Premenopausal APS and SLE women have an increased prevalence of carotid and femoral plaque that is not accounted for by other predictors of atherosclerosis, including age, lipid parameters and cumulative steroid dose.
In order to establish the normal range of values of Pulsatility (PI) and Resistance (RI) Indices in the intrarenal vasculature, a study of 50 healthy volunteers (23 males, 27 females), divided into five groups of 10 according to age, was performed with Duplex Doppler ultrasound. Both kidneys were examined in all individuals and, in 12, indices were also compared between upper and lower poles of both kidneys. In addition, repeat examinations were performed in nine subjects on three different days, in order to assess the reproducibility of the method. No differences were found in the mean values of both indices between males and females, upper and lower poles, right and left kidneys. A statistically significant increase (p < 0.01, unpaired t-test) was demonstrated when the oldest age group (7th decade) was compared to the youngest age group (3rd decade). The method appeared remarkably reproducible for RI (4.2-7%), with wider variation in the PI (9.5-22.7%).
In a prospective study 152 consecutive patients presenting with acute abdominal pain were assessed clinically and an ultrasonographic examination was performed immediately. Of these, 16 (11 per cent) patients would normally have had an immediate ultrasonographic scan requested; routine (within 24 h of admission) ultrasonographic examination would have been requested in a further 66 (43 per cent) patients. In 70 (46 per cent) patients an ultrasonographic examination would not have been requested. Ultrasonography altered the diagnosis in one patient from probable appendicitis to cholecystitis. Ultrasonography missed one abdominal aortic aneurysm and one empyema of the gallbladder. Ultrasonography had a sensitivity of 96 per cent, a specificity of 94 per cent, a positive predictive value of 96 per cent, a negative predictive value of 94 per cent and an accuracy of 95 per cent in diagnosing appendicitis. Exactly the same values were found for the clinical diagnosis of appendicitis. The study shows that routine immediate ultrasonographic examination of the acute abdomen is rarely helpful, with the possible exception of appendicitis. Where an urgent ultrasonographic scan is necessary on clinical grounds the expertise of a radiologist is probably required, whereas in specific areas, for example in the diagnosis of right iliac fossa pain, there may be a place for training the surgical trainee.
Familial hypercholesterolemia (FH) is a relatively common autosomal monogenic disease with dominant inheritance and threefold to fourfold increase in relative risk of cardiovascular death in untreated patients. For a "definitive" clinical diagnosis of FH the Simon Broome Register proposes the presence of tendon xanthomas as a key feature. However, detection of tendon xanthomas by physical examination is subjective and difficult to use for follow-up purposes. Several instrumental methods have been reported to be more sensitive than physical examination for the evaluation of xanthomas. The present case illustrates the usefulness of computed tomography (CT) to detect xanthomas in the Achilles tendons (XAT) and their regression in response to hypolipidemic drug treatment in a heterozygous FH patient. As XAT are atherosclerotic plaque-like depositions of lipids it is likely that their progression or regression follows the behavior of vascular atherosclerotic lesions.
Aims The aim of this study was to evaluate the effect of microsomal triglyceride transfer protein inhibitor (lomitapide) in patients with homozygous familial hypercholesterolaemia. Methods and results In 12 homozygous familial hypercholesterolaemia patients treated with lipid-lowering drugs ± biweekly lipoprotein apheresis sessions (nine patients), daily lomitapide was added. The lipid profile (total cholesterol, low-density lipoprotein cholesterol, triglycerides, high-density lipoprotein cholesterol) before and after lomitapide treatment was evaluated. The follow-up period with lomitapide treatment was 3–24 months (13.8 ± 7.9). The median baseline low-density lipoprotein cholesterol level was 900 mg/dl (348–1070), after lipid-lowering drugs therapy was 383.5 mg/dl (214–866) and after lipid-lowering drugs + time-averaged level was 288 mg/dl (183.7–716.6). The addition of lomitapide lowered low-density lipoprotein cholesterol levels further by 56.8% compared to lipid-lowering drugs alone (mean reduction 262, 95% confidence interval (105.5–418.7), p = 0.005) and by 54% (mean reduction 182.9, 95% confidence interval (−342 – −23), p = 0.031) comparing to lipid-lowering drugs + lipoprotein apheresis (time-averaged level). The time-averaged level of low-density lipoprotein cholesterol in lipid-lowering drugs + lipoprotein apheresis patients compared with lipid-lowering drugs + lomitapide was 54% in favour of lomitapide ( p = 0.031). Conclusions Treatment with lomitapide in homozygous familial hypercholesterolaemia patients has a beneficial effect with a constant decrease of low-density lipoprotein cholesterol by 57% compared with classical lipid-lowering therapy and by 54% compared with classical lipid-lowering therapy and time-averaged level of low-density lipoprotein cholesterol.
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