A NEW STRESS-RELATED SYNDROME OF GROWTH FAILURE AND HYPERPHAGIA IN CHILDREN, ASSOCIATED WITH REVERSIBILITY OF GROWTH-HORMONE INSUFFICIENCY

Background Growth failure without organic aetiology but associated wit h behavioural disturbance and psychosocial stress has been termed psyc hosocial short stature, This condition is not a valid diagnostic entit y, but encompasses failure to thrive, stunting secondary to chronic ma lnutrition, and idiopathic hypopituitarism. Some children show spontan eous catch-up growth when removed from the source of stress, without f urther treatment, but until now precise definition of this subgroup fo r the purpose of clinical identification has not been possible. Method s Hospital-referred children with growth failure unrelated to organic pathology, who came from stressful homes, were compared with children of short-normal stature identifed from an epidemiological survey (n=31 ). Growth-hormone dynamics were studied in the hospital group by a com bination of diurnal profiles and provocation tests, The tests were rep eated after a hospital stay of 3 weeks away from familial stress, Stan dard behavioural measures were obtained from home and school. Findings In a distinctive subgroup (n=29), growth-hormone insufficiency was as sociated with characteristic behavioural features, especially hyperpha gia and polydipsia, and a normal body-mass index. When the children we re removed from their stressful home circumstances, growth-hormone ins ufficiency spontaneously resolved only in formerly hyperphagic subject s, 74% of the non-hyperphagic cases (n=23) were anorexic, with a low b ody-mass index and normal growth-hormone responses to provocation test s. Interpretation We present explicit behavioural and developmental cr iteria by which the novel syndrome of hyperphagic short stature may be recognised clinically. Such children have a capacity for spontaneous recovery of growth-hormone production on removal from or reduction of stress, Discriminant and predictive validity of the core symptoms are demonstrated. Preliminary familial studies indicate a possible genetic predisposition.