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Biomedical subjects

N McIntyre

Publications and source records attributed to N McIntyre.

At least 91 records · Page 5Linked to original sources
PubMed1990

Clinical presentation of acute viral hepatitis.

Acute viral hepatitis may be asymptomatic, symptomatic but anicteric, or a classical icteric hepatitis; rarely it is very severe and may be fatal. Different types of illness may be caused by the various hepatitis viruses. This does not help precise diagnosis, which is based on serological tests. This paper describes hepatitis seen with the A, B, C, D and E viruses, and also some of the unusual complications which have been recognized. Serological tests allow precise diagnosis of acute hepatitis A and B, and should be used more widely, because viral hepatitis is often diagnosed when jaundice is caused by other conditions. They also allow diagnosis when viral hepatitis has an atypical presentation, and is thus not considered as the cause of the liver disease. Negative tests suggest the need for further investigation.

Acute Disease↗
PubMed1990

Intravenous albumin infusion is an effective therapy for hyponatraemia in cirrhotic patients with ascites.

The treatment of moderate to severe hyponatraemia in patients with decompensated liver disease is unsatisfactory. We report our preliminary experience using intravenous infusion of albumin to treat this condition. Three patients with cirrhosis, ascites, and hyponatraemia responded satisfactorily to treatment; one patient with fulminant hepatitis B did not respond. Intravenous albumin infusion is a safe and effective therapy for patients with cirrhosis complicated by hyponatraemia. Its main role may be in preparing patients for surgery, particularly liver transplantation.

Aged↗
PubMed1990

Severe hepatitis caused by cyproterone acetate.

A case of severe acute hepatitis caused by cyproterone acetate in a 71 year old man with prostatic carcinoma is reported with a review of the literature on hepatic reactions to this drug. The association between the use of cyproterone acetate and liver abnormalities is poorly documented. This is the fourth published report of adverse hepatic reaction to cyproterone acetate and it substantiates other evidence that cyproterone acetate is potentially hepatotoxic. Monitoring of liver function tests should be mandatory in patients receiving high doses of cyproterone acetate; the drug should be withdrawn immediately if abnormal liver function tests are found.

Adenocarcinoma↗
PubMed1990

Pancreatic pseudocyst causing portal vein thrombosis and pancreatico-pleural fistula.

Portal vein thrombosis and pancreatico-pleural fistula are unusual complications of chronic pancreatitis. We describe a patient with chronic alcoholic pancreatitis in whom erosion of the splenic vein led to portal vein thrombosis and to the development of a pancreatico-pleural fistula. We suggest that fistula formation may occur over a considerable time period as the portal vein thrombosis was diagnosed three years before the amylase-rich pleural effusions.

Adult↗
PubMed1990

How to insert a Sengstaken-Blakemore tube.

The Sengstaken-Blakemore (SB) tube is a valuable tool in the emergency treatment of patients with bleeding oesophageal varices. However, as its use may be associated with a number of serious complications it should be used judiciously and inserted with care. Once bleeding has been controlled with an SB tube, definitive treatment for the bleeding varices should be urgently considered.

Esophageal and Gastric Varices↗
PubMed1989

A comparison of sclerotherapy with staple transection of the esophagus for the emergency control of bleeding from esophageal varices.

We compared two procedures for the emergency treatment of bleeding esophageal varices in patients who did not respond to blood transfusion and vasoactive drugs. We randomly assigned 101 patients with cirrhosis of the liver and bleeding esophageal varices to undergo either emergency sclerotherapy (n = 50) or staple transection of the esophagus (n = 51). Four patients assigned to sclerotherapy and 12 assigned to staple transection did not actually undergo those procedures, but all analyses were made on an intention-to-treat basis. Total mortality did not differ significantly between the two groups; the relative risk of death for staple transection as compared with sclerotherapy was 0.88 (95 percent confidence interval, 0.51 to 1.54). Mortality at six weeks was 44 percent among those assigned to sclerotherapy and 35 percent among those assigned to staple transection. Complication rates were similar for the two groups. An interval of five days without bleeding was achieved in 88 percent of those assigned to staple transection and in 62 percent of those assigned to sclerotherapy after a single injection (P less than 0.01) and 82 percent after three injections. In only 2 of the 11 patients who received a third sclerotherapy injection was bleeding controlled for more than five days, and 9 died. We conclude that staple transection of the esophagus is as safe as sclerotherapy for the emergency treatment of bleeding esophageal varices and that it is more effective than a single sclerotherapy procedure. We currently recommend surgery after two injection treatments have failed.

Adolescent↗
PubMed1989

Cirrhotics with variceal hemorrhage: the importance of the time interval between admission and the start of analysis for survival and rebleeding rates.

The importance of variable time of entry for analysis of survival following variceal bleeding has recently been disputed. In a study of 194 cirrhotic patients with bleeding esophageal varices in whom 2-day mortality was 3%, statistically significant differences in both survival and rebleeding rates were obtained by shifting the starting point for analysis of survival by 2 weeks following admission to hospital or by 5 days for the analysis of rebleeding. In addition, the curve of hazard function for death or for failure to control bleeding following admission clearly showed that any change in entry time in a study of variceal bleeding would introduce bias and alter survival or rebleeding rates. Thus, the starting point for analysis following variceal hemorrhage is an important confounding variable when calculating both survival and rebleeding. It should always be taken into account, particularly in clinical trials, which are often performed in centers where patients are referred from other hospitals at different times following bleeding.

Epidemiologic Methods↗
PubMed1989

Significant bacteriuria has prognostic significance in primary biliary cirrhosis.

Significant bacteriuria in women has been found to be associated with increased mortality in community-based studies. We have previously reported a high prevalence of significant bacteriuria with a high recurrence rate in females with primary biliary cirrhosis (PBC), particularly those with late stage disease on liver biopsy. During a 5-year period we prospectively screened for significant bacteriuria in 187 women with primary biliary cirrhosis, (median follow-up of 47 months, range 1-83). Significant bacteriuria was found in 30 (17%) in their first urine (index bacteriuria), 90 (48%) died and 15 (8%) had liver transplants. Cox's proportional hazard models showed that age, serum bilirubin, ascites and cirrhosis were independent prognostic variables. Index bacteriuria added significantly to this model (P = 0.069) being independent from other variables, with an increased relative hazard for death of 1.65 (65% increase in risk of death) compared to non-bacteriuric patients. This effect was due mainly to non-cirrhotic patients with significant bacteriuria as shown by using multiplicative variables for histological stage and significant bacteriuria. An index of recurrent bacteriuria was significantly increased in patients with index bacteriuria (P less than 0.001) and in those who died or underwent transplantation (P less than 0.001). In this study, significant bacteriuria defined a specific sub-group of PBC patients with an increased risk of death.

Adult↗
PubMed1989

Carcinoma of the esophagus and long-term sclerotherapy.

We report a case where a chronic non-healing esophageal ulcer which developed following a course of endoscopic sclerotherapy proved to be an esophageal carcinoma. In view of 2 similar previous reports we discuss the possibility that sclerotherapy may act as a carcinogen, and suggest that all such non-healing esophageal ulcers should be biopsied.

Carcinoma, Squamous Cell↗
PubMed1988

Familial LCAT deficiency and fish-eye disease.

Familial LCAT deficiency is due to deficiency of plasma lecithin-cholesterol acyltransferase. The plasma is rich in free cholesterol and lecithin while cholesterol ester and lysolecithin levels are reduced. Analysis of the abnormal lipoproteins has helped our understanding of plasma lipid and lipoprotein metabolism in normals and in patients with liver disease. Proteinuria and anaemia are common and there is marked corneal lipid deposition. Eventually renal function deteriorates and dialysis and/or renal transplantation may be necessary. The human LCAT gene has been sequenced and been shown to be present on chromosomal segment 16q22-the region predicted on the basis of recombination studies as the site of the LCAT deficiency gene. The gene defect has been identified in some cases, but the mechanism remains unclear as the mutations were not in the region presumed to be the enzyme's active site. Only three cases of fish-eye disease have been described; all were elderly and had obvious corneal opacities. They had fasting hypertriglyceridaemia and increased VLDL. IDL and LDL were increased and were triglyceride rich. HDL, reduced by 90%, was mainly HDL3--with a high free and low ester cholesterol. LCAT activity in fish-eye plasma was normal but when measured in an exogenous substrate it was only 10-15% of normal. Fish-eye HDL is a substrate for purified LCAT, but fish-eye LCAT does not esterify free cholesterol of HDL (normal or fish-eye), although it esterifies free cholesterol of VLDL and LDL. It has been suggested that one type of LCAT activity acts on HDL (alpha-LCAT) and another on VLDL and LDL (beta-LCAT)--and that fish-eye disease is due to alpha-LCAT deficiency, and classical familial LCAT deficiency due to lack of both components.

Corneal Opacity↗
PubMed1988

Platelet aggregation and thromboxane A2 release in primary biliary cirrhosis and effect of D-penicillamine treatment.

Platelet function was assessed in 28 patients with primary biliary cirrhosis (PBC), of whom 10 were receiving D-penicillamine. Patients not on D-penicillamine treatment had platelet aggregation similar to that in the healthy control group; the group treated with D-penicillamine showed significantly enhanced platelet aggregation in response to threshold doses of adrenaline and collagen but not ADP. Median thromboxane B2 production was also higher in D-penicillamine treated patients than in controls or untreated patients; this difference did not reach statistical significance. The addition of D-penicillamine in vitro to platelet rich plasma from normal subjects was shown to enhance adrenaline- and collagen-induced platelet aggregation. Abnormalities of platelet function in PBC patients did not correlate with serum cholesterol concentration or with liver function tests but were related to the stage of disease. The present study emphasises the need to consider the aetiology, disease stage and type of treatment when assessing platelet function and prostanoid release in liver disease.

Aged↗
PubMed1988

Plasma lipid and lipoprotein response to carbohydrate feeding in cirrhotic patients.

Serum lipids and lipoproteins, and glucose and insulin, were measured after an overnight fast, and during 3 days of a eucaloric diet rich in carbohydrate, in 15 patients with cirrhosis and seven normal subjects. Following the high-carbohydrate diet triglyceride rose in all groups but the increase in cirrhotics was lower than in normals. In normals and in cirrhotics with good liver function most of the triglyceride increment was carried in VLDL; in cirrhotics with poor liver function only 31% of the increment was found in VLDL, and 56% in triglyceride-rich LDL. In an earlier study on fat feeding, our cirrhotic patients with poor liver function had an impaired chylomicron and VLDL response; they also carried most of the triglyceride increment in triglyceride-rich LDL. The markedly impaired response of triglyceride-rich lipoproteins to both carbohydrate and fat feeding suggests that sick cirrhotics may have a problem with storage of dietary energy and that this contributes to loss of their adipose tissue.

Adult↗
PubMed1987

The isolation and characterisation of cDNA and genomic clones for human lecithin: cholesterol acyltransferase.

The protein sequencing of tryptic peptides from purified human lecithin: cholesterol acyltransferase (LCAT) identified sufficient amino-acid sequence to construct a corresponding mixed oligonucleotide probe. This was used to screen an adult human cDNA liver library, from which incomplete cDNA clones were isolated. The DNA sequence of these clones allows the prediction of the entire amino-acid sequence of the mature LCAT enzyme. The mature protein consists of 416 amino acids and contains several marked stretches of hydrophobic residues and four potential glycosylation sites. The cDNA probe detects LCAT mRNA sequences approx. 1500 bases long in human liver, but not intestine, RNA. The cDNA probe was used to isolate LCAT genomic recombinants from a human genomic library. Southern blotting data, and restriction site mapping, suggest that there is a single human LCAT structural gene between 4.3 and 5.5 kb in size.

Amino Acid Sequence↗
PubMed1987

Membrane lipid changes in erythrocytes, liver and kidney in acute and chronic experimental liver disease in rats.

Lipid molecules in lipoprotein surfaces exchange with their counterparts in cell plasma membranes. In human or experimental liver disease, plasma lipoprotein surfaces are enriched in cholesterol and deficient in arachidonate; corresponding alterations occur in membrane lipids of erythrocytes. To determine whether similar changes take place in membranes of nucleated cells, the lipid content of plasma and of erythrocyte, liver and kidney membranes was measured in rats with acute (3-day) galactosamine-induced hepatitis or chronic (3-week) biliary obstruction. In both models of liver injury the cholesterol:phospholipid ratio in plasma and in erythrocytes was significantly increased (P less than 0.001). Although this ratio was also elevated in liver and kidney microsomes, only in liver microsomes of obstructed rats was the increase significant (P less than 0.001). However, the cholesterol:phospholipid ratio of kidney brush-border membranes, was significantly higher in bile-duct-ligated rats; presumably, compensating mechanisms limit cholesterol accumulation in intracellular membranes. Kidney brush-border membranes from obstructed rats were deficient in arachidonate as were plasma and erythrocytes. However, arachidonate levels were unchanged in kidney microsomes; renal delta 6-desaturase, the rate-limiting enzyme in the conversion of linoleic acid to arachidonic acid, was increased by 50% (P less than 0.001) and may have counteracted a reduced supply of exogenous lipoprotein arachidonate. We conclude that in experimental liver disease lipoprotein-induced lipid abnormalities can occur in renal membranes, although compensatory mechanisms may operate; the alterations seen, cholesterol accumulation and arachidonate depletion, would be expected to interfere with sodium transport and prostaglandin production, respectively. Our findings support the hypothesis that lipid abnormalities in kidney membranes contribute to the renal dysfunction which is a frequent complication of human liver disease.

Acute Disease↗
PubMed1987

The structural gene for lecithin:cholesterol acyl transferase (LCAT) maps to 16q22.

We have used a cDNA clone for human lecithin:cholesterol acyl transferase (LCAT) and Southern blotting techniques to identify the human LCAT gene in DNA from a series of rodent X human somatic cell hybrids. Our results are compatible with the location of the gene on human chromosome 16, and this has been confirmed using in situ hybridization of the LCAT cDNA to human metaphase chromosomes. These results confirm the earlier studies on LCAT-deficient patients, indicating that the structural gene for LCAT is on human chromosome 16q22.

Animals↗
PubMed1987

Hyperparathyroidism and low serum osteocalcin despite vitamin D replacement in primary biliary cirrhosis.

Thirty-six patients with primary biliary cirrhosis (PBC) receiving calcium and calciferol supplements (100,000 IU monthly by im injection) were investigated for their calcium, vitamin D, PTH, and osteocalcin status. The corrected plasma calcium concentrations in PBC patients were significantly greater than those in normal subjects. While the mean serum 25-hydroxycholecalciferol and 1,25-dihydroxyvitamin D concentrations in these patients were similar to those in normal subjects, the mean serum PTH concentration was significantly greater, and it was supranormal in 11 patients. Three patients had elevated corrected calcium concentrations; 1 of them had a concomitant increase in ionized calcium and a supranormal PTH level, and another had a high normal PTH. Ionized calcium concentrations were normal in the rest. Serum osteocalcin concentrations were significantly lower in the patients compared with those in normal subjects. These results indicate that PTH concentrations are frequently elevated in PBC patients despite adequate vitamin D supplementation and normal or even supranormal plasma calcium concentrations. Nonsuppression of PTH concentrations and autonomy of PTH secretion suggest that vitamin D deficiency and secondary hyperparathyroidism in such patients probably occur much earlier in the natural history of this disease than is currently realized. Persistent nonsuppressible hypersecretion of PTH probably contributes to the bone disease of primary biliary cirrhosis. The low osteocalcin concentrations probably reflect diminished osteoblastic activity, which may also contribute to osteopenia in these patients.

Adult↗