Citations

Retail medicine clinics have become widely available. However, few studies have been published that compare retail clinic costs of care to standard medical visits for similar patients. The purpose of this study was to compare standard medical costs during a 6-month period after visiting a retail medical clinic to care received in a conventional medical office setting. Medical records of primary care patients (both adults and children) seen in a large group practice in Minnesota in 2008 were analyzed for this study. Two groups of patients were studied: those who used a retail walk-in clinic (N = 141) and a comparison group who used regular office care for same-day, acute visits (N = 137). Patients treated for 5 common conditions (pink eye, sore throat, viral illness, bronchitis, and cough) were selected. The dependent variables were standard costs using federal rates and the rank of standard costs. Multiple linear regression analysis was used to adjust for differences between groups. Median costs did not differ between sites ($126.30 for usual care and $88.10 for retail, P = 0.139); mean cost ranks were 132.5 for usual care and 115.6 for retail ( P = 0.088). After adjusting for previous visit history, age, and sex, patients who received care in the retail setting had lower standard costs and lower cost rank than patients who received usual care (b = −52.9 [ P = 0.006] and b = −24.5 [ P = 0.021], respectively). After selection of cases with common conditions and adjustment for unequal variances, age, sex, and number of office visits in the previous 6 months, our retail clinic appeared to reduce medical costs for patients during the 6-month period after the index visit. ( Population Health Management 2009;12:333–335)

AbstractCertain malignant B cells rely on B-cell receptor (BCR)–mediated survival signals. Spleen tyrosine kinase (Syk) initiates and amplifies the BCR signal. In in vivo analyses of B-cell lymphoma cell lines and primary tumors, Syk inhibition induces apoptosis. These data prompted a phase 1/2 clinical trial of fostamatinib disodium, the first clinically available oral Syk inhibitor, in patients with recurrent B-cell non-Hodgkin lymphoma (B-NHL). Dose-limiting toxicity in the phase 1 portion was neutropenia, diarrhea, and thrombocytopenia, and 200 mg twice daily was chosen for phase 2 testing. Sixty-eight patients with recurrent B-NHL were then enrolled in 3 cohorts: (1) diffuse large B-cell lymphoma (DLBCL), (2) follicular lymphoma (FL), and (3) other NHL, including mantle cell lymphoma (MCL), marginal zone lymphoma (MZL), mucosa-associated lymphoid tissue lymphoma, lymphoplasmacytic lymphomas, and small lymphocytic leukemia/chronic lymphocytic leukemia (SLL/CLL). Common toxicities included diarrhea, fatigue, cytopenias, hypertension, and nausea. Objective response rates were 22% (5 of 23) for DLBCL, 10% (2 of 21) for FL, 55% (6 of 11) for SLL/CLL, and 11% (1/9) for MCL. Median progression-free survival was 4.2 months. Disrupting BCR-induced signaling by inhibiting Syk represents a novel and active therapeutic approach for NHL and SLL/CLL. This trial was registered at www.clinicaltrials.gov as #NCT00446095.

PurposeThe purpose of this systematic review was to examine the current evidence for the use of oral motor exercises (OMEs) on speech (i.e., speech physiology, speech production, and functional speech outcomes) as a means of supporting further research and clinicians' use of evidence-based practice.MethodThe peer-reviewed literature from 1960 to 2007 was searched for articles examining the use of OMEs to affect speech physiology, production, or functional outcomes (i.e., intelligibility). Articles that met selection criteria were appraised by 2 reviewers and vetted by a 3rd for methodological quality, then characterized as efficacy or exploratory studies.ResultsFifteen studies met inclusion criteria; of these, 8 included data relevant to the effects of OMEs on speech physiology, 8 on speech production, and 8 on functional speech outcomes. Considerable variation was noted in the participants, interventions, and treatment schedules. The critical appraisals identified significant weaknesses in almost all studies.ConclusionsInsufficient evidence to support or refute the use of OMEs to produce effects on speech was found in the research literature. Discussion is largely confined to a consideration of the need for more well-designed studies using well-described participant groups and alternative bases for evidence-based practice.

Background and Purpose— Previous studies of multiple-day dosing with the defibrinogenating agent, ancrod, in acute ischemic stroke yielded conflicting results but suggested that a brief dosing regimen might improve efficacy and safety. The Ancrod Stroke Program was designed to test this concept in subjects beginning ancrod or placebo within 6 hours of the onset of acute ischemic stroke. Methods— Five hundred subjects with acute ischemic stroke who could begin receiving study material within 6 hours of symptom onset were infused intravenously with either ancrod (0.167 IU/kg per hour) or placebo over 2 or 3 hours. The primary efficacy outcome was a dichotomized, modified Rankin score at 90 days with less stringent cut-points for higher prestroke modified Rankin score and pretreatment NIHSS total score (“responder analysis”). Safety variables included mortality, major bleeding, and intracranial hemorrhage. Results— Although the desired changes in fibrinogen level were seen in >90% of ancrod subjects, interim analysis for futility led to the study being halted for lack of efficacy. Positive responder status in the interim dataset was seen in 39.6% of ancrod subjects and 37.2% of placebo subjects ( P =0.47). Ninety-day mortality did not differ between the 2 groups (ancrod, 15.6%; placebo, 14.1%; P =0.32), and the incidence of symptomatic intracranial hemorrhage within the first 72 hours, although not significantly different in ancrod compared to placebo subjects ( P =0.19), was approximately twice as high (3.9% vs 2.0%; P =0.19). Conclusion— These results demonstrate that intravenous ancrod starting within 6 hours after symptom onset in a broad selection of subjects with ischemic stroke did not improve their outcome and revealed a trend to increased bleeding despite successful efforts to achieve rapid initial defibrinogenation and avoid prolonged hypofibrinogenemia.

Peripheral arterial disease (PAD) is common in patients with severe coronary artery disease (CAD) and is considered a relative contraindication to external enhanced counterpulsation (EECP), but there are no data that define the efficacy and safety of EECP in patients with PAD. The International EECP Patient Registry (IEPR) was used to compare initial post-therapy and 2-year follow-up clinical outcomes and adverse event rates in patients with and without PAD. From January 2002 to October 2004, 2126 patients were enrolled in the IEPR, of whom 493 (23%) had a history of PAD. Immediately following EECP, the reduction in angina (≥ 1 Canadian Cardiovascular Society class) was similar in patients with and without PAD (76.6% vs 79.0%, p = 0.27) as was improvement in the Duke Activity Score Index (DASI) score (+4.7% vs +6.1%, p < 0.001). Both angina reduction and DASI score improvement were sustained at 2 years. PAD patients discontinued EECP more frequently (12.0% vs 8.5%, p < 0.05), but lower extremity ulceration did not occur more frequently in patients with PAD (3.7% vs 2.7%, p = 0.26). Rates of death (17.1% vs 8.6%, p < 0.001) and myocardial infarction (9.5% vs 5.0%, p < 0.001) were, as expected, higher in patients with PAD compared to patients without PAD at 2 years. In conclusion, while PAD patients constitute a high-risk cohort with known higher adverse event rates, EECP led to similar short- and long-term improvements in angina and quality of life for individuals with PAD compared to those without PAD.