Procalcitonin as a diagnostic marker in acute exacerbation of COPD

Rational prescription of antibiotics in acute exacerbations of COPD [AECOPD] requires predictive markers. Acute phase reactants are capable of demonstrating the inflammation; however, they cannot be employed to make a difference between bacterial and nonbacterial causes of the inflammation. Recently, measurement of procalcitonin [PCT] levels appears to be useful in order to minimize this problem. We aimed to evaluate the diagnostic and prognostic role of procalcitonin in [AECOPD]. A total of 50 patients with AECOPD and 10 of apparently healthy individuals [control group] were studied. On presentation, serum PCT concentrations were measured, and quantitative sputum culture was performed for AECOPD. The patients were reevaluated when they had returned to their stable clinical state. Pathogenic bacterial microorganism [PBM] was only regarded as significant if they reached a growth 105CFU/ml, indicating the presence of bacterial exacerbation of COPD. The patients were classified into two subgroups: group A included patients with bacterial AECOPD [n = 20], group B included patients with nonbacterial AECOPD [n = 30]. On presentation, the levels of PCT for patients of group A [2.69 +/- 0.62 ng/mL] were significantly higher than group B [0.07 +/- 0.02 ng/mL] and control group [0.05 +/- 0.02 ng/mL] [p < 0.001]. When they had returned to their stable state, the levels of PCT for patients of group A decreased to [0.06 +/- 0.03 ng/mL], which was significantly lower than that in exacerbation [2.69 +/- 0.62 ng/mL] [p < 0.001]; But in patients of group B compared with exacerbation the levels of PCT did not changed [0.068 +/- 0.02 ng/mL] [p > 0.05]. In the stable state, there were no differences in the PCT measurement between the two subgroups as well as between patients and control. Furthermore, a significant correlation was recorded between PCT levels in group A at time of presentation and temperature [r = 0.898, p < 0.05], leucocytic count [r = 0.889, p < 0.05], FEV1% of predicted [r = 0.898, p < 0.05], ESR [r = 0.899, p < 0.05], CRP [r = 0.895, p < 0.05] and duration of hospital stay [r = 0.897, p < 0.05]. Procalcitonin is a good marker for differentiation between bacterial and nonbacterial AECOPD and could be used to guide antibiotic therapy and reduce antibiotic overuse in hospitalized patients with AECOPD

Insulin resistance and its fibrogenic effect in chronic hepatitis C virus patients: role of tumor necrosis factor alpha activation

Insulin resistance [IR] is one of the extrahepatic complications that occur in chronic hepatitis C virus infection [HCV], and is claimed as one of the fibrogenic factors which cause more rapid fibrosis progression. We examined the effect of HCV infection on insulin resistance states, and the possible link between IR, tumor necrosis factor-alpha [TNF-alpha] activation and development of hepatic fibrosis. Thirty patients with chronic hepatitis C infection divided into 2 groups according to presence or absence of fibrosis, 15 apparently healthy volunteer and 15 patients with hepatic fibrosis due to causes other than HCV were studied. Laboratory assessment of liver functions, fasting glucose, insulin levels, homeostasis model assessment of insulin resistance [HOMA-IR] and soluble tumor necrosis factor receptors 2 [sTNFR2] were done. HOMA-IR and sTNFR2 levels were significantly increased in patients with chronic HCV without fibrosis as compared with healthy control [p<0.01, p<0.001, respectively], and in patients with HCV induced fibrosis compared to HCV patients without fibrosis [p<0.001], and non HCV fibrosis [p<0.001, p< 0.05, respectively]. HOMA-IR was significantly correlated with sTNFR2 and fibrosis stage [p< 0.001]. IR was associated with increased risk of developing hepatic fibrosis in chronic HCV infection [OR 8.0, 95% CI 1.5-42]. Insulin resistance can be induced by chronic HCV infection per se and is correlated to fibrosis stages. Its fibrogenic role may be mediated by TNF-alpha activation

Spectroscopic studies of some ethylene oxides

Z- and E-1,2-di-[4-nitrophenyl]-1-phenyl-ethylene oxides I and II were prepared by the reaction of 4-nitrodiphenylmethyl chloride with 4-nitrobenzaldehyde in the presence of alkali in aqueous dioxane at room temperature. 1,1-di-[4-nitrophenyl] ethylene oxide III was also prepared by reacting 4,4'-dinitrodiphenylmethyl chloride with paraformaldehyde under similar conditions. The structures of these new ethylene oxides I, II and III were confirmed by IR and PMR spectra, and their mass fragmentation patterns were discussed

Substitution and elimination reactions Reaction of methyl 2,3 -dibromo-3- [P-substituted phenyl] propanoates with piperidine

The reaction of erythro-methyl 2,3-dibromo-3-[p-substituted phenyl] propanoates 1a-d with 4 molar equivalent of piperidine in methanol gave a mixture of erythro and threo-methyl 2,3-bis-piperidino-3-[p- substituted phenyl] propanoates 2a-d. The identification of the configuration of the products 2a-d was based on 1H-NMR spectra. The mechanism of the reaction is discussed

Nucleophilic ring opening of some epoxy ketones

The reaction rates of some trans P-substituted epoxybenzalacetopheaones 1[a-h] with thiophenolate and p-nitrothiophenolate have been measured at different temperatures. The reaction is unidirectional and gives W - thioaryloxy-p-substituted acetophenones and p-substituted benzaldehyde. Effect of the substituents has been analysed in terms of Hammett linear free energy relationship. The values of P and activation parameters delta Hz number sign and delta S number sign are in accordance with the proposed bimolecular S[N][2]mechanism

Synthesis, and spectral studies of some 2-halo-3-arylpropionic acid and their ester

erythro-Methyl-2,3-dibromo-3-arylpropanoates were converted to the corresponding E- and Z-2-bromo-3-arylpropenoic 1 by alcoholic pottassium hydroxide. Esterification of both isomeric acids with methanol-sulphuric acid gave Z-methyl esters 2. The assignment of the configuration was based on spectral studies

Stereochemistry of the reaction of 2,3-dibromo-ketones with phenoxide ion in DMF

The reaction of a series of erythro-2,3-dibromo-1,3-arylpropanones l[a-K] with sodium phenoxide in dimethyl-formamide [DMF] was investigated. 3-Phenoxy-l,3-diaryl-propenones 2[a-k] were obtained as a mixture of E- and Z/isomer and their configuration were established by spectral studies. A stepwise mechanism is postulated for this reaction proceeds via an intermediate carbanions

Reaction kinetics of trans-1,3-diarylpropenones with sodium thiopenoxide in ethanol

The reaction of some p-substituted trans-1,3-diarylpropenones 1a-k with sodium thiophenoxide was studied. The structure of the products was determined and the reaction kinetics were measured. The effect of substituents was analyzed in terms of Hammett free energy relationship. A suggested reaction mechanism was also proposed

New aspect of epoxide ring opening

The rates of reactions of some trans-P-substituted epoxy benzalacetophenones with morpholine in acetonitrile have been measured at different temperatures. The reactions are second order and proceeds via SN2 like mechanism to give the corresponding alpha- hydroxy-beta-morpholino-beta-[P-substituted phenyl propiophenones. Effect of substituents has been analyzed in terms of Hammett linear free energy relationship

Kinetics of aminolysis of some antibacterial vinylic ketones II Effect of solvents on aminolysis of trans -3- [p-substituted phenyl] -1- phenyl- prop -2-en -1-one

The reactions of a series of trans-3-[p-substituted phenyl]-1-phenyl- prop-2-en-1-ones Ia-e with p-toluidine and p-nitroaniline IIa, b have been studied in benzene, and their reaction rates were measured. In addition, activation parameters delta H* and delta S* were evaluated, and good Hammett correlation with positive P values of 1.2-1.9, were obtained which suggest the anionic character of the transition state