October 2011, Volume 61, Issue 10

Original Article

Polycystic ovaries in adolescent girls from Rawalpindi

Fouzia Nazir  ( Islamabad. )
Huma Tasleem  ( Department of Gyne/Obs, Shifa College of Medicine. )
Samina Tasleem  ( Department of Gynaecology, Rawalpindi General Hospital. )
Zaiba Sher  ( Pakistan Atomic Energy Commission. )
Khalida Waheed  ( Department of Gyne/Obs. )

Abstract

Objectives: To review different clinical endocrine manifestation of polycystic ovarian syndrome in adolescent girls.
Methods: A descriptive study was conducted in Holy Family Hospital, Rawalpindi, Pakistan from Nov 2001 to Oct 2002.
Adolescent girls diagnosed with polycystic ovaries on ultrasound seen in the out patients department for menstrual problems were included in the study. Their body mass index, waist hip ratio, hirsutism scoring was done. Serum FSH and LH were estimated to see the ratio. Descriptive analysis was done using SPSS v.10.
Results: A total of 52 unmarried girls between 15 to 25 years of age were included. Most of the girls were having oligomenorrhea (88%). While overweight girls were 34 (65%) and mild to moderate hirsutism was seen in 46 (88%). Serum FSH:LH ratio was normal in 25 (48%) and raised in 27 (52%). Earliest manifestation was hirsutism, and as body weight increased, there was linear increase in hirsutism and menstrual disturbances.
Conclusion: Polycystic ovarian syndrome is affecting the lives of young unmarried girls. The clinical manifestations are variable with obesity playing the key role.
Keywords: Polycystic ovarian syndrome, Obesity, Hirsutism, Oligomenorrhea, Rawalpindi (JPMA 61:960; 2011).

Introduction

Polycystic ovary syndrome (PCOS) is the most common, but perhaps least understood endocrine disturbance affecting women during their reproductive years.1 A fasting glucose-to-insulin ratio of < 7 is a useful index of insulin resistance in adolescents.2 It is well appreciated that PCOS usually becomes evident shortly after menarche. Ovarian volumes due to hyperinsulinism and raised IGF-I levels, cause increased ovarian response to gonadotropins which is an exaggerated response of normal puberty.3 The earliest recognized PCOS phenotype to date is premature pubarche characterized by excessively elevated levels of dehydroepiandosterone sulfate and hyperinsulinaemia. Such girls are at high risk for developing the full PCOS. This includes ovarian hyperandrogenism and chronic anovulation and after menarche they become oligomenorrhic.4 Sampaolo et al (1994) found obese postmenarcheal girls with PCO have large uterine and ovarian volumes.5
Polycystic ovarian syndrome is the combination of polycystic ovaries and symptoms such as oligomenorrhea,amenorrhea, dysfunctional uterine bleeding, fertility deprivation, skin problems like acne, hirsutism, acanthosis nigrans, obesity and recurrent pregnancy losses.6 The failure of the prolonged pituitary ovarian suppression with synthetic agonists of gonadotropin hormone releasing hormone agonist (LHRH) to allow resumption of the normal ovarian function upon withdrawal suggests that Polycystic ovaries is not a spontaneous aberration of an otherwise normal hypothalamo pituitary ovarian axis but rather that a defect exists which hinders the establishment of the normal ovarian control.7 The aetiology of PCOS is uncertain but there is evidence for a primary abnormality of ovarian androgen production which is manifested at puberty but may have its origins in childhood or even during foetal development.8
In adult normal women it is found in 22-33 % but it is not known at what age they first appear.9 Polycystic ovarian syndrome is a familial condition, however, its gene has not been identified yet and the effect of environmental influences such as weight changes and circulatory hormone concentrations and the age at which these occurred is unknown.10
PCOS is thought to be associated with increased weight gain and metabolic disturbances as elevated serum concentration of LH, serum Testosterone, Insulin and prolactin.
As PCOS is a life long and multisystem disorder some researchers also pointed out that adolescents with PCOS scored lower on subscales measuring general health perceptions, physical functioning, general behaviour, and limitations in family activities because of illness.10
This study was planned to suggest a need to develop interventions to reduce the distress that patients with PCOS may face as adolescents and young adults.

Patients and Methods

Adolescent unmarried girls who attended the out patients department of Gynaecology unit I of Holy Family Hospital, Rawalpindi, for menstrual disturbances, during November 2001-October 2002, were included in the study. Informed content was obtained from every participant. Unmarried girls with ultrasound reports showing features of PCOS (10 or more cysts, 2-8 mm in diameter, arranged around an echo-dense stroma)1 were included in this study. The girls who were married, those whose ultrasound report did not show evidence of PCOS and those who did not consent were excluded. Sample size was calculated and determined 52 girls for this study. Detailed history about their menarche, menstrual pattern, menstrual loss, dysmenorrhoea, past and present medical and surgical problems was taken. General physical examination especially their height in meters and weight in kilograms for body mass index, waist and hip measurements in inches, their ratio, hirsutism in Ferriman Gallways scoring system,12 thyroid enlargement and any other abnormality was noted. Body mass index of upto 23 was taken as normal, between 23 to 25 was taken as overweight, and more than 25 was considered as obese according to the WHO criteria. Ferriman Gallways score of 8 or less was taken as normal and more than 8 was considered as hirsute. Baseline sonography was done in the Radiology Department for the presence of Polycystic ovaries and other pelvic pathology. This was confirmed by the departmental ultrasound. Transabdominal sonography was conducted by using Toshiba\\\'s 3.5 MH sonography machine. Girls who were confirmed as having Polycystic ovaries were then advised serum FSH, LH, Prolactin from Pathology Department of Holy Family Hospital, Rawalpindi. Biomeriux enzyme immunoassay (EIA) kits were used for hormonal tests. FSH:LH ratio was then calculated. Serum FSH:LH ratio of 1:3 was taken as raised and below this was considered normal. All data was put on a proforma. Descriptive analysis was then calculated using SPSS version 10.1.

Results

Diagnosed 52 cases of PCOS were included in this study. Their mean age was 17.8 ± 1.65 (14-20 year). The body mass index is shown in Table-1.

Age of menarche ranged between 12-17 years (mean: 12.9 ± 1.1). Serum FSH was between 1.3-9.0 mIU/ml (mean 5.1 ± 1.9), LH was between 3.8-32 mIU/ml (mean 13.3 ± 7.6) and Prolactin ranged between 7-38 ng/ml (mean 15.4 ± 8.4). Most of the girls had secondary amennorhoea (76.9%). Oligomenorrhea was found in 15.8% of girls whereas normal menstruation was observed in 7.3% of girls.

Table-2 emphasized the presence of disturbances in ratio of FSH and LH. Earliest manifestation was hirsutism, and as body weight increased there was linear increase in hirsutism and menstrual problem.

Discussion

Body weight plays a critical role in the initiation, maintenance and successful outcome of reproductive function.13 Up to 50% of the women affected with PCOS were found to be obese.14 This study was done to see the proportion and relationship of different clinical endocrine manifestations in young girls diagnosed with Polycystic ovaries. In this study the most common complaint was oligomenorrhea and most of the girls were overweight. Obesity and PCOS have often been linked, and obesity has been found to exacerbate the underlying insulin resistance in PCOS.15 Obesity has also been linked to increased androgen production and hirsutism in women with PCOS.16 Polycystic ovary syndrome (PCOS) frequently presents during adolescence and is the commonest cause of menstrual irregularity and hirsutism.17
One recent study showed that approximately 50% of women with PCOS are overweight or obese and most of them have the abdominal phenotype. They stressed that obesity may play a pathogenetic role in the development of the syndrome in susceptible individuals. In fact, insulin possesses true gonadotrophic function and an increased insulin availability at the level of ovarian tissue may favour excess androgen synthesis. Obesity, particularly the abdominal phenotype, may be partly responsible for insulin resistance and associated hyperinsulinaemia in women with PCOS. Therefore, obesity-related hyperinsulinaemia may play a key role in favouring hyperandrogenism in these women.18 Other factors such as increased estrogen production rate, increased activity of the opioid system and of the hypothalamic-pituitary-adrenal axis, decreased sex hormone binding globulin synthesis and possibly, high dietary lipid intake, may be additional mechanisms. Irrespective of the pathogenetic mechanism involved, obese PCOS women have more severe hyperandrogenism and related clinical features (such as hirsutism, menstrual abnormalities and anovulation) than normal-weight PCOS women. In obese PCOS women with the abdominal phenotype, weight loss is associated with beneficial effects on hormones, metabolism and clinical features. A further clinical and endocrinological improvement can also be achieved by adding insulin-sensitizing agents and/or antiandrogens to weight reduction programmes.19
In the present study, 65.4 % of the girls had body mass index within the range of overweight Z zone. This is also favoured in the present study that most early symptom and sign in these girls was hirsutism.
Our study showed that serum LH levels were in linear correlation with menstrual problems. Another study also stresses the role of hyperandrogenism in \\\'programming\\\' of the hypothalamic-pituitary unit to favour excess LH secretion, and encourages preferential abdominal adiposity that predisposes to insulin resistance. Lower LH levels with increasing BMI in women with PCOS has been found by many investigators.20-21
In most of the studies it has been seen that girls with premature adrenarche (the onset of pubic hair before the age of 8 years is associated with elevated levels of adrenal androgens and no evidence of true puberty or adrenal dysfunction) may be at increased risk for development of polycystic ovarian syndrome (PCOS).22 Premature pubarche is not studied in the present data. Some researchers also influenced that because PCOS is associated with a 40% prevalence of abnormal glucose tolerance. Every adolescent patient should be evaluated regularly for glucose intolerance with a 2-hour oral glucose tolerance test and for lipid abnormalities with a fasting lipid profile.23 One local study on adolescents revealed that weight gain is associated with low work efficiency.24 Primary prevention of diabetes mellitus and cardiovascular disease by lifestyle modification, including regular exercise and a balanced diet, is particularly important in adolescents, who have the opportunity to establish healthy habits before entering adulthood.25

Conclusion

Polycystic Ovarian syndrome, a common problem of women of reproductive age group is affecting their life physically, mentally and socially. Obesity plays a leading role.

References

1.Balen A.H. Secondary Amenorrhea. In: Dewhurst\\\'s Text Book of obstetrics and Gynecology for postgraduates 6th edition (Edmonds D.K eds), Blackwell Science United Kingdom; 2000: 42-60.
2.Kent Sc, Legro RS. Polycystic ovary syndrome in adolescents. Adolescent medicine state of art reviews 2002; 13: 73-88.
3.Wiksten-Amstromer M, Hirschberg AL, Hagenfeldt K. Menstrual disorders and associated factors among adolescent girls visiting a youth clinic. Acta Obstet Gynecol Scand 2007; 86: 65-72.
4.Escobar ME, Ropelato MG, Ballerini MG, Gryngarten MG, Rudez MC, Veldhaus JD, Barontini M. Acceleration of Luteinizing hormone pulse frequency in adolescent girls with a history of central precocious puberty with versus without hyperandrogenism. Horm Res 2007; 68: 278-85.
5.Balen AH. The polycystic ovary syndrome. In: Shaw RW, ed. Gynecology 3 rd ed. Elsevier Science Philadelphia 2003; pp 259-70.
6.Blank SK, McCartney CR, Helm KD, Marshall JC. Neuroendocrine effects of androgens in adult polycystic ovary syndrome and female puberty. Semin Reprod Med 2007; 25: 352-9.
7.S Franks, Adult polycystic ovary syndrome begins in childhood. Best Practice & Research Clinical Endocrinology & Metabolism 2002; 16: 263-72.
8.Franks S, McCarthy MI, Hardy K. Development of polycystic ovary syndrome: involvement of genetic and environmental factors. Int J Androl 2006; 29: 278-85.
9.Duskova M, Hill M, Straka L. The polycystic ovary syndrome and its male equivalent. Cas Lek Cesk 2007; 146: 251-5.
10.Hollinrake E, Abreu A, Macfeld M, Van Vaorhis BJ, Dokras A. Increased risk of depressive disorders in women with polycystic ovary syndrome. Fertil Steril 2007; 87: 1369-76.
11.Ferriman D, Gallway JD. Clinical assessment of body hair growth in women. J Clin Endocrinol Metab 1961; 21: 1440-7.
12.Euling SY, Selevan SG, Pescovitz H, Skakkeback NE. Role of environmental factors in the timings of puberty. Pediatrics 2008; 21: 167-71.
13.Franks S. Genetic and environmental origins of obesity relevant to reproduction. Reprod Biomed Online 2006; 12: 526-31.
14.Morin- Papunen LC, Vauhkonen I, Koivunene RM, Ruokonen A, Tapananainen JS. Insulin sensitivity, insulin secretion and metabolic and hormonal parameters in healthy women and women with polycystic ovary syndrome. Hum Reprod 2000; 15: 1266-74.
15.Gambineri A, Pelusi C, Vicennati V, Pagotto U, Pasquali R. Obesity and the polycystic ovary syndrome. Int J of obesity and related metabolic disorders 2002; 26: 883-96.
16.Li L, Yong D, Chou X, Chen Y, Fong S, Wong L. Clinical and metabolic features of polycystic ovary syndrome. Int J Gynecol Obstet 2007; 97: 129-34.
17.Moeller R, Horejsi R, Pilz S, Lang N, Sargsyan K, Dimitrova R, Tafeit E, Giuliani A, Almer G, Mangge H. Evaluation of risk profiles by subcutaneous adipose tissue topography in obese juveniles. Obesity (silver spring) 2007; 15: 1319-24.
18.Silfen ME, Denburg M R, Mambo A M, Lobo RA, Jaffe R, Ferin M, Levine LS, Oberfield S E. Early endocrine , metabolic and sonographic characteristics of polycystic ovary syndrome (PCOS): comparison between obese and non-obese adolescents. Int J Clin Endocrinol and Metabol 2003; 88: 4682-8.
19.Taylor A E et al. Determinants of abnormal gonadotropin secretion in clinically defined women with polycystic ovary syndrome. J Clin Endocrinol Metab 1997; 82: 2248-56.
20.Abbott DH, Dumesic DA, Franks S. Developmental origin of polycystic ovary syndrome-a hypothesis. J Endocrinol 2002; 174: 1-5.
22.Battaglia C, Rognani G, Maneini F, Iugheitti L, Flamgni C, Varturoa S. Polycystic ovaries in childhood: a common finding in daughters of PCOS patients. A pilot study. Hum Reprod 2002; 17: 771-6.
23.Palmert MR, Gordon CM, Kartashov AL, Legro RS, Emans SJ, Dunaif A. Screening of abnormal glucose tolerance in adolescents with polycystic ovary syndrome. J Clin Endocrinol Metab 2002; 87: 1017-23.
24.Rehman T, Rizvi Z, Siddiqui U, Ahmad S, Sophie A, Siddiqui O, et al. Obesity in adolescents of Pakistan. J Pak Med Assoc 2003; 53: 315-9.
25.Norman RJ, Davies MJ, Lord J, Moran LJ. The role of lifestyle modification in polycystic ovary syndrome. Trends in Endocrinology & Metabolism 2002; 13: 251-7.

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