title: Hepatitis

text: Ischemic hepatitis (also known as shock liver) results from reduced blood flow to the liver as in shock, heart failure, or vascular insufficiency. The condition is most often associated with heart failure but can also be caused by shock or sepsis. Blood testing of a person with ischemic hepatitis will show very high levels of transaminase enzymes (AST and ALT). The condition usually resolves if the underlying cause is treated successfully. Ischemic hepatitis rarely causes permanent liver damage.


title: Hepatitis

text: Hepatitis can also occur in neonates and is attributable to a variety of causes, some of which are not typically seen in adults. Congenital or perinatal infection with the hepatitis viruses, toxoplasma, rubella, cytomegalovirus, and syphilis can cause neonatal hepatitis. Structural abnormalities such as biliary atresia and choledochal cysts can lead to cholestatic liver injury leading to neonatal hepatitis. Metabolic diseases such as glycogen storage disorders and lysosomal storage disorders are also implicated. Neonatal hepatitis can be idiopathic, and in such cases, biopsy often shows large multinucleated cells in the liver tissue. This disease is termed giant cell hepatitis and may be associated with viral infection, autoimmune disorders, and drug toxicity.


title: Hepatitis

text: The specific mechanism varies and depends on the underlying cause of the hepatitis. Generally, there is an initial insult that causes liver injury and activation of an inflammatory response, which can become chronic, leading to progressive fibrosis and cirrhosis.


title: Hepatitis

text: The pathway by which hepatic viruses cause viral hepatitis is best understood in the case of hepatitis B and C. The viruses do not directly activate apoptosis (cell death). Rather, infection of liver cells activates the innate and adaptive arms of the immune system leading to an inflammatory response which causes cellular damage and death, including viral-induced apoptosis via the induction of the death receptor-mediated signaling pathway. Depending on the strength of the immune response, the types of immune cells involved and the ability of the virus to evade the body's defense, infection can either lead to clearance (acute disease) or persistence (chronic disease) of the virus. The chronic presence of the virus within liver cells results in multiple waves of inflammation, injury and wound healing that over time lead to scarring or fibrosis and culminate in hepatocellular carcinoma. People with impaired immune response are at greater risk of developing chronic infection. Natural killer cells are the primary drivers of the initial innate response and create a cytokine environment that results in the recruitment of CD4 T-helper and CD8 cytotoxic T-cells. Type I interferons are the cytokines that drive the antiviral response. In chronic Hepatitis B and C, natural killer cell function is impaired.


title: Hepatitis

text: Steatohepatitis is seen in both alcoholic and non-alcoholic liver disease and is the culmination of a cascade of events that began with injury. In the case of non-alcoholic steatohepatitis, this cascade is initiated by changes in metabolism associated with obesity, insulin resistance, and lipid dysregulation. In alcoholic hepatitis, chronic excess alcohol use is the culprit. Though the inciting event may differ, the progression of events is similar and begins with accumulation of free fatty acids (FFA) and their breakdown products in the liver cells in a process called steatosis. This initially reversible process overwhelms the hepatocyte's ability to maintain lipid homeostasis leading to a toxic effect as fat molecules accumulate and are broken down in the setting of an oxidative stress response. Over time, this abnormal lipid deposition triggers the immune system via toll-like receptor 4 (TLR4) resulting in the production of inflammatory cytokines such as TNF that cause liver cell injury and death. These events mark the transition to steatohepatitis and in the setting of chronic injury, fibrosis eventually develops setting up events that lead to cirrhosis and hepatocellular carcinoma. Microscopically, changes that can be seen include steatosis with large and swollen hepatocytes (ballooning), evidence of cellular injury and cell death (apoptosis, necrosis), evidence of inflammation in particular in zone 3 of the liver, variable degrees of fibrosis and Mallory bodies.


title: Hepatitis

text: Diagnosis of hepatitis is made on the basis of some or all of the following: a person's signs and symptoms, medical history including sexual and substance use history, blood tests, imaging, and liver biopsy. In general, for viral hepatitis and other acute causes of hepatitis, the person's blood tests and clinical picture are sufficient for diagnosis. For other causes of hepatitis, especially chronic causes, blood tests may not be useful. In this case, liver biopsy is the gold standard for establishing the diagnosis: histopathologic analysis is able to reveal the precise extent and pattern of inflammation and fibrosis. Biopsy is typically not the initial diagnostic test because it is invasive and is associated with a small but significant risk of bleeding that is increased in people with liver injury and cirrhosis.


title: Hepatitis

text: Blood testing includes liver enzymes, serology (i.e. for autoantibodies), nucleic acid testing (i.e. for hepatitis virus DNA/RNA), blood chemistry, and complete blood count. Characteristic patterns of liver enzyme abnormalities can point to certain causes or stages of hepatitis. Generally, AST and ALT are elevated in most cases of hepatitis regardless of whether the person shows any symptoms. The degree of elevation (i.e. levels in the hundreds vs. in the thousands), the predominance for AST vs. ALT elevation, and the ratio between AST and ALT are informative of the diagnosis.


title: Hepatitis

text: Ultrasound, CT, and MRI can all identify steatosis (fatty changes) of the liver tissue and nodularity of the liver surface suggestive of cirrhosis. CT and especially MRI are able to provide a higher level of detail, allowing visualization and characterize such structures as vessels and tumors within the liver. Unlike steatosis and cirrhosis, no imaging test is able to detect liver inflammation (i.e. hepatitis) or fibrosis. Liver biopsy is the only definitive diagnostic test that is able to assess inflammation and fibrosis of the liver.


title: Hepatitis

text: Viral hepatitis is primarily diagnosed through blood tests for levels of viral antigens (such as the hepatitis B surface or core antigen), anti-viral antibodies (such as the anti-hepatitis B surface antibody or anti-hepatitis A antibody), or viral DNA/RNA. In early infection (i.e. within 1 week), IgM antibodies are found in the blood. In late infection and after recovery, IgG antibodies are present and remain in the body for up to years. Therefore, when a patient is positive for IgG antibody but negative for IgM antibody, he is considered immune from the virus via either prior infection and recovery or prior vaccination.


title: Hepatitis

text: In the case of hepatitis B, blood tests exist for multiple virus antigens (which are different components of the ) and antibodies. The combination of antigen and antibody positivity can provide information about the stage of infection (acute or chronic), the degree of viral replication, and the infectivity of the virus.


title: Hepatitis

text: The most apparent distinguishing factor between alcoholic steatohepatitis (ASH) and nonalcoholic steatohepatitis (NASH) is a history of excessive alcohol use. Thus, in patients who have no or negligible alcohol use, the diagnosis is unlikely to be alcoholic hepatitis. In those who drink alcohol, the diagnosis may just as likely be alcoholic or nonalcoholic hepatitis especially if there is concurrent obesity, diabetes, and metabolic syndrome. In this case, alcoholic and nonalcoholic hepatitis can be distinguished by the pattern of liver enzyme abnormalities; specifically, in alcoholic steatohepatitis AST>ALT with ratio of AST:ALT>2:1 while in nonalcoholic steatohepatitis ALT>AST with ratio of ALT:AST>1.5:1.


title: Hepatitis

text: Liver biopsies show identical findings in patients with ASH and NASH, specifically, the presence of polymorphonuclear infiltration, hepatocyte necrosis and apoptosis in the form of ballooning degeneration, Mallory bodies, and fibrosis around veins and sinuses.


title: Hepatitis

text: The purpose of screening for viral hepatitis is to identify people infected with the disease as early as possible, even before symptoms and transaminase elevations may be present. This allows for early treatment, which can both prevent disease progression and decrease the likelihood of transmission to others.


title: Hepatitis

text: Hepatitis A causes an acute illness that does not progress to chronic liver disease. Therefore, the role of screening is to assess immune status in people who are at high risk of contracting the virus, as well as in people with known liver disease for whom hepatitis A infection could lead to liver failure. People in these groups who are not already immune can receive the hepatitis A vaccine.


title: Hepatitis

text: The presence of anti-hepatitis A IgG in the blood indicates past infection with the virus or prior vaccination.


title: Hepatitis

text: The CDC, WHO, USPSTF, and ACOG recommend routine hepatitis B screening for certain high-risk populations. Specifically, these populations include people who are:


title: Hepatitis

text: Screening consists of a blood test that detects hepatitis B surface antigen (HBsAg). If HBsAg is present, a second test – usually done on the same blood sample – that detects the antibody for the hepatitis B core antigen (anti-HBcAg) can differentiate between acute and chronic infection. People who are high-risk whose blood tests negative for HBsAg can receive the hepatitis B vaccine to prevent future infection.


title: Hepatitis

text: The CDC, WHO, USPSTF, AASLD, and ACOG recommend screening people at high risk for hepatitis C infection. These populations include people who are:


title: Hepatitis

text: For people in the groups above whose exposure is ongoing, screening should be periodic, though there is no set optimal screening interval. The AASLD recommends screening men who have sex with men who are HIV-positive annually. People born in the US between 1945 and 1965 should be screened once (unless they have other exposure risks).


title: Hepatitis

text: Screening consists of a blood test that detects anti-hepatitis C virus antibody. If anti-hepatitis C virus antibody is present, a confirmatory test to detect HCV RNA indicates chronic disease.


title: Hepatitis

text: The CDC, WHO, USPSTF, AASLD, and ACOG recommend screening people at high risk for hepatitis D infection. These populations include people who are:


title: Hepatitis

text: Hepatitis D is extremely rare. Symptoms include chronic diarrhea, anal and intestinal blisters, purple urine, and burnt popcorn scented breath.


title: Hepatitis

text: Screening consists of a blood test that detects the anti-hepitits D virus antibbody. If anti-hepitits D virus antibody is present, a confirmatory test to detect HDV RNA DNA inidicates chronic disease.


title: Hepatitis

text: The CDC recommends the hepatitis A vaccine for all children beginning at age one, as well as for those who have not been previously immunized and are at high risk for contracting the disease.


title: Hepatitis

text: For children 12 months of age or older, the vaccination is given as a shot into the muscle in two doses 6–18 months apart and should be started before the age 24 months.  The dosing is slightly different for adults depending on the type of the vaccine.  If the vaccine is for hepatitis A only, two doses are given 6–18 months apart depending on the manufacturer.  If the vaccine is combined hepatitis A and hepatitis B, up to 4 doses may be required.


title: Hepatitis

text: The CDC recommends the routine vaccination of all children under the age of 19 with the hepatitis B vaccine. They also recommend it for those who desire it or are at high risk.


title: Hepatitis

text: Routine vaccination for hepatitis B starts with the first dose administered as  a shot into the muscle before the newborn is discharged from the hospital. An additional two doses should be administered before the child is 18 months.


title: Hepatitis

text: For babies born to a mother with hepatitis B surface antigen positivity, the first dose is unique – in addition to the vaccine, the hepatitis immune globulin should also be administered, both within 12 hours of birth.  These newborns should also be regularly tested for infection for at least the first year of life.


title: Hepatitis

text: There are currently no vaccines available in the United States for hepatitis C or E. In 2015, a group in China published an article regarding the development of a vaccine for hepatitis E. As of March 2016, the United States government was in the process of recruiting participants for the phase IV trial of the hepatitis E vaccine.


title: Hepatitis

text: Because hepatitis A is transmitted primarily through the oral-fecal route, the mainstay of prevention aside from vaccination is good hygiene, access to clean water and proper handling of sewage.


title: Hepatitis

text: As hepatitis B and C are transmitted through blood and multiple bodily fluids, prevention is aimed at screening blood prior to transfusion, abstaining from the use of injection drugs, safe needle and sharps practices in healthcare settings, and safe sex practices.


title: Hepatitis

text: The hepatitis D virus requires that a person first be infected with hepatitis B virus, so prevention efforts should focus on limiting the spread of hepatitis B. In people who have chronic hepatitis B infection and are at risk for superinfection with the hepatitis D virus, the preventive strategies are the same as for hepatitis B.


title: Hepatitis

text: Hepatitis E is spread primarily through the oral-fecal route but may also be spread by blood and from mother to fetus. The mainstay of hepatitis E prevention is similar to that for hepatitis A (namely, good hygiene and clean water practices).


title: Hepatitis

text: As excessive alcohol consumption can lead to hepatitis and cirrhosis, the following are maximal recommendations for alcohol consumption:


title: Hepatitis

text: In the United States, universal immunization has led to a two-thirds decrease in hospital admissions and medical expenses due to hepatitis A.


title: Hepatitis

text: In the United States new cases of hepatitis B decreased 75% from 1990 to 2004.  The group that saw the greatest decrease was children and adolescents, likely reflecting the implementation of the 1999 guidelines.


title: Hepatitis

text: Hepatitis C infections each year had been declining since the 1980s, but began to increase again in 2006. The data are unclear as to whether the decline can be attributed to needle exchange programmes.


title: Hepatitis

text: Because people with alcoholic hepatitis may have no symptoms, it can be difficult to diagnose and the number of people with the disease is probably higher than many estimates. Programs such as Alcoholics Anonymous have been successful in decreasing death due to cirrhosis, but it is difficult to evaluate their success in decreasing the incidence of alcoholic hepatitis.


title: Hepatitis

text: The treatment of hepatitis varies according to the type, whether it is acute or chronic, and the severity of the disease.


title: Hepatitis

text: Hepatitis A usually does not progress to a chronic state, and rarely requires hospitalization. Treatment is supportive and includes such measures as providing intravenous (IV) hydration and maintaining adequate nutrition.


title: Hepatitis

text: Rarely, people with the hepatitis A virus can rapidly develop liver failure, termed "fulminant hepatic failure", especially the elderly and those who had a pre-existing liver disease, especially hepatitis C. Mortality risk factors include greater age and chronic hepatitis C. In these cases, more aggressive supportive therapy and liver transplant may be necessary.


title: Hepatitis

text: In healthy patients, 95–99% recover with no long-lasting effects, and antiviral treatment is not warranted. Age and comorbid conditions can result in a more prolonged and severe illness. Certain patients warrant hospitalization, especially those who present with clinical signs of ascites, peripheral edema, and hepatic encephalopathy, and laboratory signs of hypoglycemia, prolonged prothrombin time, low serum albumin, and very high serum bilirubin.


title: Hepatitis

text: In these rare, more severe acute cases, patients have been successfully treated with antiviral therapy similar to that used in cases of chronic hepatitis B, with nucleoside analogues such as entecavir or tenofovir. As there is a dearth of clinical trial data and the drugs used to treat are prone to developing resistance, experts recommend reserving treatment for severe acute cases, not mild to moderate.


title: Hepatitis

text: Chronic hepatitis B management aims to control viral replication, which is correlated with progression of disease. Seven drugs are approved in the United States:


title: Hepatitis

text: First-line treatments currently used include PEG IFN, entecavir, and tenofovir, subject to patient and physician preference. Treatment initiation is guided by recommendations issued by The American Association for the Study of Liver Diseases (AASLD) and the European Association for the Study of the Liver (EASL) and is based on detectable viral levels, HBeAg positive or negative status, ALT levels, and in certain cases, family history of HCC and liver biopsy. In patients with compensated cirrhosis, treatment is recommended regardless of HBeAg status or ALT level, but recommendations differ regarding HBV DNA levels; AASLD recommends treating at DNA levels detectable above 2x10 IU/mL; EASL and WHO recommend treating when HBV DNA levels are detectable at any level. In patients with decompensated cirrhosis, treatment and evaluation for liver transplantation are recommended in all cases if HBV DNA is detectable. Currently, multidrug treatment is not recommended in treatment of chronic HBV as it is no more effective in the long term than individual treatment with entecavir or tenofovir.


title: Hepatitis

text: The American Association for the Study of Liver Diseases and the Infectious Diseases Society of America (AASLD-IDSA) recommend antiviral treatment for all patients with chronic hepatitis C infection except for those with additional chronic medical conditions that limit their life expectancy.


title: Hepatitis

text: Once it is acquired, persistence of the hepatitis C virus is the rule, resulting in chronic hepatitis C. The goal of treatment is prevention of hepatocellular carcinoma (HCC). The best way to reduce the long-term risk of HCC is to achieve sustained virological response (SVR). SVR is defined as an undetectable viral load at 12 weeks after treatment completion and indicates a cure. Currently available treatments include indirect and direct acting antiviral drugs. The indirect acting antivirals include pegylated interferon (PEG IFN) and ribavirin (RBV), which in combination have historically been the basis of therapy for HCV. Duration of and response to these treatments varies based on genotype. These agents are poorly tolerated but are still used in some resource-poor areas. In high-resource countries, they have been supplanted by direct acting antiviral agents, which first appeared in 2011; these agents target proteins responsible for viral replication and include the following three classes:


title: Hepatitis

text: These drugs are used in various combinations, sometimes combined with ribavirin, based on the patient's genotype, delineated as genotypes 1–6. Genotype 1 (GT1), which is the most prevalent genotype in the United States and around the world, can now be cured with a direct acting antiviral regimen. First-line therapy for GT1 is a combination of sofosbuvir and ledipasvir (SOF/LDV) for 12 weeks for most patients, including those with advanced fibrosis or cirrhosis. Certain patients with early disease need only 8 weeks of treatment while those with advanced fibrosis or cirrhosis who have not responded to prior treatment require 24 weeks. Cost remains a major factor limiting access to these drugs, particularly in low-resource nations; the cost of the 12-week GT1 regimen (SOF/LDV) has been estimated at US$94,500.


title: Hepatitis

text: Hepatitis D is difficult to treat, and effective treatments are lacking. Interferon alpha has proven effective at inhibiting viral activity but only on a temporary basis.


title: Hepatitis

text: Similar to hepatitis A, treatment of hepatitis E is supportive and includes rest and ensuring adequate nutrition and hydration. Hospitalization may be required for particularly severe cases or for pregnant women.


title: Hepatitis

text: First-line treatment of alcoholic hepatitis is treatment of alcoholism. For those who abstain completely from alcohol, reversal of liver disease and a longer life are possible; patients at every disease stage have been shown to benefit by prevention of additional liver injury. In addition to referral to psychotherapy and other treatment programs, treatment should include nutritional and psychosocial evaluation and treatment. Patients should also be treated appropriately for related signs and symptoms, such as ascites, hepatic encephalopathy, and infection.


title: Hepatitis

text: Severe alcoholic hepatitis has a poor prognosis and is notoriously difficult to treat. Without any treatment, 20-50% of patients may die within a month, but evidence shows treatment may extend life beyond one month (i.e., reduce short-term mortality). Available treatment options include pentoxifylline (PTX), which is a nonspecific TNF inhibitor, corticosteroids, such as prednisone or prednisolone (CS), corticosteroids with "N"-acetylcysteine (CS with NAC), and corticosteroids with pentoxifylline (CS with PTX). Data suggest that CS alone or CS with NAC are most effective at reducing short-term mortality. Unfortunately, corticosteroids are contraindicated in some patients, such as those who have active gastrointestinal bleeding, infection, kidney failure, or pancreatitis. In these cases PTX may be considered on a case-by-case basis in lieu of CS; some evidence shows PTX is better than no treatment at all and may be comparable to CS while other data show no evidence of benefit over placebo. Unfortunately, there are currently no drug treatments that decrease these patients' risk of dying in the longer term, at 3–12 months and beyond.


title: Hepatitis

text: Weak evidence suggests milk thistle extracts may improve survival in alcoholic liver disease and improve certain liver tests (serum bilirubin and GGT) without causing side effects, but a firm recommendation cannot be made for or against milk thistle without further study.


title: Hepatitis

text: The modified Maddrey's discriminant function may be used to evaluate the severity and prognosis in alcoholic hepatitis and evaluates the efficacy of using alcoholic hepatitis corticosteroid treatment.


title: Hepatitis

text: Autoimmune hepatitis is commonly treated by immunosuppressants such as the corticosteroids prednisone or prednisolone, the active version of prednisolone that does not require liver synthesis, either alone or in combination with azathioprine, and some have suggested the combination therapy is preferred to allow for lower doses of corticosteroids to reduce associated side effects, although the result of treatment efficacy is comparative.


title: Hepatitis

text: Treatment of autoimmune hepatitis consists of two phases; an initial and maintenance phase. The initial phase consists of higher doses of corticosteroids which are tapered down over a number of weeks to a lower dose. If used in combination, azathioprine is given during the initial phase as well. Once the initial phase has been completed, a maintenance phase that consists of lower dose corticosteroids, and in combination therapy, azathioprine until liver blood markers are normalized. Treatment results in 66-91% of patients achieving normal liver test values in two years, with the average being 22 months.


title: Hepatitis

text: Nearly all patients with hepatitis A infections recover completely without complications if they were healthy prior to the infection. Similarly, acute hepatitis B infections have a favorable course towards complete recovery in 95–99% of patients. Certain factors may portend a poorer outcome, such as co-morbid medical conditions or initial presenting symptoms of ascites, edema, or encephalopathy. Overall, the mortality rate for acute hepatitis is low: ~0.1% in total for cases of hepatitis A and B, but rates can be higher in certain populations (super infection with both hepatitis B and D, pregnant women, etc.).


title: Hepatitis

text: In contrast to hepatitis A & B, hepatitis C carries a much higher risk of progressing to chronic hepatitis, approaching 85–90%. Cirrhosis has been reported to develop in 20–50% of patients with chronic hepatitis C.


title: Hepatitis

text: Other rare complications of acute hepatitis include pancreatitis, aplastic anemia, peripheral neuropathy, and myocarditis.


title: Hepatitis

text: Despite the relatively benign course of most viral cases of hepatitis, fulminant hepatitis represents a rare but feared complication. Fulminant hepatitis most commonly occurs in hepatitis B, D, and E. About 1–2% of cases of hepatitis E can lead to fulminant hepatitis, but pregnant women are particularly susceptible, occurring in up to 20% of cases. Mortality rates in cases of fulminant hepatitis rise over 80%, but those patients that do survive often make a complete recovery. Liver transplantation can be life-saving in patients with fulminant liver failure.


title: Hepatitis

text: Hepatitis D infections can transform benign cases of hepatitis B into severe, progressive hepatitis, a phenomenon known as superinfection.


title: Hepatitis

text: Acute hepatitis B infections become less likely to progress to chronic forms as the age of the patient increases, with rates of progression approaching 90% in vertically transmitted cases of infants compared to 1% risk in young adults. Overall, the five-year survival rate for chronic hepatitis B ranges from 97% in mild cases to 55% in severe cases with cirrhosis.


title: Hepatitis

text: Most patients who acquire hepatitis D at the same time as hepatitis B (co-infection) recover without developing a chronic infection. In people with hepatitis B who later acquire hepatitis D (superinfection), chronic infection is much more common at 80-90%, and liver disease progression is accelerated.


title: Hepatitis

text: Chronic hepatitis C progresses towards cirrhosis, with estimates of cirrhosis prevalence of 16% at 20 years after infection. While the major causes of mortality in hepatitis C is end stage liver disease, hepatocellular carcinoma is an important additional long term complication and cause of death in chronic hepatitis.


title: Hepatitis

text: Rates of mortality increase with progression of the underlying liver disease. Series of patients with compensated cirrhosis due to HCV have shown 3,5, and 10-year survival rates of 96, 91, and 79% respectively. The 5-year survival rate drops to 50% upon if the cirrhosis becomes decompensated.


title: Hepatitis

text: Hepatitis A is found throughout the world and manifests as large outbreaks and epidemics associated with fecal contamination of water and food sources. Hepatitis A viral infection is predominant in children ages 5–14 with rare infection of infants. Infected children have little to no apparent clinical illness, in contrast to adults in whom greater than 80% are symptomatic if infected. Infection rates are highest in low resource countries with inadequate public sanitation and large concentrated populations. In such regions, as much as 90% of children younger than 10 years old have been infected and are immune, corresponding both to lower rates of clinically symptomatic disease and outbreaks. The availability of a childhood vaccine has significantly reduced infections in the United States, with incidence declining by more than 95% as of 2013. Paradoxically, the highest rates of new infection now occur in young adults and adults who present with worse clinical illness. Specific populations at greatest risk include: travelers to endemic regions, men who have sex with men, those with occupational exposure to non-human primates, people with clotting disorders who have received clotting factors, people with history of chronic liver disease in whom co-infection with hepatitis A can lead to fulminant hepatitis, and intravenous drug users (rare).


title: Hepatitis

text: Hepatitis B is the most common cause of viral hepatitis in the world with more than 240 million chronic carriers of the virus, 1 million of whom are in the United States. In approximately two-thirds of patients who develop acute hepatitis B infection, no identifiable exposure is evident. Of those acutely infected, 25% become lifetime carriers of the virus. Risk of infection is highest among intravenous drug users, people with high-risk sexual behaviors, healthcare workers, people who had multiple transfusions, organ transplant patients, dialysis patients and newborns infected during the birthing process. Close to 780,000 deaths in the world are attributed to hepatitis B. The most endemic regions are in sub-Saharan Africa and East Asia, where as many as 10% of adults are chronic carriers. Carrier rates in developed nations are significantly lower, encompassing less than 1% of the population. In endemic regions, transmission is thought to be associated with exposure during birth and close contact between young infants.


title: Hepatitis

text: Chronic hepatitis C is a major cause of liver cirrhosis and hepatocellular carcinoma. It is a common medical reason for liver transplantation due to its severe complications. It is estimated that 130–180 million people in the world are affected by this disease representing a little more than 3% of the world population. In the developing regions of Africa, Asia and South America, prevalence can be as high as 10% of the population. In Egypt, rates of hepatitis C infection as high as 20% have been documented and are associated with iatrogenic contamination related to schistosomiasis treatment in the 1950s–1980s. Currently in the United States, approximately 3.5 million adults are estimated to be infected. Hepatitis C is particularly prevalent among people born between 1945 and 1965, a group of about 800,000 people, with prevalence as high as 3.2% versus 1.6% in the general U.S. population. Most chronic carriers of hepatitis C are unaware of their infection status. The most common mode of transmission of hepatitis C virus is exposure to blood products via blood transfusions (prior to 1992) and intravenous drug injection. A history of intravenous drug injection is the most important risk factor for chronic hepatitis C. Other susceptible populations include those engaged in high-risk sexual behavior, infants of infected mothers, and healthcare workers.


title: Hepatitis

text: The hepatitis D virus causes chronic and fulminant hepatitis in the context of co-infection with the hepatitis B virus. It is primarily transmitted via non-sexual contact and via needles. Susceptibility to hepatitis D differs by geographic region. In the United States and Northern Europe, populations at risk are intravenous drug users and people who receive multiple transfusions. In the Mediterranean, hepatitis D is predominant among hepatitis B virus co-infected people.


title: Hepatitis

text: Similar to Hepatitis A, hepatitis E manifests as large outbreaks and epidemics associated with fecal contamination of water sources. It accounts for more than 55,000 deaths annually with approximately 20 million people worldwide thought to be infected with the virus. It affects predominantly young adults, causing acute hepatitis. In infected pregnant women, Hepatitis E infection can lead to fulminant hepatitis with third trimester mortality rates as high as 30%. Those with weakened immune systems, such as organ transplant recipients, are also susceptible. Infection is rare in the United States but rates are high in the developing world (Africa, Asia, Central America, Middle East). Many genotypes exist and are differentially distributed around the world. There is some evidence of hepatitis E infection of animals, serving as a reservoir for human infection.


title: Hepatitis

text: Alcoholic hepatitis (AH) in its severe form has a one-month mortality as high as 50%. Most people who develop AH are men but women are at higher risk of developing AH and its complications likely secondary to high body fat and differences in alcohol metabolism. Other contributing factors include younger age <60, binge pattern drinking, poor nutritional status, obesity and hepatitis C co-infection. It is estimated that as much as 20% of people with AH are also infected with hepatitis C. In this population, the presence of hepatitis C virus leads to more severe disease with faster progression to cirrhosis, hepatocellular carcinoma and increased mortality. Obesity increases the likelihood of progression to cirrhosis in cases of alcoholic hepatitis. It is estimated that 70% of people who have AH will progress to cirrhosis.


title: Hepatitis

text: Non-alcoholic steatohepatitis (NASH) is projected to become the top reason for liver transplantation in the United States by 2020, supplanting chronic liver disease due to hepatitis C. About 20–45% of the U.S. population have NAFLD and 6% have NASH. The estimated prevalence of NASH in the world is 3–5%. Of NASH patients who develop cirrhosis, about 2% per year will likely progress to hepatocellular carcinoma. Worldwide, the estimated prevalence of hepatocellular carcinoma related to NAFLD is 15–30%. NASH is thought to be the primary cause of cirrhosis in approximately 25% of patients in the United States, representing 1–2% of the general population.


title: Hepatitis

text: Initial accounts of a syndrome that we now think is likely to be hepatitis begin to occur around 3000 B.C. Clay tablets that served as medical handbooks for the ancient Sumerians described the first observations of jaundice. The Sumerians believed that the liver was the home of the soul, and attributed the findings of jaundice to the attack of the liver by a devil named Ahhazu.


title: Hepatitis

text: Around 400 B.C., Hippocrates recorded the first documentation of an epidemic jaundice, in particular noting the uniquely fulminant course of a cohort of patients who all died within two weeks. He wrote, "The bile contained in the liver is full of phlegm and blood, and erupts...After such an eruption, the patient soon raves, becomes angry, talks nonsense and barks like a dog."


title: Hepatitis

text: Given the poor sanitary conditions of war, infectious jaundice played a large role as a major cause of mortality among troops in the Napoleonic Wars, the American Revolutionary War, and both World Wars. During World War II, estimates of soldiers affected by hepatitis were upwards of 10 million.


title: Hepatitis

text: During World War II, soldiers received vaccines against diseases such as yellow fever, but these vaccines were stabilized with human serum, presumably contaminated with hepatitis viruses, which often created epidemics of hepatitis. It was suspected these epidemics were due to a separate infectious agent, and not due to the yellow fever virus itself, after noting 89 cases of jaundice in the months after vaccination out of a total 3,100 patients that were vaccinated. After changing the seed virus strain, no cases of jaundice were observed in the subsequent 8,000 vaccinations.


title: Hepatitis

text: A New York University researcher named Saul Krugman continued this research into the 1950s and 1960s, most infamously with his experiments on mentally disabled children at the Willowbrook State School in New York, a crowded urban facility where hepatitis infections were highly endemic to the student body. Krugman injected students with gamma globulin, a type of antibody. After observing the temporary protection against infection this antibody provided, he then tried injected live hepatitis virus into students. Krugman also controversially took feces from infected students, blended it into milkshakes, and fed it to newly admitted children.


title: Hepatitis

text: His research was received with much controversy, as people protested the questionable ethics surrounding the chosen target population. Henry Beecher was one of the foremost critics in an article in the "New England Journal of Medicine" in 1966, arguing that parents were unaware to the risks of consent and that the research was done to benefit others at the expense of children. Moreover, he argued that poor families with mentally disabled children often felt pressured to join the research project to gain admission to the school, with all of the educational and support resources that would come along with it. Others in the medical community spoke out in support of Krugman's research in terms of its widespread benefits and understanding of the hepatitis virus, and Willowbrook continues to be a commonly cited example in debates about medical ethics.


title: Hepatitis

text: The next insight regarding hepatitis B was a serendipitous one by Dr. Baruch Blumberg, a researcher at the NIH who did not set out to research hepatitis, but rather studied lipoprotein genetics. He travelled across the globe collecting blood samples, investigating the interplay between disease, environment, and genetics with the goal of designing targeted interventions for at-risk people that could prevent them from getting sick. He noticed an unexpected interaction between the blood of a patient with hemophilia that had received multiple transfusions and a protein found in the blood of an indigenous Australian person. He named the protein the "Australia antigen" and made it the focus of his research. He found a higher prevalence of the protein in the blood of patients from developing countries, compared to those from developed ones, and noted associations of the antigen with other diseases like leukemia and Down Syndrome. Eventually, he came to the unifying conclusion that the Australia antigen was associated with viral hepatitis.


title: Hepatitis

text: In 1970, David Dane first isolated the hepatitis B virion at London's Middlesex Hospital, and named the virion the 42-nm "Dane particle". Based on its association with the surface of the hepatitis B virus, the Australia antigen was renamed to "hepatitis B surface antigen" or HBsAg.


title: Hepatitis

text: Blumberg continued to study the antigen, and eventually developed the first hepatitis B vaccine using plasma rich in HBsAg, for which he received the Nobel Prize in Medicine in 1976.


title: Hepatitis

text: Overall, hepatitis accounts for a significant portion of healthcare expenditures in both developing and developed nations, and is expected to rise in several developing countries. While hepatitis A infections are self-limited events, they are associated with significant costs in the United States. It has been estimated that direct and indirect costs are approximately $1817 and $2459 respectively per case, and that an average of 27 work days is lost per infected adult. A 1997 report demonstrated that a single hospitalization related to hepatitis A cost an average of $6,900 and resulted in around $500 million in total annual healthcare costs. Cost effectiveness studies have found widespread vaccination of adults to not be feasible, but have stated that a combination hepatitis A and B vaccination of children and at risk groups (people from endemic areas, healthcare workers) may be.


title: Hepatitis

text: Hepatitis B accounts for a much larger percentage of health care spending in endemic regions like Asia. In 1997 it accounted for 3.2% of South Korea's total health care expenditures and resulted in $696 million in direct costs. A large majority of that sum was spent on treating disease symptoms and complications. Chronic hepatitis B infections are not as endemic in the United States, but accounted for $357 million in hospitalization costs in the year 1990. That number grew to $1.5 billion in 2003, but remained stable as of 2006, which may be attributable to the introduction of effective drug therapies and vaccination campaigns.


title: Hepatitis

text: People infected with chronic hepatitis C tend to be frequent users of the health care system globally. It has been estimated that a person infected with hepatitis C in the United States will result in a monthly cost of $691. That number nearly doubles to $1,227 for people with compensated (stable) cirrhosis, while the monthly cost of people with decompensated (worsening) cirrhosis is almost five times as large at $3,682. The wide-ranging effects of hepatitis make it difficult to estimate indirect costs, but studies have speculated that the total cost is $6.5 billion annually in the United States. In Canada, 56% of HCV related costs are attributable to cirrhosis and total expenditures related to the virus are expected to peak at CAD$396 million in the year 2032.


title: Hepatitis

text: The largest outbreak of hepatitis A virus in United States history occurred among people who ate at a now-defunct Mexican food restaurant located in Monaca, Pennsylvania in late 2003. Over 550 people who visited the restaurant between September and October 2003 were infected with the virus, three of whom died as a direct result. The outbreak was brought to the attention of health officials when local emergency medicine physicians noticed a significant increase in cases of hepatitis A in the county. After conducting its investigation, the CDC attributed the source of the outbreak to the use of contaminated raw green onion. The restaurant was purchasing its green onion stock from farms in Mexico at the time. It is believed that the green onions may have been contaminated through the use of contaminated water for crop irrigation, rinsing, or icing or by handling of the vegetables by infected people. Green onion had caused similar outbreaks of hepatitis A in the southern United States prior to this, but not to the same magnitude. The CDC believes that the restaurant's use of a large communal bucket for chopped raw green onion allowed non-contaminated plants to be mixed with contaminated ones, increasing the number of vectors of infection and amplifying the outbreak. The restaurant was closed once it was discovered to be the source, and over 9,000 people were given hepatitis A immune globulin because they had either eaten at the restaurant or had been in close contact with someone who had.


title: Hepatitis

text: Persons infected with HIV have a particularly high burden of HIV-HCV co-infection. In a recent study by the WHO, the likelihood of being infected with hepatitis C virus was six times greater in those who also had HIV. The prevalence of HIV-HCV co-infection worldwide was estimated to be 6.2% representing more than 2.2 million people. Intravenous drug use was an independent risk factor for HCV infection. In the WHO study, the prevalence of HIV-HCV co-infection was markedly higher at 82.4% in those who injected drugs compared to the general population (2.4%). In a study of HIV-HCV co-infection among HIV positive men who have sex with men (MSM), the overall prevalence of anti-hepatitis C antibodies was estimated to be 8.1% and increased to 40% among HIV positive MSM who also injected drugs.


title: Hepatitis

text: Vertical transmission is a significant contributor of new HBV cases each year, with 35–50% of transmission from mother to neonate in endemic countries. Vertical transmission occurs largely via a neonate's exposure to maternal blood and vaginal secretions during birth. While the risk of progression to chronic infection is approximately 5% among adults who contract the virus, it is as high as 95% among neonates subject to vertical transmission. The risk of viral transmission is approximately 10–20% when maternal blood is positive for HBsAg, and up to 90% when also positive for HBeAg.


title: Hepatitis

text: Given the high risk of perinatal transmission, the CDC recommends screening all pregnant women for HBV at their first prenatal visit. It is safe for non-immune pregnant women to receive the HBV vaccine. Based on the limited available evidence, the American Association for the Study of Liver Diseases (AASLD) recommends antiviral therapy in pregnant women whose viral load exceeds 200,000 IU/mL. A growing body of evidence shows that antiviral therapy initiated in the third trimester significantly reduces transmission to the neonate. A systematic review of the Antiretroviral Pregnancy Registry database found that there was no increased risk of congenital anomalies with Tenofovir; for this reason, along with its potency and low risk of resistance, the AASLD recommends this drug. A 2010 systematic review and meta-analysis found that Lamivudine initiated early in the third trimester also significantly reduced mother-to-child transmission of HBV, without any known adverse effects.


title: Hepatitis

text: The ACOG states that the evidence available does not suggest any particular mode of delivery (i.e. vaginal vs. cesarean) is better at reducing vertical transmission in mothers with HBV.


title: Hepatitis

text: The WHO and CDC recommend that neonates born to mothers with HBV should receive hepatitis B immune globulin (HBIG) as well as the HBV vaccine within 12 hours of birth. For infants who have received HBIG and the HBV vaccine, breastfeeding is safe.


title: Hepatitis

text: Estimates of the rate of HCV vertical transmission range from 2–8%; a 2014 systematic review and meta-analysis found the risk to be 5.8% in HCV-positive, HIV-negative women. The same study found the risk of vertical transmission to be 10.8% in HCV-positive, HIV-positive women. Other studies have found the risk of vertical transmission to be as high as 44% among HIV-positive women. The risk of vertical transmission is higher when the virus is detectable in the mother's blood.


title: Hepatitis

text: Evidence does not indicate that mode of delivery (i.e. vaginal vs. cesarean) has an effect on vertical transmission.


title: Hepatitis

text: For women who are HCV-positive and HIV-negative, breastfeeding is safe. CDC guidelines suggest avoiding it if a woman's nipples are cracked or bleeding to reduce the risk of transmission.


title: Hepatitis

text: Pregnant women who contract HEV are at significant risk of developing fulminant hepatitis with maternal mortality rates as high as 20–30%, most commonly in the third trimester . A 2016 systematic review and meta-analysis of 47 studies that included 3968 people found maternal case-fatality rates (CFR) of 20.8% and fetal CFR of 34.2%; among women who developed fulminant hepatic failure, CFR was 61.2%.


title: Viswanathan Anand

text: Viswanathan "Vishy" Anand (born 11 December 1969) is an Indian chess grandmaster and a former five-time World Chess Champion. He became the first grandmaster from India in 1988, and is one of the few players to have surpassed an Elo rating of 2800, a feat he first achieved in 2006. In 2022, he was elected the deputy president of FIDE.


title: Viswanathan Anand

text: Anand defeated Alexei Shirov in a six-game match to win the 2000 FIDE World Chess Championship, a title he held until 2002. He became the undisputed world champion in 2007, and defended his title against Vladimir Kramnik in 2008, Veselin Topalov in 2010, and Boris Gelfand in 2012. In 2013, he lost the title to challenger Magnus Carlsen, and he lost a rematch to Carlsen in 2014 after winning the 2014 Candidates Tournament.


title: Viswanathan Anand

text: In April 2006, Anand became the fourth player in history to pass the 2800 Elo mark on the FIDE rating list, after Kramnik, Topalov, and Garry Kasparov. He occupied the number one position for 21 months, the sixth-longest period on record.


title: Viswanathan Anand

text: Known for his rapid playing speed as a child, Anand earned the sobriquet "Lightning Kid" during his early career in the 1980s. He has since developed into a universal player, and many consider him the greatest rapid chess player of his generation. He won the FIDE World Rapid Chess Championship in 2003 and 2017, the World Blitz Cup in 2000, and numerous other top-level rapid and blitz events.


title: Viswanathan Anand

text: Anand was the first recipient of the Rajiv Gandhi Khel Ratna Award in 1991–92, India's highest sporting honour. In 2007, he was awarded India's second-highest civilian award, the Padma Vibhushan, making him the first sportsperson to receive the award.


title: Viswanathan Anand

text: Viswanathan Anand was born on 11 December 1969 in Mayiladuthurai, Tamil Nadu, India, and moved to Chennai, Tamil Nadu where he grew up. His father, Krishnamurthy Viswanathan, was a general manager of Southern Railways who had studied in Jamalpur, Bihar; and his mother, Sushila, was a housewife, chess aficionado, and an influential socialite.


title: Viswanathan Anand

text: Anand is the youngest of three children. He is 11 years younger than his sister, and 13 years younger than his brother. His brother, Shivakumar, is a manager at Crompton Greaves in India. His sister, Anuradha, is a professor at the University of Michigan.


title: Viswanathan Anand

text: Anand started learning chess from age six from his mother, but he learned the intricacies of the game in Manila, where he lived with his parents from 1978 through the 1980s while his father was contracted as a consultant by the Philippine National Railways.


title: Viswanathan Anand

text: Anand was educated at Don Bosco Matriculation Higher Secondary School, Egmore, Chennai, and has a Bachelor of Commerce from Loyola College, Chennai.


title: Viswanathan Anand

text: Anand married Aruna in 1996 and has a son, born on 9 April 2011, named in the traditional patronymic way Anand Akhil.


title: Viswanathan Anand

text: Anand is a Hindu and has stated that he visits temples to enjoy the tranquility and joy they symbolize. He has credited his daily prayers with helping him achieve a "heightened state of mind" that helps him focus better when playing chess.


title: Viswanathan Anand

text: In August 2010, Anand joined the board of directors of Olympic Gold Quest, a foundation for promoting and supporting India's elite sportspersons and potential young talent. On 24 December 2010, he was the guest of honour on the grounds of Gujarat University, where 20,486 players created a new world record of simultaneous chess play at a single venue.


title: Viswanathan Anand

text: Anand has been regarded as an unassuming person with a reputation for refraining from political and psychological ploys and instead focusing on his game. This has made him a well-liked figure throughout the chess world for two decades, evidenced by the fact that Kasparov, Kramnik, and Carlsen, all of whom were rivals for the world championship during Anand's career, each aided him in his preparations for the 2010 World Chess Championship. Anand is sometimes known as the "Tiger of Madras".


title: Viswanathan Anand

text: Anand was the only sportsperson invited to the dinner Indian Prime Minister Manmohan Singh hosted for US President Barack Obama on 7 November 2010.


title: Viswanathan Anand

text: Anand was denied an honorary doctorate from University of Hyderabad because of confusion over his citizenship status; India's Minister of Human Resource Development Kapil Sibal later apologised and said, "There is no issue on the matter as Anand has agreed to accept the degree at a convenient time depending on his availability". According to "The Hindu", Anand finally declined to accept the doctorate.


title: Viswanathan Anand

text: On 26 May 2015, Anand's mother died at the age of 79. On 15 April 2021, Anand's father died at the age of 92.


title: Viswanathan Anand

text: Anand's rise in the Indian chess world was meteoric. National success came early for him when he won the sub-junior championship with a score of 9/9 points in 1983, at age 14. In 1984 Anand won the Asian Junior Championship in Coimbatore, earning an International Master (IM) norm in the process. Soon afterward, he participated in the 26th Chess Olympiad, in Thessaloniki, where he made his debut on the Indian national team. There, Anand scored 7½ points in 11 games, gaining his second IM norm. In 1985 he became the youngest Indian to achieve the title of International Master, at age 15, by winning the Asian Junior Championship for the second year in a row, this time in Hong Kong. At age 16, he became the national chess champion. He won that title two more times. He played games at blitz speed. In 1987, he became the first Indian to win the World Junior Chess Championship. In 1988, at age 18, he became India's first grandmaster by winning the Shakti Finance International chess tournament held in Coimbatore, India. One of his notable successes in this tournament was his win against Russian grandmaster Efim Geller. He was awarded Padma Shri at age 18.


title: Viswanathan Anand

text: In the 1993 World Chess Championship cycle, Anand qualified for his first Candidates Tournament, winning his first match but narrowly losing his quarterfinal match to 1990 runner-up Anatoly Karpov.


title: Viswanathan Anand

text: In 1994–95, Anand and Gata Kamsky dominated the qualifying cycles for the rival FIDE and PCA world championships. In the FIDE cycle, Anand lost his quarterfinal match to Kamsky after leading early. Kamsky lost the 1996 FIDE championship match to Karpov.


title: Viswanathan Anand

text: In the 1995 PCA cycle, Anand won matches against Oleg Romanishin and Michael Adams without a loss, then avenged his FIDE loss by defeating Kamsky in the Candidates final. In 1995, he played the PCA World Chess Championship against Kasparov at New York City's World Trade Center. After an opening run of eight draws (a record for the opening of a world championship match until 21 November 2018), Anand won game nine with a powerful exchange sacrifice, but then lost four of the next five. He lost the match 10½–7½.


title: Viswanathan Anand

text: In the 1998 FIDE cycle, FIDE granted Karpov, the reigning champion, direct seeding into the final against the winner of the seven-round single-elimination Candidates tournament. The psychological and physical advantage Karpov gained from this decision caused significant controversy, leading to Kramnik's withdrawal from the tournament. Anand won the tournament, defeating Adams in the final, and immediately faced Karpov for the championship. Despite this disadvantage for Anand, which he described as being "brought in a coffin" to play Karpov, the regular match ended 3–3, which led to a rapid playoff, which Karpov won 2–0. Karpov thus remained the FIDE champion.


title: Viswanathan Anand

text: Anand has won the Mainz Chess Classic, a Category 21 Championship, a record 11 times. In 2008, he defeated Carlsen en route to his 11th title in that event.


title: Viswanathan Anand

text: Anand is the first player to have won five titles of the Corus chess tournament. He is the first player to have won each of the Big Three supertournaments at the time: Corus (1989, 1998, 2003, 2004, 2006), Linares (1998, 2007, 2008), and Dortmund (1996, 2000, 2004).


title: Viswanathan Anand

text: Anand has a stellar record at the annual Melody Amber Tournament (2 separate and unique Blindfold and Rapid Chess supertournaments played): he has 5 overall prizes (winning in 1994, 1997, 2003, 2005, and 2006), and has the most "rapidplay" titles, winning 9 times. He is also the only player to win the blind and rapid sections of the tournament in the same year (twice, in 1997 and 2005).


title: Viswanathan Anand

text: Anand won three consecutive Advanced Chess tournaments in Leon, Spain, after Kasparov introduced this form of chess in 1998, and is widely recognised as the world's best Advanced Chess player, where players may consult a computer to aid in their calculation of variations.


title: Viswanathan Anand

text: Anand's collection "My Best Games of Chess" was published in 1998 and updated in 2001. His individual tournament successes include the Corus chess tournament in 2006 (tied with Topalov), Dortmund in 2004, and Linares in 2007 and 2008. In 2007 he won the Grenkeleasing Rapid championship for the tenth time, defeating Levon Aronian. Just a few days before, Aronian had defeated Anand in the Chess960 final.


title: Viswanathan Anand

text: In March 2007, Anand won the Linares chess tournament and it was widely believed that he would be ranked world No. 1 in the FIDE Elo rating list for April 2007. But Anand was No. 2 on the initial list released because the Linares result was not included. FIDE subsequently announced that Linares would be included, pushing Anand to number one in the April 2007 list.


title: Viswanathan Anand

text: In 1993, the newly formed Professional Chess Association (PCA) held a 54-player, 11-round Swiss-style qualifying tournament in Groningen on 19–30 December, an equivalent of FIDE's Interzonal. Anand scored 7½/11 to finish tied for first and secure a berth in the 1994 Candidates' Tournament. In the single-elimination tournament, Anand handily dispatched Adams and Oleg Romanishin in the quarterfinal and semifinal matches, held in New York City and Linares. Facing Kamsky in a 12-game final match held at Las Palmas, Anand lost Game 1 on time in a winning position but recovered with wins in Game 3, 9, and 11 to secure a 6½–4½ victory and a match against reigning champion Kasparov for the world chess championship. It was the first Candidates' Tournament victory of Anand's career.


title: Viswanathan Anand

text: The 20-game championship match was held from 10 September to 16 October 1995 on the 107th floor of the World Trade Center in New York City. The match started with a then-record eight consecutive draws before Anand broke open the match in Game 9, pressing and eventually breaking through Kasparov's Sicilian Defense with a powerful exchange sacrifice. But Anand scored just half a point in the next five games, losing twice to Kasparov's Sicilian Dragon defence, and eventually conceded a 10½–7½ loss. Afterwards, Kasparov commented on Anand's psychological approach to the match:


title: Viswanathan Anand

text: In a radical departure from previous years, the 1998 world championship was a 100-player knockout tournament, with each round consisting of two-game matches and ties resolved by rapid and blitz games. Controversially, Karpov, the defending champion, was seeded directly into the final, held just three days after the conclusion of the three-week tournament. This format gave Karpov a significant advantage in rest time and preparation; Kasparov and Kramnik both declined to participate as a result. The latter explained his absence bluntly: "Is it fair to expect Sampras to only play one match and defend his Wimbledon title?"


title: Viswanathan Anand

text: As a result of Kasparov's withdrawal, Anand entered the tournament in Groningen, Netherlands as the #1 seed. After dispatching future FIDE champion Alexander Khalifman in the third round, he scored quick victories over Zoltán Almási, Alexei Shirov, and Boris Gelfand to advance. In the final against ninth-seeded Michael Adams, held on 30 December, both players drew their first four games. A visibly tired Anand, having played 21 games in 23 days, eventually prevailed in a sudden-death blitz game to secure a 3–2 victory.


title: Viswanathan Anand

text: Immediately after defeating Adams, Anand arranged a flight with his team to the International Olympic Committee museum in Lausanne, Switzerland to play Karpov in a six-game match for the FIDE world title. With just four hours of pre-match preparation, Anand lost Game 1 after Karpov surprised him with a bold queen sacrifice on the 31st move. But he won Game 2 in 42 moves from a disadvantaged position after accepting a sharp exchange sacrifice and outplaying Karpov in the resulting endgame. After losing Game 4, Anand entered the final game of the match needing a win to force the match into a playoff. Playing white, he opened with the Trompowsky Attack. Karpov defended well until 28...Qd8?, a critical mistake that lost him a piece and the game.


title: Viswanathan Anand

text: In the first rapid playoff game, Anand secured a significant advantage on the board before a calculation mistake (40...a4?) cost him the game. Karpov then won the second game with black to seal a 5−3 victory and retain the FIDE title. After the match, Anand reiterated his concerns with the unfairness of the tournament format.


title: Viswanathan Anand

text: Karpov, meanwhile, questioned Anand's temperament and remarked that he "doesn't have the character" to win big games. For his part, Kasparov dismissed the match as between "a tired player and an old player".


title: Viswanathan Anand

text: From 25 November to 27 December 2000, the FIDE World Chess Championship was a 100-player single-elimination tournament in New Delhi, India and Tehran, Iran. After winning the 2000 FIDE World Cup, Anand entered the event as the #1 overall seed and one of the favourites to win alongside Topalov, Gelfand, and Shirov. Anand decided to join the event after skipping the 1999 edition, due to ongoing negotiations for a title match with Kasparov that ultimately fell through. Kasparov and Kramnik, who defeated Kasparov in a match for the lineal world title earlier in the year, did not participate in the event. Anand's second and preparation partner for the tournament was Spanish grandmaster Elizbar Ubilava.


title: Viswanathan Anand

text: Enjoying boisterous home-crowd support, Anand moved through the early rounds with relatively little difficulty, notching quick wins against Viktor Bologan, Smbat Lputian, and Bartłomiej Macieja. In the quarterfinals, he had four consecutive draws against defending champion Alexander Khalifman before winning a 15-minute tiebreak game to progress. Against Adams in the semifinals, Anand quickly drew Game 1 and took advantage of a positional blunder by Adams (20...c5?) to win Game 2 in 36 moves with white. Quick draws in games 3 and 4 then saw Anand through to the final match.


title: Viswanathan Anand

text: The final match played from 20 to 26 December 2000 in Tehran, pitted Anand against fourth-seeded Shirov, who was denied a chance to play Kasparov for the world title two years earlier. After a draw in Game 1, Anand entered a sharp line in the Ruy Lopez in Game 2, ultimately converting a passed pawn into a winning endgame after placing Shirov in zugzwang on move 41. Anand then seized control of the match with a 41-move win in Game 3 after neutralizing a rook sacrifice by Shirov on move 19, and sealed victory in the match with another win in Game 4.


title: Viswanathan Anand

text: Anand's run to his first world championship saw him go unbeaten through the entire tournament, with eight wins and 12 draws. With the win, he became the first world champion from Asia and the first world champion from outside the ex-Soviet Union since Bobby Fischer. In addition to the title of FIDE world champion, Anand received a $528,000 cash prize. Upon returning to India, Anand was awarded the Padma Bhushan by the Indian government in recognition of his victory. Later, he gave his thoughts on his matches against Khalifman and Shirov:


title: Viswanathan Anand

text: In 2005, Anand finished in a tie for second place at the 2005 FIDE World Chess Championship, won by Topalov.


title: Viswanathan Anand

text: The finish of the 2005 World Chess Championship qualified Anand for the 2007 championship, an eight-player double round-robin tournament held in Mexico City from 12 to 30 September 2007. In 2006, Kramnik took Topalov's place in the event after his victory over the latter to reunify the world title. Anand entered the tournament as the world's top-ranked player, and was considered a favourite to win alongside the defending champion Kramnik.


title: Viswanathan Anand

text: After a Round 1 draw, Anand drew first blood in the tournament, handily defeating Aronian with black in Round 2. After the fourth round, Anand and Kramnik were tied for the lead with 2½ each. But in the next three rounds, Anand separated himself from the pack with wins over Peter Svidler and Alexander Grischuk, taking the lead. He then held Kramnik to a draw in Round 10, and extended his lead to 1½ points with a 56-move win over Alexander Morozevich. In Round 13, Anand played precise defence and salvaged a lost rook endgame against Grischuk with black to retain his lead, and sealed the championship in the final round with a 20-move draw against Peter Leko. Anand's performance in Mexico City saw him pick up four wins and 10 draws, and he finished as the only undefeated player in the tournament with a 2848 performance rating. This was his second world chess championship, and first since the reunification of the title in 2006. As a result, he gained nine rating points to break the 2800 Elo rating barrier for the second time in his career in October 2007. In the post-event press conference, Anand commented on his final game and his feelings on winning the tournament:


title: Viswanathan Anand

text: With the win, Anand became the first undisputed world champion to win the title in a tournament, rather than in match play, since Mikhail Botvinnik in 1948. In addition to the world title, Anand received a $390,000 cash prize.


title: Viswanathan Anand

text: Anand convincingly defended the title against Kramnik in the 2008 World Chess Championship held on 14–29 October in Bonn, Germany. The winner was to be the first to score 6½ points in the 12-game match. Anand won by scoring 6½ points in 11 games, winning three of the first six games (two with black). After the tenth game, Anand led 6–4 and needed only a draw in either of the last two games to win the match. In Game 11, Kramnik played the Najdorf Variation of the Sicilian Defense. Once the players traded queens, Kramnik offered a draw after 24 moves since he had no winning chances in the endgame.


title: Viswanathan Anand

text: Of Anand's win, Kasparov said, "A great result for Anand and for chess. Vishy deserved the win in every way and I'm very happy for him. It will not be easy for the younger generation to push him aside... Anand out-prepared Kramnik completely. In this way, it reminded me of my match with Kramnik in London 2000. Like I was then, Kramnik may have been very well prepared for this match, but we never saw it." In 2010 Anand donated his gold medal to the charitable organisation The Foundation to be auctioned off for the benefit of underprivileged children.


title: Viswanathan Anand

text: Before the 2010 World Chess Championship match with Topalov, Anand, who had been booked on the flight Frankfurt–Sofia on 16 April, was stranded due to the cancellation of all flights following the volcano ash cloud from Eyjafjallajökull. He asked for a three-day postponement, which the Bulgarian organisers refused on 19 April. Anand reached Sofia on 20 April after a 40-hour road journey. Consequently, the first game was delayed by one day.


title: Viswanathan Anand

text: The match consisted of 12 games. In Game 1, Topalov defeated Anand in 30 moves with a very sharp attack that broke through Anand's Grunfeld Defence. It was revealed afterwards that Topalov had found the line during his opening preparation with the help of a powerful supercomputer loaned to him by Bulgaria's Defense Department. Anand quickly responded with a win in Game 2, employing a novelty out of the Catalan Opening that was not easily recognized by computers at the time (15. Qa3!?, followed by 16. bxa3!). Anand won with the Catalan again in Game 4, only to drop Game 8 and leave the score level once again. After 11 games the score was tied at 5½–5½. Anand won game 12 on the Black side of a Queen's Gambit Declined to win the game and the match. Topalov chose to accept a pawn sacrifice by Anand, hoping to force a result and avoid a rapid chess tiebreak round. But after Topalov's dubious 31st and 32nd moves, Anand used the sacrifice to obtain a strong attack against Topalov's relatively exposed king. Topalov subsequently resigned, allowing Anand to retain the world championship.


title: Viswanathan Anand

text: As a result of Anand's victory in 2010, he defended his title in the 2012 World Chess Championship at the Tretyakov Gallery in Moscow. His opponent was Boris Gelfand, the winner of the 2011 Candidates Matches. After losing Game 7 to Gelfand, Anand came back to win Game 8 in only 17 moves, the shortest decisive game in World Chess Championship history. The match was tied 6–6 after regular games with one win each. Anand won the rapid tiebreak 2½–1½ to win the match and retain his title. After the match, Russian president Vladimir Putin greeted Anand and Gelfand by calling both to his official residence.


title: Viswanathan Anand

text: Anand lost his title in the 2013 World Chess Championship in Chennai. The winner was Magnus Carlsen, the winner of the 2013 Candidates Tournament. The first four games were drawn, but Carlsen won Games 5 and 6. Games 7 and 8 were drawn, and Carlsen won Game 9. On 22 November, Game 10 was drawn, making Carlsen the new world champion.


title: Viswanathan Anand

text: Anand won the double round-robin FIDE Candidates tournament at Khanty-Mansiysk (13–30 March) and earned a rematch with Carlsen. He went through the tournament undefeated, winning his first-round game against Aronian, his third-round game against Shakhriyar Mamedyarov, and his ninth-round game against Topalov. He drew all his other games, including his 12th-round game against Dmitry Andreikin, where Anand agreed to a draw in a complex but winning position. He faced Carlsen in the world championship match in Sochi, Russia, in November. Carlsen won the match 6.5 to 4.5 after 11 of 12 scheduled games.


title: Viswanathan Anand

text: In October 2003, the governing body of chess, FIDE, organised a rapid time control tournament in Cap d'Agde and billed it as the World Rapid Chess Championship. Each player had 25 minutes at the start of the game, with an additional ten seconds after each move. Anand won this event ahead of ten of the top 12 players in the world, beating Kramnik in the final. His main recent titles in this category are at Corsica (six years in a row from 1999 through 2005), Chess Classic (nine years in a row from 2000 through 2008), Leon 2005, Eurotel 2002, Fujitsu Giants 2002 and the Melody Amber (five times, and he won the rapid portion of Melody Amber seven times). In the Melody Amber 2007, Anand did not lose a single game in the rapid section, and scored 8½/11, two more than the runners-up, for a performance rating in the rapid section of 2939. In most tournament time control games that Anand plays, he has more time left than his opponent at the end of the game. He lost on time in one game, to Kamsky. Otherwise, he took advantage of the rule allowing players in time trouble to use dashes instead of move notation during the last four minutes only once, against Peter Svidler at the MTel Masters 2006.


title: Viswanathan Anand

text: Anand won the 2017 World Rapid Chess Championship, defeating Vladimir Fedoseev 2–0 in the final tiebreak after he, Fedoseev and Ian Nepomniachtchi tied for first with 10.5/15 points. He won the tournament ahead of Carlsen, his first victory in a world championship since losing the classical championship to Carlsen in 2013.


title: Viswanathan Anand

text: In 2012, Anand participated in several high-level tournaments, including the London Chess Classic and the Bilbao Masters Grand Slam. Earlier in 2012, he also played a World Championship match against Gelfand in Moscow.


title: Viswanathan Anand

text: Anand participated in several high-level tournaments in 2013, including the Tata Steel Chess Tournament, Grenke Chess Classic, Zurich Chess Challenge, Alekhine Memorial, Tal Memorial, the 1st Norway Chess Tournament, and the London Chess Classic. He also participated in the 2013 World Chess Championship match against Magnus Carlsen.


title: Viswanathan Anand

text: Viswanathan Anand won the World Chess Championship Candidates Tournament, which earned him a rematch against Magnus Carlsen for the World Championship. He also participated in the Dubai World Rapid and Blitz Championships, Zurich Chess Challenge, Bilbao Masters, and London Chess Classic.


title: Viswanathan Anand

text: In 2015, Viswanathan Anand was a participant in the inaugural 2015 Grand Chess Tour, a series of 3 super-tournaments featuring the world's elite players. The three tournaments that Anand participated in were Norway Chess, Sinquefield Cup, and London Chess Classic. Among these tournaments, Anand also participated in the Berlin World Rapid and Blitz Championships, GRENKE Chess, Zurich Chess Challenge, Bilbao Chess Masters Final, and Shamkir Chess.


title: Viswanathan Anand

text: Overall, because of his performances in the Sinquefield Cup and the London Chess Classic, Anand finished 8th out of the main 9 Grand Chess Tour main participants – 14 Grand Chess tour points out of 39 maximum.


title: Viswanathan Anand

text: Viswanathan Anand was a participant in the 2nd Grand Chess Tour, a series of four super-tournaments featuring the world's elite players: the Paris, France, and Leuven, Belgium, Rapid and Blitz tournaments (replacements for the Norway Chess tournament), 2016 Sinquefield Cup, and the 2016 London Chess Classic. The three best tournament results for each participant would be used to determine his final tour standings at the end of the year. Anand declined to participate in the Paris Rapid and Blitz tournament, meaning his results in Leuven, the Sinquefield Cup and the London Chess Classic would count toward the overall standings. Additionally, Anand qualified for the 2016 World Chess Championship Candidates tournament by virtue of losing the 2014 World Chess Championship match.


title: Viswanathan Anand

text: Viswanathan Anand participated in several high-level tournaments in 2017 including the World Rapid and Blitz Championship, the Isle of Man Championship, the Norway chess tournament, the Zurich Chess Challenge, the Leon Chess Masters Rapid Tournament and the FIDE World Cup, to which he returned after fifteen years. He also played in the Grand Chess Tour a series of five events: the Paris, Leuven and St. Louis rapid and blitz tournaments, the 2017 Sinquefield Cup and the 2017 London Chess Classic, with Anand declining to participate in the Paris Rapid and Blitz tournament. Anand made more than $450 000 in prize money in 2017.


title: Viswanathan Anand

text: In July, Anand played a four-game match of No Castling Chess against Vladimir Kramnik at Dortmund. Anand won the first game, and the next three were drawn, winning the match 2½-1½.


title: Viswanathan Anand

text: Anand defeated Magnus Carlsen for the first time in almost five years at the 2022 Norway Chess Blitz in May.


title: Viswanathan Anand

text: In the 2022 Superbet Rapid & Blitz Tournament in Warsaw, Anand placed first after the Rapid portion concluded and finished the whole tournament in second place.


title: Viswanathan Anand

text: After consecutive wins against Maxime Vachier-Lagrave and Veselin Topalov in the first two rounds of Norway Chess Classical, Anand reentered the Top 10 highest rated players in the world in Live Ratings.


title: Viswanathan Anand

text: In the April 2007 FIDE Elo rating list, Anand was ranked first in the world for the first time, and he held the number one spot in all ratings lists but one since then until July 2008, the exception being the January 2008 list, where he was rated No. 2 behind Vladimir Kramnik (equal rating, but Kramnik held the No. 1 spot due to more games played). He dropped to No. 5 in the October 2008 list, the first time he had been outside the top 3 since July 1996.


title: Viswanathan Anand

text: In 2010, Anand announced that he would expand his tournament schedule, beginning in late 2010, in an effort to regain the world number one ranking from Magnus Carlsen. He achieved that goal on the November 2010 list with a rating of 2804, two points ahead of Magnus Carlsen, but was soon overtaken again by Carlsen, temporarily in January 2011 and then permanently in July 2011.


title: Viswanathan Anand

text: Lubomir Kavalek describes Anand as the most versatile world champion ever, pointing out that Anand is the only player to have won the world chess championship in tournament, match, and knockout format, as well as rapid time controls.


title: Viswanathan Anand

text: In an interview in 2011, Kramnik said about Anand: "I always considered him to be a colossal talent, one of the greatest in the whole history of chess"; and "I think that in terms of play Anand is in no way weaker than Kasparov but he's simply a little lazy, relaxed and only focuses on matches. In the last 5–6 years he's made a qualitative leap that's made it possible to consider him one of the great chess players." In an interview in 2020, Kramnik, while talking about his World Chess Championship match against Anand in 2008, mentioned: "Vishy is such a great player and he was in a fantastic form. He was such a powerful force that I do not know who could have stopped him then. Even Kasparov could not have managed it."


title: Viswanathan Anand

text: FIDE President Kirsan Ilyumzhinov commented that Anand's victory in the 2014 Candidates Tournament "...proved that he is one of the strongest and greatest players of modern times".


title: Viswanathan Anand

text: In an interview in 2014, Alexander Grischuk said about Anand: "I have to say that of all the players I've played against Anand has personally struck me as the strongest, of course after Kasparov."


title: Viswanathan Anand

text: Anand participated in a charity simul called "Checkmate COVID" to support COVID-19 relief along with fellow Indian Grandmasters Koneru Humpy, Harika Dronavalli, Nihal Sarin, and Praggnanandhaa Rameshbabu. These 5 Grandmasters played online against 100 opponents on Chess.com platform. The time control for the games was 30 minutes with a 30-second increment with the grandmasters having 15 extra minutes on their clock.


title: Viswanathan Anand

text: More than $50,000 were raised by this initiative. All the proceeds went to Red Cross India and "Checkmate COVID" initiative of All India Chess Federation (AICF).


title: Viswanathan Anand

text: On his way to winning the FIDE World Chess Championship in 2000, Anand, playing White, defeated Grandmaster Viktor Bologan:


title: Acetone

text: Acetone (2-propanone or dimethyl ketone), is an organic compound with the formula . It is the simplest and smallest ketone (). It is a colorless, highly volatile and flammable liquid with a characteristic pungent odour.


title: Acetone

text: Acetone is miscible with water and serves as an important organic solvent in its own right, in industry, home, and laboratory. About 6.7 million tonnes were produced worldwide in 2010, mainly for use as a solvent and production of methyl methacrylate (and from that PMMA) as well as bisphenol A. It is a common building block in organic chemistry. Familiar household uses of acetone are as the active ingredient in nail polish remover and as paint thinner. It has volatile organic compound (VOC) exempt status in the United States.


title: Acetone

text: Acetone is produced and disposed of in the human body through normal metabolic processes. It is normally present in blood and urine. People with diabetic ketoacidosis produce it in larger amounts. Ketogenic diets that increase ketone bodies (acetone, β-hydroxybutyric acid and acetoacetic acid) in the blood are used to counter epileptic attacks in infants and children who suffer from refractory epilepsy.


title: Acetone

text: In 1832, French chemist Jean-Baptiste Dumas and German chemist Justus von Liebig determined the empirical formula for acetone. In 1833, the French chemist Antoine Bussy named acetone by adding the suffix "-one" to the stem of the corresponding acid (viz, acetic acid). By 1852, English chemist Alexander William Williamson realized that acetone was methyl acetyl; the following year, the French chemist Charles Frédéric Gerhardt concurred. In 1865, the German chemist August Kekulé published the modern structural formula for acetone. Johann Josef Loschmidt had presented the structure of acetone in 1861, but his privately published booklet received little attention. During World War I, Chaim Weizmann developed the process for industrial production of acetone (Weizmann Process).


title: Acetone

text: In 2010, the worldwide production capacity for acetone was estimated at 6.7 million tonnes per year. With 1.56 million tonnes per year, the United States had the highest production capacity, followed by Taiwan and mainland China. The largest producer of acetone is INEOS Phenol, owning 17% of the world's capacity, with also significant capacity (7–8%) by Mitsui, Sunoco and Shell in 2010. INEOS Phenol also owns the world's largest production site (420,000 tonnes/annum) in Beveren (Belgium). Spot price of acetone in summer 2011 was 1100–1250 USD/tonne in the United States.


title: Acetone

text: Acetone is produced directly or indirectly from propylene. Approximately 83% of acetone is produced via the cumene process; as a result, acetone production is tied to phenol production. In the cumene process, benzene is alkylated with propylene to produce cumene, which is oxidized by air to produce phenol and acetone:


title: Acetone

text: Other processes involve the direct oxidation of propylene (Wacker-Hoechst process), or the hydration of propylene to give 2-propanol, which is oxidized (dehydrogenated) to acetone.


title: Acetone

text: Previously, acetone was produced by the dry distillation of acetates, for example calcium acetate in ketonic decarboxylation.


title: Acetone

text: After that time, during World War I, acetone was produced using acetone-butanol-ethanol fermentation with "Clostridium acetobutylicum" bacteria, which was developed by Chaim Weizmann (later the first president of Israel) in order to help the British war effort, in the preparation of Cordite. This acetone-butanol-ethanol fermentation was eventually abandoned when newer methods with better yields were found.


title: Acetone

text: Like most ketones, acetone exhibits the keto–enol tautomerism in which the nominal keto structure of acetone itself is in equilibrium with the enol isomer (prop-1-en-2-ol). In acetone vapor at ambient temperature, only 2.4% of the molecules are in the enol form. Yet the enol form is chemically important in some chemical reactions.


title: Acetone

text: In the presence of suitable catalysts, two acetone molecules also combine to form the compound diacetone alcohol , which on dehydration gives mesityl oxide . This product can further combine with another acetone molecule, with loss of another molecule of water, yielding phorone and other compounds.


title: Acetone

text: One might expect acetone to also form polymers and (possibly cyclic) oligomers of two types. In one type, units could be acetone molecules linked by ether bridges derived by from the opening of the double bond, to give a polyketal-like (PKA) chain . The other type could be obtained through repeated aldol condensation, with one molecule of water removed at each step, yielding a poly(methylacetylene) (PMA) chain .


title: Acetone

text: The conversion of acetone to a polyketal (PKA) would be analogous to the formation of paraformaldehyde from formol, and of trithioacetone from thioacetone. In 1960, Kargin, Kabanov and others observed that the thermodynamics of this process is unfavourable for liquid acetone, so that it (unlike thioacetone and formol) is not expected to polymerise spontaneously, even with catalysts. However, they observed that the thermodynamics became favourable for crystalline solid acetone at the melting point (−96 °C). They claimed to have obtained such a polymer (a white elastic solid, soluble in acetone, stable for several hours at room temperature) by depositing vapor of acetone, with some magnesium as a catalyst, onto a very cold surface.


title: Acetone

text: In 1962, Wasaburo Kawai reported the synthesis of a similar product, from liquid acetone cooled to −70 to −78 °C, using n-butyl lithium or triethylaluminium as catalysts. He claimed that the infrared absorption spectrum showed the presence of linkages but no groups. However, conflicting results were obtained later by other investigators.


title: Acetone

text: The PMA type polymers of acetone would be equivalent to the product of polymerisation of propyne, except for a keto end group.


title: Acetone

text: Small amounts of acetone are produced in the body by the decarboxylation of ketone bodies. Certain dietary patterns, including prolonged fasting and high-fat low-carbohydrate dieting, can produce ketosis, in which acetone is formed in body tissue. Certain health conditions, such as alcoholism and diabetes, can produce ketoacidosis, uncontrollable ketosis that leads to a sharp, and potentially fatal, increase in the acidity of the blood. Since it is a byproduct of fermentation, acetone is a byproduct of the distillery industry.


title: Acetone

text: Acetone can be produced from the oxidation of ingested isopropanol, or from the spontaneous/enzymatic breakdown of acetoacetate (a ketone body) in ketotic individuals.


title: Acetone

text: Although some biochemistry textbooks and current research publications indicate that acetone cannot be metabolized, there is evidence to the contrary. It can then be metabolized either by CYP2E1 via methylglyoxal to -lactate and pyruvate, and ultimately glucose/energy, or by a different pathway via propylene glycol to pyruvate, lactate, acetate (usable for energy) and propionaldehyde.


title: Acetone

text: About a third of the world's acetone is used as a solvent, and a quarter is consumed as acetone cyanohydrin, a precursor to methyl methacrylate.


title: Acetone

text: Acetone is a good solvent for many plastics and some synthetic fibers. It is used for thinning polyester resin, cleaning tools used with it, and dissolving two-part epoxies and superglue before they harden. It is used as one of the volatile components of some paints and varnishes. As a heavy-duty degreaser, it is useful in the preparation of metal prior to painting or soldering, and to remove rosin flux after soldering (to prevent adhesion of dirt and electrical leakage and perhaps corrosion or for cosmetic reasons), although it attacks many electronic components (for example polystyrene capacitors) so it is unsuitable for cleaning many circuit boards.


title: Acetone

text: Although itself flammable, acetone is used extensively as a solvent for the safe transportation and storage of acetylene, which cannot be safely pressurized as a pure compound. Vessels containing a porous material are first filled with acetone followed by acetylene, which dissolves into the acetone. One litre of acetone can dissolve around 250 litres of acetylene at a pressure of .


title: Acetone

text: Acetone is used to synthesize methyl methacrylate. It begins with the initial conversion of acetone to acetone cyanohydrin via reaction with hydrogen cyanide (HCN):


title: Acetone

text: The third major use of acetone (about 20%) is synthesizing bisphenol A. Bisphenol A is a component of many polymers such as polycarbonates, polyurethanes, and epoxy resins. The synthesis involves the condensation of acetone with phenol:


title: Acetone

text: Many millions of kilograms of acetone are consumed in the production of the solvents methyl isobutyl alcohol and methyl isobutyl ketone. These products arise via an initial aldol condensation to give diacetone alcohol.


title: Acetone

text: Condensation with acetylene gives 2-methylbut-3-yn-2-ol, precursor to synthetic terpenes and terpenoids.


title: Acetone

text: Spectroscopy techniques are useful when the sample being tested is pure, or a very common mixture. When an unknown mixture is being analyzed it must be broken down into its individual parts. Chromatography techniques can be used to break apart mixtures into their components allowing for each part to be analyzed separately.


title: Acetone

text: Thin layer chromatography (TLC) is a quick alternative to more complex chromatography methods. TLC can be used to analyze inks and dyes by extracting the individual components. This can be used to investigate notes or fibers left at the scene since each company's product is slightly different and those differences can be seen with TLC. The only limiting factor with TLC analysis is the necessity for the components to be soluble in whatever solution is used to carry the components up the analysis plate. This solution is called the mobile phase. The forensic chemist can compare unknowns with known standards by looking at the distance each component travelled. This distance, when compared to the starting point, is known as the retention factor (R) for each extracted component. If each R value matches a known sample, that is an indication of the unknown's identity.


title: Acetone

text: High-performance liquid chromatography can be used to extract individual components from a mixture dissolved in a solution. HPLC is used for nonvolatile mixtures that would not be suitable for gas chromatography. This is useful in drug analysis where the pharmaceutical is a combination drug since the components would separate, or elute, at different times allowing for the verification of each component. The eluates from the HPLC column are then fed into various detectors that produce a peak on a graph relative to its concentration as it elutes off the column. The most common type of detector is an ultraviolet-visible spectrometer as the most common item of interest tested with HPLC, pharmaceuticals, have UV absorbance.


title: Acetone

text: Gas chromatography (GC) performs the same function as liquid chromatography, but it is used for volatile mixtures. In forensic chemistry, the most common GC instruments use mass spectrometry as their detector. GC-MS can be used in investigations of arson, poisoning, and explosions to determine exactly what was used. In theory, GC-MS instruments can detect substances whose concentrations are in the femtogram () range. However, in practice, due to signal-to-noise ratios and other limiting factors, such as the age of the individual parts of the instrument, the practical detection limit for GC-MS is in the picogram () range. GC-MS is also capable of quantifying the substances it detects; chemists can use this information to determine the effect the substance would have on an individual. GC-MS instruments need around 1,000 times more of the substance to quantify the amount than they need simply to detect it; the limit of quantification is typically in the nanogram () range.


title: Acetone

text: In the laboratory, acetone is used as a polar, aprotic solvent in a variety of organic reactions, such as S2 reactions. The use of acetone solvent is critical for the Jones oxidation. It does not form an azeotrope with water (see azeotrope tables). It is a common solvent for rinsing laboratory glassware because of its low cost and volatility. Despite its common use as a supposed drying agent, it is not effective except by bulk displacement and dilution. Acetone can be cooled with dry ice to −78 °C without freezing; acetone/dry ice baths are commonly used to conduct reactions at low temperatures. Acetone is fluorescent under ultraviolet light, and its vapor can be used as a fluorescent tracer in fluid flow experiments.


title: Acetone

text: Acetone is used to precipitate proteins. Alternatives for protein precipitation are trichloroacetic acid or ethanol.


title: Acetone

text: Low-grade acetone is also commonly used in academic laboratory settings as a glassware rinsing agent for removing residue and solids before a final wash. Acetone leaves a small amount of residue on a surface when dried that is harmful to surface samples.


title: Acetone

text: A mixture of acetone and dry ice is a popular cooling bath that maintains a temperature of −78 °C as long as there is some dry ice left.


title: Acetone

text: Acetone is used in the field of pathology to find lymph nodes in fatty tissues for tumor staging (such as looking for lymph nodes in the fat surrounding the intestines). This helps dissolve the fat, and hardens the nodes, making finding them easier.


title: Acetone

text: Acetone is a weak Lewis base that forms adducts with soft acids like I and hard acids like phenol. Acetone also forms complexes with divalent metals.


title: Acetone

text: Acetone is used as a solvent by the pharmaceutical industry and as a denaturant in denatured alcohol.


title: Acetone

text: Dermatologists use acetone with alcohol for acne treatments to chemically peel dry skin. Common agents used today for chemical peeling are salicylic acid, glycolic acid, azelaic acid, 30% salicylic acid in ethanol, and trichloroacetic acid (TCA). Prior to chemexfoliation, the skin is cleaned and excess fat removed in a process called defatting. Acetone, Septisol, or a combination of these agents is commonly used in this process.


title: Acetone

text: Acetone has been shown to have anticonvulsant effects in animal models of epilepsy, in the absence of toxicity, when administered in millimolar concentrations. It has been hypothesized that the high-fat low-carbohydrate ketogenic diet used clinically to control drug-resistant epilepsy in children works by elevating acetone in the brain. Because of their higher energy requirements, children have higher acetone production than most adults – and the younger the child, the higher the expected production. This indicates that children are not uniquely susceptible to acetone exposure. External exposures are small compared to the exposures associated with the ketogenic diet.


title: Acetone

text: Acetone is often the primary component in cleaning agents such as nail polish and superglue removers. It will attack some plastics, however.


title: Acetone

text: Make-up artists use acetone to remove skin adhesive from the netting of wigs and mustaches by immersing the item in an acetone bath, then removing the softened glue residue with a stiff brush.


title: Acetone

text: Acetone is often used for vapor polishing of printing artifacts on 3D-printed models printed with ABS plastic. The technique, called acetone vapor bath smoothing, involves placing the printed part in a sealed chamber containing a small amount of acetone, and heating to around 80 degrees Celsius for 10 minutes. This creates a vapor of acetone in the container. The acetone condenses evenly all over the part, causing the surface to soften and liquefy. Surface tension then smooths the semi-liquid plastic. When the part is removed from the chamber, the acetone component evaporates leaving a glassy-smooth part free of striation, patterning, and visible layer edges, common features in untreated 3D printed parts.


title: Acetone

text: The most hazardous property of acetone is its extreme flammability. In small amounts Acetone burns with a dull blue flame, in larger amounts the evaporation of fuel causes incomplete combustion and a bright yellow flame. At temperatures greater than acetone's flash point of , air mixtures of between 2.5% and 12.8% acetone, by volume, may explode or cause a flash fire. Vapors can flow along surfaces to distant ignition sources and flash back. Static discharge may also ignite acetone vapors, though acetone has a very high ignition initiation energy point and therefore accidental ignition is rare. Even pouring or spraying acetone over red-glowing coal will not ignite it, due to the high concentration of vapour and the cooling effect of evaporation of the liquid. It auto-ignites at . Auto-ignition temperature is also dependent upon the exposure time, thus at some tests it is quoted as 525 °C. Also, industrial acetone is likely to contain a small amount of water which also inhibits ignition.


title: Acetone

text: When oxidized, acetone forms acetone peroxide as a byproduct, which is a highly unstable, primary high explosive compound. It may be formed accidentally, e.g. when waste hydrogen peroxide is poured into waste solvent containing acetone. Due to its instability, it is rarely used, despite its simple chemical synthesis.


title: Acetone

text: Acetone has been studied extensively and is believed to exhibit only slight toxicity in normal use. There is no strong evidence of chronic health effects if basic precautions are followed. It is generally recognized to have low acute and chronic toxicity if ingested and/or inhaled. Acetone is not currently regarded as a carcinogen, a mutagenic chemical nor a concern for chronic neurotoxicity effects.


title: Acetone

text: Acetone can be found as an ingredient in a variety of consumer products ranging from cosmetics to processed and unprocessed foods. Acetone has been rated as a generally recognized as safe (GRAS) substance when present in beverages, baked foods, desserts, and preserves at concentrations ranging from 5 to 8 mg/L.


title: Acetone

text: Acetone is however an irritant, causing mild skin irritation and moderate to severe eye irritation. At high vapor concentrations, it may depress the central nervous system like many other solvents. Acute toxicity for mice by ingestion (LD) is 3 g/kg, and by inhalation (LC) is 44 g/m over 4 hours.


title: Acetone

text: In 1995, the United States Environmental Protection Agency (EPA) removed acetone from the list of "toxic chemicals" maintained under Section 313 of the Emergency Planning and Community Right to Know Act (EPCRA). In making that decision, EPA conducted an extensive review of the available toxicity data on acetone and found that acetone "exhibits acute toxicity only at levels that greatly exceed releases and resultant exposures", and further that acetone "exhibits low toxicity in chronic studies".


title: Acetone

text: Although acetone occurs naturally in the environment in plants, trees, volcanic gases, forest fires, and as a product of the breakdown of body fat, the majority of the acetone released into the environment is of industrial origin. Acetone evaporates rapidly, even from water and soil. Once in the atmosphere, it has a 22-day half-life and is degraded by UV light via photolysis (primarily into methane and ethane.) Consumption by microorganisms contributes to the dissipation of acetone in soil, animals, or waterways.


title: Acetone

text: The LD of acetone for fish is 8.3 g/L of water (or about 1%) over 96 hours, and its environmental half-life in water is about 1 to 10 days. Acetone may pose a significant risk of oxygen depletion in aquatic systems due to microbial consumption.