Abstract
Erythroid aplasia following the administration of drugs may be due to various mechanisms. Although the pathogenetic mechanisms involeved in drugs remain incompletely understood, a great deal of light has been shed on this problem by in vitro bone marrow cultures.
We have experienced three patients who suffered from erythroid aplasia associated with exposure to thiamphenicol, diphenylhydantoin and thiopental, respectively. These patients recovered rapidly when the offending agents were removed.
To determine the causative drug in three patients, in vitro heme synthesis and colony formation were undertaken with the addition of the drugs to the culture systems.
Thiamphenicol (10 μg/ml/plate) produced to inhibit heme synthesis in the bone marrow culture of a patient who had recovered from thiamphenicol-induced erythroid aplasia. Inhibition of in vitro heme synthesis was greater with his own serum than with fetal calf serum. However, the failure of thiamphenicol to inhibit granuloid colony formation was observed. These data suggest that some immune mechanisms with the fall in ferrochelatase activity may induce erythroid aplasia by thiamphenicol.
The specific inhibitory effect of diphenylhydantoin (20 μg/ml/plate) on in vitro heme synthesis did not occur in the bone marrow from a patient who recovered from diphenylhydantoin-induced erythroid aplasia.
Thiopental (15 μ/g/ml/plate) did affect the significant reduction of the cell viability in bone marrow cell suspensions from a patient recovered from erythroid aplasia. Her immunoglobulin G was elavated and the skin reaction test with thiopental also gave positive. These data strongly suggest that some immune mechanism may take part in causing erythroid aplasia.
