showed promising benefits of short-term (< 6 months) DAPT followed by P2Y12 inhibitors in selected patients, as well as the benefits of extended-term (> 12 months) DAPT in high risk patients. In conclusion, the optimal duration of DAPT after PCIs should be personalized after outweighing each patients risks of ischemic events and risks of bleeding events with consideration of multiple patient-related and procedure-related factors. Moreover, aspirin should be continued indefinitely after DAPT is complete. Cancer prevention
Aspirin may reduce the overall risk of both getting cancer and dying from cancer. There is substantial evidence for lowering the risk of colorectal cancer (CRC), but must be taken for at least 10–20 years to see this benefit. It may also slightly reduce the risk of endometrial cancer, breast cancer, and prostate cancer.Some conclude the benefits are greater than the risks due to bleeding in those at average risk. Others are unclear if the benefits are greater than the risk. Given this uncertainty, the 2007 United States Preventive Services Task Force (USPSTF) guidelines on this topic recommended against the use of aspirin for prevention of CRC in people with average risk.
Hereditary persistence of fetal hemoglobin (HPFH) is a benign condition in which increased fetal hemoglobin (hemoglobin F, HbF) production continues well into adulthood, disregarding the normal shutoff point after which only adult-type hemoglobin should be produced. Presentation
The condition is asymptomatic, and is only noticed when screening for other hemoglobin disorders. Sickle cell disease
In persons with sickle cell disease, high levels of fetal hemoglobin as found in a newborn or as found abnormally in persons with hereditary persistence of fetal hemoglobin, the HbF causes the sickle cell disease to be less severe. In essence the HbF inhibits polymerization of HbS. A similar mechanism occurs with persons who have sickle cell trait. Approximately 40% of the hemoglobin is in the HbS form while the rest is in normal HbA form. The HbA form interferes with HbS polymerization. Causes
HPFH can be caused by mutations in the β globin gene cluster, or the γ gene promoter region. In addition HbF levels are influenced by polymorphisms in the BCL11A gene and in the MYB gene enhancer. In HPFH the percentage of HbF varies from 0.8-1.0% to about 30% of the total hemoglobin, but levels as high as 100% can be seen in homozygotes for delta beta thalassemia. Diagnosis
Epidemiology
About 10% of the population has an HbF level >1.0%. HPFH may alleviate the severity of certain hemoglobinopathies and thalassemias, and is selected for in populations with a high prevalence of these conditions (which in turn are often selected for in areas where malaria is endemic).