Outcomes of low-weight patients with avoidant/restrictive food intake disorder and anorexia nervosa at long-term follow-up after treatment in a partial hospitalization program for eating disorders.

OBJECTIVE: To assess long-term outcomes of patients with avoidant/restrictive food intake disorder (ARFID) treated in a partial hospitalization program (PHP) for eating disorders (ED). METHOD: A cross-sectional study comparing patients with ARFID to those with anorexia nervosa (AN) who had been discharged from a PHP for at least 12 months was performed. Percent median body mass index (%MBMI), scores on the Children's Eating Attitudes Test (ChEAT), and treatment utilization were assessed, with intake and discharge data collected via retrospective chart review. RESULTS: Of the 137 eligible patients, 62 (45.3%) consented to follow-up data collection. Patients with ARFID and AN exhibited similar increases in %MBMI from intake to discharge and reported low scores on the ChEAT by discharge. Patients with ARFID and AN maintained good weight outcomes and low ChEAT scores at follow-up. Most participants were still receiving outpatient treatment from a variety of providers, although fewer with ARFID than AN continued to receive services from our multidisciplinary ED clinic. DISCUSSION: Patients with ARFID and AN exhibit similar improvements in %MBMI when treated in the same PHP and appear to maintain treatment gains at long-term follow-up. Additionally, most patients continue to utilize outpatient services after being discharged from a PHP.

Cutting Edge: Eomesodermin Is Sufficient To Direct Type 1 Innate Lymphocyte Development into the Conventional NK Lineage.

Type 1 innate lymphocytes comprise two developmentally divergent lineages, type 1 helper innate lymphoid cells (hILC1s) and conventional NK cells (cNKs). All type 1 innate lymphocytes (ILCs) express the transcription factor T-bet, but cNKs additionally express Eomesodermin (Eomes). We show that deletion of Eomes alleles at the onset of type 1 ILC maturation using NKp46-Cre imposes a substantial block in cNK development. Formation of the entire lymphoid and nonlymphoid type 1 ILC compartment appears to require the semiredundant action of both T-bet and Eomes. To determine if Eomes is sufficient to redirect hILC1 development to a cNK fate, we generated transgenic mice that express Eomes when and where T-bet is expressed using Tbx21 locus control to drive expression of Eomes codons. Ectopic Eomes induces cNK-like properties across the lymphoid and nonlymphoid type 1 ILC compartments. Subsequent to their divergent lineage specification, hILC1s and cNKs thus possess substantial developmental plasticity.