A tender sinus does not always mean rhinosinusitis.

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/cm(2)) 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

Hypertonic saline nasal provocation and acoustic rhinometry.

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.

Hypertonic saline nasal provocation stimulates nociceptive nerves, substance P release, and glandular mucous exocytosis in normal humans.

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.

IgE levels are the same in chronic fatigue syndrome (CFS) and control subjects when stratified by allergy skin test results and rhinitis types.

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.

Nasal lavage concentrations of free hemoglobin as a marker of microepistaxis during nasal provocation testing.

BACKGROUND: 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. METHODS: 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. RESULTS: fHb concentrations ranged from below the limits of detection (< 1 microg/ml) to > 164 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 (P < 0.05) and albumin (P < 0.001), but not markers of glandular secretion, were significantly increased in samples with fHb > 16.5 microg/ml compared to those < or = 16.5 microg/ml. Elevations of fHb without changes in albumin were more prevalent in nonallergic rhinitis. CONCLUSIONS: 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.