Nevo Syndrome
Synonym:
Cerebral gigantism nevo type, Sotos Syndrome
| Prevalence: | Exceptional |
| Inheritance: |
|
Causes:
Mutations in the gene encoding lysyl hydroxylase, PLOD1, (chromosome locus 1p36.3-36.2) and is thus allelic to EDS VIA.
Diagnosis:
Family history and physical examination would be the central diagnostic tools. Lymphatic dysplasia could be verified through the use of a lymphoscintigraphy test.
Symptoms: (Nevo Syndrome)
Complications:
Treatment:
Treatment might include surgery for the physical anomolies, therapy for the motor development complications and the establishment of a lymphedema mangement program.
The lymphedema treatment program would include: Manual lymphatic drainage; compression wraps or compression bandages (using short stretch bandages), compression garments, compression sleeves.
June 8, 2008
-----------------------------------------
| NEVO SYNDROME |
Nevo
et al.
(1974) described an inbred Israeli family in which 2 sibs and
their cousin
had increased growth, kyphosis, prominent forehead, volar edema,
spindle-shaped
fingers, wrist drop, talipes, hyperbilirubinemia, and generalized
hypotonia.
Although the authors considered their cases to be an autosomal
recessive variant
of Sotos syndrome (117550),
Cohen (1989) proposed that these patients had a separate entity, which
they
called the Nevo syndrome. A fourth case was reported by Hilderink
and Brunner (1995). Their patient, a boy born to
consanguineous parents, had
neither lens luxation nor aortic dilatation. 
Al-Gazali
et
al. (1997) described 2 further male cases from unrelated Arab
families with
features similar to those described by Nevo
et al. (1974) but without hyperbilirubinemia. Both had
delayed motor
development. Cognitive function was normal in one at 2 years 10 months
of age.
While the other was too young to assess, social responses appeared
normal. MRI
studies in the older child revealed extreme hyperlordosis of the
cervical spine
and a wide spinal canal suggestive of dural ectasia.
The patient
reported by Dumic
et al. (1998) manifested intrauterine and postpartum
overgrowth, accelerated
osseous maturation, dolichocephaly, highly arched palate, large and
low-set
ears, cryptorchidism, delayed neuropsychologic development, hypotonia,
edema and
contractures of the hands and feet, a single transverse palmar crease,
and
tapering digits. After meningococcal sepsis at age 6 months, he
remained
decerebrate. Thereafter, overgrowth and especially weight gain were
markedly
accelerated until his death at age 18 months, at which time his height
was 103
cm and his weight was 23 kg. In addition to low plasma concentrations
of growth
hormone and insulin-like growth factor, severe insulin resistance was
observed. Dumic
et al. (1998) presumed that a selective defect in
insulin-stimulated glucose
uptake, with preservation of anabolic effect, was one of the causes of
his
'overgrowth without growth hormone,' at least in the last 12 months of
life
after severe brain damage.
Victor A.
McKusick - updated : 3/20/1998
Michael J. Wright - updated : 7/3/1997
Iosif W. Lurie : 9/26/1996
alopez :
3/23/1998
terry : 3/20/1998
mimman : 10/3/1997
alopez : 8/27/1997
alopez : 8/7/1997
jamie : 11/1/1996
carol : 9/27/1996
Copyright © 1966-2004 Johns Hopkins University
http://www3.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=601451
............................
Nevo syndrome.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9508068&dopt=Abstract
............................
Further delineation of Nevo syndrome.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9152832&dopt=Abstract
............................
D I S E A S E : Nevo syndrome
Nevo syndrome is a rare entity characterized by prenatal and postnatal overgrowth, joint laxity, kyphosis, wrist drop and long spindle shaped fingers, and volar edema. Approximately ten cases have been described worldwide, with the majority of these patients being of Arab ethnicity. Some consider that Nevo syndrome is a variant of the kyphoscoliotic type of Ehlers-Danlos syndrome type VIA (EDS VIA), an inherited connective tissue disorder characterized by severe muscular hypotonia and kyphoscoliosis at birth, joint hypermobility, and skin fragility. In contrast, other authors consider it to be a separate entity. Additional clinical signs are a prominent forehead, delayed gross motor development, moderately advanced bone age, dorsiflexion contractures of the feet, hyperbilirubinemia, generalized hypotonia, osteopenia, and lymphedema. Nevo syndrome is transmitted as an autosomal recessive trait. It is caused by mutations in the gene encoding lysyl hydroxylase, PLOD1, (chromosome locus 1p36.3-36.2) and is thus allelic to EDS VIA. Both entities have a very similar clinical phenotype but if there is a difference between Nevo syndrome and EDS VIA, it is in the severity of the joint hypermobility and skin fragility. Management is symptomatic only. Referral to an orthopedic surgeon should be considered and prevention of the secondary complications should be offered. *Author: Orphanet (May 2007)*.
Clinical Signs:
advanced
bone age (Very frequent sign)
blepharophimosis/short
palp. fissures (Very frequent sign)
build/stature/survival
anomalies (Very frequent sign)
eyes
anomalies (Very frequent sign)
foot
anomalies (Very frequent sign)
high
vaulted/narrow palate (Very frequent sign)
hip
anomalies (Very frequent sign)
hypotonia
(Very frequent sign)
knee
anomalies (Very frequent sign)
large
hand (Very frequent sign)
long/large/bulbous
nose (Very frequent sign)
micrognatia/retrognatia
(Very frequent sign)
myopia
(Very frequent sign)
narrow
rib cage (Very frequent sign)
narrow/sloping
shoulders (Very frequent sign)
osteoporosis
(Very frequent sign)
respiratory
distress (Very frequent sign)
scoliosis
(Very frequent sign)
shoulder
dislocation (Very frequent sign)
undescended/ectopic
testes (Very frequent sign)
wrist
anomalies (Very frequent sign)
Outpatient clinic(s)
............................
Nevo syndrome with an NSD1 deletion: a variant of Sotos syndrome?
2006 Jan
Department of Pediatrics, Ibaraki Seinan Medical Center Hospital, Sakai 2190, Sashima, Ibaraki 306-0433, Japan. syouni-kanemoto@seinan-mch.or.jp
A 17-month-old girl with clinical manifestations of Nevo syndrome and NSD1 (nuclear receptor binding SET domain protein 1) deletion is described. Nevo syndrome is a rare overgrowth syndrome showing considerable phenotypic overlap with Sotos syndrome-another, more frequent overgrowth syndrome caused by NSD1 mutations or deletions. About a half of Japanese Sotos syndrome patients carry a 2.2-Mb common deletion encompassing NSD1 and present with frequent brain, cardiovascular, or urinary tract anomalies. The girl we described had the common deletion and showed patent ductus arteriosus, atrial septal defect, vesicoureteral reflux, and bilateral hydronephrosis. It was thus concluded that the clinical manifestations, including the Nevo syndrome phenotype, were caused by the microdeletion.
............................
Nevo syndrome is allelic to the kyphoscoliotic type of the Ehlers-Danlos syndrome (EDS VIA).
Am J Med Genet A. 2005 Mar
Division of Metabolism & Molecular Pediatrics, University Children's Hospital, Steinwiesstrasse 75, CH-8032 Zurich, Switzerland.
We report on seven patients affected with Nevo syndrome, a rare, autosomal recessive disorder characterized by increased perinatal length, kyphosis, muscular hypotonia, and joint laxity. Since its first description by Nevo et al. [1974], only a few cases have been reported. Because some of these patients present clinical features similar to those of the kyphoscoliotic type of Ehlers-Danlos syndrome (EDS VIA), an inherited connective tissue disorder characterized by a deficiency of lysyl hydroxylase due to mutations in PLOD1, we studied seven patients with Nevo syndrome, three of whom have previously been reported, and four of whom are new. In the five patients from whom urine was available, the ratio of total urinary lysyl pyridinoline (LP) to hydroxylysyl pyridinoline (HP) was elevated (8.2, 7.8, 8.6, 3.5, and 4.8, respectively) compared with that in controls (0.20 +/- 0.05, range 0.10-0.38), and similar to that observed in patients with EDS VIA (5.97 +/- 0.99, range 4.3-8.1). Six patients were homozygous for a point mutation in exon 9 of PLOD1 causing a p.R319X nonsense mutation, while one patient was homozygous for a large deletion comprising exon 17 of PLOD1. We conclude that the Nevo syndrome is allelic to and clinically indistinguishable from EDS VIA, and present evidence that increased length at birth and wristdrop, in addition to muscular hypotonia and kyphoscoliosis, should prompt the physician to consider EDS VIA earlier than heretofore. Wiley-Liss, Inc.
............................
| SOTOS SYNDROME |
Alternative titles; symbols
CEREBRAL GIGANTISMGene map locus 5q35A number sign (#) is used with this entry because Sotos syndrome is caused by mutation in the NSD1 gene (606681).
Sotos
et al.
(1964) described 5 children with a disorder characterized by
excessively
rapid growth, acromegalic features, and a nonprogressive cerebral
disorder with
mental retardation. High-arched palate and prominent jaw were noted in
several
of them. Birth length was between the 90th and 97th centiles in all.
Bone age
was advanced in most.
Hook
and
Reynolds (1967) reported that affected children have large
hands and feet
from birth. Growth is rapid in the first years of life but final height
may not
be excessive. Bone age is advanced. The skull is large with moderate
prognathism.
Mild dilation of the cerebral ventricles, nonspecific EEG changes, and
seizures
have been observed. Poor coordination and mental retardation are
features. In 2
patients, Bejar
et al. (1970) found abnormal dermatoglyphics, normal growth
hormone levels,
and high levels of valine, isoleucine and leucine in the blood. The
glycine-to-valine ratio seemed particularly useful in distinguishing
patients
from controls.
Ruvalcaba
et
al. (1980) found hamartomatous polyps of the intestine and
melanin spots of
the penis in 2 males with the Sotos syndrome. Halal
(1983) reported that the older of the boys she reported with
cerebral
gigantism had pigmented spots on the genitalia and that the father had
been
found to have a rectal polyp--findings like those in the 2 unrelated
adult males
reported by Ruvalcaba
et al. (1980).
Kaneko
et
al. (1987) found congenital heart defects in 5 of 10 patients
with typical
Sotos syndrome. Noreau
et al. (1998) found that 3 of 14 Sotos syndrome patients had
congenital
heart defects. In a literature review, they found another 17 patients
with
variable cardiac defects, mostly closure defects, making an overall
incidence of
approximately 8%.
Goldstein et al. (1988) described 2 unrelated children with macrocephaly, excessive growth, strabismus, hypotonia and developmental delay, and improvement with age.
In a review, Cole
and Hughes (1990) emphasized that the handicaps in Sotos
syndrome are fewer
than previously believed and tend to improve with age. The latter
feature makes
identification of affected adults difficult. Cole
and Hughes (1994) clinically assessed 79 patients with a
provisional
diagnosis of Sotos syndrome and evaluated their photographs between
ages 1 and 6
years. These photographs, together with photographs of first-degree
relatives,
also at ages 1 to 6 years, were reviewed by 4 clinical geneticists. In
41
probands, but no first-degree relatives, the facial gestalt was thought
to be
characteristic of Sotos syndrome. Comparison of anthropometric
measurements,
bone age, and developmental delay in these 41 probands showed marked
differences
between them and the remaining 38 probands. Length was identified as
the most
significantly increased prenatal parameter. In childhood,
occipitofrontal head
circumference (OFC), height, and weight were all increased. OFC
remained above
the 97th percentile in all but one case throughout childhood and
adulthood,
whereas height and weight had a tendency to return toward the mean.
This
'normalization' was more pronounced in females and was probably related
to their
early puberty. Early developmental delay and an advanced bone age were
seen in
100% and 84% of cases, respectively. Cole
and Hughes (1994) suggested that facial gestalt, growth
pattern, bone age,
and developmental delay are the major diagnostic criteria. Using these
criteria,
no affected first-degree relatives were identified.
Scarpa
et
al. (1994) described a sister and brother with macrocrania
and coarse face
(frontal bossing, highly arched palate, prognathism, pointed chin,
large ears).
Psychomotor development of the sister, who also had advanced osseous
maturation,
improved significantly at the age of 7 years. Accelerated growth with
normal
bone age, optic atrophy, renal agenesis with contralateral double
kidney, and
significant mental retardation (IQ, 45) were shown in the brother at
3.5 years
of age. The father of these children was tall, with macrocrania and
large hands
and feet. He had had learning difficulties in school and was a manual
laborer. Scarpa
et al. (1994) suggested that these children and their father
showed
different manifestations of Sotos syndrome. Allanson
and Cole (1996) presented anthropometric evaluation of the
head in 45
patients with Sotos syndrome between age 1 and 25 years. With
increasing age,
the face lengthens and the chin becomes more striking.
Opitz
et al.
(1998) reported affected mother and daughter. The mother was
described as a
large infant and 'as tall as her teacher in school.' Her adult height
was 185.4
cm, and she had mandibular prognathism and a prominent pointed chin.
The
daughter showed a prominent forehead with sparseness of frontal hair
and a
'ruddy' or flushed complexion, especially of the nose and perioral
area. She had
prominent features of the congenital hypotonia/lymphedema sequence with
hypermobile joints, especially at the knees and ankles, lymphedema
nails
(especially toenails), and a high total ridge count (TRC) of the
fingertip
dermatoglyphics. The mother also had a high TRC and a receding frontal
hairline.
Robertson
and Bankier (1999) reported 3 children with anthropometric
and
dysmorphologic features of classic Sotos syndrome in association with
redundant
skin folds, joint hypermobility, and, in 2 of the 3, vesicoureteric
reflux. Robertson
and Bankier (1999) thought the associated features suggested
a coexisting
connective tissue disorder. All the patients had a normal bone age.
Although
Sotos syndrome in its classically described form was not present, Robertson
and Bankier (1999) concluded that this entity might reflect a
related,
perhaps allelic, condition.
Maldonado
et
al. (1984) reported the association of malignant tumors in
Sotos syndrome. Nance
et al. (1990) described a 15-month-old child with Sotos
syndrome and a
paraspinal neuroblastoma. From this and other evidence, they concluded
that
children with this disorder may be at an increased risk for developing
tumors. Gorlin
et al. (1990) estimated a risk of 3.9% of benign or malignant
tumors in
Sotos syndrome. The same excess of neoplasms is present in other
overgrowth
syndromes. Le
Marec et al. (1999) reported that one of a monozygotic twin
pair, both of
whom had Sotos syndrome, developed a diffuse gastric carcinoma
containing signet
ring cells at the age of 26. The young age of occurrence of this
gastric
carcinoma suggested a genetic factor. Leonard
et al. (2000) reported 2 children with Sotos syndrome who had
benign
sacrococcygeal teratomas. Given that Sotos syndrome and sacrococcygeal
teratoma
are rare events, the authors suggested that these tumors may be due to
the
effects of overgrowth on tumor development.
Opitz
et al.
(1998) discussed the differentiation of 2 overgrowth
syndromes, Sotos
syndrome and Weaver syndrome (277590),
and the question of whether the similarities are sufficient to consider
them 1
entity. They noted that vertebrate development is constrained into only
a very
few final or common developmental pathways; therefore, no developmental
anomaly
seen in humans is unique to ('pathognomonic of') one syndrome. Possible
phenotypic differences between the syndromes of Sotos and Weaver
pointed out by Opitz
et al. (1998) were the following: the Sotos syndrome may be a
cancer
syndrome, whereas the Weaver syndrome is not (although a neuroblastoma
had been
reported in the latter disorder). In Sotos syndrome there is remarkably
advanced
dental maturation; this is rarely commented on in Weaver syndrome. In
Weaver
syndrome, there are more conspicuous contractures and a facial
appearance that
experts find convincingly different from that in Sotos syndrome. Opitz
et al. (1998) favored allelic heterogeneity as the
explanation for the
similarities between Sotos and Weaver syndromes. They suggested that
mapping and
isolation of the causative gene or genes would settle the issue.
Schaefer
et
al. (1997) concluded that neuroimaging findings of Sotos
syndrome are
distinct enough to allow differentiation of this syndrome from other
mental
retardation syndromes with macrocephaly. The most common abnormality of
the
cerebral ventricles was prominence of the trigone (90%), followed by
prominence
of the occipital horns (75%) and ventriculomegaly (63%). The
supratentorial
extracerebral fluid spaces were increased for age in 70% of the
patients and the
fluid spaces in the posterior fossa were increased in 70% also. A
variety of
midline abnormalities were noted but anomalies of the corpus callosum
were
almost universal.
Fryns (1988) referred to cases of the fragile X syndrome (309550) in which Sotos syndrome had been diagnosed; he therefore suggested that this disorder be designated the Sotos sequence or the mental retardation-overgrowth sequence.
Most reported
cases of Sotos syndrome have been sporadic and may represent
new dominant mutations. Hook
and Reynolds (1967) reported a concordant set of affected
identical twins. Hooft
et al. (1968) described cerebral gigantism in 2 first
cousins. Nevo
et al. (1974) described affected brother and sister and their
affected
double first cousin in an inbred Arab family in Israel. Two of the 3
showed
generalized edema and flexion contractures of the feet at birth. This
may
represent a distinct disorder; see Nevo syndrome (601451).
Hansen and
Friis (1976) described affected mother and child. Zonana
et al. (1976) described affected mother and 2 children (male
and female).
The mother's father may have been affected. Zonana
et al. (1977) reported 3 families showing vertical
transmission and equal
severity in males and females; no male-to-male transmission was
observed. As an
addendum, they commented on a fourth instance of affected mother and
son. Smith
et al. (1981) observed affected mother and daughter--the
presumed fifth
instance of dominant inheritance. The mother had primary hypothyroidism
due to
Hashimoto disease. Halal
(1982) reported a family in which the father and 2 of his
sons were
affected. She knew of no other instance of documented male-to-male
transmission.
Winship (1985)
described a 'Cape Coloured' family with affected father and 4 children
by 2
different, unrelated wives. Presumed Sotos syndrome was described in a
mother
and 2 daughters by Bale
et al. (1985). They suggested that instances of seemingly
autosomal
recessive inheritance may be examples of incomplete penetrance, gonadal
mosaicism, or genetic heterogeneity. Minor changes in 2 mothers of 2
unrelated
affected infants reported by Goldstein
et al. (1988) suggested dominant inheritance of a Sotos
sequence. Brown
et al. (1998) described a pair of 5-year-old male monozygotic
twins who were
discordant for Sotos syndrome.
The
possibility of uniparental disomy in Sotos syndrome was investigated by
Smith
et al. (1997). Using 112 dinucleotide repeat DNA
polymorphisms, they
examined parental inheritance of all autosomal pairs, except chromosome
15, in
29 patients with Sotos syndrome. All informative cases showed
biparental
inheritance and no cases of UPD were found.
In a study of the metacarpophalangeal pattern profile (MCPP) in Sotos syndrome, Butler et al. (1985) found no evidence of heterogeneity and developed a diagnostic tool using MCPP variables, which they suggested may be useful.
Schrander-Stumpel
et al. (1990) described a 6-year-old boy with Sotos syndrome
who also had a
de novo, apparently balanced translocation, t(3;6)(p21;p21). They
suggested that
the autosomal dominant gene for the Sotos syndrome may be located
either at 3p21
or 6p21. Tsukahara
and Kajii (1991) could find no abnormality in high
resolution-banded
chromosomes from 5 patients. Involvement of genes at 3p21 was also
suggested by
the case reported by Cole
et al. (1992); a 22-year-old female with Sotos syndrome, a
nonsmoker, died
of small cell lung carcinoma (182280)
for which genetic determinants in the 3p21 region are suggested by
loss-of-heterozygosity
studies. Maroun
et al. (1994) reported the case of a 4-year-old girl with
Sotos phenotype
and a de novo balanced translocation between 5q and 15q:
46,XX,t(5,15)(q35;q22).
They thus suggested 5q35 or 15q22 as the site of an autosomal dominant
gene
determining Sotos syndrome.
Faivre
et
al. (2000) reported a child with apparent Sotos syndrome and
mosaicism for
partial duplication of the short arm of chromosome 20
(46,XY,dup(20)(p12.1-p11.2)[12]/46,XY[66]). The somatostatin receptor-4
(SSTR4; 182454)
gene is located at 20p11.2, encompassed by the duplication. The authors
proposed
that a dosage effect of this gene might be responsible for some of
their
patient's clinical findings.
Imaizumi
et
al. (2002) described a de novo balanced reciprocal
translocation between the
long arms of chromosomes 5 and 8, 46,XX,t(5;8)(q35;q24.1), in a
15-month-old
girl with a typical Sotos syndrome phenotype. They proposed that a gene
responsible for this disorder is located in the distal long arm region
of
chromosome 5.
In patients
with Sotos syndrome harboring a chromosomal translocation, Kurotaki
et al. (2002) isolated the NSD1 (606681)
gene from the 5q35 breakpoint. They identified 1 nonsense, 3
frameshift, and 20
submicroscopic deletion mutations of NSD1 among 42 sporadic cases of
Sotos
syndrome. The results indicated that haploinsufficiency of NSD1 is the
major
cause of Sotos syndrome.
To the 42
cases of Sotos syndrome reported by Kurotaki
et al. (2002), Kurotaki
et al. (2003) added 70 more cases, 53 of whom were Japanese.
Among the 112
total cases, they identified 50 microdeletions (45%) and 16 point
mutations
(14%). They noted a large difference between Japanese and non-Japanese
patients
in the frequency of microdeletions, which occurred in 49 (52%) of the
95
Japanese but in only 1 (6%) of the 17 non-Japanese. Most of the
microdeletions
were confirmed to be identical by FISH analysis. Kurotaki
et al. (2003) identified highly homologous sequences, i.e.,
possible low
copy repeats, in regions flanking proximal and distal breakpoints of
the common
deletion. This suggested that low copy repeats may mediate the
deletion. The
frequency of such low copy repeats seemed to vary in different
populations, and
thus the differences in frequency of microdeletions between Japanese
and
non-Japanese cases may have been caused by patient selection bias.
In a Finnish father and son with Sotos syndrome, Hoglund et al. (2003) identified a heterozygous mutation in the NSD1 gene (606681.0009). The authors noted that the findings in this family confirm that familial Sotos syndrome is caused by mutation in the NSD1 gene.
Beckwith-Wiedemann
syndrome (BWS; 130650)
is, like Sotos syndrome, an overgrowth syndrome. Deregulation of
imprinted
growth regulatory genes within the 11p15 region is the major cause of
BWS.
Similarly, defects of the NSD1 gene account for more than 60% of cases
of Sotos
syndrome. Owing to the clinical overlap between the 2 syndromes, Baujat
et al. (2004) investigated whether unexplained cases of Sotos
syndrome could
be related to 11p15 anomalies and, conversely, whether unexplained BWS
cases
could be related to NSD1 deletions or mutations. Two 11p15 anomalies
were
identified in a series of 20 patients with Sotos syndrome, and 2 NSD1
mutations
(606681.0011-606681.0012)
were identified in a series of 52 patients with BWS. The results
suggested that
the 2 disorders may have more similarities than previously thought and
that NSD1
could be involved in imprinting of the 11p15 region.
Turkmen
et
al. (2003) screened the NSD1 gene for mutations in 20
patients and 1
familial case with Sotos syndrome, 5 patients with Weaver syndrome, 6
patients
with unclassified overgrowth and mental retardation, and 6 patients
with
macrocephaly and mental retardation. They identified 19 mutations, 17
previously
undescribed, in 18 Sotos patients and the familial case (90%). The best
correlation between the molecular and clinical findings was for facial
gestalt
in conjunction with overgrowth, macrocephaly, and developmental delay. Turkmen
et al. (2003) found no mutations of the NSD1 gene in the
patients with
Weaver syndrome or other overgrowth phenotypes and concluded that the
great
majority of patients with Sotos syndrome have mutations in NSD1.
Boman and Nilsson (1980); Dodge et al. (1983); Stephenson et al. (1968)
===========================
External Links:
I Have Nevo Syndrome
http://www.experienceproject.com/groups/Have-Nevo-Syndrome/93054
Patient Organizations
http://www.orpha.net/consor/cgi-bin/SupportGroup_Search_Simple.php?lng=EN&LnkId=2453&Typ=Pat
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http://www.rightdiagnosis.com/medical/nevo_syndrome.htm
Nevo Syndrome
http://www.cags.org.ae/FMPro?-DB=ctga.fp5&-Format=ctga/ctga_detail.html&-RecID=33509&-Find
Patient Organizations
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===========================
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man with lymphedema; a man with a loved one with lymphedema who you are
trying
to help and understand come join us and discover what it is to be the
master
instead of the sufferer of lymphedema.
http://health.groups.yahoo.com/group/menwithlymphedema/
Subscribe: menwithlymphedema-subscribe@yahoogroups.com
......................
All
About Lymphangiectasia
Support group for parents, patients, children who suffer from all forms
of
lymphangiectasia. This condition is caused by dilation of the
lymphatics. It can
affect the intestinal tract, lungs and other critical body areas.
http://health.groups.yahoo.com/group/allaboutlymphangiectasia/
Subscribe: allaboutlymphangiectasia-subscribe@yahoogroups.com
......................
Lymphatic
Disorders Support Group @ Yahoo Groups
While we have a number
of support groups for lymphedema... there is nothing out there for
other
lymphatic disorders. Because we have one of the most comprehensive
information
sites on all lymphatic disorders, I thought perhaps, it is time that
one be
offered.
DISCRIPTION
Information and support for rare and unusual disorders affecting the
lymph
system. Includes lymphangiomas, lymphatic malformations,
telangiectasia,
hennekam's syndrome, distichiasis, Figueroa
syndrome, ptosis syndrome, plus many more. Extensive database of
information
available through sister site Lymphedema People.
http://health.groups.yahoo.com/group/lymphaticdisorders/
Subscribe: lymphaticdisorders-subscribe@yahoogroups.com
......................
===========================
Lymphedema People New Wiki Pages
Have you seen
our new “Wiki”
pages
yet? Listed below
are just a sample
of the more than 140 pages now listed in our Wiki section. We are also
working
on hundred more. Come
and take a
stroll!
Lymphedema
Glossary
http://www.lymphedemapeople.com/wiki/doku.php?id=glossary:listing
Lymphedema
http://www.lymphedemapeople.com/wiki/doku.php?id=lymphedema
Arm Lymphedema
http://www.lymphedemapeople.com/wiki/doku.php?id=arm_lymphedema
Leg Lymphedema
http://www.lymphedemapeople.com/wiki/doku.php?id=leg_lymphedema
Acute
Lymphedema
http://www.lymphedemapeople.com/wiki/doku.php?id=acute_lymphedema
The Lymphedema
Diet
http://www.lymphedemapeople.com/wiki/doku.php?id=the_lymphedema_diet
Exercises for
Lymphedema
http://www.lymphedemapeople.com/wiki/doku.php?id=exercises_for_lymphedema
Diuretics are
not for Lymphedema
http://www.lymphedemapeople.com/wiki/doku.php?id=diuretics_are_not_for_lymphedema
Lymphedema
People Online Support Groups
http://www.lymphedemapeople.com/wiki/doku.php?id=lymphedema_people_online_support_groups
Lipedema
http://www.lymphedemapeople.com/wiki/doku.php?id=lipedema
Treatment
http://www.lymphedemapeople.com/wiki/doku.php?id=treatment
Lymphedema and
Pain Management
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: Jan. 9, 2012