The average age of onset is 40 to 60 years, and men are affected more often than women. Adults with Ménétrier disease have a higher risk of developing gastric adenocarcinoma.

Evidence does not support a role for specific foods including spicy foods and coffee in the development of peptic ulcers. People are usually advised to avoid foods that bother them.

The cause of Ménétrier disease is unknown, but it has been associated with HCMV infection in children and "H. pylori "infections in adults. Additionally, increased TGF-α has been noted in the gastric mucosa of patients with the disease.

Gastritis may also develop after major surgery or traumatic injury ("Cushing ulcer"), burns ("Curling ulcer"), or severe infections. Gastritis may also occur in those who have had weight loss surgery resulting in the banding or reconstruction of the digestive tract.

Smoking has been linked to a variety of disorders of the stomach. Tobacco is known to stimulate acid production and impairs production of the protective mucus. This leads to development of ulcers in the majority of smokers.

Chronic stomach problems have also been linked to excess intake of alcohol. It has been shown that alcohol intake can cause stomach ulcer, gastritis and even stomach cancer. Thus, avoidance of smoking and excess alcohol consumption can help prevent the majority of chronic stomach disorders.

One of the most causes of chronic stomach problems is use of medications. Use of aspirin and other non-steroidal anti-inflammatory drugs to treat various pain disorders can damage lining of the stomach and cause ulcers. Other medications like narcotics can interfere with stomach emptying and cause bloating, nausea, or vomiting.

The majority of chronic stomach problems are treated medically. However, there is evidence that a change in life style may help. Even though there is no specific food responsible for causing chronic stomach problems, experts recommend eating a healthy diet which consists of fruits and vegetables. Lean meat should be limited. Moreover, people should keep a diary of foods that cause problems and avoid them.

Recent research has shown that AMAG is a result of the immune system attacking the parietal cells.

"Environmental Metaplastic Atrophic Gastritis" (EMAG) is due to environmental factors, such as diet and "H. pylori" infection. EMAG is typically confined to the body of the stomach. Patients with EMAG are also at increased risk of gastric carcinoma.

Patients with atrophic gastritis are also at increased risk for the development of gastric adenocarcinoma. The optimal endoscopic surveillance strategy is not known but all nodules and polyps should be removed in these patients.

Cancers of the stomach are rare and the incidence has been declining worldwide. Stomach cancers usually occur due to fluctuations in acidity level and may present with vague symptoms of abdominal fullness, weight loss and pain. The actual cause of stomach cancer is not known but has been linked to infection with "Helicobacter pylori", pernicious anemia, Menetriere's disease, and nitrogenous preservatives in food.

Dietary factors such as spice consumption, were hypothesized to cause ulcers until late in the 20th century, but have been shown to be of relatively minor importance. Caffeine and coffee, also commonly thought to cause or exacerbate ulcers, appear to have little effect. Similarly, while studies have found that alcohol consumption increases risk when associated with "H. pylori" infection, it does not seem to independently increase risk. Even when coupled with "H. pylori" infection, the increase is modest in comparison to the primary risk factor.

Stress due to serious health problems such as those requiring treatment in an intensive care unit is well described as a cause of peptic ulcers, which are termed stress ulcers.

While chronic life stress was once believed to be the main cause of ulcers, this is no longer the case. It is, however, still occasionally believed to play a role. This may be by increasing the risk in those with other causes such as "H. pylori" or NSAID use.

Among those in the intensive care unit, ulceration resulting in bleeding is very rare.

This is the most common form of chronic gastritis. Involvement tends to occur in either an antral-predominant or multifocal atrophic pattern. "H. pylori" infection is also associated with development of peptic ulcer disease, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue (MALT) lymphomas.

Since 1992, chronic gastritis lesions are classified according to the Sydney system.

Reactive gastropathy has a large number of causes, including:

- Alcohol abuse.

- Bile reflux, such as may be seen post-Billroth II.

- NSAIDs.

Reactive gastropathy, also chemical gastropathy, is an abnormality in the stomach caused by chemicals, e.g. bile, alcohol, and characteristically has minimal inflammation.

In Germany, 90% of cases of infectious enteritis are caused by four pathogens, Norovirus, Rotavirus, "Campylobacter" and "Salmonella". Other common causes of infectious enteritis include bacteria such as "Shigella" and "E. coli," as well as viruses such as adenovirus, astrovirus and calicivirus. Other less common pathogens include "Bacillus cereus, Clostridium perfringens, Clostridium difficile" and "Staphylococcus aureus".

"Campylobacter jejuni" is one of the most common sources of infectious enteritis, and the most common bacterial pathogen found in 2 year old and smaller children with diarrhoea. It has been linked to consumption of contaminated water and food, most commonly poultry and milk. The disease tends to be less severe in developing countries, due to the constant exposure which people have with the antigen in the environment, leading to early development of antibodies.

Rotavirus is responsible for infecting 140 million people and causing 1 million deaths each year, mostly in children younger than 5 years. This makes it the most common cause of severe childhood diarrhoea and diarrhea-related deaths in the world. It selectively targets mature enterocytes in the small intestine, causing malabsorption, as well as inducing secretion of water. It has also been observed to cause villus ischemia, and increase intestinal motility. The net result of these changes is induced diarrhoea.

Enteritis necroticans is an often fatal illness, caused by β-toxin of "Clostridium perfringens". This causes inflammation and segments of necrosis throughout the gastrointestinal tract. It is most common in developing countries, however has also been documented in post-World War II Germany. Risk factors for enteritis necroticans include decreased trypsin activity, which prevent intestinal degradation of the toxin, and reduced intestinal motility, which increases likelihood of toxin accumulation.

Ischemic enteritis is uncommon compared to ischemic colitis due to the highly vascularised nature of the small intestine, allowing for sufficient blood flow in most situations. It develops due to circulatory shock of mesenteric vessels in the absence of major vessel occlusion, often associated with an underlying condition such as hypertension, arrhythmia or diabetes. Thus it has been considered to be associated with atherosclerosis. Surgical treatment is usually required due to the likelihood of stenosis or complete occlusion of the small intestine. Ischemic damage can range from mucosal infarction, which is limited only to the mucosa; mural infarction of the mucosa and underlying submucosa; to transmural infarction of the full thickness of the gastrointestinal wall. Mucosal and mural infarcts in and of themselves may not be fatal, however may progress further to a transmural infarct. This has the potential for perforation of the wall, leading to peritonitis.

Linitis plastica, also known as Brinton's disease or leather bottle stomach, is a morphological variant of diffuse (or infiltrating) stomach cancer.

Causes of linitis plastica could be lye ingestion or metastatic infiltration of the stomach, particularly breast and lung carcinoma. It is not associated with H. pylori infection or chronic gastritis. The risk factors are undefined, except for rare inherited mutations in E-cadherin, which are found in about 50% of diffuse-type gastric carcinomas.

Diffuse stomach cancer is characterized by the presence of poorly differentiated tumor cells. Microscopic appearance is signet ring cell carcinoma, which is tumor cells with mucin droplet that displaces the nucleus to one side.

The appearance of the stomach is like a "leather bottle". It is characterized by a thick, rigid stomach wall caused by diffuse infiltration of tumor cells and extensive fibrosis.

Diarrhea may be a presenting symptom.

Risk factors for stress ulcer formation that have been identified are numerous and varied. However, two landmark studies and one position paper exist that addresses the topic of risk factors for stress ulcer formation:

- Non-critically ill medical patients with 2 or more of the following: respiratory failure, sepsis, heart failure, hepatic encephalopathy, jaundice, kidney failure, stroke, hypertension, previous gastrointestinal disease and treatment with corticosteroids, NSAIDS, heparin, or warfarin.

- In surgical critically ill patients, only those patients who are on a mechanical ventilator for more than 48 hours and/or those with a coagulopathy.

- The American Society of Health-System Pharmacists guideline recommends against the practice of stress ulcer prophylaxis in non-critically ill patients.

The disease is typically progressive, leading to fulminant liver failure and death in childhood, in the absence of liver transplantation. Hepatocellular carcinoma may develop in PFIC-2 at a very early age; even toddlers have been affected.

Pseudopolyps are projecting masses of scar tissue that develop from granulation tissue during the healing phase in repeated cycle of ulceration (especially in inflammatory bowel disease). Inflammatory tissue without malignant potential, pseudopolyps may, according to Joffe (1977), represent either regenerating mucosal islands between areas of ulceration, edematous polypoid tags or granulation tissue covered by epithelium. There are reported cases when localized giant pseudopolyposis resulted in intestinal obstruction.

Residual mucosal islands between ulcerated and denuded areas of mucosa may have a polypoid appearance and are referred to as pseudopolyps. Polyposis syndromes, such as familial adenomatous polyposis, could give rise to a similar appearance on imaging, although the clinical presentation would differ from that of inflammatory pseudopolyposis.

Numerous, confluent ulcerations with bulging of the edematous residual mucosa determine a cobblestone appearance at endoscopy.

Causes can be:

- Mallory-Weiss syndrome: bleeding tears in the esophagal mucosa, usually caused by prolonged and vigorous retching.

- Irritation or erosion of the lining of the esophagus or stomach

- Vomiting of ingested blood after hemorrhage in the oral cavity, nose or throat

- Vascular malfunctions of the gastrointestinal tract, such as bleeding gastric varices or intestinal varices

- Tumors of the stomach or esophagus.

- Radiation poisoning

- Viral hemorrhagic fevers

- Gastroenteritis

- Gastritis

- Peptic ulcer

- Chronic viral hepatitis

- Intestinal schistosomiasis (caused by the parasite "Schistosoma mansoni")

- History of smoking

- Iatrogenic injury (invasive procedure such as endoscopy or transesophageal echocardiography)

- Zollinger–Ellison syndrome (severe peptic ulcer)

- Atrio-oesophageal fistula

- Yellow fever

Many systemic diseases can develop oral manifestations that may include gingival enlargement, some that are related to conditions and others that are related to disease:

- Conditioned enlargement

- pregnancy

- puberty

- vitamin C deficiency

- nonspecific, such as a pyogenic granuloma

- Systemic disease causing enlargement

- leukemia

- granulolomatous diseases, such as granulomatosis with polyangiitis, sarcoidosis, or orofacial granulomatosis.

- neoplasm

- benign neoplasms, such as fibromas, papillomas and giant cell granulomas

- malignant neoplasms, such as a carcinoma or malignant melanoma

- false gingival enlargements, such as when there is an underlying bony or dental tissue lesion

This type of gingival enlargement is sometimes termed "drug induced gingival enlargement" or "drug influenced gingival enlargement", abbreviated to "DIGO". Gingival enlargement may also be associated with the administration of three different classes of drugs, all producing a similar response: Gingival overgrowth is a common side effect of phenytoin, termed "Phenytoin-induced gingival overgrowth" (PIGO).

- anticonvulsants (such as phenytoin, phenobarbital, lamotrigine, vigabatrin, ethosuximide, topiramate and primidone NOT common for valproate)

- calcium channel blockers (antihypertensives such as nifedipine, amlodipine, and verapamil). The dihydropyridine derivative isradipidine can replace nifedipine and does not induce gingival overgrowth.

- cyclosporine, an immunosuppresant.

Of all cases of DIGO, about 50% are attributed to phenytoin, 30% to cyclosporins and the remaining 10-20% to calcium channel blockers.

Drug-induced enlargement has been associated with a patient's genetic predisposition, and its association with inflammation is debated. Some investigators assert that underlying inflammation is necessary for the development of drug-induced enlargement, while others purport that the existing enlargement induced by the drug effect compounds plaque retention, thus furthering the tissue response. Careful attention to oral hygiene may reduce the severity of gingival hyperplasia. In most cases, discontinuing the culprit drug resolves the hyperplasia.