Peripheral Blood Lymphocyte Surface Antigen Expression and Prognosis in Myeloma: Australian Leukaemia Study Group Study

The Australian Leukaemia Study Group myeloma study (MM1) aimed to determine the prognostic significance of clinical and immunophenotypic markers in patients with multiple myeloma. All patients were treated with standard dose melphalan and prednisone. Seventy-four patients were entered and the median survival was 27 months. Serum beta 2-microglobulin (βM) and albumin levels were the only significant clinical factors influencing survival (p = 0.007 and p = 0.008, respectively). Patients with raised levels of CD38+ lymphocytes at presentation had a significantly shorter survival than patients with normal levels (p = 0.01, logrank test, median 19 months vs 33 months). CD38 antigen expression was independent of β2M but patients with raised levels of CD38 had significantly lower levels of albumin than patients with normal levels (p = 0.001) which may explain their poorer survival. Salmon and Durie stage was not associated with antigen expression. No other B-cell antigens (CD10, CD19, CD20, CD21, CD22, CD23, FMC1 or FMC7) or plasma cell antigens tested (PCA-1) were found to be associated with prognosis. Patients who achieved plateau phase had a better prognosis than those who did not (p = 0.04 in a landmark analysis). Patients who achieved plateau phase following an objective response appeared to have a better prognosis than those who were in plateau phase at presentation (p = 0.09 in a landmark analysis). Light chain isotype suppression (LCIS) was not associated with a significant survival advantage and did not correlate with any known prognostic indicator. We conclude that phenotypic analysis of peripheral blood lymphocytes for CD38 antigen at diagnosis may be useful as a prognostic indicator in patients with myeloma.     

The impact of the Safe Kids/Healthy Neighborhoods Injury Prevention Program in Harlem, 1988 through 1991.

OBJECTIVES. This study evaluated the effectiveness of a community coalition to prevent severe injuries to children in Central Harlem, New York, NY. It was hypothesized that injury incidence rates would decline during the intervention (1989 through 1991) relative to preintervention years (1983 through 1988); that the decline would be greatest for the targeted age group (5 through 16 years) and targeted injury causes (traffic accidents, assaults, firearms, outdoor falls); and that the decline would occur in the intervention community rather than a control community. METHODS. Surveillance of injuries that result in hospitalization and/or death among children in the two communities has been under way since 1983. Data from this surveillance were used to test whether the incidence of severe injury declined during the intervention; other temporal variations were controlled by Poisson regression. RESULTS. The incidence of injury among school-aged children in central Harlem declined during the intervention. The decline was specific to the targeted age group and targeted causes. A nonspecific decline also occurred in the control community. CONCLUSIONS. The declining incidence rate in Central Harlem is consistent with a favorable program effect, but additional investigation of possible secular trend or spillover effects is needed.     

Predictors of Repeat Emergency Department Visits by Elders

Objective: To determine which characteristics of older patients who use a hospital ED are associated with repeat visits during the 90 days following the index visit.
Methods: The study was conducted in the ED of a 400-bed university-affiliated acute care community hospital in Montreal. Patients aged ≥75 years who visited the ED between 08:00 and and 16:00 on a convenience sample of days over an 8-week period (July and August 1994) were assessed using a questionnaire, physical and cognitive status instruments, and a functional problem checklist. The hospital's administrative database was used to identify repeat visits during the 90 days following the ED visit. The representativeness of the sample was assessed by analyses of ED visits made by 4,466 persons aged ≥65 years during a 12-month period (September 1993 to August 1994) using the hospital's administrative database.
Results: 256 patients aged ≥75 years visited the ED during the study period and 167 were assessed. Of these, 54 (32%) were admitted to the hospital. Among the 113 patients released from the ED, 27 (24%) made repeat visits during the next 90 days. In univariate analyses, repeat visits were significantly associated with the number of functional problems, cognitive impairment, and previous ED visits. In multiple logistic regression, male gender, living alone, and number of functional problems were independent predictors of repeat visits. In the administrative data analyses, nighttime arrival to the ED for the index visit was significantly associated with repeat visits.
Conclusions: Self-reported risk factors can help to identify a group of elders likely to make repeated ED visits; the development of a screening instrument incorporating questions on these problems and implementation of appropriate interventions might improve these patients' quality of life and reduce the demand for further ED care in this age group.     

NIFEDIPINE BLOCKS ACTH AND CORTISOL RELEASE IN MAN

1. The present study investigated the effect of prior administration of nifedipine on AVP-induced ACTH release in seven normal volunteers. Three protocols were used: 20 mg oral nifedipine; 0.14 pressor units intramuscular (i.m.) per kg bodyweight aqueous AVP; oral nifedipine plus i.m. AVP 90 min later. Plasma ACTH and cortisol were measured at intervals for 2.5 h during each test. 2. The mean peak plasma ACTH and cortisol levels and the mean peak changes from basal in these levels were significantly lower in the nifedipine/AVP test than in the AVP alone test. The integrated area under the cortisol time curve was significantly lower for the nifedipine/AVP test than that for the AVP test alone. Nifedipine alone caused no changes in ACTH or cortisol. 3. Acute administration of oral nifedipine caused an inhibition of AVP-stimulated ACTH and cortisol release in normal humans. This effect may be due to blockade of plasma membrane calcium channels normally activated during AVP stimulation of pituitary corticotrophs.