Internal medicine
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Case Reports
Rapid Progression of Autoimmune Gastritis after Helicobacter pylori Eradication Therapy: A Case Report.
We herein report a case of autoimmune gastritis (AIG) with rapid progression after Helicobacter pylori eradication therapy. The patient's previous gastritis had followed the course of type B gastritis before eradication therapy for many years. ⋯ All of these clinical findings showed significant atrophic progression in the corporal area for approximately three years. We concluded that H. pylori eradication therapy exacerbated AIG in this case.
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Case Reports
Encapsulating Peritoneal Sclerosis in Systemic Lupus Erythematosus, Rheumatoid Arthritis, and Systemic Sclerosis.
We encountered a 57-year-old Japanese woman with encapsulating peritoneal sclerosis (EPS) in systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and systemic sclerosis. The patient was admitted to our hospital because of ascites retention. ⋯ On autopsy, sclerotic thickening of the peritoneum showed diffuse infiltration of podoplanin-positive fibroblast-like cells, and a diagnosis of EPS was made. EPS rarely occurs in SLE, and tocilizumab may be a new treatment candidate for EPS.
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Case Reports
Chronic Expanding Haematoma Causing Stenosis of the Right Ventricular Outflow Tract and Pulmonary Hypertension.
A chronic expanding haematoma (CEH) is an encapsulated mass that gradually increases in size from repeated internal bleeding and neovascularization. We herein report a 69-year-old man who was admitted with dyspnoea on exertion after undergoing thymic carcinoma resection 17 years ago. ⋯ Right cardiac catheterisation revealed pulmonary hypertension that was relieved after resection of the diagnosed CEH mass. This report highlights the mechanism underlying anterior mediastinal CEH-induced stenotic compression of the right ventricle-pulmonary artery outflow and subsequent pulmonary hypertension.
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The coexistence of leucine-rich glioma-inactivated 1 (LGI1) and contactin-associated protein-like 2 (CASPR2) autoantibodies in the same individual is surprisingly often observed. We herein report the first case of LGI1 encephalitis followed by Isaacs syndrome in which LGI1 and CASPR2 antibodies in the serum and cerebrospinal fluid (CSF) were measured during the entire disease course. After the resolution of limbic encephalitis, LGI1 antibodies disappeared from the CSF simultaneously with the appearance of CASPR2 antibodies in the serum. The alternating presence of these pathogenic autoantibodies along with the clinical and phenotypic alternations suggested that LGI1 encephalitis was associated with CASPR2 autoantibody production in the peripheral tissue, leading to CASPR2-associated Isaacs syndrome.