Tag Archives: Cirrhosis

Cholangitis

Definition:
Cholangitis is an infection of the common bile duct, the tube that carries bile from the liver to the gallbladder and intestines. Bile is a liquid made by the liver that helps digest food.

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Cholangitis can be life-threatening, and is regarded as a medical emergency. Characteristic symptoms include yellow discoloration of the skin or whites of the eyes, fever, abdominal pain, and in severe cases, low blood pressure and confusion. Initial treatment is with intravenous fluids and antibiotics, but there is often an underlying problem (such as gallstones or narrowing in the bile duct) for which further tests and treatments may be necessary, usually in the form of endoscopy to relieve obstruction of the bile duct.
Symptoms:
The following symptoms may occur:

*Pain on the upper right side or upper middle part of the abdomen. It may also be felt in the back or below the right shoulder blade. The pain may come and go and feel sharp, cramp-like, or dull.

*Fever and chills

*Dark urine and clay-colored stools

*Nausea and vomiting

*Yellowing of the skin (jaundice), which may come and go
Physical examination findings typically include jaundice and right upper quadrant tenderness.Charcot’s triad is a set of three common findings in cholangitis: abdominal pain, jaundice, and fever. This was assumed in the past to be present in 50–70% of cases, although more recently the frequency has been reported as 15–20%.Reynolds’ pentad includes the findings of Charcot’s triad with the presence of septic shock and mental confusion. This combination of symptoms indicates worsening of the condition and the development of sepsis, and is seen less commonly still.

In the elderly, the presentation may be atypical; they may directly collapse due to septicemia without first showing typical features. Those with an indwelling stent in the bile duct (see below) may not develop jaundice.

Causes:
Cholangitis is most often caused by a bacterial infection. This can occur when the duct is blocked by something, such as a gallstone or tumor. The infection causing this condition may also spread to the liver.

Bile duct obstruction, which is usually present in acute cholangitis, is generally due to gallstones. 10–30% of cases, however, are due to other causes such as benign stricturing (narrowing of the bile duct without an underlying tumor), postoperative damage or an altered structure of the bile ducts such as narrowing at the site of an anastomosis (surgical connection), various tumors (cancer of the bile duct, gallbladder cancer, cancer of the ampulla of Vater, pancreatic cancer, cancer of the duodenum), anaerobic organisms such as Clostridium and Bacteroides (especially in the elderly and those who have undergone previous surgery of the biliary system). Parasites which may infect the liver and bile ducts may cause cholangitis; these include the roundworm Ascaris lumbricoides and the liver flukes Clonorchis sinensis, Opisthorchis viverrini and Opisthorchis felineus. In people with AIDS, a large number of opportunistic organisms has been known to cause AIDS cholangiopathy, but the risk has rapidly diminished since the introduction of effective AIDS treatment. Cholangitis may also complicate medical procedures involving the bile duct, especially ERCP. To prevent this, it is recommended that those undergoing ERCP for any indication receive prophylactic (preventative) antibiotics.

The presence of a permanent biliary stent (e.g. in pancreatic cancer) slightly increases the risk of cholangitis, but stents of this type are often needed to keep the bile duct patent under outside pressure

Diagnosis:
Routine blood tests show features of acute inflammation (raised white blood cell count and elevated C-reactive protein level), and usually abnormal liver function tests (LFTs). In most cases the LFTs will be consistent with obstruction: raised bilirubin, alkaline phosphatase and ?-glutamyl transpeptidase. In the early stages, however, pressure on the liver cells may be the main feature and the tests will resemble those in hepatitis, with elevations in alanine transaminase and aspartate transaminase.

Blood cultures are often performed in people with fever and evidence of acute infection. These yield the bacteria causing the infection in 36% of cases, usually after 24–48 hours of incubation. Bile, too, may be sent for culture during ERCP (see below). The most common bacteria linked to ascending cholangitis are gram-negative bacilli: Escherichia coli (25–50%), Klebsiella (15–20%) and Enterobacter (5–10%). Of the gram-positive cocci, Enterococcus causes 10–20%.

You may have the following tests to look for blockages:

*Abdominal ultrasound

*Endoscopic retrograde cholangiopancreatography (ERCP)

*Magnetic resonance cholangiopancreatography (MRCP)

*Percutaneous transhepatic cholangiogram (PTCA)

*You may also have the following blood tests:

#Bilirubin level
#Liver enzyme levels
#Liver function tests
#White blood count (WBC)
Treatment:
Quick diagnosis and treatment are very important.Antibiotics to cure infection is the first treatment done in most cases. ERCP or other surgical procedure is done when the patient is stable.Patients who are very ill or are quickly getting worse may need surgery right away.

Cholangitis requires admission to hospital. Intravenous fluids are administered, especially if the blood pressure is low, and antibiotics are commenced. Empirical treatment with broad-spectrum antibiotics is usually necessary until it is known for certain which pathogen is causing the infection, and to which antibiotics it is sensitive. Combinations of penicillins and aminoglycosides are widely used, although ciprofloxacin has been shown to be effective in most cases, and may be preferred to aminoglycosides because of fewer side effects. Metronidazole is often added to specifically treat the anaerobic pathogens, especially in those who are very ill or at risk of anaerobic infections. Antibiotics are continued for 7–10 days. Drugs that increase the blood pressure (vasopressors) may also be required to counter the low blood pressure.
Prognosis:
Acute cholangitis carries a significant risk of death, the leading cause being irreversible shock with multiple organ failure (a possible complication of severe infections). Improvements in diagnosis and treatment have led to a reduction in mortality: before 1980, the mortality rate was greater than 50%, but after 1980 it was 10–30%. Patients with signs of multiple organ failure are likely to die unless they undergo early biliary drainage and treatment with systemic antibiotics. Other causes of death following severe cholangitis include heart failure and pneumonia.

Risk Factors:
Risk factors include a previous history of gallstones, sclerosing cholangitis, HIV, narrowing of the common bile duct, and, rarely, travel to countries where you might catch a worm or parasite infection.

Risk factors indicating an increased risk of death include older age, female gender, a history of liver cirrhosis, biliary narrowing due to cancer, acute renal failure and the presence of liver abscesses. Complications following severe cholangitis include renal failure, respiratory failure (inability of the respiratory system to oxygenate blood and/or eliminate carbon dioxide), cardiac arrhythmia, wound infection, pneumonia, gastrointestinal bleeding and myocardial ischemia (lack of blood flow to the heart, leading to heart attacks).

Prevention:
Treatment of gallstones, tumors, and infestations of parasites may reduce the risk for some people. A metal or plastic stent that is placed in the bile system may be needed to prevent the infection from returning.
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.nlm.nih.gov/medlineplus/ency/article/000290.htm
http://en.wikipedia.org/wiki/Ascending_cholangitis

Aristolochia contorta

 

Botanical Name : Aristolochia contorta
Family: Aristolochiaceae
Subfamily: Aristolochioideae
Genus: Aristolochia
Species : Aristolochia contorta
Order: Piperales

Synonyms : A. nipponica.

Common Name: Ma Dou Ling

Habitat : E. Asia – China, Japan, Korea, Manchuria. .-Aug. Grows in edges of mountain woods.

Description:
Aristolochia contorta is a  perennial  herb, growing to 1.5 m (5ft). It is in flower from May to July, and the seeds ripen from Sep to October. The flowers are hermaphrodite (have both male and female organs) and are pollinated by Flies.

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The shrub  has  stout elongated rhizomes. Stem slender, glabrous. Leaves alternate, cordate or broadly ovate-cordate, 4-10 cm long, 3.5-8 cm wide, acute or obtuse at tip, cordate at base, entire, petioles 1-7 cm long.(CLICK & SEE) Peduncles axillary, 1-4 cm long, with prominent bracts at base. Flowers few in axils, fascicled, the pedicels 1-4 cm long; the calyx tubular, inflated and globose at base, loosely pilose inside; the limb dilated, obliquely truncate, narrowly deltoid, long-acuminate to a filiform point; stamens 6, ovary inferior. Fruit a capsule,globose, 3 cm in diameter, 6 valved. Jul.-Aug……...CLICK & SEE

The plant prefers light (sandy), medium (loamy) and heavy (clay) soils and requires well-drained soil.The plant prefers acid, neutral and basic (alkaline) soils..It can grow in semi-shade (light woodland) or no shade.It requires moist soil.

Cultivation:
We have very little information on this species and do not know if it will be hardy in Britain, though judging by its native range it should succeed outdoors in many parts of this country. The following notes are based on the general needs of the genus. Prefers a well-drained loamy soil, rich in organic matter, in sun or semi-shade. Succeeds in ordinary garden soil. Most species in this genus have malodorous flowers that are pollinated by flies.

Propagation
Seed – best sown in a greenhouse as soon as it is ripe in the autumn. Pre-soak stored seed for 48 hours in hand-hot water and surface sow in a greenhouse. Germination usually takes place within 1 – 3 months at 20°c. Stored seed germinates better if it is given 3 months cold stratification at 5°c. When large enough to handle, prick the seedlings out into individual pots and grow them on in the greenhouse for their first winter. Plant out in late spring or early summer after the last expected frosts. Division in autumn. Root cuttings in winter.

Edible Uses :
Edible Parts: Leaves.

Medicinal Uses;
Antiasthmatic;  Antiseptic;  Antitussive;  Cancer;  Expectorant;  Sedative.

The fruit and its capsule are antiasthmatic, antiseptic, antitussive and expectorant. A decoction of the fruit is used in the treatment of cancer, coughs, inflammation of the respiratory organs, haemorrhoids and hypertension. It is also used to resolve phlegm and lower blood pressure. It has an antibacterial action, effective against Staphylococcus aureus, Pneumococci, bacillus dysentericae etc. The root contains aristolochic acid. This has anti-cancer properties and can be used in conjunction with chemotherapy and radiotherapy. Aristolochic acid can also be used in the treatment of acute and serious infections such as TB, hepatitis, liver cirrhosis and infantile pneumonia. It also increases the cellular immunity and phagocytosis function of the phagocytic cells. Aristolochic acid is said to be too toxic for clinical use. The root is used as a purgative in the treatment of rabies and also has sedative properties.

A decoction of the fruit is used in the treatment of cancer, coughs, inflammation of the respiratory organs, hemorrhoids and hypertension. It is also used to resolve phlegm and lower blood pressure. It has an antibacterial action, effective against Staphylococcus aureus, Pneumococci, bacillus dysentericae etc. The root contains aristolochic acid. This has anti-cancer properties and can be used in conjunction with chemotherapy and radiotherapy. Aristolochic acid can also be used in the treatment of acute and serious infections such as TB, hepatitis, liver cirrhosis and infantile pneumonia. It also increases the cellular immunity and phagocytosis function of the phagocytic cells. Aristolochic acid is said to be too toxic for clinical use. The root is used as a purgative in the treatment of rabies and also has sedative properties.

Known Hazards:  No specific details for this species is found but most members of this genus have poisonous roots and stems. The plant contains aristolochic acid, this has received rather mixed reports on its toxicity. According to one report aristolochic acid stimulates white blood cell activity and speeds the healing of wounds, but is also carcinogenic and damaging to the kidneys. Another report says that it is an active antitumour agent but is too toxic for clinical use. Another report says that aristolochic acid has anti-cancer properties and can be used in conjunction with chemotherapy and radiotherapy and that it also increases the cellular immunity and phagocytosis function of the phagocytic cells.

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://www.pfaf.org/user/Plant.aspx?LatinName=Aristolochia+contorta
http://species.wikimedia.org/wiki/Aristolochia_contorta
http://www.herbnet.com/Herb%20Uses_LMN.htm

http://www.wpro.who.int/internet/files/pub/97/33.pdf

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Wilson’s Disease

Definition :
Wilson’s disease is an inherited disorder that causes too much copper to accumulate in your liver, brain and other vital organs. Another term for Wilson’s disease is hepatolenticular degeneration.

Copper plays a key role in the development of healthy nerves, bones, collagen and the skin pigment melanin. Normally, copper is absorbed from your food, and any excess is excreted through bile — a substance produced in your liver.

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Normal absorption and distribution of copper. Cu = copper, CP = ceruloplasmin, green = ATP7B carrying copper.

But in people with Wilson’s disease, copper isn’t eliminated properly and instead accumulates, possibly to a life-threatening level. Left untreated, Wilson’s disease is fatal. When diagnosed early, Wilson’s disease is treatable, and many people with the disorder live normal lives.

The excess copper can build up in the liver and/or brain causing liver damage and/or neurological problems. It can also collect in other parts of the body including the eyes and the kidneys.
Copper begins to accumulate immediately after birth but the symptoms usually appear in the 2nd to 3rd decade. The first signs are hepatic (liver) in about 40% of cases, neurological (brain) in about 35% of cases and psychiatric, renal (kidney), haematological (blood), or endocrine (glands) in the remainder.

The condition is due to mutations in the Wilson disease protein (ATP7B) gene. A single abnormal copy of the gene is present in 1 in 100 people, who do not develop any symptoms (they are carriers). If a child inherits the gene from both parents, they may develop Wilson’s disease. Symptoms usually appear between the ages of 6 and 20 years, but cases in much older people have been described. Wilson’s disease occurs in 1 to 4 per 100,000 people.  Wilson’s disease is named after Samuel Alexander Kinnier Wilson (1878–1937), the British neurologist who first described the condition in 1912


Symptoms:
The most pathognomonic sign of Wilson’s disease results from a buildup of copper in the eyes. These rings are
called Kayser – Fleischer rings. Rings are brownish, visible aroound the corneo – scleral junction (limbus).
95% of Wilson’ s disease patients presenting with neurological signs will have Kayser – Fleischer rings and 65% of Wilson’s disease patients presenting with hepatic signs will present a ring.

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Wilson’s disease causes a wide variety of signs and symptoms that are often mistaken for other diseases and conditions. Signs and symptoms vary depending on what parts of your body are affected by Wilson’s disease.
Signs and symptoms of Wilson’s disease include:

*Clumsiness
*Depression
*Difficulty speaking
*Difficulty swallowing
*Difficulty walking
*Drooling
*Easy bruising
*Fatigue
*Involuntary shaking
*Joint pain
*Loss of appetite
*Nausea
*Skin rash
*Swelling of arms and legs
*Yellowing of the skin and eyes (jaundice)

The main sites of copper accumulation are the liver and the brain, and consequently liver disease and neuropsychiatric symptoms are the main features that lead to diagnosis.  People with liver problems tend to come to medical attention earlier, generally as children or teenagers, than those with neurological and psychiatric symptoms, who tend to be in their twenties or older. Some are identified only because relatives have been diagnosed with Wilson’s disease; many of these, when tested, turn out to have been experiencing symptoms of the condition but haven’t received a diagnosis.:

Causes:
Wilson’s disease occurs when a genetic mutation leads to an accumulation of copper in  one’s body.

How the genetic mutation occurs
The genetic mutation that causes Wilson’s disease is most commonly passed from one generation to the next. Wilson’s disease is inherited as an autosomal recessive trait, which means that to develop the disease you must inherit two copies of the defective gene, one from each parent. If you receive only one abnormal gene, you won’t become ill yourself, but you’re considered a carrier and can pass the gene to your children.

How the genetic mutation causes Wilson’s disease
The mutation that causes Wilson’s disease occurs in a gene called ATP7B. When a mutation occurs on this gene, it leads to problems with a protein that’s responsible for moving excess copper out of your liver.

Your body collects copper from the food you eat during the digestive process. The copper is transported to your liver where liver cells use it for everyday tasks. Most people eat more copper than they need. In these cases, the liver takes what it needs and excretes the rest in bile, a digestive juice made by the liver.

But in people with Wilson’s disease, the extra copper doesn’t leave your body. Instead, copper builds up in the liver, where it can cause serious and sometimes irreversible damage. In time, excess copper leaves the liver and begins accumulating in and harming other organs, especially the brain, eyes and kidneys.

 

Complications:
Wilson’s disease can cause serious complications such as:

*Scarring of the liver (cirrhosis). As liver cells try to make repairs to damage done by excess copper, scar tissue forms in the liver. The scar tissue makes it more difficult for the liver to function.

*Liver failure. Liver failure can occur suddenly (acute liver failure), or it can develop slowly over many years. If liver function progresses, a liver transplant may be a treatment option.

*Liver cancer. Damage to the liver caused by Wilson’s disease may increase the risk of liver cancer.

*Persistent neurological problems. Neurological problems usually improve with treatment for Wilson’s disease. However, some people may experience persistent neurological difficulty, despite treatment.
*Kidney problems. Wilson’s disease can damage the kidneys, leading to kidney problems, such as kidney stones and an abnormal number of amino acids excreted in the urine (aminoaciduria).

Diagnosis:
Wilson’s disease may be suspected on the basis of any of the symptoms mentioned above, or when a close relative has been found to have Wilson’s. Most have slightly abnormal liver function tests such as a raised aspartate transaminase, alanine transaminase and bilirubin level. If the liver damage is significant, albumin may be decreased due to an inability of damaged liver cells to produce this protein; likewise, the prothrombin time (a test of coagulation) may be prolonged as the liver is unable to produce proteins known as clotting factors. Alkaline phosphatase levels are relatively low in those with Wilson’s-related acute liver failure. If there are neurological symptoms, magnetic resonance imaging (MRI) of the brain is usually performed; this shows hyperintensities in the part of the brain called the basal ganglia in the T2 setting.  MRI may also demonstrate the characteristic “face of the giant panda” pattern.

There is no totally reliable test for Wilson’s disease, but levels of ceruloplasmin and copper in the blood, as well of the amount of copper excreted in urine during a 24-hour period, are together used to form an impression of the amount of copper in the body. The gold standard or most ideal test is a liver biopsy

Ceruloplasmin
Levels of ceruloplasmin are abnormally low (<0.2 g/L) in 80–95% of cases. It can, however, be present at normal levels in people with ongoing inflammation as it is an acute phase protein. Low ceruloplasmin is also found in Menkes disease and aceruloplasminemia, which are related to, but much rarer than Wilson’s disease.

The combination of neurological symptoms, Kayser–Fleisher rings and a low ceruloplasmin level is considered sufficient for the diagnosis of Wilson’s disease. In many cases, however, further tests are needed.
Serum and urine copper
Serum copper is paradoxically low but urine copper is elevated in Wilson’s disease. Urine is collected for 24 hours in a bottle with a copper-free liner. Levels above 100 ?g/24h (1.6 ?mol/24h) confirm Wilson’s disease, and levels above 40 ?g/24h (0.6 ?mol/24h) are strongly indicative.[1] High urine copper levels are not unique to Wilson’s disease; they are sometimes observed in autoimmune hepatitis and in cholestasis (any disease obstructing the flow of bile from the liver to the small bowel).

In children, the penicillamine test may be used. A 500 mg oral dose of penicillamine is administered, and urine collected for 24 hours. If this contains more than 1600 ?g (25 ?mol), it is a reliable indicator of Wilson’s disease. This test has not been validated in adults.

Liver biopsy
Once other investigations have indicated Wilson’s disease, the ideal test is the removal of a small amount of liver tissue through a liver biopsy. This is assessed microscopically for the degree of steatosis and cirrhosis, and histochemistry and quantification of copper are used to measure the severity of the copper accumulation. A level of 250 ?g of copper per gram of dried liver tissue confirms Wilson’s disease. Occasionally, lower levels of copper are found; in that case, the combination of the biopsy findings with all other tests could still lead to a formal diagnosis of Wilson’s.

In the earlier stages of the disease, the biopsy typically shows steatosis (deposition of fatty material), increased glycogen in the nucleus, and areas of necrosis (cell death). In more advanced disease, the changes observed are quite similar to those seen in autoimmune hepatitis, such as infiltration by inflammatory cells, piecemeal necrosis and fibrosis (scar tissue). In advanced disease, finally, cirrhosis is the main finding. In acute liver failure, degeneration of the liver cells and collapse of the liver tissue architecture is seen, typically on a background of cirrhotic changes. Histochemical methods for detecting copper are inconsistent and unreliable, and taken alone are regarded as insufficient to establish a diagnosis.

Genetic testing
Mutation analysis of the ATP7B gene, as well as other genes linked to copper accumulation in the liver, may be performed. Once a mutation is confirmed, it is possible to screen family members for the disease as part of clinical genetics family counselling

Treatment:
DietaryIn general, a diet low in copper-containing foods is recommended, with the avoidance of mushrooms, nuts, chocolate, dried fruit, liver, and shellfish.

Medication
Various treatments are available for Wilson’s disease. Some increase the removal of copper from the body, while others prevent the absorption of copper from the diet.

Generally, penicillamine is the first treatment used. This binds copper (chelation) and leads to excretion of copper in the urine. Hence, monitoring of the amount of copper in the urine can be done to ensure a sufficiently high dose is taken. Penicillamine is not without problems: about 20% experience a side effect or complication of penicillamine treatment, such as drug-induced lupus (causing joint pains and a skin rash) or myasthenia (a nerve condition leading to muscle weakness). In those who presented with neurological symptoms, almost half experience a paradoxical worsening in their symptoms. While this phenomenon is also observed in other treatments for Wilson’s, it is usually taken as an indication for discontinuing penicillamine and commencing second-line treatment.  Intolerant to penicillamine may instead be commenced on trientine hydrochloride, which also has chelating properties. Some recommend trientine as first-line treatment, but experience with penicillamine is more extensive.  A further agent with known activity in Wilson’s disease is tetrathiomolybdate. This is still regarded as experimental,  although some studies have shown a beneficial effect.

Once all results have returned to normal, zinc (usually in the form of a zinc acetate prescription called Galzin) may be used instead of chelators to maintain stable copper levels in the body. Zinc stimulates metallothionein, a protein in gut cells that binds copper and prevents their absorption and transport to the liver. Zinc therapy is continued unless symptoms recur, or if the urinary excretion of copper increases.

In rare cases where none of the oral treatments are effective, especially in severe neurological disease, dimercaprol (British anti-Lewisite) is still occasionally necessary. This treatment is injected intramuscularly (into a muscle) every few weeks, and has a number of unpleasant side effects such as pain.

People who are asymptomatic (for instance those diagnosed through family screening or only as a result of abnormal test results) are generally treated, as the copper accumulation may cause long-term damage in the future. It is unclear whether these people are best treated with penicillamine or zinc acetate.

Physical therapy
Physiotherapy is beneficial for those patients with the neurologic form of the disease. The copper chelating treatment may take up to six months to start working, and physical therapy can assist in coping with ataxia, dystonia, and tremors, as well as preventing the development of contractures that can result from dystonia.

Transplantation
Liver transplantation is an effective cure for Wilson’s disease, but is used only in particular scenarios because of the numerous risks and complications associated with the procedure. It is used mainly in people with fulminant liver failure who fail to respond to medical treatment, or in those with advanced chronic liver disease. Liver transplantation is avoided in severe neuropsychiatric illness, in which its benefit has not been demonstrated
Lifestyle and home remedies:

Doctors sometimes recommend limiting the amount of copper you consume in your diet during the first year of your treatment for Wilson’s disease. As your signs and symptoms recede and the copper levels in your body drop, you may be able to include copper-containing foods in your diet.

Copper-containing foods
Foods that contain high levels of copper include:

*Copper-containing vitamin and mineral supplements
*Liver
*Shellfish
*Mushrooms
*Nuts
*Chocolate
*Dried fruit
*Dried peas, beans and lentils
*Avocados
*Bran products

Copper in tap water
Have your tap water’s copper levels tested if you have copper pipes in your home or if your water comes from a well. Most municipal water systems don’t contain high levels of copper.

If you have copper pipes, run the tap for several seconds before collecting water for drinking or cooking. Water that sits in the copper pipes can pick up copper particles. Running the water flushes that contaminated water out of the pipes.

Copper pots and pans
Don’t use copper pots, pans or storage containers for your food or drinks.

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://en.wikipedia.org/wiki/Wilson’s_disease
http://www.eurowilson.org/en/living/guide/what/index.phtml
http://www.mayoclinic.com/health/wilsons-disease/DS00411

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Liver

It’s important to love your liver. It performs hundreds of tasks that are vital to life, from storing energy and fighting infection, to getting rid of waste products and toxins from the body. We look at its role, the causes of damage and some of the more common liver-related conditions.

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You may click below to learn the importance of LIVER

1.Why the liver is one of the most important organs in the body.

2.How to keep liver healthy .

 

3.Causes of liver disease

4.Different Stages of liver damage

5.Liver damage symptoms and tests

6.Treatments for liver disease

7.Liver transplant

COMMON CONDITIONS AFFECTING THE LIVER
—————————————————————————

•Cirrhosis – the causes, symptoms and treatment
•Gallstones this common condition can cause abdominal pain and nausea
•Haemochromatosis when the body absorbs an excessive amount of iron
•Hepatitis A – an infection of the liver caused by a virus
•Hepatitis B – usually transmitted through contact with infected blood or body fluids
•Hepatitis C – there are a number of ways to reduce the risk of infection
Primary biliary cirrhosis – when the immune system attacks the bile ducts
Obstetric cholestasis – a condition affecting the liver that can occur during pregnancy
•Jaundice – this condition causes a yellow discolouration of the skin

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

Source:BBC Health.

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Hepatitis C

Definition;-
Hepatitis C is an infectious disease affecting the liver, caused by the hepatitis C virus (HCV). The infection is often asymptomatic, but once established, chronic infection can progress to scarring of the liver (fibrosis), and advanced scarring (cirrhosis) which is generally apparent after many years. In some cases, those with cirrhosis will go on to develop liver failure or other complications of cirrhosis, including liver cancer   or life threatening esophageal varices and gastric varices.

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Because it can take years, even decades, for symptoms to appear, many people (possibly 100,000 or more) remain unaware they have a problem. By the time they become ill and seek help, considerable damage has been done to the liver. This might have been prevented if the person had been diagnosed earlier.

The hepatitis C virus is spread by blood-to-blood contact. Most people have few, if any symptoms after the initial infection, yet the virus persists in the liver in about 85% of those infected. Persistent infection can be treated with medication, peginterferon and ribavirin being the standard-of-care therapy. Overall, 51% are cured. Those who develop cirrhosis or liver cancer may require a liver transplant, and the virus universally recurs after transplantation.

An estimated 270-300 million people worldwide are infected with hepatitis C. Hepatitis C is not known to cause disease in other animals. No vaccine against hepatitis C is currently available. The existence of hepatitis C (originally “non-A non-B hepatitis“) was postulated in the 1970s and proven in 1989. It is one of five known hepatitis viruses: A, B, C, D, and E.

According to the United States National Center for Complementary and Alternative Medicine (NCCAM), no CAM treatment has been scientifically proven to successfully
treat hepatitis C

Elsewhere in the world, hepatitis C is even more common – the World Health Organization estimates that three per cent of the world’s population (about 170 million people) have chronic hepatitis C and up to four million people are newly infected each year.

Hepatitis C is one of several hepatitis viruses and is generally considered to be among the most serious of these viruses. Hepatitis C is passed through contact with contaminated blood — most commonly through needles shared during illegal drug use.

Although there is no vaccine to protect against infection, there is effective treatment available.

Symptoms:-
In most cases, the initial infection doesn’t cause any symptoms. When it does, they tend to be vague and non-specific.

Possible symptoms of hepatitis C infection include:
*Fatigue
*Fever
*Nausea or poor appetite
*Muscle and joint pains
*Weight loss
*Loss of appetite
*Joint pains
*Flu-like symptoms (fever, headaches, sweats)
*Anxiety
*Difficulty concentrating
*Alcohol intolerance and pain in the liver area

The most common symptom experienced is fatigue, which may be mild but is sometimes extreme. Many people initially diagnosed with chronic fatigue syndrome are later found to have hepatitis C.

Unlike hepatitis A and B, hepatitis C doesn’t usually cause people to develop jaundice.

About 20-30 per cent of people clear the virus from their bodies – but in about 75 per cent of cases, the infection lasts for more than six months (chronic hepatitis C). In these cases, the immune system has been unable to clear the virus and will remain in the body long term unless medical treatment is given. Most of these people have a mild form of the disease with intermittent symptoms of fatigue or no symptoms at all.

About one in five people with chronic hepatitis C develops cirrhosis of the liver within 20 years (some experts believe that, with time, everyone with chronic hepatitis C would develop cirrhosis but this could take many decades).

 

Causes:
Hepatitis C virus is usually transmitted through blood-to-blood contact. One common route is through sharing needles when injecting recreational drugs – nearly 40 per cent of intravenous drug users have the infection and around 35 per cent of people with the virus will have contracted it this way.

Similarly, having a tattoo or body piercing with equipment that has not been properly sterilised can lead to infection.

Before 1991, blood transfusions were a common route of infection. However, since then all blood used in the UK has been screened for the virus and is only used if not present.

Hepatitis C can be sexually transmitted, but this is thought to be uncommon. It can be passed on through sharing toothbrushes and razors. It is not passed on by everyday contact such as kissing, hugging, and holding hands – you can’t catch hepatitis C from toilet seats either.

A very small percentage of pregnant women infected with hepatitis C pass the virus onto their babies. There is a small percentage of hepatitis C positive cases where no identifying risk factor can be determined.

If someone needs a blood transfusion or medical treatment while staying in a country where blood screening for hepatitis C is not routine, or where medical equipment is reused but not adequately sterilised, the virus may be transmitted.

Most people diagnosed with hepatitis C can identify at least one possible factor which may have put them at risk but for some, the likely origin of the infection isn’t clear. Because it can remain hidden and symptomless for so many years, it may be very difficult to think back through the decades to how it might have begun.

Risk Factors:
The following are the most common risk factors of Hepatitis C:

 

*Are a health care worker who has been exposed to infected blood
*Have ever injected illicit drugs
*Have HIV
*Received a piercing or tattoo in an unclean environment using unsterile equipment
*Received a blood transfusion or organ transplant before 1992
*Received clotting factor concentrates before 1987
*Received hemodialysis treatments for a long period of time
*Were born to a woman with a hepatitis C infection

Complications:-
Hepatitis C infection that continues over many years can cause significant complications,  as follows:

*Scarring of the liver tissue (cirrhosis). After 20 to 30 years of hepatitis C infection, cirrhosis may occur. Scarring in your liver makes it difficult for your liver to function.

*Liver cancer. A small number of people with hepatitis C infection may develop liver cancer

*Liver failure. A liver that is severely damaged by hepatitis C may be unable to function.

 

Diagnosis:-
The diagnosis of hepatitis C is rarely made during the acute phase of the disease, because the majority of people infected experience no symptoms during this phase. Those who do experience acute phase symptoms are rarely ill enough to seek medical attention. The diagnosis of chronic phase hepatitis C is also challenging due to the absence or lack of specificity of symptoms until advanced liver disease develops, which may not occur until decades into the disease.

Chronic hepatitis C may be suspected on the basis of the medical history (particularly if there is any history of IV drug abuse or inhaled substance usage such as cocaine), a history of piercings or tattoos, unexplained symptoms, or abnormal liver enzymes or liver function tests found during routine blood testing. Occasionally, hepatitis C is diagnosed as a result of targeted screening, such as blood donation (blood donors are screened for numerous blood-borne diseases including hepatitis C) or contact tracing.

Hepatitis C testing begins with serological blood tests used to detect antibodies to HCV. Anti-HCV antibodies can be detected in 80% of patients within 15 weeks after exposure, in >90% within 5 months after exposure, and in >97% by 6 months after exposure. Overall, HCV antibody tests have a strong positive predictive value for exposure to the hepatitis C virus, but may miss patients who have not yet developed antibodies (seroconversion), or have an insufficient level of antibodies to detect. Immunocompromised individuals infected with HCV may never develop antibodies to the virus and therefore, never test positive using HCV antibody screening. Because of this possibility, RNA testing (see nucleic acid testing methods below) should be considered when antibody testing is negative but suspicion of hepatitis C is high (e.g. because of elevated transaminases in someone with risk factors for hepatitis C). However, liver function tests alone are not useful in predicting the severity of infection and normal results do not exclude the possibility of liver disease.

Anti-HCV antibodies indicate exposure to the virus, but cannot determine if ongoing infection is present. All persons with positive anti-HCV antibody tests must undergo additional testing for the presence of the hepatitis C virus itself to determine whether current infection is present. The presence of the virus is tested for using molecular nucleic acid testing methods, such as polymerase chain reaction (PCR), transcription mediated amplification (TMA), or branched DNA (b-DNA). All HCV nucleic acid molecular tests have the capacity to detect not only whether the virus is present, but also to measure the amount of virus present in the blood (the HCV viral load). The HCV viral load is an important factor in determining the probability of response to interferon-based therapy, but does not indicate disease severity nor the likelihood of disease progression.

In people with confirmed HCV infection, genotype testing is generally recommended. HCV genotype testing is used to determine the required length and potential response to interferon-based therapy.

 

Treatment:-
People with chronic hepatitis C infection should be seen by a hospital liver specialist who may recommend antiviral drug treatments either as single drug therapy or as combination therapy.

Whether treatment is needed, and if so which type, depends on a number of factors. These include blood tests to identify which strain of hepatitis C infection is present and how well the liver is functioning, and a liver biopsy to establish whether cirrhosis is occurring.

Hepatitis C can be treated with pegylated interferon alpha and ribavirin. These drugs offer the best chance to clear the virus from the body, and are often used together as dual or combination therapy which has been shown to be effective in 55 per cent of cases. Some strains or genotypes of the hepatitis C virus are more likely to respond than others. Even if the virus isn’t completely cleared, the treatments can reduce inflammation and scarring of the liver. They may, however, cause side effects that some people find difficult to tolerate.

Many people also find that complementary and lifestyle approaches help. There is little evidence these can reduce levels of the virus, but they may help to deal with symptoms and improve quality of life.

Alternative medications:-
Several alternative therapies are claimed by their proponents to be helpful for hepatitis C, or are being researched to see if they can be effective treatments. Among them are milk thistle, ginseng, Thymus extract, colloidal silver, licorice root (or its extract glycyrrhizin), lactoferrin, TJ-108 (a mixture of herbs used in Japanese Kampo medicine), schisandra, and oxymatrine (an extract from the sophora root).

In March 2011, the United States National Center for Complementary and Alternative Medicine (NCCAM) wrote:

A review of the scientific evidence on CAM and hepatitis C found the following:
*No CAM treatment has been scientifically proven to successfully treat hepatitis C.

*A 2003 analysis of results from 13 clinical trials testing the effects of various medicinal herbs on hepatitis C concluded that there is not enough evidence to support using herbs to treat the disease.

*Two other reviews that covered a variety of CAM modalities for hepatitis C concluded that conventional therapies are the only scientifically proven treatments for the disease.

*In a 2002 NIH consensus statement on the management of hepatitis C, a panel of medical and scientific experts concluded that “alternative and nontraditional medicines” should be studied. Participants in a 2001 NIH research workshop on the benefits and risks of CAM therapies for chronic liver disease recommended research support for related laboratory and clinical studies.

Additional recommendations:
Current guidelines strongly recommend that hepatitis C patients be vaccinated for hepatitis A and B if they have not yet been exposed to these viruses, as infection with a second virus could worsen their liver disease.

Alcoholic beverage consumption accelerates HCV associated fibrosis and cirrhosis, and makes liver cancer more likely; insulin resistance and metabolic syndrome may similarly worsen the hepatic prognosis. There is also evidence that smoking increases the fibrosis (scarring) rate.

Research:
The drug viramidine, which is a prodrug of ribavirin that has better targeting for the liver, and therefore may be more effective against hepatitis C for a given tolerated dose, is in phase III experimental trials against hepatitis C. It will be used in conjunction with interferons, in the same manner as ribavirin. However, this drug is not expected to be active against ribavirin-resistant strains, and the use of the drug against infections which have already failed ribavirin/interferon treatment, is unproven.

There are new drugs under development, like the protease inhibitors (including telaprevir/VX 950), entry inhibitors (such as SP 30 and ITX 5061) and polymerase inhibitors (such as RG7128, PSI-7977 and NM 283), but development of some of these is still in the early phase. VX 950, also known as Telaprevir is currently in Phase III trials. One protease inhibitor, BILN 2061, had to be discontinued due to safety problems early in the clinical testing. Some more modern new drugs that provide some support in treating HCV are albuferon and Zadaxin. Antisense phosphorothioate oligos have been targeted to hepatitis C. Antisense Morpholino oligos have shown promise in preclinical studies however, they were found to cause a limited viral load reduction.

Some studies have shown that HCV viral replication is dependent upon the host factor miR-122. As a result, pharmaceutical companies are developing potential HCV drugs that target miR-122. HCV therapies that target this host factor necessary for viral replication, rather than the virus itself, are promising, as they show little to no potential for viral resistance.  One such drug is miravirsen, developed by Santaris Pharma a/s, a locked nucleic acid based miR-122 antagonist in Phase II clinical trials as of late 2010.

Immunoglobulins against the hepatitis C virus exist, and newer types are under development. Thus far, their roles have been unclear, as they have not been shown to help in clearing chronic infection or in the prevention of infection with acute exposures (e.g. needle sticks). They do have a limited role in transplant patients.

In addition to the standard treatment with interferon and ribavirin, some studies have shown higher success rates when the antiviral drug amantadine (Symmetrel) is added to the regimen. Sometimes called “triple therapy”, it involves the addition of 100 mg of amantadine twice a day. Studies indicate this may be especially helpful for “nonresponders” — patients who have not been successful in previous treatments using interferon and ribavirin only. Currently, amantadine is not approved for treatment of hepatitis C, and studies are ongoing to determine when it is most likely to benefit the patient and when it is a risk due to their liver deterioration.
Prognosis:-
Most people with hepatitis C infection have the chronic form.

Patients with genotypes 2 or 3 are more likely to respond to treatment than patients with genotype 1.

The chance of removing the hepatitis C virus from the blood with treatment is over 90% for some people. Even if treatment does not remove the virus, it can reduce the chance of severe liver disease.

Many doctors use the term “sustained virologic response” rather than “cure” when the virus is removed from the blood, because it is not known whether this will last a person’s entire life.

Hepatitis C is one of the most common causes of chronic liver disease in the United States today. People with this condition may have:

•Cirrhosis of the liver
•Liver cancer (also called hepatocellular cancer) — may develop in a small number of people with liver cirrhosis

Hepatitis C usually comes back after a liver transplant, which can lead to cirrhosis of the new liver.
Prevention:-
There are a number of ways to reduce the risk of the infection being transmitted. Some of them are mentioned below:-

*People with hepatitis C infection should not be allowed to register as an organ or blood donor.

*Stop using illicit drugs. If you use illicit drugs, seek help. If you can’t stop, don’t share needles or other drug paraphernalia.

*Be cautious about body piercing and tattooing. If you choose to undergo piercing or tattooing, look for a reputable shop. Ask questions beforehand about how the equipment is cleaned. Make sure the employees use sterile needles. If employees won’t answer your questions, look for another shop.

*Practice safer sex if you choose to have sex. Don’t engage in unprotected sex with multiple partners or with any partner whose health status is uncertain. Sexual transmission between monogamous couples may occur, but the risk is low.

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/hepatitisc1.shtml
http://en.wikipedia.org/wiki/Hepatitis_C
http://www.mayoclinic.com/health/hepatitis-c/DS00097
http://www.nlm.nih.gov/medlineplus/ency/article/000284.htm

http://www.medicalook.com/Viral_infections/Hepatitis_C.html

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