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Ovarian failure and polycystic ovary syndrome

Ovarian failure and polycystic ovary syndrome
Ovarian failure and polycystic ovary syndrome

Review

Ovarian failure and polycystic ovary syndrome ☆

Jana Petríková,Ivica Lazúrová?

1st Department of Internal Medicine,Medical Faculty of P.J.?afárik University,Ko ?ice,Slovakia

a b s t r a c t

a r t i c l e i n f o Available online 2December 2011Keywords:Ovary

Premature ovarian failure Polycystic ovary syndrome Autoimmunity Autoantibodies

The human ovary is commonly the target of an autoimmune attack leading to the ovarian dysfunction which can be manifested as premature ovarian failure (POF),polycystic ovary syndrome (PCOS),unexplained infertility as well as endometriosis.In case of POF,the evidence for an autoimmune etiology is based on the presence of lym-phocytic oophoritis,autoantibodies to ovarian antigens and association with other autoimmune disorders,which was clearly documented in many studies.The search for antiovarian antibodies has been undertaken in numer-ous studies,especially in patients with POF,however their results are still con ?icting particularly due to differ-ence in laboratory methods as well as many ovarian components being potential antigens.On the other side the autoimmune etiology of PCOS is still debated and was documented in some cases.Association of PCOS with non-organ speci ?c autoimmune disorders is controversial;however association with autoimmune thyroid disease was well demonstrated in some studies.

?2011Elsevier B.V.All rights reserved.

Contents 1.Introduction (4712)

Autoimmune premature ovarian failure .................................................A4722.1.Immune pathogenesis of POF................

...................................A4722.1.1.Humoral immunity ...................................................A4722.1.2.Cellular immunity....................................................A4732.1.3.Histopathology of POF...............

...................................A4732.2.Clinical manifestations and management of autoimmune POF ...................................A4732.3.Association with other autoimmune diseases ...........................................A4732.4.Impact of immunosuppressive therapy ..............................................A4743.Polycystic ovary syndrome ....................

...................................A4753.1.PCOS and autoimmunity ..................

...................................A4753.1.1.Immune dysregulation in PCOS ..........

...................................A4753.2.PCOS and ovarian autoimmunity ..............

...................................A4753.2.1.Association of PCOS with autoimmune disorders ..

...................................A4764.Conclusion...............................................................A476References ..............................

...................................A476

1.Introduction

Human ovary is commonly the target of an autoimmune attack in cases of organ or non-organ speci ?c autoimmune disorders leading to

the ovarian dysfunction which can be manifested as premature ovar-ian failure (POF)or other pathologies such as polycystic ovary disease (PCOS),unexplained infertility and endometriosis.Both humoral and cellular components of autoimmune response can be involved in the etiopathogenesis of ovarian dysfunction.

The search for antiovarian antibodies has been undertaken in nu-merous studies,especially in patients with POF,however their results are still con ?icting,and particularly due to difference in laboratory methods as well as many ovarian components being potential antigens.

Autoimmunity Reviews 11(2012)A471–A478

☆No con ?ict of interest.

?Corresponding author at:1st Department of Internal medicine,Medical Faculty of P.J.?afárik University Ko ?ice,Trieda SNP 1,04001Ko ?ice,Slovakia.Tel.:+421556403525;fax:+421556403551.

E-mail address:https://www.wendangku.net/doc/5d8733029.html,zurova@upjs.sk (I.

Lazúrová).1568-9972/$–see front matter ?2011Elsevier B.V.All rights reserved.doi:

10.1016/j.autrev.2011.11.010

Contents lists available at SciVerse ScienceDirect

Autoimmunity Reviews

j o u r n a l h om e p a g e :ww w.e l s e v i e r.c o m /l o c a t e /a u t r e v

2.Autoimmune premature ovarian failure

Premature ovarian failure is characterized by the loss of ovarian functions before the age of40years.The main symptom is absence of regular menstrual cycles,and the diagnosis is con?rmed by detec-tion of raised follicle-stimulating hormone and declined estradiol in the serum.Two mechanisms are probably involved in POF,namely follicle dysfunction and follicle depletion[1].Infertility and psycho-logical stress are common consequences of this entity,the prevalence of which is0.9to3%.It is estimated to affect about1%of women younger than40,approximately0.1%of those under30and0.01%of women under the age of20[2].The etiology includes speci?c genetic mutations(referred to oocyte,enzymes,or hormone receptors),auto-immune and environmental causes(viral infection,chemotherapy, radiotherapy and pelvic surgery),and metabolic disturbances(galac-tosemia).In most cases,however,no precise cause can be identi?ed, and these forms are referred to as idiopathic[3,4].This condition is not irreversible and permanent because residual oocytes capable of recruitment and fertilization are still present in the ovary.Autoimmune mechanism is considered to be a cause of POF in about20–30%[5].The evidence for an autoimmune etiology is threefold:the presence of lym-phocytic oophoritis,autoantibodies to ovarian antigens,and associated autoimmune disorders.

2.1.Immune pathogenesis of POF

2.1.1.Humoral immunity

Study of anti-ovarian autoantibodies has led to the identi?cation of putative ovarian epitopes,which may enable better understanding of the pathologic mechanisms involved in POF.The detection of auto-antibodies directed against various ovarian targets supports the hy-pothesis of an autoimmune etiology of POF.The?rst reports on such antibodies included mainly patients with POF and associated ad-renal autoimmune disease.These patients had antibodies that recog-nized several types of steroid-producing cells of the adrenal cortex, testis,placenta and ovary and therefore were called as steroid cell an-tibodies(SCA)[6,7].The steroid cell enzyme,3b-hydroxysteroid dehy-drogenase(3b-HSD)has been identi?ed as a target of SCA in POF.It is involved in the steroid metabolic pathway and is expressed in tissues recognized by SCA.3b-HSD autoantibodies were found in21%women with isolated idiopathic POF using immunoblotting techniques and adrenal cDNA library screening[8].However,a later study reported 3b-HSD antibodies to be rare(2%)in women with POF[9].Other anti-bodies can be directed against steroid cells or enzymes common to the ovary and adrenal glands,including cytochrome P450side-chain cleav-age enzyme(P450SCC),17-αhydroxylase/17,20-lyase(CYP17A1)and 21-hydroxylase(CYP21)enzymes.SCA in combination with P450SCC and CYP17A1enzyme antibodies are positive in a majority of this subset of POF cases[10]and[11].The prevalence of SCA depends on the clinical features:they can be detected in~60%of APS-I patients and~33%of APS II patients,but the highest prevalence,i.e.92%,has been shown in pa-tients with duration of POF less than5years[12].Among patients who have Addison's disease and POF,these autoantibodies are found to be present in more than90%of cases[13].In patients whose POF is associ-ated with autoimmune pathologies other than Addison's disease,as well as in isolated POF,the prevalence of SCA remains b10%.

The autoimmune response in POF primarily targets theca cells, yielding elevated concentrations of inhibin(useful ovarian peptides in the assessment of follicular reserve),which seems to be a useful diag-nostic marker for autoimmune etiology of ovarian insuf?ciency due to steroid cell autoimmunity[14,15].On the other hand,normal serum antimüllerian hormone concentrations were detected in two-thirds of women with recently diagnosed POF,which demonstrates that this form of ovarian insuf?ciency is associated with a preserved pool of func-tioning follicles[14].There are several other autoantibodies towards speci?c ovarian targets potentially mediated autoimmune damage in POF:gonadotropin receptor autoantibodies;zona pellucida autoanti-bodies;as well as anti-oocyte cytoplasmic antibodies towards MATER (“Maternal Antigen That Embryos Require”)[16–18].Understanding these targets in autoimmune response,Otsuka N et al.tried to induce ovarian speci?c tolerance via transgenic expression of the MATER anti-gen on potentially tolerogenic antigen-presenting cells,which typically present antigen via the major histocompatibility complex(MHC)class II molecule.They utilized a murine model of ovarian autoimmunity, whereby oophoritis develops after3rd neonatal day thymectomy (NTx).Wild-type and transgenic mice,carrying an MHC Class II-driven Mater gene(IE-Mater),were subjected to NTx and assessed for evidence of autoimmune oophoritis.After disease induction by NTx,female mice carrying the IE-Mater transgene had signi?cant reductions in histological oophoritis(56%)and circulating ovarian autoantibodies(28%)in com-parison with wild-type females(94%and82%,respectively).Incidence of other autoimmunity was unaffected as assessed by antinuclear https://www.wendangku.net/doc/5d8733029.html,ck of complete disease protection suggests that other anti-gens may also play a role in autoimmune oophoritis[19].The human ortholog of Mater,NALP5,was recently identi?ed as an autoantigen in the parathyroid gland;the presence of autoantibodies against NALP5 was associated with hypoparathyroidism and ovarian insuf?ciency in APS-1.NALP5is expressed almost exclusively in parathyroid and ovarian cells[20].

Recently,authors pointed to the concept of functional autoanti-bodies'(stimulating and/or suppressive)control in autoimmune dis-eases,particularly those comprising“sister-organs”,such as ovary, thyroid and adrenal glands[21].Lately,in a study conducted by Edas-sery et al.antigens included aldehyde(retinal)dehydrogenases (ALDH1A1,ALDH1A2,and ALDH7A1),protein disul?de isomerase A3, vimentin,α-enolase,phosphoglycerate dehydrogenase,and selenium-binding protein1(SBP1).Sixty percent(24out of40)of infertility and POF sera were positive for recombinant ALDH1A1,SBP1,or enolase;

80.7%(21out of26)of anti ovarian antibody(AOA)-positive sera had antibodies to one or more of the three antigens,and only7%(1out of 14)of AOA-negative sera had antibodies to recombinant proteins[22].

Until recently different methods have been tried to identify antio-varian antibodies the most common being enzyme-linked immuno-sorbent assay(ELISA)and immuno?uorescence(IFL).However, search for organ speci?c ovarian antibodies in POF has yielded con-?icting results so far.Such variable results were attributed to the dif-ferent stages of the disease when tested,methodological differences and by the multiplicity of potential immune targets that comprise various steroidogenic enzymes,gonadotrophins and their receptors, the corpus luteum,zona pellucida and https://www.wendangku.net/doc/5d8733029.html,ing a well estab-lished novel method[23],Khole demonstrated multiple molecular and histological autoimmune targets in the ovary using sera of infer-tile women having AOA[24]and human heat-shock protein90-beta (HSP90-beta)was identi?ed as the immunodominant target.The in-volvement of multiple antigenic targets,the high prevalence of anti-HSP90antibodies,and a broad gamut of immunological disorders,in which anti-HSP90antibodies are found,support the hypothesis that anti-HSP90antibodies could be present in patients with a putative defect in immunoregulation.In the recent study Mande et al.ob-served that31%of the total women recruited under an IVF-embryo transfer program and46%of women with premature ovarian failure tested positive for AOA[25].Three immunodominant ovarian autoan-tigens,namely non-muscleα-actinin4,heat shock70protein5and cytoplasmicβ-actin,were identi?ed.All the above antigens were found to be expressed in the ooplasm throughout follicular develop-ment.All these autoantigens are expressed speci?cally in the oocyte exceptαACTN4.

There are only a few studies addressing the role of human leukocyte antigen(HLA)in pathogenesis of POF.In a Japanese women population, 83women with idiopathic isolated POF were examined.Of86haplo-types identi?ed for MHC class I(HLA-A,B,and C)and31haplotypes detected for MHC class II(HLA-DRB1and DQB1),a single haplotype

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(A*24:02-C*03:03-B*35:01)remained signi?cant after Bonferroni and B-H corrections(frequency:4.82%in women with POI and1.06%in the control data).These results imply that a speci?c HLA haplotype (A*24:02-C*03:03-B*35:01)constitutes a susceptibility factor for appar-ently isolated POI in Japanese women[26].

2.1.2.Cellular immunity

Abnormalities of the cellular immunity,i.e.T lymphocytes(espe-cially effector helper,CD4-positive T cells),macrophages and dendrit-ic cells,also play an important role in autoimmune reactions, particularly in the development of autoimmune lesions,described also in POF supporting the autoimmune mechanism of the disease as evidenced also in animal model of autoimmune oophoritis[27,28]and [29].As in other autoimmune diseases,the absolute as well as relative count of peripheral blood T-lymphocytes,especially CD4+T cells,has been found to be increased in patients with POF and a dense in?ltration of activated T lymphocytes was observed in close contact with follicular epithelium expressing HLA-DR and CD40in a case of autoimmune oophoritis[30,31].In addition,some authors demonstrated an increase of autoantibody producing B cells independently of serum estrogen level and a low number of effector CD8+/CD57+T cytotoxic cells as well as suppressor lymphocytes in patients with POF,and an overall in-crease of the CD4+/CD8+ratio[27,32].Reduced NK cell number and impaired NK cell activity have been documented in women with POF and in murine post-thymectomy autoimmune oophoritis[33,34].The alteration of cellular immunity has also been illustrated by a cutaneous candidine(derived from Candida albicans)delayed hypersensitivity test being negative in50%of POF patients[33].The role of cytokines has also been described causing follicular atresia in POF[35,36].Finally,in vitro tests showed that blood monocytes from20to46%of POF patients had an abnormal response to chemotactic agents[37,38]whereas den-dritic cells from36%of the same patients presented a reduced capacity to aggregate with T-lymphocytes.Similar?ndings have been reported in other autoimmune diseases,such as type I diabetes or Graves'disease [38].Evidences for humoral and cellular immunity are presented in Table1.

2.1.

3.Histopathology of POF

Histological examination of ovaries from POF patients shows either a complete loss of ovarian follicles or the persistence of more or less abundant follicles.However,systematic histological screening of POF revealed detectable follicles varying from few to numerous in40%of cases[16,39].With ultrasound,residual follicular structures were docu-mented in41–60%of patients presenting clinical and biological signs of POF[40,41].

In those cases where POF is associated with adrenal autoimmuni-ty,histological examination almost always con?rms the signs of autoimmune oophoritis:in?ltration of follicles by lymphocytes,plas-ma cells and macrophages,the steroid producing cells being the main target of the immune attack.Immunohistochemical staining tech-niques have revealed in?ltrating lymphocytes being T cells(CD4+ CD8+)which is consistent with a potential role of T-lymphocytes in autoimmune ovarian disease[42].Follicular depletion might be the?nal stage of primary or secondary autoimmune process directed against ovarian structures.Hypothetically,autoantibodies to the ovary may have been present in the ovary without reaching detectable levels in the serum or inducing local in?ammation.

2.2.Clinical manifestations and management of autoimmune POF

The cardinal?nding in patients with POF is the cessation of men-ses before the age of40years.Prodromal POF may present with hot ?ushes before the development of menstrual dysfunction.In addition symptoms of estrogen de?ciency may develop in many but not all pa-tients.These include vasomotor symptoms(hot?ushes and night sweats),sleep disturbances and dyspareunia related to vaginal dryness.

A detailed medical history should be obtained from the patient present-ing with clinical picture suspicious of POF.Despite the obvious manifes-tations of serious illnesses,a history of past and current autoimmune disorders should be obtained.Inquiries should be made as to the pres-ence,in the patient or her family,of Addison's disease,thyroid disorders, diabetes mellitus,SLE,rheumatoid arthritis,vitiligo,Crohn's disease,and Sj?gren's syndrome[43].Attention should be focused to the subtle and insidious symptoms of adrenal failure,including recent weight loss,an-orexia,vague abdominal pains,weakness,increased skin pigmentation, and salt craving.All symptoms might be found in Table2.

A careful search should be made for the physical presentation of autoimmune disorders.Of particular note are premature graying of the hair associated with hypothyroidism and pernicious anemia,the sparse axillary and pubic hair with increased pigmentation of the hand skinfolds and gums of adrenal failure.Other?ndings include vit-iligo and alopecia areata or facial signs of SLE.Careful thyroid exami-nation may reveal enlargement due to autoimmune thyroid disease. Many clinicians recommend screening patients with POF for other au-toimmune endocrine problems.In the prospective screening program in119patients with POF results showed that no new cases of adrenal failure,pernicious anemia,or hypoparathyroidism were uncovered. However,screening tests revealed12new cases of thyroid disease and 2new cases of diabetes mellitus.Thyroid autoimmune disease,most commonly Hashimoto's thyroiditis,is present in14to27%of women at initial diagnosis[44].POF may occur in association with a non-organ-speci?c autoimmune disorder,and thus a complete blood count and urine analysis should be obtained.Erythrocyte sedimentation rate,anti-nuclear antibodies,immunoglobulins,and rheumatoid factor should be measured only as clinically indicated.In one of POF patient who had re-current upper respiratory infections,an isolated IgA de?ciency was con-?rmed[16].Searching for thymomas in patients with POF is not warranted unless there is coexisting myasthenia gravis.Annual screen-ing is reasonable only for serum thyroid stimulating hormone(TSH) and fasting glucose[44].

2.3.Association with other autoimmune diseases

Between10and30%of women with POF have a concurrent organ speci?c and non-organ speci?c autoimmune disorders,because there

Table1

Immune pathogenesis of POF.

Humoral immunity: (antigenic targets)Steroid cell antibodies[6,7]

3b-Hydroxysteroid dehydrogenase[8]

Cytochrome P450side-chain cleavage enzyme,17-αHydroxylase/17,20-lyase and21-hydroxylase enzymes [10,11]

Gonadotropin receptors,Zona pellucida,Oocyte cytoplasmatic Maternal Antigen That Embryos Require [16–18]

NALP5(human ortholog of MATER)[20]

Aldehyde(retinal)dehydrogenases,protein disul?de isomerase A3,vimentin,α-enolase,phosphoglycerate dehydrogenase,selenium-binding protein1[22]

Non-muscleα-actinin4,heat shock70protein5,

?-actin[25]

Cellular immunity:↑CD4+T cells[30,31]

↓CD8+/CD57+cytotoxic cells,↓Suppressor

lymphocytes[27]

↑CD4+/CD8+ratio[32]Table2

Clinical symptoms of POF.

Oligomenorrhea/amenorrhea

Dyspareunia

Vasomotor symptoms(hot?ushes,night sweats)

Sleep disturbances

Symptoms of associated autoimmune diseases

A473

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is a sharing of genetics and possibly environmental(susceptibility) factors.The most commonly reported being hypothyroidism,and the most clinically important hypoadrenalism,as well as association with myasthenia gravis,systemic lupus erythematosus,rheumatoid arthritis and Crohn's disease[16,41].

However many other organ speci?c autoimmune diseases,such as Graves'disease,diabetes mellitus,pernicious anemia,vitiligo,celiac disease,multiple sclerosis as well as non-organ speci?c diseases includ-ing idiopathic thrombocytopenia were documented to be associated with POF.

It has been recognized that POF could be associated with nearly all organ-speci?c autoimmune diseases,as well as with several autoim-mune disease in the same patients,referred to as autoimmune poly-glandular syndrome(APS)[16,41,45].APS-I,also called APECED (autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy) is a rare autosomal recessive disease caused by mutation in the AIRE (autoimmune regulator)gene on chromosome21,which may be in-volved in regulatory T cell development,and without any association with a speci?c HLA haplotype[17,39].The diagnosis is generally made in childhood,because of adrenal and parathyroid autoimmune disease, frequently associated with mucocutaneous candidiasis,ectodermal de-fects,and POF that occurs in40–60%of cases[39,46].APS-II,also called Schmidt–Carpenter syndrome,an autosomal dominant disease,and as-sociated with HLA-B8DR3DR4haplotypes,comprises Addison's disease, insulin-dependent-diabetes,and POF with the prevalence of10–25% [41,47].APS-III is quite similar to APS-II,except there is no Addison's disease,but other autoimmune diseases,such as pernicious anemia or vitiligo are often associated[48].POF may be detected before,simulta-neously and also after manifestation of APS.

Because of the particular association with Addison's disease,three different situations have to be distinguished:POF associated with ad-

renal autoimmunity;POF associated with non-adrenal immunity (most frequently associated with thyroid autoimmunity);and isolated, idiopathic POF,the latter which cannot exclude an autoimmune mech-anism,possibly provoked by environmental factors[49].Cases of POF associated with antiadrenal autoimmunity represent a homogeneous and well-characterized subgroup of ovarian failure,whereas in other forms of this disease,there is a large diversity in clinical,immunological and histological features.All the possibly associated autoimmune con-ditions with POF are listed in Table3.

2.4.Impact of immunosuppressive therapy

To evaluate prospectively the effects of high-dose,short-term treatment with a glucocorticoid in an attempt to normalize ovarian failure11women with POF desirous of pregnancy were involved.In this uncontrolled,nonrandomized prospective study,Prednisone 25mg was given four times per day for2weeks.Two women demon-strated normalization of their serum gonadotropins,an increase of serum estradiol(E2),and ultrasonographic visualization of follicular growth,with both conceiving.The other nine demonstrated no bio-chemical or clinical response.The results were most effective in women with concomitant autoimmune thyroid(AIT)disease and POF of b2years'duration[50].In another placebo-controlled,ran-domized,multicenter study one hundred patients with idiopathic POF intended to enter the study.Endocrine and immune parameters were tested on days1and15.On day1,subjects were randomized to receive either9mg of dexamethasone daily or placebo.From day 5onward,300IU of human menopausal gonadotropin daily was added for10days in both groups.The dosage of dexamethasone was decreased stepwise in the second week and discontinued after day15.Patients were monitored by transvaginal ultrasonography and by determining serum E2levels.No ovulation was recorded in the?rst36patients.Interim analysis showed that the95%con?dence intervals of an ovulation rate of0were0–17%for the dexamethasone arm(n=19)and0–19%for the placebo arm(n=17).Because the preset objective(a difference of20%)would never be reached,the study was discontinued[51].A prospective randomized study in-volved women with idiopathic karyotypically normal POF,who were treated with gonadotropin-releasing hormone(GnRH)agonist and gonadotropins with and without the addition of corticosteroids in an attempt to restore ovarian function.The study comprised58 women with idiopathic POF randomly allocated to either GnRH ago-nists(GnRHa)plus gonadotropin therapy with the addition of corti-costeroids(29patients)or GnRHa plus gonadotropin therapy with placebo(29patients).Ovulation occurred in six cases(20.7%)in the dexamethasone group versus three cases(10.3%)in the placebo group.There were two singleton pregnancies in the dexamethasone group.The combination of corticosteroids with pituitary suppression followed by ovarian stimulation with gonadotropin appeared to be bene?cial in this study[52].Two case reports of young women with POF who were treated with glucocorticoids in the hopes of restoring fertility yielded opposite results.The?rst patient with histologically proven autoimmune oophoritis was treated with alternate day pred-nisone therapy for16weeks(mean daily dose of11mg,total cumu-lative dose of1225mg).She had return of menstrual bleeding six times and ovulatory progesterone concentrations four times over a 16week period.The second patient with presumed but uncon?rmed autoimmune ovarian failure was treated with a course of up to2mg of dexamethasone per day,resulting in a total dose of255mg over a9month period.During that treatment her menses did not resume. The corticosteroid treatment was complicated by iatrogenic Cushing syndrome and osteonecrosis of the knee[53].

Moreover,some authors searched for the effect of corticosteroid on immune cells.The circulating T lymphocytes were examined uti-lizing monoclonal antibody L243to the nonpolymorphic region of the la antigen.The percentage of peripheral T cells expressing the la “immune-associated”antigen was5.6%(normal3%or less).With cor-ticosteroid therapy of Prednisone40mg daily during6months,the percentage decreased to2%and menses resumed after secondary amenorrhea of two years'duration.Following cessation of steroid Table3

Autoimmune diseases associated with POF.

Occasional associations

Non organ-speci?c diseases Organ speci?c diseases Systemic lupus erythematosus Alopecia

Idiopathic thrombocytopenic

purpura

Asthma

Haemolytic anemia Chronic active hepatitis

Sj?gren's syndrome Crohn's disease

Ulcerative colitis

Coeliac disease

Diabetes mellitus(2.5%)

Pernicious anemia

Glomerulonephritis

Hypoparathyroidism

Hypophysitis

Juvenile rheumatoid arthritis

Rheumatoid arthritis

Malabsorption syndrome

Multiple sclerosis

Myasthenia gravis

Primary biliary cirrhosis

Quantitative immunoglobulin

abnormalities

Vitiligo

Frequent associations

Thyroid disease(27%)

Autoimmune polyglandular syndrome

(APS)types I and II:

?60%of APS I have concomitant POF

?4%of APS II have concomitant POF

Addison's disease(2.5%)

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administration,the percentage of la-positive T cells rose to7.0%and secondary amenorrhea redeveloped again.After corticosteroid thera-py was reinstituted,menses resumed and the percentage of la-positive T cells fell to normal[54].Immunosuppressive therapy, using different dose and term of glucocorticoids should be considered in a selected population of well-de?ned autoimmune POF patients,as well as in idioptahic POF patients,in whom the resumption of ovarian activity is possible,spontaneously,under HRT,and/or under immuno-modulating treatment

Plasmapheresis with thymectomy has been reported to be suc-cessful in a patient with myasthenia gravis,and intravenous immuno-globulin therapy has been effective in a patient with autoimmune polyglandular syndrome[55]

3.Polycystic ovary syndrome

Polycystic ovary syndrome is the most common endocrine disor-der in women of reproductive age and the most frequent cause of in-fertility with the prevalence of5–10%.It is characterized by chronic oligo/anovulation,clinical and/or biochemical hyperandrogenism and polycystic ovaries on vaginal ultrasonography.Although the con-dition was described by Stein and Leventhal in1935[56],there is still considerable controversy on the optimal diagnostic criteria.Rotter-dam criteria proposed in2003are currently debated because they in-troduced two new nonhyperandrogenic phenotypes[57].In2006 Androgen Excess Society published a position statement which sug-gested that androgen excess is the key component of PCOS related to clinical symptoms and long-term morbidity.According to AES,diagnos-tic criteria should be modi?ed to include only those with hyperandro-genism and polycystic ovary or ovarian dysfunction[58].In agreement with current knowledge on etiopathogenesis PCOS is considered to be a genetic disorder with various phenotypic expressions.

Several mechanisms including aberration of luteinizing hormone secretion,ovarian17alpha hydroxylase dysregulation,genetics,envi-ronmental factors as well as hyperinsulinemia have been proposed to play a signi?cant role in the etiopathogenesis of PCOS.Nevertheless, its pathogenesis is still debated.Many conditions are associated with an increased prevalence of PCOS especially obesity,insulin resistance [59,60],type2diabetes mellitus(DM)[61,62]and vitamin D de?ciency. Moreover breast and endometrial carcinomas due to prolonged estro-gen stimulation unopposed by progesterone[63]have been reported. In general,higher risk of cardio-vascular diseases and a13-fold in-creased risk of acute myocardial infarction were documented.

3.1.PCOS and autoimmunity

3.1.1.Immune dysregulation in PCOS

An autoimmune mechanism has been suggested in some cases of PCOS especially those with other autoimmune disorders.Unfortu-nately the heterogeneity of the syndrome,variety of ovarian antigens as well as antibody tests lead to con?icting results.

The state of estrogens excess has been linked to different autoim-mune diseases.This was con?rmed by studies in women with reproduc-tive age documenting a higher prevalence of systemic autoimmune diseases[64]as well as studies in hypogonadal men having relative ex-cess of estrogens.For example,in patients with Klinefelter syndrome an association with rheumatic and autoimmune diseases has been reported particularly with rheumatoid arthritis,juvenile idiopathic ar-thritis,psoriatic arthritis,polymyositis/dermatomyositis,systemic lupus erythematosus,systemic sclerosis,mixed connective tissue disease,anti-phospholipid syndrome and others[65].In another study a relationship between Klinefelter syndrome and rare autoimmune diseases such as primary biliary cirrhosis was suggested[66].High levels of androgens are presented in patients who suffer from PCOS seeming to have a pro-tective role against the development of autoimmune diseases;however several mechanisms related to estrogen effects on the immune system oppose this activity.Estrogens increase the secretion of IL-4in Th2lym-phocytes,IL-1in monocytes,IL-6in T-lymphocytes and interferone-γin Th1cells.During normal ovulatory menstrual cycle in young women—follicular phase with higher levels of estrogens is characterized by eleva-tion of IL-6levels whereas its levels are decreased in the luteal phase which is also characterized by negative correlation with progesterone [67].The stimulatory effect of estrogens on the immune system could be inhibited by progesterone.Patients with PCOS present low level of progesterone due to oligo/anovulation therefore the immune system could be over-stimulated by the relative hyperestrogenism leading to production of autoantibodies in these patients.

Recent studies clearly documented that obesity is associated with a decreased vitamin D levels which was also found in obese women with PCOS.In a study of Wehr and colleagues72.8%of206PCOS women were found to be25(OH)vitamin D de?cient(b30ng/ml). These women had signi?cantly worse metabolic characteristics in comparison with those who present a suf?cient25(OH)vitamin D levels[68].Because this study had limitations of not including control group and women with metabolic syndrome but without PCOS,large intervention trials are needed to evaluate the effect of vitamin D supple-mentation on metabolic disturbances in PCOS women.Whether vitamin D de?ciency in some PCOS women may be involved in the immune path-ogenesis of PCOS remains to be elucidated.

In addition the role of vitamin D in regulations of immune mech-anism has been described.The hypothesis that vitamin D relates to autoimmune disorders emerged from the observation that people liv-ing near the equator were at a decreased risk of developing common autoimmune diseases[69].Furthermore,several authors described reduced levels of vitamin D in patients with various rheumatic disorders. In a study of Orbach et al.1029patients with different autoimmune dis-orders including scleroderma,polymyositis and dermatomyositis,anti-phospholipid syndrome,rheumatoid arthritis and SLE had lower levels (average of9.3–13.7ng/mL)of25(OH)D than controls[70].Main func-tions of vitamin D in the immune system include regulation of the differ-entiation and activation of CD4lymphocytes[71];increase in the number and function of regulatory T cells;in vitro inhibition of the differ-entiation of monocytes in dendritic cells[72];reduction in the produc-tion of cytokines,interferon-g,IL-2,and TNF-αby Th1cells,and stimulation of the function of Th2helper cells[73];inhibition of the pro-duction of IL-17by Th1cells[74];and in vivo and in vitro stimulation of NK T cells[75].

3.2.PCOS and ovarian autoimmunity

Studies of anti-ovarian antibodies that were performed so far yielded con?icting results.Evaluation of antibodies directed at human ovary using ELISA resulted in mean ratios which were signi?cantly higher for women with PCOS than for the control group(?gure:IgG (p b0.0001),IgA(p b0.003),IgM(p b0.0003).Positive anti-ovarian anti-bodies for at least one isotype were present in15(44%)of34of the PCOS[76]women:IgG nine(27%),IgA one(3%),IgM nine(27%).How-ever these results could not be con?rmed by others[77,78].A signi?cant correlation between levels of antiovarian antibodies and cycles of in vitro fertilization was found.Repeated punctures of ovarian tissue and microtraumatic changes may reveal ovarian antigens so far unknown for immune system and induce a response[79].On the other hand de-tection of anti-ovarian antibodies after laparoscopic electrocauteriza-tion in treatment of PCOS patients resistant to clomiphene citrate did not show higher rates compared to pre-operation state[80].Suh reported histological?ndings in a case of PCOS consistent with autoim-mune oophoritis[81].A group of Lonsdale demonstrated ovarian and adrenal antibodies,and lymphocytic in?ltration of ovaries in two pa-tients with PCOS[82].Some others showed antibodies to human ovarian sections and granulosa cells by immuno?uorescence in4/8patients with PCOS[83].Many other targeting antigens of opvarian immune pathology have been described in PCOS women.Anti-FSH antibodies of the IgA

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class speci?cally against the?chain of FSH were signi?cantly higher among75PCOS patients compared with85healthy controls[84].

Besides humoral immunity some researchers focused on the role of T cells and thymus.A key study in this?eld was performed by Chapman et al.,showing fundamental role of estrogen induced im-mune disruption of thymus in the development of PCOS in animal model.Na?ve mice were injected with estrogen after removing thy-mus gland.Anovulation and follicular cysts formation occurred sub-sequently.In contrary,no cysts were observed in mice in which thymectomy at3days of age preceded estrogen injection.In fact, after restoring immune function by thymocyte replacement,the ma-jority of thymectomized,estrogen-injected mice had ovaries with corpora lutea.In conclusion,when estrogen was not able to act on thymus,no cysts developed and mice had ovulation.Subsequent re-search showed that the disease is transferable by lymfocyte infusion ful?lling another condition of autoimmune diseases.Absence of regu-latory T cells seemed crucial for developing ovarian cysts[85].Glei-cher et al.claims PCOS might be an opposite condition to premature ovarian failure(POF),which in contrast is a state characterized by the loss of ovarian functions before the age of40;its prevalence is ~1%of women.They suppose that functional autoantibodies play an important role in pathogenesis of both diseases[86].

3.2.1.Association of PCOS with autoimmune disorders

3.2.1.1.PCOS and non-organ speci?c autoimmunity.Many studies clear-ly documented that estrogen excess is associated with a higher risk of autoimmune disorders which was documented in women of fertile age as well as men with Klinefelter syndrome[64,65].On the other side high testosterone levels are considered to be protective against autoimmunity.It is well known,that PCOS is a hyperandrogenic state but simultaneously it is also associated with an absolute or relative hyperestrogenic state.Whether androgen or estrogen component plays a predominant role in the immune response in PCOS patients is still unknown and data regarding the association of PCOS with other au-toimmune diseases are poor.

Recently few studies addressed the association between PCOS and autoimmunity with controversial results.He?er-Frischmuth et al. evaluated109sera from PCOS patients and performed anti-nuclear antibodies(ANA)screen,anti-histone,anti-nucleosome,and the anti ds-DNA utilizing ELISA tests.Statistical signi?cance(p b0.05) was found only in the levels of anti-histone and anti-dsDNA anti-bodies[87].In another study,36PCOS patients were evaluated for smooth muscle cell(SMA),liver–kidney microsome(LKMA),thyroid microsome(TMA),gastric parietal cell(PCA),ANA,reticulin(ARA) and mitochondrial antibodies(AMA)using indirect immuno?oures-cence method[88].Signi?cant difference in the detection of ANA and SMA was found in7PCOS patients(19.4%)versus3.6and5.1%in-cidence in control group of392women respectively(p b0.005).Other antibodies were negative.The difference in ANA levels between these studies might be explained by using distinct methods.Other autoim-mune diseases were reported in association with sexual dimorphism such as systemic lupus erythematosus and estrogen in?uence[89]. On the other hand results of Gingnell et al.indicate women with PCOS more frequently display below-median levels of IgM antibodies against phosphorylcholine,which are natural autoantibodies possibly exerting one of the atheroprotective functions of the immune system. Even more,older women with PCOS have lower median anti-PC levels suggesting a possible mechanism of higher cardiovascular risk in such patients[90].An aggressive population of T lymphocytes known as CD4(+)CD28(null)was recently associated with recurrent coronary instability and type2DM.Interestingly,PCOS patients were shown to have an expansion of such T cells which sheds new light on possible mechanisms responsible for the higher rate of cardiovascular diseases among PCOS[91].Further studies on larger cohorts of pa-tients are required.3.2.1.2.PCOS and organ speci?c autoimmunity.There are also few re-ports about association between PCOS and organ speci?c autoimmu-nity.It was studied mainly in relation to autoimmune thyroid disease. High prevalence of AIT was documented in a study of175patients with PCOS.Thyroid function and thyroid speci?c antibody tests revealed elevated thyroperoxidase(TPO)or thyroglobulin(TG)anti-bodies in14of168controls(8.3%),and in47of175patients with PCOS(26.9%)(p b0.001).On thyroid ultrasound42.3%of PCOS patients had a hypoechogenic tissue typical for AIT,in contrast to only6.5%of the control group(p b0.001).While thyroid hormone levels were nor-mal in all subjects,PCOS patients had a higher mean TSH level and a higher incidence of TSH levels above the upper limit of normal(PCOS 10.9%,controls1.8%)(p b0.001)[92].Anti-thyroid peroxidase anti-bodies exceeding the upper level of normal were found in signi?cantly more clomiphene citrate resistant patients compared to clomiphene responders and metformin responders.Elevated anti-TPO levels are as-sociated with poor treatment response in infertile women suffering from PCOS[93].On the other hand euthyroid girls with chronic lym-phocytic thyroiditis had signi?cantly higher prevalence of PCOS when compared to controls also suggesting a possible role of autoimmunity in the etiopathogenesis of PCOS.Whether autoimmune thyroiditis pre-disposes subjects to develop PCOS characteristics or if PCOS is a fore-runner of AIT still remains an unanswered speculation[94].

A case report was published of a26-years old woman having auto-immune polyglandular syndrome type II(diabetes with autoanti-bodies against GAD-65and IA-2,autoimmune thyroid disease)and PCOS with hyperandrogenic signs that had developed5years earlier [95].Recent study on50pregnant PCOS patients and59normal preg-nancies in Chilean women showed no association between anti-GAD65and anti-IA2auto-antibodies(2.0%and1.7%,respectively) known in DM[96].

4.Conclusion

Human ovary is commonly the target of an autoimmune attack leading to the ovarian dysfunction which can be manifested as pre-mature ovarian failure,polycystic ovary disease or unexplained infer-tility and endometriosis.

An autoimmune mechanism is considered to be a cause of POF in approximately20–30%of cases.The evidence for an autoimmune eti-ology is threefold:the presence of lymphocytic oophoritis,autoanti-bodies to ovarian antigens and association with other autoimmune disorders.Both humoral and cellular immunities seem to play an im-portant role in the immune pathogenesis of POF.Based on published data a short term immunosuppressive therapy using glucocorticoids may be considered in a selected population of well de?ned POF pa-tients in whom the resumption of ovarian activity could be expected.

In PCOS an autoimmune mechanism has been suggested in some cases and is probably related to estrogen excess where the stimulatory effect of estrogens on the immune system is not inhibited by progester-one levels being very low in anovulatory women.Recent studies addressed the association between PCOS and non-organ speci?c auto-immunity with controversial results.On the other side association of PCOS with thyroid autoimmunity has been well documented in some studies.Nevertheless,whether autoimmune thyroid disease predis-poses subject to develop PCOS remains still unknown.

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