[Rapidly progressive ANCA positive glomerulonephritis as the presenting feature of infectious endocarditis]. / Glomérulonéphrite rapidement progressive à ANCA révélant une endocardite infectieuse subaiguë

The association of positive cytoplasmic antineutrophil antibody (ANCA) necrotizing crescentic glomerulonephritis with endocarditis raises diagnostic issues. Indeed, it is often difficult to determine if the kidney injury is either secondary to an infectious disease or caused by an ANCA-associated small vessel vasculitis. We report a 59-year-old man admitted in nephrology for acute glomerular syndrome in whom the renal biopsy showed a crescentic necrotizing glomerulonephritis. A diagnosis of vasculitis was initially considered in the presence of high titer of ANCA (anti-proteinase 3). Because of associated Staphyloccocus aureus endocarditis the patient received both corticosteroids and antibiotics that allowed remission of both kidney injury and endocarditis. The renal presentation and the disappearance of ANCA support the infectious etiology of this glomerulonephritis rather than an ANCA-associated small vessel vasculitis. It is important to be cautious in the presence of ANCA positive extracapillary glomerulonephritis and endocarditis should be ruled out before initiation of corticosteroids that may be nevertheless necessary in severe acute glomerulonephritis.

Prospective randomized comparison between redon catheters and chest tubes in drainage after cardiac surgery.

AIM: To compare in a prospective randomized study chest tube (CT) and redon drains (RD) for effectiveness, cost, pain and complications after heart surgery using cardiopulmonary bypass. METHODS: Forty patients undergoing heart surgery were analyzed prospectively. Twenty patients had small RD with strong (-700 mmHg) vacuum and 20 others standard CT. All patients had patient controlled analgesia in the postoperative period and pain was noted. Residual pericardial effusion (RPE) was controlled and quantified at postoperative day 7 with transthoracic echocardiography. Drainage complications were noted and compared in both groups. RESULTS: Surgical statistics were comparable in both groups. Two patients underwent reoperation in CT for clotting, and 1 in RD for active surgical bleeding. One patient had orifice infection in CT. Drainage volumes and times were comparable in both groups at removal (992+/-507 ml in RD, 1154+/-571 ml in CT, p=ns). Morphine consumption and pain estimation were comparable in both groups in the postoperative period and at drainage removal. Echographic control showed important RPE for 3 patients in both groups. System cost was higher in CT compared to RD (up to 7 times). CONCLUSION: RD are comparable to CT in terms of drainage, pain and complications. Nevertheless, they offer better handling and removal conditions and limited cost.

Multiple atherosclerotic plaque rupture in acute coronary syndrome: a three-vessel intravascular ultrasound study.

BACKGROUND: To test the hypothesis of general atherosclerotic plaque destabilization during acute coronary syndrome (ACS), the present study sought to analyze the 3 coronary arteries by systematic intravascular ultrasound scan (IVUS). METHODS AND RESULTS: Seventy-two arteries were explored in 24 patients referred for percutaneous coronary intervention after a first ACS with troponin I elevation. Fifty plaque ruptures (mean, 2.08 per patient; range, 0 to 6) were diagnosed by the association of a ruptured capsule with intraplaque cavity. Plaque rupture on the culprit lesion was found in 9 patients (37.5%). At least 1 plaque rupture was found somewhere other than on the culprit lesion in 19 patients (79%). These lesions were in a different artery than the culprit artery in 70.8% and were in both other arteries in 12.5% of these 24 patients. Complete IVUS examination of all 3 coronary axes in patients who had experienced a first ACS revealed that multiple atherosclerotic plaque ruptures were detected by IVUS; these multiple ruptures were present simultaneously with the culprit lesion; they were frequent and located (in three quarters of cases) on the 3 principal coronary trunks; and the multiple plaque ruptures in locations other than on the culprit lesion were less severe, nonstenosing, and less calcified. CONCLUSION: Although one single lesion is clinically active at the time of ACS, the syndrome seems nevertheless associated with overall coronary instability.

Cell biotinylation provides a sensitive and effective detection technique for cellular adhesion assays: comparison with existing methods.

A simple, sensitive, colorimetric labelling method was devised to quantify cell adhesion, based on labelling the cell plasma membrane with biotin. This method was applied in adhesion assays, which involved the adherence of biotin-labelled, PMA-stimulated, U937 cells. These cells resemble monocytes, and were bound onto fibronectin-coated wells and to an ECV304 cell monolayer. The adherent U937 cells were detected by the addition of a peroxidase-conjugated anti-biotin antibody and a soluble colorimetric substrate. This assay is convenient, fast and sensitive, and able to detect 320-1000 U937 cells under the conditions described. This study has used titration assays to compare the biotinylation method with the existing cell quantification approaches of 51Cr radiolabelling and antibody dependent ELISA. Chromium labelling was the most sensitive technique, but we found the biotinylation method to be more convenient than radioactive labelling and more sensitive than conventional ELISA. Biotinylated cells were also used very effectively in a Stamper-Woodruff adhesion assay with U937 cells binding to histological sections of atherosclerotic plaques. The selective detection of the bound cells permitted automated quantitation by image analysis. Whole cell biotinylation may have wider applications in biological research.

A closed interatrial septum aneurysm, filled with blood, mimicking a tumour in the right atrium.

We report the case of a 70-year-old woman with rheumatic mitral stenosis and a transient ischaemic attack. Transoesophageal echocardiography revealed a cystic mass in the right atrium, hanging to the interatrial septum by a pedicle, not circulating. The mass was heterogeneous and suggested a tumour (myxoma) or a thrombus. Surgical resection showed it was an interatrial septal aneurysm, closed on itself, filled with blood. The usual causes of cardiac tumours and pathogeny of large interatrial aneurysms are discussed.

Phenotypic expression in double heterozygotes for familial hypercholesterolemia and familial defective apolipoprotein B-100.

Variability in the expression of monogenic lipid disorders may be observed in patients carrying the same DNA mutation, suggesting possible genetic or environmental interactions. Our objective was to investigate the genotype-phenotype relationships in two unrelated French patients with an aggravated expression of a dominantly inherited hypercholesterolemia. In probands, segregation analysis complemented by DNA sequencing identified heterozygous defective alleles and mutations on two nonallelic loci for two monogenic lipid disorders: familial hypercholesterolemia at the low density lipoprotein (LDL) receptor locus and familial defective apolipoprotein B-100 at the locus encoding its ligand, apolipoprotein B-100. The LDL-receptor missense mutations had been reported in French Canadians. The apolipoprotein B mutation was the Arg3500Gln founder mutation in Northern Europe. Probands had an unusual phenotype of aggravated hypercholesterolemia that was complicated with premature coronary arterial disease, although remaining responsive to lipid-lowering drugs. This phenotype was distinct from that observed in their heterozygous relatives and distinct from those observed in FH or FDB homozygotes. These cases refer to a new class of patients with digenic lipid disorders, defined by specific clinical features that result from the combined effects of two independent loci. Moreover, the observed phenotype of aggravated hypercholesterolemia gives further evidence that receptor and ligand play distinct roles in regulating LDL metabolism. Although uncommon, these cases give insight into the molecular mechanisms that underly the clinical variability of inherited hypercholesterolemia.

Decreased capacity to inhibit platelet hyperactivity and to stabilize prostacyclin of high-density lipoproteins in experimental diabetes.

Twenty-eight male Sprague Dawley rats were divided into two groups: a control group (C) of 15 animals and a streptozotocin-induced diabetes group mildly balanced by insulin (D) of 13 animals. After 15 weeks, plasma and high-density lipoprotein (HDL) lipids were determined in each group. Apoprotein A-I concentration was evaluated in HDL fractions. The capacity of the HDL fraction to inhibit thrombin and ADP-induced aggregation of normal platelets was determined for each rat, and in an additional experiment the relation dose-effect of HDL was established. The effect of HDL of the two groups on the stabilization of prostacyclin was compared by aggregation bioassay. After 15 weeks, HDL cholesterol (free + esterified). After 15 weeks, HDL cholesterol (free + esterified) tended to increase in group D compared with group C (P < 0.08). By contrast, apoprotein A-I was very significantly decreased in HDL-D compared with HDL-C (P < 0.001). These alterations were accompanied by a significantly decreased capacity of HDL (60 micrograms/ml platelet suspension) to inhibit ADP-induced aggregation (P< 0.0001) in group D compared with group C. Furthermore, HDL-D incubated 45 or 90 min with prostacyclin showed a significantly decreased capacity to stabilize prostacyclin compared with HDL-C (P<0.04; P <0.03, respectively). These alterations in HDL could be involved in thrombosis and atheromatous complications associated with this disease.