Low vitamin B6 levels in people with PSC may increase risk of liver failure
Study ties higher blood levels of vitamin to better survival in chronic liver disease
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Low blood levels of vitamin B6 — found in certain foods and essential for metabolism and immune function in the body — can increase the risk of liver failure or death in people with primary sclerosing cholangitis (PSC), a chronic liver disease. The vitamin deficiency also raised the risk of PSC patients needing a liver transplant for treatment.
That’s according to a new study involving more than 1,000 people with PSC, an autoimmune condition, in the U.S., Norway, and Germany.
“Vitamin B6 deficiency is associated with poor outcomes in multiple primary sclerosing cholangitis [patient groups],” the scientists wrote in a highlights section of the study.
Additionally, the team found that “the risk of liver complications rose faster at low vitamin B6 levels but leveled off in individuals with sufficient B6 levels.”
The study, “Vitamin B6 predicts poor outcomes in geographically distinct populations with primary sclerosing cholangitis,” was published in the Journal of Hepatology by researchers in Europe and the U.S.
PSC is characterized by inflammation and scarring of the bile ducts, the tubes that carry bile, a digestive fluid, from the liver to the intestines. As the ducts narrow due to disease, bile flow stalls — a condition known as cholestasis — and bile backs up to toxic levels in the liver, causing tissue scarring (fibrosis) and damage.
Earlier work from a research team led by scientists at Oslo University Hospital in Norway showed reduced capacity by the gut microbiota, the large community of bacteria and other microbes that live in the digestive tract, to produce the active form of vitamin B6 in people with PSC. That active form is known as PLP, fully, pyridoxal 5′-phosphate.
Earlier research had found low vitamin B6 levels in PSC patients
The team also found that vitamin B6 deficiency is common among people with PSC — though rare in the general population across Scandinavia.
Importantly, low PLP levels also predicted reduced liver transplant-free survival, which is the time a person lives without needing and undergoing a liver transplant, and PLP added value to existing predictive models for PSC, the researchers noted.
Now, these scientists, along with colleagues from both sides of the Atlantic, examined the value of vitamin B6 deficiency in predicting liver-related outcomes in a much larger group of PSC patients. Their study covered 756 people with PSC from the U.S., 315 from Norway, and 149 from Germany.
Patients in the U.S. had higher median PLP levels than those in the other two groups, the data showed. As a result, fewer individuals in the U.S. group (25%) fell within the vitamin B6 deficiency range compared with those in the Norwegian group (50%) and the German group (62%), according to the researchers.
Analyses focused on the U.S. and Norwegian groups showed that PLP levels were significantly lower in individuals who had already developed hepatic decompensation — when the liver can no longer function properly — at the time of blood sampling.
Lower PLP levels were associated with higher, or worse, scores on two established PSC risk prediction models, the Amsterdam-Oxford PSC model and the PREsTo five-year score. Low PLP was also linked with blood markers indicating cholestasis, reduced liver function, and more advanced liver fibrosis, as well as greater bodywide inflammation.
After five years of follow-up, more than twice as many patients in the Norway group had needed a liver transplant or died as those in the U.S. group (36% vs. 16%). Therefore, the median transplant-free survival was shorter in the Norway group (9.7 vs. 15.2 years).
In both groups, there was a dose-dependent relationship between vitamin B6 status and liver transplant-free survival, with PLP deficiency (PLP levels below 20 nanomole/L) associated with the shortest survival.
Longer time to liver transplant seen with higher PLP levels
In line with this finding, higher PLP was associated with better five-year liver transplant-free survival in the U.S., Norwegian, and German groups, even after accounting for patient sex and the risk scores from either the PREsTo or the Amsterdam-Oxford PSC model. PLP also added some predictive value beyond these risk scores when used alongside the PREsTo five-year score, the researchers noted.
Further analyses in the U.S. and Norwegian groups showed that 28 people in Norway and 64 in the U.S. had reached hepatic decompensation after five years, and that lower PLP was associated with a higher risk of this outcome.
Among U.S. patients, higher PLP was significantly associated with a reduced risk of hepatic decompensation, by 51%, and this link remained significant after adjusting for sex and risk scores, the scientists noted. In the Norway group, higher PLP was also associated with a 51% lower risk of hepatic decompensation, but after adjusting for the risk scores, its independent contribution became less certain.
“We show in two large, geographically distinct PSC [patient groups] with long follow-up that low levels of vitamin B6 consistently associate with an increased risk of future hepatic decompensation and liver transplantation or death,” the scientists wrote. “Future efforts to develop risk prediction models for PSC should consider PLP as a candidate prognostic factor.”
Vitamin B6 is involved in more than 100 enzyme-related reactions in the body, primarily affecting metabolism. Key sources include poultry, fish, bananas, and chickpeas.
