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Biomedical subjects

M Felder

Publications and source records attributed to M Felder.

At least 19 recordsLinked to original sources
PubMed1991

[Drug therapy of ankylosing spondylitis].

Ankylosing spondylitis has to be treated with NSAID's in order to influence the inflammatory process and thus reducing pain and slowing down the stiffening of the vertebral column. For this purpose, apart from the NSAID's Sulphasalazine is used. As a symptomatic treatment of pain and muscle spasm simple analgesics and muscle relaxants can be used. In peripheral arthritis a local treatment with intraarticular steroids can be useful, and sometimes a radiosynoviorthesis can stop the inflammation for a longer period. In case of osteoporotic fractures prescription of calcitonin may be considered.

Adrenal Cortex Hormones↗
PubMed1991

Bone loss in patients with rheumatoid arthritis--effect of steroids measured by low dose quantitative computed tomography.

For 2 years bone density changes in patients with rheumatoid arthritis were monitored to determine the effect of low dose corticosteroid treatment. Sixteen perimenopausal females were studied. Of these nine were treated with 5 to 20 mg prednisone per day and seven had no steroids. The differential effects on trabecular bone density and on cortical bone in the radius and the tibia were examined with high precision peripheral quantitative computed tomography (QCT). Steroid therapy did not influence cortical bone loss and had only a minor influence on trabecular bone density. Of greater importance was the influence of estrogen depletion. Corticosteroids and estrogen depletion, however, cannot explain fully the yearly loss of 5.7% in the trabecular and 4% in the cortical bone of the radius.

Adult↗
PubMed1990

[Assessment of the course of chronic polyarthritis].

In the following review the classical clinical and radiological parameters of rheumatoid arthritis are discussed. In our own study we made a prospective follow up of 29 patients with rheumatoid arthritis (104 years of disease) comparing the clinical and laboratory data with the radiological findings. Finally we investigated in another population with rheumatoid arthritis (315 patients) the question of quality of life using a structured questionnaire.

Arthritis, Rheumatoid↗
PubMed1990

Effect of salmon calcitonin on the infiltration of T lymphocytes in a synovium-like membrane of a rat inflammatory model.

The effect of salmon calcitonin (SCT) on the number of T lymphocytes accumulating in air pouch lining membranes produced on the back of Wistar rats was studied. SCT was given from day 0 through day seven following the air cavitation by daily injections of 2.5-20 micrograms/kg directly into the air cavity. Compared with saline controls, treatment with SCT caused a clear reduction in percentage of T lymphocytes, T helper cells and T non-helper subset in the synovial-like air pouch lining as revealed by FITC-labeled monoclonal antibodies and quantified by flow cytophotometric measurements. This effect may be due to a reduction in local vascular permeability caused by SCT.

Air↗
PubMed1988

Impaired mitogen-induced interferon-gamma production in rheumatoid arthritis and related diseases.

Peripheral blood lymphocytes from patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), progressive systemic sclerosis (PSS), Reiter's disease, osteoarthritis, and from healthy volunteers were investigated for interferon-gamma (IFN-gamma) production after mitogen activation. Phytohaemagglutinin stimulation revealed an impaired IFN-gamma production in RA, SLE, and PSS but normal levels in Reiter's disease and osteoarthritis. In RA this deficiency was also seen after pokeweed mitogen, OKT3, and concanavalin A activation. No major differences were found in interleukin 2 (IL-2) production and cell proliferation. The IL-2 receptor expression was reduced on stimulated RA lymphocytes. The deficient IFN-gamma production was compensated in RA by co-stimulation of PHA or OKT3 with phorbol myristic acetate (PMA). In addition, the combination of the calcium ionophore A 23187 and PMA induced a strong IFN-gamma secretion in all patient groups and in the controls.

Adolescent↗
PubMed1988

Quantitative computed tomography of the rheumatic knee.

A good noninvasive means to quantitate the extent and course of bone loss in rheumatoid arthritis (RA) is currently not available. We report on ways of assessing arthritic bone changes by means of quantitative computed tomography (QCT). The visualization of lesions and the quantitation of bone density diminutions are based on a stack of forty thin computed tomograms and 3D reconstructions. A pilot study shows that QCT may be a useful tool in the noninvasive assessment of the progression of RA and that it may help to evaluate the efficacy of therapeutic procedures.

Adult↗
PubMed1987

Food allergy in patients with rheumatoid arthritis.

Three hundred patients of the Swiss Rheumatoid Arthritis Patient Union were asked by questionnaire whether they had any adverse reaction from food. Of the 159 replies 52 gave a positive history. Thirty-five patients could be further evaluated. Six patients, who gave the most typical history of allergy, were investigated clinically, with laboratory tests and technetium-scintigramme after food challenge. There was no sign of an immunologic reaction in any of the measured parameters. The other patients were interviewed a second time with an extensive allergological questionnaire. None of the food intolerances could be substantiated.

Antigen-Antibody Complex↗
PubMed1986

[Vasculitic polyneuropathy as a complication in chronic polyarthritis].

Polyneuropathy due to vasculitis in connection with rheumatoid arthritis is a rare complication of the disease. Special investigations can help us to distinguish between a peripheral sensory-neuropathy with a good prognosis, the neuropathy of the autonomous nervous system and the severe form of mononeuritis multiplex. The bad prognosis of this form is due to the diffuse vasculitis of internal organs. We describe 5 patients with rheumatoid arthritis and different forms of vasculitis. The differential diagnosis, therapy and prognosis are described in detail.

Aged↗
PubMed1986

[Drug therapy of arthroses].

Osteoarthritis (OA) is one of the most common diseases requiring treatment. A clear clinical and pathophysiological understanding of the disease is required before treating a patient with OA. Drug therapy of patients with OA is mainly divided into two groups: a group receiving symptomatic therapy and a group receiving drugs intended to modify or improve the disease. Symptomatic therapy includes pure analgesics as well as non-steroidal antirheumatic drugs and muscle relaxants. Their use depends on the activity as well as on the form of clinical manifestation (activated/decompensated disease). If there are signs of severe activation, intra-articular steroids, orgotein or even synoviorthesis with yttrium are administered as local therapy. All of these therapies are used in the sense of trouble shooters, as they cannot alter the course of the disease in the long run. The disease-modifying substances have well been investigated in vitro and in animal models. Furthermore, some clinical trials have shown evidence for the usefulness of these substances in the therapy of OA.

Administration, Topical↗
PubMed1985

The effects of calcitonin on central neurons in the rat.

The effects of salmon calcitonin on central neurons were studied in anesthetized rats. Calcitonin applied iontophoretically consistently inhibited spontaneous activity in half of the neurons tested in the anterior hypothalamic nucleus and subthalamus but had virtually no effect on cortical and thalamic neurons. Calcitonin also inhibited glutamate-evoked activity in the neurons tested. Calcitonin administered into the brain ventricular system led to a marked decrease in spontaneous discharge of hypothalamic cells in the majority of cells tested. The onset of this response began within 20 and 30 min of calcitonin application.

Animals↗
PubMed1985

[Acute drug-induced pancreatitis].

93 publications concerning drug-induced pancreatitis are reviewed. A confirmed causal relationship between drug and acute pancreatitis so far exists only for 8 compounds: azathioprine, chlorothiazide, furosemide, sulfonamides, tetracycline, estrogens, valproic acid and L-asparaginase. There is less convincing, but still suggestive, evidence for a causal relationship with 5 other drugs, namely: corticosteroids, chlorthalidone, ethacrynic acid, phenformin and iatrogenic hypercalcemia. Due to inadequate or contradictory evidence, the link between a number of additional drugs and acute pancreatitis is considered possible, conditional or doubtful. Finally, the scant literature concerning the pathogenesis and histological lesions of drug-induced pancreatitis is briefly reviewed.

Acute Disease↗
PubMed1985

In vitro stimulation of lymphocytes from patients with rheumatoid arthritis.

Peripheral blood lymphocytes from patients with rheumatoid arthritis (RA) and from normal controls were compared in 20 microliters droplet cultures following stimulation with phytohemagglutinin or concanavalin A. The dynamics of proliferation were significantly changed in RA. Higher numbers of cells in culture were needed to achieve the same response. This may explain the low proliferative responses of lymphocytes from some patients with RA, and apparent changes of in vitro suppressor effects, reported by other authors. Diurnal variations of lymphocytes in RA patients were also studied. No differences in the response to mitogen of lymphocytes taken at 7 AM and 7 PM were found.

Adult↗