What is H. pylori?
Helicobacter pylori (H. pylori) is a spiral-shaped bacterium that is found in the gastric mucous layer or adherent to the epithelial lining of the stomach. H. pylori causes more than 90% of duodenal ulcers and up to 80% of gastric ulcers. Before 1982, when this bacterium was discovered, spicy food, acid, stress, and lifestyle were considered the major causes of ulcers. The majority of patients were given long-term medications, such as H2 blockers, and more recently, proton pump inhibitors, without a chance for permanent cure. These medications relieve ulcer-related symptoms, heal gastric mucosal inflammation, and may heal the ulcer, but they do NOT treat the infection. When acid suppression is removed, the majority of ulcers, particularly those caused by H. pylori, recur. Since we now know that most ulcers are caused by H. pylori, appropriate antibiotic regimens can successfully eradicate the infection in most patients, with complete resolution of mucosal inflammation and a minimal chance for recurrence of ulcers.
How common is H. pylori infection?
Approximately two-thirds of the world’s population is infected with H. pylori. In the United States, H. pylori is more prevalent among older adults, African Americans, Hispanics, and lower socioeconomic groups.
What illnesses does H. pylori cause?
Most persons who are infected with H. pylori never suffer any symptoms related to the infection; however, H. pylori causes chronic active, chronic persistent, and atrophic gastritis in adults and children. Infection with H. pylori also causes duodenal and gastric ulcers. Infected persons have a 2- to 6-fold increased risk of developing gastric cancer and mucosal-associated-lymphoid-type (MALT) lymphoma compared with their uninfected counterparts. The role of H. pylori in non-ulcer dyspepsia remains unclear.
What are the symptoms of ulcers?
Approximately 25 million Americans suffer from peptic ulcer disease at some point in their lifetime. Each year there are 500,000 to 850,000 new cases of peptic ulcer disease and more than one million ulcer-related hospitalizations. The most common ulcer symptom is gnawing or burning pain in the epigastrium. This pain typically occurs when the stomach is empty, between meals and in the early morning hours, but it can also occur at other times. It may last from minutes to hours and may be relieved by eating or by taking antacids. Less common ulcer symptoms include nausea, vomiting, and loss of appetite. Bleeding can also occur; prolonged bleeding may cause anemia leading to weakness and fatigue. If bleeding is heavy, hematemesis, hematochezia, or melena may occur.
Who should be tested and treated for H. pylori?
Persons with active gastric or duodenal ulcers or documented history of ulcers should be tested for H. pylori, and if found to be infected, they should be treated. To date, there has been no conclusive evidence that treatment of H. pylori infection in patients with non-ulcer dyspepsia is warranted. Testing for and treatment of H. pylori infection are recommended following resection of early gastric cancer and for low-grade gastric MALT lymphoma. Retesting after treatment may be prudent for patients with bleeding or otherwise complicated peptic ulcer disease. Treatment recommendations for children have not been formulated. Pediatric patients who require extensive diagnostic work-ups for abdominal symptoms should be evaluated by a specialist.
How is H. pylori infection diagnosed?
Several methods may be used to diagnose H. pylori infection. Serological tests that measure specific H. pylori IgG antibodies can determine if a person has been infected. The sensitivity and specificity of these assays range from 80% to 95% depending upon the assay used. Another diagnostic method is the breath test. In this test, the patient is given either 13C- or 14C-labeled urea to drink. H. pylori metabolizes the urea rapidly, and the labeled carbon is absorbed. This labeled carbon can then be measured as CO2 in the patient’s expired breath to determine whether H. pylori is present. The sensitivity and specificity of the breath test ranges from 94% to 98%. Upper esophagogastroduodenal endoscopy is considered the reference method of diagnosis. During endoscopy, biopsy specimens of the stomach and duodenum are obtained and the diagnosis of H. pylori can be made by several methods: The biopsy urease test – a colorimetric test based on the ability of H. pylori to produce urease; it provides rapid testing at the time of biopsy. Histologic identification of organisms – considered the gold standard of diagnostic tests. Culture of biopsy specimens for H. pylori, which requires an experienced laboratory and is necessary when antimicrobial susceptibility testing is desired.
What are the treatment regimens used for H. pylori eradication?
Therapy for H. pylori infection consists of 10 days to 2 weeks of one or two effective antibiotics, such as amoxicillin, tetracycline (not to be used for children <12 yrs.), metronidazole, or clarithromycin, plus either ranitidine bismuth citrate, bismuth subsalicylate, or a proton pump inhibitor. Acid suppression by the H2 blocker or proton pump inhibitor in conjunction with the antibiotics helps alleviate ulcer-related symptoms (i.e., abdominal pain, nausea), helps heal gastric mucosal inflammation, and may enhance efficacy of the antibiotics against H. pylori at the gastric mucosal surface. Currently, eight H. pylori treatment regimens are approved by the Food and Drug Administration (FDA) (Table 1); however, several other combinations have been used successfully. Antibiotic resistance and patient noncompliance are the two major reasons for treatment failure. Eradication rates of the eight FDA-approved regimens range from 61% to 94% depending on the regimen used. Overall, triple therapy regimens have shown better eradication rates than dual therapy. Longer length of treatment (14 days versus 10 days) results in better eradication rates.
FDA-Approved Treatment Options
One type of gastritis, called erosive gastritis, wears away the stomach lining. The most common cause of erosive gastritis is long-term use of medications called non-steroidal anti-inflammatory drugs. These include aspirin and ibuprofen. “When you stop taking the drugs, the condition usually goes away,” says Graham. Doctors might also recommend reducing the dose or switching to another class of pain medication.
Less common causes of gastritis include certain digestive disorders (such as Crohn’s disease) and autoimmune disorders, in which the body’s protective immune cells mistakenly attack healthy cells in the stomach lining.
Autoimmune atrophic gastritis is a chronic inflammatory disease in which the immune system mistakenly destroys a special type of cell (parietal cells) in the stomach. Parietal cells make stomach acid (gastric acid) and a substance our body needs to help absorb vitamin B12 (called intrinsic factor). The progressive loss of parietal cells may lead to iron deficiency and finally vitamin B12 deficiency. The clinical signs and symptoms of iron deficiency anemia include tiredness, pale complexion, and heart problems such as exercise intolerance and palpitations. B12 deficiency may lead to pernicious anemia as well as gastrointestinal and neurological problems. Autoimmune atrophic gastritis may also be associated with an increased risk of certain types of stomach cancers.
The cause of autoimmune gastritis is unknown, but affected people are likely to have other autoimmune disorders including autoimmune thyroiditis, diabetes type I, Addison’s disease, and vitiligo. Diagnosis is made through a combination of clinical findings (certain blood tests and presence of other autoimmune conditions) and biopsy of stomach lining. Treatment is based on the signs and symptoms present in each person, but may include iron infusions, vitamin B12 injections and endoscopic surveillance.
The cause of autoimmune gastritis is unknown, but affected people are likely to have other autoimmune disorders including autoimmune thyroiditis, diabetes type I, Addison’s disease, and vitiligo. Diagnosis is made through a combination of clinical findings (certain blood tests and presence of other autoimmune conditions) and biopsy of stomach lining. Treatment is based on the signs and symptoms present in each person, but may include iron infusions, vitamin B12 injections and endoscopic surveillance.
Symptoms
In some cases, autoimmune atrophic gastritis does not cause any obvious signs and symptoms. However, some people may experience nausea, vomiting, a feeling of fullness in the upper abdomen after eating, or abdominal pain. It is often associated with impaired absorption of vitamin B12 and possibly other vitamin deficiencies (such as folate and iron). People with vitamin B12 deficiency are at risk for pernicious anemia, a condition in which the body does not have enough healthy red blood cells.[4][5]
Autoimmune atrophic gastritis is considered a “precancerous” condition and it may be responsible for the development of gastric adenocarcinoma or carcinoids.[6]
Last updated: 10/20/2015
Cause
Autoimmune atrophic gastritis is considered an autoimmune disorder. In people who are affected by this condition, the immune system mistakenly attacks the healthy cells of the stomach lining. Overtime, this can wear away the stomach’s protective barrier and interfere with the absorption of several key vitamins (i.e. vitamin B12, iron, folate). This leads to the signs and symptoms of autoimmune atrophic gastritis.
Last updated: 10/20/2015
Inheritance
In some cases, more than one family member can be affected by autoimmune atrophic gastritis. Although the underlying genetic cause has not been identified, studies suggest that the condition may be inherited in an autosomal dominant manner in these families.
In autosomal dominant conditions, an affected person only needs a change (mutation) in one copy of the responsible gene in each cell. In some cases, an affected person inherits the mutation from an affected parent. Other cases may result from new (de novo) mutations in the gene. These cases occur in people with no history of the disorder in their family. A person with the condition has a 50% chance with each pregnancy of passing along the altered gene to his or her child.
Collagenous gastritis (CG) is a rare condition that primarily affects the digestive system. People with CG have increased buildup of collagen in the subepithelial layer of the stomach. This condition typically affects children and young adults up to 22 years, or older adults over 35 years of age. Features in affected people appear to vary depending on the age group. Signs and symptoms in children and young adults often begin with anemia and abdominal pain, whereas older adults often have loose stools associated with collagenous colitis, celiac disease or both. The cause of the condition is unknown. There is currently no effective treatment.
Because collagenous gastritis is very rare and its cause is unknown, there is currently no established standard therapy for the condition. Various therapies have been attempted with limited success. These have included anti-secretary agents, steroids, iron supplementation, and hypoallergenic diets. Several other therapies have also been tested. A few affected people have shown improvement of symptoms, but no randomized, controlled trials have been performed. More studies are needed to establish a standard treatment strategy.
The course and long-term outlook (prognosis) for people with collagenous gastritis (CG) is unclear. There has not yet been a comprehensive review of outcomes, and large variations in the course of the disease have been reported.
In the majority of adults, the condition seems to follow a chronic, intermittent course, with no significant mortality risk or severe progression. Diarrhea may resolve with or without treatment, although relapses may occur. In children, a less controllable course has been suspected. However, CG in children seems to follow a generally benign course, with limited long-term morbidity and no increased mortality reported to date. A few reports have documented that the abnormal collagen band in affected people persists (with or without medication) despite symptoms improving.
Sources:
https://rarediseases.info.nih.gov/diseases/10310/autoimmune-atrophic-gas…
https://rarediseases.info.nih.gov/diseases/10961/collagenous-gastritis
https://www.cdc.gov/ulcer/keytocure.htm
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