j7 R2 }1 c0 K% |6 s, k/ ?penile length in clinical studies.9 V4 Q( s& v: D
Nonetheless, we do not believe our patient is" z  u/ A5 ]% i: w  Y
going to experience any of the untoward effects from
- H. Q1 ^& p, m) G2 Qtestosterone exposure as mentioned earlier because
! Z0 J  u8 b; O; N2 n$ a! cthe exposure was not for a prolonged period of time.+ g( R( _' U5 @$ C
Although the bone age was advanced at the time of/ V+ W0 Y8 m. e) b# x% p+ n
diagnosis, the child had a normal growth velocity at& D* }. L9 o  G$ ~
the follow-up visit. It is hoped that his final adult5 b. R& |2 ]7 `5 n6 k
height will not be affected.7 p9 ^$ [' e& u2 D2 z! |
Although rarely reported, the widespread avail-8 ~1 Z9 d8 |) {( T# J
ability of androgen products in our society may( y4 f& v" _9 ~. r( x! N) d
indeed cause more virilization in male or female2 \( k( |) D4 z( A
children than one would realize. Exposure to andro-
8 a% {. a" n7 vgen products must be considered and specific ques-
4 V7 S/ m+ [  I: gtioning about the use of a testosterone product or
8 k% r: ^; P' Y7 F  Jgel should be asked of the family members during: j! S) C4 l3 ]) \, l' S& K0 G
the evaluation of any children who present with vir-+ V* E, g% L8 {2 {/ t
ilization or peripheral precocious puberty. The diag-
4 x+ u+ N; |  nnosis can be established by just a few tests and by# o# P. s# t% X" J8 O, Z) D8 X
appropriate history. The inability to obtain such a
0 V- q3 |, s: A, thistory, or failure to ask the specific questions, may
: G6 }; ~) \5 c2 Y! \6 h' Nresult in extensive, unnecessary, and expensive
4 \% N; f9 j% \( z5 c- m  J/ Xinvestigation. The primary care physician should be' z& }* U  l8 W1 ?( `6 j) {7 D
aware of this fact, because most of these children1 ?6 r& N& }# a$ B( F' U
may initially present in their practice. The Physicians’, p2 p4 w; o9 X6 H& ]) _. z
Desk Reference and package insert should also put a
! ?, p" p/ H" }1 v4 [# E& Pwarning about the virilizing effect on a male or
& V# p- {7 K. k! |$ efemale child who might come in contact with some-
' E$ Y6 N, F- N2 D. k1 _2 r0 Gone using any of these products.  m. V3 }& D" v& ^. z1 t8 k
References- q8 u9 Y; V$ |" h
1. Styne DM. The testes: disorder of sexual differentiation. Y  b9 W' K$ m# p6 _1 T
and puberty in the male. In: Sperling MA, ed. Pediatric
" D9 m( y- c- HEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;# P5 R( a, m' n% P' g& A
2002: 565-628.5 c; C2 f' h' A8 l3 X2 u2 ~
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; x# }: F! G) w% r4 C5 l
puberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
3 O9 {4 @  f5 a+ Z
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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