a high-frequency antigen may be a challenge. Autologous donations should be encouraged.

Other sources of antigennegative blood may include family members and the rare donor registry. Fortunately, because these antigens do occur so frequently, it is rare to find a patient with an antibody to one of them. Antibodies to the so-called HTLA antigens also fall under this category. Although these antibodies are usually not clinically significant themselves, up to 25 percent of patients with an HTLA antibody also make clinically significant antibodies. 44 It is not necessary to determine the specificity of the HTLA antibody, but removal of these antibodies is usually necessary to identify any underlying alloantibodies. Some HTLA antibodies, notably anti-Ch and anti-Rg, may be neutralized by normal serum, which contains complement. Routine blood bank enzymes will destroy anti-Ch, -Rg, and -JMH, whereas anti-Kna and -McCa are destroyed by dithiothreitol (DTT).

Case Three: Antibody to a Low-Frequency Antigen

Low-frequency antigens are present in less than 10 percent of the population. Antibodies to these antigens are uncommon because exposure to the antigen is rare. The antibody screen will most likely be negative, therefore no panel will have been performed. Antibodies to these antigens should be suspected when an antiglobulin crossmatch is incompatible and other sources of explanation, such as ABO incompatibility or positive donor DAT, have been eliminated. These antibodies may also be suspected when an infant has a positive DAT and there is no known blood group discrepancy between mother and infant. Testing with additional antigen-positive cells will be required to confirm the specificity. Panel cells that are positive for these rare antigens are normally indicated on the panel profile sheet or listed on the extended typing form. In Figure 1217, positive reactions were seen only with cell 4 that matched the pattern of anti-Jsa. All other antibodies could be ruled out except for the other low-frequency, antiLua. Testing two other cells positive for the Jsa antigen to satisfy the 3 and 3 rule and phenotyping the patient for the Jsa antigen should be done to complete the antibody identification workup. If additional cells are not readily available, consult a reference laboratory. Because these antigens are infrequent, finding antigen-negative units for crossmatch is usually not difficult

Case Four: Cold-Reacting Autoantibodies

Most adult sera contain low titers of cold-reacting autoantibodies, most notably autoanti-I, -H, and -IH. These antibodies are usually IgM and of no clinical significance. They are troublesome in that they may interfere with the detection of significant antibodies, resulting in prolonged workups and delayed transfusions. Cold-reacting autoantibodies may be suspected when the screening cells, panel cells, and the autocontrol are all positive at the immediate spin phase and get weaker or disappear with incubation at 37_C (Fig. 1218). In this case, reactions were reduced at 37_C and were no longer apparent at the AHG phase. The use of cord blood cells, which lack the I antigen,

confirms the presence of anti-I in this sample. Certain autoantibodies may fix complement and are only detected at the AHG phase when using complement containing AHG reagent. These autoantibodies may be mistaken for weakly reacting IgG antibodies. Many laboratories avoid detection of cold autoantibodies by omitting the immediate spin phase of the antibody screen and by using monospecific anti-IgG Coombs serum. One of the least complex methods used to prevent