Case Report: First Case of Cefotaxime-Sulbactam-Induced Acute Intravascular Hemolysis in a Newborn With ABO Blood Type Incompatibility by the Mechanism of Non-Immunologic Protein Adsorption

BackgroundABO blood type incompatibility hemolytic disease of newborn (ABO-HDN) and drug-induced immune hemolytic anemia (DIIHA) due to non-immunologic protein adsorption (NIPA) mainly cause extravascular hemolysis. All the reported severe DIIHA were caused by drug-induced antibodies, and rare report of acute intravascular hemolysis was caused by the NIPA mechanism or ABO-HDN.Case presentationWe report the first case of acute intravascular hemolysis induced by cefotaxime sodium - sulbactam sodium (CTX - SBT) in a case of ABO-HDN which resulted in death at 55 h after birth. The mother’s blood type was O and RhD-positive, and the newborn’s blood type was B and RhD-positive. No irregular red blood cell (RBC) antibodies or drug-dependent antibodies related to CTX or SBT was detected in the mother’s plasma and the plasma or the RBC acid eluent of the newborn. Before the newborn received CTX - SBT treatment, the result of direct antiglobulin test (DAT) was negative while anti-B was positive (2 +) in both plasma and acid eluent. After the newborn received CTX - SBT treatment, the results of DAT for anti-IgG and anti-C3d were both positive, while anti-B was not detected in plasma, but stronger anti-B (3 +) was detected in acid eluent. In vitro experiments confirmed that NIPA of SBT promoted the specific binding of maternal-derived IgG anti-B to B antigen on RBCs of the newborn, thereby inducing acute intravascular hemolysis.ConclusionThe NIPA effect of SBT promoted the specific binding of mother-derived IgG anti-B in newborn’s plasma to the newborn’s RBC B antigens and formed an immune complex, and then activated complement, which led to acute intravascular hemolysis. Drugs such as SBT with NIPA effect should not be used for newborns with HDN.

A Rare Case of Immune Mediated Hemolytic Anemia- Tuberculosis

Tuberculosis is one of the oldest diseases known to mankind. The disease still puzzles us with its varied clinical presentations and complications. Though tuberculosis is known to have many hematological manifestations, auto immune hemolytic anemia is extremely rare in tuberculosis. Here we report aninteresting case of tuberculosis presenting with auto immune hemolytic anemia. The treatment withanti tuberculous therapy is enough for the managing tuberculosis associated auto immune hemolyticanemia.

A Case of Rheumatoid Arthritis Associated with Microcytic Anemia

Rheumatoid arthritis (RA) is one of the most common inflammatory arthritides. It is associated with multiple systemic features, including hematological manifestations such as anemia, neutropenia and thrombocytopenia. However, immune hemolytic anemia is extremely rare with only 3 reports indexed in medline, and one of them being due to methotrexate toxicity. Microcytic anemia is a condition in which the body's tissues and organs do not get enough oxygen. This lack of oxygen can happen because the body does not have enough red blood cells, or because the red blood cells do not contain enough hemoglobin, which is a protein that transports oxygen in the blood. Case Presentation: A 60 year old female a known case of rhematoid arthritis and hypothyrodisam in 2013 for last past 3 years. Who presented to us with history of recurrent anemia . In march 2021, she was admitted to hospital because of palpitations and shortness of breath due to severe anemia. Results of laboratory studies were hemoglobin, 6.9 gm/dl and haptoglobin, less than 29.8mg/dl. A diagnosis of anemia was made on the basis of the laboratory findings She was transfused with 1units packed red blood cells (pRBCs) over less than 6 hours. High-dose PSL (50 mg/day) was started, and the anemia improved. The hemoglobin level increased to 7.0 gm/dl within the 1st week. Conclusion: The differential diagnosis of various hematological disorders should include rheumatic autoimmune diseases among other causes of blood cell and hemostasis abnormalities. It is crucial that hematologists be aware of Treatment should be administered promptly, with rheumatological consultation.

Case Report: Oral Cimetidine Administration Causes Drug-Induced Immune Hemolytic Anemia by Eliciting the Production of Cimetidine-Dependent Antibodies and Drug-Independent Non-specific Antibodies

Previously, it was reported that multiple patients had hemolytic anemia associated with cimetidine administration, while only one patient who had received intravenous cimetidine was serologically diagnosed with drug-induced immune hemolytic anemia (DIIHA) caused by cimetidine-dependent antibodies. However, the ability of oral cimetidine intake to induce the production of antibodies has not been examined. In this study, we report a 44-year-old male patient in whom oral cimetidine administration resulted in cimetidine-dependent antibodies and drug-independent non-specific antibodies, leading to the development of DIIHA. Serological tests showed that the results of direct antiglobulin test (DAT) for anti-IgG (3+) and anti-C3d (1+) were positive. The IgM and IgG cimetidine-dependent antibodies (the highest total titer reached 4,096) were detected in the plasma incubated with O-type RBCs and 1 mg/mL cimetidine or the plasma incubated with cimetidine-coated RBCs. IgG-type drug-independent non-specific antibodies were detected in blood samples collected at days 13, 34, 41, and 82 post-drug intake. This is the first study to report that oral administration of cimetidine can elicit the production of cimetidine-dependent antibodies, leading to DIIHA, and the production of drug-independent non-specific antibodies, resulting in hemolytic anemia independent of cimetidine. Presence of pathogenic antibodies were detectable longer than 41 days. This suggests that patients with DIIHA caused by cimetidine need to be given necessary medical monitoring within 41 days after cimetidine intake.

Non-immune Hemolysis in Gaucher Disease and Review of the Literature

Gaucher disease (GD) is an autosomal recessive disease characterized by the buildup of glucocerebrosides in macrophages, resulting in the formation of “Gaucher cells.” These cells predominantly infiltrate the liver, spleen, and bone marrow leading to hepatosplenomegaly, cytopenia, and bone pain. Anemia in GD is typically considered to result from non-hemolytic processes. Although rare, a higher rate of hemolytic anemia of the autoimmune type has been reported in GD than in the general population. The literature on non-immune hemolytic anemia in GD is scarce. We review the literature on hemolytic anemia in GD and report on a case of non-immune hemolytic anemia secondary to GD. We believe this is the first description of a patient with confirmed GD and symptomatic non-immune hemolytic anemia that responded to GD-specific treatment.

Cytomegalovirus-Associated Hemolytic Anemia in an Infant Born to a Mother with Lupus

A 31-day-old infant was admitted to the pediatric intensive care unit due to shock and anemia. The mother had systemic lupus erythematosus and direct antiglobulin test (DAT)-positive hemolytic anemia. The perinatal course of this infant and the mother was uneventful. Regular health check screenings revealed that activity, growth, and development were unremarkable at birth, 5, and 28 days of life. Passive immune hemolytic anemia due to neonatal lupus erythematosus was diagnosed based on a positive DAT for warm-type IgG antibodies, reticulocytosis, and lupus-specific antibodies at rehospitalization. It was complicated by cytomegalovirus (CMV) antigenemia. Umbilical cord blood and peripheral blood samples obtained from the infant at 5 days after birth were negative for CMV DNA. The infant was curatively treated by intensive care with repeated blood transfusions and antiviral therapy. This is the first report indicating that CMV infection exacerbates hemolytic anemia in patients with maternal red blood cell alloantibodies.

A RETROSPECTIVE STUDY OF THE TREATMENT RESULTS OF 40 DIVERSE PATIENTS OF ANEMIA

Background and objective: Anemia is clinical common event. There are many types of anemias, which included stem cell problems, vitamin deficiency, chronic diseases and drug antibody -induced immune hemolytic anemia. In this study, a retrospective purpose was investigated to assess the clinical efficacy of treatment and their outcome. Methods: Total 40 patients with different types of anemias were presented in the second affiliated hospital of central south University, China and my tumor institute during 1989-2019. The therapeutically design among those patients with anemias was setted to the various regimen according to diseases diagnoses. Results and conclusion: Total 23 patients achieved cure or complete remission (CR), with the exception of refractory cancers and uremic anemia. Iron supplement was provided in 5 iron deficiency anemia. One megaloblastic anemia produced an excellent response following the supplement of vitamin B12 and folic acid. 2 aplastic anemia obtained complete remission with the integrated protocol of methyl testosterone, adenine, leucogen, and levamisol. Steroid hormone (e.g. prednisone) mixed traditional medicine were occasionally promising benefit in a nephrotic syndrome and renal insufficiency. Among 2 cases with drug-induced immune hemolytic anemia (DIIHA), laboratory studies one patient's serum contained paracetamol-dependent antibody that in the presence of paracetamol, agglutinated in-vitro with "O" red cells with or without complement. Drug antibody titer was 1:4 positive. Immune hemolysis was mediated by both the immune complex and uptake of drugs, whereas hemolysis induced by another native herb was caused by absorption of the drug only. In addition, with respect to anemia induced by malignancies, the molecular genomic regulation of retinoic acid in APL has been elucidated (see illustration in full text). Therefore, promoting effective prevention and / or early preventive treatment of anemia is our concern. Peer Review History: Received 5 March 2021; Revised 27 March; Accepted 23 April, Available online 15 May 2021 UJPR follows the most transparent and toughest ‘Advanced OPEN peer review’ system. The identity of the authors and, reviewers will be known to each other. This transparent process will help to eradicate any possible malicious/purposeful interference by any person (publishing staff, reviewer, editor, author, etc) during peer review. As a result of this unique system, all reviewers will get their due recognition and respect, once their names are published in the papers. We expect that, by publishing peer review reports with published papers, will be helpful to many authors for drafting their article according to the specifications. Auhors will remove any error of their article and they will improve their article(s) according to the previous reports displayed with published article(s). The main purpose of it is ‘to improve the quality of a candidate manuscript’. Our reviewers check the ‘strength and weakness of a manuscript honestly’. There will increase in the perfection, and transparency. Received file: Reviewer's Comments: Average Peer review marks at initial stage: 6.0/10 Average Peer review marks at publication stage: 7.0/10 Reviewer(s) detail: Dr. Bilge Ahsen KARA, Ankara Gazi Mustafa Kemal Hospital, Turkey, [email protected] Prof. Dr. Hassan A.H. Al-Shamahy, Sana'a University, Yemen, [email protected] Similar Articles: THE ASSOCIATION BETWEEN LEVELS OF HEPCIDIN, IRON STATUS AND MICRO-INFLAMMATION MARKERS AMONG HAEMODIALYSIS