Professional Stress and Burnout Syndrome During the Covid Pandemic in the Medical Field.

Context: The contemporary workplace creates a challenge toward physicians and their teams. They are forced into a situation, in which to be competitive they must have skills outside of their medical specialty, such as health management, pedagogy, and information and communication technologies. Aim: To analyze the level of stress and burnout among the medical employees in the hospital care. Settings and Design: Healthcare professionals from three private, municipal, and regional hospitals filled a questionnaire in the time period January-March 2021. Methods and Material: An adapted Maslach Burnout Inventory 55 question questionnaire was used and analyzed. Statistical Analysis Used: One-way ANOVA, correlation, and multiple regression analysis in SPSS. Results: We identified high levels of emotional exhaustion (>62% report high signs or above), high levels of depersonalization (>70% report signs of depersonalization), and low levels of personal accomplishment (<39% have below average sense of achievements). Conclusions: Despite the physicians and their teams reporting high levels of workload and stress, the satisfaction from work has not diminished and the evaluation for the quality of provided work is still high. Additional research into the topic is required with focus on comparison between hospital physicians and primary care physicians.

Novel CDKL5 Mutations in Czech Patients with Phenotypes of Atypical Rett Syndrome and Early-Onset Epileptic Encephalopathy.

The X-linked CDKL5 gene, which encodes cyclin-dependent kinase-like 5 protein, has been implicated in early-onset encephalopathy and atypical Rett syndrome with early-onset seizures. The CDKL5 protein is a kinase required for neuronal development and morphogenesis, but its precise functions are still largely unexplored. Individuals with CDKL5 mutations present with severe global developmental delay, intractable epilepsy, and Rett-like features. A clear genotype-phenotype correlation has not been established due to an insufficient number of reported cases. The aim of this study was to analyse the CDKL5 gene in Czech patients with early-onset seizures and Rett-like features. We performed mutation screening in a cohort of 83 individuals using high-resolution melting analysis, DNA sequencing and multiplex ligation- dependent probe amplification. Molecular analyses revealed heterozygous pathogenic mutations in three girls with severe intellectual disability and intractable epilepsy starting at the age of two months. All three identified mutations, c.637G>A, c.902_977+29del105, and c.1757_1758delCT, are novel, thus significantly extending the growing spectrum of known pathogenic CDKL5 sequence variants. Our results support the importance of genetic testing of the CDKL5 gene in patients with early-onset epileptic encephalopathy and Rett-like features with early-onset seizures. This is the first study referring to molecular defects of CDKL5 in Czech cases.

Effects of micronized fenofibrate on insulin resistance in patients with metabolic syndrome.

BACKGROUND AND OBJECTIVE: Metabolic syndrome is characterized by insulin resistance (IR) as well as dyslipidemia, ventral overweight, hypertension and elevated fasting plasma glucose. Since diabetic and prediabetic states are commonly associated with hypertriglyceridemia, fenofibrates have been used in such patients. The aim of this pilot open trial was to study the influence of micronized fenofibrate on insulin resistance and plasma insulin levels in prediabetic and diabetic patients. SUBJECTS: From 114 dyslipidemic patients, 31 with dyslipidemia and insulin resistance were selected to take part in the study. Of the 31 patients, 20 were nondiabetic and only 11 had noninsulin-dependent diabetes mellitus. Eighteen dyslipidemic patients acted as controls. METHODS: Insulin resistance was assessed in a short-term insulin tolerance test. Plasma insulin, antiinsulin antibodies, lipid parameters and the insulin sensitivity index (ISI) were measured at entry and after a 3-month therapy with 200 mg micronized fenofibrate daily. RESULTS: Three-month therapy with micronized fenofibrate resulted in significant ISI increase and was accompanied by a decrease in plasma insulin levels in dyslipidemic patients with metabolic syndrome. ISI also improved in patients with type 2 diabetes mellitus and there was an unexpected increase in plasma insulin levels. Antiinsulin antibodies were unchanged throughout the trial. Reductions in plasma triglycerides and total cholesterol exceeding 50% and 20%, respectively, were observed in patients with metabolic syndrome. These changes were accompanied by an increase in mean levels of plasma high-density lipoprotein (HDL) cholesterol (above 35%). CONCLUSIONS: Micronized fenofibrate is an effective drug in normalizing lipid-lipoprotein levels in patients with metabolic syndrome. After a 3-month fenofibrate therapy, insulin resistance was reduced in a group of patients with dyslipidemia and metabolic syndrome.

Effects of fenofibrate and simvastatin on plasma sICAM-1 and MCP-1 concentrations in patients with hyperlipoproteinemia.

OBJECTIVE: The most important mechanism through which high plasma lipid levels trigger the formation of atherosclerotic lesions involves a change in the expression of adhesion molecules on endothelial and smooth muscle cells. The aim of this study was to evaluate an extralipid effect of fenofibrate and simvastatin by examination of MCP-1 and ICAM-1 plasma concentration after 1-month hypolipemic therapy as well as MCP-1 and ICAM-1 plasma concentration after 1-month therapy with low-fat diet alone. METHODS: Twenty patients with HLPIIb or HLPIIa, who did not respond to a low-fat diet, were treated with micronized fenofibrate or simvastatin, respectively, for 1 month. The control group included 18 normo-lipidemic, healthy age-matched participants; 10 patients with HLPIIa were effectively treated with a low-fat diet for 1 month. This group was compared to a control group of 10 healthy subjects. The plasma adhesion molecule levels were measured by an ELISA method before and after the treatment. To accurately evaluate the adhesion molecule levels, we excluded hyperlipidemic patients and control subjects with any inflammatory disease. RESULTS: sICAM-1 levels were significantly higher in HLPIIa and HLPIIb patients (331 +/- 19 ng/ml and 423 +/- 23 ng/ml, respectively) compared with the control group (236 +/- 12 mg/ml). MCP-1 levels were also significantly higher in HLPIIa and HLPIIb patients (170 +/- 9 pg/ml and 183 +/- 15 pg/ml, respectively) compared with the control group (100 +/- 4 pg/ml). Fenofibrate (200 mg daily) significantly decreased sICAM-1 (by 17%) and MCP-1 levels (by 12.5%). Simvastatin (20 mg daily) caused a significant decrease (by 10.5%) in sICAM-1 levels only. Restriction in dietary lipids resulted in a significant decrease in the levels of cholesterol (8%), LDL cholesterol (14.9%) and ApoB (12.7%), which was accompanied by a significant decrease in the levels of sICAM-1 (8.7%) and MCP-1 (16.1%). CONCLUSION: The results of this study suggest that high lipid levels are accompanied by increased levels of sICAM-1 and MCP-1 and that hypolipidemic therapy only slightly decreases the levels of these molecules compared with plasma lipids. The hypolipidemic diet-related decrease in the levels of lipids, ICAM-1 and MCP-1 suggests that it is a drug-induced decrease in lipid levels but not a direct action of the drugs on endothelial cells, smooth muscle cells or macrophages that leads to a decrease in the levels of adhesion molecules.

Effects of atorvastatin, simvastatin, and fenofibrate therapy on monocyte chemoattractant protein-1 secretion in patients with hyperlipidemia.

OBJECTIVE: Monocytes that migrate into the arterial wall participate in the development and, eventually, rupture of the atherosclerotic plaque. The aim of this study was to evaluate the secretion of monocyte chemoattractant protein-1 (MCP-1) by monocytes from hyperlipidemic patients treated with hypolipidemic drugs, namely fenofibrate, simvastatin, or atorvastatin to determine what role is played by these drugs in the development and stabilization of the atherosclerotic plaque. METHODS: Fifty-four hyperlipidemic patients, who did not respond to a low-fat diet, were treated with fenofibrate, simvastatin, or atorvastatin (18 patients in each group) for 1 month. The control group included 18 normolipidemic, healthy, age-matched participants. Ten hyperlipidemic patients were effectively treated with hypolipidemic diet alone for 1 month. This group was compared with a control group of ten healthy subjects. To accurately evaluate the adhesion molecule levels, we excluded hyperlipidemic patients and control subjects with any inflammatory disease. Before and after treatment, monocytes were isolated from peripheral blood. After stimulation with lipopolysaccharide (LPS), MCP-1 secretion was measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: MCP-1 levels were significantly higher in hyperlipidemic patients than controls: 15.8+/-0.47, 16.7+/-0.23, and 14.9+/-0.45 compared with 12.36+/-0.42 ng/ml. Fenofibrate, atorvastatin, and simvastatin significantly decreased MCP-1 levels from 15.8+/-0.47 to 8.79+/-0.89, from 16.7+/-0.23 to 7.46+/-0.73, and from 14.9+/-0.45 to 10.3+/-0.8 ng/ml, respectively. In the diet-treated group of hyperlipidemic patients, the level of MCP-1 before therapy was significantly higher than in controls (16.89+/-0.31 vs 12.45+/-0.36 ng/ml). The diet therapy caused a significant decrease in levels of MCP-1 to 15.1+/-0.36 ng/ml. There was a correlation between the decreased levels of lipids and the decreased release of MCP-1 in the patients treated with hypolipemic drugs. CONCLUSION: The drug-induced decrease in MCP-1 secretion in hyperlipidemic patients suggests that, apart from acting on lipids, the hypolipidemic drugs studied may directly inhibit the activity of monocytes.

The risk of atherosclerosis in patients with impaired glucose tolerance.

OBJECTIVES: Glucose metabolism disorders usually coexist with dyslipidemia and coagulation/fibrinolysis disturbances. Increase of insulin resistance followed by hyperinsulinemia leads to enhanced protein synthesis, including production of apolipoproteins. As a result, the structure of Low Density Lipoprotein (LDL) becomes small and dense. This augments lipid infiltration into the arterial wall. Following this process monocyte adhesion to endothelium initiates atherosclerotic injury. One of the markers of this inflammatory reaction is Monocyte Chemoattractant Peptide-1 (MCP-1). A lot of inflammatory mediators affect both oxidative modification of LDL and coagulation processes being responsible for anti-fibrinolytic predominance. Plasminogen Activator Inhibitor-1 (PAI-1) is a marker of this state. Therefore the aim of this study is to evaluate the marker of the oxidation processes (oxLDL) as well as prothrombotic (PAI-1) and inflammatory state (MCP-1) markers in patients with Impaired Glucose Tolerance (IGT). METHODS: The study was carried out on 16 subjects: 10 with biochemically confirmed IGT and 6 age-matched healthy persons without such disorders. Following tests were performed: OGTT, HbA(1c) level as well as TCh, HDL, LDL and TG. Plasma concentrations of oxLDL, PAI-1 and MCP-1 were measured using ELISA method. RESULTS: In patients with Impaired Glucose Tolerance plasma levels of oxLDL were significantly higher compared to control group (67.6 +/- 0.9 U/l vs. 57.8 +/- 4.0 U/l; p < 0.01) in spite of LDL levels, which did not reveal such difference. MCP-1 plasma concentration compared to control group occurred to be significantly increased in experimental group as well (156.4 +/- 9.2 ng/ml vs. 125.4 +/- 1.9 ng/ml; p < 0.05). PAI-1 level revealed most significant difference (84.0 +/- 1.8 ng/ml vs. 43.7 +/- 2.7 ng/ml; p < 0.0001). CONCLUSIONS: It is concluded that patients with Impaired Glucose Tolerance should be considered as a group in which atherogenic modification of lipoproteins occurred. Also plasma inflammatory as well as prothrombotic markers concentration was elevated.

Plasma cytokines as predictors of coronary heart disease.

BACKGROUND AND OBJECTIVE: Growing body of evidence explicitly suggests the significant role of inflammatory processes in vascular diseases related to atherosclerosis. Monocytes, present in every phase of atherogenesis, are the principal cells accumulating in atherosclerotic plaque. Monocyte Chemotactic Protein 1 (MCP-1) seems to influence firm adherence of rolling monocytes and infiltration into the artery wall. Although the significant meaning of inflammation in atherogenesis has been proved, potential role of antiinflammatory cytokines remains unknown. Interleukin 10 (IL-10) is a major cytokine of pleiotropic antiinflammatory function known to exert inhibitory effects on monocytes. Recent data emerging from clinical and pathological studies suggest important role of thrombosis and fibrinolytic disorders in atherosclerosis complications especially in coronary heart disease (CHD). Individuals with greater Plasminogen Activator Inhibitor 1 (PAI-1) level are believed to be more susceptible to cardiovascular disease. METHODS: In our study we measured the plasma levels of MCP-1, IL-10 and PAI-1 in 10 patients with stable angina and 10 healthy subjects. We also estimated its mutual correlations. The plasma levels of MCP-1, IL-10 and PAI-1 were determined with R&D kits (ELISA). RESULTS: Plasma levels of MCP-1 were significantly higher (261.5+/-40.7 pg/mL vs 73.3+/-3.05 pg/mL; p<0.0002) and also levels of PAI-1 were higher (79.36+/-5.8 ng/mL vs 35.88+/-1.38 ng/mL; p<0.0001) in patients with SA compared with the healthy control subjects. Whereas plasma levels of IL-10 were lower (11.6+/-0.5 pg/mL vs 16.5+/-0.4 pg/mL; p<0.0001) compared with control group and correlated with both MCP-1 plasma level (r=-0.67; p<0.0015) and PAI-1 concentration (r=-0.69; p<0.0008). CONCLUSION: The data obtained confirm the predictive role of cytokines in patients with stable coronary heart disease. The negative correlation of anti-inflammatory IL-10 and PAI-1 was also found.

Levels of sICAM-1, sVCAM-1 and MCP-1 in patients with hyperlipoproteinemia IIa and -IIb.

OBJECTIVE: Hyperlipoproteinemia is one of the factors that are involved in the development of atherosclerosis. One of the mechanisms through which these high plasma lipid levels trigger the formation of atherosclerotic lesions is a change in the expression of adhesion molecules on endothelial and smooth muscle cells. The aim of this study was to evaluate the plasma levels of soluble intracellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1) and monocyte chemoattractant protein-1 (MCP-1) in patients with Type IIa (HLP-IIa) and IIb (HLP-IIb) hyperlipoproteinemias. SUBJECTS: Twenty patients with HLP-IIa, 20 patients with HLP-IIb and 23 control subjects were studied. To accurately evaluate adhesion molecule levels, we excluded those hyperlipemic patients and control subjects who had an inflammatory disease. METHODS: Plasma sICAM-1, sVCAM-1 and MCP-1 levels were measured by the ELISA method. RESULTS: sVCAM-1 levels in HLP-IIa and HLP-IIb patients (535 +/- 27 ng/ml and 545 +/- 22 ng/ml, respectively) did not differ significantly from those in the control group (558 +/- 20 ng/ml). sICAM-1 levels were significantly higher in patients with HLP-IIa and HLP-IIb (279 +/- 10 ng/ml and 322 +/- 12 ng/ml, respectively) compared to the control group (226 +/- 10 ng/ml). MCP-1 levels were significantly higher in HLP-IIa and HLP-IIb patients (151 +/- 12 pg/ml vs 154 +/- 12 pg/ml, respectively) compared to healthy controls (98 +/- 4 pg/ml). sICAM-1 levels in the HLP-IIb group were significantly higher than in the HLP-IIa group. CONCLUSION: The results of the study suggest that lipid abnormalities affect the levels of adhesion molecules and chemokines in plasma.

A new immunological marker of atherosclerotic injury of arterial wall.

BACKGROUND AND OBJECTIVE: The atherosclerotic arterial injuries lead to many life threatening vascular incidents. It has been well documented that inflammatory processes play an important role in atherogenesis. Intensive studies are undertaken to find a serum marker of inflammatory reaction correlated with arterial injuries. METHODS: In our study we measured the level of interleukin-6 (IL-6) in patients with dyslipidemia IIa and IIb biochemically confirmed. Control estimations were done in age-matched group. Arterial injuries were evaluated as a thickening of complex intima-media in common carotid arteries by means of Doppler ultrasonography. RESULTS: Levels of IL-6 were significantly higher in both groups of patients with dyslipidemia as compared with the healthy control persons (IIa vs control p<0.001, IIb vs control p<0.001). The plasma level of IL-6 is significantly correlated to intima-media complex thickness (r=0.68, p<0.0001). CONCLUSION: We conclude that increase of serum concentration of IL-6 may be related to arterial wall injuries in the course of the most atherogenic lipid disorders.

Effects of fibrates on plasma prothrombotic activity in patients with type IIb dyslipidemia.

OBJECTIVE: Increased levels of fibrinogen and plasminogen activator inhibitor 1 (PAI-1) are associated with an increased risk of ischemic coronary disease and its complications. Since atherogenic dyslipidemias are well-known risk factors for coronary heart disease, this study aimed to determine whether Type IIb dyslipidemia, one of the most atherogenic dyslipidemias, is accompanied by increased PAI-1 and fibrinogen synthesis. The additional aim of this study was to evaluate the effect of micronized fibrates on the levels of PAI-1 and fibrinogen in patients with Type IIb dyslipidemia. SUBJECTS: Thirty patients with Type IIb dyslipidemia and 12 age-matched control subjects were studied. Fourteen patients were treated with fenofibrate and 16 were treated with ciprofibrate for 1 month. METHODS: Plasma PAI-1 levels were measured by the ELISA method with Diagnostica Stago kit. The level of fibrinogen was measured by the Clauss method. RESULTS: PAI-1 levels in dyslipidemic patients before treatment differed significantly in both the fenofibrate and ciprofibrate treatment groups (101.18 +/- 36.47 ng/ml, 87.64 +/- 32.06 ng/ml, respectively) from those in the control group (32.32 +/- 7.39 ng/ml, p < 0.001). Compared with the control subjects (2.91 +/- 0.35 g/l), fibrinogen levels before treatment were higher in patients with dyslipidemia treated with ciprofibrate (3.42 +/- 0.59 g/l, NS) and fenofibrate (3.65 +/- 1.10 g/l, p < 0.05). One-month ciprofibrate treatment resulted in an insignificant decrease in PAI-1 levels (76.28 21.60 ng/ml, NS) and in a significant decrease in fibrinogen levels (2.73 +/- 0.40 g/l, p < 0.01). After one-month fenofibrate treatment PAI-1 levels (81.22 +/- 25.01 ng/ml, p < 0.01) and fibrinogen levels (2.95 0.72 g/l, p < 0.01) decreased significantly. CONCLUSION: Type IIb dyslipidemic patients have increased levels of PAI-1 and fibrinogen. Micronized fibrates decreased not only lipid levels but also the levels of fibrinogen and PAI-1 in these patients.

Antihypertensive effect of amlodipine compared with nifedipine retard in patients with mild and moderate essential hypertension.

OBJECTIVE: The present study was undertaken to evaluate the efficacy and safety of amlodipine for hypertension treatment in comparison with nifedipine retard. METHODS: We examined 31 patients with arterial blood pressure approximately 155-165 mmHg/100-105 mm Hg at the beginning of the trial. It was a randomized double-blind, parallel-group trial including two groups of patients. Patients of the first group were given active amlodipine and nifedipine retard placebo during 6 weeks, while the second group was given active nifedipine retard and amlodipine placebo. Statistical analysis was made using the paired Student's t-test, chi-square test and ANOVA test. RESULTS: At end point we observed significant decrease in arterial blood pressure after treatment of both drugs. The treatment with nifedipine retard increased the mean heart rate of patients. Amlodipine therapy in comparison to nifedipine retard did not change the heart rate in treated patients. Safety parameters: SGOT, SGTP, creatinine and others were in laboratory norms ranges. CONCLUSION: Amlodipine proved to be an effective, more safe and better-tolerated therapeutical alternative for hypertension management than nifedipine retard.

[Levels of tumor necrosis factor alpha in serum of patients with hyperlipoproteinemia IIB before and after micronized fenofibrate therapy]. / Stezenia czynnika martwicy nowotworów alfa w surowicy pacjentów z hiperlipoproteinemia IIb przed i po podjeciu teràpii fenofibratem mikronizowanym.

UNLABELLED: Tumor necrosis factor alpha (TNF alpha) secreted by activated macrophages stimulates proliferation and migration of vascular smooth muscle in atherogenesis. Up to now, the effect of fibrates on concentration of TNF-alpha has not been investigated. The aim of this study was to estimate TNF-alpha plasma concentration in healthy subjects before and after fenofibrate therapy in patients with hyperlipoproteinaemia IIb and to correlate their levels with plasma concentration of total cholesterol (TC), low density lipoproteins (LDL) and apolipoprotein B (ApoB). METHODS: 10 patients with hyperlipoproteinaemia IIb were treated with micronized fenofibrate (Lipanthyl 200 m-Fournier) for 1 month. Cytokines levels before and after therapy was measured by the ELISA method with Genzyme kits. RESULTS: The levels of lipid parameters at the onset study were as follows: TC: 265.4 +/- 9.4 mg%, TG: 344 +/- 53 mg%, LDL: 167.2 +/- 4.7 mg%, and ApoB: 1.62 +/- 0.05 g/l. After 1-month therapy with Lipanthyl 200 m the parameters decreased: TC 206 +/- 16 mg% (p < 0.05), TG: 194 +/- 30 mg% (p < 0.05), ApoB: 1.43 +/- 0.04 g/l (p < 0.01), and LDL: 144.4 +/- 12.9 mg% (ns). The decreased level of TC, TG and LDL correlated with the decreased concentration of TNF alpha. Before treatment the TNF concentration was 19.2 +/- 1.6 pg/ml and was higher than the concentration of control subjects (9.9 +/- 1.1 pg/ml, p < 0.01). After 1-month therapy the level of TNF alpha in blood from patient was 9.2 +/- 1.0 pg/ml (p < 0.01). The results of this study indicate that the concentrations of TNF alpha in plasma from hyperlipidemic patients are higher than concentrations of healthy subjects. Fenofibrate decreased the levels of this cytokine. This effect may be of significance for the treatment of HLPIIb and of atherosclerosis prevention.

Effects of fenofibrate on plasma cytokine concentrations in patients with atherosclerosis and hyperlipoproteinemia IIb.

BACKGROUND AND OBJECTIVE: In recent studies atherosclerosis has often been referred to as immune disease. The atherosclerotic plaque consists of large amounts of inflammatory cells, mainly monocytes/macrophages and T lymphocytes. Macrophages activated by low-density lipoproteins (LDL) secrete tumor necrosis factor alpha (TNF-alpha) and interleukin-1 (IL-1) in vitro, while LDL-stimulated T lymphocytes release interferon gamma (IFN-gamma). The aim of this study was to estimate the plasma levels of TNF-alpha, IL-1, IFN-gamma in patients with hyperlipoproteinemia IIb (HLPIIb) and atherosclerosis. Since the fibrates are drugs of choice in HLPIIb, we additionally evaluated the effect of fibrates on the cytokine levels. METHODS: Ten patients with HLPIIb were treated with micronized fenofibrate for 1 month. Before and after treatment, the cytokine levels were measured by the ELISA method. To accurately evaluate cytokine levels, we excluded atherosclerotic patients and control subjects with any inflammatory disease. RESULTS: The initial lipid parameters were as follows: total cholesterol (TC): 6.9 +/- 0.24 mmol/l, triglycerides (TG): 3.44 +/- 0.53 mmol/l, LDL: 4.35 +/- 0.12 mmol/l, and apolipoprotein B (ApoB): 1.62 +/- 0.05 g/l. After 1 month of fenofibrate treatment the parameters decreased to the following values: TC 5.36 +/- 0.42 mmol/l (p < 0.05), TG 1.94 +/- 0.30 mmol/l (p < 0.05), ApoB 1.43 +/- 0.04 g/l (p < 0.01), and LDL 3.75 +/- 0.34 mmol/l (p > 0.05). Before therapy, TNF-alpha levels in atherosclerotic patients were higher than in control subjects, 19.2 +/- 1.6 and 9.9 +/- 1.1 pg/ml, respectively (p < 0.01). After 1-month therapy, TNF-alpha levels in atherosclerotic patients were 9.2 +/- 1.0 pg/ml (p < 0.01). Similarly, the initial levels of IFN-gamma were higher in atherosclerotic patients compared with healthy subjects, 44.4 +/- 5.3, and 19.4 +/- 2.1 pg/ml, respectively (p < 0.01). After fenofibrate therapy, IFN-gamma levels decreased to 24.8 +/- 2.9 pg/ml (p < 0.01). The decreased levels of TC, TG, and LDL correlated with the decreased levels of TNF-alpha and IFN-gamma. CONCLUSION: The results of this study indicate that plasma TNF-alpha and IFN-gamma levels in hyperlipidemic patients are higher than in healthy subjects, and that fenofibrate is effective in decreasing lipids and cytokines in plasma.

[Selected immunologic markers for evaluation of peripheral blood in patients with internal endometriosis]. / Wybrane wskazniki odpornosciowe oceniane we krwi obwodowej u chorych z endometrioza wewnetrzna.

In group of 16 patients with internal endometriosis verified by histopathological investigations following immunological indices in peripheral blood were estimated: 1) number of leucocytes and neutrophils, 2) neutrophil adherence to fibres, 3) phagocytic activity of neutrophil using the latex granules, 4) concentration of immunological complexes in serum. The results were compared with those in control group (20 healthy women). In patients with internal endometriosis compared to control group the increase of the number of leucocytes and neutrophils and decrease of phagocytic activity of neutrophils were observed.

[Influence of oral isosorbide dinitrate (ISDN) on parameters of blood flow in the coeliac trunk evaluated with doppler sonography]. / Wplyw doustnie podanego isosorbidinitratu (ISDN) na parametry przeplywu krwi w pniu trzewnym w ocenie sonografii dopplerowskiej.

Blood flow in the coeliac trunk was measured before and after oral application of ISDN (isosorbitol dinitrate) 10 or 20 mg. Clinical prognostic value of this test was evaluated. Investigation were carried out with a duplex-Doppler pulsatory wave. The quantitative hemodynamic method with estimation of PI and RI was applied to exclude the effect of angle and the vessel diameter. 44 healthy volunteers were examined. The ultrasonograph ACUSON 128 was used with the linear and sectorial head 3.5 MHz enabling measurement of the pulsatory wave (Doppler). All persons were divided into 4 groups: according to sex, the age, the dose of nitrate and the groups given placebo. Application of the ISDN led to increase values PI and RI. Application of placebo had no influence on the blood flow.

[Cholecystolithiasis in the urban population of Poland]. / Kamica pecherzyka zólciowego w populacji miejskiej w Polsce.

Multicentre study was carried out in three regions of Poland aimed to assess cholecystolithiasis incidence in urban population and some potential risk factors of the disease. 10133 persons in five age groups, from 16 to 70 (6071 women and 4062 men) were examined. The examination consisted of questionnaire considered sex, age, weight, dietary habits, complaints, chronic drugs use, family history and in women number of pregnancies and deliveries as well as hormone therapy. The results obtained were analysed statistically with Chi 2 test. Cholecystolithiasis was found in 1411 persons (10.7%), among them 18% women (1083 women) and 8.2% men (328 men). Incidence rate was 180.5/1000 women and 82.0/1000 men. The obtained increase in percentage of cholecystolithiasis cases with age was statistically significant. No relation were found between the number of stones and sex of the examined persons. In 1480 persons (43.5%0 the disease was asymptotic. The studies did not prove the correlation between cholecystolithiasis in women and sex of the first child or oral contraception. Positive correlation was found between cholecystolithiasis in women, obesity, number of pregnancies and family history. In men age was most significant risk factor. Incidence of cholecystolithiasis in Poland, Western Europe and USA is similar.

[Doppler examination of portal venous flow in liver neoplasms]. / Dopplerowskie badania przeplywu krwi ukladu wrotnego w nowotworach watroby.

An attempt was made to measure blood flow of portal system at various stages of neoplastic changes in the liver, which could be of some prognostic and therapeutic value. In the group of 80 studied persons, 20 patients had hepatic angioma, 6 patients hepatic cancer, 24 patients metastatic cancer affecting to the liver. Control group consisted of 50 healthy volunteers. No disturbances of blood flow in portal system in the group of patients with hepatic angioma were found. In the group with primary hepatic cancer decrease of TAV and TF in portal and splenic veins were noted, especially in 2 cases with numerous changes with relatively big sum of diameters, as compared with control method. In group with metastases of cancer to the liver slight decrease of blood flow in portal and splenic veins was observed as compared to the control group. Decrease in blood flow in the portal system was seen in cases with numerous and relatively big neoplastic focuses in the liver. Blood flow monitoring might be helpful in evaluation of the progress or regression of infiltrative changes in the liver.

[Evaluation of thyroid anti-membrane and anti-thyroglobulin antibody determination in patients with thyroid cysts treated with external drainage under ultrasonographic control]. / Ocena wyników oznaczen tarczycowych przeciwcial przeciwblonowych I przeciwtyreoglobulinowych u chorych z torbielami tarczycy leczonych drenazem zewnetrznym pod kontrola USG.

In patients (43 women and 12 men) external open drainage under ultrasonography control was performed. In 25 cases contents of serous nature, in 27 cases of colloid and in 3 cases of suppurative character were obtained. Anti-membrane thyroid antibodies (ATMA) and anti-thyroglobulin antibodies (Tg-Ab tire) were determined in the cyst contents as well as in the serum. The antibodies were present in the serum of 48% of the patients with serous cyst and in 52% with colloidal cysts. In serous cyst contents, ATMA and Tg-Ab antibodies were present in 52% of cases, while in the colloidal contents ATMA antibodies were found in 60% of patients and Tg-Ab antibodies in 68%. In 3 patients with cysts containing pus no antibodies were found. When antibodies were detected in the contents of serous and colloidal cysts their presence were also found in the serum. Among 55 cases with thyroid cysts, the antibodies were found in the serum of 47% of patients. The results indicate involvement of immunological factors the role of which has not been explained.

[Comparison of selected indices of nonspecific immunity estimated in peripheral blood of patients with untreated duodenal ulcer and after treatment with ranitidine]. / Porównanie wybranych wskazników odpornosci nieswoistej ocenianych we krwi obwodowej pochodzacej od chorych z nieleczonym wrzodem dwunastnicy i po leczeniu ich ranitydyna.

In 20 patients (8 women and 12 men) aged of 20-56 years (38 years on the average) with the yet untreated duodenal bulb ulcer selected indices of nonspecific immunity in peripheral blood (total leukocytes number and absolute neutrophils (N) number, N adherence to fibre, spontaneous leukocytes migration in a 3 hour test, N phagocytic activity and bactericidal activity of plasma and leukocytes) were estimated. Those indices were again estimated after two week of treatment with ranitidine, 150 mg every 12 hours. After ranitidine treatment reduction of the total leukocytes number and absolute N number was found, as compared with the pretreatment results. In addition to that treatment an increase of N adherence and their phagocytic activity was observed with unchanged leukocyte capacity for spontaneous migration. No statistically significant difference was observed in bactericidal activity of plasma and leukocytes. The following conclusions were reached. 1. Two-week treatment of duodenal ulcer patients with 150 mg ranitidine every 12 hours was followed by reduction of the total leukocytes and N numbers in peripheral blood, and by augmentation of their adherence and phagocytic activity. 2. Bactericidal activity of plasma and leukocytes and leukocytes capacity for spontaneous migration did not show any changes after two-week ranitidine treatment of duodenal patients.