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Airway Responsiveness to Adenosine 5′-Monophosphate and Exhaled Nitric Oxide Measurements. Part 11

By contrast, having airway hyperresponsiveness to both histamine (a direct bronchoconstric-tor) and mannitol was a clear predictor for failure of ICS reduction. In the present study, the responsiveness to a direct bronchoconstrictor agent was not determined, and so the relevance of this factor in our patients cannot be ascertained; however, the results of our study suggest that a decrease in PC20 of at least one doubling concentration 2 weeks after the dose of ICS was halved is a predictor of borderline significance for failure of ICS reduction.

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Airway Responsiveness to Adenosine 5′-Monophosphate and Exhaled Nitric Oxide Measurements. Part 10

It is important to point out that some aspects of the study design were chosen to closely emulate what might happen in the normal clinical setting when a reduction in the dose of ICS is attempted, including the single-blind design and the use of different ICS products and doses. One could argue that some patients may be prone to report more severe clinical manifestations because they were informed that the ICS dose was reduced. However, this effect would be independent of the response to inhaled AMP or ENO levels

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Airway Responsiveness to Adenosine 5′-Monophosphate and Exhaled Nitric Oxide Measurements. Part 9

At baseline, having both ENO levels of at least 15 ppb or 20 ppb and bronchoconstriction in response to AMP was a clear predictor for failure of ICS reduction, whereas having either AMP broncho-constriction or increased ENO levels alone was not a predictor. Furthermore, a doubling concentration decrease in PC20 2 weeks after the dose of ICS was halved seems to have some predictive value for failure in ICS reduction, whereas the increase in ENO levels did not have predictive value for exacerbations following ICS reduction.

In 27% (10

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Evolution of Pulmonary Injury Over Time

In severe acute pancreatitis, the early phase is associated with a systemic inflammatory response syndrome. One third of the deaths occurs during this early phase, and 50% of those deaths are associated with severe lung injury. The second phase of severe pancreatitis is closely related to the development of complications in the injured pancreas. These complications include fat necrosis, pseudocyst formation, and pancreatic abscess. Each of these complications can be related to the release of activated digestive enzymes. Release of

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Pleural effusions are often associated with acute pancreatitis

Pleural effusions are often associated with acute pancreatitis. In one study, 3 to 17% of patients with acute pancreatitis acquire pleural effusions. Most effusions were left sided, although some were bilateral. Pleural fluid amylase concentration was increased up to 30 times over the simultaneous serum value and remained elevated even after the serum concentrations had returned to a normal level. Large pleural effusions were associated with subdiaphragmatic collections of fluid. The immobility of the diaphragm induced by local inflammation seems

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Pancreatitis-Associated Acute Lung Injury

The ARDS is an important cause of mortality in critically ill patients. Its exact incidence is unknown but may be as high as 75 per 100,000 population in the United States. The risk factors for developing this syndrome include pneumonia, gastric aspiration, sepsis, shock, and multiple transfusions, as well as less common causes such as multiple trauma, multiple fractures, cardiopulmonary bypass, drug overuse, and acute pancreatitis. Although acute pancreatitis represents one of the less common clinical disorders associated with ARDS,

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The interaction with AT is mediated by a unique pentasaccharide sequence

LMWHs are polysulfated glycosaminoglycans that are about one third the molecular weight of UFH. LMWHs have a mean molecular weight of 4,000 to 5,000 d (about 15 monosaccharide units per molecule), with a range of

2,000 to 9,000 d. The various LMWHs approved for use in Europe, Canada, and the United States are shown in Table 6. Because LMWHs are prepared by different methods of depolymerization, they differ to some extent in pharmacokinetic properties and anticoagulant profiles, and are not clinically interchangeable.

The depolymerization of heparin yields low-molecular-weight

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Methods of Preparation for LMWHs and a Heparinoid

Therefore, a patient who bleeds immediately following an IV bolus of 5,000 U UFH will require the administration of 50 mg protamine. When UFH is given as an IV infusion, only heparin given during the preceding several hours needs to be included in this dose calculation, since the half-life of IV UFH is short (approximately 60 min). Therefore, a patient receiving a continuous IV infusion of 1,250 U per hour will require approximately 30 mg protamine. The neutralization of an SC dose of UFH may require a prolonged infusion

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All of the nonhemorrhagic limitations are caused by the AT-independent

All of the nonhemorrhagic limitations are caused by the AT-independent, charge-dependent binding properties of heparin to proteins and surfaces. Pharmacokinetic limitations are caused by the AT-independent binding of heparin to plasma proteins, to proteins released from platelets, and possibly to endothelial cells, which result in the variable anticoagulant response to heparin and to the phenomenon of heparin resistance; AT-independent binding to macrophages and endothelial cells also result in the dose-dependent mechanism of clearance.

The biophysical limitations occur because the hepa-rin/AT complex is unable to inactivate factor Xa in

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Although anti-IL-5 significantly reduced blood and sputum eosinophils

Although anti-IL-5 significantly reduced blood and sputum eosinophils, there was no effect on the immediate or late-phase reaction to inhaled antigen. Furthermore, there were no changes in AHR post allergen challenge; however, changes in AHR following the antigen challenge did not occur with placebo either. These studies indicate that although eosinophils parallel the development of the late-phase reaction to inhaled antigen, they do not appear causative of this event and may not contribute to an enhancement of AHR.

Further insight into how eosinophils participate in

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