SHORT COMMUNICATION: GASTROENTEROLOGY
Autoimmune Gastritis in Pediatrics:
A Review of 3 Cases

Tania Mitsinikos, yNick Shillingford, Harry Cynamon, and Vrinda Bhardwaj
ABSTRACT
Objectives: To bring heightened awareness to a condition, autoimmune
gastritis (AIG), which is a well-established entity in adults; however, rarely
described in pediatrics. Currently, the literature describes AIG in pediatric
patients who also suffer from other autoimmune disorders, which precedes
the diagnosis of AIG, and often presents with unexplained anemia. Addi-
tionally, there have been case reports describing patients with immunode-
ficiencies and AIG, which progress to gastric adenocarcinoma. AIG is a
histopathologic diagnosis, demonstrating chronic inflammatory process with
loss of parietal cells with or without intestinal metaplasia and enterochro-
maffin-like cell hyperplasia. Management of these patients includes nutri-
tional replacement as well as routine surveillance endoscopy with biopsy in
search of metaplastic and dysplastic changes.
Methods: We queried the pathology database at Children’s Hospital Los
Angeles (CHLA) for cases with a final diagnosis of AIG and for those with a
differential diagnosis that includes AIG in the diagnostic comment. All cases
that were identified were selected as long as they did not only meet the
histopathologic criteria, but also the biochemical criteria for this condition.
Results: Of the 3 patients, 2 were referred to gastroenterology for the
evaluation of iron-deficiency anemia in the context of diabetes mellitus and
Addison’s disease; and diabetes mellitus and Hashimoto’s thyroiditis. AIG
was confirmed on the biopsies, which showed a reduction in parietal cell
mass, pseudopyloric metaplasia and enterochromafin-like cell hyperplasia.
Both patients were treated with iron replacement therapy. The third patient
presented with symptomatic anemia and diagnosed with pernicious anemia
without other autoimmune disorders. She was successfully treated with oral
vitamin supplementation. In this case, serial gastric biopsies demonstrated
stable intestinal metaplasia without evidence of dysplasia.
Conclusion: Although AIG is rare in children, pediatric gastroenterologists
and pathologists should have a heightened suspicion for this entity in those
patients with a history of autoimmune disorders and/or pernicious anemia.
Key Words: autoimmune gastritis, diabetes mellitus, gastrin, iron-
deficiency anemia
(JPGN 2020;70: 252–257)
Received July 1, 2018; accepted October 13, 2019.
From the Division of Gastroenterology, Hepatology and Nutrition, and
the yDepartment of Pathology and Laboratory Medicine, Children’s
Hospital Los Angeles, Keck School of Medicine USC, Los Angeles, CA.
Address correspondence and reprint requests to Tania Mitsinikos, MD,
Attending Physician, Division of Pediatric Gastroenterology, Hepatol-
ogy and Nutrition, Children’s Hospital Los Angeles, 4650W Sunset
Boulevard, Mailstop # 78, Los Angeles, CA 90027
(e-mail: fmitsinikos@chla.usc.edu).
T.M. has been provided with research support in the way of research
coordinator and statistical analysis support through Alexion Pharma-
ceuticals, Inc. No direct financial support was provided. The remainder
of the authors have no other potential conflicts of interest to report.
Copyright # 2020 by European Society for Pediatric Gastroenterology,
Hepatology, and Nutrition and North American Society for Pediatric
Gastroenterology, Hepatology, and Nutrition
DOI: 10.1097/MPG.0000000000002547
252
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What Is Known
 Autoimmune gastritis is a rare entity in children with
strong association with autoimmune disorders and
immunodeficiencies.
 Autoimmune gastritis can progress to gastric adeno-
carcinoma in a subset of individuals/patients as
described in the literature as case reports.
What Is New
 Gastroenterologists and pathologists should consider
autoimmune gastritis in patients with autoimmune
disorders and/or pernicious anemia as the condition
can exist with no associated clinical symptoms.
 Metaplasia and dysplasia can occur in the pediatric
population, thus routine endoscopic surveillance
should be considered.
A utoimmune gastritis (AIG) is a chronic inflammatory process,
affecting the fundus and body of the stomach, where parietal
cells are replaced by atrophic glands, which may undergo meta-
plastic change (1). Although many consider this to be a condition of
older individuals, onset of inflammation may occur in adolescence,
preceding the physical and biochemical findings of iron deficiency
anemia or B12 deficiency seen in pernicious anemia (2,3). The lost
gastric oxyntic mucosa may be replaced not only by inflammatory
cells but also by metaplastic epithelium or fibrous tissue (3,4).
Although the process may start earlier in life, this still remains a
rare condition in pediatrics. However, given the potential for
metaplastic transformation and dysplasia, heightened awareness
is required, and treatment and surveillance should be initiated
wherever indicated.
In AIG, parietal cell antibodies to gastric Hþ/Kþ ATPase
are often identified and correlated with fundal gastritis (5,6). In
adult reports, antibodies are present in 7.8% to 19.5% of healthy
individuals, but little is known about the false-positive rate in
pediatrics (7). In addition to these antibodies, hypergastrinemia
and hypochlorhydria are present and progress to achlorhydria in
severe cases (1). A strong association is present with other auto-
immune disorders like thyroid disease (Hashimoto thyroiditis),
diabetes mellitus, vitiligo, and even immunodeficiency disorders
(8–11). Helicobacter pylori has been implicated as a possible
etiologic agent (7). By endoscopy, no gross changes may be
observed; however, thinning or loss of gastric rugae may be
identified. Most cases show microscopic changes, such as gastric
mucosal atrophy with loss of glands and decreased parietal cell
mass (4). We report 3 cases of AIG including their presentation,
diagnosis, and treatment.
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JPGN  Volume 70, Number 2, February 2020 Autoimmune Gastritis in Pediatrics

TABLE 1. Summary and comparison of key biochemical data

Case 1 2 3

Hemoglobin at presentation (g/dL) 9.1 (12–15.5) 9.6 (11.7–15.7) 9.9 (12–15.5)

MCV at presentation (fL) 64.5 (78–100) 70 (77–91) 99 (78–100)
Iron (mcg/dL) 25 (10–150) 14 (11–150) 138 (37–170)
Iron percentage saturation (%) 5 (15–50) 4 (15–35) 62 (15–50)
Total iron-binding capacity (TIBC) (mg/dL) 472 (250–450) 427 (250–450) 222 (250–450)
Ferritin (ng/dL) 33 (10–150) 39 (10–140) 14 (10–150)
Intrinsic factor antibody (U) Negative Negative Positive
Antiparietal cell Positive Positive Positive
Antibody (U) (115) (114.5) (60.1)
(>25) (>25) (>25)
Gastrin level (pg/mL) n/a n/a 1183 (2–168)
Vitamin B12 (pg/mL) 916 (260–935) 1285 (260–935) 303 (400–1100)

MCV, mean corpuscular volume.

METHODS persistent microcytic anemia despite oral iron supplementation. She

The pathology archives at Children’s Hospital Los Angeles
(CHLA) were queried for cases with a diagnosis of AIG and those
with a differential diagnosis that included AIG. Those with histo-
pathologic findings consistent with this condition were selected.
Charts were reviewed to confirm the presence of biochemical
evidence of AIG. All laboratory data were obtained from the CHLA
laboratory and pathology services and run through on-site labora-
tory equipment and personnel. No labs were sent to outside
laboratories or medical centers. Study approval was obtained from
the Institutional Review Board (IRB) at CHLA.
RESULTS
Case Review
Case 1
A 15 year-old girl with type I diabetes mellitus, well-con-
trolled on insulin, Addison’s disease and gastroparesis, developed
had no clinical signs or symptoms of gastroesophageal reflux. Her
physical examination was unremarkable. Laboratory data revealed
a hemoglobin of 9.1 g/dL (12–15.5) and mean corpuscular volume
of 64.5 fL (78–100). Iron studies were consistent with iron defi-
ciency (iron 25 mg/dL [10–150], iron saturation 5% [15–50], total
iron-binding capacity [TIBC] 472 mg/dL [250–450] and ferritin
33 ng/dL [10–150]). Intrinsic factor antibody was not detected by
serology. Anti-parietal cell antibody level was positive at 115.4 U
(>25 U positive; Table 1). Vitamin B12 level was 916 pg/mL (260–
935 pg/mL). Esophagogastroduodenoscopy (EGD) demonstrated
normal appearing esophagus, stomach, and duodenum (Fig. 1A
and B). Biopsies showed antral and oxyntic gastric mucosa with
diffuse mononuclear cell infiltrates in the lamina propria, focal
parietal cell pseudohypertrophy, and linear enterochromaffin-like
cell hyperplasia (Fig. 2). Immunohistochemistry (IHC) for H. pylori
was negative. She continued oral iron supplementation for 3
months, which resolved her anemia and maintained normal vitamin
B12 levels. She continued nutritional supplementation.

FIGURE 1. Endoscopic pictures at time of presentation. (A) Case 1, body. (B) Case 1, antrum. (C) Case 2, body. (D) Case 3, body. (E) Case 3,
antrum.

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Mitsinikos et al JPGN  Volume 70, Number 2, February 2020

FIGURE 2. Biopsies from patient 1. Low magnification photomicrograph of the biopsy from the corpus shows a chronic inflammatory infiltrate
extending deep into the lamina propria, and marked glandular atrophy with reduction in parietal cell mass (A). Higher magnification shows acute
(neutrophilic) inflammation involving a gastric gland (green arrow). Parietal cells are noticeably absent, a characteristic feature of autoimmune
gastritis (B). By contrast, the antral biopsy shows mild chronic lamina propria inflammation and preservation of the gastric glands with no evidence
of atrophy (C). Chromogranin immunohistochemical stain highlights linear enterochromaffin cell-like (ECL) hyperplasia. A focus of nodular
hyperplasia (red arrow) is also present (D).

Case 2
A 10 year-old-girl with type 1 diabetes mellitus, Hashimoto’s
thyroiditis, and crescentic glomerulonephritis was referred for
evaluation of anemia with hemoglobin of 9.1 g/dL (11.7–15.7),
mean corpuscular volume of 90 fL (77–91), and abdominal pain,
characterized as diffuse and rare in occurrence. Her anemia was
secondary to iron deficiency [total iron 14 ug/dL (11–150), iron
saturation 3% (15–35), and TIBC 427 ug/dL (250–450)]. Physical
examination was unremarkable. Fecal calprotectin was 171 mg/g
(reference 0–120 mg/g). EGD showed linear furrowing in the body
of the stomach (Fig. 1C); colonoscopy was normal. Gastric body
biopsies showed oxyntic type gastric mucosa with moderate-to-
severe chronic gastritis with a predominance of plasma cells and
lymphocytes, and scattered eosinophils associated with gastric
gland damage (Fig. 3). Mild glandular atrophy with decreased
parietal cell mass and pseudopyloric metaplasia were noted
(Fig. 3). IHC stain for chromogranin showed linear hyperplasia
of enterochromaffin-like cells. IHC stain for H. pylori was negative.
Serology for intrinsic factor antibody was negative; however, anti-
parietal cell antibody was elevated at 114.5 U (>25 U positive)
(Table 1). Vitamin B12 level was normal. Treatment of iron
supplementation was started, which did not improve her hemoglo-
bin; however, her concurrent renal disease was thought to contribute
to lack of normalization.
Case 3
A 17 year-old girl with no past medical history including no
gastrointestinal symptoms presented with pancytopenia identified
on routine screening by her pediatrician. After admission, a bone
marrow biopsy showed a hypercellular bone marrow with trilineage
hematopoiesis, erythroid hyperplasia, and megaloblastic changes of
the erythroid and granulocytic lineages. These findings were most
consistent with nutritional deficiency, later identified as vitamin
B12 deficiency (B12 level of 303 pg/mL [400–1100 pg/mL]).
Intrinsic factor antibody was positive (60.1 U, positive >25 U),
nonfasting gastrin level (1183 pg/mL, reference fasting 3–4 hours,
2–168 pg/mL), and anti-parietal cell antibody (60.1 U, >24.9 U
positive; Table 1). EGD revealed gastric body and antral erythema
(Fig. 4). Biopsies showed oxyntic type gastric mucosa with moder-
ate-to-severe chronic gastritis, moderate decrease of parietal cell
mass and multifocal intestinal metaplasia. Chromogranin immu-
nostain demonstrated mild hyperplasia of enterochromaffin-like

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JPGN  Volume 70, Number 2, February 2020 Autoimmune Gastritis in Pediatrics

FIGURE 3. Biopsy from patient 2. The biopsy from the gastric corpus from this patient with AIG shows glandular atrophy with loss of gastric mucin
and chronic lamina propria inflammation with scattered eosinophils (E). Pseudopyloric metaplasia, another histologic feature of AIG, is also seen in
this case (green arrow). Note the dense lymphoid aggregate to the left of the image (F). AIG ¼ autoimmune gastritis.

cells. H. pylori immunostain was negative (Fig. 2G–I). The antrum
showed mild-to-moderate chronic gastritis without any of the above
features. She was treated with oral vitamin B12 supplementation,
which normalized her B12 levels after 1 month (1221 pg/mL).
Pathologic Findings
Biopsies from the antrum and body of the stomach in all 3
cases demonstrated chronic gastritis involving the gastric body. The
mixed inflammatory infiltrate was composed of plasma cells,
lymphocytes, and scattered eosinophils. Oxyntic gland damage
and glandular atrophy were also present, and parietal cell mass
was markedly reduced. By contrast, biopsies obtained from the
antrum showed relative sparing. Pseudopyloric metaplasia charac-
terized by oxyntic glands that have assumed features of gastric
pyloric glands in the gastric body was found in 1 case. Pancreatic
acinar metaplasia was seen in another case. Immunohistochemistry
highlighted linear hyperplasia of enterochromaffin-like cells. All
biopsies were negative for H. pylori by immunohistochemical stain.
Esophageal biopsies did not demonstrate histopathologic evidence
of gastroesophageal reflux disease. None of the patients were on
acid-suppressive therapy before tissue diagnosis.
DISCUSSION
None of our cases with biopsy confirmed AIG had associated
H. pylori. Although cases described by Pogoriler et al (3) showed
AIG in the absence of H. pylori, other series, like Miguel et al (12),
demonstrated that 50% of cases (4 of 8) was associated with H.
pylori infection. Intestinal dysmotility has been described in
patients with AIG, as did one of our patients with gastroparesis.
Gastroesophageal reflux disease has also been identified in these
patients, although the majority have nonacid reflux. Our cases did
not have symptoms consistent with gastroesophageal reflux or
dyspepsia (13,14). More relevant in our cases is a strong history
of autoimmunity and/or unexplained iron deficiency or other nutri-
tional deficiency with no gross endoscopic findings, making review
of gastric biopsies by the pathologists crucial for this diagnosis.
The histologic features for AIG are not pathognomonic,
hence serologic markers are necessary in the diagnostic work-up
and exclusion of other entities that may present with similar

FIGURE 4. Biopsy from patient 3. This biopsy shows deep intestinal metaplasia (red arrows) characterized by the presence of Paneth cells (green
arrows) in addition goblet cells. Also, note the presence of pseudopyloric metaplasia (blue arrow) to the right (G). Nodules of pancreatic acinar
metaplasia are also present in this biopsy (H).

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Mitsinikos et al
findings including H. pylori and Helicobacter heilmannii-associ-
ated gastritis and inflammatory bowel disease (IBD). Most cases of
AIG are characterized by diffuse chronic atrophic gastritis restricted
to the corpus and associated with intestinal metaplasia. With H.
pylori, however, the inflammation involves both antrum and corpus
with more intense involvement of the antrum. The chronic infiltrate
may be accompanied by lymphoid follicles with germinal centers, a
feature not seen in AIG and termed follicular gastritis. The diagno-
sis of H. pylori-associated gastritis is facilitated by the use of special
stains, such as Giemsa, Warthin Starry, Thiazine, and the IHC. H
heilmannii infection is rare compared with H. pylori; however, the
histologic features are similar to that of H. pylori albeit less severe.
The diagnosis hinges on the detection of organisms facilitated with
Warthin Starry and Steiner spirochetal stains. The H. pylori IHC
will also stain H heilmannii, but only if the polyclonal stain is used.
The monoclonal H. pylori IHC is more specific and will be negative
in cases of H heilmannii. In the vast majority of cases of H. pylori
and H heilmannii-associated gastritis, the organisms are readily
identified on the routine H&E stained slides making the exclusion
of AIG less of a challenge. IBD often involves the stomach and may
pose a challenge when AIG is considered by the pathologist.
Involvement of the stomach by IBD; however, is not restricted
to the corpus as is the case with AIG. Additionally, the clinical
history of IBD in known cases is extremely helpful. In cases with no
prior history of IBD, the presence of lower gastrointestinal symp-
toms may be an important clue, and lower gastrointestinal biopsies
may prove diagnostic.
In all patients, treatment targeted management of micro-
nutrient deficiencies including either iron supplementation or, in
the case of pernicious anemia, vitamin B12 supplementation.
Vitamin B12 deficiency may have several manifestations, includ-
ing macrocytic anemia, a smooth, inflamed tongue (glossitis),
central nervous system changes like mood swings, peripheral
nervous system changes like paresthesias, and loss of proprio-
ception and vibration sensation. Bone marrow findings in one of
our patients with Vitamin B12 deficiency have been identified in
infants and children (15). Patients with AIG may also have
vitamin C, calcium, and vitamin D deficiencies, as their absorp-
tion is dependent on gastric pH and gastric secretion, both
affected in individuals with AIG (15). Thus, these vitamin levels
should be monitored routinely in patients with AIG, and supple-
ments prescribed as needed.
Treatment of AIG is limited to nutritional supplementation.
No guidelines or recommendations for endoscopic surveillance
exist, although metaplastic and dysplastic changes are expected.
Other changes reported in the literature are oxyntic pseudopolyps,
hyperplastic polyps, pyloric gland adenoma, and gastric adenocar-
cinoma (16). AIG is considered a precancerous condition, with
important risk factors being clinical evidence of pernicious ane-
mia, severe atrophy, presence of intestinal metaplasia, duration of
disease, and age over 50 years (16,17). Yamanaka et al (18)
reported a case of a 55-year-old Japanese woman with a hyper-
plastic gastric polyp, which demonstrated gastric adenocarcinoma
in the context of AIG requiring radical distal gastrectomy.
Although these case reports are rare, it is important to recognize
that metaplastic and malignant transformation occur in patients
with long-standing AIG.
For patients with autoimmune atrophic gastritis with intesti-
nal metaplasia, standard treatment is nutritional supplementation
and treatment of concurrent H. pylori infection, if present. Although
the prognosis is good in these patients, because of the malignant
potential and the risk of developing neuroendocrine tumors, a
variety of approaches have been suggested. These include the
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JPGN  Volume 70, Number 2, February 2020
use of netazepide (a gastric receptor antagonist), somatostatin, or
antrectomy to reduce the amount of circulating gastrin, which is
elevated in patients with AIG (19). Currently, no treatment recom-
mendations exist for pediatric patients with AIG, regardless of
absence or presence of metaplastic changes. Many describe the
presence of AIG as a preneoplastic condition in the development of
type-1 gastric neuroendocrine tumors and gastric adenocarcinoma
(20). The risk of gastric neoplasia in those with pernicious anemia is
increased 2.84 times in 1 adult report (21). In 1 systematic review
and meta-analysis, index upper endoscopy identified a prevalence
of 5.3% in older adults (mean age 64 years, n ¼ 150) with 50% of
those individuals diagnosed with pernicious anemia. So few cases
are in the literature that the frequency of endoscopic evaluation
cannot be recommended at the present time (20,22).
In summary, AIG should be considered in patients with
autoimmune disorders and/or unexplained nutritional deficiencies.
In pediatric patients, the disease may not present for long enough to
yield typical endoscopic changes. Thus, in suspected cases, it is
important for the clinician to take both antral and gastric body
biopsies, evaluate for H. pylori, and alert the pathologists to
suspicion of AIG. Given the chronic inflammatory state of this
condition, multicenter studies are needed to evaluate the progres-
sion of this disease in children and to establish guidelines on the
frequency of endoscopic and serologic surveillance for biomarkers,
like gastrin, to monitor disease progression.
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