Internal Medicine最新文献

Non-traumatic sternoclavicular arthritis is typically caused by either degeneration or non-infectious inflammatory conditions, although septic arthritis can often occur due to Staphylococcus aureus, particularly in immunocompromised individuals. We herein present a case of Escherichia coli (E. coli)-induced sternoclavicular arthritis in a Japanese woman with no underlying disease. As no common source of E. coli bacteremia was identified, colonoscopy revealed early-stage rectal cancer. To our knowledge, this is the first report of septic sternoclavicular arthritis in which colorectal cancer was identified as the source of infection. Clinicians should consider colorectal cancer when septic arthritis caused by gut bacteria is diagnosed without a clear source.

Objective To analyze the influence of age of the onset on myositis organ damage and to identify the factors influencing myositis organ damage, as clinical manifestations of myopathies differ by the age of onset and the background of patients. Methods Factors influencing organ damage [the Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) Damage Index (SDI)] were identified using the Japanese multicenter myositis registry (MYKO, n=220). Factors influencing organ damage were identified using a multivariate analysis. SDI was compared among juvenile-onset (<20 years old), adolescent-onset (20-64 years), and elderly-onset (>64 years) groups. Results There was a correlation between the age at onset and the SDI score (Spearman's rank correlation coefficient ρ=0.28). Elderly patients exhibited more widespread organ damage, including neuropsychiatric, renal, pulmonary, cardiovascular, peripheral vascular, gastrointestinal, skin, and diabetes, whereas juvenile-onset patients exhibited musculoskeletal damage. Adolescent-onset patients had the lowest incidence of ocular and malignant damage. A regression analysis revealed that an older onset age (coefficient, β=0.03), longer disease duration (β=0.05), and total dose of glucocorticoid (β=3.35×10^-5) influenced SDI. After adjusting for disease duration, the influences of anti-melanoma differentiation-associated gene 5 (MDA5) [hazard ratio (95% confidence interval), 4.47 (2.17-9.21)] on pulmonary fibrosis and a history of steroid pulse [2.16 (1.16-4.05)] on muscle atrophy or weakness were shown. Conclusion There were associations between the age of onset and autoantibodies with myositis organ damage. Musculoskeletal damage was greater in patients with a juvenile onset. An older age of onset is associated with severe organ damage. These findings highlight the importance of considering the age of onset and autoantibodies for assessing the prognosis and developing treatment plans for myopathies.

A 79-year-old woman was admitted to our hospital with a persistent fever, malaise, and anemia requiring frequent transfusions. A peripheral blood smear revealed erythrocyte agglutination and a high titer of cold agglutinins. Imaging examination revealed pulmonary emboli and multiple subacute cerebral infarctions. Despite the absence of lymphadenopathy or splenomegaly, the diagnosis of intravascular large B-cell lymphoma (IVLBCL) was confirmed through random skin biopsies. Immunochemotherapy successfully induced remission of her fever and anemia with normalization of her cold agglutinin titer. This case highlights that cold agglutinin syndrome can be associated with aggressive lymphomas, including IVLBCL.

The patient was an 89-year-old woman who suddenly collapsed in a hospital cafeteria. Responding medical personnel determined that the patient was in cardiac arrest. After advanced cardiac support, the patient regained spontaneous circulation. Chest compressions were continued for approximately 15 min, and the computed tomographic scan revealed kyphosis, diffuse idiopathic skeletal hyperostosis, an extension fracture of the second lumbar vertebra, and a large right Gerota's intrafascial hematoma. This case illustrates the need to consider alternative methods of chest compression to prevent spinal extension fractures and related complications when an elderly individual with a kyphotic spine experiences cardiac arrest.

Amyloid-related imaging abnormalities (ARIAs), including edema/effusion (ARIA-E) and hemosiderin deposition (ARIA-H), are complications of anti-amyloid β (Aβ) monoclonal antibody therapy for Alzheimer's disease (AD). A Japanese woman in her 70s with mild cognitive impairment due to AD, confirmed by positive amyloid positron emission tomography, developed a new lobar cerebral microbleed (CMB) after participating in aducanumab clinical trials. Magnetic resonance imaging revealed juxtacortical white matter hyperintensities on fluid-attenuated inversion recovery, which were later resolved as a novel CMB. Juxtacortical white matter hyperintensities may precede ARIA-H and may suggest cerebral amyloid angiopathy-related changes during anti-Aβ therapy. Monitoring of these lesions is essential.

Patients with anti-mitochondrial antibody positivity rarely develop tubulointerstitial nephritis with IgM-positive plasma cells (IgMPC-TIN). A previous report observed elevated serum IgM and urinary β2 microglobulin levels in all cases of IgMPC-TIN. This case involved IgA nephropathy with latent coexisting IgMPC-TIN; however, no such changes were observed. These results suggest that some patients with primary biliary cholangitis may have latent IgMPC-TIN without specific urine or blood results. Furthermore, the patient simultaneously developed IgA nephropathy and IgMPC-TIN, suggesting that the triggers and exacerbating factors for both conditions share a common underlying cause.

Although glucocorticoids are commonly used to suppress allergic reactions, systemic glucocorticoid-induced anaphylaxis has also been reported. A man with acute hepatitis B was administered intravenous methylprednisolone to prevent the progression to liver failure. Shortly thereafter, the patient developed a rash and hoarseness, and methylprednisolone-induced anaphylaxis was diagnosed. The injection was stopped, an antihistamine was administered, and the symptoms resolved quickly. Subsequently, antiviral therapy and 9.9 mg/day of dexamethasone were initiated. The patient recovered completely without persistent hepatitis B virus infection. This case highlights the importance of recognizing glucocorticoid-induced anaphylaxis and provides insights into alternative treatment strategies for acute hepatitis B.