OTHER END PRODUCTS OF HEMOGLOBIN CATABOLISM 559 



it has been observed that this is not true in the pre-icteric stage 

 of infective jaundice (2160,299la,3110). Urobilinuria disappears 

 when biHrubin no longer reaches the intestine, to reappear once 

 more in the early stage of recovery. The use of quantitative urobih'n 

 estimations for diagnosis of jaundice and other liver diseases has 

 frequently been discussed and reviewed (1206,1207,2109,2110,2112, 

 2151, 298 ]f, 2988, 2990, 3082; cf. also Chapter IV, Section 9.2.). In 

 liver diseases the ratio of urinary to fecal urobilin is greatly increased 

 and may exceed unity {2989, p. 2500; 2988). 



9.3. Other End Products of Hemoglobin Catabolism 



9.3.1. Fecal Pigments. Watson found mesobiliviolin in the feces [cf. 

 Chapter IV, Section 5.2., and 2989, p. ^iST). It is probable that this is a 

 secondary oxidation product of mesobilane, and is formed during the extrac- 

 tion of the feces; occasionally appreciable amounts of final end products of 

 hemoglobin metabolism may escape determination in this form. 



"Stercofulvin" and "stercorubrin" have been observed in the feces by 

 Baar and Hickmans {107); little is known about their properties and nothing 

 about their constitution. 



9.3.2. Urinary Pigments. According to Heilmeyer {1007 ,1208,1209,1225, 

 209If) and Bingold (274,276), "urochrome B" is also derived from hemo- 

 globin. For the earlier literature on urochrome see Garrod (980,981). Uro- 

 chrome B is an ill-defined fraction of the yellow pigment of the urine which 

 can be precipitated by ammonium sulfate. It probably contains urobilin as 

 well as uroerythrin (2989,3024) ■ Heilmeyer found it increased in hemolytic 

 anemia, after administration of phenylhydrazine, and after hemoglobin 

 injections. From the fact that injections of hematin and bilirubin also 

 increased its excretion, he concluded that it is a breakdown product of the 

 prosthetic group of hemoglobin. Fischer and Zerweck (891), however, found 

 no pyrrole in urochrome, nor did Weiss (3024) in uroerythrin. Nothhaas 

 obtained a compound resembling urochrome B by the action of 30^ hydrogen 

 peroxide on hemoglobin; on tliis slender basis Bingold assumes that uro- 

 chrome B is formed from hemoglobin by the action of hydrogen peroxide in 

 the kidney, after the protective catalase has been left behind (cf. pentdyopent, 

 below). It has been pointed out by Watson (2989) that, unlike pentdyopent, 

 urochrome B occurs in normal urine. I'roerythrin does not occur in feces; 

 Weiss assumes that the cause of uroerythrin and increased urochrome B 

 excretion is liver dysfunction rather than increased hemoglobin breakdown. 

 None of these urinary pigments can represent more than an insignificant 

 proportion of the total sum of excretory products derived from hemoglobin _ 



9.3.3. Dipyrrolic Compounds. Pentdyopent. In a series of papers Bingold 

 (269-273,278) has claimed that pentdyopent (cf. Chapter IV, and Chapter X, 

 Section 9.) plays an important part as an end product of hemoglobin 

 catabolism. 



Pentdyopent does not occur in feces, duodenal contents, or normal urine. 



