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At least 361 records · Page 20Linked to original sources
PubMed2000

Colonic inflammation found at diagnosis of juvenile retention polyps in pediatric patients.

OBJECTIVE: The finding of colonic inflammation concurrently with a juvenile retention polyp (JRP) may have prognostic value. However, the significance of abnormal mucosal histology with JRP has not been evaluated. We evaluated the significance of mucosal histology at the time of JRP removal with respect to future development of inflammatory bowel disease (IBD) and polyp recurrence. METHODS: The medical records of patients who had an endoscopic polypectomy performed at the Children's Hospital of Philadelphia (CHOP) from 1/1/87 through 4/30/98 were retrospectively reviewed. RESULTS: JRP was histologically identified in 96 patients. A total of 54 patients had colonic mucosal biopsies: 30 (55.6%) had normal histology and 24 (44.4%) had colitis. Of the 24 patients with colitis, 14 patients (58.3%) had inflammation at the polyp site. Twelve of these patients had additional inflammation elsewhere in the colon. Nine (37.5%) had inflammation elsewhere in the colon; however, biopsies around the polyp site were not obtained. One patient with inflammation did not have the location of the polyp documented. Four patients (16.7%) had IBD at the time of polypectomy; two were diagnosed prior and two coincident with JRP. None have subsequently been diagnosed with IBD. There was no difference in polyp recurrence between those with or without inflammation (16.7% [4/24] vs 10.0% [3/30]). The mean follow-up period was 72.4 months (range, 5-142 months). CONCLUSIONS: In our experience, histological mucosal inflammation is a common finding with JRP. This inflammation may be a precursor for the development of JRP but has no predictive value for polyp recurrence. This colitis does not seem to be associated with IBD.

Adolescent↗
PubMed2005

Inflammation and cytokeratin 7/20 staining of cardiac mucosa in young patients with and without Helicobacter pylori infection.

BACKGROUND: Both Helicobacter pylori and gastro-oesophageal reflux disease (GORD) may cause inflammation in cardiac mucosa. Intestinal metaplasia (IM) is found more often in GORD associated inflammation than in inflammation caused by H pylori, especially in young individuals. AIM: To examine morphological differences in chronic inflammation in these two conditions by immunohistochemistry. PATIENTS/METHODS: Tissue blocks from cardiac mucosa of patients <45 years were available as follows: 10 patients with chronic inflammation of cardiac mucosa (carditis) and H pylori gastritis (group 1); 10 patients with (possibly GORD related) carditis, but normal antrum and corpus (group 2); and 10 patients with non-inflamed cardiac mucosa and normal antrum and corpus (group 3). Haematoxylin and eosin staining and immunohistochemical staining for various inflammatory cells were performed for patients in groups 1 and 2 as follows: CD20 (B cells), CD3 (T cells), CD4 (T helper cells), CD8 (T suppressor cells), CD163 (macrophages), CD138 (plasma cells), and CD117 (mast cells). For all patients, cytokeratin 7/20 (CK7/20) staining was performed. RESULTS: No clear differences were seen in the morphology of chronic inflammation between groups 1 and 2. In both, plasma cells were most abundant. CK7/20 staining showed no differences between these groups. CONCLUSION: Helicobacter pylori negative (possibly GORD associated) and H pylori related carditis cannot be distinguished on a morphological basis. The stronger tendency towards IM in the first entity cannot be explained by differences in the type of inflammation. Barrett-type CK7/20 staining seems typical for cardiac mucosa, irrespective of the type of inflammation or presence of IM.

Adult↗
PubMed1998

The significance of cagA and vacA subtypes of Helicobacter pylori in the pathogenesis of inflammation and peptic ulceration.

AIMS: To assess the significance of cagA and vacA subtypes of Helicobacter pylori in relation to inflammation and density of bacterial colonisation in vivo within a dyspeptic UK population. METHODS: Dyspeptic patients who were Helicobacter pylori positive had antral samples taken for histology and culture. Gastroduodenal pathology was noted. The grade of bacterial density and inflammation was assessed using the Sydney system. Bacterial DNA was extracted and the vacA alleles and the cagA/gene typed using PCR. RESULTS: 120 patients were studied. There was high rate of cagA positive strains in this population. Bacterial density did not correlate with the presence of peptic ulceration. There was a significant association between cagA positive strains and increased inflammation and bacterial density. The vacA s1 type independently correlated with extensive chronic inflammation but there was no association with bacterial density. The vacA m type did not correlate with extent of inflammation or bacterial density. CONCLUSIONS: The results suggest that cagA is important in the pathogenesis of inflammation and peptic ulceration. These findings are in keeping with the hypothesis that cagA acts as a marker for a cag pathogenicity island which encodes several genes involved in inflammation. The vacA s1 allele correlates with inflammation independently of cagA, possibly through its enhanced ability to produce the vacuolating cytotoxin.

Adult↗
PubMed2003

Resolution of bronchial inflammation is related to bacterial eradication following treatment of exacerbations of chronic bronchitis.

BACKGROUND: Recent studies of the role of bacteria in chronic bronchitis have shown that bacterial colonisation is associated with enhanced inflammation and that purulent acute exacerbations of chronic bronchitis (AECB) are associated with bacteria and characterised by increased inflammation. Changes in bronchial inflammation in response to the success or failure of bacterial eradication following AECB were therefore studied. METHODS: Bacterial quantitative culture and sputum markers of inflammation (myeloperoxidase (MPO), neutrophil elastase, leukotriene B4 (LTB4), sol:serum albumin ratio, and secretory leukoprotease inhibitor) were measured in patients presenting with culture positive purulent AECB and repeated 10 days and 2 months later. 41 patients provided sputum sufficient for both bacteriology and assessment of inflammation at baseline and day 10, and 46 provided sufficient sample for bacteriology, 40 of which could also be analysed for inflammation at 2 months (when clinically stable). RESULTS: At day 10, 17 of the 41 patient samples had a positive bacterial culture. In the stable state, 18 of the 46 samples had a positive culture, but with a significantly lower bacterial load than at presentation. Although there was no difference between the groups at presentation, the concentration of MPO was lower (p<0.05) in those in whom bacteria were eradicated by day 10 than in those with persisting bacteria. The LTB4 concentration was similarly lower (p<0.001) in those in whom bacteria were eradicated than in those with persistent bacteria. In the stable clinical state the concentrations of both MPO and LTB4 were lower in those in whom bacteria were eradicated than in patients with persisting bacteria. CONCLUSION: Resolution of bronchial inflammation following AECB is related to bacterial eradication. Those in whom bacteria continue to be cultured in their sputum have partial resolution of inflammation which may reflect continued stimulation by the reduced bacterial load.

Adult↗
PubMed2007

Role of the renin-angiotensin system in the systemic microvascular inflammation of alveolar hypoxia.

Alveolar hypoxia (AH) induces widespread systemic inflammation. Previous studies have shown dissociation between microvascular Po(2) and inflammation. Furthermore, plasma from AH rats (PAHR) induces mast cell (MC) activation, inflammation, and vasoconstriction in normoxic cremasters, while plasma from normoxic rats does not produce these responses. These results suggest that inflammation of AH is triggered by a blood-carried agent. This study investigated the involvement of the renin-angiotensin system (RAS) in the inflammation of AH. Both an angiotensin-converting enzyme (ACE) inhibitor and an angiotensin II (ANG II) receptor blocker (ANG II RB) inhibited the leukocyte-endothelial adherence produced by AH, as well as the inflammation produced by PAHR in normoxic rat cremasters. MC stabilization with cromolyn blocked the effects of PAHR but not those of topical ANG II on normoxic cremasters, suggesting ANG II generation via MC activation by PAHR. This was supported by the observation that ACE inhibition and ANG II RB blocked the leukocyte-endothelial adherence produced by the MC secretagogue compound 48/80. These results suggest that the intermediary agent contained in PAHR activates MC and stimulates the RAS, leading to inflammation, and imply an RAS role in AH-induced inflammation.

Animals↗
PubMedDate not supplied

Is inflammation on Papanicolaou smear a risk factor for preterm delivery?

OBJECTIVE: Inflammation on Papanicolaou (Pap) smear has been associated with a 30-50% incidence of bacterial vaginosis (BV), a recognized risk factor for preterm delivery. We determined whether inflammation on Pap smear is associated with preterm delivery. STUDY DESIGN: 5,348 cases were studied with complete prenatal data including the potential confounder of treatment with antibiotics. Cases were categorized by presence (n = 1,139) or absence (n = 4,209) of inflammation on Pap smear. RESULTS: In the inflammation group the proportion of African Americans was lower (66.9 vs. 74.5%; p < 0.001). There were no significant differences (t test) for maternal age, gravidity, history of preterm delivery, or gestational age at delivery between inflammation and noninflammation groups. Multiple stepwise regression analysis showed that maternal age, history of preterm delivery, and African American race were all significantly positively associated with preterm delivery. Treatment with metronidazole during the pregnancy was significantly negatively associated with preterm delivery. Inflammation on Pap smear, gonorrhea detected during the pregnancy and prenatal treatment with erythromycin were not associated. CONCLUSION: Unlike bacterial vaginosis, inflammation on routine Pap smear does not appear to be a risk for subsequent preterm birth. We are unable to use inflammation on Pap smear as a surrogate for more specific diagnosis of bacterial vaginosis.

Adult↗
PubMed1992

Role of the autonomic nervous system in catheter-induced urethral inflammation.

We have studied role of the autonomic nervous system on experimentally induced urethral inflammation in the rat. Urethral inflammation was produced by inserting latex strips into the urethra. The effects of different experimental procedures were assessed by using a 4-grade inflammation scale based on histological findings. Rats pretreated with the nonspecific catecholamine depletors reserpine or quanethidine had a significantly less severe urethral inflammation than vehicle-treated controls. The severity of urethral inflammation was increased in spontaneous hypertensive rats, which have an increased sympathetic tone as compared to the normotensive rats. Propranolol, a nonselective beta-adrenergic receptor antagonist reduced and butoxamine, a beta 2-antagonist, significantly reduced the urethral inflammation. Neither phenoxybenzamine (nonselective) nor prazosin (alpha 1) or yohimbine (alpha 2), alpha-adrenergic receptor antagonists, affected the degree of urethral inflammation. These data taken together indicate that the autonomic innervation of the urethral mucosa is critically involved in the inflammatory reaction and that the use of beta 2-antagonist may be a treatment alternative in the future for the treatment of catheter-induced inflammation.

Animals↗
PubMed2001

The effect of salmeterol on markers of airway inflammation following segmental allergen challenge.

Inflammation is a critical component of asthma. Drugs that control asthma generally reduce the degree of airway inflammation. There is theoretical controversy surrounding the effects of beta(2)-agonists on airway inflammation, with some studies suggesting an anti-inflammatory effect, and others predicting a proinflammatory influence. We conducted a double-blind, placebo-controlled, crossover study of the effect of the long-acting beta(2)-agonist salmeterol on airway inflammation induced by segmental allergen challenge (SAC). We studied 13 allergic asthmatics controlled with as needed inhaled short-acting beta(2)-agonists alone, and used bronchoalveolar lavage 5 min and 48 h after SAC to assess airway inflammation, and the effects of salmeterol on this process. Salmeterol therapy improved FEV(1), but had no significant effect on the immediate or late cellular response to SAC. One measure of superoxide production was reduced, and interleukin-4 (IL-4) was reduced in baseline samples, but other indices of airway inflammation were unchanged by salmeterol therapy. We conclude that salmeterol therapy alone does not meaningfully reduce airway inflammation induced by SAC, but equally importantly, does not result in amplified inflammation.

Administration, Inhalation↗
PubMed1988

Respiratory tract infections increase susceptibility to neurogenic inflammation in the rat trachea.

This study reveals that respiratory tract infections make the tracheal mucosa of rats more susceptible to neurogenic inflammation, which is a type of inflammation mediated by neuropeptides released from sensory nerves. Neurogenic inflammation was produced in the tracheas of 2 groups of Long-Evans rats by electrical stimulation of the vagus nerve (5 V, 1 ms, 20 Hz for 5 min) or by an injection of capsaicin (15 to 200 micrograms/kg i.v.) or substance P (0.05 to 5.0 micrograms/kg i.v.). Rats of one group were pathogen-free; the others had serologic evidence of naturally occurring airway infections caused by Sendai virus, coronavirus, and Mycoplasma pulmonis. The stimuli produced neurogenic inflammation in both groups of rats, but the magnitude of this inflammation was much greater in the infected rats. The susceptibility of the infected rats to neurogenic inflammation was manifested by a 2.0 to 3.1 times larger increase in vascular permeability to Monastral blue, 5 times larger increase in number of neutrophils adhering to the endothelium of venules, and conspicuous morphologic changes in the tracheal epithelium. When pathogen-free rats acquired respiratory tract infections, they too became susceptible to neurogenic inflammation. Other experiments showed that infection by Sendai virus was essential for the change, although infection by M. pulmonis or coronavirus may also be necessary. The susceptibility to neurogenic inflammation outlasted the transient pathologic changes caused in the airway mucosa by the viral infections and may have been permanent.

Animals↗
PubMed2006

Uteroglobin-related protein 1 expression suppresses allergic airway inflammation in mice.

RATIONALE: Uteroglobin-related protein (UGRP) 1, which is highly expressed in the epithelial cells of the airways, has been suggested to play a role in lung inflammation. OBJECTIVES: The aim of study was to understand the effect of overexpressed UGRP1 on lung inflammation in a mouse model of allergic airway inflammation. METHODS: Ovalbumin-sensitized and -challenged mice, a model for allergic airway inflammation, were used in conjunction with recombinant adenovirus expressing UGRP1. MEASUREMENTS AND MAIN RESULTS: We demonstrated that intranasal administration of adeno-UGRP1 successfully delivered UGRP1 to the epithelial cells of airways and markedly reduced the number of infiltrating inflammatory cells, particularly eosinophils, in lung tissue as well as the level of proinflammatory cytokines such as interleukin (IL)-4, IL-5, and IL-13 in bronchoalveolar lavage fluids. The healed phase of inflammation was clearly seen in the peripheral areas of adeno-UGRP1-treated mouse lungs. CONCLUSION: These results demonstrate that UGRP1 can suppress inflammation in the mouse model of allergic airway inflammation. Based on this result, we propose UGRP1 as a novel therapeutic candidate for treating lung inflammation such as is found in asthma.

Adenoviridae↗
PubMed2006

Stress and inflammation as a detrimental combination for peri-implant bone loss.

The causes of peri-implant bone loss continue to be controversial. To determine the impact of biomechanical stress and inflammation, we investigated a total of 80 interforaminal implants in situ for more than 10 years. Two stress groups, with 14 patients each, were established: a low-stress situation with single-standing implants, and an increased-stress situation with splinted implants. To categorize inflammation, we introduced a Composite Inflammation Score using 4 inflammatory parameters. Peri-implant bone loss was calculated from digital panoramic radiographs. To differentiate between the effects of stress and inflammation, we compared bone loss in both stress groups at equivalent levels of inflammation. With greater Composite Inflammation Score values, a clear discrepancy between single-standing and splinted implants was evident (p = 0.117/0.000, regression analysis; p = 0.135/0.000, analysis of variance; p = 0.002, t tests). While stress and inflammation alone may not necessarily be detrimental factors, the presence of stress heightens peri-implant bone loss significantly as inflammation increases.

Aged↗
PubMed2006

Azithromycin reduces spontaneous and induced inflammation in DeltaF508 cystic fibrosis mice.

BACKGROUND: Inflammation plays a critical role in lung disease development and progression in cystic fibrosis. Azithromycin is used for the treatment of cystic fibrosis lung disease, although its mechanisms of action are poorly understood. We tested the hypothesis that azithromycin modulates lung inflammation in cystic fibrosis mice. METHODS: We monitored cellular and molecular inflammatory markers in lungs of cystic fibrosis mutant mice homozygous for the DeltaF508 mutation and their littermate controls, either in baseline conditions or after induction of acute inflammation by intratracheal instillation of lipopolysaccharide from Pseudomonas aeruginosa, which would be independent of interactions of bacteria with epithelial cells. The effect of azithromycin pretreatment (10 mg/kg/day) given by oral administration for 4 weeks was evaluated. RESULTS: In naive cystic fibrosis mice, a spontaneous lung inflammation was observed, characterized by macrophage and neutrophil infiltration, and increased intra-luminal content of the pro-inflammatory cytokine macrophage inflammatory protein-2. After induced inflammation, cystic fibrosis mice combined exaggerated cellular infiltration and lower anti-inflammatory interleukin-10 production. In cystic fibrosis mice, azithromycin attenuated cellular infiltration in both baseline and induced inflammatory condition, and inhibited cytokine (tumor necrosis factor-alpha and macrophage inflammatory protein-2) release in lipopolysaccharide-induced inflammation. CONCLUSION: Our findings further support the concept that inflammatory responses are upregulated in cystic fibrosis. Azithromycin reduces some lung inflammation outcome measures in cystic fibrosis mice. We postulate that some of the benefits of azithromycin treatment in cystic fibrosis patients are due to modulation of lung inflammation.

Animals↗
PubMed2006

Suppression of inflammation by low-dose methotrexate is mediated by adenosine A2A receptor but not A3 receptor activation in thioglycollate-induced peritonitis.

Prior studies demonstrate that adenosine, acting at one or more of its receptors, mediates the anti-inflammatory effects of methotrexate in animal models of both acute and chronic inflammation. Both adenosine A2A and A3 receptors contribute to the anti-inflammatory effects of methotrexate treatment in the air pouch model of inflammation, and the regulation of inflammation by these two receptors differs at the cellular level. Because different factors may regulate inflammation at different sites we examined the effect of low-dose weekly methotrexate treatment (0.75 mg/kg/week) in a model of acute peritoneal inflammation in adenosine A2A receptor knockout mice and A3 receptor knockout mice and their wild-type littermates. Following intraperitoneal injection of thioglycollate there was no significant difference in the number or type of leukocytes, tumor necrosis factor alpha (TNF-alpha) and IL-10 levels that accumulated in the thioglycollate-induced peritoneal exudates in adenosine A2A knockout mice or wild-type control mice. In contrast, there were more leukocytes, TNF-alpha and IL-10 in the exudates of the adenosine A3 receptor-deficient mice. Low-dose, weekly methotrexate treatment increased the adenosine concentration in the peritoneal exudates of all mice studied, and reduced the leukocyte accumulation in the wild-type mice and A3 receptor knockout mice but not in the A2A receptor knockout mice. Methotrexate reduced exudate levels of TNF-alpha in the wild-type mice and A3 receptor knockout mice but not the A2A receptor knockout mice. More strikingly, IL-10, a critical regulator of peritoneal inflammation, was increased in the methotrexate-treated wild-type mice and A3 knockout mice but decreased in the A2A knockout mice. Dexamethasone, an agent that suppresses inflammation by a different mechanism, was similarly effective in wild-type mice, A2A mice and A3 knockout mice. These findings provide further evidence that adenosine is a potent regulator of inflammation that mediates the anti-inflammatory effects of methotrexate. Moreover, these data provide strong evidence that the anti-inflammatory effects of methotrexate and adenosine are mediated by different receptors in different inflammatory loci, an observation that may explain why inflammatory diseases of some organs but not of other organs respond to methotrexate therapy.

Adenosine↗
PubMed1997

Intestinal inflammation and barrier function in HLA-B27/beta 2-microglobulin transgenic rats.

BACKGROUND: Since intestinal inflammation is correlated with impaired barrier functions, transgenic HLA-B27/human beta 2-microglobulin rats that spontaneously develop intestinal inflammation were used to investigate whether onset of inflammation or impaired barrier function was the initial event. METHODS: During the age period of 9-14 weeks, transgenic and non-transgenic (control) rats were gavaged weekly with the marker molecules, 51Cr-ethylenediaminetetraacetic acid, 1-deamino-8-D-arginine vasopressin, and albumin, which were quantified in blood or urine. RESULTS: At 12 weeks of age the first signs of inflammation appeared with decreased body weight gain, decreased urine production, and onset of diarrhea. By 14-15 weeks of age all transgenic rats had developed intestinal inflammation, as confirmed by histology and increased myeloperoxidase content, whereas no inflammation was observed in controls. Intestinal passage of the markers did, however, not differ between transgenic and control rats over the studied period. CONCLUSIONS: The results suggest that intestinal inflammation precedes altered intestinal barrier function in this inflammation model.

Animals↗
PubMed1999

Gastric cardia inflammation and intestinal metaplasia: associations with reflux esophagitis and Helicobacter pylori.

Gastric cardia inflammation and intestinal metaplasia are the subjects of recent investigation. Some authors have found associations with gastroesophageal reflux disease, whereas others have identified relationships with Helicobacter pylori (HP). We studied 150 consecutive patients who underwent upper endoscopy, had normal gastroesophageal anatomy, and had biopsies of the antrum, cardia, and lower esophagus, to evaluate relationships between reflux esophagitis, cardia inflammation, intestinal metaplasia, and HP gastritis. Forty-two patients had HP infection. Cardia inflammation was significantly related to esophageal squamous inflammation in the non-HP-infected patient group and to antral inflammation and cardia HP infection in the HP-infected patient group. The differences between the patient groups was most apparent in the patients with moderate or marked inflammation. Twenty-seven percent of patients had cardia intestinal metaplasia that was related to cardia inflammation. Cardia inflammation and intestinal metaplasia probably have multiple causes. Pathologists should refrain from applying the term Barrett's esophagus for biopsies procured from the cardia that show intestinal metaplasia in patients with a normal squamocolumnar junction.

Adolescent↗
PubMed2000

Conjunctival inflammation induces Langerhans cell migration into the cornea.

PURPOSE: The virtual absence of Langerhans cells (LC) in donor or recipient corneal epithelium is known to be an important factor in the acceptance of orthotopic corneal allografts. Though it is well known that various types of stimulation to the cornea induce LC migration into the corneal epithelium, resulting in poor graft survival, the influence of conjunctival inflammation on LC migration into the cornea has not been elucidated. Therefore we examined whether LCs migrate into the cornea in the presence of conjunctival inflammation. METHODS: Sixteen BALB/c mice were divided into four groups. Group A: 4 mice with corneal inflammation induced by two 9-0 silk interrupted sutures in the central cornea (positive control); Group B: 4 mice with conjunctival inflammation induced by two 9-0 silk interrupted sutures in the temporal and nasal bulbar conjunctiva 1 mm from the limbus; Group C: 4 mice with conjunctival inflammation by two 10-0 nylon interrupted sutures in the temporal and nasal bulbar conjunctiva 1 mm from the limbus; and Group N: 4 mice with no inflammation (untreated, naive control). Fourteen days after suturing, the mice were sacrificed and LCs migrated into the corneal epithelium were counted by immunofluorescence assay using anti-Ia antibody. RESULTS: In Group A, Ia(+) cells in the cornea totaled 29.4 +/- 3.8 cells/mm(2); in Group B, 7.9 +/- 1.2 cells/mm(2); in Group C, 7.8 +/- 0.7 cells/mm(2); and in Group N, 1. 6 +/- 0.5 cells/mm(2). Significantly greater numbers of Ia(+) cells were detected in Groups A, B and C than in Group N (p < 0.005). CONCLUSIONS: Conjunctival inflammation caused by sutures in the bulbar conjunctiva induced LC migration into the cornea. These results indicate that conjunctival inflammation influences the corneal immunological environment, and may affect the fate of orthotopic corneal allografts.

Animals↗
PubMed1992

[Pelvic inflammation after induced abortion].

A total of 949 women referred for legal termination of pregnancy in the first trimester participated in an investigation to assess the risk of pelvic inflammation in connection with the intervention in women with and without previous pelvic inflammation in connection with previous pregnancies, the gestational age and the clinical experience of the surgeon. Women who had not borne children developed pelvic inflammation more frequently after legal termination of pregnancy (p < 0.01) than women who had previously borne children. Women with previous pelvic inflammation developed renewed pelvic inflammation, if they had not previously borne children (p < 0.01) or if they had previously undergone legal termination of pregnancy (p < 0.05). Women without previous pelvic inflammation developed pelvic inflammation significantly more frequently, if they had not previously been pregnant (p < 0.05). The occurrence of pelvic inflammation was independent of the gestational age and the clinical experience of the surgeon.

Abortion, Induced↗
PubMed2005

Systemic inflammation, cachexia and prognosis in patients with cancer.

PURPOSE OF REVIEW: Cachexia remains an important cause of morbidity and mortality among cancer patients. The mechanisms underlying this syndrome remain unclear and are almost certainly multifactorial. Evidence from animal models suggests a compelling link between cachexia and inflammation, and a variety of pro-inflammatory cytokines play an integral role. This review summarizes current thinking relating to inflammation, cachexia and prognosis in cancer patients, with particular emphasis on studies relating to recent therapeutic advances. RECENT FINDINGS: Pro-inflammatory cytokines induce the acute phase protein response, a key marker of systemic inflammation. Recent evidence has also implicated other tumour-derived mediators, such as proteolysis-inducing factor and parathyroid hormone-related peptide. In addition, systemic inflammation has been found in association with many malignancies, and has been correlated with weight loss, hypermetabolism, anorexia, and adverse prognosis. Treatments such as fish oil, monoclonal antibodies, and non-steroidal anti-inflammatory drugs, have all been utilized to attenuate systemic inflammation and influence weight loss. Recent clinical studies have suggested that eicosapentaenoic acid and cyclo-oxygenase 2 inhibitors promote weight gain and downregulate the acute phase protein response. SUMMARY: Pro-inflammatory processes are clearly implicated in the hypermetabolism and weight loss associated with cancer-associated cachexia. In addition, the presence of systemic inflammation is now clearly linked with adverse prognosis in patients with cancer, which cannot be fully explained by the association with weight loss. Systemic inflammation remains an important area for novel therapeutic targets in combating cachexia, and eicosapentaenoic acid and cyclo-oxygenase 2 inhibitors appear to be efficacious in the armory against cachexia.

Acute-Phase Proteins↗