MGB1 Poor Adherence to Hypertension Treatment Guidelines: An Analysis of Therapeutic Choices

The recent Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC) reiterated long-standing recommendations that Stage 1 hypertension (BP ≥ 140/90 mm Hg) without comorbidity should be treated initially with diuretics (DI) or beta blockers (BB). Yet market research suggests that many physicians prefer to use other drug classes, such as calcium channel blockers and ACE inhibitors.
OBJECTIVES: To explore the determinants of therapeutic choice in hypertension.
METHODS: We surveyed by mail a stratified random sample of 10,000 U.S. cardiologists, internists, and family/general practitioners. Physicians were queried about their practice environment and their knowledge, attitudes, and practices regarding antihypertensive therapy, including their choice of drugs to treat patients with specified clinical profiles. The probability that physicians would follow JNC guidelines Stage 1 hypertension was analyzed using multiple logistic regression with stepwise backward elimination to select variable with p < 0.001.
RESULTS: Completed surveys were received from 1,023 physicians. 86.7% prescribe drug therapy for Stage 1 hypertension, and 19.5% (22.5% of drug prescribers) limit their choices to DI and BB. Guideline conformity was higher among physicians who: practice in academic medical centrers; are older; are general practitioners (versus general internists); have smaller caseloads; have fewer hypertensive patients; have higher proportions of HMO, Medicaid, and uninsured patients; and experience more formulary restrictions. Cardiologists and family practitioners were less likely than internists to follow guidelines.
CONCLUSION: JNC guidelines are better accepted by academic physicians, older physicians who have more expenence using DI and BB, physicians with smaller caseloads and hence more time for follow-up and therapy adjustment, and physicians who face drug reimbursement constraints.     

闭合性输尿管损伤的早期诊断

０　引言　腹部钝性伤所致闭合性输尿管损伤罕见,且早期缺乏典型症状,往往延误诊断［１］,造成严重后果．我们采用电视屏幕动态观察下大剂量静脉肾盂造影或逆行造影的方法,早期诊断闭合性输尿管损伤,取得较满意效果．１　临床资料　本组男性５例,女性１例,年龄３岁～３６岁,右侧４例,左侧２例．２例合并肾损伤,１例合并骨盆骨折,右骶髂关节分离,尿道损伤．４例为撞伤、压伤,２例坠落伤．６例均无典型输尿管损伤症状．４例在电视屏幕动态观察下行大剂量静脉肾盂造影,其中１例同时在电视屏幕动态观察下行逆行造影．本组６例,早…     

New agents for treatment of advanced transitional cell carcinoma

The prognosis for any patient with progressive or recurrentinvasive transitional cell carcinoma remains poor. In this context,the focus of clinical research in these invasive cancers concentrateson identifying systemic treatment options and new agents inorder to improve survival of patients. Cisplatin-based chemotherapyis standard treatment of patients with metastatic urothelialcancer; however, despite regimens as the cisplatin–gemcitabinecombination, the overall response rates vary between 40% and65%, with complete response in 15%–25% with survivalsup to 16 months. This survival is frequently achieved with severeand life-threatening side effects. None the less, almost allresponding patients relapse within the first year; therefore,the need for development of new and tolerable agents is urgent.This review highlights some new active chemotherapeutic as newplatinum compounds (oxaliplatin, lobaplatin), gallium nitrate,ifosfamide, the antifolates piritrexim and pemetrexed (Alimta®,LY231514), vinflunine and molecular targeting agents such asfarnesyltransferase inhibitors (lonafarnib, R115777, SCH66336),ribozyme (RPI.4610), histone deacetylase inhibitor (CI-994)and monoclonal antibodies (epidermal growth factor receptor,Her 2/neu). Key words: transitional cell carcinoma, gallium nitrate, vinflunine, platinum compounds, antifolates, molecular targeting agents Received for publication February 8, 2006. Revision received August 4, 2006. Accepted for publication August 10, 2006.     

Activated human monocytes inhibit the intracellular multiplication of legionnaires’ disease bacteria

We have examined the interaction between virulent egg yolk-grown L. pneumophila, Philadelphia 1 strain, and in vitro-activated human monocytes, under antibiotic-free conditions. Freshly explanted human monocytes activated by incubation with concanavalin A (Con A) and human lymphocytes inhibited the intracellular multiplication of L. pneumophila. Both Con A and lymphocytes were required for activation. Con A was consistently maximally effective at greater than or equal to 4 μg/ml. Monocytes activated by incubation with cell-free filtered supernatant from Con A-sensitized mononuclear cell cultures also inhibited the intracellular multiplication of L. pneumophil a. The most potent supernatant was obtained from mononuclear cell cultures incubated with greater than or equal to 15 μg/ml Con A for 48 h. The degree of monocyte inhibition of L. pneumophila multiplication was proportional to the length of time monocytes were preincubated with supernatant (48 {greater than} 24 {greater than} 12 h) and to the concentration of supernatant added (40 percent {greater than} 20 percent {greater than} 10 percent {greater than} 5 percent). Monocytes treated with supernatant daily were more inhibitory than monocytes treated initially only. With time in culture, monocytes progressively lost a limited degree of spontaneous inhibitory capacity and also lost their capacity to respond to supernatant with inhibition of L. pneumophila multiplication. Supernatant-activated monocytes inhibited L. pneumophila multiplication in two ways. They phagocytosed fewer bacteria, and they slowed the rate of intracellular multiplication of bacteria that were internalized. As was the case with nonactivated monocytes, antibody had no effect on the rate of intracellular multiplication in supernatant-activated monocytes. Neither supernatant-activated nor nonactivated monocytes killed L. pneumophila in the absence of antibody. Both killed a limited proportion of these bacteria in the presence of antibody and complement. We have previously reported that anti-L, pneumophila antibody and complement neither promote effective killing of L. pneumophila by human polymorphonuclear leukocytes and monocytes nor inhibit the rate of L. pneumophila multiplication in monocytes. These findings and our present report that activated monocytes do inhibit L. pneumophila multiplication indicate that cell-mediated immunity plays a major role in host defense against Legionnaires’ disease.