scholarly journals Chronic Immune Stimulation Might Act As a Trigger for the Development of Acute Myeloid Leukemia or Myelodysplastic Syndromes

2011 ◽  
Vol 29 (21) ◽  
pp. 2897-2903 ◽  
Author(s):  
Sigurdur Y. Kristinsson ◽  
Magnus Björkholm ◽  
Malin Hultcrantz ◽  
Åsa R. Derolf ◽  
Ola Landgren ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Autoimmune Diseases ◽  
Myeloid Leukemia ◽  
Large Population ◽  
Previous History ◽  
Population Based ◽  
Immune Stimulation ◽  
Increased Risk ◽  
History Of ◽  
Acute Myeloid

Purpose Patients with acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) often present with infections, but there are little data to assess whether a personal history of selected infections may act as pathogenic triggers. To additionally expand our knowledge on the role of immune stimulation in the causation of AML and MDS, we have conducted a large, population-based study to evaluate the risk of AML and MDS associated with a prior history of a broad range of infections or autoimmune diseases. Patients and Methods By using population-based central registries in Sweden, we included 9,219 patients with AML, 1,662 patients with MDS, and 42,878 matched controls. We used logistic regression to calculate odds ratios (ORs) and 95% CIs for the association of AML or MDS with infectious and/or autoimmune diseases. Results Overall, a history of any infectious disease was associated with a significantly increased risk of both AML (OR, 1.3; 95% CI, 1.2 to 1.4) and MDS (OR, 1.3; 95% CI, 1.1 to 1.5). These associations were significant even when we limited infections to those occurring 3 or more years before AML/MDS. A previous history of any autoimmune disease was associated with a 1.7-fold (95% CI, 1.5 to 1.9) increased risk for AML and 2.1-fold (95% CI, 1.7 to 2.6) increased risk for MDS. A large range of conditions were each significantly associated with AML and MDS. Conclusion Our novel findings indicate that chronic immune stimulation acts as a trigger for AML/MDS development. The underlying mechanisms may also be due to a common genetic predisposition or an effect of treatment for infections/autoimmune conditions.

Acute lymphoblastic leukemia in patients with Down syndrome with a previous history of acute myeloid leukemia

2016 ◽  
Vol 64 (8) ◽  
pp. e26411 ◽  
Author(s):  
Daisuke Tomizawa ◽  
Akifumi Endo ◽  
Michiko Kajiwara ◽  
Hirotoshi Sakaguchi ◽  
Kimikazu Matsumoto ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Down Syndrome ◽  
Acute Lymphoblastic Leukemia ◽  
Myeloid Leukemia ◽  
Lymphoblastic Leukemia ◽  
Previous History ◽  
History Of ◽  
Acute Myeloid

scholarly journals The association between psoriatic arthritis and venous thromboembolism: a population-based cohort study

2022 ◽  
Vol 24 (1) ◽  
Author(s):  
Tal Gazitt ◽  
Jacob Pesachov ◽  
Idit Lavi ◽  
Muna Elias ◽  
Amir Haddad ◽  
...  
Keyword(s):  
Cohort Study ◽  
Psoriatic Arthritis ◽  
Large Population ◽  
Multivariable Analysis ◽  
Previous History ◽  
Population Based ◽  
Janus Kinase ◽  
Control Group ◽  
Increased Risk ◽  
History Of

Abstract Background Although the risk of cardiovascular disease has been discussed extensively in both psoriasis (PsO) and psoriatic arthritis (PsA), very few studies have addressed the occurrence of venous thromboembolic (VTE) events among PsO patients, and even fewer in PsA. Thus, our goal was to assess the association between PsA and VTE events using a large population-based database. Methods This retrospective cohort study includes all 5,275 patients with newly diagnosed PsA from the largest health care provider in Israel between January 2003 and December 2018. Identified PsA patients were matched by age, sex, ethnicity, and index date with 21,011 controls without PsA from the same database. Both groups were followed through June 30, 2019 for the occurrence of VTE event. Cox proportional hazard regression models were used to assess the association between PsA and VTE. Results PsA cohort consisted of 53.2% females with mean age of 51.7±15.4 Sixty-two patients (1.2%) were diagnosed with VTE in the PsA group and 176 patients (0.8%) in the control group (p=0.023, HR=1.40, 95% CI 1.05-1.87). However, there was no increased risk of VTE among PsA patients on multivariable analysis (p=0.16, HR=1.27, 95% CI 0.91-1.80). Within the PsA group, patients with VTE were more often of older age and with history of VTE. Conclusions This study suggests that the increased risk of VTE in PsA patients appears to be related to the underlying comorbidities and not independently associated with PsA. Age and previous history of VTE were the only risk factors associated with increased risk of VTE in patients with PsA. Addressing VTE risk is recommended especially in the era of Janus kinase inhibitors.

Adolescents and young adult acute myeloid leukemia outcomes at pediatric versus adult centers: A population‐based study

2021 ◽  
Author(s):  
Sumit Gupta ◽  
Nancy N. Baxter ◽  
Rinku Sutradhar ◽  
Jason D. Pole ◽  
Chenthila Nagamuthu ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Young Adult ◽  
Myeloid Leukemia ◽  
Population Based ◽  
Population Based Study ◽  
Acute Myeloid

scholarly journals Melanoma is associated with an increased risk of bullous pemphigoid: a large population-based longitudinal study

2021 ◽  
Author(s):  
Khalaf Kridin ◽  
Jennifer E. Hundt ◽  
Ralf J. Ludwig ◽  
Kyle T. Amber ◽  
Dana Tzur Bitan ◽  
...  
Keyword(s):  
Bullous Pemphigoid ◽  
Statistical Significance ◽  
Large Population ◽  
Underlying Mechanism ◽  
Population Based ◽  
Control Subjects ◽  
Increased Risk ◽  
Bidirectional Association ◽  
History Of ◽  
Incident Cases

AbstractThe association between bullous pemphigoid (BP) and melanoma is yet to be investigated. We aimed to assess assess the bidirectional association between BP and melanoma and to delineate the epidemiological features of patients with both diagnoses. A population-based cohort study was performed comparing BP patients (n = 3924) with age-, sex- and ethnicity-matched control subjects (n = 19,280) with regard to incident cases of melanoma. A case–control design was additionally adopted to estimate the risk of BP in individuals with a preexisting diagnosis of melanoma. The prevalence of preexisting melanoma was higher in patients with BP than in control subjects (1.5% vs. 1.0%, respectively; P = 0.004). A history of melanoma confers a 50% increase in the risk of subsequent BP (OR 1.53; 95% CI 1.14–2.06). This risk was higher among males (OR 1.66; 95% CI 1.09–2.54) and individuals older than 80 years (OR 1.63; 95% CI 1.11–2.38), and persisted after adjustment for multiple putative confounders including PD-1/PDL-1 antagonists (adjusted OR 1.53; 95% CI 1.14–2.06). Conversely, the risk of melanoma among patients with BP was slightly elevated, but did not reach the level of statistical significance (adjusted HR 1.13; 95% CI 0.73–1.74). Patients with a dual diagnosis of BP and melanoma were older at the onset of BP and had lower body mass index. A history of melanoma is associated with a 50% increase in the incidence of subsequent BP. Physicians managing patients with both conditions should be aware of this association. Further research is warranted to reveal the underlying mechanism of these findings.

scholarly journals CMV reactivation after allogeneic HCT and relapse risk: evidence for early protection in acute myeloid leukemia

Blood ◽  
2013 ◽  
Vol 122 (7) ◽  
pp. 1316-1324 ◽  
Author(s):  
Margaret L. Green ◽  
Wendy M. Leisenring ◽  
Hu Xie ◽  
Roland B. Walter ◽  
Marco Mielcarek ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Early Relapse ◽  
Relapse Risk ◽  
Allogeneic Hct ◽  
Increased Risk ◽  
Key Points ◽  
Cmv Reactivation ◽  
Reduced Risk ◽  
Acute Myeloid

Key Points CMV reactivation after HCT is associated with a reduced risk of early relapse in patients with AML but not other disease groups. The benefit, however, is offset by an increased risk of nonrelapse mortality.

Genomics of Acute Myeloid Leukemia Diagnosis and Pathways

2017 ◽  
Vol 35 (9) ◽  
pp. 934-946 ◽  
Author(s):  
Lars Bullinger ◽  
Konstanze Döhner ◽  
Hartmut Döhner
Keyword(s):  
Acute Myeloid Leukemia ◽  
Risk Stratification ◽  
Myeloid Leukemia ◽  
Clinical Care ◽  
Clonal Expansion ◽  
Disease Classification ◽  
Disease Evolution ◽  
Myeloid Neoplasms ◽  
Increased Risk ◽  
Acute Myeloid

In recent years, our understanding of the molecular pathogenesis of myeloid neoplasms, including acute myeloid leukemia (AML), has been greatly advanced by genomics discovery studies that use novel high-throughput sequencing techniques. AML, similar to most other cancers, is characterized by multiple somatically acquired mutations that affect genes of different functional categories, a complex clonal architecture, and disease evolution over time. Patterns of mutations seem to follow specific and temporally ordered trajectories. Mutations in genes encoding epigenetic modifiers, such as DNMT3A, ASXL1, TET2, IDH1, and IDH2, are commonly acquired early and are present in the founding clone. The same genes are frequently found to be mutated in elderly individuals along with clonal expansion of hematopoiesis that confers an increased risk for the development of hematologic cancers. Furthermore, such mutations may persist after therapy, lead to clonal expansion during hematologic remission, and eventually lead to relapsed disease. In contrast, mutations involving NPM1 or signaling molecules (eg, FLT3, RAS) typically are secondary events that occur later during leukemogenesis. Genetic data are now being used to inform disease classification, risk stratification, and clinical care of patients. Two new provisional entities, AML with mutated RUNX1 and AML with BCR- ABL1, have been included in the current update of the WHO classification of myeloid neoplasms and AML, and mutations in three genes— RUNX1, ASXL1, and TP53—have been added in the risk stratification of the 2017 European LeukemiaNet recommendations for AML. Integrated evaluation of baseline genetics and assessment of minimal residual disease are expected to further improve risk stratification and selection of postremission therapy. Finally, the identification of disease alleles will guide the development and use of novel molecularly targeted therapies.

Sign in / Sign up

Export Citation Format

Share Document