scholarly journals Autoimmune Hemolytic Anemia Induced by Levofloxacin

2014 ◽  
Vol 2014 ◽  
pp. 1-2
Author(s):  
Marwan Sheikh-Taha ◽  
Pascale Frenn

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.

2013 ◽  
Vol 2013 ◽  
pp. 1-3
Author(s):  
Aram Barbaryan ◽  
Chioma Iyinagoro ◽  
Nwabundo Nwankwo ◽  
Alaa M. Ali ◽  
Raya Saba ◽  
...  

Drug-induced immune hemolytic anemia is a rare condition with an incidence of 1 per million of the population. We report the case of a 36-year-old female who presented to the emergency department complaining of shortness of breath and dark colored urine. Physical examination was significant for pale mucous membranes. The patient reported using ibuprofen for a few days prior to presentation. Complete blood count performed before starting ibuprofen revealed normal platelets and hemoglobin values. On admission, the patient had evidence of hemolytic anemia with hemoglobin of 4.9 g/dL, hematocrit of 14.2%, lactate dehydrogenase 435 IU/L, and reticulocytosis 23.2%. Further testing ruled out autoimmune disease, lymphoma, and leukemia as etiologies for the patient’s new onset hemolytic anemia. Ibuprofen was immediately stopped with a gradual hematologic recovery within 3 days.


Blood ◽  
1959 ◽  
Vol 14 (12) ◽  
pp. 1280-1301 ◽  
Author(s):  
JEAN DAUSSET ◽  
JACQUES COLOMBANI

Abstract A statistical study of 128 cases of autoimmune hemolytic anemias, serologically followed up in the same laboratory, led to some conclusions on classification, prognosis and treatment. Five forms were distinguished: 1. Idiopathic autoimmune hemolytic anemia with warm autoantibodies (IAHA-wa) was the most frequent form (65 per cent of the cases). It was observed in all peroids of life. A slight predominance among females was noted. This form was characterized clinically by a generalized or conjunctival icterus and a moderate splenomegaly. Hematologically a macrocytic normochromic anemia was present and serologically warm incomplete autoagglutinins, often nonspecific, or sometimes specific for a group antigen, were detected. Hemolysins were not found. The average course was 13 months followed by recovery (54 per cent) and 16 months followed by death (46 per cent). These two groups of patients were compared extensively. No differences in the age, sex, blood group and severity of the initial anemia were noted. A low reticulocyte count, leukopenia and association with thrombocytopenic purpura were more frequent in fatal cases. Tile persistence of a positive indirect Coombs test was unfavorable. Those with free antibodies in the plasma were the most serious. Fifty-two per cent of fatal cases had a positive indirect Coombs test. Of those who recovered, 18.5 per cent had this serologic finding. Transfusions were usually done at the begining of the disease. The efficacy of corticosteroid hormones was confirmed; the percentage of recoveries has risen since this therapy has been used fully (37.5 to 70 per cent). Early or late splenectomy had no influence on final desensitization (long-term effect), but led in 58 per cent of the cases to good clinical results (immediate effect). The spleen destroys red cells coated with noncomplement-fixing antibodies, so that splenectomy leads to compensation for the anemia. One must also describe the acute autoimmune hemolytic anemia observed especially in children, in which warm hemolysins could be detected at the very early stage of the disease. Complement was diminished or absent and the serum often showed anticomplementary activity. Complete recovery was rapid. 2. Symptomatic autoimmune hemolytic anemia with warm autoantibodies (SAHA-wa) accompanied mostly malignant conditions of the lymphocytic or reticuloendothelial systems as well as more rarely disseminated lupus erythematosus (17.6 per cent of the cases). Except for the causal disease, these cases were not different from IAHA-wa and their prognosis depended on the prognosis of the causal disorder. 3. Idiopathic autoimmune hemolytic anemia with cold antibodies (IAHAca) was less frequent (7.7 per cent of the cases). Clinically it was characterized by the rarity of splenomegaly, the chance of cold paroxysmal hemoglobinuria (1 case out of 10) and of Raynaud’s syndrome (1 case out of 10), and serologically by the presence of a cold acid-hemolysin (7 cases out of 8) along with an increased titer of complete agglutinins. Complement was diminished or absent. A positive Coombs test was possibly due to complement fixation. The course of these forms seemed to be very chronic: Nine cases of the 10 of the series were in progress for an average of 26 months, without any apparent trend to densensitization. The action of hormone therapy was less striking than in the warm variety. Splenectomy was probably not effective (1 case), since the red cells sensitized by complement-fixing antibodies were mainly recovered by the liver. 4. Symptomatic autoimmune hemolytic anemia wiith cold antibodies (SAHA-ca) was divided into two distinct forms: (a) one symptomatic of a malignant condition of the blood of the same type as in SAHA-wa (7 per cent of cases). The serology was identical to that of IAHA-ca. The prognosis was determined by that of the causal disease; (b) one symptomatic of a virus or a presumed virus infection (3.9 per cent of cases). Here an acid-hemolysin usually accompanied a very high complete cold agglutinin titer. Complete recovery occurred rapidly. In all cases with cold antibodies exposure to cold had to be carefully avoided. In cases of hemolysins, washed red cells had to be used for transfusions.


2021 ◽  
Author(s):  
Shuku Sato ◽  
Wataru Kamata ◽  
Yotaro Tamai

Abstract A 55-year-old man suffered from dyspnea, general malaise, and jaundice. His laboratory date showed pancytopenia and hemolytic anemia, and computed tomography showed splenomegaly. Bone marrow examination revealed myelofibrosis (MF)-1. The hemolytic anemia was diagnosed as IgM autoimmune hemolytic anemia (AIHA) with negative direct and indirect Coombs test but positive IgM-direct antiglobulin test. We started ruxolitinib 20 mg, which improved not only bone marrow fibrosis, symptoms related to myeloproliferative neoplasms and splenomegaly, but also AIHA. AIHA may be associated with Autoimmune MF (AIMF), and cytokines such as transforming growth factor (TGF)-β are thought to be involved in such cases. This case suggests that ruxolitinib may improve the cytokine levels and may lead to the treatment of AIHA as well as AIMF.


2021 ◽  
Author(s):  
Yingying Shen ◽  
Hangping Ge ◽  
Baodong Ye ◽  
Zhiyin Zheng ◽  
Keding Shao ◽  
...  

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.


2020 ◽  
Vol 4 (4) ◽  
pp. 668-670
Author(s):  
Zach Edwards ◽  
Stephen DeMeo

Introduction: Sepsis commonly brings patients to the emergency department (ED). Patient outcomes can vary widely. In some cases, rare complications of sepsis such as autoimmune hemolytic anemia can occur. Case Report: A 68-year-old female presented with sepsis secondary to infected nephrolithiasis. The patient had signs and symptoms consistent with hemolysis upon arrival to the ED. Her hemolysis progressively worsened over a two-day period leading to a diagnosis of warm autoimmune hemolytic anemia. She responded well to treatment; however, her condition began to worsen due to a new infection caused by perforated colonic diverticula. The patient ultimately expired from complications of her perforated colonic diverticula. Conclusion: It is crucial that emergency physicians understand the risk factors, symptoms, pathophysiology, and treatment of this rare complication of sepsis so that favorable patient outcomes can be achieved.


Blood ◽  
2021 ◽  
Author(s):  
Wilma Barcellini ◽  
Bruno Fattizzo

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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