Drug-induced antibodies can bind to red blood cells (RBCs) and lead to hemolysis by non-immunological modification of erythrocyte membranes known as adsorption of non-immunological proteins

Drug-induced antibodies can bind to red blood cells (RBCs) and lead to hemolysis by non-immunological modification of erythrocyte membranes known as adsorption of non-immunological proteins. a successful recovery of a 76-year-old patient with diclofenac-induced immune hemolytic anemia, a rare but immediate life-threatening condition of a frequently used drug in clinical practice. strong class=”kwd-title” Keywords: diclofenac, hemolysis, immune hemolytic anemia, anemia, drug-induced immune hemolytic anemia Introduction Autoimmune hemolytic anemia (AIHA) ensues when the hosts immune system acts against its own red cell antigens and has an estimated prevalence of approximately 1 in Angelicin 100,000 individuals [1]. Approximately 50% of the cases refer to primary or idiopathic AIHA, where an associated disorder is not found [2]. Secondary causes of AIHA?depend on the studied population. Current series estimate that half are associated with hematological malignancy, TUBB3 a third with infection, a sixth with collagen vascular disorders, and a tenth with drug-induced immune hemolytic anemia (DIIHA), the latter reaching an estimated incidence of one per million per year [1,3]. Diclofenac is one of the nonsteroidal anti-inflammatory drugs (NSAIDs) most used for the treatment of rheumatoid arthritis and osteoarthritis?[4]. Though generally well tolerated, over 400 adverse reactions have been documented. Most frequently, adverse reactions affect the gastrointestinal tract, the skin, and the central nervous system?[5]. Direct hematological side effects such as leukopenia, thrombocytopenia, and aplastic anemia have been described only in limited cases [6-9]. We present the case of a 76-year-old patient with?diclofenac DIIHA and a summary of the pathophysiology and therapeutic options. Case presentation A 76-year-old woman presented to the Emergency Department (ED) with recent onset of fatigue. She had a previous medical history of essential arterial hypertension, dyslipidemia, and spinal osteoarthritis with sporadic episodes of lumbosciatic pain. Angelicin Regular medications initiated several years prior included perindopril 8 mg and rosuvastatin 10 mg. No Angelicin allergies, alcohol, tobacco, toxins, or animal exposures were known, and she had no other relevant personal or familiar history. Three weeks before admission the patient had an exacerbation of right lumbosciatic pain. This Angelicin episode was similar to the previous ones, for which she usually was prescribed oral NSAIDs, acetaminophen, general physical therapy, massages, and?rest?with complete recovery. However, this time the pain was refractory to general measures, and eight days before admission, she was prescribed a combination of a daily intramuscular administration of 4 mg thiocolchicoside, 75 mg diclofenac, and 5 mg diazepam for a total of six days. On the fifth day of treatment, she developed generalized malaise, fatigue, nausea, postprandial vomiting, and diarrhea with up to six soft, brownish dejections per day. Despite resolution of nausea, vomiting, and diarrhea, she experienced progressive worsening of fatigue and Angelicin was admitted to the ED. Detailed medical history was negative for other symptoms, namely, fever, coluria, acholia, melena, and other evident blood losses, either on admission or in the past. Physical examination revealed jaundice and pallor of the skin and mucous membranes. No?epistaxis,?gingivorrhagia, adenopathies, ecchymosis, or other skin lesions were found. Blood pressure was 137/62 mmHg and heart rate was 96 beats per minute, respiratory rate was 16 beats per minute, and peripheral oxygenation saturation was 96%. No fever or other abnormalities were noted. Blood examination showed normocytic normochromic anemia (hemoglobin: 7.9 g/dL, reference median globular volume: 88 fL), reticulocytosis (9.2%), leucocytosis (white blood cells: 13.8 10 9/L), hyperbilirubinemia at the expense of unconjugated bilirubin (total bilirubin: 4.09 mg/dL, conjugated bilirubin: 0.97 mg/dL), elevated lactic dehydrogenase (805 UI/L), and sedimentation rate (VS: 76 mm). Serum iron concentration, ferritin, total iron-binding capacity, folic acid, or vitamin B12 showed no significant changes and haptoglobin levels were undetectable. Peripheral blood smear revealed exuberant erythrocyte rouleaux and spherocytes. The direct antiglobulin test (DAT) was positive for immunoglobulin G (IgG). Chest radiography, abdominal ultrasound, and electrocardiogram performed in the ED were normal. The hypothesis of AIHA was considered in the.