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Sexual Precocity in a 16-Month-Old: x$ a. g" [, @1 M. {4 B
Boy Induced by Indirect Topical
0 v/ r4 h( a" U9 NExposure to Testosterone4 }" e& c8 a) W) E( N# I- F5 L
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2' w$ V' V% B) K7 J7 t: e
and Kenneth R. Rettig, MD1
% z/ ~, d; o7 K8 _! N: Z) pClinical Pediatrics
* a! C- H) h. R$ N" X2 G5 gVolume 46 Number 6  b; P2 ]# ?" R
July 2007 540-543: p! I/ N' q) e, _- S) `+ `: V  G$ V
© 2007 Sage Publications
4 D  `2 B4 B+ K" u& B6 i, B2 Z10.1177/0009922806296651( }! }  R' q. ]2 Z5 O
http://clp.sagepub.com
* v. u7 o6 C' o3 L% ~/ Mhosted at
1 N- v  y! z6 A- q* w' fhttp://online.sagepub.com- x8 k! M6 |5 C' F
Precocious puberty in boys, central or peripheral,4 Z$ T+ e# B/ K! s* h- Y
is a significant concern for physicians. Central
4 i- b/ n+ A/ Yprecocious puberty (CPP), which is mediated2 g* C7 G; u9 z# t0 P0 G" D# ^2 R
through the hypothalamic pituitary gonadal axis, has* G9 q" z/ S7 P3 T
a higher incidence of organic central nervous system7 u5 i9 J& @; N$ p' D1 u" j8 p
lesions in boys.1,2 Virilization in boys, as manifested
! v7 E7 n: _' G/ t& w- rby enlargement of the penis, development of pubic: E9 D4 x$ z; r" `% V  P0 j
hair, and facial acne without enlargement of testi-
' z# a2 W1 {# W3 z2 O9 Icles, suggests peripheral or pseudopuberty.1-3 We
4 Z+ B7 m3 `1 P& ~, `report a 16-month-old boy who presented with the
: f4 n; j8 }" j, ?- penlargement of the phallus and pubic hair develop-  I: h3 t+ O$ M$ ?
ment without testicular enlargement, which was due: G3 R0 Q' K6 \, u* @  T. D
to the unintentional exposure to androgen gel used by" K  M8 K3 q4 T. g# y6 i
the father. The family initially concealed this infor-6 u/ u7 g3 ^% s4 A5 \9 W
mation, resulting in an extensive work-up for this5 l! q% \" Q8 V5 b
child. Given the widespread and easy availability of- N7 ?' S. q: m$ Q2 g- s+ y
testosterone gel and cream, we believe this is proba-6 v5 T2 }' J3 x5 I  z
bly more common than the rare case report in the8 W  v+ d' q7 e4 F, W. A8 G" o
literature.4
5 {/ U4 y7 L+ \; H) [Patient Report
, ^+ V4 C% A" b8 Y- |0 MA 16-month-old white child was referred to the
/ `$ l" P9 ]2 c1 P: ~4 bendocrine clinic by his pediatrician with the concern
  _5 y* e2 o  @of early sexual development. His mother noticed8 K, R) G, l" T1 }' [
light colored pubic hair development when he was- x# o4 s3 s; a1 Z( ]: T
From the 1Division of Pediatric Endocrinology, 2University of
/ `- u4 D/ n2 h; s$ e5 t4 F% n. g0 S$ @South Alabama Medical Center, Mobile, Alabama.
- k/ W5 K$ v8 k' U0 W, z3 I7 L. jAddress correspondence to: Samar K. Bhowmick, MD, FACE,8 M+ a$ `1 h$ o0 Y, ]! l
Professor of Pediatrics, University of South Alabama, College of
5 V) i  J/ g  x: q7 W+ L  AMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
. O; T- L: ^4 u; s0 @& q' L0 We-mail: [email protected].
1 A2 m2 A' X! d7 m2 N" Tabout 6 to 7 months old, which progressively became" W- o" b2 H+ g: ~# N. m
darker. She was also concerned about the enlarge-
8 X$ p; z( {3 H- o! xment of his penis and frequent erections. The child
4 G6 G% f" f; r! [# bwas the product of a full-term normal delivery, with* i3 S( y5 y3 O. P! {
a birth weight of 7 lb 14 oz, and birth length of4 W- ?) v2 ]' W4 K- M* y$ b
20 inches. He was breast-fed throughout the first year
$ g: R8 t3 S5 u' m9 A- kof life and was still receiving breast milk along with
4 H* }$ n- H$ E% }) ^+ x, `0 E; w8 \solid food. He had no hospitalizations or surgery,) B9 {# V. d" _3 ?) r" z
and his psychosocial and psychomotor development! T8 p/ ~9 R$ j( L4 L
was age appropriate.4 [2 z1 m* w" s! ]7 M! Q
The family history was remarkable for the father,7 k# w# H/ y* y1 l! Y5 D& C0 Z
who was diagnosed with hypothyroidism at age 16,9 d4 v$ ?% e. F2 @0 V
which was treated with thyroxine. The father’s7 Y3 {) e6 V) F0 k$ Z. k
height was 6 feet, and he went through a somewhat$ a+ O# G6 Z: [# s9 V- G2 r
early puberty and had stopped growing by age 14.
, [2 D) E& }9 I1 DThe father denied taking any other medication. The8 T  I. ^' |. j6 C8 F
child’s mother was in good health. Her menarche
" u" N( Y! L& \was at 11 years of age, and her height was at 5 feet
. K2 y& H3 R/ X) U" o# k6 W. v5 inches. There was no other family history of pre-$ Q9 @, S) n( a9 ~
cocious sexual development in the first-degree rela-( G& @0 z* n5 g
tives. There were no siblings.5 D1 V# L  c: P$ d+ ]! I
Physical Examination
, p( e) e! q7 p- u  SThe physical examination revealed a very active,
3 N+ y  Z1 I5 a, x. @playful, and healthy boy. The vital signs documented' u# O. E  h8 O: H6 t$ z
a blood pressure of 85/50 mm Hg, his length was, M6 ~0 q6 h0 F0 h0 s
90 cm (>97th percentile), and his weight was 14.4 kg5 _) X' E: y, H$ m
(also >97th percentile). The observed yearly growth# Z, Z) ?5 w+ P( Q
velocity was 30 cm (12 inches). The examination of" A' P! d7 v: m7 D
the neck revealed no thyroid enlargement.5 l9 p5 l5 u3 r1 h3 k6 f7 G
The genitourinary examination was remarkable for/ U+ w! z# B, j+ w
enlargement of the penis, with a stretched length of% N6 _* U% N& o8 q, C0 H
8 cm and a width of 2 cm. The glans penis was very well6 ~: h6 [6 v) E# f9 R/ ]
developed. The pubic hair was Tanner II, mostly around/ i: Q+ f  t" A0 n7 c8 s6 x
540+ e, x5 X0 Y! \8 \+ u
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 i3 _! O- s3 u9 N
the base of the phallus and was dark and curled. The
( z2 c4 j- i- m4 Jtesticular volume was prepubertal at 2 mL each.
: o' @; ?' Q1 U$ k: J; a+ VThe skin was moist and smooth and somewhat
/ G: ^$ ?- t; x9 V) u) N( I$ m, uoily. No axillary hair was noted. There were no" v$ ~+ g/ d) \& S9 R9 j4 u
abnormal skin pigmentations or café-au-lait spots.
/ x* d/ J- B3 L$ k# D' XNeurologic evaluation showed deep tendon reflex 2++ @* W' r5 U$ ]. g2 j( Y
bilateral and symmetrical. There was no suggestion8 X+ M0 C0 Q8 v8 U  {
of papilledema.
7 S1 v9 Q* A& b4 B0 G( v% }Laboratory Evaluation/ P, D( D) U1 _* ~* N7 b9 e4 O
The bone age was consistent with 28 months by1 \4 M+ Z9 h: ~7 e: a# h
using the standard of Greulich and Pyle at a chrono-- m8 n- X8 T/ y1 x- P# r/ x6 A
logic age of 16 months (advanced).5 Chromosomal
) q" g9 \  E" p- tkaryotype was 46XY. The thyroid function test' m% Z- A8 y# `5 O
showed a free T4 of 1.69 ng/dL, and thyroid stimu-7 Q: i, M+ I$ J7 O8 P. M/ g
lating hormone level was 1.3 µIU/mL (both normal).
/ F) s7 F6 A) v) N! O' OThe concentrations of serum electrolytes, blood! j/ a7 c6 R8 u9 R) y5 A
urea nitrogen, creatinine, and calcium all were
4 k4 T: f  F2 K5 e7 C# f& ^within normal range for his age. The concentration) r, e$ F) T# U# |: a2 t1 I3 i* c5 m
of serum 17-hydroxyprogesterone was 16 ng/dL: g. E" p: E0 ?1 c9 h
(normal, 3 to 90 ng/dL), androstenedione was 20
& u( y9 {' j- {" D6 u; Wng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
) ^* u6 O6 J) j* }terone was 38 ng/dL (normal, 50 to 760 ng/dL),2 C2 B& Y: x( w4 p
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
* `3 ]& i- M/ p1 E5 v, \  u- s49ng/dL), 11-desoxycortisol (specific compound S)
0 m6 W9 H. y6 F; Z( dwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-5 z# X$ `, q6 C
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
0 T4 d  U8 L. {) v& Etestosterone was 60 ng/dL (normal <3 to 10 ng/dL),+ K# T) w. K1 E
and β-human chorionic gonadotropin was less than
) G3 u5 d3 i- ~$ U9 @  M! B1 K; ^/ q5 mIU/mL (normal <5 mIU/mL). Serum follicular
2 o/ D; q( F9 C4 d7 y6 Jstimulating hormone and leuteinizing hormone
  b& y* G% M: |6 ]& dconcentrations were less than 0.05 mIU/mL/ O% C1 G% @5 u
(prepubertal).
! d2 Q* P6 d& J. ]& P8 CThe parents were notified about the laboratory: ~' }! G' ~, Q9 b4 J1 P- v( p8 ^
results and were informed that all of the tests were! X4 {  t' q7 _
normal except the testosterone level was high. The$ m+ a" Y6 P; t6 w( Q- I
follow-up visit was arranged within a few weeks to
* }& C1 Z! Q' @5 @: Y& Zobtain testicular and abdominal sonograms; how-1 R! i7 J0 C7 j2 H# q
ever, the family did not return for 4 months.
7 \' C& a8 j) KPhysical examination at this time revealed that the
* x! g% s5 N' u5 Y$ A  Jchild had grown 2.5 cm in 4 months and had gained
* ^  U/ ~' u7 l- W. }7 d$ a2 kg of weight. Physical examination remained
  ^- \) ]5 M1 ?6 Punchanged. Surprisingly, the pubic hair almost com-
+ O9 d0 L4 C" V2 t2 V4 e! hpletely disappeared except for a few vellous hairs at
5 L4 r' L' B7 |9 U3 Z8 Uthe base of the phallus. Testicular volume was still 2  I' t4 s! F1 k) U) E8 Y
mL, and the size of the penis remained unchanged.1 d0 T* v7 H( g( n0 g6 c
The mother also said that the boy was no longer hav-7 B" v$ Q% O' O! P) Z% F. z1 v
ing frequent erections.
$ ^& s4 R+ Y) M6 v! y" o" B4 R7 sBoth parents were again questioned about use of& E& a# H9 I/ F2 K
any ointment/creams that they may have applied to
2 e: t1 E8 I! R" g; {# [the child’s skin. This time the father admitted the" C% A; H: R2 Z- [8 l* L* s
Topical Testosterone Exposure / Bhowmick et al 541, L# s8 w3 W( X! U4 T/ g7 w; O, P0 s
use of testosterone gel twice daily that he was apply-1 n" F: h0 N0 F
ing over his own shoulders, chest, and back area for
) a) w: u1 K% \: R5 l6 V3 v0 S2 H! X4 Ja year. The father also revealed he was embarrassed) l6 N3 i! O, `& I/ k; }1 o/ `* @
to disclose that he was using a testosterone gel pre-4 ~" U7 o- S$ b$ M
scribed by his family physician for decreased libido
+ R. t7 }" G' [7 T) fsecondary to depression.8 \/ y) N1 m+ o! N
The child slept in the same bed with parents.
) ~8 c* n: Q1 F/ ~1 V, }The father would hug the baby and hold him on his0 Q7 h4 ^4 `7 a, ]
chest for a considerable period of time, causing sig-
! ]0 T" E2 p: [# q. H& Snificant bare skin contact between baby and father.7 k6 X: A' _) e/ F. J, G, G- z
The father also admitted that after the phone call,3 Y( O( {4 z  {0 W5 t7 e0 S
when he learned the testosterone level in the baby
: g! `# K' W) n5 |* G& F+ Cwas high, he then read the product information; }% P- ?4 Y7 Y
packet and concluded that it was most likely the rea-
, v& u: o0 T, y( Q- y* g8 json for the child’s virilization. At that time, they
9 Z8 c4 p) p9 {decided to put the baby in a separate bed, and the1 A; P* D. Q. J
father was not hugging him with bare skin and had1 z) q4 v" n/ ?4 |1 c3 u' `
been using protective clothing. A repeat testosterone$ Q+ ]3 h  a; \. Y1 d. Y2 t
test was ordered, but the family did not go to the
9 x# b' n8 p+ E' j6 mlaboratory to obtain the test.* Y6 B8 o( l5 F" }0 I4 W6 x
Discussion
! ?; D( ?, p! aPrecocious puberty in boys is defined as secondary
! }8 ?! |( l2 m. a/ \sexual development before 9 years of age.1,4; R9 [7 c. E/ c: ?* U& M
Precocious puberty is termed as central (true) when  U; ~8 }# q6 q" T3 U* H  l
it is caused by the premature activation of hypo-
, @7 O/ `5 r1 Jthalamic pituitary gonadal axis. CPP is more com-
3 C8 k3 o0 K! T8 z$ v- Fmon in girls than in boys.1,3 Most boys with CPP" Y7 M. i, n" M. m: O% T: Z( V0 l& F
may have a central nervous system lesion that is
% J/ P( W1 Z8 cresponsible for the early activation of the hypothal-/ l1 m/ Z, j- p( R7 k1 J! Q
amic pituitary gonadal axis.1-3 Thus, greater empha-" P5 O1 v3 |4 w- f# d
sis has been given to neuroradiologic imaging in( [+ _! e) i% l. O! ?4 P3 l. W
boys with precocious puberty. In addition to viril-/ x( s+ e6 i5 k& K8 [6 S
ization, the clinical hallmark of CPP is the symmet-
- U, u# s* D( yrical testicular growth secondary to stimulation by: b8 I8 Q! _5 g) i2 ]- i* P3 ^
gonadotropins.1,3
1 L/ [. V* y& d/ e9 D% k' dGonadotropin-independent peripheral preco-
4 A' G: h, j, v- z, K5 M& ecious puberty in boys also results from inappropriate) r9 a/ A, t1 b1 i
androgenic stimulation from either endogenous or
2 \1 N0 W0 X) c. ~exogenous sources, nonpituitary gonadotropin stim-# s# A. P' i0 e; e" K/ V
ulation, and rare activating mutations.3 Virilizing* j8 p' K* `2 s2 e: w
congenital adrenal hyperplasia producing excessive
$ h: m! Z' E" v5 Z( `5 X. v9 _# J$ Madrenal androgens is a common cause of precocious" I: |' C8 h' k: V
puberty in boys.3,4
' V! j9 I) R7 \: pThe most common form of congenital adrenal
. a$ N& X* \7 v, lhyperplasia is the 21-hydroxylase enzyme deficiency.
- Y8 X2 u' H/ c/ X$ j4 Q: V2 rThe 11-β hydroxylase deficiency may also result in
4 E. t4 ^6 n! R# @4 p2 S0 jexcessive adrenal androgen production, and rarely,/ l% z7 n; d8 G6 g- ^8 v8 ^
an adrenal tumor may also cause adrenal androgen
: c# S& Z1 o& [0 ]$ }$ [excess.1,34 K/ z  }% s4 Q- f# x
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 `! }3 a' q# _/ ^% |542 Clinical Pediatrics / Vol. 46, No. 6, July 2007' z( c5 P3 E; x2 P0 P7 o
A unique entity of male-limited gonadotropin-) R; A8 \% U9 x' a
independent precocious puberty, which is also known4 c# Z! T0 q1 Z8 d; K
as testotoxicosis, may cause precocious puberty at a
6 Y: m3 f" }; V: W) nvery young age. The physical findings in these boys8 i+ E7 m% Q- l* O
with this disorder are full pubertal development,2 _/ r& i/ H, ?0 w1 l, S' ~
including bilateral testicular growth, similar to boys
9 j2 z. a7 }) O! y# Owith CPP. The gonadotropin levels in this disorder! Y+ q$ ?5 Z$ ?: V* D3 z% J% A
are suppressed to prepubertal levels and do not show7 A9 q. \; y6 C7 r  I) H
pubertal response of gonadotropin after gonadotropin-2 r0 e3 p" R$ p6 ^4 ^2 q: X1 Q
releasing hormone stimulation. This is a sex-linked& c7 M1 X& h5 i5 C9 w+ d
autosomal dominant disorder that affects only5 F6 L7 E- i0 A* w+ E
males; therefore, other male members of the family
" d, o! R/ n6 n. ]; Qmay have similar precocious puberty.3! b" N# i3 x$ i; D3 j
In our patient, physical examination was incon-: b  {0 x$ V. ^% Q# [9 s
sistent with true precocious puberty since his testi-) [, k; r. Q* ^( _9 h
cles were prepubertal in size. However, testotoxicosis' R" d; M+ r5 s  \0 m  a7 u; Z
was in the differential diagnosis because his father
& q- ~  B1 W- V$ Istarted puberty somewhat early, and occasionally,
* l' v0 S. U: I% b! B1 Ltesticular enlargement is not that evident in the, W3 m# n( c5 v7 d! W* Q
beginning of this process.1 In the absence of a neg-
! d6 g( J' @: N; m; _9 fative initial history of androgen exposure, our
- z6 A+ y& Y5 b; [: N/ b& ibiggest concern was virilizing adrenal hyperplasia,
1 v% s( _. Q! F% i( Leither 21-hydroxylase deficiency or 11-β hydroxylase
2 [9 P7 Y- e( b( W" k% N2 wdeficiency. Those diagnoses were excluded by find-8 I1 n1 \, w, [: P/ N* m$ H
ing the normal level of adrenal steroids.
$ |% B# g1 A. k$ M4 JThe diagnosis of exogenous androgens was strongly
5 i; z3 C- F( B, {suspected in a follow-up visit after 4 months because8 J+ B. v$ b' m! B1 n( J5 G* @
the physical examination revealed the complete disap-% w1 w4 Q8 B1 q2 X) e( I: c; {
pearance of pubic hair, normal growth velocity, and
( e  A; e' T+ C$ {! G  o& Y. vdecreased erections. The father admitted using a testos-
  \' m, A7 i4 k9 U: }! t" [, hterone gel, which he concealed at first visit. He was* p6 p, l2 h& c& ]+ e, D
using it rather frequently, twice a day. The Physicians’3 }9 `% A: I2 @1 {; m- h" T! s
Desk Reference, or package insert of this product, gel or9 A1 ^% o# v/ Q) t/ H- \$ `
cream, cautions about dermal testosterone transfer to3 U# E( e8 K7 A; l2 ]& Q6 |
unprotected females through direct skin exposure.5 d+ \: U) A- R% n9 Y9 T
Serum testosterone level was found to be 2 times the4 I5 [$ T; G9 E2 a5 Y0 Y
baseline value in those females who were exposed to
6 k6 [8 U# y# P9 n  W1 teven 15 minutes of direct skin contact with their male
6 m% x& \7 x* J+ @/ Xpartners.6 However, when a shirt covered the applica-7 X! z. _; \8 B5 }, ?
tion site, this testosterone transfer was prevented.
) }. _2 k- Q/ O. }Our patient’s testosterone level was 60 ng/mL,& Z( }. ^* M" ?1 k% K
which was clearly high. Some studies suggest that4 r8 P7 }, P1 u& F3 b
dermal conversion of testosterone to dihydrotestos-* C# L, s: [! D: O: }& B
terone, which is a more potent metabolite, is more" e' O2 ?3 I* ]) i  y* {
active in young children exposed to testosterone: F" y$ h. x/ g9 v
exogenously7; however, we did not measure a dihy-
0 s9 ]8 u4 g  Jdrotestosterone level in our patient. In addition to
: x! B" L$ n! k. ^& J3 }: e& zvirilization, exposure to exogenous testosterone in
  x- L$ n3 ]% k! G, Z9 b' e% g4 c, Pchildren results in an increase in growth velocity and8 a& B7 v0 y* n& ^% p
advanced bone age, as seen in our patient.# W6 S; y5 ], N; `
The long-term effect of androgen exposure during
  t) @  N* c; X2 kearly childhood on pubertal development and final' u* n; E$ v. b0 ~: G1 }' u
adult height are not fully known and always remain" y3 r& a# M) H( `  b; |
a concern. Children treated with short-term testos-
" E; y# Q# U# D- bterone injection or topical androgen may exhibit some
: F4 O" ]0 e0 k; aacceleration of the skeletal maturation; however, after4 d- U9 Y9 D* O5 r) e; T) O
cessation of treatment, the rate of bone maturation
1 a1 T6 |2 l- L! |3 l% S( [decelerates and gradually returns to normal.8,95 f( a2 W( P6 L% Q7 g# c
There are conflicting reports and controversy8 s% t, ^4 [: |; A% w
over the effect of early androgen exposure on adult+ ]7 _) U: }1 n6 X' m
penile length.10,11 Some reports suggest subnormal
7 c- {. b# K9 cadult penile length, apparently because of downreg-
/ @/ P, l. B/ Y$ V. X6 e# i- m0 Hulation of androgen receptor number.10,12 However,% M2 J, I6 U" |2 x& G5 X
Sutherland et al13 did not find a correlation between$ M8 L5 Q; g! e# o& P+ W
childhood testosterone exposure and reduced adult0 C5 f9 l& j/ `! E* G
penile length in clinical studies.2 B- r- U8 g, h7 }0 a5 t8 e
Nonetheless, we do not believe our patient is
# u' ]+ ?7 e4 H9 Jgoing to experience any of the untoward effects from
1 _& X  p2 K# o9 Y1 U, Y# I6 b! x9 U  _4 Mtestosterone exposure as mentioned earlier because* }; {: S) J/ ^1 M" o' j& `
the exposure was not for a prolonged period of time.
& d9 f0 k$ U( ^8 Z+ ?9 _) EAlthough the bone age was advanced at the time of
! _/ }- `4 a7 _diagnosis, the child had a normal growth velocity at4 L* ^" k) D+ `' `" f. g4 D
the follow-up visit. It is hoped that his final adult% H% k- W( h1 M8 }) z4 R
height will not be affected.2 y7 c' G7 m" Y- a1 r, o0 I
Although rarely reported, the widespread avail-0 U1 H7 F+ E9 l6 o3 K
ability of androgen products in our society may
. a5 S4 z6 c8 E7 P) Gindeed cause more virilization in male or female
7 u) B2 }$ v5 T  f% Vchildren than one would realize. Exposure to andro-
0 M5 G+ n3 F. V6 O9 V# Fgen products must be considered and specific ques-
" ~! C5 s" x6 \- i9 ~tioning about the use of a testosterone product or  i" {, s4 Z/ Q; [; w" e, t' h
gel should be asked of the family members during/ [, g+ |! ^! c# x6 U
the evaluation of any children who present with vir-" x6 K- R$ J4 z8 B% A( i7 H
ilization or peripheral precocious puberty. The diag-( K# L3 f& D0 r# M
nosis can be established by just a few tests and by8 @" B# K1 }2 y. d. c! U2 l" N# G. F
appropriate history. The inability to obtain such a
/ w; p) R. ^  N" ^) Z- e1 Shistory, or failure to ask the specific questions, may5 J6 U5 e! W; E0 w4 m2 l4 \
result in extensive, unnecessary, and expensive
. _' k0 I3 f8 ~7 U% E6 _investigation. The primary care physician should be
2 u. h3 K6 y% L, ~; B" L4 V: k+ waware of this fact, because most of these children
" {, t& j/ ~8 Q) C4 P8 a0 D/ k# Qmay initially present in their practice. The Physicians’
9 t0 a' K/ a. P' _; ^Desk Reference and package insert should also put a0 E5 p1 H9 L, t6 `0 x) R
warning about the virilizing effect on a male or  r2 C6 K( x) H9 N
female child who might come in contact with some-
& d/ H4 ], d: Z6 B5 G1 Qone using any of these products.
0 o) a7 t! {* oReferences
- q" [6 a, z  p: K4 @/ ]$ s1. Styne DM. The testes: disorder of sexual differentiation
' K: H  N/ M$ v! G/ t* aand puberty in the male. In: Sperling MA, ed. Pediatric
9 X6 g0 b9 g! `* s  |Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;: @1 M0 f- i' t! R: v' t" w
2002: 565-628.
2 j; U$ \% C+ T( [5 n/ ~2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious" `& \+ y3 E! ?) g* V: v/ V% Q# ^
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
0 B, F! `9 ?+ R; r6 ^" }+ `Boy Induced by Indirect Topical
" o" Z; x6 G& ~8 `# w! wExposure to Testosterone
& k$ U4 R; K9 U6 x6 y8 YSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
- v9 O3 g- p+ a0 [8 band Kenneth R. Rettig, MD1
6 L' a3 A( b# tClinical Pediatrics7 \0 }2 m, |  _9 f; @6 V
Volume 46 Number 6% c4 h' v/ j5 j, v% ?- ~' \5 \
July 2007 540-543
% p* ~! C2 M" Y6 ^& z; {' K© 2007 Sage Publications5 x6 o% Y5 ~3 B  f3 w. \
10.1177/0009922806296651
/ l+ B% F$ O& R8 |. Lhttp://clp.sagepub.com
0 _$ @7 m5 }" @- G# [hosted at
$ a  @6 K* R% t, t. Ohttp://online.sagepub.com
7 V  }; w; q5 r$ U  HPrecocious puberty in boys, central or peripheral,; \$ r& P! S, a( [8 V( a9 X& O  V8 w
is a significant concern for physicians. Central# g3 |+ d: R# }0 O* T7 Z
precocious puberty (CPP), which is mediated" ^  g4 B7 k5 J( j2 A; ]7 Y
through the hypothalamic pituitary gonadal axis, has
- n! j4 e! k- A; D& v6 e# \2 \a higher incidence of organic central nervous system* k8 ~& E; `" ]4 U
lesions in boys.1,2 Virilization in boys, as manifested5 S+ r- Q# g+ H/ {2 H# C% I0 d
by enlargement of the penis, development of pubic- l$ Y5 C( l# ]/ _( X4 S% P
hair, and facial acne without enlargement of testi-7 M, w/ b. Y, P  E2 G
cles, suggests peripheral or pseudopuberty.1-3 We7 x' z. K0 l/ ]6 m! G* T% C
report a 16-month-old boy who presented with the8 I8 D5 E& m! C  |7 J) M, |
enlargement of the phallus and pubic hair develop-
4 x  q" V6 [6 r. b, p0 @ment without testicular enlargement, which was due8 m$ k2 `; h9 D2 u! \
to the unintentional exposure to androgen gel used by
1 g$ S+ A6 r  y* R& Q0 O( e: Vthe father. The family initially concealed this infor-
1 ~4 i0 G, c6 X0 Omation, resulting in an extensive work-up for this/ j; o. J2 S$ q
child. Given the widespread and easy availability of3 @2 J5 d0 ?5 @1 C' l% R* Y
testosterone gel and cream, we believe this is proba-
  S# z4 J3 y; nbly more common than the rare case report in the
- ?: a0 g  d4 c7 B' lliterature.4
3 U9 W* O# c4 B: u4 o4 {) `Patient Report, B9 N4 F- f7 i, ~7 d
A 16-month-old white child was referred to the
+ R$ Z+ K9 w  M. j# [! b! Pendocrine clinic by his pediatrician with the concern
" k+ l7 ~; _1 [of early sexual development. His mother noticed9 g5 q: I, h2 h
light colored pubic hair development when he was
* T2 u; a+ m* LFrom the 1Division of Pediatric Endocrinology, 2University of, C, v' t5 p" L3 G: `
South Alabama Medical Center, Mobile, Alabama.+ c, [" {) ^, X5 `9 ~
Address correspondence to: Samar K. Bhowmick, MD, FACE,
5 p& p* b; y2 [/ y  ~+ f$ WProfessor of Pediatrics, University of South Alabama, College of
+ D0 ^- v" t* d" ]Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ v( i5 W7 q  X4 B7 t
e-mail: [email protected]." l# I, g' \( d8 w$ L
about 6 to 7 months old, which progressively became
- I5 R1 G# S; G! V' a  g/ b) c( Z5 udarker. She was also concerned about the enlarge-
& |$ J' D0 o. e2 E9 M$ l3 ]" Oment of his penis and frequent erections. The child
2 M$ h" Y: h8 S2 Z! zwas the product of a full-term normal delivery, with
' k( B, h6 |4 L: k! ]. f' P6 P3 x3 Na birth weight of 7 lb 14 oz, and birth length of4 m2 |9 n; f5 F
20 inches. He was breast-fed throughout the first year
  L  r% a3 K1 g- i& x5 E# ]: j9 tof life and was still receiving breast milk along with
0 ]  q; ]7 j: ]" a  {solid food. He had no hospitalizations or surgery,
- ^! X8 y6 i3 _! Jand his psychosocial and psychomotor development5 P1 a4 B9 k9 @! r1 v) F' l$ _
was age appropriate.7 `, C0 C2 J- |) p7 d0 h. c6 b
The family history was remarkable for the father,* Q0 A5 U! g/ ?+ b3 a1 k9 c! i
who was diagnosed with hypothyroidism at age 16," t  y0 u2 W" P1 ]  }  _& u8 t
which was treated with thyroxine. The father’s
; y/ H8 |1 J! O. n' Mheight was 6 feet, and he went through a somewhat% \$ ]  ]8 \5 @
early puberty and had stopped growing by age 14., j$ O8 I* E" n1 o/ G$ G8 S3 b% U  [
The father denied taking any other medication. The
1 l+ V6 K0 @; H6 r& l  }child’s mother was in good health. Her menarche% n$ {9 e/ O) A' ?+ G9 h
was at 11 years of age, and her height was at 5 feet: e* S/ s/ ^) m: k$ x. U$ Q
5 inches. There was no other family history of pre-
" G; f1 M/ w4 P5 ccocious sexual development in the first-degree rela-
$ T2 |: [' a8 q$ u' n5 k# @tives. There were no siblings.$ _) H1 T/ F; G+ N% z8 L9 N
Physical Examination: w: K. J, q* ]. A
The physical examination revealed a very active,8 F6 Y, C+ s/ H  v# m! X
playful, and healthy boy. The vital signs documented
, o3 N7 G3 w+ d7 e; R! S  ~a blood pressure of 85/50 mm Hg, his length was9 b/ j7 U( e/ `+ Z9 L9 ?, n
90 cm (>97th percentile), and his weight was 14.4 kg
3 q3 k9 a7 u2 w& H- X: H(also >97th percentile). The observed yearly growth
" [/ b6 i2 G0 @1 x3 T* l* @% svelocity was 30 cm (12 inches). The examination of6 {' o; D4 c. z, R: L- ~
the neck revealed no thyroid enlargement.
1 Q, S- d! e$ d% U  _; wThe genitourinary examination was remarkable for
) G8 x# R; A1 s& I7 C0 `/ Oenlargement of the penis, with a stretched length of
4 G6 m& R! ~3 ~! M6 k8 cm and a width of 2 cm. The glans penis was very well; U0 V8 I" p; J# U! e4 `
developed. The pubic hair was Tanner II, mostly around) U& m" k" y* D3 z2 Y
540
. R% }& R& b& Bat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 g6 j3 i7 H" K3 j0 p2 Othe base of the phallus and was dark and curled. The
2 z7 C- J4 q" `0 ntesticular volume was prepubertal at 2 mL each.
6 B3 O, s: D& h5 P7 \The skin was moist and smooth and somewhat* p) {. g- P$ b$ h- z) `
oily. No axillary hair was noted. There were no, j6 ]0 X3 }+ }5 }5 Z
abnormal skin pigmentations or café-au-lait spots./ ]' c* D: a  s$ R8 Q' m
Neurologic evaluation showed deep tendon reflex 2+- o* Y! p+ {  W8 O) b& j
bilateral and symmetrical. There was no suggestion: N( B& r7 G) n: d" I
of papilledema.( _: S# D/ a* A8 ]8 O3 D, E1 a
Laboratory Evaluation  W" p5 \& o: \8 ?# ]0 s* t
The bone age was consistent with 28 months by
$ G6 ?: q2 {4 g) ?' A( ~6 C) ~using the standard of Greulich and Pyle at a chrono-
0 ?" n" \0 P$ i9 P1 D8 Ologic age of 16 months (advanced).5 Chromosomal
9 |" S9 r2 i  Q  Okaryotype was 46XY. The thyroid function test8 ~, A& s5 K, _: M: @( f  \% L7 b
showed a free T4 of 1.69 ng/dL, and thyroid stimu-: A% h- ]* A4 h$ [2 @
lating hormone level was 1.3 µIU/mL (both normal).; X1 i. H' S1 N( e: K
The concentrations of serum electrolytes, blood6 w, |& Y- p" r6 Q, ~
urea nitrogen, creatinine, and calcium all were
4 z2 Y( p8 c# ?/ p& e, Cwithin normal range for his age. The concentration
$ d: Y; d( b$ k7 N; Dof serum 17-hydroxyprogesterone was 16 ng/dL: B  ~; R3 L) K$ F0 L( `, i
(normal, 3 to 90 ng/dL), androstenedione was 20
' T/ h! |7 q; H# Nng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
* b+ ~6 X: w! i3 V4 ~; ]- D/ |$ _terone was 38 ng/dL (normal, 50 to 760 ng/dL),
0 z: r$ u# A9 B' ydesoxycorticosterone was 4.3 ng/dL (normal, 7 to
5 @% D9 W& P9 o. [+ [0 Q6 R. o- @49ng/dL), 11-desoxycortisol (specific compound S)
* R8 ?2 x& H  E- m: `( O$ V1 qwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
4 ]- m. v! r6 Q6 Ttisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# z. X% b% d+ u" L7 J( i3 i2 E$ `
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
: G8 R" K& Z: U2 u  `; s* Dand β-human chorionic gonadotropin was less than
0 a2 @  f5 `" O9 L5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 ~8 _- `, b/ @" istimulating hormone and leuteinizing hormone
6 A' R0 \& Q+ F' M) P3 Econcentrations were less than 0.05 mIU/mL( d4 Q* e/ J' r& p/ U; }9 o: x* q
(prepubertal).* H6 q0 d5 L) B' g0 p
The parents were notified about the laboratory8 f) I% [3 t8 D
results and were informed that all of the tests were% F* [; [( [! _$ h
normal except the testosterone level was high. The4 O% b! n& I& Q1 ~& |
follow-up visit was arranged within a few weeks to  e3 J( q9 e* X* p4 g
obtain testicular and abdominal sonograms; how-
$ W6 U/ R/ y2 h$ {ever, the family did not return for 4 months.
8 E0 `7 q; z7 A" j8 ?: e7 L: R1 k* CPhysical examination at this time revealed that the
. p8 v" B2 u9 J- @* Y- schild had grown 2.5 cm in 4 months and had gained0 ~2 M7 D5 a/ J( A( C: U" B+ F
2 kg of weight. Physical examination remained
2 R# K. v* |* K- Sunchanged. Surprisingly, the pubic hair almost com-
  M0 u, h3 z" }# V; A9 Lpletely disappeared except for a few vellous hairs at; A1 q- L; {+ H; T7 U' V2 j" H
the base of the phallus. Testicular volume was still 2! q6 r( `( G/ y( J
mL, and the size of the penis remained unchanged.
7 N! u, b( g: o) h& `The mother also said that the boy was no longer hav-7 E$ T( ~0 }1 F: W3 U. B
ing frequent erections.
) R- D8 G  H  d1 T3 pBoth parents were again questioned about use of" E" R& U4 P% G# S* q, C$ u) @  }. U
any ointment/creams that they may have applied to
  l- Y8 E% P  Dthe child’s skin. This time the father admitted the1 m3 d+ Y( Y# u. L8 n
Topical Testosterone Exposure / Bhowmick et al 541& M6 v7 p/ t0 ]7 s$ K1 E8 V
use of testosterone gel twice daily that he was apply-6 k$ X; M6 M4 \& p
ing over his own shoulders, chest, and back area for
# l3 _. Q" G$ I$ L, i$ ]0 Aa year. The father also revealed he was embarrassed3 U7 H4 v: W1 b9 r6 i1 {" s" |
to disclose that he was using a testosterone gel pre-& u  k( V3 L5 e, O3 q( |. H
scribed by his family physician for decreased libido. d2 w7 D4 l$ y8 }% Y
secondary to depression." z* Z9 ?. {2 j: E( @! P3 C; ^% O
The child slept in the same bed with parents." c2 |( j8 K6 A+ Q. L
The father would hug the baby and hold him on his) W/ ~1 g/ @0 E& H! p0 X$ e
chest for a considerable period of time, causing sig-  Y7 u* x0 k1 F8 U1 {
nificant bare skin contact between baby and father.
* }; y: s4 D- o) a' n0 f0 QThe father also admitted that after the phone call,
) _% Z6 \. @; Z0 k2 uwhen he learned the testosterone level in the baby! s$ w/ A3 Z+ t" S
was high, he then read the product information
* X6 c) V! g) T8 bpacket and concluded that it was most likely the rea-* D% m3 o6 f& J3 q) d5 m
son for the child’s virilization. At that time, they
3 B& U5 ^9 [2 Cdecided to put the baby in a separate bed, and the
* D% }! A+ g6 s; ?father was not hugging him with bare skin and had
) Q3 m0 a6 J% K/ c' q; ~& r, R( gbeen using protective clothing. A repeat testosterone3 k4 X  {+ U4 k. s8 v$ |6 x
test was ordered, but the family did not go to the
, d) A# m' w! x( b3 T* P5 U& rlaboratory to obtain the test.
4 K4 U+ m& Q4 D& y; j) \Discussion
+ v4 u6 ^7 y' q' V- OPrecocious puberty in boys is defined as secondary
3 g: |7 a# N3 X* O! A9 l0 b  Dsexual development before 9 years of age.1,4
9 A, F+ j' V8 ~% @: wPrecocious puberty is termed as central (true) when
  p4 R( ^- ~$ Bit is caused by the premature activation of hypo-
% N' W# C0 u4 [: Z  e3 zthalamic pituitary gonadal axis. CPP is more com-1 o! D1 D+ u( D: B% Q, S- G' u
mon in girls than in boys.1,3 Most boys with CPP
, T1 p3 \, v# T6 F+ w% Mmay have a central nervous system lesion that is
5 _3 U, H/ n& Iresponsible for the early activation of the hypothal-
9 b! M' i8 V6 j  samic pituitary gonadal axis.1-3 Thus, greater empha-8 q9 a8 D# h1 J" A2 P+ e6 B$ p) A
sis has been given to neuroradiologic imaging in' d; o# y! N0 L7 N( Y- \5 q
boys with precocious puberty. In addition to viril-
* ^: f! k( Q) p. `# C) v, wization, the clinical hallmark of CPP is the symmet-
( O/ L3 F5 M* g$ [" F6 A3 grical testicular growth secondary to stimulation by
1 d- e7 v' u/ M; L2 Q; Agonadotropins.1,3
( m! C1 i# e& }' d* K+ A0 uGonadotropin-independent peripheral preco-  N: o7 \$ N3 ~- }6 F% j3 k
cious puberty in boys also results from inappropriate& ?9 v* r. v. T2 L
androgenic stimulation from either endogenous or. K6 a/ |- Z0 L) T
exogenous sources, nonpituitary gonadotropin stim-
3 K8 f& D  U! Y, ?ulation, and rare activating mutations.3 Virilizing
" f3 s- l: P, W: u( y6 o1 rcongenital adrenal hyperplasia producing excessive/ |" q. F/ h) k$ L1 U
adrenal androgens is a common cause of precocious
" g# P- i$ I2 C+ b8 Y9 G; Xpuberty in boys.3,4
' e+ I: `( z" l. T- c* fThe most common form of congenital adrenal" J2 |0 y5 u. f" K9 N! O) U! q% l
hyperplasia is the 21-hydroxylase enzyme deficiency.& m" b3 b& c3 S" g0 Q+ j
The 11-β hydroxylase deficiency may also result in' [6 d) ?9 @9 ]& Y# v, {
excessive adrenal androgen production, and rarely,
% y5 Z5 }/ s8 c; Man adrenal tumor may also cause adrenal androgen, c8 ~+ J8 U1 @2 S2 ^5 [1 w+ ~
excess.1,35 w- z1 q4 y6 Z: k
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: ]5 N3 I) C* A/ F3 v542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
: R3 C% e8 |3 F$ C8 CA unique entity of male-limited gonadotropin-& ~2 v2 D( @% n; S" ~
independent precocious puberty, which is also known& D1 U$ B7 z, f/ b2 J" R
as testotoxicosis, may cause precocious puberty at a
$ Z+ X5 }) D  G/ `8 D! A# f$ xvery young age. The physical findings in these boys
0 ^" K& T" |4 J) F% \/ ?4 qwith this disorder are full pubertal development,2 c! I# g! i1 l
including bilateral testicular growth, similar to boys
: S" _6 Z2 [8 W/ K+ t3 V/ @with CPP. The gonadotropin levels in this disorder$ Q3 e# ~& G& ?7 Z. [# a
are suppressed to prepubertal levels and do not show  x2 o- g8 u- n6 Q+ G+ G
pubertal response of gonadotropin after gonadotropin-7 S$ R& X3 M; V+ G$ E
releasing hormone stimulation. This is a sex-linked# `$ [3 w# C2 G) |
autosomal dominant disorder that affects only
" @$ w& ?4 I" jmales; therefore, other male members of the family0 e8 R5 i7 V/ E. R$ S- A0 K$ J
may have similar precocious puberty.35 x. X7 o2 f: D+ G2 s
In our patient, physical examination was incon-% e8 L" d, `/ M9 z( m$ y: Z
sistent with true precocious puberty since his testi-
, s2 O; \$ _+ @* I$ dcles were prepubertal in size. However, testotoxicosis0 w- z& w, w1 y! W- k0 g, ?( M
was in the differential diagnosis because his father
' v% c1 [+ x$ q5 O6 Ystarted puberty somewhat early, and occasionally,; Q5 l! J3 e5 ^$ U4 K
testicular enlargement is not that evident in the
) l3 [9 S4 @. g. j! ?. D; D. X( ybeginning of this process.1 In the absence of a neg-$ a( D# f0 t8 d" |/ o4 T
ative initial history of androgen exposure, our
  {2 d% z; H- pbiggest concern was virilizing adrenal hyperplasia,5 V4 i. O4 o  ^
either 21-hydroxylase deficiency or 11-β hydroxylase6 @8 M/ m$ \  D; {6 G
deficiency. Those diagnoses were excluded by find-2 ]- Z0 t- V8 t! y; y
ing the normal level of adrenal steroids.5 D$ c% v/ ?/ v. r: N$ R# ~. ]; U
The diagnosis of exogenous androgens was strongly
. D0 U5 |  ?, Z8 v# R; B- Y2 }/ [suspected in a follow-up visit after 4 months because" ~* j- i# V3 R' D9 {% w
the physical examination revealed the complete disap-
  t, A0 f1 ?9 O5 C3 ?+ p0 vpearance of pubic hair, normal growth velocity, and# j9 D6 g, w6 o
decreased erections. The father admitted using a testos-1 S6 V% B1 G# J. |/ k) l, A+ e8 Z9 ~
terone gel, which he concealed at first visit. He was
) `+ I& W8 M5 G; \using it rather frequently, twice a day. The Physicians’
9 [- n3 t2 I9 H% VDesk Reference, or package insert of this product, gel or
6 d1 A) o' p9 v- z4 [% K; @7 {/ ~" Ocream, cautions about dermal testosterone transfer to
- {/ w1 w# p( ounprotected females through direct skin exposure.
  p+ h9 x/ L" eSerum testosterone level was found to be 2 times the
" A& y+ t$ L+ m' h8 l, q1 T- \! Bbaseline value in those females who were exposed to
9 O# A) k; x* R) Xeven 15 minutes of direct skin contact with their male
+ B. p" H6 h( h0 n$ Cpartners.6 However, when a shirt covered the applica-
! C% z( \$ p+ V3 N; rtion site, this testosterone transfer was prevented.
( D' G' Q/ R8 V. d' q6 a6 kOur patient’s testosterone level was 60 ng/mL,' U: W3 G4 Q8 M+ n
which was clearly high. Some studies suggest that3 ]: P4 B9 w# x
dermal conversion of testosterone to dihydrotestos-1 c" w: _5 L( o. F& R. i
terone, which is a more potent metabolite, is more
3 z" [+ B/ S( Q5 d9 i! k6 y  X, Uactive in young children exposed to testosterone" C; f3 D9 R/ Q4 f+ Z  G
exogenously7; however, we did not measure a dihy-
" ?- J; ^1 Q% A/ A% R. Z9 U, V% qdrotestosterone level in our patient. In addition to! I: k/ Q; k7 @: E+ j" Z9 ]# c# V
virilization, exposure to exogenous testosterone in- `5 x3 ?+ |! N/ Q: |. ^
children results in an increase in growth velocity and
- l6 ?: [9 \; q6 _6 gadvanced bone age, as seen in our patient.
# d" z8 v  n! B/ x1 Y8 TThe long-term effect of androgen exposure during/ h3 _+ N6 y* Z
early childhood on pubertal development and final( C# |* O3 X/ G9 ~( Y3 v
adult height are not fully known and always remain0 @) O! u5 X- j' s- |( ?& f
a concern. Children treated with short-term testos-
0 |/ p+ W6 E9 o0 s2 K8 `2 X5 kterone injection or topical androgen may exhibit some3 [2 b% c2 O& m. E8 M
acceleration of the skeletal maturation; however, after2 Z+ ^' W6 h. e; Y1 i( g7 t, j. I
cessation of treatment, the rate of bone maturation% U7 U2 K& j* n2 e% h) {
decelerates and gradually returns to normal.8,9
5 H0 z/ E5 g7 l! S6 OThere are conflicting reports and controversy
4 \0 I: a1 h/ v9 i1 N0 j2 X6 Sover the effect of early androgen exposure on adult- ]9 h) Q8 L3 T& e; l# J! s
penile length.10,11 Some reports suggest subnormal' e5 D# H0 F! t( i# H& E  `
adult penile length, apparently because of downreg-# m' S/ j4 w; z5 s' h7 C) }# u
ulation of androgen receptor number.10,12 However,2 _+ j. y% z4 p- Y9 j
Sutherland et al13 did not find a correlation between$ r$ O/ R) _+ I9 F& ^
childhood testosterone exposure and reduced adult' W: G* z" Q0 t5 o* e: d: ^
penile length in clinical studies.
- Y* O; ]7 x5 V: D1 [+ }8 nNonetheless, we do not believe our patient is
0 p' e" q" _& H6 J) \' }% Tgoing to experience any of the untoward effects from
6 B$ r9 g" `1 h: Z! c5 C* dtestosterone exposure as mentioned earlier because' G. y3 S9 i' a$ k6 c# \
the exposure was not for a prolonged period of time.
5 T+ I& d. S9 F- H5 K6 cAlthough the bone age was advanced at the time of
# P6 @, o6 n1 Z  G8 Ydiagnosis, the child had a normal growth velocity at/ r* q8 w, a' Z7 m% K
the follow-up visit. It is hoped that his final adult: @1 J7 h$ H) j+ g$ q; Y
height will not be affected.% C: M6 P" G3 X. H
Although rarely reported, the widespread avail-
) ?  G  u" n9 D. j- }9 g" Bability of androgen products in our society may
3 D0 E) j; f7 M4 Aindeed cause more virilization in male or female
1 }. y# O5 A' G4 `children than one would realize. Exposure to andro-
( k+ Z3 O. [% w2 Z& e' j4 Tgen products must be considered and specific ques-
& P& M9 p$ B* }4 e/ J& wtioning about the use of a testosterone product or
% [4 n% {' U* }& R5 _1 \8 E1 C! [gel should be asked of the family members during- c* f, h8 N+ l
the evaluation of any children who present with vir-# p) b/ j$ V( q  Z9 v/ ~! ~9 S+ W
ilization or peripheral precocious puberty. The diag-) m4 o9 M8 a8 Z- A( K
nosis can be established by just a few tests and by
8 @0 N! R6 L/ A/ b( ]' f* Mappropriate history. The inability to obtain such a
. s$ N5 F6 V+ T3 w" Dhistory, or failure to ask the specific questions, may
. F$ D% @7 X* }* K" [" Zresult in extensive, unnecessary, and expensive
% m0 d3 c# ]4 _2 i! m! zinvestigation. The primary care physician should be/ l* p# I  W8 B  d
aware of this fact, because most of these children7 N; o$ D, j) Q  g  s8 d, @
may initially present in their practice. The Physicians’
: [, ?  t6 D, l/ G/ K5 \( B) tDesk Reference and package insert should also put a1 b. D3 w* \# D  ?
warning about the virilizing effect on a male or! v1 c/ `# y" H, g% ~3 o2 \2 o0 h
female child who might come in contact with some-
0 q" g" U7 M0 H, p+ c( B+ f. Tone using any of these products.
4 W" T# w. L& B2 `0 q; e7 N1 xReferences$ i' W5 K* P- ]( n; I2 |/ ?! s
1. Styne DM. The testes: disorder of sexual differentiation
0 e7 v9 h: {- S0 Xand puberty in the male. In: Sperling MA, ed. Pediatric: Y+ R5 C/ j7 h
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;' [# y  i- L( m0 W2 d9 T
2002: 565-628.% W& z( j# W9 K
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
: \& n; D& M' w8 t; c5 V$ ipuberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
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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
! g; x+ f* l2 ^; E4 t" o
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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