Changing the Future

President’s Pen
Changing the Future
Wendy Book, MD
APFED President
A new year is upon us—a year full of
hope and potential. With the New
Year come opportunities to change
the future of people with eosinophilic
diseases. We at APFED have been
working hard on your behalf to educate
the public, the doctors, families,
educators, industry and legislators on
the importance of eosinophil associated
diseases. We now have several
clinical trials for patients with eosinophilic
esophagitis and Hypereosinophilic
syndrome. For a rare disease,
these initial steps are crucial, but
more work needs to be done.
Dedicated researchers, and the funding
to support their ideas, are desperately
needed. Sadly, federally funded
studies of eosinophil associated diseases
can be summarized in a few
pages. That must change. The prevalence
of eosinophil associated gastrointestinal
disorders (EGID) has risen
over the past decade, to a combined
estimated prevalence of 1 in 1200
today. Currently, diseases with
prevalence similar to eosinophilic diseases
receive many-fold more annual
research funding, and have dedicated
federal funding through the National
Institutes of Health. The National
Institutes of Health (NIH) is the primary
federal agency for conducting
and supporting medical research investigating
the causes, treatments and
cures for both common and rare diseases
(http://www.nih.gov). The NIH
attracts grant applications from the
top researchers in the country.
What can we do? I am always in awe
of the strength and enthusiasm within
our community. That remarkable energy
and drive led to the passing of
HR 296 in 2007, declaring the 3 rd
week of May National Eosinophil
Awareness Week, followed by the
passage of four ICD-9-CM codes for
eosinophilic gastrointestinal disorders
in 2008.
HR 296, the legislation which established
a National Eosinophilic Awareness
week, has language that specifically
mentions the need for funding
for improving methods of diagnosis
and developing effective treatments.
Dedicated
researchers, and
the funding to
support their ideas,
are desperately
needed.
In the two years that have passed
since HR 296, the estimated prevalence
of this debilitating group of diseases
has dramatically risen, resulting
in an even more pressing need for
research funding.
In recognition of this rapidly rising and
poorly understood group of rare diseases,
we ask that The National Institutes
of Health convene a working
group to develop a research agenda
related to eosinophil associated diseases,
and the related morbidity and
mortality due to lack of diagnostic and
treatment options. Funds are being
raised in hopes of creating a partnership
with NIH to fund research based
on the working group recommendations.
Our community will benefit from
a NIH partnership with patient associations,
such as APFED, and other appropriate
health-care agencies, to develop
education and research initiatives targeted
to the life-long needs of those
with eosinophil associated diseases.
With our proposed partnership, we
can increase our collective reach and
research dollars.
By increasing funding, we will attract
high-quality researchers, initiate important
research projects that might otherwise
not be funded, and stimulate
much-needed interest in EGID research
at the national level. Successful
research projects will also increase
public awareness, which will likely increase
funding further. Your contribution
can lead to long-term exponential
benefits to the community. Together
we can change the future for children
and adults with eosinophilic diseases.
To make this research initiative a reality,
we must raise the necessary funding.
A generous anonymous donor has
contributed $50,000 and challenged
our community to match those funds.
Contribute today to HOPE on the Horizon,
APFED’s dedicated research
fund, and make a difference in the lives
of those living with eosinophilic diseases.
3

Medical Education
Genetics
of EE and EGID
Genes are contained in chromosomes in
the nucleus of all cells. Even though
cells in different parts of the human
body appear different from each other,
they all contain the same genes. The
genes that are very active and important
for cell function in some cell types may
be completely silent in other cells.
Genes contain the information that is
essential for cell growth, development
and function. That information is transcribed,
or copied, from the DNA in the
genes to messenger RNA (mRNA),
which then brings that information
from the nucleus into the cytoplasm,
where the information is translated and
specific proteins that perform specific
functions are synthesized. Knowledge
of the genes that are active and also
inactive in disease states is crucial to
develop effective therapies and ultimately
to find cures.
Recently, the gene expression profile of
esophageal biopsies from patients with
eosinophilic esophagitis (EE) was compared
to biopsies from patients without
EE. (1) Approximately 1% of all human
genes were expressed more in esophageal
tissue containing numerous
eosinophils compared to tissue with
few or no eosinophils. The gene that
was most overexpressed in the inflamed
biopsies was eotaxin-3, a substance that
powerfully attracts eosinophils, from
blood circulating in blood vessels, to
enter tissue. The results concerning
gene expression obtained from chip
analysis were confirmed by detecting
By Margaret Collins, MD
increased amounts of both eotaxin-3
mRNA and protein in EE biopsies. A
particular type of microscopic analysis,
in situ hybridization, demonstrated that
the eotaxin-3 mRNA was increased in
the epithelial cells of the EE biopsies
compared to controls. Additional research
showed that interleukin-13 (IL-
13) mRNA was greatly increased in
biopsies from EE patients, and that
epithelial cells obtained from esophageal
biopsies of EE patients that were
cultured and grown in the lab produced
large amounts of eotaxin-3 when stimulated
with IL-13. (2) Those stimulated
esophageal epithelial cells had a gene
expression profile very similar to that
found on microarray analysis of esophageal
biopsies from EE patients,
strongly implicating IL-13 in the pathogenesis
of EE. In addition to overexpression,
a variation in a part of the
eotaxin-3 gene was significantly more
common in EE patients, among those
who had allergies as well as those who
did not. (1) The gene expression profile
identified in EE also did not vary
with patient age or sex. (1) Thus, distinct
gene alterations are present in esophageal
tissue in patients who have EE;
the alterations are independent of patient
allergy status, age or sex; and at
least one cytokine associated with
atopy induces increased expression of
genes in EE-derived esophageal epithelial
cells. Therefore, therapy that reduces
IL-13 content and/or interferes
with IL-13 function may be helpful to
treat EE. (2)
In a number of families, more than one
family member has EE. Based on estimates
of the prevalence of EE in the
general population, and in siblings
among EE patients, the estimated risk
of a sibling of an EE patient to develop
EE is significantly greater than for
other common allergic diseases such as
asthma. (3) EE is known to occur in
twins. (4) The incidence in fraternal
compared to identical twins may help to
elucidate the genetic transmission of
the disease: If the incidence of EE is
significantly higher among identical
compared to fraternal twins, that will
even further implicate genetics in the
development of the disease. In a recent
study of families with multiple members
who have EE, the clinical and histologic
characteristics of 59 members
of 26 families did not vary significantly
from those of age- and sex-matched
patients who were not known to have
other family members with EE. (4) The
gene expression profile of a subset of
the biopsies also did not differ between
familial and sporadic cases. These data
suggest that there is a common final
pathway that results in the clinical and
histologic expression of EE that is independent
of family history, allergy, etc.
There should therefore be therapies that
are effective for virtually all EE patients.
EE occurs in patients who have diseases
associated with known gene abnormalities,
such as patients who have
Rubinstein-Taybi Syndrome (RTS). (5)
Many patients who have RTS have abnormalities
of the CREB Binding Protein,
or CBP, gene. That gene product
interacts with a large number of other
proteins. There isn’t any evidence currently
that EE is more prevalent among
patients who have a particular syndrome,
including RTS. However, by
analyzing tissue from patients who
have syndromes with known genetic
abnormalities we may further advance
our understanding of the genetic abnormalities
in EE that directly participate
in disease pathogenesis.
There are virtually no publications
concerning the genetics of other
forms of EGID such as eosinophilic
gastritis, etc. (6)
DNA Continued on page 5
4

Medical Education
Pathology
Pathologists’ evaluation of biopsies is an
essential component of both the diagnosis
of eosinophilic gastrointestinal disorders
(EGIDS), and of the evaluation for
response to therapy. Pathology reports
communicate pathology diagnoses based
on review of the slides made from GI
biopsies. The communication between
pathologists and gastroenterologists may
be supplemented by discussions at conferences,
phone calls and emails. All
pathology reports display the pathologist’s
final diagnosis; a description—
called gross description—of the number
and size of the biopsy pieces from each
part of the GI tract that were submitted
to the pathology lab; and in some a microscopic
description of the features of
the tissue on the slides made from the
biopsies.
Consensus concerning the diagnosis of
EGIDS is generally lacking. The recommended
diagnosis of eosinophilic
esophagitis (EE), the most common form
of EGIDS, is characteristic clinical signs
and symptoms with an abnormal esophageal
biopsy containing at least 15
eosinophils in a high power field, in patients
who have no or incomplete response
to anti-gastroesophageal reflux
disease (GERD) therapy. (1) There are
not currently recommendations for the
diagnosis of the other forms of EGIDS
such as eosinophilic gastritis, etc. Although
the recommendations to diagnose
eosinophil
gitis
Of EGIDs
high power field
EE based on literature review and expert
experience and opinion includes
only an eosinophil count obtained from
biopsy review, in fact most biopsies
that show EE also show architectural
abnormalities. Some pathologists require
architectural abnormalities in
other sites in the GI tract in addition to
increased numbers of eosinophils to
diagnose other forms of EGIDS such
as eosinophilic gastritis. (2)
Following is a glossary of terms that
patients may find helpful to read pathology
reports and discuss their disease
with their clinicians.
High power field: Pathologists see
patterns in every biopsy. Pattern recognition
is essential for proper biopsy
interpretation. Therefore, pathologists
initially evaluate slides under the microscope
from afar to determine the
number of pieces of tissue that are on
the slide, the pattern among the pieces,
within each piece, etc. This degree of
magnification is referred to as low
power, and the circular area, or field,
seen by the pathologist is referred to as
a low power field. In order to view
more detail in the tissue, pathologists
use a different objective lens on the
microscope and see less of the total
area on the slide, but greater detail of
the smaller amount of tissue that is in
the field they see. This is referred to as
high power magnification and the cir-
mucosa
epihelium
6
By Margaret Collins, MD
Cincinnati Children’s Hospital Medical Center
crypt
cular area subtended on the slide is a
high power field. Typically high power
fields have a standard total magnification
of 400X, although the actual area
of the field varies among microscopes.
Peak count: This is the number of
eosinophils contained within one high
power field. Another means to quantitate
eosinophils in biopsies is to count
eosinophils in all the high power fields
of all the pieces to generate a mean or
average count, but that is not practical
for daily work and is essentially a research
tool. Pathologists survey the
biopsy pieces at low power magnification,
identify the area with the densest
inflammation, and generate a peak eosinophil
count by counting esoinophils in
that area. In esophageal biopsies, only
eosinophils in the epithelium are
counted.
Epithelium: Epithelium lines the inner
surface of the tube that is the GI tract.
Gastroenterologists see the epithelium
during endoscopy but cannot distinguish
individual epithelial cells.
Epithelial cells participate in multiple
processes, including a barrier function
that prevents bacteria and undigested
food or foreign material from entering
the body. The epithelium that lines the
surface of the GI tract is called surface
epithelium. In the stomach and small
and large intestines there are numerous
hyperplasia
fibrosis
esopha
lamina propria

invaginations from the surface that are
lined by epithelial cells. In the stomach
the invaginations are glands and the epithelium
lining the glands is glandular epithelium.
In the small and large intestines
the invaginations form crypts and the epithelium
lining the crypts is known as
crypt epithelium.
Basal layer: The epithelial lining of the
esophagus is different from that of the rest
of the GI tract. The epithelium of the
esophagus consists of several layers but
the surface and crypt epithelium in the
rest of the GI tract mostly consists of one
layer of cells. The esophagus is lined by
squamous epithelium that resembles the
lining of the mouth and also skin. The
basal layer of the esophageal squamous
epithelium becomes thickened in EE, described
as basal layer hyperplasia. This is
a reactive and reversible change.
Lamina propria: This is composed of
fibrous tissue, blood vessels, and other
types of tissue that provide structural support
and perform other functions for the
surrounding tissue. Since the configuration
of epithelium is different in the
esophagus from the rest of the GI tract,
the configuration of the lamina propria is
also. In the esophagus, it forms a distinct
layer below or outside of the basal layer
of the epithelium. The lamina propria
forms periodic protrusions into the epithelium
called papillae that also contain
blood vessels that supply oxygen to the
epithelium. In the rest of the GI tract, the
lamina propria resides immediately below
the single layer of surface epithelium and
surrounds the crypts. The differing configurations
of epithelium and distribution
of lamina propria explains the fact that
lamina propria is not present in some, or
most, esophageal biopsies but is virtually
always present in biopsies from the rest of
the GI tract.
Parietal cells: These are specialized
epithelial cells found in stomach glands
that secrete acid. Anti-reflux medications
block acid secretion and in response these
cells become enlarged and numerous, a
finding that pathologists report as reactive
change consistent with the use of PPIs, or
parietal cell hypertrophy and hyperplasia.
Villi: These are protrusions of the surface
into the lumen of the small intestine and
normally are found only in small intestine.
All parts of the small intestine have
these, but villi vary in length and width
somewhat among duodenum, jejunum
and ileum. Villi enormously increase the
surface of the small intestine, increasing
the area over which nutrients derived
from food can be absorbed. Villi may
become altered in numerous diseases.
The most common alteration is blunting
or a decrease in length, which is found in
celiac disease but may also be seen with
excessive numbers of eosinophils.
Muscularis mucosa: This is a layer of
muscle that separates the mucosa from
the underlying submucosa. It may be
present in biopsies from the GI tract depending
on how deeply the biopsies
were obtained. It is rarely seen in biopsies
from the esophagus, but is more
commonly present in biopsies from the
rest of the GI tract. One criterion for
making a histologic diagnosis of EGIDS
in sites other than the esophagus is finding
eosinophils in the muscularis mucosa.
Submucosa: This layer of the wall of
the GI tract is below the muscularis mucosa
and contains blood vessels and
other structures. If any submucosa is
seen in GI biopsies, it generally is only a
small amount. Eosinophilic inflammation
in the submucosa is also used as a
criterion to help to diagnose EGIDS.
Fibrosis: Fibrous tissue is a normal
component of all parts of the body and
helps to create and maintain the structure
of various organs and tissues. Fibrosis
means that there is an excessive amount
of fibrous tissue, equivalent to a scar.
Lamina propria fibrosis is seen in esophageal
biopsies showing EE, and may
be reversible
REFERENCES
1. Furuta GT, Liacouras CA, Collins
MH, Gupta SK, Justinich C, Putnam PE,
Bonis P, Hassall E, Straumann A, Rothenberg
ME: Eosinophilic Esophagitis in
Children and Adults: A Systematic Review
and Consensus Recommendations
for Diagnosis and Treatment. Sponsored
by the American Gastroenterological
Association (AGA) Institute and North
American Society of Pediatric Gastroenterology,
Hepatology, and Nutrition.
Gastroenterology 133(4):1342-63, 2007.
Collins MH: Histopathology Associated
with Eosinophilic Gastrointestinal Diseases.
Immunol Allergy Clin NA
29:109-117
7
Medical Education
Genomics of EE
Antonella Cianferoni, MD, PhD
APFED 2009 HOPE Grant Recipient
EE is a global health disease now reported
in all continents except Africa
with an incidence of ~1:10,000. Patients
with EE commonly report symptoms
that include difficulty feeding,
failure to thrive, vomiting, epigastric or
chest pain, dysphagia and food impaction.
EE patients are predominantly
young males with a high rate of atopic
disease and the diagnosis is made by
endoscopy and biopsy finding of isolated
eosinophils in the esophagus.
Accumulating evidence suggests that
EE has a strong familial association.
Nearly 10% of parents of EE patients
have a history of esophageal strictures
and ~8% have biopsy proven EE and at
least 27 multiplex families have been
described to date. EE also exhibits a
high sibling risk ratio compared with
related atopic diseases such as asthma.
While genetics is likely to have a large
role in EE susceptibility, there has been
only one candidate gene identified to
date, the eotaxin-3 gene. Eotaxin-3 is
the most overexpressed gene in the
esophagus, based on genome wide expression
profile analysis. However, the
disease-associated allele is only present
in 14% of EE patients, suggesting that
additional variants are to be found.
In collaboration with Cincinnati Children’s
Hospital Medical Center, and
The Children’s Hospital of Philadelphia
Center for Applied Genomics we have
conducted a genome wide analysis
study on children with EE aimed at
identifying a gene variation that can
make children susceptible to the disease.
We genotyped approximately
550,000 gene variation present in all
the genome in 271 EE cases from Cincinnati
Children’s Hospital Medical
Center (CCHMC), and 180 EE patients
and ~3100 controls from Children’s
Hospital of Philadelphia (CHOP). We
detected genome-wide association with
variants on one gene that has been reported
to favor allergic sensitization -
TSLP.
We are in the process of doing an extensive
Genotyping/phenotyping analysis
for the TSLP gene in the Children’s
HOPE Continued on page 9

Eos Connection 2010
2010
Eos Connection
The 8th Annual
Patient Education
Conference
Presented by
American Partnership For
Eosinophilic Disorders
in conjunction with
The Children’s Hospital Denver
and National Jewish Health
July 16-18
Denver, CO
A gathering of some of the foremost
experts in the field of EGIDs. Come to
learn, to share, to meet other families
affected by eosinophilic disorders.
Eos Connection 2010
APFED’s annual Patient Education Conference will take place in Denver,
CO. Join us to learn from the experts, to meet other families affected by
EGID and to make memories that will last a lifetime. More information
and registration at www.apfed.org .
Educational Sessions Include:
Thursday, July 15, 2010 Optional
Family Fun Day
Denver Zoo (Optional, additional fee required)
Friday July 16, 2010 Optional
Fundraising Social at the Pavilion (optional, donation required)
What’s New in Eos Research
Entertainment
Saturday July 17th
Session 1-Overview of EGIDs
What are EGIDs?
EE– What it is and how we diagnose
Endoscopy and Pathology of EE
Session 2- Allergies and Treatment of EGIDs
Allergies and EGIDs
Treatment of EGIDs
Session 3- Living Well
Diets, Medications – How do I know which treatment is best?
Six-food elimination diet: Practical tips
Celebrating the Holidays
Session 4- Eating, Nutrition and Coping with EGIDs
Concurrent Sessions
A. Feeding difficulties and EGIDs
B. Teens only
C. Nutrition: Living on an Elimination or Elemental Diet
D. Coping with Chronic Illness
Sunday July 18 th
Session 5- Hope for Today
2010 HOPE Grant lecture
Living with chronic illness
Parent-Child Panel
Speakers Include:
Dan Atkins MD
Pediatric Allergist
Nancy Creskoff–Maune
Pediatric Occupational Therapist
David Fleischer MD
Pediatric Allergist
Glenn Furuta MD
Pediatric Gastroenterologist
Angela Haas M.A.C
Pediatric Speech Pathologist, Denver, CO
Michelle L. Henry, MPH, RD
Mary Klinnert PhD
Pediatric Psychologist
Jonathan Markowitz MD
Pediatric Gastroenterologist
Philip Putnam MD
Pediatric Gastroenterologist
Speakers and Sessions are Preliminary and Subject to Change
8

EGID Myths
Fact
versus
Fiction
Eosinophilic Esophagitis: Fact or Fiction?
Philip E Putnam, MD
Pediatric Gastroenterologist, Cincinnati Children’s Hospital Medical Center
The transfer of medical information
from medical professionals to their patients
is an essential part of patient care.
The translation from medical terminology
into language that is interpretable
by individuals who may not have a
medical background plays an important
role in assuring that the patient understands
the diagnosis, disease process,
and plan for care. Arguably, the presentation,
impact, success, and comprehension
of that translation are variable.
The information that is provided to patients
and their families may undergo
some transformation when it is repeated
after the visit. The process is equivalent
to the game of “Telephone”. Each time
it is repeated to family or friends or
over the internet, it is modified in some
fa sh i on , such that th e fi nal
‘understanding’ that develops may be
accurate, mostly accurate, mostly inaccurate,
or just plain fiction.
If it’s repeated often enough and loud
enough, fiction becomes perceived
truth, but is fiction nevertheless. Fiction
stated as truth, embellished for
effect, attains mythologic status. In the
world of eosinophilic esophagitis, mythology
abounds, and the following is
an attempt to identify and demystify
some of the statements that have attained
mythologic status.
Pathology Myths
Myth: “Pathologists must count
the eosinophils.” The reality is that
pathologists look at slides as a profession,
and are extraordinarily adept at
identifying patterns of abnormality.
Well-developed eosinophilic esophagitis
is easy to recognize with little more
than a glance at the slide because it is
so different from normal esophagus.
Counting the eosinophils to “prove it”
is completely unnecessary. In borderline
cases wherein the number of eosinophils
is close to the threshold range
(15-20 per high power field that is currently
accepted as the minimum number
needed to label the inflammatory
process as “eosinophilic,”) it may be
worthwhile to count.
The actual number does not determine
cause, severity, or treatment, so knowing
whether the eosinophil count is 64
or 164/hpf is not worth the time it takes
to count. In addition, the eosinophil
number varies from area to area within
a biopsy and from biopsy specimen to
biopsy specimen (even if they are taken
millimeters apart in the same patient),
so the one number that is reported as
the peak (highest concentration identified
by inspection of all the available
tissue) is seldom representative of the
entire set of high powered fields that
are available.
Being precise and counting eosinophils
as part of a research project assures that
the result is objective and not subjective,
so the number of eosinophils/hpf
will always be reported in a research
article, but in clinical practice, the actual
number is unimportant once the
peak has exceeded the threshold for
diagnosis.
Myth: “More eosinophils = more
severe disease.” It is true that more
eosinophils makes for a really impressive
biopsy under the microscope, but
the reality is that there is a poor correlation
between the degree of inflammation
and what the patient feels (e.g.,
pain or difficulty swallowing). The
number does not determine the cause of
the esophagitis, nor does it suggest one
particular treatment over another.
Myth: “Routine biopsies are not
sufficient to ‘see’ eosinophils, they
must do a special ‘test’ to find
them.” The reality is that eosinophils
are easy to see on biopsy specimens processed
in standard fashion in all pathology
departments. “Eosinophilic” literally
means “eosin-loving,” and they are
named that because they take up a stain
called eosin more than other cells. All
biopsy specimens are stained with 2
stains, hematoxylin and eosin (referred to
commonly as H & E), because unstained
tissue on a slide is virtually impossible to
analyze. Various tissue and cells take up
the hematoxylin (which is dark blue) or
eosin (which is red) in unique patterns
predictably, which then allows the pathologist
to identify the cell types in the
specimen. Eosinophils stand out from
surrounding tissue because the tiny granules
within them stain intensely red with
eosin.
HOPE Continued from page 7
Hospital of Philadelphia cohort of patients
to see if such association is validated in a
larger group and if it could be used as a
blood biomarker in the future.
Noel, R. J., and M. E. Rothenberg. 2005. Eosinophilic
esophagitis. Curr Opin Pediatr 17:690.
Liacouras, C. A., J. M. Spergel, E. Ruchelli, R.
Verma, M. Mascarenhas, E. Semeao, J. Flick, J.
Kelly, T. Brown-Whitehorn, P. Mamula, and J. E.
Markowitz. 2005. Eosinophilic esophagitis: a 10-
year experience in 381 children. Clin Gastroenterol
Hepatol 3:1198.
Orenstein, S. R., T. M. Shalaby, C. Di Lorenzo, P.
E. Putnam, L. Sigurdsson, H. Mousa, and S. A.
Kocoshis. 2000. The spectrum of pediatric eosinophilic
esophagitis beyond infancy: a clinical series
of 30 children. Am J Gastroenterol 95:1422.
Rothenberg, M. E., A. Mishra, E. B. Brandt, and S.
P. Hogan. 2001. Gastrointestinal eosinophils in
health and disease. Adv Immunol 78:291.
Blanchard, C., N. Wang, K. F. Stringer, A. Mishra,
P. C. Fulkerson, J. P. Abonia, S. C. Jameson, C.
Kirby, M. R. Konikoff, M. H. Collins, M. B. Cohen,
R. Akers, S. P. Hogan, A.H. Assa'ad, P. E. Putnam,
B. J. Aronow, and M. E. Rothenberg. 2006. Eotaxin-
3 and a uniquely conserved gene-expression profile
in eosinophilic esophagitis. J Clin Invest 116:536
9

Events
Recent Events
Run for a Cure
Congratulations to Renea Lundin for
her finish in the PF Chang's Rock'n'Roll
Marathon in Arizona on January 17th.
Renea finished in 4 hrs, 55 minutes and
raised over $1900.00 in donations by
participating in this event.
Dance-A-Thon
Special Thanks to Megan Yanos and the
Mortar Board Honor Society of Findlay
University for hosting a Dance-A-Thon
on January 23rd. The event raised
awareness of EGIDs and a great time
was had by all who attended.
Upcoming Events
Remington Walls Golf Tournament
May 1, 2010
Wesley Chapel, Fl
K.E.'s 2nd Annual Art Show and
Bazaar to Benefit APFED.
May 16, 2010
Woodside, NY
For more info on these events, please
visit APFED Fundraising page.
Awareness Week
National Awareness Walk
May is not too far off. Spring weather,
trees and flowers blooming, birds singing...and
National Eosinophil Awareness
Week!
The third week of May is National
Eosinophil Awareness Week dedicated
to Eosinophilic Disorders. Get involved
by planning an event in your
area. Here are some great, easy ideas:
• Pass out Dum-Dums or Smarties to
classmates, with information about
Eosinophilic Disorders.
• Deliver DumDum bouquets to your
doctors’ offices, to share with other
patients.
• Host a lemonade stand, bake sale,
or car wash.
• Do a letter or email campaign, asking
friends and family to support
APFED.
Another great way to raise awareness
and support APFED is to participate in
our Virtual National Eosinophil Awareness
Walk. Grab your family, friends
and neighbors and enjoy some quality
time while raising awareness. Get together
your support group and meet
up at a local park to Walk and socialize.
Registration information and
pledge forms will be available on the
website in March. If you are interested
in hosting an event in your area, please
c o n t a c t J u l i e S p r i n g e r a t
julie@apfed.org.
Julie A. Springer
National Fundraising Coordinator
407-340-2412 julie@apfed.org
Fundraising Social
A Fundraising Social will be held in conjunction
with the Eos Connection 2010
Patient Education Conference in Denver,
CO, on July 16. An optional fundraising
event, those families raising
$100 or more for eosinophilic research
are invited to attend. Those
families raising $500 or more will receive
a free gift store item.
The whole family is invited to attend
this event, and activities for children as
well as entertainment will be provided.
Fundraising forms will be available at
www.apfed.org. Those interested in
volunteering with organization of the
event or at the fundraiser may contact
Melissa at mtierce@sbcglobal.net.
Rare Disease Day
APFED will partner with The National
Organization for Rare Diseases
(NORD) to celebrate the global observance
of Rare Disease Day on
February 28, 2010. We hope to
raise awareness of EGIDs and understanding
of the challenges faced by
patients and their families.
Last year, 39 states issues proclamations
in support of Rare Disease Day.
Requests for proclamations must come
from residents of each state. Please
consider writing a letter or sending an
email to your governor requesting that
he issue a proclamation for 2010. Sample
letters and more information can
be found at www.rarediseaseday.us.
Support APFED
There are three ways you can support
APFED when making online purchases.
Merchants will donate a portion
of your purchase amount to
APFED, with no additional cost to you.
Amazon.com
Use the links on the APFED website to
shop through Amazon.com and a portion
of all your purchases will benefit
APFED. (You must use the links on
the APFED website in order for your
purchases to benefit APFED.)
Buy for Charity
Designate APFED as your charity
of choice when shopping through Buy
for Charity and a portion of your proceeds
will benefit APFED. Buy for
Charity provides you with a variety of
s t o r e s , i n c l u d i n g B a r n e s
& Nobles, Target, Toys R Us, Sears,
Bath and Body, and many, many
more. Link is available on the APFED
website.
iGive.com
With over 757 merchants to choose
from, you should find exactly what you
are looking for with iGive.com. Register
with iGive and select APFED as
your Charity and a portion of all your
purchases will benefit APFED.
Link is available on the APFED website.
eBay Donations
A portion of your eBay sales can be
designated to benefit APFED through
Mission Fish. Sign up when you list
your item for sale.
APFED Merchandise
Visit the Gift Store at www.apfed.org
for unique merchandise that spreads
awareness of eosinophilic disorders
and supports research through its proceeds.
A variety of items are available,
including:
Two-Year Eos Calendar
Note Cards
T-Shirts
Restricted Diet Cookbook
Hats
Cooler Bag
Educational Books
10

Donations
Turkey Schnitzel
Donations
Top 6 Allergen Free
Sincere thanks to those making donation to APFED
this quarter.
In Memory of these individuals:
Ed Collins
Emma Egreczky
Ashley Fliger
In honor of the following birthdays:
Matthew Markowitz
Shannon O'Farrell
Shmuel Rosenblatt
In honor of:
Maddox Bruening
James DeLano
David Dietz and Jane Kendall
LeRoux Jooste
Andrew Kern
Ari Klosinski
Jessica Lyn Miller
Kyan Mwatha
Meredith Naylor
Ryan Piansky
Oran C. Privett
Gabby Provenzano
Charles Remquest
Edward Sarubbi
Jeremy Sable
Jacob Schwartz
Sadie Sikora
Amanda Smith
Jason and Katrina Wesson
Ryan Williams
The Robby Smith Family
The Family of Paula Eubanks and David Blume
In honor of:
Sarah Wisely through the LanConnect Golf Tournament
Renea and Mason Lundin through Running for a Cause
Ricky Springer through Racing for a Cause
Megan Yanos and the Findley University Dance-A-Thon
The Birch Wathen Lenox School donation from Dress Down
Day coordinated by APD member Andrew Frischling
IDL Worldwide donation from their Coffee Cup Fund
Many small people,
who in many small places,
do many small things,
can alter the face of the world.
-Published in Newsweek,
from the Berlin Wall
Thinly sliced turkey
Brown rice flour
Erewhon Crispy Brown rice cereal
California Rice bran oil
Rice milk
Pulverize rice cereal in food processor until fine. Place in a
bowl. Place flour and rice milk in separate bowls. Coat thinly
sliced turkey fillets first with flour, then rice milk, then coat
with rice crumb mixture. Place in a cast iron skillet then coat
with rice bran oil. Sautee for about 10 minutes each side.
Options: substitute other safe meat
Options: substitute fruit juice for rice milk
Options: substitute other safe grain for rice
APFED Membership / Donation Form
Mission: American Partnership for Eosinophilic Disorders is a nonprofit
organization dedicated to patients and their families coping
with eosinophilic disorders. APFED strives to expand education,
create awareness, and support research while promoting advocacy
among its members.
Annual Memberships now being accepted.
Become a member online at www.apfed.org or mail this form.
Name
Personal Membership
US $30
Canadian $45
International $55
Address
Country
Phone
Professional Membership
US $100
Canadian $125
International $150
Email *
∗ Please note that APFED is going Green. In an effort to save money
and the environment, the APFED newsletter will be delivered via
email unless noted otherwise.
I want to receive email notifications from APFED
I want to receive only newsletters via email from APFED
Name and age of person with eosinophilic disorder:
Donations: I would like to support APFED’s mission with a tax
deductible donation of:
$25 $50 $100 $250 $500 $1000
Other ______________
Submitted by Viv Sarubbi
Online donations welcome at www.apfed.org.
Donations by check should be made payable to APFED at:
APFED
PO Box 29545
Atlanta, GA 30359
11

American Partnership
for Eosinophilic Disorders
PO Box 29545
Atlanta, GA 30359
www.apfed.org
Phone: 713-493-7749
E-mail: mail@apfed.org
PLEASE FORWARD