Journal of Pediatric Gastroenterology and Nutrition, Publish Ahead of Print

DOI: 10.1097/MPG.0000000000002547

Manuscript Title: Autoimmune Gastritis in Pediatrics: A review of 3 cases

Tania Mitsinikos, MD

Attending Physician

Division of Gastroenterology, Hepatology and Nutrition

Children’s Hospital Los Angeles

Assistant Clinical Professor of Pediatrics

Keck School of Medicine USC

Nick Shillingford, MD

Attending Physician

Department of Pathology and Laboratory Medicine

Children’s Hospital Los Angeles

Assistant Clinical Professor of Pediatrics

Keck School of Medicine USC

Harry Cynamon, MD

Attending Physician

Division of Gastroenterology, Hepatology and Nutrition

Children’s Hospital Los Angeles

Assistant Clinical Professor of Pediatrics

Keck School of Medicine USC

Vrinda Bhardwaj, MD

Attending Physician

Division of Gastroenterology, Hepatology and Nutrition

Children’s Hospital Los Angeles

Assistant Clinical Professor of Pediatrics

Keck School of Medicine USC

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Corresponding Author: Tania Mitsinikos, MD

Division of Pediatric Gastroenterology, Hepatology and Nutrition

Children’s Hospital Los Angeles

4650 W Sunset Boulevard

Mailstop # 78

Los Angeles, CA-90027

E-mail: fmitsinikos@chla.usc.edu

Tel: 323-361-2181; Fax: 323-361-2452

Reprints:

We are not requesting reprints of the article, if accepted for publication.

Keywords: Autoimmune gastritis, gastrin, iron-deficiency anemia, diabetes mellitus

Source of Funding:

This study was not supported by a specific funding source.

Conflicts of Interest:

Potential Conflicts of Interest: Dr. Mitsinikos has been provided with research support in the way of

research coordinator and statistical analysis support through Alexion Pharmaceuticals, Inc. No direct financial

support was provided. The remainder of the authors have no other potential conflicts of interest to report.

Revised Manuscript - CLEAN

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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. Additionally, there have been case reports describing patients with
immunodeficiencies 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 enterochromaffin-like cell hyperplasia.
Management of these patients includes nutritional 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 three patients, two were referred to gastroenterology for 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: While 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.

Summary Box: What is known?

- Autoimmune gastritis is a rare entity in children with strong association with
autoimmune disorders and immunodeficiencies.
- AIG can progress to gastric adenocarcinoma in a subset of individuals/patients
as described in the literature as case reports.
What is new?
- Gastroenterologists and pathologists should consider AIG 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

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Introduction:

Autoimmune 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 metaplastic change 1. While 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

anemia2,3. The lost gastric oxyntic mucosa may be replaced by inflammatory cells but also

by metaplastic epithelium or fibrous tissue3,4. While 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 where indicated.

In AIG, parietal cell antibodies to gastric H+/K+ ATPase are often identified and

correlate with fundal gastritis5,6. In adult reports, antibodies are present in 7.8- 19.5% of

healthy individuals, but little is known about the false positive rate in pediatrics7. In addition

to these antibodies, hypergastrinemia and hypochlorhydria are present and progress to

achlorhydria in severe cases1. A strong association is present with other autoimmune

disorders like thyroid disease (Hashimoto thyroiditis), diabetes mellitus, vitiligo, and even

immunodeficiency disorders8-11. Helicobacter pylori (H.pylori) has been implicated as a

possible etiologic agent7. 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 mass4. We

report three cases of AIG including their presentation, diagnosis, and treatment.

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Methods:

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 histopathologic 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

laboratory 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: 15 year-old-girl with type I diabetes mellitus, well-controlled on insulin, Addison’s

disease and gastroparesis, developed persistent microcytic anemia despite oral iron

supplementation. She 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 MCV of 64.5 fL (78-100). Iron studies were consistent with iron deficiency

[iron 25 mcg/dL (10-150), iron saturation 5% (15-50), total iron binding capacity (TIBC) 472

mcg/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 (Figure 1a-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 (Figure 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.

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Case 2: 10 year-old-girl with type I 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), MCV 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 exam was

unremarkable. Fecal calprotectin was 171 ug/g (reference 0-120 ug/g). EGD showed linear

furrowing in the body of the stomach (Figure 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 (Figure 3). Mild glandular atrophy with decreased parietal cell mass

and pseudopyloric metaplasia were noted (Figure 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 hemoglobin, however her

concurrent renal disease was thought to contribute to lack of normalization.

Case 3: 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), non-fasting 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 (Figure 4).

Biopsies showed oxyntic type gastric mucosa with moderate to severe chronic gastritis,
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moderate decrease of parietal cell mass and multifocal intestinal metaplasia. Chromogranin

immunostain demonstrated mild hyperplasia of enterochromaffin-like cells. H.pylori

immunostain was negative (Figure 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 one month (1221 pg/mL).

Pathologic findings:

Biopsies from the antrum and body of the stomach in all three 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

characterized by oxyntic glands that have assumed features of gastric pyloric glands in the

gastric body was found in one 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 prior to tissue diagnosis.

Discussion

None of our cases with biopsy confirmed AIG had associated H.pylori. While cases

described by Pogoriler et al showed AIG in the absence of H.pylori, other series, like Miguel

et al, demonstrated that 50% of cases (four of eight) was associated with H.pylori

infection3,12. 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 non-acid reflux. Our cases did not have symptoms

consistent with gastroesophageal reflux or dyspepsia13,14. More relevant in our cases is a

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strong history of autoimmunity and/or unexplained iron deficiency or other nutritional

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 findings including H.pylori and Helicobacter heilmannii (H.heilmannii)

associated 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 diagnosis 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 to 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

symptoms may be an important clue, and lower gastrointestinal biopsies may prove

diagnostic.

In all patients, treatment targeted management of micronutrient deficiencies

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including either iron supplementation or, in the case of pernicious anemia, vitamin B12

supplementation. Vitamin B12 deficiency may have several manifestations, including

macrocytic anemia, a smooth, inflamed tongue (glossitis), CNS changes like mood

swings, peripheral nervous system changes like paresthesias and loss of proprioception

and vibration sensation. Bone marrow findings in one of our patients with Vitamin B12

deficiency have been identified in infants and children15. Patients with AIG may also

have vitamin C, calcium, and vitamin D deficiencies, as their absorption is dependent on

gastric pH and gastric secretion, both affected in individuals with AIG15. Thus, these

vitamin levels should be monitored routinely in patients with AIG, and supplements

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 adenocarcinoma16. AIG is

considered a precancerous condition, with important risk factors being clinical evidence of

pernicious anemia, severe atrophy, presence of intestinal metaplasia, duration of disease, and

age over 50 years16,17. Yamanaka et al reported a case of a 55-year-old Japanese woman

with a hyperplastic gastric polyp which demonstrated gastric adenocarcinoma in the context

of AIG requiring radical distal gastrectomy18. While 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 intestinal metaplasia, standard

treatment is nutritional supplementation and treatment of concurrent H.pylori infection, if

present. While the prognosis is good in these patients, due to the malignant potential and the

risk of developing neuroendocrine tumors, a variety of approaches have been suggested.

These include the use of netazepide (a gastric receptor antagonist), somatostatin, or

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antrectomy to

reduce the amount of circulating gastrin, which is elevated in patients with AIG19.

Currently, no treatment recommendations exist for pediatric patients with AIG, regardless of

absence or presence of metaplastic changes. Many describe the presence of AIG as a pre-

neoplastic condition in the development of Type-1 gastric neuroendocrine tumors and gastric

adenocarcinoma20. The risk of gastric neoplasia in those with pernicious anemia is increased

2.84 times in one adult report21. In one systematic review and meta-analysis, index upper

endoscopy identified a prevalence of 5.3% in older adults (mean age 64 years, n=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

time20,22.

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,

multi-center studies are needed to evaluate the progression 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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References:

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Figure 1:

A  B C

D E

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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Figure 2.

A B

C D

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).

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Figure 3

E F

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).

Figure 4

G H

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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 Table 1: Summary and comparison of key biochemical data

Case 1 2 3
Hemoglobin at presentation 9.1 9.6 9.9
(g/dL) (12-15.5) (11.7-15.7) (12-15.5)
MCV at presentation 64.5 70 99
(fL) (78-100) (77-91) (78-100)
Iron (mcg/dL) 25 14 138
(10-150) (11-150) (37-170)
Iron Percentage 5 4 62
Saturation (%) (15-50) (15-35) (15-50)
Total Iron Binding 472 427 222
Capacity (TIBC) (mcg/dL) (250-450) (250-450) (250-450)

Ferritin (ng/dL) 33 39 14
(10-150) (10-140) (10-150)
Intrinsic Factor Antibody
(U) Negative Negative Positive

Anti-parietal cell Positive Positive Positive

Antibody (U) (115) (114.5) (60.1)
(>25) (>25) (>25)
Gastrin level n/a n/a 1183
(pg/mL) (2-168)
Vitamin B12 916 1285 303
(pg/mL) (260-935) (260-935) (400-1100)

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