Vitamin B6 repletion in cirrhosis with oral pyridoxine: Failure to improve amino acid metabolism

Abstract

This study evaluated the effect of daily oral pyridoxine supplementation in patients with cirrhosis. Eight subjects were treated with 25 mg of pyridoxine for 28 days. Before and after the supplementation period, B6 status was assessed by measuring fasting plasma vitamer levels and response to a 25 mg oral pyridoxine load. In addition, a 24-hr urine collection was analyzed during each load study for B6 metabolites. The data indicated that supplementation achieved repletion of peripheral B6 stores, as evidenced by: (i) a significant (p less than 0.005) rise in fasting plasma pyridoxal phosphate after supplementation (mean +/- S.D. = 56.8 +/- 30.5 nmoles per liter) as compared to initial levels (17.0 +/- 17.8 nmoles per liter); (ii) a higher (p less than 0.05) percentage excretion of the pyridoxine load as urinary 4-pyridoxic acid (31.0 +/- 9.3%) compared to the initial load (19.6 +/- 5.8%), and (iii) a postsupplementation area under the plasma concentration vs. time curve for pyridoxal phosphate (377 +/- 529 nmoles.hr per liter), which was decreased (p less than 0.005) from the presupplementation value (934 +/- 756 nmoles.hr per liter). The postsupplementation fasting plasma pyridoxal phosphate concentrations were within the normal range. The consequences of B6 repletion on amino acid metabolism were measured by oral protein loads (n = 4) or oral methionine loads (n = 4). No significant changes were observed for methionine or any other amino acid in regard to plasma fasting concentration, peak concentration or AUC. Although the vitamin B6 deficiency of cirrhosis was corrected by daily oral pyridoxine supplementation, there was apparently no improvement in the deranged amino acid metabolism.

Vitamin B6 Deficiency

“…Unlike many causes of refractory seizures, vitamin B 6 deficiency is relatively simple to treat. Henderson et al demonstrated that supplementation with only 25 mg of oral pyridoxine daily for 28 days in patients with cirrhosis effectively replenished peripheral vitamin B 6 stores 23 . In the current report, all patients received 200 mg per day, which is double the daily dose of pyridoxine (100 mg/day) for adults recommended by the Food and Nutrition Board of the Institute of Medicine 29 .…”

“…Because none of our patients was receiving isoniazid or had a history of childhood seizures, it was assumed that dietary deficiency of vitamin B 6 was likely causative. This deficiency is unusual in adults because vitamin B 6 is so widely distributed in food, but deficiency has been associated with alcoholism and cirhossis 23 . ‐ 28 Vitamin B 6 deficiency is classically associated with peripheral neuropathy and anemia, and often other vitamin B‐complex deficiencies occur in patients with alcoholic liver disease 28 .…”

“…The third patient had a more remote history of alcohol abuse. Low concentrations of PLP have been noted in patients with cirrhosis and chronic alcoholism without liver disease 23 . ‐ 28 Pyridoxal 5′‐phosphate, the active form of vitamin B 6 , is metabolized to pyrodoxal in a 2‐way reaction.…”

Seizures caused by pyridoxine (vitamin B6) deficiency in adults: A case report and literature review

“…Insufficient dietary intakes may cause vitamin B6 deficiency which subsequently induces seizures. Gerlach and colleagues (6) reported three cases of refractory seizures consequent to vitamin B6 deficiency which may be aggravated by alcoholism or liver disease (31)(32)(33)(34)(35). Low PLP concentration in those patients may occur over time owing to a dietary deficiency coupled with intact aldehyde oxidase activity.…”

Impact of Glutathione and Vitamin B-6 in Cirrhosis Patients: A Randomized Controlled Trial and Follow-Up Study

“…Although a single dose of vitamin B-6 supplementation (50 mg/d) did not show a significant effect on the GSH and GSSG levels and activities of GSH-Px, GSH-Rd, and GSH-St in patients with hepatocellular carcinoma [14], the combination of vitamin B-6 and GSH supplementation are likely to have antioxidative effects in liver cirrhosis patients. Since an impaired vitamin B-6 and GSH status has been observed in patients with liver cirrhosis [15][16][17][18][19], a strategy is required to either maintain adequate or increase vitamin B-6 and GSH status in order to cope with the altered oxidative stress and antioxidant capacities in this specific group of patient. However, it remains unclear whether supplementation with vitamin B-6 or GSH could compensate for their reduced status, and improve the antioxidant capacity of liver cirrhosis patients.…”