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© Borgis - New Medicine 2/2002, s. 64-66
Lidia Zawadzka-Głos, Mieczysław Chmielik, Anna Bielicka
Laryngeal papillomatosis in children and their surgical treatment
Department of Paediatric Otorhinolaryngology, The Medical University of Warsaw, Poland
Head: prof. Mieczysław Chmielik M.D.
Summary
Laryngeal papillomas in children constitute a disease of viral aetiology caused by Human Papilloma Virus. Even though the changes are histologically benign, their exophytic growth may lead to a critical airway obstruction and the child´s suffocation. Due to the tendency to recur, lack of causal treatment, and risk of malignancy the optimal method of treating this condition is still being sought. The study presents methods applied nowadays in the treatment of laryngeal papillomas; especially, it concentrates on a classical papillotomy and its main advantage: the diminished risk of scar formation leading to laryngeal stenosis and vocal fold injury with speech disorders.
Recurrent respiratory papillomatosis in children is a disease of viral origin which is caused by human papillomavirus (HPV). In cases of respiratory papillomatosis types 6 and 11 (HPV 6 and HPV 11) (1, 2) are met most frequently. These same types are responsible for condyloma acuminata in women. The most common type of virus in children with tracheal and bronchial papilloma is HPV 11.
To identify the type of HPV the polymerase chain reaction (PCR), in situ hybridization, or southern blotting hybridization are used. Subtypes of HPV should be estimated at the onset of disease and at any change in the clinical course, particularly if the frequency of recurrence has increased or if papilloma has affected the lower levels of the respiratory tract.
Recurrent respiratory papillomatosis may affect children of any age; a diagnosis usually being made between 2 and 3 years of age, and below 5 years of age in 75% of small patients (3). The incidence of laryngeal papillomatosis in west European countries is about 0.6-4.0 per 100 000 children (4, 5).
The precise mode of HPV transmission remains unclear. Because the same subtypes of HPV are responsible for genital HPV infections in women and juvenile laryngeal papillomatosis, some authors have tried to find an association between maternal condylomata and the development of papilloma in the child. It is assumed that HPV infection may be passed by vertical transmission from mother to child during pregnancy via the placenta or ascending from the birth canal. In the perinatal period the most likely method of maternal-foetal HPV transmission is through direct contact in the birth canal. However, no studies have shown unequivocal confirmation that children born from a mother with condyloma acuminata are more liable to laryngeal papillomatosis. Also, it has not been proved that caesarean section or removal of viral condylomata before delivery reduce the risk of transmission of HPV infection (6). Shah et al. estimated that the risk of a child contracting the disease from a mother who has an active condylomatous lesion and delivers vaginally is only about 1 in 400 children (7).
The most common location of respiratory papillomatosis is the larynx, especially those regions which adjoin stratified squamous epithelium and ciliated epithelium. These are the vestibulum of the larynx, vocal cords, and the subglottal area. Papillomata may appear on the soft palate, in the laryngeal pharynx, in the oesophagus and in the vestibule of the nose. If laryngeal papillomatosis grows more intense the papillomatous changes may affect the trachea, or the main and segmental bronchi.
Papilloma consist of a rich vascularized connective tissue stroma, covered by non-keratinized stratified squamous epithelium. Papillomata are exophytic, irregular pinkish nodes growing up direct from the mucosa or having a petiole. Usually they grow multifocally, and have a tendency to recurrence.
The first symptom of laryngeal papillomatosis most frequently is progressive hoarseness. Other symptoms presenting in children with papillomatosis may be: stridor, beginning as an inspiratory noise and becoming biphasic with progression of the disease, haw, chronic cough, recurrent pneumonia, dysphagia, and dyspnoea. The duration of symptoms before diagnosis varies. Dyspnoea increases gradually, at first as effort dyspnea, but when the lumen of the respiratory tract becomes narrower dyspnoea may appear during rest. If the petiolate papilloma wedges in the vocal cords the dyspnoea has an acute character.
Juvenile laryngeal papillomatosis may persist to the age of maturity. In these cases there is an increased risk of malignant transformation into squamous cell carcinoma. Sommers et al. suggest that age of onset and specific viral subtypes may be correlated with severity of the disease and the clinical course. Children infected with HPV 11 appear to have a more obstructed airway course early in the disease, and a greater need for tracheotomy (8).

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Piśmiennictwo
1. Mounts P. et al.: Viral etiology of juvenile- and adult-onset squamous papilloma of the larynx. Proc. Natl. Acad. Sci. USA 1982, 79: 5425-5429. 2. Gissman H. et al.: Human papilloma virus types 6 and 11 DNA sequences in genital and laryngeal papillomas and in some cervical cancer. Proc. Natl. Acad. Sci. USA 1983, 50:560-563. 3. Cripe T.P.: Human papillomavirus: Pediatric perspectives on a family of multifaceted tumorigenic pathogens. Pediatr. Inf. Dis. J. 1990, 9:839-844. 4. Bomholt A.: Juvenile laryngeal papillomatosis: An epidemiological study from the Copenhagen region. Acta. Otolaryngol. (Stochh) 1988, 105:367-371. 5. Lindeberg H., Elbrond O.: laryngeal papillomas: The epidemiology in a Danish sub-population 1965-1984. Clin. Otolaryngol. 1991, 15:125-131. 6. Smith E.M. et al.: Perinatal vertical transmission of human papillomavirus and subsequent development of respiratory tract papillomatosis. Ann. Otol. Rhinol. Laryngol. 1991, 100:479-483. 7. Shah K. et al.: Rarity of caesarean delivery in cases of juvenil onset respiratory papillomatosis. Obstet. Gynecol. 1986, 68:795-799. 8. Somers G.R. et al.: Juvenile laryngeal papillomatosis in a pediatric population: a clinicopathologic study. Pediatr. Pathol. Lab. Med. 1977 Jan-Feb, 17 (1):53-64. 9. Lusk R.P. et al.: Three-year experience of treating recurrent respiratory papilloma with interferon. Ann. Otol. Rhinol. Laryngol. 1987 Mar-Apr, 96 (2 Pt 1):158-62. 10. Satio R. et al.: Treatment of juvenile laryngeal papilloma with combination of laser surgery and interferon. Auris Nasus Larynx 1985, 12 (2):117-24. 11. Snowden RT. et al.: The predictive value of serum interleukine in recurrent respiratory papillomatosis – a preliminary study. Laryngoscope 2001 Mar, 111 (3):404-8. 12. Bonagura VR. et al.: Recurrent respiratory papillomatosis altered CD8 (+) T-cell subsets and T(H) 1/T(H) 2 cytokine imbalance. Clin. Immunol 1999 Dec, 93 (3):302-11. 13. Swygert C.: Human papillomatosis: disease and laboratory diagnosis. Br. J. Biomed. Sci. 1997 Dec, 54 (4):299-303. 14. Bergler W.: Treatment of recurrent respiratory papillomatosis with argon plasma coagulation. The Jour. of Laryng. and Otology. 1997, Vol 111:381. 15. Bergler W. et al.: The treatment of juvenile laryngeal papillomatosis with argon plasma coagulation. Dtsch Med. Wochenschr 1997, Aug 22, 122 (34-35):1033-6. 16. Craig S., Derkay M.D.: Recurrent respiratory papillomatosis. Laryngoscope 2001, 111:57-69. 17. Chmielik M.: Otorynolaryngologia dziecięca. Warszawa, PZWL 2001.
New Medicine 2/2002
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