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      A Devastating Case of Hepatitis C-Induced Mixed Cryoglobulinemia

      case-report

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          Abstract

          Hepatitis C-induced mixed cryoglobulinemia leading to rapidly progressive gangrene, necessitating amputations, is a rare presentation. We describe a case of a 55-year-old man with untreated chronic hepatitis C virus (HCV) presenting with arthralgia and palpable purpura, which rapidly progressed to life-threatening gangrene of all extremities requiring amputations in the setting of mixed cryoglobulinemia. Treatment for HCV was initiated which led to the arrest of gangrene progression and the patient's survival. Patients with HCV-induced cryoglobulinemia should be closely monitored and started on early therapy with direct-acting antiviral therapy to prevent progression of vasculitis to gangrene. Universal screening for HCV can aid in early diagnosis and treatment to prevent devastating consequences.

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          Treatment of hepatitis C virus-associated mixed cryoglobulinemia with direct-acting antiviral agents.

          Meghan E. Sise, Allyson Bloom, Jessica Wisocky … (2016)
          Hepatitis C virus (HCV) is the most common cause of mixed cryoglobulinemia syndrome (MCS). The efficacy and safety of all-oral direct-acting antiviral (DAA) therapy in HCV-associated MCS (HCV-MCS) is largely unknown. The authors studied case series of patients with HCV-MCS who were treated with sofosbuvir-based regimens and historical controls treated with pegylated interferon and ribavirin in a single health care network. HCV-MCS was defined by circulating cryoglobulin associated with systemic vasculitis symptoms. Renal involvement (n = 7) was established by kidney biopsy (n = 5) or by two or more of the following clinical findings: reduced kidney function, proteinuria, or hematuria with other causes excluded (n = 2). Twelve patients received DAA therapy between December 2013 and September 2014. Median age was 61 years, 58% were male, and 50% had cirrhosis. Median baseline serum creatinine was 0.97 mg/dL (range 0.7-2.47). Four patients received rituximab concurrent with DAA therapy. Sustained virological response rate at 12 weeks (SVR12) was 83% overall. Patients with glomerulonephritis who achieved SVR12 experienced an improvement in serum creatinine and a reduction in proteinuria. Cryoglobulin levels decreased in 89% of patients, with median percent decreasing from 1.5% to 0.5% and completely disappearing in four of nine cases who had cryoglobulins measured after treatment. Serious adverse events were infrequent (17%). In contrast, the historical cohort treated with pegylated interferon and ribavirin experienced only 10% SVR12, with 100% experiencing at least one adverse event and 50% experiencing premature discontinuation due to adverse events.
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            Prospective study of guideline-tailored therapy with direct-acting antivirals for hepatitis C virus-associated mixed cryoglobulinemia.

            Laura Gragnani, Marcella Visentini, Elisa Fognani … (2016)
            Hepatitis C virus (HCV)-associated mixed cryoglobulinemia (MC) vasculitis commonly regresses upon virus eradication, but conventional therapy with pegylated interferon and ribavirin yields approximately 40% sustained virologic responses (SVR). We prospectively evaluated the efficacy and safety of sofosbuvir-based direct-acting antiviral therapy, individually tailored according to the latest guidelines, in a cohort of 44 consecutive patients with HCV-associated MC. In two patients MC had evolved into an indolent lymphoma with monoclonal B-cell lymphocytosis. All patients had negative HCV viremia at week 12 (SVR12) and at week 24 (SVR24) posttreatment, at which time all had a clinical response of vasculitis. The mean (±standard deviation) Birmingham Vasculitis Activity Score decreased from 5.41 (±3.53) at baseline to 2.35 (±2.25) (P < 0.001) at week 4 on treatment to 1.39 (±1.48) (P < 0.001) at SVR12 and to 1.27 (±1.68) (P < 0.001) at SVR24. The mean cryocrit value fell from 7.2 (±15.4)% at baseline to 2.9 (±7.4)% (P < 0.01) at SVR12 and to 1.8 (±5.1)% (P < 0.001) at SVR24. Intriguingly, in the 2 patients with MC and lymphoma there was a partial clinical response of vasculitis and ∼50% decrease of cryocrit, although none experienced a significant decrease of monoclonal B-cell lymphocytosis. Adverse events occurred in 59% of patients and were generally mild, with the exception of 1 patient with ribavirin-related anemia requiring blood transfusion.
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              Hepatitis C virus-induced cryoglobulinemia.

              Edgar Charles, Lynn Dustin (2009)
              In this review we discuss the clinical manifestations, pathogenesis, and treatment of hepatitis C virus (HCV)-related cryoglobulinemia. HCV is a major cause of liver-related morbidity and is increasingly recognized as an instigator of B-cell lymphoproliferative disorders such as mixed cryoglobulinemia and non-Hodgkin lymphoma. Cryoglobulinemia is characterized by the clonal expansion of rheumatoid factor-expressing B cells in the liver, lymph nodes, and peripheral blood, resulting in the presence of cryoglobulins in the circulation. Cryoglobulins are cold-insoluble immune complexes containing rheumatoid factor, polyclonal IgG, and HCV RNA that precipitate and deposit on vascular endothelium, causing vasculitis in organs such as the skin, kidneys, and peripheral nerves. A subset of patients develops a low-grade lymphoma composed of B cells that are immunophenotypically similar to the expanded B cells seen in cryoglobulinemia. HCV-related B-cell lymphoproliferative disorders likely comprise a spectrum of disease, ranging from asymptomatic clonal B-cell expansions to pathogenic cryoglobulinemia and lymphoma. It is unclear how B cells become dysregulated during the course of chronic HCV infection, and continued patient-centered research is necessary to elucidate the pathogenesis of HCV-related B-cell dysregulation.
              Article 0 comments Cited 44 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Sameeha Khalid:
                ORCID: https://orcid.org/0000-0001-9643-3473
                Journal
                Journal ID (nlm-ta): Case Reports Hepatol
                Journal ID (iso-abbrev): Case Reports Hepatol
                Journal ID (publisher-id): CRIHEP
                Title: Case Reports in Hepatology
                Publisher: Hindawi
                ISSN (Print): 2090-6587
                ISSN (Electronic): 2090-6595
                Publication date Collection: 2021
                Publication date (Electronic): 8 October 2021
                Volume: 2021
                Electronic Location Identifier: 8244432
                Affiliations
                1Department of Internal Medicine, University of California San Francisco-Fresno, Fresno, CA, USA
                2Department of Gastroenterology & Hepatology, University of California San Francisco-Fresno, Fresno, CA, USA
                3Department of Rheumatology, University of California San Francisco-Fresno, Fresno, CA, USA
                Author notes

                Academic Editor: Mauro Vigano

                Author information
                https://orcid.org/0000-0001-9643-3473
                Article
                DOI: 10.1155/2021/8244432
                PMC ID: 8519709
                SO-VID: f6371876-acf4-4203-9757-06b34d90a73d
                Copyright © Copyright © 2021 Sameeha Khalid et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 9 August 2021
                Date accepted : 24 September 2021
                Categories
                Subject: Case Report

                Data availability:

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