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Sexual Precocity in a 16-Month-Old
# `# s  ~$ T8 w3 s1 M( m" t/ r% QBoy Induced by Indirect Topical& W. ?% F# L  b# A( \& U
Exposure to Testosterone5 D/ D# `' @- d
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
3 T% A. Q$ Z$ t1 g$ Z( ~and Kenneth R. Rettig, MD1
9 W. Q' g2 M# X9 D/ wClinical Pediatrics
- z, ~/ |7 Z9 GVolume 46 Number 6
4 M" G3 L7 [+ Z% G1 {9 SJuly 2007 540-543
& S% ?& ^( }0 g* ^7 a© 2007 Sage Publications
7 X8 i; k* }" }+ x: W! N0 n10.1177/0009922806296651  |! [' \* z* F( u2 ^' S: u) B2 @
http://clp.sagepub.com
0 L. P5 @- M3 `* j6 fhosted at2 ^1 K* W3 Y8 \. V/ Z
http://online.sagepub.com
2 h' |0 [. ~4 h2 u. e  V: sPrecocious puberty in boys, central or peripheral,, U2 X# a" T3 z$ n; a& L. T( o
is a significant concern for physicians. Central
0 Y6 v8 b3 l0 B5 L3 `7 @precocious puberty (CPP), which is mediated
4 V! w$ g3 i: qthrough the hypothalamic pituitary gonadal axis, has
+ F. x. d3 S8 J+ O" Z) na higher incidence of organic central nervous system
$ J& S0 ~9 J# Z9 G* xlesions in boys.1,2 Virilization in boys, as manifested
2 i: _, H, H* f$ {# Y# Vby enlargement of the penis, development of pubic
0 n4 L5 \3 x7 O/ ~" J6 ghair, and facial acne without enlargement of testi-' f8 m+ S8 E  i$ d
cles, suggests peripheral or pseudopuberty.1-3 We& ?; c& Z7 r; ]) y* H
report a 16-month-old boy who presented with the7 n% V0 A6 s; U. U
enlargement of the phallus and pubic hair develop-
; z3 U  ~# b7 f/ U5 ]5 K9 Vment without testicular enlargement, which was due) P) q5 A  C8 K  c% n7 W
to the unintentional exposure to androgen gel used by
- t* q9 q" P8 rthe father. The family initially concealed this infor-5 \9 a5 C8 c. b7 X; h! k
mation, resulting in an extensive work-up for this
5 T. z4 ~) w. F- ~3 C. ~child. Given the widespread and easy availability of
# g7 q' `- {5 ztestosterone gel and cream, we believe this is proba-
# I' X  g! Y5 q# b" gbly more common than the rare case report in the
% y) S4 _8 X+ |! J# zliterature.4
+ w( a1 E* o* J! j9 L3 cPatient Report, {  m  ~6 }- i9 X6 H+ l: d+ @
A 16-month-old white child was referred to the
* g! S# D; M5 P" M5 x9 m9 G: qendocrine clinic by his pediatrician with the concern
1 \6 k7 ^; Q" c7 vof early sexual development. His mother noticed
/ _# u( \6 H5 L0 L5 Y0 ~+ `4 llight colored pubic hair development when he was
$ {0 P7 D! N# m- jFrom the 1Division of Pediatric Endocrinology, 2University of7 M: h# s2 n" ~" X0 A8 v" T. _
South Alabama Medical Center, Mobile, Alabama.
  q' G! P% n4 oAddress correspondence to: Samar K. Bhowmick, MD, FACE,4 C' r6 i, F: R' ?$ j7 `
Professor of Pediatrics, University of South Alabama, College of9 ?$ b  N3 k# k' _* S+ u
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
( i/ h0 T4 N5 A0 Re-mail: [email protected].
6 F* q7 W8 L2 N9 M+ tabout 6 to 7 months old, which progressively became) p& n( J* D5 n* r8 c
darker. She was also concerned about the enlarge-
* p+ X) f* `: Y( Wment of his penis and frequent erections. The child
+ x  l" \! [9 ^* iwas the product of a full-term normal delivery, with9 K( `% F7 l! C" D
a birth weight of 7 lb 14 oz, and birth length of
9 l7 p$ P* Z1 D5 T20 inches. He was breast-fed throughout the first year
8 k- x5 a! l7 L; O, Cof life and was still receiving breast milk along with
  V. O  W/ `, L* W) z7 C) s, wsolid food. He had no hospitalizations or surgery,# y, c* a; r; W( n
and his psychosocial and psychomotor development6 Y! a# J" P! W7 T+ M! U: f
was age appropriate.
8 ^" y1 R* T+ f- w" @5 o* R0 [The family history was remarkable for the father,( {* t0 b+ a* c
who was diagnosed with hypothyroidism at age 16,' I0 D0 a2 M. L; A  r9 p. N) M
which was treated with thyroxine. The father’s
  p$ K9 h: y5 w# O% y' T$ ]height was 6 feet, and he went through a somewhat
4 {$ j' y2 l9 m3 d/ yearly puberty and had stopped growing by age 14.
, q- h' [' U. q% AThe father denied taking any other medication. The' F' L! |! S/ r5 L6 K! O8 p6 z
child’s mother was in good health. Her menarche
, Y* `% v9 N) M! Wwas at 11 years of age, and her height was at 5 feet
: V# ?. p/ }0 V2 o$ `5 inches. There was no other family history of pre-2 h& i5 x- U  e' O; H/ J  C
cocious sexual development in the first-degree rela-
: }0 V8 q7 Z' P( I8 d$ I6 atives. There were no siblings.
% W7 b" `4 {4 H0 PPhysical Examination: ]) j& |* Y" k' j
The physical examination revealed a very active,
' v7 _: B/ R: @playful, and healthy boy. The vital signs documented
. z# U9 Q; V6 m7 s& A: ~2 ~( Xa blood pressure of 85/50 mm Hg, his length was, c" ]# f! N9 T5 G
90 cm (>97th percentile), and his weight was 14.4 kg$ i. W5 a1 D- T2 M3 D' `8 A9 Z
(also >97th percentile). The observed yearly growth" A# d4 E2 b' Z9 R
velocity was 30 cm (12 inches). The examination of  Z1 y9 D1 P& [- d$ \( |
the neck revealed no thyroid enlargement.
. ]% N* r2 {- c3 WThe genitourinary examination was remarkable for
8 |0 G2 z' ]) ~/ L( `+ B6 D; genlargement of the penis, with a stretched length of
1 ?! {6 ~% h& l9 x( h8 cm and a width of 2 cm. The glans penis was very well8 D! H( s* B4 L5 n3 ?; \
developed. The pubic hair was Tanner II, mostly around
& s' C7 p; j$ Z: m1 ~, ?, I  t540
1 C# v- J* q% c8 Y# S7 L( Xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! F+ m$ y; j* N. o- \. i
the base of the phallus and was dark and curled. The3 [1 B8 ~+ J4 S. D! F
testicular volume was prepubertal at 2 mL each.
+ [* M3 n) D& ^1 l& z6 P" [3 oThe skin was moist and smooth and somewhat, a8 {% `+ D# V
oily. No axillary hair was noted. There were no* v6 M/ K' v  v9 d( G# m9 H
abnormal skin pigmentations or café-au-lait spots.
9 G$ W4 J. P' z5 d3 iNeurologic evaluation showed deep tendon reflex 2+
+ i/ l: N8 k9 _. j% u' Tbilateral and symmetrical. There was no suggestion9 b- R+ \& [5 F
of papilledema.5 @  U1 B( c4 b7 ]  T
Laboratory Evaluation. h: p# o* G' _  }0 a5 I0 Q
The bone age was consistent with 28 months by+ J9 C& ^% o: y9 ^! F7 M: e
using the standard of Greulich and Pyle at a chrono-
4 ~0 ?3 O$ K/ u( {& i" J0 q* h( plogic age of 16 months (advanced).5 Chromosomal
4 P, i7 [9 c5 ^5 skaryotype was 46XY. The thyroid function test0 r- s' \! Z; k# k$ p
showed a free T4 of 1.69 ng/dL, and thyroid stimu-1 i; _, X7 P8 E( \
lating hormone level was 1.3 µIU/mL (both normal).
  n$ c" n* @! Z1 [. Y1 |/ V/ J% a, gThe concentrations of serum electrolytes, blood' v! z9 F) L3 Y% ?
urea nitrogen, creatinine, and calcium all were
) @6 G; k+ p/ Q( w. N, dwithin normal range for his age. The concentration
) d% F. j# b1 Cof serum 17-hydroxyprogesterone was 16 ng/dL; z3 v' f9 y& T. x5 u# }! c3 |
(normal, 3 to 90 ng/dL), androstenedione was 20$ S( o/ A- [6 X: Y. v+ L* E
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
7 B* r+ Q$ r$ O% _7 _3 G/ |terone was 38 ng/dL (normal, 50 to 760 ng/dL),
1 \  k) M7 v' e1 Ndesoxycorticosterone was 4.3 ng/dL (normal, 7 to
: o8 U4 f3 X* f- x) j2 I0 |3 v! {6 n49ng/dL), 11-desoxycortisol (specific compound S)' O+ }9 e& @" c$ h# }( m
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
. C8 R5 |/ J# X+ I2 i% h0 M4 ^tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total" K6 c# ?  p0 c& A& B9 |& P1 k% K  Y
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),, X$ o" N" R! W. w2 o
and β-human chorionic gonadotropin was less than
+ I( K% q2 M2 }: b& H9 x5 ]5 mIU/mL (normal <5 mIU/mL). Serum follicular
4 `# T- Z  l7 |9 v& B6 Gstimulating hormone and leuteinizing hormone0 I) @( K4 y5 c1 S0 M$ W4 ^
concentrations were less than 0.05 mIU/mL
1 O( Q2 Y' L# \, h5 r; ](prepubertal).
5 X. x) R- N% `$ p1 q5 h; s6 i4 OThe parents were notified about the laboratory
& k9 z1 h3 K$ H  Dresults and were informed that all of the tests were! s, Z$ j& O' w: S# k+ \
normal except the testosterone level was high. The
0 i/ I2 e- N% D& h  G5 u- Xfollow-up visit was arranged within a few weeks to& [& V7 E" k( K9 J+ D$ t
obtain testicular and abdominal sonograms; how-
4 B7 |" u; U) T" k$ iever, the family did not return for 4 months.$ n9 D6 g. {1 H' l9 s
Physical examination at this time revealed that the
3 U0 A  P1 g6 M0 X% Vchild had grown 2.5 cm in 4 months and had gained- E5 V0 i8 U) e- q
2 kg of weight. Physical examination remained
: T; x& U' g, H& @7 Nunchanged. Surprisingly, the pubic hair almost com-7 d! |0 e) G! T" f
pletely disappeared except for a few vellous hairs at/ Q/ @8 X" V( \, O; h
the base of the phallus. Testicular volume was still 2; |$ y% Q- A- X! S" t# g. _% G
mL, and the size of the penis remained unchanged.: L! _! t5 \: N( p# O: w9 k$ J
The mother also said that the boy was no longer hav-
( A1 a- b7 ~" v! F0 _ing frequent erections.
! h( f' z7 v5 B/ LBoth parents were again questioned about use of
0 U  `6 _: @: e5 a3 S$ |any ointment/creams that they may have applied to* n. Q* z& q! W. x# I
the child’s skin. This time the father admitted the( y( a' `/ k$ _  F
Topical Testosterone Exposure / Bhowmick et al 5414 }* W0 L! d" G( G
use of testosterone gel twice daily that he was apply-
- T- D' R+ ?! J) [4 G& Xing over his own shoulders, chest, and back area for
& V5 d/ j8 a6 [. K; a: `+ ~! ya year. The father also revealed he was embarrassed" E1 X6 N5 }% `' G- z9 \: n5 t
to disclose that he was using a testosterone gel pre-
; c2 l5 K( I. n9 ?% }& d- D! tscribed by his family physician for decreased libido
7 V* a, z; b8 S6 Esecondary to depression.
1 N, c7 {3 a' o: j& FThe child slept in the same bed with parents.
2 e8 v/ ?6 `* p/ }" ~The father would hug the baby and hold him on his
4 p: F+ a9 Z! C8 Q% E! schest for a considerable period of time, causing sig-
3 S9 w+ o0 u! F/ x# A$ C. _7 enificant bare skin contact between baby and father.' @4 r1 S7 d/ _2 c' u' e' W
The father also admitted that after the phone call,. A2 u- p  U" M2 D- y: d2 R% d
when he learned the testosterone level in the baby& k* D3 j+ A' J4 c/ c
was high, he then read the product information
5 d. \: _, b% N0 }% L2 ]+ ]packet and concluded that it was most likely the rea-
/ U& U- T. m; u/ L/ }: b1 a& tson for the child’s virilization. At that time, they
4 v# w) ~4 H' ]5 udecided to put the baby in a separate bed, and the! w0 y" v* c% \4 {: a
father was not hugging him with bare skin and had8 Y2 Y; ]& A2 L) J. K2 v
been using protective clothing. A repeat testosterone
: e8 U3 |) f! ntest was ordered, but the family did not go to the
) Z  g1 g4 g) u% ^  X8 U  Vlaboratory to obtain the test.
$ r' R8 c, Z3 ^* NDiscussion
, y) y4 D$ q. n" o# HPrecocious puberty in boys is defined as secondary
" c7 x% d. k' L5 Z$ w0 ^sexual development before 9 years of age.1,4
  g# _" s  P5 h3 S: w/ `Precocious puberty is termed as central (true) when
+ P. _% e9 d5 p* ?: R: W2 V. l! Oit is caused by the premature activation of hypo-+ P& I2 K  a# r* U' p) ?! Y1 q* P
thalamic pituitary gonadal axis. CPP is more com-' N; t3 T8 C& \2 x0 ~6 W
mon in girls than in boys.1,3 Most boys with CPP
) j% A( Q2 j, L; O$ x0 t! Wmay have a central nervous system lesion that is
6 g- ]& y6 e, g5 Wresponsible for the early activation of the hypothal-
: L% D  T- z1 U  n1 d6 A3 hamic pituitary gonadal axis.1-3 Thus, greater empha-, y/ }8 U: s" K9 J
sis has been given to neuroradiologic imaging in
4 W  z" A  \" ~5 R6 Q" @9 vboys with precocious puberty. In addition to viril-3 p% \: k) H. }- O; l" d0 O! d+ l) _
ization, the clinical hallmark of CPP is the symmet-
' B' v3 L& |$ w3 Y& Z5 E, yrical testicular growth secondary to stimulation by& X5 ]/ O- E9 @/ b# G6 d/ K
gonadotropins.1,3( S) @' S2 s2 d' ?( {  _
Gonadotropin-independent peripheral preco-
  W) j& |1 t# `cious puberty in boys also results from inappropriate
+ N3 I% ~- L+ q0 eandrogenic stimulation from either endogenous or: e7 W3 [5 X: o8 D5 Q
exogenous sources, nonpituitary gonadotropin stim-
6 s' u9 `  q/ u' D; `% Eulation, and rare activating mutations.3 Virilizing
$ u/ E  f# S$ X3 y! b' B4 _congenital adrenal hyperplasia producing excessive+ O* J5 z  q) L2 ?1 {' ?+ c
adrenal androgens is a common cause of precocious8 \1 R, s1 o4 U+ W7 n$ Y$ n, n3 Q2 g6 F
puberty in boys.3,4
, s' ~8 t5 a( G* zThe most common form of congenital adrenal0 D4 f! V  v& M5 m: l
hyperplasia is the 21-hydroxylase enzyme deficiency.
5 a; t7 v0 M; s8 q, e$ `The 11-β hydroxylase deficiency may also result in
$ R" W/ y8 ~" Y$ Fexcessive adrenal androgen production, and rarely,
6 w# z) H/ A! ]' ^4 s2 San adrenal tumor may also cause adrenal androgen4 _8 Q5 _1 i5 o# i
excess.1,3
, m: |5 B! k8 \* Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 H. [$ ]! f8 a; b) F9 ]
542 Clinical Pediatrics / Vol. 46, No. 6, July 20076 C- A/ y7 v3 K1 m7 I5 p
A unique entity of male-limited gonadotropin-
7 _( X+ @) U+ v* Z% Hindependent precocious puberty, which is also known) X+ R" R: j7 N
as testotoxicosis, may cause precocious puberty at a
3 Z; y& h% f& L3 V# x! g7 vvery young age. The physical findings in these boys+ Q( U; c" f5 F# n, b
with this disorder are full pubertal development,
" M: p! I! }  }, zincluding bilateral testicular growth, similar to boys' P9 b+ e1 `9 ?5 V" p& v
with CPP. The gonadotropin levels in this disorder3 m) h% _. r1 a6 y4 U, r
are suppressed to prepubertal levels and do not show
/ b- i1 \; S! E2 N! ?# A+ p1 |pubertal response of gonadotropin after gonadotropin-! _) J; p, `/ e; m" y
releasing hormone stimulation. This is a sex-linked# s* b6 w& C& l( s
autosomal dominant disorder that affects only' M, I' |) V# l' e' ~! D8 u
males; therefore, other male members of the family* y; }" q3 M$ F  r# J. k
may have similar precocious puberty.3
/ ~' T+ _' {# OIn our patient, physical examination was incon-2 y/ V& h  S' Q6 s! X9 C
sistent with true precocious puberty since his testi-
+ F4 E  I% ?0 `( }9 `8 F( xcles were prepubertal in size. However, testotoxicosis
0 p9 p" Q" R/ a  E) R* }7 J( Kwas in the differential diagnosis because his father
( T+ _, Y5 r  K1 p2 y( g+ f+ |) Vstarted puberty somewhat early, and occasionally,; U9 Y: B1 H6 a! Z) g) W+ G
testicular enlargement is not that evident in the
$ Y/ o" ]. B2 E3 B$ hbeginning of this process.1 In the absence of a neg-  h  a+ J: S( u. }/ m3 z$ F8 o# k: V
ative initial history of androgen exposure, our6 o" j9 c) U, p4 ]
biggest concern was virilizing adrenal hyperplasia,& ]2 F4 H! ]; F6 [% Z
either 21-hydroxylase deficiency or 11-β hydroxylase4 }: [6 i# c5 k' _; a! k' ^9 c
deficiency. Those diagnoses were excluded by find-" ^$ S, W, W6 N# O" ?$ H* c
ing the normal level of adrenal steroids.
) g9 g9 h( @: o1 I" A+ O& zThe diagnosis of exogenous androgens was strongly6 T$ O2 g. `" U6 e8 n  k! R) S2 P; v
suspected in a follow-up visit after 4 months because4 \& l! G4 k" G4 y  T, b6 u
the physical examination revealed the complete disap-
4 J' g0 @4 F3 V. V1 d5 \+ Dpearance of pubic hair, normal growth velocity, and0 E9 ^8 O& h" x* d2 ~
decreased erections. The father admitted using a testos-* p# {- Q/ e/ l! C; h  U& i
terone gel, which he concealed at first visit. He was
( i% j$ d9 a( g7 susing it rather frequently, twice a day. The Physicians’
# @- }4 P* r6 |) EDesk Reference, or package insert of this product, gel or
0 z" t0 G/ g  p' Z9 V! qcream, cautions about dermal testosterone transfer to
0 S, T9 ]$ R2 Punprotected females through direct skin exposure.0 F$ _! i' U: m
Serum testosterone level was found to be 2 times the
$ [0 B  q, J/ q, X) Jbaseline value in those females who were exposed to
# E- x  I* h0 |% \1 z* n4 Ieven 15 minutes of direct skin contact with their male
# X' L: t# H+ ~partners.6 However, when a shirt covered the applica-8 g1 ?# G, H1 t4 \
tion site, this testosterone transfer was prevented.
( Z4 a' D5 z1 h5 j" ^5 Q7 COur patient’s testosterone level was 60 ng/mL,
# B  T1 Q) g+ H5 \  n$ n9 M- T1 p7 Fwhich was clearly high. Some studies suggest that
; j) O- {5 O0 D: L, Sdermal conversion of testosterone to dihydrotestos-
* i4 a8 ]8 u, C5 b9 Q1 Oterone, which is a more potent metabolite, is more( R) j( G% [& g: H( ]; p" J- U; V# }1 ]
active in young children exposed to testosterone: v3 w9 |  `# z
exogenously7; however, we did not measure a dihy-
6 ~, t  d$ ?$ `drotestosterone level in our patient. In addition to0 ~" q, ^% l: J9 C6 A& U+ o
virilization, exposure to exogenous testosterone in$ f2 S/ R, E( p
children results in an increase in growth velocity and
2 _& M' I3 R, w) F/ ]* n9 Kadvanced bone age, as seen in our patient.  Z  q& t( D& V! ]5 I% r6 g3 b
The long-term effect of androgen exposure during8 z/ i, |- k- t
early childhood on pubertal development and final1 K# F/ d' ?7 C: o
adult height are not fully known and always remain
& l9 E4 u$ \9 W& z/ Z( I) Ea concern. Children treated with short-term testos-! t4 `/ P1 j& u5 m0 W! v9 Q9 q4 I
terone injection or topical androgen may exhibit some( k# C2 ^. [2 j$ M
acceleration of the skeletal maturation; however, after
" p( ^2 i0 o$ \! Wcessation of treatment, the rate of bone maturation% W' o& N$ u+ P# n# a
decelerates and gradually returns to normal.8,9! Q  J. o4 k) U* h: {7 e
There are conflicting reports and controversy
+ c7 t; z2 w. x9 ^" l1 `over the effect of early androgen exposure on adult
6 t2 I# r) z# cpenile length.10,11 Some reports suggest subnormal* `" r$ K! Z) ~" j$ A0 q$ ^
adult penile length, apparently because of downreg-% q. T" W5 y/ o& j, |3 m
ulation of androgen receptor number.10,12 However,
) w$ A! o$ b7 j" gSutherland et al13 did not find a correlation between
! a- W* ~+ e, rchildhood testosterone exposure and reduced adult& l# q8 o2 Y' C+ e
penile length in clinical studies.
% F$ K* S# m) N8 H. WNonetheless, we do not believe our patient is% J& R  U& U/ {2 H. H; g6 |
going to experience any of the untoward effects from+ d# z  X- u3 V1 O* X' I2 D
testosterone exposure as mentioned earlier because
& L' k  n( [5 ~  H6 k$ Jthe exposure was not for a prolonged period of time.
+ a* b3 i/ ^4 K4 _; a/ wAlthough the bone age was advanced at the time of
- o5 c, ^5 d; Xdiagnosis, the child had a normal growth velocity at
2 ~0 A1 v- Z, m! m. N+ wthe follow-up visit. It is hoped that his final adult
6 H1 L% y, E4 ~' lheight will not be affected.
/ M3 N* L  Y) D8 I  {! L' M7 SAlthough rarely reported, the widespread avail-# C2 [0 {8 R1 z5 T* t6 z! l# Q  @% F
ability of androgen products in our society may4 B; i  @1 I2 f% ^. H
indeed cause more virilization in male or female9 N' j$ L  c+ F* o+ Y) o$ ]$ `5 J
children than one would realize. Exposure to andro-
* G! D2 b0 G4 A: lgen products must be considered and specific ques-
0 n# C, X! ?, Btioning about the use of a testosterone product or
0 V5 q2 b/ j! b( a5 sgel should be asked of the family members during, m% P3 j$ j( t% c) C6 w
the evaluation of any children who present with vir-* d' i4 c5 w5 h/ ~* Y- N$ ^" f, |
ilization or peripheral precocious puberty. The diag-
, s2 G0 u! g" W) @2 L8 G* a- \nosis can be established by just a few tests and by
8 L% Z" O: t* @: O+ V& t& o  O+ dappropriate history. The inability to obtain such a, e; f- l$ A( }; R3 s6 s& x7 Y) m" I% G
history, or failure to ask the specific questions, may6 k1 n: {+ x+ F
result in extensive, unnecessary, and expensive
, h  ~* @9 H8 i& y  }7 ^  V  P6 ainvestigation. The primary care physician should be
  z0 ~) R8 a2 i+ [9 |aware of this fact, because most of these children
* z1 P6 w4 }+ I( e8 A% Umay initially present in their practice. The Physicians’
) ?. V  G, Q5 \; ~0 R( a9 cDesk Reference and package insert should also put a+ a- {! q. t3 n; h8 r: h
warning about the virilizing effect on a male or
0 ?+ y: w1 p( S5 k! j6 Hfemale child who might come in contact with some-, ^0 |; v) y' c% Q$ l
one using any of these products.+ q, \1 e* ^6 s- I$ X9 J# J% [
References  g! o. o6 B8 L6 z
1. Styne DM. The testes: disorder of sexual differentiation8 Y; d/ q2 E6 X% r* [! X
and puberty in the male. In: Sperling MA, ed. Pediatric
) ^/ |' E  R& s- u+ zEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
  L( g. G2 s. I4 e( H% w2002: 565-628.! Y$ t$ q2 m) D) x  w# `
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious1 J, x* R0 \9 H. A0 Q9 w- ?
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
' |4 x( }/ h; @Boy Induced by Indirect Topical
8 N8 I: m8 M" R- H/ v- \Exposure to Testosterone  u' v7 B- o; a
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2  Z& `8 c+ K/ O6 v
and Kenneth R. Rettig, MD13 V  g5 n( c3 I6 q( C  z
Clinical Pediatrics
2 |5 C* b9 s$ [/ j2 Z1 ^  VVolume 46 Number 6
3 w2 p  K5 w# A6 s9 {July 2007 540-543
# a! m* _# r; h& Z6 K% z© 2007 Sage Publications
$ T9 R  k) ]# w5 d10.1177/0009922806296651! L  I) A; A: ~% \8 {' v7 M& n
http://clp.sagepub.com
7 v1 `, N% [+ k( e  E" rhosted at- E+ @. E# ]6 U! h) Z* @% A
http://online.sagepub.com
  m0 ~6 R0 D1 l, _Precocious puberty in boys, central or peripheral,( _( R: b6 Y1 a* m' o1 o7 T% n! P
is a significant concern for physicians. Central$ s0 b- }; O0 d! K& U0 X( n. t
precocious puberty (CPP), which is mediated6 I. `' z% p5 |6 Z; V) r
through the hypothalamic pituitary gonadal axis, has
% ?5 J  e0 ~, ~a higher incidence of organic central nervous system
: D) T! |8 }0 n2 Jlesions in boys.1,2 Virilization in boys, as manifested
2 C* e+ }# E% j0 f+ z5 `0 kby enlargement of the penis, development of pubic3 |% r. Y$ @3 D# |
hair, and facial acne without enlargement of testi-
7 ?0 W# e3 M7 E. f$ N$ Ncles, suggests peripheral or pseudopuberty.1-3 We
2 V9 ?! U  A' {* @report a 16-month-old boy who presented with the
. W% v: g$ Q; t" uenlargement of the phallus and pubic hair develop-% Y6 [. o8 t& `  Y: F7 I, j
ment without testicular enlargement, which was due+ C5 ?" w' Q4 J7 m- [
to the unintentional exposure to androgen gel used by
) R5 O9 {" {1 u/ Gthe father. The family initially concealed this infor-' U+ T8 T2 {: q5 d, z8 O" F& m( f, l1 k
mation, resulting in an extensive work-up for this- ^1 t3 b: w  A! }. R; c1 T
child. Given the widespread and easy availability of
: W% P, @) w' p- _, Dtestosterone gel and cream, we believe this is proba-9 m  N' p5 M. U# b+ T
bly more common than the rare case report in the. `  X# Z  T+ o) ?" B) C- f( s$ P) h
literature.41 f! |0 k# O' G1 Y
Patient Report
" @" z3 O- B3 S2 N$ EA 16-month-old white child was referred to the$ X0 t: H3 g  K5 J9 f0 F, F0 s, i) c
endocrine clinic by his pediatrician with the concern
- D6 `/ ]/ r* O4 ~, v9 yof early sexual development. His mother noticed
) i# G& m, j1 b; r! \light colored pubic hair development when he was
- Y# Y8 s" M+ Y2 P& ^1 O. z$ TFrom the 1Division of Pediatric Endocrinology, 2University of  W6 E% y, W' z: I
South Alabama Medical Center, Mobile, Alabama.
, v' A' X& W" n! f8 MAddress correspondence to: Samar K. Bhowmick, MD, FACE,
+ j( F3 R: d- U* Y; KProfessor of Pediatrics, University of South Alabama, College of
7 r; c; E$ r' L  ~% b5 ]/ oMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
) `% d$ ~% T4 J2 l/ R4 D$ P3 }e-mail: [email protected].
& P: W( `. B/ @$ Z) v$ y! k1 ^about 6 to 7 months old, which progressively became2 {6 I8 Z; U6 n, R/ C& s
darker. She was also concerned about the enlarge-
4 x( b1 o% M. f4 O  `( N" wment of his penis and frequent erections. The child
: |  z9 G1 b5 i3 y+ o0 ^/ t# I5 Hwas the product of a full-term normal delivery, with
* ~; T! `* w, B$ {' O% Ra birth weight of 7 lb 14 oz, and birth length of) b; z+ R. N( v
20 inches. He was breast-fed throughout the first year
4 F! M& x( ?5 D! e, Q( E, I  jof life and was still receiving breast milk along with2 g! z! j  A( W! b- t8 w% G* {
solid food. He had no hospitalizations or surgery,- d* w3 Z6 z: h& i
and his psychosocial and psychomotor development6 ?; [! d  y+ N, X5 K
was age appropriate., X8 a0 I1 M5 P7 h  Y" x
The family history was remarkable for the father,
* q! {) s  l# r8 v) e3 [9 l3 |5 Iwho was diagnosed with hypothyroidism at age 16,3 B9 L0 o  g5 f5 V
which was treated with thyroxine. The father’s
4 L0 U' A5 h: M. ?# A% t$ Wheight was 6 feet, and he went through a somewhat
1 W+ y) S# t4 E4 I$ Eearly puberty and had stopped growing by age 14.' r, @$ f. H4 h  |
The father denied taking any other medication. The0 y5 R6 m. B9 M# S' O$ k( J
child’s mother was in good health. Her menarche
2 Q+ ~( k4 |/ ]# ~was at 11 years of age, and her height was at 5 feet1 p4 o* z% E4 _8 V( b  J) y& g9 w
5 inches. There was no other family history of pre-
8 v7 Z) s( T  _cocious sexual development in the first-degree rela-4 Z7 M( P: V6 Q
tives. There were no siblings.
' i" e  H" V1 A7 WPhysical Examination) K  t: @3 R; v) Y* B
The physical examination revealed a very active,
; b4 H3 m8 N6 ?) |+ `playful, and healthy boy. The vital signs documented
$ C4 r# g0 h7 R- n1 I+ Ba blood pressure of 85/50 mm Hg, his length was
, s, F$ e5 q' @9 B$ r- p2 G90 cm (>97th percentile), and his weight was 14.4 kg
- O2 q2 t7 z0 d( c/ s(also >97th percentile). The observed yearly growth/ j$ R5 S/ _4 k0 I( x2 U$ o$ m
velocity was 30 cm (12 inches). The examination of
# M, o; L9 O+ `1 \the neck revealed no thyroid enlargement.
% J7 n4 X  v7 ?7 l: G- z/ iThe genitourinary examination was remarkable for
+ C% J- {+ a2 _enlargement of the penis, with a stretched length of0 [! X- v5 A- Q& X7 @5 \
8 cm and a width of 2 cm. The glans penis was very well" b" [+ h& k/ O% x  x& A
developed. The pubic hair was Tanner II, mostly around' v2 S5 u1 t' Q& S7 k" K+ r
540
3 p6 W/ a3 Q; @( R) h! [at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ R8 b# z9 U  L3 l' t/ Vthe base of the phallus and was dark and curled. The
2 `. t4 b- i" S7 A/ i: `6 Ntesticular volume was prepubertal at 2 mL each.. w$ q3 w) j8 ^9 u
The skin was moist and smooth and somewhat
6 x0 p/ u5 ?9 A; d! B) m4 }9 }oily. No axillary hair was noted. There were no( d2 ?7 w7 O) V( c
abnormal skin pigmentations or café-au-lait spots.6 D6 C, k2 V6 _9 m& M6 Q
Neurologic evaluation showed deep tendon reflex 2+
/ c, [2 }* W7 D/ s" pbilateral and symmetrical. There was no suggestion! o6 A$ v: Z4 v5 `4 d' R
of papilledema.
6 B7 v$ k' _5 ^% g1 {% `5 KLaboratory Evaluation0 ]* N* n2 Z" ]& v+ H& D: `
The bone age was consistent with 28 months by
3 n! P# k5 p3 R* g7 kusing the standard of Greulich and Pyle at a chrono-
2 ^. u, c+ L. z- @4 y$ nlogic age of 16 months (advanced).5 Chromosomal; Z! L0 `; A: P# C2 q- _
karyotype was 46XY. The thyroid function test
* Q" p( t! M6 E! p7 V* V" vshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
& E9 b8 ^1 S2 j% J9 B" y  G. E4 P/ _lating hormone level was 1.3 µIU/mL (both normal).  x. v7 B5 v0 \
The concentrations of serum electrolytes, blood& Z% V0 r& v! S- @) q
urea nitrogen, creatinine, and calcium all were
9 F$ j8 A% n0 {8 h6 s1 Mwithin normal range for his age. The concentration
* ]* H) A: C( J0 Z; x) Hof serum 17-hydroxyprogesterone was 16 ng/dL
& w1 f$ @6 u& A" c- c6 M(normal, 3 to 90 ng/dL), androstenedione was 20
, R( G; K* J4 k  K& ing/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
& T, m# g: b. E% H8 Fterone was 38 ng/dL (normal, 50 to 760 ng/dL),
9 s" U9 e  H# R- l! h! Xdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
- a. H) V5 V6 s: _/ {49ng/dL), 11-desoxycortisol (specific compound S)
' i- G3 z/ J. W- z2 m0 M. jwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
. d6 e4 j) c% Y4 }" I: Ntisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total- W0 d+ u1 Z- C- @* p; O
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
5 o& ?5 h- q# aand β-human chorionic gonadotropin was less than9 K  z5 a% M) W8 e7 ^& H: M
5 mIU/mL (normal <5 mIU/mL). Serum follicular
5 S; W" j* U* I$ i) Y  wstimulating hormone and leuteinizing hormone( Y$ o6 t0 Z- C, e3 K1 j' T7 L
concentrations were less than 0.05 mIU/mL
/ Y$ j; _: o2 F- T( v1 o5 Z(prepubertal)." p4 a8 a% J% Z/ {; x
The parents were notified about the laboratory1 `+ @0 h! o  `* z/ S5 u. ?
results and were informed that all of the tests were
3 T6 n1 u7 \2 \- n1 snormal except the testosterone level was high. The9 P- e' O0 z9 |" A; b  y2 I) Y
follow-up visit was arranged within a few weeks to% I" h6 _% |% n$ q4 i1 _
obtain testicular and abdominal sonograms; how-$ _9 q7 W2 ~# i! B" n! r! }* K
ever, the family did not return for 4 months.) y( a9 [. G" }
Physical examination at this time revealed that the" Z# [- G% Y( H6 L
child had grown 2.5 cm in 4 months and had gained
9 V$ T3 j6 o6 u8 ]) I( I7 z8 q2 kg of weight. Physical examination remained# J+ N* ?$ {1 r
unchanged. Surprisingly, the pubic hair almost com-% v8 o* ?; Q" j4 S0 W
pletely disappeared except for a few vellous hairs at
2 T1 q8 U. K! |$ M# C* {+ z  g) \' }9 athe base of the phallus. Testicular volume was still 2* U' @: F3 |* k6 O9 S9 C
mL, and the size of the penis remained unchanged.
6 |; H4 H' ?% E3 e/ RThe mother also said that the boy was no longer hav-
3 Q' b7 q1 F: m* L' wing frequent erections.
) g% v2 n1 c- a. F* B: ^" }/ XBoth parents were again questioned about use of5 w8 ~0 v4 a- v  w4 |+ T
any ointment/creams that they may have applied to2 U  I3 A7 E! q- A$ `8 ?
the child’s skin. This time the father admitted the
& b6 Z9 q4 {) m# ]) b2 ?1 `' iTopical Testosterone Exposure / Bhowmick et al 541
% ?: Y, z5 ?$ n' J6 huse of testosterone gel twice daily that he was apply-* w5 y0 s: S% T, p( Z8 ~
ing over his own shoulders, chest, and back area for
4 m3 _2 X  s' V- Xa year. The father also revealed he was embarrassed
8 ?$ H4 J, c7 ^! {7 @to disclose that he was using a testosterone gel pre-3 l) [" _, k  j( q& F9 ]
scribed by his family physician for decreased libido7 I; N# `; `1 o. n& {: ~# B
secondary to depression.
! M0 R0 [8 H% ~The child slept in the same bed with parents.0 y. V5 Z0 ?8 D5 Z5 q7 w4 {
The father would hug the baby and hold him on his
( g" o( c' r3 X- z9 G) xchest for a considerable period of time, causing sig-
+ }3 Z  }1 h- W- R$ r5 q# tnificant bare skin contact between baby and father.3 J# L# H+ }0 I* W3 T
The father also admitted that after the phone call,
8 h3 X; X( ^! Y7 k+ R8 E+ Mwhen he learned the testosterone level in the baby
, g$ Y& ^0 B/ `. X# |3 m, Nwas high, he then read the product information% v; p3 W0 v* F! u  t0 K/ ?6 D/ n
packet and concluded that it was most likely the rea-
0 J) U( M. T# O) ^% w$ Rson for the child’s virilization. At that time, they
+ E# g  S7 l, j3 ndecided to put the baby in a separate bed, and the
4 _2 s3 Z: j/ R' [/ L+ e8 Qfather was not hugging him with bare skin and had* ^  E) H' y) H* i0 ?1 h/ M: t% G
been using protective clothing. A repeat testosterone
) A5 c1 L, _. [7 W1 Itest was ordered, but the family did not go to the
% q2 f, A& Y7 P1 {laboratory to obtain the test.
5 v5 b) w# T# J' m* s5 CDiscussion0 a- r. T  X8 _1 G
Precocious puberty in boys is defined as secondary
; P, E6 J% B$ R0 w2 }. bsexual development before 9 years of age.1,4* U$ n$ @4 F. N: L2 y% G
Precocious puberty is termed as central (true) when
( X3 I6 W+ {) Z. Jit is caused by the premature activation of hypo-# [$ y$ m/ @" l1 d/ Q9 R
thalamic pituitary gonadal axis. CPP is more com-  O! |; m7 |1 D) y% k/ U5 z' C
mon in girls than in boys.1,3 Most boys with CPP
, |8 k% [) h4 u7 Emay have a central nervous system lesion that is% G, K3 g3 k8 t+ a- I' m- A" Z# b
responsible for the early activation of the hypothal-
7 t7 Q. [  d* f3 N7 iamic pituitary gonadal axis.1-3 Thus, greater empha-; `- R! N4 p* M4 R! H9 a
sis has been given to neuroradiologic imaging in" o8 L, B+ P2 y' q# D* N
boys with precocious puberty. In addition to viril-
# D8 r  _* ]. O9 e0 x5 `6 aization, the clinical hallmark of CPP is the symmet-
4 X1 p7 H# ~" h/ r/ ?8 j! orical testicular growth secondary to stimulation by
% g! k7 A* \* w& ^3 u7 mgonadotropins.1,3
7 `. F. ?/ V0 I  j$ ~/ d- VGonadotropin-independent peripheral preco-
9 {* W1 S2 h1 Vcious puberty in boys also results from inappropriate# v! I5 f, S  [9 n& W5 x8 a
androgenic stimulation from either endogenous or
5 U# R; \" \, J4 h, m5 @8 Jexogenous sources, nonpituitary gonadotropin stim-
1 f& x2 M/ f! Fulation, and rare activating mutations.3 Virilizing
9 h: Z! N! s& G2 Tcongenital adrenal hyperplasia producing excessive2 y* F; _% N/ |+ p8 x
adrenal androgens is a common cause of precocious% e$ D+ X' q( s9 Q7 S# d; }
puberty in boys.3,4  M0 w  @! Y& v( F  n: F9 N; z
The most common form of congenital adrenal' b  G, c5 l- Z. B& a
hyperplasia is the 21-hydroxylase enzyme deficiency.
8 t$ f! J' ], J2 q. ?% DThe 11-β hydroxylase deficiency may also result in
3 D  G: c) t* z  r$ }' R$ v) [# G5 Pexcessive adrenal androgen production, and rarely,
! P' q1 Q2 I4 Z, `1 m3 Uan adrenal tumor may also cause adrenal androgen( P+ k3 c; U8 n! s! q; F0 y) W
excess.1,3  d$ ]7 q0 m5 [% K
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 p  M( S3 L% Q
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007# }& p) Y" E, o' o
A unique entity of male-limited gonadotropin-
; D1 `) c! b9 k, \+ kindependent precocious puberty, which is also known, a# X: W" P6 K( N9 \1 j  ]
as testotoxicosis, may cause precocious puberty at a: }$ q+ ~1 J* T. M
very young age. The physical findings in these boys. x, ]3 l* @: [: a
with this disorder are full pubertal development,
9 r5 r' a  M% \9 u9 |! mincluding bilateral testicular growth, similar to boys
2 A# X/ a- ^* R& \with CPP. The gonadotropin levels in this disorder+ \- D# g, f0 q; t  H
are suppressed to prepubertal levels and do not show
/ z2 t( U6 [  Z# v  G  ipubertal response of gonadotropin after gonadotropin-- n/ E1 T: R. w2 y5 m! |2 a4 \" K
releasing hormone stimulation. This is a sex-linked
- G" N% q9 M$ U* j: ^: I, W5 s8 a4 [% bautosomal dominant disorder that affects only9 X8 Q7 g) n+ Q' e. g
males; therefore, other male members of the family
1 s$ I- d2 f. y/ ^- D& ^may have similar precocious puberty.3
7 G; C0 J* U6 uIn our patient, physical examination was incon-, ]9 C8 @& W3 J; q! r
sistent with true precocious puberty since his testi-
+ T% z, E+ q$ e' s7 Z0 ?$ _  L3 gcles were prepubertal in size. However, testotoxicosis
4 D6 L7 l! z5 E+ vwas in the differential diagnosis because his father" O& X& Q0 E5 e  ^  E+ U
started puberty somewhat early, and occasionally,) B' F0 U" e( y8 ?
testicular enlargement is not that evident in the1 W9 n* N8 P6 O8 E/ N- O
beginning of this process.1 In the absence of a neg-* R6 P9 p( j/ y$ n, M: D
ative initial history of androgen exposure, our! q/ q% e( b; r2 @! n
biggest concern was virilizing adrenal hyperplasia,! |& v  i' |) b2 l0 S
either 21-hydroxylase deficiency or 11-β hydroxylase) _5 C7 O- ^4 D5 T( _# Y
deficiency. Those diagnoses were excluded by find-0 Z6 v% s* w; e3 s0 a2 f5 z7 s# w6 h
ing the normal level of adrenal steroids.9 ^& R# F2 ?2 p# X
The diagnosis of exogenous androgens was strongly  K# E$ ^6 B( m& v5 R  {+ D5 ~
suspected in a follow-up visit after 4 months because! ~( x$ b0 G& v6 ?1 M
the physical examination revealed the complete disap-
# A2 D0 R; i, d- z% b0 Kpearance of pubic hair, normal growth velocity, and
& M# o5 N6 x2 K6 Ldecreased erections. The father admitted using a testos-
( h* n* Z/ q+ f5 x' w- T5 J+ vterone gel, which he concealed at first visit. He was* T+ J7 Z5 y8 x- k6 w
using it rather frequently, twice a day. The Physicians’
9 I2 X' O5 J* [9 _( b& GDesk Reference, or package insert of this product, gel or& m  H% ~, Y, j5 w& t
cream, cautions about dermal testosterone transfer to- E; J: G5 U# \) {
unprotected females through direct skin exposure.
+ \, r# g* Z# N' fSerum testosterone level was found to be 2 times the9 b# i8 E* g9 t: B: \8 a
baseline value in those females who were exposed to% o6 r3 |  @  e: |: M
even 15 minutes of direct skin contact with their male
! ~0 S! M6 X, ?partners.6 However, when a shirt covered the applica-
5 x; _5 E. S- ~tion site, this testosterone transfer was prevented.
  f  ]0 J. l, Z& \, r# X, f) IOur patient’s testosterone level was 60 ng/mL,
1 \; `' o0 n) I! @9 rwhich was clearly high. Some studies suggest that
- X* a: n6 P4 z) l' e6 H8 Q& Qdermal conversion of testosterone to dihydrotestos-# A* J( s% t7 M0 y
terone, which is a more potent metabolite, is more
# I" j$ u- \  |+ G! ~4 ^6 cactive in young children exposed to testosterone
. Q: W$ `% L7 v2 |- Iexogenously7; however, we did not measure a dihy-  x) ^4 G2 }2 K7 p
drotestosterone level in our patient. In addition to
7 k, q1 ]2 n2 l) |! X8 \virilization, exposure to exogenous testosterone in
- m6 I% z& M8 G/ |$ _- {children results in an increase in growth velocity and# J! T# Z2 B. n4 W) N
advanced bone age, as seen in our patient.
+ |# R5 C1 ]$ {4 i# x8 g2 N6 R% J6 ZThe long-term effect of androgen exposure during
8 i* c! l& M5 Aearly childhood on pubertal development and final4 Y* O& G# {* B, e/ V5 s- r
adult height are not fully known and always remain
) d! w2 _# b4 f8 Z/ ~a concern. Children treated with short-term testos-
0 \- s5 D$ t3 G) i$ P% Mterone injection or topical androgen may exhibit some
# y  N2 m3 y& y! w# B( tacceleration of the skeletal maturation; however, after( y8 S% A1 U# ]# z
cessation of treatment, the rate of bone maturation! l! g7 Y. d( [/ ~& q8 }  d' k
decelerates and gradually returns to normal.8,90 ~: P& Y2 S7 ]# B7 X5 v
There are conflicting reports and controversy, g9 S' R8 M* M+ p: B, L
over the effect of early androgen exposure on adult
5 ?) a! [9 v) \penile length.10,11 Some reports suggest subnormal6 N2 A; H/ L/ s  b
adult penile length, apparently because of downreg-. a/ B  v# C1 i& o) p
ulation of androgen receptor number.10,12 However,- X. o; N( i2 L6 ^' V% I# l+ w, G* g
Sutherland et al13 did not find a correlation between
! T" `3 b+ ]) N- M) L: xchildhood testosterone exposure and reduced adult6 `" n- U) e! o& t0 N' v; w- W
penile length in clinical studies.
7 B! W2 i" Y. q" ANonetheless, we do not believe our patient is$ c  [" ^6 j) }2 m
going to experience any of the untoward effects from
4 J; x7 O, v" e- k; mtestosterone exposure as mentioned earlier because$ [/ Z; N& N/ u; J/ h
the exposure was not for a prolonged period of time.
  G+ z/ R5 v! Y! sAlthough the bone age was advanced at the time of
: i/ [6 }5 ?0 q( T! @2 H5 h0 fdiagnosis, the child had a normal growth velocity at
; M* u+ L, V5 o# Ethe follow-up visit. It is hoped that his final adult
- C( b5 a7 E- O4 d4 \2 _# f0 P/ E9 mheight will not be affected.
( @0 L, _$ i) {  ZAlthough rarely reported, the widespread avail-& h2 Z% G) K. p3 ^3 y3 O
ability of androgen products in our society may  L& u" A( P" i1 Z! k
indeed cause more virilization in male or female8 |0 l! l4 ^+ [3 p- t3 s, @) C5 E
children than one would realize. Exposure to andro-
0 `3 m8 t7 F) C% n+ }4 E2 h' Rgen products must be considered and specific ques-
; h. h$ }& d' a3 x" qtioning about the use of a testosterone product or
8 {# }. R  p: |1 W! O! D( S+ k2 C2 hgel should be asked of the family members during
  o& n5 P/ w8 cthe evaluation of any children who present with vir-. f7 r  a: T' N* J5 x+ ?
ilization or peripheral precocious puberty. The diag-2 ]" o4 s$ o  j8 p7 e
nosis can be established by just a few tests and by
$ q6 q) Q5 G) x2 v8 Q2 \) c( ?1 dappropriate history. The inability to obtain such a3 b# U; c- ^. I7 |. @0 S; N$ V
history, or failure to ask the specific questions, may
( z3 F; z! m9 r* ~: l% Kresult in extensive, unnecessary, and expensive; s/ V, ~3 c$ [- Y% \" F3 N
investigation. The primary care physician should be
5 E3 e; d7 L5 b- t6 K" Waware of this fact, because most of these children$ V1 L: N; n- q! W3 ?$ @$ B* a% X
may initially present in their practice. The Physicians’* c* x7 B% C) b, {
Desk Reference and package insert should also put a
1 k7 b4 ~) k7 a1 q; ]- [warning about the virilizing effect on a male or
  S2 V8 L) O" v4 c% X5 Yfemale child who might come in contact with some-
4 X( w" L5 ]- u* E9 ione using any of these products.
- l; ~" z+ S( h& Z( d, y& u- J" Z9 r5 kReferences
# r- u; z1 B) ?1 x8 F" B8 C1. Styne DM. The testes: disorder of sexual differentiation" [4 c& L' `4 H' b# |$ n3 _  S
and puberty in the male. In: Sperling MA, ed. Pediatric
  _) Q2 C( B( l! t; O: p3 v; _Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;) E, ^2 M! c8 ~  h
2002: 565-628.
+ ^, F" s* b6 J. a" G5 e3 I& o2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious4 e5 m' d3 E1 `( p
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

7 d6 l- S& {1 c& Y1 l) K, T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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