Acute gastritis can be caused by non-steroidal anti-inflammatory drugs, alcohol and severe stressful events such as septicaemia and shock. The mechanism by which the gastritis occurs will vary depending on the cause, although mucosal ischaemia is probably implicated in shock.

The stomach demonstrates numerous erosions. Considerable blood loss can occur from the erosions.

Mild degrees of acute gastritis are asymptomatic. At the opposite end of the spectrum there can be life-threatening haemorrhage that may necessitate an emergency gastrectomy. Intermediate degrees feature nausea, vomiting and less marked haematemesis and melaena. Pain is only sometimes present.

Helicobacter Pylori Associated Chronic Gastritis

A form of chronic gastritis can be caused by helicobacter pylori and is due to the immune response to the infection. In the majority of patients there is generalised mild chronic inflammation of the gastric mucosa and a mild reduction in the level of gastric acid secretion.

In around 5-15% the inflammation is more intense and causes atrophy of the gastric glands (atrophic gastritis). The gastric atrophy is sufficiently severe to cause a marked decrease in the level of gastric acid secretion (hypochlorhydria) and this alteration in the pH environment of the stomach favours intestinal metaplasia.

Up to 10% of patients have atrophy-related inflammation that is confined to the gastric antrum where it destroys the D cells which secrete somatostatin. Somatostatin suppresses the secretion of gastric acid. These patients therefore have excessive acid secretion.

The full blown pattern of inflammation of the gastric mucosa in response to helicobacter pylori infection is acute inflammation that affects the glands in a cryptitis distribution in conjunction with chronic inflammation that includes plasma cells and lymphoid aggregates. The majority of biopsies that contain demonstrable helicobacter pylori exhibit acute inflammation.

The gastritis can cause indigestion-type pain.

Pernicious Anaemia

Pernicious anaemia is a chronic autoimmune condition in which the autoimmune reaction is directed against gastric parietal cells and/or intrinsic factor. The disease is rare below the age of 40 years. The male : female ratio is 5 : 8. The condition is more common in people from north Europe and there is an association with fair hair, blue eyes and early greying. The condition is also associated with other organ specific autoimmune diseases.


Autoantibodies that react against either gastric parietal cells and/or intrinsic factor are present. As a consequenc pernicious anaemia features a chronic atrophic gastritis that particularly affects the fundus. The atrophy of the gastric glands is accompanied by hypochlorhydria.

The intestinal metaplasia that results from the hypochlorhydria makes pernicious anaemia a weak risk factor for the development of gastric adenocarcinoma. Carcinoid tumours of the stomach can also be encountered and almost always behave in an indolent fashion that requires very limited treatment.

The ability of pernicious anaemia to cause extragastric disease is due to the impairment of the absorption of vitamin B12.

The mechanism of absorption of vitamin B12 by the body is somewhat convoluted. The stomach secretes both intrinsic factor and R protein. The R protein binds to vitamin B12 in the stomach and protects vitamin B12 during its passage through the stomach. At this point intrinsic factor waits patiently. When the R protein-vitamin B12 complex reaches the small bowel, the higher pH in the small intestine causes vitamin B12 to dissociate from the R protein, leaving the field clear for intrinsic factor to bind vitamin B12. The intrinsic factor-vitamin B12 complex is conveyed to the terminal ileum where the enterocytes possess special receptors that recognise intrinsic factor. These receptors allow the intrinsic factor-vitamin B12 complex to be absorbed by receptor mediated endocytosis. Once the complex is inside the enterocyte the vitamin B12 is transferred to transcobalamin II, which then transports vitamin B12 in the blood.

Pernicious anaemia disrupts this complex process by either destroying the gastric parietal cells and their supply of intrinsic factor, or by interfering with the interaction between intrinsic factor and vitamin B12 by the binding of anti-intrinsic factor antibodies to intrinsic factor. In both cases there is malabsorption of vitamin B12 and once the body's reserves of vitamin B12 have been depleted (these are typically 2 to 5g; the daily dietary requirement of vitamin B12 is 6 micrograms, so a person may have several years of reserve).

Vitamin B12 is a key component of two enzymes, methylmalonyl coenzyme A mutase (MUT) and 5-methyltetrahydrofolate-homocysteine methyltransferase (MTR). MUT is involved in fat and protein based energy metabolism, as well as having a vital role in the synthesis of myelin. MTR participates in folate metabolism and is therefore integral to the synthesis of DNA.

Deficiency of vitamin B12 is felt hardest by the haematopoietic and neurological systems. The bone marrow has a very high turnover of cells and is a hotbed of DNA synthesis. The erythroid lineage suffers most and megaloblastic anaemia results; leucocyte and megakaryocyte synthesis can also be impaired.

The neurological features are based around degeneration of the myelin sheaths of nerves. The posterior columns of the lower cervical and upper thoracic segments of the spinal cord are affected first but if the disease progresses the damage extends to higher and lower segments, as well as involving the lateral and anterior parts of the spinal cord. The brain can also be affected, although the changes are less pronounced.

Subacute degeneration of the spinal cord is a marked form of these changes.

Clinical Features

The neurological aspects of pernicious anaemia impart the characteristic features of the disease. There is a loss of fine touch sensation and conscious proprioreception. Tingling and other paraesthesia of the extremeties is often present. Sensory ataxia occurs. Interruption of the long motor tracts produces upper motor neurone features but these can be coupled with loss of the ankle and knee jerks. The combination of loss of the ankle and knee jerks and upgoing plantars is characteristic but not unique.

In well established disease there can be apathy, irritability, impaired concentration and somnolence, which may progress to outright confusion and dementia. Optic atrophy is a rare complication.

Glossitis can develop and takes the form of a sore, beefy red tongue.

The patient may have symptoms related to the anaemia such as tiredness.

Gastric adenocarcinoma is a rare complication.


The initial clue that a patient may have pernicious anaemia is a raised MCV in the full blood count.

The level of vitamin B12 in the blood can be measured and is almost always paired with a measurement of folate because the two substances tend to function as a team. However, if the concentration of vitamin B12 is reduced it is necessary to determine if this is due to dietary deficiency (vegan diet), pernicious anaemia or another cause of malabsorption. This is accomplised by using a procedure that is sometimes known as the Schilling test.

The patient is given an oral dose of radiolabelled vitamin B12. The quantity that is absorbed can then be determined either by nuclear medicine imaging, or by administering an intramuscular injection of a large dose of unlabelled vitamin B12 to flush out the radiolabelled vitamin B12 into the urine, where it can be measured. The test is then repeated by giving the patient not only the oral dose of radiolabelled vitamin B12 but intrinsic factor as well.

In dietary deficiency there is normal absorption of the oral dose of vitamin B12 both with and without the intrinsic factor. A patient who has pernicious anaemia will only absorb an adequate amount of vitamin B12 if intrinsic factor is given. If the cause of the vitamin B12 deficiency is another form of malabsorption then the absorption of the oral dose of vitamin B12 will be poor with and without intrinsic factor.

The autoantibodies to gastric parietal cells can be detected in the blood.


The treatment for pernicious anaemia is vitamin B12 supplementation. This is often given in the form of intramuscular injections every three months.

If a patient has folate deficiency it is important to exclude a co-existing vitamin B12 deficiency. If the folate deficiency is corrected with oral folate but the patient has depleted vitamin B12 levels the surge in folate may overstretch the vitamin B12 reserves and precipitate subacute combined degeneration of the cord.

Reflux Gastritis

Reflux gastritis occurs when the contents of the duodenum pass backwards into the stomach. The mucosa of the stomach shows little inflammation but is oedematous and exhibits elongation and tortuosity of the gastric glands. The nuclei of these elongated glands tend to be hyperchromatic. Splicing of smooth muscle fibres into the lamina propria is observed.

Menetrier's Disease

Menetrier's disease is a rare condition in which the stomach displays large, tortuous gastric folds. It is sometimes known as hyperplastic gastropathy. The hyperplasia affects the mucinous cells primarily and these can replace the chief cells and parietal cells.

Loss of protein into the lumen of the stomach occurs and the disease falls into the category of a protein-losing enteropathy.

The disease presents with weight loss, anorexia, nausea, vomiting and epigastric pain.