Contribution To Disease Severity Research Articles

The pediatric inflammatory bowel disease INTERMED: A new clinical tool to assess psychosocial needs

ObjectiveThe adult INTERMED is used to determine case complexity and psychosocial needs. We developed and validated a pediatric version of the INTERMED for children and adolescents with inflammatory bowel disease (IBD) and assessed its utility in predicting healthcare utilization. MethodsWe performed a cross-sectional study of children (aged 8–17 y) with IBD (n = 148) and their parents, seen in a hospital-based clinic. Subjects completed semi-structured interviews that were scored on the 34 pIBD-INTERMED items. To assess inter-rater reliability, 40 interviews were videotaped and scored by a second assessor. Convergent and predictive validity were assessed by examining the relation of the pIBD-INTERMED to standardized measures of psychological, social, and family functioning, disease activity, and healthcare utilization. ResultsCorrelational analyses supported the validity of all five pIBD-INTERMED domains with very good inter-rater reliability (median r = 0.87) and internal consistency (α = 0.91) for the total complexity index. Ratings of 2–3 on the pIBD-INTERMED “mental health/cognitive threat” item were associated with greater odds of behavior and social problems (CBCL-Internalizing scale OR = 7.27, 95% CI 2.17–24.36); CBCL-Externalizing scale OR = 24.79, 95% CI 5.00–122.84), depression (Children's Depression Inventory OR = 8.52, 95% CI 1.70–43.02) and anxiety (Multidimensional Anxiety for Children OR = 11.57, 95% CI 3.00–45.37). The pIBD-INTERMED complexity index added significantly to the prediction of healthcare utilization, beyond the contribution of disease severity. ConclusionsThe pIBD-INTERMED is a reliable and valid tool for identifying psychosocial risks and needs of children with IBD. It can be used to guide planning of individualized care and enhance interdisciplinary pediatric IBD care.

Erratum to: Contributions of Disease Severity, Psychosocial Factors, and Cognition to Behavioral Functioning in US Youth Perinatally Exposed to HIV.

Erratum to: Contributions of Disease Severity, Psychosocial Factors, and Cognition to Behavioral Functioning in US Youth Perinatally Exposed to HIV.

Contributions of Disease Severity, Psychosocial Factors, and Cognition to Behavioral Functioning in US Youth Perinatally Exposed to HIV

Among perinatally HIV-infected (PHIV) and perinatally HIV-exposed, uninfected (PHEU) youth, we evaluated the contributions of home environment, psychosocial, and demographic factors and, among PHIV only, HIV disease severity and antiretroviral treatment (ART), to cognitive functioning (CF) and behavioral functioning (BF). A structural equation modeling (SEM) approach was utilized. Exploratory factor analysis was used to reduce predictor variables to major latent factors. SEMs were developed to measure associations between the latent factors and CF and BF outcomes. Participants included 231 PHIV and 151 PHEU youth (mean age=10.9years) enrolled in the PHACS adolescent master protocol. Youth and caregivers completed assessments of CF, BF, psychosocial factors and HIV health. Medical data were also collected. Clusters of predictors were identified, establishing four parsimonious SEMs: child-assessed and caregiver-assessed BF in PHIV and PHEU youth. Among both groups, higher caregiver-child stress predicted worse BF. Caregiver resources and two disease severity variables, late presenter and better past HIV health, were significant predictors of CF in PHIV youth. Higher youth CF was associated with better caregiver-reported BF in both groups. Caregiver resources predicted caregiver-reported BF in PHEU youth, which was mediated via youth CF. Among PHIV youth, better past HIV health and caregiver resources mediated the effects of CF on caregiver-assessed BF. Using SEMs, we found a deleterious impact of caregiver and child stress on BF in both groups and of HIV disease factors on the CF of PHIV youth, reinforcing the importance of early comprehensive intervention to reduce risks for impairment.

Acute care costs of patients admitted for management of chronic obstructive pulmonary disease exacerbations: contribution of disease severity, infection and chronic heart failure

In 2003, chronic obstructive pulmonary disease (COPD) accounted for 46% of the burden of chronic respiratory disease in the Australian community. In the 65-74-year-old age group, COPD was the sixth leading cause of disability for men and the seventh for women. To measure the influence of disease severity, COPD phenotype and comorbidities on acute health service utilization and direct acute care costs in patients admitted with COPD. Prospective cohort study of 80 patients admitted to the Royal Melbourne Hospital in 2001-2002 for an exacerbation of COPD. Patients were followed for 12 months and data were collected on acute care utilization. Direct hospital costs were derived using Transition II, an activity-based costing system. Individual patient costs were then modelled to ascertain which patient factors influenced total direct hospital costs. Direct costs were calculated for 225 episodes of care, the median cost per admission was AU$3124 (interquartile range $1393 to $5045). The median direct cost of acute care management per patient per year was AU$7273 (interquartile range $3957 to $14 448). In a multivariate analysis using linear regression modelling, factors predictive of higher annual costs were increasing age (P= 0.041), use of domiciliary oxygen (P= 0.008) and the presence of chronic heart failure (P= 0.006). This model has identified a number of patient factors that predict higher acute care costs and awareness of these can be used for service planning to meet the needs of patients admitted with COPD.

The contribution of disease severity, depression and negative affectivity to fatigue in multiple sclerosis: A comparison with ulcerative colitis

Background Fatigue is one of the most common and troubling symptoms of multiple sclerosis (MS) and more severe and disabling than fatigue in other somatic populations. Although fatigue seems MS specific, its pathogenesis is still poorly understood. Objective To study the disease specificity of fatigue in MS by comparing its level, its physical and psychological correlates to those of patients with ulcerative colitis (UC), a peripheral chronic auto-immune disease. We focused on the relative contribution of disease severity, depression and negative affectivity to fatigue in both patient samples. Methods A total of 88 MS and 76 UC patients were included in this cross-sectional study. Fatigue, depression and negative affectivity were assessed respectively with the physical and mental fatigue subscales of the Multidimensional Fatigue Inventory, the depression subscale of the Hospital Anxiety and Depression Scale, and the neuroticism subscale of the Dutch NEO Five-Factor Inventory. The Expanded Disability Status Scale and the Colitis Activity Index were used to measure disease severity in MS and UC patients respectively. Results While levels of both physical and mental fatigue were significantly higher in MS patients than in UC patients, there were no group differences in the contribution of disease severity, depression and negative affectivity to both physical and mental fatigue. Conclusion Although levels of fatigue are higher for MS patients when compared with UC patients, the correlates of fatigue do not indicate MS specificity. As such our results support a transdiagnostic approach to fatigue in MS.

Impact of Frontal Systems Behavioral Functioning in Dementia on Caregiver Burden

Impact of Frontal Systems Behavioral Functioning in Dementia on Caregiver Burden

Contributions of disease severity and perceptions of primary and secondary control to the prediction of psychosocial adjustment to Parkinson's disease.

Seventy-four people with Parkinson's disease (PD) completed questionnaires and were interviewed to determine the degree to which the severity of PD and perceptions of primary and secondary control over PD predicted psychosocial adjustment. Significant unique contributions to PD-related participation restrictions were made by disease severity (positive relationship) and perceived internal secondary control (negative relationship). Also, participation restrictions had a significant direct effect, and disease severity and perceived internal secondary control significant indirect effects, on both depressive symptomatology and life satisfaction. Results are consistent with theories that suggest the importance of enhancing internal secondary control processes in situations in which actual control over objective circumstances is limited, such as with chronic and progressive diseases like PD.

The molecular genetics of autoimmune liver disease.

The dual observations that human leukocyte antigens have an antigen-binding groove and that the polymorphism we study as human leukocyte antigen types is largely related to amino acid substitutions in and around that groove have provided a new focus for immunogenetic studies. In autoimmune liver disease, recent studies have described specific amino acid substitutions in the antigen-binding groove of human leukocyte antigen DR molecules that may determine both disease susceptibility, through their direct influence on antigen binding, and the severity of the disease. In autoimmune hepatitis, lysine residues at DR beta position 71 in European subjects and arginine or histidine residues at DR beta position 13 in Japanese subjects may be responsible for much human leukocyte antigen-encoded disease susceptibility. Similar claims have been made for leucine residues at DR beta 38 in primary sclerosing cholangitis and for leucine residues at DP beta 35 in Japanese patients with primary biliary cirrhosis. To date, our knowledge of genetic susceptibility to autoimmune liver disease is incomplete. Other genes may contribute to susceptibility to autoimmune liver disease--for example the contribution of TAP genes, upstream promoter sequences and class III genes on chromosome 6 and the T-cell receptor genes and complement genes elsewhere in the human genome is currently unclear. Additional information concerning the immunogenetic contribution to disease severity is needed to complete the picture.