Autoimmune hemolysis

Nausea, vomiting, and headaches, the most common side effects, are related to the blood level of sulfapyridine. If the dose is reduced, symptoms frequently improve. Fever, rash, aplastic anemia, and autoimmune hemolysis are hypersensitivity reactions to the medication. These occur less commonly and are not dose related. Sulfasalazine should not be used in patients with hypersensitivity agranulocytosis or aplastic anemia. 

The interpretation of delayed transfusion reactions can be difficult, as the occurrence of low-grade warm acquired hemolytic anemia can resemble this form of transfusion reaction (78). Careful elution of antibody, its identification, and elucidation of its relation to the transfused erythrocytes are required to establish the nature of the reaction. If the indirect antiglobulin test is negative, autoimmune hemolysis is the likely pathogenic mechanism (79). 

Autoimmune hemolytic anemia has rarely been reported with the older cephalosporins, including cefalexin (40), cefalotin (41,42), cefazolin (43), and cefaloridine (44). The main laboratory findings correspond to the drug adsorption mechanism classically found in benzylpenicil-lin-induced immune hemolysis. Antibodies cross-reacting with cefalotin and benzylpenicillin were found in both benzylpenicillin-induced and cefalotin-induced hemolysis (43,45) Cases have also been reported with cefamandole (46), cefalexin (47), ceftriaxone (48), cefotaxime (49,50), cefotetan (51,52) and ceftazidime (53). 

Ceftriaxone has been associated with autoimmune hemolytic anemia, erythroblastocytopenia, and acute hepatitis (56). The ceftriaxone in this case was given intravenously and not orally, as erroneously published (written communication from the authors). Other cases of hemolysis have been reported after ceftriaxone (57). 

Two studies have provided insights into the incidence and risk factors of the immune-mediated comphcations of interferon alfa in patients with chronic myeloid leukemia. In the first study, 13 of 46 patients had autoimmune manifestations consisting of a combination of autoimmune thyroiditis in four, a direct antiglobulin test without hemolysis in eight, cryoagglutinins in one, Raynaud s phenomenon in two, and chronic autoimmune hepatitis in one (343). Overall, six patients had chnically symptomatic manifestations after a median of 15 months of treatment. In the second study, there were autoimmune diseases in seven of 76 patients after a median of 19 months of treatment, including hypothyroidism in one, immune-mediated hemolysis in two, systemic lupus erythematosus in two, Raynaud s phenomenon in one, and mixed connective tissue disease in one (344). In... 

There have been several cases of thrombotic thrombocytopenic purpura or Moschcowitz s syndrome, characterized by intravascular coagulation, thrombocytopenia, and hemolysis, as a rare but life-threatening comphcation of penicillamine (153-156). There is one case report of Evans syndrome, thrombocytopenic purpura in combination with autoimmune hemolytic anemia, in suspected association with penicillamine (157). In this patient antiplatelet antibodies as well as antibodies against erythrocytes were detected. 

Overall, however, the reason that only some patients develop autoantibodies, and that only some of those have hemolytic disease, is not known. In an effort to explain why patients may have a positive result from a Coombs test and no hemolysis, Kelton demonstrated that methyldopa impairs the abihty of these patients to remove antibody-sensitized cells. In Coombs-positive patients receiving methyldopa, patients with impairment of the reticuloendothelial system could not clear the RBCs coated with autoantibodies from their bloodstream, and therefore hemolysis did not occur. Patients with hemolysis had no impairment of the reticuloendothelial system. Procainamide has also been reported to cause a positive result on the direct anti-human globulin test and hemolytic anemia. Other drugs that have been reported to cause autoimmune hemolytic anemia include levodopa, mefenamic acid, and diclofenac. ... 

The severity of drug-induced immune hemolytic anemia is usually a function of the rate of hemolysis. Hemolytic anemia caused by drugs via the hapten/adsorption and autoimmune mechanisms tend to be slower in onset and mild to moderate in severity. Conversely, hemolysis prompted via the neoantigen mechanism (innocent bystander) phenomenon may have a sudden onset, lead to severe hemolysis, and result in renal failure. The treatment of drug-induced immune hemolytic anemia includes the removal of the offending agent and supportive care. Glucocorticoids are usually unnecessary, and practitioners have questioned their efficacy. ... 

Primaquine GI distress, headache, dizziness, neutropenia, hemolysis. Avoid in pregnancy, G6PD deficiency, or autoimmune disorders. 

Some other drugs produce an autoimmune hemolytic anemia in which the antibodies are directed towards native antigens on the red cell surface, while the drug does not seem to function as a hapten in the reaction. This type of autoimmune hemolytic anemia has been described following treatment with levodopa, methyl-dopa, and mefenamic acid (Worrledge et al. 1966 Worrledge 1973). With a-methyldopa, clinically significant hemolysis develops in less than 1 % of individuals... 

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