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Biomedical subjects

C Friman

Publications and source records attributed to C Friman.

At least 37 records · Page 2Linked to original sources
PubMed1992

Increased risk of cancer in patients with systemic lupus erythematosus.

To evaluate the risk of cancer in patients with systemic lupus erythematosus (SLE) a series of 205 consecutive patients (182 women and 23 men) were followed up for cancer through the files of the Finnish Cancer Registry. The follow up consisted of a total of 2340 person years. Fifteen cancers were diagnosed against 5.7 expected (relative risk (RR) 2.6, 95% confidence interval (CI) 1.5 to 4.4). Among the women there were four non-Hodgkin's lymphomas against 0.09 expected (RR 44, CI 11.9 to 111) and two soft tissue sarcomas against 0.04 expected (RR 49, CI 6.0 to 177). When evaluated by a case control study previous treatment with cytostatic drugs showed no influence on the occurrence of cancer in this series of patients with SLE.

Adult↗
PubMed1991

Antibodies to Sm and SS-A demonstrated by enzyme immunoassay. Correlation to clinical manifestations and disease activity in patients with systemic lupus erythematosus.

Using commercially available antigens, enzyme-linked immunosorbent assays (ELISAs) were set up to demonstrate antibodies of IgG class against Sm and SS-A. Anti-Sm antibodies were demonstrated in 40% of patients with systemic lupus erythematosus (SLE), in 12% of patients with SJögren's syndrome, in 6% of patients with rheumatoid arthritis (RA) and in 12% of patients with miscellaneous rheumatic disorders. Anti-SS-A antibodies were seen in 63% of the SLE patients, in 37% of the patients with Sjögren's syndrome and in 23% of the patients with RA. In the patients with SLE, high levels of anti-Sm antibodies were related to the presence of Raynaud's phenomenon, whereas patients with a malar rash tended to have high levels of anti-SS-A antibodies. In 17 SLE patients followed over a period of time a correlation was seen between the levels of the anti-Sm antibodies and the disease activity. We concluded that it is useful to include ELISAs for the demonstration of anti-Sm and anti-SS-A antibodies in determining the serological profile and in the follow-up of patients with SLE.

Adolescent↗
PubMed1990

Serum baseline hyaluronate and disease activity in rheumatoid arthritis.

The baseline serum hyaluronate (HA) concentration from samples obtained five to seven hours after mobilization of the patient was quantified using a radiometric 125I-HA binding method in 58 patients with rheumatoid arthritis and compared with several clinical and laboratory parameters by means of stepwise multiple linear regression. In the age- and sex-adjusted model, the variables with independent predictive value for serum hyaluronate concentration were the erythrocyte sedimentation rate (ESR) and the joint score index measuring the extent of the synovial inflammation. The estimated synovial mass index and C-reactive protein values did not improve the fit of the model after ESR and joint score were entered, and were left out from the multiple regression equation. When ESR and joint score were studied in univariate regression analysis with serum hyaluronate, the coefficients were r = 0.492 and r = 0.397, and the P values were P less than 0.001 and P less than 0.005, respectively. It was concluded that the baseline hyaluronate level in serum is closely related to the synovitic activity of the rheumatoid inflammation and that measurement of serum hyaluronate is of value when the activity and extent of synovial inflammation is being assessed in patients with rheumatoid arthritis.

Adult↗
PubMed1990

Spontaneous and in vitro activation of synovial fluid and peripheral blood lymphocytes in rheumatoid arthritis.

Peripheral blood (PB) and synovial fluid (SF) were compared in parallel samples in rheumatoid arthritis (RA). The kinetics of in vitro T-cell activation was assessed in phytohemagglutinin (PHA) stimulated PB or SF mononuclear cell cultures on days 0, 1, 3 and 5. The early lymphocyte activation as assessed by interleukin-2 receptor expression was faster in SF than in PB cell cultures. In particular, IFN-gamma secretion was higher in SF than in PB cell cultures (p less than 0.01). Accordingly, lymphocyte major histocompatibility complex (MHC) locus II antigen expression was higher in SF than in PB cell cultures (53 +/- 7% vs. 21 +/- 5%; p less than 0.01). Our results suggest that lymphocytes, which are particularly effective producers of IFN-gamma when stimulated in vitro are sequestered in the diseased joints in RA.

Adult↗
PubMed1988

Synovial fluid lymphocytes in different subtypes of juvenile rheumatoid arthritis.

We studied the subsets of synovial fluid (SF) lymphocytes and their activation states in 4 subtypes of juvenile rheumatoid arthritis. The expression of lymphocyte differentiation antigens and activation markers (Ia and Tac) appeared to be similar in these subgroups. Tac + DNA-synthesizing T blasts represented, at most, 5% of all SF mononuclear cells. This finding was in clear contrast to the high proportion of Ia-positive SF mononuclear cells. There were no differences in Ia and Tac expression or DNA synthesis among the different juvenile rheumatoid arthritis subgroups. This finding suggests that the cell-mediated immune response may represent secondary features of the disease that are involved as a final common pathogenetic pathway.

Arthritis, Juvenile↗
PubMed1988

Class-specific rheumatoid factors, DR antigens, and amyloidosis in patients with rheumatoid arthritis.

Class-specific rheumatoid factors (RFs) were measured by enzyme immunoassay in 59 patients with rheumatoid arthritis complicated by systemic amyloidosis (RA+A), 47 patients with rheumatoid arthritis without amyloid (RA), 106 patients with other rheumatic diseases (juvenile rheumatoid arthritis, systemic lupus erythematosus, Sjögren's syndrome), and 55 blood donors. The patients with RA+A were characterised by a high prevalence of RF negativity; the IgM RF concentration was raised in only 18 of the 59 patients (31%, p less than 0.001 v RA), the IgG RF concentration in 20 of 59 (34%, p less than 0.001 v RA), and the IgA RF concentration in 24 of 59 (41%, p less than 0.001 v RA). A higher prevalence of HLA-DR4 (p less than 0.001) and a lower prevalence of DR2 (p less than 0.05) were found among 48 tested patients with RA+A when compared with a control panel consisting of 500 blood donors. No significant differences in the prevalence of DR1-DR7 or B27 antigens were observed, however, between patients with RA with or without amyloid.

Amyloidosis↗
PubMed1987

Acute transverse myelopathy successfully treated with plasmapheresis and prednisone in a patient with primary Sjögren's syndrome.

We report a case of acute transverse myelopathy in a patient with primary Sjögren's syndrome of 3 years duration. Our patient's acute transverse myelopathy developed within 1 week and resulted in complete paraparesis below the mamillary level. Extensive laboratory investigation ruled out viral, bacterial, and fungal etiology, Guillain-Barré syndrome, poliomyelitis, and multiple sclerosis. At diagnosis, treatment was initiated immediately with prednisone (80 mg/day) and plasmapheresis, which was performed as a first-aid measure. Improvement was noted as early as 10 days after the start of therapy. Within 5 1/2 months of the first symptoms of paralysis, the patient walked without difficulty and returned to her normal activities. A causal relationship between plasmapheresis/prednisone therapy and recovery has not been proven but merits further consideration.

Acute Disease↗
PubMed1987

Suppression of superoxide generation by normal polymorphonuclear leukocytes preincubated in plasma from patients with Felty's syndrome.

Polymorphonuclear leukocytes (PMN) isolated from patients with Felty's syndrome (FS) generate fewer superoxide anions (O-2) upon stimulation with fmet-leu-phe than PMN from normal controls or patients with rheumatoid arthritis (RA). In this study, plasma samples were obtained from 12 patients with RA and 12 patients with FS. Incubation of normal PMN in plasma from Felty patients resulted in a significant reduction in both the rate and total quantity of O-2 generation when activated with fmet-leu-phe. This was not observed with plasma from RA patients. The capacity of a plasma sample to suppress O-2 generation correlated with plasma IgG-PMN-binding activity (IgG-PBA) and, to a lesser extent, with the content of circulating immune complexes (CIC). These data suggest that IgG-PBA and possibly CIC have a pathogenetic role in both qualitative and quantitative defects in PMN in Felty patients.

Aged↗
PubMed1987

Plasma glycosaminoglycans in systemic lupus erythematosus.

The glycosaminoglycans (GAG) of plasma were assayed for uronic acid content in 13 female patients with systemic lupus erythematosus (SLE) and in healthy controls and compared with earlier results obtained in patients with rheumatoid arthritis (RA). The GAG were fractionated into a high charge "free" fraction known to contain chondroitin sulfate (CS) as a major and heparan-sulphate (HS) as a minor GAG and a low charge "bound" fraction known to contain low sulphated CS as the only GAG. The concentration of the free GAG was significantly increased in SLE (p less than 0.01); this increase was mainly due to the high concentrations of free GAG in patients with active disease. These patients also had an increased concentration of "bound" GAG (p less than 0.05). However, the plasma GAG concentrations did not correlate with the erythrocyte sedimentation rate, the binding of native DNA or the C4 concentration. Plasma proteoglycans and/or GAG are known to modulate certain immune functions. Whether the increase in free GAG reported here is somehow associated with the disturbed immunoregulation in SLE remains speculative.

Adult↗
PubMed1986

Effects of treadmill running on plasma glycosaminoglycans in adult rabbits.

Adult rabbits were subjected to running on a treadmill three times daily for 1, 5, and 30 days. The animals were injected with 35S-sulfate and killed 24 h later. The concentration of free and bound glycosaminoglycans (GAG) in plasma, as well as the specific radioactivities of the fractions, was determined. Thirty days of running produced a statistically significant increase in the concentrations of both free and bound plasma GAG, whereas only the latter fraction was increased after 5 days of running. Consistent changes in the specific radioactivities of the fractions were not discernible.

Animals↗
PubMed1986

Effect of diclofenac sodium, tolfenamic acid and indomethacin on the production of superoxide induced by N-formyl-methionyl-leucyl-phenylalanine in normal human polymorphonuclear leukocytes.

The effect of three non-steroidal anti-inflammatory drugs, diclofenac, indomethacin and tolfenamic acid, on the production of superoxide (O2-), by normal human polymorphonuclear leukocytes (PMNL) was studied, in vitro. The cells were activated with N-formyl-methionyl-leucyl-phenylalanine (FMLP) and O2- production was measured as superoxide dismutase inhibitable cytochrome c reduction. Cell viability was checked with assays of liberated LDH. Concentrations of the drugs considerably higher than those of therapeutic plasma were required to inhibit O2- production. The drug concentrations producing a 50% inhibition (IC50) of total O2- production were: diclofenac 2.7 X 10(-4) M, indomethacin 4.0 X 10(-4) M and tolfenamic acid 4.2 X 10(-4) M. At drug concentrations causing a significant suppression of O2- generation, diclofenac showed a slight and tolfenamic acid a marked inhibition of [3H]FMLP binding to its cellular receptor; indomethacin has earlier been shown to inhibit FMLP-binding slightly. No dismutating activity of the drugs could be demonstrated. It is concluded that the inhibition of O2- production is due to a combined effect on FMLP binding and on cellular O2- metabolism. Because of the high drug concentrations required to inhibit O2- production, this phenomenon is obviously of little significance for the anti-inflammatory effect obtained with therapeutic doses of the drugs studied.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1985

Cellular immunohistopathology of acute, subacute, and chronic synovitis in rheumatoid arthritis.

Cellular inflammation in rheumatoid arthritis (RA) synovial membrane was studied in biopsy specimens taken at different stages of synovitis and disease. Patients were classified into three subgroups: acute RA, subacute RA, and chronic RA. Inflammatory cells were characterised by a histochemical esterase method and immunohistochemical peroxidase-antiperoxidase (PAP) and avidin-biotin-peroxidase (ABC) staining. The amounts and distribution of inflammatory cells were different in various stages of the synovitis. In acute onset RA monocytes and granulocytes predominated, suggesting that the beginning of rheumatoid inflammation is similar to inflammatory reaction in general. The presence of T cells and also of plasma cells in subacute RA suggests underlying subclinical changes also in apparently healthy joints in RA. The most typical feature of prolonged synovitis in chronic RA was its intensity, characterised by the presence of large T cell and plasma cell infiltrates. Our findings suggest that the immunological mechanisms are secondary to the tissue damage caused by the initial inflammatory events of unknown cause. However, the immunological mechanisms may still play a central role in the aetiopathogenesis, because findings in chronic RA suggest a defective down-regulation of the immune response.

Acute Disease↗