Observations on the treatment of pernicious anaemia based on a study of its causation : with notes of a case / by William Hunter.

  • Hunter, William, 1861-1937.
Date:
[1890]
Catalogue details

Licence: Public Domain Mark

Credit: Observations on the treatment of pernicious anaemia based on a study of its causation : with notes of a case / by William Hunter. Source: Wellcome Collection.

Provider: This material has been provided by The Royal College of Surgeons of England. The original may be consulted at The Royal College of Surgeons of England.

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    shown in my former investigation that it is the peculiar character of the preceding blood destrnciion that determines the presence of iron in the liver in such cases. While I found it impossible to reproduce a condition of the liver similar to that found in per- nicious anaamia, by injection of such I'eagents as distilled water, glyceT'ine, or even pyrogallic acid, I succeeded, on the other hand, with toluylene-diamine. With regard to this drug I found that it had not only a peculiar destructive action on the blood, but had also a specific, not necessarily poisonous, action on the liver cells. One result of its action on the blood was that the hfemoglobin re- mained combined with the albuminous constituents of the corpuscles or plasma. As the result of its action on the liver cells part of the haemoglobin reduced in situ to the form of an albuminate of iron, which remained within the liver cell in the form of pigment granules. That under these circumstances the by-products of pigment nature split off from the original haemoglobin molecule should differ from those split off in health need occasion but little surprise. In health such by-products are the bile pigments, and the pigments and chromogens of the urine including normal urobilin. Under other conditions, for example, changes in large extravasa- tions of blood, special by-products may appear, differing, it may be slightly, but still recognisably, from the pigments usually formed. As such a by-product I regard pathological urobilin. It is formed, not only by processes of reduction or oxidation from the bile pig- ments within the intestinal canal, but also I find evidence to show from haemoglobin through the agency of cells. Between it and normal urobilin important differences exist. Its appearance in the urine in pernicious aneemia points therefore—far more than any excess of ordinary pigments —to a preceding extensive de- struction of blood of a special nature. It does not explain the presence of iron in the liver, any more than the excess of iron in the liver explains its occurrence. Both alike are, however, ex- plained by the same special cause—a destruction of blood proceed- ing along lines, and due to causes, other than those found in health. I concluded in my former investigation that the destruction was caused by the action of certain poison or poisons of specific nature. It was the object of my investigations to discover in the present case whether any such poisons were present. 2. My observations on the urine in the above case showed, secondly, occasional presence of blood-pigment in the form of