Severe immune thrombocytopenia after peg-interferon-alpha2a, ribavirin and telaprevir treatment completion: A case report and systematic review of literature

Arena, Rosario; Cecinato, Paolo; Lisotti, Andrea; Buonfiglioli, Federica; Calvanese, Claudio; Grande, Giuseppe; Montagnani, Marco; Azzaroli, Francesco; Mazzella, Giuseppe

doi:10.4254/wjh.v7.i12.1718

Cited by 3 publications

(3 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, interferon therapy induces several autoantibodies to multiple organ systems, such as anti-thyroid antibodies, auto-antibodies indicative of autoimmune hepatitis, and anti-platelet autoantibodies[ 10 ], and exhibits side effects of developing autoimmune diseases. Autoimmune thrombocytopenia sometimes occurs both during and after interferon therapy[ 11 ]. Thus, interferon therapy might have induced autoantibodies to c-Mpl in the current patient.…”

Section: Discussionmentioning

confidence: 99%

Acquired amegakaryocytic thrombocytopenia previously diagnosed as idiopathic thrombocytopenic purpura in a patient with hepatitis C virus infection

Ichimata¹,

Kobayashi²,

Honda³

et al. 2017

WJG

View full text Add to dashboard Cite

We report the first case of a patient with hepatitis C virus (HCV) infection and idiopathic thrombocytopenic purpura (ITP), who later developed acquired amegakaryocytic thrombocytopenia (AAMT), with autoantibodies to the thrombopoietin (TPO) receptor (c-Mpl). A 64-year-old woman, with chronic hepatitis C, developed severe thrombocytopenia and was diagnosed with ITP. She died of liver failure. Autopsy revealed cirrhosis and liver carcinoma. In the bone marrow, a marked reduction in the number of megakaryocytes was observed, while other cell lineages were preserved. Therefore, she was diagnosed with AAMT. Additionally, autoantibodies to c-Mpl were detected in her serum. Autoantibodies to c-Mpl are one of the causes of AAMT, acting through inhibition of TPO function, megakaryocytic maturation, and platelet formation. HCV infection induces several autoantibodies. HCV infection might also induce autoantibodies to c-Mpl, resulting in the development of AAMT. This mechanism may be one of the causes of thrombocytopenia in patients with HCV infection.

show abstract

Section: Discussionmentioning

confidence: 99%

Acquired amegakaryocytic thrombocytopenia previously diagnosed as idiopathic thrombocytopenic purpura in a patient with hepatitis C virus infection

Ichimata¹,

Kobayashi²,

Honda³

et al. 2017

WJG

View full text Add to dashboard Cite

show abstract

“…IFN-induced autoimmune ITP has been reported to develop after 4 weeks to 12 months of therapy, 79 and even after the completion of therapy. 80 In contrast to the dose-dependent thrombocytopenia caused by IFN-induced bone marrow suppression, IFN-induced autoimmune ITP can cause precipitous decreases in platelet levels; it usually responds to immunosuppression. 79 …”

Section: Increased Platelet Destructionmentioning

confidence: 99%

The pathophysiology of thrombocytopenia in chronic liver disease

Mitchell¹,

Feldman²,

Diakow³

et al. 2016

HMER

106

View full text Add to dashboard Cite

Thrombocytopenia is the most common hematological abnormality encountered in patients with chronic liver disease (CLD). In addition to being an indicator of advanced disease and poor prognosis, it frequently prevents crucial interventions. Historically, thrombocytopenia has been attributed to hypersplenism, which is the increased pooling of platelets in a spleen enlarged by congestive splenomegaly secondary to portal hypertension. Over the past decade, however, there have been significant advances in the understanding of thrombopoiesis, which, in turn, has led to an improved understanding of thrombocytopenia in cirrhosis. Multiple factors contribute to the development of thrombocytopenia and these can broadly be divided into those that cause decreased production, splenic sequestration, and increased destruction. Depressed thrombopoietin levels in CLD, together with direct bone marrow suppression, result in a reduced rate of platelet production. Thrombopoietin regulates both platelet production and maturation and is impaired in CLD. Bone marrow suppression can be caused by viruses, alcohol, iron overload, and medications. Splenic sequestration results from hypersplenism. The increased rate of platelet destruction in cirrhosis also occurs through a number of pathways: increased shear stress, increased fibrinolysis, bacterial translocation, and infection result in an increased rate of platelet aggregation, while autoimmune disease and raised titers of antiplatelet immunoglobulin result in the immunologic destruction of platelets. An in-depth understanding of the complex pathophysiology of the thrombocytopenia of CLD is crucial when considering treatment strategies. This review outlines the recent advances in our understanding of thrombocytopenia in cirrhosis and CLD.

show abstract

“…After drug‐releasing, these PEG‐related materials still remain in the body. In the past, it was believed that PEGs were inert polymers without biological effects [59–61]. However, as recently often been reported, a long‐term administration will lead to a high accumulation of PEGs in tissues, which is related to potential tissue toxicity and adverse effects [62–64].…”

Section: Introductionmentioning

confidence: 99%

Recent advances in the bioanalytical methods of polyethylene glycols and PEGylated pharmaceuticals

Zhang

Song

et al. 2020

J of Separation Science

View full text Add to dashboard Cite

Polyethylene glycols are synthetic polymers composed of repeating oxyethylene subunits, which have been known for non-toxic, non-immunogenic, non-antigenic, good solubility in water and therefore approved for pharmaceutical applications. Recently, attachment or amalgamation of polyethylene glycols to therapeutic small molecules, peptides, proteins, or nanoparticles has become a mature technology for the sake of improving their pharmacokinetic and pharmacological profiles, also referred to as PEGylation. By comparison, there are only a few PEGylated pharmaceuticals have been registered for further clinical trials and even less was approved for marketing. High failure rate of PEGylated pharmaceuticals in pre-clinical and clinical trials could be majorly attributed to their unclear pharmacokinetic behaviors. Therefore, the in vivo fate of the PEGylated pharmaceuticals for the various routes of administration needs to be thoroughly investigated An accurate in vivo pharmacological study thereof highly depends on the precise detection of polyethylene glycols as well as their fragments in biological matrixes. The goal of this review is to highlight the analytical methods that were developed and applied to evaluate the polyethylene glycols in pharmaceutical ingredients and excipients, which bring us closer to bridging

show abstract

Severe immune thrombocytopenia after peg-interferon-alpha2a, ribavirin and telaprevir treatment completion: A case report and systematic review of literature

Cited by 3 publications

References 29 publications

Acquired amegakaryocytic thrombocytopenia previously diagnosed as idiopathic thrombocytopenic purpura in a patient with hepatitis C virus infection

Acquired amegakaryocytic thrombocytopenia previously diagnosed as idiopathic thrombocytopenic purpura in a patient with hepatitis C virus infection

The pathophysiology of thrombocytopenia in chronic liver disease

Recent advances in the bioanalytical methods of polyethylene glycols and PEGylated pharmaceuticals

Contact Info

Product

Resources

About