Complete catch-up growth is
often not achieved after treatment.
Reprinted from Eating Disorders Review
November/December 2012 Volume 23, Number 6
©2012 Gürze Books
Restriction of food during anorexia nervosa (AN) can affect growth, but few studies have traced growth patterns out to final adult height in AN patients. Researchers at Chaim Sheba Medical Center, Ramat Ghan, Israel, have described their findings after studying 61 female adolescent AN patients who were hospitalized in an inpatient eating disorders department from January 1987 through December 1999. The patients’ heights were measured at admission and thereafter routinely during hospitalization and for from 2 to 10 years afterward (PLOS ONE 2012; 7:e4550504). Premorbid height data were available for 29 of these women.
The mean age on admission was 16.6 years, mean body mass index (BMI, kg/m2) was 15.7, and the mean age at menarche was 12.7 years. During hospitalization the average weight gain was almost 17 lb. During hospitalization and weight rehabilitation, the extent of growth impairment was more severe among patients admitted at an age of 13 years of younger, compared to patients admitted at an older age. This pattern was true at admission and at discharge as well. In addition, patients admitted less than one year after menarche had more severe growth impairment on admission than did patients admitted more than 1 year after menarche.
Final height data were available for 69 patients, or 32.7% of the women. Three of the original cohort of 211 women had died. On admission, the mean height of 69 patients was significantly lower than expected for a normal population, and although height standard deviation scores (SDS) increased during hospitalization, it was still significantly lower than expected in a normal population:-0.258 SDS.
What factors affected catch-up growth and final height?
Dr. Dalit Modan-Moses and colleagues had hypothesized that patients who were admitted for treatment of AN less than 1 year after they had reached menarche would have stronger catch-up growth. They feel that one reason that this did not happen could be that some of the older patients might have already achieved most of their linear growth prior to the onset of their illness. Although weight restoration led to accelerated linear growth and improved height SDS during hospitalization, complete catch-up growth was not achieved and the mean final height SDS was significantly lower than expected and not significantly different from height SDS at admission. Also, patients with greater malnutrition at admission had less catch-up growth.
Correlating weight and height led to delayed diagnosis
The researchers note that the occurrence of growth impairment in their patients well before they were hospitalized suggested that the diagnosis of AN had been considerably delayed. The authors hypothesize that weight loss in the patients may have been masked by their reduced height. Once growth retardation occurs, the severity of malnutrition may actually be underestimated because weight is related to the “stunted” height rather than to the pre-morbid projected height, resulting in a weight per height /BMI that seems reasonable. In addition, growth impairment may not have been recognized in adolescents whose heights were in the upper percentiles. In one patient, her measured height shifted from her original 90th height percentile to the 50th height percentile well before her illness was noticed. After all, she seemed normal in comparison to her peers. The authors also noted that several hormonal changes may contribute to growth retardation in AN. These include low thyroxine and triiodythyronine levels, elevated cortisol levels, and low sex hormone levels. Leptin levels were also of interest: the authors point out that leptin may act as a skeletal growth factor and can induce longitudinal growth. Since leptin levels are low in underweight AN patients and increase with refeeding, it is possible that hypoleptinemia may contribute to growth retardation in AN. In turn, increased leptin levels as weight is restored may contribute to catch-up growth.
A missed diagnosis may help compromise final height
The serious repercussions from missing a diagnosis of AN, particularly in pre-adolescent females, can include severe malnutrition and compromised final height. Since AN is associated with irreversible multi-organ damage, including brain atrophy, osteoporosis and major adverse obstetric outcomes, the authors postulate that stunting of growth should be viewed as a measurable maker of hidden tissue injury. They point out that patients admitted at a younger age, with seemingly significant growth potential, had the worst outcome and that prolonged malnutrition arising at, but not diagnosed during, early adolescence that continues around the critical time of peak height growth velocity, may interfere with growth and result in irreversible growth stunting, despite the delay in skeletal maturity.
The authors also outlined some limitations of their study. Only inpatient AN female adolescents were included, so that findings cannot be generalized to less severe forms of AN. In addition, the study did not include matched controls, and final height data were available for only a third of the original cohort of 211 women. The study also did not record Tanner states of sexual development, bone age studies, parental heights, or results of lab tests.