Hemolytic Disease of the Newborn Research Paper
Excerpt from Research Paper :
History of Pediatric Hemolytic Monitoring
Retrospect to the career of physician, Dr. James A. Wolff I and his early progress in treatment of Rh hemolytic disease as described in Pochedly (1984), looks at the development of interest in hematology in European field hospitals during World War II. After the war period, the transformation of Wolff's research in this area was advanced by research conducted during a pediatric residency at the Boston Children's Hospital, between 1945 and 1947. During his tenure at Children's he was engaged with Dr. Louis Diamond in his seminal investigation on treatment of erythroblastosis fetalis by exchange transfusion.
Collaborative efforts with Drs. Diamond and Farber focused on preliminary clinical trials of aminopterin for the treatment of acute leukemia, of which Wolff was in observation. Instrumental to the development of the concept of treating erythroblastosis fetalis by exchange transfusion; collaborative in the area of pathophysiology of disease where hemolytic conditions are found in the publication of work by colleagues, Drs. Philip Levine and Alexander Wiener. In those early studies, three techniques of exchange transfusion were implemented with Diamond's umbilical catheter technique succeeding in tests because of the ready insertion and multiple exchange facilitation made possible in what became the accepted method for treating infants diagnosed with erythroblastosis fetalis.
In Feldman and Tauber (1997), Sickle Cell Anemia: Reexamining the First "Molecular Disease" recount of the developments in molecular paradigms between 1910 and the 1950s, looks at the baseline research leading to medical classification of the pathophysiology of sickling, and definition of the term "sickle cell anemia;" used to designate two conditions: 1) hereditary predisposition to anemia occurring only in the 'negro race' characterized by crescentic distortion of the red corpuscles, and (2) chronic, severe anemia affecting only 'negroes' with this predisposition. Linus Pauling's (1949) seminal clinical study, offered foundation to molecular research on hemolytic disorders, showing that sickle cell anemia was due to an abnormal hemoglobin molecule.
Within subsequent studies, it was discovered that of a large group of the population that inherited the sickle cell trait, "an undetermined number, due to factors unknown, develop varying degrees" of sickle cell anemia "a hemolytic type of blood dyscrasia with characteristic clinical and pathological features" (Feldman and Tauber). Characterized by hemolytic jaundice, episodes of abdominal pain, and remissions and exacerbations including joint pains without inflammation and a tendency to ulcer in limbs, the persistence of the disorder found in predisposition where those affected by hemolytic anemia showed signs that the mechanism of sickle cell formation occurred in vitro.
Searching for a point of early intervention, attempts to distinguish between fetal and adult hemoglobin, Andersch, Wilson, and Menten (1944) conducted a clinical trial using a new electrophoretic technique. Although the two distinct hemoglobins had been identified through observation, according to the different rate of denaturation by alkali, the study sought information on how electrophoretic differences correlated to varying structure in the hemoglobin molecule. Using what was called a modified Tiselius apparatus, Andersch et al. tested the carbonylhemoglobin in infants ranging up to 90 days old, finding that hemoglobin types were present in varying degrees according to developmental stage, based on the hypothesis that "fetal hemoglobin is normally replaced gradually by adult hemoglobin in the first seven months of life" (Feldman and Trauber). Noting significant difference in the mobilities and in the sedimentation constants of adult and fetal hemoglobin the study confirmed the existence of two molecular species of hemoglobin in fetal and adult subjects, each differing in molecular protein constitution.
Since the studies of the mid-twentieth century, much has been done regarding diagnosis and treatment of fetal contraction of erythroblastosis, and attendant general hemolytic uremic syndrome (HUS) in infant and child patients. If the developments in molecular medicine have supported the definition and treatment of sickle cell anemia, the history of those developments has contributed greatly to knowledge on hemolytic pediatric medicine and to the History of Global Medicine more generally.
While quite a bit of the early research conducted on hemolytic related disorders is attributed to medical science in the United States and Western Europe, an important number of investigations outside the 'West' in recent decades has furthered pediatric knowledge of fetal molecular contraction and prevalence of hemolytic type of blood dyscrasia and attendant complications as patient populations in Africa, Asia, Eastern Europe, Latin America and the Middle East exhibit signs of associated autoimmune disorder or immunoregulatory abnormalities (serum imunoglobulins).
In Al Eisa and Al-Hajeri (2001) HUS was observed in twenty five, Kuwaiti Arab children in a longitudinal study from 1985 to 2000 in the P. Pediatric Nephrology Unit at Mubarak Al-Kabeer Hospital. Of the twenty five participants to the study, 14 patients (56%) exhibited typical (D+) HUS whereas 11 (44%) exhibited atypical (D-) HUS. Secondary symptoms were relatively absent, which is often not the case where HUS is diagnosed as part of spectrum of disorders, even where it is first called to the attention of physicians by way of a secondary diagnosis. In the Kuwait study, no bacterial or viral pathogens could be isolated in the majority of the cases.
Findings to the research reported that the atypical HUS group showed more severe anemia (P=0.03), significantly more prolonged in comparison with the typical HUS group (P=0.0028). However, there was no distinct indicators present between the two groups in terms of "mean maximum serum creatinine (P=0.1); blood urea nitrogen values (P=0.8) and severity of leukocytosis (P=0.4)" (Al Eisa and Al-Hajeri). Treatment factors such as anuria and the need for dialysis were not significant in outcome between the two groups, expressed as: P=0.1 and 0.05, respectively.
The incidence of mortality was significantly higher in the D- HUS patients (P<