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Anti-Hy, in a serum of a black man who had received multiple blood transfusions, was found to be a warm reactive and polyclonal IgG antibody which did not bind complement in vitro. 51Cr-labeled Hy-positive red blood cells in the patient showed a shortened "2-component" survival curve. Hy antigens were not detected on leukocytes, platelets, or in the serum of Hy-positive individuals.
A high-glycerol method for long-term storage of red cells for use in blood group serology testing is described. Total freezing-thawing-washing hemolysis was 8.05 +/- 0.3 percent. Enzyme treatment could be performed before freezing or after reconstitution. The cells performed well with manual and automated techniques. No changes in agglutinability were noted during 10 days of liquid storage at 4 degrees C following thawing.
In a retrospective study on samples from 10,000 recently transfused patients, 35 samples were found to contain an antibody that reacted with ficin-treated red cells but was not demonstrable by low-ionic-strength saline solution and indirect antiglobulin test (LISS-IAT). In those 35 patients, the specificity of the antibody was such that each patient would have been transfused with antigen-negative blood had the antibody reacted in LISS-IAT. Tests on red cells from the units already transfused showed that 19 patients had among them received, by chance, 32 antigen-positive and 74 antigen-negative units. The remaining 16 patients had among them received 57 units that were, again by chance, all antigen negative. One patient given antigen-positive blood suffered a delayed transfusion reaction; in two others the antibodies became LISS-IAT active after transfusion. However, similar changes to the LISS-IAT-active state were seen with two antibodies of patients given only antigen-negative blood. Also found in the 10,000 patients were 28 clinically insignificant antibodies, 77 sera in which the antibody was too weak to identify, and 216 autoantibodies that reacted only with ficin-treated red cells. These data support a belief, generally held in the United States but not necessarily elsewhere, that the use of protease-treated red cells for routine pretransfusion tests creates far more work than the accrued benefits justify.
Acute hepatic failure has been reported in the presence of Epstein-Barr virus (EBV) infection. Autoimmune hemolytic anemia may also occur in the course of this infection. We report a rare case of fulminant hepatic failure and autoimmune hemolytic anemia associated with Epstein-Barr virus. A seven-year-old girl was admitted with the complaints of abdominal pain, vomiting and jaundice. She was irritable, confused and had mild hepatomegaly with marked splenomegaly. Serum aminotransferase levels were moderately elevated, while direct and indirect bilirubin levels were markedly elevated. Prothrombin time was prolonged. Hemoglobin was 3.9 g/dl. Anti-HAV IgM, HbsAg, anti-HBc IgM, anti-HCV and anti-CMV IgM were negative, while IgM VCA EBV, IgG VCA EBV and anti-CMV IgG were positive. Serum copper and ceruloplasmin levels were normal. The patient received supportive therapy for hepatic failure. Meanwhile, the cause of the deep anemia was investigated and autoimmune hemolytic anemia was ascertained by means of increased reticulocyte count and positive Coombs test. Corticosteroid therapy was administered. The prognosis was good. Although not reported before, the combination of acute hepatic failure and autoimmune hemolytic anemia may complicate the course of EBV infection. Physicians need to be aware of this association.
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A 37-year-old woman developed acquired haemolytic anaemia and thrombocytopenic purpura. At the same time there were signs of hypothyroidism. Incomplete heat antibodies (direct Coombs test) were demonstrated as cause of the haemolytic changes, while high-titre thyroglobulin and microsomal thyroid antibodies as cause of the immunothyroiditis explained the hypothyroidism. Although serological demonstration of platelet antibodies did not succeed, the clinical and haematological findings suggested immunothrombocytopenia. Antibodies against smooth muscle produced no clinical symptoms. The activity of the incomplete heat autoantibodies was diminished as result of immunosuppressive treatment and haemolytic signs regressed. Platelet count rose and the haemorrhagic diathesis disappeared. Thyroid antibody titre rose at first but then markedly decreased. There was no demonstrable effect on the hypothyroidism so that it was necessary to administer thyroid hormones. This is the first published case of such immunopathological triad resulting from immunothyroiditis.
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Various studies have provided impressive evidence of the efficacy of antenatally administered anti-D in the prevention of rhesus (D) alloimmunisation in rhesus-negative women. However, possible clinical and immunohaematological problems associated with this prophylactic therapy have received little attention. We describe perinatal and immunohaematological problems, which occurred in four cases after antenatal rhesus prophylaxis. Classical immunohaematological techniques were employed, to detect and specify irregular red cell antibodies. It was found, that the antenatal administration of anti-D could mask sensitization to other red cell antigens or the production of maternal immune anti-D antibodies later in pregnancy. A further problem encountered was that of neonates with a positive direct Coombs' test (the uncertainty in the individual case being, whether this is a result of the antenatal administration of anti-D) and marked hyperbilirubinaemia. Antenatal immunoprophylaxis for rhesus disease can give rise to immunohaematological and clinical findings, of which the interpretation is extremely difficult and requires intensive cooperation between the obstetrician, neonatologist, and haematologist/clinical biochemist.
We report on a female infant with severe hemolytic disease of the newborn (HDN) secondary to anti-Gonzales antibody (anti-Go(a)) necessitating an exchange transfusion within the first day of life. The infant was born to a mother known to be Gonzales-antigen negative and a father who was Gonzales-antigen positive. The mother had an anti-Go(a) titer of 1:256 at 35 weeks' gestation. The infant was noted to have jaundice shortly after birth, with a bilirubin of 17.8 mg/dl (total) and .05 mg/dl (direct) at 11 hours of life. Coombs' test was positive and cord cells were Gonzales-antigen positive. Eluate on cord cells demonstrated anti-Go(a). Despite aggressive phototherapy, the total bilirubin reached 23.3 mg/dl by 24 hours of age and a double-volume exchange transfusion was performed. Following the exchange transfusion, phototherapy was continued for several days. The hemoglobin, which was 19.8 gm/dl at 11 hours of age, remained stable through the hospitalization, and no further transfusions were required. History revealed that two prior pregnancies resulted in Gonzales-antigen positive infants. The first child experienced mild jaundice requiring no therapy, and the second child required phototherapy for prolonged hyperbilirubinemia. Previous reported cases of anti-Go(a) suggest that this is not a cause of severe HDN. However, in view of the current case, it may be prudent to follow women with anti-Go(a) prenatally with amniotic fluid bilirubin studies, serial antibody titers, and fetal hemoglobin levels.
The case study reported here concerned an intrauterine death as a result of a Kell erythroblastosis. Allergization had been caused by the administration of Kell-positive banked blood. Irregular antibodies are on the increase as a result of the increasing number of blood transfusions. It is recommended that the Kell system be considered in the selection of banked blood for girls and women of childbearing age--a practice that has been followed at the Innsbruck University Clinics for almost four years now. The indirect Coombs' test should be performed in order to establish Kell antibodies and other clinically significant antibodies. The enzyme test is recommended as a supplementary examination, but should never be used as the sole antibody test. As with rhesus incompatibility, and insofar as the determination of the father's Kell characteristics show him to be an antigen carrier, monitoring of allergized pregnant women must be carried out with the help of antibody titer follow-ups, amniocenteses, and ultrasonographic examinations at short notice.
HISTORY AND CLINICAL FINDINGS: A 28-year-old woman in her fourth pregnancy had a positive direct Race-Coombs test in her 14th week of pregnancy. About 6 weeks later she developed marked anaemia, severe thrombocytopenia and leukopenia with nose-bleeds as well as petechiae over the lower abdomen and the inguinal regions. INVESTIGATIONS: Platelet count was 7000/microliter, haemoglobin concentration 4.8 mmol/l (7.73 g/dl) and WBC count 2600/microliter). Bleeding time was markedly prolonged. Erythrocyte-attached immunoglobulin G and complement components as well as antithrombocyte and antigranulocyte antibodies were demonstrated. Haemoblastosis or aplastic anaemia was excluded by bone marrow examination. TREATMENT AND COURSE: The pancytopenia with immune thrombocytopenia, autohaemolytic anaemia and associated leukopenia were classified as Evans syndrome. Administration of glucocorticoids and of immunoglobulins intravenously for 5 days failed to improve the blood picture significantly. But platelet count rose significantly on immunoadsorption (Ig Therasorb columns), allowing the pregnancy to proceed. CONCLUSION: In life-threatening states Ig immunoadsorption can achieve well tolerated, effective and specific elimination of pathogenetically relevant antibodies against blood cells and can also be applied in pregnant women.
In two patients, mother and daughter, with breast cancer a paraneoplastic syndrome of probably autoimmune pathogenesis developed in the course of the neoplastic disease. In the mother the cancer occurred when she was aged 51, first in the left and then, 4 years later, in the right breast. A local recurrence 18 years later caused a pericardial effusion and further tumour recurrences were associated with symptoms like those in Sjögren's syndrome, as well as bullous pemphigoid and polyneuropathy. Antinuclear antibodies, extractable nuclear antigen antibodies and rheuma factors were demonstrated in serum. Both symptoms and antibody titres regressed under treatment with tamoxifen and various cytostatic drugs. The patient died aged 74 years.--The daughter underwent a lumpectomy for breast cancer when aged 39 years, followed by mastectomy for local recurrence after 2 years. A further 2 years later she was found to be anaemic with a positive Coombs test (1:1024) and antibodies against IgG and complement. Metastases developed later. In her case, too, clinical and serological findings clearly regressed under treatment with tamoxifen and chemotherapy. She died, aged 45 years, from the consequences of further metastases.
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The premise that chronic antigenic stimulation may be involved in lymphoproliferative disorders was considered in a patient with immunoblastic lymphadenopathy who had received liver extract by injection and by mouth for many years. The salient features were lymphadenopathy and hepatosplenomegaly, a predominance of lymphocytes and plasmacytoid cells with mitotic figures in lymph-node imprints, a cryoglobulin containing IgG, IgA, IgM and bound complement components, depressed serum complement levels, and Coombs-test-positive erythrocytes. Immunoglobulin concentrations per 100 ml of serum were IgG, 5900 mg, IgA, 1480 mg, and IgM, 5640 mg, with normal ranges of 710 to 1540, 60 to 490, and 37 to 204 mg, respectively. Serum precipitins to an antigen (or antigens) in the liver extract resided in the IgA and IgM classes. Complete remission followed one course of cyclophosphamide, vincristine, and prednisone. We propose that the syndrome was caused by chronic antigenic stimulation with liver extract.
We evaluated the prevalence and specificity of smooth-muscle autoantibodies in 20 serum samples obtained from patients with angioimmunoblastic lymphadenopathy. Smooth-muscle antibodies in high titers were detected in 75 per cent of the samples. No such antibodies were found in 30 normal control serum samples or in 10 samples from patients with non-Hodgkin's lymphoma and 1 of 12 from patients with other types of polyclonal hypergammaglobulinemia were positive. The antibodies were polyclonal and belonged to the IgM, IgG, and IgA classes. They reacted with vimentin, the major polypeptide of the intermediate-filament cytoskeleton of mesenchymal cells. The pattern of tissue reactivity and absorption experiments both show that these antibodies recognize special antigenic determinants of the vimentin polypeptide that are shared by vimentin and other classes of intermediate-filament proteins - namely, keratin and desmin. The frequency of this unusual autoantibody activity in angioimmunoblastic lymphadenopathy suggests that, like hypergammaglobulinemia and a positive Coombs' test, it may represent a useful serologic marker for the disease.
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Development of the Coombs test has led to rapid progress in the recognition of various autoimmune hemolytic anemias. Cold agglutinin disease, a relatively rare disorder, occurs in idiopathic and secondary forms, the latter often in association with diseases that alter the immune status. The higher the titer of cold agglutinin, the greater is the thermal range of its activity. One of the characteristic clinical manifestations of the disease is striking cyanosis in acral areas on exposure to cold, which abates quickly on warming. This parallels the accelerated hemolysis at cold temperatures, which is reversible as heat is applied. In some patients, however, the disease is covert and is discovered only incidentally. The report of such a case is included.