The Duffy Blood Group System in Transfusion Reactions: A Review of the Literature and Report of Four Cases

1. The literature on the incidence and inheritance of the "Duffy" bloodgroup factors and their significance in blood transfusion and erythroblastosisfetalis is briefly reviewed.

2. Four new cases in which anti-Fy^a was detected are reported.

3. The necessity for the use of the Coombs’ compatibility test with apotent Coombs’ serum to prevent reactions due to anti-Fy^a is re-emphasized.

4. The inadequacy of a 15 minute incubation period for the Coombs’ compatibility test in certain cases is noted.

5. The desirability of specific identification of an antibody detected ina patient’s serum prior to transfusion whenever possible is suggested.

Submitted on January 31, 1959 Accepted on March 18, 1959     

The Lutheran blood groups: a second example of anti-Lu b and three further examples of anti-Lu a

1. An example of the blood group antibody, anti-Lu^b, was found in a patientwho had a mild hemolytic transfusion reaction. It was shown to possess thecharacteristics of an immune antibody and to be able to distinguish between asingle dose and a double dose of the Lu^b gene.

2. Three new examples of the antibody, anti-Lu^a, are presented. All of themwere found in normal blood donors and have properties which indicate that theyare naturally occurring antibodies.

Dr. R. R. Race and Dr. R. Sanger confirmed the presence of anti-Lu^b in Mrs. S.’sserum, and studied other members of her family and the three anti-Lu^a sera. We aregrateful to them for many favors and their kind encouragement.

We are obligated to Miss Marie Cutbush for making available the Lu^aLu^a cells fromMrs. R. and her sister, and for a supply of anti-Lu^b serum.

Thanks are due to Dr. A. E. Mourant who furnished our original supply of anti-Lu^aserum and to Dr. Philip Levine for the anti-Tj^a and anti-Vel sera.

We are indebted to Dr. J. M. Fine of Milwaukee for permission to study Mrs. S. andto the patient and her family for their cooperation.

The sera from 18,613 blood donors were studied by Betty McCarthy, Rosemary Polka,Pearl Lemke, Agnes Molnar, Jeannette Flagstadt and Betty Hutter.

Submitted on March 20, 1957 Accepted on July 1, 1957     

Acquired Hemolytic Anemia with Polyagglutinability of Red Blood Cells Due to a New Factor Present in Normal Human Serum (Anti-Tn)

A case of acquired hemolytic anemia of 12 years’ duration showing a permanent polyagglutinability for at least 9 years, is presented.

1. Polyagglutinability is due to the presence on the surface of the patient’serythrocytes of an antigen unknown up to the present time, which is independent of antigens T and H and does not behave like a normalantigen modified by proteolytic enzymes. It has been designated by theletters Tn. The Tn substance is not secreted in saliva. This antigen has notbeen found on the erythrocytes of 25 members of the patient’s family.

2. The substance which induces agglutination (natural anti-Tn) was foundto be present in the serum of 473 white adults and 33 adult Negroes. Itwas absent or weak in 28 sera from cord’s blood. It acts like a completeantibody, being active in saline at the temperature of laboratory and theninducing massive clumping of Tn red cells. Through absorption and elutionstudies and through sensitization in rabbits, we have been able to demonstrate that anti-T and anti-Tn are distinct.

3. There are in our patient’s serum: (a) a substance specifically activeagainst Tn erythrocytes treated by trypsin; this may be an immune anti-Tn; (b) a nonspecific incomplete antibody weaker than the anti-Tn andactive against all varieties of red cells treated by trypsin; (c) an incompleteanti-E; (d) a cold antiplatelet substance; and (e) an immune antileukocyteantibody.

These three last antibodies are very probably due to transfusions.

4. To explain the combination of an acquired hemolytic anemia and polyagglutinability, two hypotheses are presented: (a) The acquired hemolyticanemia has no relationship to the existence in the patient of a very raregroup antigen, perhaps confined to one family. (b) The hemolytic anemiais directly related to the existence of the Tn antigen on our patient’s red cellsand is due to the development of an immune anti-Tn antibody against theTn antigen, this last antigen being either a group antigen or an antigenrevealed or modified by the causal agent of the disease.

Submitted on June 18, 1958 Accepted on April 27, 1959     

Severe Mediterranean anemia (Cooley's anemia) in a Chinese child

1. The fifth known case of Cooley’s anemia in a Chinese child is reported. Deathoccurred following a febrile illness which was thought to be mumps encephalitis.Autopsy findings were consistent with this diagnosis and with Cooley’s anemia.

2. The remainder of the family showed the characteristic blood findings ofCooley’s trait.

     

Studies in Bisalbuminemia: Binding Properties of the Two Albumins

1. An abnormal serum protein pattern in a patient with Wegener’s granulomatosis and five of his relatives was identified as bisalbuminemia by electrophoretic and immunochemical methods.

2. With the exception of the patient with Wegener’s syndrome, the presenceof bisalbuminemia was not associated with a significant change in total serumproteins, total albumin, serum components other than albumin, or any disease.

3. Addition of I¹³¹-thyroxine to bisalbumin sera resulted in thyroxine binding by albumin B but not by albumin A. The failure of albumin A to bindadded I¹³¹-thyroxine leads to speculation that, in this family, neither albuminA nor B are identical to normal human serum albumin.

Submitted on December 4, 1961 Accepted on April 17, 1962     

The mechanism of the anemia associated with Hodgkin''s disease

1. The survival of autotransfused Cr⁵¹-tagged erythrocytes was shortenedin a group of five patients with the anemia of Hodgkin’s disease, but since thenormal marrow is believed to be capable of compensating for destruction ratesof six to eight times greater than normal, it is felt that the increased rate ofhemolysis was not sufficient to account for the development of anemia in anyof these patients.

2. There was evidence of an increased rate of erythropoiesis in all of thepatients with Hodgkin’s disease. This was manifested by normoblastic hyperplasia of the marrow, a moderate reticulocytosis and increased plasma ironclearance rates. The shortened red cell survival times were associated withthe increased plasma iron clearance rates. However, in view of the fact thatall of the patients were anemic, it is evident that these patients were incapableof increasing the rate of red cell production sufficiently to compensate for theincreased rate of destruction.

3. Intravenously injected Fe⁵⁹ citrate was incorporated more rapidly intothe circulating red cell mass in the patients with Hodgkin’s disease than inthe normal subjects.

4. The tissue iron stores of the liver and spleen were greatly increased,but no iron was demonstrated in the marrow of a group of seven patientswith Hodgkin’s disease.

5. The plasma iron was low and the UIBC normal in a group of 12 patientswith active Hodgkin’s disease.

6. It is suggested that one of the factors which limits the ability of themarrow to produce hemoglobin in the anemia of Hodgkin’s disease may be arelative hypoferremia caused by a defect in the mobilization of iron from tissuestores.

Submitted on April 17, 1958 Accepted on February 2, 1959     

Biochemical Lesion in Dilantin-Induced Erythroid Aplasia

Clinical and biochemical studies are reported in a patient who developedpure red cell aplasia after 2 years therapy with Dilantin but in whom aplasiacould subsequently be induced with 4-5 Gm. of the drug. Recovery occurredregularly when the drug was discontinued.

The administration of 1500 ml. of patient’s plasma obtained during theaplastic phase to a normal volunteer with Dilantin had no effect on the recipient’s reticulocyte count, number of nucleated red cells in his bone marrow,or Fe⁵⁹ clearance. Attempts to demonstrate binding of gamma globulin tothe patient’s nucleated red cells in the presence of Dilantin by immunofluorescence technic were unsuccessful.

Dilantin, in a concentration of 20 µg./ml. in vitro, caused significant inhibition of the uptake of C¹⁴ formate, glycine, adenine, orotic acid, and uridine intoDNA but not into RNA of patient’s bone marrow studied when fully recovered. There was no effect on the uptake of deoxyuridine or thymidine.

The Dilantin effect was specific to the erythroid cells as shown by radioautographic studies and by the absence of inhibition when these cells wereabsent from the bone marrow.

Vitamin B₁₂ and folinic aci dgiven to the patient in large doses did notreverse the hematologic effects of Dilantin. The daily intravenous administration of all four deoxyribonucleosides, deoxyadenosine, deoxyguanosine, deoxycytidine and thymidine had a suggestive, but not clear-cut, effect.

In an effort to examine a possible relationship of the pure red cell aplasiain this patient to riboflavin metabolism, the patient was started simultaneouslyon Dilantin and riboflavin. Dilantin was now without effect. However, thepatient remains refractory to Dilantin a year after riboflavin was discontinued.

It is concluded that Dilantin exerted its toxic effect in this patient byspecifically inhibiting DNA synthesis in erythroid cells probably at the stepof deoxyribotide formation.

The role of riboflavin in the development of resistance to the toxic effect ofDilantin in this patient remains uncertain.

Submitted on January 19, 1967 Accepted on May 5, 1967     

Studies on abnormal hemoglobins. VI. Electrophoretic demonstration of type S (sickle cell) hemoglobin in erythrocytes incapable of showing the sickle cell phenomenon

1. A family is reported in which 2 children have unmistakable sickle cellanemia, but the mother’s red cells do not sickle; the father and a third childexhibit the typical sickle cell trait. Electrophoretic studies of the hemoglobinsolution prepared from the mother’s erythrocytes demonstrated, however, thepresence of a small amount (5 per cent) of type S hemoglobin. This abnormalcomponent was identified by its mobility and by addition experiments.

2. The finding that the mother’s erythrocytes contain small quantities of Shemoglobin, but are incapable of sickling, confirms the genetic concept thatsickle cell anemia will only develop when both parents transmit the gene for Shemoglobin.

3. The physico-chemical and possible medico-legal aspects of the fact that Shemoglobin is sometimes only detectable by means of electrophoresis, are discussed.

Submitted on August 5, 1952 Accepted on September 10, 1952     

The Course of Experimentally Induced Hemolytic Anemia in a Primaquine-Sensitive Caucasian: A Case Study

Two severe hemolytic crises, in a month’s period, were induced by primaquine in a glucose-6-phosphate dehydrogenase deficient Sardinian male.

Young red blood cells tagged with Fe⁵⁹ 10 to 16 days earlier were destroyedin the second hemolytic episode.

The implications of these experiments on the nature of drug-induced hemolysis in Caucasians are briefly discussed.

Submitted on February 24, 1964 Accepted on April 24, 1964     

The genetic relation and clinical differentiation of Cooley's anemia and Cooley's trait

1. Four additional families illustrating the clinical and genetic relationshipsof Cooley’s anemia and Cooley’s trait have been presented.

2. Blood findings in an offspring of a patient with Cooley’s anemia are recorded.

3. The asymptomatic nature of Cooley’s trait and its differentiation fromCooley’s anemia has been emphasized.

4. The inheritance of Cooley’s trait and Cooley’s anemia may be best explainedin terms of an incomplete dominant or of the simultaneous appearance of twononallelomorphic genes.

Note: ACKNOWLEDGMENTWe are indebted to Dr. John H. Linner for many of the observations on the Ca family and to MissClara Gillette for observations on the Cr family.

     

Erythrokinetics in Cooley''s anemia

Blood production and destructions have been measured in four patients withCooley’s anemia. Methods employed included the determination of erythroid/myeloid ratio of the marrow, reticulocyte count, plasma iron turnover and redcell utilization, Cr⁵¹ survival and fecal urobilinogen. Rates of production obtainedby these measurements have been compared to normal.

Patients with Cooley’s anemia have been shown to have an increased turnover of hemoglobin constituents comparable to the maximal response seen inother hemolytic anemias. There is, howvever, a marked decrease in maximaldelivery of erythrocytes to the peripheral blood amounting to about 50 per centin the mildly anemic patients and 85 per cent in severely anemic patients. Therate of destruction of circulating erythrocytes was similar in the three patientsstudied. The severity of anemia was therefore largely related to the productiondefect.

It was concluded that the defect in Cooley’s anemia is not in total hemoglobin synthesis, but in the fabrications of circulating erythrocytes, which inturn have the associated manifestations of hypochromia, increased percentageof fetal hemoglobin and shortened survival time.

Submitted on May 23, 1956 Accepted on June 25, 1956     

Chediak''s anomaly of leukocytes in malignant lymphoma associated with leukemic manifestations: case report with necropsy

A case of Chediak’s anomaly of leukocytes was described, the fourth reported in the literature.

The patient was an 11-month-old boy who, in addition to Chediak’s anomalyof the leukocytes, presented a leukemic blood picture.

He died five days after admission to the hospital, and necropsy revealeda malignant lymphoma.

We consider it possible that in all the reported cases there were generalizedpathologic changes in the reticulohistiocytic system.

Submitted on December 3, 1957 Accepted on May 15, 1958     

Quantitative Serologic and Isotopic Studies on the Rho Variant--Du

1. Type D^u cells take up less than 10 per cent of the I-131 anti-D boundto D positive cells, so that the quantity of cell bound I-131 did not differ significantly from that bound nonspecifically to D negative cells.

2. Papain modification of D^u cells results in an almost threefold increasein the uptake of I-131 anti-D, whereas, D negative cells show no consistentincrease after such treatment. Enzyme modification, therefore, serves to clearlydelineate the two cell types.

3. The range of uptake of I-131 anti-D to enzyme treated D^u cells is fromapproximately 7 to 17 per cent of that by R₁R₂ cells. Most of these results wereobtained from studies on Mendelian D^u types. Studies on several bloods frommembers of a family having Rh genotypes typical of the "gene interaction" D^uconfiguration (C in transposition to D) revealed no significant reduction inI-131 anti-D uptake when compared with D positive cells.

4. Decreased antibody binding to D^u cells was confirmed by the serologicmethods used. Absorption of an anti-D serum and antiglobulin inhibitionwith sensitized D^u cells indicated that the quantity of D antigen was lessthan that observed with the isotopic technic. Elution studies did not show asmarked a reduction of D antigen on the D^u cell as the other serologic technicsindicated. Possible reasons for these differences have been discussed.

5. Although, from both the serologic and isotopic studies, the data indicate that the type D^u red cell is quantitatively deficient in D antigen, theyare inadequate to rule out other explanations for their reduced D antigenactivity. Irrespective of the mechanism(s) responsible, the effective bindingof anti-D by D^u cells is reduced several fold; this would appear to be theprimary cause of the weak second stage of red cell antigen-antibody reactionwhich characterizes type D^u blood.

Submitted on July 28, 1964 Accepted on October 8, 1964     

Studies on the anemia of disseminated malignant neoplastic disease. II. Study of the life span of the erythrocyte

1. A study of the life span of the erythrocyte in patients with advanced neoplastic disease was performed by transfusing blood from 23 hospitalized patientsinto 53 healthy volunteers.

2. The Ashby technic for red cell labeling was used alone in 16 instances, Cr⁵¹technic in 52 instances, and a combination of the 2 technics in 8 instances.

3. Normal or nearly normal life spans were suggested by the slopes of curvesin 15 instances where whole blood from patients was transfused into volunteers.

4. Some shortening of the life span of the patient’s red cells was noted whenthese cells, separated from the plasma, were transfused into volunteers or backinto patients, possibly related to the handling during plasma removal.

5. Control studies using either Cr⁵¹ or Ashby labeling technic indicated anormal life span of approximately 120 days in the volunteers employed could beachieved by each method.

6. Values obtained with Cr⁵¹ were so similar to those using Ashby labeling thatthe easier Cr⁵¹ technic is recommended for future studies.

7. The normal erythrocyte transfused into patients with neoplastic diseasemay have a moderate to considerably shortened life span.

8. These studies seem to demonstrate an absence of an intrinsic defect in theerythrocytes of patients with neoplastic disease, and further favor the presenceof a hemolytic plasma factor of considerable importance in the pathogenesis ofthe anemia of cancer.

Submitted on August 27, 1955 Accepted on January 4, 1956     

Further Cases of Hb Q-H Disease (Hb Q-agr Thalassemia)

Case reports of four patients, all Chinese, with Hb Q-H disease—also calledHb Q- thalassemia—are presented. Three were siblings. Symptoms of chronichemolytic anemia with jaundice and hepatosplenomegaly were present in allfour subjects. The red blood cells were microcytic. Slight hypochromia waspresent in three of the cases. Poikilo- and anisocytosis with target cells andsmall intraerythrocytic crystals were found in the blood. Starch-gel electrophoresis revealed the presence of a large amount of Hb Q, a small amount ofHb H, and a minor slow-moving hemoglobin component with a mobility asmuch behind Hb A₂ as Hb Q was behind Hb A. A small amount of Hb "Bart’s"was probably also present. The minor slow-moving component was thought torepresent Hb ₂^Q₂^A₂ or Hb Q₂. Hb A and Hb A₂ were not seen except afterrecent blood transfusion. Study of hemoglobin polypeptide chains showed thepresence of normal ^A-chains and abnormal ^Q-chains, without demonstrable^A-chains in the first three patients. In Patient #4 normal ^A-chains weredemonstrable only after recent blood transfusion. The mother of the threesiblings was heterozygous for Hb A; the father had -thalassemia trait.

Submitted on September 7, 1965 Accepted on April 23, 1966     

Studies concerning the pathogenesis of Gaucher's disease

1. The serum of normal individuals and of patients with Gaucher’s disease doesnot contain cerebrosides in measurable amounts. Cerebrosides in Gaucher’s diseaseare increased only in those organs containing abundant numbers of cells characteristic of the disease.

2. Normal red blood cells contain approximately 0.19 per cent cerebrosides. Thecerebroside in red blood cells is a galactosidocerebroside.

3. Red blood cells in Gaucher’s disease do not differ quantitatively and qualitatively in their cerebroside content from the red blood cells of normal individuals.

4. In four different cases of Gaucher’s disease separate determinations of splenicgalactosido- and glucosidocerebrosides were made. The spleen of two adultsshowed mainly glucosidocerebrosides and only traces of galactosidocerebrosides,while the analysis of the spleen of two other adults showed that galactosido- aswell as glucosidocerebrosides may be accumulated simultaneously in Gaucher cells.These findings are of importance, since it is demonstrated that the deviation of thecerebroside metabolism in Gaucher cells not only results in the formation of anabnormal glucosidocerebroside, but also may lead to the increased formation ofthe normal galactosidocerebroside, kerasin. It is demonstrated that the relativeproportions of galactosido- and glucosidocerebrosides in Gaucher cells may differconsiderably in individual cases.

5. The organs of infantile siblings with "generalized infantile Gaucher’s" disease were analyzed. The organs of one infant showed mainly galactosidocerebrosides while in the organs of the other sibling both kinds of cerebrosides, glucosido- as well as galactosidocerebrosides, were present.

6. The findings reported in this paper lend support to the theory that Gaucher’sdisease is the result of a deviation of the intracellular metabolism of reticulum cellsand histiocytes. The cerebrosides are not transported by the serum or by the redblood cells and secondarily deposited in the cells involved, but are formed andstored in the reticulum cells and histiocytes were they are found.

     

Thalassemia in Jews from Kurdistan

1. Seven cases of Cooley’s anemia in Jews from Kurdistan residing in theJerusalem area are presented with family studies. Four homozygous cases weresevere and progressive. One ended fatally and the remaining 3 were kept aliveby frequent blood transfusions. Three heterozygous cases showed a mildercourse.

2. It is suggested on the basis of these and other observations that the Jewsof Kurdistan constitute a hitherto unknown reservoir of the genetic abnormalityresponsible for Cooley’s anemia.

Submitted on March 30, 1954 Accepted on July 25, 1954     

The Antigenicity of Normal and Leukemic Human Leukocytes

1. A leukoagglutinin was formed in the serum of a normal human subjectwho received 10 intravenous injections of blood from a single patient withchronic myelogenous leukemia over a period of 20 weeks.

2. Coincident with development of the leukoagglutinin, first detectable oneweek after the fifth injection of leukemic blood, the normal subject experiencedprogressively more severe febrile reactions to the infusions and exhibited acharacteristic pattern of leukocyte response—namely, an immediate transientleukopenia, followed by a leukocytosis which reached its peak around 3 hoursand subsided to normal within 12 hours.

3. During the early part of the investigation immature leukocytes, presumably from the leukemic donor, could be identified in the recipient’s circulationduring the first hour immediately following injection, but none could befound following the tenth infusion of leukemic blood.

4. The leukoagglutinin which appeared in response to the injections of bloodfrom the single leukemic donor was a typical iso-antibody, showing a broadpattern of reactivity against normal leukocytes from 127 of 129 donors, leukemicleukocytes from 5 of 5 patients with chronic myelocytic leukemia and 6 of 6patients with chronic lymphocytic leukemia. No reactivity was observed againstthe recipient’s own leukocytes, and little or no reactivity was demonstrableagainst the immature leukocytes from 3 patients with acute leukemia.

5. Eighteen months after the last injection of leukemic blood, restimulationof a leukocyte iso-agglutinin in the previously immunized recipient was provoked within one week of commencing a series of intravenous infusions ofblood from a single normal donor.

6. The volume of normal leukocytes employed for the restimulation was 1/10to 1/100 the volume of leukemic leukocytes employed for the primary immunization.

7. The concept of antibody excess was demonstrable in the sensitized recipient. No evidence of in vivo absorption of leukoagglutinin activity was observedafter transfusion of 500 ml. of blood from the normal donor. The severity ofthe recipient’s reaction to the transfused blood was clearly related to the doseof donor leukocytes administered, 0.47 billion cells causing no reaction but4.16 billion causing a moderately severe reaction.

8. Fifteen months after completion of the injections of normal blood, reexposure of the normal subject to injections of blood from a second leukemicdonor resulted in prompt restimulation of leukoagglutinin activity in therecipient’s serum.

9. The leukoagglutinin could be completely absorbed in vitro by incubationwith donor leukocytes.

10. The leukoagglutinin was concentrated in the gamma globulin fraction ofthe recipient’s plasma.

11. The recipient exhibited typical symptomatic reactions and transient hematologic changes following the infusions of leukemic blood.

12. It was possible to correlate the severity of the recipient’s clinical reactionsboth with the strength of the recipient’s leukoagglutinin, as well as with thedose of donor leukocytes transfused.

13. Serologic observations, plus the results of fractionated transfusion studies,indicated that the recipient’s transfusion reactions were related to sensitivityto the donor’s buffy coat (Part II), and more specificially to donor leukocytes(Part III), rather than to donor plasma, platelets or erythrocytes.

14. Sustained stimulation of the recipient’s white cell count as a result of theinjections of leukemic blood was not observed.

15. There has thus far been no evidence of transmission of leukemia to therecipient (now 6 years after the first course of injections of leukemic bloodand 2 years since completion of the present study).

Submitted on July 15, 1960 Accepted on November 20, 1960     

Separation of Lymphocytes, Polymorphonuclear Leukocytes and Monocytes on Glass Columns, Including Tissue Culture Observations

A procedure was described for the separation of lymphocytes, polymorphonuclear (PMN) leukocytes and monocytes on Garvin’s glass bead columns. Dextran-sedimented leukocyte suspensions were added to columnsand incubated at 37 C. Lymphocytes were eluted with fresh serum. Thecolumns were then washed completely free of erythrocytes, platelets andlymphocytes while PMN leukocytes and monocytes continued to adhere. PMNleukocytes and monocytes were released from the glass with EDTA. Monocytes appeared in the effluents somewhat later than the PMN leukocytes,permitting a separation.

A fresh serum, heat labile, Ca^{+ +}- and Mg^{+ +}-requiring PMN leukocyte and monocyte adherence promoting factor was demonstrated andfound to be essential to the procedure.

The viability of column-separated cells was shown by their non-stainingwith trypan blue, motility, phagocytic ability, oxygen consumption, andsurvival or development in tissue culture.

In tissue culture, macrophages developed only from monocytes, whereasNowell’s blast-like, dividing, phytohemagglutinin cells were produced onlyin cultures containing lymphocytes.

Submitted on October 3, 1963 Accepted on December 12, 1963     

A summary of atypical antibodies,rare genotypes,and ABO hemolytic disease encountered in a one year survey

1. Among 13,000 selected blood specimens studied in 1954, there were 1882which contained atypical antibodies, mainly anti-D.

2. Of the 177 sera with atypical antibodies other than anti-D, 85 containedanti-c, anti-E or anti-K and 18 sera contained anti-Le^a.

3. There were 52 cases of intragroup hemolytic disease, more than half ofwhich were due to anti-c.

4. Intragroup isoimmunization with production of antibodies other thananti-D was detected in 47 cases as incompatibility in the crossmatching. In 31additional cases failure to detect incompatibility resulted in transfusion reactions.

5. There were 30 examples of very rare Rh genotypes due to the presence ofrare chromosomes dCe (r'), dcE (r'), DCE (R^z), and the rarest of all, dCE (R^y).All told, there were 7 bloods which contained chromosome dCE (r^y) includingone—the first of its kind—which was homozygous.

6. It is recommended that rare genotypes be registered on a world-wide basisunder the auspices of a suitable agency and that these bloods be made availableas test cells or as compatible donors.

7. Sixty-two cases of ABO hemolytic disease are reviewed briefly. In all butfour the mothers were in group O. Of the 55 group O mothers tested, all but 5showed enhancement of the specific antibody in the indirect Coombs reaction.

Submitted on April 9, 1956 Accepted on June 25, 1956