Visual disorders,the prosopometamorphopsia and prosopagnosia type in the early days after the onset of brain hemorrhagic stroke – a case report

Presented case report illustrates symptoms of prosopometamorphopsia (PM) and prosopagnosia, observed in the early days after the onset of a hemorrhagic stroke resulting from a complication of endovascular treatment of intracranial aneurysms and the use of anticoagulation therapy. PM is a visual disorder in which faces are perceived as distorted. The female patient described in the present study reported that faces she looked at seemed younger or older than in reality or as if they were dirty, swollen, or with a grimace. She also experienced symptoms of prosopagnosia, which is difficulty of recognizing familiar faces of people (e.g., of her husband and daughter). In the interview 6 months after the first examination, the patient reported spontaneous withdrawal of the visual disturbances.     

Effect of statins on platelet function in patients with hyperlipidemia

Introduction

It is generally assumed that cholesterol reduction by statins is the predominant therapeutic result underlying their beneficial effects in cardiovascular disease. However, the action of statins may be partially independent of their effects on plasma cholesterol levels, as they combine lipid lowering with positive effects on hemorheological conditions and endothelial function. We evaluated the impact of statin treatment on platelet adhesion to fibrinogen (spontaneous and ADP-activated), along with ADP, collagen or ristocetin-induced aggregation in type II hyperlipidemic patients.

Material and methods

The study group included 70 persons: 50 patients affected by type II hyperlipidemia without concomitant diseases and 20 healthy volunteers. The effects of 8-week statin treatment (atorvastatin 10 mg/day, simvastatin 20 mg/day, or pravastatin 20 mg/day) on platelet activation were evaluated.

Results

Regardless of the type of statin, a significant decrease in ADP-induced platelet aggregation was observed: for atorvastatin 50.6 ±12.8% vs. 41.1 ±15.8% (p < 0.05), for simvastatin 57.2 ±18.0% vs. 44.7 ±22.1% (p = 0.05), and for pravastatin 55.8 ±19.5% vs. 38.8 ±23.3% (p < 0.05). There was no significant effect of statins on collagen or ristocetin-induced platelet aggregation and adhesion.

Conclusions

Therapy with statins beneficially modifies ADP-induced platelet aggregation in patients with hyperlipidemia and does not affect spontaneous or ADP-induced platelet adhesion to fibrinogen and platelet aggregation induced by collagen or ristocetin.     

Treatment of non-ST-elevation myocardial infarction and ST-elevation myocardial infarction in patients with chronic kidney disease

Renal dysfunction is frequent in patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS). Chronic kidney disease (CKD) is associated with very poor prognosis and is an independent predictor of early and late mortality and major bleeding in patients with NSTE-ACS. Patients with NSTE-ACS and CKD are still rarely treated according to guidelines. Medical registers reveal that patients with CKD are usually treated with too high doses of antithrombotics, especially anticoagulants and inhibitors of platelet glycoprotein (GP) IIb/IIIa receptors, and therefore they are more prone to bleeding. Drugs which are excreted mainly or exclusively by the kidney should be administered in a reduced dose or discontinued in patients with CKD. These drugs include enoxaparin, fondaparinux, bivalirudin, and small molecule inhibitors of GP IIb/IIIa inhibitors. In long-term treatment of patients after myocardial infarction, anti-platelet therapy, lipid-lowering therapy and β-blockers are used. Chronic kidney disease patients before qualification for coronary interventions should be carefully selected in order to avoid their use in the group of patients who could not benefit from such procedures. This paper presents schemes of non-ST and ST-segment elevation myocardial infarction treatment in CKD patients in accordance with the current recommendations of the European Society of Cardiology (ESC).     

EGFR mutation testing on cytological and histological samples in non-small cell lung cancer: a Polish,single institution study and systematic review of European incidence

The targeted treatment of advanced non-small-cell lung cancer (NSCLC) depends on confirmation of activating somatic EGFR mutation. The aim of the study was to evaluate the incidence of EGFR mutations in NSCLC detected in cytological and histological material and present literature review on European EGFR mutation incidence. 273 patients with confirmed NSCLC were entered into the study: 189 histological, paraffin-embedded materials, 12 fresh and 72 fixed cytological specimens. DNA was extracted from both types of material and the EGFR mutation in exons 18-21 was analyzed by direct sequencing. In addition the EGFR gene copy number in cases with sufficient histological material (110 patients) was evaluated by fluorescent in situ hybridization (FISH) technique. The percentage of EGFR somatic mutations was 10.62%. FISH positive results (amplification or high polysomy of EGFR gene) were identified in 33 patients (30.0%). The strongest clinicopathological correlation with the EGFR mutation was found for histological type (adenocarcinoma; p < 0.01), gender (females; p < 0.01) and FISH positive result (p < 0.05). This is the first, single institution study that estimates the EGFR mutation incidence in the Polish population. Cytological material recovered from fixed preparations and stained with hematoxylin and eosin showed DNA quality comparable to fresh tumor cells and histological samples.     

The risk of atherosclerosis in patients with chronic kidney disease

Background

Chronic kidney disease (CKD) is becoming a serious health problem; the number of people with impaired renal function is rapidly rising, especially in industrialized countries. A major complication of CKD is cardiovascular disease. Accelerated atherosclerosis has been observed in early stages of renal dysfunction. The purpose of this study was to examine the relationship between the degree of renal insufficiency and both the prevalence and intensity of coronary artery disease (assessed on the basis of number of vessels with stenosis).

Methods

446 individuals with both serum creatinine >120 μmol/l (men) or >96 μmol/l (women) and acute coronary syndrome were included in the study. All patients included in this analysis underwent urgent coronarography. Data concerning glomerular filtration rate (GFR), number of vessels with stenosis, hypertension, lipid disorders, creatinine concentration, C-reactive protein, glucose and lipid profile were analyzed.

Results

This study confirmed that moderate to severe renal impairment is associated with accelerated atherosclerosis. Moreover, patients with GFR values below 60 ml/min/1.73 m² are predisposed to accelerated, multivessel cardiovascular disease.

Conclusions

GFR seems to be an independent risk factor for multivessel cardiovascular disease. Due to the fact that patients with renal dysfunction are at high risk of cardiovascular events, they should obtain optimal treatment resulting not only in kidney protection but also in the elimination of cardiovascular risk factors.     

Expression of interleukin-15 and interleukin-15Rα in monocytes of HIV type 1-infected patients with different courses of disease progression

Interleukin-15 (IL-15) enhances the effector mechanisms of anti-HIV immune responses and thus is considered a potential adjuvant of HIV-1 vaccine. However, there are a lack of data concerning the relationships between IL-15 expression and regulation in HIV-1-infected patients and the course of disease progression. We found that IL-15, but not IL-15Rα, is expressed at significantly higher levels in the CD14(+) monocytes [stimulated or not with interferon (IFN)-γ] of long-term nonprogressors (LTNP) than in those of HIV-1 progressors or healthy controls. There was no between-group difference in the amounts of soluble IL-15 released from the cells. We also found that like the healthy controls, the LTNP expressed the IL-15 and IL-15Rα genes in a more coordinated manner than the progressors. Our findings show that there are significant differences in IL-15 expression between patients with different courses of HIV infection, and that the coordinated expression of the IL-15 and IL-15Rα genes is dysregulated in patients with progressive disease. They also provide important information concerning the mechanisms of infection and the potential use of IL-15 as a therapeutic agent.