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Sexual Precocity in a 16-Month-Old
% u2 S3 i  I3 o) u0 j  BBoy Induced by Indirect Topical
. m* ]' ~2 a4 d" ~# G4 X! E; Z  R) WExposure to Testosterone- D3 K) @4 {8 F: l# y) E0 c
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 q& e* L% [- w: q) y- ^1 X4 ~8 Pand Kenneth R. Rettig, MD1
. `! m) Z# J* l1 I- _1 X2 }Clinical Pediatrics
1 H& }+ D9 w- E6 C0 B: yVolume 46 Number 6( I# {9 z) f# C. x$ m
July 2007 540-5437 V- l2 ^2 c, Z3 ^$ m8 j4 o
© 2007 Sage Publications
6 V/ Z! G8 Z. ]% N$ k10.1177/0009922806296651
& Y5 g- l- L( ?9 I$ w  y- O& d; P+ Shttp://clp.sagepub.com' {" G' v% Y. ]7 D4 u1 r7 ~
hosted at/ W0 s8 H; o! A  y
http://online.sagepub.com
; w# ^, h/ q' g0 ^Precocious puberty in boys, central or peripheral,
4 U4 R2 C2 }  _2 T" F0 O+ f6 qis a significant concern for physicians. Central6 ~- F4 Z+ E. |
precocious puberty (CPP), which is mediated+ s0 V6 }9 ~8 r
through the hypothalamic pituitary gonadal axis, has9 v4 U; A! t7 A1 u6 i) G
a higher incidence of organic central nervous system
, k+ U7 p5 I& u# T7 olesions in boys.1,2 Virilization in boys, as manifested
6 j# b0 p' Z& rby enlargement of the penis, development of pubic
1 p2 ?) }2 [  f5 H$ S; @" yhair, and facial acne without enlargement of testi-
% u9 b$ l+ W0 H* v; a$ F1 @$ V* zcles, suggests peripheral or pseudopuberty.1-3 We
) L1 M2 S9 N) C, X* ~% U- creport a 16-month-old boy who presented with the
) r" v( S8 q. S! h( k' u, U9 \enlargement of the phallus and pubic hair develop-) n* h* B) I. E* T
ment without testicular enlargement, which was due2 o; Q* m+ {& m2 @' S
to the unintentional exposure to androgen gel used by
9 B; f  o  V+ Q  @& J7 ?the father. The family initially concealed this infor-( S0 N$ V0 j( m3 l
mation, resulting in an extensive work-up for this
4 G. U# R) D5 Dchild. Given the widespread and easy availability of
' d5 ]: _. D4 e* {( Xtestosterone gel and cream, we believe this is proba-
; l# k* _: `" W1 ~6 S* O$ o% J. V, Dbly more common than the rare case report in the
  G8 z3 a) e5 L, a+ @% X' Bliterature.4
  F6 }0 d( |" ^$ N3 u4 C$ SPatient Report
3 W# E' t2 x: p# j2 X7 @0 UA 16-month-old white child was referred to the2 G! Y/ S! a1 _
endocrine clinic by his pediatrician with the concern
. ]# K3 |  t7 P" Y" b0 A8 i1 Yof early sexual development. His mother noticed* p/ P9 h$ ]& Z6 D2 e. U& ^" A
light colored pubic hair development when he was
( ]( h  H/ X! Y$ b( H) DFrom the 1Division of Pediatric Endocrinology, 2University of
7 W# g. a2 f. NSouth Alabama Medical Center, Mobile, Alabama.& I6 C- u5 g3 k5 y+ G% N- O
Address correspondence to: Samar K. Bhowmick, MD, FACE,! z3 @2 i" o& y9 {
Professor of Pediatrics, University of South Alabama, College of
, ^4 W/ g+ m" T, H" z7 ]Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;' i$ Z% P) k8 S" e2 U
e-mail: [email protected].0 \1 R) O" R* Z# n5 _2 d& W7 R+ q
about 6 to 7 months old, which progressively became! f7 J. p, m+ h# u
darker. She was also concerned about the enlarge-2 l4 Y* Y/ j% u
ment of his penis and frequent erections. The child
. h0 ]; i# X1 bwas the product of a full-term normal delivery, with: R2 g0 N" f7 W0 l' G: @
a birth weight of 7 lb 14 oz, and birth length of
7 z1 o6 e: N9 O  G0 I7 D# J: s20 inches. He was breast-fed throughout the first year4 o8 |, T  f# g' ?! d' ~5 q9 d2 X: K
of life and was still receiving breast milk along with
) w' v* s- z: Y% X/ z7 F' Csolid food. He had no hospitalizations or surgery,' ]7 r/ N: N2 v  y* B6 I* n
and his psychosocial and psychomotor development
! M; \% X% x$ i& t# U$ twas age appropriate.
, |: `9 M1 L" A, @7 n/ b4 Q7 yThe family history was remarkable for the father,
% d0 e9 t- I9 I5 s5 b% vwho was diagnosed with hypothyroidism at age 16,
1 I) Z- m8 L% L3 ~which was treated with thyroxine. The father’s1 K' H/ V$ t; o5 Z
height was 6 feet, and he went through a somewhat" V3 y& l8 |# g3 P& G! ^  I# O  n
early puberty and had stopped growing by age 14.4 w7 Y/ ^) X0 ^# s6 B  V# D) s1 V
The father denied taking any other medication. The
  C) P2 L3 `8 o7 [child’s mother was in good health. Her menarche% s: j( m9 E4 o1 i, o$ S" y! [( ~
was at 11 years of age, and her height was at 5 feet
# r2 @; C6 ?, i% |2 W5 inches. There was no other family history of pre-4 @9 s! A3 s, ^
cocious sexual development in the first-degree rela-: f6 M9 l2 n# T+ h
tives. There were no siblings.3 |( p& w/ L  k) W' T+ @
Physical Examination
9 r2 I& l: B# C2 bThe physical examination revealed a very active,7 A7 E7 t7 }2 f- M! C8 I" @
playful, and healthy boy. The vital signs documented
0 G: z1 B  J# k  h4 la blood pressure of 85/50 mm Hg, his length was
- a/ ?" u$ r% D9 x90 cm (>97th percentile), and his weight was 14.4 kg
7 }! D! C. \: q4 t(also >97th percentile). The observed yearly growth! A9 L: C0 v5 N% D1 G. k1 y
velocity was 30 cm (12 inches). The examination of7 d, m3 D. M- I; z" q6 S; E5 _
the neck revealed no thyroid enlargement.
* G+ Y  ~( M& A6 }1 XThe genitourinary examination was remarkable for! D+ a! [) a! t2 |5 U9 q* b! q; c7 m
enlargement of the penis, with a stretched length of
0 w+ {. b" S; u' q& n! w/ h8 cm and a width of 2 cm. The glans penis was very well
# t8 l, r5 l# d3 s" a. `developed. The pubic hair was Tanner II, mostly around( ]- a# V9 q$ G, n& S
5404 L2 ?8 _* k" d$ q8 k
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 Q9 y4 H4 j  q3 Q: d& Bthe base of the phallus and was dark and curled. The( j7 ]) Z3 x7 K+ n
testicular volume was prepubertal at 2 mL each.
" Z4 m" S, D! \& w% M9 a' xThe skin was moist and smooth and somewhat
# s7 [1 @6 C% loily. No axillary hair was noted. There were no
% l  r5 u- J4 ?abnormal skin pigmentations or café-au-lait spots.* G% i( C- w- Y& R4 `
Neurologic evaluation showed deep tendon reflex 2+3 L# J! ^1 X  r; b
bilateral and symmetrical. There was no suggestion! L" Q" f% M6 P
of papilledema.: X: {. X" E5 ?" r, l1 \6 P8 E* M
Laboratory Evaluation0 c4 o9 a! R( M& V
The bone age was consistent with 28 months by0 K8 r! l3 X0 E! d2 b/ c" m6 Y
using the standard of Greulich and Pyle at a chrono-/ N& u5 @, C' x3 w8 ?6 w# `, P
logic age of 16 months (advanced).5 Chromosomal
, r* I) l! Q! o. Q0 j% R( ykaryotype was 46XY. The thyroid function test4 l  z7 Z8 T, n+ }
showed a free T4 of 1.69 ng/dL, and thyroid stimu-- a! o7 H+ ]" G# p( Z
lating hormone level was 1.3 µIU/mL (both normal).
) i8 D6 Z; w2 N" B5 o% k) G7 r2 FThe concentrations of serum electrolytes, blood
  V- _4 p" H* x- V+ ~2 s2 ?5 hurea nitrogen, creatinine, and calcium all were! K, E' o. M2 v0 \/ o1 T
within normal range for his age. The concentration
3 W+ C8 s9 h; u4 I* lof serum 17-hydroxyprogesterone was 16 ng/dL' h) r0 D7 Z7 M. n' F7 q
(normal, 3 to 90 ng/dL), androstenedione was 20
% n& |$ C1 j8 v2 cng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-: F) \6 x3 O/ J' C5 d
terone was 38 ng/dL (normal, 50 to 760 ng/dL),( F$ Z" i+ S) {1 z+ G! \
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
  J& v3 c# i" z49ng/dL), 11-desoxycortisol (specific compound S)
/ Z, H" U  i, h+ w/ K. ?was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-3 y. w# K1 x# N- W) E
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total8 t1 [- N  Y& D' i9 S' l
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),0 B2 P! O/ Z9 r+ [# B
and β-human chorionic gonadotropin was less than9 L8 Y; y( s, |- K1 z
5 mIU/mL (normal <5 mIU/mL). Serum follicular/ M8 ]& R% M' n3 _1 a
stimulating hormone and leuteinizing hormone3 g. d4 c9 k% p" C
concentrations were less than 0.05 mIU/mL
3 Z# W; w7 Y% H  G/ r7 w2 c" w(prepubertal).
+ {4 p3 \" [6 L; [The parents were notified about the laboratory1 K; B) S6 h) [# P  T, F  V/ K5 h
results and were informed that all of the tests were, h$ P. x+ q2 Z' ?" I+ P: u9 w  l
normal except the testosterone level was high. The" [+ c$ P( @7 i- C+ J
follow-up visit was arranged within a few weeks to) C$ ~! e+ O1 `; J8 t3 B
obtain testicular and abdominal sonograms; how-
, d+ R: [2 ^+ K$ y1 ~ever, the family did not return for 4 months.
& y" y' J% O; {) J  u. HPhysical examination at this time revealed that the2 X8 n( q* V- t+ \1 y8 l, |
child had grown 2.5 cm in 4 months and had gained  ]; I' x0 w  c" ^
2 kg of weight. Physical examination remained
' ^7 |  U1 _3 F0 S3 _/ ounchanged. Surprisingly, the pubic hair almost com-  D2 f2 O/ ^8 j8 Q4 e
pletely disappeared except for a few vellous hairs at4 T3 t" ]3 w' A0 F) i
the base of the phallus. Testicular volume was still 2
/ B; c: N5 P$ |& I. l: kmL, and the size of the penis remained unchanged.
, A- F4 T. N7 rThe mother also said that the boy was no longer hav-# E: C5 X2 _) l0 b5 Z* H
ing frequent erections.* |& Q4 M; |3 |4 U) T
Both parents were again questioned about use of
! Q8 c$ x+ F# ^) M+ iany ointment/creams that they may have applied to
. x8 I% k3 B! Q. F/ f# Y9 ^the child’s skin. This time the father admitted the- \8 v6 v" [; S% l  k8 A: m
Topical Testosterone Exposure / Bhowmick et al 541
" U8 I' `4 O+ y5 G1 wuse of testosterone gel twice daily that he was apply-
- Z7 K/ w; A% ?1 l: ving over his own shoulders, chest, and back area for
8 u5 \, K9 z  L+ Ca year. The father also revealed he was embarrassed
6 ]. M9 M! w' a+ |- `to disclose that he was using a testosterone gel pre-+ x' v, v* ?1 c+ d/ U3 X
scribed by his family physician for decreased libido
5 X. E( k! U! o+ q: X! s# Osecondary to depression.! R* W: A" A2 e$ v6 f4 w
The child slept in the same bed with parents.4 v; K2 G" v3 p, M
The father would hug the baby and hold him on his
4 A/ M  @$ E$ l3 r0 V8 Z6 m4 ychest for a considerable period of time, causing sig-+ M2 U7 U$ J3 [# O! H. D0 e0 Y& T
nificant bare skin contact between baby and father.
+ Q4 }/ G. q  `- z+ {3 R- W8 U6 v4 UThe father also admitted that after the phone call," [: A8 L% W- J% |7 T, a
when he learned the testosterone level in the baby2 o1 `7 g! O* `% e0 i6 y9 u/ ]
was high, he then read the product information
5 e. {% X0 {6 x  |  U$ j$ Q- xpacket and concluded that it was most likely the rea-7 c7 v2 c+ e& d( y
son for the child’s virilization. At that time, they5 y$ a! j* k) k- X. `* v$ t
decided to put the baby in a separate bed, and the* a/ l' [& x+ @1 V1 @
father was not hugging him with bare skin and had! b8 I1 w. g- N* P% E- w
been using protective clothing. A repeat testosterone( u" L/ d: M0 n+ C; j3 G
test was ordered, but the family did not go to the6 k1 W# ^. u& L
laboratory to obtain the test.
2 m/ v$ |# K# u! p% B  G: yDiscussion+ {( F: I2 I$ B8 h
Precocious puberty in boys is defined as secondary. K/ f0 B8 d/ v6 A3 y
sexual development before 9 years of age.1,4
+ C! @7 `& K5 Z* `) h6 J0 Y2 F+ |Precocious puberty is termed as central (true) when5 W& d3 y7 ~! T- N
it is caused by the premature activation of hypo-$ Q: E, K' j, V
thalamic pituitary gonadal axis. CPP is more com-/ c9 o# U6 P: S. B2 U. ]
mon in girls than in boys.1,3 Most boys with CPP8 @' B9 g& S3 Z7 A
may have a central nervous system lesion that is
# R0 w; i) v1 ~/ X- m% J, Oresponsible for the early activation of the hypothal-
+ [. b8 q! I/ T; C2 Pamic pituitary gonadal axis.1-3 Thus, greater empha-
, Z; @& {% |( h* w& o. xsis has been given to neuroradiologic imaging in
! z. k6 B% g: r4 J8 oboys with precocious puberty. In addition to viril-4 y: G' D) }1 \/ C+ @
ization, the clinical hallmark of CPP is the symmet-! O! t) e1 U8 R
rical testicular growth secondary to stimulation by
0 y% L2 e5 Q! l- b, Ogonadotropins.1,3" B5 ?% X" ^- h! e9 m
Gonadotropin-independent peripheral preco-- [+ d  c2 x: }& W% j  a
cious puberty in boys also results from inappropriate
/ M8 d; x9 `. u0 |7 d8 J2 vandrogenic stimulation from either endogenous or
8 ~" C) S! n" l% ^exogenous sources, nonpituitary gonadotropin stim-
! s( g$ u" K) ~4 ]ulation, and rare activating mutations.3 Virilizing
6 V' z8 C5 a. W" o& h' g' C+ zcongenital adrenal hyperplasia producing excessive
6 O  U4 P3 e0 s$ h9 m; y# Dadrenal androgens is a common cause of precocious+ d6 _: M! `& Q! [, ~& p/ ~6 u
puberty in boys.3,4
/ F' B# {9 r2 f5 w' {9 L  ^8 iThe most common form of congenital adrenal4 j$ s2 G3 o( ?  V2 {2 a+ C
hyperplasia is the 21-hydroxylase enzyme deficiency.
! q! U: z* z  R: A. z- G7 a1 [# M) VThe 11-β hydroxylase deficiency may also result in
+ Y, M5 X1 O- W. ^& Mexcessive adrenal androgen production, and rarely,1 }* ^9 S1 |* l: n6 X& @9 D- j
an adrenal tumor may also cause adrenal androgen
7 }7 X2 i% j4 sexcess.1,30 G7 v. S7 A( ^0 P% |
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ Y2 k3 H" [9 C7 h8 k542 Clinical Pediatrics / Vol. 46, No. 6, July 2007% O6 i  U% J/ d  T# g+ T) f
A unique entity of male-limited gonadotropin-
8 i0 d" s2 q/ c* c' _6 [independent precocious puberty, which is also known
# ~7 I6 \& Z# F- Das testotoxicosis, may cause precocious puberty at a# ^! x  U, K; @4 l0 c, N+ C5 O
very young age. The physical findings in these boys( |6 N+ S5 c  q' q
with this disorder are full pubertal development,# \; V' y2 r# ^% w" G! j$ n
including bilateral testicular growth, similar to boys
; K  {$ b1 z: Y  z: A+ c7 Bwith CPP. The gonadotropin levels in this disorder
: W  L. ~2 a* J; L4 d  @8 \are suppressed to prepubertal levels and do not show- f0 \' i4 h  P$ Z
pubertal response of gonadotropin after gonadotropin-# B1 n- f8 Q" g$ @+ @7 u( x" A
releasing hormone stimulation. This is a sex-linked8 a# l, r: q3 d# F7 n8 N
autosomal dominant disorder that affects only
4 L1 q+ k7 P9 d" M* fmales; therefore, other male members of the family
& ~$ p: X5 K- T0 ~  n! T  jmay have similar precocious puberty.3
4 G. N6 N3 }. T" z! dIn our patient, physical examination was incon-4 ~  ~3 X  j- Z' R- D! @
sistent with true precocious puberty since his testi-! Y; A: f% k9 Z/ f
cles were prepubertal in size. However, testotoxicosis6 L, _  M: ^, x& Z( h
was in the differential diagnosis because his father: M0 ]" }7 }) V. u
started puberty somewhat early, and occasionally,$ B2 R$ z0 V7 w
testicular enlargement is not that evident in the
" E# J! f. b- _7 T% Kbeginning of this process.1 In the absence of a neg-% E7 w' L' q) ?' Z
ative initial history of androgen exposure, our
4 |1 G8 q* x/ ?: j1 R( vbiggest concern was virilizing adrenal hyperplasia,
$ D! F5 N" [) z& {) \: Deither 21-hydroxylase deficiency or 11-β hydroxylase; |$ I9 H0 {8 d/ K" q8 ~# w6 I
deficiency. Those diagnoses were excluded by find-* w+ t& v. @! o4 G9 p8 {% O2 V
ing the normal level of adrenal steroids.; t/ [4 ~9 Q7 y; H6 R& f
The diagnosis of exogenous androgens was strongly
9 p* U! @$ Y' M7 I, L: W* C8 Tsuspected in a follow-up visit after 4 months because
+ L1 {2 G/ L- X' i& Fthe physical examination revealed the complete disap-6 a" W  p% q9 u: `& m* V) a
pearance of pubic hair, normal growth velocity, and5 {9 o6 \4 W# _9 c! Q% I3 p
decreased erections. The father admitted using a testos-
! c' R, c6 V& i1 d7 E7 q. `, W" T8 xterone gel, which he concealed at first visit. He was
2 q2 j; X9 _8 G8 T' v1 Ausing it rather frequently, twice a day. The Physicians’
, W  G& b4 k/ i" i" k; z2 ADesk Reference, or package insert of this product, gel or
* L+ r2 e2 f. ocream, cautions about dermal testosterone transfer to' P- e4 Y1 @* B% ]# w
unprotected females through direct skin exposure.  [0 L( a2 ]' i7 C2 L
Serum testosterone level was found to be 2 times the
! j# B/ S/ U. G4 p1 G" Kbaseline value in those females who were exposed to
. b% \, m, C* Q: J3 a$ [even 15 minutes of direct skin contact with their male6 P5 `3 d! t8 n, A
partners.6 However, when a shirt covered the applica-
$ z. j- f. g  f. q6 v% b" Ution site, this testosterone transfer was prevented.$ O4 j4 H1 e  B3 x) L
Our patient’s testosterone level was 60 ng/mL,$ ^- v- ?( Y; r$ W" K! E% Q
which was clearly high. Some studies suggest that3 ]" h3 h; ]) P6 ]. W; E) o
dermal conversion of testosterone to dihydrotestos-$ C$ s: i4 `; A8 D& Y
terone, which is a more potent metabolite, is more  x" ~$ u, r+ W- @, z6 F, w$ `+ ~  r
active in young children exposed to testosterone' V% T) k/ d  o  W3 b0 ~
exogenously7; however, we did not measure a dihy-
4 p1 G0 ?4 U5 p6 k6 a5 s1 `drotestosterone level in our patient. In addition to# Y1 T8 {/ O" @  Z) b7 b  H8 p& M
virilization, exposure to exogenous testosterone in. N7 Q; d' j; `' }- d
children results in an increase in growth velocity and; w+ f6 R/ L. \; E8 @3 C
advanced bone age, as seen in our patient.
* w( Q1 ]( |. @( u) P# w/ Y0 k7 TThe long-term effect of androgen exposure during0 z5 w' p1 |4 q% P
early childhood on pubertal development and final
1 t2 I' m2 v; B- e) ^+ O& ~adult height are not fully known and always remain+ r, K/ s. v& {7 A8 c) a: G
a concern. Children treated with short-term testos-& Y: @8 Y5 E1 w3 f' j# B
terone injection or topical androgen may exhibit some9 X& b+ @' |  t- M0 }. y
acceleration of the skeletal maturation; however, after8 M7 N: b- u/ @$ o, T
cessation of treatment, the rate of bone maturation' F9 m3 |; l8 U' F& K
decelerates and gradually returns to normal.8,9
4 r, q+ @' s* O$ w' }There are conflicting reports and controversy
4 n( @  w* ~+ P+ P3 t; z1 _0 Dover the effect of early androgen exposure on adult
3 X# L: S1 l/ p, b0 I& {penile length.10,11 Some reports suggest subnormal2 i9 z0 I+ k2 E% V
adult penile length, apparently because of downreg-
1 a6 _- z4 w1 H" rulation of androgen receptor number.10,12 However,
" D) S6 D. k9 z* j4 aSutherland et al13 did not find a correlation between. M. T6 n0 L6 c0 P
childhood testosterone exposure and reduced adult
0 h+ n% u  K6 ~3 T) j6 a9 B5 ]penile length in clinical studies.
% V- @/ k0 {0 u! u8 M" JNonetheless, we do not believe our patient is
! k- R+ g/ |, g/ D: H0 ygoing to experience any of the untoward effects from$ l* [5 {! n6 }) p0 @% T4 T& a
testosterone exposure as mentioned earlier because
; {4 A% i3 A' b* }the exposure was not for a prolonged period of time.  x/ m/ L; ~1 \
Although the bone age was advanced at the time of' J. O' n7 T! ?  k; l# b
diagnosis, the child had a normal growth velocity at
2 g  Z: s' c+ I. |( C- F, u5 Wthe follow-up visit. It is hoped that his final adult3 P- I$ D! f- y& _
height will not be affected.6 _3 V5 p6 X' ?
Although rarely reported, the widespread avail-! M& @5 ?7 p3 w! F, o
ability of androgen products in our society may' x0 l2 \* e- m: y
indeed cause more virilization in male or female8 d% {+ D3 W2 u$ l
children than one would realize. Exposure to andro-% \7 r) T& K& t* a' |. Y3 J
gen products must be considered and specific ques-' |: D/ s9 v" m& r( h* S
tioning about the use of a testosterone product or
1 y% f0 i# h0 \, a& A% d+ u) ]gel should be asked of the family members during
% B2 t  @; ]$ k' pthe evaluation of any children who present with vir-8 T2 U0 J" V& S8 L
ilization or peripheral precocious puberty. The diag-
% l- c2 G. h* S* _! D7 L2 vnosis can be established by just a few tests and by/ ?* V3 g# e: K
appropriate history. The inability to obtain such a
  i) Y! z) b% }# ^history, or failure to ask the specific questions, may" M. A& y" c0 r1 w' s+ M% V8 f: f7 H
result in extensive, unnecessary, and expensive
) S& d8 N; u. ~& d5 v+ Yinvestigation. The primary care physician should be
+ v3 B, m' W% G7 s9 n; ~5 G. f7 o6 \3 _% waware of this fact, because most of these children7 v5 [; F3 K0 r
may initially present in their practice. The Physicians’8 A. T4 u' x6 `
Desk Reference and package insert should also put a
3 _/ S% F. X0 J5 @  J! [) \warning about the virilizing effect on a male or+ t: U4 F, E- ^
female child who might come in contact with some-% w% y4 D2 D3 M( x  e  e' Q
one using any of these products.. h5 Y- T/ }* q2 S, G
References1 v$ N4 w! e) A# y1 G- r
1. Styne DM. The testes: disorder of sexual differentiation
% I: ]& N/ P8 pand puberty in the male. In: Sperling MA, ed. Pediatric1 X" ?; r3 m' y$ {$ P: Z
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
( F, M/ M& P' e- F( F8 Z2002: 565-628.! E6 ^( R; P+ h% c0 f6 w, b
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
7 @( E" g5 j/ F' B3 i1 ~puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
4 J& C: }* L: b( IBoy Induced by Indirect Topical
  Y+ l% N4 y+ MExposure to Testosterone
% W* f2 t4 f- s7 v) D& i$ ~Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
2 ~5 y9 f2 F7 V7 x" fand Kenneth R. Rettig, MD1& d9 E- I/ O0 [# I- _
Clinical Pediatrics& B, ^6 B8 i/ s3 a* m8 {, _$ N2 _- u
Volume 46 Number 6& @. m4 Y6 U) L, i6 b8 U
July 2007 540-543
3 k% l/ B& {# l9 a6 t6 I0 ~© 2007 Sage Publications
. F9 O+ f, a( Z8 W1 `10.1177/00099228062966510 q" R) C7 \; c8 [3 G
http://clp.sagepub.com
# H% u: j  x  R- P8 Z' a. Shosted at9 g, W+ a4 O% n3 q
http://online.sagepub.com
, H( g% D" N2 L! J0 p! |  RPrecocious puberty in boys, central or peripheral,
7 I3 y( X( n% _% Z$ \3 G( ?" \6 tis a significant concern for physicians. Central
3 M, H8 ?/ [* Bprecocious puberty (CPP), which is mediated! {. N( ]  X8 I
through the hypothalamic pituitary gonadal axis, has& _; ]) h/ G7 b2 w( u
a higher incidence of organic central nervous system+ J9 U2 ~& ]- X$ T' H
lesions in boys.1,2 Virilization in boys, as manifested0 `) O, n! E8 T# R" m& P. m- W
by enlargement of the penis, development of pubic: z3 s. r* P# v: {$ m9 I2 h+ e% @
hair, and facial acne without enlargement of testi-2 w/ A- x0 U4 l. q7 Y) l6 w
cles, suggests peripheral or pseudopuberty.1-3 We
5 _" A' c9 w& W* J( freport a 16-month-old boy who presented with the
* d' k1 S, e- h; s8 {+ `. Lenlargement of the phallus and pubic hair develop-
  H8 L" z; t( D/ G# P" ament without testicular enlargement, which was due2 B# |. q# m1 `8 D* B0 e! v
to the unintentional exposure to androgen gel used by
% h, `! p& U0 b  d; zthe father. The family initially concealed this infor-- p* N' |! \- G/ c' r
mation, resulting in an extensive work-up for this
" h" u5 T+ h9 c3 B! i0 S4 e7 O$ tchild. Given the widespread and easy availability of
/ y# q9 ?# l/ X5 g9 ?4 j8 b1 ~testosterone gel and cream, we believe this is proba-( ]1 M& M, y& P+ @
bly more common than the rare case report in the. i5 d3 `1 u! Q* c: D
literature.4
3 y2 [& K( S2 u9 z6 B3 OPatient Report
9 ]9 Q& }  d6 a+ z( s6 F) Z1 T5 ^A 16-month-old white child was referred to the
. k/ z- Y; E$ y% ]* D' {endocrine clinic by his pediatrician with the concern
4 r' W4 F) d# o9 n2 I# pof early sexual development. His mother noticed
; s; [1 d! E: X( {light colored pubic hair development when he was( y! k$ }5 B8 v- a3 f
From the 1Division of Pediatric Endocrinology, 2University of
% P8 T0 d3 ], j* n) |South Alabama Medical Center, Mobile, Alabama.
) k" |8 o0 O0 q$ }$ P2 Z6 ?" yAddress correspondence to: Samar K. Bhowmick, MD, FACE,
# _2 X! u# a$ C8 P# HProfessor of Pediatrics, University of South Alabama, College of, }- u5 X1 x* m) ~3 U* y; {8 h
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
  b7 l# j) @3 y* X+ }; c3 `e-mail: [email protected].0 X. O% W3 }2 p2 @6 L
about 6 to 7 months old, which progressively became6 H/ F$ K& w! O$ u- J
darker. She was also concerned about the enlarge-0 B! s; R5 z4 q" p/ _: p& ?- m
ment of his penis and frequent erections. The child% |4 h, G$ ^: P; V
was the product of a full-term normal delivery, with
1 n) K3 A& g( C5 d$ P) @: v, H4 H1 Ya birth weight of 7 lb 14 oz, and birth length of/ G9 v+ ]# w, V" B9 I3 s! T( \
20 inches. He was breast-fed throughout the first year
, P8 R- q2 I6 gof life and was still receiving breast milk along with
7 C8 [) i" l5 {solid food. He had no hospitalizations or surgery,5 w  A+ Q" n- H8 \( k
and his psychosocial and psychomotor development
8 M. G; ^6 x* v; ^, ~was age appropriate.6 _3 L/ G! W% w6 R; i6 i
The family history was remarkable for the father,
* C' ]+ j8 b) swho was diagnosed with hypothyroidism at age 16,
4 ]- {+ l, p7 I+ s% M7 ?% O' {which was treated with thyroxine. The father’s& c- G$ z, M$ v5 @2 u) w% c
height was 6 feet, and he went through a somewhat" i, B& Y. O2 ^) _5 u* u9 u8 H
early puberty and had stopped growing by age 14.* f+ j# P( N4 N6 O( o; ^
The father denied taking any other medication. The, I  H- j# M5 s# _9 D
child’s mother was in good health. Her menarche
* m# a3 N! }8 l2 ]was at 11 years of age, and her height was at 5 feet8 U. ^0 s1 v. D8 g% N6 Q
5 inches. There was no other family history of pre-4 ~" e! f* V1 c2 L2 q9 F
cocious sexual development in the first-degree rela-
+ T. B% v4 x' _! X* d( I0 J+ \4 Gtives. There were no siblings.
2 P: \" W( N6 S; L% ^Physical Examination$ m: {0 {0 i2 z8 i
The physical examination revealed a very active,! \# h5 X4 [  i; B& Y
playful, and healthy boy. The vital signs documented- Y4 _' ^. |" d  y/ ^+ N
a blood pressure of 85/50 mm Hg, his length was$ ]8 j: L& r6 h* U( k
90 cm (>97th percentile), and his weight was 14.4 kg
" Z. c6 |1 [2 Q6 o5 [(also >97th percentile). The observed yearly growth
6 ]7 ~/ m) Y7 jvelocity was 30 cm (12 inches). The examination of& n9 o) q2 F; _9 `
the neck revealed no thyroid enlargement.
. ~7 T8 J7 K. {, F4 FThe genitourinary examination was remarkable for
% G) o9 Y) o- Z3 ?" \! N9 t5 k9 |" henlargement of the penis, with a stretched length of
: o7 V; n% w0 E2 A5 R- ?8 O8 cm and a width of 2 cm. The glans penis was very well! j+ @) U" ], m: m) \0 p
developed. The pubic hair was Tanner II, mostly around6 o0 p9 f$ s, V7 \$ d  R( G
540/ E2 ^) h1 w5 c8 [3 r% A
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: Y) n& j. q. B$ R: l! `the base of the phallus and was dark and curled. The: W( R9 U4 H2 ?* ?. X5 U1 ]
testicular volume was prepubertal at 2 mL each.1 H/ S( ^, m# e
The skin was moist and smooth and somewhat
! M% H; o' N2 \$ D1 I# n+ Woily. No axillary hair was noted. There were no/ A! k6 B8 j: g: F
abnormal skin pigmentations or café-au-lait spots.! g+ _' |! m# M4 n/ l: z. B( S
Neurologic evaluation showed deep tendon reflex 2+
7 |6 X. x" |8 d! a: u. w( J& @bilateral and symmetrical. There was no suggestion$ M- [' U( t' Y% N  f* ]0 h3 N
of papilledema.  o" y/ N3 u( W; h3 O, s
Laboratory Evaluation
  l( E" h. s( J) m1 {The bone age was consistent with 28 months by
  L. G' G% k/ |using the standard of Greulich and Pyle at a chrono-
! G! b- L8 x3 Z+ ]3 _+ H, l+ `' |logic age of 16 months (advanced).5 Chromosomal
4 G1 w9 X. L+ F: e6 T) W: Wkaryotype was 46XY. The thyroid function test9 V$ b& M. b* B% N0 j6 C1 j4 J
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
6 t8 h& w& J: V& @lating hormone level was 1.3 µIU/mL (both normal).. W, r( Q4 n2 z9 Y8 Q
The concentrations of serum electrolytes, blood
/ D- e7 S+ h. `9 f: Yurea nitrogen, creatinine, and calcium all were6 Y( I6 Q0 |7 _  R6 r
within normal range for his age. The concentration: c/ z& J( Q' B' J2 ~1 Y
of serum 17-hydroxyprogesterone was 16 ng/dL7 O4 {; U& s+ q! |6 [
(normal, 3 to 90 ng/dL), androstenedione was 20, u; R0 L* f+ \0 ~
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-" ^# h+ p1 j5 c  p8 ~
terone was 38 ng/dL (normal, 50 to 760 ng/dL),* }" a+ ?* D/ D, n
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
3 T+ i8 A$ w$ Z49ng/dL), 11-desoxycortisol (specific compound S)& D  @+ b& Z  n3 o
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
& [' p1 D2 @5 b5 P$ Otisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total0 S8 U% D# ^7 d3 a, B! [
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
$ G6 z3 t" J( S5 [and β-human chorionic gonadotropin was less than( u- F" y. \. W" b
5 mIU/mL (normal <5 mIU/mL). Serum follicular4 O- A/ U* E1 D
stimulating hormone and leuteinizing hormone
$ o) v8 g1 t3 @; M4 t" `concentrations were less than 0.05 mIU/mL
0 q: n5 O! W0 i5 p, R2 ]0 R(prepubertal).
! f8 m, }2 i2 U! WThe parents were notified about the laboratory
. _* s$ p# \) tresults and were informed that all of the tests were3 O8 m# i2 v% G) k* V
normal except the testosterone level was high. The' o7 ~0 h8 l$ W) v3 ^" N" t
follow-up visit was arranged within a few weeks to
4 g% Q& {1 K3 P+ z: X0 ~obtain testicular and abdominal sonograms; how-
, |1 l! ?4 U4 ^9 M" [6 H% Q6 dever, the family did not return for 4 months.8 _% E- t8 X) N& J$ k# j
Physical examination at this time revealed that the1 `0 M) i. a& {, S( {6 Z
child had grown 2.5 cm in 4 months and had gained
$ b( d8 q; k+ u# b: u8 E# [4 J2 kg of weight. Physical examination remained1 {' `7 R! e7 l3 ^8 T& J7 f
unchanged. Surprisingly, the pubic hair almost com-
1 P5 `" p' y4 c  g+ tpletely disappeared except for a few vellous hairs at
8 V7 w& n+ d. J) m; `! C4 m0 Fthe base of the phallus. Testicular volume was still 28 `" T' X" Y+ D( U: Z, C
mL, and the size of the penis remained unchanged.
( l! x! I, w1 M$ m$ @" F8 J+ C0 wThe mother also said that the boy was no longer hav-
# O, E" _" m" x9 t  a- A: eing frequent erections.8 d$ V( d, T: U* r- P9 P% l8 _2 v% m
Both parents were again questioned about use of" D3 l% [6 [/ n. n: u& A% o: U
any ointment/creams that they may have applied to
2 _" p2 d+ O8 ?! G; Z; T0 J: othe child’s skin. This time the father admitted the
" Z2 c& o9 L; v) UTopical Testosterone Exposure / Bhowmick et al 541
8 u$ w1 l( O$ v! buse of testosterone gel twice daily that he was apply-/ k! [+ _, j" p  u
ing over his own shoulders, chest, and back area for
* R4 @/ H9 C( z* _7 @a year. The father also revealed he was embarrassed- T! {+ F$ ?8 N9 N3 L  V% Z" ]
to disclose that he was using a testosterone gel pre-/ Y: v, I" W0 X$ v/ B  _9 E( H  F/ V
scribed by his family physician for decreased libido/ v; {! T( k  ^' g% d8 y$ J
secondary to depression.
0 ?& |; }1 J& J+ q1 M' X9 {* ~1 ^" V, wThe child slept in the same bed with parents.* J1 ?! Y, m" V
The father would hug the baby and hold him on his
! g- Q4 k3 _& h- jchest for a considerable period of time, causing sig-
9 k$ D6 x+ n2 p4 T# @nificant bare skin contact between baby and father./ |2 L$ L) S3 @
The father also admitted that after the phone call,
/ M( g$ L. p$ r/ m5 E  j5 Wwhen he learned the testosterone level in the baby
) F/ s0 v+ m3 o& g; B  Y: X, x0 m7 wwas high, he then read the product information' \( O8 y; [( D' n9 b: w# T! U
packet and concluded that it was most likely the rea-
; `3 f: J! p7 L# e! `son for the child’s virilization. At that time, they' v0 ?' l1 g: b2 D# r: N- F
decided to put the baby in a separate bed, and the# f( Y0 o7 ^- Y: e9 y
father was not hugging him with bare skin and had
) V6 n# I5 G% V7 tbeen using protective clothing. A repeat testosterone
+ C: s$ y7 I9 vtest was ordered, but the family did not go to the; T1 s# a1 @/ w% j8 w
laboratory to obtain the test.3 W1 [9 h! f" W2 M% R( y8 ~3 u
Discussion
' O' e% F( r" ^5 q" i9 I0 ~; G5 SPrecocious puberty in boys is defined as secondary# x! i) b0 X4 C+ @2 d6 z
sexual development before 9 years of age.1,4" G/ v2 f* t3 \' r
Precocious puberty is termed as central (true) when
! ~" p1 X/ Y$ h: |! Z% Y0 \' n+ Hit is caused by the premature activation of hypo-
4 W, c7 L9 ]% U* H: ~( L$ zthalamic pituitary gonadal axis. CPP is more com-
  U% b" g/ P% M- ]mon in girls than in boys.1,3 Most boys with CPP
  P$ p1 c, m  z" h3 gmay have a central nervous system lesion that is" G- k' r. j3 d* s
responsible for the early activation of the hypothal-
9 L) U6 u& A* t% ?. b3 `amic pituitary gonadal axis.1-3 Thus, greater empha-
7 {  _4 l" e4 j7 Y3 ~sis has been given to neuroradiologic imaging in
: _  V0 f0 a+ ^. }* Lboys with precocious puberty. In addition to viril-
" m# p% t- F: n6 d' T/ P2 j& A6 N1 jization, the clinical hallmark of CPP is the symmet-0 @4 ~3 G% [9 v1 g) _8 `2 T
rical testicular growth secondary to stimulation by$ u: E8 x: c) z+ c
gonadotropins.1,3
$ m# a( I$ V7 ^' MGonadotropin-independent peripheral preco-
. D  I5 C- M$ h( y# a8 }7 m$ D* j7 Ncious puberty in boys also results from inappropriate( Z  M& r3 Z: U" a
androgenic stimulation from either endogenous or: K5 J  @$ `& W8 ?4 e
exogenous sources, nonpituitary gonadotropin stim-
, d) h# E( H7 r% k, Rulation, and rare activating mutations.3 Virilizing
: N* V/ J% i3 S0 T2 Ccongenital adrenal hyperplasia producing excessive
, U7 f9 K; K4 Xadrenal androgens is a common cause of precocious
  t* k; N  X( J, Z/ Wpuberty in boys.3,46 p4 [& F5 N, T1 m) S
The most common form of congenital adrenal1 [: ?4 b8 @3 E* k1 D# J4 A4 W
hyperplasia is the 21-hydroxylase enzyme deficiency.; p3 D6 k8 _8 p1 k
The 11-β hydroxylase deficiency may also result in
% R( i7 d5 _, Q" zexcessive adrenal androgen production, and rarely,8 ~" C/ p- E; b' x1 c9 b+ `
an adrenal tumor may also cause adrenal androgen1 P% H/ e% h  ^$ K' r
excess.1,3
  J2 @- _* u$ N0 @" P0 Q8 p+ Nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: E+ a' r! I' K. x9 Q8 V- o( Q
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007$ Z6 \0 ?0 E, _& [
A unique entity of male-limited gonadotropin-
9 j) E9 |1 ?& M* Z" X0 S9 Pindependent precocious puberty, which is also known1 F4 Y  A' [/ B. b
as testotoxicosis, may cause precocious puberty at a
( [# u! D4 J: ?) o4 w2 |very young age. The physical findings in these boys
/ l/ }" H4 `! p' ]. c  f: Bwith this disorder are full pubertal development,/ R' z3 `4 x8 k8 k8 j% b9 X2 b" _
including bilateral testicular growth, similar to boys1 e! r$ m; V/ S5 j8 L$ W
with CPP. The gonadotropin levels in this disorder, u+ u0 l/ d2 k& \
are suppressed to prepubertal levels and do not show
5 V( ?5 c2 _+ T( l8 ]pubertal response of gonadotropin after gonadotropin-
8 w/ @# e5 ?# h1 s: Zreleasing hormone stimulation. This is a sex-linked
% s' l6 e8 b- N+ r8 ]& U" q& dautosomal dominant disorder that affects only# D4 \8 v$ v4 ^; G% ~3 [
males; therefore, other male members of the family
& J7 k  f( l% y5 \may have similar precocious puberty.3, }- ?$ o7 H  z
In our patient, physical examination was incon-4 _! G! g9 w. n' N
sistent with true precocious puberty since his testi-  b% s) _. |9 y
cles were prepubertal in size. However, testotoxicosis/ g, S0 }9 {; ]5 _3 J0 r
was in the differential diagnosis because his father" M$ G5 Z$ g/ Y2 K
started puberty somewhat early, and occasionally,
* o3 ~9 q- J4 m% C: t2 B" K" Htesticular enlargement is not that evident in the
- t! }% j6 ~9 m" _beginning of this process.1 In the absence of a neg-' l0 N+ j( r& w, v/ n8 E
ative initial history of androgen exposure, our, w$ t; m6 O& I, l+ ~+ i# f0 B
biggest concern was virilizing adrenal hyperplasia,
8 @4 r# o: C9 O% H/ geither 21-hydroxylase deficiency or 11-β hydroxylase: g* ^4 u) W' g: q
deficiency. Those diagnoses were excluded by find-
! B  Y/ M3 x6 F2 K9 E0 J) king the normal level of adrenal steroids.9 L2 z( E0 p1 o, Q! |1 ]+ ~1 }
The diagnosis of exogenous androgens was strongly
7 C1 O: ]% }9 M7 h' asuspected in a follow-up visit after 4 months because& G: \8 B1 f, {* ^  L: _( L* S
the physical examination revealed the complete disap-
9 z; i/ V  {$ G' t7 o; n, ^+ mpearance of pubic hair, normal growth velocity, and! z1 _& ]' C) P& i, S! W6 I5 _
decreased erections. The father admitted using a testos-
7 w1 u; E9 z( t! b& t! P: }% Uterone gel, which he concealed at first visit. He was
; v3 K% m/ l5 G/ \5 l. m5 o  Nusing it rather frequently, twice a day. The Physicians’
; I5 v$ @* }+ RDesk Reference, or package insert of this product, gel or/ s' ~& m! @6 D9 v. u' I
cream, cautions about dermal testosterone transfer to& w2 }2 O3 X" F2 k
unprotected females through direct skin exposure.
8 `& _. O; C9 f( KSerum testosterone level was found to be 2 times the# v: a% o- W4 j: `: ?. G
baseline value in those females who were exposed to' _5 x$ e) n& p7 `) N  K
even 15 minutes of direct skin contact with their male: W/ r8 V& t* ^9 l! f7 |% t
partners.6 However, when a shirt covered the applica-
4 Y9 p$ C4 |5 {tion site, this testosterone transfer was prevented.5 F. h6 S1 Q) m2 l- I
Our patient’s testosterone level was 60 ng/mL,  i/ b% N- Q; o
which was clearly high. Some studies suggest that% w0 y( q( L% q+ I) Y: g" Z  Y
dermal conversion of testosterone to dihydrotestos-' |  o1 B% |8 l4 V8 N* ~% A' d
terone, which is a more potent metabolite, is more7 i0 F9 c( }" ~" m* ^" V& n; \
active in young children exposed to testosterone
7 a+ ?! D4 l$ t5 \& o2 I, Mexogenously7; however, we did not measure a dihy-
" t$ e) y0 q: f/ Gdrotestosterone level in our patient. In addition to
7 b0 l# b- R5 [7 z6 R2 @. T" f3 h) ]virilization, exposure to exogenous testosterone in
9 Y& O. p/ N5 B! f9 I% ?children results in an increase in growth velocity and
# Y1 e+ f5 a% V+ T7 ~advanced bone age, as seen in our patient.. j5 }0 k/ U$ I+ `' T5 t$ [- I
The long-term effect of androgen exposure during
# c" c+ ]  Z' h5 R! w0 U$ }early childhood on pubertal development and final! [5 E7 P2 l4 z$ _" c2 O
adult height are not fully known and always remain! j# V' a4 o* a6 I7 q# W/ F
a concern. Children treated with short-term testos-: N  S& i! B1 B5 m; C$ l* v6 R' ~
terone injection or topical androgen may exhibit some# M$ D0 x; H& |1 k0 O9 N0 D
acceleration of the skeletal maturation; however, after# ?7 {2 ?+ N# }2 T
cessation of treatment, the rate of bone maturation& j; H9 h  v5 [! F1 \, ]. C5 A
decelerates and gradually returns to normal.8,9
$ X0 g/ t* }' B! V1 SThere are conflicting reports and controversy6 Q# H9 N  q- ?. k' H- M( ~. Q
over the effect of early androgen exposure on adult3 b; @$ g% k; A2 j4 y
penile length.10,11 Some reports suggest subnormal  d- H) F! q& b* |: f! z0 ?
adult penile length, apparently because of downreg-8 Q2 n5 w( g# W6 ~4 L9 W  J  D
ulation of androgen receptor number.10,12 However,4 o% Q) P- v1 `2 H6 h0 [; y
Sutherland et al13 did not find a correlation between
8 p2 |* |# V0 p, l3 g/ d  s3 k% X$ Qchildhood testosterone exposure and reduced adult
, k3 G6 v4 _) w' i% A  w8 mpenile length in clinical studies.9 }4 o. E1 O$ }0 p3 L" @! I, k6 L' H
Nonetheless, we do not believe our patient is0 F6 p! q' c) \+ I- j
going to experience any of the untoward effects from% c; j0 X% v& l1 N/ s% m
testosterone exposure as mentioned earlier because
$ f' {! o4 A+ fthe exposure was not for a prolonged period of time.
. \: K+ ~% I/ ?- r( gAlthough the bone age was advanced at the time of
6 R2 p6 D! O% X' Vdiagnosis, the child had a normal growth velocity at+ P/ Q( M, j  |
the follow-up visit. It is hoped that his final adult3 }& m! ]9 h9 p8 |* P
height will not be affected./ m$ E1 U7 p7 o" K; g4 g1 f
Although rarely reported, the widespread avail-
3 Y3 R( H* ?9 H! U: d4 lability of androgen products in our society may$ Q4 N) r# p. p8 I1 K  y
indeed cause more virilization in male or female  N0 w- U" j! z
children than one would realize. Exposure to andro-
" |. r: W4 n$ Bgen products must be considered and specific ques-0 Z) H8 K+ P" k* c* S
tioning about the use of a testosterone product or
. @5 D$ B7 I! W' f4 Q' J7 D  zgel should be asked of the family members during
) h0 N" p; |5 lthe evaluation of any children who present with vir-# r3 Z# H( k  i, t. t( l/ r5 l! u7 V
ilization or peripheral precocious puberty. The diag-7 e4 o, U; W0 i$ @
nosis can be established by just a few tests and by
9 b# K6 c& R. Q8 L- I3 z' n5 o8 |+ |appropriate history. The inability to obtain such a
# I8 P2 l0 c* c/ Q0 _! `( z  \$ |history, or failure to ask the specific questions, may
' }+ Y# G9 y; {8 s7 \/ Wresult in extensive, unnecessary, and expensive
1 k- X. M. |3 b! |$ ~/ n, }investigation. The primary care physician should be  ]" A7 X7 J5 d- W
aware of this fact, because most of these children
0 [$ o2 K2 }3 l: y; f5 y9 Cmay initially present in their practice. The Physicians’
1 v3 y# G: v6 ?; u  zDesk Reference and package insert should also put a% l7 d0 U2 F. E% d, n. o% ?
warning about the virilizing effect on a male or- o3 y0 j; Q1 w2 W/ W! D% p
female child who might come in contact with some-
7 v% e2 ]8 J% ^one using any of these products.6 ?2 ~0 M  r8 d) L4 W( s/ V
References: v0 H$ a9 ^; F1 d5 r, R
1. Styne DM. The testes: disorder of sexual differentiation1 S$ }; w% O' c: R% L  p, \% O
and puberty in the male. In: Sperling MA, ed. Pediatric% S3 }' B  D+ `5 P9 _; h1 o
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;( v3 p7 ]' Z; Y8 d) H
2002: 565-628.
2 {+ x0 o/ N7 C; h1 \$ i8 u0 A2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious4 [; t5 k8 |9 H8 |5 p
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
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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
# e) L: F% M, ^  Y( f2 y. h2 b6 Z9 e
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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