The pathological hallmark of rheumatoid arthritis (RA) is a synovial pannus that comprises proliferating and invasive fibroblast-like synoviocytes, infiltrating inflammatory cells, and an associated neoangiogenic response. Animal models have been established to study these pathological features of human RA. Spontaneous and induced animal models of RA primarily reflect inflammatory aspects of the disease. Among various induced animal models, collagen-induced arthritis (CIA) and collagen antibody-induced arthritis (CAIA) models are widely used to study the pathogenesis of RA. Improved transplantation techniques for severe combined immunodeficiency (SCID) mouse models of RA can be used to evaluate the effectiveness of potential therapeutics in human tissues and cells. This review provides basic information on various animal models of RA, including CIA and CAIA. In addition, we describe a SCID mouse coimplantation model that can measure the long-distance migration of human RA synoviocytes and cartilage destruction induced by these cells.
Microenvironmental Enzyme-Responsive Methotrexate Modified Quercetin Micelles for the Treatment of Rheumatoid Arthritis Xiuying Li, Xin Wang, Xiuwu Qu, Ningning Shi, Qinqing Li, Zhifang Yan, Yandong Li, Yingli Wang International Journal of Nanomedicine.2024; Volume 19: 3259. CrossRef
Clinical Phenotypes, Serological Biomarkers, and Synovial Features Defining Seropositive and Seronegative Rheumatoid Arthritis: A Literature Review James Perera, Chiara Aurora Delrosso, Alessandra Nerviani, Costantino Pitzalis Cells.2024; 13(9): 743. CrossRef
JAK Inhibitors in Rheumatoid Arthritis: Immunomodulatory Properties and Clinical Efficacy Kajetan Kiełbowski, Paulina Plewa, Aleksandra Wiktoria Bratborska, Estera Bakinowska, Andrzej Pawlik International Journal of Molecular Sciences.2024; 25(15): 8327. CrossRef
Astaxanthin, Compared to Other Carotenoids, Increases the Efficacy of Methotrexate in Rat Adjuvant Arthritis Katarína Pružinská, Martin Chrastina, Sasan Khademnematolahi, Veronika Vyletelová, Lívia Gajdošová, Lucia Pastvová, František Dráfi, Silvester Poništ, Ľudmila Pašková, Jarmila Kucharská, Zuzana Sumbalová, Jana Muchová, Silvia Martiniaková, Katarína Bauero International Journal of Molecular Sciences.2024; 25(16): 8710. CrossRef
In vivo murine models for evaluating anti-arthritic agents: An updated review Santenna Chenchula, Ahmad Najmi, Shubham Atal, Balakrishnan Sadasivam Future Health.2024; 2: 138. CrossRef
Impaired Development of Collagen Antibody-Induced Arthritis in Rab44-Deficient Mice Yu Yamaguchi, Tomoko Kadowaki, Eiko Sakai, Mayuko Noguromi, Shun Oyakawa, Takayuki Tsukuba Biomedicines.2024; 12(11): 2504. CrossRef
Gitelman syndrome is a condition caused by a mutation of the thiazide sensitive Na-Cl cotransporter gene on the distal convoluted tubule. It results in a variety of clinical features, including hypokalemia, hypomagnesemia, hypocalciuria, and metabolic alkalosis. It is often diagnosed in asymptomatic adults presented with unexplained hypokalemia; however, it is sometimes associated with muscular cramps, numbness, fatigue, weakness, or paralysis. We experienced a case of rheumatoid arthritis accompanied by Gitelman syndrome, presented with hand tremor. We diagnosed her using renal clearance study and genetic analysis. Here, we report our experiences regarding this case along with a literature review.
Subcutaneous tissue calcification in rheumatic diseases usually occurs in connective tissue diseases, such as systemic lupus erythematosus, scleroderma, and dermatomyositis. Domestic cases of calcification in rheumatoid arthritis have not been reported. The mechanism of subcutaneous tissue calcification may differ depending on the cause and it can develop on all parts of the body. Calcification occurring in rheumatic diseases is a major mechanism of tissue damage caused by chronic inflammation. No standard therapy for calcification has been established; however, many studies have reported on medical and surgical treatment. We report on subcutaneous tissue calcification in a rheumatoid arthritis patient tissue calcification on both sides of the buttocks, the upper limbs, and the lower limbs.
Churg-Strauss syndrome (CSS) is a necrotizing vasculitis with extra-, peri-vascular eosinophilic infiltration. Chronic symmetric polyarthritis with the presence of rheumatoid factor (RF) and anti-cyclic citrullinated peptide antibody are the mainstay of rheumatoid arthritis (RA) diagnosis. Mononeuritis multiplex is a peripheral neuropathy involving more than 2 separate nerve areas. A 62-year-old male patient was referred for left foot drop and polyarthritis of both hands and feet for 4 months. During evaluation, mononeuritis multiplex was detected on nerve conduction study and electromyography tests: vasculitis with neutrophil, eosinophil, and lymphocyte infiltration on peroneal nerve biopsy. A positive response to methacholin and bronchodilator was observed on the pulmonary function test. Radiologic tests showed peri-articular soft tissue swelling and osteopenia on both hand and foot. Marked peripheral eosinophilia, high RF, and positive perinuclear anti-neutrophil cytoplasmic antibody were detected on blood tests. Here, we report on a patient with overlap syndrome of CSS and RA with review of the relevant literature, from which a few references to overlap syndrome of CSS and RA were available.
Due to its efficacy and tolerability, low dose oral methotrexate(MTX) therapy has been widely used for treatment of rheumatoid arthritis(RA). However, it can rarely cause serious, life-threatening hematologic toxicities, such as pancytopenia. We report here on two patients with chronic kidney disease(CKD), who developed severe pancytopenia after 5 years (cumulative dose 1,240mg) and 4 years(cumulative dose 1,320mg) of low dose MTX therapy for treatment of RA, respectively. Both patients presented with renal insufficiency, hypoalbuminemia, concurrent use of nonsteroidal anti-inflammatory drugs, and elevated mean corpuscular volume of red blood cells(RBCs), all of which are known as risk factors of MTX-induced pancytopenia. Despite receiving treatment, which included RBC and platelet transfusions, antibiotic therapy, granulocyte colony stimulating factor, and leucovorin rescue, one patient died of sepsis. Based on our case study, prompt investigation of risk factors associated with MTX toxicity is required for all patients receiving MTX therapy. MTX treatment, even at a low dose, should be discontinued in patients with advanced CKD.
Pyoderma gangrenosum is uncommon neutrophilic dermatosis characterized by richness of the mature neutrophilic polynuclear dermal infiltrate. Pyoderma gangrenosum is associated with variable diseases, most commonly inflammatory bowel disease, hematological diseases, malignancies, but it is reported rarely in rheumatoid arthritis. We report a case of pyoderma gangrenosum in rheumoid arthritis patient. A 50-year-old woman admitted to our hospital due to painful pretibial ulcerative skin lesions. She had been treated as rheumatoid arthritis for 8 years. At admission, body temperature was 36.5degrees C and other vital sign was unremarkable. Physical examination revealed right pretibial ulceration, multiple pustules on left pretibial area and both palms. Laboratory studies revealed WBC count 7,600/uL (neutrophils 60.3%, eosinophil 3.2%), hemoglobin 11.4 g/dL, platelet count 319,000/uL, ESR 65 mm/hour. Other lab findings were also unremarkable. Skin biopsy was done, which showed dense dermal infiltrate of neutrophils and wound culture were negative. By 8 weeks after systemic high dose corticosteroid (1 mg/kg/day), cyclosporine A (5 mg/kg/day), sulfasalazine 2 g therapy, symptoms and skin ulceration were being improved. Without skin relapse, she is followed up our hospital with low dose corticosteroid and sulfasalazine.