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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
( _/ M" R) W' F* mBoy Induced by Indirect Topical6 a- l4 F# y( L* _% R) K) d( R7 D0 U/ _
Exposure to Testosterone% V, I. |8 l9 p) [+ X+ W
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
- }- {2 J" V) V# aand Kenneth R. Rettig, MD1
1 c+ U, i" H# S; {7 FClinical Pediatrics
- N! U! i) i* jVolume 46 Number 6  D0 K6 z# e  e+ C, t0 s) [
July 2007 540-543, T  t7 l+ n& z3 _* y
© 2007 Sage Publications' ?0 Q# A" f0 ~) S" S" w
10.1177/00099228062966514 F/ h7 y; u0 E1 N: H) p
http://clp.sagepub.com
2 L6 v1 g9 m1 p, Vhosted at
0 A1 W- l6 f6 vhttp://online.sagepub.com& M9 T) G5 b, D: _! R3 n
Precocious puberty in boys, central or peripheral,
2 h4 c% A7 a) H* u; t1 s. Iis a significant concern for physicians. Central
2 N- }6 n2 n- i8 ^3 i' @$ R0 v4 oprecocious puberty (CPP), which is mediated$ Y6 V' M2 L' K2 o9 M
through the hypothalamic pituitary gonadal axis, has
. ~& _/ l4 s% Ha higher incidence of organic central nervous system" ~& X& H6 Q1 k
lesions in boys.1,2 Virilization in boys, as manifested4 V) X# m- @3 D0 s
by enlargement of the penis, development of pubic7 ~6 ^& a/ ]& d) p, l
hair, and facial acne without enlargement of testi-
6 s& Q& c% `4 t7 {3 Mcles, suggests peripheral or pseudopuberty.1-3 We4 ~, S3 Y6 u9 [& \4 g1 E
report a 16-month-old boy who presented with the
: q  o6 T) c" S* Renlargement of the phallus and pubic hair develop-1 `) L* ]3 H. ?% z" }
ment without testicular enlargement, which was due
0 K, U. k9 h4 s9 ]9 L' |to the unintentional exposure to androgen gel used by
' a  W" Z( ^5 o9 b& N6 lthe father. The family initially concealed this infor-' d, `+ b4 K! b/ C, }4 M
mation, resulting in an extensive work-up for this
1 @% z, l5 B! P2 achild. Given the widespread and easy availability of3 u  y9 T. ^) b4 J2 T7 ]
testosterone gel and cream, we believe this is proba-
. A% r' ]5 |. o, U  c7 Qbly more common than the rare case report in the; M# x+ _* x" |* f' R' O
literature.4
9 V: I3 m, L+ B& t! J3 u  WPatient Report
4 v5 T+ A7 Q7 n/ K* H, E; PA 16-month-old white child was referred to the7 G# C1 @; T8 f
endocrine clinic by his pediatrician with the concern; x! P8 E0 F( q5 r+ {
of early sexual development. His mother noticed. Z3 f6 J0 Z" \9 w9 f4 {
light colored pubic hair development when he was7 D" y3 q+ |9 l
From the 1Division of Pediatric Endocrinology, 2University of
* o& h+ o) \* v' |' c( X# \0 c5 T: ~South Alabama Medical Center, Mobile, Alabama.. ~) p+ A' Y1 L( `2 m2 S0 H
Address correspondence to: Samar K. Bhowmick, MD, FACE,
# E" ?$ f+ R+ q# Z* nProfessor of Pediatrics, University of South Alabama, College of
0 q; }) ~4 f6 ^  N  e; a" w4 {# V. bMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 u/ h2 E5 ^* n% A+ V& g6 `
e-mail: [email protected].$ a' R. c& V$ |! O" Z
about 6 to 7 months old, which progressively became
. j0 |& Q* V" {darker. She was also concerned about the enlarge-  [% H& X2 H2 I9 z9 Q; u7 @6 ]
ment of his penis and frequent erections. The child
9 M2 O( |* {. y( Twas the product of a full-term normal delivery, with0 I( Z" f2 L0 n! M3 Z, b  U' [
a birth weight of 7 lb 14 oz, and birth length of
3 Z1 g( @- \- `! y$ V+ s. z$ a20 inches. He was breast-fed throughout the first year2 H/ i' l% T* W" l# G6 y
of life and was still receiving breast milk along with+ S$ m5 O5 Z7 j& h* r& }" S8 B
solid food. He had no hospitalizations or surgery,/ K. T4 X& ^1 E3 j9 `  q
and his psychosocial and psychomotor development
. U+ h' g0 P, ]1 Dwas age appropriate.' v) b* ^# i; b  N6 U# l/ ]3 v; Y
The family history was remarkable for the father,
1 e4 V$ e2 {7 E( N1 r5 Kwho was diagnosed with hypothyroidism at age 16,6 a2 M* D9 F5 M
which was treated with thyroxine. The father’s$ N- r. ]& _; x4 @7 i- Q- \
height was 6 feet, and he went through a somewhat
0 K' U& f5 v& w) }0 zearly puberty and had stopped growing by age 14.
5 D0 w3 r& Y1 [0 FThe father denied taking any other medication. The
# g4 [0 ~+ C( z; l' g; V; Tchild’s mother was in good health. Her menarche
% K  W8 `: t+ c. V) K$ }  uwas at 11 years of age, and her height was at 5 feet
. m) @+ J; T; a+ h" H( `0 B. ^4 h5 inches. There was no other family history of pre-! T- ]5 R! I( b4 |# G+ u" S: P1 O0 D
cocious sexual development in the first-degree rela-
! T" A/ W4 X$ n: \4 Rtives. There were no siblings.) J# C$ E& T5 [# p, \
Physical Examination* x8 c% c/ N6 U+ e  @$ z
The physical examination revealed a very active,. U- U- w8 D8 u
playful, and healthy boy. The vital signs documented
; \  B5 l7 d% p' ha blood pressure of 85/50 mm Hg, his length was
- Y# M; p4 U9 p90 cm (>97th percentile), and his weight was 14.4 kg
( y$ r) Q+ J/ T: Q& F6 l(also >97th percentile). The observed yearly growth, c- y6 R/ d6 G1 X( U
velocity was 30 cm (12 inches). The examination of* d* c; P( s8 Q* S1 m1 @7 A
the neck revealed no thyroid enlargement.8 M8 N$ Y6 K: m+ ~
The genitourinary examination was remarkable for
+ c7 D1 Y' t& q# Q, a  Zenlargement of the penis, with a stretched length of7 ~" E' c; s3 c
8 cm and a width of 2 cm. The glans penis was very well2 L0 R1 l+ S! ^$ l' M7 \
developed. The pubic hair was Tanner II, mostly around) ~9 ]" y! d+ z* r+ t
540  c0 i# i& ]' A5 m! L
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 Z( q3 @  Y/ r, p" xthe base of the phallus and was dark and curled. The0 R1 ]8 l$ v# w  k. y: n3 F# H
testicular volume was prepubertal at 2 mL each.3 K: V/ m! }7 q9 t$ f
The skin was moist and smooth and somewhat
) ?8 H' z+ D( V4 S2 w! ~, ?oily. No axillary hair was noted. There were no! r3 z9 j0 m: g! l/ U
abnormal skin pigmentations or café-au-lait spots.
2 i1 F" E7 {7 I  A  MNeurologic evaluation showed deep tendon reflex 2+& T5 k8 [. x2 L" ]; o) C' s
bilateral and symmetrical. There was no suggestion! L( x' v0 z: _- T( m' I# b" @
of papilledema.
$ S! v6 d# s3 H. \1 zLaboratory Evaluation
* S: U( Z7 b4 i5 `The bone age was consistent with 28 months by8 w; R- G7 {$ b, q6 p
using the standard of Greulich and Pyle at a chrono-
2 w% E/ F' A+ O7 h+ [logic age of 16 months (advanced).5 Chromosomal1 w9 T2 K; H2 C/ O+ F( W, o/ I
karyotype was 46XY. The thyroid function test) Y) u9 {2 ]( w9 x
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ F# y' z: n3 r( Dlating hormone level was 1.3 µIU/mL (both normal)." t' Y" {" S' t4 E, @1 \' q4 i- C* B
The concentrations of serum electrolytes, blood1 N6 N7 L% B& r5 s4 T8 X8 `
urea nitrogen, creatinine, and calcium all were
; {7 _( y2 G  e$ Z# h5 Gwithin normal range for his age. The concentration  ~8 K- W; J( ^3 M* V) M
of serum 17-hydroxyprogesterone was 16 ng/dL8 e8 D7 r0 o, ]( a# R6 _1 P' q
(normal, 3 to 90 ng/dL), androstenedione was 20
$ f! c& `# r& j: p% y: Z$ wng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
. J, g9 C# G; q1 Pterone was 38 ng/dL (normal, 50 to 760 ng/dL),7 R( g; g0 K8 \, a5 C+ }! s5 i0 G
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
9 L2 `: z* i5 b) t' i49ng/dL), 11-desoxycortisol (specific compound S): N4 A; |- h+ o
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
0 {' u4 E; y: _! Ztisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total$ L4 {( i: \9 k2 Y2 ?$ d; b- l
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),( F5 M+ c" S4 O) Q/ e. l8 v  J9 V
and β-human chorionic gonadotropin was less than1 ~. Z1 L! ?/ u' c4 }4 W5 j
5 mIU/mL (normal <5 mIU/mL). Serum follicular# D3 x( s; f$ g7 T/ @
stimulating hormone and leuteinizing hormone+ h9 J# M0 _# u$ K$ k
concentrations were less than 0.05 mIU/mL, Z8 `2 T# J& ?8 m9 o
(prepubertal).9 D1 X) z( T0 H2 s  H1 \
The parents were notified about the laboratory; L9 h5 p; _3 _& ^; M
results and were informed that all of the tests were
& t+ {- Q4 Z. B7 ynormal except the testosterone level was high. The+ i  [' U8 e  {, c! l4 u- u
follow-up visit was arranged within a few weeks to
- c% i7 |# I; h& sobtain testicular and abdominal sonograms; how-* W# [/ I3 T8 x+ j. @0 o
ever, the family did not return for 4 months." Q' Q* b2 \9 b0 k
Physical examination at this time revealed that the5 v. H) _) U% a
child had grown 2.5 cm in 4 months and had gained& j- e) A$ U( Y" u% _
2 kg of weight. Physical examination remained7 K  Z( f" G! M" o8 W( s9 a; V
unchanged. Surprisingly, the pubic hair almost com-
5 a2 p# K- p4 Tpletely disappeared except for a few vellous hairs at
5 P! h/ X' K( p0 S; o5 a  |the base of the phallus. Testicular volume was still 2
* g" s' a; L8 v! U  _mL, and the size of the penis remained unchanged.- y; U1 x0 A  ]* o4 f
The mother also said that the boy was no longer hav-
# r4 v- b. H2 Q4 U2 Jing frequent erections.' o# f# P, e  t7 b  X; R: X
Both parents were again questioned about use of3 b6 c2 t- h) V  G9 n+ h& T
any ointment/creams that they may have applied to
  w, W4 d0 g0 C0 O+ othe child’s skin. This time the father admitted the
5 {! z2 i- k* `/ m" ~Topical Testosterone Exposure / Bhowmick et al 541
" C% P5 O4 Y5 w% X) D; D  u, |use of testosterone gel twice daily that he was apply-& e% w2 O  g$ n/ F
ing over his own shoulders, chest, and back area for
2 c" g5 ^  j0 M6 sa year. The father also revealed he was embarrassed
& X3 ~) q, e3 h! {2 L" ]1 k' Qto disclose that he was using a testosterone gel pre-
+ L6 ]" X$ W) c$ {' R3 Lscribed by his family physician for decreased libido
% t. P. ]! d, J. `+ y: Z( Q; P' Msecondary to depression.
  E* Q3 U. [' [( o) v1 s+ O2 g, d% lThe child slept in the same bed with parents.
4 e3 ]1 N7 X  l( U) w5 jThe father would hug the baby and hold him on his) f; F* i" G6 p
chest for a considerable period of time, causing sig-
. {, u1 B2 x2 A1 r& J: snificant bare skin contact between baby and father.
  o2 N9 g5 u- gThe father also admitted that after the phone call,
, T/ T; f: B9 dwhen he learned the testosterone level in the baby
7 T$ T, _/ ~1 ~6 s7 mwas high, he then read the product information9 y# Q& M' h: Y6 y+ f. |
packet and concluded that it was most likely the rea-
7 d% v. N7 T( k$ o& |son for the child’s virilization. At that time, they7 n' [) L) q- h8 E. [# [6 _0 V3 ]
decided to put the baby in a separate bed, and the
' W3 s2 j$ O) F# Tfather was not hugging him with bare skin and had
% ^: x6 g) n$ i1 l; }been using protective clothing. A repeat testosterone
: g; p- y( S0 @3 d8 q7 x9 dtest was ordered, but the family did not go to the* L6 ]2 n! E% Y3 n$ }
laboratory to obtain the test.
; J% ]5 `: n2 d. F7 a( Q: |1 B9 Q; {Discussion" X2 W- S* S$ A' w- S# g
Precocious puberty in boys is defined as secondary. P% j' E" x' W2 l$ A7 H* y0 F  j
sexual development before 9 years of age.1,4; D$ ~* F7 k& x; W8 v) c
Precocious puberty is termed as central (true) when( ^) F4 y$ O# o1 D8 @4 l; M7 o
it is caused by the premature activation of hypo-# g+ K! V$ U+ z+ D
thalamic pituitary gonadal axis. CPP is more com-
! u1 \5 P7 u* Rmon in girls than in boys.1,3 Most boys with CPP
6 x9 z$ H  s9 t0 G3 m# Jmay have a central nervous system lesion that is
% n& V2 `& P  a1 v- o, ]: a/ m1 _responsible for the early activation of the hypothal-
3 `: C  I0 s4 Bamic pituitary gonadal axis.1-3 Thus, greater empha-9 Z% b8 A2 h3 X' k2 t/ I9 Y+ Z
sis has been given to neuroradiologic imaging in) X) r% @7 ]8 h4 A# P( ~, Z" t
boys with precocious puberty. In addition to viril-
2 O$ P7 r3 g0 O# Dization, the clinical hallmark of CPP is the symmet-
" B  Y0 D9 U" w/ Irical testicular growth secondary to stimulation by# n3 E) I% }, p
gonadotropins.1,3
0 [1 m8 p& U; ^9 H: K& _Gonadotropin-independent peripheral preco-
8 l$ \' l% t% @) O5 @( Pcious puberty in boys also results from inappropriate
: o* r1 i( P  P7 Y2 w6 oandrogenic stimulation from either endogenous or
2 d( Y8 Z( _, F  Q- P5 {# [exogenous sources, nonpituitary gonadotropin stim-) U) t" W0 a! Q/ z, V
ulation, and rare activating mutations.3 Virilizing* }4 H8 d4 f4 Z* W' W: a0 R
congenital adrenal hyperplasia producing excessive
1 T2 X8 h7 H* u# p) C7 oadrenal androgens is a common cause of precocious
1 a: K% s9 f; J$ {( Gpuberty in boys.3,4
$ I, d0 p* e# ]( F3 @) `The most common form of congenital adrenal
) K- o+ }$ _1 M: V3 }- {. Uhyperplasia is the 21-hydroxylase enzyme deficiency.
) G$ \, n8 n! w! c! EThe 11-β hydroxylase deficiency may also result in* c% I9 H3 j7 d* r- a
excessive adrenal androgen production, and rarely,
+ j- d. X4 l! T4 |9 kan adrenal tumor may also cause adrenal androgen
" e) n! n2 m) w. Q  zexcess.1,3
! t9 O0 F, P1 M2 A  k, V, dat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
  U$ k% {" g5 r, ~5 I, N) `/ V542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
% o8 q$ ^4 V; {1 ~( HA unique entity of male-limited gonadotropin-
2 j; T8 H: ?. Bindependent precocious puberty, which is also known
) b" V: |! k1 r5 k2 X8 [, Gas testotoxicosis, may cause precocious puberty at a! B* w0 Z* }5 z2 m
very young age. The physical findings in these boys
  w& u$ r: x, m) b# lwith this disorder are full pubertal development,! V& }( [6 a3 O" f
including bilateral testicular growth, similar to boys
( Y2 |) K4 ]$ Y  s& H+ \with CPP. The gonadotropin levels in this disorder
4 O, L5 B- b: B8 w% [are suppressed to prepubertal levels and do not show' \0 {& G$ c/ t# Q* y
pubertal response of gonadotropin after gonadotropin-4 B+ e# P# u- ^& L3 K
releasing hormone stimulation. This is a sex-linked
" K# r5 \) Y9 d6 E$ |autosomal dominant disorder that affects only
& Q4 N+ {' l" q2 w# t+ `+ y* M7 Hmales; therefore, other male members of the family& z) n6 t$ {, b
may have similar precocious puberty.3
  L, H1 I' |0 K) E* WIn our patient, physical examination was incon-
( K/ N$ f. L! |. ]" Xsistent with true precocious puberty since his testi-5 L3 J% E" b3 F6 l' D; L3 j$ N
cles were prepubertal in size. However, testotoxicosis
9 i. l3 \: ?+ U8 z0 `was in the differential diagnosis because his father
8 h* g  O( X3 g# T1 ~0 L- H0 V# Rstarted puberty somewhat early, and occasionally,
- ~) j1 O7 F; Y. l+ Xtesticular enlargement is not that evident in the
0 U1 g: _( a+ ]& m3 y+ ]beginning of this process.1 In the absence of a neg-
+ r! z! z# h5 F, U1 [ative initial history of androgen exposure, our
3 f  n( h. a+ Pbiggest concern was virilizing adrenal hyperplasia,
; N& Y3 I, x( jeither 21-hydroxylase deficiency or 11-β hydroxylase5 [5 n1 B( a: L
deficiency. Those diagnoses were excluded by find-
/ g" q3 M' v) K& T* jing the normal level of adrenal steroids.
% t* h3 v( W* L1 J) j- tThe diagnosis of exogenous androgens was strongly
6 r$ r2 g2 U$ x) z7 isuspected in a follow-up visit after 4 months because
0 V2 m8 g8 ^& i# ]. V4 Fthe physical examination revealed the complete disap-
) q" A0 V/ h# n4 l7 Q* Wpearance of pubic hair, normal growth velocity, and
5 B4 ?) f7 C, g' O3 K2 s: Tdecreased erections. The father admitted using a testos-* g' n: j5 \9 R* o( o1 c
terone gel, which he concealed at first visit. He was. U6 ~% |; J( P
using it rather frequently, twice a day. The Physicians’
5 Z- C% ]: h! U% pDesk Reference, or package insert of this product, gel or
( v( M7 T( ~- R) ycream, cautions about dermal testosterone transfer to
+ l* ?( J. t0 m2 Z1 Hunprotected females through direct skin exposure.6 d. Z9 e$ B6 ~9 O
Serum testosterone level was found to be 2 times the) L+ @/ k' J, l( k+ a& w* D
baseline value in those females who were exposed to8 U, O9 G- o* j( N6 Y
even 15 minutes of direct skin contact with their male
; v, ~( J) b/ q5 z, apartners.6 However, when a shirt covered the applica-  b! H/ Q$ j3 j
tion site, this testosterone transfer was prevented., p" ~: ]  q5 s' C; y# _' ?; ^8 [/ A
Our patient’s testosterone level was 60 ng/mL,; q& H2 R& E$ E! |2 v/ i2 e& W
which was clearly high. Some studies suggest that4 @1 Y( m7 E( w9 n4 C4 }6 h4 y4 Q+ e
dermal conversion of testosterone to dihydrotestos-
; Q' C+ W& c# F! iterone, which is a more potent metabolite, is more
: d& X5 C4 }, p) K6 F+ q2 P1 Sactive in young children exposed to testosterone* E* |6 v( v! [
exogenously7; however, we did not measure a dihy-& p  |, G3 v1 |* ]" m$ P3 ~
drotestosterone level in our patient. In addition to3 }. \' x! c4 m. g( f/ \
virilization, exposure to exogenous testosterone in( o4 \+ M9 N: g8 t2 @
children results in an increase in growth velocity and1 e" L& Q" Q1 M  T$ ~! v3 _7 L9 _
advanced bone age, as seen in our patient.
+ v+ G6 u6 d9 J% m& x! KThe long-term effect of androgen exposure during
9 E! H2 c+ J4 H" X1 C$ Iearly childhood on pubertal development and final
( v6 ^1 y6 ^5 @" u) zadult height are not fully known and always remain
3 j1 |+ w+ ~* `2 Ga concern. Children treated with short-term testos-
2 A. h% T' ~9 cterone injection or topical androgen may exhibit some# _8 V4 Q3 `+ d7 C
acceleration of the skeletal maturation; however, after3 t3 z+ K% K3 i- U$ j+ T1 D  G
cessation of treatment, the rate of bone maturation' P, j1 w9 g% i2 |) u6 P8 D
decelerates and gradually returns to normal.8,9
" J: g4 ^! |4 l- ~There are conflicting reports and controversy
6 x& I" ?% L/ B6 i$ A% bover the effect of early androgen exposure on adult, Y" f; I5 ^1 T7 O
penile length.10,11 Some reports suggest subnormal
4 D# b, c) ~7 I& i% Fadult penile length, apparently because of downreg-  q0 P( F2 R6 D; O( p
ulation of androgen receptor number.10,12 However,
- Q8 v/ {! b) J, wSutherland et al13 did not find a correlation between
. b  V2 j% Z% L0 Rchildhood testosterone exposure and reduced adult3 g) U" Q1 b1 p" S" o
penile length in clinical studies.% V! I- o5 g9 c, `  y/ s
Nonetheless, we do not believe our patient is4 {, B0 w; t1 d1 C
going to experience any of the untoward effects from6 J; n- [$ F6 u0 B5 |" P5 o
testosterone exposure as mentioned earlier because' t  o" H" G2 |& e1 S0 M
the exposure was not for a prolonged period of time.
' p$ \6 q1 E' N5 a8 w. ~Although the bone age was advanced at the time of
5 q6 h, @& @# {) P' Zdiagnosis, the child had a normal growth velocity at
2 o1 G, E9 T0 f" Z; Athe follow-up visit. It is hoped that his final adult% }( l* l& T5 {
height will not be affected.
: v8 t- G! T7 L2 x" t4 aAlthough rarely reported, the widespread avail-
' l/ R, o! Z" \ability of androgen products in our society may% F) o3 i& ?" S/ e
indeed cause more virilization in male or female1 d. E. l4 H0 w2 h
children than one would realize. Exposure to andro-
2 r2 J1 O# B. r) }gen products must be considered and specific ques-
1 Y( A% Q3 ]* i7 f& j0 P, m# o4 e; v# Xtioning about the use of a testosterone product or. p3 y7 f" ~( F, m' E
gel should be asked of the family members during; f6 w+ `, a0 y& b; r# y: H
the evaluation of any children who present with vir-
- ]0 w7 s) s3 A! ?: ^/ j9 k* vilization or peripheral precocious puberty. The diag-
1 F" T/ e  T) |% fnosis can be established by just a few tests and by
+ r) Q7 k  }' a9 Rappropriate history. The inability to obtain such a
: {& f8 S1 X6 j. g. b  m6 r: phistory, or failure to ask the specific questions, may: n$ c0 n: q% {& S& Z! v0 ~$ U
result in extensive, unnecessary, and expensive
0 O0 b1 g9 I! p2 S7 iinvestigation. The primary care physician should be
! p  Y6 L" P! f  L6 maware of this fact, because most of these children
6 T# ], G2 J) O* s. s$ nmay initially present in their practice. The Physicians’
! T3 }7 V# K# K! ]' YDesk Reference and package insert should also put a3 Y  d9 c4 V# s
warning about the virilizing effect on a male or
4 D/ ?; Q( l5 ^1 C/ afemale child who might come in contact with some-2 [4 W" }2 Y) B4 l/ U- r* C* n
one using any of these products.
% U& Q" C& R  _. ~7 F. n2 y3 ~References
, T$ B1 X9 Z7 I: A& e2 V1. Styne DM. The testes: disorder of sexual differentiation+ Q& T# g. D1 s
and puberty in the male. In: Sperling MA, ed. Pediatric' z2 |5 p7 R! }2 ^/ Y+ w
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
( W% e! ]) C2 x2002: 565-628.
' ]- [0 n  I  c  d2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious4 Q# x0 P' s# ~8 \
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
2 M( _6 G2 n* a' O/ MBoy Induced by Indirect Topical5 p, n: n/ k" J8 ]9 i* v" V) i$ I
Exposure to Testosterone, M7 P$ g" J+ h; ~: |2 R6 d! I
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2( I* N) \7 |  \" F; g! U1 u! W3 _
and Kenneth R. Rettig, MD1! \/ P- Z! t9 c/ \! z  ]
Clinical Pediatrics* ^+ A0 g- t* t( T' {
Volume 46 Number 6# q2 j1 t' P: e1 V# X3 l, l
July 2007 540-543  J* e8 c+ L0 K8 Q# [
© 2007 Sage Publications
2 g. ^9 @! S. F: R' [5 B+ f, _10.1177/0009922806296651
! }9 @. ]) T1 i6 O/ n6 X9 e8 bhttp://clp.sagepub.com
  z* n# C% b9 Ihosted at
( q1 f1 G- a" z5 D; yhttp://online.sagepub.com) u! v# g2 \1 ^( h1 f0 h$ _4 L" B
Precocious puberty in boys, central or peripheral,
. m7 C0 D# b5 K3 |is a significant concern for physicians. Central- e% k; K8 x" s
precocious puberty (CPP), which is mediated
7 u  Q2 M7 z0 V! I" s$ }7 M+ [; cthrough the hypothalamic pituitary gonadal axis, has
2 K6 n0 E# e% K5 q) a5 [0 Y; X$ \) e3 ea higher incidence of organic central nervous system2 a. F. H' y3 O% e3 ]/ c
lesions in boys.1,2 Virilization in boys, as manifested. Z! F* q2 A5 g/ f# ^
by enlargement of the penis, development of pubic' H; r% ]' F$ P0 D& R4 Y
hair, and facial acne without enlargement of testi-' {  f2 K8 D$ g! p2 e1 d
cles, suggests peripheral or pseudopuberty.1-3 We
$ B& \0 s! m" z+ W7 Oreport a 16-month-old boy who presented with the* f! d& y+ _. N# {+ [9 W; k8 ^  R
enlargement of the phallus and pubic hair develop-
- s" N+ _& K9 i- v: qment without testicular enlargement, which was due
, x! q. i+ r4 X4 c. {8 Gto the unintentional exposure to androgen gel used by8 ~7 _7 w6 ?( F7 r$ F
the father. The family initially concealed this infor-
1 L) `  M. O4 g" Hmation, resulting in an extensive work-up for this# i) e$ [& J7 b# \2 B$ v6 s
child. Given the widespread and easy availability of
; |6 p( G5 _2 l0 ntestosterone gel and cream, we believe this is proba-
; ~& _0 w" D" H! U8 [  }bly more common than the rare case report in the' u& T5 U. J, i* G! }; V
literature.4
4 z/ U. A. j0 _6 a' a9 R: V- G* m! vPatient Report
, ]% F7 ]& o! S) ]/ B' u! e+ cA 16-month-old white child was referred to the
8 W7 ~3 {7 J6 H" D' N% hendocrine clinic by his pediatrician with the concern
" O+ f% O7 u, S# s1 Tof early sexual development. His mother noticed5 m3 [. H. B+ x. q. z+ i, l: @& N
light colored pubic hair development when he was
4 {" S) m$ j5 l) D! XFrom the 1Division of Pediatric Endocrinology, 2University of
' b) l9 M3 V% ZSouth Alabama Medical Center, Mobile, Alabama.& B  K7 s$ a+ ^% _
Address correspondence to: Samar K. Bhowmick, MD, FACE,, ]" I7 g3 I. G( a- J5 f
Professor of Pediatrics, University of South Alabama, College of* P' Z- N: e7 D* R$ \! K# E
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;8 o% g" v4 a" `! H6 G+ N
e-mail: [email protected].) T+ r, |7 X3 u* A" U
about 6 to 7 months old, which progressively became
& x# p* x8 s2 w% hdarker. She was also concerned about the enlarge-
/ X7 _$ t/ q  }8 Y; xment of his penis and frequent erections. The child
( L3 @' x( R; O3 o  h0 uwas the product of a full-term normal delivery, with1 q* G6 W) \2 i
a birth weight of 7 lb 14 oz, and birth length of8 ~- s! G* X9 P6 t$ B
20 inches. He was breast-fed throughout the first year
1 z' M& i7 ~5 W$ `of life and was still receiving breast milk along with
; @2 W. e7 d' ]: s7 d; z: r3 J0 Gsolid food. He had no hospitalizations or surgery,3 n! \% _' @4 S/ `' {: T$ [
and his psychosocial and psychomotor development
: Y7 ^9 l. E0 R# G  h9 s: @: Hwas age appropriate.
& ^$ h6 K6 I: H9 d5 ^1 KThe family history was remarkable for the father,
- o/ Y2 s. @6 |3 Rwho was diagnosed with hypothyroidism at age 16,
; |# M. g4 G3 e/ Hwhich was treated with thyroxine. The father’s- @* O3 I: Q) t: a/ v9 A
height was 6 feet, and he went through a somewhat7 B) X# ~7 l+ j/ c! K
early puberty and had stopped growing by age 14.
; I# g" a- k  n8 q3 f# gThe father denied taking any other medication. The5 u" b* p! c7 I  l( L8 P' F( Z
child’s mother was in good health. Her menarche9 }8 N" |, y% B0 I& X- }
was at 11 years of age, and her height was at 5 feet
- A& s' @. {- j- m5 inches. There was no other family history of pre-
( c$ s7 N3 w+ k: P; zcocious sexual development in the first-degree rela-
0 t9 @8 \; f" i2 A7 {# n& C: stives. There were no siblings.3 y, j* n" Z# [9 \& G
Physical Examination
3 M3 J% u+ C, `+ R7 {9 o: pThe physical examination revealed a very active,+ |5 k  @: w; L' P; h- A; z0 C
playful, and healthy boy. The vital signs documented
( F  ]7 s! `8 E4 b, q* ga blood pressure of 85/50 mm Hg, his length was# y$ S# c# ]# d/ Q
90 cm (>97th percentile), and his weight was 14.4 kg# @4 R* q  ?+ f0 o/ s, S; W
(also >97th percentile). The observed yearly growth
/ B+ ]' H9 N4 M6 Cvelocity was 30 cm (12 inches). The examination of
, H4 _8 v# k* o5 m( e9 {* x1 t# lthe neck revealed no thyroid enlargement.
0 u1 z5 g% ~! m$ t9 Q7 iThe genitourinary examination was remarkable for& ?$ O4 F% [  ^% a
enlargement of the penis, with a stretched length of
9 D! r( V* ~  S5 Z7 }8 cm and a width of 2 cm. The glans penis was very well
* a$ a5 g2 o" zdeveloped. The pubic hair was Tanner II, mostly around' h% y% e$ k' Q
540
6 D% I0 @. V( W+ X( Z  }; V8 Y/ {at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from( i  ]+ [. j& w- v9 m: Q7 T" ^
the base of the phallus and was dark and curled. The4 P3 o' w2 d, r. T' K
testicular volume was prepubertal at 2 mL each.
( p  r& J2 Q" kThe skin was moist and smooth and somewhat
( _9 o& {7 `6 ~; w9 M- U7 foily. No axillary hair was noted. There were no6 }3 J; o0 c; B: z' D5 E& _/ y9 p- _
abnormal skin pigmentations or café-au-lait spots.# P5 |: W( x7 j! \
Neurologic evaluation showed deep tendon reflex 2+
1 n; E/ c; p9 ^. ~% B% dbilateral and symmetrical. There was no suggestion
8 [. c4 Z7 O% ?/ `of papilledema.
. |3 k3 s" A# D. T  h+ A% {Laboratory Evaluation
' k& x+ e. o: h0 r0 @/ ~# TThe bone age was consistent with 28 months by
+ ~: u1 X0 ^. [3 N+ Husing the standard of Greulich and Pyle at a chrono-0 \5 S/ C2 H: M  x( u8 L4 ]
logic age of 16 months (advanced).5 Chromosomal
- \* }' Q0 u2 ]karyotype was 46XY. The thyroid function test& `; ?1 F: z% e8 }  q7 s6 A0 i
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
6 @( G+ r+ B5 i0 ]# ?1 l4 Z( Wlating hormone level was 1.3 µIU/mL (both normal).
3 Q8 Y, B0 m3 _0 z# b3 MThe concentrations of serum electrolytes, blood
& u% I, g' w6 f8 wurea nitrogen, creatinine, and calcium all were
- e2 T% s9 s! |1 L5 Q4 Pwithin normal range for his age. The concentration
$ o9 U$ K) }! R" {  Hof serum 17-hydroxyprogesterone was 16 ng/dL; M" V/ c/ x* {, h! Z% L
(normal, 3 to 90 ng/dL), androstenedione was 20
  y. L' j1 j7 O) Y4 t' U$ yng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-6 V' k. c7 P) `. R  B
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
' M) i5 a+ j! Q( j. X+ udesoxycorticosterone was 4.3 ng/dL (normal, 7 to
; N1 a$ ^. r6 ^2 F5 t* o% s49ng/dL), 11-desoxycortisol (specific compound S)! W4 ^* M3 e: q/ _0 G3 G9 g! ^/ X# K
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
( ]( P% L7 b2 \5 |: C. V. O8 [' ptisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
* x9 m! x4 y) p; dtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
$ Z# s  S& Z: Q* O" m2 w" T# mand β-human chorionic gonadotropin was less than
1 I: a# A- @0 ]3 r  U5 mIU/mL (normal <5 mIU/mL). Serum follicular
* g1 n: E( L# k5 e" q1 U6 P; I+ astimulating hormone and leuteinizing hormone: j' P0 ~7 `6 k  h6 {
concentrations were less than 0.05 mIU/mL
* l! b, {0 t% `0 f( k. p5 {(prepubertal).% S2 c( e$ d, D+ [" a
The parents were notified about the laboratory0 b( J( N9 B7 q2 p( i* Q: u
results and were informed that all of the tests were
) k& M' h% `- O7 |( t9 E$ n4 Nnormal except the testosterone level was high. The% \4 L3 ~  i8 V! W: F4 ]- N
follow-up visit was arranged within a few weeks to
3 u% ~4 h/ p7 e' ?/ v) \) Fobtain testicular and abdominal sonograms; how-
  K. I+ Y0 b; G1 bever, the family did not return for 4 months.
3 C6 l6 ^; G' c- q4 h' u( ZPhysical examination at this time revealed that the9 N1 F! T% N* P$ {
child had grown 2.5 cm in 4 months and had gained+ [& W1 {- X' W
2 kg of weight. Physical examination remained* m; }* y9 @% ]+ R7 e
unchanged. Surprisingly, the pubic hair almost com-! D  H1 k2 j* b4 w/ S/ F- E! T
pletely disappeared except for a few vellous hairs at( D: k( s3 G) J; Z  b+ e/ r
the base of the phallus. Testicular volume was still 2: N% M* X7 f' H7 X0 ~' s
mL, and the size of the penis remained unchanged.3 E9 b0 Z/ M9 j6 W
The mother also said that the boy was no longer hav-
" t: w/ K( [0 H1 g$ sing frequent erections.# p: T1 K) D7 Q8 H
Both parents were again questioned about use of
, O4 X0 ?# J4 Q+ |any ointment/creams that they may have applied to
+ o- w$ x, S5 Bthe child’s skin. This time the father admitted the- z4 ?4 t/ [5 g* e; E3 h3 q
Topical Testosterone Exposure / Bhowmick et al 541
  t: A. ^9 U/ I% D+ t) Vuse of testosterone gel twice daily that he was apply-
7 p; g( k4 b3 ?9 W9 |ing over his own shoulders, chest, and back area for" D, W6 O) a6 O9 M* n( {' B3 ]
a year. The father also revealed he was embarrassed
/ C4 F8 z8 R" L; N0 _to disclose that he was using a testosterone gel pre-
$ ]/ R. b( Y3 j4 nscribed by his family physician for decreased libido
) i9 B3 c0 W' Y. A: D3 c4 p( Vsecondary to depression.$ {  m: V- q% f* i) L8 H0 ^- I
The child slept in the same bed with parents.
# A1 k. `( L6 YThe father would hug the baby and hold him on his
3 w$ E5 G$ l% l& X7 ?$ s9 @5 uchest for a considerable period of time, causing sig-
0 f6 B: u3 U; i! t7 n$ m0 Wnificant bare skin contact between baby and father.
4 ^4 q' B7 m1 CThe father also admitted that after the phone call,
* Y+ W! N: w( k( R5 y) R! l' F2 ?; nwhen he learned the testosterone level in the baby
* f9 U/ {' K% Bwas high, he then read the product information
- P3 a: @# u2 S) Y! z/ v: Ypacket and concluded that it was most likely the rea-2 t) K2 ~4 ?4 U
son for the child’s virilization. At that time, they
4 D+ p: C. B$ Ddecided to put the baby in a separate bed, and the: D$ e# {, l! A1 }! Q9 @9 T
father was not hugging him with bare skin and had8 |8 H  q5 ^5 k
been using protective clothing. A repeat testosterone
$ }+ W' \1 [  l! `6 [4 M9 vtest was ordered, but the family did not go to the) R2 i( }1 j8 C6 e6 {
laboratory to obtain the test.
$ h) |& a2 T9 w4 X5 q  |( zDiscussion
& h# E% \. G$ L- VPrecocious puberty in boys is defined as secondary
6 N/ ^- k  V+ R6 _' j4 Osexual development before 9 years of age.1,4
+ R+ ~! Q* c' e, K; y5 ?Precocious puberty is termed as central (true) when
3 P4 I& h7 W7 C' I; ~it is caused by the premature activation of hypo-
5 K9 o  {0 n" [: Ythalamic pituitary gonadal axis. CPP is more com-
3 B, Y7 K/ f* y2 h9 smon in girls than in boys.1,3 Most boys with CPP6 W4 F" ]: r, C2 X
may have a central nervous system lesion that is
4 ?3 h8 w2 G& v; e7 D2 nresponsible for the early activation of the hypothal-
) \# R4 C( Z! h# \% [- ~: Hamic pituitary gonadal axis.1-3 Thus, greater empha-: ?& }1 H+ m6 s" z3 M0 T. l: i0 j
sis has been given to neuroradiologic imaging in+ s9 T8 ~& l' Z* T
boys with precocious puberty. In addition to viril-
' Y3 ^5 s( T( f4 V7 ~ization, the clinical hallmark of CPP is the symmet-% @% m4 g9 x( |6 W/ C
rical testicular growth secondary to stimulation by5 b+ S+ m" w" ^
gonadotropins.1,31 O# {% B& u: ^7 f3 [3 K1 C
Gonadotropin-independent peripheral preco-
2 e4 |5 _9 b6 {9 u6 N5 T0 h( \cious puberty in boys also results from inappropriate  r. x) q7 v" I& P* E6 |
androgenic stimulation from either endogenous or
# }3 E% D3 j8 T0 ?exogenous sources, nonpituitary gonadotropin stim-& u/ U0 p3 I6 n7 _. o. ]
ulation, and rare activating mutations.3 Virilizing8 D1 @+ K# q# u% L* Y. d7 n
congenital adrenal hyperplasia producing excessive
3 f& I+ _3 t% Nadrenal androgens is a common cause of precocious
/ H/ G  p& U! U, upuberty in boys.3,4
" N0 b4 R9 Z5 j7 ^. @The most common form of congenital adrenal
( B$ {9 H' J0 T' Mhyperplasia is the 21-hydroxylase enzyme deficiency.
5 }, R4 |/ T. X+ CThe 11-β hydroxylase deficiency may also result in
/ i! s$ I- y. `7 M  F' eexcessive adrenal androgen production, and rarely,
' [3 W! O: Z: P& K, U& y& U! `an adrenal tumor may also cause adrenal androgen
! A) W2 p% W& U; v( b7 Gexcess.1,3
4 [% E" @* J# b  Z$ X" |/ Xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 A/ ]$ ^/ Q7 d/ J" y! |7 v+ A
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
( ?$ g2 b9 u  l' i7 G5 v+ ~9 xA unique entity of male-limited gonadotropin-
0 `' W- T2 Q0 t& mindependent precocious puberty, which is also known3 D3 J( _5 C- h5 H5 p2 J
as testotoxicosis, may cause precocious puberty at a
8 _0 @9 x$ y+ q: Z8 Q2 c9 }very young age. The physical findings in these boys
' l5 C5 m. Z: Q& _' {with this disorder are full pubertal development,
! m( D4 M" x8 Y4 w2 s: uincluding bilateral testicular growth, similar to boys: c. e) r3 Y* l# y5 w7 s8 y5 L' X% `
with CPP. The gonadotropin levels in this disorder2 \7 U6 Q' s% }3 q2 g
are suppressed to prepubertal levels and do not show, d5 P. x! V% U
pubertal response of gonadotropin after gonadotropin-
6 i1 a5 i4 J5 \6 _- c0 greleasing hormone stimulation. This is a sex-linked- w! l+ n6 z! d( K
autosomal dominant disorder that affects only4 T- ?# B4 T& F: J$ H0 q3 a% T
males; therefore, other male members of the family
6 r' U  v: Q; x- q- a4 q* Rmay have similar precocious puberty.3  r- Q3 x) {7 \9 o. u6 b- n  Y4 `
In our patient, physical examination was incon-! q9 Z# E- H" y: f* m+ t5 o
sistent with true precocious puberty since his testi-8 n* ?$ ]: E- k7 B( a- z( k# H
cles were prepubertal in size. However, testotoxicosis
& X5 U/ C3 _# y9 [7 z0 x% swas in the differential diagnosis because his father: d$ `% S$ t& W( L. i
started puberty somewhat early, and occasionally,6 h( l# i; S* B6 @0 I4 E
testicular enlargement is not that evident in the
  T% o8 k9 i) L6 D3 {beginning of this process.1 In the absence of a neg-5 f, N  Y: h8 n
ative initial history of androgen exposure, our
/ \- h/ |! ]& }  B$ Cbiggest concern was virilizing adrenal hyperplasia,
* n9 E* s4 d, }6 @! v' ~either 21-hydroxylase deficiency or 11-β hydroxylase  `3 R+ q6 }5 t' X
deficiency. Those diagnoses were excluded by find-
% @7 q7 P- S1 G) z& X3 Xing the normal level of adrenal steroids.0 T+ A" l. |8 }5 C4 d9 g( _
The diagnosis of exogenous androgens was strongly, T) J% Q/ k3 m6 B2 x, ~
suspected in a follow-up visit after 4 months because
* ~8 f& c. M7 C# x, H# c: n) Ythe physical examination revealed the complete disap-7 B( B; w( X% |/ V8 _+ `, e+ r
pearance of pubic hair, normal growth velocity, and
' q) L5 |4 V' e* P6 k- M8 f4 r' Xdecreased erections. The father admitted using a testos-; Y  P  {4 d! s! O8 C/ R
terone gel, which he concealed at first visit. He was
; ^  e, d6 [5 X2 G3 Iusing it rather frequently, twice a day. The Physicians’1 k, {6 X3 h" {+ M
Desk Reference, or package insert of this product, gel or, T# I9 S7 Z1 Y# C# O1 H
cream, cautions about dermal testosterone transfer to4 S# z- @$ L) E3 B; g6 S) j
unprotected females through direct skin exposure.  l1 w( s  }9 ?) F( v) O
Serum testosterone level was found to be 2 times the
. ?! s; J. V8 {0 sbaseline value in those females who were exposed to7 G; O2 U! M1 S, ]' e7 m+ |6 a8 H
even 15 minutes of direct skin contact with their male
: M+ r2 U6 y  j, P2 v; v0 jpartners.6 However, when a shirt covered the applica-7 D1 q' T* h* E8 V& G3 i# F% Q
tion site, this testosterone transfer was prevented.
1 @; C/ r5 \# D9 cOur patient’s testosterone level was 60 ng/mL,
! t- L# I! M7 s$ X9 @( P5 @which was clearly high. Some studies suggest that
0 @9 H: F( E1 _9 s3 ndermal conversion of testosterone to dihydrotestos-
) x- S8 I0 x5 f) Q: \9 e; J0 ]0 Gterone, which is a more potent metabolite, is more
  u" N: i: t0 E. s7 ]# K! Z! Vactive in young children exposed to testosterone
7 k8 R2 q4 l9 @3 b4 k. dexogenously7; however, we did not measure a dihy-% j: p4 s; b7 g
drotestosterone level in our patient. In addition to2 D; m2 [0 R$ a. h
virilization, exposure to exogenous testosterone in' k* B% V1 d8 z4 G. b6 W- W
children results in an increase in growth velocity and
5 `  o+ r5 c; l9 |advanced bone age, as seen in our patient.
; s) `0 D. _& A+ B1 OThe long-term effect of androgen exposure during' a4 f2 J0 ?. X3 z% ~0 o
early childhood on pubertal development and final
. ^3 ^) r9 a) badult height are not fully known and always remain
4 F. f  @, Q; Q8 C9 z2 ^- Sa concern. Children treated with short-term testos-3 o& |) e: x& ^. F& g& E
terone injection or topical androgen may exhibit some0 J1 h, S- Q$ r
acceleration of the skeletal maturation; however, after
. F) r8 M/ G3 V0 t& Jcessation of treatment, the rate of bone maturation
4 A6 q$ _9 n& W. ]decelerates and gradually returns to normal.8,9* [* L: @% A& p- Z  @
There are conflicting reports and controversy
8 B( ?; i) v4 O" N' `- H) a7 j2 yover the effect of early androgen exposure on adult( i4 @9 f8 q/ t5 G+ b5 K% B' H4 v
penile length.10,11 Some reports suggest subnormal
! F9 h, F  k% f, T/ w: B7 Yadult penile length, apparently because of downreg-
! W4 W% S) U4 d4 c4 _6 y+ k& k: pulation of androgen receptor number.10,12 However,- b# ~( Y2 ~4 |
Sutherland et al13 did not find a correlation between/ i+ N, O. D# @8 E: ^
childhood testosterone exposure and reduced adult# U6 I4 _- r. o* N, v' l1 I) {
penile length in clinical studies.
* v! T; `$ O( u1 VNonetheless, we do not believe our patient is3 W! [8 {0 c, {1 w4 \1 M2 a* d
going to experience any of the untoward effects from) B1 R7 z: {4 W% h3 \9 n. H
testosterone exposure as mentioned earlier because. W4 }; l/ z' \, ~  w
the exposure was not for a prolonged period of time.
+ H2 _; G1 T( a8 I3 w- yAlthough the bone age was advanced at the time of; d9 |+ I6 {7 b
diagnosis, the child had a normal growth velocity at
3 u! i* F8 \+ n3 N, U' W% Y9 N5 Uthe follow-up visit. It is hoped that his final adult( d/ H7 p- H  u0 P. z3 M7 ]
height will not be affected.8 n. b- R3 a' m' C0 K, K% x4 {$ C
Although rarely reported, the widespread avail-, ]+ m% @, [2 d; G1 _$ E
ability of androgen products in our society may/ y* ]. Q3 c* X# h( d  u3 Z
indeed cause more virilization in male or female( g  B$ [# w" p) v8 c
children than one would realize. Exposure to andro-
8 v5 u, f7 t2 d# k2 m. wgen products must be considered and specific ques-+ h$ O5 C% m2 R7 q% ^2 _
tioning about the use of a testosterone product or* q3 l# L* M" K+ n0 \
gel should be asked of the family members during; D6 |  t  n- G1 P2 t! N# Z9 r
the evaluation of any children who present with vir-5 ^$ q. F8 E" @6 M. u9 \8 v
ilization or peripheral precocious puberty. The diag-
( I# o3 A$ ^" P  [3 w. ?6 F8 }* Xnosis can be established by just a few tests and by- M% L8 y8 _/ ?0 X
appropriate history. The inability to obtain such a6 \* s8 l  `5 W9 L
history, or failure to ask the specific questions, may! P( L/ f$ L, H4 i; r
result in extensive, unnecessary, and expensive! }+ b# i8 n  A0 O# W+ c& l1 }
investigation. The primary care physician should be$ u  B7 v* o  I8 n
aware of this fact, because most of these children7 K# _' K$ @" b. y+ k7 I
may initially present in their practice. The Physicians’
% a& R, K. _/ lDesk Reference and package insert should also put a
) }- P" U6 ^+ j/ Nwarning about the virilizing effect on a male or
. B  J" O8 s2 N$ T' U2 W( q) X  zfemale child who might come in contact with some-+ W2 }$ R3 C! ?; ^' J  P0 v4 f6 R4 f
one using any of these products.
9 n% p! h8 E5 u% G4 YReferences
6 p* _; M- o( E. h" `' u1. Styne DM. The testes: disorder of sexual differentiation6 T3 h& L& Z$ X: ?9 |# i
and puberty in the male. In: Sperling MA, ed. Pediatric
! k3 |; p  v$ H  h9 T( }- QEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;8 l6 ^& n  [- _! J  i3 G5 j9 y
2002: 565-628.  b( g8 M  h' R1 @9 r* z
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious- e9 g1 H2 H& s/ i% d2 Q, T& h
puberty 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!
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

  }  p2 |8 [# n# G+ t7 F9 z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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