Bone marrow treatment

Laurent, G., D. Maraninchi, E. Gluckman, J.P Vernant, J.M. Derocq, M.H. Gaspard, B. Rio, M. Michalet, J. Reiffers, F. Dreyfus, et al.. Donor bone marrow treatment with TlOl Fab fragment-ricin A-chain immunotoxin prevents graft-versus-host disease. Bone Marrow Transplant, 1989. 4(4) 367-71. 

Epoetin alfa Agonist of erythropoietin receptors expressed by red cell progenitors Stimulates erythroid proliferation and differentiation, and induces the release of reticulocytes from the bone marrow Treatment of anemia, especially anemia associated with chronic renal failure, HIV infection, cancer, and prematurity prevention of the need for transfusion in patients undergoing certain types of elective surgery IV or SC administration 1-3 times per week Toxicity Hypertension, thrombotic complications, and, very rarely, pure red cell aplasia to reduce the risk of serious CV events, hemoglobin levels should be maintained < 12 g/dL... 

Adverse side effects of gold treatments include stomatitis, rash, and proteinuria. Complete blood counts and urinalysis should be performed before each or every other injection of gold compounds. Pmritic skin rash and stomatitis are more common adverse effects that may resolve, if therapy is withheld for a few weeks and then restarted cautiously at a lower dose. Oral gold causes less mucocutaneous, bone marrow, and renal toxicity than injectable gold, but more diarrhea and other gastrointestinal reactions appear. 

Acyclovir is more effective the more serious the disease and the earher it is given. It has been shown to be efficacious when used systemicaHy in the prophylaxis of HSV infections in immunosuppressed patients, ie, bone marrow transplant recipients (67). Acyclovir therapy appears to be superior to ara-A in the treatment of herpes simplex encephaUtis in humans (68). 

Treatment for chronic benzene poisoning is supportive and symptomatic, with chemotherapy and bone marrow transplants as therapeutic agents for leukemia and aplastic anemia (127). 

As regards toxicity, pyrazole itself induced hyperplasia of the thyroid, hepatomegaly, atrophy of the testis, anemia and bone marrow depression in rats and mice (72E1198). The 4-methyl derivative is well tolerated and may be more useful than pyrazole for pharmacological and metabolic studies of inhibition of ethanol metabolism. It has been shown (79MI40404) that administration of pyrazole or ethanol to rats had only moderate effects on the liver, but combined treatment resulted in severe hepatotoxic effects with liver necrosis. The fact that pyrazole strongly intensified the toxic effects of ethanol is due to inhibition of the enzymes involved in alcohol oxidation (Section 4.04.4.1.1). 

The usual dose consists of 1000 mg/m2 i.v. It is the most active single agent for treating pancreatic cancer, and it is used as a fust-line treatment for both pancreatic and small cell lung cancers. The dose-limiting toxicity is bone marrow suppression. 

Decitabine is specifically indicated for the treatment of multiple types of myelodysplastic syndromes and chronic myelomonocytic leukemia. As anticipated, use of decitabine is associated with bone marrow suppression including neutropenia and thrombocytopenia which are the most frequently observed serious adverse effects. 

This is a humanized anti-CD52 monoclonal antibody. At present it is in clinical use after bone marrow transplantation and for the treatment of refractory chronic lymphocytic leukemia. 

BENZODIAZEPINES Carbamazepine may cause aplastic anemia and agranulocytosis. During treatment blood studies are performed frequently If evidence of bone marrow depression is obtained (eg, the patient s platelet... 

Some adverse reactions are desirable, for example, the depressing effect of certain antineoplastic drugs on the bone marrow because this adverse drag reaction is essential in the treatment of the leukemias. Other adverse reactions are not desirable, for example, severe vomiting or diarrhea. 

Oral administration of 11.6 mg/kg/day of endosulfan to rats for up to 30 days also failed to induce chromosomal damage in bone marrow and spermatogonial cell systems, but it is not known how soon after treatment the animals were killed. As shown in mouse studies (Usha Rani and Reddy 1986), a latency period of 60 days was required to see chromosomal aberrations in spermatogonia. However, relatively significant changes were observed for mitotic indices (Dikshith et al. 1978). 

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