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Sexual Precocity in a 16-Month-Old! Q) C0 g& N+ u7 b0 _
Boy Induced by Indirect Topical$ M! L( v/ X; j. Q1 m
Exposure to Testosterone
* a' ]' O) T5 y7 E1 n' RSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2* P- s2 L: [' l- S2 w
and Kenneth R. Rettig, MD1
: e9 q0 v9 Y( W4 n+ s+ FClinical Pediatrics; s& `8 e( |* y6 g
Volume 46 Number 64 e: K  o8 K+ T/ z5 @; j! K
July 2007 540-543" ?5 j% P& Q4 J7 M5 A
© 2007 Sage Publications
: S+ j7 n! k1 T' }3 g) A# A10.1177/0009922806296651
* H5 A: L5 U+ C6 H6 ^http://clp.sagepub.com" P' N8 u8 q6 n9 i1 P3 N% `
hosted at
5 l, H" ^5 w: T1 k# a% d  O8 Yhttp://online.sagepub.com5 m; K- |; I+ I, W# p  z3 Z8 }# Q
Precocious puberty in boys, central or peripheral,
# N& |: e/ M; u2 X( @# Yis a significant concern for physicians. Central
$ b6 O2 m; u- W6 w* Eprecocious puberty (CPP), which is mediated
: Y$ p" V# j& q; Athrough the hypothalamic pituitary gonadal axis, has
1 Z* |' K" s2 U9 Q% Na higher incidence of organic central nervous system
* A; H7 s. z$ [: Hlesions in boys.1,2 Virilization in boys, as manifested7 @2 m+ M/ h7 B9 ], t4 U, \
by enlargement of the penis, development of pubic6 u8 n- t; ~% `7 f
hair, and facial acne without enlargement of testi-
/ S1 ^2 l1 ^6 p/ d& y/ F: ~cles, suggests peripheral or pseudopuberty.1-3 We& j& M* y9 C. |. e8 _" p
report a 16-month-old boy who presented with the; a* ~' C" Q2 [$ I% |; s& f, Z" }
enlargement of the phallus and pubic hair develop-
, b9 U, p: L8 ^) I# Xment without testicular enlargement, which was due
* g  |5 ?/ w/ rto the unintentional exposure to androgen gel used by
& k+ l; `, j2 t7 k2 x" G8 V9 M% Wthe father. The family initially concealed this infor-' z. A+ Q" e' P" @+ W2 M2 C* ?
mation, resulting in an extensive work-up for this
( t& {; D& p( bchild. Given the widespread and easy availability of
+ x3 p& c) |  a: S- B8 Itestosterone gel and cream, we believe this is proba-
) q. I8 I( l6 ^* ^bly more common than the rare case report in the
' W  |% W+ Y$ v  k1 e) fliterature.46 a, I0 r1 q1 f/ _. C" m) v3 N
Patient Report
' s7 J. A2 A$ i7 {5 p, A3 ]* W; d* OA 16-month-old white child was referred to the
% q. \. W! K* h6 C& t  `* D5 zendocrine clinic by his pediatrician with the concern
1 P! N2 w% I  M' c- Xof early sexual development. His mother noticed1 |; C' t, q2 `6 d3 Z
light colored pubic hair development when he was; @% t+ b- R/ d8 H7 @
From the 1Division of Pediatric Endocrinology, 2University of
; |  c6 {0 m1 ~4 Q! d& WSouth Alabama Medical Center, Mobile, Alabama.2 H& n. x" l. F7 U7 `3 P
Address correspondence to: Samar K. Bhowmick, MD, FACE,
% Q" @1 j2 [4 F! R: z6 A( K& @Professor of Pediatrics, University of South Alabama, College of
% i% ^9 Y# o# o6 P- WMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
6 H+ t6 r( o; U. se-mail: [email protected].
; p4 I6 q' \, e/ g! `about 6 to 7 months old, which progressively became
& `1 B1 R$ q4 C) ^& bdarker. She was also concerned about the enlarge-' ~2 C# y* m2 L% G* C
ment of his penis and frequent erections. The child; C* h: s, g5 f
was the product of a full-term normal delivery, with
9 N+ F) X# j* D4 T* h  c  U4 Ba birth weight of 7 lb 14 oz, and birth length of
: y+ V2 x3 W, T2 K2 C: Y20 inches. He was breast-fed throughout the first year
6 K7 M. c% I( l# U' b# Qof life and was still receiving breast milk along with: i% z. y; j7 M6 I) S: N  D
solid food. He had no hospitalizations or surgery,
3 [  N5 D* J# J5 D! M6 D- Aand his psychosocial and psychomotor development
( R' r8 t: A: p3 L/ \! v! \5 [' ewas age appropriate.( p6 c, Z) N( {1 E7 B6 N9 p. F
The family history was remarkable for the father,  E4 N8 [/ S3 ?( M; ^
who was diagnosed with hypothyroidism at age 16,
/ h! [  V4 H; ?6 X" Xwhich was treated with thyroxine. The father’s( O7 ]  j  r2 X1 S0 Y
height was 6 feet, and he went through a somewhat
. F$ V4 j5 i- G. w2 eearly puberty and had stopped growing by age 14.
% |1 k/ J0 h7 H% {2 @# X6 a% ~The father denied taking any other medication. The
3 D+ H' h) H$ r. R& {/ Z1 Zchild’s mother was in good health. Her menarche
" L9 O. _% |$ v1 {7 zwas at 11 years of age, and her height was at 5 feet" T! Y# z: s# x: R
5 inches. There was no other family history of pre-* R, t" a+ g. s6 ]' O# z  G
cocious sexual development in the first-degree rela-  B  g4 j% o, U+ ~
tives. There were no siblings.3 k. i$ ~1 Y, X5 w- {
Physical Examination
6 H' q) S+ q$ ~0 ^  [4 UThe physical examination revealed a very active,
4 h  N0 Z  V- g: Xplayful, and healthy boy. The vital signs documented9 A* H$ Q: _. d2 R4 d
a blood pressure of 85/50 mm Hg, his length was
6 q( l2 }1 L! \" E6 e- ?90 cm (>97th percentile), and his weight was 14.4 kg8 v) J; k1 Z" b9 W  \& m! ~0 E
(also >97th percentile). The observed yearly growth. o& X' y: j6 K8 w$ R$ H5 s
velocity was 30 cm (12 inches). The examination of- u9 M; @( u$ J* i& s* F
the neck revealed no thyroid enlargement.0 Q7 W: P2 Q! U6 |! M
The genitourinary examination was remarkable for
' W# h# z( Z' T% q8 w0 {enlargement of the penis, with a stretched length of
2 P; {3 |, X' S8 cm and a width of 2 cm. The glans penis was very well$ R1 J5 @: X8 C1 z$ b# ^( r8 R, ]
developed. The pubic hair was Tanner II, mostly around" F5 h1 S/ R! H4 V% L: H5 K7 ^
540' t2 y2 v( f! A+ V/ [8 l/ _9 }
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 v  M5 B* X* ~6 H
the base of the phallus and was dark and curled. The
0 |2 s+ y9 m  k+ p) e, utesticular volume was prepubertal at 2 mL each.
0 w$ n% b# ~0 g8 C6 Z/ T1 P% t4 JThe skin was moist and smooth and somewhat0 h" J/ F- \# Q0 o  c* I
oily. No axillary hair was noted. There were no2 B$ R( X. ]( x% |) b
abnormal skin pigmentations or café-au-lait spots.- U& o+ q' t' C, }9 ~5 J
Neurologic evaluation showed deep tendon reflex 2+" m. |. u2 p! w/ O7 N# N
bilateral and symmetrical. There was no suggestion# w& k* Q$ Q1 {0 T4 _0 h
of papilledema.& M7 N. Q8 F. D5 S# v
Laboratory Evaluation: J9 Q9 g6 E0 m; w# A8 _0 E
The bone age was consistent with 28 months by
! n" s+ h; E2 ~3 i7 Busing the standard of Greulich and Pyle at a chrono-
6 [; D8 X3 z' Q4 i8 _logic age of 16 months (advanced).5 Chromosomal
. q3 `3 g) C. e9 L  a* I9 k) nkaryotype was 46XY. The thyroid function test
  j4 G8 Q% Z# ]' z/ C  k$ X0 @showed a free T4 of 1.69 ng/dL, and thyroid stimu-1 r9 {( ~4 v2 h0 M. c* X, ?! k
lating hormone level was 1.3 µIU/mL (both normal).  z5 l, ?$ u3 |- L
The concentrations of serum electrolytes, blood
3 w& K; H) O2 D! {7 xurea nitrogen, creatinine, and calcium all were/ q3 G' p- g" {8 U
within normal range for his age. The concentration
7 ?6 A% M4 Q7 e7 H4 ]& l) p* b, R) [of serum 17-hydroxyprogesterone was 16 ng/dL
- h$ {& o- I3 |. w; T. N# S' ]6 x(normal, 3 to 90 ng/dL), androstenedione was 20
7 T0 j' w+ M3 S$ d$ O, t# Ong/dL (normal, 18 to 80 ng/dL), dehydroepiandros-' m5 Q3 W) }7 e
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
: f) b( a1 `9 }3 A. B6 ~! C) |: u& [desoxycorticosterone was 4.3 ng/dL (normal, 7 to
: W% N. @6 p5 n2 \1 D2 `* w+ U49ng/dL), 11-desoxycortisol (specific compound S)* z% s( Q% M6 p) }
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
/ a" E+ G. R# ktisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
% I9 Q- `+ C: h; Ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
' v% ]9 g9 S( i2 L) Eand β-human chorionic gonadotropin was less than/ w0 d, v5 w7 D8 @. f
5 mIU/mL (normal <5 mIU/mL). Serum follicular/ @' W8 K  j1 S0 M6 n0 A/ s8 s
stimulating hormone and leuteinizing hormone1 J& t, p( S& \# n- O3 ~# x
concentrations were less than 0.05 mIU/mL9 p: K' H% u6 t
(prepubertal).
' m+ ~0 B" x! ]% M* oThe parents were notified about the laboratory  P/ A0 N. N$ J3 Y6 M, ^
results and were informed that all of the tests were3 [5 [! P6 d  m6 m0 D
normal except the testosterone level was high. The5 z, p/ \- r; ~$ V8 W! w
follow-up visit was arranged within a few weeks to0 P" `, q- r3 z3 f' D  A$ D
obtain testicular and abdominal sonograms; how-0 Z1 M0 k9 ]; b, F/ N" L
ever, the family did not return for 4 months.( M5 U: n, k8 n; l% d
Physical examination at this time revealed that the
& Z& r2 V; ?' ~' g0 dchild had grown 2.5 cm in 4 months and had gained
6 \) G% z+ y7 y; x# v2 kg of weight. Physical examination remained
  j0 e0 I4 A, z$ _! N9 Sunchanged. Surprisingly, the pubic hair almost com-
1 M9 `! ?8 @, jpletely disappeared except for a few vellous hairs at- U$ [) d" H! ?4 i6 e5 c5 c( v/ x5 O
the base of the phallus. Testicular volume was still 2
& Z$ U% T' E* Z4 I" z1 C* RmL, and the size of the penis remained unchanged.
/ Z$ J, Y$ W) ?% V/ V6 YThe mother also said that the boy was no longer hav-
& L7 P! n* v1 }& xing frequent erections.
3 {3 R6 v; h: z% D" W: d& R) P) VBoth parents were again questioned about use of
. a6 Y7 v: M. m9 {% |any ointment/creams that they may have applied to6 }) s) g. i6 \$ G" R6 D6 f* ]; @
the child’s skin. This time the father admitted the
( B, p7 {" ^" ]Topical Testosterone Exposure / Bhowmick et al 541
4 |1 z0 d8 ^# J) r( k' V( [  suse of testosterone gel twice daily that he was apply-. a0 `* G5 P& e
ing over his own shoulders, chest, and back area for
) P  {. ~% z% c3 q. L7 ea year. The father also revealed he was embarrassed2 [8 c$ |5 A# |5 T3 e
to disclose that he was using a testosterone gel pre-
% |9 H( r* H$ j  i$ u8 o' ?, ?3 ?8 z2 |scribed by his family physician for decreased libido
, C2 N1 A7 g  H( D7 ssecondary to depression.
& R& N0 `; b& \The child slept in the same bed with parents.$ Z; H& f4 K" `/ r
The father would hug the baby and hold him on his
+ J, z! C0 F8 C# zchest for a considerable period of time, causing sig-
7 L& T5 i3 g8 q& Y2 Y$ w1 k! xnificant bare skin contact between baby and father.
/ |9 Q  r) h' g  U9 GThe father also admitted that after the phone call,
4 z& @" ~9 ^- twhen he learned the testosterone level in the baby
. x1 K: d# u& e/ b$ Z2 Awas high, he then read the product information2 h% a! u$ |5 @- ?& i
packet and concluded that it was most likely the rea-
9 F& A' ~" m7 g+ m/ E' L' p# tson for the child’s virilization. At that time, they$ z  s# M: \; ?0 W& I# ]
decided to put the baby in a separate bed, and the! r  |6 w% w: D
father was not hugging him with bare skin and had
4 Q$ ]  J' \+ [  d* Ubeen using protective clothing. A repeat testosterone
4 h9 B9 j% b) a+ p% d: K' htest was ordered, but the family did not go to the3 l& d# g4 H+ \2 K, I0 ^, {$ c
laboratory to obtain the test.
. S! I) K( ]2 q8 JDiscussion
! j8 V5 a. ^5 S6 PPrecocious puberty in boys is defined as secondary0 {6 w2 R. o; K5 {- }! U9 b2 n" t
sexual development before 9 years of age.1,48 M) T, f" \  j1 R2 x7 A
Precocious puberty is termed as central (true) when
4 g  ^; a- k" l0 `* L7 _it is caused by the premature activation of hypo-
& ^+ E4 H5 x0 ?: _( d/ z/ Tthalamic pituitary gonadal axis. CPP is more com-
" s( x* w+ T% }% q& d2 _mon in girls than in boys.1,3 Most boys with CPP/ D6 w/ {3 j4 z9 v/ R: w8 _
may have a central nervous system lesion that is' _& y1 C; X" `# \
responsible for the early activation of the hypothal-
: M9 X9 f" J$ E9 F# }7 ~amic pituitary gonadal axis.1-3 Thus, greater empha-7 |1 [7 h$ r1 T5 c- O3 x
sis has been given to neuroradiologic imaging in
* T: Y/ I) o# F; H) [6 E6 l' cboys with precocious puberty. In addition to viril-
3 `" S- e3 z' |5 N* iization, the clinical hallmark of CPP is the symmet-
7 s2 M+ \' C% I7 m. E4 Srical testicular growth secondary to stimulation by  p6 ~" C3 I6 i9 ^
gonadotropins.1,3
" t6 w1 P6 D( T! ]- [Gonadotropin-independent peripheral preco-
, J' h) q) D! p# g0 ?4 `cious puberty in boys also results from inappropriate
  k- G* [% o  T0 V4 M4 h2 O5 H8 z8 K! jandrogenic stimulation from either endogenous or
. Q: q, H4 Q- Q7 l3 [+ c8 b+ pexogenous sources, nonpituitary gonadotropin stim-
5 o4 [3 m$ ^  W% {6 V4 v0 \ulation, and rare activating mutations.3 Virilizing
7 |0 b1 n. {) _5 @( g+ O* Xcongenital adrenal hyperplasia producing excessive
8 s; R( |$ H& x! [; A2 {adrenal androgens is a common cause of precocious
2 e# }% ]  x1 c; {puberty in boys.3,4
! w* B/ c3 S7 B! D% f9 ~2 Q) e. ^9 `The most common form of congenital adrenal
/ O/ [( o& J* i, whyperplasia is the 21-hydroxylase enzyme deficiency.$ d$ G' L  Z3 A+ j" N. q
The 11-β hydroxylase deficiency may also result in9 u* v' i0 g8 x) C' a5 K9 Y1 B
excessive adrenal androgen production, and rarely,' I) O, l  v, C* h8 \  _/ I& T
an adrenal tumor may also cause adrenal androgen
7 P; y4 w; w6 z5 pexcess.1,3
. Z3 ~/ \( t6 X$ hat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 R/ |, D) Y( B3 H542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
% E$ T: m5 ]+ F+ J# }9 a2 k$ s+ xA unique entity of male-limited gonadotropin-
! i: t" [' ]8 D" O6 B6 @% \1 `+ Bindependent precocious puberty, which is also known
! W5 W6 j6 z! R5 s1 z( H0 ?! b! gas testotoxicosis, may cause precocious puberty at a
& R2 K- c1 }" p6 _+ r" ~* fvery young age. The physical findings in these boys
: x& p5 X1 a7 s# Swith this disorder are full pubertal development,
1 H8 b' K3 _4 x# zincluding bilateral testicular growth, similar to boys/ F6 [9 k+ |+ h! f
with CPP. The gonadotropin levels in this disorder
0 r1 ~0 ~+ A; y+ G1 [5 ?are suppressed to prepubertal levels and do not show
+ E6 m9 c; L6 ppubertal response of gonadotropin after gonadotropin-
& f7 u9 U/ ~6 M( G: F7 |; v7 q8 G' Treleasing hormone stimulation. This is a sex-linked5 `0 m5 _5 @( r8 ]
autosomal dominant disorder that affects only
8 ^) w6 C4 X/ S, pmales; therefore, other male members of the family; h- U# x& H& m
may have similar precocious puberty.3
( F; j2 Y. a- y( ~4 WIn our patient, physical examination was incon-# K+ u& ]( z2 D2 O/ S9 }8 P! p
sistent with true precocious puberty since his testi-  f" Z# s2 l) J
cles were prepubertal in size. However, testotoxicosis* N, q! Z6 b  a; ?% U9 m, Q; J
was in the differential diagnosis because his father2 _4 b! |" `( w9 B0 B3 m
started puberty somewhat early, and occasionally,
2 H. h, A7 N$ W4 z% Btesticular enlargement is not that evident in the
2 d9 H2 `* P! T0 v) t  Ybeginning of this process.1 In the absence of a neg-3 N  M: N! M: x1 v' Y4 O0 g
ative initial history of androgen exposure, our+ {! o0 w1 J' W* `/ J% y0 ^1 X
biggest concern was virilizing adrenal hyperplasia,) \! q( O2 K9 R9 O- N* W  {
either 21-hydroxylase deficiency or 11-β hydroxylase: N* _" R# Q3 |; M3 J' A4 j- ~
deficiency. Those diagnoses were excluded by find-8 F  q! k. c! T
ing the normal level of adrenal steroids.
; e9 f) S  a, d; ?6 a# s- L! g: [The diagnosis of exogenous androgens was strongly4 _7 T8 K  f4 T5 }1 N& a1 v
suspected in a follow-up visit after 4 months because& a# y: k! K  m
the physical examination revealed the complete disap-; ^6 x+ _$ w  _* d5 h: i
pearance of pubic hair, normal growth velocity, and
2 |' Y4 l% U& ?2 I  k+ u: xdecreased erections. The father admitted using a testos-
, K9 t1 O* y4 `9 n* Gterone gel, which he concealed at first visit. He was7 Y" D9 _% U2 V! W" G5 T* D( ^
using it rather frequently, twice a day. The Physicians’4 @  `1 }7 ^$ U, z! c
Desk Reference, or package insert of this product, gel or
2 k+ `7 ]6 o6 X- v2 \! icream, cautions about dermal testosterone transfer to. T; _$ L$ V: _( K# L, {9 R3 H
unprotected females through direct skin exposure.1 U# x& g8 q- Z- C* d* i
Serum testosterone level was found to be 2 times the
; r( y/ \! o( q7 R/ O4 I% Vbaseline value in those females who were exposed to
6 N- r3 H7 R' \/ t* F3 Oeven 15 minutes of direct skin contact with their male; i) ^& {& f/ }9 k
partners.6 However, when a shirt covered the applica-
( P8 Z1 c2 A9 K+ R8 [* U$ Htion site, this testosterone transfer was prevented.
- L, W# W5 r& ~- u+ m$ A, ZOur patient’s testosterone level was 60 ng/mL,
0 K0 @7 j; I! h' \- ywhich was clearly high. Some studies suggest that
  |7 Z0 b3 [: H6 t  K$ l5 Odermal conversion of testosterone to dihydrotestos-  j4 L* P! p, \2 g5 C+ r1 z
terone, which is a more potent metabolite, is more
; s/ h4 q$ X6 h/ |active in young children exposed to testosterone: i. J% Z/ g" E% d6 p# W' b
exogenously7; however, we did not measure a dihy-
/ K8 l" y& ]8 q1 ?& M& odrotestosterone level in our patient. In addition to
+ T; d6 \3 B3 H' m- u  gvirilization, exposure to exogenous testosterone in$ a# e5 h! V1 h, G* U9 G4 m
children results in an increase in growth velocity and
" \' G3 h8 w- S; zadvanced bone age, as seen in our patient.
8 d& _5 O- C; P" M! dThe long-term effect of androgen exposure during
( h+ n7 q1 o. h" Q3 a: {7 Bearly childhood on pubertal development and final
0 p( ?2 O) G  H8 u7 {adult height are not fully known and always remain
  j# P/ y: U. U; h( ra concern. Children treated with short-term testos-
% F* y' W: x. b" ~: m# Bterone injection or topical androgen may exhibit some) [7 J4 @2 H' x
acceleration of the skeletal maturation; however, after
4 p( u$ \0 }; X) P6 F# ccessation of treatment, the rate of bone maturation
5 s9 ~$ n; Y0 {& C! \" c; Cdecelerates and gradually returns to normal.8,93 B) X1 Z# K) u& Z
There are conflicting reports and controversy- u5 R- [8 O4 c$ f# n& k  o
over the effect of early androgen exposure on adult8 P. K5 r6 _7 m! [5 g- M! N
penile length.10,11 Some reports suggest subnormal6 @: @( O/ ~4 h  j9 l$ W# b
adult penile length, apparently because of downreg-. K% N! n+ e2 e2 R2 v
ulation of androgen receptor number.10,12 However,2 [$ f$ w, F* o& j% p; S+ {: u
Sutherland et al13 did not find a correlation between. `! y! ]% X8 g4 I1 P9 q
childhood testosterone exposure and reduced adult
& A6 w9 q) S! b8 w: \3 ~' Gpenile length in clinical studies.
% i4 G; S: }9 VNonetheless, we do not believe our patient is1 e# p$ Q) v1 I- d; K
going to experience any of the untoward effects from1 q/ C4 x& q1 i5 l
testosterone exposure as mentioned earlier because
' s" q; k  W0 i$ h0 k/ Ithe exposure was not for a prolonged period of time.' I: T9 E& m! V1 S" Q. P. i( u' A3 `
Although the bone age was advanced at the time of
4 T. t) A- p0 l9 z7 pdiagnosis, the child had a normal growth velocity at
8 M, U, ]; s. lthe follow-up visit. It is hoped that his final adult
' G& n! `  v  j- H2 y0 s! w- sheight will not be affected.
" F  v5 d' I/ ^7 jAlthough rarely reported, the widespread avail-
8 ?3 H# v. I2 h$ hability of androgen products in our society may$ O+ r, U4 [- d+ ]
indeed cause more virilization in male or female3 D% [) q8 M/ v9 _' C# l7 j
children than one would realize. Exposure to andro-
! T' l9 i- i. a4 f, i, ?gen products must be considered and specific ques-2 ]4 j7 E* o7 m1 R  d- ~2 j6 ^! @
tioning about the use of a testosterone product or% X; T/ l$ f% {) A4 Z
gel should be asked of the family members during2 E2 E* q! a8 T; Q* ^3 z' r+ M/ W% S
the evaluation of any children who present with vir-
% k0 S$ {$ h% l" E$ m, `ilization or peripheral precocious puberty. The diag-
/ l4 g, T7 n8 fnosis can be established by just a few tests and by* M: h# y5 o2 ?$ m
appropriate history. The inability to obtain such a
: j0 {! m$ h4 c; m6 O2 h$ thistory, or failure to ask the specific questions, may! p2 Y" S5 M9 j! \  I. ?+ {5 R% ]
result in extensive, unnecessary, and expensive8 v  Y$ ^! k( b' D3 d! n. y: D
investigation. The primary care physician should be
, w8 H* p2 W5 Aaware of this fact, because most of these children
3 v9 A" V+ x0 ymay initially present in their practice. The Physicians’
2 i% `& C6 e& P% Q$ M# n0 D/ b  I6 GDesk Reference and package insert should also put a% ~* Y* K/ i- O( C, D6 Z
warning about the virilizing effect on a male or
0 C' h  p/ h: X; B4 ~3 Jfemale child who might come in contact with some-
# E. q" T  u9 ?1 v" o1 \3 aone using any of these products.: J, t& ^( n$ z
References9 Q# e/ ]2 V3 ?# g% X
1. Styne DM. The testes: disorder of sexual differentiation
$ M- [8 N7 t7 c" A9 R& i/ J; rand puberty in the male. In: Sperling MA, ed. Pediatric
. v4 j) e: s; P3 s" R( Y9 S1 zEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
) G+ n6 y) H, [* M2002: 565-628.
( A0 \$ M# n5 J/ v! B8 a- H2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 Z7 P# F3 b* f+ i* _: v
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old5 \) L: U) s, o0 b, c
Boy Induced by Indirect Topical! U% l4 D3 _" f1 ~" ?1 ~
Exposure to Testosterone! G4 q, U6 `; z5 M
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 e. _: L- A" ]' {and Kenneth R. Rettig, MD1
# s' K) c$ I. zClinical Pediatrics7 f: Z6 C  f$ C% ], d: R, ]8 u
Volume 46 Number 6
# \( L+ C- i9 l; A* OJuly 2007 540-543
4 N1 G- x9 U) t0 _1 C4 m© 2007 Sage Publications! m# x( ?6 L2 q2 s$ A0 h* N7 }- {
10.1177/0009922806296651. P6 z1 ]& m; _7 l' r0 z5 ]0 ]
http://clp.sagepub.com! {1 d& p+ I( W% l; b$ V8 T
hosted at
6 t5 w' H) N1 v1 n# khttp://online.sagepub.com4 T3 _, {4 D& {& y: b: p8 a
Precocious puberty in boys, central or peripheral,( o* ]& h8 _( S2 P8 {( V
is a significant concern for physicians. Central
, K+ v7 D% g+ V# [  ~- qprecocious puberty (CPP), which is mediated' W% u- U* b3 a* Y9 W+ ]9 X6 a  G
through the hypothalamic pituitary gonadal axis, has) R3 }8 t) X, [
a higher incidence of organic central nervous system. E% E  U) [: k+ i2 G
lesions in boys.1,2 Virilization in boys, as manifested
% k6 u$ p' u! q! t- Gby enlargement of the penis, development of pubic/ m% n- ~2 B  z; Y) v- u2 O( M
hair, and facial acne without enlargement of testi-
5 q0 W+ Q# M* a- R5 Q8 }cles, suggests peripheral or pseudopuberty.1-3 We+ d/ L; Q0 t) T4 ?6 g
report a 16-month-old boy who presented with the
) y* M9 `/ {6 b2 l+ ~+ G$ D1 Uenlargement of the phallus and pubic hair develop-! Y7 P7 Y( H! u4 g, D8 ?! v
ment without testicular enlargement, which was due
% D2 s2 l' I; h+ u: A) t  |to the unintentional exposure to androgen gel used by- S7 S9 g1 K; n. f  V
the father. The family initially concealed this infor-- x2 _( T  U! ]: f9 g+ z$ Z
mation, resulting in an extensive work-up for this( T$ u. I/ _! R1 U2 H- C" T
child. Given the widespread and easy availability of+ i0 k1 ]) X* t/ V8 Y( f
testosterone gel and cream, we believe this is proba-
* P- d5 o" x' C+ t/ E4 u: ]. {: Ebly more common than the rare case report in the$ Y1 L- P( O+ T. K/ n' D
literature.4& i, f7 `! O) m3 h: V8 D
Patient Report
/ a! ~. Y' B* m% D; sA 16-month-old white child was referred to the
4 [3 B4 ^$ E; x! f% a3 vendocrine clinic by his pediatrician with the concern
; q. P5 h3 z" o1 H4 U) Wof early sexual development. His mother noticed
' b$ C( H/ c3 {6 K) \light colored pubic hair development when he was. e/ T* X* G7 r# [# X. X
From the 1Division of Pediatric Endocrinology, 2University of7 j; [# N) |6 s- @" l7 Y2 f
South Alabama Medical Center, Mobile, Alabama.2 x9 f) C' {8 |" i4 z9 @2 G
Address correspondence to: Samar K. Bhowmick, MD, FACE,
! x) k. k! @  H' W+ K2 fProfessor of Pediatrics, University of South Alabama, College of5 R  K4 O/ g1 m* v9 M- |+ m7 {
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
4 \" @6 c$ Z: J9 me-mail: [email protected].
) N1 f1 v! N. G+ y$ }& ?about 6 to 7 months old, which progressively became
3 Q9 w7 \  l) t1 D8 adarker. She was also concerned about the enlarge-' L& l  O& F9 g4 t$ l. A
ment of his penis and frequent erections. The child! U1 m9 i. P7 X
was the product of a full-term normal delivery, with
, D" U/ Z9 z5 v, m: Da birth weight of 7 lb 14 oz, and birth length of1 h  w/ F  }3 |; ^" u) h9 B: y3 _$ g
20 inches. He was breast-fed throughout the first year
# U! w" O4 A+ }/ Z; P) B4 \of life and was still receiving breast milk along with. A* k8 V8 v! }2 k' E' V( T
solid food. He had no hospitalizations or surgery,$ w7 t3 w% z; `4 H
and his psychosocial and psychomotor development6 ^! _2 A; p, u& E( v: i0 K+ ]. D6 [7 h
was age appropriate.
- i4 ~1 b. P1 c6 u* @! ?The family history was remarkable for the father,
! ~, Y3 @1 D$ L- O$ fwho was diagnosed with hypothyroidism at age 16,
# V1 C8 y8 h% h1 ywhich was treated with thyroxine. The father’s
2 Q5 w$ a" b3 y% Aheight was 6 feet, and he went through a somewhat/ D, n$ {0 t' G9 T4 l' l8 ~# C
early puberty and had stopped growing by age 14.
* A. n! u% G4 \+ M, W6 P$ b0 DThe father denied taking any other medication. The
0 H3 a8 |1 ^. y$ r" Z& f0 Dchild’s mother was in good health. Her menarche- W6 u5 g; {. }1 K  V
was at 11 years of age, and her height was at 5 feet
  N2 u; i* Y4 V$ g; K! ?5 inches. There was no other family history of pre-8 h) L4 n3 |1 _1 J6 t5 d
cocious sexual development in the first-degree rela-& l. c. {* z! ?: u; C1 v7 I8 M
tives. There were no siblings.
% s# d  p$ ?6 }  u+ FPhysical Examination- V7 V2 U7 g; v! G5 ^
The physical examination revealed a very active,' V) q; w7 p6 o$ o
playful, and healthy boy. The vital signs documented
7 m  h( H% n6 g* O0 ~a blood pressure of 85/50 mm Hg, his length was
4 ]; I! }4 z9 T6 ]1 [; d) o/ f90 cm (>97th percentile), and his weight was 14.4 kg( S- Y: a$ p( C; Y) F9 Q2 P
(also >97th percentile). The observed yearly growth! }2 Z) R% u9 y4 B* X3 e
velocity was 30 cm (12 inches). The examination of
2 H* F$ \7 i. I" a- I) O' W9 A" Jthe neck revealed no thyroid enlargement.: S8 i1 O9 T$ X. K' D7 D: B
The genitourinary examination was remarkable for
& M  X7 H2 P' I  m# g# E" ?enlargement of the penis, with a stretched length of
, Q9 _$ i  u% K( H' Q) m+ q5 d/ S8 cm and a width of 2 cm. The glans penis was very well
4 O$ Q: @7 X7 [$ edeveloped. The pubic hair was Tanner II, mostly around7 V3 a( `/ H( _# V( g) U
540- Y! z8 H+ [& R6 E" ^+ r1 M' L4 h
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) G$ N; L5 x- a, v6 J5 ?the base of the phallus and was dark and curled. The2 S% Q. L0 u# D' F/ G7 h
testicular volume was prepubertal at 2 mL each.3 j8 q! Y7 H0 U+ w1 R$ k! J& w
The skin was moist and smooth and somewhat
3 M1 l3 y3 A# T" s+ g+ ^2 j5 @1 Loily. No axillary hair was noted. There were no
1 X! |% ?* `0 rabnormal skin pigmentations or café-au-lait spots.  `1 e8 p6 e4 u) ^1 [
Neurologic evaluation showed deep tendon reflex 2+
" r  C4 e. _3 L% @8 abilateral and symmetrical. There was no suggestion* q, ]! r2 e* i( l  u! l% k* O
of papilledema., Z; |( o$ V. s" P' C% \' P
Laboratory Evaluation1 @/ X, f$ }# ^. I
The bone age was consistent with 28 months by9 Y  d' ^* s6 J( n( Q7 i( t
using the standard of Greulich and Pyle at a chrono-
( z0 Z/ }# j% @) y9 W+ `2 f* Ologic age of 16 months (advanced).5 Chromosomal4 b% r2 q8 X0 L
karyotype was 46XY. The thyroid function test
+ I2 l3 B' {' Z: z* ?3 h, Xshowed a free T4 of 1.69 ng/dL, and thyroid stimu-6 r1 ~! s; Y( z% U& l3 ^- N
lating hormone level was 1.3 µIU/mL (both normal).2 L2 a/ |7 Y" P: c4 M, F. W- i
The concentrations of serum electrolytes, blood5 A7 `2 T) T+ g+ q& x  g. I
urea nitrogen, creatinine, and calcium all were# P) G9 g. Z4 @' `. I6 L& {* y( k5 N
within normal range for his age. The concentration
4 O3 H% Z# L8 \/ ~, k7 Mof serum 17-hydroxyprogesterone was 16 ng/dL9 a4 m" Q3 o' l
(normal, 3 to 90 ng/dL), androstenedione was 20
5 r" B- Z/ H+ ]3 |ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
- \' Q: G" `" z6 r4 fterone was 38 ng/dL (normal, 50 to 760 ng/dL),, S% I6 C+ g2 S5 Z  q6 a
desoxycorticosterone was 4.3 ng/dL (normal, 7 to* A) G0 o8 y! s; v
49ng/dL), 11-desoxycortisol (specific compound S)
& H: B! k, y/ s8 Gwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-9 A3 x1 J& U. D4 V+ Q& ?
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
; G& W) M- G5 Ltestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
3 ]! ]: H# @$ k! s; ?and β-human chorionic gonadotropin was less than- r2 T& }1 K2 H6 @' [
5 mIU/mL (normal <5 mIU/mL). Serum follicular
6 C) a) t5 F$ k: t+ }stimulating hormone and leuteinizing hormone$ s" @$ Z. B% z* U
concentrations were less than 0.05 mIU/mL
8 X' P! H' n; E8 O$ z9 I) r(prepubertal).
2 Y% m3 z4 \2 s2 [' s+ KThe parents were notified about the laboratory" B. G( P- T, E$ T
results and were informed that all of the tests were
) G$ u+ n4 H# U, |normal except the testosterone level was high. The# K+ k9 u5 w4 l) d. X0 e
follow-up visit was arranged within a few weeks to
' W- N% d' U" x8 d7 i3 Jobtain testicular and abdominal sonograms; how-0 z' q1 p) a$ }( t9 N
ever, the family did not return for 4 months.! z3 Z: K3 z# _, x4 J- S
Physical examination at this time revealed that the: E! E) F- t5 b# F/ n. Z
child had grown 2.5 cm in 4 months and had gained
+ @. r5 _8 n% h2 kg of weight. Physical examination remained% _! _5 B  {3 n7 t# O
unchanged. Surprisingly, the pubic hair almost com-7 z8 V4 f( S* s4 w2 O
pletely disappeared except for a few vellous hairs at
& l; u: a9 K: a+ ~. k3 d  ?the base of the phallus. Testicular volume was still 2, a5 l9 R  U3 M& q
mL, and the size of the penis remained unchanged.: S9 R* x! R; n; A
The mother also said that the boy was no longer hav-+ B# z3 Y$ g, b
ing frequent erections.
5 J+ K8 c0 c$ v0 ?+ BBoth parents were again questioned about use of- z" O+ W* k! p: |! r" q
any ointment/creams that they may have applied to2 [8 T8 Z& G7 k3 L8 I/ }
the child’s skin. This time the father admitted the% m2 ?* f1 F0 W/ [5 R
Topical Testosterone Exposure / Bhowmick et al 5418 ~# s5 T  S9 F' O* ]! Q& s8 v
use of testosterone gel twice daily that he was apply-
4 q% p; f+ n/ E* G# }# L8 Uing over his own shoulders, chest, and back area for, S* S& o' f8 o. ^9 k* G
a year. The father also revealed he was embarrassed- h% F; |9 G8 f0 U5 S- _
to disclose that he was using a testosterone gel pre-# R+ g/ E% H& E% }+ D4 t
scribed by his family physician for decreased libido
" i  I1 j( p+ c) S$ f5 L0 A2 Usecondary to depression.
# ~8 o; y' q% F* eThe child slept in the same bed with parents." t. c- ^9 H8 w' m1 h7 @
The father would hug the baby and hold him on his5 Y( U1 A# D' e& o1 N
chest for a considerable period of time, causing sig-& G! q8 D- M' r' S' Z
nificant bare skin contact between baby and father.
$ H* q3 C, _! ]; Q) MThe father also admitted that after the phone call,
! t( l, I6 g) T! {5 n& K: fwhen he learned the testosterone level in the baby
7 {3 c: O/ m1 u  p3 ~was high, he then read the product information
6 W9 r( K$ d/ I5 [packet and concluded that it was most likely the rea-" @" g& g8 L6 f/ C9 r& @% d
son for the child’s virilization. At that time, they0 f+ ~+ j* P- [; s
decided to put the baby in a separate bed, and the& e2 a/ P1 l" D( ]9 E' }. _
father was not hugging him with bare skin and had6 N" D7 g, O% R+ ~
been using protective clothing. A repeat testosterone! ^4 n0 x6 ^- b/ ]' g! F& h+ c( N
test was ordered, but the family did not go to the
9 C: @( Y% T9 m+ s" Glaboratory to obtain the test.8 a6 A  Z; O7 A, [
Discussion
. P- W9 n$ E/ P' |* KPrecocious puberty in boys is defined as secondary# M& C) F2 R2 U" @
sexual development before 9 years of age.1,4
& X& \/ _) m9 X' ?Precocious puberty is termed as central (true) when
% b* ]& E' w: E6 r$ R* ~it is caused by the premature activation of hypo-
+ y) H. g! R5 ]. o# qthalamic pituitary gonadal axis. CPP is more com-+ X8 w9 b3 d  C2 b( r$ K
mon in girls than in boys.1,3 Most boys with CPP
- F2 O% x1 I; _& K5 n" ?- Omay have a central nervous system lesion that is
  x/ b  g6 g/ M9 @: uresponsible for the early activation of the hypothal-& M" A7 v! P* Z) q. M! l: W
amic pituitary gonadal axis.1-3 Thus, greater empha-1 {' n1 G4 P# _6 q2 \7 J! F0 C
sis has been given to neuroradiologic imaging in
; X# K8 ?3 [' w& r3 K, iboys with precocious puberty. In addition to viril-0 |% f' F5 o* B* F
ization, the clinical hallmark of CPP is the symmet-2 v( ]' f# U" l. g9 Y
rical testicular growth secondary to stimulation by
/ G; j2 m: T4 |' g; N% I1 Y5 Xgonadotropins.1,3
$ T6 ]5 k) M/ X$ G! mGonadotropin-independent peripheral preco-
* `! S' A" m9 Y2 jcious puberty in boys also results from inappropriate: d" m- y2 V0 q0 P. ?" ]
androgenic stimulation from either endogenous or4 q! k, F# z, g; R# D# P2 }) g
exogenous sources, nonpituitary gonadotropin stim-6 s) u1 _( A' f2 y
ulation, and rare activating mutations.3 Virilizing8 Q8 [) _6 c! A5 |# s/ F2 l
congenital adrenal hyperplasia producing excessive
2 Y" O% ~6 K+ t1 V6 E  y8 G/ Gadrenal androgens is a common cause of precocious
$ o) o! j* Q2 `% M; ^puberty in boys.3,4& r. Q( F8 K9 O; B% Q3 ~
The most common form of congenital adrenal
; x4 v2 K) K+ zhyperplasia is the 21-hydroxylase enzyme deficiency.7 y/ n& k; a9 c# z/ c0 a3 j5 H
The 11-β hydroxylase deficiency may also result in/ ~* h% O9 V. p' x4 Z0 N
excessive adrenal androgen production, and rarely,* w0 ]8 C4 ?4 ^
an adrenal tumor may also cause adrenal androgen5 {* }6 ^* j  w
excess.1,33 G+ U# e/ A4 e( H
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 @" C% a6 n1 K. ~7 T! P542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
( e& {$ N1 g7 o9 A  UA unique entity of male-limited gonadotropin-5 I4 z# A8 l% ?# R% M" B0 Q! L
independent precocious puberty, which is also known
& r$ U# A9 p# M  q- Sas testotoxicosis, may cause precocious puberty at a
3 r$ o* l% Y: Zvery young age. The physical findings in these boys
, {* N  y4 B+ h+ qwith this disorder are full pubertal development,5 w. x1 a) z% R$ Y+ V1 i  B
including bilateral testicular growth, similar to boys
0 y/ F0 C3 a5 mwith CPP. The gonadotropin levels in this disorder
7 J+ B9 L& E% o9 Gare suppressed to prepubertal levels and do not show( Y0 p8 {; j. Y( B* `
pubertal response of gonadotropin after gonadotropin-( `) F0 K1 \0 F% R& `
releasing hormone stimulation. This is a sex-linked6 d9 T4 h  I" S& T5 ^
autosomal dominant disorder that affects only8 G) Q/ w1 a7 l7 U) u! a$ e
males; therefore, other male members of the family
  J( J% h; ?0 [# p. }1 ^# Qmay have similar precocious puberty.3
7 s; l! J) ?4 ]) `In our patient, physical examination was incon-
8 l$ l  |4 [1 h( G) Z$ A, Lsistent with true precocious puberty since his testi-
. n  M+ N  l/ U: p% V/ g) Vcles were prepubertal in size. However, testotoxicosis+ [1 r/ S6 E, [9 H* [( H
was in the differential diagnosis because his father" R% K' `* n4 ?
started puberty somewhat early, and occasionally,
- R; q) |, G& Ytesticular enlargement is not that evident in the) l1 ~* a" C* `3 c4 H- N2 C
beginning of this process.1 In the absence of a neg-+ r; n" M: g# O& i: Y" S/ N( y2 c
ative initial history of androgen exposure, our
. o0 g  `" G+ Rbiggest concern was virilizing adrenal hyperplasia,  [; M( L3 h" ~, O9 B0 R6 M6 |, l3 O
either 21-hydroxylase deficiency or 11-β hydroxylase
) x: g/ s$ m- W( Q- [: ideficiency. Those diagnoses were excluded by find-+ I/ X8 B# m' [" }' E0 m. i& E- |
ing the normal level of adrenal steroids.# k/ ^# B" G0 ~$ v. ]& l( N' m" H
The diagnosis of exogenous androgens was strongly& J, G4 R- T2 Q# S
suspected in a follow-up visit after 4 months because
7 i# w. S9 e8 \& G! ~the physical examination revealed the complete disap-2 N; h4 u* V% c: p5 o. a5 r
pearance of pubic hair, normal growth velocity, and
( C- m4 d4 [; l% vdecreased erections. The father admitted using a testos-
& v2 A' v2 k0 v$ X3 @9 t; wterone gel, which he concealed at first visit. He was3 f) B( f0 S4 v* {# e- R
using it rather frequently, twice a day. The Physicians’2 f) s3 C! l2 X6 I6 e/ j
Desk Reference, or package insert of this product, gel or
6 K8 Q7 P" w: F* I3 l) L7 ]cream, cautions about dermal testosterone transfer to9 U" \; V  W! c
unprotected females through direct skin exposure.9 P. q. C- C3 b. {+ J/ K+ l
Serum testosterone level was found to be 2 times the4 I9 ?6 z% u) T1 A* p
baseline value in those females who were exposed to
1 d7 {6 A# X' u) m0 leven 15 minutes of direct skin contact with their male- m2 M4 {# C- n) n' K* C
partners.6 However, when a shirt covered the applica-7 c8 {& t* x9 `- ?( ?/ M
tion site, this testosterone transfer was prevented.
3 r; h& Z9 E. f) ZOur patient’s testosterone level was 60 ng/mL,
) u' r. a0 e0 O# Nwhich was clearly high. Some studies suggest that2 [7 x: \5 b+ G! a# u" X3 |8 A! U3 e
dermal conversion of testosterone to dihydrotestos-# I9 H) y5 t, M% P; J9 S* o
terone, which is a more potent metabolite, is more
+ h( K. U/ z# O$ factive in young children exposed to testosterone( D0 ~/ {3 F& m2 }1 R& B
exogenously7; however, we did not measure a dihy-
3 a) N( H+ a( zdrotestosterone level in our patient. In addition to& p9 l8 s  Y9 S& \3 r
virilization, exposure to exogenous testosterone in
8 ]+ H0 J% v5 ?' m5 G/ M) Pchildren results in an increase in growth velocity and5 W' a* ]2 U+ o0 ~5 N. _
advanced bone age, as seen in our patient.+ W; z, ]+ z( g
The long-term effect of androgen exposure during4 Z) s0 r7 J- k0 O
early childhood on pubertal development and final
3 D8 f1 c9 I+ Z$ x: Fadult height are not fully known and always remain
6 @* |/ U; {4 v' P# j! La concern. Children treated with short-term testos-
) [$ A% J* j4 P1 q- p' Fterone injection or topical androgen may exhibit some) ~, x, e7 h* z+ |$ k
acceleration of the skeletal maturation; however, after/ w# ?+ }5 A3 ~8 z
cessation of treatment, the rate of bone maturation
5 a6 X' D* ]2 R" ^, ?decelerates and gradually returns to normal.8,9
/ F; U6 E$ ]3 E$ `0 SThere are conflicting reports and controversy
1 j1 Y' K: y- D- b/ R* Oover the effect of early androgen exposure on adult3 J2 ?  j' }& s. L; w
penile length.10,11 Some reports suggest subnormal) A* L5 _4 H& q' B3 A
adult penile length, apparently because of downreg-, a2 W# ~4 a3 b: g: q
ulation of androgen receptor number.10,12 However,
6 L8 ~' I8 l0 s) ~6 t2 `' H: x/ eSutherland et al13 did not find a correlation between5 [$ G4 r; g; G$ Y. N
childhood testosterone exposure and reduced adult* d, i2 m7 t+ i% z+ ?% E
penile length in clinical studies.' w/ f, h" t) l% F$ K
Nonetheless, we do not believe our patient is
! w8 F! f; k& p6 O) R' q1 ugoing to experience any of the untoward effects from% a' ?$ o# N& z8 T$ D& I! H
testosterone exposure as mentioned earlier because
- I# E9 O% {" h1 z% {the exposure was not for a prolonged period of time.4 N, b4 p! g/ E; D# W* b- V/ n
Although the bone age was advanced at the time of; P  e# Q8 L& y
diagnosis, the child had a normal growth velocity at) E) r% b/ h: V" c& E0 S
the follow-up visit. It is hoped that his final adult! U- a: R8 l; J- o+ L+ @
height will not be affected.+ V! Z7 L1 e. ~, n
Although rarely reported, the widespread avail-* ~3 m7 S4 t7 M4 \% d
ability of androgen products in our society may
1 k; s/ O5 y4 V! p0 m8 b1 c+ L3 ^indeed cause more virilization in male or female
! ~/ u% ]5 v; d7 H5 Mchildren than one would realize. Exposure to andro-! _3 m& N+ G1 B7 p. D
gen products must be considered and specific ques-
1 A7 [6 P/ B* f5 s  Ktioning about the use of a testosterone product or: `( k5 X, ~- O) {8 o0 i- k
gel should be asked of the family members during
; h% i, A3 a1 S1 k( U/ c! M1 _6 I- Athe evaluation of any children who present with vir-
9 Y+ M) M' q+ K* N: t" I+ B2 uilization or peripheral precocious puberty. The diag-( w1 u- n6 a7 V' G  V+ r! Q; B
nosis can be established by just a few tests and by  x' R) @- S, J; c$ A
appropriate history. The inability to obtain such a
# _. ^( @6 [6 D( i. v) rhistory, or failure to ask the specific questions, may$ n. u1 Q$ g; B6 u7 Z/ u
result in extensive, unnecessary, and expensive+ U- ~. L5 E: A  u8 I" O6 J5 w
investigation. The primary care physician should be) I- s" Z% D, Q  {
aware of this fact, because most of these children
: ^# C& u" k; Mmay initially present in their practice. The Physicians’
4 q" J$ C  ?& L1 E# Z- l/ z' HDesk Reference and package insert should also put a  _& O& b5 x7 v
warning about the virilizing effect on a male or
3 w5 z% z# N* ~0 [0 |2 ]' Q$ mfemale child who might come in contact with some-
8 H# J3 I4 E, Z, hone using any of these products.' _6 K4 W4 K8 b/ X' ]
References
% K$ r2 J- ]( l2 ]; I7 C1. Styne DM. The testes: disorder of sexual differentiation: H/ k7 h' O4 R, ?  ]+ a! t
and puberty in the male. In: Sperling MA, ed. Pediatric
. ]( ~( f1 B8 Y$ DEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;. R" x0 o9 W- e0 g4 a
2002: 565-628.
: I1 z  {$ h9 Z1 {, w' Y# d2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious" b/ @$ E* U+ M) p2 X4 V$ n% i- d
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

" k0 f6 X; T6 g. v2 Z3 Y/ g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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