Which acute-phase reactant deficiency may contribute to premature emphysema in a smoker?

Which acute-phase reactant deficiency may contribute to premature emphysema in a smoker?

• A. Haptoglobin
• B. Fibrinogen
• C. Alpha1-antitrypsin
• D. Ceruloplasmin

Answer: (C)

Balance between proteases and antiproteases in the lung is the key idea. Alpha1-antitrypsin is a major antiprotease that inhibits neutrophil elastase, an enzyme that can destroy elastic tissue in the alveolar walls. When this inhibitor is deficient, elastase activity goes unchecked, so elastin and surrounding lung structure are broken down, leading to emphysema. Smoking accelerates this process by increasing neutrophil recruitment and elastase release and can also inactivate the remaining antiprotease, making lung injury more pronounced. The other acute-phase reactants listed have roles in inflammation or metabolism that do not protect the lung from elastase damage, so their deficiency wouldn’t explain premature emphysema.

Balance between proteases and antiproteases in the lung is the key idea. Alpha1-antitrypsin is a major antiprotease that inhibits neutrophil elastase, an enzyme that can destroy elastic tissue in the alveolar walls. When this inhibitor is deficient, elastase activity goes unchecked, so elastin and surrounding lung structure are broken down, leading to emphysema. Smoking accelerates this process by increasing neutrophil recruitment and elastase release and can also inactivate the remaining antiprotease, making lung injury more pronounced. The other acute-phase reactants listed have roles in inflammation or metabolism that do not protect the lung from elastase damage, so their deficiency wouldn’t explain premature emphysema.