Bone marrow dyscrasias

In humans, phenylbutazone therapy has been associated with bone marrow dyscrasias, such as agranulocytosis and aplastic anemia (Flower et al 1985). Care should be taken when handling the product to prevent human exposure. The use of phenylbutazone in horses has been banned in many European countries because of concerns for human health and because the horse is considered a food animal under European law. Nevertheless, it is still prescribed very commonly for musculoskeletal conditions in the USA and the UK. It is interesting to note that there is only one report in the literature of bone marrow suppression occurring with phenylbutazone therapy in a horse and in that case very high doses of the agent had been administered (Murray 1985). 

Bone marrow depression, anemia, blood dyscrasias, nausea, vomiting, tachycardia, itching, rash, hives, tenderness and swelling of the neck, sore throat, and cough... 

Blood dyscrasias Any abnormality in blood or bone marrow cellular components such as low white blood cells, red blood cells, or platelets. 

Biood dyscrasias Agranulocytosis, bone marrow depression, neutropenia, hypoplastic anemia and thrombocytopenia in patients receiving procainamide have been reported at a rate of approximately 0.5%. Fatalities have occurred (with approximately 20% to 25% mortality in reported cases of agranulocytosis). Perform complete blood counts including white cell, differential, and platelet counts at weekly intervals for the first 3 months of therapy, and periodically thereafter. Perform complete blood counts promptly if the patient develops any signs of infection (eg. 

Phenothiazines Suspected or established subcortical brain damage (fluphenazine) blood dyscrasias (perphenazine, trifluoperazine, fluphenazine) bone marrow depression (perphenazine, trifluoperazine, fluphenazine) preexisting liver damage (perphenazine, trifluoperazine, fluphenazine) pediatric surgery (prochlorperazine) hypertensive or hypotensive heart disease of extreme degree (thioridazine). 

Blood dyscrasias An irreversible type of marrow depression leading to aplastic anemia with a high rate of mortality is characterized by appearance of bone marrow aplasia or hypoplasia weeks or months after therapy. Peripherally, pancytopenia is most often observed, but only 1 or 2 of the 3 major cell types may be depressed. 

Patients with psoriasis or RA who have any of the following alcoholism, alcoholic liver disease, or other chronic liver disease overt or laboratory evidence of immunodeficiency syndromes preexisting blood dyscrasias (eg, bone marrow hypoplasia, leukopenia, thrombocytopenia, significant anemia). 

Contraindications Bone marrow aplasia, historyofgold-induced pathologies (including blood dyscrasias, exfoliative dermatitis, necrotizing enterocolitis, and pulmonary fibrosis), severe blood dyscrasias... 

More serious hematopoietic suppression can occur and, as noted earlier, CBZ is contraindicated with a prior history of bone marrow suppression. Aplastic anemia has been reported to occur in one out of 125,000 cases. Agranulocytosis may also rarely occur. Of some comfort, Tohen et al. ( 370) reported no serious hematological dyscrasias in more than 2,000 patients receiving either CBZ or VPA. 

Medications that cause blood dyscrasia or bone marrow suppression... 

The most serious problem associated with chloramphenicol is the potential for bone marrow aplasia, which can lead to aplastic anemia and possibly death.16,83 Chloramphenicol is also associated with other blood dyscrasias such as agranulocytosis and thrombocytopenia. Because of these risks, chloram-... 

Adverse Effects. Flucytosine may cause hepatotoxicity and may also impair bone marrow function, resulting in anemia, leukopenia, and several other blood dyscrasias.69 This drug may also produce severe gastrointestinal disturbances, including nausea, vomiting, diarrhea, and loss of appetite. 

Adverse Effects. The primary side effects of azathioprine are related to suppression of bone marrow function, including leukopenia, megaloblastic anemia, and similar blood dyscrasias. Other side effects include skin rash and gastrointestinal distress (appetite loss, nausea, vomiting) hepatic dysfunction can also occur when higher doses are used. 

AZATHIOPRINE LEFLUNOMIDE T risk of serious infections (sepsis) and of opportunistic infections (Pneumocystis jiroveci pneumonia, tuberculosis, aspergillosis) Additive immunosuppression Monitor platelets, white bloods cell, haemoglobin and haematocrit at baseline and regularly - weekly, during concomitant therapy. With evidence of bone marrow suppression, discontinue leflunomide and administer colestyramine or charcoal to T elimination of leflunomide - For signs and symptoms of immunosuppression, see Qinical Features of Some Adverse Drug Interactions, Immunosuppression and blood dyscrasias... 

Leukocyte and differential counts (including platelet counts) must be normal before starting treatment with drugs that have the potential to cause blood dyscrasias or bone marrow suppression. 

If there is the presence of blood dyscrasias, subcortical brain damage, bone marrow depression, or liver disease If there is a proven allergy to perphenazine If there is a known sensitivity to any phenothiazine... 

If fhere is fhe presence of blood dyscrasias, bone marrow depression, or liver disease... 

Because serious and fetal blood dyscrasias can occur after the administration of chloramphenicol, it should be used only in serious infections for which less potentially dangerous drugs are ineffective or contraindicated. Chloramphenicol is contraindicated in patients with known hypersensitivity or intolerance to this drug, who have blood cell or bone marrow disorders, or who are undergoing dialysis and have other complications such as cirrhosis. 

When bone marrow aplasia was complete, the fatality rate approached 100%. As a rule, it has been found that the longer the interval between the last dose of chloramphenicol and the appearance of the first sign of a blood dyscrasia, the more severe the resulting aplasia. Nearly all patients in whom the interval was longer than 2 months died as a result of this comphcation. However, fatal aplastic anemia can also occur shortly after normal doses of chloramphenicol (28). 

Of the two types of bone marrow toxicity that chloramphenicol can cause, it may cause the late type only in genetically predisposed patients. The overall risk of aplastic anemia after oral administration of chloramphenicol is 1 30 000 to 1 50 000, which is 13 times greater than the risk of idiopathic aplastic anemia in the population as a whole. Since topical administration achieves systemic effects by absorption through the conjunctival membrane or through drainage down the lacrimal duct, with eventual absorption from the gastrointestinal tract, the risk may be similar to that after oral administration. However, based on two case-control studies and a cohort study, the incidence of blood dyscrasias due to chloramphenicol eye-drops was estimated to be somewhat lower, namely 1 100 000 treated patients (40,66). 

Chloroquine inhibits myelopoiesis in vitro at therapeutic concentrations and higher. In a special test procedure, a short-lasting anti-aggregating effect could be seen with chloroquine concentrations of 3.2-32 pg/ml (SEDA-16, 303). These effects have clinical consequences. Chloroquine and related aminoquinolines have reportedly caused blood dyscrasias at antimalarial doses. Leukopenia, agranulocytosis, and the occasional case of thrombocytopenia have been reported (SEDA-13, 804) (22). There is some evidence that myelosuppression is dose-dependent. This is in line with the hypothesis that 4-aminoquinoline therapy merely accentuates the cyto-penia linked to other forms of bone marrow damage (SEDA-11, 584) (SEDA-16, 302). 

Felbamate is currently reserved for patients who are refractory to other drugs after careful consideration of the benefitrharm balance. In some countries the indication has been restricted to refractory Lennox-Gastaut syndrome. It is wise to avoid felbamate in patients with previous blood dyscrasias or autoimmune disorders, especially lupus erythematosus. Before they start to take it, patients should be informed about the potential risks and early symptoms of bone-marrow toxicity, such as bruisability, petechiae, fever of unknown origin, weakness, and fatigue. Hematology tests should be performed at baseline and during treatment, and dose escalation should be slow. 

Blood dyscrasias, ranging from thrombocytopenia and granulocytopenia to agranulocytosis and fatal pancytopenia, have been reported. (SED-9, 150). Reversible pure white cell aplasia with bone marrow plasmacytosis and complement-dependent IgG antibody has been observed in one patient (12). 

This therapy can produce urticaria and skin rashes. In addition, there can be potentially serious adverse effects, including bone marrow depression, acute leukemia, and blood dyscrasias. Symptoms of radiation sickness as well as cardiovascular complications (e.g., angina, sinus tachycardia) can also occur. 

Chloramphenicol. Chloramphenicol binds to the 508 ribosomal subunit of bacteria and prevents binding of the amino acid portion of the aminoacyl-tRNA, effectively inhibiting peptidyltransferase action. This antibiotic is used only for certain extremely serious infections, such as meningitis and typhoid fever. Chloramphenicol readily enters human mitochondria, where it inhibits protein synthesis. Cells of the bone marrow often fail to develop in patients treated with chloramphenicol, and use of this antibiotic has been linked to fatal blood dyscrasias, including an aplastic anemia. 

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