The immune status in situ of recurrent tonsillitis and idiopathic tonsillar hypertrophy

Abstract

Abstract:Objective: To analyze the immune status in situ of tonsils of patients with recurrent tonsillitis (RT) and idiopathic tonsillar hypertrophy (ITH) with the aim to discuss the indications of tonsillectomy (TE) and tonsillotomy (TT) in young children. Methods: The histological and immunohistological study of tonsillar tissue of RT and ITH in correlation with immunological parameters in peripheral blood in 13 patients with RT and 16 patients with ITH. Results: In the RT group, we found a higher degree of fi brosis with a higher density of memory lymphocytes (CD45R0 + ), B-lymphocytes (CD20 + ) and cytotoxic T-lymphocytes (CD8 + ) in surface epithelium of tonsils compared to the ITH group (NS). The density of immunoglobulin IgG in the crypt epithelium in RT was signifi cantly higher than in the ITH group (p = 0.041). We also measured a higher sera concentration of immunoglobulines (IgG, IgM, IgA) and TNF-α in RT compared to the ITH group (NS) and T H -1 immune response in tonsillar tissue based on differences between local cytokine concentration TNF-α and IL-4. Conclusions: RT has a higher infl ammatory reaction in tonsillar tissue as a result of persistent bacterial antigenic stimulation. In patients with RT, the tonsillectomy might be the only option for surgical treatment. In patients with ITH with mild symptoms, the tonsillotomy should be preferred (Tab. 3, Ref. 24). Full Text in PDF www.elis.sk.

Impact of adenotonsillectomy on the evolution of inflammatory markers

“…Children with chronic tonsillitis have an impaired immune profile due to a continuous inflammatory stimulus by pathogens that produce activation of the immune system, finally leading to an increase in the concentration of proinflammatory cytokines compared with healthy individuals …”

“…We have found that hs‐CRP values were significantly higher in the children of the study group before surgery suggesting an inflammatory systemic response. Previous studies have shown that palatine tonsils express Th1‐ and Th2‐type cytokines and are dominated by Th1‐type cytokines . In response to infection, tonsils begin production of Th1‐type cytokines, the most important being IFN‐γ, TNF‐α and IL‐1; later, tonsils secrete Th2‐type cytokines (IL‐4) …”

“…In chronic tonsillitis, elevated values of proinflammatory cytokines and cytokine‐producing cells have been detected at the site of inflammation . However, this situation does not translate into greater efficiency of the immune response but generates activation and proliferation of endothelial cells and fibroblasts, altering the immunologically active tissue and favouring the recurrence of inflammatory processes . In addition, in both adults and paediatric populations there is clear evidence of the association between obstructive sleep apnoea‐hypopnea syndrome (OSAS) linked to tonsillar hypertrophy and systemic inflammatory phenomena, as well as an increased risk of cardiovascular disease in adulthood …”

“…3 However, this situation does not translate into greater efficiency of the immune response but generates activation and proliferation of endothelial cells and fibroblasts, altering the immunologically active tissue and favouring the recurrence of inflammatory processes. 4 In addition, in both adults and paediatric populations there is clear evidence of the association between obstructive sleep apnoea-hypopnea syndrome (OSAS) linked to tonsillar hypertrophy and systemic inflammatory phenomena, as well as an increased risk of cardiovascular disease in adulthood. 5,6 Surgery performed on this immune defence system remains the most common surgical procedure in children, [7][8][9] with the highest rate of interventions between 3 and 5 years of age.…”

Intra-Capsular Tonsillotomy by Ultrasonic Method

“…Tonsil hyperplasia, also known as (idiopathic) tonsillar hypertrophy, refers to abnormal enlargement of the palatine tonsil [5,6]. It has to be distinguished from physiological pediatric palatine tonsil hyperplasia [7,8] which is not a sign or consequence of recurrent inflammation [9,10].…”