Clinical analysis of 24 adolescents with precocious puberty associated with tumors
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Objectives To analyze clinical characteristics of precocious puberty attributed to tumors. Methods Hospital-based analysis was performed for 24 adolescents with precocious puberty associated with tumors. Results Percen- tage of precocious puberty attributed to tumors in boys was 12.93%, while the percentage in girls was 0.50%. Significantly advanced bone age (BA), and obviously higher levels of LH and FSH (before and after the GnRH stimulation test) were found after the transformation from peripheral precocious puberty (PPP) to central precocious puberty (CPP). Conclu- sions The incidence of precocious puberty attributed to tumors was significantly higher in boys than that in girls. Adolescents with PPP associated with tumors will transform to CPP after operation.Keywords:
Central precocious puberty
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We have experienced three patients of autism combined with precocious puberty. Their age at diagnosis of precocious puberty ranged from 6 yr and 9 mo to 9 yr and 6 mo. All patients showed pubertal growth spurt and elevated levels of basal LH and FSH, and experienced menstruation. One patient was diagnosed as having central precocious puberty according to the diagnostic guidelines. The other two patients were on borderline sexual precocity. They have been treated with GnRH analog for the purpose of stopping menstruation, which was not tolerated for their mentality. Similar to known combination of CNS disorders and precocious puberty, patients with autism may be susceptible to the early onset of puberty.
Central precocious puberty
Menstruation
Basal (medicine)
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INTRODUCTION: Puberty is characterized by the appearance of secondary sexual features and transition from the sexually immature form to the sexually mature form. Precocious precocity is defined as the appearance of secondary sexual characteristics in an age that is less than 2-2.5 standard deviation below the mean age of puberty for general population (1, 2) or the onset of menstruation before 9.5 years in girls (3). Puberty sets in with activation of the hypothalamic-pituitary-gonadal (HPG axis). The hypothalamic-pituitary-gonadal (HPG) axis is relatively quiescent during childhood, under higher inhibitory influences that still remain incompletely understood. Any disruption to this normal inhibition of the HPG axis during childhood results in “gonadotropin dependent or central or true precocious puberty”. Abnormal secretion or exposure to sex steroids independent of the HPG axis results in “gonadotropin independent or pseudo or peripheral precocious puberty. True precocious puberty is always and the physical signs of sexual development are in keeping with the phenotypic gender of the child. In precocious pseudo puberty, the sex characteristics may be isosexual or heterosexual. Precocious pseudo puberty may induce maturation of the hypothamic - pituitary - gonadal axis and trigger the onset of true sexual precocity. Incomplete sexual precocity or variants of pubertal developments refers to those disorders in which pubertal development is mild or non progressive resulting in premature thelarche or premature adrenarche or premature menarche. AIM OF THE STUDY: 1. To evaluate the clinical and endocrine profile of patients with precocious puberty followed up in a tertiary care hospital
2. To identify predictors of central precocious puberty (CPP) that reveals central nervous system (CNS) abnormalities in girls with CPP. DISCUSSION: Wide variation exists in the clinical spectrum of premature sexual developments and its etiology is multifactorial. Precocious puberty is present more commonly in girls than boys (female to male ratio 5-10:1 approximately). (23-32) In our study 77% of children were girls and 23% were boys, therefore female to male ratio was 3.5:1. In studies by Meena Desai et al (23), Bajpai et al (30), Chemaitilly et al (26), and Taher et al (32), 72.5%, 81%, 89%, 85% and 86 %, of patients were girls respectively.
Our data demonstrate that central precocious puberty was present more commonly in girls, seen in 51% (39 / 77) than boys 17% (13/77). The majority of girls with central precocious puberty (82 %) had idiopathic CPP where no etiology has been established (idiopathic CPP to neurogenic CPP ratio, 5:1), whereas a neurogenic cause was identified in 54% of boys (idiopathic CPP to neurogenic CPP ratio, 1:1). This further signifies the fact that CPP is uncommon in boys, but when it does occur it is usually due to an underlying neurological cause (39). The incidence of neurogenic CPP in the present study 18 % is comparable to that of other reports from our country (23, 25 and 30). This increased incidence of neurogenic CPP compared to studies done earlier may be due to an improvement in radiological investigations (24, 40). Recent studies have shown an increase in the incidence of neurogenic CPP (29, 30). Our findings were consistent with Bajpai et al, where 67.5% of female patients had CPP, 80% of which were idiopathic CPP. Furthermore, 56% of boys with CPP had neurogenic cause and 44 % had Idiopathic CPP. Findings of the most studies reiterate the increased incidence of idiopathic central precocious puberty in girls and neurogenic central precocious puberty in boys. The etiology of idiopathic precocious puberty in girls is unknown. This is possibly explained by early reactivation of hypothalamic-pituitary- gonadal axis in girls in comparison to boys. Hypothalamic hamartoma was the commonest cause of neurogenic CPP (35.7%, 5/14) in our study (three girls and two boys). Gelastic seizures or laughing spells is the commonest presentation; none of our children with hypothalamic hamartoma manifested it. LH-releasing hormone containing fibers have been observed within hamartoma tissues in patients with CPP. These patients presented at an early age, as in other reports (42). These patients respond to GnRH analog therapy and surgical correction is not required (42, 43). Neurotuberculosis was the second most common cause of neurogenic CPP in this series, reflecting a greater prevalence of tuberculosis in our country. We report two girls who had all the manifestations of central precocious puberty but empty sella was the only finding on MRI brain. Empty sella syndrome in association with CPP has been reported (44), but whether it plays a role in causing CPP is debatable. Supracellar arachnoid cyst was reported in two boys with features of central precocious puberty and headache was the only presenting complaint. SUMMARY: 1. All children presenting with precocious puberty require a detailed history and clinical evaluation before commencing investigations and treatment.
2. Normal pubertal variants like premature thelarche require only reassurance and periodic follow-up. The pediatrician therefore should be adept in differentiating normal pubertal variants from pathological precocious puberty.
3. Unnecessary investigations should be avoided if features of precocious puberty are inconsistent or not clearly evident and the patient must be reviewed after a few months for reassessment.
4. All forms of PPP should be managed according to the etiology, predicted adult height and psychological concerns.
5. Suppression of CPP with GnRH analogues should be considered when there is significant compromise to adult stature and behavioral issues.
6. Urgent need for population-based studies including biological work-up and brain imaging to exclude premature thelarche, primary gonadal precocious puberty, and CPP revealing CNS abnormalities.
7. Predictors for short final height and/or CNS abnormalities, identified by rigorous statistical analysis, need to be established. CONCLUSION: 1. Precocious puberty was more common among girls. The most common etiology of precocious puberty in girls was idiopathic CPP (54.2%) followed by premature thelarche (25.4%).
2. Most common etiology of precocious puberty in boys was neurogenic CPP (38.9%) followed by peripheral precocious puberty due to CAH, non – classical 21hydroxylase deficiency (23%).
3. Central precocious puberty in girls is usually idiopathic, but in boys is more likely to be the result of a demonstrable CNS lesion. This conclusion made it mandatory for neuro imaging (either CT or MRI) in boys with CPP.
4. Neurogenic CPP was present in three girls with age of onset after 6 years, indicating the need for CNS imaging in girls with age of onset after 6 years in contrary to the current recommendations.
5. Predictors of central nervous system abnormalities in girls with neurogenic CPP were early age of onset, advanced bone age, elevated levels of serum estradiol, basal LH, basal FSH and Peak LH..
Central precocious puberty
Etiology
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Objective To explore the morbidity of children′s precocious puberty in the eastern coast in China, to take reliably clinical screening, and to investigate the epidemiology of children′s precocious puberty and analyze their correlation.Methods This study included 3 stages: preliminary screening, clinical detection and correlation analysis. The levels of FSH, LH and E 2 were detected with precocious puberty, and the LHRH test was made, children were scored according to Wenz′s scale.The uterus and ovary were detected with ultrasonic detector and compared with normal children. The epidemiology of children′s precocious puberty was evaluated in these areas, and correlation analysis was made.Results 1.Among 22 281 person-time screened, there were 84 positive cases including 9 male cases [idiopathic precocious puberty (IPP) 7 cases and partial precocious puberty(PPP) 2 cases]; there were 75 female cases (IPP 30 cases, pseudo precocious puberty 8 cases, and PPP 37 cases ) .2.There was significant difference between the female with IPP and normal children in the size of uterus and ovary with ultrasound,the levels of FSH,LH and E 2 (P0.05),whereas they were almost normal for the children with PPP and pseudo precocious puberty.3.Intelligence quotient of children with precocious puberty was slightly lower than that of normal children.but there was no significant difference.4.There may be various factors for puberty, such as urban life in industrial and polluted areas, early first menses of the mother, social environment, excessive nutrition, certain heredity factors,taking nourishment and others.Conclusions There is higher morbidity for the female (0.67 %). It is simple and reliable to detect uterus and ovary with ultrasound and test the levels of FSH, LH and E 2 for screening female IPP. There is no definite etiology for puberty, but understanding multiple factors and adopting intervention measurement may contribute to lowering the morbidity.
Central precocious puberty
Heredity
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Delayed puberty
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Precocious puberty, as early physical development and low final height might lead to psychosocial problems.To evaluate etiology and clinical feature of precocious puberty in a cohort of Iranian children.In this case-series study, 44 girls and 8 boys with precocious puberty referred to Endocrine Reserch Centre (Firouzgar), Institute of Endocrinology and Metabolism (Hemmat Campus), were examined in a 10 years period of time.Mean age of girls and boys was 7.43±1.4 years and 5.8±2.1 years respectively. Most of the patients fell within the age category of 7-7.9 years old (40.9% for girls and 50% for boys). Patients, concerning etiology of precocious puberty were classified in three categories: 42.6% of patients had central precocious puberty (CPP), including idiopathic CPP (87.5%) and neurogenic CPP (12.5%). 23.3% of patients had peripheral precocious puberty (PPP), including congenital adrenal hyperplasia (CAH) (42.8%), ovarian cysts (28.4%), McCune-Albright syndrome (14.2%) and adrenal carcinoma (14.2%). 34.1% of girls and 25% of boys had normal variant puberty including premature thelarche (57%), premature adrenarche (38%) as well as premature menarche (4.7%l).The most common etiology of precocious puberty in girls was idiopathic central precocious puberty and premature thelarche, while in boys they were neurogenic central precocious puberty and CAH. Therefore precocious puberty in girls is usually benign. In boys, CNS anomalies should first be considered in the differential diagnosis of CPP. Therefore brain Magnetic Resonance Imaging (MRI) is mandatory in all cases.
Adrenarche
Etiology
Central precocious puberty
Menarche
Pediatric endocrinology
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Sex steroid
Hypothalamic–pituitary–gonadal axis
Central precocious puberty
Hypothalamic disease
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Central precocious puberty
Sexual maturity
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Puberty is one of the most astonishing periods of human life, when significant physical alterations occur along with psychosocial maturation. Precocious Puberty (PP) is defined as the appearance and progressive development of secondary sexual characteristics at a younger age than the general population, i.e. for Caucasian girls before 8 years of age. Untreated precocious puberty usually leads to short stature and can also cause significant emotional and behavioral issues. In recent years, an increased incidence of PP has been found in many countries although several studies now suggest that this trend has slowed down over the last decade in most industrialized countries, while persisting in other countries. Some girls with idiopathic precocious puberty may also have slowly progressive pubertal development without deterioration of their predicted height over a 2-year follow-up period. It is important to determine which girls to treat and the role of the clinician remains crucial. The clinician also needs to be familiar with the terminology of pubertal progression. The aim of this review was to examine the diagnosis of central precocious puberty (CPP) taking in account clinical practice and international literature.
Central precocious puberty
Sexual maturity
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