INTRODUCTION

In simple terms the definition of gastritis is an inflammatory process in the gastric mucosa and
submucosa. Gastritis is a health disorder that is most often found in clinics, because the diagnosis is
often only based on clinical symptoms rather than histopathological examination. In most cases,
gastric mucosal inflammation does not correlate with patients' clinical complaints and symptoms. In
contrast, patients' clinical complaints and symptoms are positively correlated with complications of
gastritis. At this time a division of gastritis has been developed based on a system called the Sydney
System Update.

GASTRITISM DISTRIBUTION

The Sydney System update divides gastritis based on topography, mortology and etiology. Broadly
speaking, gastritis is divided into 3 types namely: 1. Monahopic, 2. atropic and 3. special shape. In
addition to the above divisions, there is a form of gastric abnormality which is classified as
gastropathy. So called because histopathologically does not describe inflammation. Classification of
gastritis according to the Sydney System Update requires gastroscopic action, histopathological
examination and investigations to determine its etiology. Biopsy must be done with the right
method, evaluated so that the morphology and topography of mucosal abnormalities can be
synthesized. Many gastroscopic actions ignore topography when taking specimens for
histopathological examination. As a result the results cannot be synthesized, so the classification of
gastritis cannot be arranged properly.

ETIOLOGY

of very important gastritis. In countries where the prevalence of HP infection is present in l l

Heliicobacter pylori (HP) bacterial infections are the valence of HP infections in adults approaching
90% higher. This shows the importance of infection in those who are assessed by the urea breath
test in patients with childhood toddlers. In Indonesia, the prevalence of adult infection, shows a
tendency to decline. In developed countries the prevalence of HP infection in children is very low.
Among adults the prevalence of HP germ infection is higher than that of children but lower than in
developing countries which is around 30% The use of antibiotics, especially for pulmonary infections
suspected of affecting the transmission of germs in the community because of antibiotics can
eradicate HP infection, although the percentage of success is low . At the beginning of infection by
HP germs the gastric mucosa will show an acute inflammatory response. Endoscopically it often
appears as erosion and multiple antrum ulcers or hemorrhagic lesions. Acute gastritis due to HP is
often ignored by patients so that the disease continues to be chronic Immune system impairment
associated with chronic gastritis after autoantibodies to intristic factors and to secretory canalicular s
parietal cells in patients with pernicious anemia of parietal cells correlates favorably with antibodies
to factor i with corpus chronic gastritis in a variety of patients Patients with chronic gastritis
containing parietal anu in their serum and suffering from anemia per bowel boil as follows as
atrophic chronic gastritis, corpus predomination has a characteristic characteristic that histologically
best shows on blood tests showed hypergastrinemia, these patients often also suffer from other
diseases caused by impaired immune function. It remains to be proven that HP bacterial infections
can be a booster for these immunological reactions. Suspicion of the role of HP infection begins with
the fact that patients infected with HP bacteria have antibodies to the secretory canalicular parietal
cell structure much higher than those who are not infected. There are several types of viruses that
can infect the gastric mucosa such as enteric rotavirus and calicivirus. Both types of viruses can
cause gastroenteritis, but are not specifically histopathological. Only cytomegalovirus can produce
histopathological features which are typical of gastric cytomegalovirus infection usually part of
infection in many other organs, especially in young organs and munocompromized Fungi Candida
species, Histoplasma capsulatum and Mukonaceae can infect gastric mucosa only in patients who
are compromised. Patients who have a good immune system usually cannot be infected by fungi
Similar to fungi, the gastric mucosa is not a place that is susceptible to parasitic infections. Non-
steroidal anti-inflammatory drugs are a very important cause of gastropathy infection. Gastropathy
due to NSAIDs varies widely, from only pain complaints to peptic ulcers with upper gastrointestinal
bleeding complications

DIAGNOSIS

Most symptomatic gastritis. Those who have complaints are usually not typical complaints.
Complaints often associated with gastritis are hot and painful pain in the pit of the stomach
accompanied by occasional nausea to vomiting. These complaints actually do not correlate well with
gastritis. These complaints also cannot be used as a tool to evaluate treatment success. Physical
examination also cannot provide information needed to make a diagnosis. The diagnosis is based on
endoscopic and histopathological examination. It is best to carry out biopsies systematically in
accordance with the sydney system update describing often also possible morphological changes
which require topography. Endoscopic features that can be found are erythema, exudative, flaring-
erosion, raised erosion, bleeding, edematous rugae. Histopathological changes in addition to
describing the underlying poses, for example the autoimmune adaptive response of the gastric
mucosa. changes that occur in the form of epithelial degradation, foveolar hyperplasia, neutrophil
infiltration, mononuclear cell inflammation, limpoid follicles, atrophy, intestinal metaplasia,
endocrine cell hyperplasia, parietal cell damage. Histopathological examination should also include
examination of HP bacteria.

TREATMENT

Treatment of gastritis due to bacterial infection HP aims to make the germs radicalized. At this time
a universally approved indication for eradication is an HP bacterial infection that has to do with
peptic ulceration and erection related to low grade B cell lymphoma. As if patients suffering from
non HP dyspepsia eradication of these germs are still expected to be able to suppress the incidence
of atrophy and metaplasia in patients who have been infected. Furthermore, it can prevent peptic
ulcers, gastric cancer and ulcers, even though they are associated with disputed germ infections.
Those who agree argue that germ eradication is reviewed from the epidemiology of lymphoma.
Those who do not agree to consider that not enough evidence of eradication can have such broad
implications. Eradication is done by a combination of various antibiotics and proton pump inhibitors
(PP). The recommended antibiotics are clarithomycin, amoxicillin, metronidazole and tetracycline. If
PPI and a combination of 2 failed antibiotics are recommended, add bismuth subsalicylate / subsitral
(Table 1) Management of autoimmune gastritis is aimed at 2 things, namely cobalamin deficiency
and lesions in the gastric mucosa. Gastric mucosal atrophy is an irreversible condition. Germs often
together with other autoimmune diseases, should the accompanying disease be treated. Repairing
cobalamin difficiency can often correct complications arising from these dificiency. Complications in
the form of pathological abnormalities are indeed more difficult to overcome. It is thought to
conduct surveillance of the possibility of cancer by periodic gastroscopic examination. Lymphocytic
gastritis, often related to HP infection, if it is proven, eradication can be done and often brings
improvements. There is no specific therapy for idiopathic lymphocytic gastritis. Standard dose PPIs
can be tried and often provide improvement. While lymphocytic gastritis accompanying other
diseases, such as gluten enteropathy, management is aimed at primary disease.
Referensi :

Sudoyo, Aru W. dkk. Buku Ajar Ilmu Penyakit Dalam. Jilid II Edisi VI.Jakarta: Interna Publishin
g Pusat Penerbitan Ilmu Penyakit Dalam. Hal 1770-1772