[Hypersensitivity angiitis or microscopic polyarteritis nodosa. Recent findings. III. Pathologic anatomy, etiopathogenetic aspects and therapeutic approach].

Histologically hypersensitivity angiitis produces necrotising inflammation of the small arterial and venous blood vessels. In most cases the inflammatory infiltrate presents leucocytoclasia i.e. nuclear leucocytic detritus. Unlike polyarteritis nodosa, hypersensitivity angiitis does not affect the medium sized arteries though its lesions are produced at the same stage of development. At skin level, the postcapillary venules are the vessels most often affected. Fibrinoid necrosis of the glomerular loops of the kidney may arise and is often accompanied by epithelial crescents. Aetiologically, a variety of agents--bacteria, viruses, drugs, toxic substances--have been held responsible for the disease, though very often the cause cannot be identified. The most widely based on the finding of immunocomplexes, though other immunological disorders might be involved. Treatment involves the elimination of the antigen held responsible, the suppression of the immune response, the removal of circulating immunocomplexes and the use of anti-inflammatory drugs.