BRIEF COMMUNICATIONS
A 21-year-old Hispanic woman (gravida 1, para 0) with a spontaneously conceived singleton pregnancy was admitted at 7 weeks of gestation for glucose control. Four weeks earlier, she had been diagnosed with acute pancreatitis (triglyceride 1580 mg/dL). Past medical history consisted of familial hypertriglyceridemia, hypertension, gastroesophageal reflux, pregestational diabetes, and polycystic ovary syndrome. She was taking fenofibrate (discontinued upon admission), niacin, omega-3 fatty acids (O3FA), metformin, omeprazole, and insulin. The patient was discharged 2 days later, after insulin adjustments, on a low-fat diet (20% of daily calories). Thereafter, triglyceride levels were monitored every other week; levels and interventions are shown in Table 1. At 29 weeks of pregnancy, the woman developed severe preeclampsia with persistent symptoms, necessitating delivery at 31 weeks. After failed labor induction, a male fetus (1950 g; 1-minute Apgar score 8; 5-minute Apgar score 8) was delivered via cesarean. Neonatal triglyceride levels were assessed at random on days 3 and 13 of life (66 and 56 mg/dL, respectively [normal range, 10–140 mg/dL]). The patient was discharged on postoperative day 2 in stable condition and prescribed fenofibrate, O3FA, metformin, enalapril, and insulin. Hypertriglyceridemia commonly worsens during pregnancy because of physiological elevation of lipids, thus increasing the risk of organ injury secondary to profoundly elevated triglyceride levels. Mortality rates among patients with acute pancreatitis during pregnancy and known familial hypertriglyceridemia have been reported to be as high as 20%–30% [1]. General concern for acute pancreatitis begins when triglyceride levels reach 1000 mg/dL. Plasmapheresis has been used in pregnant women with acute pancreatitis associated with spontaneous abortion and preterm delivery. Glueck et al. [2] reported 2 pregnancies in a single patient
81
with familial hypertriglyceridemia treated solely with O3FA; the patient’s triglyceride levels were never below 1000 mg/dL, despite the O3FA dose being increased in the second pregnancy. A 25%–30% reduction in triglyceride levels can be seen with an O3FA regimen of 3–4 g/day [3]. However, cases refractory to diet, O3FA, and gemfibrozil may necessitate the use of fenofibrate. Use of insulin in the present case could have contributed to the low triglyceride levels achieved because insulin is reported to potentiate the activity of lipoprotein lipase [4]. The use of gemfibrozil and fenofibrate—which are US Food and Drug Administration category C drugs (indicating animal studies with adverse fetal effects but no wellcontrolled human studies)—is limited in the pregnant population. Pregnant women with hypertriglyceridemia managed with a lowfat diet and O3FA may show improved triglyceride control with fenofibrate in place of gemfibrozil. Conflict of interest The authors have no conflicts of interest. References [1] Kulkarni A, Downes E, Crook M. Successful outcome of pregnancy in a patient with familial hypertriglyceridaemia. J Obstet Gynaecol 2006;26(1):66–7. [2] Glueck CJ, Streicher P, Wang P, Sprecher D, Falko JM. Treatment of severe familial hypertriglyceridemia during pregnancy with very-low-fat diet and n-3 fatty acids. Nutrition 1996;12(3):202–5. [3] Miller M. Current perspectives on the management of hypertriglyceridemia. Am Heart J 2000;140(2):232–40. [4] Ewald N, Hardt PD, Kloer HU. Severe hypertriglyceridemia and pancreatitis: presentation and management. Curr Opin Lipidol 2009;20(6):497–504.
0020-7292/$ – see front matter © 2014 International Federation of Gynecology and Obstetrics. Published by Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijgo.2013.11.004
Prevalence of polycystic ovary syndrome among fertile and infertile women in Minia Governorate, Egypt Ahmad S. Sanad ⁎ Department of Gynaecology and Obstetrics, Faculty of Medicine, Minia University, El-Minia, Egypt
a r t i c l e
i n f o
Article history: Received 7 February 2013 Received in revised form 13 September 2013 Accepted 9 December 2013 Keywords: Anovulation Free testosterone Hirsutism Polycystic ovary syndrome Prevalence
There is evidence that the prevalence of polycystic ovary syndrome (PCOS) is higher in populations with increased risk of insulin resistance and metabolic disease [1]. Women with PCOS most frequently present with infertility, menstrual irregularity, hirsutism, and/or other external signs of androgen excess (e.g. acne and alopecia). There is strong
⁎ Department of Gynaecology and Obstetrics, Faculty of Medicine, Minia University, El-Minia 61111, Egypt. Tel.: +20 1000222994. E-mail address: [email protected].
evidence that women with PCOS may also experience type II diabetes and cardiovascular disease, so early diagnosis and management are important. Furthermore, some studies have concluded that women with PCOS are at increased risk of obstructive sleep apnea, depression, non-alcoholic fatty liver disease, and some cancers [2]. The aim of the present study was to estimate the prevalence of PCOS in fertile and infertile women in El-Minia, Egypt. A cross-sectional observational study was conducted involving 1450 women visiting the outpatient clinic of Minia University Maternity Hospital between January 1, 2010, and April 1, 2011. Patients were classified into group 1 (n = 620; middle-aged fertile women with an intrauterine contraceptive device who gave birth more than 2 years previously) or group 2 (n = 830; all women who presented to the clinic with primary or secondary infertility). All women underwent clinical examinations, in which body weight and height were measured. Features of hyperandrogenism such as hirsutism, acne, or androgenic alopecia were looked for. All women in both groups underwent transvaginal ultrasound of the ovaries on the second or third day of their spontaneous or progesterone-induced menstrual cycles. Venous blood samples were obtained from women with clinical features of hyperandrogenism (n = 336). Using the Rotterdam diagnostic criteria, PCOS was defined by the presence of at least 2 of the following: menstrual disorders; polycystic ovaries; and clinical and/or biochemical hyperandrogenism.
82
BRIEF COMMUNICATIONS
Table 1 Characteristics of the study population.a Characteristic
Group 1 (n = 620)b
Group 2 (n = 830)c
P value
Age, y Parity Weight, kg Height, cm Body mass indexd Oligo-ovulation or anovulation Hirsutism Free testosterone, pmol/Le Polycystic ovaries Polycystic ovary syndrome
28.2 ± 4.8 (20–37) 2.5 ± 2 (1–7) 56.31 ± 11.28 (49–112) 161.78 ± 6.04 (140–177) 26.2 ± 3.4 (22.5–36.6) 83 (13.4) 73 (11.8) 49 ± 7.7 (18–60) 85 (13.7) 87 (14.0)
25.3 ± 5.1 (18–35) 0.8 ± 0.5 (0–2) 67.43 ± 10.43 (45–122) 166.23 ± 5.32 (143–175) 25 ± 3.9 (19.5–37.6) 308 (37.1) 263 (31.7) 51 ± 9.6 (20–63) 292 (35.2) 311 (37.5)
b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 0.0657f b0.001 b0.001
a b c d e f
Values are given as mean ± SD (range) or number (percentage) unless otherwise indicated. Fertile group. Infertile group. Calculated as weight in kilograms divided by the square of height in meters. Determined for patients with hirsutism only. t test with unequal variance.
Hirsutism—the clinical assessment of which is subjective—was defined by the growth of coarse dark hair in areas without hair or in which fine hair typically grows, taking a male pattern distribution (above the lip and on the chin, chest, abdomen, and back). Polycystic ovaries were identified using vaginal ultrasound in the follicular phase or when hormonal assessment revealed no follicular activity. Confirmation of polycystic ovaries required at least 12 follicles with a diameter of 2–9 mm or increased ovarian volume (10 cm) in at least 1 ovary. Statistical calculations were performed with SPSS version 16 (IBM, Armonk, NY, USA). Comparison of quantitative variables between the groups was carried out via Mann–Whitney U test for independent samples. The χ2 test was used to compare categorical data. P b 0.05 was considered to be statistically significant. The prevalence of PCOS in group 1 was 14% (87/620), compared with 37.5% (311/830) in group 2 (Table 1). In group 2, 73.3% (228/ 311) of women with PCOS experienced ovulation disorders, 60.4% (188/311) had hirsutism, and 79.4% (247/311) had polycystic ovaries. In group 1, 16.4% (12/73) of women who presented with hirsutism had normal free testosterone levels and were diagnosed with idiopathic hirsutism. In group 2, 11.4% (30/263) of women who presented with hirsutism had normal free testosterone levels and were diagnosed as having idiopathic hirsutism. Worldwide, the reported prevalence of PCOS varies between 2.2% and 26% [3]. The prevalence of PCOS—determined using Rotterdam diagnostic criteria—was reported to be 17.8% among 978 South Australian women in a retrospective birth cohort study [4]. It is clear that the prevalence of PCOS depends on the recruitment process for the study population and the criteria used for its definition; it has been reported that use of the Rotterdam diagnostic criteria doubles the reported prevalence compared with the NIH criteria [5].
In the fertile group, 14% of women had a complete picture of PCOS but confusing questions about their health complications, past reproductive history, future reproductive performance, and future fertility. Polycystic ovary syndrome is a functional disorder that does not depend on the presence of polycystic ovaries, and the absence of polycystic ovary morphology does not exclude a PCOS diagnosis. Polycystic ovary syndrome represents a major health and reproductive problem in women of reproductive age in Egypt. Conflict of interest The author has no conflicts of interest. References [1] Zhang HY, Zhu FF, Xiong J, Shi XB, Fu SX. Characteristics of different phenotypes of polycystic ovary syndrome based on the Rotterdam criteria in a large-scale Chinese population. BJOG 2009;116(12):1633–9. [2] Cerda C, Pérez-Ayuso RM, Riquelme A, Soza A, Villaseca P, Sir-Petermann T, et al. Nonalcoholic fatty liver disease in women with polycystic ovary syndrome. J Hepatol 2007;47(3):412–7. [3] Tehrani FR, Simbar M, Tohidi M, Hosseinpanah F, Azizi F. The prevalence of polycystic ovary syndrome in a community sample of Iranian population: Iranian PCOS prevalence study. Reprod Biol Endocrinol 2011;9:39. [4] March WA, Moore VM, Willson KJ, Phillips DI, Norman RJ, Davies MJ. The prevalence of polycystic ovary syndrome in a community sample assessed under contrasting diagnostic criteria. Hum Reprod 2010;25(2):544–51. [5] Kumarapeli V, Seneviratne Rde A, Wijeyaratne CN, Yapa RM, Dodampahala SH. A simple screening approach for assessing community prevalence and phenotype of polycystic ovary syndrome in a semi-urban population in Sri Lanka. Am J Epidemiol 2008;168(3):321–8.
0020-7292/$ – see front matter © 2013 International Federation of Gynecology and Obstetrics. Published by Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijgo.2013.09.025
A 21-year-old Hispanic woman (gravida 1, para 0) with a spontaneously conceived singleton pregnancy was admitted at 7 weeks of gestation for glucose control. Four weeks earlier, she had been diagnosed with acute pancreatitis (triglyceride 1580 mg/dL). Past medical history consisted of familial hypertriglyceridemia, hypertension, gastroesophageal reflux, pregestational diabetes, and polycystic ovary syndrome. She was taking fenofibrate (discontinued upon admission), niacin, omega-3 fatty acids (O3FA), metformin, omeprazole, and insulin. The patient was discharged 2 days later, after insulin adjustments, on a low-fat diet (20% of daily calories). Thereafter, triglyceride levels were monitored every other week; levels and interventions are shown in Table 1. At 29 weeks of pregnancy, the woman developed severe preeclampsia with persistent symptoms, necessitating delivery at 31 weeks. After failed labor induction, a male fetus (1950 g; 1-minute Apgar score 8; 5-minute Apgar score 8) was delivered via cesarean. Neonatal triglyceride levels were assessed at random on days 3 and 13 of life (66 and 56 mg/dL, respectively [normal range, 10–140 mg/dL]). The patient was discharged on postoperative day 2 in stable condition and prescribed fenofibrate, O3FA, metformin, enalapril, and insulin. Hypertriglyceridemia commonly worsens during pregnancy because of physiological elevation of lipids, thus increasing the risk of organ injury secondary to profoundly elevated triglyceride levels. Mortality rates among patients with acute pancreatitis during pregnancy and known familial hypertriglyceridemia have been reported to be as high as 20%–30% [1]. General concern for acute pancreatitis begins when triglyceride levels reach 1000 mg/dL. Plasmapheresis has been used in pregnant women with acute pancreatitis associated with spontaneous abortion and preterm delivery. Glueck et al. [2] reported 2 pregnancies in a single patient
81
with familial hypertriglyceridemia treated solely with O3FA; the patient’s triglyceride levels were never below 1000 mg/dL, despite the O3FA dose being increased in the second pregnancy. A 25%–30% reduction in triglyceride levels can be seen with an O3FA regimen of 3–4 g/day [3]. However, cases refractory to diet, O3FA, and gemfibrozil may necessitate the use of fenofibrate. Use of insulin in the present case could have contributed to the low triglyceride levels achieved because insulin is reported to potentiate the activity of lipoprotein lipase [4]. The use of gemfibrozil and fenofibrate—which are US Food and Drug Administration category C drugs (indicating animal studies with adverse fetal effects but no wellcontrolled human studies)—is limited in the pregnant population. Pregnant women with hypertriglyceridemia managed with a lowfat diet and O3FA may show improved triglyceride control with fenofibrate in place of gemfibrozil. Conflict of interest The authors have no conflicts of interest. References [1] Kulkarni A, Downes E, Crook M. Successful outcome of pregnancy in a patient with familial hypertriglyceridaemia. J Obstet Gynaecol 2006;26(1):66–7. [2] Glueck CJ, Streicher P, Wang P, Sprecher D, Falko JM. Treatment of severe familial hypertriglyceridemia during pregnancy with very-low-fat diet and n-3 fatty acids. Nutrition 1996;12(3):202–5. [3] Miller M. Current perspectives on the management of hypertriglyceridemia. Am Heart J 2000;140(2):232–40. [4] Ewald N, Hardt PD, Kloer HU. Severe hypertriglyceridemia and pancreatitis: presentation and management. Curr Opin Lipidol 2009;20(6):497–504.
0020-7292/$ – see front matter © 2014 International Federation of Gynecology and Obstetrics. Published by Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijgo.2013.11.004
Prevalence of polycystic ovary syndrome among fertile and infertile women in Minia Governorate, Egypt Ahmad S. Sanad ⁎ Department of Gynaecology and Obstetrics, Faculty of Medicine, Minia University, El-Minia, Egypt
a r t i c l e
i n f o
Article history: Received 7 February 2013 Received in revised form 13 September 2013 Accepted 9 December 2013 Keywords: Anovulation Free testosterone Hirsutism Polycystic ovary syndrome Prevalence
There is evidence that the prevalence of polycystic ovary syndrome (PCOS) is higher in populations with increased risk of insulin resistance and metabolic disease [1]. Women with PCOS most frequently present with infertility, menstrual irregularity, hirsutism, and/or other external signs of androgen excess (e.g. acne and alopecia). There is strong
⁎ Department of Gynaecology and Obstetrics, Faculty of Medicine, Minia University, El-Minia 61111, Egypt. Tel.: +20 1000222994. E-mail address: [email protected].
evidence that women with PCOS may also experience type II diabetes and cardiovascular disease, so early diagnosis and management are important. Furthermore, some studies have concluded that women with PCOS are at increased risk of obstructive sleep apnea, depression, non-alcoholic fatty liver disease, and some cancers [2]. The aim of the present study was to estimate the prevalence of PCOS in fertile and infertile women in El-Minia, Egypt. A cross-sectional observational study was conducted involving 1450 women visiting the outpatient clinic of Minia University Maternity Hospital between January 1, 2010, and April 1, 2011. Patients were classified into group 1 (n = 620; middle-aged fertile women with an intrauterine contraceptive device who gave birth more than 2 years previously) or group 2 (n = 830; all women who presented to the clinic with primary or secondary infertility). All women underwent clinical examinations, in which body weight and height were measured. Features of hyperandrogenism such as hirsutism, acne, or androgenic alopecia were looked for. All women in both groups underwent transvaginal ultrasound of the ovaries on the second or third day of their spontaneous or progesterone-induced menstrual cycles. Venous blood samples were obtained from women with clinical features of hyperandrogenism (n = 336). Using the Rotterdam diagnostic criteria, PCOS was defined by the presence of at least 2 of the following: menstrual disorders; polycystic ovaries; and clinical and/or biochemical hyperandrogenism.
82
BRIEF COMMUNICATIONS
Table 1 Characteristics of the study population.a Characteristic
Group 1 (n = 620)b
Group 2 (n = 830)c
P value
Age, y Parity Weight, kg Height, cm Body mass indexd Oligo-ovulation or anovulation Hirsutism Free testosterone, pmol/Le Polycystic ovaries Polycystic ovary syndrome
28.2 ± 4.8 (20–37) 2.5 ± 2 (1–7) 56.31 ± 11.28 (49–112) 161.78 ± 6.04 (140–177) 26.2 ± 3.4 (22.5–36.6) 83 (13.4) 73 (11.8) 49 ± 7.7 (18–60) 85 (13.7) 87 (14.0)
25.3 ± 5.1 (18–35) 0.8 ± 0.5 (0–2) 67.43 ± 10.43 (45–122) 166.23 ± 5.32 (143–175) 25 ± 3.9 (19.5–37.6) 308 (37.1) 263 (31.7) 51 ± 9.6 (20–63) 292 (35.2) 311 (37.5)
b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 0.0657f b0.001 b0.001
a b c d e f
Values are given as mean ± SD (range) or number (percentage) unless otherwise indicated. Fertile group. Infertile group. Calculated as weight in kilograms divided by the square of height in meters. Determined for patients with hirsutism only. t test with unequal variance.
Hirsutism—the clinical assessment of which is subjective—was defined by the growth of coarse dark hair in areas without hair or in which fine hair typically grows, taking a male pattern distribution (above the lip and on the chin, chest, abdomen, and back). Polycystic ovaries were identified using vaginal ultrasound in the follicular phase or when hormonal assessment revealed no follicular activity. Confirmation of polycystic ovaries required at least 12 follicles with a diameter of 2–9 mm or increased ovarian volume (10 cm) in at least 1 ovary. Statistical calculations were performed with SPSS version 16 (IBM, Armonk, NY, USA). Comparison of quantitative variables between the groups was carried out via Mann–Whitney U test for independent samples. The χ2 test was used to compare categorical data. P b 0.05 was considered to be statistically significant. The prevalence of PCOS in group 1 was 14% (87/620), compared with 37.5% (311/830) in group 2 (Table 1). In group 2, 73.3% (228/ 311) of women with PCOS experienced ovulation disorders, 60.4% (188/311) had hirsutism, and 79.4% (247/311) had polycystic ovaries. In group 1, 16.4% (12/73) of women who presented with hirsutism had normal free testosterone levels and were diagnosed with idiopathic hirsutism. In group 2, 11.4% (30/263) of women who presented with hirsutism had normal free testosterone levels and were diagnosed as having idiopathic hirsutism. Worldwide, the reported prevalence of PCOS varies between 2.2% and 26% [3]. The prevalence of PCOS—determined using Rotterdam diagnostic criteria—was reported to be 17.8% among 978 South Australian women in a retrospective birth cohort study [4]. It is clear that the prevalence of PCOS depends on the recruitment process for the study population and the criteria used for its definition; it has been reported that use of the Rotterdam diagnostic criteria doubles the reported prevalence compared with the NIH criteria [5].
In the fertile group, 14% of women had a complete picture of PCOS but confusing questions about their health complications, past reproductive history, future reproductive performance, and future fertility. Polycystic ovary syndrome is a functional disorder that does not depend on the presence of polycystic ovaries, and the absence of polycystic ovary morphology does not exclude a PCOS diagnosis. Polycystic ovary syndrome represents a major health and reproductive problem in women of reproductive age in Egypt. Conflict of interest The author has no conflicts of interest. References [1] Zhang HY, Zhu FF, Xiong J, Shi XB, Fu SX. Characteristics of different phenotypes of polycystic ovary syndrome based on the Rotterdam criteria in a large-scale Chinese population. BJOG 2009;116(12):1633–9. [2] Cerda C, Pérez-Ayuso RM, Riquelme A, Soza A, Villaseca P, Sir-Petermann T, et al. Nonalcoholic fatty liver disease in women with polycystic ovary syndrome. J Hepatol 2007;47(3):412–7. [3] Tehrani FR, Simbar M, Tohidi M, Hosseinpanah F, Azizi F. The prevalence of polycystic ovary syndrome in a community sample of Iranian population: Iranian PCOS prevalence study. Reprod Biol Endocrinol 2011;9:39. [4] March WA, Moore VM, Willson KJ, Phillips DI, Norman RJ, Davies MJ. The prevalence of polycystic ovary syndrome in a community sample assessed under contrasting diagnostic criteria. Hum Reprod 2010;25(2):544–51. [5] Kumarapeli V, Seneviratne Rde A, Wijeyaratne CN, Yapa RM, Dodampahala SH. A simple screening approach for assessing community prevalence and phenotype of polycystic ovary syndrome in a semi-urban population in Sri Lanka. Am J Epidemiol 2008;168(3):321–8.
0020-7292/$ – see front matter © 2013 International Federation of Gynecology and Obstetrics. Published by Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijgo.2013.09.025
