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Biomedical subjects

A Toivanen

Publications and source records attributed to A Toivanen.

At least 55 records · Page 3Linked to original sources
PubMed1996

Antibiotic prophylaxis and treatment of reactive arthritis. Lessons from an animal model.

OBJECTIVE: To study the effect of antibiotic prophylaxis and treatment of reactive arthritis (ReA), using an experimental model. METHODS: Yersinia enterocolitica O:8, when injected intravenously into Lewis rats, causes a sterile arthritis closely resembling human ReA in 70% of the animals. Arthritis develops in 1-2 weeks; in some of the animals it remains chronic, and exacerbations occur. This model was applied to study the effect of a 7-day treatment with ciprofloxacin, using 2 different dosages (20 or 100 mg/kg/day) and 4 different schedules for initiation of treatment. The effects were evaluated by determining the daily arthritis score, the number of rats developing arthritis, and fecal excretion of Yersinia. In addition, weight gain was monitored. At autopsy (35 or 60 days after inoculation with bacteria), samples were obtained for determination of Yersinia-specific antibodies in the serum. At the same time, samples were collected from mesenteric lymph nodes, lung, spleen, and liver for bacterial cultures, and from the ankle joints for histologic evaluation. In a separate experiment, ciprofloxacin concentrations in samples from serum and mesenteric lymph nodes were analyzed by high performance liquid chromatography. RESULTS: A 7-day course with 100 mg/kg/day of ciprofloxacin, started on day 3 after bacterial inoculation, completely prevented the development of ReA and eliminated Yersinia during the 60-day experiment. If a dosage of 20 mg/kg/day was used, development of acute arthritis was prevented, but some of the animals had positive fecal cultures at the end of experiment. If antibiotic treatment was started on day 5, the preventive effect was still observed, but was less pronounced. If the treatment was started at the peak of the development of arthritis, no effect on arthritis was observed. CONCLUSION: These results indicate that if any effect of antibiotic treatment in Yersinia-triggered ReA is to be expected, the treatment must be started early and given in sufficient dosage. However, antibiotic treatment has no effect on fully developed arthritis.

Animals↗
PubMed1996

Oncoprotein expression in human synovial tissue: an immunohistochemical study of different types of arthritis.

Based on the fact that synovial lining cells have some properties of transformed-appearing cells, we have examined the expression of Myc, Myb, Fos, Jun and Ras oncoproteins in synovial tissues from patients with different types of arthritis. Formalin-fixed and paraffin-embedded sections of synovial tissue from 12 patients with rheumatoid arthritis (RA), 14 with reactive arthritis (ReA), nine with other seronegative arthritis (OSA), seven with bacterial arthritis (BA), eight with probable bacterial arthritis (PBA) and eight with osteoarthritis (OA) were studied using the immunoperoxidase staining technique. The oncoproteins studied were expressed both in the synovial lining layer and in the sublining layer, consisting of lymphocytes, other inflammatory cells and blood vessels. Among the six disease entities, RA and OA appeared to be the most distinct, whereas the results obtained for ReA and OSA, and on the other hand for BA and PBA, closely resembled each other. The expression of Myc, Myb, Fos and Jun was significantly correlated both to the degree of synovial hypercellularity and the synovial lymphocytic infiltration. For Ras, such a correlation could not be seen. We conclude that we find no evidence of a cell lineage-specific or a disease-specific abnormality of proto-oncogene products in RA, and the expression of these oncoproteins is consistent with inflammation rather than with any primary abnormality of cell growth.

Adult↗
PubMed1996

Reactive arthritis.

During the past year, new information has been obtained regarding the pathogenetic process in reactive arthritis. Characterization of the triggering microbes as well as of their interaction with T cells and other host components has brought us closer to achieving a comprehensive picture of the events leading from infection to reactive arthritis. Efforts are ongoing to define clinically applicable diagnostic criteria. It is becoming apparent that chronic forms of the disease are not uncommon.

Arthritis, Reactive↗
PubMed1995

Epidemiologic, clinical, and therapeutic aspects of reactive arthritis and ankylosing spondylitis.

The role of microbes in the pathogenesis of various arthritides continues to be the focus of keen interest. In the study of genetic factors that predispose to spondyloarthropathies, HLA-B27 transgenic animal models present exciting new research possibilities. The basic principles in the management of these arthritides have not changed, but an increasing number of patients are being treated with disease-modifying antirheumatic drugs when the response to nonsteroidal anti-inflammatory drugs is inadequate.

Animals↗
PubMed1995

Synovial fluid L-lactic acid in acute arthritis of the adult knee joint.

Determination of synovial fluid (SF) lactic acid has been suggested to be an unspecific indicator of SF leukocytosis, and it is not recommended for differential diagnosis of bacterial arthritis. We analyzed the L-lactic acid content by enzymatic UV-method in 65 SF samples obtained from adult patients with acute knee arthritides. The concentration of L-lactic acid was not high in any SFs with intensive leukocytosis. The mean concentration of L-lactic acid was 13.5 mmol/l (95% confidence intervals 9.4; 17.6 mmol/l) in the synovial-fluid samples from culture-positive arthritis and 5.5 mmol/l (4.9; 6.2 mmol/l) in the synovial-fluid samples from culture-negative arthritis. Determination of SF L-lactic acid is an important part of the diagnostic setup for acute arthritis. Values > 9 mmol/l strongly support occurrence of bacterial arthritis and indicates an immediate onset of the treatment.

Acute Disease↗
PubMed1994

A statistical analysis system macro for age-standardized incidence rates.

The Statistical Analysis System (SAS) is a commercial software system for data analysis. We designed a SAS macro that produces age-specific rates of any given disease directly from the basic patient data on SAS files. The macro conforms to the statistical methods of the World Health Organization's MONICA project, which is a multinational project for MONItoring of trends and determinants in CArdiovascular disease. The data of the Coronary Register of the City of Turku, Finland, was used to test this macro. The data consists of both men and women between the ages of 35 and 64 years. Acute coronary events leading to hospitalization and acute coronary death events outside hospital have been registered since 1972. For age-standardization Segi's world population was used as the standard. The weights were then calculated for five consecutive years. Individual weights related to the population size of the reporting unit and the standard population were calculated for each subject in the population using the population size of the reporting unit and the standard population. This yielded the age-standardized rates of the acute myocardial infarction and the corresponding standard deviations. The macro permits standardization of the incidence rates of any disease. It will present the required figures instantly.

Adult↗
PubMed1994

Synovial fluid muramic acid in acute inflammatory arthritis.

Presence of muramic acid, a bacterial cell wall component, was analysed by gas chromatography-mass spectrometry in synovial fluid (SF) of 40 patients with acute inflammatory arthritis. SF muramic acid was observed in 4/14 patients with acute, culture negative inflammatory arthritis of unclear origin. Each of these four patients had a history of a recent bacterial disease (pansinuitis, purulent leg ulcer, erysipelas, unexplained fever with suspicion of cholecystitis and urinary tract infection). In the bacterial arthritis, SF muramic acid was detected in 6/12 patients (in 2/6 culture negative cases). In the reactive arthritis due to Salmonella or Yersinia, the rate of positivity was 2/14. Nineteen samples of traumatic SF effusion were muramic acid negative. These findings indicate that several cases of undefined acute inflammatory arthritis are of bacterial origin.

Acute Disease↗
PubMed1994

Epidemiologic aspects, clinical features, and management of ankylosing spondylitis and reactive arthritis.

The generally reported prevalence of 0.1% to 0.2% for ankylosing spondylitis in the white population is probably too low, because it is based almost entirely on hospital records. The incidence and clinical presentation of ankylosing spondylitis have not changed during the past few decades. For reactive arthritis, the list of microbes recognized as triggering agents is continuously increasing. Reactive arthritis is divided into urogenic, enterogenic, respiratory tract-associated, and idiopathic arthritides. In addition, several microbial diseases may be accompanied by reactive arthritis, even though the identity of the causative agent is not always known. In the diagnosis of the spondyloarthropathies, definite progress has been made in developing classification criteria. Intensive research is going on to evaluate new therapies, with special attention to the use of antimicrobial agents for the treatment of reactive arthritis.

Arthritis, Reactive↗
PubMed1994

Yersinia-specific antibodies in serum and synovial fluid in patients with Yersinia triggered reactive arthritis.

OBJECTIVES: To further evaluate the role of bacterial antigens in triggering inflammation in the joint in patients with reactive arthritis by studying local antibody synthesis in the joint. METHODS: Yersinia-specific antibodies in paired serum and synovial fluid samples from 29 patients with yersinia triggered reactive arthritis were studied using an enzyme linked immunosorbent assay (ELISA), an inhibition ELISA with six monoclonal antibodies against lipopolysaccharide or released proteins of yersinia and immunoblotting. Antibodies of IgM, IgG and IgA classes, as well as antibodies of IgA subclasses and those containing secretory component were measured against the lipopolysaccharide and the sodium dodecyl sulphate extract of whole Yersinia enterocolitica O:3 bacteria. RESULTS: It was shown that yersinia-specific antibodies, as well as antibodies against other microbial antigens (rubella, measles, Bordetella pertussis, tetanus toxoid and Candida albicans) in synovial fluid mirror those in serum by concentration, by specificity and by distribution in classes and subclasses. CONCLUSION: These results do not suggest any strong local antibody production, but indicate that the majority of yersinia antibodies in the synovial fluid are derived from the circulation.

Adolescent↗
PubMed1994

Does Yersinia induce autoimmunity?

Yersinia enterocolitica O:3 and the human thyrotropin receptor share a structural similarity, revealed by their serological cross-reactivity. The exact molecular basis of the similarity is open. In spite of this cross-reactivity, Yersinia seems not to be a major inducer of thyroid autoimmunity. Yersinia infections or avirulent Yersinia strains in the intestinal flora may rather contribute to the development of thyroid autoimmunity arising for other reasons in genetically susceptible individuals. Regarding Yersinia and spondyloarthropathies, it is undetermined whether the chronic sequelae of acute Yersinia-triggered reactive arthritis are due to the persistence of phlogistic microbial components or to autoimmunity, or to both. No convincing evidence exists for a role of molecular mimicry between Yersinia and HLA B27 or other host structures. Cytotoxic T-cell clones derived from synovial fluid, and capable of killing Yersinia-infected and uninfected autologous targets in an HLA B27-restricted fashion have recently been described. Evaluation of their significance for the potential Yersinia-induced autoimmunity is waiting for characterization of the bacterial and host peptides involved.

Animals↗
PubMed1994

Synovial-fluid D-lactic acid in bacterial and other acute joint effusions.

The use of D-lactic acid in differential diagnosis of bacterial arthritis was evaluated in a prospective study. The concentration of D-lactic acid was determined by the enzymatic UV-method in sixty-eight synovial fluids (SF) and in twenty four sera from adult patients with acute knee effusion. High concentrations of D-lactic acid (> 0.15 mmol/l) were measured most frequently in SF from bacterial arthritis, but also in individual culture-negative SF samples from patients with inflammatory culture-negative joint effusions with and without identified history of infections. Determination of SF D-lactic acid is not useful in differential diagnosis of bacterial arthritis.

Arthritis, Infectious↗
PubMed1994

Infection and arthritis.

Reactive arthritis is caused by an infection, and components of the triggering agent can be demonstrated at the site of inflammation. This fact has opened new views in studies regarding other rheumatic diseases, such as rheumatoid arthritis and ankylosing spondylitis. The possible role of infectious agents in their etiology and pathogenesis is being re-evaluated.

Arthritis, Infectious↗