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L Romics

Publications and source records attributed to L Romics.

At least 37 records · Page 2Linked to original sources
PubMed2000

Intraabdominal abscess managed successfully via the laparoscopic approach.

A rare complication of laparoscopic fundoplication-an intraabdominal abscess located between the fundus and the caudate lobe of the liver-is described. A 41-year-old man had undergone a laparoscopic Nissen-Rossetti fundoplication for longstanding gastroesophageal reflux disease. On the 5th postoperative day, the patient's general condition became worse, and he developed intermittent-remittent fever (40 degrees C), an elevated white blood cell count (WBC), and an accelerated sedimentation rate. Evidence of leakage was excluded by Gastrografin swallow. The diagnosis was finally revealed by means of ultrasound and computed tomography (CT) scan, which showed an intraabdominal fluid collection with an air cap of ~10 cm in diameter situated between the diaphragmatic crura, the caudate lobe of the liver, and the gastric fundus. The location did not allow semi-invasive management of the abscess, such as ultrasound or CT-guided puncture and drainage. On the 8th postoperative day, a laparoscopic exploration was performed utilizing the previous port sites. The adhesions were easily dissected, and evacuation of ~300 ml of white, dense fluid, and lavage and drainage were performed without intraabdominal dissemination of pus. The patient was discharged on the 12th postoperative day free of symptoms. Microbiological examination of the pus showed the presence of Peptostreptococcus. The patient remained symptom free. At 8 weeks postoperatively, barium swallow, endoscopy, 24-h pH monitoring, and stationary manometry of the esophagus yielded normal results. Because there was no direct evidence of leakage at the fundus, the development of the abscess was concluded to be due to the use of deep transmucosal stitches rather than seromuscular ones to create the wrap. The nonabsorbable multifilament suture material passing through the entire gastric wall could have facilitated bacterial contamination of the operative field.

Abdominal Abscess↗
PubMed2000

Angiotensin II type 1 receptor gene polymorphism and mitral valve prolapse syndrome.

BACKGROUND: Mitral valve prolapse syndrome (MVPS), a term applied to patients who have a variety of symptoms, has been associated with autonomic or neuroendocrine dysfunction. Recent evidence suggests that effects of angiotensin II mediated by the angiotensin II type 1 (AT(1)) receptor are involved in modulation of cardiovascular autonomic control in human beings. Association of a genetic polymorphism (A-C(1166)) of the AT(1) gene with abnormal vasomotion and low blood pressure related to autonomic control has been reported recently. Because the role of this genetic variant in MVPS has not been studied, we performed a case-control study of the A-C(1166) variant in a group of 76 white subjects with MVPS. METHODS AND RESULTS: All patients were genotyped by use of a mismatch polymerase chain reaction/Afl II restriction fragment length polymorphism analysis. Frequency of the C(1166) allele was 0.4 in patients with MVPS and 0.26 in control patients. The difference in genotype (chi square = 6.5; P <.05) and allele (chi square = 5.9; P =.02) frequencies between the groups was significant. The odds ratio in favor of carrying the C allele was 4 times greater for patients with MVP than for control patients (95% confidence interval 1.4 to 12.1). CONCLUSIONS: The current results indicate that the A-C(1166) polymorphism of the angiotensin II type 1 receptor gene is associated with MVPS in the white population.

Adult↗
PubMed2000

Association of primary biliary cirrhosis with vitamin D receptor BsmI genotype polymorphism in a Hungarian population.

We sought to determine the distribution of vitamin D receptor genotypes defined by the BsmI polymorphism and to investigate their association with bone mineral density in patients with primary biliary cirrhosis. Vitamin D receptor genotype and bone mineral density at the lumbar spine was determined in 31 female Hungarian patients with primary biliary cirrhosis and 51 age-matched healthy female controls. The genotype frequency (BB: 45%, Bb: 32%, bb: 22%) of the patients was significantly different from the control group (P = 0.01) due to an overrepresentation of the BB genotype. There was an apparent trend, not reaching statistical significance, for a lower bone mineral density in both the patient and control groups carrying a B allele. In conclusion, we found a strikingly high frequency of the BB genotype in patients with primary biliary cirrhosis, which raises questions about hormonal influences on the development of primary biliary cirrhosis.

Bone Density↗
PubMed2000

Frequencies of certain complement protein alleles and serum levels of anti-heat-shock protein antibodies in cerebrovascular diseases.

BACKGROUND AND PURPOSE: A strong correlation exists between the intensity of atherosclerotic alterations in different arteries. Marked differences exist, however, in the age and sex distribution and risk factors for coronary heart disease (CHD) and cerebrovascular disease (CVD). We therefore performed genetic and immunologic studies in patients with CVD. METHODS: We studied 292 patients with CVD (stroke or transient ischemic attack) and as control either 198 healthy blood donors and 485 healthy elderly (aged >60 years) people (genetic study) or 94 blood donors aged 45 to 60 years and 49 healthy elderly (aged >60 years) people (anti-heat-shock protein [hsp] measurements). Allele frequencies of 3 genes (C4A, C4B, and C3) encoding proteins of the complement system were determined by electrophoresis and immunofixation. Serum concentration of autoantibodies against 60-kDa heat-shock protein (anti-hsp60) was measured by the enzyme-linked immunosorbent assay method. RESULTS: Marked differences were observed between CVD patients and controls in the genetic studies. In the CVD patients aged >60 years, the frequency (11.3%) of the deficient allele of the C4B gene (C4B*Q0) was significantly (P:=0.0003) higher than that of the healthy controls (5.4%). By contrast, in the group aged 45 to 60 years, the frequency of the C4B*Q0 allele was lower in patients than in controls. Serum concentration of anti-hsp60 in the CVD patients did not differ from control values. CONCLUSIONS: In previous studies C4B*Q0 frequency was reported to be higher in CHD patients aged 45 to 60 years than in aged-matched controls. Moreover, high anti-hsp60 levels were found in CHD patients. These findings contrast with our present report of lower frequency of C4B*Q0 in CVD patients. Therefore, genetic and immunologic factors may at least partly explain the differences between the natural history and risk factors of CHD and CVD.

Cerebrovascular Disorders↗
PubMed1999

[Detection of antibodies against pancreatic islet cells in clinical practice].

Development of diabetes mellitus caused by pancreatic beta-cell destruction of autoimmune origin is the result of a long lasting process. The most easily examinable feature of this stage is the occurrence of the islet cell antibodies. The sera which are positive for islet cell cytoplasmic antibodies (ICA), examined by indirect immunofluorescence, contain a mixture of antibodies. The glutamic acid decarbocylase (GAD), the tyrosin phosphatase (IA2), the insulin, and the GM2-1 glycolipid can be the targets of these antibodies. One can routinely examine the ICA, the GADA, the IA2 antibodies. The detection of antibodies against insulin (IAA) and GM-2-1 glycolipid is not invented in the routine laboratory work. The aim of the authors was the evaluation of clinical significance of occurrence of islet cell antibodies: one hundred and eighteen nondiabetic children an adult human being without known diabetic first degree relatives and 366 type 1 diabetic children and adult patients served as controls. The authors evaluated the predictive value of the different islet cell antibodies to the development of type 1 diabetes mellitus in 596 nondiabetic children with type 1 diabetic first degree relatives. The authors looked for markers of beta-cell destruction among sera of 320 diabetics manifested after 30 years of age with at least half a year of non-insulin-dependency and in the sera of 68 females suffered from gestational diabetes after 0-14 years of the index pregnancy. Finally the authors report 7 cases in which the examination of islet cell antibodies helped the diagnosis and classification of diabetes mellitus. Indirect immunofluorescence method was used for the detection of ICA, radioimmunoassay for that of GADA and IA2 antibodies. There was no positive reaction for ICA and GADA in the nondiabetic population without diabetic first degree relatives. Among the freshly diagnosed type 1 diabetic children 39% were positive for only ICA, 44% for only GADA and 80% for any antibodies. Among the freshly manifested type 1 diabetic adults ICA positivity only was observed in 21%, GADA positivity only in 7.1% and 93% for any antibodies. From the 595 nondiabetic children with type 1 diabetic first degree relatives 23 were positive for ICA, from whom 5 became diabetic during a two years observation period. These diabetic children had multiplex autoantibodies besides ICA. One child from this group, who was negative for ICA became diabetic, too. Among type 2 diabetic patients 13% were positive for ICA alone, 17% were positive for GADA alone and 27% were positive for any antibodies. The insulin dependency manifested in a short time was associated with antibody positivity. Among the gestational diabetics 10 were found positive for ICA. From them, 7 were type 1 diabetics, and 3 were type 2 diabetics at the time of the detection of antibodies. The authors suggest the need of determination of islet cell antibodies in the group of nondiabetic first degree relatives of type 1 diabetic patients (ICA, GADA, IA2 and IAA), in the group of non-insulin-dependent diabetics (ICA and GADA) as a screening for later insulin dependency, and in gestational diabetes after delivery (ICA) as screening for type 1 diabetes mellitus.

Adolescent↗
PubMed1999

Apolipoprotein E gene polymorphism frequencies in a sample of healthy Hungarians.

Apolipoprotein E (apo E) has been found to play an important role in lipid metabolism and has been associated with cardiovascular and neurodegenerative conditions. Hungarians have some of the highest rates of cardiovascular morbidity and mortality in the world. This study examines the distribution of apo E alleles and genotypes in a population of healthy ethnic Hungarian blood donors (n = 302). Male (n = 152) and female (n = 150) subjects ranging from 18 to 62 years of age (mean 37.0) were involved. To determine the frequency of apo E alleles, polymerase chain reaction followed by restriction length polymorphism was applied. The analyses of data showed that apo E allele epsilon3 had the greatest frequency in this group (0.807), followed by apo epsilon2 (0.104) and apo epsilon4 (0.087). The highest genotype frequency was found to be epsilon3/3 at 65.2% (n = 197) followed by genotype epsilon3/4 at 15.9% (n = 48), genotype epsilon2/3 at 15.2% (n = 46), genotype epsilon2/2 at 2.3% (n = 7), genotype epsilon2/4 at 1.0% (n = 3) and genotype epsilon4/4 at 0.4% (n = 1). The apo E frequencies found in this study appear to differ from an earlier study of blood donors, where the results are based on apo E phenotyping.

Adolescent↗
PubMed1999

Elevated serum semicarbazide-sensitive amine oxidase activity in non-insulin-dependent diabetes mellitus: correlation with body mass index and serum triglyceride.

Previous clinical studies reported elevated semicarbazide-sensitive amine oxidase (SSAO) activity in insulin-dependent diabetes mellitus (IDDM), but there are not sufficient data about SSAO in non-insulin-dependent diabetes mellitus (NIDDM). The present study was conducted to investigate serum SSAO activity in NIDDM patients compared with nondiabetic and IDDM patients. Serum SSAO activity in 61 patients with diabetes (n = 34 NIDDM and n = 27 IDDM) and 36 controls was determined using 14C-benzylamine as a substrate. NIDDM and IDDM patients exhibited higher SSAO activity compared with controls ([mean +/- SD] NIDDM, 164.60+/-69.43 pmol/mg protein/h, P<.0001; IDDM, 143.91+/-72.45 pmol/mg protein/h, P<.002; control, 91.46+/-28.11 pmol/mg protein/h). There was a significant positive correlation between serum SSAO activity and the body mass index (BMI), body weight, hemoglobin A1c (HbA1c), fasting plasma glucose, and triglycerides. Within the control group, SSAO correlated with total cholesterol levels. The progression and severity of diabetic complications such as angiopathy may be exacerbated by cytotoxic metabolites (e.g., formaldehyde and hydrogen peroxide) formed by SSAO. These results reveal the possibility that elevated serum SSAO activity in association with obesity and hyperlipidemia may be a cardiovascular risk factor in diabetes mellitus.

Adult↗
PubMed1999

Antibodies against human heat-shock protein (hsp) 60 and mycobacterial hsp65 differ in their antigen specificity and complement-activating ability.

Although complement activation appears to have an important role both in the early and late phases of atherosclerosis, the exact mechanism of the initiation of this activation is still unknown. Since injuries of the endothelial cells are known to result in increased stress-protein expression we tested the complement-activating ability of recombinant human 60 kDa heat-shock protein (hsp60). Human hsp60 was found to activate the complement system in normal human serum in a dose-dependent manner. Activation took place through the classical pathway. The lack of complement activation in agammaglobulinemic serum indicates that the classical pathway is triggered by anti-hsp60 antibodies. Hsp60 activated complement in the sera of 74 patients with coronary heart disease as well, and a strong positive correlation (r = 0.459, P < 0.0001) was found between the extent of complement activation and the level of anti-hsp60 IgG antibodies but there was no correlation to the level of anti-hsp65 IgG antibodies. Further distinction between anti-hsp60 and anti-hsp65 antibodies was obtained from competitive ELISA experiments: binding of anti-hsp60 antibodies to hsp60-coated plates was inhibited only by recombinant hsp60 and vice versa. Our present findings indicate that anti-hsp60 and anti-hsp65 antibodies are distinct, showing only partial cross-reactivity. Since complement activation plays an important role in the development of atherosclerosis and the levels of complement-activating anti-hsp60 antibodies are elevated in atherosclerosis-related diseases, our present findings may have important pathological implications.

Adult↗
PubMed1999

Surgical aspects of gastro-esophageal reflux disease--indication for surgery. An update.

Gastro-esophageal reflux disease is regarded as the single most common foregut disorder mainly in Western countries. The pathophysiological background of the disease is multifactorial. The primary aim of the management of gastro-esophageal reflux disease is relieving heartburn and healing esophagitis. The therapeutic objectives are alleviating symptoms, preventing complications and avoiding recurrence. Besides the effective medical treatment nowadays we possess the minimal invasive anti-reflux surgery which gives comparable, even better results than medical therapy does, in cases of patients who are suitable for anti-reflux surgery. The key question is the appropriate patient selection. In order to achieve the most adequate patient selection, diagnostic tools like endoscopy, radiotherapy, esophageal body and sphincter manometry, 24-hour esophageal pH monitoring and occasionally 24-hour bile exposure monitoring and gastric emptying studies are mandatory to carry out preoperatively. On the basis of the results of these tests the tailored concept of anti-reflux surgery can be applied. The importance of experienced surgeon should be pointed out, too.

Antacids↗
PubMed1998

[Incidence of familial defective apolipoprotein B-100 in cases of patients diagnosed with familial hypercholesterolemia].

Familial Hypercholesterolemia (FH) and Familial Defective Apolipoprotein B-100 (FDB) are monogenic, autosome, dominantly inherited diseases appearing as type II/a primary hypercholesterolemia. The frequency of the heterozygositic forms is 1:700-1:500 in European population. Both forms of hypercholesterolemia causes early onset coronary heart diseases (CHD). According to the recommendations of the international MED-PED program (Make Early Diagnoses--Prevent Early Death), we found 73 FH cases and their 377 first relatives (parents, siblings, children) were also assessed. 156 patients were diagnosed clinically FH (131 alive and 25 deceased), and 31.8% of the males and 32.4% of females suffered from early onset CHD. One family with FH consists of 5.46 members on the average and there are 2.39 FH patients in one family. In our FH cohort four patients with FDB (R3500Q mutation) were diagnosed with allelspecific PCR, and the mutation was detectable also in 9 cases out of 11 living family members. The plasma total cholesterol level of the FDB patients--especially at younger age--was very close to the normal values, which is in contrast to the findings in FH patients. Nevertheless, FDB can be one of the independent causes of the early onset CHD. Therefore, in families with high frequency of cardiovascular diseases the R3500Q mutation has to be considered.

Adult↗
PubMed1998

Association of angiotensin II type 1 receptor polymorphism with resistant essential hypertension.

Angiotensin II type 1 receptor (AT1) mediates the vasoconstrictive and growth-promoting effect of angiotensin II in humans. It has been reported that a polymorphism of the AT1 gene (an A/C transversion at position 1166: A-C1166) occurs more frequently in resistant hypertensives taking two or more antihypertensive drugs. On the contrary, a recent study of the influence of the A-C1166 polymorphism on aortic stiffness demonstrated that the distribution of the genotypes did not differ between normotensive and hypertensive subjects. In addition, a recent population-based survey of Caucasian hypertensives reported lower blood pressure values in CC homozygotes than in heterozygotes and AA homozygotes. Because of these controversial results and the lack of a sufficient amount of data the present study was designed to assess the contribution of the AT, gene A-C1166 polymorphism to resistant essential hypertension. Forty-eight subjects with resistant essential hypertension (HT) and 48 normotensive (NT), age and sex-adjusted controls (from a population of 300 healthy blood donors) were selected. All subjects were genotyped for the A-C1166 polymorphism in the 3'-UTR of the AT1 gene using PCR-based techniques. The influence of genotype on blood pressure (BP) was investigated using ANOVA Randomized Complete Block (ANOVA RCB) design according to sex, age and BMI. There were no significant differences in allele or genotype frequencies between HT and NT subjects (X2 = 0.61; P = NS). In HT subjects higher values of systolic blood pressure were associated with the C allele of the AT1 gene only in older and overweight patients (P < 0.001 and P < 0.001, respectively). Also in HT patients an association between the presence of the C allele of the AT1 gene and higher values of diastolic blood pressure was present in overweight patients (P = 0.001). These results suggest that in resistant hypertensive subjects the AT1 A-C1166 polymorphism is potentially involved in the regulation of blood pressure. As the effects of genotypes on blood pressure are pronounced in older and overweight subjects this polymorphism may amplify the effects of age and BMI on resistant essential hypertension.

Adrenergic beta-Antagonists↗
PubMed1998

Detection of factor V Leiden mutation in severe pre-eclamptic Hungarian women.

Pre-eclampsia is a pregnancy-related disorder that complicates approximately 5% of all pregnancies and is cited as the primary cause of worldwide maternal and fetal mortality. The factor V Leiden mutation has been implicated in the development of severe pre-eclampsia. In order to investigate this association, a sample of 198 Hungarian women was recruited and enrolled in one of the three groups based on reproductive and health status: those as classified as pregnant and healthy (n = 71), those diagnosed as pregnant and severe pre-eclamptic (n = 69), and those found to be healthy and non-pregnant (n = 58). The presence of factor V Leiden mutation was determined by using polymerase chain reaction (PCR) followed by restriction fragment length polymorphism analysis (RFLP). We identified three (5.2%) heterozygous among healthy non-pregnant participants, five (7.0%) heterozygous among healthy pregnant participants and 13 (18.8%) heterozygous among pre-eclamptic women (p < 0.05, 95% CI). Our result supports the previous observation that carriers of factor V Leiden mutation are at increased risk for developing severe pre-eclampsia.

Adolescent↗
PubMed1997

Association of the apolipoprotein A-IV codon 360 mutation in patients with Alzheimer's disease.

Specific apolipoprotein E (apoE) alleles determines, in large part, the risk and mean age of onset familial and sporadic Alzheimer disease. The unresolved issues in this relationship support the contribution of other environmental and genetic parts. Among the candidates the apolipoprotein A-IV (apoA-IV) a component of plasma lipid particles similar to apoE has been suggested to play a role in brain metabolism. Since apoA-IV has a common DNA based protein polymorphism with a different function we determined apoA-IV (360:Gln:His) DNA polymorphism in 63 late-onset sporadic Alzheimer's patients. We found that the APOA-IV (360:His) heterozygosity occurs significantly more frequent (20.6% vs. 7.0%, P = 0.021, odds ratio 3.4 (confidence interval 1.1-10.2)) comparing age-matched controls with normal mental score. The significant difference in apoA-IV allelic distribution has been detected dominantly in patients with non-apoE4 genotype. Our data indicate that the apoA-IV-2 allele may confer one of the susceptibility markers for Alzheimer's disease (AD) and strengthen the polygenic risk determination of the variability in expression of AD.

Aged↗
PubMed1997

[Study of low density lipoprotein (LDL) receptor mutations, using restriction endonucleases, in familial hypercholesterolemia].

Familial hypercholesterolemia (FH) is an autosomal dominant metabolic disorder caused by different mutations in the low density lipoprotein receptor (LDLR) gene. We analyzed 13 families (23 patients) with FH and 36 subjects with normocholesterolemia by restriction fragment polymorphism (RFLP) using enzymes Xbal, BgIII and PvuII. At the 3' end of LDLR an extra 4.4 kb band has been found by Xbal digestion in one patient and it has been proved to be a "de novo" form of mutation. In the 5' end of LDLR gene a combined mutation has been identified in two FH families. The Xbal RFLP has yielded an extra band of 24.5 kb and an another extra band of 17.5 kb has been found by BgIII digestion. It has been suggested that the simultaneous occurrence of 3.3 kb extended deletion (intron 3) and 4.8 kb extended insertion (intron 1) is present. In our study the frequency of P2 allele (PvuII RFLP) in FH patients did not differ from normocholesterolemic controls.

Adolescent↗