PubMed Health⌕ Search

Biomedical subjects

A Hoffmeister

Publications and source records attributed to A Hoffmeister.

At least 19 recordsLinked to original sources
PubMed2006

[A 32-year-old patient with diarrhoea and acute kidney failure].

A 32-year-old male patient presented in the emergency department of our hospital with acute vomiting and diarrhoea. He reported occasional non-severe diarrhoea over several years in the past. Furthermore, at the time of presentation the patient had had anuria for several days. A prerenal and postrenal origin of the renal failure was excluded. A renal biopsy was performed and histopathological examination displayed findings consistent with a haemolytic-uraemic syndrome but no signs of glomerulonephritis. MRI examination of the small bowel revealed inflammatory alterations typical for Crohn's disease, even without histological verification. We describe haemolytic-waemic syndrome as manifestation of Crohn's disease for the first time.

Acute Kidney Injury↗
PubMed2003

[Moderate alcohol consumption and plasma concentration of sensitive markers of inflammation. Comment on an atheroprotective relationship].

BACKGROUND AND OBJECTIVE: Changes in lipoproteins and hemostasis only incompletely explain the reduced cardiovascular mortality associated with light to moderate alcohol consumption. Since increasing evidence suggests that atherosclerosis can be considered to be a chronic inflammatory process, we sought to assess the association between daily alcohol consumption and levels of sensitive markers of inflammation. STUDY PARTICIPANTS AND METHODS: 478 voluntary blood donors (358 men, 120 women) aged 40 to 68 years were categorized into four groups according to their self-reported amount of daily alcohol consumption: 0 g/day, >0 - 20 g/day, >20 - 40 g/day, and > 40 g/day. Means of various sensitive markers of inflammation (C-reactive protein (CRP), serum amyloid A (SAA), interleukin-6 (IL-6), intercellular adhesion molecule-1, plasma viscosity und albumin) were calculated and compared by bivariate and multivariate analyses. RESULTS: More than 80 % of the study participants reported to consume alcohol, mainly beer. We found statistically significantly decreased levels of SAA, CRP, and plasma viscosity in subjects with light-to-moderate alcohol intake (>0 - 20 g/day and > 20 - 40 g/day, respectively), and a trend for increased levels of albumin in these subjects compared to non-drinkers. After multivariable adjustment for potential confounders (age, gender, body mass index, cigarette smoking, years of school education, and physical activity) a significant U-shaped association (p = 0.02) between levels of SAA and the amount of daily alcohol intake remained: there were 0.75 mg/l and 0.70 mg/l lower mean levels, respectively, of SAA in subjects with light-to-moderate alcohol intake compared to those of non-drinkers. Subjects with an alcohol intake of > 40 grams per day showed a statistically significant increase in levels of interleukin-6 (0.50 pg/ml) compared to non-drinkers. CONCLUSION: Potential anti-inflammatory properties of moderate alcohol consumption might represent an additional mechanism to explain its atheroprotective effect.

Adult↗
PubMed2003

[Effect of molsidomine on rheological parameters and the incidence of cardiovascular events].

BACKGROUND AND OBJECTIVE: In-vitro studies revealed that nitric oxide (NO) may affect rheological parameters. We studied the effect of highly-dosed NO-donor molsidomine on blood rheology and the impact of rheological parameters on the incidence of severe cardiovascular events. PATIENTS AND METHODS: In this randomized, placebo-controlled and double-blind trial 166 patients (60 +/- 10 years) with stable angina pectoris and coronary intervention received molsidomine 3 x 8 mg t. i. d. (controlled release tablets) or placebo for 6 months. Patients with inflammatory/neoplastic disorders or elevated values of C-reactive protein were excluded from analysis. A rheological profile (plasma viscosity, blood viscosity, aggregation and flexibility of erythrocytes, filtrability of leukocytes, fibrinogen levels) was done initially and after 6 months. Adverse cardiovascular events (death, myocardial infarction, stroke, coronary/peripheral revascularization) were recorded during 12 months. Furthermore, the impact of rheological parameters regarding the occurrence of severe cardiovascular events (death, myocardial infarction, stroke) was evaluated during a follow-up of median 38 months. RESULTS: The data of 137 patients (n = 71 placebo, n = 66 molsidomine) were analysed. The difference of rheological parameters between the two measurements did not vary between the two groups. Analysis of event-free survival with Kaplan-Meier technique revealed no difference between the two groups. Multivariate Cox regression analysis with adjustment for diabetes mellitus, smoking and therapy with statin showed a significant association of fibrinogen and plasma viscosity with the occurrence of severe cardiovascular events. CONCLUSION: Treatment with molsidomine 3 x 8 mg/day for 6 months does not improve blood rheology or reduce cardiovascular events. But elevated levels of fibrinogen and plasma viscosity were associated with the occurrence of severe cardiovascular events.

Blood Viscosity↗
PubMed2002

Homocysteine and methylenetetrahydrofolate reductase genotype: association with risk of coronary heart disease and relation to inflammatory, hemostatic, and lipid parameters.

AIM: It has been suggested that homocysteine (tHcy) levels and methylenetetrahydrofolate reductase (MTHFR) genotype are primary risk factors for coronary heart disease (CHD). We performed a case-control study to investigate whether tHcy levels and MTHFR genotype (677 C-->T mutation and 1298 A-->C mutation) are associated with CHD under special consideration of the possibility for confounding. METHODS: German speaking patients aged 40-68 years who underwent coronary angiography at the University of Ulm between April 1996 and November 1997 and who had at least one coronary stenosis greater than 50% were included in the study. Controls were sampled from voluntary blood donors and were matched for sex and age. tHcy levels were measured by high performance liquid chromatography and MTHFR genotype by means of polymerase chain reaction. In addition, C-reactive protein, fibrinogen, plasma viscosity, leukocytes, HDL-cholesterol and Lp(a) were determined. RESULTS: Overall, 312 patients and 479 controls were enrolled in the study (response in patients 78%, in controls 84%). Mean tHcy value was 9.43 micromol/l in CHD patients and 8.91 micromol/l in controls (P=0.145). Prevalence of 677TT-polymorphism was 9.9% in patients and 10.4% in controls (P=0.295). Prevalence of 1298CC-polymorphism was 9.7% in patients and 13.8% in controls (P=0.346). There was a clear association of tHcy-values, but not of 677TT- or 1298CC-genotype with conventional CHD risk factors. After adjustment for these risk factors no increased risk for CHD could be associated with increased tHcy-values, with 677TT or 1298CC-genotype, or with their combination. Also no statistically significant relationships of these parameters to inflammatory, rheologic or hemostatic parameters or lipids were detectable. CONCLUSION: These results do not confirm an independent relationship of tHcy values and MTHFR genotype with risk of CHD in the population studied.

Adult↗
PubMed2001

Role of novel markers of inflammation in patients with stable coronary heart disease.

The role of novel markers of inflammation in patients with coronary heart disease (CHD) is still unclear. We conducted a case-control study to assess the association between various markers of inflammation and the presence and severity of chronic stable CHD. We included 312 clinically stable patients with angiographically documented CHD, aged 40 to 68 years. Voluntary blood donors (n = 479) matched for age and gender served as controls. High-sensitivity C-reactive protein, serum amyloid A, plasminogen activator inhibitor-1 activity, von Willebrand factor, fibrinogen, plasma viscosity, albumin, and neutrophils were determined. The severity of CHD was evaluated by 3 coronary scoring systems: the clinical 1- to 3-vessel disease score, the American Heart Association extension score (1 to 15 segments), and the Gensini score. All markers of inflammation were highly significantly elevated (all p <0.005) in patients with stable CHD compared with controls. After multivariable adjustment by means of logistic regression analysis, the association between CHD and fibrinogen, plasma viscosity, von Willebrand factor, and plasminogen activator inhibitor-1 activity remained substantial, whereas it decreased in high-sensitivity C-reactive protein, serum amyloid A, and neutrophils. The combination of > or = 2 markers of inflammation was associated with a strongly increased risk of CHD. No association between markers of inflammation and any of the coronary scores applied was found. These results document an independent association between most of the markers of inflammation and chronic CHD, even in clinically stable patients. The combination of several of these biochemical markers, i.e., the determination of an "inflammatory risk profile," may be useful to further stratify cardiovascular risk.

Adult↗
PubMed2001

Helicobacter pylori heat shock protein 60 and risk of coronary heart disease: a case control study with focus on markers of systemic inflammation and lipids.

AIM: it has been suggested that antibodies against heat shock proteins seem to be involved in the pathogenesis of coronary heart disease (CHD). We conducted a case-control study to investigate whether antibodies against Helicobacter pylori heat shock protein 60 (hsp60) are associated with CHD, and focused specifically on markers of systemic inflammation and lipids. METHODS: all patients of German nationality aged 40-68 years who underwent coronary angiography at the University of Ulm between October 1996 and November 1997 and who had at least one coronary stenosis greater than 50% were included in the study. Controls were sampled from voluntary blood donors and were matched for sex and age. H. pylori hsp60 was assessed by Western blot (H. pylori Westernblot, AID Co., Strassberg, Germany). In addition, C-reactive protein, fibrinogen, plasma viscosity, leukocytes, HDL-cholesterol and Lp(a) were determined. RESULTS: overall, 312 patients and 479 controls were enrolled in the study (response in patients 78%, in controls 84%). Whereas 25.0 and 22.4% of the cases showed a hsp60 extinction of 100 or 20-99% (according to the reference blot), respectively, only 21.3 and 14.8% of the controls did so (P=0.004). The age and sex adjusted odds ratio (OR) for CHD was 1.53 (95% confidence interval (CI) 1.14-2.06) given an extinction of 20-100% compared with an extinction of 0-19%. The OR for CHD decreased to 1.28 (95% CI 0.90-1.81) after further adjustment for other covariates. With exception of HDL-cholesterol (lowest in subjects with the highest hsp60 extinction) none of the investigated inflammatory markers was associated with the hsp60 distribution. CONCLUSION: a high H. pylori hsp60 extinction seems not to be an independent risk factor for CHD in this population.

Adult↗
PubMed2001

Characteristics of differences in Helicobacter pylori serology and 13C-urea breath-testing in an asymptomatic sample of blood donors.

Numerous tests, both invasive and non-invasive, are available for the diagnosis of Helicobacter pylori infection. The aim of this study was to evaluate the extent and determinants of differences in serology and 13C-urea breath test (13C-UBT) in diagnosing H. pylori. Four-hundred-and-seventy-four asymptomatic blood donors aged 40 to 68 years (mean age 55.8 years) and of German nationality were recruited between October 1996 and November 1997. H. pylori infection was measured with 13C-UBT and with a commercial IgG-ELISA test (Medac; Hamburg, Germany). A standardized questionnaire was applied to identify factors which could explain discrepant results of 13C-UBT and serology. Prevalence of infection was similar according to both tests (33.1% for 13C-UBT and 30.8% for serology). From the 146 subjects with a positive serology, 121 (82.7%) had a positive 13C-UBT. Previous treatment of H. pylori infection was the strongest predictor of a negative 13C-UBT given positive IgG serology (odds ratio (OR)= 12.87, 95% CI=4.10-40.36). Coffee consumption of more than 3 cups/day was also associated with an increased odds of a negative 13C-UBT given positive serology (OR = 3.12, 95% CI=1.16-8.43). No significant determinants of positive 13C-UBT given negative serology could be identified. These findings suggest a delayed fall in serum antibodies following eradication of the infection to be a major source of differences in H. pylori diagnosis using non invasive 13C-UBT and serology.

Antibodies, Bacterial↗
PubMed2001

Alcohol as a gastric disinfectant? The complex relationship between alcohol consumption and current Helicobacter pylori infection.

Alcoholic beverages have antimicrobial effects against Helicobacter pylori in vitro. To elucidate the relation between alcohol consumption and current infection with H. pylori in vivo, we carried out a pooled analysis of three recent studies from Southern Germany, comprising 1410 adults age 15 to 69. Detailed information on consumption of various alcoholic beverages was collected through standardized questionnaires. Helicobacter pylori infection was measured by 15C-urea breath test. Overall, prevalence of current H. pylori infection was lower among subjects who consumed alcohol (34.9%) than among nondrinkers (38.0%). The adjusted odds ratio was 0.79, with a 95% confidence interval of 0.58-1.08. Furthermore, alcohol consumption showed a strong inverse relation to the result of the 13C-urea breath test, a semiquantitative measure of the bacterial load, among infected subjects. The inverse association between alcohol consumption and H. pylori infection was not monotonic, however. Odds of infection were lowest at moderate levels of alcohol consumption and increased at higher levels of alcohol consumption, regardless of the type of alcoholic beverages consumed. These results support the hypothesis that moderate alcohol consumption may favor suppression and eventual elimination of H. pylori infection. At higher levels of alcohol consumption, the antimicrobial effects of alcoholic beverages may be opposed by adverse systemic effects of drinking, such as adverse effects on the immune defense.

Adolescent↗
PubMed2001

Coronary heart disease risk reduction in a predominantly beer-drinking population.

Moderate alcohol consumption protects against coronary heart disease, but there is ongoing debate about whether the effects and the underlying mechanisms differ by type of alcoholic beverage. In our case-control study from Germany, we assessed and compared the effect of alcohol consumption from various sources on risk of coronary heart disease and its underlying mechanisms. The sample included 312 patients with clinically stable, angiographically confirmed coronary heart disease and 479 healthy controls. After control for potential confounding factors, the odds ratio for coronary heart disease was 0.55 (95% confidence interval = 0.37--0.83) for drinkers compared with nondrinkers. Risk reduction was particularly strong among the majority of study participants who reported drinking predominantly or exclusively beer. Alcohol consumption from various sources was consistently associated with a more favorable profile of lipids and hemostatic factors. Nevertheless, a strong inverse association persisted between beer drinking and coronary heart disease even after control for these "intermediate variables." Our results support suggestions that the protective effect of moderate alcohol consumption against coronary heart disease is mediated in part by beneficial effects of ethanol on lipids and hemostatic factors. Additional mechanisms may account for the strong protective effect of moderate beer consumption.

Adult↗
PubMed2001

Current infection with Helicobacter pylori, but not seropositivity to Chlamydia pneumoniae or cytomegalovirus, is associated with an atherogenic, modified lipid profile.

Infectious agents may be involved in atherothrombogenesis. The potential pathogenic pathway, however, remains unclear. We investigated the association between various infectious agents and lipoproteins known to have an atherogenic effect. We recruited 470 healthy blood donors and 238 patients with angiographically proven coronary heart disease (CHD), aged 40 to 68 years. Seropositivity to Chlamydia pneumoniae (CP), chlamydial lipopolysaccharide, and cytomegalovirus (CMV) was determined; infection with Helicobacter pylori (HP) was assessed by using the [(13)C]urea breath test. In all subjects, total cholesterol, high density lipoprotein (HDL) cholesterol, lipoprotein(a), and various apolipoproteins (apos) were determined. In unadjusted analysis, mean HDL cholesterol concentration was significantly decreased in HP-positive healthy subjects (1.36 vs 1.44 mmol/L, P=0.006) compared with HP-negative subjects. The HDL cholesterol to total cholesterol ratio was significantly decreased in HP-positive (0.259 vs 0.276, P=0.01) and CP-seropositive (0.266 vs 0.280, P=0.04) healthy subjects compared with (sero)negatives. Mean apoAI levels were significantly lower in HP-positive healthy subjects (1.46 vs 1.51 g/L, P=0.03) and in CMV-positive healthy subjects (1.47 vs 1.52 g/L, P=0.01) compared with (sero)negative subjects. After multivariable adjustment by means of linear regression analysis, only the association between HP infection and decreased HDL cholesterol (P=0.002), decreased HDL cholesterol to total cholesterol ratio (P:=0.005), decreased apoAI (P=0.02), and increased apoB (P=0.02) persisted and remained significant. There was no independent association between other lipoproteins and serological markers of CP or CMV infection. Current infection with HP, but not seropositivity to CP or CMV, was associated with an atherogenic, modified lipid profile. These lipid alterations could explain, at least in part, the reported weak association between chronic HP infection and atherosclerotic diseases.

Adult↗
PubMed2001

Plasma fibrin D-dimer levels and risk of stable coronary artery disease: results of a large case-control study.

Increased levels of fibrin D-dimer are indicative of a hypercoagulable state, as found in acute coronary syndromes. Few well-controlled studies have assessed D-dimers in patients with stable coronary artery disease (CAD). We measured levels of D-dimers (in ng/mL by enzyme-linked immunosorbent assay) in 312 patients with angiographically proved CAD and stable angina pectoris and in 477 age- and sex-matched healthy blood donors. Demographic characteristics were assessed by a standardized questionnaire, and a complete lipid profile was performed for all subjects. In addition, a variety of other markers of hemostasis and inflammation were measured. The distribution of D-dimer levels was skewed to the right, and plasma median levels were higher in cases than in controls (median: 11.2 vs 2.8 ng/mL; P<0.001). In controls, correlations of D-dimer were found with fibrinogen, plasma viscosity, and interleukin-6. In logistic regression analysis, the age- and sex-adjusted odds ratio (OR) for the presence of CAD was 2.6 (95% confidence interval [CI], 1.9 to 3.5) when the highest quartile of the D-dimer distribution was compared with the combined lower 3 quartiles. The OR did not change appreciably after controlling for nonlipid risk factors (OR, 2.7; 95% CI, 1.9 to 3.9) and remained significant after further adjustment for other hemostatic parameters (OR, 2.4; 95% CI, 1.7 to 3.3) and markers of inflammation (OR, 2.1; 95% CI, 1.5 to 2.9). Plasma D-dimer levels are strongly and independently associated with the presence of CAD in patients with stable angina pectoris. These results support the concept of a contribution of intravascular fibrin to atherothrombogenesis.

Adult↗
PubMed2000

Seropositivity to chlamydial lipopolysaccharide and Chlamydia pneumoniae, systemic inflammation and stable coronary artery disease: negative results of a case-control study.

OBJECTIVES: We investigated the association between seropositivity to chlamydial lipopolysaccharide (cLPS) or Chlamydia pneumoniae (CP) and angiographically documented coronary artery disease (CAD), and we examined the relationship between serostatus and markers of systemic inflammation. BACKGROUND: The potential contribution of CP to atherogenesis is still a matter of debate, and inflammation has been suggested to represent the link between infection and atherosclerotic disease. METHODS: Subjects age 40 to 68 years were recruited for this case-control study between October 1996 and November 1997: 312 patients with at least one coronary stenosis >50% and 479 age- and sex-matched blood donors without manifest CAD or history of angina. Antibodies against cLPS and CP, C-reactive protein (CRP), fibrinogen, plasma viscosity, leukocytes and neutrophils were determined. The study had a power of >80% to detect an odds ratio (OR) of 1.55 or above for the prevalence of immunoglobulin (IgG) antibodies against cLPS at a significance level of alpha = 0.05. RESULTS: Prevalence of IgG antibodies against cLPS was not different between cases and controls (61% vs. 62%; p = 0.7). The adjusted OR for the presence of CAD given positive IgG serostatus against cLPS was 0.9 (95% CI; 0.6 to 1.3). Similarly, no difference in the prevalence of IgG antibodies against CP was seen (88% vs. 87%; p = 0.6); the adjusted OR was 1.0 (95% CI; 0.6 to 1.6). Markers of inflammation did not show any statistically significant difference between cLPS seropositives and seronegatives. CONCLUSIONS: Our results indicate no strong association between CP and CAD, and increased systemic inflammation in patients with CAD does not seem to be due to seropositivity to cLPS or CP.

Adult↗
PubMed2000

Chronic pancreatitis associated with an activation peptide mutation that facilitates trypsin activation.

BACKGROUND & AIMS: Mutations of the cationic trypsinogen have been described in hereditary pancreatitis. We report a new trypsinogen mutation in the activation peptide of the proenzyme in a family with chronic pancreatitis. METHODS: The coding region of the cationic trypsinogen gene was sequenced after polymerase chain reaction amplification. The following peptides homologous to the N-terminal end of cationic trypsinogen were synthesized (one-letter code, mutated amino acid underlined): wild-type peptide, APFDDDDKIVGG; pD22G, APFDDDGKIVGG; pK23R, APFDDDDRIVGG. The sequences of pD22G and pK23R correspond to the recently identified mutation K23R and to the mutation described here (D22G). To mimic trypsinogen activation, these peptides were digested with trypsin for 30 minutes at pH 5.0-8. 0, and the fragments were analyzed by high-performance liquid chromatography. RESULTS: In a family with clinical evidence of hereditary chronic pancreatitis, a missense mutation of codon 22 (GAC-->GGC) of the cationic trypsinogen was found. This mutation results in a substitution of aspartic acid by glycine; therefore, the mutation was called D22G. Chromatographic analysis of tryptic digests of the peptides pD22G and pK23R showed hydrolysis rates of 22% and 75%, respectively, whereas the wild-type peptide was hydrolyzed at only 6%. The cleavage rates were reduced at lower pH, and no hydrolysis occurred without trypsin. CONCLUSIONS: The activation peptides of the trypsinogen variants D22G and K23R could be released at a higher rate than in wild-type trypsinogen, resulting in increased amounts of trypsin in the pancreas, which could initiate pancreatitis.

Adult↗
PubMed1999

Infection with Helicobacter pylori is not a major independent risk factor for stable coronary heart disease: lack of a role of cytotoxin-associated protein A-positive strains and absence of a systemic inflammatory response.

BACKGROUND: There is controversy about the association between Helicobacter pylori infection and manifestations of coronary heart disease (CHD), the potential role of the more virulent H pylori strains, and whether or not a positive serostatus is related to increased levels of markers of systemic inflammation. METHODS AND RESULTS: We assessed the prevalence of an infection with H pylori and in particular the anti-cytotoxin-associated protein A (CagA) antibody response of the more virulent strains expressing CagA in 312 patients with stable CHD and in 479 control subjects. Serological prevalence of H pylori infection (IgG titer) was significantly higher in patients than in control subjects after adjustment for age and sex (44.2% versus 31.3%, P<0.001). After adjustment for various covariates in multiple logistic regression, the odds ratio (OR) for CHD was 1.3 (95% CI, 0.9 to 1.9) given a positive IgG serostatus. The prevalence of CagA-positive strains was 27.9% in patients and 21.7% in control subjects (P=0.076 adjusted for age and sex). The OR for CHD in the fully adjusted model was 1.1 (95% CI, 0.7 to 1.7). None of the inflammatory markers (C-reactive protein, fibrinogen, plasma viscosity, or leukocytes) was significantly different according to serostatus. CONCLUSIONS: In this large case-control study, the association of H pylori infection with stable CHD was strongly reduced and was no longer statistically significant after controlling for potential confounders. We also found no independent association between the more virulent strains and CHD. In addition, a positive serostatus was not associated with a systemic inflammatory response. Thus, these data do not support the hypothesis that infection with H pylori might be a major risk factor for stable CHD.

Aged↗
PubMed1999

Cytomegalovirus infection and coronary heart disease: results of a german case-control study.

This case-control study investigated whether previous infection with cytomegalovirus (CMV) was associated with coronary heart disease (CHD). In total, 312 patients of German nationality aged 40-68 years who had a coronary stenosis of >50% of the luminal diameter were recruited for study. Controls (n=479) were voluntary blood donors. CMV serology was performed to determine presence of specific CMV antibodies (IgG, IgM, IgA ELA test; Medac, Hamburg, Germany). Rheologic and inflammatory markers were determined. The prevalence of specific IgG antibodies against CMV was 54.5% in cases and 49.9% in controls (P=.116). The odds ratio for CHD was 1.21 (95% confidence interval, 0.84-1.75) given a positive serostatus of specific IgG antibodies after adjustment for covariates. With the exception of C-reactive protein in controls, none of the rheologic or inflammatory markers was associated with CMV serostatus. Thus, serologic evidence of previous infection with CMV was not a major risk factor for CHD in this population.

Adult↗