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  • 1
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 14 ( 2023-2-15)
    Abstract: The sequential progression from chronic liver disease to cirrhosis may be a risk factor for hepatocellular carcinoma (HCC) development. Although HCC originates from hepatitis B virus- or hepatitis C virus-associated liver cirrhosis, it has recently been reported in patients with non-alcoholic steatohepatitis (NASH) with advanced fibrosis. However, little is known about the pathophysiological mechanisms linking HCC to rheumatic disorders, including rheumatoid arthritis (RA). Herein, we describe the case of HCC with NASH complicated by RA and Sjögren’s syndrome (SS). A fifty-two-year-old patient with RA and diabetes was referred to our hospital for further examination of a liver tumor. She received methotrexate (4 mg/week) for 3 years and adalimumab (40 mg/biweekly) for 2 years. On admission, laboratory data showed mild thrombocytopenia and hypoalbuminemia, with normal hepatitis virus markers or liver enzymes. Anti-nuclear antibodies were positive with high titers (x640), and anti-SS-A/Ro (187.0 U/ml; normal range [NR]: ≤6.9 U/mL) and anti-SS-B/La (320 U/ml; NR: ≤6.9 U/mL) antibodies were also high. Abdominal ultrasonography and computed tomography revealed liver cirrhosis and a tumor in the left lobe (S4) of the liver. She was diagnosed with HCC based on imaging findings, and elevated levels of protein induced by vitamin K absence- II (PIVKA-II) were detected. She underwent laparoscopic partial hepatectomy, and histopathological examination revealed steatohepatitis HCC with background liver cirrhosis. The patient was discharged on the 8 th day post-operation without any complications. At the 30 months follow-up, no significant evidence of recurrence was observed. Our case suggests that clinical screening for HCC is needed in patients with RA who are at a high risk of NASH, as they may progress to HCC even without elevated liver enzymes.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2606827-8
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  • 2
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 14 ( 2023-3-21)
    Abstract: Temporal arteritis (TA) is a large-vessel vasculitis mostly seen in older patients. Amyloid A (AA) amyloidosis secondary to a chronic inflammation induces multiple organ dysfunctions, including a dysfunction of the gastrointestinal tract. Herein, we present a case of TA complicated by AA amyloidosis that was resistant to oral and intravenous steroids. An 80-year-old man with a history of new-onset headache, jaw claudication, and distended temporal arteries was referred to our department. On admission, the patient presented with tenderness and a subcutaneous temporal nodule in both temple arteries. Ultrasonography of the nodule revealed an anechoic perivascular halo surrounding the right temporal artery. Following the diagnosis of TA, high-dose prednisolone therapy was initiated. However, the patient presented with recurrent abdominal pain and refractory diarrhea. Due to the unclear origin of refractory diarrhea, an extensive workup, including biopsy of the duodenal mucosa, was performed. Endoscopy revealed chronic inflammation in the duodenum. Immunohistochemical analysis of duodenal mucosal biopsy samples revealed AA amyloid deposition resulting in the diagnosis of AA amyloidosis. After tocilizumab (TCZ) administration, refractory diarrhea reduced; however, the patient died of intestinal perforation 1 month after the start of TCZ administration. Gastrointestinal involvement was the main clinical manifestation of AA amyloidosis in the present case. This case highlights the importance of bowel biopsy screening for amyloid deposition in patients with unexplained gastrointestinal tract symptoms, even in a recent onset of large-vessel vasculitis. In the present case, the carriage of the SAA1.3 allele likely contributed to the rare association of AA amyloidosis with TA.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2606827-8
    Location Call Number Limitation Availability
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  • 3
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 13 ( 2022-10-24)
    Abstract: Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Most of the infected individuals have recovered without complications, but a few patients develop multiple organ involvements. Previous reports suggest an association between COVID-19 and various inflammatory myopathies, in addition to autoimmune diseases. COVID-19 has been known to exacerbate preexisting autoimmune diseases and trigger various autoantibodies and autoimmune disease occurrence. Here we report a case of complicated COVID-19 with anti-synthetase autoantibodies (ASSs) presenting with skin rash, muscle weakness, and interstitial lung disease (ILD) and subsequently diagnosed with dermatomyositis (DM). A 47-year-old Japanese male patient without any previous history of illness, including autoimmune diseases, presented with a high fever, sore throat, and cough. Oropharyngeal swab for SARS-Cov-2 polymerase chain reaction tested positive. He was isolated at home and did not require hospitalization. However, his respiratory symptoms continued, and he was treated with prednisolone (20 mg/day) for 14 days due to the newly developing interstitial shadows over the lower lobes of both lungs. These pulmonary manifestations remitted within a week. He presented with face edema and myalgia 4 weeks later when he was off corticosteroids. Subsequently, he presented with face erythema, V-neck skin rash, low-grade fever, and exertional dyspnea. High-resolution computed tomography of the chest showed ILD. Biochemical analysis revealed creatine kinase and aldolase elevations, in addition to transaminases. Anti-aminoacyl tRNA synthetase (ARS) was detected using an enzyme-linked immunosorbent assay (170.9 U/mL) (MESACUP™ (Medical & amp; Biological Laboratories, Japan), and the tRNA component was identified as anti-PL-7 and anti-Ro-52 antibodies using an immunoblot assay [EUROLINE Myositis Antigens Profile 3 (IgG), Euroimmun, Lübeck,Germany] . The patient was diagnosed with DM, especially anti- synthase antibody syndrome based on the presence of myositis-specific antibodies, clinical features, and pathological findings. The present case suggests that COVID-19 may have contributed to the production of anti-synthetase antibodies (ASAs) and the development of de novo DM. Our case highlights the importance of the assessment of patients who present with inflammatory myopathy post-COVID-19 and appropriate diagnostic work-up, including ASAs, against the clinical features that mimic DM after post-COVID-19.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2606827-8
    Location Call Number Limitation Availability
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