Diagnosis of depression by primary care physicians versus a structured diagnostic interview. Understanding discordance

In this paper, false-negative and false-positive cases of depressive illness are examined, differentiating levels of disagreement between a primary care physician's diagnosis and a standardized research diagnosis. Two stratified random samples of primary care patients in Seattle, USA (N = 373) and Groningen, The Netherlands (N = 340) were examined with the Composite International Diagnostic Interview-Primary Health Care Version (CIDI-PHC). Physician's severity ratings and diagnosis of psychological disorder were obtained. Three levels of disagreement between physician and CIDI diagnosis were distinguished: 1) complete disagreement about the presence of psychiatric symptoms (true false-negative and true false-positive patients); 2) disagreement over severity of recognized psychological illness (underestimated or overestimated); and 3) disagreement over the specific psychiatric diagnosis among those given a diagnosis (misdiagnosed or given another CIDI diagnosis). All three levels of disagreement were common. Only 27% of the false-negative cases were due to complete disagreement (true false-negatives), and 55% of the false-positives were due to complete disagreement (true false-positives). The true false-negative patients were younger, more often employed, rated their own health more favorably, visited their doctor for a somatic complaint and made fewer visits than the underestimated, misdiagnosed, and concordant positive patients. Complete disagreement in depressive diagnoses between the primary care physician and research interview is not as frequent as indicated by an undifferentiated false-negative/ false-positive analysis. Differentiating levels of disagreement does more justice to diagnostic practice in primary care and provides guidance on how to improve the diagnostic accuracy of primary care physicians.     

No association between an intronic presenilin-1 gene polymorphism and schizophrenia in a Chinese population

We investigated the association between schizophrenic psychosis and an intronic polymorphism of the presenilin-1 (PS1) gene in a Chinese population. Schizophrenic and control groups had similar PS1 genotype distributions and allele frequencies, indicating that this polymorphism may not be involved in the development of schizophrenia.     

Body region prevalence of injury in alcohol- and non-alcohol-related traffic injuries

OBJECTIVE: To explore the relationship between alcohol use and body region of injury in patients injured in traffic collisions. MATERIALS AND METHODS: A prospective study of 381 patients involved in traffic collisions over the past 4 months. These patients were categorized as either using alcohol or not using alcohol on the day of the accident. Eighty of 381 patients (21%) had detectable blood alcohol concentrations. Age, sex, location of injury, helmet use, clinical diagnosis, Injury Severity Score, Glasgow Coma Scale score, and blood alcohol concentrations were collected for each patient. Blood alcohol concentrations were measured by the radioactive energy attenuation method. RESULTS: The incidence of head, face, chest, abdomen, and extremity injury in patients with alcohol use was 39%, 56%, 13%, 15%, and 55%, respectively, and 26%, 32%, 15%, 12%, and 63% in those without alcohol use, respectively. The differences in the incidence of head and facial injuries were significant between these two groups (p<0.05). Mean blood alcohol concentrations in head, face, chest, abdomen, and extremity injury were 171, 204, 215, 231, and 163 mg/dL, respectively. CONCLUSION: More injuries to the head and facial areas compared with other body parts were found in patients with alcohol use. However, alcohol level did not seem to influence the region of the body injured.     

CD2 and CD3 receptor-mediated tolerance: constraints on T cell activation

BACKGROUND: Antigen specific allograft tolerance is induced in mice by anti-CD2 plus anti-CD3epsilon monoclonal antibody (mAb) treatment. Because anti-CD2 mAb inhibits several aspects of anti-CD3epsilon driven T cell activation, we investigated what components of T cell activation are required or may be dispensed with for tolerance induction. Anti-CD3epsilon-mediated T cell activation depends on FcgammaR interactions. METHODS: To assess the role of FcgammaR-mediated T cell activation in tolerance induction, FcgammaR binding IgG or non-binding IgG3 anti-CD3epsilon mAbs were examined. RESULTS: These mAbs, administered in conjunction with anti-CD2, were equally effective in inducing tolerance. Moreover, in vivo administration of a blocking mAb directed against the FcgammaR, or the use of allograft recipients deficient in FcgammaR, had no effect on tolerance induction. Blocking IL-2 using mAb directed against IL-2 or IL-2R also did not prevent the induction of tolerance. These results suggest that complete T cell activation was not required for tolerance induction. However, substitution of a partially activating mAb, directed against the T cell receptor (TCR) beta subunit for anti-CD3epsilon, failed to synergize with anti-CD2 mAb to induce tolerance. The anti-TCRbeta mAb and anti-CD3epsilon mAb were found to differentially down modulate expression of TCR/CD3 complex subunits. In particular, anti-CD3epsilon caused transient down modulation of the TCRbeta receptor subunit and the TCRzeta signaling module, and this pattern was enhanced and prolonged by anti-CD2. Anti-TCRbeta caused persistent TCRzeta modulation but no TCRbeta modulation, and anti-CD2 did not influence this pattern. CONCLUSIONS: These results suggest that, although full T cell activation is not required for the induction of tolerance by anti-CD2 plus anti-CD3epsilon mAb, a signal transduction pathway that is associated with TCRbeta and TCRzeta expression, and, specifically, is perturbed by mAb binding of the CD3epsilon epitope, is critical.     

Prevalence of microalbuminuria and relationship to the risk of cardiovascular disease in the Japanese population

The prevalence of microalbuminuria and its relationship to cardiovascular disease risk factors were examined in subjects participating in an annual physical and laboratory examination program. The urinary albumin concentration and the urinary albumin/creatinine ratio were determined in morning urine specimens. A turbidimetric immunoassay was used for the measurement of urinary albumin. Of the 731 subjects, 41 (5.6%) who were weakly positive or positive on a routine dipstick test for protein were excluded from the final analysis of data. Microalbuminuria was present in 14.5% of the men, in 12.4% of the women, and in 13.2% of the entire subject population when defined as a urinary albumin concentration of 30-299 microgram/ml. The prevalence of microalbuminuria was significantly higher in subjects with a high normal blood pressure (15.0%) or hypertension (26.2%) as compared with normotensive subjects (6.5%). Subjects with impaired glucose tolerance (24.3%) or hyperglycemic subjects (50.0%) had a significantly higher prevalence of microalbuminuria than normoglycemic subjects (11.3%). The prevalence of microalbuminuria was significantly higher in subjects with left ventricular hypertrophy (47.1%) as compared with those with normal electrocardiograms (11.3%). A good correlation was observed between urinary albumin concentration and albumin/creatinine ratio, and both showed a significant positive correlation with age, systolic and diastolic blood pressures, and fasting plasma glucose, total serum protein, albumin, and triglyceride levels, but not with angiotensin-converting enzyme activity. Multiple regression analysis demonstrated that both the urinary albumin concentration and the albumin/creatinine ratio show a significant positive correlation with systolic blood pressure and fasting plasma glucose. The prevalence of microalbuminuria was about 13% in this Japanese cohort, and the systolic blood pressure and the fasting plasma glucose level were demonstrated as independent risk indicators for both urinary microalbumin level and urinary microalbumin/creatinine ratio.     

Anesthetic management for cesarean section in a pregnant woman with impending acute liver failure--a case report

Acute liver failure includes a constellation of clinical conditions resulting from rapid loss of hepatocyte function. The anesthesiologist may often be asked to anesthetize a patient with acute liver failure before the etiological entity of disease can be completely clarified. Most of the previous reports were concentrated in obstetric or hepatological periodicals. Reports about anesthesia for such patients are scanty. We present a case about a near term pregnant woman with a complication diagnosed as impending acute liver failure, who received total intravenous anesthesia for emergent cesarean section. Pros and cons of different anesthetic techniques for this condition are discussed.     

On the use of survival analysis techniques to estimate medical care costs.

Measurement of treatment costs is important in the evaluation of medical interventions. Accurate cost estimation is problematic, when cost records are incomplete. Methods from the survival analysis literature have been proposed for estimating costs using available data. In this article, we clarify assumptions necessary for validity of these techniques. We demonstrate how assumptions needed for valid survival analysis may be violated when these methods are applied to cost estimation. Our observations are confirmed through simulations and empirical data analysis. We conclude that survival analysis approaches are not generally appropriate for the analysis of medical costs and review several valid alternatives.