Vitamin D deficiency is associated with a
poorer response to hepatitis C therapy in people who are co-infected with HIV
and hepatitis C, investigators report in the online edition of AIDS. Austrian researchers found that
people with vitamin D deficiency were significantly less likely to have an
early or sustained response to treatment than those with normal levels of the
vitamin. This was especially the case for people with established risk
factors for a poorer response to hepatitis C therapy, such as infection with
genotypes 1 or 4, or a high hepatitis C viral load.
The investigators suggest: “Vitamin D
supplementation may result in higher rates of virologic response in HIV/HCV
Previous research has shown a high
prevalence of vitamin D deficiency in co-infected people. It is also known
that the vitamin acts as an antiviral agent, inhibiting production of hepatitis
C. In hepatitis C-monoinfected patients, improved response rates to treatment
with pegylated interferon and ribavirin have been observed in those with
sufficient levels of vitamin D.
- early virological response (EVR)
A reduction in hepatitis C RNA viral load by week 12 of treatment. A partial
early virological response (pEVR) means that it has dropped by at least 2 log10 (99%). A complete early
virological response (cEVR) means that viral load is undetectable by week 12.
An inherited gene which all individuals have. There are three genotypes of IL28B; these influence response to hepatitis C and its treatment. People with CC genotype are more likely to spontaneously clear acute infection or (during chronic infection) respond well to interferon-based treatment. The other two genotypes are known as CT and TT.
Investigators in Austria therefore wanted
to see if vitamin D was associated with response to hepatitis C treatment in
They designed a study involving 65
co-infected individuals who were taking hepatitis C therapy for the first time.
Vitamin D levels were defined as normal if
they were above 30 ng/ml; insufficient when between 10 and 30 ng/ml; and
deficient if below 10 ng/ml.
Most of the participants (71%) were men; their
median age was 37 years. There was a high prevalence of risk factors associated
with a poorer response to hepatitis C treatment. Over two-thirds (68%) of
participants were infected with the harder-to-treat genotypes; 65% had a high
hepatitis C viral load; two-thirds lacked the IL28B genetic mutation; and 40%
had advanced liver fibrosis.
Only a fifth of participants had sufficient
levels of vitamin D. Levels were insufficient in 57% and deficient in 23%.
“We observed a high prevalence of vitamin D
insufficiency and deficiency in our study population,” comment the authors.
There was a higher prevalence of advanced
fibrosis in people with vitamin D deficiency compared to those with
sufficient vitamin levels (53 vs 13%, p = 0.009).
Rates of early virological response (EVR)
to hepatitis C treatment (undetectable viral load after twelve weeks) differed
according to vitamin D status. Almost all (92%) of participants with sufficient
levels of the vitamin achieved this outcome, compared to 68% of those with
vitamin D insufficiency and 47% of people with deficient levels of the
vitamin. The difference between participants with sufficient and deficient vitamin
D was significant (p = 0.0160).
The chances of achieving a sustained
virological response (SVR; undetectable hepatitis C viral load 24 weeks after
the completion of therapy) also differed according to vitamin D level. An SVR
was observed in 85% of participants with normal vitamin D; in 60% of those with
insufficiency; and 40% of individuals with vitamin D deficiency. Therefore,
people with vitamin D sufficiency were significantly more likely to achieve
an SVR than those with vitamin D deficiency (p = 0.024).
People with two or three recognised risk
factors for poorer treatment outcomes and vitamin D deficiency had lower SVR
rates than participants with the same similar numbers of risk factors and vitamin D
sufficiency (52 vs 0%, p = 0.016).
The authors conclude that low vitamin D
levels are associated with significantly poorer rates of EVR and SVR in
co-infected patients. “Prospective, randomized trials on vitamin D
supplementation in HIV/HCV co-infected patients receiving chronic hepatitis C
therapy are highly encouraged.”