2016 14 5 0 354

Detecting diseases of neglected seminal vesicles using imaging modalities: A review of current literature شناسایی بیماری های کیسه های منی نادیده گرفته شده با استفاده از روش های تصویربرداری: مروری بر متون کنونی 2 1 سمینال وزیکلز (کیسه های منی) غدد ضمیمه ای تولید مثلی و از اجزای سیستم تولید مثلی-ادراری هستند. این غدد نقش بسیار مهمی در باروری مردان دارند. بیماری­های این غدد منجر به ناباروری می­شود. این بیماری­ها بسیار کمیاب بوده و به ندرت گزارش شده­اند. در این مقاله به آسیب شناسی سمینال وزیکل، علایم، راه­های تشخیصی و درمان بیماری­های مربوط به آن پرداخته می­شود. در اینجا به اهمیت بالینی سمینال وزیکل با استفاده از PubMed می­پردازیم. روش­ها و دستگاه­های تصویربرداری موجود که کمک به تشخیص بیماری­های سمینال وزیکل می­کنند مرور می­شوند. بیماری­های شایع شامل عفونت، کیست­ها، تومورها، و بیماری­های مادرزادی اشاره می­شوند. علایمی از قبیل هماتوسپرمیا، درد، علایم مربوط به تحریک و انسداد مجاری ادراری تحتانی، و ناباروری در بیماران با بیماری­های سمینال وزیکل دیده می­شوند.  2 Seminal vesicles (SVs) are sex accessory organs and part of male genitourinary system. They play a critical role in male fertility. Diseases of the SVs, usually results in infertility. Diseases of the SVs are extremely rare and are infrequently reported in the literature. We address the current literature of SV pathologies, symptoms, diagnosis, and treatment options. We review the clinical importance of SVs from PubMed. The current imaging modalities and instrumentation that help diagnose SV diseases are reviewed. Common pathologies including, infection, cysts, tumors, and congenital diseases of the SVs are addressed. Many times symptoms of hematospermia, pain, irritative and obstructive lower urinary tract symptoms, and infertility are presented in patients with SV diseases. 293 302 2017/10/1 1396/7/9 2017/10/14 1396/7/22 Gautam Dagur Gautam Dagur Department of Physiology and Biophysics, SUNY at Stony Brook, New York, USA امریکا Kelly Warren Kelly Warren Department of Physiology and Biophysics, SUNY at Stony Brook, New York, USA امریکا Navjot Singh Navjot Singh Department of Physiology and Biophysics, SUNY at Stony Brook, New York, USA امریکا Sardar Ali Khan Sardar Ali Khan Department of Physiology and Biophysics, SUNY at Stony Brook, New York, USA امریکا skysalik@gmail.com Seminal vesicles Infertility Hematospermia Transrectal ultrasound کیسه های منی ناباروری هماتوسپرمی سونوگرافی از طریق مقعد. Aboul-Azm TE. Anatomy of the human seminal vesicles and ejaculatory ducts. Arch Androl 1979; 3: 287-292.##Donnellan P, Breathnach O, Crown JP. Odynorgasmia. Scand J Urol Nephrol 2001; 35: 158.##Du Plessis SS, Gokul S, Agarwal A. Semen hyperviscosity: causes, consequences, and cures. Front Biosci 2013; 5: 224-231.##Ates Y, Kilciler G, Bedir S, Aslan M, Kilciler M, Tuzun A, et al. Large vesicula seminalis cyst: a very rare cause of constipation and male infertility. Kaohsiung J Med Sci 2007; 23: 318-320.##Coulier B, Ramboux A, Maldague P. Emphysematous epididymitis as presentation of unusual seminal vesicle fistula secondary to sigmoid diverticulitis: case report. Abdom Imaging 2005; 30: 113-116.##Ozer T, Gundogdu S, Ozer Y, Mahmutyazicioglu K, Savranlar A, Ozdemir H. Echinococcosis involving the liver, retrovesical and seminal vesicle presented with syncope. Int J Urol 2004; 11: 922-924.##Altunrende F, Kim ED, Klein FA, Waters WB. Seminal vesicle cyst presenting as rectal obstruction. Urology 2004; 63: 584-585.##Kelm J, Duchow J, Anagnostakos K, Schneider G, Kohn D, Ahlhelm F. [Vesiculitis seminalis-a rare diagnosis in case of chronic groin pain]. Sportverletz Sportschaden 2003; 17: 84-87. (In German)##Callewaert P, De Coster M, Vuylsteke P, De Man R, Brijs S, Baert L. Anal tenesmus caused by seminal vesicle cyst. Urology 1997; 49: 139-141.##Mammen KJ, Ho KM, Fellows GJ. Cysts of seminal vesicles presenting as intra-abdominal swellings. Br J Urol 1995; 76: 141-143.##Khan A, Ahmed M, Talati J. Seminal vesicle cystic dilatation masquerading as proctalgia fugax. Br J Urol 1989; 64: 428-429.##Kitazawa M, Hiraguri M, Maeda C, Yoshiki M, Horigome N, Kaneko G. Seminal vesicle-rectal fistula secondary to anastomotic leakage after low anterior resection for rectal cancer: a case report and brief literature review. Int Surg 2014; 99: 23-27.##Inoue K, Higaki Y, Yoshida H. Inguinal hernia of seminal vesicle cyst. Int J Urol 2004; 11: 1039-1040.##van Meegen MA, Kokke F, Dik P, Fockens P, Benninga MA. A seminal vesicle cyst palpable in the rectum. Endoscopy 2006; 38 (Suppl.): E7.##Ramchandani P, Banner MP, Pollack HM. Imaging of the seminal vesicles. Semin Roentgenol 1993; 28: 83-91.##Kreiner B, Denzinger S, Ganzer R, Fritsche HM, Burger M, Wieland WF, et al. Neuroendocrine carcinoma of the seminal vesicles presenting with Lambert Eaton syndrome: a case report. J Med Case Rep 2010; 4: 320.##Cui ZQ, Wang YC, Du J, Zhou HJ, Yu ZY, Gao EJ, et al. [Transurethral seminal vesiculoscopy combined with finasteride for recurrent hematospermia]. Zhonghua Nan Ke Xue 2014; 20: 536-538. (In Chinese)##He Q, Xia M, Bai Y, Zhang JW, Wang JJ, Wang HT. [Diagnosis and treatment of seminal vesicle cyst]. Zhonghua Yi Xue Za Zhi 2012; 92: 982-983. (In Chinese)##Williams JL, Sago AL. Ureteral ectopia into seminal vesicle: embryology and clinical presentation. Urology 1983; 22: 594-596.##Gonzales GF. Function of seminal vesicles and their role on male fertility. Asian J Androl 2001; 3: 251-258.##Simpson WL Jr, Rausch DR. Imaging of male infertility: pictorial review. Am J Roentgenol 2009; 192 (Suppl.): 98-107.##Luo B, Dai YP, Wang DH, Luo DS, Deng CH, Wu RP. [Value of transrectal ultrasonography in the diagnosis of midline prostatic cysts]. Zhonghua Nan Ke Xue 2008; 14: 139-141. (In Chinese)##Dominguez C, Boronat F, Cunat E, Broseta E, Martinez R, Moreno B, et al. Agenesis of seminal vesicles in infertile males: ultrasonic diagnosis. Eur Urol 1991; 20: 129-132.##Haddock P, Wagner JR. Seminal vesicle cyst with ipsilateral renal agenesis and ectopic ureter (Zinner syndrome). Urology 2015; 85: 41-42.##Altobelli E, Bove AM, Falavolti C, Sergi F, Nguyen HT, Buscarini M. Robotic-assisted approach in the treatment for Zinner's Syndrome associated with ipsilateral megaureter and incomplete double-crossed ectopic ureter. Int Urol Nephrol 2013; 45: 635-638.##Sundar R, Sundar G. Zinner syndrome: an uncommon cause of painful ejaculation. BMJ Case Rep 2015; bcr2014207618.##Raviv G, Mor Y, Levron J, Shefi S, Zilberman D, Ramon J, et al. Role of transrectal ultrasonography in the evaluation of azoospermic men with low-volume ejaculate. J Ultrasound Med 2006; 25: 825-829.##Chiang HS, Lin YH, Wu YN, Wu CC, Liu MC, Lin CM. Advantages of magnetic resonance imaging (MRI) of the seminal vesicles and intra-abdominal vas deferens in patients with congenital absence of the vas deferens. Urology 2013; 82: 345-351.##Phillipson G. Cystic fibrosis and reproduction. Reprod Fertil Dev 1998; 10: 113-119.##Reig B, Blumenfeld J, Donahue S, Prince MR. Seminal megavesicle in autosomal dominant polycystic kidney disease. Clin Imag 2015; 39: 289-292.##Hendry WF, Rickards D, Pryor JP, Baker LR. Seminal megavesicles with adult polycystic kidney disease. Hum Reprod 1998; 13: 1567-1569.##Vasileios R, Athanasios P, Stavros T. Echinococcal cyst of the seminal vesicles: a case-report and literature review. Int Urol Nephrol 2002; 34: 527-530.##Tuygun C, Bakirtas H, Imamoglu MA, Sertcelik N, Zengin K, Bozkurt IH. The unusual mass of retrovesical space: a secondary hydatid cyst disease. Sci World J 2006; 6: 2481-2485.##Hasegawa N, Miki K, Kato N, Furuta N, Ohishi Y, Kondo N, et al. [Magnetic resonance images of hematospermia]. Nihon Hinyokika Gakkai Zasshi 1998; 89: 956-960.##La Vignera S, Condorelli RA, Di Mauro M, D'Agata R, Vicari E, Calogero AE. Seminal vesicles and diabetic neuropathy: ultrasound evaluation. J Androl 2011; 32: 478-483.##Saha S, Wright G, Arulampalam T, Corr J. An unusual groin mass. Seminal vesicle abscess: a case report. Cases J 2009; 2: 6531.##Madrid Garcia FJ, Madronero Cuevas C, Rivas Escudero JA, Parra Muntaner L, Monsalve Rodriguez M, Garcia Alonso J. [Conservative treatment of a seminal vesicle abscess. Report of one case]. Arch Esp Urol 2004; 57: 438-440. (In Spanish)##Zagoria RJ, Papanicolaou N, Pfister RC, Stafford SA, Young2nd HH. Seminal vesicle abscess after vasectomy: evaluation by transrectal sonography and CT. AJR Am J Roentgenol 1987; 149: 137-138.##Dewani CP, Dewani N, Bhatia D. Case report: tubercular cold abscess of seminal vesicle: minimally invasive endoscopic management. J Endourol 2006; 20: 436-442.##Eastham JA, Spires KS, Abreo F, Johnson JB, Venable DD. Seminal vesicle abscess due to tuberculosis: role of tissue culture in making the diagnosis. South Med J 1999; 92: 328-329.##Bayne CE, Davis WA, Rothstein CP, Engel JD. Seminal vesicle abscess following prostate biopsy requiring transgluteal percutaneous drainage. Can J Urol 2013; 20: 6811-6814.##Slim Selmi M, Hentati H, Fayala H, Riadh Ben Slama M, Chebil M. Seminal vesicle abscess: report of a new case. Tunis Med 2009; 87: 630-632.##Chandra I, Doringer E, Sarica K, Kunit G, Frick J. Bilateral seminal vesicle abscesses. Eur Urol 1991; 20: 164-166.##Monzo JI, Lledo Garcia E, Cabello Benavente R, Moralejo Garate M, Diez Cordero JM, Hernandez Fernandez C. [Primary seminal vesicle abscess: diagnosis and treatment by transrectal ultrasound]. Actas Urol Esp 2005; 29: 523-525. (In Spanish)##Liu B, Song Z, Xu A, Su S, Wang Z, Yin C. Is abnormal expression of semenogelin I involved with seminal vesiculitis? Med Hypotheses 2014; 82: 338-340.##Li YF, Liang PH, Sun ZY, Zhang Y, Bi G, Zhou B, et al. Imaging diagnosis, transurethral endoscopic observation, and management of 43 cases of persistent and refractory hematospermia. J Androl 2012; 33: 906-916.##Xu B, Li P, Niu X, Zhang X, Wang Z, Qin C, et al. A new method of chronic and recurrent seminal vesiculitis treatment. J Endourol 2011; 25: 1815-1818.##Furuya R, Takahashi S, Furuya S, Saitoh N, Ogura H, Kurimura Y, et al. Is urethritis accompanied by seminal vesiculitis? Int J Urol 2009; 16: 628-631.##Furuya R, Takahashi S, Furuya S, Takeyama K, Masumori N, Tsukamoto T. Chlamydial seminal vesiculitis without symptomatic urethritis and epididymitis. Int J Urol 2006; 13: 466-467.##Palmer WC, Patel NC, Renew JR, Bridges MD, Stancampiano FF. Acute infection of a documented seminal vesicle cyst via hematogenous seeding. Urol J 2013; 10: 1157-1159.##Xu LW, Cheng S, Zhang ZG, Li XD. [Transvesical removal of seminal vesicle mass: a report of 5 cases]. Zhonghua Nan Ke Xue 2009; 15: 357-359. (In Chinese)##Reikie BA, Yilmaz A, Medlicott S, Trpkov K. Mixed epithelial-stromal tumor (MEST) of seminal vesicle: a proposal for unified nomenclature. Adv Anat Pathol 2015; 22: 113-120.##Montironi R, Lopez-Beltran A, Cheng L, Galosi AB, Montorsi F, Scarpelli M. Seminal vesicle intraepithelial neoplasia versus basal cell hyperplasia in a seminal vesicle. Eur Urol 2014; 66: 623-627.##Crestani A, Guttilla A, Gardi M, Gardiman M, Dal Moro F, Valotto C, et al. Peripheral primitive neuroectodermal tumor of seminal vesicles: is there a role for relatively aggressive treatment modalities? Arch Ital Urol Androl 2014; 86: 291-292.##Mizuno N, Fujikawa N, Hayashi N, Murakami T, Suzuki K, Ikeda I. [A case of primary seminal vesicle cancer detected by FDG-PET/CT]. Nihon Hinyokika Gakkai Zasshi 2012; 103: 704-707. (In Japanese)##Miyajima S, Irie S, Nakamura N, Tanaka M. [A case of leiomyoma of the seminal vesicle]. Nihon Hinyokika Gakkai Zasshi 2014; 105: 144-148. (In Japanese)##Khandelwal A, Virmani V, Amin MS, George U, Khandelwal K, Gorsi U. Radiology-pathology conference: malignant solitary fibrous tumor of the seminal vesicle. Clin Imaging 2013; 37: 409-413.##Safar B, Kanmaniraja D, Herts BR. Phyllodes tumor of the seminal vesicle. J Urol 2014; 192: 554-555.##Wang J, Yue X, Zhao R, Cheng B, Wazir R, Wang K. Primary squamous cell carcinoma of seminal vesicle: an extremely rare case report with literature review. Int Urol Nephrol. 2013;45(1):135-8.##Yao XD, Hong YP, Ye DW, Wang CF. Primary yolk sac tumor of seminal vesicle: a case report and literature review. World J Surg Oncol 2012; 10: 189.##Kaminsky A, Kania U, Ortloff P, Sperling H. [Seminal vesicle cystadenoma as the cause of a retrovesical tumor]. Urologe A 2014; 53: 542-544. (In German)##Campobasso D, Fornia S, Ferretti S, Maestroni U, Cortellini P. Primary bilateral seminal vesicle carcinoma: description of a case and literature review. Int J Surg Pathol 2012; 20: 633-635.##Barnoiu OS, Gomez Pascual JA, Navarro Vilchez P, Blanco Reina F, Moreno Ramos A, Vivas Vargas E, et al. [Malacoplakia of the seminal vesicles. Case report and particularities]. Arch Esp Urol 2013; 66: 237-241. (In Spanish)##Song W, Yang JR, Wang YH, Liang QC. Primary extragastrointestinal stromal tumor of the seminal vesicles. Urology 2012; 79: 36-37.##Peng JF, Wang YM, Zhang Y, Cai SL. [Stromal tumor of the seminal vesicle: a case report and literature review]. Zhonghua Nan Ke Xue 2012; 18: 1119-1122. (In Chinese)##Gao RL. [Primary adenocarcinoma of seminal vesicle: report of a case]. Zhonghua Bing Li Xue Za Zhi 2011; 40: 775-776.##Vanzati A, Perez Pascal A, Pinto F, Eloy C. Multilocular adenomyoma of seminal vesicle. Int J Surg Pathol 2012; 20: 596-597.##Yasunaga Y, Ueda T, Kodama Y, Oka T. Poorly differentiated neuroendocrine carcinoma of the seminal vesicle. Int J Urol 2012; 19: 370-372.##He R, Yang X, Li X, He Z, Zhou L. Cystic schwannoma of a seminal vesicle. J Androl 2012; 33: 798-800.##Cauvin C, Moureau-Zabotto L, Chetaille B, Hilgers W, Denoux Y, Jacquemier J, et al. Primary leiomyosarcoma of the seminal vesicle: case report and review of the literature. BMC Cancer 2011; 11: 323.##Kojima F, Ishida M, Takikita-Suzuki M, Shiba M, Tsujimoto Y, Kinouchi T, et al. Mammary-type myofibroblastoma of seminal vesicle. Histopathology 2012; 60: 524-527.##Zhu J, Chen LR, Zhang X, Gong Y, Xu JH, Zheng S. Primary diffuse large B-cell lymphoma of the seminal vesicles: ultrasonography and computed tomography findings. Urology 2011; 78: 1073-1074.##Boeren K, De Bruecker Y, Vankan Y, Perdieus D. Schwannoma of the seminal vesicle. JBR-BTR 2011; 94: 96.##Ouyang J, Yin HL, Lu ZF, Zhou HB, Zhou XJ. [Primary Burkitt lymphoma of the seminal vesicle: a case report and review of the literature]. Zhonghua Nan Ke Xue 2009; 15: 733-737. (In Chinese)##Funahashi Y, Hattori R, Matsukawa Y, Yamamoto T, Mizutani K, Yoshino Y, et al. [Solitary fibrous tumor of the seminal vesicle]. Aktuelle Urol 2010; 41: 326-327. (In German)##Sanghvi DA, Purandare NC, Jambhekar NA, Thakur MH, Joshi MS. Primary rhabdomyosarcoma of the seminal vesicle. Br J Radiol 2004; 77: 159-160.##Han P, Wei Q, Yang YR. Neurilemmoma of a seminal vesicle. Chin Med J 2007; 120: 1383-1384.##Montie JE, Wojno K, Klein E, Pearsall C, Levin H. Transitional cell carcinoma in situ of the seminal vesicles: 8 cases with discussion of pathogenesis, and clinical and biological implications. J Urol 1997; 158: 1895-1898.##Arya M, Hayne D, Brown RS, O'Donnell PJ, Mundy AR. Hemangiopericytoma of the seminal vesicle presenting with hypoglycemia. J Urol 2001; 166: 992.##Adachi Y, Rokujyo M, Kojima H, Nagashima K. Primary seminoma of the seminal vesicle: report of a case. J Urol 1991; 146: 857-859.##Hatcher PA, Tucker JA, Carson CC. Fibromuscular hyperplasia of the seminal vesicle. J Urol 1989; 141: 957-958.##Lamont JS, Hesketh PJ, de las Morenas A, Babayan RK. Primary angiosarcoma of the seminal vesicle. J Urol 1991; 146: 165-167.##Islam M. Benign mesenchymoma of seminal vesicles. Urology 1979; 13: 203-205.##Soyer P, Rougier P, Gad M, Roche A. Primary carcinoid tumor of the seminal vesicles: CT and MR findings. J Belge Radiol 1991; 74: 117-119.##Polianichko MF, Ogorodnikova LS, Zaderin VP. [Round-cell sarcoma of the seminal vesicles]. Urol Nefrol (Mosk) 1974: 44-45. (In Russia)##Martinez-Penuela A, Rosario Mercado M, Aldave J, Martinez-Penuela JM. [Primary adenocarcinoma of the seminal vesicles]. Arch Esp Urol 2009; 62: 671-673. (In Spanish)##Lote H, Mannion E, Cook T, Cairns T, Savage P. Adenocarcinoma of the seminal vesicles complicated by antineutrophil cytoplasmic antibody vasculitis: a case report and review of the literature. J Med Case Rep 2013; 7: 59.##Tarjan M, Ottlecz I, Tot T. Primary adenocarcinoma of the seminal vesicle. Indian J Urol 2009; 25: 143-145.##Ramamurthy R, Periasamy S, Mettupalayam V. Primary malignancy of seminal vesicle: A rare entity. Indian J Urol 2011; 27: 137-139.##Mohring C, Bach P, Kosciesza S, Goepel M. [A primary adenocarcinoma of the seminal vesicles. Case report of a rare malignancy]. Urologe A 2008; 47: 616-619. (In German)##Angulo JC, Romero I, Cabrera P, Gonzalez J, Rodriguez-Barbero JM, Nunez-Mora C. [Vesiculectomy with laparoscopic partial prostatectomy in the treatment of primary adenocarcinoma of the seminal vesicle with carcinomatous transformation of the ejaculatory duct]. Actas Urol Esp 2011; 35: 304-309. (In Spanish)##Kinjo T, Nonomura D, Yamamoto Y, Yoneda S, Nomura H, Tei N, et al. [Primary adenocarcinoma of the seminal vesicle difficult to differentiate from rectal carcinoma : a case report]. Hinyokika Kiyo 2013; 59: 597-601. (In Janpanese)##Chheda N, Bolegave M, Shet T, Tongaonkar H. Recurrent mullerian adenosarcoma like tumor of seminal vesicle. Indian J Pathol Microbiol 2010; 53: 342-344.##Baschinsky DY, Niemann TH, Maximo CB, Bahnson RR. Seminal vesicle cystadenoma: a case report and literature review. Urology 1998; 51: 840-845.##Pitkanen P, Westermark P, Cornwell GG, 3rd, Murdoch W. Amyloid of the seminal vesicles. A distinctive and common localized form of senile amyloidosis. Am J Pathol 1983; 110: 64-69.##Yang Z, Laird A, Monaghan A, Seywright M, Ahmad I, Leung HY. Incidental seminal vesicle amyloidosis observed in diagnostic prostate biopsies--are routine investigations for systemic amyloidosis warranted? Asian J Androl 2013; 15: 149-151.##Kono M, Kurokawa T, Takata M, Komatsu K, Tsukahara K, Kurose N. [Localized amyloidosis of the seminal vesicle: a case report]. Hinyokika Kiyo 2011; 57: 99-101. (In Japanese)##Coyne JD, Kealy WF. Seminal vesicle amyloidosis: morphological, histochemical and immunohistochemical observations. Histopathology 1993; 22: 173-176.##Furuya S, Masumori N, Furuya R, Tsukamoto T, Isomura H, Tamakawa M. Characterization of localized seminal vesicle amyloidosis causing hemospermia: an analysis using immunohistochemistry and magnetic resonance imaging. J Urol 2005; 173: 1273-1277.##Argon A, Simsir A, Sarsik B, Tuna B, Yorukoglu K, Niflioglu GG, et al. Amyloidosis of seminal vesicles; incidence and pathologic characteristics. Turk Patoloji Derg 2012; 28: 44-48.##Vandwalle J, Dugardin F, Petit T, Surga N, Paul A, Petit J. [Haemospermia due to seminal vesicle amyloidosis. Treatment by laparoscopic vesiculectomy. A case report]. Prog Urol 2007; 17: 1382-1384. (In French)##Chang K, Sio TT, Chandan VS, Iott MJ, Hallemeier CL. Angiosarcoma of the seminal vesicle: a case report of long-term survival following multimodality therapy. Rare Tumors 2014; 6: 5202.##Corriere JN, Jr. Painful ejaculation due to seminal vesicle calculi. J Urol 1997; 157: 626.##Amano T, Kunimi K, Ohkawa M. Transrectal ultrasonography of the prostate and seminal vesicles with hemospermia. Urol Int 1994; 53: 139-142.##Prando A. Endorectal magnetic resonance imaging in persistent hemospermia. Int Braz J Urol 2008; 34: 171-177.##Vellayappan BA, Tiong HY, Chua WJ, Consigliere DT. Seminal vesicle calculus after transurethral resection of ejaculatory duct. Can J Urol 2007; 14: 3595-3597.##Han P, Yang YR, Zhang XY, Wei Q. Laparoscopic treatment of a calcium fluorophosphate stone within a seminal vesicle cyst. Asian J Androl 2008; 10: 337-340.##George SS. CAlcification of the vas deferens and the seminal vesicles. J Am Med Assoc 1906; XLVII: 103-105.##Yadav R, Goel A, Sankhwar SN, Goyal NK. Incidentally detected bilaterally symmetrical seminal and vas calcification in young infertile male: a case report, literature review and algorithm for diagnosis. Can Urol Assoc J 2012; 6: 206-208.##Stasinou T, Bourdoumis A, Owegie P, Kachrilas S, Buchholz N, Masood J. Calcification of the vas deferens and seminal vesicles: a review. Can J Urol 2015; 22: 7594-7598.##Shebel HM, Elsayes KM, Abou El Atta HM, Elguindy YM, El-Diasty TA. Genitourinary schistosomiasis: life cycle and radiologic-pathologic findings. Radiographics 2012; 32: 1031-1046.##de Oliveira MJ, Nogueira VH, Mendes MG, dos Santos AR. [Unilateral calcification of vas deferens and seminal vesicle]. Actas Urol Esp 2009; 33: 105.##Gonzalez Ortega FJ, Duque Fernandez de Vega S, Garrido Pareja F. [Bilateral calcification of seminal vesicles and vas deferens]. Actas Urol Esp 2009; 33: 216. (In Spanish)##Yassa NA, Keesara S. Role of transrectal ultrasonography in evaluating the cause of azoospermia. Can Assoc Radiol J 2001; 52: 266-268.##Lin JZ, Wu HF, Wang JC, Le MZ, Yu HB, Zhou HT. Ectopic opening of cystic dilatation of the ejaculatory duct into enlarged prostatic utricle. J Androl 2012; 33: 574-577.##Lee CB, Choi HJ, Cho DH, Ha US. Cystadenoma of the seminal vesicle. Int J Urol 2006; 13: 1138-1140.##Arora A, Sharma S, Seth A. Unusual retrovesical cystic mass in a male patient. Urology 2013; 81: 23-24.##Tambo M, Fujimoto K, Hoshiyama F, Nakanishi M, Inoue T, Hirayama A, et al. [A case of retrovesical leiomyoma]. Hinyokika Kiyo 2004; 50: 497-499.##Ahmadzadeh M, Bosse A. Leiomyoma of the seminal vesicle. Urol Int 1996; 57: 252-254.##Inan N, Fayda M, Aksu G, Akansel G, Muezzinoglu B, Arslan A. Leiomyoma of the seminal vesicle mimicking tumoral extension of prostatic carcinoma. Acta Chir Belg 2009; 109: 811-814.##Shiotani T, Kawai N, Sato M, Minamiguchi H, Takeuchi T, Tanihata H, et al. Leiomyoma of the seminal vesicle. Jpn J Radiol 2009; 27: 218-220.##Vigano P, Bonacina P, Strada GR. Leiomyoma of the seminal vesicles. Arch Ital Urol Androl 2003; 75: 230-231.##Arun G, Chakraborti S, Rai S, Prabhu GG. Seminal vesicle schwannoma presenting with left hydroureteronephrosis. Urol Ann 2014; 6: 363-365.##Furtado AM, Carrasquinho E, Ferreira M, Afonso A, Ferrito F. Schwannoma, a rare tumor of the seminal vesicle. Cent European J Urol 2011; 64: 44-46.##Latchamsetty KC, Elterman L, Coogan CL. Schwannoma of a seminal vesicle. Urology 2002; 60: 515.##Fievet L, Boissier R, Villeret J, Vidal F, Lechevallier E, Coulange C. [Pelvic kystic schwannoma evoking a tumor of the right seminal vesicle]. Prog Urol 2010; 20: 660-664. (In French)##Weingarten TN, Araka CN, Mogensen ME, Sorenson JP, Marienau ME, Watson JC, et al. Lambert-Eaton myasthenic syndrome during anesthesia: a report of 37 patients. J Clin Anesth 2014; 26: 648-653.##Giordano S, Tolonen T, Tolonen T, Hirsimaki S, Kataja V. A pure primary low-grade neuroendocrine carcinoma (carcinoid tumor) of the prostate. Int Urol Nephrol 2010; 42: 683-687.##Xu LW, Wu HY, Yu YL, Zhang ZG, Li GH. Large phyllodes tumour of the seminal vesicle: case report and literature review. J Int Med Res 2010; 38: 1861-1867.##Khan MS, Zaheer LU, Ahmed K, Cahill D, Horsfield C, Rottenberg G, et al. Low-grade phyllodes tumor of the seminal vesicle treated with laparoscopic excision. Nat Clin Pract Urol 2007; 4: 395-400.##de Paula AA, Maltez AR, Mota ED. Small round blue cell tumor of seminal vesicle in a young patient. Int Braz J Urol 2006; 32: 566-569.##Papoutsoglou N, Burger M, Riedmiller H. Persistent painless hemospermia due to metastatic melanoma of the right seminal vesicle. BMC Urol 2013; 13: 43.##Reisman Y, de Reijke TM. An unusual cause of irritable urinary bladder symptoms. Urol Int 2001; 66: 225-256.##Tornblom M, Fredriksson A, Larsson P, Zimmermann R, Hedenborg L. Seminal vesicle metastasis--an overlooked occurrence of testicular tumours? Br J Urol 1996; 77: 160-162.##Gong L, Zheng M, Li Y, Zhang W, Bu W, Shi L, et al. Seminal vesicle metastasis after partial hepatectomy for hepatocellular carcinoma. BMC Cancer 2011; 11: 111.##Mai KT, Belanger EC, Al-Maghrabi HM, Robertson S, Wang D, Margnean C. Primary prostatic central zone adenocarcinoma. Pathol Res Pract 2008; 204: 251-258.##Smith JD, Nash GM, Weiser MR, Temple LK, Guillem JG, Paty PB. Multivisceral resections for rectal cancer. Br J Surg 2012; 99: 1137-1143.##Gakis G, Efstathiou J, Lerner SP, Cookson MS, Keegan KA, Guru KA, et al. ICUD-EAU International Consultation on Bladder Cancer 2012: Radical cystectomy and bladder preservation for muscle-invasive urothelial carcinoma of the bladder. Eur Urol 2013; 63: 45-57.##Yumura Y, Noguchi K, Moriyama M, Iwasaki A. Sudden decline in semen volume due to seminal vesicle fistula in a patient with Crohn's disease: a case report. Urol J 2014; 11: 1356-1138.## ##

Impacts of morphine addiction on spermatogenesis in rats اثر اعتیاد به مواد مخدر بر باروری موش های نر 2 1 مقدمه: مطالعات اندکی درباره تأثیر اپیوئیدها بر باروری مردان و نیز ارتباط بین مواجهه پدران با مواد مخدر با شکل­گیری ویژگی­های فیزیولوژیکی و رفتاری و فرزندان وجود دارد. هدف: این مطالعه به منظور بررسی تأثیر اپیوئیدها و مشتقات آن بر باروری موش­های نر انجام شده است. مواد و روش­ها: چهل موش نر از نوع ویستار، به شکل تصادفی به 5 گروه مساوی که با مورفین، نالوکسان، نالوکسان و مورفین مواجهه داشتند و نیز یک گروه شم و یک گروه به عنوان شاهد تقسیم شدند. ویژگی­های بافت شناسی و اسپرماتوژنز بعد از 6 ماه قرار گرفتن در معرض مخدرها بر اساس اندازه گیری اسپرماتوگونی، اسپرماتوسیت اسپرماتید و اسپرم مورد بررسی قرار گرفتند. داده­های به دست آمده جهت بررسی اهمیت و معناداری تفاوت­های به دست آمده مورد تجزیه و تحلیل قرار گرفت. نتایج: در میان 5 گروه موش این مطالعه، تعداد سلول­های اسپرماتوگونی، اسپرماتوسیت، اسپرماتید، اسپرم بین گروه­ها متفاوت بودند. کمترین میانگین تعداد این سلول­ها در میان موش­های گروه مورفین، و پس از آن گروه مورفین/ نالوکسان و گروه نالوکسان وجود داشتند. این تفاوت در گروه شم و شاهد بیشتر قابل توجه بود. علاوه بر این، تفاوت مشاهده شده بین افراد از نظر آماری معنی دار بود. (001/0>p). نتیجه­ گیری: مطالعه ما نشان داد که مورفین و دیگر مشتقات اوپیوئیدی می­تواند تمام جمعیت سلولی در روند اسپرماتوژنز را کاهش دهد. 2 Background: There are numerous investigations on wide range of issues that disrupt regulatory spermatogenesis, individuals who are exposed to drug abuse faced infertility and immature spermatogenesis. Objective: The aim of this study was to evaluate the addiction effects of morphine and its derivatives on rats spermatogenesis. Materials and Methods: 40 male Wistar rats were randomly divided into 5 equal groups, which were exposed either with intravenous morphine, naloxone, naloxone and morphine, sham (with normal saline injection) and a control group without infusion. Spermatogenesis was assessed after three months via histological sections with hematoxylin and eosin staining, using a light microscope based on measurement of spermatogonia, spermatocyte, spermatid, and spermatozoa. Results: Those rats that received opioids had changes in spermatogenesis function. The population of spermatogenesis cycle cells at spermatogonia, spermatocyte, spermatid, and spermatozoa stages was significantly decreased in those rats that received opioid in comparison to the control group (p<0.05). Histological studies revealed that changes in different groups of opioid application might affect sperm formation. Sperm count in morphine group was (0±0) and in naloxone group, naloxone+morphine, sham and control were 235±3.77, 220±3.81, 247.12±6.10 and 250±6.54, respectively (p<0.001). Conclusion: Morphine could affect all spermatogenesis stages. 303 308 2017/10/12017/10/1 1396/7/9 2017/10/142017/10/14 1396/7/22 نسرین تک زارع Nasrin Takzare Department of Anatomy, Tehran University of Medical Sciences, Tehran, Iran ایران اسماعیل سمیع زاده Esmaeil Samizadeh Department of Pathology, Tehran University of Medical Sciences, Tehran, Iran ایران سعید شعار Saeed Shoar Department of Anatomy, Tehran University of Medical Sciences, Tehran, Iran ایران معصومه مجیدی ذولبین Masoumeh Majidi Zolbin Department of Anatomy, Tehran University of Medical Sciences, Tehran, Iran ایران محمد نادران Mohammad Naderan Department of Surgery, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran ایران علی لشکری Ali Lashkari Department of Pathology, Tehran University of Medical Sciences, Tehran, Iran ایران اعظم بختیاریان Azam Bakhtiarian Department of Pharmacology, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran ایران bakhtiar@sina.tums.ac.ir Opioids Morphine Spermatogenesis Sperm Rats اپیوئید مورفین اسپرماتوژنز اسپرم باروری موش نر. Cicero TJ, Davis LA, LaRegina MC, Meyer ER, Schlegel MS. Chronic opiate exposure in the male rat adversely affects fertility. Pharmacol Biochem Behav 2002; 72: 157-163.##Mattson S, Riley E. A review of the neurobehavioral deficits in children with fetal alcohol syndrome or prenatal exposure to alcohol. Clin Exp Res 1998; 22: 304-312.##Smeriglio V, HC. W. Prenatal drug exposure and child outcome. Past, present, future. Clin Perinatol 1999; 26: 1-16.##El Sawy MM, Malak HWA. Effect of tramadol abuse on testicular tissue of adult albino rats: a light and electron microscopic study. Egypt J Histol 2015; 38: 356-366.##Takzare N, Hosseini MJ, Hamideh Mortazavi S, Safaie S, Moradi R. The effect of Achillea millefolium extract on spermatogenesis of male Wistar rats. Hum Exp Toxicol 2011; 30: 328-334.##Cicero T, Adams M, Giordano A, Miller B, O'Connor L, Nock B. Influence of morphine exposure during adolescence on the sexual maturation of male rats and the development of their offspring. J Pharmacol Exp Ther 1991; 256: 1086-993.##Cicero T, Meyer E, Weist W, Olney J, RD. B. Effects of chronic morphine administration of the reproductive system of the male rat. J Pharmacol Exp Ther 1975; 192: 542-548.##Cicero T, Nock B, O'Connor L, Adams M, Meyer E. Adverse effects of paternal opiate exposure on offspring development and sensitivity to morphine-induced analgesia. J Pharmacol Exp Ther 1995; 273: 386-392.##Sharpe RM. Environmental/lifestyle effects on spermatogenesis. Biol Sci 2010; 365: 1697-1712.##Friedler G, Cicero T. Paternal pregestational opiate exposure in male mice: neuroendocrine deficits in their offspring. Res Commun Subst Abuse 1987; 8: 109-116.##Joffe J, LF. S. Paternal drug exposure: effects on reproduction and progeny. Semin Perinatol 1982; 6: 116-124.##Smith D, MJ J. Increased neonatal mortality in offspring of male rats treated with methadone or morphine before mating. Nature 1974; 253: 202-203.##Wang YH, Liu HM. The histological effect of morphine-dependence on male rat germ cell. Chin J Lab Diagnos 2011; 2: 010.##Ghowsi M, Yousofvand N. Impact of morphine dependency and detoxification by methadone on male's rat reproductive system. Iran J Reprod Med 2015; 13: 275-282.##Siddiqui A, Haq S, Shah BH. Perinatal exposure to morphine disrupts brain norepinephrine, ovarian cyclicity, and sexual receptivity in rats. Pharmacol Biochem Behav 1997; 58: 243-248.##Yilmaz B, Konar V, Kutlu S, Sandal S, Canpolat S, Gezen M, et al. Influence of chronic morphine exposure on serum LH, FSH, testosterone levels, and body and testicular weights in the developing male rat. Syst Biol Reprod Med 1999; 43: 189-196.##Karimi S, Karami M, Zardooz H, Salimi SH, Sahraei H. Biphasic Effects of Naloxone in the Rats Receiving Morphine Overdose A Place Preference Study. Iran J Pharm Res 2011; 10: 605.##Bhutta AT, Rovnaghi C, Simpson PM, Gossett JM, Scalzo FM, Anand K. Interactions of inflammatory pain and morphine in infant rats: long-term behavioral effects. Physiolv Behav 2001; 73: 51-58.##Cicero TJ, Meyer ER, Wiest WG, Olney JW, Bell R. Effects of chronic morphine administration on the reproductive system of the male rat. J Pharmacol Exp Ther 1975; 192: 542-548.##Sokol RZ. Hormonal effects of lead acetate in the male rat: mechanism of action. Biol Reprod 1987; 37: 1135-1138.##Almeida FF, Leal MC, França LR. Testis morphometry, duration of spermatogenesis, and spermatogenic efficiency in the wild boar (Sus scrofa scrofa). Biol Reprod 2006; 75: 792-799.##Burstein SR, Williams TJ, Lane DA, Knudsen MG, Pickel VM, McEwen BS, et al. The influences of reproductive status and acute stress on the levels of phosphorylated delta opioid receptor immunoreactivity in rat hippocampus. Brain Res 2013; 1518: 71-81.##Genazzani AR, Petraglia F. Opioid control of luteinizing hormone secretion in humans. J Steroid Biochem 1989; 33: 751-755.##Kalra SP. Mandatory neuropeptide-steroid signaling for the preovulatory luteinizing hormone-releasing hormone discharge. Endocr Rev 1993; 14: 507-538.##Quigley ME, Yen SSC. The role of endogenous opiates in LH secretion during the menstrual cycle. J Clin Endocrinol Metab 1980; 51: 179-181.##WANG C, Chan V, Yeung RT. The effect of heroin addiction on pituitary‐testicular function. Clin Endocrinol 1978; 9: 455-461.##El-Bermawy MI, Salem MF. Histological changes of the albino rat cerebellar cortex under the effect of different doses of tramadol administration. Egypt J Histol 2015; 38: 143-155.##El-Ghawet HA. Effects of tramadol on the reproductive function of wistar albino rats. Eur J Exp Biol 2015; 5: 56-64.##Singer R, Ben-Bassat M, Malik Z, Sagiv M, Ravid A, Shohat B, et al. Oligozoospermia, asthenozoospermia, and sperm abnormalities in ex-addict to heroin, morphine, and hashish. Syst Biol Reprod Med 1986; 16: 167-174.##Abdellatief RB, Elgamal DA, Mohamed EE. Effects of chronic tramadol administration on testicular tissue in rats: an experimental study. Andrologia 2015; 47: 674-679.##James RW, Heywood R, Crook D. Effects of morphine sulphate on pituitary-testicular morphology of rats. Toxicol Lett 1980; 7: 61-70.##Bablok L, Fracki S, Wielgos M, Czaplicki M, Marianowski L. [The naloxone test in the degenerative changes of seminiferous tubules]. Ginekol Pol 1998; 69: 374-379. (In Polish)##Blandau R. On the factors involved in sperm transport through the cervix uteri of the albino rat. Am J Anat 1945; 77: 253-272.##Carballada R, Esponda P. Structure of the vaginal plugs generated by normal rats and by rats with partially removed seminal vesicles. J Exp Zoo 1993; 256: 61-68.##Matthews L, Adler N. Systematic interrelationship of mating, vaginal plug position and sperm transport in the rat. Physiol Behav 1978; 20: 303-309.## ##

Vaginal progesterone on the prevention of preterm birth and neonatal complications in high risk women: A randomized placebo-controlled double-blind study بررسی اثر پروژسترون واژینال در جلوگیری از زایمان زودرس و عوارض نوزادی در زنان در معرض خطر زایمان زودرس : یک مطالعه کارآزمائی بالینی تصادفی دوسو کور 2 1 مقدمه: زایمان زودرس یک علت اصلی مرگ و میر و عوارض نوزادی می­باشد. هدف: هدف از این مطالعه بررسی اثرات پروفیلاکسی پروژسترون واژینال در یک جامعه پرخطر در کاهش میزان زایمان زودرس و عوارض نوزادی می­باشد. مواد و روش­ها: 100 بیمار با حاملگی تک قلو در این مطالعه کارآزمایی بالینی تصادفی، دوسوکور، قرار گرفتند. به 50 بیمار (گروه A) پروژسترون واژینال    mg 400 و به 50 بیمار (گروه B) پلاسبو، روزانه یکبار از هفته 22-16 حاملگی تا هفته 36 تجویز شد. دو گروه برای شیوع زایمان زودرس و عوارض نوزادی مقایسه شدند. نتایج: میزان شیوع تولد زودرس در این مطالعه %52 بود. میزان زایمان زودرس قبل از 37 هفته (86/2-25/1 CI %95 و 89/1=RR و %36 vs. %68) و قبل از 34 هفته (58/4-1925/1 CI %95 و 33/2=RR و %18 vs. %42) حاملگی در گروه پلاسبو بطور معنی­داری بیشتر از گروه پروژسترون بود. مطالعه ما همچنان نشان داد که مصرف پروژسترون واژینال در مقایسه با پلاسبو، با کاهش معنی­داری در میزان تولد نوزادان با وزن مساوی و کمتر از 2500 گرم، دیسترس تنفسی، و میزان بستری به بخش مراقبت­های ویژه نوزادان، همراه می­باشد. اما تفاوت معنی­داری در میزان مرگ نوزادی، طول روزهای بستری در بخش    مراقبت­های ویژه نوزادان، خونریزی داخل بطنی مغز و آنتریکولیت نکروزان بین دو گروه وجود نداشت. نتیجه­ گیری: مصرف پروژسترون واژینال بطور پروفیلاکسی، در خانم­هایی که در خطر بروز زایمان زودرس هستند، میزان زایمان زودرس را کاهش می­دهد. همچنین این مصرف با کاهش چشمگیری در میزان تولد نوزادان با وزن مساوی و کمتر از 2500 گرم، دیسترس تنفسی و بستری به بخش مراقبت­های ویژه همراه می­باشد. 2 Background: Preterm birth is the major cause of neonatal mortality and morbidity. Objective: The aim of this study was to evaluate the effect of prophylactic vaginal progesterone on decreasing preterm birth rate and neonatal complications in a high-risk population. Materials and Methods: A randomized, double-blind, placebo-controlled study was performed on 100 high-risk singleton pregnancies. Vaginal suppository progesterone (400 mg) or placebo was administered daily between 16-22 wks to 36 wks of gestation. Progesterone (n=50) and placebo (n=50) groups were compared for incidence of preterm delivery and neonatal complications. Results: The preterm birth rate was 52%. Preterm birth rate before the 37 wks of gestation (68% vs. 36%: RR=1.89, 95% CI: 1.25-2.86) and also before the 34 wks of gestation (42% vs. 18%: RR=2.33, 95% CI: 1.19-4.58) in placebo group was significantly higher than progesterone group. Our study also showed that the administration of vaginal progesterone was associated with a significant reduction in the risk of birth weight ≤2500 gr, the rates of respiratory distress syndrome (RDS) and admission to the Neonatal Intensive Care Unit (NICU) in the progesterone group when compared with the placebo group. However, there was no significant difference between the two groups in terms of neonatal death, days of admission in NICU, intraventricular hemorrhage and necrotizing enterocolitis. Conclusion: Prophylactic vaginal progesterone reduced the rate of preterm delivery, the risk of a birth weight ≤2500 gr, the rates of RDS and admission to NICU in women who were at risk of preterm delivery. 309 316 2017/10/12017/10/12017/10/1 1396/7/9 2017/10/142017/10/142017/10/14 1396/7/22 اعظم آذرگون Azam Azargoon Abnormal Uterine Bleeding Research Center, Semnan University of Medical Sciences, Semnan, Iran ایران azarmona2003@yahoo.com راهب قربانی Raheb Ghorbani Social Determinants of Health Research Center, Department of Community Medicine, Faculty of Medicine, Semnan University of Medical Sciences, Semnan, Iran ایران فرشته اصل بهار Fereshteh Aslebahar Abnormal Uterine Bleeding Research Center, Semnan University of Medical Sciences, Semnan, Iran ایران Premature birth Prevention Progesterone Randomized controlled trial پروژسترون پیشگیری تولد زودرس کارآزمائی بالینی تصادفی. Cunningham FG, Leveno KJ, Bloom SL, Hauth JC, Rouse DJ, Spong CY, editors. Williams Obstetrics. 24th Ed. New York: McGraw-Hill Medical; 2014.##Mathews J, McDonald MF. Infant mortality statistics from the 2008 period linked birth infant death data sct. Natl Vital Stat Rep 2012; 80: 1-49.##Hamilton BE, Martin JA, Ventura SJ. Births: preliminary data for 2010. Natl Vital Stat Rep 2011; 60: 1-26##Martison DR, Damus K, Fiore E, Petrini J, Alter C. Preterm delivery: a public health perspective . Paediatr Perinat Epidemiol 2001; 15 (Suppl.): 7-16.##Gluckman PD, Hanson MA. Living with the past: evolution, development and patterns of disease. Science 2004; 305: 1733-1736.##Creasy RK. Preterm birth prevention: where are we? Am J Obstet Gynecol 1993; 168: 1223-1230.##American College of Obstetricians and Gynecologist (ACOG). Assessment of risk factors for preterm birth (ACOG Practice Bulletin NO. 31). Obstet Gynecol 2001; 98: 709-716.##Papiernik E. [Double blind study of an agent to prevent pre-term delivery among women at increased risk]. In: Edition Schering; Serie4, fiche3: 1970: 65-68 (In French)##Keirse MJNC. Progestron administration in pregnancy may prevent preterm delivery. BR J Obstet Gynecol 1990; 97: 149-154.##Meis PJ, Klebanoff M, Thom E, Dombrowski MP, Sibai B, Moawad AH, et al. Prevention of recurrent preterm delivery by 17 alpha-hydroxyl progestron caproate. N Engl J Med 2003; 348: 2379-2385.##Mackenzie R, Walker M, Armson A, Hannah ME. Progestrone for the prevention of preterm birth among women at increased risk: A systematic review and meta-analysis of randomized controlled trials. Am J Obstet Gynecol 2006; 194: 1234-1242.##da Fonsceca EB, Bittar RE, Carvalho MH, Zugaib M. Prophylactic administration of progestron by vaginal suppository to reduce the incidence of spontaneous preterm birth in women at increased risk: A randomized placebo-controlled double-blind study. Am J Obstet Gynecol 2003; 188: 419-424.##Rouse DJ, Caitis SN, Peaceman AM, Sciscione A, Thom EA, Spong CY, et al. A trial of 17 alphahydroxyl progestron caproate to prevent prematurity in twins. N Engl Med 2007; 357: 454-461.##O'Brien JM, Adair CD, Lewis DF, Hall DR, Defranco EA, Fusey S, et al. progestron vaginal gel for the reduction of recurrent preterm birth : Primary results from a randomized, double blind, placebo-controlled trial. Ultrasound Obstet Gynecol 2007; 30: 687-696.##Tita AT, Rouse DJ. Progesterone for preterm birth prevention: An evolving intervention. Am J Obstet Gynecol 2009; 200: 219-224##Dodd JM, Jones L, Flenady V, Cincotta R, Crowther CA. Prenatal administration of progesterone for preventing preterm birth in women considered to be at risk of preterm birth. Cochrane Database Syst Rev 2013; 7: CD004947.##Berghella V, Figueroa D, Szychowski JM, Owent J, Hankins GD, Lams JD, et al. 17-alpha-hydroxyl progesterone caproate for the prevention of preterm birth in women with prior preterm birth and a short cervical length. Am J Obstet Gynecol 2010; 202: 351-356.##Grobman WA, ThomE, Spong CY, Lams JD, Soade GR, Mercer BM, et al. 17 alpha-hydroxyl progesterone caproate to prevent prematurity in nulliparas with cervical length less than 30 mm. Am J Obstet Gynecol 2012; 207: 390-398.##De Franco EA, O'Brien JM, Adair CD, Lewis DF, Hall DR, Fusey S, et al. Vaginal progesterone is associated with a decrease in risk for early preterm birth and improved neonatal outcome in women with a short cervix: A secondary analysis from a randomized , double blind , placebo- controlled trial. Ultrasound Obstet Gynecol 2007; 30: 697-705.##Cetingoz E, Cam C, Sakalli M, Karateke A, Celik C, Sancak A. Progesterone effects on preterm birth in high risk pregnancies: A randomized placebo-controlled trial. Arch Gynecol Obstet 2011; 283: 423-429.##Sfakianaki AK, Norwitz ER. Mechanisms of progesterone action in inhibiting prematurity. J Matern Fetal Neonatal Med 2006; 19: 763-772.##Garfield RE, Kannan MS, Daniel EE. Gap junction formation in myometrium: control by estrogens, progesterone, and prostaglandins. Am J Physiol 1980; 238: C81-C89.##Sfakianaki AK, Norwitz ER. Mechanisms of progesterone action in inhibiting prematurity. J Matern Fetal Neonatal Med 2006; 19: 763-772.##Challis JRG. Sharp increases in free circulating oestrogens immediately before parturition in sheep. Nature 1971; 229: 208.##Mitchell B, Cruickshank B, McLean D, Challis J. Local modulation of progesterone production in human fetal membranes. J Clin Endocrinol Metab 1982; 55: 1237-1239.##Frydman R, LeLaidier C, Baton-Saint-Mleux C, Fernandez H, Vial M, Bourget P. Labor induction in women at term with mifepristone(RU 486): a double-blind, randomized, placebo-controlled study. Obstet Gynecol 1992; 80: 972-975##Yellon SM, Burns AE, See JL, Lechuga TJ, Kirby MA. Progesterone withdrawal promotes remodeling processes in the nonpregnant mouse cervix. Biol Reprod 2009; 81: 16-85.##Borna S, Sahabi N. Progesterone for maintenance tocolytic therapy after threatened preterm labor: A randomized controlled trial. Aust NZ J Obstet Gynecol 2008; 48: 58-63.##Khandelwal M. Vaginal progesterone in risk reduction of preterm birth in women with short cervix in the midtrimester of pregnancy. Int J Womens Health 2012; 4: 481-490.##Berghella V, Rafael TJ, Szychowski JM, Rust OA, Owen J. Cerclage for Short Cervix on Ultrasonography in Women With Singleton Gestations and Previous reterm Birth: A Meta-Analysis. Obstet Gynecol 2011; 117: 663-671.##Hassan SS, Remero R, Vidyadhan D, Fusey S, Baxter JK, Khandelwal M, et al. Vaginal progesterone reduces the rate of preterm birth in women with a sonographic short cervix: A multicenter, randomized, double-blind, placebo-controlled trial. Ultrasound Obstet Gynecol 2011; 38: 18-31.##Berghella V, Figueroa D, Szychowski JM, Owen J, Hankins GD, Iams JD, et al. 17-alpha-hydroxyprogesterone caproate for the prevention of preterm birth in women with prior preterm birth and a short cervical length. Am J Obstet Gynecol 2010; 202: 351.##Alfirevic Z, Owen J, Carreras Moratonas E, Sharp An, Szychowski JM, Goya M. Vaginal progesterone , cerclage or cervical pessary for preventing preterm birth in asymptomatic singleton pregnant women with a history of preterm birth and a sonographic short cervix. Ultrasound Obstet Gynecol 2013; 41: 146-151.##Conde-Agudelo A, Romero R, Nicolaides K, Chaiworapongsa T, Brien JM, Cetingoz E, et al. Vaginal progesterone VS cervical cerclage for the prevention of preterm birth in women with a sonographic short cervix, previous preterm birth and singleton gestation: A systematic review and indirect comparison meta-analysis. Am J Obstet Gynecol 2013; 208: 42.## ##

Obstetrics and perinatal outcomes of dichorionic twin pregnancy following ART compared with spontaneous pregnancy بررسی نتایج بارداری در حاملگی دوقلویی ناشی از روش های کمک باروری و دوقلویی خودبخودی 2 1 مقدمه: با پیشرفت روش­های کمک باروری، فراوانی حاملگی­های دوقلویی و چند قلویی درطی سال­های اخیر به طور چشمگیری افزایش یافته است. هدف: این مطالعه با هدف بررسی نتایج بارداری در حاملگی دوقلویی تک کوریونی به دنبال استفاده از روش­های کمک باروری (ART) و دوقلویی خودبخودی انجام شد. مواد و روش­ها: در این مطالعه مقطعی که در بیمارستان قائم وابسته به دانشگاه علوم پزشکی مشهد انجام شد، تعداد 107 حاملگی دوقلویی تک کوریونی در دو گروه وارد مطالعه شدند: گروه خودبخودی (96 نفر) و گروه ART (31 نفر). معیارهای پایه و نتایج حاملگی شامل اطلاعات دموگرافیک، سن حاملگی، روش زایمان، عوارض حاملگی (پره اکلامپسی، دیابت بارداری، زایمان زودرس، IUGR، و خونریزی بعد از زایمان)، نتایج نوزادی (وزن، آپگار دقیقه 1و5، بستری در NICU، مرگ و میر، زجر تنفسی، زردی) با استفاده از پرسشنامه ای ثبت شد. نتایج: از لحاظ فاکتورهای مرتبط با مادران در بارداری و عوارض در طول بارداری و بعد از زایمان فراوانی پره اکلامپسی و دیابت بارداری و انقباضات زودرس رحمی در گروه ART به­طور معنی­داری بیشتر بود ولی سایر فاکتورها نظیر آنمی و IUGR و خونریزی بعد از زایمان و IUFD دو گروه تفاوت معنی­داری نداشتند. فاکتورهای مرتبط با نتایج نوزادی (وزن قل­ها، آپگارقل­ها، آپگار کمتر از 7 دقیقه اول و پنجم، بستری در NICU، مرگ نوزادها دیسترس تنفسی ، ایکتر) در دو گروه تفاوت معنی­داری نداشت. دو گروه همچنین از لحاظ مصرف سیگار و اعتیاد نیز تفاوتی نشان ندادند. نتیجه­ گیری: برخی عوارض مادری شامل پره اکلامپسی، دیابت بارداری، و زایمان پره ترم در گروه دوقلویی حاصل از ART بیشتر بود. از اینرو بهتر است   زوج­ها از ریسک بالاتر این عوارض قبل از استفاده از ART آگاه شوند و بعد از انتخاب آگاهانه این روش تحت مراقبت­های ویژه و غربالگری جهت تشخیص زود هنگام و مراقبت­های لازم درمانی قرار گیرند.  2 Introduction: Regarding to the recent advances in assisted reproductive techniques (ART), twin and multiple pregnancies have increased during past years. Objective: This study was performed to compare obstetrics and perinatal outcomes of dichorionic twin pregnancy following ART with spontaneous pregnancy. Materials and Methods: In this cross-sectional study which was performed in Ghaem Hospital, Mashhad University of Medical Sciences, 107 dichorionic twin pregnancy were enrolled in two groups: spontaneous group (n=96) and ART group (n=31). Basic criteria and obstetrics and neonatal outcomes information including demographic data, gestational age, mode of delivery, pregnancy complications (preeclampsia, gestational diabetes, preterm labor, and intrauterine growth retardation (IUGR), postpartum hemorrhage), neonatal outcomes (weight, first and fifth minute Apgar score, Neonatal Intensive Care Unit (NICU) admission, mortality, respiratory distress, and icterus) were recorded using a questionnaire. Results: Preterm labor, gestational diabetes, and preeclampsia were significantly higher in ART group compared to spontaneous pregnancy group. However, other factors such as anemia, IUGR, postpartum hemorrhage, and intrauterine fetal death (IUFD) were not significantly different between groups. There were no significant differences between groups in terms of neonatal outcomes (weight, 1st and 5th min Apgar score <7, NICU hospitalization, mortality, respiratory distress, and icterus). Conclusion: With regard of significantly higher poor outcomes such as preeclampsia, gestational diabetes and preterm labor in ART group, the couples should be aware of these potential risks before choosing ART. 317 322 2017/10/12017/10/12017/10/12017/10/1 1396/7/9 2017/10/142017/10/142017/10/142017/10/14 1396/7/22 لیلا پورعلی Leila Pourali Department of Obstetrics and Gynecology, Women's Health Research Center, Ghaem Hospital, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran ایران صدیقه آیتی Sedigheh Ayati Department of Obstetrics and Gynecology, Women's Health Research Center, Ghaem Hospital, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran ایران ayatis@mums.ac.ir شهرزاد جلودار Shahrzad Jelodar Ghaem Hospital, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran ایران احمدرضا ظریفیان Ahmadreza Zarifian Student Research Committee, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran ایران محمدسبحان شیخ عندلیبی Mohammad Sobhan Sheikh Andalibi Student Research Committee, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran ایران Twin pregnancy ART Preeclampsia Outcome دوقلویی تکنیک های کمک باروری نتایج پره اکلامپسی. Newman RB, Rittenberg C. Multiple gestation. In: Gibbs RS, Karlan BY, Haney AF, Nygaard I. Danforths obstetrics and gynecology. 10th Ed. Philadelphia: Lippincott Williams & Wilkins, 2008: 220.##Kanat-Pektas M, Kunt C, Gungor T, Mollamahmutoglu L. Perinatal and first year outcomes of spontaneous versus assisted twins: a single center experience. Arch Gynecol Obstet 2012; 278: 143-147.##Reddy UM, Wapner RJ, Rebar RW, Tasca RJ. Infertility assisted reproductive technology, and adverse pregnancy outcomes: executive summary of a National Institute of Child Health and Human Development workshop. Obstet Gynecol 2007; 109: 967-977.##Blickstein I. Dose assisted reproduction technology, per se, increases the risk of preterm birth? Br J Obstet Gynecol 2006; 113 (Suppl.): 68-71.##Moini A, Shiva M, Arabipoor A, Hosseini R, Chehrazi M, Sadeghi M. Obstetric and neonatal outcomes of twin pregnancies conceived by assisted reproductive technology compared with twin pregnancies conceived spontaneously: a prospective follow-up study. Eur J Obstet Gynecol Reprod Biol 2012; 165: 29-32.##Anbazhagan A, Hunter A, Breathnach FM, Mcauliffe FM, Geary MP, Daly S, et al. Comparison of outcomes of twins conceived spontaneously and by artificial reproductive therapy. J Matern Fetal Neonatal Med 2014; 27: 458-462.##Geisler ME, O'Mahony A, Meaney S, Waterstone JJ, O'Donoghue K. Obstetric and perinatal outcomes of twin pregnancies conceived following IVF/ICSI treatment compared with spontaneously conceived twin pregnancies. Eur J Obstet Gynecol Reprod Biol 2014; 181: 78-83.##Caserta D, Bordi G, Stegagno M, Filippini F, Podagrosi M, Roselli D, et al. Mathernal and perinatal outcomes in spontaneous versus assisted conception twin pregnancies. Eur J Obstet Gynecol Reprod Biol 2014; 174: 64-69.##Baxi A, Kaushal M. Outcome of twin pregnancies conceived after assisted reproductive techniques. J Hum Reprod Sci 2008; 1: 25-28.##Daniel Y, Ochshorn Y, Fait G, Geva E, Bar-Am A, Lessing JB. Analysis of 104 twin pregnancies conceived with assisted reproductive technologies and 193 spontaneously conceived twin pregnancies. Fertil Steril 2000; 74: 683-689.##Zaib-un-Nisa S, Ghazal-Aswad S, Badrinath P. Outcome of twin pregnancies after assisted reproductive techniques--a comparative study. Eur J Obstet Gynecol Reprod Biol 2003; 109: 51- 54.##Andrijasevic S, Dotlic J, Aksam S, Micic J, Terzic M. [Impact of Conception Metod on Twin Pregnancy Course and Outcome]. Geburtshilfe Frauenheilkd 2014; 74: 933-939. (In German)##Barat SH, Basirat Z, Bouzari Z, Yazdani SH, Zarinkamar Roodbari M. Comparison of Perinatal Outcomes of Twin Births Conceived Using Assisted Reproduction Technology versus Spontaneous. J Babol Univ Med Sci 2009; 11: 49-53.##Fan C, Sun Y, Yang J, Ye J, Wang S. Maternal and neonatal outcomes in dichorionic twin pregnancies following IVF treatment: a hospital-based comparative study. Int J Clin Exp Pathol 2013; 6: 2199-2207.##Beltrán Montoya J, Reyes Mu-oz E, Cruz Rivera E, López Villase-or B, Francisco de la Jara Díaz J, Herrerías Canedo T. Adverse perinatal outcomes in Mexican women with twin pregnancy achieved by assisted reproduction techniques vs. spontaneous twin pregnancies. Ginecol Obstet Mex 2012; 80: 445-453.## ##

Significant correlation of angiotensin converting enzyme and glycoprotein IIIa genes polymorphisms with unexplained recurrent pregnancy loss in north of Iran چندشکلی های ژن های آنزیم تبدیل کننده آنژیوتانسین و گلیکوپروتئین IIIa در سقط های مکرر با علت ناشناخته در شمال ایران 2 1 مقدمه: سقط خود به خودی به عنوان پیچیده­ترین مشکل دوران حاملگی شناخته شده است. ترومبوفیلی به عنوان یکی از علل سقط مکرر فرض می­شود. مطالعات بسیاری شیوع جهش در ژن­های ترومبوفیلیک خاص را در سقط­ها مورد بررسی قرار داده اند. گلیکوپروتئین IIIa یکی از ژن­های ترومبوزیس درگیر در ترومبوز و سقط جنین است. آنزیم تبدیل کننده آنژیوتانسین، آنژیوتانسین I را تبدیل به آنژیوتانسین II و باعث ترومبوز می­شود. پلی­مورفیسم (چند شکلی) شایع در این ژن موتاسیون درج / حذف می­باشد. هدف: در این مطالعه، ما ارتباط بین چند شکلی­های ژن­های گلیکوپروتئین IIIa و آنزیم تبدیل کننده آنژیوتانسین را در زنان دارای سقط مکرر با علت ناشناخته از شمال ایران، آنالیز کردیم. مواد و روش­ها: نمونه ها شامل 100 زن دارای سقط مکرر غیر قابل توضیح و 100 نفر شاهد می­باشد. ژنوتیپ­های چند شکلی­های ژن­های گلیکوپروتئین IIIa و آنزیم تبدیل­کننده آنژیوتانسین با روش PCR مشخص شدند. ارتباط بین فراوانی ژنوتیپ­ها با و سقط مکرر با استفاده از تجزیه و تحلیل آزمون­های χ2 و آزمون دقیق فیشر بررسی شدند. خطر در ارتباط با ترکیب دو ژنوتیپ نیز توسط رگرسیون لجستیک دوتایی مورد بررسی قرار گرفت. نتایج: رابطه معنی­داری بین ژنوتیپ DD آنزیم تبدیل­کننده آنژیوتانسین و سقط مکرر وجود دارد (04/2=OR و %95 44/4-94/0= CI و 036/0=p). آلل D آنزیم تبدیل کننده آنژیوتانسین نیز به طور معنی­داری با سقط مکرر مرتبط می­باشد (59/1=OR و %95 41/2-05/1= CI و 013/0=p). ارتباط آماری معنی­داری بین پلی­مورفیسم ژن GPIIIa و سقط مکرر مشاهده نشد. نتیجه گیری: پلی­مورفیسم درج/ حذف ژن آنزیم تبدیل­کننده آنژیوتانسین، احتمالا می­تواند به عنوان یک عامل پیش­بینی کننده در سقط مکرر در اعضای زن خانواده زنانی با سابقه سقط مکرر، مورد بررسی قرار گیرد. 2 Background: Spontaneous abortion is considered as the most complex problem during pregnancy. Thrombophilia is resumed as a cause of recurrent pregnancy loss (RPL). Glycoprotein IIIa (GPIIIa) gene is involved in thrombosis and abortion. Angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II and is involved in thrombosis. The most common polymorphism in this gene is the insertion/deletion (I/D). Objective: In this study, we analyzed the association between ACE I/D and GPIIIa c.98C >T polymorphisms in women with unexplained RPL from the north of Iran. Materials and Methods: Sample population consisted of 100 women with unexplained RPL and 100 controls. The ACE I/D and GPIIIa c.98C>T polymorphisms were genotyped by TETRA-ARMS PCR. The association between genotypes frequency and RPL were analyzed using χ2 and exact fisher tests. Associated risk with double genotype combinations was also investigated by binary logistic regression. Results: There was significant association between ACE DD genotype and RPL (OR=2.04; 95% CI=0.94-4.44; p=0.036). ACE D Allele was also significantly associated with the RPL (OR=1.59; 95% CI=1.05-2.41; p=0.013). No significant association was observed between GPIIIa c.98C>T polymorphism and RPL. Conclusion: ACE I/D polymorphism may probably be a prognostic factor in female family members of women with the history of recurrent abortion. 323 328 2017/10/12017/10/12017/10/12017/10/12017/10/1 1396/7/9 2017/10/142017/10/142017/10/142017/10/142017/10/14 1396/7/22 شکوفه فاضل نیا Shokoufeh Fazelnia Department of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran ایران تورج فرازمندفر Touraj Farazmandfar Medical Cellular and Molecular Research Center, Golestan University of Medical Sciences, Gorgan, Iran ایران سید محمد باقر هاشمی سوته Seyed Mohammad Bagher Hashemi-Soteh Immunogenetic Research center, Molecular and cell Biology Research Centre, Mazandaran University of Medical Sciences, Sari, Iran ایران hashemisoteh@gmail.com Angiotensin converting enzyme Platelet glycoprotein IIIa Recurrent abortion آنزیم تبدیل کننده آنژیوتانسین گلیکوپروتئین IIIa سقط مکرر. Vettriselvi V, Vijayalakshmi K, Paul SFD, Venkatachalam P. ACE and MTHFR gene polymorphisms in unexplained recurrent pregnancy loss. J Obstet Gynaecol Res 2008; 34: 301-306.##Carp H, Salomon O, Seidman D, Dardik R, Rosenberg N, Inbal A. Prevalence of genetic markers for thrombophilia in recurrent pregnancy loss. Hum Reprod 2002; 17: 1633-1637.##Kutteh WH, Triplett DA. Thrombophilias and recurrent pregnancy loss. Semin Reprod Med 2006; 24: 54-66.##Sarig G, Younis JS, Hoffman R, Lanir N, Blumenfeld Z, Brenner B. Thrombophilia is common in women with idiopathic pregnancy loss and is associated with late pregnancy wastage. Fertil Steril 2002; 77: 342-347.##Wramsby ML, Sten-Linder M, Bremme K. Primary habitual abortions are associated with high frequency of factor V Leiden mutation. Fertil Steril 2000; 74: 987-991.##Brenner B, Sarig G, Weiner Z, Younis J, Blumenfeld Z, Lanir N. Thrombophilic polymorphisms are common in women with fetal loss without apparent cause. Thromb Haemost 1999; 82: 6-9.##Goodman CS, Coulam CB, Jeyendran RS, Acosta VA, Roussev R. Which thrombophilic gene mutations are risk factors for recurrent pregnancy loss? Am J Reprod Immunol 2006; 56: 230-236.##Kovalevsky G, Gracia CR, Berlin JA, Sammel MD, Barnhart KT. Evaluation of the association between hereditary thrombophilias and recurrent pregnancy loss: a meta-analysis. Arch Intern Med 2004; 164: 558-563.##Jivraj S, Rai R, Underwood J, Regan L. Genetic thrombophilic mutations among couples with recurrent miscarriage. Hum Reprod 2006; 21: 1161-1165.##Rey E, Kahn SR, David M, Shrier I. Thrombophilic disorders and fetal loss: a meta-analysis. Lancet 2003; 361: 901-908.##Kempf Haber M, Klimek M. [Thrombophilia in pregnancy and its influence on venous thromboembolism and recurrent miscarriages]. Przegl Lek 2005; 62: 164-168. (In Polish)##Sayed-Tabatabaei FA, Oostra BA, Isaacs A, van Duijn CM, Witteman JCM. ACE polymorphisms. Circ Res 2006; 98: 1123-1133.##Ueda S, Elliott HL, Morton JJ, Connell JM. Enhanced pressor response to angiotensin I in normotensive men with the deletion genotype (DD) for angiotensin-converting enzyme. Hypertension 1995; 25: 1266-1269.##Buchholz T, Thaler CJ. Inherited thrombophilia: impact on human reproduction. Am J Reprod Immunol 2003; 50: 20-32.##Fatini C, Gensini F, Sticchi E, Battaglini B, Prisco D, Fedi S, et al. ACE DD genotype: an independent predisposition factor to venous thromboembolism. Eur J Clin Invest 2003; 33: 642-647.##Kim DK, Kim JW, Kim S, Gwon HC, Ryu JC, Huh JE, et al. Polymorphism of angiotensin converting enzyme gene is associated with circulating levels of plasminogen activator inhibitor-1. Arterioscler Thromb Vasc Biol 1997; 17: 3242-3247.##Su M-T, Lin S-H, Chen Y-C, Kuo P-L. Genetic association studies of ACE and PAI-1 genes in women with recurrent pregnancy loss: a systematic review and meta-analysis. Thromb Haemost 2013;109: 8-15.##Su MT, Lin S-H, Chen Y-C. Genetic association studies of angiogenesis- and vasoconstriction-related genes in women with recurrent pregnancy loss: a systematic review and meta-analysis. Hum Reprod Update 2011; 17: 803-812.##Casas JP, Bautista LE, Smeeth L, Sharma P, Hingorani AD. Homocysteine and stroke: evidence on a causal link from mendelianrandomisation. Lancet 2005; 365: 224-232.##Newman PJ, Derbes RS, Aster RH. The human platelet alloantigens, PlA1 and PlA2, are associated with a leucine33/proline33 amino acid polymorphism in membrane glycoprotein IIIa, and are distinguishable by DNA typing. J Clin Invest 1989; 83: 1778-1781.##Carter AM, Catto AJ, Bamford JM, Grant PJ. Platelet GP IIIaPlA and GP Ib variable number tandem repeat polymorphisms and markers of platelet activation in acute stroke. Arterioscler Thromb Vasc Biol 1998; 18: 1124-1131.##Yilmaz S, Bayan K, Tüzün Y, Batun S, Altintaş A. A comprehensive analysis of 12 thrombophilic mutations and related parameters in patients with inflammatory bowel disease: data from Turkey. J Thromb Thrombolysis 2006; 22: 205-212.##Ruzzi L, Ciarafoni I, Silvestri L, Semeraro ML, Abeni D. Association of PLA2 polymorphism of the ITGB3 gene with early fetal loss. Fertil Steril 2005; 83: 511-512.##Jeddi-Tehrani M, Torabi R, Mohammadzadeh A, Arefi S, Keramatipour M, Zeraati H, et al. Investigating Association of Three Polymorphisms of Coagulation Factor XIII and Recurrent Pregnancy Loss. Am J Reprod Immunol 2010; 64: 212-217.##Jeddi-Tehrani M, Torabi R, Zarnani AH, Mohammadzadeh A, Arefi S, Zeraati H, et al. Analysis of plasminogen activator inhibitor-1, integrin beta3, beta fibrinogen, and methylene tetra hydro folate reductase polymorphisms in Iranian women with recurrent pregnancy loss. Am J Reprod Immunol 2011; 66: 149-156.##Torabi R, Zarei S, Zeraati H, Zarnani AH, Akhondi MM, Hadavi R, et al. Combination of thrombophilic gene polymorphisms as a cause of increased the risk of recurrent pregnancy loss. J Reprod Infertil 2012; 13: 89-94.##Joung CI, Park YW, Kim SK, Uhm WS, Kim TH, Yoo DH. Angiotensin-Converting Enzyme Gene Insertion/ Deletion Polymorphism in Korean Patients with Systemic Sclerosis. J Korean Med Sci 2006; 21: 329-332.##Javaheri-Kermani M, Farazmandfar T, Ajami A, Yazdani Y. Impact of hepcidin antimicrobial peptide on iron overload in tuberculosis patients. Scand J Infect Dis 2014; 46: 693-696.##Hashemi-Soteh SMB, Sarzare F, Merat F, Salehifar E, Shiran MR. Frequencies of three CYP2D6 nonfunctional alleles (CYP2D6*3, *4, and *6) within an Iranian population (Mazandaran). Genet Test Mol Biomark 2011; 15: 821-825.##Redman CW, Sacks GP, Sargent IL. Preeclampsia: an excessive maternal inflammatory response to pregnancy. Am J Obstet Gynecol 1999; 180: 499-506.##Irani RA, Xia Y. The functional role of the renin-angiotensin system in pregnancy and preeclampsia.Placenta 2008; 29: 763-771.##Aarabi M, Memariani T, Arefi S, Aarabi M, Hantoosh Zadeh S, Akhondi MA, et al. Polymorphisms of plasminogen activator inhibitor-1, angiotensin converting enzyme and coagulation factor XIII genes in patients with recurrent spontaneous abortion. J Matern-Fetal Neonatal Med 2011; 24: 545-548.##Bagheri M, Abdi Rad I, Omrani MD, Nanbaksh F. Polymorphisms of the angiotensin converting enzyme gene in Iranian Azeri Turkish women with unexplained recurrent pregnancy loss. Hum Fertil 2010; 13: 79-82.##Buchholz T, Lohse P, Rogenhofer N, Kosian E, Pihusch R, Thaler CJ. Polymorphisms in the ACE and PAI-1 genes are associated with recurrent spontaneous miscarriages. Hum Reprod 2003; 18: 2473-2477.##Fatini C, Gensini F, Battaglini B, Prisco D, Cellai AP, Fedi S, et al. Angiotensin-converting enzyme DD genotype, angiotensin type 1 receptor CC genotype, and hyperhomocysteinemia increase first-trimester fetal-loss susceptibility. Blood Coagul Fibrinolysis 2000; 11: 657-662.##Valdez-Velazquez LL, Quintero-Ramos A, Perez SA, Mendoza-Carrera F, Montoya-Fuentes H, Rivas F et al. Genetic polymorphisms of the renin-angiotensin system in preterm delivery and premature rupture of membranes. J Renin Angiotensin Aldosterone Syst 2007; 8: 160-168.##Mello G, Parretti E, Gensini F, Sticchi E, Mecacci F, Scarselli G, et al. Maternal-fetal flow, negative events, and preeclampsia: role of ACE I/D polymorphism. Hypertension 2003; 41: 932-937.##Yenicesu GI, Cetin M, Ozdemir O, Cetin A, Ozen F, Yenicesu C, et al. A prospective case-control study analyzes 12 thrombophilic gene mutations in Turkish couples with recurrent pregnancy loss. Am J Reprod Immunol 2010; 63: 126-136.##Ozdemir O, Yenicesu GI, Silan F, Köksal B, Atik S, Ozen F et al. Recurrent pregnancy loss and its relation to combined parental thrombophilic gene mutations. Genet Test Mol Biomark 2012; 16: 279-286.##Coulam CB, Wallis D, Weinstein J, DasGupta DS, Jeyendran RS. Comparison of thrombophilic gene mutations among patients experiencing recurrent miscarriage and deep vein thrombosis. Am J Reprod Immunol 2008; 60: 426-431.##Pihusch R, Buchholz T, Lohse P, Rübsamen H, Rogenhofer N, Hasbargen U, et al. Thrombophilic gene mutations and recurrent spontaneous abortion: prothrombin mutation increases the risk in the first trimester. Am J Reprod Immunol 2001; 46: 124-131.##Hohlagschwandtner M, Unfried G, Heinze G, Huber JC, Nagele F, Tempfer C. Combined thrombophilic polymorphisms in women with idiopathic recurrent miscarriage. Fertil Steril 2003; 79: 1141-1148.## ##

H1299R in coagulation Factor V and Glu429Ala in MTHFR genes in recurrent pregnancy loss in Sari, Mazandaran در سقط مکرر در ساری، مازندران MTHFR در ژن (A1298C) Glu429Ala انعقادی و پلی مورفیسم V در فاکتور H1299R (A4070G) بررسی پلی مورفیسم 2 1 مقدمه: سقط مکرر به دلیل فاکتورهای متعددی صورت می­گیرد از جمله فاکتورهای ژنتیکی و ترومبوفیلی. علاوه بر فاکتور V لیدن، تغییر نوکلئوتیدی دیگری در ژن فاکتور V (A4070G; His1299Arg) در بروز سقط مکرر شناخته شده است و مرتبط به ترومبوفیلی ارثی می­باشد. همچنین ارتباط دو پلی­مورفیسم C677T و A1298C (Glu429A) در ژن MTHFR در سقط مکرر مطرح شده است. هدف: در این مطالعه تأثیر دو فاکتور A4070G در ژن فاکتور V و A1298C در ژن MTHFR در نژاد مازندرانی از شمال ایران مورد ارزیابی قرار گرفته است. مواد و روش­ها: جمعیت نمونه ها شامل 100 زن با سابقه سقط مکرر و 100 زن سالم مازندرانی می­باشد. ژنوتیپ پلی­مورفیسم­های A4070G از فاکتور V و A1298C از ژن MTHFR با PCR-RFLP مورد بررسی قرار گرفت. نتایج: مطالعات مولکولی نشان داد 5 زن از بیماران و 9 زن از گروه کنترل برای پلی­مورفیسم A4070G هتروزیگوت (AG) بودند. فراوانی آلل A در گروه بیماران و گروه کنترل به ترتیب 5/97% (975/0) و 5/95% (955/0) بودند و همچنین فراوانی آلل G در این دو گروه به ترتیب 5/2% (025/0) و 5/4% (045/0 ) مشاهده شد. ارتباط معنا داری بین ژنوتیپ A4070G فاکتور V لیدن و سقط مکرر مشاهده نگردید  (OR= 1.88, CI 95%= 0.6-5.82, p= 0.4). همچنین برای A1298C همه نمونه های گروه بیمار و کنترل هموزیگوت AA بودند. فراوانی آلل A در گروه بیماران و کنترل 100% و فراوانی آلل C صفر بود و تفاوت معناداری برای A1298C بین دو گروه وجود نداشت. نتیجه گیری: نتایج نشان می­دهد که پلی­مورفیسم­های A4070G و A1298C نمی­توانند عاملی برای بروز سقط مکرر در زنان استان مازندران باشند. 2 Background: Recurrent pregnancy loss (RPL) is caused by different factors, including genetics and thrombophilia. Beside Factor V Leiden, another nucleotide change in a factor V (FV) gene (A4070G; His1299Arg) has been identified linking to hereditary thrombophilia. Also, two proposed MTHFR polymorphisms, C677T and A1298C (Glu429A) are linked with RPL. Objective: In this study, the effect of two factors, A4070G in FV and A1298C in MTHFR are evaluated in RPL patients from Mazandaran province, Iran. Materials and methods: Sample population of 100 women with RPL and 100 controls with Mazandarani ethnics from northern Iran were consist. The factor V (A4070G) and MTHFR (A1298C) polymorphisms were genotyped by PCR-RFLP. Results: Molecular study showed 5 women from patients and 9 women from control group were heterozygous AG for A4070G. Frequency of "A" allele in patient and control groups was 97.5% (0.975) and 95.5% (0.955) respectively, and "G" allele frequency was 2.5% (0.025) and 4.5% (0.045) respectively. No significant association (p≤0.05) between FV A4070G genotype and RPL with an OR=1.88, CI 95%=0.6-5.82, was observed (p=0.4). Also, for A1298C, all patients and control individuals were AA genotype. "A" allele frequency in patients and control was 100% and "C" allele frequency was zero. There was no significant difference for A1298C between groups. Conclusion: Our finding showed that A4070G and A1298C polymorphisms cannot be considered as a cause of PRL in women from Mazandaran province, northern Iran. 329 334 2017/10/12017/10/12017/10/12017/10/12017/10/12017/10/1 1396/7/9 2017/10/142017/10/142017/10/142017/10/142017/10/142017/10/14 1396/7/22 نادیا عرب خزائلی Nadia Arabkhazaeli Department of Genetic, Faculty of Science, Damghan Branch, Islamic Azad University, Damghan, Iran ایران کسری قناعت Kasra Ghanaat Department of Clinical Biochemistry and Genetics, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran ایران محمد باقر هاشمی- سوته Mohammad Bagher Hashemi-Soteh Department of Clinical Biochemistry and Genetics, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran ایران Hashemisoteh@gmail.com Spontaneous Abortion Polymorphism (Genetics) Factor V Methylene tetra hydrofolate Reductase (MTHFR). سقط مکرر پلی مورفیسم (ژنتیک) فاکتور V متیلن تتراهیدروفولات ردوکتاز (MTHFR ). Vettriselvi V, Vijayalakshmi K, Paul SFD, Venkatachalam P. ACE and MTHFR gene polymorphisms in unexplained recurrent pregnancy loss. J Obstet Gynaecol Res 2008; 34: 301-306.##Carp H, Salomon O, Seidman D, Dardik R, Rosenberg N, Inbal A. Prevalence of genetic markers for thrombophilia in recurrent pregnancy loss. Hum Reprod (Oxf Engl) 2002; 17:1633-1637.##Sarig G, Younis JS, Hoffman R, Lanir N, Blumenfeld Z, Brenner B. Thrombophilia is common in women with idiopathic pregnancy loss and is associated with late pregnancy wastage. Fertil Steril 2002; 77: 342-347.##Kovalevsky G, Gracia CR, Berlin JA. Evaluation of the association between hereditary thrombophilias and recurrent pregnancy loss: a meta-analysis. Arch Intern Med 2004; 164: 558-563.##Ford HB, Schust DJ. Recurrent pregnancy loss: etiology, diagnosis, and therapy. Rev Obstet Gynecol 2009; 2: 76-83.##Rosing J, Tans G, Govers-Riemslag JW, Zwaal RF, Hemker HC. The role of phospholipids and factor Va in the prothrombinase complex. J Biol Chem 1980; 255: 274-283.##Bertina RM, Reitsma PH, Rosendaal FR, Vandenbroucke JP. Resistance to activated protein C and factor V Leiden as risk factors for venous thrombosis. Thromb Haemost 1995; 74: 449-453.##Lunghi B, Iacoviello L, Gemmati D, Dilasio MG, Castoldi E, Pinotti M, et al. Detection of new polymorphic markers in the factor V gene: association with factor V levels in plasma. Thromb Haemost 1996; 75: 45-48.##Alhenc-Gelas M, Nicaud V, Gandrille S,Van Dreden P, Amiral J, Aubry ML, et al. The factor V gene A4070G mutation and the risk of venous thrombosis. Thromb Haemost 1999; 81: 193-197.##Castaman G, Lunghi B, Missiaglia E, Bernardi F, Rodeghiero F. Phenotypic homozygous activated protein C resistance associated with compound heterozygosity for Arg506Gln (factor V Leiden) and His1299Arg substitutions in factor V. Br J Haematol 1997; 99: 257-261.##Jacques PF, Bostom AG, Williams RR, Ellison RC, Eckfeldt JH, Rosenberg IH, et al. Relation between folate status, a common mutation in methylenetetrahydrofolate reductase, and plasma homocysteine concentrations. Circulation 1996; 93: 7-9.##Frosst P, Blom HJ, Milos R, Goyette P, Sheppard CA, Matthews RG,et al. A candidate genetic risk factor for vascular disease: a common mutation in methylenetetrahydrofolate reductase. Nat Genet 1995; 10: 111-113.##Li M, Lau EM, Woo J. Methylene tetra hydrofolate reductase polymorphism (MTHFR C677T) and bone mineral density in Chinese men and women. Bone 2004; 35: 1369-1374.##Zetterberg H. Methylene tetra hydro folate reductase and trans cobalamin genetic polymorphisms in human spontaneous abortion: biological and clinical implications. Reprod Biol Endocrinol 2004; 2: 7-14.##De Re V, Cannizzaro R, Canzonieri V, Cecchin E, Caggiari L, De Mattia E,et al. MTHFR polymorphisms in gastric cancer and in first-degree relatives of patients with gastric cancer. Tumor Biol 2010; 31: 23-32.##Agodi A, Barchitta M, Cipresso R, Marzagalli R, La Rosa N, Caruso M,et al. Distribution of p53, GST, and MTHFR polymorphisms and risk of cervical intraepithelial lesions in sicily. Int J Gynecol Cancer 2010; 20: 141-146.##Nakata Y, Katsuya T, Takami S, Sato N, Fu Y, Ishikawa K, et al. Methylenetetrahydrofolate reductase gene polymorphism relation to blood pressure and cerebrovascular disease. Am J Hypertens 1998; 11: 1019-1023.##Nelen WL, Blom HJ, Steegers EA, den Heijer M, Eskes TK, et al. Hyperhomocysteinemia and recurrent early pregnancy loss: a meta-analysis. Fertil Steril 2000; 74: 1196-1199.##Doggen Carine JM, Visser Marieke CH de, Vos Hans L, Bertina RM, Cats VM, Rosendaal FR, et al. The HR2 haplotype of factor V Is not associated with the risk of myocardial infarction. Thromb Haemost 2000; 84: 815-818.##Wu X, Zeng Z, Chen B, Yu J, Xue L, Hao Y,et al. Association between polymorphisms in interleukin‐17A and interleukin‐17F genes and risks of gastric cancer. Int J Cancer 2010; 127: 86-92.##Naomi Q. Hanson, Ömer Aras, Tsai MY.C677T and A1298C polymorphisms of the Methylene tetra hydro folate reductase Gene: Incidence and effect of combined genotypes on plasma fasting and post-methionine load homocysteine in vascular disease. Clin Chem 2001; 47: 661-666.##Preston F, Rosendaal F, Walker I, Briët E, Berntorp E, Conard J, et al. Increased fetal loss in women with heritable thrombophilia. Lancet 1996; 348: 913-916.##Rai R, Shlebak A, Cohen H, Backos M, Holmes Z, Marriott K, et al. Factor V Leiden and acquired activated protein C resistance among 1000 women with recurrent miscarriage. Hum Reprod 2001; 16: 961-965.##Nowak-Göttl U, Sonntag B, Junker R, Cirkel U, von Eckardstein A. Evaluation of lipoprotein (a) and genetic prothrombotic risk factors in patients with recurrent foetal loss. Thromb Haemost 2000; 83: 350-351.##Zammiti W, Mtiraoui N, Mercier E, Abboud N, Saidi S, Mahjoub T, et al. Association of factor V gene polymorphisms (Leiden; Cambridge; Hong Kong and HR2 haplotype) with recurrent idiopathic pregnancy loss in Tunisia. A case-control study. Thromb Haemost 2009; 95: 612-617.##Goodman CS, Coulam CB, Jeyendran RS, Acosta VA, Roussev R. Which thrombophilic gene mutations are risk factors for recurrent pregnancy loss? Am J Reprod Immunol 2006; 56: 230-236.##Coulam CB, Jeyendran RS, Fishel LA, Roussev R. Multiple thrombophilic gene mutations rather than specific gene mutations are risk factors for recurrent miscarriage. Am J Reprod Immunol 2006; 55: 360-368.##Soltanpour MS, Soheili Z, Pourfathollah AA, Samiei Sh, Meshkani R, Kiani AA, et al. The A1298C mutation in methylenetetrahydrofolate reductase gene and its association with idiopathic venous thrombosis in an iranian population. Lab Med 2011; 42: 213-216.##Neagoş D, CreŃu R, Sfetea RC, Mierla D, Bohiltea LC. Investigation of the relationship between the risk of spontaneous abortion and C677T and A1298C polymorphisms of the methylenetetrahydrofolate reductase gene. Revista Română de Medicină de Laborator 2012; 20: 335-343. (In Romanian)##Rodríguez-Guillén MdR, Torres-Sánchez L, Chen J, Galván-Portillo M, Blanco-Mu-oz J, Anaya MA, et al. Maternal MTHFR polymorphisms and risk of spontaneous abortion. Salud pública Méx 2009; 51: 19-25.##Spiroski I, Kedev S, Antov S, Krstevska M, Dzhekova-Stojkova S, Bosilkova G, et al. Methylenetetrahydrofolate reductase (MTHFR-677 and MTHFR-1298) genotypes and haplotypes and plasma homocysteine levels in patients with occlusive artery disease and deep venous thrombosis. Acta Biochim Pol 2008; 55: 587- 594.##Freitas AI, Mendonça I, Guerra G, Brión M, Reis RP, Carracedo A, et al. Methylenetetrahydrofolate reductase gene, homocysteine and coronary artery disease: the A1298C polymorphism does matter. Inferences from a case study (Madeira, Portugal). Thromb Res 2008; 122: 648-656.##Bakker R, Brandjes D. Hyperhomocysteinaemia and associated disease. Pharm World Sci 1997; 19: 126-132.##Wang X, Lin Q, Ma Z, Zhao AM. [C677T and A1298C mutation of the methylenetetrahydrofolate reductase gene in unexplained recurrent spontaneous abortion]. Zhonghua Fu Chan Ke Za Zhi 2004; 39: 238-241. (In Chinese)##Mtiraoui N, Zammiti W, Ghazouani L, Braham NJ, Saidi S, Finan RR, et al. Methylenetetrahydrofolate reductase C677T and A1298C polymorphism and changes in homocysteine concentrations in women with idiopathic recurrent pregnancy losses. Reproduction 2006; 131: 395-401.##Hohlagschwandtner M, Unfried G, Heinze G, Huber JC, Nagele F, Tempfer C. Combined thrombophilic polymorphisms in women with idiopathic recurrent miscarriage. Fertil Steril 2003; 79: 1141-1148.##Khaleghparast A, Morovvati S, Noormohammadi Z. Evaluation of the association between the C677T and A1298C polymorphisms of MTHFR gene and recurrent miscarriage. Sci J Iran Blood Transfus org 2011; 8: 88-95.##PoursadeghZonouzi A, Chaparzadeh N, Asghari Estiar M, Mehrzad Sadaghiani M, Farzadi L, Ghasemzadeh A, et al. Methylene tetra hydro folate reductase C677T and A1298Cmutations in women with recurrent spontaneous abortions in the northwest of Iran. ISRN Obstet Gynecol 2012; 2012: 1-6.## ##

Low birth weight may increase body fat mass in adult women with polycystic ovarian syndrome وزن کم هنگام تولد عاملی برای افزایش توده چربی بدن در زنان بزرگسال مبتلا به سندرم تخمدان پلی کیستیک 2 1 مقدمه: زنان مبتلا به سندرم تخمدان پلی­کیستیک (PCOS)، به عنوان شایع­ترین اختلال اندوکرین زنان، فرم ویژه ای از تجمع چربی در بدن را دارا هستند. وزن هنگام تولد یکی از علل تأثیرگذار در این رابطه است. هدف: این مطالعه با هدف بررسی ارتباط میان وزن هنگام تولد و حجم توده چربی/ عضلانی بدن (BFM و BLM) در زنان مبتلا به PCOS و مقایسه آن با افراد شاهد غیرمبتلا که از نظر سن و شاخص توده بدنی همسان سازی شده بودند انجام شد. مواد و روش­ها: مجموعأ 70 زن سنین باروری با تشخیص PCOS، به همراه 70 زن که در بررسی سونوگرافیک فاقد تخمدان پلی­کیستیک و فاقد هیرسوتیسم و اختلال عملکرد تخمدان بودند، وارد مطالعه شدند. تفاوت بین گروه­ها با آزمون تی مستقل و ارتباط بین متغیرها از طریق آزمون ANCOVA آنالیز شد. نتایج: شیوع وزن کم هنگام تولد در زنان مبتلا به PCOS نسبت به گروه شاهد بالاتر بود ( 3/19 در مقابل 7/15). همچنین، این مطالعه نشان داد که حجم توده چربی و عضلانی بدن، در زنان مبتلا به PCOS که هنگام تولد کم وزن متولد شده بودند، در مقایسه با زنان سالم بیشتر بود ( به ترتیب، 05/9±8/19 در مقابل 5/4±9/12، 001/0=p و 9/6±9/48 در مقابل 8/5±2/43، 004/0=p). نتیجه­ گیری: بافت چربی دوران جنینی و وزن هنگام تولد در بروز چاقی، حجم توده چربی و عضلانی بدن در بزرگسالی تأثیر دارد که البته میزان تأثیر در بین زنان مبتلا و غیر مبتلا به PCOS متفاوت می باشد. 2 Background: Women engaged with polycystic ovarian syndrome (PCOS), as the commonest endocrine disorder, are known to have a specific type of adiposity. Birth weight is among different contributors reported to be responsible for this diversity. Objective: We aimed to compare the relation between birth weight and body fat mass (BFM)/ body lean mass (BLM) in PCOS and their age and body mass index (BMI) matched normal controls. Materials and Methods: In this case-control study, a total number of 70 reproductive aged women, diagnosed with PCOS and 70 age- BMI matched healthy women without hirsutism and/or ovulatory dysfunction were recruited., control group had no polycystic ovaries in ultrasonographic scans. A detailed history of birth weight was taken and was divided into the following categories: <2,500 (low birth weight, LBW) and 2,500-4,000 (normal birth weight; NBW). Results: Results showed that LBW prevalence was higher in women with PCOS than in controls (19.3% (27) vs. 15.7% (22)). Also body fat and lean mass (BFM, BLM) have increased in adult women with PCOS who were born underweight compared to their normal (19.8±9.05 vs. 12.9±4.5, p=0.001 and 48.9±6.9 vs. 43.2±5.8, p=0.004 respectively). Conclusion: Fetal birth weight influences on the adulthood obesity, BFM and BLM. This impact is different among women with and without PCOS. 335 340 2017/10/12017/10/12017/10/12017/10/12017/10/12017/10/12017/10/1 1396/7/9 2017/10/142017/10/142017/10/142017/10/142017/10/142017/10/142017/10/14 1396/7/22 سونیا مینویی Sonia Minooee Reproductive Endocrinology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran ایران فهیمه رمضانی تهرانی Fahimeh Ramezani Tehrani Reproductive Endocrinology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran ایران ramezani@endocrine.ac.ir پروین میرمیران Parvin Mirmiran Obesity Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran ایران فریدون عزیزی Fereidoun Azizi Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran ایران Body fat mass Body lean mass Birth weight Poly cystic ovarian syndrome حجم توده چربی حجم توده عضلانی وزن هنگام تولد سندرم تخمدان پلی کیستیک. Franks S, McCarthy MI, Hardy K. Development of polycystic ovary syndrome: involvement of genetic and environmental factors. Int J Androl 2006; 29: 278-285.##Abbott DH, Barnett DK, Bruns CM, Dumesic DA. Androgen excess fetal programming of female reproduction: a developmental aetiology for polycystic ovary syndrome? Hum Reprod Update 2005; 11: 357-374.##Carmina E, Bucchieri S, Esposito A, Del Puente A, Mansueto P, Orio F, et al. Abdominal fat quantity and distribution in women with polycystic ovary syndrome and extent of its relation to insulin resistance. J Clin Endocrinol Metab 2007; 92: 2500-2505.##Barber TM, Golding SJ, Alvey C, Wass JA, Karpe F, Franks S, et al. Global adiposity rather than abnormal regional fat distribution characterizes women with polycystic ovary syndrome. J Clin Endocrinol Metab 2008; 93: 999-1004.##Lord J, Thomas R, Fox B, Acharya U, Wilkin T. The central issue? Visceral fat mass is a good marker of insulin resistance and metabolic disturbance in women with polycystic ovary syndrome. Br J Obstet Gynaecol 2006; 113: 1203-1209.##Borruel S, Fernandez-Duran E, Alpanes M, Marti D, Alvarez-Blasco F, Luque-Ramirez M, et al. Global adiposity and thickness of intraperitoneal and mesenteric adipose tissue depots are increased in women with polycystic ovary syndrome (PCOS). J Clin Endocrinol Metab 2013; 98: 1254-1263.##Wang ET, Calderon-Margalit R, Cedars MI, Daviglus ML, Merkin SS, Schreiner PJ, et al. Polycystic ovary syndrome and risk for long-term diabetes and dyslipidemia. Obstet Gynecol 2011; 117: 6-13.##Kim JJ, Choi YM. Dyslipidemia in women with polycystic ovary syndrome. Obstet Gynecol Sci 2013; 56: 137-142.##Zabuliene L, Tutkuviene J. [Body composition and polycystic ovary syndrome]. Medicina (Kaunas, Lithuania) 2010; 46: 142-157. (In Lithuanian)##Sarr O, Yang K, Regnault TR. In utero programming of later adiposity: the role of fetal growth restriction. Pregnancy 2012; 2012: 134758.##Binkin NJ, Yip R, Fleshood L, Trowbridge FL. Birth weight and childhood growth. Pediatr 1988; 82: 828-834.##Schroeder DG, Martorell R. Fatness and body mass index from birth to young adulthood in a rural Guatemalan population. Am J Clin Nutr 1999; 70: 137s-144s.##Hediger ML, Overpeck MD, Kuczmarski RJ, McGlynn A, Maurer KR, Davis WW. Muscularity and fatness of infants and young children born small-or large-for-gestational-age. Pediatr 1998; 102: e60.##Adair LS, Gordon-Larsen P. A Study of the Birth Weight–Obesity Relation Using a Longitudinal Cohort and Sibling and Twin Pairs. Am J Epidemiol 2010; 172: 549-557.##Kirchengast S, Huber J. Body composition characteristics and body fat distribution in lean women with polycystic ovary syndrome. Hum Reprod 2001; 16: 1255-1260.##Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertil Steril 2004; 81: 19-25.##Tehrani FR, Simbar M, Tohidi M, Hosseinpanah F, Azizi F. The prevalence of polycystic ovary syndrome in a community sample of Iranian population: Iranian PCOS prevalence study. Reprod Biol Endocrinol 2011; 9: 39.##Nijland MJ, Ford SP, Nathanielsz PW. Prenatal origins of adult disease. Curr Opin Obstet Gynecol 2008; 20: 132-138.##Remacle C, Bieswal F, Bol V, Reusens B. Developmental programming of adult obesity and cardiovascular disease in rodents by maternal nutrition imbalance. Am J Clin Nutr 2011; 94 (Suppl.): 1846S-1852S.##Barker DJ, Bull AR, Osmond C, Simmonds SJ. Fetal and placental size and risk of hypertension in adult life. Br Med J 1990; 301: 259-262.##Ibá-ez L, Ong K, Dunger DB, de Zegher F. Early development of adiposity and insulin resistance after catch-up weight gain in small-for-gestational-age children. J Clin Endocrinol Metab 2006; 91: 2153-2158.##de Zegher F, Lopez-Bermejo A, Ibanez L. Adipose tissue expandability and the early origins of PCOS. Trends Endocrinol Metab 2009; 20: 418-423.##Carmina E, Guastella E, Longo RA, Rini GB, Lobo RA. Correlates of increased lean muscle mass in women with polycystic ovary syndrome. Euro J Endocrinol 2009; 161: 583-589.##Douchi T, Oki T, Yamasaki H, Kuwahata R, Nakae M, Nagata Y. Relationship of androgens to muscle size and bone mineral density in women with polycystic ovary syndrome. Obstet Gynecol 2001; 98: 445-449.##Kirchengast S, Huber J. Body composition characteristics and body fat distribution in lean women with polycystic ovary syndrome. Hum Reprod 2001; 16: 1255-1260.##Jaiswal M, Crume T, Vehik K, Scherzinger A, Stamm E, Hamman RF, et al. Is low birth weight associated with adiposity in contemporary U.S. youth? The Exploring Perinatal Outcomes among Children (EPOCH) Study. J Dev Orig Health Dis 2012; 3: 166-1672.##Mathew V, Ayyar SV. Developmental origins of adult diseases. Indian J Endocrinol Metab 2012; 16: 532-541.##Aydin K, Cinar N, Aksoy DY, Bozdag G, Yildiz BO.Body composition in lean women with polycystic ovary syndrome: effect of ethinyl estradiol and drospirenone combination. Contraception 2013; 87: 358-362.##Zabulienė L, Urboniene J, Tutkuvienė J. Body composition of lean women with polycystic ovary syndrome. Anthropol Rev 2013; 76: 183-198.## ##

Effect of granulocyte colony stimulating factor (G-CSF) on IVF outcomes in infertile women: An RCT بررسی تأثیرفاکتور محرک کولونی گرانولوسیتی بر نتایج لقاح داخل آزمایشگاهی در زنان نابارور: یک کارآزمایی بالینی 2 1 مقدمه: علیرغم پیشرفت­هایی که درتکنیک­های کمک باروری ایجاد شده است، میزان لانه­گزینی همچنان پایین است. یکی از درمان­هایی که در مطالعات سبب افزایش میزان لانه گزینی شده است انفوزیون داخل رحمی فاکتور محرک کولونی گرانولوسیتی است. هدف: بررسی تأثیر انفوزیون داخل رحمی فاکتور محرک کولونی گرانولوسیتی بر میزان حاملگی شیمیایی و بالینی و میزان لانه­گزینی و سقط در بیماران با ضخامت اندومتر نرمال. مواد و روش­ها: این مطالعه یک کارآزمایی بالینی مطالعه تصادفی شده، موازی، کور نشده و بدون دارونما می باشد. 113 بیمار با ضخامت اندومتر نرمال که کاندید لقاح داخل ازمایشگاهی بودند وارد مطالعه شدند. بیماران با سابقه بیماری­های اندوکرین، اندومتریوز شدید، ضایعات اکتسابی یا مادرزادی رحمی و وجود کنترااندیکاسیون برای فاکتور محرک کلونی گرانولوسیتی (بیماری کلیه، کم خونی داسی وبدخیمی) از مطالعه خارج شدند. بیماران پس از دادن رضایت نامه اگاهانه، به صورت تصادفی به یکی از دو گروه کنترل و مداخله وارد شدند. در گروه مداخله 55 بیماردر روز تخمک کشی 300 میکرو گرم فاکتور محرک کولونی گرانولوسیتی از طریق سرویکس به داخل حفره رحمی تزریق شد. گروه کنترل تحت لقاح ازمایشگاهی و انتقال جنین به روش معمول قرار گرفتند. متغیر پیامد اصلی: میزان حاملگی شیمیایی، حاملگی بالینی، میزان لانه گزینی و سقط. نتایج: تعداد اووسیت­های بالغ و کل اووسیت­های بدست آمده، تعداد دو پرونوکلئوس­ها، تعداد کل جنین­ها، جنین­های منتقل شده و کیفیت جنین­های انتقال داده شده و میزان باروری در بید دو گروه اختلاف معنی­داری نداشت. همچنین میزان حاملگی شیمیایی، کلینیکی، لانه گزینی، میزان باروری و سقط در بین گروه­ها اختلاف آماری معنادار نداشت. نتیجه گیری: نتایج ما نشان دادند که در بیماران نرمال کاندید لقاح داخل ازمایشگاهی که ضخامت اندومتر نرمال دارند، تزریق داخل رحمی فاکتور محرک کولونی گرانولوسیتی تأثیر مثبتی بر پیامدهای درمان ندارد. 2 Background: Despite major advances in assisted reproductive techniques, the implantation rates remain relatively low. Some studies have demonstrated that intrauterine infusion of granulocyte colony stimulating factor (G-CSF) improves implantation in infertile women. Objective: To assess the G-CSF effects on IVF outcomes in women with normal endometrial thickness. Materials and methods : In this randomized controlled clinical trial, 100 infertile women with normal endometrial thickness who were candidate for IVF were evaluated in two groups. Exclusion criteria were positive history of repeated implantation failure (RIF), endocrine disorders, severe endometriosis, congenital or acquired uterine anomaly and contraindication for G-CSF (renal disease, sickle cell disease, or malignancy). In G-CSF group (n=50), 300 µg trans cervical intrauterine of G-CSF was administered at the oocyte retrieval day. Controls (n=50) were treated with standard protocol. Chemical, clinical and ongoing pregnancy rates, implantation rate, and miscarriage rate were compared between groups. Results: Number of total and mature oocytes (MII), two pronuclei (2PN), total embryos, transferred embryos, quality of transferred embryos, and fertilization rate did not differ significantly between two groups. So there were no significant differences between groups in chemical, clinical and ongoing pregnancy rate, implantation rate, and miscarriage rate Conclusion: our result showed in normal IVF patients with normal endometrial thickness, the intrauterine infusion of G-CSF did not improve pregnancy outcomes. 341 346 2017/10/12017/10/12017/10/12017/10/12017/10/12017/10/12017/10/12017/10/1 1396/7/9 2017/10/142017/10/142017/10/142017/10/142017/10/142017/10/142017/10/142017/10/14 1396/7/22 مریم افتخار Maryam Eftekhar Research and Clinical Center for Infertility, Shahid Sadoughi University of Medical Sciences, Yazd, Iran ایران ربابه حسینی سادات Robabe Hosseinisadat Research and Clinical Center for Infertility, Shahid Sadoughi University of Medical Sciences, Yazd, Iran ایران robabehosseinisadat@yahoo.com رامش برادران Ramesh Baradaran Research and Clinical Center for Infertility, Shahid Sadoughi University of Medical Sciences, Yazd, Iran ایران الهام نقشینه Elham Naghshineh Department of Obstetrics and Gynecology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran ایران G-CSF In vitro fertilization Pregnancy rates Randomized controlled trial فاکتور محرک کولونی گرانولوسیتی لقاح داخل ازمایشگاهی میزان حاملگی مطالعه تصادفی کنترل شده. Gardner DK, Weissman A, Howles CM, Shoham Z, editors. Textbook of Assisted Reproductive Techniques. 4th Ed. Clinical Perspectives. CRC press; 2012.##Zenclussen AC, Hämmerling GJ. Cellular regulation of the uterine microenvironment that enables embryo implantation. Frontiers in immunology 2015; 6: 321.##Kunicki M, Łukaszuk K, Woclawek-Potocka I, Liss J, Kulwikowska P, Szczyptańska J. Evaluation of granulocyte colony-stimulating factor effects on treatment-resistant thin endometrium in women undergoing in vitro fertilization. BioMed Res Int 2014; 2014: 913235.##Psychoyos A. Uterine receptivity for nidationa. Ann N Y Acad Sci 1986; 476: 36-42.##Sharkey A. Cytokines and implantation. Rev Reprod 1998; 3: 52-61.##Eftekhar M, Sayadi M, Arabjahvani F. Transvaginal perfusion of G-CSF for infertile women with thin endometrium in frozen ET program: A non-randomized clinical trial. Iran J Reprod Med 2014; 12: 661.##Barad DH, Yu Y, Kushnir VA, Shohat-Tal A, Lazzaroni E, Lee HJ, et al. A randomized clinical trial of endometrial perfusion with granulocyte colony-stimulating factor in in vitro fertilization cycles: impact on endometrial thickness and clinical pregnancy rates. Fertil Steril 2014; 101:710-715.##Santjohanser C, Knieper C, Franz C, Hirv K, Meri O, Schleyer M, et al. Granulocyte-colony stimulating factor as treatment option in patients with recurrent miscarriage. Arch Immunol Ther Exp (Warsz) 2013; 61: 159-164.##Scarpellini F, Sbracia M. G-CSF treatment improves IVF outcome in women with recurrent implantation failure in IVF. J Reprod Immunol 2012; 94: 103.##Würfel W. Treatment with granulocyte colony-stimulating factor in patients with repetitive implantation failures and/or recurrent spontaneous abortions. J Reprod Immunol 2015; 108: 123-135.##Zeyneloglu HB, Onalan G, Durak T, Alyazici I, Unal E. Granulocyte macrophage colony stimulating factor (G-CSF) administration for art patients with repeated implantation failure (RIF): which route is best? Fertil Steril 2013; 100: 291-292.##Gleicher N, Vidali A, Barad DH. Successful treatment of unresponsive thin endometrium. Fertil Steril 2011; 95: 2123.##Tehraninejad E, Tanha FD, Asadi E, Kamali K, Aziminikoo E, Rezayof E. G-CSF Intrauterine for Thin Endometrium, and Pregnancy Outcome. J Fam Reprod Health 2015; 9: 107.##Lai Q, Zhang H, Zhu G, Li Y, Jin L, He L, et al. Comparison of the GnRH agonist and antagonist protocol on the same patients in assisted reproduction during controlled ovarian stimulation cycles. Int J Clin Exp Pathol 2013; 6: 1903-1910.##Lucena E, Moreno-Ortiz H. Granulocyte colony-stimulating factor (G-CSF): a mediator in endometrial receptivity for a patient with polycystic ovary (PCO) undergoing in vitro maturation (IVM). BMJ Case Reports 2013; 2013: bcr2012008115.##Li Y, Pan P, Chen X, Li L, Li Y, Yang D. Granulocyte colony-stimulating factor administration for infertile women with thin endometrium in frozen embryo transfer program. Reprod Sci 2014; 21: 381-385.##Edgell TA, Rombauts LJ, Salamonsen LA. Assessing receptivity in the endometrium: the need for a rapid, non-invasive test. Reprod Biomed Online 2013; 27: 486-496.##Momeni M, Rahbar MH, Kovanci E. A meta-analysis of the relationship between endometrial thickness and outcome of in vitro fertilization cycles. J Hum Reprod Sci 2011; 4: 130.##Garrido-Gómez T, Ruiz-Alonso M, Blesa D, Diaz-Gimeno P, Vilella F, Simón C. Profiling the gene signature of endometrial receptivity: clinical results.Fertil Steril 2013; 99:1078-1085.##Vilella F, Ramirez LB, Simón C. Lipidomics as an emerging tool to predict endometrial receptivity. Fertil Steril 2013; 99: 1100-1106.## ##

Association between electromagnetic field exposure and abortion in pregnant women living in Tehran ارتباط بین قرار گرفتن در معرض میدان الکترومغناطیسی و سقط جنین در زنان باردار شهر تهران 2 1 مقدمه: کیفیت مرتبط با سلامت زندگی که متأثر از تشعشع امواج EMF بر زندگی هر فرد می­باشد جزو مسائل بسیار بحث برانگیز می­باشد. شواهد مربوط به تأثیرات مضر آن بر روی پیامدهای بارداری در این مقاله مورد بحث قرار گرفته است. هدف: هدف از انجام مطالعه، بررسی میدان الکترومغناطیس و ارتباط آن با سقط جنین در میان زنان تهران بود. مواد و روش­ها: مطالعه طولی بر روی 462 زن باردار با سن حاملگی 12> ساکن شهر تهران با وضعیت اجتماعی و فرهنگی مشابه انجام شد. زنان توسط افراد مصاحبه­گر به صورت چهره به چهره برای جمع آوری اطلاعات در مورد ویژگی­های دموگرافیک، باروری و سابقه پزشکی و هم چنین عوامل خطر سقط جنین مورد مصاحبه قرار گرفتند. پیامدهای بارداری مقاله پژوهش ( سقط خودبخودی) با استفاده از پرونده های زایمانی آنها از بیمارستانی که به آن مراجعه کرده بودند برای همه شرکت کنندگان بدست آمد. امواج الکترومغناطیس توسط دستگاه اندازه گیری ناردا ساخت آلمان (SRM3000) با تاریخ کالیبراسیون معتبر از درب منازل افراد اندازه گیری شد. برای تجزیه و تحلیل داده ها از آزمون t، کای دو و رگرسیون لجستیک استفاده شد. نتایج: ارتباط معنی­دار بین شانس خطر سقط جنین و میزان امواج الکترومغناطیس پیدا شد. نتیجه ­گیری: یافته های این مطالعه نمی تواند شواهد منسجمی ارائه کند که تشعشعات امواج الکترومغناطیس ممکن است با خطر سقط جنین مرتبط باشد که می­تواند به دلیل حجم کوچک نمونه مورد مطالعه باشد. 2 Background: Health-related quality of life is affected by electromagnetic field exposure in each person everyday life. However, this is extremely controversial issue. Objective: Investigation of the associations between electromagnetic field exposure and miscarriage among women of Tehran. Materials and Methods: In this longitudinal study, 462 pregnant women with gestational age <12 wks from seven main regions of Tehran city in Iran with similar social and cultural status were participated. Women were interviewed face-to face to collect data. Reproductive information was collected using medical file recorded in those hospitals the subjects had delivery. The measuring device measured electromagnetic waves, Narda safety test solutions with valid calibration date at the entrance door of their houses. Results: A significant likelihood of miscarriage in women who exposed to significant level of electromagnetic wave. However, this association was not confirmed by Wald test. Conclusion: This study may not provide strong or consistent evidence that electromagnetic field exposure is associated or cause miscarriage. This issue may be due to small sample size in this study.   347 354 2017/10/12017/10/12017/10/12017/10/12017/10/12017/10/12017/10/12017/10/12017/10/5 1396/7/13 2017/10/142017/10/142017/10/142017/10/142017/10/142017/10/142017/10/142017/10/142017/10/5 1396/7/13 معصومه آباد Masoumeh Abad Department of Reproductive Health, School of Nursing and Midwifery, Shahid Beheshti University of Medical Sciences, Tehran, Iran ایران حسین ملک افضلی Hossein Malekafzali Department of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran ایران malek179@gmail.com معصومه سیمبر Masoumeh Simbar Department of TReproductive Health, Shahid Beheshti University of Medical Sciences, Tehran, Iran ایران حسن سید موسوی Hassan Seyed Mosaavi Department of Telecommunications engineering, Islamic Azad University, Garmsar Branch, Garmsar, Iran ایران عفت مرقاتی خویی Effat Merghati Khoei Department of Sexual Health Promotion, Iranian National Center for Addiction Studies (INCAS), Risk Behavior Reduction Institute, Tehran, Iran. ایران Electromagnetic field Pregnancy Abortion. امواج الکترومغناطیس حاملگی سقط جنین آنتن های BTS The World Bank Group, 2012. Retrived, 2015. Available at: 70Twww.worldbank.org70T.##70TSandström M70T, 70TWilen J70T, 70TOftedal G70T, 70THansson Mild K70T. Mobile Phone use and Subjective Symptoms. Comparison of Symptoms Experienced by Users of Analogue and Digital Mobile Phones. Occup Med 2001; 51: 25-35.##Teepen JC, Dijck JA van. Impact of High Electromagnetic Field Levels on Childhood Leukemia Incidence. J Cancer 2012; 131: 769-778.##Regan L, Rai R. Epidemiology and the medical causes of miscarriage. Baillieres Best Pract Res Clin Obstet Gynaecol 2000; 14: 839-854.##García-Enguídanos A, Calle ME, Valero J, Luna S, Domínguez-Rojas V. Dominguez-Rojas V. Risk Factors in Miscarriage: A Review. Eur J Obstet Gynecol Reprod Biol 2002; 102: 111-119.##Fan X, Wang W, Liu R, Dang S, Kang Y. Epidemiological features and risk factors of spontaneous abortion among rural Tibetan women at childbearing age. Zhonghua Liu Xing Bing Xue Za Zhi 2014; 35: 401-405.##Andersen AM, Andersen PK, Olsen J, Grønbæk M, Strandberg-Larsen K. moderate alcohol intake during pregnancy and risk of fetal Death. Int J Epidemiol 2012; 41: 405-413.##Röösli M, Hug K. Wireless communication fields and non-specific symptoms of ill health: a literature review. Wien Med Wochenschr 2011; 161: 240-250.##Auger N, Joseph D, Goneau M, Daniel M. The relationship between residential proximity to extremely low frequency power transmission lines and adverse birth outcomes. J Epidemiol Community Health 2011; 65: 83-85.##Windham GC, Fenster L, Swan SH, Neutra RR. Use of video display terminals during pregnancy and the risk of spontaneous abortion, low birthweight, or intrauterine growth retardation. Am J Ind Med 1990; 18: 675-688.##Juutilainen J, Matilainen P, Saarikoski S, Laara E, Suonio S. Early pregnancy loss and expo-sure to 50-Hz magnetic fields. Bioelectromagnetics 1993; 14: 229-236.##Lindbohm ML, Hietanen M, Kyyronen P, Sallmén M, von Nandelstadh P, Taskinen H, et al. Magnetic fields of video display terminals and spontaneous abortion. Am J Epidemiol 1992; 136: 1041-1051.##Shamsi Mahmoudabadi F, Ziaei S, Firoozabadi M, Kazemnejad A. Exposure to extremely low frequency electromagnetic fields during pregnancy and the risk of spontaneous abortion: a case-control study. J Res Health Sci 2013; 13: 131-134.##Han J, Cao Z, Liu X, Zhang W, Zhang S. Effect of early pregnancy electromagnetic field exposure on embryo growth ceasing. Wei Sheng Yan Jiu 2010; 39: 349-352.##Peduzzi P, Concato J, Kemper E, Holford TR, Feinstein AR. A simulation study of the number of events per variable in logistic regression analysis. J Clin Epidemiol 1996; 49: 1373-1379.##Cember H. Johnson Th. Introduction to Health Physics. 4th Ed. McGraw-Hill Medical; 2009: 722-759.##Lee GM, Neutra RR, Hirestova L, Yost M, Hiatt RA. A nested case-control study of residential and personal magnetic field measures and spontaneous abortions. Epidemiology 2002 ;13: 21-31.##Li DK, Odouli R, Wi S, Janevic T, Golditch I, Bracken TD, et al. A population-based prospective cohort study of personal exposure to magnetic fields during pregnancy and the risk of miscariage. Epidemiology 2002; 13: 9-20.##Davari-Tanha F, M. Shariat, M. Kaveh, M. Ebrahimi and S. Jalalvand. Threatened abortion: a risk factor for poor pregnancy outcome. Acta Medica Iranica 2008;46: 314-320.##Nielsen CV, Brandt LP. Fetal growth preterm birth and infant mortality in relation to work with video display terminals during pregnancy. Scand J Work Environ Health 1992; 18: 346-350.##Röösli M, Hug K. Wireless communication fields and non-specific symptoms of ill health: a literature review. Wien Med Wochenschr 2011; 161: 240-250.##Li De-Kun, Neutra, Raymond Richard. Magnetic fields and miscarriage. Epidemiology 2002; 13: 237-238.##Behjati Ardakani Z, Akhoundi MM, Sadeghi MR, Sadri Ardekani H. The necessity of a comprehensive study on abortion in Iran. J Reprod Infertil 2005; 6: 299-320.##Borbély AA, Huber R, Graf T, Fuchs B, Gallmann E, Achermann P. Pulsed high-frequency electromagnetic field affects human sleep and sleep electroencephalogram. Neurosci Lett 1999; 275: 207-210.##Patelarou E, Kelly FJ. Indoor exposure and adverse birth outcomes related to fetal growth, miscarriage and prematurity-a systematic review. Int J Environ Res Public Health 2014; 11: 5904-5933.## ##