PEDIATRICS Vol. 15 No. 5 May 1955, pp. 553-561
This Article
Right arrow Full Text (PDF)
Right arrow P3Rs: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when P3Rs are posted
Right arrow Alert me if a correction is posted
Services
Right arrow E-mail this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My File Cabinet
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nevé, R. A.
Right arrow Articles by Aldrich, R. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nevé, R. A.
Right arrow Articles by Aldrich, R. A.

PORPHYRIN METABOLISM. III. URINARY AND ERYTHROCYTE PORPHYRIN IN CHILDREN WITH ACUTE RHEUMATIC FEVER

Richard A. Nevé M.S.1 and Robert A. Aldrich M.D.2

1 The Department of Pediatrics, University of Oregon Medical School, Portland, Oregon.
2 The Department of Biochemistry, University of Oregon Medical School, Portland, Oregon.

1. Urinary coproporphyrin excretion of children with acute rheumatic fever is greatly increased above normal.

2. The coproporphyrin isomer isolated from urine of 15 rheumatic fever patients and 38 normal children was predominantly Type III.

3. Free erythrocyte protoporphyrin and coproporphyrin values from circulating erythrocytes of children with acute rheumatic fever were normal.

4. The Type III coproporphyrinuria of acute rheumatic fever approximately follows the fall in plasma mucoproteins during convalescence.

5. Non-toxic doses of salicylates given to rheumatic children for long periods have no significant effect on urinary coproporphyrin excretion.

6. The highest urinary excretion of coproporphyrin noted in this study was obtained from a child 2 days before the appearance of signs and symptoms of rheumatic fever following scarlet fever.

7. The liver, rather than the bone marrow, is proposed as the site of the biochemical disturbance responsible for coproporphyrinuria in rheumatic fever.

8. New information on the interrelationships between purine and porphyrin biosynthesis through delta-aminolevulinic acid affords a basis for the hypothesis offered as an explanation for the mechanism of this coproporphyrinuria.

Submitted on February 12, 1955