Abstract
The fibrinoid degeneration observed in 105 human cases of miscellaneous diseases excluding allergic or collagen diseases was investigated histologically and histochemically.
1. Fibrinoid degeneration in arterial and capillary walls and perivascular connective tissues was noticed in various lesions, such as chronic peptic, neoplastic or inflammatory ulcers, erosions, inflammatory foci, polyps, hemorrhages, anemic infarctions, atherosclerosis, uremia and so on.
2. All of the fibrinoid degenerations in various lesions or diseases were the same in nature, and moreover closely resembled the fibrinoid degeneration in vascular walls of rabbits in Arthus phenomenon, DOCA-administered rats, bilaterally nephrectomized dogs, bilaterally renal arteries-ligated dogs, renal arteries-constricted rabbits or rats, and that in so-called angionecrosis of cerebral arteries in human apoplectic cerebral hemorrhage.
3. The fibrinoid substance had spatially close relation to serofibrinous exudate and was intensely stained with fibrin stain. Most of the substance was digested by trypsin as easily as fibrin.
4. Mesenchyma l proliferative reaction, which is generally associated with fibrinoid degeneration, was scarcely noticed in the present study.
5. It is not considered that fibrinoid degeneration is characteristic merely to allergic or collagen diseases.
6. The foregoing results suggested that fibrinoid substance was derived from fibrin, fibrinogen and blood plasma proteins, all of them were exuded from vascular spaces to vascular walls as the result of increased vascular permeability by various causes including allergic phenomena. The development of increased vascular permeability was supposed to be caused by permeability-promoting factors in inflammatory lesions, hypoxidosis, fibrinolytic and other enzymatic activities, and mechanical injuries.
