Drug‐induced leukopenia and aplastic anemia

Pisciotta, Anthony V.

doi:10.1002/cpt197112113

Cited by 62 publications

(11 citation statements)

References 65 publications

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“…Agranulocytosis associated with phenothiazines has been reported most often in white, elderly women, although this was initially thought to be a function of prescribing patterns (Edwards and Barnes, 1993). It is also reported more often during treatment with high doses and within the first 10 days (Pisciotta, 1971). Grohmann et al (1989) monitored 13000 antipsychotic treated inpatients from 1979-1988.…”

Section: Discussionmentioning

confidence: 97%

Haematological safety of antipsychotic drugs

King

Wager

1998

J Psychopharmacol

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Many clinicians have become concerned about the safety of new antipsychotics particularly in view of the association of agranulocytosis with clozapine and of aplastic anaemia with remoxipride. The Committee on Safety of Medicines and Medicines Control Agency 'yellow card' post-marketing surveillance data were analysed for reports of haemopoietic disorders with the 16 antipsychotics in common use. Corrections for relative risk were made in three separate ways: (i) control for degree of use, using Northern Ireland prescribing data for 1995; (ii) percentage of total reports from 1963 to 1996; and (iii) examination of the first 5 years' post-marketing data only. After clozapine and remoxipride the highest risks of haemopoietic reactions appeared to be associated with the aliphatic phenothiazine derivatives thioridazine and chlorpromazine. There is therefore no evidence of any increased risk with high-potency drugs such as haloperidol or pimozide or with the newer drugs such as sulpiride or risperidone. Continued vigilance, however, is necessary as more new atypicals become available and begin to be widely prescribed.

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Section: Discussionmentioning

confidence: 97%

Haematological safety of antipsychotic drugs

King

Wager

1998

J Psychopharmacol

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“…One possibility to keep in mind, although it has not yet been reported for the antiepileptic drugs, is the these data are not available. Also, definition of occurrence of leukemia as a late sequel of drug-induced bone marrow damage (Pisciotta, 1971).…”

Section: The Clinical Problemmentioning

confidence: 99%

Idiosyncratic Reactions to the Antiepileptic Drugs

Booker

1975

Epilepsia

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Idiosyncratic drug reactions can be defined as those adverse drug effects caused by genetically determined enzymatic abnormalities. For the clinician, however, this definition is too limited, and other rare and unusual adverse reactions to the antiepileptic drugs are discussed, including drug interactions, drug allergies, and organ toxicities, as well as true idiosyncrasies. Responsibility for initial recognition and later diagnosis of these reactions falls heavily upon the clinician. In addition to discussing the more common or serious rare reactions, the epidemiology and general mechanisms underlying the reactions are discussed. Treatment involves drug withdrawal, plus general supportive and specific therapy determined by the type and severity of the individual reaction. If primum non nocere should guide the treatment in general, then secundum non plus nocere should guide the treatment of adverse drug reactions.

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“…The aplastic anaemia caused by clr/orci/nphcnic.ol will most often run a chronic and fatal course. but recovery has been reported (42). In a few cases it has been cured by transfusion of haematopoietic cells (2.…”

Section: Semispecu Lative Classification Of Clinically Important Aplamentioning

confidence: 99%

Aplastic Anaemia: Considerations on the Pathogenesis

Benestad

1974

Journal of Internal Medicine

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. Modern concepts of haematopoiesis and its regulation are reviewed. Observations from several forms of aplastic anaemia are analysed in the light of this new knowledge. The pathogenetic mechanism in the aplasia caused by chloramphenicol is probably a stem cell damage of an autoimmune or idiosyncratic nature. Chlorpromazine aplasia is apparently due to a constitutionally defective DNA synthesis, so that a normal compensatory reaction cannot take place against the inhibiting effects of the drug on DNA synthesis. The chlorpromazine aplasia is normally transient, since transit cells of the bone marrow—and not the stem cells—are affected. The hepatitis‐associated aplasia may possibly be precipitated by an autoimmune attack on multipotent stem cells or on transit cells of one or more cell lines after virus‐induced change of antigenicity of the cell surface. The thymoma‐associated aplasia may likewise be due to autoimmunity directed against transit cells. Finally, there are indications that the Fanconi aplasia may be pathogenetically heterogeneous, with constitutionally defective stem cells, transit cells, or stromal cells. Otherwise stromal failure rarely seems to play a role in human aplastic anaemia. Furthermore, “maturation arrest” probably does not exist. Neither “stem cell exhaustion” nor situations with missing or defective haemopoietins apparently produce aplasia on their own. A research strategy, supplementary to the routine haematological investigations, is proposed. It is recommended that modern immunological techniques in particular should be applied in combination with stem cell assays.

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Drug‐induced leukopenia and aplastic anemia

Cited by 62 publications

References 65 publications

Haematological safety of antipsychotic drugs

Haematological safety of antipsychotic drugs

Idiosyncratic Reactions to the Antiepileptic Drugs

Aplastic Anaemia: Considerations on the Pathogenesis

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