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is the infiltration wont to extend to the surrounding parenchyma, until at last the whole district of tissue to which the artery leads has experienced the change. If in an amyloid spleen we trace one of these small arteries, whilst it breaks up into a so-called penicillus, we see how its wall, in itself already a thick one, becomes thicker in proportion as the change advances, and how at the same time the calibre of the vessel becomes considerably diminished. This accounts for the circumstance, that all organs which experience the amyloid change in a considerable degree, look extremely pale; an ischaemia of the parts is produced by the obstruction which the narrowed vessels oppose to the influx of blood. If now we examine in which of the histological elements of the vessels the substance is first found, it seems to be pretty constantly seated in the little muscles of the circular-fibre coat. First of all the place of every fibre-cell is occupied by a compact, homogeneous body, in which the centre of the nucleus at first still appears as a hole, but gradually every trace of a cel

Pio. 121.

[graphic]

lular structure is lost, so that at last a kind of spindle-shaped flake (Scholle) remains, in which neither membrane, nucleus nor contents can be distinguished. In the calcification of small arteries exactly the same process takes place; the individual fibre-cells of the middle coat take up calcareous

Fig. 121. Amyloid degeneration of a small artery from the submucous tissue of the intestine, with its trunk still intact. 300 diameters.

AMYLOID DEGENERATION OF THE LIVER. 375

salts, at first in a granular, afterwards in a homogeneous form, until they are at last transformed into homogeneouslooking calcareous bodies, of a spindle-shaped form, which coalesce and produce plates of a considerable size. In like manner the amyloid substance pervades whole tracts of tissue, and the walls of the artery are transformed into a mass at last nearly completely homogeneous, compact, shining with reflected light and colourless, which not only does not possess the hardness of calcified parts, but on the contrary exhibits a high degree of friability.

Now when a change of this nature has advanced to a certain height, an analogous change takes place also in the parenchyma of the organs. This can nowhere be so distinctly traced as in the liver. Here it sometimes happens, that we meet with stages, where nothing else in the whole organ is altered, excepting the minute branches of the hepatic artery. On making fine sections through the liver, carefully washing them and applying iodine, we sometimes see, even with the naked eye, the small iodine-red lines and points which correspond to the cut branches of the hepatic artery. In a later stage, however, it is essentially the hepatic cells which are affected by the change; and indeed, what is again very characteristic, just those hepatic cells, between which lie the capillary ramifications of the hepatic artery. If namely we picture to ourselves a single acinus of the liver, we can, in accordance with the pathological changes which may often be recognized even with the naked eye, distinguish three different zones within each acinus (Fig. 110). The most external part, which lies next to the branches of the portal vein, is the chief seat of fatty infiltration ; the intermediate part, which receives the capillary terminations of the hepatic artery, belongs to the amyloid degeneration, and the central part of the acinus around the vena hepatica is the most common seat of pigmentary infiltration. Even with the naked eye the pale colourless, translucent and resistent zone of the waxy or amyloid change is sometimes recognized between the most external yellowish white, and the most internal yellowish,or greyish brown, layer.

If a single hepatic cell be watched, its previous granular contents, which give every hepatic cell a slightly cloudy appearance, are seen gradually to become homogeneous; the nucleus and cell-wall gradually disappear, and at last a stage sets in in which nothing more can be perceived than an absolutely homogeneous, slightly shining body, if you will, a simple flake (Scholle). In this manner the whole of the hepatic cells in the zone I have described are sometimes converted into amyloid flakes, and if the process attains a very high pitch, the change at last even oversteps this zone, and it may happen, that nearly the whole substance of the acinus is transformed into an amyloid mass. Thus out of the hepatic cells there is at last produced in these cases a kind of corpora amylacea, only they are not laminated like those we have already spoken of, but form, uniform, homogeneous bodies, in which no internal division, no indication of the peculiar course of their formation, can be recognized.

If we take all these facts together, it appears pretty probable, that we have here to deal with a gradual infiltration of the parts with a substance which has been conveyed to them from without. This is a view which derives essential support from the fact, that" nearly always when this change declares itself, a considerable number of organs are affected, and that the process is not confined to a single spot, but that many places in the body are simultaneously affected. Hereby the whole process really acquires au essentially dyscrasic appearance. The only place, where, until now at least, an entirely independent development of this change has been observed by me, and where it may therefore with some degree of probability be assumed that the formation is autochthonous and not imported from without,

DYSCBASIC NATURE OF THE AMYLOID DEGENERATION. 377

is permanent cartilage. The cartilages, particularly in people somewhat advanced in life, assume in various places—as for example, the sterno-clavicular articulations, the symphyses of the pelvis, and the intervertebral cartilage —a peculiarly pale-yellowish hue, and then we may be tolerably certain, that, if we try the iodine-test with them, we shall obtain the peculiar coloration. These colours are not seen so much in the cartilage-cells as in the intercellular substance, and as cases of the sort do not occur simultaneously with amyloid degeneration of large internal organs, but quite independently, in individuals, who in the rest of their body manifest nothing of the kind—it seems that we really have here to deal with a direct transformation, and not with any importation from without.

But in vain have I hitherto endeavoured to detect any definite change in the blood, from which the inference might be drawn, that this was really the source of the deposits. There exists as yet but one single observation, that points to the presence of analogous bodies in the blood, and this is so strange an one, that we can scarcely attempt to ground an explanation of the process upon it. A physician of Toronto in Canada had namely, in compliance with the wish of a patient suffering from epilepsy, examined his blood and discovered in it peculiar, pale bodies. When then he read of my observations with regard to the coloration of the corpora amylacea of the brain by iodine, his patient recurred to his mind, and, I think after the lapse of five years, he again took blood from him, and again found the bodies, which are really said to have exhibited the reaction. In opposition to this observation, it is strange that nobody else has ever seen anything of the kind, and as an extremely persistent dyscrasia must here have been in operation, we should scarcely be justified in drawing conclusions from this observation, with regard to the cases we are considering, where the disease attains its height in a much shorter time, and we have in the blood at least been able to detect nothing of the kind. Moreover great doubts must be entertained with respect to the accuracy of the observation. Starch-granules may very easily find their way into different microscopical objects, so that (with all due respect for the observer) as long as the matter turns upon a solitary observation, it must be admitted to be possible that there was perhaps an error.1 I am as yet much more inclined to admit, that the blood in this disease undergoes a chemical alteration in its fluid constituents, than that it contains the pathological substances in a material form.

At all events it is unquestionable, that the amyloid change even now holds a very high place among pathological processes. The inevitable result of the affection is, that the parts which are the seat of it, become totally incapable of discharging their special functions; that, for example, glandcells which are changed in this manner, are no longer in a condition to perform their special glandular functions, and that vessels can no longer subserve the nutrition of the tissues, or the secretion of the fluids, the duties they had been in the habit of performing.

These considerations afford a ready explanation of the circumstance that clinical disturbances so regularly concur with these anatomical ones. We find, on the one hand, well-marked conditions of cachexia, and on the other with extreme frequency, dropsy with the whole complex group of changes, which are usually included in the idea we form of Bright's disease. In nearly every instance, in which the amyloid affection reaches an advanced stage,

1 Dr. Carter of Edinburgh, and after him, M. Luys of Paris, fell into a similar error, when they imagined they were in a condition to prove that an excretion of starch took place through the skin. M. Rouget (Journal de Physiologie par Brown-Sequard, Tom, ii, p. M) has shewn that this starch is derived from external sources, from articles of food, and that its presence upon the skin therefore is merely accidental.—From a MS, note by the Author.

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