Psychosocial Correlates of Health Care Utilization for Children and Adolescents With Type 1 Diabetes Mellitus

Our objective was to examine the relation of self-reported depressive symptomatology to health care utilization (HCU) in families with a child with Type 1 diabetes mellitus (DM1). Data were obtained from a community sample (N = 88) being followed in 2 private outpatient diabetes clinics. Children and adolescents completed measures of depressive symptomatology. Mothers provided demographic information and completed measures of HCU and depressive symptomatology. Physicians provided measures of glycosylated hemoglobin (HbA1c) and illness severity. Hierarchical regression analyses indicated that higher levels of child depressive symptomatology were associated with increased HCU for children with DM1 above and beyond demographic and illness variables. However, no significant relationship was found between either adolescent or maternal depressive symptomatology and HCU. These findings suggest self-reported depressive symptomatology in children with DM1 is a salient correlate of HCU even after statistically controlling for the influence of demographics and illness parameters. The possibility that children with DM1 with symptoms of depression may have higher utilization of health services supports the need to target psychosocial variables for intervention.     

Plasminogen activator inhibitor-1 induction after experimental intracerebral hemorrhage.

Serine proteases, such as thrombin and tissue-type plasminogen activator, play an important role in brain injury after intracerebral hemorrhage and other neurologic disorders. Plasminogen activator inhibitor-1 is one of the serine protease inhibitors, or serpins. The balance between serine proteases and serpins may affect the outcome of intracerebral hemorrhage. The purpose of this study was to determine whether plasminogen activator inhibitor-1 and tissue-type plasminogen activator are upregulated after intracerebral hemorrhage and the role that thrombin plays in that induction. Plasminogen activator inhibitor-1 protein levels were upregulated after intracerebral hemorrhage. Brain plasminogen activator inhibitor-1 content also increased after thrombin infusion in a dose-dependent manner. Hirudin, a specific thrombin inhibitor, blocked the upregulation of plasminogen activator inhibitor-1 after intracerebral hemorrhage. Time courses showed that plasminogen activator inhibitor-1 levels around the hematoma peaked at the first day. Plasminogen activator inhibitor-1-positive cells were detected in the perihematomal area and the ipsilateral basal ganglia after thrombin infusion, but not in the contralateral hemisphere. Plasminogen activator inhibitor-1 messenger RNA levels were increased at 24 hours after intracerebral hemorrhage and after thrombin infusion. However, tissue-type plasminogen activator protein levels were the same in the control, whole-blood, and thrombin-infusion groups. In conclusion, intracerebral hemorrhage and thrombin infusion stimulate plasminogen activator inhibitor-1 but not tissue-type plasminogen activator production in the brain. The upregulation of plasminogen activator inhibitor-1 may be neuroprotective by limiting thrombin or other serine protease-induced toxicity.     

The Wyburn-Mason syndrome. Concomitant chiasmal and fundus vascular malformations

We report a 56-year-old female with a 50-year history of a progressive chiasmal syndrome who was found to have a suprasellar arteriovenous malformation involving the chiasm and both optic nerves associated with an unusual fundus picture consistent with the Wyburn-Mason syndrome. A review of the literature of this rare syndrome is also presented.