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Sexual Precocity in a 16-Month-Old. z$ q5 w, q' d1 z, H
Boy Induced by Indirect Topical2 b8 @; y% q: Z' l
Exposure to Testosterone" h1 N# ^6 F0 @1 m" L
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2) F" C% V' n" o2 N( T
and Kenneth R. Rettig, MD1
/ [6 J, M( u% @0 a/ q' lClinical Pediatrics
. Y& n& F% G/ w! `2 _7 UVolume 46 Number 6
$ I! K, B: u& XJuly 2007 540-543- H" F+ l. j5 B# z' _2 C
© 2007 Sage Publications
, z5 `% S1 F2 r% r10.1177/0009922806296651+ X$ y# m2 D; k
http://clp.sagepub.com
! z2 G7 x' j$ O" I7 z: o4 \6 R2 @hosted at
0 X* t3 ~2 W4 U! ~$ thttp://online.sagepub.com4 q* Q+ V) ?% ?  S. g
Precocious puberty in boys, central or peripheral,; g5 n7 k. b8 T3 j$ l: l
is a significant concern for physicians. Central
: O  Y% q" E- N( F) ^3 L8 \3 s7 s( Aprecocious puberty (CPP), which is mediated" r" _, Z+ q" O) K* q. j
through the hypothalamic pituitary gonadal axis, has
, k( V9 p. ?* I7 F. A6 l9 |4 Q# \5 ga higher incidence of organic central nervous system
! Y+ w. L4 f6 w, mlesions in boys.1,2 Virilization in boys, as manifested% |. k* B% X& e6 {
by enlargement of the penis, development of pubic
# b; Z, V% U- h4 b6 C( g. Jhair, and facial acne without enlargement of testi-
8 S! ]9 Q; G: R# }4 n$ tcles, suggests peripheral or pseudopuberty.1-3 We
. H' o' n+ k1 b" ~* n$ X/ qreport a 16-month-old boy who presented with the$ }7 |- w6 z* `1 N) l. o
enlargement of the phallus and pubic hair develop-
! ~9 Y; J& h3 S$ J  n5 o, ]4 k/ yment without testicular enlargement, which was due) j6 h: G, w& ?. f! D
to the unintentional exposure to androgen gel used by
  \3 J4 M* n, K5 Rthe father. The family initially concealed this infor-. E7 D( l2 N8 q) O
mation, resulting in an extensive work-up for this
% f: j: U  P0 b# B8 G5 Q- W% Vchild. Given the widespread and easy availability of
. M* \; ]: R8 D0 Xtestosterone gel and cream, we believe this is proba-9 f9 f  h. m& a0 W: F
bly more common than the rare case report in the9 z5 N- ?; l# f4 `) Q3 f" H
literature.4
4 j# E6 a- l7 N( v* T; EPatient Report
9 G+ L5 Z8 r/ B! l& ~& ^) XA 16-month-old white child was referred to the
8 l" F/ z9 I6 \0 lendocrine clinic by his pediatrician with the concern
/ }7 j# P. C/ q# _3 ?" n. Qof early sexual development. His mother noticed
- k7 W; c1 m+ I) b6 N& v: k* s' glight colored pubic hair development when he was
: c8 z% x4 ?6 RFrom the 1Division of Pediatric Endocrinology, 2University of$ e& x( V8 Y1 a9 U
South Alabama Medical Center, Mobile, Alabama.
: ^, z6 E: L6 r3 fAddress correspondence to: Samar K. Bhowmick, MD, FACE,
. J8 }/ Q! g2 hProfessor of Pediatrics, University of South Alabama, College of
$ l  f. @% ]& |& A  QMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;2 U0 T3 H% r! P- L* y) G5 A- H' P
e-mail: [email protected].9 W" P7 |. G' ]: Y
about 6 to 7 months old, which progressively became
! n5 E6 J# p) j( o4 ydarker. She was also concerned about the enlarge-+ Z4 v- o# O" [1 k
ment of his penis and frequent erections. The child
$ L, h* r4 o) J. g4 n3 F* B3 u. P; owas the product of a full-term normal delivery, with
, y. R* H8 t" y3 n) _a birth weight of 7 lb 14 oz, and birth length of2 M8 t& a5 R) @5 d2 `
20 inches. He was breast-fed throughout the first year5 X0 L; |. |8 _  j5 S1 ~; x) a' w+ D: z
of life and was still receiving breast milk along with
& d- |  }4 m4 X1 [0 R- v  t1 ssolid food. He had no hospitalizations or surgery,  k6 [+ ^0 n; d+ A" R
and his psychosocial and psychomotor development
3 X6 }' S9 Z- e* T* A7 xwas age appropriate.# z# s! |$ p! u0 o5 |3 j
The family history was remarkable for the father,8 P; `2 }) i1 B/ X
who was diagnosed with hypothyroidism at age 16,
1 M0 w' [6 I; i; @7 j5 [which was treated with thyroxine. The father’s
% k2 N0 k5 z) }height was 6 feet, and he went through a somewhat' f; Y7 E3 x1 B! F$ y
early puberty and had stopped growing by age 14., c" m8 s" w( S- B' z
The father denied taking any other medication. The
; x7 n9 [, U) l" @. L1 nchild’s mother was in good health. Her menarche3 z, \5 ^! P/ [+ l. w6 a! J
was at 11 years of age, and her height was at 5 feet
. m) d! g" s' Y8 g+ E5 inches. There was no other family history of pre-
$ N' F! F% c* v) I' Xcocious sexual development in the first-degree rela-
- |9 t% J! R+ m; W6 o& d2 f  E+ mtives. There were no siblings.
6 z, O, \7 U3 C. E9 @Physical Examination" L9 `0 |( G& {: r! F. ^8 J$ q
The physical examination revealed a very active,
" X) P. Q% s  W" t- aplayful, and healthy boy. The vital signs documented1 U$ e; Y8 H/ q9 ^3 Q# q$ A
a blood pressure of 85/50 mm Hg, his length was
0 J' Q/ V  m2 G7 u# G% z90 cm (>97th percentile), and his weight was 14.4 kg. b) X0 a7 G) s; W
(also >97th percentile). The observed yearly growth# J6 t0 {- u- q+ `' U7 K2 h$ O
velocity was 30 cm (12 inches). The examination of; y, j$ e+ t6 d! k
the neck revealed no thyroid enlargement.
4 R: |4 U: a. d) Q) mThe genitourinary examination was remarkable for
$ q& L2 P1 z/ }) H! ~enlargement of the penis, with a stretched length of# `$ G7 R- O8 Y' p3 f  q4 m
8 cm and a width of 2 cm. The glans penis was very well. o9 F3 ?  N# U! e" O
developed. The pubic hair was Tanner II, mostly around
4 g. k) F. N- e8 T3 z" E- M! W/ p  h540* N9 O8 ^3 X- H$ _
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# A4 k5 J0 a; l/ J: o0 O9 ?# D  @
the base of the phallus and was dark and curled. The
8 g* d, C' X, \' U5 Q( V/ G" ^0 utesticular volume was prepubertal at 2 mL each.5 [1 L$ B1 ^2 @& Q7 H) R% a/ r
The skin was moist and smooth and somewhat$ t: Q. j  s4 y5 x! Q) @' `
oily. No axillary hair was noted. There were no- t. u  K/ _% {
abnormal skin pigmentations or café-au-lait spots.  n1 H7 F! X) m/ a/ f% H
Neurologic evaluation showed deep tendon reflex 2+
6 D# Z1 g$ n  f  ~4 v3 v, abilateral and symmetrical. There was no suggestion
6 z5 |  h- c& r9 V. \' {$ G2 l" N( Sof papilledema.' f+ D$ M5 U: a/ r" Y
Laboratory Evaluation* V6 K  C8 K! N8 j7 D" q
The bone age was consistent with 28 months by
( b- ]3 _$ [3 b+ ]6 I4 T6 J. [! Pusing the standard of Greulich and Pyle at a chrono-
: t4 q3 X6 N& {  j. ?" dlogic age of 16 months (advanced).5 Chromosomal
! Q/ k, q+ \* V5 H. \! Y; Ukaryotype was 46XY. The thyroid function test3 Y9 s  ]& B1 {- q4 T! ]
showed a free T4 of 1.69 ng/dL, and thyroid stimu-& z! `4 B" o& K1 s% r6 B
lating hormone level was 1.3 µIU/mL (both normal).
+ @& [9 m1 t1 \The concentrations of serum electrolytes, blood
  |) E1 V3 Z5 u7 Vurea nitrogen, creatinine, and calcium all were
8 Y; L4 o( `% D  _5 W& P, Cwithin normal range for his age. The concentration) }, Z2 _2 V7 E' ]$ ?# L
of serum 17-hydroxyprogesterone was 16 ng/dL  F9 b0 {  O. v, ^5 z  X) ?
(normal, 3 to 90 ng/dL), androstenedione was 20( R9 K* Q# W3 l" M2 I: v
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
. p* n, B; q7 m6 t8 ^& h7 }5 [terone was 38 ng/dL (normal, 50 to 760 ng/dL),
( g1 p" M$ `: A+ `' M  b9 Ddesoxycorticosterone was 4.3 ng/dL (normal, 7 to
) v' P5 U+ N+ j. V) f0 j49ng/dL), 11-desoxycortisol (specific compound S)" y, k% `$ Q& R
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-: _" [  ^3 G  H, M
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
. t% W* y( P, M0 t4 ?0 ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
5 h6 D% H0 O% ?, i9 K  V3 A: Hand β-human chorionic gonadotropin was less than
, j: V+ S( e$ P4 o0 ~" s, m5 mIU/mL (normal <5 mIU/mL). Serum follicular/ C4 m8 V& L# q+ [# J, V
stimulating hormone and leuteinizing hormone
! m8 v0 X3 H  f, X2 fconcentrations were less than 0.05 mIU/mL' i0 j6 O& Z7 h1 ~, G1 M
(prepubertal).* [/ b9 H" n1 u
The parents were notified about the laboratory
1 \" [4 @1 t# _9 ^1 B5 Z: b  Aresults and were informed that all of the tests were, L6 q" W  R' C' P+ d' ]
normal except the testosterone level was high. The- B) L4 H1 e2 l6 j0 B: D. ^, C
follow-up visit was arranged within a few weeks to
+ [8 h* X" A% F  ~( yobtain testicular and abdominal sonograms; how-
" Y7 w3 m5 `" t; Jever, the family did not return for 4 months.
# t( H* D9 }. G0 ?' y0 zPhysical examination at this time revealed that the
6 n  U9 K' b4 @3 i# F9 Bchild had grown 2.5 cm in 4 months and had gained/ Q' ~; Y3 E; L' e7 R/ |3 A% L
2 kg of weight. Physical examination remained9 r- ?+ T7 q4 ?# _. ^2 p$ B
unchanged. Surprisingly, the pubic hair almost com-
7 m- r  Y% f# ?9 _7 [& O9 Opletely disappeared except for a few vellous hairs at! v, M/ Q! {" Q* y5 v+ N, ~
the base of the phallus. Testicular volume was still 2
0 o1 w3 D) E9 B  S0 M  RmL, and the size of the penis remained unchanged." L$ Z4 q/ M8 ?6 _
The mother also said that the boy was no longer hav-) r! P) ^1 s/ G: P
ing frequent erections.* i, Z1 z$ O" c# b- r! [% e& I
Both parents were again questioned about use of" Q! N! D! ~% i" x, n( q
any ointment/creams that they may have applied to0 f" E) _& k- b( M2 Q1 J3 e9 r; i4 O
the child’s skin. This time the father admitted the, Z9 Z, d7 x  S* D4 r4 u+ v+ f9 N
Topical Testosterone Exposure / Bhowmick et al 541
& g9 [8 v6 s. u2 l2 k& _use of testosterone gel twice daily that he was apply-
: o: r6 b7 ?  S2 ?/ ling over his own shoulders, chest, and back area for/ [3 |6 Z" x. j( D4 {
a year. The father also revealed he was embarrassed
0 r$ q4 _) Z8 A8 @% H. [9 ^to disclose that he was using a testosterone gel pre-$ v+ M$ [  U: w4 x  u5 V
scribed by his family physician for decreased libido
) Q# [  `8 f# A. I- {' D% Msecondary to depression.
; ~7 x2 V  {5 ^9 K; s' f: M3 qThe child slept in the same bed with parents.
  B5 [9 n7 m% v4 v: u1 LThe father would hug the baby and hold him on his
! d3 Q- x+ }/ w& s: Rchest for a considerable period of time, causing sig-
: r, r) }+ E9 _/ i) anificant bare skin contact between baby and father.8 z( ?, R4 u1 g
The father also admitted that after the phone call,6 x5 i% `0 t3 ?$ g
when he learned the testosterone level in the baby
$ V8 Q* E: }! X) Z& Owas high, he then read the product information
/ l: u+ ]+ q; b" ]6 `- {6 Spacket and concluded that it was most likely the rea-5 c$ p. j0 O# @+ ]2 Z5 L
son for the child’s virilization. At that time, they
$ G5 e0 Z4 v+ @1 P& \- l0 y* Vdecided to put the baby in a separate bed, and the
8 ]( N- A6 I) d. jfather was not hugging him with bare skin and had: |. r! ~7 o$ ^
been using protective clothing. A repeat testosterone, p5 O8 X# i+ h9 A1 ]( X5 H
test was ordered, but the family did not go to the! S  a# G" S; o( y. y' o7 J8 ^' Y
laboratory to obtain the test.' Z, K2 P* j3 h. z
Discussion
% P' a6 Y& z, V5 X* nPrecocious puberty in boys is defined as secondary; y4 C8 q6 w& B2 B# T, c
sexual development before 9 years of age.1,4
  I/ ~+ P0 t8 MPrecocious puberty is termed as central (true) when
$ T5 Y' _7 K1 E2 Bit is caused by the premature activation of hypo-
. k6 o0 V+ J5 a3 T2 F& t, ^( L' Pthalamic pituitary gonadal axis. CPP is more com-
8 ~; y2 k. |% r5 T/ X$ s$ Nmon in girls than in boys.1,3 Most boys with CPP
: ~/ v' {5 [' ]3 H, V2 w+ q! f6 C: {may have a central nervous system lesion that is2 a  P" f& }- {
responsible for the early activation of the hypothal-
) H2 o" R3 |# f4 ?: @amic pituitary gonadal axis.1-3 Thus, greater empha-
' l% [. M3 t: w( X2 R0 msis has been given to neuroradiologic imaging in$ P3 n3 b% ~& Q' _
boys with precocious puberty. In addition to viril-
8 w0 Y) e$ ^) i% @& Eization, the clinical hallmark of CPP is the symmet-+ u5 r+ k# c4 d' @7 u2 i+ K( J& |
rical testicular growth secondary to stimulation by
( |: h7 `( S/ h5 Q# m# I! j5 k9 Ugonadotropins.1,3
$ l" M+ {% B9 n' WGonadotropin-independent peripheral preco-3 D; J+ h" Z& u  R6 O/ F  g6 {
cious puberty in boys also results from inappropriate
1 a9 U9 k5 X) {& A# W/ Oandrogenic stimulation from either endogenous or' U, V) s# V( b5 @+ c% w4 p
exogenous sources, nonpituitary gonadotropin stim-3 Y, F6 C$ R; `4 S" U* ^
ulation, and rare activating mutations.3 Virilizing
0 c; s4 E7 G  Gcongenital adrenal hyperplasia producing excessive
0 r% O  U% i  d. Ladrenal androgens is a common cause of precocious" D: Z9 ?' b2 }( L
puberty in boys.3,4+ f; z' d. d& K7 A
The most common form of congenital adrenal
4 Z+ L' t$ R" J7 Vhyperplasia is the 21-hydroxylase enzyme deficiency.9 z4 F1 k: x3 M& W: d. ]
The 11-β hydroxylase deficiency may also result in
! ?# s, ?3 b$ Lexcessive adrenal androgen production, and rarely,
$ w" C1 j+ _! Oan adrenal tumor may also cause adrenal androgen  G3 N: @3 J+ M0 E' y- h7 p
excess.1,3
, ?, G: |1 Z8 q+ K. \at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! Y+ P& L+ z. R3 [0 C+ L542 Clinical Pediatrics / Vol. 46, No. 6, July 2007! M. U* Y) \+ Q2 x2 u6 \
A unique entity of male-limited gonadotropin-% @" C" [/ [% x' f
independent precocious puberty, which is also known
/ Y$ D7 e3 O6 _2 K# las testotoxicosis, may cause precocious puberty at a1 x' A5 |; P* T1 a6 y
very young age. The physical findings in these boys/ ^! o- I* r; Y% A& X+ l- L
with this disorder are full pubertal development,
& p) y8 Y$ C7 o. ~including bilateral testicular growth, similar to boys4 E/ E, a* x; U2 e/ F
with CPP. The gonadotropin levels in this disorder
* O! E; e$ _7 a% u* care suppressed to prepubertal levels and do not show2 J9 k5 r% v. u# Z" ~2 Y2 j8 S
pubertal response of gonadotropin after gonadotropin-
  ^6 W4 Z; N. N% yreleasing hormone stimulation. This is a sex-linked
1 \5 C; e* d0 i& b3 u7 lautosomal dominant disorder that affects only
) h* l( Z: W; \% {males; therefore, other male members of the family
( h$ d* j% Z2 M& z7 E8 Pmay have similar precocious puberty.36 u* [/ M9 K8 z3 {; V; V
In our patient, physical examination was incon-
" N' i6 t8 x1 f( S4 r. Lsistent with true precocious puberty since his testi-
1 p! q# z7 l# lcles were prepubertal in size. However, testotoxicosis
6 l3 D( a0 U; i+ ?" w( fwas in the differential diagnosis because his father
8 z: [& R5 W9 q. d  Bstarted puberty somewhat early, and occasionally,
4 Q- k& z8 l- P1 q, v! [6 ^$ Atesticular enlargement is not that evident in the
. F" y+ z4 ~% r& ebeginning of this process.1 In the absence of a neg-
0 X8 t7 P+ T9 I1 ]0 hative initial history of androgen exposure, our
$ ?  i  B6 ]$ v; abiggest concern was virilizing adrenal hyperplasia,5 u" _$ }  |2 F% ]  |) E
either 21-hydroxylase deficiency or 11-β hydroxylase
4 B1 `* o. X' ?, sdeficiency. Those diagnoses were excluded by find-5 P1 G: B, e5 \# n5 ]. M
ing the normal level of adrenal steroids.6 Z+ Y7 F$ B: k! W. s# l0 j- t  s
The diagnosis of exogenous androgens was strongly; P: a) I" W! e/ e" J" j
suspected in a follow-up visit after 4 months because' _& i9 G0 O0 f2 i5 g
the physical examination revealed the complete disap-
+ g0 K6 I/ k9 i" l' V- cpearance of pubic hair, normal growth velocity, and6 Z) b# V' d' V& B
decreased erections. The father admitted using a testos-: o8 u' c' f! f/ T
terone gel, which he concealed at first visit. He was) `" V4 j! `3 U$ v
using it rather frequently, twice a day. The Physicians’
. j- \( \3 J5 K$ Q5 w2 ~+ _( BDesk Reference, or package insert of this product, gel or
  ]. O5 u8 @$ d, N/ K. o0 @5 B5 lcream, cautions about dermal testosterone transfer to
4 U( w+ m, x, l9 Lunprotected females through direct skin exposure.
3 P3 B0 D9 U2 V) Z% h" O* Z4 I) cSerum testosterone level was found to be 2 times the5 T$ v# u; e, U+ h4 m
baseline value in those females who were exposed to
' ?4 _$ i4 b) |# S, ^even 15 minutes of direct skin contact with their male
& M* Y4 C2 Z; M  o5 E; Dpartners.6 However, when a shirt covered the applica-
4 P$ p6 f: H' e: g, rtion site, this testosterone transfer was prevented.3 y8 f- H; \; j9 B
Our patient’s testosterone level was 60 ng/mL,
+ W3 b0 K# O7 {7 Q- h1 l- G+ Kwhich was clearly high. Some studies suggest that0 m; p% l. _$ }8 S5 Z
dermal conversion of testosterone to dihydrotestos-
) F1 t. [  v8 ~/ gterone, which is a more potent metabolite, is more/ |; X2 ~9 g' ]! B  D$ |
active in young children exposed to testosterone
! H( P) z) w! I# \exogenously7; however, we did not measure a dihy-3 q+ O1 w: N& O( f2 F! c
drotestosterone level in our patient. In addition to
* Q: P- |! a5 f- Y9 q9 tvirilization, exposure to exogenous testosterone in/ c: z. p4 c7 W" ~# z$ t
children results in an increase in growth velocity and
  @: `, }. D% N% f8 Z) \- fadvanced bone age, as seen in our patient.
. |2 i& p3 Z  p% GThe long-term effect of androgen exposure during
! R) X6 Z2 m$ l5 u0 [( iearly childhood on pubertal development and final. ~( ?7 N. s8 G6 d
adult height are not fully known and always remain# t) ]) q" C  i( E' g
a concern. Children treated with short-term testos-6 P. z; C& N. A. {  ~! J6 x
terone injection or topical androgen may exhibit some( O* G: _, J- i* u7 V
acceleration of the skeletal maturation; however, after
2 j9 g3 K) K) k, V9 r3 y$ A" C, x& U8 Ccessation of treatment, the rate of bone maturation. M9 b5 D, O, K- @2 I: V
decelerates and gradually returns to normal.8,9% i- y/ d! Q/ g
There are conflicting reports and controversy
) c/ K! x3 ^& X1 D9 k1 F/ Uover the effect of early androgen exposure on adult5 v) `, x1 g- \) s1 X( \
penile length.10,11 Some reports suggest subnormal9 {  y2 T5 y# C" [! f
adult penile length, apparently because of downreg-5 e8 p0 E% y7 C  E  Y/ b7 ]
ulation of androgen receptor number.10,12 However,. |6 G+ K7 q  Q( J, O# _1 Q
Sutherland et al13 did not find a correlation between
6 z' B6 |; ?5 |childhood testosterone exposure and reduced adult
  w$ M2 _9 ~1 N) Q( O5 |penile length in clinical studies.
6 X, g" |+ W/ \- lNonetheless, we do not believe our patient is0 W# c( {" z, B! F# m6 U: f
going to experience any of the untoward effects from
3 W& J3 O& `, |3 }0 _  ~) v/ J- z) Xtestosterone exposure as mentioned earlier because
5 V5 Z6 d8 @; H. F. u- tthe exposure was not for a prolonged period of time.5 W3 M8 r6 l; a; P0 M+ l( o
Although the bone age was advanced at the time of
: [8 c2 [# D( Q1 Xdiagnosis, the child had a normal growth velocity at
3 C  @6 _4 }; B. M1 ?5 Jthe follow-up visit. It is hoped that his final adult7 }5 \5 x  m. g! u
height will not be affected.9 i8 v, K5 ~1 G- o
Although rarely reported, the widespread avail-+ h/ d7 m# H$ U: k5 N
ability of androgen products in our society may
1 K' J& A  m! A* Tindeed cause more virilization in male or female- A8 v# c$ T- F! ~( ?9 d3 D7 ^
children than one would realize. Exposure to andro-
5 ]& }$ R; T1 G0 S# q. z" [$ agen products must be considered and specific ques-$ q. @7 j. ?, h& c& @
tioning about the use of a testosterone product or* s; s3 L8 q% ~2 \) r4 D
gel should be asked of the family members during! j/ E3 |& D6 x& m3 f
the evaluation of any children who present with vir-3 Z0 B. }# Y& C- X0 L0 g' j
ilization or peripheral precocious puberty. The diag-( t0 i2 |5 W6 r) s- v, _
nosis can be established by just a few tests and by) V+ }) T' @; V# u/ m+ e
appropriate history. The inability to obtain such a
6 t$ p/ e2 y, P" f0 u0 e7 Uhistory, or failure to ask the specific questions, may8 y: v5 {8 N8 d' g
result in extensive, unnecessary, and expensive
" z. Z( g+ o/ ~investigation. The primary care physician should be& |, I- n1 l0 t# ]
aware of this fact, because most of these children- b0 M/ E3 ^+ `5 J" _. t! s% O
may initially present in their practice. The Physicians’5 M2 ]( f2 c; F2 h$ Z- ^) U
Desk Reference and package insert should also put a+ H1 Z, ^5 ?6 P) @8 |  U$ @1 g$ i7 I* C
warning about the virilizing effect on a male or' `( w7 o. d$ @$ `6 W0 o3 B* W
female child who might come in contact with some-
8 k: s: a" k& y6 l- ]one using any of these products.
( z9 A5 K8 w( w( u. `References
4 D* X5 F% u2 m7 S1. Styne DM. The testes: disorder of sexual differentiation
2 g8 J- Z8 O: F( jand puberty in the male. In: Sperling MA, ed. Pediatric9 ]0 U" N8 G- l/ W  y
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
: n/ V8 P* }% K2002: 565-628.& Y, u/ H/ z, a$ Y" x  S, [5 M
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious# |7 N5 l9 }6 [, g2 l7 J9 K
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old( x1 }) \5 z$ ?; B5 M0 Y5 F
Boy Induced by Indirect Topical
$ O) a! j4 N% hExposure to Testosterone* f9 m* Q, i0 h5 Y5 z3 W* h, U
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,24 \5 F2 w8 N: r" k
and Kenneth R. Rettig, MD1# Q5 E" ^. ?$ ]$ |/ T( k' F5 `
Clinical Pediatrics% M$ Z  ]+ E7 [
Volume 46 Number 6
  T+ Z# d% D4 m! UJuly 2007 540-543
% I+ I0 Y; ^1 M© 2007 Sage Publications$ m1 Q% n$ @1 l) {% m# A& F
10.1177/00099228062966515 g1 A  p* Y4 B! Z) W
http://clp.sagepub.com
. U. S& a' l4 Q$ ?6 @+ nhosted at: e# ^7 R' q6 `, A% L5 C! j
http://online.sagepub.com
/ l% n3 v5 N0 N, H: V; X' ]2 GPrecocious puberty in boys, central or peripheral,% d7 K5 e6 s& {1 R5 z
is a significant concern for physicians. Central
( f+ z/ x. f. C7 \precocious puberty (CPP), which is mediated
1 `  D( Y  s* K9 G6 Hthrough the hypothalamic pituitary gonadal axis, has
3 C7 F* H" f/ |( x9 wa higher incidence of organic central nervous system
) c! Z/ h& N+ s: P5 \/ Qlesions in boys.1,2 Virilization in boys, as manifested
( [  q+ p& g2 w3 n9 P) Cby enlargement of the penis, development of pubic
, D; V9 q: ^/ y; E. ahair, and facial acne without enlargement of testi-  o; W- l; l/ s9 \" L3 {5 `) r4 B
cles, suggests peripheral or pseudopuberty.1-3 We9 o8 a6 K; t8 G1 ^, c  v8 a& M9 V' {
report a 16-month-old boy who presented with the
; d/ `* a$ o1 @7 A: denlargement of the phallus and pubic hair develop-
2 P$ C1 K; {, E# e& dment without testicular enlargement, which was due
2 J- a7 @6 [( \: R7 |1 Y) Mto the unintentional exposure to androgen gel used by1 i% d' o6 |- m$ n" O- c
the father. The family initially concealed this infor-# d/ D9 N: J, Q" Q/ A
mation, resulting in an extensive work-up for this
5 C, f: R' C+ S5 G* [2 p) pchild. Given the widespread and easy availability of
. Z% ]; }  o. ytestosterone gel and cream, we believe this is proba-
2 I9 _- l( {8 N+ ~# B4 h! r% wbly more common than the rare case report in the) g+ A7 o( N) l7 b* u( d8 A0 r
literature.4
8 E- C4 t! @& N/ qPatient Report  u( z- H, x* P; s- J
A 16-month-old white child was referred to the9 |: q* n- y4 w+ I! B! q% f! @
endocrine clinic by his pediatrician with the concern
) m# \0 U2 y2 g8 h' Fof early sexual development. His mother noticed
3 b: P; Q" f, w' y' P$ h& `  {light colored pubic hair development when he was
: b( B5 ?4 Y7 f0 I0 oFrom the 1Division of Pediatric Endocrinology, 2University of4 H# P( T0 m; t$ m% k7 ]  G: a
South Alabama Medical Center, Mobile, Alabama.5 V2 y6 Z% }4 c  ?/ Z
Address correspondence to: Samar K. Bhowmick, MD, FACE,& w1 B9 K; q" l  \( Q
Professor of Pediatrics, University of South Alabama, College of, K, D/ S6 C4 R  z3 \
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
. e! A3 {8 e6 h2 c* t0 L6 Pe-mail: [email protected].1 P/ T% b- N+ o8 V2 p& Z$ f1 B
about 6 to 7 months old, which progressively became: D( Q, O7 a7 b" @* R9 ^
darker. She was also concerned about the enlarge-
+ Q2 W: K% N; m- k: o, ~4 }: Qment of his penis and frequent erections. The child
) I9 \: B: `% |( u- _! Bwas the product of a full-term normal delivery, with4 C* ^, N" u1 Q7 Z
a birth weight of 7 lb 14 oz, and birth length of
* G" H7 A/ f: P. S( D# a20 inches. He was breast-fed throughout the first year( V- v# f  @4 g  B2 W
of life and was still receiving breast milk along with
: Y- F5 s3 F  C$ S: |solid food. He had no hospitalizations or surgery,9 I+ G1 a1 a+ B$ ?, Y, w
and his psychosocial and psychomotor development
3 }+ s; z' k& l# Gwas age appropriate.
5 G9 U7 Q+ g- qThe family history was remarkable for the father,, R( c' P; n5 J4 F; m4 W
who was diagnosed with hypothyroidism at age 16,
  P$ ~4 @- G( J1 w( Qwhich was treated with thyroxine. The father’s
' ?" M. e0 N+ \0 Aheight was 6 feet, and he went through a somewhat4 q" u1 n) W# C
early puberty and had stopped growing by age 14.
8 m) L" x' B7 b& F* R! J7 w$ vThe father denied taking any other medication. The
$ L, K8 w  p' l8 Vchild’s mother was in good health. Her menarche
/ m* }/ N) o, H0 m, `& Gwas at 11 years of age, and her height was at 5 feet" e) @7 }" n9 T, b* q) D) ^1 f
5 inches. There was no other family history of pre-% `6 o1 L6 N$ |1 W# r$ b
cocious sexual development in the first-degree rela-
' Z) v4 L( M/ Y8 \5 Z2 X6 Atives. There were no siblings.
0 s- d1 K$ S+ _+ X$ A. wPhysical Examination
$ O' L; K+ ^9 Q  W  e; iThe physical examination revealed a very active,& Y6 k* b' h1 V1 z7 c! T4 W
playful, and healthy boy. The vital signs documented  ]+ H3 E9 }  E  d, b3 ^
a blood pressure of 85/50 mm Hg, his length was4 Z2 I+ Z8 i' p6 l
90 cm (>97th percentile), and his weight was 14.4 kg3 B" \9 j1 {! ^  |3 B+ X
(also >97th percentile). The observed yearly growth
6 @8 v0 E' j" l% q; [; Avelocity was 30 cm (12 inches). The examination of" `' _5 V2 ]2 x" Q5 |5 [3 D# X
the neck revealed no thyroid enlargement.4 O; D" C, f# R) A
The genitourinary examination was remarkable for6 O  M; M* k  ^' b6 ]
enlargement of the penis, with a stretched length of
/ R! ^) _3 _+ t  P' q- ?8 H& G8 cm and a width of 2 cm. The glans penis was very well
" O* |' d3 |0 |1 pdeveloped. The pubic hair was Tanner II, mostly around7 M* n5 U* s' v$ d
540
# D: F- d3 p2 L- j; [7 W6 V$ |9 Qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, ~5 d. ?7 V& W/ rthe base of the phallus and was dark and curled. The
# P! G2 F. s4 v9 X( A7 rtesticular volume was prepubertal at 2 mL each.' ~. ~6 B0 K) b
The skin was moist and smooth and somewhat
5 y9 l5 Y7 d: t% Z! loily. No axillary hair was noted. There were no; V' f5 P; Q% h
abnormal skin pigmentations or café-au-lait spots.
0 c: a! I- t! D$ |$ WNeurologic evaluation showed deep tendon reflex 2+
8 T5 {# `7 o. T" u! Ebilateral and symmetrical. There was no suggestion
4 s0 R. d- a8 U8 j; g; K* N$ @1 nof papilledema.
& t' i0 b0 r1 L" ]  A! u6 _Laboratory Evaluation
& w1 n2 k, o0 a8 fThe bone age was consistent with 28 months by
" k2 h; I2 m# V3 u4 |, Q1 [using the standard of Greulich and Pyle at a chrono-5 ^$ ]- L& C- u4 @. L! z; c
logic age of 16 months (advanced).5 Chromosomal
' R+ r" w' L! o2 ^+ Okaryotype was 46XY. The thyroid function test
. K# D9 s* p( L/ Oshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
7 s, k0 ^; D) d, glating hormone level was 1.3 µIU/mL (both normal).1 H; |! j9 u/ p, D5 k# C6 r# c
The concentrations of serum electrolytes, blood
' m& A/ o% v1 M) Y3 }urea nitrogen, creatinine, and calcium all were
' q$ O. I" u1 _$ Y, G* M$ Wwithin normal range for his age. The concentration$ M) p) G0 u( E" B$ J+ X% z
of serum 17-hydroxyprogesterone was 16 ng/dL" s* O9 }" B, u
(normal, 3 to 90 ng/dL), androstenedione was 20
( i5 X4 Z. }+ U/ d& I- g( sng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
4 Y" \5 z) _$ ?9 e) [$ Qterone was 38 ng/dL (normal, 50 to 760 ng/dL),2 @% f- s* n/ r' K
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
/ X2 O& L$ A% V49ng/dL), 11-desoxycortisol (specific compound S)# J& l. Z3 z5 d
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-+ G# ?5 F+ b0 b& `( x0 o
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
7 o; u% o- \/ n; q" N8 ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
  D, d0 d) M- k+ J1 e2 O& g7 D' Jand β-human chorionic gonadotropin was less than) K/ d8 f( {2 L7 Z4 E3 s$ [' j
5 mIU/mL (normal <5 mIU/mL). Serum follicular; N; E/ T% m$ u; i: L/ X  h
stimulating hormone and leuteinizing hormone* B5 K2 ?# }6 [; K+ t8 Y
concentrations were less than 0.05 mIU/mL
! [% s4 Z4 W2 y) e. }(prepubertal)., `: b4 Y) A: X
The parents were notified about the laboratory9 ~% I7 H4 ?, I- T2 ?
results and were informed that all of the tests were
: ?1 z* A4 \- R% c" ]normal except the testosterone level was high. The* W' v* Q" O5 {. e" u
follow-up visit was arranged within a few weeks to
4 V) c+ x+ K& D- B' wobtain testicular and abdominal sonograms; how-# u7 T) ^2 g( V" @$ L) H/ Q
ever, the family did not return for 4 months.
& O* F, ~+ e+ M8 C/ bPhysical examination at this time revealed that the
# d1 M# K, k) l  U1 ochild had grown 2.5 cm in 4 months and had gained
" `/ l7 B" }4 k: \6 k2 kg of weight. Physical examination remained# C0 ]4 |4 ^/ R6 \
unchanged. Surprisingly, the pubic hair almost com-
& \( m! M% M5 ^4 Ipletely disappeared except for a few vellous hairs at
. c! w. v9 a7 q2 b' othe base of the phallus. Testicular volume was still 2
9 C! m7 [: c6 B. z2 I6 d' }) r0 kmL, and the size of the penis remained unchanged.
% X8 U8 H5 [( x! X$ S. j! cThe mother also said that the boy was no longer hav-: i0 o& N- R6 o* j3 H
ing frequent erections.
8 C! ]( p! l2 R/ V" QBoth parents were again questioned about use of
4 L! x# h$ z4 fany ointment/creams that they may have applied to- N5 J4 R8 [1 q; N. {0 f
the child’s skin. This time the father admitted the
5 S6 ^- v! r+ [2 @8 W1 D3 ZTopical Testosterone Exposure / Bhowmick et al 5411 W* \6 b9 w4 L' \3 |! H
use of testosterone gel twice daily that he was apply-
% z7 G8 Q3 C" m$ K, W% {ing over his own shoulders, chest, and back area for
2 R: A; h; L; P* qa year. The father also revealed he was embarrassed
% v9 n* _: O9 Z% P- x& Dto disclose that he was using a testosterone gel pre-
0 Z. i9 ?% m7 e; ]6 nscribed by his family physician for decreased libido5 B) p4 p/ ?5 r+ `, X# U1 O0 j
secondary to depression.
9 K: Y. q' G) G% \! h% [) _The child slept in the same bed with parents.- C) d/ z, D/ h& p; ?1 b
The father would hug the baby and hold him on his& l& r* L; v3 s: }/ e5 }! H
chest for a considerable period of time, causing sig-: A) J: [4 v/ T' a  ]
nificant bare skin contact between baby and father.. X9 K, c- ^9 N* k
The father also admitted that after the phone call,
, I2 k# K: a+ D' `4 ]* S- hwhen he learned the testosterone level in the baby
1 B4 n3 @3 `2 G  G; x( K0 S8 |was high, he then read the product information
) t; D9 \+ I' e# \. S# L, Rpacket and concluded that it was most likely the rea-* a2 [; G' H8 W' h8 m: G
son for the child’s virilization. At that time, they
6 b! _" a& w) b/ ^- o, u9 @decided to put the baby in a separate bed, and the
' a% {: t- S3 x3 P9 ?4 Dfather was not hugging him with bare skin and had
3 H, X" a" X" v2 ^, {) i+ K. k- sbeen using protective clothing. A repeat testosterone
4 z! M, {! ^" ~  u( x  c! Rtest was ordered, but the family did not go to the
. n! e2 ~. [4 U+ e$ w( p& e' zlaboratory to obtain the test.
8 o9 W5 J; r4 n( B4 {3 \2 ~; a  ]# w3 WDiscussion
; \; K# h1 k2 `' LPrecocious puberty in boys is defined as secondary" W6 u$ v) G/ `3 }/ I3 x
sexual development before 9 years of age.1,4) R3 ~6 J% \9 ?6 Z
Precocious puberty is termed as central (true) when
; ]; O8 L$ u: Y0 w- T- Git is caused by the premature activation of hypo-8 b% ~. Q: r) r: }+ m' [
thalamic pituitary gonadal axis. CPP is more com-
# Y- W+ s$ M) N8 Cmon in girls than in boys.1,3 Most boys with CPP
8 P+ Q# I0 O& |1 U2 j: ]" h$ O; pmay have a central nervous system lesion that is/ a# Y1 v7 u$ [7 s
responsible for the early activation of the hypothal-
( Y4 |0 W3 Z  [. L) zamic pituitary gonadal axis.1-3 Thus, greater empha-# i3 X2 \" F  j/ w: D
sis has been given to neuroradiologic imaging in
( Y* a, j9 T9 zboys with precocious puberty. In addition to viril-
3 @7 X8 q9 @) [9 _& fization, the clinical hallmark of CPP is the symmet-
" p6 z# I/ n2 z& s- Jrical testicular growth secondary to stimulation by
* ^9 R5 O' X6 x( B9 [6 `- Ygonadotropins.1,3
/ _/ _' U$ v$ {8 E% oGonadotropin-independent peripheral preco-* V% W1 a2 \5 |0 ^
cious puberty in boys also results from inappropriate% @8 F2 v( m1 I2 J( c5 d$ i; X
androgenic stimulation from either endogenous or8 J3 L# K& V8 @- t$ h1 F* Q2 N# }
exogenous sources, nonpituitary gonadotropin stim-+ x" ?/ c; T/ q
ulation, and rare activating mutations.3 Virilizing
: e& a- i( k0 O( V7 Econgenital adrenal hyperplasia producing excessive2 @- h' ^2 P6 l* `
adrenal androgens is a common cause of precocious- D, O7 v# l5 {: p! ]7 j/ u
puberty in boys.3,4
/ D/ G' ?: y  B3 g3 q2 I+ ]9 ]The most common form of congenital adrenal
% }/ r4 x6 G/ ahyperplasia is the 21-hydroxylase enzyme deficiency.
" C# Q2 G7 _$ |& y% I" Z2 ZThe 11-β hydroxylase deficiency may also result in
  I9 ?# Q1 [+ r& {excessive adrenal androgen production, and rarely,1 V+ m* @; p( ?1 u9 [9 ~& F
an adrenal tumor may also cause adrenal androgen5 c# e  O& F3 O. f
excess.1,3
6 B4 O/ b) A' W4 f" {1 k7 eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 R8 O8 c/ e1 H9 ~' s5 J0 s542 Clinical Pediatrics / Vol. 46, No. 6, July 20074 N. {3 K( J1 r  K  G+ t
A unique entity of male-limited gonadotropin-
9 `( B4 Y% E: n0 {( z. i2 iindependent precocious puberty, which is also known) D2 L( l3 M6 ^$ P, {) a
as testotoxicosis, may cause precocious puberty at a
- H1 A& c9 }4 G: d8 w: Avery young age. The physical findings in these boys
+ w7 W) }2 u# l' t8 O! D) o8 @with this disorder are full pubertal development,
7 c) T  F4 R; e0 S& n5 C/ m9 kincluding bilateral testicular growth, similar to boys
8 w& E; u* s5 q- U  i  uwith CPP. The gonadotropin levels in this disorder' F5 B) S9 i, C- Z+ O
are suppressed to prepubertal levels and do not show
: ^0 v4 l% J. }: Y+ f  Q% A  }pubertal response of gonadotropin after gonadotropin-
6 A. C" a; J# n2 i  V" preleasing hormone stimulation. This is a sex-linked$ ?- L) g- q2 a4 K8 U
autosomal dominant disorder that affects only
9 g2 ?2 O; f& a& J# Mmales; therefore, other male members of the family1 m+ [8 ]) l+ \8 _& a( @7 d$ {# h
may have similar precocious puberty.38 q! {, p; A' q3 A' F" t* C
In our patient, physical examination was incon-! q) h% j% G3 t- j
sistent with true precocious puberty since his testi-% E0 M! s' K' }2 J, Y$ |. E9 t
cles were prepubertal in size. However, testotoxicosis
6 n9 O; z, ]: X) t! |was in the differential diagnosis because his father
9 B, p3 e) E9 {5 [8 Dstarted puberty somewhat early, and occasionally,. {# d/ H' v0 p& ?8 Q* l$ e! y, ]
testicular enlargement is not that evident in the- Q/ x! P- `4 e- J+ T
beginning of this process.1 In the absence of a neg-
! s" J, x( {; C2 Jative initial history of androgen exposure, our. H. B5 S5 h2 s$ N. b
biggest concern was virilizing adrenal hyperplasia,
" u2 R. S* y9 R* y. s: ^either 21-hydroxylase deficiency or 11-β hydroxylase- c" l+ p: J) `4 J; J
deficiency. Those diagnoses were excluded by find-! X2 }) ?3 W* b) {# H  v( p: F
ing the normal level of adrenal steroids.
; P& t5 H( Y& C' H* |. kThe diagnosis of exogenous androgens was strongly
6 B5 c# p3 A7 c9 q! Q9 L' V4 o  msuspected in a follow-up visit after 4 months because
2 p  e2 b  S5 C  D1 n! qthe physical examination revealed the complete disap-. d* d6 G4 m( y% {3 `1 |  q
pearance of pubic hair, normal growth velocity, and
% r# w% `4 [3 s( {decreased erections. The father admitted using a testos-
" f' Y- n$ P/ V4 W  u$ t: ~terone gel, which he concealed at first visit. He was
# c* {) i3 m" z" U2 T7 busing it rather frequently, twice a day. The Physicians’4 y0 o- N. u; V4 ^/ n
Desk Reference, or package insert of this product, gel or- s! C* p2 D3 |
cream, cautions about dermal testosterone transfer to& m* R3 \. O1 J" G
unprotected females through direct skin exposure.& h! Y) H$ ?) g7 M
Serum testosterone level was found to be 2 times the; Y" e& ]9 w% I# p% l$ z, k
baseline value in those females who were exposed to; @$ [% q: E8 O" z7 N% e
even 15 minutes of direct skin contact with their male
. _4 w5 A; C' g$ B. P9 ipartners.6 However, when a shirt covered the applica-
. m; l" C- Y8 i; Ttion site, this testosterone transfer was prevented.) ?" N* n" @( l/ Z
Our patient’s testosterone level was 60 ng/mL,
3 |5 o/ K; `! S+ m/ [9 V6 Owhich was clearly high. Some studies suggest that
* B0 k  a7 j% U% g% K+ Tdermal conversion of testosterone to dihydrotestos-
: v& Z* V! U/ r, O" b& m( I8 uterone, which is a more potent metabolite, is more+ k3 m) R4 F4 z$ W  g2 s
active in young children exposed to testosterone+ }6 T3 V1 G+ T. Y1 X5 r
exogenously7; however, we did not measure a dihy-! U- Z) o$ [  {7 H- H) y
drotestosterone level in our patient. In addition to8 z% _/ d" ~; g* ~% g
virilization, exposure to exogenous testosterone in
+ I7 t) P. o$ z3 ?children results in an increase in growth velocity and
  w6 c8 F" M3 E6 t" ~( Z% J, o9 ^2 Eadvanced bone age, as seen in our patient.9 V# i2 O+ L( ?
The long-term effect of androgen exposure during( n) v* a& N: X% \5 ?! s
early childhood on pubertal development and final7 C1 c5 S- ?6 P. N! J8 c
adult height are not fully known and always remain5 H6 h' ^, z0 z) b, N& m# z- I) u- P2 T
a concern. Children treated with short-term testos-, W) [5 Z' h. y& N) _
terone injection or topical androgen may exhibit some$ S, J" G  n! |( X" l. J0 I
acceleration of the skeletal maturation; however, after1 L; g% h+ P4 T6 V
cessation of treatment, the rate of bone maturation
! U1 l. \0 c, b* cdecelerates and gradually returns to normal.8,97 k7 }1 l' h! E8 v! o
There are conflicting reports and controversy
! _4 v# K# o1 Kover the effect of early androgen exposure on adult& {7 R6 h% R% `' L: Q1 H
penile length.10,11 Some reports suggest subnormal2 u" a5 i$ R2 q; h( r3 M2 A
adult penile length, apparently because of downreg-
8 T' p# M! h9 s2 A/ ^: |3 j% n7 ?+ Xulation of androgen receptor number.10,12 However,
% s1 o- W5 }  r( E7 Y, `: \Sutherland et al13 did not find a correlation between
+ m' Q9 K" ~" |% Ychildhood testosterone exposure and reduced adult
* R. A+ G) y6 C8 xpenile length in clinical studies.7 `3 V  E5 _5 r) b; h1 U3 j8 `
Nonetheless, we do not believe our patient is
# y. K4 [, W6 `1 r1 p; v7 cgoing to experience any of the untoward effects from( m2 H/ Z( |% U" P
testosterone exposure as mentioned earlier because
7 \* _' j' N/ V  j: R& y- J, Tthe exposure was not for a prolonged period of time.8 [/ k9 y, n2 n  D7 X& X) u2 v
Although the bone age was advanced at the time of
2 Y# q, m/ c: _diagnosis, the child had a normal growth velocity at1 R+ y: O- ~2 x0 i+ G0 X- ?& n
the follow-up visit. It is hoped that his final adult! T. W. Q- y4 t5 A+ W  l+ s
height will not be affected.4 e4 q! m" J  L" u: |
Although rarely reported, the widespread avail-2 y. i1 [. Y& {  H1 X3 F  i$ h3 ]
ability of androgen products in our society may
3 e) j' l0 q% B1 k) J6 ?0 z/ |indeed cause more virilization in male or female
0 I- ~9 Y1 x1 echildren than one would realize. Exposure to andro-
; F5 W4 V  o7 u# q! b4 I& \7 |% Wgen products must be considered and specific ques-
' |7 X( \4 I9 d: Mtioning about the use of a testosterone product or
. u. O" c4 L: V, Agel should be asked of the family members during
- c4 }' @3 y* B1 V! D" b$ a9 ythe evaluation of any children who present with vir-+ d$ C8 w- y1 J5 X1 }: q
ilization or peripheral precocious puberty. The diag-# C) B! ~8 z; ~  ]
nosis can be established by just a few tests and by2 Z3 {* ]3 S* Y7 D- S: R
appropriate history. The inability to obtain such a
: I3 ?( U4 _' d4 e) @0 |) c2 n0 Ahistory, or failure to ask the specific questions, may: H% E. G5 Y( h! g4 q) b
result in extensive, unnecessary, and expensive2 O6 A7 b2 i) A) T& q4 [
investigation. The primary care physician should be$ x4 _( N; @3 y5 @9 ~/ u1 _1 d
aware of this fact, because most of these children
5 a# B6 b, K; f: \may initially present in their practice. The Physicians’
2 t; A/ D+ q4 s+ P; vDesk Reference and package insert should also put a) E, d; h8 i7 U# {9 \: K( d) ~$ T- ?
warning about the virilizing effect on a male or
  o( e# u! v1 V% ~1 Ofemale child who might come in contact with some-
& Z  m; n7 u9 h) ?3 R; fone using any of these products.
+ F& e" ?' G1 f) Z; H0 NReferences
, C% W7 m; ?$ r. w1. Styne DM. The testes: disorder of sexual differentiation
, w3 {/ i3 ?7 A: q6 ?0 s) Kand puberty in the male. In: Sperling MA, ed. Pediatric7 C& ^& Z# L- m$ c. G- L" w
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
. L. F0 Z1 I/ _2002: 565-628.
5 [1 u+ I/ x0 I% P- |! e- \2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
" Y+ R+ O4 Y+ y1 G3 Apuberty 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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
3 z: z/ O% r( F* F2 A; L2 l$ D* e' X3 s
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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