Mistakes in the management of chronic gastritis and how to avoid them

Dyspepsia is a symptom that affects a large part of the general population, and it can be caused by numerous diverse conditions, including chronic gastritis. As most patients who have dyspepsia do not have a serious disease their symptoms can be managed conservatively, which avoids unnecessary and over treatment.

Two strategies that are based on H. pylori being a cause of dyspepsia and upper gastrointestinal disease have been proposed and assessed—‘test and treat’ and ‘test and scope’.¹ The first step for both strategies is to perform a non-invasive test for H. pylori infection (for example, the ¹³C-urea breath test, the faecal antigen test, or measurement of circulating antibodies [IgG]). For the ‘test and treat’ strategy, all patients found to have an H. pylori infection immediately receive therapy. By contrast, the ‘test and scope’ strategy directs patients to undergo gastroscopy to evaluate H.-pylori-related diseases, namely for older patients or those with alarm symptoms.

There are many studies demonstrating that ‘test and treat’ is a safe and cost-effective strategy and that it may reduce the burden on endoscopy services.1 Regardless of the strategy chosen, all patients with dyspepsia should first have the presence of H. pylori infection confirmed before additional management strategies are put in place.  

Several trials have shown a reduction in the incidence of gastric cancer after eradication of H. pylori.² Clearly, the sooner the H. pylori infection is detected and eradicated the better, but if H. pylori infection and chronic gastritis are not detected until after endoscopy has been performed and biopsy samples taken it is still worthwhile treating the infection. Indeed, although therapy for H. pylori infection has the most significant impact before atrophy and intestinal metaplasia occur, even after precancerous conditions have developed H. pylori eradication may stop progression.³ There is also evidence that after endoscopic therapy for early gastric cancer, H. pylori eradication reduces the risk of metachronous cancers.³ The take-home message is that it is never too late to eradicate H. pylori,² and eradication may represent a unique opportunity for primary prevention of gastric cancer and also of peptic ulcer disease.

An upper gastrointestinal endoscopy can be scheduled according to diverse indications and it is crucial for the detection of gastric cancer and its precursors. Regardless of the indication, the possibility that early gastric cancer might be present should always be kept in mind. In the Western world, there are indirect signs that increasing attention is being paid to early detection of gastric cancer when performing endoscopy,⁴ but it is still a challenge and one that should not be overlooked.

The estimated miss rate for gastric cancer is approximately 10%.^5,6 Therefore, it is of paramount importance that the quality of any gastroscopy is optimised, including fasting prior to the procedure, adequate observation time, photographic documentation and ensuring that any biopsy samples are taken according to the guidelines (figure 1).⁷ Of course, the a priori risk of gastric cancer must also be kept in mind (for example, in other pathologies such as Barrett oesophagus in patients with reflux, or coeliac disease in patients with anaemia).

The risk of harbouring gastric cancer varies, increasing with higher local prevalence, Asian ethnicity, older age, a family history of gastric cancer, a past diagnosis of chronic gastritis (especially its advanced forms) and the presence of alarm symptoms. To note, in an inflamed stomach proper endoscopic assessment is even more challenging.⁵ So, to avoid overlooking gastric cancer its diagnosis should always be considered when managing patients with dyspepsia and particularly those who have gastritis.

Pernicious anaemia and autoimmune gastritis (AIG) are two aspects of the same disease. The augmented risk of gastric cancer for patients with pernicious anaemia is well known. In addition, in a recently published series, around 5% of gastric cancers were associated with AIG.⁸ Considering that there is now a decline in the rates of H. pylori infection and an increase in the incidence of all autoimmune diseases, it is not unreasonable to think that the number of cases of gastric cancer attributable to pernicious anaemia and AIG will increase in the coming years.

The incidence of gastric cancer in AIG is currently reported to be 0.27% per year.⁹ The incidence is almost the same in studies from countries that have a high prevalence of gastric cancer as it is in studies from countries that have a low prevalence.⁹ Aside from the high risk of gastric cancer, AIG is associated with several other autoimmune diseases, so recognizing AIG could serve as an alert that other such concomitant conditions may be present or develop over time.¹⁰ In summary, it is of pivotal importance to recognize AIG and schedule the appropriate follow up every 1–2 years.

Approximately 5% of individuals with chronic gastritis will harbour extensive atrophic changes (including intestinal metaplasia) in their stomach.¹¹ Although the prevalence changes across different regions and countries, for different ethnicities, and with individual risk factors, once this phenotype has developed it is a valid reason for that individual to undergo future surveillance.

Frequently, these extensive atrophic changes are detected during the first endoscopic assessment through biopsy samples taken to determine the presence of H. pylori. That is, as stated already, H. pylori infection should be excluded when managing dyspeptic patients so that then when endoscopy is performed both diagnoses can be made at the same time, with appropriate biopsy samples being taken from both the antrum and corpus.¹² Biopsies must be taken from predefined sites according to the Sydney Houston protocol — they may also be taken from areas targeting endoscopic changes if adequate training has been undertaken to ensure the optimal optical diagnosis of gastric changes that are suggestive of intestinal metaplasia.¹³

To allocate individuals to the correct surveillance schedule, an adequate collection of a priori risk factors and the current phenotype must again be established. When severe atrophic changes or intestinal metaplasia is found in the antrum and the corpus, or if the changes have been identified as OLGA or OLGIM stage >III/IV disease, individuals should be followed up endoscopically in 3 years. This schedule may vary if further risk factors are present, such as H. pylori infection or family history.¹⁴

In the context of managing chronic gastritis, the correct number of adequate biopsies must be taken during endoscopy to detect H. pylori, and to stage chronic gastritis and atrophic changes if a neoplasia is found. Further biopsies indicated should be taken from the antrum and corpus because there is indirect evidence from surgical samples that distribution is patchy in the corpus and that, with age and expansion of pyloric glands, a distal-to-proximal gastric spread of H. pylori occurs.³ As a first conclusion, biopsy samples should be taken to detect whether H. pylori is present.

The need to take adequate and sufficient biopsy samples also applies to the staging of atrophic changes, as already determined. Biopsies are required to stage chronic gastritis if it is unestablished. However, importantly, once a risk phenotype has been established, biopsy samples no longer need to be taken provided the endoscopist has undergone proper training in endoscopic assessment of the gastric mucosa, except if there is a noticeable need to diagnose H. pylori infection.

Unfortunately, some individuals being managed due to chronic gastritis will harbour a lesion that is suspicious for neoplasia. In this case, it should be sampled adequately but not excessively. Early gastric neoplasia is best staged and then treated by endoscopic resection. Thus, taking extensive biopsy samples can jeopardize any subsequent endoscopic resection by inducing scarring and submucosal fibrosis. Therefore, for suspected neoplastic gastric lesions that are potentially amenable to endoscopic resection, the number of endoscopic biopsies taken should be limited.³ On the other side, for lesions that appear to be advanced when viewed endoscopically at least six biopsies should be taken.

In conclusion, when assessing the gastric mucosa via biopsy samples an integrated approach must be implemented to stage atrophic changes and to determine the nature of any neoplastic lesions, while not excluding the potential for minimal invasive therapy to be performed.

Dyspepsia can be treated by inhibiting gastric acid secretion, even if the results are only slightly better than placebo.¹⁴ However, there is no role for proton-pump inhibitors (PPIs) in the treatment of chronic gastritis in the absence of other diseases (such as reflux) or NSAID intake.¹⁴ It is worth noting that prescribing PPIs to patients who have asymptomatic chronic gastritis not only exposes them to common PPI side effects, such as headache and diarrhoea, but can also increase their risk of gastric cancer, owing to induced hypergastrinaemia, gastric atrophy and bacterial overgrowth in the stomach.¹⁵ The validity of this point has been questioned for a long time, and it has recently been demonstrated in a population study, even if the number needed to harm was greater than 1,100.¹⁵ Thus, asymptomatic individuals who have chronic gastritis do not need PPI therapy.

The most common cause of chronic gastritis is H. pylori infection. However, in addition to AIG, there are many aetiological agents that can cause chronic gastritis. They include environmental agents, transmissible and non-transmissible agents, and host-related factors. The most frequent causes of gastritis that is not attributable to H. pylori or AIG are as follows: lymphocytic gastritis, vasculitis, granulomatous diseases, inflammatory bowel disease, viral infections, bacterial diseases, alcohol abuse, and cocaine abuse. After thorough evaluation of all possible causes, there are still a few cases that remain ‘unclassified’. The malignant potential of these gastritides remains unknown. Regardless, even after exclusion of H. pylori or AIG, it is worthwhile looking for other possible causes of chronic gastritis as appropriate treatment can be helpful (figure 2).¹⁶