Search

The silicone implant controversy wavers between reassuring epidemiological studies and about 300 case reports of patients developing a definite or incomplete/atypical connective tissue disease (CTD) after receiving a silicone gel-filled breast implant (SBI). Since Hashimoto's thyroiditis (HT) is rarely reported in this context, we report here two new cases of HT associated with a history of bilateral cosmetic SBIs. The first patient was a 45-year-old white woman who had SBIs in 1976. In 1991 she developed HT, evolving to thyroid deficiency which was compensated with levothyroxine treatment. In addition, the patient complained of fatigue, arthralgia, morning stiffness and developed a sicca syndrome necessitating artificial tears. The 1995 evaluation disclosed the presence of antinuclear antibodies at a titre of 1/640, and high level anti-thyroid microsomal antibodies (1/256,000). Gamma globulins rose to 22.6%. Thyroid ultrasonography showed an enlarged thyroid gland with a diffusely hypoechogenic pattern. The implants were painful, and in 1996 they were removed. Microscope examination of the fibrous capsule surrounding the prostheses showed extremely dense connective tissue with fibrosis. The second patient was a 55-year-old white woman who had SBIs in 1984. In 1995, she developed HT with clinical pain and tenderness of the thyroid gland, with mild hyperthyroidism and positive antithyroglobulin antibodies, and was given corticosteroid treatment for 5 months. In 1996, the implants were again painful and the patient developed positive antinuclear antibodies with a titre of 1/200. Ultrasonography showed a heterogeneous thyroid gland, and implant removal was advised. Hashimoto's thyroiditis is recognized as a subset of chronic auto-immune thyroiditis, and its association with SBI is rare. In these 2 observations, an association without relation is possible, but a future survey of similar cases seems warranted.

International audience; OBJECTIVES: Anticardiolipin antibodies belong to the group of antiphospholid antibodies, and may be seen in association with endothelial damage and recurrent vascular thrombosis. The aim of our study was to determine in patients with Crohn's disease the frequency of anticardiolipin antibodies, and to correlate their presence with clinical activity and treatment of the disease. METHODS: One hundred and thirty-eight sera from patients with Crohn's disease and 118 from age-matched controls were tested for IgG anticardiolipin antibodies. In the Crohn's disease group, we determined whether the patients had a past history of vascular thrombosis, a clinically active intestinal disease, or a current immunosuppressive therapy (steroids or azathioprine). RESULTS: Anticardiolipin antibodies were found significantly more often in patients with Crohn's disease than in controls: 11.0% versus 2.5%, P < 0.02. Three patients with Crohn's disease had a past history of vascular thrombosis, but none of them had anticardiolipin antibodies. The presence of anticardiolipin antibodies was not correlated with the fact that patients had a clinically active disease (P = 0.77), or a current immunosuppressive therapy at the time of the serological test (P = 0.95). CONCLUSIONS: There is a significantly high prevalence of patients with anticardiolipin antibodies during Crohn's disease. The positivity of the test does not seem to be correlated to the existence of a past history of vascular thrombosis, nor to the clinical activity of the disease.

In order to investigate the clinical value of anti-mitochondrial antibodies type 5 (anti-M5), we carried out a retrospective study on 48 patients with these antibodies. Seventeen of these 48 patients (35%) satisfied at least 4 criteria of the revised American Rheumatism Association classification of SLE. Twenty-nine (61%) had at least one clinical manifestation of anti-phospholipid syndrome; thirteen had symptoms consistent with primary anti-phospholipid syndrome; five had isolated recurrent thrombosis; five had Evans' syndrome; four had auto-immune haemolytic anaemia; two had immunologic thrombocytopenia. Two of the 48 patients had no clinical manifestations, but only anti-M5 and a false laboratory test for syphilis (FBTS). Our data confirm that patients with anti-M5 have a high prevalence of: 1) thrombosis (42% had three or more deep thromboses) and fetal loss (21%); 2) auto-immune cytopenia with idiopathic thrombocytopenic purpura (29%) and auto-immune haemolytic anaemia (54%); 3) laboratory markers of anti-phospholipid syndrome (lupus anticoagulant (71%), FBTS (95%) and anticardiolipin antibodies (aCL) (71%). For 32 patients with anti-M5, anti-beta 2 glycoprotein I antibodies were also tested; 12 (38%) were positive, all of whom had IgG aCL, ie none had anti-beta 2GPI antibodies without aCL. There was no association between the presence of anti-beta 2GPI antibodies and recurrent thrombosis among patients with anti-M5. All these findings suggest that anti-M5 is another marker of the antiphospholipid syndrome. Even though the prevalence of anti-M5 is low, especially in SLE, it was the only marker of the anti-phospholipid syndrome in two patients; this appears to justify routine screening for these antibodies.

The aim of this study was to evaluate the prevalence and the clinical signification of non organ specific autoantibodies in chronic hepatitis C.We studied retrospectively 158 consecutive patients (97 with chronic hepatitis C, 24 with chronic hepatitis B, 67 with alcoholic cirrhosis) and 100 blood-donors.The prevalence of anti-nuclear and anti-smooth muscle antibodies was lower in blood donors than in patients (P0.001), but was comparable among the 3 groups of patients. The anti-liver-kidney microsome type 1 antibodies were detected only in patients with chronic hepatitis C (6%). The serum gammaglobulin level was significantly higher in patients with hepatitis C and anti-nuclear antibody titersor = 1/50. The anti-smooth muscle antibodies detected in patients with hepatitis C had no anti-actin specificity. The response to interferon was not related to the detection of non organ specific autoantibodies before treatment.Anti-nuclear or anti-smooth muscle antibodies are not characteristic of hepatitis C virus infection.

Anti native DNA antibodies (anti nDNA Ab), which are a highly specific feature of systemic lupus erythematosus (SLE) were measured by 3 methods: an enzyme linked immunosorbent assay (ELISA), an indirect immunofluorescence test on Crithidia luciliae (IFCL) and the Farr assay (reference test). 114 sera from patients with SLE or another connective tissue disease or without autoimmune rheumatic disease were tested. This study showed that ELISA seemed to be a more sensitive and specific test than IFCL (classical test). ELISA was also as sensitive as the Farr assay. ELISA should replace IFCL for the diagnosis and the follow up of patients with SLE. In other connective tissue diseases, ELISA might give more positive results. Thus these had to be confirmed, especially in the case of low antibodies levels, by using another method (e.g., the Farr assay).

Indirect immunofluorescent detection of anti-nuclear antibodies was conducted on sections of rat liver and on smears of human Hep 2 tumour cells in the serum of 1017 patients. Overall, the Hep 2 cells gave titres superior by 1 or 2 dilutions. Taking into account this difference, a good agreement was observed between the 2 cellular reagents in 83 per cent of the sera tested. The divergences, which affect almost one half of the positive sera, are largely due to the presence of anti-centromere antibodies, anti-nuclear antibodies giving a patchy "M3" appearance to the Hep 2 cells and, most importantly, anti-nucleolar antibodies. Such differences demonstrate that there are major qualitative or quantitative antigenic differences between the nuclei of rat hepatocytes and those of Hep 2 cells. Although technically rat liver and Hep 2 cells were found to be fairly easy to use and interpret, only a large comparative study of human pathology will be able to determine which is the better reagent for the routine detection of anti-nuclear antibodies.

The authors report a case of Waldenstrom disease in which the IgM kappa immunoglobulin had an anti-smooth-muscle activity at a very high titre (1/100 000). This activity was found in the purified IgM but not in the Fab fragment; nevertheless, the immunofluorescence inhibition by this fragment is evidence in support of the anti-smooth-muscle activity of the IgM. The IgM specificity in this patient is different from the anti-smooth-muscle antibodies already described.

Antinuclear and antinuclear membrane autoantibodies are detected by indirect immunofluorescence in sera of 62 p. 100 of primary biliary cirrhosis patients; when anti-SS-A (Ro) and anti-SS-B (La) autoantibodies were included, 70 percent of patients had at least one type of antinuclear antibody. Of 89 patients with primary biliary cirrhosis, 30 had either Raynaud's phenomenon, Sjögren's syndrome or the CREST syndrome. Some antinuclear antibodies, anticentromere and speckled S1 type, seem to correlate with the associated connective tissue disease. Antibodies showing the S3 pattern (multiple nuclear dots) and antibodies to nuclear membrane may be present independently of an association with connective tissue disease. In the classical technical conditions used to detect anti-tissue and anti-mitochondrial autoantibodies on tissue sections, antinuclear antibodies like anti-centromere or S3 may not be detected and/or identified. Primary biliary cirrhosis patient sera for antinuclear antibodies determination must be screened by at least two assays: indirect immunofluorescence on a human cell line, like HEp-2, and immunodiffusion. The last assay must be performed even if antinuclear antibodies are undetected by immunofluorescence.

Six patients developed acute, subacute or chronic hepatitis after taking tielinic acid, a new diuretic used in the treatment of hypertension. Two died of acute liver failure. The condition was characterized by marked increase in serum transaminases, parenchymal necrosis and portal and/or lobular inflammatory fibrosis. In addition, the serum of all patients contained high titers of a liver/kidney microsomal antibody, which disappeared either after tienilic acid was discontinued or after prednisolone was introduced. The study shows that tienilic acid may be responsible for acute or chronic hepatitis and suggests that a liver/kidney microsomal antibody could be a sero-immunological marker of drug-induced liver disease.

Total eosinophil count (TEC) was done in 13 normal subjects, in 8 subjects before and 90 mn after a "French" breakfast and in 29 asthmatic patients. The geometric mean is higher (p less than 0,001) in asthmatic than in normal subjects: 304 (231--391) versus 144 (101--197). The breakfast does not interfer with the result of the TEC. In asthmatic subjects, a significant inverse correlation appears (r = 0,57, p less than 0,01) between the logarithm of TEC and the quotient: formula; see text. This correlation persists whatever may be the subject's age, the duration of the asthma or age at which he first contracted the illness. Asthma appeared after 40 years in 4 of the subjects: their TEC was higher (p less than 0,01) than in subjects who had become asthmatic before the age of forty. The respiratory function was lowered more in these 4 patients than in others who had been ill for the same time (p less than 0,001). The TEC is not related to results of skin testine with usuel inhalant allergens (grass pollen, house dust, cat's or dog's dander) or by result of a provocation test (by inhalation of allergen). Eosinophilia and bronchial obstruction are connected by one (or more) factors that may be inhalant allergens in extrinsec asthma and circulating immune complexes in intrinsec asthma.

The differentiation of human B lymphocytes in vitro into Ig secreting cells, as measured by a radioimmunoassay rendered specific to IgG and IgM, in response to a polyclonal stimulant, requires the participation of several cellular types. Upon poleweed-mitogen stimulation, B-cell enriched and monocyte containing cell suspensions prepared by elution of nylon wool adherent cells, when mixed with various concentrations of T cells purified by filtration through nylon wool column and depletion of EAC-rosette forming cells, synthesize 5 to 20 times more Ig than non separated lymphocytes. These experiments which demonstrate the cooperation of certain T cells also suggest that other cells eliminated by nylon wool adherence act as suppressor cells. The cooperation of these T cells is independent of their proliferation and can be obtained with allogeneic T cell.