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Biomedical subjects

J Rossert

Publications and source records attributed to J Rossert.

At least 37 records · Page 2Linked to original sources
PubMed2000

Evaluation of FDG uptake by renal malignancies (primary tumor or metastases) using a coincidence detection gamma camera.

UNLABELLED: The aim of this study was to evaluate the usefulness of FDG scanning using an ordinary gamma camera equipped with coincidence detection (CDET) for 2 renal cancer indications: characterization and staging of renal masses before nephrectomy and search for recurrence after nephrectomy. METHODS: Between September 1997 and June 1998, a whole-body scan and at least 1 tomoscintigram were obtained on 23 occasions in 22 patients (fasting for at least 6 h) using a Prism XP 2000 CDET gamma camera; scanning was begun 45 min after intravenous injection of 150-250 MBq FDG. RESULTS: Postoperative histologic evidence was obtained from 13 of 16 patients who underwent FDG using a CDET gamma camera before renal surgery; 4 renal masses did not accumulate FDG (3 true-negatives, 1 false-negative), whereas 9 renal tumors accumulated FDG (8 true-positives, 1 false-positive). In the other 3 patients, only 1 extrarenal site of FDG uptake was checked and confirmed on histologic examination: a bone metastasis from renal cell carcinoma in 2 cases and lymph node metastasis from a squamous cell carcinoma (3 true-positives). The primary local and regional staging of the malignant renal tumors was accurate in the 9 patients who underwent nephrectomy (8 true-negatives, 1 true-positive). The primary distant staging was positive in 1 case (focus in the chest corresponding to a probable true-positive on follow-up). In the 7 examinations performed because of suspected recurrence of renal cell carcinoma several months after nephrectomy, metastases were visualized by FDG in 4 patients, confirmed by biopsy in 2 patients, and confirmed by conventional imaging or follow-up (or both) in 2 patients. The other 3 patients had negative FDG scans, corresponding to probable true-negative results on follow-up. CONCLUSION: FDG using a CDET gamma camera can be used effectively for the staging and restaging of renal tumors and might be useful for characterization of the primary renal tumor in doubtful cases.

Carcinoma, Renal Cell↗
PubMed2000

[Microscopic polyangiitis].

Microscopic polyangiitis is a non-granulomatous necrotizing vasculitis involving small vessels. Clinical manifestations are highly polymorphic, but rapidly progressive glomerulonephritis is one of the most frequent and most severe manifestations of the disease. Biopsy of an affected organ and detection of circulating anti-neutrophil cytoplasmic antibodies (ANCA) are key elements for the positive diagnosis of microscopic polyangiitis. Biopsies can disclose necrotizing vasculitis affecting small vessels, without granulomas and without immune deposits. ANCA are very specific for microscopic polyangiitis, Wegener's granulomatosis and Churg-Strauss syndrome when they are positive by indirect immunofluorescence and are directed against myeloperoxidase or proteinase 3. Such ANCA are found in about 70% of patients with microscopic polyangiitis. Treatment of severe forms of microscopic polyangiitis is based on the administration of pulse methylprednisolone, oral corticosteroids and cyclophosphamide. In the mildest forms of the disease, one can probably try either to competely avoid using immunosuppressive drugs, or to replace cyclophosphamide with azathioprine. Treatment induces a complete remission of the disease in more than 90% of cases, but about 30% of the patients will experience a relapse, and progressive worsening of renal function can occur in patients with severe chronic renal failure.

Humans↗
PubMed2000

Growth factors, cytokines, and renal fibrosis during the course of diabetic nephropathy.

Diabetic nephropathy is characterised by a progressive accumulation of extracellular matrix within the glomerular mesangium and the interstitium. The pathogenesis of this fibrotic process is still poorly understood, but in vitro and in vivo data suggest that TGF-B plays a key role. Local overproduction of TGF-B could be secondary to a synthesis of diacylglycerol, polyols, or glucosamines. It may also be secondary to an accumulation of advanced glycosylation end-products which modify the functions of neighbouring cells. Moreover, clinical as well as experimental data for TGF-B suggest that angiotensin II has a profibrotic effect; and it has been clearly demonstrated that angiotensin-converting enzyme inhibitors have a beneficial effect in patients with insulin-dependent diabetes mellitus. Other molecules such as endothelin-1, lipid peroxidation products, or IGF-1 may also play a role in this fibrotic process. Finally, heavy proteinuria secondary to glomerular lesions enhances the accumulation of extracellular matrix within the interstitium, probably through modifications of tubular cell functions, thereby inducing the release of pro-inflammatory and profibrotic molecules.

Animals↗
PubMed1998

MPO-ANCA necrotizing glomerulonephritis related to rheumatoid arthritis.

Two patients with rheumatoid arthritis (RA) developed necrotizing crescentic glomerulonephritis with high titers of anti-myeloperoxidase antibodies (MPO) in the absence of overt extrarenal vasculitis. We therefore suggest that in some patients with RA, MPO-ANCA necrotizing glomerulonephritis (GN) may occur as a kidney-limited form of rheumatoid vasculitis, and that RA should be added to the list of diseases potentially associated with necrotizing GN with anti-MPO antibodies. These observations also point out the importance of repeatedly evaluating titers of anti-MPO antibodies in the course of RA, especially if renal impairment or abnormal urinary sediment are present.

Aged↗
PubMed1998

Catastrophic antiphospholipid syndrome. Clinical and laboratory features of 50 patients.

We analyzed the clinical and laboratory characteristics of 50 patients with catastrophic antiphospholipid syndrome (APS) (5 from our clinics and 45 from a MEDLINE computer-assisted review of the literature from 1992 through 1996). Thirty-three (66%) patients were female and 17 (34%) were male. Twenty-eight (56%) patients had primary APS, 15 (30%) had defined systemic lupus erythematosus (SLE), 6 (12%) had "lupus-like" syndrome, and 1 (2%) had rheumatoid arthritis. Mean age of patients in this series was 38 +/- 14 years (range, 11-74 yr). Three (6%) patients developed the clinical picture of catastrophic APS under the age of 15 years, and 11 (22%) were 50 years old or more. In 11 (22%) patients, precipitating factors contributed to the development of catastrophic APS (infections in 3, drugs in 3, minor surgical procedures in 3, anticoagulation withdrawal in 2, and hysterectomy in 1). The presentation of the acute multi-organ failure was usually complex, involving multiple organs simultaneously or in a very short period of time. The majority of patients manifested microangiopathy--that is, occlusive vascular disease affecting predominantly small vessels of organs, particularly kidney, lungs, brain, heart, and liver--with a minority of patients experiencing only large vessel occlusions. Thrombocytopenia was reported in 34 (68%) patients, hemolytic anemia in 13 (26%), disseminated intravascular coagulation in 14 (28%), and schistocytes in 7 (14%). The following antibodies were detected: lupus anticoagulant (94%), anticardiolipin antibodies (94%), anti-dsDNA (87% of patients with SLE), antinuclear antibodies (58%), anti-Ro/SS-A (8%), anti-RNP (8%), and anti-La/SS-B (2%). Anticoagulation was used in 70% of the patients, steroids in 70%, plasmapheresis in 40%, cyclophosphamide in 34%, intravenous gammaglobulins in 16%, and splenectomy in 4%. Most patients, however, received a combination of nonsurgical therapies. Death occurred in 25 of the 50 (50%) patients. In most, cardiac problems seemed to be the major cause of death. In several of these, respiratory failure was also present, usually due to acute respiratory distress syndrome and diffuse alveolar hemorrhage. Among the 20 patients who received the combination of anticoagulation, steroids, and plasmapheresis or intravenous gammaglobulins, recovery occurred in 14 (70%) patients. The use of ancrod and defibrotide appeared to be effective in the 2 respective patients in whom they were used.

Adolescent↗
PubMed1998

[Use of Gadolinium as a contrast agent in the course of renal arterial angioplasty].

For a 72-year-old patient with chronic renal failure, and a renal artery stenosis, we used gadolinium as a contrast agent to perform a digital subtraction arteriography and subsequent arterial angioplasty. Ten ml of gadolinium were used for the arteriography, and during a second procedure 40 ml for the angioplasty, giving high quality images. Renal function remained stable after the procedure, while blood pressure was easier to control.

Aged↗
PubMed1996

A potent far-upstream enhancer in the mouse pro alpha 2(I) collagen gene regulates expression of reporter genes in transgenic mice.

We have identified three DNase I-hypersensitive sites in chromatin between 15 and 17 kb upstream of the mouse pro alpha 2 (I) collagen gene. These sites were detected in cells that produce type I collagen but not in cells that do not express these genes. A construction containing the sequences from -17 kb to +54 bp of the mouse pro alpha 2 (I) collagen gene, cloned upstream of either the Escherichia coli beta-galactosidase or the firefly luciferase reporter gene, showed strong enhancer activity in transgenic mice when compared with the levels seen previously in animals harboring shorter promoter fragments. Especially high levels of expression of the reporter gene were seen in dermis, fascia, and the fibrous layers of many internal organs. High levels of expression could also be detected in some osteoblastic cells. When various fragments of the 5' flanking sequences were cloned upstream of the 350-bp proximal pro alpha 2(I) collagen promoter linked to the lacZ gene, the cis-acting elements responsible for enhancement were localized in the region between -13.5 and -19.5 kb, the same region that contains the three DNase I-hypersensitive sites. Moreover, the DNA segment from -13.5 to -19.5 kb was also able to drive the cell-specific expression of a 220-bp mouse pro alpha 1(I) collagen promoter, which is silent in transgenic mice. Hence, our data suggest that a far-upstream enhancer element plays a role in regulating high levels of expression of the mouse pro alpha 2(I) collagen gene.

3T3 Cells↗
PubMed1995

Separate cis-acting DNA elements of the mouse pro-alpha 1(I) collagen promoter direct expression of reporter genes to different type I collagen-producing cells in transgenic mice.

The genes coding for the two type I collagen chains, which are active selectively in osteoblasts, odontoblasts, fibroblasts, and some mesenchymal cells, constitute good models for studying the mechanisms responsible for the cell-specific activity of genes which are expressed in a small number of discrete cell types. To test whether separate genetic elements could direct the activity of the mouse pro-alpha 1(I) collagen gene to different cell types in which it is expressed, transgenic mice were generated harboring various fragments of the proximal promoter of this gene cloned upstream of the Escherichia coli beta-galactosidase gene. During embryonic development, X-gal staining allows for the precise identification of the different cell types in which the beta-galactosidase gene is active. Transgenic mice harboring 900 bp of the pro-alpha 1(I) proximal promoter expressed the transgene at relatively low levels almost exclusively in skin. In mice containing 2.3 kb of this proximal promoter, the transgene was also expressed at high levels in osteoblasts and odontoblasts, but not in other type I collagen-producing cells. Transgenic mice harboring 3.2 kb of the proximal promoter showed an additional high level expression of the transgene in tendon and fascia fibroblasts. The pattern of expression of the lacZ transgene directed by the 0.9- and 2.3-kb pro-alpha 1(I) proximal promoters was confirmed by using the firefly luciferase gene as a reporter gene. The pattern of expression of this transgene, which can be detected even when it is active at very low levels, paralleled that of the beta-galactosidase gene. These data strongly suggest a modular arrangement of separate cell-specific cis-acting elements that can activate the mouse pro-alpha(I) collagen gene in different type I collagen-producing cells. At least three different types of cell-specific elements would be located in the first 3.2 kb of the promoter: (a) an element that confers low level expression in dermal fibroblasts; (b) a second that mediates high level expression in osteoblasts and odontoblasts; and (c) one responsible for high level expression in tendon and fascia fibroblasts. Our data also imply that other cis-acting cell-specific elements which direct activity of the gene to still other type I collagen-producing cells remain to be identified.

Animals↗
PubMed1995

Pharmacokinetic study of the low-molecular-weight heparin fraxiparin in patients with nephrotic syndrome.

We studied the pharmacokinetics of the low-molecular-weight heparin (LMWH) Fraxiparin in 6 patients with the nephrotic syndrome. Maximal plasma anti-Xa activity was obtained 5 h after a subcutaneous injection of 60 IU anti-Xa/kg. Anti-Xa activity was no longer detectable 24 h postinjection. These results are similar to those obtained with the same dosage in other clinical settings. The biological response to a daily subcutaneous injection of 60 IU anti-Xa/kg was studied for 8 days. No cumulative effect was observed. All the patients had an abnormal activation state of hemostasis mechanisms before treatment, as shown by high prothrombin fragment 1 + 2 and D-dimer levels, which were not decreased by Fraxiparin. It remains to be determined whether a higher dosage of LMWH might attenuate the hypercoagulability in these patients.

Adult↗
PubMed1995

Peripheral-T-cell lymphoma with hemophagocytic histiocytosis localised to the bone marrow associated with inappropriate secretion of antidiuretic hormone.

A patient with high fever, loss of weight and profound pancytopenia is reported. Peripheral T-cell lymphoma with hemophagocytosis was diagnosed. Bone marrow was the only localisation of the lymphoma. At presentation there were (i) a coagulopathy consistent with hemophagocytic histiocytosis (ii) the features of the syndrome of inappropriate antidiuretic hormone secretion (SIADH). These different abnormalities disappeared after chemotherapy and reappeared during each of the 2 periods of disease progression. The patient died 6 months after diagnosis without ever achieving complete remission. As far as we are aware this is the first case report of T-cell lymphoma with hemophagocytic syndrome localised to the bone marrow and associated with SIADH.

Aged↗
PubMed1994

Primary bilateral B-cell renal lymphoma: a case report and review of the literature.

Renal lymphoma is commonly secondary to lymphomatous infiltration of the kidneys in disseminated lymphoma and advanced stage IV disease. We describe a 57-year-old white woman presenting with an acute renal failure due to a bilateral "primary" B-cell lymphoma infiltration of the kidneys. The diagnosis of the lymphoma was made by renal biopsy. The striking feature observed was a destructive infiltration of the kidney by a malignant B-cell lymphoma that left the renal capsule intact, without any sign of secondary localization on the hilar regions. Physical examination did not reveal any peripheral lymphadenopathy or hepatosplenomegaly. A bilateral infiltration of both kidneys was the only feature shown by computed tomography and renal angiography. This case raises the question of the occurrence of a primary B-cell lymphoma in a nonlymphoid organ, which was diagnosed by renal biopsy at a time when the development was exclusively renal in origin.

Female↗
PubMed1994

Pneumocystis carinii pneumonia in the course of connective tissue disease: report of 34 cases.

OBJECTIVE: To determine the circumstances, the clinical features and the outcome of Pneumocystis carinii pneumonia (PCP) in human immunodeficiency virus (HIV)-free patients with connective tissue diseases (CTD). METHODS: Retrospective analysis of all cases referred 10 medical units in the last 10 years. RESULTS: A total of 34 cases of PCP in patients with CTD were studied (Wegener's granulomatosis, n = 12; systemic lupus erythematosus, n = 6; polyarteritis nodosa, n = 4; poly/dermatomyositis, n = 5; others, n = 7). The majority of patients (25/34 patients; 74%) presented PCP during the first 8 months following the diagnosis of CTD. At the time of diagnosis of PCP, most patients (32/34; 94%) were receiving corticosteroids (mean prednisone equivalent dose: 1.2 mg/kg/day) associated in 24 cases with cytotoxic agents (cyclophosphamide, n = 19; methotrexate, n = 5). Most patients were lymphocytopenic at the onset of PCP: 91% (31/34) of patients had fewer than 1.5 x 10(9)/l circulating lymphocytes and 76% (26/34) had fewer than 0.8 x 10(9)/l. The mean duration of prodromal symptoms was 6 days: this is much shorter than for AIDS associated PCP. Half the patients required intensive care for respiratory failure. Mortality was high (11/34 patients; 32%) although deaths were partly due to infections acquired in intensive care units. Among the 23 survivors, 10 (43%) received secondary prophylaxis for PCP and 13 (57%), received the usual therapeutic regimen. No relapse has been observed in either group with a mean followup of 22 months. CONCLUSION: Although rare, PCP must be considered in patients with any type of CTD and receiving cytotoxic agents and corticosteroids, particularly if they are lymphocytopenic. Thus, bronchoalveolar lavage must be rapidly performed in patients with CTD presenting with fever, pulmonary infiltrates, hypoxemia and lymphopenia.

Adult↗
PubMed1993

Mercury-induced autoreactive anti-class II T cell line protects from experimental autoimmune encephalomyelitis by the bias of CD8+ antiergotypic cells in Lewis rats.

Brown-Norway (BN) rats injected with HgCl2 develop a systemic autoimmune disease associated with a polyclonal B cell activation, due to autoreactive T cells specific for self-class II molecules, while Lewis (LEW) rats injected with HgCl2 do not exhibit autoimmunity and develop a non-antigen-specific, CD8-mediated immunosuppression assessed by a depression of T cell functions, and a protection against experimental autoimmune encephalomyelitis (EAE). Resistance to HgCl2-induced autoimmunity is not due to these suppressor cells since treatment with an anti-CD8 monoclonal antibody (mAb) did not allow autoimmunity to appear. The absence of autoimmunity in this strain could result from the absence of autoreactive T cells, or from quantitative or qualitative differences of these cells between susceptible and resistant strains. In the present study, we show that CD4+ anti-class II T cells are present in HgCl2-injected LEW rats and are as frequent as in BN rats when assessed by limiting dilution analysis. LEW CD4+ autoreactive T cell lines were derived. They proliferated in the presence of normal class II-bearing cells, secreted interleukin 2, and did not induce B cells to produce immunoglobulins. Transfer of one of these lines, LEW Hg A, into normal LEW rats led to the appearance of CD8+ cells responsible for a non-antigen-specific immunosuppression that induced complete protection from EAE. Immunosuppression was abrogated after treatment with an anti-CD8 mAb. In vitro, CD8+ cells from rats injected with the LEW Hg A T cell line proliferated in the presence of activated T cells whatever their origin. We conclude that HgCl2 induces CD4+ autoreactive T cells that proliferate in the presence of class II+ cells in susceptible BN as well as in resistant LEW rats. But while these cells collaborate with B cells to produce autoantibodies in BN rats, they initiate in LEW rats a suppressor circuit involving antiergotypic CD8+ suppressor cells.

Animals↗