The eradication rate of the ideal cholesterol eradication programme should exceed 95 per cent. Over time, the problem of reducing the eradication rate of cholesterosomiasis has become increasingly acute, and even where remedial treatment is provided, some patients have failed. The reasons for the failure to eradicate treatment are many, including the factors of the fungi of the cholesterol itself, host factors, environmental factors, different clinical diseases and treatment methods.
Bacteria
The most important cause of the eradication failure is the mutation of the fungus fungus via its own chromosomes, which can produce resistance to a variety of antibiotics, in particular the widespread use of fungus vistas, carracin and left-oxen fluoride resistance, which is an important factor in the treatment failure. However, about 50 per cent of those who have failed to eradicate treatment are not explained by bacterial resistance, but are related to other causes.
Discrepancies in the formation of cholesterocococcals affect the therapeutic effects of eradication treatment. Studies have found that the cholesterobacteria found in the corrosal and gastrointestinal intersections may escape the effects of antibiotics, possibly because the structure of the cortex in the cortex area is different from that of the stomach or gastric body, which makes the biological behaviour of the cipococobacteria that has been planted in the department different from that of cipocococcus in the stomach or gastrointestinal body, leading to the failure of the treatment because it is resistant to antibiotics; the study has found that, in the case of individual antiacidant treatment, the number of cluccus planted in the gastrophate is significantly lower and the number of stomachs is significantly higher, which is likely to be related to a decrease in the therapeutic effects of the use of proton pump inhibitants (PPI) by clinical patients before treatment.
Bacteria spherical reformation is one of the major causes of treatment failure following failure of antibiotic treatment, and the spherical reformation of the spherical skeletal skeletal skeletal skeletal strain is not sensitive and is now considered to exist in two forms: a dead or degenerated skeletal skeletal skeletal fungi, and a non-mortal but non-preventable fungus. After the elimination of antibiotics for 2-4 weeks or more, spherical bacteria are more likely to recover their original activity, and this spherical fungus is not only an important cause of the failure of the eradication of the scavenger.
In cases of high bacterial loads, when the success rate of eradication treatment is reduced when the bacterial loads established within the stomach are too high, the enormous bacterial loads have the effect of inoculation, which binds the fungus to the gastrogular mucous cell and forms a layer of bioprotective membranes for it, and some bacteria enter the cell, thus preventing the fungus from contact with antibiotics leading to treatment failure. Large bacterial loads can also lead to the creation of a claustrophax-type drug-resistant strain, which can still regenerate when antibiotic treatment is interrupted, leading to treatment failure.
The detection values for urea pneumatics test can be a semi-quantifiable reflection of the bacterium load, which is often suggested to be excessive when it is 10 times higher than the normal upper limit.
The increase in PH in the stomach can increase the PH for cholesterocella eradication from 2 to 7.2, most antibiotics have no apparent antibacterial activity for cholesterocella in low gastric acid settings and need to increase PH in the stomach to above 5.5 when antibiotics are applied in the body to treat the infection. Thus, anti-acid proton pump inhibitors (PPIs) need to be added to the treatment of cholesterocococcal infections to improve the pH value in the stomach, thus increasing the antibiotic antibacterial activity against cholesterocella; the new potassium ion competition acid retardants, which have been listed in recent years, offer new options for further improving the therapeutic effects of cholecella eradication treatment. The metabolic of host drug metabolism genotypes affecting the therapeutic proton pump inhibitor (PPI) for the eradication of cholesterocella is mainly through the CYP2C19 route, the CYP2C19 genetic polymorphological effects include the therapeutic effects of the PPI eradication treatment programme, the strong metabolic type of CYP2C19 is significantly lower than that of the weaker metabolist due to the high PPI clearance rate, and the strong metabolic type of CYP2C19 is an important cause of the failure to eradicate the treatment, in addition to the resistance of Hp to antibiotics. Poor patient dependence is a major cause of the failure of cholesterococcal eradication treatment, which not only tends to lead to the failure of the treatment, but also to the antibiotic resistance of cholesterocella, which makes subsequent treatment more difficult. There have been many studies of the effect of tobacco use on the treatment of cholesterococcal eradication, which have shown that smoking can reduce the eradication rate of cholesterocella, and some studies suggest that the eradication rate of cholesterocella among people with a 12-finger ulcer smoking is significantly lower than among non-smokers. Oral environments may be one of the reasons for repeated failures or relapses in the treatment of cholesterol eradication, and may be an important cause of failure or recurrence, as well as an important means of transmission. Because of the unique “biofilm” structure of the microorganisms in the oral streptomosis, the conventional eradication treatment is ineffective in the treatment of the oral cholesterocella, and the combination of oral cholesterol treatment with the eradication treatment has the potential to increase the eradication rate of the cholesterocella.
Environmental factors It is generally recommended that the success of the eradication be determined after at least four weeks after the end of the eradication treatment, but that the patient may have re-emerged or re-infected while awaiting review. Epidemiological studies suggest that cholesterococcal infections are mainly related to the living environment and habits, that there is a clear concentration of people or families, and that the important means of transmission of cholesterocella is human transmission, and that factors such as poor economic and sanitary conditions, low education, overcrowding and non-crop water sources are high risk factors for cholesteroc infections or re-infection.
