Non-Neoplastic Dermatopathology

5.5

L IPODERMATOSCLEROSIS VS MORPHEA

Lipodermatosclerosis

Morphea

Age

Middle-aged adults; women affected more than men.

Any age. Children between ages of 7 and 11 years; adults between ages of 44 and 47 years. Females affected more than males. Multiple described subtypes (circumscribed, generalized, linear, pansclerotic, and mixed) that may involve the trunk, extremities, head and neck regions. Not entirely known. Autoimmune, genetic, vascular dysfunction, and environmental factors play a role. Yellow-white indurated plaque with erythematous, violaceous border and hyper- or hypopigmentation. Lesions may be solitary or multiple. 1. Biopsy appears “squared off” due to expansion of dermis (Fig. 5.5.7) . 2. Epidermis and stratum corneum generally unremarkable. 3. Perivascular and interstitial infiltrate of lymphocytes and plasma cells; eosinophils and histiocytes in early lesions (Fig. 5.5.9) . 4. Sclerosis of collagen bundles in reticular dermis and subcutaneous septae with loss of normal fenestrations between collagen bundles (Figs. 5.5.7 and 5.5.8) . 5. Loss of fat around adnexal structures and entrapment of adnexa by sclerosis (Fig. 5.5.10) . Progressive replacement of subcutaneous fat by sclerosis. Therapy is based upon subtype, level of disease activity, depth of skin involvement, and quality of life impairment. For limited, superficial disease, topical corticosteroids are first-line therapy. Phototherapy or methotrexate is indicated for widespread superficial disease. Methotrexate None.

Location

Lower legs.

Etiology

Chronic venous insufficiency.

Presentation

Early phase of red to violaceous, mildly tender plaques that evolve into indurated, thick, hyperpigmented skin involving the lower third of the leg. Constriction in the ankle region imparts an “inverted champagne bottle” appearance to the leg. May be associated with other features of chronic venous stasis including edema, varicosities, and ulceration. 1. Grouped, thick-walled vessels within the superficial dermis (Fig. 5.5.6) . 2. Erythrocyte extravasation and hemosiderin deposition (Fig. 5.5.6) . 3. Subcutaneous septal fibrosis (Figs. 5.5.1 and 5.5.5) . 4. Membranocystic (lipomembranous) fat necrosis with lipogranuloma formation and xanthomatous macrophages (Figs. 5.5.2-5.5.4) .

Histology

Special studies

None.

Compression therapy is the conventional treatment for chronic venous insufficiency and lipodermatosclerosis. Anabolic steroids are also utilized for their fibrinolytic properties in some cases. is used in cases with deep extension of the sclerosis. Systemic corticosteroids are indicated in cases with rapid progression or development of contractures. Copyright © Wolters Kluwer, Inc. Unauthorized reproduction of the content is prohibited. 2023

Treatment

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