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Sexual Precocity in a 16-Month-Old
- X. U' x- Z* z' g* i% T4 sBoy Induced by Indirect Topical( p$ u* i* i8 g. l* G+ W% ^$ h8 e
Exposure to Testosterone
* X8 l% |# x5 x7 j' V, @Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2/ k6 h, C& Z6 A; Z$ d
and Kenneth R. Rettig, MD1
7 y, o) i; v1 N8 O& u% z5 _' H4 ~5 gClinical Pediatrics, F/ G) z/ v/ e# w9 `
Volume 46 Number 6, ~5 B9 b: v7 m* R! i! `
July 2007 540-5436 {: ]6 Q2 R4 \  Q
© 2007 Sage Publications# b' K  }. |' \7 \! c  e
10.1177/00099228062966515 @) c$ L" k2 O4 C( k
http://clp.sagepub.com( \- J; V1 G! j5 c7 T  l! o
hosted at
, \3 V9 E& d) p! k0 r, o* j" Thttp://online.sagepub.com  W( U  p% d# [1 X0 Z6 y" z+ D
Precocious puberty in boys, central or peripheral,
0 l" a8 ~) b3 f  A; Vis a significant concern for physicians. Central' Z" {/ O% m) E" j' E
precocious puberty (CPP), which is mediated
9 O; k2 S4 x) b  Dthrough the hypothalamic pituitary gonadal axis, has6 N; K. ?0 u: B+ y' J- X$ f) O# c
a higher incidence of organic central nervous system
# k" J/ i% ?1 C" C3 O) f) Ylesions in boys.1,2 Virilization in boys, as manifested
2 K( _6 p0 _0 H9 n  ]by enlargement of the penis, development of pubic: u( W% c7 ^0 f& o1 A7 W
hair, and facial acne without enlargement of testi-
& ?+ M% V. @7 m: Ocles, suggests peripheral or pseudopuberty.1-3 We8 c7 U$ i  F9 Q5 s4 u5 p0 c7 W/ P
report a 16-month-old boy who presented with the
; I: n2 j* A! b7 v. |) x2 `, Penlargement of the phallus and pubic hair develop-
+ c& {6 w  Y: h3 w% Hment without testicular enlargement, which was due; e, d( O% T7 q: K2 o/ _7 v
to the unintentional exposure to androgen gel used by& ~+ Y4 K; @5 U0 A5 L
the father. The family initially concealed this infor-9 V6 A. F3 D/ Q+ B- P9 I; ]) N7 x
mation, resulting in an extensive work-up for this
, L+ i1 x  C8 l8 ^& Bchild. Given the widespread and easy availability of
. _- ~3 m/ N- Z- o, p% Stestosterone gel and cream, we believe this is proba-
( K* w3 `/ l$ nbly more common than the rare case report in the
8 t+ W) K" ?- b, D! W6 b- a2 uliterature.4% g7 d" @" `4 l' U% ~& S: n% m
Patient Report9 O5 ]& K6 [& v. u2 n/ s
A 16-month-old white child was referred to the
- N/ m1 a. U0 x$ c. w$ e- [endocrine clinic by his pediatrician with the concern& ^% _$ R9 K5 J3 R2 }% F& H
of early sexual development. His mother noticed
- r. B0 Y) E, i3 X% Ylight colored pubic hair development when he was1 h7 M: T7 a9 h/ \+ j0 A1 l8 e
From the 1Division of Pediatric Endocrinology, 2University of
! w$ `0 i& e) g& g& q; I6 pSouth Alabama Medical Center, Mobile, Alabama.
4 B* P& s7 V  U( PAddress correspondence to: Samar K. Bhowmick, MD, FACE," X9 |9 v, Q5 E! s# ^! Y: F/ N
Professor of Pediatrics, University of South Alabama, College of
2 s& V$ H# M1 c" Z; EMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;9 D* I* ^- Z5 j
e-mail: [email protected]." Q! u. b& a6 |3 ]- {3 Q5 E
about 6 to 7 months old, which progressively became  p3 ?* d4 z! s! S. B& R
darker. She was also concerned about the enlarge-
- f3 T6 P& l' p7 }" l4 L9 `) p3 {ment of his penis and frequent erections. The child
3 p. `: V& b  |6 |0 w9 Dwas the product of a full-term normal delivery, with8 y0 L. E7 C/ G
a birth weight of 7 lb 14 oz, and birth length of5 c: [6 |0 I$ ~6 F" ]" D
20 inches. He was breast-fed throughout the first year
% N: M6 `5 g# C7 Y1 G8 Kof life and was still receiving breast milk along with
2 h/ o+ F. h; Y9 Z& q3 Usolid food. He had no hospitalizations or surgery,4 I' F$ R3 s2 ^. q
and his psychosocial and psychomotor development
$ d; n( w$ o+ J3 ~was age appropriate.
  q% l3 ^, ?8 }- a" r1 iThe family history was remarkable for the father,
. w  {  S2 _$ K+ Hwho was diagnosed with hypothyroidism at age 16,1 [6 P' N* H2 _: _6 C
which was treated with thyroxine. The father’s
$ ]- ~8 J3 i: y% H+ {/ c' Y& J7 c; qheight was 6 feet, and he went through a somewhat# ?1 s2 @4 V4 A7 y9 V6 I- c
early puberty and had stopped growing by age 14.
* R5 O( K$ j) W% T  r7 T7 T. GThe father denied taking any other medication. The
3 |+ ~+ s; L: `! H% c, n  ]4 cchild’s mother was in good health. Her menarche$ _7 s! d5 K+ b- _, C* r
was at 11 years of age, and her height was at 5 feet( l% x+ U/ D1 w; i8 y
5 inches. There was no other family history of pre-# q/ b, N( q5 q3 s  l
cocious sexual development in the first-degree rela-
7 l2 O0 N  W$ M; V7 z+ }% H, xtives. There were no siblings.
/ P, _, i. O2 ~  WPhysical Examination+ @! r# _  O9 ~' Z% v3 [
The physical examination revealed a very active,/ y3 C2 E8 O6 K2 M* g+ \
playful, and healthy boy. The vital signs documented
  u# O9 P1 S/ h, l" g1 Xa blood pressure of 85/50 mm Hg, his length was
! F% h- Y* A8 o# ]3 j+ ^  x( i8 |90 cm (>97th percentile), and his weight was 14.4 kg; B8 k' Y+ C" m! g, ?- R4 A! }
(also >97th percentile). The observed yearly growth
+ ~/ @$ N/ A1 A  f9 Vvelocity was 30 cm (12 inches). The examination of# P0 u! e3 K' Y) S  O
the neck revealed no thyroid enlargement.
& v" m5 _  j/ q4 OThe genitourinary examination was remarkable for! A& r  I  y% X) @
enlargement of the penis, with a stretched length of
8 L0 ?( O* {! L- f' C8 cm and a width of 2 cm. The glans penis was very well
7 F7 ], S" W5 ~1 ^3 Ideveloped. The pubic hair was Tanner II, mostly around
  m) |* C! N8 V' s( f( E1 n540
# T  M1 F2 p, e. Yat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
  `9 n# Y0 ~( T! ~the base of the phallus and was dark and curled. The5 A1 F( h+ c) @! V+ s& h8 }
testicular volume was prepubertal at 2 mL each.
! F" [* l0 h* i, `/ \9 a( U1 w- TThe skin was moist and smooth and somewhat
: M: h  I- A+ e6 o5 [' c7 Coily. No axillary hair was noted. There were no" [4 R4 m/ v8 j
abnormal skin pigmentations or café-au-lait spots.* h3 _" Q1 g6 r  V$ H3 h
Neurologic evaluation showed deep tendon reflex 2+1 j/ B3 a. e* y
bilateral and symmetrical. There was no suggestion) b3 v9 e- U  }9 ^( v+ _8 e$ z/ w
of papilledema.2 o% j# J, E3 x, m
Laboratory Evaluation" C# m9 R' V( I8 Z: \
The bone age was consistent with 28 months by' m+ {& A' |4 P+ m8 M7 ]
using the standard of Greulich and Pyle at a chrono-6 `/ n8 i0 W5 {' H2 b2 m
logic age of 16 months (advanced).5 Chromosomal$ w3 W4 L1 V' w& |$ g. |0 h
karyotype was 46XY. The thyroid function test& U" c' t! W- D
showed a free T4 of 1.69 ng/dL, and thyroid stimu-' Z, Y& ~9 Y' r
lating hormone level was 1.3 µIU/mL (both normal).
% F$ I0 s  E3 a# ]6 {; c% ZThe concentrations of serum electrolytes, blood
0 x4 s+ g3 W. Q3 O/ uurea nitrogen, creatinine, and calcium all were* r# G$ L) G' M# S3 c' q; j
within normal range for his age. The concentration! \% ?/ w% x7 m
of serum 17-hydroxyprogesterone was 16 ng/dL
' u2 W/ ?; Y/ h* F(normal, 3 to 90 ng/dL), androstenedione was 20
2 o; }. S3 z, q8 m: Ung/dL (normal, 18 to 80 ng/dL), dehydroepiandros-- R7 |% b" D" Z7 d7 @  M  X/ E& O
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
6 b0 g  m( w' P' }desoxycorticosterone was 4.3 ng/dL (normal, 7 to
" }! j4 e5 n0 }& [  d* _+ h49ng/dL), 11-desoxycortisol (specific compound S); L9 Y4 q* y1 }. e- q" K! ?
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-( X% W3 K! m% L& W
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
. X6 X1 V2 y9 X" z: \testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
# Q% G7 z- l8 R2 T4 ]- P/ Kand β-human chorionic gonadotropin was less than
8 I' p: c9 K+ `5 mIU/mL (normal <5 mIU/mL). Serum follicular  Y9 d9 J/ c# d( O# b" F
stimulating hormone and leuteinizing hormone
1 @8 @1 x9 K+ |: r3 Dconcentrations were less than 0.05 mIU/mL
1 m3 Z$ C( j9 ?, a: C- y& P(prepubertal).
; ?% m5 }% B( a, e3 a" V" h- `4 iThe parents were notified about the laboratory
9 }8 R3 L5 y6 u" mresults and were informed that all of the tests were& v9 q6 Z/ a# ^% m
normal except the testosterone level was high. The
5 J9 p0 _+ o1 t1 \2 D8 Qfollow-up visit was arranged within a few weeks to, q* d- @7 ^+ U, R7 E
obtain testicular and abdominal sonograms; how-' `, g. S6 T0 B% Y" A3 I
ever, the family did not return for 4 months.
0 t% T4 {0 W+ {Physical examination at this time revealed that the
6 Y% k7 P/ f* W9 J+ \6 P0 Jchild had grown 2.5 cm in 4 months and had gained
4 U( E) w$ w2 t( X6 \2 kg of weight. Physical examination remained
9 R3 `+ P: M' x& nunchanged. Surprisingly, the pubic hair almost com-1 A. q6 W" o0 `' d8 a4 c, ~
pletely disappeared except for a few vellous hairs at( k. ]& m5 Q- @, d  x1 s% J
the base of the phallus. Testicular volume was still 2+ E/ R* G, W. `  r6 {8 |( O' o8 r
mL, and the size of the penis remained unchanged.4 G) ^* k1 u8 q0 D) m$ o
The mother also said that the boy was no longer hav-# g1 q+ `, m  B8 A; l8 y5 }3 Q
ing frequent erections.8 Q$ Y' }) ~9 z9 t
Both parents were again questioned about use of$ Q' J: x4 J* H$ L6 Y+ K$ S' G
any ointment/creams that they may have applied to
  b0 P7 r6 F+ U! x9 Jthe child’s skin. This time the father admitted the
8 x& e' m; p; f. [2 @7 d- \' ~Topical Testosterone Exposure / Bhowmick et al 5418 @+ m# l$ `2 q* G9 g' Y  w
use of testosterone gel twice daily that he was apply-9 u  m& I2 ^# ~) g4 D5 K1 k
ing over his own shoulders, chest, and back area for$ I- D8 X! Y! R  `, x. ~
a year. The father also revealed he was embarrassed
4 L8 K5 b) d% L6 @* M$ mto disclose that he was using a testosterone gel pre-, h& n2 \3 N  D
scribed by his family physician for decreased libido
% G5 d+ _# K! H+ c! q+ dsecondary to depression.+ R' I. w3 U: h/ ?5 B
The child slept in the same bed with parents.
* b- u% F) }. _+ g$ ~The father would hug the baby and hold him on his
+ w3 ]0 c1 o" M) ~chest for a considerable period of time, causing sig-
9 [, s3 T3 v6 ^! l! Inificant bare skin contact between baby and father.
# q' b6 W: Z$ y! @4 N" v: PThe father also admitted that after the phone call,
. ]1 `+ X6 P0 v! l$ F# m5 Pwhen he learned the testosterone level in the baby
# g" N* H# f# `3 i! a' @was high, he then read the product information
6 L4 R/ f7 b0 Q. s8 M5 mpacket and concluded that it was most likely the rea-: O, i' D4 {( c2 Z7 F; R* M
son for the child’s virilization. At that time, they- o) X  z9 ?& U! o; ~9 [
decided to put the baby in a separate bed, and the
1 r, a: h3 G% ~+ `father was not hugging him with bare skin and had
4 `! ~( J  t7 F/ Z- M$ bbeen using protective clothing. A repeat testosterone
1 h. W1 r! X% ]: L$ v& u4 Gtest was ordered, but the family did not go to the: ?: ~! t! i0 K3 e7 Y
laboratory to obtain the test.
" X$ P+ g$ D& a) P8 \3 V/ FDiscussion
% b: N4 y6 R3 y# q/ BPrecocious puberty in boys is defined as secondary
5 F; A  X6 m& ^  W7 n& N# ksexual development before 9 years of age.1,4: O% p/ G, C# }2 h/ q4 i( y
Precocious puberty is termed as central (true) when. B/ _$ m7 z' S6 X) s+ k2 x
it is caused by the premature activation of hypo-
, e* F2 `' w5 b8 i& r$ E' o* kthalamic pituitary gonadal axis. CPP is more com-& P# ]) \9 A) n
mon in girls than in boys.1,3 Most boys with CPP; v$ W+ v6 b- ~1 [# P# N! ]2 E0 |# B
may have a central nervous system lesion that is
4 A$ G0 D  Z  y5 Dresponsible for the early activation of the hypothal-/ H* P9 R; k8 J1 e& s
amic pituitary gonadal axis.1-3 Thus, greater empha-
, k* ]! V$ A3 n! Tsis has been given to neuroradiologic imaging in0 d8 ^$ p2 W9 Q. j( ~; Y* P
boys with precocious puberty. In addition to viril-
5 N  F9 |' j8 g* oization, the clinical hallmark of CPP is the symmet-! ?9 Q& W) t4 G! e0 B7 _& y+ Y
rical testicular growth secondary to stimulation by0 M0 {0 |; N5 [9 s* P. e" A
gonadotropins.1,38 X7 S1 r: [- ?6 D# S" Y+ o1 \
Gonadotropin-independent peripheral preco-$ j; |5 e) Q! h, I- w2 ]
cious puberty in boys also results from inappropriate; `7 S; V( z/ k, o8 H
androgenic stimulation from either endogenous or
  E% ^; ]0 r+ u2 b+ p% @exogenous sources, nonpituitary gonadotropin stim-0 v" r& L; v; H) r: @
ulation, and rare activating mutations.3 Virilizing( `1 C# `2 S. @- g, n% `) p
congenital adrenal hyperplasia producing excessive
3 [9 ]: t% D( E* r9 o5 m3 Xadrenal androgens is a common cause of precocious6 h$ a- O+ W) M' y7 l) ?. q
puberty in boys.3,43 b$ v, i6 C5 f( j4 B
The most common form of congenital adrenal) D) r9 M* f+ R" e
hyperplasia is the 21-hydroxylase enzyme deficiency.
# j. [& F4 f+ ]1 X) X* S$ s5 oThe 11-β hydroxylase deficiency may also result in
0 e6 C: T$ p( s( A6 mexcessive adrenal androgen production, and rarely,
! P! x; l. u8 z0 w" @6 r; \( {- kan adrenal tumor may also cause adrenal androgen
& ~% J6 G/ m' N$ A2 \# k$ B$ sexcess.1,3
3 I" V$ l% I! p6 Gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' i. B" V  N8 ?; v4 t
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
' _& k) ^) l9 v" d- RA unique entity of male-limited gonadotropin-: _1 Q, @& w; g+ u* C
independent precocious puberty, which is also known, B2 d& }1 ]: |& i) I* o
as testotoxicosis, may cause precocious puberty at a! F7 C3 ?3 `6 V, g" p: ]8 L& V
very young age. The physical findings in these boys
. h$ t% N' ^" |* ?/ ?4 f0 W# f+ qwith this disorder are full pubertal development,2 |, w+ r0 ]" ~' M. L; s
including bilateral testicular growth, similar to boys
8 `! @) W! P$ x4 N  Fwith CPP. The gonadotropin levels in this disorder. B9 p' b0 [" a
are suppressed to prepubertal levels and do not show
! g$ K. ]& ~5 y5 \& Z4 q1 lpubertal response of gonadotropin after gonadotropin-
3 o/ f5 t3 Z: Areleasing hormone stimulation. This is a sex-linked4 E0 v& s- y8 q! M# j4 l, V
autosomal dominant disorder that affects only
) g5 `  k/ e  Z+ P, D1 d1 g+ }' kmales; therefore, other male members of the family  D. L$ E: B* D+ Q& F/ `) a; |
may have similar precocious puberty.3, e7 O: \+ ]$ ~6 O: h3 L3 J$ T
In our patient, physical examination was incon-0 i/ ^& g, U7 `( _" R5 F
sistent with true precocious puberty since his testi-# \5 U* O- S4 M! C
cles were prepubertal in size. However, testotoxicosis2 O' u4 U$ h4 d" D# s( P8 L
was in the differential diagnosis because his father
. c. ~) Q$ n* q+ B' D* _started puberty somewhat early, and occasionally,
$ @% B# S6 e* z! c" gtesticular enlargement is not that evident in the
1 |. n$ l+ c% q$ E- X0 B3 {0 U+ [- jbeginning of this process.1 In the absence of a neg-2 g( _+ Q+ m8 y' h5 `" t$ w! T+ V
ative initial history of androgen exposure, our
0 p4 x) d! w9 u! ^# rbiggest concern was virilizing adrenal hyperplasia,! p% Q  U) k+ e% t  c
either 21-hydroxylase deficiency or 11-β hydroxylase( Y6 L, u% p0 r2 z) ]( _0 X* J9 q
deficiency. Those diagnoses were excluded by find-  G3 t7 K. I5 `9 P; v0 D
ing the normal level of adrenal steroids.7 a/ `. {' T) E
The diagnosis of exogenous androgens was strongly
6 l3 O* O/ S3 Psuspected in a follow-up visit after 4 months because( ?4 N* m! g5 z0 ]
the physical examination revealed the complete disap-; @% @) D( q1 }! M" D
pearance of pubic hair, normal growth velocity, and
" \) K! N# }* u; H4 w! [# @) c2 xdecreased erections. The father admitted using a testos-
0 \1 }4 u& g2 Vterone gel, which he concealed at first visit. He was" R4 v4 a3 X/ B7 h; a; K0 Z3 o; c4 U% O
using it rather frequently, twice a day. The Physicians’
+ s) |& ^1 t7 D7 o4 cDesk Reference, or package insert of this product, gel or6 ~% u$ x' K2 b/ |# @7 k
cream, cautions about dermal testosterone transfer to$ O* u0 Q7 S2 B- o7 H# c
unprotected females through direct skin exposure.
2 v- r0 {. V# l4 a5 ~" iSerum testosterone level was found to be 2 times the1 w- j' Z- Q% u0 ]9 J& A5 D
baseline value in those females who were exposed to  A& ?3 Q1 K/ k0 c; t3 H9 Q
even 15 minutes of direct skin contact with their male
9 v- s4 D! D& f! rpartners.6 However, when a shirt covered the applica-
) B. J  u1 {& k% t# n( m6 gtion site, this testosterone transfer was prevented.% H; f4 G* B* `) ~0 N- q+ L0 j/ t
Our patient’s testosterone level was 60 ng/mL,
1 l3 |2 q4 n+ N* l- `which was clearly high. Some studies suggest that
2 r, e6 C$ U4 \) m. r) t; W5 odermal conversion of testosterone to dihydrotestos-0 p  g" B; i: y
terone, which is a more potent metabolite, is more
3 o, B1 q; S% b6 g/ b( d( b" n$ Lactive in young children exposed to testosterone! X% x* u" r0 t4 ]
exogenously7; however, we did not measure a dihy-
* _  D! ~6 X3 h" m" ]drotestosterone level in our patient. In addition to
; ^8 R7 K! \, @4 \8 A2 S. nvirilization, exposure to exogenous testosterone in4 j- z4 A7 P) r# n/ h+ d3 N
children results in an increase in growth velocity and
! P4 ]! q, r, g& ^+ ?advanced bone age, as seen in our patient.( y, H2 z1 x/ `$ O" z, p1 h3 A
The long-term effect of androgen exposure during
7 V) ^; I: q1 t) b/ i- yearly childhood on pubertal development and final
6 j9 s# l6 N3 b1 Q; Hadult height are not fully known and always remain$ j$ O& K2 j* c7 R1 _
a concern. Children treated with short-term testos-# S2 R% ?* ?, ]
terone injection or topical androgen may exhibit some
  D1 l2 b4 m3 a3 `, Jacceleration of the skeletal maturation; however, after. m, v( T. r% g6 P9 W) H3 l1 C
cessation of treatment, the rate of bone maturation7 c; k1 T1 j% q# j; M% J, L$ s
decelerates and gradually returns to normal.8,9* X1 F! z+ q. g& U8 G  S$ F
There are conflicting reports and controversy% g% J7 y0 v; U( g1 ?% m6 b- e" ]7 G
over the effect of early androgen exposure on adult
/ E- E. f4 x! p0 W& E+ ^" Cpenile length.10,11 Some reports suggest subnormal
  o* A- A( D; y' S* ladult penile length, apparently because of downreg-; R9 |. [$ _5 E) o1 s
ulation of androgen receptor number.10,12 However,
$ a" L& Z/ Z; {8 S( l6 K" bSutherland et al13 did not find a correlation between
- L; S& U2 m3 l' ~childhood testosterone exposure and reduced adult
! {5 }4 R  N8 q2 ]4 P6 I) B5 h) Z* Fpenile length in clinical studies.1 S) v( v& S; O% k
Nonetheless, we do not believe our patient is( v/ P; [+ C! S+ ~
going to experience any of the untoward effects from
1 q+ R' x' @. q% S5 ztestosterone exposure as mentioned earlier because$ g8 u/ ~! Y) X+ W# X
the exposure was not for a prolonged period of time.! u( @5 A& ^# ]8 X6 h
Although the bone age was advanced at the time of
6 y$ Y+ z; G+ k# D* t5 i# T% j; Gdiagnosis, the child had a normal growth velocity at5 R3 [' F; o" K
the follow-up visit. It is hoped that his final adult2 b- `$ ~0 B. G
height will not be affected.
8 i- s- h( [/ o) }: g  GAlthough rarely reported, the widespread avail-
0 ]+ _" i- l" E8 C8 @# oability of androgen products in our society may6 k! a1 v- D1 n- v4 d
indeed cause more virilization in male or female
2 A& v0 T5 v5 m+ n9 t) lchildren than one would realize. Exposure to andro-
$ B8 x* C) [8 O' i; Y3 ogen products must be considered and specific ques-' c: X' v9 L0 ]0 |# L
tioning about the use of a testosterone product or' E) b5 q' K% M  t7 N9 r
gel should be asked of the family members during; G( @7 w! X, E0 O
the evaluation of any children who present with vir-
1 I1 v8 J, a0 F! N9 Silization or peripheral precocious puberty. The diag-
# H6 z9 k/ }4 z( @nosis can be established by just a few tests and by- d5 Q, W, w* S3 o; }) N( q5 [
appropriate history. The inability to obtain such a" b: }' ]+ E0 q1 k. g' ~( @2 u
history, or failure to ask the specific questions, may
1 p/ W* E* |9 G0 Qresult in extensive, unnecessary, and expensive) t- p2 H6 c4 S
investigation. The primary care physician should be
4 J+ f, ]* G: o4 l  Gaware of this fact, because most of these children: M: I7 R4 K2 ^- A8 V. l- [3 D; U1 X) V
may initially present in their practice. The Physicians’
5 _4 h/ {! j  y4 M: F& ^5 [8 i4 S; PDesk Reference and package insert should also put a: ^! {' M8 P- ]: J
warning about the virilizing effect on a male or
" g& {9 I8 e0 A8 y- [3 D9 gfemale child who might come in contact with some-
6 b0 H5 {6 a8 H" m. mone using any of these products.
. [" u" Z% U. g* M/ J/ t6 K! bReferences5 V) A1 J) K  l* O
1. Styne DM. The testes: disorder of sexual differentiation
/ n" i0 F5 x. @" n. ]and puberty in the male. In: Sperling MA, ed. Pediatric
: F& U6 r/ m: X/ GEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;1 d+ z% t4 A* f# n
2002: 565-628.
) P2 }9 W  f* \  g6 C: i3 s2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious, \3 U; Z% M% P  f  A
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
! ~8 m- V( @& GBoy Induced by Indirect Topical7 d" H. N: Z( ?+ C8 K  _
Exposure to Testosterone
+ I: Q. h6 f! q- OSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
$ H& R+ v5 {. H, }and Kenneth R. Rettig, MD1
8 W) i9 B  w& T3 v, VClinical Pediatrics
2 v$ n; G8 y" p8 |+ Y7 R$ ^Volume 46 Number 6
) u9 z5 c( E2 r, _8 H: hJuly 2007 540-543
3 ^$ U8 _9 X% P( g1 H5 l) J* L© 2007 Sage Publications
/ L7 D- A+ X& A* n10.1177/0009922806296651* Z8 I: ?+ k1 G5 E
http://clp.sagepub.com. Y" V: L7 B+ q' i
hosted at
3 x$ C- t6 M2 p: O8 G* jhttp://online.sagepub.com
  z; p9 U! N" v) H; UPrecocious puberty in boys, central or peripheral,) Q& k1 R: u& x4 e
is a significant concern for physicians. Central
' I! s, E' n2 \! N# v& d0 l: Dprecocious puberty (CPP), which is mediated
0 ?7 k' W) p% j, h! ^; a% Z, f- Othrough the hypothalamic pituitary gonadal axis, has
6 H* G5 Z4 i3 l. P' Pa higher incidence of organic central nervous system5 a; ?. W5 s1 O8 b  U' b% @. {
lesions in boys.1,2 Virilization in boys, as manifested3 r9 b2 v& H: J/ X5 P
by enlargement of the penis, development of pubic
6 G% o  _' L+ b- a4 N' J5 ]5 k! ohair, and facial acne without enlargement of testi-
. d  D9 U' t) @  ]cles, suggests peripheral or pseudopuberty.1-3 We
4 u! L) J# _. Vreport a 16-month-old boy who presented with the
5 F7 _$ z8 O, F# ]enlargement of the phallus and pubic hair develop-
' n) P: G! J( q% S/ c7 tment without testicular enlargement, which was due
, W% ?* G; L& {3 X3 n5 \+ sto the unintentional exposure to androgen gel used by8 _7 @7 ?/ D5 U+ V
the father. The family initially concealed this infor-
* M' l4 E) k5 z1 ~/ ?7 Omation, resulting in an extensive work-up for this
5 {/ V' r2 v/ @1 E& a3 Q% P- g* M) @child. Given the widespread and easy availability of
  X- E; y, n8 L* W5 N4 ftestosterone gel and cream, we believe this is proba-1 o" N! h! h* K7 J7 f" @
bly more common than the rare case report in the
6 ~: i1 x; ]5 ]2 P8 Xliterature.4
0 s9 v" Z4 `$ l4 G& V( ^Patient Report! B/ ]  R$ e5 }7 f! R5 A
A 16-month-old white child was referred to the
6 O  `- Y% B' Fendocrine clinic by his pediatrician with the concern
) F, L8 N* J. D" a% Iof early sexual development. His mother noticed! o+ n& k' \" w+ X1 ^' Y  N
light colored pubic hair development when he was) V2 [6 M* W' W/ n& x: \0 Z- w" r$ Q
From the 1Division of Pediatric Endocrinology, 2University of. v2 J) l6 l7 U2 s, q9 @! `
South Alabama Medical Center, Mobile, Alabama.) L/ O) l, P0 T7 p- x7 o' ?
Address correspondence to: Samar K. Bhowmick, MD, FACE,
# }  ~+ j( I/ AProfessor of Pediatrics, University of South Alabama, College of% P: H4 ?' Z; s5 ?, g
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;1 F8 [* @9 I3 J' H) Z  B2 @- H
e-mail: [email protected].
+ n! R- s8 h& T8 tabout 6 to 7 months old, which progressively became: m, `% S6 n8 z" G% S. w6 V
darker. She was also concerned about the enlarge-8 S0 l4 ~+ |4 G' R# h
ment of his penis and frequent erections. The child0 `. X4 a+ v8 Z; ~! B
was the product of a full-term normal delivery, with
1 i" B9 A# h+ L9 [' |* z% ^, La birth weight of 7 lb 14 oz, and birth length of: @  @- t7 l( S3 [
20 inches. He was breast-fed throughout the first year
: @- ?- y! }" |3 D. O$ M! o% l4 h. Cof life and was still receiving breast milk along with, X) R! I7 s" Z+ K- F
solid food. He had no hospitalizations or surgery,8 d) O9 O, w, Q% `1 D2 S  e# h
and his psychosocial and psychomotor development! T8 B. n) @8 Z+ [
was age appropriate.
1 A5 h( i/ _# A' ^' A" Z, bThe family history was remarkable for the father,4 M0 v3 I1 y0 K! U- p: ]! i
who was diagnosed with hypothyroidism at age 16,) f4 J' z0 f( I: @
which was treated with thyroxine. The father’s0 Y$ H2 U3 _/ }& H
height was 6 feet, and he went through a somewhat
( R7 \8 b8 r3 Q* h0 ^0 x. j5 Cearly puberty and had stopped growing by age 14.
+ z/ X# J0 ~, ~* AThe father denied taking any other medication. The' k2 A+ h3 E9 j
child’s mother was in good health. Her menarche
1 f2 _! V% z3 o1 a1 Swas at 11 years of age, and her height was at 5 feet5 ]  g: p1 ^  o' w
5 inches. There was no other family history of pre-( X" A! X% v* W0 p- N5 F3 A, r
cocious sexual development in the first-degree rela-; C8 z5 C3 G+ E, n' k! G
tives. There were no siblings.
- A& k8 ~3 e& |Physical Examination
5 e% F2 e: ]/ u0 Q; TThe physical examination revealed a very active,1 h' A0 I$ F6 _# H+ y
playful, and healthy boy. The vital signs documented: s' k' Q, Q8 U; w. Q/ M
a blood pressure of 85/50 mm Hg, his length was, }# F. l  ]) T* |3 n
90 cm (>97th percentile), and his weight was 14.4 kg
6 g, D2 k  N9 j: w6 S+ Z(also >97th percentile). The observed yearly growth5 j* l7 ]2 f  r/ q2 X
velocity was 30 cm (12 inches). The examination of
: g" o- c7 Q  z3 W  ~% Q* H6 mthe neck revealed no thyroid enlargement.
. S! o! [$ n4 d& q* d( L+ RThe genitourinary examination was remarkable for: F- z1 B) a3 X# ]$ W
enlargement of the penis, with a stretched length of
1 B* P) X$ }: Q1 [3 B3 Q8 cm and a width of 2 cm. The glans penis was very well
7 k- H3 d2 s! r2 ^; x) Odeveloped. The pubic hair was Tanner II, mostly around
* \! A' I6 f7 \) ?+ Q" D* p- H* V540
9 X$ [5 u! Y  b5 t8 T. Nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) \5 v- c0 K: d1 S# f0 E
the base of the phallus and was dark and curled. The; |3 \4 K5 L; F+ G8 T
testicular volume was prepubertal at 2 mL each.
" r: p! D: T, V% j- EThe skin was moist and smooth and somewhat9 Q9 S8 t4 ~$ S6 z' W* \' s3 N
oily. No axillary hair was noted. There were no
9 i7 m* t: x* A* Mabnormal skin pigmentations or café-au-lait spots.2 }$ t' F1 j, Q
Neurologic evaluation showed deep tendon reflex 2+
1 ~. L0 s: R7 v6 r& G" V' N3 \- Wbilateral and symmetrical. There was no suggestion
6 z6 T- h. B* A+ [' C" Mof papilledema.- Z, Z  ]: H8 D: R  H3 W9 x6 {
Laboratory Evaluation: p5 i% \  c- S( i* V
The bone age was consistent with 28 months by
+ M1 m1 m( i4 g  qusing the standard of Greulich and Pyle at a chrono-/ U  A/ {  V2 [2 b9 B
logic age of 16 months (advanced).5 Chromosomal
" `  R7 v$ d3 G  Z& E2 r& ]- vkaryotype was 46XY. The thyroid function test4 [+ X% h: x4 u7 W1 u# V
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
' [3 B( B# B1 @lating hormone level was 1.3 µIU/mL (both normal).' W/ K, a5 x+ r  Y6 O; A7 j
The concentrations of serum electrolytes, blood2 H# H$ h; b9 Q1 O1 b: X
urea nitrogen, creatinine, and calcium all were
( }6 W# G) H# i/ X: e1 c# E; f1 Zwithin normal range for his age. The concentration
$ b( z' X7 x# ]0 g2 Jof serum 17-hydroxyprogesterone was 16 ng/dL& }' @- K! {& S
(normal, 3 to 90 ng/dL), androstenedione was 20
3 W# j/ J5 I& t& L* E+ Ong/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
& W- U# {/ }, O3 s1 tterone was 38 ng/dL (normal, 50 to 760 ng/dL),& W# M( C+ Z7 y. x; `* V+ y+ e4 I( H
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
2 ]0 L" L* Q/ b- q& q1 p. [49ng/dL), 11-desoxycortisol (specific compound S): r  }  J+ d2 N' Q
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
  w  N2 T! }- Htisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total" a' N# S/ y" z9 D9 ]
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
+ B5 V" e3 u* |: X; ?and β-human chorionic gonadotropin was less than, f# R- P! `* [# G# X
5 mIU/mL (normal <5 mIU/mL). Serum follicular
( I/ p7 y) m( f* K1 R7 Astimulating hormone and leuteinizing hormone
7 h: A- @( z& q- g0 i5 j7 {concentrations were less than 0.05 mIU/mL
* _# L1 }, O$ M/ Q3 D(prepubertal).7 ]/ B- p9 B% t' ~$ F& a0 Q
The parents were notified about the laboratory! S1 j: @6 e+ Z1 f3 B! X2 K
results and were informed that all of the tests were
  r4 a0 e+ {- u4 B* ^normal except the testosterone level was high. The
  u3 o  K' z. \9 o( ]  {follow-up visit was arranged within a few weeks to
% x$ l, f, q& i" H7 N" c# Mobtain testicular and abdominal sonograms; how-
7 Y6 X3 Q7 P/ U. i8 _' l  Pever, the family did not return for 4 months.7 {6 X: e4 r8 K+ U" _4 \' j! k3 `
Physical examination at this time revealed that the
) @) w3 C. R! g. y- \child had grown 2.5 cm in 4 months and had gained- G. j9 Y" j( |% Z: y
2 kg of weight. Physical examination remained
! L! h1 i* ~9 H/ e% M' B* A" ~2 runchanged. Surprisingly, the pubic hair almost com-
0 A( W$ o8 \7 A  z$ B  R( Zpletely disappeared except for a few vellous hairs at
; M; s' E& l7 f6 D9 M# nthe base of the phallus. Testicular volume was still 20 ?% E6 Y2 g, N; {7 B+ i; @2 s
mL, and the size of the penis remained unchanged.! C( q( e( x, Q1 N2 O* R4 d
The mother also said that the boy was no longer hav-
# q/ s$ T7 y7 u* uing frequent erections.
' K0 T9 }5 \9 k4 z) y5 u6 h( eBoth parents were again questioned about use of
5 _# w9 |, A& U# Nany ointment/creams that they may have applied to  r2 c0 g6 b1 [4 Q$ l2 |: |
the child’s skin. This time the father admitted the& ~: y) p; x' H1 }
Topical Testosterone Exposure / Bhowmick et al 541
  s+ A! o3 @5 f* y# Cuse of testosterone gel twice daily that he was apply-4 S+ F1 E2 P" ]7 M
ing over his own shoulders, chest, and back area for
4 A, g; d6 E" f# [5 |  ]% O- va year. The father also revealed he was embarrassed
8 Y- C, S1 F9 Jto disclose that he was using a testosterone gel pre-
" A' E) y7 N: V, d  bscribed by his family physician for decreased libido) z' ~/ J% s8 v7 ]) A( v
secondary to depression.0 n+ {" D! R" f" Y$ T
The child slept in the same bed with parents.: e( g4 R% I) ]: ~9 l$ c6 a2 r
The father would hug the baby and hold him on his& r: a2 \! s) x0 m( F
chest for a considerable period of time, causing sig-
1 f! H- m1 i" [. _' P+ inificant bare skin contact between baby and father.$ a& S& f( M, B
The father also admitted that after the phone call,
& I5 I( K* o; W. [% a! [when he learned the testosterone level in the baby/ |* J3 _7 V, l4 S2 D
was high, he then read the product information
9 C' Q0 M, l0 Y1 ?0 p' rpacket and concluded that it was most likely the rea-) S" r) L, x$ K: D% d7 R' j9 m# a
son for the child’s virilization. At that time, they  B% i) V' f# h7 B' N
decided to put the baby in a separate bed, and the- x. y# v( c9 M0 l' r6 L% \1 p
father was not hugging him with bare skin and had  o5 ]5 u( c% {6 S3 l  i
been using protective clothing. A repeat testosterone
( [3 e2 M2 Y- R# w9 @& b0 R: Qtest was ordered, but the family did not go to the: ?; S, n4 n, [' S
laboratory to obtain the test.
. F  n" G- a9 nDiscussion
- k7 q9 ~3 N; t9 |3 _Precocious puberty in boys is defined as secondary" a9 y! j2 u/ G' w' |6 N' W0 x0 t
sexual development before 9 years of age.1,4; l. }  L! S2 E: w. ^
Precocious puberty is termed as central (true) when
3 w- x1 y! n4 Eit is caused by the premature activation of hypo-
; r0 u/ D  q4 h" c: C% m4 V9 ?+ Jthalamic pituitary gonadal axis. CPP is more com-" v# p( p: g* a0 r! A, G
mon in girls than in boys.1,3 Most boys with CPP
; |. b+ Q+ a( a4 b! I1 V; Zmay have a central nervous system lesion that is
7 d/ s+ q7 o7 f$ z! l  eresponsible for the early activation of the hypothal-
1 @; t8 d) ^& D! u0 N; A5 x) u( Yamic pituitary gonadal axis.1-3 Thus, greater empha-
; ]% A6 M8 n& P6 t9 T0 j( E' hsis has been given to neuroradiologic imaging in
4 j7 d6 d' ?+ E: yboys with precocious puberty. In addition to viril-2 E% K# [/ t: h2 }
ization, the clinical hallmark of CPP is the symmet-' O' k3 T" [- U
rical testicular growth secondary to stimulation by+ N5 v' g# i( u, R) w* N
gonadotropins.1,3' G7 t% V- H, C/ `0 B1 H( d
Gonadotropin-independent peripheral preco-; h( F! ]( D+ \
cious puberty in boys also results from inappropriate6 P9 z. F! {; _! e, b
androgenic stimulation from either endogenous or
" B6 v) ^9 C/ J$ G4 m5 Q9 ^: pexogenous sources, nonpituitary gonadotropin stim-
. q  v5 @  Q; b3 ?0 P4 ~ulation, and rare activating mutations.3 Virilizing
9 y3 F9 a7 Y6 P) Q8 ]3 hcongenital adrenal hyperplasia producing excessive2 N* M; p, g* B6 m- c+ k4 Q
adrenal androgens is a common cause of precocious
0 b  |# j8 n6 e. E, ^, tpuberty in boys.3,4
# Q9 V, ^$ c" F& Z. i) [8 ]9 C4 A' VThe most common form of congenital adrenal9 Z  \! Q7 X% j2 b8 ]
hyperplasia is the 21-hydroxylase enzyme deficiency.
; l6 f8 P; k5 R9 C8 u; H( n  AThe 11-β hydroxylase deficiency may also result in% |' H/ s- w3 O$ U
excessive adrenal androgen production, and rarely,
  G5 u' J3 \7 can adrenal tumor may also cause adrenal androgen( o% |2 q# R5 Y2 M9 s( j8 r
excess.1,3
# n. j8 c0 s% rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. h2 g( j2 L5 Q; g: A% E) n
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
/ S! c8 \4 q2 r/ OA unique entity of male-limited gonadotropin-
1 ^" ]' F" f5 Z; `independent precocious puberty, which is also known
8 S( X  W* K  S4 s& ~$ \1 e# qas testotoxicosis, may cause precocious puberty at a
1 N+ y7 A1 h" C: ~2 T2 vvery young age. The physical findings in these boys
8 j' A+ F4 e% Hwith this disorder are full pubertal development,
  W; c+ u0 X  Y4 e- j* sincluding bilateral testicular growth, similar to boys4 L+ K* S, c3 W" o8 b9 p
with CPP. The gonadotropin levels in this disorder5 `4 c7 _' ?7 P
are suppressed to prepubertal levels and do not show  V& f. G" E. a9 {* F+ i4 q5 |$ ?
pubertal response of gonadotropin after gonadotropin-
2 Q( T1 F5 |% sreleasing hormone stimulation. This is a sex-linked. d3 `% C$ |0 `" r8 g. \# N6 u
autosomal dominant disorder that affects only- ], ^& b7 H5 y. V
males; therefore, other male members of the family
1 @: [) w0 {" E; Zmay have similar precocious puberty.3
" H6 Z& F: ]$ v, ~& \; ZIn our patient, physical examination was incon-& Z& [6 H7 [, H0 B5 }6 n
sistent with true precocious puberty since his testi-3 p+ M3 q6 b  a5 }! ]( R5 F* x
cles were prepubertal in size. However, testotoxicosis4 ~; r3 k' s' f* f
was in the differential diagnosis because his father% O$ i- |5 T# I5 r5 n' _3 t' j3 j
started puberty somewhat early, and occasionally,
/ w* o5 }+ s% [testicular enlargement is not that evident in the
4 n! r; X9 W, m, ibeginning of this process.1 In the absence of a neg-
/ Z8 p9 K, N; i2 Qative initial history of androgen exposure, our
" m+ N' u9 F9 N4 S+ i$ ybiggest concern was virilizing adrenal hyperplasia,3 @- }5 U* l# I
either 21-hydroxylase deficiency or 11-β hydroxylase* l% X( E) ]& }  o& p  [
deficiency. Those diagnoses were excluded by find-
+ R$ V9 R6 ~, Aing the normal level of adrenal steroids." @  H1 C; F8 L  K; r; y
The diagnosis of exogenous androgens was strongly( z" z, j0 U! e$ o4 W
suspected in a follow-up visit after 4 months because
$ {1 M5 I1 G( s  ?& Fthe physical examination revealed the complete disap-
4 d, M1 u8 i* v" S) ?pearance of pubic hair, normal growth velocity, and
# D. g$ W/ k& |9 G# Adecreased erections. The father admitted using a testos-
$ a) _5 N" a' Pterone gel, which he concealed at first visit. He was2 ~! p; c1 F" S( O
using it rather frequently, twice a day. The Physicians’% g) @  u' m: z
Desk Reference, or package insert of this product, gel or2 V1 Z1 ^% V% g& R" e
cream, cautions about dermal testosterone transfer to. n! q8 J: h$ _/ j! R1 `1 m. |
unprotected females through direct skin exposure.) y0 g/ [# U# \" O1 ~
Serum testosterone level was found to be 2 times the4 @6 p) A% Z/ L# _
baseline value in those females who were exposed to  ~) x( s* v1 l' o2 @/ a
even 15 minutes of direct skin contact with their male
! A6 x$ L  ^: C/ Npartners.6 However, when a shirt covered the applica-
/ X4 y4 P! }+ k! H. t/ Etion site, this testosterone transfer was prevented.* U( [! R2 \" Z- ^+ h
Our patient’s testosterone level was 60 ng/mL,
  k& [$ |: B8 Y( Lwhich was clearly high. Some studies suggest that3 h8 k5 b* T6 O6 }
dermal conversion of testosterone to dihydrotestos-
; a/ K7 W0 ~8 c# xterone, which is a more potent metabolite, is more
/ e/ B/ ?& L/ s+ Gactive in young children exposed to testosterone8 ~$ Q  k6 d  u! A5 L; B$ A  @
exogenously7; however, we did not measure a dihy-5 }* d% d8 ^! j# P5 }6 k, ]
drotestosterone level in our patient. In addition to
+ _/ f/ a% X6 r9 S4 F" Z2 Cvirilization, exposure to exogenous testosterone in* k& f# g! }2 @/ J" R3 D. U
children results in an increase in growth velocity and
% L6 {  o4 A+ x8 G# Gadvanced bone age, as seen in our patient.
7 ^- |. h) a: U3 EThe long-term effect of androgen exposure during
; y+ r( Z* r5 ^# T" xearly childhood on pubertal development and final
- i0 d* J- h6 J. ^/ cadult height are not fully known and always remain, E5 W0 R: `  N. G. h
a concern. Children treated with short-term testos-# i* q8 i4 z+ t3 U
terone injection or topical androgen may exhibit some
4 i4 o: `5 g: y, M7 pacceleration of the skeletal maturation; however, after
% M; Y$ ^1 z0 F* R1 R& Tcessation of treatment, the rate of bone maturation
6 F. ?+ y6 ]* Cdecelerates and gradually returns to normal.8,9: Z' ], I! X/ o- R" u# \4 A
There are conflicting reports and controversy
; \9 D+ z" B0 W+ h& G+ Nover the effect of early androgen exposure on adult+ ?* q* u6 @9 T+ U
penile length.10,11 Some reports suggest subnormal, [& {& C/ v3 f! h# z; [' ]
adult penile length, apparently because of downreg-4 q4 U$ c- M2 o" l1 [" R! }- {
ulation of androgen receptor number.10,12 However,- @/ r7 ?" i6 }8 _$ N2 V
Sutherland et al13 did not find a correlation between; R8 k. s/ @4 j' T. j* F0 h3 f; a
childhood testosterone exposure and reduced adult
$ A* J& i7 w7 rpenile length in clinical studies.! g0 w6 p9 h( B" E7 _& D
Nonetheless, we do not believe our patient is- j: y) i0 b2 U7 E
going to experience any of the untoward effects from
- s$ I- q" x7 S  @. H- ^8 p& ltestosterone exposure as mentioned earlier because
! v8 o# _6 q  F  |& f; r. jthe exposure was not for a prolonged period of time.
/ I4 l' M8 ?) S; fAlthough the bone age was advanced at the time of: D2 K! a# ?, h, E3 G8 v7 v) l
diagnosis, the child had a normal growth velocity at1 b; e3 V& s' l
the follow-up visit. It is hoped that his final adult
! _% \# \, i( eheight will not be affected.
, ]7 f5 d8 _. p# c! \. G& a: xAlthough rarely reported, the widespread avail-
# b5 e9 @9 n) s7 J9 K9 |4 q; bability of androgen products in our society may! d6 d4 P& S6 |& q$ n- T
indeed cause more virilization in male or female
( J/ I$ ~; y7 ~2 zchildren than one would realize. Exposure to andro-  Q: ^0 r. |& m$ P  t
gen products must be considered and specific ques-
1 {6 t- h6 S- \( S/ htioning about the use of a testosterone product or8 O0 ]/ ]: `2 d# Y* s
gel should be asked of the family members during) j% `: {% \1 s8 `' n# B
the evaluation of any children who present with vir-
' l+ n$ c. x  s, h/ Uilization or peripheral precocious puberty. The diag-1 X, g+ o3 W7 [8 s# ]4 O9 }
nosis can be established by just a few tests and by
( H. ^* ?4 F& k, S  ?. Z+ Uappropriate history. The inability to obtain such a& X( b& E0 {0 g" i
history, or failure to ask the specific questions, may
" H5 y3 H4 N( Y3 ]result in extensive, unnecessary, and expensive
/ ^3 y# N0 C) B2 p% P" D1 n, uinvestigation. The primary care physician should be. b9 B5 k( }( r$ b5 v- t
aware of this fact, because most of these children9 d- z* D  q. O, L: \
may initially present in their practice. The Physicians’; s" a8 ?) {. F/ \
Desk Reference and package insert should also put a
+ k" B, K1 y8 a0 P* nwarning about the virilizing effect on a male or
* [  I/ X8 ~' Q3 a) t2 d. ~' Ifemale child who might come in contact with some-* ~! F) c. Y) A
one using any of these products.
7 g, f. K* u6 m# {References
5 U! B( k7 C! ]% q1. Styne DM. The testes: disorder of sexual differentiation& ?  `& r4 A/ T8 k
and puberty in the male. In: Sperling MA, ed. Pediatric8 W7 J( W0 `9 ]4 ?' {) h
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
( X" ^- r/ `* h1 r4 j  o# \- J- h2002: 565-628.$ L. H. ?" P+ P/ P% E. n
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious' {0 m# {/ i& p3 @8 z
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
- L0 i  m0 k, R, f+ W3 B
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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