Objective-To determine the prevalence
of mucosa associated lymphoid tissue
(MALT) in the stomach and of a possible
antigen driven proliferation, in patients
with Sjogren's syndrome (SS).
Methods-Twenty one patients with primary
SS and 80 dyspeptic controls underwent
upper endoscopy. Lymphoid tissue
and Helicobacter pylon were assessed by
histopathological analysis. Epstein-Barr
virus (EBV) or human herpes virus-6
(HHV-6) genome were studied by polymerase
chain reaction (PCR) DNA amplification.
Two PCR VDJ procedures were
used to detect immunoglobulin heavy
chain (IgH) gene rearrangement.
Results-Organised MALT was found in
33.3% of the patients, compared with
21P5% of the controls (NS). H pylon
infection was seen in 71% of patients and
63% of controls. Genomic EBV or HHV-6
was found in a minor portion ofSS gastric
tissues. B celi expansion was detected in
nine ofthe 21 patients. Infectious agents in
the stomach might have contributed to B
celi clonality only in 55.50/0 ofthe cases. No
strict relationship was found between
lymphoid follicles and clonality.
Conclusion-Lymphoid accumulation in
the gastric mucosa is common in
Sjogren's syndrome, but full evidence for
an antigen driven B cell expansion could
not be demonstrated. Only a portion of
those with clonal B celi expansion had
evidence of an infectious agent. Other
unknown infectious agents or factors
related to the underlying disease (autoantigen)
and its tissue environment may
have a further role as possible causes of B
clonal expansion in the gastric mucosa.
