A Prospective Study on Triggering Factors of Gastritis and Its Management

Gastritis is the inflammation of the gastric mucosa and is often used to describe the abnormal appearance of abnormal gastric mucosa on endoscopy or radiology. Gastritis encompasses infectious or immunological inflammation of the gastric mucosa and the host response. Histopathological evidence of inflammation in the stomach lining is essential to diagnose this condition. Gastropathy is a gastric mucosal disorder without inflammation, featuring epithelial injury and subsequent regeneration. Gastritis and gastropathy are not mutually exclusive conditions and might sometimes coexist. In clinical practice, gastritis may be accompanied by signs of mucosal injury, whereas gastropathy may present with an inflammatory reaction in the gastric mucosa.¹

Gastritis is classified based on the acuity of the condition (acute versus chronic), the histological features of inflammation, or the etiology. Although the categorization and classification of gastritis are not universally accepted, understanding the histological characteristics and etiological factors associated with the different types of gastritis is essential. Appropriate histological evaluation is also essential in devising management plans for this disease. The primary objective is to equip treating clinicians with the ability to improve patient outcomes through early intervention.²

The membranes lining the stomach wall protect it from acid and germs. If this protective lining is irritated or damaged, it can become inflamed. Long-lasting inflammations can further damage the stomach lining and lead to stomach (gastric) ulcers. Inflammation of the stomach lining is called gastritis. It's usually caused by certain bacteria or the regular use of anti-inflammatory painkillers. There are two kinds of gastritis: acute and chronic. Acute gastritis is typically accompanied by very noticeable stomach and bowel problems that usually go away again on their own after a few days. Chronic gastritis, on the other hand, may go unnoticed or damage the lining of the stomach over time. Sometimes it is not discovered until stomach ulcers have developed, which then cause noticeable symptoms.³

Strictly speaking, the label ‘gastritis’ should only be applied to histologically-proven inflammatory lesions of the gastric mucosa. The etiological classification of gastritis is based on this histological definition. A semantic distinction between gastritis and gastropathies identifies the latter as gastric mucosal abnormalities with a minimal/focal inflammatory component. From a practical standpoint, however, subjective variability in the histological assessment of the inflammatory infiltrate makes the border between the two morphological entities hazy, and the diagnostic label of gastritis is the most often applied. In clinical practice as well as for research's purposes, gastric endoscopy couples the priority of assessing the topography/phenotype of the lesions, with the need of obtaining the mucosal samples for histological diagnosis. At endoscopy, gastric mucosal inflammation features either a reddening or edema of the gastric mucosa, but neither of these endoscopic features are pathognomonic. In a recent study on the accuracy of standard endoscopic imaging for the detection of Helicobacter pylori (H. pylori) gastritis, Okamura and coworkers reported an accuracy of 89% for nodularity, and 77% for mucosal swelling. High-definition endoscopy and virtual chromo-endoscopy (narrow-band imaging, blue light imaging, and linked color imaging) have significantly improved the accuracy of endoscopic gastritis assessment. Mucosal atrophy is considered the cancerization field of gastric malignancies development, which makes crucial its endoscopically/histological assessment .This review addresses the most frequently applied criteria in gastritis classification, the biological rationale behind the endoscopic biopsy sampling (including the biological diversity of the native gastric mucosa), the basic-phenotypes and the clinico-pathological “models of gastritis”, and, finally, the format a histological report potentially consistent with the clinical expectancies.⁴

SYMPTOMS

• Many people with gastritis do not have any symptoms.
• Symptoms you may notice are
• Loss of appetite.
• Nausea and vomiting.
• Pain in the upper part of the belly or abdomen.
• If gastritis is causing bleeding from the lining of the stomach, symptoms may include:

• Black stools.
• Vomiting blood or coffee-ground-like material.

Fig -1

CAUSES

Some potential causes of gastritis may include the following

1. H. pylori bacteria

Gastritis is most commonly due to H. pylori bacteria. Around 35% of people-trusted Source in the U.S. have these bacteria in their bodies.

2. Irritating substances

Reactive gastritis, which is caused by irritants, is also relatively common. It affects around 15% of people Trusted Source in the U.S. NSAIDs such as ibuprofen (Advil) and some other common pain relief drugs can cause stomach irritation and gastritis. NSAIDs represent the most common cause of stomach ulcers.⁵

3. Autoimmune conditions

Autoimmune conditions can lead to gastritis. In people with autoimmune a trophic gastritis, the immune system attacks the stomach lining.

4. Damage to the stomach

Physical trauma or damage to the stomach lining can also lead to gastritis. For example, a person who has undergone surgery to remove part of their stomach may develop postgastrectomy gastritis, which causes the lining to degenerate⁶

5. Other causes

Dietary factors do not usually cause gastritis, but food allergies can contribute to it. Some types of gastritis that stem from other issues include:

Eosinophilic gastritis:

This can result from an allergic reaction. This is rare. It involves the development of thick folds and cysts on the stomach wall.⁷

Fig - 2

RISK FACTOR

Some people, including older adults and individuals with compromised immune function, are more likely trusted Source to develop gastritis.

Some risk factors for gastritis include:

• smoking.
• high levels of stress.
• excessive use of alcohol or cocaine.
• swallowing corrosives or foreign objects.
• a history of chronic vomiting.
• a vitamin B12 deficiency.
• routine use of NSAIDs.
• regular use of prescription steroids, chemotherapy, potassium supplements, or iron supplements.
• exposure to radiation, either as a treatment option or by contamination
• bile reflux after stomach surgery.
• an autoimmune condition, such as Hashimoto’s thyroiditis or type 1 diabetes.
• HIV
• Crohn’s disease.
• Other infections that can increase the risk of gastritis include tuberculosis and syphilis.

Fig - 3

CLASSIFICATION

• Acute Gastritis

Acute gastritis is temporary stomach lining inflammation caused by stress on the gastric mucosa, manifesting as either hemorrhagic or non-hemorrhagic symptoms. This condition can develop due to various factors, including uremia, ischemia, shock, corrosive agents, medications, radiation, trauma, severe burns, sepsis, or alkaline-bile reflux. Certain infections, such as enteroviruses, can also cause a self-limited episode of gastritis. Acute gastritis may result from reduced gastric mucus secretion, mucosal barrier disruption, or decreased mucosal blood flow, depending on the underlying cause.⁸

• Chronic Gastritis

Chronic gastritis is categorized into 2 forms—atrophic and non-atrophic. The primary cause of chronic gastritis is a Helicobacter pylori infection, which typically starts with a non-atrophic morphology. The non-atrophic form of chronic gastritis can progress to atrophic without treatment. The most common cause of atrophic chronic gastritis is autoimmune gastritis, though the etiology remains unclear. Autoimmune gastritis exhibits a chronic mononuclear inflammation accompanied by severe atrophic gastritis, which usually affects the corpus, along with the presence of autoantibodies against parietal cells or the intrinsic factor. However, whether autoimmune gastritis is an independent disorder or if an H pylori infection triggers the autoimmune response in susceptible individuals is unclear.⁹

• Reactive Gastritis

Reactive gastritis or gastropathy has numerous causative factors with acute gastritis. Reactive gastritis may be caused by specific medications, alcohol consumption, radiation exposure, and duodenal (bile) reflux. These causative agents lead to histological mucosal lesions characterized by low-grade inflammation of the gastric mucosa. Although usually asymptomatic, they are revealed through endoscopy, often showing multiple erosions or ulcers without signs of atrophic changes. The use of immune checkpoint inhibitors to treat various malignancies has contributed to the incidence of reactive gastritis, although the condition remains considerably rare.¹⁰

• The Sydney System of Classification for Gastritis

The Histological Division of the Sydney System was introduced in 1990 and has since become the most widely cited classification system for the morphological features of gastritis in endoscopic biopsies. This system conveys information about the type, severity, and extent of gastric pathology. The classification system conveys the topography of gastritis, which can be restricted to the antrum or corpus or involve the entire stomach (pan gastritis). If the etiology of the disease is known, this is added as a prefix to denote the topography. For instance, the label "autoimmune corpus gastritis" is used if the disease is autoimmune.¹¹

The Sydney System of Classification further delineates 5 graded morphological variables that may be added as a suffix to the core topography. These variables include the type or chronicity of inflammation, gastritis activity, intestinal metaplasia, the extent of atrophy, and the presence or absence of Heliobacter pylori. The morphological features are graded as absent, mild, moderate, or severe. The Sydney System of Classification recommends at least 2 random biopsies from both the antrum and corpus, along with an additional biopsy from the incisura angularis. Although the classification system provides a standardized and concise means of documenting the extent and severity of gastritis, the method for predicting or forecasting future morphological changes is impossible.¹²

Classification of Gastritis Based on Etiological Factors

An alternative approach to classifying gastritis considers the etiology and chronicity of the inflammation. This approach categorizes gastritis into 3 main subtypes—acute, chronic, and special. Infectious gastritis is most commonly attributed to the global prevalence of H pylori infection. Other types of infectious gastritis include phlegmonous gastritis (caused by pyogenic bacteria), mycobacterial gastritis (caused by Mycobacterium tuberculosis), syphilitic gastritis, viral gastritis (caused by cytomegalovirus and herpes simplex virus), parasitic gastritis (caused by Anisakis, Cryptosporidium, Ascaris lumbricoides, Giardia, Toxoplasma, and Schistosoma), and fungal gastritis (caused by Candida, Aspergillus, Mucor, Coccidioides, Histoplasma, Cryptococcus neoformans, Pneumocystis carinii, and Torulosis glabrata).¹³

Granulomatous gastritis is a special gastritis observed in patients with Crohn disease and sarcoidosis. Lymphocytic gastritis, collagenous gastritis, and eosinophilic gastritis are additional special subtypes of gastritis with unclear etiologies. Lymphocytic and collagenous gastritis have been associated with celiac disease, whereas eosinophilic gastritis has a strong connection to atopic conditions and food allergens.¹⁴

According to the 2015 Kyoto Consensus Conference, a classification of gastritis based on etiological factors is outlined as follows:

with acute gastritis. Reactive gastritis may be caused by specific medications, alcohol consumption, radiation exposure, and duodenal (bile) reflux. These causative agents lead to histological mucosal lesions characterized by low-grade inflammation of the gastric mucosa. Although usually asymptomatic, they are revealed through endoscopy, often showing multiple erosions or ulcers without signs of atrophic changes. The use of immune checkpoint inhibitors to treat various malignancies has contributed to the incidence of reactive gastritis, although the condition remains considerably rare¹⁵.

The Sydney System of Classification for Gastritis

The Histological Division of the Sydney System was introduced in 1990 and has since become the most widely cited classification system for the morphological features of gastritis in endoscopic biopsies. This system conveys information about the type, severity, and extent of gastric pathology. The classification system conveys the topography of gastritis, which can be restricted to the antrum or corpus or involve the entire stomach (pan gastritis). If the etiology of the disease is known, this is added as a prefix to denote the topography. For instance, the label "autoimmune corpus gastritis" is used if the disease is autoimmune.¹⁶

The Sydney System of Classification further delineates 5 graded morphological variables that may be added as a suffix to the core topography. These variables include the type or chronicity of inflammation, gastritis activity, intestinal metaplasia, the extent of atrophy, and the presence or absence of Heliobacter pylori. The morphological features are graded as absent, mild, moderate, or severe.¹⁷ The Sydney System of Classification recommends at least 2 random biopsies from both the antrum and corpus, along with an additional biopsy from the incisura angularis. Although the classification system provides a standardized and concise means of documenting the extent and severity of gastritis, the method for predicting or forecasting future morphological changes is impossible.¹⁸

Classification of Gastritis Based on Etiological Factors

An alternative approach to classifying gastritis considers the etiology and chronicity of the inflammation. This approach categorizes gastritis into 3 main subtypes—acute, chronic, and special. Infectious gastritis is most commonly attributed to the global prevalence of H pylori infection. Other types of infectious gastritis include phlegmonous gastritis (caused by pyogenic bacteria), mycobacterial gastritis (caused by Mycobacterium tuberculosis), syphilitic gastritis, viral gastritis (caused by cytomegalovirus and herpes simplex virus), parasitic gastritis (caused by Anisakis, Cryptosporidium, Ascaris lumbricoides, Giardia, Toxoplasma, and Schistosoma), and fungal gastritis (caused by Candida, Aspergillus, Mucor, Coccidioides, Histoplasma, Cryptococcus neoformans, Pneumocystis carinii, and Torulosis glabrata).19

Granulomatous gastritis is a special gastritis observed in patients with Crohn disease and sarcoidosis. Lymphocytic gastritis, collagenous gastritis, and eosinophilic gastritis are additional special subtypes of gastritis with unclear etiologies. Lymphocytic and collagenous gastritis have been associated with celiac disease, whereas eosinophilic gastritis has a strong connection to atopic conditions and food allergens.²⁰

According to the 2015 Kyoto Consensus Conference, a classification of gastritis based on etiological factors is outlined as follows:

• Autoimmune gastritis
• Infectious gastritis
• Gastric phlegmon
• Bacterial gastritis
• H pylori-induced
• Enterococcal
• Mycobacterial
• Viral gastritis
• Cytomegaloviral
• Enteroviral
• Fungal gastritis
• Parasitic gastritis
• Gastric anisakiasis
• Cryptosporidium
• Gastritis due to other diseases
• Crohn disease
• Sarcoidosis
• Vasculitis
• Gastritis due to external causes
• Alcoholism
• Radiation
• Chemicals
• Special gastritis
• Allergic gastritis
• Gastritis due to biliary reflux
• Lymphocytic gastritis
• Eosinophilic gastritis.

Pathophysiology

H pylori–Associated Gastritis

H pylori is a flagellated gram-negative bacterium transmitted through environmental factors or the fecal-oral or oral-oral routes. The pathophysiology of H pylori–induced gastritis involves a complex interaction between bacterial virulence factors and the host's immune responses.²¹ This interplay disrupts the gastric mucosal barrier and leads to chronic inflammation. H pylori possess virulence factors that facilitate cell adhesion, cause cell damage, disrupt tight junctions, and evade the host immune response. Notably, the cytotoxin-associated gene A (CagA) is a potent inducer of inflammation and is associated with the development of gastric cancer.²²

The survival and colonization of H pylori in the stomach depend on the urease produced by the bacterium. Urease catalyzes urea hydrolysis, releasing ammonia and forming a protective layer around the bacterium.²³ The ammonia also helps neutralize the acidic micro environment of the stomach, allowing the bacterium to thrive in the stomach's low pH conditions. Subsequently, the flagellum and other mucolytic enzymes assist the organism in penetrating the mucus layer and reaching the gastric epithelium, which attaches to the epithelial cells.²⁴

which is the distinguishing characteristic of gastritis. Host macrophages and activated T-cells take up various antigenic substrates from the organism.[18] The recruited T-cells are paradoxically inhibited by the expression of B7-H1 (programmed death-1 ligand 1) on gastric epithelial cells.²⁵Studies have shown that H pylori induce B7-H1 expression on gastric epithelial cells, which is believed to contribute to the chronicity of the bacterial infection.] Further stimulation of inflammation occurs through an H pylori–induced increase in interleukin (IL)-8 production by the gastric epithelial cells.IL-8 subsequently triggers the activation of neutrophils and the recruitment of other inflammatory cells into the mucosa. Persistent inflammation ultimately leads to the depletion of gastrin-producing (G) cells and acid-producing parietal cells in the gastric mucosa. Over time, atrophy and intestinal metaplasia develop.²⁶

Autoimmune Gastritis

Autoimmune metaplastic atrophic gastritis develops due to T-cell–mediated destruction of the oxyntic mucosa and the production of autoantibodies targeting parietal cells and the intrinsic factor.²⁷ A proposed mechanism for this disease in patients with H pylori-induced atrophic gastritis outlines a crossover of antigenic activity directed against the bacterium and toward host antigens in the region, including parietal cells and the intrinsic factor.²⁸ In primary autoimmune atrophic gastritis, the immune response is directed against these antigens irrespective of an H pylori infection. However, the molecular factors driving the autoimmune response and initiating the pathogenesis of the condition remain unidentified²⁹. Over time, the immune-mediated destruction of the oxyntic mucosa leads to mucous cells and metaplastic glands within the gastric mucosa, including both intestinal and pseudo-pyloric.³⁰ 

Fig - 4

TREATMENT

Gastritis is treated in various ways, depending on what the symptoms and causes are, and how severe the inflammation is

• Treatment without medication

It is important to avoid alcohol and nicotine (smoking) if you have acute gastritis. Doctors commonly recommend eating food that is gentle on your stomach, like toast or porridge while avoiding coffee and foods that are greasy or spicy. Getting some rest is also advisable. They also often recommend eating either small portions or nothing at all for 1 to 2 days. There has hardly been any scientific research on whether these things can help, though.³¹

If you notice that stress is making your stomach problems worse, you can try coping with it differently and look for ways to relax more in your everyday life.³²

Fig - 5

• Treatment with medication

If the problems don't go away or are very severe, gastritis is usually treated with medication that reduces the amount of acid. Until the symptoms go away, the following medications can be used, depending on the type and severity of the symptoms:

Antacids like aluminium hydroxide or magnesium hydroxide neutralize the acid already in your stomach.

Proton pump inhibitors (PPIs) like omeprazole or pantoprazole reduce the production of stomach acid³³.

H2 blockers such as ranitidine and famotidine also reduce acid production.

If the gastritis is caused by a Helicobacter infection, proton pump inhibitors are combined with two or three antibiotics³⁴.

RESULTS

DATA ON DISTRIBUTION OF PATIENTS ON GENDER:

Total distribution of patient with respect to the gender shows that, out of 70 patients ,57 patients (81.4) were female and male 13 patients (17.1) were resulted with ischemic stroke.

Table 1: Gender distribution of patients

Figure 7 : Distribution of patients based on gender

DATA ON DISTRIBUTION OF PATIENTS BASED ON AGE

Total distribution of patient with respect to the age group majority of the patients were found to be between the age group of 18 year (4.3%),followed by >19 year (18.6%), and this age group >20 (38.6%),many of years are having (27%) 21-36  years.

Table 2: Age distribution of patients

Figure 8: Distribution of patients based on age

DATA ON DISTRIBUTION BASED ON SYMPTOMS:

These symptoms are associated with the gastritis were out of 70 patients, loss of appetite is having 18 patients (29%) , burning sensation are 32 (51.6%) , vomiting are having 15 patients (24.5%), heartburn are having 12 patients (19.4%), bloating are having 5 patients (8.1%) ,acid reflux are having 4 patients (6.5%).

Table 2: Symptoms of patients

Figure 8: Distribution of prescriptions based on symptoms

DATA ON DISTRIBUTION BASED ON SPICY FOOD

Out of 70 patients are having the spicy food the rarely  25 patients (35.7%) , sometimes 40 patients (57.1%) , frequently 7 patients (10%) .

Table 3: Spicy food of patients

Figure 9: Distribution of prescriptions based on spicy food

DATA ON DISTRIBUTION BASED ON SKIP MEALS

Out of 70 patients are having the skip meals were having  34 patients (48.6%) to the  yes , were having 37 patients (52.9%) to the no.

Table 4: Skip Meals Of Patients

Figure 10: Distribution of prescriptions based on skip meals

DATA ON DISTRIBUTION BASED ON DRINK COFFEE / TEA

Out of 70 patients are having the drink coffee or tea , none of the 43 patients (61.5%) ,were  1-2 are having 27 patients (38.6%), were 3 or more are having 2 patients (2.9%).

Table 5: Drink Coffee and Tea

Figure 11: Distribution of prescriptions based on drink coffee / tea

DATA ON DISTRIBUTION BASED ON CARBONATED DRINKS

Out of 70 patients are having the carbonated drinks  were having  32 patients (45.7%) to the  no , were having 38 patients (54.3%) to the yes.

Table 6: Carbonated Drinks of Patients

Figure 12: Distribution of prescriptions based on carbonated drinks

DATA ON DISTRIBUTION BASED ON DIAGNOSED WITH GASTRITIS

Out of 70 patients are having the diagnosed with gastritis were having  19 patients (27.1%) to the  yes , were having 53 patients (75.7%) to the no .

Table 7: Diagnosed with Gastritis of Patients.

Figure 13: Distribution of prescriptions based on diagnosed with gastritis.

DATA ON DISTRIBUTION BASED ON TAKING ANY REGULARLY DRUGS

Out of 70 patients are taking the regularly drug , pain killer (NSAIDS like ibuprofen, aspirin) 6 patients (8.6%) , steroids 0 patients (0%) , antacids 5 (7.1%) , none 59 patients (84.3%) .

Table 8: Any Drug Intake

Figure 14: Distribution of prescriptions based on taking any regularly drugs

DATA ON DISTRIBUTION BASED ON SMOKE

Out of 70 patients are having the smoke  were having  0  patients (0 %) to the  yes , were having 69 patients (98.6%) to the no, and sometimes 1 patients (1.4%).

Table 9: Smoke of Patients.

Figure 15 : Distribution of prescriptions based on smoke

DATA ON DISTRIBUTION BASED ON ALCOHOL

Out of 70 patients are having the alcohol  were having  1  patients (1.4 %) to the  yes , were having 69 patients (98.6%) to the no, and sometimes 1 patients (1.4%).

Table 10 : Alcohol Of Patients.

Figure 16 : Distribution of prescriptions based on alcohol

DATA ON DISTRIBUTION BASED ON STRESS FREQUENTLY

Out of 70 patients are having the alcohol  were having  24  patients (34.3 %) to the  yes , were having 10 patients (14.3%) to the no, and sometimes 1 patients (1.4%).

Table 11 : Stress Frequently of Patients.

Figure 17 : Distribution of prescriptions based on stress frequently

DATA ON DISTRIBUTION BASED ON FEEL DISCOMFORT

Out of 70 patients are having the feel discomfort  were having 14 patients (20%) to the  yes , were having 56 patients (80%) to the no .

Table 12 : Feel Discomfort of Patients.

Figure 18 : Distribution of prescriptions based on feel discomfort

DATA ON DISTRIBUTION BASED ON TROUBLE SLEEPING DUE TO STOMACH DISCOMFORT

Out of 70 patients are having the feel discomfort  were having 20 patients (29%) to the  yes , were having 49 patients (71%) to the no .

Table 12 : Trouble Sleeping Due to Stomach Discomfort of Patients.

Figure 19: Distribution of prescriptions based on trouble sleeping due to stomach discomfort

DATA ON DISTRIBUTION BASED ON DIAGNOSED

Out of 70 patients are taking the diagnosed, gastritis 18 patients (25.7%), peptic ulcer  1  patients (1.4%) , stomach pain 7 patients (10%) , none 44 patients (62.9%) .

Table 13 : Diagnosed of Patients.

Figure 20 : Distribution of prescriptions based on diagnosed

DATA ON DISTRIBUTION BASED ON GASTRIC DISCOMFORT

Out of 70 patients are taking the gastric discomfort, ignore it 6 patients (8.6%), take medicines 13 patients (18.6%) , apply home remedies 23 patients (32.9%) , visit a doctor  16  patients (22.9%) , take a rest 26 patients (37.1%).

Table 14 : Gastric Discomfort Of Patients.

Figure 21 : Distribution of prescriptions based on gastric discomfort

DATA ON DISTRIBUTION BASED ON SELF - MEDICATED FOR STOMACH ISSUES WITHOUT CONSULTING A DOCTOR

Out of 70 patients are having the self - medicated for stomach issues without consulting a doctor were having 39 patients (55.7%) to the  yes , were having 31 patients (44.3%) to the no .

Table 12 : Self - Medicated For Stomach Issues Without Consulting A Doctor Of Patients.

Figure 22 : Distribution of prescriptions based on self - medicated for stomach issues wthout consulting a doctor of patients