"Are You Talking to Me?" Confronting Behavioral Disturbances in Patients With Headache

The famous question, "Are you talking to me?," was coined by Robert DeNiro in his lead role as Travis Bickle in the Martin Scorsese classic, Taxi Driver . The phrase also characterizes the troubling encounters that many headache-treating professionals confront as they attempt to discuss serious matters of care and compliance with some of their headache patients. Although most headache patients are eager to take professional advice and guidance, there exists a minority of patients whose behavior undermines a collaborative relationship between doctor and patient. In these cases, the physician may need to directly confront this behavior in order to overcome behavioral barriers that interfere with desirable treatment outcomes. This article offers explicit means and strategies to engage difficult patients, increase the likelihood of program adherence and improvement, and develop a more satisfying doctor-patient relationship, based on clinical experience in a national referral center for difficult-to-manage headache patients.     

How do genes exert their role? Period 3 gene variants and possible influences on mood disorder phenotypes

The action of multiple liability genes is responsible for complex phenotypes at the same time, a single gene, could control several phenotypic features. This is the case of human period 3 gene (hper3), mainly involved in the setting of the biologic clock. Some variants of this gene, besides being associated with the Delayed Sleep Phase Syndrome, showed a key role in determining evening preference rather than morning one. According to this rationale, we hypothesized that this gene could influence circadian mood fluctuations, in mood disorders. Our study demonstrated that rare genetic variants of hper3 are significantly associated to a number of mood disorders features, such as age of onset, response to SSRIs treatment, circadian mood oscillations and characteristics of temperament. These preliminary results could shed further light on the involvement of circadian genes in various aspects of physiological and psychopathological mechanisms of the brain.     

What role does gemtuzumab ozogamicin have in the treatment of acute myelogenous leukemia?

Gemtuzumab ozogamicin (GO) is a novel, targeted chemotherapy designed to treat acute myeloid leukemia (AML). GO consists of an antitumor antibiotic, calicheamicin, linked to a humanized monoclonal antibody against CD33. It has been approved in the United States since 2000 to treat CD33+ AML in first relapse in older adults who are not candidates for cytotoxic therapy. Beyond this indication, the role of GO is evolving. Single-agent GO has a limited role in de novo AML. Incorporation of GO into standard induction treatment in de novo and relapsed AML is feasible. Comparative phase III studies of such an approach are ongoing. GO is associated with serious toxicities, such as infusional reactions, transient liver function test abnormalities, and veno-occlusive disease of the liver, especially in patients who undergo hematopoietic stem cell transplantation.     

Safety and effect of transforming growth factor-β2 for treatment of venous stasis ulcers

Transforming growth factor-beta(2) promotes healing in a variety of animal models and exhibits clinical effects thought to be mediated by connective tissue formation. Two clinical trials were conducted to evaluate the safety and effect of transforming growth factor-beta(2) purified from bovine bone and delivered topically to venous stasis ulcers three times per week for up to 6 weeks by means of a lyophilized collagen vehicle. The first was an open-label trial comparing transforming growth factor-beta(2) purified from bovine bone (0.5 microg/cm(2)) with a placebo consisting of lyophilized collagen vehicle-without active drug. After no safety issues arose in that trial, a prospectively randomized, closed-label, observer-blinded, three-armed trial was conducted to compare bovine transforming growth factor-beta(2) (2.5 microg/cm(2)) with the collagen matrix placebo vehicle and with a standard dressing. Standardized elastic compression was applied to all test extremities. The rate of reduction of ulcer area as measured by planimetry was the primary measure of effect. No serious safety-related events occurred in either trial. Clinical evaluation suggested that improvement in the quality and quantity of granulation tissue appeared to precede epithelialization of ulcers treated with bovine transforming growth factor-beta(2). In both studies, treatment with bovine transforming growth factor-beta(2) appeared to have a positive effect on the rate of ulcer closure, whereas ulcers in the control groups continued to exhibit impaired healing. In the open-label study, the mean rate of closure of ulcers treated with bovine transforming growth factor-beta(2) was significantly greater than that of ulcers treated with placebo. There was likewise enhanced reduction in ulcer area in the ulcers treated with bovine transforming growth factor-beta(2) in the second trial. However, because of a higher variability in patient response and a greater placebo effect, the difference was not significant. The placebo was not worse than the standard care arm, thereby showing that the vehicle is not injurious to healing. The combined results of the two trials suggest that, at doses of 0.5 to 2.5 microg/cm(2), bovine transforming growth factor-beta(2) is safe as a topically applied agent in a collagen matrix vehicle and can have a positive effect on closure of venous stasis ulcers. Large multicenter trials appear to be indicated to evaluate fully the potential utility of transforming growth factor-beta(2) in accelerating closure of chronic dermal ulcers.     

Asymptomatic metachronous metastatic renal cell adenocarcinoma to the gallbladder

Summary A case of asymptomatic metachronous metastatic unilateral renal cell adenocarcinoma to the gallbladder detected five years after resection of the primary renal neoplasm is reported here. The lesion was diagnosed by contrast enhancement of a gallbladder mass on abdominal computerized tomography scan and by color Doppler sonographic study of the gallbladder, both of which demonstrated the vascular supply to the intraluminal gallbladder mass. The biological behavior of renal cell adenocarcinoma is reviewed. Guidelines for the evaluation of intraluminal gallbladder masses are suggested.     

Accuracy of Equations to Predict Basal Metabolic Rate in Older Women

Objective To assess the accuracy of several published equations for predicting basal metabolic rate (BMR) in older women.

Design BMR was assessed in 116 healthy, older white women, aged 60 to 82 years, on three successive mornings by indirect calorimetry. Body composition was determined by dual energy X-ray absorptiometry or hydrostatic weighing. The measured BMRs were compared with values obtained from eight published prediction equations that used solely, or in various combinations, measures of height, weight, fat-free mass, age, and menopausal status.

Statistical analyses performed The root mean squared prediction error (RMSPE) was used to determine how accurately predicted BMR matched actual BMR for each subject. In addition, regression analysis was used to evaluate accuracy of predicted BMR vs directly measured BMR.

Results Predicted mean BMR determined using all eight equations was significantly correlated to measured BMR (P=.0001), accounting for 30% to 52% of the variance of measured BMR. When analyzed by RMSPE, however, the equations of Owen et al (1986), Fredrix et al (1990), and Harris-Benedict (1919) predicted actual BMR for each subject within an average of 116 kcal/day, and the equation of Cunningham (1980) resulted in the largest prediction error at 208 kcal/day.

Applications/conclusions The regression equations of Owen et al (1986), which used body weight, Fredrix et al (1990), which used body weight and age, and Harris-Benedict (1919), which used age, weight, and height as variables, were most accurate in predicting BMR in our sample of healthy older women. J Am Diet Assoc. 1995; 95:1387-1392.