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• W1972862960 abstract "See article on page 1420 Primary biliary cirrhosis (PBC) is an immune-mediated biliary disease characterized by chronic non-suppurative destructive granulomatous cholangitis, which causes persistent intrahepatic cholestasis. An immunogenetic predisposition, as well as the presence of specific autoantibodies against mitochondria (antimitochondrial antibody, AMA), and a strong association with other autoimmune-related diseases, has led to speculation that this disease may be associated with a profound immunological disturbance.1, 2 A wide range of AMA has been described (anti-M1-9), and the most specific of these for PBC is anti-M2 antibody directed against the E2 component of pyruvate dehydrogenase complex (PDC-E2) on the inner mitochondrial membrane.3, 4 Primary biliary cirrhosis is also considered to be a multisystem disease, involving many exocrine glandular structures, such as the lacrimal and salivary glands, biliary system, and pancreas, which is most likely caused by common immunopathological processes.1, 2 Strickland and Mackay proposed that chronic atrophic gastritis in humans could be classified into two categories, namely type A and type B, based on the distribution of the disease in the stomach and its pathogenesis.5 Type A predominantly involves the gastric body and fundus, and spares the antrum, whereas type B shows an involvement of the antrum as well as the body and fundus. In type A gastritis, also called autoimmune gastritis or atrophic corpus gastritis, atrophy of the glandular epithelia is invariably present, thus leading to a loss of specialized gastric glands, which also leads to the loss of the gastric parietal cells that produce both gastric acid and an intrinsic factor. Type A gastritis is usually associated with positive antiparietal cell antibody (PCA) or anti-intrinsic factor antibody reactions such as a marked impairment of acid secretion with hypergastrinemia in proportion to glandular atrophy. Pernicious anemia, which is caused by an inability to absorb vitamin B12 because of a decreased gastric intrinsic factor, occurs at the end stage of this type of gastritis. In other words, pernicious anemia evolves almost exclusively from type A gastritis. A genetic predisposition to type A gastritis is suggested by the clustering of autoimmune diseases and of gastric autoantibodies in families. Recently, the proton pump H+, K+-adenosine triphosphatase (H+, K+-ATPase) of parietal cells was confirmed to be the major humoral autoantigen in both human and experimental autoimmune gastritis characterized by an inflammatory infiltrate in the gastric mucosa and a loss of parietal cells.6-8 An association with other autoimmune endocrinopathies, such as Hashimoto's thyroiditis, Addison's disease, insulin-dependent diabetes mellitus, and idiopathic adrenocortical insufficiency has also been previously reported, and pernicious anemia is known to be one of the component disorders of autoimmune polyglandular syndrome.9, 10 One particularly attractive theory is the concept of molecular mimicry, which is based on the principle that a common epitope between the bile duct epithelial cell and the parietal cell initiates an autoimmune response and subsequent immunopathology by generating autoreactive lymphocytes and/or antibodies. As Takahashi et al. mentioned in their report, no significant amino acid sequence homology or even similarity of both PDC-E2 and H+, and K+-ATPase could be found in the Genebank database.11 An association with various kinds of autoimmune diseases is one of the characteristics of PBC. Associated diseases include Sjögren's syndrome, Hashimoto's thyroiditis, rheumatoid arthritis and calcinosis, Raynaud's phenomenon, esophageal dysfunction, sclerodactyly and telangiectasia (CREST) syndrome.1, 2, 12 However, immunoserologically, in addition to AMA, PCA is frequently detected in patients with PBC, as in the case of atrophic corpus gastritis.13 Oya et al. reported that severe and extensive gastric mucosal atrophy was manifested in autoimmune liver diseases, including PBC, which exhibited positive PCA.14 However, although the stomach can also be regarded as an exocrine organ, the association of PBC with atrophic corpus gastritis15-17 or pernicious anemia18-20 has rarely been reported to date. Culp et al. observed a link between PBC and pernicious anemia in two of 113 patients (1.8%).1 According to the literature, only seven cases including the case report by Takahashi et al. have been reported so far in the world. Renoux et al. reported four cases of PBC associated with pernicious anemia.18 Arikan et al. reported a 54-year-old woman with PBC associated with pernicious anemia.19 In Japan, only two cases of PBC associated with pernicious anemia have been reported by Takahashi et al.11 in this issue of the Journal and by us (Dohmen et al.).20 Takahashi et al. reported a 70-year-old woman associated with pernicious anemia that occurred 16 years after the onset of PBC.11 Our previously reported case was a 72-year-old woman who was simultaneously diagnosed to have PBC associated with pernicious anemia.20 To the best of my knowledge, there have been few original reports describing the relationship between atrophic corpus gastritis and PBC endoscopically and/or histologically.13, 14, 21 Wirth et al. reported no endoscopic evidence for atrophic corpus gastritis in 16 patients with PBC.13 They also found no decrease in the serum vitamin B12 level in 21 patients with PBC.13 They concluded, however, that an identical epitope between PCA and AMA in PBC patients was suggested because PCA was positive in all 24 patients with PBC, although PCA in PBC patients was an unreliable indicator for pernicious anemia.13 While Floreani et al. described that PBC patients were not characterized by chronic atrophic gastritis, even though they presented with chronic gastritis and showing the same prevalence as the dyspeptic controls.21 Floreani et al. used indirect immunofluorescence and found that none of the 33 patients with PBC were positive for PCA. In contrast, Oya et al. demonstrated that severe and extensive gastric mucosal atrophy was manifested in the autoimmune liver diseases of 16 patients with PBC and eight patients with autoimmune hepatitis.14 The issue of whether atrophic corpus gastritis is frequently complicated by PBC thus still remains controversial. Epstein et al. proposed that PBC is part of a disease complex characterized by dry eyes, dry mouth, biliary change, and hyposecretion, which should thus be regarded as a dry-gland syndrome resulting from damage to the ductular epithelia by a common autoimmune mechanism in the exocrine glandular systems.22 Atrophic corpus gastritis, however, was not mentioned in their paper. The stomach also has an exocrine glandular structure, thus making it relevant to consider whether atrophic corpus gastritis is a possible component of so-called dry-gland syndrome. At present, it is difficult to accept that this type of gastritis is involved in dry-gland syndrome. It has yet to be demonstrated that both PBC and atrophic corpus gastritis are caused by a common immunological mechanism. However, another issue of great concern is whether Helicobacter pylori (H. pylori) is involved in the early stage of corpus atrophy caused by the mucosal production of antigastric antibody,23 which eventually leads to pernicious anemia.6, 7, 24-26 At its early stage, autoimmune corpus gastritis is associated with an H. pylori infection through a molecularly mimetic immune reaction between H. pylori and parietal cells. This reaction may possibly develop mucosal atrophy.6, 7, 27, 28 An autoimmune mechanism is the most plausible factor. Negrini et al. reported that H. pylori infection could stimulate antibodies to cross-react with gastric autoantigens and thus eventually lead, over the years, to atrophic involvement.29 It has been proposed that the cross-reacting mechanism of the NH2-terminal sequence of a vacuolation toxin secreted by H. pylori is partially homologous with the internal sequences of numerous ion channnels, or transport proteins, including a 30% or more homology with the human gastric H+, K+-ATPase a subunit in the region of residues 243–25727 or 360–525.28 A high prevalence of bacteriuria with a very high recurrence rate in females with PBC, compared with other forms of chronic liver disease, has also been described.30 Likewise, monobacterial infection has also received attention in the pathogenesis of PBC. Moreover, bacteria have recently been identified from the samples of PBC patients by the use of molecular analyses, which are also suspected to initiate or trigger factors in PBC. Mayo et al. identified the COOH-terminal region of Escherichia coli ClpP protease to be a new antigen specifically reacting with the sera from PBC patients.31 Through a mimetic mechanism, the cross-reactivity of AMA against prokaryotic antigens has been reported for a number of microbes, including E. coli, Klebsiella pneumoniae, Proteus mirabilis, Staphylococcus aureus, Salmonella minnesota and Propionibacterium acnes, although the target components of AMA in these bacteria have not yet been fully determined.32, 33 Although a common epitope between PDC-E2 and H+, K+-ATPase has not yet been identified,11 another equally valid hypothesis is that the unidentified polypeptides of microbes are the antigens, while the antibodies against them coincidentally cross-react with the different peptides of both bile duct epithelial cells and parietal cells, which thus leads to the development of PBC and atrophic corpus gastritis. However, it remains unknown as to whether H. pylori or other infectious organisms act separately or are in some way interrelated to the occurrence of both PBC and atrophic corpus gastritis, which eventually leads to the development of pernicious anemia. Recent advances in molecular technologies and future epidemiologic studies are expected to further elucidate this issue." @default.
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• W1972862960 title "Primary biliary cirrhosis and pernicious anemia" @default.
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