Two cases of acquired reactive perforating collagenosis with poorly controlled diabetes mellitus were studied by histochemistry and by electron microscopy. In excoriated wound the necrotic mass on the bottom of the ulcer contained the collagen bundles which were continuous with the collagen bundles in the reticular layer. In the developing stage, the epidermis regenerated between the necrotic mass and the reticular dermis, and the collagen bundles in the reticular dermis were in continuity with those in the necrotic mass through the epithelial tunnels. The collagen in the epidermal channels did not degenerate ultrastructurally. In the mature lesion, collagen bundles being eliminated through the epidermis were surrounded by the fibroblasts at the basal cell layer. Collagen fibers were seen in the cytoplasm of these fibroblasts. From these findings, the mechanisms of the formation of the eruption in acquired reactive perforating collagenosis might be as follow: 1) In the developing stage, the regeneration of epidermis progresses between the necrotic mass and the reticular dermis, and among the collagen bundles. As a result, the collagen bundles remain in the channels of the epidermis. And then, 2) the regenerated epidermis makes the thick horny layer. As a result, the necrotic masses are lifted up and the collagen bundles are pulled up from the dermis through the epidermal channels.

IgA nephropathy(IgAN) was first reported by Berger in 1968, and characterized by diffuse IgA deposition in mesangium. Patients with IgAN have usually episodic macroscopic hematuria accompanied with pharingitis, gastroenteritis, bronchitis, or sinusitis. These findings suggest that IgAN is an immune-complex disease resulting from a poorly controlled mucosal immune response to environmental antigens to which the patients were chronically exposed. We reported glomerular deposition of outer membrane of Haemophilus parainfluenzae (OMHP) antigens and the presence of IgA antibody against OMHP in the sera of patients with IgAN. 1 These suggest that Haemophilus parainfluenzae has a role in the etiology of this disease. Furthermore, Endo et al. reported experimental IgA nephropathy induced by Gram-negative bacteria. 2 This study was conducted to determine whether intraperitoneal administration of OMHP antigens induced immunohistologically evident glomerular deposition of IgA and C3 in C3H/HeN mice.Female C3H/HeN mice (4 weeks old) were fed on commercial pellet mouse foods. The mice received intraperitoneal injection of OMHP antigens, once per week (OMHP group). The control group received intraperitoneal injection of PBS. The mice were killed at 10, 20 and 30 weeks after the experiment commenced. Throughout the experiments, hematuria and proteinuria were analyzed every 5 weeks.The OMHP group showed glomerular deposition of IgA, C3 and OMHP antigens, glomerular changes (mesangial hypercellularity and increase of mesangial matrix) at 20 and 30 weeks. The control group showed no glomerular deposition of IgA, C3 and OMHP antigens and no glomerular change. Hematuria was recognized in one of six OMHP group mice at 30 weeks.These results suggest that OMHP antigens play a role in the glomerular deposition of IgA and C3 in C3H/HeN mice. This is the first use of OMHP antigens to establish an active model of IgAN.

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