[Toxicity of low-dose methotrexate in patients with nephrotic syndrome].
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Biomedical subjects
Publications and source records attributed to M F Kahn.
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The treatment of sciatica due to lumbar disc herniation must be conservative, except if there is severe paralysis or a cauda equina syndrome. First of all, treatment needs bed rest during 15 days, non steroid antiinflammatory drugs and analgesics. In case of failure we propose 2 to 3 epidural injections of corticosteroids. Lumbar brace is often necessary. After 6 weeks of treatment including complete bed rest, radical treatment is proposed, either surgical or percutaneous. If the disc herniation is sequestered or if there is lumbar stenosis, surgery is indicated. In the other cases the choice between chemonucleolysis with chymopapain or percutaneous nucleotomy must be made with the patient informed of the results and complications of the different techniques and according to the results of CT scan or magnetic resonance imaging. Surgery remains efficacious after failure of percutaneous treatment.
Five synthetic peptides corresponding to the N-, the C- and a central domain in 60-kD SSA/Ro protein were prepared and tested with sera from 112 patients with systemic lupus erythematosus (SLE), 55 with primary Sjögren's syndrome (pSS) and 29 with rheumatoid arthritis. Among these five fragments, one representing residues 21-41, was recognized by antibodies in 57% of pSS patients. Interestingly, this peptide was recognized by only a few (less than or equal to 7%) of SLE sera, while 63% of pSS sera and 46% of SLE sera tested in parallel possessed antibodies reacting in ELISA with purified 60-kD SSA protein. The ELISA results were compared with the pattern of reactivity obtained in immunodiffusion and immunoblotting. The results indicate that the sensitivity of ELISA using peptide 21-41 and pSS sera was in the same range as immunoblotting and higher than immunodiffusion. Thus the peptide 21-41 proved useful for the detection of anti-SSA antibodies in the sera of patients with pSS. Furthermore, a positive ELISA using peptide 21-41 could be of potential use to discriminate pSS with systemic features from SLE. The fact that peptide 21-41 is recognized by antibodies in pSS but only by very few SLE sera implies that different mechanisms are involved in the anti-SSA immune response in these two autoimmune diseases.
The case is reported of a 41 year old white woman who developed systemic lupus erythematosus (SLE) seven years after primary Sjögren's syndrome and four years after the association of Sjögren's syndrome with Jaccoud's arthritis. The SLE was detected by a benign intracranial hypertension, which is a rare neuro-ophthalmic presentation of lupus. No associated conditions linked to benign intracranial hypertension syndrome were seen in this patient and the hypertension syndrome recurred one year later.
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In an attempt to establish the characteristics, circumstances leading to infection and development of polyarteritis nodosa (PN) related to hepatitis B virus (HBV), prognostic factors and outcome, and to define the most effective treatment, 66 patients observed between 1972 and 1989 were analyzed. Hepatitis was clinically present in 19/66 patients before PN. In most cases, PN occurred less than 6 months after infection. Clinical manifestations of PN were comparable to those observed in patients without HBV infection except for orchitis which was present in 13.6% and for pulmonary signs which were absent. Transaminases were normal in 38 cases for SGOT and 31 for SGPT and twice the normal range or more in the other cases. Antineutrophil cytoplasmic antibodies (ANCA) were tested in 22 patients and present in 2 (9%). Twenty-eight patients were treated with prednisone +/- oral cyclophosphamide +/- plasma exchanges. Thirty-eight patients were given a short-term treatment with prednisone followed by the association of vidarabine, 15 mg/kg bw/d for one week and 7.5 mg/kg bw/d for 2 weeks, and plasma exchanges: 14 sessions during the 3 weeks of vidarabine infusion, then tapered until stopping treatment after 2 to 3 months depending upon the clinical results obtained. The mean duration of follow-up was 50.3 +/- 46.1 months. At the end of follow-up, 13 of the 28 patients (46.4%) treated with steroids +/- cyclophosphamide +/- plasma exchanges died and 7/38 (18.4%) of those treated with vidarabine and plasma exchanges (p < 0.001) died. HBe/anti-HBe seroconversion was observed in 2 patients treated with prednisone +/- cyclophosphamide +/- plasma exchanges who were alive at the time of final analysis and in 16 patients receiving the other regimen. The outcome of patients treated with a few days of prednisone, vidarabine and plasma exchange was good and, therefore, we propose this protocol as the first viable treatment for polyarteritis nodosa related to HBV, surpassing the conventional treatment with steroids and cyclophosphamide, which stimulates viral replication.
Bilateral symmetrical polyarthritis occurred in three patients (2 males and 1 female), with no previous history of inflammatory rheumatologic disease, given alpha-interferon for 1 1/2, 7, and 10 months as treatment of chronic non A-non B hepatitis, myelofibrosis, and thrombocytopenia with myeloproliferative disorder, respectively. Joint manifestations developed 1 1/2, 3, and 10 months after initiation of alpha-interferon in a dosage of 3.10(6) U three times a week, 4.5.10(6) U per day, and 8.10(6) U three times a week. Polyarthritis persisted following withdrawal of alpha-interferon in the two last patients of whom one had rheumatoid nodules and positive rheumatoid serology and the other had scleritis, exanthema, and negative rheumatoid serology. Erosive rheumatoid arthritis was diagnosed after 28 months and 12 months, respectively, in two patients who required systemic corticosteroids with antimalarials (1 case) or azathioprine after failure of methotrexate (one case). Follow-up in the third case (12 months) is too short to allow differentiation of systemic lupus erythematosus (ANA: 1/1500 H with anti-DNA antibodies 58 U/ml) and chronic autoimmune hepatitis. Reports of chronic inflammatory rheumatologic disease during alpha interferon therapy are exceedingly few in number. In the cases reported herein, alpha-interferon may have either triggered or revealed the joint disease. To prevent occurrence of this complication, exclusion from alpha-interferon therapy of patients with autoantibodies or a positive history for clinical evidence of immune dysfunction may be considered.
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We describe 7 Achilles tendinitis occurring during fluoroquinolone treatment. Antibiotic agents used were pefloxacin and ofloxacin. In 3 cases the course was complicated by rupture of the tendon, one of which is histologically documented. The toxic effects of quinolones on tendon is discussed.
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The author reviews the locomotor problems observed in performing musicians. The overall frequency of these problems is high. Three presentations exist: overuse, entrapment and dystonic syndromes. Treatment of these problems implies not only a technical approach, but also consideration of life experience and individual personality.
SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) syndrome put together osteoarticular lesions described separately under numerous denominations, such as multifocal osteomyelitis, pustulotic arthroosteitis, acne rheumatism. The association of sterile inflammatory bone lesions and neutrophilic skin eruptions is the cornerstone of this new syndrome, which also has links with spondyloarthropathies and plain psoriasis.
In a group of 61 patients with SAPHO syndrome involving bone, 8 cases of chronic inflammatory bowel diseases have been observed. 6 cases are considered as Crohn's disease and 2 as ulcerative colitis. 5 patients presented with sacro-iliitis, 4 with palmoplantar pustulosis, 3 with plain psoriasis and 1 with disseminated acne. 4 patients have HLA B27 antigen. These findings bring some evidences to lump SAPHO syndrome with the spondylarthropathies.
To date, descriptions of bone manifestations associated with the acquired immunodeficiency syndrome (AIDS) have mostly been limited to case reports. Six such cases observed in our Departments of Rheumatology and Infectious Diseases, are reported. Three types of manifestations were observed: malignant lymphoma, infectious osteomyelitis, and reflex sympathetic dystrophy syndrome (algoneurodystrophy) secondary to central nervous system involvement.
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The purpose of this study was to establish the actual survival rate of a cohort of 51 patients with systemic lupus erythematosus (SLE) all of whom were followed during 12 years from 1976 to 1988 and to evaluate the prognostic significance of the severe complications of the disease. Forty-eight were females. The mean age was 28.5 at onset, 36.2 at diagnosis and 42 at entry; 80% had four or more 1982 ARA criteria at diagnosis and 96% in 1988. Survival rates were: 96% at two years, 86.3% at five years and 74.5% at twelve years. The main cause of death was infection (62%); SLE was directly responsible in only one case. Manifestations considered as severe occurred in almost two-thirds of the cases without any concordance in the time sufficient to recognize different severe forms of the disease.
Sarcoidosis without bone involvement or sarcoid dactylitis, is a very unusual cause of flexor synovitis. Our reported patient initially presented with chronic arthralgia of the knees and ankles. The initial diagnosis of rheumatoid arthritis was incorrect. A surgical flexor synovectomy was performed to release painful compression of the median nerve due to the synovitis. The correct diagnosis was suggested by the histopathological examination showing noncaseating epithelioid granulomas. The diagnosis was confirmed by the association of a negative tuberculin test and raised angiotensin converting enzyme. No recurrence of synovitis occurred after surgical excision and colchicine therapy but arthralgia persisted.