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

  • Fraser-Harris, David Fraser, 1867-1937.
Date:
[1898]
Catalogue details

Licence: Public Domain Mark

Credit: Hæmatoporphyminuria 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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    formation of urobilin, we have the more completely de-oxidised pigment (Pathological Urobilin) appearing in the urine. So much for the hepatic, as opposed to the biliary, origin of urobilin. On this view, urobilin or its chromogen (whichever, in the absence of positive proof, be regarded as the internal secretion of the liver) would of necessity require to be found in the blood. I may say at once that I believe urinary-pig- ment is present in blood-plasma, and therefore in blood-serum, although bile-pigment is not. M'Munn long ago discovered1 that sheep's serum yielded a spectrum with a band at F, and even then (1880) he remarked it must be due to choletelin, or a substance like it. But even at that time Maly, Neubauer, and Vogel believed it was due to urobilin; and as our knowledge of all these substances has been considerably increased in these seventeen years, we are by no means compelled to say that a pigment, choletelin, which is only known in the laboratory, is present in the blood, when we have just as much evidence for believing that another—urobilin — con- stantly in the body, is the pigment in the blood. The objection that we see no band at F in normal blood has no weight what- ever, because (1) urobilin will be in all likelihood present in blood in much less percentage than in urine, in which the urobilin present is spectroscopically invisible; and (2) because it is quite conceivable that it might exist in the blood (partly) as the colourless chromogen of the pigment. By a chromogen, we understand the precursor of a pigment, a colourless body, which on oxidation will yield the pigment, and which can be again obtained by de-oxidising the pigment. But there is evidence that the katabolism of hamiatin can proceed in other organs or tissues than the liver. It is a commonplace of clinical knowledge that in febrile diseases the urine is 'highly coloured.' In recent years, largely due to M'Munn's work, it is known that this increased depth of pigmentation is the result of either an excess of normal urobilin or the presence of 'Pathological' (originally called ' Febrile') Urobilin in the urine. Now, in fevers we have increased tissue-change, a more than im^Wl^ int° C°l0Uring MatterS 0f Human Urine< Pro- ^ Soc,