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Biomedical subjects

E Munthe

Publications and source records attributed to E Munthe.

At least 19 recordsLinked to original sources
PubMed1991

C3 activation products, C3 containing immune complexes, the terminal complement complex and native C9 in patients with rheumatoid arthritis.

Complement activation products, C9 and C3-containing circulating immune complexes (CIC), were evaluated in plasma and synovial fluid (SF) from patients with rheumatoid arthritis (RA) and osteoarthritis. C3 activation products and the fluid phase terminal complement complex were considerably elevated in SF from RA patients reaching levels five- to eighttimes that in plasma, consistant with a local activation of the whole cascade in the joints. The results emphazise the importance of detecting C3 activation by neoepitope expression instead of single fragment determinations. The concentration of native C9 was lower in synovial fluid compared with plasma, consistant with the excessive local complement activation. Increased CIC levels which correlated with the degree of complement activation were also found in the SF from the RA patients.

Adult↗
PubMed1991

The leukocyte protein L1 in plasma and synovial fluid from patients with rheumatoid arthritis and osteoarthritis.

L1 is a major granulocyte and monocyte protein, released during activation and turnover of such cells. Blood and synovial fluid (SF) from 41 patients with rheumatoid arthritis (RA) and 6 patients with osteoarthritis (OA), were analyzed for L1 and the acute phase proteins C-reactive protein, orosomucoid, haptoglobin, alpha 1-antitrypsin and albumin as well as for differential leukocyte count. L1 levels in plasma and SF showed highly significant differences (p less than 0.0001), between the RA and OA patients. All the OA patients had normal plasma concentrations of L1 and low concentrations of L1 in SF. All the RA patients had elevated plasma levels of L1 and high L1 concentrations in SF. In the RA patients, the ratios between the protein concentrations in SF and blood were 3.29 for L1 and less than or equal to 0.64 for the acute phase proteins. In the SF, the L1 levels did not correlate with the monocyte count, while a low, positive correlation was found between L1 and the granulocyte count. The high L1 concentrations observed in SF from RA patients probably reflected an increased turnover of leukocytes in the inflamed joints. In SF from RA patients, high L1 concentrations were found in joints with a high amount of swelling. The present study suggests that L1 may represent a marker of both local and systemic inflammation.

Acute-Phase Proteins↗
PubMed1990

Rheumatoid arthritis may be primarily associated with HLA-DR4 molecules sharing a particular sequence at residues 67-74.

Genomic typing of in vitro amplified DNA with sequence-specific oligonucleotide (SSO) probes was performed for DRB1, DQA1, DQB1, DPA1 and DPB1 alleles in 54 random Norwegian rheumatoid arthritis (RA) patients and 181 healthy controls. DRB1 alleles encoding the serological specificity DR4 were found in 80% of the patients, compared to 34% of the controls (relative risk = 7.9, p less than 0.0001). All DR4-positive RA patients carried either DRB1*0401 (Dw4), 0404 (Dw14), or 0405 (Dw15), while no patients were found to carry DRB1*0402 (Dw10) or 0403 (Dw13). The frequency of the DRB1*0101 allele encoding DR1 was not increased, even among DR4-negative RA patients, and we were unable to detect any sharing of other class II alleles among DR4-negative patients. No contribution of any DQA1, DQB1, DPA1 or DPB1 alleles to RA susceptibility could be detected. The results suggest that in the Norwegian population RA is primarily associated with a shared sequence at residues 67-74 of the DR beta 1 chain, but only when this sequence is expressed on DR4 molecules.

Alleles↗
PubMed1989

A longitudinal study of the leukocyte protein L1 as an indicator of disease activity in patients with rheumatoid arthritis.

L1 is a major granulocyte and monocyte protein. It is released during leukocyte activation, and the plasma level is thought to reflect the inflammatory activity. Fifteen patients with classical or definite rheumatoid arthritis were examined monthly during one year. The laboratory tests included L1, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), orosomucoid, haptoglobin, ceruloplasmin, alpha 1-antitrypsin, immunoglobulins and blood cell counts. The clinical tests included articular index, grip strength, morning stiffness and pain. The L1 protein was found to have highly significant correlations (p less than 0.0001) with orosomucoid (r = 0.86), CRP (r = 0.79), ESR (r = 0.78), haptoglobin (r = 0.75), alpha 1-antitrypsin (r = 0.63) and ceruloplasmin (r = 0.44). Significant correlation was also found between L1 and IgA. None of the laboratory variables showed significant correlation with pain, but when they were correlated with articular index, grip strength and morning stiffness, L1 was found to have the highest average correlation coefficient (p less than 0.0001).

Adult↗
PubMed1988

The major leukocyte protein L1 as an indicator of inflammatory joint disease.

L1 is a major protein in granulocytes and monocytes. It is released during activation of these cells, and the plasma level of L1 is therefore thought to reflect the turnover of leukocytes. Peripheral blood from 96 patients hospitalized in a rheumatological department, was analysed for L1, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). The total patient material was divided into groups depending on diagnosis: 47 patients with rheumatoid arthritis, 27 patients with arthritis of different etiologies, 15 patients with non-inflammatory diseases and 7 patients with arteritis. Correlation analysis were made between the different laboratory parameters. A high positive correlation was found between L1 and CRP in all the groups, and with a correlation coefficient of the total patient material of 0.68 (p less than 0.001). The correlation coefficient between L1 and ESR was 0.54 (p less than 0.001) in the total patient material, and between CRP and ESR it was 0.66 (p less than 0.001). The results indicate that the L1 protein could be a new laboratory marker of inflammation in rheumatic diseases.

Antigens, Surface↗
PubMed1986

Trace elements and rheumatoid arthritis (RA)--pathogenetic and therapeutic aspects.

Rheumatoid arthritis is characterized by increased activity of macrophages which produce toxic forms of oxygen. Such oxygen has been suggested as mediator also of rheumatoid inflammation. Gold accumulates in lysosomes of the macrophages and stabilizes lysosomal and other cell membranes leading to reduced liberation of toxic oxygen. Intracellular production of metallothionein can be induced. Zinc in high doses parenterally can immobilize macrophages and also induce metallothionein-like proteins. Copper and zinc are components of SOD which detoxifies oxygen, and copper-thiolate complexes are reported to be anti-inflammatory. The therapeutic effect of penicillamine and other thiols like aurothiomalate may also be related to an anti-oxidative action. Therapeutic induction of increased intracellular levels of glutathione or administration of selenium in such a form that it incorporates into glutathione-peroxidase and increases the efficacy of the enzyme may lead to accelerated metabolism of toxic oxygen.

Arthritis, Rheumatoid↗
PubMed1986

Analysis of cellular and membrane extracts of human leukocytes from rheumatoid arthritis patients using two-dimensional electrophoresis.

Peripheral blood leukocytes from 30 patients with classic or definite rheumatoid arthritis (RA) and 18 healthy controls were separated into lymphocytes, monocytes and granulocytes and labelled with 35S-methionine. The integral membrane proteins with an amphiphilic nature were separated from hydrophilic proteins by use of the nonionic detergent Triton X-114. Both whole cells and membrane proteins were isotope labelled and separated by high resolution two-dimensional electrophoresis under denaturing conditions. Polypeptide spots were visualised by autoradiography. No consistent differences were found when leukocytes from RA patients were compared to the controls.

Arthritis, Rheumatoid↗
PubMed1983

Is gold necessary in so called chrysotherapy?

It is postulated that the efficacy of sodium aurothiomalate and d-penicillamine could be partly dependent on the activity of sulphydryl groups. Free thiomalate, the thiol from sodium aurothiomalate was shown to be liberated in vivo and has been detected in the blood and urine of sodium aurothiomalate-treated patients. An increase in intracellular glutathione levels in response to treatment with sodium aurothiomalate and penicillamine was demonstrated and considered to be related to these drugs' properties as thiols. A pilot clinical trial using sodium thiomalate treatment demonstrated clinical improvement in four out of six patients after one course. Two patients relapsed but both improved after a second course and there were no serious adverse reactions. It is concluded that although larger controlled clinical trials are required, the role of gold in "chrysotherapy" must remain in question.

Animals↗
PubMed1982

Fate of the thiomalate part after intramuscular administration of aurothiomalate in rheumatoid arthritis.

The excretory fate and plasma level of thiomalate were studied after intramuscular administration of auro-14C-thiomalate to 3 patients with rheumatoid arthritis. The gold and the thiomalate parts separated in vivo, and the free thiomalate was excreted in the urine, rapidly at first and then slowly. After one day about 60% of the 14C-label had been recovered in the urine. The plasma level also declined rapidly. The results are in complete agreement with those previously described in animal experiments.

Adult↗
PubMed1982

Physical activity in the treatment of inflammatory rheumatic disorders.

A search of the literature in this area shows that there is little national or international documentation available on the effect of physical activity on the development of disease in inflammatory rheumatic disorders. Low capacity for physical work has been demonstrated and is based on poor circulation and reduced muscle strength in rheumatism: several studies from Norway and elsewhere have documented the value of physical training, especially in improving the rheumatic patient's physical condition (1--2, 8). No investigations have been able to document any arrest of progress of the disease, but physical training seems to be able to maintain existing joint function and also to some extent prevent progressive deterioration in condition. There is therefore no disagreement about the significance of physiotherapy, but the intensity and duration of training are more controversial.

Exercise Therapy↗