
Two CASES OF PERIARTERITIS NODOSA
Author(s) -
Tamai Sadami
Publication year - 1962
Publication title -
acta patholigica japonica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
ISSN - 0001-6632
DOI - 10.1111/j.1440-1827.1962.tb02723.x
Subject(s) - adventitia , granulation tissue , pathology , vasa vasorum , internal elastic lamina , medicine , infiltration (hvac) , lumen (anatomy) , autopsy , thrombosis , fibrosis , connective tissue , cellular infiltration , anatomy , artery , inflammation , wound healing , surgery , physics , thermodynamics
Summary Two autopsy cases of periarteritis nodosa were presented in this paper, including a 18 year and 3 month old male and a 29 year and 8 month old female. It may be that the changes in small and middle‐sized arteries of the whole body are main and secondarily gave rise to most of other lesions. Although there were various pictures in the arterial lesions, the author inclined to summarize these findings as follows:– Following primary development of fibrinoid degenerations in the intima and in the inner part of the media, infiltrations of cells occur in the adventitia and gradually replace the media and the intima, resulting in loosening of arterial walls. Fibrocytes proliferate and replace these loose walls and granulation tissues are formed here. At this time the lumens show thrombosis with intimal proliferation, developing pictures of arteritis obliterans. As the granulation tissues become old and cicatrized, recanalization occurs in the lumen and fibrosis in the adventitia. Occasionally, some cicatrized areas may show infiltration of cells with loosening of tissue connection, which suggests replacement of inflammation. Elastic fibers, when involved, may show fragmentation or even disappearance and in the granulation tissue argyrophile fibres are increased in number. That the above mentioned changes in the arteries do not occur at the same time but changes at different stages are mixed, will explain the variety of the histologic picture, and inconstancy of reactions of the internal organs will give rise to variable clinical manifestations. These changes observed in vascular walls correspond to A rkin's description at stage I to IV of periarteritis nodosa. It is of interest that in case 1, despite the presence of typical nodular sclerosis macro‐scopically, early lesions were not conspicuous histologically and in case 2, gross examination failed to find typical nodular sclerosis, but evidence of periarteritis nodosa as well as early lesions was well revealed histologically. These differences between two cases suggest that the histological changes may be influenced by the clinical course and the dose of steroid hormones given to each case.