Contributions
Abstract: PB1925
Type: Publication Only
Background
Although the pathophysiological mechanisms in chronic myeloid leukemia (CML) have been elucidated to a large degree, no etiological risk factors have been clearly established. Slightly simplified, we know a lot about what happens, but we know little of why. Peptic ulcers in CML patients have been reported for long, but it was only recently that a study found an increased incidence of ulcers before onset of CML, indicating a common etiological mechanism, rather than ulcers being a consequence of the malignancy. As Helicobacter pylori is both a known risk factor for ulcers, and a known carcinogen, it could serve as a candidate for such a common risk factor.
Aims
To evaluate a possible relationship between chronic Helicobacter infection and risk of CML by using previous gastric conditions or medication as proxy variables for Helicobacter infection.
Methods
In a matched case-control design, 980 patients registered in the Swedish CML Register and diagnosed between 2002 and 2012 were compared to 4960 control subjects, randomly selected from the Swedish population and matched on age, sex, and region of residence. Records of previous medical conditions and prescribed medications were retrieved from the National Patient Register and the Swedish Prescribed Drug Register, respectively. From these and other registers, data were further collected on potential confounders such as co-morbidities and socio-economic status.
Results
Compared to controls, CML cases significantly more often had a previous diagnosis of dyspepsia, gastritis, or peptic ulcer, with odds ratios between 1.8–2.0. Adjustments for socio-economic factors and co-morbidity did not substantially change these estimates. Furthermore, previous prescription of proton pump inhibitors was more frequent among CML cases than controls (OR 1.5, p=0.0005). Meanwhile, neither inflammatory bowel disease nor the intake of non-steroid anti-inflammatory drugs were associated with CML, indicating that it is not gastrointestinal ulcer or inflammation per se which influences risk.
Conclusion
The present study provides epidemiological evidence consistently linking certain previous gastric conditions or medications to CML risk. All of these conditions have known correlations to Helicobacter pylori infection. Although far from decisive, the data indicate that H pylori could be involved in CML carcinogenesis. H pylori is a known carcinogen, but has previously not been implicated in myeloid malignancies. The findings call for further studies with biological material from CML patients, to validate the possible relationship.
Session topic: 8. Chronic myeloid leukemia - Clinical
Keyword(s): Chronic myeloid leukemia, epidemiology, Helicobacter pylori
Abstract: PB1925
Type: Publication Only
Background
Although the pathophysiological mechanisms in chronic myeloid leukemia (CML) have been elucidated to a large degree, no etiological risk factors have been clearly established. Slightly simplified, we know a lot about what happens, but we know little of why. Peptic ulcers in CML patients have been reported for long, but it was only recently that a study found an increased incidence of ulcers before onset of CML, indicating a common etiological mechanism, rather than ulcers being a consequence of the malignancy. As Helicobacter pylori is both a known risk factor for ulcers, and a known carcinogen, it could serve as a candidate for such a common risk factor.
Aims
To evaluate a possible relationship between chronic Helicobacter infection and risk of CML by using previous gastric conditions or medication as proxy variables for Helicobacter infection.
Methods
In a matched case-control design, 980 patients registered in the Swedish CML Register and diagnosed between 2002 and 2012 were compared to 4960 control subjects, randomly selected from the Swedish population and matched on age, sex, and region of residence. Records of previous medical conditions and prescribed medications were retrieved from the National Patient Register and the Swedish Prescribed Drug Register, respectively. From these and other registers, data were further collected on potential confounders such as co-morbidities and socio-economic status.
Results
Compared to controls, CML cases significantly more often had a previous diagnosis of dyspepsia, gastritis, or peptic ulcer, with odds ratios between 1.8–2.0. Adjustments for socio-economic factors and co-morbidity did not substantially change these estimates. Furthermore, previous prescription of proton pump inhibitors was more frequent among CML cases than controls (OR 1.5, p=0.0005). Meanwhile, neither inflammatory bowel disease nor the intake of non-steroid anti-inflammatory drugs were associated with CML, indicating that it is not gastrointestinal ulcer or inflammation per se which influences risk.
Conclusion
The present study provides epidemiological evidence consistently linking certain previous gastric conditions or medications to CML risk. All of these conditions have known correlations to Helicobacter pylori infection. Although far from decisive, the data indicate that H pylori could be involved in CML carcinogenesis. H pylori is a known carcinogen, but has previously not been implicated in myeloid malignancies. The findings call for further studies with biological material from CML patients, to validate the possible relationship.
Session topic: 8. Chronic myeloid leukemia - Clinical
Keyword(s): Chronic myeloid leukemia, epidemiology, Helicobacter pylori