Tube Feeding among Elder in Long-Term Care Facilities: A Systematic Review and Meta-Analysis.

OBJECTIVE: The use of tube feeding for elderly patients with poor nutritional intake is a ubiquitous method of feeding. This systematic review and meta-analysis were carried out to compare nutritional benefits of enteral feeding versus oral feeding in long-term care facilities. SETTING: Databases including the Cochrane Library, ProQuest, PubMed, EMBASE, EBSCO, Web of Science and Google Scholar through April 2014 using keywords including enteral feeding, tube feeding or oral feeding combined with long term care facilities or nursing home. PARTICIPANTS: Eight articles, with 841 participants were included in meta-analysis and 13 articles were included in systematic review. The elderly had to live in long-term care institutions and could not be on any mechanically assisted ventilation systems or be in any type of post-operative status. MEASUREMENTS: The three investigators extracted and appraised data using the same study design, baseline characteristics, and outcomes, independently. RESULTS: Following a systematic review, 13 articles out of 8218 original research articles were selected for this analysis. Meta-analysis of tube-fed patients found lower levels of hemoglobin (Weighted Mean Difference (WMD -0.21g/dl; 95% CI -0.42 to -0.01; p=0.04) and creatinine (WMD -0.08g/dl; 95% CI -0.17 to 0.00, p=0.05). Moreover, the results showed that there were no benefits regarding body mass index (BMI), albumin, dietary intake of proteins, total calories and fat. CONCLUSIONS: The results show that tube feeding does not increase patients' nutrients absorption to improve nutritional status. Instead, these results indicate that oral feeding is better regarding some nutritional biochemical parameters.

Prognosis of advanced hepatocellular carcinoma patients enrolled in clinical trials can be classified by current staging systems.

BACKGROUND: Patients enrolled in clinical trials of advanced hepatocellular carcinoma (HCC) are usually required to have good liver reserve and organ function. However, their outcomes are still highly variable. We aimed to examine whether current staging systems can predict the survival of these highly selected patients. METHODS: Patients from clinical trials involving first-line anti-angiogenic therapy were assigned to different stage groups using the American Joint Committee on Cancer (AJCC), Barcelona Clinic Liver Cancer (BCLC), China integrated score, Cancer of the Liver Italian Program (CLIP) score, Chinese University Prognostic Index (CUPI), Groupe d'Etude et de Traitement du Carcinome Hepatocellulaire (GETCH), Japan Integrated Staging (JIS) score, Okuda, Tokyo score, and a new staging system recently proposed. Survival prediction by the 10 systems was then compared by both univariate and multivariate analyses. RESULTS: A total of 157 patients were selected for this study. In univariate analysis, all staging systems can predict patient survival except AJCC, BCLC, and JIS score. Concordance indexes for CLIP score, CUPI, and GETCH (0.752, 0.775, and 0.791, respectively) were significantly higher than those obtained for other staging systems. In multivariate analysis, the CLIP score and CUPI (P<0.001 and 0.009, respectively) predicted survival more accurately than did the other tested staging systems. Hepatitis B infection and poor performance status were also associated with poor survival. CONCLUSION: Several HCC staging systems, especially the CLIP score and CUPI, can predict prognosis of patients who are enrolled in clinical trials of advanced HCC.

Burden of tuberculosis among aboriginal and non-aboriginal Taiwanese, 1996-2006.

OBJECTIVE: To estimate the tuberculosis (TB) burden in Taiwan from 1996 to 2006, based on incidence, mortality and disability-adjusted life years (DALYs). DESIGN: Data were collected from three databases: Tuberculosis Registry Database, National Mortality Database and Taiwan Household Registration System Database. Age standardisation of the incidence/mortality rates was performed by the direct method, using the 2000 World Health Organization world population as standard. Disease burden estimation used DALY, based on the Global Burden of Disease study. RESULTS: The age-adjusted TB incidence/mortality rates decreased during the study period. The highest DALYs per 100,000 were in the ≥65 years age group among non-aboriginals, and in the 35-54 years and ≥65 years age groups in aboriginals. In general, the DALY/case increased with age among non-aboriginals, whereas the highest DALY/case was found in the 35-44 years age group in aboriginals. The DALY/100,000, DALY/case and total DALY significantly decreased from 1996 to 2006 for non-aboriginals, but fluctuated for aboriginals. CONCLUSION: This analysis provided the first comprehensive evaluation of the burden of TB in Taiwan. The prevention and treatment of TB among aboriginals in all age groups should be enhanced.

Impact of postures on blood pressure in healthy subjects.

BACKGROUND: Controversies exist on the nature of influence of body position on the level of blood pressure. This study was designed to investigate the impact of postures on blood pressures in healthy subjects. METHODS: Blood pressure was measured in 6,485 healthy subjects in both supine and sitting positions, using a standard mercury sphygmomanometer. RESULTS: The average systolic and diastolic blood pressure in all age groups in the supine position was higher than in the sitting position (P < 0.001). There was a reduced systolic pressure increment but enhanced diastolic pressure increment with aging (P < 0.05). The levels of sitting blood pressure were inversely correlated to the pressure increments in supine positions (P < 0.001). Multivariate regression analysis showed that age is an independent factor for the systolic pressure increment in the supine position (P < 0.001), whereas sex, age, body height and body mass index are independent predictors for the increment in diastolic blood pressure (P < 0.001). CONCLUSIONS: In healthy subjects, blood pressure in the supine position is higher than in the sitting position and age plays an important part in this posture-related pressure increment.

Measurement of the asymmetry in the decay Omega+-->LamdaKappa+-->rhopi+Kappa+.

The asymmetry in the rho angular distribution in the sequential decay Omega+-->LamdaKappa+-->rhopi+Kappa+. has been measured to be alphaOmegaalphaLamda=[+1.16+/-0.18(stat)+/-0.17(syst)]x10(-2) using 1.89x10(6) unpolarized Omega+ decays recorded by the HyperCP (E871) experiment at Fermilab. Using the known value of alphaLamda, and assuming that alphaLamda=-alphaLamda, alphaOmega=[-1.81+/-0.28(stat)+/-0.26(syst)]x10(-2). A comparison between this measurement of alphaOmegaalphaLamda and recent measurements of alphaOmegaalphaLamda made by HyperCP shows no evidence of a violation of CP symmetry.

Search for the lepton-number-violating decay Xi(-)-->pmu(-)mu(-).

A sensitive search for the lepton-number-violating decay Xi(-)-->pmu(-)mu(-) has been performed using a sample of approximately 10(9) Xi(-) hyperons produced in 800 GeV/c p-Cu collisions. We obtain B(Xi(-)-->pmu(-)mu(-))<4.0x10(-8) at 90% confidence, improving on the best previous limit by 4 orders of magnitude.

Search for DeltaS = 2 nonleptonic hyperon decays.

A sensitive search for the rare decays Omega(-)--> Lambdapi(-) and Xi(0)--> ppi(-) has been performed using data from the 1997 run of the HyperCP (Fermilab E871) experiment. Limits on other such processes do not exclude the possibility of observable rates for |DeltaS| = 2 nonleptonic hyperon decays, provided the decays occur through parity-odd operators. We obtain the branching-fraction limits B(Omega(-)-->Lambdapi(-)) < 2.9 x 10(-6) and B(Xi(0)--> ppi(-)) < 8.2 x 10(-6), both at 90% confidence level.

Evidence for the decay sigma+ --> pmu+ mu-.

We report the first evidence for the decay Sigma(+)-->pmu(+)mu(-) from data taken by the HyperCP (E871) experiment at Fermilab. Based on three observed events, the branching ratio is B(Sigma(+)-->pmu(+)mu(-))=[8.6(+6.6)(-5.4)(stat)+/-5.5(syst)]x10(-8). The narrow range of dimuon masses may indicate that the decay proceeds via a neutral intermediate state, Sigma(+)-->pP(0),P0-->mu(+)mu(-) with a P0 mass of 214.3+/-0.5 MeV/c(2) and branching ratio B(Sigma(+)-->pP(0),P0-->mu(+)mu(-))=[3.1(+2.4)(-1.9)(stat)+/-1.5(syst)]x10(-8).

Search for CP violation in charged-Xi and Lambda hyperon decays.

We have compared the p and p angular distributions in 117 x 10(6) Xi- -->Lambdapi- -->ppi-pi- and 41 x 10(6) Xi+ -->Lambda pi+ -->p pi+pi+ decays using a subset of the data from the HyperCP experiment (E871) at Fermilab. We find no evidence of CP violation, with the direct-CP-violating parameter AXiLambda identical with (alphaXialphaLambda-alpha Xialpha Lambda)/(alphaXialphaLambda+alphaXialphaLambda)=[0.0+/-5.1(stat)+/-4.4(syst)] x 10(-4).

Lipopolysaccharide enhances substance P-mediated neutrophil adherence to epithelial cells and cytokine release.

Lipopolysaccharide (LPS) is implicated in many respiratory tract inflammatory diseases. Tachykinins, especially substance P (SP) through the NK-1 receptor, mediate leukocyte adhesion to the endothelial or airway epithelial cells. Here we assessed the enhancement by LPS of tachykinin-mediated neutrophil adherence to alveolar epithelial cells, and associated interleukin-1 beta (IL-1beta) and tumor necrosis factor (TNF-alpha) release. Neutrophil adherence to A549 epithelial cell was not increased by LPS (100 ng/ml), or SP (10(-)(12)-10(-)(8) M) alone, but was significantly enhanced by their combination (LPS + SP). Neutrophil adherence to epithelial cells induced IL-1beta and TNF-alpha release from A549 cells either spontaneously or stimulated by SP or LPS. LPS + SP significantly enhanced IL-1beta and TNF-alpha release. The NK-1 receptor antagonist L-732,138 inhibited this enhancement response. Prevention of neutrophil adherence by CD11b/CD18 blocking antibody or by placing a filter on the epithelial monolayer diminished spontaneous or LPS + SP-enhanced IL-1beta and TNF-alpha release. Pretreatment with the serine protease inhibitor cocktail also inhibited LPS + SP-enhanced neutrophil adherence-dependent IL-1beta and TNF-alpha release as well as their mRNA expression. In conclusion, we have demonstrated LPS enhanced SP-mediated neutrophil adherence and associated IL-1beta and TNF-alpha release from the A549 epithelial monolayer, partly through NK-1 receptors. Neutrophil adherence to epithelial cells may release serine protease to induce IL-1beta and TNF-alpha release and their synthesis.

Increased apoptosis in human amnion is associated with labor at term.

PROBLEM: To characterize whether increased apoptosis in human amnion was associated with labor at term. METHOD OF STUDY: Human amnion were obtained from term patients with vaginal delivery (n = 5) or who underwent elective Cesarean section (C/S) without labor (n = 5). Apoptosis was performed by the TUNEL (Terminal dUTP Nuclear End Labeling) assay. All nucleated cells stained with propidium iodide in the amnion epithelial cells were identified in red fluorescence. TUNEL positive apoptotic nuclei were identified in green fluorescence. Five random fields of each specimen were blindly counted by investigators. The percentage of apoptotic nuclei of total nuclei (apoptotic index) was calculated and compared between the two groups (25 microscopic fields for each group, respectively). RESULTS: Patients with term labor had a significantly higher mean apoptotic index in amnion epithelial cells than that with elective C/S without labor (27.3 +/- 4.1% versus 3.6 +/- 1.6%, P < 0.001). CONCLUSIONS: Our data indicate that apoptosis in human amnion is significantly increased and associated with labor at term.

Amniotic fluid soluble fas levels in intra-amniotic infection.

OBJECTIVE: Membrane Fas can induce apoptosis in sensitive cells. It has been reported that soluble Fas (sFas) is elevated in septicemia. We examined amniotic fluid (AF) sFas levels in patients with and without intra-amniotic infection. METHODS: Forty-two AF specimens were studied. Intra-amniotic infection was defined as the presence of a positive AF culture. Twenty-one specimens were from patients with intra-amniotic infection and 21 were from patients without intra-ammotic infection. Amniotic fluid sFas was determined by an enzyme immunoassay and normalized by AF creatinine levels. The Mann-Whitney U test, contingency table method, and Spearman's rank correlation test were used for statistical analyses. Data were expressed as median with ranges. RESULTS: There were no significant differences in maternal age, gestational age, parity, and race between the groups. The median AF sFas was significantly higher with intra-amniotic infection than without it (5.07 U/mL, range 0.32-13. 25 compared with 1.95 U/mL, range 0.01-5.35; P =.004). After normalizing to AF creatinine, infected fluids also had significantly higher median sFas/creatinine than uninfected amniotic fluids (289.1 U/mg creatinine, range 16.6-920.5 compared with 126.8 U/mg creatinine, range 0.5-546.2; P =.01). Amniotic fluid sFas and sFas/creatinine were positively correlated with AF leukocytes and negatively correlated with AF glucose. CONCLUSION: Elevated AF sFas is associated with intra-amniotic infection. High production of AF sFas in intra-amniotic infection may play a role in the inhibition of apoptosis of AF leukocytes, leading to the persistence of inflammation.

Nitric oxide modulates interleukin-1beta and tumor necrosis factor-alpha synthesis by alveolar macrophages in pulmonary tuberculosis.

Interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha released from alveolar macrophages (AM) in pulmonary tuberculosis (TB) are important in host defense against mycobacterial infection. Nitric oxide (NO) production is enhanced in AM of TB patients. We examined whether NO was implicated in (IL)-1beta and TNF-alpha synthesis by AM of TB patients. Purified AM were retrieved by bronchoalveolar lavage from 11 TB patients and 10 normal subjects, and were cultured with or without the NO inhibitor N(G)-monomethyl-L-arginine (L-NMMA). The release of IL-1beta and TNF-alpha, and expression of their messenger RNAs (mRNAs), were determined by enzyme-linked immunosorbent assay and Northern blot analysis. The release of IL-1beta and TNF-alpha was greater from AM of TB patients than from AM of normal subjects. L-NMMA inhibited nitrite, IL-1beta, and TNF-alpha production in TB patients. The mRNA expression for IL-1beta and TNF-alpha was upregulated in TB patients and was depressed by L-NMMA. Immunocytochemistry done with a monoclonal antibody against the p65 subunit of nuclear factor (NF)-kappaB showed that NF-kappaB was highly expressed and translocated to the nuclei of AM from TB patients, and was inhibited by L-NMMA. Inhibition of NF-kappaB by pyrrolidine dithiocarbamate attenuated IL-1beta and TNF-alpha synthesis. In conclusion, enhanced NO generation by AM of TB patients plays an autoregulatory role in amplifying the synthesis of proinflammatory cytokines, probably through NF-kappaB activation.

Color Doppler imaging of placental masses: differential diagnosis and fetal outcome.

OBJECTIVES: To evaluate the application of Doppler imaging in the differential diagnosis of placental masses and perinatal outcome. METHODS: A retrospective study of all cases referred for suspicion of placental chorioangioma over a nine and a half year period. Only cases in which color flow mapping and pulsed Doppler examination were performed were considered. RESULTS: Fourteen cases fulfilled the criteria and included seven cases of chorioangioma, two cases of placental hemorrhage and five cases of a placental mass which resolved during pregnancy. All cases of chorioangioma could be distinguished by increased blood flow within the mass. Polyhydramnios was associated with six cases of chorioangioma. Rapid tumor growth, premature labor and neonatal death occurred in one case. Premature labor occurred in six cases of chorioangioma and both cases of placental hemorrhage. IUGR was associated with two cases of chorioangioma and both cases of placental hemorrhage. All cases of resolving placental mass delivered uneventfully at term. CONCLUSIONS: Color Doppler is a useful tool in the differentiation of placental masses. Such masses should be followed up regularly because their growth rate is variable and unpredictable.

Nitric oxide: a clinically important amniotic fluid marker to distinguish between intra-amniotic mycoplasma and non-mycoplasma infections.

The objective of this study was to determine whether the measurements of amniotic fluid nitric oxide metabolite (NOx: nitrate + nitrite) concentrations could be a clinically useful marker to differentiate between intra-amniotic mycoplasma and nonmycoplasma infections. Amniocentesis was performed on 76 pregnant women with suspicion of intra-amniotic infection. Intra-amniotic infection was defined as the presence of a positive amniotic fluid culture with either mycoplasma or nonmycoplasma infections. Rapid amniotic fluid tests for Gram stain, glucose, leukocyte counts, interleukin-6, and NOx were performed. Amniotic fluid NOx was measured with aspergillus nitrate reductase and Griess reagent. Interleukin-6 was determined by enzyme immunoassays. Amniotic fluid NOx and interleukin-6 were normalized by amniotic fluid creatinine levels. Patients with intra-amniotic mycoplasma (n = 7) and nonmycoplasma infections (n = 8) had significantly higher amniotic fluid leukocyte counts and interleukin-6 concentrations and significantly lower amniotic fluid glucose levels than noninfected controls (n = 61). Amniotic fluid concentrations of NOx were significantly higher in those with intraamniotic nonmycoplasma infection as compared to those with intraamniotic mycoplasma infection and noninfected controls (NOx: 3.35+/-0.74 vs. 2.03+/-0.41 micromol/mg creatinine, p = 0.005, and 3.35+/-0.74 vs. 1.72+/-0.07 micromol/mg creatinine, p < 0.0001, respectively). However, patients with intra-amniotic mycoplasma infection did not differ significantly from noninfected controls. Our data indicate that clinical characteristics of intra-amniotic mycoplasma infection may differ from intra-amniotic nonmycoplasma infection. As delivery is not always indicated in intra-amniotic mycoplasma infection, elevated rapid amniotic fluid tests (leukocyte counts, interleukin-6, and glucose) may not be appropriate in the clinical management of intra-amniotic mycoplasma infection. In addition to these rapid amniotic fluid tests, incorporation of the measurement of amniotic fluid NOx may be of clinical importance in the differentiation and management of patients with suspected intra-amniotic mycoplasma and nonmycoplasma infection.

Elevated amniotic fluid nucleosome levels in women with intra-amniotic infection.

OBJECTIVE: To compare amniotic fluid (AF) soluble nucleosome levels in pregnant women with and without intra-amniotic infection. METHODS: Amniocentesis was performed in 74 pregnant women with preterm contractions, labor, or premature rupture of membranes. Intra-amniotic infection was defined as a positive AF culture. Amniotic fluid tests for Gram stain, glucose, neutrophils, creatinine, pH, and specific gravity were performed. Amniotic fluid soluble nucleosome levels were determined by enzyme-linked immunosorbent assay and were normalized by AF creatinine levels. RESULTS: Twenty-eight patients had intra-amniotic infection and 46 did not. Amniotic fluid soluble nucleosome levels were significantly higher in pregnant women with intra-amniotic infection than in those without infection (48.1+/-21.3 compared with 0.0+/-0.0 U/mg creatinine; P = .005). The AF nucleosome levels were positively correlated with AF neutrophil counts and negatively correlated with AF glucose concentrations. CONCLUSION: Our data indicate that elevated AF nucleosome levels are associated with intra-amniotic infection and may have potential as a clinical marker to detect intra-amniotic infection.

Lipopolysaccharide enhances neurogenic plasma exudation in guinea-pig airways.

1. Lipopolysaccharide (LPS) is implicated in many pulmonary and airway inflammatory diseases. Tachykinins released from nerve endings increase vascular permeability. In this study, we have assessed the enhancement by LPS of tachykinin-mediated plasma exudation in guinea-pig airways, and examined the role of oxidants as well as leukocyte adherence. 2. LPS (100 microg kg(-1), i.v.) was administered 0-3 h before bilateral electrical stimulation of the cervical vagus nerves in animals anaesthetized with urethane and ventilated. Vagal stimulation increased vascular permeability in the airways. LPS enhanced the vagally-mediated plasma exudation with the peak effect at 1 h after LPS administration. LPS alone induced no significant plasma exudation. LPS also enhanced exogenous substance P (10(-8) mol kg(-1), i.v.)-induced plasma exudation. 3. The NK-1 receptor antagonist L-732,138 abolished vagally-induced plasma exudation and significantly inhibited the enhancement by LPS. Pretreatment with superoxide dismutase (SOD, 5000 U kg(-1), i.p.) did not affect the vagally-induced plasma exudation, but inhibited the LPS-enhanced neurogenic plasma leakage. The LPS-enhanced vagally-induced plasma exudation was not completely inhibited by either L-732,138 or SOD pretreatment alone, but was blocked by the combination of both pretreatments. 4. Neutrophil depletion by cyclophosphamide alone did not influence vagally-induced plasma exudation, but significantly inhibited the LPS-enhanced response. 5. In conclusion, we have demonstrated LPS enhanced neurogenic plasma exudation by augmenting the response to tachykinins, partly through NK-1 receptors, to directly increase vascular permeability or to enhance leukocyte adhesion-mediated endothelial cell injury. Tachykinins released from nerve endings may contribute to endotoxin-related airway inflammatory responses.

Elevated amniotic fluid levels of leukemia inhibitory factor, interleukin 6, and interleukin 8 in intra-amniotic infection.

OBJECTIVE: The study's objective was to determine and correlate amniotic fluid levels of leukemia inhibitory factor, interleukin 6, and interleukin 8 in patients with and without intra-amniotic infection. STUDY DESIGN: Amniocentesis was performed on 41 pregnant women with preterm contractions, labor, or premature rupture of membranes. Intra-amniotic infection was defined as the presence of a positive amniotic fluid culture result. Amniotic fluid tests for Gram stain, glucose, leukocyte counts, creatinine level, pH, and specific gravity were performed. Amniotic fluid levels of leukemia inhibitory factor, interleukin 6, and interleukin 8 were measured by an enzyme-linked immunoassay. Unlike in previous reports, cytokines were normalized by amniotic fluid creatinine levels. RESULTS: Fifteen patients had intra-amniotic infection and 26 did not. Amniotic fluid median levels of leukemia inhibitory factor, interleukin 6, and interleukin 8 were significantly higher in pregnant women with intra-amniotic infection than in those without intra-amniotic infection (leukemia inhibitory factor median 3912 pg/mg creatinine, range 0.0-199314, vs 56 pg/mg creatinine, range 0. 0-12148, P =.01; interleukin 6 median 2005 ng/mg creatinine, range 27-4071, vs 990 ng/mg creatinine, range 7.5-3409, P =.005; interleukin 8: median 4933 ng/mg creatinine, range 0.0-55058, vs 61 ng/mg creatinine, range 0.0-2399, P =.005). Amniotic fluid levels of leukemia inhibitory factor, interleukin 6, and interleukin 8 were positively correlated. CONCLUSIONS: The data indicate that leukemia inhibitory factor plays an important role in the pathogenesis of intra-amniotic infection. In addition, significant elevations of and correlations among amniotic fluid levels of leukemia inhibitory factor, interleukin 6, and interleukin 8 suggest that measurements of these cytokines in amniotic fluid may be of diagnostic and prognostic importance.

Immunohistochemical localization of inducible nitric oxide synthase on human fetal amnion in intra-amniotic infection.

OBJECTIVES: Amniotic fluid levels of nitric oxide metabolites are significantly elevated in intra-amniotic infection. We hypothesized that fetal amnion is a possible site for the production of nitric oxide. Because inducible nitric oxide synthase is the key enzyme responsible for the generation of nitric oxide in patients with intra-amniotic infection, we used immunohistochemistry to localize it on human fetal amnion. STUDY DESIGN: Human fetal amnions were obtained from patients with and without intra-amniotic infection (n = 5, respectively). Intra-amniotic infection was diagnosed by positive amniotic fluid cultures and placental pathologic features. Human fetal amniotic membranes were processed into tissue blocks and embedded in paraffin. A rabbit polyclonal antibody against human inducible nitric oxide synthase was used as the primary antibody, followed by avidin-biotin immunoperoxidase localization. Normal rabbit serum was used as a negative control and ovarian carcinoma cells were used as the positive control. RESULTS: Anti-inducible nitric oxide synthase labeling of human fetal amniotic membranes in patients with intra-amniotic infection showed positive immunostaining of epithelial cells, specifically in the cytoplasm of the perinuclear area. In contrast, no anti-inducible nitric oxide synthase immunostaining on human fetal amniotic membranes could be identified in patients without intra-amniotic infection. CONCLUSIONS: Our data provide important evidence that inducible nitric oxide synthase can be induced on human fetal amnion in intra-amniotic infection. These findings strongly support our hypothesis that human fetal amnion may be a possible site for the synthesis of nitric oxide after inducible nitric oxide synthase is induced in response to infectious products in intra-amniotic infection.

Elevated amniotic fluid nitric oxide metabolites and interleukin-6 in intra-amniotic infection.

OBJECTIVE: To compare amniotic fluid nitric oxide metabolites and interleukin-6 (IL-6) concentrations in patients with and without intra-amniotic infection. METHODS: Amniotic fluid nitric oxide metabolites, IL-6, Gram stains, glucose, leukocyte counts, leukocyte esterase activity, creatinine, pH, and specific gravity were determined in 14 patients with intra-amniotic infection and 26 patients without intra-amniotic infection. Intra-amniotic infection was defined as the presence of a positive amniotic fluid culture. The nitric oxide metabolites, nitrate and nitrite (NOx), were measured using Greiss reagent after reduction of nitrate to nitrite with aspergillus nitrate reductase. Interleukin-6 was measured by a two-site, enzyme-linked immunosorbent assay. Amniotic fluid nitric oxide metabolites and IL-6 concentrations were normalized by amniotic fluid creatinine levels. The Mann-Whitney U test, contingency table method, and Spearman's rank correlation test were used for statistical analyses. RESULTS: Amniotic fluid NOx and IL-6 levels were significantly higher in patients with intra-amniotic infection than in those without intra-amniotic infection (NOx: median = 2.06 mumol/mg creatinine, range = 0.74-6.81 versus 1.35 mumol/mg creatinine, range = 0.99-1.60, P = .01, IL-6: median = 2.00 micrograms/mg creatinine, range = 0.026-4.07 versus median = 0.04 micrograms/mg creatinine, range = 0.004-3.210, P = .0009, respectively). Patients with intra-amniotic infection had significantly elevated leukocyte counts, leukocyte esterase activity, Gram positive stains, and significantly lower amniotic fluid glucose levels compared with those without intra-amniotic infection. There were no differences in gestational age, maternal age, parity, race, pH, or specific gravity between the two groups. Amniotic fluid NOx was significantly correlated with IL-6 (r = .4, P = .02). Both amniotic fluid NOx and IL-6 were also positively correlated with amniotic fluid leukocyte counts, leukocyte esterase activity and Gram stains, and negatively correlated with glucose levels. CONCLUSIONS: Amniotic fluid NOx and IL-6 are significantly elevated and positively correlated during intra-amniotic infection. Both increased amniotic fluid IL-6 and nitric oxide may exert cytotoxic and cytostatic effects on the target cells. We suggest that measurements of amniotic fluid NOx and IL-6 may serve as useful clinical markers in patients with intra-amniotic infection.