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鄉下的妹子太便宜,一次四個都要了[12P]

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Sexual Precocity in a 16-Month-Old
# Y& ]$ z5 W5 J3 l5 p2 ?Boy Induced by Indirect Topical
; J3 a0 a( k% d2 H/ hExposure to Testosterone
" X% K% S; C* bSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2  }) F, ?- f% ^$ K
and Kenneth R. Rettig, MD1! [: g8 W7 d% T: n6 A9 {7 ?4 d6 R
Clinical Pediatrics
& _8 ]  n+ a- tVolume 46 Number 6( Y0 l: g* M( _
July 2007 540-543
5 k1 T  T' y* E7 h( s9 K$ b© 2007 Sage Publications6 v5 {. t/ k6 M+ p
10.1177/0009922806296651
& f5 }+ k# I0 w6 G6 z% C/ d: whttp://clp.sagepub.com4 }+ x4 l5 ?/ S3 c9 m- X0 u
hosted at
' s4 P3 N& f' c+ W$ E: thttp://online.sagepub.com# E# q+ ^! K, V: Q8 \  j, B0 p
Precocious puberty in boys, central or peripheral,
+ m2 J7 z( o3 |$ F. e( gis a significant concern for physicians. Central7 k6 a* f4 e4 c: J7 v. ^. e
precocious puberty (CPP), which is mediated
- j5 I) y6 c1 d$ e- x3 jthrough the hypothalamic pituitary gonadal axis, has+ M  X: y1 b4 T4 V% D
a higher incidence of organic central nervous system
% c8 x+ X$ x4 K  g( L) k7 N4 Jlesions in boys.1,2 Virilization in boys, as manifested
4 _! }! B0 d; m- k, Sby enlargement of the penis, development of pubic
& r- ^  c) f. c7 O* {7 ^hair, and facial acne without enlargement of testi-4 x4 z$ W5 w  v/ T
cles, suggests peripheral or pseudopuberty.1-3 We. v$ o; l- |5 `0 W. V- K
report a 16-month-old boy who presented with the
6 M8 X/ w6 k4 j' @' zenlargement of the phallus and pubic hair develop-
6 i# p; J* V. p5 p/ hment without testicular enlargement, which was due, Z: x" T: }, I; v! [5 I
to the unintentional exposure to androgen gel used by
# ]7 J' u; l/ n4 {3 A) Wthe father. The family initially concealed this infor-% @$ R# ?0 f7 V
mation, resulting in an extensive work-up for this2 U, h+ W0 g% v* q
child. Given the widespread and easy availability of1 b7 p" F9 s2 \. @
testosterone gel and cream, we believe this is proba-9 p4 s% \8 u4 Y( C
bly more common than the rare case report in the% j5 @. O% m: V
literature.4
, l1 z' h7 y# rPatient Report8 L' j( _9 n1 s; Z% Q# I
A 16-month-old white child was referred to the8 g' A, c( P7 Y+ ?  j: w* R
endocrine clinic by his pediatrician with the concern
7 B" Q0 j, P: r. h  L! v0 ]of early sexual development. His mother noticed
6 z' y% f0 X! e7 `; {light colored pubic hair development when he was0 K$ Q* r3 t. v6 |: n
From the 1Division of Pediatric Endocrinology, 2University of% T9 Q3 y) h# ^  D& I
South Alabama Medical Center, Mobile, Alabama.
4 a) _% ^  h! s( L; c+ gAddress correspondence to: Samar K. Bhowmick, MD, FACE,7 }; f: x  A+ d  j2 r0 |# X
Professor of Pediatrics, University of South Alabama, College of
- f, b) l( m& _+ E5 Q, k) BMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
- j4 @+ c  O. }6 Me-mail: [email protected].+ ?  ]+ D& Y  L! @) l
about 6 to 7 months old, which progressively became! @2 G8 r% G% r. B- y
darker. She was also concerned about the enlarge-# T5 |) c9 q0 {$ O' k- L4 f
ment of his penis and frequent erections. The child1 c9 u! g# f' ^) @* q
was the product of a full-term normal delivery, with7 K: J# g! ^# k
a birth weight of 7 lb 14 oz, and birth length of
/ L9 Q3 T! E: }: ?; h20 inches. He was breast-fed throughout the first year
' l9 x6 S. t. [% ~of life and was still receiving breast milk along with
( d  r/ O5 m5 K5 T9 h# G" Qsolid food. He had no hospitalizations or surgery,( q1 P) `& Y; z6 b; _6 W/ D
and his psychosocial and psychomotor development$ g& G( b+ R* ?5 H5 @
was age appropriate.' Y) a8 D* q7 C0 P
The family history was remarkable for the father,
6 {0 k1 C; K  ~3 i9 O* L% n9 }; {$ s) xwho was diagnosed with hypothyroidism at age 16,
. h& \4 W% O1 Twhich was treated with thyroxine. The father’s
/ L' q6 @$ W# V. jheight was 6 feet, and he went through a somewhat# \1 T$ n- E! S5 m) e; t0 L
early puberty and had stopped growing by age 14.
: l" I4 s( j  z/ A. DThe father denied taking any other medication. The8 z- W! l( H) E" h- _% E/ {' F
child’s mother was in good health. Her menarche
7 t  L, X9 W" U7 w/ g7 Lwas at 11 years of age, and her height was at 5 feet6 ^& }& J& O! V5 T; A+ x! x2 c
5 inches. There was no other family history of pre-, Q5 _8 o" U/ C6 H% T
cocious sexual development in the first-degree rela-6 Y; U1 h& R; e% A7 x. j$ \
tives. There were no siblings.
# o( J) J! a) j, t1 i: kPhysical Examination1 k2 s4 G+ c  P0 s5 {
The physical examination revealed a very active,# w9 h. M) K9 C$ y$ t9 f
playful, and healthy boy. The vital signs documented
. s' g" S* ]; t8 r8 a1 J2 aa blood pressure of 85/50 mm Hg, his length was8 `& I  T7 K* S* X& o6 @  d7 c
90 cm (>97th percentile), and his weight was 14.4 kg& ~  q/ C+ @6 `/ }9 e, J
(also >97th percentile). The observed yearly growth* }# g/ l  @) P& N' U/ J
velocity was 30 cm (12 inches). The examination of5 w& Q2 Q+ d7 }
the neck revealed no thyroid enlargement.( ^. T" k0 _+ D! z' A
The genitourinary examination was remarkable for
" |1 @: N% ^$ L5 F0 s9 tenlargement of the penis, with a stretched length of
' x1 H( ?1 q! q/ v6 O: E8 cm and a width of 2 cm. The glans penis was very well
. b' f' y; s6 s6 C: vdeveloped. The pubic hair was Tanner II, mostly around( B3 z: ]& E+ S+ Q# f7 @
5400 K1 ^6 t1 {, o7 p, G
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ s7 p5 _/ `! k( `- Q; S6 Y
the base of the phallus and was dark and curled. The
: `( ~& L5 m0 [! y  k9 h: p/ jtesticular volume was prepubertal at 2 mL each.
% C8 \1 Q9 f. R* y1 F* pThe skin was moist and smooth and somewhat
$ v$ F  W6 R0 N4 O8 G  _oily. No axillary hair was noted. There were no6 P/ F0 f+ @$ y( o( `. ~
abnormal skin pigmentations or café-au-lait spots.5 |5 a+ S7 N5 l1 d6 u% g
Neurologic evaluation showed deep tendon reflex 2+' y$ \2 d' H4 A7 j9 G
bilateral and symmetrical. There was no suggestion
$ e9 R$ p) H/ v3 ^4 o, }9 Vof papilledema.% Z" t8 D  ^( x. Q" X7 R% G
Laboratory Evaluation
) V) f# @: \$ l+ R, W$ e4 SThe bone age was consistent with 28 months by
$ d# ?7 S( E$ W& O9 i" F2 Dusing the standard of Greulich and Pyle at a chrono-1 z! Q2 l. H& `
logic age of 16 months (advanced).5 Chromosomal" O  ^& e/ ]1 [' K' x4 Y! ^" \
karyotype was 46XY. The thyroid function test- d/ p. [" a/ U( X# B5 I* u
showed a free T4 of 1.69 ng/dL, and thyroid stimu-% N( R: x. k% o- Q' w+ n0 c& I
lating hormone level was 1.3 µIU/mL (both normal).
; L* [& ^, P7 ?; p3 CThe concentrations of serum electrolytes, blood8 u7 }6 _; O7 f0 D' {/ W
urea nitrogen, creatinine, and calcium all were
2 L) |& W- E( E0 @5 G" Z$ zwithin normal range for his age. The concentration+ j( \; H" q% y! k; m4 Q) ?
of serum 17-hydroxyprogesterone was 16 ng/dL
, }+ k0 o' N- a) y(normal, 3 to 90 ng/dL), androstenedione was 20
: r, R( S& C: |6 D2 m6 T& ~  A" {ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
# `1 w0 K0 s! r+ c! M  ^$ kterone was 38 ng/dL (normal, 50 to 760 ng/dL),9 a4 w4 @8 n# I& u
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
% D. `% Q0 }& g49ng/dL), 11-desoxycortisol (specific compound S)
8 l9 S7 g! i" ?; Ewas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-  n/ q) i2 g, |$ P
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total4 c# {1 h4 a2 q9 K. T
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
4 g5 ^- ?  w& _7 S& J. Sand β-human chorionic gonadotropin was less than# m4 ^- T# u6 m5 e" G1 T; v' |
5 mIU/mL (normal <5 mIU/mL). Serum follicular
  }) h& ^2 P9 b) \7 r1 t& `* estimulating hormone and leuteinizing hormone/ R) u# S) K, M( q2 j
concentrations were less than 0.05 mIU/mL$ y/ a0 @0 K9 c  `  z
(prepubertal).+ {; J2 l3 e  F) g
The parents were notified about the laboratory( v: G! ^& w: @
results and were informed that all of the tests were7 k2 _* Z$ Y! J' P! f
normal except the testosterone level was high. The
: y- z/ ~! q* V1 afollow-up visit was arranged within a few weeks to# r. \# e: m9 n/ p
obtain testicular and abdominal sonograms; how-
& X! V9 A/ X. @7 ^3 Vever, the family did not return for 4 months.0 m  u2 q7 ]% o& ^; f- L
Physical examination at this time revealed that the1 A, F1 _' U2 T4 i/ p4 C
child had grown 2.5 cm in 4 months and had gained3 S8 D. X3 o- q, @7 c
2 kg of weight. Physical examination remained; v5 j/ s3 n3 A2 o( N+ M
unchanged. Surprisingly, the pubic hair almost com-
5 w5 y0 H- B! Ppletely disappeared except for a few vellous hairs at
9 G9 _4 \4 J4 ]7 _2 ?the base of the phallus. Testicular volume was still 2
" J& ~: b- Z( L- O/ n+ G1 W  WmL, and the size of the penis remained unchanged.9 Z7 u: ]8 e% u' J: B- {
The mother also said that the boy was no longer hav-6 V, i6 R$ P8 x$ F# v8 [
ing frequent erections.
! q" y+ S& R' u1 r: N. w8 E, k0 \, R$ s+ qBoth parents were again questioned about use of7 g2 `8 `6 ^: I! \( ?
any ointment/creams that they may have applied to
3 O' E, F5 V) O# {$ Rthe child’s skin. This time the father admitted the
9 z3 E( y" z& N/ a9 y" {6 lTopical Testosterone Exposure / Bhowmick et al 541' i3 N4 ~! n. ^9 V+ r. h9 i
use of testosterone gel twice daily that he was apply-' ?- F1 }0 D, r0 s
ing over his own shoulders, chest, and back area for' Y) B9 G; ~: s( h
a year. The father also revealed he was embarrassed
# _* F; A4 {  S9 r: T* f% Zto disclose that he was using a testosterone gel pre-/ A1 a# ^* i0 J5 A8 A7 U
scribed by his family physician for decreased libido
+ z4 h  ?8 d' l7 M) n4 }secondary to depression.
! ~7 A% v/ @! v& K7 b0 }7 }The child slept in the same bed with parents.
# ^! D! t  j: ~# Q' H3 mThe father would hug the baby and hold him on his& @) O8 l" h7 I3 S2 B
chest for a considerable period of time, causing sig-3 Z' `) ^+ q6 e; {* I. s: D8 L5 R- a
nificant bare skin contact between baby and father.* w# H# K" P% c! N5 G
The father also admitted that after the phone call,' O- a( ?* U; U( J( n2 f' n1 O3 @
when he learned the testosterone level in the baby# Y) w8 t2 b) A# j: I6 d
was high, he then read the product information. {7 C) T& f& D" p$ J/ K
packet and concluded that it was most likely the rea-; A; c  l& z0 m$ c; e" n9 X
son for the child’s virilization. At that time, they  ?0 S" E7 u7 P) p
decided to put the baby in a separate bed, and the/ b% x9 m: }3 ~# z, _$ g, g
father was not hugging him with bare skin and had3 V. G- k, D/ W% t$ s7 z' g. U
been using protective clothing. A repeat testosterone
6 |# ]/ z7 Y# M1 E: v: |9 `test was ordered, but the family did not go to the
* e, `' h' O2 K# G6 E0 ?8 Wlaboratory to obtain the test.1 F4 n3 b3 w) B4 I
Discussion
  X' ^+ R8 r+ G7 H8 r* \Precocious puberty in boys is defined as secondary
# T. P' S1 f6 K5 M) c7 E; Jsexual development before 9 years of age.1,4, V" N  C- r: c* @8 b
Precocious puberty is termed as central (true) when3 X. e. z7 V3 s9 K+ ~
it is caused by the premature activation of hypo-
# A7 U1 S! d4 c8 d9 ]thalamic pituitary gonadal axis. CPP is more com-. u% F9 q- c, G- r
mon in girls than in boys.1,3 Most boys with CPP
9 q- T9 O- X% ~* i+ \may have a central nervous system lesion that is
# y( \0 d# Y" `9 k+ tresponsible for the early activation of the hypothal-3 [: \" J. ~0 f0 c; @
amic pituitary gonadal axis.1-3 Thus, greater empha-
7 p4 l% y: g+ V! r' ?- M  ~/ ~sis has been given to neuroradiologic imaging in
3 h* t/ F, q8 u1 vboys with precocious puberty. In addition to viril-: B- d% O/ X5 b  H
ization, the clinical hallmark of CPP is the symmet-3 Z7 K1 W; N8 g; O/ e8 J
rical testicular growth secondary to stimulation by5 v$ h  f; U3 M: Q5 O
gonadotropins.1,3% D# ^/ \# u4 ?; Q/ b7 u
Gonadotropin-independent peripheral preco-9 n1 k5 [2 ~- T2 k/ O) u
cious puberty in boys also results from inappropriate3 \1 b5 W  K- G4 a- |7 {& W& P
androgenic stimulation from either endogenous or' s0 Z1 F% o  q  m( z! i/ r
exogenous sources, nonpituitary gonadotropin stim-' D5 [8 g4 t: S4 t3 n0 i+ S
ulation, and rare activating mutations.3 Virilizing* g* c8 b! ?; G4 v* W
congenital adrenal hyperplasia producing excessive
* f6 F* C6 h  o: |( s, P) m  k' iadrenal androgens is a common cause of precocious
* H# }2 o% l! Zpuberty in boys.3,47 d2 U; @4 c* a2 X- d) X" R3 i! T
The most common form of congenital adrenal
5 C0 S- a, H; b, N' ^$ W3 shyperplasia is the 21-hydroxylase enzyme deficiency.  V9 a2 T; A* j
The 11-β hydroxylase deficiency may also result in
& ]# t* q2 Z5 uexcessive adrenal androgen production, and rarely,; N; z, v, o; F& b0 o  s: h
an adrenal tumor may also cause adrenal androgen
* |' `! w4 d) X( gexcess.1,3; w6 S' b& w- i- J2 G% E0 O
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% f. L; M" X' [( o: M' X: K. |
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
( K- P* Q3 s; z6 }2 sA unique entity of male-limited gonadotropin-; j, X% b/ R- @& y0 R) t
independent precocious puberty, which is also known* V8 `$ q/ q8 S$ R
as testotoxicosis, may cause precocious puberty at a* C2 @, M0 c6 u* `! S
very young age. The physical findings in these boys1 t# l$ i$ C, ^1 i
with this disorder are full pubertal development," _3 ^+ H! \& b( W+ F+ W% T7 {
including bilateral testicular growth, similar to boys
+ g: U, f7 q  |. r% d0 iwith CPP. The gonadotropin levels in this disorder5 x* G) K$ \# u) I, V6 q5 A6 t
are suppressed to prepubertal levels and do not show/ I, \: G9 `* N, J1 Q
pubertal response of gonadotropin after gonadotropin-
6 }" k% H. C8 w" Wreleasing hormone stimulation. This is a sex-linked
- D$ \: U& i/ X3 a' Kautosomal dominant disorder that affects only
2 b: B7 _5 J5 S& v% Hmales; therefore, other male members of the family5 ~% o- l# |1 L" i) O9 H  R
may have similar precocious puberty.3. R4 r9 H+ |' @! Q7 o
In our patient, physical examination was incon-, E5 E- e* w( p  Q
sistent with true precocious puberty since his testi-7 g$ l" j3 ~4 v+ G$ J6 G+ p# G
cles were prepubertal in size. However, testotoxicosis4 x5 x/ H- i( y1 P3 A) I
was in the differential diagnosis because his father7 _5 l5 Z" {) ~0 Q- T4 _9 m
started puberty somewhat early, and occasionally,, q: k" b$ R) O$ d+ b
testicular enlargement is not that evident in the- j7 Q2 k5 w+ v6 V
beginning of this process.1 In the absence of a neg-
, D& @- ~2 U5 X9 {# T0 l8 q# }ative initial history of androgen exposure, our) w9 ]. ~) Z: W
biggest concern was virilizing adrenal hyperplasia,8 {5 M; O/ I/ }% p6 q. s7 ~
either 21-hydroxylase deficiency or 11-β hydroxylase' S- g0 s3 o  b$ t6 T& `
deficiency. Those diagnoses were excluded by find-
4 [/ m  y& G, v2 y( ling the normal level of adrenal steroids., J* w! q8 G9 ]  f/ R
The diagnosis of exogenous androgens was strongly" e8 s9 d+ \3 }( |5 b
suspected in a follow-up visit after 4 months because- y, d+ N, g7 l
the physical examination revealed the complete disap-  F" J# G! ~$ C$ g& s# F
pearance of pubic hair, normal growth velocity, and
2 r1 e4 w7 ?5 a9 ^8 odecreased erections. The father admitted using a testos-, ^8 D( C% g# q2 p( r( C
terone gel, which he concealed at first visit. He was( ]3 W9 R5 W  T: y
using it rather frequently, twice a day. The Physicians’
0 \1 w* b+ A# h/ y, q% RDesk Reference, or package insert of this product, gel or8 K$ ]% H$ l) }, G  A
cream, cautions about dermal testosterone transfer to
' h4 h$ h' v& D% N' ?/ o  s, funprotected females through direct skin exposure.1 n6 Y( T/ q* i* X3 X& \
Serum testosterone level was found to be 2 times the$ t- g% L* f9 H+ S+ G
baseline value in those females who were exposed to
$ g7 R, U1 A- i# `even 15 minutes of direct skin contact with their male3 \0 y& h+ p8 |4 @+ h2 J1 Y
partners.6 However, when a shirt covered the applica-, X8 V1 }; _$ c" l$ h
tion site, this testosterone transfer was prevented.) S/ v% Q7 i( @  b& P# V9 Z
Our patient’s testosterone level was 60 ng/mL,
) b) R8 N& Y4 m; wwhich was clearly high. Some studies suggest that
0 n/ R1 l' S7 u1 B. T3 U  R& i1 @dermal conversion of testosterone to dihydrotestos-
' A% d: |/ M& |* @$ H4 E$ Nterone, which is a more potent metabolite, is more
/ D' }6 Y5 ~: m& E) o/ |active in young children exposed to testosterone
1 l) i" k$ p+ U7 r" C) jexogenously7; however, we did not measure a dihy-
6 b1 s: c8 j" g4 K9 S/ Gdrotestosterone level in our patient. In addition to
& f, t: o: Y5 x9 K$ @8 I: Tvirilization, exposure to exogenous testosterone in6 f, W' Z& r3 e% J8 u0 l
children results in an increase in growth velocity and3 d' d! q) j( K$ ~4 `" c4 a1 B/ e; \
advanced bone age, as seen in our patient.
; h4 j: ?+ }* K+ Z7 wThe long-term effect of androgen exposure during% B3 {0 b5 g. k- u: W) P& l) f! c& g
early childhood on pubertal development and final
8 ?2 e8 K4 F7 r2 }; Y7 y, M% padult height are not fully known and always remain: ]8 U0 S  T, Z9 R6 F  A
a concern. Children treated with short-term testos-
! t) I) Z4 F6 A$ ?) P6 ~! N7 hterone injection or topical androgen may exhibit some4 T2 d5 d' ~& |- R6 {- e( Z/ V
acceleration of the skeletal maturation; however, after
6 I# X0 S2 {# E- zcessation of treatment, the rate of bone maturation
6 @! a& H  P. Idecelerates and gradually returns to normal.8,9
# ~( z* _/ D7 B1 o7 `6 p& E$ tThere are conflicting reports and controversy; Q9 w# Z: z$ O5 n5 v
over the effect of early androgen exposure on adult; o; ^. d: m1 Y+ [; s; d$ s( M
penile length.10,11 Some reports suggest subnormal
! a4 A* R+ \! @2 C+ oadult penile length, apparently because of downreg-
$ _5 s8 x8 h; gulation of androgen receptor number.10,12 However,
8 P$ N' {7 S* ]$ m0 @2 `. `Sutherland et al13 did not find a correlation between
( d: A4 ]0 X1 y* ichildhood testosterone exposure and reduced adult
2 |- j7 F8 ?, p( Z; R. U$ h( Dpenile length in clinical studies.
; B) ^' {; F5 F% x/ wNonetheless, we do not believe our patient is
- i4 |" |2 F5 ggoing to experience any of the untoward effects from
0 i. p1 B2 {& {4 J, ]2 xtestosterone exposure as mentioned earlier because1 S' N) ?5 l0 v2 }" t
the exposure was not for a prolonged period of time.
* V* P, D/ f2 ]( K' d  uAlthough the bone age was advanced at the time of" D0 E' [% C/ c! J9 I9 \: g0 h
diagnosis, the child had a normal growth velocity at% t: c: v, D3 h) }2 `
the follow-up visit. It is hoped that his final adult. S; z( d* E. f* F, _% ~( u
height will not be affected.
! C8 }4 X. r) D( u! T2 W, yAlthough rarely reported, the widespread avail-1 o. x* O/ `: E
ability of androgen products in our society may
$ B' H- f5 J8 L, _9 I, J# g! Rindeed cause more virilization in male or female
" e- P" Q# w5 i$ cchildren than one would realize. Exposure to andro-
8 s$ }9 B3 h: r# }* }5 V6 agen products must be considered and specific ques-9 T9 s3 J" N+ B( `& U, K, h
tioning about the use of a testosterone product or
- ~& S- |9 w. {gel should be asked of the family members during2 Q- h  }! Q* s, t0 w7 T- L( c; g" M
the evaluation of any children who present with vir-
) G5 }9 f3 c7 P0 ]ilization or peripheral precocious puberty. The diag-8 e* `6 f/ b$ s
nosis can be established by just a few tests and by0 ]' g+ s, H  x" d0 ^
appropriate history. The inability to obtain such a
; R" _5 \; o. jhistory, or failure to ask the specific questions, may; n' Y, O! j& Y# b  T
result in extensive, unnecessary, and expensive
$ o4 Y; |% `6 V* l6 ^# c( tinvestigation. The primary care physician should be1 M7 q7 S# _, c
aware of this fact, because most of these children) z5 q4 {8 R& O
may initially present in their practice. The Physicians’
. R4 {. u$ `5 }4 X% Q$ M. RDesk Reference and package insert should also put a
0 r4 f- S7 Y% v# \warning about the virilizing effect on a male or
3 \- b* O- {* U6 l) Ffemale child who might come in contact with some-4 o# M$ p( A# r
one using any of these products.
% P. g) [- K+ N9 S2 [0 AReferences
1 V% `6 o" T) K- x, x2 s$ n6 F1. Styne DM. The testes: disorder of sexual differentiation
: M, x4 X5 j* uand puberty in the male. In: Sperling MA, ed. Pediatric
5 l6 Y# t' M8 g# W9 oEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
# U; L4 |" ?4 N; Q& @( o2002: 565-628.. d* R+ D9 }4 }  H  H
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; U& T+ J* k. `! ?
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old4 [% z+ W8 d9 n" a0 p& C
Boy Induced by Indirect Topical/ T, j+ x% g% _- F9 C
Exposure to Testosterone. k- @: V1 U! }) A
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,27 f) {2 S3 S6 Q  y5 e2 T
and Kenneth R. Rettig, MD1
& I" P" r; U2 U9 W4 P/ PClinical Pediatrics, W: `  z5 h8 t0 {" J/ q# q+ \
Volume 46 Number 6! u; Y/ }$ M  s3 L3 k. v- w
July 2007 540-543
- V; v' F3 S( h  j% F/ G© 2007 Sage Publications
* a0 Y  E# z  A1 y! X8 T10.1177/0009922806296651
5 t! j2 p' @+ a, d1 n6 Khttp://clp.sagepub.com* B2 I8 k0 F+ u* O1 ?: M$ u; o
hosted at
9 P" W9 V# @8 Lhttp://online.sagepub.com
" e8 J4 W( n3 ?$ k2 e( K, `$ fPrecocious puberty in boys, central or peripheral,5 s% B) Q& H& j+ l5 a
is a significant concern for physicians. Central* y2 T! V; W) X4 r$ S
precocious puberty (CPP), which is mediated/ w5 h5 u/ j' ?) A. n  `. I
through the hypothalamic pituitary gonadal axis, has
. {) o. I. i5 k* }. C: \a higher incidence of organic central nervous system$ ?- s' q, J' \7 k7 X0 C; a
lesions in boys.1,2 Virilization in boys, as manifested# W6 ~$ k4 ^' F+ o1 c7 W4 z2 V$ F9 @
by enlargement of the penis, development of pubic
5 w. S. |$ [% a  s: `/ _6 z* n- `hair, and facial acne without enlargement of testi-* u5 ?: G- F) |3 ^
cles, suggests peripheral or pseudopuberty.1-3 We, k# S6 P' {& q; S; o( j
report a 16-month-old boy who presented with the
- N$ J: @$ K1 U( ^4 `6 t. renlargement of the phallus and pubic hair develop-
' P( Y% F- v5 e4 mment without testicular enlargement, which was due
5 D6 R$ M) D2 K4 f  K& ato the unintentional exposure to androgen gel used by
$ X' X) Q3 H% H( |" W  i5 Cthe father. The family initially concealed this infor-
2 Q) f: V, F  a) ?1 k. `) o/ Smation, resulting in an extensive work-up for this
# `+ |% G* S- X, D$ C, l9 T! \child. Given the widespread and easy availability of+ g+ @* M* d1 V; D
testosterone gel and cream, we believe this is proba-
( b4 ~3 z: r2 X+ g) S% S! Z6 Jbly more common than the rare case report in the9 ^  W1 b4 i, k. c7 g- U
literature.4/ _% X* Y0 P) l5 q, K" t
Patient Report
- o5 g) L) W0 m# q$ \+ l& j" z. bA 16-month-old white child was referred to the
2 O* Z# J, N. _8 _( d1 Wendocrine clinic by his pediatrician with the concern
$ F+ c5 |: V  ?. }8 ^8 n3 yof early sexual development. His mother noticed3 @4 i& M& R; L; ?! U6 g7 I; Q
light colored pubic hair development when he was+ s' V. P" u) d9 Y
From the 1Division of Pediatric Endocrinology, 2University of
+ x" w/ I4 V7 Y6 `' ^8 m, p2 |South Alabama Medical Center, Mobile, Alabama.! n; [. P3 u: o1 E# A
Address correspondence to: Samar K. Bhowmick, MD, FACE,
7 u, ~7 `) Z+ Z2 h1 hProfessor of Pediatrics, University of South Alabama, College of
9 v' ^' c1 D* ^7 OMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;& e4 |5 f# o, x* E  E
e-mail: [email protected].6 T/ \: }( F0 c, H4 v% V* }. T+ V
about 6 to 7 months old, which progressively became
7 r+ F, {7 l/ l# ~. Odarker. She was also concerned about the enlarge-
* ~1 d/ U" F+ C. M" S7 g5 g# B, }ment of his penis and frequent erections. The child- C- g( L" N0 I7 T& d+ U# u- X
was the product of a full-term normal delivery, with
1 M5 w: j. B# s+ s" g" Ra birth weight of 7 lb 14 oz, and birth length of9 O( p# g& f% x6 _% a" P( i
20 inches. He was breast-fed throughout the first year
+ m# U3 `+ v' H  l! `7 lof life and was still receiving breast milk along with
" p& C( L* R2 Psolid food. He had no hospitalizations or surgery,) y1 y6 D  P- R
and his psychosocial and psychomotor development
8 o3 c% T3 s$ X% s4 nwas age appropriate.
7 X" m  o8 i% ]2 g1 ]' _+ yThe family history was remarkable for the father,6 B* c- q# t) o% x# p1 W
who was diagnosed with hypothyroidism at age 16," ]( ?0 d7 s4 @8 y( B
which was treated with thyroxine. The father’s
4 a( p: }2 I* Mheight was 6 feet, and he went through a somewhat
( Z8 O7 p" q( x0 o. iearly puberty and had stopped growing by age 14.
$ T5 _2 I1 i3 f' v- l' X& [The father denied taking any other medication. The
+ V0 b2 `3 e! |: V* Q: Vchild’s mother was in good health. Her menarche  E, R5 [: a+ n$ `8 ^
was at 11 years of age, and her height was at 5 feet
7 C% \1 }- s6 o7 l' I$ a% R5 inches. There was no other family history of pre-6 e/ \( G0 A: C3 T4 a# Q, o' I
cocious sexual development in the first-degree rela-
: J5 H' O; L: [/ P) Atives. There were no siblings.
! Z3 U0 _; E8 o& m# F" \Physical Examination( z5 Y8 ?) |8 q6 g' m9 l9 @
The physical examination revealed a very active,
. U, _. z" |  _- }7 ?  m' h2 R2 }playful, and healthy boy. The vital signs documented0 m! `6 z2 a8 D- M$ z+ a$ g
a blood pressure of 85/50 mm Hg, his length was
4 F; y* x8 d5 x! Y8 R9 l90 cm (>97th percentile), and his weight was 14.4 kg. r' q. n% m& v* g7 r% O
(also >97th percentile). The observed yearly growth
+ \2 K% U# O! zvelocity was 30 cm (12 inches). The examination of8 s, H+ o. z1 G+ S3 o4 A) y
the neck revealed no thyroid enlargement.; ~0 l; t7 D+ v
The genitourinary examination was remarkable for
1 A1 y( q9 f; W: }/ e! |enlargement of the penis, with a stretched length of
$ ]8 T3 J4 Z0 }/ N/ q  v8 cm and a width of 2 cm. The glans penis was very well: |# D. @, W  ]% Z
developed. The pubic hair was Tanner II, mostly around% {( \2 X6 b+ D/ ^
540
+ }4 H7 {4 a8 _; b* L& ]! oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- |* l4 J# v1 c# ?9 \  b+ Gthe base of the phallus and was dark and curled. The
: \- ?* C- A8 R5 Xtesticular volume was prepubertal at 2 mL each., E" h5 f, b7 x# |  \5 T# n# U7 k4 e( C
The skin was moist and smooth and somewhat, p! z  r: _; c/ {
oily. No axillary hair was noted. There were no) A. Y1 g" L% K! i; M/ ~: L% \
abnormal skin pigmentations or café-au-lait spots.
% I; Y& {* E: D; nNeurologic evaluation showed deep tendon reflex 2+7 N: E, \9 U: P% A" T3 g7 Z" C1 z0 ^& C; s
bilateral and symmetrical. There was no suggestion
( ^2 y# I8 c4 Z) jof papilledema.
, z: x7 a0 f" s* m' |Laboratory Evaluation. k9 F( t4 \7 l* \
The bone age was consistent with 28 months by/ ?2 @' x$ {' F. o
using the standard of Greulich and Pyle at a chrono-
8 h- H" K  e  x, Flogic age of 16 months (advanced).5 Chromosomal
% Z, Z# Y! `% i/ {karyotype was 46XY. The thyroid function test$ H6 o* m- D. c8 m4 A
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
- D9 c/ |, r, @lating hormone level was 1.3 µIU/mL (both normal).; G# {8 J: p# Z" t' d7 A% |
The concentrations of serum electrolytes, blood) m& g) Q/ b7 |0 i: z' |- b
urea nitrogen, creatinine, and calcium all were/ i8 U: L% [: S% ?3 V  p
within normal range for his age. The concentration
% D$ w5 |9 \. C& eof serum 17-hydroxyprogesterone was 16 ng/dL
- a) E2 }& r" j" z& _4 o% d9 d4 X(normal, 3 to 90 ng/dL), androstenedione was 20: L0 A  x# b; i
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
- G0 {* l4 ]* I0 n9 R5 Z/ V8 Oterone was 38 ng/dL (normal, 50 to 760 ng/dL),+ g; U- W8 ~: D* [* u
desoxycorticosterone was 4.3 ng/dL (normal, 7 to9 p5 w: r, L4 e5 l/ n# |
49ng/dL), 11-desoxycortisol (specific compound S)
# {3 o' R) _" Rwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
+ x' g4 N& p- W7 O4 o1 b* ]6 ptisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
+ a5 P# m% Q! o+ Dtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),, l+ a: D" i1 i0 R
and β-human chorionic gonadotropin was less than
6 A& A( K1 f( j4 W1 B/ S5 mIU/mL (normal <5 mIU/mL). Serum follicular" m# m7 j& ^$ c  ~2 U  Z' ~! y
stimulating hormone and leuteinizing hormone
& K' M8 u( F2 e* _# z; f0 R1 R9 c1 {concentrations were less than 0.05 mIU/mL
3 U% w/ g$ L8 q(prepubertal).
' W  L$ @# ?3 R4 oThe parents were notified about the laboratory
' ~/ k5 I0 c; J: kresults and were informed that all of the tests were# N6 N) T- ^# t3 X2 M* t
normal except the testosterone level was high. The  u4 A% L! _8 ~  N4 ]# l+ Y
follow-up visit was arranged within a few weeks to
% U& I! ~' q/ W/ Zobtain testicular and abdominal sonograms; how-3 ]2 S$ V5 V& n, m$ f5 G# `( r
ever, the family did not return for 4 months.. F9 @3 i, _6 F0 q/ j9 _! v" ^2 L
Physical examination at this time revealed that the: [8 o8 `' m# S/ d" o$ n* i. U# s
child had grown 2.5 cm in 4 months and had gained
' w- }& o  r0 z  t( ?/ Z* r; O2 kg of weight. Physical examination remained
6 \' e" h* ^: \  [unchanged. Surprisingly, the pubic hair almost com-* `( d/ {5 b, [9 E( B2 k
pletely disappeared except for a few vellous hairs at7 q/ s9 ?/ V# X( }, v+ J" o
the base of the phallus. Testicular volume was still 2$ u* V, W! A5 i& A2 W
mL, and the size of the penis remained unchanged.
& k; S9 p% {/ w: U  sThe mother also said that the boy was no longer hav-' N! L3 f# v: ^1 ?2 _6 k6 }
ing frequent erections.
" Z' c* q# f! V- c4 n$ a, s; GBoth parents were again questioned about use of
- Q0 S( p# t+ v. B" g8 Kany ointment/creams that they may have applied to6 j+ v3 C  c- h! n' k
the child’s skin. This time the father admitted the% b! K" u8 p& s0 |. y0 T
Topical Testosterone Exposure / Bhowmick et al 5416 ?  o- C/ D% j8 K% a# D% x2 e
use of testosterone gel twice daily that he was apply-
- E" ~7 G8 @  D- S) jing over his own shoulders, chest, and back area for0 m% j8 y; b2 e! h
a year. The father also revealed he was embarrassed
2 G0 ]% }. C; x* ^' L/ Cto disclose that he was using a testosterone gel pre-9 |/ [) R. g' N' a" I: Q
scribed by his family physician for decreased libido
4 L4 i( ~* s; h% a4 r0 csecondary to depression.
8 ?: v* I6 s3 v: b' LThe child slept in the same bed with parents.
; K3 O% o% A) p  ^* f, L2 _+ r& ~; jThe father would hug the baby and hold him on his
3 {; T+ Q! n$ F4 a5 t( g0 Q" `' k: Dchest for a considerable period of time, causing sig-* B1 f6 J% O- A
nificant bare skin contact between baby and father.3 }  T8 S* r2 m2 i$ W
The father also admitted that after the phone call,+ e& y. s4 o7 k: A9 E
when he learned the testosterone level in the baby6 i% Q" O' n3 u! `! ?
was high, he then read the product information9 Q1 w2 G( J& T/ I
packet and concluded that it was most likely the rea-0 {) R+ s9 C* i9 T: G4 U% m4 w
son for the child’s virilization. At that time, they2 [( A& p: K1 L
decided to put the baby in a separate bed, and the
7 @6 @* B7 A$ D. ]father was not hugging him with bare skin and had
6 |. W# c3 o; [9 x; Y( @been using protective clothing. A repeat testosterone3 ?0 p. `) w# G; B7 f/ |! F8 w
test was ordered, but the family did not go to the5 l; a* E% e. ?, X
laboratory to obtain the test.6 t1 U9 A7 E1 o; ]: R+ m8 R
Discussion
; Z; s% r6 |3 w2 b/ ePrecocious puberty in boys is defined as secondary
# L6 u# z) |& u" L& E+ Xsexual development before 9 years of age.1,4- X1 |6 S7 r! ]# S2 ~3 W: m+ L- n
Precocious puberty is termed as central (true) when
$ ~* r- N+ z/ o4 o$ p# e3 Yit is caused by the premature activation of hypo-
2 ?# u7 {7 j) y: R2 Y  ]8 f" M6 |9 bthalamic pituitary gonadal axis. CPP is more com-
: `9 }. M3 ?, dmon in girls than in boys.1,3 Most boys with CPP
  F& E$ k, v* |, ~2 J! \5 y! Omay have a central nervous system lesion that is
* V* i% Z2 Q' }7 fresponsible for the early activation of the hypothal-
7 h+ P; c# \; ?& {1 x9 Y# |. bamic pituitary gonadal axis.1-3 Thus, greater empha-2 C0 }6 c0 D% c! j, ^% A/ A- ~
sis has been given to neuroradiologic imaging in
) Q# s2 a& ~8 }5 w; Cboys with precocious puberty. In addition to viril-* e- f$ p9 j6 D. _! `: P& f  X" f% H
ization, the clinical hallmark of CPP is the symmet-, q( o& _) r, Z7 F) r
rical testicular growth secondary to stimulation by
6 B( H' B$ J/ X8 T# {% W+ Cgonadotropins.1,39 d2 Y/ [1 B$ e. o8 ^7 F: ^4 n
Gonadotropin-independent peripheral preco-; l# N5 k# d9 j" c( W/ W6 x
cious puberty in boys also results from inappropriate
% F8 O& X! |8 T+ Q. }) Bandrogenic stimulation from either endogenous or
9 z& z# F9 L5 f0 J! `* Uexogenous sources, nonpituitary gonadotropin stim-
$ i+ c9 Y# N1 a% L  B* D1 }# tulation, and rare activating mutations.3 Virilizing4 P  h; @- {9 U; g8 @$ ]7 J
congenital adrenal hyperplasia producing excessive' [! k2 c5 T( J" G
adrenal androgens is a common cause of precocious9 K6 p! ^* Z/ {% S) W4 Y
puberty in boys.3,4
% w' R6 I& P6 D5 YThe most common form of congenital adrenal; }, p3 C% R6 l% b+ H' ^
hyperplasia is the 21-hydroxylase enzyme deficiency.
/ J7 U  S8 h" Q" |2 h( CThe 11-β hydroxylase deficiency may also result in
, Q% y5 ]% a* h" |3 q5 K6 iexcessive adrenal androgen production, and rarely,4 Z( m1 E  F- y, ~! h! V5 O) {
an adrenal tumor may also cause adrenal androgen! e% R5 k0 w0 G) W, \, d/ T
excess.1,3
1 n: a+ V* L3 h1 f, C; Fat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- Q' |4 P: [" E1 \8 F# ]542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
( C1 f/ ?0 e( E3 n+ s7 S+ h9 ?A unique entity of male-limited gonadotropin-
1 J4 i3 K* j1 n* k$ M. Lindependent precocious puberty, which is also known( Q# r% l! Y6 Y! {
as testotoxicosis, may cause precocious puberty at a
* _" l7 w% ~& f: _! ivery young age. The physical findings in these boys, T- o9 ]' M8 v
with this disorder are full pubertal development,
0 A  \4 O3 h- [4 N& lincluding bilateral testicular growth, similar to boys* [9 N. ?* R0 E: E, W$ e4 x1 Y
with CPP. The gonadotropin levels in this disorder. p0 o! G* N9 P7 d
are suppressed to prepubertal levels and do not show
* y; _1 _* w1 ]( f0 N. N/ n$ }pubertal response of gonadotropin after gonadotropin-
3 o3 M% q3 k  I9 x% B* {releasing hormone stimulation. This is a sex-linked
- x6 S) g* k2 D  g2 x# Sautosomal dominant disorder that affects only
# ?+ H) i" l# P1 J9 z+ s$ jmales; therefore, other male members of the family# \( h9 B1 o1 B* E2 V% f' ^" n
may have similar precocious puberty.3
8 m% f3 C# w. A1 u1 ?3 Y7 AIn our patient, physical examination was incon-
: K' u: f8 Y6 e4 U: B( y% bsistent with true precocious puberty since his testi-; t* J9 y8 q$ k: @8 s) [6 @
cles were prepubertal in size. However, testotoxicosis* w$ ^; \9 x% f7 W1 S+ [
was in the differential diagnosis because his father
+ i9 T9 b, }; n, gstarted puberty somewhat early, and occasionally,
" Y, S2 J1 q, D- ztesticular enlargement is not that evident in the3 U3 ^# A* C6 w) S2 o5 w8 o
beginning of this process.1 In the absence of a neg-
) `, X; t' u# Z, C% N# p" J0 Oative initial history of androgen exposure, our+ t0 x0 |- c. L- T" h
biggest concern was virilizing adrenal hyperplasia,
, ^. G; {! k  D, A7 @either 21-hydroxylase deficiency or 11-β hydroxylase
3 M1 q3 p6 s& ~- P% z4 Vdeficiency. Those diagnoses were excluded by find-) D6 Q* \2 [% A2 T7 R
ing the normal level of adrenal steroids.
+ v, d2 Q$ `, [% y1 UThe diagnosis of exogenous androgens was strongly' a1 _( |1 q5 g' n* v0 N
suspected in a follow-up visit after 4 months because' P4 }" q5 o/ R8 o' }: @
the physical examination revealed the complete disap-
3 F' l  l$ ~5 A4 |0 Ypearance of pubic hair, normal growth velocity, and
+ E  X$ U6 I, B1 w5 _decreased erections. The father admitted using a testos-! p  e5 n; l6 g# I4 j/ G
terone gel, which he concealed at first visit. He was
4 {% `/ u. O" F) z9 u8 R& susing it rather frequently, twice a day. The Physicians’! b9 F: r) m8 i5 X4 J  h
Desk Reference, or package insert of this product, gel or4 }1 Q4 {& _3 z
cream, cautions about dermal testosterone transfer to
) P6 y: s# V( s1 D- ~7 funprotected females through direct skin exposure.
- f" a! i! x& ^! \Serum testosterone level was found to be 2 times the( y7 e& f0 e7 p7 X$ i0 l
baseline value in those females who were exposed to8 T. _+ u! {4 C9 _  a
even 15 minutes of direct skin contact with their male% I1 z  u+ ?: _
partners.6 However, when a shirt covered the applica-4 @& Y$ D! }8 c- Z* [7 b
tion site, this testosterone transfer was prevented.
1 M7 d1 O7 l5 NOur patient’s testosterone level was 60 ng/mL,
* @" U, |; P# o1 u) pwhich was clearly high. Some studies suggest that5 T& P  P( Q" k% K" Q# N
dermal conversion of testosterone to dihydrotestos-
" _8 k# J' E8 W: \9 Fterone, which is a more potent metabolite, is more
9 j0 Z) X) c+ C4 Uactive in young children exposed to testosterone
( p* }5 }7 S" ^4 B7 q% t- sexogenously7; however, we did not measure a dihy-
3 i. p$ K( p% {0 Zdrotestosterone level in our patient. In addition to  S2 Z) }+ Y0 r7 C6 N% S
virilization, exposure to exogenous testosterone in% d) ^, M' q  g: g
children results in an increase in growth velocity and0 Y  x( n# a2 K* R: p0 ]# r
advanced bone age, as seen in our patient.! _7 z' g( P9 T6 H) g  U
The long-term effect of androgen exposure during+ a. W2 y0 \9 n
early childhood on pubertal development and final0 U* y$ {) G# q
adult height are not fully known and always remain, \0 l) M) q) C9 o
a concern. Children treated with short-term testos-4 }& }" u7 O; t( h$ p
terone injection or topical androgen may exhibit some$ V: H# b2 L" j2 y; O4 h
acceleration of the skeletal maturation; however, after
/ _. Y/ j5 {" O* F% x- B- jcessation of treatment, the rate of bone maturation
8 {! A2 _" ]/ t+ @$ M4 vdecelerates and gradually returns to normal.8,9
  t& A! ^- D3 w$ U- HThere are conflicting reports and controversy1 }, w; O2 s' g1 Y% M
over the effect of early androgen exposure on adult
6 L; j9 V6 X- s, i0 @penile length.10,11 Some reports suggest subnormal" J. D5 p7 `" @
adult penile length, apparently because of downreg-
+ \. {4 e; Z( W$ T; o- }/ C& O" pulation of androgen receptor number.10,12 However,
' `" ?" L  G# c8 ~2 I. ESutherland et al13 did not find a correlation between
' f& p1 V1 N( ]9 Q9 @+ ?( H; `childhood testosterone exposure and reduced adult
2 d- d3 W2 n! X/ _penile length in clinical studies.0 Z& M/ C( y) z. e; u1 m
Nonetheless, we do not believe our patient is
& g) e: {1 D; T( H2 Tgoing to experience any of the untoward effects from' s3 N' U5 A9 \$ N
testosterone exposure as mentioned earlier because
+ @& s* ?. R: e  S2 t) qthe exposure was not for a prolonged period of time.
6 n' c& c8 x* Y- A9 ^Although the bone age was advanced at the time of6 }* O1 G- y- h) v2 _
diagnosis, the child had a normal growth velocity at+ J$ k' {) S& Z2 L* V0 D
the follow-up visit. It is hoped that his final adult8 c; F1 T& O0 c# e  Y3 L0 G
height will not be affected.
9 W+ s8 }# }9 DAlthough rarely reported, the widespread avail-% Y3 l$ c, k1 y; [9 ~# Z
ability of androgen products in our society may
  z) u" `( R) P2 x" d+ |% t0 b% _indeed cause more virilization in male or female
" S2 a( h8 A4 X/ hchildren than one would realize. Exposure to andro-
$ i1 N, z& U) ^gen products must be considered and specific ques-
6 }) [' w" E% m- K; `1 [& t, _tioning about the use of a testosterone product or- k' F9 t6 G$ J' q. K( Z9 E" ~
gel should be asked of the family members during
3 D9 i1 u; ^1 N* Z( T; d3 \the evaluation of any children who present with vir-( Y- s" T* Z+ O' O  o
ilization or peripheral precocious puberty. The diag-# H) X' N' C! `* g# \! U: l# U
nosis can be established by just a few tests and by
: H8 Y: z0 l: W4 t" L# t4 @* kappropriate history. The inability to obtain such a
. c+ O' n9 m, v0 M" `# c9 E4 |history, or failure to ask the specific questions, may" N9 U1 [; R0 I2 ^  ]) i
result in extensive, unnecessary, and expensive
% F% Q' Q4 E. `1 Y2 ]investigation. The primary care physician should be; ^1 f+ f1 ?! L
aware of this fact, because most of these children$ r, Q* P4 a6 t' B" E, I. h
may initially present in their practice. The Physicians’
1 |4 k# j$ U, d3 o5 u9 a- g, D0 {Desk Reference and package insert should also put a4 ?% u' m- t* @$ y
warning about the virilizing effect on a male or5 ^  a/ t$ z* f1 O9 A0 O
female child who might come in contact with some-
- j& @, F7 K" s+ A0 Y+ Gone using any of these products.
- @/ o& V2 N, h, u7 U) ~References$ B; U& S- L/ \
1. Styne DM. The testes: disorder of sexual differentiation% `  c) c4 [8 S
and puberty in the male. In: Sperling MA, ed. Pediatric) z+ _# c8 [6 \, N2 Y6 Z4 r
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;" v" a6 |* k8 [. p$ p: V
2002: 565-628.; Y& l; t" l# t0 j
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious: ?7 A/ d/ b- l: I
puberty in children with tumours of the suprasellar pineal
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VIP精品區,資源無限好賺金任務區,輕松賺金幣
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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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

: H* Q, y2 _0 P/ F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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