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Fatty Liver

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CME Article Non-alcoholic fatty liver disease
Jamali R1*, Jamali A 2 1- Anatomical Sciences Research Center, Kashan University of Medical Sciences, Kashan, I. R. Iran 2-Student Scientific Research Center, Tehran University of Medical Sciences, Tehran, I.R. Iran Received March 2, 2010; Accepted May 22, 2010

Abstract: Background: Non-alcoholic fatty liver disease is among the prevalent causes of chronic hepatitis and cirrhosis. Here, we discuss the best diagnostic and therapeutic approaches for the disease. Materials and Methods: Epidemiology, pathogenesis, etiologies, natural course, differential diagnosis, treatment options, complications and follow up of the disease are reviewed in this paper. Results: Non-alcoholic fatty liver disease seems to be the hepatic manifestation of the metabolic syndrome. Liver function tests and sonography can be used as the appropriate screening tests for diagnosis. Weight loss and control of hyperlipidemia and diabetes mellitus might be the best therapeutic approaches. Conclusion: Early diagnosis and appropriate treatment may decrease mortality and morbidity rate associated to the cardiovascular complications of the metabolic syndrome. Keywords: Fatty liver, Insulin resistance, Metabolic syndrome x, Diabetes mellitus, Obesity, Therapy
* Corresponding Author. Email: raika.jamali@gmail.com Tel: 0098 361 555 0026 Fax: 0098 361 555 8900

Conflict of Interests: No
Feyz, Journal of Kashan University of Medical Sciences, Summer 2010; Vol 14, No 2, Pages 169-181

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‫‪Archive of SID‬‬
‫ﻣﺮوري ﺑﺮ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب‬
‫2‬ ‫1*‬

‫راﻳﻜﺎ ﺟﻤﺎﻟﻲ ، ارﺳﻴﺎ ﺟﻤﺎﻟﻲ‬
‫ﺧﻼﺻﻪ‬

‫ﺳﺎﺑﻘﻪ و ﻫﺪف: ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻳﻜﻲ از ﻋﻠﻞ ﺷﺎﻳﻊ ﺑﻴﻤﺎري ﻣﺰﻣﻦ ﻛﺒﺪي و ﺳﻴﺮوز ﻣﻲﺑﺎﺷﺪ. ﻫﺪف اﻳﻦ ﻣﻘﺎﻟﻪ ﻣﻌﺮﻓﻲ و ﺑﺮرﺳﻲ‬ ‫ﺑﻬﺘﺮﻳﻦ روشﻫﺎي ﺗﺸﺨﻴﺼﻲ و درﻣﺎﻧﻲ ﺟﻬﺖ اﻳﻦ ﺑﻴﻤﺎري ﻣﻲ ﺑﺎﺷﺪ.‬ ‫ﻣﻮاد و روشﻫﺎ: در اﻳﻦ ﻣﻘﺎﻟﻪ ﭘﺲ از اراﺋﻪ ﺧﻼﺻﻪاي از ﻫﻤﻪ ﮔﻴﺮ ﺷﻨﺎﺳﻲ، ﻓﺮآﻳﻨﺪ اﻳﺠﺎد ﺑﻴﻤﺎري، ﻋﻠﻞ، ﻋﻮارض و ﺳﻴﺮ ﺑﻴﻤﺎري،‬ ‫روشﻫﺎي ﺗﺸﺨﻴﺺ اﻓﺘﺮاﻗﻲ، درﻣﺎن و ﭘﻴﮕﻴﺮي ﺑﻴﻤﺎري ﺗﻮﺿﻴﺢ داده ﺷﺪهاﻧﺪ.‬ ‫ﻧﺘﺎﻳﺞ: ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﺗﻈﺎﻫﺮ ﻛﺒﺪي ﺳﻨﺪروم ﻣﺘﺎﺑﻮﻟﻴﻚ ﻳﺎ ﻫﻤﺎن ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ ﻣﻲﺑﺎﺷﺪ. از آزﻣﺎﻳﺶﻫﺎي ﻋﻤﻠﻜﺮد ﻛﺒﺪ و‬ ‫ﺳﻮﻧﻮﮔﺮاﻓﻲ ﺷﻜﻢ ﻣﻲﺗﻮان ﺑﻪ ﻋﻨﻮان آزﻣﻮن ﻏﺮﺑﺎﻟﮕﺮي ﺟﻬﺖ ﺗﺸﺨﻴﺺ ﺑﻴﻤﺎري اﺳﺘﻔﺎده ﻛﺮد و ﻛﺎﻫﺶ وزن و ﺗﻨﻈﻴﻢ ﭼﺮﺑﻲ و ﻗﻨﺪ‬ ‫ﺧﻮن از ﺑﻬﺘﺮﻳﻦ روشﻫﺎي درﻣﺎﻧﻲ ﻣﻲﺑﺎﺷﻨﺪ.‬ ‫ﻧﺘﻴﺠﻪ ﮔﻴﺮي: ﺗﺸﺨﻴﺺ و درﻣﺎن زود ﻫﻨﮕﺎم و ﺻﺤﻴﺢ اﻳﻦ ﺑﻴﻤﺎري ﻣﻲﺗﻮاﻧﺪ ﻣﻨﺠﺮ ﺑﻪ ﻛﺎﻫﺶ ﻣﺮگ و ﻣﻴﺮ و ﻋﻮارض ﻧﺎﺷﻲ از‬ ‫ﺑﻴﻤﺎري ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ ﮔﺮدد.ك‬ ‫واژﮔﺎن ﻛﻠﻴﺪي: ﻛﺒﺪ ﭼﺮب، ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ، ﺳﻨﺪروم ﻣﺘﺎﺑﻮﻟﻴﻚ، دﻳﺎﺑﺖ ﺷﻴﺮﻳﻦ، ﭼﺎﻗﻲ، درﻣﺎن‬ ‫ﻓﺼﻠﻨﺎﻣﻪ ﻋﻠﻤﻲ – ﭘﮋوﻫﺸﻲ ﻓﻴﺾ، دوره ﭼﻬﺎردﻫﻢ، ﺷﻤﺎره 2، ﺗﺎﺑﺴﺘﺎن 9831، ﺻﻔﺤﺎت 181-961‬

‫ﻫﻤﺮاﻫﻲ ﺑﻴﻤﺎري ﭘﺮﻓﺸﺎري ﺧﻮن، اﻓﺰاﻳﺶ ﭼﺮﺑﻲ ﺧﻮن، ﭼﺎﻗﻲ و دﻳﺎﺑﺖ‬ ‫ﻛﻪ ﻫﻤﮕﻲ از اﺟﺰاء ﺳﻨﺪروم ﻣﺘﺎﺑﻮﻟﻴﻚ ﻣﻲﺑﺎﺷﻨﺪ، ﺑﺎ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب‬ ‫ﻣﺸﺎﻫﺪه ﺷﺪه اﺳﺖ. ﺑﻪ ﻫﻤﻴﻦ دﻟﻴﻞ ﺑﻌﻀﻲ از ﻣﺤﻘﻘﻴﻦ، ﺑﻴﻤﺎري ﻛﺒﺪ‬ ‫ﭼﺮب را ﺗﻈﺎﻫﺮ ﻛﺒﺪي ﺑﻴﻤﺎري ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ ﻳﺎ ﻫﻤﺎن ﺳﻨﺪروم‬ ‫ﻣﺘﺎﺑﻮﻟﻴﻚ ﻣﻲداﻧﻨﺪ. ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ ﻋﻮارض ﺳﻮﻳﻲ ﺑﺮ دﺳﺘﮕﺎه-‬ ‫ﻫﺎي ﺣﻴﺎﺗﻲ ﺑﺪن ﻣﺎﻧﻨﺪ ﻗﻠﺐ و ﻋﺮوق، ﻛﻠﻴﻪﻫﺎ، ﻣﻐﺰ، اﻋﺼﺎب ﻣﺤﻴﻄﻲ‬ ‫و ﺑﺎﻻﺧﺮه ﻛﺒﺪ ﻣﻲﮔﺬارد؛ ﺑﻪ ﻋﺒﺎرت دﻳﮕﺮ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻣﻲ-‬ ‫ﺗﻮاﻧﺪ ﻧﺸﺎﻧﻪاي از ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ ﺑﺎﺷﺪ و ﺑﻪ ﻫﻤﻴﻦ ﺧﺎﻃﺮ اﺳﺖ‬ ‫ﻛﻪ ﺗﺸﺨﻴﺺ زود ﻫﻨﮕﺎم و درﻣﺎن ﻣﻨﺎﺳﺐ آن ﻧﻪ ﺗﻨﻬﺎ از آﺳﻴﺐ‬ ‫ﺳﻠﻮلﻫﺎي ﻛﺒﺪي، ﻛﻪ از ﻋﻮارض ﻣﻬﻢ ﻗﻠﺒﻲ و ﻋﺮوﻗﻲ آن ﻛﻪ‬ ‫ﻣﻬﻤﺘﺮﻳﻦ ﻋﻠﺖ ﻣﺮگ و ﻣﻴﺮ ﺑﻴﻤﺎران ﻣﺒﺘﻼ ﺑﻪ ﻛﺒﺪ ﭼﺮب اﺳﺖ ﻧﻴﺰ‬ ‫ﺟﻠﻮﮔﻴﺮي ﺧﻮاﻫﺪ ﻛﺮد ]1[. ﺧﻮﺷﺒﺨﺘﺎﻧﻪ اﻛﺜﺮ ﻣﻮارد ﺑﻴﻤﺎري ﻛﺒﺪ‬ ‫ﭼﺮب ﺑﺎ آزﻣﺎﻳﺸﺎت ﺳﺎده ﻛﺒﺪي در ﻧﻤﻮﻧﻪ ﺧﻮن اﻓﺮاد و ﻳﺎ ﺑﺎ اﻧﺠﺎم‬ ‫روشﻫﺎي ﺗﺼﻮﻳﺮ ﺑﺮداري ﺳﺎده ﻣﺎﻧﻨﺪ ﺳﻮﻧﻮﮔﺮاﻓﻲ ﻛﺒﺪ ﻗﺎﺑﻞ ﺗﺸﺨﻴﺺ‬ ‫اﺳﺖ. ﻛﺎﻫﺶ وزن و ﺗﻨﻈﻴﻢ ﻣﻴﺰان ﭼﺮﺑﻲ ﺧﻮن ﺑﻴﻤﺎران در ﭘﻴﺸﮕﻴﺮي از‬ ‫ﭘﻴﺸﺮﻓﺖ آﺳﻴﺐ ﻛﺒﺪي ﻣﻮﺛﺮ اﺳﺖ. ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﺑﺮاي اوﻟﻴﻦ ﺑﺎر‬ ‫در ﺳﺎل 0891 ﺗﻮﺳﻂ ‪ Ludwig‬و ﻫﻤﻜﺎراﻧﺶ ﺷﻨﺎﺳﺎﻳﻲ و ﻣﻌﺮﻓﻲ‬ ‫ﺷﺪ. ﻣﺸﺎﻫﺪه ﺷﺪه ﺑﻮد ﻛﻪ در ﮔﺮوﻫﻲ از ﺑﻴﻤﺎران ﻣﺸﺎﺑﻪ ﻛﺴﺎﻧﻲ ﻛﻪ‬ ‫اﻟﻜﻞ ﻣﺼﺮف ﻣﻲﻛﻨﻨﺪ، آﺳﻴﺐ ﺳﻠﻮلﻫﺎي ﻛﺒﺪي اﺗﻔﺎق ﻣﻲاﻓﺘﺪ، وﻟﻲ‬ ‫در اﻳﻦ ﺑﻴﻤﺎران ﺳﺎﺑﻘﻪاي از ﻣﺼﺮف اﻟﻜﻞ وﺟﻮد ﻧﺪارد. در اﻳﻦ‬ ‫ﺑﻴﻤﺎران ﺷﻮاﻫﺪي از ﺳﺎﻳﺮ ﺑﻴﻤﺎريﻫﺎي ﺳﻠﻮل ﻛﺒﺪ ﻧﻴﺰ وﺟﻮد ﻧﺪاﺷﺖ،‬ ‫وﻟﻲ ﻣﺸﺎﻫﺪه ﺷﺪ ﻛﻪ 09 درﺻﺪ آﻧﺎن ﭼﺎق ﺑﻮده و 52 درﺻﺪ آﻧﺎن‬ ‫اﻓﺰاﻳﺶ ﻣﻴﺰان ﭼﺮﺑﻲ ﺧﻮن و 52 درﺻﺪ ﻧﻴﺰ ﺑﻴﻤﺎري دﻳﺎﺑﺖ دارﻧﺪ ]2[.‬
‫دورﻧﻮﻳﺲ:0098555 1630‬

‫ﻣﻌﺮﻓﻲ ﺑﻴﻤﺎري‬ ‫ﻛﺒﺪ ﻳﻜﻲ از اﻋﻀﺎء ﻣﻬﻢ ﺑﺪن اﺳﺖ ﻛﻪ ﺳﻢزداﻳﻲ از داروﻫﺎ،‬ ‫دﻓﻊ ﻣﺤﺼﻮﻻت زاﻳﺪ ﻧﺎﺷﻲ از ﺗﺨﺮﻳﺐ و ﻧﻮﺳﺎزي ﮔﻠﺒﻮلﻫﺎي ﻗﺮﻣﺰ‬ ‫ﺧﻮن ﺑﻪ ﺻﻮرت ﺻﻔﺮا، ﺗﻮﻟﻴﺪ ﻋﻮاﻣﻞ اﻧﻌﻘﺎدي ﺧﻮن، ذﺧﻴﺮه ﻗﻨﺪ ﺑﻪ‬ ‫ﺻﻮرت ﮔﻠﻴﻜﻮژن و ﻧﻴﺰ ﺗﻨﻈﻴﻢ ﺳﻮﺧﺖ و ﺳﺎز ﻗﻨﺪ و ﭼﺮﺑﻲ از‬ ‫ﻣﻬﻤﺘﺮﻳﻦ ﻧﻘﺶﻫﺎي آن در ﺑﺪن ﻣﻲﺑﺎﺷﺪ؛ اﻟﺒﺘﻪ ﻧﻘﺶ ﻛﺒﺪ در ﺟﺬب‬ ‫ﭼﺮﺑﻲ و دﻓﺎع در ﻣﻘﺎﺑﻞ ﻣﻴﻜﺮوبﻫﺎ و ﺳﻤﻮم ﺟﺬب ﺷﺪه از راه ﻣﻮاد‬ ‫ﻏﺬاﻳﻲ را ﻧﻴﺰ ﻧﺒﺎﻳﺪ ﻧﺎدﻳﺪه ﮔﺮﻓﺖ ]1[. ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﺑﻴﻤﺎري‬ ‫ﺳﻠﻮلﻫﺎي ﻛﺒﺪ اﻧﺴﺎن اﺳﺖ ﻛﻪ اﺧﻴﺮا ﺑﻪ ﻋﻠﺖ اﻓﺰاﻳﺶ ﻣﻴﺰان ﭼﺎﻗﻲ‬ ‫در ﺟﺎﻣﻌﻪ ﻣﺎ اﻓﺰاﻳﺶ ﻳﺎﻓﺘﻪ اﺳﺖ. اﻫﻤﻴﺖ اﻳﻦ ﺑﻴﻤﺎري ﺑﻪ ﺧﺎﻃﺮ‬ ‫ﺗﺨﺮﻳﺐ ﺳﻠﻮلﻫﺎي ﻛﺒﺪي اﺳﺖ و در ﺻﻮرت ﻋﺪم ﺗﺸﺨﻴﺺ‬ ‫زودرس و درﻣﺎن ﻣﻨﺎﺳﺐ ﻣﻲﺗﻮاﻧﺪ ﻣﻨﺠﺮ ﺑﻪ ﺑﻴﻤﺎري ﭘﻴﺸﺮﻓﺘﻪ و ﻏﻴﺮ‬ ‫ﻗﺎﺑﻞ ﺑﺮﮔﺸﺖ ﻛﺒﺪي ﺑﻪ ﻧﺎم »ﺳﻴﺮوز« ﺷﻮد ]1[. ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب‬ ‫ﺷﺎﻣﻞ ﻃﻴﻔﻲ از ﺑﻴﻤﺎري ﺧﻔﻴﻒ ﻛﺒﺪ ﺑﻪ ﺻﻮرت ﺗﺠﻤﻊ ﭼﺮﺑﻲ در‬ ‫ﺳﻠﻮلﻫﺎي ﻛﺒﺪي اﺳﺖ ﻛﻪ در ﺳﻴﺮ ﺧﻮد ﻣﻤﻜﻦ اﺳﺖ در ﮔﺮوﻫﻲ از‬ ‫ﺑﻴﻤﺎران اﻟﺘﻬﺎب ﺳﻠﻮل ﻛﺒﺪي اﻳﺠﺎد ﺷﺪه و ﺑﺎ ﺗﺨﺮﻳﺐ ﺳﻠﻮل ﻛﺒﺪي ﺑﻪ‬ ‫ﺑﻴﻤﺎري ﻣﺰﻣﻦ و ﻏﻴﺮ ﻗﺎﺑﻞ ﺑﺮﮔﺸﺖ ﺑﻪ ﻧﺎم ﺳﻴﺮوز ﻣﻨﺘﻬﻲ ﺷﻮد.‬
‫1 اﺳﺘﺎدﻳﺎر، ﻣﺮﻛﺰ ﺗﺤﻘﻴﻘﺎت ﻋﻠﻮم ﺗﺸﺮﻳﺢ، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﻛﺎﺷﺎن‬ ‫2 دﺑﻴﺮ ﻣﺮﻛﺰ ﺗﺤﻘﻴﻘﺎت ﻋﻠﻤﻲ داﻧﺸﺠﻮﻳﺎن، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان‬ ‫* ﻧﺸﺎﻧﻲ ﻧﻮﻳﺴﻨﺪه ﻣﺴﻮول:‬ ‫ﻛﺎﺷﺎن، ﻛﻴﻠﻮﻣﺘﺮ 5 ﺑﻠﻮار ﻗﻄﺐ راوﻧﺪي، ﺑﻴﻤﺎرﺳﺘﺎن ﺷﻬﻴﺪ ﺑﻬﺸﺘﻲ‬ ‫ﺗﻠﻔﻦ: 6200555 1630‬

‫ﭘﺴﺖ اﻟﻜﺘﺮوﻧﻴﻚ: ‪raika.jamali@gmail.com‬‬ ‫ﺗﺎرﻳﺦ ﭘﺬﻳﺮش ﻧﻬﺎﻳﻲ: 1/3/98‬ ‫ﺗﺎرﻳﺦ درﻳﺎﻓﺖ: 11/21/88‬

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‫‪... ، of SID‬‬ ‫ﻣﺮوري ﺑﺮ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب‪Archive‬‬ ‫ﻫﭙﺎﺗﻴﺖ وﻳﺮوﺳﻲ ‪ A‬و ‪ B‬در اﻳﺮان رو ﺑﻪ ﻛﺎﻫﺶ اﺳﺖ، در ﻋﻮض‬ ‫ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ ﻫﻤﻪﮔﻴﺮي ﭼﺎﻗﻲ در ﻛﺸﻮرﻫﺎي ﺷﺮﻗﻲ ﺑﻪ ﺧﺎﻃﺮ اﻓﺰاﻳﺶ‬ ‫ﺑﻲ ﺗﺤﺮﻛﻲ و روي آوردن ﺑﻪ رژﻳﻢﻫﺎي ﻏﺬاﻳﻲ ﭘﺮﻛﺎﻟﺮي ﺑﻪ ﺳﺒﻚ‬ ‫ﺟﻮاﻣﻊ ﻏﺮﺑﻲ، ﺑﻪ ﻧﻈﺮ ﻣﻲرﺳﺪ ﻛﻪ در ﻛﺸﻮرﻣﺎن ﺷﺎﻫﺪ اﻳﻦ روﻧﺪ‬ ‫ﺻﻌﻮدي اﻓﺰاﻳﺶ ﻣﻴﺰان ﭼﺎﻗﻲ و ﻋﻮارض ﺳﻮء ﻧﺎﺷﻲ از آن ﻣﺎﻧﻨﺪ‬ ‫اﻓﺰاﻳﺶ ﻣﻴﺰان ﭼﺮﺑﻲ ﺧﻮن، ﭘﺮﻓﺸﺎري ﺧﻮن، ﻋﻮارض ﻗﻠﺒﻲ ﻋﺮوﻗﻲ و‬ ‫ﺑﺎﻻﺧﺮه ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﺑﺎﺷﻴﻢ ]21-01[. در ﮔﺰارش وزارت‬ ‫ﺑﻬﺪاﺷﺖ ﻛﺸﻮرﻣﺎن در ﺳﺎل 0831، ﺑﻴﻤﺎري ﭘﻴﺸﺮﻓﺘﻪ و ﻏﻴﺮﻗﺎﺑﻞ‬ ‫ﺑﺮﮔﺸﺖ ﻛﺒﺪي ﻳﺎ ﻫﻤﺎن ﺳﻴﺮوز ﻋﺎﻣﻞ 1 درﺻﺪ ﻣﺮگ و ﻣﻴﺮ اﻓﺮاد‬ ‫ﺑﺎﻻﺗﺮ از 51 ﺳﺎل در اﻳﺮان ﺑﻮده اﺳﺖ ]31[. ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ اﻳﻨﻜﻪ ﻛﺒﺪ‬ ‫ﭼﺮب ﻧﺸﺎﻧﻪاي از درﮔﻴﺮي ﻛﺒﺪ در ﺑﻴﻤﺎري ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ‬ ‫)ﺳﻨﺪروم ﻣﺘﺎﺑﻮﻟﻴﻚ( اﺳﺖ، ﻣﺮگ و ﻣﻴﺮ ﻧﺎﺷﻲ از آن ﺑﻪ ﺻﻮرت‬ ‫اﻓﺰاﻳﺶ ﻣﺮگ و ﻣﻴﺮ ﺑﻪ ﻋﻠﺖ ﻋﻮارض ﻗﻠﺒﻲ ﻋﺮوﻗﻲ اﺳﺖ و آﺳﻴﺐ‬ ‫ﺳﻠﻮلﻫﺎي ﻛﺒﺪي روﻧﺪ ﺑﺴﻴﺎر ﻛﻨﺪي داﺷﺘﻪ و در ﺻﻮرت ﻛﻨﺘﺮل‬ ‫ﻋﻮارض ﻗﻠﺒﻲ در اﻧﺘﻬﺎ ﻣﻲﺗﻮاﻧﺪ ﻣﻨﺠﺮ ﺑﻪ ﺳﻴﺮوز ﻛﺒﺪي ﺷﻮد. ﺑﻪ‬ ‫ﻋﺒﺎرﺗﻲ دﻳﮕﺮ ﺑﻪ ﻧﻈﺮ ﻣﻲرﺳﺪ ﻛﻪ اﻛﺜﺮ ﻣﺒﺘﻼﻳﺎن ﺑﻪ ﻛﺒﺪ ﭼﺮب ﻗﺒﻞ از‬ ‫اﻳﺠﺎد ﺳﻴﺮوز از ﻋﻮارض ﻗﻠﺒﻲ و ﻋﺮوﻗﻲ ﺳﻨﺪروم ﻣﺘﺎﺑﻮﻟﻴﻚ ﻓﻮت‬ ‫ﻣﻲﻛﻨﻨﺪ ]41[.‬ ‫ﻋﻼﺋﻢ ﺑﻴﻤﺎري‬ ‫در اﻛﺜﺮ ﻣﻮارد، ﺑﻴﻤﺎري ﺑﺪون ﻋﻼﻣﺖ اﺳﺖ و ﺑﺎ ﻣﺸﺎﻫﺪه‬ ‫ﺑﺎﻻ ﺑﻮدن آﻧﺰﻳﻢﻫﺎي ﻛﺒﺪي در آزﻣﺎﻳﺶ ﺧﻮن ﻛﻪ ﺑﻪ ﻣﻨﻈﻮر ﺑﺮرﺳﻲ-‬ ‫ﻫﺎي دورهاي ﺳﻼﻣﺖ اﻧﺠﺎم ﻣﻲﺷﻮد و ﻳﺎ در ﺳﻮﻧﻮﮔﺮاﻓﻲ ﺷﻜﻢ ﻛﻪ ﺑﻪ‬ ‫ﻋﻠﻞ دﻳﮕﺮ اﻧﺠﺎم ﻣﻲﺷﻮد، ﺑﻪ ﺻﻮرت اﺗﻔﺎﻗﻲ ﻛﺸﻒ ﻣﻲﮔﺮدد. اﮔﺮ ﭼﻪ‬ ‫ﺑﻌﻀﻲ ﺑﻴﻤﺎران ﺑﻪ ﻧﺪرت از درد ﻣﺒﻬﻢ ﻗﺴﻤﺖ ﺑﺎﻻ و راﺳﺖ ﺷﻜﻢ و‬ ‫ﻳﺎ اﺣﺴﺎس ﺧﺴﺘﮕﻲ زودرس ﺷﻜﺎﻳﺖ دارﻧﺪ.‬ ‫ﻣﻌﺎﻳﻨﻪ ﺑﺎﻟﻴﻨﻲ‬ ‫اﻓﺰاﻳﺶ اﻧﺪازه ﻛﺒﺪ در ﺣﺪود 57 درﺻﺪ ﺑﻴﻤﺎران در ﻣﻌﺎﻳﻨﻪ‬ ‫ﺑﺎﻟﻴﻨﻲ ﻗﺎﺑﻞ ﺗﺸﺨﻴﺺ اﺳﺖ. ﻋﻼﺋﻢ ﺑﻴﻤﺎري ﻣﺰﻣﻦ و ﭘﻴﺸﺮﻓﺘﻪ ﻛﺒﺪي‬ ‫ﻣﺎﻧﻨﺪ آﻧﮋﻳﻮم ﻋﻨﻜﺒﻮﺗﻲ )‪ ،(Spider Angioma‬ﺳﺮﺧﻲ ﻛﻒ دﺳﺖ‬ ‫)‪ ،(Palmar Erythema‬ﺗﺠﻤﻊ ﻣﺎﻳﻊ در ﺷﻜﻢ و ﺑﺰرﮔﻲ ﻃﺤﺎل در‬ ‫ﺗﻌﺪاد ﺑﺴﻴﺎر اﻧﺪﻛﻲ از ﺑﻴﻤﺎران ﻛﻪ ﺗﺸﺨﻴﺺ در آنﻫﺎ ﺑﻪ ﺗﺎﺧﻴﺮ اﻓﺘﺎده‬ ‫اﺳﺖ، ﻗﺎﺑﻞ ﻣﺸﺎﻫﺪه اﺳﺖ.‬ ‫ﻋﻠﻞ‬ ‫ﻋﻠﻞ ﺑﻴﻤﺎري را ﻣﻲﺗﻮان ﺑﻪ دو ﮔﺮوه ﻛﻠﻲ ﺗﻘﺴﻴﻢ ﻛﺮد. ﮔﺮوه‬ ‫اول داروﻫﺎ و ﺳﻤﻮم و ﮔﺮوه دوم اﺧﺘﻼﻻت ﺳﻮﺧﺖ و ﺳﺎز ﻣﻲﺑﺎﺷﻨﺪ.‬ ‫ﻋﻠﻞ اﺣﺘﻤﺎﻟﻲ اﻳﺠﺎد ﻛﻨﻨﺪه ﺑﻴﻤﺎري در ﺟﺪول ﺷﻤﺎره 1 ﻧﺸﺎن داده‬ ‫ﺷﺪهاﻧﺪ.‬ ‫ﻫﻤﻪ ﮔﻴﺮ ﺷﻨﺎﺳﻲ‬ ‫ﺑﻪ ﻧﻈﺮ ﻣﻲرﺳﺪ ﻛﻪ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب از ﺷﺎﻳﻊﺗﺮﻳﻦ‬ ‫ﺑﻴﻤﺎريﻫﺎي ﻛﺒﺪي در دﻧﻴﺎ ﺑﺎﺷﺪ و ﻣﻴﺰان ﺷﻴﻮع آن در ﺟﻮاﻣﻊ‬ ‫ﻣﺨﺘﻠﻒ از 8/2 درﺻﺪ ﺗﺎ 42 درﺻﺪ ﻣﺘﻔﺎوت اﺳﺖ ]3،4[. ﺣﺴﺎﺳﻴﺖ‬ ‫ﺗﺸﺨﻴﺼﻲ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﺑﺎ روشﻫﺎي آزﻣﺎﻳﺸﮕﺎﻫﻲ ﺑﺴﺘﮕﻲ ﺑﻪ‬ ‫ﺗﻌﺮﻳﻒ ﺳﻄﺢ ﻃﺒﻴﻌﻲ آﻧﺰﻳﻢﻫﺎي ﻛﺒﺪ در ﺳﺮم دارد ]5[. در ﻣﻄﺎﻟﻌﻪاي‬ ‫ﻛﻪ در اﻳﺮان ﺑﺮ روي ﺟﻤﻌﻴﺖ ﻋﻤﻮﻣﻲ اﻧﺠﺎم ﺷﺪ، ﻣﺸﺎﻫﺪه ﺷﺪه اﺳﺖ‬ ‫ﻛﻪ ﺳﻄﺢ ﻃﺒﻴﻌﻲ اﻳﻦ آﻧﺰﻳﻢﻫﺎ در ﺳﺮم از ﺳﻄﺢ ﻃﺒﻴﻌﻲ اراﺋﻪ ﺷﺪه‬ ‫ﺗﻮﺳﻂ ﺷﺮﻛﺖﻫﺎي ﺳﺎزﻧﺪه اﺑﺰار اﻧﺪازهﮔﻴﺮي آزﻣﺎﻳﺸﮕﺎﻫﻲ ﭘﺎﺋﻴﻦﺗﺮ‬ ‫اﺳﺖ و ﺑﻪ ﻧﻈﺮ ﻣﻲرﺳﺪ ﻛﻪ ﻣﻴﺰان ﻃﺒﻴﻌﻲ آﻧﺰﻳﻢﻫﺎي ﻛﺒﺪي ﺑﺮ اﺳﺎس‬ ‫ﺟﻨﺲ و وزن ﺑﺎﻳﺪ ﺑﻪﻃﻮر ﺟﺪاﮔﺎﻧﻪ ﺗﻌﻴﻴﻦ و ﺗﻔﺴﻴﺮ ﺷﻮد ]5[؛ ﺑﻪ‬ ‫ﻋﺒﺎرت دﻳﮕﺮ ﺑﺎ ﺗﻐﻴﻴﺮ ﺳﻄﺢ ﻃﺒﻴﻌﻲ ﺳﺮﻣﻲ آﻧﺰﻳﻢﻫﺎي ﻛﺒﺪي‬ ‫ﺣﺴﺎﺳﻴﺖ روشﻫﺎي آزﻣﺎﻳﺸﮕﺎﻫﻲ در ﺗﺸﺨﻴﺺ ﺑﻴﻤﺎري ﺗﻐﻴﻴﺮ ﻣﻲﻛﻨﺪ‬ ‫]5[. ﻫﻤﭽﻨﻴﻦ ﻣﻴﺰان ﺷﻨﺎﺳﺎﻳﻲ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﺑﺮ اﺳﺎس ﺣﺴﺎﺳﻴﺖ‬ ‫روش ﺗﺼﻮﻳﺮﺑﺮداري ﺑﻪ ﻛﺎر رﻓﺘﻪ ﻣﺘﻔﺎوت اﺳﺖ؛ در ﻧﺘﻴﺠﻪ ﺷﻴﻮع اﻳﻦ‬ ‫ﺑﻴﻤﺎري ﻧﻴﺰ در ﻣﻄﺎﻟﻌﺎت ﻣﺨﺘﻠﻒ ﺑﺮ اﺳﺎس روش ﺗﺼﻮﻳﺮﺑﺮداري ﺑﻪ‬ ‫ﻛﺎر رﻓﺘﻪ، ﻣﺘﻔﺎوت ﺧﻮاﻫﺪ ﺑﻮد. در ﻣﻄﺎﻟﻌﻪاي ﻣﻴﺰان ﺷﻴﻮع ﻛﺒﺪ ﭼﺮب‬ ‫ﺑﺮ اﺳﺎس ﻳﺎﻓﺘﻪﻫﺎي ﺳﻮﻧﻮﮔﺮاﻓﻲ ﻛﺒﺪ 86 درﺻﺪ ﺑﻮده اﺳﺖ. زﻣﺎﻧﻲ ﻛﻪ‬ ‫از روش »ام آر آي« ﺟﻬﺖ ﺗﺸﺨﻴﺺ ﺑﻴﻤﺎري اﺳﺘﻔﺎده ﺷﻮد، ﺷﻴﻮع‬ ‫ﺑﻴﻤﺎري در ﻫﻤﻴﻦ ﺟﻤﻌﻴﺖ ﺑﻪ ﺣﺪود 04 درﺻﺪ ﻣﻲرﺳﺪ ]6[. ﺷﺎﻳﺎن‬ ‫ذﻛﺮ اﺳﺖ ﻛﻪ 08 درﺻﺪ اﻓﺮادي ﻛﻪ در »ام آر آي« ﻛﺒﺪ ﭼﺮب‬ ‫دارﻧﺪ، آزﻣﺎﻳﺸﺎت ﻛﺒﺪي ﻃﺒﻴﻌﻲ دارﻧﺪ. اﻳﻦ ﻧﻜﺘﻪ ﻧﺸﺎن دﻫﻨﺪهي‬ ‫ﺿﻌﻒ روشﻫﺎي آزﻣﺎﻳﺸﮕﺎﻫﻲ در ﺗﺸﺨﻴﺺ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب‬ ‫اﺳﺖ. در ﺻﻮرﺗﻲ ﻛﻪ از روشﻫﺎي آزﻣﺎﻳﺸﮕﺎﻫﻲ ﺟﻬﺖ ﺗﺸﺨﻴﺺ‬ ‫ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب اﺳﺘﻔﺎده ﺷﻮد، ﻓﻘﻂ 5 ﺗﺎ 8 درﺻﺪ ﺑﻴﻤﺎران ﻗﺎﺑﻞ‬ ‫ﺷﻨﺎﺳﺎﻳﻲ ﺧﻮاﻫﻨﺪ ﺑﻮد؛ ﺑﻨﺎﺑﺮاﻳﻦ روشﻫﺎي آزﻣﺎﻳﺸﮕﺎﻫﻲ ﺑﻪ ﺗﻨﻬﺎﻳﻲ‬ ‫آزﻣﻮن ﻣﻨﺎﺳﺒﻲ ﺟﻬﺖ ﺷﻨﺎﺳﺎﻳﻲ اﻳﻦ ﺑﻴﻤﺎري ﻧﻴﺴﺘﻨﺪ ]7[. ﺑﺮ اﺳﺎس‬ ‫ﻣﻄﺎﻟﻌﺎﺗﻲ ﻛﻪ از روش ﻧﻤﻮﻧﻪﺑﺮداري ﺑﺎﻓﺘﻲ ﻛﺒﺪ ﺟﻬﺖ ﺷﻨﺎﺳﺎﻳﻲ‬ ‫ﺑﻴﻤﺎري در ﺟﺎﻣﻌﻪ اﺳﺘﻔﺎده ﻛﺮده اﻧﺪ، ﻣﺸﺎﻫﺪه ﺷﺪه اﺳﺖ ﻛﻪ ﺷﻴﻮع‬ ‫ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﺣﺪود 64 درﺻﺪ ﺑﻮده اﺳﺖ ]8[. ﻣﻴﺰان ﺷﻴﻮع‬ ‫ﻛﺒﺪ ﭼﺮب در ﺟﺎﻣﻌﻪ ﺑﺎ ﺷﻴﻮع ﭼﺎﻗﻲ ارﺗﺒﺎط دارد ]7[ و ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ‬ ‫اﻃﻼﻋﺎت ﻣﻮﺟﻮد، ﺷﻴﻮع ﺑﻴﻤﺎري در ﻣﺮد و زن ﻳﻜﺴﺎن اﺳﺖ ]9[. اﮔﺮ‬ ‫ﭼﻪ ﺗﺎﻛﻨﻮن در اﻳﻦ ﺑﻴﻤﺎري ﻫﻴﭻ ﺷﺎﺧﺺ ژﻧﺘﻴﻜﻲ ﻛﺸﻒ ﻧﺸﺪه اﺳﺖ،‬ ‫اﻣﺎ اﻓﺰاﻳﺶ ﺷﻴﻮع ﺑﻴﻤﺎري در ﺑﻌﻀﻲ ﺧﺎﻧﻮادهﻫﺎ ﻣﺸﺎﻫﺪه ﺷﺪه اﺳﺖ.‬ ‫اﻳﻦ ﺑﻴﻤﺎري ﺷﺎﻳﻊﺗﺮﻳﻦ ﻋﻠﺖ اﻓﺰاﻳﺶ آﻧﺰﻳﻢﻫﺎي ﻛﺒﺪي و ﻧﻴﺰ ﺑﻴﻤﺎري‬ ‫ﺳﻴﺮوز ﻛﺒﺪي ﺑﺎ ﻋﻠﺖ ﻧﺎﺷﻨﺎﺧﺘﻪ ﻣﻲﺑﺎﺷﺪ ]7[. ﻣﻄﺎﻟﻌﺎت اﻧﺠﺎم ﺷﺪه در‬ ‫اﻳﻦ زﻣﻴﻨﻪ در اﻳﺮان ﻣﺤﺪود اﺳﺖ. در ﻣﻄﺎﻟﻌﻪاي ﻛﻪ در اﺳﺘﺎن ﮔﻠﺴﺘﺎن‬ ‫در ﺳﺎل 5831 اﻧﺠﺎم ﺷﺪ، ﻣﻴﺰان ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب 2 درﺻﺪ در‬ ‫ﺟﻤﻌﻴﺖ ﻋﻤﻮﻣﻲ ﺑﺎﻻﺗﺮ از 81 ﺳﺎل ﮔﺰارش ﺷﺪ ]7[. اﮔﺮ ﭼﻪ ﻣﻴﺰان‬

‫ﻓﺼﻠﻨﺎﻣﻪ ﻓﻴﺾ| ﺗﺎﺑﺴﺘﺎن 9831| دوره 41| ﺷﻤﺎره 2‬

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‫ﺟﺪول ﺷﻤﺎره 1 – ﻋﻠﻞ ﺑﺮوز ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب‬
‫ﻣﻮارد ﻣﺘﻔﺮﻗﻪ‬ ‫ﺳﻨﺪروم رﺷﺪ ﺑﻴﺶ از ﺣﺪ ﺑﺎﻛﺘﺮيﻫﺎي روده‬ ‫ﻛﻢ ﺧﻮﻧﻲ ﺷﺪﻳﺪ‬ ‫ﺗﻐﺬﻳﻪ ورﻳﺪي ﻛﺎﻣﻞ‬ ‫ﺑﻴﻤﺎري اﻟﺘﻬﺎﺑﻲ روده‬ ‫ﻟﻴﭙﻮدﻳﺴﺘﺮوﻓﻲ‬ ‫ﺑﻴﻤﺎري ﻫﺎي ﻣﺎدرزادي ﻛﺒﺪ‬ ‫ﮔﺎﻻﻛﺘﻮزﻣﻲ‬ ‫ﺑﻴﻤﺎريﻫﺎي ذﺧﻴﺮه ﮔﻠﻴﻜﻮژن‬ ‫ﻫﻮﻣﻮﺳﻴﺴﺘﻴﻦ اوري‬ ‫ﺗﻴﺮوزﻳﻨﻤﻲ‬ ‫ﺑﻴﻤﺎري وﻳﻠﺴﻮن‬ ‫داروﻫﺎ‬ ‫ﻣﺘﻮﺗﺮوﻛﺴﺎت‬ ‫ال آﺳﭙﺎرژﻳﻨﺎز‬ ‫ﺑﻠﺌﻮﻣﺎﻳﺴﻴﻦ‬ ‫ﺗﺘﺮاﺳﻴﻜﻠﻴﻦ‬ ‫آﻣﻴﻮ دارون‬ ‫اﺳﺘﺮوژن‬ ‫داروﻫﺎي ﺿﺪ وﻳﺮوس اﻳﺪز‬ ‫ﻫﻴﺪرازﻳﻦ‬ ‫ﺗﺎﻣﻮﻛﺴﻴﻔﻦ‬ ‫اﻋﻤﺎل ﺟﺮاﺣﻲ‬ ‫ﺑﺮداﺷﺘﻦ ﻗﺴﻤﺖ وﺳﻴﻌﻲ از روده ﺑﺎرﻳﻚ‬ ‫ﻣﻴﺎنﺑﺮ زدن ﻣﻌﺪه ﻳﺎ ژژوﻧﻮم‬

‫راﻳﻜﺎ و ارﺳﻴﺎ ﺟﻤﺎﻟﻲ‬

‫ﻓﻠﺰات‬ ‫ﻓﺴﻔﺮ‬ ‫ﺗﺮﻛﻴﺒﺎت اوراﻧﻴﻮم‬ ‫ﺗﺮﻛﻴﺒﺎت ﺗﺎﻟﻴﻮم‬ ‫ﻛﺮوﻣﺎت‬ ‫آﻧﺘﻴﻤﻮان‬

‫اﺧﺘﻼﻻت ﻣﺘﺎﺑﻮﻟﻴﻚ‬ ‫دﻳﺎﺑﺖ‬ ‫ﭼﺎﻗﻲ‬ ‫اﻓﺰاﻳﺶ ﭼﺮﺑﻲ ﺧﻮن‬ ‫ﮔﺮﺳﻨﮕﻲ ﻃﻮﻻﻧﻲ‬

‫* اﻳﻦ ﺟﺪول ﺑﺮﮔﺮﻓﺘﻪ از ﻣﺒﺤﺚ ﻋﻠﻞ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب از ﻛﺘﺎب ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻧﻮﺷﺘﻪ ﻣﻮﻟﻔﻴﻦ ﻫﻤﻴﻦ ﻣﻘﺎﻟﻪ ﻣﻲ ﺑﺎﺷﺪ.‬

‫ﻛﺒﺪ ﺧﺎرج ﻣﻲﺷﻮﻧﺪ. اﻳﻦ روﻧﺪ ﺗﺤﺖ ﺗﺎﺛﻴﺮ ﻫﻮرﻣﻮنﻫﺎ و ﺑﻪ ﺧﺼﻮص‬ ‫اﻧﺴﻮﻟﻴﻦ ﺗﻨﻈﻴﻢ ﻣﻲﺷﻮد. اﻧﺒﺎﺷﺘﻪ ﺷﺪن ﭼﺮﺑﻲ در ﺳﻠﻮل ﻛﺒﺪي ﻫﻨﮕﺎﻣﻲ‬ ‫اﺗﻔﺎق ﻣﻲاﻓﺘﺪ ﻛﻪ روﻧﺪ ﺗﻮﻟﻴﺪ ﭼﺮﺑﻲﻫﺎ اﻓﺰاﻳﺶ ﻳﺎﻓﺘﻪ و ﺗﺮﺷﺢ آنﻫﺎ از‬ ‫ﻛﺒﺪ ﻣﺨﺘﻞ ﺷﻮد. اﻳﻦ ﭘﺪﻳﺪه زﻣﺎﻧﻲ اﺗﻔﺎق ﻣﻲاﻓﺘﺪ ﻛﻪ ﻣﻴﺰان ﭼﺮﺑﻲﻫﺎي‬ ‫ورودي ﺑﻪ ﻛﺒﺪ اﻓﺰاﻳﺶ ﻳﺎﻓﺘﻪ و ﻳﺎ ﺑﻪ ﻋﻠﺖ اﺧﺘﻼل در ﻣﻴﺘﻮﻛﻨﺪري ﻫﺎ‬ ‫روﻧﺪ ﺗﻮﻟﻴﺪ و ﺗﺮﺷﺢ ﻓﺴﻔﻮﻟﻴﭙﻴﺪﻫﺎ ﻛﺎﻫﺶ ﻳﺎﺑﺪ. ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ ﺑﻪ‬ ‫ﻋﻨﻮان اوﻟﻴﻦ ﻋﺎﻣﻞ دﺧﻴﻞ در روﻧﺪ ﻓﻮق ﻣﻮرد ﻣﻄﺎﻟﻌﻪ ﻗﺮار ﮔﺮﻓﺘﻪ‬ ‫اﺳﺖ ) ﺷﻜﻞ ﺷﻤﺎره 1(. اﻓﺮاد ﻣﺒﺘﻼ ﺑﻪ ﺑﻴﻤﺎري ﻗﻨﺪ و ﻳﺎ ﭼﺎﻗﻲ، داراي‬ ‫ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ ﻫﺴﺘﻨﺪ ﻛﻪ اﻳﻦ اﻣﺮ ﺧﻮد ﺑﺎﻋﺚ اﻓﺰاﻳﺶ اﺳﻴﺪﻫﺎي‬ ‫ﭼﺮب ﻣﻮﺟﻮد در ﻛﺒﺪ ﻣﻲﺷﻮد. اﻧﺒﺎﺷﺘﻪ ﺷﺪن اﻳﻦ ﻣﻮاد در ﺳﻠﻮل‬ ‫ﻛﺒﺪي ﻣﺨﺮب ﻣﻲﺑﺎﺷﺪ و ﻣﻲﺗﻮاﻧﺪ ﻣﻨﺠﺮ ﺑﻪ ﻣﺮگ ﺳﻠﻮل ﻛﺒﺪي ﺷﻮد‬ ‫]81[. ﺑﺎ ﺗﻀﻌﻴﻒ ﻋﻮاﻣﻠﻲ ﻛﻪ ﺳﺒﺐ ﺧﺮوج ﭼﺮﺑﻲ از ﺳﻠﻮلﻫﺎي‬ ‫ﻛﺒﺪي ﻣﻲﺷﻮﻧﺪ )اﻛﺴﻴﺪاﺳﻴﻮن و ﺳﻮﺧﺖ ﭼﺮﺑﻲ( و ﻏﻠﺒﻪ ﻋﻮاﻣﻠﻲ ﻛﻪ‬ ‫ﺳﺒﺐ اﻓﺰاﻳﺶ ورود ﭼﺮﺑﻲ ﺑﻪ ﺳﻠﻮل ﻛﺒﺪي ﻣﻲﺷﻮﻧﺪ )ﻣﻘﺎوﻣﺖ ﺑﻪ‬ ‫اﻧﺴﻮﻟﻴﻦ( اﻧﺒﺎﺷﺘﮕﻲ ﭼﺮﺑﻲ در داﺧﻞ ﺳﻠﻮلﻫﺎي ﻛﺒﺪي ﺑﻪ وﺟﻮد ﻣﻲ-‬ ‫آﻳﺪ.‬

‫ﭼﺎﻗﻲ از ﻣﻬﻤﺘﺮﻳﻦ ﺑﻴﻤﺎريﻫﺎي ﻫﻤﺮاه ﺑﺎ ﻛﺒﺪ ﭼﺮب اﺳﺖ. اﻟﺒﺘﻪ‬ ‫اﻓﺰاﻳﺶ ﻣﻴﺰان ﭼﺮﺑﻲ ﺷﻜﻤﻲ ﻛﻪ ﺑﺎ ﺷﺎﺧﺺ اﻧﺪازه دور ﻛﻤﺮ ﺑﻪ دور‬ ‫ﺑﺎﺳﻦ اﻧﺪازهﮔﻴﺮي ﻣﻲﺷﻮد، ﻧﺴﺒﺖ ﺑﻪ ﭼﺎﻗﻲ ﻛﻞ ﺑﺪن ﺷﺎﺧﺺ‬ ‫ﻣﻬﻤﺘﺮي ﺑﺮاي ﺑﺮوز ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب اﺳﺖ ]51[. اﻓﺰاﻳﺶ ﭼﺮﺑﻲ‬ ‫ﺧﻮن از دﻳﮕﺮ اﺟﺰاء ﺳﻨﺪروم ﻣﺘﺎﺑﻮﻟﻴﻚ اﺳﺖ ﻛﻪ ﺑﺎ ﺑﻴﻤﺎري ﻛﺒﺪ‬ ‫ﭼﺮب ارﺗﺒﺎط دارد و درﻣﺎن ﻣﻨﺎﺳﺐ اﻓﺰاﻳﺶ ﭼﺮﺑﻲ ﺧﻮن ﻣﻨﺠﺮ ﺑﻪ‬ ‫ﻛﺎﻫﺶ روﻧﺪ ﺗﺨﺮﻳﺐ ﺳﻠﻮلﻫﺎي ﻛﺒﺪي در ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻣﻲ-‬ ‫ﮔﺮدد. ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ ﻛﻪ ﻣﻘﺪﻣﻪاي در اﻳﺠﺎد ﺑﻴﻤﺎري ﻗﻨﺪ‬ ‫)دﻳﺎﺑﺖ( اﺳﺖ، اﺳﺎس اﻳﺠﺎد ﺳﻨﺪروم ﻣﺘﺎﺑﻮﻟﻴﻚ ﺑﻮده و ﺣﺘﻲ ﻗﺒﻞ از‬ ‫ﺑﺮوز دﻳﺎﺑﺖ آﺷﻜﺎر ﻣﻲﺗﻮاﻧﺪ ﺑﺮ ﺳﻠﻮلﻫﺎي ﻛﺒﺪي آﺛﺎر ﺳﻮء ﺑﮕﺬارد.‬ ‫ﺳﻨﺪروم ﻣﺘﺎﺑﻮﻟﻴﻚ ﻣﺠﻤﻮﻋﻪاي از ﺑﻴﻤﺎريﻫﺎي ﭘﺮﻓﺸﺎري ﺧﻮن،‬ ‫اﻓﺰاﻳﺶ ﭼﺮﺑﻲ ﺧﻮن، ﭼﺎﻗﻲ و دﻳﺎﺑﺖ اﺳﺖ و ﻣﻄﺎﻟﻌﺎت اﺧﻴﺮ ﺣﺎﻛﻲ‬ ‫از آن ﻫﺴﺘﻨﺪ ﻛﻪ ﺑﺎ اﻓﺰاﻳﺶ ﺗﻌﺪاد ﺑﻴﻤﺎريﻫﺎي ﺗﺸﻜﻴﻞ دﻫﻨﺪهي اﻳﻦ‬ ‫ﺳﻨﺪروم، ﺷﺪت ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻧﻴﺰ اﻓﺰاﻳﺶ ﻣﻲﻳﺎﺑﺪ ]61[.‬ ‫ﻓﺮآﻳﻨﺪ اﻳﺠﺎد ﺑﻴﻤﺎري‬ ‫ﺑﻪ دﻟﻴﻞ ﻛﻢ ﺑﻮدن اﻟﮕﻮﻫﺎي ﺣﻴﻮاﻧﻲ ﻣﻨﺎﺳﺐ ﺟﻬﺖ ﻣﻘﺎﻳﺴﻪ ﺑﺎ‬ ‫ﻛﺒﺪ ﭼﺮب اﻧﺴﺎن، روﻧﺪ اﻳﺠﺎد ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﺑﻪ ﺧﻮﺑﻲ ﺷﻨﺎﺧﺘﻪ‬ ‫ﺷﺪه ﻧﻴﺴﺖ. ﻗﺎﺑﻞ ﻗﺒﻮل ﺗﺮﻳﻦ ﻓﺮﺿﻴﻪ در ﺳﺎل 8991 ﺗﻮﺳﻂ ‪ Day‬و‬ ‫‪ James‬ﺑﻪ اﻳﻦ ﺻﻮرت ﺑﻴﺎن ﺷﺪ ﻛﻪ اوﻟﻴﻦ اﺗﻔﺎق، اﺧﺘﻼل در‬ ‫ﺳﻮﺧﺖ و ﺳﺎز اﺳﻴﺪﻫﺎي ﭼﺮب در ﻛﺒﺪ اﺳﺖ ﻛﻪ ﺗﺤﺖ ﺗﺎﺛﻴﺮ ﻳﻚ ﻳﺎ‬ ‫ﭼﻨﺪ ﻣﺤﺮك ﻣﺤﻴﻄﻲ و ﻳﺎ ژﻧﺘﻴﻜﻲ ﻣﻨﺠﺮ ﺑﻪ اﻳﺠﺎد اﻟﺘﻬﺎب و ﺗﺨﺮﻳﺐ‬

‫ﺷﻜﻞ ﺷﻤﺎره 1- ﻧﻘﺶ ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ دراﻳﺠﺎد ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب‬ ‫ﺳﻪ ﻋﺎﻣﻞ ﻣﻬﻢ در روﻧﺪ اﻳﺠﺎد ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﺷﻨﺎﺧﺘﻪ ﺷﺪهاﻧﺪ ﻛﻪ‬ ‫ﺷﺎﻣﻞ اﺳﻴﺪﻫﺎي ﭼﺮب، واﺳﻄﻪ ﻫﺎي ﺷﻴﻤﻴﺎﻳﻲ ﺑﻪ ﻧﺎمﻫﺎي »‪ «TNFα‬و‬ ‫»آدﻳﭙﻮﻧﻜﺘﻴﻦ« ﻣﻲﺑﺎﺷﻨﺪ ]91[. اﺳﻴﺪﻫﺎي ﭼﺮب ﺑﻪ ﻃﻮر ﻃﺒﻴﻌﻲ ﺑﻴﻦ‬ ‫ﺑﺎﻓﺖ ﭼﺮﺑﻲ و ﺳﻠﻮلﻫﺎي ﻛﺒﺪي ﻣﺒﺎدﻟﻪ ﻣﻲﺷﻮﻧﺪ. واﺳﻄﻪﻫﺎي ﺷﻴﻤﻴﺎﻳﻲ‬ ‫ذﻛﺮ ﺷﺪه ﻧﻴﺰ در ﺑﺎﻓﺖ ﭼﺮﺑﻲ و ﻛﺒﺪ وﺟﻮد دارﻧﺪ. »آدﻳﭙﻮﻧﻜﺘﻴﻦ« ﺑﺎ‬

‫ﺳﻠﻮلﻫﺎي ﻛﺒﺪي و در ﻧﻬﺎﻳﺖ اﻳﺠﺎد ﺑﺎﻓﺖ ﺟﻮﺷﮕﺎﻫﻲ در ﻛﺒﺪ و‬ ‫ﺳﻴﺮوز ﻣﻲﺷﻮد ]71[. اﻓﺰاﻳﺶ ﻣﻴﺰان ﭼﺮﺑﻲ ﺳﻠﻮلﻫﺎي ﻛﺒﺪي‬ ‫ﻣﻬﻤﺘﺮﻳﻦ ﻳﺎﻓﺘﻪ ﺑﺎﻓﺖ ﺷﻨﺎﺳﻲ اﺳﺖ. در ﺣﺎﻟﺖ ﻃﺒﻴﻌﻲ اﺳﻴﺪﻫﺎي ﭼﺮب‬ ‫از ﻃﺮﻳﻖ ﺟﺮﻳﺎن ﺧﻮن رودهﻫﺎ ﺑﻪ ﻛﺒﺪ ﻣﻨﺘﻘﻞ ﺷﺪه، در آﻧﺠﺎ ﺗﻮﺳﻂ‬ ‫ﻳﻜﻲ از اﻋﻀﺎء ﻣﻬﻢ ﺳﻠﻮلﻫﺎي ﻛﺒﺪي ﺑﻪ ﻧﺎم ﻣﻴﺘﻮﻛﻨﺪري ﻛﻪ ﻣﻨﺒﻊ‬ ‫ﺗﻮﻟﻴﺪ اﻧﺮژي ﺳﻠﻮﻟﻲ ﻫﺴﺘﻨﺪ، ﺗﻐﻴﻴﺮ ﻳﺎﻓﺘﻪ و ﺑﻪ ﺻﻮرت ﻓﺴﻔﻮﻟﻴﭙﻴﺪ از‬

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‫ﻓﺼﻠﻨﺎﻣﻪ ﻓﻴﺾ| ﺗﺎﺑﺴﺘﺎن 9831| دوره 41| ﺷﻤﺎره 2‬ ‫‪www.SID.ir‬‬

‫‪... ، of SID‬‬ ‫ﻣﺮوري ﺑﺮ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب‪Archive‬‬ ‫ﭼﻪ ﺑﺎﻳﺪ در ﻧﻈﺮ داﺷﺖ ﻛﻪ در ﮔﺮوه اﻧﺪﻛﻲ از ﺑﻴﻤﺎران ﻛﻪ اﻟﺘﻬﺎب‬ ‫ﺳﻠﻮل ﻛﺒﺪي و ﺗﺨﺮﻳﺐ ﺑﺎﻓﺘﻲ و ﺑﻪ دﻧﺒﺎل آن ﺟﺎي ﮔﺰﻳﻨﻲ ﺑﺎﻓﺖ‬ ‫ﺟﻮﺷﮕﺎﻫﻲ)ﻓﻴﺒﺮوز( وﺟﻮد دارد، ﻣﻤﻜﻦ اﺳﺖ ﺑﻴﻤﺎر ﺑﻪ ﺳﻤﺖ ﺑﻴﻤﺎري‬ ‫ﭘﻴﺸﺮﻓﺘﻪ و ﻣﺰﻣﻦ ﻛﺒﺪي )ﺳﻴﺮوز( و ﺣﺘﻲ ﺑﺪﺧﻴﻤﻲ ﺳﻠﻮل ﻛﺒﺪي‬ ‫ﻣﻨﺘﻬﻲ ﺷﻮد ]02[. در ﻳﻚ ﻣﻄﺎﻟﻌﻪ ﻣﻴﺰان ﭘﻴﺸﺮﻓﺖ آﺳﻴﺐ ﻛﺒﺪي در 23‬ ‫ﺗﺎ 05 درﺻﺪ ﺑﻴﻤﺎران و ﺳﻴﺮوز در 02 درﺻﺪ ﺑﻴﻤﺎران ﮔﺰارش ﺷﺪ‬ ‫]12[. در ﺣﺎل ﺣﺎﺿﺮ ﻧﻤﻮﻧﻪ ﺑﺎﻓﺖ ﺷﻨﺎﺳﻲ ﻛﺒﺪ ﺑﻬﺘﺮﻳﻦ ﻣﻌﻴﺎر ﺟﻬﺖ‬ ‫ﺑﺮرﺳﻲ ﺳﻴﺮ و ﺷﺪت درﮔﻴﺮي ﻛﺒﺪ ﻣﻲﺑﺎﺷﺪ؛ ﺑﻪ ﻃﻮري ﻛﻪ ﻫﺮ ﭼﻪ‬ ‫ﻣﻴﺰان اﻟﺘﻬﺎب و وﺳﻌﺖ درﮔﻴﺮي ﺳﻠﻮل ﻛﺒﺪي ﺑﻴﺸﺘﺮ ﺑﺎﺷﺪ، ﺳﻴﺮ‬ ‫ﺑﻴﻤﺎري ﺳﺮﻳﻊﺗﺮ ﺧﻮاﻫﺪ ﺑﻮد ]22[. ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب اﺣﺘﻤﺎﻻ ﺷﺎﻳﻊ-‬ ‫ﺗﺮﻳﻦ ﻋﻠﺖ ﺳﻴﺮوز ﺑﺎ ﻋﻠﺖ ﻧﺎﺷﻨﺎﺧﺘﻪ ﻣﻲﺑﺎﺷﺪ ]32[. در ﻣﻄﺎﻟﻌﻪاي ﻛﻪ‬ ‫ﺟﻬﺖ ﻣﻘﺎﻳﺴﻪ ﻋﻮارض ﺳﻴﺮوز و اﻳﺠﺎد ﺑﺪﺧﻴﻤﻲ ﺳﻠﻮل ﻛﺒﺪي ﺑﻴﻦ‬ ‫ﺑﻴﻤﺎران ﺳﻴﺮوزي ﺑﻪ ﻋﻠﺖ وﻳﺮوس ﻫﭙﺎﺗﻴﺖ ‪ C‬و ﻛﺒﺪ ﭼﺮب اﻧﺠﺎم‬ ‫ﺷﺪ، ﻣﺸﺎﻫﺪه ﮔﺮدﻳﺪ ﻛﻪ ﻣﺮگ و ﻣﻴﺮ و ﻋﻮارض ﻧﺎﺷﻲ از ﺳﻴﺮوز در‬ ‫ﻫﺮ 2 ﮔﺮوه از ﺑﻴﻤﺎران ﻣﺸﺎﺑﻪ ﺑﻮده، وﻟﻲ ﻣﻴﺰان اﺑﺘﻼء ﺑﻪ ﺑﺪﺧﻴﻤﻲ‬ ‫ﺳﻠﻮل ﻛﺒﺪي در ﻣﺒﺘﻼﻳﺎن ﺑﻪ ﺳﻴﺮوز ﻧﺎﺷﻲ از ﻛﺒﺪ ﭼﺮب از ﻣﺒﺘﻼﻳﺎن‬ ‫ﺑﻪ ﺳﻴﺮوز ﻧﺎﺷﻲ از ﻫﭙﺎﺗﻴﺖ ‪ C‬ﻛﻤﺘﺮ اﺳﺖ ]42[. ﻫﻤﺎن ﻃﻮر ﻛﻪ ﻗﺒﻼ‬ ‫اﺷﺎره ﺷﺪ، در ﺣﺎل ﺣﺎﺿﺮ ﻧﻤﻮﻧﻪ ﺑﺎﻓﺖ ﺷﻨﺎﺳﻲ ﻛﺒﺪ ﺑﻬﺘﺮﻳﻦ ﻣﻌﻴﺎر‬ ‫ﺟﻬﺖ ﺑﺮرﺳﻲ ﻣﻴﺰان و ﺷﺪت آﺳﻴﺐ ﻛﺒﺪي و ﻧﻴﺰ ﺗﻌﻴﻴﻦ ﭘﻴﺶ آﮔﻬﻲ‬ ‫و ﺳﻴﺮ ﺑﻴﻤﺎري ﻣﻲﺑﺎﺷﺪ. ﻫﻢ اﻛﻨﻮن ﻣﻄﺎﻟﻌﻪ ﺑﺮ روي ﻣﻌﻴﺎرﻫﺎي ﺑﺎﻟﻴﻨﻲ و‬ ‫آزﻣﺎﻳﺸﮕﺎﻫﻲ ﻏﻴﺮﺗﻬﺎﺟﻤﻲ ﺟﻬﺖ ﺑﺮرﺳﻲ ﭘﻴﺶ آﮔﻬﻲ ﻣﻮرد ﺗﻮﺟﻪ ﻗﺮار‬ ‫ﮔﺮﻓﺘﻪ اﺳﺖ؛ ﭼﺮا ﻛﻪ اﻧﺠﺎم ﻧﻤﻮﻧﻪ ﺑﺮداري ﻛﺒﺪ روﺷﻲ ﺗﻬﺎﺟﻤﻲ ﺑﻮده‬ ‫و در ﻣﻮاردي ﻧﻴﺰ ﻋﻮارﺿﻲ از آن ﮔﺰارش ﺷﺪه اﺳﺖ. ﺳﻦ ﺑﺎﻻﺗﺮ از‬ ‫05 ﺳﺎل، ﭼﺎﻗﻲ، ﺑﻴﻤﺎري ﻗﻨﺪ و ﭘﺮ ﻓﺸﺎري ﺧﻮن از ﻣﻌﻴﺎرﻫﺎي ﺑﺎﻟﻴﻨﻲ‬ ‫ﻧﺸﺎﻧﻪ ﺷﺪت ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻣﻲ ﺑﺎﺷﻨﺪ ]72-52[. اﻓﺰاﻳﺶ آﻧﺰﻳﻢ-‬ ‫ﻫﺎي ﻛﺒﺪي ﺑﻴﺶ از 2 ﺑﺮاﺑﺮ ﺣﺪ ﻃﺒﻴﻌﻲ و ﻣﻴﺰان »ﺗﺮي ﮔﻠﻴﺴﻴﺮﻳﺪ«‬ ‫ﺧﻮن ﺑﻴﺶ از 052 ﻣﻴﻠﻲﮔﺮم در دﺳﻲ ﻟﻴﺘﺮ ﻧﻴﺰ از ﻣﻌﻴﺎرﻫﺎي‬ ‫آزﻣﺎﻳﺸﮕﺎﻫﻲ ﻧﺸﺎﻧﻪ ﺷﺪت ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻣﻲﺑﺎﺷﻨﺪ ]82[.‬ ‫روش ﻫﺎي ﺗﺸﺨﻴﺺ‬ ‫ﺟﻠﻮﮔﻴﺮي از ورود اﺳﻴﺪﻫﺎي ﭼﺮب ﺑﻪ داﺧﻞ ﺳﻠﻮلﻫﺎي ﻛﺒﺪي و‬ ‫اﻓﺰاﻳﺶ ﺳﻮﺧﺖ و ﺳﺎز ﭼﺮﺑﻲ در داﺧﻞ ﺳﻠﻮلﻫﺎي ﻛﺒﺪي از ﺗﺠﻤﻊ‬ ‫ﭼﺮﺑﻲ در ﻛﺒﺪ ﺟﻠﻮﮔﻴﺮي ﻣﻲﻛﻨﺪ. اﻳﻦ واﺳﻄﻪ ﺷﻴﻤﻴﺎﻳﻲ ﻳﻚ ﻋﺎﻣﻞ‬ ‫ﻣﻬﻢ ﺣﺴﺎس ﻛﻨﻨﺪه ﻛﺒﺪ ﺑﻪ اﺛﺮ اﻧﺴﻮﻟﻴﻦ ﻣﻲﺑﺎﺷﺪ. »‪ «TNFα‬واﺳﻄﻪ‬ ‫ﺷﻴﻤﻴﺎﻳﻲ دﻳﮕﺮي اﺳﺖ ﻛﻪ اﺛﺮي ﻣﺨﺎﻟﻒ اﺛﺮ واﺳﻄﻪ ﺷﻴﻤﻴﺎﻳﻲ اول ﻳﺎ‬ ‫ﻫﻤﺎن »آدﻳﭙﻮﻧﻜﺘﻴﻦ« را داﺷﺘﻪ و ﺳﺒﺐ اﻓﺰاﻳﺶ ﺗﺠﻤﻊ ﭼﺮﺑﻲ در ﻛﺒﺪ و‬ ‫اﻳﺠﺎد ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ ﻣﻲﺷﻮد ]91[. ﺑﺎ اﻓﺰاﻳﺶ اﺛﺮ »‪«TNFα‬‬ ‫ﻧﺴﺒﺖ ﺑﻪ »آدﻳﭙﻮﻧﻜﺘﻴﻦ« ﻧﻪ ﺗﻨﻬﺎ اﻧﺒﺎﺷﺘﮕﻲ ﭼﺮﺑﻲ در ﻛﺒﺪ ﺑﻮﺟﻮد ﻣﻲ-‬ ‫آﻳﺪ، ﻛﻪ اﻳﻦ اﻓﺰاﻳﺶ ﺳﺒﺐ ﺗﻮﻟﻴﺪ ﻣﻮاد ﺳﻤﻲ )رادﻳﻜﺎلﻫﺎي اﻛﺴﻴﮋن(‬ ‫در ﻣﻴﺘﻮﻛﻨﺪريﻫﺎ ﻣﻲﺷﻮد و در ﻧﻬﺎﻳﺖ ﻣﻨﺠﺮ ﺑﻪ اﻳﺠﺎد اﻟﺘﻬﺎب،‬ ‫ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ و ﻣﺮگ ﺳﻠﻮل ﻛﺒﺪي ﻣﻲﺷﻮد. اﻧﺒﺎﺷﺘﮕﻲ ﭼﺮﺑﻲ‬ ‫در ﺳﻠﻮل ﻛﺒﺪي ﺑﺎ اﻳﺠﺎد ﻳﻚ ﺳﺮي واﺳﻄﻪﻫﺎي ﺷﻴﻤﻴﺎﻳﻲ ﺳﺒﺐ ﺗﻮﻟﻴﺪ‬ ‫واﺳﻄﻪﻫﺎي اﻟﺘﻬﺎﺑﻲ از ﺟﻤﻠﻪ »اﻳﻨﺘﺮﻟﻮﻛﻴﻦ 6« ﻣﻲﺷﻮد ﻛﻪ از ﻣﻬﻤﺘﺮﻳﻦ‬ ‫ﻋﻮاﻣﻞ ﻣﺮگ ﺳﻠﻮل ﻛﺒﺪي ﺧﻮاﻫﺪ ﺑﻮد ]91[. ﻣﻴﻜﺮوبﻫﺎي روده اي‬ ‫ﻋﻼوه ﺑﺮ ﺗﻨﻈﻴﻢ ﺟﺬب ﭼﺮﺑﻲﻫﺎ از دﺳﺘﮕﺎه ﮔﻮارش، در ﺗﻮﻟﻴﺪ‬ ‫اﺳﻴﺪﻫﺎي ﭼﺮب در ﻛﺒﺪ ﻧﻴﺰ ﻧﻘﺶ دارﻧﺪ. ﻣﺸﺎﻫﺪه ﺷﺪه ﻛﻪ ﻣﻴﻜﺮوب-‬ ‫ﻫﺎي رودهاي در ﺑﺮﺧﻲ اﻓﺮاد ﻻﻏﺮ ﻣﻲﺗﻮاﻧﻨﺪ ﺳﺒﺐ اﻓﺰاﻳﺶ ﺗﺠﻤﻊ‬ ‫اﺳﻴﺪﻫﺎي ﭼﺮب در ﻛﺒﺪ ﺷﺪه و ﺑﺎﻋﺚ اﻳﺠﺎد واﺳﻄﻪﻫﺎي ﺷﻴﻤﻴﺎﻳﻲ‬ ‫اﻟﺘﻬﺎب ﻣﺎﻧﻨﺪ »اﻳﻨﺘﺮﻟﻮﻛﻴﻦ 6« و »‪ «TNFα‬ﺷﻮﻧﺪ. در ﺣﺎل ﺣﺎﺿﺮ‬ ‫ﻋﻘﻴﺪه ﺑﺮ اﻳﻦ اﺳﺖ ﻛﻪ ﭘﻴﺸﺮﻓﺖ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﺑﻪ ﺳﻤﺖ ﺳﻴﺮوز‬ ‫ﺑﺮ اﺳﺎس ﺷﺪت ﺗﻮﻟﻴﺪ واﺳﻄﻪﻫﺎي ﺷﻴﻤﻴﺎﻳﻲ اﻟﺘﻬﺎب و روﻧﺪ اﻟﺘﻬﺎب‬ ‫در ﺳﻠﻮل ﻛﺒﺪي ﺗﻌﻴﻴﻦ ﻣﻲﺷﻮد؛ اﻟﺒﺘﻪ در اﻳﻦ ﻣﺴﻴﺮ واﺳﻄﻪﻫﺎي‬ ‫ﺷﻴﻤﻴﺎﻳﻲ ﻣﺘﻌﺪد دﻳﮕﺮي ﻧﻴﺰ ﻧﻘﺶ دارﻧﺪ ﻛﻪ ﺗﺎﻛﻨﻮن ﺷﻨﺎﺧﺘﻪ ﻧﺸﺪهاﻧﺪ.‬ ‫ﺑﻪ ﻫﻤﻴﻦ دﻟﻴﻞ اﺳﺖ ﻛﻪ در ﺑﻌﻀﻲ ﺑﻴﻤﺎران ﻋﻠﻲرﻏﻢ ﭼﺮﺑﻲ ﻓﺮاوان‬ ‫ﻛﺒﺪ، ﭘﻴﺸﺮﻓﺖ ﺑﻪ ﺳﻤﺖ ﺳﻴﺮوز ﺑﺴﻴﺎر ﻛﻨﺪ ﺑﻮده، در ﺣﺎﻟﻲ ﻛﻪ در‬ ‫ﺑﻌﻀﻲ ﺑﻴﻤﺎران ﺑﺎ ﻣﺨﺘﺼﺮي ﺗﺠﻤﻊ ﭼﺮﺑﻲ در ﻛﺒﺪ، اﻟﺘﻬﺎب ﺷﺪﻳﺪ‬ ‫اﻳﺠﺎد ﺷﺪه و ﺳﻴﺮ ﺑﻴﻤﺎري ﺑﻪ ﺳﻤﺖ ﺳﻴﺮوز ﺳﺮﻳﻊ اﺳﺖ. در اﻳﻦ ﻣﻴﺎن‬ ‫ﻧﻘﺶ واﺳﻄﻪﻫﺎﻳﻲ ﻣﺎﻧﻨﺪ »ﻟﭙﺘﻴﻦ«، »آﻧﮋﻳﻮﺗﺎﻧﺴﻴﻦ« و »ﻧﻮراﭘﻲ ﻧﻔﺮﻳﻦ« ﻛﻪ‬ ‫ﺳﺒﺐ اﻓﺰاﻳﺶ ﺗﻜﺜﻴﺮ ﺳﻠﻮلﻫﺎي ﺗﻮﻟﻴﺪ ﻛﻨﻨﺪه ﺑﺎﻓﺖ ﺟﻮﺷﮕﺎﻫﻲ ﻣﻲ-‬ ‫ﺷﻮﻧﺪ، ﻧﻴﺎز ﺑﻪ ﻣﻄﺎﻟﻌﺎت ﺑﻴﺸﺘﺮي دارد. اﻳﻦ واﺳﻄﻪﻫﺎي ﺷﻴﻤﻴﺎﻳﻲ ﺑﺮ‬ ‫ﺧﻼف »آدﻳﭙﻮﻧﻜﺘﻴﻦ« ﻋﻤﻞ ﻛﺮده و ﺑﺎ اﻓﺰاﻳﺶ ﺑﺎﻓﺖ ﺟﻮﺷﮕﺎﻫﻲ ﺑﻪ‬ ‫دﻧﺒﺎل ﺗﺨﺮﻳﺐ ﺳﻠﻮلﻫﺎي ﻛﺒﺪي ﺳﺒﺐ ﺳﻴﺮ ﺳﺮﻳﻊﺗﺮ ﺑﻴﻤﺎري ﺑﻪ ﺳﻮي‬ ‫ﺑﻴﻤﺎري ﻣﺰﻣﻦ و ﻏﻴﺮ ﻗﺎﺑﻞ ﺑﺮﮔﺸﺖ ﻛﺒﺪي ﻳﺎ ﻫﻤﺎن ﺳﻴﺮوز ﻣﻲﺷﻮﻧﺪ‬ ‫]91[.‬ ‫ﺳﻴﺮ ﺑﻴﻤﺎري‬ ‫در اﻛﺜﺮ ﻣﻮارد، ﺑﻴﻤﺎري داراي ﺳﻴﺮ آﻫﺴﺘﻪ و ﺧﻮش ﺧﻴﻢ‬ ‫ﻣﻲﺑﺎﺷﺪ. در ﺻﻮرت ﻋﺪم وﺟﻮد اﻟﺘﻬﺎب و ﻣﺮگ ﺳﻠﻮلﻫﺎي ﻛﺒﺪي‬ ‫در ﻧﻤﻮﻧﻪﻫﺎي ﺑﺎﻓﺖ ﺷﻨﺎﺳﻲ، ﭘﻴﺶ آﮔﻬﻲ ﺑﻴﻤﺎري ﺧﻮب اﺳﺖ. اﮔﺮ‬

‫1( روشﻫﺎي آزﻣﺎﻳﺸﮕﺎﻫﻲ‬
‫آﻧﺰﻳﻢﻫﺎي ﻛﺒﺪي )آﺳﭙﺎرﺗﺎت آﻣﻴﻨﻮ ﺗﺮاﻧﺴﻔﺮاز و آﻻﻧﻴﻦ آﻣﻴﻨﻮ‬ ‫ﺗﺮاﻧﺴﻔﺮاز( در ﺳﻠﻮلﻫﺎي ﻛﺒﺪي ﻣﻮﺟﻮد ﺑﻮده و ﺑﺎ ﺗﺨﺮﻳﺐ ﺳﻠﻮل‬ ‫ﻛﺒﺪي در ﺳﺮم ﺑﻴﻤﺎران وارد ﻣﻲ ﺷﻮﻧﺪ. اﻓﺰاﻳﺶ آﻧﻬﺎ ﻧﺸﺎﻧﻪ ﺗﺨﺮﻳﺐ‬ ‫ﺳﻠﻮل ﻛﺒﺪي اﺳﺖ ]7[. اﻓﺰاﻳﺶ ﻣﻴﺰان آﻧﺰﻳﻢﻫﺎي ﻛﺒﺪي ﺑﺎ ﺷﺪت‬ ‫ﺑﻴﻤﺎري ارﺗﺒﺎط ﻣﺴﺘﻘﻴﻢ ﻧﺪاﺷﺘﻪ و در05 درﺻﺪ ﻣﺒﺘﻼﻳﺎن ﺑﻪ ﻛﺒﺪ ﭼﺮب‬ ‫ﻣﺸﺎﻫﺪه ﻣﻲﺷﻮد. اﻳﻦ اﻓﺰاﻳﺶ در ﻣﺮاﺣﻞ ﭘﻴﺸﺮﻓﺘﻪ ﺑﻴﻤﺎري ﺑﻪ 08‬ ‫درﺻﺪ ﻣﻲرﺳﺪ. »آﻻﻧﻴﻦ آﻣﻴﻨﻮ ﺗﺮاﻧﺴﻔﺮاز« و »آﺳﭙﺎرﺗﺎت آﻣﻴﻨﻮ‬ ‫ﺗﺮاﻧﺴﻔﺮاز« ﻣﻬﻤﺘﺮﻳﻦ آﻧﺰﻳﻢﻫﺎي ﻛﺒﺪي ﺑﻮده ﻛﻪ در اﻳﻦ ﺑﻴﻤﺎري‬

‫ﻓﺼﻠﻨﺎﻣﻪ ﻓﻴﺾ| ﺗﺎﺑﺴﺘﺎن 9831| دوره 41| ﺷﻤﺎره 2‬

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‫‪Archive of SID‬‬
‫ﺷﻮد و در واﻗﻊ ﻧﺸﺎﻧﻪاي از ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ ﻣﻲﺑﺎﺷﺪ ]13[. از‬ ‫ﺷﺎﺧﺺﻫﺎي ﺳﺮﻣﻲ ﺟﺪﻳﺪ ﻛﻪ اﺣﺘﻤﺎﻻ ﺑﻴﺎن ﻛﻨﻨﺪه ﺷﺪت ﺑﻴﻤﺎري ﻧﻴﺰ‬ ‫ﻣﻲﺑﺎﺷﻨﺪ، ﻣﻲﺗﻮان از »‪ «TNFα‬و »اﻳﻨﺘﺮﻟﻮﻛﻴﻦ6« ﻧﺎم ﺑﺮد ]61[.‬ ‫ﻣﺠﺪدا ﺗﺄﻛﻴﺪ ﻣﻲﺷﻮد ﻛﻪ ﻳﺎﻓﺘﻪﻫﺎي آزﻣﺎﻳﺸﮕﺎﻫﻲ و ﺑﺎﻟﻴﻨﻲ ﻧﺸﺎﻧﻪ‬ ‫ﺷﺪت ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻧﺒﻮده و ﻓﻘﻂ ﺑﺮرﺳﻲ ﺑﺎﻓﺖ ﺷﻨﺎﺳﻲ ﻛﺒﺪ‬ ‫اﺳﺖ ﻛﻪ ﻣﻲﺗﻮاﻧﺪ ﺗﻌﻴﻴﻦ ﻛﻨﻨﺪه ﺷﺪت و ﭘﻴﺶ آﮔﻬﻲ ﺑﺎﺷﺪ.‬

‫راﻳﻜﺎ و ارﺳﻴﺎ ﺟﻤﺎﻟﻲ‬

‫اﻓﺰاﻳﺶ ﻣﻲﻳﺎﺑﻨﺪ ]7[. در ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﺑﺮ ﺧﻼف اﺧﺘﻼل ﻛﺒﺪ‬ ‫ﻧﺎﺷﻲ از ﻣﺼﺮف اﻟﻜﻞ، اﻓﺰاﻳﺶ ﻣﻴﺰان »آﻻﻧﻴﻦ آﻣﻴﻨﻮ ﺗﺮاﻧﺴﻔﺮاز« از‬ ‫»آﺳﭙﺎرﺗﺎت آﻣﻴﻨﻮ ﺗﺮاﻧﺴﻔﺮاز« ﺑﻴﺸﺘﺮ اﺳﺖ و ﻓﻘﻂ در ﻣﺮاﺣﻞ ﭘﻴﺸﺮﻓﺘﻪ‬ ‫ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب )ﺳﻴﺮوز( اﺳﺖ ﻛﻪ ﻏﻠﺒﻪ اﻓﺰاﻳﺶ ﻣﻴﺰان »آﺳﭙﺎرﺗﺎت‬ ‫آﻣﻴﻨﻮ ﺗﺮاﻧﺴﻔﺮاز« ﺑﺮ »آﻻﻧﻴﻦ آﻣﻴﻨﻮ ﺗﺮاﻧﺴﻔﺮاز« دﻳﺪه ﻣﻲﺷﻮد. اﻓﺰاﻳﺶ‬ ‫آﻧﺰﻳﻢﻫﺎي ﻛﺒﺪي ﻓﻮق در اﻛﺜﺮ ﻣﻮارد ﺑﻴﻦ 5/1 ﺗﺎ 2 ﺑﺮاﺑﺮ ﺣﺪ ﻃﺒﻴﻌﻲ‬ ‫ﻣﻲﺑﺎﺷﺪ. اﻓﺰاﻳﺶ ﺑﺴﻴﺎر ﺑﺎﻻي آﻧﺰﻳﻢﻫﺎي ﻛﺒﺪي )ﺑﻴﺶ از 01 ﺑﺮاﺑﺮ‬ ‫ﺣﺪ ﻃﺒﻴﻌﻲ ﺳﺮم( در ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﺑﺴﻴﺎر ﻧﺎدر ﺑﻮده و اﺣﺘﻤﺎل‬ ‫ﺑﻴﻤﺎريﻫﺎي ﻛﺒﺪي دﻳﮕﺮ را ﻣﻄﺮح ﻣﻲﺳﺎزد. اﻓﺰاﻳﺶ ﻣﻴﺰان‬ ‫»ﮔﺎﻣﺎﮔﻠﻮﺗﺎﻣﻴﻞ ﺗﺮاﻧﺲ ﭘﭙﺘﻴﺪاز« ﺳﺮم ﻛﻪ از آﻧﺰﻳﻢﻫﺎي ﻣﺘﺮﺷﺤﻪ از ﻛﺒﺪ‬ ‫اﺳﺖ، در ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻏﻴﺮ اﻟﻜﻠﻲ ﻣﺎﻧﻨﺪ ﻛﺒﺪ ﭼﺮب اﻟﻜﻠﻲ دﻳﺪه‬ ‫ﻣﻲﺷﻮد و ﻧﺸﺎﻧﻪ ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ اﺳﺖ ]92[. ﻣﻴﺰان ﺑﻴﻠﻲ روﺑﻴﻦ،‬ ‫آﻟﺒﻮﻣﻴﻦ، زﻣﺎن ﭘﺮوﺗﺮوﻣﺒﻴﻦ و ﭘﻼﻛﺖﻫﺎي ﺧﻮن ﻛﻪ ﻧﺸﺎﻧﻪ ﻋﻤﻠﻜﺮد‬ ‫ﺳﻠﻮل ﻛﺒﺪي ﻣﻲﺑﺎﺷﻨﺪ، در ﻣﺮاﺣﻞ اﺑﺘﺪاﻳﻲ ﺑﻴﻤﺎري ﻃﺒﻴﻌﻲ ﺑﻮده و‬ ‫اﺧﺘﻼل در آﻧﻬﺎ اﺣﺘﻤﺎل ﺳﻴﺮوز را ﻣﻄﺮح ﻣﻲﻛﻨﺪ. ﺑﻴﻠﻲ روﺑﻴﻦ از ﻣﻮاد‬ ‫زاﺋﺪ ﺧﻮن ﻣﻲ ﺑﺎﺷﺪ ﻛﻪ ﺗﻮﺳﻂ ﻛﺒﺪ از ﺗﺨﺮﻳﺐ ﮔﻠﺒﻮلﻫﺎي ﻗﺮﻣﺰ ﭘﻴﺮ‬ ‫ﺧﻮن ﺳﺎﺧﺘﻪ ﺷﺪه و ﭘﺲ از ﺳﻢ زداﻳﻲ ﺗﻮﺳﻂ ﻛﺒﺪ از ﺻﻔﺮا و ادرار‬ ‫دﻓﻊ ﻣﻲﺷﻮد. اﻓﺰاﻳﺶ ﻣﻴﺰان ﺑﻴﻠﻲ روﺑﻴﻦ ﺷﺎﺧﺼﻲ از ﺑﻴﻤﺎري ﻛﺒﺪ‬ ‫اﺳﺖ. آﻟﺒﻮﻣﻴﻦ ﻳﻚ ﭘﺮوﺗﺌﻴﻦ اﺳﺖ ﻛﻪ ﺗﻮﺳﻂ ﻛﺒﺪ ﺳﺎﺧﺘﻪ ﺷﺪه و‬ ‫ﻣﺴﺌﻮﻟﻴﺖ ﺑﺮﻗﺮاري ﺗﻌﺎدل ﻓﺸﺎرﻫﺎي اﺳﻤﺰي ﺧﺎرج ﺳﻠﻮلﻫﺎي ﺑﺪن را‬ ‫ﺑﻪ ﻋﻬﺪه دارد. ﺑﺎ ﻛﺎﻫﺶ آﻟﺒﻮﻣﻴﻦ ﺳﺮم، اﺣﺘﺒﺎس آب ﺑﻪ ﺻﻮرت ﺗﻮرم‬ ‫در اﻧﺪامﻫﺎ و ﺷﻜﻢ ﺑﻪ وﺟﻮد ﻣﻲآﻳﺪ. ﭘﺮوﺗﺮوﻣﺒﻴﻦ از ﻋﻮاﻣﻞ اﻧﻌﻘﺎدي‬ ‫ﺧﻮن ﻣﻲﺑﺎﺷﺪ ﻛﻪ ﺗﻮﺳﻂ ﻛﺒﺪ ﺳﺎﺧﺘﻪ ﻣﻲﺷﻮد و ﻛﺎﻫﺶ آن ﺳﺒﺐ‬ ‫اﻓﺰاﻳﺶ اﺳﺘﻌﺪاد ﺑﻪ ﺧﻮﻧﺮﻳﺰي در ﺑﺪن ﻣﻲﮔﺮدد. ﺳﺎﻳﺮ ﺷﺎﺧﺺﻫﺎي‬ ‫آزﻣﺎﻳﺸﮕﺎﻫﻲ ﻋﻤﻠﻜﺮد ﻛﺒﺪ در ﻣﺮاﺣﻞ اﺑﺘﺪاﻳﻲ ﻛﺒﺪ ﭼﺮب ﻃﺒﻴﻌﻲ ﺑﻮده‬ ‫و ﻓﻘﻂ در ﻣﺮاﺣﻞ ﭘﻴﺸﺮﻓﺘﻪ )ﺳﻴﺮوز( ﻣﺨﺘﻞ ﻣﻲﺷﻮﻧﺪ؛ اﻟﺒﺘﻪ ﻣﻤﻜﻦ‬ ‫اﺳﺖ ﺑﺮﺧﻲ ﺑﻴﻤﺎران داراي ﺑﻴﻤﺎري ﭘﻴﺸﺮﻓﺘﻪ ﻛﺒﺪي ﺑﻪ ﺷﻜﻞ ﺳﻴﺮوز‬ ‫ﺑﺎﺷﻨﺪ، وﻟﻲ آﻧﺰﻳﻢﻫﺎي ﻛﺒﺪي در آﻧﻬﺎ ﻃﺒﻴﻌﻲ ﺑﺎﺷﺪ. در ﺑﻴﻤﺎري ﻛﺒﺪ‬ ‫ﭼﺮب ﺷﺎﺧﺺﻫﺎي وﻳﺮوس ﻫﭙﺎﺗﻴﺖ ‪ B‬و ‪ C‬ﻣﻨﻔﻲ اﺳﺖ ]7[؛ اﻟﺒﺘﻪ‬ ‫ﻫﻤﺰﻣﺎﻧﻲ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﺑﺎ ﻫﭙﺎﺗﻴﺖ ‪ C‬وﺟﻮد داﺷﺘﻪ و ﻫﻤﺰﻣﺎن‬ ‫ﺑﻮدن اﻳﻦ دو ﺑﻴﻤﺎري ﺳﺒﺐ ﺗﺴﺮﻳﻊ روﻧﺪ آﺳﻴﺐ ﻛﺒﺪي ﻧﺴﺒﺖ ﺑﻪ وﻗﺘﻲ‬ ‫اﺳﺖ ﻛﻪ اﻳﻦ ﺑﻴﻤﺎريﻫﺎ ﻫﺮ ﻛﺪام ﺑﻪ ﺗﻨﻬﺎﻳﻲ وﺟﻮد داﺷﺘﻪ ﺑﺎﺷﻨﺪ.‬ ‫اﻓﺰاﻳﺶ ﻣﻴﺰان ﭼﺮﺑﻲﻫﺎي ﺧﻮن ﺑﻪ ﺻﻮرت اﻓﺰاﻳﺶ ﻣﻴﺰان »ﺗﺮي‬ ‫ﮔﻠﻴﺴﻴﺮﻳﺪ«، »ﻛﻠﺴﺘﺮول« و ﺑﻪ ﺧﺼﻮص ﺟﺰء » ﻛﻠﺴﺘﺮول ﺑﺎ ﭼﮕﺎﻟﻲ‬ ‫ﻛﻢ اﻛﺴﻴﺪ ﺷﺪه« و ﻧﻴﺰ اﻓﺰاﻳﺶ ﻗﻨﺪ ﺧﻮن در ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب‬ ‫ﻣﺸﺎﻫﺪه ﻣﻲﺷﻮد ﻛﻪ ﻫﻤﮕﻲ دﻟﻴﻠﻲ ﺑﺮ وﺟﻮد ﺳﻨﺪروم ﻣﺘﺎﺑﻮﻟﻴﻚ ﻣﻲ-‬ ‫ﺑﺎﺷﻨﺪ ]03[. ﻣﻴﺰان آﻫﻦ ﺳﺮم ﻧﻴﺰ در ﻣﺮاﺣﻞ ﭘﻴﺸﺮﻓﺘﻪ ﺑﻴﻤﺎري ﻣﻲﺗﻮاﻧﺪ‬ ‫ﺑﺎﻻ ﺑﺎﺷﺪ ﻛﻪ ﻧﺸﺎﻧﻪ ﺷﺪت ﺑﻴﻤﺎري ﻛﺒﺪ اﺳﺖ. اﻓﺰاﻳﺶ »ﻓﺮﻳﺘﻴﻦ« ﻛﻪ‬ ‫ﻧﺸﺎﻧﻪ ذﺧﺎﻳﺮ آﻫﻦ ﺑﺪن اﺳﺖ، در ﻧﻴﻤﻲ از ﻣﻮارد ﻛﺒﺪ ﭼﺮب دﻳﺪه ﻣﻲ-‬

‫2( روش ﻫﺎي ﺗﺼﻮﻳﺮ ﺑﺮداري‬
‫ﺳﻮﻧﻮﮔﺮاﻓﻲ از ﻛﺒﺪ ﻣﺘﺪاول ﺗﺮﻳﻦ روش ﺗﺸﺨﻴﺼﻲ ﺑﻮده ﻛﻪ‬ ‫ﻏﻴﺮ ﺗﻬﺎﺟﻤﻲ، ﻧﺴﺒﺘﺎ ارزان و در دﺳﺘﺮس اﺳﺖ. ﻧﻤﺎي ﺑﺎﻓﺖ ﻛﺒﺪ در‬ ‫اﻳﻦ ﺑﻴﻤﺎري درﺧﺸﺎنﺗﺮ و ﺑﻪ اﺻﻄﻼح ﭘﺮﺗﻮ ﺷﻨﺎﺳﻲ »اﻛﻮژن« ﺗﺮ از‬ ‫ﺳﺎﻳﺮ ﻣﻨﺎﻃﻖ ﺑﺎﻓﺖ ﻛﺒﺪي ﺧﻮاﻫﺪ ﺑﻮد. ﺳﻲ ﺗﻲ اﺳﻜﻦ از ﻛﺒﺪ روش‬ ‫ﺗﺸﺨﻴﺼﻲ دﻳﮕﺮي اﺳﺖ ﻛﻪ ﻧﺴﺒﺖ ﺑﻪ ﺳﻮﻧﻮﮔﺮاﻓﻲ ﮔﺮانﺗﺮ ﺑﻮده و در‬ ‫اﻳﻦ روش ﺑﻪ ﺟﺎي اﻣﻮاج ﻣﺎوراي ﺻﻮت از ﭘﺮﺗﻮ اﻳﻜﺲ اﺳﺘﻔﺎده ﻣﻲ-‬ ‫ﺷﻮد. در ﻳﻚ ﻣﻄﺎﻟﻌﻪ ﺣﺴﺎﺳﻴﺖ اﻳﻦ روش در ﺷﻨﺎﺳﺎﻳﻲ ﻛﺒﺪ ﭼﺮب‬ ‫ﻛﻤﺘﺮ از ﺳﻮﻧﻮﮔﺮاﻓﻲ ﮔﺰارش ﺷﺪه اﺳﺖ ]23[. »ام آر آي« روش‬ ‫ﺗﺼﻮﻳﺮ ﺑﺮداري دﻳﮕﺮي اﺳﺖ ﻛﻪ اﺳﺘﻔﺎده از آن ﺟﻬﺖ ﺗﺸﺨﻴﺺ‬ ‫ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﺑﻪ ﺗﺪرﻳﺞ در ﺣﺎل اﻓﺰاﻳﺶ اﺳﺖ؛ اﮔﺮﭼﻪ در ﺣﺎل‬ ‫ﺣﺎﺿﺮ ﻛﺎرﺑﺮد آن ﺟﻬﺖ ﺗﺸﺨﻴﺺ ﻛﺒﺪ ﭼﺮب ﺑﻪ دﻟﻴﻞ ﮔﺮان ﺑﻮدن‬ ‫ﻣﺘﺪاول ﻧﻴﺴﺖ. ﻫﻴﭻﻛﺪام از روشﻫﺎي ﺗﺼﻮﻳﺮ ﺑﺮداري ﻓﻮق ﻧﺸﺎن‬ ‫دﻫﻨﺪه ﺷﺪت ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻧﻤﻲﺑﺎﺷﻨﺪ و ﻗﻄﻌﺎ ﻧﻤﻲﺗﻮاﻧﻨﺪ‬ ‫ﺟﺎﻳﮕﺰﻳﻦ ﻧﻤﻮﻧﻪ ﺑﺎﻓﺖ ﺷﻨﺎﺳﻲ ﻛﺒﺪ ﺟﻬﺖ ﺗﻌﻴﻴﻦ ﺷﺪت و ﭘﻴﺶ آﮔﻬﻲ‬ ‫ﺑﻴﻤﺎري ﺑﺎﺷﻨﺪ.‬

‫3( روشﻫﺎي ﺑﺎﻓﺖ ﺷﻨﺎﺳﻲ‬
‫ﻧﻤﻮﻧﻪ ﺑﺮداري از ﻛﺒﺪ دﻗﻴﻖ ﺗﺮﻳﻦ روش ارزﻳﺎﺑﻲ ﻣﻴﺰان و‬ ‫وﺳﻌﺖ آﺳﻴﺐ ﻛﺒﺪي در اﻓﺮاد ﺑﺎ ﺗﺎرﻳﺨﭽﻪ ﻳﺎ ﻣﻌﺎﻳﻨﻪ ﺑﺎﻟﻴﻨﻲ ﻣﺸﻜﻮك‬ ‫ﺑﻪ ﻛﺒﺪ ﭼﺮب ﻣﻲﺑﺎﺷﺪ. اﻳﻦ روش ﺳﺒﺐ ﺗﺸﺨﻴﺺ درﺳﺖ و ﻛﻨﺎر‬ ‫ﮔﺬاﺷﺘﻦ ﺗﺸﺨﻴﺺﻫﺎي اﻓﺘﺮاﻗﻲ ﺷﺪه و ﻫﻤﺰﻣﺎن ﻣﻲﺗﻮان از آن ﺑﻪ‬ ‫ﻋﻨﻮان ﻣﻌﻴﺎري از ﺷﺪت ﺑﻴﻤﺎري اﺳﺘﻔﺎده ﻛﺮد. ﻧﻤﻮﻧﻪ ﺑﺎﻓﺘﻲ ﻛﺒﺪ‬ ‫اﻃﻼﻋﺎت زﻳﺎدي در ﻣﻮرد روﻧﺪ ﭘﻴﺸﺮﻓﺖ ﺑﻴﻤﺎري و ﭘﻴﺶ آﮔﻬﻲ ﻧﻴﺰ‬ ‫ﻣﻲدﻫﺪ و ﻣﻲﺗﻮان ﻧﻮع درﻣﺎن ﻣﻨﺎﺳﺐ را ﺑﺮ اﺳﺎس ﻳﺎﻓﺘﻪﻫﺎي آن‬ ‫ﺗﻌﻴﻴﻦ ﻛﺮد. ﺑﺎز ﻫﻢ ﺗﺎﻛﻴﺪ ﻣﻲﺷﻮد ﻛﻪ در ﺣﺎل ﺣﺎﺿﺮ ﻫﻴﭻﻛﺪام از‬ ‫ﻣﻌﻴﺎرﻫﺎي ﺳﺮﻣﻲ و ﺗﺼﻮﻳﺮ ﺑﺮداري ﻗﺎﺑﻠﻴﺖ ارزﻳﺎﺑﻲ وﺿﻌﻴﺖ ﻛﺒﺪ را‬ ‫ﺑﻪ ﺧﻮﺑﻲ روش ﺑﺎﻓﺖ ﺷﻨﺎﺳﻲ ﻛﺒﺪ ﻧﺪارﻧﺪ. ﻧﻤﻮﻧﻪ ﺑﺮداري ﻛﺒﺪ روﺷﻲ‬ ‫اﺳﺖ ﻛﻪ در آن ﻧﻤﻮﻧﻪ ﺑﺎﻓﺘﻲ ﻛﺒﺪ ﺑﻪ روشﻫﺎي ﻣﺨﺘﻠﻔﻲ ﻛﻪ ﺗﻮﺿﻴﺢ‬ ‫داده ﻣﻲﺷﻮد، ﺑﻪ دﺳﺖ آﻣﺪه و ﺗﻮﺳﻂ ﻣﻴﻜﺮوﺳﻜﻮپ ﻣﻮرد ﺑﺮرﺳﻲ‬ ‫دﻗﻴﻖ ﺳﻠﻮﻟﻲ ﻗﺮار ﻣﻲﮔﻴﺮد. اﻳﻦ روش اوﻟﻴﻦ ﺑﺎر در ﺳﺎل 3881‬ ‫ﺗﻮﺳﻂ ‪ Paul Ehrlich‬در آﻟﻤﺎن اﻧﺠﺎم ﮔﺮﻓﺖ. در اواﺧﺮ دﻫﻪ‬ ‫0591، ‪ Mengini‬روش آﺳﭙﻴﺮاﺳﻴﻮن ﺛﺎﻧﻴﻪاي ﻧﻤﻮﻧﻪ ﺑﺮداري ﻛﺒﺪ را‬ ‫اﺑﺪاع ﻛﺮد ﻛﻪ ﻣﻮرد ﺗﻮﺟﻪ ﻗﺮار ﮔﺮﻓﺖ و اﻳﻦ روش ﻛﺎرﺑﺮدﻫﺎي‬

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‫ﻓﺼﻠﻨﺎﻣﻪ ﻓﻴﺾ| ﺗﺎﺑﺴﺘﺎن 9831| دوره 41| ﺷﻤﺎره 2‬ ‫‪www.SID.ir‬‬

‫‪... ، of SID‬‬ ‫ﻣﺮوري ﺑﺮ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب‪Archive‬‬ ‫ﺑﺎﻓﺖﺷﻨﺎﺳﻲ ﻛﺒﺪ اﺳﺖ. ﻣﺠﻤﻮﻋﻪاي از ﻋﻼﻳﻢ ﺑﺎﻟﻴﻨﻲ، ﺗﺎرﻳﺨﭽﻪ‬ ‫ﺑﻴﻤﺎر، ﺑﺮرﺳﻲ ﺧﻮن و روشﻫﺎي ﭘﺮﺗﻮ ﺷﻨﺎﺳﻲ ﺑﻪ ﻣﻨﻈﻮر رد ﻛﺮدن‬ ‫ﺗﺸﺨﻴﺺﻫﺎي اﻓﺘﺮاﻗﻲ ﺿﺮوري ﺑﻪ ﻧﻈﺮ ﻣﻲرﺳﺪ. ﻓﻬﺮﺳﺘﻲ از ﺗﺸﺨﻴﺺ-‬ ‫ﻫﺎي اﻓﺘﺮاﻗﻲ در ﺟﺪول ﺷﻤﺎره 2 ﻧﻤﺎﻳﺶ داده ﺷﺪه اﺳﺖ.‬ ‫ﺟﺪول ﺷﻤﺎره 2 – ﺗﺸﺨﻴﺺﻫﺎي اﻓﺘﺮاﻗﻲ‬
‫ﺑﻴﻤﺎري وﻳﻠﺴﻮن‬ ‫ﻫﻤﻮﻛﺮوﻣﺎﺗﻮزﻳﺲ‬ ‫ﻛﻤﺒﻮد آﻟﻔﺎ آﻧﺘﻲ ﺗﺮﻳﭙﺴﻴﻦ‬ ‫ﺑﻴﻤﺎري ﺳﻠﻴﺎك‬ ‫ﻫﭙﺎﺗﻴﺖ اﻟﻜﻠﻲ‬ ‫ﻫﭙﺎﺗﻴﺖ وﻳﺮوﺳﻲ ‪E,C,B,A‬‬ ‫ﻫﭙﺎﺗﻴﺖ ﺧﻮد اﻳﻤﻨﻲ‬ ‫ﻫﭙﺎﺗﻴﺖ داروﺋﻲ‬ ‫ﻫﭙﺎﺗﻴﺖ اﻳﺴﻜﻤﻴﻚ‬

‫زﻳﺎدي در ﺑﺮرﺳﻲ ﺑﻴﻤﺎريﻫﺎي ﻛﺒﺪي ﭘﻴﺪا ﻛﺮد. ﻧﻤﻮﻧﻪ ﺑﺮداري ﻛﺒﺪ‬ ‫ﻋﻼوه ﺑﺮ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب در ﺑﺴﻴﺎري از درﮔﻴﺮيﻫﺎي ﻛﺒﺪي ﻣﺎﻧﻨﺪ‬ ‫ﺑﻴﻤﺎريﻫﺎي اﻟﺘﻬﺎﺑﻲ ﻛﺒﺪ ﻧﺎﺷﻲ از وﻳﺮوسﻫﺎي ﻫﭙﺎﺗﻴﺖ ‪ B‬و ‪،C‬‬ ‫واﻛﻨﺶﻫﺎي داروﻳﻲ، ﺑﻴﻤﺎريﻫﺎي ﻣﺘﺎﺑﻮﻟﻴﻚ ﻣﺎﻧﻨﺪ ﺑﻴﻤﺎري وﻳﻠﺴﻮن و‬ ‫ﻫﻤﻮﻛﺮوﻣﺎﺗﻮز و ﺑﺎﻻﺧﺮه ﺳﺮﻃﺎنﻫﺎي ﻛﺒﺪ، ﻧﻘﺶ ﺗﺸﺨﻴﺼﻲ داﺷﺘﻪ و‬ ‫ﻣﻲﺗﻮان ﺑﺮ اﺳﺎس ﻳﺎﻓﺘﻪﻫﺎي آن ﻧﻮع درﻣﺎن ﻣﻨﺎﺳﺐ را ﺗﻌﻴﻴﻦ ﻛﺮد؛‬ ‫ﺑﻪ ﻧﻈﺮ ﻣﻲرﺳﺪ در ﺣﺎل ﺣﺎﺿﺮ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﺷﺎﻳﻊﺗﺮﻳﻦ ﻋﻠﺖ‬ ‫ﻧﻤﻮﻧﻪ ﺑﺮداري ﻛﺒﺪ در ﺑﻴﻦ ﺑﻴﻤﺎريﻫﺎي ﻛﺒﺪي ﺑﺎﺷﺪ. از آﻧﺠﺎ ﻛﻪ‬ ‫ﻣﻬﻤﺘﺮﻳﻦ ﻋﺎﻣﻞ ﺗﻌﻴﻴﻦ ﻛﻨﻨﺪه ﭘﻴﺶ آﮔﻬﻲ ﺑﻴﻤﺎري ﺑﺮرﺳﻲ ﻧﻤﻮﻧﻪ ﺑﺎﻓﺖ-‬ ‫ﺷﻨﺎﺳﻲ ﻛﺒﺪ اﺳﺖ، ﺑﻪ ﺧﻼﺻﻪاي از اﻳﻦ ﻳﺎﻓﺘﻪﻫﺎ اﺷﺎره ﻣﻲﻛﻨﻴﻢ. اﻳﻦ‬ ‫ﻳﺎﻓﺘﻪﻫﺎ ﻣﺸﺎﺑﻪ درﮔﻴﺮي ﻛﺒﺪ در اﻓﺮاد اﻟﻜﻠﻲ اﺳﺖ. ﺧﻔﻴﻒﺗﺮﻳﻦ ﺷﻜﻞ‬ ‫درﮔﻴﺮي ﻛﺒﺪ ﺗﺠﻤﻊ ﭼﺮﺑﻲ در ﺳﻠﻮلﻫﺎي ﻛﺒﺪي اﺳﺖ. ) ﺷﻜﻞ ﺷﻤﺎره‬ ‫2(‬ ‫ﺷﻜﻞ ﺷﻤﺎره 2- اﻧﺒﺎﺷﺘﮕﻲ ﭼﺮﺑﻲ در ﻧﻤﻮﻧﻪ ﺑﺎﻓﺖ ﺷﻨﺎﺳﻲ ﻛﺒﺪ در‬ ‫ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب در ﻣﻴﻜﺮوﺳﻜﻮپ ﻧﻮري‬ ‫در ﻣﺮاﺣﻞ ﭘﻴﺸﺮﻓﺘﻪﺗﺮ ﺑﻴﻤﺎري و ﺑﺎ اﻓﺰاﻳﺶ ﻣﻴﺰان ﭼﺮﺑﻲ در ﺑﺎﻓﺖ‬

‫وﺟﻮد ﻳﺎﻓﺘﻪﻫﺎي ﭘﺮﺗﻮ ﻧﮕﺎري ﺑﻪ ﺗﺄﻛﻴﺪ ﺗﺸﺨﻴﺺ ﻛﻤﻚ ﻣﻲﻛﻨﺪ، وﻟﻲ‬ ‫ﻋﺪم رؤﻳﺖ ﻳﺎﻓﺘﻪﻫﺎي ﺑﻴﻤﺎري در روشﻫﺎي ﭘﺮﺗﻮ ﻧﮕﺎري رد ﻛﻨﻨﺪه‬ ‫ﺑﻴﻤﺎري ﻧﻤﻲﺑﺎﺷﺪ. ﻫﻤﺎنﻃﻮر ﻛﻪ ﭘﻴﺸﺘﺮ ﻧﻴﺰ اﺷﺎره ﺷﺪ ﺑﺮرﺳﻲ ﻧﻤﻮﻧﻪ‬ ‫ﺑﺎﻓﺖ ﺷﻨﺎﺳﻲ ﻛﺒﺪ روش ﻣﻄﻤﺌﻨﻲ ﺟﻬﺖ ﺗﺸﺨﻴﺺ و ﺗﻌﻴﻴﻦ ﺷﺪت‬ ‫درﮔﻴﺮي ﻛﺒﺪ و ﭘﻴﺶ آﮔﻬﻲ ﺑﻴﻤﺎري اﺳﺖ. ﺷﺎﻳﺎن ذﻛﺮاﺳﺖ ﻛﻪ‬ ‫ﻣﻬﻤﺘﺮﻳﻦ ﺗﺸﺨﻴﺺ اﻓﺘﺮاﻗﻲ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب، اﺧﺘﻼل ﻛﺒﺪ ﻧﺎﺷﻲ از‬ ‫اﻟﻜﻞ ﻣﻲﺑﺎﺷﺪ. ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب وﻗﺘﻲ اﻃﻼق ﻣﻲﺷﻮد ﻛﻪ ﻣﻴﺰان‬ ‫ﻣﺼﺮف اﻟﻜﻞ ﻛﻤﺘﺮ از 02 ﮔﺮم در روز ﺑﺎﺷﺪ ]6[. در ﺑﻴﻤﺎري ﻛﺒﺪ‬ ‫ﭼﺮب ﺷﺎﺧﺺﻫﺎي ﺳﺮﻣﻲ ﻫﭙﺎﺗﻴﺖ وﻳﺮوﺳﻲ ‪ B‬و ‪ C‬و ﻧﻴﺰ ﺳﺎﻳﺮ‬ ‫وﻳﺮوسﻫﺎ ﻣﻨﻔﻲ ﺑﻮده و ﺷﻮاﻫﺪ ﺳﺮﻣﻲ ﺑﻴﻤﺎري ﻫﭙﺎﺗﻴﺖ ﺧﻮد اﻳﻤﻨﻲ‬ ‫ﻧﻴﺰ وﺟﻮد ﻧﺪارد ]7[.‬

‫ﻛﺒﺪ، اﻟﺘﻬﺎب اﻳﺠﺎد ﻣﻲﺷﻮد ﻛﻪ ﻧﺘﻴﺠﻪ آن ﻣﺮگ ﺳﻠﻮلﻫﺎي ﻛﺒﺪي‬ ‫درﻣﺎن‬ ‫ﺗﺎ ﺷﻨﺎﺧﺖ ﺑﻬﺘﺮﻳﻦ روش درﻣﺎن ﺑﻴﻤﺎري ﻣﺴﻴﺮ ﻃﻮﻻﻧﻲ در‬ ‫ﭘﻴﺶ اﺳﺖ و ﻣﻄﺎﻟﻌﺎت ﻣﺤﺪودي در اﻳﻦ زﻣﻴﻨﻪ اﻧﺠﺎم ﺷﺪه اﺳﺖ. ﺑﺮ‬ ‫اﺳﺎس اﻃﻼﻋﺎت ﻣﻮﺟﻮد اﺳﺎس درﻣﺎن ﺑﺮﭘﺎﻳﻪ ﻛﺎﻫﺶ وزن، ﺣﺬف‬ ‫داروﻫﺎ و ﺳﻤﻮم اﺣﺘﻤﺎﻟﻲ و ﻧﻴﺰ ﻛﻨﺘﺮل دﻳﺎﺑﺖ و ﭼﺮﺑﻲ ﺧﻮن ﺑﻴﻤﺎران‬ ‫ﻣﻲﺑﺎﺷﺪ.‬ ‫اﺳﺖ. ﺟﻬﺖ ﺗﻌﻴﻴﻦ ﺷﺪت اﻟﺘﻬﺎب، ﻣﺮگ ﺳﻠﻮﻟﻲ و ﻓﻴﺒﺮوز، ﻃﺒﻘﻪ-‬ ‫ﺑﻨﺪيﻫﺎي ﻣﺨﺘﻠﻔﻲ وﺟﻮد دارد ﻛﻪ در آﻧﻬﺎ ﻳﺎﻓﺘﻪﻫﺎي ﺑﺎﻓﺖ ﺷﻨﺎﺳﻲ‬ ‫ﻣﻴﺰان اﻟﺘﻬﺎب، ﻣﺮگ ﺳﻠﻮﻟﻲ و ﻓﻴﺒﺮوز ﻛﺒﺪ اﻣﺘﻴﺎز ﺑﻨﺪي ﻣﻲﺷﻮﻧﺪ. ﻳﻜﻲ‬ ‫از اﻳﻦ روشﻫﺎي ﻃﺒﻘﻪ ﺑﻨﺪي، روش ‪ Knodell‬و ‪ Ishak‬اﺳﺖ ﻛﻪ‬ ‫در آن ﻣﻴﺰان اﻟﺘﻬﺎب و ﻣﺮگ ﺳﻠﻮﻟﻲ ﺑﻴﻦ ﺻﻔﺮ ﺗﺎ 41 اﻣﺘﻴﺎز و ﻣﻴﺰان‬ ‫ﻓﻴﺒﺮوز ﺑﺎﻓﺖ ﻛﺒﺪ ﺑﻴﻦ ﺻﻔﺮ ﺗﺎ 6 اﻣﺘﻴﺎز ﻣﻲﮔﻴﺮﻧﺪ )ﺷﺎﺧﺺ ﻓﻌﺎﻟﻴﺖ‬ ‫ﻛﺒﺪي(. ﭘﺲ از ﻣﺮگ ﺳﻠﻮل ﻛﺒﺪي ﺑﺎﻓﺖ ﺟﺎﻳﮕﺰﻳﻦ ﻳﺎ ﺑﺎﻓﺖ ﻓﻴﺒﺮوز ﺑﻪ‬ ‫ﺟﺎي ﺑﺎﻓﺖ ﻣﺮده ﻛﺒﺪ رﺷﺪ ﻣﻲﻛﻨﺪ ﻛﻪ دﻳﮕﺮ ﻋﻤﻠﻜﺮدﻫﺎي ﺳﻠﻮل‬ ‫ﻛﺒﺪي را ﻧﺪاﺷﺘﻪ و در اﻧﺘﻬﺎ اﻓﺰاﻳﺶ ﺑﺎﻓﺖ ﻓﻴﺒﺮوز ﺑﻪ ﺳﻴﺮوز ﻛﺒﺪي‬ ‫ﻣﻲاﻧﺠﺎﻣﺪ. اﺟﺴﺎم ﻣﺎﻟﻮري )‪ (Mallory body‬از ﻳﺎﻓﺘﻪﻫﺎي ﻣﻬﻢ در‬ ‫ﻧﻤﻮﻧﻪ ﺑﺎﻓﺘﻲ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻣﻲﺑﺎﺷﻨﺪ ﻛﻪ ﺑﻪ ﻋﻠﺖ ﺗﻐﻴﻴﺮات اﻟﺘﻬﺎﺑﻲ‬ ‫و ﺗﺠﻤﻊ ﭼﺮﺑﻲ در ﺳﻠﻮل ﻛﺒﺪي ﺑﻪ وﺟﻮد آﻣﺪه و ﻣﻴﺰان آﻧﻬﺎ در‬ ‫ﺑﻴﻤﺎري ﻛﺒﺪ ﻧﺎﺷﻲ از اﻟﻜﻞ از ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻏﻴﺮ اﻟﻜﻠﻲ‬ ‫ﺑﻴﺸﺘﺮاﺳﺖ.‬ ‫ﺗﺸﺨﻴﺺ و ﺗﺸﺨﻴﺺ ﻫﺎي اﻓﺘﺮاﻗﻲ‬ ‫ﺗﺸﺨﻴﺺ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﺑﺮاﺳﺎس ﺷﻮاﻫﺪ ﺑﺎﻟﻴﻨﻲ و‬

‫درﻣﺎنﻫﺎي ﻏﻴﺮداروﻳﻲ‬
‫اﻧﺠﺎم ﻣﻄﺎﻟﻌﺎت ﻣﺘﻌﺪد ﺑﺮ روي ﺑﺎﻟﻐﻴﻦ و ﺑﭽﻪﻫﺎ ﻧﺸﺎن دﻫﻨﺪه‬ ‫اﺛﺮ ﺗﻐﺬﻳﻪ و ورزش در روﻧﺪ ﺑﻴﻤﺎري ﺑﻮده اﺳﺖ ]53-33[. در ﺑﻴﻦ‬ ‫درﻣﺎنﻫﺎي ﻛﻨﻮﻧﻲ ﻛﺎﻫﺶ وزن و رﺳﻴﺪن ﺑﻪ وزن اﻳﺪه آل ﻣﻮﺛﺮﺗﺮﻳﻦ‬ ‫درﻣﺎن ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻣﻲﺑﺎﺷﺪ. ﻛﺎﻫﺶ وزن ﺳﺮﻳﻊ ﺑﻪ ﺧﺼﻮص‬ ‫ﭘﺲ از ﺟﺮاﺣﻲﻫﺎي اﻧﺠﺎم ﺷﺪه ﺑﻪ ﻣﻨﻈﻮر درﻣﺎن ﭼﺎﻗﻲ ﺳﺒﺐ ﺗﺸﺪﻳﺪ‬ ‫ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻣﻲﺷﻮد ]63[.‬

‫ﻣﺸﺎوره و آﻣﻮزش ﺑﻴﻤﺎران‬
‫ﺟﻬﺖ رﺳﻴﺪن ﺑﻪ وزن اﻳﺪه آل و ﺗﻨﻈﻴﻢ ﺳﺮﻋﺖ ﻛﺎﻫﺶ‬ ‫وزن، ﻣﺸﺎوره ﺑﺎ ﻣﺘﺨﺼﺺ ﺗﻐﺬﻳﻪ ﻫﻤﺮاه ﺑﺎ ﻳﻚ ﺑﺮﻧﺎﻣﻪرﻳﺰي و ﭘﻴﮕﻴﺮي‬ ‫دﻗﻴﻖ ﻣﻨﻄﻘﻲ ﺑﻪ ﻧﻈﺮ ﻣﻲرﺳﺪ. ﭼﺮا ﻛﻪ رژﻳﻢﻫﺎي ﻏﻴﺮ ﻋﻠﻤﻲ ﻧﻪ ﺗﻨﻬﺎ‬ ‫ﻓﺼﻠﻨﺎﻣﻪ ﻓﻴﺾ| ﺗﺎﺑﺴﺘﺎن 9831| دوره 41| ﺷﻤﺎره 2‬

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‫ﻣﻨﻈﻮر اﺳﺘﻔﺎده در ﻛﺒﺪ ﭼﺮب ﻧﻤﻮﻧﻪﻫﺎي اﻧﺴﺎﻧﻲ ﻣﻲﺑﺎﺷﻨﺪ.‬

‫راﻳﻜﺎ و ارﺳﻴﺎ ﺟﻤﺎﻟﻲ‬

‫ﻣﻮﺛﺮ ﻧﺒﻮده، ﻛﻪ ﺻﺪﻣﺎت ﺟﺒﺮان ﻧﺎﭘﺬﻳﺮي در ﻣﺒﺘﻼﻳﺎن ﺑﻪ ﻛﺒﺪ ﭼﺮب‬ ‫اﻳﺠﺎد ﻣﻲﻛﻨﻨﺪ. اﺳﺘﻔﺎده از داروﻫﺎي ﻣﺨﺘﻠﻒ ﺑﻪ ﻣﻨﻈﻮر ﻛﺎﻫﺶ وزن‬ ‫در ﻣﺠﻤﻮع رﺿﺎﻳﺖ ﺑﺨﺶ ﻧﺒﻮده و ﺑﺎ ﻋﻮارض ﻫﻤﺮاه اﺳﺖ. ﻳﻜﻲ از‬ ‫اﻳﻦ داروﻫﺎ »ارﻟﻲ اﺳﺘﺎت« ﻣﻲﺑﺎﺷﺪ ﻛﻪ ﻣﻬﺎر ﻛﻨﻨﺪه آﻧﺰﻳﻢ ﻫﻀﻢ ﻛﻨﻨﺪه‬ ‫ﭼﺮﺑﻲ ﻣﺘﺮﺷﺤﻪ از ﻟﻮزاﻟﻤﻌﺪه و ﻣﻌﺪه ﺑﻮده و از ﺟﺬب ﭼﺮﺑﻲﻫﺎ ﻛﻪ‬ ‫ﻣﻨﺒﻊ ﻏﻨﻲ ﺗﻮﻟﻴﺪ اﻧﺮژي ﻣﻲﺑﺎﺷﻨﺪ، ﺟﻠﻮﮔﻴﺮي ﻣﻲﻛﻨﺪ. از ﻋﻮارض اﻳﻦ‬ ‫دارو اﻳﺠﺎد ﻧﻔﺦ ﻣﻲﺑﺎﺷﺪ ﻛﻪ ﺑﻪ ﻋﻠﺖ ﺗﻮﻟﻴﺪ ﮔﺎز ﻧﺎﺷﻲ از ﻣﺼﺮف‬ ‫ﭼﺮﺑﻲﻫﺎي ﺟﺬب ﻧﺸﺪه در روده ﺗﻮﺳﻂ ﺑﺎﻛﺘﺮيﻫﺎي روده اﺳﺖ.‬

‫داروﻫﺎي ﺣﺴﺎس ﻛﻨﻨﺪه ﺑﻪ اﻧﺴﻮﻟﻴﻦ‬
‫ﻫﻤﺎنﻃﻮر ﻛﻪ ﭘﻴﺸﺘﺮ اﺷﺎره ﺷﺪه ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ ﻛﻪ‬ ‫اﺳﺎس ﺑﻴﻤﺎري زاﻳﻲ در ﺳﻨﺪروم ﻣﺘﺎﺑﻮﻟﻴﻚ اﺳﺖ از ﻓﺮآﻳﻨﺪﻫﺎي اﺻﻠﻲ‬ ‫آﺳﻴﺐ ﺳﻠﻮل ﻛﺒﺪي در ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻣﻲ ﺑﺎﺷﺪ. ﺑﻪ ﻧﻈﺮ ﻣﻲرﺳﺪ‬ ‫ﺑﺎ اﻓﺰاﻳﺶ ﺣﺴﺎﺳﻴﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ و از ﺑﻴﻦ ﺑﺮدن ﻣﻘﺎوﻣﺖ ﺑﻪ آن ﺑﺎ‬ ‫درﻣﺎنﻫﺎي داروﻳﻲ ﻣﻲ ﺗﻮان ﺑﻪ ﻧﺘﺎﻳﺞ درﻣﺎﻧﻲ ﻣﻄﻠﻮﺑﻲ در ﺑﻴﻤﺎري‬ ‫ﻛﺒﺪ ﭼﺮب رﺳﻴﺪ. در ﻳﻚ ﻣﻄﺎﻟﻌﻪ ﻛﻪ ﺑﺮ روي ﻣﻮشﻫﺎي آزﻣﺎﻳﺸﮕﺎﻫﻲ‬ ‫ﭼﺎق اﻧﺠﺎم ﺷﺪه، ﻣﺖ ﻓﻮرﻣﻴﻦ ﺗﻮاﻧﺴﺘﻪ اﺳﺖ ﺑﺎ ﻛﺎﻫﺶ ﻣﻘﺎوﻣﺖ ﺑﻪ‬ ‫اﻧﺴﻮﻟﻴﻦ ﺳﺒﺐ ﻛﺎﻫﺶ ﭼﺮﺑﻲ در ﺳﻠﻮل ﻛﺒﺪي ﺷﻮد ]14[؛ اﮔﺮﭼﻪ اﻳﻦ‬ ‫ﻣﻄﺎﻟﻌﺎت در اﻧﺴﺎن ﺗﺎﻛﻨﻮن ﺑﻪ ﻧﺘﺎﻳﺞ ﻣﻄﻠﻮﺑﻲ ﻧﺮﺳﻴﺪه اﺳﺖ ]24،34[.‬ ‫»ﺗﻴﺎزوﻟﻴﺪﻳﻦ دﻳﻮنﻫﺎي« از دﻳﮕﺮ داروﻫﺎي ﺣﺴﺎس ﻛﻨﻨﺪه ﺳﻠﻮل‬ ‫ﻛﺒﺪي ﺑﻪ اﻧﺴﻮﻟﻴﻦ ﻫﺴﺘﻨﺪ در ﻣﻄﺎﻟﻌﻪاي ﻛﻪ ﺑﺮروي ﭘﻴﻮﮔﻠﻴﺘﺎزون اﻧﺠﺎم‬ ‫ﺷﺪه، ﻣﺸﺎﻫﺪه ﺷﺪه اﺳﺖ ﻛﻪ اﻳﻦ داروﻫﺎ ﺑﺎ ﻛﺎﻫﺶ ﻣﻘﺎوﻣﺖ ﺑﻪ‬ ‫اﻧﺴﻮﻟﻴﻦ ﺳﺒﺐ ﺑﻬﺒﻮد ﺷﺎﺧﺺﻫﺎي آزﻣﺎﻳﺸﮕﺎﻫﻲ و ﺑﺎﻓﺖ ﺷﻨﺎﺳﻲ‬ ‫ﻣﺒﺘﻼﻳﺎن ﺑﻪ ﻛﺒﺪ ﭼﺮب ﺷﺪهاﻧﺪ ]44،54[؛ اﻟﺒﺘﻪ ﮔﺰارﺷﺎت ﺑﺴﻴﺎر‬ ‫ﻣﺤﺪودي از ﻋﻮارض ﻛﺒﺪي اﻳﻦ دﺳﺘﻪ داروﻫﺎ و ﺑﻪ ﺧﺼﻮص ﻧﺴﻞ‬ ‫اول اﻳﻦ داروﻫﺎ ﻣﺎﻧﻨﺪ ﺗﺮوﮔﻠﻴﺘﺎزون وﺟﻮد دارد ]64[.‬

‫رژﻳﻢ ﻏﺬاﻳﻲ‬
‫ﺟﻬﺖ رﺳﻴﺪن ﺑﻪ وزن اﻳﺪهآل ﻣﺤﺪود ﻛﺮدن ﻛﺎﻟﺮي درﻳﺎﻓﺘﻲ‬ ‫ﻳﺎ ﻫﻤﺎن ﻣﺤﺪودﻳﺖ ﻛﺎﻟﺮي رژﻳﻢ ﻏﺬاﻳﻲ ﻣﻮﺛﺮﺗﺮﻳﻦ روش ﻣﻲﺑﺎﺷﺪ.‬ ‫اﺳﺘﻔﺎده از رژﻳﻢ ﻛﻢ ﻛﺎﻟﺮي ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ ﻣﻴﺰان ﻛﺎﻫﺶ وزن و اﺳﺘﻔﺎده‬ ‫درﺳﺖ از وﻳﺘﺎﻣﻴﻦﻫﺎ و ﭘﺮوﺗﺌﻴﻦﻫﺎ در رژﻳﻢﻫﺎي ﻏﺬاﻳﻲ ﺑﺴﻴﺎر ﻣﻔﻴﺪ‬ ‫ﺑﻮده و ﺗﺎرﺳﻴﺪن ﺑﻪ وزن اﻳﺪهآل ﺑﺎﻳﺪ اداﻣﻪ ﻳﺎﺑﺪ. آﻧﭽﻪ ﺑﻴﻤﺎران ﺑﺎﻳﺪ‬ ‫ﺗﻮﺟﻪ داﺷﺘﻪ ﺑﺎﺷﻨﺪ اﻳﻦ اﺳﺖ ﻛﻪ ﭘﺲ از رﺳﻴﺪن ﺑﻪ وزن اﻳﺪهآل ﺑﺎﻳﺪ‬ ‫ﺑﺎ ورزش و رژﻳﻢ ﻏﺬاﻳﻲ ﻣﻨﺎﺳﺐ، آن را ﺣﻔﻆ ﻛﻨﻨﺪ. ﭼﺮا ﻛﻪ در‬ ‫ﺻﻮرت ﻋﺪم ﺗﻮﺟﻪ و اﻓﺰاﻳﺶ ﻣﻴﺰان درﻳﺎﻓﺖ ﻛﺎﻟﺮي )ﭘﺮﺧﻮري(‬ ‫ﻣﺠﺪداً در ﻣﻌﺮض ﻋﻮارض ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻗﺮار ﺧﻮاﻫﻨﺪ ﮔﺮﻓﺖ.‬ ‫ﻳﻜﻲ از روشﻫﺎي ﺑﺴﻴﺎر ﻣﻨﺎﺳﺐ ورزش اﺳﺖ ﻛﻪ ﻋﻤﺪﺗﺎ از ﻃﺮﻳﻖ‬ ‫ﻛﻨﺘﺮل اﺷﺘﻬﺎ ﺳﺒﺐ ﺣﻔﻆ وزن اﻳﺪهآل ﻣﻲﺷﻮد. ﻧﻘﺶ ورزش در‬ ‫ﻛﺎﻫﺶ وزن ﻛﻢ اﻫﻤﻴﺖ ﺑﻮده و ﻧﻘﺶ اﺻﻠﻲ آن در ﺣﻔﻆ وزن اﻳﺪهآل‬ ‫اﺳﺖ. ﺑﻪ ﻧﻈﺮ ﻣﻲرﺳﺪ ﭘﺲ از رﺳﻴﺪن ﺑﻪ وزن اﻳﺪهآل ﺑﺎ رژﻳﻢ ﻏﺬاﻳﻲ‬ ‫درﺳﺖ، ورزش ﻣﻲﺗﻮاﻧﺪ وزن ﻣﻨﺎﺳﺐ را ﺣﻔﻆ ﻧﻤﺎﻳﺪ. ﺟﺮاﺣﻲ ﺑﺎ‬ ‫روشﻫﺎي ﻣﺘﻌﺪد ﻓﻘﻂ در ﺑﻴﻤﺎران ﻣﺒﺘﻼ ﺑﻪ ﭼﺎﻗﻲ ﻛﺸﻨﺪه ﻛﻪ ﺑﻪ درﻣﺎن‬ ‫ﻃﺒﻲ ﭘﺎﺳﺦ ﻧﻤﻲدﻫﻨﺪ، ﺗﻮﺻﻴﻪ ﻣﻲﺷﻮد. اﻋﻤﺎل ﺟﺮاﺣﻲ در ﺑﻬﺘﺮﻳﻦ‬ ‫ﺷﺮاﻳﻂ ﻧﻴﺰ داراي ﻋﻮارض ﺑﻮده و ﺑﻪ ﻋﻨﻮان آﺧﺮﻳﻦ ﺧﻂ درﻣﺎن‬ ‫ﭼﺎﻗﻲ اﺳﺖ و ﻓﻘﻂ در ﺑﻌﻀﻲ اﻓﺮاد ﻗﺎﺑﻞ ﺗﻮﺻﻴﻪ اﺳﺖ.‬

‫داروﻫﺎي ﭘﺎﻳﻴﻦ آورﻧﺪه ﭼﺮﺑﻲ ﺧﻮن‬
‫داروي »ﺟﻢ ﻓﻴﺒﺮوزﻳﻞ« ﻛﻪ از داروﻫﺎي ﭘﺎﻳﻴﻦ آورﻧﺪه ﭼﺮﺑﻲ‬ ‫ﺧﻮن ﻣﻲﺑﺎﺷﺪ، ﺳﺒﺐ ﺑﻬﺒﻮد ﻋﻼﻳﻢ آزﻣﺎﻳﺸﮕﺎﻫﻲ ﻣﺒﺘﻼﻳﺎن ﺑﻪ ﻛﺒﺪ‬ ‫ﭼﺮب ﻣﻲﺷﻮد ]74[. اﺳﺘﺎﺗﻴﻦﻫﺎ از دﻳﮕﺮ داروﻫﺎي ﭘﺎﺋﻴﻦ آورﻧﺪه‬ ‫ﭼﺮﺑﻲ ﺧﻮن و ﺑﻪ ﺧﺼﻮص ﻣﻴﺰان ﻛﻠﺴﺘﺮول ﻣﻲﺑﺎﺷﻨﺪ ﻛﻪ آﻧﺎن ﻧﻴﺰ‬ ‫ﺳﺒﺐ ﺑﻬﺒﻮد ﻋﻼﻳﻢ آزﻣﺎﻳﺸﮕﺎﻫﻲ ﺷﺪهاﻧﺪ ]84[. اورزوداﻛﺴﻲ ﻛﻮﻟﻴﻚ‬ ‫اﺳﻴﺪ ﻛﻪ ﻳﻚ ﻣﺤﺎﻓﻈﺖ ﻛﻨﻨﺪه ﺳﻠﻮلﻫﺎي ﻛﺒﺪي اﺳﺖ، در ﻣﻄﺎﻟﻌﺎت‬ ‫اﺧﻴﺮ ﭼﻨﺪان ﻣﻔﻴﺪ ﻧﺒﻮده اﺳﺖ ]94[.‬

‫ﭘﻴﻮﻧﺪ ﻛﺒﺪ‬
‫در ﻣﺒﺘﻼﻳﺎﻧﻲ ﻛﻪ دﻳﺮ ﻣﺮاﺟﻌﻪ ﻛﺮدهاﻧﺪ و ﺗﺤﺖ درﻣﺎن‬ ‫ﻣﻨﺎﺳﺐ داروﻳﻲ و ﭘﻴﮕﻴﺮيﻫﺎي دورهاي ﻗﺮار ﻧﮕﺮﻓﺘﻪاﻧﺪ و ﻣﻴﺰان‬ ‫آﺳﻴﺐ ﻛﺒﺪي آﻧﺎن ﺑﻪ ﻣﺮﺣﻠﻪ ﭘﻴﺸﺮﻓﺘﻪ و ﻏﻴﺮ ﻗﺎﺑﻞ ﺑﺮﮔﺸﺖ ﻛﺒﺪ‬ ‫)ﺳﻴﺮوز( رﺳﻴﺪه اﺳﺖ، ﭘﻴﻮﻧﺪ ﻛﺒﺪ ﺑﻪ ﻋﻨﻮان آﺧﺮﻳﻦ ﺧﻂ درﻣﺎﻧﻲ‬ ‫ﻣﺤﺴﻮب ﻣﻲ ﺷﻮد. ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﺑﻌﺪ از ﭘﻴﻮﻧﺪ ﻧﻴﺰ ﻣﻲﺗﻮاﻧﺪ در‬ ‫ﻛﺒﺪ ﭘﻴﻮﻧﺪي اﻳﺠﺎد ﺷﻮد. ﻣﻬﻤﺘﺮﻳﻦ ﻋﻠﻞ ﻋﻮد آن در ﻛﺒﺪ ﭘﻴﻮﻧﺪي‬ ‫وﺟﻮد اﺟﺰاي ﺳﻨﺪروم ﻣﺘﺎﺑﻮﻟﻴﻚ ﺑﻪ ﺻﻮرت اﻓﺰاﻳﺶ ﭼﺮﺑﻲ ﺧﻮن،‬ ‫ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ، ﭼﺎﻗﻲ و دﻳﺎﺑﺖ ﻣﻲﺑﺎﺷﺪ.‬

‫ﻣﻮاد آﻧﺘﻲ اﻛﺴﻴﺪان‬
‫ﻣﻄﺎﻟﻌﺎت اﺧﻴﺮ ﻧﺸﺎن دادهاﻧﺪ ﻛﻪ ﻣﻮاد »آﻧﺘﻲ اﻛﺴﻴﺪان« ﻣﺎﻧﻨﺪ‬ ‫وﻳﺘﺎﻣﻴﻦ ‪ E‬و ‪ C‬و »ﺑﺘﺎﺋﻴﻦ« ﻣﻲﺗﻮاﻧﻨﺪ در اﻧﺴﺎن از ﭘﻴﺸﺮﻓﺖ ﺑﻴﻤﺎري‬ ‫ﻛﺒﺪ ﭼﺮب ﺟﻠﻮﮔﻴﺮي ﻛﻨﻨﺪ. اﻳﻦ ﻣﻮاد ﺑﺎ ﻛﺎﻫﺶ اﺛﺮ ﻣﻮاد »اﻛﺴﻴﺪان«‬ ‫ﻛﻪ در روﻧﺪ ﺑﻴﻤﺎري در ﺳﻠﻮل ﻛﺒﺪي ﺗﻮﻟﻴﺪ ﻣﻲﺷﻮﻧﺪ، اﺛﺮ درﻣﺎﻧﻲ‬ ‫ﺧﻮد را اﻳﻔﺎ ﻣﻲﻛﻨﻨﺪ. اﺛﺮ درﻣﺎﻧﻲ وﻳﺘﺎﻣﻴﻦ ‪ E‬ﻛﻪ ﻳﻚ آﻧﺘﻲ اﻛﺴﻴﺪان‬ ‫ﻗﻮي و ﻧﺴﺒﺘﺎ ارزان اﺳﺖ، در ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب در ﺑﺎﻟﻐﻴﻦ و‬ ‫ﻛﻮدﻛﺎن ﺗﺎﺋﻴﺪ ﺷﺪه اﺳﺖ ]93-73[. در ﺗﻤﺎم اﻳﻦ ﻣﻄﺎﻟﻌﺎت وﻳﺘﺎﻣﻴﻦ ‪E‬‬ ‫ﺗﺤﻤﻞ ﺷﺪه و ﺑﺎ ﺑﻬﺒﻮد ﻣﻴﺰان آﻧﺰﻳﻢﻫﺎي ﻛﺒﺪي، ﻳﺎﻓﺘﻪﻫﺎي‬ ‫ﺳﻮﻧﻮﮔﺮاﻓﻴﻚ و ﻫﻤﭽﻨﻴﻦ ﺑﺎﻓﺖ ﺷﻨﺎﺳﻲ ﻛﺒﺪ ﻫﻤﺮاه ﺑﻮده اﺳﺖ ]04[.‬ ‫ﻫﻢاﻛﻨﻮن ﮔﺮوه ﺑﺰرﮔﻲ از ﻣﻮاد آﻧﺘﻲ اﻛﺴﻴﺪان ﻣﺎﻧﻨﺪ »ان اﺳﺘﻴﻞ‬ ‫ﺳﻴﺴﺘﺌﻴﻦ« و »ﺳﻮﭘﺮ اﻛﺴﻴﺪ دﺳﻤﻮﺗﺎز« در ﻣﺮاﺣﻞ اﺑﺘﺪاﻳﻲ ﺗﺤﻘﻴﻘﺎﺗﻲ ﺑﻪ‬

‫ﭘﻴﮕﻴﺮي و ﻣﺮاﻗﺒﺖﻫﺎي دورهاي‬
‫ﭘﺲ از ﺗﺸﺨﻴﺺ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب اوﻟﻴﻦ ﻗﺪم درﻣﺎﻧﻲ‬ ‫رﺳﻴﺪن ﺑﻪ وزن اﻳﺪه آل و ﺳﭙﺲ ﺣﻔﻆ آن ﺑﺎ اﻧﺠﺎم ﻓﻌﺎﻟﻴﺖ ﺑﺪﻧﻲ‬ ‫ﻣﺮﺗﺐ و ﻣﺴﺘﻤﺮ اﺳﺖ. در ﺑﻴﻤﺎران ﻣﺒﺘﻼ ﺑﻪ دﻳﺎﺑﺖ ﻛﻨﺘﺮل دﻗﻴﻖ ﻗﻨﺪ‬

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‫ﻓﺼﻠﻨﺎﻣﻪ ﻓﻴﺾ| ﺗﺎﺑﺴﺘﺎن 9831| دوره 41| ﺷﻤﺎره 2‬ ‫‪www.SID.ir‬‬

‫‪... ، of SID‬‬ ‫ﻣﺮوري ﺑﺮ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب‪Archive‬‬ ‫ﭼﺮب ﻧﺎﺷﻲ از اﺛﺮات ﺳﻨﺪروم ﻣﺘﺎﺑﻮﻟﻴﻚ و ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ ﺑﺮ‬ ‫روي اﻋﻀﺎء ﺣﻴﺎﺗﻲ ﺑﺪن ﻣﺎﻧﻨﺪ ﺳﻴﺴﺘﻢ ﻗﻠﺐ و ﻋﺮوق و ﺳﻴﺴﺘﻢ‬ ‫اﻋﺼﺎب ﻣﻲﺑﺎﺷﺪ. ﻣﻬﻤﺘﺮﻳﻦ ﻋﻠﺖ ﻣﺮگ و ﻣﻴﺮ در اﻳﻦ ﺑﻴﻤﺎري ﻧﻴﺰ‬ ‫ﻧﺎﺷﻲ از ﻋﻮارض ﻗﻠﺒﻲ ﻋﺮوﻗﻲ اﺳﺖ. در ﺻﻮرت ﻛﻨﺘﺮل ﻋﻮارض‬ ‫ﻗﻠﺒﻲ و ﻋﺮوﻗﻲ، ﺳﻴﺮ ﺑﻴﻤﺎري ﻛﺒﺪ ﺑﻪ ﺳﻮي ازﻣﺎن اداﻣﻪ ﭘﻴﺪا ﻛﺮده و‬ ‫ﺗﻐﻴﻴﺮات ﻏﻴﺮ ﻗﺎﺑﻞ ﺑﺮﮔﺸﺖ ﺑﺎﻓﺖ ﻛﺒﺪ )ﺳﻴﺮوز( ﺑﻪ وﺟﻮد آﻣﺪه، ﻛﻪ‬ ‫در اﻳﻦ ﻣﺮﺣﻠﻪ درﻣﺎن، ﺑﺴﻴﺎر ﮔﺮان و ﻣﺸﻜﻞ ﺧﻮاﻫﺪ ﺑﻮد. ﭼﺎﻗﻲ،‬ ‫ﺑﻴﻤﺎري دﻳﺎﺑﺖ و ﺳﻦ ﺑﺎﻻ از ﻋﻮاﻣﻞ ﺑﺴﻴﺎر ﻣﻬﻢ در ﭘﻴﺸﺮﻓﺖ ﺑﻴﻤﺎري‬ ‫ﻛﺒﺪ ﭼﺮب ﺑﻪ ﺳﻤﺖ ﺳﻴﺮوز ﻣﻲ ﺑﺎﺷﻨﺪ. در ﻣﺮﺣﻠﻪاي ﻛﻪ ﺑﻴﻤﺎري ﺑﻪ‬ ‫ﺳﻴﺮوز رﺳﻴﺪه ﺑﺎﺷﺪ، ﻋﻼﺋﻤﻲ ﻧﻈﻴﺮ ﺧﻮﻧﺮﻳﺰي ﮔﻮارﺷﻲ، اﻏﻤﺎي‬ ‫ﻛﺒﺪي، ﺗﻮرم ﺷﻜﻢ ﻧﺎﺷﻲ از اﺣﺘﺒﺎس ﻣﺎﻳﻊ و ﺑﺪﺧﻴﻤﻲ ﺳﻠﻮل ﻛﺒﺪي‬ ‫دﻳﺪه ﻣﻲﺷﻮد. ﻳﻜﻲ از ﻋﻮارض ﻧﺎدر ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب در ﻣﺮﺣﻠﻪ‬ ‫ﺳﻴﺮوز اﻳﺠﺎد ﺳﺮﻃﺎن ﺳﻠﻮل ﻛﺒﺪي ﻣﻲﺑﺎﺷﺪ. ﺑﺪﻳﻬﻲ اﺳﺖ ﺑﺎ ﻛﻨﺘﺮل‬ ‫ﺑﻴﻤﺎري و ﻋﺪم اﻳﺠﺎد ﺳﻴﺮوز اﻳﻦ ﻋﺎرﺿﻪ ﻗﺎﺑﻞ ﭘﻴﺸﮕﻴﺮي اﺳﺖ؛ اﮔﺮ‬ ‫ﭼﻪ ﻣﻄﺎﻟﻌﺎت ﺑﻴﺸﺘﺮ در ﺧﺼﻮص اﻳﻨﻜﻪ ﭼﻪ ﮔﺮوﻫﻲ از ﻣﺒﺘﻼﻳﺎن ﺑﻪ‬ ‫ﻛﺒﺪ ﭼﺮب ﻣﺴﺘﻌﺪ اﺑﺘﻼء ﺑﻪ ﺳﺮﻃﺎن ﺳﻠﻮل ﻛﺒﺪي ﻣﻲﺑﺎﺷﻨﺪ، ﺿﺮوري‬ ‫ﺑﻪ ﻧﻈﺮ ﻣﻲرﺳﺪ. ﺟﻬﺖ ﺷﻨﺎﺳﺎﻳﻲ زودرس ﺑﺪﺧﻴﻤﻲ ﻛﺒﺪ در ﻣﺒﺘﻼﻳﺎن‬ ‫ﺑﻪ ﺳﻴﺮوز ﻧﺎﺷﻲ از ﻛﺒﺪ ﭼﺮب ﻋﻼوه ﺑﺮ ﻣﻌﺎﻳﻨﺎت دورهاي، اﻧﺠﺎم‬ ‫ﺳﻮﻧﻮﮔﺮاﻓﻲ ﻛﺒﺪ و ﺑﺮرﺳﻲ ﻣﻴﺰان ﻳﻚ ﺷﺎﺧﺺ ﺳﺮﻃﺎن ﻛﺒﺪي ﺑﻪ ﻧﺎم‬ ‫آﻟﻔﺎ ﻓﻴﺘﻮ ﭘﺮوﺗﺌﻴﻦ، ﺗﻮﺻﻴﻪ ﻣﻲﺷﻮد.‬ ‫ﭘﻴﺸﮕﻴﺮي‬ ‫ﻧﺘﻴﺠﻪ ﮔﻴﺮي‬ ‫ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﺗﻈﺎﻫﺮ ﻛﺒﺪي ﺳﻨﺪروم ﻣﺘﺎﺑﻮﻟﻴﻚ ﻳﺎ ﻫﻤﺎن‬ ‫ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ ﻣﻲﺑﺎﺷﺪ. از آزﻣﺎﻳﺶﻫﺎي ﻋﻤﻠﻜﺮد ﻛﺒﺪ و‬ ‫ﺳﻮﻧﻮﮔﺮاﻓﻲ ﻣﻲﺗﻮان ﺑﻪ ﻋﻨﻮان آزﻣﻮن ﻏﺮﺑﺎﻟﮕﺮي ﺟﻬﺖ ﺗﺸﺨﻴﺺ‬ ‫ﺑﻴﻤﺎري اﺳﺘﻔﺎده ﻛﺮد. ﻛﺎﻫﺶ وزن و ﺗﻨﻈﻴﻢ ﭼﺮﺑﻲ و ﻗﻨﺪ ﺧﻮن از‬ ‫ﺑﻬﺘﺮﻳﻦ روشﻫﺎي درﻣﺎﻧﻲ ﻣﻲﺑﺎﺷﻨﺪ. ﺗﺸﺨﻴﺺ و درﻣﺎن زود ﻫﻨﮕﺎم و‬ ‫ﺻﺤﻴﺢ اﻳﻦ ﺑﻴﻤﺎري ﻣﻲﺗﻮاﻧﺪ ﻣﻨﺠﺮ ﺑﻪ ﻛﺎﻫﺶ ﻣﺮگ و ﻣﻴﺮ و ﻋﻮارض‬ ‫ﻧﺎﺷﻲ از ﺑﻴﻤﺎري ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ ﮔﺮدد.‬ ‫ﻫﻤﺎن ﻃﻮر ﻛﻪ ﻗﺒﻼ اﺷﺎره ﺷﺪ اﻛﺜﺮ ﻋﻮارض ﺑﻴﻤﺎري ﻛﺒﺪ‬ ‫ﻋﻮارض‬ ‫ﺟﻬﺖ ﭘﻴﺸﮕﻴﺮي از اﻳﻦ ﺑﻴﻤﺎري ﺣﻔﻆ وزن اﻳﺪه آل و ﻛﻨﺘﺮل‬ ‫ﭼﺮﺑﻲ و ﻗﻨﺪ ﺧﻮن و ﻧﻴﺰ ﺳﺎﻳﺮ اﺟﺰاء ﺳﻨﺪروم ﻣﺘﺎﺑﻮﻟﻴﻚ ﺗﻮﺻﻴﻪ ﻣﻲ-‬ ‫ﺷﻮد. در اﻓﺮاد در ﻣﻌﺮض ﺧﻄﺮ آزﻣﺎﻳﺸﺎت دورهاي ﺧﻮن ﺟﻬﺖ‬ ‫ﺑﺮرﺳﻲ آﻧﺰﻳﻢﻫﺎي ﻛﺒﺪي، ﭼﺮﺑﻲ و ﻗﻨﺪ ﺗﻮﺻﻴﻪ ﻣﻲﺷﻮد ﺗﺎ ﺑﺎ ﺗﺸﺨﻴﺺ‬ ‫و درﻣﺎن زودرس از ﭘﻴﺸﺮﻓﺖ ﺑﻴﻤﺎري ﺟﻠﻮﮔﻴﺮي ﺷﻮد.‬ ‫ﺧﻮن از اﻫﻤﻴﺖ ﺑﺎﻻﻳﻲ ﺑﺮﺧﻮردار اﺳﺖ. در اﻓﺮاد ﺑﺎ اﻓﺰاﻳﺶ ﭼﺮﺑﻲ‬ ‫ﺧﻮن، ﺗﻨﻈﻴﻢ آن ﺑﺎ رژﻳﻢ ﻏﺬاﻳﻲ، ورزش و ﺑﺎﻻﺧﺮه درﻣﺎن داروﻳﻲ‬ ‫ﺗﻮﺻﻴﻪ ﻣﻲﺷﻮد. در ﺗﻤﺎم ﺑﻴﻤﺎران ﻣﺼﺮف آﻧﺘﻲ اﻛﺴﻴﺪانﻫﺎي ﻃﺒﻴﻌﻲ‬ ‫ﻣﺎﻧﻨﺪ اﻧﻮاع ﻣﻴﻮهﺟﺎت و ﻳﺎ وﻳﺘﺎﻣﻴﻦ ‪ E‬و ‪ C‬ﺗﺤﺖ ﻧﻈﺮ ﭘﺰﺷﻚ ﻣﻮﺛﺮ‬ ‫ﺑﻮده و در آﺧﺮ ﺑﺎ ﺷﻨﺎﺧﺘﻪ ﺷﺪن ﻋﻮاﻣﻞ ﺟﺪﻳﺪ دﺧﻴﻞ در ﺑﻴﻤﺎري ﻛﺒﺪ‬ ‫ﭼﺮب، درﻣﺎنﻫﺎ ﺑﺮ اﺳﺎس ﻛﻨﺘﺮل اﻳﻦ ﻋﻮاﻣﻞ اﺳﺘﻮار ﺧﻮاﻫﺪ ﺑﻮد. در‬ ‫ﻣﺒﺘﻼﻳﺎن ﺑﻪ ﻛﺒﺪ ﭼﺮب ﺧﻔﻴﻒ، ﭘﻴﮕﻴﺮي دورهاي ﺑﻪ ﺻﻮرت ﺑﺮرﺳﻲ‬ ‫آﻧﺰﻳﻢ ﻫﺎي ﻛﺒﺪي ﻫﺮ 2 ﺗﺎ 3 ﻣﺎه ﻳﻚﺑﺎر ﺗﻮﺻﻴﻪ ﻣﻲﺷﻮد. در اﻳﻦ‬ ‫ﻣﻮارد ﻋﻤﻮﻣﺎ ﻧﻴﺎز ﺑﻪ ﻧﻤﻮﻧﻪ ﺑﺮداري ﻛﺒﺪ ﻧﻤﻲﺑﺎﺷﺪ، ﻣﮕﺮ اﻳﻨﻜﻪ ﺑﻴﻤﺎر از‬ ‫ﭘﺰﺷﻚ ﻣﻌﺎﻟﺞ ﺑﺨﻮاﻫﺪ ﺗﺎ ﺟﻬﺖ ﺑﺮرﺳﻲ دﻗﻴﻖ ﻣﻴﺰان آﺳﻴﺐ ﻛﺒﺪي‬ ‫ﻧﻤﻮﻧﻪ ﺑﺮداري از ﻛﺒﺪ اﻧﺠﺎم ﺷﻮد. در ﻣﺒﺘﻼﻳﺎن ﺑﻪ ﻛﺒﺪ ﭼﺮب ﻣﺘﻮﺳﻂ‬ ‫ﺗﺎ ﺷﺪﻳﺪ ﻛﻪ ﺳﻦ ﺑﺎﻻﺗﺮ از 05 ﺳﺎل داﺷﺘﻪ، ﭼﺎق ﻫﺴﺘﻨﺪ، دﻳﺎﺑﺖ ﻳﺎ‬ ‫ﻓﺸﺎر ﺧﻮن دارﻧﺪ و ﻧﻴﺰ در ﻛﺴﺎﻧﻲ ﻛﻪ اﻓﺰاﻳﺶ ﻣﻴﺰان »آﺳﭙﺎرﺗﺎت‬ ‫آﻣﻴﻨﻮ ﺗﺮاﻧﺴﻔﺮاز« آﻧﺎن از ﻣﻴﺰان »آﻻﻧﻴﻦ آﻣﻴﻨﻮ ﺗﺮاﻧﺴﻔﺮاز« ﺑﻴﺸﺘﺮاﺳﺖ و‬ ‫ﻳﺎ ﻣﻴﺰان اﻳﻦ 2 آﻧﺰﻳﻢ ﺑﻴﺸﺘﺮ از 2 ﺑﺮاﺑﺮ ﺣﺪ ﻃﺒﻴﻌﻲ اﺳﺖ ﺑﻪ ﻣﻨﻈﻮر‬ ‫ﺷﻨﺎﺳﺎﻳﻲ وﺳﻌﺖ درﮔﻴﺮي ﻛﺒﺪ ﻧﻤﻮﻧﻪ ﺑﺮداري ﻛﺒﺪ ﺗﻮﺻﻴﻪ ﺷﺪه، وﻟﻲ‬ ‫ﺑﻪ ﻧﻈﺮ ﻣﻲرﺳﺪ ﻛﻪ ﺑﺮرﺳﻲ آﻧﺰﻳﻢﻫﺎي ﻛﺒﺪي ﺑﺎ ﻓﻮاﺻﻞ ﻧﺰدﻳﻚﺗﺮ ﻳﻚ‬ ‫ﺗﺎ 2 ﻣﺎه ﻳﻚﺑﺎر ﻛﺎﻓﻲ ﺑﺎﺷﺪ؛ اﮔﺮﭼﻪ ﺗﺎ ﺑﻪ ﺣﺎل در اﻳﻦ زﻣﻴﻨﻪ‬ ‫دﺳﺘﻮاﻟﻌﻤﻞ ﺧﺎﺻﻲ از ﺳﻮي ﻣﺤﻘﻘﻴﻦ اﻳﻦ رﺷﺘﻪ اراﺋﻪ ﻧﺸﺪه اﺳﺖ.‬

‫:‪References‬‬
‫.01-9 .‪[1] Jamali R, Jamali A. Fatty Liver Disease. 1st ed. Kashan: Davat; 2010. p‬‬ ‫‪[2] Ludwig J, Viggiano TR, McGill DB, Oh BJ. Nonalcoholic steatohepatitis: Mayo Clinic experiences with a‬‬ ‫.8-434 :)7(55 ;0891 ‪hitherto unnamed disease. Mayo Clin Proc‬‬ ‫‪[3] Neuschwander-Tetri BA, Caldwell SH. Nonalcoholic steato-hepatitis: Summary of an AASLD single topic‬‬ ‫.91-2021 :)5(73 ;3002 ‪conference. Hepatology‬‬ ‫‪[4] Bellentani S, Saccoccio G, Masutti F, Crocè LS, Brandi G, Sasso F, et al. Prevalence of and risk factors for‬‬ ‫.7-211 :)2(231 ;0002 ‪hepatic steatosis in Northern Italy. Ann Intern Med‬‬ ‫‪[5] Jamali R, Pourshams A, Amini S, Deyhim MR, Rezvan H, Malekzadeh R. The Upper normal limit of serum‬‬ ‫.7–206 :)6(11 ;8002 ‪alanine aminotransferase in Golestan Province, Northeast of Iran. Arch Iranian Med‬‬ ‫‪[6] Pacifico L, Celestre M, Anania C, Paolantonio P, Chiesa C, Laghi A. MRI and ultrasound for hepatic fat‬‬ ‫‪quantification:relationships to clinical and metabolic characteristics of pediatric nonalcoholic fatty liver‬‬ ‫.7-245 :)4(69 ;7002 ‪disease. Acta Paediatr‬‬

‫ﻓﺼﻠﻨﺎﻣﻪ ﻓﻴﺾ| ﺗﺎﺑﺴﺘﺎن 9831| دوره 41| ﺷﻤﺎره 2‬

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Archive of SID

‫راﻳﻜﺎ و ارﺳﻴﺎ ﺟﻤﺎﻟﻲ‬

[7] Jamali R, Khonsari M, Merat S, Khoshnia M, Jafari E, Bahram Kalhori A, et al. Persistent alanine aminotransferase elevation among Iranian general population: prevalence and causes. World J Gastroenterol 2008; 14(18): 2867-71. [8] Söderberg C, Stål P, Askling J, Glaumann H, Lindberg G, Marmur J, et al. Decreased survival of subjects with elevated liver function tests during a 28-year follow-up. Hepatology 2010; 51(2): 595-602. [9] Adams LA, Lymp JF, St Sauver J, Sanderson SO, Lindor KD, Feldstein A, et al. The natural history of nonalcoholic fatty liver disease: a population-based cohort study. Gastroenterology 2005; 129(1): 113-21. [10] Chitturi S, Farrell GC, George J. Non-alcoholic steatohepatitis in the Asia-Pacific region: future shock? J Gastroenterol Hepatol 2004; 19(4): 368-74. [11] Merat S, Rezvan H, Nouraie M, Abolghasemi H, Jamali R, Amini-Kafiabad S, et al. Seroprevalence and risk factors of hepatitis A virus infection in Iran: a population based study. 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[in Persian] [23] Poonawala A, Nair S, Thuluvath P. Prevalence of obesity and diabetes in patients with cryptogenic cirrhosis: A case-control study. Hepatology 2002; 32(4 Pt 1): 689-92. [24] Hui JM, Kench JG, Chitturi S, Sud A, Farrell GC, Byth K, et al. Long-term outcomes of cirrhosis in nonalcoholic steatohepatitis compared with hepatitis C. Hepatology 2003; 38(2): 420-7. [25] Dixon J, Bhathal P, O'Brien P. Nonalcoholic fatty liver disease: Predictors of nonalcoholic steatohepatitis and liver fibrosis in the severely obese. Gastroenterology 2001; 121(1): 91-100. [26] Tsang SW, Ng WF, Wu BP, Chow DA, Li ET, Wong TC. Predictors of fibrosis in Asian patients with non-alcoholic steatohepatitis. J Gastroenterol Hepatol 2006; 21(1 Pt 1): 116-21. [27] Ratziu V, Giral P, Charlotte F, Bruckert E, Thibault V, Theodorou I, et al. Liver fibrosis in overweight patients. Gastroenterology 2000; 118(6): 1117-23. [28] Leite NC, Salles GF, Araujo AL, Villela-Nogueira CA, Cardoso CR. Prevalence and associated factors of nonalcoholic fatty liver disease in patients with type-2 diabetes mellitus. Liver Int 2009;29: 113-9. [29] Lee DS, Evans JC, Robins SJ, Wilson PW, Albano I, Fox CS, et al. Gamma glutamyl transferase and metabolic syndrome, cardiovascular disease, and mortality risk: the Framingham Heart Study. Arterioscler Thromb Vasc Biol 2007; 27(1): 127-33. [30] Nakhjavani M, Khalilzadeh O, Khajeali L, Esteghamati A, Morteza A, Jamali A, et al. Serum oxidizedLDL is associated with diabetes duration independent of maintaining optimized levels of LDL-cholesterol. Lipids 2010; 45(4): 321-7. [31] Bugianesi E, Manzini P, D'Antico S, Vanni E, Longo F, Leone N, et al. Relative contribution of iron burden, HFE mutations, and insulin resistance to fibrosis in nonalcoholic fatty liver. Hepatology 2004; 39(1): 179-87. [32] Saadeh S, Younossi ZM, Remer EM, Gramlich T, Ong JP, Hurley M, et al. The utility of radiological imaging in nonalcoholic fatty liver disease. Gastroenterology 2002; 123(3): 745-50. [33] Hickman IJ, Jonsson JR, Prins JB, Ash S, Purdie DM, Clouston AD, et al. Modest weight loss and physical activity in overweight patients with chronic liver disease results in sustained improvements in alanine aminotransferase, fasting insulin, and quality of life. Gut 2004; 53(3): 413-9.

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... ، of SID Archive‫ﻣﺮوري ﺑﺮ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب‬ [34] Knobler H, Schattner A, Zhornicki T, Malnick SD, Keter D, Sokolovskaya N, et al. Knobler H, Schattner A, Zhornicki T, et al. Fatty liver-an additional and treatable feature of the insulin resistance syndrome. QJM 1999; 92(2): 87-96. [35] Kugelmas M, Hill DB, Vivian B, Marsano L, McClain CJ. Cytokines and NASH: A pilot study of the effects of lifestyle modification and vitamin E. Hepatology 2003; 38: 413-9. [36] Luyckx F, Lefebvre P, Scheen A. Nonalcoholic steatohepatitis: Association with obesity and insulin resistance, and influence of weight loss. Diabetes Metab 2000; 26: 98-106. [37] Hasegawa T, Yoneda M, Nakamura K, Makino I, Terano A. Plasma transforming growth factor-β1 and efficacy of alpha-tocopherol in patients with nonalcoholic steatohepatitis: A pilot study. Aliment Pharmacol Ther 2001; 15: 1667-72. [38] Harrison S, Torgerson S, Hayashi P, et al. Vitamin E and vitamin C treatment improves fibrosis in patients with nonalcoholic steatohepatitis. Am J Gastroenterol 2003; 98(11): 2485-90. [39] Lavine J. Vitamin E treatment of nonalcoholic steatohepatitis in children: A pilot study. J Pediatr 2000; 136(6): 734-8. [40] Sanyal AJ, Chalasani N, Kowdley KV, McCullough A, Diehl AM, Bass NM, et al. Pioglitazone, vitamin E, or placebo for nonalcoholic steatohepatitis. 2010; 362(18): 1675-85. [41] Marchesini G, Brizi M, Bianchi G, Tomasetti S, Zoli M, Melachionda N. Metformin in nonalcoholic steatohepatitis. Lancet 2001; 358: 893-4. [42] Nair S, Diehl AM, Wiseman M, Farr GH Jr, Perrillo RP. Metformin in the treatment of nonalcoholic steatohepatitis: A pilot open label trial. Aliment Pharmacol Ther 2004; 20: 23-8. [43] Duvnjak M, Tomasic V, Gomercic M, Smircic Duvnjak L, Barsic N, Lerotic I. J Physiol Pharmacol. Therapy of nonalcoholic fatty liver disease: current status. J Physiol Pharmacol 2009; 60 Suppl 7: 57-66. [44] Neuschwander-Tetri BA, Brunt EM, Wehmeier KR, Oliver D, Bacon BR. Improved nonalcoholic steatohepatitis after 48 weeks of treatment with the PPAR-γ ligand rosiglitazone. Hepatology 2003; 38(4):1008-17. [45] Promrat K, Lutchman G, Uwaifo GI, Freedman RJ, Soza A, Heller T, et al. A pilot study of pioglitazone treatment for nonalcoholic steatohepatitis. Hepatology 2004; 39(1):188-96. [46] Caldwell SH, Hespenheide EE, Redick JA, Iezzoni JC, Battle EH, Sheppard BL. A pilot study of a thiazolidinedione, troglitazone, in nonalcoholic steatohepatitis. Am J Gastroenterol 2001; 96(2): 519-25. [47] Basaranoglu M, Acbay O, Sonsuz A. A controlled trial of gemfibrozil in the treatment of patients with nonalcoholic steatohepatitis. J Hepatol 1999; 31(2): 384-92. [48] Kiyici M, Gulten M, Gurel S, Nak SG, Dolar E, Savci G, et al. Ursodeoxycholic acid and atorvastatin in the treatment of nonalcoholic steatohepatitis. Can J Gastroenterol 2003; 17(12): 713-8. [49] Lindor KD, Kowdley KV, Heathcote EJ, Harrison ME, Jorgensen R, Angulo P, et al. Ursodeoxycholic acid for treatment of nonalcoholic steatohepatitis: Results of a randomized trial. Hepatology 2004; 39(3): 770-8.

2 ‫ﻓﺼﻠﻨﺎﻣﻪ ﻓﻴﺾ| ﺗﺎﺑﺴﺘﺎن 9831| دوره 41| ﺷﻤﺎره‬

179 www.SID.ir

‫‪Archive of SID‬‬

‫راﻳﻜﺎ و ارﺳﻴﺎ ﺟﻤﺎﻟﻲ‬

‫ﮔﺮوه ﻫﺎي ﻫﺪف ﻣﻘﺎﻟﻪ ﺧﻮد آﻣﻮزي: ﭘﺰﺷﻜﺎن ﻋﻤﻮﻣﻲ، ﻣﺘﺨﺼﺼﻴﻦ داﺧﻠﻲ، ﻋﻔﻮﻧﻲ، آﺳﻴﺐ ﺷﻨﺎﺳﻲ، زﻧﺎن و زاﻳﻤﺎن، ﺟﺮاﺣﻲ‬ ‫ﻋﻤﻮﻣﻲ و ﻛﺎرﺷﻨﺎﺳﺎن ﻋﻠﻮم آزﻣﺎﻳﺸﮕﺎﻫﻲ و ﭘﺮﺳﺘﺎري‬
‫ﭼﺮب دارد.‬ ‫ج- ﺑﺎ وﺟﻮد ﭼﺎﻗﻲ ﺷﺪت ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﺑﻴﺸﺘﺮ ﻣﻲﺷﻮد.‬ ‫د- ﭼﺎﻗﻲ از اﺟﺰاي ﺳﻨﺪروم ﻣﺘﺎﺑﻮﻟﻴﻚ ﺑﻮده و ارﺗﺒﺎط ﭼﻨﺪاﻧﻲ ﺑﺎ ﺑﻴﻤﺎري‬ ‫ﻛﺒﺪ ﭼﺮب ﻧﺪارد.‬ ‫8- در راﺑﻄﻪ ﺑﺎ ﺗﺸﺨﻴﺺ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻛﺪام ﮔﺰﻳﻨﻪ‬ ‫ﻧﺎدرﺳﺖ اﺳﺖ؟‬ ‫اﻟﻒ- ﺷﻨﺎﺳﺎﻳﻲ ﺑﻴﻤﺎري ﺑﺮ اﺳﺎس ﺣﺴﺎﺳﻴﺖ روش ﺗﺼﻮﻳﺮ ﺑﺮداري ﺑﻪ ﻛﺎر‬ ‫رﻓﺘﻪ ﻣﺘﻔﺎوت اﺳﺖ.‬ ‫ب- ﺑﺎ ﺗﻐﻴﻴﺮ ﺳﻄﺢ ﺳﺮﻣﻲ آﻧﺰﻳﻢﻫﺎي ﻛﺒﺪي ﺣﺴﺎﺳﻴﺖ روشﻫﺎي‬ ‫آزﻣﺎﻳﺸﮕﺎﻫﻲ در ﺗﺸﺨﻴﺺ ﺑﻴﻤﺎري ﺗﻐﻴﻴﺮ ﻣﻲﻛﻨﺪ.‬ ‫ج- اﺳﺘﻔﺎده از روشﻫﺎي آزﻣﺎﻳﺸﮕﺎﻫﻲ ﺑﻪ ﺗﻨﻬﺎﻳﻲ ﻣﻌﻴﺎر ﺧﻮﺑﻲ ﺟﻬﺖ‬ ‫ﺗﺸﺨﻴﺺ ﺑﻴﻤﺎري ﻧﻴﺴﺖ.‬ ‫د- ﺗﺸﺨﻴﺺ ﺑﻴﻤﺎري ﻛﻤﻚ ﭼﻨﺪاﻧﻲ ﺟﻬﺖ اﻓﺰاﻳﺶ ﻃﻮل ﻋﻤﺮ ﺑﻴﻤﺎر‬ ‫ﻧﺨﻮاﻫﺪ ﻛﺮد.‬ ‫9- در ﻣﻮرد ﺑﻴﻤﺎري زاﻳﻲ ﻛﺒﺪ ﭼﺮب ﻛﺪام ﮔﺰﻳﻨﻪ ﻧﺎدرﺳﺖ اﺳﺖ؟‬ ‫اﻟﻒ- اوﻟﻴﻦ ﻣﺮﺣﻠﻪ اﺧﺘﻼل در ﺳﻮﺧﺖ و ﺳﺎز اﺳﻴﺪﻫﺎي ﭼﺮب در ﻛﺒﺪ‬ ‫اﺳﺖ.‬ ‫ب- اﻓﺰاﻳﺶ ﻣﻴﺰان ﭼﺮﺑﻲ ﻛﺒﺪ ﺑﻪ دﻟﻴﻞ ﺑﻪ ﻫﻢ ﺧﻮردن روﻧﺪ ﺗﻮﻟﻴﺪ ﭼﺮﺑﻲ و‬ ‫ﺗﺮﺷﺢ آن از ﻛﺒﺪ اﺳﺖ.‬ ‫ج- اﻓﺰاﻳﺶ ﺗﺮﺷﺢ ﻓﺴﻔﻮﻟﻴﭙﻴﺪﻫﺎ ﻣﺸﺎﻫﺪه ﻣﻲ ﺷﻮد.‬ ‫د- ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ ﺑﻪ ﻋﻨﻮان اوﻟﻴﻦ ﻋﺎﻣﻞ ﺑﻴﻤﺎري ﺷﻨﺎﺧﺘﻪ ﺷﺪه اﺳﺖ.‬ ‫01- ﻛﺪام ﻳﻚ از ﻋﻮاﻣﻞ ﻣﻬﻢ در اﻳﺠﺎد ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻧﻤﻲ-‬ ‫ﺑﺎﺷﺪ؟‬ ‫ب- ﻓﻴﺒﺮوﻧﻜﺘﻴﻦ‬ ‫د- آدﻳﭙﻮﻧﻜﺘﻴﻦ‬ ‫اﻟﻒ- اﺳﻴﺪ ﭼﺮب‬ ‫ج- ﺗﻲ ان اف آﻟﻔﺎ‬ ‫1- ﻛﺪام ﮔﺰﻳﻨﻪ در ﻣﻮرد ﺑﻴﻤﺎري ﭼﺮب ﻧﺎدرﺳﺖ اﺳﺖ؟‬ ‫اﻟﻒ- ﺷﻴﻮع ﺑﻴﻤﺎري در ﺟﺎﻣﻌﻪ ﻣﺎ روﺑﻪ اﻓﺰاﻳﺶ اﺳﺖ.‬ ‫ب- اﻳﻦ ﺑﻴﻤﺎري ﻣﻲ ﺗﻮاﻧﺪ ﻣﻨﺠﺮ ﺑﻪ ﺑﻴﻤﺎري ﻣﺰﻣﻦ و ﻏﻴﺮ ﻗﺎﺑﻞ ﺑﺮﮔﺸﺖ‬ ‫ﻛﺒﺪي ﻣﻲ ﺷﻮد.‬ ‫ج- ارﺗﺒﺎﻃﻲ ﺑﻴﻦ اﻳﻦ ﺑﻴﻤﺎري و ﺑﻴﻤﺎري ﭘﺮﻓﺸﺎري ﺧﻮن و ﻧﻴﺰ اﻓﺰاﻳﺶ ﭼﺮﺑﻲ‬ ‫ﺧﻮن وﺟﻮد ﻧﺪارد.‬ ‫د- اﻳﻦ ﺑﻴﻤﺎري ﺗﻈﺎﻫﺮ ﻛﺒﺪي ﺳﻨﺪروم ﻣﺘﺎﺑﻮﻟﻴﻚ اﺳﺖ.‬ ‫2- ﻛﺪام ﮔﺰﻳﻨﻪ در ﻣﻮرد ﻫﻤﻪ ﮔﻴﺮﺷﻨﺎﺳﻲ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب‬ ‫ﻧﺎدرﺳﺖ اﺳﺖ؟‬ ‫اﻟﻒ- ﺑﻪ ﻧﻈﺮ ﻣﻲ رﺳﺪ از ﺷﺎﻳﻊ ﺗﺮﻳﻦ ﺑﻴﻤﺎري ﻫﺎي ﻣﺰﻣﻦ ﻛﺒﺪي در دﻧﻴﺎ‬ ‫ﺑﺎﺷﺪ.‬ ‫ب- ﻣﻴﺰان ﺷﻴﻮع ﺑﻴﻤﺎري ﺑﺎ ﻣﻴﺰان ﭼﺎﻗﻲ در ﺟﺎﻣﻌﻪ راﺑﻄﻪ دارد.‬ ‫ج- ﺷﻴﻮع ﺑﻴﻤﺎري در ﺟﻨﺲ ﻣﺮد ﺑﻴﺸﺘﺮ اﺳﺖ.‬ ‫د- اﻳﻦ ﺑﻴﻤﺎري ﺷﺎﻳﻊ ﺗﺮﻳﻦ ﻋﻠﺖ اﺳﻴﺪوز ﺑﺎ ﻋﻠﺖ ﻧﺎﺷﻨﺎﺧﺘﻪ ﻣﻲ ﺑﺎﺷﺪ.‬ ‫3- ﻛﺪام ﮔﺰﻳﻨﻪ در ﻣﻮرد ﺷﻴﻮع ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻧﺎدرﺳﺖ‬ ‫اﺳﺖ؟‬ ‫اﻟﻒ- ﻣﻴﺰان ﺷﻴﻮع آن رو ﺑﻪ ﻛﺎﻫﺶ اﺳﺖ.‬ ‫ب- ﺷﻴﻮع اﻳﻦ ﺑﻴﻤﺎري در اﻳﺮان ﺣﺪود 2 درﺻﺪ در ﺟﻤﻌﻴﺖ ﺑﺎﻻﺗﺮ از 81‬ ‫ﺳﺎل اﺳﺖ.‬ ‫ج- اﻳﻦ ﺑﻴﻤﺎري در ﺑﻌﻀﻲ ﺧﺎﻧﻮاده ﻫﺎ ﺷﻴﻮع ﺑﻴﺸﺘﺮي ﻧﺴﺒﺖ ﺑﻪ ﺟﺎﻣﻌﻪ دارد.‬ ‫د- ﺷﻴﻮع ﺑﻴﻤﺎري ﺑﺎﺗﻮﺟﻪ ﺑﻪ ﻧﻮع روش ﺗﺸﺨﻴﺼﻲ ﺑﻪ ﻛﺎر رﻓﺘﻪ ﻣﺘﻔﺎوت‬ ‫اﺳﺖ.‬ ‫4- در ﻣﻮرد ﻋﻼﺋﻢ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻛﺪام ﮔﺰﻳﻨﻪ ﻧﺎدرﺳﺖ اﺳﺖ؟‬ ‫اﻟﻒ- اﻛﺜﺮ ﺑﻴﻤﺎران از درد ﻧﺎﺣﻴﻪ ﻗﺴﻤﺖ راﺳﺖ و ﺑﺎﻻي ﺷﻜﻢ ﺷﻜﺎﻳﺖ‬ ‫دارﻧﺪ.‬ ‫ب- اﺣﺴﺎس ﺳﻨﮕﻴﻨﻲ و درد ﺷﻜﻢ از ﻋﻼﻳﻢ ﺑﻴﻤﺎري اﺳﺖ.‬ ‫ج- اﻛﺜﺮ ﺑﻴﻤﺎران ﺑﻪ ﺻﻮرت ﺗﺼﺎدﻓﻲ ﺗﺸﺨﻴﺺ داده ﻣﻲ ﺷﻮﻧﺪ.‬ ‫د- اﺣﺴﺎس ﺧﺴﺘﮕﻲ زودرس ﻣﻲﺗﻮاﻧﺪ از ﻋﻼﻳﻢ ﺑﻴﻤﺎري ﺑﺎﺷﺪ.‬ ‫5- ﻛﺪام ﻳﻚ از ﻣﻮارد زﻳﺮ از ﻋﻼﻳﻢ ﺑﺎﻟﻴﻨﻲ ﻛﺒﺪ ﭼﺮب ﻧﻴﺴﺖ؟‬ ‫ب- ﺑﺮزﮔﻲ ﻃﺤﺎل‬ ‫د- ﻣﺎﻳﻊ در ﺷﻜﻢ‬ ‫ب- اﻟﻜﻞ‬ ‫د- آﻣﻴﻮدارون‬ ‫اﻟﻒ- ﺑﺰرﮔﻲ ﻛﺒﺪ‬ ‫ج- رﻳﺰش ﻣﻮي ﺳﺮ‬ ‫اﻟﻒ- ﭼﺎﻗﻲ‬ ‫ج- ﻟﻴﭙﻮدﻳﺴﺘﺮوﻓﻲ‬ ‫اﺳﺖ؟‬ ‫اﻟﻒ- ﭼﺎﻗﻲ از ﻣﻬﻢﺗﺮﻳﻦ ﺑﻴﻤﺎريﻫﺎي ﻫﻤﺮاه ﺑﺎ ﻛﺒﺪ ﭼﺮب اﺳﺖ.‬ ‫ب- ﭼﺮﺑﻲ ﺷﻜﻤﻲ ﻧﻘﺶ ﻣﻬﻤﺘﺮي از ﭼﺎﻗﻲ ﻛﻞ ﺑﺪن در ﺑﺮوز ﺑﻴﻤﺎري ﻛﺒﺪ‬

‫11- در ﻣﻮرد ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻛﺪام ﮔﺰﻳﻨﻪ ﺻﺤﻴﺢ اﺳﺖ؟‬ ‫اﻟﻒ- ﻣﻴﻜﺮوبﻫﺎي روده اي ﻧﻘﺸﻲ در ﺑﻴﻤﺎري زاﻳﻲ ﻧﺪارﻧﺪ.‬ ‫ب- واﺳﻄﻪ ﻫﺎي ﺷﻴﻤﻴﺎﻳﻲ اﻟﺘﻬﺎب ﻣﺎﻧﻨﺪ اﻳﻨﺘﺮﻟﻮﻛﻴﻦ 21 در ﺑﻴﻤﺎري زاﻳﻲ‬ ‫ﻧﻘﺶ دارﻧﺪ.‬ ‫ج- ﭘﻴﺸﺮﻓﺖ ﺑﻴﻤﺎري ﺑﺮ اﺳﺎس ﺷﺪت ﺗﻮﻟﻴﺪ واﺳﻄﻪﻫﺎي ﺷﻴﻤﻴﺎﻳﻲ اﻟﺘﻬﺎب‬ ‫ﭘﻴﺶ ﺑﻴﻨﻲ ﻣﻲﺷﻮد.‬ ‫د- ﻟﭙﺘﻴﻦ و آﻧﮋﻳﻮﺗﺎﻧﺴﻴﻦ ﻣﻲﺗﻮاﻧﻨﺪ از واﺳﻄﻪﻫﺎي ﻣﻮﺛﺮ در ﻣﻴﺰان ﺑﺎﻓﺖ‬ ‫ﺟﻮﺷﮕﺎﻫﻲ ﺑﺎﺷﻨﺪ.‬ ‫21- ﺑﻬﺘﺮﻳﻦ ﻣﻌﻴﺎر ﺟﻬﺖ ﺑﺮرﺳﻲ ﻣﻴﺰان و ﺷﺪت آﺳﻴﺐ ﻛﺒﺪي‬ ‫ﻛﺪام اﺳﺖ؟‬ ‫ب- ﻧﻤﻮﻧﻪ ﺑﺎﻓﺖ ﺷﻨﺎﺳﻲ ﻛﺒﺪ‬ ‫د- ﺷﺮح ﺣﺎل‬ ‫اﻟﻒ- روشﻫﺎي ﺗﺼﻮﻳﺮ ﺑﺮداري‬ ‫ج- روش ﻫﺎي آزﻣﺎﻳﺸﮕﺎﻫﻲ‬

‫6- ﻛﺪام ﻳﻚ از ﻣﻮارد ذﻳﻞ از ﻋﻠﻞ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻧﻴﺴﺖ؟‬

‫7- در راﺑﻄﻪ ﺑﺎ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب و ﭼﺎﻗﻲ ﻛﺪام ﮔﺰﻳﻨﻪ ﻧﺎدرﺳﺖ‬

‫31- ﻛﺪام ﻳﻚ از ﻣﻌﻴﺎرﻫﺎي ﺷﺪت ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻣﻲ ﺑﺎﺷﺪ؟‬

‫081‬

‫ﻓﺼﻠﻨﺎﻣﻪ ﻓﻴﺾ| ﺗﺎﺑﺴﺘﺎن 9831| دوره 41| ﺷﻤﺎره 2‬ ‫‪www.SID.ir‬‬

‫‪... ، of SID‬‬ ‫ﻣﺮوري ﺑﺮ ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب‪Archive‬‬ ‫د- ﻫﻴﺮﺷﭙﺮوﻧﮓ‬ ‫ج- ﻫﭙﺎﺗﻴﺖ داروﻳﻲ‬ ‫ﻣﻮﺛﺮ در درﻣﺎن ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻧﻤﻲ ﺑﺎﺷﻨﺪ؟‬ ‫ب- وﻳﺘﺎﻣﻴﻦ ‪C‬‬ ‫د- ﺑﺘﺎﻳﻴﻦ‬ ‫اﻟﻒ- اﺳﺘﺎﺗﻴﻦﻫﺎ‬ ‫ج- وﻳﺘﺎﻣﻴﻦ ‪E‬‬ ‫اﻟﻒ- داروﻫﺎي ﭘﺎﺋﻴﻦ آورﻧﺪه ﭼﺮﺑﻲ ﺧﻮن‬ ‫ب- داروﻫﺎي ﺣﺴﺎس ﻛﻨﻨﺪه ﺑﻪ اﻧﺴﻮﻟﻴﻦ‬ ‫ج- رژﻳﻢ ﻏﺬاﻳﻲ و رﺳﻴﺪن ﺑﻪ وزن اﻳﺪه آل‬ ‫د- ﭘﻴﻮﻧﺪ ﻛﺒﺪ‬ ‫02- ﻛﺪام ﻳﻚ از ﻣﻬﻢﺗﺮﻳﻦ ﻋﻮارض ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻣﻲ-‬ ‫ﺑﺎﺷﻨﺪ؟‬ ‫اﻟﻒ- ﺧﻮﻧﺮﻳﺰي ﮔﻮارﺷﻲ‬ ‫ب- ﺳﺮﻃﺎن ﺳﻠﻮل ﻛﺒﺪي‬ ‫ج- ﻋﻮارض ﻗﻠﺒﻲ ﻋﺮوﻗﻲ ﻧﺎﺷﻲ از ﺳﻨﺪروم ﻣﺘﺎﺑﻮﻟﻴﻚ‬ ‫د- اﻋﻀﺎي ﻛﺒﺪي‬ ‫12- ﭘﻴﮕﻴﺮي ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﭼﮕﻮﻧﻪ اﺳﺖ؟‬ ‫اﻟﻒ- ﻛﻨﺘﺮل وزن، ﭼﺮﺑﻲ ﺧﻮن و ﻗﻨﺪ ﺧﻮن‬ ‫ب- ﺳﻮﻧﻮﮔﺮاﻓﻲ ﻛﺒﺪ ﺑﻪ ﺻﻮرت دوره اي‬ ‫ج- ﻧﻤﻮﻧﻪ ﺑﺮداري ﺑﺎﻓﺖ ﺷﻨﺎﺳﻲ ﻛﺒﺪ‬ ‫د- ‪ MRI‬از ﻛﺒﺪ ﺑﻪ ﺻﻮرت دورهاي‬ ‫ب- وﻳﻠﺴﻮن‬ ‫ب- آﻟﻜﺎﻟﻴﻦ ﻓﺴﻔﺎﺗﺎز‬ ‫د- ﻓﺮﻳﺘﻴﻦ‬ ‫ب- ﻛﺎﻫﺶ اﻧﺴﻮﻟﻴﻦ‬ ‫د- ﻛﺎﻫﺶ "ﺗﻲ ان اف آﻟﻔﺎ"‬ ‫ب- ﭼﺎﻗﻲ‬ ‫د- اﻟﻜﻞ‬ ‫اﻟﻒ- ﺳﻦ زﻳﺮ 04 ﺳﺎل‬ ‫ج- ﺳﻴﮕﺎر‬ ‫ﺷﻮد؟‬ ‫اﻟﻒ- اﻓﺰاﻳﺶ ‪ LDL‬ﻛﻠﺴﺘﺮول‬ ‫ج- ﻛﺎﻫﺶ ﻓﺮﻳﺘﻴﻦ‬ ‫ﻣﻲ ﻛﻨﻨﺪ؟‬ ‫اﻟﻒ- آﻻﻧﻴﻦ آﻣﻴﻨﻮ ﺗﺮاﻧﺴﻔﺮاز، آﺳﭙﺎرﺗﺎت آﻣﻴﻨﻮ ﺗﺮاﻧﺴﻔﺮاز، ﮔﺎﻣﺎﮔﻠﻮﺗﺎﻣﻴﻞ‬ ‫ﺗﺮاﻧﺲ ﭘﭙﺘﻴﺪاز‬ ‫ب- اﻳﻨﺘﺮﻟﻮﻛﻴﻦ 03، اﻳﻨﺘﺮﻓﺮون ﺑﺘﺎ‬ ‫ج- آﻧﺘﻲ ﺑﺎدي ﺿﺪ ﻫﺴﺘﻪاي‬ ‫د- آﻧﺘﻲ ﺑﺎدي ﺿﺪ ﻣﻴﺘﻮﻛﻨﺪري‬ ‫61- ﻛﺎﻫﺶ ﻛﺪام ﻳﻚ از اﺟﺰاء ﺳﺮﻣﻲ ﺳﺒﺐ ورم اﻧﺪامﻫﺎ و‬ ‫اﺣﺘﺒﺎس آب در ﺷﻜﻢ ﺑﻪ ﻫﻨﮕﺎم ﺑﺮوز ﺳﻴﺮوز ﻧﺎﺷﻲ از ﻛﺒﺪ ﭼﺮب‬ ‫ﻣﻲ ﺷﻮد؟‬ ‫اﻟﻒ- ﺑﻴﻠﻲ روﺑﻴﻦ‬ ‫ج- آﻟﺒﻮﻣﻴﻦ‬ ‫ﭼﺮب ﻧﻴﺴﺘﻨﺪ؟‬ ‫اﻟﻒ- ﻫﭙﺎﺗﻴﺖ اﻟﻜﻠﻲ‬

‫81- ﻛﺪام ﻳﻚ از ﻣﻮارد زﻳﺮ از ﮔﺮوه داروﻫﺎي آﻧﺘﻲ اﻛﺴﻴﺪان‬

‫41- ﻛﺪام ﻳﻚ از ﻣﻮارد زﻳﺮ در ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻣﺸﺎﻫﺪه ﻣﻲ-‬

‫91- آﺧﺮﻳﻦ ﺧﻂ درﻣﺎﻧﻲ ﺑﺮاي ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب ﻛﺪام اﺳﺖ؟‬

‫51- ﻛﺪام ﻳﻚ از ﻣﻮارد زﻳﺮ در ﺑﻴﻤﺎري ﻛﺒﺪ ﭼﺮب اﺧﺘﻼل ﭘﻴﺪا‬

‫71- ﻛﺪام ﻳﻚ از ﺑﻴﻤﺎري ﻫﺎي زﻳﺮ در ﺗﺸﺨﻴﺺ اﻓﺘﺮاﻗﻲ ﻛﺒﺪ‬

‫ﻓﺼﻠﻨﺎﻣﻪ ﻓﻴﺾ| ﺗﺎﺑﺴﺘﺎن 9831| دوره 41| ﺷﻤﺎره 2‬

‫181‬ ‫‪www.SID.ir‬‬

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