Urticaria and Arthralgias as Manifestations of Necrotizing Angiitis (Vasculitis)**From the Departments of Dermatology and Medicine. Harvard Medical School, and the Division of Dermatology, Departments of Medicine, Peter Bent Brigham and Robert B. Brigham Hospitals. Boston, Massachusetts. (Reprint requests to: Dr. Soter, Robert B. Brigham Hospital, 125 Parker Hill Avenue, Boston, Mass. 02120.)

Although necrotizing angiitis (vasculitis) of the superficial venules and capillaries of the skin is usually appreciated visually as a purpuric papule, a group of patients has been defined in whom all of the skin lesions were urticarial. Microscopic examination of skin biopsy specimens showed fibrinoid necrosis of the blood-vessel walls, an infiltrate containing polymorphonuclear leukocytes, fragmentation of cell nuclei, and extravasation of erythrocytes. Arthralgias were present in 7 of the 8 patients and arthritis in 3 of these. Two of the patients experienced episodes of abdominal pain. A syndrome of chronic refractory urticaria accompanied by arthralgias and occasionally arthritis or abdominal pain and an elevated erythrocyte sedimentation rate was recognized in nonatopic female patients and appears to be a manifestation of an underlying necrotizing angiitis

Delayed phase of Hematoporphyrin-Induced Phototoxicity: Modulation by Complement, Leukocytes, and Antihistamines

We have investigated the role of complement, leukocytes, and histamine in the delayed phase of hematoporphyrin-induced phototoxicity in guinea pigs. The phototoxic response was quantified by the accumulation of intravenously injected [125I]bovine serum albumin in the skin. There was a greater than 6-fold increase in the vascular response at the completion of irradiation, which subsided partially to reach a plateau of twice the preirradiation level between 0.5 h and 12 h. At 18 h the vascular responsiveness returned to the baseline value. The 7 h timepoint was selected in this study to evaluate the modulation of the delayed phase. In complement-depleted guinea pigs, as well as in leukopenic animals, the enhancement in the vascular response was significantly suppressed (p vs control, < 0.0001 and 0.0022. respectively). Cimetidine, when administered prior to irradiation, significantly suppressed the phototoxic response (p vs control, 0.0365). The combination of diphenhydramine and cimetidine, administered 6 h after the induction of phototoxicity, also suppressed the vascular response (p vs control, < 0.0001). These data indicate that the expression of the delayed phase of hematoporphyrin-iuduced phototoxicity, similar to the early phase, requires the presence of an intact complement system, leukocytes, and histamine

Leprosy: Altered Complement Receptors in Disseminated Disease

We have studied the expression of the C3b receptor (CR1) on erythrocytes of 55 patients with Hansen's disease. We developed a radioimmunoassay utilizing a monoclonal antibody that recognized an epitope different from the C3b binding site, which therefore enabled us to measure total number of CR1 regardless of receptor occupancy. We observed that patients in the lepromatous pole of the disease had a mean of 310 CR1/erythrocyte, whereas the ones in the tuberculoid pole showed a mean of 577 CR1/erythrocyte; 77 normal controls had a mean of 512 CR1/erythrocyte. The number of C3b receptors on the cells of lepromatous patients was significantly decreased (p < .001) when compared to the normal population or tuberculoid patients. The presence of receptors for the C3b fragment of complement (CR1) on the surface of human erythrocytes enables these cells to participate in a number of immune functions including the clearance of circulating immune complexes. These findings could bear importance in the ability of the host to clear immune complexes from the circulation in patients with lepromatous leprosy