Erratum: Intravenous ketamine for adolescents with treatment-resistant depression: An Open-Label Study, by Cullen KR, Amatya P, Roback MG, Albott CS, Westlund Schreiner M, Ren Y, Eberly LE, Carstedt P, Samikoglu A, Gunlicks-Stoessel M, Reigstad K, Horek N, Tye S, Lim KO, Klimes-Dougan B. (J Child Adolesc Psychopharmacol (2018) 28:7 (437-444) DOI: 10.1089/cap.2018.0030)

In the September 2018 issue of Journal of Child and Adolescent Psychopharmacology (vol. 28, no. 7, pp. 437-444), the article "Intravenous Ketamine for Adolescents with Treatment-Resistant Depression: An Open-Label Study," by Dr. Kathryn R. Cullen et al., was missing the financial support information as follows: This research was supported by the National Institutes of Health's National Center for Advancing Translational Sciences (UL1TR002494), the Biotechnology Research Center (P41 EB015 894), the NINDS Institutional Center Core Grants to Support Neuroscience Research (P30 NS076408), the High Performance Connectome Upgrade for Human 3TMR Scanner (1S10OD017974-01), and the University Foundation, Amplatz Scholarship. The online version of the article has been corrected to reflect this additional information. The authors wish to apologize for the omission

Genotype-phenotype relationships in Berardinelli-Seip congenital lipodystrophy

Generalised lipodystrophy of the Berardinelli-Seip type (BSCL) is a rare autosomal recessive human disorder with severe adverse metabolic consequences. A gene on chromosome 9 (BSCL1) has recently been identified, predominantly in African-American families. More recently, mutations in a previously undescribed gene of unknown function (BSCL2) on chromosome 11, termed seipin, have been found to be responsible for this disorder in a number of European and Middle Eastern families. We have studied the genotype/phenotype relationships in 70 affected subjects from 44 apparently unrelated pedigrees of diverse ethnic origin. In all subjects, hepatic dysfunction, hyperlipidaemia, diabetes mellitus, and hypertrophic cardiomyopathy were significant contributors to morbidity with no clear differences in their prevalence between subjects with BSCL1 or BSCL2 and those with evidence against cosegregation with either chromosome 9 or 11 (designated BSCLX). BSCL2 appears to be a more severe disorder than BSCL1 with a higher incidence of premature death and a lower prevalence of partial and/or delayed onset of lipodystrophy. Notably, subjects with BSCL2 had a significantly higher prevalence of intellectual impairment than those with BSCL1 or BSCLX (p<0.0001, OR 17.0, CI 3.6 to 79.0). The higher prevalence of intellectual impairment and the increased risk of premature death in BSCL2 compared to BSCL1 emphasise the importance of molecular diagnosis of this syndrome and have clear implications for genetic counselling