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鄉下的妹子太便宜,一次四個都要了[12P]

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Sexual Precocity in a 16-Month-Old
3 o: Y% O6 s! v( M& qBoy Induced by Indirect Topical1 L+ _9 [: ?5 \" p8 q1 Y) w* Q
Exposure to Testosterone7 N5 @+ K  i; |+ R6 a
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2! e$ T0 |! V( x% e1 E2 n
and Kenneth R. Rettig, MD1& N/ j# ?9 x- P) j0 @. _
Clinical Pediatrics
5 h7 Q$ J) T7 S# P; c$ PVolume 46 Number 60 L0 O: R! |! V! J& U' Y( u9 a8 u
July 2007 540-543
8 w5 X& L* b# l© 2007 Sage Publications4 t+ l+ C3 p7 ^, y% m
10.1177/0009922806296651
' r8 A4 X( P/ U: ^' mhttp://clp.sagepub.com% ?! t) m  g- d5 X
hosted at
+ {9 l: G! y  e& Chttp://online.sagepub.com) c" S2 n2 |! g3 M( o
Precocious puberty in boys, central or peripheral,
7 n: G! ~$ [, J- N7 g- g' gis a significant concern for physicians. Central( z0 ]0 {( u7 T# e1 x, N0 X
precocious puberty (CPP), which is mediated
3 u7 U" A, w/ q% }6 z/ ?through the hypothalamic pituitary gonadal axis, has* P% i+ z# U) P
a higher incidence of organic central nervous system6 Y. _8 A( @; N1 `# m5 _
lesions in boys.1,2 Virilization in boys, as manifested
+ o2 R  _: L+ Q9 Xby enlargement of the penis, development of pubic& ^! l: E/ D4 W
hair, and facial acne without enlargement of testi-
$ m8 w, X5 f; V8 |% _+ {& C9 f, Fcles, suggests peripheral or pseudopuberty.1-3 We
+ u5 l9 u7 u3 G7 h' xreport a 16-month-old boy who presented with the. M' q! B: w6 e% Z! X
enlargement of the phallus and pubic hair develop-
. a$ R8 E! ^$ \0 r) tment without testicular enlargement, which was due; Q# y. S1 b2 B3 U" P
to the unintentional exposure to androgen gel used by9 x2 x  V* X' d8 j/ \
the father. The family initially concealed this infor-
% A- P7 t$ T/ |" ?mation, resulting in an extensive work-up for this4 D% h9 h6 Z' j
child. Given the widespread and easy availability of' e4 {/ q! H2 I$ q* D
testosterone gel and cream, we believe this is proba-: p4 D  P1 k- D8 |8 g
bly more common than the rare case report in the
: g0 Q' T8 x$ p. v0 fliterature.45 D" Q' s/ o3 l! I+ `' ^# c
Patient Report
/ {% s& {- j! G4 ~4 cA 16-month-old white child was referred to the+ _% M* A9 B. V1 D; C. H/ z" |2 w
endocrine clinic by his pediatrician with the concern
! G: R, w# W# Jof early sexual development. His mother noticed  T; d( w: s6 n) @
light colored pubic hair development when he was
: p! N5 C+ v" d1 g. B4 R' VFrom the 1Division of Pediatric Endocrinology, 2University of
1 a  p; C! |9 N; c! z8 k5 V0 F, SSouth Alabama Medical Center, Mobile, Alabama.
1 m$ D3 d) x$ B7 D2 o+ o) @Address correspondence to: Samar K. Bhowmick, MD, FACE,6 [& D# M3 Z& |( L# v/ P# P5 M
Professor of Pediatrics, University of South Alabama, College of
+ N" }* D; a& v" s4 e# ZMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
7 z/ K% }- w- \. ee-mail: [email protected].
& w$ G& i- }5 J! l2 Kabout 6 to 7 months old, which progressively became
  M. l; j  s+ q3 i! ndarker. She was also concerned about the enlarge-& s/ e3 v$ H/ ^# j! G* J  P
ment of his penis and frequent erections. The child! m6 B; z1 q1 g8 @, Y
was the product of a full-term normal delivery, with
$ d" v2 v! U. k6 q( za birth weight of 7 lb 14 oz, and birth length of. |. g7 M. a1 O2 }# |: j" M
20 inches. He was breast-fed throughout the first year
% G9 O4 S( M' S5 R- p/ i- U6 }of life and was still receiving breast milk along with
' q& C$ Q  A$ E/ msolid food. He had no hospitalizations or surgery,4 U: S6 ]) @9 n
and his psychosocial and psychomotor development8 Y0 x% x2 w+ A+ |0 X( \8 m
was age appropriate.& _% @5 P7 [) y3 p
The family history was remarkable for the father,0 s2 v+ I+ \, Q
who was diagnosed with hypothyroidism at age 16,
( t% s) ?; }0 Y& e* [which was treated with thyroxine. The father’s
) o* w; h% k# [. w! `- mheight was 6 feet, and he went through a somewhat
5 R6 q# `; q3 e. zearly puberty and had stopped growing by age 14.
! S- }; M1 T0 e2 p6 g) ZThe father denied taking any other medication. The
2 L/ J8 k0 @( y! G- U4 X  qchild’s mother was in good health. Her menarche7 H; J, \) q0 q: n. N/ F
was at 11 years of age, and her height was at 5 feet
. |: H, M5 J$ u5 inches. There was no other family history of pre-
# f  \, [7 L' _* W* |0 Ncocious sexual development in the first-degree rela-( m. ^6 L' [& u- P$ k! Q
tives. There were no siblings.
* g1 K; p, ~. ^6 Q8 w3 [( X+ _Physical Examination
2 f0 J- @  v5 X% @% i0 DThe physical examination revealed a very active,
* z( N) e( M' l' t/ `* vplayful, and healthy boy. The vital signs documented
& l+ y9 h: T$ Q# R' k+ |a blood pressure of 85/50 mm Hg, his length was+ ?" p& i( G$ _+ n; Q) p/ u" k& E
90 cm (>97th percentile), and his weight was 14.4 kg; T) L7 ]& }& N) T+ X4 ^
(also >97th percentile). The observed yearly growth
1 o# t4 N- X& `velocity was 30 cm (12 inches). The examination of3 @& E1 [4 `  ?- f
the neck revealed no thyroid enlargement.
; q  ^( [" j. {9 UThe genitourinary examination was remarkable for
: t/ ]: P9 M% D, _/ M/ J+ senlargement of the penis, with a stretched length of" s( p( |- {& l
8 cm and a width of 2 cm. The glans penis was very well
% j: v. b& n# N) G0 J# [6 rdeveloped. The pubic hair was Tanner II, mostly around. |2 P6 K; ?! N" b0 {5 K0 W
540
# i/ _$ U% `5 u; b' v2 |, qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, R) Z( W# b8 f- rthe base of the phallus and was dark and curled. The
: k- w' B+ a1 V8 q+ M1 [( @) jtesticular volume was prepubertal at 2 mL each.7 j! A" h+ k- b2 f
The skin was moist and smooth and somewhat' F. ~9 u0 D8 y. K8 v- \7 |# S
oily. No axillary hair was noted. There were no
2 \4 R0 _# G9 Q( y1 L/ f2 Cabnormal skin pigmentations or café-au-lait spots.
8 n; h$ ]( U2 b+ H/ NNeurologic evaluation showed deep tendon reflex 2+5 [4 J: j1 N: O0 R, ^, G+ M
bilateral and symmetrical. There was no suggestion
8 L1 o. A/ I8 v8 {of papilledema.1 D  R7 I. m9 ^( Q
Laboratory Evaluation7 |2 H9 _5 t0 O/ K
The bone age was consistent with 28 months by$ G' E' C# ?& o( b
using the standard of Greulich and Pyle at a chrono-
% y& [( `7 \; E1 x/ m" Z7 v) Glogic age of 16 months (advanced).5 Chromosomal* L# X8 R7 V5 P6 R) q/ }
karyotype was 46XY. The thyroid function test; t; r! u9 Y* S" L
showed a free T4 of 1.69 ng/dL, and thyroid stimu-0 e" n( d- \$ G: k3 ^
lating hormone level was 1.3 µIU/mL (both normal).
, z) y! T2 n9 ~The concentrations of serum electrolytes, blood
; @3 g; \1 t0 Curea nitrogen, creatinine, and calcium all were$ S+ G6 D8 u' L, M
within normal range for his age. The concentration1 k4 N- a* |% D: v" t/ O7 h
of serum 17-hydroxyprogesterone was 16 ng/dL: c7 v6 f; E' S8 o! O5 U
(normal, 3 to 90 ng/dL), androstenedione was 20
0 o) f& |# z% M0 B# qng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-2 t: a& [. |- \) w
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
% S2 L. W8 m4 w" J+ Xdesoxycorticosterone was 4.3 ng/dL (normal, 7 to& ^3 l5 j! [8 ~/ j* I  f. g
49ng/dL), 11-desoxycortisol (specific compound S)$ k/ a' ^- j4 U  p
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-: _+ g* t* L+ ^" W; e2 K+ i
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total; \" ?- T4 R: W9 ]' g% Q
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
% p3 ^! C" k+ C  O$ x& E  s. ~and β-human chorionic gonadotropin was less than  B! H9 n9 o% q! h
5 mIU/mL (normal <5 mIU/mL). Serum follicular% s* t! P: @% l- ]6 k
stimulating hormone and leuteinizing hormone+ r) f, T3 C0 s1 z8 X  ^: d- g
concentrations were less than 0.05 mIU/mL
) A, J& D" r2 ~: D5 K! L6 ](prepubertal).
+ Z+ N0 e- Z: ^: ^4 X- Q! |The parents were notified about the laboratory) P6 O" r$ g& F0 m
results and were informed that all of the tests were
! B- k' c" P1 vnormal except the testosterone level was high. The
- r( W) n7 H2 A. K, g+ Jfollow-up visit was arranged within a few weeks to
9 V  W1 _  M" U# K' f7 mobtain testicular and abdominal sonograms; how-. \3 f0 E1 r( \5 r
ever, the family did not return for 4 months.9 B2 r, z9 y0 F
Physical examination at this time revealed that the( a/ {5 D$ ^7 R1 L
child had grown 2.5 cm in 4 months and had gained
% l; t% l6 I6 Z, Q2 kg of weight. Physical examination remained
6 l; {" c" L7 Dunchanged. Surprisingly, the pubic hair almost com-7 g( f' c* w0 e6 B' V, b- k
pletely disappeared except for a few vellous hairs at3 X1 N5 _* N" f( D6 `% [
the base of the phallus. Testicular volume was still 2: j+ g) Z5 ^+ w9 W4 [2 H$ Y
mL, and the size of the penis remained unchanged.3 I: |! W+ d0 [9 Y: y) P
The mother also said that the boy was no longer hav-7 }; k2 T3 l3 Z. ^# @
ing frequent erections.% D/ x: v: m3 `3 v8 @2 d/ m
Both parents were again questioned about use of
  d; ^' L8 J* A6 H& S6 zany ointment/creams that they may have applied to
' [+ |8 U1 y+ P' q; uthe child’s skin. This time the father admitted the, @2 s7 U2 e" Y5 u6 t5 z$ Q
Topical Testosterone Exposure / Bhowmick et al 541! r$ c- ?/ @' V: E7 E
use of testosterone gel twice daily that he was apply-
6 b& `5 P& v+ wing over his own shoulders, chest, and back area for
0 g3 I. {# s- `3 N; t! va year. The father also revealed he was embarrassed
7 @0 `. I# I1 W; Eto disclose that he was using a testosterone gel pre-) v# e: J2 D. |$ L$ g# a
scribed by his family physician for decreased libido
6 [' z: k& [% A7 O7 T6 `% fsecondary to depression.
+ J( e! `- ~  T9 J2 h9 QThe child slept in the same bed with parents.
8 g; J3 N) j% k  b; q% ?The father would hug the baby and hold him on his& z  W/ a% j- X/ s4 ]
chest for a considerable period of time, causing sig-' E+ h+ Z0 [% r- g
nificant bare skin contact between baby and father.; D1 j* ^+ @7 h/ e
The father also admitted that after the phone call,6 W+ \4 B$ V4 s1 ?& [6 c
when he learned the testosterone level in the baby' V# {& X/ ^, k9 X, w5 [' x: h' Q
was high, he then read the product information& @' l9 w2 \/ l( z
packet and concluded that it was most likely the rea-. J5 t+ J% @% R9 G
son for the child’s virilization. At that time, they  u: g+ L  Q- q
decided to put the baby in a separate bed, and the
. Y" n( z3 o: S+ n. Z% C$ z4 tfather was not hugging him with bare skin and had! z1 J& y9 h8 `& u/ E8 g
been using protective clothing. A repeat testosterone
7 p1 |: b! H, |% `5 ~1 a5 @test was ordered, but the family did not go to the- R( O8 T+ m  D' ?: |* `' O
laboratory to obtain the test.
4 g; C1 h$ ^% B4 T" s( h& f. _1 {Discussion
2 P4 k  e( P: V% z) ^0 n. u1 K6 ZPrecocious puberty in boys is defined as secondary/ V- s$ w4 q- Q! [/ a
sexual development before 9 years of age.1,4+ p% D: w, F% s# \: O) e
Precocious puberty is termed as central (true) when5 e0 S# ^7 l9 a8 R+ E
it is caused by the premature activation of hypo-7 i8 y9 ?, O; Z6 X! U% y& y6 Q
thalamic pituitary gonadal axis. CPP is more com-* Q- D+ G. m% ]. w8 v6 @( l
mon in girls than in boys.1,3 Most boys with CPP
3 m+ c3 {! ^% R! t, ?" j8 Fmay have a central nervous system lesion that is/ P2 k3 y  \5 D+ }* t% Z, K
responsible for the early activation of the hypothal-* n( V# c. g6 t/ k! Q5 X
amic pituitary gonadal axis.1-3 Thus, greater empha-, R! S+ s! R* q7 L+ H8 e' ^" x8 b  E$ ]
sis has been given to neuroradiologic imaging in
6 F' V1 t. |4 aboys with precocious puberty. In addition to viril-
/ `! Z6 m- A5 e" [- zization, the clinical hallmark of CPP is the symmet-
1 X* o) I" w2 Trical testicular growth secondary to stimulation by1 B: l4 n. X1 H8 i, G& r
gonadotropins.1,3
3 Z% Z9 L# J* q) ?. i- @Gonadotropin-independent peripheral preco-
! p4 w9 I" W# k6 e! B8 K3 hcious puberty in boys also results from inappropriate
9 A# i3 p* ]! A$ l" O) p* L# @7 N+ Candrogenic stimulation from either endogenous or3 j/ u9 c$ A2 m2 u, S$ T
exogenous sources, nonpituitary gonadotropin stim-' b1 o" L5 `' h& k( n7 w, I# j  X3 c
ulation, and rare activating mutations.3 Virilizing
: [5 z7 C8 r  w8 z" {congenital adrenal hyperplasia producing excessive
1 N% A) V7 Z# a& Y1 D( oadrenal androgens is a common cause of precocious' n0 s! m% @# P( j$ B& m% z
puberty in boys.3,4
% X5 Q# N. I& W% w0 l7 R% M. wThe most common form of congenital adrenal6 l& n; W( W( W+ C2 Z. w. j
hyperplasia is the 21-hydroxylase enzyme deficiency.
2 K4 q* ]7 Q) ?+ \  S+ m, U: \9 d$ iThe 11-β hydroxylase deficiency may also result in5 a  r( C% C9 N
excessive adrenal androgen production, and rarely,
3 n5 O+ D0 R5 |' e) c# c6 lan adrenal tumor may also cause adrenal androgen( [: ^1 e) O& l% D( ?/ X4 C
excess.1,3
& t3 I$ C/ d2 T' u$ x9 f  w% U0 cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ ^* _- c. k" N% l, Q6 k
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
5 [0 e6 o4 f% }7 a* u9 G& EA unique entity of male-limited gonadotropin-2 y) R5 t) S( b4 C" b/ \8 t
independent precocious puberty, which is also known/ h; S0 r: o* a1 R0 h! W
as testotoxicosis, may cause precocious puberty at a  v" q3 c. l& I- L
very young age. The physical findings in these boys6 A  _3 D  l6 ]" ^
with this disorder are full pubertal development,7 Z9 ]2 i5 g: E$ F7 Q  D
including bilateral testicular growth, similar to boys
& L) s* V9 h0 P. k, u! hwith CPP. The gonadotropin levels in this disorder  h; H4 X3 S( @2 e' `; o3 ?0 N8 G, O
are suppressed to prepubertal levels and do not show, `" j5 H' \/ a6 |' O0 C3 K0 f+ Y7 b
pubertal response of gonadotropin after gonadotropin-
3 }, b* M, {& k/ jreleasing hormone stimulation. This is a sex-linked. w9 S# e+ R) ^8 _0 s1 `5 G, X
autosomal dominant disorder that affects only; A* I/ }( R9 t
males; therefore, other male members of the family' X% k) ^+ F- t
may have similar precocious puberty.3
8 T/ D' z3 ?) }" g0 EIn our patient, physical examination was incon-
( {" @3 n& T) q% T. Ysistent with true precocious puberty since his testi-2 f$ s  b& K8 E  C; F) b
cles were prepubertal in size. However, testotoxicosis1 O% n% e( ^, ~
was in the differential diagnosis because his father
! m8 V# Q$ l8 `started puberty somewhat early, and occasionally,
; _/ _6 M2 U+ x# f' Dtesticular enlargement is not that evident in the+ E& |( C5 O) p: B6 V7 a7 t
beginning of this process.1 In the absence of a neg-+ V. q, q2 C6 p3 h+ {) ~6 F
ative initial history of androgen exposure, our
% Y" U% n. t1 T0 X7 {0 Bbiggest concern was virilizing adrenal hyperplasia,. I  R* z2 h, H; H0 v$ q  m3 j
either 21-hydroxylase deficiency or 11-β hydroxylase* {) C" [7 O; c" ]
deficiency. Those diagnoses were excluded by find-
" N" [5 _+ C2 A8 `% Xing the normal level of adrenal steroids.
9 U' S, N: A" N: h3 ?' k) sThe diagnosis of exogenous androgens was strongly
, V& b0 K' S+ |6 u2 H3 d2 q$ bsuspected in a follow-up visit after 4 months because3 d2 O9 b& Q, n- |" _
the physical examination revealed the complete disap-& q8 H/ o5 W8 P/ q$ ^) g
pearance of pubic hair, normal growth velocity, and
9 L3 u* p* b5 Q% }decreased erections. The father admitted using a testos-
. H0 B# G/ M, }' a0 hterone gel, which he concealed at first visit. He was
- Y; w& ?8 T+ g# J+ [. ^using it rather frequently, twice a day. The Physicians’* e9 |9 s, k1 B) ~1 e- _1 z' b
Desk Reference, or package insert of this product, gel or
' H- z- b9 l: c' d$ y8 Scream, cautions about dermal testosterone transfer to5 [$ P5 x+ |$ F, s
unprotected females through direct skin exposure.
7 N  l/ a$ F# N7 e, dSerum testosterone level was found to be 2 times the
& Z/ ~; v; ?  Z  S$ {0 jbaseline value in those females who were exposed to
  z6 ^8 y! i/ geven 15 minutes of direct skin contact with their male: V4 u. ]; j+ H
partners.6 However, when a shirt covered the applica-6 A' \. y/ D+ p0 q* F
tion site, this testosterone transfer was prevented.
% z$ R# L, x, r7 N4 \; o5 LOur patient’s testosterone level was 60 ng/mL,; [4 d8 S! z5 X4 E; q% H2 A1 L
which was clearly high. Some studies suggest that0 r/ P4 w4 F8 B! b
dermal conversion of testosterone to dihydrotestos-
' M1 B) e8 h- H, F( dterone, which is a more potent metabolite, is more
3 \7 h+ N  v6 ]  c6 O( Tactive in young children exposed to testosterone
; }  G! U3 @9 H- a8 R* k5 c4 \exogenously7; however, we did not measure a dihy-
# H" \) ~1 ^$ {5 z; w' T) Q, Ydrotestosterone level in our patient. In addition to
! I1 T% O, B$ I& e0 b, {7 Gvirilization, exposure to exogenous testosterone in$ T: a4 D6 a5 j' P# O  Q7 p$ B& l
children results in an increase in growth velocity and7 f; g* v* d( t# C% K5 \( k
advanced bone age, as seen in our patient.
6 y/ |% z; Z; d1 d2 CThe long-term effect of androgen exposure during. _( `5 L# O- p" i! N. ]
early childhood on pubertal development and final+ V: m2 k5 C7 R' a/ c0 b
adult height are not fully known and always remain
- G0 k3 Z8 `$ W/ ta concern. Children treated with short-term testos-  e4 H5 D+ {1 v8 h
terone injection or topical androgen may exhibit some
% q+ v5 S! G/ P- b, Yacceleration of the skeletal maturation; however, after
4 w5 H4 ]/ |' M, |+ w# ecessation of treatment, the rate of bone maturation
6 A, _( O" C/ K. m. h  S4 adecelerates and gradually returns to normal.8,9
2 s, U  r4 ~3 I0 p. h" nThere are conflicting reports and controversy8 W/ m2 e6 N% G# T0 [; B6 b" a
over the effect of early androgen exposure on adult4 U& _- F' `4 j% Y, |/ T. G
penile length.10,11 Some reports suggest subnormal
; f5 X! |3 B" F) Y7 sadult penile length, apparently because of downreg-
/ g% Q/ o" G( Q+ O4 A7 P7 qulation of androgen receptor number.10,12 However,( i- W5 Y7 M4 M9 k1 }
Sutherland et al13 did not find a correlation between- n& |# I8 i) n! P( X
childhood testosterone exposure and reduced adult
# J' I& Q  p' I" M9 spenile length in clinical studies.
# E3 {8 ^% _: Z$ Y) j9 Y0 z/ {Nonetheless, we do not believe our patient is/ D# J/ F5 m5 F0 @' T
going to experience any of the untoward effects from
/ U+ V) W$ m+ {- Mtestosterone exposure as mentioned earlier because
$ h$ H  q5 l4 x+ M, N6 R) Mthe exposure was not for a prolonged period of time.5 u0 s' M" u) ?) \
Although the bone age was advanced at the time of
1 v- K) O) z+ z  ^; D0 {diagnosis, the child had a normal growth velocity at+ j/ `  X" ]: b
the follow-up visit. It is hoped that his final adult
$ \6 v# G5 r% N; K) u$ C' k9 lheight will not be affected.
. s* ?8 N, ?* c. s" O+ Z- ^Although rarely reported, the widespread avail-
; ?! k, ^: o; B9 Bability of androgen products in our society may9 l) a2 `# }/ b
indeed cause more virilization in male or female
) C6 O  M9 c/ o+ w4 A6 n! ^: E5 Kchildren than one would realize. Exposure to andro-
% a% ?: U: N: X2 `gen products must be considered and specific ques-
1 W! U8 r9 P3 `. ttioning about the use of a testosterone product or
' O: @. e, l; qgel should be asked of the family members during
( U( y! R( z, A9 Wthe evaluation of any children who present with vir-+ e+ h& t: }) n4 \
ilization or peripheral precocious puberty. The diag-. s+ Q4 s6 V8 f- z6 z
nosis can be established by just a few tests and by
! r& T1 A& a# e# W, o) eappropriate history. The inability to obtain such a0 `$ C- `( n2 x" s; _' p
history, or failure to ask the specific questions, may, D: a4 Q. V4 }7 T8 T3 j4 h7 b
result in extensive, unnecessary, and expensive
& f* B$ }; h- T  K8 Jinvestigation. The primary care physician should be
% ?  ?5 p- j  C& _' `( E. aaware of this fact, because most of these children
( v- H7 j% V+ h( o  Bmay initially present in their practice. The Physicians’
* {6 L) Z  ~' |7 l/ J& BDesk Reference and package insert should also put a  z6 u* u1 [( x" n9 k
warning about the virilizing effect on a male or
3 H$ e/ J0 s# @/ V' j) Z/ jfemale child who might come in contact with some-+ V! r, W8 j6 |" F( t5 r3 N
one using any of these products., ?( i: R7 B, i9 L& Y
References
. C% e+ F# [1 R' Y- b1. Styne DM. The testes: disorder of sexual differentiation
0 W  j2 ^  H" P! |+ U) r% S$ p/ q: |and puberty in the male. In: Sperling MA, ed. Pediatric5 i+ |7 ~& z: X1 }& q. Y3 r. ^% w9 S
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
# b1 Z  X- N2 Q2002: 565-628.
: k2 s/ P$ Y# R7 s2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
! U4 L& z3 X( A( G/ ?9 vpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old3 j1 M) y3 T& c* P6 p9 `" |; h3 U6 I
Boy Induced by Indirect Topical
- z' q9 ?9 Z! {Exposure to Testosterone& `$ y  C1 h, W/ d
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
% V- `+ r$ \$ f3 X( i( P" e- ~and Kenneth R. Rettig, MD1
% G- i9 w. j& x; f( [+ g' SClinical Pediatrics% k: ]3 ]1 a" h* T) V" n
Volume 46 Number 6$ S* G3 u) R5 Q: A, B5 O2 E
July 2007 540-5433 w' P3 V' U6 f% Q! \
© 2007 Sage Publications' S5 }; [+ k3 I
10.1177/0009922806296651& U% [2 l% b( F
http://clp.sagepub.com* |$ [* |. k) k& O0 f) Z# N
hosted at
6 Q' n  N/ F4 h0 Ihttp://online.sagepub.com
% ?$ k' v) t" W3 |+ F3 aPrecocious puberty in boys, central or peripheral,
- I2 |; `0 h. U+ v2 w, tis a significant concern for physicians. Central6 k4 D( L/ v. t. _
precocious puberty (CPP), which is mediated
4 B+ \' H  F' Tthrough the hypothalamic pituitary gonadal axis, has
3 Q$ @- O) e# Y9 j3 ?. v4 sa higher incidence of organic central nervous system8 s6 [; z' h+ ^& v+ V
lesions in boys.1,2 Virilization in boys, as manifested
4 w* ?+ c4 v" @0 ?4 W% _9 M, M! Sby enlargement of the penis, development of pubic0 |  R6 {) [! \9 m5 q0 x
hair, and facial acne without enlargement of testi-1 G4 i! U5 I$ Q8 F5 v5 Z+ C8 B, Z0 H* d
cles, suggests peripheral or pseudopuberty.1-3 We
( [' ?% l5 t/ z, |3 N  oreport a 16-month-old boy who presented with the
. |' ~3 u7 C2 }: H# `6 D  K1 Aenlargement of the phallus and pubic hair develop-1 a" u3 @) {% s' ?
ment without testicular enlargement, which was due
6 j1 w: B5 E5 r, D" Q" h7 rto the unintentional exposure to androgen gel used by
- p  y- {5 U: C: X3 H, @( s3 P7 }the father. The family initially concealed this infor-
  v1 \0 n8 }8 X+ _mation, resulting in an extensive work-up for this
, O2 u. p8 k( g- ?; N. wchild. Given the widespread and easy availability of
, s1 F) M" F2 H; i4 U7 l& Btestosterone gel and cream, we believe this is proba-
+ E; Y. g5 u0 z! `9 y  a0 Z4 ?bly more common than the rare case report in the
7 u  a1 J1 g( K2 K1 ]. N% C$ tliterature.4
! K5 L% R6 d. `. b3 v+ k1 aPatient Report" U( X, d' @7 t+ r
A 16-month-old white child was referred to the
) J( }& |: ~) u+ |! d# sendocrine clinic by his pediatrician with the concern, k- N/ S4 R: U( z- I
of early sexual development. His mother noticed5 s& Y: S( k; v4 W2 ?
light colored pubic hair development when he was4 z' A' C; Q# {" q$ _$ c- O- D
From the 1Division of Pediatric Endocrinology, 2University of
( H  ?& L1 N" t5 C( A! n+ GSouth Alabama Medical Center, Mobile, Alabama.
6 X9 z% t% r/ [" b  d; K& fAddress correspondence to: Samar K. Bhowmick, MD, FACE,
( Z8 J; N: @1 E% N2 J: DProfessor of Pediatrics, University of South Alabama, College of8 x2 k5 p8 j9 u, s. O
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;% h7 J7 m; e; ~6 U
e-mail: [email protected].
- [6 e* e) A, i3 d) \about 6 to 7 months old, which progressively became3 d6 n' C& u. A% T
darker. She was also concerned about the enlarge-* N: p$ ]9 P0 S+ G! j
ment of his penis and frequent erections. The child% W0 Y, X, y% w
was the product of a full-term normal delivery, with/ X/ F! K4 X! |/ U
a birth weight of 7 lb 14 oz, and birth length of
; s. M( `5 X/ q+ O% m# |! h20 inches. He was breast-fed throughout the first year  O/ z/ P$ ]# H! m
of life and was still receiving breast milk along with& r1 K9 ?0 F) `4 R- U4 T1 h4 L1 k
solid food. He had no hospitalizations or surgery,2 T2 R8 k& x: B6 [; s0 n7 N
and his psychosocial and psychomotor development
2 Z- F- C6 r, L, h# kwas age appropriate.
$ N6 c3 b! c/ r  ^The family history was remarkable for the father,2 y' D8 w8 b6 d
who was diagnosed with hypothyroidism at age 16,: g; ~& Y( ]0 X% Q4 `' l% r& v
which was treated with thyroxine. The father’s
( J0 G8 m0 `3 K& M5 L6 Dheight was 6 feet, and he went through a somewhat+ X  g7 k' Q) K# Q4 i3 m0 O2 R
early puberty and had stopped growing by age 14.6 ?" {( B! O, _$ K* k" `$ P3 K
The father denied taking any other medication. The
6 _. k  S% w7 R% Nchild’s mother was in good health. Her menarche9 g7 f8 H# O! X% K! r6 D
was at 11 years of age, and her height was at 5 feet. Y% C6 K. |5 W
5 inches. There was no other family history of pre-
2 v/ n( y2 ?% q$ v' w% ]2 f' z# ^cocious sexual development in the first-degree rela-
8 @2 i% v/ ~$ Y* ltives. There were no siblings.
& Q% Z5 O! N: R" ~Physical Examination
2 `- ]& H, `) t( O, B0 Q8 }The physical examination revealed a very active,2 G- x4 u1 e5 w6 K1 G7 U
playful, and healthy boy. The vital signs documented' R4 }7 q4 ~/ f# G0 |, j1 ]
a blood pressure of 85/50 mm Hg, his length was' D0 q/ m) k7 b( E. \7 k
90 cm (>97th percentile), and his weight was 14.4 kg5 ^8 G+ m- |2 m1 k% S
(also >97th percentile). The observed yearly growth
2 V$ |! l( V) ?( T" W! P% pvelocity was 30 cm (12 inches). The examination of
8 h4 o) N$ J0 ^" c$ V& i2 Cthe neck revealed no thyroid enlargement.% ~& j3 @% I6 e
The genitourinary examination was remarkable for
6 L3 S3 N0 t5 {' O% K# J, renlargement of the penis, with a stretched length of, [! Q0 u5 W( y
8 cm and a width of 2 cm. The glans penis was very well& v- Y$ l$ m% j
developed. The pubic hair was Tanner II, mostly around' P3 u. x& {1 n# U# _9 n! W
540
" b6 Z" u+ g) W$ k2 D1 rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; T! b7 C! _6 V5 gthe base of the phallus and was dark and curled. The
. z# s# g/ f( o' S* Wtesticular volume was prepubertal at 2 mL each.8 u, L! p! Z! C) J. W  T" t
The skin was moist and smooth and somewhat
% Z" Z' {" [2 Qoily. No axillary hair was noted. There were no
1 p* g' K' M* Z/ W2 v/ y2 x- L) tabnormal skin pigmentations or café-au-lait spots.
7 q9 |: C- e2 B4 [& t" KNeurologic evaluation showed deep tendon reflex 2+
  w) ?7 e: p- \1 @- B* |bilateral and symmetrical. There was no suggestion# M0 T' t1 F' S( U4 p
of papilledema.3 {; Y7 [* A: B2 }
Laboratory Evaluation
( G6 k) H, W8 [4 i8 j; R/ SThe bone age was consistent with 28 months by
  t+ @- d9 ^3 ~$ V; @' _using the standard of Greulich and Pyle at a chrono-  M' A6 V4 R* k4 J  o% I) L* @" r
logic age of 16 months (advanced).5 Chromosomal9 `+ i' K/ _/ M: v1 N+ ?$ E
karyotype was 46XY. The thyroid function test
$ b6 z, x  y3 T7 Jshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
0 J- n( F* S3 ?+ }lating hormone level was 1.3 µIU/mL (both normal).
. ~2 ?4 w+ R# i: J( TThe concentrations of serum electrolytes, blood
$ t' F9 w, i7 z7 U0 j8 {7 E3 uurea nitrogen, creatinine, and calcium all were9 w. C3 L% M, r  M5 y- \
within normal range for his age. The concentration
7 s6 \# G% w% E( V2 d) Eof serum 17-hydroxyprogesterone was 16 ng/dL
- A4 A+ d# h/ n+ \2 ?; e+ B2 }' I(normal, 3 to 90 ng/dL), androstenedione was 20. R6 @0 p* W& t) _% q0 B# q
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-, s8 {4 i# S$ A, r3 p; d: ~
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
, j, N: e, H* L; L% X% O) A6 ^desoxycorticosterone was 4.3 ng/dL (normal, 7 to% d( g1 |" P! O/ n) P& O: i/ T4 X4 e
49ng/dL), 11-desoxycortisol (specific compound S)
3 p$ F8 W1 Y8 v: m. ~4 P  Wwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
$ P0 `9 \. ]1 P9 Ltisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
' g/ A( x) w7 G7 X! x, g! Y8 w8 @2 Ntestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
* s; X/ O: j( `  d! hand β-human chorionic gonadotropin was less than
5 j: j/ b4 J, e; Z. k6 N8 o5 mIU/mL (normal <5 mIU/mL). Serum follicular% [& }/ t% }+ Y; P
stimulating hormone and leuteinizing hormone
2 g0 i  z! s2 \concentrations were less than 0.05 mIU/mL
3 K; a! F/ _9 O, p$ L4 n: H7 z(prepubertal).9 Y/ l# j; y8 p
The parents were notified about the laboratory
) \2 D" a. {7 l" V) }- x+ G% oresults and were informed that all of the tests were
. e5 K' F1 Z9 X2 ]; Z# D5 L+ J) Mnormal except the testosterone level was high. The& b- n2 j1 [/ l3 b" w9 x
follow-up visit was arranged within a few weeks to6 Z( c+ g; n% j
obtain testicular and abdominal sonograms; how-
6 h, j7 @- `7 S( Uever, the family did not return for 4 months.
2 T! `# b" h4 K- C0 I$ HPhysical examination at this time revealed that the
3 o  v% G. Z7 g' i$ @4 w% ychild had grown 2.5 cm in 4 months and had gained; |' [5 \- }: w3 K5 _. e% k& l
2 kg of weight. Physical examination remained
+ H# S+ S3 d; m& \) funchanged. Surprisingly, the pubic hair almost com-
- G+ W3 R5 J3 I+ J  @0 Spletely disappeared except for a few vellous hairs at
. L: {; M5 |& j1 C8 z  Z0 U6 Wthe base of the phallus. Testicular volume was still 28 z  d# M8 E7 |/ ?( q8 F1 b
mL, and the size of the penis remained unchanged.
% t7 y& v) M. Q8 l! |! pThe mother also said that the boy was no longer hav-# ~. x, s* `" T5 e! Y+ I$ ~
ing frequent erections.
9 d; W7 S4 J. S; D! z  M  _Both parents were again questioned about use of
# w$ t  k& Q1 h; O. h7 B0 jany ointment/creams that they may have applied to
% R( a/ p) ]; m! t- Athe child’s skin. This time the father admitted the& Z2 J1 s7 C/ @1 a& P7 D
Topical Testosterone Exposure / Bhowmick et al 541
* \6 r; @1 B2 D1 z+ ^use of testosterone gel twice daily that he was apply-9 p; F5 q/ _& }9 b* p9 X
ing over his own shoulders, chest, and back area for
. @8 d, e" g4 y, O5 W# i- na year. The father also revealed he was embarrassed
& G  I& ?! E! r4 c! d6 xto disclose that he was using a testosterone gel pre-
/ }$ P6 O8 t, M+ X9 x2 [) i5 hscribed by his family physician for decreased libido1 _; X5 e$ g% Y
secondary to depression.
" {# |/ O3 I: y& Y" D- g0 n9 m, mThe child slept in the same bed with parents.
8 D, A& y/ `9 j6 C8 B$ z8 f+ jThe father would hug the baby and hold him on his; P; C3 |( `1 P5 n6 f1 i0 M) u9 i1 E9 @
chest for a considerable period of time, causing sig-0 K3 G$ |1 z- c* p; ^
nificant bare skin contact between baby and father./ ]- A- S- C) r# o
The father also admitted that after the phone call,. _& T! p; R2 J: ]3 w0 x
when he learned the testosterone level in the baby
+ f8 T, P/ @. J1 y" w0 f9 Jwas high, he then read the product information
6 T6 l' P/ O3 Z# R3 P2 hpacket and concluded that it was most likely the rea-
: y9 M9 O# G7 @) json for the child’s virilization. At that time, they
, _8 Z& P" f9 b' ^( h9 Sdecided to put the baby in a separate bed, and the
& N8 S1 ]* u# O9 @father was not hugging him with bare skin and had5 ~. P+ G) M* u+ [2 B! h8 x* D
been using protective clothing. A repeat testosterone/ a! ]8 ~! r; S9 P
test was ordered, but the family did not go to the* C* {& Y2 h- _9 |8 G
laboratory to obtain the test.
4 g; d$ ]) n9 XDiscussion
* ]2 b; l% w5 D8 _! k- rPrecocious puberty in boys is defined as secondary* R  \, c3 m! G0 i
sexual development before 9 years of age.1,4
7 p6 l6 }$ r% w0 g& K  Y2 RPrecocious puberty is termed as central (true) when0 q9 g) l- c, [0 L9 `
it is caused by the premature activation of hypo-# c! ^' N' i  ~- ~4 \3 Y
thalamic pituitary gonadal axis. CPP is more com-
# B0 y# a: H2 L9 n: Amon in girls than in boys.1,3 Most boys with CPP
, n' e# ^6 R) h" [$ J* t! s- Qmay have a central nervous system lesion that is
3 T& p! `6 f6 ?3 Kresponsible for the early activation of the hypothal-+ o! L* a/ E: n6 {2 u8 V7 K% q
amic pituitary gonadal axis.1-3 Thus, greater empha-
- ?4 z" Y, V1 z9 M, tsis has been given to neuroradiologic imaging in
: n" b* Y+ g2 L$ ^( c9 L3 X4 E- r( qboys with precocious puberty. In addition to viril-6 p5 E1 ]' i9 `: F/ h/ i
ization, the clinical hallmark of CPP is the symmet-# g; ~1 f" V' }5 J8 {: Q/ e; z, D
rical testicular growth secondary to stimulation by' Z, f5 z8 P5 @0 d; G1 f3 P0 x. H% G
gonadotropins.1,3( G1 ?1 l. T7 \7 X4 U9 n3 C, h
Gonadotropin-independent peripheral preco-
# g, p6 p: u% ~& W! K$ [, M, P; [6 ]cious puberty in boys also results from inappropriate
8 p5 K4 x/ n3 s+ h3 ]* iandrogenic stimulation from either endogenous or
7 J6 w+ I" a2 }9 W, Z+ Q! iexogenous sources, nonpituitary gonadotropin stim-! {# @: Z' P$ u" L" c' f2 ~# y% ?" ~
ulation, and rare activating mutations.3 Virilizing
9 {& P2 O1 ?  n% w5 ^- T4 i& U# mcongenital adrenal hyperplasia producing excessive/ T: o5 u" j) j
adrenal androgens is a common cause of precocious
! ]# [. {% _$ m) Dpuberty in boys.3,4
, W; K- }( K8 `) |' H) ~# E5 jThe most common form of congenital adrenal
* N- }: h2 K; |7 i/ e! v& v% _! s% n' ?hyperplasia is the 21-hydroxylase enzyme deficiency.
% h3 g* H$ c9 D; GThe 11-β hydroxylase deficiency may also result in7 b  w( `: p, e' ]/ z
excessive adrenal androgen production, and rarely,
5 J1 n1 `/ l5 g3 }an adrenal tumor may also cause adrenal androgen$ c* p  K4 ~9 d( N, C0 ~
excess.1,31 @% y# N2 E( Z, m, l0 v: x9 ?
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* ]& N) A1 z" k) E
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007- C( Z& w7 W: O5 `6 b
A unique entity of male-limited gonadotropin-
7 \9 ^" Z6 b3 c8 Q4 zindependent precocious puberty, which is also known* E- E( ^, y% V
as testotoxicosis, may cause precocious puberty at a( |& C8 L$ D( [
very young age. The physical findings in these boys# D( x# D3 l7 m, }7 K9 U
with this disorder are full pubertal development,  L$ o, L1 Q  s% z0 S
including bilateral testicular growth, similar to boys- |6 x0 T% Q9 y0 U7 [# D( m" t
with CPP. The gonadotropin levels in this disorder4 Y9 |, P0 s9 T6 z6 J; _. l. g
are suppressed to prepubertal levels and do not show. g3 c8 H  r0 x4 X0 u$ d4 t
pubertal response of gonadotropin after gonadotropin-
* I( S+ `* C" Yreleasing hormone stimulation. This is a sex-linked9 y8 S. E+ v) T$ {
autosomal dominant disorder that affects only
( r/ |1 a' H6 g' }males; therefore, other male members of the family
5 Q8 ]) G  F1 U8 m( tmay have similar precocious puberty.32 K, T0 i+ U# Q* V) [; ?/ c
In our patient, physical examination was incon-5 H0 H, }" a2 s- t. z4 p
sistent with true precocious puberty since his testi-
0 y, X, S7 e4 hcles were prepubertal in size. However, testotoxicosis4 }* y+ C% N* G. W* V3 @
was in the differential diagnosis because his father/ \. f6 w8 e6 @+ y) I7 h7 i" e' [- M
started puberty somewhat early, and occasionally,
1 N, T& X. ~; e/ w4 K+ otesticular enlargement is not that evident in the
% y. I+ l+ {& v$ O+ m9 h% `beginning of this process.1 In the absence of a neg-
5 A, a, B6 u, q! d* @/ H6 a' rative initial history of androgen exposure, our4 b' s. m6 M+ g6 m+ x  S+ Z! Y: b
biggest concern was virilizing adrenal hyperplasia,, T0 \/ y5 y; F3 x
either 21-hydroxylase deficiency or 11-β hydroxylase
, A; p8 T8 [( h. Ydeficiency. Those diagnoses were excluded by find-- {/ c8 u* q9 J2 s
ing the normal level of adrenal steroids.
* B) f3 }+ s' A+ fThe diagnosis of exogenous androgens was strongly
* f+ X  t% f3 ?1 Asuspected in a follow-up visit after 4 months because
3 D; |9 r/ a4 X% }the physical examination revealed the complete disap-3 G7 N/ _4 b7 `0 z, s$ G3 N
pearance of pubic hair, normal growth velocity, and
% O2 j. y* J3 g& c' K* _, Tdecreased erections. The father admitted using a testos-
8 w% ]; u+ `5 ]terone gel, which he concealed at first visit. He was) T& v$ z: e% u8 R; J: ]* k- v2 Y
using it rather frequently, twice a day. The Physicians’# D( r( J6 T; e$ R
Desk Reference, or package insert of this product, gel or/ w0 {3 }9 T1 D% J6 i9 W: O% b
cream, cautions about dermal testosterone transfer to
; v+ I1 r* W& ~, X; Q' R7 runprotected females through direct skin exposure.
7 w$ q$ L  e4 |' W- k$ nSerum testosterone level was found to be 2 times the
' `4 H9 e( s: z' Cbaseline value in those females who were exposed to7 k. _5 Y% `3 S
even 15 minutes of direct skin contact with their male; }+ j/ @/ u; Z& w& Q* ~5 l
partners.6 However, when a shirt covered the applica-' \, s# L! y# A, s: a
tion site, this testosterone transfer was prevented.
5 A3 m! M1 x/ i7 x/ ZOur patient’s testosterone level was 60 ng/mL,
# l2 F, H9 M  M0 Uwhich was clearly high. Some studies suggest that
1 g; T# D0 Q* sdermal conversion of testosterone to dihydrotestos-
* {! V' U. Y: E( Y$ _$ [terone, which is a more potent metabolite, is more
' ~+ S3 j9 r" {* O# ?* R% A; eactive in young children exposed to testosterone
5 x. c1 r* v' Q/ b" O- vexogenously7; however, we did not measure a dihy-
3 ~- F6 O1 a3 Odrotestosterone level in our patient. In addition to/ t! K+ F2 O7 }4 a* P& b% X1 A
virilization, exposure to exogenous testosterone in% g' z1 j+ N5 O( p& O- g+ U1 K! g
children results in an increase in growth velocity and+ l: k& ^, h* u8 L( ~
advanced bone age, as seen in our patient.& r" z' K0 y. _, P
The long-term effect of androgen exposure during
' e0 N! U; K( ^* F) B8 Uearly childhood on pubertal development and final
+ |8 ~# B* `( s+ q" F( c; gadult height are not fully known and always remain
$ g% `( R: d& h' Q  D3 Ba concern. Children treated with short-term testos-
- E3 p8 B  `2 J; C1 n( a; [terone injection or topical androgen may exhibit some$ {2 b9 s% U# |+ H: b
acceleration of the skeletal maturation; however, after
- t$ f) l3 s  X' Z7 G" bcessation of treatment, the rate of bone maturation
, ^/ T9 g) c* N. Pdecelerates and gradually returns to normal.8,9. @/ F6 {+ y- E7 y4 N$ ~
There are conflicting reports and controversy) x& S: N7 K* k# L
over the effect of early androgen exposure on adult! I. b/ _; X7 d3 B9 e" Q  \- [& Y4 l
penile length.10,11 Some reports suggest subnormal' L6 \9 T+ b4 a" ~3 }" P: d) e
adult penile length, apparently because of downreg-/ W. E) n. {/ N
ulation of androgen receptor number.10,12 However,
0 z- k1 U0 @- E$ mSutherland et al13 did not find a correlation between" M  D* x* {5 G- N2 r1 k8 I
childhood testosterone exposure and reduced adult
6 f; P# ?: }7 Gpenile length in clinical studies.
# u; y% i# D6 ]Nonetheless, we do not believe our patient is& m% f  i2 A7 [) t
going to experience any of the untoward effects from5 H. x9 k5 M( T* t
testosterone exposure as mentioned earlier because3 m. U+ C- |2 ~) Q7 l* E4 I, L( r
the exposure was not for a prolonged period of time.! k9 I9 k; m$ ^3 h( [; K3 `8 j
Although the bone age was advanced at the time of
* a- \7 S8 p0 ^+ P  j( kdiagnosis, the child had a normal growth velocity at& o" N" }8 |6 ?
the follow-up visit. It is hoped that his final adult
* Q% f: b6 |9 g. @height will not be affected.. e$ B9 N2 J( a- N0 g! S  h& [
Although rarely reported, the widespread avail-5 H) T/ c2 i, I. _4 x( U, o# X+ w
ability of androgen products in our society may. j- R. c  _0 N! W  J1 R; d
indeed cause more virilization in male or female4 W1 ?+ P1 F2 I) s. B/ d
children than one would realize. Exposure to andro-
0 h0 E  O9 i0 p& W1 C3 ggen products must be considered and specific ques-: J) S3 Y$ X% d& g0 j
tioning about the use of a testosterone product or) e% D/ F0 y% ?3 h" ?
gel should be asked of the family members during
7 f6 e! G# {* U, I* Y. Jthe evaluation of any children who present with vir-
$ c7 t, |2 Z8 Y. ~  cilization or peripheral precocious puberty. The diag-
* C+ y2 k4 a7 l. r: v) J' e+ Znosis can be established by just a few tests and by
$ J  C1 I! K* }appropriate history. The inability to obtain such a$ o! _9 h7 V# P! z; ~+ ~
history, or failure to ask the specific questions, may
% J/ d+ L0 s8 U- s1 Aresult in extensive, unnecessary, and expensive
9 f0 r- I: W- S, D6 @9 iinvestigation. The primary care physician should be
4 N5 j8 F8 q/ ]8 p1 k  i4 saware of this fact, because most of these children
) p% M* `5 Q$ wmay initially present in their practice. The Physicians’; o0 g8 y# u! e# N6 d& {
Desk Reference and package insert should also put a
) N- C8 F  a3 I" \. d' nwarning about the virilizing effect on a male or
* g/ p- H6 t, ^0 ~+ yfemale child who might come in contact with some-
7 i; Q1 j$ x# s& yone using any of these products.4 Q0 F8 i! j( X3 J
References3 B- h4 O3 E' M4 c, g9 _
1. Styne DM. The testes: disorder of sexual differentiation
' S, Y  M; D) vand puberty in the male. In: Sperling MA, ed. Pediatric
8 v: T% M: V4 k2 zEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
6 q, D. Q7 ]$ b3 H3 ^7 i: ?  t0 T2002: 565-628.- a' F/ A' f7 ]6 I9 V
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious" F* k1 Q7 D! S/ [  Q4 p1 J
puberty 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
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
' i; @/ W' P( C, p
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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