discussion

• The aim of this study was to investigate the risk factors for PTH and to
assess the impact of smoking history on PTH rates. In the present
study, overall PTH rate was %14.6 which is higher than previous
findings [2,7].
• In our study, 48.3% of the patients were smokers which is slightly
higher than reported smoking incidence in Turkey. In a recent report
by ‘International Union Against Tuberculosis and Lung Disease’, 40%
percent of population aged between 25 and 44 are smokers. Our
study population has a slightly higher smoking rate which can be tied
to increased incidence of recurrent tonsillitis in smokers.
• Smoking has significant adverse effects on healing. Impairment in
epithelialization, decrease in tissue oxygenation, microvascular injury
are some of the known effects of smoking [14].
• Torre et al. [15] showed a dose-dependent correlation with smoking
and clinical findings of recurrent infections and histological and
ultrastructural damages to the palatine tonsils. We found that mean
pack/year smoking history of patients in PTH group was significantly
higher than patients without PTH group (p = .004).
• In a study by Demars et al. [16],a significant correlation was found
with smoking history of patient and PTH in patients who underwent
uvulopalatopharyngoplasty for obstructive sleep apnea. But they did
not find a significant relationship with smoking and PTH in patients
who underwent tonsillectomy for chronic tonsillitis. This finding might
be due to longer operative time of uvulopalatopharyngoplasty
operations, and besides they did not specify the patient's exposure to
tobacco.
• In our study, we analyzed the smoking history using pack/year
formula, and we found a significant correlation with PTH and mean
pack/year smoking history of patient which increases the strength of
our study.
• In our study, 40 patients in Group 1 had a prior history of peritonsillar abscess, and 4
patients had prior history of peritonsillar abscess in Group 2 and there was no
statistically significant association between peritonsillar abscess history and PTH
rates which was not consistent with previous studies. Prior peritonsillar abscess
history was relatively low in our study and we believe that this might be the factor
affecting our outcome.
• In our study, 10 patients in Group 1 had a history of hypertension, whereas only 1
patient in Group 2 had a history of hypertension. The only patient with hypertension
in Group 2 experienced 3 episodes of bleeding, first episode ceased spontaneously,
in other two episodes, hemostasis was obtained via surgical intervention (Tables 1,
3). We did not find any significant relationship with hypertension and the risk of PTH.
Mean age in our study group was 25,9 ± 9,8, and prevalence of hypertension is
relatively low compared to older population. Larger studies are needed to reveal the
relationship, if any, with hypertension and the risk of PTH.
• In our study, mean IT of patients without PTH was 23.8 ± 12.3 (4–80), and mean IT of
patients with PTH was 29.0 ± 16.1 (7–90), which was significantly higher in PTH
group (p = .031)(Table 1) and was found to be a significant risk factor for PTH in
logistic regression analysis(p = .001)(Table 4). The underlying mechanism of this
finding might be the sclerotic process caused by chronic and recurrent inflammation
in tonsils and tonsillar fossa.