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Year : 2018  |  Volume : 7  |  Issue : 5  |  Page : 963-966

Stature–weight growth delays: Clinical and etiological aspects

1 Department of Endocrinology and Diabetology, University Hospital of Fez, Fez, Morocco
2 Department of Biophysics and Clinical MRI Methods, Faculty of Medicine and Pharmacy, University of Fez, Fez, Morocco
3 Department of Endocrinology, Faculty of Medicine and Pharmacy, Ibn Zohr University, Agadir, Morocco

Correspondence Address:
Prof. Saïd Boujraf
Department of Biophysics and Clinical MRI Methods, Faculty of Medicine and Pharmacy, University of Fez, BP. 1893; Km 2.200, Sidi Hrazem Road, Fez 30000
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jfmpc.jfmpc_207_16

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Background: Stature–weight growth delay (SWGD) is a frequent motivation of consultation. It could be a consequence of a known chronic affection, congenital or acquired affection. The purpose of this study is to describe epidemiological, clinical, paraclinical, and etiological aspects of SWGD. Patients and Methods: This retrospective study included 103 patients presenting a growth delay with an average age of 14.44 years and ranging between 5 and 21 years. Male predominance was noticed in 68.93% of cases. Patients showed a stature lower to −2 standard deviation (SD) for corresponding age compared to Sempe and Pedron reference. Patients were hospitalized in Endocrinology and Metabolic Diseases Department of the University Hospital of Fez, Fez, Morocco. Results: Patient's history included a perinatal suffering in 6.7% of cases, a chronic pathology follow-up in 17.6% of cases, and psychomotor development disorder in 10.6% of cases. The average weight was −2.37 SD with extremes varying from −4 to −0.5 SD. The stature values varied between −4.5 and −2 SD for the given age, with an average of −3.12 SD. A severe stature delay (< −3 SD) was recorded in 39.6% of cases and the targeted average size was −2.44 SD with extremes varying from −4 to −1.5 SD. Growth delay etiologies were dominated by a deficit in growth hormones (GHs) in 60% of cases. Discussion and Conclusion: Dynamic tests objectified a total deficit and partial deficits in GH in 41.7 and 30% of patients, respectively. The hypothalamo–pituitary magnetic resonance imaging was pathological in 23.3% of patients and showed a syndrome of interruption of pituitary stem in seven patients, pituitary hail gland in three patients, a craniopharyngioma in two patients, prolactin microadenoma in one patient, and nonfunctional pituitary microadenoma in one patient. GH treatment was established in 16 children that were presenting a deficit in GH, and two girls presenting Turner syndrome, whereas etiological treatment was suggested in all remaining cases.

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