The frequency, clinical picture and prognosis of pulmonary sarcoidosis in Finland.
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A solid phase ELISA was developed for the simple and rapid determination of rheumatoid factors (RF) of all major immunoglobulin classes. Micro-ELISA-plates were coated with human Fc-fragments and incubated with various dilutions of serum samples as well as with an international RF reference serum. Rheumatoid factors were quantitatively detected by rabbit antibodies (RaHIgA(alpha), RaHIgM(mu), RaHIgG(Fab] conjugated with alkaline phosphatase. The specificity of the ELISA was proved by means of binding inhibition of all rheumatoid factor classes by heat aggregated human IgG. A comparison of the IgM-RF titres of the latex fixation test with the IgM-RF concentration values of the ELISA yielded high correlation (r = .81).
Fifteen patients (with dysglobulinemia, ranging in age from 35 to 52 years, were studied over a period of 6 years. The following parameters of immune response and immunoelectrophoresis of serum proteins were checked: total hemolytic complement (CH50), serum cryoglobulins, presence of circulating immune complexes (CIC), beta 2-microglobulins, rheumatoid factor (RF). Of the 15 patients investigated, 6 (40%) developed during the period of study severe forms of rheumatoid arthritis (RA) which required the introduction of continuous cortisone therapy. In a control group, ranging between the same age limits but without immune disturbances, no case of RA was observed. It should be noted that polyclonal hypergammaglobulinemia preceded by at least 5 years the appearance of articular inflammation. The changes of serum complement were also significant. CH50 was found constantly decreased below 40 HU/ml, particularly in the patients with febrile forms of RA; positive latex fixation test greater than 1/80 was observed at least 6 months before the appearance of articular tumefactions. Increase of beta 2-microglobulins in the serum and the presence of cryoglobulins was also observed in the 4 patients with RA. Dysglobulinemia has often been observed in the course of RA but it has seldom been presented as a preceding disturbance predicting the disease. The originality of the observations reported in this paper consists in a case of malignant RA appeared in the course of dysglobulinemia.
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A retrospective analysis of 20 patients with amoebic liver abscesses was performed. Seven of 20 patients had more than one abscess. In all, 33 separate abscesses were observed. The diagnosis was based on clinical findings such as malaise, fever, abdominal discomfort, and pain in the right abdomen, haematological and serological anomalies, such as leukocytosis, elevated erythrocyte sedimentation rate, and slightly elevated liver enzymes. The serological investigation included complement fixation, indirect haemagglutination, and latex fixation test; this latter test produced strong reactions in all patients with acute symptoms. The typical ultrasonographic pattern resembled that of a minor echogenic lesion at the time of diagnosis and initiation of therapy. However, in a few acutely ill patients the lesions could not be identified by ultrasonography on first examination, but were clearly identifiable on second investigation on the following days. This finding has not been published previously. It may be observed in a very early stage of the disease only and is, therefore, dependent on rapid diagnosis of amoebiasis. During the follow-up investigations of three months to one year, the majority of abscesses could still be identified.
56 healthy rabbits were inoculated with the active Cysticercus each into lateral ventricle of the brain, the white substance of the brain and into Spatium subarachnoideale. Rabbits were killed after 32 weeks p.i. Then their brains were macro- ev. microscopically investigated. The positive seroreactions (ringpreciptitation reaction and the latex-test) were observed at the beginning of the second week after infection. Curve of the titers was revealed two tops: first one between 6-7 weeks, second one 16-22 weeks after infection. All rabbits except one reacted positive on the application of the Cysticercus antigen. The control group consisted of the 8 rabbits revealed negative serological and immunological reactions. Three groups of the cerebral cysticercosis, dependent on the localization of the cysticerci in the brains, were observed: oedema form, hydrocephalous form and tumor form. These forms as well as the symptoms are similar to the human cerebral cysticercosis.
We reviewed 11 patients with rheumatoid subcutaneous bursitis involving the olecranon bursa in 10 and an adventitious bursa in 1. All patients had a positive latex fixation test for rheumatoid factors. The mean bursal fluid white blood count (WBC) was 2,924/mm3 compared with a mean joint fluid WBC of 15,608/mm3 in 32 consecutive cases of classical or definite rheumatoid arthritis (p less than 0.001). Bursal fluid glucose and complement concentrations were low. Cholesterol crystals were present in 5 of 6 nodular bursae, and in none of the 5 non-nodular bursae (p less than 0.05). Two patients had acicular cholesterol crystals that had previously led to an erroneous diagnosis of gout.
Two assay systems for fibrinogen-fibrin degradation products (FDP) in canine serum, the glutaraldehyde erythrocyte hemagglutination-inhibition immunoassay (GEHII) and the staphylococcal clumping test (SCT), were compared for reactivity with the plasmin digests of canine fibrinogen and with sera obtained from dogs suspected of having circulating FDP, The GEHII reacted well with early and late plasmin digests of fibrinogen. With early-stage fibrinogen digests, the SCT was more reactive than was GEHII. However, after the appearance of D and E fragments in the digests, SCT reactivity decreased progressively during plasminolysis. The sensitivities of GEHII and SCT for assaying FDP were 0.5 and 0.125 microgram of fibrinogen equivalent/ml, respectively. Serum FDP values for dogs with desease were comparable, with values ranging from 1 to 122 micrograms/ml by GEHII and 8 to 64 micrograms/ml by SCT. One dog with fulminating disseminated intravascular coagulation had a serum FDP value of 128 micrograms/ml by SCT and 179 micrograms/ml by GEHII. Howeever, normal canine sera had values by SCT of 4 to 16 micrograms of fibrinogen equivalent/ml, whereas normal values by GEHII were 0.5 to 2 micrograms/ml. Serum FDP concentrations were also determined for healthy and diseased dogs by latex-agglutination test. The dog with fulminating disseminqated intravascular coagulation had a FDP value of greater than 40 micrograms/ml, and only 1 other diseased dog had greater than 10, but less than 40 micrograms of fibrinogen equivalent/ml. All other dogs were considered negative, with FDP values of less than 10 micrograms/ml.
The Clq assay for antigen-antibody complexes was performed on 79 blood samples from 43 patients with juvenile rheumatoid arthritis (JRA). The results were compared with assays for the activation products of C3 (C3c,d), for the concentration of C3, for rheumatoid factor, and for antinuclear antibodies. A statistically significant association was found between Clq binding and positive tests for latex fixation and C3c,d in systemic and polyarticular JRA, but positive results of each assay were found independently. These 3 assays were usually negative in pauciarticular JRA. No relationship was found between Clq binding and C3 concentration or antinuclear antibodies.
During the hunting season of 1993, hearts from 28 black bears (Ursus americanus) from Pennsylvania were examined for Toxoplasma gondii infection. Serum samples from heart blood were examined for T. gondii antibodies by the use of the modified agglutination test (MAT), the Sabin-Feldman dye test (DT), the latex agglutination test (LAT), and the indirect hemagglutination test (IHA). One-hundred grams of myocardium from each bear were bioassayed in mice. Approximately 500 g of myocardium from 11 bears were fed to 11 cats, and feces from those cats were examined for T. gondii oocysts. Toxoplasma gondii MAT antibodies (> or = 1:40) were found in 22 bears in titers of 1:40 (4 bears), 1:80 (3 bears), 1:160 (7 bears), 1:320 (4 bears), and > or = 1:2,000 (4 bears). Antibodies to T. gondii by DT (> or = 1:10), LAT (> or = 1:32), and IHA (> or = 1:64) tests were found in 21, 9, and 6 bears, respectively. All 6 bears that did not have T. gondii antibodies in MAT were also negative in DT, IHA, and LAT. Viable T. gondii was isolated from 3 bears by bioassays in mice and from an additional 7 bears by bioassays in cats. All 10 bears that had viable T. gondii had MAT and DT antibodies but only 6 and 5 of them had antibodies by LAT and IHA, respectively.
Hidden 19S IgM rheumatoid factor (RF) and 7S IgG RF were assayed in 24 children with juvenile chronic arthritis (JCA) and 26 controls, in whole sera and in the IgM and IgG containing fractions of the serum after separation by acid gel filtration. When non-fractioned serum was used, IgM RF detection was positive in 4.2% by latex fixation test and 4.2% by ELISA. IgG RF was positive in 91.7% by ELISA. In the IgM containing fraction of the serum, the positivity for IgM RF was 41.7% by LFT and 54.2% by ELISA. In the IgG containing fraction the positivity for IgG RF was 100%. These results suggest toward the need of previous serum dissociation before hidden 19S IgM RF is assayed and demonstrate high prevalence of 7S IgG RF.
The latex- and hemagglutination tests were applied to determination of the titres of anthrax antibodies in the sera of 982 immunized sheep. Monodispersive standard colur latex of polymethylmetacrylate and protective anthrax antigen was used in these tests. On the basis of the results of titration of control sera titres of anthrax antibodies over 1:16 in the latex- and hemagglutination tests were accepted as positive. There was revealed no difference between the sera of the immunized animals reacting positively in both tests (d = 1.87 less than delta = 2.94 at P = 0.95). The difference between the positive titres determined in the latex-agglutination (55.78%) and hemagglutination (44.41%) tests was significant (d = 11.37 less than delta = 4.39 at P = 0.95). Consequently, both tests could be used for the purpose of determination of anthrax antibody titres, but the latex-agglutination test was more sensitive of the two.
Four-week-old chickens were inoculated orally with 1,000 or 100,000 oocysts of the ME-49 or GT-1 strain of Toxoplasma gondii, and their antibody responses were measured, using the direct modified agglutination test, latex agglutination test, indirect hemagglutination test, ELISA, and the Sabin-Feldman dye test. Antibodies against T gondii were detected by use of the modified agglutination test and ELISA within 2 weeks of oocyst inoculation, and antibodies persisted until termination of the study by postinoculation day 68. The latex agglutination test was insensitive in detecting T gondii antibodies, and antibodies were not detected by use of the dye and indirect hemagglutination tests. Of tissues bioassayed in mice for tissue cysts by pepsin digestion of individual organs of chickens on postinoculation day 68, tissue cysts were found in the brain of all 5, heart of 3, and leg muscles of 2, but not in the liver and breast muscles. None of the birds developed clinical toxoplasmosis.
Hidden rheumatoid factor (HRF) was detected in rheumatoid arthritis (RA) serum with ELISA after separation and dissociation of immune complex (IC). It was found that 60% of the patients with active RA has positive latex fixation test, whereas 96% of them has been demonstrated to have IgM hidden rheumatoid factor (HIgMRF) and 70% of them IgG hidden rheumatoid factor (HIgGRF). When the disease was controlled, HIgMRF and HIgGRF was found in 24% and 12% respectively. The difference was significant with P < 0.01. Our results show that the presence of HRF in RA patients is related with the activity of the disease, but not with duration of disease, sex and age.
Twenty-four 3-5-mo-old battery-hatched bobwhite quail were inoculated orally with 10(5) (ME 49 strain, group A, 6 birds), 10(4) (ME 49 strain, group B, 6 birds), 10(5) (GT-1 strain, group C, 6 birds), and 10(4) (GT-1 strain, group D, 6 birds) Toxoplasma gondii oocysts. One quail in group B died 18 days after inoculation (DAI) due to undetermined etiology. Two quail from group C and 1 quail from group D given GT-1 oocysts died of acute toxoplasmosis 6, 7, and 8 DAI, respectively; numerous T. gondii tachyzoites were found in lesions in visceral tissues. The surviving quail in group A and B were killed 106 DAI and those in groups C and D were killed 60 DAI. Toxoplasma gondii was isolated from pooled tissues of 4 of 5 quail in group B. Brains, hearts, and skeletal muscles from quail in groups A, C, and D were bioassayed individually in mice; T. gondii was isolated from the brains of all 6, hearts of 3, and skeletal muscles of 2 of the 6 quail in group A; from the brains of all 4, hearts of 1, and skeletal muscles of 2 of the 4 quail in group C; and from the brains of all 5, hearts of 1, and skeletal muscles of 3 of the 5 quail in group D. Toxoplasma gondii antibodies were found in sera of all 20 quail killed 60 or 106 DAI. Antibody titers detected in the modified agglutination test using whole tachyzoites were higher than in latex agglutination and indirect hemagglutination tests that used soluble antigens. Antibodies were not detected in a 1:4 dilution of 19 of 20 quail sera in the Sabin-Feldman dye test.
Fourteen 2-3-wk-old turkeys were inoculated orally with 10(5) or 10(4) infective oocysts of the ME 49 strain of Toxoplasma gondii. Of the 8 turkeys given 10(5) oocysts in experiment 1, 3 died or were killed 12 or 14 days after inoculation (DAI) because of respiratory distress associated with a concomitant Aspergillus-like fungus infection. The remaining 5 turkeys remained normal and were killed 62 DAI. Toxoplasma gondii was isolated in mice from the heart of all 5, from the breast muscles of 2, leg muscles of 3, and from the brains and livers of none of the turkeys. All 6 turkeys fed 10(4) oocysts in experiment 2 remained clinically normal until necropsy on 41 DAI; T. gondii was isolated from pooled tissues from each turkey. All 14 turkeys developed high antibody titers to T. gondii in the modified agglutination test (MAT) using formalinized tachyzoites. The enzyme-linked immunosorbent assay (ELISA) was as sensitive as MAT for detecting T. gondii antibodies in turkey sera. The latex agglutination and indirect hemagglutination tests were less sensitive than the MAT and ELISA. No dye-test-measurable antibodies were found in sera of any turkey.
BACKGROUND: In the treatment of rheumatoid arthritis an irreplaceable position is held by so-called disease modifying drugs. Recently among the latter cyclosporin A was included. The objective of the present study was to assess its therapeutic effect in patients with rheumatoid arthritis refractory to treatment. METHODS AND RESULTS: To a group of 20 patients with the refractory form of rheumatoid arthritis cyclosporin A (Consupren-Galena) was administered for 6 months in a mean daily dose of 3.5 mg. Clinical and laboratory examinations were made after one-month intervals. Cyclosporin administration influenced the clinical indicators of disease activity but did not lead to changes of red cell sedimentation values or the titre of the latex fixation test. Three patients did not complete the study because of serious undesirable effects. CONCLUSIONS: The results of the investigation indicate the clinical effectiveness of cyclosporin in patients with rheumatoid arthritis who do not react to other forms of disease modifying drugs. It is not clear whether cyclosporin affects the progression of rheumatoid tissue changes or whether is its effect is close to symptomatic treatment.