Higher Plasma Homocysteine Is Associated With Lower Vitamin B₆ Status in Critically Ill Surgical Patients

Abstract

Background: Hyperhomocysteinemia might be at least partially due to compromised B vitamin status in critically ill patients and has been linked with critical illness. This study was conducted to examine the association between plasma homocysteine with B vitamins and clinical outcomes in critically ill surgical patients. Methods: Thirty‐two patients in the surgical intensive care unit (SICU) were enrolled. Disease severity (Acute Physiology and Chronic Health Evaluation II score), hematological values, serum and erythrocyte folate, serum vitamin B12, plasma, and erythrocyte pyridoxal 5′‐phosphate (PLP) were determined within 24 hours of admission and again after 7 days. Results: The prevalence of hyperhomocysteinemia in the patients was either 46.9% (plasma homocysteine ≥12 µmol/L) or 31.3% (plasma homocysteine ≥15 µmol/L) on day 1 in the SICU and increased to 62.5% (plasma homocysteine ≥12 µmol/L) and 37.5% (plasma homocysteine ≥15 µmol/L) on day 7 after admission to the SICU. Plasma homocysteine, serum folate, and vitamin B12 significantly increased by day 7, whereas plasma and erythrocyte PLP remained constant throughout the study. Plasma homocysteine was not correlated with serum folate and vitamin B12. However, plasma and erythrocyte PLP on day 1 were adversely associated with day 1 levels of plasma homocysteine after adjusting for potential confounders. Plasma homocysteine on day 1 or changes (Δ day 7 – day 1) did not show any association with clinical outcomes. Conclusions: Lower plasma PLP might be a significant factor for increased plasma homocysteine in critically ill surgical patients. The association between plasma homocysteine and clinical outcomes was not found.

Pyridoxal-5′-phosphate deficiency is associated with hyperhomocysteinemia regardless of antioxidant, thiamine, riboflavin, cobalamine, and folate status in critically ill patients

“…Critical care patients have higher risk of stress and inflammation, which causes a hypercatabolic state during the acute phase of the disease [10]. Many factors are associated with HHcy prevalence, particularly folate, cobalamine and pyridoxine deficiencies needed Values are expressed as mean (SD).…”

“…Because erythrocyte PLP is an important indicator of Hcy levels in blood, the interpretation of a role of this coenzyme must be approached primarily through its association with Hcy metabolism [10] and the stress in critically ill patients. As previously discussed the main objective of this study was to assess the nutritional status of PLP in critically ill patients with SIRS admitted to the ICU for 7 days in comparison with a group of healthy people, studying it's association with factors involved in the pyridoxine and other B vitamins metabolism, as the total antioxidant capacity and Hcy as cardiovascular risk biomarker.…”

Inadequate Vitamin B-6 Status in Critical Care

“…Hyperhomocysteinemia might be due, at least in part, to compromised B-vitamin status and may cause and further exacerbate oxidative stress and inflammatory responses in critically ill patients. However, studies on the association between plasma homocysteine and status of B-vitamins have yielded conflicting results (Schindler et al 2002;Abilés et al 2008;Hou et al 2012). Maintenance of an adequate vitamin B-6 status is warranted for critically ill patients, regardless of whether or not lower plasma PLP significantly contributes to increased plasma homocysteine concentration in this patient population.…”

“…The high prevalence of hyperhomocysteinemia (plasma homocysteine concentration >12 or >15 μmol/L) in critically ill patients at admission is a particularly challenging problem. The prevalence rate of hyperhomocysteinemia has been reported to be approximately 12-55 % in critically ill patients (Schindler et al 2002;Abilés et al 2008;Ploder et al 2010;Hou et al 2012). Hyperhomocysteinemia might be due, at least in part, to compromised B-vitamin status and may cause and further exacerbate oxidative stress and inflammatory responses in critically ill patients.…”

“…The binding of PLP to serum albumin in the circulation serves to protect it from hydrolysis and allows for the delivery of PLP to other tissues. Critically ill patients often have a compromised albumin concentration (Bassili and Deitel 1981;Larca and Greenbaum 1982;Christman and McCain 1993;Huang et al 2000;Kan et al 2003;Hou et al 2012); therefore, low serum albumin levels (<3 g/dL) in critically ill patients may affect the binding of PLP and lead to the dephosphorylation of plasma PLP into PL (Merrill and Henderson 1987). Another possibility might be that patients' critical clinical condition causes hepatic PLP reserves to decrease or to be prescribed drugs, such as gentamicin, which could affect vitamin B-6 status.…”