Sicca Syndrome (sicca + syndrome)

Distribution by Scientific Domains


Selected Abstracts


Primary biliary cirrhosis in Singapore: Evaluation of demography, prognostic factors and natural course in a multi-ethnic population

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 4 2008
Reuben-Km Wong
Abstract Background and Aim:, Primary biliary cirrhosis (PBC) is infrequent in Asians. Among Asian patients with PBC, information on natural course is scarce. The aim of this study was to study the clinical course and prognosticators among Asians with PBC. Methods:, During 1990,2005, patients diagnosed with PBC at the National University Hospital, Singapore, constituted the retrospective cohort. Their demographic characteristics were evaluated. To evaluate the prognostic factors and natural course, two outcome measures were assessed: hepatic decompensation and death or liver transplant. Multivariate analysis was undertaken to identify factors associated with hepatic decompensation and terminal event (death or liver transplantation). Results:, Thirty-four PBC patients aged 56.8 ± 1.8 years (mean ± SEM) of whom 32 (94%) were women were included. Thirty-two (94%) of them were of Chinese origin. At presentation, 18 (53%) were symptomatic in the form of jaundice (n = 9, 26.5%), pruritus (n = 6, 17.6%) and fatigue (n = 5, 14.7%). During 4.80 ± 0.7 (range 0.02,15.03) years follow up, 6/16 (37.5%) asymptomatic patients developed symptoms. After 5 years, 17.6% (n = 6) and 8.8% (n = 3) had hepatic decompensation and terminal event, respectively. Sicca syndrome was present in 26% (n = 9) of patients. Multivariate analysis revealed that serum bilirubin level at presentation was the sole determinant of decompensation. Rate of change of laboratory indices did not predict either event. Conclusion:, In Singapore, Chinese women constitute most of the PBC patients. Elevated serum bilirubin level at presentation was the sole predictive marker associated with dismal outcome. [source]


Course and outcome of hepatitis C

HEPATOLOGY, Issue 5B 2002
31 Center Dr., Jay H. Hoofnagle Bldg. 3, Room 9A2
The hepatitis C virus (HCV) is a small enveloped RNA virus belonging to the family flaviviridae and genus hepacivirus. The HCV RNA genome is 9,600 nucleotides in length and encodes a single polyprotein that is post-translationally cleaved into 10 polypeptides including t3 structural (C, E1, and E2) and multiple nonstructural proteins ([NS] NS2 to NS5). The NS proteins include enzymes necessary for protein processing (proteases) and viral replication (RNA polymerase). The virus replicates at a high rate in the liver and has marked sequence heterogeneity. There are 6 genotypes and more than 90 subtypes of HCV, the most common in the United States being 1a and 1b (approximately 75%), 2a and 2b (approximately 15%), and 3 (approximately 7%). Acute hepatitis C is marked by appearance of HCV RNA in serum within 1 to 2 weeks of exposure followed by serum alanine aminotransferase (ALT) elevations, and then symptoms and jaundice. Antibody to HCV (anti-HCV) tends to arise late. In acute resolving hepatitis, HCV RNA is cleared and serum ALT levels fall to normal. However, 55% to 85% of patients do not clear virus, but develop chronic hepatitis C. Chronic hepatitis C is often asymptomatic, but is usually associated with persistent or fluctuating elevations in ALT levels. The chronic sequelae of hepatitis C include progressive hepatic fibrosis, cirrhosis, and hepatocellular carcinoma. Extra-hepatic manifestations include sicca syndrome, cryoglobulinemia, glomerulonephritis, and porphyria cutanea tarda. Knowledge of the course and outcome of hepatitis C is important in developing approaches to management and therapy. [source]


Increased expression of interleukin-7 in labial salivary glands of patients with primary Sjögren's syndrome correlates with increased inflammation

ARTHRITIS & RHEUMATISM, Issue 4 2010
A. Bikker
Objective To study the expression levels and immunostimulatory capacities of interleukin-7 (IL-7) in primary Sjögren's syndrome. Methods Labial salivary gland (LSG) IL-7 expression was determined by immunohistochemistry, using a quantitative scoring system, in 30 patients with sicca syndrome: 15 patients with primary Sjögren's syndrome (SS) and 15 patients with non-SS sicca syndrome. The correlation of IL-7 expression in LSGs with parameters of local and peripheral disease was studied, and serum and salivary IL-7 levels were determined. Additionally, the effects of IL-7 on cytokine production by peripheral blood mononuclear cells (PBMCs) from patients with primary SS were determined in vitro by Luminex multicytokine assay and compared with the effects in control subjects. Results The expression of IL-7 in LSGs was higher in patients with primary SS compared with that in patients with non-SS sicca syndrome. IL-7 was observed primarily in the vicinity of lymphocytic infiltrates. Salivary IL-7 levels in patients with primary SS were higher than those in control subjects. In all 30 patients with sicca syndrome, IL-7 expression in LSGs correlated with parameters of both local and peripheral disease. Furthermore, IL-7 stimulated T cell,attracting and T cell,differentiating cytokines (monokine induced by interferon-, [IFN,], IFN,-inducible 10-kd protein, IL-12, and IL-15), as well as Th1 (IFN,), Th2 (IL-4), Th17 (IL-17A), proinflammatory (tumor necrosis factor , and IL-1,), and regulatory (IL-10 and IL-13) cytokine production by PBMCs. All of these cytokines were previously shown to be associated with primary SS. The IL-7,induced increase in IL-10 production in patients with primary SS was reduced compared with that in control subjects. Conclusion The correlation between LSG IL-7 expression and (local) disease parameters in primary SS as well as the IL-7,mediated induction of inflammatory cytokines indicate that IL-7 might contribute to the immunopathology of primary SS. [source]


Rheumatoid arthritis does not share most of the newly identified systemic lupus erythematosus genetic factors

ARTHRITIS & RHEUMATISM, Issue 9 2009
Marian Suarez-Gestal
Objective Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) share some genetic factors such as HLA, PTPN22, STAT4, and 6q23. The aim of this study was to determine whether 9 other SLE genetic factors are also implicated in RA susceptibility. Methods A characteristic single-nucleotide polymorphism (SNP) in each of 9 genetic factors, ITGAM (rs1143679), C8orf13,BLK (rs13277113), TYK2 (rs2304256), 1q25.1 (rs10798269), PXK (rs6445975), KIAA1542 (rs4963128), MECP2 (rs17435), BANK1 (rs17266594), and LY9 (rs509749), was studied in 1,635 patients with RA and 1,906 control subjects from Spain. The rs7574865 SNP in STAT4 was also included. Analyses were conducted globally and after stratification by sex and clinical features (anti,cyclic citrullinated peptide and rheumatoid factor, shared epitope, rheumatoid nodules, radiographic changes, sicca syndrome, and pneumonitis). Results No association was observed between RA and any of the 9 newly identified SLE genetic factors. A meta-analysis using previous data was consistent with these results. In addition, there were no significant differences between individuals with and those without each of the clinical features analyzed, except the frequency of the minor allele in the C8orf13,BLK locus that was decreased in patients with sicca syndrome (14.6% versus 22.4% in controls; P = 0.003). Conclusion None of the 9 recently identified SLE risk factors showed association with RA. Therefore, common genetic factors affecting the pathogenesis of these 2 disorders seem to be limited, revealing that the genetic component contributes to the different expression of these diseases. [source]


Marked swollen erythema of the face together with sicca syndrome as a sign for chronic active Epstein,Barr virus infection

BRITISH JOURNAL OF DERMATOLOGY, Issue 6 2000
K.C. Sato-Matsumura
No abstract is available for this article. [source]