UNASSIGNED: precocious puberty is defined as the development of sexual characteristics before 8 years of age in girls and 9 years of age in boys. The purpose of our study was to describe the clinical, paraclinical and etiological profile of precocious puberty.
UNASSIGNED: we conducted a retrospective descriptive study from 1999 to 2017 in the Pediatric Endocrinology Unit at the Rabat Children\'s Hospital.
UNASSIGNED: ninety-nine children were included in the study. The average age of girls was 4.25 ± 2.6 years, while that of boys was 3.6 ± 1.8 years. There was a female predominance (90%; 90 girls). The telltale signs in girls were dominated by breast development (77.77%). In boys, the most common reason for consultation was pubic hair (70%). Biologically, in central precocious puberty, the mean peak LH level after GnRH stimulation was high (17 IU/L) with a mean peak LH to peak FSH ratio of 1.30. The causes included: dissociated early puberty (60.60%), pathological early puberty (39.40%). In the latter, we noted a predominance of precocious pseudopuberty (58.98%). Concerning the central precocious puberty, idiopathic central precocious puberty was the most common etiology in girls (62.5%). In all boys, central nervous system lesion was found.
UNASSIGNED: our study confirms that central pathological precocious puberty is often related to a lesion of the central nervous system in boys, thus justifying systematic brain imaging.

BACKGROUND: Van Wyk Grumbach syndrome (VWGS) and Kocher-Debre Semelaigne syndrome (KDSS) are rare forms of pseudo-precocious puberty and myopathy in patients with longstanding untreated hypothyroidism. We present the case of an adolescent girl who developed pseudo-precocious puberty and myopathy caused by long-term untreated hypothyroidism.
METHODS: A 17-year-old female patient was referred to our outpatient clinic due to menstrual irregularities. She had muscle pain and multiple cystic ovaries in addition to clinical signs of severe congenital hypothyroidism. High levels of creatinine and creatinine kinase and accompanying muscle hypertrophy were present. After the initiation of L-thyroxine therapy, the symptoms were alleviated in a short time.
CONCLUSIONS: Congenital and acquired hypothyroidism should be considered in the differential diagnosis of pseudo-precocious puberty and myopathy that presents with muscle pain, muscle hypertrophy, and elevated creatinine kinase levels.

Steroid cell tumor, not otherwise specified (NOS), are rare ovarian tumor, in addition, it is more rare in children. The majority of these tumors produce several steroid hormones, particularly testosterone. Estrogen also secreted by steroid cell tumor, NOS, but it is uncommon. Furthermore, hypertension is an infrequent sign in steroid cell tumor, NOS. An 8.5-yr-old girl with hypertension and frequent vaginal spotting visited at our clinic. On laboratory evaluation, secondary hypertension due to an elevated plasma renin level and isosexual pseudoprecocious puberty was diagnosed. Right solid ovarian mass was detected in radiologic tests. She underwent a right ooporectomy and it revealed renin and progesterone receptor positive steroid cell tumor, NOS. After operation, her blood pressure returned to normal level and vaginal bleeding disappeared. Even though this case is very rare, when hypertension coincides with virilization or feminization, a renin-secreting ovarian steroid cell tumor, NOS, should be considered.