Hæmatoporphyrinuria and its relations to the source of urobilin / by David Fraser Harris.

  • David Fraser Fraser-Harris
Date:
[1897]
Catalogue details

Licence: Public Domain Mark

Credit: Hæmatoporphyrinuria and its relations to the source of urobilin / by David Fraser Harris. Source: Wellcome Collection.

Provider: This material has been provided by The University of Glasgow Library. The original may be consulted at The University of Glasgow Library.

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    neurotic fatal cases in women, and once in a case with grave cutaneous lesion (reported above). It is noteworthy that in muscles we have a haemoglobin derivative, myo-haematin, whose spectrum is very similar to urohaematoporphyrin. Whatever else it is, it is a reduction product, for oxidation causes its bands to dis- appear. We might note the anaemia in Addison's and Hodgkin'.s diseases; and as to System II., that if it be destroyed over a pretty extensive area, as in a severe burn, we have haemoglobinuria— a paralysis of Hb02-transforming power. Normally, then, we may regard muscles, skin, and connective- tissues as seats of a subsidiary formation of urobilin from a haematin derivative, which, if it be excessively reduced, gives rise to pathological urobilin; if, owing to as yet most obscure devia- tions from healthy metabolism in these systems, it be only imper- fectly reduced, we then have, in not a few cases, urohaematopor- phyrin, and in very rare ones its less reduced dark red ally. The degree of completeness of the initial reduction determines which of these haematin derivatives is to appear, for the amount of subse- quent pulmonary oxidation and renal reduction is probably the same for all. [In certain diseases this would, of course, not be so, as in pneumonia, where pulmonary oxidation is deficient, more, tlu , of the chromogen and less of the pigment from the system in which the prominent lesion existed would be excreted.]