{'fraction_non_alphanumeric': 0.02187966185977126, 'fraction_numerical': 0.018398806563898557, 'mean_word_length': 5.64026402640264, 'pattern_counts': {'":': 0, '<': 3, '<?xml version=': 0, '>': 1, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Plasma homocysteine in relation to serum cobalamin and blood folate in a psychogeriatric population

Abstract Plasma homocysteine, serum cobalamin and blood folate were analysed in 296 consecutive patients referred to a psychogeriatric department for diagnosis of mental disease. Plasma homocysteine correlated with positive significance with age and serum creatinine, and with negative significance with serum cobalamin and blood folate. Approximately 35–40% of the patients with low serum cobalamin (<150 pmol l‐1) or low blood folates (<150 nmol l‐1) exhibited normal values of plasma homocysteine (<19·9 μmol l‐1). Possibly, these patients do not have a deficiency of the vitamins in the tissue. At least 7·5% of the patients with serum cobalamin levels (>150 pmol l‐1) showed an inexplicably increased level of plasma homocysteine. These patients might have a deficiency of tissue cobalamin despite the normal serum cobalamin levels. The effect of cobalamin supplementation for 7–10 days on plasma homocysteine was tested in 62 patients with different levels of serum cobalamins. We found the most pronounced decrease of plasma homocysteine in the patients with lowest serum cobalamin levels and in the patients with highest plasma homocysteine, indicating that the percentage decrease of the initial concentration of plasma homocysteine could reflect the degree of cobalamin deficiency. Folate supplementation for 7–10 days reduced plasma homocysteine not only in patients with folate deficiency but also in those with a normal folate status, and even in patients with cobalamin deficiency. The latter patients further reduced their plasma homocysteine after additional cobalamin treatment. The findings in this study support the view that, in elderly patients with co‐existing organic brain disease, cobalamin substitution should be started when serum cobalamin concentrations are below 200 pmol l‐1 and plasma homocysteine is elevated, to prevent further organic lesions related to cobalamin deficiency.