Gastritis

The most common symptom of gastritis is epigastric pain which is often described as burning by patients. Sometimes, this burning pain extends up to the sternum. There may also be nausea and vomiting, feeling of fullness, easy satiety, hiccups and flatulence. Symptoms like bleeding occur when complications set in and they could be accompanied by symptoms of anemia. They usually manifest as blood in stool or coffee stained vomitus [5].

Laboratory tests

• Complete blood count
• Coagulation profile
• Urea breath test
• Liver function test
• Renal function test
• Stool for occult blood
• Gastric biopsy 
• Pregnancy test
• Helicobacter pylori stool antigen test
• Test for gall bladder and pancreatic function

Imaging

• Plain abdominal X-ray
• Double contrast barium studies
• CT scan
• Endoscopy

The treatment of gastritis can either be medical or surgical. Medical treatment involves identifying the root cause of gastritis and eradicating it as well as instituting supportive treatment. Supportive treatment involves setting up an IV line to replace lost fluid and electrolytes for patients who are vomiting and blood transfusion for anemic patients [6].

Drugs treatments are targeted at reducing acid secretion, increasing mucosal resistance and eradicating infectious organisms. They include:

• Antacids to neutralize the acidity of the stomach.
• H2 blockers like cimetidine and ranitidine.
• Proton pump inhibitors like omeprazole.
• Antibiotics include metronidazole, amoxicillin, clarithromycin, and tetracycline. They are usually used in combination.
• Other antibiotics for target specific causes like anti-tuberculosis drugs for gastritis caused by mycobacterium.

Surgical intervention is rare and mostly involves resection and it is limited to cases of phlegmonous gastritis [7].

The prognosis of simple gastritis is generally very good. Once the causative organism is identified and treated, the individual makes good recovery. However, when it becomes complicated by hemorrhage, perforation, or in minute cases gastric cancer, the clinical outcome becomes worse.

The cause could be infective or non-infective. The infective causes could be bacteria, Helicobacter pylori is the commonest of this group. It is also the commonest cause of gastritis. Others infective causes include viruses, fungi, mycobacteria and parasites.

Non-infective causes include drugs, the most implicated drugs here are non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen. Other non-infective causes are stress, food poison, food allergy, radiation, bile, autoimmune diseases, ischemia, uremia and trauma. It could also be autoimmune [2].

Gastritis is a curable condition and it is treatable as soon as the cause can be determined. The incidence ad prevalence as well as distribution among age, race and gender is largely dependent on the cause of gastritis. The acute form affects both sexes equally and affects all age groups. It is has a slightly higher prevalence in blacks and Hispanics.

The chronic form also has no sexual predilection and affects all age groups although it usually begins to manifest after childhood.
It is important to note that about half of the world’s population is infected with Helicobacter pylori which is the number one cause of gastritis with the underdeveloped world contributing a large percentage. Not all of them are however symptomatic [3].

The gastric mucosa is usually kept intact by an equilibrium of the aggressive stomach acid forces and the forces of the protective gastric mucosal barrier. As a rule, anything that increases the force of the acid or reduces the defenses of the barrier such that the acid overwhelms the protective barrier would lead to gastritis and this could happen suddenly or over time. 

Examples of substances that increase the acidic contents are bile and pancreatic acids. Occasionally, they reflux into the stomach overwhelming the stomach mucus. NSAIDs act by inhibiting prostaglandin synthesis. Prostaglandin is necessary for formation of the gastric mucosal lining. Effects like radiation and ischemia affect the mucus producing cells in the stomach wall by killing them thereby reducing the capacity of the stomach to defend itself against acids.

Helicobacter pylori has a different pathway however. When a person is infected, the bacteria finds its way to the stomach wall where it colonizes and begins to form a substance known as urease. Urease is an enzyme that protects the bacteria from stomach acids by breaking urea down to the more alkaline ammonia while it causes a severe inflammatory reaction in the stomach wall [4].

• Avoid long term use of NSAIDs.
• Avoid hot and spicy foods.
• Avoid foods that irritate the stomach.
• Avoid prolonged hunger by eating small meals frequently.
• Reduce stress.
• Exercise regularly.
• Maintain a good BMI.
• Route of transmission of Helicobacter pylori is thought to be from fecal to the oral route so good food hygiene like hand washing before a meal is advocated [8].

Gastritis is a fairly common condition and is usually classified as acute or chronic and erosive or non-erosive. It can either affect the whole stomach or part of it. However, all cases present with the same set of symptoms, regardless of the underlying etiology [1].

Definition

Gastritis is a condition that result when the walls of the stomach are either partially or wholly inflamed.

Cause

It could be acute (occurring suddenly) or chronic (occurring over time) and causes of this include infections from bacteria, the commonest one being Helicobacter pylori. Other infective agents could be viruses, fungi, parasites and mycobacterium. Other causes are prolonged used of the pain relieving NSAIDs like ibuprofen, exposure to radiation, injuries, stress and food allergy and food poison. Sometimes the body cells attacking itself can lead to gastritis [9].

Signs and symptoms

The most common symptom is a burning pain at the upper part of the abdomen, it can also be felt in the middle of the chest. This pain is usually worse after eating. Other symptoms are nausea, vomiting, feeling of full abdomen, inability to eat normally, and passing of gas. Sometimes, vomitus or stool might be blood stained and this is a sign of internal bleeding.

Diagnosis

Many tests would be carried out. They include blood tests, urine tests and stool tests to test for bacteria and blood. Imaging tests like X-ray (including special x-rays) and CT scan might be carried out. A live view of the stomach wall might also be done using an endoscope.

Treatment

Treatment is usually with drugs and often requires a combination of drugs. Surgery is required only in rare types and when complication arises [10].

1. Drepper MD, Spahr L, Frossard JL. Clopidogrel and proton pump inhibitors--where do we stand in 2012?. World J Gastroenterol. May 14 2012;18(18):2161-71
2. Saad RJ, Schoenfeld P, Kim HM, Chey WD. Levofloxacin-based triple therapy versus bismuth-based quadruple therapy for persistent Helicobacter pylori infection: a meta-analysis. Am J Gastroenterol. Mar 2006;101(3):488-96.
3. Chen CH, Yang JC, Uang YS, Lin CJ. Differential inhibitory effects of proton pump inhibitors on the metabolism and antiplatelet activities of clopidogrel and prasugrel. Biopharm Drug Dispos. Jul 2012;33(5):278-83.
4. Feldman. Sleisenger and Fordtran's Gastrointestinal and Liver Disease. 7th ed. 2002:810-823.
5. Gisbert JP, Pajares JM. Diagnosis of Helicobacter pylori infection by stool antigen determination: a systematic review. Am J Gastroenterol. Oct 2001;96(10):2829-38.
6. Soltermann A, Koetzer S, Eigenmann F, et al. Correlation of Helicobacter pylori virulence genotypes vacA and cagA with histological parameters of gastritis and patient's age. Mod Pathol. Aug 2007;20(8):878-83.
7. Odze RD, Goldblum JR. Inflammatory disorders of the stomach. In: Surgical Pathology of the GI Tract, Liver, Biliary Tract, and Pancreas, Lash RH, Lauwers GY, et al. (Eds), Saunders, Philadelphia 2009. p.285.
8. van der Hulst RW, van der Ende A, Dekker FW, et al. Effect of Helicobacter pylori eradication on gastritis in relation to cagA: a prospective 1-year follow-up study. Gastroenterology 1997; 113:25.
9. Morgner A, Bayerdörffer E, Meining A, et al. Helicobacter heilmannii and gastric cancer. Lancet 1995; 346:511.
10. Hazell SL, Lee A, Brady L, Hennessy W. Campylobacter pyloridis and gastritis: association with intercellular spaces and adaptation to an environment of mucus as important factors in colonization of the gastric epithelium. J Infect Dis 1986; 153:658.

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