Two Cases of Acute Gastric Mucosal Lesions Due to Helicobacter pylori Infection Confirmed to be Transient Infection

Abstract

Two adult cases of acute gastric mucosal lesions (AGML) caused by Helicobacter pylori infection were confirmed by spontaneous eradication during the follow-up period. The clinical course of the initial infection by H. pylori in adults with AGML remains unclear, whether it is transient or progresses to a persistent infection. In these two reported cases, gastric biopsies at the time of the onset revealed the presence of H. pylori; however, serum H. pylori antibodies performed at the same time were negative. Retesting for H. pylori serum antibody, after six months in one and after two months in the other, was negative, confirming spontaneous eradication.

Introduction

Many reports of acute gastric mucosal lesions (AGML) diagnosed using endoscopy have been published (1-5), but with the establishment of disinfection methods for endoscopes and the decrease in the infection rate of Helicobacter pylori itself (6), the number of reported cases of AGML caused by H. pylori has been decreasing. However, despite the reduced frequency of occurrence of such cases, we still experience sporadic cases and need to know how to deal with them.

At present, AGML due to H. pylori infection is known to occur in many cases where the route of infection is unknown (7), and it is not clear how many cases of initial infection progress to persistent infections. To prove that AGML due to H. pylori infection is the first infection, the presence of H. pylori must be confirmed by a histological examination or culture using gastric biopsy tissue, a rapid urease test, urea breath test (UBT), or stool antigen test during the acute phase, and serum or urine antibodies to H. pylori must be negative.

We encountered two cases in which the presence of H. pylori was confirmed in gastric biopsy tissue at the onset of acute gastritis, and serum antibodies on the same day were negative, suggesting an initial infection with H. pylori. Furthermore, these two cases were spontaneously cleared of H. pylori in the subsequent course of the disease.

We herein report these cases because it is valuable to consider the diagnostic method to prove the initial infection with H. pylori and to consider the course of H. pylori infection in adults.

Case Report

Case 1

A 38-year-old man presented with periodic chest pain, epigastric pain, and watery diarrhea for the past day. The patient visited our hospital for intensification. He had no history of drinking or smoking and no history of taking non-steroidal anti-inflammatory drugs (NSAIDs).

A physical examination revealed tenderness of the epigastric region. Blood chemistry tests were normal. Serum H. pylori antibody IgG was <3 U/mL, negative. Computed tomography (CT) of the abdomen showed edematous mucosa from the gastric angle to the antrum, confirming the diagnosis of acute gastritis, and the patient was given Omeprazole.

Endoscopy was performed the following day, revealing edematous mucosa from the gastric angle to the antrum, with shallow erosions in some areas, as well as narrowing of the pylorus (Fig. 1a, b). The erosions were clearly visible by narrow-band imaging (NBI) (Fig. 1c). The mucosa of the gastric body showed a red streak but no mucosal atrophy (Fig. 1d). Gastric biopsy specimens from the antrum showed marked inflammatory cell infiltration with disruption of mucosal superficial glandular ducts and increased capillaries (Fig. 2a), and staining with H. pylori monoclonal antibody showed a small population of H. pylori (Fig. 2b). Six months later, repeat endoscopy was performed, but there were no abnormalities in the gastric mucosa, and a histological examination of a gastric biopsy specimen and serum H. pylori antibody findings were negative (<3 U/mL).

Figure 1.

Endoscopic findings of Case 1. (a, b) Edematous mucosa extending from the gastric angle to the antrum. Surface erosion with white moss and partly covered with creamy mucus. (c) Erosion clearly visible on narrow-band imaging (NBI). (d) Absence of atrophy in the gastric body, suggestive of an initial infection with H. pylori.

Figure 2.

Gastric biopsy tissue from the antrum of Case 1. (a) Histological findings from the antrum showed marked inflammatory cell infiltration with disruption of mucosal superficial glandular ducts and increased capillaries. (b) Staining with H. pylori monoclonal antibody showed a small number of H. pylori (arrow).

Case 2

A 34-year-old man was admitted to the emergency room with epigastric pain and nausea that had persisted for 2 days. The patient had no medical history and no history of smoking. He had a history of alcohol consumption (350 mL of beer per day) but no history of taking NSAIDs.

A physical examination revealed tenderness of the epigastric region. No abnormalities were observed on blood chemistry tests. Serum H. pylori antibody IgG was <3 U/mL, negative. CT of the abdomen revealed mucosal edema in the gastric antrum region, and acute gastritis was diagnosed (Fig. 3a, b).

Figure 3.

CT images of the abdomen of Case 2 at the initial examination. Gastric antrum shows circumferential peaked thickening, mainly in the submucosa (a, b).

Vonoprazan was administered immediately, and endoscopy was performed one week later, revealing that the mucosa of the antrum was generally erythematous, with a healing ulcer spotted at the lesser curvature (Fig. 4a, b). The mucosa of the gastric body was slightly erythematous but without gastric mucosal atrophy (Fig. 4c). Biopsy tissue from the gastric fundus showed a regenerated epithelium and inflammation marked with the presence of neutrophils in the mucosa (Fig. 5a), which may have represented the convalescent phase of acute gastritis. Giemsa staining showed bacilli in the superficial layer of the gland ducts (Fig. 5b). Retesting of H. pylori serum IgG antibodies 2 months later was negative (<3 U/mL).

Figure 4.

Endoscopic images of Case 2. (a, b) Generalized erythematous mucosa of the antrum with a healing ulcer at the lesser curvature. (c, d) Slightly erythematous mucosa of the gastric body without gastric mucosal atrophy.

Figure 5.

Biopsy tissue from the body of the stomach. (a) Inflammation marked with presence of neutrophils is seen in the mucosa. (b) Giemsa staining shows bacilli in the superficial layer of the gland ducts (arrow).

Discussion

We present two cases of acute gastritis due to primary infection with H. pylori. Since the authors had experienced three similar cases in the past (8), and two of them were transient infections, the present two cases were also observed without administering eradication treatment, and both cases were confirmed to be transient infections.

To our knowledge, based on a literature search in the databases of the Central Journal of Medicine and PubMed, there have been nine previous cases that were followed up without eradication therapy after the initial infection and had the status of the infection subsequently checked. Table shows the nine cases previously encountered and the two cases described in the present study (8-13). Of the 11 total cases, 2 were confirmed to be persistent infections, and 9 were transient infections, suggesting that majority were transient infections. In general, H. pylori was transmitted at an early age, and once infection was established, it likely progressed to a chronic persistent infection that developed over time into atrophy of the gastric mucosa (14). Since the eradication therapy can cause serious side effects in rare cases (15), it should be performed when persistent infection is confirmed.

Table.

A Case Report in Japan of Initial Helicobacter Pylori Infection Diagnosed and Untreated, with Subsequent Follow-up to Confirm the Presence of H. Pylori Infection.

Reference		Age		Sex		Time of decision		Final diagnosis method and results of H. pylori infection
(9)		24		M		16 months		RUT(-), Histology(-), UBT(-), serum antibody(-)
(10)		27		F		6 months		Histology(-), culture(-)
(11)		39		F		1 month		RUT(-), immunohistology(-), serum antibody(-)
(12)		41		M		2 years		RUT(-), UBT(-), serum antibody(-), stool antigen(-)
		23		F		174 days		Histology(+), immunohistology(+), culture(+), serum antibody(-), stool antigen(+)
(13)		60		F		4 months		RUT(-)
(14)		27		F		2 months		UBT(+), serum antibody(+)
		65		M		2 months		Histology(-), culture(-)
		62		M		42 days		Culture(-)
Our case		38		M		6 months		Histology(-), serum antibody(-)
		34		M		2 months		UBT(-), serum antibody(-)

RUT: rapid urease test, UBT: urea breath test

The pathogenesis of acute H. pylori infection in adults, particularly whether it is transient or progresses to a persistent infection, is unclear. Two previous reports have suggested that once H. pylori enters the stomach, the infection persists (16,17). To prove that an H. pylori infection is the first, it is necessary to prove that H. pylori is present and that there is no history of H. pylori infection. In the two cases reported in our study, there was no history of H. pylori infection, the serum H. pylori antibodies were negative, and gastric biopsy tissue revealed the presence of H. pylori. In addition, there was no atrophy in the gastric body mucosa, and the presence of regular arrangement of collecting venules (RAC) was confirmed, as reported by Yagi et al (10). In our patients, the histological diagnosis by a gastric biopsy showed spiral bacilli, which were considered to be H. pylori, and serum H. pylori antibodies at the time of onset of AGML had a cut-off value of ≤3; therefore, we considered the gastric mucosal background at the time of endoscopy to be primary H. pylori infection. In addition, the two patients were followed up without immediate eradication therapy and retested for H. pylori serum antibody (after six months in one and after two months in the other), showing negative findings, which confirmed spontaneous eradication. The infection in our patients was considered to have been eliminated spontaneously. In general, upon detection of infection with H. pylori, eradication therapy is initiated immediately. However, there are cases of patients in whom spontaneous eradication occurs, as presented here, so we believe that eradication therapy should be started only after persistent infection is confirmed.

The route of transmission of H. pylori infection in adults is often unknown (8), but it has been reported to be transmitted through dental procedures (14), endoscopy (1-5), drinking water (18), and contact with infected partners (19). Similarly, the route of infection was not clear in the two patients in our study, as they had no recent history of dental visits, endoscopic examinations, overseas travel, or drinking well water.

When AGML due to H. pylori infection is suspected, there are several methods of diagnosing the infection, including culture and speculum examination using gastric biopsy tissue, measurement of serum and urine antibodies, a rapid urease test, a urea breath test, and a stool antigen test. Itano et al. performed rapid urease tests in 36 cases of AGML that developed after endoscopy and reported that all of them were negative (20). Sakai et al. also reported that the rapid urease test and urea breath test in two cases may have produced false-negative results due to the low number of bacteria (21). In any case, negative serum antibodies are necessary to prove initial infection with H. pylori.

Culture using a gastric biopsy specimen requires a special medium for the culture of H. pylori that is not used regularly outside of certain facilities where this culture method is used to check for resistant bacteria. In addition, in AGML, proton pump inhibitors (PPIs) may have already been administered before endoscopy due to the presence of severe pain, so the rapid urease test may show a false positive in PPI-treated cases due to an increased intragastric pH. In our patients, a PPI or vonoprazan had already been administered at the time of endoscopy.

Regarding the pathological diagnosis using gastric biopsy tissue, Watanabe et al. pointed out that the distribution of H. pylori is high around the lesion and that biopsies collected at a distance from the lesion or 7 to 21 days after the onset of the disease, after the acute phase, are likely to show false negatives due to a decrease in or the elimination of the bacteria (22). Although we are hesitant to perform gastric biopsies when multiple ulcers with clots are seen, there have been no reports of complications, including bleeding on an examination, when gastric biopsies were performed in the acute phase, including in our two cases.

Acute gastritis is diagnosed by clinical symptoms and endoscopic findings and can also be caused by sources other than H. pylori infection, such as stress or drugs. Acute gastritis is associated with symptoms, such as severe pain in the pericardial area and hematemesis, so once diagnosed, patients need to be treated with strong gastric acid secretion inhibitors, PPIs, or vonoprazan. Regarding the timing of eradication of acute gastritis due to H. pylori infection, H. pylori infection initially occurs in childhood, and its persistent infection can lead to peptic ulcers and gastric cancer after decades of long-term follow-up (23). Therefore, there is no need for hasty eradication in cases of acute H. pylori infection.

We encountered two cases of AGML that appeared to have achieved spontaneous eradication after acute infection with H. pylori. In addition, we reviewed the literature on similar cases of spontaneous eradication after acute infection and recommended that eradication not be started immediately - only after persistent infection is confirmed - as the initial infection with H. pylori is often transient.

The authors state that they have no Conflict of Interest (COI).