Toxic porphyria.

By ARIF I. CETINGIL AND MUHLIS A. OZEN T HE EXCESSIVE porphyrin excretion seen in idiopathic disturbances of porphyrin metabolism must be differentiated from the porphyrinuria that occurs in various diseases associated with alterations in porphyrin metabolism. Porphyrinuria can he observed in the course of various diseases and may result from the intake of various drugs and poisons. It is well known that certain drugs and poisonS can produce porphyrinuria. Coproporphyrinuria was observed by Garrod in 1849 and by Stokvis in 1895 following lead intoxication. The porphyrinogenic action of sulfonal and related compounds was described by Salkowsky in 1891.1 Brownlee noted the porphyrinogenic action of certain aromatic groups in rats.2 Porphyrinuria was observed in man treated with sulfanilamide and in rats fed with sulfanilamides, other sulfa drugs and anilin.3’4 Coproporphyrinuria occurs following methyichioride intoxication.5 Occasionally it has been observed after administration of arsphenamine, barbiturates, choral, cinchophen and thiosinamine. The porphyrinogenic action of these drugs in man and animals usually consists in an increase of urinary and fecal coproporphyrin excretion. In the toxemia produced by trional and sulfonal, Ellinger and Riesser (1916) found in the urine uro-type porphyrins which are insoluble in ether. Later Fischer and Duesberg detected traces of similar etherinsoluble porphyrins in the urine of rabbits fed sulfonal.6 Waldenstr#{246}m and Wendt repeated these experiments with negative results.7 During the last few years, a new classification of human porphyria has been proposed based on the work done in the laboratories of Watson,8’9 which is as follows: