1896-97.] Mr D. F. Harris on Haemaloporphyrinuria. 389 
of urobilin or pathological urobilin, which also occurs in acute 
muscular rheumatism and in other fevers. 
[The presence of an increase of urobilin in febrile urine may 
possibly be due not only to an excessive initial production of 
pigment-antecedent normally oxidised to urobilin, but also to a 
diminished reduction to chromogen by the relatively inactive renal 
epithelium.] 
Tissue, other than hepatic, can katabolise blood-pigment, but 
urobilin is not always the end-product — the initial reduction may 
not proceed so far as that. These other tissues may be included 
under three heads : — 
I. muscles ; II. skin ; III. connective tissues, with bones, 
cartilages, etc. Now, it is of blood from these three systems, in 
addition to the hepatic supply, that the blood in the right auricle 
may be chemically viewed as constituted : blood from these four 
sources contributes to arterial and therefore renal blood. 
Under certain diseased conditions of one or more of these three 
systems, urohaematoporphyrin replaced urobilin in the urine, 
notably in acute rheumatism (muscular and articular), effusion of 
blood into the peritoneum, and Addison’s disease ; but the follow- 
ing is a complete list of M‘Munn’s cases,* with the seats of de- 
praved metabolism indicated (as above numbered) : — 
Acute rheumatism (I. and III.) 
Pericarditis 
Peritonitis 
Meningitis 
Cirrhosis of liver 
Peritoneal blood effusion 
Croupous pneumonia. 
Typhoid fever 
Measles 
Addison’s disease 
Hodgkin’s disease. 
Sulphonal overdosing.! 
The less de-oxidised ally, meio-de-oxyhaematoporphyrin, has 
appeared as the pigment on one or two occasions — twice in obscure 
* Journal of Physiology, vol. x. 
t Oswald, Glas. Mecl. Journal , 1895. 
(in.) 
1 
r (ii.) 
