Neonatal jaundice historical perspective
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]
Overview
Historical Perspective
- In the 19th century, the authors of some pediatric texts described cases of yellowish discolouration in the newborns at which they named it "Icterus neonatorum". They described the condition of icterus neonatorum as benign self-resolved disease.
- Between 1885 and 1891, some medical records from the original Providence hospital showed several cases of icterum neonatourm through the first week of life.
- In 1940, the Rh body antigens were discovered and that's assured the genetic basis of the neonatul jaundice disease.
- Between 1940 and 1950, some studies were held on the hemolytic disease of the newborn in order to know the pathogenesis of neonatal jaundice. These studies had a great role in developing a good perinatal and neonatal care.[1]
- In 1950, Dr. London published an article describing the mechanism of bile degradation inside the human body.[2]
- In the 1960s, some pediatricians like Dr. John Barrett, Dr. Frank Giunta, and Edwin Forman formed consultation team for the newborns with jaundice in order to perform blood transfusion when needed.[3]
- In 1964, Dr. Arias was the first to describe the breast milk jaundice.[4]
- In 1968, it was the development of Rh antiglobin and it had been given during pregnancy. After that the Rh erythroblastosis has been a rare disease now.
History of the inhereted syndromes:
- Gilbert syndrome:[5]
- In 1901, Dr. Gilbert and Dr. Lereboulet described the Gilbert syndrome as a cause of neonatal jaundice.
- It is now considered as the most common hereditary cause of hyperbilirubinemia in the neonates.
- Crigler-Najjar syndrome:[6]
- In 1952, Dr. Crigler and Dr. Najjar describe the type one of this syndrome which is the abscence of UGT1A1 enzyme activity.
- In 1962, Dr. Arias described another variation of the syndrome at which the UGT1A1 enzyme activity is just reduced not abscent. The syndrome named either Crigler-Najjar syndrome type 2 or Arias syndrome.
- Lucey-Driscoll syndrome:[7]
- In 1965, Dr. Lucey described another cause of severe hyperbilirubinemia in the newborns during the first few days of life.
References
- ↑ LILEY AW (1965). "THE USE OF AMNIOCENTESIS AND FETAL TRANSFUSION IN ERYTHROBLASTOSIS FETALIS". Pediatrics. 35: 836–47. PMID 14277636.
- ↑ LONDON IM, WEST R, SHEMIN D, RITTENBERG D (1950). "On the origin of bile pigment in normal man". J Biol Chem. 184 (1): 351–8. PMID 15422003.
- ↑ Phibbs RH (1966). "Advances in the theory and practice of exchange transfusions". Calif Med. 105 (6): 442–53. PMC 1516609. PMID 5342893.
- ↑ ARIAS IM, GARTNER LM, SEIFTER S, FURMAN M (1964). "PROLONGED NEONATAL UNCONJUGATED HYPERBILIRUBINEMIA ASSOCIATED WITH BREAST FEEDING AND A STEROID, PREGNANE-3(ALPHA), 20(BETA)-DIOL, IN MATERNAL MILK THAT INHIBITS GLUCURONIDE FORMATION IN VITRO". J Clin Invest. 43: 2037–47. doi:10.1172/JCI105078. PMC 441992. PMID 14228539.
- ↑ Owens D, Evans J (1975). "Population studies on Gilbert's syndrome". J Med Genet. 12 (2): 152–6. PMC 1013257. PMID 1142378.
- ↑ CRIGLER JF, NAJJAR VA (1952). "Congenital familial nonhemolytic jaundice with kernicterus". Pediatrics. 10 (2): 169–80. PMID 12983120.
- ↑ ARIAS IM, WOLFSON S, LUCEY JF, MCKAY RJ (1965). "TRANSIENT FAMILIAL NEONATAL HYPERBILIRUBINEMIA". J Clin Invest. 44: 1442–50. doi:10.1172/JCI105250. PMC 292625. PMID 14332157.