-tumor necrosis factor TNF-, and a number of studies have reported increased production of TNF in COPD patients. This increased production has been linked to weight loss, muscle weakness and muscle loss.
In addition, animal studies supported the prospect using the drug in COPD. When TNF- was infused into rats, they developed emphysema, which, along with chronic bronchitis, makes up most COPD cases. When the TNF- receptor was turned off in mice, they were less likely than mice that had not be genetically altered to develop emphysema when exposed to chronic cigarette smoke.
The latest study, however, did confirm a recently reported pilot study that found no improvement among the 14 COPD patients given infliximab.
In attempting to explain the disappointing results, the study authors speculate that, despite infliximab's efficacy in treating other inflammatory diseases, it may not be effective in COPD because other mediators, in addition to TNF-, are necessary to cause COPD. They also concede that six months may simply be too short a time period to see improvement.
However, an increased number of malignancies observed in infliximab-treated subjects, the authors said, raised concern about the safety of this drug in lung patients. Although the malignancies may have been present when the patients enrolled in the study, "the possibility that infliximab contributed to the progession, and thus the diagnosis, of malignancies remains a serious concern."
This safety issue, coupled with the "resoundingly negative results," make in unlikely that a longer trial will be undertaken, according to the accompanying editorial.
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