medical

1. Presented by supervised by
Dr. Saleh salman Dr.Adnan Al-Asosi

3.  Mr. N I
 Age : 48
 Gender : male
 Nationality : Bangladeshi
 Date of admission : 16/8/2014
 Date of discharge : 26/8/2014

4. Situation and background
 48 years , male patient , previously healthy , non smoker , not
alcoholic , come to medical causality complaining of
abdominal pain and vomiting .
 this was the 4th visit to causality ( seen before by surgical and
medical doctors ) .
 The patient has history of five days duration of peri-umbilical
abdominal pain of moderate severity , colicky in nature ,
associated with multiple episodes of vomiting ( 3 times per
day in average )
 there is no ( fever, weight loss , change in bowel habits ,
dysuria , melena , hematemesis , skin lesions, or joint pain …)
 There is no clear aggravating or relaxing factors
 There is no clear radiation

5. Assessment
 The patient vitally stable :
Bp= 143/95 HR=86 TEMP=36.6
 He has no jaundice , pallor, or cyanosis…….
 CVS: S1S2+ O
 Chest : clear bilaterally
 Abdomen : soft and lax , +ve bowel sounds, no rigidity
or rebound , mild peri umbilical and RT iliac fosa
tenderness
 CNS : no focal deficit , no abnormal movement , no
abnormal behavior
 LL: no edema , no signs of DVT , Intact perpheral
pulsation

6. Initial investigation:
 X-ray chest : normal
 X-ray abdomen : no air under diaphragm, no air fluid
level
 ECG : normal
WBC 20000 PH 7.40
SEG 33 % Amylase 44
LYM 13 % Glu ( random) 7.5
mono 5 % Cr 99
Eosin 42 % Na 138
8770 K 3.8
Hgb 159 TNT negative
PLT 312 Urine RM unremarkable
INR 1.05
APTT 29

7. SUGGESTION

8. Further work up

10. CRP negative ESR 6
Blood film eosinophilia
Stool R/M WBC=0-1 No parasite or ova seen
Alb 38 Alt 41
Uric acid 304 Alk-pho 73
T.G 1.9 Ca 2.22
Cholesterol 4.3
T bil 22
Widdal test Negative Brucellosis test Negative
Skin PPD test Negative

11.  During hospital stay :
the patient received empirical treatment for
gastroenteritis as well as parasitic infection but still
has abdominal pain and Eosinophilia
He received also supportive treatment with IV fluid,
losec and anti-emetics
Surgical doctors was consulted again : no acute surgical
emergency

12. In summary
 48 years , male patient , previously healthy
 complaining of abdominal pain and vomiting
 Positive lab finding : eosinophilia
 Imaging studies : suggestive for distal ileal inflammation

13. DIAGNOSIS ?

14. Next step = endoscopy

17. Eosinophilic gastroentritis

18. INTRODUCTION
 Eosinophilic gastroenteritis (EG) represents one member of a
family of diseases that includes (eosinophilic esophagitis,
gastritis, enteritis, and colitis ), collectively referred to as
eosinophilic gastrointestinal disorders (EGIDs) .
 Despite its rarity, eosinophilic gastroenteritis needs to be
recognized by the clinician because this treatable disease can
masquerade as irritable bowel syndrome. The diagnosis of EG
is confirmed by a characteristic biopsy and/or Eosinophilic
ascitic fluid in the absence of infection by intestinal parasites
or other causes of intestinal eosinophilia.
 Eosinophilic esophagitis is a distinct clinical entity and it is
discussed elsewhere.

19.  The clinical features of EG are related to the layer(s)
and extent of bowel involved with eosinophilic
infiltration: mucosa; muscle; and/or subserosa .
 The prevalence of each subtype is unknown because
of reporting and referral biases. Surgical series
report a predominance of muscular disease with
obstruction , while medical series primarily
describe patients with mucosal involvement .
 The disease can affect patients of any age, but typical
presentations are in the third through fifth decade
(a peak age of onset in the third decade ) with a
male predominance

20. MUCOSAL DISEASE
 Eosinophilic mucosal infiltration produces nonspecific
symptoms which depend upon the organ(s) involved. The entire
gastrointestinal tract from esophagus to colon, including bile
ducts, can be affected .
 In a retrospective study of 40 patients, the most common
symptoms were abdominal pain, nausea, vomiting, early satiety,
and diarrhea, suggesting a possible diagnosis of irritable bowel
syndrome .
 Only one-third of patients had a weight loss of 2.4 kg or more.
 Patients with diffuse small bowel disease can develop
malabsorption

21. Laboratory findings :
 Peripheral eosinophil counts are usually elevated, ranging from
5 to 35 % with an average absolute eosinophil count of 2000 cells/μL
, but may be normal in about 20 % of patients .
The absolute eosinophil count rather than percent eosinophils is
the best indicator to document eosinophilia.
 Patients with malabsorption may have the typical laboratory
findings of this disorder: abnormal D-xylose test, increased fecal fat
excretion, prolonged prothrombin time, and reduced serum iron
concentration.
 Hypoalbuminemia can be induced by a protein-losing enteropathy,
 anemia can be induced by impaired iron absorption, and occult
gastrointestinal bleeding.

22.  The ESR is usually normal , but can be elevated modestly
in about 25 percent of patients .
 Serum IgE levels can be elevated, especially in children,
and up to 50 percent may be atopic or have a history of
food intolerance or allergy.
 Barium studies of the gastrointestinal tract may
suggest the diagnosis but are neither sensitive nor specific.
They typically reveal thickening or nodularity in the
antrum and a thickened or "saw-tooth" mucosa in the
small bowel .

23. Diagnosis :
The diagnosis of mucosal EG is typically confirmed by endoscopic biopsies,
which reveal ≥20 to 25 eosinophils /HPF on microscopic
examination.
Upper endoscopy with biopsy of the stomach and small intestine is
diagnostic in at least 80 percent of patients . Typical endoscopic
findings in mucosal disease include nodular or polypoid gastric mucosa,
erythema, or erosions .

24. There are specific recommendations with respect to the diagnosis
 Biopsies should be taken from both normal and abnormal
appearing mucosa because even normal appearing mucosa can
demonstrate eosinophilic inflammation .
 Multiple biopsy samples (at least four to five biopsies per site)
should be taken from both the stomach and small intestine
including areas with visual abnormalities to overcome sampling
error . Biopsies that reveal increased eosinophils in sheets in
conjunction with mucosal architectural abnormalities are
diagnostic in the appropriate clinical setting.
On the other hand, given its patchy mucosal involvement, even
multiple normal mucosal biopsy specimens cannot exclude the
diagnosis of EG in some patients.

25. MUSCLE LAYER DISEASE
 Eosinophilic infiltration of the muscle layer of the
gastrointestinal tract results in a thickened, rigid gut and
symptoms of intestinal obstruction such as nausea, vomiting,
and abdominal distention .
 Pseudo-achalasia, esophageal stricture, perforation, or
obstruction of the gastric outlet, small bowel, or rarely the
colon can occur depending on the site of infiltration.
(? Impairing motility )
 Food intolerance or allergic history IS NOT usually present in
patients with this form of eosinophilic gastroenteritis (EG).
 Patients may present with a peripheral eosinophilia with
absolute eosinophil counts averaging 1000 cells/μL .

26. Diagnosis :
 The diagnosis of muscle layer disease is typically made after
resection of small bowel for obstruction.
 In less acute presentations, Barium studies usually reveal
irregular luminal narrowing, especially in the distal antrum
and proximal small bowel. These findings can mimic those
induced by cancer, lymphoma, or other malignancies.
 Endoscopic biopsies should be performed, but they are often
nondiagnostic because mucosal involvement is lacking.
 In these cases, laparoscopic FULL THICKNESS biopsy is
usually necessary to exclude malignancy, thereby avoiding
unnecessary radical resectional surgery by confirming the
diagnosis

27. SUBSEROSAL DISEASE
 Patients with subserosal eosinophilic gastroenteritis (EG)
present with isolated ascites or ascites in combination
with symptoms characteristic of mucosal or muscular EG .
 The diagnostic feature is a marked eosinophilia, up to 88 %,
in the ascitic fluid.
 Patients in this subgroup MAY HAVE an allergic history and
peripheral eosinophil counts as high as 8000 cells/μL .
 An eosinophilic pleural effusion may also be present

28. PATHOGENESIS
The pathogenesis of eosinophilic gastroenteritis (EG) is not
well understood. Several epidemiologic and clinical features
suggest an allergic component:
 Approximately one-half of patients have allergic disease, such
as asthma, defined food sensitivities, eczema, or rhinitis
 Some patients have elevated serum IgE levels.
The role of food allergy as a stimulus to EG has not been as
clearly defined as for eosinophilic esophagitis. However,
several reports have described an allergic response to food
allergens with improvement in disease activity with allergen
avoidance with an elemental or elimination diet .

29.  In allergic EG patients, but not those with conventional
anaphylactic food allergy, a population of IL-5 expressing food
allergen specific T cells have been characterized . This
suggests that food exposure activates IL-5+ T cells in EG,
leading to gut eosinophilia.
As a result, a thorough allergy history and workup are important
in management of this illness.
Although food hypersensitivity may play an important role in
EG pathogenesis, no food allergy test (skin, patch,
or RAST/ImmunoCAP test) has been shown to effectively
identify specific culprit foods leading to clinical improvement.

30.  Once eosinophils are recruited to the gastrointestinal tract,
they are able to persist through the release of eosinophil
active cytokines such as interleukin-3, interleukin-5, and
granulocyte macrophage-colony stimulating factor (GM-CSF)
 Eotaxin, a chemokine, appears to have a central role in the
recruitment of eosinophils into the small intestine in
response to antigen challenge .
 Eosinophils may cause local inflammation by release of
eosinophil major basic protein, a cytotoxic cationic protein .

31. DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS
Eosinophilic gastroenteritis (EG) should be suspected
in any patient with
gastrointestinal symptoms
associated with
peripheral eosinophilia.
It should also be considered before making a diagnosis
of irritable bowel syndrome. As noted above, the
diagnosis of EG can be made in almost all cases by
suspicion in the appropriate clinical context and
endoscopic or full thickness biopsy or paracentesis.

32. Other diseases in which gastrointestinal symptoms are
associated with peripheral eosinophilia usually can be
distinguished from EG with simple laboratory
tests and/or endoscopic biopsies:
 Intestinal parasites.
 Malignancies
 Crohn's disease
 Polyarteritis nodosa
 Hypereosinophilic syndrome (HES)
 Eosinophilic granuloma (Langerhans cell histiocytosis),

33.  Intestinal parasites ( such as Ancylostoma, Anisakis, Ascaris,
Strongyloides, Toxocara, Trichiura, Capillaria, and Trichinella )
all cause eosinophilia and should be excluded with careful
examination of the stool for ova or
parasites and/or appropriate serologic testing. Such stool
examination may reveal Charcot-Leyden crystals, which are the
product of eosinophil granules.
Infection with the dog hookworm, Ancylostoma caninum, mimics
EG clinically and pathologically with eosinophilic infiltration of
the gut wall and even ascites. Although reported so far only from
Australia, the worm has a worldwide distribution and is easy to
overlook even on pathologic specimens .

34.  Malignancies, such as lymphoma, gastric cancer, and colon
cancer, can present with intestinal obstruction, masses on
barium radiography, and eosinophilia. They can be differentiated
from EG by endoscopic or full thickness biopsy.
Conversely, EG can mimic some of the features of a MALT
lymphoma, with bowel wall thickening and marked
retroperitoneal lymphadenopathy.
 Crohn's disease can usually be differentiated by the typical
architectural distortion that is not found in EG. Rarely, Crohn's
disease or ulcerative colitis may be associated with peripheral
eosinophilia and/or an eosinophil rich tissue infiltrate.

35.  Polyarteritis nodosa is associated with systemic
manifestations, a markedly elevated ESR , and perivascular
eosinophilia .
 Hypereosinophilic syndrome (HES) is an idiopathic
condition associated with marked peripheral eosinophilia
and may rarely present with predominantly gastrointestinal
symptoms.
Many EG patients may formally fulfill the diagnostic criterion
for HES (AEC ≥1500 cells/mL present for over six months).
However, HES, in contrast to EG, involves other organs
such as the heart, lungs, brain, and kidneys and generally has
a progressively fatal course . Because of the potential for
confusion, patients with EG should be counseled that their
prognosis is generally good and that they do not have HES.

36.  Eosinophilic granuloma (Langerhans cell histiocytosis),
which can present as an antral mass, is diagnosed by
its typical GRANULOMATOUS appearance on biopsy
specimens .
An eosinophilic gastroenteritis, characterized by
abdominal pain, diarrhea, gastrointestinal bleeding,
and colitis, may precede or coincide with the vasculitic
phase of the Churg-Strauss syndrome. Asthma is the
cardinal feature of this disorder (occurring in more
than 95 percent of patients) and usually precedes the
vasculitic phase by approximately 8 to 10 years.

37. PROGNOSIS AND TREATMENT
 Data on the natural history and therapy of (EG) are limited to case
reports and retrospective series of less than 20 patients.
 Untreated patients with EG may rarely remit spontaneously or
progress to severe malabsorption and malnutrition .
 There have been no prospective, randomized therapeutic clinical
trials. Thus, TREATMENT IS EMPIRIC and based upon the severity
of the clinical manifestations.
 Patients who are SYMPTOMATIC or have evidence of
MALABSORPTION may be treated with systemic glucocorticoids.
Micronutrient deficiencies should be sought and replaced as
needed. [ In cases of severe malabsorption, a dietary consultation
may be valuable to help identify nutritional deficits] .

38.  Although food hypersensitivity plays an important role in EG
pathogenesis, no food allergy test (skin, patch or allergen
specific IgE) has been shown to effectively identify specific
culprit foods leading to clinical improvement of EG symptoms
or tissue eosinophilia.
Thus, at present there is no evidence base to support routine
food allergy testing of EG patients for use in clinical decision
making.
A prospective trial in adults with EG has demonstrated clinical
remission with a six-week course of dietary elimination. In this
study, three of seven adults undergoing an empiric six food
elimination diet and six of six adults undergoing elemental diet
had significant reduction in symptoms, complete histologic
remission, endoscopic improvement and normalization of
peripheral eosinophilia within six weeks .

39.  The empiric elimination diet is similar to the six-food
elimination diets employed in EoE, with the patient avoiding
soy, wheat, corn, egg, milk, peanut, and seafood .
 limitations exist due to patient tolerance.
 Dietary therapy should be pursued in motivated patients
under the guidance of a dietitian trained in eosinophilic
gastrointestinal disorders.

40.  If dietary measures do not result in decreased symptoms
and tissue eosinophilia, we suggest a trial
of prednisone (typically 20 to 40 mg/day).Improvement
usually occurs within two weeks regardless of the layer of
bowel involved .
Prednisone should then be tapered rapidly over the next
two weeks. However, some patients require more
prolonged therapy (up to several months) to produce
resolution of symptoms .
 Patients not responding to prednisone can be tried on
intravenous glucocorticoids.

41.  The subsequent course is variable.
Some patients have no recurrences , or only require
periodic glucocorticoid bursts, while most experience
recurrent symptoms during or immediately after
the Predniaon taper. The latter patients may
require long-term, low-dose maintenance therapy
with prednisone (eg, 5 to 10 mg/day). Other patients
experience periodic flares months to years after the
initial episode. They can be treated with another short
course of oral prednisone, 20 to 40 mg/day, followed
by a rapid taper

42. Several other approaches have been described in case
reports or small series:
 Successful transition from oral, conventional
glucocorticoids to budesonide (non-enterically
coated) was described in patients with EG involving
the gastric antrum and small intestine . It should be
noted that the formulation of budesonide currently
available for gastrointestinal use is in controlled ileal
release capsules, which largely bypass the upper
gastrointestinal tract.

43.  Oral cromolyn (800 mg/day in four divided doses)
has been effective for short- and long-term
management in some , but not all case reports. This
agent works by preventing the release of mast cell
mediators, including histamine, platelet-activating
factor, and leukotrienes, and also is thought to reduce
absorption of antigens by the small intestine.
 Ketotifen (Zaditen), an H1-antihistamine, has been
helpful in individual cases . The drug is approved for
treatment of urticaria in Canada, Europe, and Japan,
but is not available in the United States. In adults, it is
administered at a starting dose of 1 mg at night and
increased to 2 to 4 mg per day for one to four months.

44.  The leukotriene antagonist,montelukast , was
effective in some reported cases, but not in others
 A clinical response to suplatast tosilate (a novel
antiallergic drug that suppresses cytokine production
including interleukin-4 and interleukin-5 from T
helper 2 cells) was described in a single patient .

45.  In a preliminary report of four patients, treatment with a
humanized anti-interleukin-5 antibody was
associated with reduced peripheral and tissue eosinophil
counts but had NO effect on symptoms . Rebound
eosinophilia has been observed after the drug was
discontinued .
 A report of nine patients treated with omalizumab
( which is a recombinant humanized IgG1 monoclonal
antibody that binds IgE with high affinity and has been
developed for the treatment of allergic diseases) described
significant improvement in symptoms and measures of
IgE mediated allergy . Tissue eosinophilia was reduced but
results were not statistically significant.

46. SUMMARY AND RECOMMENDATIONS
 The signs and symptoms of eosinophilic gastroenteritis (EG)
are related to the layer(s) and extent of bowel involvement .
Eosinophilic mucosal infiltration produces NONSPECIFIC
symptoms, which depend upon the organ(s) involved. Most
common symptoms are abdominal pain, nausea, early satiety,
vomiting, diarrhea, and weight loss.
Eosinophilic infiltration of the muscle layer of the
gastrointestinal tract results in a thickened, rigid gut and
symptoms of intestinal OBSTRUCTION such as nausea,
vomiting, and abdominal distention.
Patients with subserosal EG present with isolated ASCITES or
ascites in combination with symptoms characteristic of
mucosal or muscular EG.

47. We suggest the following approach, which is based upon
observational data and clinical experience:
 In patients who are symptomatic or have evidence of
malabsorption, we suggest an initial attempt at an empiric
elimination diet, an elemental diet, or a six-food elimination
diet for six weeks. This approach is similar to dietary
interventions used to treat eosinophilic esophagitis.
 If a dietary approach is undertaken, patients should be
referred to a dietitian to obtain proper education on the foods
to avoid. If a history of environmental allergens is identified,
these should be treated in conjunction with the diet.
 If the dietary changes are successful at reducing symptoms,
peripheral eosinophilia, and tissue eosinophilia, foods can be
added back slowly in a systematic fashion from least allergenic
to most allergenic.

48.  We follow patients based upon their symptoms and the
changes in peripheral eosinophilia. We perform a repeat
endoscopy when there is uncertainty regarding the response to
treatment and/or degree of ongoing disease activity.
 In patients who decline a dietary approach or whose symptoms,
tissue and peripheral eosinophilia do not improve after the diet,
we suggest a trial of prednisone (20 to 40 mg/day).
Improvement usually occurs within two weeks regardless of the
layer of bowel involved. Prednisone should then be tapered
rapidly over the next two weeks. However, some patients require
more prolonged therapy (up to several months) to produce
resolution of symptoms.
Patients who relapse immediately after steroid cessation may need
chronic low dose steroids or transition to budesonide or other
agents as outlined above.

49. Refference
 Prussin C et al . Eosinophilic gastroenteritis .
UpToDate 2014; 2536 : 10.0.