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Biomedical subjects

J Cledes

Publications and source records attributed to J Cledes.

At least 73 records · Page 4Linked to original sources
PubMed1984

[Current status of Wegener's syndrome. Apropos of 2 cases].

In the context of two recent cases, the authors briefly review the clinical, laboratory and anatomical features of Wegener's granulomatosis and, in particular, its clinical course in response to treatment. These 2 cases include fairly original features: one case presented with abundant haemoptysis with a radiological picture of extensive diffuse bilateral pneumonia; the other case presented with a very large pleural effusion with no E.N.T. involvement whatsoever. The authors then summarise the classical features of this severe form of granulomatous vasculitis, which essentially affects the lungs, the kidneys and the ear, nose and throat. The lesions have a typical histological appearance. The major interest of this disease lies in its treatment. The natural evolution of this disease is very serious with a mean survival of 5 months. However, with immunosuppressant and corticosteroid treatment, a complete remission is obtained and maintained in more than 90% of cases. The therapeutic protocol used, as in one of the present cases, prevents the development of the lesion responsible for the very serious prognosis, irreversible renal failure.

Adult↗
PubMed1983

Low-affinity E-rosette-blocking factor in hemodialysis-treated patients in chronic renal failure.

Enumeration of total E-rosette-forming cells (t-ERFC) enabled 30 renal failure patients on hemodialysis to be classified into three groups: group 1 with normal numbers of t-ERFC, and groups 2A and 2B with reversibly and irreversibly reduced numbers, respectively. Duration of dialysis treatment was the only distinguishing feature between these three groups, being shorter for group 1 than for group 2A (P less than 0.02) and shorter for group 2A than for group 2B (P less than 0.001). However, a rosette-blocking factor (RBF) was demonstrated in all three groups which predominantly affected the low-affinity ERFC (i.e., total ERFC minus active ERFC). This factor could be partially absorbed (P less than 0.01) on normal lymphocytes and showed increased activity after a single dialysis session, suggesting the removal by dialysis of a putative anti-RBF substance.

ABO Blood-Group System↗
PubMed1983

A study of familial lupus erythematosus-like disease and hereditary angio-oedema treated with danazol.

Immunological and genetic studies were performed in a family in which the mother and five siblings had hereditary angio-oedema (HAE). LE cells, antinuclear factors, antibodies to double-stranded DNA and positive direct Coombs' test were not found in any of the subjects. One female sibling had a lupus erythematosus-like illness with skin lesions of the face which responded to danazol treatment. Laboratory evidence of HAE was obtained in the entire kindred and all the siblings shared HLA haplotype AIB7 inherited from the deceased mother.

Adolescent↗
PubMed1983

[Pulmonary silicosis and disseminated lupus erythematosus].

In a 59-year old sand-blaster, histologically proven silicosis was complicated by systemic lupus erythematosus (SLE) and focal glomerulonephritis with IgG, IgA and ClQ deposits. Nothing likely to facilitate SLE was detected by investigating the familial background, the HLA phenotype and the complement system. This type of SLE differs from drug-induced lupus-like syndromes by a high level of anti-double helix DNA antibodies and by the renal lesions observed. The connection between silicosis and SLE lies in changes in humoral immunity, i.e. polyclonal activation and production of antinuclear antibodies. A decrease in the number of suppressor T-cells may also be held responsible.

Humans↗
PubMed1982

[Mytomycin C nephrotoxicity. 3 new cases and review of the literature].

Three women with adenocarcinoma of cardia, adenocarcinoma of liver or ileum carcinoid tumor, respectively, were treated with mitomycin C (MMC) and 5-fluoro-uracil (5-FU). Two patients had renal impairment 6 and 11 months, the third as early as 8 weeks after initiation of MMC therapy. In the three cases, blood transfusions appeared to play an aggravating role inducing respiratory distress, microangiopathic hemolytic anemia and thrombocytopenia, and to accelerate progression of renal failure. Death occurred in the first patient; terminal renal insufficiency necessitated hemodialysis treatment in the second, and after 10 plasma exchanges, renal failure remained stable in the third. Light and electron microscopy study of the kidney revealed renal lesions compatible with thrombotic microangiopathy in all cases. Mesangiolysis with swollen nuclei of endothelial cells in most glomeruli was also seen in two cases. We compared our observations with the findings found in 30 previously reported cases. These observations substantiate the renal toxicity of mitomycin C.

Adenocarcinoma↗