A controlled trial of prednisolone treatment in primary biliary cirrhosis

Mitchison, H.; Palmer, Jeremy M.; Bassendine, Margaret F.; Watson, Alexander; Record, C. O.; James, Oliver

doi:10.1016/0168-8278(92)90065-w

Cited by 188 publications

(75 citation statements)

References 15 publications

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“…36 Against this hypothesis stands the insidious clinical course, without flares or remissions in disease activity and, most strikingly, the failure of immunosuppressive therapy to alter disease progression. 37 Furthermore, one might expect a T-cell mediated disease to show a close association with HLA phenotype, and this has not been shown. The closest association, with HLA DR8 accounts for about one third of Caucasian patients; furthermore, PBC, unlike other autoimmune liver diseases, has no counterpart in children.…”

Section: Pbc As a Paradigm Of Autoimmunitymentioning

confidence: 99%

PBC and AMA?what is the connection?

Neuberger

Thomson²

1999

Hepatology

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Primary Biliary Cirrhosis (PBC) is very closely associated with the presence of antimitochondrial antibodies (AMA); indeed, the presence of these antibodies is virtually disease specific. Despite the major advances made during the last decade in identifying the antigens with which these antibodies react, the reason for the close association remains uncertain. In this review, we examine the clinical correlates of AMA with features of PBC and discuss the possible implications of the association. CLINICAL CORRELATES Epidemiology of PBCThere is geographical variation in the prevalence of PBC, being highest in areas such as the north of England and parts of North America but rare in Africa and the Indian subcontinent. 1 Studies from the north of England suggest that the incidence of PBC is increasing. Clustering of cases is well described. 2 PBC may occur in families, and up to 4% of first-degree relatives may have PBC. Where PBC does occur in families, it may be related to maternally inherited factors and tends to present earlier in the second generation. 3 AMA Are Detectable Before the Clinical and Histological Features of PBCOf 29 asymptomatic patients who were found to have AMA in serum (later confirmed to be reactive with E2 components of pyruvate dehydrogenase) but with normal liver tests only two had normal liver histology. 4 A decade later, 76% had developed symptoms of PBC and 83% had cholestatic liver tests. None had progressed to cirrhosis. 5

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Section: Pbc As a Paradigm Of Autoimmunitymentioning

confidence: 99%

PBC and AMA?what is the connection?

Neuberger

Thomson²

1999

Hepatology

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“…Most of these drugs also have been used to treat PBC. [18][19][20] Clinical manifestations have been minimal, even in well-documented cases of recurrent PBC, but the condition still is of great interest because it may offer insights into the pathogenesis of PBC, especially the role of HLA-restricted mechanisms.…”

mentioning

confidence: 99%

Disease recurrence after living liver transplantation for primary biliary cirrhosis: A clinical and histological follow-up study

Hashimoto¹,

Shimada²,

Noguchi³

et al. 2001

Liver Transplantation

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“…In autoimmune hepatitis, patients responding to corticosteroids progress more slowly to fibrosis and cirrhosis (196). However, it is not effective in autoimmune cholestatic diseases such as primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC) (197,198). Malotilate is another agent with anti-inflammatory effects that is under investigation for treating liver fibrosis.…”

Section: Reduction Of Inflammation and Immune Responsementioning

confidence: 99%

Bioconjugation of Oligonucleotides for Treating Liver Fibrosis

Houssein

Mahato

2007

Oligonucleotides

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Liver fibrosis results from chronic liver injury due to hepatitis B and C, excessive alcohol ingestion, and metal ion overload. Fibrosis culminates in cirrhosis and results in liver failure. Therefore, a potent antifibrotic therapy is in urgent need to reverse scarring and eliminate progression to cirrhosis. Although activated hepatic stellate cells (HSCs) remains the principle cell type responsible for liver fibrosis, perivascular fibroblasts of portal and central veins as well as periductular fibroblasts are other sources of fibrogenic cells. This review will critically discuss various treatment strategies for liver fibrosis, including prevention of liver injury, reduction of inflammation, inhibition of HSC activation, degradation of scar matrix, and inhibition of aberrant collagen synthesis. Oligonucleotides (ODNs) are short, single-stranded nucleic acids, which disrupt expression of target protein by binding to complementary mRNA or forming triplex with genomic DNA. Triplex forming oligonucleotides (TFOs) provide an attractive strategy for treating liver fibrosis. A series of TFOs have been developed for inhibiting the transcription of α1(I) collagen gene, which opens a new area for antifibrotic drugs. There will be in depth discussion on the use of TFOs and how different bioconjugation strategies can be utilized for their site-specific delivery to HSCs or hepatocytes for enhanced antifibrotic activities. Various insights developed in individual strategy and the need for multipronged approaches will also be discussed.

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A controlled trial of prednisolone treatment in primary biliary cirrhosis

Cited by 188 publications

References 15 publications

PBC and AMA?what is the connection?

PBC and AMA?what is the connection?

Disease recurrence after living liver transplantation for primary biliary cirrhosis: A clinical and histological follow-up study

Bioconjugation of Oligonucleotides for Treating Liver Fibrosis

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