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Biomedical subjects

J P Reckless

Publications and source records attributed to J P Reckless.

At least 19 recordsLinked to original sources
PubMed1992

Screening programme for microvascular complications and hypertension in a community diabetic population.

The role of a community-based screening programme for microvascular complications of diabetes and hypertension was evaluated in the semi-rural town of Trowbridge (population 31,000). Of 405 diabetic patients identified (prevalence 1.31%), 358 (88%) attended for screening, 94 (26%) of whom were under hospital review for diabetes. In only 136 patients (38%) were all aspects of diabetes care found to be satisfactory. The remaining 222 patients included 162 patients with poor metabolic control (HbA1 greater than or equal to 12%), 118 who were hypertensive at screening, 13 with previously undiagnosed diabetic nephropathy, and 29 with undiagnosed potentially sight-threatening retinopathy. Overall standards of diabetes care in this community population appear inadequate, and might be improved by introduction of a simple screening programme for diabetic complications.

Adult↗
PubMed1992

Laboratory facilities for investigating lipid disorders in the United Kingdom: results of the British Hyperlipidaemia Association survey.

AIMS: To determine the availability of facilities for the investigation of hyperlipidaemia in the United Kingdom. METHODS: A questionnaire was sent to all health districts in the United Kingdom. RESULTS: The response rate was 81%. All laboratories used enzymatic techniques to measure serum triglyceride and cholesterol concentrations, although there were differences in standardisation procedures. Reference ranges for serum lipids were quoted by 58% of laboratories while 50% quoted "desirable limits". Almost half specified that fasting blood samples were required. High density lipoprotein cholesterol concentrations were estimated by 75% and apolipoproteins AI and B by 14% of laboratories; there were differences in specimen type and considerable diversity in procedures used for measurement. CONCLUSIONS: Many laboratories were unaware of current recommendations for screening for hypercholesterolaemia in the community. The present survey indicated an urgent need for the introduction of better reference methods, standardisation, and quality assurance procedures before apolipoproteins become a routine part of coronary heart disease risk assessment.

Apolipoproteins↗
PubMed1991

Garlic.

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Blood Coagulation↗
PubMed1991

Effects of pravastatin and cholestyramine on gonadal and adrenal steroid production in familial hypercholesterolaemia.

1. Adrenal and gonadal steroids are derived from cholesterol, which may be derived from plasma lipoproteins or de novo synthesis. 2. Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, the rate limiting enzyme in cholesterol synthesis, may therefore affect steroidogenesis when used as lipid-lowering agents in hypercholesterolaemia. 3. We have assessed gonadal and adrenal function in subjects with heterozygous familial hypercholesterolaemia (FH) before and after 12 weeks treatment with pravastatin, an HMG CoA reductase inhibitor, or cholestyramine as a control in maximal recommended doses. 4. No changes in measured plasma cortisol responses to tetracosactrin injection were seen in 11 patients on cholestyramine or 12 on pravastatin. 5. No changes were seen in testosterone, sex hormone binding globulin, androstenedione, dehydroepiandrosterone sulphate, oestradiol or 17 alpha-hydroxyprogesterone. 6. Gonadotrophin levels were unaffected in 10 male subjects on cholestyramine and 7 on pravastatin. 7. Measurements on a subset of subjects continuing to 24 weeks treatment also showed no changes. 8. No adverse effect on adrenal or gonadal function could be demonstrated in patients with familial hypercholesterolaemia on maximal recommended doses of pravastatin.

Adrenal Glands↗
PubMed1991

Detection of diabetic retinopathy in the community using a non-mydriatic camera.

The role of the non-mydriatic fundus camera in detection of diabetic retinopathy was evaluated as part of a comprehensive screening programme for diabetic complications offered to all diabetic patients in a rural town. Retinopathy was demonstrated in 124/358 (35%) of patients screened. Forty-eight patients (13%) were judged to have sight-threatening retinopathy, of whom 29 patients (8% of the total) were not already under the care of an ophthalmologist. However, in only 66% of patients were photographs of both eyes of adequate quality to assess for retinopathy. The percentage of poor quality photographs increased with age in those aged greater than 50 years. It is concluded that the non-mydriatic camera can increase the detection of sight-threatening retinopathy in the community. Although this method of screening is not perfect, because of the number of poor quality photographs, it may be as good as or better than existing screening practices in unselected diabetic populations.

Adolescent↗
PubMed1990

Combination of insulin with glipizide increases peripheral glucose disposal in secondary failure type 2 diabetic patients.

Twenty Type 2 diabetic patients, recently converted to insulin because of inadequate control on oral hypoglycaemic agents, were studied. Endogenous insulin reserve was measured by glucagon stimulation, and insulin-mediated peripheral glucose disposal by a hyperglycaemic (11 mmol l-1) clamp, measurements being repeated after 8 weeks of glipizide or placebo therapy in addition to the patients' usual insulin. The study was randomized and double blind. Fasting and stimulated C-peptide levels did not change on glipizide or placebo. Insulin-mediated glucose disposal rose from 2.5 (1.5-8.0) (median (range] to 4.2 (2.3-8.4) mg kg-1 min-1 in the glipizide group (n = 9, p less than 0.01), but did not change in the placebo group. Glycosylated haemoglobin did not change in either group, but median fasting plasma glucose fell from 10.6 (6.1-15.1) to 9.0 (6.4-11.2) mmol l-1 in the glipizide group (p less than 0.02). Fasting insulin rose on glipizide from 10.1 (4.0-23.2) to 13.0 (6.4-33.8) mU l-1 (p less than 0.02). Insulin dosage fell in the glipizide group from 36 to 26 U day-1, as 4 patients experienced hypoglycaemic symptoms. HDL-Cholesterol fell in all patients on glipizide, from 0.94 (0.79-2.13) to 0.79 (0.62-1.95) mmol l-1 (p less than 0.01). Combination of insulin with the sulphonylurea glipizide in secondary failure Type 2 diabetic patients leads to increased insulin-mediated peripheral glucose disposal. Glipizide may have an adverse effect on HDL-cholesterol, which is unrelated to change in diabetic control.

Aged↗
PubMed1990

Isoform patterns of apolipoprotein E in diabetes mellitus.

Apolipoproteins in delipidated VLDL preparations from normal, diabetic, and non-diabetic hyperlipidaemic subjects were analysed by SDS-polyacrylamide gel electrophoresis, and by isoelectric focusing. On electrophoresis, diabetic VLDL contained more apolipoprotein E (17.3 +/- 7.3 (+/- SD) %, n = 54) than did VLDL from hyperlipidaemic (13.4 +/- 4.2%, n = 52; p less than 0.005) or normal (12.4 +/- 2.6%, n = 29; p less than 0.001) subjects. Apolipoprotein E excess was also seen when subgroups were characterized by apolipoprotein E phenotype. In diabetic patients of E3/E3 phenotype, apolipoprotein E was 16.4 +/- 6.0% (n = 25), compared with 12.9 +/- 2.5% in control subjects (n = 14; p = 0.008). Acidic isoforms were more common in 44 diabetic patients with E3/E3 phenotype; E3, E2, E1, and E1' as percentage of total E apolipoprotein were 58.3 +/- 7.6, 24.5 +/- 4.4, 13.7 +/- 4.5, and 3.8 +/- 4.3% respectively, compared with 63.5 +/- 10.4 (p = 0.034), 19.1 +/- 5.3 (p less than 0.001), 13.7 +/- 6.5 (NS), and 3.7 +/- 2.1% (NS) in 21 normal subjects. In 31 diabetic patients, of apolipoprotein E3/E3 phenotype, E3, E2, E1 and E1' were 60.2 +/- 7.3, 23.4 +/- 9.4, 11.1 +/- 4.1, and 5.4 +/- 3.7%, respectively, compared with 68.0 +/- 7.1 (p less than 0.001), 21.9 +/- 6.4 (NS), 6.3 +/- 3.9 (p less than 0.001), and 3.7 +/- 2.5 (p less than 0.05) % in 32 hyperlipidaemic patients. Diabetic patients of E3/E2 phenotype showed less apolipoprotein E3 than normal or hyperlipidaemic subjects, with a similar trend for apolipoprotein E4 in those of E4/E3 phenotype.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoproteins↗
PubMed1989

Proliferative diabetic retinopathy in a patient with maturity-onset diabetes of the young (MODY).

Maturity-onset diabetes of the young (MODY) has been described as being characteristically free from severe complications. This has led to speculation that the type of diabetes may be important in the pathogenesis of complications in diabetes. We report a case of classical MODY in which severe proliferative diabetic retinopathy developed. The retinopathy was detected shortly after the diagnosis of diabetes was made when the patient was 32 years old, and did not progress subsequently. No further complications developed during the subsequent 29 years in which normal postprandial plasma glucose levels were maintained with chlorpropamide therapy (mean 4.7, range 4.1-6.0 mmol I-1). This case demonstrates that severe retinopathy can occur in MODY and we suggest that in this patient there may have been a period of hyperglycaemia prior to diagnosis which was sufficient to lead to the microvascular complication.

Adolescent↗
PubMed1988

Clinical and laboratory responses to niceritrol in the treatment of hypercholesterolaemia.

Twenty-five hypercholesterolaemic patients from three centres in the UK were investigated in an open study of the efficacy and side effects of niceritrol. Five patients dropped out of the study at an early stage and had insufficient data for analysis. There were 13 males and 7 females (mean age 49.2 years, range 18-69). Fourteen patients had heterozygous familial hypercholesterolaemia, and six polygenic hypercholesterolaemia. Niceritrol was started at a dose of 750 mg/day and this was increased at weekly intervals over 4 weeks to the maximum tolerated dosage up to 3 g/day. This was then maintained for a further 8 weeks. There were statistically significant decreases in total plasma cholesterol, total triglyceride, LDL cholesterol and VLDL triglyceride; HDL cholesterol remained unchanged after 12 weeks of treatment (Wilcoxon matched pairs, signed ranks test). The 14 patients with familial hypercholesterolaemia showed a 13.9% fall in total cholesterol and a 19.8% fall in LDL cholesterol. All patients reported flushing and some had gastrointestinal symptoms but 19 would have been prepared to continue with the therapy at doses up to 3 g/day. Thus niceritrol has been found to be beneficial in the treatment of both familial and polygenic hypercholesterolaemia.

Adolescent↗
PubMed1987

Glycaemic control in diabetic patients transferred from therapy with animal insulins to human crystalline zinc insulin of recombinant DNA origin: a multicentre study.

87 stable insulin-dependent diabetic patients from 6 diabetic clinics within the UK were transferred from their existing once or twice daily regimen of subcutaneous animal insulin to a similar regimen of human insulin of recombinant DNA origin in neutral soluble and crystalline zinc suspension formulations. Seven point blood glucose profiles, glycosylated haemoglobin concentrations and insulin dose were examined, in each patient, before and after 6 weeks therapy with human insulins. The 67 patients on twice daily insulin showed no significant change in mean blood glucose values or glycosylated haemoglobin but required a significantly higher dose of human crystalline zinc suspension than their previous long-acting animal insulin. In contrast the 17 patients on a once daily regimen experienced a significant deterioration in glycaemic control without a significant change in insulin dose or glycosylated haemoglobin. Three patients on twice daily insulin withdrew shortly after transfer to human insulin. The combination of human soluble and crystalline zinc suspension appears to be a more satisfactory substitute for animal insulin when used in a multi-dose regime rather than on a once daily basis.

Animals↗
PubMed1986

Paradoxical platelet behaviour in diabetic ketoacidosis.

Thrombotic events may occur in patients who present with severe uncontrolled diabetes or with diabetic coma. As a possible explanation for this, platelet function was investigated at presentation with diabetic ketoacidosis and during treatment in 10 patients. Concentrations of the platelet-specific proteins, platelet factor 4 (PF4) and beta-thromboglobulin (beta TG) were elevated and fell towards normal with treatment. Despite evidence of increased aggregation in vivo, platelets from subjects with ketoacidosis were insensitive to adenosine 5'-diphosphate (ADP), sensitivity increasing with correction of ketoacidosis. Platelets from ketoacidotic diabetics were initially insensitive to the anti-aggregatory action of prostacyclin (PGI2) and became normal with treatment. Initial blood glucose concentrations correlated with log10 ADP concentrations (r = 0.72, p less than 0.01) and with log10 PGI2 ID50 (the PGI2 concentration required to half-inhibit ADP-induced aggregation) (r = 0.66, p less than 0.025). Glucose concentrations throughout the 2-week study period correlated with all log10 ADP concentrations (r = 0.32, p less than 0.005) and all log10 PGI2 ID50 concentrations (r = 0.51, p less than 0.001). The decrease in ADP sensitivity in ketoacidosis, paradoxical in view of the evidence of increased in vivo platelet aggregation, may result from an acquired platelet storage pool deficiency.

Adenosine Diphosphate↗