Patients with hepatitis C who have a low level of Vitamin D do not obtain a sustained virus fighting effect from medication

December 17, 2009

Hepatitis C is a virus that attacks the liver and in once established, chronic infection can progress to scarring of the liver (fibrosis), and advanced scarring (cirrhosis) which is generally apparent after many years. In some cases, those with cirrhosis will go on to develop liver failure or other complications of cirrhosis, including liver cancer .

The hepatitis C virus (HCV) is spread by blood-to-blood contact. Most people have few symptoms after the initial infection, yet the virus persists in the liver in about 85% of those infected; this is referred to as chronic infection. Persistent infection can be treated with medication, interferon and Ribavirin being the standard-of-care therapy. 51% are cured overall. Those who develop cirrhosis or liver cancer may require a liver transplant, and the virus universally recurs after transplantation.

Patients with chronic hepatitis C virus (HCV) infection have lower serum levels of 25-hydroxyvitamin D than healthy individuals, and as their vitamin D level falls, so does the likelihood of a sustained virologic (anti-viral) response to interferon and Ribavirin, new research shows.

Disturbances in vitamin D metabolism can affect the inflammatory response and fibrogenesis, Dr. Salvatore Petta, from the University of Palermo, Italy, and co-researchers state. Exactly how vitamin D levels influence the progression of chronic hepatitis C and response to treatment, however, was not known, according to the report in the November 15th issue of Hepatology.

To investigate this topic, the researchers analyzed data from 197 patients with biopsy-proven genotype 1 chronic hepatitis C and from 49 healthy matched controls. Most of the patients were treated with peg-interferon and Ribavirin. Tissue expression of two liver 25-hydroxylating enzymes, CYP27A1 and CYP2R1, was evaluated in 34 patients and 8 controls.

Average serum levels of 25-hydroxyvitamin D were 25 in patients and 43 in healthy people (controls). Significant correlates of lower levels included female gender and inflammation of liver tissue. Expression of CYP27A1, but not CYP2R1, was directly linked to the level of 25-hydroxyvitamin D and inversely related to inflammation.

On multivariate analysis, low 25-hydroxyvitamin D levels, low cholesterol levels, older age, high ferritin, and liver cell inflammation were all independent predictors of severe fibrosis.

Seventy patients (42%) treated with interferon and Ribavirin achieved a sustained virologic response. Hepatic steatosis (fat infiltrating into the liver) and lower levels of 25-hydroxyvitamin D and cholesterol predicted that patients would not achieve a sustained response. The study is published in the medical textbook Hepatology, 2009.