Drug-induced Hemolytic Anemia Research Articles

Drug-Induced Autoimmune Hemolytic Anemia: Detection of New Signals in the World Pharmacovigilance Database and Risk Assessment in a Nationwide Cohort Study in France

Drug-Induced Autoimmune Hemolytic Anemia: Detection of New Signals in the World Pharmacovigilance Database and Risk Assessment in a Nationwide Cohort Study in France

Acute Hemolytic Anemia Induced by Levofloxacin in A Woman With G6PD Deficiency: A Case Report

Introduction: Glucose 6-Phosphate Dehydrogenase deficiency (G6PD) is an X-linked recessive disorder recognized as the most prevalent enzyme deficiency around the world. G6PD deficiency has a high prevalence in Iran, especially in the northern regions. As we know, hemolysis in G6PD patients was not reported with levofloxacin previously.
 Case Report: In this report, we introduce a 54-year-old G6PD deficient woman who experienced the symptoms of hemolytic anemia following completion of treatment with levofloxacin.
 Result: After ruling out other causes of hemolysis, by using the Naranjo scale, levofloxacin was considered as a possible cause of hemolysis.
 Conclusion: Though the hemolytic anemia induced by levofloxacin is extremely rare in G6PD deficient patients, drug-induced hemolytic anemia should be considered as one of the differential diagnoses. It would be appropriate to use an alternative antibiotic instead of levofloxacin in a G6PD deficient patient.

Population pharmacogenomics: an update on ethnogeographic differences and opportunities for precision public health.

Both safety and efficacy of medical treatment can vary depending on the ethnogeographic background of the patient. One of the reasons underlying this variability is differences in pharmacogenetic polymorphisms in genes involved in drug disposition, as well as in drug targets. Knowledge and appreciation of these differences is thus essential to optimize population-stratified care. Here, we provide an extensive updated analysis of population pharmacogenomics in ten pharmacokinetic genes (CYP2D6, CYP2C19, DPYD, TPMT, NUDT15 and SLC22A1), drug targets (CFTR) and genes involved in drug hypersensitivity (HLA-A, HLA-B) or drug-induced acute hemolytic anemia (G6PD). Combined, polymorphisms in the analyzed genes affect the pharmacology, efficacy or safety of 141 different drugs and therapeutic regimens. The data reveal pronounced differences in the genetic landscape, complexity and variant frequencies between ethnogeographic groups. Reduced function alleles of CYP2D6, SLC22A1 and CFTR were most prevalent in individuals of European descent, whereas DPYD and TPMT deficiencies were most common in Sub-Saharan Africa. Oceanian populations showed the highest frequencies of CYP2C19 loss-of-function alleles while their inferred CYP2D6 activity was among the highest worldwide. Frequencies of HLA-B*15:02 and HLA-B*58:01 were highest across Asia, which has important implications for the risk of severe cutaneous adverse reactions upon treatment with carbamazepine and allopurinol. G6PD deficiencies were most frequent in Africa, the Middle East and Southeast Asia with pronounced differences in variant composition. These variability data provide an important resource to inform cost-effectiveness modeling and guide population-specific genotyping strategies with the goal of optimizing the implementation of precision public health.Supplementary InformationThe online version contains supplementary material available at 10.1007/s00439-021-02385-x.

Safety of Ibuprofen in Children With G6PD Deficiency: A Systematic Review.

Ibuprofen is included on websites and frequently referenced lists as medium risk for inducing hemolysis in children with glucose-6-phosphate dehydrogenase (G6PD) deficiency. This presents a challenge for otolaryngologists who perform tonsillectomy and other surgeries in children, as ibuprofen serves as an important alternative to opioids for perioperative pain control. We systematically review published literature and national medication databases to evaluate the risk of hemolytic anemia and related complications when ibuprofen is used in children with G6PD deficiency. Systematic literature review using preferred reporting items for systematic reviews and meta-analyses methodology. National drug adverse reaction database inquiry. Our search yielded 774 results for review consideration. Of these, three studies were included in our final analysis (two retrospective case-series, and one nonrandomized prospective study). The prospective study showed no evidence of hemolysis from perioperative exposure to ibuprofen or other non-steroidal anti-inflammatory drugs (NSAIDs) in children with G6PD deficiency at high risk. Two population studies in the Middle East suggested extremely low incidence of ibuprofen-related hemolysis (approximate 1/100,000 affected children per year). United States Food and Drug Administration (FDA), European Medicine Agency, and Health Canada adverse drug reaction databases reveled reported ibuprofen-related hematologic adverse reactions of approximate 1/100 million affected children per year. There is scant, low-quality evidence of hemolytic anemia caused by ibuprofen in children with G6PD deficiency. If an association does exist, it is extremely rare. Drug-induced hemolytic anemias are recognizable and reversible following discontinuation of the inciting medication. Given these low risks, ibuprofen should be considered an appropriate choice in the management of perioperative pain in children with G6PD deficiency. NA Laryngoscope, 132:1300-1305, 2022.

Drug‑induced hemolytic anemia

One of the reasons for the development of hemolytic anemia (HA) can be drugs, including some antibacterial, non-steroidal anti-inflammatory, antitumor and antihypertensive drugs. It was found that the most common drug-induced hemolytic anemia (DIHA) develops against the background of taking antibacterial drugs. The true prevalence of DIHA is not known and is approximately one case per 1.0–1.2 million patients. The mechanisms of the occurrence of DIHA are divided into immune and metabolic (non-immune). The first mechanism is associated with the formation of haptens, the second option – with the formation of immune complexes, the third option is mediated by the formation of true autoantibodies to red blood cells, the fourth option of the immune mechanism of the occurrence of DIHA is non-immunological protein absorption on the membranes of red blood cells. The risk factors for the development of DIHA are not fully established. The most common hereditary risk factor for DIHA is glucose-6-phosphate dehydrogenase deficiency. The main method of diagnosing DIHA is a direct antiglobulin test (direct Coombs’ test). The temporal relationship between the use of the inducer drug and the development of HA symptoms is important. The treatment strategy of DIHA is determined by the severity of the disease. In all cases, treatment should be initiated with the identification and withdrawal of the drug that initiated the occurrence of HA. With the development of severe HA, hemodialysis may be required. Prevention of DIHA involves avoiding the use of drugs associated with a high risk of its development.

Drug-induced autoimmune hemolytic anemia in pregnancy: A case report

Introduction. About 10 - 20% of patients taking methyldopa therapy for more than 4 months develop autoantibodies to antigens on the surface of their own red blood cells, while less than 1% develop autoimmune hemolytic anemia. Methyldopa-induced red cell autoantibodies not associated with autoimmune hemolytic anemia are five times more common in pregnant women than in non-pregnant women. Case Report. We present a case of methyldopa-induced immune hemolytic anemia in a 23-year-old woman in her first pregnancy with and an estimated gestational age of 30 weeks. The woman presented with obesity and preeclampsia and there was no information that she has ever received a blood transfusion. The hemoglobin concentration was 10.8 g/dL. The woman started taking methyldopa tablets in the twelfth week of pregnancy and 14 weeks later she developed anemia. Warm type autoantibodies were detected in the 30th week of gestation. Conclusion. Although methyldopa- induced hemolytic anemia is rare during pregnancy, it is necessary to monitor pregnant women who take this therapy, because only discontinuation of the drug leads to termination of hemolysis and correction of anemia.

Immune-Mediated Hemolytic Anemia in a Bitch Triggered by Drugs

Background: Immune-mediated hemolytic anemia (IMHA) is characterized by an autoimmune response with production of auto-antibodies and destruction of erythrocytes resulting in anemia. Primary IMHA is referred to a condition when the cause is unknown (idiopathic), whereas secondary IMHA involves changes in red blood cells caused by the action of drugs, neoplasms, or infectious diseases. The diagnosis can be made through changes in the blood count, usually of a regenerative character, Coombs test, and autoagglutination test. The present study aimed to report a case of drug-induced hemolytic anemia, with emphasis on the clinical signs, diagnostic methods, and treatment, in a female dog.Case: A 9-year-old mixed-breed bitch weighing 29.6 kg was referred to the Veterinary Medical Teaching Hospital (HCV-UFRGS) with a previous diagnosis of gallbladder mucocele that was unresponsive to clinical treatment. After laboratory tests, cholecystectomy was performed, and the procedure required conversion from laparoscopic to open cholecystectomy. Therapy included administration of amoxicillin, dipyrone, tramadol hydrochloride, and meloxicam. Three days after surgery, the dog presented with apathy, lethargy, hyporexia, and a pale and subicteric mucosa. The patient developed hypochromic macrocytic anemia with reticulocytosis, spherocytosis, anisocytosis, and leukocytosis with neutrophilia. The result of the autoagglutination test was positive, confirming the diagnosis. All medications were suspended, and immunosuppressive treatment with dexamethasone was included, with a subsequent switch to prednisolone. After 10 days of treatment, the patient experienced significant improvement, and therapy was discontinued.Discussion: Based on the patient's history, the cause of the IMHA was secondary to drug administration, and it is not possible to distinguish if it was due to one or a combination of drugs, as they were all started and stopped simultaneously. The patient had hypothyroidism, which may have contributed to the production of antibodies against TSH receptors, blocking the hormone's action, thereby causing tissue damage due to T cell-mediated cytotoxicity and the effect of cytokines. The pale and subicteric mucosa, apathy, weakness, lethargy, exercise intolerance, and dyspnea resulted from extravascular hemolysis and bilirubin released from erythrocyte rupture with a subsequent decrease in the number of red blood cells, leading to oxygen transport deficiency. The diagnosis is based on the blood count and results of autoagglutination supported by the response to immunosuppressive therapy. Anemia results in increased production and release of precursor cells from the bone marrow, accompanied by reticulocytosis and increased mean corpuscular volume (MCV) and mean corpuscular hemoglobin concentration (MCHC). The treatment of IMHA consists of supportive care and immunosuppressive therapy with corticosteroids to ensure suppression of the immune system, preventing response against erythrocytes. Initially, tramadol hydrochloride, dipyrone, and amoxicillin with potassium clavulanate were suspended to interrupt the cause of IMHA, and administration of dexamethasone in an immunosuppressive dose was started. Therefore, it is important to include drug-induced IMHA in the differential diagnosis of patients who present with anemia after using medications. Early diagnosis, initiation of therapy, and adequate care were important factors for the recovery of the animal.Título: Anemia hemolítica imunomediada medicamentosa em uma cadelaKeywords: dog, hypochromic macrocytic anemia, erythrocyte, hemoglobin, spherocyte.Descritores: cão, anemia macrocítica hipocrômica, eritrócito, hemoglobina, esferócito.

10-Year Mortality in Patients with Sickle Cell Disease from a Large Population-Based Cohort

Background Mortality rates and causes of death in children with sickle cell disease (SCD) have changed significantly over the past several decades. With ongoing improvements in standards of care, modern mortality estimates must be updated. Children's Healthcare of Atlanta (CHOA) houses one of the largest pediatric SCD programs in the country. This analysis reviews mortality in children with SCD who were treated at CHOA between June 2010-June 2020. Methods We reviewed the CHOA's Sickle Cell Clinical Database (SCCD) for deceased patients. Demographics, SCD genotype, date and age at death, healthcare utilization, hydroxyurea (HU) use, chronic transfusion therapy (CTT), and bone marrow transplant (BMT) were obtained from the SCCD. Cause of death and history of significant comorbidities were abstracted from the medical record. Mortality rates were calculated using person-time for all CHOA SCD patients and population-based mortality was obtained from CDC WONDER Online Database. Results A total of 3,698 patients with SCD were seen at CHOA from June 2010-June 2020 and accounted for 19,998 person-years. Of the 46 patients who died during that time, all but 1 patient had been seen in the CHOA Sickle Cell Outpatient Clinic at least once. That patient received SCD care at a different institution, died from complications of a non-SCD related disease following transfer to CHOA, and was excluded from analysis. Of the 45 remaining patients (178 person-years), the majority were sickle cell anemia genotypes (n=37, 82%; Hb SS or Hb S β0 thalassemia), followed by Hb SC (n=5, 11.1%) and Hb S β+ thalassemia (n=3, 6.7%); 53% (n=24) were female. The average age at death was 12.8 years (1.0-22.8 years). Twenty-one (46.7%) patients had ever been treated with HU and 11 (24.4%) were currently on HU at the time of last contact (either death or last CHOA encounter). Eleven (24.4%) patients had ever been treated with CTT, and 3 (8.9%) were being treated with CTT at time of last contact. In comparison, during the same time period an average of 58% and 12% of the overall CHOA SCD population were being treated with HU and CTT, respectively. Forty-one patients had at least 1 SCD-related encounter at CHOA within 12 months prior to death. For the 4 patients who had not been seen at CHOA within 12 months, the average time since last contact was 1.72 years (1.03 - 2.7 years). Eighty percent (n=8) of the 10 patients who died at age >19 had either recently transitioned to adult care or had documentation of a transition plan. During this 10-year period, the crude death rate was 2.3 per 1,000 person-years. The majority of deaths (62%, n=28) were attributable SCD-related causes and corresponded to a cause-specific mortality rate of 1.40 per 1,000 person-years. The remaining 38% (n=17) of deaths were caused by complex non-SCD comorbidities or accidental trauma and corresponded to a non-SCD related mortality rate of 0.85 per 1,000 person-years. In comparison, the mortality rate for African American persons age <22 in Georgia from 2009-2018 was 0.9 per 1,000 person-years. Of the 28 patients who died due to an SCD-related cause: 12 (27%) experienced an acute illness related to SCD, 4 (9%) succumbed to acute bacterial infections, 3 (7%) died from complications of SCD treatment (1 procedure-related, 2 drug-induced hemolytic anemia), and 1 (2%) died from complications of BMT. Nine (20%) had either recently transitioned to adult care or were lost to follow-up and had no significant non-SCD comorbidities, therefore cause of death was unknown. Of the 17 non-SCD related deaths, 16 (36%) were due to complex non-SCD comorbidities (including cancers, autoimmune disorders, and congenital heart disease) and 1 (2%) from an accidental trauma. Conclusions To our knowledge, this is the largest and most recent study of mortality in patients with SCD from a single institution. Overall, the demographics of deceased patients were similar to those of the CHOA SCD population as a whole. This cohort indicates that trends in mortality of children with SCD have largely shifted away from bacterial infections to other complications of SCD, subsequent treatments, or comorbidities. Our data confirm that patients nearing transition to adult care are at high risk of mortality. This study is limited to deaths that are known to the CHOA system, so future analyses will expand this cohort to include data from death certificates and CDC's National Death Index. Disclosures Lane: FORMA Therapeutics: Membership on an entity's Board of Directors or advisory committees; Global Blood Therapeutics: Membership on an entity's Board of Directors or advisory committees.

A Study on the Relevance of Glucose-6-Phosphate Dehydrogenase Level Screening in Patients with Rheumatic Diseases Prior to Initiating Treatment With Hydroxychloroquine.

ObjectiveDrug-induced hemolytic anemia can occur in patients with glucose-6-phosphate-dehydrogenase (G6PD) deficiency. The practice of G6PD-deficiency screening in the rheumatology field has been inconsistent. This study aimed to determine the utility of screening prior to the initiation of hydroxychloroquine and/or sulfasalazine in rheumatology patients in the ambulatory clinics at Stony Brook University Hospital, New York.MethodsWe conducted a retrospective chart review of cases of rheumatic diseases that were screened for G6PD deficiency at Stony Brook University Hospital ambulatory clinics. Demographic details and relevant clinical and laboratory data of the patients were collected. The data from similar studies in the literature were searched for and reviewed.ResultsThis study consisted of 228 patients with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and Sjögren’s syndrome. Among those patients, 94.7% received hydroxychloroquine, sulfasalazine, or dapsone; 41% (89/228) of patients were screened for G6PD deficiency, and the majority of them were on treatment with hydroxychloroquine. Of those patients, 7.9% (five Caucasians and two African Americans) were found to have G6PD deficiency, and two of the G6PD-deficient patients received hydroxychloroquine. There was no incidence of hemolytic anemia documented in any of the seven patients with G6PD deficiency. We reviewed the literature and found three similar studies of patients receiving hydroxychloroquine with no reported hemolytic anemia from different medical centers in the US, and the frequency of G6PD deficiency reported in these studies was 1.4%, 4.0%, and 4.2%, respectively.ConclusionsOur study suggests that the frequency of G6PD deficiency in our rheumatic population is similar to that of the general population, and the risk of hemolytic anemia in G6PD deficiency associated with hydroxychloroquine is extremely rare. Hence, G6PD screening may not be recommended prior to starting treatment with hydroxychloroquine.

Detection of Autoimmune Hemolytic Anemia Induced by Salvianolate and Evaluation of Blood Transfusion Efficacy

To evaluate the characteristics of autoimmune hemolytic anemia caused by salvianolate by antibody detection and clinical index monitoring. Micro-column gel anti-human globulin method was used for irregular antibody screening and antibody identification. Salvianolate, sodium creatine phosphate and levocarnitine were used to sensitize red blood cells that were compatible with the patient's plasma, and the RBCs were used to test drug antibody in patient plasma respectively. The patient's clinical examination of hemolysis index and blood transfusion effect were analyed retrospectively. The patients were positive for irregular antibody screening, and there were antoanti-Ce antibodies in serum. The erythrocytes sensitized with salvianolate in the patient's serum were positive, while those sensitized with sodium creatine phosphate and levocarnitine were negative. Salvianolate causes drug-induced autoimmune hemolytic anemia in this patient.

Drug-induced autoimmune haemolytic anaemia in a patient treated with artesunate for malaria infection

A 54-year-old woman was diagnosed with severe Plasmodium falciparum malaria following travel to Guinea. Her haemoglobin (Hb) at presentation was 138 g/L (ref range 115–160), with an initial parasite density of 5% and otherwise normal red cell morphology. The patient showed a good response to second line anti-malarial therapy with artesunate but re-presented 16 days post treatment initiation with symptomatic anaemia (Hb of 64 g/L), and displayed typical laboratory features consistent with haemolysis. The direct antiglobulin test (DAT) was positive (3/4) showing IgG and C3d specificity. The antibody screen was also positive, with grade 4+ reactions against all screening cells. Drug-induced autoimmune haemolytic anaemia (DIIHA) from artesunate therapy was suspected. Prednisolone 1 mg/kg therapy was commenced, and transfusion was avoided due to the presence of the autoantibody and high risk of transfusion reaction. Treatment was successful with rapid resolution of haemolysis and Hb completely normalised on follow-up testing within 2 weeks. Response was sustained with tapering of prednisolone. Post-artesunate delayed haemolysis (PADH) is estimated to occur in about 15–30% of patients treated with the drug.1 Cases with a positive DAT are less common but are increasingly being reported and raise the possibility that artesunate may cause DIIHA. Reference1.Camprubi D, Pereira A, Rodriguez-Valero N, et al. Positive direct antiglobulin test in post-artesunate delayed haemolysis: more than a coincidence? Malar J 2019; 15: 123.

How to Manage Antibiotic Allergy in Cystic Fibrosis? Epidemiologic, Diagnostic, and Therapeutic Aspects

Cystic fibrosis (CF) is a complex genetic disease with high mortality, of which 85% is a result of lung disease characterized by serious endobronchial infections. Antibiotic therapy is one of the main treatments of CF, both during acute exacerbations and as chronic maintenance medications, contributing to a prolonged survival. Since neonatal CF screening programs have been implemented universally and the longevity of patients with CF steadily increases, antibiotic hypersensitivity reactions (HSRs) are becoming more important. HSR to antibiotics in CF has been reported since the 1980s and was estimated to occur up to three times more frequently in these patients, probably owing to high rates of antibiotic exposure and boosting stimuli such as infections and inflammation. However, recent studies including large groups of CF patients with a suspicion of antibiotic allergy have used diagnostic algorithms including skin tests and drug provocation tests and showed that true incidence was much lower. The mechanism of the reactions and the clinical presentations are not different in CF than in the general population. Both the immediate and nonimmediate type HSRs are seen, and among the latter, drug fever and drug-induced hemolytic anemia are distinctive presentations. Beta-lactam (BL) agents are the most common cause, with higher rates for ureidopenicillins (piperacillin, mezlocillin, and piperacillin/tazobactam) and cephalosporins (especially ceftazidime), intermediate rates for carbapenems, and lowest rates for aztreonam, and also HSRs to aminoglycosides, macrolides, and quinolones are encountered. Since the available choices for antibiotic therapy are limited due to relevant organisms, management becomes a challenge. It is essential to evaluate the patients according to the mechanism of the HSR and determine the risk of repeat administration of the culprit drug and also safety of alternative drugs with prior skin and provocation tests. The chemical structure and side chains must be taken into account when selecting a safe alternative drug. Contrary to what was previously thought, recent data on cross-reactions between BL antibiotics showed that some BLs can be an option of treatment for patients allergic to other BLs. Desensitization is a useful procedure in immediate and some delayed reactions, if a suitable alternative antibiotic is not available.

Drug-induced hemolytic anemia: Pharmacological aspects

Drug-induced hemolytic anemia is a very rare but potentially lethal adverse drug reaction, which can take the form of oxidative damage to vulnerable erythrocytes (as in glucose-6-phosphate dehydrogenase deficiency), drug-induced thrombotic microangiopathy, or immune-mediated hemolytic anemia. For each form, distinctive drugs are documented as potential triggers. When a formal diagnosis of hemolytic anemia is made following drug administration, a structured approach is recommended to assess the plausibility of an adverse drug reaction based on chronological sequence, epidemiological data, objective evidence (when available), and ruling out of non-drug causes. For suspicions of immune-mediated hemolytic anemia, investigations by a laboratory with specific expertise are crucial given the complexity of the field. If there is good reason to believe hemolytic anemia is drug-induced, immediate drug discontinuation is necessary and corticosteroid administration can be considered. The clinical pharmacology specialist can support evaluation of drug imputability and report the case to the pharmacovigilance system, an important last step in managing such events.

Drug-Induced Hemolytic Anemia: A Fatal Complication Further Under-Recognized in Sickle Cell Disease

Drug-induced immune hemolytic anemia (DIIHA) is commonly attributed to cephalosporins. Ceftriaxone is the most frequently administered cephalosporin in patients with sickle cell disease. We present a pediatric patient with severe DIIHA (hemoglobin

Protective role of tocopherol and ascorbic acid in taxol-treated human erythrocytes in vitro

Taxol is a well-known anticancer agent. It is used for the treatment of several kinds of cancer, including breast cancer, lung cancer and ovarian cancer. In spite of being a good chemotherapeutic agent, taxol has several side effects. Drug-induced haemolytic anaemia is one of the most common side effects of taxol. This study investigated the haemolytic effect of taxol on normal erythrocytes and the protective effect of natural antioxidants ascorbic acid and tocopherol in the presence of taxol. We evaluated the osmotic fragility and the activity of enzymes superoxide dismutase and catalase of erythrocytes in the presence of taxol alone and taxol in combination with tocopherol and ascorbic acid. Taxol-induced haematological perturbation significantly caused haemolysis and reduced the activities of superoxide dismutase and catalase in erythrocytes. The antioxidants tocopherol and ascorbic acid demonstrated a protective effect when added to taxol. The combination of tocopherol with taxol significantly protected the osmotic lysis of erythrocytes and increased the activities of superoxide dismutase but had less effect on catalase. Ascorbic acid showed significant protection of erythrocytes from osmotic lysis but didn’t show any significant effect on superoxide and catalase. The results suggest that both antioxidants, especially tocopherol, could exhibit a protective effect against taxol-induced haematological toxicity.

An unusual side effect by atomoxetine use: hemolytic anemia

Drug-induced autoimmune hemolytic anemia, inducing by antibodies that bind to the erythrocyte surface antigen and resulting by interaction between the immune system and red blood cell membrane, an immunological status characterized by erythrocyte destruction is rare in children. There is enough evidence that about 130 drug caused hemolytic anemia. Hematological side effects due to psychotropic drugs is rare and in the literature there is no case developing hemolytic anemia with the use of atomoxetine. Therefore, this case report is found worthy to be presented and expected to contribute to the literature and possible mechanisms

Unusual serological findings associated with ceftriaxone‐induced immune hemolytic anemia in a child with disseminated low‐grade glioma

Ceftriaxone-induced immune hemolytic anemia (CIHA) is the second most common cause of drug-induced hemolytic anemia. Prompt recognition of this drug reaction is essential because brisk hemolysis can be deadly. The extent to which ceftriaxone antibodies persist after CIHA is unknown; rechallenging patients who have experienced CIHA is not recommended. We report a case of CIHA in a neurooncology patient, which is the first to show anticeftriaxone antibodies with Rh specificity and persisted for 8 months after the drug reaction. These findings have implications for understanding the mechanism of CIHA.

Drug-Induced Hemolytic Anemia. Case Report

Drug-Induced Hemolytic Anemia. Case Report

Hemolytic anemias and vitamin B12 deficieny

Hemolytic anemias consist of corpuscular, immun-hemolytic and toxic hemolytic anemias. Within the group of corpuscular hemolytic anemias, except for the paroxysmal nocturnal hemoglobinuria (PNH), all symptoms are caused by underlying heredetiary disorders within the red blood cell membran (hereditary spherocytosis), deficiencies of red cell enzymes (G6PDH- and pyrovatkinase deficiency) or disorders in the hemoglobin molecule (thalassaemia and sickle cell disease). Immune-hemolytic anemias are acquired hemolytic anemias and hemolysis is caused by auto- or allo-antibodies which are directed against red blood cell antigens. They are classified as warm, cold, mixed type or drug-induced hemolytic anemia. Therapy consists of glucocorticoids and other immunsuppressive drugs. Pernicious anemia is the most important vitamin B12 deficiency disorder. Diagnosis relies on cobalamin deficiency and antibodies to intrinsic factor. The management should focus on a possibly life-long replacement treatment with cobalamin.

Phenazopyridine‐Induced Hemolytic Anemia in Advanced Kidney Disease

Phenazopyridine‐Induced Hemolytic Anemia in Advanced Kidney Disease