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Sexual Precocity in a 16-Month-Old
. D, ~& P9 N( b9 \Boy Induced by Indirect Topical
& @4 B& F7 P* B" |* pExposure to Testosterone
; u2 B3 \6 m: }- K7 P2 b/ U* ~Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
" _, \/ Q) R1 u  [5 n" A+ }2 f# k% }and Kenneth R. Rettig, MD1
" d$ N- g3 L3 m. a( L7 cClinical Pediatrics
6 W8 d4 L% @) K- i- a* CVolume 46 Number 6
& C+ P2 _* v* Y# d# ^" zJuly 2007 540-543( N/ S2 C% n6 Y, j
© 2007 Sage Publications
$ _6 S  X+ d4 F8 Y9 N" z* S10.1177/0009922806296651
3 _2 I% F) x; l* G8 L+ j7 G% whttp://clp.sagepub.com+ y' m) Y; X2 m1 j/ d  O; m$ @
hosted at+ Q9 X: @# g5 ?- ?9 m( O
http://online.sagepub.com
4 [+ T6 z* G- ]5 |4 f' p' YPrecocious puberty in boys, central or peripheral,! _% v( G4 Y6 t) ~4 q# c5 @
is a significant concern for physicians. Central3 C$ m, d! B3 T* T" f! {
precocious puberty (CPP), which is mediated
; C5 F  V* T; {through the hypothalamic pituitary gonadal axis, has
; |9 e3 J$ u) Q5 Ca higher incidence of organic central nervous system
) p( ^- ]  w' K1 g1 Q/ C' clesions in boys.1,2 Virilization in boys, as manifested0 Q7 p$ w* O) f3 e. _
by enlargement of the penis, development of pubic, W. q! f- `, X! I
hair, and facial acne without enlargement of testi-3 Q$ ?. t- r* g2 K
cles, suggests peripheral or pseudopuberty.1-3 We
5 t; c% |! L9 v' j* Areport a 16-month-old boy who presented with the) q( J% ?. q0 {: q
enlargement of the phallus and pubic hair develop-+ m. \% t: l% |/ T8 t5 }3 x$ x
ment without testicular enlargement, which was due0 Y$ U' S- j' r! C' u8 I0 B" i5 B
to the unintentional exposure to androgen gel used by
& ^: T$ R0 ^" {the father. The family initially concealed this infor-3 W  Z- e0 V- ^# ~/ d# |( m
mation, resulting in an extensive work-up for this. O% F4 K; |; A) Y( i0 P
child. Given the widespread and easy availability of9 K) D. T' o* [# s. B2 I) m6 A
testosterone gel and cream, we believe this is proba-
2 e, g! v! `4 |0 d, H3 Vbly more common than the rare case report in the* S0 D- _  K, u; I. k
literature.4* ?& _: R# m( a: }7 d+ T$ Y" |
Patient Report
2 ?& I) y0 M5 ~5 k1 ?8 V0 uA 16-month-old white child was referred to the
3 ~) ~6 X3 w/ J) V' qendocrine clinic by his pediatrician with the concern
/ x- I/ {: X# R# ^/ lof early sexual development. His mother noticed
. t7 ^4 d( L: `light colored pubic hair development when he was4 b# k- \7 ]( ]9 F7 v& J$ Z
From the 1Division of Pediatric Endocrinology, 2University of
( S5 N7 y8 s. r/ Y, P$ wSouth Alabama Medical Center, Mobile, Alabama.3 a5 P; i0 e! H8 _1 m' `# M! b
Address correspondence to: Samar K. Bhowmick, MD, FACE,: {' T; D& G: V. T' _) W7 w
Professor of Pediatrics, University of South Alabama, College of0 E- j8 H  M2 i' E1 b4 m" `
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
4 ?1 s5 |7 Z2 {+ ie-mail: [email protected].
+ M, |' w- U9 I6 Oabout 6 to 7 months old, which progressively became% m3 r# D3 n' b: M5 C
darker. She was also concerned about the enlarge-6 W5 c: [2 W" E" N' N! O7 A
ment of his penis and frequent erections. The child0 d% M. `  @2 V4 \. g3 l
was the product of a full-term normal delivery, with
1 o$ B5 y+ p  j6 J. ~9 U; Da birth weight of 7 lb 14 oz, and birth length of' D4 P5 [3 S; r0 C$ [
20 inches. He was breast-fed throughout the first year, ?6 H+ R/ X8 d
of life and was still receiving breast milk along with% m6 g, a5 |3 ^+ M- _. S8 d- v6 Q
solid food. He had no hospitalizations or surgery,* G! s3 c  Q* ^. t
and his psychosocial and psychomotor development3 [9 A; a2 P/ ]( R2 _4 e
was age appropriate.
, J+ L: {/ q) p- ^2 P: Y. d" b2 O  J) `The family history was remarkable for the father,$ Z$ A: Y9 |+ s& _% h0 b4 r8 K
who was diagnosed with hypothyroidism at age 16,$ V# n- L# \6 f& U! `
which was treated with thyroxine. The father’s$ j5 U. y, x6 y; [2 Y  H; ]
height was 6 feet, and he went through a somewhat
8 f" D& J/ i; g# z  Q0 S9 zearly puberty and had stopped growing by age 14.
% g4 r0 t( ^4 _0 w- PThe father denied taking any other medication. The. T' n# l% u& k* O7 d5 C3 n: r
child’s mother was in good health. Her menarche
! X' ~/ e. O7 M" L6 d9 F4 @" B* s8 Dwas at 11 years of age, and her height was at 5 feet
! Y" e5 i, j* ^* n5 inches. There was no other family history of pre-
9 Z" x$ n1 q" Xcocious sexual development in the first-degree rela-4 ~& ], n* `8 ]. e
tives. There were no siblings.
) k8 d8 }9 Q5 U/ o0 f( W- h" TPhysical Examination
( M+ u( I- b7 A, r0 s# k- p6 |The physical examination revealed a very active,- R" o7 E3 A- H0 `/ y  j$ I
playful, and healthy boy. The vital signs documented
9 B- m6 j0 ?! ga blood pressure of 85/50 mm Hg, his length was
4 J+ B- B+ O7 A* L& ]' n90 cm (>97th percentile), and his weight was 14.4 kg
: h" x$ h0 E) \  K9 Z(also >97th percentile). The observed yearly growth
7 o- `1 h( E) {4 |5 |# w- ~& zvelocity was 30 cm (12 inches). The examination of5 u' z+ \$ u- F3 v: \
the neck revealed no thyroid enlargement.
. n+ e% s# e/ H- [7 p5 h( LThe genitourinary examination was remarkable for
  N  g  d- A  Senlargement of the penis, with a stretched length of: E1 u* Z* H7 {8 T- N
8 cm and a width of 2 cm. The glans penis was very well
9 r; ^0 R# G3 A; Ideveloped. The pubic hair was Tanner II, mostly around6 S8 X% m5 L- a/ V) r4 e
540$ m( G" u& p2 p( v* U7 V" T( _: y2 h/ ~
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, c# j6 D1 J* h. H: Uthe base of the phallus and was dark and curled. The1 ?' e8 w3 O9 h1 {6 e! {
testicular volume was prepubertal at 2 mL each.
0 I! W( Z% {9 [3 g2 y  rThe skin was moist and smooth and somewhat
' I3 I4 a/ y2 [, r. e- ^" E( ~- i) v' Xoily. No axillary hair was noted. There were no
5 I" I, U& q7 R! j9 P# C/ U  m$ mabnormal skin pigmentations or café-au-lait spots.
% z6 K, i% {/ e: zNeurologic evaluation showed deep tendon reflex 2+3 u  O$ }$ X# M/ V: Y- \
bilateral and symmetrical. There was no suggestion
8 A, b, Z7 t9 L! a1 t' ^: F, t* Dof papilledema.3 v, r( Z4 D# q0 R# {
Laboratory Evaluation
9 U( G0 A0 w+ e* eThe bone age was consistent with 28 months by
) Z% @' ?8 E* b# _3 Susing the standard of Greulich and Pyle at a chrono-' P" ]  k  h: T) |4 L* u& W2 u
logic age of 16 months (advanced).5 Chromosomal  y: m0 P5 s1 X& w- _8 ]# B0 ~% d
karyotype was 46XY. The thyroid function test0 H7 u" W0 x. P9 ]( K/ M) K, ~
showed a free T4 of 1.69 ng/dL, and thyroid stimu-0 U$ _) v, O% E( s( n! u
lating hormone level was 1.3 µIU/mL (both normal).' I; D1 _8 S" l
The concentrations of serum electrolytes, blood
' E( b  w: Y4 B/ E+ |3 |1 eurea nitrogen, creatinine, and calcium all were+ F) N7 J+ o/ k0 u; h( K' l
within normal range for his age. The concentration) Y. s2 a. a: j) S1 W0 [' h
of serum 17-hydroxyprogesterone was 16 ng/dL5 e1 L5 y% x9 G. I! U
(normal, 3 to 90 ng/dL), androstenedione was 20: n& `0 d( d' U) Q/ O# W
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
1 L0 F3 t/ \+ @$ c' iterone was 38 ng/dL (normal, 50 to 760 ng/dL),$ [0 U# B. i" [3 R0 L5 _( M
desoxycorticosterone was 4.3 ng/dL (normal, 7 to7 z4 o' O+ z* D/ X3 Q* l( Q4 O
49ng/dL), 11-desoxycortisol (specific compound S)
) ~. l8 O, G) a9 n& [9 d# Nwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-* U- A: `, l& G7 f9 F8 j
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total; K% b( Q2 R; \7 ~" R
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
  M* K3 t8 D! e5 t; g; I) Band β-human chorionic gonadotropin was less than
' ^; D$ l  r& z, D& M9 @3 q5 G# C5 mIU/mL (normal <5 mIU/mL). Serum follicular
) U1 _  {# ^. wstimulating hormone and leuteinizing hormone$ j( ]  A8 y+ B% v
concentrations were less than 0.05 mIU/mL% R6 j# G) U% U2 b- f
(prepubertal).
" n  t5 e$ B6 t  w1 c% EThe parents were notified about the laboratory$ {/ y+ Q) l. U
results and were informed that all of the tests were* @$ n# U' \# B* I1 h
normal except the testosterone level was high. The
, x4 e& q$ U" x! {follow-up visit was arranged within a few weeks to0 e4 Q$ L8 o# W6 `' E' i2 a  ]+ f
obtain testicular and abdominal sonograms; how-
3 v: s/ h9 P* j( Tever, the family did not return for 4 months.: O8 N8 n% r9 |1 C5 A
Physical examination at this time revealed that the9 r! H$ T% e8 r2 h) R7 D
child had grown 2.5 cm in 4 months and had gained# c. ?# z* Y) u5 ^% P# A9 D, {4 w
2 kg of weight. Physical examination remained
* y( I/ V: h; Tunchanged. Surprisingly, the pubic hair almost com-
1 [: B" c7 ]7 c1 C, U) Zpletely disappeared except for a few vellous hairs at% H: I8 H: E* i2 M0 E
the base of the phallus. Testicular volume was still 2
2 T% s( ?/ w/ b8 _mL, and the size of the penis remained unchanged.
, |. ^! y* N% t" r( N: G$ w, vThe mother also said that the boy was no longer hav-7 {$ w' G+ U. o' ?
ing frequent erections.& J: I' {8 J/ E" I9 l7 ~# Q
Both parents were again questioned about use of
1 X. I+ R( B7 _5 x3 yany ointment/creams that they may have applied to) \9 B- {) q( ^1 M) }+ {& B9 D
the child’s skin. This time the father admitted the
! H2 }: w0 ?2 n' Q" _( HTopical Testosterone Exposure / Bhowmick et al 541
0 C5 t! r7 Q* a# D' ?use of testosterone gel twice daily that he was apply-
9 k2 n- ]+ P0 ]" G: ging over his own shoulders, chest, and back area for
6 B4 T1 T; I8 r+ l' r; Ta year. The father also revealed he was embarrassed% r" J* M3 j" K' j9 X& M- }' S
to disclose that he was using a testosterone gel pre-* V6 [$ s6 V5 X3 T# U- g
scribed by his family physician for decreased libido
  c3 w2 d$ E: }9 J8 b! F0 [secondary to depression.
; A9 `+ P0 h/ _/ Q# j5 @The child slept in the same bed with parents.2 f. A4 w9 P6 ]) ?
The father would hug the baby and hold him on his9 [, d* Z' r8 o: ?# R4 L
chest for a considerable period of time, causing sig-
, W, R0 f8 q$ m* l( knificant bare skin contact between baby and father.
5 r0 k5 w9 L2 NThe father also admitted that after the phone call,* o1 P& i( Z$ H+ x7 y
when he learned the testosterone level in the baby5 q# y# A6 b# v* X7 l/ Q9 _
was high, he then read the product information
* }$ l  V2 B5 @1 @packet and concluded that it was most likely the rea-- C( M8 T- H" z
son for the child’s virilization. At that time, they
! b; H  i& A$ k8 ~decided to put the baby in a separate bed, and the! `. t$ `* |4 Z
father was not hugging him with bare skin and had
& g: E. F7 T* _# B' Ibeen using protective clothing. A repeat testosterone
- {0 t% l0 B. A: xtest was ordered, but the family did not go to the! p( |( P. I& Z+ |  t, L; R
laboratory to obtain the test.
9 n% O/ C3 ^/ LDiscussion
) t: a6 @. |+ N- u) _" B3 mPrecocious puberty in boys is defined as secondary
8 o% l0 ?: u# nsexual development before 9 years of age.1,4
3 |& A* R  ~+ ]/ ?Precocious puberty is termed as central (true) when# x" o3 b, K, ^' |* f
it is caused by the premature activation of hypo-& C/ n5 a- c8 t" t
thalamic pituitary gonadal axis. CPP is more com-
! H4 C' X- K2 [" Y9 d9 O- Qmon in girls than in boys.1,3 Most boys with CPP: h3 |& U- a$ F9 r% a- O* f
may have a central nervous system lesion that is/ P4 l2 m7 [# ]  K
responsible for the early activation of the hypothal-
2 N6 v9 s& I. l" |7 D( Gamic pituitary gonadal axis.1-3 Thus, greater empha-
( u" L6 X- N9 k; E- Y5 o" J6 ysis has been given to neuroradiologic imaging in
/ Q4 j& Y% c: B1 b5 qboys with precocious puberty. In addition to viril-
' A' a* J! ]: P) w% jization, the clinical hallmark of CPP is the symmet-
* s5 k/ F% I, o* S4 Frical testicular growth secondary to stimulation by1 H' e3 }8 Q% d' }  e; V
gonadotropins.1,32 H/ L$ U. L3 N
Gonadotropin-independent peripheral preco-
! H1 Q+ e! L% D1 E7 V, Ecious puberty in boys also results from inappropriate4 r" ^7 y: `$ l9 W; G
androgenic stimulation from either endogenous or( m3 b" r- {" Y, F7 \5 S$ B$ _9 o4 _
exogenous sources, nonpituitary gonadotropin stim-
/ E" C$ B" C, r5 B0 gulation, and rare activating mutations.3 Virilizing
4 w3 Z+ O! y# Z. ~( n& ~congenital adrenal hyperplasia producing excessive/ L. t( j6 o' Y2 S. E, I
adrenal androgens is a common cause of precocious
1 m8 O8 Q" \/ F! i& A7 [( \puberty in boys.3,4& V$ }9 ~3 h) C
The most common form of congenital adrenal2 U/ L! |, V0 ]* ^
hyperplasia is the 21-hydroxylase enzyme deficiency.
4 N% K  o% V5 s0 YThe 11-β hydroxylase deficiency may also result in6 ?& V" A. y% }* j) P/ q
excessive adrenal androgen production, and rarely,! v1 F: L/ [2 q+ f- ^! C2 h5 B
an adrenal tumor may also cause adrenal androgen0 r& |4 a/ c, ?; V0 N+ A
excess.1,3
  a* m3 g6 C$ W0 \* h" gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  n; z6 W# t. q, I* G
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
% G0 c% P6 g/ k8 C5 L; X! A' WA unique entity of male-limited gonadotropin-/ M# S" c0 F4 r& D+ y
independent precocious puberty, which is also known9 o4 |; s4 X6 o) p  @
as testotoxicosis, may cause precocious puberty at a
" ]6 b7 f6 c8 h6 Nvery young age. The physical findings in these boys7 ], Y, ~& h" e$ k1 |
with this disorder are full pubertal development,+ x# X; @  x+ x# @: [. u1 M
including bilateral testicular growth, similar to boys) Y5 g. D1 B6 T. [
with CPP. The gonadotropin levels in this disorder4 \9 K) t; l# N7 X
are suppressed to prepubertal levels and do not show/ z# f9 ?0 n5 i) R  _
pubertal response of gonadotropin after gonadotropin-! @+ W& C' q2 q( c
releasing hormone stimulation. This is a sex-linked; q, s2 @; i- U* f
autosomal dominant disorder that affects only* a( |: x% Z4 V# u" q
males; therefore, other male members of the family
! [  r0 M& M& Z6 amay have similar precocious puberty.3
( \* D5 l# q; v: K  @6 J' ~In our patient, physical examination was incon-0 R3 F; ]4 o" q
sistent with true precocious puberty since his testi-8 K) H9 }. U" _* r- G: r
cles were prepubertal in size. However, testotoxicosis' N# V5 E4 K+ q, q( i  T
was in the differential diagnosis because his father
5 d/ K+ _1 Y* ~- P" j6 a" I+ Dstarted puberty somewhat early, and occasionally,
3 H% W4 s) K# w7 P/ t! x( ptesticular enlargement is not that evident in the0 M9 ~, P; _& [, v4 v
beginning of this process.1 In the absence of a neg-2 D) {4 m) L7 E9 Q, K4 Y- g% ], a$ D
ative initial history of androgen exposure, our
  X) m6 H1 n3 ^" mbiggest concern was virilizing adrenal hyperplasia,
7 b, Q% m4 r( F# C/ m9 Ieither 21-hydroxylase deficiency or 11-β hydroxylase+ l4 q1 u3 M. T* @
deficiency. Those diagnoses were excluded by find-' K& ?, m6 y& J, D- y7 k, E# E+ l: Z
ing the normal level of adrenal steroids.! v, n: x5 |+ i% E3 I) K
The diagnosis of exogenous androgens was strongly* Q9 L* k# B3 W- ^
suspected in a follow-up visit after 4 months because: i5 {7 w. n8 i$ c
the physical examination revealed the complete disap-1 k. t3 S% C0 r! E! x: g3 P; B
pearance of pubic hair, normal growth velocity, and
6 D% e4 J0 U3 ^# W7 n& Kdecreased erections. The father admitted using a testos-
1 M, }( r7 c, k- g. ^. lterone gel, which he concealed at first visit. He was
7 ^) E2 X- k# M3 l1 {2 p' musing it rather frequently, twice a day. The Physicians’
0 u  `! G5 t( q5 p- ODesk Reference, or package insert of this product, gel or+ }8 k" \5 ~3 g4 u
cream, cautions about dermal testosterone transfer to% p$ x! x! ]: G! Z, U# {+ P
unprotected females through direct skin exposure.
9 x7 M) Z+ Y: m# r( Y. D/ c, e0 eSerum testosterone level was found to be 2 times the; R$ Q+ t. ]) ]. `; ~2 O
baseline value in those females who were exposed to  i! }1 R* A5 \- m2 P* ?0 U: n/ ?
even 15 minutes of direct skin contact with their male- q) c( A$ Q% Q
partners.6 However, when a shirt covered the applica-8 T& u. {" t0 k+ x3 H: g( v, `9 E
tion site, this testosterone transfer was prevented.
: d, o# D4 b7 _/ C1 U1 pOur patient’s testosterone level was 60 ng/mL,2 O) Y0 ~& N/ g( c0 o* Z
which was clearly high. Some studies suggest that9 d' F& h, {# m( S0 k
dermal conversion of testosterone to dihydrotestos-
0 c, S$ J% y% `' b/ ~terone, which is a more potent metabolite, is more( L3 l0 B5 U  f( F0 c
active in young children exposed to testosterone
3 J8 z+ P: K' L1 o+ a3 j( Gexogenously7; however, we did not measure a dihy-3 C8 p1 F6 f0 `) @: s
drotestosterone level in our patient. In addition to9 x) j. N8 D) F9 x0 X- A
virilization, exposure to exogenous testosterone in8 h) {2 B% N; G+ n3 |4 P4 q' C
children results in an increase in growth velocity and. E5 n+ W# d6 `1 b  `
advanced bone age, as seen in our patient.0 X. S! r4 j, W; E% V
The long-term effect of androgen exposure during8 H+ Q$ r: O7 F$ R
early childhood on pubertal development and final
! w$ ~& J; |2 s9 d4 jadult height are not fully known and always remain; r# @7 [1 X, e6 |, u
a concern. Children treated with short-term testos-0 r) x) _8 |4 P# K( c& M( R/ i; g
terone injection or topical androgen may exhibit some' w7 X6 p! a% K8 F; O, @, R3 Q
acceleration of the skeletal maturation; however, after! c& A, I9 K; ~9 ~; a7 `" j
cessation of treatment, the rate of bone maturation
$ N4 J; D: G, n$ Edecelerates and gradually returns to normal.8,9, g3 J" C  U6 U) V2 B3 ~- c
There are conflicting reports and controversy
: L% ]( \% d) w2 Q" Yover the effect of early androgen exposure on adult
; |- i# t; K" K- ~% c/ ?penile length.10,11 Some reports suggest subnormal: H! B, s" o2 l0 `
adult penile length, apparently because of downreg-
. W3 K8 x/ M; L& t! _ulation of androgen receptor number.10,12 However,
$ s; a1 c% C: p- iSutherland et al13 did not find a correlation between* R, @0 H- Z0 D3 G
childhood testosterone exposure and reduced adult& p" O( g4 D6 r: [+ h) h
penile length in clinical studies.* H* q1 \& N& u/ k: A: @. V' t
Nonetheless, we do not believe our patient is
. x0 D+ d- p) G( cgoing to experience any of the untoward effects from5 _2 t" C3 p) }5 a6 g5 v. F
testosterone exposure as mentioned earlier because: ]  i- w- [$ _2 J/ P
the exposure was not for a prolonged period of time.
+ ~- v- q+ z' G4 P2 PAlthough the bone age was advanced at the time of
- P; S, k: |1 {* c$ ?diagnosis, the child had a normal growth velocity at
' i( s; N7 t% g. B! ]6 r6 c/ }$ lthe follow-up visit. It is hoped that his final adult5 }: A# @9 L. N* p; S* }
height will not be affected.2 {# V* W2 {, y" x. [2 ^. J! l4 _
Although rarely reported, the widespread avail-" l# M) q! f1 Z' F: ]8 q0 u
ability of androgen products in our society may8 f- r; L5 G3 g% N5 a! ^6 P6 J) o
indeed cause more virilization in male or female
. W! I6 O& W3 }* ^children than one would realize. Exposure to andro-5 W' @: m' v( `6 V6 x
gen products must be considered and specific ques-
3 H8 N. ^& ?& Z- Y, h% Gtioning about the use of a testosterone product or! ~/ }& ]) p! g& ?* ~6 F2 s/ y
gel should be asked of the family members during& I+ ?7 A( I5 I
the evaluation of any children who present with vir-
! x% ]. V$ c) U" }& Gilization or peripheral precocious puberty. The diag-
& i4 b- d; J: D5 dnosis can be established by just a few tests and by
1 ^' e0 x- ]8 s& ^9 L9 h9 c! G% h( Sappropriate history. The inability to obtain such a
1 ~" n5 k6 j! }) Chistory, or failure to ask the specific questions, may
2 v; l0 a& f( i2 Rresult in extensive, unnecessary, and expensive+ k* [3 V1 o5 ], X, L3 s0 u* C7 p
investigation. The primary care physician should be# L+ r6 p2 Y0 V7 {
aware of this fact, because most of these children! h! P' J! i( d& T& p
may initially present in their practice. The Physicians’
* b( @& A: T% ?9 `2 {Desk Reference and package insert should also put a
2 ^$ [2 U8 B- rwarning about the virilizing effect on a male or8 {& G' y* w; h6 y% a" g# ?
female child who might come in contact with some-
5 H7 `2 o+ ^2 e) B: u/ {3 Mone using any of these products.
% g+ I  n  {, H2 SReferences
; @# d! W( |+ J# D$ w! K1. Styne DM. The testes: disorder of sexual differentiation; m5 Y, m. n1 D
and puberty in the male. In: Sperling MA, ed. Pediatric
3 ^" b( _9 N! e8 Z' f% \Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;5 E7 @5 R% w) w6 d
2002: 565-628.
% M: r& ?5 v, K1 e0 G0 P" Y' m9 g2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
( D' G  C7 Q: [0 O! Ppuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
; \0 M- j0 V! a6 h$ D  BBoy Induced by Indirect Topical; [. S; R% R7 S9 H8 Y
Exposure to Testosterone
0 e8 S( t$ j5 }& _Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,26 P$ |- l+ i& A! J7 U9 s
and Kenneth R. Rettig, MD1) Y" Z4 a8 A9 z1 n# Z6 C
Clinical Pediatrics
7 Z$ _9 c' o3 hVolume 46 Number 6
5 Q5 `. {0 p; S" W9 ?+ YJuly 2007 540-543
) i9 m: q- h' F& E© 2007 Sage Publications0 d$ t: A( F5 b9 ^! r
10.1177/0009922806296651
! k( O, ~9 {* }+ nhttp://clp.sagepub.com
- W% X1 I1 z3 G1 q  y# ^! Yhosted at; I! m: t' K' y0 e. ]
http://online.sagepub.com- m% k  A' W+ @$ n( P! r' f
Precocious puberty in boys, central or peripheral,9 P* I2 B+ a! y2 q$ \
is a significant concern for physicians. Central
/ _0 o! d' R# J; b9 b3 @precocious puberty (CPP), which is mediated
  b- O) n# P4 }) @$ qthrough the hypothalamic pituitary gonadal axis, has
; u5 ~6 y! v* _$ V1 N1 A# _a higher incidence of organic central nervous system
& ~" [% G  r& U2 X% elesions in boys.1,2 Virilization in boys, as manifested
; F1 R9 k* p. i; Pby enlargement of the penis, development of pubic
$ j- n! ]6 X) _1 Whair, and facial acne without enlargement of testi-7 a3 o9 Y$ q, P8 w5 n; F8 q7 o9 n
cles, suggests peripheral or pseudopuberty.1-3 We5 S8 f/ G+ \! P! c3 U0 P
report a 16-month-old boy who presented with the
& \' p3 j) L1 {# m0 H% V: R2 ~enlargement of the phallus and pubic hair develop-& t7 Q$ j, p- {6 o( [. A
ment without testicular enlargement, which was due
7 ~2 s8 k' Y6 y* }7 kto the unintentional exposure to androgen gel used by  F! h7 ?# O" G+ {
the father. The family initially concealed this infor-
1 P/ L2 G0 G0 j8 W6 s  O$ Bmation, resulting in an extensive work-up for this
% w- G% x- S+ V/ T4 x, u: Vchild. Given the widespread and easy availability of
. B0 W: ~0 ?0 e# a/ c2 ?testosterone gel and cream, we believe this is proba-! }/ d* @" }& }9 A3 U
bly more common than the rare case report in the
- S) |% r( w9 f, e- l. oliterature.4
2 `+ @3 V' m) `3 xPatient Report5 G% z6 _. n- d
A 16-month-old white child was referred to the' [. C) t6 @/ n7 ]
endocrine clinic by his pediatrician with the concern
$ y  t8 x* }/ V3 _8 {& P# {- {of early sexual development. His mother noticed
9 X' l# g) k  t% [: y% V  y* glight colored pubic hair development when he was  M' D8 f7 b. k5 u6 U
From the 1Division of Pediatric Endocrinology, 2University of7 t0 q* x( }: Z4 R# n7 T; `
South Alabama Medical Center, Mobile, Alabama.- J- e) A: S/ M) |9 c6 _
Address correspondence to: Samar K. Bhowmick, MD, FACE,; L. v1 V+ i" A$ g/ t: R! f$ G( t0 e
Professor of Pediatrics, University of South Alabama, College of
% l, ~: H- p% \; j. a9 ~Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;1 E2 N. G- i+ \, `) ~* |
e-mail: [email protected].0 {0 t+ s1 h" V4 T. f3 H. G( n/ ?
about 6 to 7 months old, which progressively became( q/ O4 |' M  L
darker. She was also concerned about the enlarge-* r4 M9 B3 c! \8 c( {, |
ment of his penis and frequent erections. The child
2 n& ?- ~0 ?+ U/ z" Zwas the product of a full-term normal delivery, with
  r* F' r' h( S/ |" fa birth weight of 7 lb 14 oz, and birth length of' f6 W0 n6 d# i( i
20 inches. He was breast-fed throughout the first year
5 d( }) }% H5 s+ y2 t0 Z1 rof life and was still receiving breast milk along with
. G8 d; S3 j3 ]$ d. d0 zsolid food. He had no hospitalizations or surgery,( E) Y: |: Q* Z# K* m+ j; Y8 k
and his psychosocial and psychomotor development
6 z6 }' _3 W7 ?5 Y0 ewas age appropriate.
5 k/ h6 Q7 q! Q' G# iThe family history was remarkable for the father,* X) X) B& e6 e, [2 J& W1 g$ t* l
who was diagnosed with hypothyroidism at age 16,& f- |1 K( R7 R" G
which was treated with thyroxine. The father’s  L' f/ k3 O3 B9 N# M+ Q
height was 6 feet, and he went through a somewhat) [! K5 A6 z: ^
early puberty and had stopped growing by age 14.7 n4 S  C& l# k6 l9 e
The father denied taking any other medication. The
! G# c6 ~* @7 l; J9 q' v0 ]  Bchild’s mother was in good health. Her menarche2 D7 D7 @* W- F# x+ b
was at 11 years of age, and her height was at 5 feet: y9 ^# W( w  X1 U; Y; N+ Y' u; g# `
5 inches. There was no other family history of pre-9 m" d5 R; u9 t) Z
cocious sexual development in the first-degree rela-
  B: _8 V3 ^9 _; htives. There were no siblings.
7 l* U9 U2 U9 V" I4 s4 F; uPhysical Examination
3 j3 h4 p7 ~/ a' r4 QThe physical examination revealed a very active,, Z( _: F1 i, Y1 w6 I8 `
playful, and healthy boy. The vital signs documented! ]& \5 G5 m% N1 N
a blood pressure of 85/50 mm Hg, his length was" h! I4 N8 n6 F5 c% C
90 cm (>97th percentile), and his weight was 14.4 kg
" |+ ?5 \* I, O# c. S(also >97th percentile). The observed yearly growth! {, @  W0 X2 V: m
velocity was 30 cm (12 inches). The examination of
1 l/ Z6 K- ~( B  cthe neck revealed no thyroid enlargement.
( D) f) F- W! z  `+ wThe genitourinary examination was remarkable for3 @& Z3 Y5 q2 `8 t* B5 H. Q
enlargement of the penis, with a stretched length of
3 P  x% p+ _: X5 E% q7 k3 M8 cm and a width of 2 cm. The glans penis was very well9 a* A/ a, k$ k; a+ [, a' P
developed. The pubic hair was Tanner II, mostly around
8 M  G. z, D9 U" Y) l: X& M540* i: |1 H2 n, R
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 B( s6 \; j  r2 L; r4 _$ i7 N
the base of the phallus and was dark and curled. The
0 v, z% T7 C) }testicular volume was prepubertal at 2 mL each.' k: H# @8 m+ x4 {0 x+ a
The skin was moist and smooth and somewhat
+ a9 e/ G0 K" [* c( v' G4 }; l. Toily. No axillary hair was noted. There were no
3 b. s, A6 [# j5 s4 `abnormal skin pigmentations or café-au-lait spots.
7 g3 @! q' W6 k" a: L! i8 f& oNeurologic evaluation showed deep tendon reflex 2+- z: n5 m; S3 _% G- G8 K5 T8 O
bilateral and symmetrical. There was no suggestion
8 r2 x/ F" Q9 n9 V& K% rof papilledema., O* |5 h) g: E& W- s" \* ]* U
Laboratory Evaluation% |/ X  B" ^6 J1 M1 N" j) v  x
The bone age was consistent with 28 months by# H' {4 \8 a) ~" V
using the standard of Greulich and Pyle at a chrono-+ F# P- S( N( R/ f8 {! s
logic age of 16 months (advanced).5 Chromosomal
& t5 @& u' e" {* ]5 vkaryotype was 46XY. The thyroid function test
& e& Q+ K" `7 z% r2 G4 Z4 B: p9 C& Yshowed a free T4 of 1.69 ng/dL, and thyroid stimu-8 ?/ {; R* \. [1 @
lating hormone level was 1.3 µIU/mL (both normal).
( M) f; D3 p! O4 {The concentrations of serum electrolytes, blood( I1 L. ~9 W! t0 z+ h+ v, T
urea nitrogen, creatinine, and calcium all were( y( G* j6 z( v( a0 f* D  w3 O0 M
within normal range for his age. The concentration
! v1 }1 f. y2 R! Zof serum 17-hydroxyprogesterone was 16 ng/dL/ O; L( ]; m4 A# T% S* e
(normal, 3 to 90 ng/dL), androstenedione was 20
! q, m% j9 q* l' K; b) L- ~9 }, Lng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-& ~2 C6 h9 `9 v4 n2 ]! b; S
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
0 ]9 }- t& F, y2 }0 ?desoxycorticosterone was 4.3 ng/dL (normal, 7 to
! o. L( E9 [" [6 D. b49ng/dL), 11-desoxycortisol (specific compound S)0 V* L. g1 W9 t- }7 O8 w$ e9 H
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
% f( ]; h  _: |6 ~+ s5 p; l- Htisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total. y, y, ^. `; d" `" R0 I9 B
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
" @" k& _0 p2 @- rand β-human chorionic gonadotropin was less than
8 X  o% |. B  U5 mIU/mL (normal <5 mIU/mL). Serum follicular7 j6 D) W2 m* G5 Q% y; k9 ]  |, x
stimulating hormone and leuteinizing hormone8 q# _# R4 {8 p0 M3 }2 G  l  H
concentrations were less than 0.05 mIU/mL9 a9 N, R  V: A
(prepubertal).
8 q' F4 F3 r4 K' UThe parents were notified about the laboratory
, e4 @& O9 q  Kresults and were informed that all of the tests were
; N7 v3 n4 A4 F8 d1 a* Bnormal except the testosterone level was high. The
4 E, E& O7 _6 r. dfollow-up visit was arranged within a few weeks to- f; p$ ?5 v7 U: P! P
obtain testicular and abdominal sonograms; how-
* f0 R# l) Q3 o' ?$ gever, the family did not return for 4 months.
7 ?6 k7 W" R2 j7 N/ _: I6 hPhysical examination at this time revealed that the
( h8 A: L4 \  h! J% ?child had grown 2.5 cm in 4 months and had gained9 T# b4 K! K! ]  g( B' U
2 kg of weight. Physical examination remained
$ e1 ?1 c. c5 E7 \3 b" \+ |3 k6 sunchanged. Surprisingly, the pubic hair almost com-
2 x& g& |" `8 ^/ Z2 l: w4 Lpletely disappeared except for a few vellous hairs at& [) F7 B* Z) X" |: h: i
the base of the phallus. Testicular volume was still 21 X6 ~8 y. i& o1 f* x
mL, and the size of the penis remained unchanged.
( e/ ^' a0 w" g" j; t, {) yThe mother also said that the boy was no longer hav-( X; J  M' T$ w, E& l9 r; B$ S3 B
ing frequent erections.: _+ u! L- }6 I0 p. V# Z& {
Both parents were again questioned about use of; n( `( u$ f4 ^  t
any ointment/creams that they may have applied to  [  t) `& ~/ ]9 {. b$ M4 t
the child’s skin. This time the father admitted the  F" Q$ w* ]9 r4 w5 A1 g1 A& Y! C
Topical Testosterone Exposure / Bhowmick et al 541
  x) x. M% U- E/ \use of testosterone gel twice daily that he was apply-
) ~" }9 L4 J; n: L+ j( H1 E/ f+ cing over his own shoulders, chest, and back area for8 |9 m7 W. b. h1 s
a year. The father also revealed he was embarrassed
( c: i$ o- P" @8 q; Pto disclose that he was using a testosterone gel pre-
) V% J7 Z3 |; R7 ]* Kscribed by his family physician for decreased libido
3 k4 S! D% S# ?8 R4 \. Tsecondary to depression.7 n; E, u/ e1 v1 ~$ C
The child slept in the same bed with parents.  h1 N% U# g, @0 F
The father would hug the baby and hold him on his9 n8 W! P7 n. I. T
chest for a considerable period of time, causing sig-
% l$ b6 W+ L% Mnificant bare skin contact between baby and father.( U5 ?% i) t8 M+ b6 E4 y
The father also admitted that after the phone call,
) r/ i' {/ Z) h. ^( k3 b6 u2 }8 @when he learned the testosterone level in the baby
) P; b0 B/ X5 h: {8 C4 ?was high, he then read the product information
( u9 g) }3 a0 B  Dpacket and concluded that it was most likely the rea-
7 O* E3 r. e. Y) H- Wson for the child’s virilization. At that time, they" d2 t- I* E8 U3 `8 |+ ]0 f
decided to put the baby in a separate bed, and the. h5 S( \( H' W/ P/ F
father was not hugging him with bare skin and had( Z* m# v" M! ^) `
been using protective clothing. A repeat testosterone
5 G/ n: n# m; h; R) I9 Ltest was ordered, but the family did not go to the
1 N% F& P  Y+ q' o: Q& \# h8 Q# [' L" Olaboratory to obtain the test.; i6 t! c  S" f# x' r& H
Discussion
6 o9 Q) t1 A% G. E% m- [1 PPrecocious puberty in boys is defined as secondary% y" B0 P: R' A
sexual development before 9 years of age.1,4- A  E/ A' j/ F/ W# |
Precocious puberty is termed as central (true) when& n8 p4 _4 U. H, j# ?' P& k
it is caused by the premature activation of hypo-! H* S  X( g4 D" R8 W
thalamic pituitary gonadal axis. CPP is more com-; S0 ]! e0 [) i7 U: }
mon in girls than in boys.1,3 Most boys with CPP
# T) o3 h) K, W9 ]; imay have a central nervous system lesion that is" x  V) H+ B) P: T
responsible for the early activation of the hypothal-
) i- u7 A  W$ [0 R5 `8 h3 Jamic pituitary gonadal axis.1-3 Thus, greater empha-
5 r6 c8 g$ C$ psis has been given to neuroradiologic imaging in
. W7 _. D! Z( M4 jboys with precocious puberty. In addition to viril-+ R% k* H: \$ O
ization, the clinical hallmark of CPP is the symmet-
0 ^8 M* b( H$ |, f* Grical testicular growth secondary to stimulation by
1 g  d0 H/ G  F) Y; Z6 [: X) X6 j: G" dgonadotropins.1,3/ K' c$ W* ]0 Z" y* b0 g8 q
Gonadotropin-independent peripheral preco-/ L: c9 f+ R/ F. m
cious puberty in boys also results from inappropriate7 K0 }5 O, a, N8 H) f
androgenic stimulation from either endogenous or
9 S% a# y- t0 ]7 {& G1 hexogenous sources, nonpituitary gonadotropin stim-
9 _4 S- b  r, O1 D, pulation, and rare activating mutations.3 Virilizing
# N. f, a5 O4 F( F4 E- tcongenital adrenal hyperplasia producing excessive
2 n/ F2 o1 a& sadrenal androgens is a common cause of precocious( V0 _5 q; ~! F/ V/ ~0 H$ y' W
puberty in boys.3,4) @' v. p5 F$ [
The most common form of congenital adrenal
% ^$ M8 `) g* Q* ?: U% L) p) thyperplasia is the 21-hydroxylase enzyme deficiency.
" A% _& {/ a) V" u5 K2 ?0 P& c+ P' qThe 11-β hydroxylase deficiency may also result in
" x' \# J1 p( ~  m8 X) ^2 v9 Cexcessive adrenal androgen production, and rarely,
) `. i/ I3 j8 m) l1 H' zan adrenal tumor may also cause adrenal androgen
  o) v" W6 ~5 ^: B2 X4 _excess.1,3& W8 f7 |6 e0 u* I1 t& h  L1 ~$ l+ s
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" V+ h$ N& w$ y) d0 s2 m3 w542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
1 ^7 y. p9 `# |3 [, wA unique entity of male-limited gonadotropin-. ]5 i1 w- T% }! e% e+ c3 l6 x+ y
independent precocious puberty, which is also known
* ~; n! h* {4 x; J3 q; E0 \# v6 j) xas testotoxicosis, may cause precocious puberty at a3 x0 h% B9 B) c! ], ]" l! i# Y3 S
very young age. The physical findings in these boys# }4 P: F3 D# c8 o- m* C
with this disorder are full pubertal development,
: p1 w3 `  f7 Q# dincluding bilateral testicular growth, similar to boys* e2 S# q9 r# T$ D
with CPP. The gonadotropin levels in this disorder
* A! C. Z# D( uare suppressed to prepubertal levels and do not show5 X+ y4 p% T0 g: O
pubertal response of gonadotropin after gonadotropin-
5 D( }! \! f, T; xreleasing hormone stimulation. This is a sex-linked
9 d* \" e& l- w  ]1 b" N8 Oautosomal dominant disorder that affects only
" E- `5 j3 y3 J; o3 B7 {  Gmales; therefore, other male members of the family
, N* O6 O$ u5 emay have similar precocious puberty.33 T5 K1 Y. o+ X! g' o  p' ~) E
In our patient, physical examination was incon-
; I4 t/ N0 z) ysistent with true precocious puberty since his testi-
& F) h0 Z2 J* V  T! ^: U0 |9 Ccles were prepubertal in size. However, testotoxicosis3 \* V: O. r1 d" S1 n: c9 @& `
was in the differential diagnosis because his father( `. a2 v, S& o6 b$ Z; I0 W3 ~
started puberty somewhat early, and occasionally,
/ s5 e  O+ b% H+ d+ S! ~% qtesticular enlargement is not that evident in the
5 q, S4 E" S4 X' t* H; o" ~beginning of this process.1 In the absence of a neg-4 s/ |! }7 w4 S" Z7 I) s7 D
ative initial history of androgen exposure, our3 i$ W( F  |4 \' I
biggest concern was virilizing adrenal hyperplasia,; x1 ^3 d5 B! |  u4 l+ q0 ~/ z; }: n& a: P
either 21-hydroxylase deficiency or 11-β hydroxylase
, U' g4 K/ ~  _) ]deficiency. Those diagnoses were excluded by find-
' l/ [; |% h& A% Ting the normal level of adrenal steroids.
' J0 l$ b# _% TThe diagnosis of exogenous androgens was strongly
5 [! w4 v, K& _- ~% esuspected in a follow-up visit after 4 months because
6 T( N0 S3 P5 Y7 h8 qthe physical examination revealed the complete disap-1 ^5 N2 s1 W: R  c: s
pearance of pubic hair, normal growth velocity, and
& B0 U( a: b% Idecreased erections. The father admitted using a testos-
6 k5 n5 {/ H+ ?& f6 \terone gel, which he concealed at first visit. He was- r. R' J0 o4 i3 f1 u7 Z5 P* h
using it rather frequently, twice a day. The Physicians’& v2 P- ?- G4 j: d4 n6 G0 j- g2 r
Desk Reference, or package insert of this product, gel or
; i/ ^( b5 g6 U! T; w2 Lcream, cautions about dermal testosterone transfer to
  _) J: C& K" ~unprotected females through direct skin exposure.
, b: d9 Z1 {- |& \6 y3 RSerum testosterone level was found to be 2 times the
) N1 _. k0 _% e) N( V: mbaseline value in those females who were exposed to% D. [( P& S* g- U8 e
even 15 minutes of direct skin contact with their male
5 k) I9 R$ V- f4 s/ Vpartners.6 However, when a shirt covered the applica-) v* s" q) Z5 q4 `7 K5 f* A3 f3 x
tion site, this testosterone transfer was prevented.
' c' E! C0 W; X- Y% V3 I8 q# D, nOur patient’s testosterone level was 60 ng/mL,
# ~4 _9 _& m; x  _which was clearly high. Some studies suggest that
- Y' c( V3 b: `8 f& @( Bdermal conversion of testosterone to dihydrotestos-& u8 `3 G$ O  V7 r
terone, which is a more potent metabolite, is more  r3 C# J8 N5 R
active in young children exposed to testosterone
4 _9 T2 ~3 F2 a+ E: }exogenously7; however, we did not measure a dihy-
7 N3 G5 @; m; sdrotestosterone level in our patient. In addition to
. I; j7 h  U# L# ]: C( P$ Fvirilization, exposure to exogenous testosterone in% C4 a5 T+ d, g
children results in an increase in growth velocity and2 Z/ r/ |+ Y+ E; a( r4 l; Q, E
advanced bone age, as seen in our patient.
- \7 X6 q) X& z* @# g! zThe long-term effect of androgen exposure during9 H" o9 v: e% M/ D9 y7 q; ?% z+ ~
early childhood on pubertal development and final9 |* Q2 @3 a9 U& u) o
adult height are not fully known and always remain
/ T2 H1 V) a+ P0 D9 w# `1 Ba concern. Children treated with short-term testos-
7 R6 }* b( Z/ n1 \* {- g+ jterone injection or topical androgen may exhibit some7 S& L& @0 i* P- I) F0 t- s
acceleration of the skeletal maturation; however, after+ k) c4 N  I' f8 D- A
cessation of treatment, the rate of bone maturation& B& r9 A/ |) z/ m# ?8 ?- A- x
decelerates and gradually returns to normal.8,91 h# q& v- t) I+ m' b" p, M3 e# r! Y
There are conflicting reports and controversy
/ ~3 q' \* I- ], c6 `over the effect of early androgen exposure on adult4 e( b  r1 W, U
penile length.10,11 Some reports suggest subnormal
; [" ?- `$ E0 K7 s7 |0 E( vadult penile length, apparently because of downreg-
* Z, c$ J) Z+ l; w  ]ulation of androgen receptor number.10,12 However,
' f% s( j. P; p+ o4 f" U! r+ h% O6 RSutherland et al13 did not find a correlation between
2 e2 Z! @& R. }2 e( h. m6 ^# o$ W/ y) Zchildhood testosterone exposure and reduced adult# ~' _: s9 A0 P: M4 V; R' ^
penile length in clinical studies.
0 L$ s3 J0 C8 l+ A5 {8 DNonetheless, we do not believe our patient is
( D( A1 U1 a1 _1 w3 Sgoing to experience any of the untoward effects from
- i" b+ ]& V$ I! ?1 W. p/ _testosterone exposure as mentioned earlier because+ x2 Q% E! C6 n
the exposure was not for a prolonged period of time.- X: I" j! A+ c# ^
Although the bone age was advanced at the time of8 F3 ?# j: Y8 w  a) I! y; b/ b( \
diagnosis, the child had a normal growth velocity at
  x1 O8 I) T! L2 M& Athe follow-up visit. It is hoped that his final adult3 N- c9 Y7 y& Z$ v+ U& e
height will not be affected.
+ w7 q/ k3 \5 W6 R% y9 XAlthough rarely reported, the widespread avail-; |/ H7 A! [4 s1 l
ability of androgen products in our society may' L8 ?/ ?+ N+ g1 J+ r
indeed cause more virilization in male or female
9 e1 O0 s/ g  z+ B4 cchildren than one would realize. Exposure to andro-
. X& o( |% Q6 n; vgen products must be considered and specific ques-
& c: ]2 x( @5 z& D2 R9 h0 @& L& otioning about the use of a testosterone product or2 ~% v9 k: Z6 o- }, x; W/ |
gel should be asked of the family members during" [9 c% A/ A9 r1 t! g- R
the evaluation of any children who present with vir-. f) W' e2 j2 y# z
ilization or peripheral precocious puberty. The diag-- v5 T4 \* N$ `5 x
nosis can be established by just a few tests and by0 D: Q8 t- E" \9 p
appropriate history. The inability to obtain such a
: u3 e6 c5 r( p  Q% M6 chistory, or failure to ask the specific questions, may. g! C4 L, W1 W2 v& I
result in extensive, unnecessary, and expensive
$ _0 j4 Z8 M* F& Q) |investigation. The primary care physician should be
5 ?7 Q# y' G: b8 j5 m8 M  zaware of this fact, because most of these children" a3 a* I7 D' Q. w( _1 i8 H
may initially present in their practice. The Physicians’+ H% O0 b, ?: M5 Y( c5 n0 ~2 L
Desk Reference and package insert should also put a8 c6 N- I( v& w) W1 f( Y
warning about the virilizing effect on a male or
  v( a/ p( O( q& ~female child who might come in contact with some-
8 e: v% t2 O2 }. N$ j$ @one using any of these products.3 M' K3 Y% |' W) M; ]
References
2 k5 }( i: b0 J0 O* X1. Styne DM. The testes: disorder of sexual differentiation8 g0 u; k0 ?/ X( M" T5 L+ M
and puberty in the male. In: Sperling MA, ed. Pediatric
. Z" ^  x) b6 g5 sEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
( @. d( `* v2 p% e" Q0 X2002: 565-628." ?9 x) X1 E% E, u) l
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
& O+ V, r6 y8 z9 \0 Spuberty 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
* e0 z. k% E5 m
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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