[Rheumatoid arthritis and HLA class II antigens].
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Biomedical subjects
Publications and source records attributed to T Bardin.
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We studied 56 patients who had been receiving peritoneal dialysis for greater than 3 years, to investigate the prevalence of rheumatic diseases suggestive of beta 2-microglobulin (beta 2m) amyloid deposition. Eight patients were found to have carpal tunnel syndrome, 16 had chronic shoulder pain, 8 had subchondral bone cysts, and 13 had destructive arthropathies. Amyloid reacting with anti-beta 2m was demonstrated in the hip synovium of 1 patient. Serum beta 2m levels were elevated in all patients. These data suggest that peritoneal dialysis, like hemodialysis, may lead to the development of an arthropathy associated with beta 2m accumulation and beta 2m amyloid deposition.
We describe a patient undergoing long-term hemodialysis, in whom severe chondrolysis of the hip joint developed. The chondrolysis evolved in the absence of synovial inflammation and articular chondrocalcinosis. Biochemical studies of articular cartilage retained at surgery revealed deposition of exclusively small proteoglycans in the matrix. This may have been an important factor leading to the rapid chondrolysis in this patient.
Heparinotherapy and systemic mastocytosis are two unusual aetiologies of diffuse osteopenia, possibly linked by common pathophysiological factors. Osteoporosis related to heparinotherapy has only been observed in patients treated with doses higher than 10,000 units per day and for more than 4 months. Even in these, it is a rare disorder which has only been reported approximately 15 times in the world literature. Bone histomorphometry has demonstrated the occurrence of marked hyperresorption. In vitro, heparin appears to have resorptive and collagenolytic effects which could play a pathophysiological part in the disorder. Diagnosis of the osteopenic form of systemic mastocytosis may be difficult. Urticaria pigmentosa is a very important clue but may be misdiagnosed or even missing. Hepato or splenomegaly are inconstant. X-rays may show the coexistence of osteosclerotic lesions. Standard biochemical tests are of little help. The urinary excretions of the histamine metabolites methyl histamine and methyl imidazolacetic acid have been found increased when measured. Finally, the diagnosis is made by bone histology which must be performed without decalcification and read by a pathologist informed of the potential diagnosis. Toluidine blue stain shows that mastocytes are numerous in the bone marrow where they are grouped in foci. Histomorphometry demonstrates a high bone turnover with excessive resorption, which could be mediated by heparin or PG E 2 contained in mastocyte granules. Treatment is difficult and may involve cytostatic drugs and/or inhibitors of bone resorption: Clodronate has recently been reported to be at least transiently effective.
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A sporadic case of camptodactyly and arthropathy is described in a 54-year-old man. Polyepiphyseal dysplasia complicated by the so called "chondrodysplastic rheumatism" was a main feature of the arthropathy which included early onset osteoarthritis, calcium pyrophosphate dihydrate and calcium phosphate deposition diseases. We suggest that epiphyseal dysplasia, chondrocalcinosis and mixed crystal deposition disease could be an additional cause of a camptodactyly-arthropathy syndrome.
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A series of 121 consecutive patients with abdominal (96 cases) and retroperitoneal (25 cases) masses was studied in order to evaluate the contribution of cytology in establishing a definite diagnosis of the tumors. The cytologic results on aspirates were obtained with 22 or 23 gauge Chiba needles. At the same time, percutaneous fine needle aspiration biopsy was performed with 19 or 21 gauge fine needles having circumferentially bevelled tips that produced tiny tissue cores suitable for histologic study in 88 cases. These diagnoses were controlled with larger pathological specimens in 78 cases and appeared to be consistent with the clinical and biological course in 43 cases. The sensitivity of the cytologic diagnosis was 83 per cent, and its overall accuracy 87.6 per cent. There were no false-positive results. Furthermore, the method proved to be safe and well-tolerated, with low morbidity (0.8 per cent) and no mortality.
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The noninvasive diagnosis of amyloid arthropathy in dialysis patients is still uncertain. Therefore, we investigated the potential diagnostic value of the 99mTc-methylene diphosphonate scan in seven long-term hemodialysis patients suffering from chronic joint pain who had biopsy-proven osteoarticular amyloidosis of the recently discovered beta 2-microglobulin (beta 2-M) type. In six, but in none of five control patients on short-term hemodialysis, increased tracer uptake was found at the site of one or several articular and/or periarticular regions. Increased uptake at a given joint was often, but not always, associated with joint pain. It appeared to precede radiologically visible changes. In conclusion, the 99mTc-methylene diphosphonate scan may be of help in the early diagnosis of dialysis amyloidosis.
In long-term haemodialysis patients a new type of amyloidosis composed of beta 2-microglobulin (beta 2-M) has recently been described. The amyloid deposition has a particular predilection for articular structures. In the pathogenesis of this complication markedly elevated plasma beta 2-M concentrations, such as those observed in anuric patients, have a role. However, other as yet ill-defined factors must also be implicated, possible candidates being aluminium intoxication and the widely used regenerated cellulose (cuprophan) membrane. In the present experimental study, we examined tissue distribution of exogenous beta 2-M after i.v. injection of 125I-beta 2-M to bilaterally nephrectomised rats. One hundred and twenty minutes after injection, most radioactivity remained in the vascular compartment. The accumulation in tissues was weak, and no predilection for a particular tissue became apparent. Interestingly, chronically aluminium-overloaded, acutely anephric rats accumulated a significantly greater amount of 125I-beta 2-M in their spleens than anephric rats without prior aluminium intoxication. We then attempted to induce beta 2-M amyloid deposition in rats and mice, some of whom had undergone chronic aluminium intoxication and subcutaneous implantation of regenerated cellulose fragments for various periods of time. They were subsequently made anephric to obtain high plasma beta 2-M concentrations. None of the animals developed beta 2-M amyloidosis in spleen, liver, skin and mechanically altered joint synovium. In conclusion, chronic aluminium intoxication enhances splenic accumulation of exogenous 125I-beta 2-M in anephric rats. The factors required to form beta 2-M-amyloidosis in vivo have still to be defined.
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