| Abstrakt: |
Background: We tried to understand the underlying mechanism of pulmonary hypertension (PHT) in the sickle cell diseases (SCD). Methods: All patients with the SCD were included. Results: The study included 434 patients (212 females) with similar mean ages in males and females (30.8 versus 30.3 years, respectively, p>0.05). Smoking (23.8% versus 6.1%, p<0.001) and alcohol (4.9% versus 0.4%, p<0.001) were higher in males, significantly. Transfused units of red blood cells (RBC) in their lives (48.1 versus 28.5, p=0.000), disseminated teeth losses (<20 teeth present) (5.4% versus 1.4%, p<0.001), chronic obstructive pulmonary disease (COPD) (25.2% versus 7.0%, p<0.001), ileus (7.2% versus 1.4%, p<0.001), cirrhosis (8.1% versus 1.8%, p<0.001), leg ulcers (19.8% versus 7.0%, p<0.001), digital clubbing (14.8% versus 6.6%, p<0.001), coronary heart disease (CHD) (18.0% versus 13.2%, p<0.05), chronic renal disease (CRD) (9.9% versus 6.1%, p<0.05), and stroke (12.1% versus 7.5%, p<0.05) were all higher but not PHT (12.6% versus 11.7%, p>0.05) in males, significantly. Conclusion: SCD are severe inflammatory processes on vascular endothelium, particularly at the capillary level since the capillary system is the main distributor of hardened RBC into the tissues. Although the higher smoking, alcohol, and disseminated teeth losses, COPD, ileus, cirrhosis, leg ulcers, digital clubbing, CHD, CRD, and stroke-like atherosclerotic consequences in male sex, PHT was not higher in them in the present study. In another definition, PHT may not have an atherosclerotic background in the SCD. Instead, the hardened RBC-induced capillary endothelial damage, inflammation, edema, and fibrosis around the alveoli may be the major underlying cause. [ABSTRACT FROM AUTHOR] |
