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Biomedical subjects

C R Tomson

Publications and source records attributed to C R Tomson.

At least 19 recordsLinked to original sources
PubMed1992

Crossover comparison of intravenous and subcutaneous erythropoietin in haemodialysis patients.

To examine the suggestion that s.c. administration of recombinant human erythropoietin (rHuEpo) may be more effective than i.v. administration, we changed the route of administration in 11 patients, previously established on a stable dose of rHuEpo given twice or thrice weekly, from i.v. to s.c. administration without altering the dose. All patients were iron replete (serum ferritin greater than 100 micrograms/l). In one patient the haemoglobin concentration declined at the time of conversion due to poor compliance, and another patient died shortly after conversion. In the remainder there was a significant increase in haemoglobin concentration from 9.30 (SD 0.78) at the time of conversion to 9.84 (0.59) at 1 month, 10.35 (1.22) at 2 months, and 10.39 (1.42) at 3 months. The increase in haemoglobin concentration was greater than 1 g/dl at 3 months in only five of the patients. Serum ferritin prior to conversion was similar in 'responders' and 'non-responders', but all responders had a transferrin saturation of greater than 16%, whereas three of four non-responders had transferrin saturation of less than or equal to 16%. Subcutaneous administration of rHuEpo is more effective, dose for dose, than i.v. administration, but poor iron mobilization may limit the response.

Adult↗
PubMed1992

Deterioration in renal function associated with angiotensin converting enzyme inhibitor therapy is not always reversible.

Fifteen patients presented between January 1986 and January 1991 with deterioration in renal function coincident with the introduction of angiotensin converting enzyme inhibitors. There was evidence of extrarenal vascular disease in 12 patients and preexisting renal impairment in 13. Four patients remained dialysis-dependent and died within 4 weeks of presentation. Five patients required short-term dialysis. Serum creatinine remained above pre-treatment values in seven patients. Conventional explanations of the decline in renal function with ACE inhibition do not account for irreversible decrements in renal function. Possible mechanisms for this observation and clinical guidelines to identify patients at risk are suggested. We conclude that these agents should be used with great care in patients in whom atherosclerotic vascular disease is likely.

Acute Kidney Injury↗
PubMed1992

Effect of recombinant human erythropoietin on erythropoiesis in homozygous sickle-cell anaemia and renal failure.

The development of end-stage renal disease (ESRD) in patients with sickle-cell anaemia results in increased transfusion dependence, increasing the risk of iron overload. Correction of anaemia with recombinant human erythropoietin (rHuEpo) in dialysis patients might also result in stimulation of haemoglobin F production, which protects against sickling, although very high doses were required to achieve this effect in non-uraemic animals. rHuEpo was administered to three transfusion-dependent patients with ESRD and homozygous sickle-cell disease (initial dose 100 U/kg twice weekly, increasing to 125 U/kg at 6 weeks, and to 150 U/kg at 9 weeks in two patients). This resulted in reticulocytosis and increased circulating erythroid blast-forming units. Total haemoglobin was predominantly HbA (i.e. transfused blood) at the start of the study, reflecting transfusion dependence, but after 3 months' treatment was between 60 and 94% HbS. No sickling crises occurred. Haemoglobin F remained at less than 3% of total haemoglobin. One patient was withdrawn at 10 weeks with CAPD peritonitis. The other two patients completed 12 weeks' treatment without transfusion but final Hb concentrations were 4.5 and 5.5 g/dl. Whether larger doses of rHuEpo will be more successful in managing such patients remains unclear. No effect on HbF production can be expected.

Adult↗
PubMed1991

Plasma erythropoietin levels and acquired cystic disease of the kidney in patients receiving regular haemodialysis treatment.

Acquired cystic disease of the kidney (ACDK) in patients with end-stage renal failure can be associated with development of polycythaemia. The relationship between plasma erythropoietin levels and ACDK in 17 patients on long-term haemodialysis treatment was studied. There was a significantly higher level of plasma erythropoietin in patients with multiple renal cysts than in those patients with less than five cysts or no cysts. Haemoglobin tended to be higher in the ACDK group, but the difference was not significant. These results indicate that the development of renal cysts results in increased secretion of erythropoietin.

Erythrocyte Indices↗
PubMed1991

Does treated essential hypertension result in renal impairment? A cohort study.

To determine how frequently essential hypertension results in significant renal impairment we undertook a follow-up study of 176 patients with well documented essential hypertension first seen in 1975-1977. Six patients were Asian, two Negro, and the remainder Europid. Follow-up was achieved in 92% of the cohort at five years and in 87% at 12-14 years. At five years 13 (7%) patients had moved away or were lost, and 15 (9%) patients had died (11 cardiovascular deaths). Treated blood pressure was greater than 160/95 mmHg in 60/148 patients and greater than 200/100 mmHg in 16 patients. Despite this, no significant change in serum creatinine was detected in the group as a whole. Increments in serum creatinine of at least 35 mumol/l occurred in six patients. Over the ensuing 6-9 years serum creatinine had returned to normal in three of these patients and stabilized in two; the sixth patient died from myocardial infarction. No patient reached end-stage renal failure. We conclude that progressive deterioration in renal function in essential hypertension is rarely a significant problem in Caucasian patients. A decline in renal function should prompt a search for underlying primary renal disease.

Adult↗
PubMed1990

Echocardiographic assessment of systolic function in dialysis patients.

Echocardiography has been widely used to investigate cardiac function in uraemic patients. There is no doubt about the validity of this technique in certain situations, particularly the demonstration of structural abnormalities and pericardial effusions. However, the assessment of cardiac function by measurement of cardiac dimensions and their rate of change is complicated by the profound influence of altered loading conditions, common in uraemia, on the measurements obtained. This is a particular problem in the assessment of changes in cardiac function during haemodialysis. Even studies utilising isovolaemic dialysis are open to criticism, due to the effects of altered afterload on cardiac emptying. Recently the experimental finding that end-systolic volume is independent of end-diastolic volume and linearly related to afterload has raised the possibility that non-invasive assessment of end-systolic indices may allow load-independent assessment of intrinsic cardiac contractility in patients. However, none of the studies using these indices in uraemic patients has validated the assumption that they are indeed load-independent in this clinical situation. Evidence is presented suggesting that the end-systolic pressure:volume relationship is altered by the administration of a volume load and that manipulation of afterload without autonomic blockade results in markedly increased contractility, presumably due to reflex sympathetic activity. More work is required before these indices are used uncritically in dialysis patients.

Echocardiography↗
PubMed1990

Ascorbate-induced hyperoxalaemia has no significant effect on lactate generation or erythrocyte 2,3,diphosphoglycerate in dialysis patients.

To examine the possible effects of hyperoxalaemia on anaerobic metabolism and erythrocyte pyruvate kinase activity, we induced a rise in plasma oxalate in 11 dialysis patients by the oral administration of ascorbic acid, 500 mg day-1 for 3 weeks. Blood samples were taken from the same antecubital vein before and after the supplementation period, without venous stasis, after an overnight fast. This protocol allowed patients to be used as their own controls. Five healthy subjects underwent an identical protocol to exclude any effect of ascorbate per se. Mean (SEM) plasma oxalate (mumol l-1) rose from 30.3 (3.5) to 48.4 (6.1) in patients and from 1.4 (0.2) to 6.8 (0.9) in healthy subjects. Whole blood ascorbate (mg l-1) rose from 7.0 (0.7) to 26.6 (2.5) in patients and from 9.3 (1.2) to 17.8 (1.8) in healthy subjects (reference range 7.5-20.0 mg l-1). No changes were observed in either group in plasma creatinine, bicarbonate, haemoglobin, or erythrocyte 2,3,diphosphoglycerate (2,3 DPG) after the 3 week supplementation period. Before supplementation lactate generation (area under curve, mmol min l-1) in the 5 min following a 60 s period of standardized ischaemic forearm exercise was significantly (P = 0.026) greater in patients [69.1 (4.7)] than in healthy subjects [46.9 (6.7)]; no significant change in lactate generation occurred in either group after ascorbate-induced hyperoxalaemia. We conclude that changes in plasma oxalate of the order of 20 mumol l-1 have no significant effect on lactate generation or 2,3,DPG levels in uraemic subjects.

2,3-Diphosphoglycerate↗
PubMed1990

Acetonitrile ingestion: delayed onset of cyanide poisoning due to concurrent ingestion of acetone.

A fatal case of acetonitrile ingestion is reported. The patient presented having apparently taken an overdose but was well until around 24 hours after the supposed ingestion, when cardiovascular collapse and profound metabolic acidosis developed. Later investigation revealed that the patient had taken acetone and acetonitrile. Acetone is known to slow the metabolism of acetonitrile to cyanide, thereby delaying the appearance of toxicity.

Acetone↗
PubMed1990

Long term survival on haemodialysis in primary hyperoxaluria.

Results of treatment of end-stage renal failure (ESRF) in patients with primary hyperoxaluria have been generally poor, largely due to the inability of any treatment regime to match the endogenous overproduction of oxalate. The severity of the disease varies widely, as reflected by the differences in age at onset of ESRF. This variability may influence the results of treatment of ESRF in these patients. The longest reported survival on haemodialysis of a patient with primary hyperoxaluria is eight and a half years. We report a patient who survived for eleven years on haemodialysis after reaching ESRF due to primary hyperoxaluria, and suggest that this prolonged survival was due to relatively mild disease severity rather than exceptional treatment.

Female↗
PubMed1989

Correction of subclinical ascorbate deficiency in patients receiving dialysis: effects on plasma oxalate, serum cholesterol, and capillary fragility.

Whole blood ascorbate, plasma oxalate, serum cholesterol, and capillary fragility were measured at monthly intervals for 3 mth in 7 patients receiving continuous ambulatory peritoneal dialysis and 4 receiving haemodialysis, to whom ascorbate supplements had not been prescribed for at least 12 mth. Ascorbate supplements, 25 mg/day, were prescribed for the first month and 50 mg/day for the second month; in the final month patients received no supplements. Whole blood ascorbate was below normal in 6/11 patients at the start of the study but was normal in 10/11 patients when taking ascorbate 50 mg/day. No significant changes in plasma oxalate were observed with these doses of ascorbate, and correction of ascorbate deficiency had no effect on serum cholesterol, mean cell volume, or the results of capillary fragility tests. In a supplementary study, ascorbic acid 500 mg/day was administered for 3 wk to 11 patients. This resulted in a significant rise in mean plasma oxalate from 30.3 (SEM 3.5) to 48.4 (SEM 20.3) mumol/l.

Ascorbic Acid↗
PubMed1989

The determination of plasma oxalate concentrations using an enzyme/bioluminescent assay. 2. Co-immobilisation of bioluminescent enzymes and studies of in vitro oxalogenesis.

An inexpensive, continuous flow assay for the determination of oxalate in plasma is described. The assay is based on the bioluminescent determination of NADH, a product of the degradation of oxalate by oxalate decarboxylase and formate dehydrogenase, using bioluminescent enzymes immobilized on cyanogen bromide-activated sepharose. The detection limit of the assay is 0.8 mumol/l. Intra-batch CV values of 5.2 and 3.8% were obtained at oxalate concentrations of 18 and 60 mumol/l. Recovery of added oxalate averaged 100.7%. Plasma oxalate ranged from less than 0.8 to 2 mumol/l in 14 healthy subjects, and from 6 to 134 mumol/l in 125 patients with renal disease treated by continuous ambulatory peritoneal dialysis. Ascorbic and dehydroascorbic acid did not directly interfere in the assay. In vitro oxalogenesis was observed in blood from 12 healthy subjects, but only after samples had stood at room temperature for more than 6 h. No significant oxalate generation occurred in blood from 24 patients with impaired renal function, even after standing at room temperature for 24 h. Oxalate generation was inhibited by the addition of oxalate to plasma, but the addition of urea and creatinine was without effect.

Creatinine↗