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| {{DiseaseDisorder infobox | | | __NOTOC__ |
| Name = Dysmetabolic syndrome X |
| | '''For patient information click [[{{PAGENAME}} (patient information)|here]]''' |
| ICD10 = |
| | {{Metabolic syndrome}} |
| ICD9 = {{ICD9|277.7}} |
| | {{CMG}}; {{AE}} [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh13579@gmail.com]; {{RT}}; {{AN}} |
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| ICDO = |
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| OMIM = 605552 |
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| DiseasesDB = 31955 |
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| MedlinePlus = |
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| eMedicineSubj = |
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| eMedicineTopic = |
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| MeshID = D024821 |
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| {{Search infobox}} | |
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| Synonyms and Keywords: '''Metabolic syndrome X''', '''[[Insulin resistance]] syndrome''', '''[[Gerald Reaven|Reaven's]] syndrome''' or '''CHAOS''' (Australia)
| | {{SK}} Metabolic syndrome X; insulin resistance syndrome; Reaven syndrome; CHAOS (Australia); abdominal obesity-metabolic syndrome; dysmetabolic syndrome; plurimetabolic syndrome; hypertriglyceridemia waist syndrome; visceral fat syndrome; cardiometabolic syndrome; general cardiovascular syndrome |
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| ==Overview== | | ==[[Metabolic syndrome overview|Overview]]== |
| '''Metabolic syndrome''' is a combination of [[medicine|medical]] disorders that increase one's risk for [[cardiovascular disease]] and [[Diabetes mellitus|diabetes]]. It affects a large number of people in a clustered fashion. In some studies, the [[prevalence]] in the USA is calculated as being up to 25% of the population.
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| ==Associated Conditions== | | ==[[Metabolic syndrome historical perspective|Historical Perspective]]== |
| *[[Polycystic ovarian syndrome]]
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| *[[Hemochromatosis]](iron overload)
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| ==Diagnosis== | | ==[[Metabolic syndrome classification|Classification]]== |
| ===Physical Examination===
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| ====Vitals====
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| * [[High blood pressure]]
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| ====Skin==== | | ==[[Metabolic syndrome pathophysiology|Pathophysiology]]== |
| *[[Acanthosis nigricans]] (a skin condition featuring dark patches)
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| ====Abdomen==== | | ==[[Metabolic syndrome causes|Causes]]== |
| * [[Central obesity]] (also known as visceral, male-pattern or apple-shaped adiposity), overweight with fat deposits mainly around the waist;
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| ===Laboratory Studies=== | | ==[[Differentiating Metabolic syndrome from other diseases|Differentiating Metabolic Syndrome from other Diseases]]== |
| * Fasting hyperglycemia — [[diabetes mellitus type 2]] or [[impaired fasting glucose]], [[impaired glucose tolerance]], or [[insulin resistance]]
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| * Decreased [[High density lipoprotein|HDL]] cholesterol
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| * Elevated [[triglyceride]]s
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| * Elevated [[uric acid]] levels
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| *[[Fatty liver]] (especially in concurrent [[obesity]]), progressing to [[non-alcoholic fatty liver disease]],
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| ===Diagnostic Criteria== | | ==[[Metabolic syndrome epidemiology and demographics|Epidemiology and Demographics]]== |
| There are currently two major definitions for metabolic syndrome provided by 1) [[International Diabetes Federation]]<ref>The IDF consensus worldwide definition of the metabolic syndrome. [http://www.idf.org/webdata/docs/IDF_Metasyndrome_definition.pdf PDF]</ref> and 2) the revised [[National Cholesterol Education Program]], respectively. The revised NCEP and IDF definitions of metabolic syndrome are very similar and it can be expected that they will identify many of the same individuals as having metabolic syndrome. The two differences are that IDF excludes any subject without increased waist circumference, while in the NCEP definition metabolic syndrome can be diagnosed based on other criteria and the IDF uses geography-specific cut points for waist circumference, while NCEP uses only one set of cut points for waist circumference regardless of geography. These two definitions are much closer to each other than the original NCEP and WHO definitions.
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| ===WHO=== | | ==[[Metabolic syndrome risk factors|Risk Factors]]== |
| The World Health Organization criteria (1999) require presence of diabetes mellitus, impaired glucose tolerance, impaired fasting glucose or insulin resistance, AND two of the following:
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| * blood pressure: ≥ 140/90 mmHg
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| * dyslipidaemia: triglycerides (TG): ≥ 1.695 mmol/L and/or high-density lipoprotein cholesterol (HDL-C) ≤ 0.9 mmol/L (male), ≤ 1.0 mmol/L (female)
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| * central obesity: waist:hip ratio > 0.90 (male), > 0.85 (female), and/or body mass index > 30 kg/m<sup>2</sup>
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| * microalbuminuria: urinary albumin excretion ratio ≥ 20 mg/min or albumin:creatinine ratio ≥ 30 mg/g
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| ===EGIR=== | | ==[[Metabolic syndrome natural history, complications and prognosis |Natural History, Complications and Prognosis]]== |
| European Group for the Study of Insulin Resistance (1999) requires insulin resistance defined as the top 25% of the fasting insulin values among non-diabetic individuals AND two or more of the following:
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| * central obesity: waist circumference ≥ 94 cm (male), ≥ 80 cm (female)
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| * dyslipidaemia: TG ≥ 2.0 mmol/L and/or HDL-C < 1.0 mg/dL or treated for dyslipidaemia
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| * hypertension: blood pressure ≥ 140/90 mmHg or antihypertensive medication
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| * fasting plasma glucose ≥ 6.1 mmol/L
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| ===NCEP=== | | ==Diagnosis== |
| The National Cholesterol Education Program Adult Treatment Panel III (2001) requires at least three of the following:<ref>Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. ''Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III).'' JAMA 2001;285:2486-97. PMID 11368702.</ref>
| | [[Metabolic syndrome diagnostic criteria|Diagnostic Criteria]] | [[Metabolic syndrome history and symptoms|History and Symptoms]] | [[Metabolic syndrome physical examination|Physical Examination]] | [[Metabolic syndrome laboratory findings|Laboratory Findings]] | [[Metabolic syndrome electrocardiogram|Electrocardiogram]] | [[Metabolic syndrome chest x ray|Chest X Ray]] | [[Metabolic syndrome CT|CT]] | [[Metabolic syndrome MRI|MRI]] | [[Metabolic syndrome echocardiography or ultrasound|Echocardiography or Ultrasound]] | [[Metabolic syndrome other imaging findings|Other Imaging Findings]] |[[Metabolic syndrome other diagnostic studies|Other Diagnostic Studies]] |
| * central obesity: waist circumference ≥ 102 cm or 40 inches (male), ≥ 88 cm or 36 inches(female)
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| * dyslipidaemia: TG ≥ 1.695 mmol/L (150 mg/dl)
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| * dyslipidaemia: HDL-C < 40 mg/dL (male), < 50 mg/dL (female)
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| * blood pressure ≥ 130/85 mmHg
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| * fasting plasma glucose ≥ 6.1 mmol/L (110 mg/dl)
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| ===American Heart Association/Updated NCEP=== | | ==Treatment== |
| | [[Metabolic syndrome dietary therapy|Dietary Therapy]] | [[Metabolic syndrome physical activity|Physical Activity]] | [[Metabolic syndrome medical therapy|Medical Therapy]] | [[Metabolic syndrome surgery|Surgery]] | [[Metabolic syndrome primary prevention|Primary Prevention]] | [[Metabolic syndrome secondary prevention|Secondary Prevention]] | [[Metabolic syndrome tertiary prevention|Tertiary Prevention]] | [[Metabolic syndrome cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Metabolic syndrome future or investigational therapies|Future or Investigational Therapies]] |
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| There is quite a bit of confusion about whether AHA/NHLBI intended to create another set of guidelines or simply update the NCEP ATP III definition. According to Scott Grundy, University of Texas Southwestern Medical School, Dallas, Texas, the intent was just to update the NCEP ATP III definition and not create a new definition.<ref name="Grundy">[http://circ.ahajournals.org/cgi/reprint/109/3/433.pdf Grundy SM, Brewer HB, Cleeman JI, Smith SC, Lenfant D, for the Conference Participants. Definition of metabolic syndrome: report of the National, Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition.] Circulation. 2004;109:433-438.</ref>:
| | ==Case Studies== |
| * Elevated waist circumference: Men — Equal to or greater than 40 inches (102 cm) Women — Equal to or greater than 35 inches (88 cm)
| | [[Metabolic syndrome case study one|Case #1]] |
| * Elevated triglycerides: Equal to or greater than 150 mg/dL
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| * Reduced HDL (“good”) cholesterol: Men — Less than 40 mg/dL Women — Less than 50 mg/dL
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| * Elevated blood pressure: Equal to or greater than 130/85 mm Hg or use of medication for hypertension
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| * Elevated fasting glucose: Equal to or greater than 100 mg/dL (5.6 mmol/L) or use of medication for hyperglycemia
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| ==Etiology== | | ==Related Chapters== |
| The cause of the metabolic syndrome is unknown. The pathophysiology is extremely complex and has only been partially elucidated. Most patients are older, obese, sedentary, and have a degree of [[insulin resistance]]. The most important factors in order are 1) aging, 2) genetics and 3) lifestyle (i.e., decreased physical activity and excess caloric intake). There is debate regarding whether obesity or insulin resistance is the ''cause'' of the metabolic syndrome or if it is a by-product of a more far-reaching metabolic derangement. Systemic [[inflammation]]: a number of inflammatory markers (including [[C-reactive protein]]) are often increased, as are [[fibrinogen]], [[interleukin 6]] (IL−6), [[Tumor necrosis factor-alpha]] (TNFα) and others. Some have pointed to [[oxidative stress]] due to a variety of causes including dietary [[fructose]] mediated increased uric acid levels.<ref>{{cite journal | author=Nakagawa T, Hu H, Zharikov S, Tuttle KR, Short RA, Glushakova O, Ouyang X, Feig DI, Block ER, Herrera-Acosta J, Patel JM, Johnson RJ | title=A causal role for uric acid in fructose-induced metabolic syndrome | journal=Am J Phys Renal Phys | year=2006 | volume=290 | issue=3 | pages= F625–F631 | id=PMID 16234313}}</ref><ref>{{cite journal | author=Hallfrisch J | title=Metabolic effects of dietary fructose | journal=FASEB J | year=1990 | volume=4 | issue=9 | pages= 2652–2660 | id=PMID 2189777}}</ref><ref>{{cite journal | author=Reiser S, Powell AS, Scholfield DJ, Panda P, Ellwood KC, Canary JJ | title=Blood lipids, lipoproteins, apoproteins, and uric acid in men fed diets containing fructose or high-amylose cornstarch | journal= Am J Clin Nutr | year=1989 | volume=49 | issue=5 | pages= 832–839 | id=PMID 2497634}}</ref>
| | * [[Chronic Somogyi rebound]] |
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| ==Pathophysiology==
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| Commonly, there is development of [[visceral fat]] followed by the [[adipocyte]]s (fat [[Cell (biology)|cell]]s) of the visceral fat increasing [[blood plasma|plasma]] levels of TNFα and altering levels of a number of other substances (e.g., adiponectin, resistin, PAI-1). TNFα has been shown to not only cause the production of inflammatory [[cytokine]]s, but may also trigger cell signalling by interaction with a TNFα [[Receptor (biochemistry)|receptor]] that may lead to insulin resistance. An experiment with rats that were fed a diet one-third of which was [[sucrose]] has been proposed as a model for the development of the metabolic syndrome. The sucrose first elevated blood levels of [[triglyceride]]s, which induced [[visceral]] fat and ultimately resulted in insulin resistance <ref>{{cite journal | author=Fukuchi S, Hamaguchi K, Seike M, Himeno K, Sakata T, Yoshimatsu H. | title=Role of Fatty Acid Composition in the Development of Metabolic Disorders in Sucrose-Induced Obese Rats | journal=Exp Biol Med | year=2004 | volume=229 | issue=6 | pages= 486–493 | url=http://www.ebmonline.org/cgi/content/full/229/6/486 | id=PMID 15169967}}</ref>. The progression from visceral fat to increased TNFα to insulin resistance has some parallels to human development of metabolic syndrome.
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| == Therapy ==
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| The goal is to get the LDL down to < 100 mg/dl. The first line treatment is change of lifestyle (i.e., caloric restriction and physical activity). However, drug treatment is frequently required. Generally, the individual diseases that comprise the metabolic syndrome are treated separately (e.g. [[diuretic]]s and [[ACE inhibitor]]s for [[hypertension]]). Cholesterol drugs may be used to lower LDL cholesterol and triglyceride levels, if they are elevated, and to raise HDL levels if they are low. Use of drugs that decrease [[insulin resistance]] e.g., [[metformin]] and [[thiazolidinedione]]s is controversial and not FDA approved.
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| A recent study indicated that cardiovascular exercise was therapeutic in approximately 31% of cases. The most probable benefit was to triglyceride levels, with 43% showing improvement; conversely 91% of test subjects did not exhibit a decrease in fasting plasma glucose or insulin resistance.<ref name="katzmaryk">{{cite journal
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| | last = Katzmaryk,
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| | first = Peter T
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| | coauthors = Leon, Arthur S.; Wilmore, Jack H.; Skinner, James S.; Rao, D. C.; Rankinen, Tuomo; Bouchard, Claude
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| | title = Targeting the Metabolic Syndrome with Exercise: Evidence from the HERITAGE Family Study.
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| | journal = Med. Sci. Sports Exerc
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| | volume = 35
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| | issue = 10
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| | pages = 1703-1709
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| | date = [[October 2003]]
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| | url = http://www.ms-se.com/pt/re/msse/abstract.00005768-200310000-00013.htm
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| | accessdate = 2007-06-24 }}
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| </ref>
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| Many other studies have supported the value of increased physical activity along with restricted calories in metabolic syndrome.
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| ==Prevention==
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| Various strategies have been proposed to prevent the development of metabolic syndrome. These include increased physical activity (such as walking 30 minutes every day),<ref>{{cite journal |author=Lakka TA, Laaksonen DE |title=Physical activity in prevention and treatment of the metabolic syndrome |journal=Applied physiology, nutrition, and metabolism = Physiologie appliquée, nutrition et métabolisme |volume=32 |issue=1 |pages=76-88 |year=2007 |pmid=17332786 |doi=10.1139/h06-113}}</ref> and a healthy, reduced calorie diet.<ref>{{cite journal |author=Feldeisen SE, Tucker KL |title=Nutritional strategies in the prevention and treatment of metabolic syndrome |journal=Appl Physiol Nutr Metab |volume=32 |issue=1 |pages=46-60 |year=2007 |pmid=17332784 |doi=10.1139/h06-101}}</ref> There are many studies that support the value of a healthy lifestyle as above. However, one study stated that these measures are effective in only a minority of people.<ref name="katzmaryk" /> The International Obesity Taskforce states that interventions on a sociopolitical level are required to reduce development of the metabolic syndrome in populations.<ref>{{cite journal |author=James PT, Rigby N, Leach R |title=The obesity epidemic, metabolic syndrome and future prevention strategies |journal=Eur J Cardiovasc Prev Rehabil |volume=11 |issue=1 |pages=3-8 |year=2004 |pmid=15167200 |doi=}}</ref>
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| A 2007 study of 2,375 male subjects over 20 years suggested that daily intake of a pint of milk or equivalent dairy products more than halved the risk of metabolic syndrome.<ref>{{cite journal |last=Elwood |first=PC |coauthors=Pickering JE, Fehily AM |year=2007 |title=Milk and dairy consumption, diabetes and the metabolic syndrome: the Caerphilly prospective study |journal= J Epidemiol Community Health |volume=61 |issue=8 |pages=695-698 |id=PMID 17630368 |url=http://jech.bmj.com/cgi/content/abstract/61/8/695 |doi=10.1136/jech.2006.053157}}</ref> Other studies both support and dispute the authors' findings.<ref>{{cite journal |author=Snijder MB, van der Heijden AA, van Dam RM, ''et al'' |title=Is higher dairy consumption associated with lower body weight and fewer metabolic disturbances? The Hoorn Study |journal=Am. J. Clin. Nutr. |volume=85 |issue=4 |pages=989-95 |year=2007 |pmid=17413097 |doi=}}</ref>
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| ==History==
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| The term "metabolic syndrome" dates back to at least the late 1950s, but came into common usage in the late 1970s to describe various associations of risk factors with diabetes, that had been noted as early as the 1920s.<ref>Joslin EP. The prevention of diabetes mellitus. ''JAMA'' 1921;76:79–84.</ref><ref>Kylin E. [Studies of the hypertension-hyperglycemia-hyperuricemia syndrome] (German). ''Zentralbl Inn Med'' 1923;44: 105-27.</ref>
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| * The Marseilles physician Dr. Jean Vague, in 1947, made the interesting observation that upper body obesity appeared to predispose to diabetes, atherosclerosis, gout, and calculi.<ref>Vague J. La diffférenciacion sexuelle, facteur déterminant des formes de l'obésité. Presse Med 1947;30:339-40.</ref>
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| * Avogaro, Crepaldi and co-workers described six moderately obese patients with diabetes, hypercholesterolemia, and marked hypertriglyceridemia all of which improved when the patients were put on a hypocaloric, low carbohydrate diet.<ref>Avogaro P, Crepaldi G, Enzi G, Tiengo A. Associazione di iperlipidemia, diabete mellito e obesità di medio grado. ''Acta Diabetol Lat'' 1967;4:572-590.<!--No PMID--></ref>
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| * In 1977, Haller used the term "metabolic syndrome" for associations of obesity, diabetes mellitus, hyperlipoproteinemia, hyperuricemia and steatosis hepatis when describing the additive effects of risk factors on atherosclerosis.<ref>Haller H. [Epidemiology and associated risk factors of hyperlipoproteinemia] (German). ''Z Gesamte Inn Med'' 1977;32(8):124-8. PMID 883354.</ref> | |
| * The same year, Singer used the term for associations of obesity, gout, diabetes mellitus, and hypertension with hyperlipoprotenemia.<ref>Singer P. [Diagnosis of primary hyperlipoproteinemias] (German). ''Z Gesamte Inn Med'' 1977;32(9):129-33. PMID 906591.</ref>
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| * In 1977 and 1978, Gerald B. Phillips developed the concept that risk factors for myocardial infarction concur to form a "constellation of abnormalities" (i.e., glucose intolerance, hyperinsulinemia, hyperlipidemia [hypercholesterolemia and hypertriglyceridemia] and hypertension) that is associated not only with heart disease, but also with aging, obesity and other clinical states. He suggested there must be an underlying linking factor, the identification of which could lead to the prevention of cardiovascular disease; he hypothesized that this factor was sex hormones.<ref>Phillips GB. Sex hormones, risk factors and cardiovascular disease. ''Am J Med'' 1978;65:7-11. PMID 356599.</ref><ref>Phillips GB. Relationship between serum sex hormones and glucose, insulin, and lipid abnormalities in men with myocardial infarction. ''Proc Natl Acad Sci U S A'' 1977;74:1729-1733. PMID 193114.</ref>
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| * In 1988, in his Banting lecture, Gerald M. Reaven proposed insulin resistance as the underlying factor and named the constellation of abnormalities Syndrome X. Reaven did not include abdominal obesity, which has also been hypothesized as the underlying factor, as part of the condition.<ref>Reaven GM. Banting lecture 1988. Role of insulin resistance in human disease. Diabetes 1988;37:1595-607. PMID 3056758.</ref>
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| The terms "metabolic syndrome," "insulin resistance syndrome," and "syndrome X" are now used specifically to define a constellation of abnormalities that is associated with increased risk for the development of type 2 diabetes and atherosclerotic vascular disease (e.g. heart disease and stroke).
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| ==See also==
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| * [[Hyperinsulinemia]] | | * [[Hyperinsulinemia]] |
| * [[Insulin resistance]] | | * [[Insulin resistance]] |
| * [[Chronic Somogyi rebound]]
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| ==References==
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| {{Reflist|2}} | | {{WS}} |
| | {{WH}} |
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| [[Category:Cardiology]] | | [[Category:Cardiology]] |
| [[Category:Endocrinology]] | | [[Category:Endocrinology]] |
| [[Category:Medical conditions related to obesity]] | | [[Category:Rheumatology]] |
| [[Category:Syndromes]]
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| {{Circulatory system pathology}}
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| [[de:Metabolisches Syndrom]]
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| [[es:Síndrome metabólico]]
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| [[ko:대사증후군]]
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| [[nl:Metabool syndroom]]
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| [[ja:メタボリックシンドローム]]
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| [[pl:Zespół metaboliczny]]
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| [[pt:Síndrome metabólica]]
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| [[ru:Метаболический синдром]]
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| [[fi:Metabolinen oireyhtymä]]
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| [[sv:Metabolt syndrom]]
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| [[zh:代謝症候群]]
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