PHOTODYNAMIC ACTION 717 



hydroa and presumed that faulty technique was responsible for failure to 

 reproduce the natural syndrome. 



Numerous attempts have been made to resolve some of these apparent 

 inconsistencies, but none has proved satisfactory. For example, expla- 

 nations based on the occurrence of the porphyrins in the tissues as color- 

 less precursors, on protection by pigments such as urofuscin, or on the 

 variation of the photosensitizing power of different porphyrins all fail to 

 account for the difference between hydroa lesions and those resulting from 

 photosensitivity. 



The relation of porphyrin metabolism to diseases of the skin was 

 reviewed by Turner and Obermayer (1938) and by Brunsting et al. 

 (1939), and the general conclusion from both reviews is that there has 

 been no clear demonstration that porphyrin photosensitization is directly 

 responsible for the skin lesions seen in diseases involving a derangement 

 of porphyrin metabolism. Essentially the same conclusion was drawn 

 by Blum (1941a) in a comprehensive discussion of attempts that have 

 been made to reproduce these lesions experimentally and to determine 

 action spectra. 



Blum and Pace (1937) could not elicit typical symptoms in a patient 

 with hydroa vacciniforme by exposure to sunlight or to artificial sources 

 of radiation. In the course of these experiments, however, one of the 

 normal subjects, in whom local reactions had been produced by injection 

 of hematoporphyrin and repeated exposure to sunhght, developed papulo- 

 vesicles 9 weeks later at the site of injection. Blum (1941a) suggested 

 that these lesions may be similar to those obtained by Meineri (1931), 

 who found that successive exposures of a hydroa patient to light did not 

 give lesions directly but made the skin more sensitive to slight trauma. 

 Blum considered that Meineri's explanation of the development of 

 hydroa-like lesions is the one most consistent with the known evidence 

 and justifies further study. Whether such increased sensitivity to 

 trauma can be a delayed result of photodynamic action when other 

 reactions are not elicited has yet to be determined. 



The whole subject of the relation of endogenous porphyrins to photo- 

 sensitivity diseases remains in an unsatisfactory state. Although the 

 ability of certain porphyrins (more especially the artifact hematopor- 

 phyrin) to produce photosensitivity is well estabhshed, there appears to 

 have been no clear demonstration of photodynamic action by porphyrins 

 in any of the diseases of man. Too frequently investigators of photo- 

 sensitivity in such diseases have made no attempt to determine the 

 nature, isomeric type, and amount of the porphyrins in the urine and 

 blood of their patient — observations that may influence future interpre- 

 tation of their work — and those interested in porphyrin metabolism have 

 often neglected the photosensitivity. This subject well illustrates the 

 need, in all work on photodynamic action, for careful experiments along 



