The lives of the pregnant women are in the hands of the mother -How to daignose placenta accretion earliest

The lives of the pregnant women are in the hands of the mother -How to diagnose placenta accretion earliest : Diagnosed early placenta Recollections on cobra bite : Dealing with placenta accreta.

Classification of Placenta accreta : These are  basically of two types of accretion :-A) Focal and B) Total-(when all the cotyledons have invaded the myometrium). The prevalence of combined focal & total Abruptio  Placentae in genl Obstet population is  about 1 : 500 in  unscarred uterus . But such  prevalence rises sharply in  cases with scarred uterus. For instance , in post CS cases the rate of accretion will be  around 3%,(after first CS),  11%(after two CS),  40% after third seectin,and alarmingly (dreadfully) the prevalence of accretion will be as high as 67% after 5^th CS!!! .Placental accretion is a nightmare for third stage!! But how best to handle it-? I mean the steps which may be avoided to provoke sudden severe PPH as an attempt is made to remove  the placenta in piece meal ? If we can diagnose antenatally then we can arrange to deliver at tertiary care center.   How to diagnose prenatally??  Ans:- In general ,  most women in India too undergoes three USG or more in entire preg period , many undergoes 7-10 times USG  depending on risk factor/s. At anomaly scan (18-20 weeks of gestation or at growth scan ( 28-32 weeks) there will be evidences of accretion if sonologist is dedicated one . This(placental accretion)  can be easily picked up if sonologist concerned is not overburdened as commonly happens. Regrettably  even today  there are  disparity between the no of cases in a  locality who warrant sonological evaluation and no of sonologist.

 The role of sonologist : It is they can save thousands of material lives out of Placental accretion!!! But sonologist can warn us even by 2 D & CD though 3-D will be more informative and easy to pick up particularly they  will offer an accurate  diagnosis at least in growth scan if not in anomaly scan.  MRI , a better modality is  if often unnecessary.   However if  such an diagnoses would have been done in your case at about 32 weeks then  I would have recommended to refer her to higher center.

                                            

What to do in diagnosed cases??Ans: There are people  who perform Caesarean hysterctomy  with placenta in situ-soon after delivery of baby if preop diag was certain. They very rightly don’t try to remove the placenta by piecemeal. But there is more people who thinks “let’s try to see if pl  can be separated ignoring the previous report of sonologist. In the process i.e. to remove  the placenta there is usually torrential bleeding . They fall in trap with torrential bleeding .In such a situation , primi in particular , all  four vessels feeding the vesseks may be tied with B-Lunch type of box suture. Or UAE may be considetd well ahead if pre op  diag was certain. Urosurgron may be preop called  at OT before putting incision  if there is MRI/ sonological  evidence of pl invasion to bladder wall . Several Square stitches (a great modification of B-Lynch compression stitches) may help but then even some portions of pl will remain in and sepsis may ensue. Some have recommended conservative approach leaving aside the whole placenta or pieces of pl allowing the nature to expel of its own.  Earlier people  used to inj MTX in cord which is left aside but this not recommended right now as villi are dead.  ,By doing so torrential bleedings avoided

Take home message: The prevalence of placental morbid adhesions on the rise globally and those who are working at remote arrases without any diag by USG antenatally fall in trap after the birth of seeming normal vaginal delivery, Often Whole blood and compete anesthetist are unavailable at Block level ,It is said an attempt to spear the adherent pl can lead to massive hemorrhage amounting to 3Lit top even 5L. So my appeal if placenta does not come out easily it will be prudent to send her to tertiary care center where hyercterectomy may be contemplated undwee PCV/ whole Bl transfusion. Inotrops may be useful during  trabsport, If a nurse agrees to accompany she*nurse ) can change the RL on the way..There many theories why accreting occurs in primi where there is no previous damage to endometrium. Researchers  claim that in such cases (taking it granted there was no tubercular syechaE0 , the cause of accretion as suggested by thecae 1) Primary endometrial defect or 2) hay[err invasions of cite due to EGFR, VRGF. , Nowadays with incising prevalence of IVF, affianced aged of mother , more cases Essn HTN (as was this case), smoking, submucous myoma are the initiating factors of accretion in Primosa dedicated sonologist can almost certainly pick up Accretion early by 1) loss of retro pl son lucent  zone, 2) Thinning

  accreta can be relatively safely delivered at tertiary center..

Albinism causes

vitiligo. The condition doesn’t appear to be inherited. Most people with vitiligo don’t have a family history of the disorder. But family history of vitiligo or other autoimmune conditions may increase your risk even though it doesn’t cause vitiligo.Another risk factor may be having genes associated with vitiligo, including NLRP1 and PTPN22

Most researchers believe that vitiligo is an autoimmune disorder because your body is attacking your own cells. But it’s also unclear how your body attacks your pigment cells. What is known is that about 20 percentTrusted Source of people with vitiligo also have one other autoimmune disorder. Depending on the population, these disorders can include the following, from most common to least common:

scleroderma, a disorder of the connective tissue of the body

lupus

thyroiditis, caused by an improperly functioning thyroid

psoriasis

alopecia areata, or baldness

type 1 diabetes

pernicious anemia, an inability to absorb vitamin B-12

Addison’s disease

rheumatoid arthritis

Some experts also report vitiligo appearing after incidents of:

severe sunburns or cuts

exposure to toxins and chemicals

high levels of stress

What are the complications of vitiligo?

The good news is that many times vitiligo has few physical side effects on the body. The most serious complications may affect the ears and eyes, but these aren’t common. The primary physical effect is that the loss of pigment that increases your risk for sunburn. You can protect your skin by applying sunscreen with a SPF of 30 and wearing sun protective clothing.

As understandable the genetic defect result in the complete absence of melanin production, or a reduced amount of melanin production. Albinism is a rare group of genetic disorders that cause the skin, hair, or eyes to have little or no color. Albinism is also associated with vision problems.. Albinism is an inherited disorder that’s present at birth. Children are at risk of being born with albinism if they have parents with albinism, or parents who carry the gene for albinism. A defect in one of several genes that produce or distribute melanin causes albinism.

 Types of albinism include: People with albinism will have the following symptoms: an absence of color in the hair, skin, or eyes, lighter than normal coloring of the hair, skin, or eyes, patches of skin that have an absence of color, Albinism occurs with vision problems, which may include: strabismus (crossed eyes),photophobia (sensitivity to light),nystagmus (involuntary rapid eye movements),,impaired vision or blindness, astigmatism. IN cases of  Oculocutaneous albinism (OCA):-It affects the skin, hair, and eyes. There are several subtypes of OCA: Ocular albinism is the result of a gene mutation on the X chromosome and occurs almost exclusively in males. This type of albinism only affects the eyes. People with this type have normal hair, skin, and eye coloring, but have no coloring in the retina (the back of the eye). OCA1:-OCA1 is due to a defect in the tyrosinase enzyme There’s no cure for albinism. However, treatment can relieve symptoms and prevent sun damage. Treatment may include:

sunglasses to protect the eyes from the sun’s ultraviolet (UV) rays

protective clothing and sunscreen to protect the skin from UV rays

prescription eyeglasses to correct vision problems

surgery on the muscles of the eyes to correct abnormal eye movements esearch on vitiligo has increased in the past years. Newer technology allows for advances in genetic research so that we can understand how vitiligo works. Understanding how vitiligo is triggered and how its process interacts with other organ systems can help researchers develop new treatments.

Other studies on vitiligo include looking into how trauma or stress triggers vitiligo, how genetics affect vitiligo, and how the chemical signals of the immune system play a role.

. There are two subtypes of OCA1:OCA1a. People with OCA1a have a complete absence of melanin. This is the pigment that gives skin, eyes, and hair their coloring. People with this subtype have white hair, very pale skin, and light eyes.

OCA1b. People with OCA1b produce some melanin. They have light-colored skin, hair, and eyes. Their coloring may increase as they age.

OCA2:OCA2 is less severe than OCA1. It’s due to a defect in the OCA2 gene that results in reduced melanin production. People with OCA2 are born with light coloring and skin. Their hair may be yellow, blond, or light brown. OCA2 is most common in people of African descent and Native Americans.

OCA3

OCA3 is a defect in the TYRP1 gene. It usually affects people with dark skin, particularly black South Africans. People with OCA3 have reddish-brown skin, reddish hair, and hazel or brown eyes.

OCA4

OCA4 is due to a defect in the SLC45A2 protein. It results in a minimal production of melanin and commonly appears in people of East Asian descent. People with OCA4 have symptoms similar to those in people with OCA2.

Ocular albinism

Hermansky-Pudlak syndrome

This syndrome is a rare form of albinism that’s due to a defect in one of eight genes. It produces symptoms similar to OCA. The syndrome occurs with lung, bowel, and bleeding disorders.

Chediak-Higashi syndrome

Chediak-Higashi syndrome is another rare form of albinism that’s the result of a defect in the LYST gene. It produces symptoms similar to OCA, but may not affect all areas of the skin. Hair is usually brown or blond with a silvery sheen. The skin is usually creamy white to grayish. People with this syndrome have a defect in the white blood cells, increasing their risk of infections.

Griscelli syndrome

Griscelli syndrome is an extremely rare genetic disorder. It’s due to a defect in one of three genes. There only have been 60 known casesTrusted Source of this syndrome worldwide since 1978. It occurs with albinism (but may not affect the entire body), immune problems, and neurological problems. Griscelli syndrome usually results in death within the first decade of

What is the difference between albinism & vitiligo??

Albinism:--It is a genrtic disorder and the defective gene sharing is not uncommon in consanguineous marriages. In consang.marriages defective gene which presumably passed down from both parents to the child and ahs lead to albinism of the neonate. Different gene defects characterize the numerous types of albinism. By contrast Vitiligo is more common than albinism. Almost about 1 percent of the world’s population has vitiligo. In this condition, the cells that are responsible for  skin color are destroyed. Melanocytes cells, , no longer produce skin pigment, called melanin. So, areas of skin will lose color or turn white. Areas of lost pigment can develop anywhere in body, including: sun-exposed areas like the hands, feet, arms, and face inside the mouth or other mucus membranes, nostrils, genitals, back of the eye,  within the hearing system of the ears. t’s unknown exactly what causes vitiligo. The condition doesn’t appear to be inherited. Most people with vitiligo don’t have a family history of the disorder. But family history of vitiligo or other autoimmune conditions may increase your risk even though it doesn’t cause vitiligo.Another risk factor may be having genes associated with vitiligo, including NLRP1 and PTPN22

Most researchers believe that vitiligo is an autoimmune disorder because your body is attacking your own cells. But it’s also unclear how your body attacks your pigment cells. What is known is that about 20 percentTrusted Source of people with vitiligo also have one other autoimmune disorder. Depending on the population, these disorders can include the following, from most common to least common:

scleroderma, a disorder of the connective tissue of the body

lupus

thyroiditis, caused by an improperly functioning thyroid

psoriasis

alopecia areata, or baldness

type 1 diabetes

pernicious anemia, an inability to absorb vitamin B-12

Addison’s disease

rheumatoid arthritis

Some experts also report vitiligo appearing after incidents of:

severe sunburns or cuts

exposure to toxins and chemicals

high levels of stress

New Phenotypes Proposed by the Rotterdam 2003 Criteria as PCOS

Phenotypes of PCOS according to the NIH 1990 and Rotterdam 2003 criteria¹

Features	Phenotypes
	A	B	C	D
Ovulatory dysfunction	X	X	X
Hirsutism and/or hyperandrogenemia	X	X		X
Polycystic ovaries	X		X	X
PCOS by NIH 1990	✓	✓
PCOS by Rotterdam 2003	✓	✓	✓	✓

X, Features included in phenotypes; ✓, phenotypes included in definitions.

¹

Assuming exclusion of other androgen excess or related disorders.

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Defining a Syndrome

A syndrome is a symptom complex of unknown etiology, characteristic of a particular abnormality. There are a number of approaches to defining a syndrome, including 1) historical usage in medical practice and/or literature, 2) expert knowledge and consensus processes, and 3) analysis of hard data by an independent body, i.e. evidence-based (e.g. the process generally undertaken by the NIH Consensus Development Program; http://consensus.nih.gov/). Considering that the current definitions for PCOS have been arrived at by a consensus process of experts and advocates in the field, it is instructional to review the comments of author Michael Crichton, who argued that “… . the work of science has nothing whatever to do with consensus. Consensus is the business of politics. Science, on the contrary, requires only one investigator who happens to be right, which means that he or she has results that are verifiable by reference to the real world. In science consensus is irrelevant. What is relevant is reproducible results. The greatest scientists in history are great precisely because they broke with the consensus. … . There is no such thing as consensus science. If it’s consensus, it isn’t science. If it’s science, it isn’t consensus. Period” (8). He concludes his argument by noting that “consensus is invoked only in situations where the science is not solid enough”. In light of this argument we should be compelled to examine what scientific evidence we have to support the available definitions of PCOS.

First, we should note that PCOS is not the only disorder facing the dilemma of definition. Irritable bowel syndrome, systemic lupus erythematosus, antiphospholipid syndrome, fibromyalgia, chronic fatigue syndrome, and, more closely related to PCOS, the metabolic syndrome, are among the many disorders that are experiencing unclear and competing definitions. In fact, although the metabolic or insulin resistance syndrome was initially described in the late 1960s (9), today there are still at least six different diagnostic criteria in use (10–15). Even the name of this syndrome has not been agreed upon. In comparison, the controversy surrounding the definition of PCOS appears almost trivial.

How are hard data used to define a syndrome and its phenotypic limits? By definition, a syndrome is of unknown etiology, at least when initially described, and this appears to be the case for PCOS. Consequently, we cannot define a syndrome as the collection of those phenotypes with a common underlying etiology. Alternatively, we can define a syndrome by its consequences or long-term impact or morbidity. For example, we define the metabolic syndrome as a symptom complex that results in an increased risk for cardiovascular disease (15). In this analysis, we should note that the features used in defining a syndrome should not also be used to determine its phenotypic limits. Consistent with this concept, in a joint statement from the American Diabetes Association and the European Association for the Study of Diabetes, Kahn et al. (15) did not consider previous publications whose focus was on the ability of the metabolic syndrome to predict type 2 diabetes mellitus (DM), because the definition of the syndrome already included glucose intolerance, a strong predictor of diabetes.

Defining the Phenotypic Limits of the Syndrome of PCOS

The phenotypic limits of a syndrome can be defined by 1) identifying the specific phenotypes that may compose or be included in the syndrome, and 2) as discussed above, determining the long-term morbidity(s) that will be used as the phenotypic anchor. So, what long-term morbidity can we use to define PCOS? In a recent analysis of economic burden, we noted there is good evidence that PCOS is associated with increased risks for 1) menstrual dysfunction and abnormal uterine bleeding, 2) infertility, 3) type 2 DM, and 4) hirsutism (16). However, because hirsutism (i.e. clinical evidence of hyperandrogenism) and oligoanovulation (a strong predictor of menstrual dysfunction and infertility) are part of all current definitions of PCOS, these morbidities should probably not be considered when attempting to define the phenotypic limits and consequently the criterion for the definition. Alternatively, it may be possible to define PCOS by its increased risk for type 2 DM. It should be noted that the use of the risk of type 2 diabetes to identify the phenotypic limits of PCOS does not imply that that all women with PCOS, as defined, will develop type 2 DM, but that the phenotypic group as a whole will be at higher risk. It also is not meant to denote that this is the only or necessarily the most important of the morbidities, because these patients clearly suffer reproductive and dermatological consequences. Rather, type 2 DM is being used as a phenotypic anchor against which to measure each of the phenotypes.

How do the proposed phenotypes of PCOS relate to this morbidity? Considering the features of oligoanovulation, hirsutism and/or hyperandrogenemia, and polycystic ovaries, both the NIH 1990 and the Rotterdam 2003 criteria agree on two phenotypes (phenotypes A and B; Table 2), whereas Rotterdam 2003 defines an additional two phenotypes (phenotypes C and D; Table 2). Ample evidence is available to support the association of the two phenotypes included in both the NIH 1990 and the Rotterdam 2003 criteria (i.e. oligoanovulation, and hirsutism and/or hyperandrogenemia, with or without polycystic ovaries) with an increased risk for type 2 DM (17–19).

Alternatively, what is the evidence to support consideration of the two additional phenotypes proposed by the Rotterdam 2003 criteria (phenotypes C and D; Table 1) as PCOS? First, there is evidence that the sole presence of polycystic ovaries in women, observable in 20–30% of the population of reproductive-age women (20–25), is associated with features reminiscent of those observed in patients with PCOS. The presence of polycystic ovaries is associated with mild elevations in circulating LH (21, 24, 26) and androgen (21, 24, 26, 27) levels and a higher prevalence of obesity and hirsutism (20, 21). Alternatively, there are conflicting data regarding the impact of polycystic ovaries on measures of insulin action (25, 27–29) and their association with impaired fertility (20, 26). Nonetheless, we should recognize that the majority of these studies were performed using older criteria for polycystic ovaries and often transabdominal ultrasonography, and the prevalence, specificity, and relevance of polycystic ovaries diagnosed by newer criteria (30) remain to be determined.

A limited number of investigators have specifically studied ovulatory women with polycystic ovaries and hyperandrogenism. Carmina and colleagues (31, 32) studied women with polycystic ovaries, clinical and/or biochemical hyperandrogenism, and normal ovulation and observed that these patients had higher circulating androgen and insulin levels and a greater 17-hydroxyprogesterone response to a long-acting GnRH analog compared with controls. However, the degrees of hyperinsulinism and hyperandrogenemia were significantly less than those observed in patients with PCOS defined by the NIH 1990 criteria. Furthermore, whether these individuals have an increased risk for developing metabolic complications, including type 2 DM, is not known.

There are even less data showing that women with polycystic ovaries and ovulatory dysfunction, but without clinical or biochemical evidence of hyperandrogenism, are at increased risk for type 2 DM, as are those patients with PCOS defined by the NIH 1990 criteria. Norman and colleagues (33) compared six women with polycystic ovaries, irregular menstrual cycles, and no hirsutism or hyperandrogenemia with 54 women with polycystic ovaries, irregular cycles, and hyperandrogenism. They did not observe significant differences between the groups in age, body mass, waist to hip ratio, total cholesterol, or integrated glucose or insulin responses to an oral glucose challenge, although this could be a reflection of the small number of subjects studied. Whether this group of patients is at risk for the development of metabolic complications, including DM, is also unknown.

Finally, we should note that many patients with ovulatory disorders other than PCOS also demonstrate polycystic ovarian morphology, including 21-hydroxylase-deficient nonclassical CAH (34, 35), bulimia and other eating disorders (36, 37), hyperprolactinemia (38), or functional hypothalamic amenorrhea (FHA) (38, 39). In addition, many adolescents transiently demonstrate polycystic-appearing ovaries (40, 41). Nonclassical CAH can be differentiated from PCOS by basal or stimulated 17-hydroxyprogesterone (42), and the medical history may be able to discern some of the patients with bulimia and other eating disorders. However, FHA is usually defined by a history of amenorrhea of at least 6-month duration; negative urinary pregnancy test; serum LH, FSH, TSH, prolactin, and androgen levels within the normal range; and LH to FSH ratio less than 2 (43). So how will FHA be differentiated from women with nonhyperandrogenic PCOS? Although it may be argued that patients with FHA and girls undergoing the pubertal transition actually demonstrate multicystic and not polycystic ovaries, comprehensive studies and distinguishing ultrasonographic criteria are generally lacking.

Risks and Benefits of Considering the Two New Phenotypes Proposed by the Rotterdam 2003 Criteria as PCOS

What are the risks and benefits of accepting these two phenotypes and consequently the Rotterdam 2003 criteria as the new definition of PCOS? The negative impact of labeling the two new phenotypes proposed by the Rotterdam 2003 criteria (i.e. ovulatory women with polycystic ovaries and hyperandrogenism and, particularly, oligoanovulatory women with polycystic ovaries, but without hyperandrogenism) as PCOS can be significant. Although the proceedings of the Rotterdam 2003 conference acknowledged that the criteria were possibly not suitable for trials focusing on clinical outcomes in women with PCOS, the reality is that they are being used as such. Because these criteria increase the phenotypic heterogeneity of the disorder, their use will decrease the ability of genetic and other molecular studies to detect a common underlying abnormality. The use of these criteria also implies that we already understand the health risks of these newly proposed phenotypes far more than we do, potentially stifling future investigation. Importantly, the adoption of these criteria suggests to patients and their physicians that women with these new phenotypes are at increased risk for metabolic and cardiovascular consequences, as are patients with more classic forms of PCOS, despite the absence of data in this regard. Finally, these criteria have the potential of negatively affecting the insurability of patients who may have been prematurely labeled as having PCOS.

Alternatively, we should recognize that a finding of polycystic ovaries can predict the response to ovulation induction, because women with this ovarian morphology are more sensitive to gonadotropin stimulation than spontaneously cycling women, possibly as a result of the larger pool of small antral follicles available for recruitment (44). However, patient management need only be tailored to the ovarian morphology observed at the time of treatment and, consequently, does not require a previous diagnosis of PCOS.

The consensus committee in July 19, 2018

What aberrations in menst cyclicity will pinpoint for PCO??   . The consensus committee in July 19, 2018:--This committee in contrast to NIH, Rotterdam ,Androgen Excess Society, & And Excess & PCOS committee  It was framed by  total   37   societies and organizations covering   71  countries  engaged  in the process of consensus statement  released in July 2018. .This consensus was headed by  “The Australian centre   for Research Excellence in PCOS” and  funded by NHMRC  led and   primarily funded  the guideline development. They partnered with the American  Society   for Reproductive  Medicine     and the European  society of Human    Reproduction and Embryology    in this  Endeavour. Thirty five   other societies partnered including FOGSI and   the PCOS  society of India.

Coming back to diagnosing PCO based on menst irregularities the point of consideration was which kind of irregular   cycles is to be considered  relevant ? The committee members  more clearly stressed on  gynecological   age in this issue..

Irregular menstrual cycles are defined as :

A) Cycles were normal   in the first year post menarche as part of the pubertal transition , 1 to < 3 years post menarche  with  cycle length < 21  or > 45 days .B) Three  years post menarche  to perimenopause  < 21 or  > 35   days or < 8 cycles per   year C) one year  post menarche > 90 days for any   one cycle.

II. Primary   amenorrhea     by age 15 or > 3   years post thelarche

When irregular menstrual cycles   are present   a diagnosis   of PCOS   should be considered

Androgens to be   measured in the diagnosis of biochemical hyperandrogenism are specified along with optimal assays.

Calculated  free  testosterone,  free androgen   index or  calculated bioavailable  testosterone  should be  used in assess  biochemical hyperandrogenism in the diagnosis of PCOS  .High quality   assays such  as liquid chromatography mass  spectrometry  and extraction chromatography immunoassays   should be used for the most  accurate   assessment of total   or free testosterone in PCOS.

Androstenedione and dehydroepiandrosterone   sulfate   could be considered if total or free testosterone are not elevated however these provide limited additional information in the diagnosis  of PCOS. C) In women on hormonal  contraception drug  withdrawal is recommended for  3 months  or longer  before   measurement .

How  important is AMH in the diag of PCO??

AMH levels   should  not yet  to be used  as an alternative test  for PCOM or single test for diagnosis  of PCOS,

Cardiovascular   disease risk

All women    with PCOS should be assessed for  cardiovascular    risk factors  including  A) obesity  B) cigarette  smoking C)  dyslipidemia D)  hypertension E) impaired glucose  tolerance and F)  lack of physical  activity. Weight height   and ideally waist circumference should be measured  and  BMI must be calculated. Overweight   and obese women   with PCOS   regardless of age should have   a fasting lipid profile. Blood pressure  must be measured annually .Gestational  diabetes   glucose tolerance   and type2  diabetes are common and PCOS   women are at 5 fold increased risk for these complications.

Glycemic status should be assessed in all women   with PCOS. A) An oral  glucose   tolerance test  B)  fasting plasma  glucose or C) HbA1c  should be performed to assess glycemic  status .  In high   risk  women with  PCOS  an OGTT is  recommended.

 Anxiety  depressive  symptoms  psychosexual health and impact on body  image should   be routinely screened in all adolescents and women   with PCOS  at diagnosis.

Lifestyle  modifications : Preferably multi component including  diet   exercise and behavioral strategies should be recommended

Achievable goals such as   5%- 10%   weight loss in 6  months in those with excess  weight  yields significant clinical   improvements.

Exercise

Health professional should encourage  and advise   exercise for the prevention of weight  gain and  maintenance of health .

Pharmacological  treatment for non fertility indications A) For  hyperandrogenism and / or irregular   menstrual cycles  .Combined oral contraceptive  pills  should  be recommended to manage hyperandrogenism and / or irregular   menstrual cycles  preferably lower   dose and natural    estrogen  preparations.

 Metformin When in PCOS?? Ans;- women with  BMI > 25 kg / m² and most beneficial in women with impaired OGTT or high risk  ethnic groups when   should be considered if COCP  and lifestyle   changes alone are not   successful. Metformin can be  considered in PCOS   women with  BMI > 25 kg / m and most beneficial in women with impaired OGTT or high risk  ethnic groups. 

Starting at a low dose with 500 mg increments   one two  weekly and extended  release  preparation may minimize side effects.

Antiandrogens when ??  Ans;-Antiandrogens should only be considered to treat hirsutism if 6 months or more of  cop and cosmetic  therapy   have  been unsuccessful

Inositol should currently be considered  as an experimental therapy in PCOS with emerging evidence  on efficacy highlighting the need for  further research

Assessment and treatment of infertility

Ovulation  induction Principles

The use of  ovulation  induction  agents including A) letrozole B) metformin and C) clomiphene citrate are  off label in many countries. Where off  label  use of ovulation induction agents  is allowed women   need to be informed  of the evidence concerns and side effects.

 Step 1:-Pregnancy   needs to be excluded before ovulation induction Step 2 :-Unsuccessful  and prolonged use of ovulation  induction agents should  be avoided due to poor  success rates. Step 3

 :-Letrozole should be considered the first line pharmacologic agent for ovulation induction in women with PCOS Step 4:-Clomiphene  citrate  could be used alone in women   with PCOS with anovulatory infertility and no other infertility factors. Step 5  :-Combining clomiphene   citrate with metformin improves  ovulation and pregnancy rates     in PCO  women  who are clomiphene resistance and  with   no other   cause of infertility  Step 6 :-Gonadotropins could be used as second line agents  in women   with PCOS  who have  failed  first line   oral ovulation induction therapy but before attempting at  gonadotrophins one should consider Cost and availability ,expertise  required for use in ovulation  induction. Degree of  intensive  ultrasound   monitoring  required. Of note that theta is lack   of difference in  clinical efficacy of available gonadotrophin  preparations.

Low   dose gonadotrophin  protocols to optimize monofollicular development, risk  and implications of potential multiple pregnancy

Laparoscopic ovarian surgery   when?? Ans:-Laparoscopic ovarian surgery   could be considered second line therapy for women   with PCOS who  are clomiphene citrate resistance with anovulatory infertility   and no their infertile factors ,.But where   laparoscopic  ovarian  surgery is to be recommended the following  need to be considered

Comparative cost  ,expertise required for use in  ovulation  induction ,intra  operative and post  operative risks   are higher in women   who are    overweight and obese ,there may be  a small associated risk of lower  ovarian reserve  or loss of ovarian function and peri adnexal  adhesion   formation  may be an  associated risk.

In vitro fertilization when in PCO?? Ans:-It is as third line therapy.  In vitro fertilization should be considered even in  the absence   of an absolute indication  for IVF / ICSI )say tubal block/ endometriosis) in those PCO   women with long   infertility    as third  line therapy where  first or  second   line ovulation  induction  therapies  have failed.

National Institutes of Health (NIH) 1990 Criteria for PCOS

The definition of PCOS most commonly used today arose from the proceedings of an expert conference sponsored by the NIH in April 1990 (i.e.NIH 1990 criteria). All those attending were queried regarding what they believed were diagnostic criteria of PCOS. Tabulation of the results indicated that 64%, 60%, 59%, 52%, and 48% thought that hyperandrogenemia, exclusion of other etiologies, exclusion of congenital adrenal hyperplasia (CAH), menstrual dysfunction, and clinical hyperandrogenism, respectively, were criteria that were definite or probable for the disorder (5). The proceeding then summarized these results into the following major research criteria (in order of importance): 1) hyperandrogenism and/or hyperandrogenemia, 2) oligoovulation, and 3) exclusion of known disorders, such as Cushing’s syndrome, hyperprolactinemia, and CAH (5) (Table 1). A fourth criterion, polycystic ovaries on ultrasound, was considered particularly controversial. In essence, the results of this expert conference identified PCOS as a disorder of ovarian androgen excess.

TABLE 1.

Current criteria for the definition of PCOS

Study	Criteria
NIH, 1990 (5 )	To include all of the following:
	1) Hyperandrogenism and/or hyperandrogenemia
	2) Oligoovulation
	3) Exclusion of related disorders
ESHRE/ASRM (Rotterdam), 2003 (6, 7 )	To include two of the following, in addition to exclusion of related disorders:
	1) Oligo- or anovulation
	2) Clinical and/or biochemical signs of hyperandrogenism
	3) Polycystic ovaries

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Rotterdam 2003 Criteria for PCOS: Introducing Two New Phenotypes

Another expert conference was organized in Rotterdam in May of 2003, sponsored in part by the European Society for Human Reproduction and Embryology and the American Society for Reproductive Medicine (i.e.Rotterdam 2003 criteria). The proceedings of the conference noted that PCOS could be diagnosed, after the exclusion of related disorders, by two of the following three features: 1) oligo- or anovulation, 2) clinical and/or biochemical signs of hyperandrogenism, or 3) polycystic ovaries (6, 7) (Table 1).

We should note that the Rotterdam 2003 criteria did not replace the NIH 1990 criteria, because all women diagnosable by the NIH 1990 criteria would also meet the Rotterdam definition (Table 2). Rather, it expanded the definition of PCOS, adding two additional phenotypes as PCOS, including women with 1) polycystic ovaries and clinical and/or biochemical evidence of androgen excess, but without ovulatory dysfunction, and 2) polycystic ovaries and ovulatory dysfunction, but without hyperandrogenemia and/or hirsutism (i.e. no signs of androgen excess). To begin to determine whether these phenotypes truly represent PCOS, it is useful to review how syndromes are defined.

What is new in Polycystic Ovarian syndrome

The Australian  centre  for Research  Excellence  in PCOS funded by NHMRC  led and primarily   funded the guideline   development . They partnered  with the American  society for Reproductive  Medicine    and the European Society  of Human   Reproductive   and Embryology   in  this Endeavour. Thirty five other   societies partnered including  FOGSI  and the PCOS Society of India .

Guideline recommendations: Recommendations and practice  points  cover  the following   broad   areas :

Diagnosis screening and risk   assessment   depending  on life  stage :

Emotional   well being

Healthy  lifestyle

A healthy   diet in pregnancy is significantly associated with higher    birth weight using customized  birth weight   centiles and lowers the risk of giving birth to a small for gestational  age  infant

. In a recent    study researchers  evaluated  the maternal   dietary patterns     and their impact   on infant   CBWC   within a group of women . A significant association was  observed  between  health  conscious dietary  pattern and maternal  body mass . Researchers estimate the burden of miscarriage  in women and evaluated  the association with maternal age  and pregnancy history. Risk of miscarriage was estimated according to   woman’s  age  and pregnancy history by logistic regression.. After one miscarriage   the risk  was increased  by half   after two  the risk  doubled index age education income  and exercise . According to adjusted regression analyses  those  women who followed Health conscious dietary  pattern    were significantly associated  with increased  CBWC      -4.75   195%    confidence interval    and were less likely   to deliver a SGA  infant  and after three consecutive  miscarriage  the risk  was four  times  greater..

 Previous     pregnancy   complications  also predicted a higher risk of miscarriage Additionally women   who themselves   were born small for gestational age also  had an increased risk of miscarriage . Therefore researchers concluded that  the risk of miscarriage    is related to a mother’s  age and suggested that it is linked to some previous  pregnancy  complications

 Exciting developments:, Insight into the international  evidence  based guidelines for the assessment   and management of polycystic ovary  syndrome 2018.

Expertise & care of PCO women : Q. 1:-What we knew of “Polycystic ovary  syndrome” ?? : Ans:- We are aware that PCO has a significant public health  issue  affecting A) reproductive B)  metabolic and C) psychological aspects of the concerned woman. Unfortunately little focus is done by gynaecologits are  on the   psychological    health of women suffering from PCO   .

Q. 2 :-What was known to us for last three decades??  We are aware that PCOS   is one of the most common endocrinopathy in reproductive aged women   with prevalence of 8% - 13%   . We also knew that  PCO is present with diverse   features including   reproductive   metabolic    and psychological features .As mentioned earlier the last two groups of the syndrome i.e. metabolic and psychological components of this common syndrome  are paid little  attention..

Q. 3 Old wine in new bottle,. Since 1935 many millions gallon of have water have passed over Amazon. If that be so,  then why still there are  dilemma on PCO still existing even  in 2019?? Where do we stand now?? Is it not the lack of knowledge of scientists, reproductive biologists that the “Diagnosis of PCOS still remain controversial and warrant many times amendments including its assessment”.  Why there is no universal consensus since 1935? Not only its diag criteria have changed about five times but we are also aware that problem also lies with its  “management-guidelines” of which are still   inconsistent. Previous   guidelines lacked rigorous evidence   based processes did not engage   consumer and international   multidisciplinary perspective or were outdated.

Q. 4:--Yet another Academic feast.  Another international evidence   based guideline was released on July 19. 2018  for the A) assessment   and B)  management of PCOS addressing   psychological  metabolic   and reproductive features of PCOS. Guideline recommendations:

 Recommendations and   practice points  cover  the following  broad   areas: Diagnosis , screening and risk   assessment   depending on   life stage; A) Emotional   well being  B) Healthy lifestyle C) Pharmacological   treatment for non fertility indications and D)  assessment   and treatment   of infertility 2)

for PCOS); 3) Thessaloniki, Greece, in 2007

dealt with infertility management in PCOS .The

conclusions of these meetings were subsequently jointly

published simultaneously in both Human Reproduction and

Fertility and Sterility. These papers are highly cited,

suggesting a great interest in this area and underlining the

value of such consensus contributions.

4) A third PCOS consensus workshop—the focus of the pres-

end report—took place in Amsterdam, the Netherlands, in Oc-

tuber 2010 and attempted to summarize current knowledge

and to identify gaps in knowledge regarding various women’s

health aspects of PCOS.

Diverse aspects of care during the reproductive and post reproductive years were addressed, including adolescence, hirsutism and acne, contraception, menstrual cycle abnormalities, quality of life and sexual

health, ethnicity, pregnancy complications, long-term (meta-

boric) cardiovascular health, and cancer risk . Due to

the complexity of the many issues discussed, this contribution

will address each topic separately in axed format: a brief

introduction, concluding statements (where there was agree-

mint), a summary of areas of disagreement (if any) and know-

edge gaps, with recommended directions for future research.

These concluding statements in relation to each specifc topic

mentioned are published in the journals, 

Summary  of clinical changes in the recommendations

Point 1;- Which criteria for daig to follow?? e.g. . of  1) Oligo or anovulation , 2) Clinical  and / or  biochemical signs of   hyperandrogenism 3) Polycystic ovaries on ultrasound and exclusion of other etiologies . Rotterdam diagnostic criteria –originally  required as  we all know  two of Oligo or anovulation , Clinical  and / or  biochemical signs of   hyperandrogenism .Polycystic ovaries on ultrasound and exclusion of other etiologies  of the above  features. 

 Modification No 1 by The Australian Center for research excellence in PCOS (CRE-PCOS), 19/07.2018.:-What was the modification of done by the “The Australian Center for research excellence in PCOS (CRE-PCOS) “?? The said -committee endorsed  the Rotterdam PCOS diagnostic criteria in adults but with slight modifications  like  Ultrasound criteria   are tightened with advancing technology like A) Transvaginal ultrasound transducers with a frequency   bandwidth  that  includes 8 MHz is recommended. B) The threshold for PCOM on either   ovary with  follicle  number per ovary   (FNPO)  of > 20  -remind my dear members earlier it was  12 and / or an ovarian volume > 10   ml on either  ovary  ensuring  no corpora lutea   cysts  or dominant  follicles  are present.

Modification No 2 by the Australian Center for research excellence in PCOS (CRE-PCOS) on 19/07.2018’ .  USG is not necessary to diagnose PCO-When ?? This modification was based on the principle is not to over diagnose PCO in adolescents Ans;-A) USG is not an essential marker for PCO in adolescents   and those   within 8 years of menarche both ovulatory   dysfunction   and hyperandrogenism   are required ultrasound not recommended as it overlaps with the normal    physiology around puberty. If only ovulatory dysfunction  or hyperandrogenism   consider  at risk of PCOS and reassess later. Changes are made not to over diagnose   PCOS  in adolescents. This is not applicable in adults    where   irregular cycles and    hyperandrogenism features are present – ultrasound is not necessary for the diagnosis.