Clinical practice. Diagnosis of diabetes.
N Engl J Med. 2012 Aug 9;367(6):542-50
Authors: Inzucchi SE
PMID: 22873534 [PubMed - in process]Link to Article at PubMed
Toward Safer Transitions: How Can We Reduce Post-Discharge Adverse Events?
Healthc Q. 2012 Apr;15(SP):63-67
Authors: Dhalla IA, O'Brien T, Ko F, Laupacis A
Ranjit Kaur is an 83-year-old woman who is brought to the hospital by her son because of worsening shortness of breath over the previous week. The emergency room physician correctly diagnoses a heart failure exacerbation (Wang et al. 2005), initiates appropriate treatment (Felker et al. 2011) and consults the hospitalist physician for admission and ongoing care (Wachter 2004).The hospitalist learns that the patient has been prescribed the various medications recommended by clinical practice guidelines and that her adherence to this medication regimen is excellent. No specific trigger for the heart failure exacerbation is found, and the hospitalist concludes that the most likely explanation is a gradual decline in cardiovascular function, perhaps combined with excessive sodium intake. The day after admission, a dietitian meets with the patient and her daughter-in-law to discuss how her diet could be modified to reduce her sodium intake. Three days after admission, Ms. Kaur is "back to baseline" and ready for discharge. The hospitalist discharges her on a slightly higher dose of her diuretic and instructs Ms. Kaur to see her family physician within a week of discharge. She is sent home with a discharge summary in hand that clearly explains the care provided in hospital and the follow-up plan. In other words, the emergency department and in-patient care are "textbook." The admission is brief and efficient, there are no complications and Ms. Kaur's symptoms are substantially improved. Nevertheless, three weeks after discharge, Ms. Kaur is brought back to the emergency department because of confusion. Her blood work in the emergency department shows a dangerously low sodium level. This adverse event may occur after a change in diuretic dose, and can be prevented or managed with careful follow-up after discharge.
PMID: 22874449 [PubMed - as supplied by publisher]Link to Article at PubMed
Lancet. 2012 Aug 3;
Authors: Maron BJ, Maron MS
Hypertrophic cardiomyopathy is a common inherited cardiovascular disease present in one in 500 of the general population. It is caused by more than 1400 mutations in 11 or more genes encoding proteins of the cardiac sarcomere. Although hypertrophic cardiomyopathy is the most frequent cause of sudden death in young people (including trained athletes), and can lead to functional disability from heart failure and stroke, the majority of affected individuals probably remain undiagnosed and many do not experience greatly reduced life expectancy or substantial symptoms. Clinical diagnosis is based on otherwise unexplained left-ventricular hypertrophy identified by echocardiography or cardiovascular MRI. While presenting with a heterogeneous clinical profile and complex pathophysiology, effective treatment strategies are available, including implantable defibrillators to prevent sudden death, drugs and surgical myectomy (or, alternatively, alcohol septal ablation) for relief of outflow obstruction and symptoms of heart failure, and pharmacological strategies (and possibly radiofrequency ablation) to control atrial fibrillation and prevent embolic stroke. A subgroup of patients with genetic mutations but without left-ventricular hypertrophy has emerged, with unresolved natural history. Now, after more than 50 years, hypertrophic cardiomyopathy has been transformed from a rare and largely untreatable disorder to a common genetic disease with management strategies that permit realistic aspirations for restored quality of life and advanced longevity.
PMID: 22874472 [PubMed - as supplied by publisher]Link to Article at PubMed
Activity of delafloxacin against methicillin-resistant Staphylococcus aureus: resistance selection and characterization.
J Antimicrob Chemother. 2012 Aug 8;
Authors: Remy JM, Tow-Keogh CA, McConnell TS, Dalton JM, Devito JA
OBJECTIVES: To determine the potential for delafloxacin to select for resistant mutants in methicillin-resistant Staphylococcus aureus (MRSA), including isolates with existing mutations in the quinolone resistance determining region (QRDR). METHODS: Susceptibility testing by broth microdilution was performed on 30 MRSA clinical isolates. For four of these isolates, the presence or absence of mutations in the QRDR was characterized. Resistance selection was performed on these four isolates by spreading cells on drug-containing agar plates followed by incubation for 48 h. Resistance frequencies and mutant prevention concentrations (MPCs) were calculated for each; PCR amplification and sequencing were performed using standard methods to characterize mutations in the QRDR. Growth rate analysis was performed and relative fitness was determined. RESULTS: Delafloxacin demonstrated potent in vitro activity against this set of MRSA isolates, with MICs of 0.008-1 mg/L and an MIC(50) and MIC(90) of 0.03 and 0.5 mg/L, respectively. Spontaneous delafloxacin resistance frequencies for the MRSA strains were 2?×?10(-9) to <9.5?×?10(-11). Delafloxacin MPCs were one to four times the MIC for any isolate, lower than those of comparator quinolones. Some delafloxacin-selected mutants showed a fitness cost when co-cultured with the parent strain. CONCLUSIONS: Delafloxacin demonstrates excellent antibacterial potency and exhibits a low probability for the selection of resistant mutants in MRSA. Although mutants can be selected at low frequencies in vitro from quinolone-resistant isolates, delafloxacin MICs and MPCs remain low and a fitness cost can be observed. Consequently delafloxacin warrants further investigation for the potential treatment of drug-resistant MRSA infections.
PMID: 22875850 [PubMed - as supplied by publisher]Link to Article at PubMed