Published online Nov 26, 2020. doi: 10.4252/wjsc.v12.i11.1429
Peer-review started: February 14, 2020
First decision: September 11, 2020
Revised: September 20, 2020
Accepted: September 25, 2020
Article in press: September 25, 2020
Published online: November 26, 2020
Processing time: 286 Days and 9.1 Hours
We previously reported a serendipitous finding from a patient with refractory severe aplastic anemia who had gotten an unexpected hematological response to treatment with gut-cleansing preparations (GCPs). This patient experienced three recurrences over the ensuing one year of intermittent GCP treatments, with each recurrence occurring 7-8 wk from a GCP. After his third recurrence, he was prescribed successive treatment with rifampicin, berberine, and monthly administered GCP for 4 mo, and he developed an erythroid proliferative neoplasma and an overwhelming enteropathy, and eventually died of septic shock. Laboratory investigations had validated the resolution of myelosuppression and the appearance of malignant clonal hematopoiesis. From the treatment process and laboratory investigations, it is reasonably inferred that the engagement of gut inflammation is critically required in sustaining the overall pathophysiology of acquired aplastic anemia probably by creating a chronic inflammatory state. Incorporation of rifampicin, berberine, and monthly GCP into cyclosporine can enhance the immunosuppressive effect. In a subgroup of acquired aplastic anemia patients whose pathogenesis is associated with genotoxic exposure, the suppressed normal hematopoiesis may result from the bystander insult that is mediated by the soluble inflammatory cytokines generated in response to the immunogenic products of damaged hematopoietic cells in the context of chronic inflammatory state and may offer a protective antineoplastic mechanism against malignant proliferation.
Core Tip: We previously reported a severe aplastic anemia patient who had gotten an unexpected hematological response to treatment with intermittent gut-cleansing preparations. After his third recurrence, he was prescribed successive treatment with rifampicin, berberine, and monthly administered gut-cleansing preparations for 4 mo, and he developed an erythroid proliferative neoplasma and an overwhelming enteropathy. We hereby make an extrapolation that, in a subgroup of aplastic anemia patients, the suppressed normal hematopoiesis may result from the bystander insult that is generated in response to the antigenic products of damaged hematopoietic cells, and may offer a protective antineoplastic mechanism against malignant proliferation.