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Biomedical subjects

J Laurent

Publications and source records attributed to J Laurent.

At least 91 records · Page 5Linked to original sources
PubMed1988

Renal survival in membranoproliferative glomerulonephritis (MPGN): role of long-term treatment with non-steroid anti-inflammatory drugs (NSAID).

The renal survival of 53 MPGN patients treated on a long-term basis by non-steroid anti-inflammatory drugs (NSAID) was compared to that of untreated MPGN patients previously reported in the literature. The difference between NSAID-treated and untreated patients (Habib's and Legrain's series) was significant by chi-square and logrank test performed during 10 and 14 years of follow-up. Our results were not significantly different from those observed by West in 45 MPGN children treated by steroids alone or in association with cytotoxic agents. After a follow-up of 14 years, 21 among our NSAID patients were in renal survival and 8 in end-stage renal disease (ESRD). They were respectively 11 and 3 in West' series, and for the untreated groups, 4 and 19 in Legrain's series and 1 and 33 in Habib's series.

Adolescent↗
PubMed1988

Postradiation meningioma in a child.

Tumors caused by radiation treatment are not unknown. They may be benign or malignant. Among these, postradiation meningiomas (PRM) are considered to be a distinct entity. A case of a child who developed a PRM is presented. She received radiation therapy for a presumed thalamic glioma 11 years earlier. An unusual and interesting aspect of this tumor was its attachment to the membrane of the old subdural hematoma, following a shunting procedure. There was no dural attachment. The pathology of PRMs and meningiomas in children are discussed in light of our recent experience.

Brain Neoplasms↗
PubMed1988

Enhanced beta 2-microglobulin levels in lymphocyte culture supernatants from patients with idiopathic nephrotic syndrome: inhibition of lymphocyte activation by cyclosporine.

Idiopathic nephrotic syndrome (INS) is associated with a disorder of T-lymphocyte function, and an enhanced production of a vasoactive lymphokine, the vascular permeability factor (VPF). In an attempt to evaluate lymphocyte activation in various phases of INS, we measured beta 2-microglobulin (beta 2m) levels in lymphocyte culture supernatants (LCS). In 23 cases of untreated active INS, beta 2m levels in unstimulated LCS were significantly increased in comparison with those of 13 cases of untreated INS in complete remission (p less than 0.001), of 17 cases of active membranous nephropathy (p less than 0.01) and of 14 controls (p less than 0.001). In 13 patients treated with cyclosporine (Cs) (3-4.5 mg/kg/d) during 3 months, beta 2m levels were within the normal range. Although the beta 2m of 7 Cs patients without proteinuria was lower than 5 Cs patients with residual proteinuria, the difference was not statistically significant. In 15 prednisone(Pr)-treated INS patients, beta 2m levels were normalized. However their beta 2m levels were lower in 8 cases of complete remission than in 7 cases of persistent proteinuria (p less than 0.05). Concanavalin-A stimulation increased beta 2m amounts in all groups with a similar magnitude. In vitro addition of Cs (100 ng/ml) inhibited both beta 2m and VPF elevations observed in active INS. beta 2m level and VPF activity were significantly correlated (r = 0.54, p less than 0.01). High levels of beta 2m in LCS from INS are the consequence of an enhanced cellular synthesis and they are inhibited by Pr and Cs. Thus beta 2m increase in INS indeed reflects lymphocyte activation.

Adolescent↗
PubMed1988

[Idiopathic nephrotic syndrome and food hypersensitivity. Value of an exclusion diet].

A case of idiopathic nephrotic syndrome (INS) evolving since more than 7 years with 4 successive corticosensitive relapses is reported. At the time of a 5th relapse corticosteroid treatment was refused by the parents and evolution went on without any spontaneous tendency to remission. Three months later, allergy tests detected various sensitizations, especially for food allergens. An antiallergic treatment including dietary exclusions induced a complete and durable remission. Five similar cases are reported. These facts, compared to data from the literature, indicate the possible role of food hypersensitivity in INS. Its mechanism has been discussed; the possible part of a lymphocyte activation has been emphasized.

Adrenal Cortex Hormones↗
PubMed1987

Altered C1 inhibitor genes in type I hereditary angioedema.

Hereditary angioedema is an inherited disease transmitted as an autosomal dominant trait and characterized by deficient activity of C1 inhibitor, a glycoprotein that limits intravascular activation of complement. The unavailability of markers for the C1 inhibitor locus has so far precluded access to the genetic bases of the disorder. Using a recombinant-DNA probe for the C1 inhibitor gene, we identified a cluster of four distinctive DNA restriction sites in a multigeneration family. The strict cosegregation of these markers with a low C1 inhibitor level supports the conclusion that a defective structural gene is responsible for the disease. The occurrence of distinct DNA markers in patients from unrelated kinships indicates that, like forms of the condition displaying dysfunctional C1 inhibitor variants, those characterized by protein deficiency are also genetically heterogeneous. Although multiple restriction-site changes in the C1 inhibitor gene are carried by certain patients, DNA markers for this locus are strikingly infrequent among normal persons. These findings indicate that the gene alterations responsible for hereditary angioedema arise more often from DNA rearrangements than from nucleotide substitutions. Such variations in the structure of the C1 inhibitor gene may provide the basis for early and direct identification of persons at risk.

Angioedema↗
PubMed1987

[Hereditary angioneurotic edema. Treatment of a pseudosurgical digestive attack with C1 inhibitor concentrate].

Although anabolic androgens can be used to prevent acute attacks of hereditary angioneurotic oedema, these are still observed. When they are severe, and even more so when they involve the larynx or the abdominal viscera, an emergency treatment is necessary, ideally with the purified C1-inhibitor (C1-INH) administered by intravenous infusion. In a case with pseudo-surgical abdominal symptoms, this treatment was followed by an unusually dramatic regression of all symptoms. Serial laboratory examinations showed an increase in C1-INH and C2 plasma levels and in the number of basophils within less than 30 minutes; the increase in C4 levels occurred later. Thus, C1-INH is very effective in the treatment of acute hereditary angioneurotic oedema, but the product is not widely available; it should be reserved to severe forms affecting the larynx and the viscera.

Abdomen, Acute↗
PubMed1987

[Membranoproliferative glomerulonephritis associated with Buckley's syndrome treated with cyclosporin].

A 38-year old patient had been suffering, since the age of 17, from membranoproliferative glomerulonephritis associated with chronic atopic eczema and recurrent sinusitis. Bouts of eczema with severe itching occurred simultaneously with sinusitis and proteinuria. Permanently extreme serum IgE levels (greater than 10,000 IU/ml), defective neutrophil chemotaxis and monocyte phagocytic function (Buckley's syndrome) were present. Because cyclosporin reduces excessive IgE levels in Brown Norway rats with mercuric chloride nephritis, we gave the patient this drug in daily doses of 3-4 mg/kg. A dramatic improvement resulted within a few days: itching disappeared, the eczema progressively cleared, proteinuria decreased to less than 0.5 g/day and serum IgE levels to 4000 KIU/l. Reduction of dosage was followed by recurrence of all clinical and biological signs. In spite of the improvement obtained, serum creatinine levels, which were initially high (200-250 mumol/l) rose up to 300 mumol/l after one year of treatment.

Adult↗
PubMed1987

An increase in circulating IgA antibodies to gliadin in IgA mesangial glomerulonephritis.

In IgA glomerulonephritis (GN), the pathogenic role of IgA is well documented, but the specificity of these IgA is unknown. Cases of celiac disease associated with IgA GN have been reported and led us to investigate the role of gliadin sensitivity. We measured IgA, IgG and IgM antibodies to gliadin, beta-lactoglobulin and ovalbumin by ELISA (results expressed as optical density; OD) in 27 patients with primary IgA GN, 14 with membranous GN (MGN), 21 with idiopathic nephrotic syndrome (INS) and 21 healthy controls. The normal value for antigliadin IgA was less than 0.650 OD. 19/27 patients with IgA GN had a raised level versus 2/14 in MGN and 2/21 INS (p less than 0.001: IgA GN vs. MGN, INS and controls). Antibodies to beta-lactoglobulin were rarely found and were not more frequent in IgA GN. Cross-reactivity with reticulin was investigated in 16 patients who were serum-positive for IgA antigliadin: no reticulin antibodies were detected by immunofluorescence. Antigliadin IgA are of diagnostic value for distinguishing IgA GN from other GN, with a sensitivity of 70%, a specificity of 89%, a positive predictive value of 83% and a negative one of 79%.

Adult↗
PubMed1987

Diclofenac, a nonsteroidal anti-inflammatory drug, decreases proteinuria in some glomerular diseases: a controlled study.

Treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) was first used in glomerulonephritis (GN) in 1966 but its efficiency is still debated. We studied the antiproteinuric effect of such a treatment in a double-blind study. 29 GN patients with normal renal function (17 membranoproliferative GN, 12 IgA GN) were randomly assigned to receive 100 mg/day of diclofenac or placebo for at least 2 months. There was a significant antiproteinuric effect of diclofenac versus placebo with a fall of 70% in the diclofenac group versus 6% in the placebo group (p less than 0.001 with the Mann-Whitney test). The median was 3 mg/min at onset and 2.45 mg/min after 2 months treatment with the placebo. In the diclofenac group, it was 2.2 and 0.95 mg/min, respectively (p less than 0.01). Diclofenac did not significantly increase creatinine levels. Gastric irritation was noted only once. This study establishes the short-term antiproteinuric action of diclofenac. Whether this action affects the final outcome is not yet determined.

Adolescent↗