Component
Peripheral large-fiber axonal loss
Peripheral large-fiber axonal loss
1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What acts on it
Large-fiber-predominant axonal loss characterized the thiamine-deficiency group, whereas small-fiber loss predominated in the pure alcoholic-neuropathy group.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- evidence_location
- Abstract: sural-nerve pathology comparison
- evidence_span
- Large-fiber-predominant axonal loss predominated in TDN
- experimental_model
- Clinical and sural-nerve pathology comparison of 64 alcoholic-neuropathy patients subdivided by coexisting thiamine deficiency and 32 nonalcoholic thiamine-deficiency neuropathy patients.
- exposure
- Nonalcoholic thiamine-deficiency neuropathy identified in a clinical cohort
- limitations
- Biopsy association does not identify a single biochemical injury step or imply that every thiamine-deficient patient loses only large fibers.
- nutrient_topic
- Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
- organism
- Homo sapiens
- plain_language
- The nerve biopsies also distinguished the dominant injury patterns.
- primary_references
- [koike-2003-neuropathy-subtypes] Alcoholic neuropathy is clinicopathologically distinct from thiamine-deficiency neuropathy (2003). https://pubmed.ncbi.nlm.nih.gov/12838517/ DOI: 10.1002/ana.10550
- tissue_or_cell_type
- Sural nerve biopsy specimens
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1549–1561
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Clinical and sural-nerve pathology comparison of 64 alcoholic-neuropathy patients subdivided by coexisting thiamine deficiency and 32 nonalcoholic thiamine-deficiency neuropathy patients. · source_derived_draft · unverified_draft
### thiamine-def-large-fiber-neuropathy-pathology Large-fiber-predominant axonal loss characterized the thiamine-deficiency group, whereas small-fiber loss predominated in the pure alcoholic-neuropathy group. Condition category: nutrient_deficiency nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The nerve biopsies also distinguished the dominant injury patterns. organism: Homo sapiens tissue_or_cell_type: Sural nerve biopsy specimens experimental_model: Clinical and sural-nerve pathology comparison of 64 alcoholic-neuropathy patients subdivided by coexisting thiamine deficiency and 32 nonalcoholic thiamine-deficiency neuropathy patients. limitations: Biopsy association does not identify a single biochemical injury step or imply that every thiamine-deficient patient loses only large fibers. evidence_location: Abstract: sural-nerve pathology comparison evidence_span: Large-fiber-predominant axonal loss predominated in TDN exposure: Nonalcoholic thiamine-deficiency neuropathy identified in a clinical cohort [koike-2003-neuropathy-subtypes] Alcoholic neuropathy is clinicopathologically distinct from thiamine-deficiency neuropathy (2003). https://pubmed.ncbi.nlm.nih.gov/12838517/ DOI: 10.1002/ana.10550
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.