Ethnic-specific Polycystic Ovary Syndrome

Epidemiology, Significance and Implications

Chandrika N Wijeyaratne; SA Dilini Udayangani; Adam H Balen

Expert Rev Endocrinol Metab. 2013;8(1):71-79.

Abstract and Introduction

Abstract

Being the most common endocrinopathy of young women, polycystic ovary syndrome has much variation in its clinical expression based on ancestry. Ethnic differences of the phenotype are closely linked to its complex pathophysiology. This paper reviews data of the past three decades ensuring a precise diagnosis and taking into account underlying factors, effects of migration including heterogeneity, and diversity within each identified ethnic group. Differing expressions of hyperandrogenism, obesity, insulin resistance and metabolic manifestations of polycystic ovary syndrome occur among women from distinct geographic locations and ancestry. These ethnic phenotypes correlate with their inherent metabolic risks, skin sensitivity to androgens and social outlook that particularly affects their quality of life and health-seeking behavior. It is recommended that such ethnic variations are recognized in routine clinical practice and longitudinal data be maintained to study the true impact of such differences on disease outcomes.

Introduction

Polycystic ovary syndrome (PCOS), the most common endocrine problem that afflicts young women all over the world, has the potential for much variation in its clinical expression, co-morbidities and management outcomes based on ethnicity.^[1] Although from the same species, the world's populations vary in physical, behavioral and social distinctiveness based particularly on ancestry and geographic segregation. Natural selection of genes and adaptation to environmental conditions has caused these variations, which in turn impacts disease phenotype.^[2] Additionally, sociocultural differences, particularly diet, impact on chronic diseases and their health-related behavior.^[3,101] Therefore, the occurrence, manifestations and management problems of PCOS commonly encountered in clinical practice must be viewed within the context of the ethnic origin of the affected woman.

This review addresses the following on PCOS and ethnicity: how its defining characteristics (hyperandrogenism, anovulation, polycystic ovarian morphology) and subphenotypes differ among ethnic groups worldwide; how the metabolic risks differ based on ethnicity, both in their homeland and after migration to more developed countries; how the sociologic implications of its diagnosis vary among ethnic groups and countries in perceived quality-of-life, care-seeking behavior and preference for treatment modality. Standard biomedical classification of ethnic groups in the USA are black or African–American, Hispanic and non-Hispanic that includes whites and blacks, Asians, Native Hawaiian and Pacific Islanders, and American Indians or Alaskan Natives.^[101] This review of the world's populations will be on a continental basis: African, caucasian (Europe and the Middle East), Asian, Pacific Islander (Australian, New Guinean and Melanesian) and Native American.^[3,4] Nevertheless, diversity within a given continent must be taken into account, especially in Eurasia – the world's largest landmass occupied by nearly two-thirds of its population.

The study of ethnic differences of PCOS requires in-depth analysis of its epidemiology that would also help decipher its complex etiology. This ideally entails an 'accurate' diagnosis and proper classification of ethnicity.^[102] However, a gold standard definition of PCOS is not possible due to symptom heterogeneity and lack of a unique phenotype. Therefore, a pragmatic approach to the diagnosis of PCOS using standard international criteria must be applied for this purpose to ensure that comparable groups of affected women are reviewed (Table 1).^[5–7]

Furthermore, the phenotype of PCOS can vary over time in an affected woman, which is age and weight dependent. One must also be cautious to translate observed ethnic differences in small studies to reflect inherent characteristics of entire populations. Further, socioeconomic differences cause health disparities that can alter disease manifestation and complications, which must also be taken into account in the analysis.

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Table 1. Summary of international recommendations for the diagnosis of polycystic ovary syndrome in adults.
	Diagnostic criteria				Ref.
	Oligo/amenorrhea or oligo/anovulation	Hyperandrogenism or hyperandrogenaemia	PCO	Essential prerequisite
NIH conference (1990)	+	+	–	Exclude secondary causes such as hypothyroidism, hyperprolactinemia, Cushing's syndrome and other causes of hyperandrogenemia such as congenital adrenal hyperplasia, androgen-secreting tumors, medications, and so on	[5]
Rotterdam consensus^† (2003)	±	±	±		[6]
AE-PCOS^‡ (2009)	±	+	±		[7]

†Rotterdam Consensus – any combination of two criteria (includes nonhyperadnrogenic and ovulatory groups).
‡AEPCOS Criteria – hyperandrogenism and one other criterion (recognizes PCO).
+ mandatory; – not a criterion; ± may or may not be present.
AE-PCOS: Androgen Excess and Polycystic Ovary Syndrome Society; PCO: Polycystic ovary on ultrasound.

Table 2. Summary of phenotypic variations of polycystic ovary syndrome among distinct ethnic groups.
Ethnic group/geographic region	Key phenotypic variations	Ref.
Asian
East Asian (Japanese, Chinese, Taiwanese, Korean)	Japanese low BMI (<25 kg/m²); less hirsute Chinese – age 25 years; BMI 22 kg/m2; FG = 3; PCO 96%; MetS 22–28%Taiwanese – age 26 years; BMI 28 kg/m2; acanthosis 31%; AGT 42% BMI better predictor of IR than testosterone. No major difference in insulin sensitivity between phenotypes Southern Chinese – community prevalence 2% (Rotterdam) USA based – 'milder phenotype', short stature; MetS 50%	[11,21,36,52,58,62,63]
South Asian (Sri Lankan, Indian, Pakistani)	Mean BMI 26 kg/m²; >central obesity; greater risk of diabetes Severe symptoms at younger age (25 years) than white Europeans; lower SHBG; greater IR than caucasians; MetS 30%; similar prevalence of MetS among phenotypes Acanthosis nigricans ++; family history of T2DM common Pakistanis more hirsute than Sri Lankans/south Indians Sri Lankan – community prevalence 6.3% (Rotterdam) Migrant south Asians – greater insulin response to oral glucose PCO prevalence 52 vs 20–33% (white caucasians) Infertility, rather than obesity, affects their QoL	[8,9,13,14,18,46]
Southeast Asian (Thai, Singaporean, Malay)	Mean BMI ~27 kg/m²; mean age 27 years MetS 35%; AGT in 42% Acanthosis nigricans important predictor Thai – community prevalence 5% (Rotterdam)	[22,23,53]
*White European (caucasian)*
Hispanic:	MetS 31% (USA)	[25]
∂ Caribbean	>IR than non-Hispanic blacks and whites; PCOS has an additive effect	[12]
∂ Mexican	>IR 73 vs 44% in whites	[15,64,65]
∂ American	Greater prevalence (13%) ∂ (selected population)
North European:	Mean BMI 35 kg/m²; mean age 32 years; less insulin resistant; SHBG higher
∂ UK, Dutch, Icelandic	PCO prevalence 20∂33%; PCOS (Rotterdam) ~8%	[9,14,48,54]
∂ USA (non-Hispanic)	Caucasians taller; Icelandics less hirsute	[21,26,62]
	MetS 43% (NIH criteria) PCOS; BMI 35.2 kg/m²
	Mean age 28 years; PCO in 90%
Mediterranean:	MetS and AGT ~20∂24%; HA in 10%	[38]
∂ Greek, Turkish	Prevalence 6.8% (NIH criteria)	[37]
	Hirsutism marked 88% FG = 13; IR greater
South European:	BMI 30∂35 kg/m², AGT 25%; hirsutism FG = 8 (71%); MetS	[11,39]
∂ Italian, Spanish	Prevalence 6.5% (NIH criteria)
East European:	Hirsutism not marked; MetS less prevalent	[44]
∂ Chez	IGT in 12%; higher CVD risk than matched controls
∂ South American Brazilian	MetS in 31%; indicators of central obesity (waist circumference and waist-to-height ratio) were accurate predictors of MetS; frequency of MetS similar in the phenotypes	[47]
*Middle Eastern (caucasian)*
Arab	Overweight/obesity in 79%; BMI >30 kg/m² in 51%
∂ Iranian, Saudi Arabian	Similar prevalence of MetS among phenotypes	[48∂51]
∂ Migrants (Canada and Austria)	High insulin response to glucose; infertility, rather than their obesity, affecting QoL	[51,61]
*African origin*
American black	More obese than whites; more hypertension than T2DM; central obesity, IR, elevated TG; MetS 26% (less than Asians and Hispanics); community prevalence similar to white Europeans	[25,28,55]
*Native indigenous groups*
New Zealand, Indian, Maori, Pacific Islanders	>BMI, IR, SBP; lower SHBG; less perception of obesity; infertility more common Birth cohort prevalence Australia 11% (Rotterdam)	[24,27,56]
Alaskans, Pacific Islanders	Higher rate of obesity and MetS than caucasians	[27]

AGT: Abnormal glucose tolerance (includes impaired fasting glucose, impaired glucose tolerance or IGT, frank diabetes); IR: Insulin resistance quantified by validated mathematical formulae using fasting plasma glucose and insulin; MetS: Metabolic syndrome; QoL: Quality of life; SBP: Systolic blood pressure; SHBG: Sex hormone-binding globulin.

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Ethnic-specific Polycystic Ovary Syndrome

Epidemiology, Significance and Implications

Abstract and Introduction

Abstract

Introduction

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