Individuals with the disease present with upper abdominal pain (epigastric), at times accompanied by nausea, vomiting, loss of appetite, edema, and weight loss. A small amount of gastrointestinal bleeding may occur, which is typically due to superficial mucosal erosions; large volume bleeding is rare. 20% to 100% of patients, depending on time of presentation, develop a protein-losing gastropathy accompanied by low blood albumin and edema.

Symptoms and pathological features of Ménétrier disease in children are similar to those in adults, but disease in children is usually self-limited and often follows respiratory infection.

With Ménétrier disease, the stomach is characterized by large, tortuous gastric folds in the fundus and body of the stomach, with antrum generally spared, giving the mucosa a cobblestone or cerebriform (brain-like) appearance. Histologically, the most characteristic feature is massive foveolar hyperplasia (hyperplasia of surface and glandular mucous cells). The glands are elongated with a corkscrew-like appearance and cystic dilation is common. Inflammation is usually only modest, although some cases show marked intraepithelial lymphocytosis. Diffuse or patchy glandular atrophy, evident as hypoplasia of parietal and chief cells, is typical.

Although ICD-10 classifies it under "Other gastritis" (K29.6), and the lamina propria may contain mild chronic inflammatory infiltrate, Ménétrier disease is not considered a form of gastritis. It is rather considered as one of the two most well understood hypertrophic gastropathies; the other being Zollinger–Ellison syndrome.

Many people with gastritis experience no symptoms at all. However, upper central abdominal pain is the most common symptom; the pain may be dull, vague, burning, aching, gnawing, sore, or sharp. Pain is usually located in the upper central portion of the abdomen, but it may occur anywhere from the upper left portion of the abdomen around to the back.

Other signs and symptoms may include the following:

- Nausea

- Vomiting (if present, may be clear, green or yellow, blood-streaked, or completely bloody, depending on the severity of the stomach inflammation)

- Belching (if present, usually does not relieve the pain much)

- Bloating

- Early satiety

- Loss of appetite

- Unexplained weight loss

Common causes include "Helicobacter pylori" and NSAIDs. Less common causes include alcohol, cocaine, severe illness and Crohn disease, among others.

Crohn's disease is an inflammatory bowel disease that can affect any part of the digestive tract, even the stomach, although it's a rare presentation. Its main feature is inflammatory ulcers that can affect the total thickness of the stomach wall and can bleed but rarely perforate.

Symptoms include abdominal pain, loss of appetite, and weight loss. Diarrhea is also a symptom that can develop, so checking stools for the appearance of blood is important. It is possible for symptoms of Crohn's disease to remain with a person for weeks or go away on their own. Reporting the symptoms to a doctor is recommended to prevent further complications.

Reactive gastropathy is morphologically distinct entity that can be separated from gastritis, which by definition has a significant inflammatory component.

As a reactive gastropathy may mimic a (true) gastritis symptomatically and visually in an endoscopic examination, it may incorrectly be referred to as a gastritis. Even aware of the underlying etiology of the pathologic process, e.g. NSAID use, the label "chemical gastritis" is applied to a chemical gastropathy.

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.

Atrophic gastritis (also known as Type A or Type B Gastritis more specifically) is a process of chronic inflammation of the stomach mucosa, leading to loss of gastric glandular cells and their eventual replacement by intestinal and fibrous tissues. As a result, the stomach's secretion of essential substances such as hydrochloric acid, pepsin, and intrinsic factor is impaired, leading to digestive problems. The most common are vitamin B deficiency which results in a megaloblastic anemia and malabsorbtion of iron, leading to iron deficiency anaemia. It can be caused by persistent infection with "Helicobacter pylori", or can be autoimmune in origin. Those with the autoimmune version of atrophic gastritis are statistically more likely to develop gastric carcinoma, Hashimoto's thyroiditis, and achlorhydria.

Type A gastritis primarily affects the body/fundus of the stomach, and is more common with pernicious anemia.

Type B gastritis primarily affects the antrum, and is more common with "H. pylori" infection.

In the stomach there is a slight balance between acid and the wall lining which is protected by mucus. When this mucus lining is disrupted for whatever reason, signs and symptoms of acidity result. This may result in upper abdominal pain, indigestion, loss of appetite, nausea, vomiting and heartburn. When the condition is allowed to progress, the pain may become continuous; blood may start to leak and be seen in the stools. If the bleeding is rapid and of adequate volume it may even result in vomiting of bright red blood (hematemesis). When the acidity is uncontrolled, it can even cause severe blood loss (anemia) or lead to perforation (hole) in the stomach which is a surgical emergency. In many individuals, the progressive bleeding from an ulcer mixes with the feces and presents as black stools. Presence of blood in stools is often the first sign that there is a problem in the stomach.

Many people who have chronic gastritis do not experience any noticeable symptoms. Those who do, claim to experience one or several of the following: upper abdominal pain, indigestion, bloating, nausea, vomiting, belching, loss of appetite, and weight loss. Stomach bleeding or black stool has been reported in extreme cases.

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.

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.

The diagnosis is by examination of tissue, e.g. a stomach biopsy.

It is characterized, histologically, by:

1. foveolar hyperplasia with gland tortuosity and dilation,

2. smooth muscle hyperplasia in the lamina propria, and

3. scant or minimal inflammation, i.e. lack of large numbers of neutrophils and plasma cells.

Signs and symptoms of a peptic ulcer can include one or more of the following:

- abdominal pain, classically epigastric strongly correlated to mealtimes. In case of duodenal ulcers the pain appears about three hours after taking a meal;

- bloating and abdominal fullness;

- waterbrash (rush of saliva after an episode of regurgitation to dilute the acid in esophagus - although this is more associated with gastroesophageal reflux disease);

- nausea and copious vomiting;

- loss of appetite and weight loss;

- hematemesis (vomiting of blood); this can occur due to bleeding directly from a gastric ulcer, or from damage to the esophagus from severe/continuing vomiting.

- melena (tarry, foul-smelling feces due to presence of oxidized iron from hemoglobin);

- rarely, an ulcer can lead to a gastric or duodenal perforation, which leads to acute peritonitis, extreme, stabbing pain, and requires immediate surgery.

A history of heartburn, gastroesophageal reflux disease (GERD) and use of certain forms of medication can raise the suspicion for peptic ulcer. Medicines associated with peptic ulcer include NSAIDs (non-steroid anti-inflammatory drugs) that inhibit cyclooxygenase, and most glucocorticoids (e.g. dexamethasone and prednisolone).

In people over the age of 45 with more than two weeks of the above symptoms, the odds for peptic ulceration are high enough to warrant rapid investigation by esophagogastroduodenoscopy.

The timing of the symptoms in relation to the meal may differentiate between gastric and duodenal ulcers: A gastric ulcer would give epigastric pain during the meal, as gastric acid production is increased as food enters the stomach. Symptoms of duodenal ulcers would initially be relieved by a meal, as the pyloric sphincter closes to concentrate the stomach contents, therefore acid is not reaching the duodenum. Duodenal ulcer pain would manifest mostly 2–3 hours after the meal, when the stomach begins to release digested food and acid into the duodenum.

Also, the symptoms of peptic ulcers may vary with the location of the ulcer and the person's age. Furthermore, typical ulcers tend to heal and recur and as a result the pain may occur for few days and weeks and then wane or disappear. Usually, children and the elderly do not develop any symptoms unless complications have arisen.

Burning or gnawing feeling in the stomach area lasting between 30 minutes and 3 hours commonly accompanies ulcers. This pain can be misinterpreted as hunger, indigestion or heartburn. Pain is usually caused by the ulcer but it may be aggravated by the stomach acid when it comes into contact with the ulcerated area. The pain caused by peptic ulcers can be felt anywhere from the navel up to the sternum, it may last from few minutes to several hours and it may be worse when the stomach is empty. Also, sometimes the pain may flare at night and it can commonly be temporarily relieved by eating foods that buffer stomach acid or by taking anti-acid medication. However, peptic ulcer disease symptoms may be different for every sufferer.

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.

Peptic ulcer disease (PUD) is a break in the lining of the stomach, first part of the small intestine or occasionally the lower esophagus. An ulcer in the stomach is known as a gastric ulcer while that in the first part of the intestines is known as a duodenal ulcer. The most common symptoms of a duodenal ulcer are waking at night with upper abdominal pain or upper abdominal pain that improves with eating. With a gastric ulcer the pain may worsen with eating. The pain is often described as a burning or dull ache. Other symptoms include belching, vomiting, weight loss, or poor appetite. About a third of older people have no symptoms. Complications may include bleeding, perforation and blockage of the stomach. Bleeding occurs in as many as 15% of people.

Common causes include the bacteria "Helicobacter pylori" and non-steroidal anti-inflammatory drugs (NSAIDs). Other less common causes include tobacco smoking, stress due to serious illness, Behcet disease, Zollinger-Ellison syndrome, Crohn disease and liver cirrhosis, among others. Older people are more sensitive to the ulcer-causing effects of NSAIDs. The diagnosis is typically suspected due to the presenting symptoms with confirmation by either endoscopy or barium swallow. "H. pylori" can be diagnosed by testing the blood for antibodies, a urea breath test, testing the stool for signs of the bacteria, or a biopsy of the stomach. Other conditions that produce similar symptoms include stomach cancer, coronary heart disease, and inflammation of the stomach lining or gallbladder inflammation.

Diet does not play an important role in either causing or preventing ulcers. Treatment includes stopping smoking, stopping NSAIDs, stopping alcohol and giving medications to decrease stomach acid. The medication used to decrease acid is usually either a proton pump inhibitor (PPI) or an H2 blocker with four weeks of treatment initially recommended. Ulcers due to "H. pylori" are treated with a combination of medications such as amoxicillin, clarithromycin and a PPI. Antibiotic resistance is increasing and thus treatment may not always be effective. Bleeding ulcers may be treated by endoscopy, with open surgery typically only used in cases in which it is not successful.

Peptic ulcers are present in around 4% of the population. Newly ulcers were found in around 87.4 million people worldwide during 2015. About 10% of people develop a peptic ulcer at some point in their life. They resulted in 267,500 deaths in 2015 down from 327,000 deaths in 1990. The first description of a perforated peptic ulcer was in 1670 in Princess Henrietta of England. "H. pylori" was first identified as causing peptic ulcers by Barry Marshall and Robin Warren in the late 20th century, a discovery for which they received the Nobel Prize in 2005.

Signs and symptoms of enteritis are highly variable and vary based on the specific cause and other factors such as individual variance and stage of disease.

Symptoms may include abdominal pain, cramping, diarrhoea, dehydration, fever, nausea, vomiting and weight loss.

Inflammation of the gastrointestinal tract is common after treatment with radiation therapy to the abdomen or pelvis. It is classified as early if it manifests within the first 3 months, and delayed if it manifests 3 months after treatment. Early radiation enteritis is caused by cell death of the crypt epithelium and subsequent mucosal inflammation, however usually subsides after the course of radiation therapy is completed. Delayed radiation enteritis is a chronic disease which has a complex pathogenesis involving changes in the majority of the intestinal wall.

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.

The ulcerations may be superficial and confined to the mucosa, in which case they are more appropriately called erosions, or they may penetrate deeper into the submucosa. The former may cause diffuse mucosal oozing of blood, whereas the latter may erode into a submucosal vessel and produce frank hemorrhage.

The characteristic lesions may be multiple, superficial mucosal erosions similar to erosive gastroduodenitis. Occasionally, there may be a large acute ulcer in the duodenum (Curling’s ulcer).

Generally, there are multiple lesions located mainly in the stomach and occasionally in the duodenum. They range in depth from mere shedding of the superficial epithelium (erosion) to deeper lesions that involve the entire mucosal thickness (ulceration).

The age of onset is almost always before 3 months of age. Many infants are born preterm (1/3 cases) and dysmature. The babies are frequently small for dates. The placenta may be abnormal with non-specific inflammation on histology. Umbilical cord anomalies have occasionally been reported. In severe cases, signs in the brain may be detected on prenatal ultrasound.

The presentation is pleiomorphic, making the diagnosis difficult, but the most common features of this disease involve the skin, joints, and central nervous system.

All have a maculopapular urticarial skin rash that is often present at birth (75% cases). It is probably more correctly described as an urticarial-like rash. The presence of the rash varies with time, and biopsy of these skin lesions shows a perivascular inflammatory infiltrate including granulocytes.

In about 35-65% of cases, arthritis occurs. Joint signs are variably expressed and can lead to transient swelling without sequelae between crises, or to unpredictable anomalies of growth cartilage and long bones epiphyses suggestive of a pseudo-tumour. Biopsies reveal hypertrophic cartilage without inflammatory cells. This most commonly affects the large joints (knees, ankles, elbows, and wrists) but may also involve the small joints of the hands and feet. It is usually bilateral and painful. A common and characteristic feature is giant kneecaps. Severe cases may result in contractures (joint deformities).

Most patients eventually have neurological problems. These manifest themselves in three principal ways: chronic meningitis, involvement of both the optic tract and eye, and sensorineural hearing loss. The chronic meningitis presents with the features of chronically raised intracranial pressure: headaches, vomiting, ventriculomegaly, hydrocephalus, macromegaly, cerebral atrophy, and optic atrophy. Some of these features may be evidenced on prenatal ultrasound. In 50% of cases, intellectual deficit occurs. Seizures occur in 25% of cases, but other manifestations are rare. Histological examination shows infiltration of the meninges with polymorphs.

Ocular manifestations occur in 80% of cases and include uveitis (70%), papillary involvement, conjunctivitis, and optical neuritis. If untreated, these may result in blindness (25%). The sensorineural hearing loss occurs in 75%, and tends to be progressive leading to deafness in 20% of cases.

Almost all children are remarkably short and have growth delay. Fever is extremely common but inconstant and is most often mild. Anemia is frequent. Other findings that have been reported include macrocephaly (95%), large fontanelle, prominent forehead, flattening of the nasal bridge (saddleback nose), short and thick extremities, and finger clubbing. The liver and/or spleen may be enlarged. Lymph node enlargement may also be present.

Later in life, secondary amyloidosis may occur. Delayed puberty and secondary amenorrhoea are not uncommon. Hoarseness due to inflammation of the laryngeal cartilage has also been reported.

Gingival enlargement, (also termed gingival overgrowth, hypertrophic gingivitis, gingival hyperplasia, or gingival hypertrophy, and sometimes abbreviated to GO), is an increase in the size of the gingiva (gums). It is a common feature of gingival disease. Gingival enlargement can be caused by a number of factors, including inflammatory conditions and the side effects of certain medications. The treatment is based on the cause. A closely related term is epulis, denoting a localized tumor (i.e. lump) on the gingiva.

The terms gingival hyperplasia and gingival hypertrophy have been used to describe this topic in the past. These are not precise descriptions of gingival enlargement because these terms are strictly histologic diagnoses, and such diagnoses require microscopic analysis of a tissue sample. Hyperplasia refers to an increased number of cells, and hypertrophy refers to an increase in the size of individual cells. As these identifications obviously cannot be performed with a clinical examination and evaluation of the tissue, the term "gingival enlargement" is more properly applied. Gingival enlargement has been classified according to cause into 5 general groups:

- Inflammatory enlargement

- Drug induced enlargement

- Enlargement associated with systemic diseases or conditions

- Neoplastic enlargement

- False enlargement.

The disease usually affects the lower legs or scrotum. The swelling is accompanied by rough nodules or wart-like plaques on the skin. If the disease is not treated, it eventually results in pain and immobility.