Autoimmune Oophoritis: Clinical Presentation of an Unusual Clinical

Total Page:16

File Type:pdf, Size:1020Kb

Autoimmune Oophoritis: Clinical Presentation of an Unusual Clinical Page 1 of 5 Case report Autoimmune oophoritis: clinical presentation of an unusual clinical entity Obstetrics & Gynecology M Varras1*, A Anastasiadis2, J Panelos3, E Balassi3, A Demou3, CH Akrivis4 Abstract infertility in women before the age and had regular menses on a 28-day Introduction of 40 years1-4. The aetiologies of this cycle. She had five full-term normal condition include chromosomal pregnancies without any miscar- anomalies (such as X chromosome riages. Autoimmune oophoritis is a rare co- monosomy, translocations or partial On pelvic bimanual examination, ndition, which provokes ovarian fail- deletions), genetic predisposition an anteverted uterus was palpated, ure with either primary amenorrhea (such as fragile X pre-mutations, while both fallopian tubes and ovaries or secondary amenorrhea and a sub- BMP15 or DIAPH2 mutations), infec- were impalpable. Pelvic ultrasonog- sequent loss of fertility and ovarian tious diseases, complications of chem- raphy disclosed normal-sized ovaries hormonal function. The purpose of t- otherapy, pelvic radiotherapy, surgical with bilateral multicystic structures, his report is to document the clinical interventions or surgery, enzymatic with the largest follicle measuring Casesfindings report from two patients with aut- disorders and endometriosis. Prema- 1.2 cm. The thickness of the endo- oimmune oophoritis. ture ovarian failure might also be idio- metrium was 3.5 mm. Initial inves- manuscript. nal pathic or autoimmune2. Among a total tigation showed her serum gonado- fi Two cases of autoimmune oophorit- of 266 patients with spontaneous POF, tropin concentrations to be elevated: is are presented whose histopathol- 4% were diagnosed to have autoim- follicle stimulating hormone (FSH) at ogical findings were consistent with mune oophoritis3,4. 40 mIU/ml and luteinizing hormone international literature. Both cases Ovarian autoimmunity was first (LH) at 56 mIU/ml. 17-beta oestra- were histopathologically characteri- reported and serologically docu- diol was at 30 pg/ml (normal range: sed by lymphocytic and plasmacytic mented by Vallotton and Forbes in 30–100 pg/ml). Serum prolactin inflammatory infiltrations around t- 19665. Autoimmune oophoritis is a levels were normal and there was he cystic follicles. The inflammation distinct clinical entity and one of the no evidence of hypoparathyroidism. Conclusionwas located both in the theca and gr- causes of POF, particularly in women Thyroid function tests were normal. anular layers. with secondary amenorrhea6-8. Auto- Also, kidneys and liver function tests immune oophoritis generally occurs were normal. Serum electrolytes Patients with autoimmune oophorit- in the setting of autoimmune poly- were normal. Proteinuria was nega- is should be recognised by the histo- endocrine syndromes and is asso- tive. Serum adrenocorticotropin pathology of the ovarian biopsies as ciated commonly with other major hormone levels were normal. The they are at an increased risk of deve- endocrine failures such as diabetes progesterone challenge test was loping other autoimmune disorders. mellitus, Addison’s disease, hypopar- negative. Introduction athyroidism or hypothyroidism8-10. A At exploratory laparoscopy, her wide clinical spectrum has also been ovaries appeared small and inactive. Premature ovarian failure (POF) is on of the manuscript, as well read and approved a condition characterised by amen- demonstrated11. There were no signs of abdominal or Ɵ orrhea, some hot flushes, elevated The aim of this was to pelvic inflammatory processes. Biop- serum gonadotropin levels and describe the clinical spectrum and sies from both ovaries were obtained hypo- oestrogenism with associated the interesting pathologicalreport findings and endometrial curettage was originating from small ovarian biop- performed as well. sies from two patients with autoim- Grossly, two specimens had been * Corresponding author Email: [email protected] mune oophoritis. obtained from the right ovary with none declared. ict of Interests: a whitish-grey colour, measuring fl 1 Third Department of Obstetrics and Gynecol- on, design, and prepara ogy, ‘Elena Venizelou’ General Maternity Hos- Case report 0.7 cm and 1.2 cm in their greatest Ɵ pital, Athens, Greece Case 1 dimension, respectively, and one 2 rules of disclosure. (AME) ethical Ethics Medical on for Fourth Department of Obstetrics and Gyne- A 33-year-old woman presented with specimen had been obtained from Ɵ cology, ‘Elena Venizelou’ General Maternity Hospital, Athens, Greece a 10-month history of secondary the left ovary with white tan to 3 Department of Pathology, ‘G. Chatzikosta’ amenorrhoea and hot flushes. grey colour measuring 1.6 cm in its General State Hospital, Ioannina, Greece Menarche had occurred at an age of 14 greatest dimension. Also, the spec- 4 Department of Obstetrics and Gynecology, ‘G. Chatzikosta’ General State Hospital, Ioannina, years, she had developed secondary imen from the endometrial biopsy Greece sex characteristics appropriately measured 3.5 × 3 × 0.2 cm. At micro- Licensee OA Publishing London 2013. Creative Commons Attribution Licence (CC-BY) none declared. Con ng interests: Ɵ F : Varras M, Anastasiadis A, Panelos J, Balassi E, Demou A, Akrivis CH. Autoimmune oophoritis: All authors abide by the Associa All authors contributed to the concep to All authors contributed clinical presentation of an unusual clinical entity. OA Case Reports 2013 Jan 31;2(1):7. Compe Page 2 of 5 Case report Figure 1: Case 1: dense inflammation of Figure 3: Case 1: primordial folli- Figure 5: Case 1: T8 positive lympho- the ovary (haematoxylin-eosin × 100). cles are spared by the inflammation cytes (CD8 stain × 200). (haematoxylin-eosin × 400). nal manuscript. nal fi Figure 2: Case 1: dense inflamma- Figure 6: Case 1: CD138 positive tory infiltrate destroys the follicle Figure 4: Case 1: T4 positive lympho- plasma cells (× 100). (haematoxylin-eosin × 200). cytes (CD4 stain × 200). history of hypothyroidism; she was was i dentified in the endometrium. scopic examination, the ovarian biop- stable on thyroxine 0.1 mg daily. The final pathological diagnosis was sies contained primordial, developing On pelvic bimanual examination, autoimmune oophoritis. and atretic follicles. Dense inflamma- an anteverted uterus was palpated The patient was diagnosed as tion of the ovary was found (Figure and a painful cystic mass in the having POF due to autoimmune 1). The most striking feature was right adnexa was palpated as well. oophoritis, and she was started on the destruction of the developing Pelvic ultrasonography revealed oestrogen and progesterone replace- follicles by lymphocytic and plasma- a well-defined cystic mass with a ment therapy. Laboratory tests were cytic infiltration (Figure 2), while the hypoechogenic appearance in the negative for rheumatoid factor, anti- primordial follicles were apparently right adnexa uteri, measuring 8 cm nuclear antibodies (ANA), compo- and entirely spared from this process in its maximum diameter and a on of the manuscript, as well read and approved nents 3 and 4 of the complement (C3 Ɵ (Figure 3). The inflammation was small multicystic structure in the left and C4), immunoglobulin (Ig) G and located both in the theca and granular adnexa. Free liquid in the posterior IgM alpha cardiolipin antibodies and layers. The ovarian stroma was unre- space of Douglas was not found. C-reactive protein (CRP). The patient markable. Immunohistochemically, Initial investigation showed was missed from further follow-up. the inflammatory population was normal blood cell counts, as well composed mainly from T-lympho- Case 2 as normal function tests for liver, cytes (CD4+, CD8+) (Figures 4 A 32-year-old woman presented with kidneys and thyroid. The INR and none declared. ict of interests: and 5) and plasma cells (CD138+) acute lower abdominal pain. Last activated partial thromboplastin fl on, design, and prepara (Figure 6). The endometrium had menstrual period was three months time ratios were normal. Elevated Ɵ an oedematous appearance with previous to the date of presentation. levels of serum carbohydrate antigen rules of disclosure. (AME) ethical Ethics Medical on for focal haemorrhagic infiltration of the Menarche had occurred at the age (CA)-19.9 (81 IU/ml, normal range Ɵ stroma. The endometrial glands were of 15 years and her menstrual cycle <37) and CA-125 (39.7 U/ml, normal small, round, coated with cylinder had been regular previously on a range: <37) were found, while the epithelium and without any remark- 29-day cycle. She had two previous serum levels of CA-15.3, carcinoem- able mitotic activity. No inflammation caesarean sections and a medical bryonic antigen and alpha fetoprotein Licensee OA Publishing London 2013. Creative Commons Attribution Licence (CC-BY) none declared. Con ng interests: Ɵ F : Varras M, Anastasiadis A, Panelos J, Balassi E, Demou A, Akrivis CH. Autoimmune oophoritis: All authors abide by the Associa All authors contributed to the concep to All authors contributed clinical presentation of an unusual clinical entity. OA Case Reports 2013 Jan 31;2(1):7. Compe Page 3 of 5 Case report Figure 7: Case 2: severe inflamma- Figure 9: Case 2: characteristic Figure 11: Case 2: PanT (CD45RO) tory infiltrate destroys the follicle destruction of the developing follicle (haematoxylin- eosin × 200). by the inflammatory infiltration stain × 100. (haematoxylin-eosin × 400). virus. Also, the serum Ig concentra- tions were negative for IgM (162 mg/ dl; normal range: 46–304 mg/dl) and IgA (165 mg/dl; normal range: 82–453 mg/dl). Positive serum labo- ratory tests were found for antistrep- nal manuscript. nal tolysin O (333 IU/ml; normal range: fi 0–116 IU/ml) and IgG (1730 mg/dl; normal: 751–1560 mg/dl). Also, the titres of ANA were positive. During the six-month follow-up Figure 8: Case 2: dense inflamma- postoperatively, her serum gonado- tory infiltrations around the follicle tropins were slightly elevated with (haematoxylin-eosin × 200). Figure 10: Case 2: layers of granu- FSH levels of 15.8 mIU/ml and losa cells surround an unremark- LH levels of 18.4 mIU/ml. 17-beta able oocyte in a secondary follicle were in normal ranges. The patient (haematoxylin-eosin × 400).
Recommended publications
  • The Role of Autoimmunity in Premature Ovarian Failure
    Iran J Reprod Med Vol. 13. No. 8. pp: 461-472, August 2015 Review article The role of autoimmunity in premature ovarian failure Mahbod Ebrahimi M.D., Firouzeh Akbari Asbagh M.D. Department of Obstetrics and Abstract Gynecology, Moheb-e-Yas Women General Hospital, Faculty of Premature ovarian failure (POF) is a heterogeneous syndrome with several causative Medicine, Tehran University of factors. Autoimmune mechanisms are involved in pathogenesis of 4-30 % of POF Medical Sciences and Health cases. The present review focuses on the role of autoimmunity in the Services, Tehran, Iran. pathophysiology of POF. The evidences for an autoimmune etiology are: demonstration of ovarian autoantibodies, the presence of lymphocytic oophoritis, and association with other autoimmune disorders. Several ovarian antigenic targets have been identified in POF patients. The oocyte seems to be the most often targeted cell. Lymphocytic oophoritis is widely present in POF associated adrenal s disease is one of the most common autoimmune disordersۥinsufficiency. Addison associated with POF. Early detection of this potentially life threatening disease was recommended in several studies. The gold standard for detecting autoimmune POF is ovarian biopsy. This procedure is not recommended due to unknown clinical value, expense, and risks. Several immunoassays have been proposed as substitute diagnostic tools. Nevertheless, there is no clinically proven sensitive and specific serum test to confirm the diagnosis of autoimmune POF or to anticipate the patient’s chance of developing POF or Corresponding Author: Mahbod Ebrahimi,, Department of associated diseases. Obstetrics and Gynecology, Some authors suggested the possible effects of immuno-modulating therapy on the Moheb-e-Yas Women General resumption of ovarian function and fertility in a selected group of autoimmune POF Hospital, North Oustad Nejatollahi patients.
    [Show full text]
  • Management of Women with Premature Ovarian Insufficiency
    Management of women with premature ovarian insufficiency Guideline of the European Society of Human Reproduction and Embryology POI Guideline Development Group December 2015 1 Disclaimer The European Society of Human Reproduction and Embryology (hereinafter referred to as 'ESHRE') developed the current clinical practice guideline, to provide clinical recommendations to improve the quality of healthcare delivery within the European field of human reproduction and embryology. This guideline represents the views of ESHRE, which were achieved after careful consideration of the scientific evidence available at the time of preparation. In the absence of scientific evidence on certain aspects, a consensus between the relevant ESHRE stakeholders has been obtained. The aim of clinical practice guidelines is to aid healthcare professionals in everyday clinical decisions about appropriate and effective care of their patients. However, adherence to these clinical practice guidelines does not guarantee a successful or specific outcome, nor does it establish a standard of care. Clinical practice guidelines do not override the healthcare professional's clinical judgment in diagnosis and treatment of particular patients. Ultimately, healthcare professionals must make their own clinical decisions on a case-by-case basis, using their clinical judgment, knowledge, and expertise, and taking into account the condition, circumstances, and wishes of the individual patient, in consultation with that patient and/or the guardian or carer. ESHRE makes no warranty, express or implied, regarding the clinical practice guidelines and specifically excludes any warranties of merchantability and fitness for a particular use or purpose. ESHRE shall not be liable for direct, indirect, special, incidental, or consequential damages related to the use of the information contained herein.
    [Show full text]
  • Anti-Müllerian Hormone in African-American Women With
    Reproductive health and APS Lupus Sci Med: first published as 10.1136/lupus-2020-000439 on 1 November 2020. Downloaded from Anti- Müllerian hormone in African- American women with systemic lupus erythematosus Meghan Angley ,1 Jessica B Spencer,2 S Sam Lim ,1,3 Penelope P Howards1 To cite: Angley M, Spencer JB, ABSTRACT organs include the skin, musculoskeletal Lim SS, et al. Anti- Müllerian Objective Women with SLE may experience ovarian system, and heart. In women, organ damage hormone in African- American insufficiency or dysfunction due to treatment or disease can also manifest as ovarian insufficiency or women with systemic effects. Anti- Müllerian hormone (AMH), a marker of ovarian lupus erythematosus. dysfunction. reserve, has been examined in small populations of women Lupus Science & Medicine Anti- Müllerian hormone (AMH) is a with SLE with conflicting results. To date, these studies 2020;7:e000439. doi:10.1136/ marker of ovarian reserve. Unlike follicle- lupus-2020-000439 have included very few African- American women, the racial/ethnic group at greatest risk of SLE. stimulating hormone, AMH levels remain Methods We enrolled African- American women aged 22– relatively constant throughout a woman’s Received 20 August 2020 40 years diagnosed with SLE after age 17 from the Atlanta menstrual cycle so they can be measured at Revised 18 September 2020 Metropolitan area. Women without SLE from the same any point during the menstrual cycle. AMH Accepted 1 October 2020 area were recruited from a marketing list for comparison. is a hormone secreted by granulosa cells of AMH was measured in serum using the Ansh Labs assay small antral follicles and correlates with the (Webster, Texas, USA).
    [Show full text]
  • Antigen Mimicry in Autoimmune Disease Sharing of Amino Acid Residues Critical for Pathogenic T Cell Activation
    Antigen mimicry in autoimmune disease sharing of amino acid residues critical for pathogenic T cell activation. A M Luo, … , D Hunt, K S Tung J Clin Invest. 1993;92(5):2117-2123. https://doi.org/10.1172/JCI116812. Research Article A nonamer peptide from murine nicotinic acetylcholine receptor delta chain (ACR delta), which shared four amino acid residues with a nonamer peptide of murine ovarian zona pellucida glycoprotein ZP3, induced murine autoimmune oophoritis and IgG autoantibody to the zona pellucida. Crossreaction between the ACR delta and ZP3 peptides was established by the response of a ZP3 peptide-specific, oophoritogenic T cell clone to both peptides in association with IA (alpha k beta b). By substituting the ZP3 peptides with a single alanine, four amino acids within the ZP3 peptide were found to be important for ovarian autoimmune disease, autoantibody response, and stimulation of the ZP3-specific T cell clone. Substitution with conservative amino acids of three residues also ablated activity, whereas the fourth, a phenylalanine, was replaceable by tyrosine without loss of activity. Of the four critical amino acids, three were shared between the ZP3 peptide and the ACR delta peptide. Moreover, polyalanine peptides with the four critical ZP3 amino acids or the four amino acids common to the ZP3 and ACR delta peptides induced immune response to ZP3 and elicited severe ovarian autoimmune disease. Thus, organ-specific autoimmune disease can occur through immune response against unrelated self (or foreign) peptides that share with a self-peptide sufficient common amino acid residues critical for activation of pathogenic, autoreactive T cells.
    [Show full text]
  • The Patient Was Monitored Monthly for 3 Months Until a Maintenance Dose
    IMMUNOLOGIC BASIS OF MYASTHENIA GRAVIS WITH SUBSEQUENT PREMATURE OVARIAN INSUFFICIENCY: A CASE REPORT Cialuj Teza A. Agbayani, MDa and Maria Antonia E. Habana, MD, MScb * Fellow in-training, Section of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, Philippine General Hospital, University of the Philippines Manila ** Professor 12, Department of Obstetrics and Gynecology, College of Medicine and Philippine General Hospital, University of the Philippines Manila CASE DISCUSSION A 25-year old nulligravid had regularly occurring menstrual Patients who have POI with MG are fewer than 1%.(1) There is ovarian resistance to endogenous or exogenous hormonal activation as the autoantibodies cycles until she noted amenorrhea 2 years after presenting with lower competitively antagonize FSH or luteinizing hormone (LH). Uncontrolled thymic expression of extremity weakness. antigens specific to the ovaries may contribute to the ovarian autoimmune disease.(2) In 2014, she experienced lower extremity weakness which There are 8 documented cases of MG accompanied by POI and are summarized in Table 2.(3) The women were in the first decade of their reproductive debut with spontaneously resolved after one month. In 2016, the diagnosis of ages ranging from 15-27 years all presenting with symptoms of MG. Fifty percent manifested MG was made.A month into starting immunomodulating therapy, she with symptoms of MG first followed by POI after several years. Six of the cases (75%) were positive with AChR Ab. Other antibodies seen were anti-leutinizing hormone antibody (12.5%), had myasthenic crisis occurring during menses. Oligomenorrhea was AOA (12.5%), and thyroglobulin antibody (12.5%), each occurring solely in 3 separate cases.
    [Show full text]
  • Proteome-Wide Survey of the Autoimmune Target Repertoire in Autoimmune Polyendocrine Syndrome Type 1
    Proteome-wide survey of the autoimmune target repertoire in autoimmune polyendocrine syndrome type 1 Nils Landegren, Donald Sharon, Eva Freyhult, Asa Hallgren, Daniel Eriksson, Per-Henrik Edqvist, Sophie Bensing, Jeanette Wahlberg Topp, Lawrence M. Nelson, Jan Gustafsson, Eystein S. Husebye, Mark S. Anderson, Michael Snyder and Olle Kampe Linköping University Post Print N.B.: When citing this work, cite the original article. Original Publication: Nils Landegren, Donald Sharon, Eva Freyhult, Asa Hallgren, Daniel Eriksson, Per-Henrik Edqvist, Sophie Bensing, Jeanette Wahlberg Topp, Lawrence M. Nelson, Jan Gustafsson, Eystein S. Husebye, Mark S. Anderson, Michael Snyder and Olle Kampe, Proteome-wide survey of the autoimmune target repertoire in autoimmune polyendocrine syndrome type 1, 2016, Scientific Reports, (6), 20104. http://dx.doi.org/10.1038/srep20104 Copyright: Nature Publishing Group: Open Access Journals - Option C / Nature Publishing Group http://www.nature.com/ Postprint available at: Linköping University Electronic Press http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-125308 www.nature.com/scientificreports OPEN Proteome-wide survey of the autoimmune target repertoire in autoimmune polyendocrine Received: 28 October 2015 Accepted: 23 December 2015 syndrome type 1 Published: 01 February 2016 Nils Landegren1,2,*, Donald Sharon3,4,*, Eva Freyhult2,5,6, Åsa Hallgren1,2, Daniel Eriksson1,2, Per-Henrik Edqvist7, Sophie Bensing8, Jeanette Wahlberg9, Lawrence M. Nelson10, Jan Gustafsson11, Eystein S Husebye12, Mark S Anderson13, Michael Snyder3 & Olle Kämpe1,2 Autoimmune polyendocrine syndrome type 1 (APS1) is a monogenic disorder that features multiple autoimmune disease manifestations. It is caused by mutations in the Autoimmune regulator (AIRE) gene, which promote thymic display of thousands of peripheral tissue antigens in a process critical for establishing central immune tolerance.
    [Show full text]
  • And Sialoadenitis Mice to Suppress Lupus Glomerulonephritis T Cells
    Failure of CD25+ T Cells from Lupus-Prone Mice to Suppress Lupus Glomerulonephritis and Sialoadenitis This information is current as Harini Bagavant and Kenneth S. K. Tung of September 28, 2021. J Immunol 2005; 175:944-950; ; doi: 10.4049/jimmunol.175.2.944 http://www.jimmunol.org/content/175/2/944 Downloaded from References This article cites 29 articles, 12 of which you can access for free at: http://www.jimmunol.org/content/175/2/944.full#ref-list-1 Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on September 28, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2005 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Failure of CD25؉ T Cells from Lupus-Prone Mice to Suppress Lupus Glomerulonephritis and Sialoadenitis1 Harini Bagavant2 and Kenneth S. K. Tung The development of organ-specific autoimmune diseases in mice thymectomized on day 3 of life (d3tx mice) can be prevented by transferring CD4؉CD25؉ T cells from syngeneic, normal adult mice.
    [Show full text]
  • Impact of Autoimmunity on Oogenesis and Ovarian Morphology Maya Markova*, Stefka Delimitreva, Anton Kolarov, Ralitsa Zhivkova
    Institute of Experimental Morphology, Pathology and Anthropology with Museum Bulgarian Anatomical Society Acta morphologica et anthropologica, 25 (1-2) Sofia • 2018 Impact of Autoimmunity on Oogenesis and Ovarian Morphology Maya Markova*, Stefka Delimitreva, Anton Kolarov, Ralitsa Zhivkova Department of Biology, Medical Faculty, Medical University, Sofia, Bulgaria * Corresponding author e-mail:[email protected] Compromised tolerance to ovarian components can lead to autoimmune oophoritis. Histological examina- tion of affected ovaries reveals a mononuclear infiltrate, in many cases initially restricted to the follicular theca and sometimes associated with polycystic appearance. Autoimmune oophoritis interferes with fol- licle maturation and eventually diminishes the number of growing follicles, with a corresponding impact on fertility and hormonal secretion. In severe cases, all follicles advanced beyond the primordial stage are destroyed, leading to premature ovarian insufficiency (failure). Among known autoantigens, most im- portant are the components of zona pellucida and of steroidogenic cells. Autoimmune ovarian disease is often associated with Addison’s disease. In some cases, it is a manifestation of autoimmune polyendocrine syndrome. Little is known at present about the effects of systemic autoimmune diseases on the ovary, but data from patients and animal models show decreased ovarian reserve. Key words: autoimmunity, oophoritis, premature ovarian failure, oocyte, fertility Autoimmune diseases result from loss of normal immune tolerance to self-antigens. Due to the involvement of multiple complex regulatory mechanisms in their etiology and development, they are difficult to diagnose and especially to treat. This review ad- dresses the effects of autoimmune diseases on oogenesis and overall ovarian morpho- logy, which in recent years have been revealed as much more diverse and profound than previously estimated.
    [Show full text]
  • Acquired Aplastic Anemia • Acute Disseminated Encephalomyelitis
    • Acquired aplastic anemia • Acute disseminated encephalomyelitis (ADEM) • Acute hemorrhagic leukoencephalitis (AHLE) / Hurst’s disease • Agammaglobulinemia, primary • Alopecia areata • Ankylosing spondylitis (AS) • Anti-NMDA receptor encephalitis • Antiphospholipid syndrome (APS) • Arteriosclerosis • Autism spectrum disorders (ASD) • Autoimmune Addison’s disease (AAD) • Autoimmune dysautonomia / Autoimmune autonomic ganglionopathy (AAG) • Autoimmune encephalitis • Autoimmune gastritis • Autoimmune hemolytic anemia (AIHA) • Autoimmune hepatitis (AIH) • Autoimmune hyperlipidemia • Autoimmune hypophysitis / lymphocytic hypophysitis • Autoimmune inner ear disease (AIED) • Autoimmune lymphoproliferative syndrome (ALPS) • Autoimmune myocarditis • Autoimmune oophoritis • Autoimmune orchitis • Autoimmune pancreatitis (AIP) / Immunoglobulin G4-Related Disease (IgG4-RD) • Autoimmune polyglandular syndromes, Types I, II, & III • Autoimmune progesterone dermatitis • Autoimmune sudden sensorineural hearing loss (SNHL) • Balo disease • Behçet’s disease • Birdshot chorioretinopathy / birdshot uveitis • Bullous pemphigoid • Castleman disease • Celiac disease • Chagas disease • Chronic fatigue syndrome (CFS) / myalgic encephalomyelitis (ME) • Chronic inflammatory demyelinating polyneuropathy (CIDP) • Chronic Lyme disease / post-treatment Lyme disease syndrome (PTLDS) • Chronic urticaria (CU) www.Stemedix.com 601 7th Street South, Suite 565 T: 800-531-0831 [email protected] Saint Petersburg, FL 33701 F: 727-362-4630 • Churg-Strauss syndrome / eosinophilic
    [Show full text]
  • Premature Ovarian Failure
    Human Reproduction Update, Vol.11, No.4 pp. 391–410, 2005 doi:10.1093/humupd/dmi012 Advance Access publication May 26, 2005 Premature ovarian failure Deepti Goswami and Gerard S.Conway1 Department of Endocrinology, The Middlesex Hospital, London W1T 3AA, UK 1To whom correspondence should be addressed. E-mail: [email protected] Premature ovarian failure (POF) causing hypergonadotrophic hypogonadism occurs in 1% of women. In majority of cases the underlying cause is not identified. The known causes include: (a) Genetic aberrations, which could involve the X chromosome or autosomes. A large number of genes have been screened as candidates for causing POF; however, few clear causal mutations have been identified. (b) Autoimmune ovarian damage, as suggested by the observed association of POF with other autoimmune disorders. Anti-ovarian antibodies are reported in POF by several studies, but their specificity and pathogenic role are questionable. (c) Iatrogenic following surgical, radiotherapeutic or chemotherapeutic interventions as in malignancies. (d) Environmental factors like viral infec- tions and toxins for whom no clear mechanism is known. The diagnosis is based on finding of amenorrhoea before age 40 associated with FSH levels in the menopausal range. Screening for associated autoimmune disorders and karyotyping, particularly in early onset disease, constitute part of the diagnostic work-up. There is no role of ovarian biopsy or ultrasound in making the diagnosis. Management essentially involves hormone replacement and infertility treatment, the only proven means for the latter being assisted conception with donated oocytes. Embryo cryopreservation, ovarian tissue cryopreservation and oocyte cryopreservation hold promise in cases where ovarian failure is foreseeable as in women undergoing cancer treatments.
    [Show full text]
  • Gender Characteristics of Autoimmune Hypogonadism* G
    UDC 618 Вестник СПбГУ. Медицина. 2020. Т. 15. Вып. 1 Gender characteristics of autoimmune hypogonadism* G. Kh. Safarian1,2, D. A. Niauri1,2, Ye. S. Borodina1, L. Kh. Dzhemlikhanova1,2, A. M. Gzgzyan1,2 1 St. Petersburg State University, 7–9, Universitetskaya nab., St. Petersburg, 199034, Russian Federation 2 D. O. Ott Research Institute of Obstetrics, Gynecology and Reproductology, 3, Mendeleevskaya liniia, St. Petersburg, 199034, Russian Federation For citation: Safarian G. Kh., Niauri D. A., Borodina Ye. S., Dzhemlikhanova L. Kh., Gzgzyan A. M. Gender characteristics of autoimmune hypogonadism. Vestnik of Saint Petersburg University. Medi- cine, 2020, vol. 15, issue 1, pp. 9–23. http://doi.org/10.21638/spbu11.2020.102 Autoimmune gonadal lesions represent a highly heterogenous conditions affecting men and women of reproductive age and resulting in loss of endocrine function and, eventually, infer- tility. Well-known and well-documented risk factors exist, and the presence or suspicion of autoimmune disorder should be regarded as an important one. For the purpose of the present study, ELISA kits according to the proprietary technology for detection of antitesticular and antiovarian antibodies were developed. Among men with autoimmune orchitis an increased level of antibodies to steroid-producing testicular cells, decreased serum total and free tes- tosterone and altered semen parameters were found. Combined autoimmune diseases were present (autoimmune thyroiditis, vitiligo, type 1 diabetes) in 13.5 % of cases. In women with autoimmune oophoritis the main finding was anovulation with preserved serum FSH and LH levels (91.6 %) and luteal insufficiency (8.4 %). In total, 19.4 % of patients had other autoim- mune diseases (autoimmune thyroiditis, vitiligo, chronic autoimmune hepatitis, rheumatoid arthritis, systemic lupus erythematosus).
    [Show full text]
  • Autoimmune Diseases in Patients with Premature Ovarian Insufficiency—Our Current State of Knowledge
    International Journal of Molecular Sciences Review Autoimmune Diseases in Patients with Premature Ovarian Insufficiency—Our Current State of Knowledge Anna Szeliga 1,†, Anna Calik-Ksepka 2,†, Marzena Maciejewska-Jeske 1, Monika Grymowicz 2, Katarzyna Smolarczyk 3 , Anna Kostrzak 1, Roman Smolarczyk 2 , Ewa Rudnicka 2,*,‡ and Blazej Meczekalski 1,*,‡ 1 Department of Gynecological Endocrinology, Poznan University of Medical Sciences, 60-535 Poznan, Poland; [email protected] (A.S.); [email protected] (M.M.-J.); [email protected] (A.K.) 2 Department of Gynaecological Endocrinology, Medical University of Warsaw, 00-315 Warsaw, Poland; [email protected] (A.C.-K.); [email protected] (M.G.); [email protected] (R.S.) 3 Department of Dermatology and Venereology, Medical University of Warsaw, 00-315 Warsaw, Poland; [email protected] * Correspondence: [email protected] (E.R.); [email protected] (B.M.); Tel.: +48-22-59-66-470 (E.R.); +48-61-65-99-366 (B.M.); Fax: +48-61-65-99-454 (B.M.) † These authors contributed equally to this work. ‡ These authors contributed equally to this work. Abstract: Premature ovarian insufficiency (POI), previously known as premature ovarian failure or premature menopause, is defined as loss of ovarian function before the age of 40 years. The risk of Citation: Szeliga, A.; Calik-Ksepka, POI before the age of 40 is 1%. Clinical symptoms develop as a result of estrogen deficiency and A.; Maciejewska-Jeske, M.; may include amenorrhea, oligomenorrhea, vasomotor instability (hot flushes, night sweats), sleep Grymowicz, M.; Smolarczyk, K.; disturbances, vulvovaginal atrophy, altered urinary frequency, dyspareunia, low libido, and lack of Kostrzak, A.; Smolarczyk, R.; energy.
    [Show full text]