Erythema Nodosum: Pathogenesis and clinical findings
Authors: Merna Adly Reviewers: Taylor Evart Woo Crystal Liu Yan Yu* Laurie Parsons* * MD at time of publication
Epidermal layer Dermal-Epidermal Junction
Dermal layer
Subcutaneous Fat Layer
Phase 1-5. Septal Fibrosis made of inflammatory cells, such as T lymphocytes, histocytes and eosinophils
Genetic Dysregulation
Infections (Ex.
Streptococcal
Pharyngitis) ~28-48% of cases
Medications (Ex. Birth Control Pills, Sulfa drugs) ~3-10% of cases
Malignancy (ex. Lymphoma)
Autoimmune conditions (ex. Sarcoidosis and
Inflammatory Bowel Disease) ~11-25% of cases
Pregnancy ~1-3% of cases
Antigenic Stimuli / Bacteria / Viruses / Chemical Agents all could trigger the following process: Phase 1. Neutrophils Infiltrate the fibrous septa between fat lobules in the subcutaneous fat
Phase 2. Neutrophils release reactive oxygen species, leading to oxidative tissue damage and inflammation
Phase 3. Opening of inter-endothelial junction and the migration of more inflammatory cells into the septal venules, including macrophages, histocytes, and eosinophils
Phase 4. Macrophages secrete inflammatory cytokines, which stimulates the proliferation of more helper T cells (Th1)
Phase 5. Th1 cells secrete more cytokines, leading to the further release of Th1 cytokines and mediating the immune complexes deposition in the septal venules of the subcutaneous fat (panniculitis). The Th1 immune reaction is called Type IV Delayed Hypersensitivity Reaction
Phase 6. Activated macrophages produce hydrolytic enzymes and transform into multi- nucleated giant cells, called Miescher’s Radial Granulomas. These consist of small, well defined aggregations of small histocytes arranged radially around a small cleft of variable shapes in the septal venules of the subcutaneous fat
Phase 1-4. Lesions are red tender nodules, poorly defined, vary in size from 2-6 cm, and usually on shins ( 1st week)
Fat Lobules T lymphocytes
Macrophages
Note: we’ve done extensive research and can’t figure out why erythema nodosum happens mostly on the shins. If you have an answer, please email us!
Phase 5. Lesions become tense, hard, and painful; and they change in color into bluish or livid. (2nd week)
Phase 6. Lesions become fluctuant as in abscess, but do not ulcerate. Lesions fade to a yellowish color
Epidermal layer Dermal-Epidermal Junction
Dermal layer Subcutaneous Fat Layer
Phase 6. Miescher’s Radial Granulomas
Fat Lobules
T lymphocytes
Macrophages
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published August 25, 2019 on www.thecalgaryguide.com