2. Introduction
Primary gastric lymphoma : rare tumour, <5% of
primary gastric neoplasms.
median age of diagnosis = 60 years old
Male=female
Symptoms :abdominal pain , loss of appetite ,weight
loss, gastrointestinal bleeding, and Vomiting
The primary risk factor for gastric lymphoma is
infection with H. pylori

3. Endoscopic findings
gastritis and superficial ulcers
diffuse thickening and irregularities of mucosal folds
submucosal mass-like effect
Frankly exophytic masses with the appearance of
carcinoma

4. Grading , by EUS
low-grade or indolent
high-grade or aggressive
grading is extremely important in the prognosis and
treatment

5. Treatment
*H. pylori eradication therapy.
* Surgery, chemotherapy, and/or radiation therapy
for patients with less than complete response to
treatment

6. Prevalence of H. pylori Infection
eradicating therapy and thus tumour regression in a
high percentage of cases
• highly variable , almost 90% in low-grade
lymphomas
• depend on the number and type of diagnostic
techniques used for diagnosis, on histological
grade, and on tumour invasion depth

7. *negativity in at least two diagnostic modalities should be
required to definitely consider a patient as non-infected
• H. pylori mucosal colonisation is in patches
• Extensive mucosal lesion secondary to lymphoma may
reduce the density of the infection to even
undetectable levels
• Histological grade: H. pylori infection is cleared by
lymphoma progression and blastic transformation
• Invasion depth : The prevalence of infection decreases
with the progression of gastric wall invasion –it is very
high in tumours confined to the mucosa or superficial
submucosa (90%), and lower than 50% in neoplasms
extending beyond the lamina propria.

8. H. pylori Eradication and MALT
Lymphoma Remission
*low grade : effective in treating approximately 80%
endoscopic surveillance every 3-6months.
time interval between eradication and lymphoma
regression : 4 weeks - 14 months
If failure >> 2nd line trt
*High grade : not considered standard therapy
unlikely to respond (transformed, antigen independent,
autonomously growing tumours )
*H.pylori negative :no guideline, under discussion, may
be beneficial
( low bacterial counts and urease-negative H. pylori
mutant strains may escape detection by the diagnostic
tests )

9. Histological Regression of the
Lymphoma after H. pylori Eradication
can vary and can take even longer than 12
months.
Accordingly, most protocols recommend to wait
at least for 12 months after successful
eradication therapy before a nonresponder is
defined and second-line therapy is applied

10. Molecular Regression After H. pylori
Eradication
lags histological regression by 1–2 years
despite the response of localized gastric MALT lymphoma to H. pylori
eradication, a relatively high proportion of patients in histological remission
have persistent monoclonal immunoglobulin heavy chain variable (IgVH) gene
rearrangements for as long as 10 years
in most patients achieving a histological regression of the gastric MALT
lymphoma, a minimal residual disease persists for years.
This may indicate that the eradication therapy suppresses, but does not
completely eradicate the tumour clone
although the finding of persistent monoclonal populations at the molecular
level would appear to be a risk factor for lymphoma relapse, patients with
histological regression but with a persistent clonal band should not be treated
unless the lymphoma can be histologically demonstrated