Comparison of the Systemic Levels of Inflammatory Markers after Percutaneous Coronary Intervention with Bare Metal versus Sirolimus-Eluting Stents

Background: Percutaneous coronary intervention (PCI) with bare metal stent (BMS) deployment causes plaque disruption and a rise in systemic levels of C-reactive protein (CRP), interleukin (IL)-6, and monocyte chemoattractant protein (MCP)-1. Our aim is to study whether PCI with sirolimus-eluting stent (SES) use attenuates this response.
Methods: Patients with stable angina undergoing single-vessel PCI were enrolled in a randomized, open-label fashion into a BMS group or an SES group. Blood samples were drawn pre-PCI, 24 hours post-PCI, and 30 days post-PCI. Systemic concentrations of CRP, IL-6, and MCP-1 were measured at all time points.
Results: In total, 41 patients were enrolled (21 in the BMS group and 20 in the SES group). The baseline plasma concentrations of all markers were comparable between groups. At 24 hours, the mean plasma CRP concentration in the SES group was 20.21 mg/dL versus 8.95 mg/dL in the BMS group (P = 0.15). The mean plasma IL-6 concentration at 24 hours was 25.41 pg/mL in the SES group versus 17.44 pg/mL in the BMS group (P = 0.17). The mean plasma MCP-1 concentration at 24 hours was 382.38 pg/mL in the SES group versus 329.04 pg/mL in the BMS group (P = 0.2). At 30 days, plasma concentrations of all three markers decreased to similar values between groups.
Conclusions: The use of SES did not inhibit the rise in systemic concentrations of CRP, IL-6, and MCP-1 at 24 hours or 30 days post-PCI, compared with BMS. Moreover, at 24 hours, there was a trend for higher systemic levels of all proinflammatory markers in the SES group compared with the BMS cohort.     

Inhibitor development and successful immune tolerance in an HIV-infected patient with haemophilia A and after immune reconstitution with HAART

This is the case of a 28-year-old man with severe congenital haemophilia A, who had a relatively mild bleeding course during early childhood, with limited factor VIII (FVIII) exposure. He was infected with HIV before the age of 7 years, and demonstrated profound immunodeficiency from childhood, with very low CD4+ cell counts for more than a decade. Following initiation of highly active anti-retroviral therapy (HAART) and gradually increasing CD4+ cells, he presented for the first time with a high-titre inhibitor at age 26, despite over 1000 previous FVIII exposures. Subsequently, his inhibitor was successfully eradicated with a standard immune tolerance protocol. It is likely that the effects of chronic HIV infection on T-lymphocyte pathways, and the partial immune reconstitution resulting from HAART, led to this patient's unusual inhibitor course. Such a case serves to augment knowledge gained in animal studies about the immunobiology of FVIII inhibitors.     

High Incidence of Sudden Death with Conduction System and Myocardial Disease Due to Lamins A and C Gene Mutation

BÉCANE, H.–M., et al. : High Incidence of Sudden Death with Conduction System and Myocardial Disease Due to Lamins A and C Gene Mutation. We studied 54 living relatives from a large French kindred, among which 17 members presented with a cardiomyopathy transmitted on an autosomal dominant mode. Five of these individuals had clinical manifestations of muscle disease phenotypically consistent with Emery-Dreifuss muscular dystrophy. Genetic analysis of this kindred had demonstrated a nonsense mutation in the LMNA gene located on chromosome 1q11–q23. This gene encodes lamins A and C, proteins of the nuclear lamina located on the inner face of the nuclear envelope. We retrospectively determined the cause of death of 15 deceased family members, 8 of whom had died suddenly, 2 as a first and single manifestation of the disease. The six other cases had histories of arrhythmias and left ventricular dysfunction before dying suddenly, and three of them died despite the prior implantation of a permanent pacemaker. The mean age of onset of cardiac symptoms among affected living family members was 33 years (range 15–47 years), and the first symptoms were due to marked atrioventricular conduction defects or sinus dysfunction, requiring the implantation of permanent pacemakers in seven cases. Myocardial dysfunction accompanied by ventricular arrhythmias developed rapidly in the course of the disease and resulted in severe dilated cardiomyopathy requiring cardiac transplantation in three cases. In conclusion, in patients presenting a life-threatening familial or sporadic cardiac restricted phenotype similar to that described here, mutations in the lamins A and C gene should be looked for. In the genotypically affected individuals, cardiological and electrophysiological follow-up should be performed to prevent sudden death that could occur rapidly in the evolution of such disease.     

Ultrasonographic features of amoebic abscess: Study in 59 patients

Sonographic examination was carried out in 59 patients with a clinical diagnosis of amoebic liver abscess during the previous 4 years (January 1982 to December 1985). The amoebic liver abscess was located in the right lobe in 45 patients, in the left lobe in eight patients, and in both lobes in six patients. The ultrasonic diagnosis was confirmed in the majority of patients by the indirect haemaglutination test (titres 1:512 or greater) coupled with excellent response to metronidazole, or by ultrasonic-guided percutaneous aspiration producing anchovy sauce pus.
The sonographic patterns of the abscess were evaluated. All patients had well-defined hypoechoic lesions near the surface, which demonstrated fine homogeneous low-level echoes throughout at a normal and a high-gain setting, without a peripheral echo-free halo. The configuration of the abscess was round, oval or lobulated. The walls were irregular in 53 patients, and showed a slight distal sonic enhancement. This ultrasonic feature is suggestive of amoebic liver abscess. The specific ultrasonographic features of amoebic liver abscess, combined with a feature of pleural effusion, pericardial effusion, or an abdominal abscess, were suggestive of the complications of liver abscess found in 19 patients.
It is concluded that ultrasonography is a valuable aid in the diagnosis of amoebic liver abscess. It is of value not only for detection, but also for determination of the site, depth, size, and location of the complicating rupture of the abscess.     

CELL NUMBER IN THE INFERIOR OLIVE OF NERVOUS AND LEANER MUTANT MICE

Naturally occurring cell death is an important feature of neuronal network development: the absence of adequate postsynaptic target neurons during a critical period may result in the death of presynaptic neurons, the degree of death varying inversely with the size of the target population. Studies of mouse mutants with abnormal cerebellar development provide support for this neuron/target relationship in circuits within the CNS. In the present study we analysed the inferior olivary cell population in two cerebellar mutant mice, nervous (nr/nr) and leaner (Cacna1a^la/la). In these mice Purkinje cell degeneration begins near the end of the first postnatal month. In nervous mice the loss starts at postnatal day 20 (P20) and by the end of second month almost 90% of the Purkinje cells in the hemisphere and 50% in the vermis have disappeared. In leaner mice Purkinje cell loss starts after P30 and by P60 almost 50% of these cells are lost. We report here a loss of one third of inferior olivary neurons in the nervous mutation while the entire population appears intact in the leaner mouse. These results allow better definition of the end of the period of target dependency of inferior olive neurons. Their implications for the cell-cell interactions in the developing olivo-cerebellar system are discussed.