ASHM Report Back

Clinical posts from members and guests of the Australasian Society for HIV, Viral Hepatitis and Sexual Health Medicine (ASHM) from various international medical and scientific conferences on HIV, AIDS, viral hepatitis, and sexual health.

HIV Co-infections, hepatitis B, hepatitis C and TB

Normal 0 false false false EN-AU X-NONE X-NONE /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-priority:99; mso-style-parent:""; mso-padding-alt:0cm 5.4pt 0cm 5.4pt; mso-para-margin-top:0cm; mso-para-margin-right:0cm; mso-para-margin-bottom:10.0pt; mso-para-margin-left:0cm; line-height:115%; mso-pagination:widow-orphan; font-size:11.0pt; font-family:"Calibri","sans-serif"; mso-ascii-font-family:Calibri; mso-ascii-theme-font:minor-latin; mso-hansi-font-family:Calibri; mso-hansi-theme-font:minor-latin; mso-bidi-font-family:"Times New Roman"; mso-bidi-theme-font:minor-bidi;}

CROI formally opened yesterday evening. The format for the opening session of this conference is reliable and runs to its own format. Very little formality, straight into the science and accessible.

This year the first plenary, dedicated to Bernard Fields, was on Hepatitis C, a tiny bit of co-infection but largely monoinfection. It was given by Charlie Rice from the Rockerfeller. Hepatitis C has increasingly been making inroads into CROI and I think this is a great move. Rice commented on the prominence of HCV in this program. While it is not a retrovirus, it is a common opportunistic infection of HIV and we were told that globally about a third of people with HIV also have hepatitis C.

Like all good plenaries the lecture was general enough to be understood by a wide audience, covered the history, outlined some of the challenges and did some speculating. If you are looking for a comprehensive timeline for HCV science have a look at the earlier slides in this presentation. I found it very informative.

Hearing about the problems scientists have experienced in working with the virus were interesting, but I couldn't help thinking "they can't have been that difficult or you wouldn't have got to a cure so quickly." Charlie then went on to summarise the great leaps in treatment efficacy, which I think most of the Australians are familiar with.

In closing he revisited his comments about the difficulties in not have animal models and the practical issues this causes in looking at things like:

  • why some people don't respond to treatment
  • why others do or don't have improvement in their liver health, and
  • why still other's go on to develop liver disease or cancer even if the virus is cleared.

At that stage I ate my words about cure.

The last few minutes of this talk were very poignant:

  • about a trillion visions are produced each day,
  • the drugs have the potential for resistance resistance, and
  • efforts have been focused on treatment rather than vaccine development.

Lastly, accompanied by a photo of the lab dog, he summarised some of the potential animal models. I recommend that you have a look at the presentation. It is up on the CROI webcast site http://www.croiwebcasts.org

 

Tagged in: croi2015

Take- home messages for GPs with patients with HCV

1. There are much more effective Hep C drug regimes becoming available that produce high cure rates.

- in general terms the newer drug regimes, called Interferon-free Direct acting antivirals (DAAs), are achieving >95% cure rates in HCV genotype 1, and not much less in HIV co-infected patients.They are daily oral tablets as opposed to previous injections, better tolerated and require much shorter durations of treatment (usually 12wks) than previous regimes.

- HCV genotype 3 requires a different drug regime to Genotype 1. More recently treatment has changed from Pegylated Interferon and Ribavirin (PEG/INF/RBV) regimes to Sofosbuvir and Ribavirin for 24wks.

- in HIV co- infected patients on cART( combination anti-retroviral treatment) some regimes increase risk of renal toxicity and renal impairment and so regular renal monitoring, including  serum Creat, eGFR, Phosphate and urine Protein/ Creat Ratio, usually  on a 2-4 wkly basis is suggested in early treatment.

- remember to consider cART and HCV drug-drug interactions.

2. Diagnostic testing- "if you can't identify who your patient's are you can't treat them"

- in at risk patients test antibody to Hep C (Anti-HCV) and if positive then do HCV RNA , understanding that in early infection there is a sero-negative window where HCV RNA won't be present and hence you should repeat the test again a few weeks later.

- early diagnosis is even more important in order to enable early treatment with a view to preventing progression to cirrhosis, liver failure and cancer in those who develop chronic hepatitis but also importantly to prevent virus transmission to others ( treatment as prevention).

- remember that upto 50% of patients spontaneously clear the virus, most of those within 2-6 months.

3. In HCV/ HIV Co- infection liver disease is accelerated. There is a 3x risk of progression, which is also more rapid, to cirrhosis and decompensated liver disease.

4. Clinicians, including GPs should determine the severity of liver disease using clinical examination, laboratory tests- including Bilirubin, PT, INR, Albumin. In addition, other specialist investigations are used to determine hepatic fibrosis, include non- invasive imaging such as Fibroscan and direct serum biomarkers such as Fibrospect II. Liver biopsy is usually preserved for instances where there is discordance in the other results. Tools such as the Child- Pugh- Turcotte Score ( CTP) and the Model for End stage Liver disease (MELD) help to determine disease severity and to guide management decisions

5. Be aware that 5-7% of Child's A ( mild) cirrhotics progress to decompensated liver disease each year and hence regular review, at least 6 monthly, is recommended.

6. Screen for Hepatocarcinoma. Remember that in those with chronic disease and liver fibrosis cure does not remove the risk of hepatocarcinoma.

7. Consider organising Gastroscopy to screen for oesophageal varices.

Tagged in: croi2015

Tracy Swan from the Treatment Action Group in New Your provided a brief yet comprehensive over view of where we are at in relation to hepatitis C treatment access. The webcast from this session is now available on  the HIV Drug Therapy Glasgow 2014 website http://hivglasgow.org/

Or you can go to the specific talk. http://aps.mediasite.com/mediasite/Play/aae59f4f5518478ab61316c0e86530581d There is also an excellent talk at the end of this session which tries to explain the drug regulatory system, and role of generics, predominantly in Europe.  by Pauline Londeix

 

Tagged in: Glasgow2014 VH 2014

I caught up with Sanjay Bhagani and asked him about his comments from day 1 about the timing of hepatitis C treatment commencement:

Could you elaborate on the safety of delaying treatment in people with advancing hepatitis C disease both in mono infection and HIV co-infection:

The question is 'When is it too late to treat hepatitis C?' In other words, when are people started on hepatitis C treatment not going to benefit; when are you are not going to prevent decompensating and needing liver transplant? This is a key area where we are going to get data over the next year or two. A number of countries are advocating the treatment of people with end-stage liver disease because of the high cost of treatment. The NHS has put in an scheme to treat 500 people with advanced disease Child-Pugh B or liver cirrhosis and I can tell you that at the Royal Free we have a number of people who are decompensating despite having started treatment. This will certainly give us an idea of when is it too late to treat people.

So when should we start?

Hepatitis C is not just a disease affecting the liver. It is a multi-system disease. It can cause renal disease, brain disease, cardio vascular disease as well as liver disease. All of these need to be considered. The concept of simply waiting until the liver is diseased might be delaying too late.

Many of these comorbidities are seen in HIV. Do they have a cumulative effect?

Certainly the data is emerging that having another virus as well as hepatitis C means that you are doubling-up on your inflammatory response. Controlling HIV is all well and good and we have been able to do that fairly effectively for some time. But if you have another virus that causes inflammation that may defeat the objective of reducing the inflammatory effect.

Thank you.

 

 

Tagged in: Glasgow2014

The Conference started yesterday and I attended a very interesting workshop on the ongoing relevance of Drug Drug Interactions. The debate, which found ongoing interested and need for attention to drug drug interactions, gave way to three very important case disucssions about DDIs in the context of coinfection and comorbidities.

Sanjay Bhagani presented on the HIV/HCV coinfected patient. While a complex case it was illustrative of some of the issues in managing not just coinfected, but also HCV mono-infected patients and just how long it is safe to delay the commencement of treatment and how much DAAs can rescue patients with advanced liver disease. I am going to try and talk to him in more detail about this during the conference.

Marta Boffito presented on recreational drug interactions with HIV therapy and suggested that some presumed interactions could simply be poor dosing or understanding of the variability of rereational drugs on the part of the patient.

Lastly Kelly Dooley, reporting on TB HIV coinfection raised the issue of whether to treat TB before starting HIV Therapy. Cautioning that the emergence of multi drug and XDRTB suggests treating HIV at the same time. Fortunately we do not see a lot of TB in Australia, but with changing epidemiology this may become more important.

Levinia

Tagged in: Glasgow2014

Please join us for a memorial event celebrating the life of one of Australia’s leading HIV advocates, Levinia Crook… https://t.co/N7dof5xaGa

ASHM ASHM