Salivary and serum interleukin 6 in primary Sjögren's syndrome.

OBJECTIVE: To measure interleukin 6 (IL-6) salivary and serum concentrations in primary Sjögren's syndrome (SS), to correlate these data with the clinical presentation in patients, and to determine if salivary IL-6 is reflective of local exocrine involvement or of the underlying autoimmune disorder. METHODS: Thirty-one patients with primary SS, 15 with primary biliary cirrhosis (PBC), and 14 healthy controls were studied. Parotid secretion was stimulated with 2% citric acid and collected using a Carlson-Crittenden collector. Concentrations of salivary and serum IL-6 were determined using a high sensitivity ELISA. Serologic autoimmune disease markers and salivary functional and histopathologic disease markers in the patients with SS were correlated with salivary and serum IL-6 levels. RESULTS: Mean serum IL-6 concentrations were elevated in both patient groups (SS = 3.05 pg/ml, PBC = 3.07 pg/ml, healthy subjects = 0.843 pg/ml). Mean stimulated salivary IL-6 concentrations were elevated only in the patients with SS (16.21 pg/ml) compared to the PBC (1.07 pg/ml) and healthy subjects (0.769 pg/ml). No correlation was found between serum and salivary IL-6 concentrations for any group. Positive correlations were found between salivary IL-6 concentrations and serum IgG concentrations and between salivary IL-6 and erythrocyte sedimentation rate. Higher IL-6 concentrations were associated with increased disease activity. CONCLUSION: Salivary IL-6 concentration is elevated in SS compared to healthy subjects and patients with another systemic autoimmune disease without salivary gland involvement. Elevated salivary IL-6 concentrations in SS are reflective of local exocrine involvement and may serve as a useful monitor of disease activity.

Oral defense mechanisms are impaired early in HIV-1 infected patients.

We have examined the hypothesis that individuals infected with human immune deficiency virus type 1 (HIV-1) experience significant, specific alterations in mechanisms protecting the oral cavity prior to the appearance of AIDS-related systemic opportunistic infections. In a study of 13 early-stage, stable anti-HIV antibody positive patients, parotid salivary function was found to be generally intact. In contrast, several indicators of submandibular gland dysfunction were detected. In particular, stimulated fluid output was decreased and salivary lysozyme levels were increased relative to controls by 50-60% for both resting (p less than 0.05) and stimulated (p less than 0.001) conditions. Also, the frequency of albumin detection in submandibular saliva samples was approximately 65% in HIV-1 infected patients vs. 0% in controls (p less than 0.05). In addition, cytologic evaluation of oral mucosa revealed a fivefold increase in the prevalence of candidal hyphae in HIV-1 infected patients compared to controls (41% vs. 8%, p less than 0.05). We conclude that normal oral defense mechanisms show signs of compromise in HIV-1 infected individuals. We suggest that (a) effects of HIV-1 infection are seen early in the oral cavity, (b) impairment of oral defense mechanisms may facilitate entry of microorganisms with an attendant increased risk of morbidity and mortality, and (c) intensive oral surveillance and prophylactic care should be part of the routine management afforded to AIDS patients soon after HIV-1 infection is recognized.