Hepatitis B Annual

: 2010  |  Volume : 7  |  Issue : 1  |  Page : 57--72

Treatment options for HBV with co-morbid conditions

AK Seth 
 Dr BL Kapur Memorial Hospital, Pusa Road, New Delhi, India

Correspondence Address:
A K Seth
Dr BL Kapur Memorial Hospital, Pusa Road, New Delhi - 110 005


The treatment for Hepatitis B viral infection without any co-morbidities is relatively simpler, although the outcome remains suboptimal. However in a large number of these patients, the matter is complicated by co-morbid conditions which exist in these patients and the treatment in such patients has to be tailored to individual settings and demands. All patients of chronic hepatitis B [CHB] must be evaluated for co-morbidities especially those which can complicate treatment. This overview attempts to provide clinicians with guidance for treatment of CHB patients who have coexisting co-morbidities.

How to cite this article:
Seth A K. Treatment options for HBV with co-morbid conditions.Hep B Annual 2010;7:57-72

How to cite this URL:
Seth A K. Treatment options for HBV with co-morbid conditions. Hep B Annual [serial online] 2010 [cited 2023 Sep 26 ];7:57-72
Available from: https://www.hepatitisbannual.org/text.asp?2010/7/1/57/162141

Full Text


The prevalence of HBV co-infection in HIV-infected patients is approximately 10%. Both share transmission patterns and risk factors. Among the estimated 40 million persons infected with HIV worldwide, an estimated 2-4 million have CHB. In HIV-infected persons, an estimated 2-4 million have chronic HBV co-infection and 4-5 million have HCV co-infection. HBV, HCV and HIV share common routes of transmission, but they differ in their prevalence by geographic region and the efficiency by which certain types of exposures transmit them. Among HIV-positive persons studied from Western Europe and the USA, chronic HBV infection has been found in 6-14% overall, including 4-6% of heterosexuals, 9-17% of men who have sex with men (MSM), and 7-10% of injection drug users. HCV infection has been found in 25-30% of HIV-positive persons overall; 72-95% of injection drug users, 1-12% of MSM and 9-27% of heterosexuals. The characteristics of HIV infected persons differ according to the co-infecting hepatitis virus, their epidemiologic patterns may change over time, and surveillance systems are needed to monitor their infection patterns in order to ensure that prevention measures are targeted appropriately. [1]

CHB prevalence is higher among HIV-infected persons than among the general population. HIV co-infection tends to accelerate the natural history of HBV and co-infected patients tend to have more histologically advanced disease and higher rates of liver related mortality. All HIV positive individuals should be screened for HBsAg and anti-HBs and if negative should be vaccinated (three double doses is recommend for such immunosuppressed individuals). The treatment of the co-infected individual is complex and ideally these patients should be managed by a multidisciplinary approach by specialists with an understanding of both infectious disease and liver disease. An understanding of the activity of various nucleoside analogues against both viruses, the potential for hepatotoxicity with certain HIV medications and issues regarding timing of HIV therapy are required. [2]

CHB does not significantly affect the course of HIV disease, but HIV does alter the course of CHB.

HIV-infected persons are less likely to clear acute HBV infection spontaneously, will more likely have a higher level of HBV replication, and face a higher risk of liver-related death than those monoinfected with either virus. Conditions associated with CHB are currently among the leading causes of hospital admission and death in the HIV-infected population. Therefore, the adequate management of CHB is now being considered a priority in HIV/HBV co-infected patients. [3]

 Goal of Therapy

The principal goal of treatment in co-infection are the same as monoinfection, i.e., prevent or delay the development of complications of cirrhosis, decompensation and hepatocellular carcinoma. To achieve this, treatment objectives are:

HBV DNA suppression (<2000 IU/mL; preferably PCR undetectable <50 IU/mL)ALT within normal limitsHistological improvement.

All patients with detectable HBV DNA should be treated. The optimal time to initiate CHB treatment in HIV co-infected patients has not been established. Based on available evidence, consensus suggests using the HBV DNA criteria applied to CHB-monoinfected patients. These depend on HBeAg serostatus. In HBeAg-positive patients, a serum HBV DNA level >20,000 IU/ml justifies consideration of treatment. In HBeAg-negative patients, the cut off is a serum HBV DNA level >2,000 IU/ml. ALT levels also should be considered. If the results of liver function tests are out of proportion to HBV DNA levels, check for other causes of liver disease. Patients who do not meet criteria for anti-HIV treatment should undergo a biopsy to evaluate the hepatic inflammation and fibrosis stage. Those with a METAVIR ≥A2 and/or ≥F2 should receive CHB therapy.

 Treatment Considerations

[Table 1] {Table 1}

Co-infected patients who do not meet criteria for anti-HIV highly active antiretroviral therapy (HAART) treatment

In HBeAg-positive patients, consider pegIFN or ADV. Typically, pegIFN is not preferred for the treatment of HBeAg negative patients, because the chance to achieve HBsAg seroconversion and to maintain HBV DNA suppression off therapy is low. These patients should not receive agents with dual (anti-HIV) activity (e.g. LAM, ETV,TDF, and FTC) as it raises the risk of early HIV resistance, and may limit future HIV therapeutic options. Patients generally need long-term maintenance therapy and combination therapy.

Co-infected patients who meet criteria for anti-HIV (HAART) and CHB treatment

The immune restoration associated with highly active antiretroviral therapy (HAART) can improve control of HBV replication and loss of HBeAg in some patients, but can also lead to increased immune-mediated liver injury. On balance, use of HAART before severe immunosuppression develops may be beneficial. Still, the complexity of CHB, HIV, and HAART interactions must be evaluated for each individual. HAART that includes two dual-acting drugs (e.g. LAM, TDF, FTC) constitutes the preferred option for these patients. The best choice is to combine a nucleoside and a nucleotide analogue to prevent long-term resistance (i.e., TDF plus LAM or FTC). ADV can be substituted for TDF if the latter is contraindicated or otherwise not a desirable option. Similarly, ETV offers an alternative to FTC or LAM.

If HAART treatment is altered because of intolerance or lack of efficacy, the CHB component should be continued, or substituted with another agent. Stopping CHB therapy has been associated with HBV reactivation and ALT flares. If the patient has achieved HBeAg seroconversion an adequate course of consolidation treatment must be undertaken prior to discontinuation of CHB treatment.

Co-infected patients who meet criteria for HAART only

Individuals with persistent controlled HBV replication may not need agents with dual activity. Monitor ALT and serum HBV DNA every 3 or 4 months. If CHB treatment does not begin at the same time as ART, delay its introduction until HIV replication is controlled or there is evidence of liver disease. Specifically, monitor HBV DNA for the anti-HBV treatment thresholds.

Co-infected patients with LAM-Resistance

LAM resistance is reported to be higher in HBV/HIV coinfection. Detectable HBV viraemia >200 IU/mL at 48 weeks is a risk factor for the development of CHB drug resistance. These patients require a HAART regimen with maximum activity against both viruses. LAM should be maintained and ADV or TDF should be added.

Co-infected patients with cirrhosis

As preventing resistance and ensuring compliance are paramount considerations, cirrhotic patients should receive combination CHB therapy (e.g., TDF plus FTC or LAM included in the HAART regimen or ADV plus ETV or LdT, if there is no indication for anti-HIV therapy). Patients with cirrhosis should be monitored closely during the first 12 to 24 weeks of therapy because of risk of ALT flare and immune reconstitution hepatitis. Serum HBV DNA should be assessed every 12 weeks. This is especially true for those with CD4 counts <200 cells/mm 3 . Patients with liver decompensation should be treated with combination anti-HBV therapy and considered for liver transplantation.

 Co-Infection HBV / HCV

HBV and hepatitis C virus (HCV) co-infection is common. Patients who are co-infected represent a unique group with diverse serologic profiles. In patients with CHB, estimates of the rates of HCV coinfection vary from 9 to 30%, depending on the geographic region. These numbers may underestimate the true number of patients with both viral infections because no large-scale studies have been performed, and there is a well-described phenomenon of "serologically silent" occult HBV infection (i.e., patients with negative HBsAg but detectable serum HBV DNA) in patients with chronic hepatitis C (CHC). Combined CHB and C leads to more severe liver disease, higher rates of cirrhosis with decompenation and an increased risk of hepatocellular carcinoma. Co-infected HBV/HCV patients represent a treatment challenge. Several studies have shown that the two infections interact with each other, affect immune responses and can reciprocally (and simultaneously) inhibit each other. Either virus can play a dominant role and both viruses have the ability to induce seroconversion of the other. The chronology of infection has a role in determining the dominant virus; and HBV and HCV can alternate their dominance. However, the overall dominant effect appears to be HCV suppression of HBV. Furthermore, co-infected patients have been demonstrated to have lower levels of both HBV DNA and HCV RNA than corresponding monoinfected controls, indicating that concurrent suppression of both viruses by the other virus can also occur.

In most patients, HBV replication is suppressed while HCV replication remains active. However, the opposite has also been observed. Patients with HCV and HBV co-infection tend to have more severe chronic hepatitis, and cirrhosis and HCC are more common. There is little information on the efficacy of antiviral treatment in such patients. [4]

 Goal of Therapy

The principal goal of treatment in co-infection are the same as monoinfection, i.e., prevent or delay the development of complications of cirrhosis, decompensation and hepatocellular carcinoma. To achieve this, treatment objectives are:

HBV DNA suppression (<2000 IU/ml; preferably PCR undetectable <50 IU/ml)ALT within normal limitsHistological improvement.


 When to Treat

There is no currently established standard of care for patients who are co-infected with HBV and HCV, although assessment of the "dominant" virus is helpful in determining a treatment strategy.

Thorough serologic and virologic testing is required in dually infected patients prior to consideration of therapy. Caution must be taken with treatment of co-infected individuals, as exacerbations of liver disease after initiation of therapy have been described, likely due to loss of viral suppression from the successfully treated dominant virus. Patients are candidates for therapy if they meet the inclusion criteria for standard treatment guidelines for either HBV or HCV monoinfection.

 Treatment Considerations

Treatment should be individualised based on patient variables such as serologic and virologic profiles, patient's prior exposure to antiviral treatment, and the presence of other parenterally transmitted viruses such as hepatitis D virus and HIV [Table 2]. In general, the same treatment criteria should be applied to patients who are HBV/HCV dually infected as are applied to monoinfected patients.{Table 2}

Co-infected patients with HCV dominant disease

PegIFN plus ribavirin treatment in standard doses is a possible option. To date, IFN plus ribavirin treatment has been well studied and has proven efficacy. An initial study using the addition of LAM to IFN was effective in coinfected patients with CHC and active HBV replication. Future studies are needed to assess the effectiveness of pegIFN as well as triple therapy with an antiviral, IFN and ribavirin in coinfected patients.

Co-infected patients with HBV dominant disease

PegIFN/IFN, with or without ADV or ETV, is a reasonable option.

Co-infected patients with decompensated cirrhosis

Referral to a transplant centre is indicated for patients with decompensated cirrhosis, fulminant hepatitis, or HCC in appropriate patients. A few studies have found the survival of patients with CHB/CHC monoinfection was worse than that of dually infected patients, suggesting a possible beneficial role of HCV in the immunosuppressed post-transplant population.

Triple infection with HCV/HBV/HDV

Few treatment studies have been published, but pegIFN/ IFN is a reasonable treatment option despite the lack of data to support its use.

Triple infection with HCV/HBV/HIV

Infection of HIV must be controlled before treatment of viral hepatitis can be considered. Few studies have been performed on treatment of patients with triple infection, so treatment algorithms are often extrapolated from results of trials of patients with either HBV/HIV or HCV/HIV co-infection. As no standard of care exists for these patients, individual care plans should be coordinated with an HIV specialist and hepatologist.

 Co-Infection HBV/HDV

Hepatitis delta virus (HDV) can be considered as a satellite of HBV and only infects patients with preexisting HBV infection. HDV is most often transmitted by contact with contaminated blood and body fluid, similar to HBV infection. Approximately 5% of the global HBsAg carriers are also co-infected with HDV, leading to a total of 10 - 15 million HDV carriers worldwide. Seroprevalence studies of anti-HD in HBsAg-positive patients has shown a worldwide but not uniform distribution. High prevalence areas of HDV infection include some Pacific Islands, Pakistan, Western Asia, Italy, some parts of Eastern Europe, the Amazon basin, Venezuela and Columbia. Foci of high HDV prevalence continue to be identified as in the case of the island of Okinawa in Japan, areas of China, Northern India and Albania. Acute HDV infection can occur concurrently with HBV infection (co-infection) or in a patient with established HBV infection (superinfection). Around 70-90% will progress to chronicity and follow a rapid progressive course to cirrhosis (up to 70% of CHD patients develop cirrhosis). In the superinfection setting, about 15% developed cirrhosis within 1-2 years and 21% within 5 years of disease onset. This indicates HDV infection plays an important role in the progression of HBV related liver diseases. As the spread of HDV is linked with HBV, strategies to decrease the incidence of HBV will result in a corresponding decrease in CHD, e.g. universal HBV vaccination and post-exposure prophylaxis will help eliminate HDV co-infection in the future. Education to reduce high risk behaviours among persons with CHB will also reduce the incidence of HDV superinfection.

 Goal of Therapy

The principal goal of treatment in co-infection are the same as monoinfection, i.e. prevent or delay the development of complications of cirrhosis, decompensation and hepatocellular carcinoma. To achieve this, treatment objectives are:

HBV DNA suppression (<2000 IU/mL; preferably PCR undetectable < 50 IU/mL)ALT within normal limitsHistological improvement.



 Treatment Considerations

CHD is difficult to treat but, as the risks of end-stage liver disease are higher, active therapeutic intervention for CHB and D is required. IFN treatment has proven efficacy in CHD. Although the response to IFN varies and occurs at different time points, sometimes after discontinuation, the rate of response is generally proportional to the dose of IFN, with 9 million units (MIU) three times a week being more effective than 3 MIU thrice weekly. In CHD patients, there is no evidence that ribavirin, acyclovir or LAM, alone or in combination with IFN-based therapy, enhances treatment outcomes.

As side effects may prohibit IFN use, pegIFN treatment in standard doses for one year is a promising option. Persistent disappearance of HDV RNA after 6-12 months of treatment with pegIFN in previous IFN nonresponders has recently been reported. In small studies, a sustained virological response (categorized as undetectable HDV RNA by PCR and normalisation of ALT six months after treatment) was achieved in 17- 43% of CHD patients. Sustained biochemical responses were higher in these studies. Nonresponders were identified by a <3 log decrease of HDV RNA at 6 months of treatment.

 Chemotherapy and Immunosuppressive Therapy

Reactivation of HBV is a serious cause of morbidity / mortality in patients undergoing cytotoxic or immunosuppressive therapy. While the majority of cases have been reported among patients who are HBsAg positive, any previous exposure to HBV infection (HBsAg-negative, anti-HBc) increases risk of reactivation. Patients in this group can suffer from reactivation in response to immune suppression either as a result of cancer chemotherapy, short courses of corticosteroids, immunomodulatory agents (anti-cytokines), heart, kidney and liver transplantation and even as a result of advancing immune deficiency due to HIV infection. Rates of HBV reactivation in HBsAg positive patients receiving chemotherapy can be as high as 70%. Mortality rates, primarily related to liver failure, range from 4 - 60%. Reactivation also leads to interruption of anticancer treatment and jeopardise the patient's prognosis. Treatment delays for up to 100 days contribute to lower disease free and lower overall survival for these patients. In a study of breast cancer patients, over 70% with HBV reactivation required premature termination of chemotherapy or disruption of treatment.

Reactivation of HBV infection may occur during or after completing a full course of chemo- or immunosuppressive therapy. Enhanced viral replication may occur during intense cytotoxic or immunosuppressive therapy or may be related to the restoration of immune function following withdrawal of cytotoxic or immunosuppressive therapy, which causes rapid immune-mediated destruction of infected hepatocytes.

 When to Treat

HBsAg screening (and HBcAb measurements) should be performed in all patients prior to initiation of chemo- or immunosuppressive therapy. All patients undergoing bone marrow or solid organ transplantation and some forms of monoclonal antibody therapy (rituximab, infliximab, etc.) should be screened for HBV markers prior to treatment. Recipients of organs (e.g. kidney, lung) should receive LAM prophylaxis for at least the first post-transplant year during which time immunosuppression levels are at their highest.

 Treatment Considerations

HBV naïve patients should be immunized against hepatitis B, as should haematopoietic stem cell donors.

HBsAg or HBV DNA positive patients

Prophylactic antiviral therapy is recommended in all HBsAg positive patients at the onset of chemo- or immunosuppressive therapy to improve clinical outcomes. The greatest experience in preventing HBV reactivation with chemotherapy has been with LAM. Several studies have shown that preemptive prophylactic LAM can prevent or at least ameliorate the course of reactivation. Delaying therapy until HBV DNA levels rise is ineffective. Preemptive prophylactic LAM therapy has also increases the likelihood of patients completing their chemotherapy without interruption. In immunosuppressed patients, a cumulative resistance rate of 41% after 31 months in HBsAg positive patients receiving LAM has been observed. In these cases, the administration of additional or alternative antiviral drugs such as ADV may be necessary. The optimal duration of LAM prophylaxis remains controversial. People with high baseline HBV DNA > 2,000 IU/ml should continue treatment until they reach treatment end points for CHB. Those with baseline HBV DNA < 2,000 IU/ml should continue treatment for at least 1 year following the completion of chemotherapy. However, some patients, based on their liver histology and viral status may require treatment indefinitely. While studies to date have focused on LAM, ETV with an improved resistance profile may be an alternate treatment, particularly in patients who require more than 12 months of therapy in whom there is a higher risk of resistance to LAM. PegIFN / IFN should be avoided in view of the bone marrow suppressive effect and the risk of exacerbating immune-mediated diseases (autoimmune disorder, graft rejection, or graft vs host disease).

HBsAg negative patients

Although the risk of reactivation may be low (<5%) in these patients, reemergence of HBV may be severe and even fatal. If nucleoside analogues are not used prophylactically in anti-HBc positive patients, these individuals should be monitored regularly with ALT and HBsAg testing every 1-3 months and antiviral therapy should be initiated as soon as there is evidence of HBV reactivation, without waiting for a rise in ALT. While HBV reactivation can occur in persons who are HBsAg negative but anti-HBc and anti-HBs positive, and in those with isolated anti-HBc, this is infrequent, and there is not enough information to recommend routine prophylaxis for these individuals. All patients undergoing cytotoxic / immunosuppressive therapy should be checked for HBV serologic markers and serum HBV DNA levels.

 Organ Transplant Patients

CHB frequently requires liver transplantation. Reactivation of HBV after organ transplantation in HBsAg carriers may be fatal. Other solid (non-liver) organ transplants can also get infected de novo or through reactivation from previous active or inactive infections. CHB infection in kidney, heart, and other organs has become a serious long-term problem and an important co-morbidity affecting graft and patient survival.

For much of the 1990s, CHB was considered a formal contraindication for liver transplantation, since recurrence of infection without prophylaxis occurs in 75 - 90% of the patients, with significant morbidity and mortality and few therapeutic alternatives. Significant improvements in surgical techniques and immunosuppressive regimens, means organ transplantation has become the most effective and lifesaving therapy for patients with chronic renal failure, acute and chronic liver failure, hepatocellular carcinoma, heart failure and respiratory failure.

 Goal of Therapy

The principal goal of treatment is to prevent or delay the development of complications of cirrhosis, decompensation and hepatocellular carcinoma. To achieve this, treatment objectives are:

HBV DNA suppression (<2000 IU/ml; preferably PCR undetectable <50 IU/ml)ALT within normal limitsHistological improvement.

 Treatment Considerations

All patients awaiting solid organ transplantation should be vaccinated against HBV, although the likelihood of an effective antibody response is low. Recipients with documented seroconversion following HBV vaccination and persistent protective levels of anti-HBs (>10 IU/ml) do not require antiviral prophylaxis.

HBeAg-negative/HBV DNA-negative

No treatment is necessary prior to transplantation. HCC screening with alpha-fetoprotein levels and imaging of the liver every 6 months is recommended.

High-risk group (HBeAg-positive/HBV DNA-detectable)

In order to prevent HBV recurrence post-transplant, and control viral replication to the lowest possible level at the time of surgery, patients should be commenced on antiviral therapy at the time of placement on the transplant waiting list (if not before) and started on combination LAM plus HBIG during the anhepatic phase or immediately post-operatively. Resistance occurs more frequently, and at an earlier time point in the transplantation setting with immunosuppressed patients. Life-long combination prophylaxis with low-dose intramuscular HBIG and LAM is effective in preventing recurrent HBV, may protect against the emergence of resistant mutants, and is significantly more cost-effective than HBIG monotherapy, or high dose HBIG combination therapy. In patients with YMDD mutations and evidence of viral reactivation, combination of LAM and ADV, or the latter alone, is recommended. ADV is effective and safe in wait-listed or post-transplantation CHB patients with LAM-R and prevents graft reinfection with or without HBIG.

Low-risk group (HBeAg-Negative/HBV DNA-Negative)

HBIG should be initiated during the anhepatic phase. LAM and/or ADV (in presence of YMDD mutations) should be given starting the day of the transplant and both monthly intramuscular low dose HBIG and an antiviral drug should be given indefinitely.

HBsAg-negative/HBV DNA-negative/anti-HBc-positive/anti-HBs-positive

No treatment is necessary prior to transplant since the risk of recurrence is very low.

 Pregnancy / Lactation

Women with CHB generally do quite well during pregnancy, provided they have not progressed to decompensated cirrhosis. While there are case reports and studies indicating an increased incidence of maternal and neonatal morbidity (e.g. premature delivery, raised incidence of antepartum haemorrhage, foetal distress, meconium peritonitis, and gestational diabetes), as a general rule, a stable liver equals a safe pregnancy.

During pregnancy all markers of liver function (e.g. AST, ALT and total bilirubin) are generally reduced or low due to the expansion of extracellular fluid and pregnancy-associated immunosuppression.

The only exception is serum alkaline phosphatase, elevated due to ALP of placental origin. In late in pregnancy, or shortly after delivery, many HBeAg-negative and positive women experience significant increases in both ALT and viral load. Vertical transmission, in one study, was only seen in HBeAg positive mothers with very high levels of viraemia.

HBsAg-positive women who become pregnant may continue treatment only if the potential benefit of treatment outweighs the risk to the foetus. Careful consideration should be given to discontinuing pegIFN / IFN (Category B3) and antiviral therapy (Category B3) unless absolutely indicated. Given the uncertainties regarding foetal risks, no clear recommendations on treatment can be made at this time.

Mother to child transmission occurs often, either in utero or through exposure to blood or blood contaminated fluids at, or around, birth. The risk of perinatal transmission is associated with the HBeAg status of the mother. If a mother is positive for both HBsAg and HBeAg, 70% to 90% of her children become chronically infected. If a mother is HBsAg-positive but HBeAg-negative the risk of transmission is significantly lower.

HBsAg screening

All pregnant women should be screened for HBsAg, even if previously tested or vaccinated.

Modes of delivery

Although elective caesarean delivery has been proposed as a means of reducing mother to child transmission, the mode of delivery does not appear to have a significant effect.

Management of infants

All infants born to HBsAg positive women should receive hepatitis B vaccine and Hepatitis B Immunoglobulin (HBIG) (0.5 ml) ≤12 hours of birth, administered at different injection sites. HBIG and concurrent hepatitis B vaccine have been shown to be 95% efficacious in the prevention of perinatal transmission of HBV. The evidence on immunization for infants of HBsAg positive mothers is strong, and weaker for HBeAg-negative patients. In general, the risk of perinatal transmission from HBeAg-negative mothers for hepatitis is considered much lower than that from mothers who are HBeAg-positive. Further, the infants of HBeAg-negative mothers often clear an asymptomatic infection.

Management of pregnant women with high viral loads

The efficacy of HBIG and the hepatitis B vaccine may be lower in mothers with very high serum HBV DNA levels (>8 log10 IU/ml) at the time of delivery. In these patients there is some limited evidence to suggest LAM, taken in the last month of pregnancy, may reduce high viral load and reduce, but not eliminate, the risk of child vaccination breakthrough. At this stage the evidence does not support routine use of antiviral agents during the third trimester of pregnancy to reduce the risk of vertical transmission and pregnant women with high levels of HBV DNA should be referred to specialists for consideration of this treatment.


HBsAg-positive mothers are encouraged to breastfeed their babies. The benefits of breast-feeding for the health of an infant far outweigh any theoretical increased risk. While HBV has been isolated in breast milk, the risk of HBV transmission is very low and comparable for both breast-fed and formula-fed infants. Transmission may be more common in women with the HBeAg.

It is recommended that the baby breast feeds after the administration of the HBIG. As the virus is most commonly passed by blood-to-blood routes, mothers should be counselled to take good care of their nipples, ensure proper latch-on and allow the nipples to dry before covering to avoid cracking or bleeding. Breastfeeding should be avoided if the mother has cracked or bleeding nipples.


Testing for comorbidities should include a comprehensive medical history that focuses on cofactors associated with more progressive liver injury, and it should cover other viral liver diseases, tuberculosis pregnancy, etc . Co-infection can complicate treatment. People with liver damage due to chronic hepatitis are more likely to experience hepatotoxicity (liver toxicity) related to anti-HIV drugs. In addition, drugs used to treat HIV and hepatitis can interact and side effects may be exacerbated.

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Conflict of interest

There are no conflicts of interest.


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