Гепатит Б+Д

У близкого человека (Б, естественно тоже есть). Это приговор? Терапия от Б не поможет?
Сижу реву.
Есть излечившиеся?



[Сообщение изменено пользователем 02.10.2013 20:42]

В алфавите еще много буков, не ревите.

[Сообщение удалено пользователем 01.10.2013 17:01]

Насколько эффективна 2-х годичная терапия Пегасисом?
Играет ли при d какую-то роль диета?

Treatment and prevention of hepatitis D virus infection
Authors
Francesco Negro, MD
Anna SF Lok, MD
Section Editor
Rafael Esteban, MD
Deputy Editor
Jennifer Mitty, MD, MPH
Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Aug 2013. | This topic last updated: אוק 18, 2012.
INTRODUCTION — The clinical manifestations of hepatitis D virus (HDV) infection vary from benign acute hepatitis to fulminant hepatitis, and from an asymptomatic carrier state to rapidly progressive chronic liver disease. HDV is a defective virus requiring the simultaneous presence of hepatitis B virus (HBV) to fully express its pathogenicity; thus, hepatitis D always occurs in the presence of HBV. (See "Pathogenesis, epidemiology, natural history, and clinical manifestations of hepatitis D virus infection".)

In most cases of HDV infection, HBV replication is suppressed to low levels by HDV [1,2]. Liver damage in these patients is essentially due to HDV only. Occasionally, HBV and HDV replicate simultaneously, each virus contributing to the liver damage, thereby resulting in more severe liver disease [3].

CLINICAL COURSE OF HDV INFECTION — The clinical course is influenced by several factors, including the HDV genotype [4]. This issue is discussed in detail elsewhere but a brief review is warranted to provide the rationale for antiviral therapy. (See "Pathogenesis, epidemiology, natural history, and clinical manifestations of hepatitis D virus infection".)

The predominant genotype in the Western world is genotype I. Once chronic HDV infection is established, it usually exacerbates the preexisting liver disease due to HBV. Progression towards cirrhosis may be rapid, but does not occur in all patients. HDV-associated chronic liver disease may run an indolent course and asymptomatic HDV carriers have been found in some geographical areas.

Patients who are currently referred for HDV infection appear to represent cohorts infected many years ago in whom the HDV-related disease rapidly developed to cirrhosis, but whose subsequent disease progression has been slow. This was illustrated in a report from Italy in which the estimated 5- and 10-year probability of survival free of liver transplantation in patients who had already developed clinically overt cirrhosis was 49 and 40 percent, respectively [5]. A more ominous course toward liver decompensation has been documented in patients with active HBV and HDV replication [5]. In the Far East, where the predominant genotype is genotype II, there is a less frequent association of chronic HDV infection with progressive liver disease [4].

AIMS OF TREATMENT — The aim of treatment of hepatitis D is to eradicate or to achieve long-term suppression of both HDV and HBV.


■The primary endpoint of treatment is the suppression of HDV replication, which is accompanied by normalization of the serum aminotransferase (ALT) level and amelioration of necroinflammatory activity on liver biopsy. Suppression of HDV replication is documented by loss of detectable HDV RNA in serum and of HDAg in the liver. (See "Diagnosis of hepatitis D virus infection".)
■A secondary endpoint is the eradication of HBV infection, with HBsAg to anti-HBs seroconversion. There is very little information to support that current treatment is effective in achieving this goal. Eradication of HBV infection with development of anti-HBs will protect the individual from reinfection with HBV as well as HDV. Patients who have cleared HDV but who remain HBsAg positive are still at risk of reinfection with HDV. This phenomenon has been observed in chimpanzees. However, reexposure to HDV appears to cause only a mild and self-limiting hepatitis [6].

INTERFERON ALFA — The only drug approved at present for treatment of chronic hepatitis D is interferon alfa (IFNa). Peginterferon appears to be more effective than standard interferon, but data are limited. Unfortunately, only a minority of patients treated with interferon clear HDV infection. A meta-analysis of five trials comparing interferon with observation (including a total of 169 participants) concluded that there was a modest benefit in suppressing viral and liver disease activity in some patients, but such benefits were not sustained in the majority of patients [7].

The mechanism of action of IFNa in hepatitis D is unclear. IFNa does not have any antiviral activity against HDV when tested in vitro [8,9]. Thus, the efficacy of IFNa in patients with chronic hepatitis D may depend upon its antiviral effects on the helper virus (HBV) or its immunomodulatory effects. Interestingly, in vitro studies have found that HDV subverts the effect of IFNa signaling, possibly contributing to viral persistence and treatment resistance [10]. (See "Standard and pegylated interferon for chronic hepatitis B virus infection".)

Trials of standard interferon therapy — The absolute number of reported patients with chronic hepatitis D who have been treated with standard IFNa is small and the available data have shown mixed results [11-18].

Eradication of HDV infection and resolution of liver disease after IFNa treatment have been reported anecdotally in uncontrolled studies [11-13]. In one of these reports, long-term therapy with high doses of IFNa permanently suppressed HDV replication in some patients and dramatically improved liver fibrosis [13]. However, the favorable effects of IFNa have not been confirmed in all controlled trials.

In the largest multicenter trial, 61 Italian patients with chronic hepatitis D were randomly assigned to receive IFNa in doses of 5 MU/m2 three times weekly for four months, followed by 3 MU/m2 three times weekly for an additional eight months, or placebo [14]. They were then followed for another 12 months. The following results were noted:


■Eight (25 percent) of the 31 treated patients had a normal serum ALT level versus none of the 30 controls at the end of the 12-month treatment period. However, all but one of the responders had biochemical relapse after discontinuation of therapy. Only one patient had a normal ALT level at the end of the follow-up period.
■Fourteen (45 percent) treated patients were HDV RNA-negative at the end of treatment; however, a similar proportion (27 percent) of controls also became HDV RNA-negative, suggesting that spontaneous fluctuations in HDV viremia may occur. The frequency of undetectable HDV-RNA at the end of the follow-up period was not significantly different (45 versus 33 percent with placebo). The only patient with persistently normal ALT level was also HDV RNA-negative at the end of the follow-up period.
■Improvement in liver histology at the end of therapy occurred with similar frequency in the two groups (57 versus 36 percent, p = NS).

The authors concluded that IFNa therapy did not produce any appreciable benefit in patients with chronic hepatitis D.

In another smaller Italian study, 42 patients with chronic hepatitis D were randomly assigned to receive two different doses (9 versus 3 MU three times weekly) of IFNa for 48 weeks or placebo [15].


■Normal serum ALT levels at the end of treatment occurred more frequently in the patients receiving 9 MU doses of IFNa than in the other two groups (70, 29, and 8 percent, respectively).
■Complete response (normal ALT level and undetectable serum HDV RNA at the end of treatment) was also more frequent with 9 MU dosing (50, 21, and 0 percent, respectively).
■Treatment with 9 MU doses of IFNa was also associated with a marked improvement in liver histology. Five of the 10 responders in the 9 MU dose group had normal ALT levels that lasted for up to four years. However, none of the patients had sustained clearance of HDV RNA.

The authors concluded that high-dose interferon was effective in suppressing HDV replication but that the antiviral effect was not sustained. Furthermore, in a follow-up report they found that ALT normalization correlated with improved hepatic function and loss of IgM anti-HDV [16]. Compared to treatment with low-dose interferon or placebo, those who received high doses of IFNa were more likely to have clearance of HDV RNA and HBV DNA as well as improvement in histologic activity and fibrosis (including reversal of cirrhosis in some patients).

However, these optimistic conclusions have not been confirmed by another randomized, controlled trial performed in Italy that used a similarly aggressive regimen [17]. The reasons for these discrepant findings are unknown.

Factors predicting response to standard IFNa — In view of the poor overall response, it is difficult to identify factors that predict response. The only feature that may be associated with an increased likelihood of response is a short duration of disease [11,12,14].

Peginterferon — There is little published experience with peginterferon in the treatment of chronic hepatitis D [19-21]. The largest published study included 38 patients who were treated with pegylated IFN alfa-2b (1.5 MU/kg per week) alone or in combination with ribavirin for 48 weeks [19]. Most patients had previously failed treatment with standard IFN. All patients were maintained on pegylated IFN for an additional 24 weeks, and then followed off therapy for 24 weeks. At the end of follow-up, HDV RNA was undetectable in eight patients (21 percent). Treatment had to be discontinued in 25 percent of patients while 58 percent required dose modification. The response rate was similar in the monotherapy and combination therapy groups suggesting that ribavirin had no effect on the viral clearance rate. The response rate was somewhat higher in a subset of patients who had not previously received interferon-based therapy (three of eight patients).

A higher virologic response rate (43 percent) was found in another study involving 14 patients treated with 12 months of pegylated IFN [20]. The higher response rate may have been due to a lower proportion of patients with cirrhosis in the second study (28 versus 74 percent).

Peginterferon plus adefovir dipivoxil — Few studies have evaluated combination therapy for HDV using nucleoside analogues. One of the largest controlled trials included 90 patients with compensated chronic hepatitis D who were randomly assigned to peginterferon alone or in combination with adefovir, or adefovir monotherapy [22]. After 48 weeks, HDV RNA was negative in approximately 25 percent of patients in both peginterferon arms and none in the adefovir monotherapy arm. The response was sustained up to 24 weeks after stopping therapy. Thus, combination therapy appeared to offer no advantage to peginterferon monotherapy, while adefovir monotherapy was ineffective. A significant decline in HBsAg levels was observed in patients receiving peginterferon (especially when combined with adefovir) but not in patients treated with adefovir monotherapy, the clinical significance of which requires further study.

ALTERNATIVE TREATMENTS — Several drugs have been evaluated as alternatives to interferon. Overall, the results are discouraging.


■Ribavirin inhibits HDV replication in vitro [23]. It has been tested in two small trials in humans without any biochemical or virological response [24,25]. The addition of ribavirin to pegylated IFNa did not improve response [19].
■Foscarnet and acyclovir have a paradoxical stimulatory effect on HDV replication, at least in vitro [23]. However, anecdotal reports suggest that foscarnet may be beneficial in fulminant liver failure due to HBV/HDV coinfection. (See 'Treatment of acute hepatitis D' below.)
■Suramin inhibits HDV infection in vitro, possibly by blocking virus uptake or uncoating [23,26]. When administered in vivo, suramin was effective in preventing HDV infection in woodchucks only when they were inoculated with a low infecting dose [27].
■THF gamma 2, a synthetic octapeptide of thymic origin, has been shown to have some efficacy in HBV infection. However, a pilot study in 11 patients with hepatitis D found that it was ineffective [28].
■Lamivudine, a potent inhibitor of HBV replication, had little or no effect on HDV replication in two series [29,30], and no synergistic effect with high dose IFNa in two other reports [31,32].
■Antisense oligonucleotides are nucleic acid sequences that bind to RNA or DNA with a high degree of specificity, and can thereby block expression of a specific protein. Antisense therapy is being developed for treatment of HDV, but its efficacy has not yet been established [33].
■"Prenylation" involves the covalent addition of a farnesyl or geranylgeranyl isoprenoid molecule to a conserved cysteine residue at or near the C-terminus of a protein [34]. This link promotes membrane interactions with the prenylated protein, since the isoprenoid chain is hydrophobic. Specific inhibitors of HDV prenylation have been developed. In particular, the farnesyltransferase inhibitor FTI-277 prevented the production of complete infectious HDV virions of different genotypes, including the genotypes associated with most severe disease [35]. The prenylation inhibitors FTI-277 and FTI-2153 were highly effective in clearing HDV viremia in mice [36].
■Famciclovir, an acyclic deoxyguanosine analog, was of no benefit in a pilot study [37].

TREATMENT OF ACUTE HEPATITIS D — There is no specific treatment for acute hepatitis D. In one report, all three patients treated with foscarnet for fulminant hepatitis due to HDV recovered, as did two additional patients with fulminant hepatitis due to HBV alone [38]. Although these results are encouraging, they need to be confirmed. Foscarnet is an inhibitor of some viral DNA polymerases. However, it was shown to have a paradoxical stimulatory effect on HDV replication in vitro [23]. Thus, the efficacy of foscarnet in fulminant hepatitis due to HBV/HDV coinfection may be secondary to its inhibition of HBV.

PREVENTION OF HDV INFECTION — The mainstay of prevention of HDV infection is vaccination against its helper virus, the HBV. Anti-HBs-positive chimpanzees are protected against experimental HDV infection [39]. However, passive prophylaxis with hepatitis B immunoglobulin has not completely prevented reinfection of transplanted livers by HDV. In some patients, HDV virions were able to infect and replicate within the liver allograft. Nonetheless, HDV infection is abortive and does not result in recurrent liver disease unless the allograft is simultaneously reinfected with HBV. (See "Hepatitis D virus reinfection following liver transplantation".)

Vaccination against HDV — Chronic HBV infection is a serious health problem affecting approximately 300 million individuals worldwide. Apart from the morbidity and mortality associated with HBV infection, these individuals are at risk of HDV infection. Thus, every effort should be made to reduce the risk of HDV transmission to HBV carriers. The observation that chimpanzees rechallenged with HDV many years after recovery from the initial HDV infection were partially protected [6] suggests that a protective immune response is present and that vaccine strategies for preventing HDV superinfection may be feasible.

Early attempts to vaccinate woodchuck hepatitis virus (WHV) carrier woodchucks with liver derived HDAg [40] or the N-terminal portion of recombinant HDAg that contain a major immunogenic epitope [41] were unsuccessful. (See "Pathogenesis, epidemiology, natural history, and clinical manifestations of hepatitis D virus infection", section on 'Hepatitis D antigen'.)

In a later experiment, six WHV carrier woodchucks were repeatedly immunized with the full-size, recombinant, yeast-derived small form of HDAg [42]. Upon challenge with HDV, two woodchucks were not infected, as serum HDV RNA was never detected by polymerase chain reaction; two showed a transient, low level HDV viremia, and only two had a typical acute HDV infection. All control animals developed full-blown acute hepatitis D. These data showed for the first time that partial protection against HDV superinfection could be achieved by active immunization.

A similar study used the short form of HDAg expressed by recombinant baculovirus or vaccinia virus as immunogen [43]. Again, after challenge of the woodchucks with HDV, partial protection was observed even though anti-HDV was not detected. It is possible that the protection was related to induction of cytotoxic T-cell response.

However, these encouraging results were not confirmed by other investigators who used live recombinant vaccinia virus expressing either the small or the large form of HDAg [44]. The explanations for the different outcomes using vaccines that are manufactured by very similar approaches are unknown.

In another approach, three synthetic HDAg peptides were administered to four woodchucks, resulting in the production of specific antibodies. These woodchucks developed transient, low-level viremia after inoculation with HDV but none developed chronic HDV infection [45].

Thus, partial protection of HBsAg carriers from HDV infection through active immunization is feasible. The woodchucks serve as a useful animal model for evaluating HDV vaccines. However, worldwide implementation of a vaccination policy against HDV would probably prove too costly and impractical due to the need to screen for HBsAg carriers. Vaccination against HBV remains the most cost effective means to prevent HDV infection, except for individuals who are already infected with HBV.

SUMMARY AND RECOMMENDATIONS


■Although the rate of success is low, we suggest that patients with chronic hepatitis D and active liver disease, as evidenced by elevated ALT levels and/or chronic hepatitis on liver biopsy be treated and treated early, particularly if there is advanced fibrosis (Grade 2B). This is based upon the observation that chronic hepatitis D can be a severe liver disease, and that response is more likely to be attained in patients with a short duration of infection. Asymptomatic HDV carriers with normal ALT levels do not require therapy but should be monitored for signs of active disease. (See 'Aims of treatment' above.)
■The optimal treatment of HDV is uncertain. Thus, patients should ideally be treated as part of a clinical trial. As noted above, the only treatment approved for chronic HDV is interferon alfa. Before the availability of peginterferon, the recommended dose regimen was standard IFNa 9 MU three times weekly for at least 12 months, although longer treatment had been advocated. However, in light of emerging data, we suggest pegylated IFNa replace standard IFNa as the treatment of choice for chronic hepatitis D (Grade 2C). Treatment should be administered for one year; whether longer duration of treatment will improve response rates remains to be established. (See 'Peginterferon' above.)
■Available data have not demonstrated an advantage from the addition of a nucleos/tide analogue. (See 'Alternative treatments' above.)

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Это из последнего UpToDate. Достаточно авторитетный и подробный разбор, ориентированный в основном на врачей. Извините, на английском. Если есть интерес - переводите.

Если острая форма, то может и есть вариант излечиться. Если это хроническая форма, то скорей всего лечение бесполезно, потратите деньги и дополнительно здоровье различных органов.
Сдайте 1.общие анализы крови 2. кол-во вируса+маркеры к гепатиту 3. желательно проверить печень на фиброз(обязательно, если анализы плохие или общее состояние).
Если все анализы в норме-1.антиалкоголь(строго!!! он с вирусом напару убивает печень, длительное время незаметно) 2.антижирное-острое 3.душевное спокойствие(у всех при появлении этой шняги появляются депресняки, как следствие сложности в семье и на работе, люди держите себя в руках!!!!)
Но вообще, если с гепатитом Д, течение болезни проходит намного тяжелей, чем просто"В",кто-то сидит на Бароклюде пожизненно.

Фиброскан сегодня будет, остальное - в процессе.


А разве Бараклюд влияет на д?

Вот чего не понимаю, того не понимаю. Идти на публичный форум, где какие-то незнакомые юзеры без имени и регалий напишут тебе что де не тратьте деньги и время. Вместо того чтобы проконсультироваться с лечащим врачом и задать все вопросы ему при очной встрече. Я понимаю желание найти "второе мнение", но не обывательское же.

ЗЫ. Текст на английслом, который вы так яростно минусите - между прочим последний и самый актуальный обзор по сабжу и он дает ответы на Ваши вопросы. И между прочим, это платная база данных (600$ в год индивидуальная лицензия), т/е/ информация, которую вы вряд ли найдете в открытом доступе.

Да, мой первый пост, по большей части, был написан на эмоциях. С врачом говорили, наметили кое-какие этапы в дальнейшем обследовании.
Но, мой вопрос

остается актуальным.
Было бы здорово, если бы на этом форуме нашлись люди с такой же проблемой (а именно гепатит б+д), прошедшие терапию интерферонами удачно.
В поиске смотрела, там, в основном, только гепатит с обсуждается.



[Сообщение изменено пользователем 02.10.2013 13:55]

Я полгода пробегал по врачам(у меня ГепВ), не зная что нужно делать, много денег и времени потратил на лишние поездки, не зная какие анализы нужны и где их сдавать. Я человеку посоветовал, чтобы он был подготовлен в случае похода к врачу, а не так чтобы его каждый раз отправляли за новыми анализами и похихикивали над ним. И выразил общесложившееся мнение по поводу лечения.

http://www.hv-info.ru/gepatit-forum/
Зарегистрируйтесь здесь, много чего дельного можете узнать, там есть болные б+д.
Скорей всего Вам назначили гепотапротекторы, очень внимательно изучайте их, большая часть из них бесполезна!

Не знаю, но знаю двоих людей Б+Д, вроде как принимают Бараклюд с диагнозом "пожизненно".

Все, приплыли. По фиброскану F4, цирроз.

Пока ничего не назначили.

Мы готовы и Пегасисом лечиться, лишь бы помогло.

С терапией не торопитесь, внимательно все изучите, как следует проконсультируйтесь с врачами, есть разные терапии, которые могут быть бестолковыми и пагубно влиять на другие органы. Еще есть программы бесплатного лечения, я на такой стою, но ждать около 2лет.
F4 это очень серьезно и терапия скорей всего нужна будет. Очень важно отнеситесь к алкоголю и диетам. У меня после отказа от алкоголя и боле-менее правильного питания через два месяца анализы почти в два раза улучшились и почти пришли в норму. Главное не отчаивайтесь и моральная поддержка, если лечение назначат, то оно длительное.
на сайте зарегистрируйтесь, там по маленьку консультируют, врачи с центральных городов, ну и больные с опытом лечения есть.

Уже консультируемся



Если не сложно скиньте в личку как встать в очередь. Может, пригодится для второго курса.


Диету соблюдаем, алкоголь вообще не принимает.


Спасибо за информацию. Уже регистрируюсь.

У кого-где?
Сходите к Тихомировой (Доктор Плюс) на прием

Сколько там кПа?

IQR (Kpa) 3.1
CS (KPa) 13.5
Stiffness (KPa) 14.3

[Сообщение изменено пользователем 02.10.2013 22:29]

Самое начало
Надо убирать вирусную нагрузку и ждать что печень восстановится до приемлемого уровня - это реально.
Ссылку на один из многих гепатитфорумов уже дали - вперед!

Спасибо!