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Helicobacter pylroscopic research progress
< "text-line: left;" > Helicobacter pylbo and its infection1 overview
< p style"text-align:left;" > study of stomach bacteriology has long been a neglected area. The separation of Marshall and Warren from a biopsy specimen of gastric mucous membranes in patients with chronic active gastritis in 1983 to Helicobacter pylori (Hp) is an important breakthrough in this field.caused a huge stir in the international digestive community shortly thereafter, and its discovery played a huge role in the development of digestive disease, especially gastroenterology. It is now clear that it is an important causative factor in the development of many chronic stomach diseases (chronic gastritis, peptic ulcers, stomach cancer, etc.).
1.1 Hp history, discovery and naming
1.1.1 1.1 Historical background
Marshall, after separating to Hp, went back to explore the historical literature and found that this type of bacteria had actually been noticed for a long time. In dogs in 1893, in 1896, rats and cats were reported to have stumbled upon snails in their stomachs. The same bacteria were found in the stomach contents of ulcerative stomach cancer patients at the beginning of this century.
other reports confirm these findings. It has also been noted that these bacteria are not found in healthy people. After 30 years of effort, the bacteria were found in the stomachs of patients with benign peptic ulcers in scattered reports. In a comprehensive autopsy study in 1938, Doenges suggested a 43 percent prevalence of snails in the stomach, but did not examine the relationship between the bacteria and different stomach diseases.
< p-style is "text-align:left;" > there has been a debate about the possible role of these bacteria in stomach diseases. Some researchers suggest that the bacteria seen in biopsy specimens are contaminants swallowed or mouthfuls. This hypothesis prevailed in 1959 when Palmer, then an influential scholar, published a report on a large number of histological studies of 1,000 gastric biopsy specimens. After that, interest in stomach bacteriology was poured with cold water.In 1975, Steer and Colin-Jones reported the discovery of bacteria in the stomach mucous membranes under the mucus layer in patients with stomach ulcers, re- sparking interest in the role of stomach bacteria in the mechanisms of peptic ulcer disease, suggesting that bacteria may reduce the resistance of the stomach mucous membranes and are therefore susceptible to ulcers. Steer and others tried to isolate the bacteria.
result is the growth of green pus. A closer look at the images in the article suggests that what is seen in the mucous membrane is a screw-shaped bacteria unrelated to the bacteria. It now appears that the green pus isolated by these authors may have been contaminated bacteria from endoscopes, and what is seen in the pictures is the HP that we are all interested in now.
is now known to produce a large number of urea enzymes, and many scholars have demonstrated the presence of endogenetic urea enzyme activity in the stomachs of many animals prior to the discovery of Hp. Luck and Seth first described this activity in 1924. In 1955, Kornber and Devies concluded in a review that gastric urea enzymes were mainly present in the stomach and originated from bacteria. Later studies in human dung have also confirmed the relationship between these enzymes and ulcer disease, and some have even used urea to treat certain patients.
With hp's discovery, people can now put these studies together to get a clear understanding that hp in the stomach is linked to urea enzymes. Separating HP from gastric mucous membrane biopsy specimens is a key factor in this process. Without this finding, awareness of stomach diseases will remain limited.
1.1.2 Discovery and Naming
In the above historical context and gastroscopy has been greatly popular, separation and culture of enterobacteria micro-needs O2 method has matured conditions, Marshall and other sensitive to the stomach seen in the form of isolated intestinal bacillus. Since the conventional O2 and O2 methods can not be separated, why not separate the method of cultured enterobacteria to try it? As a result, they succeeded.
was successful in 1985. It was initially believed to be morphologically similar to the Campylobacter genus bacteria, and the separation culture method was similar, but isolated from the stomach specimen, so it was called gas camptriclobacter like organism, GCLO.
soon changed its name to campylobacter pyloridis Chinese (CP) because it was common in the sinuses of the stomach, and later changed to cacpylobater pylori because the name did not conform to the bacteria's uniform Latin naming principle.
As the study of the biological characteristics of the bacteria continues to develop, it has been found that although the bacteria are similar in morphological and culture characteristics to the Campylobacter genus bacteria, there are many properties that are significantly different from the Campylobacter genus bacteria. It has been suggested that the nucleotide sequence of HP's 16SrRNA is different from that of Campylobacter, and similar to that of the Wolinella succinogenes, which should be classified as the wolinella genus.
1989 Goodwin and other representative strains of CP and Campylobacter genus and wolinella genus from the superstructage, fatty acid composition, respiratory tantalum, growth characteristics, enzyme activity and other five expressive characteristics made a systematic comparison. They believe that CP should not belong to the Genobacteria genus, nor to the Wollinella genus, and that a new genus, called the Genus Bacillus (helicobacter, H), should be established.
, CP should be renamed Helicobacter pylori (Hp) accordingly. At that time, a hp-like campylobacter mustelae, which had been separated from the otter's stomach, was changed to helicobacter mustelae (Hm).
Since the new genus, there have been people in the world from a variety of animal gastrointestinal isolation to the new strain is considered to belong to the genus of Scum, and some people from the past has belonged to the Genus Campylobacter and other genus bacteria pulled out certain bacteria to think that should be attributed to Bacillus. According to the available reports, there are no less than 10 species of bacteria in the genus Bacillus. In addition to Hp and Hm, there is also a cat screw bacteria (helicobacter felis, Hf) has been more people's approval, other are still recognized.
1.2 hp infection and upper digestive disease
< p style"text-align:left;">Hp infection and upper digestive tract disease has been widely reported, and has achieved a basically consistent understanding as follows.1.2.1 Hp infection and chronic gastritis
Hp and chronic shallow gastritis are fully established. The evidence is as follows: (1) In fact, all HP-positive people have been confirmed to have sinusitis. (2) If hp infection is treated with antibacterial drugs, gastritis can subside after Hp is eradicated. (3) In some animal models, the loss of chronic shallow gastritis can be replicated after inoculation of hp obtained by separation from the patient's stomach. (4) Marshall and Morris, who infected themselves with the patient's HP, respectively, achieved the same results.
1.2.2 Hp infection and peptic ulcers
From available information to establish the etiology relationship between hp and peptic ulcer diseases(PUD), including stomach ulcers, duod ulcers. This is partly due to the lack of suitable animal models and the fact that only a few people infected with HP develop ulcers. However, almost all PUD patients have HP-infected gastritis.
So, when there are no other triggers, such as taking steroidal anti-inflammatory drugs (NSAIDs) or Zollinger-Ellison syndrome, the correlation between Hp infection and stomach ulcers is slightly weaker, and 80 percent of patients with gastric ulcers induced by NSAID have hp infection. However, it is important to note that most people infected with HP do not have tit-for-ting or stomach ulcers.
< p style is "text-align:left;" > these facts mean that the host's genetic characteristics, strain variability, or other factors play a role. After the eradication of Hp infection, the recurrence rate of ulcer disease decreased significantly, which is the strongest evidence of hp's estigation in PUD. Hp prevents the recurrence of ulcer disease after eradication, which is not as well-evidenced in stomach ulcers as in duoon ulcers.In cases of duobial ulcers, it is strange that in some studies, Hp is more common in the sinuses of the stomach than in the duobium area where ulcers occur. Why does Hp in the sinuses of the stomach cause duoon lesions? Factors that have been proposed include: Hp's settlement on heteroentialized cells, secondary changes in stomach acid or heterointestinal bicarbonate, or lesions caused by the product of the infected bacteria and/or the host inflammatory response.
1.2.3 Hp infection and non-ulcerative indigestion
Hp infection is not convincingly associated with non-ulcerative indigestion (Nonulcer Dyspepsia, NUD). So there is still debate. The infection rate of HP in NUD patients is not higher than that of the general population.
1.2.4 Hp infection and stomach malignancies
< p style"text-align:left;">Hp infection and stomach adenocarcinoma: gastric adenocarcinoma is one of the most common malignant tumors in the world. The incidence rate in our country is second only to lung cancer. There is evidence that HP infection is associated with stomach and sinus adenocarcinoma. However, stomach cancer also occurs in people with no evidence of HP infection. The prevention and treatment of Hp infection has insufficient evidence on the risk of stomach cancer. Epidemiological data show that the incidence of stomach cancer is higher in some people with high rates of HP infection. Hp infection rate and stomach cancer incidence were negatively related to socioeconomic status and increased with age.has declined in the study of continuous births in developed countries. In the United States, African-Americans and Latinos have a higher rate of occurrence than whites. A regionally distributed correlation between Hp infection rates and gastric cancer mortality has been found. However, there are some significant epidemiological insiss between the two diseases. For example, men with stomach cancer have a higher incidence than women, and there is no difference between the sexes in the rate of HP infection.
reported high hp infection rates in some populations, but low incidence of stomach cancer. These insopties indicate that factors other than hp infection rates are also important in gastric cancer risk factors. In some, but not all, retrospectiveserum studies have shown that patients with stomach cancer have higher rates of HP infection than the control group.
< the most powerful evidence of a > infection associated with stomach cancer came from three prospective serological studies. These studies show a significant increase in the incidence of stomach cancer in people infected with HP. In these studies, no hp infection was associated with throttle cancer and gastroesophageal disease