[Placental growth factor (PlGF) is a member of the proangiogenic VEGF-family; it is mainly produced by throphoblast cells. During the last years numerous studies have shown that circulating PlGF-level in maternal plasma is decreased and its suluble receptor sFlt-1 shows increased expression. In the present study we examined the prognostic accuracy of Alere Triage® PlGF-Assay in hypertensive disorders of pregnancy and its relation with the length of pregnancy. 130 pregnant women were involved in this case-control study (PE: 23, HELLP-syndrome: 20, superimposed praeeclampsia: 17, chronic hypertension: 25, gestational hypertension: 18 and normal control: 27). Blood draw occured between the 22nd and 34th gestational week. PlGF levels were measured by the Alere Triage® PlGF Assay using samples from the maternal plasma. The plasma PlGF-levels of women whose pregnancies were complicated by hypertensive disorders were significantnormotoly lower compared to those who had uncomplicated pregnancies and the decrease were greater in those patients who delivered before the 35th gestational week. The PlGF-test was positive in 93,7% of those women who delivered before the 35th gestational week and in 90,5% of those who delivered before the 37. gestational week. The vast majority of preeclamptic (PE: 95,7%, SIPE: 82,4%) and HELLP-syndrome (95%) patients had positive PlGF tests, the 60% of the chronic hypertension and the 44,4% of the gestational hypertension patients have also shown positive results. The main conclusion of this study is that the PlGF levels using maternal plasma are lower in those pregnancies which are complicated by hypertension and show strong correlation with the severity of the hypertensive disorder. We perceived high sensitivity values in detecting preeclampsia, HELLP-syndrome and superimposed preeclampsia. In the future we may use this method to separate high risk women for hypertensive disorders and it may improve the perinatal outcome]

[Hypertensive disorders represent the most common and dangerous medical disorder in pregnancy. Furthermore, its prevalence is rising. According the recent studies the initiation of antihypertensive treatment should be withhold in mild chronic hypertension (140-159/90-109 mmHg) in pregnancy, excepting associated subclinical hypertensive organ damage or hypertensive complications because of risk of compromising uteroplacental perfusion and fatal circulation. In preeclampsia, however, early antihypertensive treatment is necessary for the prevention of maternal cerebrovascular events.]

[The Reiter-syndrome is the complex of sterile arthritis, urethritis and conjunctivitis and involvement of other organs (skin, mucosal membranes, cardiac conducting system) following bacterial enteric or urogenital infec tion. Systemic signs can also occur with polyarthritis. This syndrome belongs to the reactive arthritis group. In each year there are 30 40 new cases among 100 000 citizens. The disease can occur at any age, but most of the patients are 20-40 years old. It is the patient's genetic background and the type of invading microbes that play a leading role in the pathomechanism of the disease. The exact pathomechanism is yet unknown, therefore our treatment is symptomatic. It is advised to immobilize the involved joint and aspirate the excess fluid and to take non-steroidal antiinflammatory drugs. The patient's medical history is most important to diagnose the disease, because laboratory tests may show signs of inflammation, the serology can only prove antecedent infection, viable organism can not be cultured from the involved organs and the imaging procedures and histology shows non-specific inflammation only. The importance of diagnostic procedures is to exclude the presence of other diseases. Other causes of monarticular inflammation (infection, crystal induced arthritis, sarcoid arthritis) and rheumatic fever should be excluded. The disease lasts for 3-6 months. 2 to 18% of the patients develop chronic arthritis and 12 to 26% of the patients develop ankylosing spondylitis. ]

[Systemic lupus erythematosus is an autoimmune disorder. It stands at the focus of medical interest: basic scientists, clinicians and innovative biotechnologists all pay attention to lupus. Authors of this article present the novel scientific results on the etiopathogenesis, clinical and laboratory characteristics of SLE. Furthermore, authors discuss diagnostic problems and the possible therapeutic modalities. One of the most important results is the characterisation and mapping of the susceptibility genes as well as the analysis of their functional features. More and more is known about the relationship between natural and adaptive immunity, about the cooperation of T and B cells. The abnormalities of intracellular biochemical processes and signal transduction pathways have been cleared. The importance of cytokine network and infective agents in the pathogenesis of SLE has largely been investigated recently. With regards to the outcome of the disease, there is growing attention paid on chronic organ damages, such as end-stage renal disease, osteoporosis and atherosclerosis - in connection with the increased life expectancy. Evidence accumulates on the importance of immune-inflammatory processes in the initiation and perpetuation of osteoporosis and atherosclerosis. There is an urgent need for validated biomarkers which can predict the susceptibility, prognosis, clinical manifestations, activity and severity of SLE. To follow and measure the effectiveness of treatment is also required. Although the principals of lupus management have not changed, novel immune modulators, biological therapy and non-medical treatments (e.g. stem-cell transplantation) have become available. Further research and clinical observations may help to find the real place of such therapeutics.]

[In the development of a cholesterol granuloma both cellular and vascular permeability factors have to be taken into consideration. It may arise as a special degradation product in a chronic cerebral infarct because of the partial insufficient activity of the macrophages. Consequently, the degradation of brain sphingolipids and other compounds does not follow the usual route of degradation and transportation by granular cells to the stage of neutral fat but the necrotic mass transforms into cholesterol esters. Cholesterol crystals produce an irritative effect to neighbouring tissues which may result in the formation of young fibroblasts with proliferative tendency in the vessel wall. Some of the fibroblasts take part in the proliferation of connective tissue, while the rest degenerate, producing more cholesterol or xanthomatous material. Inflammatory changes may also be associated with these lesions. The amount of cholesterol sometimes increases in the inner side of the thickening connective tissue layer. The final result may be an intracranial space occupying mass or it may end as a small cholesterol granuloma, as demonstrated in our incidental cases. By the time a granuloma has developed, the original vessel usually disappears completely, but sometimes remnants of vessels might prove the vascular origin. Other pathomechanisms should also be taken into consideration, such as a cholesterol embolus or anomalous vessel with a large cholesterol plaque in the wall. This also explains why trauma (hemorrhage, granulation), cholesterol embolus, inflammation, metabolic imbalance may predispose to the formation of a granuloma, as well as the hypercholesterolaemia. The nine cases demonstrate the significance of the intracranial granuloma from pathological, clinical and neurosurgical points of view. Such cases have not yet been reported in the national or international literature.]