Salivary Secretory Immunoglobulin A as a Candidate Biomarker of Oral Mucosal Vulnerability in Paediatric Acute Lymphoblastic Leukaemia: A Prospective Pilot Cohort Study.
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Background: Acute lymphoblastic leukaemia (ALL) is the most common paediatric haematological malignancy. Treatment-related immunosuppression compromises mucosal integrity and contributes to oral and dento-maxillary complications, which remain a clinically relevant but insufficiently characterised source of morbidity. Salivary secretory immunoglobulin A (sIgA), the principal antibody of mucosal surfaces, may provide a non-invasive surrogate measure of local immune competence; however, its longitudinal behaviour and relationship with oral morbidity in paediatric ALL remain incompletely characterised. Methods: This prospective, single-centre pilot cohort study included 21 children with newly diagnosed ALL treated at the Fundeni Clinical Institute, Bucharest (March-November 2024). Salivary sIgA was measured at diagnosis (TP1) and after completion of intravenous chemotherapy (TP3). Oral mucositis (OM) was clinically assessed and graded according to WHO criteria at induction (TP2), as well as the predominant WHO grade across the post-induction chemotherapy course. Stomatological evaluation included DMFT/dmft and PUFA/pufa indices, and microbiological screening was performed at predefined time points. Statistical analyses were exploratory and included non-parametric tests and correlation analyses. Results: All patients developed OM at induction (TP2), with 38% experiencing severe forms (WHO grades 3-4). Baseline salivary sIgA (TP1) (n = 15) showed a non-significant weak inverse association with mucositis severity (Spearman ρ = -0.35, p = 0.20); differences across severity groups did not reach statistical significance (Kruskal-Wallis p = 0.43). When grouped, lower median salivary sIgA levels were observed in patients with severe mucositis compared with mild-to-moderate forms (median 91.0 mg/L (IQR 65.0-123.0) vs. 170.5 mg/L (IQR 125.0-231.8); non-significant p = 0.13). A non-significant decline in salivary sIgA was observed from TP1 to TP3 (median 174.5, IQR 127.2-213.8 versus median 111.5, IQR 33.2-142.7; Wilcoxon signed-rank p = 0.084; n = 10 paired measurements). Pre-existing dento-maxillary morbidity was substantial (median DMFT 4.0 (IQR 2.5-5.5), PUFA 3.0 (IQR 1.5-4); dmft 4.0 (IQR 3.0-5.0), pufa 3.0 (IQR 2.0-3.5)), but showed no statistically significant association with either mucositis grade or salivary sIgA levels. No clinically meaningful correlation was observed between salivary and intestinal sIgA levels (Spearman ρ = 0.33 overall; ρ = 0.16 after exclusion of an extreme outlier; p > 0.05 in both analyses), consistent with immunological compartmental independence. Conclusions: In this exploratory pilot cohort, no statistically significant associations were observed between salivary sIgA and oral mucositis severity or dento-maxillary indices. Although trends toward lower baseline salivary sIgA in severe mucositis and declining sIgA during induction therapy were observed, larger adequately powered studies are needed to determine whether these findings represent true biological associations.