Managing Cutaneous Vasculitis in a Patient With Lupus Erythematosus
Managing Cutaneous Vasculitis in a Patient With Lupus Erythematosus
Cutaneous vasculitis (CV) is a term used for inflammation of the blood vessels in the skin that occurs in up to 70% of patients with lupus erythematosus (LE). The inflammation affects the smaller vessels of the skin such as the capillaries and the medium-size vessels that include venules and arterioles. Small vessel vasculitis is the most common cause of vasculitis in patients with LE and may be secondary to other rheumatic diseases such as rheumatoid arthritis, dermatomyositis, and Sjogren's syndrome, or present as a primary disease (see Table 1 ). Small vessel vasculitis may present as palpable purpura, urticaria, pustules, vesicles, petechiae, painful red bumps and hard spots, small bruises, or erythema multiforme-like lesions. Sub cut aneous nodules and livedo reticularis may be observed when the patient has small and medium vessel involvement. If untreated, CV can lead to ulceration and gangrene (Akrekar, Bichile, & Kale, 2005; Arroyo, 2002; Golan, 2002; Weyand & Goronzy, 2003).
Histopathologic features of skin lesions include inflammation of the vessel wall associated with fibrinoid necrosis, extravasation of erythrocytes, granulocytic debris, granulomatous or lymphocytic inflammation, and immune complex deposition within the vessel wall. Peri vascular infiltration is a nonspecific histologic finding observed in a variety of disease processes and is not considered diagnostic of vasculitis, even though it may coexist in vasculitic tissues. Leukocytoclastic vasculitis (LCV), where neutrophils are predominant, and lymphocytic vasculitis, where lymphocytes are predominant, are inflammatory cells seen in the biopsy of skin lesions from patients with LE (Jennette & Falk, 2005; Norton, 2004).
The vascular injury in CV is caused by the deposition of immune complexes in the vessel wall with activation of complement, leading to migration of mononuclear cells and polymorphonuclear neutro phils. Com plement are a group of proteins that, when activated, promote and are consumed during inflammation. The antigens causing the immune complexes are sometimes not known. However, anti-DNA antigens, anti-Ro (also known as SS-A) or Ro antigens, anticardiolipin antibody, and antineutrophil cytoplasm antibody are implicated in many vasculitic syndromes in LE (Lupus Foundation of America, 2005; Mansi, Opran, & Rosner, 2002).
Introduction
Cutaneous vasculitis (CV) is a term used for inflammation of the blood vessels in the skin that occurs in up to 70% of patients with lupus erythematosus (LE). The inflammation affects the smaller vessels of the skin such as the capillaries and the medium-size vessels that include venules and arterioles. Small vessel vasculitis is the most common cause of vasculitis in patients with LE and may be secondary to other rheumatic diseases such as rheumatoid arthritis, dermatomyositis, and Sjogren's syndrome, or present as a primary disease (see Table 1 ). Small vessel vasculitis may present as palpable purpura, urticaria, pustules, vesicles, petechiae, painful red bumps and hard spots, small bruises, or erythema multiforme-like lesions. Sub cut aneous nodules and livedo reticularis may be observed when the patient has small and medium vessel involvement. If untreated, CV can lead to ulceration and gangrene (Akrekar, Bichile, & Kale, 2005; Arroyo, 2002; Golan, 2002; Weyand & Goronzy, 2003).
Histopathologic features of skin lesions include inflammation of the vessel wall associated with fibrinoid necrosis, extravasation of erythrocytes, granulocytic debris, granulomatous or lymphocytic inflammation, and immune complex deposition within the vessel wall. Peri vascular infiltration is a nonspecific histologic finding observed in a variety of disease processes and is not considered diagnostic of vasculitis, even though it may coexist in vasculitic tissues. Leukocytoclastic vasculitis (LCV), where neutrophils are predominant, and lymphocytic vasculitis, where lymphocytes are predominant, are inflammatory cells seen in the biopsy of skin lesions from patients with LE (Jennette & Falk, 2005; Norton, 2004).
The vascular injury in CV is caused by the deposition of immune complexes in the vessel wall with activation of complement, leading to migration of mononuclear cells and polymorphonuclear neutro phils. Com plement are a group of proteins that, when activated, promote and are consumed during inflammation. The antigens causing the immune complexes are sometimes not known. However, anti-DNA antigens, anti-Ro (also known as SS-A) or Ro antigens, anticardiolipin antibody, and antineutrophil cytoplasm antibody are implicated in many vasculitic syndromes in LE (Lupus Foundation of America, 2005; Mansi, Opran, & Rosner, 2002).