Necrotizing Angiitis: I. A Clinical Review of Twenty-Seven Autopsied Cases

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SINCE its description by Kussmaul and Maier1 in 1866, polyarteritis nodosa has been variously classified, and yet its precise etiology is still unknown. In the first quarter of this century, numerous unsuccessful attempts were made to indict infection as an etiologic factor. Ever since 1925, when Gruber2 suggested that a systemic hyperallergic reaction to various infections and toxic agents might be incriminated, there has been much speculation concerning the possible role of hypersensitivity. In 1952, Zeek3 suggested that hypertension might play an important role in the precipitation of what she called ‘necrotizing angiitis.’ The term necrotizing angiitis includes all vascular lesions showing inflammation and necrosis; this term was designated by Zeek to include the entire spectrum of entities which had come to be known as polyarteritis nodosa. Zeek3 sought to differentiate between the two entities, polyarteritis nodosa and hypersensitivity angiitis; the distinctive pathologic features of these two entities were outlined as follows:

  1. Involvement of large arteries in polyarteritis nodosa; involvement of small arteries, venules, and arterioles in hypersensitivity angiitis.

  2. Acute and healing lesions in polyarteritis nodosa; all lesions tending to be of the same age in what was considered to be the more lethal entity, hypersensitivity angiitis.

The concept that hypersensitivity angiitis of the type defined by Zeek3 can be clinically differentiated from polyarteritis nodosa described by Kussmaul and Maier1 has been challenged. Recently Austen and Fitzpatrick suggested that a unifying concept is needed in approaching this group of diseases, and that a classification based on clinicopathologic correlations . . .



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