Introduction

Polycystic ovarian syndrome (PCOS) is the most common metabolic and endocrine disorders in women of reproductive age group. It is the first leading cause of infertility in females with incidence of 5-10%.1

The cause of polycystic ovarian syndrome is indefinite but a few genetic factors triggered by certain environmental and behavioral factors have been suggested in various reports.2 In some studies, insulin resistance secondary to obesity is strongly correlated to PCOS as causal factor.3

Insulin resistance plays a key role in pathophysiology of polycystic ovarian syndrome by stimulating lipolysis and alteration of hepatic lipase and lipoprotein lipase. 4

In PCOS subjects there is relative inadequacy of insulin receptors binding to insulin which causes inappropriate transfer of glucose to intracellular compartment and this lead to relative hyperglycemia, despite raised insulin producing beta cells.1

Dyslipidemia is most common malformation seen in most of PCOS women characterized by lower levels of high density lipoproteins and high triglycerides. In PCOS the causes for dyslipidemia are multi-factorial and this altered lipid profile is a crucial risk element for progression of cardiovascular pathology in women with PCOS.5

The clinical diagnosis of PCOS was rested on trio of amenorrhea, obesity and hirsuitism in earlier studies.6 As per Rotterdam criteria (2003) the diagnosis of PCOS is defined by the presence of any two of the following three criteria i) Chronic oligo or anovulation. ii) Polycystic ovaries by ultrasonography with exclusion of other related disorders. iii) Clinical or biochemical signs of hyperandrogenism.1, 5

Women with PCOS are often obese and at increased risk of developing diabetes mellitus and cardiovascular diseases. With this background the present study was undertaken to study lipid profile in polycystic ovarian syndrome women in order to anticipate early diagnosis of complications and its management.

Materials and Methods

This observational study was carried out over a period of six months from November 2019 to April 2020 at Department of Biochemistry in association with Department of Gynecology of a tertiary care hospital after approval of Ethics Committee.

The present study included 60 diagnosed PCOS women in the age group of 16-40 years.

Women under treatment of diabetes mellitus, renal diseases, thyroid disorders, hypertension, cardiovascular diseases, pregnant or lactating women, women on drugs like oral contraceptives or lipid lowering drugs, hypoglycemic agents and on hormonal medicines within six weeks were excluded from the study.

An appropriate informed consent from the patient was taken.

After overnight fasting, the blood samples were collected in plain and fluoride bulbs for analysis. Fasting plasma glucose was measured by GOD POD method by semiautoanalyser. Serum fasting insulin was measured by chemiluminescence immunoassay in Maglumi 800.Lipid profile (TC, TG and HDL) was done on fully automatic Meril 400 biochemistry analyzer. LDL was calculated from TC, TG and HDL cholesterol as per Friedewald calculation.1

LDL cholesterol = Total cholesterol – HDL cholesterol –Triglycerides/five The values were expressed in mg/dl

Adult treatment panel III considers levels of LDL below 100 mg/dl as optimal and 100 to 129 mg/dl as near optimal, TG below 150 mg/dl as normal, TC below 200 mg/dl as desirable and HDL more than or equal to 50 mg/dl as normal for women.

Dyslipidemia levels includes LDL as borderline high (130 to 150 mg/dl), high (160 to 189 mg/dl) and very high (more than or equal to 190 mg/dl) ; TG as borderline high (150 to 199 mg/dl), high (200 to 499 mg/dl) and very high (more than 500mg/dl); TC as borderline high (200 to 239 mg/dl), high (more than or equal to 240 mg/dl); HDL (below 50 mg/dl) is considered as a risk factor in women.7

Insulin resistance (IR) was calculated by using HOMA model (HOMA-IR)1 with the formula

HOMA-IR = Fasting plasma glucose (mg/dl) x Fasting serum insulin (µiu/ml)/405

If HOMA-IR > 2.7, the patient was considered to be insulin resistant.

Data was analyzed using descriptive statistics. The values were expressed as Mean ± Standard deviation. Frequency was calculated in terms of percentage. Pearson’s correlation coefficient was calculated to assess the correlation HOMA IR and lipid profile.

Observations and Results

The Table 1 shows that mean serum levels of TC, TG, LDL and HDL were 160.65 ± 24.72, 110.21 ± 28.66, 99.44 ± 21.47, and 38.76 ±4.36 respectively.

Figure 1

Showing mean values of TC, TG, LDL and HDL in PCOS women

This Table 2 shows mean level of FBG as 100.53 ±19.24, mean level of serum insulin as 14.39 ± 3.76.

Discussion

In 1935, for the first time Irving F. Stein and Michael L.Levental stated a symptom complex –polycystic ovarian syndrome. PCOS is a major public health issue now a days and the incidence is increasing because of high stress level and change in the life style. It is also becoming a very common problem in adolescents developing after puberty.20%women are attributed to anovulation caused by PCOS amongst infertile women. Some women who develop Type II diabetes, hypertension, cardiovascular disease, endometrial cancer later in life appear to have suffered from PCOS in earlier years.6 Insulin resistance is the central key point in the genesis of PCOS. Obesity is important cause of insulin resistance and compensatory hyperinsulinemia. Since the exact cause of PCOS is still not known, we cannot cure this disease completely. This syndrome can only be controlled and the symptoms can be reduced or eliminated by lifestyle modification and some effective drugs but not the pathology of it.

Altered lipid profile is very common metabolic malformation in women with PCOS. Insulin resistance is the principal pathogenesis of PCOS, thus deranged lipid profile in PCOS patient may be persistent with those found in an insulin resistant state. In PCOS women TG, LDL cholesterol levels were higher and HDL cholesterol level was on lower side.8

The mean value of serum TC in present study was 160.65±24.72 with range from 120 to 230. The mean value of serum TG level in present study was 110.21±28.66 with range from 46.32-190. The mean value of serum LDL was 99 ± 21.47 with range from 60 to 169. The findings were comparable to Koppalli S et al who reported mean value of TC, TG and LDL as 159.11 ± 26.95, 117.34 ± 33.86 and 94.66 ± 26.74, respectively.

The mean value of serum HDL level in present study was 38.76 ± 4.36 with range from 22.89 to 54. The findings were consistent with those reported by Singh G et al (2017) and Halasawadekar NR et al (2016). Singh G et al (2017) reported HDL levels of 38.16±4.838. Halasawadekar NR et al (2016) reported HDL levels of 39 ±4.7 respectively.

A deranged serum lipid in the present study was mainly in the form of decreased HDL levels. 96.67% women had lower serum HDL levels. Serum TG levels was raised in 16.6% women, serum TC level in 6.67% and serum LDL in 8.33% PCOS women in the present study.

The main reason for lowered HDL levels may be due to insulin resistance, which is seen in PCOS women. Insulin resistance results in more catabolism of HDL particles and LDL particles are formed. Cholesterol ester transfer protein may play role in this process.

PCOS is frequently associated with altered lipid profile as reported in various studies. The pattern of alteration of lipid profile is not alike in all populations. This is due to influence of age, BMI, insulin resistance, hyperandrogenism, genetics and environmental factors.9

Insulin resistance resulting in hyperinsulinemia is associated with diverse adverse effects on regulating lipid metabolism in PCOS subjects. Hyperinsulinemia appears to be a leading factor for development of cardiovascular diseases.5

Insulin plays a crucial role in triglyceride metabolism. In insulin resistant cases, insulin hormone fails to suppress synthesis of large very low density lipoprotein particles. Insulin resistance is also associated with increased flow of FFA(free fatty acid) to liver, increased synthesis of lipid in the liver and clearance of VLDL particles decreased, all these resulting in elevated concentration of VLDL in plasma and this lead to elevated plasma TG concentration. By the activity of cholesterol ester (CE) transfer protein triglycerides are transferred for cholesterol esters. The above process lead in HDL enriched with triglyceride that are catabolised rapidly and VLDL enriched with cholesterol ester converted in to LDL particle.10

Conclusion

PCOS is frequently associated with dyslipidemia. In the present study, dyslipidemia was mainly in the form of deranged serum HDL. HOMA-IR was increased in the present study which indicates presence of insulin resistance in PCOS women. Hence, the women with PCOS should be screened for lipid profile which can be helpful in assessing the risk of cardiovascular disease. Also, counseling should be conducted on routine basis of PCOS women for diet and lifestyle modification.

Source of Funding

None.

Conflict of Interest

None.