Key result
Salivary uric acid levels are ~3-fold higher in hypertensive patients compared to healthy controls.
Why the study?
Uric acid is implicated in hypertensive pathophysiology, and salivary uric acid offers a non-invasive, cost-effective alternative to serum analysis whose levels and diagnostic utility in hypertensive adults required comparison against normotensive controls.
Does salivary uric acid measurement accurately differentiate hypertensive patients from normotensive controls in adults?
Case-Control (n=120)
No
Does salivary uric acid measurement accurately differentiate hypertensive patients from normotensive controls in adults?
Stimulated salivary uric acid is significantly elevated in hypertensive patients, correlates strongly with blood pressure and serum uric acid, and demonstrates high diagnostic accuracy (AUC 0.97) as a non-invasive biomarker for hypertension.
Salivary UA may aid non-invasive hypertension assessment; hypothesis-generating and requires validation before clinical adoption.
Background. Hypertension is a leading global cause of cardiovascular morbidity and mortality. Uric acid (UA) is implicated in oxidative stress, endothelial dysfunction, and hypertensive pathophysiology. Salivary UA offers a non-invasive, cost-effective alternative to serum analysis. Aim: To compare salivary UA levels in hypertensive adults against normotensive controls and evaluate its diagnostic utility. Material and Methods. This prospective case-control study enrolled 60 adult hypertensive patients and 60 age- and sex-matched normotensive controls. Non-stimulated whole saliva (NWS) and stimulated whole saliva (SWS) were collected following a standardised protocol. Salivary UA concentrations were measured spectrophotometrically using a commercial QuantiChrom™ Uric Acid Assay Kit. Serum UA, total antioxidant capacity (TAC), and salivary flow rates were also assessed. Pearson correlation coefficients and receiver operating characteristic (ROC) analysis were applied for statistical evaluation. Results. SWS UA was significantly higher in the hypertensive group (18.62 ± 3.27 µg/mg protein) versus controls (6.14 ± 1.92 µg/mg protein; p < 0.001). NWS UA was similarly elevated. Salivary UA in SWS correlated positively with systolic blood pressure ( r = 0.79, p < 0.001), diastolic blood pressure ( r = 0.81, p < 0.001), and serum UA ( r = 0.84, p < 0.001). ROC analysis showed SWS UA had an AUC of 0.97 with sensitivity of 92% and specificity of 93% in differentiating hypertensive from normotensive individuals. Stimulated salivary flow was significantly lower in the hypertensive group. Conclusion. Salivary UA, particularly measured in stimulated saliva, is markedly elevated in hypertensive patients and demonstrates strong diagnostic performance. It represents a promising non-invasive biomarker for hypertension screening and monitoring, warranting validation in larger multicentre studies.
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Ahmed et al. (2026) conducted a case-control in Hypertension (n=120). Salivary uric acid measurement vs. Normotensive controls was evaluated on Stimulated whole saliva (SWS) uric acid concentration (µg/mg protein) (AUC 0.97, p=<0.001). Salivary uric acid in stimulated saliva was significantly higher in hypertensive patients vs controls (18.62 vs 6.14 µg/mg protein; p<0.001; AUC 0.97).
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