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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. (Otolaryngol Head Neck Surg 2002;127:387-97.)

BACKGROUND Hypertonic saline (HTS) acts as an airway irritant in human nasal mucosa by stimulating nociceptive nerves and glandular secretion. HTS does not change vascular permeability. In asthma, HTS causes airflow obstruction. OBJECTIVE To determine the effect of HTS on mucosal swelling using acoustic rhinometry (AcRh). Potential vasodilator effects were controlled by maximally constricting mucosal vessels with oxymetazoline (Oxy). METHOD Normal subjects had AcRh before and 30 min after either 0.05% Oxy or saline (0.9% NaCl) nasal treatments. Nasal provocations followed immediately with five step-wise incremental escalating doses of HTS administered at 6-min intervals. AcRh was performed 1, 3 and 5 min after each HTS administration, and then after blowing the nose at 5 min. The minimum cross-sectional area (Amin), volume of the anterior 6 cm of nasal cavity (V6) and incremental changes from pre-drug treatment baseline levels (delta, mean +/- SEM) were calculated. RESULTS Oxy increased Amin by 46% (delta = 0.48 +/- 0.07 cm2, P = 0.0001) and V6 by 53% (Delta = 9.9 +/- 1.5 mL, P < 1 x 10-7) during the first 30 min. Saline (vehicle) treatment had no effect. The maximum HTS dose had no effect after 1 or 3 min. However, in the 4th and 5th minutes there were reductions in Amin (delta = 0.07 +/- 0.03 cm2, P = 0.035) and V6 (delta = 1.57 +/- 0.42 mL, P = 0.004) with an increase in the weight of secretions (delta = 700 +/- 100 mg, P < 0.05). Blowing the nose returned Amin and V6 towards baseline. Oxy had no effect on HTS-induced changes in Amin, V6, pain, rhinorrhea or weight of secretions. CONCLUSION HTS induced nociceptive nerve stimulation and mucus secretion, and reduced V6 and Amin. Oxy caused vasoconstriction but did not alter HTS-induced effects. HTS may stimulate neurogenic axon response-mediated glandular secretion that contributes to perceptions of nasal obstruction in normal subjects.

Objective: To assess potential mechanism(s) for the rhinitis found in Chronic Fatigue Syndrome (CFS) subjects.Methods: The concentrations of mucus constituents were measured in basal nasal lavage fluids of 103 CFS and 92 non-CFS control subjects. Subjects were further characterized by their Rhinitis Score and allergy skin test results into nonallergic and allergic rhinitis, atopic, and negative subgroups to determine if differences were related to atopy. Other questionnaires of irritant sensitivity and medicine use were completed.Results: Mucin polysaccharide (p = 0.043, ANOVA), free hemoglobin (p = 0.0044), mucin/total protein (p = 0.039) and hemoglobin/total protein (p = 0.043) were higher in CFS than controls. CFS subjects with positive Rhinitis Scores (p = 0.023) or skin tests (p = 0.047) had higher mucin levels than those with negative values. For all subjects, increased mucin was correlated with total protein (Pearson's r2 = 0.188) and inhaled corticosteroid use (r2 = 0.091), while hemoglobi...

Background Chronic fatigue syndrome (CFS) has an uncertain pathogenesis. Allergies have been suggested as one cause. Objective The aim of this study was to compare serum immunoglobulin (Ig)E in CFS and control subjects to determine whether IgE levels were elevated in CFS. This would be suggestive of increased atopy in CFS. Methods IgE was measured by quantitative ELISA (sandwich) immunoassay in 95 CFS and 109 non-CFS control subjects. Subjects were classified by positive or negative allergy skin tests (AST) and rhinitis questionnaires (rhinitis score, RhSc) into four rhinitis types: nonallergic rhinitis (NAR with positive RhSc and negative AST); allergic rhinitis (AR with positive AST and RhSc); atopic/no rhinitis (AST positive/RhSc negative); and nonatopic/no rhinitis (both AST and RhSc negative) subjects. Results IgE was not significantly different between control (128 ± 18 IU/mL, mean ± SEM) and CFS (133 ± 43 IU/mL) groups, or between control and CFS groups classified into the four rhinitis types. IgE was significantly higher in subjects with positive AST whether or not they had positive RhSc or CFS symptoms. Conclusions Elevated IgE and positive AST indicate allergen sensitization, but are not necessarily indicators of symptomatic allergic diseases. There was no association between IgE levels and CFS, indicating that atopy was probably not more prevalent in CFS. Therefore, TH2-lymphocyte and IgE-mast cell mechanisms are unlikely causes of CFS.

Background: Irritation symptoms after exposure to “nonspecific” stimuli are often attributed to nonallergic rhinitis (vaso-motor rhinitis). This is a heterogeneous syndrome of exclusion based on nasal symptoms with negative allergy skin tests.Method: Control (n = 114) and Chronic Fatigue Syndrome (CFS, n = 120) subjects scored the severity of nasal congestion and rhinorrhea sensations that they attributed to 9 irritants. The sum was the “Irritant Rhinitis Score” (IRS maximum 72). A positive IRS of > 19 defined “Irritant Rhinitis.” Demographic, allergy skin test and other assessments were done to characterize the Irritant Rhinitis population.Results: Irritant Rhinitis was present in 11% of control and 47% of CFS subjects. In multivariate analysis, positive IRS was correlated with a history of rhinitis complaints, systemic complaints such as fatigue, sensations of congestion and rhinorrhea induced by meteorological conditions, tobacco smoke, odors, perfumes, and other volatile materials, and diagnos...

Hypertonic saline (HTS) induces bronchoconstriction. Potential mechanisms were evaluated in a human nasal provocation model. Aliquots of normal saline (1 x NS, 100 microliters) and higher concentrations (3 x NS, 6 x NS, 12 x NS, 24 x NS) were sprayed into one nostril at 5-min intervals. Lavage fluids were collected from the ipsilateral and contralateral sides to determine the concentrations of specific mucus constituents. Nasal cavity air-space volume was assessed by acoustic rhinometry (AcRh). The distribution of substance-P-preferring neurokinin-1 (NK-1) receptor mRNA was assessed by in situ reverse transcriptase-polymerase chain reaction. Unilateral HTS induced unilateral dose-dependent increases in sensations of pain, blockage, and rhinorrhea, the weights of recovered lavage fluids, and concentrations of total protein, lactoferrin, mucoglycoprotein markers, and substance P. Contralateral, reflex-mediated effects were minor. There were no changes in IgG or AcRh measurements. NK-1 receptor mRNA was localized to submucosal glands. HTS caused pain with unilateral substance P release. The presumed nociceptive nerve efferent axon response led to glandular exocytosis, presumably through actions on submucosal gland NK-1 receptors. Vascular processes, including plasma exudation, filling of venous sinusoids, and mucosal edema were not induced in these normal subjects.

Hypertonic saline (HTS) acts as an airway irritant in human nasal mucosa by stimulating nociceptive nerves and glandular secretion. HTS does not change vascular permeability. In asthma, HTS causes airflow obstruction.To determine the effect of HTS on mucosal swelling using acoustic rhinometry (AcRh). Potential vasodilator effects were controlled by maximally constricting mucosal vessels with oxymetazoline (Oxy).Normal subjects had AcRh before and 30 min after either 0.05% Oxy or saline (0.9% NaCl) nasal treatments. Nasal provocations followed immediately with five step-wise incremental escalating doses of HTS administered at 6-min intervals. AcRh was performed 1, 3 and 5 min after each HTS administration, and then after blowing the nose at 5 min. The minimum cross-sectional area (Amin), volume of the anterior 6 cm of nasal cavity (V6) and incremental changes from pre-drug treatment baseline levels (delta, mean +/- SEM) were calculated.Oxy increased Amin by 46% (delta = 0.48 +/- 0.07 cm2, P = 0.0001) and V6 by 53% (Delta = 9.9 +/- 1.5 mL, P1 x 10-7) during the first 30 min. Saline (vehicle) treatment had no effect. The maximum HTS dose had no effect after 1 or 3 min. However, in the 4th and 5th minutes there were reductions in Amin (delta = 0.07 +/- 0.03 cm2, P = 0.035) and V6 (delta = 1.57 +/- 0.42 mL, P = 0.004) with an increase in the weight of secretions (delta = 700 +/- 100 mg, P0.05). Blowing the nose returned Amin and V6 towards baseline. Oxy had no effect on HTS-induced changes in Amin, V6, pain, rhinorrhea or weight of secretions.HTS induced nociceptive nerve stimulation and mucus secretion, and reduced V6 and Amin. Oxy caused vasoconstriction but did not alter HTS-induced effects. HTS may stimulate neurogenic axon response-mediated glandular secretion that contributes to perceptions of nasal obstruction in normal subjects.

The constituents of nasal mucus may be contaminated by plasma if there is epistaxis. Gross epistaxis is apparent as a red lavage fluid, while microepistaxis may yield a clear fluid. If gross or microepistaxis are present, it will be difficult to decide whether plasma protein concentrations are elevated because of plasma exudation or bleeding. In order to discriminate between these two possibilities, we measured erythrocyte-derived free hemoglobin (fHb) in nasal lavage fluids.Single-blinded subjects underwent standard hypertonic saline nasal provocation. Unilateral hypertonic nasal provocation was performed in normal, allergic rhinitis (AR) and nonallergic rhinitis (NAR) subjects (total of 1316 specimens). fHb was measured using the Sigma-Aldrich kit (St. Louis, MO). Grossly bloody specimens were analyzed separately from the remainder. Statistical analysis defined the means and 95th percentiles for fHb and albumin in the nonbloody normal group.fHb concentrations ranged from below the limits of detection (1 microg/ml) to164 microg/ml fHb was 79.3 microg/ml +/- 4.7 (mean +/- SEM) in four normal, 31 AR and 25 NAR grossly bloody specimens. The 95th percentile of fHb in the nonbloody normal samples (n = 68 subjects, n = 681 specimens) was 16.5 microg/ml. This value was defined as the threshold to detect potential microepistaxis, and corresponded to approximately 245 000 erythrocytes per ml of lavage fluid. Total protein (P0.05) and albumin (P0.001), but not markers of glandular secretion, were significantly increased in samples with fHb16.5 microg/ml compared to thoseor = 16.5 microg/ml. Elevations of fHb without changes in albumin were more prevalent in nonallergic rhinitis.Significant bleeding into nasal lavage samples can contaminate the specimens and increase the concentrations of both fHb and plasma proteins. Increased albumin alone would indicate increased vascular permeability. The mechanism(s) leading to elevated fHb without increased plasma proteins require further investigation.