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Sexual Precocity in a 16-Month-Old
( A' x$ S; }2 T) oBoy Induced by Indirect Topical0 _( i: f& P9 |: p
Exposure to Testosterone" L0 {1 {" [6 L/ X) e
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2% V- ?" _( M  v( J9 W$ j% y% u2 I
and Kenneth R. Rettig, MD1
! K+ L( i* p! E4 zClinical Pediatrics8 u' L+ V2 c% D' T. \8 Y, {
Volume 46 Number 6
: ~( w0 ~4 ?$ k" }! s/ |July 2007 540-543
" C! v+ t( V2 }" p" v5 P& M© 2007 Sage Publications; j- n% t9 g# P
10.1177/00099228062966512 Z; h7 P: |8 E* D& }2 O
http://clp.sagepub.com
: H4 D8 D8 Y  F1 Uhosted at
/ r4 Y& m; c$ p! H* e3 Rhttp://online.sagepub.com
2 B# C" @! y9 h7 P9 I2 L) iPrecocious puberty in boys, central or peripheral,8 x9 J9 G1 j5 G+ X4 G. k
is a significant concern for physicians. Central
6 f. x% D' p  Aprecocious puberty (CPP), which is mediated% J4 E% {6 z* i; L) w  ~1 `
through the hypothalamic pituitary gonadal axis, has
+ Q( b' P$ M, V$ Fa higher incidence of organic central nervous system
2 n/ v$ w& f1 N) Alesions in boys.1,2 Virilization in boys, as manifested
" O- _5 |0 n7 t: q: r' S1 {by enlargement of the penis, development of pubic5 d9 D2 \- O/ t6 E$ [5 ~
hair, and facial acne without enlargement of testi-
$ o  [: \4 d  K! ncles, suggests peripheral or pseudopuberty.1-3 We
# k3 h, m5 X, Jreport a 16-month-old boy who presented with the: m9 Z: _: U' X, a# K
enlargement of the phallus and pubic hair develop-
2 n! e* o9 I* f. H0 \# yment without testicular enlargement, which was due5 V2 `+ R8 p" W  h' f4 e
to the unintentional exposure to androgen gel used by" g, L& g8 Z$ H$ X" s/ O+ |
the father. The family initially concealed this infor-0 E1 N$ D" _. B" ?, \
mation, resulting in an extensive work-up for this
" E! V( D6 M$ b& O- _& H, @child. Given the widespread and easy availability of0 Y: H9 M- L# }: ~3 X& I
testosterone gel and cream, we believe this is proba-
# _8 \8 d; G# O0 ?+ e* f; V/ kbly more common than the rare case report in the3 }, @; x: X& n( K+ u1 w: |( ~# Q
literature.4) s0 K9 l2 I5 t1 g
Patient Report1 v! i. [3 D9 h2 {
A 16-month-old white child was referred to the: V% D! F. i. N% `7 R+ U/ ^' I/ ]) ?
endocrine clinic by his pediatrician with the concern
! C9 P/ r6 ~7 Q  g# ?! B$ bof early sexual development. His mother noticed+ O, j2 e0 L' ^1 T! W8 w& K( u
light colored pubic hair development when he was9 r5 G( w( t: T& \# t! l. m6 K2 m
From the 1Division of Pediatric Endocrinology, 2University of
6 j! ?2 b: A: m0 t: ^" j9 oSouth Alabama Medical Center, Mobile, Alabama.9 C$ X8 T8 u: I9 o
Address correspondence to: Samar K. Bhowmick, MD, FACE,* w& T+ [, p6 A
Professor of Pediatrics, University of South Alabama, College of+ Z* v, S7 _, n& ^$ l
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;% Y& {  h' b: ?9 c# p8 q# D9 _
e-mail: [email protected].% d% S. `4 m! l! u3 u
about 6 to 7 months old, which progressively became
) C9 [0 v2 F8 \4 }7 y6 Zdarker. She was also concerned about the enlarge-
5 ?4 _  G1 o9 d4 `ment of his penis and frequent erections. The child( C0 h1 q9 w! j5 b: }: p
was the product of a full-term normal delivery, with
$ ?! x5 O: x  N7 u" S# A7 K6 \a birth weight of 7 lb 14 oz, and birth length of
& X, M* ]# v2 e2 P, H3 |# w20 inches. He was breast-fed throughout the first year
# S4 d' [& f0 z5 o0 z" o2 ]4 Iof life and was still receiving breast milk along with
% j) a& P( P  z7 M0 Ysolid food. He had no hospitalizations or surgery,6 |( T' M9 ?& |0 P
and his psychosocial and psychomotor development! Q' C6 Z8 f( Z8 T3 v" e8 \$ T
was age appropriate.
6 l! Y* t# U" K$ c& pThe family history was remarkable for the father,
9 f$ i* Z3 ^3 {" l+ R: ?who was diagnosed with hypothyroidism at age 16,- S  o0 T  b- ]/ S/ V
which was treated with thyroxine. The father’s
8 n/ x2 l& }+ y% Bheight was 6 feet, and he went through a somewhat
& ]' T+ I+ V% s( T% b% ^  s& e  eearly puberty and had stopped growing by age 14.8 Y6 x' a. X$ I4 h- G
The father denied taking any other medication. The5 F" L; m' I* ?4 O/ k. Q, I& B) d! [
child’s mother was in good health. Her menarche
6 k& D9 o/ x) l9 [: d  P/ N4 F: X( fwas at 11 years of age, and her height was at 5 feet
  \4 J: c. A' e( y' H5 inches. There was no other family history of pre-" c4 Y+ j5 A0 |6 G
cocious sexual development in the first-degree rela-
& N# B4 r5 J5 D, ]# ntives. There were no siblings.
+ }) R% u% n, q9 @2 x- IPhysical Examination0 j2 v) p2 J; G" t3 v6 g; f
The physical examination revealed a very active,& f0 Z& P: y7 d
playful, and healthy boy. The vital signs documented; n7 d: Q% ^* r5 v0 D; Z2 r( O+ ]2 b
a blood pressure of 85/50 mm Hg, his length was3 V3 `2 f" C4 Q$ v2 ~
90 cm (>97th percentile), and his weight was 14.4 kg( n! S5 ?' i) }6 Z' b: N
(also >97th percentile). The observed yearly growth* g7 \2 y1 V; W3 c+ Z- d6 \
velocity was 30 cm (12 inches). The examination of1 ]8 ^9 d2 Z: r
the neck revealed no thyroid enlargement.' ^" Z) [* `. _5 q
The genitourinary examination was remarkable for
6 j- g% C2 Q! J! }. e. o, _enlargement of the penis, with a stretched length of) t4 `4 l6 P9 K0 |+ t
8 cm and a width of 2 cm. The glans penis was very well
  y! f) [! n2 {8 K( e* Edeveloped. The pubic hair was Tanner II, mostly around. D1 D: b6 Z0 O9 t& p
5408 [' n; Z% @% x
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 j4 c3 m' C1 t/ s7 o8 Nthe base of the phallus and was dark and curled. The  j4 P9 h5 x& j& R; a1 S# X" m
testicular volume was prepubertal at 2 mL each.! [" E* w1 q5 h
The skin was moist and smooth and somewhat
& a9 |% |$ T6 F9 [2 a0 L0 H' Ooily. No axillary hair was noted. There were no
$ H' q; H. Q0 v5 h8 Mabnormal skin pigmentations or café-au-lait spots.% V3 z% F, U) x3 P
Neurologic evaluation showed deep tendon reflex 2+
4 C! J! D9 o. [; {2 fbilateral and symmetrical. There was no suggestion
/ f+ ^  ^; j: G! q* H/ {2 Fof papilledema.5 ]5 L( c  W; g* v+ p$ l
Laboratory Evaluation7 z: Y$ ^) F$ z# |6 v3 m- z4 A2 S
The bone age was consistent with 28 months by
0 H+ k/ Q& O, g4 b- yusing the standard of Greulich and Pyle at a chrono-
7 n" E+ h5 P7 f- _# h) P6 Llogic age of 16 months (advanced).5 Chromosomal" V" @/ G  C. H9 M
karyotype was 46XY. The thyroid function test' T- N0 X# m5 R" i3 L4 G9 ^* \' T! F
showed a free T4 of 1.69 ng/dL, and thyroid stimu-, D7 o: \0 z# B& D- M) N
lating hormone level was 1.3 µIU/mL (both normal).6 I* V- I* Y* C
The concentrations of serum electrolytes, blood
3 y! a% O! G% ~" Vurea nitrogen, creatinine, and calcium all were# Q- ]# l$ Z2 C/ _
within normal range for his age. The concentration& W5 x" M% q7 G! k
of serum 17-hydroxyprogesterone was 16 ng/dL
5 s8 G$ [4 y  }4 V. W(normal, 3 to 90 ng/dL), androstenedione was 20
  Y4 Q  L0 u- I6 |4 B5 ^ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
) T; `9 _3 n4 e' dterone was 38 ng/dL (normal, 50 to 760 ng/dL),
8 @4 u. H2 f: |- ]) {3 H: x  Idesoxycorticosterone was 4.3 ng/dL (normal, 7 to0 v+ p& ]8 u, m# s& L$ y$ m
49ng/dL), 11-desoxycortisol (specific compound S): C: P0 {# J6 \0 B" k7 z  o
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-% j8 A  X7 F4 T, N# V  S6 [
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total5 u# H. I& l- j* }4 b$ _, v% l. m
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),6 I& Z. x5 M+ w$ V. y1 C; Z
and β-human chorionic gonadotropin was less than
' N9 ^) e) @& T& V  T5 mIU/mL (normal <5 mIU/mL). Serum follicular
* w- `% K0 \( q: }' t+ X$ Pstimulating hormone and leuteinizing hormone( ]. u% {( J7 L6 w
concentrations were less than 0.05 mIU/mL* g7 p" q8 |2 O1 p" [* ^
(prepubertal).# ?" C3 l: P$ i5 F! @" L7 M! O% A2 s% f
The parents were notified about the laboratory
% {* p4 ^7 t3 u( aresults and were informed that all of the tests were
( u# A5 h( d, pnormal except the testosterone level was high. The+ g  h4 T, q+ p7 d
follow-up visit was arranged within a few weeks to
: {# j, g7 V% x9 A, b& P3 vobtain testicular and abdominal sonograms; how-' G5 Q0 |4 Q. d
ever, the family did not return for 4 months.$ _7 {( b9 E) o4 n) Q2 G
Physical examination at this time revealed that the! U6 M4 g$ t' ?" g  K3 w5 h/ d5 G) ]
child had grown 2.5 cm in 4 months and had gained
1 l' |3 y/ b1 x* {, t7 t/ D& i5 V! K; d4 k2 kg of weight. Physical examination remained
$ L' q8 B5 C* j5 Z1 F5 b7 G/ a3 wunchanged. Surprisingly, the pubic hair almost com-  ^* a& K% h! I2 U. ?, H6 r8 L
pletely disappeared except for a few vellous hairs at
% |7 {% F! y$ r; k7 f2 jthe base of the phallus. Testicular volume was still 24 c9 v  ]+ E3 Z
mL, and the size of the penis remained unchanged.' U5 h  Y# i6 r" D# F5 e
The mother also said that the boy was no longer hav-
7 `5 |; C/ m# Y6 L; T7 V( Xing frequent erections.
9 s7 i, N6 {" D# A/ mBoth parents were again questioned about use of" Q+ q7 Y* d! e) v" N0 D0 l
any ointment/creams that they may have applied to
1 q  ^4 J, L: D" P: q6 Z; t7 ~8 Wthe child’s skin. This time the father admitted the5 Z3 \' L1 g9 g4 Z- |1 H
Topical Testosterone Exposure / Bhowmick et al 5412 N$ k2 u9 p+ S' ^# l' |: _7 v2 P
use of testosterone gel twice daily that he was apply-
& j9 o, d  c; U! c& K  M, b" m: L" oing over his own shoulders, chest, and back area for& r9 I) N/ N7 N
a year. The father also revealed he was embarrassed% G+ [5 N& g3 f* L/ ^
to disclose that he was using a testosterone gel pre-
* V, ?. ]" V5 f$ i5 c8 ascribed by his family physician for decreased libido4 Y. @9 o6 r6 P) a7 z4 R0 z6 A
secondary to depression.0 w# b  G) R; P% q! F  z* T
The child slept in the same bed with parents.
2 m6 F& I  B$ }0 \, k+ BThe father would hug the baby and hold him on his
1 `" P# q; Q; m& l( W  ]. Mchest for a considerable period of time, causing sig-0 G9 G: U, N* c) c. B  F
nificant bare skin contact between baby and father.' n2 x% [) Q( w& F
The father also admitted that after the phone call," k3 T; u6 Y8 Y8 Y  s
when he learned the testosterone level in the baby
: a3 u, r, L) V) U1 bwas high, he then read the product information
7 q1 g+ a& c  bpacket and concluded that it was most likely the rea-) g) r% A  y  O* W# A
son for the child’s virilization. At that time, they
. D% h% m# t+ |2 e4 Udecided to put the baby in a separate bed, and the
3 b% f6 M6 n0 E! R# O" _9 w  r( Pfather was not hugging him with bare skin and had, ?# d5 L$ o/ Z9 R/ s0 O1 S2 x4 B
been using protective clothing. A repeat testosterone4 l3 `3 i9 m* H- m5 }
test was ordered, but the family did not go to the9 T1 H! n# p9 f* q0 L
laboratory to obtain the test.
; x0 z' i4 K2 `: ~4 QDiscussion
2 Y$ {2 Y; v6 e8 }3 I* k- l5 LPrecocious puberty in boys is defined as secondary
  c1 S, E2 x& U) Z, ssexual development before 9 years of age.1,4$ r* ^$ Y- b" f' J
Precocious puberty is termed as central (true) when0 m7 C3 b  Q1 \9 K' c) @
it is caused by the premature activation of hypo-
  i) r' x: B- Nthalamic pituitary gonadal axis. CPP is more com-
- m8 A4 c, R& m6 d+ D4 kmon in girls than in boys.1,3 Most boys with CPP4 @- V* r3 v8 u6 e) I2 [- _! n
may have a central nervous system lesion that is
) u; Y5 u& }. I' n1 vresponsible for the early activation of the hypothal-' g& e# g( }. N- A# d+ w7 S
amic pituitary gonadal axis.1-3 Thus, greater empha-
0 |: o' j( c& Y% Msis has been given to neuroradiologic imaging in
- g; O+ K5 I% P5 o  c* O3 L% dboys with precocious puberty. In addition to viril-- u8 Z- l0 s8 K# d
ization, the clinical hallmark of CPP is the symmet-
& z7 ?8 K$ s1 f9 f+ T; k4 Erical testicular growth secondary to stimulation by
; C( j: Q# v% ^) _9 x7 k/ vgonadotropins.1,3
+ h, s; M5 F+ F+ v% o, P" {Gonadotropin-independent peripheral preco-
. x: F" c/ r2 q# ]- Ucious puberty in boys also results from inappropriate
' L- V7 B5 Y3 t# K! b+ J3 nandrogenic stimulation from either endogenous or( u; w7 p- }; f( o0 g* W/ E
exogenous sources, nonpituitary gonadotropin stim-
: Q7 p3 |2 H; W" X6 V- Zulation, and rare activating mutations.3 Virilizing
7 j/ [7 E7 l: ^7 D( h( K7 zcongenital adrenal hyperplasia producing excessive
4 [" ^- E# `+ f, Radrenal androgens is a common cause of precocious
1 U0 L) \# f" J7 Cpuberty in boys.3,4
1 j0 f6 b5 l; l' b+ b0 s: ]9 d/ [The most common form of congenital adrenal
: N& f3 I4 `' t7 }* w/ V! Jhyperplasia is the 21-hydroxylase enzyme deficiency.* h& P8 h$ B7 X2 e2 U
The 11-β hydroxylase deficiency may also result in# s# I1 k  w/ v; z" \' V6 u" H
excessive adrenal androgen production, and rarely,; i7 W$ [- u6 x6 k) E$ P
an adrenal tumor may also cause adrenal androgen4 l, T5 q5 a" u" b: m  G3 V4 h$ ?3 T
excess.1,3
0 k8 Y* K! a) e0 s! U8 Bat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ o. _% h1 l- L# S" q
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007$ I. S3 |( |! a1 K# {0 f8 q  I4 a
A unique entity of male-limited gonadotropin-
) M( a2 Q! {6 l' P% ~: cindependent precocious puberty, which is also known
5 F5 F- g! K8 i/ s* z3 d! ras testotoxicosis, may cause precocious puberty at a
/ p4 T% {- V" ]9 _3 Yvery young age. The physical findings in these boys: u0 J) a8 v/ {, n4 K
with this disorder are full pubertal development,6 z- B% s# f/ A5 {
including bilateral testicular growth, similar to boys
  d* d. p, O. M. O% y9 ^$ ]with CPP. The gonadotropin levels in this disorder
' ^- D# [- P5 z0 y6 Jare suppressed to prepubertal levels and do not show# E' _3 T1 {" h
pubertal response of gonadotropin after gonadotropin-
, i, |4 g; H9 K  rreleasing hormone stimulation. This is a sex-linked) w" H# L0 S8 k3 X
autosomal dominant disorder that affects only$ W/ n+ D! x* b7 Q2 G
males; therefore, other male members of the family
0 s$ {4 k1 n: A3 q7 W' p: K- Lmay have similar precocious puberty.37 U! [: f, A& O8 r; p. e3 Q
In our patient, physical examination was incon-5 a. M: W: `. S) |8 A
sistent with true precocious puberty since his testi-0 O7 ~6 m# Z5 t
cles were prepubertal in size. However, testotoxicosis" L: P  V8 Q  o5 D" {
was in the differential diagnosis because his father
$ x7 h& \3 v( ustarted puberty somewhat early, and occasionally," C. D2 y) d# P0 T& ^6 U& q
testicular enlargement is not that evident in the
4 B1 l3 m( ]' n% X) ^: F( |beginning of this process.1 In the absence of a neg-
4 j* a( x& c- V7 C1 eative initial history of androgen exposure, our
' W! o1 i4 u( B% A/ M+ ibiggest concern was virilizing adrenal hyperplasia,
7 K3 j2 i- a( N- a1 O& _. Aeither 21-hydroxylase deficiency or 11-β hydroxylase
/ J0 E% P0 e" |& q( u/ M( ydeficiency. Those diagnoses were excluded by find-
. j6 ^5 _2 n' T, ving the normal level of adrenal steroids.
7 U1 G$ z! o6 jThe diagnosis of exogenous androgens was strongly5 `" ?3 ?+ h, I& y6 t- k
suspected in a follow-up visit after 4 months because0 i$ P/ O6 e  H* U- C& L
the physical examination revealed the complete disap-
! Q% y. U; t5 a* N5 U- apearance of pubic hair, normal growth velocity, and! O2 P% K3 p2 n+ @* Z
decreased erections. The father admitted using a testos-! s- d" {* `* l4 \& r
terone gel, which he concealed at first visit. He was( i" l( ]% N1 H; x! a0 ]
using it rather frequently, twice a day. The Physicians’
1 X5 f2 c9 c9 qDesk Reference, or package insert of this product, gel or& b* Y2 e/ ~- I/ K0 w& i5 \7 @& N2 ]
cream, cautions about dermal testosterone transfer to* ~& F* _7 ]( L/ A$ ~. u) K
unprotected females through direct skin exposure.
) p: }* J3 q' e2 \+ ]+ k2 KSerum testosterone level was found to be 2 times the
' t& V: \3 Y% J3 b6 nbaseline value in those females who were exposed to
5 p" }# Q/ O# B$ geven 15 minutes of direct skin contact with their male  |4 ]" z! L8 v% |' P; z! t
partners.6 However, when a shirt covered the applica-
3 D6 ^/ r1 O0 k7 X% _! qtion site, this testosterone transfer was prevented.5 u( [% K% j  t
Our patient’s testosterone level was 60 ng/mL,& c1 H7 |" C& [6 ^9 h
which was clearly high. Some studies suggest that7 S1 d# b, D: I- v7 E
dermal conversion of testosterone to dihydrotestos-
! _, E$ k' o% @8 {  Dterone, which is a more potent metabolite, is more/ p; B6 H* \3 V) O% U9 S( S
active in young children exposed to testosterone
0 j# Z8 {1 I1 Xexogenously7; however, we did not measure a dihy-
4 |( U" a. d4 O5 I3 L. L( gdrotestosterone level in our patient. In addition to3 h& h2 `/ A- `
virilization, exposure to exogenous testosterone in
9 t) P* N3 W1 H; V7 L* Dchildren results in an increase in growth velocity and
8 l0 A( o& v* g- ~6 ~1 O& m* dadvanced bone age, as seen in our patient.- I& [1 D8 \6 |
The long-term effect of androgen exposure during
# j" }0 M& Q6 ~. Vearly childhood on pubertal development and final5 v+ Q! k6 G+ C! Q+ u
adult height are not fully known and always remain! w; m5 P1 M8 ?# W
a concern. Children treated with short-term testos-
" F4 f- v5 u! U2 d+ }$ S* Hterone injection or topical androgen may exhibit some5 X2 ^4 R. h0 {& u: O  c
acceleration of the skeletal maturation; however, after
7 r, i) ]; {, p: g8 ~: Zcessation of treatment, the rate of bone maturation' E1 X0 {3 j5 c) b" x
decelerates and gradually returns to normal.8,9* _( w+ }6 h4 I9 x' R. M' M. o
There are conflicting reports and controversy/ V, u! W) y5 o& X! b
over the effect of early androgen exposure on adult& p1 W0 {" S% H
penile length.10,11 Some reports suggest subnormal
# i; K, d! M0 O8 qadult penile length, apparently because of downreg-
. L8 E6 @% u& n* ?. c, Lulation of androgen receptor number.10,12 However,; {8 D  Y% v" `+ j9 F
Sutherland et al13 did not find a correlation between3 g6 E; b1 H3 R8 u; l1 S
childhood testosterone exposure and reduced adult
* d. L  R2 V, ]% Gpenile length in clinical studies.
; B% p! a# {; X0 y2 l4 S& o4 ]Nonetheless, we do not believe our patient is
$ d; _% \  l- |, C% Agoing to experience any of the untoward effects from: k9 s/ i" t! k, U
testosterone exposure as mentioned earlier because: y; K" B" o% J; _$ _  K& J
the exposure was not for a prolonged period of time.
2 U& H8 A; s+ i6 PAlthough the bone age was advanced at the time of
  i" r7 _' |/ }, r) A# Xdiagnosis, the child had a normal growth velocity at
9 h; s8 |! X0 S" Sthe follow-up visit. It is hoped that his final adult
$ {/ h$ V/ X  B' A, n9 l3 A3 vheight will not be affected.
3 u% U9 A' D, W$ ^0 G7 ]Although rarely reported, the widespread avail-
5 h: U% m& j. }% Z! Kability of androgen products in our society may3 G2 L- X6 p$ s- Q; [
indeed cause more virilization in male or female
' |+ C' Z6 E7 O$ ?children than one would realize. Exposure to andro-, f) }% Q0 O* g6 j$ e
gen products must be considered and specific ques-6 y+ P3 w+ S& K) D: F( s( q
tioning about the use of a testosterone product or% K4 @5 q1 {; h+ I6 L2 x  r
gel should be asked of the family members during# r" T) u, B& C3 F# L6 h1 @- u0 L7 H
the evaluation of any children who present with vir-
7 F( K! w, R, F- a* milization or peripheral precocious puberty. The diag-
, M$ d) }4 g( F" Y9 ~; Snosis can be established by just a few tests and by  u, p8 h9 a' ~# ]( w- ^' y% {
appropriate history. The inability to obtain such a# }' `8 u& M: D1 V$ O. o4 M3 \+ W
history, or failure to ask the specific questions, may' T: F$ I: Z9 [# Y3 |
result in extensive, unnecessary, and expensive# D' [7 `; \6 H- M  ~% g
investigation. The primary care physician should be! R# g1 \# ?. T2 g0 b, l2 C
aware of this fact, because most of these children
/ r3 x( B$ n1 M" b3 }0 Lmay initially present in their practice. The Physicians’
& }& j' _3 L0 j4 a' S/ sDesk Reference and package insert should also put a
& U5 `7 G7 Y6 O4 D( W! Cwarning about the virilizing effect on a male or
( d% Q/ r1 ?- ]1 H- R7 g; T, zfemale child who might come in contact with some-
, }& k$ E/ m" c5 J: j4 x# Lone using any of these products.; C/ s! X6 Y9 r; `* w
References* u1 X  z+ i0 ~+ P1 a
1. Styne DM. The testes: disorder of sexual differentiation
4 Z' ?" ?/ m' Qand puberty in the male. In: Sperling MA, ed. Pediatric' `1 j& o0 m5 x5 p7 S) s
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;2 n% \# f8 t& C4 s+ N
2002: 565-628.$ e- D' ?+ @7 z# _0 ]5 S$ _
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious  u+ S; R' g7 k  _, B- J
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
3 j; G) l. ]7 g$ V7 e0 r: g% H/ NBoy Induced by Indirect Topical: @- v  P. K! o1 a% V
Exposure to Testosterone
  R* b9 ]0 _7 ~. g2 `* D9 H+ nSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,20 H: Z  a* i7 P4 e$ X' r
and Kenneth R. Rettig, MD1" d! M+ z& v% h: n
Clinical Pediatrics
! w! n7 U% M9 ~$ t# |$ F& O3 wVolume 46 Number 66 m+ ~2 q* l6 F
July 2007 540-5430 v5 \" A, q( n! q# G: _! T) I
© 2007 Sage Publications  V2 Z, w$ e- M. ~, l
10.1177/00099228062966510 D4 H8 H3 c: Y
http://clp.sagepub.com
0 I4 S- m  t& ]7 x6 r7 thosted at
& a( X! u3 e8 {* E, uhttp://online.sagepub.com8 D( ]0 t3 n# W3 C) Q6 \! L, v! @
Precocious puberty in boys, central or peripheral,
7 f$ `: q+ D% V. Ais a significant concern for physicians. Central
: t, \- F+ H. d$ y  {precocious puberty (CPP), which is mediated
5 h  l( U6 H2 K) Ythrough the hypothalamic pituitary gonadal axis, has
1 d3 y: [3 A2 y! d- N9 ja higher incidence of organic central nervous system
) `. j6 Y( h' s/ A  g" \% Jlesions in boys.1,2 Virilization in boys, as manifested
8 n7 ?& H4 |- ?8 X6 I) Xby enlargement of the penis, development of pubic8 b% x  \& i7 d1 B2 m! H5 P
hair, and facial acne without enlargement of testi-: X9 j0 `+ s& S0 F: P5 Z- P5 N
cles, suggests peripheral or pseudopuberty.1-3 We- y3 d4 S# o, @; L, m- ^
report a 16-month-old boy who presented with the
3 j8 j+ P9 ~* wenlargement of the phallus and pubic hair develop-
  j: @5 }- Z& `% p% {ment without testicular enlargement, which was due
8 U0 ~# v8 E! }' I8 m  vto the unintentional exposure to androgen gel used by
7 f2 r4 a: [7 r) [the father. The family initially concealed this infor-
7 C: z3 [+ E3 `) K! n+ vmation, resulting in an extensive work-up for this2 Y0 ?5 C! u; {" l, S2 Y% n
child. Given the widespread and easy availability of4 t  g% z/ @4 L8 A4 D4 d
testosterone gel and cream, we believe this is proba-8 @4 l+ n% G/ m/ P. E: i( x  H
bly more common than the rare case report in the
: x% {  H" J5 n9 a& F; Wliterature.4
+ S! e  {$ \; g, Y- F( gPatient Report6 u' k9 f3 U# F
A 16-month-old white child was referred to the
& }4 C8 Y+ F5 e8 l) \  C6 A, Cendocrine clinic by his pediatrician with the concern
$ J- @2 z' L6 I( zof early sexual development. His mother noticed
' H2 b% H1 Q7 Elight colored pubic hair development when he was
3 i% _6 Q0 Y2 c* MFrom the 1Division of Pediatric Endocrinology, 2University of
6 W) j- I; T: u  o* p$ m& J$ ]9 PSouth Alabama Medical Center, Mobile, Alabama.4 q7 d: D( l3 V
Address correspondence to: Samar K. Bhowmick, MD, FACE,4 l3 l* C$ o7 {+ g) Z+ e
Professor of Pediatrics, University of South Alabama, College of2 `$ B+ Y: M( f  i" c  E
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;9 e3 m, R, Q& x; h: t1 c
e-mail: [email protected].
& \3 p0 y4 ~0 W4 ^% b+ m) \0 }about 6 to 7 months old, which progressively became
# u" T% `4 D, W. Q. Z- W/ Edarker. She was also concerned about the enlarge-4 j! S6 D7 a" k. l; t$ ?) q
ment of his penis and frequent erections. The child
- f* [$ l  i# `% a- uwas the product of a full-term normal delivery, with
: j5 l* N; ?# I/ @6 S  La birth weight of 7 lb 14 oz, and birth length of
& U% c' x" N; ^& ^5 z20 inches. He was breast-fed throughout the first year
7 l, |, R5 D. E, `- M( ^0 Dof life and was still receiving breast milk along with, _& V8 r, E) t; r' R
solid food. He had no hospitalizations or surgery,
9 I9 F7 o8 l: v5 Eand his psychosocial and psychomotor development& _+ |, d9 h; m1 z, F8 ~# n; L
was age appropriate.
; N- x8 m. U/ A$ I0 JThe family history was remarkable for the father,
, H. Z( N. D6 J9 S+ xwho was diagnosed with hypothyroidism at age 16,
, u: Z) Y) ?" k) U# u9 d  S/ Jwhich was treated with thyroxine. The father’s6 @) d, {5 N4 v$ ]: O! N$ B6 m1 n; G( R
height was 6 feet, and he went through a somewhat
! \" J' E2 }- P7 {/ M' E3 Cearly puberty and had stopped growing by age 14.( s; b( W; x8 S/ ~% Y. z
The father denied taking any other medication. The
# K% u- R" j: i! y3 Bchild’s mother was in good health. Her menarche
2 G4 k: q5 k" \) p% \$ ]2 |; @7 Ewas at 11 years of age, and her height was at 5 feet
" ^! m. F; K# Q+ f& |1 v. k, u5 inches. There was no other family history of pre-
- n3 G) T4 o* ^2 n! {& s. Q: D0 ucocious sexual development in the first-degree rela-! c5 e8 y+ Y: C* \- \( b4 e
tives. There were no siblings.# C3 L1 d% h0 e! N$ f
Physical Examination. F, P; [& e! t! v) K
The physical examination revealed a very active,
' S3 F' l- X# _( D. b8 @4 @" jplayful, and healthy boy. The vital signs documented
5 g7 T, H4 B( S/ k7 K8 x; ~( `a blood pressure of 85/50 mm Hg, his length was5 X* ^: n; T& v1 A; @
90 cm (>97th percentile), and his weight was 14.4 kg  p9 v# k% m% B3 D% O
(also >97th percentile). The observed yearly growth' T: w' n2 j+ J) @4 @. N4 O
velocity was 30 cm (12 inches). The examination of
: B+ @! F' M# I; @. Z! Y0 G" Mthe neck revealed no thyroid enlargement.
7 m& t0 b# o' d2 X9 R; m2 LThe genitourinary examination was remarkable for" @7 G, N( C$ e  [' W8 u
enlargement of the penis, with a stretched length of' D' J9 D: m/ _
8 cm and a width of 2 cm. The glans penis was very well
7 ?3 H; F/ x* {developed. The pubic hair was Tanner II, mostly around  S3 i! n1 O  Q9 F7 O
540
8 G; ~0 F+ d) [* Xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 o1 J8 ^! `- p  m- ~
the base of the phallus and was dark and curled. The1 J7 g5 V0 m& z3 B+ G+ h
testicular volume was prepubertal at 2 mL each.
- O! g- t$ o( ^* H' q9 nThe skin was moist and smooth and somewhat
0 ~1 D- x8 Z3 R* f( t' koily. No axillary hair was noted. There were no/ w- q" v7 y: |; S( `* w
abnormal skin pigmentations or café-au-lait spots.
% e& R- p& N' E# ?Neurologic evaluation showed deep tendon reflex 2+
$ p* e5 m$ y9 h. u4 O( I$ Ybilateral and symmetrical. There was no suggestion
' u8 ]( N7 B9 k: @of papilledema.
- w1 ~% H8 ]' K2 J- H3 yLaboratory Evaluation
( ^8 S1 Y* H, V$ y3 p) JThe bone age was consistent with 28 months by& r9 x* F/ L9 [
using the standard of Greulich and Pyle at a chrono-
) ~7 W6 u6 _, I, p- w. Rlogic age of 16 months (advanced).5 Chromosomal6 [( x( p) f4 Z
karyotype was 46XY. The thyroid function test- F. U) J( U4 m1 X0 d6 d
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
3 |) l1 V1 c1 ^/ Z& Q7 C" clating hormone level was 1.3 µIU/mL (both normal).* L! l' N* U/ ^1 m9 [7 U, ?2 J
The concentrations of serum electrolytes, blood. L% l* B' ~9 L- W& Y# X! M
urea nitrogen, creatinine, and calcium all were
7 ]: @7 k4 W$ h3 t4 b5 p: bwithin normal range for his age. The concentration: _) {" d5 T+ w7 _9 `
of serum 17-hydroxyprogesterone was 16 ng/dL/ |3 f+ z: T) S3 T! w/ r* A0 U* i
(normal, 3 to 90 ng/dL), androstenedione was 203 D; Z9 l- Q  @8 A' J0 a, r
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
6 }5 G* t# ^3 n" K0 T6 T( J3 Cterone was 38 ng/dL (normal, 50 to 760 ng/dL),& s1 E8 T* B5 U: a" {
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
( ]1 N) h* p2 a: h49ng/dL), 11-desoxycortisol (specific compound S)
  r$ S( J5 G* X" I! I4 \$ ?' Wwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
4 [- R7 t4 p+ F0 ]/ g9 ntisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total9 f# a9 x* @$ w( t4 C" f  W* l
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),( ]0 K: v# g) o' |
and β-human chorionic gonadotropin was less than& L2 O9 x/ S+ C4 Z) l% x1 `. [
5 mIU/mL (normal <5 mIU/mL). Serum follicular
  M1 g6 A- [) dstimulating hormone and leuteinizing hormone) a  p/ y9 A. F2 T. F! P% z( D- [
concentrations were less than 0.05 mIU/mL
* c: e7 i" @0 H* L(prepubertal).
: J$ x# w" M# s$ s, D5 u/ V+ f' tThe parents were notified about the laboratory# l& ?5 O8 [- o, z1 \1 A( J
results and were informed that all of the tests were
* |5 Q. @& a# L* ynormal except the testosterone level was high. The* ?& K) @) ^! n, ?
follow-up visit was arranged within a few weeks to
8 i5 D" n) b, m. ?/ p" E9 @obtain testicular and abdominal sonograms; how-
2 c7 m' j+ b2 W& h: ^0 |ever, the family did not return for 4 months.0 @3 S. Z/ J; i+ Z# D6 D
Physical examination at this time revealed that the; N4 O" K' C& O$ V8 |. c
child had grown 2.5 cm in 4 months and had gained
- C7 D) ]6 y3 j$ m2 kg of weight. Physical examination remained% r9 s4 L" [# o! o' P0 \, |
unchanged. Surprisingly, the pubic hair almost com-
3 f$ C6 X1 \4 R$ H* ]! cpletely disappeared except for a few vellous hairs at
3 N5 ~& L  l. |the base of the phallus. Testicular volume was still 2
6 E  k9 O. W- ~# D: }2 zmL, and the size of the penis remained unchanged." I: X) U$ J3 ?' [7 S, f. k& ~
The mother also said that the boy was no longer hav-4 ^4 C! x/ l. Y, i8 d8 @9 ]
ing frequent erections.
% s' T6 F6 R) H. f$ D/ m% t3 s) bBoth parents were again questioned about use of/ s" Z. z  }8 i7 Q( C% [
any ointment/creams that they may have applied to
* A& g" F1 @! r1 A7 cthe child’s skin. This time the father admitted the* v, Q3 f) r; l
Topical Testosterone Exposure / Bhowmick et al 541
* T3 |0 R* ~0 e0 n( y7 Huse of testosterone gel twice daily that he was apply-5 S" V3 V8 i% G( E1 r! C  _
ing over his own shoulders, chest, and back area for
- w  V! }% q( X4 O  v3 J6 Aa year. The father also revealed he was embarrassed3 g, @, f' j' b% Q; ]
to disclose that he was using a testosterone gel pre-
5 z( d8 K2 w0 T" `; q. D+ ?scribed by his family physician for decreased libido2 W/ O: _- o' C' ?! Y
secondary to depression.7 \$ d" s5 j" {) [( F, _( @' g
The child slept in the same bed with parents.
6 L% P' k5 r! U& pThe father would hug the baby and hold him on his2 o) F3 [* ^) W
chest for a considerable period of time, causing sig-
3 b6 e4 ]& m0 Vnificant bare skin contact between baby and father., Y0 S2 F. t( B4 S
The father also admitted that after the phone call,. H1 W7 D, `6 d- X
when he learned the testosterone level in the baby: [" }9 e! _9 O7 U# c6 L8 T1 F! m, }
was high, he then read the product information" F( i4 j! i4 B- W
packet and concluded that it was most likely the rea-
/ v  F5 S& K, y- ason for the child’s virilization. At that time, they' {) ?& ~# U, g3 B3 D
decided to put the baby in a separate bed, and the
9 ]3 ^5 P) O( t0 g1 |father was not hugging him with bare skin and had
; p4 Z; G. y- L3 p/ x$ A# S; o! Gbeen using protective clothing. A repeat testosterone
2 J$ }! z* t* u, Q% R+ _' Xtest was ordered, but the family did not go to the1 d+ q6 G+ t4 o0 ~
laboratory to obtain the test.
$ {% C% e( C7 a5 NDiscussion
( e" D& J; l5 r. z( P9 B; ]Precocious puberty in boys is defined as secondary7 ]$ G* H7 J/ O  f
sexual development before 9 years of age.1,4' a- n) z+ h; R: Y0 I9 H
Precocious puberty is termed as central (true) when
7 I- p; h( Y( s3 p% kit is caused by the premature activation of hypo-
- m2 Q  G7 }; Z+ x( b: R8 Ithalamic pituitary gonadal axis. CPP is more com-# f* m' M1 [& v2 K
mon in girls than in boys.1,3 Most boys with CPP
, S: p7 e* _- }) U: xmay have a central nervous system lesion that is
) B2 z9 g' }$ k$ g4 w" Fresponsible for the early activation of the hypothal-
- y- A& Z" l6 Camic pituitary gonadal axis.1-3 Thus, greater empha-! M6 N9 f4 o+ f3 h
sis has been given to neuroradiologic imaging in% e9 d6 s+ g, B7 D9 f+ ~
boys with precocious puberty. In addition to viril-5 O3 j4 C% s5 m* Q9 o3 F
ization, the clinical hallmark of CPP is the symmet-
* }5 G3 {5 e2 q% k  B. m  F# a( |rical testicular growth secondary to stimulation by* V9 k1 x7 l4 O% \
gonadotropins.1,3
8 a- x0 j  b. z4 h# p/ }1 s2 JGonadotropin-independent peripheral preco-
# e, V9 A6 D0 x; R/ Mcious puberty in boys also results from inappropriate
0 C- `  j; J! V& ~8 K' Aandrogenic stimulation from either endogenous or
& _; B( z3 N0 E" Eexogenous sources, nonpituitary gonadotropin stim-
8 l' b  K! t$ pulation, and rare activating mutations.3 Virilizing6 F8 {+ h; ]2 D' n7 D. x1 T2 L' Y+ `
congenital adrenal hyperplasia producing excessive
3 c7 j# V* z7 h* r8 w* Yadrenal androgens is a common cause of precocious
, @' C% o" p4 G& tpuberty in boys.3,4
' l0 I7 A! k5 X! f# QThe most common form of congenital adrenal0 s8 a3 F3 n2 M$ X
hyperplasia is the 21-hydroxylase enzyme deficiency." Y  k1 d2 m  r( u
The 11-β hydroxylase deficiency may also result in
/ C: [' [  h. b9 Texcessive adrenal androgen production, and rarely,
" F  M* z1 \9 r8 f, W3 kan adrenal tumor may also cause adrenal androgen
! P  o2 y! V. S0 ]5 v) Eexcess.1,3: h- w* J' o, G, h, a; {
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 r  j, [  L9 @& {! Y( M( y
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
2 f' j- Z4 l% b8 n) H/ @A unique entity of male-limited gonadotropin-
1 T; B2 G. m8 p6 D. uindependent precocious puberty, which is also known
' a+ @( L( a* U( X7 o% t2 d; Fas testotoxicosis, may cause precocious puberty at a
8 N/ ?3 G8 P5 a1 y" D5 rvery young age. The physical findings in these boys6 H. `) j0 o9 \! X
with this disorder are full pubertal development,% S$ [; Y! \" v2 O0 ^. q
including bilateral testicular growth, similar to boys
; A  L+ _; m* }+ p. V/ Lwith CPP. The gonadotropin levels in this disorder
0 ^( r6 o0 {$ w+ N) j8 Lare suppressed to prepubertal levels and do not show
6 |  N/ T" |* M6 p: }pubertal response of gonadotropin after gonadotropin-% @) u8 P+ J- y7 P" o8 M( n
releasing hormone stimulation. This is a sex-linked
: K1 i" C) H6 S' O3 |; V* aautosomal dominant disorder that affects only
1 `% h2 y" g+ {7 {; c/ Q& K. H, Hmales; therefore, other male members of the family' y5 z4 s* F8 G* H# c8 n, c* c1 e
may have similar precocious puberty.3/ n+ B2 z3 ?- l0 c' O; ]
In our patient, physical examination was incon-0 N$ d* ]6 \0 C/ a7 a2 H( z, I
sistent with true precocious puberty since his testi-
  I% X6 V# P; {/ m% Qcles were prepubertal in size. However, testotoxicosis8 F7 a, K5 A4 S) m% T
was in the differential diagnosis because his father* ~' P: F% F5 x+ P+ W8 g
started puberty somewhat early, and occasionally,+ E( f! r* v: S7 I9 N
testicular enlargement is not that evident in the. Q! b5 L% g; R8 A0 X7 v
beginning of this process.1 In the absence of a neg-
: ~$ S0 z5 a, E7 I" ^! y" A2 Cative initial history of androgen exposure, our
2 |( ]' a  R: z, |6 v" U% Z, s$ Ubiggest concern was virilizing adrenal hyperplasia,
0 @$ F( a, K6 l% z/ h6 }either 21-hydroxylase deficiency or 11-β hydroxylase
3 w* h7 @+ a7 Zdeficiency. Those diagnoses were excluded by find-
1 S* S" l: u* W. w2 ]* w9 wing the normal level of adrenal steroids.3 T$ n% ^5 T# M2 p+ Y; l/ J
The diagnosis of exogenous androgens was strongly7 f( K" O7 c9 ?
suspected in a follow-up visit after 4 months because
3 R) N  u( n2 m5 f: s$ wthe physical examination revealed the complete disap-; A: b& y7 S; |: H  K/ e
pearance of pubic hair, normal growth velocity, and
1 Y3 q& C) M, mdecreased erections. The father admitted using a testos-
+ O- D0 E- q' j8 i7 zterone gel, which he concealed at first visit. He was! o! S2 o4 \7 o& |
using it rather frequently, twice a day. The Physicians’, C; h3 Y( m; T8 @. @7 O
Desk Reference, or package insert of this product, gel or
/ j3 b/ h  N4 _cream, cautions about dermal testosterone transfer to9 m5 d! o/ ~6 ]2 o6 v1 B0 k3 u
unprotected females through direct skin exposure.+ F, y5 h. e$ z! p: C( g2 T' \
Serum testosterone level was found to be 2 times the0 B! m3 _6 H* p! S# H/ l
baseline value in those females who were exposed to' Q4 t8 t# o7 Q# S: H8 g3 s
even 15 minutes of direct skin contact with their male
2 Q0 q  J3 f$ ?6 Ppartners.6 However, when a shirt covered the applica-& @4 H4 m4 Y( y* [5 Z; S
tion site, this testosterone transfer was prevented.' j! r  {5 B) [# k6 Y6 o! [
Our patient’s testosterone level was 60 ng/mL,
1 _5 T; v9 r; u( z3 ewhich was clearly high. Some studies suggest that
1 P7 k, k. R, M( ?. E! Odermal conversion of testosterone to dihydrotestos-& {5 x6 o9 S0 t
terone, which is a more potent metabolite, is more
( y) v  f7 L* e5 G1 ~active in young children exposed to testosterone( j. X3 I+ J8 u$ |6 l
exogenously7; however, we did not measure a dihy-/ |; s3 j% E, c5 M
drotestosterone level in our patient. In addition to
" q2 `1 d: R5 u9 o  A: Nvirilization, exposure to exogenous testosterone in7 Q4 y" C9 K) X4 n- q! L" f
children results in an increase in growth velocity and
  l% x6 H* D( Qadvanced bone age, as seen in our patient.# ~+ j6 Y6 W: n; L5 U  i
The long-term effect of androgen exposure during
1 G5 \/ |" k7 K0 N/ @. Fearly childhood on pubertal development and final
( h2 Q9 |- ?, E% A; I/ iadult height are not fully known and always remain7 D' A9 P% h+ g" N8 J( p6 u
a concern. Children treated with short-term testos-  y. L, V$ G( h: y$ i2 L- B  l
terone injection or topical androgen may exhibit some
" r  x* @8 a, g# h) macceleration of the skeletal maturation; however, after) S9 I4 G7 n0 r6 |% {+ W
cessation of treatment, the rate of bone maturation3 z/ v+ E8 ?* ~2 k9 {, z0 i
decelerates and gradually returns to normal.8,9
) i, g2 `- t+ i  P$ J3 c" dThere are conflicting reports and controversy
& d5 i/ s5 w9 ~! A0 w/ \2 h5 ?3 _over the effect of early androgen exposure on adult
2 ]5 T5 [7 S+ U+ H9 a* apenile length.10,11 Some reports suggest subnormal
' r- \  a7 a" e5 _* yadult penile length, apparently because of downreg-
$ ?( i2 ^, B  J, v* Z. z% Kulation of androgen receptor number.10,12 However,; O5 z# C8 A: ^* J+ V- s: Q" x3 F5 P) w
Sutherland et al13 did not find a correlation between% H' h6 s, O5 M# s; i1 D8 N
childhood testosterone exposure and reduced adult7 q9 j  S( i& s8 `9 J! T+ U# f/ R
penile length in clinical studies.) Z2 F, R- q  `$ M8 f& a
Nonetheless, we do not believe our patient is( X0 N- k' b2 B1 {
going to experience any of the untoward effects from
$ f: Z$ X& J* `) itestosterone exposure as mentioned earlier because
# @* L  ^6 F2 p; t. Z' K& athe exposure was not for a prolonged period of time." j8 E8 {- @7 ]0 h7 Y4 j2 O
Although the bone age was advanced at the time of
6 `; j. F! g; e" ediagnosis, the child had a normal growth velocity at
) m/ ~  \- |. C" Q/ dthe follow-up visit. It is hoped that his final adult. [& Q# _( E& B$ p7 N
height will not be affected.0 t  N( f' w- l+ r/ _. ]
Although rarely reported, the widespread avail-
' C$ k! A2 _8 l/ k, }) T/ Vability of androgen products in our society may
0 [/ [4 L' j1 I; `! zindeed cause more virilization in male or female" y2 V6 v2 I, e' m0 R! N' ~6 }
children than one would realize. Exposure to andro-
) |* o" A$ E7 b8 M! U0 Q" u2 sgen products must be considered and specific ques-" \; t. f! Z( s8 \
tioning about the use of a testosterone product or
& M& a( J5 Y5 C% r( M/ J; cgel should be asked of the family members during# p* N- L4 D" Y- r4 i2 m3 B& d
the evaluation of any children who present with vir-0 [7 c7 B& @' W2 E# o4 ~* H
ilization or peripheral precocious puberty. The diag-
9 T4 U5 f* o, I. e" mnosis can be established by just a few tests and by, U" k0 N7 z1 P1 A/ j
appropriate history. The inability to obtain such a4 A- q6 A4 E1 L9 s" P! g4 P( Z
history, or failure to ask the specific questions, may" y5 p. z+ e# K9 @, C
result in extensive, unnecessary, and expensive8 V7 d5 z# y, }1 Z4 c# K
investigation. The primary care physician should be  z: O7 I( G/ \+ J8 v
aware of this fact, because most of these children  J2 v1 k2 n; q
may initially present in their practice. The Physicians’+ w( Z0 z: F: a7 `0 ]
Desk Reference and package insert should also put a
6 l+ {, {6 T4 |1 ~. lwarning about the virilizing effect on a male or2 V0 H0 c. f# Y+ b* V
female child who might come in contact with some-
" t- m  z0 ]+ L- q& ?one using any of these products.
# n2 b5 D  n! A0 LReferences
  q9 p2 u% q  k8 q1 w2 p1. Styne DM. The testes: disorder of sexual differentiation& F; y2 ^4 M* J% B
and puberty in the male. In: Sperling MA, ed. Pediatric' R- v6 ^1 J. B% s) U6 B4 @
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- Z5 h5 q! N4 C3 s5 |* ^8 B2002: 565-628.
: P# p* P( _, a  k0 p: {2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
# A! w9 G3 e; d) Y# U2 Fpuberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
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
+ d; q' X' b, k5 _' }
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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