Biomedical subjects

Zoltán Prohászka

Publications and source records attributed to Zoltán Prohászka.

At least 19 recordsLinked to original sources

PubMed2007

Relationship between copy number of genes (C4A, C4B) encoding the fourth component of complement and the clinical course of hereditary angioedema (HAE).

In order to study if in patients with hereditary angioedema (HAE), copy number of the two genes (C4A and C4A) encoded in the central region of main histocompatibility complex (MHC) influences the diagnostically important C4 serum concentration as well as the clinical course of the disease, we determined copy number of the complement C4A and C4B genes in DNA samples of 95 HAE patients and 246 healthy controls. Distribution of both the C4A and C4B copy numbers significantly (p=0.0183 and 0.0318, respectively) differed between the two groups, the most marked difference we observed was the lower frequency of the high (3 or 4) C4A copy numbers in the patients. As it expected, the dosage of both C4A and C4B genes positively correlated to the longitudinally measured serum C4 concentrations. Moreover, we found an unexpected clinical correlation with the dosage of the C4B gene. The course of the disease was milder in the 9/95 patients carrying 3 or 4 copies of C4B gene, compared to the rest of patients, i.e. diagnosis was established at significantly (p=0.0052) older age (36.0 (31.0-39.5)) years versus 20.5 (7.5-31.5 years), bi-yearly attack rate was significantly (p=0.0145) lower (1.0 (0.0-11.0)) versus 11.0 (3.5-21.5), and the over-all activity of the classical pathway and the enzyme-inhibitor activity of the C1-inhibitor (C1-INH) was closer to the normal values. These observations indicate that high copy number of the C4B gene can be a protective factor against disease severity in HAE and therefore its determination is warranted.

Adolescent↗

PubMed2007

Chaperones as part of immune networks.

Network theory is increasingly accepted as a basic regulatory mechanism in diverse immunological functions. Heat shock proteins (Hsps) are involved in multiple networks in the immune system. Hsps themselves (foreign or endogenous) activate innate immunity and play important roles to deliver self or nonself materials to antigen presenting cells. However, Hsps are immunodominant antigens during infectious diseases making self Hsps endangered targets of autoimmunity by cross-reactive clones. Therefore, it is not surprising that the mechanism of protection of self Hsps is not clonal deletion in natural self tolerance; rather, self Hsps are protected by active regulating natural autoimmunity. The active regulatory/protective immunity is accomplished by natural autoantibodies and regulatory T cells, both recognizing Hsps. The multiple involvements of Hsps in immune networks make them ideal targets of therapy in autoimmune diseases. Indeed, immunotherapy with Hsps was recently reported to be effective treatment modality against cancer, arthritis or diabetes mellitus.

Animals↗

PubMed2006

Factor V Leiden and apolipoprotein E genotypes in severe femoropopliteal atherosclerosis with restenosis.

BACKGROUND: The role of factor V (Leiden) mutation, thrombophilia, and apolipoprotein E (apoE) alleles in the pathogenesis of accelerated atherosclerosis and restenosis was studied in patients requiring reoperation within five years after femoropopliteal angioplasty with artificial grafts. METHODS: One hundred ninety-eight consecutive patients with femoropopliteal atherosclerotic disease, reoperated for restenosis were contacted by phone and 100 of them returned for laboratory and clinical work-up. In addition to clinical evaluation and routine laboratory investigations, parameters of lipoprotein metabolism, factor V (Leiden) mutation and apolipoprotein E (apoE) allele were studied by PCR amplification of DNA and endonuclease digestion techniques. RESULTS: A significantly higher incidence of factor V (Leiden) mutation was found in patients with atherosclerosis and restenosis, compared to 445 healthy blood donors (13/200, 6.5% vs. 34/890, 3.8%, p=0.0379). Distribution of the alleles of the apolipoprotein E (apoE) gene was different, when the patients were compared to 372 controls; however, the difference only approached the level of statistical significance (25/200, 12.5% vs. 56/744, 7.5%, p=0.0515). Comparing the two groups, the number of epsilon4 allele carriers was significantly higher among patients with restenosis (25/100, 25% vs. 53/272, 14%, p=0.0147). CONCLUSION: Factor V (Leiden) mutation may influence the progression of atherosclerosis and the development of restenosis after revascularization in patients with accelerated femoropopliteal atherosclerosis. Further investigation is needed whether long-term anticoagulation has an impact or not on the course of disease in such cases. ApoE epsilon4 allele should be screened in patients with femoropopliteal atherosclerosis, because it indicates a faster progression of atherosclerosis and may predict restenosis after revascularization procedure.

Adult↗

PubMed2006

Associations between interleukin-6 genetic polymorphisms and levels of autoantibodies to 60-kDa heat-shock proteins.

AIMS: Previously we reported an association between levels of anti-Hsp60 autoantibodies and interleukin-6 (IL-6) -174 SNP in Finnish population. The aim of this study was to investigate the same association in an independent population and to study four recently described SNP in IL-6. MATERIALS AND METHODS: 313 healthy Hungarian subjects were recruited and genotyped for IL-6 -174(G-->C), -9316(T-->C), -1363(G-->T), +1753(C-->G), +2954(G-->C). IgG antibodies to Hsp60 were measured by ELISA. LD between SNPs was computed by Haploview 3.2 software. RESULTS: A strong association between IL-6 -174 polymorphism and anti-Hsp60 autoantibody levels was observed. Carriers of -174 CC genotype had significantly lower levels of anti-Hsp60 (p = 0.0052). Eight haplotypes were observed with five SNP-s and autoantibody levels in individuals carrying the most common haplotype (containing allele C of -174) were significantly lower than in all other genotype combinations (p = 0.026). CONCLUSIONS: Allele C of -174 promoter polymorphism of the IL-6 gene was repeatedly shown to be associated with low anti-Hsp60 autoantibody levels. Strong linkage in the IL-6 gene was observed and the most frequent haplotype containing the -174 C allele was significantly associated with autoantibody levels. Since the -174 SNP of IL-6 is a functional polymorphism, our results indicate for a direct regulatory effect of IL-6 genotypes in the determination of autoantibody levels.

Adult↗

PubMed2006

Association of increased serum heat shock protein 70 and C-reactive protein concentrations and decreased serum alpha(2)-HS glycoprotein concentration with the syndrome of hemolysis, elevated liver enzymes, and low platelet count.

The primary aim of this study was to determine serum Hsp70 concentrations in HELLP syndrome. We measured also the serum concentrations of three acute phase proteins: C-reactive protein (CRP), alpha(2)-macroglobulin (AMG) and alpha(2)-HS glycoprotein (AHSG). Ten severe preeclamptic patients with HELLP syndrome, 20 severe preeclamptic patients without HELLP syndrome and 20 normotensive, healthy pregnant women were included in this case-control study. Serum concentrations of Hsp70, CRP, AMG and AHSG were measured using an enzyme-linked immunosorbent assay (Hsp70), particle-enhanced immunoturbidimetric assay (CRP) and radial immunodiffusion (AMG, AHSG). The serum Hsp70 and CRP concentrations were significantly higher, whereas the serum AHSG concentration was significantly lower in the HELLP group (H) than the severe preeclamptic (P) and control (C) groups (median (25-75 percentile); Hsp70: 2.02 ng/ml (0.76-2.23) (H) versus 0.54 ng/ml (0.47-0.79) (P), p<0.01, and 0.30 ng/ml (0.27-0.33) (C), p<0.001; CRP: 43.9 mg/l (27.1-84.5) (H) versus 6.5 mg/l (2.7-10.7) (P), p<0.001, and 2.5 mg/l (1.1-6.7) (C), p<0.001; AHSG: 588 microg/ml (492-660) (H) versus 654 microg/ml (576-768) (P), p<0.05, and 738 microg/ml (666-804) (C), p<0.01, respectively). The serum AMG concentration did not differ between the study groups. In the HELLP group, there was a statistically significant negative correlation between serum Hsp70 concentration and platelet count (Spearman R=-0.69, p=0.026). In conclusion, serum Hsp70 and CRP concentrations are increased, whereas serum AHSG concentration is decreased, in HELLP syndrome. The maternal systemic inflammation seems to be more pronounced in HELLP syndrome than preeclampsia without HELLP syndrome, as suggested by the alterations in serum CRP and AHSG levels. However, it requires further investigation to determine whether these changes are causes or consequences of the disease.

Adult↗

PubMed2006

The 8.1 ancestral MHC haplotype is associated with delayed onset of colonization in cystic fibrosis.

Major cause of death in patients with cystic fibrosis (CF) is colonization with Staphylococcus aureus and Pseudomonas aeruginosa. The wide phenotypic variation in CF patients suggests that genes other than the cystic fibrosis transmembrane conductance regulator (CFTR) gene modify the disease. The 8.1 ancestral haplotype (8.1AH) in main histocompatibility complex is associated with alterations of the immune response. To study the influence of carriage of 8.1AH on frequency and onset of colonization in CF patients, DNA samples of 72 CF patients (39 homozygous and 33 heterozygous for DeltaF508) were genotyped for member alleles of the 8.1AH: HLA-DQB1*0201, HLA-DRB1*0301, receptor for advanced glycation end products (AGER) -429C, HSP70-2 -1267G (HSP70-2G) and tumor necrosis factor-alpha (TNF-alpha) -308A (TNF2). Colonization was verified by regular clinical and bacteriological screening. Frequency of colonization was significantly (P = 0.012) lower in the 8.1AH carriers; age, gender and DeltaF508 genotype-adjusted odds ratio to be colonized of the carriers versus non-carriers was 0.112 (0.024-0.520). According to survival analysis, patients with 8.1AH had significantly (P < 0.0001) longer colonization-free period compared with non-carriers. Our novel observations demonstrate that the 8.1AH is associated with delayed onset of colonization in CF, presumably by influencing defense mechanisms against infections.

Adolescent↗

PubMed2006

MBL and C1q compete for interaction with human endothelial cells.

C1q, the recognition molecule of the classical pathway of complement, binds to endothelial cells, leading to cell activation. Mannose-binding lectin (MBL), a recognition molecule of the lectin pathway, is structurally and functionally related to C1q. Therefore, we investigated the interaction of MBL with human umbilical vein endothelial cells (HUVEC). C1q and MBL were purified from normal human plasma and binding to HUVEC was evaluated by flow cytometry. Cross-competition experiments were performed using MBL and C1q labeled with digoxygenin. MBL, similar to C1q, exhibited a dose-dependent binding to HUVEC under calcium-free conditions, suggesting involvement of its collagenous domains. Pre-incubation of HUVEC with MBL inhibited the binding of digoxygenin-labeled MBL at equimolar concentrations, confirming the specificity of the interaction. Pre-incubation of HUVEC with MBL inhibited the binding of C1q and vice versa. Activation of HUVEC with LPS resulted in increased C1q and MBL binding. Stimulation of HUVEC with MBL did not result in a detectable increase in cytokine production. Based on these results, we propose that MBL and C1q bind to a shared receptor on endothelial cells. Interaction of MBL and C1q with receptors on endothelial cells may be involved in inflammatory processes, and in clearance of pathogens and apoptotic cells.

Apoptosis↗

PubMed2006

Modified low density lipoproteins differentially bind and activate the C1 complex of complement.

Several studies suggest that complement plays an important role in atherogenesis. To further investigate this question, we have studied the ability of native and modified forms of low density lipoprotein (LDL) to bind and activate C1, the complex that triggers the classical pathway of complement. For this purpose, LDL was both obtained commercially and purified according to an established procedure, and oxidized (oxLDL) and enzymatically modified (E-LDL) derivatives were generated from each preparation. Whereas the unmodified LDL and oxLDL samples did not activate C1 in the presence of excess C1 inhibitor, the E-LDL derivatives obtained by sequential treatment of LDL with a protease and then with cholesterol esterase triggered efficient C1 activation under these conditions, with activation levels approximately 60% upon incubation with 1 microM E-LDL for 90 min at 37 degrees C. In agreement with these findings, as shown by surface plasmon resonance spectroscopy (SPR), the C1q recognition subunit of C1 showed no interaction with unmodified LDL but bound to both E-LDL samples with high affinity (K(D)=58-75 nM). More unexpectedly, although they did not trigger direct C1 activation, both oxLDL samples were also efficiently recognized by C1q. Whereas the oxLDL derivative of commercial LDL activated C1 to a significant extent ( approximately 30%) in the presence of C-reactive protein (CRP), much lower activation levels (<10%) were obtained using the oxLDL derivative of purified LDL. As measured by SPR, CRP bound equally well to the oxLDL and E-LDL derivatives obtained from purified LDL. These data provide the first experimental evidence that E-LDL triggers efficient C1 activation under conditions close to the physiological situation, suggesting that activation of the classical complement pathway by this derivative may be a crucial factor in the pathogenesis of atherosclerosis. In contrast, it appears unlikely that oxLDL significantly activates C1 directly or in a CRP-dependent manner in vivo.

Animals↗

PubMed2006

Proinflammatory changes in human umbilical cord vein endothelial cells can be induced neither by native nor by modified CRP.

The role of C-reactive protein (CRP) in atherosclerosis is controversial. It is not clear, either, if the presumed endothelium-activating effect of CRP resides in native CRP (nCRP) or in a conformational isoform of CRP known as modified CRP (mCRP). In the present study we evaluated and compared the effect of nCRP, recombinant modified CRP (rmCRP) and urea-modified CRP (umCRP) on human umbilical vein endothelial cells (HUVECs). CRP preparations were carefully analyzed by biochemical, immunological and cell biological methods in order to avoid endotoxin or sodium azide contamination as well as inappropriate conformational changes, which together had possibly been the main reason for the previously published controversial results. Neither nCRP nor mCRP showed significant cytotoxicity up to 100 microg ml(-1) at 24 h but high concentrations of CRPs induced cell death at 48 h. rmCRP but not nCRP nor umCRP showed membrane binding to HUVEC by confocal microscopy. However, none of the CRP forms induced intercellular cell adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin expression or IL-8 production. Monocyte chemotactic protein-1 production was weakly inhibited by high concentration of both nCRP and rmCRP, analyzed by sandwich ELISA. Neither nCRP nor mCRP could induce pro-inflammatory changes in the phenotype of HUVECs. Therefore, our present findings do not support the notion that different isoforms of CRP alone have significant effects on inflammation of the vessel wall via an interaction with endothelial cells (ECs), although one cannot exclude the possibility that there may be significant differences among various types of ECs in the response to CRP.

Atherosclerosis↗

PubMed2006

Determination of complement factor H functional polymorphisms (V62I, Y402H, and E936D) using sequence-specific primer PCR and restriction fragment length polymorphisms.

BACKGROUND: Complement factor H (CFH; HF) is an essential regulatory protein that plays a critical role in the homeostasis of the complement system in plasma. Several polymorphisms and mutations in the complement factor H gene (CFH; HF1) have been identified. These have revealed interesting associations with hemolytic-uremic syndrome and age-related macular degeneration. METHODS AND RESULTS: The aim of this study was to develop a rapid and reliable assay for determining genotypic variants of the CFH gene. Sequence-specific primer PCR and restriction fragment length polymorphism techniques were chosen for the analysis of CFH polymorphisms. The assays detected the following published single nucleotide polymorphisms of CFH in our Caucasian population (n = 271): rs800292, 257G-->A (V62I); rs1061170, 1277T-->C (Y402H); and rs1065489, 2881G-->T (E936D). The allele frequencies (257G = 0.850, 1277T = 0.574, and 2881G = 0.839) that we obtained from a healthy Hungarian population were consistent with previously published results. CONCLUSION: These analytical methods are simple, reliable, and rapid to perform, and are amenable to automation. Therefore, they could facilitate large-scale genotypic analyses of the CFH gene in various diseases, such as hemolytic-uremic syndrome, age-related macular degeneration, and cardiovascular diseases.

Adult↗

PubMed2006

Elevated complement C3 is associated with early restenosis after eversion carotid endarterectomy.

Early restenosis following carotid endarterectomy (CEA) is an inflammatory process leading to myointimal hyperplasia of smooth muscle cells. The risk for restenosis is increased in homozygous carriers of the normal (A) allele of mannose-binding lectin (MBL2) gene. Our objective was to study the associations of C3 and as control three non-complement acute-phase reactants (APRs) (C-reactive protein, haptoglobin and alpha2HSglycoprotein) with early restenosis following CEA. We also considered, whether MBL2 genotype relates to C3 levels and to the risk of restenosis. Concentrations of the APRs were determined by radial immunodiffusion or immunoturbidimetric methods in 64 patients who underwent eversion CEA and were followed up with carotid duplex scan (CDS) examinations for at least one year. MBL2 genotypes were determined by a PCR-SSP method. C3 levels increased during the follow-up and correlated with the percentage of restenosis detected by CDS at 14 months postsurgery, in MBL2 A/A allele carriers. Patients with high C3 levels had nearly five-fold higher odds for the presence of significant restenosis (>50% reduction in diameter) even after adjusting for MBL2 genotype, age and gender. By contrast, no such associations were detected between the non-complement APRs and early restenosis. C3 is associated with and might have a direct role in the development of an early restenosis following CEA, which is partially related to an intact MBL lectin pathway, thus determining C3 levels might have clinical importance. On the other hand, our results indicate that the regulation of C3 differs from non-complement APRs.

Adult↗

PubMed2005

Chaperone-related immune dysfunction: an emergent property of distorted chaperone networks.

Molecular chaperones (heat shock proteins) are important components of cellular networks, such as protein-protein and gene regulatory networks. Chaperones participate in the folding of immunologically important proteins, presentation of antigens and activation of the immune system. Here, we propose that chaperone-related immune dysfunction might be more general than was previously thought. Mutations and polymorphism of chaperones and the regulators of their synthesis, heat shock factor-1, chaperone diseases, sick chaperones and chaperone overload might all affect (mostly impairing) immune responses.

Animals↗

PubMed2005

High rate of early restenosis after carotid eversion endarterectomy in homozygous carriers of the normal mannose-binding lectin genotype.

BACKGROUND AND PURPOSE: Mannose-binding lectin (MBL) is thought to influence the pathophysiology of cardiovascular disease by decreasing the risk of advanced atherosclerosis and by contributing to enhanced ischemia reperfusion injury. Thus, we investigated the role of MBL in restenosis after eversion endarterectomy in patients with severe carotid atherosclerosis. METHODS: In a prospective study, 123 patients who underwent carotid endarterectomy were followed-up by carotid duplex scan (CDS) sonography for 14 months. In a retrospective study, we examined 17 patients and 29 patients, respectively, who had or had not at least 50% restenosis 29 months after carotid eversion endarterectomy. MBL genotypes were analyzed by a polymerase chain reaction-based method, and MBL serum concentrations were measured. RESULTS: In the prospective study in the patients homozygous for the normal MBL genotype, CDS values were significantly higher after 14 months of follow-up compared with the values measured 6 weeks after surgery (P<0.001). In contrast, only a slight increase was registered in patients carrying MBL variant alleles. The differences were much more pronounced in female than in male patients. Similar differences were observed when patients with high and low MBL serum concentrations were compared. In the retrospective study, a significant increase in the frequency of MBL variant genotypes was observed in patients not experiencing restenosis compared with the patients with restenosis (P=0.007). CONCLUSIONS: These results indicate that reoccurrence of stenosis after carotid endarterectomy is partially genetically determined and imply that MBL contributes significantly to the pathophysiology of this condition.

Aged↗

PubMed2005

Dramatic changes in the serum levels of anti-cholesterol antibodies after eversion endarterectomy in patients with severe carotid atherosclerosis.

Our goal was to study changes in anti-cholesterol antibodies (ACHA) levels in patients with severe carotid stenosis after eversion endarterectomy. Seventy consecutive patients who underwent eversion endarterectomy at the Department of Cardiovascular Surgery, Semmelweis University, Budapest, were included in the study. Serum samples from 66 healthy volunteers served as controls. Patients had medical check up at 5.7 (4.6-8.0) weeks (median (interquartile range)), 6.8 (6.2-7.9) months as well as 13.8 (12.3-19.0) months after endarterectomy. In all patients the carotid arteries were investigated by color duplex ultrasound. ACHA concentrations were determined in the serum samples taken before operation as well as at the first and last follow-up visits by using an ELISA method. ACHA concentrations (median (interquartile range) were found to be significantly (p<0.0001) lower in the sera of the patients with carotid atherosclerosis (13.5 (8.4-21.3)AU/ml) than in the healthy subjects (26.1 (20.9-33.2)AU/ml) (Mann-Whitney test). Strong negative correlation was found between the preoperative ACHA and LDL-cholesterol levels (r=-0.413, p=0.0004). Serum ACHA concentrations significantly (p<0.0001) increased from the values measured before operation (13.5 (8.4-21.3)AU/ml) to 27.1 (19.9-34.7)AU/ml measured at the end of the 14 months long follow-up. Increase occurred only in patients with low or medium baseline ACHA concentration. Our present findings indicate that after surgical removal of atherosclerotic plaques from the carotid arteries the reduced baseline levels of ACHA reach normal values in 1 year. Different not mutually exclusive mechanisms (binding of ACHA to lipid/lipoproteins particles, to advanced plaques or reversibly injured endothelial cells in CNS) can be responsible for this novel finding.

Acute-Phase Proteins↗

PubMed2005

Development of a sensitive assay for the measurement of antibodies against heat shock protein binding protein 1 (HspBP1): increased levels of anti-HspBP1 IgG are prevalent in HIV infected subjects.

The 70 kDa heat shock protein (Hsp70) is generally considered to be an intracellular protein, however, there is evidence that Hsp70 can be found in the extracellular environment. Hsp70 and antibodies against Hsp70 have been reported in human serum. Recent evidence has shown that Hsp70 antibodies are elevated in HIV infected individuals. This study reports on the antibody levels against a co-chaperone, HspBP1, that regulates Hsp70 activity. We have developed a solid-phase enzyme linked assay for the determination of anti-HspBP1 IgG antibodies. We report here that HspBP1 antibodies are present in human serum and the levels are elevated approximately twofold in HIV infected patients. There was no correlation between HspBP1 antibody levels and clinical parameters nor was there a relation between anti-Hsp70 levels and anti-HspBP1 levels. The presence of HspBP1 antibodies in human serum suggests that the protein may also be present in the serum. The increased level of HspBP1 antibodies in HIV infected individuals suggests a relationship directly to the virus or indirectly to secondary consequences of HIV infection.

Adaptor Proteins, Signal Transducing↗

PubMed2005

Antibodies against heat shock proteins and cholesterol in HIV infection.

This review summarizes data on the presence and function of different heat shock proteins (Hsp) in the HIV virions and the infected cells. A 60 kD heat shock protein-like molecule is present in the envelope of the human immunodeficiency virus type 1 which can specifically interact with the transmembrane glycoprotein gp41. The role of cholesterol in the so-called cholesterol-rich lipid raft where HIV is budding from the infected cells as well as the consequential insertion of cholesterol into the envelope of HIV virion are also discussed. Natural antibodies against 60 kD (Hsp60) and 70 kD (Hsp70) families of Hsp and cholesterol can be detected in most healthy individuals. HIV infection results in a sharp increase in the serum concentration of anti-Hsp70 and cholesterol antibodies whereas no difference in the concentration of anti-Hsp60 antibodies can be detected. Highly active antiretroviral therapy leads to normalization of the levels of both anti-Hsp70 and anti-cholesterol antibodies.

Autoantibodies↗

PubMed2004

Genetic basis of tobacco smoking: strong association of a specific major histocompatibility complex haplotype on chromosome 6 with smoking behavior.

The genetic basis for addiction to tobacco smoking--particularly that of the perception of olfactory stimuli that may be important in reinforcing smoking addiction--is largely unknown. A cluster of genes for olfactory receptors is in close proximity to the MHC region on chromosome 6. Polymorphisms of MHC class III genes (RCCX modules, TNFA promoter polymorphisms) were determined in 101 healthy subjects and 232 coronary artery disease (CAD) patients from Hungary with defined tobacco smoking habits. A highly significant association between ever smoking (past + current smokers) and a specific MHC haplotype was observed (odds ratios = 2.14-4.13; P-values = 0.012 to <0.001). This haplotype is characterized by the presence of C4A null alleles and a solitary short C4B gene linked to the TNF2 allele of the promoter for TNFA gene. This haplotype occurred more frequently in the ever smokers than in the never smokers [odds ratio: 4.97 (1.96-12.62); P = 0.001], and such associations were stronger in women (odds ratio = 13.6) than in men (odds ratio = 2.79). An independent study of complement C4 protein polymorphism and smoking habits in Icelandic subjects (n = 351) yielded similar and confirmative results. Considering the documented link between olfactory stimuli and smoking in females, and the presence of a cluster of odorant receptor genes close to the MHC class I region, our findings implicate a potential role of the MHC-linked olfactory receptor genes in the initiation of smoking.

Adult↗

PubMed2004

[C-reactive protein levels determined by an ultrasensitive method in a healthy Hungarian population].

INTRODUCTION: C-reactive protein (CRP) is a well-known acute phase protein. The concentration of CRP in serum is increased in response to inflammatory stimuli. Increased levels serve to identify organic disease, to monitor disease activity and to assist differential diagnosis. AIM: The aim of the authors' cross-sectional study was to determine CRP distribution of the healthy Hungarian population. METHOD: 207 (79 male, 128 female; mean age: 4 +/- 68 years) healthy blood donors were enrolled for the study. The following parameters were registered: sex, age, body mass index, smoking habits, diabetes mellitus and blood pressure. Serum samples were assayed for total serum cholesterol, triglyceride, erythrocyte sedimentation rate, hemoglobin and for white blood cell count. CRP was measured by ultrasensitive, particle enhanced immunoturbidimetric assay. RESULTS: CRP levels were less than 5 mg/L in 81% of the blood donors. Mean level of CRP in the study population was 3.57 mg/L (SD +/- 5.33); the distribution was comparable to the data of already published studies. Comparing laboratory parameters and the risk status stratified according to CRP levels (less or more than 5 mg/L) significant differences were found in BMI (p = 0.0015), in total serum cholesterol (p = 0.0136), in triglyceride (p < 0.0001), in erythrocyte sedimentation rate (p < 0.0001), in white blood cell (p = 0.0007) and granulocyte count (p = 0.0014). Significant correlation was found between age and the concentration CRP (r = 0.22; p = 0.0011). CONCLUSION: The CRP measurement by ultrasensitive method is suitable for cardiovascular risk estimation in apparently healthy men and women. Risk prediction adapted for the Hungarian situation may be stimulated by these data.

Adult↗