Understanding and use of inhaler medication by asthmatics in specialty care in Trinidad: a study following development of Caribbean guidelines for asthma management and prevention

STUDY OBJECTIVES: Following the development of the Caribbean Guidelines for Asthma Care, we examined the utilization of inhaled medications in asthmatic patients in Trinidad, West Indies. SETTING: Chest Clinic, Ministry of Health, Trinidad. PARTICIPANTS: Physician-diagnosed asthmatic patients who attended the Chest Clinic between July 1998 and August 2000. MEASUREMENTS AND RESULTS: A consecutive sample of patients who were > 7 years of age (n = 402) was interviewed about compliance with, understanding of, and use of inhaler medication. The inhaler technique of these patients was directly observed. Inhaled steroid therapy was prescribed in 83% of patients but were prescribed the least in elderly patients (63%) and children (62%). Salbutamol was prescribed in 98% of patients, and ipratropium and sodium cromoglycate were selectively prescribed in elderly men and children, respectively. Only 33% of patients used the inhaler correctly, and children and the elderly were the least efficient in its use. The use of a spacer device was advised in 19% of patients, including only 6% of the elderly patients. Explanations for different inhaler therapies were given to 62% of patients, and 53% of patients could describe these reasons. The reported 40% noncompliance rate among patients in the sample was primarily a result of long waiting periods at the pharmacy (58%) and the personal cost incurred on purchasing the medication (52%). CONCLUSIONS: Educating patients, with a focus on children and the elderly, in inhaler techniques and reinforcing understanding of asthma medications can improve asthma management in Trinidad. Asthma caregivers in the Caribbean should ensure the appropriate dissemination of the guidelines and should outline strategies for their implementation.     

Cardiopulmonary Resuscitation Feedback: A Comparison of Device-Measured and Self-Assessed Chest Compression Quality

BackgroundHigh-quality cardiopulmonary resuscitation is the foundation of cardiac arrest care. Guidelines specify chest compression depth, recoil, and rate, but providers often fail to achieve these targets. Furthermore, providers are largely unable assess the quality of their own or other peoples’ chest compressions. Chest compression feedback devices can improve chest compression quality; their use is endorsed internationally, but they remain largely absent in clinical care.This article analyzes preclinical data collected during a quality improvement project. It describes provider demographics and perceptions about their chest compression quality and correlates them to measured chest compression quality, compares clinician perception of chest compressions to objective measures, and describes the effect of feedback on compression quality.MethodsClinicians were recruited from 2 metropolitan emergency departments. A questionnaire was used to assess participants’ levels of training and experience. A before-and-after assessment of chest compression quality was performed using a Laerdal CPRmeter 2 and a CPR mannequin. Pretest measures of chest compression quality were made by covering the device screen thereby blinding providers to feedback; repeat measures were then collected from the same participants but unblinded to feedback. Provider charecteristic were collected by survey. Correlations between blinded chest compression quality and provider charecteristics; the reliability of providers estimated compared to measured quality; and the effects of feedback on chest compression quality were assessed using Pearsons correlations, Cohens κ, and paired t testing.Results84 participants were assessed. The mean years of certification were 11.74. Ninty-five percent of the providers self-assessed as more experienced than novice and 81% reported performing cardiopulmonary resuscitation at least occasionally. The frequency of performing chest compressions was correlated with self-assessed skill (r = 0.58, P < .001). However, self-assessed skill was only weakly correlated with chest compression quality (r = 0.29, P = .01) and not at all with the frequency of performing chest compressions or years of certification. There was no agreement between self-assessed and device-measured chest compression depth (κ = ?0.10, P = 0.11), recoil (κ = ?0.14, P = .03), or rate (κ = 0.06, P =.30). The overall quality of compressions improved by 16.9%; the percentage of chest compressions achieving target depth by 3.58%; recoil by 22.82%; and rate by 23.66% with feedback. A total of 97.6% of the staff rated chest compression feedback helpful.ConclusionsOur findings suggest that participants’ demographics were not correlated with chest compression quality and that providers cannot reliably assess chest compression quality. The data also demonstrate that with minimal training, feedback can significantly improve chest compression quality.     

Prostaglandin E2 potentiates platelet aggregation by priming protein kinase C

Prostaglandin E2 (PGE2) is produced by activated platelets and by several other cells, including capillary endothelial cells. PGE2 exerts a dual effect on platelet aggregation: inhibitory, at high, supraphysiologic concentrations, and potentiating, at low concentrations. No information exists on the biochemical mechanisms through which PGE2 exerts its proaggregatory effect on human platelets. We have evaluated the activity of PGE2 on human platelets and have analyzed the second messenger pathways involved. PGE2 (5 to 500 nmol/L) significantly enhanced aggregation induced by subthreshold concentrations of U46619, thrombin, adenosine diphosphate (ADP), and phorbol 12-myristate 13-acetate (PMA) without simultaneously increasing calcium transients. At a high concentration (50 mumol/L), PGE2 inhibited both aggregation and calcium movements. PGE2 (5 to 500 nmol/L) significantly enhanced secretion of beta-thromboglobulin (beta TG) and adenosine triphosphate from U46619- and ADP-stimulated platelets, but it did not affect platelet shape change. PGE2 also increased the binding of radiolabeled fibrinogen to the platelet surface and increased the phosphorylation of the 47-kD protein in 32P- labeled platelets stimulated with subthreshold doses of U46619. Finally, the amplification of U46619-induced aggregation by PGE2 (500 nmol/L) was abolished by four different protein kinase C (PKC) inhibitors (calphostin C, staurosporine, H7, and TMB8). Our results suggest that PGE2 exerts its facilitating activity on agonist-induced platelet activation by priming PKC to activation by other agonists. PGE2 potentiates platelet activation at concentrations produced by activated platelets and may thus be of pathophysiologic relevance.     

Autologous bone marrow transplantation in acute myelogenous leukemia: in vitro treatment with myeloid cell-specific monoclonal antibodies

Second or third chemotherapy-induced remissions in acute myelogenous leukemia (AML) are limited by early relapse of the leukemia. We developed monoclonal antibodies (MoAbs) that are cytotoxic to myeloid leukemia cells to treat bone marrow from these patients ex vivo for autologous transplantation. In this pilot study, bone marrow was harvested from ten patients with AML in remission, treated with one or two complement-fixing MoAbs, PM-81 and AML-2-23, which react with myeloid differentiation antigens, incubated with rabbit complement, and cryopreserved. These MoAbs were chosen because they have broad reactivity with AML cells but not with pluripotent progenitor cells. At the time of transplant, 6 patients were in second complete remission, 1 each was in third complete or partial remission, and 2 were in early first relapse. The patients were treated with cyclophosphamide (60 mg/kg a day for 2 days) and total body irradiation (200 cGy twice a day for 3 days) and given infusions of MoAb-treated bone marrow. Full bone marrow reconstitution was observed in eight patients; two patients did not recover platelets. Seven of the ten patients are surviving and disease-free at 21.0, 15.0, 13.0, 10.0, 6.0, 3.0, and 2.0 months posttransplant. Treating bone marrow with MoAbs to myeloid differentiation antigens does not interfere with pluripotential stem cell engraftment. Longer follow-up and a controlled study are necessary to prove that the apparent efficacy of this therapeutic approach in some patients is attributable to MoAb-mediated killing of leukemia cells.     

General and specific brain regions involved in encoding and retrieval of events: what, where, and when.

Remembering an event involves not only what happened, but also where and when it occurred. We measured regional cerebral blood flow by positron emission tomography during initial encoding and subsequent retrieval of item, location, and time information. Multivariate image analysis showed that left frontal brain regions were always activated during encoding, and right superior frontal regions were always activated at retrieval. Pairwise image subtraction analyses revealed information-specific activations at (i) encoding, item information in left hippocampal, location information in right parietal, and time information in left fusiform regions; and (ii) retrieval, item in right inferior frontal and temporal, location in left frontal, and time in anterior cingulate cortices. These results point to the existence of general encoding and retrieval networks of episodic memory whose operations are augmented by unique brain areas recruited for processing specific aspects of remembered events.     

A Mediterranean-style, low-glycemic-load diet decreases atherogenic lipoproteins and reduces lipoprotein (a) and oxidized low-density lipoprotein in women with metabolic syndrome

The objective was to assess the impact of a Mediterranean-style, low-glycemic-load diet (control group, n = 41) and the same diet plus a medical food (MF) containing phytosterols, soy protein, and extracts from hops and Acacia (MF group, n = 42) on lipoprotein atherogenicity in women with metabolic syndrome. Plasma lipids, apolipoproteins (apos), lipoprotein subfractions and particle size, low-density lipoprotein (LDL) oxidation, and lipoprotein (a) were measured at baseline, week 8, and week 12 of the intervention. Three-day dietary records were collected at the same time points to assess compliance. Compared with baseline, women decreased energy intake from carbohydrate (P < .001) and fat (P < .001), whereas they increased energy intake from protein (P < .001). A significant increase in energy from monounsaturated fatty acids was also observed as well as increases in eicosapentaenoic acid and docosahexaenoic acid, whereas trans-fatty acid intake was reduced (P < .00001). The atherogenic lipoproteins, large very low-density lipoprotein (P < .0001) and small LDL (P < .0001), were reduced, whereas the ratio of large high-density lipoprotein to smaller high-density lipoprotein particles was increased (P < .0001). Apolipoprotein B was reduced for all women (P < .0001), with a greater reduction in the MF group (P < .025). Oxidized LDL (P < .05) and lipoprotein (a) (P < .001) were reduced in both groups at the end of the intervention. Consumption of a Mediterranean-style diet reduces the risk for cardiovascular disease by decreasing atherogenic lipoproteins, oxidized LDL, and apo B. Inclusion of an MF may have an additional effect in reducing apo B.     

Inhibition of Porphyromonas gingivalis‐induced periodontal bone loss by CXCR4 antagonist treatment

Microbial pathogens have evolved mechanisms to proactively manipulate innate immunity, thereby improving their fitness in mammalian hosts. We have previously shown that Porphyromonas gingivalis exploits CXC‐chemokine receptor‐4 (CXCR4) to instigate a subversive crosstalk with Toll‐like receptor 2 that inhibits leukocyte killing of this periodontal pathogen. However, whether CXCR4 plays a role in periodontal disease pathogenesis has not been previously addressed. Here, we hypothesized that CXCR4 is required for P. gingivalis virulence in the periodontium and that treatment with AMD3100, a potent CXCR4 antagonist, would inhibit P. gingivalis‐induced periodontitis. Indeed, mice given AMD3100 via osmotic minipumps became resistant to induction of periodontal bone loss following oral inoculation with P. gingivalis. AMD3100 appeared to act in an antimicrobial manner, because mice treated with AMD3100 were protected against P. gingivalis colonization and the associated elevation of the total microbiota counts in the periodontal tissue. Moreover, even when administered 2 weeks after infection, AMD3100 halted the progression of P. gingivalis‐induced periodontal bone loss. Therefore, AMD3100 can act in both preventive and therapeutic ways and CXCR4 antagonism could be a promising novel approach to treat human periodontitis.