Vitamin D deficiency associated with a poorer response to HCV treatment in HIV/HCV-co-infected patients

Michael Carter
Published: 11 October 2012

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 coinfected patients.”

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.

Investigators in Austria therefore wanted to see if vitamin D was associated with response to hepatitis C treatment in co-infected people.

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.”


Mandorfer M et al. Low vitamin D levels are associated with impaired virologic response to PEGIFN+RBV therapy in HIV/HCV coinfected patients. AIDS 26, online edition. DOI: 10.1097/QAD.0b013e32835aa161, 2012.

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