Delayed Puberty of nutritional origin : Analysis of a cases serie from an academic center of eastern Algeria

Introduction. Malnutrition is one of main reasons for growth and puberty delay. Objective. To determine the prevalence of functional hypogonadotropic hypogonadism (FHH) from nutritional origin, and to study its clinical and biological characteristics. Population and methods. This retrospective study was conducted on 32 cases of FHH [secondary to Chronic Diseases + Constitutional Delay of Growth and Puberty (CDGP)], from a series of 125 patients evaluated for delayed puberty (DP) in the Endocrinology Department of the University Hospital Center of Constantine, between 2000 and 2010, and follow-up for at least 5 years. The diagnosis of malnutrition was clinical, according to the American Academy of Nutrition and Dietetics consensus. Each patient received a general check-up and a gonadotropic and thyrotropic hormonal assay. Other etiological explorations were clinically guided. FHH group was compared with isolated hypogonadotropic hypogonadism (IHH) group. Results. FHH constituted 26% of the series [21 boys/11 girls, (p<0.5)] vs 24% of IHH group. Secondary HHF represented 20% of cases in the series against 6% of CDGP. Malnutrition represented 27% of the series, 11% of which were directly responsible for delayed puberty (DP). Protein-energy undernutrition and iron deficiency anemia, due to inadequate intake, accounted for 62% of nutritional causes. There was a break in the growth curve in 97% of FHH vs 26% of IHH patients (p<0.001). FHH tripled the risk for developing growth retardation. Testicular volume of FHH group was 2.82±0.73 mL (2.69±0.4 mL in patients with malnutrition) vs 2.09±0.87 mL for IHH group (p<0.05). Conclusion. Despite therapeutic progress, DP in CD is common, representing a severity indicator, and poor control of CD. Prevention of FHH requires early detection, nutritional supplementation, and good control disease.