Evaluation of metabolic, hormonal and clinical parameters in different phenotypes of polycystic ovary syndrome: an observational study from a tertiary care centre in Eastern India

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Introduction
Polycystic ovary syndrome (PCOS) is most common endocrine
abnormality in women of reproductive age. Several studies of
diverse populations have estimated its prevalence at 6%-10%.1‒2
They described a constellation of amenorrhea, oligomenorrhea,
obesity and hirsutism in presence of polycystic ovary.3 The disorder
has since been known as PCOS, although considerable changes
in its denition and path physiology have occurred. The endocrine
abnormalities in PCOS include hyperandrogenism of ovarian and/
or adrenal origin, which vary in clinical presentation, leading to
arrested follicular development and consequently an ovulation and
polycystic ovarian morphology. The majority of women with PCOS
have increased luteinizing hormone (LH) secretion further worsening
the hyperandrogenemic. Metabolic characteristics of PCOS include
central adiposity and hyperinsulinemia with consequential insulin
resistance further exacerbating hyperandrogenism. Endocrine and
metabolic abnormalities seen in PCOS may vary among affected
women, thus creating a heterogeneous biochemical and clinical
phenotype producing difculties in establishing a diagnosis. Most
patients with PCOS have metabolic abnormalities such as insulin
resistance with compensatory hyperinsulinemia, obesity, and
dyslipidemia. All of these metabolic features may play a role in the
development of glucose intolerance or type 2 diabetes mellitus and
hypertension, thereby increasing risk of cardiovascular diseases.4
However, it is important to note that an attempt to generalize data
obtained from any single ethnic group should be approached with
caution. Although a true prevalence study would survey a community,
our tertiary care centre represents a reference centre for women with
all types of menstrual irregularities and clinical signs of androgen
excess, hence this study could be a representative sample of the
Eastern Indian population. As a result, the aim of this study was to
report the relative prevalence of all four Rotterdam PCOS phenotypes
in a tertiary care setting and compare all phenotypes for clinical,
hormonal, and metabolic differences.
J Diabetes Metab Disord Control. 2018;5(6):195‒200. 195
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Evaluation of metabolic, hormonal and clinical
parameters in different phenotypes of polycystic
ovary syndrome: an observational study from a
tertiary care centre in Eastern India
Volume 5 Issue 6 - 2018
Devarbhavi Praveen,1 Maiti Animesh,1 Swar
Subir Chandra,1 Sinha Anirban,1 Basu Asish
Kumar,1 Bhattacharjee Kingshuk,2
1Department of Endocrinology & Metabolism, Medical College
& Hospital, India
2Medical Sciences, JJT University, India
Correspondence: Praveen Devarbhavi, Department of
Endocrinology & Metabolism, Medical College & Hospital, India,
Tel +91 9986108182 Email praveen.devavbhavi@gmail.com
Received: August 06, 2018 | Published: November 06, 2018
Abstract
Aim and Objective: To evaluate the metabolic, hormonal and clinical proles of
adolescents and young women of polycystic ovary syndrome (PCOS).
Materials and Methods: An Observational cross-sectional study was carried out in the
department of Endocrinology and metabolism, Medical College, Kolkata. We included 120
patients of PCOS, diagnosed according to Rotterdam criteria 2003, in the age group of 16
to 40 years.
Results: All phenotypes of PCOS had higher BMI with respect to controls (P<0.05). Among
hyperandrogenemic phenotypes, hirsutism was more common in anovulatory classic
phenotypes A (92%) and B (87.5%) than ovulatory phenotype C (14.2%). However, all
phenotypes had signicantly higher testosterone level than control. Normo-androgenemic
phenotype D had mean testosterone signicantly higher (p<0.001) than control. LH and
LH/FSH ratio was highest in classical phenotype A followed by phenotype B than newer
phenotypes C and D, all being signicantly higher than controls. Total cholesterol was
signicantly higher in phenotype A (172.62± 28.48mg/dl) than control (150.22± 18.3mg/
dl). Phenotype A, C and D had signicantly lower (p<0.05) HDL cholesterol and higher
(p>0.05) triglyceride than control. Phenotype B had HDL and triglyceride similar to
control. LDL was high in phenotype A compared to control (p<0.001). Mean FPG was
higher in phenotype A and D being 91.17±10.51 and 92.1±14.51 respectively, which were
signicantly higher (p<0.05) than control. Insulin resistance by HOMA-IR in phenotype
A, B, C, D and control are 3.98 ± 2.26, 2.73±1.79, 2.34 ±0.89, 3.35±0.98 and 1.29±0.98
respectively. Prevalence of metabolic syndrome was highest in phenotype A (52.83%). All
phenotypes had higher prevalence of metabolic syndrome than controls.
Conclusion: Phenotype A represents the most common and severe form of PCOS. This group
presented with higher modied FG score, more severe biochemical hyperandrogenemic and
increased levels of LH and LH/FSH ratio than rest of the sub-groups. Metabolic aberrations
were greatest for phenotype A with abdominal obesity, elevated insulin and insulin
resistance, higher prevalence of impaired glucose tolerance, atherogenic dyslipidemia.
Journal of Diabetes, Metabolic Disorders & Control
Research Article Open Access

Evaluation of metabolic, hormonal and clinical parameters in different phenotypes of polycystic ovary
syndrome: an observational study from a tertiary care centre in Eastern India 196
Copyright:
©2018 Praveen et al.
Citation: Praveen D, Animesh M, Chandra SS, et al. Evaluation of metabolic, hormonal and clinical parameters in different phenotypes of polycystic ovary
syndrome: an observational study from a tertiary care centre in Eastern India. J Diabetes Metab Disord Control. 2018;5(6):195‒200.
DOI: 10.15406/jdmdc.2018.05.00164
Materials and methods
Observational, cross-sectional single centred study performed in
adolescent girls and young women of reproductive age group between
16 to 40 years attending the department of Endocrinology, diagnosed
to have PCOS by Rotterdam criteria 2003. A total of 120 patients were
recruited consecutively for the study. 32 healthy age matched women
with normal menstrual cycles and without clinical or biochemical
evidence of hyperandrogenism were recruited as controls. These
patients were divided in to four phenotypes based on Rotterdam
criteria 2003.
I. Classic PCOS (H+O+P); phenotype A
II. Classic PCOS but normal ovaries (H+O); phenotype B
III. Ovulatory PCOS (H+P) phenotype C
IV. Norm androgenic PCOS (O+P) phenotype D
Then various clinical metabolic and hormonal proles are studied
in these populations.
A pre-specied proforma was used for obtaining demographic and
clinical features. Clinical evaluation of each patient comprised of a
thorough menstrual, obstetrics, personal, past, family history followed
by complete physical examination. Hirsutism was assessed by
Ferriman–Galway (FG) score≥8 or elevated serum total testosterone
(TT)≥60ng/dL. Pelvic Ultrasonography was performed to assess
ovarian morphology including size, echogenicity, stromal thickness,
number and distribution of the cyst typical of PCOM and ovarian
volume of each ovary. History of depression was assessed by validated
Patient Health Questionnaire 2(PHQ-2).5 Physical examination
included anthropometric data namely weight, height, BMI, waist
circumference, hip circumference. Presence and distribution of acne
(Grade 1 to 4) and acanthosis nigricans (grade 1 to 4) were assessed.6
Statistical methods
In the statistical analysis of our study, Continuous variables were
presented as mean for parametric data and median if the data is non-
parametric or skewed. Student t test was applied for calculation
of statistical signicance whenever the data followed normative
distribution. Mann-Whitney test was applied whenever data followed
non normative distribution. A categorical variable was expressed as
frequencies and percentages. Nominal categorical data between the
groups was compared using Chi-square test or Fisher’s exact test as
appropriate. Analysis of variance (ANOVA) or kruskal-wallis test
with multiple comparisons. Correlation coefcient was assessed
by Pearson’s correlation test depending on the distribution of data.
Multivariate logistic regression analysis was carried out to identify
the predictors of outcome (for binary variables) P<0.05 was taken to
indicate a statistically signicant difference. Minitab version 17 was
used for computation of statistics.
Observations and results
CLINICAL PROFILE: Clinical prole of all phenotypes of
PCOS and controls is given in Table 1. Most prevalent phenotype
in our study was phenotype A (44.16%) followed by Phenotype
D (25%), phenotype C(17.5%) and phenotype B(13.3%). Waist
circumference was higher in Phenotype A and D with mean WC of
88.08±8.68 and 88.97±7.23 cm respectively than phenotype B and
C. Hirsutism was more common in anovulatory classic phenotypes
A(92%) and B (87.5%) than ovulatory phenotype C (14.2%) among
hyperandrogenemic phenotypes. Phenotype A had more severe
hirsutism among all phenotypes( FG score 12.96±3.69) followed
by phenotype B(FG -11.38±4.03) which was signicantly higher
than ovulatory phenotype C. FG score of phenotype D was similar
to control. Blood pressure among all phenotypes was similar to
control except systolic BP of phenotype B which was signicantly
higher compared to other phenotypes and control. Depression was
signicantly higher among hyperandrogenemic PCOS phenotypes
(35.85% in A, 31.25% in B and 66.67% in C) than norm androgenic
phenotype D (6.67% with P<0.05). Snoring and features of sleep
apnea were higher among all phenotypes compared to control. Forty
percent of phenotype D demonstrated snoring with higher BMI and
WC than other phenotypes.
Table 1 Clinical prole of all phenotypes of PCOS and controls
Variables
Phenotype A
(P+H+O)
N=53
Phenotype B
(H+O)
N=16
Phenotype C
(H+P)
N=21
Phenotype D
(P+O)
N=30
Control
N=32
Number of Individuals (%) 44.16% 13.33% 17.50% 25%
Age in years 23.08 ± 3.93 25.5 ± 4.47 25.62 ± 6.09 24.1 ± 5.62 24.78 ± 5.62
BMI(Kg/m2) 26.51 ± 4 27.42 ± 6.14 25.08 ± 4.12 26.69 ± 2.57 22.16 ± 2.57
Infertility in married 17 (32.08%) 8 (50%) 16(76.19%) 18 (60%) 5 (15.63%)
m FG Score 12.96 ± 3.69 11.38 ± 4.03 4.1 ± 3.83 2.66 ± 1.48 2.47 ± 1.48
Hirsutism(mFG>8) 49 (92.45%) 14 (87.5%) 3 (14.29%) 0 (0%) 0 (0%)
Anxiety 22 (41.51%) 10 (62.5%) 13 (61.9%) 12 (40%) 2 (6.25%)
Depression-PHQ2 score>3 19 (35.85%) 5 (31.25%) 14 (66.67%) 2 (6.67%) 4 (12.5%)
Snoring 6 (11.32%) 3 (18.75%) 2 (9.52%) 12 (40%) 0 (0%)
Acanthosis 39 (73.58 %) 6 (37.5 %) 14 (66.67 %) 16 ( 53.33 % 8 (25 %)
SBP 114.68 ± 8.7 123.25±13.68 109.9±5.95 117.93±11.47 114.06±11.47
DBP 78.26 ± 8.15 78.88 ± 8.2 71.43±4.34 74.48 ± 9.21 75.13 ± 9.21

Evaluation of metabolic, hormonal and clinical parameters in different phenotypes of polycystic ovary
syndrome: an observational study from a tertiary care centre in Eastern India 197
Copyright:
©2018 Praveen et al.
Citation: Praveen D, Animesh M, Chandra SS, et al. Evaluation of metabolic, hormonal and clinical parameters in different phenotypes of polycystic ovary
syndrome: an observational study from a tertiary care centre in Eastern India. J Diabetes Metab Disord Control. 2018;5(6):195‒200.
DOI: 10.15406/jdmdc.2018.05.00164
Endocrine prole
Endocrine prole of all phenotypes of PCOS and controls is
given in Table 2.Mean Testosterone level was highest in women with
PCOS phenotype A, intermediate in phenotype B and C and lowest
in women with phenotype D. All phenotypes had signicantly high
testosterone level than control. Normoandrogenic phenotype D had
mean testosterone signicantly higher (p<0.001) than control. Similar
trend was noted with adrenal androgen DHEAS. LH and LH/FSH
ratio was highest in classical phenotype A followed by phenotype B
than newer phenotype C and D, all which were signicantly higher
than controls.
Table 2 Endocrine prole of all phenotypes of PCOS and controls
Variables
Phenotype A
(P+H+O)
N=53
Phenotype B
(H+O)
N=16
Phenotype C
(H+P)
N=21
Phenotype D
(P+O)
N=30
Control
N=32
Testosterone 79.05 ± 42.54 58.58 ± 23.51 44.5 ± 12.42 36.98 ± 10.83 26.93 ± 10.83
DHEAS 254.53 ± 89.63 229.67 ± 73.38 200.33 ± 39.91 207.83 ± 39.16 156.06 ± 39.16
LH 7.85 ± 3.88 6.7 ± 1.76 6.52 ± 1.06 4.53 ± 1.51 3.49 ± 1.51
FSH 5.99 ± 3.17 5.03 ± 1.75 6.31 ± 1.11 4.02 ± 1.84 4.78 ± 1.84
LH/FSH 1.74 ± 0.83 1.55 ± 0.5 1.4 ± 0.82 1.06 ± 0.2 0.59 ± 0.2
17OHP 1.28 ± 0.59 1.36 ± 0.7 0.94 ± 0.25 0.94 ± 0.4 1.18 ± 0.4
TSH 3.5 ± 4.29 2.11 ± 0.56 1.9 ± 1.13 2.04 ± 1.08 2.13 ± 1.08
Prolactin 12.58 ± 4.89 16.41 ± 5.79 15.35 ± 4.69 8.95 ± 4.02 12.94 ± 4.02
Metabolic prole
Lipid prole of all phenotypes of PCOS and controls is given in
Table 3. Total cholesterol was signicantly higher in phenotype A
(172.62±28.48mg/dl) than control (150.22±18.3mg.dl) . Rest of the
phenotypes did not differ from control. Phenotype A, C and D had
signicantly lower (p<0.05) HDL cholesterol and higher (p>0.05)
triglyceride than control. Phenotype B had HDL and triglyceride
similar to control. LDL was high in phenotype A compared to control
(p<0.001).
Table 3 Lipid prole of all phenotypes of PCOS and controls
Variables
Phenotype A
(P+H+O)
N=53
Phenotype B
(H+O)
N=16
Phenotype C
(H+P)
N=21
Phenotype D
(P+O)
N=30
Control
N=32
TC 172.64 ± 28.48 160.56 ± 33.43 154 ± 22.7 145.28±18.3 150.22±18.3
HDL 40.57 ± 5.38 42.5 ± 7.26 39.62 ± 6.24 35.51±6.29 46.31±6.29
LDL 102.57 ± 22.81 92.25 ± 27.07 90.6 ± 7.58 87.07±17.07 83.09±17.07
TG 139.09 ± 33.27 131.44 ± 41.18 155.48±38.78 122.55±34.33 105.69±34.33
Insulin resistance
Prole of insulin resistance of all phenotypes of PCOS and
controls is given in Table 4. Mean FPG was higher in phenotype A
and D were 91.17±10.51 and 92.1±14.51 respectively, which were
signicantly higher (p<0.05) than control. FPG of phenotype B and
C did not differ from control. Average post 75 gm glucose plasma
glucose in phenotype A (123.68±22.94) was signicantly higher than
control (103.69±14.48) with other phenotypes having similar plasma
glucose as control. Insulin resistance by HOMA-IR in phenotype A,
B, C, D and control are 3.98±2.26, 2.73±1.79, 2.34±0.89, 3.35±0.98
and 1.29±0.98 respectively. Insulin resistance was signicantly higher
in all phenotypes compared to control. Phenotype A and D exhibited
severe IR than other two phenotypes. Insulin sensitivity by QUICKI
index was lowest in Phenotype A compared to all other phenotypes.
HOMA B was signicantly lower in all PCOS phenotypes compared
to control.
Table 4 Prole of insulin resistance of all phenotypes of PCOS and controls
Variables
Phenotype A
(P+H+O)
N=53
Phenotype B
(H+O)
N=16
Phenotype C
(H+P)
N=21
Phenotype D
(P+O)
N=30
Control
N=32
FPG in mg/dl 91.17±10.51 88.23±13.98 88.81±10.58 92.1±14.51 83.72±14.51
2 hr post 75 Gm Glucose (mg/dl) 123.68±2.94 114.06±26.77 107.57±7.19 106.59±14.48 103.69±14.48
Fasting insulin µU/ml 17.3±8.61 12.17±6.46 11.14±3.41 12.71±3.24 6.12±3.24
HOMAIR 3.98±2.26 2.73±1.79 2.34±0.89 3.35±0.98 1.29±0.98
QUICKi 0.31±0.03 0.34±0.03 0.34±0.02 0.34±0.02 0.37±0.02
HOMA B 401.41±180.37 286.24±131.05 287.73±91.52 302.12±876.44 1477.25±876.44

Evaluation of metabolic, hormonal and clinical parameters in different phenotypes of polycystic ovary
syndrome: an observational study from a tertiary care centre in Eastern India 198
Copyright:
©2018 Praveen et al.
Citation: Praveen D, Animesh M, Chandra SS, et al. Evaluation of metabolic, hormonal and clinical parameters in different phenotypes of polycystic ovary
syndrome: an observational study from a tertiary care centre in Eastern India. J Diabetes Metab Disord Control. 2018;5(6):195‒200.
DOI: 10.15406/jdmdc.2018.05.00164
Metabolic syndrome
Prevalence of metabolic syndrome in different phenotypes and
control groups is given in Figure 1. There were 28, 6,8,7,4 subjects
with metabolic syndrome in PCOS phenotype A, B, C, D and
control respectively. Metabolic syndrome was highest in phenotype
A (52.83%). All phenotypes had higher prevalence of metabolic
syndrome than control subjects.
Figure 1 Prevalence of metabolic syndrome in different phenotypes and control groups.
Discussion
Present study evaluated clinical, hormonal and metabolic prole
of 120 PCOS patients. The Rotterdam criteria for women with PCOS
resulted in four phenotypes. The most common phenotype in our study
was phenotype A (H+O+P; 44.16%), followed by phenotype D (O+P;
25 %), phenotype C (H+P; 17.5 %) and phenotype B (H+O; 13.33%).
Most published studies reported phenotype A to be the most prevalent
which is similar to our study.7‒8 This phenotype is included in all
three-consensus criteria and certainly represents the basis of PCOS
diagnosis.9‒10 The prevalence of the other three phenotypes differs
between published studies across the world. Prevalence of Phenotype
A in studies from Croatian, Turkish, Bulgarian, and American
population were 56.7, 44.09, 53.6, and 60% respectively.7,11,12
Distribution of phenotypes, A, B,C,D from studies of Asian countries
like Iran was 32.1, 46.8, 14.8, and 6.3%, and Chinese was 33.2,15.2
,17.5, 34,1% respectively.13‒14 Study by S. Kar et al. from India found
distribution of phenotype A,B,C,D, to be 65.6, 11.2, 0.9, and 22.2%
respectively.15 Pikee et al.16 found most common phenotype to be
D(P+O) in a north Indian population.16 Beena joshi from Western
India found phenotype D (52.6%) to be most prevalent phenotype.17
This difference in prevalence of different phenotypes was probably
due to complex genetic, ethnic, cultural differences across different
geographic areas of Indian subcontinent. This also depends on the
study population recruited by different specialities like Gynaecology,
Endocrinology and dermatology, who are involved in management of
this heterogeneous disorder.
BMI was signicantly higher in PCOS and had more truncal
obesity than controls. This nding was similar to study by Welt et
al.18 In present study obesity was present in 57%. Thathpudi et al
used similar cut off by Asia specic denition (BMI>25) for dening
obesity found higher prevalence of obesity (70%). Phenotype A had
signicantly higher BMI compared to other phenotypes.
Fasting serum insulin and HOMA-IR is signicantly higher in
PCOS than controls. 66% of PCOS patients had Insulin Resistance
(cut off of 2.5). Previous study by Aziz have shown similar prevalence
(64%) of IR in US population.19 In an Indian study the prevalence
of IR was 50.52% when cut off of HOMA IR was 2.5. All PCOS
subgroups had higher HOMA IR compared to control, similar to the
ndings of Chae SJ et al.20 The present study showed higher level of
insulin and HOMA scores in the phenotype A (P+H+O) followed by
Normo-androgenemic phenotype D which was more than other two
hyperandrogenemic sub group. Our nding is in disagreement with
general opinion that norm androgenic phenotype D is metabolically
similar to control. Conicting reports are reported with respect to
metabolic derangement in this controversial sub group.21,22 In our
study IR was positively correlated with central obesity (r= 0.489), BMI
(r=0.311) and hyperandrogenemic (r= 0.262). Strongest correlation
was with truncal obesity. Both phenotype A and D had higher central
obesity than other phenotypes.
Both fasting plasma glucose and 2hr OGTT (75gm anhydrous
glucose) was more in PCOS than control. Prevalence of IGT was 30%
and diabetes was 9.1% which is consistent with study by Ehrmann et
al (IGT in 35% and Type 2 DM in 10%).23 abnormal glucose tolerance
and diabetes was more prevalent in phenotype A and D and was
consistent with higher truncal obesity and insulin resistance in these
two groups.
In our study mean total cholesterol, LDL, triglyceride was higher
and HDL was lower in PCOS group compared to Control. These
Phenotype A, C and D had higher triglyceride and low HDL compared
to control which is characteristic of metabolic syndrome expected
in PCOS. Mean LDLc was highest in phenotype A (102.mg/dl±
22.81) than other sub groups and control (83.09±17.07) conferring
additional cardiovascular risk. Phenotype A represents more severe
cardiovascular risk prone subgroup with respect to lipid prole.
This nding was similar to study by Teharani et al.8 who reported
phenotype A to have more adverse lipid prole but other phenotypes
in their study did not differ from control.

Evaluation of metabolic, hormonal and clinical parameters in different phenotypes of polycystic ovary
syndrome: an observational study from a tertiary care centre in Eastern India 199
Copyright:
©2018 Praveen et al.
Citation: Praveen D, Animesh M, Chandra SS, et al. Evaluation of metabolic, hormonal and clinical parameters in different phenotypes of polycystic ovary
syndrome: an observational study from a tertiary care centre in Eastern India. J Diabetes Metab Disord Control. 2018;5(6):195‒200.
DOI: 10.15406/jdmdc.2018.05.00164
Overall prevalence of metabolic syndrome (MS) in our PCOS
population was 40.8%. Studies have reported varied prevalence of
metabolic syndrome like 47.3% in the U.S.24,25 25.6% in southeast
China, 23.8% in Sweden,26 19.9% in Greece,27 12.5% in Turkey,28 and
1.6% in the Czech Republic.29 The prevalence of metabolic syndrome
(MS) ranges from 33% to 45% in Brazilian women with PCOS.30,31
Studies from India have reported MS in 35–46.2%.15,30 Prevalence
of metabolic syndrome in current study was 52.83% in phenotype
A (P+H+O) followed by 38.1% in Phenotype C (H+P), 37.5% in
B(H+O) and 23.3% in D.
Prevalence of hirsutism was higher in PCOS than control. Among
hyperandrogenemic sub-groups’ classic phenotype A (92%) and
phenotype B (87%) had higher prevalence of hirsutism than ovulatory
phenotype C. Similar trend was seen with severity of hirsutism.
Modied FG score was signicantly higher in Phenotype A and B
than ovulatory phenotype C. This is consistent with various studies.7,8.
The testosterone levels were elevated in all three groups with
hyperandrogenism (A, B, C), when compared to the group D without
the signs of hyperandrogenism. It was highest with phenotype a when
compared with a particular group with hyperandrogenism. Our data
conrms the report by Dewailly et al.7 that patients with non hyper
androgenic PCOS (phenotype D) had in fact slightly but signicantly
higher mean androgen levels than controls,(36.98 ±10.83 ng/dl Vs 26
. 93±10.83ng/dl) although by denition, all individual values were
within the normal range.
Limitations of the study
Our study population had the potential for bias since participants
were recruited based on self-reported concerns over PCOS not from
population survey. It would be expected that those with the most
concerns over PCOS would be selected for evaluation (i.e. overt
PCOS). Secondly our study was not designed to assess the prevalence
of PCOS phenotypes in general population rather it was planned
for looking at the prevalence of PCOS phenotypes in women who
were concerned with the symptoms suggestive of PCOS. Thirdly our
PCOS and control populations were not matched for adiposity. The
cross -sectional design of our study only allowed for the report of
associations among metabolic disturbances and PCOS phenotypes.
Therefore future longitudinal and prospective study may address
potential causal mechanisms for phenotypic variation in PCOS in our
country.
Conclusion
Appropriate diagnosis of PCOS and accurate identication of
phenotype is very important due to its long-term health implications,
and it is essential that these women are informed and counselled
about their present and long-term risks. Classic PCOS, Phenotype A
represents the most common and severe form of PCOS. These patients
presented as group with hirsutism with higher modied FG score,
more severe biochemical hyperandrogenism, increased levels of LH
and LH/FSH ratio, than rest of the sub groups. Metabolic aberrations
were greatest for phenotype A with abdominal obesity, elevated
insulin and insulin resistance, higher prevalence of impaired glucose
tolerance, atherogenic dyslipidemia and metabolic syndrome. In our
setting, these patients represented almost 45% of all PCOS patients.
Acknowledgments
None.
Conict of interest
The author declares that there is no conict interest.
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Evaluation of metabolic, hormonal and clinical parameters in different phenotypes of polycystic ovary
syndrome: an observational study from a tertiary care centre in Eastern India 200
Copyright:
©2018 Praveen et al.
Citation: Praveen D, Animesh M, Chandra SS, et al. Evaluation of metabolic, hormonal and clinical parameters in different phenotypes of polycystic ovary
syndrome: an observational study from a tertiary care centre in Eastern India. J Diabetes Metab Disord Control. 2018;5(6):195‒200.
DOI: 10.15406/jdmdc.2018.05.00164
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