Hepatitus C Made Simple (video) (Hepatitis C / Liver Transplant & Biopsy (Hep C) HCV Blog)

Monday, 25 April 2011

Hi to everyone, just a video about Hep C explaining what the virus is and how it operates. In this vid it says "HepatitisC can be cured" - I suppose they sound very optimistic as it was created by Vertex Pharmaceuticals, the company who are just about to launch 'Teleprevir', the latest drug for the war on HCV.
There is no doubt that this drug, and 'Boceprevir' that is also about to be launched, represent a huge leap forward in the fight against this terrible virus that affects 4 times as many people in the world than Aids and for so many people who are infected, they have no idea that they have it until it becomes a life threatening illness. What it doesn't say is that even with these new drugs, there is still no definitive cure...
take care everyone... Ian


Another Letter to Ali (Hepatitis C / Liver Transplant & Biopsy (Hep C) HCV Blog)

Friday, 22 April 2011

I thought I would share this letter that I sent to Ali and readers of this blog will know this is not the first time I have posted our letters here.
Ali's a good friend of mine whom I've known since way back when, through good times and bad. I sometimes wish I was as good a friend to her as she has always been for me and even though we are now many miles and countries apart, she continues to support me in so many ways.

Dear Ali, How are you and how is beautiful Chamonix?
Well, I finally managed to track down my HepC nurse at our local hospital and after badgering her a bit (It has been nearly a month and a half since St Jimmy's handed me over to them to start my treatment) I finally got a date from her for the start of my treatment... I think.
Friday 6th May is when I'll be going to see them to start treatment. Apparently she's been having to study the protocol for dealing with transplant patients as she's never dealt with one before.... Yikes!!
I'm sure it will be OK and she will be in regular touch with my doctors at Jimmy's and I'll be very closely monitored. You know my old saying "It'll be all-right!!!"

Thank-you to you and Mo for doing the healing meditations, I can't believe how well they've worked. I know you think Benny would frown on spiritual meditation as "a load of bollocks and all that" (and at one time I would've been right there with him) but if he ever needed proof that it works then he needn't look any further.

It really has lifted me in my mind and I feel physically better than I have done for a long time and don't just take my word for it, even Mandy's amazed. And Mandy is not a spiritual believer in the way we are but she can't believe the change in me.

I've also had Jenny saying Buddhist 'chants' or prayers for me as apparently shes quite into that, It was great to see her again and she hasn't changed a bit, the rotten cow!
Anyway, it was quite interesting hearing her talking about her religion but I don't think I could ever embrace it in it's entirety but as with the spiritual meditations, I think there must be something to it. 
I've been looking into meditation quite a bit anyway after our success with it. I certainly haven't 'found God'  or 'seen the light' yet but Jenn probably put it right when she said "I think they're all paths to the same thing" and essentially I think shes probably right.

I'm not sure if, since we started the meditation, everything is going exactly to plan (far from it sometimes) but I certainly feel like I'm coping with it a lot better.
I'm better at dealing with the fear of the unknown so much better now and that's got to be a good thing. I've certainly had plenty of that in the last couple of years. 
But although the fear never quite goes away entirely, it just feels like I've got a kind of scary, hairy creature thumping around inside me all the time at the back of my mind.
It's all the things that have haunted me and now I no longer see 'it' staring me in the face. But sometimes I can hear it moving around and I can hear it's breathing and grunting somewhere way back in the darkness of my mind where I have put it and I just have to tell myself that it cant hurt me anymore because it's locked up in it's cage back there.
And then I try and think back to the meditations and I can feel it getting further and further away, like I'm walking out from a dark passage where it lives and out into the light where you and Mo are and all the other people who are fighting this thing with me. I can hear their voices and see their smiles and feel the warmth and the safety and then I'm back, and that's it - life can go on again without all that weight on me.

I'm so glad we spoke on the phone when we did, I was pretty low at that point, as anyone who's had or has this virus knows, you get good days and some very bad. It's difficult to explain to people, now that I've recovered from the transplant op and you look okay on the outside and some days you feel okay too, and then others when you can't get out of bed because you feel so fatigued or you just can't face the world and are in a place that I though I would never go. I suppose people will have to live and learn as I have had to.

OK chicken, I'll get off, write me back soon and I guess we'll both keep looking out for each other.

Take care.... Rio xx


Adverse Effects: Management of Hepatitis C Antiviral Therapy (Hepatitis C / Liver Transplant & Biopsy (Hep C) HCV Blog)

Sunday, 17 April 2011

Hi folks, I thought it was time I researched and put something on my blog about my forthcoming treatment. And, as everyone I talk to who doesn't have HepC keeps asking me about the treatment and about the side effects I thought I'd post some information for all of us to read.
The treatment I will be having is standard Ribavirin & Pegylated Interferon therapy and will hopefully rid me of the Hepatitis C Virus (HCV) - this is the reason why I had a Liver Transplant just over 14 months ago.
I understand that if I clear this virus it will be considered extraordinary and to date, I have not come across any geno 1a (my geno-type) who has been cured or achieved 'Sustained Virological Response' (SVR) as it is known medically.
I found this info on the very excellent 'HCV New Drug Research' blog, sorry if it's heavy reading but I'm aware that they're very heavy drugs to treat a very heavy virus and I will be entering into this treatment with some trepidation but overall positive attitude.
take care everyone... Ian
Management of Hepatitis C Antiviral Therapy Adverse Effects

Hepatitis C is one of the leading causes of liver disease in the United States, affecting more than 4 million individuals. The current treatment regimen involves pegylated interferon in combination with ribavirin. Although antiviral treatment has been associated with a greater than 50% sustained viral response rate, the adverse effects have proven to be detrimental to quality of life and therapy adherence, and consequently lead to lower sustained viral response rates. This article identifies the most frequently described complications associated with pegylated interferon and ribavirin. The active management of these complications is discussed, including both preventive and empiric treatments.

Keywords: Hepatitis C virus, Pegylated interferon, Ribavirin, Side effects, Management


Hepatitis C is a major public health concern. With almost 4 million Americans with chronic infection, hepatitis C is the one of the leading causes of chronic liver disease and is the single most common indication for liver transplantation [1–3]. Antiviral therapy is effective in more than half of infected patients, but the actual rate of sustained viral response depends on viral, host, and adherence factors. Viral and host factors tend to be nonmodifiable, whereas interventions may increase adherence.

The current standard of care for hepatitis C therapy is the combination of pegylated interferon and ribavirin [4]. Sustained viral response for antiviral therapy is about 55% [5•, 6•]. However, adverse effects from antiviral therapy directly affect treatment adherence and can decrease the likelihood of a sustained viral response. These complications can severely compromise quality of life [7]. Both interferon and ribavirin are associated with signature effects that are predictable, manageable, and improve with dose modification or discontinuation [8••]. Rarely is an adverse effect from hepatitis C antiviral therapy permanent. Adverse effects can arise from both interferon and ribavirin, and may lead to treatment termination and dose modifications in 10% to 15% and 32% to 42% of patients, respectively [5•, 6•, 9]. When interferon and ribavirin doses are reduced by a certain threshold, the sustained viral response may also decrease [10]. For instance, the results of a recent study by Reddy et al. [11••] demonstrated the sustained viral response is 34% when a patient’s cumulative ribavirin dose decreases below 60%.

An understanding of the antiviral adverse effects is essential to effectively deal with adverse effects in a timely manner. The goal during therapy is to maximize the likelihood of achieving a sustained viral response while improving tolerability and maintaining quality of life. Providers should discuss the potential issues with patients and with their social support. During clinic follow-up, patients should be queried about treatment adverse effects. Many times, the adverse effects can accumulate over time and lead to early treatment discontinuation. The current paper reviews the most frequent adverse effects associated with hepatitis C therapy, and proposes interventions to ameliorate complications. The adverse effects from pegylated interferon and ribavirin are considered separately.

Pegylated Interferon

The efficacy and therapeutic value of hepatitis C treatment is dependent on the degree of tolerability and adherence to the drugs, which in turn are related to the management of the side effects. The frequency and number of side effects related to interferon therapy are common, with most clinical trials reporting at least one interferon-related adverse effect in 95% of the patient group [5•, 10, 12]. The most frequently reported adverse effects from interferon include constitutional, hematologic, neuropsychiatric, and endocrinologic complications See; (Table 1). The onset of the adverse effects differ. The onset can be from minutes after the interferon injection, to months See; (Table 2).

Constitutional Effects

The most common adverse effects from interferon are constitutional symptoms. The severity of these side effects is inversely related to the amount of time after the interferon injection. Fatigue, headache, and fever were each reported in about 50% to 60% of treated patients [6•, 9, 12].

Constitutional effects can manifest early during therapy, even after the first dose of interferon [12]. However, several constitutional effects (e.g., fever) resolve or wane after the first several injections. Certain precautions can assist with the effects, such as maintaining adequate hydration and light to moderate exercise. The suggested intake of water in ounces is equivalent to half the patient’s body weight in pounds. To prevent interferon therapy from interfering with work, injections should occur on Fridays. As a result, most of the constitutional effects will occur on Saturday. By Monday, treated patients tend to feel better. The use of acetaminophen or ibuprofen before the injection can also ameliorate many of the constitutional adverse effects. Other adverse effects (e.g., arthralgia) can respond to acetaminophen or ibuprofen. However, ibuprofen should be avoided in patients with liver cirrhosis.

Hematologic Effects

Hematologic side effects are the most recurrent abnormal laboratory values that can lead to dosage reductions and premature treatment termination [9]. Because of its myelosuppressive effect, interferon can affect hemoglobin, white blood cell, and platelet values. However, the anemia seen during combination treatment is mostly associated with ribavirin-induced hemolytic anemia.

The definition of neutropenia varies between the two commercially available pegylated interferons. For instance, neutropenia is defined as an absolute neutrophil count less than 500 cells/mm3 when using pegylated interferon α-2a, and below 750 cells/mm3 when using pegylated interferon α-2b [13, 14]. Certain populations appear to be more likely affected by the neutropenic effects of interferon, such as the elderly and non-African Americans [15]. Although African Americans are prone to constitutional neutropenia, initiation of interferon treatment usually only leads to minimal further decreases in neutrophil count. However, the clinical impact of neutropenia on significant infection is controversial. In a study of 119 subjects, 22 infections were documented and were dominated by sinusitis, pharyngitis, and urinary tract infections [15].

In most clinical trials, neutropenia is treated with dose modification. Interferon dose reduction occurs in about 17% to 20% of patients and treatment termination in 2% to 3% of patients [16••, 17, 18]. The rapid decline in neutrophils usually occurs within the first 2 weeks of treatment initiation, with stabilization occurring over the next 4–6 weeks [9]. One study of 25 patients illustrated a median drop of 21% in neutrophils following the first dose of interferon [19].

Another option for patients who develop neutropenia from interferon therapy is the use of granulocyte colony-stimulating factor (GCSF) [20–22]. Few clinical studies have included the use of GCSF [20, 21]. These studies have indicated that the GCSF is able to raise neutrophil counts during interferon therapy. However, the results of a recent study failed to show a correlation between interferon-induced neutropenia and incidence or severity of infections [15]. Thus, although GCSF can improve neutrophil counts, future studies are required to determine the utility of GCSF in clinical practice, particularly given its increased costs and its own associated adverse effects. Regardless of the intervention of neutropenia, affected patients need regular cell counts to monitor neutrophil levels.

Another interferon-induced hematologic adverse effect is thrombocytopenia. Several mechanisms exist for the development of thrombocytopenia. It has been shown that platelet count can fall up to 50% because of posttranscriptional suppression of megakaryopoiesis or platelet sequestration in capillaries [23]. In addition, there have been rare cases of immune-mediated thrombocytopenia leading to significant decreases in platelet count, which can be rectified by termination of interferon treatment or corticosteroid therapy [24, 25]. Platelet reduction often occurs within the first 24 h of interferon administration, with nadir being reached within 8 weeks of therapy. Platelet levels will then stabilize at this low level during the length of therapy [23, 24]. However, it may compound the already present thrombocytopenia associated with cirrhosis and portal hypertension. With pegylated interferon α-2a, dose reduction is suggested when platelet counts fall below 50,000/mL and therapy termination when counts fall below 25,000/mL [13]. The threshold is set a little higher with respect to pegylated interferon α-2b, with limits of 80,000/mL for dose reduction and 50,000/mL for discontinuation [14]. Discontinuation of therapy is often followed by normalization of platelet counts within 4–8 weeks [23, 24]. Recent studies have shown eltrombopag, a thrombopoietin receptor agonist, to effectively increase platelet counts to greater than 250,000/mm3 in thrombocytopenic patients with hepatitis C virus [26]. However, its safety and utility in patients with advanced liver disease remains to be determined, because it may increase the risk of thrombosis [27].

Neuropsychiatric Effects

Not only is the prevalence of depression in patients with hepatitis C higher than the general population, antiviral therapy increases the likelihood of a variety of neuropsychiatric complications, including worsening depression, anxiety, and suicidal ideation [28]. Thus, it is imperative to assess for underlying depression and other preexisting psychiatric illness before considering antiviral therapy. In fact, antiviral therapy is contraindicated in patients with uncontrolled neuropsychiatric disorders. With a treated patient’s approval, it is helpful for their social support to provide feedback on mood changes because patients themselves may not notice changes in their disposition.

About 20% to 30% of patients treated with interferons report depression during therapy or the exacerbation of a preexisting depressive state [6•, 29]. Depending on the type and severity of neuropsychiatric effects, patients may be monitored or may be treated with more frequent clinic visits or telephone calls, antidepressant medications, psychiatric referral, or dose modification or even discontinuation.

The selection of antidepressant medication requires tailoring, because depression may have nuances that improve or worsen with the choice of therapy [30]. The greatest experience with antidepressant medications is with selective serotonin reuptake inhibitors (SSRIs) [31, 32]. Although the use of antidepressant medication may not necessarily significantly improve the likelihood of a sustained viral response, it does improve adherence and help maintain quality of life [33]. In patients believed at increased risk of interferon-associated depression, preemptive treatment with SSRIs was associated with a significant reduction in the incidence of major depression [33].

Endocrinologic Effects

Thyroid abnormalities are the most commonly associated interferon-induced endocrinologic adverse effect, occurring in 1% to 6% of interferon-treated patients [34, 35]. Both hypo- and hyperthyroidism can develop. Patients with hepatitis C may be predisposed to developing thyroid abnormalities because of an increased rate of thyroid autoantibodies prior to starting antiviral therapy [36]. For instance, one study described the development of thyroid disorder in 60% of patients with antithyroid microsome antibodies present prior to the initiation of interferon therapy, compared to only 3.3% of patients without these antibodies [35]. In a similar study, 38.5% of females with antithyroid peroxidase antibodies developed hypothyroidism versus only 7.8% of females lacking these antibodies [37].

Thyroid function tests should be obtained at baseline and every 12 weeks during antiviral treatment, and after treatment completion. If a patient develops symptomatic hypothyroidism, hormone replacement should be initiated while continuing antiviral therapy. Moreover, if the patient develops hyperthyroidism, the patient should be referred to an endocrinologist for further management with reevaluation of the antiviral regimen. Similar to the autoantibody destruction seen in the thyroid, antibodies to the adrenal cortex, pancreatic islet cells, and antiphospholipid antibodies have been reported with the use of interferon [38, 39]. Although rare, new-onset insulin-dependent diabetes mellitus with the presence of antibodies directed toward islet cells and insulin has been reported [40].

Dermatologic Effects

Many dermatologic adverse effects are associated with interferons, with an incidence ranging from 13% to 87% [5•, 41]. Besides nonspecific symptoms, reactions at the site of interferon injection are common, with 30% to 40% of patients complaining of erythema, pruritus, and tenderness [6•, 42]. Because the lesions may take weeks to resolve, it is recommended to rotate between unique injection sites. After injection, the sites are often warm and raised, expanding to a circumference of 5 cm or more. If the site continues to enlarge and remains warm and tender, the patient must be examined for possible abscess formation. Rarely, infection and skin necrosis are seen at the injection site. However, these symptoms do not necessarily warrant termination of treatment.

An additional major complaint from interferon therapy is skin dryness, which occurs in two of three treated patients [43]. Skin dryness can be exacerbated in cold weather, and may be accompanied by intense pruritus. Topical steroids, emollients, and soothing baths may help to alleviate these symptoms, but studies have not shown a significant response [43]. Another typical adverse effect seen with interferons is alopecia, occurring in about one third of patients, with a higher prevalence in females [44]. To combat alopecia, the patient can cut his/her hair short prior to interferon initiation and avoid pulling, braiding, or vigorously combing the hair. In addition, patients should avoid the use of harsh hair-care products, harsh hair dyes, hair dryers, and other products that may be detrimental to hair growth.

Other Effects

Neurologic, pulmonary, and ophthalmologic adverse effects associated with interferon use have been reported. Sensory and autonomic neuropathies, as well as Bell’s palsy, have been documented with interferon use, most likely arising from an autoimmune phenomenon or neuronal injury caused by interferon stimulation of the immune system [45]. Neuropathy usually resolves with the termination of interferon treatment, but additional steroids and/or cyclophosphamide may be beneficial [12]. In addition to the neuropathies stated, there have been rare cases of myasthenia gravis. In such cases, interferon therapy is withdrawn and pyridostigmine therapy is initiated [46]. During interferon treatment, multiple pulmonary adverse effects can occur, such as interstitial pneumonitis, alveolar disease, and sarcoidosis reactivation. If a patient complains of continual cough and dyspnea on exertion or rest, a chest radiograph should be obtained to exclude pneumonitis. Possible bacterial pneumonia should be treated with proper antibiotics in conjunction with halting antiviral therapy, which can be reinitiated when there is clinical improvement. Occasionally, pulmonary function tests may be indicated, including forced vital capacity, forced expiratory volume, and carbon monoxide diffusion capacity, as well as a thoracic CT scan. Interferon-induced interstitial pneumonitis can be life-threatening, although it usually resolves with withdrawal of interferon. However, the most common cause for cough and shortness of breath is likely ribavirin-induced [43].

In addition to the pulmonary and neurologic effects, interferons have been associated with retinopathy (e.g., retinal hemorrhages and cotton wool spots), particularly in patients with diabetes [47]. In one study of 63 patients treated with antiviral therapy, 40% of patients developed retinal hemorrhages and 44% developed cotton wool spots [48]. Diabetes and hypertension were risk factors for retinopathy [47, 49]. It is important for patients with pre-treatment risk factors for retinopathy to undergo retinal examination prior to treatment, and if any visual changes occur during treatment, to undergo ocular re-evaluation. Antiviral treatment must be halted if retinopathy worsens during therapy.


Ribavirin is used with interferon to treat hepatitis C. Like interferon, it is associated with several adverse effects. Although the adverse effects from ribavirin appear to be less severe than those from interferon, maintaining ribavirin dose appears more critical to the likelihood of achieving a sustained viral response than sustaining the interferon dose [6•]. Thus, it is still imperative to understand and be able to manage ribavirin-associated complications.

Hematologic Effects

The signature adverse effect of ribavirin is anemia, occurring in up to 30% of treated individuals [5•, 6•]. Ribavirin-related anemia is one the most common reasons for dosage reduction or discontinuation of the drug, resulting in 9% to 22% of patients requiring dosage reduction [5•, 6•]. Anemia can result in persistent fatigue, shortness of breath, and lower quality-of-life scores [12]. Treatment with ribavirin displays a drop in hemoglobin during the first 4 weeks of treatment, followed by stabilization, then normalization after treatment completion [9]. The mechanism of ribavirin-associated hemolytic anemia is unclear, but is believed to be related to impaired antioxidant defenses and red blood cell oxidative damages through its metabolites [51]. The degree of hemolytic anemia is directly related to ribavirin dose, renal function, and perhaps patient age [52, 53]. Recently, ITPA gene variants have been found to be protective of anemia in patients treated with ribavirin [54••].

The definition of anemia can vary. Although anemia may be suggested by the rate of hemoglobin drop, it is commonly defined by an absolute value of less than 10 g/dL [55]. Intervention for ribavirin-induced anemia depends on the rate of hemoglobin decrease, absolute hemoglobin value, comorbidities, and symptoms. Therapeutic options include frequent monitoring, blood transfusion, erythropoietin grown factor, and ribavirin dose modification [6•, 8••, 50••]. The risk of significant anemia can be predicted by hemoglobin trends. For instance, a decrease in hemoglobin of at least of 1.5 g/dL after 2 weeks predicts significant decreases after 4 weeks of therapy [56]. Recognition of impending anemia may prompt small reductions of ribavirin to avoid significant decline in hemoglobin.

There is a discrepancy between the intervention for anemia according to package inserts, and what is often done in clinical practice. The respective package inserts recommend decreasing the ribavirin dose by 200 mg/day when using peginterferon α-2b/ribavirin and by 600 mg/day when using peginterferon α-2a/ribavirin, if hemoglobin decreases to less than 10 g/dL in a patient without cardiac risk factors [13, 14, 55]. The package inserts also recommend termination of ribavirin if the hemoglobin levels decrease below 8.5 g/dL.

Studies have shown erythropoietin can improve hemoglobin values, maintain ribavirin dosage levels, and improve quality of life in patients with symptomatic ribavirin-induced anemia [57]. Despite improved adherence with erythropoietin, no studies have shown that the use of erythropoietin translates to higher sustained viral response. This may be due to the large cohort of treated patients needed to show a beneficial effect. There have been reported cases of antibody-mediated pure red-cell aplasia induced by erythropoietin, which is potentially life-threatening, but resolves with termination of erythropoietin treatment and initiation of danazol [58]. A recent study highlighted the correlation between the magnitude of hemoglobin decline and the likelihood of sustained viral response, and indicated an association between the magnitude of hemoglobin decline and ribavirin exposure [59]. Erythropoietin use in early-onset anemia minimized treatment discontinuation and led to higher sustained viral response rates. However, erythropoietin for anemia after 8 weeks of therapy was not associated with higher sustained viral response rates. Moreover, erythropoietin has been linked to a greater incidence of mortality with its use in ischemic stroke patients [60]. These recent concerns regarding raised risks of thromboembolic events and aplastic anemia with erythropoietin justify the judicious use of this agent.

Other Effects

Other ribavirin-associated complications include nausea and pulmonary, dermatologic, and teratogenic effects. Studies have shown that 25% to 40% of patients complain of nausea [5•, 6•, 12]. However, this symptom can be managed with alterations in the patient’s dietary regimen. More specifically, along with maintaining adequate hydration, patients should avoid acidic, spicy, sweet, or greasy foods. Instead, dietary intake should consist of clear beverages and dry foods (e.g., toast and crackers). If nausea persists after dietary changes, antiemetics may be prescribed.

Ribavirin therapy is often associated with a dry, nonproductive cough, which resolves only upon termination of treatment. Most patients can tolerate this adverse effect, and thus it is not a major cause of dose reductions or treatment termination. However, if the cough becomes productive or other clinical indications are present, a chest radiograph should be considered.

The addition of ribavirin in combination therapy increases the incidence of dermatologic adverse effects. More specifically, one study compared the incidence of skin rash in two groups, one receiving interferon monotherapy and one receiving interferon and ribavirin. Monotherapy resulted in an 8% incidence, whereas combination therapy resulted in 28% incidence [41]. Dermatologic side effects with combination therapy are typified by generalized pruritus, skin xerosis, and eczematiform lesions, which are localized to the extremities. Although ribavirin is shown to increase the incidence of dermatologic conditions when added to interferon treatment, it should be noted that ribavirin alone may cause rash and pruritus. Ribavirin must be discontinued if an acute hypersensitivity reaction develops. However, transient rashes do not require ribavirin treatment interruption [55]. Management entails topical corticosteroids, which may be tapered once signs of inflammation and irritation begin to recede. Preventive measures can be taken, with daily emollient therapy and skin moisturizers to commonly affected areas.

Ribavirin has been associated with significant teratogenic or embryocidal effects in nonhuman animal species exposed to it; therefore, patients must take proper precautions when beginning ribavirin treatment. Moreover, ribavirin therapy, which according to the Food and Drug Administration is pregnancy category X, is contraindicated in pregnant woman and in the male partners of women who are pregnant. It is imperative for patients to avoid pregnancy during ribavirin treatment and for 6 months after treatment completion. It is suggested that two reliable forms of effective contraception be used during this time. Upon cessation of treatment, recovery from ribavirin-induced testicular toxicity was apparent within one or two spermatogenesis cycles. Although human studies are lacking, there is a ribavirin pregnancy registry that enrolls pregnant women who have been directly or indirectly exposed to ribavirin [61]. Although underpowered, the results of a recent registry questioned the association between ribavirin and human teratogenicity [62].


References Conclusions The current standard of care for the treatment of hepatitis C infection involves the use of pegylated interferon and ribavirin. This antiviral combination therapy is associated with several potentially serious adverse effects. Fortunately, pegylated interferon and ribavirin have been available for almost a decade, and most of the adverse effects regarding incidence and time of onset have been defined. The management of these antiviral complications has also been well described, including preventive and empiric strategies. Understanding the limitations of current treatment is essential to assure quality of life and adherence during therapy, and may provide insight to deal with the finer points of future treatment strategies.

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Source with thanks: HCV New Drug Research: Adverse Effects: Management of Hepatitis C Antivir...


Questions to the HepC Community (Hepatitis C / Liver Transplant & Biopsy (Hep C) HCV Blog)

Monday, 11 April 2011

Hi all, still waiting to start tx (treatment) as my HepC nurse and Consultant have had holidays- one straight after the other...bloody frustrating as I want to get cracking.

I have been told that as a (HCV) geno 1a, post (liver) transplant, I only stand a 30% chance of clearing the virus but hey, it’s worth a shot – it might get rid of it or at least knock it back until some new drugs come along – I think it’s gonna be another couple of years before transplant patients get Teleprevir / Boceprevir (new HepC drugs) on the NHS in the UK and I can’t wait that long – Still hanging in there folks!
(Pictured - 'injecting Interferon')

They also said that there is a chance that the HepC treatment drugs, being fairly bloody powerful, could react badly with my immunosuppressant drugs and that I could end up rejecting my new liver - eeek. I suppose if my docs have put me forward tx then they must think its worthwhile...?

Just wondered if any of you within the HepC community had any info on 'pre-dosing' with Ribavarin for a couple of weeks prior to commencing with Interferon?

I have heard of a few people who have done this (geno 1a's like myself) and said it was very successful, especially as they had been non-responders 1st time around and had tried this on their 2nd attempt and WON, any info would be greatly appreciated as been told I am to start tx any time soon .

This is the 1st attempt for me even though HCV took my first liver (my liver was too damaged by the time I was diagnosed with HepC) so anything to improve my chances 'post-transplant' would be good.

I realise also that the jury’s out on this issue as it seems that the people who have 'pre-dosed', highly recommend this action and those that didn’t tend to say ‘stick to yr doctors orders’ – I have to say that I haven’t come across anyone who has 'pre-dosed' and then not achieved the hallowed 'SVR' (Sustained Virological Response - or cured to you and me). If anyone does feel that it’s so contentious an issue that they would rather email me rather than post a comment, then I understand – whether they are for, or against it, I’m trying to get info to make an informed choice.

I also wanted to ask you folks about Anti-Depressants, I was reading an article on HepatitisC NewDrugs  (http://goo.gl/fb/v51BG) saying that patients who start treatment from the outset on anti-depressants are far more likely to complete tx than those who don’t. And I wondered if anyone felt they needed pain-killers at any point – I get a lot of abdominal pain but wonder if that’s just because I had a transplant.

Other than that folks all is good and I’m waiting to get on with it, my Hep C Special Nurse rang me to say she has no problem treating me but I have to see the Consultant who got back to work last Friday, once he’s gets to his admin I’ll get an appointment and we should be getting going! Keep everything crossed for me.

Take care everyone… Ian


Tackling Hepatitis C: A Tale of Two Countries (Hepatitis C / Liver Transplant & Biopsy (Hep C) HCV Blog)

Friday, 8 April 2011

I found this article on the Hepatitis C Trust website and was originally published in The Lancet. As a a Hep C sufferer living in England, it backs up what I have known for some time, having been admitted to my local Hospital twice with symptoms of the virus and misdiagnosed and released thereafter, only for it to be picked up on a blood test done by my GP who didn't accept the hospitals findings. I think this country is in denial of the condition and with 250,000 people suspected of carrying this virus in Britain undetected, it is a disaster waiting to happen!

Hepatitis C remains underdiagnosed and undertreated in parts of the UK. Kelly Morris asks whether the National Liver Strategy for England will deliver what Scotland is already achieving.

20 years after the hepatitis C virus was identified, mortality and hospitalisations are steeply rising in the UK as people infected 20—30 years ago develop end-stage liver disease and hepatocellular carcinoma. At least 250 000 people in the UK might have the infection, mostly undiagnosed, and more likely to present with advanced disease.

Graham Foster, professor of hepatology at Queen Mary's University, London, UK, has “no doubt that more people are being diagnosed with an increase in awareness and testing, but still we are way behind Europe and the rest of the developed world in diagnosing patients and our flow through from diagnosis to treatment is still woefully inadequate”. Foster, who also works as a clinician in east London, tells The Lancet that “treatment services in general are very poor throughout the UK”; he fears that excellent treatment performance and high standards of care are found in few services.

Injection drug use is the main, but not sole risk factor, for contracting hepatitis C, hence the infection is stigmatised and misunderstood in the general population. Prevalence among people who inject drugs is about 50%, yet local provision of testing and treatment varies widely in this often marginalised and unheard of group, despite clear evidence of its usefulness to reduce disease burden and ongoing transmission.

Moreover, treatment and testing are inextricably linked. “If you have a good treatment service, then GPs [general practitioners] become aware that their patients are being cured and that drives them to find the virus and refer patients on”, Foster explains. “If treatment is available at a very low level, GPs stop referring patients because they see nothing happens.” But if specialist services are poorly resourced, then consultants have to place severe restrictions on who gets treatment, he says.

These disparities are increasingly seen now at country level, because action to tackle the virus has widely differed especially between the UK countries Scotland and England, which have similar high prevalence epidemics compared with other countries in the UK and much of the developed world.

England launched a national hepatitis C strategy in 2002 and then an action plan in 2004. This plan, say critics, had few outcome measures, no clear timetable, no attached financing, and the political environment, which focused on priority setting at local National Health Service (NHS) level, was such that the government would not stipulate what was required of local clinical services. “There were absolutely no levers whatsoever to have this actioned. The result is that largely it hasn't been”, says Charles Gore, chief executive officer of the Hepatitis C Trust, which has been campaigning for 10 years for England to develop an actionable plan.

Scotland launched its two-phase action plan in 2006. The 3-year first phase was completed early so that progress and outcomes of the second phase (2008—11) have now been reported for 2 years. From 2007 to 2009, Scotland had a 34% increase in new diagnoses, and a further increase is expected as a consequence of professional and public awareness campaigns, which began early in 2010. Testing has also been enhanced by the roll out of dried blood-spot collection by finger prick, which allows sampling in non-clinical settings.

Development of clinical services has doubled the number of patients started on treatment in 2007—09, while treatment of prison inmates has increased six times. Provision of clean injecting equipment has increased several times since guidelines were approved in 2009. This year, the governance structure and data-generating initiatives now in place will further monitor progress and outcomes. In April, the plan will become part of the Sexual Health and Blood-Borne Virus Framework.

The Scotland Hepatitis C Action Plan “is regarded globally as a model of good practice”, says Gore, who is also president of the World Hepatitis Alliance. To make progress in England, Foster says, Scotland's example “shows how a government-supported initiative can produce enormous dividends in numbers diagnosed and numbers treated”. Gore concurs: “what we in England need to learn is to have outcome measures as a key part of a strategy, to put some money towards it, and to have a clear timetable.” Scotland's total investment in the action plan is about £43 million.

England's action now depends on the forthcoming National Liver Strategy, which is currently in development by the Department of Health and the national clinical director for liver services, Martin Lombard of the Royal Liverpool University Hospital NHS Trust, Liverpool, UK. Lombard has spent the past 12 months working with government policy officials, patient and professional groups, the National Institute for Health and Clinical Excellence, and industry “to develop an understanding of how to tackle the escalating burden of liver disease in England”. Through the strategy, expected in autumn, “we want to transform outcomes for people with liver disease and the various underlying conditions that lead to liver disease”, he says.

Provision of clean injecting equipment has increased in Scotland over the past 2 years

Government commitment to tackling liver disease, including hepatitis, is clear by inclusion of chronic liver disease in outcome frameworks for the NHS and public health, says Lombard, and the National Liver Strategy must link in with the government's vision for the NHS and for public health, published in the white papers Liberating the NHS and Healthy Lives, Healthy People. “Across liver disease, there are significant numbers of patients who need help in their lifestyles to achieve optimum benefit from such a programme. This is an area where we need to do more work with key partners and different agencies”, he says.

“The temptation is going to be to focus very much on alcohol with obesity next as big headline problems”, Gore tells The Lancet. He would like hepatitis C to be the primary focus of strategy: “Out of the main causes of liver disease—alcohol, obesity, and viral hepatitis—hepatitis C is the one bit that is actually solvable in a reasonable amount of time. We could all but eradicate hepatitis C in England within the next 30 years, and make a huge dent in the prevalence in a reasonably short time, if there are clear directions to local NHS on how to go about it in a way that is easy to action.”

Alcohol and obesity must be part of the National Liver Strategy, Foster comments, “but the half million or so people with viral hepatitis deserve a very significant place. There are very large numbers of people infected, the disease burden in terms of cancer and transplantation is huge, and it's a tractable problem where we have solutions”. Conversely, he says, reducing problem drinking requires strategies that are more social than medical, to tackle marketing and availability of alcohol.

Broadly speaking, there is consensus on hepatitis C, “that we need to identify patients earlier”, says Lombard. “Key to this is the need to engage with and up-skill primary and community care services to help us to do this. We also need to do more work with those areas and populations identified as having a higher prevalence of hepatitis C such as drug treatment units, prisons, and within some ethnic groups…many more patients could be treated and prevented from progressing to advanced liver disease if we can achieve this”, he tells The Lancet.

With a new NHS structure and government looking for savings across the board, Gore wonders what will be the levers and incentives to increase testing and treatment. Without safeguards, he says, GP consortia might fail to prioritise or even reduce testing and commissioning of the expensive recommended treatments, with concomitant effects on specialist care. England already ranks second lowest of 14 comparable countries in use of drug treatments, while about a third of patients referred to hospitals in 2009 were not offered treatment, according to the 2010 audit report from the All-Party Parliamentary Hepatology Group and the Hepatitis C Trust.

Amid this uncertainty, the clinical outlook for patients is about to change radically, with the launch of new drugs boceprevir and telaprevir expected within 1 year. When added to existing treatments, these drugs can increase response rates from 40% to 70% in patients with genotype 1 virus and greatly reduce treatment times. “This will transform the picture, both for those who have failed to respond to previous treatment and for naive patients”, says Foster, but could “expose some terrible holes in our service provision”, he warns.

Lombard acknowledges that “some patients who have not responded to treatment programmes in the past may benefit from the availability of newer treatments in the future”. However, he urges, “we need to understand better, and explain better, which particular patients will benefit and what services are needed to treat them”, especially given future financial pressures, and the need to optimise efficiency in services.

Globally, Gore describes the increasing awareness of viral hepatitis B and C infection, as raised last year in a World Health Assembly resolution. July 28 will be the first annual WHO-supported World Hepatitis Day, and WHO is currently drafting a global viral hepatitis strategy. In January, the US Institute of Medicine released a report that recommends steps to improve awareness, recognition, and surveillance, plus integration of care services, to tackle hepatitis B and C in the USA. Foster comments that, “the message from Scotland is absolutely clear. If you set clear targets and you nominate individuals with clear tasks, action happens. If you set rather vague, pious wishes, nothing effective will take place.”

Source: http://www.thelancet.com/ via http://www.hepctrust.org.uk/


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What Is Hepatitis C?

Hepatitis C Information:

Hepatits C is a blood-borne viral disease which can cause liver inflamation, fibrosis, cirrhosis and liver cancer. The Hepatitis C virus (HCV) is spread by blood-to-blood contact with infected person's blood. Many people with HCV infection have no symptoms and are unaware of the need to seek treatment. Hepatitis C infects an estimated 150-200 million people worldwide. It is the leading cause of liver Transplant...

Hepatitis C is an inflamation of the liver caused by infection with the Hepatitis C virus is one of the five known hepatitis viruses: A, B, C, D & E. Hepatitis C was previousley known as non-A non-B hepatitis prior to isolation of the virus in 1989.

Symptoms of Acute Hepatitis C:

Acute Hepatitis C refers to first 6 months after infection with HCV. Remarkably, 60% - 70% of people develop no symptoms during the acute phase. In the minority of patients who experience acute phase symptoms, thet are generally mild and non-specific, and rarely lead to specific diagnoses of Hepatitis C. Symptoms of acute hepatitis C include decreased appetite, fatigue, abdominal pain, jaundice, itching and flu-like symptoms.

Symptoms of Chronic Hepatitis C:

Chronic Hepatitis C is defined as infection with the Hepatitis C virus persisting for more than six months. The course of chronic hepatitis C varies considerably from one person to another. Virtually all people infected with HCV have evidence of inflamation on liver biopsy however, the rate of progression of liver scarring (fibrosis) shows significant inter-individual variability.

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