Autoimmune Gastritis: Interpreting the Diagnostic Curve

By Rex Wiig – Engineer, Author, and Autoimmune Advocate

This article takes a closer look at the diagnostic curve of autoimmune gastritis (AIG) and why it can be so confusing — even for doctors.

You can’t take a single snapshot of lab results and rule out this disease. Test results can change over time. If you test positive, you’re diagnosed. If you test negative, you’re often left undiagnosed — stuck in a kind of medical purgatory. It can feel like a coin toss, and that’s what frustrates so many of us.

I’m not a doctor — just someone who has lived through every stage of this condition. Think of me as a regular guy who’s learned a little something about something.
Please feel free to share this article with your physician if it helps open a conversation or shed light on your own journey.

What’s Really Happening

Autoimmune gastritis is a slow, progressive condition in which the body’s immune system attacks the stomach’s acid-producing parietal cells.
Over time, this damages two essential parts of digestion:

The proton pump (H⁺/K⁺-ATPase) — the acid-producing pumps located inside the parietal cells.
Intrinsic Factor (IF) — a protein also produced by the parietal cells, required for the absorption of vitamin B₁₂.

This doesn’t happen overnight. It can take decades before symptoms or anemia appear. Understanding that long timeline helps explain why so many people are misdiagnosed — or told their results are “normal” — when the disease is already underway.

The Slow Timeline of Change

Early Stage

The first antibody to appear is usually the Parietal Cell Antibody (PCA).
PCA can show up years — often decades — before symptoms or B₁₂ deficiency.
It signals inflammation in the stomach’s acid-producing region (the oxyntic mucosa).

Middle Stage

The immune system begins attacking Intrinsic Factor, producing IF Antibodies (IFAB).
IFAB is more specific but peaks for a shorter time.
Acid secretion starts to fail, and gastrin levels begin to climb.

Late Stage

Once most parietal cells are destroyed, stomach acid disappears (achlorhydria).
Gastrin surges in a futile attempt to restart acid production.
As intrinsic factor production collapses, vitamin B₁₂ can no longer be absorbed from food — even though liver stores may still be full.
Those stores become biologically unavailable, leaving only what’s maintained through parenteral (injection) supplementation.
This is when pernicious anemia and neurological symptoms appear — not because the body ran out of B₁₂, but because it lost its ability to naturally absorb it.

In summary:

PCA rises first and lasts longest.
IFAB peaks later and then fades.
Gastrin rises as acid vanishes.
Once intrinsic factor is lost, dietary B₁₂ becomes inaccessible — only injected B₁₂ supports serum levels.

🩸 Figure: The Autoimmune Gastritis Diagnostic Curve

For those who like visuals, here’s a conceptual chart showing how PCA, IFAB, gastrin, and B₁₂change across decades of autoimmune gastritis.

Conceptual model for education purposes only. Actual disease course and antibody and kinetics vary among individuals

Why the IFAB Test Often Misses the Diagnosis

The Intrinsic Factor Antibody (IFAB) test is intentionally designed to be very specific, meaning a positive result is almost always correct — but that same design makes it less sensitive.

Early disease: antibody levels are too low to detect yet.
Late disease: once parietal cells and intrinsic factor are gone, the immune system has nothing left to attack, so antibodies fade.

That’s why many people with proven AIG or pernicious anemia still see a “negative” IFAB result.
The test isn’t wrong — it’s just blind to certain stages of the disease.

How Doctors Combine Clues

Because no single test tells the full story, doctors combine clues:

PCA positive + high gastrin → strong evidence of autoimmune gastritis.
IFAB positive → almost diagnostic for pernicious anemia.
Endoscopy with biopsy (EGD) → the gold standard showing direct parietal-cell loss.

Interpreting these findings together, rather than separately, gives the clearest picture of where a patient lies on the AIG continuum.

After the Immune System Goes Quiet

When the immune attack ends, the battlefield it leaves behind is scarred.
The parietal cells and rugae don’t regenerate.

That means the damage is permanent — and autoimmune gastritis requires lifelong management, not a short-term fix.

And as I often remind others:

“It ain’t just B₁₂!”

Loss of stomach acid affects far more than B₁₂.
It changes how the body absorbs iron, magnesium, calcium, and zinc, and even how certain medications work.
It shifts gut bacteria and alters the rhythm of digestion itself.
Living well afterward means learning how to support the body’s new chemistry.

The Takeaway

Autoimmune gastritis develops slowly and quietly.
A negative test doesn’t always mean “no disease.”

Understanding these diagnostic curves helps patients and physicians recognize the pattern earlier — when intervention can still prevent serious complications.

Selected References

Neumann WL et al. Gastroenterology Clinics of North America. 2013.
Lahner E & Annibale B. Nature Reviews Gastroenterology & Hepatology. 2009.
De Block CE et al. Journal of Clinical Endocrinology & Metabolism. 2008.
Toh BH et al. Gastroenterology. 1997.
Kulnigg-Dabsch S. Autoimmunity Reviews. 2016.

About the Author

Rex Wiig is an author, engineer, and founder of Subsurface Press. After developing autoimmune atrophic gastritis, he applied his background in systems engineering to study how the body’s feedback networks fail — and how awareness can help restore their rhythm.

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© 2025 Rex Wiig / Subsurface Press™
Engineer, Author, and Autoimmune Advocate
Adapted from the forthcoming book Thank God for Oxes.

Permission is granted to share this article for educational or patient-advocacy use only if unaltered and properly attributed to the author.