Categories
Ailmemts & Remedies

Haemochromatosis

Definition:
Haemochromatosis is a disease caused by excess iron in the body.

Iron is needed in the diet to maintain good health, particularly for making red blood cells that carry oxygen around the body. These red blood cells contain large amounts of iron.

Lack of iron can cause anaemia, but excessive iron is toxic. The body has few ways of disposing of unwanted iron, so it builds up in tissues causing damage and disease.

Haemochromatosis – or genetic haemochromatosis (GH) – is a disorder that causes the body to absorb an excessive amount of iron from the diet.

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We can only use a limited amount of iron and any excess is deposited around the body. This accumulates mainly in the liver, but can also affect the heart, pancreas and pituitary gland, damaging these vital body organs and resulting in a deterioration of their functional capacity.

Haemochromatosis is more common in Caucasian or white populations, with about 1 in 300 to 1 in 400 affected. About half that number are affected in black populations.

Men are more likely to have hereditary haemochromatosis and suffer from it at an earlier age, as women regularly lose iron in menstruation or use stores in pregnancy.

Symptoms:
Although haemochromatosis and the potential for the condition to cause problems is present from birth, symptoms don’t usually become apparent until middle age.

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Common symptoms that might be noticed then include:

•weakness, tiredness and lack of energy
•joint pain and stiffness – particularly in the hands and fingers
•a tanned or bronzed appearance of the skin
•impotence in men
•shrinking of testicles
•weight loss
•abdominal pain
.
Later, more serious symptoms may develop including:

•diabetes
•arthritis
•heart problems
•enlargement or damage to the liver

Clinical presentation:
Organs commonly affected by haemochromatosis are the liver, heart, and endocrine glands.

Haemochromatosis may present with the following clinical syndromes:

*Cirrhosis of the liver
*Diabetes due to pancreatic islet cell failure
*Cardiomyopathy
*Arthritis (iron deposition in joints)
*Testicular failure
*Tanning of the skin

Causes:
The causes can be distinguished between primary cases (hereditary or genetically determined) and less frequent secondary cases (acquired during life). People of Celtic (Irish, Scottish, Welsh) origin have a particularly high incidence of whom about 10% are carriers of the gene and 1% sufferers from the condition.

Primary haemochromatosis:
The fact that most cases of haemochromatosis were inherited was well known for most of the 20th century, though they were incorrectly assumed to depend on a single gene. The overwhelming majority actually depend on mutations of the HFE gene discovered in 1996, but since then others have been discovered and sometimes are grouped together as “non-classical hereditary haemochromatosis”, “non-HFE related hereditary haemochromatosis”, or “non-HFE haemochromatosis

It is thought to be mainly caused by a mutation of a gene called HFE, which probably allows excess iron to be absorbed from the diet. This mutation is known as C282Y and to develop haemochromatosis you usually need two genes (one from each parent) to be C282Y.

However, not everyone with the mutation may develop the disease, and it may occur if only one C282Y gene is present.

Confusingly, another mutation labelled H63D elsewhere on the HFE gene may occur alone or with C282Y and also influence iron levels.

Other rare mutations may give rise to haemochromatosis, especially in children.

Secondary haemochromatosis:
*Severe chronic haemolysis of any cause, including intravascular haemolysis and ineffective erythropoiesis (haemolysis within the bone marrow).
*Multiple frequent blood transfusions (either whole blood or just red blood cells), which are usually needed either by individuals with hereditary anaemias (such as beta-thalassaemia major, sickle cell anaemia, and Diamond–Blackfan anaemia) or by older patients with severe acquired anaemias such as in myelodysplastic syndromes.
*Excess parenteral iron supplements, such as can acutely happen in iron poisoning
*Excess dietary iron
*Some disorders do not normally cause haemochromatosis on their own, but may do so in the presence of other predisposing factors. These include cirrhosis (especially related to alcohol abuse), steatohepatitis of any cause, porphyria cutanea tarda, prolonged haemodialysis, post-portacaval shunting.

Risk Factors:
The onset of hereditary haemochromatosis usually occurs between the ages of 30 and 60 as the build up of iron takes years.

However, a rapid form of the disease does affect children. If left untreated excess iron builds up in the organs especially the liver, heart and pancreas. This may cause heart or liver failure, which can be fatal.

Diagnosis:
There are several methods available for diagnosing and monitoring iron loading including:

*Serum ferritin
*Liver biopsy
*HFE
*MRI

Serum ferritin is a low-cost, readily available, and minimally invasive method for assessing body iron stores. However, the major problem with using it as an indicator of iron overload is that it can be elevated in a range of other medical conditions unrelated to iron levels including infection, inflammation, fever, liver disease, renal disease, and cancer. Also, total iron binding capacity may be low, but can also be normal.

The standard of practice in diagnosis of hemochromatosis was recently reviewed by Pietrangelo. Positive HFE analysis confirms the clinical diagnosis of hemochromatosis in asymptomatic individuals with blood tests showing increased iron stores, or for predictive testing of individuals with a family history of hemochromatosis. The alleles evaluated by HFE gene analysis are evident in ~80% of patients with hemochromatosis; a negative report for HFE gene does not rule out hemochromatosis. In a patient with negative HFE gene testing, elevated iron status for no other obvious reason, and family history of liver disease, additional evaluation of liver iron concentration is indicated. In this case, diagnosis of hemochromatosis is based on biochemical analysis and histologic examination of a liver biopsy. Assessment of the hepatic iron index (HII) is considered the “gold standard” for diagnosis of hemochromatosis.

MRI is emerging as an alternative to liver biopsy for measuring liver iron loading. For measuring liver iron concentrations, R2-MRI (also known as FerriScan)  has been validated and is coming into use in medical centers. It is not recommended in practice guidelines at this time

Prognosis:
A third of those untreated develop hepatocellular carcinoma.

Treatment:
Routine treatment in an otherwise-healthy person consists of regularly scheduled phlebotomies (bloodletting). When first diagnosed, the phlebotomies may be fairly frequent, perhaps as often as once a week, until iron levels can be brought to within normal range. Once iron and other markers are within the normal range, phlebotomies may be scheduled every other month or every three months depending upon the patient’s rate of iron loading.

For those unable to tolerate routine blood draws, there is a chelating agent available for use. The drug Deferoxamine binds with iron in the bloodstream and enhances its elimination via urine and faeces. Typical treatment for chronic iron overload requires subcutaneous injection over a period of 8–12 hours daily. Two newer iron chelating drugs that are licensed for use in patients receiving regular blood transfusions to treat thalassemia (and, thus, who develop iron overload as a result) are deferasirox and deferiprone.

Haemochromatosis is treated by:

•Reducing the amount of iron absorbed by the body – patients are advised to avoid iron-rich foods and alcohol.
•Removing excess iron from the body by removing blood from the body (venesection therapy or phlebotomy). Initially this may involve removing a unit of blood a week (sometimes for many months) until iron levels in the blood are normal. Then most people can be kept stable by removing a unit of blood every 2-3 months.

If phlebotomy is started before liver damage occurs the outlook is good, and the affected person can expect to live an otherwise normal life.

Acquired haemochromatosis is normally treated by a drug that binds iron and allows it to be excreted from the body.

Associated problems such as heart failure and diabetes are treated as appropriate.

Good advice:-
*Limit the amount of iron in your diet.
*Eating red or organ meats (such as liver) is not recommended.
*Iron supplements should also be avoided, including iron combined with other multivitamins.
*Vitamin C increases iron absorption from the gut and intake should also be limited.
*Avoid excess alcohol as this may make liver disease worse

Future prospects:
Your prospects largely depend on the stage at which the disease was diagnosed. Symptoms of tiredness and general weakness often improve, but joint problems may not.

Abdominal pain and liver enlargement can also lessen or disappear, and heart function may also improve with treatment.

However, liver cirrhosis is irreversible and a liver transplant may be required.

Patients with liver disease are also usually monitored for liver cancer, which can be a long-term complication.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://www.bbc.co.uk/health/physical_health/conditions/haemochromatosis1.shtml
http://en.wikipedia.org/wiki/Iron_overload
http://www.netdoctor.co.uk/diseases/facts/haemochromatosis.htm

https://runkle-science.wikispaces.com/Haemochromatosis

http://www.ironxs.com.au/the-symptoms-of-haemochromatosis.html

http://www.goldbamboo.com/topic-t1404-a1-6Haemochromatosis.html

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Categories
Ailmemts & Remedies Pediatric

Biliary Atresia

DEfinition:
Biliary atresia is a rare condition in newborn infants in which the common bile duct(that carry a liquid called bile from the liver to the gallbladder) between the liver and the small intestine is blocked or absent. If unrecognized, the condition leads to liver failure — but not kernicterus, as the liver is still able to conjugate bilirubin, and conjugated bilirubin is unable to cross the blood-brain barrier. The cause of the condition is unknown. The only effective treatments are certain surgeries such as the kasai procedure, or liver transplantation.

..You may click to see the picture

Biliary atresia is a very rare disorder. About one in 10,000 to 20,000 babies in the U.S are affected every year. Biliary atresia seems to affect girls slightly more often than boys. Within the same family, it is common for only one child in a pair of twins or only one child within the same family to have it. Asians and African-Americans are affected more frequently than Caucasians. There does not appear to be any link to medications or immunizations given immediately before or during pregnancy.

This is now effective surgery which can relieve symptoms in most cases. Liver transplant is also an option, and as a result, survival rates are now above 90 per cent.

Causes & b Risk Factors:
Biliary atresia is due to a progressive fibrosis or scarring of the bile ducts responsible for draining bile from the liver, which eventually leads to atresia or loss of the biliary system. It’s not clear how or why this occurs, and many factors may be involved. It may be due to a problem in the developing embryo (10 to 20 per cent – other congenital abnormalities may also be present) or around the time of birth or shortly afterwards (80 to 90 per cent). It occurs more often in Asian and African-American newborns than Caucasian.

Bile is made by the liver and helps with the digestion of fats. If bile is not removed from the liver, it builds up and begins to damage it. The baby will then develop jaundice, or a yellow colour of the skin as levels of the bile chemical bilirubin rise in the blood. Other symptoms include dark coloured urine and pale stools. Many newborn babies become jaundiced but this is usually temporary. Jaundice lasting for longer than 14 days, especially if there are other symptoms such as an enlarged liver or failure to thrive, is a worrying sign and must be investigated further.

Pathophysiology:
There is no known cause of biliary atresia. There have been many theories about ethiopathogenesis such as Reovirus 3 infection, congenital malformation, congenital CMV infection, autoimmune theory. This means that the etiology and pathogenesis of biliary atresia are largely unknown. However, there have been extensive studies about the pathogenesis and proper management of progressive liver fibrosis, which is arguably one of the most important aspects of biliary atresia patients. As the biliary tract cannot transport bile to the intestine, bile is retained in the liver (known as stasis) and results in cirrhosis of the liver. Proliferation of the small bile ductules occur, and peribiliary fibroblasts become activated. These “reactive” biliary epithelial cells in cholestasis, unlike normal condition, produce and secrete various cytokines such as CCL-2 or MCP-1, Tumor necrosis factor (TNF), Interleukin-6 (IL-6), TGF-beta, Endothelin (ET), and nitric oxide (NO). Among these, TGF-beta is the most important profibrogenic cytokine that can be seen in liver fibrosis in chronic cholestasis. During the chronic activation of biliary epithelium and progressive fibrosis, afflicted patients eventually show signs and symptoms of portal hypertension (esophagogastric varix bleeding, hypersplenism, hepatorenal syndrome(HRS), hepatopulmonary syndrome(HPS)). The latter two syndromes are essentially caused by systemic mediators that maintain the body within the hyperdynamic states. There are three main types of extrahepatic biliary atresia:- Type I: atresia restricted to the common bile duct. Type II: atresia of the common hepatic duct. Type III: atresia of the right and left hepatic duct. Associated anomalies include, in about 20% cases, cardiac lesions, polysplenia, situs inversus, absent vena cava and a preduodenal portal vein.

Symptoms:
Newborns with this condition may appear normal at birth. However, jaundice (a yellow color to the skin and mucous membranes) develops by the second or third week of life. The infant may gain weight normally for the first month, but then will lose weight and become irritable, and have worsening jaundice.

Other symptoms may include:

•Dark urine
•Enlarged spleen
•Floating stools
•Foul-smelling stools
•Pale or clay-colored stools
•Slow growth
•Slow or no weight gain

Diagnosis:
The health care provider will perform a physical exam, which includes feeling the patient’s belly area. The doctor may feel an enlarged liver.

Tests to diagnose biliary atresia include:

•Abdominal x-ray
•Abdominal ultrasound to examine the liver and bile ducts
•A blood test to look for raised levels of bilirubin and check liver enzyme levels and blood clotting
•Hepatobiliary iminodiacetic acid (HIDA) scan, also called cholescintigraphy, to help determine whether the bile ducts and gallbladder are working properly
•Liver biopsy to determine the severity of cirrhosis or to rule out other causes of jaundice
•An abdominal x-ray to look for an enlarged liver and spleen
•X-ray of the bile ducts (cholangiogram)
•An scan to determine how well bile is flowing (HIDA or TEBIDA)

Treatment :
TreatmentIf the intrahepatic biliary tree is unaffected, surgical reconstruction of the extrahepatic biliary tract is possible. This surgery is called a Kasai procedure (after the Japanese surgeon who developed the surgery, Dr. Morio Kasai) or hepatoportoenterostomy.

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If the atresia is complete, liver transplantation is the only option(currently has a greater than 95 per cent survival rate at one year). Timely Kasai portoenterostomy (e.g. < 60 postnatal days) has shown better outcomes. Nevertheless, a considerable number of the patients, even if Kasai portoenterostomy has been successful, eventually undergo liver transplantation within a couple of years after Kasai portoenterostomy.

Recent large volume studies from Davenport et al. (Ann Surg, 2008) show that age of the patient is not an absolute clinical factor affecting the prognosis. In the latter study, influence of age differs according to the disease etiology—i.e., whether isolated BA, BASM (BA with splenic malformation ), or CBA(cystic biliary atresia).

It is widely accepted that corticosteroid treatment after a Kasai operation, with or without choleretics and antibiotics, has a beneficial effect on the postoperative bile flow and can clear the jaundice; but the dosing and duration of the ideal steroid protocol have been controversial (“blast dose” vs. “high dose” vs. “low dose”). Furthermore, it has been observed in many retrospective longitudinal studies that steroid does not prolong survival of the native liver or transplant-free survival. Davenport at al. also showed (hepatology 2007) that short-term low-dose steroid therapy following a Kasai operation has no effect on the mid- and long-term prognosis of biliary atresia patients.

Prognosis:
Early surgery will improve the survival of more than a third of babies with this condition. The long-term benefit of liver transplant is not yet known, but is expected to improve survival.

Possible Complications:
•Infection
•Irreversible cirrhosis
•Liver failure
•Surgical complications, including failure of the Kasai procedure

Prevention:
The earlier biliary atresia is detected, the less damage it will have done to the liver and the better the chance of a successful outcome to treatment. The current target is to treat babies before they are eight weeks old.

If the liver has not yet been damaged by cirrhosis, the condition is usually treated through an operation called a Kasai portoenterostomy (or a similar procedure). This involves using a loop of bowel to form a duct to drain the bile from the liver. The operation is named after the Japanese surgeon, Professor Morio Kasai, who developed it in 1959. It was first introduced in the UK in the 1960s.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://www.bbc.co.uk/health/physical_health/conditions/biliary_atresia.shtml
http://www.nlm.nih.gov/medlineplus/ency/article/001145.htm
http://en.wikipedia.org/wiki/Biliary_atresia

http://www.mikylah.com/pictures.html

http://www.chw.health.nsw.gov.au/parents/factsheets/biliary_atresia.htm

Categories
News on Health & Science

Coffee Good for Chronic Hepatitis C Patients

Patients of chronic hepatitis C, who drink three or more cups of coffee daily, have a 53 percent lower risk of liver disease progression than non-coffee drinkers, says a new study
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The study, led by Neal Freedman of National Cancer Institute (NCI), found that patients with hepatitis C related cirrhosis who did not respond to treatment benefited from increased coffee intake. No effect on liver was observed in patients who drank black or green tea.

Hepatitis C virus (HCV) infects approximately 2.2 percent of the world’s population, including three million Americans. A centre for Disease Control and Prevention (CDC) cites HCV as the leading cause of liver transplantation in US, accounting for 8,000 to 10,000 deaths, annually.

The World Health Organisation (WHO) estimated that three to four million people contract HCV each year with 70 percent becoming chronic cases that can lead to cirrhosis of the liver and liver cancer.

This study included 766 participants enrolled in the Hepatitis C Antiviral Long-Term Treatment against Cirrhosis (HALT-C) trial who had hepatitis C-related cirrhosis and failed to respond to standard treatment of the anti-viral drugs peginterferon and ribavirin, according to an NCI release.

Participants were seen every three months during the 3.8-year study period to assess clinical outcomes. Liver biopsies were also taken at 1.5 and 3.5 five years to determine the progression of liver disease.

“Results from our study suggest that patients with high coffee intake had a lower risk of disease progression,” said Freedman.

These findings will appear in the November issue of Hepatology

Sources: The Times Of India

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Ailmemts & Remedies

Hepatitis B

Hepatitis B virus surface antigen. Transmission electron Micrograph

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Definition:
Hepatitis B is the most common serious liver infection in the world. It is thought to be the leading cause of liver cancer.The World Health Organization estimates that hepatitis B infections lead to more than one million deaths every year.

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Virus classification:-
Group: Group VII (dsDNA-RT)
Family: Hepadnaviridae
Genus: Orthohepadnavirus
Species: Hepatitis B virus

Hepatitis B virus infects the liver of hominoidae, including humans, and causes an inflammation called hepatitis. It is a DNA virus and one of many unrelated viruses that cause viral hepatitis. The disease was originally known as “serum hepatitis” and has caused epidemics in parts of Asia and Africa. Hepatitis B is endemic in China and various other parts of Asia. The proportion of the world’s population currently infected with the virus is estimated at 3 to 6%, but up to a third have been exposed. Symptoms of the acute illness caused by the virus include liver inflammation, vomiting, jaundice, and rarely, death. Chronic hepatitis B may eventually cause liver cirrhosis and liver cancer, a fatal disease with very poor response to current chemotherapy. The infection is preventable by vaccination.

Symptoms:
The virus can cause a range of problems, including fever, fatigue, muscle or joint pain, loss of appetite, nausea and vomiting.

Chronic carriers have an increased risk of developing liver disease such as cirrhosis or liver cancer, because the hepatitis B virus steadily attacks the liver.

Chronic carriers will usually have on going inflammation of the liver and may eventually develop cirrhosis and liver cancer.

About 1% of people who are infected develop an extreme form of disease called acute fulminant hepatitis.

This condition can be fatal if not treated quickly. Sufferers may collapse with fatigue, have yellowing of the skin and eyes (jaundice) and develop swelling in their abdomen.

Hepatitis B virus infection may either be acute (self-limiting) or chronic (long-standing). Persons with self-limiting infection clear the infection spontaneously within weeks to months.

Children are less likely than adults to clear the infection. More than 95% of people who become infected as adults or older children will stage a full recovery and develop protective immunity to the virus. However, only 5% of newborns that acquire the infection from their mother at birth will clear the infection. Of those infected between the age of one to six, 70% will clear the infection.

Acute infection with hepatitis B virus is associated with acute viral hepatitis – an illness that begins with general ill-health, loss of appetite, nausea, vomiting, body aches, mild fever, dark urine, and then progresses to development of jaundice. It has been noted that itchy skin has been an indication as a possible symptom of all hepatitis virus types. The illness lasts for a few weeks and then gradually improves in most affected people. A few patients may have more severe liver disease (fulminant hepatic failure), and may die as a result of it. The infection may be entirely asymptomatic and may go unrecognized.

Chronic infection with Hepatitis B virus may be either asymptomatic or may be associated with a chronic inflammation of the liver (chronic hepatitis), leading to cirrhosis over a period of several years. This type of infection dramatically increases the incidence of hepatocellular carcinoma (liver cancer). Chronic carriers are encouraged to avoid consuming alcohol as it increases their risk for cirrhosis and liver cancer. Hepatitis B virus has been linked to the development of Membranous glomerulonephritis (MGN).

Hepatitis D infection can only occur with a concomitant infection with Hepatitis B virus because the Hepatitis D virus uses the Hepatitis B virus surface antigen to form a capsid. Co-infection with hepatitis D increases the risk of liver cirrhosis and liver cancer. Polyarteritis nodosa is more common in people with hepatitis B infection.

Causes:The disease is caused by the hepatitis B virus (HBV) that attacks the liver. The virus is transmitted through blood and bodily fluids that contain blood.This can occur through direct blood-to-blood contact, unprotected sex, and illicit drug use. It can also be passed from an infected woman to her new-born during the delivery process.

Risk Factor:It is thought that about one in three of the world’s population is infected by HBV.However, about 50% of those who carry the virus never develop any symptoms.
About nine out of ten people infected with HBV will eventually clear the virus from their bodies. But about 5-10% of infected adults will become chronic hepatitis B carriers, often without even knowing it.

Diagnosis:The tests, called assays, for detection of hepatitis B virus infection involve serum or blood tests that detect either viral antigens (proteins produced by the virus) or antibodies produced by the host. Interpretation of these assays is complex.

The hepatitis B surface antigen (HBsAg) is most frequently used to screen for the presence of this infection. It is the first detectable viral antigen to appear during infection. However, early in an infection, this antigen may not be present and it may be undetectable later in the infection as it is being cleared by the host. The infectious virion contains an inner “core particle” enclosing viral genome. The icosahedral core particle is made of 180 or 240 copies of core protein, alternatively known as hepatitis B core antigen, or HBcAg. During this ‘window’ in which the host remains infected but is successfully clearing the virus, IgM antibodies to the hepatitis B core antigen (anti-HBc IgM) may be the only serological evidence of disease.

Shortly after the appearance of the HBsAg, another antigen named as the hepatitis B e antigen (HBeAg) will appear. Traditionally, the presence of HBeAg in a host’s serum is associated with much higher rates of viral replication and enhanced infectivity; however, variants of the hepatitis B virus do not produce the ‘e’ antigen, so this rule does not always hold true. During the natural course of an infection, the HBeAg may be cleared, and antibodies to the ‘e’ antigen (anti-HBe) will arise immediately afterwards. This conversion is usually associated with a dramatic decline in viral replication.

If the host is able to clear the infection, eventually the HBsAg will become undetectable and will be followed by IgG antibodies to the hepatitis B surface antigen and core antigen, (anti-HBs and anti HBc IgG). A person negative for HBsAg but positive for anti-HBs has either cleared an infection or has been vaccinated previously.

Individuals who remain HBsAg positive for at least six months are considered to be hepatitis B carriers. Carriers of the virus may have chronic hepatitis B, which would be reflected by elevated serum alanine aminotransferase levels and inflammation of the liver, as revealed by biopsy. Carriers who have seroconverted to HBeAg negative status, particularly those who acquired the infection as adults, have very little viral multiplication and hence may be at little risk of long-term complications or of transmitting infection to others.

More recently, PCR tests have been developed to detect and measure the amount of viral nucleic acid in clinical specimens. These tests are called viral loads and are used to assess a person’s infection status and to monitor treatment.


Treatment:-
Acute hepatitis B infection does not usually require treatment because most adults clear the infection spontaneously. Early antiviral treatment may only be required in fewer than 1% of patients, whose infection takes a very aggressive course (“fulminant hepatitis”) or who are immunocompromised. On the other hand, treatment of chronic infection may be necessary to reduce the risk of cirrhosis and liver cancer. Chronically infected individuals with persistently elevated serum alanine aminotransferase, a marker of liver damage, and HBV DNA levels are candidates for therapy.

There are several drug treatments available to treat hepatitis B.Patients may be put on a four month course of injections of the drug interferon.

An alternative treatment is a drug called lamivudine which is taken orally once a day. Treatment is usually for one year. Sometimes lamivudine is combined with interferon.

Although none of the available drugs can clear the infection, they can stop the virus from replicating, and prevent liver damage such as cirrhosis and liver cancer. Treatments include antiviral drugs such as lamivudine, adefovir and entecavir, and immune system modulators such as interferon alpha. However, some individuals are much more likely to respond than others and this might be because of the genotype of the infecting virus or the patient’s heredity. The treatment works by reducing the viral load, (the amount of virus particles as measured in the blood), which in turn reduces viral replication in the liver.

On March 29, 2005, the US Food and Drug Administration (FDA) approved Entecavir for the treatment of Hepatitis B. On February 25, 2005, the EU Commission approved Peginterferon alfa-2a (Pegasys). On October 27, 2006, telbivudine gained FDA approval. It is marketed under the brand name Tyzeka in the US and Sebivo outside the US. It is approved in Switzerland.

Infants born to mothers known to carry hepatitis B can be treated with antibodies to the hepatitis B virus (hepatitis B immune globulin or HBIg). When given with the vaccine within twelve hours of birth, the risk of acquiring hepatitis B is reduced 95%. This treatment allows a mother to safely breastfeed her child.

Chronic patients may require a liver transplant…....CLICK & SEE

Prevention:It can be prevented by the use of a safe and effective vaccine.However, for the 400 million people world-wide who are already carriers of HBV, the vaccine is of no use.

Vaccination: Several vaccines have been developed for the prevention of hepatitis B virus infection. These rely on the use of one of the viral envelope proteins (hepatitis B surface antigen or HBsAg). The vaccine was originally prepared from plasma obtained from patients who had long-standing hepatitis B virus infection. However, currently, these are more often made using recombinant DNA technology, though plasma-derived vaccines continue to be used; the two types of vaccines are equally effective and safe.

Following vaccination Hepatitis B Surface antigen may be detected in serum for several days; this is known as vaccine antigenaemia .

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.
Resources:
http://news.bbc.co.uk/2/hi/health/1505615.stm
http://en.wikipedia.org/wiki/Hepatitis_B

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Herbs & Plants

Milk Thistle

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Botanical Name: Silybum marianum
Family: N.O. Compositae,Asteraceae
Subfamily: Lactucoideae
Tribe: Cynareae
Genus: Silybum
Species: S. marianum
Kingdom: Plantae
Order: Asterales

Synonym-:Marian Thistle.  Carduus lactifolius. Carduus marianus. Centaurea dalmatica. Mariana lactea.
Common Names-:- Cardus marianus,  Milk thistle,  Blessed milkthistle,   Marian thistle, Mary thistle, Saint Mary‘s thistle, Mediterranean milk thistle, Variegated thistle and Scotch thistle,  Mary thistle, holy thistle. Milk thistle is sometimes called silymarin, which is actually a mixture of the herb’s active components, including silybinin (also called silibinin or silybin).

Latin Name-:-Silybum marianum

Habitat : Milk Thistle is native to  S. Europe, N. Africa and W. Asia. Naturalized in Britain.  It grows on  waste places, usually close to the sea, especially if the ground is dry and rocky.  .

Parts Used-: Whole herb, root, leaves, seeds and hull.

Description: Members of this genus grow as annual or biennial plants. The erect stem is tall, branched and furrowed but not spiny. The large, alternate leaves are waxy-lobed, toothed and thorny, as in other genera of thistle. The lower leaves are cauline (attached to the stem without petiole). The upper leaves have a clasping base. They have large, disc-shaped pink-to-purple, rarely white, solitary flower heads at the end of the stem. The flowers consist of tubular florets. The phyllaries under the flowers occur in many rows, with the outer row with spine-tipped lobes and apical spines. The fruit is a black achene with a white pappus

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Only two species are currently classified in this genus:

Silybum eburneum Coss. & Dur., known as the Silver Milk Thistle, Elephant Thistle, or Ivory Thistle
Silybum eburneum Coss. & Dur. var. hispanicum
Silybum marianum (L.) Gaertner, the Blessed Milk Thistle, which has a large number of other common names, such as Variegated Thistle.
The two species hybridise naturally, the hybrid being known as Silybum × gonzaloi Cantó , Sánchez Mata & Rivas Mart. (S. eburneum var. hispanicum x S. marianum)

A number of other plants have been classified in this genus in the past but have since been relocated elsewhere in the light of additional research.

S. marianum is by far the more widely known species. It is believed to give some remedy for liver diseases (e.g. viral hepatitis) and an extract, silymarin, is used in medicine. The adverse effect of the medicinal use of milk thistle is loose stools.

This handsome plant is not unworthy of a place in our gardens and shrubberies and was formerly frequently cultivated. The stalks, like those of most of our larger Thistles, may be eaten, and are palatable and nutritious. The leaves also may be eaten as a salad when young. Bryant, in his Flora Dietetica, writes of it: ‘The young shoots in the spring, cut close to the root with part of the stalk on, is one of the best boiling salads that is eaten, and surpasses the finest cabbage. They were sometimes baked in pies. The roots may be eaten like those of Salsify.’ In some districts the leaves are called ‘Pig Leaves,’ probably because pigs like them, and the seeds are a favourite food of goldfinches.

The common statement that this bird lines its nest with thistledown is scarcely accurate, the substance being in most cases the down of Colt’s-foot (Tussilago), or the cotton down from the willow, both of which are procurable at the building season, whereas thistledown is at that time immature.

Westmacott, writing in 1694, says of this Thistle: ‘It is a Friend to the Liver and Blood: the prickles cut off, they were formerly used to be boiled in the Spring and eaten with other herbs; but as the World decays, so doth the Use of good old things and others more delicate and less virtuous brought in.’

The heads of this Thistle formerly were eaten, boiled, treated like those of the Artichoke.

There is a tradition that the milk-white veins of the leaves originated in the milk of the Virgin which once fell upon a plant of Thistle, hence it was called Our Lady’s Thistle, and the Latin name of the species has the same derivation.
Cultivation:
Succeeds in any well-drained fertile garden soil. Prefers a calcareous soil and a sunny position. Hardy to about -15°c. The blessed thistle is a very ornamental plant that was formerly cultivated as a vegetable crop. Young plants are prone to damage from snails and slugs. Plants will often self sow freely.

Propagation:
Seed – if sown in situ during March or April, the plant will usually flower in the summer and complete its life cycle in one growing season. The seed can also be sown from May to August when the plant will normally wait until the following year to flower and thus behave as a biennial. The best edible roots should be produced from a May/June sowing, whilst sowing the seed in the spring as well as the summer should ensure a supply of edible leaves all year round.

Edible Uses :
Edible Parts: Flowers; Leaves; Oil; Oil; Root; Stem.
Edible Uses: Coffee; Oil; Oil.

Root – raw or cooked. A mild flavour and somewhat mucilaginous texture. When boiled, the roots resemble salsify (Tragopogon hispanicus). Leaves – raw or cooked. The very sharp leaf-spines must be removed first, which is quite a fiddly operation. The leaves are quite thick and have a mild flavour when young, at this time they are quite an acceptable ingredient of mixed salads, though they can become bitter in hot dry weather. When cooked they make an acceptable spinach substitute. It is possible to have leaves available all year round from successional sowings. Flower buds – cooked. A globe artichoke substitute, they are used before the flowers open. The flavour is mild and acceptable, but the buds are quite small and even more fiddly to use than globe artichokes. Stems – raw or cooked. They are best peeled and can be soaked to reduce the bitterness. Palatable and nutritious, they can be used like asparagus or rhubarb or added to salads. They are best used in spring when they are young. A good quality oil is obtained from the seeds. The roasted seed is a coffee substitute

HEALTH BENEFITS:

The seeds of this plant are used nowadays for the same purpose as Blessed Thistle, and on this point John Evelyn wrote: ‘Disarmed of its prickles and boiled, it is worthy of esteem, and thought to be a great breeder of milk and proper diet for women who are nurses.’

It is in popular use in Germany for curing jaundice and kindred biliary derangements. It also acts as a demulcent in catarrh and pleurisy. The decoction when applied externally is said to have proved beneficial in cases of cancer.

Gerard wrote of the Milk Thistle that:
‘the root if borne about one doth expel melancholy and remove all diseases connected therewith. . . . My opinion is that this is the best remedy that grows against all melancholy diseases,’
which was another way of saying that it had good action on the liver. He also tells us:
‘Dioscorides affirmed that the seeds being drunke are a remedy for infants that have their sinews drawn together, and for those that be bitten of serpents:’and we find in a record of old Saxon remedies that ‘this wort if hung upon a man’s neck it setteth snakes to flight.’ The seeds were also formerly thought to cure hydrophobia.
Culpepper considered the Milk Thistle to be as efficient as Carduus benedictus for agues, and preventing and curing the infection of the plague, and also for removal of obstructions of the liver and spleen. He recommends the infusion of the fresh root and seeds, not only as good against jaundice, also for breaking and expelling stone and being good for dropsy when taken internally, but in addition, to be applied externally, with cloths, to the liver. With other writers, he recommends the young, tender plant (after removing the prickles) to be boiled and eaten in the spring as a blood cleanser.
A tincture is prepared by homoeopathists for medicinal use from equal parts of the root and the seeds with the hull attached.

It is said that the empirical nostrum, antiglaireux, of Count Mattaei, is prepared from this species of Thistle.

Thistles in general, according to Culpepper, are under the dominion of Jupiter.
Milk thistles have been reported to have protective effects on the liver and to improve its function. They are typically used to treat liver cirrhosis, chronic hepatitis (liver inflammation), and gallbladder disorders. The active compound in Milk thistle credited with this effect is “silymarin”, and is typically administered in amount ranging from 200-500mg per day (common Milk Thistle supplements have an 80% standardized extract of silymarin). Increasing research is being carried out into its possible medical uses and the mechanisms of such effects. However, a previous literature review using only studies with both double-blind and placebo protocols concluded that milk thistle and its derivatives “does not seem to significantly influence the course of patients with alcoholic and/or hepatitis B or C liver diseases.”

Medicinal Uses:
Silymarin is poorly soluble in water, so aqueous preparations such as teas are ineffective, except for use as supportive treatment in gallbladder disorders because of cholagogic and spasmolytic effects. The drug is best administered parenterally because of poor absorption of silymarin from the gastrointestinal tract. The drug must be concentrated for oral use.   Silymarin’s hepatoprotective effects may be explained by its altering of the outer liver cell membrane structure, as to disallow entrance of toxins into the cell.  This alteration involves silymarin’s ability to block the toxin’s binding sites, thus hindering uptake by the cell.  Hepatoprotection by silymarin can also be attributed to its antioxidant properties by scavenging prooxidant free radicals and increasing intracellular concentration of glutathione, a substance required for detoxicating reactions in liver cells.

Silymarin’s mechanisms offer many types of therapeutic benefit in cirrhosis with the main benefit being hepatoprotection. Use of milk thistle, however, is inadvisable in decompensated cirrhosis.  In patients with acute viral hepatitis, silymarin shortened treatement time and showed improvement in serum levels of bilirubin, AST and ALT.

Treatment claims also include:

1.Lowering cholesterol levels
2.Reducing insulin resistance in people with type 2 diabetes who also have cirrhosis
3.Reducing the growth of cancer cells in breast, cervical, and prostate cancers.

4.Milk thistle is also used in many products claiming to reduce the effects of a hangover.

5.Milk thistle can also be found as an ingredient in some energy drinks like the AriZona Beverage Company Green Tea energy drink and Rockstar Energy Drink.


How It Is Used:

Milk thistle is a flowering herb. Silymarin, which can be extracted from the seeds (fruit), is believed to be the biologically active part of the herb. The seeds are used to prepare capsules containing powdered herb or seed; extracts; and infusions (strong teas).

What the Science Says:
There have been some studies of milk thistle on liver disease in humans, but these have been small. Some promising data have been reported, but study results at this time are mixed.
Although some studies conducted outside the United States support claims of oral milk thistle to improve liver function, there have been flaws in study design and reporting. To date, there is no conclusive evidence to prove its claimed uses.
NCCAM is supporting a phase II research study to better understand the use of milk thistle for chronic hepatitis C. With the National Institute of Diabetes and Digestive and Kidney Diseases, NCCAM is planning further studies of milk thistle for chronic hepatitis C and nonalcoholic steatohepatitis (liver disease that occurs in people who drink little or no alcohol).
The National Cancer Institute and the National Institute of Nursing Research are also studying milk thistle, for cancer prevention and to treat complications in HIV patients.

Other Uses:
Green manure; Oil; Oil..……A good green manure plant, producing a lot of bulk for incorporation into the soil.

Known Hazards  : When grown on nitrogen rich soils, especially those that have been fed with chemical fertilizers, this plant can concentrate nitrates in the leaves. Nitrates are implicated in stomach cancers. Diabetics should monitor blood glucose when using. Avoid if decompensated liver cirrhosis. Possible headaches, nausea, irritability and minor gastrointestinal upset

Disclaimer:
The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider
Resources:
http://en.wikipedia.org/wiki/Milk_Thistle
http://nccam.nih.gov/health/milkthistle/
http://botanical.com/botanical/mgmh/t/thistl11.html#mil

http://www.herbnet.com/Herb%20Uses_LMN.htm

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