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Biomedical subjects

Y J Huskisson

Publications and source records attributed to Y J Huskisson.

2 recordsLinked to original sources

Folate binders in body fluids.

In normal serum, saline dialysis for 48 hours in Visking casing resulted in folate clearance closely comparable to that produced by haemoglobin-coated charcoal adsorption, except in kwashiorkor where charcoal removed a greater proportion of folate. Pre- and post-dialysis values probably represented total and bound folate, respectively. Urinary folate consisted almost exclusively of dialyzable or free folate. Folate in saliva, bile, and erythrocytes consisted of dialyzable and non-dialyzable fractions; gastric juice contained minimal amounts of folate. In spite of low serum albumin in kwashiorkor the bound folate fraction was increased rather than decreased; in myeloma with hyperglobulinaemia there was no increase in the bound folate fraction. Nephrotic urine did not contain excess folate, but pregnancy urine (third trimester) showed increased total folate.Serum, chromatographed on Sephadex G-25, produced two folate peaks, only the first being associated with serum proteins. Urine contained only a second folate peak corresponding to the elution peak of pteroyl-monoglutamic acid (PGA). Adsorption studies with charcoal coated with ;molecular sieves' of varying size suggested that the predominant serum folate binder was of molecular weight 70,000-120,000. It is unlikely to be albumin.

Agammaglobulinemia↗

Serum and urinary folate in liver disease.

During the active phase of viral hepatitis urinary folate loss was found to be 8.0 to 48.3 (mean 31.1) mug./day, compared with a normal urinary folate excretion of 0.1 to 18.0 (mean 9.5) mug./day. In cirrhosis and cardiac failure with congestive hepatomegaly the corresponding values were 25.8 to 55.0 (mean 35.7) mug./day and 2.5 to 61.6 (mean 26.9) mug./day, respectively. Urinary folate loss may be a significant factor in the aetiology of folate deficiency of chronic liver disease, particularly when dietary intake is poor.After prolonged dialysis in Visking casing urinary folate was almost totally dialysable, but an appreciable fraction of serum folate was not, even after 72 hours. The dialysable (free) folate fraction of serum and urine disappeared maximally during the first six hours' dialysis, and was virtually cleared after 24 hours' dialysis; clearance curves in normal individuals and in liver disease were comparable. The non-dialysable serum folate fraction was of similar magnitude in all subjects studied, in spite of marked variation in total folate, and probably represented protein-bound folate.

Adult↗