Comorbid Anxiety Increases Suicidal Risk in Bipolar Depression: Analysis of 9720 Adolescent Inpatients

Objective: To evaluate the risk of association between suicidal behaviors and comorbid anxiety disorders in adolescents with bipolar depression. Methods: We conducted a cross-sectional study using the nationwide inpatient sample (NIS) from the United States. This study included 9720 adolescent inpatients with bipolar depression and further grouped by co-diagnosis of anxiety disorders. Logistic regression analysis was used to evaluate the odds ratio (OR) of suicidal behaviors due to comorbid anxiety after controlling demographic confounders and psychiatric comorbidities. Results: Out of total inpatients, 34.8% (n = 3385) had comorbid anxiety disorders with a predominance in females (70.3%) and White patients (67.7%). About 54.1% of inpatients with comorbid anxiety had suicidal behaviors versus 44.6% in the non-anxiety cohort (p < 0.001). Comorbid anxiety disorders were associated with 1.35 times higher odds (95% CI 1.23–1.47, p < 0.001) for suicidal behaviors. Conclusion: Suicidal behaviors are significantly prevalent in bipolar depression adolescents with comorbid anxiety disorders. Anxiety disorders are an independent risk factor in bipolar depression that increase the risk of suicidal behaviors by 35%. This necessitates careful assessment and management of comorbid anxiety disorders in bipolar youth to mitigate suicidality

Late-onset polyucosan body myopathy in five patients with a homozygous mutation in GYG1

International audienceFive Sardinian patients presented in their 5th or 6th decade with progressive limb girdle muscle weakness but their muscle biopsies showed vacuolar myopathy. The more or less abundant subsarcolemmal and intermyofibrillar vacuoles showed intense, partially α-amylase resistant, PAS-positive deposits consistent with polyglucosan. The recent description of late-onset polyglucosan myopathy has prompted us to find new genetic defects in the gene (GYG1) encoding glycogenin-1, the crucial primer enzyme of glycogen synthesis in muscle.We found a single homozygous intronic mutation harbored by five patients, who, except for two siblings, appear to be unrelated but all five live in central or south Sardinian villages