scholarly journals Polymorphisms of the mannose binding lectin gene in patients with Sjogren's syndrome

2001 ◽  
Vol 60 (5) ◽  
pp. 483-486 ◽  
Author(s):  
Z-Y Wang
Keyword(s):  
Sjögren’S Syndrome ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Mannose Binding Lectin ◽  
Lectin Gene ◽  
Mannose Binding ◽  
Binding Lectin ◽  
Sjögren‘S Syndrome

scholarly journals Clinical significance of C4d deposition in renal tissues from patients with primary Sjögren’s syndrome—A preliminary study

2019 ◽  
Author(s):  
Wenli Xia ◽  
Bixia Gao ◽  
Lin Duan ◽  
Yan Li ◽  
Yubing Wen ◽  
...  
Keyword(s):  
Sjögren’S Syndrome ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Primary Sjögren’S Syndrome ◽  
Primary Sjogren’S Syndrome ◽  
Primary Sjögren's Syndrome ◽  
Mannose Binding ◽  
Binding Lectin ◽  
Sjögren‘S Syndrome

AbstractObjectivesTo evaluate renal expression of C4d, a complement component in the classical/mannose binding lectin (MBL) pathway, in patients with primary Sjögren’s syndrome (pSS)-associated renal impairments.MethodsWe retrospectively reviewed the clinical and pathological data from 39 patients with pSS presenting with renal impairments. C4d was examined in paraffin-embedded biopsy tissues using immunohistochemistry. Glomerular C4d positive was defined when >75% glomeruli were globally stained. Tubulointerstitial C4d (TI-C4d) were scored semi-quantitatively as 0 (absent), 1 (spotty or weak), 2 (patchy) and 3 (diffuse). A TI-C4d score ≥2 was considered TI-C4d positive and included in the TI-C4d+ group and vice versa. Peritubular capillary (PTC) C4d was scored as 0 (absent), 1 (0∼10%, minimal), 2 (10%∼50%, focal), and 3 (>50%, diffuse).ResultsGlomerular C4d deposition was observed in all 8 patients with pSS-related membranous nephropathy (MN) without obvious C1q deposition. Two of 5 patients with mesangial proliferative glomerulonephritis and 1 of 2 patients with IgA nephropathy had mild mesangial C4d deposition. Sixteen patients (6 glomerular dominant and 10 tubulointerstitial dominant) presented TI-C4d score ≥2. Patients in the TI-C4d+ group exhibited a higher serum creatinine level at the time of renal biopsy (TI-C4d+ 132.5 [89.7, 165.5] vs. TI-C4d- 83.0 [70.7, 102.0] μmol/L, P=0.008). PTC C4d was observed in 12 patients, with each of minimal, focal and diffuse staining being noted in 4 patients.ConclusionsThe MBL pathway of complement activation was potentially involved in pSS-related MN. Tubulointerstitial C4d might be a pathological marker of severe renal injury in patients with pSS-related renal impairments.

The association of Raynaud’s phenomenon/syndrome with scleroderma and Sjögren’s syndrome – a meta-analysis

VASA ◽  
2008 ◽  
Vol 37 (Supplement 73) ◽  
pp. 26-32 ◽  
Author(s):  
Schlattmann ◽  
Höhne ◽  
Plümper ◽  
Heidrich
Keyword(s):  
Quantitative Analysis ◽  
Sjögren’S Syndrome ◽  
Mixture Model ◽  
Sjögren's Syndrome ◽  
Meta Analysis ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Raynaud’S Syndrome ◽  
Raynaud's Syndrome ◽  
Sjögren‘S Syndrome

Background: In order to analyze the prevalence of Raynaud’s syndrome in diseases such as scleroderma and Sjögren’s syndrom – a meta-analysis of published data was performed. Methods: The PubMed data base of the National Library of Medicine was used for studies dealing with Raynaud’s syndrome and scleroderma or Raynaud’s syndroem and Sjögren’s syndrom respectively. The studies found provided data sufficient to estimate the prevalence of Raynaud’s syndrome. The statistical analysis was based on methods for a fixed effects meta-analysis and finite mixture model for proportions. Results: For scleroderma a pooled prevalence of 80.9% and 95% CI (0.78, 0.83) was obtained. A mixture model analysis found four latent classes. We identified a class with a very low prevalence of 11%, weighted with 0.15. On the other hand there is a class with a very high prevalence of 96%. Analysing the association with Sjögren’s syndrome, the pooled analysis leads to a prevalence of Raynaud’s syndrome of 32%, 95% CI(26.7%, 37.7%). A mixture model finds a solution with two latent classes. Here, 38% of the studies show a prevalence of 18.8% whereas 62% observe a prevalence of 38.3%. Conclusion: There is strong variability of studies reporting the prevalence of Raynaud’s syndrome in patients suffering from scleroderma or Sjögren’s syndrome. The available data are insufficient to perform a proper quantitative analysis of the association of Raynaud’s phenomenon with scleroderma or Sjögren’s syndrome. Properly planned and reported epidemiological studies are needed in order to perform a thorough quantitative analysis of risk factors for Raynaud’s syndrome.

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