Causes of Alpers Syndrome
Alpers Syndrome Causes: Book Excerpts
What causes Alpers Syndrome?
Causes: Alpers Syndrome:
While some researchers believe that Alpers'
disease is caused by an underlying metabolic defect, no consistent defect
has been identified.
(Source: excerpt from NINDS Alpers' Disease Information Page: NINDS)
Related information on causes of Alpers Syndrome:
As with all medical conditions,
there may be many causal factors.
Further relevant information on causes of Alpers Syndrome may be found in:
Causes of Alpers Syndrome: Online Medical Books
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for more information about the causes of Alpers Syndrome.
Viral hepatitis:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
The major forms of viral hepatitis result from infection with the causative viruses: A, B, C, D, E, or G.
Type A hepatitis is highly contagious and is usually transmitted by the fecal-oral route. However, it may also be transmitted parenterally. Hepatitis A usually results from ingestion of contaminated food, milk, or water. Many outbreaks of this type are traced to ingestion of seafood from polluted water. In 2001, there were more than 10,000 acute cases of hepatitis A infection reported in the United States.
Type B hepatitis, once thought to be transmitted only by the direct exchange of contaminated blood, is now known to be transmitted also by contact with human secretions and feces. As a result, nurses, physicians, laboratory technicians, and dentists are frequently exposed to type B hepatitis, in many cases as a result of wearing defective gloves. Transmission also occurs during intimate sexual contact as well as through perinatal transmission. An estimated 200,000 new cases of hepatitis B virus (HBV) and 5,000 deaths from HBV occur annually in the United States.
Although specific type C hepatitis viruses have been isolated, only a small percentage of patients have tested positive for them — perhaps reflecting the test’s poor specificity. Usually, this type of hepatitis is transmitted through transfused blood from asymptomatic donors. Hepatitis C accounts for 30,000 new infections and 8,000 to 10,000 deaths each year in the United States. Most exposures (60%) occur through the use of illicit I.V. drugs. However, sexual transmission is responsible for 20% of cases. More than 170 million people have the hepatitis C virus worldwide.
Type D hepatitis is found only in patients with an acute or chronic episode of hepatitis B and requires the presence of HBsAg. The type D virus depends on the double-shelled type B virus to replicate. For this reason, type D infection can’t outlast a type B infection. About 15 million people are infected with hepatitis D worldwide. It’s more common in adults than in children. People with a history of illicit I.V. drug use and people who live in the Mediterranean basin have a higher incidence.
Type E hepatitis is transmitted enterically, much like type A. Because this virus is inconsistently shed in feces, detection is difficult. In the United States, the prevalence of hepatitis E is less than 2%. It’s typically found in developing countries that lie near the equator. Incidence is highest among people ages 15 to 40.
Type G may be transmitted in a manner similar to that of hepatitis C. It may also be transmitted by sexual contact, and its incidence may be higher than previously suspected. It’s associated with acute and chronic liver disease, but studies haven’t clearly implicated the hepatitis G virus as an etiologic agent.
Other proposed causative factors, such as non-ABCDE viral hepatitis and type F, are under investigation.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Hepatic encephalopathy:
Causes
(Professional Guide to Diseases (Eighth Edition))
Hepatic encephalopathy follows rising blood ammonia levels. Normally, the ammonia produced by protein breakdown in the bowel is metabolized to urea in the liver. When portal blood shunts past the liver, ammonia directly enters the systemic circulation and is carried to the brain. Such shunting may result from the collateral venous circulation that develops in portal hypertension or from surgically created portosystemic shunts. Cirrhosis further compounds this problem because impaired hepatocellular function prevents conversion of ammonia that reaches the liver.
Other factors that predispose rising ammonia levels include excessive protein intake, sepsis, excessive accumulation of nitrogenous body wastes (from constipation or GI hemorrhage), and bacterial action on protein and urea to form ammonia. Certain other factors heighten the brain’s sensitivity to ammonia intoxication: hypoxia, azotemia, impaired glucose metabolism, infection, and administration of sedatives, narcotics, and general anesthetics. Depletion of the intravascular volume, from bleeding or diuresis, reduces hepatic and renal perfusion and leads to contraction alkalosis. In turn, hypokalemia and alkalosis increase ammonia production and impair its excretion.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Nonviral hepatitis:
Causes
(Professional Guide to Diseases (Eighth Edition))
Various hepatotoxins — carbon tetrachloride, acetaminophen, trichloroethylene, poisonous mushrooms, and vinyl chloride — can cause the toxic form of this disease. Following exposure to these agents, liver damage usually occurs within 24 to 48 hours, depending on the size of the dose or degree of exposure. Alcohol, anoxia, and preexisting liver disease exacerbate the toxic effects of some of these agents.
Drug-induced (idiosyncratic) hepatitis may stem from a hypersensitivity reaction unique to the affected individual, unlike toxic hepatitis, which appears to affect all people indiscriminately. Among the drugs that may cause this type of hepatitis are niacin, halothane, sulfonamides, isoniazid, methyldopa, and phenothiazines (cholestasis-induced hepatitis). In hypersensitive people, symptoms of hepatic dysfunction may appear at any time during or after exposure to these drugs but usually emerge after 2 to 5 weeks of therapy. Not all adverse drug reactions are toxic. Hormonal contraceptives, for example, may impair liver function and produce jaundice without causing necrosis, fatty infiltration of liver cells, or hypersensitivity.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Cirrhosis and fibrosis:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
These clinical types of cirrhosis reflect its diverse etiology:
❑ Portal, nutritional, or alcoholic (Laennec’s) cirrhosis, the most common type, occurs in 30% to 50% of cirrhotic patients, up to 90% of whom have a history of alcoholism. Liver damage results from malnutrition, especially of dietary protein, and chronic alcohol ingestion. Fibrous tissue forms in portal areas and around central veins.
❑ Biliary cirrhosis (15% to 20% of patients) results from injury or prolonged obstruction.
❑ Postnecrotic (posthepatic) cirrhosis (10% to 30% of patients) stems from various types of hepatitis.
❑ Pigment cirrhosis (5% to 10% of patients) may result from disorders such as hemochromatosis.
❑ Cardiac cirrhosis (rare) refers to liver damage caused by right-sided heart failure.
❑ Idiopathic cirrhosis (about 10% of patients) has no known cause.
Noncirrhotic fibrosis may result from schistosomiasis or congenital hepatic fibrosis or may be idiopathic.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Hepatitis, viral:
Causes
(Handbook of Diseases)
The major forms of viral hepatitis result from infection with the causative viruses: A, B, C, D, E, or G.
Type A hepatitis
Hepatitis A is highly contagious and usually transmitted by the fecal-oral route. It may also be transmitted parenterally.
Clinical tip I.V. drug abusers and recipients of multiple blood product transfusions are at increased risk for hepatitis A.
Hepatitis A usually results from ingestion of contaminated food, milk, or water. Outbreaks of this type are commonly traced to ingestion of seafood from polluted water.
Type B hepatitis
Once thought to be transmitted only by the direct exchange of contaminated blood, hepatitis B is now also known to be transmitted by contact with human secretions and stool passed by health care workers, recipients of plasma-derived products, and hemodialysis patients. As a result, nurses, physicians, laboratory technicians, and dentists are frequently exposed to type B hepatitis, commonly as a result of wearing defective gloves.
Transmission also occurs during intimate sexual contact and through perinatal transmission.
Type C hepatitis
Although hepatitis C viruses have been isolated, only a small percentage of patients have tested positive for them, perhaps reflecting the test’s poor specificity. Usually, this type of hepatitis is transmitted through transfused blood from asymptomatic donors and receiving tattoos.
Clinical tip Most patients with hepatitis C are asymptomatic. Hepatitis C virus is associated with a high rate of chronic liver disease (chronic hepatitis, cirrhosis, and an increased risk of hepatocellular carcinoma), which develops in 50% to 80% of those infected. People who have chronic hepatitis C are considered infectious.
Type D hepatitis
Hepatitis D is found only in patients with an acute or a chronic episode of hepatitis B and requires the presence of HBsAg. The type D virus depends on the double-shelled type B virus to replicate. For this reason, a type D infection can’t outlast a type B infection.
Hepatitis D is rare in the United States, except in I.V. drug abusers.
Type E hepatitis
Hepatitis E is transmitted enterically (oral-fecal and waterborne routes), much like type A. Because this virus is inconsistently shed in feces, detection is difficult.
Type G hepatitis
Hepatitis G, a newly identified virus, is transmitted by the blood-borne route, similar to hepatitis C.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Hepatic encephalopathy:
Causes
(Handbook of Diseases)
Hepatic encephalopathy develops as a result of rising blood ammonia levels. Several factors cause these levels to rise.
Improper shunting of blood
Normally, the ammonia produced by protein breakdown in the bowel is metabolized to urea in the liver. When portal blood shunts past the liver, ammonia directly enters the systemic circulation and is carried to the brain.
Such shunting may result from the collateral venous circulation that develops in portal hypertension or from surgically created portal-systemic shunts. Cirrhosis further compounds this problem because impaired hepatocellular function prevents conversion of ammonia that reaches the liver.
Other factors
Other factors that predispose to rising ammonia levels include excessive protein intake, sepsis, excessive accumulation of nitrogenous body wastes (from constipation or GI hemorrhage), and bacterial action on protein and urea to form ammonia.
Certain other factors heighten the brain’s sensitivity to ammonia intoxication, including fluid and electrolyte imbalances (especially metabolic alkalosis), hypoxia, azotemia, impaired glucose metabolism, infection, and administration of sedatives, narcotics, and general anesthetics.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Hepatitis, nonviral:
Causes
(Handbook of Diseases)
Nonviral hepatitis results from various causes, including:
❑ alcohol overuse — follows heavy alcohol consumption
❑ direct hepatotoxicity — hepatocellular damage and necrosis usually caused by toxins; it’s dose-dependent and occurs primarily in connection with acetaminophen overdose
❑ idiosyncratic hepatotoxicity — follows a sensitization period of several weeks; caused by a host hypersensitivity to medications (isoniazid, methyldopa, mercaptopurine, lovastatin, pravastatin, dipyridamole, and halothane)
❑ cholestatic reactions — caused by lack of bile excretion; possibly direct hepatotoxicity from hormonal contraceptives or anabolic steroids; hypersensitivity to phenothiazine derivatives, such as chlorpromazine, antibiotics, thyroid medications, antidiabetic drugs, and cytotoxic drugs
❑ metabolic and autoimmune disorders — acute exacerbations of subclinical liver disease, such as autoimmune hepatitis and Wilson’s disease
❑ infectious agents — systemic viruses, such as cytomegalovirus, mononucleosis or Epstein-Barr virus, measles virus, varicella zoster, adenovirus, herpes simplex virus, coxsackievirus, and human immunodeficiency virus; spirochetes such as those that cause syphilis and leptospirosis.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Cirrhosis:
Causes
(Handbook of Diseases)
Cirrhosis has various causes, depending on the type.
Hepatocellular disease
Postnecrotic cirrhosis accounts for 10% to 30% of patients and stems from various types of hepatitis (such as types A, B, C, D viral hepatitis) or toxic exposures.
Laënnec’s cirrhosis — also called portal, nutritional, or alcoholic cirrhosis — is the most common type and is commonly caused by hepatitis C. Liver damage results from malnutrition (especially dietary protein) and overuse of alcohol. Fibrous tissue forms in portal areas and around central veins.
Autoimmune disease, such as sarcoidosis and chronic inflammatory bowel disease, may result in cirrhosis.
Cholestatic diseases
Cholestatic diseases include diseases of the biliary tree (biliary cirrhosis resulting from bile duct diseases suppressing bile flow) and sclerosing cholangitis.
Metabolic diseases
Metabolic diseases include disorders such as Wilson’s disease, alpha1-antitrypsin deficiency, and hemochromatosis (pigment cirrhosis).
Other types of cirrhosis
Other types of cirrhosis include Budd-Chiari syndrome, cardiac cirrhosis, and cryptogenic cirrhosis. Cardiac cirrhosis is rare; the liver damage results from right-sided heart failure. Cryptogenic refers to cirrhosis of unknown cause.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Chronic Hepatitis:
Chronic Hepatitis - pathophysiology
(The 5-Minute Pediatric Consult)
Pathology has been traditionally classified as chronic persistent hepatitis, chronic aggressive hepatitis, and chronic lobular hepatitis. The hepatocytes are damaged, with inflammatory cellular infiltration accompanied by liver regeneration.
- Chronic persistent hepatitis:
- Minimal portal tract fibrosis
- Slightly widened portal tracts
- Limiting plate is intact and inflammation does not extend beyond this.
- No bridging fibrosis between portal tracts
- Chronic aggressive hepatitis:
- Perilobular hepatitis, with inflammatory cells extending from portal tracts into parenchyma with fibrosis
- Piecemeal necrosis: Necrotic hepatocytes surrounded by lymphocytes and fibroblasts
- In advanced disease, fibrosis bridges the portal tracts (bridging fibrosis).
- Cirrhosis occurs when there is loss of architecture owing to fibrosis.
- Chronic lobular hepatitis:
- Liver architecture is preserved with scattered changes of acute hepatitis with hepatocyte necrosis in the lobules (perivenular regions).
- These changes are most often associated with hepatitis B and non-A, non-B hepatitis.
Chronic Hepatitis - etiology
- Autoimmune liver disease
- Viral hepatitis
- Obesity (NASH)
- Progressive familial intrahepatic cholestasis syndromes
- Congenital hepatic fibrosis
- Cystic fibrosis
- Metabolic disease:
- Mitochondrial disease
- Lysosomal storage disorders
- Peroxisomal disease
- Lipid storage disease
- Glycogen storage disease
- Wilson disease and others
- Drug hepatotoxicity:
- Methotrexate
- Isoniazid
- Thioguanine
- 6-Mercaptopurine
- Valproate
- Liver disease associated with other chronic diseases:
- Cardiac disease
- Autosomal recessive polycystic kidney disease
- Diabetes mellitus
- Langerhans cell histiocytosis
- Immunodeficiency
- Total parenteral nutrition cholestasis
» READ BOOK EXCERPT ONLINE »
Source: The 5-Minute Pediatric Consult, 2008
Hepatitis:
Epidemiology and Etiology
(Pediatric Infectious Disease)
Hepatitis A is the most common viral etiology of pediatric hepatitis. The mode
of transmission is person to person, resulting from fecal contamination of
food. Sexual contact and nosocomial transmission have also been documented.
» READ BOOK EXCERPT ONLINE »
Source: Pediatric Infectious Disease, 2004
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