尿道壁細動脈の病変形態観察(膠原病観)に基づく尿道狹窄成因に関しての考察

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A resume of investigations on urethral stricture as outlined in the reports of Rrof. Tabayashi and Midorikawa was published by our department in 1958. It was then noted that in the area Of urethral stricture a definite sequence of changes was taking place in the locations neighboring the connective tissue and its arteriolar walls. The present report is concerned with the details of these changes. Urethral stricture has hitherto been regarded as a sequela of gonorrhoeal infection, but at present there is an increasing incidence of traumatic origin, which, though somewhat differing according to geographic locations, is largely due to the rapid advances in mechanical civilization such as heavy industry, skyscraper construction and automobile manufacture. Tuberculosis also plays a role in a relatively small percentage of cases. There is also a group of urethral stricture In which the cause is unknown as judged from the past history or routine examination. A statistical summary of all cases seen in our department is herewith attempted: [table] The stricture occurred at the bulba and pars membranecea urethra in 35 cases, while it involved the anterior urethra in 5 cases. The materials for the present investigation consisted of the transverse or longitudinal serial sections prepared from 1-4.5 cm circular blocks of stricture tissue obtained from these 40 patients. The sections were stained by 10 different methods, namely hamatoxylineosin, Van Gieson's stain, Weigert's method, Mallory's stain, Mallory's phosphotungstic acid-hematoxylin stain, PAS stain and others. The general and pathological findings of the tissue may here be omitted, since they agree fairly well with the description published by Midorikawa in his on "Clinical and histopathological studies on urethral stricture " (Japan 'J. Urolcgy. Vol 49, No, 11, 1958). Of the histological [table] observations those presenting various changes of peripheral arterioles may be classified as follows: This table indicates that the cases with vasculitic type are by far most numerous, followed in order by those showing hypertrophy of middle layer and sclerrotic changes, while only a few presented no systematic changes. These changes may be summarized as follows: 1) Internal meatus. The internal meatus presented varying degrees and shapes of narrowing, such as central or marginal, oval or similunar, narrowing as well as dendritic or even obstructive in nature. Occasional thrombosis containing erythrocytes and desquamated endothelial cells. 2) Internal layer. The internal layer was seen to have undergone hypertrophy in various manners, such as fibrotic and proliferative hypertrophy, or hyaline degeneration, producing the narrowing of the internal meatus. 3) Middle layer. The middle layer exhibited pictures of degenerative changes In almost all cases, including the irregularities in the arrangement as well as swelling,dissolution and even disappearance of smooth muscles. 4) External layer. The extanal layer wes generally indistinct in appearance, although there were a few wich presented fibrotic proliferation or cicatrization. 5) Many cases showed cellular infiltrations, hypertrophied internal layer and degenerative changes in the middle layer, while inflammatory cellular infiltrations around the blood vessels were frequently encountered. Generally speaking, the infiltrative changes were most remarkable in the perivascular areas. These cells were recognaized to have migrated from the internal layer into the perivascular tissues, or from the perivascular areas into the vessel walls. 6) Elastic fibers. There were many instances of vasculitic type in which degenerative pictures consisted of semicircular remains of tissues resulting from the well demarkated partial dissolution or disappearance of swollen, proliffiferative and internal elastic layer. In addition to the above cases, there were 6 instances of so-called hypertrophy of middle layer and 5 of sclerotic type in the materials for the present investigation. Since these are tissues taken from the patients complaining of difficulties in urination or even anuric developing. after a lapse 8 time from 3 to 20 years, the atypical changes seen in these may also be regarded as maintaining some etiological relations to those involved in producing the stricture, particularly the inflammation of the blood vessels and the sclerosis of perivascular tissues. The above stated changes were common to all the cases of urethral stricture whatever the cause may be. Pathogenesis of vasculitic tissue changes. The diseases characterized by perivascular changes such as rheumatism and allergy have in the past been chiefly explained on the basis of Kling's allergy hypothesis. In recent years, however, a new theory of collagen disease has been proposed by Klemperer who, having noted the fibrinoid dhanges of connective tissues irrespective of causes, reclassified all conditions. characterized by such changes as collagen diseases. The basic changes as seen in the present series of materials consisted of vasculitis typified by fibrinoid swelling or degeneration in addition to interstitial inflammation accompanied by mesenchymal cell proliferatisn. Hence, it seems proper to include these conditions in the category of collagen diseases, and not be subjected to the outmoded explanation even if not of allergic etiology. Pathogenesis of urethral stricture As to the pathogenesis of urethral stricture, the condition has long been explained as a type of residual changes following purulent inflammations consisting of the sclerosis, callus formation and cicatrization of connective tissues. However, in view of the nature of vasculitic changes as, elucidated in the present in vestigation, the changes favor decidedly its inclusion in the category of collagen diseases, presenting resemblances to the pathogenesis of allergic or rheumatic conditions.
社団法人日本泌尿器科学会の論文

尿道壁細動脈の病変形態観察(膠原病観)に基づく尿道狹窄成因に関しての考察

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