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Sexual Precocity in a 16-Month-Old
/ Q" x8 T, [6 J" Z+ b2 Q4 z  O( h  _Boy Induced by Indirect Topical, f2 S6 ^2 V* H
Exposure to Testosterone3 g. s/ `; |1 Y/ e, d
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. ?4 I5 H% _* h$ e  I, p
and Kenneth R. Rettig, MD1
) a( V8 Z- A' O" f4 ?5 qClinical Pediatrics( J( |, [% h; R4 v% |
Volume 46 Number 6
  d! D, n) n8 S+ y. g2 t0 tJuly 2007 540-543
' R. ~; M8 A" h+ X© 2007 Sage Publications
7 A) y8 b5 [" e5 e) h& A0 Q10.1177/0009922806296651
2 b( A. Z2 K# xhttp://clp.sagepub.com! t, Y2 _8 [6 C
hosted at
# m9 }, F$ |# R3 Y  Bhttp://online.sagepub.com7 N1 I8 W8 Z4 z0 {! V
Precocious puberty in boys, central or peripheral,
& l. c, s* d0 {; m$ z5 dis a significant concern for physicians. Central
$ g- o. p4 h: T2 g9 I5 v: [precocious puberty (CPP), which is mediated! j2 t7 {. l' a
through the hypothalamic pituitary gonadal axis, has5 ]; a! `. M8 q. G( t9 C% m* X
a higher incidence of organic central nervous system
9 i# p# G2 @# C! f: S  @1 Qlesions in boys.1,2 Virilization in boys, as manifested
4 l$ `5 c: Q0 e& ~0 b% oby enlargement of the penis, development of pubic
, x: y% ~3 g4 o% P) D3 b7 Ihair, and facial acne without enlargement of testi-2 d$ z$ P; `, |2 w+ T" y
cles, suggests peripheral or pseudopuberty.1-3 We
: ]0 {6 t. U. H% ~! yreport a 16-month-old boy who presented with the& W) {4 ^; {9 @6 n5 f
enlargement of the phallus and pubic hair develop-
& s1 T' w: D  }- G- m& }ment without testicular enlargement, which was due7 t4 T- g5 o% l
to the unintentional exposure to androgen gel used by
- ]: E8 O" [- u0 n1 Y1 o# t; Pthe father. The family initially concealed this infor-$ H% }! o3 o, l: |% N
mation, resulting in an extensive work-up for this
' x( k& S1 b& r: {7 M8 _+ S8 Tchild. Given the widespread and easy availability of  z: w2 E( v5 j/ }/ W3 x
testosterone gel and cream, we believe this is proba-
  A9 R4 I* Z# x/ dbly more common than the rare case report in the9 V9 [5 g8 L1 F1 P4 I( c" B
literature.45 D. j/ E6 A0 r6 W
Patient Report
+ D: m2 f5 s6 P( w1 z  NA 16-month-old white child was referred to the
# S* f" t1 N, _& `5 k! s9 Jendocrine clinic by his pediatrician with the concern- ]4 e0 x: n4 v8 f5 R2 F
of early sexual development. His mother noticed
2 ^4 \# l- n( l4 g6 Nlight colored pubic hair development when he was
& a3 D5 S: R, g% u8 ?2 aFrom the 1Division of Pediatric Endocrinology, 2University of* v4 i3 J" }- j( \% v" Q# c
South Alabama Medical Center, Mobile, Alabama.% z+ |" `: c" \/ v
Address correspondence to: Samar K. Bhowmick, MD, FACE,  ~: c4 A  V1 S* f" b# Y' v7 T
Professor of Pediatrics, University of South Alabama, College of
/ D9 ]  b4 r4 \3 x3 M" K6 Q2 @Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
' [/ W6 f. O+ l1 R7 Q8 ue-mail: [email protected].  X6 p6 y8 O: J
about 6 to 7 months old, which progressively became$ _7 Q$ q  n- Q" J; j/ B  O% _5 ^
darker. She was also concerned about the enlarge-; S7 F6 g6 _/ q4 K
ment of his penis and frequent erections. The child1 K, r( R8 Z4 E0 K; s1 }( ?5 b: `( o& ]
was the product of a full-term normal delivery, with
; _+ k& a/ n; g6 ?a birth weight of 7 lb 14 oz, and birth length of1 t" C6 ^& @$ X3 M! d: E1 D
20 inches. He was breast-fed throughout the first year
  F6 J" p' R! B7 wof life and was still receiving breast milk along with
$ I  D9 ^+ l$ r) A1 n# dsolid food. He had no hospitalizations or surgery,& Q, U0 D; r& {2 h
and his psychosocial and psychomotor development
5 T" G$ w1 a5 h* d& M; \was age appropriate.
% V+ a) \/ X3 p5 T% y% F% eThe family history was remarkable for the father,' {& R/ Y6 t8 v, M$ A
who was diagnosed with hypothyroidism at age 16,% A" j7 j# j7 d; x9 S  l3 q
which was treated with thyroxine. The father’s+ B7 ]6 Y* O( f2 m% \# R- Y& t: I
height was 6 feet, and he went through a somewhat" {$ q# ?0 {- f: i, k8 u
early puberty and had stopped growing by age 14.; o  ], D! l& u' N
The father denied taking any other medication. The
- [" X: O4 y$ s9 V( p( h$ Uchild’s mother was in good health. Her menarche
* d' s, U- u+ h3 nwas at 11 years of age, and her height was at 5 feet" M8 j% E; h8 v) G7 y
5 inches. There was no other family history of pre-6 N3 J7 Z1 p0 x- E4 z' X' A
cocious sexual development in the first-degree rela-' @7 e5 O  r% W5 u4 b+ V. Y* K- j
tives. There were no siblings.. ], T. O6 t: L
Physical Examination: |7 @; W/ y/ R$ K+ f
The physical examination revealed a very active,4 `. t4 {1 i, Z  l
playful, and healthy boy. The vital signs documented
/ E: }3 D, Z  ?. }& [% _a blood pressure of 85/50 mm Hg, his length was
) C' @1 o# X) d90 cm (>97th percentile), and his weight was 14.4 kg
5 q4 F! Y2 r. f9 @( q(also >97th percentile). The observed yearly growth
  S6 G% S& _+ ~" |velocity was 30 cm (12 inches). The examination of
0 o0 r/ n# J* F; A- O  q4 }/ S' Pthe neck revealed no thyroid enlargement.
' B! V& ]; U$ a# ]' A9 S. x  VThe genitourinary examination was remarkable for8 u; L) k9 h5 m+ f
enlargement of the penis, with a stretched length of' Z* q1 m! x. `- L4 V1 i
8 cm and a width of 2 cm. The glans penis was very well( C& b  a7 R! u3 q7 X7 [
developed. The pubic hair was Tanner II, mostly around
! o* K0 e, j) {; T8 o540
5 N2 }& d+ X7 n( Q8 X) Wat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; p( L' F" _3 rthe base of the phallus and was dark and curled. The
4 f1 z! q1 Q: Q5 {testicular volume was prepubertal at 2 mL each.1 x6 T7 K# a3 @6 T( R6 f' L& @
The skin was moist and smooth and somewhat2 |" Y; b5 g+ @3 t8 t
oily. No axillary hair was noted. There were no; A) o1 V7 a. l8 p' [; }
abnormal skin pigmentations or café-au-lait spots.
0 g& V  C2 V' uNeurologic evaluation showed deep tendon reflex 2+
2 v( ^; H2 p5 b1 Hbilateral and symmetrical. There was no suggestion; b3 k7 C+ g0 X* }' S3 z) k" [
of papilledema.
; i" _. Z2 {& q' y9 N2 ^5 d& kLaboratory Evaluation
* i. s6 n+ R7 h, `The bone age was consistent with 28 months by
( B- [* _8 v$ t) L; jusing the standard of Greulich and Pyle at a chrono-
) s( d! @5 M( _5 m6 ^logic age of 16 months (advanced).5 Chromosomal
9 g9 E1 n$ r" E' skaryotype was 46XY. The thyroid function test
) r! o& u; y" p' {; H" x) Vshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
3 @( F; ?7 q. O; {lating hormone level was 1.3 µIU/mL (both normal).& K0 J& I! A, j/ b: H( i
The concentrations of serum electrolytes, blood" e1 ?$ X9 M& [7 M  l: X( Y
urea nitrogen, creatinine, and calcium all were8 D  k7 Y( N, C3 J, d1 y; f! @1 I  \
within normal range for his age. The concentration( x$ z  L2 t1 `
of serum 17-hydroxyprogesterone was 16 ng/dL
9 [4 Q$ c! J7 {7 d# q; ](normal, 3 to 90 ng/dL), androstenedione was 202 p& k2 ?5 r! v3 |
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-: ?' Z. e9 _" j  M/ d0 Q1 S6 k
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
1 V& q* ], p/ `8 X) [4 G/ X: b& z( }8 hdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
- l& ~0 p1 a4 c: T* x49ng/dL), 11-desoxycortisol (specific compound S)
( j' w/ }9 w1 e9 G8 nwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
* V8 Q! ?+ p! y$ d) z5 @/ p6 R; y0 ptisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total5 U" ?7 f* I7 M' C# H0 \8 R5 m
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),8 n* K6 q" S& ~1 ?9 f
and β-human chorionic gonadotropin was less than
3 G+ O0 X* t6 W7 `" N/ W5 mIU/mL (normal <5 mIU/mL). Serum follicular
# v# `7 {, r: ?0 Z8 _6 `stimulating hormone and leuteinizing hormone' s2 ?3 s$ u" k! d9 [% U+ @5 y
concentrations were less than 0.05 mIU/mL0 |7 g% z, c& n' P: Y4 @( X
(prepubertal)./ E  ?; @) F" ?  B) r" c. b
The parents were notified about the laboratory
% b( [5 X7 t0 r3 @/ n7 Uresults and were informed that all of the tests were5 h" L2 I6 K8 e2 n; D& f3 w& B( q+ A) r
normal except the testosterone level was high. The' i1 @5 ]0 c; A
follow-up visit was arranged within a few weeks to
: ?- T  _; q5 ]$ b; `obtain testicular and abdominal sonograms; how-) c/ I* B: N  _
ever, the family did not return for 4 months.
6 l0 s; I  r' u9 X+ LPhysical examination at this time revealed that the6 K8 ?& `2 K( J3 d% ?
child had grown 2.5 cm in 4 months and had gained
% g& V, ]9 D5 V/ `2 kg of weight. Physical examination remained
# a' _5 p) s9 {% v3 [unchanged. Surprisingly, the pubic hair almost com-! X9 z$ H6 p* m* z2 O2 x- R
pletely disappeared except for a few vellous hairs at/ ^( M# C- {5 `4 t0 D1 v5 b6 o
the base of the phallus. Testicular volume was still 2( c3 u& B  Y9 a& N# x
mL, and the size of the penis remained unchanged./ m/ j3 B/ ^- Q* X4 S
The mother also said that the boy was no longer hav-% V7 V( f6 I8 Z# H8 L; H5 y
ing frequent erections.
3 q/ F; Y; Z# W8 z1 fBoth parents were again questioned about use of
0 {! x& H. X$ p! d1 F  Many ointment/creams that they may have applied to/ }$ p! ]$ ^1 C  {9 U7 ^- j
the child’s skin. This time the father admitted the
3 x& E- z) X$ s( WTopical Testosterone Exposure / Bhowmick et al 541; B! M$ b, `9 R# K# ?
use of testosterone gel twice daily that he was apply-
2 N6 t8 u) w( V# X. L0 J" ging over his own shoulders, chest, and back area for
4 \& n4 y2 D! l. Q1 }. Ha year. The father also revealed he was embarrassed+ B4 A7 Q7 u. K/ V  E/ t8 i
to disclose that he was using a testosterone gel pre-
! W1 e* y1 Z3 Q3 Iscribed by his family physician for decreased libido
" I) x4 W8 j' @secondary to depression.2 g  [% r$ b$ z1 c: W
The child slept in the same bed with parents.
8 I" ]; a* J' E; u  E9 uThe father would hug the baby and hold him on his
7 p6 S, ^( m! J+ cchest for a considerable period of time, causing sig-$ f4 @$ q  F& v9 @. P/ u
nificant bare skin contact between baby and father.
# `7 w+ _: j. a6 I0 h; X  lThe father also admitted that after the phone call,- i0 k. ?: y' y5 I
when he learned the testosterone level in the baby
+ z0 F) e9 X7 k  F- \6 o+ B5 @was high, he then read the product information
5 L9 r0 S; J7 o+ [3 k' ~" S% jpacket and concluded that it was most likely the rea-% l! Y2 A1 T( l: k' x5 g) r: }
son for the child’s virilization. At that time, they/ q' s0 j" |% ^: o8 u
decided to put the baby in a separate bed, and the& C  B$ h, G, ?3 w4 `/ r- x
father was not hugging him with bare skin and had
- E' S% i8 K1 H% kbeen using protective clothing. A repeat testosterone
8 g* ]6 [; y2 J+ Atest was ordered, but the family did not go to the. v  D, D+ W0 A" O
laboratory to obtain the test.
' v8 L% R) ]/ k. `+ T* kDiscussion
0 t* w- d8 m3 c' I9 `2 uPrecocious puberty in boys is defined as secondary
) U" Y/ t- O5 Msexual development before 9 years of age.1,45 u$ ]- F% Q; N+ J0 s
Precocious puberty is termed as central (true) when, H$ B4 i# Z+ `9 R$ J" Z* t4 J8 h
it is caused by the premature activation of hypo-
8 S" L4 I. N7 d! P( }6 ythalamic pituitary gonadal axis. CPP is more com-
  `& h0 L( h- U$ }8 y; mmon in girls than in boys.1,3 Most boys with CPP) P, S1 \0 |2 z
may have a central nervous system lesion that is
& }3 [! Z1 p/ s( H( Mresponsible for the early activation of the hypothal-( o: z* |7 T. g( K+ r- R: i2 Y7 y- U
amic pituitary gonadal axis.1-3 Thus, greater empha-
# u+ _0 f9 l6 b1 z. B! f8 y7 b( Msis has been given to neuroradiologic imaging in9 l! A: y7 D% P# c& Y+ K9 h
boys with precocious puberty. In addition to viril-6 L3 Y" H6 T- X' `9 Z
ization, the clinical hallmark of CPP is the symmet-
1 |' [# a3 y! nrical testicular growth secondary to stimulation by
4 c/ C# _$ x. ngonadotropins.1,3) _3 F9 ~  P  M5 w
Gonadotropin-independent peripheral preco-
! C+ c7 X3 U: z1 w4 t" icious puberty in boys also results from inappropriate9 a( \( |  t& J& f
androgenic stimulation from either endogenous or2 k. W9 u7 z" _+ B4 Y3 t
exogenous sources, nonpituitary gonadotropin stim-0 Q* b5 i% h' Q+ z# k
ulation, and rare activating mutations.3 Virilizing, Z$ G7 P* H; Q3 U  T
congenital adrenal hyperplasia producing excessive
& D# J9 O$ Y% e7 f. R$ _adrenal androgens is a common cause of precocious- o& `/ I  i5 r- C' z7 d8 P
puberty in boys.3,4, F! w' w& M% P0 P# }
The most common form of congenital adrenal, V. a5 A) i- b/ C/ Z
hyperplasia is the 21-hydroxylase enzyme deficiency.% j' \& h$ C) B5 o8 ?1 ]) v
The 11-β hydroxylase deficiency may also result in
) G$ x2 J5 |1 X9 G8 x& Zexcessive adrenal androgen production, and rarely,
" X( y/ Y& U8 O7 W8 wan adrenal tumor may also cause adrenal androgen- F" S3 O# [1 O, f% l8 D
excess.1,3$ T! M5 b* A: Z9 k
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) `  Y2 S, O" r6 w5 X4 i542 Clinical Pediatrics / Vol. 46, No. 6, July 2007! Z( h' |& Y# m5 a
A unique entity of male-limited gonadotropin-" O* V: z  E+ `, N: z/ z; z3 d5 P6 u
independent precocious puberty, which is also known# A- U& t  D. y; d9 a$ l% e+ B
as testotoxicosis, may cause precocious puberty at a
9 w9 M, \# P8 O! D" o* a0 Uvery young age. The physical findings in these boys
8 m8 H2 q2 ^& c2 L2 xwith this disorder are full pubertal development,8 Z' l0 f& F  k; `2 r% D
including bilateral testicular growth, similar to boys0 y$ L! m+ [8 f) e8 A2 f
with CPP. The gonadotropin levels in this disorder$ ~" G- W+ a! ~& G
are suppressed to prepubertal levels and do not show
4 \, n/ v5 T* q8 lpubertal response of gonadotropin after gonadotropin-
1 C& ^: T( u0 dreleasing hormone stimulation. This is a sex-linked
& `: p1 Z0 x% u, Mautosomal dominant disorder that affects only
) L; h- E! h  xmales; therefore, other male members of the family
' X& _2 G: q; n. ?5 [) jmay have similar precocious puberty.3
* q1 y8 ^: I+ [4 XIn our patient, physical examination was incon-7 a* b1 w" ~' a+ {! g3 ^
sistent with true precocious puberty since his testi-4 ~, w( f! e1 y2 e3 J. W
cles were prepubertal in size. However, testotoxicosis, C% k# Q( j$ Z0 _& D
was in the differential diagnosis because his father7 j4 a$ m1 z+ W% @4 @) f
started puberty somewhat early, and occasionally,
, {4 g$ `6 `* Qtesticular enlargement is not that evident in the
6 C: \+ Y7 r2 f" Y& l% K, ybeginning of this process.1 In the absence of a neg-) W$ J; r6 D- e8 ?" O
ative initial history of androgen exposure, our* K5 C/ [; S5 u  z
biggest concern was virilizing adrenal hyperplasia,0 U  J" t, k6 e  M
either 21-hydroxylase deficiency or 11-β hydroxylase2 P: ~& [- U4 m
deficiency. Those diagnoses were excluded by find-: ^6 g0 I4 A; o: g3 z" D
ing the normal level of adrenal steroids.7 j' c& I' I+ S  J# ~# `: u( R
The diagnosis of exogenous androgens was strongly, T7 m8 X4 B1 D6 S, B
suspected in a follow-up visit after 4 months because3 M9 ~7 ?! F8 n5 [& l
the physical examination revealed the complete disap-
( U9 F1 ?# ^" @* q; n. }pearance of pubic hair, normal growth velocity, and
, Z5 p) n! q. C( ldecreased erections. The father admitted using a testos-
3 d) k3 x6 L; c6 s( w' V) Y$ u0 pterone gel, which he concealed at first visit. He was! x' t# r" E% p5 _3 [7 U
using it rather frequently, twice a day. The Physicians’# s) ?( e1 |# p
Desk Reference, or package insert of this product, gel or
0 _+ C7 A9 @- A7 ?; scream, cautions about dermal testosterone transfer to% }) _$ }" Y0 H% Z8 O
unprotected females through direct skin exposure.
! r8 F: x5 q4 y0 W  ]9 [Serum testosterone level was found to be 2 times the
9 j3 X8 s6 e7 t8 G5 O% gbaseline value in those females who were exposed to  X4 g3 B$ M0 b( t* ]& Q
even 15 minutes of direct skin contact with their male
7 x/ R. h, d5 o2 x7 epartners.6 However, when a shirt covered the applica-0 a7 u: r( }, F9 W! k9 m
tion site, this testosterone transfer was prevented.; ?' k/ M% E2 F6 j* p
Our patient’s testosterone level was 60 ng/mL,( u1 d, x9 o3 e1 a' X+ L! k1 ~
which was clearly high. Some studies suggest that
" d: s- @; D. L2 tdermal conversion of testosterone to dihydrotestos-
. Q* Q6 V" F' t2 V( V9 cterone, which is a more potent metabolite, is more
4 P; h/ E- K  T5 J; V" hactive in young children exposed to testosterone
0 ?& e- y+ K2 I* Sexogenously7; however, we did not measure a dihy-
8 W- |- X) ?% b2 c" G0 sdrotestosterone level in our patient. In addition to' e5 ^  j% Z8 l: G4 d$ p
virilization, exposure to exogenous testosterone in
8 R2 s$ `% A  nchildren results in an increase in growth velocity and+ @& T* l, Q+ e& N. e# K9 k
advanced bone age, as seen in our patient.% `4 P9 r8 o' d2 D- p+ v0 u0 j
The long-term effect of androgen exposure during3 S$ S# Y4 ^5 }$ V8 K6 O
early childhood on pubertal development and final: H7 J; {9 N) a8 b- T: N; v$ E
adult height are not fully known and always remain
* h/ g, a: c& _6 C$ fa concern. Children treated with short-term testos-
. e$ Z( U8 W' w2 L; v' C* q; P8 }terone injection or topical androgen may exhibit some0 n5 r. v; M: H4 |: o& x$ i0 \1 c
acceleration of the skeletal maturation; however, after
/ S# F/ g8 v. E" }3 L& @cessation of treatment, the rate of bone maturation
( u7 G! g  v: c& ~, ydecelerates and gradually returns to normal.8,91 w4 A- u! I1 D0 x
There are conflicting reports and controversy5 y" W9 I1 U4 P6 t/ G# n4 q  K
over the effect of early androgen exposure on adult$ l, U( b# d8 v& B
penile length.10,11 Some reports suggest subnormal- v3 I) f$ u3 l2 F
adult penile length, apparently because of downreg-& F2 ]7 k/ R4 S" `: {
ulation of androgen receptor number.10,12 However,
! v8 h" z; d) @Sutherland et al13 did not find a correlation between, d0 R+ F7 Q5 s* `: S
childhood testosterone exposure and reduced adult
3 c: Q, Z3 Z' ?# E( A& G3 d1 wpenile length in clinical studies.
) K! c- t, F6 ~" ~8 J' gNonetheless, we do not believe our patient is( s2 y  W- T/ F
going to experience any of the untoward effects from
2 l0 ^. t7 t( x2 t" y2 f% B) `! Utestosterone exposure as mentioned earlier because- `4 a9 v6 _' ^3 \
the exposure was not for a prolonged period of time.
' \8 y. R# E8 c' ?Although the bone age was advanced at the time of
' B; f4 l/ r0 Q: K+ A: r1 mdiagnosis, the child had a normal growth velocity at
3 n+ j2 s2 I8 K* \' Y( F9 ethe follow-up visit. It is hoped that his final adult; g! s* b$ L' c( i2 E
height will not be affected.
, s8 ~+ ~* J& ^5 }$ N2 e7 v# qAlthough rarely reported, the widespread avail-
0 J5 Q2 y( B6 [. o( v* [2 dability of androgen products in our society may
, |- s* s: v, V* |& C4 m- [  z3 ?; T' Eindeed cause more virilization in male or female' L3 B) z7 y! {2 J+ A! _  ~' ]
children than one would realize. Exposure to andro-7 q# V3 L$ l! k2 Z8 p" a
gen products must be considered and specific ques-
. A5 M. L: `" {- e3 J5 Ftioning about the use of a testosterone product or! Q# e; B, E6 B
gel should be asked of the family members during
6 q+ T8 D  v0 M, ethe evaluation of any children who present with vir-
% _. \: Q+ W1 i; y2 h& xilization or peripheral precocious puberty. The diag-2 n+ U- U" \3 t3 k5 _
nosis can be established by just a few tests and by
+ O" f$ p( x) h  {9 Tappropriate history. The inability to obtain such a
: U6 w1 r! N! O2 ^) b9 fhistory, or failure to ask the specific questions, may
# U6 k* x5 P2 g9 E0 L% s( u( Cresult in extensive, unnecessary, and expensive7 s8 d; f2 u# n* s$ F; \* O6 ^
investigation. The primary care physician should be
* \1 \( U+ O% S7 paware of this fact, because most of these children
/ y. Y5 n9 D( N, z0 L3 fmay initially present in their practice. The Physicians’
' q$ |1 ~9 h' |4 e7 uDesk Reference and package insert should also put a) H+ }! ~9 D- D8 G
warning about the virilizing effect on a male or
( \! @% v7 s0 u! c7 a! `- Q4 {female child who might come in contact with some-6 [1 y& M6 f; y5 {; j* x, o
one using any of these products.& h* m" Q2 D# o7 q0 o- p1 B& C
References8 p" ^8 P8 }- [0 u/ k
1. Styne DM. The testes: disorder of sexual differentiation# T1 K. T$ c' _1 d6 C
and puberty in the male. In: Sperling MA, ed. Pediatric
( b2 w- A, u/ i. a3 V* N8 NEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;  r+ E7 N* a6 C3 o' _
2002: 565-628.5 _5 K4 ]5 t& ]2 S) N
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious+ _/ v; Z: j3 ~" `  ?& B4 `( _1 i
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
4 w3 l$ U; c& q, u2 VBoy Induced by Indirect Topical
& P% u: H. w+ O( o% m" RExposure to Testosterone
9 m! h7 {8 z# L" o) iSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2- l/ M( i6 c+ `4 ]
and Kenneth R. Rettig, MD1
0 o3 A0 y1 n  V  a" f; ?Clinical Pediatrics6 x( I7 H) @- w. W1 D8 {
Volume 46 Number 61 u* R+ j/ y: t1 e
July 2007 540-5431 ~9 f  S1 M; H: G$ c
© 2007 Sage Publications- ~' \  ~" W# P$ G% v/ R' J) v
10.1177/0009922806296651: f, L3 a" M" F* e9 E0 w# G
http://clp.sagepub.com5 t% i/ h' S/ w2 Z* V3 a: v- q
hosted at
3 F& c& W, Y; h; N: _: fhttp://online.sagepub.com$ Y0 y/ I% b" [. ?+ `8 l" i
Precocious puberty in boys, central or peripheral,7 r+ b2 _: [! u0 D& F. R1 x5 _
is a significant concern for physicians. Central; c1 B1 Q+ V- n0 K: }# T! `
precocious puberty (CPP), which is mediated: F* V8 L0 O) |" ]+ w
through the hypothalamic pituitary gonadal axis, has4 P, h3 U; u$ j1 H6 `) H
a higher incidence of organic central nervous system/ v" @) q6 q9 d( ^: w* p
lesions in boys.1,2 Virilization in boys, as manifested0 j8 |6 s; v5 e9 i- j- ^& `6 E
by enlargement of the penis, development of pubic
) N/ o' |2 G8 F* L7 k$ Dhair, and facial acne without enlargement of testi-
5 M% m" [# p  D) T3 |. vcles, suggests peripheral or pseudopuberty.1-3 We
2 o, }; p3 o7 x! k2 d  Y/ V* hreport a 16-month-old boy who presented with the
, d6 _- J4 k1 r$ M/ E8 D. v' denlargement of the phallus and pubic hair develop-) O+ J. I; R  o! m
ment without testicular enlargement, which was due* s/ q: ?. Q9 f& u0 f
to the unintentional exposure to androgen gel used by
" M8 B/ p* e' rthe father. The family initially concealed this infor-8 L" S0 o% p' n2 g$ ~* d& w
mation, resulting in an extensive work-up for this
1 i5 e" V4 k: Pchild. Given the widespread and easy availability of5 {& I- C; ~1 H5 c/ a
testosterone gel and cream, we believe this is proba-7 d0 Q' l) d8 u. r# Z
bly more common than the rare case report in the
. Q; I  ?" T3 Z/ D; {+ j+ I% nliterature.43 W* j* M- D0 ^1 Z" b7 K! p2 J7 w
Patient Report2 V) O- v6 m" w" s: p
A 16-month-old white child was referred to the
4 R% q) e  e( nendocrine clinic by his pediatrician with the concern
, i- g$ B) j( A& }* oof early sexual development. His mother noticed: \' r: ~& i  B3 H" @. l' v, T
light colored pubic hair development when he was
) }* x5 w8 p4 C7 K% M  @& YFrom the 1Division of Pediatric Endocrinology, 2University of
  l5 K2 o9 z6 E0 e# p6 y& lSouth Alabama Medical Center, Mobile, Alabama.. w0 J- d& D2 O! _
Address correspondence to: Samar K. Bhowmick, MD, FACE,. ^$ ]  \! F5 N, [5 s. b
Professor of Pediatrics, University of South Alabama, College of
- s4 j% [+ K/ I' ]5 [Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 @& u% V/ e9 X1 w1 g, \; v1 |8 e
e-mail: [email protected].
1 @- `0 t. X) U. o. u4 Dabout 6 to 7 months old, which progressively became2 @. e2 ^% ~; m7 v
darker. She was also concerned about the enlarge-
) N# w4 Q- B: I3 o- F$ Z( iment of his penis and frequent erections. The child
$ O, J' R/ ~' d$ T1 \) z/ Y8 D$ Bwas the product of a full-term normal delivery, with
7 `  `  L. R9 H! B! sa birth weight of 7 lb 14 oz, and birth length of
: E* `  O+ z) A: W20 inches. He was breast-fed throughout the first year
0 D  ^$ W- E6 l% Z- Zof life and was still receiving breast milk along with
  b$ Y6 M, F( a7 @# T& \solid food. He had no hospitalizations or surgery,5 ~8 B7 v8 i" q3 M% A, e, \7 b1 w3 o
and his psychosocial and psychomotor development; g; ?7 [6 z& H9 A( c- k2 \
was age appropriate.
2 X$ Y- f; A+ {The family history was remarkable for the father,
9 e) T/ `7 \; T9 Uwho was diagnosed with hypothyroidism at age 16,7 M' T; ~: ]1 N8 g$ M. K( }/ [
which was treated with thyroxine. The father’s
  i! r( R) |- c! P" `4 ]height was 6 feet, and he went through a somewhat
' b# t$ p7 [: s" bearly puberty and had stopped growing by age 14., C" C! q3 v3 N$ O2 c
The father denied taking any other medication. The
/ k" q# I& l4 R# m; B1 |child’s mother was in good health. Her menarche
% Q, i' L6 q" j) uwas at 11 years of age, and her height was at 5 feet
/ o+ }. \+ Z5 S" T4 \2 _8 K5 inches. There was no other family history of pre-
  j; e# P/ F; ccocious sexual development in the first-degree rela-
# U+ _' _& \2 i) ?tives. There were no siblings.
2 c, j0 R, v' k( r4 ?9 q( CPhysical Examination5 j9 K4 G3 M% B6 N5 R4 a
The physical examination revealed a very active,9 l" K+ T, ?* V) |* M. |
playful, and healthy boy. The vital signs documented5 h: X5 X4 t% o4 F5 ]1 x
a blood pressure of 85/50 mm Hg, his length was
1 n0 x0 l3 T( }3 P90 cm (>97th percentile), and his weight was 14.4 kg# o' n8 C. E/ I+ ^, l- ]3 m* h! Y6 V
(also >97th percentile). The observed yearly growth/ K" E0 w2 F9 l' V$ d
velocity was 30 cm (12 inches). The examination of: C5 p6 s- l' X& b/ i: T
the neck revealed no thyroid enlargement.
+ t( O5 [  Y: U7 A" r4 C8 T% J* {The genitourinary examination was remarkable for6 y6 q3 }4 m0 i0 s* G' S9 S
enlargement of the penis, with a stretched length of
0 o0 o* ~; O8 j; g! \/ N. T8 cm and a width of 2 cm. The glans penis was very well0 Y' R+ E' P# t1 k4 @' X/ L9 r8 L
developed. The pubic hair was Tanner II, mostly around4 T8 M$ w* l  X, \
5405 m5 q3 p- W1 d  H, O5 S
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: U- Y9 S; l( R; {the base of the phallus and was dark and curled. The' s8 n3 s2 {, p7 i
testicular volume was prepubertal at 2 mL each.
3 }& r6 U- {( X+ |The skin was moist and smooth and somewhat
0 f7 z$ n) b- u! S' O3 N1 poily. No axillary hair was noted. There were no- c+ r# |2 w# T+ `2 k, C/ o
abnormal skin pigmentations or café-au-lait spots.
3 Y6 u* `) ]7 }( u7 }9 [4 E2 J$ P# r' w) INeurologic evaluation showed deep tendon reflex 2+" q' U$ f8 H/ b9 z1 G7 N8 r- d
bilateral and symmetrical. There was no suggestion% {5 E3 S" k& C: J4 r' ?# }1 S
of papilledema.
% s$ ?5 ~: L5 jLaboratory Evaluation
4 ^  T% h+ c' V' l* N3 dThe bone age was consistent with 28 months by
* r: E* o) j1 [1 b/ Musing the standard of Greulich and Pyle at a chrono-% q1 J0 |, h. m4 Y- H: D3 b9 X
logic age of 16 months (advanced).5 Chromosomal
" a9 i+ u5 }: I) A: R/ u/ Bkaryotype was 46XY. The thyroid function test; Y1 K2 R8 m0 _+ r3 \  e
showed a free T4 of 1.69 ng/dL, and thyroid stimu-7 I$ E8 g" R4 t0 F
lating hormone level was 1.3 µIU/mL (both normal).
+ A' D8 b1 J2 a* j+ V: uThe concentrations of serum electrolytes, blood0 F* t. d! z2 N3 ]9 w% Z' r/ S
urea nitrogen, creatinine, and calcium all were7 [9 _8 V0 y3 d
within normal range for his age. The concentration9 y' T% p6 j. B- p6 M) m+ z' a
of serum 17-hydroxyprogesterone was 16 ng/dL
8 E/ a7 c- E) `% A1 I9 e2 v(normal, 3 to 90 ng/dL), androstenedione was 20: |  o" @  K8 y( M  m
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-& E8 J/ X: b; B/ E) c, W9 ^9 X
terone was 38 ng/dL (normal, 50 to 760 ng/dL),! F$ }/ C! \* u
desoxycorticosterone was 4.3 ng/dL (normal, 7 to$ d+ n& w% U, [( O! k4 q8 j
49ng/dL), 11-desoxycortisol (specific compound S)
# ^! L, q' i7 b# r+ c1 bwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-, f3 V# X+ \! V/ \! z3 ?4 x
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total7 x" Q8 T' I% _% F
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),, V2 P* ^; ?* r0 x! d; b, h
and β-human chorionic gonadotropin was less than
0 c4 @. w' t% d5 mIU/mL (normal <5 mIU/mL). Serum follicular9 ]" X  R9 R' l8 k; |% g& ?; ^7 h
stimulating hormone and leuteinizing hormone& D# F# e$ c8 x  n0 A  U, G/ |5 _/ v
concentrations were less than 0.05 mIU/mL
1 _& t! N/ G3 e( r( w(prepubertal).3 D/ o! R( h' _2 J# l) H
The parents were notified about the laboratory) I0 d# E: F9 v1 l5 k
results and were informed that all of the tests were5 s$ _. R0 n$ S2 u6 l! G
normal except the testosterone level was high. The8 L) ]! K6 j$ [( U* F
follow-up visit was arranged within a few weeks to4 G9 d5 n9 q8 X4 V
obtain testicular and abdominal sonograms; how-
; j+ n  a' }4 L5 d2 Aever, the family did not return for 4 months.5 L6 K! Y1 r( K( T2 z  f0 |
Physical examination at this time revealed that the7 a2 o4 A% Z2 f, }4 s
child had grown 2.5 cm in 4 months and had gained
4 g1 J/ F& `# P3 k$ g% Q: y( O# Y+ a2 kg of weight. Physical examination remained
& f- g* u1 y1 z6 S( a- tunchanged. Surprisingly, the pubic hair almost com-( t6 [7 u) I+ F( t( n
pletely disappeared except for a few vellous hairs at
8 k) q1 w7 g. N0 ~4 w0 x1 I8 Rthe base of the phallus. Testicular volume was still 2* j( A: u! C3 n* A3 I$ W1 W
mL, and the size of the penis remained unchanged.
1 L* j3 r  j7 Q* v4 `/ X6 {) v  u/ UThe mother also said that the boy was no longer hav-
! R7 \0 z1 Q6 _: n+ ~# king frequent erections.
% P0 h' E+ G0 t% ?  X0 p3 k+ ]/ ^Both parents were again questioned about use of
+ Y. E9 o! z! `: F' b0 dany ointment/creams that they may have applied to
5 i- L0 {  f! S; [the child’s skin. This time the father admitted the
; `  h# W1 a4 B  _Topical Testosterone Exposure / Bhowmick et al 541
: m% x; M0 x4 j1 O- ~use of testosterone gel twice daily that he was apply-2 f: Q0 C4 K& t1 V
ing over his own shoulders, chest, and back area for7 ~1 I# y5 B1 J1 G; q
a year. The father also revealed he was embarrassed
- d# H: `5 |9 K* q5 cto disclose that he was using a testosterone gel pre-& b0 O' I# c1 r3 i1 @* m
scribed by his family physician for decreased libido( A( P! J, n3 K7 W* K$ Y4 ~
secondary to depression.; m$ y+ \- A6 J2 l+ `- h
The child slept in the same bed with parents.
; J7 E% Z" V! p6 g4 ^8 dThe father would hug the baby and hold him on his
- T+ l% |4 p$ Q$ }- h& Hchest for a considerable period of time, causing sig-
9 T6 J2 Z- _- Y3 W$ A. hnificant bare skin contact between baby and father.
& ]7 N: v& U* _- K" @$ f6 nThe father also admitted that after the phone call,: u: l! k1 d& V5 I( r
when he learned the testosterone level in the baby
! _8 G! D7 p9 w/ D+ J4 F/ ?was high, he then read the product information
# h% `; y: [3 ]9 F1 Tpacket and concluded that it was most likely the rea-- d* |8 ]6 A) ?  y
son for the child’s virilization. At that time, they
6 I! ^8 V* V! w- x! cdecided to put the baby in a separate bed, and the0 u& Z: Z) L! T& t, I: V8 D( |
father was not hugging him with bare skin and had
! O0 i. H/ r: y2 P" cbeen using protective clothing. A repeat testosterone
3 X7 w" Q6 `% h5 h' G2 t0 itest was ordered, but the family did not go to the0 b6 a2 Y8 f+ @* [; R4 h( S
laboratory to obtain the test.
  L) k. `7 Y7 G% d- f8 D2 @Discussion
2 g; Y! f( n# r" T  {Precocious puberty in boys is defined as secondary, }0 q+ h5 A$ w$ l% M: H, s
sexual development before 9 years of age.1,4: a& y6 C+ V4 r  m9 I0 O
Precocious puberty is termed as central (true) when
" T! R( n# v) C! C+ ]1 p3 H5 Pit is caused by the premature activation of hypo-; \- n9 W: F2 S. M& w3 a
thalamic pituitary gonadal axis. CPP is more com-
1 h# C* Y9 `7 b9 J8 U) A# }) H, [mon in girls than in boys.1,3 Most boys with CPP8 @- T% I6 S# C; Z
may have a central nervous system lesion that is
% {. G: J6 P7 \* C; q* Z) Aresponsible for the early activation of the hypothal-, f; A% {6 j* R8 O
amic pituitary gonadal axis.1-3 Thus, greater empha-
( j' Z, C& N1 l9 Y4 n& I0 q; Fsis has been given to neuroradiologic imaging in& f: O  N6 K. c# g8 m  i8 _0 H& l
boys with precocious puberty. In addition to viril-
4 J: `9 O2 p# Hization, the clinical hallmark of CPP is the symmet-( \7 M$ d2 Q3 l
rical testicular growth secondary to stimulation by4 [; i+ E9 E' L
gonadotropins.1,3
# i" j9 n' e( x7 w: q' n- \7 [Gonadotropin-independent peripheral preco-
" I  C7 q/ \& k4 f/ Mcious puberty in boys also results from inappropriate- a  P5 b& m, C+ |3 V: ]# T  C
androgenic stimulation from either endogenous or/ E, l% [; t! h2 r% `  d; \1 L
exogenous sources, nonpituitary gonadotropin stim-8 R& ]5 h9 B1 W0 ]
ulation, and rare activating mutations.3 Virilizing
: o9 B' Z' v0 O" W' @, ]. wcongenital adrenal hyperplasia producing excessive
8 m. w1 E& B. Y% N- ~& p. yadrenal androgens is a common cause of precocious, N$ g+ A) v1 r# A9 F5 J  e! G' Z
puberty in boys.3,4
) p( l7 v/ ~1 y$ [The most common form of congenital adrenal
* [* d- `/ ?7 Q' v& p) s' v2 Yhyperplasia is the 21-hydroxylase enzyme deficiency.
: t# m! x- l6 k7 S0 e( T8 VThe 11-β hydroxylase deficiency may also result in
1 ]8 [7 v3 p9 @4 yexcessive adrenal androgen production, and rarely,0 r& G9 u7 g4 i- x
an adrenal tumor may also cause adrenal androgen
2 x* N( F+ ?8 f/ M, sexcess.1,33 t4 W/ ]7 H- C& O) I
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; ^$ o. O6 g/ e' ^( A542 Clinical Pediatrics / Vol. 46, No. 6, July 2007, s0 p# C1 E4 c5 ]9 F( l
A unique entity of male-limited gonadotropin-* O" |4 @' x  ~9 q
independent precocious puberty, which is also known
3 d) h! r5 S, `, k) F, b4 \9 Jas testotoxicosis, may cause precocious puberty at a0 \/ c) _: @  L+ |0 d
very young age. The physical findings in these boys
& C& S2 E4 R0 s8 q) y; o2 u/ Pwith this disorder are full pubertal development,) C: c( d, }$ ?0 t% @. ]9 @
including bilateral testicular growth, similar to boys
# g6 D0 G1 k7 L% K- Xwith CPP. The gonadotropin levels in this disorder
2 V& r7 X, H7 S$ }" P) ^are suppressed to prepubertal levels and do not show
- u& m9 ^. j: B" U4 Dpubertal response of gonadotropin after gonadotropin-
6 O" }8 W# I# g- s0 areleasing hormone stimulation. This is a sex-linked; j! C. x) U- c( R' i
autosomal dominant disorder that affects only. Y, X- |- d; |
males; therefore, other male members of the family
% C' r/ X+ M3 \2 Umay have similar precocious puberty.3
! s1 p6 |! b" r9 mIn our patient, physical examination was incon-9 f* U5 O  r/ o6 T. Y' H
sistent with true precocious puberty since his testi-
$ p8 L  G) p; Y* Ncles were prepubertal in size. However, testotoxicosis
3 K! O) W9 v' e/ P! D+ g$ w: ywas in the differential diagnosis because his father, w8 d3 z0 \1 X  D; ?
started puberty somewhat early, and occasionally,3 [# J. j6 B6 Y( s+ D% `
testicular enlargement is not that evident in the1 M% e( n% S' m# o4 _
beginning of this process.1 In the absence of a neg-
' |4 Y1 B' ?' s- t9 hative initial history of androgen exposure, our1 I9 r/ E6 E8 f9 z
biggest concern was virilizing adrenal hyperplasia,  @7 ~5 V0 V* C' |- f
either 21-hydroxylase deficiency or 11-β hydroxylase! F7 w1 Q$ C4 D/ T" Y
deficiency. Those diagnoses were excluded by find-& B% k' I, R2 C! {& P! R* g
ing the normal level of adrenal steroids.; O  r' n5 T% ~
The diagnosis of exogenous androgens was strongly" w2 Y; _  ]- S. O4 G+ v+ k
suspected in a follow-up visit after 4 months because
# m( }% m( i- q" [the physical examination revealed the complete disap-, j( e( C) W8 q3 \7 j
pearance of pubic hair, normal growth velocity, and
. c0 p) X( x3 u2 G( t# ?8 ddecreased erections. The father admitted using a testos-
) S; V) A- ]1 x9 k3 Y) bterone gel, which he concealed at first visit. He was/ Y* R" N. Z4 f/ j8 t
using it rather frequently, twice a day. The Physicians’
) Z& \8 h3 [7 g5 H# wDesk Reference, or package insert of this product, gel or
* l1 C, b6 R7 Q: [$ a1 S( O  e( U0 vcream, cautions about dermal testosterone transfer to7 ?7 }8 K' m8 \! U( i
unprotected females through direct skin exposure.
# a3 |7 E8 U( Q+ i1 v' d) t. tSerum testosterone level was found to be 2 times the# C9 C( \# u7 g
baseline value in those females who were exposed to
* h/ c5 u3 U+ ^- C7 K0 m# |* B( teven 15 minutes of direct skin contact with their male# d% w! ]: x4 F* \
partners.6 However, when a shirt covered the applica-% }0 D" [3 U+ R1 m+ s
tion site, this testosterone transfer was prevented.
/ W4 X8 P+ q+ QOur patient’s testosterone level was 60 ng/mL,# j' t/ {; M- R7 F3 V+ q5 {& F
which was clearly high. Some studies suggest that
; {) M8 a/ |7 j( m# X7 D  ^dermal conversion of testosterone to dihydrotestos-) R/ F. U6 {4 Z: e% D, u5 e0 q
terone, which is a more potent metabolite, is more
  w( C7 M9 N% J2 ^/ R$ u+ W: tactive in young children exposed to testosterone8 w$ \0 I1 q7 M% M, o2 ]2 L9 C
exogenously7; however, we did not measure a dihy-4 v. {; X$ v: T) f( z
drotestosterone level in our patient. In addition to
& K3 Z: v: }  ]- U1 |; jvirilization, exposure to exogenous testosterone in5 K# S: P  Y, w* S" n' m5 `$ |# }
children results in an increase in growth velocity and
2 _9 f4 p0 U0 Q  j: l3 x2 |* \advanced bone age, as seen in our patient.
" `' s) ]$ F$ C& `4 D; c& LThe long-term effect of androgen exposure during8 f+ u: @- M. N% ~, L: g
early childhood on pubertal development and final, r( |+ t" J+ K  m. m
adult height are not fully known and always remain7 [4 ?, |' i0 Y; j
a concern. Children treated with short-term testos-
7 ]9 T, d3 Y& i" X/ a6 V" [terone injection or topical androgen may exhibit some
) H7 }+ f/ v$ g& X& ^: Aacceleration of the skeletal maturation; however, after0 M2 r9 h$ Q+ I1 `# g% O" u
cessation of treatment, the rate of bone maturation
6 T$ @) y" k! p! S- k2 \decelerates and gradually returns to normal.8,92 Y3 o4 F4 Y- j. Z) V
There are conflicting reports and controversy6 B# h  g0 _; s
over the effect of early androgen exposure on adult) T8 r" |, T# V0 L) c
penile length.10,11 Some reports suggest subnormal& I1 D9 x) o6 A9 H' m
adult penile length, apparently because of downreg-
  {  S5 L0 M; [* t% z4 Bulation of androgen receptor number.10,12 However,
5 n1 l5 ^/ e3 ?" nSutherland et al13 did not find a correlation between+ P0 u% O% C7 h  n7 W4 Y$ @
childhood testosterone exposure and reduced adult
! @) y) U' c; O8 A# Ipenile length in clinical studies.
/ [+ F2 S& U1 o" r- kNonetheless, we do not believe our patient is/ _$ U# |& Q* J; j/ p0 v  `
going to experience any of the untoward effects from- ~" E8 v% W0 y  N( V! R
testosterone exposure as mentioned earlier because, m% N/ v) Y" p( G/ o; r
the exposure was not for a prolonged period of time.
( p7 c3 `4 e. v! gAlthough the bone age was advanced at the time of" ^# T1 L/ s; R
diagnosis, the child had a normal growth velocity at
4 U# T3 w* I6 bthe follow-up visit. It is hoped that his final adult: o+ Q" q1 t- l9 y  H
height will not be affected.7 ?" j* K- o1 M$ _# O$ p, A
Although rarely reported, the widespread avail-/ U8 h3 T- X! N- H6 E* {
ability of androgen products in our society may' v4 j3 b0 U- n: j6 V
indeed cause more virilization in male or female
: p$ v: T  \/ {* m# s# g8 Mchildren than one would realize. Exposure to andro-8 T1 \6 z# h( H! h3 i
gen products must be considered and specific ques-, A/ m5 f2 d" t" C
tioning about the use of a testosterone product or5 O0 V! K3 w5 }: L9 F
gel should be asked of the family members during' u; [3 l% H; T2 c; T! ]% K
the evaluation of any children who present with vir-, Q# O4 c. P6 C9 o2 d4 Z
ilization or peripheral precocious puberty. The diag-, _! ~5 A5 g; d+ j7 X
nosis can be established by just a few tests and by8 P1 z. U+ u6 O
appropriate history. The inability to obtain such a& g  `8 E/ Q0 e( W
history, or failure to ask the specific questions, may8 L5 ?$ q' j* L" M8 n. }- v3 o
result in extensive, unnecessary, and expensive( D, P* f% j8 ^% Q3 v* m4 z% F% t
investigation. The primary care physician should be' P* l& n% G5 k. z3 d& u
aware of this fact, because most of these children* i. W; y: ~* S% d; |
may initially present in their practice. The Physicians’) G) k* b$ E+ v: r' N$ h; }
Desk Reference and package insert should also put a0 G( J" |% i" B! P/ I! {% m
warning about the virilizing effect on a male or. w6 Y/ ?; M. @( J0 Z5 N7 y- }7 Y
female child who might come in contact with some-
. g! \1 y! _' s! D" @one using any of these products.
+ l9 k5 E) Y6 c' R0 e* a) X7 Y0 nReferences
- b; ?" `" E! t2 N) w' d1. Styne DM. The testes: disorder of sexual differentiation% b# m! d+ f: U; _: }  @6 X
and puberty in the male. In: Sperling MA, ed. Pediatric
: }7 C3 v3 w) fEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
" T3 r6 o) R8 ]* Y2002: 565-628.
; ]8 v$ _; c; t, `9 ^, b, b# f+ y9 r% w2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
% r  X  X7 S0 s% {" {, g# D& ~puberty in children with tumours of the suprasellar pineal
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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!

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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
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
累計簽到:11 天
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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

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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?
累計簽到:3 天
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發表於 2025-1-19 02:41:05 | 顯示全部樓層

7 o/ D+ C3 F8 O; H8 m精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!

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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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