PORPHYRINS IN PATHOLOGIC EXCRETA 589 



feces (600,2986), meconium {2907,2908) and normal bile {2986) so 

 far only the type I isomeride of coproporphyrin has been isolated. 

 Uroporphyrin does not occur in normal feces and has also not been 

 found in the feces in porphyria, unless the ester of melting point 

 208°C., isolated by Watson and co-workers (3002) from feces in 

 acute porphyria is a uroporphyrin ester (c/. Chapter III). Uropor- 

 phyrin, being hydrophilic, is evidently not taken up by the liver, but 

 passes into the urine. By subcutaneous injection of coproporphyrin, 

 the coproporphyrin content of bile and feces was increased (Fischer 

 and Hilmer, 832), while only traces of injected uroporphyrin are 

 excreted in the feces (832,1070). 



3.3.4. Porphyrins in Pathologic Excreta. Porphyrinuria. A dis- 

 tinction is now drawn between porphyrinuria and the porphyrias. 

 Porphyrinuria is a symptom accompanying a variety of diseases, or is 

 caused by the intake of certain drugs and poisons. The copropor- 

 phyrin content of the urine is moderately increased, rarely above 

 1 mg. per day, in lead poisoning occasionally up to several mg. per 

 day. Porphyrias are rather rare congenital diseases in which the 

 excretion of porphyrin (or its precursor) is greatly increased and is 

 counted in milligrams rather than in micrograms. Here the porphyrin 

 consists predominantly of uroporphyrin. The classic patient of 

 congenital chronic porphyria, Petry, excreted no less than 200-600 

 mg. uroporphyrin per day. 



Occasionally complex salts of porphyrins have been found in the urine. 

 Porphyrins easily combine with traces of metal, hut there is reliable evi- 

 dence that the zinc salts of coproporphyrin and of uroporphyrin occur in 

 the unne(201427.659,U64,Uf>oJ01-J.^!)i0.2o06,2S37). The two absorption 

 bands of zinc coproporphyrin at .577 and .541 m^ can be mistaken for the 

 bands of oxyhemoglobin, l)ut are easily differentiated by acidification with 

 hydrochloric acid, which splits the zinc complex and develops the typical, 

 absorption spectrum of the porphyrin hydrochloride. 



Porphyrin excretion in the urine is increased in a large number of diseases, 

 in fever, liver diseases, anemias, polycythemia, pellagra, and skin and mental 

 diseases (cf. the review of Dobriner and Rh(5ads, 60S). In pernicious anemia 

 this was first observed by Taylor (27Jf(>) in 1897. The porphyrinuria in lead 

 intoxication was discovered early by Garrod (980) and Stokvis (2671). 

 Francke and Litzner ('JV>) found the porphyrin excretion to parallel the 

 degree of lead intoxication so exactly tiiat they suggested porphyrin estima- 

 tions as a means of studying progress in lead poisoning. 



The porphyrinogenic action of sulfonal and related drugs was discovered 

 even before that of lead by Salkowsky {2JtlS\ cf. also 383, 2041, U64)- Bar- 



