The Experts below are selected from a list of 240 Experts worldwide ranked by ideXlab platform

Marc D. Cohen - One of the best experts on this subject based on the ideXlab platform.

  • An unusual case of carcinoma Polyarthritis with associated vasculitis
    Arthritis and rheumatism, 1997
    Co-Authors: Jose M. Acosta Madiedo, Anant Murthy, Denis A. Cortese, Marc D. Cohen
    Abstract:

    This report describes a patient who presented with an unusual Polyarthritis syndrome. After extensive evaluation, squamous cell carcinoma of the lung was diagnosed. During the course of the illness, the patient developed vasculitic features and "rheumatoid-like" nodules. Two months after the administration of combined-modality therapy for stage IIIA non-small cell lung carcinoma, the signs and symptoms of Polyarthritis and vasculitis had disappeared completely. Ten months later, the patient remains in clinical remission. This is the first published report of simultaneous vasculitic and polyarticular manifestations in a patient with carcinoma Polyarthritis.

S. Okamoto - One of the best experts on this subject based on the ideXlab platform.

  • Polyarthritis ASSOCIATED WITH HEPATITIS C VIRUS INFECTION
    British journal of rheumatology, 1994
    Co-Authors: Y. Ueno, R. Kinoshita, I. Kishimoto, S. Okamoto
    Abstract:

    Two cases of Polyarthritis associated with hepatitis C infection are reported. In Patient 1, stiffness and Polyarthritis occurred during the acute stage of hepatitis. The arthritic symptoms lasted for 4 months. A transient Polyarthritis recurred 4 yr later. The persistent presence of anti-hepatitis C viral antibodies was noted. Hepatitis C viral RNA (HCV RNA) was identified in the serum using the polymerase chain reaction proving that the patient was a carrier. In Patient 2, Polyarthritis occurred associated with chronic hepatitis C liver disease. Synovial biopsy showed infiltration of mononuclear cells. HCV RNA was demonstrated in both serum and SF. These cases suggest an aetiologic association between arthritis and hepatitis C antigenaemia.

John J Cush - One of the best experts on this subject based on the ideXlab platform.

  • Acute Polyarthritis.
    Best practice & research. Clinical rheumatology, 2006
    Co-Authors: Kathryn Dao, John J Cush
    Abstract:

    Arthritis is the most common cause of disability. Hence, prompt recognition and management of acute-onset Polyarthritis are paramount to prevent progressive damage. When rheumatoid arthritis is considered as a prototypical example of Polyarthritis, the stakes of early and accurate evaluation are evident. The challenge is in determining when undifferentiated Polyarthritis ends and rheumatoid arthritis begins. This chapter reviews the evidence to help clinicians identify and manage patients who present with acute polyarticular inflammation.

Hongquan Zhang - One of the best experts on this subject based on the ideXlab platform.

  • therapeutic effect of syringin on adjuvant arthritis in rats and its mechanisms
    Acta pharmaceutica Sinica, 2010
    Co-Authors: Yuanyuan Song, Hongquan Zhang
    Abstract:

    : This study is to investigate the therapeutic effect of syringin on adjuvant arthritis (AA) in rats and its mechanisms. Complete Freund's adjuvant (FCA) was used to induce AA in rats. Secondary paw swelling of AA rats was measured with volume meter. Pain response and Polyarthritis index were scored. Meanwhile, splenic lymphocyte proliferation response induced by concanavalin A (ConA) or lipopolysaccharide (LPS) was examined with MTT assay. IL-2 production of splenic lymphocytes and IL-1 beta, TNF-alpha production of peritoneal macrophage (PM phi) were estimated by enzyme linked immunosorbent assay (ELISA). The secondary inflammation of AA rats appeared on the 14th day after injection of FCA. Syringin and tripterygium glycosides (TG) were given by intragastric administration for 16 days from the 14th day. Treatment of AA rats with syringin and TG from the 22th day significantly attenuated the secondary hind paw swelling, as well as relieved the pain response and the polyarthritic symptoms of the whole body as compared with that of the AA model group. The suppressed lymphocyte proliferation and IL-2 production of splenic lymphocytes in AA rats were reversed by treatment with syringin. Meanwhile, syringin remarkably down-regulated IL-1 beta, TNF-alpha productions from PM phi. These results indicate that anti-inflammatory effects of syringin on AA rats are mediated by modulating the immune function of abnormal cells and the balance of cytokines.

Gregory Keenan - One of the best experts on this subject based on the ideXlab platform.

  • juvenile rheumatoid arthritis like Polyarthritis in chromosome 22q11 2 deletion syndrome digeorge anomalad velocardiofacial syndrome conotruncal anomaly face syndrome
    Arthritis & Rheumatism, 1997
    Co-Authors: Kathleen E Sullivan, Donna M Mcdonaldmcginn, Deborah A Driscoll, Chester M Zmijewski, Abdou S Ellabban, Lori Reed, Beverly S Emanuel, Elaine H Zackai, Balu H Athreya, Gregory Keenan
    Abstract:

    Objective. To investigate the association of Polyarthritis and chromosome 22q11.2 deletions. Methods. Eighty patients with chromosome 22q11.2 deletion syndrome followed up at The Children's Hospital of Philadelphia were examined for evidence of arthropathy or arthritis. Patients with chromosome 22q11.2 deletion syndrome and Polyarthritis underwent laboratory evaluations of immunologic function to determine the relationship of their immunodeficiency to the Polyarthritis. Results. The prevalence of Polyarthritis in patients with chromosome 22q11.2 deletion syndrome was markedly increased over the prevalence of polyarticular juvenile rheumatoid arthritis (JRA) in the general population. All 3 patients with Polyarthritis had evidence of impaired T cell function. Two of the patients with Polyarthritis also had IgA deficiency. Conclusion. The chromosome 22q11.2 deletion syndrome represents a primary T cell disorder which can be associated with a JRA-like Polyarthritis. All 3 patients with Polyarthritis had evidence of more extensive immunoregulatory derangements than those typically seen in patients with chromosome 22q11.2 deletion, and these derangements may have predisposed to the development of Polyarthritis.