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The efficacies of Coombs' test and the polybrene test, heretofore not used in this country, for the diagnosis of autoimmune hemolytic anemias are compared in examinations of 27 donors and 62 patients with this condition. The results evidence a high efficacy of the polybrene test. The test is simple and available for wide use at clinical laboratories.
Anemia occurs in more than one half of patients with systemic lupus erythematosus and is usually attributed to "chronic disease." Approximately 10% of patients with a positive Coombs' test manifest clinically significant hemolysis. Leukopenia affects both granulocytic and lymphocytic lines and may be caused by autoantibodies. Nevertheless, enhancement of B lymphocyte function occurs in active disease, perhaps due to a loss of regulatory T cells. Most patients have increased production and increased peripheral destruction of thrombocytes, with a normal circulation platelet count. Thrombocytopenia is usually caused by increased destruction. Qualitative abnormalities of platelet aggregation also occur. Circulation anticoagulants are not rare; however, spontaneous bleeding is uncommon. The anticoagulants, immunoglobulins directed against clotting factors, assume importance for invasive procedures. Most clinically significant hematopoietic abnormalities can be suppressed by corticosteroids; however, splenectomy, or immunosuppressive agents, or both, may be indicated for patients who respond inadequately to corticosteroids.
The charts of newborn infants with positive direct Coombs' test were studied. Only cases in which the mother's blood was group O and the infant's group A or group B were studied. There was no difference between group A and group B infants in the frequency and severity of the hemolytic process caused by maternal antibodies. In group B infants, monospecific antibodies (anti-B) were associated with more severe hemolytic process than cross-reacting antibodies (anti-A,B). In group A infants there was no difference in the severity of the disease between monospecific antibodies (anti-A) and cross reacting antibodies (anti-A,B). Even though there was no significant difference in the sex distribution of affected infants, there was a higher number of boys in the more severely affected group.
Antiglobulin Coombs' test was included into the complex of sero-allergic reactions used for selection of the groups of population to be vaccinated by epidemiological indications, for the purpose of studying the incomplete antibodies in age aspect under conditions of the existing foci of brucellosis infection. A total of 1904 persons were examined. Incomplete antibodies were found with equal frequency in the blood serum of children and in adults of the population of the Kashka-Dariya region of Uzbek SSR residing in the foci of cattle brucellosis; it was revealed in 40.3% of children aged from 7 to 10 to 10 years, in 45.6% of children aged from 11 to 14 years, and in 42.3% of adults aged from 31 to 40 years.
Children with acute Plasmodium falciparum malaria and anemia were investigated to see if immunological factors could be implicated in the pathogenesis of their anaemia. Direct Coombs tests using an anti-whole immunoglobulin antiserum were negative in all 12 children tested but two had positive tests with antisera to C3b and C3d. Low plasma levels of C3 and C4 were found but these were not significantly different from values found in a group of children with acute malaria who were not anaemic. Serum levels of immune complexes were normal at the time of their presentation at hospital with anaemia but were elevated one month later. Incubation of group O rhesus-negative red cells in a serum pool obtained from children with acute malaria and anaemia did not cause enhanced haemolysis or reduce their survival time on injection into mice. Splenic uptake of red cells was, however, significantly enhanced. We conclude that the anaemia of acute malaria is due mainly to destruction of red cells by malaria parasites and to enhanced erythrophagocytosis of normal cells.
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Serum complement levels and hematological data were evaluated in five patients with immunoblastic lymphadenopathy (IBL) and four with IBL-like T cell lymphoma (IBL-T). Anemia with Hb values below 10.0 g/dl was seen in four patients. A direct Coombs test was positive in five patients and the bone marrow of two of these showed features of pure red cell aplasia. Seven patients were thrombocytopenic with platelet counts below 100 x 10(9)/l. Six of the seven patients had splenomegaly. Platelet-associated IgG was elevated in all three thrombocytopenic patients examined. Whole complement activity (CH50) was reduced in eight patients (89%) at presentation and subsequently normalized in five who were treated either with prednisolone (two patients with IBL) or with multidrug combination chemotherapy (three with IBL-T). One patient achieved complete remission and four partial remission. Remission was accompanied by normalization of hematological abnormalities and elevation of complement activity to the normal range in all cases. These results suggested that complement-mediated mechanisms are responsible, at least in part, for some of the hematological abnormalities observed in IBL and IBL-T and that hypocomplementemia is a common abnormality with significance as a laboratory marker for the disease activity.
We identified 3 patients with autoimmune myelofibrosis (AM) lacking American Rheumatism Association criteria for systemic lupus erythematosus (SLE). They had 1 or 2 cytopenias and lacked serologic evidence for SLE. Autoimmune features included psoriatic arthritis and positive direct Coombs test (DCT) result, DCT-positive autoimmune hemolytic anemia, and synovitis with polyclonal hypergammaglobulinemia. Bone marrow biopsy specimens from each patient were evaluated by routine morphologic and immunohistochemical examination. They demonstrated marked hypercellularity (2 cases) or hypocellularity (1 case), moderate erythroid hyperplasia (all cases) with left-shifted maturation (2 cases), intrasinusoidal hematopoiesis (all cases), slightly to moderately increased megakaryocytes (2 cases), and grade 3 to 4 reticulin fibrosis (all cases). All lacked basophilia, eosinophilia, bizarre megakaryocytes, clusters of megakaryocytes, and osteosclerosis. Mild to moderate bone marrow lymphocytosis was noted in all cases. In 2 cases, increased small T cells and B cells formed nonparatrabecular, loose aggregates. AM is a clinicopathologic entity that may lack features of SLE. Loose aggregates of bone marrow T and B lymphocytes and the absence of morphologic and clinical features of myeloproliferative disease or low-grade lymphoproliferative disease are clues that distinguish AM from better known causes of bone marrow fibrosis.
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Clinical, haematological and immunological data are presented from 14 dogs with autoimmune haemolytic anaemia (AIHA) serially monitored for up to 945 days after initial presentation. At the time of diagnosis, all dogs had severe anaemia (mean packed cell volume [PCV] 17.6 +/- 7.1 per cent) with leucocytosis in seven cases and thrombocytopenia in four dogs. The Coombs' test was positive in all cases. Immunoglobulin G (IgG) autoantibody alone was identified in eight cases, a combination of IgG and IgM autoantibodies was recognised in three cases, and in two dogs only IgM autoantibody was recorded (complement fixing in one of these dogs). All dogs were treated with immunosuppressive doses of corticosteroids and some animals also received cyclophosphamide (four cases), azathioprine (two cases), blood transfusion (four cases) or underwent splenectomy (two cases). Two dogs died during the initial episode of AIHA. In 12 dogs, the anaemia was resolved by an average of 36.3 +/- 16.0 days after initial presentation, but autoantibody titre often persisted after clinical improvement and normalisation of PCV. Four dogs had a clinical relapse 67 to 170 days after initial presentation and one of these dogs subsequently died from thromboembolic disease. One dog developed lymphocytic thyroiditis and serum antinuclear antibody at day 691 after initial presentation, and two cases developed disease consistent with autoimmune thrombocytopenia (AITP) at 365 and 618 days post initial presentation. In one of these dogs, AITP was concurrent with multicentric lymphoma. No correlation was recorded between haematological and immunological parameters at presentation and subsequent response to therapy or long-term clinical behaviour.
We have examined IgG and complement factor C3d deposition on erythrocytes by means of the direct Coombs' test (DAT) and looked for an association with the anaemia seen in falciparum malaria in children living in an area of hyperendemic malaria transmission (in Ghana). In one study (in 1997), 53 out of 199 patients had a positive DAT. Of these, 45 samples reacted with anti-C3d antibodies, 2 with anti-IgG and 6 with both reagents. There were significantly lower haemoglobin (Hb)-levels and higher prevalence of spleen enlargement in DAT-positive than in DAT-negative patients. Hb-levels were independently associated with DAT and age. This initial study was designed to investigate the role of intravascular haemolysis (IVH), but we found no association between IVH and either DAT result or anaemia. Because of the risk of selection bias we repeated the study using consecutive enrollment of malaria patients and were able to confirm the results in a total of 49 DAT-positive and 183 DAT-negative patients. This second study (in 1998) was designed to look at the importance of erythrophagocytosis through measurement of plasma neopterin levels and total nitrite and nitrate as markers of NO-release. Both parameters were significantly higher in DAT-positive than in DAT-negative patients (P < 0.001), indicating that complement binding to erythrocytes was associated with macrophage activation. Plasma levels of haptoglobin, interleukin-10 and tumour necrosis factor-alpha did not vary between the groups. The studies support the role of complement activation and erythrophagocytosis in the pathogenesis of anaemia in falciparum malaria in African children.
We report six cases of children presenting with paroxysmal cold haemoglobinuria occurring in a 3-year period in the north-west of England. In all six cases the onset of the illness was dramatic and its duration brief. We note the prominent red cell agglutination was evident in the blood film, the absence of a prompt reticulocyte response and a negative classical direct Donath Landsteiner test in each of these cases. The Direct Coombs Test (DCT) was positive when anticomplement reagents were used but high titres of free autoantibody were not demonstrated in the serum.
BACKGROUND: The postpartum administration of an adequate amount of anti-D immunoglobulin to the mother in cases of Rhesus incompatibility requires the exact quantification of the amount of Rh-positive fetal cells that may be present in the Rh-negative maternal circulation. The classical methods to detect an intrapartum fetomaternal hemorrhage are either time-intensive (such as the Kleihauer-Betke test), of low specificity (such as the indirect Coombs test), or technically cumbersome (such as flow cytometry). The goals of our study were to develop a simple screening test that may be used routinely to quantify fetomaternal hemorrhage in cases of Rhesus incompatability and to evaluate this test in clinical practice. STUDY DESIGN AND METHODS: In cases of Rhesus-negative mothers of Rhesus-positive neonates, 2.5 ml of maternal Rhesus negative blood was sampled in an EDTA tubes immediately postpartum and was incubated with anti-D antibodies. Thereafter, a semiquantitative determination was made of the amount of antibody that remained unbound in the serum via a gel agglutination test (GAT) (DiaMed., Switzerland) after mixing with test red blood cells. The amount of anti-D consumed (bound to fetal cells in the first phase) is the semi-quantitatively indicated by the degree of positivity in the second phase the weaker reaction--the more anti-D absorbed in the first phase--the more Rhesus-positive fetal cells present in the maternal sample--the larger the fetomaternal hemorrhage. Following the development of a discrimination zone using this GAT which could ascertain an Rhesus-positive erythrocyte concentration of over 0.2%, the test was applied in a clinical setting. Between September 1995 and April 1998 in unselected postpartum blood samples from 603 Rhesus negative parturients, the GAT was used to test the same blood samples as those requiring evaluation for HbF concentration using the traditional Kleihauer-Betke test. RESULTS: In 585 of the 603 cases (97%) there was no evidence of a fetomaternal transfusion following testing using both methods. Furthermore, both tests showed significant evidence for a fetomaternal transfusion in five cases. The Kleihauer-Betke test was false-positive in three cases of mothers who had a hereditary elevation of the HbF concentration. The GAT showed three false-positive reaction due to a Dweak maternal varient. In two cases, the disparity between the GAT and the Kleihauer-Betke test could be attributed to an antecedant dose of anti-D antibody. In the two cases, the Kleihauer-Betke test results were 0.3% while the GAT was only 0.2%. CONCLUSION: The GAT may be used as a screening method in routine clinical practice. This is a quick test that allows for the specific determination and semiquantitative evaluation of the Rh-positive erythrocyte concentration in clinically relevant concentrations. Thus, following a positive GAT screening test, a further specific test such as the Kleihauer-Betke test may be utilized to absolutely quantify the amount of blood transfused from fetus to mother. It is also possible to perform such a quantification test with the GAT by eventually using a diluted maternal blood sample.
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The effects of synthetic thymopoeitin32-36 and purified ubiquitin, in daily doses of 1 or 10 microgram, were studied in New Zealand mice. The most striking result was a 4-month delay in the appearance of Coombs' positive tests or Coombs' antibodies in New Zealand black (NZB) mice treated from 4 wk of age with ubiquitin. Ubiquitin also reduced the spleen weight in the animals and stimulated suppressor T cell activity in shorter term studies of older NZB and black and white (B/W) mice. Thymopoietin was also active in this assay and improved the mitogen responsiveness of lymph node cells in older treated NZB and B/W mice. Thymopoietin injections, from 4 wk of age, reduced the titer of Coombs' antibodies and thymocytotoxic antibodies in NZB mice and caused an increase in Thy 1+ spleen cells in these animals. In correspondingly treated B/W mice, thymopoietin reduced the anti-DNA antibody titer. While our present injection protocol did not result in clinical cure of the genetically determined autoimmune diseases of NZB and B/W mice, they do point to the feasibility of selective immunoregulation by these peptides in diseases associated with altered states of immune reactivity.
The term lupus anticoagulant (LAC) refers to antiphospholipid antibodies assessed by means of phospholipid-dependent coagulation tests. About two-thirds of LAC-positive patients described in the literature have systemic lupus erythematosus (SLE) or a lupus-like syndrome. The estimated prevalence in SLE is about 30%. LAC is a marker of a subset of patients characterized by a high prevalence of thromboembolic complications (present in 40% of the LAC-positive patients), fetal loss (related to placental infarction), thrombocytopenia, biologically false positive tests for syphilis, antinuclear antibodies and a positive Coombs' test. There is a strong correlation between the presence of LAC and antibodies to the phospholipid cardiolipin, which can be estimated with relatively simple solid phase assays. Studies demonstrating in some patients interactions between LAC and either humoral factors with important functions in the (patho-) physiology of thrombosis, endothelial cells or platelets strongly suggest that LAC represents autoantibodies with pathogenic significance.
A 45-year-old woman with Bence-Jones type multiple myeloma was treated with natural type alpha-interferon (Namalwa interferon), 3 million IU every other day subcutaneously. After about 5 months, she developed hemolytic anemia. However, screening tests for autoantibodies, including direct and indirect antiglobulin (Coombs' tests), were negative. This report is the first case in which hemolytic anemia appeared to be caused by natural type alpha-interferon. It is likely that interferons will be used in treating increasing numbers of patients and that more patients will develop this complication.