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Sexual Precocity in a 16-Month-Old
2 U& L1 W% ?/ yBoy Induced by Indirect Topical$ ~+ Q; i% z$ m5 J) S9 @: V1 Z
Exposure to Testosterone# G$ {4 u' _) B+ W3 i# m
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2' p2 r& l. ?5 L5 N
and Kenneth R. Rettig, MD1& F* G% W- M( t. o4 n! c4 i' i9 B
Clinical Pediatrics( T' o) P& E3 d3 C' _7 Q9 X0 h* N
Volume 46 Number 6
8 m  d( I! `- `: ~, x. d; \July 2007 540-543" s3 ~+ T! V$ X7 n
© 2007 Sage Publications
' _# D9 @% M+ H9 [10.1177/0009922806296651. m1 K6 C3 o# M7 M
http://clp.sagepub.com
' g6 \, u) q2 p( U1 W6 r# ^hosted at( \, b% A1 J7 X7 `/ _5 c
http://online.sagepub.com% g. b  t' M- H( K  Q- t: [
Precocious puberty in boys, central or peripheral,( F& u2 ?8 t4 Z
is a significant concern for physicians. Central
3 i% d! `8 J$ f" z, W8 K& B' S. eprecocious puberty (CPP), which is mediated
$ U: W- `! B+ y5 ethrough the hypothalamic pituitary gonadal axis, has1 r. [- u" A" I8 n& w" B
a higher incidence of organic central nervous system
/ Y9 p8 p7 ^, v1 S, jlesions in boys.1,2 Virilization in boys, as manifested) R0 r! J9 |* ~, _
by enlargement of the penis, development of pubic
. |" o7 C4 c& xhair, and facial acne without enlargement of testi-* p8 Q3 f: i; z$ e" u9 Q
cles, suggests peripheral or pseudopuberty.1-3 We
. V( V; g8 o) ^; Z" T' b/ greport a 16-month-old boy who presented with the( l8 y) S% h+ P2 E
enlargement of the phallus and pubic hair develop-9 I: x$ D; b8 T# V# [7 h
ment without testicular enlargement, which was due4 _' `! w5 L9 v8 d
to the unintentional exposure to androgen gel used by
& w8 U# [/ V, a3 ~) m! @9 Uthe father. The family initially concealed this infor-. z' @% j) {2 A0 H
mation, resulting in an extensive work-up for this$ y4 N. t+ I$ g) n
child. Given the widespread and easy availability of# L/ _- h  H) A2 o. ?6 N% {
testosterone gel and cream, we believe this is proba-
' X. Z( V0 j' m8 y# ^% vbly more common than the rare case report in the
8 g! t# E& R" l# Oliterature.4# G3 g9 Z9 ^. V2 E7 [. C
Patient Report2 h$ \+ y: ?) a, z% ~
A 16-month-old white child was referred to the: q/ M1 l6 q' m4 o! [" p# a6 e
endocrine clinic by his pediatrician with the concern$ y  g1 u3 E- V" x$ w0 a/ ?( z/ }
of early sexual development. His mother noticed
+ i7 ~* x5 F& Alight colored pubic hair development when he was
. E6 C  m4 _9 X0 L& u" T! M& I1 {From the 1Division of Pediatric Endocrinology, 2University of
' Z5 j6 B' d3 H/ t( \% RSouth Alabama Medical Center, Mobile, Alabama.
" ^& I* C6 v3 P: R" AAddress correspondence to: Samar K. Bhowmick, MD, FACE,
5 j4 O: F; `0 {9 L# i2 dProfessor of Pediatrics, University of South Alabama, College of. b) W( s, Q- H2 T% B! A8 w  P& \9 _
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;2 ~. j' ^. g3 z$ ^
e-mail: [email protected].  E& X* k/ `, u- X2 h
about 6 to 7 months old, which progressively became
* [. B; ^  C0 l. mdarker. She was also concerned about the enlarge-
2 K! ]  |4 I5 U0 E7 {ment of his penis and frequent erections. The child, U5 D1 n6 x( N( w! D6 P
was the product of a full-term normal delivery, with
: s1 I, B, m) j4 `6 i% ^* F+ ]a birth weight of 7 lb 14 oz, and birth length of& E! R+ @) a2 [5 K& A$ @2 _
20 inches. He was breast-fed throughout the first year, m3 A+ u' `. ~% i+ J1 `+ ]
of life and was still receiving breast milk along with
9 g) R; j: L  e+ x7 B3 I9 l; Rsolid food. He had no hospitalizations or surgery,+ Z  [6 d* X& J0 D
and his psychosocial and psychomotor development
/ I7 Z7 p: H2 p, A" G1 g2 iwas age appropriate.
7 W+ N' S& Y8 j( o! CThe family history was remarkable for the father,
0 f1 s$ H1 Z# x# t0 Ywho was diagnosed with hypothyroidism at age 16,5 h" }6 B' {0 T+ D8 v
which was treated with thyroxine. The father’s
& l& m3 N' A+ W2 W- T0 G2 Jheight was 6 feet, and he went through a somewhat0 R* Y$ F& j) u
early puberty and had stopped growing by age 14.' ?: x, V4 F  y* g
The father denied taking any other medication. The1 U+ `" t) d1 D& n- ?5 F) I/ M2 p
child’s mother was in good health. Her menarche5 o3 g, A0 D% ^2 W& v: E
was at 11 years of age, and her height was at 5 feet
/ q( t" U0 M6 G. W( z5 inches. There was no other family history of pre-
5 d/ F+ i$ A, ]1 d: V6 dcocious sexual development in the first-degree rela-, _( n! J( \* Q, @" w0 l/ e
tives. There were no siblings.
- y; V4 A7 c9 M5 \: n: |+ jPhysical Examination
' g; ^5 i3 i' }1 Z/ m( aThe physical examination revealed a very active,
: y1 V/ C* n& _! J  k8 K$ N) Qplayful, and healthy boy. The vital signs documented
; P- @3 E- Q0 m: F; K- pa blood pressure of 85/50 mm Hg, his length was( J5 U5 |; M  j3 q4 m7 U, F! D/ `" R
90 cm (>97th percentile), and his weight was 14.4 kg
# s# G+ h' U$ \* ~: i6 G(also >97th percentile). The observed yearly growth
% {- c8 y1 @4 E* Dvelocity was 30 cm (12 inches). The examination of* e. e: K, O- ~2 s% J; J
the neck revealed no thyroid enlargement.
' A7 N: L3 `9 ]9 v) H: EThe genitourinary examination was remarkable for
1 Z$ j+ u- y" f6 H6 T% A. l& fenlargement of the penis, with a stretched length of
; ]# u9 J" h  ]+ D: c! I8 cm and a width of 2 cm. The glans penis was very well
* }& C% M- F  U* c5 K0 B/ ^& ^developed. The pubic hair was Tanner II, mostly around
: i4 l3 Q; w: {9 C7 e540
6 s9 e7 B. `* g: g" b, Qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 Q7 C8 }, Z- g+ C5 [7 ~the base of the phallus and was dark and curled. The- ~2 E: V/ Z" g, G; U
testicular volume was prepubertal at 2 mL each.
, |7 A& t9 }8 y  cThe skin was moist and smooth and somewhat
+ E$ b7 F9 H; z, O0 b  V- ooily. No axillary hair was noted. There were no9 d2 x: Y, c% }% l* g
abnormal skin pigmentations or café-au-lait spots.
0 i0 t% p( T( P8 g0 S7 Q! rNeurologic evaluation showed deep tendon reflex 2+' V9 e! d# d; {, D$ [. q" Q
bilateral and symmetrical. There was no suggestion
; D( N7 r/ n& B- O8 k! G3 Q% S6 Lof papilledema.
, w$ [5 f  ]& ]; z; k7 D5 k4 TLaboratory Evaluation
, H6 F% Q  b$ eThe bone age was consistent with 28 months by
; f) X1 }  v! K& J% m8 Dusing the standard of Greulich and Pyle at a chrono-) U. g& f4 x( l1 J. H0 Y
logic age of 16 months (advanced).5 Chromosomal
4 f$ q7 J# O1 v5 }* z; Akaryotype was 46XY. The thyroid function test
2 ]. o& ~  p# |; @. V" u$ _showed a free T4 of 1.69 ng/dL, and thyroid stimu-
% B6 \: p( h/ I; blating hormone level was 1.3 µIU/mL (both normal).
- d) u' X0 B  M+ Q2 `The concentrations of serum electrolytes, blood
+ T- n. V9 k7 F5 Yurea nitrogen, creatinine, and calcium all were( F* I4 O  u2 e/ [) G$ F; [/ P
within normal range for his age. The concentration9 N* v8 ?8 y3 m$ D/ ~5 m
of serum 17-hydroxyprogesterone was 16 ng/dL
. P& N  P+ r+ N0 d- _5 m(normal, 3 to 90 ng/dL), androstenedione was 206 q, J- A) e9 P  W+ O; y0 w4 e& {
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-' n! Z. @* L% P
terone was 38 ng/dL (normal, 50 to 760 ng/dL),2 J8 d; `& G  Z1 N8 d
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
$ {0 ]; s- d) H- e( B4 U# k49ng/dL), 11-desoxycortisol (specific compound S)4 O3 l9 _  {2 K% v& {
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-( ~% ?3 p5 b' R. ?$ _
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total1 P& W3 N( K! T& w: R5 h* Y
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),3 K9 |! X" F% O+ {5 b4 V
and β-human chorionic gonadotropin was less than6 S/ ?8 i# ]' \( t
5 mIU/mL (normal <5 mIU/mL). Serum follicular
0 D3 D$ a2 @, ]7 D6 ?- f% `+ Hstimulating hormone and leuteinizing hormone. ~" I. g" x5 Y1 U& q7 z& t
concentrations were less than 0.05 mIU/mL
: {1 S' i7 u9 [5 F- q0 ^(prepubertal).
0 W' R0 }+ i) DThe parents were notified about the laboratory5 t' I: W5 r, W& E! c( i
results and were informed that all of the tests were5 F! h9 y; ?+ p1 W0 l
normal except the testosterone level was high. The/ C. _& P2 O" @( j" Q# q
follow-up visit was arranged within a few weeks to
9 ^  f) M4 c) q$ [% \obtain testicular and abdominal sonograms; how-
4 d5 t4 C5 u/ U3 M' T, z) pever, the family did not return for 4 months.. @3 h/ ]3 H+ z1 c" Y6 F
Physical examination at this time revealed that the
7 ~5 \9 _9 H0 ichild had grown 2.5 cm in 4 months and had gained
) \6 }) N' U# S5 t$ ?5 ~2 kg of weight. Physical examination remained+ ~% D+ G5 Q% u! n0 d
unchanged. Surprisingly, the pubic hair almost com-4 @0 C. T; E6 [9 c; X. S
pletely disappeared except for a few vellous hairs at
. j: f1 s( Q: g9 {0 M- l6 Q6 X) x2 |the base of the phallus. Testicular volume was still 2
* C- r& n8 W% dmL, and the size of the penis remained unchanged.
& T8 N. a8 U- b4 bThe mother also said that the boy was no longer hav-
7 X$ M/ ~7 V" `' j$ B; J. s6 |ing frequent erections.
: v! G6 i* I! KBoth parents were again questioned about use of
) f2 X, [6 R, Q# s) F$ S) K0 Wany ointment/creams that they may have applied to: {9 j; ]  o5 Z' ]" M. J
the child’s skin. This time the father admitted the& n, V7 R& M7 h( g4 n
Topical Testosterone Exposure / Bhowmick et al 541
8 g. L0 S( x% A5 \8 @. C7 [0 Quse of testosterone gel twice daily that he was apply-
) {1 D9 p6 R- t- w; b1 }ing over his own shoulders, chest, and back area for
5 H% a! U: a  s& [a year. The father also revealed he was embarrassed& A' }: T+ g& i+ }5 U
to disclose that he was using a testosterone gel pre-) ~) D4 A! m, T- ~; _: w
scribed by his family physician for decreased libido
8 w; O1 Q3 ]$ `8 l# f( S( qsecondary to depression.* ~- e* X8 Q- q" y/ Q
The child slept in the same bed with parents.
9 C. w5 f5 I# W9 w- \The father would hug the baby and hold him on his4 E% P/ `" x) r+ g' Q- K% o$ r. y
chest for a considerable period of time, causing sig-
$ c8 P$ D5 c7 F9 Z* ]4 Inificant bare skin contact between baby and father.
3 u. d3 h2 q+ sThe father also admitted that after the phone call,  t0 ?. _+ @% v& x, X5 F  l# H
when he learned the testosterone level in the baby3 B' A$ u, r, J6 W/ B1 R2 ~' r* U+ u
was high, he then read the product information' b0 F6 }6 P+ Z: u9 @
packet and concluded that it was most likely the rea-
' v0 E- m. u2 ~4 R! u0 Y! ?son for the child’s virilization. At that time, they
( Q$ e% z3 S. M7 n$ x! X  d4 j/ [decided to put the baby in a separate bed, and the2 M5 i, x" J" q/ p& E
father was not hugging him with bare skin and had, @3 W. R: n, s* l: U
been using protective clothing. A repeat testosterone+ \7 m& q/ x+ w# I% G8 l" w
test was ordered, but the family did not go to the/ Z# z8 N8 d! f2 W, S# I$ ~+ O
laboratory to obtain the test., c0 Q2 p1 v' y5 \  @- k7 L/ R
Discussion+ u0 ]0 C1 R; R& s" W
Precocious puberty in boys is defined as secondary! C% n$ o6 P9 c! w- O6 ?
sexual development before 9 years of age.1,4
- S8 y4 x7 Y' W* x% z; qPrecocious puberty is termed as central (true) when
" _" ]3 P% @: Vit is caused by the premature activation of hypo-2 l; G1 w+ W* F8 l$ Y
thalamic pituitary gonadal axis. CPP is more com-5 ]- O& q  D2 M: d
mon in girls than in boys.1,3 Most boys with CPP
% [: l9 M$ Y* L6 u6 o. O$ e0 v: Umay have a central nervous system lesion that is
5 Z& _& H& G# W! h3 K' W" jresponsible for the early activation of the hypothal-. f) \8 y3 L9 e1 X1 Z3 B& g) a
amic pituitary gonadal axis.1-3 Thus, greater empha-9 ^; g* f" b" N0 T' A9 O; }
sis has been given to neuroradiologic imaging in/ _9 P" p& G0 y  R$ E
boys with precocious puberty. In addition to viril-
$ I/ K; [8 A3 n" Qization, the clinical hallmark of CPP is the symmet-
2 K& f6 i% q% E! Q& Q* hrical testicular growth secondary to stimulation by0 ~  o5 X, f6 `& p* ^4 j+ G
gonadotropins.1,3$ O1 w8 f; p* q' A, \# |# s* y( M% X
Gonadotropin-independent peripheral preco-- k* i; p5 c- o4 I
cious puberty in boys also results from inappropriate4 K0 O; `& `3 @6 r; o1 ?: ?5 Y
androgenic stimulation from either endogenous or$ f, N% Y: P% u- N8 f
exogenous sources, nonpituitary gonadotropin stim-6 @* }4 b! Z* W3 ]- M+ M
ulation, and rare activating mutations.3 Virilizing
# I* p9 m8 s. `0 jcongenital adrenal hyperplasia producing excessive
, s2 j9 m1 ^6 Y3 u* N/ z- Kadrenal androgens is a common cause of precocious
& c. R/ t' b' J% ?' ~! apuberty in boys.3,40 h: C5 r* u" C, @
The most common form of congenital adrenal0 z5 S2 n, o, V7 N# w% _' ?
hyperplasia is the 21-hydroxylase enzyme deficiency.. H0 n+ c6 c3 C: @) D* J
The 11-β hydroxylase deficiency may also result in! Y( n! q% m" G. \
excessive adrenal androgen production, and rarely,
$ ^& y' Q/ ^5 M1 pan adrenal tumor may also cause adrenal androgen6 w* b; y, H) u, s
excess.1,3
$ ]- }1 g9 z+ I: w& ?! h4 F/ pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 S' U  Q( W4 C5 q; D542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
$ }0 ?0 ^6 k; N" T  T; o9 @1 pA unique entity of male-limited gonadotropin-
+ x) ^. O3 A' F& {independent precocious puberty, which is also known, C+ }9 p8 W" q$ k, R! h
as testotoxicosis, may cause precocious puberty at a; F/ q8 a+ l1 F- B- U4 h. b4 g
very young age. The physical findings in these boys
& P, L0 A* [& h; U. `* T! z' Pwith this disorder are full pubertal development,6 j+ _2 T% ]5 W
including bilateral testicular growth, similar to boys
: u: u# X6 F' c5 L) I) Q2 V! Y  \with CPP. The gonadotropin levels in this disorder. Z% `4 g. F4 x. O& I
are suppressed to prepubertal levels and do not show
7 `" I! _* }. _. v( H$ I2 h' x# Ipubertal response of gonadotropin after gonadotropin-# P& P% L% Z4 W2 y9 K/ X* t
releasing hormone stimulation. This is a sex-linked: ^: B# F. t* }# b5 s% C4 t
autosomal dominant disorder that affects only
& K; E5 U4 E! O9 v: Omales; therefore, other male members of the family
# v; J/ U" W" x0 ]6 gmay have similar precocious puberty.3" H3 s" t- V  |) J
In our patient, physical examination was incon-  t7 K* Y9 Q+ t7 r  A
sistent with true precocious puberty since his testi-/ S/ F: B1 S" X. x
cles were prepubertal in size. However, testotoxicosis
! f% J- j0 ]; Uwas in the differential diagnosis because his father1 L$ t& T8 |3 O& F8 H* v
started puberty somewhat early, and occasionally,
! d. Z3 a, F1 p. Ztesticular enlargement is not that evident in the
9 Y3 t9 e$ C0 U: b. ~  G3 Nbeginning of this process.1 In the absence of a neg-
  P! F6 k8 R4 K; jative initial history of androgen exposure, our
. M' V9 d7 m9 Z; m% |) |$ }biggest concern was virilizing adrenal hyperplasia,
/ }3 _9 B! o. b7 U4 O% {$ l1 Keither 21-hydroxylase deficiency or 11-β hydroxylase
* s- z" E* T: k( }deficiency. Those diagnoses were excluded by find-9 ]$ I  f) A( W$ [. F3 |
ing the normal level of adrenal steroids.; P8 U) Y& J& ^1 C. u
The diagnosis of exogenous androgens was strongly
. G' H5 i$ \' |; S% X- Y+ lsuspected in a follow-up visit after 4 months because
" |6 Q8 s9 p, L/ Nthe physical examination revealed the complete disap-
6 b  o' F$ r9 @+ Z' V+ F0 k7 _3 ypearance of pubic hair, normal growth velocity, and# t' K8 [( o' r/ Y+ L9 g5 ^! Y
decreased erections. The father admitted using a testos-
" v7 Q4 |( J4 z5 W; {" Fterone gel, which he concealed at first visit. He was
) [# n; R& _( d7 Y/ t2 g1 Wusing it rather frequently, twice a day. The Physicians’/ X0 r3 U2 _, ^2 ?  V
Desk Reference, or package insert of this product, gel or
& q6 S2 P) f7 N* x! d2 Ycream, cautions about dermal testosterone transfer to
5 v% s. K$ n8 L) G* yunprotected females through direct skin exposure.
" V6 |- `4 P: f9 i! _. K+ {Serum testosterone level was found to be 2 times the
2 P& W" ^  _$ f- D3 R: Cbaseline value in those females who were exposed to
# Z/ h$ @  c, s1 n5 veven 15 minutes of direct skin contact with their male$ c" F  C" O& u! v- n. Z
partners.6 However, when a shirt covered the applica-, D% W  w, v9 v# ~9 Z+ h4 E7 j
tion site, this testosterone transfer was prevented.
: [/ x/ H  D8 L1 Y; J" S8 XOur patient’s testosterone level was 60 ng/mL,
! Y) ]# p$ v, ^which was clearly high. Some studies suggest that
. j7 H2 ~) H  w( J( vdermal conversion of testosterone to dihydrotestos-% }$ g' E5 x+ g# |
terone, which is a more potent metabolite, is more1 F+ p" Y3 A5 Y9 L- x
active in young children exposed to testosterone
: l% z2 e  f! U( F1 Fexogenously7; however, we did not measure a dihy-$ N7 y  {$ Y; Z1 P
drotestosterone level in our patient. In addition to. f/ P+ N: a8 `: h, ]7 |% S" k5 c
virilization, exposure to exogenous testosterone in$ d; K& m1 N2 H9 w5 d
children results in an increase in growth velocity and
/ r. F( {# z6 v; W0 ^8 w4 S$ H% jadvanced bone age, as seen in our patient.
/ t  {9 ~$ a8 |% kThe long-term effect of androgen exposure during
! @. P* d4 C3 x9 M4 dearly childhood on pubertal development and final1 }: J$ [- g+ v; F
adult height are not fully known and always remain
/ F8 Z) \# e8 D8 ma concern. Children treated with short-term testos-- H4 Z8 p3 Q' R# _
terone injection or topical androgen may exhibit some; \  e& W% I/ w7 i' G
acceleration of the skeletal maturation; however, after( f3 Z3 c. w9 g) W
cessation of treatment, the rate of bone maturation. W8 b: ]( S; Z7 q# V# I" P
decelerates and gradually returns to normal.8,9
$ E, K5 E3 X. R+ WThere are conflicting reports and controversy: ~5 h+ J2 `9 y! M6 S: ?* }
over the effect of early androgen exposure on adult
6 }( @* p  j- c+ {penile length.10,11 Some reports suggest subnormal( N; R) H& R" P! z- O- C2 r
adult penile length, apparently because of downreg-1 a, H. E" g8 ]0 z: U
ulation of androgen receptor number.10,12 However,( U) R2 b+ N  f) ^; j( z7 S1 n
Sutherland et al13 did not find a correlation between, ?$ Q1 l2 T  R6 Z
childhood testosterone exposure and reduced adult
1 T( m8 b1 }( g. K- a! r5 apenile length in clinical studies.0 c( b) s( e% ^
Nonetheless, we do not believe our patient is
( E, H: C: L6 f- ^# j; X( l2 V: zgoing to experience any of the untoward effects from( {! ]2 g) M+ @: o4 D. @
testosterone exposure as mentioned earlier because: T# r+ O$ E2 s7 O
the exposure was not for a prolonged period of time.9 f9 H& Q* v) f* p/ T2 J0 ~6 F
Although the bone age was advanced at the time of
! d* u/ z& h' pdiagnosis, the child had a normal growth velocity at( G4 Y' {6 t/ P* g
the follow-up visit. It is hoped that his final adult1 V0 b0 `* J( o
height will not be affected.
7 ]) Q, Y" Y% U8 @. }" [/ GAlthough rarely reported, the widespread avail-
; }9 M: r0 B6 ~( L- x" Dability of androgen products in our society may
5 _, D& r" N: z" qindeed cause more virilization in male or female
2 n4 I: B, r1 m" x$ w  y( ]; o8 Bchildren than one would realize. Exposure to andro-
9 t, T$ q* W( Z  |, Pgen products must be considered and specific ques-: @7 N" w8 ?% q) c% J$ R/ X  `
tioning about the use of a testosterone product or
6 o) m" C% \/ u/ u. f& kgel should be asked of the family members during9 J1 v, ]. N* `  u# o
the evaluation of any children who present with vir-7 i" j0 h1 Y1 o+ E) T9 ^
ilization or peripheral precocious puberty. The diag-6 f7 {0 Q3 q2 q- ]' z! E
nosis can be established by just a few tests and by" c3 B1 C. P+ c, N& T- F& o
appropriate history. The inability to obtain such a
7 _8 s, i' B& c5 Q5 B& [+ yhistory, or failure to ask the specific questions, may
! t& p% }( B( u4 S5 J% kresult in extensive, unnecessary, and expensive7 a) u) x  Z2 j7 r
investigation. The primary care physician should be
1 D. Y; d" ~8 r! ~! C) n2 Aaware of this fact, because most of these children
% \; Q7 n8 ]6 C; j/ vmay initially present in their practice. The Physicians’: G) O, s! C- F  Z
Desk Reference and package insert should also put a
. l- i+ }9 U7 M( D9 Z6 Kwarning about the virilizing effect on a male or
- ~+ Z& N$ V, m9 C8 \+ Q" D+ ~& ^female child who might come in contact with some-
7 L0 |9 ~& |2 @9 C# S2 u9 }one using any of these products.
; S, I% x) P7 k6 N* AReferences, K  P9 U( k( m! o, l
1. Styne DM. The testes: disorder of sexual differentiation. F) C/ a6 ?% {! s) i2 \/ \
and puberty in the male. In: Sperling MA, ed. Pediatric, ^; Y+ v  q3 ]6 d7 t- w& i% n
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
+ a3 e. F! Z* _# ]/ Y2002: 565-628.: P+ n8 r9 }4 M4 t
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
- }. m2 l; d( t; bpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
5 l) w; a7 C6 T' D5 XBoy Induced by Indirect Topical
  N7 s0 e3 {2 ?" RExposure to Testosterone
3 y. A4 B" U( m$ ~Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. t/ c$ V+ m5 ^
and Kenneth R. Rettig, MD1: `* K; M0 x7 ?4 [
Clinical Pediatrics
5 y3 P( q' C) m: c! d  GVolume 46 Number 6% V& ]1 [0 S& u$ C+ l
July 2007 540-5432 L7 T& J& l+ [3 _
© 2007 Sage Publications
( \( ?1 @/ _- U' W4 c) i10.1177/0009922806296651
! ], g. Z3 T! ~, p" yhttp://clp.sagepub.com  e$ v% n% k' |, Y" ^4 v+ r
hosted at- ^# ~2 }# Z- x
http://online.sagepub.com2 p- ?; T5 x9 G+ J3 [# ^
Precocious puberty in boys, central or peripheral,
& ]7 t+ Q8 }  kis a significant concern for physicians. Central8 |# r9 Y  Q. D, K! J
precocious puberty (CPP), which is mediated. O! L, @) x9 R. F
through the hypothalamic pituitary gonadal axis, has8 w5 j9 V1 c. L* Z" @2 Z
a higher incidence of organic central nervous system7 N* s+ g+ R5 z9 K% V) j
lesions in boys.1,2 Virilization in boys, as manifested! d+ F: E/ Z$ s9 ^
by enlargement of the penis, development of pubic: P. E3 t9 T3 `- d8 K- A/ o" z
hair, and facial acne without enlargement of testi-
6 M% ~5 ~' Q" F1 scles, suggests peripheral or pseudopuberty.1-3 We
/ D, T6 {7 O8 Q. L, z  }report a 16-month-old boy who presented with the; @( N6 a: t9 t* S* {4 R  ^. D& V
enlargement of the phallus and pubic hair develop-
0 ]* L4 S8 X0 Q1 V0 p; Lment without testicular enlargement, which was due
8 C( K0 e$ ^& }; Fto the unintentional exposure to androgen gel used by% C) \% O' f2 S7 d9 I' H4 T: ?& Q; q
the father. The family initially concealed this infor-
7 O* A2 m- z! m2 imation, resulting in an extensive work-up for this
* h( z# D/ }) c3 [+ uchild. Given the widespread and easy availability of( h% v" m' b* d2 C
testosterone gel and cream, we believe this is proba-+ y5 |4 ^; s2 K
bly more common than the rare case report in the
+ K% `* w, i3 v2 hliterature.4
% r: b" i4 A' q# O, OPatient Report
9 m8 ?5 a5 u: D7 S. mA 16-month-old white child was referred to the
& W' m# i: W9 b4 @4 [2 e6 Iendocrine clinic by his pediatrician with the concern+ u* y5 I) m) O  a/ {+ x/ ]
of early sexual development. His mother noticed
6 {, @/ [) Y4 {$ g& K1 Slight colored pubic hair development when he was1 T" H; N, Y6 n( \# z  W; T) C
From the 1Division of Pediatric Endocrinology, 2University of+ u6 F8 ~; }; [* ~: g( l
South Alabama Medical Center, Mobile, Alabama.
- F6 W3 u  g2 p5 CAddress correspondence to: Samar K. Bhowmick, MD, FACE,
1 V. a- ]8 e( W' E/ b" \" m# U, ZProfessor of Pediatrics, University of South Alabama, College of
8 y* c7 ^7 X1 p0 r. P) iMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
+ F( ]1 I% ?. u: X! u- U$ V5 c) s1 Le-mail: [email protected].: f) z) A7 X1 d# }# Z0 L0 B5 U) K
about 6 to 7 months old, which progressively became
' E7 a( C$ J# \% g- L3 m  Odarker. She was also concerned about the enlarge-
, i7 ]" C6 p. ?1 j% Iment of his penis and frequent erections. The child3 W& @" d% n9 y" s) y1 x0 L9 r- W
was the product of a full-term normal delivery, with
) j& F; H3 z; `# @' Ea birth weight of 7 lb 14 oz, and birth length of
& p# S% r( d2 _6 X# E3 t6 p, T3 v/ S20 inches. He was breast-fed throughout the first year
( f. a. L% J1 n* v2 Qof life and was still receiving breast milk along with
1 ?8 S% D' S/ W9 e% \solid food. He had no hospitalizations or surgery,
5 i7 u- H, J$ W/ U& {5 l8 T& dand his psychosocial and psychomotor development4 X+ h+ ?" A3 @; u
was age appropriate.# w1 c3 E- x0 P9 W# {
The family history was remarkable for the father,
7 H( {# W1 E0 ?' l' Y6 O, Owho was diagnosed with hypothyroidism at age 16,
0 @% w! X4 ~$ r$ g0 Jwhich was treated with thyroxine. The father’s
4 z: X/ e7 }/ ?; fheight was 6 feet, and he went through a somewhat2 T5 C" O: w$ \' H$ h8 o( S& A
early puberty and had stopped growing by age 14.
% a* k$ b9 g, S( R. _0 C& CThe father denied taking any other medication. The
+ F; x0 i) V- ?+ ~/ f+ hchild’s mother was in good health. Her menarche
- C9 s6 F$ T" ]( I  r) [was at 11 years of age, and her height was at 5 feet4 l7 n0 x+ e9 e4 H- }  E: ?
5 inches. There was no other family history of pre-; e0 P/ y9 G( `, h
cocious sexual development in the first-degree rela-' Y+ \4 L: z7 n. T
tives. There were no siblings., f! B0 P) H7 m4 q+ S' H2 U- Z$ [
Physical Examination0 _8 Y8 F6 _' F  ?7 [
The physical examination revealed a very active,
  n& v8 r' f5 \: _! Y8 B7 i' Nplayful, and healthy boy. The vital signs documented$ P& J3 a7 M- N5 k
a blood pressure of 85/50 mm Hg, his length was
5 d$ V7 P9 W) u" G. m7 e+ }# `90 cm (>97th percentile), and his weight was 14.4 kg
5 \8 H0 t5 X( v4 {6 w7 \& W(also >97th percentile). The observed yearly growth: Q! |& r& e4 [0 W' r2 u, J6 y. {
velocity was 30 cm (12 inches). The examination of) T( e/ u) z4 {2 K) B' |
the neck revealed no thyroid enlargement." t& I+ z- f7 J6 s* D
The genitourinary examination was remarkable for4 d( Q: b: k% }1 q
enlargement of the penis, with a stretched length of
. Z3 z% ]! D( d: T" V% |( ]) f8 cm and a width of 2 cm. The glans penis was very well$ m8 t5 v# V7 e  ^6 a7 E
developed. The pubic hair was Tanner II, mostly around: B! I4 H/ }: Q0 Q. Q: U# ~& Y7 D
540
/ L7 D% v  h; v0 m# ?4 \& S# eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; w" c" [  ~* Z" S4 X( ythe base of the phallus and was dark and curled. The$ Y6 {: ?8 l& G) t8 D, g
testicular volume was prepubertal at 2 mL each.
( g& `0 ~; T5 _5 }7 Z+ R0 @; l$ T8 vThe skin was moist and smooth and somewhat. U6 g7 ^9 L, V) i/ r
oily. No axillary hair was noted. There were no3 \: [$ q, A+ Q+ h; b
abnormal skin pigmentations or café-au-lait spots.3 F) I/ r5 |5 b, h& z
Neurologic evaluation showed deep tendon reflex 2+
; f3 u2 m% u3 D" pbilateral and symmetrical. There was no suggestion
+ W+ y- @- w) s. c& lof papilledema.3 {% }3 }; I# `9 i8 e
Laboratory Evaluation! S/ p" t- T1 Q3 R4 Q) v
The bone age was consistent with 28 months by$ v0 ^( ~5 ?  K% F3 m4 E# O
using the standard of Greulich and Pyle at a chrono-% @6 Y8 B0 Y1 T" R
logic age of 16 months (advanced).5 Chromosomal3 ~+ a$ G) p& Y( j
karyotype was 46XY. The thyroid function test( K1 _% a* v3 A
showed a free T4 of 1.69 ng/dL, and thyroid stimu-, [$ d! J+ G8 Z* D5 n, t
lating hormone level was 1.3 µIU/mL (both normal).
+ a3 F" c9 e4 _' i* w' o. K# KThe concentrations of serum electrolytes, blood
. G  p  Y+ j# burea nitrogen, creatinine, and calcium all were
9 J7 O5 [6 ], Y& z/ ~within normal range for his age. The concentration# L9 P- w: A" F4 a
of serum 17-hydroxyprogesterone was 16 ng/dL
0 u; Z4 C) q. A, _9 Q(normal, 3 to 90 ng/dL), androstenedione was 201 [( O# t  l7 S  X2 s
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-& a! d1 p+ {7 q5 w3 P
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
% j* T+ {$ G7 hdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
! Z- m- `  m' u0 D3 b1 T49ng/dL), 11-desoxycortisol (specific compound S)
9 _" J0 e. q; Cwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
1 \) t, p" h- |+ ~5 {; J9 a) Z# ~: Ytisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total* u8 ~  P4 E. e. C; j
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),* t6 E! y3 S3 r/ V' D, J& }
and β-human chorionic gonadotropin was less than5 U+ Q: A% x& _
5 mIU/mL (normal <5 mIU/mL). Serum follicular
9 t% k5 P; e( F6 j) p9 Ystimulating hormone and leuteinizing hormone3 a9 Y: c' a/ g! d8 m2 W  C- A
concentrations were less than 0.05 mIU/mL
" @. L+ J" X, f% E(prepubertal).
* ~0 V( I: _+ A2 R7 uThe parents were notified about the laboratory) Q- r% z9 x" ?# ]3 l( c
results and were informed that all of the tests were; y* c; M4 v8 n% Q+ N( l7 u
normal except the testosterone level was high. The
4 P8 l- J3 c  L( u8 efollow-up visit was arranged within a few weeks to" {) `* W& s3 j* j
obtain testicular and abdominal sonograms; how-" t7 @: `! Y1 x) @
ever, the family did not return for 4 months.5 m1 C9 {5 K6 |- L* e, l0 G1 b
Physical examination at this time revealed that the
+ @* i8 y" ^1 Y0 ^child had grown 2.5 cm in 4 months and had gained
2 o0 R5 W1 R/ j6 ]: z, ^! E0 n% _' r5 h2 kg of weight. Physical examination remained
2 @: c% [& T+ s' X! U- Xunchanged. Surprisingly, the pubic hair almost com-+ K0 O) v0 P. L& }9 y( U' J7 G
pletely disappeared except for a few vellous hairs at
- S* V4 G' a7 p. [& D6 x' u: Mthe base of the phallus. Testicular volume was still 2
' w7 D) J# [; I  V/ t  QmL, and the size of the penis remained unchanged.
  G9 `6 V% {3 X% B/ {0 EThe mother also said that the boy was no longer hav-
7 }! B5 K0 N( F0 h, H3 aing frequent erections.
8 L3 B* n; ]( T, D8 H  e1 u0 VBoth parents were again questioned about use of
) {6 B" C8 t. Oany ointment/creams that they may have applied to
* d- h7 s  b9 q* y" ithe child’s skin. This time the father admitted the
. V: X: C  M+ ?Topical Testosterone Exposure / Bhowmick et al 541) U) j# d  j7 F# r
use of testosterone gel twice daily that he was apply-, H% Q6 z2 J! h6 \
ing over his own shoulders, chest, and back area for9 o4 r3 u( ], F1 Z
a year. The father also revealed he was embarrassed/ p. Q1 T* ], {
to disclose that he was using a testosterone gel pre-
5 W. {* E, G& M4 h/ l+ a; }. _) oscribed by his family physician for decreased libido6 V9 X3 s! W3 x9 I5 ^
secondary to depression.
3 h' `8 [' R7 EThe child slept in the same bed with parents.2 N; D; H  n) `0 v/ k! F: h% U
The father would hug the baby and hold him on his
4 J0 a7 C/ m+ O& cchest for a considerable period of time, causing sig-
, M' d5 x1 b8 u' @nificant bare skin contact between baby and father.* x2 p# {4 S# k. ~
The father also admitted that after the phone call,. g- R* n+ |/ I' y% j% J9 Z' @. e5 o( q
when he learned the testosterone level in the baby
( [: g4 u- l, v! d& ?was high, he then read the product information
/ `7 @6 Z* o' `& Mpacket and concluded that it was most likely the rea-( L+ k5 l8 A1 u5 h  T) L7 d
son for the child’s virilization. At that time, they
( \+ t% t8 |+ ^+ K- n: bdecided to put the baby in a separate bed, and the# w% z# S! k% v' d& t4 N3 b
father was not hugging him with bare skin and had" K* M9 O7 T: t" [
been using protective clothing. A repeat testosterone
! s: }' f1 W% M% O4 P' ]: h; [test was ordered, but the family did not go to the
& O* h8 t$ a# f, v% Tlaboratory to obtain the test.: q8 u7 }' Z, @( E% V8 P1 C
Discussion
" l* ~7 y% Q% |  x4 u# Q+ iPrecocious puberty in boys is defined as secondary
7 [* g7 I5 P# Gsexual development before 9 years of age.1,4: \2 P. o5 S# O! l) _! s3 X
Precocious puberty is termed as central (true) when5 H0 \' |3 ~: E% j6 L
it is caused by the premature activation of hypo-
. G; c$ v$ u9 z3 K, Vthalamic pituitary gonadal axis. CPP is more com-9 C1 t$ O6 r$ [( u
mon in girls than in boys.1,3 Most boys with CPP
( g: d# I; W; ]" G- X5 Q- u: i" Hmay have a central nervous system lesion that is. s4 M% |+ f8 K3 M# [$ y* Z5 h( `
responsible for the early activation of the hypothal-( }& z- ^3 \9 q" k
amic pituitary gonadal axis.1-3 Thus, greater empha-5 O! {, K: C. A& S0 z
sis has been given to neuroradiologic imaging in  U* B4 x: o$ i! A3 t
boys with precocious puberty. In addition to viril-5 \6 `: W  L+ I2 X% x3 a, J* c
ization, the clinical hallmark of CPP is the symmet-
# L2 t7 R# E% Trical testicular growth secondary to stimulation by2 A# }& B% h  I* m) p
gonadotropins.1,38 q4 H7 ^* K+ y0 q7 U7 S
Gonadotropin-independent peripheral preco-* b7 Z' O( O  V* ^) [7 z
cious puberty in boys also results from inappropriate+ ^, N/ V' g. J) h. Y. B: I& m
androgenic stimulation from either endogenous or) s; y' E, W1 }5 {: N( D
exogenous sources, nonpituitary gonadotropin stim-
7 G9 _$ o" J6 c& u4 @, ^( V4 uulation, and rare activating mutations.3 Virilizing
4 ^+ V, ]6 j! @4 ncongenital adrenal hyperplasia producing excessive
! D" ^/ ^2 B: j& T/ radrenal androgens is a common cause of precocious
- t4 S) E6 }& }! d, k5 Y5 b0 p. Cpuberty in boys.3,4* p0 |$ d  l5 Y, D# x0 i$ c- n
The most common form of congenital adrenal  A% K' g: h" a9 T4 @/ L
hyperplasia is the 21-hydroxylase enzyme deficiency.
/ T/ _2 U/ f2 v: K& e. U4 Z: SThe 11-β hydroxylase deficiency may also result in
; r: ~" d$ |! v; aexcessive adrenal androgen production, and rarely,
& O' j! W( @: X- i  J" |2 a* {an adrenal tumor may also cause adrenal androgen6 S, F. d4 n' p  ]2 S$ X: ?2 q7 @
excess.1,3
; I* ]! \6 R* t, ]at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ H* F2 X0 I( g7 z* Q. k4 G
542 Clinical Pediatrics / Vol. 46, No. 6, July 20073 Z9 s6 R3 Q/ B. h( P
A unique entity of male-limited gonadotropin-/ s, o, O  a& D' T. s+ v) i# a
independent precocious puberty, which is also known
/ H+ o9 t1 W+ T( P8 e0 w) j3 das testotoxicosis, may cause precocious puberty at a
7 h& f: S. y# {$ avery young age. The physical findings in these boys
6 \. Q! k) i: M% ^" L7 M8 iwith this disorder are full pubertal development,
; J# ~0 U3 u! e5 E+ nincluding bilateral testicular growth, similar to boys2 h6 `' E. p( c" I8 F+ a
with CPP. The gonadotropin levels in this disorder
6 C/ U0 l" g* w& u0 m6 ?are suppressed to prepubertal levels and do not show
+ H0 \& i6 d* V* z4 w+ Vpubertal response of gonadotropin after gonadotropin-
- ], S* k7 }0 ^6 x4 J- I% zreleasing hormone stimulation. This is a sex-linked
0 A5 \' v4 t9 k5 Fautosomal dominant disorder that affects only
( J- ]) o7 Q+ o% G6 J1 N) J$ omales; therefore, other male members of the family% A6 u9 D5 x* ?" X% u5 U
may have similar precocious puberty.3
1 H/ a0 O0 ]/ f* \0 V1 `In our patient, physical examination was incon-
$ `/ f4 I/ _$ W! \0 K. V# Lsistent with true precocious puberty since his testi-! w$ I: M! [4 r9 Y/ M' {- t
cles were prepubertal in size. However, testotoxicosis
. e7 U. g2 R/ N4 Lwas in the differential diagnosis because his father2 l6 e( d3 D" G  w
started puberty somewhat early, and occasionally,) S5 X2 X0 e  F  f  @) `% L* J4 o) s
testicular enlargement is not that evident in the; ~! F/ u, V  `/ k* @0 K
beginning of this process.1 In the absence of a neg-. v) r. W; `& W, _/ U! [
ative initial history of androgen exposure, our( \1 y  q; ~# o5 u
biggest concern was virilizing adrenal hyperplasia,
" `7 Z, C+ Q1 reither 21-hydroxylase deficiency or 11-β hydroxylase
1 c! [, |0 s- p' F  x2 A0 ndeficiency. Those diagnoses were excluded by find-+ x7 @2 H. o/ J' w: B
ing the normal level of adrenal steroids.' m5 J0 ?. s' T/ Q/ F) |
The diagnosis of exogenous androgens was strongly
. E( Q& Z% Z- R! Hsuspected in a follow-up visit after 4 months because
1 ^' A# f, V; Z# M5 u9 r1 h- d4 ~the physical examination revealed the complete disap-
' \% b) |0 h/ ], A: Gpearance of pubic hair, normal growth velocity, and, N% p5 H+ s* ]/ t# J4 v
decreased erections. The father admitted using a testos-( `) f- Q! r  N' G' P
terone gel, which he concealed at first visit. He was3 r4 {" S" \# v' I# X
using it rather frequently, twice a day. The Physicians’& m) G) L& p: V
Desk Reference, or package insert of this product, gel or
5 F% m# W4 j" U- F  I1 A6 ucream, cautions about dermal testosterone transfer to
3 b& h2 i4 G7 U7 `: bunprotected females through direct skin exposure.3 z) B5 [$ B1 q. g- _3 _. U
Serum testosterone level was found to be 2 times the: s1 Y6 d; f0 G) _* S; U
baseline value in those females who were exposed to
8 u( u5 N, T& r# m' E% A( |5 d5 ceven 15 minutes of direct skin contact with their male& f+ W  r* b- f7 b9 f! [
partners.6 However, when a shirt covered the applica-6 R# W% n* A/ ]! l" [7 `, E
tion site, this testosterone transfer was prevented.
7 p! D+ M* Q: q0 d$ x; b3 n7 eOur patient’s testosterone level was 60 ng/mL,
1 L0 K- c) g. |5 _# _6 A- G& owhich was clearly high. Some studies suggest that! u: |* b0 m- t3 m: I0 ^0 \4 l2 p
dermal conversion of testosterone to dihydrotestos-1 P  E) D6 S8 Z1 {9 a
terone, which is a more potent metabolite, is more
' V8 k: t8 y* g+ T3 sactive in young children exposed to testosterone+ l1 ^$ s( m. \
exogenously7; however, we did not measure a dihy-
  ]! a2 s$ S, K0 N# Ldrotestosterone level in our patient. In addition to
! p0 y3 N/ |$ I$ c- `( rvirilization, exposure to exogenous testosterone in# A: o+ W$ ]9 f# u2 E& h& F
children results in an increase in growth velocity and% D/ ?( }, t; D
advanced bone age, as seen in our patient.
- r& q8 K8 {( O; ?3 GThe long-term effect of androgen exposure during
8 x  r' ?. r5 bearly childhood on pubertal development and final1 V* \! H1 W% ]$ a- p
adult height are not fully known and always remain$ x- c" h; V9 g$ ~. y. m! z5 T
a concern. Children treated with short-term testos-
! G  v7 v" S) C- c+ g& `% }terone injection or topical androgen may exhibit some
8 p( U. F* C4 s+ w5 J- kacceleration of the skeletal maturation; however, after/ y5 C# E$ l$ w% p
cessation of treatment, the rate of bone maturation
  n: v/ I$ H# l+ j/ \3 g: Tdecelerates and gradually returns to normal.8,9, E( x) M8 Y- J- v: `
There are conflicting reports and controversy) f6 k7 i; K1 p0 w
over the effect of early androgen exposure on adult
2 v4 e" D( ~* ^penile length.10,11 Some reports suggest subnormal2 @+ P2 t% \# {8 g3 w, X
adult penile length, apparently because of downreg-
) H! {  Y* @+ e6 W- `ulation of androgen receptor number.10,12 However,
: \& b1 O* M% b! ISutherland et al13 did not find a correlation between- p8 a' P6 C" A1 l, x
childhood testosterone exposure and reduced adult( l/ Z! ?6 K# k: S8 W
penile length in clinical studies.( _1 [7 A# Y& Y- F4 V! G( m
Nonetheless, we do not believe our patient is
, }2 u- I% i  O% ^going to experience any of the untoward effects from
! h& B! ~" Y0 [9 K1 ]) Stestosterone exposure as mentioned earlier because# F/ |9 K8 f1 o: T2 q1 a' w1 j
the exposure was not for a prolonged period of time.! r  R$ x) s! }: K: r
Although the bone age was advanced at the time of
# P; ^$ M+ ~9 [  L! \diagnosis, the child had a normal growth velocity at4 B1 r) {% O& c2 N' V; i
the follow-up visit. It is hoped that his final adult: b8 w5 d: [7 @5 L( q8 q
height will not be affected.  ]- K8 V- |6 {# z' m7 F( m
Although rarely reported, the widespread avail-
) ~; w9 e+ p8 @. b  M  t9 ^ability of androgen products in our society may# ~- N9 b0 v2 B+ j1 F
indeed cause more virilization in male or female% z) {% G/ f" U- @8 |+ d( y
children than one would realize. Exposure to andro-- w, x+ C- _/ d# r: p
gen products must be considered and specific ques-
7 ~' E4 H' u! @8 ^/ g: k8 [tioning about the use of a testosterone product or( g' N9 s% k4 y4 q+ W/ ^! A6 J
gel should be asked of the family members during
$ C: n) L% \, D6 P+ mthe evaluation of any children who present with vir-/ s% ?6 h9 {& @4 T  u' d
ilization or peripheral precocious puberty. The diag-( w' F' F: E, {3 e/ ?9 S% y
nosis can be established by just a few tests and by- I; ]- U& Z" ~0 T+ u+ m0 y1 b
appropriate history. The inability to obtain such a4 c: ~  F- B1 o( [% W
history, or failure to ask the specific questions, may% D7 {6 w' B! {& O/ h" F
result in extensive, unnecessary, and expensive
/ u4 R1 S9 G8 |" Finvestigation. The primary care physician should be
5 A2 ?% q2 d$ i! H& O/ E* u& Waware of this fact, because most of these children) V) m7 B% q# H, j
may initially present in their practice. The Physicians’
* V) |: n( _3 U9 GDesk Reference and package insert should also put a
  s& q. a0 v# o2 u% y4 ~warning about the virilizing effect on a male or" S: M: |+ `6 m
female child who might come in contact with some-
+ q1 I+ @& n6 s4 k& @9 J  Bone using any of these products.( q; R6 H2 ]8 L0 c* `0 G
References
4 Z5 A2 y) U4 u& H6 ^0 I1. Styne DM. The testes: disorder of sexual differentiation
; x, x1 s3 b+ J1 [+ }7 Hand puberty in the male. In: Sperling MA, ed. Pediatric
! M- i  f% D1 [& y/ LEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
( J$ B5 E6 m, E! }$ v* H# i2002: 565-628.
% W" L% H7 p/ g$ w- Z; a2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
1 v' [( p" r0 d, b. M0 Mpuberty in children with tumours of the suprasellar pineal
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VIP精品區,資源無限好賺金任務區,輕松賺金幣
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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
) o3 ~$ n* s; \% k" T- A; `
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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