CHICAGO-Recurrent respiratory papillomatosis (RRP) begins with a pretty small virus, relatively speaking, but it can lead to some pretty big problems for both the patient and the treating physician. Recent surgical and pharmaceutical advances, however, are already making a difference and researchers may be on the verge of answering some big questions that may lead to improved treatments and, ultimately perhaps, prevention.
Explore this issue:September 2006
The American Laryngological Association (ALA) and the American Society of Pediatric Otolaryngology (ASPO) joined forces to present a special panel discussion here at the 2006 Combined Otolaryngology Spring Meetings (COSM). Robert T. Sataloff, MD, Professor of Otolaryngology-Head and Neck Surgery at Thomas Jefferson University Hospital in Philadelphia, Pa., served as moderator of the discussion, which covered some of the current issues surrounding the treatment of RRP.
Etiology and Natural History
The viral etiology of RRP is the human papilloma virus (HPV), which is also associated with genital warts and cervical cancer.
It is a fiendishly simple virus, said Andrew Inglis, MD, Associate Professor of Otolaryngology-Head and Neck Surgery at the University of Washington Medical Center in Seattle. It only has about 8000 base pairs-there’s not a lot of kilobytes of information in that virus.
I find [the microdebrider] a much more elegant way to remove papilloma and I find it is as effective as the CO2 laser. – -Marvin Fried, MD
HPV encompasses a large family of types that are based on the homology of the genome; more than 100 types and subtypes have been characterized, with types 6 and 11 being the most common in RRP. Many others have also been reported, including types 16 and 18, which are considered the most carcinogenic.
It only has eight proteins that it codes for, so it’s very efficient, Dr. Inglis said. There are two capsid proteins, four kind of housekeeping proteins, and then the two oncogenes-E6 and E7 oncoproteins.
Initially, the virus particle enters the stem cells at the basal layers, where it may remain latent or it may express the viral proteins. Expression of the E6 and E7 oncogenes then leads to continued proliferation in the upper mucosal layer.
The cells don’t divide faster, they just continue to divide when they should be differentiating, Dr. Inglis said. It also stimulates angiogenesis and that’s what leads to a papilloma forming.
Investigating Juvenile RRP
There are two types of RRP-juvenile onset, which is generally observed to be most severe, and adult onset. The conventional wisdom is that the juvenile RRP viral infection is acquired in the birth canal, according to Dr. Inglis, who noted a recently published Danish study suggesting that the biggest risk factor is maternal history of genital warts.