Researchers determined that no relationship existed between haptoglobin polymorphism and frequent exacerbator status, though a negative one existed between exacerbator status and current smoking habits.
A new study evidences a significant association between current smoking habits and chronic obstructive pulmonary disease (COPD) exacerbators.
In a recent analysis designed to determine the relationship between haptoglobin phenotypes and the frequent exacerbator status, compared to COPD non-exacerbators, a team of Israel-based investigators found that the exacerbator phenotype is inversely association with smoking rather than the haptoglobin—a protein produced predominately by the liver—phenotype.
It has been long established that smoking is significantly correlated with COPD. The American Lung Association currently estimates that 85 to 90% of all COPD cases are caused by cigarette smoking. Though the main cause of COPD is generally smoking, nonsmokers are also susceptible, according to the association.
“When a cigarette burns, it creates more than 7,000 chemicals, many of which are harmful,” the ALA noted. “The toxins in cigarette smoke weaken your lungs' defense against infections, narrow air passages, cause swelling in air tubes and destroy air sacs—all contributing factors for COPD.”
Investigators, from the Pulmonology Institute at Carmel Medical Center in Haifa, observed that frequent COPD exacerbators are at an increased risk of “adverse health outcomes when compared to infrequent exacerbators.”
“Haptoglobin (Hp) polymorphism has been associated with differing clinical outcomes in cardiovascular and renal disease,” investigators wrote.
In humans, 2 types of genes for Hp exist: Hp1 and Hp2, with potential combinations of the genes, according to a 2016 Carmel Medical Center study. The Hp2 phenotype has been found to have bacteriostatic properties, investigators noted, while the Hp1 phenotype is more associated with infections.
Inclusion criteria for the study included patients with a previous COPD diagnosis, as well as the presence of at least 2 documented COPD exacerbations in the previous year, or absence of such exacerbations in the previous 2 years.
Investigators analyzed the data utilizing Fisher’s exact test and the nonparametric Kruskal-Wallis test, in addition to performing a multivariate logistic regression analysis.
Ultimately, the researchers determined that no relationship existed between haptoglobin polymorphism and frequent exacerbator status.
“Despite its importance, haptoglobin may not be an important contributor to airway uptake of hemoglobin and iron, which may explain the lack of effect of haptoglobin phenotype in these two studies,” the team wrote.
Conversely, the frequent exacerbator status had a statistically significant association with COPD Assessment Test scores and pack-years, as well as a negative correlation with current smoking status.
Smoking status was found to be negatively related with the frequent exacerbator status, with an odds ratio of 0.240. Number of pack-years was negatively related to being a frequent exacerbator, according to the study.
“The impact of smoking status and number of cigarettes smoked on frequent exacerbator status supports the hypothesis that certain people are susceptible to exacerbations due to factors irrespective of smoking history,” investigators wrote. “Our analysis, paradoxically, found that those who continued to smoke at the time of the study were less likely to be frequent exacerbators.”
The team concluded that more studies assessing the observed positive correlation between current smoking and patients being a non-exacerbator should be explored. Such studies, which should also consider the findings that haptoglobin phenotype is not associated with exacerbation status, should include larger patient populations.
The study, “COPD Exacerbator Phenotype is Inversely Associated with Current Smoking But Not with Haptoglobin Phenotype,” was published online in the Israel Medical Association Journal.