The Rho Variant-Du

A simplified test for the D^u factor employing a reagent containing 25 per cent serum albumin, the "stick" technic to introduce cells and forceful cen-trifugation has been given an extensive trial in a routine blood bank operation. A routine preliminary test with anti-D gave 5,051 negative reactions among 26,753 bloods tested. The D^u tube test was then performed on the former with an anti-CDE reagent in parallel with the indirect antiglobulin test done with anti-D. All bloods positive by one or both tests were tested further for D antigens by an anti-D elution technic; they were also tested for Rh-Hr factors.
Among the 126 bloods positive by elution for the D^ufactor, 122 and 126 were positive respectively by the antiglobulin and the D^u tube tests. The two tests were in agreement on all eight of the type ccD^uee bloods found in the study. The D^utube test, as done with anti-CDE, gave no false negative reactions. It is, thus, concluded that bloods which are negative with this test will be type ccddee and can be labeled "Rh negative tested for D^u. Serological factors which might account for sensitivity of the D^u tube test's being the equal of the antiglobulin test are considered, as are the probabilities of the existence of D variants so weak that they could not be detected by either test.     

The Rho Variant — Du

In a survey of 18,365 bloods for the incidence of the D^u factor, in a population comprised approximately of 72 per cent Caucasoids, 15 per cent Negroids, 10 per cent Mexicans and 3 per cent Orientals, 78 D^u bloods were found of which seven were type ccD^uee. Of the latter, five came from Negroids and two from Caucasoids; the frequency among the two populations approximates respectively one in 6,000 and one in 500. In the general population of this region it is one in 2,500.
The degree of reactivity of the type ccD^uee found in this study was that of the "low grade" variety. However, from the remaining 71 "low grade" D^u bloods, substantially weaker examples were found among type CcD^uee and ccD^uEe. The indirect antiglobulin and ficinized cell method readily detected type ccD^uee; however, among the weaker variants, the antiglobulin method gave the more consistent results.
It is concluded, therefore, that type ccD^uee does occur in this area with a frequency that is considered significant and that its detection rests on the antiglobulin or other equally sensitive methods.     

A New Rh Phenotype, Rhorh, G-Negative

A new Rh phenotype, Rh_orh, G-negative is described in a Negro woman who developed anti-G (rhG) antibodies during pregnancy. The baby was Rh_o, G-positive and had mild hemolytic disease with a positive direct antiglobulin test. The mother's titer was 1:1024 at delivery, dropping to 1:8 after 14 months. The baby's direct antiglobulin test became negative after two months. The mother most likely became sensitized alter a blood transfusion five years prior.     

The Serology of Rho Variants (Rho)

Eighty-two Rh_o samples were tested with a battery of ten anti-Rh_o sera by the antiglobulin, bromelin and albumen replacement technics. The varying ability of different anti-Rh_o sera to react with Rh_o variant cells was clearly demonstrated. Anti-Rh_o used for the detection of Rh_o variants should be specially selected for this purpose. It is suggested that the Rh_o factor results from a genetically determined absence or abnormality of the primary Rh_o factor, and the serologic reactions characterizing it are dependent on the reactions of the subsidiary factors Rh^A, Rh^B, Rh^C, and Rh^D.     

Another Example of Phenotype Rhnull

Blood‐donor typing provided the sixth example of a person with the rare phenotype, Rh_null. Serologic investigation of the propositus and his family gives indirect support for the theory that the homozygous state of amorphic genes ( X ⁰r/X⁰r) at a locus independent of Rh can block the production of the precursor substance upon which the Rh genes act to form the Rh antigenic determinants on red blood cells.     

Another Example of Anti-Jsa

Anti-Js^a resulting from transfusions is reported. The antibody was not detectable six months later. Repeated antibody screening is advised in patients treated by frequent transfusions.     

Another Example of Anti-Jsa

The fourth example of anti-Js^a probably stimulated by blood transfusion is described. Thirty-four of 244 Negroid bloods were Js(a+). All 103 Caucasians and three Indian blood samples were Js(a–).     

Immunization to Rho(D) Observed in Pregnancy of a Woman with Type rhG(G)

A Negro woman was tested during her third pregnancy and found to have type rh^G(G). When the patient was re-tested during the sixth month of her fourth pregnancy, she was found to have a weak antibody of questionable identity. During the last two months of the pregnancy, the titer of the antibody rose sharply and it was established to be specific for Rh_o(D). The infant, delivered by cesarean section shortly before term, had evidence of mild hemolytic disease; it recovered without transfusion therapy. Since this indicates that isoimmunization to Rh_o can occur in a person of type rh^G, such persons should receive only Rh_o-negative blood for transfusion. They should be regarded as Rh-negative for prenatal purposes, but it might be considered preferable not to use them as blood donors for Rh-negative recipients.     

Identification of a Specific Leukocyte Antigen: Another Presumed Example of 5b

A leukocyte agglutinating antibody obtained from a multiparous normal female was studied. By means of cross-absorption and antibody elution methods, it was established that this antibody detected a single leukocyte antigen, designated as "Ke." The data suggest a gene frequency of 0.8 for "Ke" and 0.2 for "ke," the postulated allelic gene. The antigen is shared by granulocytes, lymphocytes-monocytes, eosinophils and also platelets, but is absent from red cells. The cross reaction studies indicate that this antigen may be identical with group 5^b already described by Van Rood.     

Further Observations on the Blood Factors RhA, RhB, RhC and RhD

The findings in 18 cases of individuals with Rh_o-positive blood who had antibodies in their serum resembling anti-Rh_o in specificity are briefly summarized. One interesting finding is the relatively high frequency of such individuals among Negroes, especially with the blood type Rh^d_o and Rh^abd_o. The significance of these findings is discussed.     

Familial Autohemolytic Anemia and Runting Syndrome with Rho-specific Autoantibody

A case of autohemolytic anemia with hypergammaglobulinemia and specific anti-Rh_o autoantibody is reported. The patient had the clinical syndrome of simulated runt disease as it occurs in experimental animals. Thymic atrophy and generalized lymphocytic depletion were found at autopsy. Four siblings of the proposita died in infancy of similar affections. The sera of the two living siblings and the parents disclose abnormal serum globulin patterns. It is suggested that dysglobulinemia favors the survival of lymphoid cells acquired trans-placentally from the mother and that the autohemolytic anemia and other pathologic manifestations in this case are the result of a graft-versus-host reaction. The anti-Rh_o specificity of the autoantibody is ascribed to isosensitization of a clone of grafted lymphoid cells which have sustained a loss of Rh genes in the process of somatic mitosis.     

The Rh Antigen EW

A second white family carrying E^w is reported, the antigen being traced through three generations.     

The Third Example of Anti-hrS

A third example of anti-hr^S, first described by Shapiro in 1960, was detected in the serum of a Bantu woman whose newborn infant suffered from mild hemolytic disease of the newborn.     

The Expected "Bombay" Groups OhA1 and OhA2

An American family of English extraction is reported in which two Oh ("Bombay") members have transmitted A ₂ genes to their children thus demonstrating that the expression of the gene A ₂, like that of the gene B , can be suppressed in this phenotype. Another American family, of French extraction, shows with a high degree of probability that the expression of the gene A ₁ can be similarly suppressed.     

Quantitative Studies of the Rho(D) Antigenic Determinants on Gorilla Erythrocytes

Human and simian red blood cells were tested for ¹²⁵I anti-D binding at equilibrium and for their ability to adsorb ¹²⁵I anti-D. On the basis of the equilibrium quantity of red blood cell-bound anti-D at different ionic strengths, the rate of binding of anti-D, and adsorption studies, evidence has been obtained that D-antigenic specificities occur on the erythrocytes of orangutans ( Pongo pygmaeus ), chimpanzees ( Pan troglocytes ) and gorillas ( Gorilla gorilla ). Gorillas, like chimpanzees, appear to be polymorphic with respect to the presence of D-components on their erythrocytes. Individual animals have been found whose red blood cells take up very little anti-D and are similar to human D-negative cells. The quantity of anti-D bound at equilibrium, as a fraction of that bound to human D-positive red blood cells was: for gorillas 0.6 to 4.0; for chimpanzees 0.08 to 0.51; for orangutans 0.06 to 0.09, and for human D^u red blood cells 0.04. At low ionic strength there was almost a twofold increase in anti-D binding. At low ionic strength, the adsorbing capacities of these erythrocytes, as compared to a human D-positive cell, were: orangutans 10 to 20 per cent; chimpanzees about 50 per cent; human D^u 86 per cent; and gorillas 97 per cent. Evidence is presented to indicate that the discrepancy between adsorbing capacity and the binding of anti-D at equilibrium, for D^u and simian erythrocytes, is due to absence of some of the D-antigenic components found on human D-positive red blood cells.     

Erythrocyte Li+/Na+ and Na+/H+ exchange, cardiac anatomy and function in insulin-dependent diabetics

It has been proposed that an increased activity of cell membrane Na+/H+ exchange, mirrored by increased erythrocyte Li+/Na+ exchange, may facilitate cell hypertrophy and hyperplasia. Patients with insulin-dependent diabetes mellitus may develop a specific cardiomyopathy with systolic and diastolic abnormalities and increased thickness of the left ventricle. Therefore, we have investigated the relationships between erythrocyte Li+/Na+ and Na+/H+ exchange and echocardiographic parameters in 31 male insulin-dependent diabetics (aged 17-68), in good metabolic control. Three had untreated mild hypertension. In all patients the urinary albumin excretion rate was less than 200 micrograms min-1. Ten patients had a Li+/Na+ countertransport higher than 0.37 mmol l-1 cell h-1, the upper normal limit for our laboratory (0.49 +/- 0.10, mean +/- SD). In comparison with the patients with normal countertransport, they had increased interventricular septum thickness and relative wall thickness (h/r). End diastolic volume and cardiac index were reduced while blood pressure and urinary albumin excretion rate were similar. In the whole study group, interventricular septum thickness was significantly correlated to Li+/Na+ exchange (r = 0.61, P less than 0.001) and Na+/H+ exchange (r = 0.35, P less than 0.05), independently of the effect of age and blood pressure. Posterior wall thickness was correlated to Li+/Na+ exchange (r = 0.38, P less than 0.05) and h/r to Li+/Na+ exchange (r = 0.41, P less than 0.05) and to Na+/H+ exchange (r = 0.44, P less than 0.05). Li+/Na+ exchange was negatively correlated to cardiac index (r = -0.37, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

IgG anti-Jka/Jkb antibodies are unlikely to fix complement

Antibodies in the Kidd blood group system show a great deal of serological variability, are notoriously elusive and hence evoke difficulties in detection. However, they have been regularly reported as causing severe immediate or delayed haemolytic transfusion reactions and this clinical potential has been largely attributed to their complement binding ability.
In initial investigations on 43 anti-Jk^a/Jk^b sera with a range of titres of IgG antibody only a few seemed to fix complement, though following repeated tests on 20 of these sera a further five were shown to bind complement, making a total of 12 (27.9%) showing evidence of complement binding. Twenty-three sera were unavailable for re-testing. Subsequent tests revealed that only those sera which showed direct agglutination or were positive with an anti-IgM reagent in an indirect antiglobulin test (IAT) fixed complement. Evaluations on the IgG fractions of six selected potent anti-Jk^a sera failed to reveal any complement-fixing ability although all the original sera bound complement avidly and contained variable amounts of IgM antibody, some at very low subagglutinating levels.
These findings challenge past perceptions and give cause for reflection on the changing methodologies and strategies which could unduly compromise the detection of these potentially clinically damaging antibodies.