Immunofluorescence studies were made by the indirect method in 54 cases of pemphigus erythematosus, in 50 of which skin specimens from light-exposed and unexposed regions were investigated also by the direct IF method. IF Band was shown to be demonstrable in skin specimens from exposed regions in 81% of cases and from unexposed regions in 23%. ANA were found in some 31% of patients, though usually in titers below those of IC antibodies. There were 2 cases each of coexistence with myastenia gravis and thymoma and with SLE. Virus-like particles, however, were found by electron microscopy only in 1 case with coexisting SLE. Detection of IF Band in skin specimens from a significant majority of patients with pemphigus erythematosus, presence of ANA in some, and occasional coexistence of SLE suggest some relation of the disease with lupus erythematosus.

Cardiac manifestations are reported in 0.3%-4.0% of European patients with Borrelia burgdorferi (B.b.) infection. Usually symptoms disappear within 6 weeks. We report a case with persistent impairment of atrioventricular (AV) conduction. Diagnosis was confirmed by demonstration of IgM antibodies and increase of IgG antibody titers against B.b. in serum, by isolation of the spirochete from skin biopsy material and by the typical clinical combination of erythema migrans, Bannwarth syndrome (meningoradiculitis), and complete heart block. Despite immediate antibiotic therapy with ceftriaxone, first degree AV block and second degree block Wenckebach with atrial pacing at 100 beats/minute persisted for 2 years. We conclude, that Lyme carditis can cause long-standing or irreversible AV conduction defects despite adequate and early antimicrobial therapy.

In 4 cases of allergic vasculitis circulating immune complexes (IC) were demonstrated. Spontaneous and histamine induced vascular changes were studied by immunofluorescence microscopy. The early events in IC vasculitis were investigated at the ultrastructural level by immunoelectronmicroscopy using the peroxidase-antiperoxidase multistep technique. Our findings support the concept that human IC vasculitis is triggered by the deposition of circulating IC in the walls of postcapillary venules between endothelial cells, pericytes and the layers of the basal lamina. Tissue destruction is only secondary due to local complement activation and the release of lysosomal enzymes from chemotactically attracted leukocytes.

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