Hemolytic anemia treatment

As the above mentioned studies with high supplementation dosages exemplarily show, there is no known toxicity for phylloquinone (vitamin Kl), although allergic reactions are possible. This is NOT true for menadione (vitamin K3) that can interfere with glutathione, a natural antioxidant, resulting in oxidative stress and cell membrane damage. Injections of menadione in infants led to jaundice and hemolytic anemia and therefore should not be used for the treatment of vitamin K deficiency. 

Ribavirin causes a dose-related hemolytic anemia. Once treatment has been initiated, the hemoglobin concentration may... 

The answers are 484-k 485-j. (tlardman, pp 1061-1062, 1682-1685.) Sulfonamides can cause acute hemolytic anemia. In some patients it mayr be related to a sensitization phenomenon, and in other patients the hemolysis is due to a glucose-6-phosphate dehydrogenase deficiency Sulfamethoxazole alone or in combination with trimethoprim is used to treat UTls. The sulfonamide sulfasalazine is employed in the treatment of ulcerative colitis. Daps one, a drug that is used in the treatment of leprosy, and primaquine, an anti mala rial agent, can produce hemolysis, particularly in patients with a glucose-6-phosphate dehydrogenase deficiency. 

Treatment of hemolytic anemia should focus on correcting the underlying cause. There is no specific therapy for glucose-6-phosphate dehydrogenase deficiency, so treatment consists of avoiding oxidant medications and chemicals. Steroids, other immunosuppressants, and even splenectomy can be indicated to reduce RBC destruction. 

Autoantibodies to red blood cells and autoimmune hemolytic anemia have been observed in patients treated with numerous drugs, including procainamide, chlor-propaminde, captopril, cefalexin, penicillin, and methyldopa (Logue et al., 1970 Kleinman et al., 1984). Hydralazine- and procainamide-induced autoantibodies may also result in SLE. Approximately 20% of patients administered methyldopa for several weeks for the treatment of essential hypertension developed a dose-related titer and incidence of autoantibodies to erythrocytes, 1% of which presented with hemolytic anemia. Methlydopa does not appear to act as a hapten but appears to act by modifying erythrocyte surface antigens. IgG autoantibodies then develop against the modified erythrocytes. 

Hematological Effects. A decrease in red blood cell counts was observed in persons exposed to a wood treatment liquid containing phenol, formaldehyde, and organic chlorohydrocarbons (Baj et al. 1994). Although only limited data were identified, hemolytic anemia and methemoglobinemia are considered to be well-documented complications of phenol poisoning in humans (ACGIH 1991). 

Zaja, R, lacona, L, Masolini, P, Russo, D., Sperotto, A., Prosdocimo, S., Patriarca, R, de Vita, S., Regazzi, M., Baccarani, M., and Panin, R., B-cell depletion with rituximab as treatment for immune hemolytic anemia and chronic thrombocytopenia, Haematologica, 87, 189-195, 2002. 

Toxicoiogy At 17 times the maximum human dose (on mg/kg basis), dogs developed reversible neutropenia and/or reversible hemolytic anemia between 1 and 10 months of treatment. Mice given doses twice the maximum human dose (on mg/kg basis) showed a decrease in lymphocytes and neutrophils in studies of 3 months duration. 

Sequential determination of platelet counts in patients receiving vincristine during early studies unexpectedly occasionally revealed thrombocytosis, which could not be accounted for by systemic response to treatment alone 10,11). Ultimately shown to most likely be the result of increased megakaryocytic endomitosis II), the observation led to the use of vincristine, and later vinblastine, both alone and bound to platelets, in a variety of thrombocytopenic disorders. These include idiopathic thrombocytopenic purpura, thrombotic thrombocytopenic purpura, and chemotherapy-induced microangiopathic hemolytic anemia. 

Finally, the successful use of vincristine in the treatment of drug-induced microangiopathic hemolytic anemia, a disease resembling the hemolytic uremic syndrome rarely seen subsequent to administration of mitomycin C or other chemotherapy has been described in two patients with this disorder (79). 

In a subacute inhalation toxicity study, rats of both sexes were exposed for 6 hours/day, 5 days/week for 4 weeks. Recovery groups were kept for an observation period of 14 days without treatment. At 891, 441, or 142 ppm hemolytic anemia was observed. Mild hemolytic anemia was found in female rats exposed to 100 ppm, but it had disappeared after the 14-day recovery period. 

Skin reactions Severe or life-threatening skin reactions, including Stevens-Johnson syndrome, were reported in less than 1% of patients treated with fosamprenavir in the clinical studies. Discontinue treatment with fosamprenavir for severe or life-threatening rashes and moderate rashes accompanied by systemic symptoms. Hemolytic anem/a.-Acute hemolytic anemia has been reported. 

Vitamin E may be indicated in some rare forms of anemia such as macrocytic, megaloblastic anemia observed in children with severe malnutrition and the hemolytic anemia seen in premature infants on a diet rich in polyunsaturated fatty acids. Also anemia s in malabsorption syndromes have shown to be responsive to vitamin E treatment. Finally, hemolysis in patients with the acanthocytosis syndrome, a rare genetic disorder where there is a lack of plasma jS-lipoprotein and consequently no circulating alpha tocopherol, responds to vitamin E treatment. In neonates requiring oxygen therapy vitamin E has been used for its antioxidant properties to prevent the development retrolental fibroplasia. It should be noted that high dose vitamin E supplements are associated with an increased risk in allcause mortality. 

Although dapsone (Avlosulfon) was once used in the treatment and prophylaxis of chloroquine-resistant P. falciparum malaria, the toxicities associated with its administration (e.g., agranulocytosis, methemoglobinemia, hemolytic anemia) have severely reduced its use. 

Immune globulin, given intramuscularly or intravenously, is recommended in the treatment of primary humoral immunodeficiency, congenital agammaglobulinemias, common variable immunodeficiency, severe combined immunodeficiency, idiopathic thrombocytopenic purpura, and autoimmune hemolytic anemia. There are six licensed preparations of immune globulin. 

Subsequent analysis of stored serum samples showed reduction of HCV RNA levels during treatment and durable eradication of virus in some cases [38]. These early results were confirmed by randomized controlled trials in patients with chronic hepatitis C [39-41]. Durable viral eradication (termed sustained virologic response, or SVR) was achieved in 6% to 15% of patients after six months of treatment with recombinant interferon at doses of 3 to 6 MU administered subcutaneously three times per week. SVR increased to 13% to 25% if treatment was extended to 12 months [41]. The combination of the oral nucleoside analogue ribavirin with recombinant interferon increased SVR to 41% [42-44]. Ribavirin, however, is potentially embryotoxic and induces a dose-dependent hemolytic anemia, a situation that calls for close monitoring during therapy. 

In the past, large doses of androgens were employed in the treatment of refractory anemias such as aplastic anemia, Fanconi s anemia, sickle cell anemia, myelofibrosis, and hemolytic anemias. Recombinant erythropoietin has largely replaced androgens for this purpose. 

Wollheim FA, Ljunggren HO, Blom-Bulow B. Hemolytic anemia during cyclofenil treatment of scleroderma. Acta Med Scand 1981 210(5) 429-30. 

The most dangerous adverse reaction of sulfonylureas is agranulocytosis. Aplastic anemia (79), red cell aplasia (80), pure white cell aplasia (81), bone marrow aplasia, and hemolytic anemia have been described during treatment with chlorpropamide (82), glibenclamide (83), or tolbutamide (84). 

Serum Total Iron and Total Iron Binding Capacity The results for the determination of serum total iron and total iron-binding capacity of rats fed treatment diets for 18 months are also listed in Table VI. A significant increase in serum total iron was detected in rats fed the Maillard browned egg albumin over their control group. Increased serum total iron with normal total iron binding capacity is associated with hemolytic anemia, hemochromatosis, hemosiderosis, and hepatitis (30 ). On the basis of other clinical and histopathological data, however, none of these causes are likely. 

---