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Biomedical subjects

B A Chapman

Publications and source records attributed to B A Chapman.

At least 37 records · Page 2Linked to original sources
PubMed1996

Comparison of histological and biochemical hepatic iron indexes in the diagnosis of genetic haemochromatosis.

AIMS: To compare a histological hepatic iron index with a biochemical hepatic iron index, derived from atomic absorption spectroscopy measurements of hepatic iron content, for the diagnosis of genetic haemochromatosis (GH). METHODS: Histological sections of liver biopsy specimens from 70 subjects, who had previously had their biochemical hepatic iron index measured, were examined. The iron stores were scored to derive a histological hepatic iron index and were also graded from 0 to 4 by a standard grading system. The case history of each patient was then reviewed to establish a definitive clinical diagnosis and patients were classified as GH, non-GH or indeterminate. RESULTS: There were 26 cases of GH, 40 cases of non-GH and four indeterminate cases in whom a definite clinical diagnosis was not established. Using a biochemical hepatic iron index cut off level of 2.0, two cases were misclassified, with one case of GH having a biochemical hepatic iron index of 1.8 and one non-GH case having a biochemical hepatic iron index of 3.1. This could not have been improved by altering the cut off level. Using the recommended cut off level of 0.15, the histological hepatic iron index was raised in all cases of GH, but was also increased in 11 of the 40 non-GH patients. The specificity of this histological index can be improved by increasing the cut off level to 0.30. A histological iron grade of > or = 3 is more specific than the histological index but has a lower sensitivity, which particularly affects the diagnosis of younger patients with GH. CONCLUSIONS: The biochemical hepatic iron index is a reliable method for establishing a diagnosis of homozygous GH. In contrast, the histological hepatic iron index as originally described is non-specific and does not reliably distinguish patients with GH from others with a raised hepatic iron index due to other causes. The specificity of this index can be improved by increasing the cut off level used, but the discrimination provided by the histological index is still inferior to that provided by the biochemical hepatic iron index.

Adult↗
PubMed1995

Treatment of chronic hepatitis C with interferon alpha.

AIM: To evaluate the response to interferon alpha in patients with chronic hepatitis C in Christchurch. METHOD: Fifteen patients with chronic HCV were given interferon alpha 3 million units subcutaneously three times a week for up to 24 weeks. A complete and partial biochemical response was defined by relative changes in the serum alanine aminotransferase (ALT) during the treatment period. Detection of HCV RNA by the polymerase chain reaction was used to determine the virological response to treatment. RESULT: A complete or partial response was seen in nine of the 15 patients (60%). Histological improvement was demonstrated in all patients for whom paired liver biopsies were taken. Following treatment two of the five complete responders have shown a sustained biochemical response but only one has remained PCR negative, ie, a sustained virological responder. The other three, complete responders and all four partial responders relapsed. CONCLUSION: The response to treatment and relapse was comparable with other studies. It remains to be shown whether investigation of the viral titre and/or viral type will help to explain the high relapse rate in these patients with chronic HCV.

Adult↗
PubMed1994

Investigation of subjects with abnormal iron studies: role of the hepatic iron index.

AIM: Genetic haemochromatosis is a common disorder resulting in increased iron deposition in the liver and other organs but can be difficult to diagnose. The aim of this study was to assess the diagnostic value of the conventional tests for iron overload (percentage saturation of transferrin, serum ferritin and grading of iron staining on liver biopsy) and compare these with the newer quantitative biochemical measurements of liver iron. METHOD: A retrospective analysis was made of 108 consecutive patients referred for quantitative liver iron measurements. Iron studies were obtained in 66 of the 108 subjects of whom 60 had abnormal screening tests defined as percent saturation of transferrin (> 60%) and/or ferritin > 350 micrograms/L for females and > 450 micrograms/L for males. Based on clinical features, biochemical data and treatment outcome these 60 subjects were classified as either genetic haemochromatosis, nongenetic haemochromatosis or indeterminate. One patient with treated genetic haemochromatosis was excluded from subsequent analysis. RESULTS: Although the serum ferritin (p < 0.002), percentage saturation of transferrin (p < 0.001), histological iron grade (p < 0.0001) were significantly higher in the genetic haemochromatosis than nongenetic haemochromatosis group there was considerable overlap. Similarly for the hepatic iron concentration (HIC) (p < 0.0001) overlap occurred. The hepatic iron index (HIC/age) gave the best separation with only three cases being misclassified. A correlation between the HII and histological iron index (visualised iron score corrected for age) in 15 subjects gave an r value of 0.72. CONCLUSION: Based on this study we feel that in addition to visual grading of iron in liver biopsies, the hepatic iron index is helpful in establishing a diagnosis of genetic haemochromatosis.

Adult↗
PubMed1994

Variation in the estimation of gallbladder volume using the sum-of-cylinders method.

RATIONALE AND OBJECTIVES: Gallbladder contraction was measured by ultrasound, using the sum-of-cylinders method, as part of a study of the effects of lipid-lowering drugs. Although this method of measurement has been validated in the literature, paired measurements were obtained to provide an additional check on reproducibility. METHODS: A total of 136 pairs of gallbladder measurements were made on 17 patients using the sum-of-cylinders method of calculating gallbladder volume. Each pair comprised a left posterior oblique and a supine measurement performed at the same ultrasound examination to assess measurement error. RESULTS: There was a large average coefficient of variation of 21%. CONCLUSIONS: Marked measurement variability limited the ability of the sum-of-cylinders technique to detect even modest alterations in gallbladder contractility, at least in this population subgroup.

Bezafibrate↗
PubMed1994

Primary biliary cirrhosis presenting with granulomatous skin lesions.

A case is described of primary biliary cirrhosis in a 59 year old woman who initially presented with a rash over her lower legs 18 months before diagnosis. Skin biopsy examination showed non-caseating granulomas of the sarcoid type. It is believed that this is the first reported case of primary biliary cirrhosis presenting with a granulomatous rash.

Female↗
PubMed1993

The fate of ingested 14C-urea in the urea breath test for Helicobacter pylori infection.

The metabolic fate of the radioactive carbon in the 14C-urea breath test for Helicobacter pylori was investigated in 18 subjects. After ingestion of labelled urea, breath was sampled for 24 h, and urine was collected for 3 days. Subjects were designated high or low expirers on the basis of their breath counts, and this agreed well with H. pylori serologic analyses. When given 185 or 37 kBq of 14C-urea, 51% (SD = 16%, n = 11) of the label was recovered from the breath of high expirers, and 7% (SD = 3%, n = 7) from the breath of low expirers. The mean combined urinary and breath recovery for high expirers was 86% (SD = 7%), and for low expirers it was 97% (SD = 3%). It is concluded that the long-term retention of 14C from ingested 14C-urea is low. The results enable a more accurate estimation to be made of radiation exposure resulting from the 14C-urea breath test.

Breath Tests↗
PubMed1992

Viral hepatitis in the Christchurch community.

AIM: To determine the relative frequency of known causes of viral hepatitis in the Christchurch community. METHODS: Serum samples were collected at a private laboratory from patients aged 15-75 years who had an elevated transaminase of at least twice normal. RESULTS: One hundred and thirty-three subjects entered the study of whom 32 were positive for Epstein Barr virus, three for cytomegalovirus, nine for hepatitis A virus, and eight for hepatitis B virus. Paired convalescent samples were obtained from 64 of the remaining 81 subjects (17 lost or declined) and seven of these were positive for hepatitis C. Assuming a similar percentage in the lost/declined group this corrects to nine. CONCLUSION: The relative frequency of viral agents causing hepatitis was Epstein Barr virus 52%, cytomegalovirus 5%, hepatitis A virus 15%, hepatitis B virus 13% and hepatitis C virus 15%. Hepatitis C virus is a common cause of viral hepatitis in the Christchurch community.

Adolescent↗
PubMed1992

The prevalence of antibodies to hepatitis C virus in patients with chronic liver disease.

OBJECT: to determine the prevalence of antibodies to hepatitis C virus in selected groups of patients with chronic liver disease. METHODS: serum specimens were obtained from 39 patients with chronic liver function abnormalities of uncertain cause (group A), from 15 patients with autoimmune chronic active hepatitis (group B) and from 10 patients with chronic hepatitis B (group C). In an extension of the study, serum was collected from sexual partners of patients found to be HCV seropositive. A second generation ELISA assay (Abbott) was used to analyse the specimens. RESULTS: ten patients (26%) in group A were seropositive, one (7%) in group B and three (30%) in group C. Risk factors for infection included blood transfusion in three, intravenous drug use in six (including the only positive patient in group B) and both factors in another patient. Only one of the 10 sexual partners tested was positive but this subject was also an intravenous drug user. CONCLUSIONS: hepatitis C virus is a significant cause of chronic liver disease in Christchurch. Important risk factors include blood transfusion and intravenous drug use although sporadic cases occur. Transmission to sexual partners is uncommon. The second generation assay does not appear to give false positive results in autoimmune chronic active hepatitis.

Adult↗
PubMed1991

Pyogenic liver abscesses: a retrospective review of 24 cases.

OBJECTS: to review our experience of pyogenic liver abscess with attention to the value of ultrasound and computerised tomography, and the duration of antimicrobial therapy. METHOD: retrospective review of all pyogenic liver abscesses in Christchurch hospitals between 1972 and 1989. RESULTS: twenty-four cases were identified. The presentation of these cases was typical of those described in other series. Ultrasound scanning was positive in 69% of cases, and computerised tomography in 94%. Enteric organisms were isolated from blood or abscess cavities in all but two cases. Two patients died soon after admission and three were treated with antimicrobial therapy alone. The remainder underwent either a percutaneous or surgical drainage procedure, and received antimicrobial therapy. The antimicrobial therapy was clearly inappropriate in two patients. Eight patients (67%) with single abscesses received less than 10 days of antimicrobial therapy. Four patients (50%) with multiple abscesses received less than 18 days therapy. No patient relapsed. CONCLUSIONS: ultrasound is a convenient initial imaging technique, but may give false negative results. Computerised tomography should be done promptly if clinical suspicion of a liver abscess persists. Both surgical and percutaneous drainage techniques gave good results in combination with antimicrobial therapy. It is probably unnecessary to give prolonged courses of antimicrobial therapy following drainage of single liver abscess, provided there is rapid resolution. Multiple abscesses, or those which are not drained, may require longer courses of antimicrobial therapy.

Adolescent↗
PubMed1990

Apolipoprotein localization in the human bile duct and gallbladder.

Apolipoproteins AI, AII and B were identified in the normal and pathological human bile duct and the gallbladder epithelium using an avidin-biotin immunoperoxidase technique. Small intestine and stomach sections served as positive and negative controls respectively. Staining was focal for apolipoproteins AI and AII, and continuous for apolipoprotein B. In addition to homogenous and granular cytoplasmic staining, foamy cytoplasmic staining, particularly for apolipoproteins AI and AII, was observed around lipid droplets in cells containing much lipid. No correlation between a particular pathological condition of the gallbladder (acute cholecystitis, mucocele, chronic cholecystitis, cholesterolosis) and staining pattern or intensity of staining was found for any of the apolipoproteins, although both apolipoproteins AI and AII stained more intensely than apolipoprotein B in each group. Positive staining was also found for all apolipoproteins in epithelial cells which had invaded the underlying connective tissue (gallbladder carcinoma), suggesting that the epithelial cells are capable of synthesizing apolipoproteins de novo. In this latter case, apolipoprotein B stained more intensely than for either AI or AII, and significantly (p less than 0.05) more strongly than that found in the other pathological groups. The identification of apolipoproteins in the gallbladder epithelium raises the interesting question of their origin and functional role.

Apolipoproteins↗
PubMed1988

The effect of ethanol on phospholipid metabolism in rat pancreas.

The phospholipid effect involves agonist-induced breakdown of phosphatidyl inositol (or polyinositides) generating second messengers followed by increased incorporation of 32P during the resynthetic phase of the cycle. Ethanol, an aetiological factor in pancreatitis, has been shown to have various effects on pancreatic secretion. In this study ethanol decreased the incorporation of 32P into phosphatidyl inositol but had no effect on the stimulated breakdown of prelabelled phosphatidyl inositol. However, in addition to recycling of phosphatidyl inositol stimulation of pancreatic tissue results in increased incorporation of precursors into other phospholipids. Cholecystokinin increased the incorporation of both [U-14C] glucose and 32P into phosphatidyl ethanolamine 3-fold but had no effect on 32P incorporation into phosphatidyl choline. As well as increased incorporation of 32P into phosphatidyl inositol (8-fold) cholecystokinin also increased the incorporation of [U-14C] glucose into phosphatidyl inositol (4-5-fold) implying significant de novo synthesis of 1,2 diacyl glycerol in addition to the currently accepted recycling of the 1,2 diacyl glycerol back to phosphatidyl inositol. Ethanol caused an inhibition of 32P incorporation into total phospholipid of rat pancreas during basal and stimulated conditions. When individual phospholipids were separated ethanol was found to decrease the incorporation of 32P into phosphatidyl choline under basal conditions and into all phospholipids during cholecystokinin stimulation. With [U-14C] glucose as the precursor, ethanol inhibited its incorporation into phosphatidyl choline only. Ethanol did not alter the total 32P radioactivity in the aqueous phase of the pancreatic extract nor the percent incorporated into nucleotides. This excluded decreased uptake of 32P and incorporation into nucleotides as a mechanism for the differential inhibition of 32P versus [U-14C] glucose incorporation into phospholipids other than phosphatidyl choline under stimulated conditions.

Animals↗
PubMed1987

The effect of ethanol on enzyme synthesis and secretion in isolated rat pancreatic lobules.

This study investigates the effect of ethanol on enzyme synthesis and secretion in rat pancreatic lobules. Ethanol caused a dose-dependent inhibition of 3H-leucine incorporation into total protein. Examination of the time dependence showed that ethanol inhibited protein synthesis at each time point. Removal of ethanol partially reversed this inhibition. An autoradiograph of the newly synthesized proteins separated on SDS-PAGE showed that ethanol inhibited synthesis of all proteins. 14C-cycloleucine uptake was not altered by ethanol, excluding inhibition of amino acid uptake as the mechanism for the decreased protein synthesis induced by ethanol. Electron microscopy revealed no ultrastructural damage. Ethanol had no effect on the stimulated release of (i) amylase from zymogen granules nor (ii) newly synthesized pulse labelled enzymes. Acetaldehyde had no inhibitory effect on enzyme synthesis or secretion indicating that ethanol per se and not its metabolite is inhibitory. The decreased synthesis after acute exposure to ethanol with preservation of exocytosis would limit the autodigestive potential of pancreatic tissue. This may explain why isolated toxic doses of ethanol are rarely if ever associated with pancreatitis.

Acetaldehyde↗
PubMed1987

Dientamoeba fragilis: a bowel pathogen?

Although many patients infected with Dientamoeba fragilis suffer gastrointestinal symptoms, controversy still surrounds the pathogenic role of this intestinal protozoan. We describe three patients infected with D fragilis who had gastrointestinal symptoms. In the first patient symptoms resolved with therapy before the protozoan was eradicated from the stool, however in the second, symptoms persisted unabated despite clearing of the organism. In the third patient, symptoms resolution was associated with effective treatment. We discuss the life cycle, diagnosis and treatment of this organism and its role as a pathogen.

Adult↗
PubMed1987

Inhibition of biliary phospholipid and cholesterol secretion by cefoperazone.

The effect of cefoperazone, a third-generation cephalosporin, on biliary lipid secretion in rats was examined. Rats were anesthetized with ether and the mid-lumbar vein and common bile duct cannulated. Bile acid secretion was maintained by intravenous taurocholic acid infusion (28 mumol/hr). A 1-hr control period was followed by intravenous cefoperazone infusion at either submaximal (20 mumol/hr), or supramaximal (60 mumol/hr) concentrations. At the cefoperazone infusion rate of 20 mumol/hr (biliary secretion of 7.1 +/- 1.6 mumol/hr) phospholipid secretion fell 19% and cholesterol secretion fell 31%; at a cefoperazone infusion rate of 60 mumol/hr (biliary secretion rate of 27.1 +/- 5.1 mumol/hr) phospholipid and cholesterol secretion were further reduced 40% and 56%, respectively, of controls. All changes were significant (P less than 0.01). Inhibition of both cholesterol and phospholipid secretion paralleled each other, was dose-dependent, and reversible. Cefoperazone's inhibitory action was abolished at a bile acid infusion rate of 108 mumol/hr. Cefoperazone was not found to be associated with bile acid micelles or mixed micelles as determined by ultracentrifugation and gel filtration. Thus, the effect of cefoperazone on biliary lipid secretion is not due to the impairment of mixed micelle formation in the canalicular lumen but rather its inhibitory effect appears to be due to a presecretory event.

Animals↗
PubMed1987

The incorporation of [myo-2-3H] inositol into phosphatidyl inositol of stimulated rat pancreas.

The 'phospholipid effect' involves agonist induced breakdown of phosphatidyl inositol (PI) or its phosphorylated derivates with increased incorporation of 32P or [myo-2-3H] inositol during resynthesis. In rat pancreas pancreozymin and bethanecol resulted in the standard dose dependent increased incorporation of 32P into PI which was paralleled by increased amylase secretion. By contrast the incorporation of [myo-2-3H] inositol into PI was significantly decreased by pancreozymin whereas bethanecol had no effect. However, pancreozymin caused a 30% decrease in labelled PI irrespective of whether it was prelabelled with 32P or [myo-2-3H] inositol. Thus in rat pancreas, pancreozymin resulted in the standard agonist induced breakdown of pre-labelled PI but inhibited the incorporation [2-3H-myo] inositol during the resynthetic phase.

Amylases↗
PubMed1987

Biliary secretion of cefoperazone and its inter-relationship with bile acid transport in the rat.

Cefoperazone is a third generation cephalosporin which is secreted predominantly in bile. This study set out to examine the effect of stimulating bile choleresis on the biliary secretion of cefoperazone. Stimulation of both bile acid-dependent and independent bile flow (phenobarbitone pretreatment) hastened the peak appearance of a pulse of cefoperazone into bile. Although the biliary secretion rate of cefoperazone was enhanced by bile acid infusion, the % recovery and maximal biliary concentration were reduced. The reciprocal effect of continuous cefoperazone infusion on the rate of biliary transport of a pulse of bile acid was examined. Cefoperazone infusion hastened the biliary transport of glycocholate. Net recovery of glycocholate was unaffected.

Animals↗