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Table
Table 1: Differentiating features between Non drug‑induced erythroderma and drug‑induced erythroderma
Non drug‑induced erythroderma Drug‑induced erythroderma
Onset Insidious Acute or subacute
Progression Gradual Rapid
Clinical features In the initial stages, morphology is that of disease It usually starts with pruritic maculopapular rash or lichenoid
responsible for causing erythroderma. In later or urticarial rash which evolves into erythroderma. Scales are
stages, there is diffuse scaling and erythema usually large, especially during acute phase
Resolution Slow to subside Faster (after drug discontinuation)
Causative factors Extensive or unstable psoriasis, eczema, Many drugs can cause erythroderma. In clinical practice, drugs
infections, GVHD, immunobullous disorder, and such as dapsone, phenytoin, AKT, antibacterial, beta-blockers
malignancy are likely causes. In clinical practice, carbamazepine, proton-pump inhibitor, and phenylbutazone
the most common cause is psoriatic erythroderma can cause erythroderma[3]
Sites involved Skin Skin. Mucous membranes may also be involved
Temperature Present Fever mostly present (associated)
Nail changes, arthritis, Seen Not seen
palmoplantar keratoderma
Lymphadenopathy Present Present
Relapse Seen No relapse
Hospitalization time Long duration stay Short duration stay
Skin and lymph node biopsy Presents with changes of preexisting dermatosis Histology is like pseudolymphoma. Changes suggestive of a
drug reaction such as necrosis of epidermis and dense dermal
infiltrate of lymphocytes with/without eosinophils
Systemic involvement Usually secondary to the erythroderma Deranged liver function test and leukocytosis with
predominant eosinophilia (AEC> 1000) can be seen in DRESS
GVHD: Graft versus host disease, AEC: Absolute eosinophil count, DRESS: Drug reaction, eosinophilia and systemic symptoms, AKT: Antitubercular drugs