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Query: UMLS:C0021311 (Infection)
 38,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the association among elevations in acute phase proteins, reported illness, and hyporetinolemia in 234 pregnant Nepali women with (cases) and without (controls) night blindness. Serum alpha1-acid glycoprotein (AGP) and C-reactive protein (CRP) were inversely associated with serum retinol concentrations. Elevations in the concentration of CRP in both cases and controls and of AGP in cases were associated with significant reductions (approximately 0.2-0.3 micromol/L) in serum retinol. The risk of a low serum retinol concentration (< 0.7 micromol/L) with elevated AGP (> or = 1 g/L) and CRP (> or = 5 mg/L) concentrations was significantly higher in cases (odds ratios = 8.6 and 4.3, respectively) than in controls (odd ratios = 1.9 and 2.4, respectively). A 7-d morbidity history indicated that cases were significantly more likely than controls to report symptoms of infections of the urinary, reproductive, and gastrointestinal tracts. Only a few of these symptoms (diarrhea, nausea, and vomiting) were significantly associated with low serum retinol concentrations. Illness in the previous week and elevated CRP or AGP concentrations were synergistically associated with lower serum retinol. For example, the reduction in serum retinol in women with diarrhea and elevated AGP was 0.54 micromol/L, compared with a reduction of 0.03 micromol/L in those with diarrhea only. AGP and CRP may provide useful information about the effect of reported illness on hyporetinolemia in pregnancy. Infection-related hyporetinolemia may predispose women to night blindness during pregnancy in Nepal.
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PMID:Hyporetinolemia, illness symptoms, and acute phase protein response in pregnant women with and without night blindness. 1087 52

Lipopolysaccharide (LPS) of gram-negative bacteria is capable of activating the immune system of higher animals, which may lead to cytokine-induced lethal shock and death. LPS has little toxicity for the frog and fish, but it kills the horseshoe crab instantly by causing intravascular blood coagulation. The response to LPS evolved from simple reactions in lower animals into an intense reaction in mammals that involves a massive immune activation leading to a profound neuroendocrine and metabolic response. This is now known as the acute-phase response (APR). During APR, LPS-binding proteins (LBP) are produced by the liver in rapidly increasing quantities under the influence of interleukin-6, glucocorticoids, and catecholamines. After combination with LPS, LPB is capable of activating monocyte-macrophages and granulocytes via the CD14 surface receptor. Other receptors (CD18, 80-kDa receptor) allow for direct action by LPS of phagocytes, B and T lymphocytes, and other cells. Numerous other acute-phase proteins are produced in the liver, including C-reactive protein, complement components, fibrinogen, enzyme inhibitors, and anti-inflammatory proteins. Similar responses may be stimulated by subtoxic doses of LPS or by detoxified LPS, which manifest in endotoxin tolerance. Tolerant animals and man show increased resistance to LPS, to infections, and to various noxious insults. Infection and various forms of tissue injury are also capable of causing APR. There is much evidence to indicate that APR, which manifests in febrile illness, is an efficient host defense reaction. It is an emergency response in cases where specific immunity fails to protect the host. Therefore, the neuroimmunoregulatory network converts the immune system to a less specific, but rapid and more efficient response, APR. The hypothesis is presented that intestinal LPS serves to amplify the APR in response to various insults, which contribute to host defense, regeneration, and healing.
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PMID:Neurohormonal host defense in endotoxin shock. 962 5

A prospective study was performed to assess the potential value of interleukin (IL)-8, IL-6, and C-reactive protein (CRP) serum levels to predict fever, gram-negative bacteremia and complicated infection in neutropenic patients with cancer. Serum samples were obtained three times a week during 208 neutropenic episodes following cytotoxic chemotherapy. Fever of any cause developed during 104 out of 191 evaluable episodes. Serum levels of neither cytokine nor CRP were predictive of fever within more than 24 h before its onset. Unlike CRP, both IL-6 and IL-8 serum levels were significantly different between microbiologically documented infections and unexplained fevers. The highest values of IL-6 and IL-8 were observed in episodes of gram-negative bacteremia. Using receiver-operating-characteristic curves, the analysis of cytokine levels measured around the onset of fever indicated that IL-8 is potentially useful for predicting gram-negative bacteremia, with a high negative predictive value of > 90% and a moderate positive predictive value of 50% (sensitivity, 70%; specificity, 91%). In patients with persistent fever, predictions of further clinical complications, defined as prolonged fever of more than 7 days' duration, pneumonia, shock and/or death due to infection, were best predicted by IL-6. With an IL-6 cutoff value of 250 pg/ml in samples obtained 8 to 32 h after onset of fever, the positive predictive value was 92%, the negative predictive value 91% (sensitivity, 85%; specificity, 95%). The positive predictive value of IL-6 in samples obtained another 24 h later from patients still febrile remained > 90%, but the negative predictive value dropped to 47%. In any of the analyses, the predictive values of CRP levels were poor and inferior to either cytokine. These findings may have clinical value in identifying subgroups of patients requiring different therapeutic approaches.
Infection
PMID:An analysis of interleukin-8, interleukin-6 and C-reactive protein serum concentrations to predict fever, gram-negative bacteremia and complicated infection in neutropenic cancer patients. 971 78

It has been suggested that chronic infection with Helicobacter pylori (H. pylori), in particular infection with virulent strains producing the cytotoxin-associated protein CagA, may increase the risk of coronary heart disease by generation of a persistent low-grade inflammatory stimulus. We assessed the relation between serological markers of H. pylori infection and various markers of systemic inflammation in a population-based sample of 1834 men and women aged 18-88. A total of 39.3% of the sample had a positive IgG response, and among these a slight majority was CagA positive. Infection with H. pylori was unrelated to C-reactive protein and the leukocyte count, regardless of CagA status. There was an inverse relation between H. pylori infection and serum albumin. The adjusted OR (95% CI) of an albumin level in the bottom versus the top third were 2.2 (1.5-3.1) and 2.0 (1.4-3.1) for infection with CagA-positive and CagA-negative H. pylori strains, respectively. These results do not support the hypothesis that chronic infection with virulent H. pylori strains provokes major systemic inflammation. The mechanisms underlying the inverse association between H. pylori infection and serum albumin and the clinical relevance of this finding require further research.
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PMID:Chronic infection with Helicobacter pylori does not provoke major systemic inflammation in healthy adults: results from a large population-based study. 1055 26

A rare case of spontaneous spondylodiscitis caused by Klebsiella pneumoniae in a 55-year-old man who presented with thoracolumbar pain is described. Increased erythrocyte sedimentation rate and C-reactive protein level were pertinent laboratory findings. Computed tomography revealed a paravertebral mass and destruction of the 10th and 11th vertebrae. Magnetic resonance imaging (MRI) showed spondylodiscitis in the same area. Culture of a biopsy sample from the mass grew Klebsiella pneumoniae, while histological examination confirmed the inflammation. A combination of ceftazidime, amikacin and ciprofloxacin resulted in disappearance of the pain. Two months later, MRI showed substantial improvement of the lesions.
Infection
PMID:Spontaneous spondylodiscitis caused by Klebsiella pneumoniae. 1062

In adult postoperative intensive care patients, the biallelic Ncol polymorphism within the tumor necrosis factor (TNF) locus has been shown to be a genomic marker for individuals with increased TNF-alpha response and poor prognosis in severe sepsis. We characterized the genomic distribution and allele frequency of the Ncol polymorphism in 23 preterm and term neonatal intensive care unit (NICU) patients with culture-proven sepsis and compared it with clinical and laboratory characteristics to assess its prognostic value for disease progression. Genotype analysis demonstrated the following absolute (relative) frequencies: 7 (0.31) infants were homozygous for the allele TNFB2 (Group A). 12 (0.52) infants were heterozygous (TNFB1/TNFB2) and four (0.17) infants homozygous for the allele TNFB1 (Group B). There was no significant difference compared to adult intensive care patients with severe sepsis (p = 0.31). The median gestational age of all infants (13 female and ten male) as well as for either group was 28 weeks (range 23-37) with a median birth weight of 845 g (range 560-2,720). The study population included a total of 16 very low birth weight (VLBW) infants, four in Group A and 12 in Group B. However, there was no significant difference for gestational age and birth weight in both groups (p = 0.82 and 0.71, respectively). Laboratory parameters as maximum and minimum leukocyte and thrombocyte counts, maximum immature to total neutrophil ratios (ITR), maximum C-reactive protein (CRP) levels, days of CRP levels > 5 mg/l and total days of antibiotic treatment, were not statistically different in both groups. In total, three infants (13%) died in consequence of their underlying disease. Two infants belonged to Group A and one to Group B. The statistical analysis of outcome variables (mortality, neurological impairment, failure to thrive) was not possible, because the study population was small and the reasons for poor outcome and death in these high-risk patients had to be considered multifactorial. In conclusion, in this pilot study the biallelic Ncol polymorphism within the TNF locus was not a prognostic marker for disease progression in high-risk NICU-admitted term and preterm infants with culture-proven sepsis. In order to detect differences in outcome similar to adult postsurgical patients with severe sepsis, an unfeasibly high number of NICU patients with culture-proven sepsis would need to be included for a similar study.
Infection
PMID:Pilot study assessing TNF gene polymorphism as a prognostic marker for disease progression in neonates with sepsis. 1078 94

Chlamydia pneumoniae, a common cause of respiratory infection, is vasotropic and frequently found in human atheromas. Whether it plays a causal role in coronary artery disease (CAD) is uncertain. The effects of 3 months of azithromycin treatment or placebo were tested in 302 patients with chronic CAD seropositive to C. pneumoniae at 3-6 months. Azithromycin reduced a global rank sum score of 4 inflammatory markers (C-reactive protein [CRP], interleukin [IL]-1, IL-6, tumor necrosis factor-alpha; P=.011) and a global rank sum change score (+/-SD) (from 535+/-201 to 587+/-190; P=.027) at 6 (but not 3) months. Change scores for CRP and IL-6 and median IL-1 levels were lower. C. pneumoniae IgG and IgA antibody titers were unchanged. Clinical cardiovascular events at 6 months did not differ between groups (azithromycin, 9; placebo, 7). Infections were reduced and drug was well tolerated. Thus, azithromycin caused modest but significant reductions in markers of inflammation, but differences in clinical events were not evident at 6 months. However, power was limited and conclusions should await results of the 2-year evaluation and larger studies.
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PMID:The ACADEMIC study in perspective (Azithromycin in coronary artery disease: elimination of myocardial infection with Chlamydia). 1083 61

Nutritional status and some iron metabolism parameters of acute phase response (APR) positive and APR-negative AIDS patients were studied. Twenty-nine AIDS patients were submitted to 24h food intake recall, anthropometry, and albumin, C-reactive protein (CRP), hemoglobin, ferritin, and total iron binding capacity (TIBC) measurements. Infection plus serum CRP > 7 mg/dl were criteria for APR presence. Protein-energy malnutrition (PEM) was ascertained by body mass index (BMI) lower than 18.5 kg/m2 and height-creatinine index (HCI < 70%). PEM (77.8 vs 40%) and pulmonary tuberculosis (44. 4 vs 9.5%) were more frequent in APR-positive patients, which also had lower serum albumin (3.7 +/- 0.9 vs 4.3 +/- 0.9 g/dl), TIBC (165. 8 +/- 110.7 vs 265.9 +/- 74.6 mg/dl) and blood hemoglobin (10.5 +/- 1. 8 vs 12.6 +/- 2.3g/dl). Iron intake was similar between groups; however, serum ferritin levels (median, range) were higher among APR-positive (568, 45.3-1814 vs 246, 18.4-1577 ng/ml) patients. HIV-positive adults with systemic response to invading pathogens showed worse nutritional status than those APR-negative. In APR-positive AIDS patients, anemia appears to be unrelated to recent iron intake.
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PMID:[Iron status, malnutrition and acute phase response in HIV-positive patients]. 1088 Nov 30

Four cases of reactive arthritis (ReA) related to Helicobacter pylori (HP) are presented. These were identified by IgG, IgM and IgA ELISA tests performed on sera obtained from a 2-year prospective study on 186 patients with a clinical picture suggesting ReA as a possible diagnosis. If anti-HP IgM and IgA or IgG were positive, the case was considered related to HP. Three out of four HP ReA patients were originally classified as "possible ReA", i.e. having a clinical picture of ReA but without any identified triggering microorganism. IgG antibodies against cagA and vacA were detected in three and two cases respectively. The HP ReA patients did not present with typical clinical or laboratory features differentiating them from ReA induced by Chlamydia trachomatis (N = 25) or enteropathogenic bacteria (N = 27). However, compared to findings in patients with ReA due to enteropathogenic bacteria the number of active joints was higher (six versus two), duration of arthritis longer (3.9 weeks versus 2 weeks) and the CRP (C-reactive protein) lower (43 versus 59). Our findings suggest that HP may be included in the list of possible arthritis triggering microbes.
Infection 1999
PMID:Helicobacter pylori--a trigger of reactive arthritis? 1088 36

Infection and inflammation have been suggested to play roles in coronary artery disease (CAD). We hypothesized that: (1) CAD risk is associated with the aggregate number of pathogens (pathogen burden), and (2) increased pathogen burden is associated with elevated levels of C-reactive protein (CRP), a marker of inflammation. We evaluated 233 patients for CAD. Blood samples from each patient were tested for immunoglobulin-G (IgG) antibodies to cytomegalovirus (CMV), Chlamydia pneumoniae, hepatitis A virus (HAV), herpes simplex virus type 1 (HSV-1) and HSV type 2 (HSV-2), and for the CRP levels. Of the 233 study subjects, 68% had evidence of CAD by coronary angiography. Although the prevalence of seropositivity for each pathogen tended to be higher in the patients with CAD than those without, only the association between CAD and seropositivity to HAV was significant in multivariate analysis. Over 75% of study subjects had been exposed to > or =3 of the 5 pathogens tested, and analysis determined that increasing pathogen burden was significantly associated with increasing CAD risk, even after adjustment for traditional CAD risk factors. The prevalence of CAD was 48%, 69%, and 85% in individuals with antibodies to < or =2 pathogens, to 3 or 4 pathogens, and to 5 pathogens, respectively. A similar association between increasing pathogen burden and CRP levels was also found. The pathogen burden remained a significant predictor of CRP levels after multivariate analysis. Our data suggest that infection does play a role in the genesis of atherosclerosis. However, the risk posed by infection is related to the pathogen burden that may contribute to CAD through inflammatory responses.
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PMID:Effects of total pathogen burden on coronary artery disease risk and C-reactive protein levels. 1095 67


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