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Pulmonary
hypertension may not have an atherosclerotic background
in sickle cell diseases
......................................................................................................................................................................
Mehmet Rami Helvaci (1)
Zeki Arslanoglu (2)
Atilla Yalcin (1)
Orhan Ekrem Muftuoglu (1)
Abdulrazak Abyad (3)
Lesley Pocock (4)
(1) Specialist of Internal Medicine,
MD
(2) Specialist of Dentistry, PhD
(3) Middle-East Academy for Medicine of Aging,
MD
(4) medi-WORLD International
Corresponding author:
Prof Dr Mehmet Rami Helvaci,
07400, ALANYA, Turkey
Phone: 00-90-506-4708759
Email: mramihelvaci@hotmail.com
Received April 2021. Accepted
May 2021. Published June 1, 2021.Please cite this
article as: Mehmet Rami Helvaci et al. A much
higher prevalence of chronic obstructive pulmonary
disease in males with sickle cell diseases even
in the absence of smoking and alcohol.. Middle
East J Intern Med 2021; 14(1): 17-25
DOI: 10.5742/MEJIM2021.93794.
.....................................................................................................................................
ABSTRACT
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.
Key words: Sickle cell
diseases, chronic endothelial damage, pulmonary
hypertension, atherosclerosis, male sex, smoking,
alcohol
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