Serum markers of infections in patients with primary biliary cirrhosis: evidence of infection burden

Shapira, Yinon; Agmon‐Levin, Nancy; Renaudineau, Yves; Porat-Katz, Bat Sheva; Barzilai, Ori; Ram, Maya; Youinou, Pierre; Shoenfeld, Yehuda

doi:10.1016/j.yexmp.2012.09.012

Cited by 54 publications

(34 citation statements)

References 45 publications

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“…pylori prevalence has been studied in patients with SLE, but the results vary amongst reports. A recent study has failed to find significantly higher prevalence of anti-H. pylori antibodies in SLE patients compared to controls [41] . Of note, this study showed an increased prevalence of anti-H. pylori antibodies in patients with anti-phospholipid syndrome, giant cell arteritis, SSc and PBC [41] .…”

Section: Systemic Lupus Erythematosusmentioning

confidence: 93%

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Helicobacter pyloriand autoimmune disease: Cause or bystander

Smyk¹,

Κουτσουμπασ²,

Mytilinaiou³

et al. 2014

WJG

148

108

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Helicobacter pylori (H. pylori) is the main cause of chronic gastritis and a major risk factor for gastric cancer. This pathogen has also been considered a potential trigger of gastric autoimmunity, and in particular of autoimmune gastritis. However, a considerable number of reports have attempted to link H. pylori infection with the development of extra-gastrointestinal autoimmune disorders, affecting organs not immediately relevant to the stomach. This review discusses the current evidence in support or against the role of H. pylori as a potential trigger of autoimmune rheumatic and skin diseases, as well as organ specific autoimmune diseases. We discuss epidemiological, serological, immunological and experimental evidence associating this pathogen with autoimmune diseases. Although over one hundred autoimmune diseases have been investigated in relation to H. pylori, we discuss a select number of papers with a larger literature base, and include Sjögrens syndrome, rheumatoid arthritis, systemic lupus erythematosus, vasculitides, autoimmune skin conditions, idiopathic thrombocytopenic purpura, autoimmune thyroid disease, multiple sclerosis, neuromyelitis optica and autoimmune liver diseases. Specific mention is given to those studies reporting an association of anti-H. pylori antibodies with the presence of autoimmune disease-specific clinical parameters, as well as those failing to find such associations. We also provide helpful hints for future research.

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Section: Systemic Lupus Erythematosusmentioning

confidence: 93%

“…For example, Shapira et al [41] reported anti-H. pylori antibodies in 54% of patients with PBC compared to 31% (P < 0.01) of patients with other conditions, while Tanaka et al [140] have failed to find any differences between patients and demographically-matched controls (51% vs 46%, respectively).…”

Section: Primary Biliary Cirrhosismentioning

confidence: 99%

Helicobacter pyloriand autoimmune disease: Cause or bystander

Smyk¹,

Κουτσουμπασ²,

Mytilinaiou³

et al. 2014

WJG

148

108

View full text Add to dashboard Cite

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“…Another study has shown that giant cell arteritis, SSc and PBC increased the prevalence of anti-H. Pylori antibodies [8]. In an early study, a negative relationship was determined between H. Pylori seropositivity and the development of SLE in Afro-American females [9].…”

Section: H Pylorı and Slementioning

confidence: 99%

The Relationship of Systemic Lupus Erythematosus and Helicobacter Pylori

Yıldırım¹,

Yıldırım²

2015

Med-Science

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Systemic lupus erythematosus (SLE) is an inflammatory disease of unknown etiology. In the pathogenesis of SLE, several infectious agents have been held responsible such as cytomegalovirus, parvovirus B19 and Epstein Barr virus (EBV). There is a variable relationship between SLE and helicobacter, which is different from that of lupus and other infections. We would like to emphasize the interrelation between these entities.

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“…Moreover, the prevalence of anti- Toxoplasma IgG is significantly higher among the primary biliary cirrhosis patients (71%) compared with controls without cirrhosis (40%, p < 0.0001), whereas the infection burden is rare in healthy subjects (20% vs. 3%, respectively, p < 0.0001). It is predicted that Toxoplasma to increase the risk of primary biliary cirrhosis in patients (Shapira et al, 2012). Since, latent infection is fairly common, and once infected organisms reside for the lifelong; the Toxoplasma interventions with safe and effective regimens will have a great impact on health related concerns in vulnerable individuals.…”

Section: Discussionmentioning

confidence: 99%

Toxoplasmosis complications and novel therapeutic synergism combination of diclazuril plus atovaquone

2014

Front. Microbiol.

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Toxoplasmosis is a major cause of foodborne disease, congenital complication, and morbidity. There is an urgent need for safe and effective therapies to encounter congenital and persisting toxoplasmosis. The hypothesis was: combination diclazuril plus atovaquone to exert a novel therapeutic synergy to prevent toxoplasmosis syndromes.Methods: Pregnant dams were treated with diclazuril and atovaquone monotherapy or combination therapy and infected i.p with Toxoplasma tachyzoites.Results: Infected dams developed severe toxoplasmosis associated syndrome with increases in the abdominal adiposity surrounding uteri, gansterointestinal and other internal organs and excessive weight gain. Numerous organisms along with infiltration of inflammatory cells were detected scattered into adipose tissues. Combination therapy (p < 0.01) and to a lesser extent diclazuril (p < 0.05) protected dams from inflammatory fat and excess weight gains. This was consistent with pancreatitis development in infected dams (versus normal p < 0.05) with infiltration of inflammatory cells, degeneration and necrosis of pancreatic cells followed by the degeneration and loss of islets. Combination and monotherapy protected dams from these inflammatory and pathological aspects of pancreatitis. Infected dams exhibited severe colitis, and colonic tissues significantly shortened in length. Brush border epithelial cells were replaced with infiltration of lymphocytes, granulocytes, and microabscess formations into cryptic microstructures. Combination therapy synergistically preserved colonic structure and normalized pathological damages (p < 0.001) and to a lesser degree diclazuril monotherapy protected dams from colitis (p < 0.05) and gastrointestinal toxoplasmosis. Other complications included severe splenitis (p < 0.001) and hepatitis (p < 0.001) which were normalized with combination therapy.Conclusion: Combination diclazuril plus atovaquone was safe and with a novel therapeutic synergism protected dams and fetuses from toxoplasmosis.

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Serum markers of infections in patients with primary biliary cirrhosis: evidence of infection burden

Cited by 54 publications

References 45 publications

Helicobacter pyloriand autoimmune disease: Cause or bystander

Helicobacter pyloriand autoimmune disease: Cause or bystander

The Relationship of Systemic Lupus Erythematosus and Helicobacter Pylori

Toxoplasmosis complications and novel therapeutic synergism combination of diclazuril plus atovaquone

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