[Evaluation of terminal parathormone NH2 and COOH and plasma calcitonin in the blood of uremic patients under hemodialysis therapy].
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Biomedical subjects
Publications and source records attributed to A Ruffatti.
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An antinuclear antibody specific for nuclear membrane (ANMA) was observed by the immunofluorescence method in sera from patients with primary biliary cirrhosis (PBC). ANMA was present in 18 of 63 PBC sera (28.5) and in 1 of 431 control sera (0.2%). Its reaction appeared as a thin fluorescent ring confined to the nuclear envelope and was more evident when the sera were highly diluted and the fluorescence, due to frequently associated antimitochondrial antibody, faded. The ANMA fluorescent pattern was confirmed by indirect immunoperoxidase staining. ANMA was seen on both tissue cryostat sections and HEp-2 cells. It was a poorly or non-complement-fixing IgG, specific for an antigen resistant to DNase I, RNase, and trypsin. The significance of its presence in PBC in unknown at present. Identification of its antigen with one of the centromeric antigens is suggested.
In testing for antinuclear antibodies the sera of 121 patients affected with scleroderma, we found in 2 of them the concurrent presence of anti-centromere and anti-Scl 70 antibodies. Since the association of these antibodies has never been reported, to the best of our knowledge, we report the clinical and serological features of the 2 patients. Both subjects were women with an incomplete CREST syndrome (RST), a relatively limited involvement of the skin, a mild pulmonary fibrosis without apparent signs of other visceral involvement. On the other hand, the clinical course of the disease was different in the 2 cases. One patient had a longer disease duration and up to date the clinical features appear to be unchanged; the other had a shorter disease duration, when suddenly she died of cardiac arrest.
Anticentromere antibody (ACA) was investigated in 116 blood relatives of 22 ACA positive patients affected with scleroderma and, for comparison, in 82 healthy subjects matched for age and sex who belonged to 25 families. No relative showed any evident scleroderma symptom although in 8 an unusual cold sensitivity of the extremities was present. ACA at a low titer (40), was found in 4 relatives (3.44%), while it was absent in control sera. The 4 ACA positive relatives were first as well as second degree relatives of probands. Two had familial disease: one idiopathic chronic hypoparathyroidism and the other mental retardation. The third had myasthenia gravis and the fourth unusual cold sensitivity and allergic dermatitis. At present we cannot explain the significance of ACA occurrence in relatives of ACA positive patients. Followup clinical and serological studies could show a possible association of low titer of ACA with subclinical scleroderma features in patients who later develop overt disease.
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Sera from 69 patients affected with rheumatoid arthritis were examined for IgM, IgG and IgA rheumatoid factors (RF) by a indirect immunofluorescence method. The results were compared with those obtained from the classical rheumatoid factor latex test. By this technique we have demonstrated antigammaglobulin activity in a high proportion (23%) of sera from latex test seronegative rheumatoid patients. Moreover, by fractionated antisera it was possible to detect also IgG and IgA factors. Indirect immunofluorescence results to be a simple and available technique for detection of RF, also in many "seronegative" patients.
IgM, IgA, IgG rheumatoid factors were investigated by a indirect immunofluorescence method in three groups of patients affected with rheumatoid arthritis of various picture: 30 patients with mild articular disease, 20 with severe joint involvement and 19 with articular and systemic symptoms. Rheumatoid factors occurred more frequently in patients with articular and extraarticular severe rheumatoid arthritis; moreover these patients showed higher titres and higher incidence of different immunoglobulin class rheumatoid factors in comparison with rheumatoid patients having mild joint disease.
Tissue antibodies (Ab) were investigated in 85 patients affected with pulmonary malignancy of different histologic type and, as control, in 40 non-smoker healthy subjects and in 40 smoker subjects with chronic bronchitis. A significantly higher number of patients (64, 7%) had tissue Ab in comparison with both control groups (17% in non smoker group and 25% in smoker and chronic bronchitis group, respectively). Antinuclear antibodies were found in 29.4% of patients, antismooth muscle in 31.7%, anti-mitochondrial Ab in 4.7%, antityroid microsomes Ab in 4.7%, anti-gastric parietal cells Ab in 4.7%, anti-reticulin Ab in 11.7%. The patients at third stage of disease showed all antibodies as well as anti-nuclear more frequently that patients at first and second stage. Antibodies to cytoplasmic antigens were found in patients with anaplastic and squamous cancer, but not in patients with adenocarcinoma. Our observations suggest that immunologic abnormalities similar to those present in autoimmune disease, may be associated to pulmonary malignancy.
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In 20 patients affected with rheumatoid arthritis, tissue autoantibodies were studied during a year of treatment with levamisole. Before therapy, antinuclear antibodies were present in 11 cases, anti-thyroid microsomes in 1 and anti-smooth muscle in 6. During therapy, autoantibodies remained almost unchanged in all patients, thus indicating that levamisole does not influence this aspect of humoral immunity in rheumatoid arthritis. Furthermore, no correlation was found between autoantibody pattern before treatment and effects of levamisole on clinical course of disease.
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Twenty patients found LKM antibody positive during the routine screening for autoantibodies, were studied for the association with other autoantibodies. Sixteen sera (80%) were found positive either for ANA (50%) or SMA (50%) or both (20%). Eleven patients (55%) were over 40 years old, 3 patients were HBsAg+ve, 4 have toxic and alcohol-related liver disease. These results provide evidence that the LKM antibody is not confined to young people chronic active hepatitis, but is present also in CALD of adult with various etiology. Its association with other autoantibodies (especially ANA) suggest that also LKM could be a marker of autoimmunity. The presence of ANA may be an expression of more severe stages of the disease.
OBJECTIVE: To determine the clinical significance of anti-NuMA and anti-HsEg5 antibodies in a group of patients affected with rheumatic diseases. MATERIALS AND METHODS: Indirect immunofluorescence on HEp-2000 cells at serum dilution of 1:40 was used to examine 26 sera which had previously showed a "mitotic spindle" fluoroscopic pattern type during laboratory routine. RESULTS: 21 sera (80,7%) were identified with NuMA and 5 (19,3%) with HsEg5 patterns alone or associated with other ANA patterns. However only patients with isolated positivity and that is 15 with NuMA and 4 with HsEg5 stainings were included in this study. Of the NuMA positive patients 5 were affected with arthropathies associated to different forms of thyroiditis, 2 with seronegative arthritis, 2 with antiphospholipid syndrome, 1 with systemic lupus erythematosus (SLE), 1 with rheumatoid arthritis, 1 with sicca syndrome, 1 with undifferentiated connective tissue disease, 1 with Mycoplasma pneumoniae infection and 1 with retinal thrombosis. Of the HsEg5 positive patients 3 were affected with SLE and 1 with seronegative arthritis. CONCLUSIONS: NuMA does not prevail in any defined rheumatic disease, while HsEg5 staining were more frequent (75%) in patients affected with SLE all of whom showing high antibody titres.
OBJECTIVES: To evaluate the prevalence and clinical significance of cathepsin G antibodies in patients affected with systemic sclerosis (SSc, scleroderma). METHODS: 115 patients affected by SSc, 55 (47,8%) with diffuse scleroderma (dSSc) and 60 (52,2%) with limited scleroderma (lSSc), were tested for cathepsin G antibodies by ELISA method. Moreover these sera were evaluated by indirect immunofluorescence (IIF) on ethanol and formalin fixed human neutrophils. RESULTS: By means of the ELISA method 16 (13,9%) patients were found to be sera positive for anti-cathepsin G, 2 (12.5%) of which showed a perinuclear fluorescence pattern (P-ANCA) and 4 (25%) an atypical ANCA staining, while 10 (62,5%) were negative on IIF. The IIF on scleroderma sera revealed 5 (4,3%) P-ANCA and 18 (15,7%) atypical ANCA patterns. The anti-cathepsin G antibodies significantly prevailed in scleroderma sera (p=0.02) when their frequency was compared with that of healthy controls; while they were not significantly associated to any clinical or serological features of SSc patients. CONCLUSIONS: The anti-cathepsin G antibodies were significantly frequent in scleroderma sera; however, no clinical correlations were found. Thus, the significance of their presence in SSc still needs to be clarified.
OBJECTIVE: To study the incidence and the features of congenital heart block (CHB) in patients with undifferentiated connective tissue disease (UCTD) and primary Sjögren's syndrome (pSS). METHODS: We studied 81 pregnancies of 41 women attending the Outpatients' Clinic of the Rheumatology Unit of University Hospital of Padova from July 1989 to March 2004. Twenty five of these (61%) were affected with UCTD and 16 (39%) with pSS. Serologic inclusion criteria was anti-Ro/La positivity, assessed by counterimmunoelectrophoresis and ELISA. RESULTS: CHB was found in 2 out of the 46 (4.3%) pregnancies followed by our Staff and in 2 out of the 35 (5.7%) included in the retrospective part of the study. In 3 cases CHB was a 3rd degree block, causing pregnancy termination in 2. The only 2nd degree block was identified in one patient at the 22nd week of gestation and treated with dexamethasone and plasma-exchange. All of the women were positive to 52 kd and 60 kd Ro autoantibodies. CHB mothers had higher titer antibodies to 52 kd Ro protein than did the mothers with healthy infants (P = 0.026). Electrocardiographic abnormalities at birth were found in 3 out of 29 asymptomatic infants. One presented sinus bradycardia, the second abnormalities of ventricular repolarization, both regressed spontaneously, while the third ventricular extrasystoles which continue even now at 5 months. CONCLUSIONS: These results showed that in UCTD and pSS there is a higher incidence of CHB than that reported in Systemic Lupus Erythematosus. Electrocardiographic screening in all infants born to mothers with anti-Ro/La antibodies would seem an important measure to identify those with irreversible heart conduction abnormalities.
OBJECTIVE: We evaluated the induction and clinical significance of ANA, anti-dsDNA and anti-ENA during infliximab therapy in patients with Rheumatoid Arthritis (RA) or Ankylosing Spondylitis (AS). METHODS: We tested sera from 30 RA and 30 AS patients before and during treatment with infliximab. ANA and antidsDNA were determined by indirect immunofluorescence and anti-ENA by an "in house" counterimmunoelectrophoresis. Statistical analysis was performed by X2 and McNemar's tests and U-test of Mann-Whitney. RESULTS: Eight of the 30 RA patients and 1 of the 30 AS patients were positive for ANA before treatment with infliximab. Eighteen of the 22 (81.8%) negative patients with RA and 11 of the 29 (37.9%) negative patients with AS became positive for ANA during infliximab treatment. No ANA positive patients became negative during the therapy. The difference between ANA before and after treatment resulted significant in both RA and AS patients (p=0.001). The frequency of anti-dsDNA and anti-ENA did not change significantly from baseline, in both RA and AS patients. Acquired ANA positivity was not associated with clinical signs of lupus syndrome and was not correlated with adverse events. The mean values of ESR and CRP in RA patients who became positive for ANA were significantly decreased (p=0.01 and p=0.02 respectively). CONCLUSIONS: Infliximab treatment induced a significant increase in the frequency of ANA in RA and AS patients. The significance of ANA development in these diseases is at present unknown. The significant decrease of ESR and CRP in RA patients who became positive for ANA after treatment should be investigated in a larger number of patients.
OBJECTIVE: In order to investigate the potential role of hyperhomocysteinemia as an additional risk factor for thrombotic events, we studied its prevalence in patients with primary antiphospholipid syndrome (APS) and evaluated its association with different clinical features. METHODS: We enrolled 29 patients without any current evidence of underlying connective tissue disorder and fulfilling the Sapporo preliminary classification criteria for APS. RESULTS: Ten (34,4%) patients showed mild hyperhomocysteinemia (18,34 micromol/L +/- 2,04 DS). Nine had history of cerebrovascular disease, isolated (3 cases) or more often (6 cases) in association with other APS features. All patients, but one, showed multiple ischemic cerebral lesions. Seven of the 10 patients with hyperhomocysteinemia had multiple antiphospholipid antibody positivity and presented more frequently (6 cases) multi-site vascular involvement. CONCLUSIONS: The frequency of hyperhomocysteinemia in patients with primary APS is not negligible and appears to be associated with cerebral microangiopathic disease, multiple antiphospholipid antibody positivity and the simultaneous involvement of different vascular districts. For this reason and because hyperhomocysteinemia can be easily corrected with safe and relatively inexpensive therapeutic interventions, we advocate the measurement of homocysteinemia in every patient affected by APS and possibly in subjects with positive antiphospholipid antibody without a history of thrombosis.