Table 1.

Review of body mass index (BMI) changes before, during and after GnRHa treatment

Authors and references	Results
Kamp GA et al. J Clin Endocrinol Metab. 1991;72:301-7.	The increased BMI SDS during treatment seems to be a transient phenomenon.
Boot AM et al. J Clin Endocrinol Metabol. 1998;83:370-3.	The Authors performed dual-energy x-ray absorptiometry (DEXA) before and during treatment with GnRHa in girls with CPP and early puberty. Their findings showed that BMI SDS, fat mass, and percent of body fat for chronological age increased during GnRHa therapy.
Heger S et al. J Clin Endocrinol Metab. 1999;84:4583-90.	Many CPP patients were obese prior to GnRHa treatment but experienced no changes in BMI SDS following treatment. The BMI SDS before treatment correlated strongly with the BMI SDS after treatment discontinuation.
Palmert MR et al. J Clin Endocrinol Metab. 1999;84:4480-8.	Obesity occured at a high rate among children with CPP, but did not appear to be related to long term pituitary-gonadal suppression induced by GnRHa administration.
Feuillan PP et al. J Clin Invest. 2001; 24:734-6.	The increased BMI, at initial presentation and during therapy, persisted after discontinuation of therapy and progressed to frank obesity.
van der Sluis IM et al. J Clin Endocrinol Metab. 2002;87:506-12.	After an initial increase of percentage body fat during treatment, percentage body fat decreased and normalized within 1 yr after cessation of treatment.
Arrigo T et al. Eur J Endocrinol. 2004;150:533-7.	23.8% of CPP patients were obese prior to GnRHa treatment but experienced BMI decreases after at least 2 years of treatment.
Paterson WF et al. Clin Endocrinol (Oxf). 2004;61:626-34.	The mean BMI SD scores of CPP patients increased from 0.93 to 1.2. The frequency of overweight increased from 41% to 59%, and the frequency of obese patients increased from 28% to 39%.
Traggiai C et al. Eur J Endocrinol. 2005;153:463-4.	The Authors compared 29 ICPP girls with 45 healthy girls with normal onset puberty. Regarding BMI SDS few changes were observed during the first year of therapy, while an increasing trend was observed at the end of therapy and a complete recovery after 2.5 years of the end of therapy.
Pasquino AM et al. J Clin Endocrinol Metab. 2008;93:190-5.	CPP patients maintained their previous BMI SDS during treatment regardless of the overall increase in BMI after GnRHa treatment.
Authors and references	Results
Glab E et al. Pediatr Endocrinol Diabetes Metab. 2009;15:7-11.	No significant correlation between overweight and obesity at the end of treatment and the duration of the therapy, and with the duration of CPP before introduction of GnRHa therapy was observed.
Magiakou MA et al. J Clin Endocrinol Metab. 2010;95:109-17.	No difference in the BMI SDS between GnRHa-treated group and a nontreated group was observed. Therefore, it appears likely that GnRHa treatment is not associated with an increase in fat mass
Ko JH et al. Horm Res Paediatr. 2011;75: 174-9.	The Authors assessed the percentage of body fat with DEXA method, at baseline and after one year of GnRHa therapy in 121 Korean girls and concluded that GnRHa therapy does not increase the prevalence of obesity in girls with CPP.
Yoon JY et al. J Korean Soc Pediatr Endocrinol.2011;16:165- 71.	BMI z-score increased from 0.26 ± 1.03 to 0.4 ± 0.89 during a year of GnRHa treatment.
Wolters B et al. Horm Res Paediatr. 2012;78:304-11.	Patients who were normal-weight at the start of the GnRHa treatment, exhibited an increase in BMI z-score (0.08±1.02 at baseline vs. 0.40±0.85 at the end of treatment vs. 0.41±0.89 at 6-month follow-up). In the overweight group, there was an insignificant change in BMI z-score (2.01±0.69 at baseline vs. 2.03 ± 0.54 at the end of treatment vs. 1.9 ± 0.51 at 6 months after the end of treatment).
Lee SJ et al. Chonnam Med J. 2012; 48:27-31.	BMI z-score of a Korean girl with CPP significantly increased from 0.58± 1.18 to 0.96 ± 0.83, after 18 months of GnRHa treatment.
Sorensen K et al. Eur J Endocrinol. 2012;166:903-10.	A year of GnRHa treatment increased BMI from 18.1 to 18.6 kg/m2.
Karamizadeh Z et al. Acta Med Iran. 2013;51:41-6.	GnRHa therapy cause central obesity and hyperlipidemia. The maximum weight gain of was observed at sixth months of therapy.
Gillis D et al. J Pediatr. 2013; 163: 532-6.	34 girls with CPP treated with a GnRHa were evaluated before, and the end of treatment until menarche. Changes of BMI-SDS was not significant in neither group.
Anik A et al. Indian J Endocrinol Metab. 2015;19:267-71.	GnRHa treatment did not induce significant changes in BMI z-score for chronological age, but it increased BMI z-score for bone age. The percentage of overweight/ obese CPP patients increased from 59.4% to 65.7%, after a year of treatment.
Arani KS and Heidari F. Int J Endocrinol Metab. 2015 July; 13(3): e23085. DOI: 10.5812/ijem.23085v2	The prevalence of obesity was significantly different between study groups at baseline and at sixth and 12th months of therapy (P = 0.11, P = 0.068, and P = 0.052, respectively).
Chemaitilly W et al. Clin Endocrinol (Oxf). 2016;84:361-71.	Obesity was more prevalent at the last follow-up than at the completion of GnRHa or the puberty onset (37,7%, 22,6% and 20,8%, respectively, P = 0.03).
Park J et al. Ann Pediatr Endocrinol Metab.2017; 22:27-35.	GnRHa treatment increased BMI z-score within a year of treatment, regardless of the subject’s obesity status.
Arcari AJ et al. J Pediatr Endocrinol Metab. 2019;32:181-6.	An increase of BMI in girls with normal weight was observed.