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Biomedical subjects

N McIntyre

Publications and source records attributed to N McIntyre.

At least 109 records · Page 6Linked to original sources
PubMed1986

Computer aided diagnosis of acute abdominal pain: a multicentre study.

A multicentre study of computer aided diagnosis for patients with acute abdominal pain was performed in eight centres with over 250 participating doctors and 16,737 patients. Performance in diagnosis and decision making was compared over two periods: a test period (when a small computer system was provided to aid diagnosis) and a baseline period (before the system was installed). The two periods were well matched for type of case and rate of accrual. The system proved reliable and was used in 75.1% of possible cases. User reaction was broadly favourable. During the test period improvements were noted in diagnosis, decision making, and patient outcome. Initial diagnostic accuracy rose from 45.6% to 65.3%. The negative laparotomy rate fell by almost half, as did the perforation rate among patients with appendicitis (from 23.7% to 11.5%). The bad management error rate fell from 0.9% to 0.2%, and the observed mortality fell by 22.0%. The savings made were estimated as amounting to 278 laparotomies and 8,516 bed nights during the trial period--equivalent throughout the National Health Service to annual savings in resources worth over 20m pounds and direct cost savings of over 5m pounds. Computer aided diagnosis is a useful system for improving diagnosis and encouraging better clinical practice.

Abdomen↗
PubMed1986

Serum immunoreactive trypsin and pancreatic lipase in primary biliary cirrhosis.

Immunoreactive trypsin concentration and pancreatic lipase activity were measured in the sera of 33 patients with primary biliary cirrhosis. Immunoreactive trypsin was increased (above the normal range) in 16 (48%) and pancreatic lipase activity in 18 (55%) patients. Both enzymes were increased in 10 (30%) patients. Twenty four patients (73%) had an increase of either one or both enzymes. There was a significant correlation between immunoreactive trypsin and pancreatic lipase activity. This abnormality was not related to treatment with D-penicillamine, the age of the patients, the stage of the disease, or the severity of cholestasis. Thus most patients with primary biliary cirrhosis have increased pancreatic enzyme activity and immunoreactive trypsin concentration in their sera. These data are indicative of damage to the exocrine pancreas. The cause of this damage is as yet unknown.

Age Factors↗
PubMed1985

Desmopressin and bleeding time in patients with cirrhosis.

Desmopressin acetate 0.3 microgram/kg was given intravenously to nine patients with chronic liver disease and to a further six such patients in a double blind controlled study versus placebo. Desmopressin acetate significantly shortened the bleeding time compared with basal values in both groups and compared with placebo. There was also a significant decrease in partial thromboplastin time (but not prothrombin time) and significant increases in factor VIII and its components, von Willebrand factor and ristocetin cofactor activity, but not in factors VII, IX, X, XI, or XII. Increased fibrinolysis could be blocked by concomitant administration of tranexamic acid. No important side effects were seen. The multimer pattern of von Willebrand factor was studied for the first time in chronic liver disease. It was normal, but after administration of desmopressin acetate the percentage of multimers of higher molecular weight increased significantly. This may be an important mechanism in the shortening of the bleeding time in cirrhosis, as has been shown in uraemia and other conditions after administration of desmopressin acetate. Desmopressin acetate may be useful in correcting defects in primary haemostasis in chronic liver disease.

Bleeding Time↗
PubMed1985

Erythrocyte echinocytosis in liver disease. Role of abnormal plasma high density lipoproteins.

Echinocytes were frequently found in patients with liver disease when their blood was examined in wet films, but rarely detected in dried, stained smears. When normal erythrocytes (discocytes) were incubated with physiologic concentrations of the abnormal high density lipoproteins (HDL) from some jaundiced patients, echinocytosis developed within seconds. Other plasma fractions were not echinocytogenic. There was a close correlation between the number of echinocytes found in vivo and the ability of the corresponding HDL to induce discocyte-echinocyte transformation. On incubation with normal HDL, echinocytes generated in vitro rapidly reverted to a normal shape, and echinocytes from patients showed a similar trend. Echinocytosis occurred without change in membrane cholesterol content, as did its reversal, and was not caused by membrane uptake of lysolecithin or bile acids. Abnormal, echinocytogenic HDL showed saturable binding to approximately 5,000 sites per normal erythrocyte with an association constant of 10(8) M-1. Nonechinocytogenic patient HDL and normal HDL showed only nonsaturable binding. Several minor components of electrophoretically separated erythrocyte membrane proteins bound the abnormal HDL; pretreatment of the cells with trypsin or pronase reduced or eliminated binding. Echinocytosis by abnormal HDL required receptor occupancy, rather than transfer of constituents to or from the membrane, because cells reversibly prefixed in the discoid shape by wheat germ agglutinin, and then exposed to abnormal HDL, did not become echinocytes when the HDL and lectin were successively removed. Binding did not cause dephosphorylation of spectrin. We conclude that the echinocytes of liver disease are generated from discocytes by abnormal HDL, and we infer that the shape change is mediated by cell-surface receptors for abnormal HDL molecules.

Carcinoma↗
PubMed1984

Abnormal high density lipoproteins from patients with liver disease regulate cholesterol metabolism in cultured human skin fibroblasts.

Apolipoprotein B (apoB) of plasma low density lipoproteins (LDL) binds to high affinity receptors on many cell types. A minor subclass of high density lipoproteins (HDL), termed HDL1, which contains apoE but lacks apoB, binds to the same receptor. Bound lipoproteins are engulfed, degraded, and regulate intracellular cholesterol metabolism and receptor activity. The HDL of many patients with liver disease is rich in apoE. We tested the hypothesis that such patient HDL would reduce LDL binding and would themselves regulate cellular cholesterol metabolism. Normal HDL had little effect on binding, uptake, and degradation of 125I-labeled LDL by cultured human skin fibroblasts. Patient HDL (d 1.063-1.21 g/ml) inhibited these processes, and in 15 of the 25 samples studied there was more than 50% inhibition at 125I-labeled LDL and HDL protein concentrations of 10 micrograms/ml and 25 micrograms/ml, respectively. There was a significant negative correlation between the percentage of 125I-labeled LDL bound and the apoE content of the competing HDL (r = -0.54, P less than 0.01). Patient 125I-labeled HDL was also taken up and degraded by the fibroblasts, apparently through the LDL-receptor pathway, stimulated cellular cholesterol esterification, increased cell cholesteryl ester content, and suppressed cholesterol synthesis and receptor activity. We conclude that LDL catabolism by the receptor-mediated pathway may be impaired in liver disease and that patient HDL may deliver cholesterol to cells.

Adult↗
PubMed1982

Decreased erythrocyte membrane fluidity and altered lipid composition in human liver disease.

Abnormal plasma lipoproteins in patients with liver disease are associated with characteristic changes in erythrocyte membrane lipid composition. The membranes are enriched in cholesterol and phosphatidylcholine and both the cholesterol/phospholipid and phosphatidylcholine/sphingomyelin molar ratios are increased. Phospholipid fatty acid composition is also abnormal; the proportions of arachidonic acid and stearic acid are decreased and that of palmitic acid raised. In this study we have examined the effects of these membrane lipid abnormalities on membrane fluidity. Erythrocyte membrane fluidity was assessed in 30 patients with a variety of liver diseases and in 25 normal subjects using the hydrophobic, fluorescent probe 1,6-diphenylhexa-1,3,5-triene and the values were related to their lipid composition. Membrane fluidity was significantly decreased in the patient erythrocytes (lipid order parameter, S(v)[37 degrees C] = 0.713 +/- 0.018, mean +/- S.D. compared to 0.686 +/- 0.008 in the normal subjects, P < 0.001) and correlated significantly with the cholesterol/phospholipid ratio (r = 0.88, P < 0.001). The fluidity of lipid extracts from the membranes of patient erythrocytes was also decreased, suggesting that decreased membrane fluidity was mainly a consequence of altered lipid composition rather than protein abnormalities. Incubation of patient erythrocytes for 20 hr with normal, heated plasma removed the excess cholesterol without affecting the phosphatidylcholine/sphingomyelin ratio or phospholipid fatty acid composition; following incubation the fluidity of these membranes was similar to that of normal membranes. We conclude that in liver disease changes in the composition of the phospholipid bilayer matrix in the erythrocyte membrane have little influence on its fluidity; the reduced fluidity is predominantly a result of increases in cholesterol relative to phospholipid.-Owen, J. S., K. R. Bruckdorfer, R. C. Day, and N. McIntyre. Decreased erythrocyte membrane fluidity and altered lipid composition in human liver disease.

Abetalipoproteinemia↗
PubMed1981

Platelet lipid composition and platelet aggregation in human liver disease.

Abnormal plasma lipoproteins in patients with liver disease are associated with an increase in erythrocyte cholesterol concentration and a raised erythrocyte cholesterol/phospholipid molar ratio. We hypothesized that their platelets would also have an increased cholesterol/phospholipid ratio and that this might affect aggregation in vitro. Platelet aggregates by adrenaline and ADP was measured in 34 patients with a variety of liver diseases and in 20 normal subjects and the values were related to platelet lipid composition. The platelet cholesterol/phospholipid ratio was 13% higher in the patients and correlated closely with erythrocyte cholesterol/phospholipid ratio. Platelet aggregation was reduced in most of the patients and inversely correlated with the cholesterol/phospholipid ratio. Cross-incubation and hemostasis studies indicated that there were no inhibitory factors present in the plasma; the defect was in the platelets. In contrast, other workers have shown that cholesterol-rich platelets, either from patients with Type IIa hyperlipoproteinemia or prepared in vitro, aggregate more readily than normal platelets. However, the phospholipid and fatty acid compositions of our patient platelets were also abnormal: the lecithin/sphingomyelin ratio was increased and was inversely correlated with aggregation; the proportion of arachidonic acid was decreased and positively correlated with the aggregation. In our patients with liver diseases the effects of the altered phospholipid and fatty acid composition presumably overrode those of the increased cholesterol content so that instead of enhanced aggregation, only reduced or normal aggregation was seen. We conclude that the reduced platelet aggregation seen in liver disease may reflect a decrease in arachidonic acid availability for prostaglandin and/or thromboxane production.

Blood Platelets↗
PubMed1980

Dimethylsulphoxide-induced toxicity.

Two elderly people were given intravenous infusion of dimethylsulphoxide (DMSO) as treatment for arthritis. One became seriously ill, the other remained well. Both had similar changes in aspartate transaminase, hydroxybutyrate dehydrogenase, and creatine kinase and evidence of haemolysis. This is the first report of serum enzyme changes and anaemia after intravenous DMSO in man.

Acute Kidney Injury↗