Antiglobulin Test Research Articles

Tuberculosis-induced Autoimmune Hemolytic Anemia

Abstract Autoimmune hemolytic anemia (AIHA) is a rare disorder characterized by antibodies against one’s own red blood cells, often difficult to diagnose and treat in the elderly. It can be secondary to an infection, drug, or a myeloproliferative disorder. We report a rare case of tuberculosis (TB)-induced AIHA in an older woman. A 70-year-old woman complained of progressive weakness, weight loss, and abdominal pain over 6 months. Examination revealed anemia, jaundice, and splenomegaly. Routine blood investigations showed pancytopenia and Coombs test that was positive for autoantibodies. Workup for autoimmune disease like systemic lupus erythematosis was negative. Lymphoma, disseminated TB, and lymphoproliferative disorders were considered. Bone marrow biopsy was reported as normal. Mycobacterium tuberculosis was isolated from the bronchoalveolar lavage. A diagnosis of autoimmune hemolytic anemia secondary to disseminated TB was made. She was treated with steroids and antitubercular therapy, which improved her health and laboratory parameters. A positron emission tomography–computed tomography showed the resolution of splenic lesions and reduced metabolic activity of mediastinal and abdominal lymph nodes.

Donor vs. Donor or Recipient vs. Recipient? A Singular Case of Post Hematopoietic Stem Cell Transplantation Autoimmune Hemolytic Anemia in a Pediatric Patient

Hematopoietic Stem Cell Transplantation (HSCT) is a curative treatment for certain blood disorders, but can lead to complications such as Autoimmune Cytopenia (AIC), particularly Autoimmune Hemolytic Anemia (AIHA). AIHA after HSCT often involves donor-derived antibodies attacking donor red blood cells, but this case report describes a unique case in a 7-year-old male with beta-thalassemia major. Following HSCT, he developed AIHA nine months after transplantation from an unrelated donor. Despite initially successful engraftment, chimerism analysis revealed a decline in donor cells coincident with the onset of AIHA. The patient had severe hemolysis, a positive Direct Coombs Test (DAT) for IgG and C3d, and several antibodies including anti-e, anti- C, and anti-D. Treatment with cyclosporine and prednisone initially stabilized his condition, but discontinuation resulted in relapse, worsening chimerism, and increased antibody titers. Analysis confirmed the predominance of recipient immune cells, suggesting that AIHA was driven by the recipient's immune response against his own red blood cells. This case emphasizes the complexity of immune reconstitution after HSCT and highlights a recipient-versus-recipient mechanism in post-transplant AIHA.

The Effect of the Direct Anti-Human Globulin Test on the Clinical Outcome of Patients Receiving Blood Transfusion

Objective: To study the effect of the direct anti-human globulin test on the clinical efficacy of blood transfusion patients. Methods: 52 transfused patients were selected for this study, of which 26 cases with positive direct anti-human globulin tests were included in the positive group, and another 26 cases with negative direct anti-human globulin tests were included in the negative group. The apparent efficacy of the patients in the two groups after blood transfusion was compared. Results: After blood transfusion, the apparent efficacy of the negative group was significantly higher, P < 0.05; in the positive group, the proportion of the predominantly multi-antibody group was the highest; after blood transfusion, the post-transfusion apparent efficacy of the simple IgG group was higher than that of the multi-antibody group, P < 0.05; comparing the intensity of the different antibodies resulted in the 1+ group, and the 3+ to 4+ groups were significantly lower after blood transfusion, P < 0.05. Conclusion: The use of the direct antiglobulin test in transfused patients showed that patients with positive results would have better clinical efficacy. Direct anti-human globulin tests will have an impact on the clinical efficacy of blood transfusion in patients with positive results, so it is very important to carry out a direct anti-human globulin test on blood transfusion patients.

Mixed autoimmune hemolytic anemia during recovery from Immune Thrombocytopenia (ITP): A Case Report

Mixed autoimmune hemolytic anemia (AIHA) is characterized by hemolysis with the coexistence of warm and cold autoantibodies. It is a relatively rare condition, accounting for 6.5-8.3% of AIHA cases. It is diagnosed by identifying IgG and C3d with cold agglutinins on monospecific direct antiglobulin testing. We present a unique case of a 69-year-old female who developed mixed hemolytic anemia while she was being treated for chronic idiopathic thrombocytopenic purpura (ITP).

A case of infectious mononucleosis caused by Epstein-Barr virus complicated by autoimmune hemolytic anemia

We represent a rare clinical case of infectious mononucleosis with hepatitis, caused by Epstein-Barr virus, complicated by rare secondary autoimmune hemolytic anemia associated with warm agglutinins in a 16-year-old patient. The disease was long-lasting, with a two-wave course of febrile fever. Signs of hepatitis with the development of anemia of moderate severity appeared during the second wave of febrile fever. The etiology of the disease was confirmed by the detection of Epstein-Barr virus DNA in blood and the detection of anti-VCA IgM antibodies to Epstein-Barr virus in the absence of anti-EBNA IgG antibodies. Hemolytic anemia was verified using markers of hemolysis (increased lactate dehydrogenase activity, decreased haptoglobin concentration), and positive results of a direct Coombs test. After successful initiation of prednisone therapy and clinical improvement, the patient was discharged from the hospital on the 24th day of disease to continue treatment on an outpatient basis (prednisone was replaced by methylprednisolone).This case demonstrates the development of a rare autoimmune complication in infectious mononucleosis caused by the Epstein-Barr virus.

Insight Into Aetiology and Severity of Hemolysis Associated with Immunoproteins on Red Cell Surface in Direct Antiglobulin Test Positive Auto-immune Hemolytic Anemia

Insight Into Aetiology and Severity of Hemolysis Associated with Immunoproteins on Red Cell Surface in Direct Antiglobulin Test Positive Auto-immune Hemolytic Anemia

Acute hemolytic transfusion reaction caused by anti-M antibodies: a case report and literature review.

We report a rare case of acute hemolytic reactions caused by immunoglobulin (Ig)M anti-M antibody and present a literature review. A 61-year-old male patient who underwent blood transfusion developed fever, chills, soy sauce-colored urine, and changes in laboratory test results, including persistently decreased hemoglobin levels, neutrophilia, elevated lactate dehydrogenase level, acute kidney injury, mild acute liver injury, and activation of the coagulation system, indicating acute hemolytic transfusion reaction (AHTR). Antibody screening and major crossmatching results indicated weak positive at 37°C for both posttransfusion and pretransfusion sample. Subsequent serological examinations indicated the presence of IgM anti-M antibodies in plasma but the direct antiglobulin and elution tests were negative. Antibody hemolytic activity assay confirmed AHTR caused by anti-M. The transfused red blood cells were MM and the patient is NN. These signs and symptoms disappeared rapidly and required no additional interventions before discharge. The accurate diagnosis of anti-M antibody-mediated acute hemolysis is essential for guiding treatment decisions.

A Case of Immune-Mediated Coombs-Negative Hemolytic Anemia in a Patient with Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is an auto-immune connective tissue disorder that can involve any organ in the body. The American College of Rheumatology criteria (ACR) include autoimmune hemolytic anemia with reticulocytosis as one of the criteria in the diagnosis of SLE. Anti-erythrocyte antibodies in SLE are mainly warm-type IgG. We present a case of systemic lupus erythematosus presenting with immune-mediated Coombs-negative hemolytic anemia. This case highlights the possibility of autoimmune hemolysis occurring with a negative Coombs test, where the autoantibody levels are too low to be detected by a conventional direct antiglobulin test. (DAT)

A national survey of current immunohematologic testing practices for the diagnosis of autoimmune hemolytic anemia in India.

Autoimmune hemolytic anemia (AIHA) is a common term for several disorders that differ from one another in terms of etiology, pathogenesis, clinical features, and treatment. Management of patients with AIHA has become increasingly evidence-based in recent years. While this development has resulted in therapeutic improvements, it also carries increased requirements for optimal diagnosis using more advanced laboratory tests. Unfortunately, limited data are available from developing countries regarding the testing and transfusion management of patients with AIHA. The main objective of this survey was to explore the current immunohematologic testing practices for the diagnosis of AIHA in India. This online survey consisted of 30 questions, covering the place of work, the number of AIHA cases encountered in the 3 preceding years, testing method(s), transfusion management, and so forth. Individuals representing 89 laboratories completed the survey; only 78 of which responded that AIHA testing was performed in their facility's laboratory. The majority of respondents agreed that the most commonly affected age-group comprised individuals of older than 20 years, with a female preponderance. Regarding transfusion management, respondents indicated that transfusion with "best-match" red blood cell units remains the most common practice. Column-agglutination technology is used by 92 percent of respondents as the primary testing method. Although a monospecific direct antiglobulin test is available at 73 percent of the sites, most of them have limited access to other resources that could diagnose cold or mixed AIHA. Merely 49 percent of responding laboratories have the resources to perform adsorption studies for the detection of alloantibodies. Furthermore, three-cell antibody screening reagents are unavailable at 32 percent of laboratories. In 72 percent of centers, clinical hematologists would prefer to consult a transfusion medicine specialist before administering treatment to AIHA patients. There is unanimous agreement regarding the need for a national registry. The survey data indicate wide variability in testing practices for patients with AIHA in India. Future studies are needed to focus on the feasibility and cost-effectiveness of different testing strategies for developing countries.

Acute paroxysmal cold hemoglobinuria upon dengue fever: A case report

Rationale: Dengue fever is capable of inciting the formation of transient polyclonal antibodies directed at red blood cell antigens, resulting in complement-mediated hemolysis, leading to intravascular hemolysis and hemoglobinuria. Patient’s concern: A 12-year-old male patient who recovered from dengue fever a week ago had red blood cell agglutination, spherocytes, and engulfment of red blood cells (erythrophagocytosis) by monocytes and neutrophils on routine hematological peripheral blood smear. The unexpected blood smear results prompted the lab physicians to investigate autoimmune hemolytic anemia, which revealed a monospecific positive direct antiglobulin test for complement (C3d, C3b) and the presence of Donath-Landsteiner antibody. Diagnosis: Paroxysmal cold hemoglobinuria (PCH), secondary to dengue fever. Interventions: Oxygen supplements, antibiotics, intravenous immunoglobulins, steroid therapy, and packed cell transfusions were administered. Outcomes: The patient’s condition was improved following the therapy. Lessons: Post-dengue PCH is a rare complication that requires a thorough peripheral smear examination for erythrophagocytosis, as advanced hematology analyzers fail to detect such findings.

The Identification Idea of Antibodies Against Ku and Other High-Frequency Antigens

This study was aimed to provide ideas for identifying the antibodies to high-frequency antigens by analyzing a female case of high-frequency antigen antibody (anti-Ku) using serological and sequencing method. The methods for identification of blood group, erythrocyte antigen, screening and identification of antibody were used to detect the blood type and antibody in the proband. The proband's serum and reagent screening cells treated with Sulfhydryl reagent were applied to judge the type and characteristics of this antibodies when reacted with the regaent screening cells or proband's serum respectively. Gene sequencing was used to determine the genotype of the proband's blood group. The proband's red blood cells were determined as O type RhD positive, whose serum showed strong positive reaction to antibody-screening cells and antibody identification cells with the same intensity in saline and IAT medium, however, the self-cells showed negative effect. The Direct Antihuman Globulin of proband's red blood cells also showed weak positive reaction, and the other blood types were CcEe, Jk(a+b-), P1-, Le(a-b -), Lu (a-b +), K-, k-, Kp(a-b-). Serum of the proband treated with 2-ME still react with three groups of screening cells in IAT medium. The reaction intensity of proband's serum was also unchanged with the cells modified with papain and bromelain, but showed negative effect when the cells were treated with sulfhydryl agents including DTT and 2-ME. Gene sequencing revealed that the KEL genotype of the patient was KEL*02N.24 . This patient had a rare K0 phenotype. The rare Kell-null blood group (also known as K0) were identified by serological and molecular tests in the proband who produced both IgG and IgM type of antibody to high-frequency antigen (anti-Ku). These two methods are of great significance in the identification of this rare blood group as well as the antibody to high frequency antigen.

Autoimmune Hemolytic Anemia Associated with Mature Ovarian Cystic Teratoma Containing Monoclonal Immunoglobulin G: A Case Report and Review of Literature

Background. Autoimmune hemolytic anemia (AIHA) associated with solid tumors such as mature cystic teratomas is rare and poorly understood. Here, we report a successfully treated case of secondary AIHA in a mature cystic teratoma containing antibodies against red blood cells. Case description. A 22-year-old woman was referred to our hospital with progressive anemia. Laboratory findings revealed hemolysis with a positive direct and indirect antiglobulin test. Imaging studies identified a left ovarian mass, suspected to be a mature cystic teratoma, which was later confirmed by histopathology after laparoscopic oophorocystectomy. The patient was treated with prednisolone, resulting in improved anemia. To examine the relationship between the tumor and AIHA, an indirect antiglobulin test was performed on the tumor contents. Stronger aggregations were observed at any concentration diluted by 10 times from 10 to 10,000 times of the tumor contents compared to the patient’s serum. Additionally, immunofixation electrophoresis of the tumor contents revealed the presence of monoclonal immunoglobulin G-κ. Conclusion. The presence of monoclonal IgG-κ in the tumor suggests intratumoral antibody production as a possible mechanism. Further research is necessary to elucidate the pathogenic relationship between such tumors and AIHA. The report also highlights the importance of considering secondary AIHA in patients with unexplained anemia and solid tumors.

#1572 Recurrent parvovirus B19 infection-associated pure red cell aplasia in kidney transplantation

Abstract Background and Aims Anemia is frequent in kidney transplant (KT) recipients, with multiple potential causes. Parvovirus B19 (PVB19) infection-associated pure red cell aplasia (PRCA) becomes an important diagnosis in KT recipients experiencing persistent anemia, in whom other etiologies have been excluded. PVB19-associated PRCA is described in up to 27% of KT recipients with anemia and recurrent disease in up to 33% of cases. The authors describe a case of a recurrent PVB19-associated PRCA in a KT recipient. Method - Results A 42-year-old male with chronic kidney disease of unknown etiology underwent KT from a deceased donor after circulatory death in January 2021. He received induction immunosuppression (IS) with thymoglobulin and maintenance IS with prednisolone, tacrolimus, and mycophenolate mofetil (MMF). Three months after KT, the patient complained of progressive asthenia, and normocytic normochromic (NN) anemia was detected. A thorough investigation revealed normal leucocyte and platelet counts, low reticulocyte count, and no signs of bacterial infection, iron deficiency, or hemolysis; thyroid function, erythropoietin, folate, and vitamin B12 levels were normal, direct Coombs test was negative and no monoclonal spike was detected on protein electrophoresis. Endoscopic studies and cervico-thoraco-abdomino-pelvic computer tomography were unremarkable. Serum PCR of PVB19 was positive and confirmed the diagnosis of PVB19-associated PRCA. MMF was discontinued but anemia continued aggravating (nadir hemoglobin [Hg] level of 6.6 g/dL) with a sustained PVB19 load. He was admitted to the hospital, received blood transfusions, and was started on intravenous immunoglobulin (IVIG) 2 g/kg. A bone marrow aspirate was performed and was compatible with recovery after erythroid aplasia. The patient was discharged with Hg 8 g/dL and reduced PVB19 load. Although MMF remained suspended, and close monitoring of Hg and PVB19 load was performed, four months later he developed recurrent PVB19-associated PRCA, which motivated another hospital admission for IVIG with excellent response. In addition, he presented kidney dysfunction, and a kidney biopsy revealed borderline acute T-cell mediated rejection. In this setting, IS was altered to TRANSFORM SCHEEME. Four months later, he presented a second recurrence of PVB19-associated PRCA, requiring new hospitalization and treatment with IVIG. Considering the recurrent PVB19-associated PRCA, in a patient with chronic allograft dysfunction, high immunologic risk, and the foscarnet's probable nephrotoxicity, preventive therapy with IVIG (0.4 mg/kg) every 4 weeks was started. After 7 months of preventive IVIG infusion, no relapse was identified, the Hg is 11.5 g/dL (and increasing, without erythropoiesis stimulants) and the PVB19 load remains low. Conclusion PVB19-associated PRCA is characterized by persistent NN anemia with low reticulocyte counts, which is unresponsive to erythropoietin. One significant risk factor is induction IS, particularly thymoglobulin. In the setting of solid organ transplants, the absence of PVB19 antibodies does not exclude this diagnosis and viral detection should be performed. The initial therapeutic approach involves reducing IS. However, the risk of allograft rejection must be acknowledged. If this approach proves insufficient, IVIG treatment is usually successful. In our patient, considering the facts that allograft rejection limits the reduction of IS, the need for blood transfusions, and the inherent immunization, in a young patient that will possibly require a second KT, the undesirable nephrotoxicity of foscarnet, the successful response to IVIG, and patient's quality of life, chronic IVIG therapy was thought to be the best choice and proved efficacious in preventing relapses. Despite the absence of precise guidelines for chronic PVB19 infection management, maintenance therapy with prolonged IVIG infusions may be a therapeutic option for recurrent PRCA, but more studies are necessary to define the appropriate duration of treatment.

#2262 Renal outcomes of postpartum atypical hemolytic uremic syndrome treated with plasma exchange

Abstract Background and Aims Postpartum acute kidney injury (AKI) with features of thrombotic microangiopathy (TMA) are particularly challenging and complex cases. Causes include Preeclampsia (PE), hemolysis, elevated liver enzymes and low platelet count syndrome (HELLP) and atypical hemolytic uremic syndrome (aHUS). In a limited resource setting, it is difficult to diagnose such cases with more than standard blood tests. Therapeutic Plasma exchange (TPE) is the only available option for treatment in the absence of complement inhibitors. This study evaluates renal outcomes in patients with aHUS treated with plasma exchange. Method This is a single centre observational study conducted in a Tertiary Obstetric Intensive Care unit. The data of women who were admitted with postpartum AKI from January 2021 to October 2023 was retrospectively collected and analyzed. We used the following criteria to diagnose postpartum atypical HUS (Serum creatinine ≥1.9 mg/dL, Lactate dehydrogenase (LDH) ≥1832 U/L, or serum creatinine ≥1.9 mg/dL in combination with LDH ≥600 U/L) [1]. Inclusion criteria include women older than 18 yrs with microangiopathic hemolytic anaemia, schistocytes on peripheral blood film, negative direct antiglobulin test (DAT) and platelet count <100 /mm3.Lack of improvement of kidney functions and hemolysis 72 hours after delivery. Patients with sepsis, disseminated intravascular coagulopathy (DIC), postpartum hemorrhage (PPH) and chronic kidney disease were excluded. We identified 10 patients with postpartum aHUS. Peak creatinine, LDH, AST and Nadir platelet count and hemoglobin were recorded. Patients were followed up in the nephrology outpatient clinic. Results Fifty-two patients developed postpartum AKI in the study period. Ten patients (19%) were diagnosed with aHUS according to the above-mentioned criteria. Mean age was 24.5 ± 6.9 yrs. Median peak creatinine 5.1 (2.6-7) mg/dl, LDH 1950 (612-4000) U/L, AST 246 (150-699) U/L. Median nadir hemoglobin 7.25 (6-8.2) g/dl and platelets 57 (41-95)/mm3. All 10 patients received 3 to 6 sessions of TPE guided by platelets and LDH levels. All patients required at least 3 sessions of hemodialysis. Eight patients received TPE with plasma filter and 2 had centrifugal TPE (due to lack of plasma filters). Two patients died during ICU admission. Two months after discharge 4 (50%) patients had partial recovery of kidney functions average creatinine (3.5 ± 0.8) mg/dl and four (50%) remained dialysis dependent. Six of these patients had kidney biopsies, three biopsies showed a picture of thrombotic microangiopathy and two showed thrombotic microangiopathy with renal cortical necrosis. The other patient was lost to follow up. Conclusion It is difficult to diagnose and treat aHUS in a resource limited setting. The available treatment with therapeutic plasma exchange has poor renal outcomes.

#2487 Deleterious renal outcome in patients with thrombotic microangiopathy after lung transplantation: the lung TMA trial

Abstract Background and Aims Thrombotic microangiopathy (TMA) is a rare but severe complication following lung transplantation. The pathogenesis is poorly understood, involving endothelial damage and various risk factors, including calcineurin inhibitor (CNI) toxicity. We aimed to evaluate diagnostic accuracy, identify risk factors for and assess the renal and overall survival of TMA in this patient group. Method We performed a retrospective study of patients with TMA after lung transplant between 01/01/2000-01/01/2021. Matching controls were selected based on underlying lung disease, age, gender, CMV risk, and immunosuppressive regimen. Overall survival and baseline data (age, gender) were collected for the whole lung transplant group. Results A total of 29 TMA cases (2.9%) were identified out of 1025 lung transplantations. 48% of patients had a complete hematological assessment with Coombs testing as the most frequent (52%) missing test. The median time from transplantation to TMA was 5.9 months. 76% of the episodes occurred before 12 months. 77% of patients had organ damage with acute kidney injury in 72%. At the time of TMA 38% of patients had a cytomegalovirus (CMV) infection. Arterial hypertension was found in 31% and acute rejection in 11%. The immunosuppressive scheme consisted of tacrolimus/mycophenolate mofetil and corticosteroids in the majority of cases (56%). Tacrolimus (n = 22) and cyclosporine (n = 7) trough levels were respectively 11.8 and 207 µg/l at the time of TMA. Treatment consisted of change in immunosuppressive regimen (72%), 31% received plasmapheresis. When comparing the TMA patients with the control group a higher rate of donor specific antibodies were found (11% vs 1%), a lower median time till chronic lung allograft dysfunction (37 m vs 91 m) and a higher prevalence of end-stage renal disease (24% vs 6%) and overall death (97% vs 44%) with mortality being significantly higher (p < 0.01). Fig. 1 illustrates the overall outcome. Conclusion This study illustrates the clinical characteristics and outcomes of TMA after lung transplantation. Even though the prevalence is low the effects are deleterious with acute kidney injury in the majority of cases and higher risk of end-stage renal disease and mortality. Our study emphasizes the need for higher further research into risk factors, and therapeutic strategies to prevent and improve patient outcomes. Furthermore, the findings underscore the importance of vigilant monitoring and tailored interventions for TMA in lung transplant patients.

#2996 Diffuse alveolar haemorrhage in antiphospholipid syndrome—a rare case

Abstract Background and Aims Diffuse alveolar haemorrhage (DAH) is a serious manifestation of diseases such as systemic lupus erythematosus (SLE) and, apparently in a paradoxical manner, antiphospholipid syndrome (APS). Inflammation resulting from the deposition of immune complexes in alveolar capillaries appears to contribute to the pathophysiology of DAH, SLE and APS. Symptoms include cough, dyspnoea, haemoptysis or fever. It is associated with a drop in haemoglobin, respiratory failure and diffuse infiltrates on imaging exams. Bronchoscopy is diagnostic. It is important to exclude infection as treatment includes high-dose corticosteroid therapy and other immunosuppressive drugs. We present a challenging case regarding the diagnostic and therapeutic approach to this pathology. Case report This is the case of a 52-year-old Caucasian female, with a history of SLE, APS, splenectomy due to thrombocytopenia, IgM Kappa monoclonal gammopathy and indolent non-Hodgkin lymphoma. She was medicated with prednisolone 5 mg and warfarin (target INR between 2 and 3). The patient was observed due to a 1-day history of fever, nasal obstruction and odynophagia, associated with progressively worsening fatigue. On examination, she was pale, eupnoeic, tachycardic, with bibasal rales and a hyperaemic oropharynx. Lab workup results were the following: haemoglobin 7 g/dL (11.7 g/dL 3 months before), VGM 71 fL, presence of schistocytes, leukocytes 13.7 G/L, neutrophils 11.1 G/L, PCR 4.6 mg/dL, platelets 170 G/L, INR 3.6, aPTT 45 sec, negative D-Dimers, urea 54 mg/dL, creatinine 1.4 mg/dL, LDH 431 IU/L, normal haptoglobin, negative Coombs test. In arterial blood gas analysis, pO2 was 61 mmHg and lactate was 5 mmol/L. Chest X-ray showed bilateral basal cotton-wool infiltrates and chest CT showed bilateral ground-glass pattern. The rest of the investigation included no complement consumption, negative anti-ds-DNA antibody, positive lupus anticoagulant, anticardiolipin and anti-beta2-glycoprotein antibodies, negative cryoglobulins and no evidence of progression of the lymphoproliferative disease. She was admitted to the intensive care unit due to suspicion of atypical/viral pneumonia vs. DAH. Oxygen therapy, empirical antibiotic therapy with ceftriaxone and clarithromycin and oral methylprednisolone 1 mg/Kg/day were started. She needed blood transfusion, although without visible blood loss. Bronchofibroscopy was performed, with bronchoalveolar lavage suggestive of DAH, so it was decided to start intravenous pulses of methylprednisolone, plasmapheresis, and intravenous immunoglobulin (IVIG). Warfarin was changed to unfractionated heparin. The patient had clinical, analytical and radiological improvement. Due to the lack of evidence of infection, antibiotics were stopped after 7 days. The patient was discharged under weaning corticosteroid therapy and monthly IVIG (during 5 months), without recurrence in the following year. Conclusion This is a rare case of oligosymptomatic DAH in a patient with SLE and APS. The literature currently available on DAH in the context of SLE or APS is scarce and its treatment is mainly dependent on the experience of each medical centre. Corticosteroid therapy is consensual, with greater variability in other corticosteroid-sparing therapies. In the case of patients with APS, anticoagulation is a challenge, and it is important to resume it as soon as the bleeding is controlled due to the risk of thrombotic events.

Neonatal Jaundice, Risk Factors and Implication of Direct Coombs Test as a Model of Severity. A Retrospective Study from One Single Center in South Lebanon

Neonatal Jaundice, Risk Factors and Implication of Direct Coombs Test as a Model of Severity. A Retrospective Study from One Single Center in South Lebanon

How do transfusion services manage patients taking therapies such as anti-CD38 and anti-CD47 known to interfere with red blood cell compatibility testing?

Drugs such as daratumumab (Darzalex, anti-CD38) and Hu5F9-G4 (magrolimab, anti-CD47) may interfere with red blood cell compatibility testing as CD38 and CD47 are expressed on red blood cells. A survey of AABB member transfusion services was undertaken to understand their experiences of managing patients taking therapeutic monoclonal antibodies that are known to interfere with blood grouping and compatibility testing. The survey was distributed to the contact person at US-based AABB member transfusion services. The response rate was 27%. 172 of 240 (72%) indicated they had difficulties in performing compatibility testing in patients taking daratumumab and 66 of 91 (73%) reported difficulties in performing compatibility testing in patients taking magrolimab. Actions taken to provide compatible blood for these patients included referral of all samples to a reference center, blood group pheno/genotyping the patient in advance of starting the drug, treating reagent cells with 0.2 M dithiothreitol and using K-negative red cell units for patients taking daratumumab, and Gamma-clone (Immucor) anti-IgG for indirect antiglobulin testing for patients taking magrolimab. Lack of communication from clinical services about drug treatment was identified as a concern. The results of the survey demonstrate that transfusion services are having challenges with the transfusion management of patients taking therapeutic monoclonal antibodies, and further education is needed.

Neonatal screening of ABO/RhD blood group and direct antiglobulin Coombs test. Experience of a single institution.

Evaluating the ABO/RhD blood group and the direct antiglobulin Coombs test (DAT) at birth is recommended good practice, but there is variability in its universal implementation. This study aims to show the comparative results in various variables of clinical impact during the hospital stay of neonates with positive DAT compared with those with negative DAT, based on the systematic detection of the ABO/RhD group and DAT at birth. Newborns between 2017 and 2020 in a high-risk pregnancy care hospital were included. The ABO/RhD and DAT group was determined in umbilical cord samples or the first 24 hours of life. Demographic, maternal, and neonatal variables were recorded. The association between the variables was estimated using the odds ratio (OR). 8721 pairs were included. The DAT was positive in 239 newborns (2.7%), with the variables associated with positive PDC being maternal age > 40 years (OR: 1.5; 95% CI: 1.0 to 2.3), birth by cesarean section (1.4; 1.1-2.0), mother group O (6.4; 3.8-11.8), prematurity (3.6; 2.6-5.0), birth weight < 2500 g (2.1; 1.6-2.8), newborn group A (15.7; 10.7-23.1) and group B (17.6; 11.4-27.2), hemoglobin at birth < 13.5 g/dl (4.5; 2.8-7.1) and reticulocytosis > 9% (1.9; 1.2 to 3.1). The frequency of neonatal positive PDC was 2.7%, with a significant association with maternal/neonatal incompatibility to the ABO and RhD group, with a substantial impact on various neonatal variables. These results support the policy of universal implementation at the birth of the ABO/RhD and DAT determination.

RHD Genotyping to Resolve Weak and Discrepant RHD Phenotypes: The “Serenissima” Experience

Background: A considerable number of RHD alleles responsible for weak and partial D phenotypes have been identified. Serological determination of these phenotypes is often doubtful and makes genetic analysis of RHD gene highly desirable in transfusion recipients and pregnant women. Aim: We report the experience of Mestre Blood Bank in analysis of the RHD gene in six years from 2018 to 2023. Methods: Subjects for RHD gene analysis were selected for presence of a serological weak D phenotype, defined as reactivity of RBCs with an anti-D reagent giving no or weak (≤2+) score in initial testing but agglutinating moderately or strongly with anti human globulin (AHG). These samples were selected for genotyping using the microarray-based method Bead-Chip supplied by Werfen. Results: From 2018 to 2023, we selected, for RHD gene analysis, 555 subject with D weak phenotype; 86 subjects (15.5%) were D positive and 56 (10.1%) were D negative, without variant, in 413 subjects a D weak or a D variant was observed. Discussion: Many serological weak D phenotypes are associated to RHD gene mutations leading to one or more amino acids substitutions in the RhD protein predicted to be within or below the RBC membrane, causing decreased antigen expression on the red cell surface. Prevalence of serological weak D phenotypes varies by race and ethnicity. Serological weak D phenotypes are the most common D variants detected in Caucasians (0.2%-1.0%). The majority, as in our series, are associated with weak D type 1, 2 or 3. Our data confirmed a high prevalence of weak D type 1 and type 2, but we observed a high prevalence of type 11 and 15 and of the uncommon type 18 too. The most common partial D phenotypes in Europe are DNB, DVI, and DVII. Our data confirmed a high prevalence of D partial type VI. Studies indicate that D partial transfusion recipients are at risk of forming alloanti-D when exposed to conventional RhD-positive blood units.