Differences in hip axis and femoral neck length in premenopausal women of Polynesian, Asian and European origin

There are substantial inter-racial differences in hip fracture incidence. Studies in several different ethnic groups have suggested that differences in the length of the femoral neck may contribute to these. The present study assesses femoral neck and hip axis lengths in three ethnic groups in which it has not been documented previously (Chinese, Indians and Polynesians) and compares these values with those in Europeans. Lengths were measured from dual-energy X-ray absorptiometry scans of the proximal femur in normal premenopausal women (n=225). The Polynesian (1.65 m) and European (1.64 m) women were significantly taller than the two Asian groups (mean height in each, 1.58 m). There were also differences in mean body weight, the Polynesians being the heaviest (76 kg) and the Chinese the lightest (53 kg). Femoral neck lengths were (mean + SD) Chinese 61.5+4.4 mm, Indian 61.5+5.1 mm, Polynesian 68.2+4.3 mm and Europeans 66.0+4.8 mm. Hip axis lengths were Chinese 98.0+5.6 mm, Indian 94.5+5.2 mm, Polynesian 106.4 ± 5.3 mm and European 102.3+5.3 mm. Each of the other groups were significantly different from the Europeans for both variables and, in general, this remained so after height adjustment. These data suggest that shorter femoral necks are common to the major Asian racial groups. However, in contrast to all other ethnic groups studied, Polynesians have longer femoral necks than Europeans and their low incidence of hip fracture is not explicable, therefore, in terms of their femoral neck length. This suggests that either higher bone density or other more subtle differences in proximal femoral geometry must account for the low hip fracture incidence in Polynesians.     

Active and passive surveillance for communicable diseases in child care facilities, Seattle-King County, Washington.

OBJECTIVES: The purpose of this study was to develop and evaluate models for public health surveillance of illnesses among children in out-of-home child care facilities. METHODS: Between July 1992 and March 1994, 200 Seattle-King County child care facilities participated in active or enhanced passive surveillance, or both. Reporting was based on easily recognized signs, symptoms, and sentinel events. Published criteria were used in evaluating surveillance effectiveness, and notifiable disease reporting of participating and nonparticipating facilities was compared. RESULTS: Neither surveillance model was well accepted by child care providers. Enhanced passive and active surveillance had comparable sensitivity. Reporting delays and the large amount of time needed for data entry led to problems with timeliness, especially in terms of written reporting during active surveillance. CONCLUSIONS: Widespread active public health surveillance in child care facilities is not feasible for most local health departments. Improvements in public health surveillance in child care settings will depend on acceptability to providers.     

Catheter-induced tricuspid regurgitation. Incidence and clinical significance

The incidence and severity of catheter-induced tricuspid regurgitation has not been studied extensively. Given the frequency with which right heart catheters are employed to measure cardiac output, it is important to know whether the severity of catheter-induced tricuspid regurgitation is sufficient to invalidate the measurement of thermodilution cardiac output. Accordingly, the purpose of the present prospective study was to determine the incidence and severity of catheter-induced tricuspid regurgitation in 25 men (mean age, 58.1 +/- 1.4 years) using Doppler ultrasound. The tricuspid valve was interrogated from two orthogonal views using pulsed-wave and color flow Doppler, either in the presence or absence of a 7-French catheter across the tricuspid valve. The severity of catheter-induced tricuspid regurgitation was graded semiquantitatively using a validated scoring system. Pulsed-wave Doppler studies showed that the incidence of catheter-induced tricuspid regurgitation was 48 percent, and that the average tricuspid regurgitation score increased from 0.41 +/- 0.16 to 0.61 +/- 0.17 (p less than 0.01). Color flow Doppler studies showed similar findings. Further, the incidence of catheter-induced tricuspid regurgitation was not related to the patient's underlying hemodynamic status or right ventricular geometry. In conclusion, this study shows for the first time that the quantitative extent of catheter-induced tricuspid regurgitation is small, and is therefore unlikely to be important clinically, particularly with regard to the assessment of thermodilution cardiac output.     

Fine T-Cell Subsets in Alcoholics as Determined by the Expression of l-Selectin, Leukocyte Common Antigen, and β-Integrin

Alcoholics admitted to the hospital solely for detoxication have been studied by flow cytometry to evaluate changes in the surface markers of peripheral blood leukocytes. As we have shown previously, such patients have an elevated percentage of CD8^hl lymphocytes that are HLA DR⁺; we now demonstrate that they also have striking alterations in the quantitative relationships of the fine T-cell subsets. Both CD4⁺ and CD8^hl lymphocytes have a sharply reduced percentage of the l -selectin⁺ CD45RA⁺ subset, increased percentages of the CD45RA-subsets, and several other fine subset alterations. The fine subset profile suggests, according to current correlations of phenotype and function, that both CD4⁺ suppressor inducer and CD4-dependent CD8⁺ suppressor effector cells are reduced, whereas other subsets, including CD8⁺ CTL or their precursors, are increased in relative percentages. Some of the phenotypic changes are reversible over the several days following withdrawal. In other results, the percentage of CD8^hl lymphocytes expressing CD11b (β-integrin) is shown to be reciprocal with the percentage expressing l -selectin both in normals and alcoholics. However, the regression function of CD11b vs. l -selectin on CD8^hl cells is different for the alcoholics than for the normals, indicating an abnormality in the regulation of the expression of these two adhesion markers. Taken together, this abnormality of adhesion molecules and the fine subset alterations previously described indicate widespread changes in the peripheral lymphocytes of currently drinking alcoholics. These changes suggest functional deficiencies that may include alterations of lymphocyte traffic and other adhesion-dependent functions, and a shift in the balance of regulatory interactions.     

Treatment of acute graft-versus-host disease with a nonmitogenic anti-CD3 monoclonal antibody.

Treatment with the monoclonal antibody OKT3 specific for the CD3 complex associated with the T cell antigen receptor can reverse acute rejection of human renal allografts. However, efficacy of anti-CD3 antibodies for treatment of patients with acute graft-versus-host disease after marrow transplantation has not been established. The dose-limiting side effects resulting from T cell activation induced by some anti-CD3 antibodies in vivo have discouraged their use for this application. We now report a phase I-II study of GVHD treatment with the anti-CD3 antibody BC3, a monoclonal murine IgG2b that, unlike OKT3, does not activate T cells. Fourteen patients were treated with BC3 after progression of acute GVHD despite treatment with cyclosporine and corticosteroids, and three patients received BC3 as primary treatment for GVHD. BC3 was administered at a dose of 0.1 or 0.2 mg/kg/day for seven or eight days. Five patients achieved complete resolution of GVHD, eight patients had partial improvement, two patients had no change, and two patients had progression of GVHD on therapy. Responses were sustained in 8 of 13 patients. Mild chills, fever, hypertension, and chest discomfort occurred in various combinations following 6 of 17 (35%) initial infusions of BC3 and following 4 of 99 (4%) subsequent infusions. In each instance it was possible to continue BC3 therapy without adjusting the dose or treatment schedule. In each patient treated, the absolute count of peripheral blood lymphocytes decreased transiently but returned to baseline within 22 hr after the first infusion. Circulating T cells had surface CD3 molecules saturated by the infused antibody in all but one patient. Four patients survived longer than one year after treatment with antibody BC3, and 13 patients died of infection or organ failure. Administration of the nonmitogenic anti-CD3 antibody BC3 was associated with improvement in the clinical manifestations of GVHD with minimal acute toxicity. Efficacy of antibody treatment did not depend on depletion of circulating T cells. Therefore, antibody BC3 may be achieving therapeutic immunosuppression by modulating T cell function. Controlled studies in patients treated earlier in the course of GVHD should determine whether antibody BC3 can improve survival.     

Role of EDRF in the Regulation of Shear Rate in Large Coronary Arteries in Conscious Dogs

To determine whether dilation of large coronary arteries normalizes shear during increased flow following brief occlusion, six dogs were instrumented to measure aortic and left ventricular pressures, left circumflex coronary artery external diameter, and coronary blood flow. The coronary artery was occluded for 15 or 30 s. Data were obtained before and after blockade of EDRF synthesis with nitro-L-arginine. Internal coronary artery diameter and wall shear were calculated on a moment-to-moment basis and the area under the flow curve was measured. Peak flow and shear rate were unaffected by NLA or by the occlusion duration. Flow curve area increased with the duration of occlusion. Internal and external diameters increased significantly for 15 s occlusions before NLA (by 4 ± 1% in external diameter and by 11 ± 4% in internal diameter) and for 30 s occlusions before NLA (by 5 ± 1% in external diameter and by 14 ± 5% in internal diameter) but not after NLA. Adenosine infusions of 0.05, 0.10, 0.50, and 1.0 μmol/kg/min were also used to dilate the coronary arteries. With each infusion, flow, shear and diameter were allowed to reach steady state. Steady state shear was reduced only slightly and did not approach the baseline state. We conclude that increased shear rate causes an increase in coronary artery diameter which is EDRF dependent. Increased coronary artery diameter during reactive hyperemia and adenosine infusions did not normalize wall shear.     

Nutritional issues in pediatric inflammatory bowel disease.

Malnutrition, characterized by weight loss, growth failure and micronutrient depletion, are prominent features of inflammatory bowel disease (IBD) in the pediatric age group. Accurate evaluation of the patient's nutritional status and appropriate nutritional support, whether enteral or parenteral, constitute integral parts of the management of the growing child with IBD. Over the past two decades, a number of studies have supported the potential use of nutritional therapy to induce remission and to control disease activity in symptomatic Crohn's disease. More recently, preliminary studies on the use of dietary supplements of marine-oil-derived omega-3 fatty acids have also indicated a beneficial effect in IBD patients. In parallel with these clinical trials, scientific research has recently focused on the concept that specific dietary alterations can modulate the immune response. Components of the diet that may have particular relevance to mucosal immunity and the pathogenesis of IBD include polyunsaturated fatty acids, nucleotides, and amino acids such as glutamine and arginine. Future research in the interactions between specific nutrients and the immune system will likely increase our understanding of the causes of IBD, as well as enhance the development of novel nutritional therapies for IBD patients.     

Surveillance of congenital cytomegalovirus disease, 1990-1991. Collaborating Registry Group.

In January 1990, a registry was initiated for surveillance of infants with the often severe symptoms of congenital cytomegalovirus (CMV) disease. In the first 2 years, 100 cases were reported to the registry. Petechiae, the most commonly noted clinical sign, were reported for approximately 50% of infants, usually accompanied by hepatomegaly and splenomegaly. Of the various severe neurologic conditions that can result from congenital CMV infection, the most frequent was intracranial calcifications, which were noted in 43% of the cases. The most common laboratory abnormality was low platelet count, which was observed in 52% of the cases. Infants with severe neurologic damage were about twice as likely as infants with less severe damage to have most other clinical signs and laboratory abnormalities. Databases will be developed to facilitate comparisons among symptomatically infected infants and asymptomatically infected as well as noninfected infants.