Celiac Index

This file is the human-readable companion to skos-lexicon.ttl. It records the concept-selection threshold and the patterns that emerge from the current corpus.

Inclusion Threshold

A term is included when it is at least one of:

a recurring domain concept needed to explain multiple pages
a bridge term connecting mechanism, diagnosis, and management
a disease subtype, complication, or adjacent disorder with independent explanatory value
an active therapeutic class or research target

Excluded for now:

one-off proper names
low-level biochemical detail that appears only once
generic medical words that do not organize the corpus

Core Concept Clusters

1. Disease Core

celiac disease
small intestine
gluten-free diet

2. Mechanism / Pathogenesis

prolamins
gliadin
tissue transglutaminase
deamidation
zonulin
tight junctions
intestinal permeability
HLA-DQ2 / HLA-DQ8
CD4+ T cells
intraepithelial lymphocytes
cytokines
IL-15
villous atrophy
crypt hyperplasia
malabsorption

3. Diagnosis

serology
TTG IgA
IgA deficiency
endoscopy and biopsy
Marsh classification
gluten challenge

4. Management / Failure States

gluten-free diet
cross-contact
non-responsive celiac disease
refractory celiac disease

5. Complications / Systemic Spread

dermatitis herpetiformis
enteropathy-associated T-cell lymphoma
osteoporosis
iron-deficiency anemia
peripheral neuropathy
gluten ataxia

6. Borderland / Differential Cluster

non-celiac gluten sensitivity
small intestinal bacterial overgrowth
oats

7. Practical Management / Threshold Logic

gluten threshold

8. Therapeutics Research

glutenases
latiglutenase
AN-PEP
EP-B2
SC-PEP
Kuma030
larazotide acetate
ZED1227
tolerance induction
Nexvax2
KAN-101
IL-15 inhibitors

Trends Emerging from the Lexicon

Trend A: The corpus has a strong mechanistic spine

The densest concept network runs:

prolamins -> gliadin -> zonulin / tight junctions -> tissue transglutaminase -> deamidation -> HLA-DQ2/DQ8 -> CD4+ T cells -> cytokines / IL-15 -> villous atrophy -> malabsorption

This suggests the KB is already good at explaining why disease happens, not just what it is.

Trend B: Diagnosis is conceptually dense but under-articled

The corpus repeatedly uses:

serology
TTG IgA
IgA deficiency
biopsy logic
Marsh staging
gluten challenge

But these are spread across multiple pages rather than consolidated into a higher-level diagnostic sub-ontology.

Trend C: The disease-boundary region is important

The lexicon repeatedly brushes against adjacent categories:

NCGS
SIBO
oats tolerance
dermatitis herpetiformis
gluten ataxia
wheat allergy

That means the KB increasingly needs pages that explain where celiac ends and neighboring entities begin.

Trend D: Research targets map cleanly onto mechanistic nodes

The main experimental therapies line up with specific points in the mechanism:

glutenases -> before absorption
larazotide -> barrier level
ZED1227 -> transglutaminase/deamidation level
tolerance induction -> adaptive immune retraining
IL-15 inhibitors -> innate/refractory axis

This is a good sign: the research space can be organized as interventions on the disease pathway.

Expansion Result

This iteration used the lexicon to add the following bridge pages:

celiac-serology — the diagnostic antibody/testing layer
antigen-presentation — APC / MHC II / HLA-DQ / epitope logic
gluten-related-disorders — celiac vs neighboring entities and mimics
oats — the special-case grain question
wheat-allergy — allergic differential adjacent to celiac

Likely Next Expansion Targets

microbiome and disease onset/modulation
nutrient deficiency cascade as its own synthesis page
family/risk-group screening logic
article-level pages for EMA and DGP as serology subcomponents

Backlinks

INDEX | glossary | mechanism | diagnosis | research_plan