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PubMed2000

Markers of inflammation as predictors in cardiovascular disease.

Recent research suggests that inflammation in the coronary arteries may be intimately involved in the development of atherosclerosis and its associated acute coronary syndromes. Experimental and clinical studies based on the biochemical markers of inflammation and vascular perturbation in plasma as well as in atherosclerotic tissue have provided substantial evidence of ongoing inflammation in coronary heart disease. These studies have suggested a potential role for biochemical markers of inflammation in the prediction of risk for the development of coronary heart disease as well as in the prediction of adverse cardiac-related outcomes in patients with known coronary syndromes. Markers of inflammation appear to offer risk prediction information that is independent of, and possibly complementary to, traditional risk factors for the development of cardiovascular disease. There are numerous potential markers for these inflammatory processes and their interdependence remains somewhat unclear. Clinical studies have investigated some, but not all of these markers in a critical and comparative fashion. Therefore, further well-designed prospective studies should elucidate the role of markers of inflammation in the prediction, diagnosis, and management of cardiovascular disease.

Animals↗
PubMed1998

Subtherapeutic corticosteroids potentiate the ability of interleukin 10 to prevent chronic inflammation in rats.

BACKGROUND & AIMS: Interleukin (IL)-10, which inhibits macrophages and T-helper lymphocyte type 1 (TH1) lymphocytes, attenuates chronic granulomatous inflammation induced by bacterial cell wall polymers. This study determines whether corticosteroids enhance the protective effects of IL-10 in cultured peripheral blood mononuclear cells (PBMNCs) and in vivo when started before or after the onset of experimental chronic granulomatous inflammation. METHODS: Intestines of Lewis rats were injected intramurally with streptococcal peptidoglycan-polysaccharide (PG-APS) polymers. Daily murine recombinant IL-10 and/or dexamethasone (DEX) therapy was started 12 hours before or at several intervals after PG-APS injection. RESULTS: IL-10 plus corticosteroids additively inhibited IL-1beta secretion in human PBMNCs but preserved the beneficial IL-1RA/IL-1beta ratio induced by IL-10. IL-10 started before PG-APS injection significantly attenuated intestinal and extraintestinal inflammation, with even more pronounced effects in combination with subtherapeutic doses of DEX. The combination of DEX decreased the effective dose of IL-10 by at least one half. After onset of systemic inflammation using doses effective for prevention, IL-10 monotherapy had nearly no benefit and DEX plus IL-10 was similar to the mild therapeutic effect of DEX alone. CONCLUSIONS: The combination of IL-10 and corticosteroids allows lower doses of both agents in preventing chronic intestinal and systemic inflammation. However, timing of IL-10 administration is a critical variable in regulating inflammation.

Animals↗
PubMed2003

Multi-organ inflammation after hepatic cryoablation in BALB/c mice.

BACKGROUND: There is increasing evidence that injury to the liver can precipitate or exaggerate lung injury. We have previously shown that hepatic cryoablation (cryo) causes activation of nuclear factor (NF)-kappaB, cytokinemia (tumor necrosis factor-alpha, Mouse Macrophage Inflammatory Protein-2 [MIP-2]), and lung inflammation in transgenic HLL (5'HIV-LTR-Luciferase gene) mice and in Sprague-Dawley rats. It has been reported that BALB/c mice are susceptible to traumatic injury and are active immune responders. We tested whether activation of NF-kappaB and the development of multiple-organ inflammation in response to hepatic injury from 35% cryo were demonstrable in the BALB/c mouse. METHODS: BALB/c mice (n = 9) were anesthetized, and midline laparotomy was performed. Cryoablation was performed with careful isolation of adjacent structures to avoid inadvertent organ injury to the gastrointestinal tract. A freeze-thaw cycle of the left lobe of the liver was induced, encompassing approximately 35% (by weight). Animals were sacrificed at 1, 2, 4, and 24 h after cryoablation. Serum was collected via IVC puncture and liver, lungs, and kidneys were harvested and freeze-clamped. Two animals were sacrificed without undergoing cryo surgery to serve as a baseline control. NF-kappaB activity was monitored by electrophoretic mobility shift assays. MIP-2 levels and Mouse KC levels from tissue and serum were measured using enzyme-linked immunosorbent assay. Organs were submitted for histological review. We characterized lung inflammation induced by cryosurgery by measuring total and differential cell counts in lung lavage fluid 4 h after hepatic cryoablation. RESULTS: After cryo, NF-kappaB activation was demonstrated in the 1, 2, and 4-h time points by electrophoretic mobility shift assay in the liver and lungs. Mouse KC and MIP-2 levels increased from baseline, peaked at the 4-h time point, and returned to baseline after 24 h in both liver and lung. Lung lavage 4 h after cryoablation showed increased total cells and neutrophilic lung inflammation. CONCLUSIONS: BALB/c mice demonstrate evidence of multi-organ inflammation in response to 35% hepatic cryo. These data demonstrate that this model provides for assessment of liver-mediated multi-system inflammation after direct liver injury.

Animals↗
PubMed2002

Assessment of the relationship between hyperalgesia and peripheral inflammation in magnesium-deficient rats.

Magnesium-deficient rats develop simultaneously a significant lowering of nociceptive threshold and a generalized inflammation. We investigated the relationship between these two phenomena by testing drugs that are able to suppress the inflammation in this model. In weaning rats fed a magnesium-depleted diet for ten days, the nociceptive threshold was assessed by the paw pressure test and the inflammation by a clinical score. A non-steroidal anti-inflammatory drug (piroxicam); antagonists of H1 and H2 receptors (astemizole and cimetidine. respectively); a glucocorticoid (dexamethasone); an inhibitor of mastocyte degranulation (cromoglycate); and estradiol benzoate were used to block the inflammatory response. Dexamethasone and estradiol significantly suppressed the inflammation (p < 0.001 vs control group). Cromoglycate showed a delayed anti-inflammatory effect (p < 0.01 vs control group on D10). The combination of astemizole and cimetidine partially blocked the inflammation process, whereas astemizole and piroxicam were without effect. Regardless of the effect of the test drugs on inflammation, no change in the time course of hyperalgesia was observed. These data support the view that hyperalgesia induced by the magnesium-depleted diet is not a consequence of the inflammatory process.

Animals↗
PubMed2001

Selective upregulation of the flip-flop splice variants of AMPA receptor subunits in the rat spinal cord after hindpaw inflammation.

Glutamate receptors are involved in spinal nociceptive transmission and the development of persistent inflammatory hyperalgesia. It is unclear, however, whether there are changes in glutamate receptor gene expression associated with tissue injury. In the present study, we used reverse transcription-polymerase chain reaction (RT-PCR) to examine the modulation of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor gene expression in the rat spinal cord by inflammation. Inflammation was introduced into the hindpaw by intraplantar injection of 0.2 ml of complete Freund's adjuvant (CFA). At 2 h-14 d after inflammation, total RNAs from L4,5 spinal cord were used for RT-PCR with primers targeted at eight flip-flop splice variants of the AMPA receptor subunits. It was found that the GluR1-flop mRNA was up-regulated at 2 h-5 h (P<0.05), down-regulated at 3 d (P=0.05), and returned to control levels at 7 d following inflammation. The GluR2-flip and GluR3-flop mRNAs were up-regulated at 5 h-1 d (P<0.05) and returned to control levels at 3 d after inflammation. The GluR1-flip mRNA was not detected in the samples and the mRNAs for other splice variants did not exhibit significant changes. Immunocytochemical analysis of GluR1 and GluR2 subunits indicate that the protein translation products of these subunits were also increased in the spinal cord. These results demonstrate an increased expression of AMPA receptor subunits that correlates with the acute phase of CFA-induced inflammation and hyperalgesia. Selective changes in the expression of the flip-flop splice variants of the AMPA receptor suggest a reorganization of the composition of the AMPA receptor complex and its involvement in the development of inflammatory hyperalgesia.

Alternative Splicing↗
PubMed2003

Neonatal inflammation and primary afferent terminal plasticity in the rat dorsal horn.

Abnormal or excessive activity related to pain and injury in early life may alter normal synaptic development and lead to changes in somatosensory processing. The aim of the current study was to define the critical factors that determine long-term plasticity in spinal cord afferent terminals following neonatal inflammation. Hindpaw inflammation was produced in neonatal rat pups with 5 or 25 microl 2% carrageenan, and 5 or 25 microl complete Freund's adjuvant (CFA). All groups displayed a clear inflammatory response that recovered in 2 weeks in all but the 25 microl CFA group, who had persistent chronic inflammation confirmed by histological examination of the paw at 8 weeks. The 25 microl CFA group was also the only group that displayed a significant expansion of the sciatic and saphenous nerve terminal field in lamina II of the dorsal horn at 8 weeks, using wheat-germ agglutinin-horse radish peroxidase transganglionic labelling. This effect was not accompanied by changes in dorsal root ganglion (DRG) cell number, expression of activating transcription factor 3 (ATF3), or alterations in calcitonin gene related peptide (CGRP) or isolectin B4 binding; and was not mimicked by partial nerve damage. No long-term change in mechanical or thermal behavioural sensory thresholds was seen in any group. Lower dose CFA caused an acute, reversible expansion of terminal fields in lamina II in neonatal animals, while CFA did not produce this effect in adults. The duration and effect of neonatal inflammation is therefore dependent on the type and volume of inflammatory agent used. The expansion of afferent terminals in lamina II following neonatal CFA inflammation is maintained into adulthood if the inflammation is also maintained, as seen following 25 microl CFA. This effect is not seen in adult animals, emphasising the plasticity of the nervous system early in development.

Afferent Pathways↗
PubMed2001

Increased conduction velocity of nociceptive primary afferent neurons during unilateral hindlimb inflammation in the anaesthetised guinea-pig.

Decreases in durations of action potentials (C- and Adelta-fibre units) and afterhyperpolarisations (A-fibre units) occur in somata of nociceptive dorsal root ganglion neurons during hindlimb inflammation induced in young guinea-pigs by intradermal injections of Complete Freund's Adjuvant into the ipsilateral leg and foot. Here we present evidence that the single-point conduction velocity (i.e. estimated over a single conduction distance) of these nociceptive neurons is increased during this type of inflammation. The single-point conduction velocities in anaesthetised untreated guinea-pigs (control) were compared with those two and four days after Complete Freund's Adjuvant treatment in two types of experiment. The first involved intracellular voltage recordings from somata of ipsilateral L6 and S1 dorsal root ganglion neurons. Units were classified as C, Adelta or Aalpha/beta on the basis of their dorsal root conduction velocities and characterised as nociceptive, low-threshold mechanoreceptive or unresponsive according to their responses to mechanical and thermal stimuli. Compared with untreated animals, significant increases of 54% for C-fibre nociceptive units and 46% for A-fibre nociceptive units in the medians of dorsal root single-point conduction velocities were found four days after Complete Freund's Adjuvant treatment. These increases were greater at four days than at two days after Complete Freund's Adjuvant. A slight tendency in the same direction (10%) that was not significant was also seen in low-threshold mechanoreceptors four days after treatment, but not after two days. The increased velocities were confirmed with compound action potential recordings from ipsilateral S2 dorsal roots and sural nerves, in treated and control animals. Recordings showed a tendency for increased single-point velocities in C, Adelta and Aalpha/beta waves, with the upper border of the Adelta wave (i.e. the border between Adelta and Aalpha/beta waves) falling at a significantly higher conduction velocity in treated than control animals. This was seen both in S2 dorsal roots and in sural nerves. There was also a significant decrease in the mean electrical threshold for eliciting the C and Adelta components of compound action potentials of both dorsal root and sural nerves during inflammation. No evidence was found for a reduction in utilisation time for any components of the sural nerve compound action potential (C, Adelta or Aalpha/beta). The conduction velocity increases may be due to altered expression or activation/inactivation of certain ion channel types, such as Na(+) channels. The present experiments demonstrate that hindlimb inflammation caused a significant increase in conduction velocity of nociceptive but not of low-threshold mechanoreceptive primary afferent neurons during inflammation, as well as a significant decrease in the mean electrical threshold for eliciting the C and Adelta components of compound action potentials of both dorsal root and sural nerves. These changes, together with the previously described changes in the action potential shape of nociceptive neurons during inflammation, probably reflect alterations in membrane function that contribute to inflammatory hyperalgesia.

Action Potentials↗
PubMed2003

Effect of anti-nerve growth factor treatment on pituitary adenylate cyclase activating polypeptide expression in adult sensory neurons exposed to adjuvant induced inflammation.

Expression of pituitary adenylate cyclase activating polypeptide (PACAP) is increased in sensory neurons exposed to adjuvant induced peripheral inflammation. Local elevation in expression of the neurotrophin nerve growth factor (NGF) is a main factor contributing to the neuronal response to inflammation. This study examines the role of endogenous NGF in inflammation-associated increases in PACAP expression using the adjuvant-induced peripheral inflammation model with or without systemic administration of antibodies against NGF. Quantitative in situ hybridization was used to detect changes in neuronal PACAP mRNA expression and to correlate this expression with neuronal mRNA expression of the NGF receptor tyrosine kinase (trk) A. The results from this study show that inflammation triggered increases in PACAP expression occurs in small- to medium-sized dorsal root ganglion (DRG) neurons that also express trkA, and that this elevation in PACAP expression is prevented by systemic injection of anti-NGF. This supports a role for NGF as a positive regulator of PACAP expression during inflammation.

Animals↗
PubMed1997

Acute and chronic effects of different bile acids on indomethacin-induced intestinal inflammation.

The role of bile acids in the pathogenesis of bowel inflammation is unknown. The objective of this study was to determine whether urso- (UDC), cheno- (CDC), and taurochenodeoxycholic acid (TCDC) exert a pro- or antiinflammatory action in the acute and chronic phase of the indomethacin model of a long lasting ileitis in rats. Short-term and long-term inflammatory responses (48 h and 10 days, respectively) after two subcutaneous indomethacin (Indo) injections were elicited in rat small bowel and mesentery. To distinguish between common and model-specific effects bile acids were tested also in another model of acute inflammation induced by mesenteric superfusion with leukotriene B4(LTB4). The number of adherent and emigrated leukocytes, leukocyte rolling velocity, and venular wall shear rate were monitored in normal and inflamed postcapillary venules, and fecal pH of ileal contents which has been shown to correlate with degree of inflammation was measured, 6.5- and 2.3-fold increases in leukocyte adherence and comparable increments in leukocyte emigration were observed 48 h and ten days after indomethacin treatment, respectively. UDC, CDC, and TCDC (10 mg/kg) given daily from Indo administration until the experiment attenuated the leukocyte adherence and emigration responses elicited by indomethacin in short- and long-term inflammation. This effect was accompanied by a significant increase of fecal pH which had been lowered by indomethacin. None of the bile acids reduced the LTB4-induced increases in adherence and emigration. Oral administration of UDC, CDC, and TCDC reduces leukocyte adhesion and emigration in acute and chronic stages of Indo-induced inflammation. This could be due to the alkalizing effect of these bile acids on fecal pH which has been shown to correlate with a decrease of leukocyte-endothelial cell interactions but--according to the missing effectiveness in another model of intestinal inflammation--not to specific influences on leukocyte-endothelial cell adhesion.

Animals↗
PubMed1988

Bradykinin is increased during acute and chronic inflammation: therapeutic implications.

Bradykinin is a potent pain-producing substance, yet little is known about its role in inflammation. The present study measured circulating levels of immunoreactive bradykinin in a clinical model of acute inflammation (oral surgery) and chronic inflammation (rheumatoid arthritis) and in the rat carrageenan model of inflammation. The effects of a kallikrein inhibitor (soybean trypsin inhibitor) on blocking bradykinin synthesis in vitro and its analgesic actions in the rat model were also evaluated. Levels of immunoreactive bradykinin increased threefold to fourfold during oral surgery. Levels were twofold to threefold greater in patients with rheumatoid arthritis compared with control subjects. Levels of immunoreactive bradykinin increased twofold in rats during carrageenan inflammation. Soybean trypsin inhibitor blocked synthesis of bradykinin in vitro and possessed analgesic activity in rats. The results indicate that the bradykinin system is activated during inflammation. Kallikrein inhibitors may represent a new class of analgesic/antiinflammatory drugs.

Adult↗
PubMed2005

Myocardial injury occurs earlier than myocardial inflammation in acute experimental viral myocarditis.

Endomyocardial biopsy often fails to show myocardial inflammation for patients with clinically suspected myocarditis. The serum isoforms of troponin T (cTnT) level is a very sensitive marker of myocardial injury and it is elevated even in the absence of myocardial inflammation. We investigated the correlations for myocardial injury, virus titers and inflammation in acute viral infection. Using the murine coxsackievirus group B3 (CVB3) myocarditis model, the histopathologic findings and virus titers in mouse hearts were compared with the serum cTnT levels measured by ELISA at various time points. Viable virus titers in the hearts peaked at 3 days after infection (8.22 +/- 0.13 log10 PFU/100 mg of heart); they decreased at day 7 and no viable virus was detected from day 14. Myocardial inflammation was minimal at day 3, peaked at day 7 and markedly decreased at day 14. The individual serum TnT levels were significantly increased at day 3 (7.37 +/- 1.46 ng/ml), persisted to day 7 (0.73 +/- 0.08 ng/ml), and normalized at day 14. Serum cTnT levels were correlatable with virus titers in the heart (r = 0.744, P <0.01), but the serum cTnT levels were not correlated with the degrees of inflammation. Using the less myocarditic strain of CVB3, similar relationships were observed between the changes for the serum cTnT levels and the heart virus titers. During the course of viral infection, myocardial injury precedes the pathologic evidence of inflammation, and the elevated cTnT levels provide evidence of myocardial injury even in the absence of any histologic findings of myocarditis.

Acute Disease↗
PubMed2001

Possible new role for NF-kappaB in the resolution of inflammation.

Inflammation involves the sequential activation of signaling pathways leading to the production of both pro- and anti-inflammatory mediators. Although much attention has focused on pro-inflammatory pathways that initiate inflammation, relatively little is known about the mechanisms that switch off inflammation and resolve the inflammatory response. The transcription factor NF-kappaB is thought to have a central role in the induction of pro-inflammatory gene expression and has attracted interest as a new target for the treatment of inflammatory disease. We show here that NF-kappaB activation in leukocytes recruited during the onset of inflammation is associated with pro-inflammatory gene expression, whereas such activation during the resolution of inflammation is associated with the expression of anti-inflammatory genes and the induction of apoptosis. Inhibition of NF-kappaB during the resolution of inflammation protracts the inflammatory response and prevents apoptosis. This suggests that NF-kappaB has an anti-inflammatory role in vivo involving the regulation of inflammatory resolution.

Animals↗
PubMed2003

Despite increased plasma concentration, inflammation reduces potency of calcium channel antagonists due to lower binding to the rat heart.

1. Rheumatoid arthritis reduces verapamil oral clearance thereby increases plasma concentration of the drug. This coincides with reduced drug effects through an unknown mechanism. 2. The effect of interferon-induced acute inflammation on the pharmacokinetics and electrocardiogram of verapamil (20 mg kg(-1), p.o.) and nifedipine (0.1 mg kg(-1), i.v.) was studied in Sprague-Dawley rats. 3. The effect of both acute and chronic inflammation on radioligand binding to cardiac L-type calcium channels was also investigated. 4. Acute inflammation resulted in increased plasma concentration of verapamil but had no effect on that of nifedipine. Verapamil binding to plasma proteins was unaffected. 5. As has been reported for humans, the increased verapamil concentration coincided with a reduction in the degree to which PR interval is prolonged by the drug. The effect of nifedipine on PR interval was also reduced by inflammation. 6. Maximum binding of (3)H-nitrendipine to cardiac cell membrane was significantly reduced from 63.2+/-2.5 fmol mg(-1) protein in controls to 46.4+/-2.0 in acute inflammation and from 66.8+/-2.2 fmol mg(-1) protein in controls to 42.2+/-2.0 in chronic inflammation. 7. Incubation of the normal cardiac cell membranes with 100 and 1000 pg ml(-1) of rat tissue necrosis factor-alpha did not influence the binding indices to the calcium channels. 8. Our data suggest that the reduced calcium channel responsiveness is because of altered binding to channels.

Animals↗
PubMed2004

Relationship of vitamin A deficiency, iron deficiency, and inflammation to anemia among preschool children in the Republic of the Marshall Islands.

INTRODUCTION: Although vitamin A deficiency, iron deficiency, and inflammation may contribute to anemia, their relative contribution to anemia has not been well characterized in preschool children in developing countries. OBJECTIVE: To characterize the contributions of vitamin A and iron deficiencies and inflammation to anemia among preschool children in the Republic of the Marshall Islands. SUBJECTS AND METHODS: A community-based survey, the Republic of the Marshall Islands Vitamin A Deficiency Study, was conducted among 919 preschool children. The relationship of vitamin A and iron status and markers of inflammation, tumor necrosis factor-alpha, alpha1-acid glycoprotein, and interleukin-10, to anemia were studied in a subsample of 367 children. RESULTS: Among the 367 children, the prevalence of anemia was 42.5%. The prevalence of severe vitamin A deficiency (serum vitamin A < 0.35 micromol/l) and iron deficiency (serum ferritin < 12 microg/dl) were 10.9 and 51.7%, respectively. The respective prevalence of iron deficiency anemia (hemoglobin < 110 g/l and iron deficiency), anemia with inflammation (anemia with TNF-alpha > 2 pg/ml and/or AGP > 1000 mg/l), and severe vitamin A deficiency combined with anemia was 26.7, 35.6, and 7.6%. In multivariate linear regression models that adjusted for age, sex, and inflammation, both iron deficiency (odds ratio (OR) 1.74, 95% confidence interval (CI) 1.08-2.83, P = 0.023) and severe vitamin A deficiency (OR 4.85, 95% CI 2.14-10.9, P < 0.0001) were significantly associated with anemia. CONCLUSIONS: Both iron and vitamin A deficiencies were independent risk factors for anemia, but inflammation was not a significant risk factor for anemia among these preschool children.

Anemia↗
PubMed2006

The association of markers of inflammation with weight change in older adults: the Cardiovascular Health Study.

OBJECTIVE: Elevated levels of inflammation factors often precede weight loss and may be causally related to it. Newer studies suggest that elevated levels of inflammation factors also precede weight gain. In this study, we examined whether inflammation factors are elevated in individuals, age >or=65 years, who lost or gained >5% weight over a 3 year follow-up period compared to those with stable weight. SUBJECTS: In total, 3254 participants in the Cardiovascular Health Study whose weight was stable; 661 who gained >5% weight; and 842 who lost >5% weight. MEASUREMENTS: C-reactive protein (CRP), fibrinogen, factor VIIIc, white blood cell (WBC) and platelet counts, and interleukin-6 (IL-6) levels. RESULTS: As compared to participants whose weight was stable, those who lost >5% weight had higher baseline CRP concentration (1.05 (95% CI, 1.02, 1.08) per interquartile increase) and WBC count (1.10 (1.01, 1.19) per interquartile increase) on adjusted analyses. Those who gained >5% weight had higher baseline CRP (1.05 (1.01, 1.08)), fibrinogen (1.13 (1.01, 1.27)), and factor VIIIc (1.15 (1.03, 1.30)). CONCLUSIONS: Inflammation factors are associated with weight gain and weight loss in older individuals. These findings suggest that subclinical inflammation, or unknown factors associated with subclinical inflammation, contribute to weight change.

Aged↗
PubMed1999

Serum eosinophilic cationic protein and blood eosinophil counts for the prediction of the presence of airways inflammation in children with wheezing.

BACKGROUND: Serum eosinophilic cationic protein (ECP) concentrations may be useful noninvasive markers of airways inflammation in atopic asthma. However, the usefulness of serum ECP measurement for the prediction of airways inflammation in children with a history of wheezing is unknown. OBJECTIVE: To determine the test accuracy of serum ECP and blood eosinophil percentage as noninvasive markers of eosinophilic airways inflammation. METHODS: Bronchoalveolar lavage (BAL) fluid and peripheral blood samples for eosinophil percentages and serum ECP were obtained from children undergoing elective surgery and who gave a history of wheezing in the previous year. Sensitivity, specificity and likelihood ratios (LH) and the area under the curve (AUC) for the receiver operator characteristic (ROC) curve were calculated for each blood marker for the prediction of airways inflammation defined by a BAL eosinophil percentage > 0.86. Data were analysed on the basis of how recently symptoms had occurred. RESULTS: Seventy-seven children (median age 6.75 years) were studied. An AUC of 0.75 (log serum ECP concentration) and 0.76 (log blood eosinophil percentage) was obtained for predicting airways inflammation. A serum ECP > 13 microg/L yielded a LH of 4.4, whereas using a cutoff blood eosinophils > 4% yielded a LH of 1.9, for the prediction of elevated eosinophils in BAL. Serum ECP and eosinophil percentages in BAL and blood were lowest (not statistically significant) when last symptoms had occurred more than 12 weeks previously. CONCLUSIONS: Serum ECP and blood eosinophil percentages are useful markers for predicting eosinophilic airways inflammation in wheezing children.

Adolescent↗
PubMed1998

Appendiceal inflammation in ulcerative colitis.

AIMS: Previous uncontrolled reports have suggested that appendiceal inflammation may occur as a discontinuous lesion in ulcerative colitis. This study aims semiquantitatively to compare the prevalence and histological features of appendiceal inflammation in patients with ulcerative colitis and Crohn's disease, using colonic carcinoma and acute appendicitis specimens as controls. METHODS AND RESULTS: Surgical pathology records and original histological slides for the period 1980-1994 were examined. The prevalence of appendiceal inflammation in ulcerative colitis (24/50, 48%), was higher than in colonic carcinoma (5/65, 8%, P < 0.001), but was similar to that in Crohn's disease (14/27, 52%). Appendiceal inflammation with caecal sparing was seen in nine out of 24 specimens with ulcerative colitis (37%), two out of nine (22%) with Crohn's disease and five out of 65 (8%) with colonic carcinoma. Inflamed appendixes from patients with inflammatory bowel disease showed histological features typical of ulcerative colitis and Crohn's disease rather than acute appendicitis and were significantly less likely to have transmural inflammation. There had been a previous appendicectomy in 3% of ulcerative colitis patients compared with 8% of colonic carcinoma specimens and 21% (P < 0.01) Crohn's disease controls. CONCLUSION: In ulcerative colitis, as in Crohn's disease, appendiceal inflammation commonly occurs as a skip lesion and histologically resembles the colonic disease rather than acute appendicitis. The low prevalence of appendicectomy supports the hypothesis that the appendix itself may have a central role in the pathogenesis of ulcerative colitis.

Adolescent↗
PubMedDate not supplied

Characteristics and effects of inflammation in end-stage renal disease.

Malnutrition and cardiovascular disease are associated with end-stage renal disease (ESRD) and both are closely associated with one another, both in cross-sectional analysis and when the courses of individual patients are followed over time. Inflammation, by suppressing synthesis of albumin, transferrin, and other negative acute-phase proteins and increasing their catabolic rates, either combines with modest malnutrition or mimics malnutrition, resulting in decreased levels of these proteins in dialysis patients. Inflammation also leads to reduced muscle mass by increasing muscle protein catabolism and blocking synthesis of muscle protein. More importantly, inflammation alters plasma protein composition and endothelial structure and function so as to promote vascular disease. Markers of inflammation, C-reactive protein (CRP), and interleukin (IL)-6 powerfully predict death from all causes and from cardiovascular disease in dialysis patients as well as progression of vascular injury. The causes of inflammation are likely multifactorial, including oxidative modification of plasma proteins, interaction of blood with nonbiocompatible membranes and lipopolysaccharides in dialysate, subclinical infection of vascular access materials, oxidative catabolism of endothelium-derived nitric oxide, and other infectious processes. Treatment should be focused on identifying potential causes of inflammation, if obvious, and reduction of other risk factor for cardiovascular disease.

Biomarkers↗