[Back pain--one more comment].
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Biomedical subjects
Publications and source records attributed to L Remvig.
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This study is a comparison of treatments of idiopathic "Frozen Shoulder" (adhesive capsulitis), distension combined with steroid is compared with steroid alone. Evaluation was based on pain scales, analgesic usage, and range of motion outcome scales. Out of one-hundred twenty patients (age, mean 51, range 21-70) that were referred under the diagnosis FS, twenty-six fulfilled the criteria for inclusion in the study, but four patients did not want to participate in the trial, giving a total of 22 patients (age, mean 53, range 40-65) in the study. Patients were randomised by the envelope method. Two patients dropped-out, one in each treatment group thus leaving the study with 20 patients for the final statistical analysis. Eight were treated with steroid alone and 12 with distension combined with steroid. Patients received one treatment per week for a six weeks period with a follow-up at 12 weeks. They were evaluated by pain VAS on function and at rest within the study period, the different ranges of motion (ROM) were measured at inclusion time and subsequent afterwards at 3, 6, and 12 weeks. The VAS outcomes showed no difference between the treatments (VAS-function p=0,1; VAS-rest p=0.1), while in the distension group ROM showed significant improvement in all directions except extension (external p=0.0007, flexion p=0.03, extension p=0,01). The analgesic usage was significantly lower in the group treated with distension at the end of the study (p=0.008). A blinded clinical assessment of ROM also showed significant improvement (p=0.002). It is concluded that distension with steroid can seem to help in management of "Frozen Shoulder". Other studies seems to support the conclusion.
OBJECTIVES: Most randomised trials of anticoagulant therapy for suspected acute myocardial infarction have been small and, in some, aspirin and fibrinolytic therapy were not used routinely. A systematic overview (meta-analysis) of their results is needed, in particular to assess the clinical effects of adding heparin to aspirin. DESIGN: Computer aided searches, scrutiny of reference lists, and inquiry of investigators and companies were used to identify potentially eligible studies. On central review, 26 studies were found to involve unconfounded randomised comparisons of anticoagulant therapy versus control in suspected acute myocardial infarction. Additional information on study design and outcome was sought by correspondence with study investigators. SUBJECTS: Patients with suspected acute myocardial infarction. INTERVENTIONS: No routine aspirin was used among about 5000 patients in 21 trials (including half of one small trial) that assessed heparin alone or heparin plus oral anticoagulants, and aspirin was used routinely among 68,000 patients in six trials (including the other half of one small trial) that assessed the addition of intravenous or high dose subcutaneous heparin. MAIN OUTCOME MEASUREMENTS: Death, reinfarction, stroke, pulmonary embolism, and major bleeds (average follow up of about 10 days). RESULTS: In the absence of aspirin, anticoagulant therapy reduced mortality by 25% (SD 8%; 95% confidence interval 10% to 38%; 2P = 0.002), representing 35 (11) fewer deaths per 1000. There were also 10 (4) fewer strokes per 1000 (2P = 0.01), 19 (5) fewer pulmonary emboli per 1000 (2P < 0.001), and non-significantly fewer reinfarctions, with about 13 (5) extra major bleeds per 1000 (2P = 0.01). Similar sized effects were seen with the different anticoagulant regimens studied. In the presence of aspirin, however, heparin reduced mortality by only 6% (SD 3%; 0% to 10%; 2P = 0.03), representing just 5 (2) fewer deaths per 1000. There were 3 (1.3) fewer reinfarctions per 1000 (2P = 0.04) and 1 (0.5) fewer pulmonary emboli per 1000 (2P = 0.01), but there was a small non-significant excess of stroke and a definite excess of 3 (1) major bleeds per 1000 (2P < 0.0001). CONCLUSIONS: The clinical evidence from randomised trials dose not justify the routine addition of either intravenous or subcutaneous heparin to aspirin in the treatment of acute myocardial infarction (irrespective of whether any type of fibrinolytic therapy is used).
Different training models are effective for the treatment of chronic low back pain, but no consensus has been found. Earlier studies have emphasized training of spinal mobility and back strength. To evaluate if other physiological parameters, such as coordination, are of equal importance, we performed a randomized trial on 40 consecutive patients with chronic low back pain. Two training models were compared: 1) intensive training of muscle endurance and 2) muscle training, including coordination. In both groups, training was performed 1 hour twice a week for 3 months. Pain score, disability score, and spinal mobility improved in both training groups without differences between the two groups. Only intensive training of muscle endurance improved isokinetic back muscle strength. At study entry, we found a significant correlation between spinal mobility and dysfunction, but after the training, no correlation was found between improvement of spinal mobility or isokinetic back extension strength and improvement of function or pain level. We conclude that coordination training for patients with chronic low back pain is as equally effective as endurance training.
Low energy laser (LEL) is a widely used treatment for a variety of musculoskeletal disorders although convincing documentation of the effect is missing. We have examined the LEL effect on Rheumatoid Arthritis (RA) in a double blind placebo controlled study. Twenty-two patients completed the study (10 receiving LEL treatment) according to the protocol. A significant effect on pain score was found due to LEL treatment, but when data were corrected for disease variation the effect disappeared. No effect of LEL could be demonstrated on the other assessed variables: grip strength, morning stiffness, flexibility, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP). In conclusion, we did not find that LEL had any clinically relevant effects on RA.
We report the case of a 46-year old man who presented with symptomatic myopathy. Muscle biopsy revealed epithelioid granulomas consistent with sarcoidosis. The patient had no symptoms other than those of muscle involvement. He responded well to a moderate dose of corticosteroid. We discuss the differential diagnosis of this rare illness.
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Eight adult patients with hypoimmunoglobulinaemia were randomly allocated to initiation of low- or high-level IgG-substitution. IgG was administered subcutaneously, at 50 or 150 mg ml-1, 20 ml per infusion, by means of a pocket-portable electric infusion pump. Infusions were given 2 to 4 times weekly for 24 months, with a change of dose regimen after 12 months. The desired plasma IgG levels were reached after a mean lag phase of 3 months (range 1-5 months). The median (and ranges) of the individual mean plasma IgG levels during the ensuing 9-month periods were as follows: high-level period, 6.5 g l-1 (range 6.2-7.8 g l-1); low-level period, 3.2 g l-1 (range 3.0-4.0 g l-1). During the high-level period, compared to the low-level period, there was a significant decrease in the following parameters: 'days in bed at home', 'days missed work' and 'days with fever'. No serious side-effects were observed. It is concluded that a plasma IgG concentration of 6 g l-1 can readily be achieved by subcutaneous IgG substitution, and the prophylactic effect is superior to that obtained with a plasma IgG concentration of 3 g l-1.
Various biological assays are used for qualitative and quantitative measurements of interleukin 1 (IL-1) in supernatants from cell cultures. The purpose of the present study was to compare the specificity and variability of three cellular IL-1 bioassays: the PHA co-stimulatory human T lymphocyte proliferation assay, the PHA co-stimulatory murine thymocyte (THY) proliferation assay, and the 2-step NOB-1 conversion assay. Three different ways of IL-1 unit calculation, based on a semi-logarithmic plot, a double-logarithmic plot, or a probit-analysis plot were also compared. The T lymphocyte assay can be used only to demonstrate qualitative differences in IL-1-like activity, whereas the THY assay is excellent as a semi-quantitative assay, with a low intra-assay variability, but also with a low specificity. The NOB-1 assay is probably more specific with respect to IL-1 measurement, although, with a high intra-assay variance. The THY and the NOB-1 assays both have a high inter-assay variability, and measurement of samples from longitudinal clinical studies must be done in one and the same analysis if quantitative differences are to be illustrated. Probit analysis for unit calculation is recommended. To generate a consensus view as to assay performance, collaborative laboratory studies are needed.
Immune complexes (IC) are believed to play a role in the pathogenesis of some autoimmune diseases in which interleukin 1 (IL-1) and probably other cytokines also take part. This investigation shows that tetanus toxoid-human anti-tetanus toxoid IC induce human monocytes to release IL-1. The activity was identified as being mainly IL-1 beta by molecular size chromatography, isoelectric focusing, and anti-IL-1 beta affinity chromatography. Endotoxins were eliminated by repetitive washing of the IC suspension and by preincubation of IC with polymyxin B. The IL-1-inducing effect of IC was destroyed by heating at 80 degrees C, and it was not blocked by the cytoskeleton inhibitor cytochalasin B. IL-1 inhibitors were not detected in the supernatants.
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Monocytes (M phi) were simultaneously preincubated with salicylazosulfapyridine (Salazopyrin) (SAZ), 0.78-12.5 mM, and lipopolysaccharide from E. coli, 1 X 10(-9) g/ml. Presence of SAZ resulted in a dose-dependent decrease in the co-stimulatory activity in M phi culture supernatants, corresponding to a 50% reduction by SAZ, 2.0 mM. Co-stimulatory activity was estimated by the mitogen-induced thymocyte proliferation assay (THY assay). The results indicate an inhibitory effect of SAZ in vitro on the production of IL-1 and other possible co-stimulatory factors. This inhibitory effect was not due to decreased M phi viability, production of suppressive substances, or to drug interference with the THY assay. Equimolar preincubations with sulfapyridine, 5-aminosalicylic acid and N-acety-1-5-aminosalicylic acid were without effect on the production of co-stimulatory factors.
Dialysis with cellulose acetate membranes is frequently performed in the laboratory in order to remove possible interfering substances from various biological fluids. However, retentates from dialysis, compared to undialysed samples, inhibited the sub-maximal phytohaemagglutinin-induced proliferation of human T-lymphocytes. This inhibition was accentuated when the samples to be dialysed contained normal human serum. Four different membranes all produced similar degrees of inhibition when samples of varied composition were dialysed. It is unlikely that the inhibitory effect on the MNC/M phi-DC proliferations is due to glycerol, heavy metals or sulphuric compounds in the retentate. The most likely explanation of the inhibition is liberation of a substance from the membrane to the retentate during dialysis. Our experiments suggested two solutions. Simply boiling the dialysis tubing--internal as well as external--solved the problem. Another way to circumvent the problem is to use a commercially available dialysis membrane which is completely devoid of this inhibitory effect.
The continuous presence of Auranofin (AF), 1.0 microgram/ml and above, or sodium aurothiomalate (GST), 2.0 micrograms/ml and above, inhibited the phytohaemagglutinin-induced proliferation of monocyte-depleted mononuclear cells. Preincubation of monocytes (M phi) with AF, 1.0 microgram/ml, caused a minor increase in the co-stimulatory effect of LPS-induced M phi-culture supernatants, whereas preincubation with AF 2.5 micrograms/ml and above resulted in a dose-dependent decrease in production of the co-stimulatory factor--probably interleukin-1 (IL-1). This inhibition is not due to decreased M phi viability, production of suppressive substances, or drug interference with the IL-1 test assays. A similar preincubation with GST up to 100 micrograms/ml had no effect on IL-1 production, nor did preincubation with thioglucopyranose, triethylphosphine or chloroauric acid, the three molecular sub-components of AF. The inhibitory effect of AF on the production of IL-1--as well as other co-stimulatory monokines--and on lymphocyte proliferation might explain the anti-inflammatory and disease-modifying effect of the drug.
The variability in measurements of the interleukin-1 (IL-1) responsiveness of human monocyte (M phi)-depleted mononuclear cells (MDC) and in IL-1 production of human M phi has been estimated. Subjects were grouped so that inter- and intra-donor biological variability were evaluated, as well as day-to-day and basic intrinsic test-to-test methodological variability. IL-1 responsiveness was measured by the co-mitogenic effect of unstimulated and LPS-stimulated IL-1 standards on the PHA-induced proliferation of MDC. IL-1 production was measured by the enhancing effect of unstimulated and LPS-stimulated M phi-culture supernatants on PHA-stimulated allogeneic MDC. The variability of the IL-1 responsiveness of MDC was influenced mainly by biological factors, and this variability was effectively reduced by calculating the difference between the response of unstimulated and stimulated cultures, or by using cryopreserved MDC originating from a single stock of cells. In contrast, IL-1 production from both unstimulated and LPS-stimulated M phi was subjected to less biological and methodological variability, and this variability was not reduced by the above mentioned procedures. The results indicate that when assaying IL-1 production in clinical investigations involving longitudinal or comparative studies, a test system consisting of cryopreserved MDC from one stock of cells should be used. Alternatively the difference between the IL-1 activity from unstimulated and LPS-stimulated cultures should be calculated, since these procedures enhance the reproducibility of the measurements.
Interleukin 1 (IL-1) is a monocyte-derived mediator that participates in the regulation of various T-lymphocyte activities, among them IL-2 production. Since IL-2 deficiency is a central feature in the immunological profile of the acquired immunodeficiency syndrome (AIDS), the production of IL-1 from peripheral blood monocytes from male homosexuals with AIDS was investigated at the same time as the IL-1 responsiveness of monocyte-depleted mononuclear cells (MDC) from the same patients. The IL-1 was produced by lipopolysaccharide-stimulated monocytes and assayed by the capacity of monocyte supernatants to amplify the proliferation of phytohaemagglutinin-stimulated allogeneic MDC from healthy donors as well as murine thymocytes. The IL-1 responsiveness was measured by measuring the enhancing effect of an IL-1 standard on the proliferative response of patients' MDC. The IL-1 production was not reduced compared to the IL-1 production in a control group, but the IL-1 responsiveness of the patients' MDC was depressed. The results indicate that depressed IL-1 production is not one of the immunological disturbances in AIDS, but that the T-lymphocyte accessory properties of IL-1 are affected.
Depletion of agarose for endotoxins resulted in a low spontaneous migration of polymorphnuclear cells (PMNC). Re-addition of endotoxin, in casu lipopolysaccharide from E. coli 026:B6 (LPS), enhanced the spontaneous PMNC migration in a two-phased dose-response pattern, reaching maximum migration with LPS 1 x 10(-7) g/ml. Thus, the migration of PMNC under agarose seems to be a chemokinesis. Leucocyte migration inhibition factor (LIF), induced by PPD 50 micrograms/ml at endotoxin-free conditions, significantly reduced the PMNC migration compared to supernatants from control cultures, however not compared to the conventional limit of significance, MI = 0.80. With increasing PMNC migration there was an insignificant decrease in the MI. Addition of LPS, 1 x 10(-9) g/ml, during LIF induction caused a significant increase in LIF production, an effect which overshadowed the effect of PPD. Thus, the application of the conventional limit of significance, MI = 0.80, may result in false-negative or false-positive conclusions, depending upon the endotoxin contamination. A standardization of the endotoxin content in both steps of the indirect leucocyte migration inhibition assay seems mandatory in order to obtain a reliable and reproducible bioassay.