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Sexual Precocity in a 16-Month-Old9 _  v. Z, Y" U" E% O" }6 p/ b  B
Boy Induced by Indirect Topical
5 h8 j& Y/ d) a3 O/ n( y$ P& tExposure to Testosterone
. n: K3 V# e: X! l" S5 ESamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
! o/ Q! K' d3 i( {. E0 K. M% Cand Kenneth R. Rettig, MD1, Q8 `: D6 u- h* s. k
Clinical Pediatrics7 \. U: R* ?: M, c, |/ u
Volume 46 Number 6' B: X: D2 ]& G* N, I+ X- [! ]
July 2007 540-543
3 A) o* R# {. g/ F© 2007 Sage Publications1 n: f5 n5 g, v- U  r4 M2 d6 `3 Q
10.1177/00099228062966519 M- k, Q5 j9 s$ `+ `9 c& d+ B
http://clp.sagepub.com
' T# v# e" V% H4 J7 _hosted at
0 O: H8 [, A2 _% n$ J8 m$ ^http://online.sagepub.com
0 [2 }7 \, U  E/ J5 ePrecocious puberty in boys, central or peripheral,) H! X; [9 @4 g6 k1 V6 t4 _
is a significant concern for physicians. Central3 P5 b$ u& l4 q* S" D9 J, m
precocious puberty (CPP), which is mediated
% I# {/ S& S6 p. t! C) cthrough the hypothalamic pituitary gonadal axis, has, r) E- K+ K$ _4 G: ?4 T5 T! }
a higher incidence of organic central nervous system
; e1 u3 b3 |' t& v5 v6 `lesions in boys.1,2 Virilization in boys, as manifested! Z! R$ f: d+ G$ A
by enlargement of the penis, development of pubic
  A) ]; E, Y/ ]6 O* c3 A1 ^hair, and facial acne without enlargement of testi-
/ X0 C0 A" @- T/ Z& `cles, suggests peripheral or pseudopuberty.1-3 We
9 C6 o# L8 @1 ?! U$ b; c/ v& }report a 16-month-old boy who presented with the
6 H/ i8 n  h9 U$ U5 v: Penlargement of the phallus and pubic hair develop-
: S* R4 Q( U* ?0 D1 iment without testicular enlargement, which was due5 Y. q8 c1 p" h" `  S; m1 Z8 H
to the unintentional exposure to androgen gel used by1 ?7 W. z2 J& n" N  ]8 c3 w
the father. The family initially concealed this infor-. h2 Y  i/ I. U# M' y
mation, resulting in an extensive work-up for this7 G3 a! v( ^& w
child. Given the widespread and easy availability of5 w  t9 a: W  _3 Z1 q7 L# d
testosterone gel and cream, we believe this is proba-
( J% F+ u, l0 E' n- Gbly more common than the rare case report in the( \  c& j' T: }
literature.4
5 T7 u( t$ B6 H- t% B5 p5 q% ?Patient Report
4 s+ o$ n" R* J) U" H8 u0 C( x5 eA 16-month-old white child was referred to the6 E) ?2 @6 v' Z3 q
endocrine clinic by his pediatrician with the concern
# \0 O3 b& F. e2 Nof early sexual development. His mother noticed
, T0 n. z" S: W/ ?light colored pubic hair development when he was
! A- l2 h3 t9 C  C& {From the 1Division of Pediatric Endocrinology, 2University of3 ~. b; W# j! P$ Q$ Q/ |7 ]
South Alabama Medical Center, Mobile, Alabama.
  v. R  B1 j6 g, U; y7 EAddress correspondence to: Samar K. Bhowmick, MD, FACE,
% s. {0 \1 m% a$ X4 AProfessor of Pediatrics, University of South Alabama, College of
5 E. M4 o5 M! ]; R: s* YMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
9 E2 L) z, G, n, ?* g+ Ne-mail: [email protected].& ~, X( p; @6 S
about 6 to 7 months old, which progressively became8 O" ?  y; U$ F; U) z! e# C
darker. She was also concerned about the enlarge-
/ O5 j" ^" K0 p) @ment of his penis and frequent erections. The child4 R! h3 r. `5 N% R+ P+ m. i2 q
was the product of a full-term normal delivery, with& l) h6 |- E8 \' R
a birth weight of 7 lb 14 oz, and birth length of6 c0 E6 N& B! V- O) w. [+ ]
20 inches. He was breast-fed throughout the first year
8 |; a# n( v2 Q: N, e6 D; N, }of life and was still receiving breast milk along with
6 C, K4 \5 U8 Y+ Y8 a. q& ^! N# Z1 `solid food. He had no hospitalizations or surgery,
1 G3 L; v+ o1 m, {% p1 Q" Nand his psychosocial and psychomotor development
! ?7 y% g; T# F+ H0 [; P' ewas age appropriate." {8 M$ u8 S5 g) \, b; |
The family history was remarkable for the father,9 p( b1 A2 s* N: L9 @
who was diagnosed with hypothyroidism at age 16,- P4 m8 @$ Z, f" G& o! l; R
which was treated with thyroxine. The father’s- b: d; \6 B& W9 j) h
height was 6 feet, and he went through a somewhat
1 [5 B& D9 K9 Z/ r% ~, qearly puberty and had stopped growing by age 14.6 g2 M4 C, u2 c6 H! s
The father denied taking any other medication. The9 M, i- k0 k9 Y
child’s mother was in good health. Her menarche( Q/ r9 Y5 ^/ U5 {7 U( b0 K) \
was at 11 years of age, and her height was at 5 feet6 v4 v9 c  c  [7 f% T
5 inches. There was no other family history of pre-6 n6 D1 T. d- i7 ?7 v
cocious sexual development in the first-degree rela-6 E" p% f" N3 a% \" J
tives. There were no siblings.  Q4 D7 I0 p* I  r
Physical Examination
3 {  Y) M/ U9 g3 MThe physical examination revealed a very active,
  Q9 g) i- P) x' K! }playful, and healthy boy. The vital signs documented
( r. H+ T5 k1 r7 h3 r) V+ O. ?3 Za blood pressure of 85/50 mm Hg, his length was
/ Y3 m0 U5 g( r) Y% S' _90 cm (>97th percentile), and his weight was 14.4 kg
3 x$ u2 T, v- o/ C(also >97th percentile). The observed yearly growth9 q% Q( w9 J% Z$ x" N
velocity was 30 cm (12 inches). The examination of) p3 _$ L( Q: n/ i
the neck revealed no thyroid enlargement.4 X8 `. u2 }6 ^2 ]8 v
The genitourinary examination was remarkable for1 F8 V! S; G* m3 n9 S4 U6 @/ ~
enlargement of the penis, with a stretched length of# }/ {" [! g) e2 f
8 cm and a width of 2 cm. The glans penis was very well9 y7 ], u3 S. o3 ^& h
developed. The pubic hair was Tanner II, mostly around2 Y3 d/ p1 D# [; N& ~& M& z
540
/ p4 D( w" M( p7 cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# v) w8 {1 T/ h8 |the base of the phallus and was dark and curled. The
$ z, Q( A& e/ S& u1 d/ jtesticular volume was prepubertal at 2 mL each.* o8 m2 w5 M" h  e+ p5 ~% X
The skin was moist and smooth and somewhat6 `4 b) b) [! ~. P' p
oily. No axillary hair was noted. There were no
  p5 m; X9 K7 J) i* Jabnormal skin pigmentations or café-au-lait spots.
9 ^8 R8 p2 p' ?% O1 H% N$ c5 T* q' gNeurologic evaluation showed deep tendon reflex 2+( U& c* ^3 j, j' d) M) ?3 ?) `
bilateral and symmetrical. There was no suggestion0 ~* R5 B8 @0 G% [% X: C
of papilledema.
8 p5 U* T3 b2 _5 J' a/ ~6 P; H. cLaboratory Evaluation) {0 f, v$ c/ {, Y. s. b' V
The bone age was consistent with 28 months by$ i/ r9 m$ W; Z5 n* _4 ?
using the standard of Greulich and Pyle at a chrono-
* o* p7 ^7 j6 s- |. z' e4 @logic age of 16 months (advanced).5 Chromosomal
# Z: S4 ^# C7 u; ~karyotype was 46XY. The thyroid function test
: A  g) F5 }& X( f7 ~4 P6 X" vshowed a free T4 of 1.69 ng/dL, and thyroid stimu-5 ~: Y# j( t5 ^" K, f
lating hormone level was 1.3 µIU/mL (both normal).- g0 [1 H$ P$ z( x7 p! c9 ^8 {
The concentrations of serum electrolytes, blood
; b9 W1 t7 g" ~1 k3 Lurea nitrogen, creatinine, and calcium all were# i% }% G* h/ ]- V7 i" D& `
within normal range for his age. The concentration
3 F' W3 T1 u/ V% c% v7 _5 V- nof serum 17-hydroxyprogesterone was 16 ng/dL
" S8 }  R9 z  P1 \(normal, 3 to 90 ng/dL), androstenedione was 20
, j; l1 O9 j: ?; u3 p0 a" Kng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
  Q+ U" b5 k7 N+ B6 U* Sterone was 38 ng/dL (normal, 50 to 760 ng/dL),- @& c6 x! p: T0 n+ J; {
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
2 D. O1 {) O- p49ng/dL), 11-desoxycortisol (specific compound S)
! B1 U# k$ _* C% \% m/ V; jwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-! |6 e5 D9 m1 @
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
- U+ v- M9 l) b' R4 Ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL),) c$ S5 a; j( n+ `$ z, d/ @! m
and β-human chorionic gonadotropin was less than
1 H/ u4 k0 [! Z. t5 d5 mIU/mL (normal <5 mIU/mL). Serum follicular  y9 ]% v. G7 L3 b( J$ ^& `
stimulating hormone and leuteinizing hormone
+ s6 \2 K# y$ pconcentrations were less than 0.05 mIU/mL
* k* H1 W' s' ?/ {; Y( g- e(prepubertal).! k; n/ S" p. i6 w* R
The parents were notified about the laboratory  N4 o, g& E6 }1 t" L
results and were informed that all of the tests were) C& z$ \- `- c' k. K% ]' {& F
normal except the testosterone level was high. The
6 y# _5 G, K# @. l8 J6 mfollow-up visit was arranged within a few weeks to0 |) i. j' Q% R4 o- \0 u# O' E
obtain testicular and abdominal sonograms; how-
8 \: T; m$ \( x2 k1 Vever, the family did not return for 4 months.& K/ O/ N& [, {* k4 w% e$ b
Physical examination at this time revealed that the
1 k8 v$ A8 v$ w2 a9 V2 B" i6 W+ |+ Vchild had grown 2.5 cm in 4 months and had gained, G5 [' X) C4 }) {. f
2 kg of weight. Physical examination remained
' b' o8 q0 R% p6 J6 i7 Gunchanged. Surprisingly, the pubic hair almost com-
- A6 u' U% x6 ]( U/ `) cpletely disappeared except for a few vellous hairs at
3 M7 G- Q/ O- n( Y; Wthe base of the phallus. Testicular volume was still 2
" s/ {2 V* K) D. j, ?; BmL, and the size of the penis remained unchanged.1 u- b$ z1 q1 G& i( V
The mother also said that the boy was no longer hav-
. j2 B6 n. b$ j4 ting frequent erections.% {+ A* A4 u" N0 J5 V
Both parents were again questioned about use of
5 k+ i8 O6 R: _- ]2 G# r0 c9 ]any ointment/creams that they may have applied to" ?2 ]) X) C9 Y3 ?$ q8 x9 ?9 K3 G- v
the child’s skin. This time the father admitted the: t+ t, t4 A# P8 h. ]
Topical Testosterone Exposure / Bhowmick et al 5418 ^% V5 s8 P; q* _8 H5 W" W9 X4 V- [
use of testosterone gel twice daily that he was apply-3 G) E" }9 {6 x( b
ing over his own shoulders, chest, and back area for
; o& H/ Y! y1 W/ `; la year. The father also revealed he was embarrassed
* `0 G/ I- t& `$ Y% n* qto disclose that he was using a testosterone gel pre-- [/ c, A, u% X" m' `* z
scribed by his family physician for decreased libido
/ |, A  N. Q. E6 Y" b( \0 `secondary to depression.( b) Y2 S$ v* g
The child slept in the same bed with parents.
0 p5 Q! u, _- X. g/ X* m7 d6 aThe father would hug the baby and hold him on his5 Q4 O2 n! @7 o+ f, ?
chest for a considerable period of time, causing sig-+ U. e2 F; V3 d4 P. j
nificant bare skin contact between baby and father.
: x& m; L+ \- u, {The father also admitted that after the phone call,
) p* N& m7 g! o& awhen he learned the testosterone level in the baby
& W* i& ]; P6 n8 i7 V  p/ t. Twas high, he then read the product information
' |, V2 D. G2 n9 G1 ], \1 }packet and concluded that it was most likely the rea-6 u, J5 C% Y& l3 w2 I
son for the child’s virilization. At that time, they
3 m6 v' t* i7 U: ]$ xdecided to put the baby in a separate bed, and the
% @8 t2 J: O4 J" V5 w5 D7 k  }& \father was not hugging him with bare skin and had$ ^* ]+ B( [; \' t
been using protective clothing. A repeat testosterone2 B+ n0 c. P( n; K
test was ordered, but the family did not go to the
. X% t: t, H7 Nlaboratory to obtain the test.
" M( `: Q7 u. j7 l* S8 Y3 Q/ UDiscussion
6 l" p2 P! B" iPrecocious puberty in boys is defined as secondary3 U2 G- O- D* ]' d: e
sexual development before 9 years of age.1,4
  D  c9 Z7 V% }$ J) W) X* N* WPrecocious puberty is termed as central (true) when8 x7 r" |' T. A6 t1 E
it is caused by the premature activation of hypo-2 h+ `% |, j; J7 z
thalamic pituitary gonadal axis. CPP is more com-
4 [$ }& [  J0 k7 ]8 Lmon in girls than in boys.1,3 Most boys with CPP1 w5 q8 G2 \1 t. d
may have a central nervous system lesion that is
+ M" l& F6 C7 [' k9 `( g7 j, a% cresponsible for the early activation of the hypothal-1 j, n0 h+ V+ m# k) O
amic pituitary gonadal axis.1-3 Thus, greater empha-. C$ |8 e. S& J" C
sis has been given to neuroradiologic imaging in! ^0 T' M/ w) b. M: k$ f0 |6 K* o
boys with precocious puberty. In addition to viril-
5 N5 m0 y; {2 y% y7 @ization, the clinical hallmark of CPP is the symmet-
$ U, ]* E1 f# o- j' }4 Rrical testicular growth secondary to stimulation by
4 r' `* p: G( A6 Fgonadotropins.1,3
. g/ Z% E1 S* c8 j& @) u$ h- nGonadotropin-independent peripheral preco-
& m$ e+ X& \9 F. ~2 w9 Xcious puberty in boys also results from inappropriate
$ P: F0 B9 t) xandrogenic stimulation from either endogenous or7 q! K5 u5 p" C' V
exogenous sources, nonpituitary gonadotropin stim-- R% u" V. [1 U" P, q  `6 n9 {3 W; d
ulation, and rare activating mutations.3 Virilizing
9 p( o6 m$ u: f/ fcongenital adrenal hyperplasia producing excessive2 H5 ~5 o5 u$ i& y3 Z' n4 A, G4 J4 ]
adrenal androgens is a common cause of precocious2 D# {* ]* T0 d' i6 J/ y5 T  i' j# O
puberty in boys.3,4
$ c/ Z& O& r" X# X1 OThe most common form of congenital adrenal
) i$ E+ W. X( q% u2 _hyperplasia is the 21-hydroxylase enzyme deficiency.
5 Q  i3 v! A; cThe 11-β hydroxylase deficiency may also result in' N# S; J6 R% g; Z, \. e
excessive adrenal androgen production, and rarely,
6 F' }' B% w- O5 @2 m5 G: r% M1 man adrenal tumor may also cause adrenal androgen
/ U0 R/ \4 d7 W- ?; {7 ]excess.1,3  s2 E6 e, M- j3 j* i
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 ^- h4 b  i( ^/ E4 f3 `. J2 W542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
3 f' d  o3 t  P$ S% q7 a$ ?A unique entity of male-limited gonadotropin-
1 s4 v$ Z5 F# \8 i- \- h' ?independent precocious puberty, which is also known. r/ k: ?! @6 Y" O* K
as testotoxicosis, may cause precocious puberty at a  m9 ?+ S2 n" Y0 e( q/ U' ?; M) `
very young age. The physical findings in these boys6 g( G6 t$ o7 Y  c# ~7 A2 s
with this disorder are full pubertal development,( t: K% Y. d  I5 e
including bilateral testicular growth, similar to boys
& {% w) d1 L- t; }with CPP. The gonadotropin levels in this disorder8 j% U* X# n2 ]9 I0 f
are suppressed to prepubertal levels and do not show! \' j7 }0 }2 E: [7 w! d
pubertal response of gonadotropin after gonadotropin-
! ~& L5 j1 ]  D7 V! g9 `8 D, [releasing hormone stimulation. This is a sex-linked
* D0 D( o* D8 @/ A5 ~autosomal dominant disorder that affects only: r7 g- |3 ~( L. V
males; therefore, other male members of the family
7 `! l" N  X3 M( omay have similar precocious puberty.3
; }0 n  w  i4 a5 GIn our patient, physical examination was incon-( o  u5 I0 V0 C6 B) u
sistent with true precocious puberty since his testi-! e% [( Y7 R% K$ j5 M  K
cles were prepubertal in size. However, testotoxicosis2 Q7 t* f6 p, m! m: v2 I! W6 F
was in the differential diagnosis because his father8 c% i1 D  z' ^! m
started puberty somewhat early, and occasionally,
1 T/ d8 C9 n' Atesticular enlargement is not that evident in the
  P# ~" P. A$ X2 B  s4 t9 T2 L9 s) z4 |' Obeginning of this process.1 In the absence of a neg-3 X  r8 z0 x. o2 ?7 h! L/ M* k
ative initial history of androgen exposure, our
7 A6 Q: A7 H; h* w/ Bbiggest concern was virilizing adrenal hyperplasia,
6 r) M6 M* M$ |6 i. ^+ m3 Meither 21-hydroxylase deficiency or 11-β hydroxylase+ |0 g. H: _5 L9 U
deficiency. Those diagnoses were excluded by find-
4 t. o, h' P" Ving the normal level of adrenal steroids.# b% R, Z9 W. m6 @% n: w
The diagnosis of exogenous androgens was strongly6 ~1 x2 o' I, l: S9 V
suspected in a follow-up visit after 4 months because
. K9 M# }4 I' M7 ethe physical examination revealed the complete disap-0 y8 J5 V% O' y
pearance of pubic hair, normal growth velocity, and: z* {/ O  F0 {5 h- j2 z3 N
decreased erections. The father admitted using a testos-
9 ]3 t  H) R- yterone gel, which he concealed at first visit. He was
- n% X$ U! E) K6 a) }3 Ousing it rather frequently, twice a day. The Physicians’
0 e- D) G0 o4 M% D, RDesk Reference, or package insert of this product, gel or
! Z- h7 s% \( [( K4 |4 Lcream, cautions about dermal testosterone transfer to3 j( Q' O. p" n! q2 Q7 V* W4 Q7 A
unprotected females through direct skin exposure.
5 K; z0 G! H+ F% [. [Serum testosterone level was found to be 2 times the* N& X+ N# S% V& |  M$ o% }$ Z
baseline value in those females who were exposed to& M# s3 e, E6 g9 s' |
even 15 minutes of direct skin contact with their male$ r7 `! ]' U1 p) k6 L/ k
partners.6 However, when a shirt covered the applica-7 e* `3 ?7 u' G7 @; X7 a/ F
tion site, this testosterone transfer was prevented.6 f/ t, j- F/ i; Z( g& Z3 \, D, z4 B5 ~8 W
Our patient’s testosterone level was 60 ng/mL,# V5 P( N! {0 f+ h$ x7 N7 j" }+ M; L
which was clearly high. Some studies suggest that
: P( K. l# U5 P) R3 v, qdermal conversion of testosterone to dihydrotestos-
* t% H) g" r+ b- t2 D, ?( v* j2 I. Qterone, which is a more potent metabolite, is more
: v$ W7 }  h+ ?# _8 t- m1 Cactive in young children exposed to testosterone1 V8 m; A: Z$ i- C
exogenously7; however, we did not measure a dihy-
# X0 x, i+ Q* c- \6 Idrotestosterone level in our patient. In addition to
2 V% P; s2 A9 S' m) i1 Q% Fvirilization, exposure to exogenous testosterone in. A5 I. \; S! X! c
children results in an increase in growth velocity and: k, y+ x! y# d" O2 Q( X1 R7 g
advanced bone age, as seen in our patient.
( ~, J; b0 E+ Y# _# p# ]+ _The long-term effect of androgen exposure during3 _3 S% S% l5 h0 F2 {& ?: z8 L7 J
early childhood on pubertal development and final# F: }% a2 Q2 z! b! U
adult height are not fully known and always remain
* m* X4 R: @" E: k1 K& F/ [+ qa concern. Children treated with short-term testos-
$ s6 @6 [( ~- ?8 \terone injection or topical androgen may exhibit some
2 m/ O9 A, l9 n9 k* ^9 u& Vacceleration of the skeletal maturation; however, after$ y+ |% B  R0 Q  y4 ]
cessation of treatment, the rate of bone maturation1 j" t% M5 c; q- c2 T
decelerates and gradually returns to normal.8,9$ m8 g* b6 O$ B- c6 V4 E
There are conflicting reports and controversy
( J: D- V6 u; e2 }1 c$ K7 C% zover the effect of early androgen exposure on adult
. d: P+ |) n& rpenile length.10,11 Some reports suggest subnormal
. f4 [, |. s, M- j' a& ?8 g$ oadult penile length, apparently because of downreg-
2 D9 A+ n) i$ X. p' e  Z- Iulation of androgen receptor number.10,12 However,! l7 ?( v2 ?  @9 c
Sutherland et al13 did not find a correlation between" p; [  Q" _9 w. s* j! b
childhood testosterone exposure and reduced adult2 M( y" k/ Y9 ~" \. F
penile length in clinical studies.5 y3 T2 b% [/ b! E* @
Nonetheless, we do not believe our patient is
) B1 U% v8 _) T( y% g+ Kgoing to experience any of the untoward effects from6 S; U3 [) X8 s
testosterone exposure as mentioned earlier because! f6 j* z. t& F
the exposure was not for a prolonged period of time.
1 {) Y$ y0 \" pAlthough the bone age was advanced at the time of- a$ i9 X: U- }9 |. O, ?1 N
diagnosis, the child had a normal growth velocity at
1 W# ~# e2 W+ E+ u  v$ x* nthe follow-up visit. It is hoped that his final adult
4 n' G( j; ]4 W  {height will not be affected.
" o) f1 @3 Y5 WAlthough rarely reported, the widespread avail-
1 d! u: H( b. X- P4 v, g1 [ability of androgen products in our society may
2 c4 ^: ?! G% ]( _1 }indeed cause more virilization in male or female- q; B4 d* i1 e9 [& w
children than one would realize. Exposure to andro-6 `' l4 x; ~' v0 B. s* Y. A
gen products must be considered and specific ques-
1 `+ R4 v1 a; q+ C* w8 G+ o. Vtioning about the use of a testosterone product or
, P) B4 p  L: W) c5 [% Mgel should be asked of the family members during
9 J, s  T( i8 K7 J7 @/ F8 J3 O$ Xthe evaluation of any children who present with vir-
4 m2 o, D4 B5 y3 [: p/ f/ q# U, X" z: jilization or peripheral precocious puberty. The diag-% D, G0 C3 `+ ~0 u- B
nosis can be established by just a few tests and by2 O$ t) Y6 `) D" w) V+ R1 u! A1 U
appropriate history. The inability to obtain such a; t* C5 g% J/ E- x% c( Y" i
history, or failure to ask the specific questions, may
  w2 d# L  S; @. Sresult in extensive, unnecessary, and expensive
: B, w& x1 A! D. l; hinvestigation. The primary care physician should be
, e8 a& h. r( Z3 x" m% taware of this fact, because most of these children
7 P4 c+ W" \: G' ymay initially present in their practice. The Physicians’
6 j( w, f. h) l2 n; B& [Desk Reference and package insert should also put a" {& f" r( ~( _4 i
warning about the virilizing effect on a male or
2 \4 B! v: \" `2 xfemale child who might come in contact with some-
& H" T1 G. W5 V! E5 Zone using any of these products.6 h! V. ~. ]0 }. [3 S, r* i
References
" O2 p; `" g! V2 u; k1. Styne DM. The testes: disorder of sexual differentiation& b% {7 R& K" i6 s8 Q; r' q
and puberty in the male. In: Sperling MA, ed. Pediatric5 P, q1 j5 S  t! Q- w
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;2 u; K$ G4 \9 b$ B: o
2002: 565-628.  P/ }  G5 H% T
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
3 y4 x- D( v2 mpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old; Z2 D& L; M0 s' T
Boy Induced by Indirect Topical8 `, ^) d2 P3 ^+ l+ Q
Exposure to Testosterone
' B$ \& c8 [' }0 h/ W( KSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,24 @" C& ~7 _2 r, @
and Kenneth R. Rettig, MD1
1 g& U- e+ w6 }2 K* tClinical Pediatrics
8 x3 b' @$ I  uVolume 46 Number 6* T% D1 b7 `, ^  e! Z5 g1 t
July 2007 540-543
4 p3 K! L- W& n. D' X7 Z! U' l  R© 2007 Sage Publications/ P9 C% J: v2 Q  U% |# m( h# g
10.1177/0009922806296651% L- |+ l+ d5 ^+ i
http://clp.sagepub.com
# i9 P  d0 U9 f1 J7 K3 f% O5 ]hosted at
' o- @; K/ P' e! phttp://online.sagepub.com
& h; a& c+ S5 V0 d3 P( qPrecocious puberty in boys, central or peripheral," T! r/ i, [3 R  c" a! e( S7 Q5 h( |
is a significant concern for physicians. Central
5 i3 O; R0 Q1 B0 Uprecocious puberty (CPP), which is mediated% w1 A( j) [) E4 I" g  T) a1 q
through the hypothalamic pituitary gonadal axis, has/ }) ^4 J/ y4 M
a higher incidence of organic central nervous system, {, Y! N; r% c
lesions in boys.1,2 Virilization in boys, as manifested
* [( R4 ]6 X: x% a3 Vby enlargement of the penis, development of pubic* U) y6 Q( k7 \) e  L
hair, and facial acne without enlargement of testi-. @. M% O* T6 Q: {4 p; r
cles, suggests peripheral or pseudopuberty.1-3 We
  N5 I# M7 F( d  q5 v; Breport a 16-month-old boy who presented with the' h8 @! \0 U& @" @
enlargement of the phallus and pubic hair develop-
, i7 k/ Y5 p) u% k8 Y, ement without testicular enlargement, which was due
3 k: r0 I3 a, W  G6 J' N6 j. N) a& Mto the unintentional exposure to androgen gel used by
5 D0 G  H. b, a3 s) Ythe father. The family initially concealed this infor-
3 [: M+ t  h! Y3 I4 [mation, resulting in an extensive work-up for this
4 @& }- k  ?+ S1 V" p0 v+ Q% Cchild. Given the widespread and easy availability of
4 N! @3 Q+ G+ Q- }8 O% Ytestosterone gel and cream, we believe this is proba-5 ~! \; j; D1 X# Y. c
bly more common than the rare case report in the
0 O$ K: m) S4 q2 ]0 a7 y% D) vliterature.4* A8 z% d8 B, o6 o  l, x: I# K
Patient Report) l% Y' l% }, U
A 16-month-old white child was referred to the
8 f5 p% t( x3 L$ |, n0 Jendocrine clinic by his pediatrician with the concern
: B8 Q) l* V+ E9 o, L" lof early sexual development. His mother noticed% u0 V9 Z  Y# O* }
light colored pubic hair development when he was
4 O' {3 `  ?: t' I2 s0 P$ z3 [( yFrom the 1Division of Pediatric Endocrinology, 2University of
$ P$ x; ]5 x" J  ^: H' L; ]) TSouth Alabama Medical Center, Mobile, Alabama.
' d& ~5 Y0 ]5 M2 k' P1 R+ PAddress correspondence to: Samar K. Bhowmick, MD, FACE,
' V; x, K% I: qProfessor of Pediatrics, University of South Alabama, College of: c- }# x: K; `$ M8 a
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
' R: g3 D7 m$ k: ae-mail: [email protected].9 w. h$ h, n% [0 E" q4 q+ ~" r9 [
about 6 to 7 months old, which progressively became
& i. x' p8 U6 [2 ~8 b0 Xdarker. She was also concerned about the enlarge-
$ \$ [: g8 a4 T" f0 W, Lment of his penis and frequent erections. The child/ n* O3 {4 y4 C: _- P" J0 l
was the product of a full-term normal delivery, with
: ~1 h3 i! m4 d" la birth weight of 7 lb 14 oz, and birth length of! y- H  Y2 ]- t
20 inches. He was breast-fed throughout the first year
* W( D% Y* A& x  W( |- [8 Sof life and was still receiving breast milk along with
7 ]# U! d+ j$ ]" V3 g+ ]3 Isolid food. He had no hospitalizations or surgery,
& a4 X4 C: S6 {0 _, z8 `5 Gand his psychosocial and psychomotor development: _4 b1 l) h4 C3 ^* S& T  a9 d
was age appropriate.
2 ^: I7 @( z+ LThe family history was remarkable for the father,% p" u& r: G$ Y. z/ f5 R5 l! x
who was diagnosed with hypothyroidism at age 16,
6 c$ T, k6 ^0 R& |6 ]) `( kwhich was treated with thyroxine. The father’s  G  L* }/ L- R5 D
height was 6 feet, and he went through a somewhat7 L6 ]) a2 a7 b) M' [
early puberty and had stopped growing by age 14.
  I; o6 K8 W# ^  P( CThe father denied taking any other medication. The
4 R. g0 k* Y: M2 a5 @. d- fchild’s mother was in good health. Her menarche
5 {6 V5 H0 ~: [3 j. Kwas at 11 years of age, and her height was at 5 feet2 [) V  H3 O! b; ?
5 inches. There was no other family history of pre-
, B  ?1 m6 @# ^; icocious sexual development in the first-degree rela-, e3 W9 W8 [# q8 N5 o' b
tives. There were no siblings." p& U6 U3 L3 p! i' x  B6 B% [
Physical Examination7 C3 S( s3 W# H
The physical examination revealed a very active,
# I# J4 }2 I9 l1 z8 a/ Yplayful, and healthy boy. The vital signs documented4 }& S& H, G. O" ?. {+ x
a blood pressure of 85/50 mm Hg, his length was
# Z( q, ?  ]/ C8 {4 }: a$ x2 f6 N90 cm (>97th percentile), and his weight was 14.4 kg
6 ?1 t# u9 F0 f(also >97th percentile). The observed yearly growth
+ p, h7 i5 j' t9 b) c/ P. P' Qvelocity was 30 cm (12 inches). The examination of3 ?2 _  l8 p- k3 n
the neck revealed no thyroid enlargement.9 P: T" F% L# ?4 M
The genitourinary examination was remarkable for
% \% U, x+ t+ e& Oenlargement of the penis, with a stretched length of
! I1 E- B: k9 j" G3 v8 cm and a width of 2 cm. The glans penis was very well5 L* y- j* v+ J" |% J* A) h
developed. The pubic hair was Tanner II, mostly around3 C# z% a/ E% [2 p7 G
540$ B% i% S% u, c
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& Y5 u0 Q0 J: h2 C! `* i
the base of the phallus and was dark and curled. The; O; n5 @7 d" i5 e
testicular volume was prepubertal at 2 mL each.( b9 G2 s2 X& g5 }
The skin was moist and smooth and somewhat5 ~) Y9 v1 R8 S/ u
oily. No axillary hair was noted. There were no
0 r6 `$ O) C2 m& i- X( ?abnormal skin pigmentations or café-au-lait spots.6 m' Y2 X) F3 q; ?- ?2 Z( O5 I
Neurologic evaluation showed deep tendon reflex 2+- a  j( B/ ~0 ?
bilateral and symmetrical. There was no suggestion7 k) q) _4 f2 d9 [! o7 k5 ?9 v* D
of papilledema.( g5 h' j2 h8 U1 K
Laboratory Evaluation
! m+ w5 j8 ~1 ?# J! E2 yThe bone age was consistent with 28 months by3 X5 ^4 E' D  G5 |0 ?7 C" t/ R
using the standard of Greulich and Pyle at a chrono-& }3 a: E% z( e& W! T
logic age of 16 months (advanced).5 Chromosomal6 f7 b/ ?6 F; k
karyotype was 46XY. The thyroid function test
  |/ q+ F- B. ~$ X! Cshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
4 r' `9 q5 v% Hlating hormone level was 1.3 µIU/mL (both normal).
6 v0 @3 _' S8 N0 e$ |4 H1 R9 YThe concentrations of serum electrolytes, blood, t% f+ |( T% t
urea nitrogen, creatinine, and calcium all were. S. D- `- N& R; S( T
within normal range for his age. The concentration3 d8 F3 y, }, g4 H1 ~7 R
of serum 17-hydroxyprogesterone was 16 ng/dL
% E, H& H- G9 U9 }& w0 ~" i2 d6 s3 U(normal, 3 to 90 ng/dL), androstenedione was 206 V- J1 C# S* D; B( W1 g* S8 M* @9 B
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
( q% N" K5 s* ]5 l/ e- Q/ |8 zterone was 38 ng/dL (normal, 50 to 760 ng/dL),& m$ H  |8 T$ g0 y2 c
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
+ T! M8 ^7 x0 Z' ?8 k# R1 N1 [49ng/dL), 11-desoxycortisol (specific compound S)
6 i: D" d- }7 O3 Lwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
# E- }. q7 j3 M+ `) w1 Utisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
! q% X2 e5 n/ g$ y1 }* stestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
; O  U- @& A  e4 a# O# g9 g' jand β-human chorionic gonadotropin was less than
4 n7 p6 M$ _' p  m5 mIU/mL (normal <5 mIU/mL). Serum follicular9 J2 T/ I, H7 i3 C5 S, }- s  F
stimulating hormone and leuteinizing hormone) j6 X0 G7 Q2 j5 M
concentrations were less than 0.05 mIU/mL7 C. @/ Q+ ~6 Z6 L
(prepubertal).
6 z8 M$ q( Y* ]" k9 lThe parents were notified about the laboratory% s# M& p3 S9 u, f
results and were informed that all of the tests were5 e1 J2 z5 M/ J9 o# n
normal except the testosterone level was high. The* o. m9 Q) a8 q" v) G0 H
follow-up visit was arranged within a few weeks to4 ?, s+ f1 ^  o5 q1 B: r$ m9 {- x: E  b
obtain testicular and abdominal sonograms; how-
- ]7 [, D* e9 m  Uever, the family did not return for 4 months.
) X" U9 G; ~' D" B! {! dPhysical examination at this time revealed that the! y% |0 j0 I% c) b- R; E
child had grown 2.5 cm in 4 months and had gained8 V; `$ M/ k7 D4 k8 {, f$ {- C# V, r
2 kg of weight. Physical examination remained8 _( e8 Y$ S, e- q3 Q+ s
unchanged. Surprisingly, the pubic hair almost com-
" }2 ?' j" Q7 Z  n) tpletely disappeared except for a few vellous hairs at8 p4 n5 W8 H: W" i- b) R4 j' f! r
the base of the phallus. Testicular volume was still 2
; [; e! b/ o: w2 k6 XmL, and the size of the penis remained unchanged.
9 V5 m+ G; H( n2 \# o: ?: `& VThe mother also said that the boy was no longer hav-. |- Q# {7 o% d5 E1 x9 d, L0 l0 y! s
ing frequent erections.9 T; @, K, g- G
Both parents were again questioned about use of/ C  E" {- u# C/ b
any ointment/creams that they may have applied to
0 ~2 I" d  p( t9 |7 V& i) P: Jthe child’s skin. This time the father admitted the5 b/ p/ L2 u( A4 f  i
Topical Testosterone Exposure / Bhowmick et al 541
+ b* v. z6 h/ H. f8 E& T9 Muse of testosterone gel twice daily that he was apply-4 p6 W( l: Z8 Y) ?5 f
ing over his own shoulders, chest, and back area for
3 L' B( D% L1 Q, j% @( |1 d4 ta year. The father also revealed he was embarrassed# [' v9 e6 V8 n6 s$ E% q. R
to disclose that he was using a testosterone gel pre-& ~; o" D1 y0 U3 S  A
scribed by his family physician for decreased libido8 F4 W& t; d3 h: g% o# `
secondary to depression.2 F# h9 |' O" D3 v8 x' l
The child slept in the same bed with parents.
8 V! w; d" H* M3 tThe father would hug the baby and hold him on his, L+ ~6 _7 ?% U
chest for a considerable period of time, causing sig-
! z" [, a- F/ t  b! qnificant bare skin contact between baby and father.
) p3 f0 [3 r1 OThe father also admitted that after the phone call," V0 D6 o# V4 V0 D5 k
when he learned the testosterone level in the baby# f, H& t6 _3 p5 F/ e& @/ @2 o3 v
was high, he then read the product information
( t4 U9 t' X2 {- J" npacket and concluded that it was most likely the rea-. ~" O* Y6 _+ L+ c
son for the child’s virilization. At that time, they" w8 f3 A+ W/ {- J9 a! a1 }$ G
decided to put the baby in a separate bed, and the
) _$ |( @0 m0 L% |0 }4 rfather was not hugging him with bare skin and had* n! x! R  h" e* c8 j6 u3 Y
been using protective clothing. A repeat testosterone9 L; }# h/ T& A; w6 e6 ?3 X
test was ordered, but the family did not go to the0 P# m: Q' S! c" m  |3 @  F
laboratory to obtain the test.7 Z. M9 w( f( b
Discussion
$ t- C5 e/ Z% V+ ]* uPrecocious puberty in boys is defined as secondary: e4 r$ b$ a1 x; J3 P6 P7 y
sexual development before 9 years of age.1,4
  V) X* k  v7 @  N1 u' C9 C8 WPrecocious puberty is termed as central (true) when
1 O0 z9 D; r1 `6 z2 }! g# u# Xit is caused by the premature activation of hypo-* r; T8 Y3 E& W3 l8 K2 e% e
thalamic pituitary gonadal axis. CPP is more com-0 S/ Y1 o9 t5 `# y! b4 Q' t9 n
mon in girls than in boys.1,3 Most boys with CPP1 H0 c# D) _5 G* T+ R( X( M
may have a central nervous system lesion that is1 o4 Z( _, P1 k8 n( y+ T0 W
responsible for the early activation of the hypothal-
( B' U) {8 v* G. L3 samic pituitary gonadal axis.1-3 Thus, greater empha-4 b% c* `- A4 Q4 L( H' ]
sis has been given to neuroradiologic imaging in* M, ^+ `, x( |
boys with precocious puberty. In addition to viril-
# n, V7 e% ?% E5 c& e( gization, the clinical hallmark of CPP is the symmet-( e! C, Z3 W0 k
rical testicular growth secondary to stimulation by
1 _/ Y# J' Z3 W+ E7 e# ogonadotropins.1,3) Y3 x- Y' k' W$ F
Gonadotropin-independent peripheral preco-
; N) G# }0 ~. x, }, f) pcious puberty in boys also results from inappropriate) H6 |( E5 O7 o4 M# E. Q" `
androgenic stimulation from either endogenous or! ]) p+ `$ `3 Q% k3 p
exogenous sources, nonpituitary gonadotropin stim-# r7 c, T- c& M3 }. ^
ulation, and rare activating mutations.3 Virilizing6 t- {, X; q( M. F5 L2 J
congenital adrenal hyperplasia producing excessive
/ v# J; ]( \" Nadrenal androgens is a common cause of precocious0 R% k% J/ f1 ]0 }' S: E& O+ a
puberty in boys.3,4$ B9 H4 d; G, H: s
The most common form of congenital adrenal
" |. i" \1 T  fhyperplasia is the 21-hydroxylase enzyme deficiency./ f' K/ t, R' J5 d
The 11-β hydroxylase deficiency may also result in4 T% \9 H! e" l2 }2 S4 M  Z3 T
excessive adrenal androgen production, and rarely,
1 T# s  G* ]8 ?  c0 {8 P' Wan adrenal tumor may also cause adrenal androgen
  p' B4 k: C. \- T' u5 p: Oexcess.1,31 @: O  ^/ J+ N( n
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) F" S+ d- u0 |9 V9 Z- }0 P0 {
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007/ h& q% _, |* U$ T3 P, }: d
A unique entity of male-limited gonadotropin-2 X7 Z& N" d4 \9 ~6 e
independent precocious puberty, which is also known
9 ^0 J3 G. v0 o9 u' R+ Xas testotoxicosis, may cause precocious puberty at a) c* v! b4 T  U0 V& W( \1 L
very young age. The physical findings in these boys
( i3 @) |& G1 X: Fwith this disorder are full pubertal development,- `0 S" U1 T. ^) c, F( z9 r8 r$ u
including bilateral testicular growth, similar to boys
# h) @% C1 s2 [with CPP. The gonadotropin levels in this disorder& s: n/ w6 X, }
are suppressed to prepubertal levels and do not show4 {0 B5 B% w& T  ]; F. l" u
pubertal response of gonadotropin after gonadotropin-% D: X7 V) E$ B
releasing hormone stimulation. This is a sex-linked" F7 j, r& N0 E3 i5 v6 ?( d9 r
autosomal dominant disorder that affects only# t6 o0 p( d" L9 A3 d' H
males; therefore, other male members of the family! A  u+ S7 @9 y. R9 W6 [
may have similar precocious puberty.32 U: }$ L  `; H6 ]6 s  L! \, S6 g
In our patient, physical examination was incon-
' K  L  Z+ B( Ksistent with true precocious puberty since his testi-  r* T/ K1 T; m2 F" ]. G8 B
cles were prepubertal in size. However, testotoxicosis, Z6 L: n: ]1 G* S0 r; F
was in the differential diagnosis because his father2 O- a/ i; f3 t. \9 y1 q
started puberty somewhat early, and occasionally,
6 \) x5 w/ t2 n8 P! y& Q, f  [testicular enlargement is not that evident in the, j% N; q/ y4 W" ]* I7 D
beginning of this process.1 In the absence of a neg-
. m( d( T" l6 Z9 z# o5 Z5 Zative initial history of androgen exposure, our
0 l$ j% A4 B3 {# y# t% Pbiggest concern was virilizing adrenal hyperplasia,
) h4 `% W4 D, D* @+ veither 21-hydroxylase deficiency or 11-β hydroxylase! w1 E" }" {8 n- Z7 j; x0 A$ c
deficiency. Those diagnoses were excluded by find-8 j" B2 B: h& [7 V" j7 I% ^
ing the normal level of adrenal steroids.1 u' i: N1 _$ i9 O. @. h
The diagnosis of exogenous androgens was strongly
/ b/ G9 m( Y4 [. A$ P4 U; z3 vsuspected in a follow-up visit after 4 months because. T( F9 O# M, B
the physical examination revealed the complete disap-3 h5 i- K" N0 F8 d6 q( W
pearance of pubic hair, normal growth velocity, and
/ v' O. F# ?% t8 r. O  rdecreased erections. The father admitted using a testos-
2 r6 W+ \, z, w- A, b6 k: O: Qterone gel, which he concealed at first visit. He was, l" |3 e( h" Y
using it rather frequently, twice a day. The Physicians’
- a* p* L  a& hDesk Reference, or package insert of this product, gel or8 v& s5 Z6 q4 j* ]
cream, cautions about dermal testosterone transfer to, U1 J. m4 F  l$ a# n  O
unprotected females through direct skin exposure.
! U& X# L! S. p/ S' B! p- E5 A+ B! a( zSerum testosterone level was found to be 2 times the+ [, }/ Z  u" ]# ?9 v
baseline value in those females who were exposed to- F; c! }! r7 G+ h' J
even 15 minutes of direct skin contact with their male
2 k/ h0 D6 _6 p  {) {$ J; c5 z' tpartners.6 However, when a shirt covered the applica-
1 i; A) t) d3 H# w) ]# h' ation site, this testosterone transfer was prevented.. {6 k) I# W$ \$ v
Our patient’s testosterone level was 60 ng/mL,
4 l$ s+ {7 f1 m8 d8 \which was clearly high. Some studies suggest that
; N* q6 G$ M, `4 E. b) V5 Xdermal conversion of testosterone to dihydrotestos-. s/ m3 y" u3 B, n1 o8 n
terone, which is a more potent metabolite, is more& E% S4 ~& i! M5 T% j1 m+ f6 J
active in young children exposed to testosterone2 ?! [4 ^2 C' D0 d6 j% y6 V
exogenously7; however, we did not measure a dihy-
( N2 G- p! B+ Adrotestosterone level in our patient. In addition to
2 y/ V0 P2 V$ x" [/ Jvirilization, exposure to exogenous testosterone in
; J: r. \$ u8 M4 W# x9 M2 W6 Z  Uchildren results in an increase in growth velocity and
8 M$ Y* ]5 ^; U! y  zadvanced bone age, as seen in our patient.
' e1 }. w% x3 d$ c9 H7 ^The long-term effect of androgen exposure during
- a/ n" _8 H  q2 {1 gearly childhood on pubertal development and final, @8 [  }0 p- |" }1 C% E
adult height are not fully known and always remain
9 I0 s/ u- ?4 U% e& p# xa concern. Children treated with short-term testos-
8 m) K5 f% f1 B9 f1 s/ Gterone injection or topical androgen may exhibit some7 @' F: M* S3 ]
acceleration of the skeletal maturation; however, after
; V7 T" h, b! _0 g3 q9 \5 \5 k/ t( Ucessation of treatment, the rate of bone maturation+ O$ j4 x2 `" p, ~( G6 u' B
decelerates and gradually returns to normal.8,9
: F' j7 S9 p- k' b; NThere are conflicting reports and controversy, h# a2 ~1 X2 k0 X& b
over the effect of early androgen exposure on adult
) C* b+ M& u- L5 [2 \4 _* ]penile length.10,11 Some reports suggest subnormal7 S# h4 m9 r6 q5 r
adult penile length, apparently because of downreg-; R  J4 D& U5 \, C" A! f
ulation of androgen receptor number.10,12 However,6 w& J! y* b/ z: J: I
Sutherland et al13 did not find a correlation between  N, `  A* H: }4 t) N- h
childhood testosterone exposure and reduced adult
5 x" s6 C/ F7 `& Mpenile length in clinical studies.
: i2 U# \. q% ~( H& u( n3 oNonetheless, we do not believe our patient is
% m- x" b8 ?" n: F) J( dgoing to experience any of the untoward effects from
4 G( M) l9 ]7 l' Ztestosterone exposure as mentioned earlier because1 e  E8 ^# x) w; t  {3 y6 B
the exposure was not for a prolonged period of time.
5 ^+ O" l1 F* U8 T. m' ^Although the bone age was advanced at the time of
, Z  W9 G* a7 {/ Ldiagnosis, the child had a normal growth velocity at
3 s6 u5 }9 K  G' ithe follow-up visit. It is hoped that his final adult
. |7 l% I6 q6 V0 O! cheight will not be affected.
4 `" z" A. T0 n7 F! a* s1 n1 EAlthough rarely reported, the widespread avail-6 k- E' J! t$ M+ B
ability of androgen products in our society may& h1 X# L- Y  J0 Y  M7 B4 g/ y
indeed cause more virilization in male or female0 B; |; y9 Z9 ^# W6 a3 Z4 y* l
children than one would realize. Exposure to andro-8 j% z1 O& L& K" @4 H: @/ i& s
gen products must be considered and specific ques-* t4 h2 Q/ s2 d9 o5 d2 X$ P
tioning about the use of a testosterone product or
5 {: q. r7 Z! C7 y) z7 n/ Pgel should be asked of the family members during! f+ c) M! ]% ?1 s1 k* h
the evaluation of any children who present with vir-
" l% f  [4 B3 Ailization or peripheral precocious puberty. The diag-
' t( `) I9 K+ ~& Cnosis can be established by just a few tests and by
- U, R5 l' d( q1 }  Y. Eappropriate history. The inability to obtain such a
; ~& R% t5 B4 C: N' mhistory, or failure to ask the specific questions, may; M4 W; k% v' w
result in extensive, unnecessary, and expensive
9 i& G! Y% |5 A9 s/ Linvestigation. The primary care physician should be
+ b* n2 m; w+ a  Raware of this fact, because most of these children
- |4 C* @! m0 t$ q7 O: v5 V! Vmay initially present in their practice. The Physicians’+ L# ~/ D3 x( O" L* p6 u
Desk Reference and package insert should also put a
1 r8 [6 F+ o" x8 p) r$ Xwarning about the virilizing effect on a male or
3 ]4 E+ i+ w/ y3 z6 C1 c3 Z0 hfemale child who might come in contact with some-
8 w6 ~% G6 [* ~# R: v+ Hone using any of these products.& Z! T. b5 a8 w9 Z# j/ d
References! c6 ]; A0 h7 L9 C5 u& d
1. Styne DM. The testes: disorder of sexual differentiation
- @- I8 H5 c1 T6 f2 o# k# \and puberty in the male. In: Sperling MA, ed. Pediatric
, T& p8 U* N, jEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;- g, H0 [4 _/ s$ d/ x
2002: 565-628.. z9 ~3 }7 B8 f/ f" l( a
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
; @5 n2 ~/ u4 O8 a$ ]puberty 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

" i* J4 U2 ^+ Z8 x' h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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