Biomedical subjects
Publications and source records attributed to J M Barragry.
We describe a 79 year old lady who presented with a cytologically confirmed anaplastic carcinoma of the thyroid gland eleven years after administration of radio-iodine for thyrotoxicosis. This is, we believe, the first such occurrence documented in the Irish literature.
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1. Vitamin D deficiency was induced in anicteric Wistar rats, Wistar rats before common bile-duct ligation was performed and Gunn rats with unconjugated hyperbilirubinaemia. 2. The effect of ultraviolet radiation on plasma concentrations of 25-hydroxy-vitamin D was studied in a group of control anicteric Wistar rats (n = 11), Wistar rats 8 days after common bile-duct ligation (n = 7) with conjugated hyperbilirubinaemia and in Gunn rats (n = 11). 3. The plasma 25-hydroxy-vitamin D response to ultraviolet radiation was similar in the three groups. 4. It is suggested that neither conjugated nor unconjugated hyperbilirubinaemia prevent cutaneous vitamin D3 synthesis or 25-hydroxylation in the rat.
A patient is described who had a long history of abuse of kaolin and morphine mixture which ultimately proved fatal.
A patient with an apparent abnormality of cortisol binding globulin (CBG) is reported. Investigations showed that while the plasma CBG binding capacity (equivalent to the plasma CBG concentration) was normal, the binding affinity was reduced by a factor of four. The significance of this observation is discussed with regard to its possible role in the development of the adrenocortical hyperfunction also seen in this patient.
Following intravenous injection of (3H) cholecalciferol into healthy subjects the disappearance of label from the plasma was followed by the reappearance ("rebound") of (3H) radioactivity associated exclusively with cholecalciferol. Lipoprotein fractionation of plasma revealed an increasing association of label with protein rather than lipoprotein during the rebound phase. We conclude that the rebound of plasma radioactivity reflects the transfer of label from lipoprotein to Vitamin D-binding globulin in the liver followed by its release into plasma.
The intestinal absorption of (3H)cholecalciferol was studied in five patients with alcoholic liver disease, six patients with primary biliary cirrhosis, and 15 healthy subjects. The rate of appearance in plasma of (3H)cholecalciferol after oral ingestion and the subsequent appearance of (3H) polar metabolites in the alcoholic subjects were similar to those in the healthy subjects. In subjects with primary biliary cirrhosis the rate of appearance in plasma of (3H)cholecalciferol was significantly reduced. The rate of appearance of labelled polar metabolites of cholecalciferol was also lower in this group, suggesting that increased removal of labelled vitamin by conversion into more polar metabolites could not account for the reduced plasma (3H)cholecalciferol response. It is suggested that intestinal absorption of cholecalciferol is usually normal in alcoholic liver disease but impaired in primary biliary cirrhosis. Hepatic 25-hydroxylation is normal in alcoholic liver disease but may be defective in primary biliary cirrhosis.
The response of plasma-25-hydroxyvitamin D (25[OH]D) to different exposures to ultraviolet irradiation has been studied in patients in long-stay geriatric wards. Increases sufficient to bring the plasma-25(OH)D into the normal range may be obtained with doses less than those required to produce erythema. The provision of such background irradiation may be a suitable method of preventing vitamin-D deficiency in elderly subjects who receive very little exposure to sunlight.
Plasma concentrations of vitamin D-binding globulin were measured by radial immunodiffusion in healthy subjects, pregnancy, and during oestrogen therapy. Subjects with disorders of vitamin D metabolism (dietary deficiency, malabsorption, anticonvulsant therapy, chronic liver disease) were also studied. Neither sex nor age influenced the plasma vitamin D-binding globulin concentration in healthy subjects, but there was a significant increase in concentration during pregnancy and oestrogen therapy. Elevated levels were found in vitamin D deficient elderly but not younger subjects, while levels in subjects with chronic liver disease were significantly reduced. Normal levels of vitamin D-binding globulin were present in hypervitaminosis D and no vitamin D-binding globulin was detected in human milk. No correlation was observed between plasma 25-hydroxycholecalciferol levels and plasma vitamin D-binding globulin concentrations.
1. A method for assessing cholecalciferol absorption in man is described. 2. The intestinal absorption of [3H]cholecalciferol was studied in 20 female geriatric patients, most of whom were vitamin D-depleted. 3. The plasma [3H]cholecalciferol response after oral ingestion was significantly lower than that of a group of younger female subjects. 4. The plasma response of labelled polar metabolites of cholecalciferol was also lower in the geriatric than in the younger group, suggesting that increased removal of label by conversion into more polar metabolites could not account for the reduced plasma [3H]cholecalciferol response. 5. There was no evidence that alteration in gastrointestinal motility could account for the different rate of appearance of the labelled vitamin in the plasma in the two groups. 6. It is suggested that there is a defect in intestinal absorption of cholecalciferol in the elderly.
Plasma sex hormone binding globulin (SHBG) and testosterone levels were measured in 29 patients with epilepsy (16 men and 13 women), most of them on chronic therapy with anticonvulsant drugs. Sex hormone binding globulin concentrations were increased in both sexes and testosterone levels in male patients. It is postulated that anticonvulsants may induce hepatic synthesis of SHBG.
Plasma concentrations of 25-hydroxy-cholecalciferol (25-OHD3) and vitamin-D-binding globulin (V.D.B.G.) were significantly reduced in ten nephrotic subjects. V.D.B.G., which is undetectable in normal urine, was present in substantial amounts in the urine of each nephrotic subject. Administration of 3H-labelled cholecalciferol to three subjects resulted in the rapid appearance of the labelled vitamin in the urine, mainly as the 25-hydroxylated metabolite bound to V.D.B.G. in amounts which could largely account for the low plasma-25-OHD3. The plasma half-life of 25-OHD3 was substantially reduced in the nephrotic syndrome.
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A 46XY individual with incomplete male pseudohermaphroditism was studied. The phenotype was distinctive, with a masculine habitus despite a small phallus, gynaecomastia and diminished virilization. Plasma levels of testosterone, oestrogens, gonadotrophins and sex-hormone binding globulin were elevated. It is proposed that this syndrome is a variant of Type I incomplete male pseudohermaphroditism.
Erythrocyte carbonic-anhydrase-I (C.A.I.) concentration was measured by radial immunodiffusion in 30 thyrotoxic patients and 15 myxoedemic patients, the results being compared with those found in a control group of 90 euthyroid individuals. In thyrotoxicosis the erythrocyte-C.A.I. concentration was found to be below 10-29 mg/g haemoglobin, whereas the normal range varied from 11-1 to 22-5 mg C.A.I./g Hb. Low values were found in 4 patients with triiodothyronine(T3)-toxicosis. In myxoedema, the mean erythrocyte-C.A.I. concentration, though elevated at 20-37 mg/g Hb, fell within the normal range. In pregnancy, the erythrocyte-C.A.I. concentration rose with time, the mean value at tern being 20-6 +/-S.D. 3-3 mg/g Hb. In a group of women taking oral contraceptives, a low erythrocyte-C.A.I. concentration was noted--an effect which was most obvious among those taking low-oestrogen contraceptives. It is suggested that erythrocyte-C.A.I. estimation provdes a rapid screening test for thyrotoxicosis.
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