Multiple OralCandidaInfections in Patients with Sjögren’s Syndrome — Prevalence and Clinical and Drug Susceptibility Profiles

2011 ◽  
Vol 38 (11) ◽  
pp. 2428-2431 ◽  
Author(s):  
ZHIMIN YAN ◽  
ANDREW L. YOUNG ◽  
HONG HUA ◽  
YANYING XU

Objective.To determine the prevalence of oral candidiasis and multiple oralCandidainfections in patients with primary Sjögren’s syndrome (SS), and the clinical and drug susceptibility profile.Methods.Thirty patients with primary SS were enrolled in our study. The diagnosis of oral candidiasis was based on the clinical manifestation, and confirmed by a concentrated rinse culture.Candidaspp. assessment was accomplished using standard methods: Sabouraud dextrose agar with 50 mg/l chloramphenicol and CHROMagar were used for the rapid screening of clinical species, followed by the API 20C system for further species identification.In vitroantifungal drug susceptibility ofCandidaisolates was determined by the minimal inhibitory concentrations.Results.In our study, 87% (26/30) of subjects had oral candidiasis, in which 42% (11/26) had multipleCandidaspp. infection. AlthoughC. albicansremains the predominant isolate, other rare species such asC. tropicalis,C. glabrata,C. parapsilosis, andC. kruseiwere present, alone or in combination. Chronic atrophic candidiasis is the most common clinical type of oral candidiasis in patients with SS. The susceptibilities of the 44Candidaisolates to 7 antifungal agents varied dramatically. The resistance to azoles was remarkable, and the phenomenon of cross-resistance between itraconazole and fluconazole was observed.Conclusion.Patients with primary SS carry a high risk of oral candidiasis and a high frequency of multipleCandidainfections. The azole resistance patterns ofCandidaspp. support the necessity for drug susceptibility testing as a routine procedure for patients with oralCandidainfections.

Author(s):  
Mirjana Sijan Gobeljic ◽  
Vera Milic ◽  
Nada Pejnovic ◽  
Nemanja Damjanov

Abstract Sjogren’s syndrome (SS) is a complex, chronic, systemic, autoimmune disease that mainly affects the exocrine glands, especially the salivary and lacrimal glands, leading to the dryness of the mouth and eyes, along with fatigue, joint and muscle pain. The prevalence of SS is estimated to be between 0.05% and 1% in European population. Diagnosis of SS is based on the revised criteria of the American-European consensus group (AECG). Sjogren’s syndrome can be subclassified into primary disease (primary Sjogren syndrome, pSS) and a secondary disease (secondary Sjogren syndrome, sSS) when present with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and systemic sclerosis. The decrease in salivary flow and qualitative alterations in saliva could explain many of the oral manifestations frequently present in patients with SS. Low salivary flow may affect chewing, swallowing, speech and sleeping in pSS patients. Oral manifestations include dental erosion, dental caries, mucosal infection, ulcers and oral candidiasis. Recent studies reveal that pSS patients experience impaired olfactory and gustatory functions and have higher occurrence of oral complications such as dysgeusia, burning sensation in the tongue (BST) and halitosis. The exocrine manifestations and systemic involvement in SS significantly impact the patient’s perception of oral healthrelated quality of life (OHRQoL).


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Tsutomu Tanaka ◽  
Blake M. Warner ◽  
Toshio Odani ◽  
Youngmi Ji ◽  
Ying-Qian Mo ◽  
...  

Abstract Primary Sjögren’s syndrome (pSS) is a complex autoimmune disease characterized by dysfunction of secretory epithelia with only palliative therapy. Patients present with a constellation of symptoms, and the diversity of symptomatic presentation has made it difficult to understand the underlying disease mechanisms. In this study, aggregation of unbiased transcriptome profiling data sets of minor salivary gland biopsies from controls and Sjögren’s syndrome patients identified increased expression of lysosome-associated membrane protein 3 (LAMP3/CD208/DC-LAMP) in a subset of Sjögren’s syndrome cases. Stratification of patients based on their clinical characteristics suggested an association between increased LAMP3 expression and the presence of serum autoantibodies including anti-Ro/SSA, anti-La/SSB, anti-nuclear antibodies. In vitro studies demonstrated that LAMP3 expression induces epithelial cell dysfunction leading to apoptosis. Interestingly, LAMP3 expression resulted in the accumulation and release of intracellular TRIM21 (one component of SSA), La (SSB), and α-fodrin protein, common autoantigens in Sjögren’s syndrome, via extracellular vesicles in an apoptosis-independent mechanism. This study defines a clear role for LAMP3 in the initiation of apoptosis and an independent pathway for the extracellular release of known autoantigens leading to the formation of autoantibodies associated with this disease. ClinicalTrials.gov Identifier: NCT00001196, NCT00001390, NCT02327884.


2015 ◽  
Vol 75 (3) ◽  
pp. 617-622 ◽  
Author(s):  
Barbara M Szczerba ◽  
Paulina Kaplonek ◽  
Nina Wolska ◽  
Anna Podsiadlowska ◽  
Paulina D Rybakowska ◽  
...  

ObjectivesAutoantibodies reactive with Ro52 are often found in sera of patients with Sjögren's syndrome (SS). This study was undertaken to investigate the role of Ro52-induced immune responses in pathogenesis of SS.MethodsNew Zealand Mixed (NZM) 2758 mice were immunised with Ro52 in alum adjuvant. Control mice were immunised either with maltose-binding protein or injected with alum alone. Mice were monitored for anti-Ro52 antibody, sialoadenitis and pilocarpine-induced salivation. Antibody binding to salivary gland (SG) cells was analysed in vivo and in vitro by immunofluorescence. Sera from immunised mice were passively transferred into untreated or alum injected NZM2758 mice.ResultsBy day 30 post-immunisation, Ro52 immunised mice generated immunoprecipitating anti-Ro52 antibodies and they had the maximum drop in saliva production. Both Ro52 immunised and control mice showed evidence of mild sialoadenitis. However, only Ro52 immunised mice had antibody deposition in their SG. Passive transfer of Ro52-immune sera induced SG dysfunction in recipient mice, only if the recipients were primed with alum. In vitro, antibodies from Ro52-immune sera were internalised by a SG cell line and this uptake was inhibited by cytochalasin D treatment.ConclusionsOur data show for the first time that antibodies induced by Ro52 are capable of inducing SG dysfunction, and that this phenomenon is dependent on the activation of innate immunity. The mouse model described in this study implies that autoantibody deposition in the SG might be an important step in the induction of xerostomia and pathogenesis of SS.


2019 ◽  
Vol 2019 ◽  
pp. 1-7
Author(s):  
Raouaa Belkacem Chebil ◽  
Yassine Oueslati ◽  
Marwa Marzouk ◽  
Fatma Ben Fredj ◽  
Lamia Oualha ◽  
...  

Objective. The aim of this study was to investigate the prevalence and characteristics of oral lichen planus (OLP) and oral lichenoid lesions (OLL) in Sjogren’s syndrome (SS) patients. Patients and Methods. A prospective clinical study was conducted at the Department of Oral Medicine and Oral Surgery in Sahloul Hospital, Sousse, from January 2012 to June 2018. The patients involved in this study were diagnosed with Sjogren’s syndrome according to the AECG (American-European consensus group) diagnostic criteria. Among these patients, we searched for those affected by OLP or OLL as determined by the WHO (World Health Organisation) classification of 2003. Clinical variables such as age, sex, medical conditions and medications, type of SS (primary or secondary), clinical form of OLP, and treatment were analyzed. The assessment of the results was performed using SPSS software. Results. We evaluated 30 patients (27 females and 3 males) diagnosed with SS (24 had primary SS) with a mean age of 55 years and 11 months (±11,714). Overall, 9 patients had oral lesions (30%). Two patients had OLP associated with secondary SS (25%). Primary Sjogren’s syndrome patients had 6 OLP lesions and one erythematous lichenoid lesion. OLP was erosive in eight patients, among them two had vulvo-vaginal-gingival syndrome. OLP lesions showed improvement in symptoms after topical or general corticosteroids treatment, while OLL showed improvement only under antibiotic treatment. Conclusion. The results of our analysis suggest that patients with SS have 30% prevalence of OLP and OLL. This possible association shows the importance of screening for oral dryness in patients with OLP or OLL. Treatment includes topical or general corticosteroids for erosive forms associated or not with topical antifungal treatment to treat or prevent oral candidiasis.


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