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Biomedical subjects

P Janson

Publications and source records attributed to P Janson.

12 recordsLinked to original sources

Loneliness as a predictor of hospital emergency department use.

BACKGROUND: Recent studies indicate that loneliness is a significant risk factor for many ailments from colds to heart disease. If lonely patients are at greater risk for illness, then we might expect that they would use the emergency department (ED) more often and incur greater medical costs than those who are not lonely. Our goal was to determine the prevalence of loneliness in patients in an ED and to evaluate it as a predictor of ED use, hospital admission, and chronic illness. METHODS: We evaluated a convenience sample of 164 ED patients with the University of California-Los Angeles Loneliness Scale, Version 3 and a survey of patient characteristics. Using medical record review and patient self-report, we determined total ED visits, the presence of chronic illness, and discharge diagnoses during a 1-year retrospective period. We evaluated data with least mean square regression and a 2-tailed t test. RESULTS: We found a statistically significant correlation between loneliness score and total hospital ED visits (P <.001). The mean loneliness score (39) was equal to that of normal populations. Patients scoring higher than the mean used the ED 60% more per year than patients who scored lower (P = .008). There was no association between a patient's loneliness score and baseline chronic illness or severity of current illness (P = .56). Spanish-speaking patients had higher loneliness scores than English-speaking patients (P = .001). CONCLUSION: Loneliness is a predictor of hospital ED use independent of chronic illness and is potentially very expensive to society. We recommend further studies be done to examine if allocating resources for preventing, diagnosing, and treating loneliness would be cost effective.

Ambulatory Care↗

The bleeding time response to aspirin. Identifying the hyperresponder.

The authors measured the template bleeding time in 11 normal people before and 2, 4, 12, 24, and 48 hours after the subjects ingested a single dose of 74 mg of aspirin (ASA). The entire experiment was repeated twice at two-week intervals, with the dose of ASA increased to 325 mg and finally 3,900 mg. The mean increase was maximal at 4 and 12 hours, regardless of the dose administered, with a return to baseline by 48 hours. The authors then performed bleeding times in a prospective randomized double-blinded fashion on an additional 39 subjects at baseline and seven hours after they ingested either placebo or ASA 325 mg. The mean baseline bleeding time was 5.2 minutes (SD +/- 1.4), with a mean prolongation after ASA of 2.1 minutes (SD +/- 1.9). The authors identified 5 of 37 (14%) subjects as hyper-responders (HRs) using the criterion of a bleeding time prolongation of greater than 5.9 minutes (greater than 2 SD beyond the mean prolongation). Neither baseline bleeding time, threshold sensitivity of collagen-induced platelet aggregation, nor other tests of hemostatic function discriminated HRs from normals. The authors conclude that in subjects with normal baseline bleeding times, a prolongation of greater than 5.9 minutes when measured seven hours after the administration of a single dose of 325 mg of ASA can discriminate HRs from normals.

Adult↗

Abnormal factor VIII coagulant antigen in patients with renal dysfunction and in those with disseminated intravascular coagulation.

Factor VIII antigen (VIII:CAg) exhibits molecular weight heterogeneity in normal plasma. We have compared the relative quantities of VIII:CAg forms present in normal individuals (n = 22) with VIII:CAg forms in renal dysfunction patients (n = 19) and in patients with disseminated intravascular coagulation (DIC; n = 7). In normal plasma, the predominant VIII: CAg form, detectable by sodium dodecyl sulfate polyacrylamide gel electrophoresis, was of molecular weight 2.4 X 10(5), with minor forms ranging from 8 X 10(4) to 2.6 X 10(5) D. A high proportion of VIII:CAg in renal dysfunction patients, in contrast, was of 1 X 10(5) mol wt. The patients' high 1 X 10(5) mol wt VIII: CAg level correlated with increased concentrations of serum creatinine, F1+2 (a polypeptide released upon prothrombin activation), and with von Willebrand factor. Despite the high proportion of the 1 X 10(5) mol wt VIII:CAg form, which suggests VIII:CAg proteolysis, the ratio of Factor VIII coagulant activity to total VIII:CAg concentration was normal in renal dysfunction patients. These results could be simulated in vitro by thrombin treatment of normal plasma, which yielded similar VIII:CAg gel patterns and Factor VIII coagulant activity to antigen ratios. DIC patients with high F1+2 levels but no evidence of renal dysfunction had an VIII:CAg gel pattern distinct from renal dysfunction patients. DIC patients had elevated concentrations of both the 1 X 10(5) and 8 X 10(4) mol wt VIII:CAg forms. We conclude that an increase in a particular VIII:CAg form correlates with the severity of renal dysfunction. The antigen abnormality may be the result of VIII:CAg proteolysis by a thrombinlike enzyme and/or prolonged retention of proteolyzed VIII:CAg fragments.

Aged↗