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Biomedical subjects

L W Powell

Publications and source records attributed to L W Powell.

At least 163 records · Page 9Linked to original sources
PubMed1985

Cohort study of internal malignancy in genetic hemochromatosis and other chronic nonalcoholic liver diseases.

The risk of hepatocellular carcinoma (HCC) and other internal malignancies was examined in patients with genetic hemochromatosis (GH) by following 208 patients from the time of diagnosis to June 1983 and by comparing the numbers of cancers they developed with expected values constructed from cancer registry incidence data by means of actuarial methods. In addition, cancers occurring in a comparison group of 148 subjects with other chronic nonalcoholic liver diseases (CLD) were determined. Among the GH group, 16 new cases of HCC occurred subsequent to the diagnosis of GH, together with 8 other malignancies. The 16 cases of HCC reflect a 200-fold excess risk, which from all indications represents the first quantitation of the risk of this tumor in GH. There appears to be no increased risk of other malignancies in this disease. Among the CLD group only 1 HCC and 1 other malignancy occurred.

Adolescent↗
PubMed1985

The effect of acute liver damage on circulating ferritin levels in vivo and in the isolated perfused rat liver.

The effects of minimal acute liver injury on circulating ferritin levels have been examined in the rat both in vivo and in the isolated perfused liver. Liver damage produced by 6 mmol/kg of D-galactosamine (GalN) in vivo resulted in a marked rise in plasma ferritin levels 4 h after administration, 2 h before any significant increase in plasma aspartate transaminase. In the isolated perfused liver, damage produced by 5mM GalN introduced into the perfusate also produced an early increase in circulating ferritin before any evidence of release of intracellular enzymes, or alteration in liver histology as assessed by light microscopy was apparent. It is concluded that minimal acute liver damage results in a pronounced increase in circulating ferritin levels before other evidence of liver dysfunction. This is unlikely to be due solely to increased release from damaged cells but may rather result from an alteration in the mechanism responsible for ferritin homeostasis.

Animals↗
PubMed1985

Use of chromatofocusing to detect a transferrin variant in serum of alcoholic subjects.

We describe a technique for detecting an abnormal (pl 5.7) transferrin component in serum, which appears after prolonged heavy consumption of alcohol. Serum transferrin was purified by chromatography on DEAE-Affi-Gel Blue and analyzed by chromatofocusing on an ion-exchange column (Mono P). The abnormal transferrin component was detected in 17 of 20 patients (85%) with a history or prolonged consumption of alcohol (100 g per day), and in control subjects who ingested up to 80 g of alcohol per day for seven days, but not in 14 normal control subjects or 14 patients with liver disease unrelated to alcohol. The variant consistently disappeared from the serum within three weeks of cessation of alcohol consumption. It is apparently produced by desialylation of ordinary human transferrin. We find that chromatofocusing on an ion-exchange column is a sensitive and reliable technique for its identification and conclude that detection of this desialylated transferrin indicates recent prolonged alcohol ingestion.

Adult↗
PubMed1985

The detection of IgG anti-hepatocyte antibodies by ELISA in sera of patients with chronic active hepatitis: correlation with disease activity.

Anti-hepatocyte membrane IgG antibodies were detected in serial dilutions of sera from patients with chronic active hepatitis using an enzyme linked immunosorbent assay with isolated rat hepatocytes as the antigenic substrate. The assay is rapid, reliable and reproducible. Antibodies to hepatocyte membrane antigens were detected in 24 out of 31 (77%) patients with autoimmune chronic active hepatitis. Four of these patients were negative in a 1/10 dilution but became positive on progressive dilution. In 12 patients, liver biopsy was performed at the same time as serum was obtained. In these patients, the titre of antibodies to hepatocyte membrane antigen correlated significantly with the overall biopsy score of disease activity and particularly with the degree of portal tract infiltration. In 2 patients followed serially, titres of anti-hepatocyte membrane antibodies fell progressively in parallel with clinical, biochemical and histological evidence of improvement in the liver disease. The estimation of titres of antibodies to hepatocyte membrane antigens using isolated rat hepatocytes as the antigenic substrate may assist in the diagnosis, assessment of disease activity and follow-up of individual patients with chronic active hepatitis.

Autoantibodies↗
PubMed1984

Pyogenic liver abscess--a neglected diagnosis.

Twenty-five patients with pyogenic liver abscess admitted to the Royal Brisbane Hospital between 1970 and 1982 have been reviewed. The mortality rate was 32%; however, all patients who were diagnosed before death survived. In seven patients there was a history of biliary obstruction or biliary surgery of whom six died. The mean age of the patients who died was significantly higher than those surviving and it is suggested that this resulted from overdiagnosis of malignancy in the elderly, some hesitancy in investigating older patients, and a tendency to attribute multiple space-filling defects to metastatic tumour. If liver biopsy or even exploratory laparotomy have failed to confirm the diagnosis of hepatic abscess the clinician should not discard the possibility. It is concluded that the continuing high mortality from liver abscess is in large part due to lack of clinical awareness and failure in diagnosis rather than to inadequate therapy.

Age Factors↗
PubMed1984

Chronic hepatitis. Aetiology and current management.

The entity of chronic hepatitis has long been an enigma, and its treatment confusing. Recent studies have indicated the importance of excluding causes such as drugs, Wilson's disease and alpha 1-antitrypsin deficiency. After excluding such causes, there are 3 major groups--'autoimmune', hepatitis B, and non-A, non-B (NANB) in all of which an immunological basis for pathogenesis exists. The autoimmune group has been subdivided into a milder type (chronic persistent hepatitis) and a more severe type (chronic active hepatitis) on histological grounds. Corticosteroids are indicated in chronic active hepatitis if cirrhosis or bridging necrosis is present. However, corticosteroids are contraindicated in disease due to the hepatitis B virus where chronic active hepatitis correlates with the presence of replicating virus (serum positive for e antigen, DNA polymerase and HBV-DNA), and in such cases antiviral agents and immunomodulation are being studied. Very little is known about NANB hepatitis in the absence of an assay and there may be more than a single agent. In hepatitis B, the development of serological markers, molecular probes (HBV-DNA), natural animal hepatitis with near-identical viruses, and delta antigen (a virus requiring co-infection with hepatitis B) have all extended our knowledge so dramatically that it is hoped that the enigma of chronic hepatitis will be solved when an assay for NANB hepatitis becomes available.

Adrenal Cortex Hormones↗
PubMed1984

Are the causes and presentation of chronic hepatitis changing? An analysis of 104 cases over 15 years.

We describe the features at presentation of 104 patients with biopsy-proven chronic hepatitis who presented in Brisbane in the period 1968-32. The mean period of follow-up was 59 months. Sex ratio (female : male) was 70 : 34 and the mean age was 37 years (range 3-83). Eighty-five (82 per cent) were born in Australia. Serological evidence of hepatitis B (HBV) infection was present in 24 (23 per cent). Analysis of the HBV marker positive and negative (non-B) groups revealed that the clinical and laboratory features of HBsAg positive chronic hepatitis were much less florid than those of non-B patients. However, the disturbances seen in hepatic histopathology were similar in severity, and the mortality in the HBsAg positive group exceeded that in the non-B group. The relative risk calculated on an actuarial basis was higher in HBsAg positive patients. In contrast to the experience of others, severe chronic active hepatitis remains an important problem in Brisbane but some features of the disease are altering. Several changes may be attributable to the increasing incidence of HBV-associated disease, and in addition, patients aged under 20 with non-B chronic hepatitis are now rarely seen. This is of interest in view of recent reports of decreased incidence of another disease of disordered immune response, rheumatoid arthritis.

Adolescent↗
PubMed1984

Diagnosis of hemochromatosis in young subjects: predictive accuracy of biochemical screening tests.

The reliability of serum iron, transferrin saturation, and serum ferritin in the detection of early iron overload in hemochromatosis was determined in 120 young (less than 35 yr old) relatives whose genetic susceptibility for the disease was determined by HLA typing of families. Serum ferritin and transferrin saturation demonstrated high levels of sensitivity and specificity, whereas serum iron concentration was an unreliable test in the detection of hemochromatosis. In hemochromatosis homozygotes there was an excellent correlation between serum ferritin and mobilized body iron (r = 0.92), 1 microgram/L of serum ferritin corresponding to approximately 7.5 mg of body iron stores. For a given age, serum ferritin values were higher in homozygotes compared with heterozygotes or homozygous-normal subjects and increased by approximately 65 micrograms/L X yr, reflecting the progressive accumulation of iron in hemochromatosis homozygotes. All hemochromatosis subjects with either hepatic fibrosis or cirrhosis had serum ferritin concentrations greater than 700 micrograms/L. We conclude that the combination of serum ferritin and transferrin saturation is a reliable screening regimen for the detection of hemochromatosis and for predicting the level of body iron stores in young hemochromatosis subjects.

Adolescent↗
PubMed1983

Detection and isolation of a hepatic membrane receptor for ferritin.

A ferritin receptor has been detected on isolated rat hepatocytes and has been partially purified from rat liver using affinity chromatography. Isolated hepatocytes exhibit approximately 30,000 ferritin binding sites/cell with a binding association constant (Ka) of 1 x 10(8) mol-1 liter. A binding assay has been developed which utilizes a hepatic ferritin receptor coupled to a microparticulate support to facilitate separation of bound and free ligand. This method yielded a Ka of 3 x 10(8) mol-1 liter for the purified hepatic ferritin receptor. Binding of ferritin to the insolubilized receptor was partially inhibited by human lactoferrin but unaffected by 200-fold molar excess of bovine albumin, rat transferrin, or human asialoorosomucoid.

Animals↗
PubMed1983

Mononuclear cell factors that inhibit fibroblast collagen synthesis. I. In vitro conditions determining their production and expression.

Peripheral blood mononuclear cells (PBMC) incubated either with phytohaemagglutinin-P (PHA) under serum-free conditions or with tuberculin purified protein derivative in the presence of 5% human blood group AB serum released into the culture medium factors that decreased collagen synthesis by dermal fibroblasts. These factors were first detected after incubation of PBMC with PHA for 24 h and were produced by non-adherent cells. The decrease in collagen synthesis was observed despite changes in conditions of fibroblast culture, the addition of a cross-linking inhibitor, and the use of different fibroblast cell lines.

Aminopropionitrile↗
PubMed1983

Mononuclear cell factors that inhibit fibroblast collagen synthesis. II. Properties of the factors.

Supernatants harvested from peripheral blood mononuclear cells (PBMC) incubated either with the non-specific mitogen phytohaemagglutinin-P (PHA) or with the specific antigen tuberculin purified protein derivative for 72 h decreased collagen synthesis by dermal fibroblasts. PHA-induced mononuclear cell factors (PHA-MCF) responsible for decreases in collagen synthesis by dermal fibroblasts were localized by column chromatography on Sephacryl S-200 to fractions of 30,000-60,000 daltons. Proteolytic enzymes destroyed the activity of PHA-MCF, but after incubation with neuraminidase some activity of these factors remained. The activity of PHA-MCF was not inhibited by incubation with the monosaccharides L-fucose, L-rhamnose, N-acetylglucosamine, and alpha-methyl-D-mannoside but was partially destroyed by heating at 80 degrees C for 10 min. The factors were not mitogenic to PBMC. These factors did not appear to resemble any previously characterized factors produced by non-adherent mononuclear cells. The mechanism by which these factors decreased fibroblast collagen synthesis appeared complex. There was no detectable increase in the release of collagenase by fibroblasts, nor was a cytotoxic effect apparent. Increased PGE2 production by fibroblasts could not be related to the factor-induced decrease in fibroblast collagen synthesis.

Collagen↗