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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report describes a patient with active systemic lupus erythematosus (SLE) who evidenced severe bleeding consequent to a profound and isolated reduction in plasma factor II (prothrombin) activity. Absence of the factor is documented by immunologic means and its return after corticosteroid therapy is demonstrated. The authors recommend inclusion of this acquired coagulopathy among other more traditional diagnostic manifestations of SLE.
Arthritis Rheum
PMID:Absent factor II in systemic lupus erythematosus. Immunologic studies and response to corticosteroid therapy. 81 6

The clinical and laboratory experience with the lupus anticoagulant was reviewed in 37 patients. The anti-coagulant is thought to act by blocking the activation of prothrombin by the prothrombin activator comlex of factors Xa, V, and phospholipid. Although the anticoagulant has been principally associated with diseases of immune origin, 14 of the present patients had disorders not thought to be immune in nature. Eighteen patients underwent twenty-one operative procedures with only a single episode of excessive bleeding. In the author's experience, the lupus anticoagulant is a rare cause of bleeding.
Arthritis Rheum
PMID:The lupus anticoagulant. 99 35

A wide spectrum of hemostatic abnormalities is found in patients with SLE. Thrombocytopenia and qualitative platelet disorder (impaired aggregation to collagen) are probably both due to antiplatelet antibodies, which can be found in most patients with the disease. About 10% of patients with SLE have a circulating anticoagulant. These circulating anticoagulants are broadly heterogeneous. Although most reported cases act at the level of the prothrombin converting complex, 15 of the 74 cases here reviewed had other points of action. The anticoagulants are probably all antibodies; they differ (with rare exceptions) from other naturally occurring circulating anticoagulants in having an immediate rather than a progressive effect, and in acting, not against pre-existing procoagulants, but against unstable complexes. An anticoagulant of the type found in SLE is only rarely observed in the absence of SLE; its presence in a patient is thus of some diagnostic importance. Hypoprothrombinemia is a common second lesion in patients with circulating anticoagulants. Its pathogenesis is obscure. Two patients with acquired von Willebrand's disease have been observed. All the hemostatic abnormalities found in SLE probably have immunologic bases; all respond to glucocorticoid treatment.
Semin Arthritis Rheum 1975 Feb
PMID:Disorders of hemostatic function in patients with systemic lupus erythematosus. 109 75

Recent reports of and our own experience with biochemical alterations of liver function secondary to salicylate therapy stimulated this prospective study. Thirty-four children with juvenile rheumatoid arthritis, 6 children with acute cartilagenous necrosis of the hipfollowing slipped capital femoral epiphysis, and 2 children with ulcerative colitis and hip disease who were on salicylates were followed over a period of 1-27 months with serial determinations of serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), lactic dehydrogenase (LDH), alkaline phosphatase (AP), bilirubin, and serum salicylate. Prothrombin time was measured in 14 children. Twenty-two of 34 children with rheumatoid arthritis and none of the 8 controls demonstrated abnormalities of various liver functions at serum salicylate levels between 7.0 and mg%. Three children demonstrated severe abnormalities characterized by marked elevation of SGOT, SGPT, LDH, and AP, prolongation of prothrombin time, and epistaxis. This type of reaction occurred within 5-14 days of initiation of aspirin therapy and occurred at serum salicylate levels between 18 and 43 mg%. Moderate changes in various liver function tests were observed in 19 other children. None of those children who were tested showed prolongation of prothrombin time. The serum salicylate level in this group varied between 7.0 and 38.2 mg%. The abnormal liver function tests returned to normal in 6 children upon withdrawal of aspirin and in 12 others even when salicylates were continued. Therefore, despite the occurrence of biochemical abnormalities following chronic salicylate therapy, it does not appear to be necessary to discontinue their use except in those children who develop bleeding.
Arthritis Rheum
PMID:Aspirin-induced hepatotoxicity in juvenile rheumatoid arthritis. A prospective study. 115 54

Three patients with hemarthrosis of the knee joint complicating sodium warfarin oral anticoagulation therapy are described. In all 3 the prothrombin time was at least 2.4 times the control value at the time of hemarthrosis. After initial bleeding was controlled, 2 patients had recurrences at times when their prothrombin times were again more than 2.5 times greater than those of the normal control subject. Joint symptoms persisted in all patients until the warfarin dose was substantially decreased or discontinued. Underlying joint disease was present in 1 individual and may have predisposed him to the occurrence of hemarthrosis. No long-term joint damage was recognized as resulting from the hemarthrosis at followup 1 to 2 years later. The authors conclude that hemathrosis associated with oral anticoagulant therapy occurs when the prothrombin time is excessively prolonged any may remain symptomatic until anticoagulation is reduced or discontinued. Management includes careful diagnostic aspiration, despite the prolonged prothrombin time, and discontinuation of anticoagulation.
Arthritis Rheum
PMID:Hemarthrosis associated with sodium warfarin therapy. 125 72

Sixty-seven patients were treated with moxalactam in a noncomparative trial of hospitalized patients; 32 had endometritis or chorioamnionitis, 12 had skin and soft tissue infections, 5 had osteomyelitis, 5 had pneumonia, 5 had urinary tract infections, 4 had arthritis, 2 had sepsis from an unknown source, 1 had endocarditis, and 1 had peritonitis. Bacteremia was present in 12 of these patients. Patients were given 3 to 12 g of moxalactam per day (mean, 6.24 g/day) in divided doses every 6 to 8 h. Seven patients were given intramuscular treatment for 3 to 20 days for part or all of their therapy. The rest were given intravenous treatment exclusively. Treatment was continued for 2 to 42 days (mean, 10 days). The dose and the duration of therapy were determined by the type of infection and the response of each patient. There were four treatment failures and one enterococcal-clostridial superinfection. Moxalactam was well tolerated. Allergic reactions led to the discontinuation of the antibiotic in three patients. Prolonged prothrombin and partial thromboplastin times were observed in 2 of 11 patients tested; in both instances in patients had severe underlying diseases, including malnutrition and alcoholism. Pain on intramuscular injection was noted in two patients receiving 1,500 mg, but not in five receiving a lower dose; in one case the pain forced the use of intravenous therapy after one dose, and in the other case the pain was mild and the patient was treated for 20 days. We concluded that moxalactam was effective in the treatment of the types of infections included in this study and produced few adverse reactions.
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PMID:Moxalactam in the therapy of serious infections. 621 Nov 40

Goats, sheep and calves were inoculated intravenously with strain Y3343 of the large colony type of Mycoplasma mycoides subsp. mycoides isolated from a goat with polyarthritis. The goats and sheep died of septicemia (one was killed in extremis) within eight days. The goats had leukopenia and granulocytopenia. Coagulopathy was indicated in some goats; the fibrinogen titer, prothrombin and partial thromboplastin times increased with the progress of disease and the number of platelets decreased dramatically in one goat. Goats and sheep had cellulitis at the site of inoculation, pleural hemorrhages, pneumonia, myocarditis, renal infarcts, glomerulitis, adrenal cortical necrosis, enteritis, focal splenic necrosis, polyarthritis and lymphadenitis. Vasculitis and thrombi were seen occasionally, suggesting that vascular changes, perhaps together with coagulopathy, had a role in pathogenesis. One of two experimental calves developed a slight fever, arthritis and minor inflammation of adrenal tissue. Calves seen less susceptible to the mycoplasma organism given intravenously than do goats or sheep.
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PMID:Experimental infection of goats, sheep and calves with the large colony type of Mycoplasma mycoides subsp. mycoides. 700 31

Three children with systemic lupus erythematosus who developed hemorrhagic tendencies as a consequence of a clotting factor II (prothrombin) deficiency are described. All three responded rapidly to treatment with corticosteroids. A literature review added 25 case reports, with the following findings. First, factor II deficiency occurs in the presence of the lupus anticoagulant, although the interrelationship between the two is not understood. Second, the deficiency is presumed to be secondary to rapid clearing of the antigen/antibody factor II complex in the liver. Finally, most cases respond to corticosteroid therapy with or without the coadministration of vitamin K or fresh frozen plasma. In corticosteroid-dependent patients, the addition of antimetabolites such as azathioprine has enabled reduction in steroid doses.
Semin Arthritis Rheum 1994 Aug
PMID:Hypoprothrombinemia in childhood systemic lupus erythematosus. 798 33

Because fibrin is commonly observed within arthritic joints, studies were undertaken to determine whether purified coagulation and fibrinolytic proteases degrade cartilage in vitro and to seek evidence for the activation of coagulation in arthritic joints through measurements of the levels of inhibitor-enzyme complexes and several other proteins associated with coagulation and fibrinolysis. The concentrations of 13 plasma proteins and complexes of thrombin and Factor Xa with antithrombin III were measured in synovial fluids recovered at the time of knee replacement surgery. All zymogens necessary to constitute the coagulation cascade were present. Thrombin and the combination of prothrombin plus prothrombinase induced proteoglycan release from both normal and arthritic cartilages. Factor Xa and plasmin induced release from diseased cartilage only, and urokinase, tissue plasminogen activator, and activated protein C were without effect at the levels used. At saturating levels of thrombin (> or = 2.0 microM) 80% of the proteoglycan content of normal cartilage was released within 24 h. Thrombin, which is cationic, reversibly binds cartilage with Kd = 7.0 +/- 1.0 microM and Bmax = 820 +/- 70 ng/mg of human cartilage. Levels of thrombin-antithrombin III complexes in synovial fluids and arthritis were 4-fold higher in osteo (OA) and 43-fold higher in rheumatoid (RA) than in controls (0.98 nM). Factor Xa-antithrombin III complex levels were threefold lower in OA and fivefold higher in RA than in controls (0.24 nM). These elevated levels of enzyme-inhibitor complexes imply a history of activation of coagulation within the joint, especially in RA. Since thrombin degrades cartilage in vitro and had been generated in vivo, as inferred by the existence of thrombin-antithrombin III complexes, intraarticular activation of coagulation may both contribute to the pathology of arthritis and comprise a target for therapy and diagnosis.
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PMID:Studies of thrombin-induced proteoglycan release in the degradation of human and bovine cartilage. 804 Mar

Great progress has been made within the past 10 years in characterizing, assaying, and describing mechanism(s) of action in vitro of antiphospholipid antibodies (a-PL Abs); three prominent members are reagin, anticardiolipin antibodies (a-CL Abs), and the lupus anticoagulants (LAC). The major focus of this review is on basic and current biochemical and immunologic research. First, the biochemistry, structural composition, and sources of anionic and dipolar ionic (zwitterionic) phospholipids are discussed together with several serum antibodies directed to these phospholipids. Cardiolipin, the most acidic phospholipid (net negative charge of 2 at pH 7.0) has been historically important as an antigen for testing reagin in syphilis serology, and currently is part of the antigenic composition used in the Venereal Disease Research Laboratory (VDRL) tests. In this connection, the chronic biological false-positive test for syphilis and the LAC are discussed in association with autoimmune disorders such as systemic lupus erythematosus. Second, a naturally occurring plasma anticoagulant in vitro and a critical cofactor for binding of purified autoimmune a-CL Abs to cardiolipin is considered, the beta 2-glycoprotein I (beta 2-gpI). This single-chain plasma polypeptide is highly glycosylated, has 326 amino acids, a molecular weight of 50 kD, and is characterized by repeating amino acid motifs or domains that structurally resemble multiple loops. The highly cationic C-terminal fifth domain binds to anionic phospholipids. The beta 2-gpI is a member of the short consensus repeat superfamily of proteins, and is compared with other proteins with similar domains. Third, experiments are detailed for defining LAC and distinguishing it from other a-CL Abs. Cofactors are also associated with LAC and include beta 2-gpI, prothrombin, protein C, protein S, tissue factor, and factor XI. Thus, LAC antibodies are heterogeneous, and no individual assay can detect all LACs. Because patients with syphilis and other infectious diseases have no cofactor associated with a-CL Abs, their plasma LACs are negative. The a-CL Abs found in infection are not associated with the clinical features of the antiphospholipid syndrome. LAC assays are important because of the pathogenetic association with clinical observations of venous and arterial thrombosis, thrombocytopenia, and recurrent fetal loss. Finally, reports leading to development of currently used direct solid-phase enzyme-linked immunosorbent assays (ELISA) for testing a-PL Abs are outlined; these developments have greatly increased understanding of the basic immunology of target antigens and their respective antibodies. Of significance, a-CL Abs cross-react with other anionic phospholipids. Additionally, the results of these assays led to the realization that high levels of circulating a-PL Abs over long periods are associated with a number of clinical problems now known collectively as the antiphospholipid syndrome.
Semin Arthritis Rheum 1997 Apr
PMID:Antiphospholipid antibodies: basic immunology and assays. 914 49


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