Repeated spontaneous remission of acute myeloid leukemia in response to various infections: a case report

Abstract

Background Acute myeloid leukemia (AML) is a progressive hematological malignancy that can be fatal when left untreated. However, spontaneous remission is rarely observed in the presence of infectious diseases. Case presentation We treated an 80-year-old woman with AML who spontaneously underwent remission after infections. Spontaneous remission was observed after each of three independent clinical infections caused by different pathogens—nontuberculous Mycobacterium infection, pulmonary aspergillosis, and Escherichia coli bacteremia. All infections were treated promptly with antimicrobials. Mycobacterium avium infection was treated with azithromycin, rifampin, and ethambutol. Pulmonary aspergillosis was treated with itraconazole followed by voriconazole. E. coli infection was treated with meropenem. During each infectious episode, leukemic cells disappeared from the patient’s peripheral blood and pancytopenia improved without routine blood transfusion. These clinical effects lasted for several months. The patient has survived for > 2 years beyond the median survival time of end-stage AML. Thus, this case represents an immunological antileukemic effect of systemic infections. Conclusions We have discussed a common mechanism of spontaneous remission of AML without chemotherapy, clinically exhibited by infection immunology. We believe that infections exert a limited immunological effect against AML, which may prolong survival among elderly individuals with AML.

When inflammatory stressors dramatically change, disease phenotypes may transform between autoimmune hematopoietic failure and myeloid neoplasms

“…This process simulates spontaneous remission in AML patients after an infectious episode and aplastic crisis ( 245 – 252 ). The mechanism is presumed to be due to reversion of the immune exhaustion state and restoration of antileukemic immunity through activation of immune cells and their secretion of proinflammatory cytokines in response to invading pathogens ( 250 – 253 ).…”

“…To date, spontaneous remission has been reported in more than 200 AML patients. The remission duration usually lasts for 2–6 months, which indicates that leukemic clones cannot be eradicated even under inflammatory stress-powered antileukemic immunity ( 245 , 254 ). This may be due to the low expression of neoplastic antigens on dormant leukemic cells ( 255 – 258 ).…”

“…This may be due to the low expression of neoplastic antigens on dormant leukemic cells ( 255 – 258 ). However, repeated spontaneous remissions occur in a paucity of patients ( 245 , 247 ), which suggests that patients do not completely lose the hematopoietic regulatory mechanisms and the inflammatory stress-powered antileukemic immunity. Another interesting phenomenon also suggests the existence of inflammatory stress-powered antileukemic activities ( 243 , 244 ).…”

“…Neoplastic epitopes from genetic or epigenetic products of transformed HPCs ( 42 , 93 , 95 , 97 , 100 , 232 ) are likely the targeting molecules responsible for the primary inflammatory BME. However, effective repression of leukemic blasts also requires the engagement of additional inflammatory stressors that are strong Th1 responses for the sustenance of antileukemic immunity ( 95 , 161 , 245 , 246 , 250 ). This is perhaps due to the low immunogenicity of neoplastic antigens on leukemic cells ( 255 – 258 ).…”

“…A reasonable explanation is that leukemic clones preexist but are repressed in AHF stages ( 19 – 27 ) and rapidly expand after the resolution of inflammatory stressors ( 95 , 245 , 250 , 254 ). The persistence of autoantibodies ( 42 , 99 , 100 , 258 , 330 ) and autoimmune responses ( 59 , 78 , 93 , 273 , 321 ) in AA, MDS, and AML suggests that autoantigens are persistent and their immunogenicity is less intensive.…”