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Sexual Precocity in a 16-Month-Old  ?. }. @: u' k. [$ R4 H
Boy Induced by Indirect Topical1 W( g' h4 Z4 R- S& K1 B9 Q2 F
Exposure to Testosterone
* B* Y$ W1 U9 O3 y1 KSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
# g4 R' J; y0 E8 rand Kenneth R. Rettig, MD1) r* Y& u' d2 C6 ~
Clinical Pediatrics
2 g( G* H. y, `) J, l2 H' TVolume 46 Number 6
+ \. Q) I8 E4 f: HJuly 2007 540-543  F( h9 P/ s! Z1 o+ j9 A4 i) N
© 2007 Sage Publications
. g; ]6 X& @: K. E: d  H/ w7 k10.1177/0009922806296651& Y+ K7 ?9 Z4 f2 _3 F( a
http://clp.sagepub.com
; _$ q+ R. _) n' A# ahosted at
- w; o, O) t5 Nhttp://online.sagepub.com% g' {7 e: O$ K
Precocious puberty in boys, central or peripheral,7 W* ^6 s2 v% c
is a significant concern for physicians. Central
, I1 I8 I9 @4 k$ m, h5 \precocious puberty (CPP), which is mediated- q1 f! v! f) B, n. z
through the hypothalamic pituitary gonadal axis, has
! N; O: B) _! Y% Ra higher incidence of organic central nervous system8 j* I3 c; G1 b! g* B; f
lesions in boys.1,2 Virilization in boys, as manifested
( l# |  I0 X/ W& T* eby enlargement of the penis, development of pubic* Y2 N$ B- u/ V/ v
hair, and facial acne without enlargement of testi-
* E5 i5 S& Z! E$ Ncles, suggests peripheral or pseudopuberty.1-3 We& I3 O2 q( E+ C/ a8 e  k$ n, G1 A; n
report a 16-month-old boy who presented with the
+ E. V  G% X- ~- ?/ uenlargement of the phallus and pubic hair develop-9 ]" N7 O; j% z. q. O
ment without testicular enlargement, which was due
0 E$ {2 D2 E$ l7 T3 ]* Dto the unintentional exposure to androgen gel used by
) S+ r# }3 b6 b1 \9 a. W" Q8 s5 p, sthe father. The family initially concealed this infor-
9 [' e' B2 z9 K1 ]+ Y1 dmation, resulting in an extensive work-up for this
. t6 m* ?' T' m* g9 k6 n/ S# }child. Given the widespread and easy availability of0 C- Y+ U% ?" E8 p; j# M
testosterone gel and cream, we believe this is proba-
" n9 A8 d: [+ P. E* x% [bly more common than the rare case report in the
& R2 _2 h9 r- I; o8 B- j- jliterature.47 }3 `6 L7 F9 E/ S8 t2 N
Patient Report
- l+ S1 x1 r8 fA 16-month-old white child was referred to the
9 S; ^# H8 T6 p8 A+ Kendocrine clinic by his pediatrician with the concern
2 @, T) D" n5 D- v0 _) }of early sexual development. His mother noticed
7 p6 H' i, S  H0 K8 I8 vlight colored pubic hair development when he was
6 j0 ^  W1 }* Y  p: Q9 W8 tFrom the 1Division of Pediatric Endocrinology, 2University of
( p5 L; f; g: l) XSouth Alabama Medical Center, Mobile, Alabama.
- e& h, b3 C! t5 L8 d  y2 tAddress correspondence to: Samar K. Bhowmick, MD, FACE,
. S/ Q* g8 T9 z  b, ~8 w3 o! lProfessor of Pediatrics, University of South Alabama, College of
. i4 T6 b7 u7 I6 Q$ p* @( n+ x8 |Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ @. }0 Q& [! v
e-mail: [email protected].
; J# t3 V  h  F4 U5 h, p1 H! K# ?about 6 to 7 months old, which progressively became
3 J1 m% B, V1 W( s+ {3 A7 f% {darker. She was also concerned about the enlarge-& E. ~3 q0 e" j. R, r, b
ment of his penis and frequent erections. The child, G0 {8 F/ U, l1 w
was the product of a full-term normal delivery, with
6 J8 p- F; M* N/ r8 {1 e" D/ Ka birth weight of 7 lb 14 oz, and birth length of, |" Q7 \. }: U! I) N( x  l) ^9 i, T/ F
20 inches. He was breast-fed throughout the first year
" V4 d) X& G* r% a- F9 ~of life and was still receiving breast milk along with
2 |. {  K. n. [% E6 nsolid food. He had no hospitalizations or surgery,
* J6 r9 M  O1 W0 I, \$ `and his psychosocial and psychomotor development
2 n* ]+ i8 U+ owas age appropriate.
5 S' c% I! R3 qThe family history was remarkable for the father,: E+ ^: Z: x3 A9 Q# Z; t2 T
who was diagnosed with hypothyroidism at age 16," k% ], R( i% F9 W
which was treated with thyroxine. The father’s
& E( s  J: ?& m) vheight was 6 feet, and he went through a somewhat$ h4 ?( P3 q) Z' Z8 N# w2 e
early puberty and had stopped growing by age 14.
( i6 T+ ^! l/ K7 W2 p) S3 `' u9 wThe father denied taking any other medication. The
( |$ h6 Y. q8 v- Jchild’s mother was in good health. Her menarche
* S# u& c/ X2 q- Mwas at 11 years of age, and her height was at 5 feet
; F/ w, g' B, i$ a5 inches. There was no other family history of pre-# y0 ~  Q# V1 @1 r/ C, w$ t( G8 L8 {. k
cocious sexual development in the first-degree rela-
: D0 Q9 ~" |) [8 `; Dtives. There were no siblings.; B/ {& x" K: ~# Z7 ]9 m
Physical Examination
+ p7 U3 K3 z; H. i: UThe physical examination revealed a very active,2 c/ ]( [  b0 W
playful, and healthy boy. The vital signs documented' x! l3 g% E0 Y3 D9 n6 z5 Y# i
a blood pressure of 85/50 mm Hg, his length was) B7 W3 V" f9 A
90 cm (>97th percentile), and his weight was 14.4 kg- w3 r6 q: }; l! L
(also >97th percentile). The observed yearly growth- M# f4 M  y4 m) j  ?
velocity was 30 cm (12 inches). The examination of
8 j. Q' I* |! m  G" Y' `$ l1 jthe neck revealed no thyroid enlargement.: e( u+ E9 Q) ?- s3 D+ W6 X
The genitourinary examination was remarkable for
( b  X5 t8 v% L; zenlargement of the penis, with a stretched length of# f2 o, x2 S& @% s( N- k
8 cm and a width of 2 cm. The glans penis was very well
& G6 ^7 I4 U9 Q) ?developed. The pubic hair was Tanner II, mostly around
! r9 P0 w2 I" W1 x5 Z! v( w540
( Q; A5 u. G! j! }at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from8 b+ X3 `1 _* |0 p9 U
the base of the phallus and was dark and curled. The3 J% L3 n# B! \5 m3 W' V* `
testicular volume was prepubertal at 2 mL each., M: i  E) w/ x: I4 L9 E/ M7 Z; u
The skin was moist and smooth and somewhat/ M! N' L- E! J
oily. No axillary hair was noted. There were no- b. \2 O) O3 o/ y9 q
abnormal skin pigmentations or café-au-lait spots., z* w; h5 O' x* b* z$ a
Neurologic evaluation showed deep tendon reflex 2+
( ?, @2 j: }7 X$ m  Ibilateral and symmetrical. There was no suggestion
, x2 O9 b3 L# B6 nof papilledema.
' Q4 q5 ^: I) p% q8 V' DLaboratory Evaluation, c5 T* G8 G  Y0 M" O2 n" J
The bone age was consistent with 28 months by5 X! ~/ w1 }* h( a+ S, ]
using the standard of Greulich and Pyle at a chrono-. m4 B0 a' P3 f6 I  d+ \+ r8 [
logic age of 16 months (advanced).5 Chromosomal
2 `. t- [- b8 `! @+ a7 \5 k, L+ Mkaryotype was 46XY. The thyroid function test
0 j( D5 L3 n" {5 b% n- E7 wshowed a free T4 of 1.69 ng/dL, and thyroid stimu-$ k* ?7 |' |/ S7 F" c
lating hormone level was 1.3 µIU/mL (both normal).# h( z8 R+ I' ?( n, B+ \' s# ?
The concentrations of serum electrolytes, blood
9 F4 O$ |( L8 N' `: Curea nitrogen, creatinine, and calcium all were
8 e. q& Y2 I  T  rwithin normal range for his age. The concentration
1 P; f, |+ _. N; A- w* uof serum 17-hydroxyprogesterone was 16 ng/dL5 y4 P" A" X) @. P
(normal, 3 to 90 ng/dL), androstenedione was 20
7 `) I, I. V) P9 k7 u! M1 `ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
& C/ ]0 O, Z7 ~8 c& yterone was 38 ng/dL (normal, 50 to 760 ng/dL),) r: J' P! h% R/ D( c; O1 p
desoxycorticosterone was 4.3 ng/dL (normal, 7 to6 Y; _; }$ Z4 i8 i) V
49ng/dL), 11-desoxycortisol (specific compound S)
1 e- T6 V* g) T. ?/ F5 r6 R; Kwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
( n  J1 C4 e% w! D1 P: C8 otisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total; x( {( Z3 }( d" k# e4 X; I
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
  M( h  n% e4 a! j/ y( m" cand β-human chorionic gonadotropin was less than5 O( l0 N; m5 K/ R4 G/ X
5 mIU/mL (normal <5 mIU/mL). Serum follicular
. b( a6 |9 |4 X7 \stimulating hormone and leuteinizing hormone& u4 B4 @/ p0 s  K) s5 O/ T) [
concentrations were less than 0.05 mIU/mL% P# C" u! a2 R/ V+ X+ A7 f
(prepubertal).
) d- W3 L8 }7 }/ J1 T+ oThe parents were notified about the laboratory" a& }5 U; \0 P2 I4 l) w
results and were informed that all of the tests were
7 h% N, {8 t/ f/ @0 \5 Q! w! {' [- Znormal except the testosterone level was high. The8 L3 P: d3 i' j$ l
follow-up visit was arranged within a few weeks to, N, g7 J# Q+ N8 Y+ Y
obtain testicular and abdominal sonograms; how-
2 W4 e2 y3 K0 Iever, the family did not return for 4 months.! b3 N9 \0 m' R% S) E6 F* j' t
Physical examination at this time revealed that the
1 X' d& j0 ?) ^. Q  q5 ~4 P% Z' Tchild had grown 2.5 cm in 4 months and had gained
6 o4 n' y7 ~+ }7 t) ~- o2 kg of weight. Physical examination remained  ?) M0 r) q. u6 |' E
unchanged. Surprisingly, the pubic hair almost com-* j6 n: Y% b- t$ Q) ?
pletely disappeared except for a few vellous hairs at5 b" S8 o. a8 \/ J. b& i8 A1 c( Z
the base of the phallus. Testicular volume was still 29 Z  ^- O* x, E0 Q9 M
mL, and the size of the penis remained unchanged.
# |7 z' R9 P) o. x* gThe mother also said that the boy was no longer hav-
" j: z; W  [/ Ding frequent erections.
4 u5 T6 X4 H" L& C, RBoth parents were again questioned about use of
0 {% [' S# n  ~6 s2 i. `9 b( eany ointment/creams that they may have applied to0 q/ j& W; n! h2 W5 t
the child’s skin. This time the father admitted the" U# L7 a5 N/ m% s5 |% e6 T0 D* G* C
Topical Testosterone Exposure / Bhowmick et al 541
) t/ g1 Y5 w+ o4 {2 ^! uuse of testosterone gel twice daily that he was apply-7 ^& V" O. J" Z
ing over his own shoulders, chest, and back area for  I" |0 {, ?: p0 m  S) T0 M! D
a year. The father also revealed he was embarrassed# ]: |* A: i0 u' I
to disclose that he was using a testosterone gel pre-9 _  w' h. r" I4 G/ C8 p8 J$ x
scribed by his family physician for decreased libido- P3 E+ t! Q% G. j: m
secondary to depression.' T+ Y) l  d8 C% |, ]8 k
The child slept in the same bed with parents.9 t( F" R1 l5 N% H* A
The father would hug the baby and hold him on his3 p) G( M. w: Y# F" v7 q
chest for a considerable period of time, causing sig-
4 p6 i% }1 O: }  X6 Knificant bare skin contact between baby and father.0 X( L2 Q( w. y! I$ W( L
The father also admitted that after the phone call,
. W* J8 v4 S, {9 G' Owhen he learned the testosterone level in the baby& k) r+ Q) {. w5 {) `% P" A8 _
was high, he then read the product information
1 M. M( J- d/ Ypacket and concluded that it was most likely the rea-6 Q0 I- a* d7 l+ N5 f
son for the child’s virilization. At that time, they4 E+ ]# t4 n) y
decided to put the baby in a separate bed, and the
* R2 ]  I$ @+ _) ]father was not hugging him with bare skin and had, x3 X0 U( w& @' s
been using protective clothing. A repeat testosterone+ r) N. y5 n# \+ W( Y* {% P
test was ordered, but the family did not go to the
$ [8 S6 I5 b) g4 B  r4 ]1 _laboratory to obtain the test.5 L7 s) c% {" O3 K, U
Discussion2 |$ q% k! j$ O& U
Precocious puberty in boys is defined as secondary0 |8 i1 ?; |6 W7 }2 m. Q8 g
sexual development before 9 years of age.1,4
3 O3 Y) r2 E* N2 IPrecocious puberty is termed as central (true) when
2 K. `! L1 e0 O& a# f- [3 M7 _/ lit is caused by the premature activation of hypo-
* k1 ^  c. K) Y6 }, ]: jthalamic pituitary gonadal axis. CPP is more com-! k1 |7 p5 E+ \4 k" B7 i- h1 D
mon in girls than in boys.1,3 Most boys with CPP% A, `2 J" X8 u' u
may have a central nervous system lesion that is+ R; B' D  i* J( B, z9 v0 Q
responsible for the early activation of the hypothal-1 _( V2 X5 i# O5 Z6 F# W4 u0 ?
amic pituitary gonadal axis.1-3 Thus, greater empha-
& y, \2 `& k, j5 f- A" N, G1 q: asis has been given to neuroradiologic imaging in8 \# v7 P9 V! g/ l# E1 |5 `& N
boys with precocious puberty. In addition to viril-
4 h; t3 G2 O) m. ^ization, the clinical hallmark of CPP is the symmet-# e' t. w. y1 e6 n7 F/ A
rical testicular growth secondary to stimulation by9 O% S7 I' e8 g) }5 c
gonadotropins.1,3
* v4 T4 y5 ^2 {3 z- l# VGonadotropin-independent peripheral preco-' E8 j" Y" E; [! N$ u0 m
cious puberty in boys also results from inappropriate
" W3 n/ c5 \0 d/ ~7 V$ b3 Sandrogenic stimulation from either endogenous or
; S- m7 |) l/ z6 o  G1 I6 K% m7 U# d* @exogenous sources, nonpituitary gonadotropin stim-
$ R; p& x% _1 ^% o7 tulation, and rare activating mutations.3 Virilizing7 V! K2 {  O# C' f  Q" n
congenital adrenal hyperplasia producing excessive
7 b' O# i  |' P# ~! |8 Uadrenal androgens is a common cause of precocious" \# K/ D3 P* _* t! o  s
puberty in boys.3,4* k: e. D; Q! c. a
The most common form of congenital adrenal; A$ ?. t/ U2 M9 E9 Z. J
hyperplasia is the 21-hydroxylase enzyme deficiency.9 t+ q1 R# p( \+ _  X
The 11-β hydroxylase deficiency may also result in; ~% c7 m0 d1 G$ I3 ~7 K$ B& J+ q
excessive adrenal androgen production, and rarely,4 i2 {/ f6 V) ^$ f" }5 b
an adrenal tumor may also cause adrenal androgen
0 C; b! W+ B+ }- w& aexcess.1,3
7 X/ n* [% U/ ?; dat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  m) [2 d! v1 y" _9 M  n3 N9 l% E
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007* r: V# Q6 y) S7 @0 B7 H
A unique entity of male-limited gonadotropin-6 z7 n0 t/ g) n' Q
independent precocious puberty, which is also known
, D; V9 Q! E, W. v  T( Z- W* vas testotoxicosis, may cause precocious puberty at a
% }8 F0 B2 ]# H) Mvery young age. The physical findings in these boys
5 N& {5 I7 h  ~" F5 ~with this disorder are full pubertal development,) X4 v* c, G. Z8 ^2 u+ e$ H  m
including bilateral testicular growth, similar to boys
4 |! U! A1 `7 i0 R! T2 ^with CPP. The gonadotropin levels in this disorder
7 e7 c) l1 O9 e3 v; h' x) ?are suppressed to prepubertal levels and do not show% Z" V  o# {3 G7 L3 @! E5 K4 x
pubertal response of gonadotropin after gonadotropin-
1 C5 \$ C7 [4 u/ X. f+ areleasing hormone stimulation. This is a sex-linked
/ F  w9 Z0 ?7 K; r5 Dautosomal dominant disorder that affects only& v! y3 N- D$ W
males; therefore, other male members of the family
8 n) N# q' Y2 x' q% ?may have similar precocious puberty.3
) T" H, |) h: J0 BIn our patient, physical examination was incon-
$ Y3 T9 u3 G! Z; Lsistent with true precocious puberty since his testi-
0 Y* v$ E  z0 \6 D# b% bcles were prepubertal in size. However, testotoxicosis; N3 C2 |1 u3 ?
was in the differential diagnosis because his father
* U9 p) V1 u/ i+ r6 v( `7 l4 Qstarted puberty somewhat early, and occasionally,
7 h* Y- c; _5 Etesticular enlargement is not that evident in the* G0 s6 n. M4 h+ f- y
beginning of this process.1 In the absence of a neg-
/ H2 x- x$ n3 x; X4 Xative initial history of androgen exposure, our
- H8 |  ]! p$ @, |biggest concern was virilizing adrenal hyperplasia,
+ F& g4 j& {2 I% \6 `! heither 21-hydroxylase deficiency or 11-β hydroxylase  a- |) A* e# R7 X  H! i  x
deficiency. Those diagnoses were excluded by find-# i; F9 R- j7 e. O- v4 [6 ?  {( e: K
ing the normal level of adrenal steroids.
6 \. q* D6 }1 N0 \; b7 q% QThe diagnosis of exogenous androgens was strongly
& D( L$ b/ r3 J' ~suspected in a follow-up visit after 4 months because0 f2 d. w# m; l7 M2 d& S1 j. v. C
the physical examination revealed the complete disap-. j/ v! E* O1 E
pearance of pubic hair, normal growth velocity, and
3 x# H: I" e, B/ x4 p+ h6 j* zdecreased erections. The father admitted using a testos-
' w! M. o7 r+ Y; }6 [0 o0 Oterone gel, which he concealed at first visit. He was0 ~. _! M" B9 i
using it rather frequently, twice a day. The Physicians’
) a) f* f3 {. p. \1 @  w2 CDesk Reference, or package insert of this product, gel or$ }1 O3 X5 ?- b! K: z+ `
cream, cautions about dermal testosterone transfer to: c% ~/ L- m  l# ^2 z$ e% {- [
unprotected females through direct skin exposure.4 p0 k. d" M8 ?8 r: ~; Q
Serum testosterone level was found to be 2 times the$ ~7 |0 p2 O; e
baseline value in those females who were exposed to
$ n- A% V8 e4 I7 ueven 15 minutes of direct skin contact with their male
( `+ ?: l1 ?  _) L% Lpartners.6 However, when a shirt covered the applica-0 W/ B  v+ L5 I; a3 _. V" `, K+ |
tion site, this testosterone transfer was prevented.
' p1 |, b' v& Q1 ~( f9 @& ^Our patient’s testosterone level was 60 ng/mL,
1 @+ q2 _/ p& V: Z$ awhich was clearly high. Some studies suggest that
% }# u( s' U+ gdermal conversion of testosterone to dihydrotestos-
3 u& b& a$ O1 C5 ~" lterone, which is a more potent metabolite, is more' D2 X& d- S: `% {/ ^4 L" u
active in young children exposed to testosterone0 M) s- o) D1 y) I5 ~0 |: d3 D
exogenously7; however, we did not measure a dihy-2 }+ U' }4 b! {' p
drotestosterone level in our patient. In addition to
2 i5 a2 ]5 L2 y; t# p0 }% Lvirilization, exposure to exogenous testosterone in0 {$ j' z. {, d- ]1 Q( {" \' d
children results in an increase in growth velocity and
, D* B# A+ l+ _advanced bone age, as seen in our patient.
& Q9 r6 n5 G& Q+ NThe long-term effect of androgen exposure during6 S6 Z7 T0 Y' Q& d4 ~) B! w
early childhood on pubertal development and final, \9 ~  [; L: \2 m' z+ B) u* w8 V
adult height are not fully known and always remain% H+ a) b& |: ]4 i5 ^3 @8 S% @9 i
a concern. Children treated with short-term testos-9 T. p# U7 Y  ^7 H
terone injection or topical androgen may exhibit some, Z; l: V: b6 d5 J: w
acceleration of the skeletal maturation; however, after1 m8 w1 X4 c( c. m8 k
cessation of treatment, the rate of bone maturation7 ~/ s: U, E( ?; Y' ^2 ]
decelerates and gradually returns to normal.8,9
0 N, L+ d3 K! ^, SThere are conflicting reports and controversy
* \0 U0 [# I- L6 {: Z. a, Dover the effect of early androgen exposure on adult
! P' `% U5 H: r3 x) y/ e5 ~penile length.10,11 Some reports suggest subnormal3 {( m: q. l$ v( |2 n/ S' @
adult penile length, apparently because of downreg-$ [: I* _# g' V6 l2 B: l5 c
ulation of androgen receptor number.10,12 However,# d1 W% w2 D: `( }4 Q
Sutherland et al13 did not find a correlation between
7 \4 `/ D. b0 O4 b) Jchildhood testosterone exposure and reduced adult
4 |, p! g4 b! _) G" z/ kpenile length in clinical studies.
- S) s9 [; E% G- XNonetheless, we do not believe our patient is2 F2 u& J: O' R9 Y3 P$ E% m
going to experience any of the untoward effects from5 o9 L* m& b; X' e
testosterone exposure as mentioned earlier because: o0 t6 \/ {, k7 L* {
the exposure was not for a prolonged period of time." f$ z: @( A2 X- v
Although the bone age was advanced at the time of
& n) Y" k5 y. \  W! Adiagnosis, the child had a normal growth velocity at# o4 A3 {  X2 w& r& M# Z& ^3 {' ]
the follow-up visit. It is hoped that his final adult
6 A" M8 f$ d7 r$ W  q4 a4 H; \3 Eheight will not be affected.9 h  W6 q! w! S. \1 P$ L
Although rarely reported, the widespread avail-
8 o) t- g+ n/ u6 w: Tability of androgen products in our society may' b/ u. l! H- S& e7 w: R. s
indeed cause more virilization in male or female. b- V& H: u4 V. P
children than one would realize. Exposure to andro-$ G0 a6 T5 d' J4 [; x
gen products must be considered and specific ques-+ b, l: c7 t- I5 ^3 p* b0 X
tioning about the use of a testosterone product or
4 X" I, b1 D7 X" D' R6 |gel should be asked of the family members during
' i: }  o$ h+ F% G* Z$ Hthe evaluation of any children who present with vir-
+ r1 T* B, ]3 {5 Z( n! ]. Cilization or peripheral precocious puberty. The diag-, ]! O: K; }3 @" x1 |+ ?
nosis can be established by just a few tests and by  z2 U( o' V* V% q) Y+ ]
appropriate history. The inability to obtain such a' n/ F/ ?: P$ I! D
history, or failure to ask the specific questions, may
  k8 M" F* V1 I) K' ?' D+ nresult in extensive, unnecessary, and expensive2 }3 o' ^6 \, t; b7 k2 D
investigation. The primary care physician should be& M7 F% _/ k% K6 K
aware of this fact, because most of these children
7 T$ \7 g5 e% ~9 f; }6 Emay initially present in their practice. The Physicians’
: x( f9 m. w! o! l5 r9 KDesk Reference and package insert should also put a) L- s: |* f: _! D
warning about the virilizing effect on a male or% _- O4 ?, g3 J+ u4 b# B
female child who might come in contact with some-# Z/ y4 u! }4 y0 _0 l: m
one using any of these products.% v! v' D+ V: q# {) A  ]
References
5 Z/ U- J( ?8 j5 J1. Styne DM. The testes: disorder of sexual differentiation
' ~4 T  F; D% r# X, n$ N3 cand puberty in the male. In: Sperling MA, ed. Pediatric1 C: ^3 {7 d) ?# f/ `( e3 X) Z! ]
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;. ~2 ]9 A: {( B9 c  f0 U
2002: 565-628.
7 T; L: x! ~2 i1 w% N$ A2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious5 W* ~% U" E  k  O, {
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
% Z  p9 z# y% H, H, e& kBoy Induced by Indirect Topical
3 Y5 Z7 v6 |( E" w* H* N; FExposure to Testosterone& G$ z6 h# d9 L
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
: S& d: Z. u" U! `6 ]and Kenneth R. Rettig, MD1, J* y5 t8 w+ [5 C" l; \& g$ x
Clinical Pediatrics- }! j; W9 I8 Y
Volume 46 Number 64 Y! F% c2 ^  Z
July 2007 540-5439 O( V' N* B% O2 p  g
© 2007 Sage Publications( S/ C) a. T. H" S) j6 ^
10.1177/0009922806296651. r/ J9 [/ R! z: d3 @$ L! b( m$ T
http://clp.sagepub.com5 u7 u$ i2 T! B( S8 F
hosted at
* w) W! Y# y8 O" E2 Y8 _; jhttp://online.sagepub.com  N  L. ~: f' k3 R9 v, y. u7 U- _
Precocious puberty in boys, central or peripheral,8 l% C: p9 j0 W9 `  e7 x/ l
is a significant concern for physicians. Central3 p! [3 c% \# B" y
precocious puberty (CPP), which is mediated; c6 W9 T1 u7 r; H
through the hypothalamic pituitary gonadal axis, has% L  m5 `8 i( a$ ?3 E- H: ~
a higher incidence of organic central nervous system3 w( q* n) \+ T, [! L
lesions in boys.1,2 Virilization in boys, as manifested: A! K$ ?/ b1 {3 H
by enlargement of the penis, development of pubic8 }$ q2 S% C* [) V3 Y( ]
hair, and facial acne without enlargement of testi-2 S, ]2 l0 Z' i1 g
cles, suggests peripheral or pseudopuberty.1-3 We
* ^1 B- _0 V: b) r! I; k# [5 sreport a 16-month-old boy who presented with the- d, Y% A- ?( E! D, B! H, T
enlargement of the phallus and pubic hair develop-
* r8 N0 y. r" c0 U. ~  y( ]ment without testicular enlargement, which was due
# ~: H; f% y- Y' mto the unintentional exposure to androgen gel used by
# g2 t4 ^: V, e5 q& Q) c3 c! sthe father. The family initially concealed this infor-5 ?  I3 ~2 h+ s# }: {
mation, resulting in an extensive work-up for this
8 i9 L6 ]  e: M; s. y; L6 e( Ichild. Given the widespread and easy availability of
& ~5 A* }$ J- a6 ^% ?  p/ M: gtestosterone gel and cream, we believe this is proba-4 t$ o- x/ J% l1 I2 P8 M; j+ L
bly more common than the rare case report in the
* @5 ~$ p) d' ^# v! }5 g" vliterature.4- P( c2 I' g$ [8 m6 s) n0 S
Patient Report
+ A1 [' ?# ?" {% y' _- [A 16-month-old white child was referred to the( F  ~  m  s" ]5 A# n  T
endocrine clinic by his pediatrician with the concern" s1 G# r; z$ E# j! V& O) h
of early sexual development. His mother noticed
; }3 O* e8 {/ a1 glight colored pubic hair development when he was
0 Z4 t' q+ A$ _% q0 C' VFrom the 1Division of Pediatric Endocrinology, 2University of' B7 n9 A# k4 e/ O$ u, }' V
South Alabama Medical Center, Mobile, Alabama.3 F" U2 a4 `8 t4 v
Address correspondence to: Samar K. Bhowmick, MD, FACE,
* Z) c+ i* \7 H* t& T: s3 N8 TProfessor of Pediatrics, University of South Alabama, College of
$ C- W! v2 ~0 R0 `# }Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;8 @6 u0 E" ]1 l" V, C! \6 {
e-mail: [email protected].; o" x# R8 h) s& P, w
about 6 to 7 months old, which progressively became. V! i0 x+ t! W; P: z
darker. She was also concerned about the enlarge-
# R2 E3 |, h$ W, ~9 W5 Qment of his penis and frequent erections. The child& i  I2 B6 {6 o$ ]5 C- g
was the product of a full-term normal delivery, with+ s% i; R1 U( o1 X
a birth weight of 7 lb 14 oz, and birth length of5 U$ ], g3 m9 r5 _3 F- b
20 inches. He was breast-fed throughout the first year- S/ L& [; k) F8 Y; M* ]" u; T
of life and was still receiving breast milk along with
1 a- g& K) P) x& L) r' `solid food. He had no hospitalizations or surgery,
6 ~; n8 G( e$ w, {5 pand his psychosocial and psychomotor development
+ a( g" f0 M. ?6 j" k+ Y. Zwas age appropriate.+ V" G! d: G. [
The family history was remarkable for the father,
/ [9 z) O! B8 h) q: \3 E8 [1 Uwho was diagnosed with hypothyroidism at age 16,
+ w7 S9 |5 j# L. H& Rwhich was treated with thyroxine. The father’s
; y: l7 b1 z, o& @. Sheight was 6 feet, and he went through a somewhat* ?7 a. L; T! b4 m" p: E! L. u, e
early puberty and had stopped growing by age 14.
* H2 e: ?2 }" o" ^* @9 m& tThe father denied taking any other medication. The* N+ ?9 C" {3 g% q1 @
child’s mother was in good health. Her menarche
. s, q) e" Q- A7 gwas at 11 years of age, and her height was at 5 feet9 M$ N% m' J3 L9 r/ j8 s$ W7 R. g
5 inches. There was no other family history of pre-  B2 G$ u. J% P
cocious sexual development in the first-degree rela-, x6 @/ Y) y. }: w& i! `( R
tives. There were no siblings.0 ?) J6 q9 f0 n4 ]2 ^7 }% q9 s) u# V7 j
Physical Examination
: d7 V4 D; V/ e( C) {' AThe physical examination revealed a very active,
; v: T) R- ~: |* l8 `playful, and healthy boy. The vital signs documented
' l) b* T% j8 x/ n; ^8 sa blood pressure of 85/50 mm Hg, his length was
# J  A9 {& i# L90 cm (>97th percentile), and his weight was 14.4 kg. q$ N3 A+ T' t$ R( }" `1 k
(also >97th percentile). The observed yearly growth: _, E2 k* r" Z
velocity was 30 cm (12 inches). The examination of
; s: ?8 W0 H8 S3 j# D* |the neck revealed no thyroid enlargement.2 _. b: L5 u$ e9 |& @7 f6 [" z( U
The genitourinary examination was remarkable for' y0 i' Q7 ?) D4 u2 k$ T
enlargement of the penis, with a stretched length of
2 \4 _  g9 A9 Y# s2 ?8 cm and a width of 2 cm. The glans penis was very well
/ L6 p. }  k# P. adeveloped. The pubic hair was Tanner II, mostly around5 R0 W% |% L2 d; u3 J( |; A# j* X
540
1 G3 k$ {5 v& @0 v; _( rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ k9 H. G7 L8 d: S! l; D% b) fthe base of the phallus and was dark and curled. The' D) |5 J8 t# P' t( M
testicular volume was prepubertal at 2 mL each." @7 U* |  _( \
The skin was moist and smooth and somewhat
- o+ ?- n& T  L; R( t* Coily. No axillary hair was noted. There were no
* Y* }$ L) y# |) u( l3 P9 habnormal skin pigmentations or café-au-lait spots.
+ Q, k* W5 o3 k$ `Neurologic evaluation showed deep tendon reflex 2+
3 }/ n. K0 e' x& p% kbilateral and symmetrical. There was no suggestion
+ l( k2 M2 v& @& [of papilledema.
4 T5 ]7 p4 d. v+ DLaboratory Evaluation
8 j5 H, h5 k8 h6 WThe bone age was consistent with 28 months by
1 U  Y  j/ ]& C( [9 t  ^0 @  Musing the standard of Greulich and Pyle at a chrono-# C2 ]+ |+ K1 A
logic age of 16 months (advanced).5 Chromosomal
5 B0 j% d- k: V  lkaryotype was 46XY. The thyroid function test  n1 W3 ^+ C, R& F# r4 I* W
showed a free T4 of 1.69 ng/dL, and thyroid stimu-; K* z1 B. h' n9 W6 o" a
lating hormone level was 1.3 µIU/mL (both normal).
) ~& o( A. q. b9 V) I& VThe concentrations of serum electrolytes, blood
% j% f; {2 Q$ H$ v/ X* D/ c; }urea nitrogen, creatinine, and calcium all were
# J* B! B3 t8 ^  T5 }( nwithin normal range for his age. The concentration
1 R- k; q1 o8 r7 q  H; }of serum 17-hydroxyprogesterone was 16 ng/dL+ E) i; ^' [5 @2 @1 y7 q( j; I
(normal, 3 to 90 ng/dL), androstenedione was 20
0 q$ R) ]" v' O/ X1 xng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-% t/ ]% {# N* G- a! A
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
; b" L4 o& g) y* U: V% i5 ^desoxycorticosterone was 4.3 ng/dL (normal, 7 to2 D# o1 M. {/ ~) Y
49ng/dL), 11-desoxycortisol (specific compound S)* r% w9 m2 v3 p$ e; Z5 E; H% X3 [
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
& G# }$ K1 O* V. e4 i( m9 s! ftisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
0 _. D0 d* z( W: g2 Jtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),) w* s, `4 C, `: W' n# ~$ L$ w
and β-human chorionic gonadotropin was less than
2 ^2 k1 v1 b3 }5 t5 mIU/mL (normal <5 mIU/mL). Serum follicular5 u% @1 L  L7 U* {
stimulating hormone and leuteinizing hormone8 f3 z6 w6 C0 e+ B/ Y2 E& |. y
concentrations were less than 0.05 mIU/mL- V% r) x1 `8 V3 @
(prepubertal).
# z# x) C+ f$ `$ @% O; J4 P' OThe parents were notified about the laboratory0 K" n4 {* W7 C  x- d
results and were informed that all of the tests were( c3 x$ d! v8 ~3 o  @* }
normal except the testosterone level was high. The9 w$ x) S$ X0 M  @3 O
follow-up visit was arranged within a few weeks to
1 m7 d* c. I% }9 W7 ^0 V$ gobtain testicular and abdominal sonograms; how-1 X* |, J. F: \7 J# _+ Z9 q
ever, the family did not return for 4 months.
! S6 `4 J8 U7 w" w/ e& {$ ~Physical examination at this time revealed that the* ^$ q; w& I9 @' x0 R. |
child had grown 2.5 cm in 4 months and had gained
* H2 {5 X5 D6 n$ q2 kg of weight. Physical examination remained
! X. U8 _( A0 ], e1 @unchanged. Surprisingly, the pubic hair almost com-) _4 ]1 `" a% n0 m
pletely disappeared except for a few vellous hairs at
4 A) h( h, W9 {' \7 g1 Z. Qthe base of the phallus. Testicular volume was still 2
) _) C! v+ {: z: L; v" EmL, and the size of the penis remained unchanged.( y$ T6 f6 {5 q
The mother also said that the boy was no longer hav-# v+ I! W. P. g+ D
ing frequent erections.8 p! U; K% V! z! z3 t0 N2 M6 U  U
Both parents were again questioned about use of
4 L: H, |$ D5 m/ P% P7 `& h/ Oany ointment/creams that they may have applied to, n! J  L1 \: R9 s( D2 D2 w" W" X
the child’s skin. This time the father admitted the
& A- S9 K- }1 y+ x3 h* g" ~Topical Testosterone Exposure / Bhowmick et al 541* M3 w/ S$ t* d9 ~, H6 K' X9 W
use of testosterone gel twice daily that he was apply-( {8 @8 L  I# h7 U3 S
ing over his own shoulders, chest, and back area for$ H+ Z0 @9 U7 `7 q4 X( x5 |
a year. The father also revealed he was embarrassed6 x- |. y5 ?6 C1 C! l
to disclose that he was using a testosterone gel pre-
. l5 _9 f" R8 ^! ~7 p, ~scribed by his family physician for decreased libido
3 p: r& ]! u; @7 u; ?3 Zsecondary to depression.
4 l  r0 q; A! ~1 Y4 W2 BThe child slept in the same bed with parents.  U  d0 O! M$ r4 D, F8 l1 N4 e/ {
The father would hug the baby and hold him on his# I" k, K6 }9 |1 B+ P5 e4 S
chest for a considerable period of time, causing sig-
- z! s* r( p2 Y/ ?nificant bare skin contact between baby and father., @0 I; }( G. H8 q( v$ g$ d
The father also admitted that after the phone call,
7 T+ B5 {& T! L8 U$ {when he learned the testosterone level in the baby
* U/ }( ^# D3 G4 ]- n; Fwas high, he then read the product information2 o4 V; _% w4 \/ b) \* L8 x) K. X
packet and concluded that it was most likely the rea-! z' d5 A; x+ F# e# T
son for the child’s virilization. At that time, they
: i# T7 O' U) }; a+ b  A7 m' ?decided to put the baby in a separate bed, and the
, x7 W: [' M! L# pfather was not hugging him with bare skin and had- r. G7 o, m# k5 V/ s' ?- F
been using protective clothing. A repeat testosterone
2 O2 ]  I% [* g# o2 Xtest was ordered, but the family did not go to the* b; N& m4 B1 K" ?; z
laboratory to obtain the test.
' a  _9 O% K& o) N6 o  pDiscussion
1 C8 `! U: S/ ]/ B  T, gPrecocious puberty in boys is defined as secondary+ g0 k0 J3 U) r! X
sexual development before 9 years of age.1,4
( z, z' d+ E( K/ r' D9 p! ?7 FPrecocious puberty is termed as central (true) when" e# y2 v& V% z( d
it is caused by the premature activation of hypo-* i/ q! q; f2 L  X8 ~! d
thalamic pituitary gonadal axis. CPP is more com-
2 }2 d: h& u% `% p" xmon in girls than in boys.1,3 Most boys with CPP0 G3 B& [0 F' ?7 v2 |$ C
may have a central nervous system lesion that is; R3 J$ e6 P1 z( `5 M
responsible for the early activation of the hypothal-2 {0 N- Q. s7 `/ a2 M9 c
amic pituitary gonadal axis.1-3 Thus, greater empha-# f- L, A+ w/ i8 d2 T
sis has been given to neuroradiologic imaging in
" C: }" u: ^9 A3 I1 A. Wboys with precocious puberty. In addition to viril-
! Y/ W" {! u0 Q) V1 u* i6 C0 iization, the clinical hallmark of CPP is the symmet-- |* e/ W/ M' \
rical testicular growth secondary to stimulation by4 s) X/ f+ D3 p" L
gonadotropins.1,3# _1 j& V9 Y: W5 ^3 N
Gonadotropin-independent peripheral preco-
. c+ }3 j3 `4 r  h% Gcious puberty in boys also results from inappropriate% L% c; N: x. G+ i% [
androgenic stimulation from either endogenous or7 U8 t/ q: B" l
exogenous sources, nonpituitary gonadotropin stim-
$ J+ }9 ~5 }/ [ulation, and rare activating mutations.3 Virilizing  l+ x* N- g0 |2 x( F
congenital adrenal hyperplasia producing excessive
* j* Y" O# Z( Wadrenal androgens is a common cause of precocious* B8 |' l. T8 e% W6 q" A; u
puberty in boys.3,4
: i, Y- T! M, J7 a5 N+ bThe most common form of congenital adrenal$ I  M* O! O$ K, X0 q
hyperplasia is the 21-hydroxylase enzyme deficiency.
" _% B# M; c/ oThe 11-β hydroxylase deficiency may also result in
6 x6 F0 d9 f* `7 Oexcessive adrenal androgen production, and rarely,
& G# I( I- [! d: C; H$ m$ a+ m3 ean adrenal tumor may also cause adrenal androgen3 p* W5 k% \4 @& T2 C
excess.1,3  C; @/ P) F  [: B9 b% X: ^% j
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( ?9 C& C& t1 G6 B* N' ~# r: B, _; Q: Y542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
9 e  @( f: Z4 _) l0 vA unique entity of male-limited gonadotropin-
) M  r+ U5 l9 X9 l+ sindependent precocious puberty, which is also known% k) j. K% \2 h  ^" j! d
as testotoxicosis, may cause precocious puberty at a1 `# _/ \, i9 }) q$ M2 F  z$ a2 S
very young age. The physical findings in these boys
( ~& U" [# _& r! r" ywith this disorder are full pubertal development,
* M) d- v8 O9 d2 f9 Y0 z% u4 {3 _$ o2 yincluding bilateral testicular growth, similar to boys
* v6 N* y2 g8 kwith CPP. The gonadotropin levels in this disorder
% Q- X/ |8 D: I- g. aare suppressed to prepubertal levels and do not show0 B6 x, L1 t( q5 n0 K: P# Q
pubertal response of gonadotropin after gonadotropin-
, Q( L. D1 M9 r, Preleasing hormone stimulation. This is a sex-linked+ N+ d' E# v" n8 `
autosomal dominant disorder that affects only
3 ]" l0 L* n/ @males; therefore, other male members of the family
* x1 r0 V8 {* h9 M0 F+ q2 H0 hmay have similar precocious puberty.3
( t1 X/ g3 D) k9 z- fIn our patient, physical examination was incon-
! Z1 z! v# e" n1 Bsistent with true precocious puberty since his testi-
! W) y3 M: I; Y( X+ c' gcles were prepubertal in size. However, testotoxicosis
- P8 g1 ?( a+ X3 x! jwas in the differential diagnosis because his father
3 s, [% ~  L7 k2 {started puberty somewhat early, and occasionally,
' L  `+ [2 h/ J8 Ftesticular enlargement is not that evident in the# K) t, V' J& c: F/ W
beginning of this process.1 In the absence of a neg-" m# F6 j" z- A" O/ i9 j# H, Z
ative initial history of androgen exposure, our
; ~# Q, @8 N- R5 W$ u  g% m" @biggest concern was virilizing adrenal hyperplasia,
% @. @( K" H. N. U1 j3 B  s8 w: l' Neither 21-hydroxylase deficiency or 11-β hydroxylase
* P  u# h$ I2 n; p$ |! F& i9 ^" `deficiency. Those diagnoses were excluded by find-+ R6 i: s& c3 Z: z
ing the normal level of adrenal steroids.
% P& _# K8 d$ w; O- H7 ~The diagnosis of exogenous androgens was strongly
( X( i4 m( q( j0 N* b3 h$ dsuspected in a follow-up visit after 4 months because. ~9 Y/ |$ s0 H0 S5 c# k; C$ H
the physical examination revealed the complete disap-
4 a( X7 t* o: \4 vpearance of pubic hair, normal growth velocity, and
( R( x6 N! R+ p4 j, f7 Mdecreased erections. The father admitted using a testos-
" @# H! W+ }# x7 z8 B4 K) tterone gel, which he concealed at first visit. He was
+ u: |; h& @+ k) v0 o! u2 Dusing it rather frequently, twice a day. The Physicians’
' Q: M$ Z8 ^$ KDesk Reference, or package insert of this product, gel or4 Z: @* k3 J, q- ?3 I. T5 V
cream, cautions about dermal testosterone transfer to" g5 }" ]) d) ^% Z" d! q0 r
unprotected females through direct skin exposure.2 O4 W, }( u1 s8 ?
Serum testosterone level was found to be 2 times the
) c) T5 `; c+ }9 Q) f* }8 P! j# wbaseline value in those females who were exposed to. k& d1 ?/ f* G" P0 R) g8 _
even 15 minutes of direct skin contact with their male4 f5 I' Q- ]% r' V
partners.6 However, when a shirt covered the applica-' l9 R# x; y2 \/ i4 }' `$ x
tion site, this testosterone transfer was prevented.5 W* R3 h. x# X  f* B
Our patient’s testosterone level was 60 ng/mL,
4 x1 t# b* f7 G8 p" k- u* d! Q: kwhich was clearly high. Some studies suggest that
; ~% ?9 @8 f5 m* s' Gdermal conversion of testosterone to dihydrotestos-
9 I4 ^& Z4 @  H! M- D! aterone, which is a more potent metabolite, is more
- F* {# C" A7 l% Qactive in young children exposed to testosterone
6 |% C7 Y5 [' P( fexogenously7; however, we did not measure a dihy-( d/ a, w, N/ m& y1 d
drotestosterone level in our patient. In addition to
- K6 b; d1 x0 C9 e# ?7 q8 Jvirilization, exposure to exogenous testosterone in# G. ^, z: V! ]7 a" g
children results in an increase in growth velocity and
. Q' @' h# Q: t( @) @1 E+ Aadvanced bone age, as seen in our patient.
7 {4 a5 [% h8 N3 NThe long-term effect of androgen exposure during
4 k4 O2 O! y( s, z$ ^) q1 q$ \/ eearly childhood on pubertal development and final/ `+ A/ P+ w! {! _1 c
adult height are not fully known and always remain
$ q" V; o) g9 X/ E9 n+ e/ Z/ ia concern. Children treated with short-term testos-
" r" V: }3 F1 x5 ]$ f- ]terone injection or topical androgen may exhibit some  l3 k2 W' l1 n1 l7 P. \
acceleration of the skeletal maturation; however, after
. T1 o- _- `1 ?/ ]4 Y, Ocessation of treatment, the rate of bone maturation
8 J, \1 p0 s! g6 W" l# qdecelerates and gradually returns to normal.8,9
: t+ {* E+ n( A5 w: i. [There are conflicting reports and controversy1 }- `1 ]0 m/ b' V% C' W
over the effect of early androgen exposure on adult  H  j9 K1 ~2 {  C3 W7 b+ c
penile length.10,11 Some reports suggest subnormal
: b* T9 O5 N$ v( Z  U* Y7 Hadult penile length, apparently because of downreg-) \4 J! M1 ~. A% {
ulation of androgen receptor number.10,12 However,
: E6 x9 _$ \, F$ ~: P) L& ?Sutherland et al13 did not find a correlation between6 l/ E8 S+ I" h; p
childhood testosterone exposure and reduced adult
1 ]7 b7 u6 P% X" P5 T+ Z! ~penile length in clinical studies., N9 e  a2 g, n; J, z0 P8 a4 X
Nonetheless, we do not believe our patient is
! ]7 v# p8 f1 K; }going to experience any of the untoward effects from
2 x  \* o! J+ T1 Qtestosterone exposure as mentioned earlier because
: V6 h) C& g% n% othe exposure was not for a prolonged period of time.
. G" k( b1 Z( Q8 c( j6 M, e# u" AAlthough the bone age was advanced at the time of
! X% l5 l# g6 Q& Cdiagnosis, the child had a normal growth velocity at
( F, ?' t0 ~& ~/ xthe follow-up visit. It is hoped that his final adult
" W: K, i+ I1 w5 \9 C# _height will not be affected.
6 o" ?' X, z' K7 O, B: t7 qAlthough rarely reported, the widespread avail-3 G6 [. G8 O. T4 Q+ U
ability of androgen products in our society may
, m  B1 L; z- g- zindeed cause more virilization in male or female1 r$ g# K: B. k0 m' R! N
children than one would realize. Exposure to andro-
& H1 k  B- e+ ngen products must be considered and specific ques-( O" k! O% M3 @) i
tioning about the use of a testosterone product or+ M6 ~: L; f7 {7 O6 {+ W- f
gel should be asked of the family members during% Z! n, L$ w6 o6 v- G) i. w1 S% i
the evaluation of any children who present with vir-
3 h) n! L% Q# V6 milization or peripheral precocious puberty. The diag-
& B1 Q1 b& g) V: s9 s: ~* X4 E! hnosis can be established by just a few tests and by( s/ x9 h1 d; y& e% E* l$ d. n
appropriate history. The inability to obtain such a
% J$ P6 a& U% O) I* c+ S+ r3 }# phistory, or failure to ask the specific questions, may
4 e- d7 N( h7 l2 \result in extensive, unnecessary, and expensive
5 ?3 k* X& ]0 B- T" Kinvestigation. The primary care physician should be9 K: i/ H' ^0 W9 p% u
aware of this fact, because most of these children- e2 l  ]' ^& g4 `( b8 Y
may initially present in their practice. The Physicians’- e5 Z  ^1 [: X. u0 y# N* Y
Desk Reference and package insert should also put a) g0 C: D0 ]) y
warning about the virilizing effect on a male or
: i( n. Q! g+ n( h$ ^female child who might come in contact with some-) T5 N2 Q0 Y7 i
one using any of these products.
' G4 F4 l1 Z' r2 e6 f5 {/ hReferences( ?% ]; ^* Y2 v+ y6 ^( K$ k
1. Styne DM. The testes: disorder of sexual differentiation+ H4 B! H, g: h- X+ V7 h) F
and puberty in the male. In: Sperling MA, ed. Pediatric
% X$ r5 ^2 o# |; c: `; aEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
0 w/ q. r$ Y' \% h) l2 g. g2002: 565-628.
8 f  O& T7 V5 X2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious6 L8 Z% [$ T+ W. S( R7 d
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
9 {1 e- m! j7 D0 N/ |
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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