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The Case of the Probable anti-Lw INTRODUCTION AND HISTORY 1940 - Landsteiner and Wiener injected Rhesus-monkey red blood cells into rabbits. They called this antibody anti-Rh 1941- Levine & Stetson's human antibody was shown to have the same pattern of reactivity as the rabbit anti-Rh antibody. 1942 - Fisk and Foord demonstrate a difference between rabbit and human anti-Rh. 1963 - Levin et al prove that human and rabbit anti-Rh do not react with the same antigen. 1982 - Lw is divided into a three antigen system Development of the Lw antigen system - The Lw antigen is independent of the Rh genes, but, in order to express itself, the Lw glycoprotein (ICAM 4) still requires interaction with the Rh protein. For example, Rh+ red cells express LW more strongly than Rh negative cells. - Initially a numerical system was used to identify Lw. E.g. LW1, 2 etc. - After the Nea gene was shown to be allelic to Lw, it was then renamed Lwa and Lwb. - Lw (a+b+) is defined by an alloantibody produced by an individual with an inherited Lw (a-b-) phenotype. - The null phenotype Lw (a-b-) is the result of a partial gene deletion and is extremely rare. Phenotypes and frequencies in Europeans: Reactions with Anti – Lwa Lwb Phenotype % + 0 Lw (a+b-) 97 0 + Lw (a-b+) 3 + + Lw (a+b+) Very rare 0 0 Lw (a-b-) Very rare FREQUENCY: In most populations, Lwa has a higher frequency, occurring in essentially 100% of donors, compared to Lwb which occurs in only 1–8% of Europeans. Characteristics of Lw: - Lw is expressed strongly on the red cells of neonates in equal amounts regardless of D type - Frequently appears as autoantibodies - IgM and IgG - Reactive at room temperature or on the IAT - do not bind complement - react to anti-human globulin - Resistant to papain, trypsin, sialidase and acid, but are sensitive to pronase and DTT. - are stimulated by blood transfusions CASE STUDY: - A 69 year old female patient with a history of cold agglutinin disease presented to Wollongong Hospital and was diagnosed with Waldenstom's Macroglobulinaemia. - Initial Group and Screen was O Positive with an anti – E, cold agglutinins and a C3d positive DAT on a pre-warmed sample. She then develops an anti-Jka, then an autoantibody and an IgG positive DAT. - A sample showing a preference for D+ cells was then sent to Red Cross to investigate a possible anti-D. - Their report indicated a possible anti – Lw specificity as the sample reacted against both D- and D+ cord cells. A negative reaction was also observed with an Rhnull cell. Specimen not signed - a new signed form and specimsen will be needed if blood products are required. CLINICAL SIGNIFICANCE Although no Lw antibody has been responsible for any serious HTR or HDFN it is still important to be careful about its possible identification. This is particularly important in women during their fertile period due to the need for anti-RhD prophylaxis. However, as is evident in this case study, they predominantly do not present clinical problems from a transfusion therapy perspective.