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American Journal of Public Health Research
DOI: 10.12691/ajphr-1-1-3

The Implementation of a Tele-Homecare System with Service Oriented Architecture and HL7 Message Transmission Standard
Ching-Sung Wang

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The Influence of Ethanol on Pyruvate Kinases Activity in Vivo, in Vitro, in Silico
Lelevich Sergey Vladimirovich, Khrustalev Vladislav Victorovich, Barkovsky Eugene Victorovich, Shedogubova Tatyana Aleksandrovna

American Journal of Medical Sciences and Medicine
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Clinical and Histological Features in Wegener Granulomatosis
Li Cavoli Gioacchino, Passantino Rita, Bono Luisa, Tortorici Calogera, Ferrantelli Angelo, Giammarresi Carlo, Rotolo Ugo

American Journal of Infectious Diseases and Microbiology
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The Curse of Lymphatic Filariasis: Would the Continual Use of Diethylcarbamazine Eliminate this Scourge in Papua New Guinea?
Anne Lanham, Lillian Mwanri

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Hypercoagulability State in Celiac Disease and Hepatitis C Association

Cornel Aldea, Daniel Sur, Ciprian Silaghi*

Emergency Clinical Hospital for Children, Cluj-Napoca, Romania

Abstract: A concerning pathological and serological aspect that is found in both HCV and celiac disease is the hypercoagulability state which can lead to various complications.

Keywords: celiac disease, hepatitis C, hypercoagulability state

Received September 17, 2018; Revised October 28, 2018; Accepted January 04, 2019

Citation: Cornel Aldea, Daniel Sur, Ciprian Silaghi, Hypercoagulability State in Celiac Disease and Hepatitis C Association. International Journal of Celiac Disease, 6 (3). 74-75. January 2018. doi:10.12691/ijcd-6-3-3

1. Introduction

Is there any connection between celiac disease and hepatitis C? [1]. Celiac disease (CD) is characterized by heterogeneous clinical manifestations of variable severity that can occurat any age [2]. It is worth paying attention to one warning sign that occurs in advanced cases of CD and liver complications in HCV patients, namely the hypercoagulant state.

2. Hipercoagulabity State in CD Patients

In CD patients, the pathogenesis of hypercoagulant state is the result of various interplay between genetic factors (methylenetetrahydrofolate reductase mutations), autoimmunity (thrombophilic autoantibodies), haematological factors (abnormality of platelets and endothelial dysfunction) and vitamin deficiencies (folate, vitamin B12 or vitamin K) [3]. It is well known that vitamin K is necessary for the carboxylation of coagulation factors (II, VII, IX, X), anticoagulation factors (protein C and S), but also for the carboxylation of extrahepatic vitamin K dependent proteins, such as osteocalcin in bone [4], growth arrest specific protein 6 (Gas6) [5] and matrix Gla protein (Mgp) in arterial wall [6,7]. In a case report was noticed that low vitamin K supplies, due to malabsorption or poorly dietary intake of vitamin K, were assigned to a defectively controlled CD [8]. Furthermore, Berthoux et al have identified risk factors for thrombosis, such as deficiency of protein C and S due to vitamin K insufficiency, which could be associated to CD [9].

3. Hipercoagulabity State in HCV Patients

On the contrary,in HCV patients with liver fibrosis, there is an apparent paradox: a manifest decline in procoagulant factorsactivity leading to prolonged common coagulation tests [10,11] coexist with theevidence of hypercoagulabilitycaused by an impaired synthesis of anticoagulant factors, such as protein C and antithrombin III [12,13]. Moreover, it has been assessed that in patients with progressive HCV liver disease the promotion of thrombin formation will lead to the activation of hepatic stellate cells therefore via PAR-1 cleavage, promoting liver fibrosis [14,15]. Other findings strengthen the link between liver fibrosis in HCV patients, activated protein C resistance and acquired protein C deficiency [16,17], these patients being prone to thrombotic events.A study on 3686 patients with newly diagnosed HCV compared the incidence ofvenous thromboembolism in the HCV group and a 14,744 healthy control group, the risk of venous thromboembolism was significantly higher in the HCV group than in the control group [18]. Following the idea of assessing the carboxylating status, the most sensitive marker for vitamin K deficiency is the prothrombin induced by vitamin K absence-II (PIVKA-II), which is a functional marker of coagulation [19]. Kamel et al have found elevated PIVKA-II serum levels in patients with hepatocellular carcinoma, the most significant complication of viral hepatitis, concluding that PIVKA-II could be a sensitive and specific marker for its early detection [20].

4. Conclusion

Accordingly, to ascertain whether hypercoagulant state is actually (and to what extent) established in CD or HCV patients with liver complications, laboratory analyses should go beyond the common coagulation tests. In this regard, vitamin K deficiency has to be assessed by using non-invasive serum markers, e.g. PIVKA-II for liver, different carboxylated / uncarboxylated conformations of osteocalcin for bones and Mgp for vasculature.

References

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[2]   | Sur ML, Colceriu M, Aldea C, Sur G, Floca E. Celiac Disease a Road Paved with Many Obstacles. Differential Diagnosis in Children. International Journal of Celiac Disease 2018; 6(1): 7-10.
[3]   | Lerner A, Blank M. Hypercoagulability in celiac disease - an update. Autoimmun Rev. 2014; 13(11): 1138-41.
[4]   | Lacombe J, Ferron M. Gamma-carboxylation regulates osteocalcin function. Oncotarget. 2015; 6(24): 19924-5.
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[14]   | Gonzalez-Reimers E, Quintero-Platt G, Martin-Gonzalez C, Perez-Hernandez O, Romero-Acevedo L, Santolaria-Fernandez F. Thrombin activation and liver inflammation in advanced hepatitis C virus infection. World J Gastroenterol. 2016; 22(18): 4427-37.
[15]   | Poujol-Robert A, Boëlle PY, Poupon R, Robert A. Factor V Leiden as a risk factor for cirrhosis in chronic hepatitis C. Hepatology. 2004; 39(4): 1174-5.
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[17]   | Wang C-C, Chang C-T, Lin C-L, Lin I-C, Kao C-H. Hepatitis C Virus Infection Associated With an Increased Risk of Deep Vein Thrombosis: A Population-Based Cohort Study. Medicine (Baltimore). 2015; 94(38): e1585.
[18]   | Liebman HA, Furie BC, Tong MJ, Blanchard RA, Lo KJ, Lee SD, et al. Des-gamma-carboxy (abnormal) prothrombin as a serum marker of primary hepatocellular carcinoma. N Engl J Med. 1984; 310(22): 1427-31.
[19]   | Kamel MM, Saad MF, Mahmoud AA, Edries AA, Abdel-Moneim AS. Evaluation of serum PIVKA-II and MIF as diagnostic markers for HCV/HBV induced hepatocellular carcinoma. Microb Pathog. 2014; 77: 31-5.
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