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In order to characterize the nature of the mononuclear cells in the perivascular infiltrates in the skin of 11 patients with CU, skin biopsy specimens were analyzed in situ by an avidin-biotin immunoperoxidase technique. Serial frozen sections were stained for total T cells, helper-inducer T cells, suppressor-cytotoxic T cells, B cells, monocytes/macrophages, and HLA-DR antigen. The infiltrates were found to consist mainly of T cells, whereas B cells and macrophages were rarely seen. Most of the T cells possessed the T4+ helper phenotypes, whereas smaller numbers of infiltrating cells were defined as suppressor-cytotoxic cells. Most of the helper-inducer T cells coexpressed the Ia (HLA-DR) antigen. Several potential pathogenic mechanisms could be implicated in CU based on these observations.

In a comprehensive study of 80 patients with vasculitis, 4 had concurrent hepatitis B virus (HBV) infection. Polyarteritis nodosa was present in 2 and in the other 2, cutaneous vasculitis, presenting clinically as palpable or Henoch-Schonlein purpura. In one of these patients skin biopsies demonstrated granular deposits of IgM, C3, C4, and the hepatitis B surface antigen (HBsAg) and electron-dense deposits of aggregated 20-nm particles resembling HBsAg in postcapillary venules. Evidence for circulating HBsAg-immune complexes included increased serum Clq binding activity, decreased serum complement, and a cryoprecipitate containing both HBsAg and IgM anti-HBs. Aggregated 20-nm particles resembling intact HBsAg were also seen by negative staining electron microscopy of the serum cryoprecipitate. This patient fulfills all the criteria for a specific immune complex vasculitis caused by his immune response to a chronic HBV infection. These findings emphasize that HBV infection may be associated with small vessel vasculitis as well as polyarteritis nodosa, mixed cryoglobulinemia, and glomerulonephritis. A similar immune response to other viral infections may be expressed as palpable (Henoch-Schonlein) purpura also.

Intestinal lymphoid hyperplasia and recurrent pulmonary infections by pyogenic bacteria are well-recognized accompaniments of common variable (late onset) hypogammaglobulinemia. A 35-yr-old woman with this illness had progressive pulmonary insufficiency caused by nodular lymphoid interstitial pneumonitis, rather than by infectious lung damage, and intestinal lymphoid nodular hyperplasia. B cells were abundant in the intestinal nodules but absent in the pulmonary nodules by immunoperoxidase staining. Pulmonary lymphocytes isolated in single-cell suspension from the biopsy were 0.5% B cells and 82% T cells. Prednisone therapy improved pulmonary function and decreased the intestinal lymphoid nodules. Lymphocytic interstitial pneumonitis should be considered in patients with hypogammaglobulinemia and restrictive lung disease.

Late cutaneous reactions preceded by an immediate wheal-and-flare reaction have been described after allergen skin testing, intradermal 48/80 injection, and skin testing with heterologous antihuman IgE. We report the finding of delayed cutaneous reactions after prick food skin testing in a subgroup of five patients with delayed pressure urticaria. This subgroup is also defined by symptomatic clearing after fasting. We demonstrate a correlation of food challenge with skin test response in this same subgroup. Some patients who had previously required prednisone for control of urticaria were able to be managed without it while they were receiving the exclusion diet. In addition, their pressure symptoms and challenge disappeared while they were receiving the restricted diet. These findings suggest that an underlying food sensitivity may be an important precipitating factor in some patients with delayed pressure urticaria.

We report a patient with hypocomplementemic urticarial-vasculitis syndrome. This case illustrates the continuum between urticaria and purpura characteristic of hypocomplementemic urticarial-vasculitis syndrome. Clq precipitin was demonstrated in the patient's serum and in the diethylaminoethylcellulose-ion exchange fraction containing only IgG. A skin biopsy specimen of urticarial and purpuric lesions demonstrated leukocytoclastic vasculitis and granular deposition of C3 and Clq in the basement membrane with IgA, IgM, C3, and Clq in postcapillary venules. Serial total hemolytic complement activity and Clq determinations were performed, and the response to several treatment regimens is presented. Symptomatic and serologic improvement was observed only with hydroxychloroquine.

Electroimmunodiffusion (EID) was adapted for the detection of hepatitis-associated antigen (HAA) and compared with immunoelectroosmophoresis (IEOP) and double diffusion (DD) with respect to sensitivity and applicability to rapid screening of large numbers of sera. EID is as sensitive as IEOP, requires less antiserum, and is quantitative. Results may be obtained within 45 minutes if high-titer antiserum is available. Using this technique, 26 HAA-positive sera were identified among 10,303 potential blood donors during a 3 month period.

Do allergists really need to be well informed about circulating antigen-antibody or immune complexes (CIC)? The answer to this rhetorical question is “yes” for a number of reasons. First, over the past year four articles have appeared. Three of them were in this JOURNAL. The most recent is by Yang and colleagues on page 300 of this issue. It concerns CIC in patients with atopic respiratory disease, comparing those on hyposensitization thera.py with untreated atopic controls and with normals without IgE-related disease. rw4 In these studies, two of them from the same laboratory,‘, 4 the hypothesis was tested that long-term hyposensitization, intended to increase IgG blocking antibody, might also induce CIC composed of allergen and IgG blocking antibody. To me this is a very unlikely hypothesis when the small amounts of allergenic extracts injected and the sensitivity of the CIC detection assays are considered. For examlple, Stein and associates3 collected serum from patients 2 hr after injections of 0.5 ml of 1: 100 w/v allergenic extracts when “significant antigen absorption” appeared. CIC were measured with a radiolabeled Clq-polyethylene glycol assay, which had a detection sensitivity equivalent to 5 pg/ml of human