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Biomedical subjects

J P Mery

Publications and source records attributed to J P Mery.

At least 19 recordsLinked to original sources
PubMed1991

Induction of tumour necrosis factor-alpha during haemodialysis. Influence of the membrane type.

Some of the secondary clinical effects induced by long-term haemodialysis in patients with end-stage renal failure have been related to an increased production of interleukin-1 (IL-1). We investigated the role of another cytokine which shares a number of biological properties with IL-1, tumour necrosis factor-alpha (TNF-alpha). In long-term haemodialysed patients, we found at the beginning of the dialysis increased plasma TNF-alpha levels and enhanced monocyte capacity to produce TNF-alpha spontaneously ex vivo. Non-haemodialysed uraemic patients also presented increased plasma TNF-alpha levels. During dialysis with cellulose acetate (CA) or polysulphone (PS) membranes, plasma TNF-alpha levels and the spontaneous and lipopolysaccharide-induced production of TNF-alpha by monocytes remained at predialysis levels. In contrast, when cuprophane membranes were used, there was a significant increase in plasma TNF-alpha levels and in both spontaneous (10-fold) and lipopolysaccharide-induced (seven-fold) ex vivo TNF-alpha production by monocytes. These results suggest that monocytes are stimulated during haemodialysis with the poorly biocompatible cuprophane membrane.

Adult↗
PubMed1989

Immunoblotting profiles in 55 systemic lupus erythematosus sera lacking precipitating antibodies to extractable nuclear antigens.

Serum samples from 55 patients with systemic lupus erythematosus (SLE) were selected for the absence of anti-extractable nuclear antigen antibodies after routine immunodiffusion tests. These sera were immunoblotted for anti-Sm and anti-RNP antibodies on a HeLa cell nuclear extract. Ten (18%) were negative and 45 (82%) produced complex patterns: 10 (18%) suggestive of anti-Sm, three (5%) anti-RNP, and 32 (58%) a combination of anti-Sm and anti-RNP antibodies. These data were very similar to those obtained from sera from a control group of 28 SLE sera selected for positivity of anti-Sm and anti-RNP precipitins with the immunodiffusion test. IgM isotype antibodies to the D peptide were significantly more prevalent than IgG isotype antibodies, whereas antibodies to the 68 kD polypeptide were of both IgM and IgG isotypes. Sera with an anti-Sm/RNP immunoblotting pattern stemmed from a group of patients with SLE with a higher titre of anti-dsDNA antibodies. Among clinical symptoms, the incidence of haemolytic anaemia was higher in the group of patients with the anti-Sm immunoblotting profile. Patients with an anti-RNP immunoblotting profile showed a higher incidence of cutaneous symptoms. It is concluded that immunoblotting for anti-Sm or anti-RNP antibody determination is a very sensitive diagnostic tool in patients with SLE.

Adult↗
PubMed1987

[Components of the classical complement pathway in systemic lupus erythematosus].

Measurements of complement components in sera from patients with systemic lupus erythematosus (SLE) and some of their relatives indicated that decreased levels of CH50, C4 and C2 were mostly related to a genetic deficiency at one or both of the loci coding for C4, at least in those patients in whom decreased C4 levels were associated with normal C1 hemolytic activity. C4 deficiency is either isolated or associated with complement activation. In some patients with C4 deficiency, complement activation could only be demonstrated by measuring plasma level of the C3 cleavage fragment, C3a des Arg. Decreased concentration and/or hemolytic activity of C4 and C2 in SLE cannot be used to assess the activity of the disease.

Complement Activation↗
PubMed1986

Anti-C3b-receptor (CR1) antibodies in patients with systemic lupus erythematosus.

Using an enzyme-linked immunoadsorbent assay, IgG in the plasma and purified IgG from 2 patients with systemic lupus erythematosus (SLE) were found to strongly react with purified C3b receptor (CR1) insolubilized on microtiter plates. The amount of IgG that bound to CR1 in 201 plasma samples from 179 other patients with SLE did not significantly differ from that which bound in 72 control samples from normal individuals. Purified IgG from the patients with anti-CR1 reactivity did not inhibit CR1 function in vitro. The number of CR1 antigenic sites expressed on erythrocytes from both patients was much lower than that observed in a normal population and in the lowest range of the decreased numbers found in patients with SLE. The occurrence of anti-CR1 antibodies in patients with SLE could provide an acquired mechanism for decreased expression of CR1 through antigenic modulation of the receptor on precursor cells and/or alter the function of cells of the immune system bearing C3b receptors.

Animals↗
PubMed1986

[Vesical amyloidosis. Apropos of a case and a review of the literature].

A case of primary localized amyloidosis of the bladder in a 60 years old male is described. The initial symptom was hematuria. Cystoscopy revealed a redish angioma-like lesion on the trigone, and the diagnosis was pointed out with biopsy, complementary data, and a close follow-up during two years. In the literature we found 47 cases of primary localized amyloidosis of the bladder and 10 others cases of amyloidosis of the bladder which were part of generalized amyloid disease. The interest of the Wright's special staining method is underlined specifying, on light microscopic study, the AA or AL type of the amyloid disease.

Amyloidosis↗
PubMed1983

Immunopathological studies of polyarteritis nodosa and Wegener's granulomatosis: a report of 43 patients with 51 renal biopsies.

Although it is generally considered that vasculitis of the polyarteritis nodosa (PAN) group and Wegener's granulomatosis (WG) is immune complex (IC) mediated, there are no simultaneous data on circulating IC, complement levels and deposits of Ig and complement in the kidney. Therefore we have performed a retrospective study of 43 patients suffering from PAN and WG. Ig glomerular deposits were uncommon and scanty, except in two patients with WG; C3 deposits were detected in 12 patients, whereas fibrinogen was constantly found when lesions were recent and active. Similar data were obtained for the renal vessel walls. Contrasting with these results, rheumatoid factors and cryoglobulins, suggestive of the presence of circulating IC, were detected respectively in nine of 39 and seven of 37 patients, and IC 'activity' assessed by the Raji cell assay and the Clq binding assay was found respectively in six of 17 and nine of 10 patients before treatment, and in none of 10 and five of seven patients in remission. Haemolytic complement activity and complement components were never decreased, but the C3d breakdown product of C3 was elevated in all the eight patients studied before treatment. Signs of persistent hepatitis B virus (HBV) infection were detected in five of 25 patients of the PAN group, whereas three of eight patients with WG had only anti-HBV antibodies. Furthermore, cytomegalovirus (CMV) could be isolated from the blood in a case of WG before the treatment was started. Persistent interferonaemia was detected in one of five patients. These results suggest either that renal deposition of CIC is transient, the paucity of Ig deposits being due to rapid clearance of IC by phagocytic cells; or alternatively that vascular and glomerular lesions are not caused by CIC, as in some cases of experimental vasculitis induced by infectious agents.

Adolescent↗
PubMed1983

Acute interstitial nephritis due to drug hypersensitivity. An up-to-date review with a report of 19 cases.

The clinical, biologic, and pathologic features and the course and treatment of acute interstitial nephritis (AIN) due to drug hypersensitivity are reviewed. The authors report 19 additional cases of AIN, outlining some particular and unusual features. The drugs most often responsible now are penicillins and cephalosporins, cotrimoxazole, thiazide diuretics, glafenin and its derivatives, and nonsteroid anti-inflammatory agents. Diagnosis of AIN should be considered in any case of rapidly progressive renal failure occurring during drug therapy, especially when fever, skin rash, arthralgias, macroscopic hematuria, and blood or urinary eosinophilia are present. In the absence of the preceding symptoms, systematic early renal biopsy may be helpful to detect intersitial infiltrates containing lymphocytes, plasma cells, and eosinophils and/or granulomas with epithelioid cells. Immunologic tests are inconstantly positive. Their sensitivity and specificity often are doubtful in the absence of precise knowledge of the pathogenetic factors involved. Recovery may be hastened in some cases by corticoid therapy. Recurrence of the disease will be avoided by definitive suppression of offending and related drug(s).

Acute Disease↗
PubMed1983

Drug-induced granulomatous interstitial nephritis.

Among 22 cases of drug-induced acute interstitial nephritis (AIN), noncaseating interstitial granulomas were found in eight cases (36%). Acute renal failure (ARF), oliguric in three patients, appeared within 1-20 days after the beginning of therapy. Clinical symptoms suggesting a hypersensitivity reaction were unusual, marked blood eosinophilia was absent, and immunologic tests were inconstantly positive. The discovery of interstitial granulomas may be a clue to the diagnosis of drug-induced AIN, especially when the inflammatory infiltrates do not contain eosinophils. Since significant residual renal impairment may be observed the benefit of early steroid therapy must be debated.

Adolescent↗
PubMed1982

[Bacterial endocarditis on a mitral prosthesis with negative blood cultures. Case evolving over a 3 year period in the absence of fever].

A 38 year-old man, operated upon two years previously for combined mitral and tricuspid valve disease of rheumatic origin, presented with signs of a severe biological inflammatory syndrome, and a mild proliferative glomerulonephritis (normal complement with exclusively mesangial deposits of IgM, Clq, and C3 on immunofluorescence), which developed slowly over a period of 3 years in the absence of any fever. Blood cultures were always negative, and prolonged antibiotic therapy on two occasions had no effect on the clinical or biological picture. Mitral prosthesis replacement was necessary 6 months after the onset of the affection, a second leakage 16 months later leading to rapidly fatal heart failure. Pathological examination confirmed the presence of an endocarditis at the zone of insertion of the prosthesis. The slow progression of the disorder in this case, and the absence of fever, emphasize diagnostic difficulties of certain cases of endocarditis, due to low virulence germs, that progress under cover of a generalized disease of renal expression. The value of renal biopsy, which provided almost specific indications in the present case, is also stressed.

Adult↗
PubMed1980

Synthesis of abnormal heavy and light chains in multiple myeloma with visceral deposition of monoclonal immunoglobulin.

In a patient treated for IgA kappa myeloma, bone marrow relapse and a sharp drop in the serum IgA level paralleled tissue deposition of non-amyloid material reactive with anti-kappa anti-alpha sera in immunofluorescence studies of kidney and liver biopsies. Clinical manifestations were progressive renal failure with nephrotic syndrome, with both tubular and glomerular lesions (including nodular glomerulosclerosis), hepatomegaly, cardiac and neurological symptoms. Biosynthesis experiments showed the production of alpha chains diminished in length by about one domain which were rapidly degraded predominantly after secretion and of two species of light chains; normal-sized light chains which assembled with alpha chains and abnormally short ones which were secreted as free light chains. The apparent molecular weight of the light chains was larger in secretions than in cytoplasmic extracts, suggesting their glycosylation. These results suggest a causal relationship between tissue deposition and production of abnormal immunoglobulins by a variant clone, the emergence of which was possibly induced by Melphalan therapy.

Bone Marrow↗
PubMed1977

[Successive connective tissue diseases (scleroderma, then lupus). Clinical and biological study of 4 cases].

The authors present 4 patients who had suffered for several years from isolated systemic scleroderma and in whom, after 3, 10, 19 and 22 years, clinical, biological and histological signs of DLE appeared. There was no current further progression of the scleroderma in two cases, at the time of onset of DLE. In the oter two cases, it had disappeared. All four patients had a serum cryoglobulin. In all cases the kidneys were involved histologically : extra membranous glomerulitis in one, segmental glomerulitis in a second, and diffuse progressive glomerulitis in the last two. The authors analyse the biological changes which accompanied the clinical transformation. One of the patients had anti-ribonucleoprotein antibodies. She died from severe renal involvement which would be against the good prognosis usually associated with the presence of this type of antibody.

Adult↗