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Sexual Precocity in a 16-Month-Old$ B; e! i- S, Z' ?, U! m
Boy Induced by Indirect Topical
/ }& `# J5 |) pExposure to Testosterone
1 ~0 y5 V5 s% }0 G' p. c' y$ X, tSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 f: I2 @2 R2 Zand Kenneth R. Rettig, MD1
; [- C2 l9 T3 F( DClinical Pediatrics" P) M4 `- k4 P" {% X
Volume 46 Number 62 \! |$ R/ y6 p; Z
July 2007 540-5438 l" u9 b& K; s$ A- {
© 2007 Sage Publications$ C/ b; K! j$ G" h8 O
10.1177/0009922806296651
3 X0 [5 x" |9 H4 T* Uhttp://clp.sagepub.com0 S- g" [% j5 `& Q7 T% n8 r
hosted at
5 I% k7 \1 w. m7 ihttp://online.sagepub.com$ q4 O2 M1 x! m' I5 ~# B; `
Precocious puberty in boys, central or peripheral,
/ i6 A: X( P5 T! [2 @5 P' Yis a significant concern for physicians. Central. p3 L% D# Y5 h" X
precocious puberty (CPP), which is mediated
; q8 O& t1 q1 O) B4 m: Ethrough the hypothalamic pituitary gonadal axis, has
% Y( X* Q9 @( j7 \0 q  z6 ]a higher incidence of organic central nervous system' N$ K9 b$ t. c& @% _1 A' t6 ^( {# N
lesions in boys.1,2 Virilization in boys, as manifested
/ O6 Q) y8 d  z, F( P! V5 Lby enlargement of the penis, development of pubic+ K5 f; E' J5 `8 q7 A
hair, and facial acne without enlargement of testi-: a  e' L! f% u% D/ P6 W
cles, suggests peripheral or pseudopuberty.1-3 We, o8 e8 K, v2 c) b4 m) B* w
report a 16-month-old boy who presented with the) @; h. @. ]! i' F4 R" ^
enlargement of the phallus and pubic hair develop-  k) t% P4 U- I: @1 y& R; v
ment without testicular enlargement, which was due
4 _; U: T# A0 R" n" sto the unintentional exposure to androgen gel used by
9 Q& S3 u$ F& l6 B( }8 H( H1 rthe father. The family initially concealed this infor-, X- [2 q: @! y
mation, resulting in an extensive work-up for this9 [, O# ]! B* C2 F- g9 M2 M
child. Given the widespread and easy availability of
" d+ k' ~& ]; k& ptestosterone gel and cream, we believe this is proba-
( v: }& n3 s; i' ]% @9 K7 ?! ^0 o$ xbly more common than the rare case report in the& ~! V' M; ]3 h, M- q$ E8 l) G
literature.4/ }1 t1 h5 Y' ^* w" o; A6 v  h
Patient Report2 c7 q1 v0 S# a5 Z8 \, J
A 16-month-old white child was referred to the
9 J5 B& v, p2 y! h) J, Fendocrine clinic by his pediatrician with the concern
$ c! J3 ?1 F3 r# ?1 Lof early sexual development. His mother noticed+ J0 z( Y! q9 L! b, w) x; G& V
light colored pubic hair development when he was
5 Y5 y: j+ }/ e# ^$ E; ^) ]From the 1Division of Pediatric Endocrinology, 2University of
5 [$ L5 J  `  t5 M% c# v2 JSouth Alabama Medical Center, Mobile, Alabama.( Y/ r: ~/ ?# b, {  c
Address correspondence to: Samar K. Bhowmick, MD, FACE,
5 Z8 H; Y% T8 W) h; mProfessor of Pediatrics, University of South Alabama, College of
8 X+ r4 r$ O  z% V& RMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;( T8 K# C7 _4 `
e-mail: [email protected].3 U6 J6 p1 H; Y+ j, t" s7 h' t, n
about 6 to 7 months old, which progressively became
- u# R9 R- A3 E) B: l. [9 `& qdarker. She was also concerned about the enlarge-
# G0 J5 ?# [/ q6 q, `  _$ N( Dment of his penis and frequent erections. The child
: a/ }$ j. E3 z; H6 mwas the product of a full-term normal delivery, with; q4 a: o" r! v3 I1 R, {: b
a birth weight of 7 lb 14 oz, and birth length of
1 k( W8 G1 Q( c7 I2 k# r20 inches. He was breast-fed throughout the first year
$ ]8 Q6 u7 D0 B0 R* I% gof life and was still receiving breast milk along with
& z4 I/ h8 Y" i; Ksolid food. He had no hospitalizations or surgery,7 S/ A5 z$ a- m0 P; Z8 f8 P% S
and his psychosocial and psychomotor development
2 t3 n9 n5 {7 I- x4 e; zwas age appropriate.
9 m: C& I% {. J  \The family history was remarkable for the father,
: U5 ]. H, b1 y. A( m5 Uwho was diagnosed with hypothyroidism at age 16,
5 a, f5 O( x/ L$ uwhich was treated with thyroxine. The father’s; D8 R( Q. w2 }& y5 ?# S9 f
height was 6 feet, and he went through a somewhat: ^3 a  K# F$ ~; U/ F9 Z" u
early puberty and had stopped growing by age 14.. F' u7 q! {9 @9 c# U9 b+ k
The father denied taking any other medication. The
0 g) U  s. s5 v+ g: nchild’s mother was in good health. Her menarche
4 c. h' v) M+ S' G7 O" }2 p" ywas at 11 years of age, and her height was at 5 feet! L; f0 r1 `' u3 _; ]0 `; R
5 inches. There was no other family history of pre-. G7 _* m; v' @7 U* L7 J- z8 W
cocious sexual development in the first-degree rela-9 d- r/ I1 V0 y# ?$ [4 W5 q0 {
tives. There were no siblings.0 t2 h5 g. }6 i, Q1 q
Physical Examination  h" k- U# o) I
The physical examination revealed a very active,
, s$ y. z' e% E" a% splayful, and healthy boy. The vital signs documented) z* i# Z) q4 v5 N. H
a blood pressure of 85/50 mm Hg, his length was
: F3 D' p5 N4 O& U' Y90 cm (>97th percentile), and his weight was 14.4 kg
8 e: O% ~( w7 W  a1 ^9 `- C8 ^; R(also >97th percentile). The observed yearly growth
6 G' F. w4 x" w' O! xvelocity was 30 cm (12 inches). The examination of
2 N1 O5 B" B' M( I9 J: dthe neck revealed no thyroid enlargement.
3 B$ Z  h- [6 y+ {6 mThe genitourinary examination was remarkable for
9 O7 q5 v, \) r4 qenlargement of the penis, with a stretched length of
' _* e+ [6 x1 q7 p& h; W7 n8 cm and a width of 2 cm. The glans penis was very well
  X- e6 w& l) z& \2 U, n- e3 Edeveloped. The pubic hair was Tanner II, mostly around! a+ D  z: _& g1 @
5409 ?, O8 X' \) r
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from" [$ O3 m' a+ u6 D) t
the base of the phallus and was dark and curled. The
, L9 ~% k. ^! Itesticular volume was prepubertal at 2 mL each.
" H- }, N, [- ?, s% y) {* E+ VThe skin was moist and smooth and somewhat3 F; \5 k2 h% X# A) c' }
oily. No axillary hair was noted. There were no
5 z' c' d  }- A# g8 k' u2 fabnormal skin pigmentations or café-au-lait spots./ G% ~) X/ n0 G
Neurologic evaluation showed deep tendon reflex 2+
' J: e3 ]; S4 Z+ ?bilateral and symmetrical. There was no suggestion  I; K' P) b3 H9 F
of papilledema., e9 g2 d2 e9 v; u
Laboratory Evaluation
9 S. b% b" v2 w7 i/ T5 D  pThe bone age was consistent with 28 months by
* p/ b  D( _, {8 \2 U6 P& K+ [% Husing the standard of Greulich and Pyle at a chrono-
% L7 L5 l& Q4 o" g$ {  klogic age of 16 months (advanced).5 Chromosomal+ R/ z, q- C; `. D6 \
karyotype was 46XY. The thyroid function test% S' }* {5 h/ O. k- O: `1 G
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
# [9 D5 G* a, a+ Ulating hormone level was 1.3 µIU/mL (both normal).
) r- v! B$ m$ c$ }+ w/ ^The concentrations of serum electrolytes, blood
$ a1 Y3 C2 i0 x+ ]8 K: Furea nitrogen, creatinine, and calcium all were4 r- T  Q7 g2 v0 C& M5 ^+ k  \
within normal range for his age. The concentration" `, d9 T6 W) D: L
of serum 17-hydroxyprogesterone was 16 ng/dL
! S# v1 F4 {1 K  C3 N6 \$ K" P1 R; |(normal, 3 to 90 ng/dL), androstenedione was 20
# _5 m% n" G2 }  k; v7 n# zng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
  g2 j8 H% e0 v% y* aterone was 38 ng/dL (normal, 50 to 760 ng/dL),7 G6 y1 V1 [) i
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
0 z; x1 R! }' o/ Q3 G* {49ng/dL), 11-desoxycortisol (specific compound S)
/ o7 C& o- \. Z1 b$ ?& Jwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-5 @# }( K8 l, E
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
+ T( H/ _* l* @( I5 Z; D" G9 h( `testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
& B" h- L0 |1 t' C$ J4 j* T. wand β-human chorionic gonadotropin was less than2 _% G, U! o$ w) V; H$ w1 t4 Z2 g
5 mIU/mL (normal <5 mIU/mL). Serum follicular
" c5 w' K( {2 Zstimulating hormone and leuteinizing hormone
- Q: c7 h' \" n2 r. d: kconcentrations were less than 0.05 mIU/mL
- |$ I  [' R: p' K) y: |(prepubertal).
: a' [" o+ w& c* WThe parents were notified about the laboratory+ {- W: R& J7 b
results and were informed that all of the tests were
1 Z/ x1 g4 [% }* z, M- c2 `" ^normal except the testosterone level was high. The
! K; @9 R7 s  ~  efollow-up visit was arranged within a few weeks to
- P6 Q; v( n$ gobtain testicular and abdominal sonograms; how-
3 _: A" P9 Y; ]  C/ Cever, the family did not return for 4 months.
0 p) P0 T6 b" e( t" @0 UPhysical examination at this time revealed that the
& c" Y& H: k1 I6 j9 F: e+ Xchild had grown 2.5 cm in 4 months and had gained
* n, @4 g$ O1 i$ @' a2 kg of weight. Physical examination remained
; P- c2 \$ X( _4 Y( f* sunchanged. Surprisingly, the pubic hair almost com-6 O- B/ o# @7 [% n6 Z
pletely disappeared except for a few vellous hairs at
( E1 b4 w( m* b% f3 Ethe base of the phallus. Testicular volume was still 24 g4 \* \5 y6 u- D2 d
mL, and the size of the penis remained unchanged.
  [9 U# v6 f' _" TThe mother also said that the boy was no longer hav-
5 s; B/ O; X3 n2 g6 M% X, eing frequent erections.
* x8 |: n0 T' |4 o: p9 ~Both parents were again questioned about use of5 R: y+ c- P5 P4 Q3 z" J7 E
any ointment/creams that they may have applied to6 f; N: N% j0 z' z* ]4 U
the child’s skin. This time the father admitted the9 U# m  n0 O. x9 Y
Topical Testosterone Exposure / Bhowmick et al 541
8 n% N7 L9 d/ z/ F  q0 Z* u% Euse of testosterone gel twice daily that he was apply-
5 E0 N1 z) @1 H( G! Ping over his own shoulders, chest, and back area for0 m, @" K7 d. B
a year. The father also revealed he was embarrassed
# V+ I  R7 V" F" Zto disclose that he was using a testosterone gel pre-
) W% m# L5 w. D; p* {4 q3 F/ f9 Y0 sscribed by his family physician for decreased libido1 w2 t+ p* t( w* a& o5 ?
secondary to depression.# u1 _& ?5 o* M$ ]: h2 M
The child slept in the same bed with parents.7 z  p3 ]: z  g
The father would hug the baby and hold him on his" b) L' G7 t. f; o
chest for a considerable period of time, causing sig-
3 d6 O  `: c! H' x5 \, Y( @  xnificant bare skin contact between baby and father.6 z9 R4 }8 Q1 C! {& _
The father also admitted that after the phone call," z* L9 U" S6 x! Z" l' a
when he learned the testosterone level in the baby! |1 ]1 Y5 p! B+ {
was high, he then read the product information
, l6 ~* I/ j! U# o: ]% v) {packet and concluded that it was most likely the rea-
1 i; r. R; t) U2 @, sson for the child’s virilization. At that time, they' d6 B& E; N" x& F
decided to put the baby in a separate bed, and the
$ A! a, j) d1 J9 d( ~* Z) Ifather was not hugging him with bare skin and had
! L2 i( e1 ?# k8 Dbeen using protective clothing. A repeat testosterone
# b+ v+ O7 l3 v( y8 mtest was ordered, but the family did not go to the+ I( o5 Z7 S2 _! E
laboratory to obtain the test.
6 ~6 \) t  |8 f0 ^2 C( m( [' NDiscussion# |: b. N- ~' D) S$ h+ `
Precocious puberty in boys is defined as secondary& J) B+ A8 h1 L& ]/ a
sexual development before 9 years of age.1,41 i* ^; |' A7 P3 H% M+ l* X$ r
Precocious puberty is termed as central (true) when
" g+ Z0 `, P* c/ i6 X6 v$ \& hit is caused by the premature activation of hypo-
! z- u- y: g" _0 V0 rthalamic pituitary gonadal axis. CPP is more com-
3 n4 Y' {. X- y! Rmon in girls than in boys.1,3 Most boys with CPP$ Y. S0 A2 O9 s# X) T- ]# b# F
may have a central nervous system lesion that is7 x0 s- C- E  @4 v+ _8 u
responsible for the early activation of the hypothal-$ s( e% V" ]6 K2 {" Z* l3 I
amic pituitary gonadal axis.1-3 Thus, greater empha-
, r" G" w1 @" B" [7 p! Dsis has been given to neuroradiologic imaging in
9 p& {3 R: t" E5 M; Iboys with precocious puberty. In addition to viril-* q" ^0 Q& O/ k* U& b
ization, the clinical hallmark of CPP is the symmet-
; n5 K6 q: t- jrical testicular growth secondary to stimulation by
3 A% q6 s- V7 n# H1 Igonadotropins.1,3( G6 f- O  c/ L% `
Gonadotropin-independent peripheral preco-
9 F* L& O  L! }. i5 ~% z! Ycious puberty in boys also results from inappropriate+ B* A- F$ ?9 x' @) O* N% R
androgenic stimulation from either endogenous or+ X( ]; T: E2 P4 A( S
exogenous sources, nonpituitary gonadotropin stim-
6 L; G7 C3 o  ^  A) A$ R* |ulation, and rare activating mutations.3 Virilizing0 R3 ^3 j4 a8 x& b9 k3 V% }* f
congenital adrenal hyperplasia producing excessive
6 V3 l7 A8 P2 i) F6 _! J+ T4 iadrenal androgens is a common cause of precocious) t2 ]7 ]+ a- d7 A, F' Y
puberty in boys.3,4
% m9 l) o; y4 rThe most common form of congenital adrenal2 }4 b/ d- i' p
hyperplasia is the 21-hydroxylase enzyme deficiency.
$ r8 l  S* t( z( F9 `The 11-β hydroxylase deficiency may also result in
0 B( z' M5 c" T6 Y5 i: j% wexcessive adrenal androgen production, and rarely,
2 T; G% r( ]- j& X- N+ xan adrenal tumor may also cause adrenal androgen
9 y0 Z; u( E# h. B) zexcess.1,3( k/ \" G6 F% d) u  ^) N4 L- r: G, `
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. v9 E* S4 x3 b" _
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007# W, z  }2 Z4 r! g  e" H
A unique entity of male-limited gonadotropin-
: p5 I& M+ I4 h# g, ?+ S; V% kindependent precocious puberty, which is also known
$ B- E2 W4 i8 M9 |# _8 ?as testotoxicosis, may cause precocious puberty at a$ i! b7 X0 @- V1 p' h" q; B
very young age. The physical findings in these boys# ~- D; E: E6 l5 ?0 V( Y7 n; S
with this disorder are full pubertal development,7 S% R1 P+ t* F, I& Q
including bilateral testicular growth, similar to boys
+ \4 N  k( P( `  |- qwith CPP. The gonadotropin levels in this disorder, }# K1 s/ f9 t8 m( {4 u" _
are suppressed to prepubertal levels and do not show
/ S& h- q( {1 {- b  Xpubertal response of gonadotropin after gonadotropin-
4 a& n+ h: ~( Ireleasing hormone stimulation. This is a sex-linked
9 \+ u/ N$ ~, |autosomal dominant disorder that affects only+ l2 r3 q5 O6 [5 @; v- i2 S
males; therefore, other male members of the family$ [/ x* V+ c, e+ d; Y2 n% g8 Y  ]
may have similar precocious puberty.3# t& i# o! |+ x7 R4 i1 L
In our patient, physical examination was incon-6 T" U4 X% _: h
sistent with true precocious puberty since his testi-/ \& J7 X  U9 `! x1 |# |* A
cles were prepubertal in size. However, testotoxicosis! i4 w0 _$ c. X/ @3 c2 z' f
was in the differential diagnosis because his father8 y6 Z# F# t: o4 o: W# i. }
started puberty somewhat early, and occasionally,
) E4 m: D9 a2 Y/ N- y, \testicular enlargement is not that evident in the
+ V7 z# H, ^. h) T2 M9 obeginning of this process.1 In the absence of a neg-
3 |( E! e, J- Y! `ative initial history of androgen exposure, our
# F* k# x+ Z* \3 I+ `biggest concern was virilizing adrenal hyperplasia,% I* S& v( v  h. F5 M; X
either 21-hydroxylase deficiency or 11-β hydroxylase% \. F% f/ R+ [" c! W
deficiency. Those diagnoses were excluded by find-; ]& T  d: H9 a' C  R1 E
ing the normal level of adrenal steroids.
  ]! L- x1 g2 H9 \  i1 k! qThe diagnosis of exogenous androgens was strongly
) t/ m% \, a( u0 u9 fsuspected in a follow-up visit after 4 months because
6 Q4 @% S3 o+ A# L6 u8 Z; gthe physical examination revealed the complete disap-' c# ]4 q/ a  F6 D! {$ ]
pearance of pubic hair, normal growth velocity, and
. c/ n5 i' X8 _" edecreased erections. The father admitted using a testos-5 m5 m2 e* @; i6 g( ]* e
terone gel, which he concealed at first visit. He was* ~5 ]" O3 D4 r1 j9 x
using it rather frequently, twice a day. The Physicians’
; e+ g  g7 b( T$ C  LDesk Reference, or package insert of this product, gel or6 ]6 E2 |3 T; h7 e& S5 p
cream, cautions about dermal testosterone transfer to
$ h$ j$ W" U5 M+ c. s  ounprotected females through direct skin exposure.3 e/ Y9 L7 [$ V$ }! I
Serum testosterone level was found to be 2 times the
% v+ V! t5 {5 U9 A' j* l: ibaseline value in those females who were exposed to
7 u+ i5 Y- \9 \8 ]2 a, X- deven 15 minutes of direct skin contact with their male# p2 D' l/ A( Q  b
partners.6 However, when a shirt covered the applica-: H* |/ |- ~( r
tion site, this testosterone transfer was prevented.9 g9 }- m; Y! J
Our patient’s testosterone level was 60 ng/mL,
% I  V# X) Q; B/ h0 _) k8 jwhich was clearly high. Some studies suggest that
+ ?6 q' F! H8 Odermal conversion of testosterone to dihydrotestos-
% l$ e! N1 N! L7 vterone, which is a more potent metabolite, is more
: O# _! b& Q6 v0 V# S5 ~active in young children exposed to testosterone( x7 p, I6 K( I2 Z2 e( k0 b
exogenously7; however, we did not measure a dihy-4 U2 ^* D/ A* H% `9 {& M
drotestosterone level in our patient. In addition to8 Z8 x& _( g4 K0 _: N$ m# H
virilization, exposure to exogenous testosterone in
! E# t/ m1 R$ C3 g; Xchildren results in an increase in growth velocity and
% ~8 v' X- |: p  e! |6 o. Aadvanced bone age, as seen in our patient.# f% M/ E# W: |8 a9 V2 @! q3 j, {
The long-term effect of androgen exposure during
# E" V2 `+ I2 V2 T4 H4 x& T6 Xearly childhood on pubertal development and final* B* d; k, b8 O) Z% q6 ~, M
adult height are not fully known and always remain
6 D. B8 O+ H  J. [3 ka concern. Children treated with short-term testos-9 o( Q) L( f9 ]. s
terone injection or topical androgen may exhibit some! ?3 b( p1 c+ U) L
acceleration of the skeletal maturation; however, after
0 A+ D- o% c, bcessation of treatment, the rate of bone maturation' W: Q) {8 Y% M/ V5 m. }
decelerates and gradually returns to normal.8,9
2 L, c* R8 @2 w% DThere are conflicting reports and controversy
, m  S# Y" ~4 W# K6 m3 }2 Uover the effect of early androgen exposure on adult1 ^# j! p: T( r: W! o8 {& M/ ^2 z
penile length.10,11 Some reports suggest subnormal( m. ]! T8 _% C- o! O
adult penile length, apparently because of downreg-
7 j3 B" X* P4 B. n  `& kulation of androgen receptor number.10,12 However,5 ~4 N" A9 Q* y; W
Sutherland et al13 did not find a correlation between
+ A. i" u0 }: R( ]# k, _# vchildhood testosterone exposure and reduced adult
4 g( }  J' g' X& j( ~! ~penile length in clinical studies.) F- E! f$ p7 M* |! j/ z9 q
Nonetheless, we do not believe our patient is
& _" q/ N" g7 Ogoing to experience any of the untoward effects from/ q1 G8 q4 y( y  S; {* ]
testosterone exposure as mentioned earlier because
' }/ A3 Y& J5 _the exposure was not for a prolonged period of time.- `! k8 N1 v4 w6 J/ p
Although the bone age was advanced at the time of! b, S$ N; G; L4 |
diagnosis, the child had a normal growth velocity at1 ]) q* h. T0 t
the follow-up visit. It is hoped that his final adult
, D: f+ t  @% v7 B5 n8 Vheight will not be affected.
  \# H& @8 ?' Q$ L- ~+ r  v: vAlthough rarely reported, the widespread avail-# k* N* d. }% g
ability of androgen products in our society may
" u3 E/ E  N' Vindeed cause more virilization in male or female
) R( s4 ]4 D- d9 N! Q) j. g+ Z3 c) Pchildren than one would realize. Exposure to andro-* d/ G) ~/ e1 ?# @  T
gen products must be considered and specific ques-* U" S) X5 d6 V0 R( y3 F% U8 o2 o
tioning about the use of a testosterone product or
8 _% w3 B4 H/ s+ g/ n* B: l, ]gel should be asked of the family members during
/ w8 H. G7 s. M5 ]the evaluation of any children who present with vir-- E* ?+ P0 V/ w$ O
ilization or peripheral precocious puberty. The diag-& e5 n7 K" ]" j1 {( z
nosis can be established by just a few tests and by4 s. X( I  f/ T7 h8 y' N' H
appropriate history. The inability to obtain such a
. f2 S, F6 P$ r* h0 N& uhistory, or failure to ask the specific questions, may2 ?6 k8 Z. d, l8 n
result in extensive, unnecessary, and expensive
  d, v4 }8 D3 w4 Y5 Binvestigation. The primary care physician should be  P* [6 I' y: [% H- N0 c8 W
aware of this fact, because most of these children- E9 V% i# O1 ~8 O1 _( Q
may initially present in their practice. The Physicians’" B2 a: a- l) d# }7 ?( O
Desk Reference and package insert should also put a
7 \! Z  o/ W) G- t+ \warning about the virilizing effect on a male or+ z4 S' l& }# q$ ~& _1 [3 @( H
female child who might come in contact with some-
& Q' e, E; {5 \1 ]) w! N+ Ione using any of these products.! e, |- r0 F: }3 ^/ Q1 J
References/ w: e! |  \! K9 X: R
1. Styne DM. The testes: disorder of sexual differentiation
* f5 a5 p! h' ?$ eand puberty in the male. In: Sperling MA, ed. Pediatric8 \3 Q6 s* R+ u+ h/ Q5 J9 \- L
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;; ~; T( |/ L& D$ o7 ^- J, p
2002: 565-628.
2 i3 `' ~" S* F2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious( d# p4 S$ d! r6 S( z0 R
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
. ~6 L) s/ G3 U' W8 b0 hBoy Induced by Indirect Topical, Q7 S4 Z1 p  _" r) T9 z; i, X
Exposure to Testosterone
' q1 o0 ^- ~  B2 n% `$ TSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2  ^% r4 J1 n2 K% n6 w' f# \
and Kenneth R. Rettig, MD1
+ ^! N7 p5 g: }  p" T7 qClinical Pediatrics0 D# C. H) Z# S, S( R, K. h. e
Volume 46 Number 6
& _" L2 }5 G% ~$ PJuly 2007 540-543
9 z: Z0 u7 {7 W" D) \& P7 d© 2007 Sage Publications; o# ~' k, m$ T/ g5 b$ }* v
10.1177/0009922806296651( y2 Y# @5 m  N  B0 K
http://clp.sagepub.com) _; d6 i0 G9 X1 e- ^+ ~. ^7 B% b
hosted at
* f. q* z; M. w! j6 D3 T$ d8 ^$ Xhttp://online.sagepub.com
+ s/ N7 R9 t: ?) g1 q/ vPrecocious puberty in boys, central or peripheral,0 r0 u- e# O: v7 z9 `5 D% Z0 p
is a significant concern for physicians. Central# {8 [. R+ ?7 q
precocious puberty (CPP), which is mediated; \  @# G7 h2 M
through the hypothalamic pituitary gonadal axis, has9 M8 z- t( u# l
a higher incidence of organic central nervous system
. `. L1 Z% x( T0 k) C$ ylesions in boys.1,2 Virilization in boys, as manifested+ c  c2 K# o" c( `& t& B
by enlargement of the penis, development of pubic4 \: [2 D( D0 l$ O& A6 l9 c
hair, and facial acne without enlargement of testi-
. y, a& K( [4 k% e1 t2 ycles, suggests peripheral or pseudopuberty.1-3 We  k& X7 w# Y1 b# C
report a 16-month-old boy who presented with the
  o9 o# C' n, D: y( Nenlargement of the phallus and pubic hair develop-
. c$ j! U0 |5 I$ Bment without testicular enlargement, which was due
( Q2 `% {7 Y( k' n# C( F0 hto the unintentional exposure to androgen gel used by
! [$ n4 p6 U5 C3 ~2 [& hthe father. The family initially concealed this infor-/ `# K% j3 H& {3 h9 D, u6 D8 i
mation, resulting in an extensive work-up for this( }$ y: A- J2 W' k
child. Given the widespread and easy availability of
5 a2 \' d0 T/ r/ P" D( {. ]testosterone gel and cream, we believe this is proba-- O9 G. b- c/ G# ]/ ]# {
bly more common than the rare case report in the5 N, t/ ?# Z8 T2 ?+ c. X
literature.46 f3 E  C" v/ ~  T9 H2 j
Patient Report# v* ^/ G* g2 T- t6 B  a. z5 D
A 16-month-old white child was referred to the; H, C% W+ f7 m0 L
endocrine clinic by his pediatrician with the concern
, ~, k- p, h7 W2 x. R+ R" }of early sexual development. His mother noticed
# `7 t* z0 S- Z0 f2 \; s% Vlight colored pubic hair development when he was" ^$ q2 v; B5 e7 P9 w! A5 C
From the 1Division of Pediatric Endocrinology, 2University of; P/ m# I8 t' Y: u9 V# s! X
South Alabama Medical Center, Mobile, Alabama.
6 T+ W0 I" Z3 R  S: d" lAddress correspondence to: Samar K. Bhowmick, MD, FACE,
! f# H# o7 I8 L) l; ~Professor of Pediatrics, University of South Alabama, College of- `. P- O/ B# x; U
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
8 \6 G! e( g9 Q, ve-mail: [email protected].
  ^; n$ W9 n1 @7 F; a+ d2 s* w& Pabout 6 to 7 months old, which progressively became
; g% ]+ r/ M- }darker. She was also concerned about the enlarge-
$ N, {' X, S  Oment of his penis and frequent erections. The child0 o, K9 k( H; }) l- ]
was the product of a full-term normal delivery, with( {0 E6 Z9 s' h6 r) B* v6 m
a birth weight of 7 lb 14 oz, and birth length of6 [3 D: d9 P" W# t/ Z" `0 W) M
20 inches. He was breast-fed throughout the first year$ l7 |- u9 c: H1 I& x
of life and was still receiving breast milk along with5 ~0 s; m! x/ F5 S' b0 K# Y
solid food. He had no hospitalizations or surgery,
$ W: ^: w9 f+ Q% D: c) g$ g0 Yand his psychosocial and psychomotor development: k- i+ i5 W2 d( u6 t+ _
was age appropriate.
7 d) v* k# ^: S" c3 MThe family history was remarkable for the father,1 q2 S" f+ `  R8 ~; {1 x9 C0 e
who was diagnosed with hypothyroidism at age 16,
& U; K0 [. ?5 p+ W: y; r  xwhich was treated with thyroxine. The father’s
' n8 ?! d6 m' p: jheight was 6 feet, and he went through a somewhat, S3 I0 d7 G/ i. b- q& h8 a" b
early puberty and had stopped growing by age 14.4 t& @! u4 w* |
The father denied taking any other medication. The+ m) o2 `7 A$ L* Y/ D1 K- z1 V
child’s mother was in good health. Her menarche3 K7 M; w  [2 {, t" b! ~4 m
was at 11 years of age, and her height was at 5 feet
0 |: Q3 G4 w" j2 ~5 inches. There was no other family history of pre-
0 I6 e$ e+ C9 A. K+ {cocious sexual development in the first-degree rela-2 i! b9 `: r4 [) ?8 G- M) [
tives. There were no siblings.
4 A# c: u) O) t4 `Physical Examination
: [9 o0 x6 p! v# d2 Q. q0 v. uThe physical examination revealed a very active,2 G; T6 f& |- D1 P. f$ C' w
playful, and healthy boy. The vital signs documented
5 }) W8 a1 n" H; X) W" {8 P9 ya blood pressure of 85/50 mm Hg, his length was
% S& k* d& N' k, c' |: N90 cm (>97th percentile), and his weight was 14.4 kg
( O, W2 o# p0 ?6 L1 D9 d* J9 r  ](also >97th percentile). The observed yearly growth
+ |" g! q! p+ F3 m5 zvelocity was 30 cm (12 inches). The examination of
- I" z. K- Y% @; `6 A0 k+ mthe neck revealed no thyroid enlargement.2 i; p; U+ I2 d" a- S4 ^
The genitourinary examination was remarkable for
  V- N% [  D1 e8 ?% X# qenlargement of the penis, with a stretched length of
# \, y! E2 e7 ?  s3 g  r9 \' O8 cm and a width of 2 cm. The glans penis was very well3 t* S7 E8 I8 u+ [1 K
developed. The pubic hair was Tanner II, mostly around
( y$ M) J  e# U+ c6 x: d4 n; h% n0 d540  k9 {4 ?: f6 N* v; o
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ ]( h. |' G) i( {1 [
the base of the phallus and was dark and curled. The1 I8 u; _3 y0 l+ |+ `
testicular volume was prepubertal at 2 mL each.
; d: J% r$ w8 z0 M" S  gThe skin was moist and smooth and somewhat
  U5 Q! M6 I6 Aoily. No axillary hair was noted. There were no
$ O. G1 j8 {' h+ z8 L9 H! vabnormal skin pigmentations or café-au-lait spots.7 m2 f, ~: j) L: D4 I
Neurologic evaluation showed deep tendon reflex 2+( o% A0 p! K1 V& L
bilateral and symmetrical. There was no suggestion, [& P$ S: R; b) u
of papilledema.  W( x, H; \1 I" W( D' j  h
Laboratory Evaluation
% q0 U, e2 i9 dThe bone age was consistent with 28 months by2 {( w# n7 h+ s% j5 p  ?
using the standard of Greulich and Pyle at a chrono-
* d' T2 p9 A3 R7 w3 ?/ P9 \1 jlogic age of 16 months (advanced).5 Chromosomal
( g, V) ~9 e7 b8 Tkaryotype was 46XY. The thyroid function test) n; {0 q" K7 P0 D$ _
showed a free T4 of 1.69 ng/dL, and thyroid stimu-9 x+ b9 C0 [: n: Z% L0 Z/ s
lating hormone level was 1.3 µIU/mL (both normal).
1 s5 d/ L! G  C3 y- I: @. }( |( D2 dThe concentrations of serum electrolytes, blood5 u/ N  p( h6 v; Y: @4 F) I
urea nitrogen, creatinine, and calcium all were
* _0 Y( r  i( ~, y) P! kwithin normal range for his age. The concentration3 v2 _* q( `/ y8 y7 \3 W
of serum 17-hydroxyprogesterone was 16 ng/dL$ E8 m! d' s4 E) u8 _1 f
(normal, 3 to 90 ng/dL), androstenedione was 20% }) l2 N: U/ S8 x; o! P
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-! _" [5 Q7 T5 z4 p# v/ a0 T) W# ~
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
# O) `4 n0 X6 {5 v9 d' Odesoxycorticosterone was 4.3 ng/dL (normal, 7 to0 L3 U) {0 Q. t0 [1 `2 f. \" a
49ng/dL), 11-desoxycortisol (specific compound S)& w& O' s2 q9 e& Z
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-  g, K  d. S) [( B8 A. m/ a
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total8 T/ F  r/ ]' [1 n; ^/ T( J1 z
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),7 ~9 A  m2 L$ L/ ~0 i8 M
and β-human chorionic gonadotropin was less than; D, s4 @' S  h3 b; s& C
5 mIU/mL (normal <5 mIU/mL). Serum follicular  V  q* H% @/ I* h: @
stimulating hormone and leuteinizing hormone1 ^$ d9 Y9 d. j# A; w6 F* C3 A
concentrations were less than 0.05 mIU/mL
2 ^/ i: T( z7 V- o1 n5 J(prepubertal).
! f' Q  @8 j, AThe parents were notified about the laboratory
* |3 R. A9 E3 s; ~) {, nresults and were informed that all of the tests were* d- O5 Y, W0 F& i4 `( \5 t
normal except the testosterone level was high. The
: O/ W/ k, W) X5 d# A2 \$ G1 h+ gfollow-up visit was arranged within a few weeks to
' }. M3 B* j+ j6 |& A6 yobtain testicular and abdominal sonograms; how-
1 J8 p* q% Y5 c- xever, the family did not return for 4 months.
9 c1 _1 j! F# X8 k0 Q8 d4 }6 ZPhysical examination at this time revealed that the3 C  b1 p# |2 z# e, e! ^
child had grown 2.5 cm in 4 months and had gained
0 @( ~* T. o: b) z2 `2 kg of weight. Physical examination remained
8 {1 |: u- `* m5 [unchanged. Surprisingly, the pubic hair almost com-2 ]3 h( j- _- b% j& r
pletely disappeared except for a few vellous hairs at
$ B% ^2 _2 c6 H* g2 ]4 Ithe base of the phallus. Testicular volume was still 2
# A: ?8 F6 [& q9 Y. p$ z9 AmL, and the size of the penis remained unchanged.( Z8 M) F( t. O' M$ P/ }7 x8 m/ m% Q
The mother also said that the boy was no longer hav-4 J$ n* ?, }( r3 M  f2 E1 y
ing frequent erections.
. S: D1 S8 v& g" y2 |$ u' \9 R- JBoth parents were again questioned about use of% y2 H" d& v2 n4 B( p' B4 V; Q; y
any ointment/creams that they may have applied to
. |+ t. J# @7 J) v+ f( bthe child’s skin. This time the father admitted the
' @. y3 _3 z0 l  g+ _Topical Testosterone Exposure / Bhowmick et al 541: x: i5 {( g' J% F
use of testosterone gel twice daily that he was apply-# @' |+ S3 z3 J+ q) y
ing over his own shoulders, chest, and back area for
& g- A! ~" G$ b/ o% e3 x/ Va year. The father also revealed he was embarrassed6 b0 G/ X2 ^& p; f1 {2 h. B1 m$ z) T7 U
to disclose that he was using a testosterone gel pre-
$ Q9 N( h4 v) o& `scribed by his family physician for decreased libido
/ W% \4 v# I4 p7 y) Lsecondary to depression.
/ o! U' c$ d" d+ L3 m5 Q1 z& h" @0 QThe child slept in the same bed with parents.
. t6 N  x9 ~! E7 yThe father would hug the baby and hold him on his
! [# Q$ a% s& P" X: @: ochest for a considerable period of time, causing sig-
8 j: r! W" L0 |nificant bare skin contact between baby and father.
9 I& @, A! Z; MThe father also admitted that after the phone call,7 K& k; {. p! w5 B. a8 O
when he learned the testosterone level in the baby: ~  |1 ?5 ]2 u0 M! |
was high, he then read the product information
2 G' Z$ t; W# y: rpacket and concluded that it was most likely the rea-
. s( t/ b& `/ @9 uson for the child’s virilization. At that time, they
) j# |, V$ |5 P8 v2 Q! ~: C; qdecided to put the baby in a separate bed, and the
: B- c0 o6 \0 V# vfather was not hugging him with bare skin and had' k# ~, N: `& Q, D0 g+ p
been using protective clothing. A repeat testosterone; m6 g8 I! e% y- w5 v  a! L9 l
test was ordered, but the family did not go to the8 {3 f* o) g9 B5 v# G
laboratory to obtain the test.
( p& y2 l2 L( m- fDiscussion; z7 Y; D/ ^4 Q2 y7 P9 N
Precocious puberty in boys is defined as secondary
/ v) R5 z- V  L% b7 Tsexual development before 9 years of age.1,4
7 q/ ?8 m  v3 z$ [Precocious puberty is termed as central (true) when
+ E. |0 ^& @# H8 ^- T% L7 ^" ?. zit is caused by the premature activation of hypo-
8 I7 s) Q6 p( c; M) @thalamic pituitary gonadal axis. CPP is more com-- `4 Y+ q. h: Y/ V1 L) o+ ?
mon in girls than in boys.1,3 Most boys with CPP
% w9 A2 g, E2 h) t2 h3 nmay have a central nervous system lesion that is& ?# z5 R( d7 c9 d
responsible for the early activation of the hypothal-
- I: y* b- J: N* t8 camic pituitary gonadal axis.1-3 Thus, greater empha-
3 r, u' n0 Z+ o! t* |7 Jsis has been given to neuroradiologic imaging in
+ I3 q: S" N1 h5 i0 ]7 H+ H- a' Q; |boys with precocious puberty. In addition to viril-  B% O' Z- u: X6 }" y+ z
ization, the clinical hallmark of CPP is the symmet-5 \, D% `1 o  i, n3 Y) w3 x
rical testicular growth secondary to stimulation by
- f# ~( J- l  c. {3 ~; D. p2 _gonadotropins.1,3
# F- _$ n9 k1 jGonadotropin-independent peripheral preco-
5 [' x3 M, a6 Y, ]cious puberty in boys also results from inappropriate3 I; @# r5 n+ _( \
androgenic stimulation from either endogenous or
9 ?4 d1 u, v# T" o" _# D3 t' Hexogenous sources, nonpituitary gonadotropin stim-
# f% }9 v$ L5 L' _ulation, and rare activating mutations.3 Virilizing- z' i6 `2 ?/ Z# ]% W# @
congenital adrenal hyperplasia producing excessive
+ k# h  ~; X/ f6 m2 ^adrenal androgens is a common cause of precocious
/ D0 _' X- N9 K) l& X, z% Gpuberty in boys.3,4
0 ]% ~5 L1 }6 \; bThe most common form of congenital adrenal0 ?: J& H) e6 P: n
hyperplasia is the 21-hydroxylase enzyme deficiency.& w! X7 Y6 [- d
The 11-β hydroxylase deficiency may also result in0 M% i4 |5 D  X9 c" i# C9 v
excessive adrenal androgen production, and rarely,
9 s/ P1 `2 x& f: s5 nan adrenal tumor may also cause adrenal androgen
6 |& G0 g2 u8 |- Y. J& p- pexcess.1,3& T$ Z# e" b7 O' R; W
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ Y$ P4 [1 K1 P! z9 W$ y( A542 Clinical Pediatrics / Vol. 46, No. 6, July 2007" G# T& I+ Z' |
A unique entity of male-limited gonadotropin-
, W: W3 N0 R* k# l' _& vindependent precocious puberty, which is also known$ x% g4 {5 u! ^
as testotoxicosis, may cause precocious puberty at a/ O+ I. U- t% b7 A4 x, d2 N0 L) R
very young age. The physical findings in these boys5 L2 }1 R: _( U" L/ s
with this disorder are full pubertal development,8 ]$ f5 X* H; N: r! l* T
including bilateral testicular growth, similar to boys
) z$ w3 s+ N+ U+ p+ `- _1 @with CPP. The gonadotropin levels in this disorder
. ^% u' h+ G; w5 }% C( Hare suppressed to prepubertal levels and do not show
  i& @# V, |+ K& t5 ~' apubertal response of gonadotropin after gonadotropin-
+ p! d- k9 x+ g0 p$ m1 x. ?/ Breleasing hormone stimulation. This is a sex-linked% e, K+ o  i+ C. U: k
autosomal dominant disorder that affects only+ `( N/ t5 B. z. Z! r
males; therefore, other male members of the family
+ z) [: l' H, R4 omay have similar precocious puberty.3; [) F- T5 H8 B- E, }
In our patient, physical examination was incon-
% q( \; |: q  csistent with true precocious puberty since his testi-- Z* C9 }  k5 T) D' E
cles were prepubertal in size. However, testotoxicosis
" Q. p$ W( ?) d2 r" \1 wwas in the differential diagnosis because his father
+ j" \- Z2 N: q: H' xstarted puberty somewhat early, and occasionally,4 W7 S. @2 ?. r) h
testicular enlargement is not that evident in the
+ A! M0 I0 O1 W  Ybeginning of this process.1 In the absence of a neg-
" q# ^9 e# W) X  Cative initial history of androgen exposure, our
/ `$ @, a2 a0 y+ T' F& bbiggest concern was virilizing adrenal hyperplasia,
5 ?/ W2 B8 w& C; w0 yeither 21-hydroxylase deficiency or 11-β hydroxylase) g" f. ?, H" M9 w8 |' `; B8 U
deficiency. Those diagnoses were excluded by find-
; I- n, B" B) V6 [6 T5 Z5 ~ing the normal level of adrenal steroids.5 l: ~5 G' ~( k8 [, L4 X
The diagnosis of exogenous androgens was strongly
5 P3 }) y) `% J& z4 k: esuspected in a follow-up visit after 4 months because  t7 o* W0 ^, n" t2 @: l
the physical examination revealed the complete disap-' b$ Z/ x) F  s" d4 e
pearance of pubic hair, normal growth velocity, and, ?$ N& n' N- B) A; L* R
decreased erections. The father admitted using a testos-- F8 j! q$ E/ y: G4 h% p" b5 j7 X
terone gel, which he concealed at first visit. He was
4 \! I0 ]% T& w% ]using it rather frequently, twice a day. The Physicians’
0 L2 z. @% y& N  n+ n2 T# y7 YDesk Reference, or package insert of this product, gel or
" T& C2 ?. z* {cream, cautions about dermal testosterone transfer to
3 u- C; Y4 G$ Z: g) wunprotected females through direct skin exposure.9 X) A0 ~6 ?# V2 z7 r; Z. o/ u$ @; F
Serum testosterone level was found to be 2 times the
" L. k0 z$ k4 M% l: z# Nbaseline value in those females who were exposed to) @3 @# j0 F8 T! q: R
even 15 minutes of direct skin contact with their male9 S, m% E5 Y/ [& l  `3 w
partners.6 However, when a shirt covered the applica-: b4 r! y$ g. m1 y0 V: g7 G
tion site, this testosterone transfer was prevented.
* R4 T' \) Y% I" {Our patient’s testosterone level was 60 ng/mL,
2 t& W) |0 M' ~1 P; }9 Q2 Mwhich was clearly high. Some studies suggest that1 k' b/ R: N. F& c8 E- ^1 X
dermal conversion of testosterone to dihydrotestos-
- m" [  @7 K- b% a& Hterone, which is a more potent metabolite, is more
7 W2 T& v% d6 `, Xactive in young children exposed to testosterone. p7 V" l. {: N7 F' [
exogenously7; however, we did not measure a dihy-- j8 {# X1 [5 T
drotestosterone level in our patient. In addition to
- s7 @- P7 L0 ]9 ?7 ~& qvirilization, exposure to exogenous testosterone in
  A3 s4 G3 W* T6 m/ P9 o" qchildren results in an increase in growth velocity and4 _* n3 ~; J6 D6 p( T) ^' k
advanced bone age, as seen in our patient.* ^; q# y. y7 {$ F1 L
The long-term effect of androgen exposure during1 B. v8 R; |0 v/ s4 e$ r# E
early childhood on pubertal development and final
; r: L. \/ \$ ?# Iadult height are not fully known and always remain* p* d3 ^) a+ F& q' m
a concern. Children treated with short-term testos-
  i4 J4 T0 p2 J: a+ w8 Xterone injection or topical androgen may exhibit some0 X2 ~) E- i# E( v/ z' p( Q
acceleration of the skeletal maturation; however, after
. N1 K( M- }5 C; _( E1 H" Scessation of treatment, the rate of bone maturation6 u9 c7 b" h! d0 y1 ^7 C" f. z! [
decelerates and gradually returns to normal.8,9
7 ~1 v9 F" ?9 B; qThere are conflicting reports and controversy9 A! e9 }! e# N* r) }, I
over the effect of early androgen exposure on adult# K% q& [  E5 z" P' Z- f1 Z
penile length.10,11 Some reports suggest subnormal  Y- V, N: S1 D, P' i6 ?* `
adult penile length, apparently because of downreg-* M, a9 A. z( Q; G8 N
ulation of androgen receptor number.10,12 However,
+ @$ A6 S- n! sSutherland et al13 did not find a correlation between
) ~" v5 r; o2 Achildhood testosterone exposure and reduced adult8 o! o6 N& T7 V: L
penile length in clinical studies.1 q" R! H5 P/ R
Nonetheless, we do not believe our patient is* G' {; ], R, b4 f
going to experience any of the untoward effects from
5 k" `2 A+ K. `6 S6 h  E( g; u$ m6 o" ftestosterone exposure as mentioned earlier because
8 t) V5 o9 H' C& p! ethe exposure was not for a prolonged period of time.
4 m$ U- ~- s+ l  D, G2 K5 N5 [Although the bone age was advanced at the time of
) I! b8 P+ [" h$ k3 r, Y& H- _diagnosis, the child had a normal growth velocity at6 n8 Y& P/ y' O; i$ t; P
the follow-up visit. It is hoped that his final adult
; L+ F# q' D  c0 _1 }. E4 Z+ Gheight will not be affected.
( s5 ^+ n, u2 E5 oAlthough rarely reported, the widespread avail-/ U; g$ L. \! ?2 y( O5 v3 S
ability of androgen products in our society may% y( ?$ o" T0 D4 V5 n
indeed cause more virilization in male or female
/ t8 a# J+ _6 v* i3 _children than one would realize. Exposure to andro-
% a, T. _# C/ q9 T2 W$ T" Y9 u9 `gen products must be considered and specific ques-" m8 c; [: _/ ?" `# [6 m
tioning about the use of a testosterone product or6 q: G: k  ]: K+ A! V) r' N# H
gel should be asked of the family members during. N6 v: |0 z! |/ N9 L
the evaluation of any children who present with vir-! Z: F* L+ y7 y+ t
ilization or peripheral precocious puberty. The diag-
' `) o6 e) {: P; Ynosis can be established by just a few tests and by+ S+ c# g: P. f& J8 k
appropriate history. The inability to obtain such a8 O9 C6 w, U0 n2 o( F
history, or failure to ask the specific questions, may
& R% g+ E- W$ J/ Uresult in extensive, unnecessary, and expensive6 H* l) x. Q7 u" R7 P$ i7 v# [
investigation. The primary care physician should be( ~/ V/ V6 w/ D, ]: ?" B
aware of this fact, because most of these children
6 {9 y0 @( Q. M7 W) G( n, Wmay initially present in their practice. The Physicians’
7 B# ]9 K- r( ], ^Desk Reference and package insert should also put a
# m5 n# e8 f/ x! Z0 p: @1 Mwarning about the virilizing effect on a male or
6 U/ V0 I5 k; D  B1 a, a- Jfemale child who might come in contact with some-5 a# i3 o" T6 }& f+ i0 F
one using any of these products.
6 x5 s* W- l8 W; K0 ^+ `References
- V- ]) J8 r( h" F0 L% t1. Styne DM. The testes: disorder of sexual differentiation& Z5 L1 p* z  d9 [8 }
and puberty in the male. In: Sperling MA, ed. Pediatric, g0 w0 \4 |( f. E" e6 |& i
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;. |9 Z; K& M3 e8 Z* _0 C! f' ^
2002: 565-628.
, j' X6 E' s; {5 W! L; K2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious/ V) t5 _% x, _* ?
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
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

9 Z: D! a0 f9 q$ K3 M% P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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