Peptic ulcers
H. pylori infection significantly increases the risk of developing duodenal and gastric ulcers. Approximately 1 in 6 people with H. pylori infection may develop peptic ulcer disease. Treatment of H. pylori infection accelerates ulcer healing and greatly reduces the recurrence rate of ulcers. Treatment with anti-H. pylori drugs alone, without acid suppressants, has been shown to be effective in healing gastric and duodenal ulcers as well.
H. pylori infection has been found to be linked to a number of causes of ulcer disease. For example, increased gastric acid, duodenal gastric chemosis, changes in the nature of the mucosal barrier, and production of inflammatory metabolites in the gastric sinus mucosa. These findings in patients have been tentatively demonstrated in animal experiments. In fact peptic ulcer involves several complex interacting mechanisms.
Such as virulence factors of bacteria (vaca and caga, etc.), host reactivity (e.g. genetics of susceptibility, gastric chemotaxis of the duodenal epithelium, interaction of mucosal barrier and inflammation, acid secretion response, neuromodulation) and environmental factors (e.g. diet, age of acquisition of infection) combine to lead to the final outcome of ulceration. There used to be a clinical proverb for the development of ulcers, “no acid, no ulcer”. Now, from the modern theory, “no hp, no ulcer” should be emphasized more.
The cause of peptic ulcer (including gastric ulcer and duodenal bulb ulcer) has long been considered to be related to genetics, excessive gastric acid, bile reflux, smoking and other factors, among which gastric acid is considered to be the main factor in the development. For nearly 80 years, stomach acid has been considered the cause of gastric ulcer formation, so there is a traditional saying of “no acid, no ulcer”.
The traditional treatment for peptic ulcers is to neutralize gastric acid or inhibit acid secretion. In the past, alkaline drugs were used, but nowadays, Hz receptor inhibitors or other inhibitors of gastric acid secretion are commonly used. The application of these anti-acid and anti-acid drugs is indeed beneficial to the healing of ulcers, but these drugs have a common drawback, once the drug is discontinued, the ulcer will soon recur. Therefore, some patients have to take the drug intermittently, and some need to take a long-term maintenance dose. There are also many patients with ulcers that heal repeatedly.
Gastric fluid analysis found that duodenal ulcer patients, gastric acid secretion is too high; and gastric ulcer patients in gastric acid secretion increased only 16%, while many patients with normal gastric acid secretion, some even below normal. It can be seen that the amount of gastric acid secretion is not an important factor in the development of gastric ulcer, but the decrease of gastric mucosal defense ability, so that the relative increase of gastric acid and other attacks, may be the main reason for the formation of gastric ulcer.
Stomach tumor
Many possible mechanisms of H. pylori causing gastric cancer have been proposed from a large number of studies on H. pylori infection in recent years.
(1) Direct transformation of the mucosa by metabolites of the bacteria;
(2) Similar to the pathogenic mechanism of viruses, some fragments of hp dna are transferred into the host cell, causing transformation;
(3) H. pylori causes an inflammatory response, which itself has genotoxic effects. Of these mechanisms, the latter seems to be consistent with the most widely available information.
Barry J. Marshall and J. Robin Warren (for which both were awarded the 2005 Nobel Prize in Physiology or Medicine)
Chronic gastric disease
Chronic gastric disease refers to chronic gastritis (superficial gastritis and atrophic gastritis) and ulcer disease (gastric ulcer and duodenal ulcer). The gastroscopy survey confirmed that the incidence of chronic gastritis in our population is up to 60% or more, and the incidence of ulcer disease is about 10%.
In 1982, the Australian scholar Marshall observed that a bacterium called Helicobacter pylori (HP) in the gastric mucosa was associated with the development of chronic gastric disease. After that, scholars at home and abroad made a lot of research on this bacterium and found that.
(1) In volunteers with normal gastric mucosa, oral administration of HP suspension can cause gastritis symptoms and pathological changes.
(2) The detection rate of HP is very high in chronic gastritis, while the bacteria cannot be detected in those with normal gastric mucosa.
(3) HP antibodies are significantly higher in the serum of patients with chronic gastritis.
(4) Treatment for HP can result in significant improvement of gastric mucosa in patients with chronic gastritis.
(5) HP can be detected in the gastric sinus of 60%-80% of patients with gastric ulcer and 70%-100% of patients with duodenal ulcer, and serological examination confirms that these people have high titers of serum HP antibodies.
(6) The recurrence rate of ulcer disease cured with anti-HP drugs was significantly reduced.
(7) Infection of rhesus monkeys with HP can cause chronic gastritis and pathological changes of gastric mucosa with human infection.
Now the medical community has the following consensus: HP is definitely the causative agent of chronic gastritis, and is also extremely close to ulcer disease and gastric cancer. That is to say, HP is the culprit and culprit of chronic gastric disease.
Therefore, in addition to traditional drugs, anti-HP drugs should be given for the treatment of chronic gastric disease. The drugs that are considered to be more effective in the treatment of this bacterium are: colloidal bismuth subcitrate (also known as Denox), amoxicillin, dysentery and metronidazole, etc.
Urticaria
In 1998, Dr. Gasparini successively found that the rate of H. pylori in the stomach of patients with chronic intractable urticaria could be as high as 55%, and after elimination of H. pylori by antibacterial therapy, urticaria no longer occurred in 81% of patients. According to this analysis, the H. pylori bacteria associated with chronic gastritis and peptic ulcer may become an allergen and trigger allergic reactions and allergic diseases such as urticaria.
Therefore, patients suffering from chronic intractable urticaria that has not been cured for a long time should go to the hospital to check whether there is H. pylori parasites in the stomach. If there is, anti-H. pylori treatment can be carried out, and the main drugs commonly used are hydroxybenzyl penicillin (amoxicillin), metronidazole, and methylerythromycin. Of course, those who are allergic to penicillin should not use amoxicillin. Patients with chronic intractable urticaria may be cured unexpectedly after debridement treatment.
Other diseases
H. pylori (Hp), which lives deep in the gastric mucosa and makes waves, has been found to be not so honest in recent years. It is not only associated with chronic gastritis, peptic ulcer and gastric cancer, but also causes other organ and tissue diseases, especially cardiovascular diseases, anemia and idiopathic thrombocytopenic purpura. With the elimination of Hp, these diseases can be improved or recovered unexpectedly.
H. pylori infection is one of the most prevalent chronic diseases in our country and is the main cause of chronic gastritis, which initiates a series of pathogenic events leading to the development of atrophic gastritis, chemosis, heterogeneous hyperplasia and eventually gastric cancer. Eradication of H. pylori prevents the development and progression of precancerous changes in the gastric mucosa (atrophic gastritis, intestinal chemosis). Removal of H. pylori infection from the stomach leads to a significant reduction in the risk of precancerous gastric lesions and gastric cancer. H. pylori is very stubborn and once infected, the rate of self-healing is close to zero unless a regular treatment plan is used.