Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 73-year-old woman with rheumatoid arthritis was treated with Levamisole, 150 mg per day, on 2 days a week. Her arthritis improved, but she developed a severely itching rash, and the treatment was stopped after 6 months. Penicillamine was subsequently given and tolerated without skin complications. 15 months after regular Levamisole was stopped, she was given a single dose of 150 mg which provoked fever of 40 degrees C and rash. Thirteen punch-biopsy specimens were examined by direct immunofluorescence microscopy. During the Levamisole treatment, granular deposits of IgG and C3 were found at the dermal--epidermal junction. Subsequently, the deposits disappeared, but reappeared after Levamisole challenge. The patient's leukocytes were exposed in vitro to Levamisole, and 36% of the total histamine content in the basophils was released. Our results provide further evidence that Levamisole can cause type-I as well as type-III hypersensitivity.
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PMID:Levamisole-induced hypersensitivity. 8 40

Levamisole, an anthelminthic agent with immunostimulatory properties, was used in a double-blind, controlled therapeutic trial in rheumatoid arthritis. Patients received either levamisole 100 mg 4 days a week, or placebo, for a period of 4 months. Significant improvement in the treated group, as compared with the control group, was found in the number of tender and swollen joints, grip strength, range of joint motion, sedimentation rate, and C-reactive protein. On double-blind global evaluation by the examining physicians, 9 of 14 patients on levamisole and none of 13 on placebo were considered to have improved. Adverse effects did not differ in frequency between the two groups except for mild alteration in taste, which was more common with levamisole.
Arthritis Rheum
PMID:Treatment of rheumatoid arthritis with levamisole. A controlled trial. 33 52

Three experimental animal models have been used in the studies on the stimulatory effect of coumarin and levamisole. Both coumarin and levamisole increases cell coverage on subcutaneous implanted glass coverslip in mice. An increase in intracellular phosphatase activity was also observed. Stimulated mouse peritoneal cells when treated in vivo with coumarin or levamisole and then cultured in vitro showed increases acid phosphatase secretion (both extracellular and intracellular) as compared to control. Coumarin reduced the primary lesion of adjuvant-induced arthritis in rats. However, it potentiates the secondary lesions. Levamisole has no effect on the primary lesion but potentiates the secondary lesions. There was an increase in spleen and adrenal weights which correlate well with the severity of the secondary lesions. Increase in liver weight was only observed in coumarin-treated animals, an observation which suggests that coumarin may be a powerful mononuclear phagocytes system stimulant. The similarities and differences between coumarin and levamisole in their mode of action will be discussed.
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PMID:A comparison of coumarin and levamisole on parameters of the inflammatory response. 49 45

The immuno-modulatory effect of Levamisole in the treatment of rheumatic diseases was studied in an open trial. Nine patients with theumatoid arthritis (RA), 13 with ankylosing spondylitis (AS) and one with Reiter's syndrome (RS) were treated initially with 150 mg Levmisole daily for 4 weeks, then intermittently 3 days a week. Significant clinical improvement was observed in 7 out of 9 patients with RA, in 4 out of 13 patients with AS, and in the one patient with RS. An increased skin sensitivity to a panel of antigens was noted in 3 out of 9 RA patients and in 6 out of 13 AS patients. A fall in rheumatoid factor titre was observed in 2 out of 5 patients with seropositive RA. No development of other auto-antibodies was observed. No significant changes in the absolute lymphocyte counts either of the total counts or of the T, B, and null cell counts, were noted. Drug-related adverse reactions were seen in 13 patients, mostly allergic skin rash which required a short interruption in therapy. Severe leucopenia was observed in 2 patients, whereupon therapy was definitely withdrawn. Levamisole seems to have a definite beneficial effect on RA and a possible effect on AS and RS. Severe adverse reactions, mostly on the haemopoietic system, demonstrated some potential hazardous complications of the drug and required physical and laboratory examinations at short intervals.
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PMID:Immunotherapy with levamisole in rheumatic diseases. 79 21

Rat adjuvant arthritis (AA) was used as a model to evaluate several blood markers as possible predictive indicators of drug efficacy. AA was induced in Sprague-Dawley rats by the injection of complete Freund's adjuvant into the right hind foot pad. The rats were dosed p.o. from day 18 to day 31 with levamisole (10 mg/kg), indomethacin (1 mg/kg), diclofenac sodium (0.5 & 1 mg/kg), and prinomide (10 & 20 mg/kg). Disease severity was assessed by paw circumference on day 31. The following blood markers were analyzed: hyaluronate by ELISA, prostaglandin E2 by RIA, ESR by micro-dispette, total PMN by Technicon H-1, and albumin by BCG dye. Blood marker correlation (r) to disease severity was: hyaluronate (0.71), prostaglandin E2 (0.58), ESR (0.52), PMN (0.58), and albumin (-0.71). The relative rank order of drug efficacy (indomethacin, diclofenac sodium, and prinomide) did not differ using the change in paw circumference (day 31-day 17) or blood markers. Levamisole exacerbated the disease as measured by all the above parameters. Thus, these blood markers provide additional information for the statistical evaluation of drugs in rat adjuvant arthritis.
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PMID:Relationship of blood markers to disease severity and drug efficacy in rat adjuvant arthritis. 179 16

Angioimmunoblastic lymphadenopathy (AILD) is a lymphoproliferative disorder with well established clinical and histological features, one of the clinical manifestations being a peripheral polyarthritis. A case of AILD with a symmetrical non-erosive peripheral polyarthritis is described, including the findings in the synovial fluid and histology of the synovium. There was a marked reduction in the number of peripheral blood T lymphocytes bearing the CDT8 phenotype in both the peripheral blood and synovial fluid. The arthritis was difficult to control, requiring large doses of corticosteroids, which produced significant side effects. Levamisole 150 mg, one day each week, was effective in controlling the arthritis and returning the numbers of CDT8 lymphocytes to normal. The aetiology of AILD is unknown, though a defect in T cell regulation, in particular T cell suppression, with a secondary B cell proliferation has been postulated. The demonstration of reduced numbers of lymphocytes bearing the CDT8 phenotype in this patient supports that theory.
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PMID:Polyarthritis and angioimmunoblastic lymphadenopathy. 366 44

Type II collagen- and adjuvant-induced arthritis in outbred Wistar rats were compared using parameters that measured the inflammatory response, cellular and humoral immunity, blood protein changes, drug metabolism and histopathological and bony changes of the inflamed paws. There was a lesser incidence (40-70%) and severity of collagen disease than the adjuvant model (incidence approximately 100%). The use of MDP increased the incidence and severity of collagen arthritis. The acute phase protein response (plasma fibrinogen) was similar in both models during the peak of inflammatory response. Drug metabolism was inhibited in both type II collagen boosted with MDP or M. butyricum sensitized rats with arthritis; however, arthritic rats sensitized with collagen alone produced no inhibition. Only collagen arthritic rats produced type II collagen antibody and exhibited delayed hypersensitivity to type II collagen. Bony changes as assessed by radiographic evaluation were more severe in adjuvant arthritic rats than in the collagen arthritic model; histopathological findings from these animals confirmed this observation. The primary lesions in both models were periosteal reaction of the bone and ankylosis. Several classes of antiarthritic drugs were compared in both models using paw edema measurements and bony changes by radiographic evaluation. Drugs with inhibitory activity in both models were indomethacin, methylprednisolone, D-penicillamine and gold sodium thiomalate. Levamisole, chloroquine and auranofin were inactive in both models.
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PMID:Comparison of inflammatory changes in established type II collagen- and adjuvant-induced arthritis using outbred Wistar rats. 407 44

Adjuvant arthritis is an experimental immunopathy that is thought to share many features of human rheumatoid arthritis and, as such, is one of the most widely used models for studying the anti-inflammatory properties of compounds. Adjuvant arthritis can be induced in the rat by the injection of various bacterial cell walls or their components; however, the exact immunogen remains unknown. Recently, an autoantibody response to type II collagen was described not only in the collagen-induced arthritic model but in the adjuvant-induced disease as well. This response thus suggests that shared antigenic determinants exist between type II collagen and the responsible immunogen in the bacterial cell wall components. The contribution of the T lymphocyte to the pathogenesis of adjuvant arthritis is well known. It has now been shown that under specific conditions, adjuvant arthritis can be either enhanced or suppressed with pharmacologic or surgical manipulation, thus suggesting the heterogenicity of T lymphocytes capable of influencing the course of the disease. Levamisole was shown to reverse the augmentation of adjuvant disease seen after adult thymectomy, which suggests that levamisole can restore an aberrant immune response. Monoclonal antibodies are now being developed to evaluate T cell subsets in the rat. The use of these antibodies to study or selectively deplete lymphocyte subpopulations in this disease model promises to reveal immunologic characteristics that may lead to the development of new classes of immunoregulant drugs. Finally, the adjuvant rat has been found useful as a pain model capable of detecting the analgesic properties of both central and the newer peripheral analgesics. The above studies further corroborate the similarities between the immunopathological and hyperalgesic features of human rheumatoid arthritis and adjuvant disease. Recently developed immunologic technology may allow a new look at an old model and may result in the ability to evaluate new classes of immunoregulating agents.
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PMID:Adjuvant arthritis: immunopathological and hyperalgesic features. 617 58

During levamisole therapy, 14 of 20 patients with previously unresponsive rheumatoid arthritis had significant improvement (P less than 0.05) in clinical measures of disease activity, erythrocyte sedimentation rate, and rheumatoid factor titer in a 32-week double-blind placebo controlled crossover trial. Levamisole was shown to alter antibody responses to tetanus and typhoid antigens, lymphocyte blastogenesis to phytohemagglutinins, and the number of null cells in peripheral blood. Agranulocytosis and rash resulted in discontinuation of the drug in one patient in each group. Though clearly effective, routine use of levamisole as a disease suppressant in rheumatoid arthritis must await more complete clarification of its association with agranulocytosis.
Arthritis Rheum 1980 Feb
PMID:Double-blind placebo controlled crossover evaluation of levamisole in rheumatoid arthritis. 698 88

The clinical response to levamisole in 11 patients with complete Behcet's syndrome was reviewed. Nine patients responded, 3 completely and 6 partially, with reduction in the number and severity of buccal and genital lesions. In 3 patients each, ocular inflammation and gastrointestinal involvement responded to levamisole, and in 1 patient neurologic status improved. Levamisole was purposely discontinued in 3 patients to assess its true role in disease control. Each patient experienced a flare. Reintroduction of therapy controlled the flare in all cases, although 1 patient subsequently relapsed while continuing therapy. Two patients failed to respond. Side effects necessitated permanent discontinuation of the drug in 2 respondent patients, but in no case did neutropenia or agranulocytosis develop. These preliminary results suggest that levamisole may be useful in the therapy of the various manifestations of Behcet's syndrome and that a controlled prospective study is indicated.
Arthritis Rheum 1981 Jan
PMID:Treatment of Behcet's syndrome with levamisole. 700 1


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