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Sexual Precocity in a 16-Month-Old, T1 E4 o: g  a3 w% S7 \6 Y
Boy Induced by Indirect Topical6 E$ k4 d5 k3 }$ K" [. C$ d
Exposure to Testosterone1 S5 O. |8 _: d: v6 [1 B  C
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
3 a: e5 ^, s. T2 e3 C5 H  n# S3 p# Kand Kenneth R. Rettig, MD16 Z* {  X' [4 e% w
Clinical Pediatrics+ y( u5 w* }5 K1 x
Volume 46 Number 6
+ i# {9 y! j  CJuly 2007 540-543
8 {# p( R2 ]/ h* b5 {) m) x© 2007 Sage Publications3 g: W( W. E% K# e* n
10.1177/0009922806296651
# ?. E* C% C! |http://clp.sagepub.com
7 R/ O$ Q9 m: X7 f! k6 D4 s! }hosted at
. p7 k1 B; \  G$ q) Z7 A1 uhttp://online.sagepub.com4 K- T' v9 }- \0 K1 x2 M6 h7 r
Precocious puberty in boys, central or peripheral,
% Q3 T& r9 n8 u5 T6 v9 A) sis a significant concern for physicians. Central
* o# X% ~/ B9 l9 G+ R4 P+ Vprecocious puberty (CPP), which is mediated
2 l  m4 P# N2 X2 l& Ythrough the hypothalamic pituitary gonadal axis, has  X) W# o$ h" ^6 f- H
a higher incidence of organic central nervous system  Z0 K. B7 X# c2 u, M
lesions in boys.1,2 Virilization in boys, as manifested! I$ }! K1 G3 j& Y
by enlargement of the penis, development of pubic
! t' f2 p+ d; n( G& N5 _hair, and facial acne without enlargement of testi-
# E$ ^; e9 f) s  L7 f5 S4 ucles, suggests peripheral or pseudopuberty.1-3 We( \5 l. R( }* t9 K' j' C7 ?
report a 16-month-old boy who presented with the* u' L( f* q! j, G4 C: N
enlargement of the phallus and pubic hair develop-9 @2 @9 x+ W: F# d2 G3 x
ment without testicular enlargement, which was due
6 b2 Y$ _/ @, ~  a  Q" u1 ato the unintentional exposure to androgen gel used by" T! D& c2 ~) I2 U* ]
the father. The family initially concealed this infor-
7 s  k/ B* V5 i; Tmation, resulting in an extensive work-up for this
7 @$ [! C/ U' U; U: C3 Z+ b  ?! Zchild. Given the widespread and easy availability of
0 P4 Q/ O2 l! S, k' a7 p1 dtestosterone gel and cream, we believe this is proba-
- N' r6 S* W9 I  O: y& Z$ ^0 Sbly more common than the rare case report in the# O" {) \! e/ n( j! C) n( a/ t# N
literature.4
* u& K. X' X0 m5 K; S5 qPatient Report* S8 |- |' i' \5 r% w
A 16-month-old white child was referred to the
) J1 Y: \! m; s5 a4 @: G8 Eendocrine clinic by his pediatrician with the concern
+ q7 a9 m" G7 R+ u. F0 F$ P- {of early sexual development. His mother noticed
6 C$ _( B1 Z& qlight colored pubic hair development when he was
, D: y" z0 R+ W& @From the 1Division of Pediatric Endocrinology, 2University of
' W  X' n7 T0 i* Y) E) [. q4 O: fSouth Alabama Medical Center, Mobile, Alabama.
& d" r. N& \0 f) P. z$ A9 ^Address correspondence to: Samar K. Bhowmick, MD, FACE,
$ v+ l: L  x4 x$ a" l; rProfessor of Pediatrics, University of South Alabama, College of' B& X& U& h2 J. m+ Y) |
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
9 R- P6 Y; e/ P2 ^e-mail: [email protected].9 E# D( c$ r3 g& l" t
about 6 to 7 months old, which progressively became
% Y9 j1 @$ w- F0 }" b7 r. C* C+ z* rdarker. She was also concerned about the enlarge-
' z1 Y3 S9 v" S8 Dment of his penis and frequent erections. The child
# P  _  D+ b- S) t6 ^was the product of a full-term normal delivery, with9 A" t& p- O, ~5 Z& k( p+ y6 }
a birth weight of 7 lb 14 oz, and birth length of0 k0 v7 L5 n1 x5 Z% a$ L  c
20 inches. He was breast-fed throughout the first year
8 Q2 V) E7 }3 ]0 ~3 @of life and was still receiving breast milk along with4 O' G7 B9 O$ g1 T$ J
solid food. He had no hospitalizations or surgery,
' H9 E, m+ Z0 f% H7 Qand his psychosocial and psychomotor development- w5 _* H7 I6 ^
was age appropriate.; @4 j1 A6 k; S, A3 \
The family history was remarkable for the father,  Z; ^- v2 r4 `+ ]9 y0 ^/ f# o/ ]
who was diagnosed with hypothyroidism at age 16,
1 b. |$ G& _9 ywhich was treated with thyroxine. The father’s9 s6 h6 f; J$ i2 F) p
height was 6 feet, and he went through a somewhat( J3 c: W1 H6 Q2 q( T
early puberty and had stopped growing by age 14.: r5 ?3 p5 _2 I3 f
The father denied taking any other medication. The. U: N7 p$ ^- ]% |8 }+ v
child’s mother was in good health. Her menarche- c, C2 G. M2 X" E( w$ V" T4 V' g" P
was at 11 years of age, and her height was at 5 feet+ _1 Q$ `3 _! R) d$ `$ [
5 inches. There was no other family history of pre-
( ]) ?1 V. ~; O, p; kcocious sexual development in the first-degree rela-
* K* j: m; ~0 N7 v8 e) J7 Ztives. There were no siblings.
1 g$ p% c8 l# k' B9 mPhysical Examination5 P0 C0 M0 H- h$ l& Q$ F
The physical examination revealed a very active,7 U. ^2 n4 P: C2 F4 \1 y7 `
playful, and healthy boy. The vital signs documented1 C6 ~$ i9 }( _; E  O( e
a blood pressure of 85/50 mm Hg, his length was1 c2 F0 I6 p1 w8 }' s) E
90 cm (>97th percentile), and his weight was 14.4 kg
% U0 y/ U# o; `/ ~(also >97th percentile). The observed yearly growth
  w- a( @5 h3 F' @8 E# J; Mvelocity was 30 cm (12 inches). The examination of+ i9 o4 x8 j* ]( x  I
the neck revealed no thyroid enlargement.
- t$ i" G- C% S' J) @) U0 [( b. _The genitourinary examination was remarkable for0 ^2 ~* m( ?. U# d
enlargement of the penis, with a stretched length of/ z" o7 G- ?7 `0 H
8 cm and a width of 2 cm. The glans penis was very well
/ @% k- ^7 d4 s: i/ f/ |6 A3 ~; Ldeveloped. The pubic hair was Tanner II, mostly around/ y% J& b& |" @% ?/ e  f
540% _: k& V: w- V
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
. w: J$ Q, G1 w- J. }4 Xthe base of the phallus and was dark and curled. The0 n/ Q' g# n* N
testicular volume was prepubertal at 2 mL each.- P! j3 |+ H+ y4 R5 `
The skin was moist and smooth and somewhat
) P: x+ \2 E! e) q2 z, voily. No axillary hair was noted. There were no
9 |9 a, f* a  n# ~abnormal skin pigmentations or café-au-lait spots.) R! M+ f- ?3 `! U7 Z3 b
Neurologic evaluation showed deep tendon reflex 2+* O  Q2 K5 b3 e. ~  w. f$ w0 R( _7 w
bilateral and symmetrical. There was no suggestion
: p& ]3 H8 u5 s; z7 P; Oof papilledema.
$ W# j% e1 o- H1 A; ]% J) TLaboratory Evaluation# q; ]/ q1 m/ D* j6 H2 r
The bone age was consistent with 28 months by
' R- w' |2 D$ l$ ~4 O& Qusing the standard of Greulich and Pyle at a chrono-2 c( N' f, m; d, C  F
logic age of 16 months (advanced).5 Chromosomal! t/ @, c$ z+ |+ p7 z
karyotype was 46XY. The thyroid function test
) ]8 M/ D! m7 h- Oshowed a free T4 of 1.69 ng/dL, and thyroid stimu-! w! a6 N( c+ S+ d+ X4 i
lating hormone level was 1.3 µIU/mL (both normal).
: i! K' K  i% ]The concentrations of serum electrolytes, blood2 ?: F" `& F6 c! b9 S
urea nitrogen, creatinine, and calcium all were
! l2 e) a* S: j6 B2 j1 D2 Nwithin normal range for his age. The concentration
; ~/ n  J6 t, n) ]( w- w  p4 }8 @, _of serum 17-hydroxyprogesterone was 16 ng/dL
9 b) _+ O' T* C! ?: h# [(normal, 3 to 90 ng/dL), androstenedione was 20
" t3 x& L; T2 k" ]4 d* ing/dL (normal, 18 to 80 ng/dL), dehydroepiandros-5 P/ v4 y/ F: z  o; M2 l
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
. p7 C3 Q8 O0 H9 G- L, A/ L. tdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
0 |3 G6 k/ |: R% \49ng/dL), 11-desoxycortisol (specific compound S). Y% A1 F$ ^& s6 F* D& s4 @1 K
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-+ Y5 u2 g. g2 {% a6 X& \. v9 W  U
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
% H5 K3 _8 _; ^1 o' k$ L& utestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
& V7 z/ `/ d1 C  Kand β-human chorionic gonadotropin was less than8 q9 b* S# X2 U" U
5 mIU/mL (normal <5 mIU/mL). Serum follicular! K  `0 B- E4 d4 q" Z
stimulating hormone and leuteinizing hormone
0 @5 A" G, w' U) }* \: X' qconcentrations were less than 0.05 mIU/mL
6 u2 @  j# h7 K; }- f7 f4 _5 P(prepubertal).
* u! j# t5 R  W3 U1 ^: M5 |$ N/ tThe parents were notified about the laboratory4 S7 p% W/ J, `1 F7 u' }
results and were informed that all of the tests were' C/ L/ w5 _- y0 k' ~
normal except the testosterone level was high. The
  {* U# f! ^' t! tfollow-up visit was arranged within a few weeks to/ r2 R$ w+ W6 p* N
obtain testicular and abdominal sonograms; how-
# z) x6 \' q+ ^& d) Tever, the family did not return for 4 months.
- h3 u. b! b9 f- I; sPhysical examination at this time revealed that the- U$ p1 \( |. l9 v3 m# g8 ~  Y, Z9 k
child had grown 2.5 cm in 4 months and had gained
3 K& K* S  [; G! l/ G2 kg of weight. Physical examination remained
3 f& B+ x1 B3 f- uunchanged. Surprisingly, the pubic hair almost com-, a3 r- c5 p4 X. N; B# `6 H
pletely disappeared except for a few vellous hairs at$ S" q0 E4 W( ?8 Y* ?( E: b
the base of the phallus. Testicular volume was still 2
9 c7 W3 _: b# H) {6 x* kmL, and the size of the penis remained unchanged.( P/ s- `; h' C& x
The mother also said that the boy was no longer hav-
. f, R+ l3 i$ H# S0 w# ging frequent erections.  a  S7 k. X! g3 B: `+ o) ~' j
Both parents were again questioned about use of1 b# W  e+ Z; j9 K" F$ G2 v
any ointment/creams that they may have applied to
& l8 d( Y0 S7 b# E# sthe child’s skin. This time the father admitted the
. B! g9 P8 V1 P# wTopical Testosterone Exposure / Bhowmick et al 541
; c$ h$ s* o# ]6 X) Euse of testosterone gel twice daily that he was apply-  c9 X9 ?9 X3 l( ?( e' p" }
ing over his own shoulders, chest, and back area for, o" c* w9 u: E% p- }
a year. The father also revealed he was embarrassed8 p- r( j; P" P8 z& D& `
to disclose that he was using a testosterone gel pre-
8 n" ]2 b- L% Z0 O6 Pscribed by his family physician for decreased libido9 u; t/ y# ]; V" B3 Y& f0 A: A
secondary to depression.4 y' q0 b1 {, ^5 O( e5 E7 G
The child slept in the same bed with parents.2 ?% o, p" S" i+ j
The father would hug the baby and hold him on his
6 I# o8 {1 z4 Zchest for a considerable period of time, causing sig-/ w# |/ t1 F* c2 M1 r
nificant bare skin contact between baby and father.
- Q8 R7 @( ?2 \* [( ^5 B3 u8 a( aThe father also admitted that after the phone call,
" L' \! H' c* h( G+ cwhen he learned the testosterone level in the baby& m! b# V* X7 i! s$ H; d/ g
was high, he then read the product information' @! ]  A' a, Y  ~' Z
packet and concluded that it was most likely the rea-
6 Y5 Y" x- |, `2 mson for the child’s virilization. At that time, they7 t- j- s- w) ?
decided to put the baby in a separate bed, and the
# ?4 n  k$ N! d& D7 n; V! ffather was not hugging him with bare skin and had
7 s- I" M" S3 B! kbeen using protective clothing. A repeat testosterone
/ U/ c" Y, \( t5 Etest was ordered, but the family did not go to the
7 B& V: c' a, M- q. x) F7 }0 Blaboratory to obtain the test.( C! W9 _, v* T6 ?! g- E
Discussion
4 l. b  A( s) a$ M$ x# m" FPrecocious puberty in boys is defined as secondary
2 E3 N; _( ]8 L$ b8 H. Usexual development before 9 years of age.1,4
* m- s' e1 J) N5 w# e) [5 zPrecocious puberty is termed as central (true) when
9 \/ }% c) U/ S* B4 Dit is caused by the premature activation of hypo-" S& Y% T" t6 v1 k6 P
thalamic pituitary gonadal axis. CPP is more com-+ K+ l, _' d6 H$ L& e2 C
mon in girls than in boys.1,3 Most boys with CPP
, w. q2 h6 ^) z. H7 o' z  u; ^* Imay have a central nervous system lesion that is
# |% B2 N; T# D, t8 p2 E& L! eresponsible for the early activation of the hypothal-
; J; P7 O' H! Q+ q$ g7 ^: M4 samic pituitary gonadal axis.1-3 Thus, greater empha-% g: X  V* ?3 R+ n- b* V6 d8 g
sis has been given to neuroradiologic imaging in
1 |& f, @0 W3 j& z* D" H5 ?; Kboys with precocious puberty. In addition to viril-
0 E& P; K2 J* W4 @; ?ization, the clinical hallmark of CPP is the symmet-
* z8 }- m1 }% _& f+ L! r& I4 F# }% yrical testicular growth secondary to stimulation by2 h  X, c0 R" v# s# \
gonadotropins.1,3
, O( {; {* H/ W9 [0 E) s& EGonadotropin-independent peripheral preco-6 [5 _0 M2 y, M+ w, t6 E' O
cious puberty in boys also results from inappropriate9 }' b: ~' {5 b( F; C+ t; x
androgenic stimulation from either endogenous or, \0 t3 R3 R+ _( [/ _
exogenous sources, nonpituitary gonadotropin stim-
9 e+ F! _7 E; U8 tulation, and rare activating mutations.3 Virilizing
+ O4 F7 ^% c) z) O, Wcongenital adrenal hyperplasia producing excessive
4 ~. v; a. t. b$ ^adrenal androgens is a common cause of precocious5 i4 i; ~8 I  [" |
puberty in boys.3,4
' g0 B. Z" q4 fThe most common form of congenital adrenal
) r/ Z4 T6 e: P! O0 Dhyperplasia is the 21-hydroxylase enzyme deficiency.
9 \8 H9 l+ V6 ~8 x' Y1 ^7 [The 11-β hydroxylase deficiency may also result in. I1 e6 W2 B& }) i  E$ j+ W
excessive adrenal androgen production, and rarely,, a6 ]2 _' G: [- F, O6 w
an adrenal tumor may also cause adrenal androgen
3 O; `1 M  T3 O; n$ L5 R" [- Mexcess.1,34 H) z# \- d# K' s
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" y  H# @; @, w+ O) ?# c, T: ^* A5 _542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
+ ~! H5 V7 C! |* b- I+ mA unique entity of male-limited gonadotropin-
5 w8 ]( J3 X$ c4 V) l" B& k& Findependent precocious puberty, which is also known( N/ R- e: Z9 |0 l& d1 a1 k
as testotoxicosis, may cause precocious puberty at a
4 C. G# N/ ~3 Y( V3 Mvery young age. The physical findings in these boys
5 ], G0 {% W  c4 F/ K/ S1 V8 l5 Z0 swith this disorder are full pubertal development," {/ e4 X* X# x2 V' P' ]- {
including bilateral testicular growth, similar to boys4 C" m: ^% j/ j2 }1 w! }2 I) l
with CPP. The gonadotropin levels in this disorder2 z9 z- Z9 g, i% a* d2 k  {0 Z, Y
are suppressed to prepubertal levels and do not show
9 i% Z( T. \4 j7 zpubertal response of gonadotropin after gonadotropin-5 x" T! X" g' U3 q; S7 I
releasing hormone stimulation. This is a sex-linked7 ]& J3 j& F4 |% W+ Z" O& k( d2 }
autosomal dominant disorder that affects only. `5 D9 i) ^3 F* M( x" t
males; therefore, other male members of the family
) M  b. V' Y6 y$ ?* |may have similar precocious puberty.3
" L- `+ s$ J9 ]- f. D7 [( r* LIn our patient, physical examination was incon-1 J% c1 x# r! \; X+ U! e& I' N
sistent with true precocious puberty since his testi-
" r! H( a* Y2 ~5 ]' p* @# [2 {, Ycles were prepubertal in size. However, testotoxicosis3 }; G/ Q! q: q3 P. Y" p
was in the differential diagnosis because his father
0 S/ h$ N# u/ B6 j5 Estarted puberty somewhat early, and occasionally,; v' j6 o( n3 K, H
testicular enlargement is not that evident in the& l3 m. M: s. A* g2 U( k% o8 d$ D$ z
beginning of this process.1 In the absence of a neg-* W) i# T3 x' o1 A/ d% o
ative initial history of androgen exposure, our) M/ ~% v2 n5 N( T7 A
biggest concern was virilizing adrenal hyperplasia,
/ _* E. D3 {( g# U% ?1 u1 m! O7 Leither 21-hydroxylase deficiency or 11-β hydroxylase4 T6 x4 x# s+ p- U% d; ?
deficiency. Those diagnoses were excluded by find-" Z9 `3 b  p/ y' _% |
ing the normal level of adrenal steroids.
- Z. k" b: a) q5 KThe diagnosis of exogenous androgens was strongly
; j' n- F4 J- v4 ?8 Hsuspected in a follow-up visit after 4 months because8 L; M9 q& y' S  i
the physical examination revealed the complete disap-- ^6 Q$ _  j' P0 U: w  l& ?
pearance of pubic hair, normal growth velocity, and$ r7 w" T# `7 k. F
decreased erections. The father admitted using a testos-, Y, x5 {7 S$ _1 _8 b% Z; f
terone gel, which he concealed at first visit. He was
% F$ V$ Q1 L% z8 vusing it rather frequently, twice a day. The Physicians’
8 R& r- C6 i5 V' ~; vDesk Reference, or package insert of this product, gel or4 R6 [1 c) N( ~8 r" |* d
cream, cautions about dermal testosterone transfer to
, X( x% L" i5 I8 cunprotected females through direct skin exposure.
$ `! b* `3 J! t1 GSerum testosterone level was found to be 2 times the* n8 g3 C" q, Z  e* R
baseline value in those females who were exposed to$ s1 ], ?' K  @  V+ e  p; n! j
even 15 minutes of direct skin contact with their male
9 T9 V6 {5 w: [partners.6 However, when a shirt covered the applica-' z7 l& y$ D3 h
tion site, this testosterone transfer was prevented.; r& d% Y6 F" q) S" r4 w  s: f1 M
Our patient’s testosterone level was 60 ng/mL,8 x# g* U% s) S  B# D( e7 x
which was clearly high. Some studies suggest that
4 {$ u; x- H( T' A) }5 Sdermal conversion of testosterone to dihydrotestos-) E5 w% L6 e7 S4 k, H( ?$ r) a
terone, which is a more potent metabolite, is more
# y$ E% d/ Y( d! m$ `# Kactive in young children exposed to testosterone
% e" z8 b7 `1 l1 n8 k- l& ~) w0 ?exogenously7; however, we did not measure a dihy-
; t' R3 h. m# Y% J4 r. mdrotestosterone level in our patient. In addition to
, y( X: S6 L& L1 {# X% m8 Z/ Lvirilization, exposure to exogenous testosterone in" n7 |0 d* L7 F- c
children results in an increase in growth velocity and
, E9 l& @% c" u/ p! n& P! i# Oadvanced bone age, as seen in our patient.
) M* G. B/ h( @; B  s7 x. RThe long-term effect of androgen exposure during6 b. L0 o# E; I# N' C6 G/ S! `
early childhood on pubertal development and final
' i3 {4 M9 Q- j. }7 Nadult height are not fully known and always remain7 L. @( F/ h" y( h
a concern. Children treated with short-term testos-
, W% Y% H" \8 G- gterone injection or topical androgen may exhibit some# M0 U. ?9 z3 N9 J+ ]- N
acceleration of the skeletal maturation; however, after
) g$ ~2 _  R3 {cessation of treatment, the rate of bone maturation/ l% O" H1 U9 P5 V" B" Y
decelerates and gradually returns to normal.8,9
; @# A% a! [3 U8 T, lThere are conflicting reports and controversy
3 s, n; p, C3 |/ Pover the effect of early androgen exposure on adult
4 s- e. V& E2 s1 U, p* {  ?0 apenile length.10,11 Some reports suggest subnormal) |& M* H/ F- {" k9 z
adult penile length, apparently because of downreg-% D) S, V- X/ O
ulation of androgen receptor number.10,12 However,9 J$ Z# [2 m! n3 T9 \4 D
Sutherland et al13 did not find a correlation between
( i, w4 l2 C% V8 ]6 k' J+ f; @6 `childhood testosterone exposure and reduced adult. m4 ^9 j( f/ ?$ c
penile length in clinical studies.- {  O0 X4 Q: v; @- D+ L+ E
Nonetheless, we do not believe our patient is' M5 f% S, s1 \6 L
going to experience any of the untoward effects from, `$ J2 r8 {( ~
testosterone exposure as mentioned earlier because3 t' ]  k. v5 h+ n0 x( g
the exposure was not for a prolonged period of time.
1 @" a4 }3 ~% K% q$ u. ~* J5 jAlthough the bone age was advanced at the time of2 L/ _  W& n5 F( q  l$ v
diagnosis, the child had a normal growth velocity at- a+ L4 {3 b3 Z! O! _( ^5 t
the follow-up visit. It is hoped that his final adult
: K) m7 f1 T6 ^4 {3 \  nheight will not be affected.4 \+ V% [8 U  q) s
Although rarely reported, the widespread avail-
3 E3 r! W( r1 _7 r: Wability of androgen products in our society may
: s3 p. d6 `$ O  Y. _% Yindeed cause more virilization in male or female. c" @( D" w8 J2 T
children than one would realize. Exposure to andro-
5 C7 g* E4 ~5 h4 igen products must be considered and specific ques-; Q  j( t, q7 a+ K
tioning about the use of a testosterone product or
  h2 q' A; @. }# `# E2 o/ |gel should be asked of the family members during
3 b6 c& Y( U+ _/ Hthe evaluation of any children who present with vir-7 ]7 z" O2 R% A+ C; l; X2 R
ilization or peripheral precocious puberty. The diag-" u7 O6 |4 ?! C& ?0 |/ v
nosis can be established by just a few tests and by
6 N' A  E# M' o" ~1 Dappropriate history. The inability to obtain such a
5 b9 y0 l! b2 M2 n) e9 C: dhistory, or failure to ask the specific questions, may
- ^9 c/ K5 \, \1 M- Uresult in extensive, unnecessary, and expensive/ K7 [% w% s+ ?& o% R
investigation. The primary care physician should be# x7 u2 l5 d! C  h6 ^4 x5 _
aware of this fact, because most of these children
8 D/ @* p9 s2 R+ bmay initially present in their practice. The Physicians’+ X! m9 z  o' h8 w% t7 b6 _
Desk Reference and package insert should also put a! b/ p. m$ V) @! p& a, a
warning about the virilizing effect on a male or  J" n- H) y4 |
female child who might come in contact with some-! d8 ^! r. f0 I/ P+ B( e1 U
one using any of these products.; N0 K3 \: d  I
References. V$ [2 V/ Y3 L$ s8 G' x. W
1. Styne DM. The testes: disorder of sexual differentiation. V: N: A$ a( i, C- O- C* s9 @
and puberty in the male. In: Sperling MA, ed. Pediatric/ k- h6 e8 G5 ~# w
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
; C: q# e" F1 P2 L' E' ~2002: 565-628.# a* n$ l- i6 `9 h6 G
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious2 ^7 R1 ]% |7 t; E/ R& o, f7 A% {+ x
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
4 J0 o5 H5 k5 Q1 p6 w) }# CBoy Induced by Indirect Topical5 S& K& h1 ]# {, C! C
Exposure to Testosterone/ E% ^  E/ t7 ^4 f6 d# R0 n
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
$ D& [: r; t3 S  jand Kenneth R. Rettig, MD1$ S  V1 R5 p, e$ P' n( `
Clinical Pediatrics
& c- Z% Z) l0 ?0 q! q* f7 `Volume 46 Number 6
; @3 K& p5 A9 z8 [July 2007 540-543- W* k' {" `1 P3 c' i- ]! K# y# P# I
© 2007 Sage Publications/ a+ s; D5 A) U' ^9 ~8 P( E
10.1177/0009922806296651  m, v0 |) p+ K- ^: n) z  e
http://clp.sagepub.com+ F: V- z, j/ ]  Q+ l; S. ~
hosted at  _( i% {' m2 `/ Z
http://online.sagepub.com, c  h' V& ~" [' R
Precocious puberty in boys, central or peripheral,
0 V' u/ S, r2 b! cis a significant concern for physicians. Central
: I( Y" N# |  tprecocious puberty (CPP), which is mediated
2 u: x3 i% [. G+ O# w( B3 ^through the hypothalamic pituitary gonadal axis, has
" l/ j2 B0 K$ K& ?a higher incidence of organic central nervous system: P# B$ B; A# U
lesions in boys.1,2 Virilization in boys, as manifested" K% r9 O! f6 F' B8 h# p
by enlargement of the penis, development of pubic
: U. _2 @, N# g, x/ s9 r1 ^hair, and facial acne without enlargement of testi-
' M+ ^/ @- Z+ ~( x# R; ocles, suggests peripheral or pseudopuberty.1-3 We3 k" l3 `+ B- j  q# ^8 Q
report a 16-month-old boy who presented with the, g) W* O, t2 M; x+ Z* i& `
enlargement of the phallus and pubic hair develop-
" Q) ~6 F) X; o" rment without testicular enlargement, which was due6 m' c. C, B5 n: g, [9 f7 E" Q
to the unintentional exposure to androgen gel used by
! ~4 o: ]3 m2 _% j$ ]the father. The family initially concealed this infor-
' Z0 R8 v: Q( I/ k% s8 W" L! hmation, resulting in an extensive work-up for this
, f' X  T& M! u$ g7 a& uchild. Given the widespread and easy availability of9 d& D: w3 Q" ^% F
testosterone gel and cream, we believe this is proba-0 n3 d: g+ W  K; T% u
bly more common than the rare case report in the
4 {) ~, m4 O4 H* L1 Bliterature.4
! i/ E/ O: C# N0 @, U( FPatient Report  t3 Y7 N+ P2 e' ]
A 16-month-old white child was referred to the' u: P; Y- C  Z% {1 B% c$ B
endocrine clinic by his pediatrician with the concern4 X! A; G; Y$ V9 O8 m) {  ^
of early sexual development. His mother noticed
6 b. C" r- Y  l- A( j* @  Zlight colored pubic hair development when he was
/ w& `4 b; j3 X7 j4 P: ^! UFrom the 1Division of Pediatric Endocrinology, 2University of. N# P# X9 S+ t# |
South Alabama Medical Center, Mobile, Alabama.8 e% |2 \( `: t5 p# @9 y& ~
Address correspondence to: Samar K. Bhowmick, MD, FACE,* M! T2 `9 t: E: h# v- _* I
Professor of Pediatrics, University of South Alabama, College of
  z2 n7 U2 l, K$ S' ?7 jMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
9 d" X% N% U6 Y$ d& g/ u8 M3 l  R$ le-mail: [email protected].. A; C/ H0 n% P' g# Q6 k- V. V' ~
about 6 to 7 months old, which progressively became
: U( j9 O- o) n- |& n3 ydarker. She was also concerned about the enlarge-* n0 \9 z4 A3 ]6 P. J8 T
ment of his penis and frequent erections. The child2 M6 ~, o" S  K! C: g8 D: u. Y, L
was the product of a full-term normal delivery, with
1 b' H! l( m) L& [a birth weight of 7 lb 14 oz, and birth length of
" I( W& D2 a" r- r0 E20 inches. He was breast-fed throughout the first year( c* Q! ]& _4 D
of life and was still receiving breast milk along with
+ _* Q) n, B. T3 K9 y& y+ Nsolid food. He had no hospitalizations or surgery,
+ x4 F( {5 y/ }and his psychosocial and psychomotor development
3 w  ~! e+ \! d" l) dwas age appropriate.& G5 p1 D0 s/ b0 F  [
The family history was remarkable for the father,
' T) Z  M  k. v* c$ y6 }' zwho was diagnosed with hypothyroidism at age 16,
: G/ |* m* L2 I- I( m, Fwhich was treated with thyroxine. The father’s* }+ b, o, i% ^
height was 6 feet, and he went through a somewhat& \* _, t+ @* g2 B% G
early puberty and had stopped growing by age 14.) }% K, E0 n( C
The father denied taking any other medication. The
4 `' I/ Y7 N* G9 ochild’s mother was in good health. Her menarche0 `: e6 h  _$ b6 A
was at 11 years of age, and her height was at 5 feet9 j0 r! V, X, @7 F& M1 E5 }
5 inches. There was no other family history of pre-& z; p) Z# X, u  i" o
cocious sexual development in the first-degree rela-4 Y1 @. v; `, r; ]* M
tives. There were no siblings." h) ]: S+ d; w- D; R  g
Physical Examination: n7 i5 V4 k3 J: H0 ?3 |. F$ u
The physical examination revealed a very active,7 }$ C) ~* x+ v9 f! }0 ]# m2 K6 f
playful, and healthy boy. The vital signs documented
" s7 X) u7 L6 J8 Ta blood pressure of 85/50 mm Hg, his length was
6 L' s# O* p; Q( s5 m90 cm (>97th percentile), and his weight was 14.4 kg
9 O4 P' `$ q1 p7 b(also >97th percentile). The observed yearly growth$ V9 d. A6 K9 M, \6 ]  J0 F% r( a; L0 w
velocity was 30 cm (12 inches). The examination of
: V' l8 }0 P& Pthe neck revealed no thyroid enlargement.
' M; p6 u0 P  yThe genitourinary examination was remarkable for! j- @8 p5 m. Q( a8 ]
enlargement of the penis, with a stretched length of
! v/ z& S( o4 _+ o0 S8 cm and a width of 2 cm. The glans penis was very well4 T. |) X/ z) c) y7 u9 S5 c
developed. The pubic hair was Tanner II, mostly around& h( i8 s2 @9 `6 G# X; K
540+ y3 A- Y+ c) s. @; q/ z. N( Y, ~
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' }* n: L  B+ w6 c
the base of the phallus and was dark and curled. The# G& T/ z9 T/ [, P6 b5 @' y
testicular volume was prepubertal at 2 mL each.$ f8 o6 K5 T" I9 j1 O/ D
The skin was moist and smooth and somewhat8 ~1 j0 I* X" v# t1 b
oily. No axillary hair was noted. There were no
( ?, E& J' {& R' r- ?9 ^8 Y+ ]4 ^abnormal skin pigmentations or café-au-lait spots." ]$ f1 A" D# M% S0 ^5 c- s# u
Neurologic evaluation showed deep tendon reflex 2+
% B( V$ M! F! e' m! O6 mbilateral and symmetrical. There was no suggestion$ J1 U4 V  k# ^$ ?# c
of papilledema.
, B* e" H* M. |5 ~1 A/ p2 {9 DLaboratory Evaluation
  l# M$ K8 B# O: J' n- ]1 lThe bone age was consistent with 28 months by
9 s% R1 ?+ q- g4 n* H) ^  ~using the standard of Greulich and Pyle at a chrono-
# r! m5 g6 Q1 S% T1 v! P% ulogic age of 16 months (advanced).5 Chromosomal. q# d: H4 t' Q. Q1 a4 b
karyotype was 46XY. The thyroid function test) q2 h3 m, l6 {  r: q
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
: B+ {" g9 p% w% U" wlating hormone level was 1.3 µIU/mL (both normal).
9 ~5 y3 h+ r% F" v& c$ _9 U% o5 xThe concentrations of serum electrolytes, blood! |  S2 M6 U. L0 ]& K
urea nitrogen, creatinine, and calcium all were
9 a1 f$ K3 @+ @; I: G0 j% uwithin normal range for his age. The concentration8 u: V5 X. ]! w9 \0 @$ p+ l: J
of serum 17-hydroxyprogesterone was 16 ng/dL
& l2 j# I( x; @(normal, 3 to 90 ng/dL), androstenedione was 205 k9 B7 m5 b' l% P5 i; m; H" l, B
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
1 S9 t: v: ]3 Z, n7 G, f% m+ e7 Tterone was 38 ng/dL (normal, 50 to 760 ng/dL),) O+ a7 W) e7 t. U! J9 h- e/ Z1 G
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
" U  E0 H$ H; R" q- A5 [3 c4 R8 z49ng/dL), 11-desoxycortisol (specific compound S)
8 f( B9 g( i- Z; Xwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-7 j$ Y0 R8 q2 L4 d0 F3 ]
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total5 [/ s  K* p9 V2 F3 d$ M
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),' ]! H! f- C3 g, f' x
and β-human chorionic gonadotropin was less than2 G5 W  ]: f6 J, f% a
5 mIU/mL (normal <5 mIU/mL). Serum follicular
6 g) o6 v  a  T4 g6 _/ _7 Zstimulating hormone and leuteinizing hormone# ^) v/ J  E. e! w
concentrations were less than 0.05 mIU/mL9 }1 `# _) ~+ G; U* w9 W' A5 L2 L
(prepubertal).
, T8 `. n% `$ g  VThe parents were notified about the laboratory5 ?) ]3 H# M! f9 ]1 m4 A' n7 ^2 T
results and were informed that all of the tests were+ G; b. O7 N$ `  T# N, _( u- p
normal except the testosterone level was high. The. x. |4 f7 P' M/ L
follow-up visit was arranged within a few weeks to
2 j- x+ t* Y3 ^# b+ t$ D: Nobtain testicular and abdominal sonograms; how-
' D& U+ s" F8 m( bever, the family did not return for 4 months.
0 e( M, z1 e: |- A$ ~. ?! G! lPhysical examination at this time revealed that the' e* N( p& F) b' n/ M
child had grown 2.5 cm in 4 months and had gained
" o$ v9 E; m7 b. W: u" [8 k) R2 kg of weight. Physical examination remained3 p; U0 q7 k1 s& _9 @7 k
unchanged. Surprisingly, the pubic hair almost com-- R& A4 S! {4 s8 L8 T" y  A! ?
pletely disappeared except for a few vellous hairs at/ n0 s2 y. W6 Q5 [" M/ l2 Y$ X
the base of the phallus. Testicular volume was still 20 ~# W! [9 f- ^' X7 n! p& p
mL, and the size of the penis remained unchanged.
. b& @5 t$ v% }" w1 T2 |( qThe mother also said that the boy was no longer hav-
9 L2 B0 R6 Q8 O% y( Ving frequent erections.
3 ~$ i; S" n4 I1 RBoth parents were again questioned about use of
  r* o. R7 n8 C( N4 ?+ Many ointment/creams that they may have applied to
' Q* p- p9 j, ?$ {the child’s skin. This time the father admitted the
7 Y$ y- H9 I; n' ]* _8 fTopical Testosterone Exposure / Bhowmick et al 5413 t9 Y! h# o6 c( p) F
use of testosterone gel twice daily that he was apply-) m. s4 d. s. P
ing over his own shoulders, chest, and back area for9 o5 ~  i' a4 k: ~" w1 q4 G2 K) H
a year. The father also revealed he was embarrassed
. y2 R, R# O. T- Bto disclose that he was using a testosterone gel pre-
% \. E8 C8 a5 n4 l) Vscribed by his family physician for decreased libido
- t5 F1 y1 E: x% dsecondary to depression.; n; p6 Q0 J  y6 t( F% ^2 g
The child slept in the same bed with parents.
" d7 i' O! j. [" [  ~& [. cThe father would hug the baby and hold him on his1 N) G2 G* i- v! `
chest for a considerable period of time, causing sig-
2 a' C& Z8 J! t0 f  g) R+ }nificant bare skin contact between baby and father.
/ C$ G6 |5 O5 p# LThe father also admitted that after the phone call,
( V9 E5 J4 Q4 Y; Iwhen he learned the testosterone level in the baby
" @: `8 M" r( z) H5 G! P( |was high, he then read the product information6 g1 @% Z; U) F; R$ z
packet and concluded that it was most likely the rea-
6 J, Q, {# A" U1 j7 E* [$ fson for the child’s virilization. At that time, they
7 o5 F  i* v0 F* W5 p+ M/ p+ {# Xdecided to put the baby in a separate bed, and the* w* K4 F8 l; R* l' Y5 J" c
father was not hugging him with bare skin and had
8 U$ T, X- j8 |) H. u7 b1 ybeen using protective clothing. A repeat testosterone
( z: \' g% O" _1 Q/ M" _test was ordered, but the family did not go to the9 P2 C' u& r, m5 Y8 O- Y$ g
laboratory to obtain the test.
! s$ U, j# s- i" ^Discussion
9 a; b# a' T! gPrecocious puberty in boys is defined as secondary( N' P! q/ F. [/ a  `
sexual development before 9 years of age.1,4! ?5 i; M2 a- j4 ^7 X( T
Precocious puberty is termed as central (true) when
) h& T8 ?7 k! \1 m. iit is caused by the premature activation of hypo-
* J$ E. Y& L/ P) e1 Rthalamic pituitary gonadal axis. CPP is more com-+ Q- Q" A# e6 |6 T( [; _
mon in girls than in boys.1,3 Most boys with CPP$ ^  a/ m. k5 t
may have a central nervous system lesion that is8 I, X7 r/ W2 W7 D
responsible for the early activation of the hypothal-
. P% }8 w& k, z( {; ~amic pituitary gonadal axis.1-3 Thus, greater empha-. q6 _0 w( z2 E: ^5 B/ ~, @: T. G  a% H
sis has been given to neuroradiologic imaging in
8 j- l% c  J' }5 D1 k' C$ vboys with precocious puberty. In addition to viril-2 ?  r5 h( m5 ]( o2 M4 o3 S
ization, the clinical hallmark of CPP is the symmet-+ C: X, }; a! j
rical testicular growth secondary to stimulation by3 W7 ]; }8 \8 J/ [; W: F
gonadotropins.1,33 c, P4 a/ [0 _5 e: m
Gonadotropin-independent peripheral preco-
! N6 _, U5 x# r+ Mcious puberty in boys also results from inappropriate
- d% Y$ _( R1 O' P. V4 G4 _) D9 Xandrogenic stimulation from either endogenous or! m% c) b+ p1 ~: n. A  Y2 [
exogenous sources, nonpituitary gonadotropin stim-
) @3 Z' o& j6 `- c1 Aulation, and rare activating mutations.3 Virilizing
7 Q7 a4 g8 t7 U2 {congenital adrenal hyperplasia producing excessive, j; g) D# _8 L- T: b+ H
adrenal androgens is a common cause of precocious' ~+ O2 @- t: c
puberty in boys.3,4% M. V9 h% Q  U" }+ n& l: e7 f' R
The most common form of congenital adrenal# O2 K- e2 W6 t8 t
hyperplasia is the 21-hydroxylase enzyme deficiency.( v; t8 Z8 G( k/ u( s$ n
The 11-β hydroxylase deficiency may also result in- g- N/ r" m) z! y- r5 R0 y
excessive adrenal androgen production, and rarely,
+ A3 z: m9 S7 X8 ~. Y& r4 f( |  m9 Pan adrenal tumor may also cause adrenal androgen
- g8 y6 y& ]& l! T! [" vexcess.1,3
6 ]' ^: x9 a2 y: v+ Y& _$ r/ Sat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 i; h) w8 K6 G9 l; q3 z
542 Clinical Pediatrics / Vol. 46, No. 6, July 20077 t& n# F, q8 D$ ~5 j7 L
A unique entity of male-limited gonadotropin-
, j; J! N/ a+ D  Eindependent precocious puberty, which is also known! B0 V/ [* D. |( {/ j  w
as testotoxicosis, may cause precocious puberty at a
- o- E' V) f7 q5 I3 ?very young age. The physical findings in these boys
4 i  R- W' C' `with this disorder are full pubertal development,
: h( H  |3 {6 f4 mincluding bilateral testicular growth, similar to boys3 n9 h( `* d$ |, B, P
with CPP. The gonadotropin levels in this disorder
% M  f6 z1 R- q8 H7 V& care suppressed to prepubertal levels and do not show
0 s( U0 D6 n" J6 f+ xpubertal response of gonadotropin after gonadotropin-
' J- g" F  e1 X1 s# nreleasing hormone stimulation. This is a sex-linked7 g6 V& x. o, p5 w/ k$ j
autosomal dominant disorder that affects only
! I% G4 A2 H$ s0 j. a$ a: u9 Mmales; therefore, other male members of the family3 J8 O' u% T7 o( Q; K. q9 N
may have similar precocious puberty.3! @0 D! A( y$ Y# m
In our patient, physical examination was incon-9 C5 C' R, p. J
sistent with true precocious puberty since his testi-
1 [/ G4 Z+ h# e& Ocles were prepubertal in size. However, testotoxicosis3 {3 r- R2 w5 i3 i
was in the differential diagnosis because his father& Z2 V' n7 n* G. {' o  B
started puberty somewhat early, and occasionally,
9 I6 ~$ v0 v- c7 Stesticular enlargement is not that evident in the8 C' a( J5 }, l' m  W5 c" X5 W
beginning of this process.1 In the absence of a neg-
0 u  a' s8 |% N& E4 {( L% f% jative initial history of androgen exposure, our/ {( {2 K% q9 E- e" b3 ]
biggest concern was virilizing adrenal hyperplasia,4 m4 @4 d+ T3 [* F! m" Z6 x1 Z
either 21-hydroxylase deficiency or 11-β hydroxylase
# }+ D2 \6 y. }0 N% r7 jdeficiency. Those diagnoses were excluded by find-
0 G: \% r8 o1 `# s# R* Fing the normal level of adrenal steroids.
" c& ?* N* n  s  X. ]The diagnosis of exogenous androgens was strongly
* H6 D% c3 `# ~/ J, lsuspected in a follow-up visit after 4 months because
0 L) a( i' H6 X1 j9 F& J& g! Hthe physical examination revealed the complete disap-
+ k" B5 p2 w- \" Dpearance of pubic hair, normal growth velocity, and6 {& U2 |' y' @  |
decreased erections. The father admitted using a testos-& e3 ]6 M# i, ?) X+ N# E
terone gel, which he concealed at first visit. He was8 ?5 c! P+ G7 j5 O% D& @& p2 E
using it rather frequently, twice a day. The Physicians’
9 ^( k) B' N. n1 b3 O) w! X( |Desk Reference, or package insert of this product, gel or  r! F7 \* i2 [/ k% m% H
cream, cautions about dermal testosterone transfer to
9 d3 X$ C$ v- k6 C# c! Ounprotected females through direct skin exposure.
1 X5 h: u1 `/ @Serum testosterone level was found to be 2 times the
3 w/ q( ^$ I2 f2 T  ?- C) z, Nbaseline value in those females who were exposed to+ R) j2 J: }/ I
even 15 minutes of direct skin contact with their male3 Y1 A, G; `& ~1 k
partners.6 However, when a shirt covered the applica-6 `/ G) d& K, p- w5 y& b8 d* R
tion site, this testosterone transfer was prevented.
6 q$ w1 l* h  Y: NOur patient’s testosterone level was 60 ng/mL,5 h& {8 h7 G3 \0 ]6 i, t' W
which was clearly high. Some studies suggest that
( L3 }' P# {9 K, M$ Ndermal conversion of testosterone to dihydrotestos-8 b& X6 R+ n7 ~" V/ ]- N
terone, which is a more potent metabolite, is more
* g* [+ d3 `/ k0 Vactive in young children exposed to testosterone& q: D3 `0 Y$ E5 e
exogenously7; however, we did not measure a dihy-
5 E: A2 U- d4 }) I: ~6 C4 udrotestosterone level in our patient. In addition to
8 V2 c' f& q2 Gvirilization, exposure to exogenous testosterone in
5 c; _5 k/ q7 pchildren results in an increase in growth velocity and- u9 Q) n# T3 K) k+ _+ a, f# H
advanced bone age, as seen in our patient.
, Q! d! i4 g$ B3 J5 }, gThe long-term effect of androgen exposure during
" J; |9 o+ K4 l2 [$ z' nearly childhood on pubertal development and final+ v$ t: k4 n- G
adult height are not fully known and always remain/ w1 |  D& j7 z+ n6 R
a concern. Children treated with short-term testos-
6 R1 x+ x: W8 k1 T7 B, Yterone injection or topical androgen may exhibit some
& K$ N( r0 Y1 |) @% Dacceleration of the skeletal maturation; however, after
2 H7 F. H% A3 T/ I& R8 z+ E1 }cessation of treatment, the rate of bone maturation
3 S+ ~$ I* h, u0 T) l7 y! H& ?decelerates and gradually returns to normal.8,9* B! C1 ^5 g# ^; l
There are conflicting reports and controversy% M( o' f8 s8 I# i+ E7 d
over the effect of early androgen exposure on adult
+ N3 W& g( M' h5 }' H: }% L5 D1 upenile length.10,11 Some reports suggest subnormal
4 V/ a6 D9 t3 n. v5 x* dadult penile length, apparently because of downreg-: |8 P  H4 [  F
ulation of androgen receptor number.10,12 However,! w! K4 v& o4 w0 {9 G5 c
Sutherland et al13 did not find a correlation between- B* v% D0 B4 H5 _9 ^! b0 p7 ~
childhood testosterone exposure and reduced adult* \; {+ D- }* U0 \
penile length in clinical studies.1 @% ~* G9 _+ \* K; r% F6 c3 ^9 U
Nonetheless, we do not believe our patient is
. a2 F, b6 b+ b: d9 `going to experience any of the untoward effects from
: k1 x/ h4 e( \# R" F  U; Ntestosterone exposure as mentioned earlier because
+ ]0 j' b+ K( @6 L' L6 ethe exposure was not for a prolonged period of time.
; I* k5 _2 u; \" L! o" O* CAlthough the bone age was advanced at the time of
7 T& r, r) O2 V9 }+ ^diagnosis, the child had a normal growth velocity at
9 \2 u* p; E$ i' N; X6 Pthe follow-up visit. It is hoped that his final adult
4 t. L. X- B+ y! \0 x) xheight will not be affected.3 H# \# S/ e! z; x6 I
Although rarely reported, the widespread avail-
" y: f$ t0 h+ W0 d3 `* Vability of androgen products in our society may
. D( s8 v% t% s3 V; q3 l, m/ eindeed cause more virilization in male or female
8 c; V) W6 B) t- X3 D" A1 zchildren than one would realize. Exposure to andro-
$ V5 `$ E( D" M- Kgen products must be considered and specific ques-
5 r, m8 x# o( d; F. C- wtioning about the use of a testosterone product or
5 r9 R+ v; E5 F! H8 k" ^( e, ugel should be asked of the family members during
6 ^' i1 R4 ~6 ithe evaluation of any children who present with vir-% R; A/ r$ z9 y. C7 }* g, z
ilization or peripheral precocious puberty. The diag-
6 z+ Q5 k' v5 d! R2 ?2 |nosis can be established by just a few tests and by
0 f: ~% Z* D6 N2 c. Z5 Cappropriate history. The inability to obtain such a2 J2 W8 {  B& ]0 W, _+ M
history, or failure to ask the specific questions, may, ^  n; b7 M7 e* B
result in extensive, unnecessary, and expensive
2 `, @+ F$ [8 z. w/ h. g0 Iinvestigation. The primary care physician should be
) t2 T- V. T9 B' E+ |aware of this fact, because most of these children
  o  E9 k6 f" [" ^) K4 F9 T4 kmay initially present in their practice. The Physicians’
  H6 X7 w" _; k3 i/ o9 jDesk Reference and package insert should also put a" z- w. Z3 }- U! f* m  |
warning about the virilizing effect on a male or
4 [9 a" d. j0 @female child who might come in contact with some-$ |& D: Y0 U# O& |
one using any of these products.7 Z( k( }+ d3 j8 n2 O9 K$ y8 U
References
- ]3 }1 Z' |% C  s  T8 i( c1. Styne DM. The testes: disorder of sexual differentiation/ u5 Z0 e9 g. M, a# B
and puberty in the male. In: Sperling MA, ed. Pediatric
4 @( U, M3 T. R$ V6 x5 yEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;" I/ n' w4 W  p1 X% ^
2002: 565-628.2 Z  q) X9 H4 ?; ?6 y2 M
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious) o9 f' K2 d- r3 Z0 T, v
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

2 e$ p; U  P! O; J( `6 `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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