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Sexual Precocity in a 16-Month-Old
% U$ s. K! S: RBoy Induced by Indirect Topical, i7 Z6 K5 x+ ]9 T$ S
Exposure to Testosterone
3 i/ W, `+ {9 _) h) nSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
  \9 [/ }; s$ y$ land Kenneth R. Rettig, MD1
& |2 f3 U- T% |: P* l  Y6 FClinical Pediatrics. k( k( i( b  G' L
Volume 46 Number 69 U, E6 b/ b8 g& N3 k  T8 P
July 2007 540-543
( Z  R! g4 k/ c8 a© 2007 Sage Publications
1 B2 A: H( k9 B2 l& A10.1177/0009922806296651
6 U# f% E0 X" N- b# A) m2 s9 {6 bhttp://clp.sagepub.com
( }8 e& P- K5 y1 r# k1 Zhosted at
+ s- N# C  ?4 n, i7 k0 vhttp://online.sagepub.com8 b4 S- F% x$ }; a2 U4 R
Precocious puberty in boys, central or peripheral,6 ?, N9 E4 I- R
is a significant concern for physicians. Central" f8 D( ]2 g! Q- J3 O
precocious puberty (CPP), which is mediated
4 x- @  D) H: I. pthrough the hypothalamic pituitary gonadal axis, has% k" P& {' v. S4 _# y: |7 H! E! B# f
a higher incidence of organic central nervous system5 Z7 W, ~2 ?4 d( K% F
lesions in boys.1,2 Virilization in boys, as manifested
3 |9 b# v1 |* p# D3 Iby enlargement of the penis, development of pubic* w9 M# t5 Q4 W7 x% x
hair, and facial acne without enlargement of testi-3 h2 |/ V' j: o
cles, suggests peripheral or pseudopuberty.1-3 We: L0 p2 i( x4 K/ n
report a 16-month-old boy who presented with the
) \  p. W2 C  x3 i8 W# Renlargement of the phallus and pubic hair develop-9 s1 h4 I: q0 ]* p* E) z. B8 O. w
ment without testicular enlargement, which was due
3 C; _: P# n. b- D; i7 g" z8 m6 ?to the unintentional exposure to androgen gel used by
% X8 \! C! o( z( b# g7 Ythe father. The family initially concealed this infor-# ]0 M2 \1 b$ |5 _" q6 r2 ~
mation, resulting in an extensive work-up for this9 B9 B2 V/ q) u: F: A1 V
child. Given the widespread and easy availability of
% o3 v2 Q1 F' H8 s. rtestosterone gel and cream, we believe this is proba-& O8 s! P2 ]* L/ ^4 b: E- t
bly more common than the rare case report in the0 B! Z/ F$ Q, K; A% Z. s+ Z
literature.4
2 c0 k6 g7 T' {3 r* E# S( B4 |Patient Report. l( h& e9 b% A4 N; {7 D: C* s' ]3 |' u
A 16-month-old white child was referred to the* @* M$ U# g0 q, I  n1 {0 d& g
endocrine clinic by his pediatrician with the concern
  p2 z$ z0 E7 W5 O6 E& W% sof early sexual development. His mother noticed
+ m; G2 U& }4 F5 @light colored pubic hair development when he was
6 H5 o' X& B( L6 w/ _From the 1Division of Pediatric Endocrinology, 2University of
% k. l7 u7 K! _1 n" W% TSouth Alabama Medical Center, Mobile, Alabama.
# E0 M4 b) D8 f( DAddress correspondence to: Samar K. Bhowmick, MD, FACE,& J& N  n/ y- M! B7 F) l2 ]- {/ T
Professor of Pediatrics, University of South Alabama, College of& U# g. L7 R6 k1 ~+ }- b9 S; g7 ~
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;5 f- P1 S; I' ?
e-mail: [email protected].0 z5 l4 W$ e3 W3 e8 L8 n  K2 z+ C
about 6 to 7 months old, which progressively became
5 q, V7 f! s4 p. q9 l3 a+ F! @2 kdarker. She was also concerned about the enlarge-9 a4 q( f5 l3 a+ |0 }1 O
ment of his penis and frequent erections. The child! @1 }2 D! O6 I7 h4 f
was the product of a full-term normal delivery, with
9 w9 W3 F3 X: Y/ ~- Aa birth weight of 7 lb 14 oz, and birth length of
0 L* _% m1 j# H. p7 s20 inches. He was breast-fed throughout the first year% c% }' Q: y; J) G3 n) p. L
of life and was still receiving breast milk along with
6 U- S1 H$ g/ {# m# O' E! }solid food. He had no hospitalizations or surgery,
, U. I; ^9 G6 N' U- _, [and his psychosocial and psychomotor development; X. f% x) [7 U1 _. }
was age appropriate.
8 G( A0 w: X3 e' lThe family history was remarkable for the father,
) h* h7 }* z9 b) {+ c4 D3 lwho was diagnosed with hypothyroidism at age 16,
$ s3 C: Y/ M. g0 Wwhich was treated with thyroxine. The father’s
6 d3 h/ l+ L4 a+ }. i4 V  aheight was 6 feet, and he went through a somewhat7 {5 M! Y! x9 Q. d
early puberty and had stopped growing by age 14.% l# V1 ~9 g% @% l7 z
The father denied taking any other medication. The2 B% W9 o% [# p, `
child’s mother was in good health. Her menarche" F" F" D/ Y- `  ^% o, e9 Z
was at 11 years of age, and her height was at 5 feet
6 L3 g/ {' D1 F' P9 g8 T5 inches. There was no other family history of pre-2 H1 s3 ^2 `. R! A- [
cocious sexual development in the first-degree rela-! y) i2 k) Q. p. j" s
tives. There were no siblings.
! \. F' G) p' @! R9 j1 `Physical Examination: i- D; L" y3 i1 q# x0 m2 ~
The physical examination revealed a very active,
6 S. W& }' q7 h7 eplayful, and healthy boy. The vital signs documented
  B1 u0 p, S' n, u- F8 Q; y; N8 @! ha blood pressure of 85/50 mm Hg, his length was: e; P* ~+ I5 _/ L" t1 N! p
90 cm (>97th percentile), and his weight was 14.4 kg" h2 u9 W6 U, D. r6 e4 W" i
(also >97th percentile). The observed yearly growth
+ o1 `/ n0 M3 G" F' |& y4 Lvelocity was 30 cm (12 inches). The examination of
% v# k% B; F4 y+ d) [the neck revealed no thyroid enlargement.( S* M( H) t. f. z: J- S% V
The genitourinary examination was remarkable for1 l  t. m) c# J" L1 {7 p* F
enlargement of the penis, with a stretched length of
/ B" L7 c6 ~, o5 A8 C) {$ ~8 cm and a width of 2 cm. The glans penis was very well+ H- W9 y6 r% j; v; B
developed. The pubic hair was Tanner II, mostly around6 j# W; D  ~7 l- B& ^) l
5402 R5 d5 i  v0 A7 s% Y# a
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' m" @) \; ^" b% S5 z/ `
the base of the phallus and was dark and curled. The" L: S/ G6 m  B/ z! Z% u" k4 `
testicular volume was prepubertal at 2 mL each.
4 R4 b1 s6 E0 c% _) G7 `; @The skin was moist and smooth and somewhat7 d" Q0 r% r, r1 u! U
oily. No axillary hair was noted. There were no2 z5 m+ E+ ~" y0 x: B
abnormal skin pigmentations or café-au-lait spots.3 k( d7 _- C$ z
Neurologic evaluation showed deep tendon reflex 2+
/ i, Y; V1 {! rbilateral and symmetrical. There was no suggestion2 P7 r) }- i: |7 z4 Q6 i
of papilledema.
0 K- F6 |$ ?/ \Laboratory Evaluation% M; }. B( \! `
The bone age was consistent with 28 months by3 H" K# Z  W8 g
using the standard of Greulich and Pyle at a chrono-
" B' h, f$ q# F3 |# Q% m: Blogic age of 16 months (advanced).5 Chromosomal6 h$ a! u; m  S  j6 p' S+ A+ V
karyotype was 46XY. The thyroid function test/ {2 w7 A1 Q% J. O5 o
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
) E& F+ q* G% q# c" W5 }8 [. alating hormone level was 1.3 µIU/mL (both normal).1 M) ?+ O' H* X2 v- U8 G# b
The concentrations of serum electrolytes, blood+ a# K% l; ]# W* w1 k* S' j9 s5 h& K
urea nitrogen, creatinine, and calcium all were& |; H8 g7 ?& c; s3 F
within normal range for his age. The concentration5 [* a, C: d7 E! [2 a. n
of serum 17-hydroxyprogesterone was 16 ng/dL
( ~% W- H' t. Z6 m) ?(normal, 3 to 90 ng/dL), androstenedione was 209 `+ [: N0 e0 A+ V6 W
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
" C3 t3 F. Y7 Qterone was 38 ng/dL (normal, 50 to 760 ng/dL),: |8 A% U: F- y+ f
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
* R1 ~9 n: Z* b! E49ng/dL), 11-desoxycortisol (specific compound S)7 F5 m# A( M1 ^
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
7 C6 v5 |; ]8 Q/ ^: p4 Ztisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total! N7 S7 B: s6 B$ J2 C8 @: L* Z; c
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
( z/ m. H* o, e/ ^. Tand β-human chorionic gonadotropin was less than
$ B( F- E7 J3 s5 mIU/mL (normal <5 mIU/mL). Serum follicular9 |0 e8 J7 r$ b9 h/ Z% a
stimulating hormone and leuteinizing hormone
* r* X6 t& G  [; J' o% bconcentrations were less than 0.05 mIU/mL, P- o8 i! J% i% h$ b
(prepubertal).
- S2 b$ \" c2 J  Z% [9 Z. y/ kThe parents were notified about the laboratory
. m; ~/ N+ r1 n7 I! z8 q. }; {7 @results and were informed that all of the tests were# s9 q3 }9 E6 h% g" @' x
normal except the testosterone level was high. The
* z" d) X( X, [follow-up visit was arranged within a few weeks to
% d1 t: |0 o0 t  z& _6 Z+ mobtain testicular and abdominal sonograms; how-! |. s3 w  }& h- S% @5 W
ever, the family did not return for 4 months.
: ~, I8 k& G" }, s* v5 o- xPhysical examination at this time revealed that the# q; S( M4 ?# O3 V. k# H7 O# v
child had grown 2.5 cm in 4 months and had gained
6 q( I. |! J- }6 J3 i1 P, `  D% s4 m2 kg of weight. Physical examination remained* N9 [; I0 U  X+ i6 X7 h; O1 J
unchanged. Surprisingly, the pubic hair almost com-! i- m$ l+ A' T: N
pletely disappeared except for a few vellous hairs at& f- u6 g' A4 r: e+ n/ u0 `
the base of the phallus. Testicular volume was still 2
# ~( @$ m- a  A; K3 SmL, and the size of the penis remained unchanged.
% H9 l& q; L: e8 Q# Z# A5 o6 j+ JThe mother also said that the boy was no longer hav-( I; O0 Q" A) I1 C
ing frequent erections.! V' u" n' N* P  v0 Y( Z: k0 f
Both parents were again questioned about use of, E0 k# U7 x7 s
any ointment/creams that they may have applied to
2 f  q8 x0 X# _- y0 W7 B6 K# Fthe child’s skin. This time the father admitted the
5 f- j, G# Y, P4 p6 i8 ]' e* [8 pTopical Testosterone Exposure / Bhowmick et al 541
& O- z& ?7 G5 O& Q) ]3 K* j7 Vuse of testosterone gel twice daily that he was apply-
8 g  E  {, l6 R& }6 |ing over his own shoulders, chest, and back area for
; F2 _# u. K9 I1 q; Oa year. The father also revealed he was embarrassed! h5 W/ l" A4 B) |$ `
to disclose that he was using a testosterone gel pre-
; H0 l. `* D: G& ~scribed by his family physician for decreased libido" y1 o/ i0 I! I: q5 _! `! G& ]
secondary to depression.
% U& X4 e) v  `2 u2 _; DThe child slept in the same bed with parents.: ~5 Z* Q$ t* `; A
The father would hug the baby and hold him on his
1 q. ~; d  ]; r$ t- W* Echest for a considerable period of time, causing sig-2 ^# j; A9 O. Z3 [' d5 E+ j
nificant bare skin contact between baby and father.
) z: \, W, V/ }$ j: FThe father also admitted that after the phone call,* z- p9 f6 P- i
when he learned the testosterone level in the baby4 G# }2 m" I4 w2 w8 S) g
was high, he then read the product information
# k# ]  t) R* L/ `- i; Vpacket and concluded that it was most likely the rea-  Y1 p3 n' \' X2 b; j* G+ ~& C& u! h
son for the child’s virilization. At that time, they
" s5 z- p# P2 P0 X: wdecided to put the baby in a separate bed, and the
& M# V0 c8 T6 \- ^/ H/ S  P" x" wfather was not hugging him with bare skin and had
9 ]6 m4 s" P  b# mbeen using protective clothing. A repeat testosterone: T  R. S. [% Z9 ?+ c0 @
test was ordered, but the family did not go to the
8 u) W& m0 ]; `" R  m5 slaboratory to obtain the test.( e- Z3 @0 \  E! F& N- d; y
Discussion' e$ b& P1 s; m
Precocious puberty in boys is defined as secondary
6 q4 c5 ?$ C4 I0 G6 Dsexual development before 9 years of age.1,4
: U) p. C4 G5 J( I+ f3 y8 ?Precocious puberty is termed as central (true) when
( V* Q$ i7 r7 A5 N/ ]it is caused by the premature activation of hypo-( X2 k# q& z1 Q7 w6 D$ I
thalamic pituitary gonadal axis. CPP is more com-
) Y& K& i+ \4 m3 i5 S! Amon in girls than in boys.1,3 Most boys with CPP
6 Q4 `: W0 ^& W/ {may have a central nervous system lesion that is: u4 A* E7 \7 i/ t: _
responsible for the early activation of the hypothal-/ g( S- U5 {7 b3 N9 z( k% z( n  j
amic pituitary gonadal axis.1-3 Thus, greater empha-
" w: u9 m, R5 ]2 Dsis has been given to neuroradiologic imaging in
% M8 e) B3 P$ K3 ^4 P3 Fboys with precocious puberty. In addition to viril-! \- V2 M5 I: X2 y/ @) S
ization, the clinical hallmark of CPP is the symmet-
2 D! q/ }& b. ^: w* Y1 L& Wrical testicular growth secondary to stimulation by
, I8 U# B1 t! w8 Ogonadotropins.1,3
' c: ^' h8 U. W5 l1 cGonadotropin-independent peripheral preco-. i: \- L: T+ S% `
cious puberty in boys also results from inappropriate
' P( _6 v8 s5 N2 t  E3 gandrogenic stimulation from either endogenous or
7 p7 r/ R7 `* ?3 k# jexogenous sources, nonpituitary gonadotropin stim-
% ]! ^( o  @2 i) b$ d- }6 Bulation, and rare activating mutations.3 Virilizing
$ s; H- v) E# j4 a1 _' Y1 g: p6 |congenital adrenal hyperplasia producing excessive, }* |' A; i8 m* I
adrenal androgens is a common cause of precocious$ Y; P% ?0 h9 o
puberty in boys.3,4
7 t' g+ Q; n& r; g1 L2 F0 NThe most common form of congenital adrenal$ d4 g1 t: A% O, b; x
hyperplasia is the 21-hydroxylase enzyme deficiency.
# h! f' p5 p# a# u! M% NThe 11-β hydroxylase deficiency may also result in9 y0 `$ t; k; \) k' c: t
excessive adrenal androgen production, and rarely,
* D5 x9 Q2 z6 x" M; X: y- Pan adrenal tumor may also cause adrenal androgen
% p' w2 \) R1 o5 Sexcess.1,3
; \& g1 G: E, B9 U. R. x' H& Lat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- X- S. v7 D5 o/ W) q/ h! |542 Clinical Pediatrics / Vol. 46, No. 6, July 2007* D2 y* w" s9 U
A unique entity of male-limited gonadotropin-
; z; o, j( e' ~" o# J' K1 Pindependent precocious puberty, which is also known
* B; s6 ~7 B9 J  A- \$ ^/ kas testotoxicosis, may cause precocious puberty at a2 C! s* p9 _) z6 U- ^- S! j
very young age. The physical findings in these boys3 Y) }/ M4 w5 J# n7 x1 p8 T+ g
with this disorder are full pubertal development,
4 F+ }* R3 W% O( {including bilateral testicular growth, similar to boys! c, r) t6 y, `1 P% x6 V1 X/ O, G
with CPP. The gonadotropin levels in this disorder
' Y1 t% N0 B& j7 nare suppressed to prepubertal levels and do not show: Y" S' ]9 f' x, D5 J& K
pubertal response of gonadotropin after gonadotropin-( v4 p! Z! [7 R) n9 n' x
releasing hormone stimulation. This is a sex-linked6 e$ F0 f2 L1 ?4 g0 m
autosomal dominant disorder that affects only6 k7 u7 S1 |3 i$ D1 h
males; therefore, other male members of the family* U* S, B9 w# Z& f# X1 ~( y
may have similar precocious puberty.3( N! m7 s# B. o) O+ _' Q
In our patient, physical examination was incon-
% t2 ^6 C  N& d; D  @sistent with true precocious puberty since his testi-
4 I& X: l7 @  s9 X8 ~: h  ^cles were prepubertal in size. However, testotoxicosis
/ u5 T3 D4 v( s, {- X* z0 Xwas in the differential diagnosis because his father
5 f. `' b) b: r$ V3 }started puberty somewhat early, and occasionally,7 J9 A. d; m& p$ s0 C0 V
testicular enlargement is not that evident in the
% _+ a) j; F# n0 R1 V5 ~beginning of this process.1 In the absence of a neg-
; [2 R6 |+ s  L; X# I# Vative initial history of androgen exposure, our% N1 K) n6 b/ {
biggest concern was virilizing adrenal hyperplasia,% L2 B. y* A/ W3 R  H3 m
either 21-hydroxylase deficiency or 11-β hydroxylase. V( k! n" I* ?0 r7 N9 u- T
deficiency. Those diagnoses were excluded by find-  P6 j5 b  c1 J4 m
ing the normal level of adrenal steroids.8 M5 Z# k7 W( U, p4 f
The diagnosis of exogenous androgens was strongly
# k6 K4 `% f& Z9 @) }( r: ]; I: Csuspected in a follow-up visit after 4 months because0 \" w9 y  [( X! p& G
the physical examination revealed the complete disap-( d' n/ Y" K, L+ ^" ]1 w
pearance of pubic hair, normal growth velocity, and
* p2 K: D) l: j/ O8 ]decreased erections. The father admitted using a testos-
& q7 Q/ `. O; Q5 }: jterone gel, which he concealed at first visit. He was
8 I$ F5 H% U! c/ B6 qusing it rather frequently, twice a day. The Physicians’
* R, s$ g% o2 G" D) @Desk Reference, or package insert of this product, gel or1 J/ n# @: ^8 ^5 \! ?/ q
cream, cautions about dermal testosterone transfer to
/ S6 C! e- e4 m/ Eunprotected females through direct skin exposure.
$ D3 Z& L! M; h) f/ T9 RSerum testosterone level was found to be 2 times the
( l' g' G+ I& g* xbaseline value in those females who were exposed to
1 h& G3 i) i% Q* R" Qeven 15 minutes of direct skin contact with their male
& r9 V" I/ R# I+ _+ j5 z  @. Tpartners.6 However, when a shirt covered the applica-
8 z! T3 w# n# J0 t5 R' ~( u  J/ Stion site, this testosterone transfer was prevented.
, Y, P5 n% ?8 J- y  M) ^2 j4 ?Our patient’s testosterone level was 60 ng/mL,0 e& ^. b4 ]( P, H
which was clearly high. Some studies suggest that) {2 q& B0 p) l5 _7 @* P9 O
dermal conversion of testosterone to dihydrotestos-( |4 c, m( c) M- k+ c3 S0 t
terone, which is a more potent metabolite, is more
# s' o/ j/ N7 xactive in young children exposed to testosterone
! M! m' U3 z5 O0 a( @$ A. S, Texogenously7; however, we did not measure a dihy-2 W' R9 f' s. N/ i: e6 \4 v
drotestosterone level in our patient. In addition to9 a2 l: r5 K. F9 K7 U# Q
virilization, exposure to exogenous testosterone in+ _0 h. K8 n- J- ^
children results in an increase in growth velocity and
8 Q5 M/ x: _% t! ]) r. N# |advanced bone age, as seen in our patient., e2 [. q' b- {9 E; |/ v" r/ r/ y
The long-term effect of androgen exposure during
& p' X# T8 b! O7 h0 P# oearly childhood on pubertal development and final2 P* p" T- O* k6 c/ B& }- A$ f  b
adult height are not fully known and always remain
/ M" k6 p' L1 [" ^: F9 ma concern. Children treated with short-term testos-
9 K9 \3 k6 z; B9 L( S" }+ oterone injection or topical androgen may exhibit some% ^3 Y6 L# l2 ^3 s! b+ x
acceleration of the skeletal maturation; however, after
( L2 p$ f  N: Q; e3 e. R# Y* I) ocessation of treatment, the rate of bone maturation" o# z/ }, U+ t. z) c# f. ~
decelerates and gradually returns to normal.8,9
2 j; O  u7 ]# C' D5 k' R" sThere are conflicting reports and controversy3 K* \1 k( }5 n6 \' ?/ y
over the effect of early androgen exposure on adult. c, L7 P1 j# T2 `& ~4 {8 H+ Z! U
penile length.10,11 Some reports suggest subnormal
7 E2 I( W2 _- aadult penile length, apparently because of downreg-
" C; z5 t7 D& Z* e* Oulation of androgen receptor number.10,12 However,
2 J, @: O" w5 q( K4 ?6 L- qSutherland et al13 did not find a correlation between" X, [7 k8 K( a# M
childhood testosterone exposure and reduced adult
  ]9 w  ^/ n/ e" c) Kpenile length in clinical studies.& k/ r, I  u( Q1 p: F+ a
Nonetheless, we do not believe our patient is
+ j# s, ?( y3 V) tgoing to experience any of the untoward effects from
% j: z3 z" ]3 r: \$ b; C5 ~% L  t' m5 dtestosterone exposure as mentioned earlier because
+ x0 q3 H5 x* h+ ^8 h) @0 u6 `, [the exposure was not for a prolonged period of time.
+ A/ y% G9 e+ I# sAlthough the bone age was advanced at the time of7 D" S, [3 K- D) t6 O
diagnosis, the child had a normal growth velocity at4 b6 L3 s& g" {! Z2 m
the follow-up visit. It is hoped that his final adult  u" g2 L: [( d  X8 R4 Q) s9 V) Q( w2 c
height will not be affected.4 N8 q7 X2 j% _# R& E3 C
Although rarely reported, the widespread avail-9 V- j/ c' @7 I6 W! I
ability of androgen products in our society may+ b  U  B4 j3 R
indeed cause more virilization in male or female
8 u. F+ m- R& g5 Q1 c4 Y% {) ?7 mchildren than one would realize. Exposure to andro-  j" G9 x$ s3 l! W. }0 x
gen products must be considered and specific ques-
/ H1 U6 C7 y, s  q$ E0 I' Z6 |7 _/ utioning about the use of a testosterone product or
8 l1 P$ f2 ~9 n- C" s% P$ Qgel should be asked of the family members during
7 \/ G/ _! q  a2 |7 vthe evaluation of any children who present with vir-
: }. B- H: u$ Z9 m! ]1 Cilization or peripheral precocious puberty. The diag-
) n, e9 Y5 {: w3 E( Knosis can be established by just a few tests and by
" X; X. Y' j3 N) J& T# ^# K5 O. Dappropriate history. The inability to obtain such a
! T: }4 L4 q. [% ~4 ~- Chistory, or failure to ask the specific questions, may' `8 e* Q: Q7 j4 q
result in extensive, unnecessary, and expensive) u& M1 g$ k" R9 x1 g' W* I: a3 j
investigation. The primary care physician should be! ~1 d& H$ J: m
aware of this fact, because most of these children1 w% ]( n0 i5 V
may initially present in their practice. The Physicians’9 v! G$ e1 y# w" m) K% y& P
Desk Reference and package insert should also put a$ |/ P/ V& B' u9 @6 Y
warning about the virilizing effect on a male or$ m% F& x& X: m: Y; ]" m
female child who might come in contact with some-' \0 L9 `% ]3 X3 x
one using any of these products.
/ @8 T! ^: G$ H/ }. Y1 \References/ e( T  @. D; w4 n7 B- b7 _
1. Styne DM. The testes: disorder of sexual differentiation
6 `7 e7 \9 z# Band puberty in the male. In: Sperling MA, ed. Pediatric' I1 i: z2 H( O6 s
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
+ e7 A9 n/ H9 |2002: 565-628.) Y- q# e, g2 P! v5 a- d
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious9 V5 h" j- R, y1 P7 e- y
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
- Z) T. ]" V1 R) E8 d' i, kBoy Induced by Indirect Topical* S- o" d$ C: V- H7 v
Exposure to Testosterone
2 Z- [7 `3 h5 h( x. KSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2- g8 p  D: b' E8 L+ t) f: K$ L
and Kenneth R. Rettig, MD1
6 a  e. j. z, k7 HClinical Pediatrics3 l. C1 f, |' P
Volume 46 Number 69 [7 K/ ~& I  T
July 2007 540-543
6 D+ w; V) T% G8 i0 p© 2007 Sage Publications; A/ V- i( s9 P" s+ }( ~0 M5 T
10.1177/0009922806296651
0 k! G1 U, _- ?" Mhttp://clp.sagepub.com
4 D5 M* z! K1 H( V! e. g1 lhosted at
3 v4 Z* p3 O; P' hhttp://online.sagepub.com1 H6 d: O- l, j
Precocious puberty in boys, central or peripheral,
# v% ^$ Y2 W/ x, r, }is a significant concern for physicians. Central
( n* L* r, ^& K4 f& Z' ]1 r: x3 vprecocious puberty (CPP), which is mediated0 t5 r( `5 K2 X6 ~$ j$ B
through the hypothalamic pituitary gonadal axis, has
" _- b1 ^  E" _7 y, pa higher incidence of organic central nervous system
0 R+ x3 h. T* n" M/ vlesions in boys.1,2 Virilization in boys, as manifested
, N/ }/ `9 G( N- M2 Sby enlargement of the penis, development of pubic
, N3 F; O! G. w& ^1 Z% x- khair, and facial acne without enlargement of testi-
1 Q7 `. {) }# L* C& Lcles, suggests peripheral or pseudopuberty.1-3 We  L1 C  u: i0 O1 f; d( H" F
report a 16-month-old boy who presented with the7 [5 J) {0 ~0 m5 w
enlargement of the phallus and pubic hair develop-
/ T7 k( i$ j2 g9 [5 U# \! @ment without testicular enlargement, which was due7 a0 e& Y( {8 P* a: x4 k2 i
to the unintentional exposure to androgen gel used by
3 {  B$ M1 k- y0 k* F, i6 w) s( z% `the father. The family initially concealed this infor-
8 {' n' E7 o( A- @3 f$ Ymation, resulting in an extensive work-up for this! x: W( \. }4 y+ M2 X( v
child. Given the widespread and easy availability of
+ X9 d" }; K# I/ m* ttestosterone gel and cream, we believe this is proba-
0 e# _: B7 S( m# Gbly more common than the rare case report in the# G* w4 s) v& q1 O+ Y2 P
literature.42 D  X9 v6 v# ~" H) ?8 o& d
Patient Report1 I6 k5 h! q1 k
A 16-month-old white child was referred to the# _% t1 |4 w$ Z' S
endocrine clinic by his pediatrician with the concern
7 u0 t: f/ a5 ?- I. Uof early sexual development. His mother noticed
7 M  c( {9 Z! Dlight colored pubic hair development when he was
& l% Y2 t: P0 @5 U6 L, kFrom the 1Division of Pediatric Endocrinology, 2University of
- F; V, o4 t4 JSouth Alabama Medical Center, Mobile, Alabama.' C! Q) \- E& ~7 ?1 G6 T- ^, x
Address correspondence to: Samar K. Bhowmick, MD, FACE,
9 k, a% t% s5 K$ y% |& N2 s2 EProfessor of Pediatrics, University of South Alabama, College of. s: i, c' b7 l: }
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;' V. H; j+ y7 Z5 z: y
e-mail: [email protected].
* ^8 [4 r; w! `! I4 R! Xabout 6 to 7 months old, which progressively became
; R/ A, W, T. B9 f- S# Ydarker. She was also concerned about the enlarge-
% o; {' x1 H3 I) K& jment of his penis and frequent erections. The child
$ u8 Y2 V/ f" _3 k! {was the product of a full-term normal delivery, with
8 k( u* i- i% R' D6 f, T3 _, `% ta birth weight of 7 lb 14 oz, and birth length of1 u6 {6 h7 ]4 {/ c( p2 r
20 inches. He was breast-fed throughout the first year
, K* V1 Q# d  E& Xof life and was still receiving breast milk along with) q" ~+ |3 m6 _- a8 c- c# Z" S. S
solid food. He had no hospitalizations or surgery,; T6 K: f- F+ w* u
and his psychosocial and psychomotor development# G( J3 W6 y! o& f$ [+ T% j
was age appropriate.1 ~: w$ H0 p% ~# n
The family history was remarkable for the father,3 f3 s  ^1 G6 O( r# S
who was diagnosed with hypothyroidism at age 16,8 k% ~) @/ Q, b3 ]
which was treated with thyroxine. The father’s
: ~; f1 D, `2 O1 {height was 6 feet, and he went through a somewhat
, J& ], ]5 E: S6 L. x3 _; J! S/ E8 Aearly puberty and had stopped growing by age 14.
7 ?; e- h1 f- X( F; p# [, a& YThe father denied taking any other medication. The) p+ k- F5 m9 ]( A* `
child’s mother was in good health. Her menarche4 s4 L3 }6 y9 l( C' j
was at 11 years of age, and her height was at 5 feet
; _: q0 U5 y3 p$ B, h8 V5 inches. There was no other family history of pre-
8 _( O9 s: p1 L1 Q6 Ucocious sexual development in the first-degree rela-7 @1 ^/ P* ?( V6 j# u5 K- G5 y3 m
tives. There were no siblings.8 [- c- Q; C" H1 t+ w
Physical Examination! ~( S0 {% ]  f0 |1 x
The physical examination revealed a very active,7 N6 g7 ^) C7 x  B. r- Z/ R, z
playful, and healthy boy. The vital signs documented3 y4 B' |$ X. B' \8 V( {1 X) [0 j
a blood pressure of 85/50 mm Hg, his length was" u0 Z4 u9 C: w0 E( ]
90 cm (>97th percentile), and his weight was 14.4 kg4 i! q, u, c$ P  `% x# z$ o1 B
(also >97th percentile). The observed yearly growth5 W) }0 T& D% ~+ s( s, `
velocity was 30 cm (12 inches). The examination of
" \6 f0 u- U1 B! xthe neck revealed no thyroid enlargement.4 v$ d& K1 d7 w: |" a, m5 u( c
The genitourinary examination was remarkable for
, A- Q5 Q1 m: x: ?; W, t, P% oenlargement of the penis, with a stretched length of
( `9 r  G, A! I8 c! L" i4 N- D8 cm and a width of 2 cm. The glans penis was very well
1 i% Q$ l2 s; `& G! b: `developed. The pubic hair was Tanner II, mostly around
+ o* P6 R2 Z" k+ h% [540
9 c+ e5 p0 Q/ p: U# vat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# \( L6 |5 m3 ^- D! P) Fthe base of the phallus and was dark and curled. The' p0 s: N' x* A, o$ i
testicular volume was prepubertal at 2 mL each.' U5 z7 b) v! q: @: ~
The skin was moist and smooth and somewhat
# {: X3 \4 b' A' G) w- }oily. No axillary hair was noted. There were no% E2 W; t5 T( m8 I# d. R. S1 U
abnormal skin pigmentations or café-au-lait spots.
$ z2 y' L* m# V4 ]1 }Neurologic evaluation showed deep tendon reflex 2+- {8 p: c% ^3 ?$ m
bilateral and symmetrical. There was no suggestion6 R, C1 U, m7 u$ D- n
of papilledema.
- J8 `/ q4 a: s) o; ]Laboratory Evaluation
3 g9 ?0 k7 ~& i" AThe bone age was consistent with 28 months by
+ N. l0 d3 h5 u7 Y  a# z# G" G& w: P5 _using the standard of Greulich and Pyle at a chrono-
: T5 o; ?+ i9 dlogic age of 16 months (advanced).5 Chromosomal
+ x  \! R! `+ M! l/ vkaryotype was 46XY. The thyroid function test* K; I$ \) A/ d, L9 @( }5 G
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
" Q% h8 \; {' l! X6 dlating hormone level was 1.3 µIU/mL (both normal).( k( h1 U, }9 X: }6 E7 E
The concentrations of serum electrolytes, blood  U: l0 ~- |) d9 h% B
urea nitrogen, creatinine, and calcium all were
% S5 J5 n6 Y; h8 i0 twithin normal range for his age. The concentration
+ {  F7 m* z, b+ Y  G: |of serum 17-hydroxyprogesterone was 16 ng/dL
, f: W+ z- Z! x0 A8 {; X(normal, 3 to 90 ng/dL), androstenedione was 20
. i3 W1 }/ S2 T& Y( a' wng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 @' T. |: I5 p& y9 uterone was 38 ng/dL (normal, 50 to 760 ng/dL),
$ w' H2 o6 f! J) Edesoxycorticosterone was 4.3 ng/dL (normal, 7 to- l$ Z, d9 l6 A- ?, D9 g" f8 G; m
49ng/dL), 11-desoxycortisol (specific compound S)
, o' r9 z$ _+ }9 ^& Qwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-7 a  C0 x7 `7 h, T) x9 H
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' Z+ R7 l1 A  h" d/ Z+ a# N8 v
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),: @: ^; e/ G8 W7 E4 l
and β-human chorionic gonadotropin was less than' E1 g1 S8 W! c# G1 Y' R
5 mIU/mL (normal <5 mIU/mL). Serum follicular; ^+ ?; k# C1 ^8 E+ K
stimulating hormone and leuteinizing hormone
4 z8 n' C+ B4 y5 E! o# u" vconcentrations were less than 0.05 mIU/mL( L& j) y, W5 i- X) W
(prepubertal).
% _* n: w/ t! o; r' t3 wThe parents were notified about the laboratory
# r9 E2 o5 C2 V: z) s$ t; K9 Uresults and were informed that all of the tests were8 o. ^: p; L. S: j
normal except the testosterone level was high. The) x! n3 H+ ^1 y- r& s+ P, K
follow-up visit was arranged within a few weeks to5 h1 [  P9 r4 G; J2 a( F7 u9 S
obtain testicular and abdominal sonograms; how-
" [9 q6 m( G+ l0 B% yever, the family did not return for 4 months.
) ^0 o) N+ ~$ @4 z7 SPhysical examination at this time revealed that the
2 ~4 C3 u2 v8 v: N9 gchild had grown 2.5 cm in 4 months and had gained
" i) P+ I/ S/ k9 Z# R2 kg of weight. Physical examination remained6 f) V* Y9 M1 m: o7 y8 l. X
unchanged. Surprisingly, the pubic hair almost com-
! Y5 m4 y9 ]  O" F! ypletely disappeared except for a few vellous hairs at
' V4 y! G  I4 f" b9 `6 ~; d1 Ithe base of the phallus. Testicular volume was still 2! }1 l' K% S% n. `* B9 _
mL, and the size of the penis remained unchanged.3 |  t  j2 C+ U4 F) z8 V3 W# Y
The mother also said that the boy was no longer hav-
6 p0 q' D2 Z8 Q3 j, A6 {. ^ing frequent erections.. @+ {9 n: R$ F4 I+ L; }
Both parents were again questioned about use of/ t! ~' g" B6 r' T0 z3 f0 X
any ointment/creams that they may have applied to
2 L" O' {- k2 r5 Q3 Rthe child’s skin. This time the father admitted the
: {: J# ?) K) l1 _& f+ ~Topical Testosterone Exposure / Bhowmick et al 541; f0 _/ ~) i" Z1 |  p$ G* _
use of testosterone gel twice daily that he was apply-
$ i$ y  {" \0 ^+ _6 u! X) W) ^! Hing over his own shoulders, chest, and back area for, B# ^& B' L) M# @1 T' g7 ~" a  Y0 Q
a year. The father also revealed he was embarrassed, Z7 \7 s# C: c, V; J+ r$ \) {' G- a
to disclose that he was using a testosterone gel pre-
8 {7 F  d. [8 b/ s! Wscribed by his family physician for decreased libido
. O" E1 O; c& f; K5 ksecondary to depression.$ [% X. a3 N6 {1 F
The child slept in the same bed with parents.3 P# C/ L) A5 `, ^; |
The father would hug the baby and hold him on his
3 a( s, x% Q2 C; M) jchest for a considerable period of time, causing sig-& U: V* {2 y$ L
nificant bare skin contact between baby and father.: U, w* J% {3 W/ a% k0 K, t
The father also admitted that after the phone call,6 T! Z6 m9 I8 u  t7 z
when he learned the testosterone level in the baby
0 l, O4 S8 z; E  lwas high, he then read the product information% n' s; V' c" c) l: T: R
packet and concluded that it was most likely the rea-
, _; c) \/ D4 u+ J( e/ G. oson for the child’s virilization. At that time, they) D9 l, ]+ A0 g, U
decided to put the baby in a separate bed, and the
1 M5 h% p$ A. n, k/ G/ R  ffather was not hugging him with bare skin and had1 Z  y3 q- L* L! G! a. K- f
been using protective clothing. A repeat testosterone
; _! p# W( w7 g7 X# Htest was ordered, but the family did not go to the
" ]" O( K7 g$ e) C) nlaboratory to obtain the test.  k# L) l. h2 ?  R; o7 q( w
Discussion- D* e9 H. F) x6 v: |
Precocious puberty in boys is defined as secondary1 U2 {- K4 B4 e! Q) x% `, b8 V
sexual development before 9 years of age.1,4
0 t. }- p1 D6 ?) y. ?) _Precocious puberty is termed as central (true) when6 E4 a0 g2 S0 p) f: G6 m
it is caused by the premature activation of hypo-
% m0 n( z5 Q6 o( Uthalamic pituitary gonadal axis. CPP is more com-
5 n% o+ R5 r- E3 l& ]7 i" hmon in girls than in boys.1,3 Most boys with CPP. h+ w) T  ]+ l6 @  s9 v
may have a central nervous system lesion that is0 _# u- z& B7 T4 M- f
responsible for the early activation of the hypothal-
, Z* ~& K  W: s) v/ Z! F8 qamic pituitary gonadal axis.1-3 Thus, greater empha-% `9 T7 ^1 I- a& ?! R  L# b
sis has been given to neuroradiologic imaging in4 e, ~2 Y" [, ~! X2 N- q+ G
boys with precocious puberty. In addition to viril-# J% h( Z4 S# T8 [- \6 f# z
ization, the clinical hallmark of CPP is the symmet-# g! D8 s. U5 c2 Z: t
rical testicular growth secondary to stimulation by
  }; L& f! R( h- _# v9 H# b* lgonadotropins.1,3) P: I8 z' y6 H$ t" a! t  @
Gonadotropin-independent peripheral preco-
& s; ]) J2 I! j! K1 K# x% V6 Ecious puberty in boys also results from inappropriate
" J8 p9 B' M$ q/ D6 Q% k& ~& yandrogenic stimulation from either endogenous or
; N' G& }( [8 V, F. @. d/ w' {exogenous sources, nonpituitary gonadotropin stim-+ X: i; [2 X! F- i2 H: T
ulation, and rare activating mutations.3 Virilizing
: t- t( u; `4 Z4 g9 ?congenital adrenal hyperplasia producing excessive
) N- u* o8 h) S4 badrenal androgens is a common cause of precocious
: W5 w+ J4 V7 A3 d! ypuberty in boys.3,4" t3 o; q# H  M  \* Y, Q
The most common form of congenital adrenal2 B7 A. Z+ q; }+ ~. Z4 q" q
hyperplasia is the 21-hydroxylase enzyme deficiency.
$ X! u2 W; O6 }9 I( lThe 11-β hydroxylase deficiency may also result in- P4 A/ k7 Z3 Y' ^# D4 ~9 n
excessive adrenal androgen production, and rarely,/ p4 y- x6 c- M) x+ z" ?* C
an adrenal tumor may also cause adrenal androgen3 Z" {2 \" h5 r3 w1 O) l
excess.1,33 J7 }$ `- R% i  c3 n+ L/ ?& z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- P2 J# ]7 f- T+ H
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007, c7 X0 X6 x; x, s; `2 X: ^- b: `
A unique entity of male-limited gonadotropin-
9 @# v$ a4 {5 Y" ~2 pindependent precocious puberty, which is also known
, y- d' D" p$ V& `% ^$ [) M/ Cas testotoxicosis, may cause precocious puberty at a6 ~- }5 p9 R7 q7 z; X
very young age. The physical findings in these boys
+ ^9 \5 j3 S( y, f" R; |/ Mwith this disorder are full pubertal development,
* p. x( k0 P% r, h* X, S) t2 Sincluding bilateral testicular growth, similar to boys& j3 n+ i& X& p) ?# n% q
with CPP. The gonadotropin levels in this disorder
$ h, A0 M- r2 D0 H  C7 mare suppressed to prepubertal levels and do not show
5 M: j8 R1 k+ m" M2 h$ h6 c  q( xpubertal response of gonadotropin after gonadotropin-0 u1 P& d) U$ g3 z9 @# l
releasing hormone stimulation. This is a sex-linked' k% M* i, r; H6 t6 ^
autosomal dominant disorder that affects only
0 m3 Q2 n1 ~# ~* N- D4 dmales; therefore, other male members of the family
! D2 P; {9 H$ m) P, [6 @may have similar precocious puberty.3% @; B. B" r  A" w. W# [7 A9 C
In our patient, physical examination was incon-& V. h- d$ u0 B' D
sistent with true precocious puberty since his testi-& f! G& T; p; z  W8 M6 y6 Q
cles were prepubertal in size. However, testotoxicosis% g% m8 C" [( }' P
was in the differential diagnosis because his father
& q* {7 E" L; r  I" z5 ustarted puberty somewhat early, and occasionally,1 V5 u: e; ]( V
testicular enlargement is not that evident in the
, T7 R2 C% D" V% B4 Z/ Z+ l2 @( k1 E. ?beginning of this process.1 In the absence of a neg-
/ J  G5 m' E- P: Iative initial history of androgen exposure, our4 W- R# M5 }- X+ s
biggest concern was virilizing adrenal hyperplasia,
1 [" a  I/ }  H' ]) xeither 21-hydroxylase deficiency or 11-β hydroxylase
) K: c0 |3 K+ r" n+ Jdeficiency. Those diagnoses were excluded by find-
& O' M8 x7 E7 b( \# {ing the normal level of adrenal steroids.
/ P, W+ T2 J$ R, ^) PThe diagnosis of exogenous androgens was strongly/ _6 @: @$ w, ^/ r) N! v5 K
suspected in a follow-up visit after 4 months because/ b' }8 g: X* l
the physical examination revealed the complete disap-
  a" ~1 w6 K2 \pearance of pubic hair, normal growth velocity, and
, L# d# z9 a' h5 b- Hdecreased erections. The father admitted using a testos-
* o0 l4 ]1 E5 ~3 i+ E& x. h, g( kterone gel, which he concealed at first visit. He was$ f+ S8 m5 f5 h" J2 O9 U# O
using it rather frequently, twice a day. The Physicians’
( h, P/ l7 u" u. PDesk Reference, or package insert of this product, gel or4 I4 d0 Z6 e( Y% b7 O% X
cream, cautions about dermal testosterone transfer to# o. n! B5 s! |3 @1 f
unprotected females through direct skin exposure.
. [+ P9 v. J- ]2 g0 O, xSerum testosterone level was found to be 2 times the( X! b$ G5 V' E' t; Q
baseline value in those females who were exposed to
$ `8 V: _7 D9 beven 15 minutes of direct skin contact with their male
7 j" I) G4 g1 ^1 E% N- W5 Kpartners.6 However, when a shirt covered the applica-. [. O( u9 [0 ?% I: W5 Q
tion site, this testosterone transfer was prevented." o+ k# P* q6 r1 E6 P5 p
Our patient’s testosterone level was 60 ng/mL,# Q6 ?4 b2 s* x" }' \' U& y
which was clearly high. Some studies suggest that/ a7 D: }1 n5 `+ ^8 q: y7 h4 V! g
dermal conversion of testosterone to dihydrotestos-
2 Z3 U7 E; r$ @! Z/ Q9 {9 L/ I8 Uterone, which is a more potent metabolite, is more( N' i1 N( {. v1 ^7 a) @
active in young children exposed to testosterone
: d4 r- l# Z" c' v$ U, [2 P' P6 Nexogenously7; however, we did not measure a dihy-
' B% M1 T9 S) Q( I5 @9 Pdrotestosterone level in our patient. In addition to1 r9 A) X* ^3 N* Z; p0 w2 k6 i
virilization, exposure to exogenous testosterone in
2 ~  y' Z0 h0 ?* @$ F, r5 schildren results in an increase in growth velocity and
) k8 w; a1 T2 D  \; badvanced bone age, as seen in our patient.
" F- ^( F. N' s, }: I, WThe long-term effect of androgen exposure during3 Y; j, G+ f6 ~: b, \+ m+ \. a
early childhood on pubertal development and final; J5 T: B5 t; R0 l! O; m: J
adult height are not fully known and always remain
, k4 b3 I  U0 @* }, f9 M. x9 r/ ]a concern. Children treated with short-term testos-# k; F& V& G4 u
terone injection or topical androgen may exhibit some
+ F: u, ]4 n9 D0 W& |7 qacceleration of the skeletal maturation; however, after
) h) U; Q4 ^# ^1 J- P& G/ Dcessation of treatment, the rate of bone maturation" |5 A# D( m/ v7 @' t
decelerates and gradually returns to normal.8,9
: _6 H) G2 q3 B- q) `- qThere are conflicting reports and controversy
# F  w/ j0 n: w: l( `% p" tover the effect of early androgen exposure on adult/ d* k- I$ p, F3 V& U! Z
penile length.10,11 Some reports suggest subnormal
7 H$ d+ L; n& R3 V9 Xadult penile length, apparently because of downreg-
* Y2 y+ N% {/ f/ H) k. qulation of androgen receptor number.10,12 However,
4 Q* ^  u! K) d4 ?Sutherland et al13 did not find a correlation between' u7 @  F" K/ p: s
childhood testosterone exposure and reduced adult: Y7 r! _/ t2 e, p! @! @/ E4 R
penile length in clinical studies.3 H  c$ G! d9 \" P8 j
Nonetheless, we do not believe our patient is9 J) P% R2 V, h2 D2 n! C; v* T
going to experience any of the untoward effects from6 v" [: i# @+ a9 T  F7 i! o7 [
testosterone exposure as mentioned earlier because
) a* O9 O- v& h( M, b) H6 athe exposure was not for a prolonged period of time.5 g8 `; U% m- R4 J4 m0 s0 |% X
Although the bone age was advanced at the time of7 `3 {4 F/ X6 ]: ~5 Z: ^/ ~
diagnosis, the child had a normal growth velocity at
) R# r6 A9 f$ j; Z- @& uthe follow-up visit. It is hoped that his final adult
$ x5 |  r' A: a* e3 l8 Rheight will not be affected.
! G! ^$ i2 x, ?! ]' h9 FAlthough rarely reported, the widespread avail-0 {6 v2 G7 @( f  I
ability of androgen products in our society may
" [8 d+ ~+ N& T5 M' Q6 P* N: d- findeed cause more virilization in male or female
$ k$ H) ]/ C& D' D) `children than one would realize. Exposure to andro-4 |1 ]: X, w9 |
gen products must be considered and specific ques-- ^' x& n5 v' u# M' P
tioning about the use of a testosterone product or
4 Q/ r9 G% I4 C2 mgel should be asked of the family members during) n- }" i! {5 ~) N2 S; R. h
the evaluation of any children who present with vir-
6 O$ i: d) E+ n/ w/ Q9 Z- Pilization or peripheral precocious puberty. The diag-
* z9 z8 N- A1 wnosis can be established by just a few tests and by# z' Z( y& @6 H, k6 s1 `$ w5 A
appropriate history. The inability to obtain such a
. K/ P; c! u; [7 uhistory, or failure to ask the specific questions, may
& i1 E! M; l1 E2 B$ Lresult in extensive, unnecessary, and expensive: a4 e6 E5 u# k
investigation. The primary care physician should be
+ d* O! B) X6 ^* a7 c5 Taware of this fact, because most of these children
; Z2 P- m4 Z% m$ G1 emay initially present in their practice. The Physicians’
7 C  p* B0 w# Y0 M3 {" ADesk Reference and package insert should also put a' _$ o$ A( U% E* M
warning about the virilizing effect on a male or
4 i8 F) J+ n7 Qfemale child who might come in contact with some-  N* d6 Q* X6 y6 ]$ y& b
one using any of these products.0 r, H4 u) H$ a
References
7 o9 G4 i) B  p. t0 u1. Styne DM. The testes: disorder of sexual differentiation
3 p% `6 K( a3 E8 |& Z8 \& land puberty in the male. In: Sperling MA, ed. Pediatric
. O. y6 D& U8 z) L0 UEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
& f. y( J. Z' {  f& c4 U2002: 565-628.
% t6 p7 a* q# O  {& B) V% B2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious. r' h1 G2 m5 X# n! r( S
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

8 u; E( H1 k. C1 B* K# Z6 Y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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