ﭘﻴﺸﮕﻴﺮي از دورهدر واﻛﺴﻴﻨﺎﺳﻴﻮن ﻋﻠﻮمو ﻧﻘﺶ ﺳﺮوﻳﻜﺲ ،12آناﺳﻔﻨﺪ 1-8 ،1385 ، 64ﺷﻤﺎره ﭘﺰﺷﻜﻲ ﺗﻬﺮان، ﺳﺮﻃﺎنداﻧﺸﮕﺎه ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ، 1 ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ :ﻧﻘﺶ واﻛﺴﻦ HPVدر ﭘﻴﺸﮕﻴﺮي )ﻣﻘﺎﻟﻪ ﻣﺮوري( * ﻣﮋﮔﺎن ﻛﺮﻳﻤﻲ زارﭼﻲ زﻣﻴﻨﻪ و ﻫﺪف :ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ دوﻣﻴﻦ ﺳﺮﻃﺎن ﺷﺎﻳﻊ زﻧﺎن در دﻧﻴﺎ ﻣﻲﺑﺎﺷﺪ .اﻧﺠﺎم ﺑﺮﻧﺎﻣﻪﻫﺎي 50ﺳﺎﻟﻪ ﻏﺮﺑﺎﻟﮕﺮي ،در ﺑﺮﺧﻲ ﻛﺸﻮرﻫﺎ ﺗﻮاﻧﺴﺘﻪ ﺷﻴﻮع و ﺑﺮوز آن را ﺗﺎ ﺣﺪود %70ﻛﺎﻫﺶ دﻫﺪ .در ﺣﺎﻟﻴﻜﻪ در ﺑﻴﺸﺘﺮ ﮔﺮوه زﻧﺎن و ﻣﺎﻣﺎﻳﻲ ،ﺑﺨﺶ اﻧﻜﻮﻟﻮژي زﻧﺎن داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ﻧﻘﺎط ﺟﻬﺎن ،اﻳﻦ ﺳﺮﻃﺎن دوﻣﻴﻦ ﻳﺎ ﺳﻮﻣﻴﻦ ﺳﺮﻃﺎن ﺷﺎﻳﻊ زﻧﺎن ﻣﻲﺑﺎﺷﺪ .از آﻧﺠﺎﺋﻴﻜﻪ وﻳﺮوس ﭘﺎﭘﻴﻠﻮم اﻧﺴﺎﻧﻲ) (HPVﻋﺎﻣﻞ ﺷﻨﺎﺧﺘﻪ ﺷﺪه اﻳﺠﺎد ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ اﺳﺖ ،ﻣﻄﺎﻟﻌﺎت اﻧﺠﺎم ﺷﺪه در زﻣﻴﻨﻪ ﭘﻴﺸﮕﻴﺮي از آن ﻃﻲ دو دﻫﻪ اﺧﻴﺮ ،ﻣﻨﺠﺮ ﺑﻪ ﺗﻮﻟﻴﺪ واﻛﺴﻦ و ﻣﻌﺮﻓﻲ آن ﺑﻪ ﺑﺎزار در ﺳﺎل ﮔﺬﺷﺘﻪ ﺷﺪه اﺳﺖ .در اﻳﻦ ﻣﻘﺎﻟﻪ ﺳﻌﻲ ﺑﺮ آن اﺳﺖ ﻛﻪ ﻋﻮاﻣﻞ اﻳﺠﺎد ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ و ﺟﺰﺋﻴﺎت واﻛﺴﻴﻨﺎﺳﻴﻮن ﻣﻮرد ﺑﺤﺚ ﻗﺮار ﮔﻴﺮد .ﺑﻨﻈﺮ ﻣﻲرﺳﺪ در ﺻﻮرت اﺟﺮاي ﺑﺮﻧﺎﻣﻪ واﻛﺴﻴﻨﺎﺳﻴﻮن در دﺧﺘﺮان ﺟﻮان ،اﻣﻜﺎن رﻳﺸﻪﻛﻦ ﻛﺮدن ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ در ﺳﻪ دﻫﻪ آﻳﻨﺪه وﺟﻮد داﺷﺘﻪ ﺑﺎﺷﺪ. *ﻧﻮﻳــﺴﻨﺪه ﻣــﺴﺌﻮل ،ﺗﻬــﺮان ،اﻧﺘﻬــﺎي ﺑﻠــﻮار ﻛــﺸﺎورز، ﺑﻴﻤﺎرﺳﺘﺎن اﻣﺎم ﺧﻤﻴﻨﻲ ،ﺑﺨﺶ اﻧﻜﻮﻟﻮژي زﻧﺎن ﻛﻠﻤﺎت ﻛﻠﻴﺪي :ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ ،واﻛﺴﻴﻨﺎﺳﻴﻮن ،HPV ،ﭘﻴﺸﮕﻴﺮي ،ﺗﻠﻔﻦ66930666 : Email:nadbehtash@yahoo.com ﻣﻘﺪﻣﻪ ﺷﻴﻮع ،ﺑﺮوز و ﻣﺮگ و ﻣﻴﺮ ﻧﺎﺷـﻲ از آن در ﻃـﻲ 50ﺳـﺎل ﮔﺬﺷـﺘﻪ ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ دوﻣﻴﻦ ﻋﻠﺖ ﻣـﺮگ ﻧﺎﺷـﻲ از ﺳـﺮﻃﺎن در زﻧـﺎن ﻣــﻲﺑﺎﺷــﺪ .در ﺳــﺎل ،2006ﺣــﺪود 500ﻫــﺰار ﻣــﻮرد ﺟﺪﻳــﺪ ﺳــﺮﻃﺎن ﺳﺮوﻳﻜﺲ ﮔﺰارش ﺷﺪه و ﭘﻴﺶﺑﻴﻨﻲ ﻣﻲ ﺷﻮد در ﺣﺪود 280,000ﻣﺮگ ﺣﺪود %70ﻛﺎﻫﺶ ﻳﺎﻓﺘﻪ و اﻳﻦ ﻛﺎﻫﺶ در ﻛﺸﻮرﻫﺎي داراي ﺑﺮﻧﺎﻣﻪﻫـﺎي ﻏﺮﺑﺎﻟﮕﺮي و ﺑﺪﻟﻴﻞ اﻧﺠﺎم ﻣﻨﻈﻢ ﭘﺎپ اﺳﻤﻴﺮ ﻣﻲﺑﺎﺷﺪ. ﻋﻔﻮﻧﺖ : HPVﺗﺎ ﺣﺪود ﺳﺎﻟﻬﺎي ،1997ﻋﻔﻮﻧﺖ HPV ﻫﻤﺎﻧﻨﺪ ﻧﺎﺷﻲ از آن واﻗﻊ ﺧﻮاﻫﺪ ﺷﺪ .اﻛﺜﺮ اﻳﻦ ﺑﻴﻤﺎران در ﻛـﺸﻮرﻫﺎي در ﺣـﺎل ﺳﺎﻳﺮ ﻋﻔﻮﻧﺖﻫﺎي دﺳﺘﮕﺎه ﺗﻨﺎﺳﻠﻲ ﺑﻪ ﻋﻨﻮان ﻋﻮاﻣﻞ ﻣﺴﺘﻌﺪ ﻛﻨﻨﺪه ﺑﺮوز ﺗﻮﺳــﻌﻪ؛ در آﻓﺮﻳﻘــﺎ ،آﻣﺮﻳﻜــﺎي ﻣﺮﻛــﺰي و آﻣﺮﻳﻜــﺎي ﺟﻨــﻮﺑﻲ زﻧــﺪﮔﻲ ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ ﺷﻨﺎﺧﺘﻪ ﻣﻲﺷﺪ .در ﺳﺎل 2000و ﺑﻌﺪ از آن اﻳﻦ ﻣﻲﻛﻨﻨﺪ 1.اﻳﻦ ﺟﻮاﻣﻊ ﻋﻤﻮﻣﺎً ﻓﺎﻗﺪ ﺑﺮﻧﺎﻣﻪﻫﺎي ﻣﻨﻈﻢ ﻏﺮﺑـﺎﻟﮕﺮي ﻛـﺸﻮري وﻳﺮوس ﺑﻌﻨﻮان ﻋﺎﻣﻞ اﺗﻴﻮﻟﻮژﻳﻚ ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ ﻣﻌﺮﻓﻲ ﺷﺪ و در ﺗﺸﺨﻴﺺ زودرس ﺳﺮﻃﺎن ﻣﻲﺑﺎﺷﻨﺪ. ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ ﺑﻪ ﻋﻨﻮان ﺗﻨﻬﺎ ﺳﺮﻃﺎن ﺳﺎﻟﻴﺪ ﺑﺎ ﻋﻠﺖ ﻣﺸﺨﺺ وﻳﺮال ﺑﺎ وﺟﻮد ﮔﺰارﺷﺎت ﺑﻴﻦاﻟﻤﻠﻠﻲ در زﻣﻴﻨﻪﻫـﺎي ﻣﺨﺘﻠـﻒ ﻏﺮﺑـﺎﻟﮕﺮي، در زﻧﺎن ﻣﻲﺑﺎﺷﺪ .وﻳﺮوس HPVﺑﺎ ﻣﻬﺎر ) apoptosisﻣﺮگ ﺑﺮﻧﺎﻣﻪ رﻳﺰي ﺗﺸﺨﻴﺺ و درﻣﺎن ﺳﺮﻃﺎن ﺳـﺮوﻳﻜﺲ از اﻳـﺮان 2-7،ﺑـﻪ دﻟﻴـﻞ ﻧﺪاﺷـﺘﻦ ﺷﺪه ﺳﻠﻮل( و ﺗﻮﻟﻴﺪ ﭘﺮوﺗﺌﻴﻦﻫﺎي ﻣﻬﺎرﻛﻨﻨﺪه ژﻧﻬﺎي p53و ﺷﺒﻜﻪ ﺛﺒﺖ ﺳﺮﻃﺎن در ﻛـﺸﻮر ،آﻣـﺎر روﺷـﻨﻲ از ﺑـﺮوز و ﻣـﺮگ و ﻣﻴـﺮ رﺗﻴﻨﻮﺑﻼﺳﺘﻮﻣﺎ )ژنﻫﺎي ﻣﻬﺎرﻛﻨﻨﺪه رﺷﺪ ﺳﻠﻮﻟﻲ( ﻣﻮﺟﺒﺎت ﺗﻮﻟﻴﺪ ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ در دﺳﺖ ﻧﻴﺴﺖ .ﺑﺮ اﺳﺎس ﮔﺰارش ﺛﺒﺖ ﺳـﺮﻃﺎن در 3-6 ﺗﻮدهﻫﺎي ﺳﺮﻃﺎﻧﻲ ﺳﻠﻮﻟﻲ را ﻓﺮاﻫﻢ ﻣﻲﺳﺎزد. HPV ﺑﻴﺶ از 40ﮔﻮﻧﻪ از ﻛﻪ در ﻣﺨﺎط ﻧﺎﺣﻴﻪ ﺗﻨﺎﺳﻠﻲ آﻟﻮدﮔﻲ اﻳﺠﺎد ﻣﻲﻛﻨﺪ، اﻧﺴﺘﻴﺘﻮ ﻛﺎﻧﺴﺮ ،ﺷﻴﻮع ﺳﺮﻃﺎن رﺣﻢ و ﺳﺮوﻳﻜــﺲ ﺣـﺪود 6-7درﺻـﺪ وﻳﺮوس ﻫﺰار ﻣﻲﺑﺎﺷﺪ .اﻳـﻦ ﺳـﺮﻃﺎن ﻋﻤﻮﻣـﺎ در ﺳـﻨﻴﻦ 30ﺗـﺎ 55ﺳـﺎﻟﮕﻲ رخ ﺷﻨﺎﺳﺎﻳﻲ ﺷﺪه اﺳﺖ ﺗﻘﺮﻳﺒﺎ 15ﺗﺎي آﻧﻬﺎ ﺳﺮﻃﺎنزا ﻫﺴﺘﻨﺪ و ﺳﺒﺐ ﻣﻲدﻫﺪ ،اﻣﺎ اﺧﻴﺮاً در زﻧﺎن ﺟﻮان ﮔﺰارﺷﺎت ﻣﺘﻌﺪدي دﻳﺪه ﻣﻲﺷﻮد. 1 ﺳﺮﻃﺎن دﻫﺎﻧﻪ رﺣﻢ و ﺿﺎﻳﻌﺎت ﭘﻴﺶﺑﺪﺧﻴﻢ ﻣﺜﻞ CIN III ﻣﻲﺷﻮﻧﺪ. ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 64ﺷﻤﺎره ،12اﺳﻔﻨﺪ 1385 Downloaded from tumj.tums.ac.ir at 16:09 IRST on Tuesday September 22nd 2020 ﻧﺎدره ﺑﻬﺘﺎش ﭼﻜﻴﺪه ﻧﺎدزه ﺑﻬﺘﺎش و ﻫﻤﻜﺎران 2 ﺗﺎﻳﭗ 16و 18وﻳﺮوس ،HPVﺷﺎﻳﻊﺗﺮﻳﻦ ﻧﻮع ﻣﻮﺛﺮ در اﻳﺠﺎد ﺳﺮﻃﺎن HPV ﺳﺮوﻳﻜﺲ ﻫﺴﺘﻨﺪ .ﺗﺎﻳﭗ ،16در 60درﺻﺪ ﻫﻤﻪ ﺳﺮﻃﺎنﻫﺎي ﺳﺮوﻳﻜﺲ در ﻣﻄﺎﻟﻌﻪ ﺟﺪﻳﺪ دﻳﮕﺮي ،ﺷﻴﻮع ﻋﻔﻮﻧﺖ و ﻧﻮع 18در 10ﺗﺎ 20درﺻﺪ از ﻣﻮارد دﻳﺪه ﻣﻲﺷﻮد. 8-9 ﻧﻜﺘﻪ ﻣﻬﻢﺗﺮ درﺻﺪ ﺳﺮﻃﺎن آﻧﺎل 60 ،ﺗﺎ 65درﺻﺪ ﺳﺮﻃﺎنﻫﺎي واژن و 40-60 11و10 HPV در زﻧﺎن ﺟﻮاﻧﺘﺮ از 25 ﺳﺎل %36 ،در 45ﺳﺎل و ﺑﻴﺸﺘﺮ %2/8 ،اﺳﺖ .ﺷﻴﻮع ﻋﻔﻮﻧﺖ HPV ﺑﻲﻧﻬﺎﻳﺖ در زﻧﺎن ﻓﻌﺎل ﺟﻨﺴﻲ ﺑﺎﻻﺳﺖ و ﺣﺪود %64از زﻧﺎن ﺟﻮان، DNAي وﻳﺮوس HPVرا دارﻧﺪ. 13-14 از ﻓﺎﻛﺘﻮرﻫﺎي ﺧﻄﺮ ﻣﺴﺘﻘﻞ ﺷﻴﻮع ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ در ﺑﺴﻴﺎري از ﻣﻤﺎﻟﻚ دﻧﻴﺎ ﺑﺎ ﺑﺮﻧﺎﻣﻪﻫﺎي دﻳﮕﺮ در ﺑﺮوز ﺳﺮﻃﺎن دﻫﺎﻧﻪ رﺣﻢ ،ﺳﻦ ﭘﺎﺋﻴﻦ زن در اوﻟﻴﻦ ﻧﺰدﻳﻜﻲ، ﻏﺮﺑﺎﻟﮕﺮي زﻳﺮ ده درﺻﺪ ﻫﺰار ﻣﻲﺑﺎﺷﺪ .ﺑﻨﻈﺮ ﻣﻲرﺳﺪ ﻛﻪ در ﻣﻮارد HIV اﻧﺪﻛﻲ ﻋﻔﻮﻧﺖ HPVﻣﻲﺗﻮاﻧﺪ ﻣﻨﺠﺮ ﺑﻪ ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ ﺷﻮد .ﻋﻮاﻣﻞ ﻳﻚ ﻣﻮﺛﺮ در اﻳﻦ ﻣﺴﻴﺮ ﻋﺒﺎرﺗﻨﺪ از :وﺟﻮد ﺳﺎب ﺗﺎﻳﭗﻫﺎي ﭘﺮﺧﻄﺮ ﻋﻔﻮﻧﺖ درﺻﺪ ﺳﺮﻃﺎنﻫﺎي وﻟﻮ ﻧﻘﺶ دارد. ﻣﻮﻟﺘﻲ ﭘﺎرﻳﺘﻲ ،وﺟﻮد ﭼﻨﺪ ﺷﺮﻳﻚ ﺟﻨﺴﻲ ،ﺳﻴﮕﺎر و ﻋﻔﻮﻧﺖ )وﻳﺮوس ﻧﻘﺺ اﻳﻤﻨﻲ اﻧﺴﺎﻧﻲ( ﺑﻪ ﺷﻤﺎر ﻣﻲرود 10.ﻋﻔﻮﻧﺖ HPV ﺑﻴﻤﺎري ﻣﻨﺘﻘﻠﻪ از راه ارﺗﺒﺎط ﺟﻨﺴﻲ اﺳﺖ و در ﺟﻮاﻣﻌﻲ ﻛﻪ اﻓﺮاد ،HPVﻋﻔﻮﻧﺖ ﭼﻨﺪﻳﻦ ﺷﺮﻳﻚ ﺟﻨﺴﻲ دارﻧﺪ ﻣﻴﺰان آن ﺗﺎ ﺣﺪ زﻳﺎدي اﻓﺰاﻳﺶ ﻣﻲﻳﺎﺑﺪ. ﺳﺎﻟﮕﻲ ،ﻫﻤﺮاه ﺑﻮدن ﺳﺎﻳﺮ رﻳﺴﻚ ﻓﺎﻛﺘﻮرﻫﺎ ﻣﺜﻞ ﻣﻮﻟﺘﻲﭘﺎرﺗﻨﺮ ﺑﻮدن، زﻧﺎﻧﻲ ﻛﻪ دﭼﺎر ﻋﻔﻮﻧﺖ ﭘﺎﻳﺪار HPV ﻫﺴﺘﻨﺪ ،ﺑﻴﺸﺘﺮﻳﻦ اﺣﺘﻤﺎل ﭘﻴﺸﺮﻓﺖ 9و8 ﺑﻪ ﺳﻤﺖ ﺿﺎﻳﻌﺎت ﭘﻴﺶ ﺑﺪﺧﻴﻤﻲ و ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ دارﻧﺪ. ﭘﺎﻳﺪارHPV ﺑﻪ ﻣﺪت ﺑﻴﺶ از دو ﺳﺎل و ﺑﻌﺪ از 30 ﻋﻔﻮﻧﺖ ،HIVﺳﻴﮕﺎر و ﻏﻴﺮه. ﻧﻘﺶ ﻏﺮﺑﺎﻟﮕﺮي در ﭘﻴﺸﮕﻴﺮي از ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ :ﻋﻠﻲرﻏﻢ اﻳﻦ ﺳﻴﺮ اﻳﺠﺎد ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ :ﺳﺮوﻳﻜﺲ ﻋﻀﻮ ﻣﻨﺤﺼﺮ ﺑﻪ ﻓﺮدي ﻛﻪ ﺑﻴﺶ از ﻧﻴﻢ ﻗﺮن از اﻧﺠﺎم ﺗﺴﺖ ﭘﺎﭘﺎﻧﻴﻜﻮﻻﺋﻮ ) (Pap testﻣﻲﮔﺬرد، اﺳﺖ ﻛﻪ از زﻧﺪﮔﻲ ﺟﻨﻴﻨﻲ دو ﻧﻮع اﭘﻲﺗﻠﻴﻮم ﻣﺘﻔﺎوت در آن ﺑﻬﻢ ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ ﻫﻨﻮز ﻳﻚ ﻋﻠﺖ ﻣﻮرﺑﻴﺪﻳﺘﻲ واﺑﺴﺘﻪ ﺑﻪ ﺳﺮﻃﺎن و ﻣﻲرﺳﻨﺪ و در ﻣﺤﻞ ﺗﻼﻗﻲ اﻳﻦ دو ﻧﻮع اﭘﻲﺗﻠﻴﻮم اﺳﻜﻮاﻣﻮس و ﻣﺮگ و ﻣﻴﺮ زﻧﺎن در آﻣﺮﻳﻜﺎ و دﻳﮕﺮ ﻛﺸﻮرﻫﺎ ﺑﻪ ﺷﻤﺎر ﻣﻲرود .اﺟﺮاي ﮔﻼﻧﺪوﻻر وﺳﻴﻊ ، Squamo-Collumnar Junction(S-C-J) ،در ﻫﻨﮕﺎم ﺑﺮﻧﺎﻣﻪ ﻏﺮﺑﺎﻟﮕﺮي ﺑﺎ ﺳﻴﺘﻮﻟﻮژي ،ﺳﺒﺐ ﻛﺎﻫﺶ ﻗﺎﺑﻞ ﺗﻮﺟﻪ در ﺑﺮوز ﻣﺮگ ﺑﻠﻮغ ﭘﻮﺷﺶ ﺟﺪﻳﺪي از ﺑﺎﻓﺖ ﻣﺘﺎﭘﻼزﻳﻚ ﻧﺎﺑﺎﻟﻎ ﺑﺮ روي ﻣﺨﺎط و ﻣﻴﺮ ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ در ﻛﺸﻮرﻫﺎي ﭘﻴﺸﺮﻓﺘﻪ ﺷﺪه اﺳﺖ .اﻣﺎ در اﺳﺘﻮاﻧﻪاي اﻳﺠﺎد ﺷﺪه و اﻳﻦ ﻧﺎﺣﻴﻪ ﺟﺪﻳﺪ ﻧﺎﺣﻴﻪ ﺗﻐﻴﻴﺮ ﺷﻜﻞ ﻛﺸﻮرﻫﺎي در ﺣﺎل ﺗﻮﺳﻌﻪ ﻫﻨﻮز ﻋﻠﻲرﻏﻢ اﻧﺠﺎم ﺗﺴﺖ ﭘﺎپ در ﺧﻴﻠﻲ )Transformation Zoneﻳﺎ (T-Zﻧﺎم ﻣﻲﮔﻴﺮد .اﻏﻠﺐ ﺳﺮﻃﺎنﻫﺎي اﺳﻜﻮاﻣﻮس ﻛﻪ ﺷﺎﻳﻊﺗﺮﻳﻦ ﺳﺮﻃﺎنﻫﺎي ﺳﺮوﻳﻜﺲ ﻣﻲﺑﺎﺷﻨﺪ از ﻧﺎﺣﻴﻪ T-Zﻣﻨﺸﺎء ﻣﻲﮔﻴﺮﻧﺪ .ﺑﺎ ورود HPV ﺑﺎﻓﺖ اﻳﻤﭽﻮر ﻣﺘﺎﭘﻼزي در ﻧﺎﺣﻴﻪ 14 ﻣﻮارد ،ﻓﺮم ﭘﻴﺸﺮﻓﺘﻪ ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ دﻳﺪه ﻣﻲﺷﻮد. ﻫﺪف از اﻧﺠـﺎم ﻏﺮﺑـﺎﻟﮕﺮي ﺑـﺎ ﺳـﻴﺘﻮﻟﻮژي ﺳـﺮوﻳﻜﺲ ،ﺗـﺸﺨﻴﺺ ﺳﺮﻃﺎن و ﺿﺎﻳﻌﺎت ﭘﻴﺶ زﻣﻴﻨﻪ آن ﻣﻲﺑﺎﺷﺪ ،ﺑﺎ ﺗﺴﺖ ﭘﺎپ ،ﺳـﻠﻮلﻫـﺎي 15 T-Zﻣﺴﺘﻘﺮ و ﺗﺒﺪﻳﻞ ﺑﻪ ﺑﺎﻓﺖ دﻳﺴﭙﻼزﻳﻚ ﻣﻲﮔﺮدد و ﺑﺘﺪرﻳﺞ ﻻﻳﻪﻫﺎي ﺳﻄﺤﻲ و رﻳﺰشﻛﻨﻨﺪه ﺳﺮوﻳﻜﺲ ﺑﺮرﺳﻲ ﻣﻴﻜﺮوﺳﻜﻮﭘﻲ ﻣﻲﺷﻮد .اﻣـﺎ ﺑﻴﺸﺘﺮي از ﺑﺎزال ﻣﻤﺒﺮان درﮔﻴﺮ ﺗﻮده ﻧﺌﻮﭘﻼزﻳﻚ ﻣﻲﺷﻮﻧﺪ .اﻳﻦ ﻣﺮاﺣﻞ ﻋﻠﻲرﻏﻢ ﻣﻮﻓﻘﻴـﺖ ﺑﺮرﺳـﻲﻫـﺎي ﻏﺮﺑـﺎﻟﮕﺮي در ﺳـﻄﺢ وﺳـﻴﻊ ،اﻧﺠـﺎم CIN2 ﻏﺮﺑﺎﻟﮕﺮي ﺑﺎ ﺳﻴﺘﻮﻟﻮژي ارزش ﻣﺤـﺪودي دارد .ﺣـﺴﺎﺳﻴﺖ اﻳـﻦ روش ﺑﻪ ﺗﺮﺗﻴﺐ ﻧﺌﻮﭘﻼزي داﺧﻞ اﭘﻲﺗﻠﻴﺎل اﺳﻜﻮاﻣﻮس،(CIN1) 1- و CIN 3ﻣﻲﺑﺎﺷﺪCIN 3. ﻫﻤﺎن ﺳﺮﻃﺎن )Carcinoma in Situ (CIS ﻣﻲﺑﺎﺷﺪ .ﺑﻨﻈﺮ ﻣﻲرﺳﺪ از زﻣﺎن ورود ﻋﻔﻮﻧﺖ HPV ﺗﺎ ﺗﻐﻴﻴﺮات ﻣﺮﺣﻠﻪ 11و10 داﺷﺖ ﻛﻪ اﻛﺜﺮﻳﺖ ﻗﺮﻳﺐ ﺑﻪ اﺗﻔﺎق ﻣﻮارد III و CIN II ﺑﻴﻦ 30ﺗﺎ %87و اﺧﺘﺼﺎﺻﻲ ﺑﻮدن آن ﺑﻴﻦ 68ﺗﺎ %100ﻣﻲﺑﺎﺷﺪ. ﻋﻠﺖ ﻣﺘﻐﻴﺮ ﺑﻮدن ﺣﺴﺎﺳﻴﺖ و اﺧﺘﺼﺎﺻﻲ ﺑﻮدن روش ﺳﻴﺘﻮﻟﻮژي، ﺑﺎﻳﺪ ﺗﻮﺟﻪ وﺟﻮد ﺿﺎﻳﻌﺎت ﻛﻮﭼﻚ ﺳﺮوﻳﻜﺲ ،ﻧﻤﻮﻧﻪ ﻧﺎﻣﻨﺎﺳﺐ ،آﻟﻮده ﺷﺪن ﻧﻤﻮﻧﻪ و ﺣﺪود دوﺳﻮم ﻣﻮارد ﺑﺎ ﺧﻮن و ﺗﺮﺷﺤﺎت ﻣﻲﺑﺎﺷﺪ .ﺑﻪ دﻟﻴﻞ ﭘﺎﻳﻴﻦ ﺑﻮدن ﺣﺴﺎﺳﻴﺖ ﺗﺴﺖ CIS Liquid Based Cytology ﻓﻮق و ﺳﺮﻃﺎن ﻣﻬﺎﺟﻢ 10-15ﺳﺎل ﻃﻮل ﺧﻮاﻫﺪ ﻛﺸﻴﺪ. CIN1 15و14 ﭘﺴﺮﻓﺖ ﻛﺮده و ﺑﻬﺒﻮدي ﺣﺎﺻﻞ ﻣﻲﻛﻨﺪ .در ﺣﺎﻟﻴﻜﻪ 13و12 ﺷﺎﻧﺲ ﺑﺎﻻﺋﻲ ﺑﺮاي ﺗﺒﺪﻳﻞ ﺑﻪ ﺳﺮﻃﺎن ﻣﻬﺎﺟﻢ دارد. ﻋﻔﻮﻧﺖ ﭘﺎپ ،روش ﺳﻴﺘﻮﻟﻮژي ﻏﻮﻃﻪور در ﻣﺎﻳﻊ ) (LBCدر ﺑﺮﻧﺎﻣﻪﻫﺎي ﻏﺮﺑﺎﻟﮕﺮي ﺟﺎﻳﮕﺰﻳﻦ اﻳﻦ روش ﺷﺪه اﺳﺖ. 15 HPVﺑﺨﺼﻮص در ﺟﻮاﻣﻊ ﻏﺮﺑﻲ در زﻧﺎن ﺟﻮان ﺑﺴﻴﺎر ﺷﺎﻳﻊ اﺳﺖ .در ﺳﻴﺘﻮﻟﻮژي ﺑﺮ ﭘﺎﻳﻪ ﻣﺎﻳﻊ ،ﻣﻴﺰان ﺗﺸﺨﻴﺺ ﺿﺎﻳﻌﺎت ﺑﺎ درﺟﻪ ﺑﺎﻻ را آﻣﺮﻳﻜﺎ ،ﺗﺎ %70ﻧﻮﺟﻮاﻧﺎن ﻓﻌﺎل از ﻧﻈﺮ ﺟﻨﺴﻲ ،ﻋﻔﻮﻧﺖ HPVدارﻧﺪ .در اﻓﺰاﻳﺶ ﻣﻲدﻫﺪ وﻟﻲ ﻣﻤﻜﻦ اﺳﺖ ﻣﻴﺰان اﺧﺘﺼﺎﺻﻲ ﺑﻮدن آن ﺑﺮاي وﻳﺮوس ﺗﺸﺨﻴﺺ اﻳﻦ ﺿﺎﻳﻌﺎت ﻛﺎﻫﺶ ﻳﺎﺑﺪ .در ﺑﻌﻀﻲ ﻣﻄﺎﻟﻌﺎت ،ﺳﻴﺘﻮﻟﻮژي ﺑﺮ ﻳﻚ ﻣﻄﺎﻟﻌﻪ ﻧﺸﺎن داده ﺷﺪ %32زﻧﺎن 16-24ﺳﺎﻟﻪ، DNA ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 64ﺷﻤﺎره ،12اﺳﻔﻨﺪ 1385 Downloaded from tumj.tums.ac.ir at 16:09 IRST on Tuesday September 22nd 2020 اﻳﻦ اﺳﺖ ﻛﻪ HPVدر 30درﺻﺪ ﺳﺮﻃﺎنﻫﺎي اوروﻓﺎرﻧﻜﺲ 45 ،ﺗﺎ 95 را دارﻧﺪ وﻟﻲ اﻳﻦ رﻗﻢ ﺑﺮاي زﻧﺎن 45ﺳﺎﻟﻪ ﻳﺎ ﺑﻴﺸﺘﺮ %4ﻣﻲﺑﺎﺷﺪ. ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ و ﻧﻘﺶ واﻛﺴﻴﻨﺎﺳﻴﻮن در ﭘﻴﺸﮕﻴﺮي از آن Atypical Squamous Cell of ﭘﺎﻳﻪ ﻣﺎﻳﻊ ،ﺳﺒﺐ اﻓﺰاﻳﺶ ﻧﻤﻮﻧﻪﻫﺎي )Undetermined Significance (ASCUS ﺷﺪه اﺳﺖ. 14-16 روش دﻳﮕﺮ ﻛﻪ ﻣﻲﺗﻮاﻧﺪ ﭘﺎﻳﻴﻦ ﺑﻮدن ﺣﺴﺎﺳﻴﺖ ﺗﺴﺖ ﭘﺎپ را ﺗﺎ ﺣﺪي ﺟﺒﺮان ﻛﻨﺪ، ﺑﻌﻨﻮان روش ﻏﺮﺑﺎﻟﮕﺮي اوﻟﻴﻪ ﺑﻜﺎر رود .ﻣﺘﺎآﻧﺎﻟﻴﺰﻫﺎي اﻧﺠﺎم ﺷﺪه در اﻳﻦ ﻣﻮرد ﻧﺸﺎن داده اﺳﺖ ﻛﻪ ﺗﺴﺖ DNAي HPV ﺣﺴﺎسﺗﺮ از ﺳﻴﺘﻮﻟﻮژي ﻏﺮﺑﺎﻟﮕﺮي در ﻧﻮﺟﻮاﻧﺎن و ﺟﻮاﻧﺎن :ﻏﺮﺑﺎﻟﮕﺮي ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ در ﻧﻮﺟﻮاﻧﺎن ﺗﺎ ﺣﺪي ﺗﻐﻴﻴﺮ ﻳﺎﻓﺘﻪ اﺳﺖ .ﺷﻴﻮع ﻣﻮارد ﻣﺜﺒﺖ 32و31 زﻧﺎن ﺟﻮان ﺑﺎﻻﺳﺖ. HPV در در ﻳﻚ ﺑﺮرﺳﻲ ﻛﻪ در 1075زن 15ﺗﺎ 19 ﺳﺎﻟﻪ اﻧﺠﺎم ﺷﺪ ،ﻃﻲ ﻣﺪت ﭘﻨﺞ ﺳﺎل %60ﻣﻮارد ﻋﻠﻲرﻏﻢ ﻣﻴﺰان ﺑﺮوز ﺑﺎﻻي ﻋﻔﻮﻧﺖ HPV ﻋﻔﻮﻧﺖﻫﺎ ﮔﺬرا ﺑﻮده و ﺑﺎ ﺿﺎﻳﻌﺎت HPV 33 ﻣﺜﺒﺖ ﺑﻮدﻧﺪ. در اﻳﻦ ﮔﺮوه ﺳﻨﻲ ،اﻛﺜﺮ Low Grade Squamous اﺳﺖ اﻣﺎ ﻛﻤﺘﺮ اﺧﺘﺼﺎﺻﻲ ﻣﻲﺑﺎﺷﺪ .ﻣﺘﻮﺳﻂ ﺣﺴﺎﺳﻴﺖ ﺗﺸﺨﻴﺺ ) Intraepithelial Lesion (LG-SILﻫﻤﺮاه ﻫﺴﺘﻨﺪ ،ﺑﻪ ﻫﺮ ﺣﺎل ﺑﺮوز ﺑﻴﻤﺎريﻫﺎي ﺑﺎ درﺟﻪ ﺑﺎﻻ ﺑﺎ ﺗﺴﺖ %85 ،HPVﺑﻮده وﻟﻲ %84اﺧﺘﺼﺎﺻﻲ اﺧﺘﻼﻻت ﺳﻴﺘﻮﻟﻮژي در زﻧﺎن ﺟﻮان ،در ﺣﺎل اﻓﺰاﻳﺶ اﺳﺖ .در ﭼﻨﺪﻳﻦ اﺳﺖ در ﺣﺎﻟﻲ ﻛﻪ ﺳﻴﺘﻮﻟﻮژي ،ﺣﺴﺎﺳﻴﺖ %60و اﺧﺘﺼﺎﺻﻴﺖ %95 ﺑﺮرﺳﻲ ،ﻣﻴﺰان Atypical Squamous Cell Undetermined Significant دارد. 17-18 اﻳﻦ ﻧﺘﺎﻳﺞ در ﺳﻨﻴﻦ ﺑﺎﻻي 30ﺳﺎل ﺑﻬﺘﺮ ﻣﻲﺷﻮد .ﻃﺒﻖ ﺗﻮﺻﻴﻪﻫﺎي اﻧﺠﻤﻦ زﻧﺎن و ﻣﺎﻣﺎﻳﻲ و اﻧﺠﻤﻦ ﺳﺮﻃﺎن زﻧﺎن آﻣﺮﻳﻜﺎ، آزﻣﺎﻳﺶ HPV ﺑﻪ ﻫﻤﺮاه ﺗﺴﺖ ﺳﻴﺘﻮﻟﻮژي ﺳﺮوﻳﻜﺲ ﻣﻲﺗﻮاﻧﺪ ﺑﻪ ﻋﻨﻮان ) (ASCUSو LSIL در ﻧﻮﺟﻮاﻧﺎن و ﺟﻮاﻧﺎن ﺑﻪ ﺗﺮﺗﻴﺐ ﺣﺪود %7-16و High %3-13ﮔﺰارش ﺷﺪه اﺳﺖ ،در ﺣﺎﻟﻴﻜﻪ اﻳﻦ ﻣﻴﺰان ﺑﺮاي ﺿﺎﻳﻌﺎت )(HG-SIL Grade Squamous Intraepithelial Lesionﺣﺪود 0/2ﺗﺎ 34-38 روش ﻏﺮﺑﺎﻟﮕﺮي ﺑﻪ ﻛﺎر رود وﻟﻲ در زﻧﺎن 30ﺳﺎل و ﺑﻴﺸﺘﺮ ،اﮔﺮ اﻳﻦ دو %3ﻣﻲﺑﺎﺷﺪ ﺗﺴﺖ ﻣﻨﻔﻲ ﺑﺎﺷﻨﺪ ،ﻣﻲﺗﻮان ﻓﺎﺻﻠﻪ ﻏﺮﺑﺎﻟﮕﺮي را ﺑﻪ ﻫﺮ ﺳﻪ ﺳﺎل اﻓﺰاﻳﺶ ﺳﻨﻲ ﻧﺎدر اﺳﺖ .ﻟﺬا ﺑﻪ واﺳﻄﻪ ﺧﻄﺮات درﻣﺎن دﻳﺴﭙﻼزي و زﻳﺮا ﺣﺴﺎﺳﻴﺖ اﻳﻦ ﺗﺴﺖﻫﺎ ﺑﺎﻻ و ارزش ﺗﺸﺨﻴﺺ آﻧﻬﺎ ﻗﺎﺑﻞ ﻧﻤﻮﻧﻪﺑﺮداريﻫﺎي ﺗﻬﺎﺟﻤﻲ ) ،(Excisionalﺗﻮﺻﻴﻪ ﻣﻲﺷﻮد ﻛﻪ اﻳﻦ ﻗﺒﻮل اﺳﺖ ﺑﻪ ﺧﺼﻮص اﮔﺮ ﺑﻴﻤﺎر ﻋﻼﻣﺖ دار ﺑﺎﺷﺪ .اﮔﺮ ﺳﻴﺘﻮﻟﻮژي اﻗﺪاﻣﺎت ﺑﺮ اﺳﺎس ﺗﺎرﻳﺨﭽﻪ واﻗﻌﻲ دﻳﺴﭙﻼزي ﺳﺮوﻳﻜﺲ و ﺑﺎ اﺣﺘﻴﺎط داد، 19-24 ﻓﺮدي ﻧﺮﻣﺎل ﺑﻮده ،وﻟﻲ از ﻧﻈﺮ DNAي وﻳﺮوس ) HPVﻓﺮم ﺳﺮﻃﺎنزاي و ﺑﺮوز ﺳﺮﻃﺎنﻫﺎي ﻣﻬﺎﺟﻢ ﺳﺮوﻳﻜﺲ در اﻳﻦ ﮔﺮوه در اﻳﻦ ﺳﻨﻴﻦ اﻧﺠﺎم ﺷﻮد. 38-41 آن( ﻣﺜﺒﺖ ﺑﺎﺷﺪ ،ﺑﺎﻳﺪ ﻣﺠﺪدا ﻏﺮﺑﺎﻟﮕﺮي ﺷﻮد .اﮔﺮﭼﻪ ﺑﺮﻧﺎﻣﻪ ﻏﺮﺑﺎﻟﮕﺮي ﭘﺮوﻓﻴﻼﻛﺴﻲ ﺑﺎ واﻛﺴﻦ ﺣﺎوي ذرات ﺷﺒﻪ وﻳﺮوس :HPV ﺟﻤﻌﻲ ﺑﻪ ﻃﻮر واﺿﺢ در ﻛﺎﻫﺶ ﻣﺮگ و ﻣﻴﺮ ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ ﻧﻘﺶ واﻛﺴﻴﻨﺎﺳﻴﻮن ﻳﻚ روش ﻣﻘﺮون ﺑﻪ ﺻﺮﻓﻪ ﺑﺮاي ﺟﻠﻮﮔﻴﺮي از ﺑﻴﻤﺎري و ﺑﻪ ﺳﺰاﻳﻲ دارد اﻣﺎ اﻳﻦ ﺳﺮﻃﺎن در ﻛﺸﻮرﻫﺎي ﺟﻬﺎن ﺳﻮم ﻫﻤﭽﻨﺎن رخ از ﺟﻤﻠﻪ ﻋﻮاﻣﻞ ﻣﻴﻜﺮوﺑﻴﺎل اﺳﺖ .از اﻫﺪاف اﺻﻠﻲ اراﺋﻪ واﻛﺴﻦ ،HPV ﻣﻲدﻫﺪ و اﻛﺜﺮ زﻧﺎن ﻛﻪ ﺑﻪ ﺳﻤﺖ ﺳﺮﻃﺎن ﭘﻴﺸﺮﻓﺘﻪ ﺳﺮوﻳﻜﺲ ﭘﻴﺶ ﻛﺎﻫﺶ ﺑﺮوز ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ و ﺿﺎﻳﻌﺎت ﭘﻴﺶزﻣﻴﻨﻪ آن ﻣﻲﺑﺎﺷﺪ. ﻣﻲروﻧﺪ ﻫﺮﮔﺰ ﻏﺮﺑﺎﻟﮕﺮي ﻧﺸﺪه اﻧﺪ ﻳﺎ ﻏﺮﺑﺎﻟﮕﺮي ﻧﺎﻣﻨﺎﺳﺐ داﺷﺘﻪاﻧﺪ. اﻫﻤﻴﺖ ﻏﺮﺑﺎﻟﮕﺮي در اﻳﻦ اﺳﺖ ﻛﻪ ﭘﺲ از ﺷﻨﺎﺳﺎﺋﻲ ﭘﺎپ اﺳﻤﻴﺮﻫﺎي ﻏﻴﺮﻃﺒﻴﻌﻲ ،ﺑﻴﻤﺎر ﺟﻬﺖ ﻛﻮﻟﭙﻮﺳﻜﻮﭘﻲ ﺑﻴﻮﭘﺴﻲ ارﺟﺎع داده ﺧﻮاﻫﺪ ﺷﺪ و ﻫﺪف ﺑﻌﺪي ،ﺗﻼش ﺑﺮاي ﻛﺎﻫﺶ ﺑﺮوز ﺳﺮﻃﺎنﻫﺎي واﺑﺴﺘﻪ ﺑﻪ HPV و 38و37 ﺷﺮاﻳﻂ ﺧﻮشﺧﻴﻢ واﺑﺴﺘﻪ ﺑﻪ HPVاﺳﺖ. دو ﻧﻮع واﻛﺴﻦ HPV ﺟﻬﺖ ﭘﻴﺸﮕﻴﺮي ﻋﻔﻮﻧﺖﻫﺎي HPV و CIN ﺑﺮ اﺳﺎس ﻧﺘﻴﺠﻪ آن اﻗﺪاﻣﺎت درﻣﺎﻧﻲ ﻻزم ﺑﻌﻤﻞ ﻣﻲآﻳﺪ .در ﺟﺪول ﺗﻮﺿﻴﺢ داده ﺷﺪهاﻧﺪ ﻛﻪ اﺛﺮات ﭘﺎﻳﺪار آﻧﻬﺎ 2ﺗﺎ 4/5ﺳﺎل ﻣﻲﺑﺎﺷﺪ. ﺷﻤﺎره ،1ﻣﺠﻤﻮﻋﻪ راﻫﻨﻤﺎﻳﻲﻫﺎي ﻣﻮﺟﻮد در زﻣﻴﻨﻪ ﻏﺮﺑﺎﻟﮕﺮي ﺳﺮﻃﺎن ﺷﺎﻣﻞ -1 :ﻓﺮم ﭼﻬﺎرﮔﺎﻧﻪ ﻳﺎ ) (Gardasilو ﻓﺮم دوﮔﺎﻧﻪ ) .(Cervarixﻫﺮ ﺳﺮوﻳﻜﺲ ﻛﻪ ﺗﻮﺳﻂ اﻧﺠﻤﻦ ﺳﺮﻃﺎن آﻣﺮﻳﻜﺎ ) ،(ACSاﻧﺠﻤﻦ زﻧﺎن و دو ﺷﻜﻞ ﺣﺎوي ذرات ﺷﺒﻪ وﻳﺮوس HPVﺗﺎﻳﭗ 16و 18ﻣﻲﺑﺎﺷﺪ ﻛﻪ و ﮔﺮوه اراﺋﻪدﻫﻨﺪه ﺧﺪﻣﺎت ﭘﻴﺸﮕﻴﺮي در ﺣﺪود %70ﻫﻤﻪ ﺳﺮﻃﺎنﻫﺎي ﺳﺮوﻳﻜﺲ در دﻧﻴﺎ واﺑﺴﺘﻪ ﺑﻪ اﻳﻦ دو ﺗﺎﻳﭗ آﻣﺮﻳﻜﺎ ) (USPSTFاراﺋﻪ ﺷﺪه اﺳﺖ .ﺗﻮﺻﻴﻪﻫﺎي اﺧﻴﺮ ﻣﺒﻨﻲ ﺑﺮ ﺷﺮوع ﻫﺴﺘﻨﺪ 39-43.ﻓﺮم Gardasilواﻛﺴﻦ ﻫﻤﭽﻨﻴﻦ ﺣﺎوي ذرات ﺷﺒﻪ وﻳﺮوس ﻏﺮﺑﺎﻟﮕﺮي ﺗﺎ ﺳﻦ 21ﺳﺎﻟﮕﻲ ﻳﺎ ﻃﻲ ﺳﻪ ﺳﺎل اول ﭘﺲ از ﺷﺮوع ) (VLPﺗﺎﻳﭗ 6و 11ﺑﻮده ﻛﻪ در ارﺗﺒﺎط ﺑﺎ اﻛﺜﺮ زﮔﻴﻞﻫﺎي ﺗﻨﺎﺳﻠﻲ ﻧﺰدﻳﻜﻲ ﻣﻲﺑﺎﺷﺪ .ﺗﺎ ﺳﻦ 30ﺳﺎﻟﮕﻲ ﻏﺮﺑﺎﻟﮕﺮي ﺑﺎ ﻓﺎﺻﻠﻪ ﻫﺮ 1-2ﺳﺎل اﺳﺖ .ﻫﺮ دو واﻛﺴﻦ ﺣﺎوي ﭘﺮوﺗﺌﻴﻦ ﻛﭙﺴﻴﺪال ﺑﻮده وﻟﻲ DNAو RNA اﻧﺠﺎم ﻣﻲﺷﻮد )ﺑﺴﺘﻪ ﺑﻪ ﻧﻮع روش ﻏﺮﺑﺎﻟﮕﺮي( .اﮔﺮ ﺑﻴﻤﺎر ﺟﺰء ﮔﺮوه ﻛﻢ ﻧﺪارﻧﺪ اﻣﺎ ﻣﻲﺗﻮاﻧﻨﺪ ﺳﻴﺴﺘﻢ اﻳﻤﻨﻲ را ﺑﺮاﻧﮕﻴﺰاﻧﻨﺪ و آﻧﺘﻲﺑﺎديﻫﺎي ﺧﻄﺮ ﺑﺎﺷﺪ از 30ﺳﺎﻟﮕﻲ ﻣﻲﺗﻮان ﻓﺎﺻﻠﻪ ﻏﺮﺑﺎﻟﮕﺮي را ﺑﻪ ﻫﺮ دو ﺗﺎ ﺳﻪ ﺧﻨﺜﻲﻛﻨﻨﺪه HPVرا ﻓﻌﺎل ﻛﻨﻨﺪ اﻣﺎ ﺑﻪ دﻟﻴﻞ ﻧﺪاﺷﺘﻦ DNAﺗﻮاﻧﺎﻳﻲ اﻳﺠﺎد ﻣﺎﻣﺎﻳﻲ آﻣﺮﻳﻜﺎﻳﻲ )(ACOG ﺳﺎل ﻳﻚ ﺑﺎر اﻓﺰاﻳﺶ داد. 25-30 ﻋﻔﻮﻧﺖ را در ﻓﺮد ﻧﺪارﻧﺪ. ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 64ﺷﻤﺎره ،12اﺳﻔﻨﺪ 1385 Downloaded from tumj.tums.ac.ir at 16:09 IRST on Tuesday September 22nd 2020 اﻧﺠﺎم آزﻣﺎﻳﺶ DNA وﻳﺮوس HPV اﺳﺖ .اﻣﺎ اﻳﻦ ﺗﺴﺖ ﻧﻤﻲﺗﻮاﻧﺪ 3 ﻧﺎدزه ﺑﻬﺘﺎش و ﻫﻤﻜﺎران 4 ) Gardasilواﻛﺴﻦ ﭼﻬﺎرﮔﺎﻧﻪ ﻳﺎ :(Quadrivalent ﻋﻠﻴﻪ اﻧﻮاع 11-6-18-16وﻳﺮوس HPV دارد .ﺑﻨﺎﺑﺮاﻳﻦ واﻛﺴﻴﻨﺎﺳﻴﻮن در زﻧـﺎن 13-26ﺳـﺎل ﻛـﻪ ﻗـﺒﻼ واﻛـﺴﻴﻨﻪ آﻟﻮﻣﻴﻨﻴﻮم ﺑﻪ ﻋﻨﻮان اﻓﺰاﻳﻨﺪه )ادﺟﻮاﻧﺖ( ﻣﻲﺑﺎﺷﺪ .در ﺑﺮرﺳﻲﻫﺎي اﻧﺠﺎم ﻣﻮرد آﻣﻮزش واﻛﺴﻴﻨﺎﺳﻴﻮن ﻋﺒﺎرﺗﺴﺖ از :واﻛﺴﻴﻨﺎﺳﻴﻮن ﺑﺎﻳـﺴﺘﻲ ﺑـﺮاي ﺷﺪه ﭘﻴﺶ از 25000زن و دﺧﺘﺮ ﺑﻴﻦ 9-26ﺳﺎﻟﻪ ﺑﺮرﺳﻲ ﺷﺪه اﻧﺪ .اﻳﻦ زﻧﺎن 9-26ﺳﺎﻟﻪ ﻛﻪ ﻧﺘﺎﻳﺞ ﺗﺴﺖ ﭘﺎپ آﻧﻬـﺎ ﻏﻴﺮﻃﺒﻴﻌـﻲ ﺑـﻮده ﻳـﺎ زﮔﻴـﻞ واﻛﺴﻦ در 500ﻣﺮد ﺑﻴﻦ 9-15ﺳﺎل ﻧﻴﺰ ﺑﺮرﺳﻲ ﺷﺪه اﺳﺖ .ﻫﺪف ﺗﻨﺎﺳﻠﻲ دارﻧﺪ و ﻳﺎ ﺗﺴﺖ HPVآﻧﻬﺎ از ﻧﻈﺮ اﻧﻮاع ﭘﺮﺧﻄﺮ وﻳﺮوس ﻣﺜﺒـﺖ و اﺳﺖ در ﻧﻈﺮ ﮔﺮﻓﺘﻪ ﺷﻮد .واﻛﺴﻴﻨﺎﺳﻴﻮن ﺑﺮ ﻋﻠﻴﻪ اﻧﻮاع HPVاﻳﻤﻨﻲزاﻳـﻲ دﻳﺴﭙﻼزي ﺳﺮوﻳﻜﺲ ﺑﻮد .اﻳﻦ واﻛﺴﻦ ﺣﺎوي 20mgاز HPVﺗﺎﻳﭗ 16 اﻳﺠﺎد ﻣﻲﻛﻨﺪ ،اﻣﺎ اﻃﻼﻋﺎﺗﻲ در ﻣﻮرد اﻳﻦ ﻛﻪ واﻛﺴﻦ ﺑﺘﻮاﻧﺪ اﺛـﺮ درﻣـﺎﻧﻲ ﻧﻬﺎﻳﻲ ﺷﺎﻣﻞ اﻧﻮاع ﻋﻔﻮﻧﺖﻫﺎي ﻣﺸﺨﺼﻪ ﺗﺎﻳﭗ ﺧﺎﺻﻲ از HPV ﺗﺎ 18و 40 mgاز ﺗﺎﻳﭗ 11و 16ﻣﻲﺑﺎﺷﺪ .ﺣﺠﻢ آن 0/5mlﺑﻮده و 41-47 روي ﺑﻌﻀﻲ ﺿﺎﻳﻌﺎت ﺳﺮوﻳﻜﺲ -واژن داﺷﺘﻪ ﺑﺎﺷﺪ وﺟﻮد ﻧﺪارد. ﺑﻪ روش داﺧﻞ ﻋﻀﻼﻧﻲ ﺗﺰرﻳﻖ ﻣﻲﺷﻮد .ﻓﻮاﺻﻞ ﺗﺰرﻳﻖ ،ﺻﻔﺮ – دو و ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ اﺣﺘﻤﺎل ﺧﻄﺮ ﺑﺎﻻي ﻋﻔﻮﻧﺖ HPVﭘﺎﻳﺪار در زﻧﺎن دﭼﺎر ﺷﺶ ﻣﺎه ﻣﻲﺑﺎﺷﺪ .ﻫﻤﻪ ﺑﺮرﺳﻲﻫﺎ و ﻛﺎرآزﻣﺎﻳﻲﻫﺎي ﺑﺎﻟﻴﻨﻲ ﻧﺸﺎن داد ﻛﻪ ﻧﻘﺺ ﺳﻴﺴﺘﻢ اﻳﻤﻨﻲ ،اﻧﺠﺎم واﻛﺴﻴﻨﺎﺳﻴﻮن ﻣﻲﺗﻮاﻧﺪ آﻧﻬﺎ ﭘﻴﺸﻨﻬﺎد ﺷﻮد اﻣﺎ ﺗﺠﻮﻳﺰ واﻛﺴﻦ Gardasilﺑﺎﻋﺚ ﭘﻴﺸﮕﻴﺮي ﺿﺎﻳﻌﺎت ﺳﺮوﻳﻜﺲ و ﻧﺎﺣﻴﻪ ﻫﻴﭻ ﺑﺮرﺳﻲ از اﺛﺮﺑﺨﺸﻲ واﻛﺴﻦ ﻳﺎ اﻳﻤﻨﻲزاﻳﻲ آﻧﻬﺎ وﻳﺮوس زﻧﺪه ﺗﻨﺎﺳﻠﻲ زﻧﺎن ﻧﺎﺷﻲ از اﻧﻮاع 18-16-11-6وﻳﺮوس HPVو ﻧﻴﺰ ﻛﺎﻫﺶ ﻧﻴﺴﺖ و اﻣﻨﻴﺖ ﻣﺸﺨﺼﻲ ﻧﺪارد ،ﻟﺬا ﻛﺎرﺑﺮد آن در زﻧﺎﻧﻲ ﻛﻪ در ﻣﻌﺮض ﻧﻴﺎز ﺑﻪ ﺗﻜﻨﻴﻚﻫﺎي ﺗﺸﺨﻴﺼﻲ و درﻣﺎﻧﻲ ﻋﻔﻮﻧﺖ ﻣﻲﺷﻮد .ﻃﻲ 30ﻣﺎه ﺑﻴﻤﺎري ﻣﻴﻬﻤﺎن ﻋﻠﻴﻪ ﻣﻴﺰﺑﺎن ) (Graft- Versus Hostﻫﺴﺘﻨﺪ ﺑﺎﻳﺪ ﺑﺎ ﭘﻲﮔﻴﺮي ،ﻣﻴـﺰان ﺑـﺮوز ﻋﻔﻮﻧـﺖ ﭘـﺎﻳﺪار در اﺛﺮ اﻧﻮاع 16-11-6و 18 اﺣﺘﻴﺎط ﺑﻪ ﻛﺎر رود .از واﻛﺴﻴﻨﺎﺳﻴﻮن ﺣﻴﻦ ﺣﺎﻣﻠﮕﻲ ﺑﺎﻳﺪ اﺟﺘﻨﺎب ﺷﻮد. وﻳﺮوس HPVدر اﻓﺮادي ﻛﻪ ﺣﺪاﻗﻞ ﻳﻚ دوز واﻛﺴﻦ درﻳﺎﻓﺖ ﻛﺮدهاﻧﺪ اﮔﺮ زن ﺣﺎﻣﻠﻪاي ﺑﻪ ﻃﻮر اﺗﻔﺎﻗﻲ واﻛﺴﻴﻨﻪ ﺷﻮد ،ﻧﺸﺎن داده ﺷﺪه ﻛﻪ ﻃﻲ در ﻣﻘﺎﻳﺴﻪ ﺑﺎ ﻋﺪم درﻳﺎﻓﺖ واﻛﺴﻦ ،ﺗﺎ %89ﻛﺎﻫﺶ ﻣﻲدﻫﺪ .ﻫﻤﭽﻨﻴﻦ 30روز از واﻛﺴﻴﻨﺎﺳﻴﻮن ﻣﻤﻜﻦ اﺳﺖ ﺗﺎ ﺣﺪ ﻧﺎﭼﻴﺰي آﻧﻮﻣﺎﻟﻲﻫﺎي CIN ﻣﺎدرزادي در ﺟﻨﻴﻦ وي اﻓﺰاﻳﺶ ﻳﺎﺑﺪ .واﻛﺴﻴﻨﺎﺳﻴﻮن ﻃﻲ ﺷﻴﺮدﻫﻲ ﻣﻨﻌﻲ )ﻧﺌﻮﭘﻼزي اﻳﻨﺘﺮااﭘﻲﺗﻠﻴﺎل(، ﻧﺪارد ،اﻣﺎ ﻣﺎدران ﺑﺎﻳﺪ آﮔﺎﻫﻲ داﺷﺘﻪ ﺑﺎﺷﻨﺪ ﻛﻪ ﻃﻲ ﻳﻚ ﻣﺎه ﭘﺲ از )ﻧﺌﻮﭘﻼزي اﻳﻨﺘﺮااﭘﻲﺗﻠﻴﺎل واژن( ،زﮔﻴﻞ ﺗﻨﺎﺳﻠﻲ و ﺳﺮﻃﺎن ﺗﺰرﻳﻖ واﻛﺴﻦ ﻣﻤﻜﻦ اﺳﺖ اﺣﺘﻤﺎل وﻗﻮع اﺧﺘﻼﻻت ﺗﻨﻔﺴﻲ در ﺗﻬﺎﺟﻤﻲ ﺳﺮوﻳﻜﺲ ،ﺗﺎ %100ﻛﺎﻫﺶ ﺧﻮاﻫﺪ ﻳﺎﻓﺖ .ﻣﺪت اﺛﺮ ﺣﻔﺎﻇﺘﻲ ﺷﻴﺮﺧﻮار ﺗﻐﺬﻳﻪﻛﻨﻨﺪه از ﺷﻴﺮﻣﺎدر اﻓﺰاﻳﺶ ﻳﺎﺑﺪ .در ﻣﻮارد ﺿﻌﻒ ﻣﺘﻮﺳﻂ واﻛﺴﻦ ﺗﺎ 3/5ﺳﺎل ﭘﺲ از ﺗﻜﻤﻴﻞ دوره واﻛﺴﻴﻨﺎﺳﻴﻮن ﺑﺮ ﻋﻠﻴﻪ ﺗﺎﻳﭗ ﺗﺎ ﺷﺪﻳﺪ ﺣﺎد ،واﻛﺴﻴﻨﺎﺳﻴﻮن ﺑﺎﻳﺪ ﺗﺎ زﻣﺎن ﺑﻬﺒﻮدي از آن ﺑﻪ ﺗﻌﻮﻳﻖ اﻓﺘﺪ. ﺑﻴﻤﺎريﻫﺎﻳﻲ ﻛﻪ ﺑﺎ ﺑﻴﻮﭘﺴﻲ ﺗﺸﺨﻴﺺ داده ﻣﻲﺷﻮد از ﺟﻤﻠﻪ )ﻧﺌﻮﭘﻼزي اﻳﻨﺘﺮااﭘﻲﺗﻠﻴﺎل ﺳﺮوﻳﻜﺲ(، VAIN 16 HPV VIN و 2/5ﺳﺎل ﭘﺲ از ﺗﻜﻤﻴﻞ ﺳﻪ دوره واﻛﺴﻴﻨﺎﺳﻴﻮن ﺑﺮﻋﻠﻴﻪ ﺗﺎﻳﭗ 18-11-6وﻳﺮوس HPVﻣﻲﺑﺎﺷﺪ. ﻣﺮاﻗﺐ واﻛﻨﺶﻫﺎي آﻟﺮژﻳﻚ در ﻓﺮد واﻛﺴﻴﻨﻪ ﺷﺪه ﺑﺎﺷﻴﻢ. ﻓﺮم دوﮔﺎﻧﻪ واﻛﺴﻦ ) :(Cervarixﺣﺎوي ذرات وﻳﺮوس Gardasilدر زﻧﺎن 9-26ﺳﺎﻟﻪ ﺑﻪ ﺧﻮﺑﻲ ﺗﺤﻤﻞ ﻣﻲﺷﻮد وﻟﻲ HPV ﺑﻮده و ﺣﺎوي ﺗﺎﻳﭗ 16و 18وﻳﺮوس HPVﻣﻲﺑﺎﺷﺪ. low ادﺟﻮاﻧﺖ آن آﻟﻮﻣﻴﻨﻴﻮم و ﺣﺎوي ﻳﻚ ﻋﺎﻣﻞ ﻟﻴﭙﻴﺪي اﺳﺖ .ﺑﺎ اﺳﺘﻔﺎده gradeﻣﻲﺑﺎﺷﺪ .ﺷﺎﻳﻊﺗﺮﻳﻦ ﻋﺎرﺿﻪ ﺟﺎﻧﺒﻲ ﺳﻴﺴﺘﻤﻴﻚ آن ،ﺳﺮدرد از اﻳﻦ واﻛﺴﻦ ،روي 27000زن و دﺧﺘـﺮ 11-55ﺳـﺎﻟﻪ ﺑﺮرﺳـﻲﻫـﺎﻳﻲ ﻣﻲﺑﺎﺷﺪ .ﺗﺰرﻳﻖ واﻛﺴﻦ ،ﺳﺒﺐ ﺗﺄﺛﻴﺮ روي ﻋﺎﻗﺒﺖ ﺣﺎﻣﻠﮕﻲ ﻧﻤﻲﺷﻮد. اﻧﺠﺎم ﺷﺪه اﺳﺖ .اﻳﻦ واﻛﺴﻦ ﻫﻨـﻮز در ﻣﺮدﻫـﺎ آزﻣـﺎﻳﺶ ﻧـﺸﺪه اﺳـﺖ. ﻋﻮارض ﻣﺤﻞ ﺗﺰرﻳﻖ ﺷﺎﻣﻞ درد ،ﺧﻮﻧﺮﻳﺰي ﻣﺤﻞ ﺗﺰرﻳﻖ و ﺗﺐ اﺳﺘﻔﺎده از واﻛﺴﻦ Gardasilﻳﺎ ﻓﺮم ﭼﻬﺎرﮔﺎﻧﻪ واﻛﺴﻦ HPV ﺗﻮﺳﻂ ﻫﺪف ﻧﻬﺎﻳﻲ ) (End pointدر اﻳﻦ ﺑﺮرﺳﻲﻫﺎ ﻋﻔﻮﻧـﺖﻫـﺎي واﺑـﺴﺘﻪ ﺑـﻪ )ﻛﻤﻴﺘﻪ ﻏﺬا و داروي آﻣﺮﻳﻜﺎ( در زﻧﺎن و دﺧﺘﺮان 9-26ﺳﺎﻟﻪ اﻧﻮاع ﻣﺸﺨﺺ HPVاﺳﺖ .اﻳﻦ واﻛﺴﻦ ﺣﺎوي ﭘﺮوﺗﺌﻴﻦ ﻛﭙـﺴﻴﺪ ﺑـﻮده و ﻣﻮرد ﺗﺄﻳﻴﺪ ﻗﺮار ﮔﺮﻓﺘﻪ اﺳﺖ .در ﺳﺎل 2006در ﻣﻮرد واﻛﺴﻴﻨﺎﺳﻴﻮن ﭘﻮﺷــﺶ DNAﻧــﺪارد ،زﻧــﺪه ﻧﻴــﺴﺖ وﻟــﻲ ﺗﺰرﻳــﻖ آن ﺳــﺒﺐ ﺗﻮﻟﻴــﺪ در زﻧﺎن 11-12ﺳﺎﻟﻪ ﺑﺎ ﺳﻪ دوز واﻛﺴﻦ ﺗﻮﺻﻴﻪ ﺷﺪه آﻧﺘﻲﺑﺎديﻫﺎي واﺑﺴﺘﻪ ﺑﻪ اﻧﻮاع ﻣﺸﺨﺺ HPVﺧﻮاﻫﺪ ﺷﺪ .ﺑﺮرﺳﻲﻫـﺎﻳﻲ FDA روﺗﻴﻦ HPV اﺳﺖ .واﻛﺴﻴﻨﺎﺳﻴﻮن ﻣﻲﺗﻮاﻧﺪ از ﺳﻦ 9ﺳﺎﻟﮕﻲ ﻧﻴﺰ ﺷﺮوع ﺷﻮد. ﻛﻪ ﻃﻲ ﺳﺎل ﻫﺎي 2004ﺗﺎ 2006اﻧﺠﺎم ﺷﺪ ﻧـﺸـﺎن داد ﻛــﻪ در زﻧـﺎن ﻫﺪف از اﻳﻦ ﺗﻮﺻﻴﻪﻫﺎ ،اﻳﻤﻨﻲﺳﺎزي ﻗﺒﻞ از ﺷﺮوع ﻓﻌﺎﻟﻴـﺖ ﺟﻨـﺴﻲ 15-25ﺳﺎﻟﻪ واﻛﺴﻴﻨﺎﺳﻴﻮن ﻓﺮم دوﮔﺎﻧﻪ در ﻛﺎﻫﺶ ﻋﻔﻮﻧﺖﻫـﺎي واﺑـﺴﺘﻪ ﻗﺒﻼ واﻛﺴﻴﻨﻪ ﻧﺸﺪه اﻧﺪ ﻧﻴﺰ ﻛـﺎرﺑﺮد ﻣﻲﺑﺎﺷﺪ اﻣﺎ ﺣﺘﻲ در زﻧﺎن ﺟﻮاﻧﻲ ﻛﻪ ً ﺑﻪ HPVﻣﻮﺛﺮ ﺑﻮده اﺳﺖ 43-44.ﺑﺮرﺳﻲ ﺳﺎل ،2004ﻛﺎﻫﺶ ﻣـﺸﺨﺺ در ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 64ﺷﻤﺎره ،12اﺳﻔﻨﺪ 1385 Downloaded from tumj.tums.ac.ir at 16:09 IRST on Tuesday September 22nd 2020 ﻣﻮﺛﺮ اﺳﺖ و داراي ﻧﺸﺪﻧﺪ ﻧﻴﺰ ﻗﺎﺑﻞ اﺳﺘﻔﺎده اﺳﺖ .راﻫﻨﻤﺎﻳﻲ اﻧﺠـﺎم ﺳـﺮﻃﺎنﻫـﺎي زﻧـﺎن در ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ و ﻧﻘﺶ واﻛﺴﻴﻨﺎﺳﻴﻮن در ﭘﻴﺸﮕﻴﺮي از آن 5 اﺛﺮﺑﺨﺸﻲ واﻛﺴﻦ Cervarixرا ﺗﺎ %95/1ﺑﺮ ﻋﻠﻴﻪ ﻋﻔﻮﻧـﺖﻫـﺎي ﭘﺎﻳـﺪار ﺑﻴﻤﺎري ﻣﻨﺘﻘﻠﻪ از راه ﺟﻨﺴﻲ اﺳﺖ و ﻫﻢ ﺗﻮﺳﻂ ﻣﺮدان و ﻫﻢ زﻧﺎن اﻧﺘﺸﺎر ﺳﺮوﻳﻜﺲ ﻛﻪ ﺑﺎ HPVارﺗﺒﺎط دارﻧـﺪ ﻧـﺸﺎن داد .ﺣﺘـﻲ در ﻳـﻚ آﻧـﺎﻟﻴﺰ، ﻣﻲﻳﺎﺑﺪ ،ﻟﺬا واﻛﺴﻴﻨﺎﺳﻴﻮن در ﻣﺮدان و زﻧﺎن اﻧﺠـﺎم ﮔﻴـﺮد اﻣـﺎ در ﻣـﻮرد اﺛﺮﺑﺨﺸﻲ واﻛﺴﻦ ﺗﺎ %100ﺑﺮاي ﺿـﺎﻳﻌﺎت CINواﺑـﺴﺘﻪ HPVﮔـﺰارش اﺛﺮﺑﺨﺸﻲ واﻛﺴﻦ روي ﻣـﺮدان ﻫﻨـﻮز ﺗﺤﻘﻴﻘـﺎت ﺑﻴـﺸﺘﺮي ﺑﺎﻳـﺪ اﻧﺠـﺎم 45-46 آﻳﺎ واﻛﺴﻴﻨﺎﺳﻴﻮن در ﻣﺒﺘﻼﻳـﺎن ) HIVوﻳـﺮوس ﻧﻘـﺺ اﻳﻤﻨـﻲ ﺷﺪ .ﻫﻤﭽﻨﻴﻦ اﻳﻦ ﻧﻮع واﻛﺴﻦ ﺳﺒﺐ ﻛﺎﻫﺶ ﻋﻔﻮﻧـﺖﻫـﺎي واﺑـﺴﺘﻪ ﺑـﻪ ﺷﻮد. ﺗﺎﻳﭗ 45و 31وﻳﺮوس HPVﻣﻲﺷﻮد 45.ﻋﻮارض ﺗﺰرﻳﻖ واﻛﺴﻦ ﺷﺎﻣﻞ اﻧﺴﺎن( ﻧﻴـﺰ در ﺟﻠـﻮﮔﻴﺮي از ﻋﻔﻮﻧـﺖﻫـﺎي ﻧﺎﺣﻴـﻪ ﺗﻨﺎﺳـﻠﻲ و ﻣﻘﻌـﺪي ﺧﺴﺘﮕﻲ ،ﻋﻮارض ﮔﻮارﺷﻲ ،ﺗﺐ Low gradeو ﺳﺮدرد اﺳـﺖ .ﻣـﺪت )آﻧﻮژﻧﻴﺘﺎل( ﻣﻮﺛﺮ اﺳﺖ؟ ﺗـﺄﺛﻴﺮ آن در ﻣﺒﺘﻼﻳـﺎن HIVﻧﺎﺷـﻨﺎﺧﺘﻪ اﺳـﺖ و اﺛﺮﺑﺨﺸﻲ و ﺣﻔﺎﻇﺖ واﻛﺴﻦ دوﮔﺎﻧﻪ ﻣﺸﺨﺺ ﻧﺸﺪه اﺳـﺖ و ﻫﻨـﻮز ﺑـﻪ ﻛﻠﻴــﺪ اﺻــﻠﻲ ﻣﻮﻓﻘﻴــﺖ واﻛــﺴﻴﻨﺎﺳﻴﻮن ،آﻣــﻮزش ﻣﻨﺎﺳــﺐ و ﺟﺎﻣﻌــﻪ- 47 ﻧﺘﻴﺠﻪﮔﻴﺮي ﻧﻬﺎﻳﻲ :ﭘﻴـﺸﮕﻴﺮي از ﻋﻔﻮﻧـﺖ ﻣﺪت اﻳﺪه آل )از زﻣﺎن ﺷﺮوع ﻓﻌﺎﻟﻴﺖ ﺟﻨﺴﻲ ﺗﺎ اﺗﻤﺎم آن ﻛﻪ ﭼﻨﺪ دﻫـﻪ ﺧﺎﻧﻮادهﻫﺎ و ﺑﻴﻤﺎران اﺳﺖ. ﺑﻪ ﻃﻮل ﻣﻲاﻧﺠﺎﻣﺪ( ﻧﺮﺳﻴﺪه اﺳﺖ 46.ﭘﺲ از دوره ﺳـﻮم واﻛـﺴﻴﻨﺎﺳﻴﻮن، HPVﻧﺎﺣﻴﻪ ﺗﻨﺎﺳﻠﻲ ﺗﺤﺘﺎﻧﻲ اﺳﺎس ﺑﺮرﺳﻲﻫﺎي اﺧﻴﺮ را ﺗﺸﻜﻴﻞ ﻣﻲدﻫﺪ. ﻃﻲ ﻳﻚ ﻣﺎه ﺑﻌﺪ اﺛﺮ ﺣﻔﺎﻇﺘﻲ آن ﺷﺮوع ﺷﺪه و ﺣﺪاﻗﻞ 18ﻣـﺎه ﭘـﺲ از ﺑﺎ واﻛﺴﻴﻨﺎﺳﻴﻮن ﻣﻲﺗﻮان %70ﺳﺮﻃﺎنﻫﺎي ﺳﺮوﻳﻜﺲ ﻣﺮﺗﺒﻂ ﺑـﺎ HPVرا ﺷﺮوع ﺑﻪ ﺣﺪ ﭘﺎﻳﺪار ) (Plateauﻣﻲرﺳﺪ 42-46.ﺑﻪ ﻃﻮر ﻛﻠﻲ اﻓﺰاﻳﺶ 133 ﻛﺎﻫﺶ و ﺣﺘﻲ از ﺿﺎﻳﻌﺎت ﭘﻴﺶﺑﺪﺧﻴﻢ و دﻳﮕـﺮ ﺑـﺪﺧﻴﻤﻲﻫـﺎي ﻧﺎﺣﻴـﻪ ﺑﺮاﺑﺮي در ﻣﻴـﺎﻧﮕﻴﻦ ﺳـﻄﺢ آﻧﺘـﻲﺑـﺎدي HPV-16و HPV-18در ﭘﺎﻳـﺎن ﺗﻨﺎﺳﻠﻲ زﻧﺎن ﺟﻠـﻮﮔﻴﺮي ﻛـﺮد .ﺑﺮﻧﺎﻣـﻪ ﻏﺮﺑـﺎﻟﮕﺮي ﺑـﺮاي ﺟﻠـﻮﮔﻴﺮي از 46 ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ ﻳﻚ اﻣﺮ ﻣﻬﻢ اﺳﺖ وﻟﻲ ﺑﺮرﺳﻲﻫـﺎي ﺑﻴـﺸﺘﺮ در اﻳـﻦ واﻛﺴﻦ ﭼﻬﺎرﮔﺎﻧﻪ ﻃﻲ 36ﻣﺎه ﺳـﺒﺐ اﻓـﺰاﻳﺶ ﺳـﻄﺢ آﻧﺘـﻲﺑـﺎدي ﺿـﺪ زﻣﻴﻨﻪ و اﻧﺠـﺎم واﻛـﺴﻴﻨﺎﺳﻴﻮن ﺑـﺮ ﻋﻠﻴـﻪ HPVدر ﺣـﺎل اﻧﺠـﺎم اﺳـﺖ و وﻳﺮوس HPVﻣﻲﺷﻮد ﻛﻪ اﻳﻦ ﺳﻄﺢ ﺣﺘﻲ از اﻓﺰاﻳﺶ ﻣﻮﺟﻮد در ﺳـﻄﺢ آﻣﻮزش و آﮔﺎﻫﻲ اﻓﺮاد ﺟﺎﻣﻌﻪ ﻧﻘﺶ ﺑﻪ ﺳﺰاﻳﻲ در ﻣﻮﻓﻘﻴـﺖ ﻏﺮﺑـﺎﻟﮕﺮي ﺧﻮﻧﻲ ﻓـﺮد ﻣﺒـﺘﻼ ﺑـﻪ ﻋﻔﻮﻧـﺖ HPVﻧﻴـﺰ ﺑﻴـﺸﺘﺮ ﻣـﻲﺑﺎﺷـﺪ 44.اﻣـﺎ آﻳـﺎ ﺟﻤﻌﻲ ﺟﺎﻣﻌﻪ ﺧﻮاﻫﺪ داﺷﺖ. ﻣﺪت 4/5ﺳﺎﻟﻪ ﭘﺲ از واﻛـﺴﻴﻨﺎﺳﻴﻮن ﻓـﺮم دوﮔﺎﻧـﻪ رخ ﺧﻮاﻫـﺪ داد. ﺟﺪول :1-راﻫﻨﻤﺎﻳﻲ ﻫﺎﻳﻲ در ﻣﻮرد ﻏﺮﺑﺎﻟﮕﺮي ﺳﺮﻃﺎن ﺳﺮوﻳﻜﺲ * ACS راﻫﻨﻤﺎﻳﻲ 3ﺳﺎل ﭘﺲ از اوﻟﻴﻦ ﻧﺰدﻳﻜﻲ وﻟﻲ دﻳﺮﺗﺮ زﻣﺎن ﺷﺮوع ﻏﺮﺑﺎﻟﮕﺮي ﻓﺎﺻﻠﻪ ﻏﺮﺑﺎﻟﮕﺮي در ﺳﻨﻴﻦ ﻗﺒـﻞ از ** ACOG 3ﺳﺎل ﭘﺲ از اوﻟﻴﻦ ﻧﺰدﻳﻜﻲ دﻳﺮﺗﺮ از 21ﺳﺎل USPSTF *** 3ﺳﺎل ﭘﺲ از اوﻟﻴﻦ ﻧﺰدﻳﻜﻲ وﻟﻲ دﻳﺮﺗﺮ از 21ﺳﺎل ﻧﺸﻮد. ﻧﺸﻮد. از 21ﺳﺎل ﻧﺸﻮد. ﺳﺎﻻﻧﻪ :اﮔﺮ ﺗﺴﺖ ﭘﺎپ ﭘﺎﭘﺎﻧﻴﻜﻮﻻﺋﻮ اﻧﺠﺎم ﺳﺎﻻﻧﻪ ﺳﺎﻻﻧﻪ ﺷﻮد. 30ﺳﺎﻟﮕﻲ ﻫﺮ دو ﺳﺎل :اﮔﺮ روش ﺳﻴﺘﻮﻟﻮژي ﺑﺮ ﭘﺎﻳﻪ ﻣﺎﻳﻊ اﻧﺠﺎم ﺷﻮد. ﻓﺎﺻﻠﻪ ﻏﺮﺑـﺎﻟﮕﺮي در زﻧـﺎن ≤30 ﻫﺮ 3-2ﺳﺎل اﮔﺮ 3ﺗﺴﺖ ﻗﺒﻠﻲ ﻧﺮﻣﺎل ﻫﺮ 2ﺗﺎ 3ﺳﺎل اﮔﺮ 3ﺗﺴﺖ ﻗﺒﻠﻲ ﻧﺮﻣﺎل ﺑﺎﺷﺪ. ﺑﺎﺷﺪ. ﺳﺎل آزﻣـــﺎﻳﺶ DNAوﻳـــﺮوس ﺟﻬﺖ ﻏﺮﺑﺎﻟﮕﺮي زﻣﺎن ﺗﻮﻗﻒ ﻏﺮﺑﺎﻟﮕﺮي HPV ﻫﺮ 3ﺳﺎل اﮔﺮ 2ﻳﺎ 3ﺗﺴﺖ ﻗﺒﻠﻲ ﻧﺮﻣﺎل ﺑﺎﺷﺪ. در زﻧﺎن ≤ 30ﺳﺎﻟﮕﻲ ،ﻫﺮ 3ﺳﺎل ﻫﻤﺮاه ﻳﻚ ﭘﻴﺸﻨﻬﺎد ﺑﺮاي زﻧﺎن ≤ 30ﺳﺎل ،ﺑﻪ ﻓﺎﺻﻠﻪ ﺑﺎ ﺳﻴﺘﻮﻟﻮژي ﻫﺮ 3ﺳﺎل ﻫﻤﺮاه ﺑﺎ ﺳﻴﺘﻮﻟﻮژي ﺳﻦ ≤ 70ﺳﺎل .اﮔﺮ 3ﺗﺴﺖ ﻗﺒﻠﻲ ﻧﺮﻣﺎل ﻣﺪارك ﻧﺎﻣﺸﺨﺺ اﺳﺖ و ﺳﻦ ﻧﻬﺎﻳﻲ ﺗﻮﻗﻒ ﺳﻦ ≤ 65ﺳﺎل اﮔﺮ ﺑﺮﻧﺎﻣﻪ ﻏﺮﺑﺎﻟﮕﺮي ﺑﺎﺷﺪ و ﻫﻴﭻ ﻧﺘﻴﺠﻪ ﻏﻴﺮﻃﺒﻴﻌﻲ ﻃﻲ 10 ﻣﺸﺨﺺ ﻧﺸﺪه اﺳﺖ. ﻣﻨﺎﺳﺐ ﺑﻮده و ﺗﺴﺖ ﭘﺎپ ﻧﻴﺰ ﻧﺮﻣﺎل ﺑﺎﺷﺪ. ﻣﺪارك ﻣﺸﺨﺼﻲ وﺟﻮد ﻧﺪارد. ﺳﺎل ﻧﺪاﺷﺘﻪ ﺑﺎﺷﻴﻢ. :aزﻧﺎن ﮔﺮوه ﭘﺮﺧﻄﺮ ﺷﺎﻣﻞ ﻛﺴﺎﻧﻲ ﻛﻪ در ﺗﻤﺎس ﺑﺎ DESﺑﻮده اﻧﺪ ﻳﺎ ﻣﻮارد ﻧﻘﺺ اﻳﻤﻨﻲ ﻳﺎ ﻋﻔﻮﻧﺖ ،HIVدر اﻳﻦ ﻣﻮارد ﺑﺎﻳﺪ ﺳﺎﻻﻧﻪ ﻏﺮﺑﺎﻟﮕﺮي ﺷﻮﻧﺪ. *Atypical Cell Squamous **American College of Obstetrics & Gynecology ***U.S. Preventive Services Task Force ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 64ﺷﻤﺎره ،12اﺳﻔﻨﺪ 1385 Downloaded from tumj.tums.ac.ir at 16:09 IRST on Tuesday September 22nd 2020 ﻣﻴﺰان ﻣﻮارد ﻣﺜﺒﺖ HPV-16و HPV-18را ﻧﺸﺎن داد 82.اﻳـﻦ ﻣﻄﺎﻟﻌـﺎت واﻛﺴﻴﻨﺎﺳﻴﻮن HPVدر ﻣﺮدان ﻧﻴﺰ ﺑﺎﻳﺪ اﻧﺠﺎم ﺷﻮد؟ از آﻧﺠﺎ ﻛﻪ HPVﻳﻚ Behtash N. et al. Evaluation of two surveillance methods for surgical site infection و ﻫﻤﻜﺎران 6 Downloaded from tumj.tums.ac.ir at 16:09 IRST on Tuesday September 22nd 2020 References 1. Announcement the society of Gynecologic oncologists statement on a cervix cancer vaccine. Gynecol Oncol 2006; 10: 377. 2. Behtash N, Ghaemmaghami F, Ayatollahi H, Khaledi H, Hanjani P. A case-control study to evaluate urinary tract complications in radical hysterectomy. World J Surg Oncol 2005; 3: 12. 3. Behtash N, Mousavi A, Mohit M, Modares M, Khanafshar N, Hanjani P. Simple hysterectomy in the presence of invasive cervical cancer in Iran. Int J Gynecol Cancer 2003; 13: 177-81. 4. Behtash N, Mousavi A, Tehranian A, Khanafshar N, Hanjani P. Embryonal rhabdomyosarcoma of the uterine cervix: case report and review of the literature. Gynecol Oncol 2003; 91: 452-5. 5. Behtash N, Nazari Z, Ayatollahi H, Modarres M, Ghaemmaghami F, Mousavi A. Neoadjuvant chemotherapy and radical surgery compared to radical surgery alone in bulky stage IB-IIA cervical cancer. Eur J Surg Oncol 2006; 32: 1226-30. 6. Behtash N, Ghaemmaghami F, Yarandi F, Ardalan FA, Khanafshar N. Cutaneous metastasis from carcinoma of the cervix at the drain site. Gynecol Oncol 2002; 85: 20911. 7. Nazari Z, Behtash N, Gilan MM, Ganjoei TA. Cervical carcinoma simulating advanced ovarian cancer. Eur J Surg Oncol 2007; 33: 123-4. 8. Munoz N, Bosch FX, de Sanjose S, Herrero R, Castellsague X, Shah KV, et al. Epidemiologic classification of human papillomavirus types associated with cervical cancer. N Engl J Med 2003; 348: 489-90. 9. Castellsague X, Diaz M, De Sanjose S, et al. Worldwide human papillomavirus etiology of cervical adenocarcinoma and its cofactors: implications for screening and prevention. J Natl Cancer Inst 2006; 98: 303-15. 10. Daling JR, Madeleine MM, Johnson LG, Schwartz SM, Shera KA, Wurscher MA, et al. Human papillomavirus, smoking, and sexual practices in the etiology of anal cancer. Cancer 2004; 101: 270-80. 11. Schiffman M, Kjaer SK. Chapter 2: Natural history of anogenital human papilloma virus infection and neoplasia. J Natl Cancer Inst Monogr 2003; 31: 14-19. 12. Jemal A, Siegel R, Ward E, Murray T, Xu J, Smigal C, et al. Cancer statistics 2006; CA Cancer J Clin 2006; 56: 106-30. 13. Freeman HP, Wingrove BK. Excess cervical cancer mortality: a marker for low access to health care in poor communities. Rockville, MD: National Cancer Institute, Center to Reduce Cancer Health Disparities 2005; No. 05-5282. 14. Behbakht K, Lynch A, Teal S, Degeest K, Massad S. Social and cultural barriers to Papanicolaou test screening in an urban population. Obstet Gynecol 2004; 104: 1355-61. 15. Cooper CP, Saraiya M, McLean TA, et al. Report from the CDC. Pap test intervals used by physicians serving low-income women through the National Breast and 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. Cervical Cancer Early Detection Program. J Womens Health 2005; 14: 670-8. Hoyo C, Yarnall KS, Skinner CS, Moorman PG, Sellers D, Reid L. Pain predicts nonadherence to pap smear screening among middle-aged African American women. Prev Med 2005; 41: 439-45. Jacobs EA, Karavolos K, Rathouz PJ, Ferris TG, Powell LH. Limited English proficiency and breast and cervical cancer screening in a multiethnic population. Am J Public Health 2005; 95: 1410-6. Wright Jr TC, Schiffman M. Adding a test for human papillomavirus DNA to cervical-cancer screening. N Engl J Med 2003; 348: 489-90. Kjaer SK, van den Brule AJ, Paull G, Svare EI, Sherman ME, Thomsen BL, et al. Type specific persistence of high risk human papillomavirus (HPV) as indicator of high grade cervical squamous intraepithelial lesions in young women: population based prospective follow up study. BMJ 2002; 325: 572-6. Khan MJ, Castle PE, Lorincz AT, Wacholder S, Sherman M, Scott DR, Rush BB, Glass AG, Schiffman M. The elevated 10-year risk of cervical precancer and cancer in women with human papillomavirus (HPV) type 16 or 18 and the possible utility of type-specific HPV testing in clinical practice. J Natl Cancer Inst 2005; 97: 1072-9. Castle PE, Solomon D, Schiffman M, Wheeler CM. Human papillomavirus type 16 infections and 2-year absolute risk of cervical precancer in women with equivocal or mild cytologic abnormalities. J Natl Cancer Inst 2005; 97: 106671. Einstein MH, Cruz Y, El-Awady MK, Popescu NC, DiPaolo JA, van Ranst M, et al. Utilization of the human genome sequence localizes human papillomavirus type 16 DNA integrated into the TNFAIP2 gene in a fatal cervical cancer from a 39-year-old woman. Clinn Cancer Res 2002; 8: 54954. Wang SS, Sherman ME, Hildesheim A, Lacey JV, Devesa S. Cervical adenocarcinoma and squamous cell carcinoma incidence trends among white women and black women in the United States for 1976-2000. Cancer 2004; 100: 103544. Kyndi M, Frederiksen K, Kruger-Kjaer S. Cervical cancer incidence in Denmark over six decades (1994-2000). Acta Obstet Gynecol Scand 2006; 85: 106-11. Clavel C, Masure M, Bory JP, Putaud I, Mangeonjean C, Lorenzato M, et al. Hybrid Capture II-based human papillomavirus detection, a sensitive test to detect in routine high-grade cervical lesions: a preliminary study on 1518 women. Br J Cancer 1999; 80: 1306-11. Nanda K, McCrory DC, Myers ER, Bastian LA, Hasselblad V, Hickey JD, et al. Accuracy of the Papanicolaou test in screening for and follow-up of cervical cytologic abnormalities: a systematic review. Ann Intern Med 2000; 132: 810-9. Bernstein SJ, Sanchez-Ramos L, Ndubisi B. Liquid-based cervical cytologic smear study and conventional Papanicolaou smears: a metaanalysis of prospective studies 1385 اﺳﻔﻨﺪ،12 ﺷﻤﺎره، 64 دوره، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ Cervical cancer: The role of HPV vaccine in prevention of this 7 Downloaded from tumj.tums.ac.ir at 16:09 IRST on Tuesday September 22nd 2020 28. 29. 30. 31. 32. 33. 34. 35. 36. 37. ﻛﺎراﻳﻲ دو روش ﭘﺎﻳﺶ ﺑﺮاي ﺗﺸﺨﻴﺺ ﻋﻔﻮﻧﺖ ﻣﺤﻞ ﺟﺮاﺣﻲ در ﺑﺨﺸﻬﺎي ﺟﺮاﺣﻲ ﻋﻤﻮﻣﻲ comparing cytologic diagnosis and sample adequacy. Am J Obstet Gynecol 2001; 185: 308-17. Marino JF, Fremont-Smith M. Direct-to-vial experience with autoCyte PREP in a small New England cytology practice. J Reprod Med 2001; 46: 353-8. Belinson J, Qiao YL, Pretorius R, Zhang WH, Elson P, Li L, et al. Shanxi Province Cervical Cancer Screening Study: a cross-sectional comparative trial of multiple techniques to detect cervical neoplasia. Gyncecol Oncol 2001; 83: 439-44. Obwegeser JH, Brack S. Does liquid-based technology really improve detection of cervical neoplasia? A prospective, randomized trial comparing the ThinPrep Pap Test with the conventional Pap Test, including follow-up of HSIL cases. Acta Cytol 2001; 45: 709-14. Saslow D, Runowicz CD, Solomon D, et al. American Cancer Society guideline for the early detection of cervical neoplasia and cancer. CA Cancer J Clin 2002; 52: 342-62. American College of Obstetricians and Gynecologists. ACOG practice Bulletin 45: Cervical Cytology Screening. Obstet Gynecol 2003; 102: 417-27. Bundrick JB, Cook DA, Gostout BS. Screening for cervical cancer and initial treatment of patients with abnomal results from papanicolaou testing. Mayo Clin Proc 2005; 80: 1063-8. Jacobs MV, Walboomers JM, Snijders PJ, Voorhorst FJ, Verheijen RH, Fransen-Daalmeijer N, et al. Distribution of 37 mucosotropic HPV types in women with cytologically normal cervical smears: the age-related patterns for high-risk and low-risk types. Int J Cancer 2000; 87: 221-7. Cuzick J, Szarewski A, Cubie H, Hulman G, Kitchener H, Luesley D, et al. Management of women who test positive for high-risk types of human papillomavirus: the HART study. Lancet 2003; 362: 1871-6. Kulasingam SL, Hughes JP, Kiviat NB, et al. Evaluation of human papillomavirus testing in primary screening for cervical abnormalities: comparison of sensitivity, specificity, and frequency of referral. JAMA 2002; 288: 1749-57. Clavel C, Masure M, Bory JP, Putaud I, Mangeonjean C, Lorenzato M, et al. Human papillomavirus testing in primary screening for the detection of high-grade cervical 1385 اﺳﻔﻨﺪ،12 ﺷﻤﺎره، 64 دوره، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ 38. 39. 40. 41. 42. 43. 44. 45. 46. 47. lesions: a study of 7932 women. Br J Cancer 2001; 84: 1616-23. Cuzick J, Beverley E, Ho L, Terry G, Sapper H, Mielzynska I et al. HPV testing in primary screening of older women. Br J cancer 1999; 81: 554-8. Franco EL. Chapter 13: Primary screening of cervical cancer with human papillomavirus tests. J Natl Cancer Inst Monogr 2003; 31: 89-96. Schneider A, Hoyer H, Lotz B, Leistritza S, Kuhne-Heid R, Nindl I, et al. Screening for high-grade cervical intraepithelial neoplasia and cancer by testing for high-risk HPV, routine cytology or colposcopy. Int J Cancer 2000; 89: 52934. Blumenthal PD, Gaffikin L, Chirenje ZM, McGrath J, Womack S, Shah K. A Adjunctive testing for cervical cancer in low resource settings with visual inspection, HPV, and the Pap smear. Int J Gynaecol Obstet 2001; 72: 47-53. Sherman ME, Lorincz AT, Scott DR, Wacholder S, Castle PE, Glass AG, et al. Baseline cytology, human papillomavirus testing, and risk for cervical neoplasia: a 10year cohort analysis. J Natl Cancer Inst 2003; 95: 46-52. Wright TC Jr, Schiffman M, Solomon D, Cox JT, Garcia F, Goldie S, et al. Interim guidance for the use of human papillomavirus DNA testing as an adjunct to cervical cytology for screening. Obstet Gynecol 2004; 103: 304-9. Villa LL, Costa RL, Petta CA, Andrade RP, Ault KA, Giuliano AR, et al. Prophylactic quadrivalent human papillomavirus (types 6, 11, 16, and 18) L1 virus-like particle vaccine in young women: a randomised double-blind placebo-controlled multicentre phase II efficacy trial. Lancet Oncol 2005; 6: 271-8. Harper DM, Franco EL, Wheeler CM, Moscicki AB, Romanowski B, Roteli-Martins CM, et al. Sustained efficacy up to 4.5 years of a bivalent L1 virus-like particle vaccine against human papillomavirus types 16 and 18: follow-up from a randomised control trial. Lancet 2006; 367: 1247-55. Mao C, Koutsky LA, Ault KA, Wheeler CM, Brown DR, Wiley DJ, et al. Efficacy of human papillomaviurs-16 vaccine to prevent cervical intraepithelial neoplasia: a randomized controlled trial. Obstet Gynecol 2006; 107: 1827. Erratum in: Obstet Gynecol 2006; 107: 1425. Frisch M, Biggar RJ, Goedert JJ. Human Papillomavirusassociated cancers in patients with human immunodeficiency virus infection and acquired immunodeficiency syndrome. J Natl Cancer Inst 2000; 92: 1500-10. Tehran University Medical Journal; Vol. 64, No.12, Mar 2007: 1-8 Evaluation of two surveillance methods for surgical site infection و ﻫﻤﻜﺎران 8 Downloaded from tumj.tums.ac.ir at 16:09 IRST on Tuesday September 22nd 2020 Cervical cancer: The preventive role of HPV vaccine (review article) N. Behtash* M. Karimizarchi Department of Obstetrics & Gynecology, Division of Gynecology Oncology Tehran University of Medical Sciences. Abstract Cervical cancer is the second most common gynecologic cancer. A steady 70% annual decline in mortality from cervical cancers has been observed since the mid 20th century after the introduction of widespread papanicolaou cytological screening. But also cervical cancer continues to be an important world health problem for women. Cervical cancer is one of the best- understood neoplasm given its well known viral cause of persistent infection with high risk human papillomavirus (HPV). To date, two manufacturers have developed HPV vaccines composed of noninfectious, recombinant HPV viral-like particles (VLPs). This article presents current advances and perspectives on HPV vaccines.The vaccine is administered by intramuscular injection, and the recommended schedule is a 3-dose series with the second and third doses administered 2 and 6 months after the first dose. The recommended age for vaccination of females is 11-12 years. Vaccine can be administered as young as age 9 years. Catch-up vaccination is recommended for females aged 13--26 years who have not been previously vaccinated. Vaccination is not a substitute for routine cervical cancer screening, and vaccinated females should have cervical cancer screening as recommended. Keywords: Cervical cancer, vaccination, HPV, prevention. *Corresponding autho, Depart of Gynecology Oncology, Vali-e-Asr Hospital, Keshavarz Blvd., Tehran. Tel: +98-21-66930666 Email: nadbehtash@yahoo.com 1385 اﺳﻔﻨﺪ،12 ﺷﻤﺎره، 64 دوره، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ