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Vol. 17. Issue 6.
Pages 1078-1080 (November - December 2018)
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Vol. 17. Issue 6.
Pages 1078-1080 (November - December 2018)
DOI: 10.5604/01.3001.0012.7209
Open Access
Thrombosis of the Portal Venous System in Cirrhotic Patients
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Antonio Ponzetto*, Natale Figura**, Vania Cruz-Ramón*, Paulina Chinchilla-López*, Oscar Ramírez-Pérez*, Nancy E. Aguilar-Olivos*, Luis F. Alva-López, Ericka Fajardo-Ordoñez, Guadalupe Ponciano-Rodríguez, Patrick G. Northup§, Nicolas Intagliata§, Stephen H. Caldwell§, Xingshun Qi, Nahum Méndez-Sánchez*
* Professor of Gastroenterology. Department of Medical Sciences, University of Torino Corso AM, Siena, Italy
** Department of Medical, Surgical and Neurological Sciences, University of Siena, Siena, Italy
* Liver Research Unit. Medica Sur Clinic & Foundation, Mexico City, Mexico
Radiology Department. Medica Sur Clinic & Foundation, Mexico City, Mexico
Public Health Department. Faculty of Medicine, National Autonomous University of Mexico, Mexico City, Mexico
§ Division of Gastroenterology and Hepatology. University of Virginia Medical Center, Charlottesville, USA
Department of Gastroenterology. General Hospital of Shenyang, Military Area Command, Shenyang, China
* Liver Research Unit. Medica Sur Clinic & Foundation, Mexico City, Mexico
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Dear editor

Cruz-Ramon, et al. report on portal vein thrombosis (PVT) in patients with liver cirrhosis.1 We feel the necessity to avert and cure such underestimated and undertreated complication: PVT often proceeds to severe portal hypertension and bleeding, and correlates with lower life expectancy. A major problem is the wide disparity of treatments. We believe that a comment is warranted, as other possible mechanisms leading to PVT are often overlooked. These mechanisms include neutrophilic infiltration, a cause of neutrophilic extracellular traps or NETosis,2 and anti-phospholipid syndrome (APS). Both conditions can be elicited by Helicobacter pylori (H. pylori) infection.3 APS is characterized by anti-cardiolipin antibodies which are also increased in cirrhotics. H. pylori infection is a frequent finding in cirrhosis patients,4 and a well-established cause of autoimmunity, including that one against endothelial cells, as bacterial proteins cross reacts with human endothelial antigens via antigenic mimicry.5 Moreover, the bacterium secretes a neutrophilic-activating protein (NAP); neutrophilic infiltration of vascular walls may lead to venous thrombosis, that has been recognized involved in atherosclerosis as well, as reviewed by Mozzini.2 Cirrhotic patients very frequently are also infected by pathogenic strains of H. Pylori,6 which are also known to correlate with acute ischemic stroke and autoimmune thrombotic thrombocytemia. Hence, PVT might benefit by the simple cure of H.pylori, which in turn will lower serum levels of anti-phospholipid antibodies,7 rescind endothelial activation,8 and decrease circulating levels of pro-inflammatory cytokines.

Ap Conceived the Writing

All authors contributed to the final manuscript and approved it.

Copyright Assignment

In consideration of the Fundación Clínica Médica Sur (FCMS) taking action to review and edit my submission, the undersigned authors, jointly and severally, hereby transfer, convey, and assign all right, title, and interest therein, including any and all copyrights in all forms and media now or hereafter known, to the FCMS. The authors retain the nonexclusive right to use all or part of the Article in future works of their own in a noncompeting way, provided proper copyright credit is given to the Foundation.

Should the FCMS not publish the aforesaid submission, the FCMS agrees to release its rights therein

Authorship Responsibility

I, the undersigned author, certify that I have participated sufficiently in the intellectual content, the analysis of data, if applicable, and the writing of the Article, to take public responsibility for it. I have reviewed the final version of the Article, believe it represents valid work, and approve it for publication. As an author of this Article, I certify that none of the material in the manuscript has been published previously, is included in another manuscript, or is currently under consideration for publication elsewhere. I also certify that the Article has not been accepted for publication elsewhere, nor have I assigned any right or interest in the Article to any third party.

Financial Disclosure

I, the undersigned author, certify that I have no commercial associations (e.g., consultancies,stock ownership, equity interests, patent-licensing arrangements) that might pose a conflict of interest in connection with the submitted Article, Antonio Ponzetto, Natale Figura.

Conflict of Interest

The authors declare that they have no conflict of interest as regards this work. No grant or funding was received for this work.

Reply

We would like to thank you for your interest in our paper and for taking the time to express your concerns. In your letter to the editor, you note other potential causes of portal vein thrombosis (PVT) as well as the challenge of choosing the appropriate treatment option. We know that treatments and outcomes of acute PVT depend on several factors such as the involvement of the remaining splanchnic circulation, malignancy, liver cirrhosis, inflammatory disorders, and infections.1

In this regard, you have postulated the importance of antiphospholipid syndrome in the pathogenesis of PVT in liver cirrhosis. However, a previous meta-analysis did not fully support the association between antiphospholipid antibodies and PVT.2 In details, the results suggested a significant association of unclassified anticardiolipin antibody with PVT in liver cirrhosis, but not that of IgG anticardiolipin antibody, IgM anticardiolipin antibody, lupus anticoagulant, or anti-b2-glycoprotein-I antibody.

Nowadays, the recommendations for treatment of non-cirrhotic, non-malignant and cirrhotic acute PVT are different.3,4 Fortunately, at present we have some recommendations for the screening, diagnosis and treatment of patients with PVT by the proceedings of the 7th International Coagulation in Liver Disease Conference.5

Conflicts of Interest

The authors declare that there is no conflict of interest regarding the publication of this article.

References
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Thrombosis of the Portal Venous System in Cirrhotic vs. Non-Cirrhotic Patients..
Annals Hepatology, 17 (2018), pp. 476-481
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Mozzini C., Garbin U., Fratta Pasini A., Cominacini L..
An exploratory look at NETosis in atherosclerosis..
Internal Emergency Medicine, 12 (2017), pp. 13-22
[3.]
Figura N., Moretti E., Collodel G., Langone F., Fiorilli G., Campagna M., Giordano N., et al.
Helicobacter pylori infection and antiphospholipid syndrome: a case report and meta-analysis of the world literature..
Gastro open access, 3 (2015), pp. 120-124
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High prevalence of Helicobacter pylori in liver cirrhosis: relationship with clinical and endoscopic features and the risk of peptic ulcer..
Digestive Diseases Science, 42 (1997), pp. 2024-2030
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Circulation, 106 (2002), pp. 430-434
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Helicobacter pylori seroprevalence in patients with cirrhosis of the liver and hepatocellular carcinoma..
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Cicconi V., Carloni E., Franceschi F., Nocente R., Silveri N.G., Manna R., Servidei S., et al.
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Sharma A.M., Zhu D., Henry Z..
Portal vein thrombosis: When to treat and how.
Vascular Medicine, 21 (2016), pp. 61-69
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Qi X., De Stefano V., Su C., Bai M., Guo X., Fan D..
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Concepts and Controversies in Haemostasis and Thrombosis Associated with Liver Disease: Proceedings of the 7th International Coagulation in Liver Disease Conference.
Thromb Haemost, 118 (2018), pp. 1491-1506
Copyright © 2018. Fundación Clínica Médica Sur, A.C.
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