A layered skin block with grouped rounded subepidermal bodies appears beside a separate small-intestinal villus model.
Dermatologic orientation reconstruction Editorially reviewed

Representative skin-layer and small-intestinal orientation for dermatitis herpetiformis. This reconstruction does not depict herpes infection, a patient, rash distribution, biopsy, diagnostic stain, severity, or diagnosis.

WikiBiome / Microbiome MedicineNLM-MeSH-condition-, NIDDK-celiac-association-, skin-and-intestinal-, and literal-output-audit-informed reconstruction
Scientific media record1 verified identifier
Subject
Dermatitis Herpetiformiscondition
Identifiers
MeSH:D003874
Review
Editorial review completeIdentifiers authority-verified · Accessibility validated · · dermatitis-herpetiformis|dermatitis-herpetiformis-pathology-v1.webp
Digital source
Trained-algorithmic mediaCreated with a trained generative algorithm and reviewed by WikiBiome for subject identity, scientific framing, identifiers, provenance, and accessibility.
License
CC BY-SA 4.0Created

Dermatitis herpetiformis (DH) is the cutaneous manifestation of Celiac Disease, presenting as intensely pruritic, grouped vesicles on the elbows, knees, buttocks, and scalp. It is driven by IgA antibodies against epidermal transglutaminase (eTG), the skin homolog of tissue transglutaminase (tTG) targeted in celiac disease.

Virtually all DH patients have underlying celiac enteropathy, though intestinal symptoms may be subclinical.

Integrated microbiome signature

One disease. Five evidence layers.

A generated systems view of the metals, organisms, host sequestration signals, ecological conditions, and microbial functions indexed for Dermatitis Herpetiformis.

01

Evidence layer

Metallomic signature

Elements and antioxidants reported as elevated, accumulated, depleted, or systemically altered.

Elevated or accumulated

0

No structured signals indexed yet.

Depleted or redistributed

0

No structured signals indexed yet.

02

Evidence layer

Taxonomic signature

Organisms reported as enriched or depleted, with their indexed functional context kept beside the name.
Enriched taxa0

No structured taxa indexed yet.

Depleted taxa0

No structured taxa indexed yet.

03

Evidence layer

Nutritional immunity

Host metal-withholding, inflammatory, antioxidant, and microbial-metabolite signals indexed in the signature.

Elevated host signals

0

No structured signals indexed yet.

Depleted protective signals

0

No structured signals indexed yet.

04

Evidence layer

Ecological state

The environmental conditions that connect the organism-level observations into a system.
WB.ECO / SYSTEM MODEL0 connected states

No structured ecological features indexed yet.

EnvironmentCommunity structureHost response
05

Evidence layer

Virulence functions

Microbial structures, enzymes, and acquisition systems implicated by the linked evidence.

No structured virulence functions indexed yet.

Encyclopedia article

The disease record, in full.

The original WikiBiome disease narrative remains intact beneath the generated signature atlas.

Microbiome Associations#

DH shares the Gut Microbiome alterations documented in celiac disease: reduced Bifidobacterium and Lactobacillus, increased Proteobacteria and Bacteroides. The gut-skin axis in DH likely operates through immune-mediated pathways—intestinal Dysbiosis promotes systemic Metal-Driven Inflammation and aberrant IgA production that deposits in dermal papillae.

Whether skin-resident microbiome changes contribute to lesion formation remains under investigation.

Metal Associations#

The subclinical celiac enteropathy in DH patients impairs absorption of iron, zinc, and selenium through villous atrophy. Iron deficiency is common even without overt anemia. Zinc malabsorption may contribute to impaired wound healing and skin barrier dysfunction.

These micronutrient deficiencies compound the immune dysregulation driving the disease.

Associated Conditions#

DH clusters with other autoimmune conditions: Celiac Disease (virtually universal), autoimmune thyroid disease, and Type 1 Diabetes. This autoimmune clustering suggests shared genetic susceptibility (HLA-DQ2/DQ8) and potentially shared gut microbiome-immune interactions.

Cross-References#

Generated evidence record

References 8

Numbered by first appearance in the article, then reconciled with its declared source list.

  1. 1

    Flyvholm MA, Nielsen GD, Andersen A (1984). Nickel Content of Food and Estimation of Dietary Intake. Zeitschrift fur Lebensmittel-Untersuchung und Forschung.

  2. 2

    Monisha Jaishankar, Tenzin Tseten, Naresh Anbalagan et al. (2014). Toxicity, Mechanism and Health Effects of Some Heavy Metals. Interdisciplinary Toxicology.

  3. 3

    Di Gioacchino M, Gatta A, Della Valle L et al. (2018). Systemic Nickel Allergy Syndrome. Metal Allergy (book chapter).

  4. 4

    Veien NK, Hattel T, Laurberg G (1993). Low nickel diet: An open, prospective trial. Journal of the American Academy of Dermatology.

  5. 5

    Borghini R, Porpora MG, Casale R et al. (2020). Irritable Bowel Syndrome-Like Disorders in Endometriosis: Prevalence of Nickel Sensitivity and Effects of a Low-Nickel Diet. An Open-Label Pilot Study. Nutrients.

  6. 6

    Sharma AD (2006). Disulfiram and low nickel diet in the management of hand eczema: A clinical study. Indian Journal of Dermatology, Venereology and Leprology.

  7. 7

    Genchi G, Carocci A, Lauria G et al. (2020). Genchi 2020 — Nickel: Human Health and Environmental Toxicology. International Journal of Environmental Research and Public Health.

  8. 8

    Braga M, Quecchia C, Perotta C et al. (2013). Systemic Nickel Allergy Syndrome: Nosologic Framework and Usefulness of Diet Regimen for Diagnosis. International Journal of Immunopathology and Pharmacology.

Knowledge graph

Article network

Researcher discussion

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Publicly readable discussion by ORCID-authenticated researchers. Questions, interpretation, methods, corrections, and new evidence stay attached to this record.

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Transparent record

Activity and accepted changes

Accepted researcher context, editorial status, public discussion, and upstream Git revisions are shown together. Pending, declined, and withdrawn proposals remain private.

5 events
  1. published revision

    Backfill gut microbiome concept links

    Karen Pendergrass · +1 −1

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  2. published revision

    Backfill inflammation concept links

    Karen Pendergrass · +1 −1

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  3. published revision

    Complete corpus-wide Dysbiosis linking

    Karen Pendergrass · +1 −1

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  4. published revision

    massive wiki expansion: 149 stubs fixed, 100+ new pages, Rule 15 scan, keystone papers

    WikiBiome Deploy Bot · +13 −7

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  5. published revision

    maintenance: 409 source fixes, 34 entity updates, 17 concept updates, 30 analysis outputs

    WikiBiome Deploy Bot · +60 −0

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8 references · 1 content records · 822 corpus pages