In twenty patients with erythema multiforme we investigated circulating immune complexes and their deposition in the skin lesions. CIq-binding activity was elevated in ten of twenty patients, and the platelet aggregation titre was high in three of twelve tested sera. Decreased levels of C3 were seen in two and of C4 in one out of eighteen patients. Direct immunofluorescence showed a deposition of C3, IgM or IgG in the blood vessel walls of the upper dermis in four of twelve patients. These findings may suggest that transient production of circulating immune complexes and their deposition play an important role in the pathogenesis of this disease.

The case is described of a 39-year-old man with acute generalized pustular bacterid and high Clq-binding activity in the sera during the active stage. Histamine-induced vascular changes studied by immunofluorescence microscopy revealed a perivascular deposition of IgM and C3. These findings support the view that leukocytoclastic vasculitis underlying the subcorneal pustules is mediated by immune complex deposition.

The effect of sera from patients with untreated leukocytoclastic vasculitis was investigated on the generation of oxygen intermediates by normal polymorphonuclear leukocytes. Sera from untreated patients induced increased hydroxyl radical generation, which is one of the most potent oxidants capable of causing tissue damage. It is suggested that vascular injury may be mediated in part by enhanced production of hydroxyl radical by polymorphonuclear leukocytes. Circulating immune complexes in the sera of the patients are considered to be one of the factors responsible for enhanced generation of hydroxyl radical.

Since the observation of immune complexes in the circulation of patients with systemic lupus erythematosus (SLE) and rheumatoid arthritis, much attention has been drawn to immune complexes as pathogenic factors. We here report the presence of immune complexes in the sera of patients with several kinds of skin diseases using the platelet aggregation (PA) test (Penttinen, 1977).The 128 fresh or stored (-8o°C) sera were from patients with the active stage of several skin diseases. Detection of immune complexes was performed by the PA test (Penttinen, 1977) with some modifications. Platelet suspensions were prepared as follows: 20 ml of venous blood were collected into 5 ml of anticoagulant solution. The platelet rich plasma was obtained by centrifugation at 200 g for 15 min. Platelets were then sedimented by centrifugation at 1000 g for 15 min and the pellet was washed with PBS. Finally, the platelets were suspended i-5-2-ox io'/mm^ in PBS (pH 7-8). The PA test was performed by using disposable U-microplates. PBS (pH 7-8, 100 /il) and twofold serial dilutions of tested sera (100 /il) were mixed in a U-microplate, and then the platelet suspensions (50 fil) were added to each well. After pipettings, the plates were incubated at 4°C for 18-20 h in a moisture chamber and aggregation patterns were read.The sensitivity of the PA test was shown by its ability to detect i /fg/ml of BSA, 2-5 /ig/ml of anti-BSA antibody and 6-3 ;Ug/ml of aggregated human IgG.PA titres of the tested sera are shown in Fig. i. All of the twenty-three sera from healthy volunteers showed PA titres of below 8. PA titres above 8 were noted in a considerable number of sera from the patients with erythema nodosum (78%), progressive systemic sclerosis (PSS) (71%), SLE (69%), pemphigus (56%), cutaneous angiitis (50%), generalized drug eruption (40%) and erythema multiforme (36%).The PA test is based on the phenomenon of interaction of immune complexes with the Fc receptors on the surface of platelets and has been proven to be one of the most sensitive assays for the detection of circulating large (19 s) immune complexes, although factors other than immune complexes (e.g. aggregated IgG, platelet antibodies and enzymes such as trypsin and thrombin) are also potent platelet agglutinators (Penttinen, 1977).In the present study, we have found the high PA titres in a considerable number of sera from patients with erythema nodosum, PSS, SLE, pemphigus, cutaneous angiitis, generalized drug eruption and erythema multiforme.With regard to collagen diseases such as SLE and PSS, the presence of circulating immune complexes has been mentioned by many authors. Jordon et al. (1976) suggested that pemphigus was an immune complex disease where local activation of complement was noted in blister fluids. Tappeiner et al. (1977) showed immune complexes in pemphigus sera by Clq-binding assay. Our results confirmed this.There have been several reports suggestive of immune complex formation in the sera of patients with erythema multiforme (Kazmierowski & Wuepper, 1977) and c...

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