Assessment of Total Serum Prostate Specific Antigen (TPSA), Anti Mullerian Hormone (AMH) Level among Sudanese Women with Polycystic Ovarian Syndrome

Abstract Back ground: Polycystic ovarian syndrome (PCOS) is one of the commonest endocrine disorders in women of reproductive age group, cause of androgen excess in women. (PSA) may be a new one diagnostic tool for PCOS. Serum AMH is synthesized by small antral follicles, which are precisely those seen on ultrasound and could help us to diagnose PCOS. The aim of this study to evaluate the levels of serum TPSA, AMH among Sudanese women with polycystic ovary syndrome and to determine the performance of PSA in diagnosis of PCOS. Material and Method: In a cross sectional case control study, 50 women newly diagnosed with polycystic ovary syndrome and 50 apparently healthy controls were enrolled. Sample were collected during the period between February to May 2017 from Elsir Abo Alhassen Center for Infertility in Khartoum State, serum TPSA , AMH levels were measured using an ultrasensitive method (Electrochemiluminesent (ECL) immunoassay method) . Results were analyzed using statistical package for social science (SPSS) computer program. Result: Serum levels of TPSA, AMH were significant higher in polycystic ovary syndrome group versus control group with mean ± SD for TPSA (0.019 ±0.009 ng/ml) versus control group (0.001 ± 0.001 ng/ml) and a p.value=0.00. AMH was (14.11±9.2 ng/ml) versus control group (2.404 ± 1.00ng/ml) p.value 0.00. There was a slight decrease in level of TPSA in females who had regular cycle in contrast to females that had irregular cycle with p.value = 0.04, where there was no difference in AMH p.value = 0.6. Also, this study showed that there was positive correlation between TPSA and BMI (P.value=0.00, r=.893) and negative correlation between AMH and BMI (P.value=0.025, r = -.317). The majority of females had irregular cycle were obese 36%, overweight 24% and those with normal weight were12%. Also there was significant increase in TPSA and AMH in PCO patients who had family history, TPSA (mean+ SD 0.022 ± 0.021 IV ng/mL versus 0.0165±0.006 ng/ml) value 0.03, and AMH (mean+ SD 21.3±10.0 ng/ml versus 10.6± 5.6 ng/ml) p-value 0.00. Conclusion: The study concluded that the serum levels of TPSA and AMH are increased in PCOS. TPSA and AMH were significantly increased in patients who had a family history.

Contents

No Title Pages

1 Dedication I

2 Acknowledge II

3 Abstract III

4 المستخلص V

5 Content VII

6 List of Tables X

7 List of Figures XI

CHAPTER ONE

1.1 Introduction 1

1.2 Rationale 2

1.3 Objectives 3

CHAPTER TWO

2 Literature review 4

2.1 Polycystic Ovary Syndrome 4

2.1.1 Etiology of PCOS 5

2.1.1.1 Genetic of PCOS 6

2.1.2 Pathophysiology of PCOS 7

2.1.2.1 Hyperandrogenism 7

2.1.2.2 Hirsutism 8

2.1.2.3 Acne 9

2.1.2.4 Androgenic alopecia 10

2.1.3 Specific steroidogenic enzyme defects in PCOS 11

2.1.4 Gonadotropins 12

2.1.5 Intraovarian factors 12

2.1.6 Adrenal hyperandrogenism 13

VIII

2.1.7 Poly cystic ovary syndrome and ovarian

dysfunction

13

2.1.7.1 Amenorrhoea 14

2.1.7.2 Intraovarian Androgens 17

2.2 AMH 18

2.2.1 AMH physiology 18

2.2.2 AMH in PCOS 19

2.2.3 AMH and its relation to obesity and insulin

resistance in PCOS

20

2.3 Prostate specific antigen 20

2.3.1 Biochemistry of PSA 20

2.3.2 Molecular Forms of PSA 21

2.3.3 Non Prostatic-PSA 22

CHAPTER THREE

3 Material and Methods 24

3.1 Study design 24

3.2 Study area and duration 24

3.3 Study population 24

3.4 Selection criteria 24

3.5 Ethical consideration of the study 24

3.6 Sampling 25

3.6.1 Data collection 25

3.6.2 Sample collection 25

3.7 Biochemical measurements 25

IX

3.7.1 Total prostatic specific Antigen

(TPSA)measurement

25

3.7.1.1 Principle of the method 25

3.7.1.2 Procedure of TPSA measurement 26

3.7.2 AMH measurement 26

3.7.2.1 Principle of the method 26

3.7.2.2 Procedure of AMH measurement 26

3.8 Quality control 26

3.9 Statistical analysis 27

CHAPTER FOUR

4 Result 28

CHAPTER FIVE

5.1 Discussion 36

5.2 Conclusion 38

5.3 Recommendation 38

Reference 39

Appendices