S. Imaizumi

Successful treatment of chromoblastomycosis with topical heat therapy

Four female patients with chromoblastomycosis were completely cured by prolonged topical application of tolerable heat from pocket warmers. The lesions involuted after 2, 3, and 6 months, respectively, in three patients who faithfully followed our strict treatment schedule, in contrast to the fourth patient who performed the topical heat therapy in an irregular manner at home over a 12-month period. In vitro studies showed that the mature colonies of Fonsecaea pedrosoi, isolated from three of the patients, withstood persistent heating at 42.5 degrees C for more than 1 month. This suggested that heat killing of the causative organisms is unlikely to have been the sole reason for the effectiveness of this simple therapeutic modality.

In vivo binding site of pemphigus vulgaris antibodies and their fate during acantholysis

Ultrastructural localization of pemphigus vulgaris antigen-antibody complexes and their fate during acantholysis were studied in epidermal sheets obtained from the area surrounding the bullae and in acantholytic cells in blister fluid. The distribution of pemphigus vulgaris antibodies already bound to the keratinocytes in early acantholytic lesions was detected with ferritin-conjugated goat antihuman IgG. Ferritin particles were observed on the surface of keratinocytes with particular affinity for desmosomal structures. The acantholytic cells in the blister fluid bound only a small number of ferritin particles on their surface. During incubation at 37 degrees C, pemphigus vulgaris antigen-antibody complexes on the surface of separated desmosomes were internalized and recognized in cytoplasmic vesicles. Endocytosis of separated desmosomes also was observed in vivo when freshly obtained epidermal sheets were immediately processed for routine electron microscopic study. These findings suggest that pemphigus vulgaris antibodies are densely located on desmosomes and that the antigen-antibody complexes, together with other serum proteins on the keratinocyte surface, are internalized by a process of endocytosis.

The speckled epidermal nuclear immunofluorescence of mixed connective tissue disease seems to develop as an in vitro phenomenon

The pathogenesis of speckled epidermal nuclear immunofluorescence in patients with mixed connective tissue disease (MCTD) was studied by reproducing this reaction in guinea‐pigs, using serum samples containing high litre antibody to ribonucleoprotein (RNP). Immunofluorescence studies on specimens obtained from guinea‐pig skin into which scrum samples containing high titre RNP antibody had been injected intradermally, revealed positive epidermal nuclear staining for IgG. This speckled immunofluorescence was demonstrable immediately after injection and remained so for 24 or 48 h. The pattern of fluorescence was similar in all cases, and there was no penetration of RNP antibody through the cell membrane. The epidermal nudear fluorescence was not detected with sera at a dilution of 1:100 or more. These results provide strong evidence that the epidermal nuclear immunofluorescence observed in patients with high titre antibody to RNP develops as an in vitro phenomenon.

Alterations of surface receptors on intralesional neutrophils in pustular psoriasis and palmo‐plantar pustulosis

Alterations of binding capacity of surface IgG‐Fc and complement receptors were demonstrated in polymorphonuclear neutrophils (PMNs) obtained from the pustular lesions of psoriasis. A marked decrease of C3 receptors, but not of IgG‐Fc, was found in PMNs from the lesions of palmo‐plantar pustulosis (PPP) and bacterial pustules. PMNs from pustular lesions of psoriasis exhibited only a slight decrease in the number of C3 receptors. No significant decrease in membrane receptors was noted in circulating PMNs from psoriatic patients. We suggest that mechanisms of formation of aseptic subcorneal pustules, mediated by PMN membrane receptors for C3 fragments, are different in pustular psoriasis and PPP.

Production of antikeratin autoantibodies by hybrid spleen cells of naive mice.

The mechanism of the occurrence of natural antikeratin antibodies in human sera was studied using hybrid spleen cells obtained from experimentally naive or from immunized mice. Antikeratin antibodies were detected by enzyme‐linked immunosorbent assay (ELISA) in 5·9–9·5% of the culture supcrnatants of fused spleen cells taken from naive mice. When mice were immunized with keratins, the number of supernatants containing antikeratin antibodies was increased to eight out of 51 (15.7%). When immunized with non‐keratin materials such as activated human T cells, adult T‐cell leukaemia cell lysates, and human T‐cell lymphotropic virus type‐1 (HTLV‐1), 16·7–20·8% of the supernatants were found to contain antikeratin antibodies by ELISA.

Congenital Cutis laxa

We have encountered 2 cases (mother and son) with an autosomal dominant form of cutis laxa, which is clinically characterized by inelastic, loose, and pendulous skin without systemic organ involvement. The histopathological findings disclosed that the elastic fibers were decreased in number and had abnormalities in shape. Furthermore, electron microscopic observations showed some variations in structural abnormalities of the elastic fibers between the 2 cases. These findings may suggest that the elastic fibers seen in congenital cutis laxa give various features for elastogenesis and elastolysis in the individual cases, perhaps due to aging.

Mechanisms of pustule formation in cutaneous bacterial and viral infections: alterations of neutrophil membrane surface receptors

Changes in membrane surface receptors have been demonstrated by rosetting methods in polymorphonuclear leukocytes obtained from the pustules of different infectious dermatoses. There was a distinct difference in numbers of receptors in neutrophils from bacterial and viral pustules, i.e., C3b receptors were decreased on neutrophils from both bacterial and viral pustules, whereas IgG‐Fc receptors were decreased only in neutrophils from viral pustules. The difference appears to be due to variations in the defence mechanisms against the invading micro‐organisms.