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Sexual Precocity in a 16-Month-Old
: ~4 G2 t+ B1 h! t* |% |Boy Induced by Indirect Topical6 }; L  b* T2 o
Exposure to Testosterone
5 v) ^1 s8 w% Y  Q9 G* uSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
# ~/ ]- v9 P4 }2 Q% K! Nand Kenneth R. Rettig, MD1+ m( _% S* Z  O2 o
Clinical Pediatrics
* J5 A  c5 N2 x# [1 i$ U2 q! M  hVolume 46 Number 6
7 R2 s+ B/ ^5 t" ?& d; S3 cJuly 2007 540-543
: K; A+ ^( f! Q, [1 o% t© 2007 Sage Publications
3 G0 N# f% r4 j# I10.1177/0009922806296651/ a; Q& |( p; I+ q! s+ H# \. O2 G
http://clp.sagepub.com0 n# V$ ~# z% o3 l; r; J' f
hosted at
( x8 u3 H8 j9 ihttp://online.sagepub.com! m! R% p8 {* E8 g& Q
Precocious puberty in boys, central or peripheral,
5 r7 R" ]9 I2 _* |; Uis a significant concern for physicians. Central/ s( P1 e1 Y) S0 k
precocious puberty (CPP), which is mediated7 f) |) u# R& i  x. ?+ F& o
through the hypothalamic pituitary gonadal axis, has
  I( C! D$ C3 N! r( W5 B# o2 La higher incidence of organic central nervous system* G! }9 D$ C# P7 S! v
lesions in boys.1,2 Virilization in boys, as manifested
2 U1 a( M- J8 Zby enlargement of the penis, development of pubic
+ D$ `, P$ H- K5 k; ghair, and facial acne without enlargement of testi-$ N- E" p5 r2 ]1 F* K: V* E
cles, suggests peripheral or pseudopuberty.1-3 We8 ^; ^7 g6 \, O* ?' }
report a 16-month-old boy who presented with the! ~( \* A3 @& G, E/ |  t
enlargement of the phallus and pubic hair develop-
' Y& ^- f/ n( p9 d0 gment without testicular enlargement, which was due
7 n. g7 ^& \  ]9 O* Rto the unintentional exposure to androgen gel used by
' v1 ~1 r3 ]/ A/ A1 bthe father. The family initially concealed this infor-$ F$ y8 \4 L7 j: [0 |/ G
mation, resulting in an extensive work-up for this
" ~1 }/ |" p8 S7 rchild. Given the widespread and easy availability of) [8 Y2 j# R, \7 a) @: l
testosterone gel and cream, we believe this is proba-
( I, }. s' |+ U, B: lbly more common than the rare case report in the: Y4 G! O' _& d7 l3 ~* j9 C7 M" T
literature.4
7 }% l+ C. C; a" s9 S. G* QPatient Report% Z$ P. ^1 f4 W: t" o/ u
A 16-month-old white child was referred to the
, L( _5 ]6 K4 j2 `endocrine clinic by his pediatrician with the concern  E) C( o' w. R& d4 ?
of early sexual development. His mother noticed
, F2 |+ n2 s  o7 ?7 w* Z6 dlight colored pubic hair development when he was. U) n0 w9 y3 k! r$ V
From the 1Division of Pediatric Endocrinology, 2University of- y5 E: S! }, b3 k9 k* p$ V6 Q
South Alabama Medical Center, Mobile, Alabama.; f% t: X% f: A4 p/ j" V: a1 G+ S5 K
Address correspondence to: Samar K. Bhowmick, MD, FACE,/ ?# w! O- j4 [" ?, K
Professor of Pediatrics, University of South Alabama, College of
3 V+ g$ {" L* j5 {/ m" }8 \6 e' ]Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;# Q0 ?: R1 R# V/ f; E+ n. I) O
e-mail: [email protected]., [8 m3 U6 d$ a0 |
about 6 to 7 months old, which progressively became
- e8 ?+ A: k$ n- F* N! y) Udarker. She was also concerned about the enlarge-: I* y5 o9 N' Y$ |4 F& a8 i8 Q
ment of his penis and frequent erections. The child+ d/ K! g) M( t8 Y$ k
was the product of a full-term normal delivery, with
' e7 \$ q4 H6 M* d7 ba birth weight of 7 lb 14 oz, and birth length of
/ Y; S5 X, p$ x: D) G1 Z20 inches. He was breast-fed throughout the first year
6 a, ]9 s6 r, c* P9 H  Eof life and was still receiving breast milk along with' ^" U3 F9 b- ?
solid food. He had no hospitalizations or surgery,
# ?+ u, W5 s/ `* n. j# aand his psychosocial and psychomotor development
2 T% N5 k- ~) Kwas age appropriate.
. Q/ J  v* ~$ ^0 G* U& `The family history was remarkable for the father,1 E+ w/ n  x& F+ f  \3 e
who was diagnosed with hypothyroidism at age 16,* V  ^3 q8 L" Z& ^! l
which was treated with thyroxine. The father’s
2 f% @/ m9 u" v/ M3 kheight was 6 feet, and he went through a somewhat$ P! p2 i5 G. Q5 a# @5 h
early puberty and had stopped growing by age 14.
" y; t/ r( `8 |  L/ _The father denied taking any other medication. The
6 `2 i0 [- {5 `. v: Kchild’s mother was in good health. Her menarche
/ y6 @/ [+ ?. w, N* \9 Awas at 11 years of age, and her height was at 5 feet
; O; o6 S) \" }: h" f6 n* J5 inches. There was no other family history of pre-
' f4 Z6 G2 L  ecocious sexual development in the first-degree rela-+ E" M& B1 i. V- ?$ E; U+ i
tives. There were no siblings.
3 P; t0 x5 E2 X% TPhysical Examination
6 J  H/ G$ O2 _% J, {) P- |The physical examination revealed a very active,! x; m' S/ _$ S3 y8 I/ w6 S& c
playful, and healthy boy. The vital signs documented
: T7 c, X1 A& G. j; ]9 M* \1 Ga blood pressure of 85/50 mm Hg, his length was
$ u3 ?1 b2 i9 z# U! c9 t90 cm (>97th percentile), and his weight was 14.4 kg+ m# E- ?% ?3 ?, |
(also >97th percentile). The observed yearly growth
0 K  F1 }, \& evelocity was 30 cm (12 inches). The examination of
: t- }5 f# d" X- Rthe neck revealed no thyroid enlargement.
' G# A8 M0 n, }1 r0 r3 a. r2 D' f0 P7 GThe genitourinary examination was remarkable for/ L3 z& M1 J8 U
enlargement of the penis, with a stretched length of+ ^! K/ {/ G9 O& l# u; p
8 cm and a width of 2 cm. The glans penis was very well
; L7 i$ e1 T/ v& P! k+ Vdeveloped. The pubic hair was Tanner II, mostly around3 [. O! y1 g8 B9 E2 R2 I
5403 S; g& ^, ~8 l: S2 G6 \, H" `( S
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 o2 ~! j4 ^1 P; I7 T
the base of the phallus and was dark and curled. The
( I, P+ {, b" B! d9 `testicular volume was prepubertal at 2 mL each.- C6 k& F0 r* r7 d7 j
The skin was moist and smooth and somewhat
( L' E' s5 g6 f+ s" v- Zoily. No axillary hair was noted. There were no! N* ?5 m8 Y2 S
abnormal skin pigmentations or café-au-lait spots.
6 I" Y% j+ l# t9 p  M; k! M% WNeurologic evaluation showed deep tendon reflex 2++ g9 d* N+ V* [- D- q
bilateral and symmetrical. There was no suggestion& b) ]# ]( T/ \7 W5 H$ e) g# g
of papilledema.
. a: H  N, L/ i) R+ v' Q# r; PLaboratory Evaluation
3 t+ E* p& h- D/ ^The bone age was consistent with 28 months by
7 L! n6 Z4 d) `6 N' C0 F' \: uusing the standard of Greulich and Pyle at a chrono-, z2 p+ M: m2 ]; e+ y
logic age of 16 months (advanced).5 Chromosomal
1 n' U2 g& X5 zkaryotype was 46XY. The thyroid function test2 O9 l0 J  ?- q" j
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
$ C7 x6 r  e$ olating hormone level was 1.3 µIU/mL (both normal).
3 B! U8 x' p2 F- V: U, w: t# f/ ?The concentrations of serum electrolytes, blood' |; Q1 c) n& m* B/ m
urea nitrogen, creatinine, and calcium all were
- @+ k* Y" h7 @# k2 awithin normal range for his age. The concentration
  u/ M0 E4 U. lof serum 17-hydroxyprogesterone was 16 ng/dL) P, b! B0 F  X7 B
(normal, 3 to 90 ng/dL), androstenedione was 20
5 x. m/ N& g8 {6 E! k- A9 Eng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
( A, B( T1 N4 dterone was 38 ng/dL (normal, 50 to 760 ng/dL),
7 S4 Y7 }6 x% u+ ^( ]6 E7 Udesoxycorticosterone was 4.3 ng/dL (normal, 7 to7 Q5 p1 g  h1 A& f# a2 q
49ng/dL), 11-desoxycortisol (specific compound S)
$ N/ j+ _) l. A3 n$ d* m+ h  s1 J- Cwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-! U7 u: O  _8 E7 w# y  e
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
- c7 Q5 O; G0 I8 ~( B) g3 xtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),0 g$ n! h' d6 t% P# r% H& t4 ^
and β-human chorionic gonadotropin was less than0 a2 @! O/ f. h' \, A
5 mIU/mL (normal <5 mIU/mL). Serum follicular  O' v- _  n! r) P; ^  A
stimulating hormone and leuteinizing hormone
- y  R4 L4 W% }2 a: L5 S. d4 \concentrations were less than 0.05 mIU/mL
8 z: ]: `) r' L; V2 G- S3 o) K(prepubertal).2 J+ W& o, r/ Y+ j9 D5 w6 |
The parents were notified about the laboratory" P9 @6 _) A1 K) ^+ S+ d6 S  x
results and were informed that all of the tests were9 q& T8 r: g% T* u
normal except the testosterone level was high. The
7 w- |1 G# x# d  o7 G: ]follow-up visit was arranged within a few weeks to3 R% s, y: c6 r3 |$ j1 [
obtain testicular and abdominal sonograms; how-9 t8 P* r4 I" [6 U+ J& Z
ever, the family did not return for 4 months.
5 v5 z$ |8 g( s7 }Physical examination at this time revealed that the
7 ]) k; K$ g. ]4 D$ v# ^- f: z7 uchild had grown 2.5 cm in 4 months and had gained
9 W* L) }6 \3 t, L) T( g# o2 kg of weight. Physical examination remained# l' X" V: d' S* L. }# g
unchanged. Surprisingly, the pubic hair almost com-
; E' e+ j  C# G- d0 Lpletely disappeared except for a few vellous hairs at
- r" Q( ]2 S5 o+ Ithe base of the phallus. Testicular volume was still 2
+ ], @. {+ a3 Q4 M! WmL, and the size of the penis remained unchanged.! `4 I1 B, E3 g
The mother also said that the boy was no longer hav-
6 b; Y, \' R4 H5 x9 Ding frequent erections.
* x6 e* ?0 E' X* SBoth parents were again questioned about use of
$ Y! e$ E6 |: p( P2 wany ointment/creams that they may have applied to
- H9 o5 P0 z* R9 e4 Fthe child’s skin. This time the father admitted the
( z; m: x# A: u4 f+ h2 j% ATopical Testosterone Exposure / Bhowmick et al 541  e3 x5 `# R% m) H" w
use of testosterone gel twice daily that he was apply-
9 e. M* e! {, p- L% E, sing over his own shoulders, chest, and back area for  r: n+ X6 b4 F: P1 v
a year. The father also revealed he was embarrassed
( m9 v3 ^; B3 U7 }8 J  Y# j2 cto disclose that he was using a testosterone gel pre-
/ q9 P- `& H! O0 D: hscribed by his family physician for decreased libido
+ I, N6 U% n6 B5 X7 S3 L6 esecondary to depression.7 x; V% S7 [  G9 Z7 ^
The child slept in the same bed with parents.
* ~) l% F- I; Z) E# N7 {+ nThe father would hug the baby and hold him on his% q5 \( J; a5 R
chest for a considerable period of time, causing sig-
0 S4 R6 R$ Y+ H' o8 rnificant bare skin contact between baby and father.0 \" R0 z* B" r* e* U
The father also admitted that after the phone call,  M/ o+ ]( x% P" @$ p$ c
when he learned the testosterone level in the baby
; r+ u; f" A5 b9 `was high, he then read the product information
6 M7 {7 ]2 V0 o% k* G- w- o2 ]packet and concluded that it was most likely the rea-! m# @5 F3 @+ Q$ f8 A% \1 e
son for the child’s virilization. At that time, they
8 `/ v. o9 v) K" Fdecided to put the baby in a separate bed, and the) i2 @+ m7 v" U" I8 \
father was not hugging him with bare skin and had( W3 s) P; M' _* Y9 G
been using protective clothing. A repeat testosterone8 Q, P; d, M7 Y" z& L  a
test was ordered, but the family did not go to the
) o. N, \# o5 t4 mlaboratory to obtain the test.- I. N* x- Q7 i+ P3 v
Discussion6 X9 r7 Q, d7 h5 O5 c
Precocious puberty in boys is defined as secondary, ]  C% j& z' |, b8 e3 y, p3 K5 o9 X% k
sexual development before 9 years of age.1,4' J' H. D/ C# B$ Y* L2 ~
Precocious puberty is termed as central (true) when$ u- f6 F5 J6 s* l" C. V, d" g$ P4 ?
it is caused by the premature activation of hypo-
. \+ T. B! L9 e" Z6 p$ Fthalamic pituitary gonadal axis. CPP is more com-
, t3 B% Z' Y- v3 H8 ymon in girls than in boys.1,3 Most boys with CPP
$ a$ L$ c% N$ P, |may have a central nervous system lesion that is, Z+ M6 Q" Y; L9 |6 q: {5 m9 f
responsible for the early activation of the hypothal-
' t7 S/ m' m: U( X# Wamic pituitary gonadal axis.1-3 Thus, greater empha-
1 U8 q8 M* P$ {4 r" F$ N7 Jsis has been given to neuroradiologic imaging in
7 O2 }) H9 k  j4 a; l4 @boys with precocious puberty. In addition to viril-
) t0 [6 v0 ?( T. s/ \" Y3 vization, the clinical hallmark of CPP is the symmet-
7 W/ o, |) H8 {$ Z! B6 |% vrical testicular growth secondary to stimulation by
2 |5 D: p! o' Bgonadotropins.1,3
- k: U. c5 ^3 Y8 x6 @Gonadotropin-independent peripheral preco-
6 R+ B6 P3 n5 F* jcious puberty in boys also results from inappropriate
1 L1 p! y: [# v1 Q( R5 C% Vandrogenic stimulation from either endogenous or! i" ~/ q3 L0 Z/ T9 ?
exogenous sources, nonpituitary gonadotropin stim-- d5 X8 G8 t; n+ \6 G2 n
ulation, and rare activating mutations.3 Virilizing, T( f8 V( Q3 T/ k  B9 [
congenital adrenal hyperplasia producing excessive
3 k& P' u9 y- J" Kadrenal androgens is a common cause of precocious' p! q( Y3 `1 u( s# k' s8 k, I
puberty in boys.3,4: N+ }- w6 W! X) B* I. s
The most common form of congenital adrenal2 T! L7 m3 t" J/ C6 F5 |& [
hyperplasia is the 21-hydroxylase enzyme deficiency.7 m5 l9 p& B4 s. Y! c( h5 n
The 11-β hydroxylase deficiency may also result in
, w: a9 j* _0 z  Uexcessive adrenal androgen production, and rarely,
: W; {$ |/ a/ c+ z$ Aan adrenal tumor may also cause adrenal androgen
1 U( y0 {5 x6 {, T: F6 f, ^: l/ M% }$ uexcess.1,3* k) }" _; M* Q7 U% E; Q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& `7 {9 b/ x6 F+ L) d5 _( F542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
: x3 q9 Y6 h' q, N: Y: H( n; f- j( UA unique entity of male-limited gonadotropin-  O" C6 _+ X2 `! R6 B$ e. F
independent precocious puberty, which is also known- _" r' j8 X* D$ n& ?
as testotoxicosis, may cause precocious puberty at a/ x; w* K: n( @' M
very young age. The physical findings in these boys  J* y6 P6 Q: |, _& A
with this disorder are full pubertal development,
( T/ T; }* s( S/ @) Wincluding bilateral testicular growth, similar to boys
" u8 J& F/ W" ]/ hwith CPP. The gonadotropin levels in this disorder) p' X! R, }' `5 J/ @8 D6 Q  }# e
are suppressed to prepubertal levels and do not show
# ^( V( R' ^% ]& W4 Ppubertal response of gonadotropin after gonadotropin-* _; |9 i, m' O4 b
releasing hormone stimulation. This is a sex-linked" @) |: I2 i' J  G7 j" D  u; Q
autosomal dominant disorder that affects only
2 \( b* C7 O* ?& w9 gmales; therefore, other male members of the family
/ J: g. c/ v  N! q2 k1 P: Cmay have similar precocious puberty.3
) d; R' ?7 u! ^In our patient, physical examination was incon-
# P. x# B3 {6 P% A/ e5 I9 Qsistent with true precocious puberty since his testi-
7 n; U) V! m! [2 u1 h" `cles were prepubertal in size. However, testotoxicosis
: X, R1 _( C5 q( Awas in the differential diagnosis because his father
; j3 r- ^; C# ?0 n( d/ l; u/ F7 ]started puberty somewhat early, and occasionally,
4 Z6 `1 l4 |& Y/ Utesticular enlargement is not that evident in the, g) o* a7 {4 {% ~) i3 }% y& N: L
beginning of this process.1 In the absence of a neg-
; U. J' k0 y: L6 [! kative initial history of androgen exposure, our
4 z. v+ x$ J# l- ?$ Z- qbiggest concern was virilizing adrenal hyperplasia,
9 ]5 A! k7 q5 d, I% ]7 w* Ceither 21-hydroxylase deficiency or 11-β hydroxylase
$ z) J3 r! }0 T8 |, ]deficiency. Those diagnoses were excluded by find-
* |% o3 d+ l  M8 ^8 a' ying the normal level of adrenal steroids.. Z' ~$ i* i6 m& B
The diagnosis of exogenous androgens was strongly
$ }$ w( p1 C) Y/ `suspected in a follow-up visit after 4 months because
' H0 ?9 q) G2 g2 {' b" zthe physical examination revealed the complete disap-
6 C$ |' B- q. M1 ^; q3 Bpearance of pubic hair, normal growth velocity, and
0 j' ~, z7 O3 J1 X7 u$ C8 V8 G. L/ _decreased erections. The father admitted using a testos-2 g! @  C, ]! P4 u2 O: B
terone gel, which he concealed at first visit. He was2 e9 z/ V3 M: L0 A( ^
using it rather frequently, twice a day. The Physicians’
: r% C$ V' h( T/ o% b+ L" jDesk Reference, or package insert of this product, gel or
, P7 S+ P' C7 y# C3 [$ V4 f8 u3 fcream, cautions about dermal testosterone transfer to
- T+ Z) O* v- |# X/ N/ Gunprotected females through direct skin exposure.) H) h8 h6 [/ g
Serum testosterone level was found to be 2 times the, C0 J' `1 F) d1 z
baseline value in those females who were exposed to
0 K8 J% @7 M; @' t" B# ^even 15 minutes of direct skin contact with their male" s0 t, c8 @- g- F# ]6 b& s
partners.6 However, when a shirt covered the applica-) r2 k6 F7 S4 r! r5 ~9 {* k
tion site, this testosterone transfer was prevented.
, _6 l0 s" D1 y' `; Y$ D- N- x3 tOur patient’s testosterone level was 60 ng/mL,
' Q. {7 h: Q1 w- Pwhich was clearly high. Some studies suggest that! n; K7 u9 B; z9 a$ u
dermal conversion of testosterone to dihydrotestos-" F; Y+ B  i( }8 D, v) q0 G3 f  Z5 a
terone, which is a more potent metabolite, is more
$ a; s8 Y% N1 G2 ]active in young children exposed to testosterone" p1 v0 R. A1 T9 `# b$ z) [: K9 j
exogenously7; however, we did not measure a dihy-5 }* Z  d, X" |
drotestosterone level in our patient. In addition to  u7 c: o. I5 y1 N
virilization, exposure to exogenous testosterone in
) S. Z7 |5 c1 K) y$ P2 Z, x' \children results in an increase in growth velocity and
7 i  G9 e+ d6 H: Y$ c( c4 Fadvanced bone age, as seen in our patient.
6 h+ [8 g. A% ]1 kThe long-term effect of androgen exposure during4 A, k8 v7 @- I
early childhood on pubertal development and final+ ], y9 O2 M/ I( B* b6 D
adult height are not fully known and always remain/ N5 y2 g! r* E  p4 C
a concern. Children treated with short-term testos-1 [5 H& k. O0 O) [1 ?6 c' Y
terone injection or topical androgen may exhibit some
/ `' W9 d: }2 F' H% N0 a2 V2 Yacceleration of the skeletal maturation; however, after
) {# ?5 N( y. z9 N# U" Icessation of treatment, the rate of bone maturation6 U% Z: p+ n' ^+ x5 ~
decelerates and gradually returns to normal.8,9  J+ a; m/ s' M. x& n! R$ z  Q1 s
There are conflicting reports and controversy; `0 v2 L4 h* A7 P; f8 m
over the effect of early androgen exposure on adult) d1 a  w$ q: t3 k
penile length.10,11 Some reports suggest subnormal
1 k; d* t+ N7 S' \7 c) o: N) cadult penile length, apparently because of downreg-' Y# z  i7 N- w3 l) n* x0 Y
ulation of androgen receptor number.10,12 However,! @. _0 [# o9 a1 v8 ]
Sutherland et al13 did not find a correlation between' W6 ?( g. U2 [2 J: @& v8 c
childhood testosterone exposure and reduced adult2 \6 p6 o: c2 D9 H+ h2 b& s+ y9 I1 J/ L
penile length in clinical studies.
6 k: D" q7 U# |! r0 ~Nonetheless, we do not believe our patient is
1 B, P7 {; k1 c8 O2 B, @" f2 Ggoing to experience any of the untoward effects from% f) F% S4 k" F9 y  h9 U
testosterone exposure as mentioned earlier because2 G$ B: V  ]' y' I+ [
the exposure was not for a prolonged period of time.
) z- w$ p2 ]# dAlthough the bone age was advanced at the time of
7 d( z( T4 Y6 w% c4 E3 Xdiagnosis, the child had a normal growth velocity at) o  }+ j9 @( A* L# ]. F
the follow-up visit. It is hoped that his final adult
/ b+ {* N, o6 c; |height will not be affected.# w+ Z, N: U" M+ R8 I
Although rarely reported, the widespread avail-
- u% S) E. \# L/ P0 e8 yability of androgen products in our society may
; w& b2 n$ h7 T* x! Nindeed cause more virilization in male or female9 k3 j) [: v. v7 e0 o
children than one would realize. Exposure to andro-
& V* F# ^7 O- P6 r4 Ggen products must be considered and specific ques-
7 e9 s; h+ y. w1 i8 ~# Q$ o# R- ~tioning about the use of a testosterone product or( X4 ?( ~3 v  T0 _# {9 a9 m2 b: a
gel should be asked of the family members during3 K. J, t4 a3 h6 W) z
the evaluation of any children who present with vir-6 s6 y$ C- w" F2 I" x/ h
ilization or peripheral precocious puberty. The diag-1 l* P+ L( s+ T, p/ O2 t
nosis can be established by just a few tests and by
0 v2 ]1 M4 Q1 Oappropriate history. The inability to obtain such a
* L6 J* n4 O7 e% k) \4 I( Fhistory, or failure to ask the specific questions, may/ h5 v1 c2 F3 b3 S1 c! }# j! M! ~
result in extensive, unnecessary, and expensive
* c8 A. K4 s& t5 D) F: l; @investigation. The primary care physician should be
% O+ H* A3 P& E; `aware of this fact, because most of these children$ m! U) H4 v: e3 @% m4 g
may initially present in their practice. The Physicians’
8 ~3 W5 o9 \) hDesk Reference and package insert should also put a
& T/ U! _5 b+ F7 Y' [& ~1 p7 ~: D' Zwarning about the virilizing effect on a male or1 |. i3 k& H/ [* S+ f, x
female child who might come in contact with some-9 I+ `4 u) a) ]  ?" T
one using any of these products.
- A; c$ \; B# KReferences# H  p; \- `/ D6 A
1. Styne DM. The testes: disorder of sexual differentiation" l" g' {$ I: [  I7 T" J
and puberty in the male. In: Sperling MA, ed. Pediatric. N7 a2 y! G5 Q  Y1 I, h; q7 r
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;. S: I- V; V, ^+ C
2002: 565-628.9 A9 {8 d0 A! Z7 Q+ _7 |) i/ X
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious* U$ H( X$ L% C: i
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old4 j+ U/ \9 \6 h+ F. A
Boy Induced by Indirect Topical7 v. w# t2 q8 x# y( X
Exposure to Testosterone
' ~! e9 V# b5 W4 LSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
% d" m/ v' T  K8 o9 O* wand Kenneth R. Rettig, MD1
2 C. C$ G& P, r3 f2 X1 uClinical Pediatrics
. f  c8 _! Y* D8 i, X% hVolume 46 Number 6
8 S8 g2 g' S$ U3 IJuly 2007 540-543
2 V, w. V4 b% o9 ]8 u© 2007 Sage Publications# ], W: d3 r' M/ ]  e
10.1177/0009922806296651& X9 @7 D: P& I# g  `
http://clp.sagepub.com9 Y9 U% y2 Q$ N& y9 `2 }- l" Q: l
hosted at
$ V1 |1 v* V4 n0 n2 p  D* ~http://online.sagepub.com7 m. R* w$ J. i- \! z
Precocious puberty in boys, central or peripheral,, T8 ^. c3 [, U3 z% i' \0 X1 N
is a significant concern for physicians. Central
% f" N1 U( }! a* @precocious puberty (CPP), which is mediated
1 P7 o( _' e% Z( }+ e: Dthrough the hypothalamic pituitary gonadal axis, has
. V( a; p3 A  ]$ C0 F$ p! oa higher incidence of organic central nervous system# }: `+ E3 {: L/ q: X
lesions in boys.1,2 Virilization in boys, as manifested# K8 j$ P3 c1 A
by enlargement of the penis, development of pubic
6 F- ~& c: ]  I/ Z$ ihair, and facial acne without enlargement of testi-
6 H2 c* W5 [! O4 ~0 Qcles, suggests peripheral or pseudopuberty.1-3 We
# p' i7 k2 O( W  a; [report a 16-month-old boy who presented with the
7 l9 Q: D" z4 D5 |/ h" Oenlargement of the phallus and pubic hair develop-  J0 G- G1 I- {: i8 g3 P
ment without testicular enlargement, which was due
6 R  b7 N& ~! v  d. qto the unintentional exposure to androgen gel used by
& b& ]+ L- ~! ]5 Y* pthe father. The family initially concealed this infor-( w' |7 |0 o2 o. N
mation, resulting in an extensive work-up for this
8 N1 G7 O& B! ^3 Nchild. Given the widespread and easy availability of
4 W  L! L' z1 }6 @7 O& f$ Jtestosterone gel and cream, we believe this is proba-5 W( i( _' g9 ]+ m0 E4 H
bly more common than the rare case report in the/ n) d7 M5 g! B8 T. K2 X% _
literature.4: J2 P5 D9 k" `
Patient Report+ j5 H8 J; D% t: y( m& d/ \" [
A 16-month-old white child was referred to the
8 G$ [1 T8 w; Iendocrine clinic by his pediatrician with the concern
+ y. U# c- \* ~of early sexual development. His mother noticed4 H% T# A% ?4 u7 y3 w$ p! q
light colored pubic hair development when he was# r2 S; @- U) y% c% G3 f1 Y; L% j4 A
From the 1Division of Pediatric Endocrinology, 2University of
8 t4 }1 X! N/ y( _South Alabama Medical Center, Mobile, Alabama.
* A9 ^* N2 `6 j! wAddress correspondence to: Samar K. Bhowmick, MD, FACE,0 C9 I0 n* O, H% [4 P7 w
Professor of Pediatrics, University of South Alabama, College of" v: K9 X' s! Y' ^
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;. T' a) k( C9 s: o2 }2 c
e-mail: [email protected].% z& I$ v4 D2 D4 S  V' d
about 6 to 7 months old, which progressively became
* R. ~8 A4 @5 b1 `darker. She was also concerned about the enlarge-& Z) @, [) a* D5 W. s8 K; ]7 s
ment of his penis and frequent erections. The child/ I1 ~1 P0 ^6 }# c: K" U- C0 A% B
was the product of a full-term normal delivery, with
) Q6 y% O* w% w6 ha birth weight of 7 lb 14 oz, and birth length of
+ a6 ^$ i4 I1 T$ h; j- F6 V, A" a20 inches. He was breast-fed throughout the first year8 V9 U  C( l% @
of life and was still receiving breast milk along with
3 h" Z% ^4 C) h, F8 nsolid food. He had no hospitalizations or surgery,
& ~$ }2 k, N0 d3 aand his psychosocial and psychomotor development
8 f$ ^% D& l7 a' }was age appropriate.
: B- ]% ]2 o( DThe family history was remarkable for the father,
8 y% q4 @9 s- h' owho was diagnosed with hypothyroidism at age 16,
4 n- Q- ]7 m. y' _which was treated with thyroxine. The father’s
3 G$ `, M% c% K/ R0 C# `: yheight was 6 feet, and he went through a somewhat2 \+ }# z- r+ q
early puberty and had stopped growing by age 14.- ?4 }# F0 Q2 u, d
The father denied taking any other medication. The! s% V: l& j4 f* X0 r# E- R9 [
child’s mother was in good health. Her menarche
8 D0 f$ r( j) R& Owas at 11 years of age, and her height was at 5 feet
8 M& d- |+ ?3 }8 U; |( U5 X' d' W& i5 inches. There was no other family history of pre-
- D) u, Q/ c- w- }$ L5 ]cocious sexual development in the first-degree rela-+ N, G6 x$ P# b/ S5 [+ l2 a
tives. There were no siblings.
: O  p+ v/ X; j6 L) jPhysical Examination
' k  L- v, o' n; U$ NThe physical examination revealed a very active,
( {! l) o+ Z/ F& C( Eplayful, and healthy boy. The vital signs documented, [5 ?( U. [- p
a blood pressure of 85/50 mm Hg, his length was$ c) A5 n* w7 ~2 P6 L
90 cm (>97th percentile), and his weight was 14.4 kg. Q5 R1 L" h% S: |6 v
(also >97th percentile). The observed yearly growth$ b2 \7 b: t6 T4 i
velocity was 30 cm (12 inches). The examination of
9 D: `# E7 l: F/ {3 B3 N, }! fthe neck revealed no thyroid enlargement.  e2 k# |3 Q0 C4 ~
The genitourinary examination was remarkable for
5 Q2 A; S" }3 k) v8 Benlargement of the penis, with a stretched length of: Y$ S1 l5 ~& W- [- O# D4 g
8 cm and a width of 2 cm. The glans penis was very well5 F: e: k* Y" {) n5 L
developed. The pubic hair was Tanner II, mostly around( Y) O+ G2 {# L9 f
540
# X8 f3 m! ?6 ^, i( s6 yat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 V, \2 F# V' u+ Nthe base of the phallus and was dark and curled. The
. m& b& b  F  O! ]7 {5 ltesticular volume was prepubertal at 2 mL each.# M; d0 o  o8 Z7 ~8 h
The skin was moist and smooth and somewhat" |4 w0 J6 \4 Z2 R  ^
oily. No axillary hair was noted. There were no
- ?& r8 N# j: U1 E% \abnormal skin pigmentations or café-au-lait spots.* b% c* h% o% r. h
Neurologic evaluation showed deep tendon reflex 2+0 c2 K$ v. h) V& Q- g
bilateral and symmetrical. There was no suggestion( b& K8 V9 p! U
of papilledema.2 D7 g! E( f# ?6 h
Laboratory Evaluation7 A3 L6 g  ^$ ?1 K$ ~3 L3 O, k
The bone age was consistent with 28 months by
6 A1 H% B: g/ t5 D0 y  L2 jusing the standard of Greulich and Pyle at a chrono-
, Q, ~9 M9 k/ Mlogic age of 16 months (advanced).5 Chromosomal, g: Q5 v4 s: X
karyotype was 46XY. The thyroid function test" Q7 e" F; j8 e2 E' ~) _* J9 d8 N
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
# p; ?5 d8 ^# L+ U9 M/ Llating hormone level was 1.3 µIU/mL (both normal).$ W* B" \. D# K0 B
The concentrations of serum electrolytes, blood
; x+ \6 q( F/ q/ j# A4 p. [1 Purea nitrogen, creatinine, and calcium all were* Z- ^6 L( ^6 f  e- J4 D
within normal range for his age. The concentration
: A. F* {4 m' x* `3 nof serum 17-hydroxyprogesterone was 16 ng/dL
/ z) b$ ^. k6 q) T3 B8 o3 s( _(normal, 3 to 90 ng/dL), androstenedione was 20
# M! ]* I( r" A  L, X$ P2 sng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-/ j$ z7 r1 {  n. i3 g
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
4 q* [6 I1 T1 D! _desoxycorticosterone was 4.3 ng/dL (normal, 7 to; w$ l4 `& `# R( T) z. Q
49ng/dL), 11-desoxycortisol (specific compound S)
( n0 t, p1 |- q- Q2 Y4 z( |5 twas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-! I1 O1 H- @: s2 w2 m. K
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
2 [- E( H( _8 q8 Ntestosterone was 60 ng/dL (normal <3 to 10 ng/dL),! R, M) R. O9 L9 N, i/ `+ p3 f, E. t8 h
and β-human chorionic gonadotropin was less than- T) q6 w1 |% `5 N5 _
5 mIU/mL (normal <5 mIU/mL). Serum follicular! D. R( {) l! j& t
stimulating hormone and leuteinizing hormone- B. r# o) y. C; ~+ f' p
concentrations were less than 0.05 mIU/mL& B; ?) o7 X  w) v- n# h+ g! D
(prepubertal).7 d: N# g/ l! y7 }: H6 x
The parents were notified about the laboratory
) f0 n. \$ V! G# X" {results and were informed that all of the tests were
0 `4 Y7 E4 z  d; g; v: Dnormal except the testosterone level was high. The6 D' S& z& R$ w2 l. V: y
follow-up visit was arranged within a few weeks to
5 G" p5 S0 i8 J7 L. Aobtain testicular and abdominal sonograms; how-
' R# I9 {' i9 v# Q" q2 @3 Hever, the family did not return for 4 months.
7 D! p" A8 c/ h8 c- i) w( j. `Physical examination at this time revealed that the
6 r3 b; J4 N0 l: W' \child had grown 2.5 cm in 4 months and had gained0 y8 n! c, O& L6 P% s! B* }5 l* e6 D8 B
2 kg of weight. Physical examination remained* |8 x: T, \' c. c! I+ x
unchanged. Surprisingly, the pubic hair almost com-8 f' C; X4 T) X3 }* `4 p7 H
pletely disappeared except for a few vellous hairs at. Y7 s& f9 e8 V+ M
the base of the phallus. Testicular volume was still 26 p4 c7 n. M2 q0 C5 c7 u3 C
mL, and the size of the penis remained unchanged.
3 @. a; w  ?+ X2 wThe mother also said that the boy was no longer hav-
+ b& {' S3 D4 Jing frequent erections.
& M5 `. f1 W; B3 f2 iBoth parents were again questioned about use of6 `5 w3 p% u6 b$ v, c
any ointment/creams that they may have applied to
" y! E1 o' }' m# N4 `the child’s skin. This time the father admitted the
) Y8 p0 W# Q6 ?" R2 STopical Testosterone Exposure / Bhowmick et al 541
0 E  O' B  h# M# {  O5 B$ Q8 Quse of testosterone gel twice daily that he was apply-& Z, |1 Z/ s7 ^% c0 }) T3 N% ?- f
ing over his own shoulders, chest, and back area for. q6 [( ^! ]7 k
a year. The father also revealed he was embarrassed
; G. d. t8 a2 K3 r9 U1 v. Mto disclose that he was using a testosterone gel pre-
& A. T! |2 A+ E# t2 Z4 n0 Uscribed by his family physician for decreased libido. U9 L/ ^& [" d) ]$ b( {2 X
secondary to depression.( f5 \, o* i& y* n
The child slept in the same bed with parents.; N: d3 p+ ?9 y. ]+ g7 |7 D9 c
The father would hug the baby and hold him on his
) K& \6 d3 B1 K6 [! wchest for a considerable period of time, causing sig-
# T* g) W; X- M- lnificant bare skin contact between baby and father.
2 `* t3 ^* B/ v: D* BThe father also admitted that after the phone call,' b2 o2 G# T5 X! U
when he learned the testosterone level in the baby
! ?! P9 S! P3 E+ i. @was high, he then read the product information5 F: ]. z, T- t" |1 n
packet and concluded that it was most likely the rea-9 g. `2 t5 j1 J- c7 y$ k
son for the child’s virilization. At that time, they
$ n# U: o- s. Y8 ~decided to put the baby in a separate bed, and the& r+ g; v6 Z  n7 h; T
father was not hugging him with bare skin and had- s" v+ g- K( v
been using protective clothing. A repeat testosterone" i' Y! W, d% u! i1 t; J
test was ordered, but the family did not go to the& l) t; F- H# Z' X4 e4 I
laboratory to obtain the test.' a0 x  d2 ?$ {' x" |# r" O
Discussion
! M  F7 S( U) k; T( [Precocious puberty in boys is defined as secondary# ^  y. p. U6 l; Z- c7 C
sexual development before 9 years of age.1,4
) ^/ c: e$ Q% U! E: n0 gPrecocious puberty is termed as central (true) when
  O8 R  w8 Q( A* t2 K7 Iit is caused by the premature activation of hypo-! U% k. N5 I& q
thalamic pituitary gonadal axis. CPP is more com-
' m; n3 @+ D# w3 Mmon in girls than in boys.1,3 Most boys with CPP
& q! d% \2 f; \: y4 u) Lmay have a central nervous system lesion that is
8 S' l& \& |& h5 B$ A' _+ p$ eresponsible for the early activation of the hypothal-6 ~9 p0 R: l2 v/ C
amic pituitary gonadal axis.1-3 Thus, greater empha-
$ Y' D; ~3 u" g) ]( [sis has been given to neuroradiologic imaging in, j" m) T( }) U* @: {" m
boys with precocious puberty. In addition to viril-
6 ~) J! A# S$ ?$ {8 m, iization, the clinical hallmark of CPP is the symmet-
+ Z0 `. a. k2 i6 T" S+ srical testicular growth secondary to stimulation by
* t1 A8 ^5 j8 ~; m# B% Agonadotropins.1,3
( R- @0 s% v8 L" p. O& m7 dGonadotropin-independent peripheral preco-! P. @4 D0 P% \: h$ u4 L
cious puberty in boys also results from inappropriate0 Q3 s4 S; [1 v* @
androgenic stimulation from either endogenous or
8 U' r0 ~# x. y7 d8 V$ Q2 c* hexogenous sources, nonpituitary gonadotropin stim-' C) v0 S' a3 g+ }  O* \" ~
ulation, and rare activating mutations.3 Virilizing' Z/ I" g* g% |1 P8 u
congenital adrenal hyperplasia producing excessive, Q$ k$ E# Q4 N
adrenal androgens is a common cause of precocious% }4 }8 W2 a6 u) L2 ~$ A
puberty in boys.3,4& i1 Z$ K3 k' h; R
The most common form of congenital adrenal7 O$ y& d  S1 a4 I: E
hyperplasia is the 21-hydroxylase enzyme deficiency.
" _$ n6 |/ \! o) z9 b8 n# |The 11-β hydroxylase deficiency may also result in9 j! l; U6 X& N1 I
excessive adrenal androgen production, and rarely,
& r; {# d" K8 [6 X$ lan adrenal tumor may also cause adrenal androgen
* Z1 t: g0 b* Eexcess.1,3, ]8 a0 K2 \# f: L+ F3 P
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' L* U' ~) T! Q
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
7 R) b% G! h5 ~A unique entity of male-limited gonadotropin-) K0 m0 J/ f% ]# {2 I  Y( c5 H9 L
independent precocious puberty, which is also known
5 l! ~+ ]+ |  j! Has testotoxicosis, may cause precocious puberty at a
7 X# r; }* p- U0 ]% w2 Zvery young age. The physical findings in these boys
0 v4 y  a: H1 C. y& O2 g/ Jwith this disorder are full pubertal development,
1 n# d& a2 }. n% \  Oincluding bilateral testicular growth, similar to boys
* u3 k3 Y. C1 Nwith CPP. The gonadotropin levels in this disorder
( v9 j7 f) X7 D8 P* A: `1 P/ fare suppressed to prepubertal levels and do not show4 R+ H7 V4 W7 w' h9 P% O
pubertal response of gonadotropin after gonadotropin-
1 H) e& W$ e* s, B7 }9 s6 Rreleasing hormone stimulation. This is a sex-linked' j; r& i+ D; k
autosomal dominant disorder that affects only: b0 `* I, w8 b
males; therefore, other male members of the family! P5 _5 s- T. d$ i4 ^$ [1 _8 q
may have similar precocious puberty.3
3 C7 w$ y1 R, Z4 _+ ]6 j( a8 }5 DIn our patient, physical examination was incon-
, g$ @/ @& d1 Wsistent with true precocious puberty since his testi-
- d0 `; f/ S, }- c! Q% Q- l6 Ccles were prepubertal in size. However, testotoxicosis
. m3 q% S  P1 m$ mwas in the differential diagnosis because his father
; M* u7 b6 ?, A7 p# _started puberty somewhat early, and occasionally,; K0 n+ P- u2 l" W
testicular enlargement is not that evident in the
3 y3 x6 l( M& g" J( W+ }8 u2 e- g8 C8 Nbeginning of this process.1 In the absence of a neg-) c3 i7 s4 t! ?5 S+ ^0 t9 I$ S
ative initial history of androgen exposure, our/ u+ K; y" b+ O- ?0 l! k- w8 G
biggest concern was virilizing adrenal hyperplasia,
! `9 n" W* h7 j- R) F: i" j3 teither 21-hydroxylase deficiency or 11-β hydroxylase1 G+ A( d5 D$ k0 Z- i- O' i
deficiency. Those diagnoses were excluded by find-9 ?6 b4 J( V8 D  t
ing the normal level of adrenal steroids.
3 F5 a1 p& l' h4 ]$ Z  m* ZThe diagnosis of exogenous androgens was strongly/ \9 w3 P2 g' i7 S" O2 n
suspected in a follow-up visit after 4 months because
! H4 {$ o7 B1 A2 C; P5 s3 ?the physical examination revealed the complete disap-
/ ]. O# T6 \" Q) @pearance of pubic hair, normal growth velocity, and9 Y6 ]5 c' U) r" o9 R
decreased erections. The father admitted using a testos-
# Y+ h. A& W1 w. j* n5 C8 \% Tterone gel, which he concealed at first visit. He was; _9 k7 Q. k$ E4 T
using it rather frequently, twice a day. The Physicians’
1 r0 r: O' a3 h+ X6 y/ sDesk Reference, or package insert of this product, gel or
, l) T" D. I& h+ ?* gcream, cautions about dermal testosterone transfer to8 S- c7 z% s" o% t
unprotected females through direct skin exposure.
* w7 b+ b1 ?- o9 @+ r4 [Serum testosterone level was found to be 2 times the$ j$ \) L/ s# ~' n8 B5 e- t( p
baseline value in those females who were exposed to
+ }, U' i9 Y; N! A) h/ s+ ]: Seven 15 minutes of direct skin contact with their male
) W. X0 D/ ~/ y) \6 a6 Dpartners.6 However, when a shirt covered the applica-
& g  g1 x3 S$ O  z$ Otion site, this testosterone transfer was prevented.
- @. C0 w4 k: }& ^; }Our patient’s testosterone level was 60 ng/mL,
" l3 l0 x, A# x+ f# swhich was clearly high. Some studies suggest that
" I7 A% q  |/ S$ Jdermal conversion of testosterone to dihydrotestos-
  @6 R4 c! B7 h% r0 l5 b4 Nterone, which is a more potent metabolite, is more
0 d: T" J; y1 D' I2 ~active in young children exposed to testosterone
/ j+ G6 D1 M" b) _- Aexogenously7; however, we did not measure a dihy-5 t! ]( {$ B( r5 }: Y. l
drotestosterone level in our patient. In addition to
7 }( k8 G  f' e- zvirilization, exposure to exogenous testosterone in
- t& R* z& V9 B- Hchildren results in an increase in growth velocity and) F, g+ `# c# o2 q
advanced bone age, as seen in our patient./ a) n4 @) e4 Y, w" w7 v
The long-term effect of androgen exposure during
) x) m# d" ]$ n, d; c" bearly childhood on pubertal development and final
7 Z6 S  ]+ F4 F# F* {2 aadult height are not fully known and always remain4 A- f7 o: H9 \8 {1 Q! d% o
a concern. Children treated with short-term testos-
. @8 Y9 M6 X0 N/ m( w. T1 vterone injection or topical androgen may exhibit some
5 [/ c: {3 i0 y4 N' m0 Bacceleration of the skeletal maturation; however, after
# |$ q; v. R+ H: \; _cessation of treatment, the rate of bone maturation
4 p$ W. q6 g2 i6 v3 ~/ Odecelerates and gradually returns to normal.8,9: u# M, _5 M% w* S
There are conflicting reports and controversy% P% t, `# [& V5 W; V' c
over the effect of early androgen exposure on adult
# u/ s/ F' L& Y8 p+ L/ I  Vpenile length.10,11 Some reports suggest subnormal
0 V1 f* G9 J$ \$ P' ]adult penile length, apparently because of downreg-7 n1 M' B& o) e( z  [4 o" C
ulation of androgen receptor number.10,12 However,# a6 r7 {" A, e% `! @" @- y
Sutherland et al13 did not find a correlation between
- t& y* x# U4 z7 {2 A% N& i, kchildhood testosterone exposure and reduced adult
0 [# c) f' O5 l5 ~4 G/ Ipenile length in clinical studies.
& K6 B1 o: \6 q9 Y) ?! g$ I& fNonetheless, we do not believe our patient is( \; P: D% t, c3 Z
going to experience any of the untoward effects from& X! s, ?: g: X4 y% j. S3 K
testosterone exposure as mentioned earlier because' s' I. s/ O* O
the exposure was not for a prolonged period of time.0 w+ y9 k8 b0 K4 i
Although the bone age was advanced at the time of% b4 O: F6 B8 v% K' {
diagnosis, the child had a normal growth velocity at
' t# v( M7 B; S, k2 k+ hthe follow-up visit. It is hoped that his final adult+ _- F) L9 r; o3 C( t
height will not be affected.
" H/ _1 M* v: |2 MAlthough rarely reported, the widespread avail-
' B/ C: K2 X. k8 E( cability of androgen products in our society may* T* d* ]3 ~9 p+ T  d
indeed cause more virilization in male or female# t7 |5 O6 L+ v- I" n. o7 o
children than one would realize. Exposure to andro-& G4 S6 a, x; i2 E5 E" [
gen products must be considered and specific ques-! {* d7 w0 T( X6 b; P
tioning about the use of a testosterone product or
& c; [0 B/ I# [6 X4 ~- @gel should be asked of the family members during/ }, G4 [, z  N+ [) }, g
the evaluation of any children who present with vir-
9 V- M9 X0 W3 ]+ a7 b% L1 pilization or peripheral precocious puberty. The diag-: v  I" D5 ^" [  ^- e* ]* u
nosis can be established by just a few tests and by
; e0 d3 j% Z) Q1 i- H. aappropriate history. The inability to obtain such a
% k# ~3 h7 W  c5 Ehistory, or failure to ask the specific questions, may
- a( q4 x9 {5 T* Mresult in extensive, unnecessary, and expensive
+ L! r! u- j% R. ]investigation. The primary care physician should be8 r( `0 K* J7 T3 P
aware of this fact, because most of these children
" ^3 e, s1 [1 y: {4 u* T# n% ?may initially present in their practice. The Physicians’# j2 M# a( N4 K5 I/ {' U
Desk Reference and package insert should also put a" [: ?+ i: Y1 \: X
warning about the virilizing effect on a male or& I7 a; A2 ~" w
female child who might come in contact with some-7 V! L! r6 t: G4 k/ n) W1 ?1 ]
one using any of these products.' a# u; C* ~5 h8 |8 ~8 x
References
! D6 v- h- k1 V1. Styne DM. The testes: disorder of sexual differentiation: ~- d' H. B6 a  n8 _
and puberty in the male. In: Sperling MA, ed. Pediatric* o$ ]  q: Y$ ~! A' w4 E
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;) p+ w/ N. \# z6 j) J5 e; S' M
2002: 565-628.
8 |- U& |1 T* f) `" U5 j" s2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
$ j' b3 u% c1 ?% v3 U- Npuberty in children with tumours of the suprasellar pineal
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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!
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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
0 d% X, x# I) c& M0 T: X
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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