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LOUIS A. BRUNSTING, M.D.; JOACHIM T. BRUGSCH, M.D.; PAUL A. O'LEARY, M.D.

Arch Derm Syphilol. 1939;39(2):294-307.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

The dermatologist's interest in porphyrin metabolism has been concerned mainly with abnormal formation and excretion of porphyrin in rare cases of chronic or congenital sensitivity to light.¹ It was first thought that hematoporphyrin was the porphyrin which accounted for the clinical symptoms of hydroa aestivale, as it could be shown that hematoporphyrin was possessed of photosensitizing powers when injected experimentally into animals² and into human beings.³ Later Fischer⁴ proved that hematoporphyrin, which is readily prepared in the laboratory from blood, does not appear to play any important role in porphyrin metabolism in nature. In a long series of investigations in the case of congenital porphyria of Petry, Fischer was able to show that the excreted porphyrins differed fundamentally from hematoporphyrin in the melting point of the esters and in a greater number of carboxyl groups in the molecule. These porphyrins were labeled uroporphyrin and coproporphyrin. Coproporphyrin, . . . [Full Text PDF of this Article]

Author Affiliations
Fellow in Biochemistry, the Mayo Foundation; ROCHESTER, MINN.

From the Section on Dermatology and Syphilology, the Mayo Clinic.

Footnotes
Now residing in Berlin, Germany.

Read before the Sixty-First Annual Meeting of the American Dermatological Association, Inc., Del Monte, Calif., June 10, 1938.

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