Biomedical subjects
Publications and source records attributed to B J Boucher.
Evidence is presented that two levels of glycosylated haemoglobin can be defined which when exceeded indicate respectively the presence of diabetes mellitus and a significant risk for the development of microvascular complications, as judged by current glucose tolerance test criteria for such risk.
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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.
In order to assess the quality of care in a community-wide sample of diabetic patients, a study was performed on 217 such patients identified in three group practices in an east London health district. Only 46% of the patients were currently attending a hospital. In the two years before review, 64% of patients had had their blood pressure recorded and 59% had had retinal examinations. Levels of glycosylated haemoglobin were significantly higher in patients on insulin than in those on oral regimes (P = 0.0004). The mean level of glycosylated haemoglobin was higher in patients from Social Classes III, IV, and V than in patients from Social Classes I and II (P = 0.005), but there was no difference in level between those patients attending hospital and those attending their general practitioners after accounting for differences in these two populations (P = 0.19). Over 50% of all diabetic patients in this study had levels of glycosylated haemoglobin which may indicate vulnerability to microvascular disease.
The results are reported of 2830 radioisotope brain scans, the records for which have been reviewed one year after scanning over a period of ten years before CT scan facilities were available on site. Out of 766 lesions confirmed by other means 672 were detected by scanning. The majority of the space-occupying lesions that went undetected did so either because they were situated low down in the brain, e.g. small acoustic neuromas, pituitary fossa tumours and brain stem lesions, or they were astrocytomas or cystic lesions. Of 2064 cases with a negative clinical diagnosis all but 28 had negative brain scans. The high accuracy with which many types of space-occupying lesion can be excluded by this non-invasive, atraumatic technique confirms its continuing value where access to a CT scanner is limited.
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1. Concentrations of high-density-lipoprotein cholesterol and of glycosylated haemoglobins [HbA1(a+b+c)] were measured in non-fasting blood samples taken from 171 diabetic patients. 2. Mean concentrations of high-density-lipoprotein cholesterol were lower in men, and in patients not requiring insulin. 3. There was no correlation between concentrations of high-density-lipoprotein cholesterol and of HbA1(a+b+c) in the patients as a whole, but a significant positive correlation was found between these values in male diabetics not requiring insulin. 4. Changes in the concentrations of HbA1(a+b+c) were not correlated with changes in concentrations of high-density-lipoprotein cholesterol.
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 vitamin D status of residents of an old people's home and long-stay patients was assessed by means of plasma 25-hydroxycholecalciferol (25-OHD) estimations. The residents of the old people's home had a higher mean plasma 25-OHD concentration than long-stay patients. Both groups had diets with vitamin D intakes of less than 2.5 micrograms (100 IU) per day and the conclusion is that solar exposure is the major determinant of the concentration of circulating 25-OHD.
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.
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A case of chronic myelogenous leukemia in which the disease pursued an atypical course is described. The presence of a previously unreported translocation t(1;20), in addition to a Ph' chromosome t(9;22), is demonstrated, and its possible significance and relationship to the disease are discussed.
A rapid method is described for the measurement of total glycosylated haemoglobins (HbA1(a+b+c). The procedure utilizes 0.05 ml of blood and takes forty minutes to complete manually. Eighty blood samples can be analysed without automation by one person in a day. Each analysis uses less than 2 mg of potassium cyanide, resulting in a method that is both safe and rapid for routine hospital laboratories. The inter-assay coefficient of variation was 4% and that for intra-assay measurements 3%, over the range 5-20%, HbA1(a+b+c). The method confirmed that the level of HbA1(a+b+c) is elevated in imperfectly controlled diabetics. Amongst patients with blood glucose levels of less than 10 mmol/l the mean level of HbA1(a+b+c) was found to be 8.5%; samples from 14 known diabetics gave a mean value of 10.9%, whereas 17 known non-diabetic samples gave a mean value of 8.3%. In the group of samples from 27 diabetic individuals with blood glucose levels above 10 mmol/l the mean level of HbA1(a+b+c) was found to be 13.5%.
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 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.
Investigation of the serum complement system in 25 patients with various forms of lipodystrophy showed no abnormality in three patients with total lipodystrophy; a single patient with limb lipodystrophy had evidence of activation of the classical complement pathway. However, of the 21 patients with partial lipodystrophy, 17 had low serum C3, with normal C4 and C2, concentrations, accompanied in 14 by a serum C3 splitting factor indistinguishable from nephritic factor, suggesting activation of the alternative pathway. These abnormalities occurred in 10 patients without clinically overt renal disease. Seven patients had overt nephritis; renal biopsies obtained in six showed mesangiocapillary (membranoproliferative) nephritis in all. Thus, the majority of patients with partial lipodystrophy have hypocomplementemia. Although nephritis may not invariably develop, the high rate of mesangiocapillary nephritis in these patients suggests that complement activation via the alternative pathway predisposes to the development of this form of glomerular disease.