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Biomedical subjects

C R Tomson

Publications and source records attributed to C R Tomson.

At least 55 records · Page 3Linked to original sources
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↗
PubMed1989

Effect of pyridoxine supplementation on plasma oxalate concentrations in patients receiving dialysis.

Plasma oxalate and erythrocyte glutamic oxaloacetate transaminase activity (EGOT) (an indicator of nutritional status with respect to pyridoxine) were measured in 21 patients maintained on regular continuous ambulatory peritoneal dialysis or haemodialysis before and after a 4-month period of supplementation with pyridoxine, 100 mg day-1. Prior to supplementation 10/21 patients showed subnormal EGOT activity, although the increment in activity on addition of pyridoxal-5-phosphate in vitro was within the normal range in all cases. Mean plasma oxalate was 31.5 mumol l-1 (SEM 2.9) prior to supplementation and did not change significantly with supplementation, despite normalization of EGOT activity in all but 2/21 patients. We conclude that pyridoxine deficiency does not contribute significantly to hyperoxalaemia in patients receiving dialysis and that 100 mg of pyridoxine daily is insufficient to reduce oxalate generation by a pharmacological action on glycine transamination.

Aspartate Aminotransferases↗
PubMed1989

Strychnine poisoning as an unusual cause of convulsions.

A fatal case of strychnine poisoning is presented. The patient vomited then suffered a series of tonic convulsions which were triggered by tactile stimulation. In between paroxysms he was initially alert. Eventually the patient became comatosed due to anoxia and had a cardiac arrest. He presented with a marked metabolic acidosis and rapidly developed renal failure caused by acute rhabdomyolysis. This clinical picture is classical for strychnine poisoning and the complications which the intoxication produces. Attention is drawn to the fact that survival can even follow the ingestion of very large doses of strychnine providing there is no delay in diagnosis and treatment.

Adult↗
PubMed1989

Plasma oxalate concentration, oxalate clearance and cardiac function in patients receiving haemodialysis.

Pre-dialysis plasma oxalate concentration was measured in a cross-sectional study of 75 patients receiving maintenance haemodialysis. The aims of this study were to enable formulation of hypotheses regarding the determinants of plasma oxalate concentration and to allow preliminary examination of the possibility that hyperoxalaemia confers an increased risk of cardiac and vascular disease even in the absence of primary hyperoxaluria. Plasma oxalate concentration ranged between 7 and 76 mumol/l, mean (SD) 34.6 (18.1) mumol/l (normal range less than 0.8-2.0 mumol/l). Significant correlations were found between plasma oxalate concentration and plasma creatinine, duration of dialysis, current dose of ascorbic acid, and serum phosphate, and each of these variables retained significance on multiple linear regression. Oxalate clearance across a 1 m2 hollow-fibre Cuprophan dialyser, at 500 ml/min dialysate flow and blood flow between 175 and 225 ml/min, was measured 1 h after commencement of dialysis (n = 19). Mean (SD) clearance was 96.5 (27.0) ml/min. No significant association was found between self-reported maximum walking distance or the occurrence of symptoms of cardiac failure and plasma oxalate concentration. No relationship was found between plasma oxalate concentration and electrocardiographic conduction disturbances (n = 8) 'major' ST/T wave changes (n = 22), 'minor' ST/T wave changes (n = 49). Plasma oxalate was significantly greater in patients with radiologically detectable calcification of medium-sized arteries than in those without calcification, but duration of dialysis was also significantly longer in these patients. Routine haemodialysis results in marked hyperoxalaemia, which may be exacerbated by ascorbate supplementation. Oxalate clearance is similar to that of other small molecules such as creatinine and phosphate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Seizures in haemodialysis patients treated with recombinant human erythropoietin.

Administration of recombinant erythropoietin (r-HuEPO) is an effective treatment for the anaemia of chronic renal failure, but in some patients it has been accompanied by elevated blood pressure. This study focuses on seven patients with end-stage renal failure, managed on haemodialysis, who developed probable hypertensive encephalopathy with seizures during treatment with r-HuEPO. All made a full recovery. The events were not clearly related to the haemoglobin concentrations achieved, and four patients have subsequently been restarted on r-HuEPO therapy at a reduced dose, resulting in a slower increase in haemoglobin with no recurrence of episodes of severe hypertension. Close attention needs to be paid to blood pressure in patients commencing erythropoietin therapy, and it seems prudent to aim for a gradual increase in haemoglobin concentration to allow the circulation to adapt to changes in oxygen delivery and haematocrit.

Adult↗
PubMed1989

Oxalate retention in chronic renal failure: tubular vs glomerular diseases.

Plasma oxalate concentration was measured using an enzyme/bioluminescent assay in 289 patients (178 males, 111 females) with chronic renal failure (plasma creatinine greater than 200 mumol/l), age (SD) 55.5 (13.8) years. Plasma oxalate ranged between less than 0.8 and 48 mumol/l and showed a positive correlation with plasma creatinine (r = 0.57, p less than 0.0001). The slope of the regression line in 55 patients with glomerulonephritis (GN) was significantly lower than in patients with tubulointerstitial disease (TI); however the intercept was significantly higher in GN than in TI. Analysis of covariance showed no relationship between plasma oxalate concentration and age, duration of renal impairment, or administration of diuretics, vitamin D analogues, or phosphate binders. Longitudinal analysis of plasma oxalate measured 3-monthly in selected patients showed marked variability of oxalate/creatinine and oxalate/urea ratios.

Adolescent↗
PubMed1988

Plasma oxalate concentration and secondary oxalosis in patients with chronic renal failure.

To examine the association between hyperoxalaemia and secondary oxalosis, measurement of plasma oxalate concentration was combined with a search for tissue deposition of calcium oxalate crystals in patients with chronic renal disease. Two groups of patients were studied. In the first, samples of the inferior epigastric artery were taken from 35 patients at the time of renal transplantation. In the second, sections taken at necropsy from 23 patients with chronic renal failure in whom plasma oxalate had been measured before death were examined. Though plasma oxalate concentrations ranged between 6 and 116 mumol/l (four to 78 times greater than the upper limit of the reference range), no extrarenal deposits of oxalate were found in either study. Renal deposition of oxalate was associated with a plasma oxalate concentration of greater than 20 mumol/l. This study gives no support to the suggestion that hyperoxalaemia of the degree seen in patients with the type of chronic renal failure that is not due to primary hyperoxaluria confers an appreciable risk of extrarenal oxalosis.

Adolescent↗
PubMed1988

Cardiac arrest associated with hypokalaemia in a patient receiving mithramycin.

The case is reported of a patient who developed severe hypokalaemia, leading to cardiac arrest, while receiving mithramycin for painful Paget's disease. The patient was also receiving antihypertensive and anti-anginal treatment including bendrofluazide, but plasma potassium before the administration of mithramycin was normal. Hypokalaemia has been reported in previous studies of the use of mithramycin but has received little attention. The drug should be used with great care in patients with cardiovascular disease and in those receiving diuretics.

Aged↗
PubMed1988

Plasma oxalate in patients receiving continuous ambulatory peritoneal dialysis.

Plasma oxalate has been measured in 125 patients maintained on continuous ambulatory peritoneal dialysis using an enzyme/bioluminescent assay. Values ranged between 6 and 134 mumol/l, with a positively skewed distribution. Multiple linear regression analysis with plasma oxalate as the dependent variable showed highly significant associations with the dose of ascorbic acid, dose of alfacalcidol, and plasma creatinine, and weaker associations with serum phosphate, serum calcium, and body weight. When the presence of other potential risk factors was taken into account, no significant relationship could be found between the presence of clinically evident cardiac or vascular disease and plasma oxalate.

Ascorbic Acid↗