BACKGROUND: Sinus tenderness has not been quantitatively assessed. OBJECTIVE: We sought to compare sinus and systemic tenderness in rhinosinusitis, allergic rhinitis, and chronic fatigue syndrome (CFS), and healthy (non-CFS) groups. METHODS: Cutaneous pressures (kg/cm2) causing pain at 5 sinus and 18 systemic sites were measured in acute and chronic rhinosinusitis, active allergic rhinitis, healthy non-CFS/no rhinosinusitis, and CFS subjects. RESULTS: Sinus thresholds differed significantly ( P ≤ 10−11, ANOVA) between non-CFS/no rhinosinusitis (1.59 ± 0.14 kg/cm2, mean ± 95% CI, n = 117), allergic rhinitis (1.19 ± 0.31, n = 30), exacerbations of chronic rhinosinusitis (1.25 ± 0.26, n = 25), non-CFS/chronic rhinosinusitis (1.23 ± 0.27, n = 23), acute rhinosinusitis (1.10 ± 0.20, n = 22), CFS/no rhinosinusitis (0.98 ± 0.15, n = 70), and CFS/chronic rhinosinusitis (0.78 ± 0.12, n = 56). Systemic pressure thresholds were lower for CFS (1.46 ± 0.15) than for non-CFS (2.67 ± 0.22, P ≤ 10−11). CONCLUSIONS: The lower sinus thresholds of rhinosinusitis groups validated the sign of sinus tenderness. Sinus and systemic thresholds were both 44% lower in CFS than in non-CFS subjects, suggesting that systemic hyperalgesia contributed to CFS sinus tenderness and “rhinosinusitis” complaints. Tenderness to palpation or percussion is one of the clinical hallmarks of acute and chronic rhinosinusitis. 1,2 This sign may equate with the subjective sensation of pain experienced by rhinosinusitis subjects and so may be indicative of either excessive nociceptive nerve depolarization or centrally mediated hyperalgesia. Several peripheral mechanisms may contribute, including the release of excessive amounts of mediators that activate sensory neurons (eg, bradykinin); increased sensitivity of type C fibers to mediators generated during acute or chronic inflammation (eg, endothelin, bradykinin); or hyperresponsiveness due to facilitation of neural depolarization induced by prostaglandins, leukotriene B4, and neurotropic cytokines (eg, nerve growth factor). 3 Central factors may also cause hyperalgesia by modulating the spinal cord actions of large-diameter, low-threshold A$bT-fiber touch or other sensory nerves that innervate the trigeminal dermatome and mucosal areas (“ mucotome”). Sites of alteration may include the spinal dorsal horn somatosensory region and higher central nervous system sites of nociceptive regulation 4 and dysfunction of descending antinociceptive aminergic neural circuits. 3 Although the sign of tenderness is commonly used to diagnose rhinosinusitis, the degree of hyperalgesia has not been quantified in comparison to the sensitivity of control subjects. Therefore, we used dolorimetry (algometry) to measure sinus tenderness. 4 A strain gauge was pressed against the sinus regions until pain was elicited. The mean pressure required to cause pain was considered to be the sinus pressure threshold (kg/cm2). Systemic pressure threshold was determined for 18 “tender points” that are used to diagnose fibromyalgia. 4 Sinus and systemic tenderness were compared in acute rhinosinusitis, chronic rhinosinusitis, chronic rhinosinusitis with acute exacerbations, active allergic rhinitis, and control groups. Chronic fatigue syndrome (CFS) subjects formed one control group. They have a high prevalence of rhinitis complaints (60% to 80%) but there is no evidence of mucosal inflammation based on measures of mucus constituents including neutrophil elastase and eosinophil cationic protein, 5 cytokines, 6 or any bias toward atopic disease as assessed by serum IgE levels. 4 Another reference population consisted of healthy subjects not fulfilling the criteria for CFS (non-CFS subjects). The impact of chronic rhinosinusitis complaints was assessed in CFS/chronic rhinosinusitis, non-CFS/chronic rhinosinusitis, and their corresponding no-rhinosinusitis subpopulations.
Erythromycin reduces nasal inflammation by inhibiting immunoglobulin production, attenuating mucus secretion, and modulating cytokine expression
