Obsetrical outcome of pregnancy in patients with systemic lupus erythematosus

To assess the impact of systemic lupus erythematous [SLE] on the outcome of pregnancy and the course of disease during pregnancy. During a period of three years we prospectively followed thirty pregnancies in thirty SLE patients in a tertiary care centre, for each case two age and parity-matched healthy control [60] were chosen. The management protocol included: * Planning of conception when disease was inactive. * Frequent follow-up visits by an internist-obstetrician team. * Use of sequential ultrasonographic, Doppler and fetal echo cardiographic examination. * Serial evaluation of maternal immunological condition. * The same dose of steroids or immunosuppressives as before pregnancy was continued. In the study group the mean age of patients was 27.1 +/- 3.8 years and mean previous duration of SLE at booking was [4.2 +/- 2.5]. SLE was active at conception in four cases [13.3%]; at that time all patients were taking prednisolone. In control group the mean age of patients was 25.3 +/- 3.2 years. In the study group there were 23 live birth [88.6%] with 15 full term and 8 premature deliveries, 4 [13.3] spontaneous abortion, 3 [10%] intra uterine foetal death. In the control group the were 54 live birth [98.1%] with 39 full term and 15 premature deliveries, 5 [8.3%] spontaneous abortion one [1.0%] intra uterine foetal death. The mean gestational age of live births were 35.8 weeks and 37.5 weeks respectively p<0.05. The mean birth weight of live births were 2108gm and 2750gm respectively p<0.05. Flares up of disease activity occur in 4 of 26 pregnancies. We conclude from our study that pregnancy induce SLE flare-up is uncommon but SLE is associated with increased incidence of intrauterine growth retardation. All of our patients were on corticosteroid therapy during pregnancy and it is possible that steroid therapy may have contributed to the low flare-up rate

ACE gene polymorphism: a predictor of instent restenosis

Restenosis is the maladaptive response of the coronary artery to Restenosis occurs in 20-50% of patients [Pts] after balloon angioplasty and in 10-30% of patients receiving a stent. Neointimal proliferation is one distinct processes involved and the rennin-angiotensin system has been implicated in its pathogenesis. The level of plasma has been implicated in its pathogenesis. The level of plasma ACE is party under genetic control and the plasma and cellular levels pf ACE are associated with the insertion/deletion [I/D] polymorphism in the ACE gene where DD genotype bearers have higher levels of ACE than either ID or II genotype bearers. Aim: To assess the possible role of ACE gene polymorphism in the pathogenesis of instent restenosis [ISR]. We studies 136 patients having elective or emergency successful angioplasty and of a previously untreated native single coronary artery, including 117 males and 19 females, with a mean age of 52.5 +/- 9.8 years. Besides clinical evaluation, all pts were subjected to routine laboratory measurements, followed by DNA extraction for a peripheral venous sample using the QUIAmp Blood Kit. ACE gene was amplified by PCR-technique [30cycles], then were electrophoresed in agars gel and visualized directly with ethidium bromide staining under an ultraviolet light source to determine the ACE I/D genotypes. Clinical follow-up was performed on monthly basis up to six months for the occurrence of major adverse cardiac events. Angiographic follow-up was done in 93 patients at a mean of 6.17 +/- 2.3 months after PCI using edge detection and segment analysis by the Xcelera catch Philips Intruris QCA program to detect the minimal lumen diameter, reference vessel diameter and segment length before and after PCI and after 6 months follow up in the same views at baseline, to detect acute gain, late lumen loss and binary restenosis rate. ISR was expressed as >/= 50% diameter loss. Out of 136 pts, 93 were available for angiographic follow- up. Those were divided into two groups: 41 pts with angiographic evidence of restenosis [ISR], and 52pts without angiographic evidence of restenosis [NO-ISR]. The homozygous DD genotype was significantly more frequent in the ISR group compared to the NO-ISR group [51.2% vs 11.5%, p=0.005]. The heterozygous ID genotype was significantly more frequent in the NO-ISR group compared to the ISR group [76.9% vs 39%, p=0.005]. The homozygous II genotype was equal in both group [11.5% in ISR vs 9.8% in No ISR, p=0.79]. Compared to the heterozygous ID and the homozygous II, genotypes the homozygous DD genotype, of the ACE gene was more significantly associated with in-stent restenosis. This knowledge may help in the selection of subgroups of patients who will benefit form alternative therapeutic strategies such as CABG surgery or intensive preventive treatment or drug-eluting stent