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Annual Meeting—1968Midwest Society for Pediatric Research October 30–31, Chicago, Ill.
ABSTRACTS
Annual Meeting-1968 Midwest Societyfor Pediatric Research October 30-31, Chicago, Ill.
1. The mechanism of blue light on neonatal jaundice. S. O. Porto* and D. Y.-Y. Hsia, Chicago, IlL 2. Serum biliruhin binding determined by sephadex column chromatography. W. J. Keenan,* J. E. Arnold,* and J. M. Sutherland, Cincinnati, Ohio. 3. Hypoglycemia in severely affected Rh erythroblastotic infants. W. Oh, L. L. Yap, ~ and M. D. D'Amodio,* Chicago, Ill, 4. Initiation of breathing in fetal sheep: Appraisal of the role of systemic arterial mean pressure. V. Chernick, R. D. Pagtakkan,* and E. E. Faridy,* Winnipeg, Manitoba. 5. A defect in epinephrine synthesis in ascorhic acid-deficlent premature infants. I. J. Light, J. M. Sutherland, J. M. Loggie, and H. K. Berry,* Cincinnati, Ohio. 6. Congenital cytomegalovirus infection associated with low birth weight. J. Starr* and E. Gold, Cleveland, Ohio. 7. Studies of bactericidal activity and metabolism of the leukocyte in full-term infants. R. W. Coen,* O. C. Grush,* and E. Kauder, Cincinnati, Ohio. 8. Serum bacterial opsonins and polymorphonuclear leukocytes in mothers and newborns. J. H. Dossett and P. G. Quie, Minneapolis, Minn. 9. Rhinovirus infections in nursery school children. M. Beem, Chicago, IlL 10. Methotrexate liver toxicity. H. Sharp,* M. *By invitation. Asterisk indicates the same throughout;
Nesbit,* J. White, and W. Krivit, Minneapolis, Minn. 11. Metabolic data on the handling of NaCI by infants. C. F. Whitten, Detroit, Mich. 12. Initial hydrating solutions. S. Hellerstein and L. Surapathana,* Kansas City, Mo. 13. Plasma renin in Bartter's syndrome: Response of depression of stimuli for renin release. R. C. Kelsch,* G. W. Geelhoed,* A. J. Vander,* and W. J. Oliver, Ann Arbor, Mich. 14. Variations of diabetes insipidus associated with histiocytosis X. H. Helbock,* W. Krivit, and M. Nesbit,* Minneapolis, Minn. 15. Salivary gland enlargement and functional changes during feeding of pancreatin to rats (possible relationship to pathophysiology of cystic fibrosis). J. A. Mangos, P. J. Benke,* and N. R. McSherry,* Madison, Wis. 16. Metachromatic granules in cultivated fibroblasts derived from patients with genetic disorders. H. L. Nadler, Chicago, Ill. 17. Metabolic studies in a child with ring one chromosome. C. B. Wolf,* Detroit, Mich. 18. A case of glycogen storage disease. L. A. Reyes* and P. W. K. Wong,* Chicago, Ill. 19. Orotic aciduria in a girl with normal growth and development. D. G. Tubergen,* R. M. Heyn, R. S. Krooth,* Y. L. Pan,* and K. D. Wuu,* Ann Arbor, Mich. 20. Pyruvic acidemia with hyperalaninemia: Vitamin B 1 dependency. D. Lonsdale, W. R. Faulkner, W. Price, and R. R. Smeby, Cleveland, Ohio. VoL 74, No. 5, pp. ,311-834
8 12
Abstracts
21. Metabolism and serum protein binding of ZH-vitamin D~ in vitamin D-resistant rickets. H. Rikkers* and H. D e L u c a , * Madison, Wis.
22. Growth in familial hypophosphatemic vitamin D-resistant rickets. S. L. M c N a i r * and G. B. Stickler, Rochester, Minn.
23. Effect of surgery on cortisol secretion rate (CSR) in normal and steroid-treated children. N. F. Iturzaeta, ~ J. Fine, ~ C. Richards, r and F. Kenny, Pittsburgh, Pa. 24. Plasma testosterone and dehydroepiandrosterone sulfate during puberty. R. L. Rosenfield, ~ A. M. Bongiovanni,* and W. R. Eberlein, e Chicago, Ill. 25. Insulin reserve in children with chemical
1. The mechanism oJ blue light on neonatal iaundice S. O. Porto and D. Y.-Y. Hsia, Chicago,
Ill. This paper will describe in vitro and in vivo studies performed to determine the degradation products of bilirubin exposed to blue light. When solutions of bilirubin are exposed to blue light, the bilirubin peak at 435 mtz shifts to 380 In~ and there is an increase in the optical density in the 600 to 700 m# region. The solution turns green, indicating the formation of biliverdin. When solutions of bilirubin-albumin are similarly treated, there is only a gradual disappearance of the bilirubin peak at 460 m# and a slight change in the 600 to 700 m/~ region. The solution turns slowly into yellow-brown, but not green. If the Stokvis (pentdyopent) reaction is carried out, the bilirubin solution shows a slow and the bilirubin-albumin solutions show a rapid formation of a peak at 520 m/~, indicating the formation of sodium dipyrroles. When low birth weight infants exposed to blue light are compared with controls, there is a decrease of serum bilirubin, accumulation of dark brown pigments in the stool and urine, and a much stronger Stokvis reaction. The latter reaction is absent 'in the urine of adults and older infants and is increasingly positive in normal birth weight infants, low birth weight infants, and low birth weight infants treated with blue light. These observations indicate that the photooxidation of biiirubin results in the formation of dipyrroles which can be identified by their conversion to sodium dipyrroles by the Stokvis reaction. This mechanism of bilirubin disposal is particularly active when there is an excess of bilirubin formation, an immaturity or absence of the conjugating system for bilirubin, or when babies are exposed to light.
The Journal of Pediatrics May 1969
diabetes. D. Y. N. Murthy, ~ R. A. Guthrie, ~' W. N. Womack, ~ and R. L. Jackson, Columbia, Mo. 26. Partial exchange transfusion in sickle cell anemia: Viscosity determination as a guide to therapy. A. Sommer, r J. G. Bodenbender,* and S. B. Kontras, Columbus, Ohio. 27. Chronic granulomatous disease in females: evidence for dominant transmission. S. B. Kontras, J. G. Bodenbender, ~ R. L. Hintz, ~ and P. Azimi, ~ Columbus, Ohio. 28. Tyrosine hydroxylase activity in neurohlastoma. N. Sanpitak, ~ R. H. Kathan, ~ and I. Rosenthal, Chicago, Ill.
DISCUSSION DR. SV.OAR, Rochester. What was the size of your groups and was there a proportionate number of Negro babies in both groups? Second, were the differences significant ? DR. PORTO. We had 12 infants in each group, and one Negro in the control and one in the study group. The differences were significant on the fourth and fifth days of life, not in the first 2 days of life. DR. KRIVlT, Minneapolis. Was there any anemia associated with dipyrroles or a Heinz b o d y type anemia? Was there any evidence of red cell damage ? DR. PORTO. NO. We had hemoglobin and hematocrit determinations on all of these babies, and we didn't find any anemia. DR. HSlA, Chicago. There was also a series of studies done on older children with various hemolytic anemias, and all of the children with hemolytic anemias during the period of hyperbilirubinemia showed a positive Stokvis reaction. DR. RIKKERS, Madison. What is the specific wavelength of light that is effective, and are you aware of how far the light penetrates into the skin ? DR. PORTO. I don't know how far the light penetrates into the skin; I don't think it has been measured. The wavelength efficient for treatment is that emitted by a blue fluorescent lamp which is between 380 to 500 m#. This is exactly the area in which bilirubin is absorbed. The blue fluorescent lamp has a weak emission in the ultraviolet part of the spectrum, so there is no h a r m to the baby from this type of emission. The greatest emission of a fluorescent lamp is in the visual part of the spectrum, 380 to 600. DR. NACI-IMAN, Columbus. I wonder if the significance of this reaction differs among babies of different gestational ages. Have you looked at
Annual Meeting-1968 Midwest Societyfor Pediatric Research October 30-31, Chicago, Ill.
1. The mechanism of blue light on neonatal jaundice. S. O. Porto* and D. Y.-Y. Hsia, Chicago, IlL 2. Serum biliruhin binding determined by sephadex column chromatography. W. J. Keenan,* J. E. Arnold,* and J. M. Sutherland, Cincinnati, Ohio. 3. Hypoglycemia in severely affected Rh erythroblastotic infants. W. Oh, L. L. Yap, ~ and M. D. D'Amodio,* Chicago, Ill, 4. Initiation of breathing in fetal sheep: Appraisal of the role of systemic arterial mean pressure. V. Chernick, R. D. Pagtakkan,* and E. E. Faridy,* Winnipeg, Manitoba. 5. A defect in epinephrine synthesis in ascorhic acid-deficlent premature infants. I. J. Light, J. M. Sutherland, J. M. Loggie, and H. K. Berry,* Cincinnati, Ohio. 6. Congenital cytomegalovirus infection associated with low birth weight. J. Starr* and E. Gold, Cleveland, Ohio. 7. Studies of bactericidal activity and metabolism of the leukocyte in full-term infants. R. W. Coen,* O. C. Grush,* and E. Kauder, Cincinnati, Ohio. 8. Serum bacterial opsonins and polymorphonuclear leukocytes in mothers and newborns. J. H. Dossett and P. G. Quie, Minneapolis, Minn. 9. Rhinovirus infections in nursery school children. M. Beem, Chicago, IlL 10. Methotrexate liver toxicity. H. Sharp,* M. *By invitation. Asterisk indicates the same throughout;
Nesbit,* J. White, and W. Krivit, Minneapolis, Minn. 11. Metabolic data on the handling of NaCI by infants. C. F. Whitten, Detroit, Mich. 12. Initial hydrating solutions. S. Hellerstein and L. Surapathana,* Kansas City, Mo. 13. Plasma renin in Bartter's syndrome: Response of depression of stimuli for renin release. R. C. Kelsch,* G. W. Geelhoed,* A. J. Vander,* and W. J. Oliver, Ann Arbor, Mich. 14. Variations of diabetes insipidus associated with histiocytosis X. H. Helbock,* W. Krivit, and M. Nesbit,* Minneapolis, Minn. 15. Salivary gland enlargement and functional changes during feeding of pancreatin to rats (possible relationship to pathophysiology of cystic fibrosis). J. A. Mangos, P. J. Benke,* and N. R. McSherry,* Madison, Wis. 16. Metachromatic granules in cultivated fibroblasts derived from patients with genetic disorders. H. L. Nadler, Chicago, Ill. 17. Metabolic studies in a child with ring one chromosome. C. B. Wolf,* Detroit, Mich. 18. A case of glycogen storage disease. L. A. Reyes* and P. W. K. Wong,* Chicago, Ill. 19. Orotic aciduria in a girl with normal growth and development. D. G. Tubergen,* R. M. Heyn, R. S. Krooth,* Y. L. Pan,* and K. D. Wuu,* Ann Arbor, Mich. 20. Pyruvic acidemia with hyperalaninemia: Vitamin B 1 dependency. D. Lonsdale, W. R. Faulkner, W. Price, and R. R. Smeby, Cleveland, Ohio. VoL 74, No. 5, pp. ,311-834
8 12
Abstracts
21. Metabolism and serum protein binding of ZH-vitamin D~ in vitamin D-resistant rickets. H. Rikkers* and H. D e L u c a , * Madison, Wis.
22. Growth in familial hypophosphatemic vitamin D-resistant rickets. S. L. M c N a i r * and G. B. Stickler, Rochester, Minn.
23. Effect of surgery on cortisol secretion rate (CSR) in normal and steroid-treated children. N. F. Iturzaeta, ~ J. Fine, ~ C. Richards, r and F. Kenny, Pittsburgh, Pa. 24. Plasma testosterone and dehydroepiandrosterone sulfate during puberty. R. L. Rosenfield, ~ A. M. Bongiovanni,* and W. R. Eberlein, e Chicago, Ill. 25. Insulin reserve in children with chemical
1. The mechanism oJ blue light on neonatal iaundice S. O. Porto and D. Y.-Y. Hsia, Chicago,
Ill. This paper will describe in vitro and in vivo studies performed to determine the degradation products of bilirubin exposed to blue light. When solutions of bilirubin are exposed to blue light, the bilirubin peak at 435 mtz shifts to 380 In~ and there is an increase in the optical density in the 600 to 700 m# region. The solution turns green, indicating the formation of biliverdin. When solutions of bilirubin-albumin are similarly treated, there is only a gradual disappearance of the bilirubin peak at 460 m# and a slight change in the 600 to 700 m/~ region. The solution turns slowly into yellow-brown, but not green. If the Stokvis (pentdyopent) reaction is carried out, the bilirubin solution shows a slow and the bilirubin-albumin solutions show a rapid formation of a peak at 520 m/~, indicating the formation of sodium dipyrroles. When low birth weight infants exposed to blue light are compared with controls, there is a decrease of serum bilirubin, accumulation of dark brown pigments in the stool and urine, and a much stronger Stokvis reaction. The latter reaction is absent 'in the urine of adults and older infants and is increasingly positive in normal birth weight infants, low birth weight infants, and low birth weight infants treated with blue light. These observations indicate that the photooxidation of biiirubin results in the formation of dipyrroles which can be identified by their conversion to sodium dipyrroles by the Stokvis reaction. This mechanism of bilirubin disposal is particularly active when there is an excess of bilirubin formation, an immaturity or absence of the conjugating system for bilirubin, or when babies are exposed to light.
The Journal of Pediatrics May 1969
diabetes. D. Y. N. Murthy, ~ R. A. Guthrie, ~' W. N. Womack, ~ and R. L. Jackson, Columbia, Mo. 26. Partial exchange transfusion in sickle cell anemia: Viscosity determination as a guide to therapy. A. Sommer, r J. G. Bodenbender,* and S. B. Kontras, Columbus, Ohio. 27. Chronic granulomatous disease in females: evidence for dominant transmission. S. B. Kontras, J. G. Bodenbender, ~ R. L. Hintz, ~ and P. Azimi, ~ Columbus, Ohio. 28. Tyrosine hydroxylase activity in neurohlastoma. N. Sanpitak, ~ R. H. Kathan, ~ and I. Rosenthal, Chicago, Ill.
DISCUSSION DR. SV.OAR, Rochester. What was the size of your groups and was there a proportionate number of Negro babies in both groups? Second, were the differences significant ? DR. PORTO. We had 12 infants in each group, and one Negro in the control and one in the study group. The differences were significant on the fourth and fifth days of life, not in the first 2 days of life. DR. KRIVlT, Minneapolis. Was there any anemia associated with dipyrroles or a Heinz b o d y type anemia? Was there any evidence of red cell damage ? DR. PORTO. NO. We had hemoglobin and hematocrit determinations on all of these babies, and we didn't find any anemia. DR. HSlA, Chicago. There was also a series of studies done on older children with various hemolytic anemias, and all of the children with hemolytic anemias during the period of hyperbilirubinemia showed a positive Stokvis reaction. DR. RIKKERS, Madison. What is the specific wavelength of light that is effective, and are you aware of how far the light penetrates into the skin ? DR. PORTO. I don't know how far the light penetrates into the skin; I don't think it has been measured. The wavelength efficient for treatment is that emitted by a blue fluorescent lamp which is between 380 to 500 m#. This is exactly the area in which bilirubin is absorbed. The blue fluorescent lamp has a weak emission in the ultraviolet part of the spectrum, so there is no h a r m to the baby from this type of emission. The greatest emission of a fluorescent lamp is in the visual part of the spectrum, 380 to 600. DR. NACI-IMAN, Columbus. I wonder if the significance of this reaction differs among babies of different gestational ages. Have you looked at