Cases reported "Hepatitis C, Chronic"

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1/8. Bell's palsy during interferon therapy for chronic hepatitis c infection in patients with haemorrhagic disorders.

    Two adult patients with life-long severe haemorrhagic disorders commenced on interferon-alpha2b therapy for chronic hepatitis c infection. Both developed Bell's palsy several weeks after commencing therapy, They were started on steroids and, in addition, the first patient discontinued interferon-alpha2b therapy while the second patient elected to continue with therapy. In both cases facial paralysis improved over the ensuing weeks. Bell's palsy is often idiopathic but has been reported. in association with herpesviruses. It is not a recognised complication of chronic hepatitis b or C infection, or interferon-alpha2b therapy. However, the interferons are associated with numerous adverse reactions including various neuropsychiatric manifestations and neurological syndromes. There are several reports of nerve palsies, including optic tract neuropathy, occurring during interferon therapy, and immune-based mechanisms are thought to play a role in the aetiopathogenesis. No reports of Bell's palsy in association with interferon therapy were identified in our literature search, although one possible case has been reported to the Committee of safety in medicine. Although Bell's palsy in our patients may have occurred by chance, a neuropathic effect of interferon-alpha2b on the facial nerve cannot be excluded and we urge physicians using interferons to be aware of this potential side-effect.
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2/8. Intra-hepatic haematoma complicating transjugular intra-hepatic portosystemic shunt for budd-chiari syndrome associated with anti-phospholipid antibodies, aplastic anaemia and chronic hepatitis c.

    Portal venous decompression with transjugular intra-hepatic portosystemic shunt (TIPS) is a new approach in the treatment of budd-chiari syndrome. We report on a 31-year-old female with budd-chiari syndrome due to anti-phospholipid antibodies with compression of the inferior vena cava treated with TIPS and stenting of the inferior vena cava. TIPS was complicated by massive intra-hepatic haematoma which was managed conservatively. Treatment options and pathogenic mechanisms of budd-chiari syndrome under the rare coincidence of aplastic anaemia and anti-phospholipid syndrome are discussed. TIPS may be considered for venous decompression in budd-chiari syndrome, but physicians should be aware of potential TIPS' complications in these patients.
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3/8. Reactivation of sarcoidosis during interferon therapy.

    The exacerbation of a co-existing autoimmune disease is often a concern for physicians who use immunomodulating agents for the treatment of a concomitant process. As physicians begin to treat chronic hepatitis c more often and more aggressively, this potential problem with occur more frequently. Herein we reported a case of reactivation of sarcoidosis occurring during the treatment of chronic hepatitis c, and we present a literature review of other centers' experiences with this problem. Depending upon the severity of the exacerbation and the type of organ involvement, reactivation of sarcoidosis may require discontinuation of the interferon therapy, with or without the use of additional steroids. The majority of patients, however, do not require the use of steroids. Interestingly, continuation of the interferon therapy in the presence of a mild-to-moderate exacerbation of sarcoidosis may be safe in a minority of patients with noncritical organ involvement.
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4/8. Approach to the patient with chronic hepatitis c virus infection.

    Chronic hepatitis c virus (HCV) infection is common and often asymptomatic. antibodies against HCV are a highly sensitive marker of infection. Molecular testing for HCV is used to confirm a positive result on antibody testing and to provide prognostic information for treatment; however, quantitative HCV rna does not correlate with disease severity or risk for progression. Chronic HCV infection is most frequently associated with remote or current intravenous drug use and blood transfusion before 1992, although as many as 20% of infected patients have no identifiable risk factor. In an estimated 15% to 20% of persons infected with HCV, the infection progresses to cirrhosis; alcohol intake is an important cofactor in this progression. Most specialists prefer to include an examination of liver histology in the management of patients with chronic HCV infection to aid prognostic and treatment decisions. The current standard of pharmacologic treatment of chronic HCV is weekly subcutaneous peginterferon in combination with daily oral ribavirin, which results in sustained virologic response in approximately 55% of chronically infected patients. Side effects of interferon therapy include myalgias, fever, nausea, irritability, and depression. The cost-effectiveness of interferon therapy is similar to that of many commonly accepted medical interventions. The primary care physician serves a vital role in identifying patients with chronic HCV infection, educating patients about risk factors for transmission, advising patients about the avoidance of alcohol, and aiding patients in making treatment decisions.
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5/8. Nephrotoxicity of interferon alfa-ribavirin therapy for chronic hepatitis c.

    The nephrotoxicity associated with interferon therapy for chronic hepatitis c infection has not been clearly defined. We describe a patient with chronic hepatitis c infection who developed the nephrotic syndrome during treatment with interferon and ribavirin. Renal biopsy revealed focal segmental glomerulosclerosis. She had a virologic and biochemical response to the antiviral therapy, and the nephrotic syndrome improved after termination of antiviral therapy. We place our case report in context with a review of the literature on nephrotoxicity associated with interferon therapy. Because our patient had no other obvious reason for the nephrotic syndrome, we are postulating that it may be secondary to interferon-ribavirin therapy. The temporal relation between the administration of the drug and the detection of toxic affects (nephrotic syndrome) and subsequent improvement upon withdrawal also supports a causative role for interferon-ribavirin. Although nephrotoxicity is rare, it should be emphasized that it can occur anytime after the start of interferon therapy, and physicians treating patients with chronic hepatitis c must be aware of this idiosyncratic, unpredictable, and potentially serious adverse event.
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6/8. Visual side effects of pegylated interferon during therapy for chronic hepatitis C infection.

    Ocular toxicity, including retinopathy, optic neuropathy and ocular loss, has been infrequently (<1%) reported as a potentially serious adverse event associated with standard interferon therapy. The new pegylated interferons have improved pharmacokinetics which translates to better antiviral efficacy, however, this improved pharmacokinetic profile also has the potential to alter the frequency and extent of their adverse events. We describe a case of chronic hepatitis c infection that developed visual complaints after one month of pegylated interferon, and retinopathy confirmed on ophthalmologic examination. We place our report in context with a review of the literature related to visual complications associated with interferon therapy. From our compilation of case reports, it is apparent that variable doses and duration of interferon therapy have been associated with ocular toxicity, which in turn suggests an idiosyncratic drug reaction. In as much as this adverse event is unpredictable, and its frequency undefined with pegylated interferon therapy, further surveillance will be required for patients undergoing pegylated-interferon therapy. Although ocular toxicity is uncommon, it should be emphasized that it can occur any time after the start of interferon therapy, and physicians now treating chronic hepatitis c patients with pegylated interferon must be aware of this potentially serious adverse event.
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7/8. Acute sensorineural hearing loss associated with peginterferon and ribavirin combination therapy during hepatitis c treatment: outcome after resumption of therapy.

    Peginterferon and ribavirin combination therapy for the treatment of hepatitis c virus (HCV) is well known to be associated with significant adverse effects. Sensorineural hearing loss, that in most cases is unilateral, has been reported as a consequence of therapy with both non-pegylated and pegylated interferon (pegIFN) but is not a well-known adverse effect. We report a 45-year-old Caucasian woman who developed acute sensorineural hearing loss 2 mo after starting therapy with pegIFN-alpha 2b and ribavirin for the treatment of chronic HCV, genotype 1a. She did not report the hearing loss to the hepatitis clinic until 1 mo, later whereupon therapy was promptly discontinued. Although her serum alanine aminotransferase (ALT) normalized and her HCV-rna became undetectable after 12 wk of pegIFN and ribavirin therapy, after discontinuation, her HCV-rna became detectable with significant elevations of serum ALT. Four months after initial discontinuation, the patient re-commenced pegIFN and ribavirin combination therapy. After 44 of 48 wk of therapy, the patient's liver biochemistry has normalized and the HCV-rna is undetectable. She has not developed worsening of her hearing loss and hearing on the left-side is unaffected. Both patients and physicians should be aware that sensorineural hearing loss may occur with pegIFN therapy. Our experience suggests that re-institution of therapy is not always associated with further hearing impairment.
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8/8. Disseminated aspergillosis following infliximab therapy in an immunosuppressed patient with Crohn's disease and chronic hepatitis c: a case study and review of the literature.

    A 55-year-old white woman with a greater than 25-year history of Crohn's disease developed disseminated aspergillosis following combination therapy with methylprednisolone, azathioprine, and infliximab. The patient was hospitalized 11 days after initiation of infliximab for respiratory symptoms and developed respiratory failure, coma, and died. Postmortem examination revealed disseminated aspergillus fumigatus involving multiple organs. This case demonstrates that combined treatment with infliximab, methylprednisone, and azathioprine may induce severe immunosuppression and depressed cellular immunity, leading to severe opportunistic infections. Given the increasing use of antitumor necrosis factor agents, physicians should be aware of the risk of opportunistic infections and be vigilant about diagnosing and aggressively treating these infections to reduce the risk of disseminated disease.
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