In 1963 Carl-Bertil Laurell, the Head of the Clinical Chemistry Department at Malmö General Hospital, University of Lund, Sweden in collaboration with Sten Eriksson published their observations on the relationship between serum deficiency of the Alpha-1-Antitrypsin (AAT) protein and hereditary emphysema. He continued his work on AAT and other disorders until his death in 2001.

Dr. Laurell, who had a major interest in studies of protein biochemistry, together with his Research Fellow Sten Eriksson, used paper electrophoresis studies of serum proteins to investigate subjects with deficient bands in the Alpha-1 globulin region. This region showed the greatest inhibition of trypsin, and the major protein within the band became known as Alpha-1-Antitrypsin. Three of the original five patients had severe early-onset pulmonary emphysema suggesting a cause and effect.

Further work showed that enzymes inhibited by Alpha-1-Antitrypsin were capable of producing many of the pathological features of COPD including emphysema, mucus gland hyperplasia and mucus secretion. Because most of the lung Alpha-1-Antitrypsin is derived from the circulation by diffusion, low serum levels were associated with low lung concentrations. This resulted in insufficient amounts of Alpha-1-Antitrypsin in the lung to protect the tissues from the damage by the enzymes, predominantly neutrophil elastase, normally controlled by this inhibitor.

Recognition of the role of serum deficiency in the emphysematous process led to the introduction of augmentation therapy with purified Alpha-1-Antitrypsin from Bayer in 1988. This treatment leads to an increase in both the serum Alpha-1-Antitrypsin and lung Alpha-1-Antitrypsin levels to concentrations considered protective.

In honor of Dr. Laurell’s major contributions to the discovery and understanding of AAT deficiency, Bayer HealthCare has initiated an annual fellowship award program in 2004.