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Sexual Precocity in a 16-Month-Old
8 y. v' H; z/ K6 m9 [8 WBoy Induced by Indirect Topical
3 I' t$ N- f% [7 ~Exposure to Testosterone
. q1 e& V% M5 V) [2 _% ?Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2% ?# f( J4 p" k& f2 e& N# Z' B1 I
and Kenneth R. Rettig, MD1
- @4 a* Z7 m) y6 Q: V8 U0 yClinical Pediatrics% ~" J: ~- m4 x3 }' r- o
Volume 46 Number 62 f6 s1 n& v) U& r
July 2007 540-543
" Y% M) L, F) i2 ~# i© 2007 Sage Publications
$ |! q4 l; V3 m: ~' P( u  I( d10.1177/00099228062966516 l% `4 u7 W9 P* F7 E& ?# n/ b9 j6 z7 Y
http://clp.sagepub.com
# v, |6 e7 p- ^4 {2 p2 T5 n& }hosted at
" K9 v) u7 [+ U/ R" Phttp://online.sagepub.com6 m- b& {! a1 P) I
Precocious puberty in boys, central or peripheral,
7 `& [" x6 y, @$ d; I1 O; Yis a significant concern for physicians. Central8 r1 s7 U. U; |
precocious puberty (CPP), which is mediated
8 k2 X' t/ n, }6 p  uthrough the hypothalamic pituitary gonadal axis, has
7 |" x: ^* N  J# Ua higher incidence of organic central nervous system
9 c) ]4 F7 Q4 ^% I4 hlesions in boys.1,2 Virilization in boys, as manifested
" r; N7 J% d7 V) @* O3 G8 L) lby enlargement of the penis, development of pubic
+ q8 L  I/ R. Q% [hair, and facial acne without enlargement of testi-* S% {$ z; z' }1 z! Z& h
cles, suggests peripheral or pseudopuberty.1-3 We
: ?/ T7 e. d" }report a 16-month-old boy who presented with the
/ K, E( K' g' q9 wenlargement of the phallus and pubic hair develop-( |+ y  x4 U+ k! c
ment without testicular enlargement, which was due  \$ e  s: z; ^) s
to the unintentional exposure to androgen gel used by
. u! q& h. h  V7 H& Gthe father. The family initially concealed this infor-) S$ H0 ]+ A" S0 \+ u
mation, resulting in an extensive work-up for this
  {9 e6 B) j: _- z) R9 `& Qchild. Given the widespread and easy availability of
# _6 ~" Y  I0 g* ctestosterone gel and cream, we believe this is proba-
  R" ~. ]. P' Vbly more common than the rare case report in the
4 M8 s: Q! a7 J5 f9 d/ s! Cliterature.4" y9 Q6 T' P$ A7 S# k4 w" x
Patient Report
# \  g4 W/ j6 {9 {# Q9 AA 16-month-old white child was referred to the
- [, S1 r: r! l% U. I, Uendocrine clinic by his pediatrician with the concern% |0 e4 z9 c2 t8 e4 b7 n
of early sexual development. His mother noticed
+ x/ E! ]# S5 X* l/ h& _% w9 wlight colored pubic hair development when he was$ T4 N) k4 m  P" w
From the 1Division of Pediatric Endocrinology, 2University of
& C0 s) `& K) g: y. K4 m5 nSouth Alabama Medical Center, Mobile, Alabama.
3 n3 B. U( h5 X8 e/ rAddress correspondence to: Samar K. Bhowmick, MD, FACE,! T, Y) {  Q0 ~* K
Professor of Pediatrics, University of South Alabama, College of
8 Q1 ?6 `0 v4 \1 c. v6 Q6 ]6 f- nMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
; j+ H( b9 A* Q7 |5 ?- {9 J' ?& K3 We-mail: [email protected].
% g; w; [/ I! X+ `8 d& i2 `about 6 to 7 months old, which progressively became
6 i! n1 g+ s8 }4 v* M9 I2 k9 |$ idarker. She was also concerned about the enlarge-- Q0 o  J7 x8 f/ {& C* j
ment of his penis and frequent erections. The child
( Y, q% O$ c( P" Y: Q  w! Z0 zwas the product of a full-term normal delivery, with8 a7 v8 `1 }2 d9 {
a birth weight of 7 lb 14 oz, and birth length of
* U0 A3 q( g. T20 inches. He was breast-fed throughout the first year
* S  f6 \3 }- M, j# Q; y* ?of life and was still receiving breast milk along with% t  _5 @0 P* g" U6 }5 o
solid food. He had no hospitalizations or surgery,
& _2 s- d7 s. ^4 @! P# dand his psychosocial and psychomotor development. a! q( @7 O9 L# F* A5 f* f
was age appropriate.. G3 _/ e0 B1 ?. |8 W
The family history was remarkable for the father,, Z/ i" R$ Z; N0 T" W
who was diagnosed with hypothyroidism at age 16,
+ S0 O2 _3 t: k5 |, o. I; X# Ewhich was treated with thyroxine. The father’s
+ O7 x: S! |9 L/ z* H. Kheight was 6 feet, and he went through a somewhat
, G9 }6 T* t' q: K" D) V; hearly puberty and had stopped growing by age 14.8 \9 N8 m  _! i$ b3 n. S, }; |4 j- ^! v
The father denied taking any other medication. The
2 g9 W4 b* V) H0 U1 q! f+ mchild’s mother was in good health. Her menarche1 [2 h+ }# [2 w6 S# I+ e) Q) A
was at 11 years of age, and her height was at 5 feet* a$ O* K6 {9 b6 f. h
5 inches. There was no other family history of pre-
, Y, R8 K9 r- I5 ccocious sexual development in the first-degree rela-
: N, H/ o7 d# X, @: X1 p' Ktives. There were no siblings.
; t4 U& ~$ R7 e4 t/ T7 OPhysical Examination1 W4 U6 a% }- [; X) p9 B2 V$ R
The physical examination revealed a very active,
8 z. J) J2 O! F( u) ?playful, and healthy boy. The vital signs documented; m7 J" o. y! v- ~3 f3 o* }- j
a blood pressure of 85/50 mm Hg, his length was# G; s- h2 w: D
90 cm (>97th percentile), and his weight was 14.4 kg
" q0 l' i# E0 ^(also >97th percentile). The observed yearly growth
. m2 [" z( Q, _" j, k* W! Qvelocity was 30 cm (12 inches). The examination of
: K, V/ a0 ?9 W3 L8 Mthe neck revealed no thyroid enlargement.2 {3 b* G+ @, ^! [+ |
The genitourinary examination was remarkable for) ^5 p2 C- u7 v6 }9 ?4 S& ?* c
enlargement of the penis, with a stretched length of8 N6 m6 P8 U5 B* B3 m3 O
8 cm and a width of 2 cm. The glans penis was very well0 C3 j0 r8 @* L' r7 j
developed. The pubic hair was Tanner II, mostly around
; c5 Y6 E& v& b* P6 w+ A540* T/ {7 h) [6 F1 Y9 P- f) Y
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 r; H% D. Q: _. }; }* Z
the base of the phallus and was dark and curled. The5 b+ K# h, U0 F3 A1 U
testicular volume was prepubertal at 2 mL each.
# _5 R& M0 i& S. k: E/ p& G8 tThe skin was moist and smooth and somewhat
" E, Z2 x$ O: poily. No axillary hair was noted. There were no
5 X  l2 k/ G0 P- Kabnormal skin pigmentations or café-au-lait spots.
0 K$ [# u/ c) R  X0 [# s$ XNeurologic evaluation showed deep tendon reflex 2+: M% }/ O  K- M5 Z  N% w
bilateral and symmetrical. There was no suggestion
8 t2 J5 j5 Z- l: G" @) Qof papilledema.% E& M0 i# @& j) a( B
Laboratory Evaluation( B$ j- W! o( ]6 n( Y
The bone age was consistent with 28 months by
; o5 n3 h5 @, d, xusing the standard of Greulich and Pyle at a chrono-
3 a5 g% M9 y; glogic age of 16 months (advanced).5 Chromosomal
4 q" R% b2 H& \1 Ckaryotype was 46XY. The thyroid function test* T! k- [  E9 H) E, F2 I
showed a free T4 of 1.69 ng/dL, and thyroid stimu-+ P9 c+ y9 I9 {- q/ N/ R7 t
lating hormone level was 1.3 µIU/mL (both normal).0 `" X! ?  }4 Z. ^* K4 l
The concentrations of serum electrolytes, blood% \, [6 ~: z% g  l) _) h% x, C# x1 _
urea nitrogen, creatinine, and calcium all were
6 n) o/ O1 W, c" Qwithin normal range for his age. The concentration' d. a3 M+ E7 r0 o
of serum 17-hydroxyprogesterone was 16 ng/dL
( E- _! T; P. x$ Z2 N. k(normal, 3 to 90 ng/dL), androstenedione was 20
) `+ ^0 |" k2 e& x. K) cng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-* J, ]* m" y; X$ c" @0 U
terone was 38 ng/dL (normal, 50 to 760 ng/dL),9 M5 E. X- i" @0 w
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
5 }/ {+ V# m  w% b" C  S* f1 `49ng/dL), 11-desoxycortisol (specific compound S)
+ u) v6 P. G  ]9 a) w6 s4 h* |was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-: n( p' u; K4 @6 H$ g( @' a( Y
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
2 J% L* M: |" w) P6 A: ~; _, d6 _testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
( h. H9 A3 B. u8 |1 e  @and β-human chorionic gonadotropin was less than7 J$ z2 S: J& \- {. w% d. A
5 mIU/mL (normal <5 mIU/mL). Serum follicular
0 n) w8 X, o, F% g& X! Bstimulating hormone and leuteinizing hormone. Y  K; u. _/ l; q1 H! Y
concentrations were less than 0.05 mIU/mL
6 P6 e( Q! }* ], s1 n(prepubertal).6 ?& f1 _8 h& l6 U  C: T# L# V$ h
The parents were notified about the laboratory
- k+ F5 D: H0 i2 o- ?" Iresults and were informed that all of the tests were
# l. ^3 a0 X7 s% w7 |0 Pnormal except the testosterone level was high. The
) @& X) n, o" f) J0 u1 G$ W$ Lfollow-up visit was arranged within a few weeks to, a# c  N1 A1 _3 l9 I
obtain testicular and abdominal sonograms; how-* M0 P$ `8 g# u' {
ever, the family did not return for 4 months.1 E% n8 O2 W1 v1 Y/ I$ }1 C/ h
Physical examination at this time revealed that the
. ~' C+ h' [- H7 T% fchild had grown 2.5 cm in 4 months and had gained: ]3 z) x$ a; @5 |: v  k. |
2 kg of weight. Physical examination remained6 u5 N% c) }* f! Y+ q2 Q7 U
unchanged. Surprisingly, the pubic hair almost com-
, c- R2 q( D* q' ^- O, ^pletely disappeared except for a few vellous hairs at
0 S3 p0 R5 i+ K* o) I8 k, \- a! Zthe base of the phallus. Testicular volume was still 2+ D2 H" K. N; A' v6 C
mL, and the size of the penis remained unchanged.
+ M2 O( Z# Q+ v* ]4 _; pThe mother also said that the boy was no longer hav-! u; J1 ^: d5 J+ o# P0 G
ing frequent erections.
) G5 N; K% }# Y& b0 l* _Both parents were again questioned about use of
7 `, v" J1 Z- P& z8 fany ointment/creams that they may have applied to
, R, L6 i; ?# ?, hthe child’s skin. This time the father admitted the- I2 ?, d' j' H2 I" A$ q( v
Topical Testosterone Exposure / Bhowmick et al 541
' n+ l9 O4 v2 {9 y" W+ F0 Kuse of testosterone gel twice daily that he was apply-% G* O$ `) }( d# |) S7 f
ing over his own shoulders, chest, and back area for
# n2 q1 n6 b9 {  x; H6 p8 t1 J% H2 Wa year. The father also revealed he was embarrassed
/ I! l! F4 e; W) t* t6 Mto disclose that he was using a testosterone gel pre-
2 a" O$ H, f. H5 |/ }, h4 ?scribed by his family physician for decreased libido
5 d, x+ u* W6 ~secondary to depression.; x9 W4 a% N4 c: c( B% R
The child slept in the same bed with parents.
: J, E( Y: o/ F$ f. c7 p/ C5 RThe father would hug the baby and hold him on his; g2 L4 ]- x/ m' Y. ~- h
chest for a considerable period of time, causing sig-
. ~6 P6 b+ Q/ b- X5 x2 a' cnificant bare skin contact between baby and father." R, Y" d% I, y) [/ e. D0 t5 J) h
The father also admitted that after the phone call,
1 C( y+ S5 E7 |when he learned the testosterone level in the baby
  a) S1 E4 l8 _5 J6 h2 gwas high, he then read the product information, a- a; @' X6 T+ t% y
packet and concluded that it was most likely the rea-
; {  q7 Q: |; K. b8 z) V  vson for the child’s virilization. At that time, they
* u$ V2 ]& W  v% @decided to put the baby in a separate bed, and the
# R  n4 T& L% g8 vfather was not hugging him with bare skin and had0 O/ p( ]! B2 P  s
been using protective clothing. A repeat testosterone
$ ^, k* ~) F; h7 P/ qtest was ordered, but the family did not go to the
) Q+ d& n2 t" e0 `5 B6 x6 claboratory to obtain the test.
: r1 {. Y# g2 O4 M: w; K- ]5 RDiscussion3 g* y( g1 I$ y! v2 z" g6 Y; h
Precocious puberty in boys is defined as secondary5 X. z3 Q6 D  S- L
sexual development before 9 years of age.1,4
* |, q+ J7 [# v& s0 `% ePrecocious puberty is termed as central (true) when
1 ^3 `" U& F4 s* g! U. `it is caused by the premature activation of hypo-6 `4 F" z- K# {" E; _: v
thalamic pituitary gonadal axis. CPP is more com-) }; ]7 |  W, t8 |2 m
mon in girls than in boys.1,3 Most boys with CPP5 a& u2 q+ S* i: e, N; d. [" G
may have a central nervous system lesion that is/ }/ F5 m  T+ N+ w
responsible for the early activation of the hypothal-% n: Q7 r& X" j# z- m& E
amic pituitary gonadal axis.1-3 Thus, greater empha-9 A% d7 K& B1 M" m* K5 }. j7 S
sis has been given to neuroradiologic imaging in
7 P/ ]! {% p, E# S( B4 fboys with precocious puberty. In addition to viril-* w, E) F2 c4 Q' P, p1 ^
ization, the clinical hallmark of CPP is the symmet-
, Z4 H" Y5 Y; e* wrical testicular growth secondary to stimulation by4 R# K# K9 S  w9 k
gonadotropins.1,3; Y3 ]0 D% o/ Q6 O1 `8 ]
Gonadotropin-independent peripheral preco-1 _  c# y8 u! j1 Q4 T, a
cious puberty in boys also results from inappropriate+ @3 ~; ]* |% |
androgenic stimulation from either endogenous or6 a( X# [; ?" y$ |5 X+ p9 q7 o
exogenous sources, nonpituitary gonadotropin stim-
1 T4 _4 a. I" q4 sulation, and rare activating mutations.3 Virilizing, }' f# ^9 c  y. V, j
congenital adrenal hyperplasia producing excessive& d* g. W8 H, z- m! n0 E% u* M2 u
adrenal androgens is a common cause of precocious, j; ^  k3 Q" c1 t. P
puberty in boys.3,4
% Y) c- I! d/ T( C( T. b3 V0 qThe most common form of congenital adrenal
6 H" m8 Z) c; s& Bhyperplasia is the 21-hydroxylase enzyme deficiency.
! X, M5 d% K8 E& OThe 11-β hydroxylase deficiency may also result in- p8 u8 |8 ^( O2 D( ^7 U: B: O4 S
excessive adrenal androgen production, and rarely,
+ b# Q5 f. v" n. z  s4 s. Man adrenal tumor may also cause adrenal androgen
1 b) ^0 i6 L4 k  Uexcess.1,3
# {, o# _$ f" Z: d3 X/ Y" g# V6 T8 wat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 p7 a3 d$ [# B/ _5 ~" n542 Clinical Pediatrics / Vol. 46, No. 6, July 20072 x1 F+ I- n% D' g) O
A unique entity of male-limited gonadotropin-5 K# Q% T' s. i
independent precocious puberty, which is also known
# V& @2 l6 V! G6 g) s) [3 e( c. |, ]as testotoxicosis, may cause precocious puberty at a; {& B( c* w% v0 c% u
very young age. The physical findings in these boys
* b7 p% L* {) a, Xwith this disorder are full pubertal development,2 o( M  h8 E8 R* a& t
including bilateral testicular growth, similar to boys
  t  n8 I% ?/ Ywith CPP. The gonadotropin levels in this disorder* d. u0 [8 ^5 S( h8 v; Y
are suppressed to prepubertal levels and do not show
' J  ~: {- @7 T8 Zpubertal response of gonadotropin after gonadotropin-
' U& I0 r" P9 o5 W! preleasing hormone stimulation. This is a sex-linked
; P0 N" V6 U1 R0 i! e' Yautosomal dominant disorder that affects only
" i% V( {) m% V/ k1 y5 i3 {- ]4 Rmales; therefore, other male members of the family
7 O2 B7 k4 {! F3 S* j! {9 V6 Mmay have similar precocious puberty.36 M& `1 S2 B& F) ?( W. Z$ D
In our patient, physical examination was incon-8 ]0 u0 D! x4 c3 d, a& V: l
sistent with true precocious puberty since his testi-! p7 A  d/ r& F  U) G/ t
cles were prepubertal in size. However, testotoxicosis3 D: u4 r, q9 w4 s: S
was in the differential diagnosis because his father; _( m8 b3 }  K+ b3 T
started puberty somewhat early, and occasionally,% I( L- f+ k5 D' I1 }' c3 l2 _
testicular enlargement is not that evident in the
" [- n% G2 D9 Y9 Vbeginning of this process.1 In the absence of a neg-
; G7 W2 h9 G4 }! i4 s3 Cative initial history of androgen exposure, our
- r0 R# e. M/ @% W) W. kbiggest concern was virilizing adrenal hyperplasia,
8 k! o* ?( d- k% P# keither 21-hydroxylase deficiency or 11-β hydroxylase
4 C. r6 A8 i+ }0 x& _deficiency. Those diagnoses were excluded by find-9 d( |# K5 ]5 N  }9 Q! q9 ?) k( S& s
ing the normal level of adrenal steroids.9 C- t  w2 x) g6 `: }7 H
The diagnosis of exogenous androgens was strongly. r3 P& G- n% M! N2 O6 _) }
suspected in a follow-up visit after 4 months because
! I4 i' W+ b- H5 q$ Zthe physical examination revealed the complete disap-
( h+ m  u/ e. cpearance of pubic hair, normal growth velocity, and4 m( i# a+ P' c: u
decreased erections. The father admitted using a testos-
( [. k' R2 m& v- h7 x* Cterone gel, which he concealed at first visit. He was9 {& R1 x9 x& n( u: F
using it rather frequently, twice a day. The Physicians’+ b+ w' Y" W& {8 ^& s1 s3 b0 k
Desk Reference, or package insert of this product, gel or5 q4 C1 F2 E  j% n2 }8 R3 ?8 f
cream, cautions about dermal testosterone transfer to
$ I' k6 |6 V1 J! sunprotected females through direct skin exposure." D8 t. Z, w6 n: h$ r
Serum testosterone level was found to be 2 times the% q: m0 e2 s5 e3 g) I
baseline value in those females who were exposed to
1 N5 c0 r& i( ?& o1 [even 15 minutes of direct skin contact with their male8 e& i: w( E1 V
partners.6 However, when a shirt covered the applica-
! I* N3 d1 b2 I- s; I9 K  Dtion site, this testosterone transfer was prevented.
1 n6 l9 T, \/ C- @& _) F7 D; dOur patient’s testosterone level was 60 ng/mL,$ `, |1 o8 J8 j
which was clearly high. Some studies suggest that
# z( _. `8 Y. v  G: `: \& z, hdermal conversion of testosterone to dihydrotestos-
: E. Z+ N2 A2 ?  {4 i( fterone, which is a more potent metabolite, is more
8 z0 U: y0 r% kactive in young children exposed to testosterone- V  G- J' \9 R$ H% L  e
exogenously7; however, we did not measure a dihy-
6 O; w/ U$ X0 V8 v- `1 o8 wdrotestosterone level in our patient. In addition to
- O/ b. F$ [9 ]4 U. S& L- tvirilization, exposure to exogenous testosterone in
8 n# W% @( k/ ]children results in an increase in growth velocity and- A5 W# Z8 a3 F% `% q1 I
advanced bone age, as seen in our patient.
4 b( ~& [8 i" \4 s# S. aThe long-term effect of androgen exposure during" [! f! o* X  f6 t! Z
early childhood on pubertal development and final
; H6 |: \) k6 Nadult height are not fully known and always remain
  ^) H* M+ ^# ha concern. Children treated with short-term testos-3 o: ^- b# {' ]% F/ b( N  `
terone injection or topical androgen may exhibit some* l$ Y6 u$ W( s
acceleration of the skeletal maturation; however, after
2 R" l, N. @7 lcessation of treatment, the rate of bone maturation
5 L; d& c9 e7 _5 Tdecelerates and gradually returns to normal.8,9
9 d9 I# J" D! S3 j1 ]+ c! ]1 F4 [There are conflicting reports and controversy
5 X, h/ Q& S" l! x8 b, {  j2 ~. uover the effect of early androgen exposure on adult
& m( {1 ?6 f3 s. `& B# gpenile length.10,11 Some reports suggest subnormal* q- ]! p! D- O9 ]* y- M, T
adult penile length, apparently because of downreg-8 J$ N7 h+ c4 i! |0 F
ulation of androgen receptor number.10,12 However,
3 E# I$ z. P3 k, s- t/ ?Sutherland et al13 did not find a correlation between; L) Q# s9 z7 n6 h& k- U
childhood testosterone exposure and reduced adult
$ q6 R$ L! h. s" @penile length in clinical studies.4 q# q4 s$ M' L; K/ o
Nonetheless, we do not believe our patient is
& W8 u: B8 q) X3 Y' x" C+ Egoing to experience any of the untoward effects from9 V' Z+ R) N2 S& X1 i! B
testosterone exposure as mentioned earlier because
$ [# c9 Y% N, B; j. n; ?3 Athe exposure was not for a prolonged period of time.1 U9 r, b9 o( B. e1 U( \% s
Although the bone age was advanced at the time of5 ~3 ^- y, L0 d2 I: J
diagnosis, the child had a normal growth velocity at
+ R# u; q* V) x( `2 C% [$ mthe follow-up visit. It is hoped that his final adult: i7 b7 `, r; f6 i. ^4 a  p
height will not be affected.
# R* i9 K4 J6 N( S- tAlthough rarely reported, the widespread avail-
+ s% V8 A) i7 t- b9 }  gability of androgen products in our society may
0 [: ^7 |- s- A+ |1 u: a0 z4 kindeed cause more virilization in male or female
* c1 u6 P7 W' r# X7 P! @children than one would realize. Exposure to andro-
: V7 v# t; `4 M6 ~$ I1 d! ]& rgen products must be considered and specific ques-
0 b4 i  H5 T2 Utioning about the use of a testosterone product or# K" L4 c! N# m/ b5 L' z3 ~
gel should be asked of the family members during
; z0 x  [  Z* _8 p) |the evaluation of any children who present with vir-* E* ~# b( K( Y% O8 v, I* x0 H
ilization or peripheral precocious puberty. The diag-
( H  l& C+ U  hnosis can be established by just a few tests and by) _8 c: u9 B, H( X2 `0 R
appropriate history. The inability to obtain such a; M: L, L' g* _" B' X# _7 c$ A
history, or failure to ask the specific questions, may$ ?% ^+ C' g6 n/ [6 U+ ~/ t
result in extensive, unnecessary, and expensive
0 Z7 X+ _, e# c3 S6 a7 Oinvestigation. The primary care physician should be) y9 T- l+ h- N* Z6 J3 t
aware of this fact, because most of these children
' y$ ?% C0 ~1 }+ e' umay initially present in their practice. The Physicians’
' @8 p! j( v4 t* ^5 r, W6 k! oDesk Reference and package insert should also put a; Q- K. N# q9 r8 U
warning about the virilizing effect on a male or- e2 \0 h! r3 ?/ @' O& s% [+ P
female child who might come in contact with some-6 G1 w2 F  L8 n5 _7 H
one using any of these products.
/ _" _" q0 B* C6 r$ e+ @References" J" Z0 Q7 r% ~( c
1. Styne DM. The testes: disorder of sexual differentiation& p/ K5 Q, t/ Z! @
and puberty in the male. In: Sperling MA, ed. Pediatric
* M2 G1 c+ S! h  |$ wEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
7 @" l2 @# i4 @( E) x# Z* x9 M2 e2002: 565-628.
4 R7 F6 {5 N' J9 ]! L9 @0 Z2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious$ _% y% h. f( V" M' P2 h. W
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
* h5 w$ n/ T( v% M/ @* H( h3 |6 O( dBoy Induced by Indirect Topical
: w8 T# j+ g7 j- m* U! d) YExposure to Testosterone
8 P+ B2 |3 ^& P3 C; q4 @" TSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
2 Y7 g' H9 Z1 J7 U8 M( M9 q  tand Kenneth R. Rettig, MD1
' \" c- D6 b( |9 CClinical Pediatrics
6 \/ o) ]: {" ^* y: V+ ~Volume 46 Number 6, ]9 C+ y/ w# E9 Y
July 2007 540-543' D! f1 P; j5 y7 E
© 2007 Sage Publications  s6 L) @7 p' Y9 G0 ~
10.1177/0009922806296651
: I& i/ |# D1 r# Ihttp://clp.sagepub.com$ U* [0 C4 J8 `  }; k* [3 F, s
hosted at* g8 {: C9 b& P1 Z0 U" m+ T
http://online.sagepub.com
" r9 R' l7 ]; v0 l. m) S8 CPrecocious puberty in boys, central or peripheral,% p- g  a$ Q: e9 v
is a significant concern for physicians. Central. O( d. I- g$ `  ~6 {
precocious puberty (CPP), which is mediated
' w" v+ t$ L+ f4 ]through the hypothalamic pituitary gonadal axis, has6 g+ s) y8 k) M2 \6 b
a higher incidence of organic central nervous system; q% M( y! _6 S0 h# \
lesions in boys.1,2 Virilization in boys, as manifested
1 B8 ]- j0 |9 ^/ r7 lby enlargement of the penis, development of pubic
( S" j) \# g. j& P* }hair, and facial acne without enlargement of testi-4 @5 o1 B, u5 X! J3 f1 o; W
cles, suggests peripheral or pseudopuberty.1-3 We9 N0 l  v, p- V* m: S
report a 16-month-old boy who presented with the
$ L9 P0 Y8 \9 `$ _' Oenlargement of the phallus and pubic hair develop-) r% [: M0 O2 V$ b& c, Y
ment without testicular enlargement, which was due
/ m' j! f. h* [7 h  Yto the unintentional exposure to androgen gel used by2 }; O1 j1 h  F/ [
the father. The family initially concealed this infor-6 D5 N! h3 j1 a! G
mation, resulting in an extensive work-up for this* F9 I/ n0 O* o8 T
child. Given the widespread and easy availability of
3 T9 |* k! N  _# M; ]9 B$ T& utestosterone gel and cream, we believe this is proba-
' O: I$ K9 j! ~8 u: I, Lbly more common than the rare case report in the. f1 R. ~6 v- Y/ p3 N% o) s
literature.4
4 y' K' y4 Z4 Q8 ~Patient Report
7 e+ j/ j( ~7 N$ k0 k! ?  wA 16-month-old white child was referred to the) [* Q* m# d: d8 t
endocrine clinic by his pediatrician with the concern
* Q0 Z, k& n: d/ ^6 ^+ g. L6 ~of early sexual development. His mother noticed
2 ^# S8 T# M$ f5 ]0 g$ O/ o7 rlight colored pubic hair development when he was) O. o% i* }2 y( L8 W  T, a! v6 J% r
From the 1Division of Pediatric Endocrinology, 2University of
- A1 P0 A: R  F  RSouth Alabama Medical Center, Mobile, Alabama.
; M  i* X# l+ eAddress correspondence to: Samar K. Bhowmick, MD, FACE,
# a% i+ z- D( _( v' Y7 f; ^9 TProfessor of Pediatrics, University of South Alabama, College of7 X$ K( g' J. L
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;, p6 Q& O4 `; x5 v5 s7 H7 K
e-mail: [email protected]." r) m8 T& E# f, E: r
about 6 to 7 months old, which progressively became
! k  S' r% R5 ~, ddarker. She was also concerned about the enlarge-
& R5 J; E" k# F' Tment of his penis and frequent erections. The child8 A1 g  S' U  [( u7 q$ N
was the product of a full-term normal delivery, with
, q3 c, ]3 M5 V. L; t" g! La birth weight of 7 lb 14 oz, and birth length of; Y5 I/ B" w9 |. P6 f4 m' p
20 inches. He was breast-fed throughout the first year: e, {" \$ I8 j$ u
of life and was still receiving breast milk along with
5 ]: x0 G9 K# ~+ l: S+ n& F; esolid food. He had no hospitalizations or surgery,8 W/ D4 @0 f8 s8 x
and his psychosocial and psychomotor development
- F3 n1 c0 ~" N$ ^1 f6 w! [; V7 hwas age appropriate.! G. z+ m# a. {& j
The family history was remarkable for the father,* m8 M9 G. e! K' o
who was diagnosed with hypothyroidism at age 16,
( T0 L; ^3 ], t) G3 W$ b: }8 ewhich was treated with thyroxine. The father’s
6 f6 e1 Y4 m6 K3 b- d( G/ sheight was 6 feet, and he went through a somewhat
$ L% j5 d( a6 gearly puberty and had stopped growing by age 14.6 _: c/ [. l/ s0 d6 n# S
The father denied taking any other medication. The3 t$ V  Y8 I# I' O8 G# V) `
child’s mother was in good health. Her menarche
. k( X& C4 z" ~0 I" Zwas at 11 years of age, and her height was at 5 feet
: ~1 ^0 p, Y, I$ }8 n5 inches. There was no other family history of pre-
6 O3 B3 P/ n( i' Z: ^cocious sexual development in the first-degree rela-' i: {( Z) r) I1 p
tives. There were no siblings.
# @& X( O- r! }% jPhysical Examination, }0 K- X4 k  B5 A( d
The physical examination revealed a very active,! d! b; N( ^: v4 S; j
playful, and healthy boy. The vital signs documented, x" l8 N6 R: v9 E
a blood pressure of 85/50 mm Hg, his length was8 U5 m3 ]- S" M
90 cm (>97th percentile), and his weight was 14.4 kg
, Z7 s; M6 p2 k(also >97th percentile). The observed yearly growth
4 F7 ]- d. ]" Zvelocity was 30 cm (12 inches). The examination of, c# T, B/ `2 t' [; q
the neck revealed no thyroid enlargement.
# w% }; E+ W8 k/ O/ B1 HThe genitourinary examination was remarkable for, B; _  C: |; A- s  R7 E7 h
enlargement of the penis, with a stretched length of
7 b: H# m" f) O! G& |9 [8 cm and a width of 2 cm. The glans penis was very well
! X) T6 E! P7 R/ q  Bdeveloped. The pubic hair was Tanner II, mostly around8 [% r3 [9 w$ r2 h8 T
540$ J- n6 Q/ \& I
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
. Q& ^; f2 a) g1 kthe base of the phallus and was dark and curled. The
9 J2 V0 V& {2 G7 [% U" Mtesticular volume was prepubertal at 2 mL each.3 q  Y5 Y, [$ F2 k% F5 M
The skin was moist and smooth and somewhat0 V. M, w6 k! p2 R' z8 M
oily. No axillary hair was noted. There were no
& ~4 k6 y) V" x0 Z- W2 habnormal skin pigmentations or café-au-lait spots.
! r* z7 x7 t6 F/ rNeurologic evaluation showed deep tendon reflex 2+
& t0 B& G9 Q! B& obilateral and symmetrical. There was no suggestion
% j: }4 N! o) [7 I6 ?. ~of papilledema.3 V' D2 ~4 ^, x
Laboratory Evaluation
( g! V" j2 m7 ^& y0 {+ x1 @2 _The bone age was consistent with 28 months by
( r4 r$ |) K& N% w$ c# P5 n1 Cusing the standard of Greulich and Pyle at a chrono-4 l+ J6 Y: Q2 k/ [: ?0 B+ P
logic age of 16 months (advanced).5 Chromosomal
, L( A; T! M2 ?7 _. @+ F5 _6 qkaryotype was 46XY. The thyroid function test
8 V7 I: ~% s+ ?: Dshowed a free T4 of 1.69 ng/dL, and thyroid stimu-) K0 ~& m1 e; w. G8 W. F" p
lating hormone level was 1.3 µIU/mL (both normal).
( K5 K7 i8 T% O# E" c8 `! XThe concentrations of serum electrolytes, blood
1 P' f. S5 |4 d. surea nitrogen, creatinine, and calcium all were' B7 K2 c8 o- S  I0 s
within normal range for his age. The concentration
6 }( ^- P: y* h$ q7 O1 F5 Lof serum 17-hydroxyprogesterone was 16 ng/dL- g! s$ I. P/ r& C4 k
(normal, 3 to 90 ng/dL), androstenedione was 20. [0 h9 m8 l9 L. e
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-7 g# s! }0 u9 u4 t8 _3 v: V8 B
terone was 38 ng/dL (normal, 50 to 760 ng/dL),! h/ q0 ?- V2 l8 ]
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
7 j4 @) c- S& c; k% w' v49ng/dL), 11-desoxycortisol (specific compound S)# p' {- }' y2 n4 ]
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
; ^) `" L0 x: V$ Y! W% R8 Vtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
; S3 E9 P9 ?* d+ W8 ptestosterone was 60 ng/dL (normal <3 to 10 ng/dL),* X2 r) c' \0 A4 m* s
and β-human chorionic gonadotropin was less than
. G- Y$ F/ H! j, f8 k& A1 y5 mIU/mL (normal <5 mIU/mL). Serum follicular
( ~& J0 w( q9 w- `: Ostimulating hormone and leuteinizing hormone( m2 B5 ~3 j* c
concentrations were less than 0.05 mIU/mL
* j; m5 n- R8 a(prepubertal).
% n  S- E% u& l' ^, Q- a) r  `The parents were notified about the laboratory
! g7 P, y4 I* ?0 Q6 gresults and were informed that all of the tests were  r9 B9 _* E6 u
normal except the testosterone level was high. The: [9 _  D$ N- Y2 M& D0 l2 t/ u
follow-up visit was arranged within a few weeks to8 H7 q2 i6 n) O' b1 U  t8 M
obtain testicular and abdominal sonograms; how-
- C2 t7 k. O! D2 tever, the family did not return for 4 months.( ~9 e" Z- y8 h- K; v7 w# Y
Physical examination at this time revealed that the
* P3 @% S1 x0 r- C$ K% Dchild had grown 2.5 cm in 4 months and had gained
% `" b' Q  `& Y  r' H" s9 P  Z* w2 kg of weight. Physical examination remained9 `5 Z8 N6 C* y8 B" o! U# @; ?
unchanged. Surprisingly, the pubic hair almost com-( ?4 B- S- m5 ]6 I
pletely disappeared except for a few vellous hairs at
' Z4 J  w6 \2 H+ Sthe base of the phallus. Testicular volume was still 2
+ G# q3 i# v! g5 ~2 V$ J) XmL, and the size of the penis remained unchanged.
* g+ n4 C1 p/ R3 [+ ~3 @The mother also said that the boy was no longer hav-
% l# H" V. b. P/ K/ v4 sing frequent erections.
* f( ?" x; L. C6 o2 ]' cBoth parents were again questioned about use of
; p* P& L  |) @) r/ g: g" uany ointment/creams that they may have applied to, g  j+ P" i" A+ R8 K+ R0 M6 d
the child’s skin. This time the father admitted the
, }* P* T9 C! a, }/ y% i* V- V, ?Topical Testosterone Exposure / Bhowmick et al 541
4 ~2 p* q8 M+ `- k/ Guse of testosterone gel twice daily that he was apply-
* X' a- d$ z5 m/ d0 Wing over his own shoulders, chest, and back area for
; h& I: ]7 v) K( }% |4 Ua year. The father also revealed he was embarrassed
7 R5 E2 e  c/ _4 |2 K0 D8 qto disclose that he was using a testosterone gel pre-
4 t' p) f8 x; x, ^scribed by his family physician for decreased libido
: K+ D. Y( c# ^' c/ N) g# O1 Osecondary to depression.
. j9 E2 S" Y9 q2 iThe child slept in the same bed with parents.
0 F+ m& W- w$ h: _6 p* q5 w+ pThe father would hug the baby and hold him on his( \" O7 }3 t& i! {6 D8 i: k1 M; J0 d
chest for a considerable period of time, causing sig-/ a% K9 Q' e) G: z" z1 H. i' @7 D8 i
nificant bare skin contact between baby and father.' j: A5 p) u1 P% p0 \
The father also admitted that after the phone call,
  `2 J8 Q8 r# P/ Q, U! n# c1 Pwhen he learned the testosterone level in the baby
4 R" _+ r! E7 ?& mwas high, he then read the product information
$ s/ \! y* V% o( n7 hpacket and concluded that it was most likely the rea-
" K/ a' K8 M  Yson for the child’s virilization. At that time, they# r! R! G, g2 ?6 e" \' Y7 L/ c
decided to put the baby in a separate bed, and the2 e" O1 {2 ^, ~7 C- I% W7 i
father was not hugging him with bare skin and had
- Z% t, j7 f+ \  t& s% f" B; W& }been using protective clothing. A repeat testosterone
7 Q; Z( g7 w# F1 R) atest was ordered, but the family did not go to the* k% [- [. r8 Y9 ^
laboratory to obtain the test.
( g1 T! w- p4 c; n3 X* k) ^Discussion% d) P, W- V3 w% r7 j$ X! ]2 n
Precocious puberty in boys is defined as secondary
8 j& m6 }: H2 _! L" q1 T) {sexual development before 9 years of age.1,4
+ R/ P+ Y' H/ H+ _$ mPrecocious puberty is termed as central (true) when4 A0 L4 |) z6 ?7 ~) {! }; Z$ \
it is caused by the premature activation of hypo-, z9 L( y/ r+ m$ a* O. B, ~- s
thalamic pituitary gonadal axis. CPP is more com-
" g) u: b! {& y: F" T, }# O: ?2 [mon in girls than in boys.1,3 Most boys with CPP6 ~/ B5 d$ y' v) m! Q
may have a central nervous system lesion that is$ W7 H$ C5 ^1 Q9 G
responsible for the early activation of the hypothal-
8 ]8 @. a  k( i. N9 i7 u- o5 a% `amic pituitary gonadal axis.1-3 Thus, greater empha-
2 w1 R( P: o; ?+ s# Ssis has been given to neuroradiologic imaging in2 `3 w* ~3 D7 i1 V
boys with precocious puberty. In addition to viril-. D$ j- D. k& Z0 @( [- K9 B( {
ization, the clinical hallmark of CPP is the symmet-
6 C9 z2 U0 S4 Trical testicular growth secondary to stimulation by0 Z: P6 Y/ ~1 n9 F  T2 q
gonadotropins.1,3! ~! g3 V# t% K, M( f3 n
Gonadotropin-independent peripheral preco-
" j1 T* H5 i* e" E, F3 Tcious puberty in boys also results from inappropriate
- M7 H+ H# K8 Eandrogenic stimulation from either endogenous or
) u0 I8 v- H3 hexogenous sources, nonpituitary gonadotropin stim-# a! j8 @: K8 o
ulation, and rare activating mutations.3 Virilizing6 N& V. D# H* |  p; t9 c; b
congenital adrenal hyperplasia producing excessive
) ~7 M% P- D. [2 J# dadrenal androgens is a common cause of precocious( N0 V- I8 ^3 Q$ ~! e
puberty in boys.3,4
" q0 {' ]; e. \- l1 xThe most common form of congenital adrenal5 ?) Z4 U5 j; w$ Q& h7 W1 J
hyperplasia is the 21-hydroxylase enzyme deficiency.7 ?  q  W) y* B
The 11-β hydroxylase deficiency may also result in. f8 @$ W1 U9 d. U& w
excessive adrenal androgen production, and rarely,
3 r. f& C2 O& a! @: oan adrenal tumor may also cause adrenal androgen% R! n4 q! W: G( p
excess.1,3
/ S5 S/ s5 Z  y5 L- ~at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 i' G5 D/ d* ~. J' M. ~( [542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
( z9 ^% {' O; d% D3 Y2 Z3 y' hA unique entity of male-limited gonadotropin-! V$ r/ M7 _  l/ c, Z
independent precocious puberty, which is also known
+ n) U! t5 @8 J/ j" g) D8 T3 D2 ias testotoxicosis, may cause precocious puberty at a
! b* {  i8 _5 _2 b. a' \very young age. The physical findings in these boys
  E3 \: E% @6 Y+ l& z  }with this disorder are full pubertal development,4 f. w0 T$ X( `$ s& w
including bilateral testicular growth, similar to boys
$ s6 @; `) c, M7 Fwith CPP. The gonadotropin levels in this disorder
3 Q: m' o' y0 N( Dare suppressed to prepubertal levels and do not show
$ ^7 i$ p/ p4 W* Z: U/ gpubertal response of gonadotropin after gonadotropin-6 n( P! z3 f  w  h! ?& S, g0 X
releasing hormone stimulation. This is a sex-linked6 A7 [; I, F/ }& Q
autosomal dominant disorder that affects only
, I8 b, L. |2 C0 Amales; therefore, other male members of the family4 f  y  r" T3 M6 k6 V8 @
may have similar precocious puberty.3* z4 l% U- A2 u
In our patient, physical examination was incon-. N! j) }8 p9 d
sistent with true precocious puberty since his testi-% R9 V  j/ R+ Q# m" @
cles were prepubertal in size. However, testotoxicosis% O; r' ^. _  m1 z& |8 ]- i, y; V
was in the differential diagnosis because his father$ ?! l; G: p( P( V, b, m
started puberty somewhat early, and occasionally,+ g3 m; P2 d. v' \
testicular enlargement is not that evident in the) N7 Y4 N$ a6 P5 g4 _& p# C0 \! `" z
beginning of this process.1 In the absence of a neg-
* s$ J/ w, h) bative initial history of androgen exposure, our1 _2 \9 b' P1 H! `% d
biggest concern was virilizing adrenal hyperplasia,
% }# ~* y- `0 t7 v: g: E0 eeither 21-hydroxylase deficiency or 11-β hydroxylase5 K4 Y* R0 H2 [9 m
deficiency. Those diagnoses were excluded by find-
% p& r  `* I5 Ving the normal level of adrenal steroids.
* g/ a# C$ l: w7 K& Q+ CThe diagnosis of exogenous androgens was strongly0 w, e6 Z6 C8 b: W, ~5 [
suspected in a follow-up visit after 4 months because
$ M, P7 B! `) p  P3 C$ S! G; i: w0 h4 Vthe physical examination revealed the complete disap-7 \" ^2 M5 D6 I8 H  }$ v
pearance of pubic hair, normal growth velocity, and
5 f+ J  m" o% Y+ y- Y6 ndecreased erections. The father admitted using a testos-
, N. N; N$ ?8 {& q' _0 lterone gel, which he concealed at first visit. He was( W6 l2 N6 [  o0 p- D0 q0 ~. W
using it rather frequently, twice a day. The Physicians’6 d" f, B7 a8 e0 P. d/ f; M; O
Desk Reference, or package insert of this product, gel or  Z5 f7 C# K: l1 _2 l/ O8 E+ }8 N
cream, cautions about dermal testosterone transfer to. g+ l, d6 }" e
unprotected females through direct skin exposure.+ H! w. ]* A, s* m9 J2 d" L
Serum testosterone level was found to be 2 times the
! ^& D5 r, ?2 O' C1 B5 l$ U7 Xbaseline value in those females who were exposed to
) H2 @  L: o6 ^% Ceven 15 minutes of direct skin contact with their male' r, P  h* x* j: P
partners.6 However, when a shirt covered the applica-. L$ S% J& c$ w! ?! l5 k2 O
tion site, this testosterone transfer was prevented.) n; U5 O* n& a+ t5 n2 A3 h& z7 {
Our patient’s testosterone level was 60 ng/mL,
/ z1 z' I/ D2 k$ Q. N4 h( Lwhich was clearly high. Some studies suggest that2 @" Z9 O* z0 X+ `! n, n
dermal conversion of testosterone to dihydrotestos-6 L( o' o! X, [) _1 Q, S' r
terone, which is a more potent metabolite, is more
* v4 G# a+ g  nactive in young children exposed to testosterone
/ }8 _* w! M7 ~3 f# ]5 t; zexogenously7; however, we did not measure a dihy-
& d+ D9 Q4 L2 U% B( e4 g' k4 \drotestosterone level in our patient. In addition to
! d! }+ B9 g/ Tvirilization, exposure to exogenous testosterone in. ?7 h# k1 ~* ^; C7 S0 w) }# v
children results in an increase in growth velocity and. i8 s& z  Y# D- C/ `: R/ t
advanced bone age, as seen in our patient.3 H5 k: y  m  B& i
The long-term effect of androgen exposure during
8 P0 b2 k9 B8 p$ k; Aearly childhood on pubertal development and final
: k7 U/ ~, w/ v( t1 ~adult height are not fully known and always remain
  o6 L/ ]& ~) B) fa concern. Children treated with short-term testos-9 t/ M6 i  r' u: h  H% b
terone injection or topical androgen may exhibit some
, l: r" \  s* H- E# A4 b% cacceleration of the skeletal maturation; however, after$ y6 J% _% M0 M4 e9 L( q: v3 h/ R
cessation of treatment, the rate of bone maturation* ]' }9 j3 x6 Z9 f" u8 s
decelerates and gradually returns to normal.8,9
7 M; k" {6 U. Y3 E; QThere are conflicting reports and controversy  ^/ Y' _& V0 T7 o8 X( s
over the effect of early androgen exposure on adult
  Q# N8 B' d+ Xpenile length.10,11 Some reports suggest subnormal" I2 [3 F4 R  A5 x2 ^+ @
adult penile length, apparently because of downreg-
) @' b5 s1 y3 m5 S0 |; tulation of androgen receptor number.10,12 However,
! q! N2 D- t! ~+ Q/ bSutherland et al13 did not find a correlation between
/ L+ }3 M6 v, Z, @% ychildhood testosterone exposure and reduced adult
6 ~5 f  {& {. \# Qpenile length in clinical studies.
2 ?/ f! m! |& P1 P1 G8 @" O, z1 E( iNonetheless, we do not believe our patient is
3 P3 D- y- ^" P* t' x5 m8 S3 Rgoing to experience any of the untoward effects from
) {$ E; \5 G! x2 Q/ w% M8 S7 Z+ ltestosterone exposure as mentioned earlier because, D' [# t( ~7 ^
the exposure was not for a prolonged period of time.# s  t5 Q8 f$ ^+ H
Although the bone age was advanced at the time of/ N* g- O) b* a/ i& [: W
diagnosis, the child had a normal growth velocity at# V, K. i0 `8 t* \% r, _* O  S/ C( v
the follow-up visit. It is hoped that his final adult" |; ~, v1 D2 @( _
height will not be affected.- O% w& u2 j0 S4 J! ~. `1 }7 C
Although rarely reported, the widespread avail-
' h. p- \, f5 n- L3 e2 aability of androgen products in our society may3 v1 K' z5 q9 l, N' J
indeed cause more virilization in male or female
% h( M( T' b' X! P" K8 gchildren than one would realize. Exposure to andro-/ S7 D; Q; W- F8 V
gen products must be considered and specific ques-$ q7 a! ^4 Z/ T- M
tioning about the use of a testosterone product or
+ i, ?9 \: K' _. W% b- w8 m" l7 wgel should be asked of the family members during
) {9 h5 `  H9 [6 B  M, Qthe evaluation of any children who present with vir-
; w& w5 u3 ?; W: B9 filization or peripheral precocious puberty. The diag-
- n. y6 G7 {# |9 _, g! Cnosis can be established by just a few tests and by
) _; `0 a) L8 X$ s* ~appropriate history. The inability to obtain such a# v" x) c2 {. D0 h. k, a
history, or failure to ask the specific questions, may
+ b( \4 |% j$ K; hresult in extensive, unnecessary, and expensive
4 D% Z! ]  C5 s( S$ L$ jinvestigation. The primary care physician should be  o% ?% T; e- R4 _0 ?' K3 N
aware of this fact, because most of these children+ q6 l7 d! P$ ]
may initially present in their practice. The Physicians’' @7 B' b9 B9 J3 [5 C( v& ]: K
Desk Reference and package insert should also put a# I/ n2 H$ L1 S. }
warning about the virilizing effect on a male or
9 |# V# t9 L* Rfemale child who might come in contact with some-4 N2 u8 r+ |, T* \" z, h
one using any of these products.
6 P, `. a- c6 L( R! s" M8 _2 |; WReferences' s# B' ~1 d2 ^# b# D8 ]: I3 Y
1. Styne DM. The testes: disorder of sexual differentiation
1 U- ~/ G* L' E1 _: T' Qand puberty in the male. In: Sperling MA, ed. Pediatric8 X. i) f* s/ r+ x3 L
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;+ p/ f0 Q$ `, Y
2002: 565-628.: J. g4 S, s3 t  T9 u& t% O
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
( G5 F! e; Z; W4 ~* Wpuberty in children with tumours of the suprasellar pineal
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這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

: D5 Q$ b+ }- O+ H9 W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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