scholarly journals Diagnosis and Management of Autoimmune Hemolytic Anemia in Patients with Liver and Bowel Disorders

2021 ◽  
Vol 10 (3) ◽  
pp. 423
Author(s):  
Cristiana Bianco ◽  
Elena Coluccio ◽  
Daniele Prati ◽  
Luca Valenti
Keyword(s):  
Hemolytic Anemia ◽  
Autoimmune Hemolytic Anemia ◽  
Primary Biliary Cholangitis ◽  
Drug Induced ◽  
Adequate Treatment ◽  
High Clinical Suspicion ◽  
Bowel Diseases ◽  
Choice Of Treatment ◽  
Bowel Disorders ◽  
Biochemical Indices

Anemia is a common feature of liver and bowel diseases. Although the main causes of anemia in these conditions are represented by gastrointestinal bleeding and iron deficiency, autoimmune hemolytic anemia should be considered in the differential diagnosis. Due to the epidemiological association, autoimmune hemolytic anemia should particularly be suspected in patients affected by inflammatory and autoimmune diseases, such as autoimmune or acute viral hepatitis, primary biliary cholangitis, and inflammatory bowel disease. In the presence of biochemical indices of hemolysis, the direct antiglobulin test can detect the presence of warm or cold reacting antibodies, allowing for a prompt treatment. Drug-induced, immune-mediated hemolytic anemia should be ruled out. On the other hand, the choice of treatment should consider possible adverse events related to the underlying conditions. Given the adverse impact of anemia on clinical outcomes, maintaining a high clinical suspicion to reach a prompt diagnosis is the key to establishing an adequate treatment.

Primary biliary cholangitis associated with warm autoimmune hemolytic anemia

2016 ◽  
Vol 17 (2) ◽  
pp. 128-131 ◽  
Author(s):  
Emmanuel I. Gonzalez-Moreno ◽  
Sylvia A. Martinez-Cabriales ◽  
Miguel A. Cruz-Moreno ◽  
Omar D. Borjas-Almaguer ◽  
Carlos A. Cortez-Hernandez ◽  
...  
Keyword(s):  
Hemolytic Anemia ◽  
Autoimmune Hemolytic Anemia ◽  
Primary Biliary Cholangitis

A Rare Cause of Anemia in Inflammatory Bowel Diseases: A Case Report and Review of Literature

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 5385-5385
Author(s):  
Waqas Ahmed ◽  
Kevin Monroe ◽  
James Essell ◽  
E. Randolph Broun
Keyword(s):  
Case Report ◽  
Hemolytic Anemia ◽  
Inflammatory Bowel Diseases ◽  
Autoimmune Hemolytic Anemia ◽  
Blood Smear ◽  
Rare Complication ◽  
Peripheral Blood Smear ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Abstract Introduction: Anemia is a common problem in patients with inflammatory bowel diseases (IBD), and its etiology is usually multifactorial. It can be produced by chronic blood loss, nutritional deficiencies, and drugs such as salazopyrine; however it can also due to auto immune hemolysis, which is a rare complication of IBD. We report a case of coombs positive autoimmune hemolytic anemia associated with ulcerative colitis both diagnosed at the same presentation. Case Report: A 32 year old man with no significant past medical history presented with complaint of dark colored urine, jaundiced skin and fatigue for 4 weeks. He also reported diarrhea mixed intermittently with blood for last few months. Physical exam was consistent with jaundice and anemia (pallor and icterus) with slightly palpable spleen. Initial lab work up showed Hb of 3.8 with normal platelet and WBC count, high reticulocytes count of 7% .LFT showed serum bilirubin of 3.6 (direct 0.4) with normal serum ALT and AST levels .Serum LDH was high (1032 U/l) while serum haptoglobin was low (0.11 mg/dl). Peripheral smear showed anisopoikilocytosis & spherocytosis. (See Figure 1) Further investigations revealed a positive direct Coombs test consistent with diagnosis of autoimmune hemolytic anemia. CT abdomen and pelvis showed mild splenomegaly & non-specific enlarged mesenteric lymph nodes. Colonoscopy revealed ulcerative pancolitis confirmed by histological findings of biopsies taken. Patient received PRBC transfusions and was started on steroids and mesalamine and was discharged on maintenance dose. His symptoms resolved in 4 weeks and Hb remained stable with no evidence of further hemolysis at 4 month follow up .Repeated CT abdomen & pelvis showed resolution of the lymphadenopathy. Figure 1: Peripheral Blood smear showing anisopoikilocytosis & spherocytosis. Figure 1:. Peripheral Blood smear showing anisopoikilocytosis & spherocytosis. Discussion: Autoimmune hemolytic anemia (AIHA) is a rare complication of IBD. The exact underlying pathogenesis of this association remains obscure; however it has been attributed to the production of cross reacting anti erythrocyte antibodies. In AIHA associated with IBD, corticosteroids are considered to be first line therapy and often cause remission of hemolysis along with treatment for IBD Immunomodulators and splenectomy has been used for patients with refractory AIHA. Colectomy done for fulminant colitis has also been reported to induce remission of AIHA. Further studies for long term follow up and pathogenesis of this association are warranted.

scholarly journals First Report of Eltrombopag Induced Severe Autoimmune Hemolytic Anemia in the Management of Waldenström Macroglobulinemia-associated Autoimmune Thrombocytopenia

2021 ◽  
Author(s):  
Yingying Shen ◽  
Hangping Ge ◽  
Baodong Ye ◽  
Zhiyin Zheng ◽  
Keding Shao ◽  
...  
Keyword(s):  
Hemolytic Anemia ◽  
Autoimmune Hemolytic Anemia ◽  
Single Treatment ◽  
Autoimmune Thrombocytopenia ◽  
Drug Induced ◽  
Case Presentation ◽  
Waldenström Macroglobulinemia ◽  
First Report ◽  
Waldenstrom Macroglobulinemia ◽  
Platelet Level

Abstract Background: Autoimmune thrombocytopenia (ITP) and autoimmune hemolytic anemia (AIHA) can be observed in Waldenström Macroglobulinemia (WM). The cause of AIHA should be carefully distinguished during the disease management. Case Presentation: A 63-year-old female WM patient complicated with thrombocytopenia, who was admitted to our department with a complaint of abdominal pain. After first half of bortezomib/dexamethasone/rituximab (BRD) chemotherapy, her platelet level recovered, but subsequently decreased to extremely low level (around 1-2×109/L), and the patient suffered from platelet transfusion refractoriness. During the management of refractory thrombocytopenia, the patient developed severe hemolytic anemia, and further tests confirmed warm AIHA. FcγRIIα polymorphism test showed that the patient had FcγRIIα-131RH, which implied that the AIHA may not be WM-related. Given the effects of ibrutinib in controlling WM, ibrutinib single treatment was started, which quickly corrected the thrombocytopenia within five days, but not hemolysis. With a relatively safe platelet level, eltrombopag was stopped, and the hemolysis alleviated within three days after eltrombopag withdrawal. Conclusion: This is the first report on eltrombopag-induced AIHA, and we should always keep in mind of the drug induced hemolysis even in disorders with autoimmune background.

An Interesting Case of EBV-Associated Autoimmune Hemolytic Anemia

2019 ◽  
Vol 152 (Supplement_1) ◽  
pp. S87-S88
Author(s):  
Sapna Desai ◽  
Jeffrey West ◽  
Salvador Sena
Keyword(s):  
Hemolytic Anemia ◽  
Autoimmune Hemolytic Anemia ◽  
Cell Function ◽  
Hepatitis B Surface Antigen ◽  
Rare Complication ◽  
Macrocytic Anemia ◽  
Interesting Case ◽  
Significant Past Medical History ◽  
Adequate Treatment ◽  
Laboratory Test Results

Abstract We report a case of a 28-year-old male with no significant past medical history who presented with a weeklong history of flu-like symptoms, dark urine, and cold-induced pain and discoloration in his fingers. Upon presentation, he was noted to be significantly jaundiced. Abdominal ultrasound showed splenomegaly. Laboratory test results returned as follows: hematocrit, 26.4%; hemoglobin, 9.0 g/dL; WBC count, 9.8 × 109/L; and automated differential, 0.42 segmented neutrophils, 0.44 lymphocytes, and 0.08 monocytes. Manual differential showed 0.26 atypical lymphocytes, 0.21 lymphocytes, 0.10 monocytes, 0.03 metamyelocytes, and 0.05 segmented neutrophils. He was found to have a normochromic macrocytic anemia with absolute lymphocytosis, monocytosis, and thrombocytopenia. Peripheral blood smear revealed normochromic macrocytic RBCs with anisocytosis. Downey type II cells, plasmacytoid lymphocytes, large activated lymphocytes, and monocytes were present in addition to a neutrophilic left shift up to metamyelocytes. Liver function tests showed elevated levels of total bilirubin (8.4 mg/dL), direct bilirubin (2.6 mg/dL), aspartate aminotransferase (193 U/L), alanine aminotransferase (102 U/L), and alkaline phosphatase (132 U/L). Urinalysis was positive for urobilinogen. Serology was nonreactive for anti–hepatitis A IgM, hepatitis B surface antigen, and anti–hepatitis C antibody. Positive results were obtained for a rapid monoscreening test and Epstein-Barr virus viral capsid antigen IgM. Direct antiglobulin testing showed positivity for IgG, and complement and cold autoantibody were detected. He was transfused and treated with prednisone, IVIG, and external warmth. After improvement, the patient was discharged with recommendations for follow-up. Hemolytic anemia is a relatively rare complication of patients with infectious mononucleosis and occurs in approximately 1% to 3% of these patients. The pathogenesis of EBV-related autoimmune hemolytic anemia is unknown, with a suspicion for inadequate B-cell function after infection. Appropriate laboratory testing and analysis are critical for rapid diagnosis in these patients to ensure adequate treatment with no long-term sequelae.

scholarly journals Autoimmune Hemolytic Anemia Induced by Levofloxacin

2014 ◽  
Vol 2014 ◽  
pp. 1-2
Author(s):  
Marwan Sheikh-Taha ◽  
Pascale Frenn
Keyword(s):  
Emergency Department ◽  
Urinary Tract Infection ◽  
Hemolytic Anemia ◽  
Autoimmune Hemolytic Anemia ◽  
Rare Condition ◽  
White Female ◽  
Coombs Test ◽  
Drug Induced ◽  
Indirect Bilirubin ◽  
Patient Reported

Drug-induced autoimmune hemolytic anemia is a rare condition. We report the case of a 32-year-old white female who presented to the emergency department with generalized fatigue, fever, and jaundice. The patient reported using levofloxacin few days prior to presentation for urinary tract infection. The patient had evidence of hemolytic anemia with a hemoglobin of 6.7 g/dL which dropped to 5 g/dL on day 2, the direct Coombs test was positive, indirect bilirubin was 5.5 mg/dL, and LDH was 1283 IU/L. Further testing ruled out autoimmune disease, lymphoma, and leukemia as etiologies for the patient’s hemolytic anemia. Levofloxacin was immediately stopped with a gradual hematologic recovery within few days.

scholarly journals How I treat warm autoimmune hemolytic anemia

Blood ◽  
2021 ◽  
Author(s):  
Wilma Barcellini ◽  
Bruno Fattizzo
Keyword(s):  
Bone Marrow ◽  
Hemolytic Anemia ◽  
Autoimmune Hemolytic Anemia ◽  
Bone Marrow Failure ◽  
Clinical Severity ◽  
Therapeutic Interventions ◽  
Drug Induced ◽  
Bone Marrow Failure Syndromes ◽  
Dependent Cell ◽  
Changes Over Time

Warm autoimmune hemolytic anemia (wAIHA) is caused by increased erythrocyte destruction by IgG autoantibodies, with or without complement activation. Antibody-dependent cell-mediated cytotoxicity by macrophages/activated lymphocytes occurs in the lymphoid organs and spleen (extravascular hemolysis). The ability of the bone marrow to compensate determines clinical severity. The different pathogenic mechanisms, their complex interplay, and changes over time may explain wAIHA's great clinical heterogeneity and unpredictable course. The disease may be primary, drug-induced, or associated with lymphoproliferative neoplasms, autoimmune and infectious diseases, immunodeficiencies, solid tumors, or transplants. Therapeutic interventions include steroids, splenectomy, immunosuppressants, and rituximab; the latter is increasingly used in steroid refractory cases based on evidence from the literature and a few prospective trials. We present five patient case studies highlighting important issues: 1) the diagnosis and proper use of steroid therapy; 2) the concerns about the choice between rituximab and splenectomy in second-line treatment; 3) the need of periodical re-evaluation of the disease to assess the possible evolution of relapsed/refractory cases in myelodysplastic and bone marrow failure syndromes; and 4) the difficulties in managing cases of severe/acute disease which are at high risk of relapse. Incorporating novel targeted therapies into clinical practice will be an exciting challenge in the future.

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