Swyer syndrome
Hereditary/Genetic:
Gonadal
dysgenesis, XY female type; Gene
map locus Xp22.11-p21.2;
point mutations or
deletions of the SRY gene
Description:
This type of gonadal defect is characterized by a female phenotype, normal to tall stature, bilateral streak or dysgenetic gonads, and a 46,XY karyotype. This XY gonadal dysgenesis is a heterogenous condition with variant forms resulting from a structural abnormality on Y chromosome, a mutation in SRY gene or a mutation in autosomal genes. The syndrome is sometimes called "pure gonadal dysgenesis," but this designation may also refer to gonadal dysgenesis with a 46,XX karyotype (GONADAL DYSGENESIS, 46,XX).
Symptoms:
Very frequentMay also include: Small fallopian tubes; Small uterus; Dysgenetic testes; Eunuchoid proportion; Absence of puberty. Generalized edema or lymphedema
In females with delayed puberty, a pelvic ultrasound can be performed to confirm the presence or absence of ovaries.
Additionally, blood can be taken for a karyogram, which identifies the full set of chromoomes of the female. Females with Swyer syndrome will have both X and Y chromosomes rather than a set of two X chromosomes, which is normal for females.
Treatment:
Symptoms of Swyer syndrome can be treated with hormone replacement therapy (HRT), although surgical procedures are not uncommon. A typical HRT regimen includes estrogen and progesterone treatment to regulate menstruation and induce the female's secondary sexual characteristics. In some cases, the fibrous streak gonads are surgically removed as a precautionary measure against the development of gonadoblastomas a type of cancer of the gonads.
May 30, 2008
-----------------------------------------
306100
Swyer syndrome
| GONADAL DYSGENESIS, XY FEMALE TYPE; GDXY |
Alternative titles; symbols
SWYER SYNDROMEGonadal dysgenesis, XY female type, is associated with point mutations or deletions of the SRY gene (480000), but also in some cases with changes in the X chromosome.
At birth the patients with the XY female type of gonadal dysgenesis (Swyer syndrome) appear to be normal females; however, they do not develop secondary sexual characteristics at puberty, do not menstruate, and have 'streak gonads.' They are chromatin negative and have a 46,XY karyotype.
Affected
sisters were reported by Cohen
and Shaw (1965), and twins by Frasier
et al. (1964). Sternberg
et al. (1968) observed 3 cases, each in a different sibship
of a family
connected through normal females (proposita, maternal cousin, and
maternal
aunt). A high incidence of neoplasia (gonadoblastomas and germinomas)
in streak
gonads of patients with the XY karyotype was claimed by Taylor
et al. (1966). 
Patients are
of normal stature and have no somatic stigmata of Turner
syndrome except, of course, the lack of secondary sexual
characteristics and
streak gonads. In this condition, as in the testicular feminization
syndrome (300068),
it was at first unclear whether the gene that was responsible was on
the X
chromosome or on an autosome and expressed only in chromosomal males.
Whether
the abnormal gene directly suppresses testis-determining loci on the
chromosome
or blocks some early stage of testicular morphogenesis was also
unknown. The
sisters reported by Cohen
and Shaw (1965) had a marker autosome, which was present also
in the mother.
They referred to another instance of XY 'sisters' with an abnormal
autosome. One
of their 2 patients had gonadoblastoma.
Two sisters
reported by Fine
et al. (1962) were of normal stature but were chromatin
negative. One of
these cases and 1 of those reported by Baron
et al. (1962) had gonadoblastoma. In the last family, 2
'females' and a male
were affected, the male showing no testes. All 3 sibs were
sex-chromatin
negative. Barr
et al. (1967) reported on a sibship containing 2 genetic
males. The first,
who had male pseudohermaphroditism, was reared as a female; he
developed signs
of masculinization at puberty and had undescended but otherwise normal
testes
and small fallopian tubes. The second genetic male (180 cm tall) had
pure
gonadal dysgenesis with small uterus and streak gonads. This patient
was at
first thought to have the testicular feminization syndrome. An
unaffected sister
had a son with perineal hypospadias (urethral orifice at the base of
the penis).
The sibship reported by Chemke
et al. (1970) was similar to that of Barr
et al. (1967). Espiner
et al. (1970) described 5 XY females in 3 sibships of 2
generations. They
emphasized that the affected persons were unusually tall for females.
The height
of patients with XY gonadal dysgenesis (unusually great for females) is
probably
explained by androgen production in the streak gonad (Rose
et al., 1974). Clitoromegaly is present in some cases.
Rushton
(1979) pointed out that the streak gonads of this disorder
differ from those
of the 45,X Turner syndrome in the presence of calcification and the
increased
hazard of gonadoblastoma. Comparative studies of the frequency of
gonadoblastoma
in Turner mosaics with normal or rearranged Y chromosomes have
suggested that
the integrity of the Y chromosome, and in particular the presence of
the distal
fluorescent band Yqh, is required in these mosaics for the tumor to
develop; no
cases with distal deletions of the fluorescent band on Yq had been
reported (Lukusa
et al., 1986).
Moreira-Filho
et al. (1979) suggested that there are 3 forms of Swyer
syndrome (defined as
streak gonads without other somatic features of the Turner syndrome and
with a
normal 46,XY karyotype). (1) Sporadic testicular agenesis syndrome
(STAS)
corresponds to H-Y negative Swyer syndrome. (2) Familial testicular
agenesis
syndrome (FTAS) is H-Y negative Swyer syndrome showing an X-linked
recessive
pedigree pattern. The mutation is probably homologous to that of the
wood
lemming. The phenotype of STAS and FTAS is identical even though the
mutation is
probably on the Y in STAS and on the X in FTAS. (3) In familial
testicular
dysgenesis syndrome (FTDS), the patients are H-Y positive and have a
female
phenotype and streak gonads; the streak gonads may contain testis-like
tumoral
structures. (See report of 3 sisters by Moreira-Filho
et al. (1979) and cases of Wolf
(1979).) The XY gonadal agenesis syndrome is a separate
disorder (see 273250).
Passarge
and
Wolf (1981) pointed out that there are 2 groups of patients
with XY gonadal
dysgenesis (Swyer syndrome) and that each of these may be
heterogeneous. One
group is the H-Y antigen-positive form, which may represent a 'receptor
disease.' The second is the H-Y antigen-negative form, which may be due
to
mutation in the H-Y generating system, either of the structural gene
(presumably
autosomal) or of a controlling gene (on the sex chromosomes). It may be
only the
H-Y antigen-positive cases that are at risk for gonadoblastoma or
dysgerminoma.
See 233300 for discussion of the XX type of gonadal dysgenesis.
Simpson et al. (1981) reported 3 pedigrees of XY gonadal dysgenesis consistent with X-linked inheritance.
German
et
al. (1978) suggested that there is a gene on the X chromosome
that blocks
the testis-determining function of H-Y (which was then a leading
candidate for
TDF, testis-determining factor). However, it was later shown that TDF
and H-Y
antigen map to different parts of the Y chromosome with TDF being
absent and H-Y
antigen being present in XY females with Y short arm deletions (Simpson
et al., 1987). See 278850.
It appeared that 46,XY women had premature ovarian involution, with
resulting
'streak gonads.' Families such as that of Barr
et al. (1967) described above may indicate that the mutation
is 'leaky.' The
pedigree pattern was equally consistent with X-linked recessive or
autosomal
dominant inheritance. Indeed, Allard
et al. (1972) observed transmission through a normal male,
arguing for
autosomal inheritance.
Nazareth et al. (1979) found H-Y positivity in a sporadic case occurring in an offspring of first-cousin parents. They favored recessive inheritance; see 233420.
De
Arce et
al. (1992) contributed further support of this hypothesis by
demonstrating
lack of gonadoblastoma in a 14-year-old girl who was a mosaic for
45X/46X-isodicentric Y. The anomalous Y chromosome showed no
fluorescent distal
Yq. In another patient, an 8-year-old girl with 45X/46XY karyotype,
bilateral
gonadoblastoma developed in her rudimentary ovaries at the age of 8.
Her normal
Y chromosome showed the characteristic distal fluorescence seen in her
father's
Y chromosome. Using Y chromosome probes, De
Arce et al. (1992) demonstrated the Y chromosome in the
paraffin blocks of
the ovarian tissue of both girls.
Wachtel
(1979) and Wachtel
et al. (1980) suggested the existence of 4 'causes' of XY
gonadal dysgenesis:
(1) mutational suppression of H-Y structural genes by regulatory
elements of the
X chromosome or failure of an X-linked structural gene (in association
with H-Y
negative somatic cell phenotype); (2) failure of H-Y antigen to engage
its
gonadal receptor (in association with the H-Y positive somatic cell
phenotype);
(3) loss of the critical moiety of H-Y genes in deleted or translocated
Y
chromosome (in association with H-Y negative or intermediate somatic
cell
phenotype); and (4) presence of XY-XO mosaicism.
(Small
deletions in the short arm of the Y chromosome can result in 46,XY
females (Disteche
et al., 1986). The 2 patients reported by Disteche
et al. (1986) had some signs of Turner syndrome, including
congenital
lymphedema and primary amenorrhea with streak gonads, but were of
normal height.
One of the patients had bilateral gonadoblastoma. Several
Y-chromosome-specific
DNA probes were found to be deleted in the 2 patients. DNA analysis
showed that
the 2 deletions were different, but included a common overlapping
region likely
to contain the testis-determining factor (TDF) gene.)
Bernstein
et
al. (1980) observed an abnormal band on Xp in a 46,XY female
and her 46,XY
female fetal sib. Despite the presence of an intact Y chromosome,
neither had
testicular differentiation and both were H-Y negative. Giemsa banding
suggested
duplication of p21 and p22. The maternal grandmother, mother and a
younger
sister, all phenotypically normal, had a karyotype 46,XXp+. The proband
had
profound psychomotor retardation, and both sibs had multiple congenital
malformations. (The second sib was ascertained by amniocentesis for
prenatal
diagnosis followed by elective abortion.) Multiple congenital anomalies
in the
proband included ventricular septal defect, cleft palate, asymmetric
skull and
facies, prognathic jaw, low-set ears, and clinodactyly V. When the girl
died at
5 year of age, postmortem studies showed hypoplastic uterus and
fallopian tubes.
Histologic examination of the uterine adnexa revealed an area of
ovarian stroma
with scattered degenerative follicles. There was no testicular
morphology, and
the external genitalia were those of a normal 5-year-old female. The
second
affected sib, the product of a pregnancy terminated at 20 weeks, showed
ovaries
containing numerous follicles and germ cells. As in the proband, there
was no
evidence of testicular morphology. Wachtel
(1998) referred to other cases of XY sex reversal in subjects
with Xp
duplication and chromosomal abnormalities resembling those in the
family
reported by Bernstein
et al. (1980). This suggested occurrence of a gene on Xp,
duplication of
which can block development of the testis in an XY fetus. The gonads
begin to
develop as ovaries, but in the absence of the second X chromosome, the
germ
cells die, the follicles become atretic, and the ovaries degenerate.
Cytogenetic
duplication of the X chromosome in males is a rare event usually
characterized by a significant degree of phenotypic abnormality, which
can
include sex reversal despite an apparently normal Y chromosome. Arn
et al. (1994) reported 2 half brothers with maternally
inherited cytogenetic
duplications of Xp and sex reversal; the absence of dysmorphic features
in
mother and children was thought to be because of the relatively small
extent of
the duplication. Comparison with previous reports allowed the putative
sex
reversing locus (SRVX) to be assigned to a 5- to 10-Mb segment between
Xp22.11
and Xp21.2, which includes the DMD locus. The regional assignment may
help in
the isolation of SRVX mutations that may cause sex reversal in the 90%
of
sex-reversed women with XY gonadal dysgenesis who do not have
detectable
mutations of the SRY gene.
Mapping
studies by hybridization to DNA from somatic cell hybrids containing
various fragments of the X chromosome suggested that the sequence on
the X
chromosome maps to region Xp22.3-p21 (Page
et al., 1987). Arn
et al. (1994) mapped the SRVX gene to a 5- to 10-Mb segment
between Xp22.11
and Xp21.2, which includes the DMD locus.
Page
et al.
(1987) cloned a 230-kb segment of the human Y chromosome
thought to contain
some or all of the TDF gene. The cloned region spanned the deletion in
a female
who carried all but 160 kb of the Y. Homologous sequences were found
within the
sex-determining region of the mouse Y chromosome.
Jager
et al.
(1990) demonstrated a mutation in SRY in 1 out of 12
sex-reversed XY females
with gonadal dysgenesis who had no large deletions of the short arm of
the Y
chromosome. They found a 4-nucleotide deletion in the part of the SRY
gene that
encodes a conserved DNA-binding motif. A frameshift presumably led to a
nonfunctional protein. Mutation occurred de novo, because the father
had a
normal SRY sequence. This is strong evidence that SRY is TDF. The de
novo G-to-A
mutation led to a change from methionine to isoleucine at a residue
that lies
within the putative DNA-binding motif of SRY and is identical in all
SRY and SRY-related
genes. (TDF and SRY are written Tdy and Sry in the mouse.)
Vilain
et
al. (1992) described a family in which all 5 XY individuals
in 2 generations
had a single basepair substitution resulting in an amino acid change in
the
conserved domain of the SRY open reading frame (480000.0004).
A G-to-C change at nucleotide 588 resulted in substitution of leucine
for valine.
Three of the individuals were XY sex-reversed females and 2 were XY
males. One
of the males had 8 children; all were phenotypic females, 2 of whom
were
sex-reversed XY females carrying the mutation mentioned. Several models
were
proposed to explain association between a sequence variant in SRY and 2
alternative sex phenotypes. These included the existence of alleles at
an
unlinked locus.
McElreavey
et al. (1992) described an XY sex-reversed female with pure
gonadal
dysgenesis who harbored a de novo nonsense mutation in SRY, which
resulted
directly in the formation of a stop codon in the putative DNA-binding
motif. A
C-to-T transition at nucleotide 687 changed a glutamine codon (CAG) to
a
termination codon (TAG); see 480000.0005.
The patient, referred to as the 'propositus,' was a phenotypic female
who
presented at age 20 years for primary amenorrhea. Treatment with
estrogen
induced menstruation and slight enlargement of the breasts which were
underdeveloped. Laparotomy showed 2 streak gonads without germ cells or
remnants
of tubes.
Harley
et
al. (1992) found point mutations in the region of the SRY
gene encoding the
high mobility group (HMG) box in 5 XY females. (The HMG box is related
to that
present in the T-cell-specific, DNA binding protein TCF-1 (142410).)
In 4 cases, the binding activity of mutant SRY protein for the AACAAAG
core
sequence was negligible; in the fifth case, DNA binding was reduced. In
the SRY
gene in a 46,XY female, Muller
et al. (1992) demonstrated an A-to-T transversion of
nucleotide 684 in the
open reading frame, resulting in a change of lysine (AAG) to a stop
codon (UAG).
The patient had gonadoblastoma.
Page
et al.
(1987) advanced several hypotheses to explain the existence
of the X-linked
locus. One hypothesis was inconsistent with the prevailing notion of a
dominantly acting sex-determining factor unique to the Y chromosome and
suggested that the X and Y loci are functionally interchangeable, that
both are
testis determining, and that the X locus is subject to X-chromosome
inactivation. According to this model, sex is determined by the total
number of
expressed X and Y loci: a single dose is female determining, while a
double (or
greater) dose is male determining. The addition of an X-derived
transgene to the
genome of an XX embryo should result in testis differentiation, as long
as that
transgene is not subject to X inactivation. Increased expression of the
X-chromosomal locus could explain the presence of testicular tissue in
XX
hermaphrodites and the rare Y-negative XX males, who lack the TDF locus
of the Y
chromosome. Although some XY females lack TDF as judged by Y-DNA
analysis,
others do not have discernible deletions. These unexplained XY females
may have
point mutations in TDF or in genes that function in conjunction with or
downstream of TDF. The model mentioned above suggests that mutation in
the
X-chromosomal locus (at Xp22.3-p21) could cause XY embryos to develop
as
females.
However, Berta
et al. (1990) and Jager
et al. (1990) presented compelling evidence that the mutation
in one type of
XY female gonadal dysgenesis is not on the X but on the Y chromosome.
In the
human sex-determining region in a 35-kb interval near the
pseudoautosomal
boundary of the Y chromosome, there is a candidate gene for
testis-determining
factor, termed SRY ('sex-reversed, Y,' from mouse terminology), which
is
conserved and specific to the Y chromosome in all mammals tested (Sinclair
et al., 1990); see 480000.
(Cherfas (1991)
stated that SRY stands for 'sex-determining region Y.' This is a nice
presumption and perhaps in its present usage should be so considered,
but it
does not indicate the true historical derivation.)
Moreira-Filho et al. (1979) suggested that the H-Y antigen status in the Swyer syndrome may be a useful indicator of whether removal of the gonads is necessary to avoid malignancy.
Boczkowski (1976); Ghosh et al. (1978); Herbst et al. (1978); Judd et al. (1970); Koopman et al. (1991); Koopman et al. (1990); Mann et al. (1983); Wolf et al. (1980)
Victor A. McKusick - updated : 11/4/1998
Victor A. McKusick : 6/4/1986
terry :
6/3/2004
carol : 3/17/2004
http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=306100
....................................
Swyer syndrome
[Pure gonadal dysgenesis with 46 XY karyotyping (Swyer's syndrome) with gonadoblastoma, dysgerminoma and embryonal carcinoma]PMID: 3370322 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3370322&dopt=Abstract
....................................
Swyer syndrome
http://ghr.nlm.nih.gov/condition/swyer-syndrome
....................................
Swyer syndrome
D I S E A S E : Gonadal dysgenesis, XY female type
Clinical Signs
abnormal
ovaries (Very frequent sign)
external
female genitalia anomalies (Very frequent sign)
late
puberty/hypogonadism (Very frequent sign)
small/atrophic
testes (Very frequent sign)
x-linked
recessive inheritance (Very frequent sign)
Outpatient clinic(s)
http://www.orpha.net/consor/cgi-bin/OC_Exp.php?Lng=GB&Expert=242
....................................
Gonadoblastoma and dysgerminoma associated with 46,XY pure gonadal dysgenesis--a case report....................................
46,XY pure gonadal dysgenesis with gonadoblastoma. A case report.....................................
Association of Turner's syndrome and Swyer's syndrome in the same family.PMID: 10803875 [PubMed - indexed for MEDLINE]
..................
http://www.medhelp.org/www/ais/24_RELATED.HTM
===========================
Abstracts and Studies
..................
Swyer syndrome: presentation and outcomes - May 2008
..................
A Case of 46,XY Pure Gonadal Dysgenesis with Loss of the Sex-Determining Region of Y Chromosome - April 2008
..................
Swyer syndrome: A five-cases report - Jan 2008..................
Tumors of dysgenetic gonads in Swyer syndrome - Oct 2007
..................
http://www.ncbi.nlm.nih.gov/pubmed/22032815
http://www.jstage.jst.go.jp/article/internalmedicine/50/17/50_1829/_article
http://www.fertstert.org/article/S0015-0282(11)00846-6/abstract
==============================
Support Groups
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Intersex Society of North America
The Intersex Society of North America (ISNA) is devoted to systemic change to end shame, secrecy, and unwanted genital surgeries for people born with an anatomy that someone decided is not standard for male or female.
..................
Androgen
Insensitivity Syndrome
Support Group (AISSG)
..................
AIS Support Group Australia
http://home.vicnet.net.au/~aissg/index.htm
..................
List of International AIS Support Groups
http://www.medhelp.org/www/ais/11_GROUP.HTM
===========================
Codes and external resources
..................
ICD - 10
Q97.3 - Female with 46,XY karyotype
See also:
Q56
| Indeterminate sex and pseudohermaphroditism | ||||||||
| Excludes: | pseudohermaphroditism: · female, with adrenocortical disorder · male, with androgen resistance · with specified chromosomal anomaly |
|||||||
| Q56.0 | Hermaphroditism, not elsewhere classified | |||||||
| Ovotestis |
||||||||
| Q56.1 | Male pseudohermaphroditism, not elsewhere classified | |||||||
| Male pseudohermaphroditism NOS |
||||||||
| Q56.2 | Female pseudohermaphroditism, not elsewhere classified | |||||||
| Female pseudohermaphroditism NOS |
||||||||
| Q56.3 | Pseudohermaphroditism, unspecified | |||||||
| Q56.4 | Indeterminate sex, unspecified | |||||||
| Ambiguous genitalia |
||||||||
ICD - 9
OMIM
-
306100;
MeSH - D006061
Inheritance: X-linked recessive
| Age of onset | Adolescence / Young adulthood |
===========================
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http://www.lymphedemapeople.com/wiki/doku.php?id=lymphedema_and_pain_management
Manual
Lymphatic Drainage (MLD) and Complex Decongestive Therapy (CDT)
Infections
Associated with Lymphedema
http://www.lymphedemapeople.com/wiki/doku.php?id=infections_associated_with_lymphedema
How to Treat a
Lymphedema Wound
http://www.lymphedemapeople.com/wiki/doku.php?id=how_to_treat_a_lymphedema_wound
Fungal
Infections Associated with Lymphe
http://www.lymphedemapeople.com/wiki/doku.php?id=fungal_infections_associated_with_lymphedema
Lymphedema in
Children
http://www.lymphedemapeople.com/wiki/doku.php?id=lymphedema_in_children
Lymphoscintigraphy
http://www.lymphedemapeople.com/wiki/doku.php?id=lymphoscintigraphy
Magnetic
Resonance Imaging
http://www.lymphedemapeople.com/wiki/doku.php?id=magnetic_resonance_imaging
Extraperitoneal
para-aortic lymph node dissection (EPLND)
Axillary
node biopsy
http://www.lymphedemapeople.com/wiki/doku.php?id=axillary_node_biopsy
Sentinel Node
Biopsy
http://www.lymphedemapeople.com/wiki/doku.php?id=sentinel_node_biopsy
Small
Needle Biopsy - Fine Needle Aspiration
http://www.lymphedemapeople.com/wiki/doku.php?id=small_needle_biopsy
Magnetic
Resonance Imaging
http://www.lymphedemapeople.com/wiki/doku.php?id=magnetic_resonance_imaging
Lymphedema
Gene FOXC2
http://www.lymphedemapeople.com/wiki/doku.php?id=lymphedema_gene_foxc2
Lymphedema Gene VEGFC
http://www.lymphedemapeople.com/wiki/doku.php?id=lymphedema_gene_vegfc
Lymphedema Gene SOX18
http://www.lymphedemapeople.com/wiki/doku.php?id=lymphedema_gene_sox18
Lymphedema
and Pregnancy
http://www.lymphedemapeople.com/wiki/doku.php?id=lymphedema_and_pregnancy
Home page: Lymphedema People
http://www.lymphedemapeople.com
Page Updated: Nov. 28, 2011