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Sexual Precocity in a 16-Month-Old8 m0 Z2 m* k; o0 m0 j- \4 z  f
Boy Induced by Indirect Topical  M1 D  e, m! H& k' _
Exposure to Testosterone  v* r8 y- s9 H& K3 v
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2: k( K& ~" L) R! v+ y6 I8 i( t$ z# U
and Kenneth R. Rettig, MD1) ?+ P& G6 r0 F4 Y- E& ?
Clinical Pediatrics
+ b0 R) c) u: z' b* m+ gVolume 46 Number 6
% w4 v0 s# `/ W* E" oJuly 2007 540-543! W' |/ V8 v  y) p' N7 z
© 2007 Sage Publications
$ F* k9 Z- B1 Z4 N5 `& j& z3 V10.1177/00099228062966512 u. ^2 |  k! d( d
http://clp.sagepub.com2 x( q0 c. a3 O; V. |
hosted at0 j& a4 e( T9 d% H. F) I" v
http://online.sagepub.com0 [: f' ~4 E# H9 u5 I* i& ]1 @$ ?6 J0 C
Precocious puberty in boys, central or peripheral,) u5 f9 K% E, |% p- e9 g% ~2 {
is a significant concern for physicians. Central1 n, O2 b8 g# ]5 i6 U) H! p- w
precocious puberty (CPP), which is mediated" R9 e: r; l0 J# `9 }" h/ E, s% N
through the hypothalamic pituitary gonadal axis, has- Q+ K5 R# U0 P  z
a higher incidence of organic central nervous system3 f4 w2 I2 @; [' @
lesions in boys.1,2 Virilization in boys, as manifested
  D  _  G' B) |0 ?by enlargement of the penis, development of pubic
( e" h7 z: j: D+ rhair, and facial acne without enlargement of testi-% d: C& }8 R7 U5 Y! w
cles, suggests peripheral or pseudopuberty.1-3 We
5 l0 T4 N% Q& I, k* Ureport a 16-month-old boy who presented with the& f2 B. c2 X1 }; P8 s* m5 {0 C
enlargement of the phallus and pubic hair develop-
- R& U1 P0 a9 T( U8 s4 }ment without testicular enlargement, which was due
7 s! T% L3 o9 ^& R2 m+ oto the unintentional exposure to androgen gel used by
/ M3 i; x6 ]- D" E- y3 Ithe father. The family initially concealed this infor-9 D, p: b1 ~. B+ s1 K, v
mation, resulting in an extensive work-up for this
' ]  ?; d% P) K, Rchild. Given the widespread and easy availability of" \. d3 L: P* ~% _9 F! @9 M
testosterone gel and cream, we believe this is proba-& p' \* K$ O- _
bly more common than the rare case report in the, l3 |' J3 b% W7 A: C/ U
literature.4
* i5 T& M5 k, YPatient Report
+ }( Z7 s7 h9 k: S3 oA 16-month-old white child was referred to the
  A9 @9 g4 [$ rendocrine clinic by his pediatrician with the concern: U, p, W; R; K: s* M9 y) {* m
of early sexual development. His mother noticed
$ Q9 N; j- I& }5 A' z1 R& ~* Dlight colored pubic hair development when he was' K" t( P" F7 h3 i
From the 1Division of Pediatric Endocrinology, 2University of
' ^; p% u% x& K6 {South Alabama Medical Center, Mobile, Alabama., q' Q3 n6 Z' }0 c: W6 j3 m- h
Address correspondence to: Samar K. Bhowmick, MD, FACE,: m! R( e1 Y5 k
Professor of Pediatrics, University of South Alabama, College of
3 A6 Y2 B5 ?* C' W" M+ ^" J' J4 i, ^Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
1 R/ R$ z! ^, P' Me-mail: [email protected].
  Z2 D( I8 ~3 ^) t% }2 k9 o6 ^about 6 to 7 months old, which progressively became
' R# q' X6 |8 J6 l; ^darker. She was also concerned about the enlarge-* H  c* L- k3 ?4 W
ment of his penis and frequent erections. The child' a! Z0 r. t8 [1 H' B8 |
was the product of a full-term normal delivery, with
/ A1 _& u9 A. O" W  S1 Q8 S5 ta birth weight of 7 lb 14 oz, and birth length of
  I/ V' O$ |; N$ N! W# x# r20 inches. He was breast-fed throughout the first year5 g- T6 z8 u4 i5 d7 V- Q8 ]/ I- I7 ~
of life and was still receiving breast milk along with2 ^( G8 _( W! a! |+ f
solid food. He had no hospitalizations or surgery,
& \  B% T8 D4 F2 ~7 v: N- f( X- yand his psychosocial and psychomotor development' b) {9 r' ^+ i$ R9 D; `8 p
was age appropriate.. d/ U( q! `! w4 p7 v
The family history was remarkable for the father,
/ y; x5 T1 x& U7 E( M% nwho was diagnosed with hypothyroidism at age 16,+ {9 |! s! H) \) W5 o5 g. F- y
which was treated with thyroxine. The father’s% ?. v, o. x4 g' y" w6 k
height was 6 feet, and he went through a somewhat
+ f' S+ N( M+ ?- n+ i" Bearly puberty and had stopped growing by age 14.  B, v$ e; P" X3 N  L
The father denied taking any other medication. The
/ X2 s$ H* Y' P" S, |( Q2 Ychild’s mother was in good health. Her menarche
7 s8 N  t! C, K! Xwas at 11 years of age, and her height was at 5 feet
4 A8 ^6 x9 Q! v: X/ I- i* W5 inches. There was no other family history of pre-
: o3 H2 S7 w, b/ E3 ?cocious sexual development in the first-degree rela-+ c/ @) t$ z# b7 h% b
tives. There were no siblings.; }3 x! \) \" P" h! t
Physical Examination5 G; u! V; a/ L# k/ _" ~
The physical examination revealed a very active,9 p8 [( U" C  h9 ~2 t5 X
playful, and healthy boy. The vital signs documented
0 ]& X' j& E' h" x9 E1 l! Ha blood pressure of 85/50 mm Hg, his length was5 f" C9 Q% D9 [! R( g4 i% s
90 cm (>97th percentile), and his weight was 14.4 kg
2 q9 K2 x+ h, v$ p(also >97th percentile). The observed yearly growth
% {' |6 t1 u9 K+ X5 N( L3 V% \velocity was 30 cm (12 inches). The examination of1 q$ h/ ~0 X: z' q
the neck revealed no thyroid enlargement.  k) q% W3 J& e4 A0 Z( Z
The genitourinary examination was remarkable for
  x  W3 H8 L6 g; henlargement of the penis, with a stretched length of
( L( h5 K  k" N; @+ W/ }* B8 j8 cm and a width of 2 cm. The glans penis was very well
' C2 x8 x; ]) z" s/ ldeveloped. The pubic hair was Tanner II, mostly around3 w! t6 s* |: L5 G4 \
540
9 n. i" `* [: A" o! Bat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 r( {* Z5 O, i/ tthe base of the phallus and was dark and curled. The8 U$ Y: X* U5 G6 I; d. s; ~* p
testicular volume was prepubertal at 2 mL each.
% o2 ]7 R, I7 aThe skin was moist and smooth and somewhat
( S4 G8 W% ~$ g8 {# Moily. No axillary hair was noted. There were no
* P7 M; r( {& b2 Q5 g3 Q6 S4 n* Eabnormal skin pigmentations or café-au-lait spots.
, `$ I7 [' f. G+ I5 b6 HNeurologic evaluation showed deep tendon reflex 2+3 g. Q; v; Z4 B# l' E! E' U
bilateral and symmetrical. There was no suggestion% v" p: f5 q( Q2 U
of papilledema.
1 g# R& n1 d" M' A$ I; dLaboratory Evaluation0 k, n. l/ u& f# U: o
The bone age was consistent with 28 months by
; z* S. p; u8 _" c, cusing the standard of Greulich and Pyle at a chrono-
; M. E+ I7 j5 W8 x3 tlogic age of 16 months (advanced).5 Chromosomal7 L* ]: t7 r* k* G
karyotype was 46XY. The thyroid function test" H( v% l/ R' _  D/ k, F3 B
showed a free T4 of 1.69 ng/dL, and thyroid stimu-. A* X# z! j0 f6 n
lating hormone level was 1.3 µIU/mL (both normal).
3 x" U) W- I. H. W6 Q9 ^The concentrations of serum electrolytes, blood
7 F6 G5 N3 Y  u3 ^urea nitrogen, creatinine, and calcium all were
% y  Y6 o* G) I- Pwithin normal range for his age. The concentration; m: R* f5 V1 i# B6 Z$ [
of serum 17-hydroxyprogesterone was 16 ng/dL# r+ {  f0 x% c+ A- ]
(normal, 3 to 90 ng/dL), androstenedione was 20
# n2 r' g/ R8 c6 L3 q6 Kng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
5 j' E3 V! ^3 K" n, k3 p5 M# \  Oterone was 38 ng/dL (normal, 50 to 760 ng/dL),$ ?1 D: k9 D( ^6 S: S5 \
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
* s4 ~' e+ L6 e49ng/dL), 11-desoxycortisol (specific compound S)* Q1 b" O# B& k) U% I1 s
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
, J1 b; d# q, y5 F* dtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total* s' C2 p) p4 `
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
5 M, s, G7 t( N0 u; d/ W' ?+ P6 Uand β-human chorionic gonadotropin was less than- s$ |- r: _. n! S8 o) {/ X
5 mIU/mL (normal <5 mIU/mL). Serum follicular
% N7 O% ~5 {' V: `; qstimulating hormone and leuteinizing hormone
( b" Q# B" W( e! c: nconcentrations were less than 0.05 mIU/mL
" X! ?$ r6 i( f4 |( \1 j(prepubertal).
$ u( U: s8 R0 |& C. c7 o! o. `The parents were notified about the laboratory% {, k7 M; N5 d! u+ Q+ G. C8 |
results and were informed that all of the tests were
3 K  p- s) A2 x' K) k" Anormal except the testosterone level was high. The' J  i5 @# C" B% {) N% E  q
follow-up visit was arranged within a few weeks to* ]$ L8 a7 G: M$ m" I; z
obtain testicular and abdominal sonograms; how-
3 d8 d+ I9 t, t+ Q: Gever, the family did not return for 4 months.
3 p" \8 Q/ e5 Z# g" oPhysical examination at this time revealed that the# E7 o( u1 n5 x5 k
child had grown 2.5 cm in 4 months and had gained% O7 V# \; d# a. b5 T1 r9 C; Z9 [
2 kg of weight. Physical examination remained9 O% v- G  V% Z
unchanged. Surprisingly, the pubic hair almost com-3 P! P! A) S& Q. W! u+ l% |
pletely disappeared except for a few vellous hairs at
5 z9 M( T8 A4 t2 h8 d4 ythe base of the phallus. Testicular volume was still 2
) Z0 s9 x9 |8 ?8 QmL, and the size of the penis remained unchanged.* u# R$ P( i7 ?  M6 u1 d! w
The mother also said that the boy was no longer hav-" p/ L) n4 a+ R4 r' K
ing frequent erections.+ ~  N+ h  n/ x8 K+ ]+ s
Both parents were again questioned about use of3 z* q8 J3 P+ [+ c% Z$ @
any ointment/creams that they may have applied to
; O5 U; D4 y9 F% e! M9 E/ `. Gthe child’s skin. This time the father admitted the* S5 k2 V+ t2 {4 f
Topical Testosterone Exposure / Bhowmick et al 541
1 J2 H# N3 J, A: f2 Yuse of testosterone gel twice daily that he was apply-+ z& z0 `; t2 A! M
ing over his own shoulders, chest, and back area for; t9 {( z% K& d8 k& X- R
a year. The father also revealed he was embarrassed% ~( P; D% }: i4 L
to disclose that he was using a testosterone gel pre-7 j- x! o& x" f9 s; z( ?
scribed by his family physician for decreased libido6 p4 j& n) m) W) [) P/ j" q
secondary to depression.1 E/ }' J: \. k* n; \0 o, `
The child slept in the same bed with parents., U5 S3 S* |# D; r6 H! V' T( C
The father would hug the baby and hold him on his% R9 {( N7 k" Y+ G. V* e
chest for a considerable period of time, causing sig-0 \; v' q9 [6 }+ a
nificant bare skin contact between baby and father.; n! b- k5 V" E0 [% Z. B
The father also admitted that after the phone call,4 |. ]' i+ C2 s$ C( I/ @
when he learned the testosterone level in the baby
3 A5 O5 ^9 d! _% M: k3 qwas high, he then read the product information2 M2 N* n: a+ I* S4 H* M4 F
packet and concluded that it was most likely the rea-4 X' P" L5 M. ?) b/ r
son for the child’s virilization. At that time, they: k) x$ q9 J* o, |- P+ U( P2 U
decided to put the baby in a separate bed, and the* r0 A$ p$ Y1 v. z
father was not hugging him with bare skin and had7 Z, N( L! @. Q) s
been using protective clothing. A repeat testosterone
4 t. P# ]* J5 u1 t8 Ktest was ordered, but the family did not go to the7 p" l* B* ~6 T; I+ q: C
laboratory to obtain the test.
2 n! _8 I# Q& A# w3 `Discussion' P/ G0 P, S, j
Precocious puberty in boys is defined as secondary2 G* _% B) z4 j' a+ E0 K
sexual development before 9 years of age.1,4) B7 D1 r# y- T1 d' C
Precocious puberty is termed as central (true) when: H; y+ o* R0 c* _% }- r" v
it is caused by the premature activation of hypo-9 s- I4 P2 d% A9 g8 S
thalamic pituitary gonadal axis. CPP is more com-
% ]% H9 Z' `6 r- D  Ymon in girls than in boys.1,3 Most boys with CPP, x. g6 i$ K5 }9 m4 n7 d1 y7 Y* [) j
may have a central nervous system lesion that is$ N4 d7 }9 {% d  X. l: g
responsible for the early activation of the hypothal-
8 Y3 C% ~# v: a6 ^% j8 @/ r4 j) Eamic pituitary gonadal axis.1-3 Thus, greater empha-
% K- T9 `1 J9 }sis has been given to neuroradiologic imaging in7 I! J; g7 r2 Y% }, a" c. `% b& ~7 c
boys with precocious puberty. In addition to viril-
9 E+ J7 K) Q5 gization, the clinical hallmark of CPP is the symmet-
4 W, m- Y6 z9 Mrical testicular growth secondary to stimulation by1 C2 J0 L$ x0 A$ a4 Q8 e9 {/ D
gonadotropins.1,3
4 m' m# K9 ~" ?) v* w; p- mGonadotropin-independent peripheral preco-
0 X# x  ]& h1 C: Fcious puberty in boys also results from inappropriate9 X0 D4 d' v3 B7 C0 o7 V
androgenic stimulation from either endogenous or
9 v* D& C" @) J" s* }exogenous sources, nonpituitary gonadotropin stim-
: s- L% B/ U8 \/ f/ M  V$ Pulation, and rare activating mutations.3 Virilizing8 K, X, R$ `8 R6 {
congenital adrenal hyperplasia producing excessive/ ~. h4 f" C# c8 F4 j' A; e4 m
adrenal androgens is a common cause of precocious7 A* [" D1 ~; ]  ~3 m. O7 F6 {
puberty in boys.3,4& |4 D+ K2 r4 c1 I3 n  |! B
The most common form of congenital adrenal: y- T( R: }9 S# K8 S
hyperplasia is the 21-hydroxylase enzyme deficiency.
5 v! G/ T4 _2 j* UThe 11-β hydroxylase deficiency may also result in$ x: C2 F$ l( }: E
excessive adrenal androgen production, and rarely,
# O! n9 g$ E- h, Uan adrenal tumor may also cause adrenal androgen
) \; G+ o8 c( l" x, R9 sexcess.1,33 b7 S5 s$ q3 M" g1 R1 c! z7 w' g
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ d6 K5 e( N: h1 G2 E) l3 a6 }* N
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
6 j9 W8 ^9 x' f# _" l& E  ]- eA unique entity of male-limited gonadotropin-
: |! W) D0 w" y# Nindependent precocious puberty, which is also known
6 c5 k- ]  d# eas testotoxicosis, may cause precocious puberty at a
# g3 ]& E. O3 `/ J8 V5 Uvery young age. The physical findings in these boys
  R: l' q1 Y* Z, z/ xwith this disorder are full pubertal development,
4 A% N' [) Z( j: q  h; \8 E. `including bilateral testicular growth, similar to boys' @0 {: \# y  {' [6 S
with CPP. The gonadotropin levels in this disorder
/ C. R4 T% R" [$ |" ^+ `+ Pare suppressed to prepubertal levels and do not show
3 L) ]9 t) [8 Z0 h: i- @4 q1 Vpubertal response of gonadotropin after gonadotropin-" g! N$ g4 _: P0 m  P/ m# ~, s
releasing hormone stimulation. This is a sex-linked
& B) ^2 j. D5 {; hautosomal dominant disorder that affects only$ M6 B8 h0 n* U- n  @
males; therefore, other male members of the family
$ z) \. s0 I: Q  Q# y' {: omay have similar precocious puberty.3
8 j. f3 ^- U3 r# q- U" k. o1 Z8 l9 YIn our patient, physical examination was incon-
! W/ |3 I8 t! Z# k" Csistent with true precocious puberty since his testi-: Y+ h$ P) s' |2 W+ h6 v
cles were prepubertal in size. However, testotoxicosis
/ }9 ~2 {9 v8 Z. _( c6 }5 e5 }7 Rwas in the differential diagnosis because his father
4 n2 s4 n5 T% P# }; `started puberty somewhat early, and occasionally,
  V  O1 i$ M) f5 Btesticular enlargement is not that evident in the5 o8 p1 Z; T& X2 c# l! Y
beginning of this process.1 In the absence of a neg-
; @! {8 d$ x2 g' X! b! Jative initial history of androgen exposure, our
7 O  b" i% c/ t! R4 ?3 ^biggest concern was virilizing adrenal hyperplasia,. @$ O, G. w  Q' n* Z0 F& {" C$ |0 B
either 21-hydroxylase deficiency or 11-β hydroxylase
9 `6 n, C7 i# e/ ~0 T* H1 Udeficiency. Those diagnoses were excluded by find-
/ {3 i( Y& M8 Uing the normal level of adrenal steroids.
0 S: c/ }# O7 O# C# k, {; H# cThe diagnosis of exogenous androgens was strongly8 _+ O0 o; k8 d+ ?6 ]
suspected in a follow-up visit after 4 months because  o4 s* B' ?/ b# B* B; A
the physical examination revealed the complete disap-# T) {6 R' p7 s1 s" M# O, T. T
pearance of pubic hair, normal growth velocity, and' m2 F! {. ~" p9 X
decreased erections. The father admitted using a testos-
7 A0 l% r$ ?+ D* R6 K% X. pterone gel, which he concealed at first visit. He was
+ f+ [& a7 E- b$ O  cusing it rather frequently, twice a day. The Physicians’
/ z  \5 Y: V: r: kDesk Reference, or package insert of this product, gel or
! J1 B9 R4 n; s$ t  |2 Dcream, cautions about dermal testosterone transfer to
! K& j' d# v: G+ gunprotected females through direct skin exposure.
6 u3 O* }/ r! XSerum testosterone level was found to be 2 times the
. j  M9 |0 e' v( K8 |: Ebaseline value in those females who were exposed to
& h! ~" ~  r/ Teven 15 minutes of direct skin contact with their male
, l3 v8 a2 m. c9 zpartners.6 However, when a shirt covered the applica-
' z' ^' l! |  x- ?0 N2 n. ^; b" }; ^tion site, this testosterone transfer was prevented.
% p9 Y) f* g3 w/ v" u' XOur patient’s testosterone level was 60 ng/mL,
2 n4 d& M: f0 p5 t9 f  H% swhich was clearly high. Some studies suggest that
1 }' {8 ]% d" `7 wdermal conversion of testosterone to dihydrotestos-: F9 x8 V1 p8 _( O# I
terone, which is a more potent metabolite, is more
( b: k1 d: ?  P( X* g8 dactive in young children exposed to testosterone" r! P+ T4 h$ Y8 P% J; s, U
exogenously7; however, we did not measure a dihy-
4 r+ k2 P3 ^% b" V0 S; ?drotestosterone level in our patient. In addition to
& F3 C: S8 |: _! t" j% X2 p' _virilization, exposure to exogenous testosterone in3 @  w2 l; l3 B- ?
children results in an increase in growth velocity and
& S# g4 {! K. @8 h4 _2 S6 kadvanced bone age, as seen in our patient.' p0 G" _3 L, n: b
The long-term effect of androgen exposure during
3 o( `3 q! R( ?( b; h3 |4 Qearly childhood on pubertal development and final! m8 i) ], _% }& E
adult height are not fully known and always remain* V9 x# Y: y0 x$ Z
a concern. Children treated with short-term testos-$ j" ]1 N) r* |) o! @/ J6 ?2 C
terone injection or topical androgen may exhibit some: @( [# d7 B8 I
acceleration of the skeletal maturation; however, after5 t1 s8 b/ M: d3 u' h0 N
cessation of treatment, the rate of bone maturation
7 Z- u" [8 Y! K, |- J1 S' ?decelerates and gradually returns to normal.8,9
5 m) ]( C5 i3 }9 a3 T; rThere are conflicting reports and controversy7 K6 f- s9 O8 T$ _/ V- G
over the effect of early androgen exposure on adult
/ X, X9 Z; s& Kpenile length.10,11 Some reports suggest subnormal
6 w* F4 v3 I8 ]! ?" radult penile length, apparently because of downreg-: m5 C1 }- h2 V7 h0 D2 m; H7 A
ulation of androgen receptor number.10,12 However,
& q- y% q1 D# f( r( D/ Y8 N- ?Sutherland et al13 did not find a correlation between9 U2 [" l8 F: ~3 f; }
childhood testosterone exposure and reduced adult
7 u* y$ l* m' R! f4 g9 Vpenile length in clinical studies.
5 n6 m( O9 ?0 e  z# q- h6 HNonetheless, we do not believe our patient is& q7 j8 J8 f1 J7 Q8 a6 e8 x
going to experience any of the untoward effects from+ h* ~+ A$ t8 Z! T
testosterone exposure as mentioned earlier because
5 m, p% `: i; u+ M; [: ~the exposure was not for a prolonged period of time.- {+ h: f/ l7 [2 K8 \( W7 G. ?3 Q! i
Although the bone age was advanced at the time of
& ]( [9 ^5 u5 A- B; \5 n% Mdiagnosis, the child had a normal growth velocity at
3 z  O, s% [+ g1 Q* P! }* _the follow-up visit. It is hoped that his final adult
2 a/ r4 E  T  H( ?& ^/ s8 r$ A( Rheight will not be affected.% o% B* l: V$ j& x4 {
Although rarely reported, the widespread avail-" \9 e: p& [) h& `, j' {
ability of androgen products in our society may1 U& n6 S7 w* D2 E0 ?; j
indeed cause more virilization in male or female2 S6 |( `1 N4 r3 @7 P
children than one would realize. Exposure to andro-
- y2 M6 M7 O5 ^' \gen products must be considered and specific ques-  G7 P, @: k+ X- {" k& n
tioning about the use of a testosterone product or
$ n# U" \: G' }0 X; Pgel should be asked of the family members during
% x/ @$ ~7 b6 e8 K) Z. L" c! Ithe evaluation of any children who present with vir-
  ]) O. M/ E" y6 `: Bilization or peripheral precocious puberty. The diag-
) ^* r$ a0 D" w/ m& o2 y/ T. Anosis can be established by just a few tests and by  f  D& t6 i( s7 |' T  N
appropriate history. The inability to obtain such a
' ]+ q* W) G+ R5 ^history, or failure to ask the specific questions, may0 @* m5 y# V( X5 b( h
result in extensive, unnecessary, and expensive5 r8 z/ v% p  |% C+ S) \; m
investigation. The primary care physician should be
( {# F. s/ e5 O. j; b" T) b* f9 @3 }) Iaware of this fact, because most of these children
2 `# K9 w4 u! u# _& P" G$ mmay initially present in their practice. The Physicians’
- d; A* D9 x5 S% N6 a6 r* TDesk Reference and package insert should also put a5 W5 e: r* b* S7 `
warning about the virilizing effect on a male or8 g3 i& s8 P. G4 B+ v7 z6 s
female child who might come in contact with some-
% q% m4 \$ W/ qone using any of these products.
8 D) R) D( J" \+ x/ nReferences! c2 m4 q; ~9 }+ _) ]3 d
1. Styne DM. The testes: disorder of sexual differentiation' S; w/ d% X! C
and puberty in the male. In: Sperling MA, ed. Pediatric
) p* P. P4 r$ t  Y7 t" IEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
  F+ v' O# }0 Y& Z2002: 565-628.% g0 B8 Q  {! ]- I# ~! |" D
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
0 z5 [4 J# Y6 Jpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
( F$ Y* Q0 Y" z; IBoy Induced by Indirect Topical2 p$ V) Z3 l& p9 u# s+ |2 k8 v- }
Exposure to Testosterone
* Y. Q% `% a0 \2 Q+ |/ b; ASamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,23 y# A5 z1 `7 e/ D* H; S
and Kenneth R. Rettig, MD1/ b' s+ X, z# s
Clinical Pediatrics9 e% d8 z9 v+ D% a& k2 u/ G( \# }4 i
Volume 46 Number 6
* \. G  E: ^7 x+ tJuly 2007 540-5437 p4 T/ j" |1 X* g5 O& F
© 2007 Sage Publications" ^% |& c6 `( K) B8 b- E
10.1177/0009922806296651% i: C$ j5 B+ D$ O: B
http://clp.sagepub.com1 p. K8 L" u. P; v8 o) |
hosted at
' r! P# d/ V. p8 Yhttp://online.sagepub.com& v/ x$ l6 n1 t, [
Precocious puberty in boys, central or peripheral,: m* D# D: ^' u8 d: V! W9 g; ^9 Z
is a significant concern for physicians. Central% g' U4 p7 f( `5 j' k
precocious puberty (CPP), which is mediated: i9 M1 w, ?; U+ S0 y
through the hypothalamic pituitary gonadal axis, has
- N( S- g9 T  H4 P: w+ B1 X) Ea higher incidence of organic central nervous system" \7 w2 U0 m* U7 z3 Q
lesions in boys.1,2 Virilization in boys, as manifested
; N2 V$ G" Y& Z7 Xby enlargement of the penis, development of pubic
% m; A' ^7 r- @9 Hhair, and facial acne without enlargement of testi-
, p  ~* r- r( z" y) D- }0 Icles, suggests peripheral or pseudopuberty.1-3 We: I# I$ r6 `7 ~: c4 _* u
report a 16-month-old boy who presented with the  Y$ W8 o; X" A0 a0 `5 h
enlargement of the phallus and pubic hair develop-% u3 A. n* f# @4 ^; r! P4 r
ment without testicular enlargement, which was due. N( ^: D  J5 l: I5 r) U
to the unintentional exposure to androgen gel used by9 n/ G& w( S5 v& m
the father. The family initially concealed this infor-
. l. c" B" M) _* q( `mation, resulting in an extensive work-up for this
" [- I* C  c1 n3 A/ [" p  tchild. Given the widespread and easy availability of* C# o; p) j) B/ e3 t' G; i
testosterone gel and cream, we believe this is proba-
) Y9 Y& H+ Z* W1 {bly more common than the rare case report in the7 Y# g0 v2 u1 X1 h; ]* G' Q
literature.45 }: `' X3 \, ^* @; L  l
Patient Report
- z# j# j8 D6 \/ p$ RA 16-month-old white child was referred to the+ @) R6 v/ M/ l7 H$ v+ f$ V
endocrine clinic by his pediatrician with the concern" [2 P) ]- c( W) M1 h" H- a$ m
of early sexual development. His mother noticed9 D: |4 h( j; H# k  ?3 G
light colored pubic hair development when he was
& L! e: T1 S% g* l. S+ ~( _From the 1Division of Pediatric Endocrinology, 2University of
6 p1 R# ~+ E  @6 [1 |South Alabama Medical Center, Mobile, Alabama.
$ h# [) J/ `+ `: D7 a/ u2 CAddress correspondence to: Samar K. Bhowmick, MD, FACE,+ r) b. n% w+ g6 \8 o1 D
Professor of Pediatrics, University of South Alabama, College of8 X+ l0 w) m& _9 f8 v6 s- V
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
1 z% o5 y4 F! ]! m( Pe-mail: [email protected].- M* u1 F" b! M$ b% `- E
about 6 to 7 months old, which progressively became
! Q# u. F& s7 tdarker. She was also concerned about the enlarge-. z2 Y+ _7 s5 p0 L& `6 @% K* f/ [" x
ment of his penis and frequent erections. The child
: v1 {. K  ]' t  Gwas the product of a full-term normal delivery, with# I% `5 Z9 n* I" z5 U( [
a birth weight of 7 lb 14 oz, and birth length of
' E* k6 d! Y5 r9 S  f8 p  X  I20 inches. He was breast-fed throughout the first year2 Y* s# X( M, {& G: K  T) c
of life and was still receiving breast milk along with
! {1 _/ N% ?  I( g; Jsolid food. He had no hospitalizations or surgery,
, K8 f- W! C) @$ \! g0 c# O9 O0 p; z, vand his psychosocial and psychomotor development; J* s% T* w' O& P; ^1 ^+ n
was age appropriate.# p' F! D. [2 w
The family history was remarkable for the father,
+ |; L8 F/ W, W4 p! n7 Cwho was diagnosed with hypothyroidism at age 16,, p3 ^6 I) P1 f- i* p: J, ^
which was treated with thyroxine. The father’s
; v4 t* ?. N  m5 Pheight was 6 feet, and he went through a somewhat! z7 N  g4 M  e, n# q; B2 L
early puberty and had stopped growing by age 14.
" ?8 R. p$ |; p4 c1 \  F  v- CThe father denied taking any other medication. The& _: w: J2 F6 @  s4 h1 c
child’s mother was in good health. Her menarche
2 [$ z/ j- X2 x/ ]- S% I* Z/ r8 s( Twas at 11 years of age, and her height was at 5 feet$ j2 I% G# v* N
5 inches. There was no other family history of pre-3 z) D$ h0 I- N; [$ [
cocious sexual development in the first-degree rela-
& S$ y" v/ g: W  L3 g5 T* ltives. There were no siblings.
0 }- U8 [$ L7 o1 DPhysical Examination
' H) h6 e6 U6 z& U  R! A) V+ qThe physical examination revealed a very active,
! d/ ^7 \7 ]! }% dplayful, and healthy boy. The vital signs documented8 b  z1 U  o( g
a blood pressure of 85/50 mm Hg, his length was. l# g0 k2 z1 Y6 y  g
90 cm (>97th percentile), and his weight was 14.4 kg' o& ]& h: P9 l# W) O1 h# u
(also >97th percentile). The observed yearly growth
" O6 j5 A+ N6 N* O( J! P7 dvelocity was 30 cm (12 inches). The examination of& \' B$ q/ w! A' D
the neck revealed no thyroid enlargement.5 k; p# {+ J( a- G  z
The genitourinary examination was remarkable for7 w/ \# b, e8 [* R
enlargement of the penis, with a stretched length of: i& M- Z2 W4 I$ J4 ]4 _
8 cm and a width of 2 cm. The glans penis was very well3 f% H# M4 V8 ~- `
developed. The pubic hair was Tanner II, mostly around( A3 ?$ B1 o/ }0 n4 Z1 z7 n
540% n: g, A; H  x+ f3 S6 N7 Z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& r+ l7 P) a# Y* nthe base of the phallus and was dark and curled. The. Z8 P' U- {0 W+ m. J0 F8 L9 t
testicular volume was prepubertal at 2 mL each.
" \4 ^6 d; O. n! eThe skin was moist and smooth and somewhat3 m. R; i) i; E2 s$ Y, @
oily. No axillary hair was noted. There were no
- i" ]; d' d9 Z$ B; h3 H6 R. uabnormal skin pigmentations or café-au-lait spots.
6 L; ?3 \: k5 `Neurologic evaluation showed deep tendon reflex 2+
$ U3 x+ P  _/ u) L9 `( wbilateral and symmetrical. There was no suggestion
; f  X* E' l3 {of papilledema.; ^' _9 A" h7 R" ^/ I
Laboratory Evaluation& x4 j; C. \" b% c
The bone age was consistent with 28 months by
0 c" J  x9 ]7 _" J# z  ]+ {using the standard of Greulich and Pyle at a chrono-
/ W0 z8 ^6 {8 P7 Z+ y& U# ulogic age of 16 months (advanced).5 Chromosomal$ b! g1 q9 v* y. J: A
karyotype was 46XY. The thyroid function test* x0 V& o% M0 x1 ]" I2 [2 n
showed a free T4 of 1.69 ng/dL, and thyroid stimu-: B! X4 g) I. R% R
lating hormone level was 1.3 µIU/mL (both normal).
, Z$ d5 C: I3 x4 T1 gThe concentrations of serum electrolytes, blood) t! D' A" i* Q5 N9 k+ t" Q- x7 p
urea nitrogen, creatinine, and calcium all were2 Q5 m7 h2 d1 |) @' @/ r, |9 I
within normal range for his age. The concentration
, K( o4 u7 y: K  X* zof serum 17-hydroxyprogesterone was 16 ng/dL# \9 ~# m* P9 x
(normal, 3 to 90 ng/dL), androstenedione was 201 V, ~" a% c: E' s% G0 C8 z% p
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
9 E0 H& d. ~" p7 Q; S. }terone was 38 ng/dL (normal, 50 to 760 ng/dL),
2 X$ {( F$ F, Cdesoxycorticosterone was 4.3 ng/dL (normal, 7 to+ ]7 U$ m, `, D; ~2 G4 N
49ng/dL), 11-desoxycortisol (specific compound S)& ]8 M2 q' Z. ?6 g
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
/ A1 ?8 u# _3 v, Z: q/ W( Ctisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# T4 K# j7 c0 a. j6 e
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),' ]8 g/ ^) i4 d  ~6 k6 F' Q# m
and β-human chorionic gonadotropin was less than, e+ \7 M- O$ D. `
5 mIU/mL (normal <5 mIU/mL). Serum follicular
9 r! p4 f- ]  r) i0 ]stimulating hormone and leuteinizing hormone: w7 [) U" _/ L$ x1 M% e
concentrations were less than 0.05 mIU/mL
, `$ D- O$ D& X6 ?! K1 H" S0 f* z(prepubertal).
" h9 H: K+ r$ T$ t8 {3 o& Z: WThe parents were notified about the laboratory
5 u$ r" r1 R( wresults and were informed that all of the tests were# I6 l! g  }$ Z& f
normal except the testosterone level was high. The+ J1 M# N+ }0 a1 a0 `% A
follow-up visit was arranged within a few weeks to: t/ p" B7 h" O, s. E1 h+ h: M% z
obtain testicular and abdominal sonograms; how-
& _8 {- z# a9 Zever, the family did not return for 4 months.. q/ |* `, O. N2 t9 x- J/ [
Physical examination at this time revealed that the
3 e, ]+ G9 h9 }child had grown 2.5 cm in 4 months and had gained* Y& g# U6 B8 v) W2 b8 ?
2 kg of weight. Physical examination remained
' @7 t& K% q$ Q7 H0 eunchanged. Surprisingly, the pubic hair almost com-, k' }* y/ Q  p- Y4 U
pletely disappeared except for a few vellous hairs at) \5 m1 F. D2 O% k5 ~
the base of the phallus. Testicular volume was still 2& p  C6 V, D0 W/ J1 X4 S/ l* m& x
mL, and the size of the penis remained unchanged.! N! P: B3 t, |# J
The mother also said that the boy was no longer hav-
. u7 I+ Z! O$ @" x- V. cing frequent erections.2 m" N; r) l9 Q3 B% q0 J
Both parents were again questioned about use of3 K1 D. Q* D% ]6 N% S5 d, F
any ointment/creams that they may have applied to
  m; X3 J6 L$ `the child’s skin. This time the father admitted the
: ~2 f: w: l* I  ~. ETopical Testosterone Exposure / Bhowmick et al 5412 s0 k1 A! c' |, X
use of testosterone gel twice daily that he was apply-
( q6 W/ L. }. b1 I+ `4 Z! N/ C5 y; Ping over his own shoulders, chest, and back area for
4 `( j* Q' t' u5 |" n' l1 ja year. The father also revealed he was embarrassed. ?- s5 @( Z5 _+ F2 L, z! {" X
to disclose that he was using a testosterone gel pre-
* p& q! ?. z5 T( |* M( `scribed by his family physician for decreased libido3 k/ L1 B! N. @1 @+ b
secondary to depression.% z& }' [' C' o7 h
The child slept in the same bed with parents.9 o, O: T- ?3 U! }
The father would hug the baby and hold him on his6 L' r' I4 q/ }# [' P
chest for a considerable period of time, causing sig-' R  Z& ~$ o$ u& S
nificant bare skin contact between baby and father.
+ h# D5 y, \" n; S$ Z8 }) `2 kThe father also admitted that after the phone call,4 P/ z) [' ^8 ?% j5 B" k# X
when he learned the testosterone level in the baby7 X3 \" S8 I! |! G% l
was high, he then read the product information
) I) b0 L2 G3 x* {0 x6 gpacket and concluded that it was most likely the rea-; _9 P0 A, g: X2 Q% K5 _
son for the child’s virilization. At that time, they
. H3 S. }; G; R, k) T" f4 g$ M: udecided to put the baby in a separate bed, and the4 b$ d! f6 ]3 ^7 w4 |
father was not hugging him with bare skin and had
, E- q  ~. _* q6 o# k1 i$ mbeen using protective clothing. A repeat testosterone
, b6 b# L. y! D% M  J) j+ {, X! t9 Jtest was ordered, but the family did not go to the
: s2 N- }& a  V9 hlaboratory to obtain the test.; o3 B! g3 ]" L  Z7 u* Z
Discussion: E4 T; z/ r" f" K/ w( X& A- A3 k
Precocious puberty in boys is defined as secondary' [3 Y% |, r) z$ n  B0 k
sexual development before 9 years of age.1,4
# d- M3 D( \- Y1 `5 kPrecocious puberty is termed as central (true) when
& u: @3 e9 O% [7 X3 kit is caused by the premature activation of hypo-
/ C4 S' P. B; f5 K1 K2 r/ B3 V  ]thalamic pituitary gonadal axis. CPP is more com-' d/ c. `! D- X7 s% v3 c
mon in girls than in boys.1,3 Most boys with CPP4 l! L& A1 r/ |/ N3 h2 p( U
may have a central nervous system lesion that is2 o6 c0 ]: ?% N9 q7 B/ C
responsible for the early activation of the hypothal-9 o/ q- y8 i% Z  i
amic pituitary gonadal axis.1-3 Thus, greater empha-- ~4 R2 R4 Y& V. k8 u3 f$ ?. Y/ d
sis has been given to neuroradiologic imaging in
/ w: e, W, w, z4 I" P. Aboys with precocious puberty. In addition to viril-( ^" z& a4 c8 A" A% M
ization, the clinical hallmark of CPP is the symmet-  I3 O1 W& e) A$ ~/ r* E& A+ Y
rical testicular growth secondary to stimulation by
) }, w7 {. n2 `" ?" w7 r" o0 ^+ o# ugonadotropins.1,3
' f- M  }! |, D0 Z4 n! f2 W, rGonadotropin-independent peripheral preco-* k- Z& h: H3 B5 t2 H8 E# }
cious puberty in boys also results from inappropriate5 q, A6 {9 J* R/ ~, E
androgenic stimulation from either endogenous or' l+ N3 {  H$ N0 \6 d
exogenous sources, nonpituitary gonadotropin stim-
9 e( Q6 K/ f! iulation, and rare activating mutations.3 Virilizing& v8 |+ g. A# H5 r# n
congenital adrenal hyperplasia producing excessive
( Q  e3 o7 K- B, A, J0 `1 yadrenal androgens is a common cause of precocious/ ]0 F3 T! E0 o
puberty in boys.3,4
5 y4 o* q$ N1 RThe most common form of congenital adrenal
- P) O2 b- S2 _  G! thyperplasia is the 21-hydroxylase enzyme deficiency.3 D( \6 c7 |0 Z% L2 g& |/ l" A# E. m
The 11-β hydroxylase deficiency may also result in* d) v, {( F. {# [9 M6 j. E
excessive adrenal androgen production, and rarely,
: Q/ ^: h2 O$ l. T" |6 l( a; Aan adrenal tumor may also cause adrenal androgen6 @: _- s, K: X/ U3 o1 |
excess.1,3( {- w: o2 t) x! t5 Q' J$ m% d% ^5 i
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. O- Z1 W; o( f, P5 x
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
1 S2 N* q  U, SA unique entity of male-limited gonadotropin-: D. A# K7 H+ T' w- a
independent precocious puberty, which is also known
  O8 m: ^# k9 B* \- ~! O, [0 Bas testotoxicosis, may cause precocious puberty at a
* K+ b0 d; Q5 z2 [: Qvery young age. The physical findings in these boys
% v1 y* x8 B4 X+ M( q* Uwith this disorder are full pubertal development,
( o! M% A( y! |5 k0 mincluding bilateral testicular growth, similar to boys# M& p2 K9 x( L. t1 d8 N% @
with CPP. The gonadotropin levels in this disorder; ~/ ^4 ]9 y1 |- K1 E" }
are suppressed to prepubertal levels and do not show
- m# {- s% D- N% J5 J/ cpubertal response of gonadotropin after gonadotropin-
) V9 a+ |1 H5 h9 wreleasing hormone stimulation. This is a sex-linked6 C4 \4 t6 ^. U
autosomal dominant disorder that affects only
4 z, w: t: p! M5 Dmales; therefore, other male members of the family/ p0 c% p: T" |, n% }% a8 o/ U
may have similar precocious puberty.3+ W3 V+ Y; |8 C$ L) q
In our patient, physical examination was incon-  H! `0 x" [6 j1 w! B  O1 ?
sistent with true precocious puberty since his testi-
" h' T8 u1 w3 K8 Q" |# a  e+ |. Bcles were prepubertal in size. However, testotoxicosis( [. q6 j4 i. ]$ B$ V
was in the differential diagnosis because his father
+ }& P. p! p4 Y  u2 Ystarted puberty somewhat early, and occasionally,7 }) y1 t! a4 X1 {
testicular enlargement is not that evident in the
% A" u: I9 s- t/ g4 v% Wbeginning of this process.1 In the absence of a neg-5 s8 _& k; P+ i) A
ative initial history of androgen exposure, our
2 p5 Y# P. Q5 H% `biggest concern was virilizing adrenal hyperplasia,, w+ j6 F- ^5 j0 R8 W% Q5 }
either 21-hydroxylase deficiency or 11-β hydroxylase* x$ u% A3 j; w* O# U$ Q  l
deficiency. Those diagnoses were excluded by find-( K4 c7 q4 v+ }1 n
ing the normal level of adrenal steroids.
: o+ q% [, |8 b9 O2 x9 WThe diagnosis of exogenous androgens was strongly
3 @6 h8 g5 e& P# @8 Q# F& |suspected in a follow-up visit after 4 months because4 ?- {7 Q* {  O  V5 S7 Q
the physical examination revealed the complete disap-! n) _) W" H+ ?' y7 x
pearance of pubic hair, normal growth velocity, and
# Z7 `) a& h" D0 b" Q" xdecreased erections. The father admitted using a testos-
6 E( |0 [' n2 i; i+ {# r& K) B% i9 Iterone gel, which he concealed at first visit. He was
: C6 u5 |2 a5 j0 m5 ?% I6 V- H* Vusing it rather frequently, twice a day. The Physicians’
/ k. x/ z9 i; i) K' m# |' L5 GDesk Reference, or package insert of this product, gel or
, D: _& Z9 G, S! A3 ?5 vcream, cautions about dermal testosterone transfer to7 t3 U: V# i; R6 f: S) k
unprotected females through direct skin exposure.& o$ l" H, x. [" J$ n% O1 k
Serum testosterone level was found to be 2 times the" @" s: b! D' A" y4 a* u+ ^  H+ d: c
baseline value in those females who were exposed to
! Y* ], \' [4 p# E" f! Eeven 15 minutes of direct skin contact with their male2 f7 J/ U/ D1 R9 w2 I
partners.6 However, when a shirt covered the applica-
- F% P% [: }& H$ s, h+ Y* u% Qtion site, this testosterone transfer was prevented., Z7 k  c# W) g
Our patient’s testosterone level was 60 ng/mL,  w; w3 u8 ?3 w) p+ Q, M
which was clearly high. Some studies suggest that
+ L* a" `' h  D/ udermal conversion of testosterone to dihydrotestos-
( s' w% T; a* t1 i2 Nterone, which is a more potent metabolite, is more
+ q) C; d) |. J* kactive in young children exposed to testosterone
9 A6 S% L5 s7 }3 ]8 iexogenously7; however, we did not measure a dihy-
4 g' k7 ?3 E- v' cdrotestosterone level in our patient. In addition to
$ ^  Q% H/ I- d% b# a0 uvirilization, exposure to exogenous testosterone in, ~5 L2 t9 _' n- G3 y9 h
children results in an increase in growth velocity and
9 N4 r* ^) u  p( m9 Q* H7 Cadvanced bone age, as seen in our patient.. c7 w7 ]5 F8 `( `2 \. L
The long-term effect of androgen exposure during
$ e- O, f" D0 H# i7 b9 kearly childhood on pubertal development and final
3 b( L. v+ }: [0 [; [0 Xadult height are not fully known and always remain- m! ?2 }7 U( ?. n: H
a concern. Children treated with short-term testos-
3 @0 l  y, {. K- J; N' |  h8 E4 c3 m. xterone injection or topical androgen may exhibit some# @- V  Q2 \$ R% ~) i; R+ D% [. L
acceleration of the skeletal maturation; however, after% r) s7 q. _7 x7 V9 t
cessation of treatment, the rate of bone maturation1 H  C$ d! I4 T0 V
decelerates and gradually returns to normal.8,98 e2 f# J. Y6 x  U
There are conflicting reports and controversy
' c/ E  g$ h% v; f  sover the effect of early androgen exposure on adult
) p& B- g$ b1 E) r0 Y9 lpenile length.10,11 Some reports suggest subnormal8 @9 n5 J6 l& A  A# O$ s. T
adult penile length, apparently because of downreg-! c/ ?# v0 Z3 l: z/ ?  O
ulation of androgen receptor number.10,12 However,
2 J6 e5 Z. C) I1 G/ fSutherland et al13 did not find a correlation between. S& M, L  ~7 ]' B
childhood testosterone exposure and reduced adult
1 s- C6 l; z8 f0 ]& @1 c6 Rpenile length in clinical studies.
6 B; C! ]) t" p  TNonetheless, we do not believe our patient is
4 F% z* \& M7 a) pgoing to experience any of the untoward effects from* t! Q% c+ U2 y  n, h: }
testosterone exposure as mentioned earlier because
0 |% E4 Y6 w, wthe exposure was not for a prolonged period of time.# ]( @% F: F& R
Although the bone age was advanced at the time of) ]0 V. t. y$ C2 Z' D7 O- O
diagnosis, the child had a normal growth velocity at; p% ?8 ^& Y5 A5 P. ~: X4 z
the follow-up visit. It is hoped that his final adult& n# E, s1 f  g
height will not be affected.
: a' ]! d- b* s4 b6 v8 J, xAlthough rarely reported, the widespread avail-
* Z0 D! a6 ?$ x( Wability of androgen products in our society may
* I* `/ x) v- t. A6 oindeed cause more virilization in male or female% y. k8 c- r' E
children than one would realize. Exposure to andro-6 v6 x' L+ r* r3 r, @% ^
gen products must be considered and specific ques-
0 M; T" F3 v. e2 xtioning about the use of a testosterone product or0 ?+ [* f  O3 w) @2 w
gel should be asked of the family members during
/ z+ R( L6 j/ {3 k: F- {the evaluation of any children who present with vir-$ b) o; J/ B% D, ~( O; ]& A5 k! R$ L
ilization or peripheral precocious puberty. The diag-7 w1 X2 G, m( v* Z. D
nosis can be established by just a few tests and by0 ~7 Y( ?$ z  k2 o, V  v
appropriate history. The inability to obtain such a+ L1 i% _7 t6 u" B
history, or failure to ask the specific questions, may
! c9 W  x0 ~0 w1 gresult in extensive, unnecessary, and expensive
/ Y6 W& K# I  F, U6 Ginvestigation. The primary care physician should be
0 K0 a; V  a  k. |0 ], y3 |) caware of this fact, because most of these children
  ?5 @) G4 Z* K" ~1 {! y$ Nmay initially present in their practice. The Physicians’. J" ]& r$ W  W" g4 `8 E
Desk Reference and package insert should also put a
0 d( Z" ^$ M2 T+ f& ]+ I8 c% {warning about the virilizing effect on a male or  o: \) m' }5 j- |9 L
female child who might come in contact with some-
" k5 q4 S* a+ M; y$ hone using any of these products.( O5 \* k+ o( e+ K
References
8 {8 F) l  o' z' h* E+ R0 M1. Styne DM. The testes: disorder of sexual differentiation
$ B  }8 V% w4 L5 Kand puberty in the male. In: Sperling MA, ed. Pediatric: R6 d/ ~# j1 h0 V( J) S# f, x8 B& h
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
% T* r5 E5 o( {/ \) s2002: 565-628.
: P& F8 O# n# Q$ _8 n1 u2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
7 X$ Q+ f/ }$ Ppuberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
2 I4 q1 s  y$ e/ {' X
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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