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Sexual Precocity in a 16-Month-Old0 g2 o7 _4 ]- ?8 e% I8 r
Boy Induced by Indirect Topical5 o7 V: a0 z3 h
Exposure to Testosterone
  A. J! H) _4 o: X5 F/ o4 L* Z3 }Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,28 X( x. V, `7 g& j3 i3 R4 V' k$ D# Q
and Kenneth R. Rettig, MD12 x" ?# ^2 x1 {4 M1 l4 I% G; s. R
Clinical Pediatrics
( D% U- {, h) UVolume 46 Number 6
9 `  v1 x, k9 s. T+ ^0 ?July 2007 540-543
' x9 x, t5 v5 y, R© 2007 Sage Publications
) j% V$ B/ q) C( \( t10.1177/0009922806296651
' e& P, m; U6 N2 {5 shttp://clp.sagepub.com
0 }6 R7 [' U* e. F% ^" vhosted at" T% m" f6 g0 Q# X
http://online.sagepub.com  O+ u" d/ Z; b& v1 l0 i, n0 R2 C1 i
Precocious puberty in boys, central or peripheral,
3 Y( n% O4 B. y/ ]+ S6 T& [9 Dis a significant concern for physicians. Central
! @) G  j# F) T  n7 Fprecocious puberty (CPP), which is mediated
& ^# W8 C0 ~1 ^4 Y5 othrough the hypothalamic pituitary gonadal axis, has
2 I( c4 R$ E: B8 m' Fa higher incidence of organic central nervous system* ^6 J2 j6 P+ }$ M! g5 ]
lesions in boys.1,2 Virilization in boys, as manifested# I. L- K$ b& c# h1 C" R
by enlargement of the penis, development of pubic
9 [+ p; k4 ~0 D( B. R0 ?; l5 Fhair, and facial acne without enlargement of testi-; ^4 V" {( Y0 J% {0 C
cles, suggests peripheral or pseudopuberty.1-3 We
6 y  Z! K/ _* A+ Ireport a 16-month-old boy who presented with the
$ n7 h5 [$ U2 X- ~5 \enlargement of the phallus and pubic hair develop-/ K5 w7 M- N) L( \6 l
ment without testicular enlargement, which was due
- i/ v6 V7 P7 R3 T# s. C6 ?7 qto the unintentional exposure to androgen gel used by
7 {) f3 z: `- \2 a' Rthe father. The family initially concealed this infor-
& x  `9 E2 P! Q$ o  gmation, resulting in an extensive work-up for this
' A/ F! b4 X/ I! S, bchild. Given the widespread and easy availability of
7 s9 [( t; E1 f) `% E# K5 utestosterone gel and cream, we believe this is proba-/ o- W+ d8 J6 _  Y4 r+ ]$ x7 u
bly more common than the rare case report in the: X# t7 P/ g5 Y! P
literature.48 D% S8 X, z1 o0 d" x5 y' @
Patient Report
$ i. c1 O/ E- Q4 j2 O4 R9 sA 16-month-old white child was referred to the& B. K- L! C9 A# X
endocrine clinic by his pediatrician with the concern
' u/ `2 f1 F% s* Y* V, tof early sexual development. His mother noticed
& x" t4 ~/ F/ S/ w- Mlight colored pubic hair development when he was8 d7 K7 {& f8 i+ g. S4 j( u
From the 1Division of Pediatric Endocrinology, 2University of+ h5 B4 z$ C, |, v1 R7 Z: _
South Alabama Medical Center, Mobile, Alabama.
9 e/ c3 x; X0 v1 T( z7 X: ]Address correspondence to: Samar K. Bhowmick, MD, FACE,& e6 z, T. ]" n8 E0 P0 }2 k
Professor of Pediatrics, University of South Alabama, College of
* q$ l4 F0 O/ c8 ]Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 c1 O  N" T3 f( X  C* x6 v
e-mail: [email protected].# Q. ?0 _1 l& R
about 6 to 7 months old, which progressively became
) Q! f# e7 H0 q& j0 o7 b) Adarker. She was also concerned about the enlarge-2 v2 l) z$ k$ H3 _- y
ment of his penis and frequent erections. The child
* X" p6 `3 h  r5 ~! h' Twas the product of a full-term normal delivery, with) k2 a2 ]/ M7 O* l- }! z5 V$ z5 L
a birth weight of 7 lb 14 oz, and birth length of
: L0 [6 V& Q+ b" O3 `7 L20 inches. He was breast-fed throughout the first year
2 D" Z" [* M" ~* M% Lof life and was still receiving breast milk along with
- l9 j% @+ e9 Zsolid food. He had no hospitalizations or surgery,
7 y( H% ]( o; ^* `1 \/ K) cand his psychosocial and psychomotor development, V; b2 P0 @. t, j
was age appropriate.# W/ ]  C5 p8 G' o
The family history was remarkable for the father,  [2 f) _, r- G  d+ ?$ Q+ b8 ?$ h  B
who was diagnosed with hypothyroidism at age 16,
3 R! Y% s5 \& k) R  v$ Jwhich was treated with thyroxine. The father’s, ~7 |' a3 |/ R8 e: E# X3 n1 L9 G
height was 6 feet, and he went through a somewhat: c) `+ ~; ~/ @  V3 v
early puberty and had stopped growing by age 14.
* v% M1 U% m" v4 L7 N" n3 v) [! l  AThe father denied taking any other medication. The
% ~( L" p# a3 E* X$ x* {child’s mother was in good health. Her menarche
+ Z: }8 |1 s. j9 ~was at 11 years of age, and her height was at 5 feet2 j  ^8 p1 ?/ G$ {
5 inches. There was no other family history of pre-6 d* a/ ~& F4 C5 p& H0 e: I0 D, c
cocious sexual development in the first-degree rela-
2 r+ [$ ]6 G0 A! ], Ytives. There were no siblings., E" }" E, T3 F4 Y. c+ A; Y
Physical Examination
% I  U3 v! C$ S- _' Y/ b) }& p. D* bThe physical examination revealed a very active,
- Z3 Q+ `3 X( ]0 p# O' oplayful, and healthy boy. The vital signs documented/ J5 x9 c& E, R3 O
a blood pressure of 85/50 mm Hg, his length was
$ @/ U) C# z4 x. m90 cm (>97th percentile), and his weight was 14.4 kg
+ c( o5 \8 y: p6 p/ r$ G$ X(also >97th percentile). The observed yearly growth! g* O" i1 K+ S) e. E0 a
velocity was 30 cm (12 inches). The examination of
. x& p3 O9 ~+ X+ [8 Sthe neck revealed no thyroid enlargement.
; Q4 d! b4 A  }: u) }4 [0 p2 aThe genitourinary examination was remarkable for$ J& w! e" B! Q0 G  ~8 }
enlargement of the penis, with a stretched length of# j  ^+ P! ]: n2 z3 ^+ H  D! F
8 cm and a width of 2 cm. The glans penis was very well
6 X" j8 P% t/ J8 P6 vdeveloped. The pubic hair was Tanner II, mostly around
9 j6 D4 E# q" i' p540
# w2 z$ k9 s& y! I. y$ gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: H* Z) H6 X; Wthe base of the phallus and was dark and curled. The1 \7 o8 T! K8 U6 h2 Z) N
testicular volume was prepubertal at 2 mL each.
: `& W: l( k2 tThe skin was moist and smooth and somewhat& ?% n. b' i3 F& W5 ?$ O# {3 g" y
oily. No axillary hair was noted. There were no
$ s, J5 n2 Y" o# {" x* Kabnormal skin pigmentations or café-au-lait spots.
! o) `5 H* h$ p# S3 \- I5 ~Neurologic evaluation showed deep tendon reflex 2++ O1 z" I& ?8 Q9 Z
bilateral and symmetrical. There was no suggestion
! \2 V( M, O# W8 D5 N5 |" Oof papilledema.
: v7 L9 W9 J3 P- d' y- rLaboratory Evaluation
- ^3 X1 m2 g2 P. S- v7 lThe bone age was consistent with 28 months by. p* ?2 k! l! |/ N# Q4 O
using the standard of Greulich and Pyle at a chrono-) d& o3 U$ S5 G+ J
logic age of 16 months (advanced).5 Chromosomal
' q; G0 ^3 A! l) `( h! Jkaryotype was 46XY. The thyroid function test
/ @( @3 d# Y! m  d* b3 `showed a free T4 of 1.69 ng/dL, and thyroid stimu-. K/ r0 Q; h3 d% e7 v' X  ?
lating hormone level was 1.3 µIU/mL (both normal).
6 P# K& C' H. t" _/ x( e& JThe concentrations of serum electrolytes, blood
# k# G' Q" M4 s0 B' ~4 V3 lurea nitrogen, creatinine, and calcium all were1 u, G/ g- v+ c$ k/ b; u6 ?
within normal range for his age. The concentration8 L# r1 H* c7 j6 j) K- g, ]
of serum 17-hydroxyprogesterone was 16 ng/dL
0 m9 g' H6 q9 ~% w9 B7 n: }9 B(normal, 3 to 90 ng/dL), androstenedione was 20+ l" b5 f  b9 Y' N- N8 Z
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-; x, D  \/ q- P2 f3 u
terone was 38 ng/dL (normal, 50 to 760 ng/dL),1 Y/ |+ @0 q' d" ]! V
desoxycorticosterone was 4.3 ng/dL (normal, 7 to5 l' r2 ^$ E- x! ]/ G% O
49ng/dL), 11-desoxycortisol (specific compound S)! l( Y9 r2 T) T  _
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-, Y' t7 j" U5 S0 S3 I0 i% G
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total+ ~2 Y/ q4 d, w
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
7 J! b! V. t  hand β-human chorionic gonadotropin was less than
& g: F% E! i0 p5 mIU/mL (normal <5 mIU/mL). Serum follicular
! \; f. M, W4 ?" ?stimulating hormone and leuteinizing hormone
+ V5 p. C; h  X( v4 h2 e3 xconcentrations were less than 0.05 mIU/mL
" ^+ |! q1 l! R( w% k/ ~! B(prepubertal).# U: ]0 Z( ~! k$ f. q0 l6 a- `" M1 I# v
The parents were notified about the laboratory( _3 M) c% A7 h
results and were informed that all of the tests were
6 m, o" T: U. G4 `* b1 ]6 D1 Pnormal except the testosterone level was high. The! a1 h: j+ ]/ ]8 A& v
follow-up visit was arranged within a few weeks to
! t4 u& m5 j- V+ l  A' _obtain testicular and abdominal sonograms; how-" W; G% n9 ?- }  X( u3 K0 K
ever, the family did not return for 4 months.6 d% f/ q% ~4 ~7 @2 [3 W
Physical examination at this time revealed that the" D( K+ }  {9 c& Q* R
child had grown 2.5 cm in 4 months and had gained; h1 O+ c" {# L2 i
2 kg of weight. Physical examination remained
! `' o! c* i3 z7 r7 Funchanged. Surprisingly, the pubic hair almost com-' k4 X& m" N; M  W6 _8 f
pletely disappeared except for a few vellous hairs at
1 U( u; P1 V! s; `the base of the phallus. Testicular volume was still 26 r! w' a( p% I. u& A/ ]% Y
mL, and the size of the penis remained unchanged.
* [1 Z, s# Y, v+ L, c) ^The mother also said that the boy was no longer hav-  H/ x( C( J- S+ e
ing frequent erections.+ ~+ l7 y2 `2 t9 H: f
Both parents were again questioned about use of
! c. }$ {0 ]1 z/ N# U" I1 cany ointment/creams that they may have applied to6 A9 L: x' g$ v1 h2 W0 s
the child’s skin. This time the father admitted the
) n. J: p7 F( U& p$ }Topical Testosterone Exposure / Bhowmick et al 541
" j* u) t% s" q6 Q: Iuse of testosterone gel twice daily that he was apply-' A5 U$ f' b% P! ?
ing over his own shoulders, chest, and back area for& A# Y3 @3 ]& V8 ^
a year. The father also revealed he was embarrassed
$ V) V/ F6 I# w4 @& uto disclose that he was using a testosterone gel pre-& t( H+ Q' b* r
scribed by his family physician for decreased libido! c% ]% t0 \0 y7 _9 F- L  Q4 W0 r
secondary to depression.; U3 a) u  h9 `) [: L# f9 ^# ?
The child slept in the same bed with parents.
8 f/ G' \4 B- h8 w5 [The father would hug the baby and hold him on his0 i- p0 u1 n2 W; e+ I) H' H7 u
chest for a considerable period of time, causing sig-
+ `$ u/ `# ^4 e* X/ R3 Cnificant bare skin contact between baby and father.- ]( H, @& u9 Q
The father also admitted that after the phone call,) O# z5 i& P0 a* K, H) ^$ Y6 {
when he learned the testosterone level in the baby
# `; v" D, \: nwas high, he then read the product information
2 ^: l' P1 J- Spacket and concluded that it was most likely the rea-
" J! a- D8 }8 {/ k( ~son for the child’s virilization. At that time, they: b% Z% L) d% D2 x/ M$ o
decided to put the baby in a separate bed, and the  h. {+ C) i: j7 ~3 u* D6 j* `
father was not hugging him with bare skin and had1 A- E. ]- J. }  ?5 v6 u
been using protective clothing. A repeat testosterone2 v* i9 a; U6 f( T
test was ordered, but the family did not go to the1 Z) H# N8 e) i9 r, ?7 `! L
laboratory to obtain the test.% X# I, _( b  }: j7 I% a
Discussion& I- W7 ^& f; u
Precocious puberty in boys is defined as secondary; b8 e; m1 j2 \- G
sexual development before 9 years of age.1,4& e' p+ v* h& L. ]2 ~, [
Precocious puberty is termed as central (true) when- {( B  o4 H& R. J
it is caused by the premature activation of hypo-) A& t" t4 I( F/ J) p) K
thalamic pituitary gonadal axis. CPP is more com-  d& Y4 V$ M% O- _2 `
mon in girls than in boys.1,3 Most boys with CPP( K5 O0 R, K, F
may have a central nervous system lesion that is4 A2 W9 v+ K' C% m
responsible for the early activation of the hypothal-" x1 q8 N" ^4 a  H
amic pituitary gonadal axis.1-3 Thus, greater empha-
# k+ p" P# F+ v: ~sis has been given to neuroradiologic imaging in
& M4 C6 J" X) m9 o1 C( I7 lboys with precocious puberty. In addition to viril-8 Z; q) S9 C7 |
ization, the clinical hallmark of CPP is the symmet-3 e  E* }5 m2 P6 r: {
rical testicular growth secondary to stimulation by
0 i! d2 Q4 ?9 {' h6 m. u" Ngonadotropins.1,3' }5 O1 a9 t' S: \
Gonadotropin-independent peripheral preco-! M6 V5 Y# h' o; f6 M  }
cious puberty in boys also results from inappropriate
( {5 l$ a" p6 \( handrogenic stimulation from either endogenous or0 K! V* W9 b. D. S" M. w
exogenous sources, nonpituitary gonadotropin stim-1 X3 l2 M# e$ F( V
ulation, and rare activating mutations.3 Virilizing
5 U1 `) ~3 ]  s3 d6 qcongenital adrenal hyperplasia producing excessive5 m! v6 z! u1 v
adrenal androgens is a common cause of precocious
) w2 l; F, e% W9 z. g% W  }; v0 spuberty in boys.3,4
( ]. g/ R7 J5 I- X7 P7 q+ zThe most common form of congenital adrenal% S1 X! B, R# o$ U
hyperplasia is the 21-hydroxylase enzyme deficiency.0 s3 z8 D( M$ T/ _+ ?. e/ f
The 11-β hydroxylase deficiency may also result in
2 n6 y2 n# |, t+ gexcessive adrenal androgen production, and rarely,) Q7 R2 Z, B; l* A/ x* i
an adrenal tumor may also cause adrenal androgen7 j( y' D" V9 C, `( z
excess.1,3
, I! t) ?7 K& {- q  G* n5 qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 I9 A8 D6 l5 l/ ^) b2 r: m
542 Clinical Pediatrics / Vol. 46, No. 6, July 20071 u& j/ U; g3 w0 B& H2 v0 H! {
A unique entity of male-limited gonadotropin-
: v2 z3 F6 J& |, x! l% a- B3 z6 {independent precocious puberty, which is also known
% V1 Q* l% A) U% P* Zas testotoxicosis, may cause precocious puberty at a6 f& }" H% A. K$ d( f$ P7 g  U; {/ O
very young age. The physical findings in these boys0 o* o0 Y0 Y7 o
with this disorder are full pubertal development,+ G' u/ K8 T9 j' \9 c+ F: T7 `8 s
including bilateral testicular growth, similar to boys% a2 o6 l. _: q. c
with CPP. The gonadotropin levels in this disorder
  o* }0 n* v" v4 A% w: Bare suppressed to prepubertal levels and do not show
1 {. v/ M$ G. u8 |7 X, M8 k: R  Kpubertal response of gonadotropin after gonadotropin-
1 V5 g( b5 |0 m# x5 ^9 E, Breleasing hormone stimulation. This is a sex-linked0 P+ L& D% r. H0 }$ @1 V1 V: r8 h
autosomal dominant disorder that affects only
6 U" c5 f  R& Z& x" B2 ?4 @males; therefore, other male members of the family
' j* c- `/ v! A8 Q; i+ pmay have similar precocious puberty.3
; I$ P, ]: X7 w% \0 L2 g+ d8 l' n1 k9 kIn our patient, physical examination was incon-7 G7 w: w9 E1 ]
sistent with true precocious puberty since his testi-
% n6 w  ]5 U8 Ccles were prepubertal in size. However, testotoxicosis
) J! Q9 B6 E/ h5 Q2 d5 W, |was in the differential diagnosis because his father
& ?" Z) f4 b7 l4 P4 [  A) H$ L# jstarted puberty somewhat early, and occasionally,$ K) a6 B. {+ \
testicular enlargement is not that evident in the; y: }. d+ f: t( @+ e  [# z1 G3 |
beginning of this process.1 In the absence of a neg-
% D. L' e; J3 ]' Rative initial history of androgen exposure, our
  p8 g( L/ w2 F  `. Y- Fbiggest concern was virilizing adrenal hyperplasia,
! l  G, m$ X+ T! F0 w3 Eeither 21-hydroxylase deficiency or 11-β hydroxylase1 L7 j' a" L0 T( G1 f( J
deficiency. Those diagnoses were excluded by find-( B! b2 O+ ]9 M- F) b" P& m! x
ing the normal level of adrenal steroids.
$ k* K) P  W1 [8 W, O& PThe diagnosis of exogenous androgens was strongly
( N8 ]) W% k0 u! O8 j+ o$ ?suspected in a follow-up visit after 4 months because
3 _# e; P4 x# ?7 h; t0 U% E  Cthe physical examination revealed the complete disap-% E1 A: B& J: u2 y7 @
pearance of pubic hair, normal growth velocity, and/ @) w/ O0 p% T% W9 i
decreased erections. The father admitted using a testos-$ X) S0 M6 g' }$ G- p
terone gel, which he concealed at first visit. He was
( u. r# t) a  V# wusing it rather frequently, twice a day. The Physicians’
, L6 l* o: ]& ODesk Reference, or package insert of this product, gel or
% B; p. D" p% r) Q. ~cream, cautions about dermal testosterone transfer to
1 t; m/ X1 T4 j- D# ]' i. A; funprotected females through direct skin exposure.
* }9 J- R, I2 ?& P0 {, hSerum testosterone level was found to be 2 times the1 j3 [* Y0 J1 z0 h- H$ }& ~4 s
baseline value in those females who were exposed to
) @" v- F/ ?" B# q: Weven 15 minutes of direct skin contact with their male
* I  m" _% k9 B' b  o( G, @8 m) ipartners.6 However, when a shirt covered the applica-
6 D" r, D4 d7 u# q  xtion site, this testosterone transfer was prevented." A; @, Y+ b" A) ?" B
Our patient’s testosterone level was 60 ng/mL,/ ?5 S) R4 i& ^
which was clearly high. Some studies suggest that
! U9 [0 J  M7 ^% S' s8 @( _dermal conversion of testosterone to dihydrotestos-( `% C' A% g) B( M. y+ u
terone, which is a more potent metabolite, is more/ X. _4 u* ^( I1 Q. o
active in young children exposed to testosterone  R4 q: }# N9 z, T  J& H9 _
exogenously7; however, we did not measure a dihy-, f, w9 u+ _, T% U+ r$ B
drotestosterone level in our patient. In addition to
1 [+ c9 a" [2 ~$ Mvirilization, exposure to exogenous testosterone in
! E* Y' K+ F2 b7 T6 Nchildren results in an increase in growth velocity and
: m+ v0 J& o+ V1 v0 zadvanced bone age, as seen in our patient.0 b5 s+ f; \4 x9 G
The long-term effect of androgen exposure during- z; c: E4 p% P) d8 i1 f  \$ U
early childhood on pubertal development and final8 X: f9 s1 C  g! u" ?
adult height are not fully known and always remain
5 S* T2 }) S% ^" I+ U- m! ga concern. Children treated with short-term testos-
4 F8 R# s* u6 ?: r0 q2 Nterone injection or topical androgen may exhibit some
' t! \  j" T' v  A) ^! S8 y$ ~, `) Zacceleration of the skeletal maturation; however, after# C) X1 r. r. G& ^" v
cessation of treatment, the rate of bone maturation: c1 {2 T0 C" k( M% M4 f: p2 R
decelerates and gradually returns to normal.8,9
5 A% D. Q1 w2 C' v* n7 m3 bThere are conflicting reports and controversy
6 A5 X! ?: ~; j/ Q9 P, G5 wover the effect of early androgen exposure on adult# Y! ]8 E$ T; |& o2 E) x
penile length.10,11 Some reports suggest subnormal7 d0 R, c2 W# y+ {/ S4 B
adult penile length, apparently because of downreg-
0 I- B+ L: S8 l% j2 a3 fulation of androgen receptor number.10,12 However,; H1 l: y& I7 v( \- w
Sutherland et al13 did not find a correlation between4 Q* e/ j4 d% B" \% M' j1 F
childhood testosterone exposure and reduced adult
& t+ j1 r7 `! gpenile length in clinical studies.; q0 ]: x, v& b; x( F8 n( A
Nonetheless, we do not believe our patient is
% U8 c7 a( u: ~" E3 p: J+ Sgoing to experience any of the untoward effects from/ q1 b% E9 M. y  |6 j# o
testosterone exposure as mentioned earlier because
8 H5 ~  s; _* c0 l0 l1 M6 Pthe exposure was not for a prolonged period of time.
9 g0 Y% y8 T  y2 c! \. J% c" mAlthough the bone age was advanced at the time of; X$ V, P8 Y: u: V) ^
diagnosis, the child had a normal growth velocity at
2 l% N+ c7 p) r9 t/ l8 Lthe follow-up visit. It is hoped that his final adult7 a2 }" [7 u* R' A( e2 g
height will not be affected.3 T2 d6 p  d( e" ~( E$ C$ f) w2 `
Although rarely reported, the widespread avail-" X% _- b' _: d4 ^
ability of androgen products in our society may
% E3 |! Y9 Z" a* J+ uindeed cause more virilization in male or female0 o  N1 J2 t) r( q! m9 u+ k
children than one would realize. Exposure to andro-- f' l5 N, P& e9 ~
gen products must be considered and specific ques-
6 P. r% c: C" ?" G6 `# R$ @1 |tioning about the use of a testosterone product or
  E* K/ s. g/ r  j# n" J3 J0 Vgel should be asked of the family members during0 T/ t, s- x' `" E
the evaluation of any children who present with vir-
5 B/ g4 z/ F& a2 F/ ailization or peripheral precocious puberty. The diag-7 f+ W  n1 E; c4 h' T
nosis can be established by just a few tests and by
( b! `- |, s5 V- \+ z  W% Yappropriate history. The inability to obtain such a  c* U1 R9 O+ d3 j# X
history, or failure to ask the specific questions, may3 W! @. G2 |3 K3 _+ _. c
result in extensive, unnecessary, and expensive% J) V# b5 ?$ N; B
investigation. The primary care physician should be9 b7 b( v3 e' q
aware of this fact, because most of these children
2 M0 q# v" b* N+ m7 Hmay initially present in their practice. The Physicians’" l; z7 y  N5 E+ L9 q
Desk Reference and package insert should also put a' H$ j# G% N9 n
warning about the virilizing effect on a male or1 p" U+ C9 T" w" J0 a0 v2 O
female child who might come in contact with some-
2 [9 B7 G* m1 W7 B5 Z1 s/ C) {one using any of these products.& a+ y; R8 I. Q9 J  I% Y
References* {8 b5 w9 @5 l% g# y8 S  h+ J6 Y
1. Styne DM. The testes: disorder of sexual differentiation
  G* {, f; w# ^3 e/ k' xand puberty in the male. In: Sperling MA, ed. Pediatric" a6 y9 x, A: m
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;8 D5 W5 \* J4 D4 F  U
2002: 565-628.  ^: r. Y# M! a
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
/ x. F* B# Z2 `8 j, L# w/ M* b& Opuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
5 b7 [$ A* d& Q  O4 I5 j5 ^8 k# y8 YBoy Induced by Indirect Topical# B+ S5 a- H. a! L% V
Exposure to Testosterone
9 G1 h0 o& |. p) X. B/ ASamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. X& ]* V* w7 I8 B! d, J
and Kenneth R. Rettig, MD1! O; L1 m) m7 |4 H5 q0 h1 l
Clinical Pediatrics5 d+ C* B- N# D
Volume 46 Number 6: P- r; B) q$ o4 H2 g% D
July 2007 540-543
' d; j9 X- U8 Y* i/ m3 W, m& w© 2007 Sage Publications7 W' d5 q$ J8 `( H# d0 `7 f
10.1177/0009922806296651
& K3 O7 z$ m: c3 z" \" x- Lhttp://clp.sagepub.com
8 K' L5 @0 h4 e( Lhosted at
  e8 \3 A2 x3 C1 x' A3 ^http://online.sagepub.com
, t. R6 a% B" z' ?+ dPrecocious puberty in boys, central or peripheral,0 h- b+ H* M, S! n. ]
is a significant concern for physicians. Central
0 i% M+ L9 M' p" vprecocious puberty (CPP), which is mediated
8 }" ~. l5 U7 wthrough the hypothalamic pituitary gonadal axis, has
7 f/ v" c% M+ F& e. U% `) Sa higher incidence of organic central nervous system
. A+ B: `( f& {; u! ulesions in boys.1,2 Virilization in boys, as manifested3 _! _1 y  R4 f' A9 L
by enlargement of the penis, development of pubic; w0 u2 u, _& y$ ~& a
hair, and facial acne without enlargement of testi-8 u& b" Z' m/ p
cles, suggests peripheral or pseudopuberty.1-3 We: \) F+ {0 _2 e/ ~2 C* R
report a 16-month-old boy who presented with the
" m5 F. U  E* ?, I7 g6 N. Q1 S- henlargement of the phallus and pubic hair develop-" d; B/ S, _# |# v- y
ment without testicular enlargement, which was due
. p& l9 a3 T1 z9 ~to the unintentional exposure to androgen gel used by1 L+ T* l- y( s' E  v9 X9 J' x
the father. The family initially concealed this infor-" y- p2 T, ^4 ~8 M& P) x: D5 }& g4 L
mation, resulting in an extensive work-up for this3 E. N& m( p3 w( `
child. Given the widespread and easy availability of
: i/ }, m' i( v0 Q& t4 i4 R) t% ytestosterone gel and cream, we believe this is proba-: }% x) ^% S4 s- f4 A3 \( R
bly more common than the rare case report in the
9 k: R7 V  A, V9 S3 Cliterature.4/ j0 F/ H2 a* I$ [
Patient Report/ \3 u; E# I6 v7 _& w
A 16-month-old white child was referred to the
' [7 q( y3 O3 `! `% cendocrine clinic by his pediatrician with the concern
2 h, o+ m; U; O6 [: N3 ^of early sexual development. His mother noticed* A! Z5 M/ v. H( Y$ I: _3 E
light colored pubic hair development when he was8 N# K; c: W; y' n$ J# a8 E* e4 j
From the 1Division of Pediatric Endocrinology, 2University of
+ m8 k- h. ~7 w# W! B! g1 GSouth Alabama Medical Center, Mobile, Alabama.0 e: w4 T4 U' E) Z, V
Address correspondence to: Samar K. Bhowmick, MD, FACE,
4 Q6 Y9 c  ~) I2 C) v; ?Professor of Pediatrics, University of South Alabama, College of9 C- d; X+ Q0 F0 E9 x
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
4 [1 B0 _7 Y: i$ E9 y$ U7 {e-mail: [email protected].
; V! T; r  p& P5 {1 h. y9 {about 6 to 7 months old, which progressively became
5 J: X5 G0 b: W* ydarker. She was also concerned about the enlarge-
3 ^" N9 x" g2 }6 Lment of his penis and frequent erections. The child
1 a0 e2 Z* F9 }% M$ k" Q( v2 Lwas the product of a full-term normal delivery, with; ]7 I6 @+ u* l0 ]" q' K: N
a birth weight of 7 lb 14 oz, and birth length of
0 b2 C* V( ~' _% ?( J7 W" {20 inches. He was breast-fed throughout the first year
1 `, h7 C" y( S: Z, lof life and was still receiving breast milk along with; K6 W. o. t, N; w) m3 d" w/ U
solid food. He had no hospitalizations or surgery,2 p1 S$ Q& d0 W
and his psychosocial and psychomotor development% j. x/ C6 j7 M+ b" {' q# o: N
was age appropriate.& x- N% i6 r/ h5 K0 E4 K# o1 ^
The family history was remarkable for the father,  c1 I8 f& E; F, C5 o. A
who was diagnosed with hypothyroidism at age 16,
& K( b' u( f# {which was treated with thyroxine. The father’s
# s+ Y3 T$ q% X( l8 ?9 Pheight was 6 feet, and he went through a somewhat9 J, E6 J0 [% D' Q7 T: Y
early puberty and had stopped growing by age 14.7 f* r/ c7 I' P/ e5 K
The father denied taking any other medication. The
3 c0 l: G0 I& h" vchild’s mother was in good health. Her menarche4 j" q# n  ~- ^* O/ l
was at 11 years of age, and her height was at 5 feet
0 E5 N6 z( r5 h. q$ N5 inches. There was no other family history of pre-
, b" S" {( H" R- bcocious sexual development in the first-degree rela-
/ p8 s! W7 r. q* g* L* X8 ^6 Stives. There were no siblings.
2 c2 ~7 u+ v/ v  [Physical Examination
' v+ T& W& h5 W$ _- _( FThe physical examination revealed a very active,
# H# z- t* N! Rplayful, and healthy boy. The vital signs documented
; Y0 M4 E+ a5 [8 Q  J6 A1 Ka blood pressure of 85/50 mm Hg, his length was
6 q. P  X4 r  w/ F, T9 J) {; G90 cm (>97th percentile), and his weight was 14.4 kg
! q! H7 `6 _: q5 {; O# \& Y(also >97th percentile). The observed yearly growth
* A$ H8 G7 Y$ W& X- O2 x. Mvelocity was 30 cm (12 inches). The examination of7 u& h4 B0 `, j
the neck revealed no thyroid enlargement.* ~6 p1 w9 ?6 S/ w4 s7 N; P2 E
The genitourinary examination was remarkable for
, n" J# p7 {. ]8 C2 }! kenlargement of the penis, with a stretched length of' B" B. X2 N. @/ m/ @
8 cm and a width of 2 cm. The glans penis was very well
3 i% k* \9 \% i- T' w* B  S; C* {- mdeveloped. The pubic hair was Tanner II, mostly around
( B3 w. ~* h* ?6 A) J- ?* ^" v540
( k' Y) w) k! l( ?at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 Z6 e6 J5 z9 I7 [( b3 ?! Cthe base of the phallus and was dark and curled. The
& d1 M' p9 f; T8 z' s' c' gtesticular volume was prepubertal at 2 mL each.
9 T$ L( A2 Z6 F/ l  O) m& l4 UThe skin was moist and smooth and somewhat2 r# k6 r) O- o8 |2 R
oily. No axillary hair was noted. There were no: W1 h; z0 N5 b
abnormal skin pigmentations or café-au-lait spots.
) C2 Y  Z$ w& J0 s, L: \  DNeurologic evaluation showed deep tendon reflex 2+
* V7 B8 F  w. }# h, ~bilateral and symmetrical. There was no suggestion
0 d. i. T0 ?1 M7 ~- Kof papilledema.0 I/ b( g$ ]( M, O! `6 y
Laboratory Evaluation
$ y: J  [3 e0 G! Z: h+ p$ ?% bThe bone age was consistent with 28 months by6 i3 X; e- J  _5 \) F, {9 q( s
using the standard of Greulich and Pyle at a chrono-5 Y! v# y) C4 _6 L
logic age of 16 months (advanced).5 Chromosomal9 V( y! b, V1 [4 I- {
karyotype was 46XY. The thyroid function test
! p/ E, h: w3 l, b4 Y( y. E4 ashowed a free T4 of 1.69 ng/dL, and thyroid stimu-
! |9 C* U1 W% f9 K) @. p/ F2 [lating hormone level was 1.3 µIU/mL (both normal).
; e- x4 w' Y$ G) `The concentrations of serum electrolytes, blood
5 l) c9 |& l+ b  e; G3 H) Curea nitrogen, creatinine, and calcium all were/ ?% W* `' M4 x1 A
within normal range for his age. The concentration
! j" Z. G2 e) A) Uof serum 17-hydroxyprogesterone was 16 ng/dL) `9 j7 _- M9 m6 O5 O- E
(normal, 3 to 90 ng/dL), androstenedione was 20  p) n- [1 v4 a* F. X: z
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-* w: F2 l$ j% ]2 h7 I3 T6 T3 c) G
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
4 e3 Y2 D! `, F% cdesoxycorticosterone was 4.3 ng/dL (normal, 7 to9 [7 n- G) X& R3 {2 I
49ng/dL), 11-desoxycortisol (specific compound S)- g( k6 c6 ~: c, F4 b
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
4 v) V, f) ~$ m1 p6 utisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total, e# Z6 E8 H# S6 Z$ e
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),( y- |5 X) t6 ~
and β-human chorionic gonadotropin was less than
& m% J( u, y0 l/ F' v. x5 mIU/mL (normal <5 mIU/mL). Serum follicular  W, T2 R! q- M9 ^5 \
stimulating hormone and leuteinizing hormone
; m2 u, b* x! P* k6 }# B; ^concentrations were less than 0.05 mIU/mL
( D  ]% x' r6 D(prepubertal).& t+ J$ {' V0 H1 ~, R1 W7 _
The parents were notified about the laboratory
- u4 Q/ ?4 W+ G( Fresults and were informed that all of the tests were. H3 b8 V1 m9 [5 P: p) f
normal except the testosterone level was high. The
# C( N1 G- J: w3 jfollow-up visit was arranged within a few weeks to
8 z* U. x  b3 }; x: G+ @obtain testicular and abdominal sonograms; how-8 V& _6 k- {6 Y) p* B$ z
ever, the family did not return for 4 months.7 h- m4 w* P. L
Physical examination at this time revealed that the
' y- U9 ~" K8 E4 i! r" n& w0 fchild had grown 2.5 cm in 4 months and had gained
1 v1 q7 v- ~0 v3 B. H2 kg of weight. Physical examination remained, X+ X4 j: o2 {; G( y! A1 }
unchanged. Surprisingly, the pubic hair almost com-2 \& N: w4 y0 G* v4 h
pletely disappeared except for a few vellous hairs at
" X* \7 [3 @& s2 T0 r3 M+ X; gthe base of the phallus. Testicular volume was still 2
1 ~- L3 O8 t$ P5 A2 VmL, and the size of the penis remained unchanged.
% n& A* M8 P$ e7 q( n5 ~The mother also said that the boy was no longer hav-7 F) }- L$ ^7 s
ing frequent erections.
$ A# [& ]& Y, V: @* i% dBoth parents were again questioned about use of! G* b8 ]/ t. h7 a9 k$ r
any ointment/creams that they may have applied to: S8 N2 {4 j5 h9 |! Y- C3 _; D
the child’s skin. This time the father admitted the
& H& M* W% R# k+ M4 OTopical Testosterone Exposure / Bhowmick et al 541. E$ n) ?- _, Y% H. W
use of testosterone gel twice daily that he was apply-
  \9 C# o$ H* H; r) Ving over his own shoulders, chest, and back area for
  F& r6 A+ f! h' a0 E' C; q; Xa year. The father also revealed he was embarrassed3 R. N( A% P  y( k$ i
to disclose that he was using a testosterone gel pre-0 H* g: R4 V0 }2 B
scribed by his family physician for decreased libido3 Z# F5 s; N( s3 O* W6 c# m  ~  c
secondary to depression.
' N+ C7 g) w) `. G5 v% w9 kThe child slept in the same bed with parents.5 n. R9 R# Y: Q- [) M) |
The father would hug the baby and hold him on his
$ C8 x, [2 x  Bchest for a considerable period of time, causing sig-
' s) C* Y, X  C" N# E( N( p4 [& Qnificant bare skin contact between baby and father.0 `8 G: P! _3 y# z9 ^
The father also admitted that after the phone call,
" F1 a# c$ t* a# G. Rwhen he learned the testosterone level in the baby; Y. A" w/ H) X# G7 m/ e/ Y
was high, he then read the product information
3 P5 d/ E+ W0 ?' u9 Tpacket and concluded that it was most likely the rea-
5 E8 N4 a( v3 R1 ^, U2 ason for the child’s virilization. At that time, they
0 k% M7 @2 r1 wdecided to put the baby in a separate bed, and the# v- o) `3 T! {6 {
father was not hugging him with bare skin and had' h  D+ y8 H0 b% S% n4 [
been using protective clothing. A repeat testosterone
5 O( L1 v& u( b5 W/ N3 Atest was ordered, but the family did not go to the( E# y7 {3 V% j2 Q
laboratory to obtain the test.' `) l5 b4 I2 f/ n
Discussion
* _- z5 E2 B( J2 d+ L! IPrecocious puberty in boys is defined as secondary: n- M; E) E2 T7 }& k4 A
sexual development before 9 years of age.1,4! V7 D7 J, \3 p; i
Precocious puberty is termed as central (true) when
2 ^, q$ c7 I3 u6 kit is caused by the premature activation of hypo-
* k" T( n  b6 K+ H3 wthalamic pituitary gonadal axis. CPP is more com-- ~6 f4 K3 ]$ E
mon in girls than in boys.1,3 Most boys with CPP
8 q, s' ?2 I( g! mmay have a central nervous system lesion that is
( A1 {/ E, q8 s6 ]% V" _2 mresponsible for the early activation of the hypothal-! e# a5 H. r3 X9 ^1 `
amic pituitary gonadal axis.1-3 Thus, greater empha-0 a2 N. }; i: x
sis has been given to neuroradiologic imaging in1 o3 \4 t: P2 l, p6 U4 h- r8 T
boys with precocious puberty. In addition to viril-
: f, v6 ]6 a8 j' u8 u5 zization, the clinical hallmark of CPP is the symmet-
1 U+ z; T( ]" D4 w% erical testicular growth secondary to stimulation by
! C5 r1 q# l" h% G% D  dgonadotropins.1,3- u2 R* @) @1 l' s, u2 A
Gonadotropin-independent peripheral preco-
9 R+ n4 a6 c( _, Lcious puberty in boys also results from inappropriate
$ ^2 S+ D/ G( w: o2 }& V9 ?androgenic stimulation from either endogenous or
, o; B- H' V) z8 K/ `exogenous sources, nonpituitary gonadotropin stim-! i: u' `3 ?0 y/ ~+ V8 P* z
ulation, and rare activating mutations.3 Virilizing
3 y$ L! L' z- a/ B( Pcongenital adrenal hyperplasia producing excessive: D8 V9 Q7 I+ I- ?% m
adrenal androgens is a common cause of precocious
. c! i% z8 a$ B( {- bpuberty in boys.3,45 h6 @- H. j+ E# \; l
The most common form of congenital adrenal, k5 T" D9 Z6 n4 ?# m$ Y1 q- {% [5 h
hyperplasia is the 21-hydroxylase enzyme deficiency.
. t" O3 O  m' c% [The 11-β hydroxylase deficiency may also result in% s& h- i5 f% h$ q, L
excessive adrenal androgen production, and rarely,
  m- n+ a* j( w+ J9 b9 r; Ban adrenal tumor may also cause adrenal androgen( x) p0 k! B6 O
excess.1,3; k/ E# E' ]& K9 q; \" }
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 o; ?% a4 s( d8 Y6 M  x3 r
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007' R9 y  ?8 v( h/ ?
A unique entity of male-limited gonadotropin-
# s5 M; B2 Q5 c1 v* [% Cindependent precocious puberty, which is also known# z- b: W4 t1 l2 X6 G2 L# {$ W' w
as testotoxicosis, may cause precocious puberty at a8 j9 H  m; {1 g8 `6 T3 v2 s; m  }$ d
very young age. The physical findings in these boys9 M+ E, ]2 Q2 o* U$ @, f
with this disorder are full pubertal development,: i3 x! I$ S' n: z+ i
including bilateral testicular growth, similar to boys" W. @2 Y+ v" }, a7 e. d* z
with CPP. The gonadotropin levels in this disorder# ^. T- p# {5 M9 v* B: a# O
are suppressed to prepubertal levels and do not show
* B: T3 v6 ?: p% tpubertal response of gonadotropin after gonadotropin-/ i9 |0 G0 f) K7 n7 F0 t
releasing hormone stimulation. This is a sex-linked' F5 a- H9 N7 ], m6 s1 h6 k
autosomal dominant disorder that affects only
  Y$ N3 V7 }& Umales; therefore, other male members of the family9 q4 @* `  e) [5 f, n% V
may have similar precocious puberty.38 ^/ I1 n- Y' ?- j3 A4 Y- J4 D: T7 {
In our patient, physical examination was incon-  j; i/ d2 z3 P+ [. v9 x8 e
sistent with true precocious puberty since his testi-2 x) x5 I( C' y) Z. N! I( z
cles were prepubertal in size. However, testotoxicosis- T" M* A9 C! I% Y% w
was in the differential diagnosis because his father% n5 U5 ]  Y2 F3 Q% y7 p* m
started puberty somewhat early, and occasionally,
8 G. D* A- T4 G0 S8 ^/ P, G3 Ztesticular enlargement is not that evident in the
+ b7 s& _! m1 ]0 p. J( J  W6 fbeginning of this process.1 In the absence of a neg-
5 s4 A% h! G: g4 {ative initial history of androgen exposure, our9 u: d2 k' ?4 U
biggest concern was virilizing adrenal hyperplasia,) q% S  Q, u; Y: K, n1 K6 p
either 21-hydroxylase deficiency or 11-β hydroxylase
. o2 d( ?4 a& G6 Q& U9 Mdeficiency. Those diagnoses were excluded by find-- s4 S, u9 H$ Z, l- E9 G! G4 n( H" t
ing the normal level of adrenal steroids.  s3 q! i+ @2 v* X1 v& |+ i) x
The diagnosis of exogenous androgens was strongly
7 q( o+ A; q8 e/ o( L4 e! C* ssuspected in a follow-up visit after 4 months because
1 E- Y* V4 e% E# _2 u8 rthe physical examination revealed the complete disap-: i2 X3 k) E' f* d/ ]# h
pearance of pubic hair, normal growth velocity, and
9 ^; D- M& r' t- _& A# w0 Wdecreased erections. The father admitted using a testos-5 {# K5 `8 O0 G- X
terone gel, which he concealed at first visit. He was
2 x: ?8 S4 u4 c1 Y( A0 h& k# `; Xusing it rather frequently, twice a day. The Physicians’! z' p6 w3 E  U8 }+ Y2 n
Desk Reference, or package insert of this product, gel or& I2 \9 T9 {2 @
cream, cautions about dermal testosterone transfer to* d6 Y9 h% f! Z- F
unprotected females through direct skin exposure.4 g4 J# u  o# u- Y- o! X
Serum testosterone level was found to be 2 times the' O! a/ ]0 I! M: K( P, q
baseline value in those females who were exposed to0 e9 j$ o1 T8 f% k+ I1 R
even 15 minutes of direct skin contact with their male2 o) g% j5 D7 ]  ^
partners.6 However, when a shirt covered the applica-
% K3 |& n. D4 s, b# N& _1 [tion site, this testosterone transfer was prevented.
, R" Q* @4 |6 U/ |; IOur patient’s testosterone level was 60 ng/mL," p2 J2 r- |5 |, j2 @1 x! x
which was clearly high. Some studies suggest that6 Q$ }. W# b2 n) i3 N- q
dermal conversion of testosterone to dihydrotestos-& M8 A. i  G: l& @' H  m
terone, which is a more potent metabolite, is more: D5 _. ]0 r- X' S9 w! N
active in young children exposed to testosterone5 M: U' l* z1 v3 s+ w9 m
exogenously7; however, we did not measure a dihy-
7 Y: f1 H3 @# Edrotestosterone level in our patient. In addition to3 r+ M$ S& ]! m4 E5 |7 v8 |0 Z
virilization, exposure to exogenous testosterone in
( K1 E& m4 J, [' n- gchildren results in an increase in growth velocity and: K2 D7 x0 M* h# M
advanced bone age, as seen in our patient.
5 P) g2 @! Z4 Z3 y! }The long-term effect of androgen exposure during5 G3 l# q+ T' \2 N
early childhood on pubertal development and final
$ D0 x! U6 `2 Y0 ~adult height are not fully known and always remain% `1 h% D4 T+ O5 s! a, z
a concern. Children treated with short-term testos-
8 @+ R4 M& W* S# @# Rterone injection or topical androgen may exhibit some
8 P/ z; E* ~# r8 U2 i: Y8 \8 @5 jacceleration of the skeletal maturation; however, after
8 F1 ^, h+ M- z4 s* ^3 p9 Vcessation of treatment, the rate of bone maturation2 f: c. L+ C# {6 m
decelerates and gradually returns to normal.8,9) U4 ^* }; X$ v$ x4 n. ?5 m. w* Z
There are conflicting reports and controversy
& X+ |1 U9 \2 m" g* Y6 Gover the effect of early androgen exposure on adult7 w4 K% z, H+ R! ?; e1 }- ^) Y
penile length.10,11 Some reports suggest subnormal6 J, c' [8 |, O
adult penile length, apparently because of downreg-# z3 h$ ~& `. E9 f  e! C' d) H3 J
ulation of androgen receptor number.10,12 However,4 K  h0 l) N) k; a  g& P) G5 u
Sutherland et al13 did not find a correlation between
+ N/ p% ]0 i# o  ?4 ?+ _childhood testosterone exposure and reduced adult
0 P! Y/ Z) g  [; jpenile length in clinical studies.
( h' ]* U4 M4 v& yNonetheless, we do not believe our patient is
; l7 w4 g7 _" l) [8 Kgoing to experience any of the untoward effects from
  M/ c  N% R$ a2 V5 ]testosterone exposure as mentioned earlier because
1 m% _( Q  b1 R8 a, F- Lthe exposure was not for a prolonged period of time.: Z& \( a2 P9 n$ f
Although the bone age was advanced at the time of$ z, K1 B1 [$ x+ S
diagnosis, the child had a normal growth velocity at) v" r& B9 l* L% s4 |0 v1 q* d
the follow-up visit. It is hoped that his final adult) q; M- s8 B, F# T% m
height will not be affected.
% p3 a8 k3 E# E+ f$ p, yAlthough rarely reported, the widespread avail-$ `6 D9 \# J+ V, j
ability of androgen products in our society may( O% v) _1 _+ `, C, a) A& l
indeed cause more virilization in male or female9 m1 c6 |' B/ q, J, }) {
children than one would realize. Exposure to andro-  n2 g3 Z! t) n9 O: O/ _- E2 C
gen products must be considered and specific ques-4 {) }7 w; J$ M- V6 g  L6 W7 A
tioning about the use of a testosterone product or
9 h( J5 j% V! _/ Ngel should be asked of the family members during* {8 p, z( h7 \: V/ f) z
the evaluation of any children who present with vir-' X: U# k( V2 e& b+ Y! `3 K" Y0 L9 |# n
ilization or peripheral precocious puberty. The diag-
9 p/ M, |4 P6 t) N+ dnosis can be established by just a few tests and by6 v6 C/ F3 p, A  l% B0 y8 B# e( h: _
appropriate history. The inability to obtain such a
7 m  r+ s$ w9 D2 s- n! ]5 T' whistory, or failure to ask the specific questions, may
4 p" |1 H0 q3 m9 a  H* i  hresult in extensive, unnecessary, and expensive' a) \& Z; q6 y
investigation. The primary care physician should be
% |! z- R/ K- i2 M4 {' `8 Zaware of this fact, because most of these children
! P' U6 T! F) i4 W$ O2 e$ kmay initially present in their practice. The Physicians’5 M5 X6 j6 K4 m: d7 u6 h
Desk Reference and package insert should also put a
6 P6 k4 g( G# T# c) Vwarning about the virilizing effect on a male or
4 o# d  A, v; y& Qfemale child who might come in contact with some-
: Z3 W% `1 k+ d9 l9 B* Y6 Rone using any of these products.7 M- v% o$ e" f* B8 z. T+ `
References0 s& r0 H" s8 m
1. Styne DM. The testes: disorder of sexual differentiation
/ B) A0 Z: \$ W  c0 |, w) kand puberty in the male. In: Sperling MA, ed. Pediatric
% f( h7 ^: c" R5 nEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;; k! @  z9 V4 q4 m5 {8 p4 n
2002: 565-628.! `- Z, v. S( K# |
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
- F) P& W7 X( G- epuberty 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
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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
, c& t) J. z: w) [0 X" [: z
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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