ABSTRACT
Adenomas of the nonpigmented ciliary epithelium (NPCE) are often clinically indistinguishable from amelanotic malignant melanomas of the ciliary body or metastatic carcinomas. This paper reports a case study of a distinctive variant of adenoma of the NPCE, which clinically appears as epiretinal membrane in the macular region. Histopathologic studies have revealed this is an adenoma of the NPCE. Identification of this clinic feature is important because it will miss the diagnosis of the adenoma of the NPCE. In this case study, B-scan ultrasonography as well as computerized tomography (CT) has been used to provide help in diagnosing the ciliary body tumor. Because of their anterior location in the ciliary body, partial lamellar sclerouvectomy is an effective method of treatment.
Subject(s)
Adult , Humans , Male , Adenoma , Pathology , Ciliary Body , Pathology , Epithelium, Corneal , Pathology , Pigment Epithelium of Eye , Pathology , Uveal Neoplasms , PathologyABSTRACT
<p><b>OBJECTIVES</b>To establish a primary biliary cirrhosis (PBC) model by AMAM2 autoantigen injection into C57BL/6 mice.</p><p><b>METHODS</b>Mice of the model group were immunized intraperitonealy with 200 microl of purified recombinant AMAM2 autoantigen in complete Freund's adjuvant (CFA). Mice immunized with bovine serum albumin and CFA in the same way were used as negative controls. Sixty-six weeks later, mice were sacrificed and their sera were collected. Sera samples were assayed for AMAM2 autoantibody, alkaline phosphatase (ALP), ALT and total bilirubin (TBil). Their liver, stomach, muscle and kidney tissues were sectioned and stained using HE to observe the pathological changes.</p><p><b>RESULTS</b>Antibodies to AMAM2 autoantigen were readily induced in the model group. The mice in the model group had no significant changes in the level of serum ALT and TBil but had an obvious increase of ALP (P<0.05). The stomach, muscle and kidney tissues showed no evident damage while the livers had obvious pathological changes, including bile duct degeneration or proliferation, and mononuclear cell infiltration.</p><p><b>CONCLUSION</b>The AMAM2 autoantigen-induced PBC animal model was successfully established in C57BL/6 mice in our experiment and its characteristic biochemical and pathology are quite similar to that in the early stage of human PBC. This model may provide a useful experimental approach for further study of the pathogenesis and clinical treatment of human PBC.</p>