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Biomedical subjects

D Droz

Publications and source records attributed to D Droz.

At least 127 records · Page 7Linked to original sources
PubMed1981

Systemic lambda light-chain deposition in a patient with myeloma.

Systemic lambda light-chain deposition occurred in a 73-year-old man with myeloma. An initial renal biopsy specimen showed the features of myeloma kidney. When he died 22 months later lambda light chains were detected by immunofluorescence in kidneys, liver, spleen, and heart. They were probably responsible for cardiac dysfunction and the fatal arrhythmia. It is suggested that in this patient deposition was due to a structural alteration of the light chains, possibly induced by cyclophosphamide.

Aged↗
PubMed1981

Clq deposits at the dermoepidermal junction: a marker discriminating for discoid and systemic lupus erythematosus.

Discoid lupus (DL) and systemic lupus erythematosus (SLE) patients have been comparatively evaluated for complement and immunoglobulin deposits at the dermoepidermal junction (DEJ) by immunofluorescence (IF). When IF was positive, Clq deposits were quasi-constantly found in SLE patients with or without skin lesions (90%), while Clq was found in only 29% of the DL patients. Of the 42 DL patients followed-up to at least 2 years, 4 have eventually evolved a systemic disease. In these 4, neither cryoglobulinemia nor significant titers of ANA had been found at the time of presentation. Only 1 of these 4 patients had initially circulating immune complexes (P.E.G) and a positive IF in a normal sunprotected area. Clq deposits at the DEJ were present in all these 4. Of the remaining 38 DL patients, none has progressed to SLE: 8 had had significant titers of ANA, 5 had had circulating immune complexes, and 3 others had had cryoglobulinemia. Thus Clq deposits in DL cases are associated with a relatively high incidence of eventual systemic disease. Taken together, these data suggest that Clq deposits in skin may be a marker for systemic lupus.

Adolescent↗
PubMed1980

[Immunological tests as guide-lines for the treatment of systemic lupus erythematosus (author's transl)].

Sixty-five patients with systemic lupus erythematosus were followed up for periods of 8 to 48 months. Sixty-six clinical exacerbations of the disease were observed and treated with various, non-randomized therapeutic regimens. The relationship between the results of immunological tests (DNA binding rate, serum levels of C3 and C4, presence of immune complexes and number of E rosettes) and the clinical and histological changes detected during treatment with corticosteroids or immunosuppressants was studied. In most cases a correlation was found between clinical and histological activities and the intensity of immunological reactions. Immunological abnormalities usually preceded clinical exacerbations but were rarely seen in patients with stable remission. However, exceptions occurred, which limit the value of these tests as sole therapeutic guide-lines in systemic lupus erythematosus.

Adolescent↗
PubMed1980

Effect of long-term treatment with circulating thymic factor on murine lupus.

Mice from three different strains (NZB, B/W, and Swan) which spontaneously develop a lupus-like disease and show a premature decline of their secretion of the circulating thymic factor, Facteur Thymique Sérique (FTS), were treated repeatedly with FTS and followed for the evolution of their autoimmune disease. The autoimmune sialoadenoitis (Sjögren's syndrome) appearing in NZB and B/W mice, evaluated here by a scintigraphic method, was completely prevented or even cured by FTS treatment. The increase in anti-erythrocyte autoantibody production was transiently delayed in aged NZB mice. Conversely, antiDNA antibody production either remained unaffected or was accelerated (in B/W mice) by FTS treatment. These results demonstrate that the restoration of the failing thymic secretion does influence autoantibody production, in a manner depending primarily on the autoantigen eliciting the autoimmune response. However, caution is urged in the application of this approach to human lupus without further studies.

Age Factors↗
PubMed1980

The dense deposits disease of the renal basement membranes.

Dense-deposits disease is characterized by an original morphological aspect of the renal basement membranes which have an electron-dense appearance. The immunofluorescence studies showed C3 alone in kidney. Low serum C3 levels and the presence of C3 NF activity have been detected in this disease, demonstrating an activation of the complement alternative pathway. The observation of recurrence in transplanted kidneys contributed to establish the sequence of the morphological events and showed the dissociation between the serological complement profiles and the lesions. Although the nature of the dense deposits remains still unknown, the altered membranes are recognized by at least some anti-GBM antibodies.

Antigens↗
PubMed1980

Dense deposit disease with rapidly progressive renal failure in a narcotic addict.

A girl aged 17 developed a nephrotic syndrome with renal insufficiency after narcotic abuse. Renal biopsy showed a diffuse glomerulonephritis with crescents and dense deposits within the glomerular basement membrane; glomerular C3 deposits were present without immunoglobulin. The serum complement profile was typical of activation via the alternative pathway, and tests for C3 nephritic factor were strongly positive. Terminal renal failure occurred within 6 months and required chronic hemodialysis. It is likely that the narcotics used or their contaminants were responsible for the renal damage, presumably by activating the complement system via the alternative pathway.

Adolescent↗
PubMed1979

Immunologically-mediated acute renal failure of nonglomerular origin in the course of systemic lupus erythematosus [SLE]. Report of two cases.

Acute anuric renal failure was observed in two patients with systemic lupus erythematosus (SLE) during the clinical and serologic active phase of the disease. Renal biopsies, performed during the acute episodes, showed only mild and focal mesangial cell proliferation without deposits. In contrast, tubulointerstitial lesions were predominant. Intense granular immune deposits along the tubular basement membrane, or immunofluorescence examination, were suggestive of immune complex deposition. One of these patients had severe high blood pressure and vascular lesions likely induced by immune complexes. In both, renal function was recovered. Immunologically-mediated tubular and vascular lesions in the course of SLE are discussed.

Acute Kidney Injury↗
PubMed1979

Recurrence of dense deposits in transplanted kidneys: I. Sequential survey of the lesions.

Serial specimens from transplanted kidneys were obtained in 11 patients with dense deposit disease (DDD). The recurrence of DDD was obvious in 9 patients and appeared very early after grafting. Three different types of evolution of the lesions were observed. In 4 patients no modification of the lesions occurred with time, and in 2 of them the dense alteration alone persisted without any other glomerular changes. In 3 patients a progression of the lesions was observed, whereas a regression occurred in 1 other patient. From these observations the following sequence of the morphologic changes can be proposed: the dense alteration appears first and constitutes the specific marker of that disease; the C3 deposition in the kidney occurs later following the appearance of the dense lesion.

Basement Membrane↗
PubMed1979

Recurrence of dense deposits in transplanted kidney: II. Serum complement and nephritic factor profiles.

Dense deposit disease of the kidney is a rare form of chronic glomerulonephritis frequently associated with serum complement abnormalities (low C3 levels) and a circulating C3 convertase activator of the alternative pathway, the C3 nephritic factor (NF). Eleven patients with end-stage dense deposit disease underwent kidney transplantation. Of the 11, 7 had pretransplant low C3 and NF. In the posttransplant period, persisting low C3 levels were associated with persisting NF, although not quantitatively so. The original glomerular lesion recurred in the graft within 6 months in 9 of 11. Of these 9, 2 had no complement abnormalities either prior to or after transplantation. Pretransplant complement abnormalities were rapidly corrected in 4 of 7 patients whether or not recurrence of the original lesion occurred. Thus, serum complement profiles before and after transplantation are neither predictive nor indicative of recurrence.

Complement C3↗
PubMed1979

The role of circulating immune complexes in the glomerular disease of experimental hepatosplenic schistosomiasis.

The serological and renal changes were studied simultaneously in 115 mice infected with Schistosoma mansoni. IgG and IgM, but not IgA anti-S. mansoni antibodies were detected in the sera, together with circulating immune complexes containing schistosomal antigen. Glomerular mesangial deposits of IgA, IgM and C3 were observed. Despite the strong correlation observed between the occurrence of the circulating immune complexes containing schistosomal antigen and the glomerular deposits, results concerning the behaviour of IgA suggest that portal hypertension and liver damage have a role in the pathogenesis of glomerular lesions.

Animals↗