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Sexual Precocity in a 16-Month-Old
/ y% C) i+ {, l9 ?Boy Induced by Indirect Topical
# G# o  t+ t/ J! jExposure to Testosterone8 W( m0 {  j9 }: }  B
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
  U* b/ B% V' ]. X0 u' ]- p: m1 h; Band Kenneth R. Rettig, MD1
, L5 r7 M$ V. X' c6 ]Clinical Pediatrics% ~7 @* @! l( l/ e, T0 o: @2 D0 b/ d" ~
Volume 46 Number 69 \, c* ?$ H% D7 f, Z1 V
July 2007 540-543, S3 [3 u5 O1 N8 R, l
© 2007 Sage Publications
, k4 c# {$ _- D/ R10.1177/0009922806296651& d9 p' T7 q# F, _  E
http://clp.sagepub.com: I- v& J. T- V5 G3 B2 z" y4 E) [$ O+ X
hosted at: ~( J- j1 T; ?- B1 }- ~4 K
http://online.sagepub.com
2 c1 C, p9 {7 s0 Z$ F( yPrecocious puberty in boys, central or peripheral,
0 H/ J" W! Q9 b9 F3 b* [5 D. {) Lis a significant concern for physicians. Central* W; N4 U. p  v- I9 X: Q: \7 Z
precocious puberty (CPP), which is mediated
! r" x  Y) G  @# L3 Ithrough the hypothalamic pituitary gonadal axis, has" \' Y" k. \' `4 Y
a higher incidence of organic central nervous system# W  q- L/ t3 A$ J
lesions in boys.1,2 Virilization in boys, as manifested
& c' v" X- o' C# Eby enlargement of the penis, development of pubic( U( V( H: K) _, E
hair, and facial acne without enlargement of testi-4 }: I. g- x7 {9 [- r' x9 ^5 j: ?
cles, suggests peripheral or pseudopuberty.1-3 We9 t3 g! q' F+ W! p$ u
report a 16-month-old boy who presented with the
1 q, }) c+ _: `8 H4 Yenlargement of the phallus and pubic hair develop-% m/ f7 I$ v# q7 \) P3 q( X! ]' l
ment without testicular enlargement, which was due
$ D- m+ z( ~5 @1 ^to the unintentional exposure to androgen gel used by3 ~# T, ]2 }0 R4 S6 P1 Q' p1 |
the father. The family initially concealed this infor-
8 H! a/ F- q4 imation, resulting in an extensive work-up for this7 s6 M: b4 }% e& ?" ]! c0 @( q
child. Given the widespread and easy availability of: t% l- \$ m6 k* [
testosterone gel and cream, we believe this is proba-
- F& j4 ^: k8 f. l- D" G" k) ^' [bly more common than the rare case report in the
* D1 ~  ?2 y  ?" C# _9 Yliterature.4
+ {: C6 q% F: f& w- X! A( Y" Z/ oPatient Report
5 ^; P$ m: m& J' |* KA 16-month-old white child was referred to the
% O% J" J% j2 C: v4 m! W$ G: ]endocrine clinic by his pediatrician with the concern
2 X/ q$ Y/ a2 c+ k! X+ Zof early sexual development. His mother noticed
' L# I2 u' X$ z/ n( P; `light colored pubic hair development when he was. M: _$ {* C; s0 T1 e
From the 1Division of Pediatric Endocrinology, 2University of& l  k& O5 T' G1 n; ^$ B
South Alabama Medical Center, Mobile, Alabama.
, u% W% r3 r! a# y/ WAddress correspondence to: Samar K. Bhowmick, MD, FACE,* z3 h- ?- x% b- x
Professor of Pediatrics, University of South Alabama, College of
; T2 v- K: s! M7 sMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
8 X: ]+ g: p: ~8 L* ?4 ve-mail: [email protected].% j7 S& A+ y% q
about 6 to 7 months old, which progressively became5 }2 d, R& `- \2 y. Z
darker. She was also concerned about the enlarge-# @: Z$ _: @$ I& }* l$ K
ment of his penis and frequent erections. The child
0 @2 F' q5 X, T* C; P4 |was the product of a full-term normal delivery, with
, \6 ]3 U  o/ \$ C# z+ K" Ka birth weight of 7 lb 14 oz, and birth length of5 M+ o1 o# a1 V7 {7 g
20 inches. He was breast-fed throughout the first year
' ]% |; V& `( N9 kof life and was still receiving breast milk along with
0 T) C9 m2 L9 F( }5 t7 }solid food. He had no hospitalizations or surgery,
# Z" \- E8 a  T8 m! B0 Dand his psychosocial and psychomotor development
9 H) f! f  M6 h4 Z1 ^! ]: y% Twas age appropriate.% [% z9 y) _" V% T& t
The family history was remarkable for the father,% q- a5 {  u  g
who was diagnosed with hypothyroidism at age 16,
% A3 J' b: h" awhich was treated with thyroxine. The father’s" b8 b" y) j: O4 g& \" i. \5 m5 h: Z
height was 6 feet, and he went through a somewhat  S( `, L1 W; h2 Y
early puberty and had stopped growing by age 14.
" q9 A- I) X$ _" xThe father denied taking any other medication. The
0 h; M: h  a3 g$ |5 vchild’s mother was in good health. Her menarche
# \' c# B" ^9 m; _, l  F( X, C  Nwas at 11 years of age, and her height was at 5 feet9 A) a/ ^: e: ]. t" p
5 inches. There was no other family history of pre-" u! j* A: `" e% r5 w7 C
cocious sexual development in the first-degree rela-/ `. S& p0 j! {& ^5 c& t
tives. There were no siblings.
. f* [( }2 L' P" lPhysical Examination1 _- l3 H/ L* Q: ?- m+ `0 B
The physical examination revealed a very active,
  _# r4 `) K: Splayful, and healthy boy. The vital signs documented+ s$ L2 v, a/ \6 t, l
a blood pressure of 85/50 mm Hg, his length was. X; U3 h& L  l# m8 j
90 cm (>97th percentile), and his weight was 14.4 kg
6 \1 v* \) G$ [( |0 ](also >97th percentile). The observed yearly growth" O$ k$ _; r. p1 }  L3 Q4 e
velocity was 30 cm (12 inches). The examination of
9 M" g7 _% |: U/ \8 j% ?  ]+ _the neck revealed no thyroid enlargement.* z3 q! O' W: Y% A) [5 L& P
The genitourinary examination was remarkable for
6 O# k3 m" r' D+ ^: e; yenlargement of the penis, with a stretched length of5 @( f$ Z# D- b
8 cm and a width of 2 cm. The glans penis was very well8 ~  E: G2 {, \
developed. The pubic hair was Tanner II, mostly around1 `) k, m+ O3 _( {% L/ b& S0 Z
540
5 F! r  `/ u( g9 i0 z8 Yat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 e) C( o" m# p- Bthe base of the phallus and was dark and curled. The
7 Z* w4 p0 ?0 s9 W( Q$ x4 Atesticular volume was prepubertal at 2 mL each.8 K4 x2 J# M7 ^$ Z, p  P  D
The skin was moist and smooth and somewhat2 ^: |0 m9 a3 ^' V; J
oily. No axillary hair was noted. There were no4 v3 Z. m" ]7 ]6 C$ N
abnormal skin pigmentations or café-au-lait spots.
$ z- d# {- |3 f+ }" j5 E$ HNeurologic evaluation showed deep tendon reflex 2+" i3 @2 k1 f" c6 t! L
bilateral and symmetrical. There was no suggestion
7 O) P( a; F1 T" dof papilledema./ _* {8 n1 G  M! V& @: m; l
Laboratory Evaluation- T& A5 l: }; _  ?9 p2 B! F5 c
The bone age was consistent with 28 months by
3 S" @  a+ P5 z0 Rusing the standard of Greulich and Pyle at a chrono-2 V2 U) c+ d) b$ d: {% s
logic age of 16 months (advanced).5 Chromosomal8 L( {5 _6 \4 K' m6 X' y) w
karyotype was 46XY. The thyroid function test
% v* F/ m& d0 [! J- f  B7 a+ sshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
2 x" V- |. R1 N$ x) h' z2 X' tlating hormone level was 1.3 µIU/mL (both normal).6 r0 J+ P* H# [8 K
The concentrations of serum electrolytes, blood/ l9 ?$ _4 [- y6 O  E
urea nitrogen, creatinine, and calcium all were
2 ]' K  F1 M+ Z: H9 p9 twithin normal range for his age. The concentration
. Y/ P9 W/ U. s# w; K, Dof serum 17-hydroxyprogesterone was 16 ng/dL
( [: t3 Y6 i* V* T' q3 y(normal, 3 to 90 ng/dL), androstenedione was 20
! J7 I- H0 c, o2 e4 F9 @ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
* n9 j. N, K4 b% A6 Aterone was 38 ng/dL (normal, 50 to 760 ng/dL),; l. _6 F+ t0 J& s0 c/ L% f% i
desoxycorticosterone was 4.3 ng/dL (normal, 7 to' z/ o. i" E& U. j: d1 m" G& B
49ng/dL), 11-desoxycortisol (specific compound S): e5 G: E. \) w2 u# Y9 x# k# D
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
! a+ K9 I$ J/ P$ t8 a# L8 ztisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
1 I  b7 _3 p9 x" D* N, q( Gtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
  y. g4 x4 }1 ~4 [$ Hand β-human chorionic gonadotropin was less than3 |5 ^/ f# h% k6 P" J
5 mIU/mL (normal <5 mIU/mL). Serum follicular2 P; z: {( E5 h
stimulating hormone and leuteinizing hormone
& r5 L4 V7 k! i" ~9 k  ]) t/ ^concentrations were less than 0.05 mIU/mL* H* b! i! s/ e( D1 w6 a# [5 f
(prepubertal).
$ S, C" w. v( G9 F6 qThe parents were notified about the laboratory
3 L) U1 ~& Y+ S2 |results and were informed that all of the tests were
( A5 ~' S7 L  b# L# m$ Xnormal except the testosterone level was high. The
3 u; x1 j0 a" J: @follow-up visit was arranged within a few weeks to
( j+ G! ?" g: Z  F# Robtain testicular and abdominal sonograms; how-
1 B* o2 A2 v5 ~- lever, the family did not return for 4 months.: A' H3 h* o$ M7 m9 u& t: M
Physical examination at this time revealed that the3 l/ Z0 p/ C! \3 q) q
child had grown 2.5 cm in 4 months and had gained
9 q3 a) Y! J, X) B2 kg of weight. Physical examination remained! B! {- k: E* H% k7 V" k2 T% K9 z5 w
unchanged. Surprisingly, the pubic hair almost com-: l0 H" S7 i4 x, N
pletely disappeared except for a few vellous hairs at
4 d6 h3 M  m8 O$ _7 x# |the base of the phallus. Testicular volume was still 22 w/ S2 _5 @( r! e9 E# T: B) l
mL, and the size of the penis remained unchanged.
2 J; Z& x7 ~. t3 z" [( AThe mother also said that the boy was no longer hav-! g, m5 H4 X4 ?+ {; w
ing frequent erections.' Q4 R! X, R9 h' b
Both parents were again questioned about use of5 k" L* k9 w# b* a% H
any ointment/creams that they may have applied to
! X: Q0 `6 R! _: s7 I/ f7 F' W5 Rthe child’s skin. This time the father admitted the0 p7 l- n& }4 d5 T% c) ^
Topical Testosterone Exposure / Bhowmick et al 541
* s! h9 t# G: Y: A2 R! @use of testosterone gel twice daily that he was apply-7 R& }0 y/ L% k; ]1 \6 |
ing over his own shoulders, chest, and back area for
. o2 |8 l& B& s, V/ m! s* Wa year. The father also revealed he was embarrassed& P* ^3 M: p% z0 E4 D
to disclose that he was using a testosterone gel pre-
0 O) b  H8 f; Z# F3 j  Q& xscribed by his family physician for decreased libido
9 r2 `8 A0 {2 u/ [6 f. ?4 i! C3 K& Lsecondary to depression.3 g% S1 N4 ^$ N8 F0 i5 w$ h( q5 z
The child slept in the same bed with parents.% ?8 |" f( S0 w* k3 l- B* I
The father would hug the baby and hold him on his
0 ^# O! j3 z; l9 \7 @chest for a considerable period of time, causing sig-: i6 Q1 s5 \/ ]$ l! P  D
nificant bare skin contact between baby and father.
' w2 I9 C3 m: n0 W! H0 o3 y# A3 B: @The father also admitted that after the phone call,
6 n& C7 r/ u# c7 |4 l- _  w1 V. uwhen he learned the testosterone level in the baby: G8 _/ h5 N. u' y9 Y# i% O# F
was high, he then read the product information* b3 L# ?# |% J# C
packet and concluded that it was most likely the rea-
2 `: i5 h! h5 K! g8 F4 d* ison for the child’s virilization. At that time, they' a  @0 |& ~) E9 j1 X
decided to put the baby in a separate bed, and the
! o6 R' Z9 H+ m# v# ifather was not hugging him with bare skin and had: C1 O5 h: f& H! T2 Y4 Q) i
been using protective clothing. A repeat testosterone
' L- L( `" d4 ]  P- H! ttest was ordered, but the family did not go to the
6 l- @6 {/ j# F0 y$ D4 |' I* mlaboratory to obtain the test.& m! d" O; ?7 G( b
Discussion
( ]' i6 J) y, ~Precocious puberty in boys is defined as secondary
9 K6 I- V! M9 |* l# H2 zsexual development before 9 years of age.1,49 J8 Z3 {. U! Q
Precocious puberty is termed as central (true) when
; L) W% K6 v  [* yit is caused by the premature activation of hypo-. U- Q2 x! Q/ k+ V
thalamic pituitary gonadal axis. CPP is more com-7 c7 A/ {# _. p0 @+ J5 ~! [, G
mon in girls than in boys.1,3 Most boys with CPP6 c+ V) U# C+ q! Q  A( R& N% [4 i
may have a central nervous system lesion that is
' @+ i/ k  Y; q6 y  h2 |1 C0 ^: Aresponsible for the early activation of the hypothal-
% E3 N$ r/ j$ a7 [5 wamic pituitary gonadal axis.1-3 Thus, greater empha-* H! ~' |! b& ]3 f7 [
sis has been given to neuroradiologic imaging in
# U$ H- p' ]0 O+ N7 ?0 [: {$ Gboys with precocious puberty. In addition to viril-
6 T* c0 ^" O! T, i" p- sization, the clinical hallmark of CPP is the symmet-8 g- U3 y) N! N( s  A7 ]
rical testicular growth secondary to stimulation by
" [, M0 n0 D! B# ygonadotropins.1,37 ~' D4 w& b, d
Gonadotropin-independent peripheral preco-2 o+ ?/ @" P1 A5 ~
cious puberty in boys also results from inappropriate# Z  u, v- A; H. m$ l1 S
androgenic stimulation from either endogenous or8 B( m% Y, y, p* ]# E
exogenous sources, nonpituitary gonadotropin stim-( Q4 m( Z8 M3 y/ ^
ulation, and rare activating mutations.3 Virilizing4 M. w& W5 B9 C
congenital adrenal hyperplasia producing excessive% Q1 W$ h9 W, E5 V
adrenal androgens is a common cause of precocious
  N: o# A  e& ^8 D, r$ ^puberty in boys.3,48 h. o. U2 J8 x# y! n
The most common form of congenital adrenal
0 W# [1 d1 J  J  w# Qhyperplasia is the 21-hydroxylase enzyme deficiency.
0 a0 u  m* I+ L& b1 @4 X0 GThe 11-β hydroxylase deficiency may also result in
' Q+ t" ], ?  k/ s4 z, L2 ^- pexcessive adrenal androgen production, and rarely,
: }" P2 |) g. ?0 Xan adrenal tumor may also cause adrenal androgen
/ ^! I# v+ d/ Z. e1 t% e$ ]6 L) Nexcess.1,3
$ u% E1 E4 i* g8 ?% Bat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ X' {1 f; a5 `, S542 Clinical Pediatrics / Vol. 46, No. 6, July 20070 @1 c8 q6 o  }/ O: V
A unique entity of male-limited gonadotropin-
6 T: e) }/ M+ Z+ Y1 a% G; L! J- j& findependent precocious puberty, which is also known$ q* T, |: L& W" j$ u* G  r; \  N0 Z3 f
as testotoxicosis, may cause precocious puberty at a
8 l0 P2 c/ s6 y4 k7 Cvery young age. The physical findings in these boys- |$ g1 y. ~6 {- p
with this disorder are full pubertal development,
1 y& K" X" {* dincluding bilateral testicular growth, similar to boys& D( A+ A7 N. f) a* I- m
with CPP. The gonadotropin levels in this disorder
. v3 o$ t' f( j! @3 q! pare suppressed to prepubertal levels and do not show
* M, A4 U) N0 D0 S6 A, npubertal response of gonadotropin after gonadotropin-
0 m* W& d0 @& s0 Qreleasing hormone stimulation. This is a sex-linked% R2 z7 K- j2 `0 X1 H
autosomal dominant disorder that affects only3 h* z. R& j4 J$ ^2 a
males; therefore, other male members of the family
2 y* ~8 _, M  R, n, @may have similar precocious puberty.3. o2 A, }: E2 }& U1 J3 C! }1 g
In our patient, physical examination was incon-
3 g$ a2 k* o" s0 @- Q# Z$ fsistent with true precocious puberty since his testi-
3 F( t& [; I# d( b5 D7 u- a7 Scles were prepubertal in size. However, testotoxicosis
: d  C% u4 r0 `. u: Dwas in the differential diagnosis because his father
1 v; S; D, K3 {; q# K$ x/ _" @$ Z! gstarted puberty somewhat early, and occasionally,
" @* @$ ~" w+ K9 O. Itesticular enlargement is not that evident in the9 ?) K! C) Z( c+ Q$ r' ]0 e
beginning of this process.1 In the absence of a neg-
/ D% n* }% f5 @ative initial history of androgen exposure, our
& B* e" O. W  `- N* A3 lbiggest concern was virilizing adrenal hyperplasia,( Q, f3 K( g. R" E' g$ @
either 21-hydroxylase deficiency or 11-β hydroxylase; @9 j* E: Q3 l, t2 M+ u
deficiency. Those diagnoses were excluded by find-
9 V1 V2 L8 |2 P" F9 oing the normal level of adrenal steroids., K' X: ~* r& x, d
The diagnosis of exogenous androgens was strongly
# n" r- Q4 `: v' p0 H3 [suspected in a follow-up visit after 4 months because% E# \+ E/ i. f
the physical examination revealed the complete disap-: b( o# K) _+ V' g# J5 m' Y
pearance of pubic hair, normal growth velocity, and3 k; ]) b/ L: e- W( L9 c
decreased erections. The father admitted using a testos-
2 I5 G6 R7 n0 W. l: {8 Z9 ?* nterone gel, which he concealed at first visit. He was( E/ e( ]% B* C2 @
using it rather frequently, twice a day. The Physicians’& R; ^8 }: s5 v  T: ~
Desk Reference, or package insert of this product, gel or$ T( ]. W6 t4 g: S; V
cream, cautions about dermal testosterone transfer to
7 K7 D& s2 T+ eunprotected females through direct skin exposure.
7 F+ N4 w' B* }+ d0 ^" S3 tSerum testosterone level was found to be 2 times the
% h  G3 `2 Q5 A' k, _1 H) Kbaseline value in those females who were exposed to
, _' i- x$ N) w: deven 15 minutes of direct skin contact with their male/ a& @% k/ @" t& v
partners.6 However, when a shirt covered the applica-
7 c" W0 B2 S2 r' X% U* P$ ?5 ttion site, this testosterone transfer was prevented.
: u! M, \) I3 D3 jOur patient’s testosterone level was 60 ng/mL,
! Y* c% M& D) n9 N* F$ w. q- Pwhich was clearly high. Some studies suggest that8 Q  [' Q4 A9 r& e7 t
dermal conversion of testosterone to dihydrotestos-' V) |5 f; A, i* J
terone, which is a more potent metabolite, is more. O( Z+ ?! t7 u% \* P4 T
active in young children exposed to testosterone
) A9 Z9 q3 y" b  B' M" M( i2 wexogenously7; however, we did not measure a dihy-7 y' c; F& l; G/ ^" G5 X3 d0 H5 f2 B. w& @
drotestosterone level in our patient. In addition to
5 V- i: Q/ F; rvirilization, exposure to exogenous testosterone in
7 c) ?% \# N7 e" l) Rchildren results in an increase in growth velocity and0 L+ O! \5 f9 C) T/ H. i; N6 r
advanced bone age, as seen in our patient.
' Z2 G' o4 I8 e9 ~! ~" j2 D$ fThe long-term effect of androgen exposure during
/ z) P- w7 U+ I  o; A. ]4 Bearly childhood on pubertal development and final
" k# m  H/ D* w. S/ x, b+ y/ |adult height are not fully known and always remain/ a' K$ B/ o1 |
a concern. Children treated with short-term testos-
  e. M: P2 I) N: dterone injection or topical androgen may exhibit some
  b. f& x& }8 ^& F2 i- ]; Eacceleration of the skeletal maturation; however, after* [1 z  |5 p" E- J6 S% e5 h) y! t
cessation of treatment, the rate of bone maturation
+ c7 m% C: L8 n1 [9 H! Xdecelerates and gradually returns to normal.8,9
2 H  o. G/ U, D; o3 vThere are conflicting reports and controversy
: [( E  U$ x8 {0 H8 c$ Jover the effect of early androgen exposure on adult0 G: z' y' c$ b# c% ]5 g
penile length.10,11 Some reports suggest subnormal
3 m& L  d. `/ N, hadult penile length, apparently because of downreg-8 s( @/ B# V' p5 c0 y$ l0 U6 k
ulation of androgen receptor number.10,12 However,
; V$ n/ w6 Z& K4 O; X% P- _1 rSutherland et al13 did not find a correlation between3 K& z2 b, T2 F" K5 y! O4 C. _
childhood testosterone exposure and reduced adult( @, i4 H7 x& h% {
penile length in clinical studies.
  n/ o5 C" v1 ]; m$ ?& bNonetheless, we do not believe our patient is
: x- w! {3 I! T# ?going to experience any of the untoward effects from
: `- r; L* n6 a- f. rtestosterone exposure as mentioned earlier because
7 `; C, V5 W2 y) q3 tthe exposure was not for a prolonged period of time.
, p$ `/ C6 j' |Although the bone age was advanced at the time of- @2 H, A( }+ @7 l+ N* z6 v
diagnosis, the child had a normal growth velocity at
% i: E+ [1 `% Uthe follow-up visit. It is hoped that his final adult
+ o- D3 S- c4 p/ ]# v5 s; K# jheight will not be affected.
5 Y0 Q9 o: W  T' l# M2 q( SAlthough rarely reported, the widespread avail-
3 W/ a' f; t1 Z4 O  `ability of androgen products in our society may# z5 ^. `/ d3 E
indeed cause more virilization in male or female
3 T8 R6 Y: X2 ^children than one would realize. Exposure to andro-  H1 X$ P1 I! v+ z+ N6 @
gen products must be considered and specific ques-$ {0 Y  v- @( M, C, h* ~0 O/ i& @
tioning about the use of a testosterone product or
* m  v& E1 t; w3 r2 K. U* \gel should be asked of the family members during; I& _3 \" L+ I4 ]6 F6 X
the evaluation of any children who present with vir-
, N8 D' s" t- p* W  R  qilization or peripheral precocious puberty. The diag-1 g2 _  s/ ]$ f8 _9 x2 p8 w
nosis can be established by just a few tests and by, K0 R' r$ y2 `0 H' z
appropriate history. The inability to obtain such a0 |1 \. r: c9 l9 I6 [
history, or failure to ask the specific questions, may5 \$ ^; |7 S$ |7 t8 m
result in extensive, unnecessary, and expensive1 H  }8 t7 e3 G/ Q
investigation. The primary care physician should be
3 [# T' R  P6 q; z# Maware of this fact, because most of these children
  r" I+ h) o' ?) Y5 h: fmay initially present in their practice. The Physicians’! ~  ~- h- q' ?( e* W7 M/ a
Desk Reference and package insert should also put a
  N9 ~, s+ x! ?1 O/ z3 D# t3 mwarning about the virilizing effect on a male or
  o) m: L1 m) O4 V# B% l# Pfemale child who might come in contact with some-
0 h; U5 _0 q2 D7 ~# Aone using any of these products.
/ \9 @' _! \4 H8 q2 _0 nReferences; R' C. |% E' {7 g5 D
1. Styne DM. The testes: disorder of sexual differentiation$ D* N( z9 G* k  r5 I& w
and puberty in the male. In: Sperling MA, ed. Pediatric
- o$ P1 o3 [9 @/ B2 |Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;( a" I4 d4 S5 D) E3 T9 n
2002: 565-628.
5 d' ?4 E; m! j4 i  ^6 y  @2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
$ A! a8 F) V0 o: E# a% fpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
' n! b3 ?( e" ^3 F5 j* yBoy Induced by Indirect Topical
9 P/ m5 M7 j9 a! FExposure to Testosterone
% f9 ^6 {' S2 {7 [! Y8 gSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
  I' V3 Y8 b( O! q% @and Kenneth R. Rettig, MD1
! z7 P' n- J# ^6 ~0 d% ZClinical Pediatrics
( O1 G$ [+ F: e5 _Volume 46 Number 60 U6 j5 k( C1 |. T* _
July 2007 540-543, K. W/ K: l" E1 c# m
© 2007 Sage Publications, A- ?" _" B1 J% H
10.1177/00099228062966512 O" H& x  E$ \' I: S+ h$ n
http://clp.sagepub.com
1 T' [3 `; h5 B) r' nhosted at% J% R% M% N, S# a  O, o; H
http://online.sagepub.com
  a7 v! P$ D2 C( I- K6 `Precocious puberty in boys, central or peripheral,0 x/ }7 j6 Q# D$ a" S9 V4 M
is a significant concern for physicians. Central
( D6 a9 Q0 V7 g3 u' nprecocious puberty (CPP), which is mediated$ l1 r, t( m& j* ~, ?
through the hypothalamic pituitary gonadal axis, has
7 ~3 @8 A) L8 ?; q0 k5 U+ Ta higher incidence of organic central nervous system
4 D3 H. K! U: v* Blesions in boys.1,2 Virilization in boys, as manifested
. z# k# L0 }/ a( }* S0 Q, F# }by enlargement of the penis, development of pubic
. u* r" d) ], c! e4 t; t7 Uhair, and facial acne without enlargement of testi-
4 `8 @! a! Z7 X8 K2 P, r: jcles, suggests peripheral or pseudopuberty.1-3 We
' U2 J) K9 ]9 xreport a 16-month-old boy who presented with the
% j; D1 f3 H, N) tenlargement of the phallus and pubic hair develop-( ~3 a) ]$ [4 h1 ~
ment without testicular enlargement, which was due
! f3 f2 F7 w6 x1 X6 z1 U1 S% Gto the unintentional exposure to androgen gel used by: U7 E3 f2 Y3 H% ]6 K
the father. The family initially concealed this infor-
* E# s6 Q- F3 P7 i) e! Xmation, resulting in an extensive work-up for this0 b* l; j) B3 n
child. Given the widespread and easy availability of+ A" ]6 |) A' u, j9 b$ b% `
testosterone gel and cream, we believe this is proba-
& B% C6 U) f8 {3 E" J/ s4 ebly more common than the rare case report in the3 i- ?8 ]" {- j% @/ k) Z- X
literature.4
, f( N& b6 c8 M* r" R( _Patient Report1 b. r, Q; l- x& N1 X
A 16-month-old white child was referred to the
& Z% O) k9 r! E* ]/ G0 qendocrine clinic by his pediatrician with the concern! R$ Z/ V, o3 d  H2 e% |- F, S
of early sexual development. His mother noticed: o' R7 T4 W$ f5 q- w1 f  U
light colored pubic hair development when he was7 f+ w1 a  P* N+ `7 ]# p
From the 1Division of Pediatric Endocrinology, 2University of
  g3 t# r5 {2 {  }. XSouth Alabama Medical Center, Mobile, Alabama.
% i3 \+ f# h7 z& [; g' D# R8 ]( bAddress correspondence to: Samar K. Bhowmick, MD, FACE,
5 W/ |$ B2 [$ h9 UProfessor of Pediatrics, University of South Alabama, College of4 e# S/ `+ n  S# p
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;9 h7 ^  S, @: G8 [9 l
e-mail: [email protected].
' p) ~6 E; b$ k: p' habout 6 to 7 months old, which progressively became4 _5 @, ]) z% U' h* T' t* ?* [; W
darker. She was also concerned about the enlarge-; t8 F8 l& v# Q& l& x! d2 U
ment of his penis and frequent erections. The child
. H* _  s% W8 d0 p$ z; Y" hwas the product of a full-term normal delivery, with5 Q6 b6 {& @4 f' N: Z6 q0 S6 p
a birth weight of 7 lb 14 oz, and birth length of
4 l& m) u: f$ Y5 n& Z20 inches. He was breast-fed throughout the first year) o4 |. [, a1 g6 ?$ d
of life and was still receiving breast milk along with
0 F1 O" ~( s) h( z, G6 @3 L4 e, @solid food. He had no hospitalizations or surgery,
& V. p8 `7 y# x+ `and his psychosocial and psychomotor development
( C: Y0 p# Z- l( d) \5 `8 t. Fwas age appropriate.& x  ]3 \# E* I7 W6 h" q
The family history was remarkable for the father,: x4 y* `! y# F- R$ ~
who was diagnosed with hypothyroidism at age 16,
5 R' d5 |- {, T: iwhich was treated with thyroxine. The father’s0 ?: U, U) l( T; j1 j& D, r6 ?$ y: s
height was 6 feet, and he went through a somewhat& n9 Z, m6 V6 q2 C4 `
early puberty and had stopped growing by age 14.0 w) p4 S; {7 H$ ]7 O
The father denied taking any other medication. The3 B! b( R  q9 J# N
child’s mother was in good health. Her menarche
# K5 B2 n6 Z  q5 E2 ~$ zwas at 11 years of age, and her height was at 5 feet- |" [( K1 d' J) B# \  t7 g0 u8 J
5 inches. There was no other family history of pre-
- M3 K8 T7 q9 d" M- t+ q9 y- `# ecocious sexual development in the first-degree rela-
% F' x- D; X2 F9 I" ^4 N8 E: X9 Ftives. There were no siblings.
7 u% j( G( c2 xPhysical Examination
: N0 _' ^0 o: S: C& o* zThe physical examination revealed a very active,/ v0 ^/ U7 v- }, S% D9 a/ r
playful, and healthy boy. The vital signs documented
6 U* }0 }: ~- b& I& oa blood pressure of 85/50 mm Hg, his length was
6 ^/ f. E& `! z( p  o90 cm (>97th percentile), and his weight was 14.4 kg
/ b# U/ u6 I6 ?( I- i0 g  B(also >97th percentile). The observed yearly growth6 `5 ]& }0 \" u, X9 D% q
velocity was 30 cm (12 inches). The examination of
: |4 D# z4 j# f5 f+ N( I, K8 Tthe neck revealed no thyroid enlargement.
9 W, R6 p3 }" Z0 HThe genitourinary examination was remarkable for
+ i7 H- x6 J3 T0 \! c1 R1 M# |enlargement of the penis, with a stretched length of
; Z; G6 }4 X. [/ S' f% k8 cm and a width of 2 cm. The glans penis was very well8 A) O9 @: ]8 T# e6 O: n
developed. The pubic hair was Tanner II, mostly around6 \& x  p* _$ c* E4 o7 z% v
540
3 u# c( ^, c' }at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 J1 @/ j9 l4 x1 d1 O. m2 v
the base of the phallus and was dark and curled. The5 d6 G4 {" e! W. l
testicular volume was prepubertal at 2 mL each.
# W- R; D) b' E% B  h% l) fThe skin was moist and smooth and somewhat
  Q' U% V% [/ F; i4 P* D! ^oily. No axillary hair was noted. There were no1 a6 b( ~3 j" c) u; x& A3 S  Q8 w
abnormal skin pigmentations or café-au-lait spots./ w. E9 L# a4 ]% ?# y
Neurologic evaluation showed deep tendon reflex 2+
* q6 Q7 I5 F3 r9 U3 qbilateral and symmetrical. There was no suggestion
( L7 W: ~5 B+ G" Tof papilledema.
1 Q( Z  ?7 g3 @' ILaboratory Evaluation
% d: X5 [! b/ i1 I- G- [2 A; XThe bone age was consistent with 28 months by
: F  `: }2 {! V; v7 ~! yusing the standard of Greulich and Pyle at a chrono-
+ `1 D9 ^. `2 r: Q, elogic age of 16 months (advanced).5 Chromosomal
! U' l" u: f4 l$ C+ d& V% o+ Ekaryotype was 46XY. The thyroid function test' \- x5 m& L; y
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
% x* }) C/ C: T; tlating hormone level was 1.3 µIU/mL (both normal).
$ R* H1 Q9 r3 F+ gThe concentrations of serum electrolytes, blood
& T" k8 c* _5 J# ~urea nitrogen, creatinine, and calcium all were
; |* c" [3 Q( h+ \$ Swithin normal range for his age. The concentration8 Y$ g. I; u. H( @0 b- J5 S8 Q
of serum 17-hydroxyprogesterone was 16 ng/dL1 z4 W- x5 @6 }" Y+ V$ {0 m( [
(normal, 3 to 90 ng/dL), androstenedione was 20
, f0 L( x& q* R9 O0 Kng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-( @2 Q  g1 L. ~  Z! J
terone was 38 ng/dL (normal, 50 to 760 ng/dL),. m7 b8 b4 n: r* H9 n$ X, D
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
( m& c1 D1 S+ p. \% D3 o; d: I49ng/dL), 11-desoxycortisol (specific compound S)
6 C. w6 z( {( Y5 }- O1 t3 Gwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
8 b1 G) t2 e, Q! V, }. z7 d2 j; atisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total4 C9 J6 A1 r6 u" f" A& @
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),& R8 ?, I4 l6 A6 J. h7 c  ~5 N4 x
and β-human chorionic gonadotropin was less than6 K0 H: q8 j' `9 B0 z
5 mIU/mL (normal <5 mIU/mL). Serum follicular
% y& f8 q* D/ }( b( rstimulating hormone and leuteinizing hormone
/ P* Q2 F# Z# t2 R7 p$ M& lconcentrations were less than 0.05 mIU/mL' n/ N* t% A1 P# W# E
(prepubertal).
- e' g& s% V( U$ ^The parents were notified about the laboratory6 t3 Q: {8 i. D" X
results and were informed that all of the tests were! j3 |: }7 F* F
normal except the testosterone level was high. The
1 M* p# i1 s6 }/ Mfollow-up visit was arranged within a few weeks to2 e) O  F$ ]( L/ y/ p/ x6 k; `( [
obtain testicular and abdominal sonograms; how-& C2 ]$ Z$ N; E8 V+ g( f
ever, the family did not return for 4 months." T; W% k9 K$ o9 D4 @& t
Physical examination at this time revealed that the
1 @3 J  C3 }" w- F1 G. h/ Gchild had grown 2.5 cm in 4 months and had gained
7 m0 [$ m- v, g) l" j. Z. @( n# z2 kg of weight. Physical examination remained
% H3 _, Z: ^5 r# _unchanged. Surprisingly, the pubic hair almost com-; h3 }9 y1 s8 x
pletely disappeared except for a few vellous hairs at
2 D; v6 X7 n; lthe base of the phallus. Testicular volume was still 24 f# ~: O  n9 D7 C! c: R
mL, and the size of the penis remained unchanged.* \, D& F  x. B4 b: f* {
The mother also said that the boy was no longer hav-
- `8 V5 f& B" B# M( |* V: ]: Jing frequent erections.
4 R: z3 J: g+ J& i" zBoth parents were again questioned about use of8 J( e1 n, i. U: n3 y1 h( f7 d! j
any ointment/creams that they may have applied to/ K+ ~; E4 P) o# v
the child’s skin. This time the father admitted the1 Y. ]* T0 z# a- {, {8 p3 G
Topical Testosterone Exposure / Bhowmick et al 541# Z# ^- v' Z$ h3 F
use of testosterone gel twice daily that he was apply-, s* t, k% k/ e/ w! i8 d
ing over his own shoulders, chest, and back area for9 Z6 K: u9 C& f6 F1 u& N, N
a year. The father also revealed he was embarrassed% ]; i( X$ s' U: z& e
to disclose that he was using a testosterone gel pre-
% m8 a: O+ k8 B; s. j% ascribed by his family physician for decreased libido/ S: x5 H1 h" [( Q1 Q5 Z* G
secondary to depression.5 G' Q- `# Z: Z' b% P! H2 N( ]
The child slept in the same bed with parents.
' E' n0 B( R/ [  M9 m" JThe father would hug the baby and hold him on his
# |8 F1 X$ q0 @5 B# Xchest for a considerable period of time, causing sig-/ s) s; H8 }5 {( {5 e- q! L
nificant bare skin contact between baby and father.
$ B4 O- g2 R8 \3 V# |; @The father also admitted that after the phone call,) B7 t  s0 }7 }% U0 k
when he learned the testosterone level in the baby/ K$ s- q: l  ?' N$ Z) \
was high, he then read the product information% P0 p/ E" j; a7 C7 S* G
packet and concluded that it was most likely the rea-" L1 j' B  s. h+ M" o$ W
son for the child’s virilization. At that time, they1 W9 ~! ^8 `( U9 n6 ~/ U* k& X
decided to put the baby in a separate bed, and the
/ x% q' r% k, s; X. bfather was not hugging him with bare skin and had; s: C7 b$ `) J6 h
been using protective clothing. A repeat testosterone. _) Y& A) v0 q9 r  G8 B0 ]* N' i
test was ordered, but the family did not go to the1 }% V6 C6 c" g/ A$ E  q$ B
laboratory to obtain the test.2 \7 D- b: x2 |' [
Discussion5 g5 U5 a. e! B* h6 q
Precocious puberty in boys is defined as secondary
0 S( k8 Q1 P" R7 fsexual development before 9 years of age.1,4
! s$ y5 v0 Z9 t9 A7 n4 {% |8 ePrecocious puberty is termed as central (true) when
0 ~4 K, a' h% o% W0 x0 }it is caused by the premature activation of hypo-, f: k& d* e$ ?% ?( k, s% k% j
thalamic pituitary gonadal axis. CPP is more com-9 ?6 ]: b7 v7 n0 D2 A  c) o' E
mon in girls than in boys.1,3 Most boys with CPP
5 ]4 G6 y6 @# U% \' @: Fmay have a central nervous system lesion that is
9 z' I4 t2 N  i( t6 rresponsible for the early activation of the hypothal-
, L2 i* g; w5 U  P! R- v; I' xamic pituitary gonadal axis.1-3 Thus, greater empha-
4 \( a; B6 m' b4 m/ Gsis has been given to neuroradiologic imaging in
5 k: y" X+ I4 B1 Lboys with precocious puberty. In addition to viril-
" R* u$ @# a5 o( P7 J: Rization, the clinical hallmark of CPP is the symmet-
; S) g1 D: k& Zrical testicular growth secondary to stimulation by( C" z( B3 ^+ ^: t
gonadotropins.1,3
  p4 c. s. B/ `5 |7 d) Y5 B1 rGonadotropin-independent peripheral preco-+ y6 h! B0 f% @, P+ p3 j6 r. a$ t2 C
cious puberty in boys also results from inappropriate9 p9 ~9 ^3 a) h1 ~! U/ o* i  J
androgenic stimulation from either endogenous or9 i8 E8 X9 r# {# P
exogenous sources, nonpituitary gonadotropin stim-
0 j/ T4 ]3 i& `8 n! pulation, and rare activating mutations.3 Virilizing+ `6 T% B! {) c( M/ H& d
congenital adrenal hyperplasia producing excessive2 v7 X7 ]- q5 B* ?! |+ e/ _9 |, T3 o
adrenal androgens is a common cause of precocious
4 [- t9 V# Y2 T4 d7 bpuberty in boys.3,4
0 r' q. _1 V. x) m- q7 PThe most common form of congenital adrenal6 C4 C; n- k$ d) }5 Y) Y, H
hyperplasia is the 21-hydroxylase enzyme deficiency.
/ P% a: k, b( r" Q4 x" C0 j1 AThe 11-β hydroxylase deficiency may also result in
9 e) p6 y9 g+ D0 K/ dexcessive adrenal androgen production, and rarely,+ d" \9 M. u9 j( @: n# b0 M
an adrenal tumor may also cause adrenal androgen
( [; X, l2 l, m4 }5 }. Rexcess.1,3/ ^5 m( D  K, X5 `1 F( i, {
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
  l$ g4 ]# C0 K+ @8 _  v& ?& ?% l542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
2 q8 d% U3 y( \" ^3 ZA unique entity of male-limited gonadotropin-- n0 ^7 A6 l5 q7 \. G# m; v9 \
independent precocious puberty, which is also known
. [5 u( q5 y3 Y" u2 \9 E9 Vas testotoxicosis, may cause precocious puberty at a
. j" r- Z5 j6 z1 {! Lvery young age. The physical findings in these boys
) s) O/ N  Z% q6 k% L. owith this disorder are full pubertal development,
$ a& ?7 y# P* F, [/ nincluding bilateral testicular growth, similar to boys
# t, N/ H! y3 f$ Y& S- Twith CPP. The gonadotropin levels in this disorder- X7 S; P0 ^: ?& }* R
are suppressed to prepubertal levels and do not show# e  |  }4 m0 |
pubertal response of gonadotropin after gonadotropin-/ U- i" z- G  F, v% A8 z
releasing hormone stimulation. This is a sex-linked
* H, F) T* |6 e: Y$ B. A' }( l% Jautosomal dominant disorder that affects only9 `& Y% X3 ~+ D' B% x$ }
males; therefore, other male members of the family+ n: B, y: j6 k4 e- _
may have similar precocious puberty.3# t. {7 {) t; G' B/ p- P6 ], R
In our patient, physical examination was incon-0 I/ l! T6 c# H8 O- J: H( K
sistent with true precocious puberty since his testi-
5 I& V9 o' K1 zcles were prepubertal in size. However, testotoxicosis
$ n' D% ?6 K1 G7 X! mwas in the differential diagnosis because his father
( n/ j0 i; y4 C6 Rstarted puberty somewhat early, and occasionally,
0 F7 X8 W5 b. gtesticular enlargement is not that evident in the' V8 [" v2 p& C0 f# t
beginning of this process.1 In the absence of a neg-0 ^; ?. o- u1 e- C+ U+ ?
ative initial history of androgen exposure, our
5 P! H7 F. v6 W, d' y- h7 ?* bbiggest concern was virilizing adrenal hyperplasia,& l3 s# a9 t+ m6 c/ P7 m
either 21-hydroxylase deficiency or 11-β hydroxylase* `3 I9 b; [  n4 j5 k
deficiency. Those diagnoses were excluded by find-1 d& S* K: _" `' G& K  p
ing the normal level of adrenal steroids.
; C& A- K0 V5 S/ G8 IThe diagnosis of exogenous androgens was strongly6 v. W, [: o' S+ f& k
suspected in a follow-up visit after 4 months because
; K0 m: w* G& F0 u' Wthe physical examination revealed the complete disap-/ G7 y7 v3 h  v2 D( T0 R
pearance of pubic hair, normal growth velocity, and
" `3 Z5 Y# Y; N! o& @. u/ X, Udecreased erections. The father admitted using a testos-
0 x* G1 J5 S8 m: ]terone gel, which he concealed at first visit. He was5 e  O; r; j3 S( b
using it rather frequently, twice a day. The Physicians’
0 j3 p. u/ h) K& ?Desk Reference, or package insert of this product, gel or
1 p% h! i4 O: Vcream, cautions about dermal testosterone transfer to( b- f6 R, B" }
unprotected females through direct skin exposure.
8 }$ \) h- ]! iSerum testosterone level was found to be 2 times the
. Z, Y# _' M0 ^: l3 _baseline value in those females who were exposed to
) q8 D7 t+ R  _& B% meven 15 minutes of direct skin contact with their male) I3 @) }: D6 D/ w% L. p8 j4 O
partners.6 However, when a shirt covered the applica-' g4 {0 b. n% J& B5 j0 @+ W0 H. |( ^
tion site, this testosterone transfer was prevented.; l( s; F& K9 q2 s# v, j# \3 D- {' l
Our patient’s testosterone level was 60 ng/mL,
+ r* `9 ?0 ^) A" G6 L' owhich was clearly high. Some studies suggest that( ?' J% M7 u" ~" t5 J
dermal conversion of testosterone to dihydrotestos-
7 I$ @. P4 f4 W2 f- g$ T  I" dterone, which is a more potent metabolite, is more
& t. y- l7 e7 D. ]9 t/ b" jactive in young children exposed to testosterone
& _& @. ~; a" V  M4 Mexogenously7; however, we did not measure a dihy-
  I6 K: Q# ]8 Q' g+ u, [drotestosterone level in our patient. In addition to
; M5 ^4 v2 ?' ^+ Svirilization, exposure to exogenous testosterone in
  R8 x8 B. [  }' ]children results in an increase in growth velocity and
* Q& b' E; T! G! Nadvanced bone age, as seen in our patient.
) a! n' I2 @% j( z& s/ qThe long-term effect of androgen exposure during
3 l& F; _* N. ~& @, rearly childhood on pubertal development and final
% T( e, o' q% Zadult height are not fully known and always remain% n; x# _" q5 E9 P' `; W
a concern. Children treated with short-term testos-7 p6 c$ A7 |) V* b  g( \) B
terone injection or topical androgen may exhibit some2 X) n" k$ s: h5 x
acceleration of the skeletal maturation; however, after
& w2 f! W3 ^6 n7 tcessation of treatment, the rate of bone maturation
$ M: D7 F5 N+ [* edecelerates and gradually returns to normal.8,9
6 d7 |# d& S. AThere are conflicting reports and controversy# r+ H- `, F- C! \2 P
over the effect of early androgen exposure on adult
) s. Q8 X9 [- `+ ]4 y- ~4 n7 Jpenile length.10,11 Some reports suggest subnormal
! _. |0 l  e* C$ N% Gadult penile length, apparently because of downreg-
, c; J  N! {' Y. D0 t2 Y1 xulation of androgen receptor number.10,12 However,
- M" n1 T9 i7 \; O8 d; B+ wSutherland et al13 did not find a correlation between" s; o. h. u1 Z2 O& [9 J. e4 W; n, w
childhood testosterone exposure and reduced adult
, h7 w: L9 v* Y( ~penile length in clinical studies.
5 O8 t& ?9 }% X# ^. t( H& ~3 [Nonetheless, we do not believe our patient is
7 V( V7 B, N; ]6 i+ Xgoing to experience any of the untoward effects from  y* }6 y  o4 v0 J% V
testosterone exposure as mentioned earlier because
( W* K2 U/ W; [3 E9 O1 V+ S& b4 \) ethe exposure was not for a prolonged period of time.
8 m/ p! Z* P: GAlthough the bone age was advanced at the time of1 a& J8 ^$ w5 A! O2 o% z, b7 V
diagnosis, the child had a normal growth velocity at! E6 ?' V: ~4 o6 ^) ~& z
the follow-up visit. It is hoped that his final adult
0 i$ H  n& c* cheight will not be affected.9 ~- g) P0 g% Z1 P
Although rarely reported, the widespread avail-
7 O8 B# H% q& L9 Sability of androgen products in our society may& u# G( t7 b+ E& l
indeed cause more virilization in male or female3 F1 P/ E' @  m+ X  A, y; L4 f
children than one would realize. Exposure to andro-
8 \; w  {# r$ x! Ggen products must be considered and specific ques-
1 u6 h9 ?: R. I" ~8 J0 Y- Gtioning about the use of a testosterone product or
4 C! ~6 ?; E5 Y& K- K7 O# h- Jgel should be asked of the family members during
, w/ z3 c* T1 S0 `# sthe evaluation of any children who present with vir-! C; q- b( c. `
ilization or peripheral precocious puberty. The diag-
8 `1 f4 U( E$ _nosis can be established by just a few tests and by& J7 ?& I) _% A- y1 m
appropriate history. The inability to obtain such a
' w. m8 d/ n& ]9 ?7 r( ohistory, or failure to ask the specific questions, may
! w! e" K; N( S) Z8 M9 Gresult in extensive, unnecessary, and expensive( T& s/ o% j7 C  y  O
investigation. The primary care physician should be0 @" @) s/ l2 ^( {1 Q
aware of this fact, because most of these children
) |# v+ q- k# y* ]- o' Lmay initially present in their practice. The Physicians’
% ?* s% M  G0 A: |& I1 EDesk Reference and package insert should also put a
% M8 D3 I1 q& U( m3 k3 fwarning about the virilizing effect on a male or
, ?; ~2 O' ]/ }. xfemale child who might come in contact with some-2 T; H2 P3 N9 Q5 x. i) ~
one using any of these products." @4 m3 o* j$ W0 R1 n
References
( n: u/ S2 B5 R1. Styne DM. The testes: disorder of sexual differentiation( v; O- o2 m  N8 i
and puberty in the male. In: Sperling MA, ed. Pediatric( i4 @- S2 t/ ]1 |& X3 O
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
! Z/ |% n& k% D7 i) d$ d2002: 565-628.9 R/ }0 }4 l& ^7 P) m4 D, _
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious& W% p$ ~6 e7 w. Z0 K; \6 X
puberty in children with tumours of the suprasellar pineal
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這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
6 L% s; m4 {' s' G* `2 ^, c( F" q3 b6 }
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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