CNUH-2015-049). both T and B cell activation, their presence within the glandular infiltrates of SS patients is thought to play a significant role disease progression (20). In several previous studies (12,13,21,22,23,24), SS patients exhibiting GC-like structures in the minor salivary glands have showed a higher prevalence of anti-SS-A/Ro or anti-SS-B/La antibodies (Ab) or rheumatoid factor (RF), higher lymphocyte focus score in minor salivary gland biopsy, enhanced levels of local and systemic proinflammatory mediators, and higher risk of lymphoma development compared with GC-negative SS patients. While the presence of ectopic GC-like structures in chronic inflammatory diseases is not a new finding, the role of GCs in SS is still being defined. Here, we analyzed the prevalence of GCs in minor salivary glands of patients with SS, and compared their laboratory and clinical profiles with that of GC-negative patients. MATERIALS AND METHODS Population and study design We performed a retrospective analysis of medical records from 93 SS patients seen in our outpatient clinic from January 2006 to March 2012. We included patients who underwent minor salivary gland biopsies in the process of diagnosing SS and finally confirmed the diagnosis using the revised criteria proposed by the American-European Rabbit Polyclonal to HTR5A Consensus Group (AECG). As part of routine evaluation for SS, all patients underwent ophthalmologic test, 99-mTc salivary glands scintigraphy, and laboratory tests. Schirmers tests were performed by an ophthalmologist, with a positive diagnosis defined as 5 mm in 5 minutes. Next, a tear film break-up time (BUT) test was performed, with a positive result defined as 10 seconds. Salivary glands scintigraphy with 99-mTc was considered positive when the tracer showed delayed uptake, reduced concentration, or delayed excretion. Clinical and laboratory manifestations Sociodemographic, clinical, and laboratory data were collected at the time of minor salivary gland biopsy and again during follow-up period. Patients were examined by an experienced rheumatologist to assess common disease symptoms, including sicca symptoms and Alvimopan dihydrate symptom onset age, enlargement of parotid glands, and experience of Alvimopan dihydrate extraglandular manifestations such as photosensitivity, purpura, Raynauds phenomenon, sclerodactyly, arthritis, psychosis and lymphadenopathy. Interstitial lung disease or pulmonary fibrosis was documented based on chest radiograph or high-resolution computed tomography (HRCT). Renal involvement was defined as proteinuria ( 500 mg/day), active urine sediment, impaired glomerular filtration rate (GFR) ( 60 mL/minute) or renal tubular acidosis. Serositis was defined by radiologic pleural effusion or pericardial effusion. Gastroesophageal reflux was diagnosed by gastroscopy in patients with symptoms of heartburn or regurgitation. Carpal tunnel syndrome was diagnosed based upon complaints of abnormal sensation and confirmed using a nerve conduction study. Autoimmune thyroiditis was defined as hypothyroidism in combination with increased autoantibody levels such as anti-thyroid peroxidase or anti-thyroglobulin antibodies. Lymphoma was confirmed by lymph node biopsy. To measure disease activity and degree of damage, we used the EULAR SS disease activity index (ESSDAI) and SS disease damage index (SSDDI), respectively. ESSDAI and SSDDI were completed retrospectively by reviewing the medical records carefully. Routine laboratory profiles were performed at the time of the labial salivary gland biopsy to measure Alvimopan dihydrate white blood cell (WBC) count, lymphocyte, hemoglobin, platelets, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), immunoglobulin G (IgG), IgA, IgM, and complement level (C3, C4, CH50). CRP was measured with a turbidimetric immunoassay (Wako, Osaka, Japan), IgG, IgA, IgM, C3, and C4 were measured using nephelometric assays (Siemens, Marburg, Germany) and CH50 was measured with an liposome immunoassay (Wako, Osaka, Japan). The presence of autoantibodies against SS-A/Ro, SS-B/La (ORGENTEC Diagnostika, Mainz, Germany), and dsDNA (Trinity Biotec, Wicklow, Ireland) was determined by ELISA; rheumatoid factor was assessed by nephelometry (Beckman Coulter, Galway, Ireland). Tissue samples and immunohistochemistry A labial salivary gland biopsy was performed for all SS patients. The focus score (FS) was determined using the classification method of Chisholm and Mason, defined as the number of.