Search PubMed⌕ Search

Biomedical subjects

Francis Berenbaum

Publications and source records attributed to Francis Berenbaum.

25 records · Page 2Linked to original sources
PubMed2003

Anti-tumor necrosis factor alpha therapy in fifteen patients with AA amyloidosis secondary to inflammatory arthritides: a followup report of tolerability and efficacy.

OBJECTIVE: Because anti-tumor necrosis factor alpha (anti-TNF) has emerged as a highly effective treatment for numerous inflammatory arthritides, which are a common cause of AA amyloidosis, we retrospectively evaluated the safety and efficacy of anti-TNF in a nationwide study. METHODS: The rheumatology departments of all French teaching hospitals were contacted by mail to obtain the files of patients with histologically proven secondary AA amyloidosis and renal involvement who were treated with anti-TNF. Efficacy was assessed as a sustained decrease in 24-hour proteinuria and a stable/improved glomerular filtration rate (GFR). RESULTS: Among the 15 patients studied, the 24-hour proteinuria was 4.5 +/- 3.6 gm (mean +/- SD), creatininemia was 178.4 +/- 74.9 micromoles/liter, and GFR was 46 +/- 23 ml/minute before starting anti-TNF. Ten patients received infliximab, 4 received etanercept, and 1 received both types of treatment. The mean followup was 10.4 months. No severe adverse events were recorded; one episode of herpes zoster in the first branch of the trigeminal nerve occurred after one infusion of infliximab. Amyloidosis progressed in 7 patients and was stabilized in 5 patients. Three patients (receiving infliximab alone, infliximab plus methotrexate [MTX], or etanercept plus MTX) experienced rapid, dramatic, and sustained decreases in proteinuria (>or=80%), with the GFR increasing 15-78%. CONCLUSION: Anti-TNF was well-tolerated and safe in the 15 patients with AA amyloidosis and renal involvement. The pathogenic role of TNF in AA amyloidosis, the sustained proteinuria decrease in 3 patients, and the stabilization of renal parameters in 5 other patients make anti-TNF a promising candidate to treat AA amyloidosis secondary to inflammatory arthritides.

Adult↗
PubMed2002

Design of a chimeric promoter induced by pro-inflammatory mediators in articular chondrocytes.

We have designed a chimeric promoter that can be stimulated by various pro-inflammatory mediators and so drive the expression of therapeutic genes under inflammatory conditions. The promoter has two parts, the [-247/+20] fragment of the human type IIA secreted phospholipase A2 gene promoter, which is stimulated by the pro-inflammatory cytokine interleukin-1beta (IL-1beta), and a double peroxisome proliferator-activated receptor response element that is activated by some eicosanoids and by non-steroidal anti-inflammatory drugs (NSAIDs). Transfection experiments using rabbit articular chondrocytes in primary culture showed that this chimeric promoter produced a low basal activity and was induced by NSAIDs, WY-14643, IL-1beta, and 15-deoxy Delta12,14 prostaglandin J2. The latter two compounds stimulated the promoter synergistically.

Animals↗
PubMed2002

Differentiation regulates interleukin-1beta-induced cyclo-oxygenase-2 in human articular chondrocytes: role of p38 mitogen-activated protein kinase.

Chondrocyte dedifferentiation has been noted in osteoarthritic cartilage, but the contribution of this phenomenon is poorly understood. Interleukin (IL)-1beta, the major pro-inflammatory cytokine found in osteoarthritic synovial fluid, induces the dedifferentiation of cultured articular chondrocytes, whereas E-series prostaglandins (PGE) are capable of inducing cell differentiation. Since PGE(2) synthesis is up-regulated by IL-1beta, we addressed the question of whether the state of chondrocyte differentiation may influence the production of IL-1-induced PGE(2) by modulating cyclooxygenase (COX)-2 expression. Immortalized human articular chondrocytes, (tsT/AC62) cultured in monolayer after passage through alginate matrix (alg+) produced 5-fold greater amounts of PGE(2) than continuous monolayer cultures (alg-) after stimulation with IL-1beta. Moreover, IL-1beta induced COX-2 expression at 0.01 ng/ml in (alg+) cells, whereas a 100-fold higher dose of cytokine was necessary for stimulation in (alg-) cells. SB203580, a selective p38 mitogen-activated protein kinase (MAPK) inhibitor, completely abolished the IL-1beta-induced COX-2 mRNA. Overexpression of p38 MAPK induces a COX-2 reporter, whereas overexpression of dominant negative p38 MAPK represses IL-1beta-induced promoter expression. Interestingly, IL-1beta-induced p38 MAPK activity was greatly enhanced in (alg+) compared with (alg-) cells. Our results suggest that differentiated articular chondrocytes are highly responsive to IL-1beta and that p38 MAPK mediates this response by inducing COX-2 gene expression.

Alginates↗
PubMed2002

Bone loss in primary biliary cirrhosis: absence of association with severity of liver disease.

OBJECTIVES: The aim of the study was to measure the lumbar bone mineral density in women with primary biliary cirrhosis and to evaluate whether bone mineral density was related to the liver disease, hormonal status and corticosteroid use in these women. METHODS: Bone mineral density of the lumbar spine (L2-L4) was assessed by dual emission X-ray absorptiometry in 40 women with primary biliary cirrhosis. Hormonal, bone and liver status were compared with bone mineral density and analyzed by nonparametric statistical tests. RESULTS: Bone loss was evidenced in women with primary biliary cirrhosis compared with control age-matched women (Z-score: -0.9 SD), 32.5% had osteoporosis and 32.5% had osteopenia. The main risk factor of bone loss was the hormonal status: T-score was -1 SD in premenopausal women, -1.1 SD in postmenopausal women receiving an hormonal replacementtherapy and - 2.7SD in postmenopausal untreated women. There was no statistically significant relationship between bone mineral density and biological and histological liver characteristics. CONCLUSION: Primary biliary cirrhosis-associated bone loss was significantly related to postmenopausal estrogen deficiency, and efficiently prevented by hormonal replacement therapy. Interestingly, the severity of primary biliary cirrhosis was not a determinant factor for bone loss in these women.

Absorptiometry, Photon↗