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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$ H4 f- Y# J% X
Boy Induced by Indirect Topical
* S9 ^1 q, V1 @( wExposure to Testosterone3 y! V  @" L& d! o
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
) f0 w; E7 b/ j8 i) Y- Y& V% x% D# uand Kenneth R. Rettig, MD1" v; h4 e; ]& @) q
Clinical Pediatrics6 U/ M& _+ m5 p' q7 n, Z: j4 T
Volume 46 Number 6( x( R7 {* V, }$ F
July 2007 540-543
# ]0 X. V; K# p7 K$ w# A© 2007 Sage Publications  k* E% S- J1 _+ D* \2 C
10.1177/0009922806296651
( f% M/ E) n3 f: vhttp://clp.sagepub.com
' y4 x1 W  ?" U* {7 {- `% ]hosted at7 H- C( ]2 _2 P4 i
http://online.sagepub.com! q2 M0 X* c$ J$ c- P* J
Precocious puberty in boys, central or peripheral,1 g4 s0 `0 ^* j4 q9 W
is a significant concern for physicians. Central: r+ v7 e; C& k$ B
precocious puberty (CPP), which is mediated
  p, x+ t& \: ?& d' `& N$ jthrough the hypothalamic pituitary gonadal axis, has
+ q& F" z9 `  S) F+ U/ `# |a higher incidence of organic central nervous system
9 ^4 Z, L5 c; e, {/ \& i  Llesions in boys.1,2 Virilization in boys, as manifested
0 l% [2 k3 L4 J9 C/ C) iby enlargement of the penis, development of pubic
& _5 o( E# G. \5 B3 }2 }2 {4 M9 r8 Fhair, and facial acne without enlargement of testi-, w* E+ Y: ~( `& @$ x
cles, suggests peripheral or pseudopuberty.1-3 We7 c- P  |6 T. `) v! r
report a 16-month-old boy who presented with the' S3 a% d9 D- f( N9 t  p: p
enlargement of the phallus and pubic hair develop-
4 ~  H+ b2 p. [/ iment without testicular enlargement, which was due" _& H- L- U0 F" n- \6 A5 M
to the unintentional exposure to androgen gel used by$ R! D; [$ N3 l1 e3 ^0 c7 O
the father. The family initially concealed this infor-! A$ ?3 q& t$ C+ p4 Y8 D7 I! y
mation, resulting in an extensive work-up for this
$ H! I, z6 L5 f# }; x! _3 I& bchild. Given the widespread and easy availability of: m5 V9 F6 U8 H9 l9 Z; X! P3 b) |
testosterone gel and cream, we believe this is proba-0 y+ Z. B1 k7 M% T
bly more common than the rare case report in the
  G  [; Q6 c9 I$ j! Iliterature.4
& {8 z6 t1 ^. u( K" _, \! [6 @! aPatient Report3 _; k. t3 Z+ V2 P* b! R
A 16-month-old white child was referred to the! {' ]) I8 c& E. y: m
endocrine clinic by his pediatrician with the concern
5 h6 R( I/ j* H# W$ @' \( L% hof early sexual development. His mother noticed
% d  X1 a& @% w1 dlight colored pubic hair development when he was2 x- u4 {7 y1 ?4 d2 T
From the 1Division of Pediatric Endocrinology, 2University of
; @. v, o& D$ a% x" RSouth Alabama Medical Center, Mobile, Alabama.
" Z! C! G" a% uAddress correspondence to: Samar K. Bhowmick, MD, FACE,/ a, O- h& s7 ?+ F* I& Y8 N
Professor of Pediatrics, University of South Alabama, College of% y( T$ F7 w+ m$ t4 a
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
- X1 ~6 r; u' H0 r; P/ D0 l5 ~e-mail: [email protected].9 u+ @7 b+ g3 O) U1 X+ H2 h9 k9 @' y
about 6 to 7 months old, which progressively became
, k' v  r1 }5 ?$ Vdarker. She was also concerned about the enlarge-
4 A: \9 X' ~& U( ^! [! W7 H" sment of his penis and frequent erections. The child
3 }% l' a7 Q# d, _6 U+ U; owas the product of a full-term normal delivery, with! U( U0 k- Q, J. T' _" c
a birth weight of 7 lb 14 oz, and birth length of
, Y) K+ q4 ?" H7 z4 Z. J; a, D20 inches. He was breast-fed throughout the first year. B, N  m+ b2 J9 s) V
of life and was still receiving breast milk along with# M& x) ~# I- o+ g' u
solid food. He had no hospitalizations or surgery,
, o3 V) w/ ^1 Qand his psychosocial and psychomotor development) B9 O) a* u5 ]* s
was age appropriate.
# V7 p; P' d' l7 FThe family history was remarkable for the father,
5 e8 T1 D- {) ?who was diagnosed with hypothyroidism at age 16,/ _) @5 d# k1 @5 @. t2 ]! a
which was treated with thyroxine. The father’s
2 ?# q7 `* G6 m/ ]* ]height was 6 feet, and he went through a somewhat
" G2 a' k+ I. Dearly puberty and had stopped growing by age 14.
2 }) ?0 d) _; M9 a! Z& T% aThe father denied taking any other medication. The
" f! }) `5 E% W3 I6 b0 |0 s* Lchild’s mother was in good health. Her menarche
+ s- X0 `5 V) mwas at 11 years of age, and her height was at 5 feet6 u0 Q- L8 f. q# R5 ?
5 inches. There was no other family history of pre-& v5 i+ b$ a$ q& b% y. b
cocious sexual development in the first-degree rela-0 f) }. v( K" C, o& z' v2 r
tives. There were no siblings.
! [: j4 x2 m! h' M0 h+ oPhysical Examination
4 T/ n! s% Z4 XThe physical examination revealed a very active,& ?/ E; _! J" V+ Q. o
playful, and healthy boy. The vital signs documented3 k! l: f  y* r# J
a blood pressure of 85/50 mm Hg, his length was
0 L  X# Z4 N: B. k; P' X& b90 cm (>97th percentile), and his weight was 14.4 kg
2 e2 r2 {) F4 A(also >97th percentile). The observed yearly growth
' Q& I' N. N# e* h, j" `1 @6 Bvelocity was 30 cm (12 inches). The examination of
9 K( X' H  E  L1 F& R; R# L8 Kthe neck revealed no thyroid enlargement.
# b; J7 N, G; A( e- WThe genitourinary examination was remarkable for3 i: [8 }$ W0 U% K
enlargement of the penis, with a stretched length of
9 P4 {6 P- J1 R# I' v  \8 cm and a width of 2 cm. The glans penis was very well
+ j, |; `' I) z# k3 |developed. The pubic hair was Tanner II, mostly around: t  }* ~2 U3 T. b: ]1 Q9 P
540
2 D) D6 }4 n5 }  Y/ L, g" ^5 Q& N' g1 [at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 I( w/ q4 U# N$ @the base of the phallus and was dark and curled. The: @! p+ k6 ^$ B, B& {
testicular volume was prepubertal at 2 mL each.& @7 w6 W( ]+ B# q& A4 m7 M0 V; H
The skin was moist and smooth and somewhat
- N/ L0 @. j/ t! aoily. No axillary hair was noted. There were no
0 e( G( E1 ]1 Q; R% M  A9 xabnormal skin pigmentations or café-au-lait spots.5 @. X+ Y7 W' i2 c/ ^' \
Neurologic evaluation showed deep tendon reflex 2+! m1 ^- }( F" X! ?! V6 v: ^
bilateral and symmetrical. There was no suggestion* W7 s& _. _- c3 u
of papilledema.
5 ^" `$ I$ |( i* ~Laboratory Evaluation; t$ }: T, A9 c' V
The bone age was consistent with 28 months by
- v- ?, g0 R, E+ V) susing the standard of Greulich and Pyle at a chrono-: f: z" K) e" L
logic age of 16 months (advanced).5 Chromosomal. Z1 Y+ Q2 t8 J! m0 f
karyotype was 46XY. The thyroid function test
; `  a& M& [  U0 Lshowed a free T4 of 1.69 ng/dL, and thyroid stimu-) e+ _: E3 L( Z1 g$ b
lating hormone level was 1.3 µIU/mL (both normal).; o! ~9 u* {* _$ ?( Z- ^1 e
The concentrations of serum electrolytes, blood9 R! E5 C8 Z8 U: l0 h9 F
urea nitrogen, creatinine, and calcium all were& `. t$ y* p0 k; G0 Z
within normal range for his age. The concentration; [' c. {+ [; J6 u( \( ^
of serum 17-hydroxyprogesterone was 16 ng/dL
8 g( q; r) W$ p# T" p/ d(normal, 3 to 90 ng/dL), androstenedione was 20
" k9 }% B  I7 r* ]/ Yng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-! @- g) `5 o, O0 d
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
2 v% M' B) F( n, H; edesoxycorticosterone was 4.3 ng/dL (normal, 7 to( V* I( f8 ]# \4 \6 Q% L  E' n
49ng/dL), 11-desoxycortisol (specific compound S)8 J9 V8 n/ s' a
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
; B5 ^* R0 g7 m5 stisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total* X9 o' W) u' o  c, m  ?, H9 P: y
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
( U2 n. Q: T1 c9 c' q$ C) q4 F# `and β-human chorionic gonadotropin was less than
1 Q2 t8 A8 ?6 S: a$ g6 M. P5 mIU/mL (normal <5 mIU/mL). Serum follicular
6 S  {) U9 X' k+ P5 s" j& jstimulating hormone and leuteinizing hormone
8 {1 b4 v( V, r; dconcentrations were less than 0.05 mIU/mL
% \: I, U3 a( g, L4 g1 L7 }/ h6 _(prepubertal).* M: A, L! N+ s/ h; o
The parents were notified about the laboratory/ M8 J: m' e: O7 m
results and were informed that all of the tests were# F8 j$ d; H; J- F1 K3 ]; K
normal except the testosterone level was high. The
- i( ?* o: U: c1 dfollow-up visit was arranged within a few weeks to
& O+ u+ ^% \! X5 ?$ Z" ^obtain testicular and abdominal sonograms; how-
6 J; G- w: K- B: ~: r. C5 H- oever, the family did not return for 4 months.
0 [; f0 {4 _# K# P& k% p+ r0 SPhysical examination at this time revealed that the% E) b, H( Q7 t- C- b
child had grown 2.5 cm in 4 months and had gained
; e% K/ x% R. P4 q  F2 kg of weight. Physical examination remained7 @! F( m* o9 U( b0 D. u$ Z( @" H
unchanged. Surprisingly, the pubic hair almost com-7 g, X. o; v- ?1 a+ Z
pletely disappeared except for a few vellous hairs at
( A/ Z/ ~# ]3 zthe base of the phallus. Testicular volume was still 2
9 A" a( o; ]) A( T; y; bmL, and the size of the penis remained unchanged.
3 L! n8 F8 `5 a5 G5 M$ V+ K5 t! sThe mother also said that the boy was no longer hav-
( J* P! ?( X6 m3 b( \ing frequent erections.6 k8 |; y8 A0 F# m- m) A9 ^, I
Both parents were again questioned about use of
! \: k5 f2 z  q; y) ^' }5 ^, `any ointment/creams that they may have applied to' l* w: P- j2 }0 R1 d+ l
the child’s skin. This time the father admitted the; d  n, O7 F' D- X% |1 Z
Topical Testosterone Exposure / Bhowmick et al 541
. {* O3 e/ x3 Luse of testosterone gel twice daily that he was apply-8 Z1 v; L4 a% U7 q2 O7 |
ing over his own shoulders, chest, and back area for
0 l( v) r$ {- ~- s  O: Na year. The father also revealed he was embarrassed
. c" `, j  Y/ m9 f) p1 w: fto disclose that he was using a testosterone gel pre-
8 v8 D: H( ]% X" [- K" Tscribed by his family physician for decreased libido- l9 d  ~! E" ]/ U
secondary to depression.
% o, x+ B& p' O: h1 N) s, P9 j$ v$ HThe child slept in the same bed with parents.
5 {6 u* o7 i+ f( U/ x9 ?The father would hug the baby and hold him on his
3 ^3 D. a7 L# P9 h% J) r  echest for a considerable period of time, causing sig-
) F0 z6 m) \" I" V0 O$ }2 [nificant bare skin contact between baby and father.
9 A1 j' d/ d5 uThe father also admitted that after the phone call,, a/ Q' M; J) N: l- b" m4 Q/ k; D
when he learned the testosterone level in the baby
0 s  ]+ L3 \! ?' Jwas high, he then read the product information" J% M' x* w" Q& ^8 ]
packet and concluded that it was most likely the rea-
: z# b2 o. m4 nson for the child’s virilization. At that time, they
- z7 Y, O2 L. f' F) ]decided to put the baby in a separate bed, and the0 S* e8 @6 z; v' o2 Y5 A
father was not hugging him with bare skin and had
. l1 }5 p; r4 J& s' J( q2 Kbeen using protective clothing. A repeat testosterone
* i4 i& X+ z" R; I2 `1 ?( Htest was ordered, but the family did not go to the, o3 k, g5 m. }5 w) k2 m( W
laboratory to obtain the test.
: [% q. U7 t* V; U) s' \, g' q* p% GDiscussion' A$ l6 r) H& ?. F; o, z
Precocious puberty in boys is defined as secondary7 W- ]3 [1 N/ r. e
sexual development before 9 years of age.1,42 Z- Z: H3 F+ o5 y
Precocious puberty is termed as central (true) when: V& y( q9 D" a; C& i. c
it is caused by the premature activation of hypo-
2 P; L; c! V- ~, _, A# A1 }thalamic pituitary gonadal axis. CPP is more com-
7 E: k; Z- \- l- p6 N' smon in girls than in boys.1,3 Most boys with CPP' V2 G- ?$ z  R; b- G4 l) m
may have a central nervous system lesion that is' l' u5 L+ W9 T3 X" d# U2 t" a
responsible for the early activation of the hypothal-
1 p/ K8 G+ T/ [* Q0 O- |' yamic pituitary gonadal axis.1-3 Thus, greater empha-
  l9 S0 x/ G& asis has been given to neuroradiologic imaging in
3 Y1 S9 T0 J7 j; m9 }! xboys with precocious puberty. In addition to viril-
& C0 G9 f, O% m* wization, the clinical hallmark of CPP is the symmet-
8 B- Y% f& @' srical testicular growth secondary to stimulation by
0 I- f; g2 E" H4 A. f3 Cgonadotropins.1,3
0 f2 z' K# a  k/ SGonadotropin-independent peripheral preco-, K+ v, u/ o2 s" F  v! Y
cious puberty in boys also results from inappropriate
' U- d, D5 e% d5 m6 [1 F# i8 ^* Y2 j0 u8 Landrogenic stimulation from either endogenous or( O; H3 i' b+ u. {$ O9 j
exogenous sources, nonpituitary gonadotropin stim-
. g" B5 V  j( W7 X) t" M7 Iulation, and rare activating mutations.3 Virilizing
7 q* b3 a+ F& j: k8 _! y% ?  Zcongenital adrenal hyperplasia producing excessive4 v# G, o2 Q6 o% [6 S0 h
adrenal androgens is a common cause of precocious7 u4 z* T2 f. W: m1 t8 J; e
puberty in boys.3,4* V" K7 J4 E4 M2 F+ c* e' L9 r
The most common form of congenital adrenal
9 D) T6 V% F" d2 z$ O) Bhyperplasia is the 21-hydroxylase enzyme deficiency.* a$ |! S6 J1 C' |) O
The 11-β hydroxylase deficiency may also result in
# q3 `/ Z% b+ }excessive adrenal androgen production, and rarely,
+ T% z/ P5 a: T% U, Gan adrenal tumor may also cause adrenal androgen
! v+ k, I1 Q$ L) o/ wexcess.1,3
7 W; w9 U7 J" M/ V1 jat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% L9 J& T0 Y% L$ p2 g% B
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007. J% J) k6 G: n. n9 y; H6 O
A unique entity of male-limited gonadotropin-
+ g6 o# G% a  ^+ N9 `* u8 j; Tindependent precocious puberty, which is also known
* H. Q6 ?& j; M2 f2 uas testotoxicosis, may cause precocious puberty at a& F! q' a0 d' |
very young age. The physical findings in these boys
, O4 ~2 a( P1 Ywith this disorder are full pubertal development,1 ^& t# P2 K0 T2 v8 m
including bilateral testicular growth, similar to boys9 C' j# T5 {8 r) ]
with CPP. The gonadotropin levels in this disorder
4 O: x# c8 k5 v0 }  Pare suppressed to prepubertal levels and do not show) A* |/ \3 Y+ q" z+ e3 ?
pubertal response of gonadotropin after gonadotropin-- N8 ^6 s4 e8 }
releasing hormone stimulation. This is a sex-linked
; b- E; `) p! b7 \" g  mautosomal dominant disorder that affects only
+ y) ~0 E1 {; J/ Zmales; therefore, other male members of the family+ u( ~1 q6 P" _9 A: x+ F& m
may have similar precocious puberty.3
' [" J" r$ Y. a# AIn our patient, physical examination was incon-
# j; Y: s8 Z& e6 asistent with true precocious puberty since his testi-
! ^. a+ V% `; X9 x0 Rcles were prepubertal in size. However, testotoxicosis
7 Z) X, z# |: a  Lwas in the differential diagnosis because his father
1 l" n% R- Y/ M1 g2 Lstarted puberty somewhat early, and occasionally,/ k% h1 I: Q4 Z) i
testicular enlargement is not that evident in the% [/ c3 e! n7 T( a; U) A
beginning of this process.1 In the absence of a neg-+ ]/ [5 o. B* c! T* ?! J
ative initial history of androgen exposure, our' P0 }' W* k1 U0 q4 v4 a/ M* N
biggest concern was virilizing adrenal hyperplasia,% H8 A6 ?: X6 |( Q0 A$ d
either 21-hydroxylase deficiency or 11-β hydroxylase
$ L4 ^# _# p" Z1 ?  ~$ o. J: ]deficiency. Those diagnoses were excluded by find-5 @7 @+ n! b  e  G; ?- _
ing the normal level of adrenal steroids.
* R: ^9 |9 d0 n' R- q/ tThe diagnosis of exogenous androgens was strongly3 \$ E) |& X. A2 m/ x' T
suspected in a follow-up visit after 4 months because' J0 a+ h& |8 a/ k0 u1 R9 W) ?  s
the physical examination revealed the complete disap-$ {# U/ ~+ _' d8 t
pearance of pubic hair, normal growth velocity, and9 C$ `+ i; n' F8 f7 [$ p/ m$ h+ e
decreased erections. The father admitted using a testos-
) M0 h/ C6 j# Jterone gel, which he concealed at first visit. He was
3 z' [$ N, U0 T* M. a- K; Ousing it rather frequently, twice a day. The Physicians’/ x5 V7 Q* T. f. E
Desk Reference, or package insert of this product, gel or) j/ A: B. e4 b* n0 e( u
cream, cautions about dermal testosterone transfer to
& u2 c! [/ U5 yunprotected females through direct skin exposure.
* e/ g' @, w3 C: k4 F5 LSerum testosterone level was found to be 2 times the  P+ h" R* ?' U3 X2 d
baseline value in those females who were exposed to; z( ^: ^) o! Z6 e8 |: G, u; L( b! C6 q
even 15 minutes of direct skin contact with their male
6 ~0 z& K6 E& N3 z2 X# J5 Q# Lpartners.6 However, when a shirt covered the applica-2 }2 }' o' ], v! @  a! k
tion site, this testosterone transfer was prevented.
; E: t$ e  Q* _5 _Our patient’s testosterone level was 60 ng/mL,
* V0 V. Y4 ]2 Kwhich was clearly high. Some studies suggest that1 Q5 }6 p; y2 O$ p
dermal conversion of testosterone to dihydrotestos-! x0 T4 C+ B+ m* j0 J* {
terone, which is a more potent metabolite, is more5 Y  m5 I5 J9 k4 t8 _
active in young children exposed to testosterone
9 {5 p& _) {6 {4 Hexogenously7; however, we did not measure a dihy-
/ |, H$ v. E* `8 ^drotestosterone level in our patient. In addition to
4 Z. N2 F9 ~& s! Y8 `virilization, exposure to exogenous testosterone in, P- U7 ^. R9 \4 x  l' ~) B, G
children results in an increase in growth velocity and
' X  R, Q: K4 s0 z$ oadvanced bone age, as seen in our patient.$ }9 h+ ^8 \5 ]6 T; F+ Y  c
The long-term effect of androgen exposure during
3 A( t5 x4 L6 Y) M7 X7 Nearly childhood on pubertal development and final( E( F+ u+ X! ~  ]) c, i
adult height are not fully known and always remain
! V& X( e% t; N# j# Ba concern. Children treated with short-term testos-* G2 t- T% X$ r* k( f# f
terone injection or topical androgen may exhibit some
- z3 V; |" T& O5 ~7 Macceleration of the skeletal maturation; however, after
7 g4 r* z* U' x6 P5 p8 ecessation of treatment, the rate of bone maturation
3 x4 u* P+ k  M5 f; h, Y) b* x* A* z0 pdecelerates and gradually returns to normal.8,90 U+ w. J9 _6 _
There are conflicting reports and controversy( [2 U& e* d- i( z- b
over the effect of early androgen exposure on adult; c$ N$ ]0 b( i) V, h$ p$ e
penile length.10,11 Some reports suggest subnormal/ h9 G8 [' a6 {1 p
adult penile length, apparently because of downreg-
3 Q. e- z! c8 z/ P0 a- Fulation of androgen receptor number.10,12 However,3 i/ K4 S. O2 S, D* Y3 q
Sutherland et al13 did not find a correlation between- B$ C8 g; T: H% a0 e) ?( U, `
childhood testosterone exposure and reduced adult
- ]0 \: W; a3 z; \3 p% y$ Hpenile length in clinical studies.
8 N8 g5 R+ L7 w- N) RNonetheless, we do not believe our patient is0 U/ {3 g1 {' C7 E; K
going to experience any of the untoward effects from. @2 p. `& Y, J) k& D
testosterone exposure as mentioned earlier because9 ~0 n5 Y# i' v2 Q
the exposure was not for a prolonged period of time." n; l+ ]& J5 q& L) ?. L, h
Although the bone age was advanced at the time of
0 V2 k& w: w( }. v, Z' [diagnosis, the child had a normal growth velocity at
5 D5 g$ _" ]! uthe follow-up visit. It is hoped that his final adult1 a/ L) `" ]3 s# `: a. A# @) u. [
height will not be affected.
7 `. c9 u2 V; Q5 S" dAlthough rarely reported, the widespread avail-7 w; @  q5 F3 T  G2 [# P5 x  J0 }( _
ability of androgen products in our society may
& f& h: }& M/ p$ S, t2 z0 \indeed cause more virilization in male or female
0 Y# D! W: m, i8 F. T" {children than one would realize. Exposure to andro-
& Z, I( r( p* r0 ]% s6 Bgen products must be considered and specific ques-5 m* f  }4 B2 K5 ^( U
tioning about the use of a testosterone product or
( l; r8 u7 y3 Y/ Z' p, }gel should be asked of the family members during' x0 y6 M4 r, F4 `2 @; E
the evaluation of any children who present with vir-
8 j, l4 C1 h* Y1 e0 D, U6 Ailization or peripheral precocious puberty. The diag-- w# ]4 A; w! h" T4 Y
nosis can be established by just a few tests and by  Q  d5 a- i- z
appropriate history. The inability to obtain such a9 a9 @( _5 I; @' Y0 s7 X8 G5 O' h
history, or failure to ask the specific questions, may
5 M, `  W6 B) G0 Gresult in extensive, unnecessary, and expensive
* u/ Y# e! g6 ^6 k! B" finvestigation. The primary care physician should be7 T6 _* N) A4 ~0 M: [' i' x
aware of this fact, because most of these children
, z" ]$ M* u) Y, `8 g$ smay initially present in their practice. The Physicians’
# T) C" Q6 K* mDesk Reference and package insert should also put a
7 N. R" f2 \9 C! m. Mwarning about the virilizing effect on a male or
2 D* z& \9 Z2 ~0 V0 o1 \9 {female child who might come in contact with some-
' Q+ Z. J, X7 R# ^one using any of these products.
9 {( k! e. N0 P8 [" U! pReferences
' z- Y- W; R4 m. Y9 A1. Styne DM. The testes: disorder of sexual differentiation7 C$ u7 F6 w, j1 h
and puberty in the male. In: Sperling MA, ed. Pediatric' s4 r# L3 F- p: X  U4 M
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
: Q6 n$ T) C" _2 u2002: 565-628.9 G6 M; z1 G' g" T! a
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious5 J6 a9 O0 P! X9 ~7 \; q
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old0 K8 G( W: S! r! V) E  a6 j
Boy Induced by Indirect Topical% I  g& ?1 f$ r( @
Exposure to Testosterone! p5 `* {5 V8 j( o0 R% A( b2 O
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
4 l4 U# z+ t/ |and Kenneth R. Rettig, MD1
9 C6 Y6 O4 e' B# a: wClinical Pediatrics
2 u" y" m1 |2 u# {- O$ MVolume 46 Number 6
; }" K) G) m* Z+ b! W1 {July 2007 540-543
  ~& s1 ]% h1 D2 G© 2007 Sage Publications: ^4 E! v  ~; ^. l( o  `1 Z# H
10.1177/0009922806296651
- Y$ ?) u; G! |4 F' E, i) [http://clp.sagepub.com3 I+ S; J; O# U/ l
hosted at
; j' n6 l! W! V. r) L% vhttp://online.sagepub.com
) p" a# S3 H) c% K0 o, z+ PPrecocious puberty in boys, central or peripheral,
: ?# K  ?& ^3 u- qis a significant concern for physicians. Central
) U1 L& m( o1 Uprecocious puberty (CPP), which is mediated
0 M/ }) O; T9 Y6 [; h8 T; j" G' G4 Y" Ythrough the hypothalamic pituitary gonadal axis, has( c2 M9 z: b8 A# ^( f7 ]+ U. {8 u
a higher incidence of organic central nervous system
' Y. v- T$ d- ?8 f* N* p  L2 ilesions in boys.1,2 Virilization in boys, as manifested
$ u- L; ]3 [& U8 c7 aby enlargement of the penis, development of pubic
% X: ~4 j. j2 Xhair, and facial acne without enlargement of testi-' T2 w7 l: w8 q% k- t
cles, suggests peripheral or pseudopuberty.1-3 We5 l- I2 z) r* J2 H
report a 16-month-old boy who presented with the
4 k% O: R" b: d' E/ Q. M" |enlargement of the phallus and pubic hair develop-
( M) S+ M5 g  E4 c( t) L4 ]ment without testicular enlargement, which was due
9 K! l2 b( e" H/ y3 z# I3 ^to the unintentional exposure to androgen gel used by& X7 Q8 x+ x: Q% ]( k
the father. The family initially concealed this infor-
% u4 `) {$ w$ r% Y% E1 w7 o1 nmation, resulting in an extensive work-up for this3 {* a# P; O2 A; y8 }% M# d
child. Given the widespread and easy availability of/ L( E, U" g+ F$ x1 T3 r, q
testosterone gel and cream, we believe this is proba-5 d+ E1 X& a  v) G- V/ l0 x; Z
bly more common than the rare case report in the
3 d3 X  x6 P/ Dliterature.4( e8 U) p7 [5 K4 L4 [- H7 `
Patient Report
7 h$ M" q+ t3 ?- q: n3 ]5 eA 16-month-old white child was referred to the. |& t5 I! {+ T  w. E  y$ z/ J
endocrine clinic by his pediatrician with the concern
* L$ B0 m: k( B2 G6 eof early sexual development. His mother noticed. U: V' p5 a) m7 w$ r0 `) y
light colored pubic hair development when he was
0 E- B0 H% e5 U/ w8 eFrom the 1Division of Pediatric Endocrinology, 2University of# ], v. U' L% M- G
South Alabama Medical Center, Mobile, Alabama.
; ?+ c# k3 Z& i% N& t+ B6 m3 l8 AAddress correspondence to: Samar K. Bhowmick, MD, FACE,
6 G/ _; l2 E( c& v7 e9 kProfessor of Pediatrics, University of South Alabama, College of9 N$ u9 @* B3 h! E% y
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;- U3 X. N9 z" n( N1 P
e-mail: [email protected].# _! B+ W8 {8 K" y0 g
about 6 to 7 months old, which progressively became
7 E( h- _3 b0 P, Z$ \darker. She was also concerned about the enlarge-# h/ H2 L: N' ]: C" v6 U0 O- @
ment of his penis and frequent erections. The child( a& Y- D$ v: ]! O! z  b1 E
was the product of a full-term normal delivery, with8 {4 k* T; a, Q2 F9 S: i
a birth weight of 7 lb 14 oz, and birth length of
9 A( H; T% i3 S% u) |0 F. G" ]20 inches. He was breast-fed throughout the first year
, ^9 j+ V! r& p, P: y5 A0 O8 eof life and was still receiving breast milk along with, E% Z1 x- M7 x( }6 _1 H; y% g
solid food. He had no hospitalizations or surgery,
$ k  x) I8 b6 \+ l* O/ @. l2 {and his psychosocial and psychomotor development$ _4 i, F; D4 i2 N- W  N
was age appropriate.' {% @9 A4 Q5 V! J6 ~7 X
The family history was remarkable for the father,
2 y0 T, k0 m% O* `; {who was diagnosed with hypothyroidism at age 16,
$ \6 E' a" q/ {, F! Iwhich was treated with thyroxine. The father’s
' M& c; W" w7 U4 j3 Wheight was 6 feet, and he went through a somewhat
7 J0 E( @& p! }0 b; Cearly puberty and had stopped growing by age 14.$ p# X: a  M7 e
The father denied taking any other medication. The
6 e  C: }0 T% U# {! ichild’s mother was in good health. Her menarche
) s4 N* l7 }/ C$ u. jwas at 11 years of age, and her height was at 5 feet  E# S1 m. m4 J& E- V
5 inches. There was no other family history of pre-: d: X% w; j% H; H) D# f9 W
cocious sexual development in the first-degree rela-2 D& r! c4 r9 ~! P
tives. There were no siblings.
) W& p  Q! h1 C) h/ JPhysical Examination. _2 Y% q- W; U$ Q& ^( }
The physical examination revealed a very active,
2 L7 P1 c% N5 Z3 m; J, F3 pplayful, and healthy boy. The vital signs documented8 s! A3 Q3 y! [! Z
a blood pressure of 85/50 mm Hg, his length was/ ]  c; p# w$ a( D+ ^% i& `
90 cm (>97th percentile), and his weight was 14.4 kg
5 P* `6 x# ]9 E: ]* E(also >97th percentile). The observed yearly growth
4 E1 G7 Y+ w2 [% z0 q! kvelocity was 30 cm (12 inches). The examination of
! e$ v+ D1 `( _0 u; L: K# d. tthe neck revealed no thyroid enlargement., H8 w3 q: a' b; _6 a# `) B
The genitourinary examination was remarkable for8 t: g) ~& q' b) q
enlargement of the penis, with a stretched length of
# K9 o  x6 _; u5 S$ n8 K8 cm and a width of 2 cm. The glans penis was very well. e5 T+ e" u  G0 t% L# F% D: L
developed. The pubic hair was Tanner II, mostly around  c: S" |. C$ r) ?/ i+ K
540
# X4 C7 w6 A5 t+ p' V4 B$ qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& \4 h# q2 s) B) V$ |* |3 z5 Dthe base of the phallus and was dark and curled. The# A& R4 @% j; e
testicular volume was prepubertal at 2 mL each., Q; V/ ?/ o. u0 T1 U& R
The skin was moist and smooth and somewhat
* L( B! e7 L, G9 n4 S3 m. ioily. No axillary hair was noted. There were no5 L# O3 L! y& t# l4 Q
abnormal skin pigmentations or café-au-lait spots.( D# \( N& d( H5 @- J* E
Neurologic evaluation showed deep tendon reflex 2+) `3 z( f' J4 E8 [( N7 \/ a5 ~. a
bilateral and symmetrical. There was no suggestion
0 t$ ?! R1 H& {) x" kof papilledema.% q8 I! d% i" I- i# t, E. p
Laboratory Evaluation
; ~* x- Y6 A! t* @" n% c7 z* EThe bone age was consistent with 28 months by6 o1 [  h  T2 c$ b- t# F) T+ j, n
using the standard of Greulich and Pyle at a chrono-2 b5 d- r, ?- V* F5 X% z- h
logic age of 16 months (advanced).5 Chromosomal
# t' n1 N. X' w: _3 ?' {5 T, |( d1 Kkaryotype was 46XY. The thyroid function test# u6 `6 P- b& B& F/ {4 @5 n
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
6 k! C$ [6 s: g2 ~" E% rlating hormone level was 1.3 µIU/mL (both normal).! B) c- R6 s9 M* R0 v' h
The concentrations of serum electrolytes, blood
& P/ l) t4 o" t1 r5 q$ Y* ]4 z2 Y& ?urea nitrogen, creatinine, and calcium all were
7 O3 y  Q; J2 B; c+ pwithin normal range for his age. The concentration
; r3 q1 w2 D0 ~2 n* Y( N- E" qof serum 17-hydroxyprogesterone was 16 ng/dL
" P+ B# G. X. `) k0 C$ I(normal, 3 to 90 ng/dL), androstenedione was 20
, R5 c: U  S8 q! `ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
- p0 C% Q3 }8 i- c/ L- eterone was 38 ng/dL (normal, 50 to 760 ng/dL),
; |) m; C; A2 d2 }; tdesoxycorticosterone was 4.3 ng/dL (normal, 7 to) i; g0 w' A6 d/ Q$ B
49ng/dL), 11-desoxycortisol (specific compound S)) Q: c/ w$ a' ^6 G3 ]
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
' i, E6 l5 V& g, l) L4 k' ]tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
3 w- t: P5 u" y" P& htestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
# V. Q. _6 L5 @5 iand β-human chorionic gonadotropin was less than
' ]" |- W; r; O# y4 h6 X/ ]5 mIU/mL (normal <5 mIU/mL). Serum follicular: X6 A: E# I* B8 ?( A. B) K
stimulating hormone and leuteinizing hormone1 J0 Z% L' E- t0 n
concentrations were less than 0.05 mIU/mL& m% m* D$ X1 V: N
(prepubertal).: b" _8 @$ @6 @1 N2 w5 Z$ Z
The parents were notified about the laboratory2 H- v" O9 ^: G( t! f: n0 X$ I
results and were informed that all of the tests were; y' _( O2 y& ?# A6 n
normal except the testosterone level was high. The& X3 t( A& E- C
follow-up visit was arranged within a few weeks to
# M# j  V" }2 s, v5 T5 z% A. Aobtain testicular and abdominal sonograms; how-0 l# M' V( {9 H6 i1 W9 G
ever, the family did not return for 4 months.3 W) B5 V: c$ g9 L5 E
Physical examination at this time revealed that the
# y3 {2 a  V6 @& e2 y, Vchild had grown 2.5 cm in 4 months and had gained
4 S* j! }" h, S: u2 kg of weight. Physical examination remained
$ X  |8 h4 V' e  I. L! g) Qunchanged. Surprisingly, the pubic hair almost com-6 l6 q0 p" O/ E  x  ^2 {
pletely disappeared except for a few vellous hairs at) P* ~6 ^7 h4 Q4 D
the base of the phallus. Testicular volume was still 2
7 s( ]' c, b' Z# _) k! @mL, and the size of the penis remained unchanged.
" F5 C( h6 v' z, u3 jThe mother also said that the boy was no longer hav-0 L, ~& ~7 o9 r2 c' B, N' C
ing frequent erections.# ~7 X: A* |& a9 m" O* v
Both parents were again questioned about use of
3 G, n# j$ f" r' Vany ointment/creams that they may have applied to* e/ p& h. a) ?, D  X
the child’s skin. This time the father admitted the
0 d( k4 P+ m% k/ zTopical Testosterone Exposure / Bhowmick et al 541' a1 {0 d8 G/ J& A$ d3 E
use of testosterone gel twice daily that he was apply-2 m% x6 j4 N6 H4 s( \  B  T
ing over his own shoulders, chest, and back area for% l! e/ Q# g* m( Z
a year. The father also revealed he was embarrassed
, h6 o- k2 Y# q8 T$ sto disclose that he was using a testosterone gel pre-0 ?4 l" ~# s8 d, g5 [) c3 x/ }- e
scribed by his family physician for decreased libido
* @3 J$ N5 m" O8 Z3 f" Gsecondary to depression.7 C6 s3 E' c- j% G8 S  Y* w
The child slept in the same bed with parents.) ?. d- F7 j0 w5 F1 m
The father would hug the baby and hold him on his
( E( F+ i( ~8 Gchest for a considerable period of time, causing sig-
( V' K( |7 z: N+ K, F+ t1 pnificant bare skin contact between baby and father.
1 s$ _6 ^2 U+ y$ o1 V: d: dThe father also admitted that after the phone call,
( s# _8 w2 \# e! n3 D' ~when he learned the testosterone level in the baby$ X3 M, [) Z) b- Y/ K
was high, he then read the product information3 `( f3 |4 a9 g9 h3 p$ ^
packet and concluded that it was most likely the rea-
0 j5 s& n" N# x& I6 vson for the child’s virilization. At that time, they
3 P' D% w: x9 ?5 U! Z$ Adecided to put the baby in a separate bed, and the  D7 S1 H# P7 P: k) z$ a
father was not hugging him with bare skin and had3 Z, U0 r+ c. g5 a2 H; y( x
been using protective clothing. A repeat testosterone
8 C8 l' p2 Q" A+ {3 @3 {8 N# ?' l) Atest was ordered, but the family did not go to the
) W. y% H3 |! U. I6 B  j$ S6 P- rlaboratory to obtain the test.
- M: h( f0 N$ r( w) N2 V: PDiscussion- K( `1 C  y7 R  i0 R
Precocious puberty in boys is defined as secondary: X9 E  |9 ]8 P# o) o4 s5 [
sexual development before 9 years of age.1,41 B- Q! {" Q9 k
Precocious puberty is termed as central (true) when/ |, \2 r# N! t+ s, d5 b
it is caused by the premature activation of hypo-' T9 l) P# b$ j
thalamic pituitary gonadal axis. CPP is more com-, D/ T# |: `2 S$ j
mon in girls than in boys.1,3 Most boys with CPP
3 R  l/ M8 E2 \* {0 L& v6 E- \may have a central nervous system lesion that is7 z2 e. q) ?' Q2 o) D2 C1 E
responsible for the early activation of the hypothal-, n( r) Q6 g9 Z2 k" Q5 Z, _2 _
amic pituitary gonadal axis.1-3 Thus, greater empha-& l* F& ?+ f7 m* |+ d+ Z
sis has been given to neuroradiologic imaging in
4 p3 h' M! b: d* E* E& t- \6 Wboys with precocious puberty. In addition to viril-
. E! e! O  R. V4 A5 a; Vization, the clinical hallmark of CPP is the symmet-% y* h7 j7 m$ u# t( c$ d( W
rical testicular growth secondary to stimulation by8 |; \; R% X" {" l! c* K
gonadotropins.1,3
0 m( B2 O$ E7 W* H1 [Gonadotropin-independent peripheral preco-, h- a8 l  }4 z6 m* x5 D" u3 c- D7 T
cious puberty in boys also results from inappropriate
' w2 U/ i' k' R& p, N; xandrogenic stimulation from either endogenous or
0 ], P, u2 n; V3 j7 a2 p' u( yexogenous sources, nonpituitary gonadotropin stim-/ n* ?! l9 ?; N# K$ T
ulation, and rare activating mutations.3 Virilizing% {0 x8 g* M( V( {" g
congenital adrenal hyperplasia producing excessive
' Y1 h9 h1 r9 j$ S1 w. I) Padrenal androgens is a common cause of precocious
2 z5 f3 q3 ~8 ipuberty in boys.3,4: h" i# @3 ]4 y4 t, W* L
The most common form of congenital adrenal
5 K6 j& Y) [* v  jhyperplasia is the 21-hydroxylase enzyme deficiency.
5 m( l- q: J2 qThe 11-β hydroxylase deficiency may also result in
% T% X5 C/ L% C7 |4 z  q; C' yexcessive adrenal androgen production, and rarely,) k' J9 i& d& w+ u9 `
an adrenal tumor may also cause adrenal androgen: ?& \, }& n8 e! `
excess.1,31 ]% I3 y" t; O1 r' z. D; Q2 E" C
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 E/ g% a% W! D& v* H) F/ @
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007. V* G) \0 I3 p
A unique entity of male-limited gonadotropin-* P! `1 k* V# p$ I$ ]3 [( w
independent precocious puberty, which is also known
7 o/ |0 e6 f- y' e% V& X* ?1 H& ^5 b  Sas testotoxicosis, may cause precocious puberty at a
) \$ A3 ~* H8 M8 Y3 g$ y' Zvery young age. The physical findings in these boys2 ]2 a. [% r! v) m. d8 N" C8 x$ |  u
with this disorder are full pubertal development,+ Y, S* S+ Z6 k1 X( J3 s/ }7 Q
including bilateral testicular growth, similar to boys
* v- ~. H8 ?3 x& B( i) Z0 l1 X0 `" C0 ^with CPP. The gonadotropin levels in this disorder4 o" t0 U- T4 b4 g
are suppressed to prepubertal levels and do not show
- X2 s/ w3 w0 L; Epubertal response of gonadotropin after gonadotropin-( A( ]) ]" T2 F6 C
releasing hormone stimulation. This is a sex-linked# r0 D2 P& L# W: O- R( c$ x
autosomal dominant disorder that affects only
0 f, N# W% z2 z) s; y% E( Wmales; therefore, other male members of the family( D% P! j5 Q$ f) B. L0 s1 O
may have similar precocious puberty.3( A1 Y0 |" V8 x
In our patient, physical examination was incon-5 g. G& A8 i. ?6 D; V, N: [
sistent with true precocious puberty since his testi-1 g8 f+ ]. G, }- q0 ~4 U2 k: M3 K
cles were prepubertal in size. However, testotoxicosis- @( W" `" C# P9 ?  H
was in the differential diagnosis because his father+ p( R& ?! Z8 W1 v
started puberty somewhat early, and occasionally,
$ F+ L, I/ \& {testicular enlargement is not that evident in the, V( z3 U1 ^( M. n7 I- }2 e) u
beginning of this process.1 In the absence of a neg-
9 B: ~2 G! d( b/ N" G3 Q  oative initial history of androgen exposure, our0 k  |& q  K& |5 V
biggest concern was virilizing adrenal hyperplasia,8 P+ `5 B2 R0 K' k: Y+ J
either 21-hydroxylase deficiency or 11-β hydroxylase
$ P8 b/ W, O& g! K( i* rdeficiency. Those diagnoses were excluded by find-% @/ x% I5 K6 n. y2 W( x
ing the normal level of adrenal steroids.. P8 x: I: U' A6 |  t# v; p" q
The diagnosis of exogenous androgens was strongly& ?+ g  O. ~; Q# e+ |& `8 E/ b
suspected in a follow-up visit after 4 months because0 B" d/ w5 \) V, `- z2 R) V
the physical examination revealed the complete disap-
$ g# w6 H* Z" c( vpearance of pubic hair, normal growth velocity, and! a+ Y# n+ d6 D' G$ G8 ~
decreased erections. The father admitted using a testos-
# {& ]1 b0 @4 T0 ?5 ^terone gel, which he concealed at first visit. He was8 f' o1 Y7 Y" W# F; Z# [
using it rather frequently, twice a day. The Physicians’/ o1 V- o2 F# s8 n/ b: T; d
Desk Reference, or package insert of this product, gel or
4 h( R: [7 I% i7 p* K! r1 f5 E8 ~$ @; acream, cautions about dermal testosterone transfer to) X/ u$ A, X/ Z) b
unprotected females through direct skin exposure.& L1 b$ y3 J& g/ b# |. e2 a
Serum testosterone level was found to be 2 times the3 l+ a) u: I& \+ P. [
baseline value in those females who were exposed to
  }% H" b/ C' K4 i1 ~: Teven 15 minutes of direct skin contact with their male
0 U. f( L4 ]4 H% z% k1 ppartners.6 However, when a shirt covered the applica-
5 n) z0 w2 x9 S" C" I& u/ X% b2 ltion site, this testosterone transfer was prevented.
; A5 C$ j0 b9 E# NOur patient’s testosterone level was 60 ng/mL,
8 R4 G" g# k- J8 x9 A5 Qwhich was clearly high. Some studies suggest that
+ B& t  r0 O* L6 Wdermal conversion of testosterone to dihydrotestos-
/ R) o8 c7 u9 `! lterone, which is a more potent metabolite, is more
. s3 Z6 f( W- V2 e6 N& ?active in young children exposed to testosterone
3 z0 J3 p& P, s6 D  a9 }, Yexogenously7; however, we did not measure a dihy-
- d& M  G* L  g2 _. Qdrotestosterone level in our patient. In addition to
0 P% v* H3 Y. ^' ^0 ^3 ~; c0 Cvirilization, exposure to exogenous testosterone in
) q# p  @. f. V9 i" {: ~children results in an increase in growth velocity and4 a+ j6 T  \: z, r" ?" j; Z" q
advanced bone age, as seen in our patient.# M4 A2 _: C( f
The long-term effect of androgen exposure during
: u' n: w3 T, E; A* @& {, D0 T4 @early childhood on pubertal development and final
6 h6 S5 P3 x# ^$ [" \( kadult height are not fully known and always remain& u% U, |! d+ O9 S1 g! P6 E
a concern. Children treated with short-term testos-% c3 \# s# g8 q2 ]% \2 s; v, O! h% P
terone injection or topical androgen may exhibit some) z& D' N7 a! i% c5 N& Z
acceleration of the skeletal maturation; however, after
! [& q2 U0 I0 M4 F% t8 pcessation of treatment, the rate of bone maturation# c9 L" Y- q3 }8 g3 b  T
decelerates and gradually returns to normal.8,9. {' ^/ \; r2 b' {0 o6 D
There are conflicting reports and controversy1 m1 ^; Q! m" r1 H3 Z
over the effect of early androgen exposure on adult
) h. w0 {* s0 Fpenile length.10,11 Some reports suggest subnormal
% @# P& u" f9 y) [1 B0 U, l' Sadult penile length, apparently because of downreg-- L6 B8 x7 W2 q/ Y4 T5 Y- O
ulation of androgen receptor number.10,12 However,
. J& G1 o$ C2 vSutherland et al13 did not find a correlation between4 x( p; A' I' A: Y
childhood testosterone exposure and reduced adult
4 V. o7 v9 ]- A& x2 X0 U: M& _penile length in clinical studies.- l" N$ B( _0 a
Nonetheless, we do not believe our patient is
4 w' I' {% ]  l; t; v* j/ bgoing to experience any of the untoward effects from
! a* E% f! c# Z/ l+ O" [. _testosterone exposure as mentioned earlier because
$ V: y' y! X/ |' othe exposure was not for a prolonged period of time.
2 N" ~7 q. D; i* k+ tAlthough the bone age was advanced at the time of( r' w9 i/ w, i, A
diagnosis, the child had a normal growth velocity at
2 L- \7 A0 D( T9 P4 fthe follow-up visit. It is hoped that his final adult; d/ p5 [  q' J+ A  U' F9 b
height will not be affected.+ ^2 V' ?) j0 G
Although rarely reported, the widespread avail-
: B& s  l2 s" N" Y9 sability of androgen products in our society may7 l; `4 G0 w$ ]2 P# \3 e/ y7 B3 _
indeed cause more virilization in male or female3 [# H# e$ B( J2 \  p
children than one would realize. Exposure to andro-9 p& H' E9 I6 X" ]; i4 k
gen products must be considered and specific ques-; k$ {  U! v6 ]: K
tioning about the use of a testosterone product or
+ R- P; s' j5 }gel should be asked of the family members during
: Y8 Q" e6 Z1 Z- J  jthe evaluation of any children who present with vir-4 H' `9 q, z1 a  u3 n* B
ilization or peripheral precocious puberty. The diag-
1 O# W0 p0 G8 Tnosis can be established by just a few tests and by
0 R" r) W/ ~. b2 c' V: }6 i; lappropriate history. The inability to obtain such a
! U1 H( w  e! h/ S% o6 W# qhistory, or failure to ask the specific questions, may" a+ M) y' k8 c# L' Q/ M
result in extensive, unnecessary, and expensive
( B! V) Q2 E7 }) L0 [. B8 Z. Ainvestigation. The primary care physician should be
/ J: T/ |0 y' G: \2 jaware of this fact, because most of these children
' c/ B3 |4 ~) nmay initially present in their practice. The Physicians’
* p( b9 J( Z4 H7 \+ @% _0 p' }Desk Reference and package insert should also put a$ N; x! R) T; U
warning about the virilizing effect on a male or
- \- r# x4 a- @1 L7 wfemale child who might come in contact with some-
" a& i8 Q  h+ C& m3 Y, v6 U9 B4 q8 Qone using any of these products.# W, {0 o. }! f0 t2 c7 ]- C: S& m
References6 v7 c* R  J& j6 ^9 b, P9 [
1. Styne DM. The testes: disorder of sexual differentiation- z4 {* T2 b: @. q
and puberty in the male. In: Sperling MA, ed. Pediatric
1 n0 H. Q' r% o" A8 fEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
) t$ c3 X' x, o5 `% T% z, ~2002: 565-628.
, V+ u2 L3 R) k2 ~3 Q( Q2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious+ A5 [1 z5 A" z( t
puberty in children with tumours of the suprasellar pineal
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這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

9 E/ ^8 }* m5 a% a( C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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