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Sexual Precocity in a 16-Month-Old
4 g# Y7 }; H+ v% i" Q8 i6 E; O2 ]Boy Induced by Indirect Topical0 m2 b) J4 Q7 e
Exposure to Testosterone3 q7 H  M4 c0 s4 t8 @
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
( W; z( [8 b$ e4 J$ X# nand Kenneth R. Rettig, MD1" N1 m0 K5 u1 w4 ]
Clinical Pediatrics
6 O' c5 s. V% O7 k, a' B: DVolume 46 Number 6  J( G- K/ I$ |
July 2007 540-543
/ s$ @. t+ i1 u4 G6 }7 y© 2007 Sage Publications' N2 \' ^9 B6 ]; s
10.1177/0009922806296651/ d; v" S2 `7 z3 L! {! e
http://clp.sagepub.com8 l& N1 {7 r8 u) y
hosted at
3 w& L6 L. q1 U" [: O3 Phttp://online.sagepub.com) I% ?* L. N/ k, N  u/ k" o% A
Precocious puberty in boys, central or peripheral,% o- |0 ]. q% M; a. ]7 \6 S
is a significant concern for physicians. Central- n8 T+ c0 C! h0 L& C* @0 `9 ^2 _
precocious puberty (CPP), which is mediated5 N4 x4 s# \6 q( g. F4 q- |' c
through the hypothalamic pituitary gonadal axis, has
( _+ T. e2 M) ea higher incidence of organic central nervous system
$ v, }) a/ B& z) [6 [6 x: @lesions in boys.1,2 Virilization in boys, as manifested
) o- Z2 n8 _" o0 C0 Nby enlargement of the penis, development of pubic: P2 w' a6 A- A5 p# e
hair, and facial acne without enlargement of testi-
( }( p9 s  ]% w3 S/ S4 Gcles, suggests peripheral or pseudopuberty.1-3 We
0 N. [+ M- D  m# v( oreport a 16-month-old boy who presented with the
% A  s' X2 w' `: q$ r: L5 ^8 t) zenlargement of the phallus and pubic hair develop-5 U9 m) J1 y! C4 j8 {
ment without testicular enlargement, which was due
, U% T$ D; E4 {0 h- d. Eto the unintentional exposure to androgen gel used by
: u- w( |" d; I% a( @5 sthe father. The family initially concealed this infor-
7 c+ I" m' R3 N+ Ymation, resulting in an extensive work-up for this( b% ]' F7 k6 A6 o: v
child. Given the widespread and easy availability of# t# P7 E: C" l# q' r, `# u# x
testosterone gel and cream, we believe this is proba-; M( g3 S! H/ ~* b. L1 N
bly more common than the rare case report in the
% I( F/ N# I$ @literature.44 n0 Z) |0 ]$ m7 m
Patient Report
: k7 n; y" s8 Z6 E3 z, WA 16-month-old white child was referred to the
- o. a* G; c! _  ~8 iendocrine clinic by his pediatrician with the concern
& o+ N& l" x: W7 Vof early sexual development. His mother noticed" A& e; |& I( O5 l+ |9 l% z/ v* g! x
light colored pubic hair development when he was
5 @6 D( g9 T1 v1 OFrom the 1Division of Pediatric Endocrinology, 2University of% `+ F) T+ P' q5 ?8 N7 K
South Alabama Medical Center, Mobile, Alabama.
9 k- R7 ~$ w7 H" o1 wAddress correspondence to: Samar K. Bhowmick, MD, FACE,
4 |/ T' F7 Z/ VProfessor of Pediatrics, University of South Alabama, College of
/ i: U- ~4 @5 |0 l# {Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;/ L9 T6 n9 [/ z* ?& Y* O
e-mail: [email protected].
6 b. A+ N4 `4 _$ h& \' C% S! }5 [about 6 to 7 months old, which progressively became: p$ ^/ Y2 r  Y- m
darker. She was also concerned about the enlarge-
: v5 g( D) z$ v. [ment of his penis and frequent erections. The child; g, |# _9 ~3 W2 f) b
was the product of a full-term normal delivery, with
7 {0 r" A2 o. ~$ `. _* Za birth weight of 7 lb 14 oz, and birth length of
) t9 |2 u+ k0 u( l' @) i8 E2 y, g) v2 [20 inches. He was breast-fed throughout the first year
6 o- F2 E! J1 \6 A! [5 o, @/ G' Rof life and was still receiving breast milk along with" i2 [$ v1 R- o
solid food. He had no hospitalizations or surgery,4 t! D0 K3 S5 m+ l
and his psychosocial and psychomotor development
2 q' c& c" `9 b8 L$ k7 Nwas age appropriate.$ ~/ s6 t* l0 J: S
The family history was remarkable for the father,' @& T" W& q" B/ B0 L+ Q( o
who was diagnosed with hypothyroidism at age 16," V# e; @$ p/ W% e
which was treated with thyroxine. The father’s
+ o' o, E5 T1 c* _" Zheight was 6 feet, and he went through a somewhat
* @8 ^* s$ l' G7 {# [* K+ p( kearly puberty and had stopped growing by age 14.; _  @7 e& h% C
The father denied taking any other medication. The
. ~4 a3 ?2 a0 @child’s mother was in good health. Her menarche
& P, M! b" L* n5 Y, z% g# Qwas at 11 years of age, and her height was at 5 feet' ~/ r# J1 Q5 c6 r3 k8 Q1 [4 Z  o
5 inches. There was no other family history of pre-+ t/ f" H) q& Z7 ?) l/ F
cocious sexual development in the first-degree rela-
( I% k6 q2 m5 i/ {1 E3 E) Utives. There were no siblings.8 n0 V6 q  c& J" J
Physical Examination
0 b% I5 s% D, X& s$ D: [( X8 Q( K0 bThe physical examination revealed a very active,
+ t$ O3 u4 K8 Q# d) l8 D0 ~1 zplayful, and healthy boy. The vital signs documented
' X$ O- H0 T) |a blood pressure of 85/50 mm Hg, his length was1 r. [! s: g2 s! ~# M+ A3 B8 \
90 cm (>97th percentile), and his weight was 14.4 kg
  u7 h8 u7 i( n(also >97th percentile). The observed yearly growth
0 }- ]2 x& b1 b2 d0 Ivelocity was 30 cm (12 inches). The examination of& _/ e( m" {& D" z
the neck revealed no thyroid enlargement.7 {1 s: ?3 l! O' U% q
The genitourinary examination was remarkable for
0 K' m6 R8 X# v+ E0 ienlargement of the penis, with a stretched length of
+ x7 @3 p5 W+ R2 }3 s8 cm and a width of 2 cm. The glans penis was very well
* E' a% Y) J7 k$ Y: S8 m  v( i/ kdeveloped. The pubic hair was Tanner II, mostly around
% n' y0 o6 J3 D6 A3 p540
8 t. w& Y+ w" _+ s6 pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- H( k$ q' q4 Ethe base of the phallus and was dark and curled. The, @/ {2 E4 m* s4 q9 W
testicular volume was prepubertal at 2 mL each.% y: l6 X' o7 H' ^- J) s
The skin was moist and smooth and somewhat" P7 P5 D& m9 V! i6 e' g+ i/ c4 M
oily. No axillary hair was noted. There were no* U' R% i8 ^, }- G" f( O
abnormal skin pigmentations or café-au-lait spots.
2 g5 h+ w: d8 N- pNeurologic evaluation showed deep tendon reflex 2+
  p& b1 L6 q& P- Z7 x9 cbilateral and symmetrical. There was no suggestion
1 ]3 _+ q8 c5 T# Z: L( r1 Lof papilledema.4 x. i6 e& k8 K  v
Laboratory Evaluation
5 b5 J3 B$ \( T' e( c/ e5 ]The bone age was consistent with 28 months by
. I5 Y; N8 C5 K; a7 p$ N$ ?using the standard of Greulich and Pyle at a chrono-* h2 S- a* Z8 N
logic age of 16 months (advanced).5 Chromosomal, I9 @: h1 c6 k
karyotype was 46XY. The thyroid function test
+ T2 E3 }3 k5 h9 o. B: u# |- Sshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
  y1 r6 {2 d, h5 Elating hormone level was 1.3 µIU/mL (both normal).8 t2 g$ Y) y: ]+ q+ r3 k
The concentrations of serum electrolytes, blood2 h+ n" @+ |* b. _- P- N! c! ~5 [
urea nitrogen, creatinine, and calcium all were
  c4 J* c; {9 Iwithin normal range for his age. The concentration
" A5 ^% y; y1 q4 v: J  D5 Tof serum 17-hydroxyprogesterone was 16 ng/dL
# W4 H* e$ ~# [6 {( P(normal, 3 to 90 ng/dL), androstenedione was 20
- b9 Q! c+ s4 ?8 Zng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
& M3 `6 t- _. n# p8 @! Z, `* Gterone was 38 ng/dL (normal, 50 to 760 ng/dL),8 J, J- R5 W& N% J3 N/ s
desoxycorticosterone was 4.3 ng/dL (normal, 7 to- }; R0 n( ~$ H8 A2 {/ {
49ng/dL), 11-desoxycortisol (specific compound S)- W; C: d5 a3 w) T1 F* S
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
8 i, J' a9 h! T. M- Ytisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total1 S. V& d, q5 t# e- z  K4 b
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),; D! Q; c7 v* W9 Q" U7 o% Z
and β-human chorionic gonadotropin was less than
" |' q( a& u2 Q7 j% g$ T5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 x) H: F: I4 Cstimulating hormone and leuteinizing hormone% F. F1 i  X: a  D& T+ B5 W
concentrations were less than 0.05 mIU/mL) d! q, [7 m0 o+ F$ r
(prepubertal).4 {/ @' N/ e' D: d9 L
The parents were notified about the laboratory
- Q8 |/ ^8 i9 r- }/ D; q; vresults and were informed that all of the tests were
1 w! d4 t- _8 g' ?  xnormal except the testosterone level was high. The2 Y6 f: v0 p* C
follow-up visit was arranged within a few weeks to
; C) K4 x3 t6 h! vobtain testicular and abdominal sonograms; how-6 t. {  B+ b$ c
ever, the family did not return for 4 months.
8 p( z- T1 {, C: W6 H/ APhysical examination at this time revealed that the
' p' K4 n6 E- h' ~  Pchild had grown 2.5 cm in 4 months and had gained& Q  c1 x6 h0 T+ m7 B
2 kg of weight. Physical examination remained4 B1 [2 k6 l" m) J& z: F
unchanged. Surprisingly, the pubic hair almost com-
! ~, ^! v1 N* b3 V8 l  epletely disappeared except for a few vellous hairs at5 F: i3 C+ V6 l/ A
the base of the phallus. Testicular volume was still 2
1 H7 x3 l' k6 _- P' A- gmL, and the size of the penis remained unchanged.; {7 v% J! s. h  y
The mother also said that the boy was no longer hav-8 X8 b8 y7 r- R
ing frequent erections.
" ]  N( B6 X+ D7 L+ tBoth parents were again questioned about use of  w, I! z6 y/ K0 y$ B
any ointment/creams that they may have applied to
4 P. t, F. H/ ~% B) f+ M8 ?the child’s skin. This time the father admitted the! H5 ?6 P0 E/ F& W: S* P
Topical Testosterone Exposure / Bhowmick et al 541
& h& p; G3 H/ D) E* juse of testosterone gel twice daily that he was apply-
2 o0 l) F6 E% m6 l3 wing over his own shoulders, chest, and back area for: F, \2 |; z9 }# ^6 t
a year. The father also revealed he was embarrassed
; m& S) Z' X3 J; A# H# pto disclose that he was using a testosterone gel pre-) o  |: ^( Y5 t
scribed by his family physician for decreased libido
: b% Y. n% w7 X2 isecondary to depression.2 P% ~. K  n  P! P$ r) z- j3 ]/ i) ?; ^
The child slept in the same bed with parents.2 r& n& ~+ P" x+ _6 G; E
The father would hug the baby and hold him on his4 S8 Q9 l8 Z) o
chest for a considerable period of time, causing sig-8 d8 G$ ]6 ~. s
nificant bare skin contact between baby and father., d: l+ z. d2 W  c
The father also admitted that after the phone call,
, O9 g" Y) e2 v! w( w3 [+ ^when he learned the testosterone level in the baby9 u- S6 C# u0 ?* {
was high, he then read the product information
( J. L: `4 d9 F4 h; }+ gpacket and concluded that it was most likely the rea-9 c& d  q- z5 h) ], X" A( f
son for the child’s virilization. At that time, they
) I; T; e6 Q3 H2 M+ ?, ?decided to put the baby in a separate bed, and the; c' I# U+ A2 b9 F
father was not hugging him with bare skin and had! s# O; g" M) @3 ]1 J8 y
been using protective clothing. A repeat testosterone8 ^1 P1 Y' E0 {
test was ordered, but the family did not go to the4 y. n" H6 l( ?+ v% u. b
laboratory to obtain the test.
) F( z! |$ {) P, CDiscussion& U1 i& s8 F. s3 c" J  a; N3 O! G
Precocious puberty in boys is defined as secondary
  P. c5 _/ V8 P0 Ysexual development before 9 years of age.1,4
* z9 B. ~- S8 q; z# F. z8 HPrecocious puberty is termed as central (true) when
& ]! `8 S" `( P& s! d$ t( iit is caused by the premature activation of hypo-
. T' F2 `) W- `/ q3 b) f% Uthalamic pituitary gonadal axis. CPP is more com-9 y' l* ?2 f; c
mon in girls than in boys.1,3 Most boys with CPP' y* G4 R0 c$ K
may have a central nervous system lesion that is
7 n/ N, M$ X3 t0 ]' z- P# L& `6 |responsible for the early activation of the hypothal-9 r5 a* G2 {  u2 C) f6 ]
amic pituitary gonadal axis.1-3 Thus, greater empha-$ C* ]# ^. F2 C9 `
sis has been given to neuroradiologic imaging in: g/ J7 i' S  u( H9 ~
boys with precocious puberty. In addition to viril-
. A7 V- V& N* d' [ization, the clinical hallmark of CPP is the symmet-
; x9 f* ]. N( d7 J( ?; A2 }( Srical testicular growth secondary to stimulation by
: m" N) g8 R( ?" w8 egonadotropins.1,3! G  V/ a: d: j: s) e& t* l
Gonadotropin-independent peripheral preco-4 |# W  q% ~$ k0 l6 v1 {: }
cious puberty in boys also results from inappropriate
$ V+ _6 E- F) V6 xandrogenic stimulation from either endogenous or, g% t# e( f+ n1 \8 e" \$ Z3 ]  Q4 S
exogenous sources, nonpituitary gonadotropin stim-8 t8 G1 z( ?+ `9 q  p% }  o. J
ulation, and rare activating mutations.3 Virilizing
/ b: d) ?% S( c. ?" i7 \4 \* Zcongenital adrenal hyperplasia producing excessive
4 l/ J& i/ p8 \  x  Ladrenal androgens is a common cause of precocious* b/ @" w3 c/ Y5 N( g7 q+ ]1 {) t
puberty in boys.3,4( q/ z7 f2 f) p# |! N  C9 E8 E
The most common form of congenital adrenal
; ], Q6 t; e4 O$ W: Lhyperplasia is the 21-hydroxylase enzyme deficiency.! M- ^4 C3 M- F+ o5 c
The 11-β hydroxylase deficiency may also result in8 s8 w. h. v; W0 K- Z4 x" k1 G) Y7 W
excessive adrenal androgen production, and rarely,
( X! f3 m1 i( \1 m% uan adrenal tumor may also cause adrenal androgen/ w& M8 d) _" @$ V3 J0 u- @9 ^/ N
excess.1,3% h( b* l& y, D4 r3 u* }' \! [
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! u: r1 s8 K) {6 [
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
' W1 }  |7 }. o+ t$ t. h+ N) cA unique entity of male-limited gonadotropin-
( ^* x& N( i: ]# N" pindependent precocious puberty, which is also known# d0 X  P# s6 D  J4 D+ X/ h$ h+ W4 D
as testotoxicosis, may cause precocious puberty at a% \% r' L  P& b5 Q6 U
very young age. The physical findings in these boys
1 U; d& g; v$ Q2 g9 Q" d- iwith this disorder are full pubertal development,
/ ]* r0 k' d) w* L5 q+ {3 j) A/ T# dincluding bilateral testicular growth, similar to boys
* K+ r$ N1 N" {3 T3 {$ G$ hwith CPP. The gonadotropin levels in this disorder
- o$ i$ ~( q; {are suppressed to prepubertal levels and do not show
/ S: L6 h# d2 ?- H/ r+ y  qpubertal response of gonadotropin after gonadotropin-
3 S/ ^5 S- [* P; I$ D( hreleasing hormone stimulation. This is a sex-linked) A7 S# b6 A' M* b% a
autosomal dominant disorder that affects only4 J, h' e. t: Z$ s
males; therefore, other male members of the family- {; |. v. I; d& l. I
may have similar precocious puberty.3
- o! M3 r$ k6 l) ?/ B2 ZIn our patient, physical examination was incon-
& Q9 P. N8 m6 v6 S# w4 t  K7 bsistent with true precocious puberty since his testi-
4 H1 c) @. @( K% @' [6 N  C4 T& T! Dcles were prepubertal in size. However, testotoxicosis! n& J% g6 U0 C' R7 l2 u
was in the differential diagnosis because his father7 {: W1 _  \) S' F
started puberty somewhat early, and occasionally,# N3 e! L7 B9 `  F- o' ^3 {+ J: `$ t
testicular enlargement is not that evident in the0 ]" r9 R. L8 }  G2 n" B
beginning of this process.1 In the absence of a neg-5 g* r  t* P; F/ {, k& ]
ative initial history of androgen exposure, our
9 D4 o$ b: [3 Sbiggest concern was virilizing adrenal hyperplasia,
2 {: X% W* g* |0 _" Peither 21-hydroxylase deficiency or 11-β hydroxylase* h2 @. C" c/ `0 ?: [  C* D
deficiency. Those diagnoses were excluded by find-- X( r5 y, E3 m! w$ j
ing the normal level of adrenal steroids.4 v% _/ C( |1 [0 a) S
The diagnosis of exogenous androgens was strongly9 d' ~% E4 i2 w5 A  X$ ^7 L
suspected in a follow-up visit after 4 months because# O; \" j# S( t2 x) m
the physical examination revealed the complete disap-
5 x  B9 Z6 c. H3 X3 s; C  y# w, rpearance of pubic hair, normal growth velocity, and  \/ c& h4 C) A) G& u% w. L
decreased erections. The father admitted using a testos-
  n% S1 A: p  @- Wterone gel, which he concealed at first visit. He was% N) w+ n3 `+ X
using it rather frequently, twice a day. The Physicians’2 b/ ^& s3 A, O; P2 |
Desk Reference, or package insert of this product, gel or7 y& N* @$ b3 P2 A: z+ D
cream, cautions about dermal testosterone transfer to2 n& j! B  O& p* a( o& |
unprotected females through direct skin exposure.
# y4 U! Z* g3 o; I0 MSerum testosterone level was found to be 2 times the
% P1 _; P- U( N0 p0 T7 fbaseline value in those females who were exposed to$ v( w; Z( @& _4 L5 [. d0 D
even 15 minutes of direct skin contact with their male# R# j5 N7 X# N  m
partners.6 However, when a shirt covered the applica-1 R  g! A) q1 p/ ~7 K: M- f
tion site, this testosterone transfer was prevented.: `" g" b' \- J" \) B. n% E9 H3 x
Our patient’s testosterone level was 60 ng/mL,
- H5 l! e1 Z9 q3 N+ ywhich was clearly high. Some studies suggest that+ ]* G, H7 e! _
dermal conversion of testosterone to dihydrotestos-$ K8 _7 \, e8 l
terone, which is a more potent metabolite, is more
, Y; V0 v) C1 u/ gactive in young children exposed to testosterone
& T* n8 G9 A: _2 |# L5 Y$ R! @1 Qexogenously7; however, we did not measure a dihy-
5 q+ m7 ?- ?) E" ^: H  }) h1 ~8 udrotestosterone level in our patient. In addition to
5 c0 t0 K" V( ]: }' `virilization, exposure to exogenous testosterone in: T6 b$ E/ d1 j7 s7 n
children results in an increase in growth velocity and# x3 ]8 ?8 y4 B8 {4 q9 r, m) ^0 [1 G
advanced bone age, as seen in our patient.
% }8 m4 p& F( f) B. `: C& K( q: }The long-term effect of androgen exposure during+ W4 u4 n' j+ T, e( T: V# K5 P3 u
early childhood on pubertal development and final+ R$ v- q( o. V9 c* U3 {
adult height are not fully known and always remain
. K8 A7 F2 K3 _0 E) M5 Xa concern. Children treated with short-term testos-" j$ H: |+ m. g7 [9 r1 i9 ~7 ~, {
terone injection or topical androgen may exhibit some2 C! T+ x5 l) F/ N. l5 I$ h# M( d( }
acceleration of the skeletal maturation; however, after
; {+ ~/ ^* c# |cessation of treatment, the rate of bone maturation
* ^) U/ ]6 U1 o8 S, B: N$ Ddecelerates and gradually returns to normal.8,9# g6 I$ O  m, o8 F0 y  y/ {
There are conflicting reports and controversy/ `2 h- _  c4 R4 I8 x8 F) U3 m2 |
over the effect of early androgen exposure on adult
* z2 U+ u: o3 q0 c! {% ypenile length.10,11 Some reports suggest subnormal8 T; H* z: n8 ~3 G* K( E
adult penile length, apparently because of downreg-
! q) O" c! Z# h! O5 e0 aulation of androgen receptor number.10,12 However,, t" s: g" z8 V+ d' V! }
Sutherland et al13 did not find a correlation between
5 a- b0 s) L# N8 `+ |" B6 r4 u6 a+ Cchildhood testosterone exposure and reduced adult
1 ^, m& X2 C9 Fpenile length in clinical studies.8 s+ [. p% |- y* r( P' @* x
Nonetheless, we do not believe our patient is" O* b5 s) N6 r+ w0 V7 s
going to experience any of the untoward effects from
$ [; v% W2 O8 Y- ftestosterone exposure as mentioned earlier because
5 ]+ w7 J# ~# bthe exposure was not for a prolonged period of time.6 F3 T+ S) U) L/ s" D
Although the bone age was advanced at the time of
7 T$ h0 o) j8 b- mdiagnosis, the child had a normal growth velocity at2 l. Q- X  \- v% y2 f" A, k3 @0 d
the follow-up visit. It is hoped that his final adult
$ J: a( s% I2 E2 X" Gheight will not be affected.. i. v+ S: f- d2 V) ~5 o* @
Although rarely reported, the widespread avail-; E3 [% g( _+ b. U; h5 q5 I
ability of androgen products in our society may1 r# ]  ?8 K7 j
indeed cause more virilization in male or female
. u" Q$ {4 F- h# D, `" ]& c  gchildren than one would realize. Exposure to andro-
3 t* q4 r. ?2 _4 O5 ^gen products must be considered and specific ques-  ?+ X& a0 y. P/ x; t
tioning about the use of a testosterone product or
( u: ~' F, ~9 `- u, L3 n$ K* }gel should be asked of the family members during
3 }3 Z& {. z* c1 a3 Vthe evaluation of any children who present with vir-
/ l9 G. R  x- x& z3 `/ n) ?ilization or peripheral precocious puberty. The diag-
" U7 Y# W4 U6 n/ V2 @nosis can be established by just a few tests and by, c- [/ @- |' ?/ b  c
appropriate history. The inability to obtain such a
" g6 a2 n1 @/ q4 b, V, Bhistory, or failure to ask the specific questions, may
. G4 l2 w) i( B$ s. x2 s/ Xresult in extensive, unnecessary, and expensive
: o$ R, G2 @8 u. G  D# ginvestigation. The primary care physician should be
- E, Q9 }, O; q! U. p4 `5 R% p# [3 saware of this fact, because most of these children% ~* Y7 P# Z" q# A# w9 Q( t9 v( ~
may initially present in their practice. The Physicians’
$ f! f& {" R8 c, n  RDesk Reference and package insert should also put a
2 O3 R# H: G0 j( q* n& d8 ?warning about the virilizing effect on a male or: O: ^9 o7 u/ D$ p$ `; m& `+ L  w
female child who might come in contact with some-
4 P  u4 q2 M* _9 @1 Uone using any of these products.
) y7 ~# }4 o$ R! O. w7 X, XReferences- L0 M2 |4 x% B1 l1 v7 n9 D  O
1. Styne DM. The testes: disorder of sexual differentiation
1 f! J& v, R1 D: c9 j( `$ s5 nand puberty in the male. In: Sperling MA, ed. Pediatric
/ s; K7 y. \6 ~7 |Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;. g4 C8 f; [7 T, y# s2 g
2002: 565-628.! t# K; `7 L7 K6 u) r" z
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious* Q6 M/ `0 e# S8 v! |$ _
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
9 v$ d& ^9 X' f! }Boy Induced by Indirect Topical9 E+ i5 ~( ]9 F0 r3 f, A' i0 R
Exposure to Testosterone
2 J/ ]- O9 y% p- W* ZSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
  K; B9 T( W5 Yand Kenneth R. Rettig, MD1& @0 Y7 X2 G% d0 Q1 K9 {
Clinical Pediatrics  H- [1 G$ v( p* M! @
Volume 46 Number 6
" s1 x, l# o1 ~) N$ T) kJuly 2007 540-543. r6 r% O/ ?# w4 x1 F. @
© 2007 Sage Publications$ ], r- Q: O7 a% E% E8 J4 N
10.1177/0009922806296651
- r/ m: v$ h3 J  G$ bhttp://clp.sagepub.com+ [5 e: L( d/ ~5 Q: g  T9 B
hosted at
) q1 U" T8 G& W+ d6 phttp://online.sagepub.com$ f# w" C2 v8 b' O
Precocious puberty in boys, central or peripheral,, R) b% L4 q# \/ [4 E  K
is a significant concern for physicians. Central7 g9 z$ W2 ^5 j
precocious puberty (CPP), which is mediated; A, ?) X) _; o  Q: m: t! Q' }4 u
through the hypothalamic pituitary gonadal axis, has
4 H; n* q; }' J0 E! Y1 P8 Sa higher incidence of organic central nervous system
4 t+ s- c# M4 \, glesions in boys.1,2 Virilization in boys, as manifested0 B# x4 X5 N) m/ u1 I3 J1 j0 D
by enlargement of the penis, development of pubic* L' k; I4 ]3 K% E* X
hair, and facial acne without enlargement of testi-4 w1 d9 z4 z* e7 ~! e% J9 O  J
cles, suggests peripheral or pseudopuberty.1-3 We
/ v2 G* ]  C7 I$ R: e( a, D5 T5 freport a 16-month-old boy who presented with the
; M* S) H0 D' _0 @. X" U' tenlargement of the phallus and pubic hair develop-
5 F5 M2 }2 Y2 S- Tment without testicular enlargement, which was due
) A, T5 D- c; P/ uto the unintentional exposure to androgen gel used by' ^* ?: n, K9 V; I
the father. The family initially concealed this infor-0 V( b3 h: S5 c2 w$ r7 T' g
mation, resulting in an extensive work-up for this% j& D, S6 {4 ], R( r, F  L
child. Given the widespread and easy availability of1 J5 @3 N' U& N& Y' f
testosterone gel and cream, we believe this is proba-  s1 F( C3 w4 ?' J* c' ~/ g/ t+ f
bly more common than the rare case report in the  j. k1 o! m6 [( q3 `
literature.42 O8 Y; b& _  `: r
Patient Report
  S( _" l4 V% q+ x# b8 V/ tA 16-month-old white child was referred to the, M/ a% D) ?- y/ x. D
endocrine clinic by his pediatrician with the concern
2 w: f/ a/ Q2 @* e5 c/ I' X8 s/ Wof early sexual development. His mother noticed' F, |: s  h5 ~$ H2 r# C
light colored pubic hair development when he was; v$ [/ {; |, {+ o: x% R5 |
From the 1Division of Pediatric Endocrinology, 2University of
- I% j, v! _2 i% O8 k% _0 @7 USouth Alabama Medical Center, Mobile, Alabama.3 M2 c2 S2 B( d( z$ i: e  K9 @8 S
Address correspondence to: Samar K. Bhowmick, MD, FACE,. e9 {, c# f7 b7 s% ~1 W
Professor of Pediatrics, University of South Alabama, College of  m+ O8 ?( a. a. }% m$ w) B
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;- b, d7 u- Y  W1 `* A4 U% x& v
e-mail: [email protected].4 c; u; ~# K) L4 L" a, o3 _3 {
about 6 to 7 months old, which progressively became; p: ]* N& m" H5 t. Z
darker. She was also concerned about the enlarge-% [: u4 U& L$ T5 F, F
ment of his penis and frequent erections. The child
; L% R! B1 D0 a9 d+ a8 Swas the product of a full-term normal delivery, with/ s6 g' Q# C  X- r; u
a birth weight of 7 lb 14 oz, and birth length of
. u" t4 O7 p4 c: c) ]3 p: j* Q" J6 N( B20 inches. He was breast-fed throughout the first year
( }' ?* m8 r8 e. i; B; z/ W$ i1 gof life and was still receiving breast milk along with
6 Q6 [% w+ l- _; `solid food. He had no hospitalizations or surgery,8 i# n5 ?: T: r( F9 x, a
and his psychosocial and psychomotor development, o. q2 d! `4 {: B- s5 d& Z/ k1 ]; T3 {
was age appropriate.8 }% r8 M& l# q# R% X: @
The family history was remarkable for the father,- z5 p% v, w1 c& O+ b' r5 O- o
who was diagnosed with hypothyroidism at age 16,
- ^1 \4 I9 L/ Xwhich was treated with thyroxine. The father’s( H4 q  t5 c+ V
height was 6 feet, and he went through a somewhat
5 A4 Y% Y8 ^5 x9 r1 O5 _early puberty and had stopped growing by age 14.
. Q% j( n9 q# K0 c% vThe father denied taking any other medication. The
6 G+ W' E1 i9 b, t3 gchild’s mother was in good health. Her menarche7 w$ X( M1 J6 k' Z: k% e) S1 A+ n+ J
was at 11 years of age, and her height was at 5 feet  M8 c6 B( N7 E! l
5 inches. There was no other family history of pre-
: |' V( K9 o$ d4 R" l  ^cocious sexual development in the first-degree rela-2 @  x) O$ b" l
tives. There were no siblings." |& \. ^" e% s. O3 p: o  L& t9 G
Physical Examination
6 ~. n0 G1 B9 i& QThe physical examination revealed a very active," s& \( Q6 L+ \8 r
playful, and healthy boy. The vital signs documented! G# E7 p8 W4 l5 @9 t. M
a blood pressure of 85/50 mm Hg, his length was2 k9 n9 N8 m; t8 V: C9 f3 c% ^
90 cm (>97th percentile), and his weight was 14.4 kg7 r( t/ H& t) P( Z9 R- w
(also >97th percentile). The observed yearly growth
9 P9 x! Y' F, Z* L' |; b& J* Pvelocity was 30 cm (12 inches). The examination of: s+ {" s! s, x7 J( ^& I/ d. Q
the neck revealed no thyroid enlargement.! b" n( S# z# I4 K0 w6 a) p
The genitourinary examination was remarkable for
" v% ?5 a' J7 y5 {3 R- senlargement of the penis, with a stretched length of
4 r% Y, v) d1 c8 s# Z8 cm and a width of 2 cm. The glans penis was very well5 I7 T) X9 P7 e
developed. The pubic hair was Tanner II, mostly around
6 e7 t8 \. F. w% A$ x540
, P& v! x( Z5 u% aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" T( i' y( V, t0 R2 F' _0 w; Gthe base of the phallus and was dark and curled. The
4 ^/ ]- b# z8 F/ M6 S- X2 Otesticular volume was prepubertal at 2 mL each.
/ C* A) w. a8 Y$ u7 x% K6 oThe skin was moist and smooth and somewhat
1 ]6 s$ ^( z3 w+ Hoily. No axillary hair was noted. There were no+ ~, q$ V; P8 P$ R. {" X; \
abnormal skin pigmentations or café-au-lait spots.
0 R4 j4 Z5 m  m, R5 v4 I+ k5 U7 yNeurologic evaluation showed deep tendon reflex 2+
6 |5 m) ~# y* c& pbilateral and symmetrical. There was no suggestion
/ p( m3 ^& j# d( Gof papilledema.
' ]( E7 Z# R0 oLaboratory Evaluation
2 A: L5 y8 |) M  v* T9 ]The bone age was consistent with 28 months by
1 U+ E: A0 y6 K9 z" Musing the standard of Greulich and Pyle at a chrono-1 G3 `2 [& q* N. F! s
logic age of 16 months (advanced).5 Chromosomal8 T$ P2 ]( @# [5 a0 ^
karyotype was 46XY. The thyroid function test; ?% ]4 o8 `5 {" I1 Y1 ?" V6 X: p
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
. e0 u! }0 s* ]! P3 r' Llating hormone level was 1.3 µIU/mL (both normal).0 ^, N6 R( D8 Q+ v) W4 z' }( e1 L
The concentrations of serum electrolytes, blood
1 j0 W1 y- [3 murea nitrogen, creatinine, and calcium all were/ z# m. W0 a. J: d  s
within normal range for his age. The concentration
! Y5 c' R. s: D9 c& Aof serum 17-hydroxyprogesterone was 16 ng/dL
4 x* h7 o9 t& U" }! _5 U2 G+ H3 \(normal, 3 to 90 ng/dL), androstenedione was 20% J; Y: N0 Q6 h& ?# n3 s
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-% C: u8 [+ T, K5 I* v- c) @& m
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
4 h4 W: E, L. H- Ydesoxycorticosterone was 4.3 ng/dL (normal, 7 to
! G5 @; j1 `& A$ b# V+ [8 y49ng/dL), 11-desoxycortisol (specific compound S)3 m% e5 R- D9 w/ C( D- u- O
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-1 ~. ]- U3 V# l, r# h
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total7 E! {6 b- H4 f% p* V$ q5 b% y- X
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
  K$ C1 G% c4 @- O% Q- c, ]and β-human chorionic gonadotropin was less than" B5 w. |5 B2 w: n9 ?
5 mIU/mL (normal <5 mIU/mL). Serum follicular
3 [3 a2 c+ j% P# f1 G2 R; [stimulating hormone and leuteinizing hormone
$ f* k' t1 @9 O% @' o  b2 i  Wconcentrations were less than 0.05 mIU/mL
3 w; ]8 u: @! h3 Q% ?- B- ~(prepubertal).
5 y% A+ l/ m+ s: @The parents were notified about the laboratory
! [+ R* U8 b( g1 v" A, ~results and were informed that all of the tests were
- @2 u  j6 n& `9 I$ Jnormal except the testosterone level was high. The; m, \, m* v1 I& J1 ]/ C! S
follow-up visit was arranged within a few weeks to- v9 X$ D5 `1 F' o. |$ Q
obtain testicular and abdominal sonograms; how-( Z: ~. V! p" A+ k
ever, the family did not return for 4 months." E" \/ X" O# n( @9 ^
Physical examination at this time revealed that the% p3 g" N2 L7 o% i7 I, t% w0 |
child had grown 2.5 cm in 4 months and had gained7 J% n% `. C: A2 e6 x- B! t' C+ Y
2 kg of weight. Physical examination remained
" D8 {$ f4 n' ^. m6 j4 E4 wunchanged. Surprisingly, the pubic hair almost com-
5 w* h! \. s9 x- y1 q- Zpletely disappeared except for a few vellous hairs at
3 J4 D3 r3 c, Athe base of the phallus. Testicular volume was still 22 V8 R4 S( |' o0 t; G* O6 W6 p$ C! s
mL, and the size of the penis remained unchanged., W: k9 c( E" a9 Y
The mother also said that the boy was no longer hav-
- G. G0 f  P% i. {, ling frequent erections.
* \6 |' J" l7 a" [5 r( gBoth parents were again questioned about use of! {0 N* Q( e" u) s; O4 H- L
any ointment/creams that they may have applied to
1 r( A3 c) T) B: Ithe child’s skin. This time the father admitted the
3 M3 }$ ~& x1 C/ ETopical Testosterone Exposure / Bhowmick et al 541
' R' ]2 ^' [) I+ F+ d& Z' suse of testosterone gel twice daily that he was apply-
/ O8 z+ \( {* M& W* j! E. uing over his own shoulders, chest, and back area for2 H8 Q# d% R$ l8 B
a year. The father also revealed he was embarrassed5 w$ C$ m- i, {( C* u
to disclose that he was using a testosterone gel pre-" {; T4 S# t* [5 M6 W
scribed by his family physician for decreased libido
  s0 m7 l, D2 P6 F" W+ a$ M. v: s7 t- r3 zsecondary to depression.! h; V1 S2 ?4 e& h  H! L
The child slept in the same bed with parents.
" G# |+ ~8 z' kThe father would hug the baby and hold him on his
' @5 u+ ~" C6 y9 ~chest for a considerable period of time, causing sig-! l7 q# s/ [/ s0 I/ O! J) z& X
nificant bare skin contact between baby and father.
+ q  X5 a* Y3 v6 j- w# n, {The father also admitted that after the phone call,
' g8 P# U, A6 [  t9 Pwhen he learned the testosterone level in the baby! U' b! E; M4 F0 W' X, M( i  D
was high, he then read the product information
% R  Y6 l5 {; N5 |packet and concluded that it was most likely the rea-
0 i& F2 x0 h6 j( q  {son for the child’s virilization. At that time, they& [7 Q. [" D" d
decided to put the baby in a separate bed, and the
: T- l* L# S0 F, L0 v- s* Ffather was not hugging him with bare skin and had; N) n3 C$ @5 d) E9 v
been using protective clothing. A repeat testosterone
! w0 M; @' G% r" F" G* xtest was ordered, but the family did not go to the6 n3 z5 _0 R9 Q3 e+ ^5 C5 N
laboratory to obtain the test.. H! v$ Y/ ^5 O6 v
Discussion
7 x. A. Y# M; U$ ]( F, s' EPrecocious puberty in boys is defined as secondary( v, R4 _- {0 H$ R1 n
sexual development before 9 years of age.1,4
$ r" n0 V. D3 Z1 Q, A4 k6 \Precocious puberty is termed as central (true) when
- h; T6 g' A; }1 z& L$ qit is caused by the premature activation of hypo-
: K0 \: B1 |1 H3 E! q3 Nthalamic pituitary gonadal axis. CPP is more com-3 b6 ]% a7 z+ v5 P5 I* K
mon in girls than in boys.1,3 Most boys with CPP3 N) }5 Z8 y0 ~# w( T
may have a central nervous system lesion that is$ Q# L8 i- ?6 D' v2 c, w
responsible for the early activation of the hypothal-
$ t/ o* @: Z4 o/ y; gamic pituitary gonadal axis.1-3 Thus, greater empha-
  ^8 ~) x- [% }' o6 W' ?' v0 esis has been given to neuroradiologic imaging in& g$ N% t: A; m9 O% |
boys with precocious puberty. In addition to viril-
; c2 r7 I. G5 O9 q( Hization, the clinical hallmark of CPP is the symmet-
5 W/ Y& A' n. w; X( `6 U  B( Orical testicular growth secondary to stimulation by# G; a& a# z3 i/ l
gonadotropins.1,3/ h( F7 Q# p  j* \0 X, ~# A* `
Gonadotropin-independent peripheral preco-: J* Y5 V5 L- x  V
cious puberty in boys also results from inappropriate: s/ W# k5 |7 D! g$ ]& u$ i8 r6 h/ l
androgenic stimulation from either endogenous or  F4 L% Y8 P$ U1 N5 ~( p0 R
exogenous sources, nonpituitary gonadotropin stim-
- L: h( s5 Z& Y8 b) a' [0 Culation, and rare activating mutations.3 Virilizing
, q1 Y$ {! J/ K( `congenital adrenal hyperplasia producing excessive" d  k/ J. C: M0 F8 i7 d4 T
adrenal androgens is a common cause of precocious9 Y2 u6 Y" g  w5 ?) P; u! N
puberty in boys.3,4$ y9 k1 K# L' f
The most common form of congenital adrenal
& x+ o" G$ }" Khyperplasia is the 21-hydroxylase enzyme deficiency.# @+ H* T6 s, ?8 L
The 11-β hydroxylase deficiency may also result in
( a( {/ M4 G7 D+ f  o; t) `excessive adrenal androgen production, and rarely,
0 n2 k( `' |- {- O) @8 X4 Tan adrenal tumor may also cause adrenal androgen
' }1 s; e, \* d) h% Texcess.1,3  D+ a4 s7 w6 ?
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. b/ \- |' A) {- d8 w) U
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007, n) d! f8 C( t  j- Q% O
A unique entity of male-limited gonadotropin-
$ \7 A) B1 \: o; ?8 N1 U: R! U. H3 ?independent precocious puberty, which is also known4 a  f! }. q, a& E, L7 b- P
as testotoxicosis, may cause precocious puberty at a
0 n# F3 Q* P+ y1 {& d9 _6 ^) [9 fvery young age. The physical findings in these boys
: i/ {* k3 @0 r+ _* @& q5 k: _with this disorder are full pubertal development,! S# C- h$ w) d! B2 G1 r+ U
including bilateral testicular growth, similar to boys
6 [# E/ {- k8 \# xwith CPP. The gonadotropin levels in this disorder
# O+ y/ p, [  W( Mare suppressed to prepubertal levels and do not show' v& x$ w$ P: e  B
pubertal response of gonadotropin after gonadotropin-
' d, s( a; |5 f- ?( B; s  y' `releasing hormone stimulation. This is a sex-linked: z+ i; X/ |) t; O, ?1 u
autosomal dominant disorder that affects only! `+ }  @; L& c  @0 K
males; therefore, other male members of the family
. W% v" c) g/ u* [4 Wmay have similar precocious puberty.3) u+ f# e. Z+ [+ T
In our patient, physical examination was incon-
5 m' S; E8 b0 V# a+ Y7 _sistent with true precocious puberty since his testi-
; M$ m% m7 N1 Kcles were prepubertal in size. However, testotoxicosis5 `1 T, u" O4 {* P* d
was in the differential diagnosis because his father. u. a5 }3 O( f' n9 X& N
started puberty somewhat early, and occasionally,5 O" e% ^+ O6 a( ~. y
testicular enlargement is not that evident in the$ q3 I* ^$ b* r; N
beginning of this process.1 In the absence of a neg-: I, Z7 m' V& g( M3 [5 M+ |! v
ative initial history of androgen exposure, our4 o0 x4 t4 J3 \! Q; l8 M
biggest concern was virilizing adrenal hyperplasia,1 s+ |- A+ O; H% p
either 21-hydroxylase deficiency or 11-β hydroxylase) m: g( E' a# F5 V* u) V
deficiency. Those diagnoses were excluded by find-& ^% K1 F: J, I* c  @  o- i
ing the normal level of adrenal steroids.5 Y" j' W) W( P2 Q) l
The diagnosis of exogenous androgens was strongly
) L. L3 {2 V4 [: _4 o* ksuspected in a follow-up visit after 4 months because4 S8 f; g0 `1 u& r/ Y# a) ^
the physical examination revealed the complete disap-
4 Q# _9 I' ]- U& w4 M! y( V& c/ Ipearance of pubic hair, normal growth velocity, and" o7 x* r- p  M. T" l: J6 Y0 g
decreased erections. The father admitted using a testos-
# a4 U2 c/ [8 a. ?: l: N# fterone gel, which he concealed at first visit. He was% u$ ~. E- P7 W! b* x- s# q: B  o
using it rather frequently, twice a day. The Physicians’
7 O6 `0 X9 l/ J& N% RDesk Reference, or package insert of this product, gel or
# k; R% V5 g" _5 j8 }cream, cautions about dermal testosterone transfer to
, Z# x6 p. k! o. f( V1 xunprotected females through direct skin exposure.0 y$ m, e: w- ]2 Q. ]4 ?! i8 n
Serum testosterone level was found to be 2 times the% u* D" M* @  E  Q
baseline value in those females who were exposed to5 F% |3 I+ m( V3 L) Q
even 15 minutes of direct skin contact with their male6 C9 S6 o$ Q5 Q
partners.6 However, when a shirt covered the applica-
) U/ @$ V- m$ _7 otion site, this testosterone transfer was prevented.4 m2 b# F: G7 f) l
Our patient’s testosterone level was 60 ng/mL,
7 l  U+ r& B6 G& rwhich was clearly high. Some studies suggest that
& u4 s# g. L4 K3 }dermal conversion of testosterone to dihydrotestos-
* ^6 g% E9 P9 {1 Aterone, which is a more potent metabolite, is more
% Y8 g. F* X* Lactive in young children exposed to testosterone
# H: |0 y. `5 E5 `exogenously7; however, we did not measure a dihy-/ s+ C: w: [6 H2 q3 C
drotestosterone level in our patient. In addition to$ Z9 B* j+ s9 I& r& F! _
virilization, exposure to exogenous testosterone in
1 ~$ U$ T; w, ^& S$ M  Pchildren results in an increase in growth velocity and6 |' M7 h$ G  i/ x0 D
advanced bone age, as seen in our patient.
) r$ N) C  t: QThe long-term effect of androgen exposure during
3 B7 e8 N5 m, w& c6 c9 h2 `early childhood on pubertal development and final( `0 a$ e  i3 H
adult height are not fully known and always remain
$ z+ k( W6 j, H% I7 Aa concern. Children treated with short-term testos-. M  }; ~2 T* T1 r/ r& x+ f4 F( f
terone injection or topical androgen may exhibit some
3 ^9 d5 _' F  `" x# W1 L; Lacceleration of the skeletal maturation; however, after$ r3 Z% z; U% z* {
cessation of treatment, the rate of bone maturation
' b- m* d- G% hdecelerates and gradually returns to normal.8,94 H: L( \- |1 L$ O9 p
There are conflicting reports and controversy
( M+ W* N+ J& U" vover the effect of early androgen exposure on adult0 U/ a8 C, x: x9 y4 \
penile length.10,11 Some reports suggest subnormal; u+ N* Q" K( G  {+ ~7 K
adult penile length, apparently because of downreg-
0 b' L$ E2 a! G. [0 ?ulation of androgen receptor number.10,12 However,
2 g& V4 i1 h8 ]5 x5 H( F/ Q. LSutherland et al13 did not find a correlation between! V. ?& U' E2 A$ P$ Y
childhood testosterone exposure and reduced adult
) B  s6 o2 G0 s  W1 C9 @penile length in clinical studies.0 U/ Q8 _* L; ^% S* L- y/ j
Nonetheless, we do not believe our patient is% z; U2 W( Q3 m# D! H' |
going to experience any of the untoward effects from6 D; ~0 |0 K; t3 |8 H0 U0 C1 ?
testosterone exposure as mentioned earlier because  q3 g0 ]% ~6 h3 f8 ?
the exposure was not for a prolonged period of time.
, {3 c' N: m3 p* G: CAlthough the bone age was advanced at the time of
  }' j% l. c$ g* Mdiagnosis, the child had a normal growth velocity at3 O) y8 Y; u/ U5 M) \" n
the follow-up visit. It is hoped that his final adult
- b, w% h8 O3 w* B9 N9 Theight will not be affected.
% v5 [, I9 t5 e( T9 R! ?Although rarely reported, the widespread avail-4 x" v; b2 l! C- {/ B$ ~) D' Z+ X, n
ability of androgen products in our society may5 c- }5 D' X% p* c! h
indeed cause more virilization in male or female& p' M& S; C$ X$ J2 o) U
children than one would realize. Exposure to andro-) h2 _, D3 ]2 `% Z: w9 F7 q
gen products must be considered and specific ques-; ?* P* l, E# E) U3 P
tioning about the use of a testosterone product or1 H" \6 l: w* p5 v
gel should be asked of the family members during
) O6 c# N6 P3 `- lthe evaluation of any children who present with vir-2 o% h4 a8 g6 F. [
ilization or peripheral precocious puberty. The diag-0 U9 v, N- A- ]- p$ }! i
nosis can be established by just a few tests and by" s, a+ ]8 l1 `! n& R
appropriate history. The inability to obtain such a
' h6 S$ J! j% ]& P! E$ e' y4 ~history, or failure to ask the specific questions, may" O# e$ ~) ~. j1 d* y
result in extensive, unnecessary, and expensive
# K  N9 D* s& L1 ]. C9 n0 g; @investigation. The primary care physician should be
" n% {& o9 u1 q0 e( R4 aaware of this fact, because most of these children7 N; C% ^% B4 Z, j' g5 }6 A0 t
may initially present in their practice. The Physicians’
4 u# N9 g3 E: F! o5 NDesk Reference and package insert should also put a
  h9 f# C; r# xwarning about the virilizing effect on a male or
5 s( }5 }& s; X. |6 Z( K% ~female child who might come in contact with some-/ m9 {/ @) y& `: a9 r: z5 Y
one using any of these products.. @3 Q6 g0 z. C! W" [* K
References9 P/ Q' r3 ^' o: B3 Q
1. Styne DM. The testes: disorder of sexual differentiation- Q3 h/ Y( }* f: h3 z
and puberty in the male. In: Sperling MA, ed. Pediatric& p, q" H4 D. y, }% l! M! U! u
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
5 ^. x9 x9 y$ }- f; ^2002: 565-628.
4 N5 V$ [- P7 i8 T" ~+ Z0 q2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
6 v3 [1 O9 X4 O- T3 l) {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

- G- E& b( ^4 m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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