Table 1.
Similarities between MPNs, Alzheimer’s disease, type II DM, chronic inflammatory diseases, and smoking
| Clinical | MPNs | AD | Type II DM | Smoking | CI | Comments |
|---|---|---|---|---|---|---|
| Risk of CVE | Increased | Increased | Increased | Increased | Increased | Chronic inflammation is involved in disease pathogenesis in all five disease entities |
| Risk of CKD | Increased | ? | Increased | Increased | Increased | Chronic inflammation contributes in all five disease entities |
| Risk of PA | Increased | ? | Increased | Increased | Increased | PA is well described in smokers and in CI in MPNs, CI has recently been hypothesized to elicit and drive clonal evolution |
| Risk of VT | Increased | ? | Increased | Increased | Increased | CI significantly increases risk of thromboembolic diseases |
| Risk of MS and type II DM | Increased | ? | – | Increased | Increased | A recent study has found an association between MS and ET |
| Risk of AD | ? | – | Increased | Increased | ? | Epidemiological studies are ongoing to investigate, whether AD is more common among patients with MPNs. |
| Risk of COPD | Increased | – | Increased | Increased | Smokers and patients with CI and MPNs have an increased risk of developing COPD | |
| Risk of neuroinflammation | ? | – | Increased | Increased | Increased | Neuroinflammation is prone to develop in patients with MPNs due to a chronic inflammatory state with elevated cell counts, in vivo cell activation, and recurrent ischemic cerebral multi-infarctions with chronic cerebral hypoperfusion—one of the hallmarks of AD |
| Risk of cancer | Increased | ? | Increased | Increased | Increased | Smokers have an increased risk of cancer, in particular lung and bladder cancer; MPNs are associated with a 40% increased risk of second cancers. CI precedes several cancers |
| Biochemical | ||||||
| CI markers | Increased | Increased | Increased | Increased | Increased | Chronic inflammation is the common denominator for elevated inflammatory markers in all diseases and smoking as well |
| In vivo activation of leukocytes, platelets, and endothelium | Increased | Increased | Increased | Increased | Increased | Chronic inflammation is the common denominator for in vivo cell activation in all diseases and smoking as well |
| Markers of endothelial dysfunction | Increased | Increased | Increased | Increased | Increased | Chronic inflammation is considered to play a major role for endothelial dysfunction in all diseases and smoking as well |
| Markers of oxidative stress | Increased | Increased | Increased | Increased | Increased | Chronic inflammation with induction of increased oxidative stress is considered of major pathogenetic importance for organ dysfunction and organ failure in all disease entities |
| Molecular pathways | ||||||
| JAK-STAT/NF-kB, HIF, NF-E2 | Increased | Increased ? | Increased | Increased | Increased | The JAK-STAT, NF-kB, and HIF are activated in both smokers and in patients with MPNs, type II DM, and chronic inflammatory disease patients |
| Stalling of cerebral capillaries | Yes | Yes | ? | ? | ? | Elevated cell counts, in vivo cell activation with adherence of neutrophils to monocytes and platelets, and adherence of these cells to dysfunctional endothelium predispose to stalling of cerebral capillaries and cerebral hypoperfusion |
MPNs myeloproliferative neoplasms, AD Alzheimer’s disease, DM diabetes mellitus, CVE cardiovascular events, CKD chronic kidney disease, PA peripheral atherosclerosis, VT venous thromboembolism, CI chronic inflammatory diseases, MS metabolic syndrome, COPD chronic obstructive pulmonary disease