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Herbs & Plants

Sabatia angularis

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Botanical Name :Sabatia angularis
Family: Gentianaceae
Genus: Sabatia
Species: S. angularis
Kingdom: Plantae
Order: Gentianales

Common Names :Rosepink, Rose Pink, American centaury, Bitterbloom, Bitter floom, Square-stemmed Sabbatia)
Habitat :Sabatia angularis is native to the United States.Occurring over much of the eastern United States, rosepink is distributed from New York west to Illinois and eastern Kansas, ranging south to the Florida panhandle and Texas. It is considered rare in Kansas and New York, and is considered to be extirpated in Ontario (NatureServe 2007). Rocky open woods, glades, thickets, fields, prairies, roadsides.

Description:
It is a herbaceous flowering plant.
Stems – To +60cm tall, branching above, herbaceous, erect, glabrous, 4-angled, winged on angles, from thickened roots.

Leaves – Opposite, sessile, clasping, ovate, entire, acute, glabrous, decussate, reduced upward, to +4cm long, +3cm broad, with 3 conspicuous veins and 4 faint veins (best seen from below).

Inflorescence – Typically flat-topped cymes with many flowers, dichotomously branching. Each division of inflorescence subtended by small foliaceous bracts.

Flowers – Corolla tube greenish, 4mm long, glabrous, 5-lobed. Lobes spreading, pink or white, to 1.3cm long, +/-6mm broad, oblanceolate to spatulate, glabrous, greenish-yellow at very base. Stamens 5, alternating with corolla lobes, erect. Filaments to 5mm long, glabrous, yellowish. Anthers curling, 3mm long, brownish. Style 6mm long, glabrous, whitish to pale yellow. Stigma 2-lobed. Lobes curled, yellow. Ovary superior, unilocular. Placentation parietal. Calyx tube 1.5mm long(in flower), green, glabrous, 5-lobed. Lobes linear, 8-9mm long, 1mm broad, glabrous, ascending to erect, acute, entire. Calyx accrescent. Capsule to 8mm long, cylindric, glabrous, green, many seeded.
...CLICK & SEE THE PICTURES
Flowering period – June – September.

Propagation : : Seed – best sown as soon as it is ripe in late summer or early autumn. Sow in a peaty soil in a moist shady border or sow in pots in a shady part of the cold frame and keep the soil moist by standing the pot in 2 – 3cm of water.

Cultivation :  Rich soils in open woods, clearings, fields and prairies.

Medicinal Uses:
This herb, which should be gathered when in full bloom, is an active tonic, of the more stimulating class, with moderate and somewhat diffusive relaxing qualities, allied to the American  gentian, but rather milder.   Its chief power is exerted upon the stomach, gall-ducts, and spleen; and the general circulation and uterus feel it moderately.  A warm infusion gently promotes the menstrual secretion, in cases of debility.   Cold preparations increase appetite and digestion in weak and flaccid conditions of the stomach, and may be used for chronic dyspepsia and general debility.  By maintaining the portal circulation somewhat vigorously,  it proves of eminent service for the intermediate treatment of agues; and though not a nervine stimulant and antiperiodic as cinchona is, it is of decided value against intermittents where the cinchona preparations (and similar antiperiodics) prove too exciting to the nerve centers.  In cases of this class, I have several times arrested ague paroxysms by the fluid extract of this plant alone, with suitable daily hepatics; yet it is not strong enough to meet the chills of deeply-prostrated or congested cases.   It makes an excellent tonic addendum to such agents as fraxinus, angustura, or euonymus, in treating chronic biliousness with indigestion; and may be used to advantage with caulophyllum, convallaria, and similar uterine remedies, in chronic prolapsus, leucorrhea, hysteria, etc.   Its sustaining influence is shown to excellent advantage in the treatment of night sweats, exhaustion from excessive purulent discharges, recovery from malignant scarlatina, and other prostrated conditions.  Some use it for worms, as a tonic.   Usually given by infusion, made by digesting an ounce of the herb in a pint of hot water; of which a fluid ounce may be given every two or three hours during the intermission of an ague, or half a fluid ounce every three hours as a tonic.

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.missouriplants.com/Pinkopp/Sabatia_angularis_page.html
http://en.wikipedia.org/wiki/Sabatia_angularis
http://beetlesinthebush.wordpress.com/2009/08/28/friday-flower-sabatia-angularis/
http://www.cas.vanderbilt.edu/bioimages/species/saan.htm

http://www.ct-botanical-society.org/galleries/sabatiaangu.html

http://www.naturalmedicinalherbs.net/herbs/s/sabatia-angularis=bitter-bloom.php

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Ailmemts & Remedies

Tourette Syndrome

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Alternative Names: Tourette’s syndrome, Tourette’s disorder, Gilles de la Tourette syndrome, GTS or, more commonly, simply Tourette’s or TS

Definition:
Tourette syndrome  is an inherited neuropsychiatric disorder with onset in childhood, characterized by multiple physical (motor) tics and at least one vocal (phonic) tic; these tics characteristically wax and wane. Tourette’s is defined as part of a spectrum of tic disorders, which includes transient and chronic tics.

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Tourette’s was once considered a rare and bizarre syndrome, most often associated with the exclamation of obscene words or socially inappropriate and derogatory remarks (coprolalia), but this symptom is present in only a small minority of people with Tourette’s. Tourette’s is no longer considered a rare condition, but it may not always be correctly identified because most cases are classified as mild. Between 1 and 10 children per 1,000 have Tourette’s; as many as 10 per 1,000 people may have tic disorders, with the more common tics of eye blinking, coughing, throat clearing, sniffing, and facial movements. Tourette’s does not adversely affect intelligence or life expectancy. The severity of the tics decreases for most children as they pass through adolescence, and extreme Tourette’s in adulthood is a rarity. Notable individuals with Tourette’s are found in all walks of life.

Tourette syndrome can be a chronic condition with symptoms lasting a lifetime, most people with the condition experience their worst symptoms in their early teens, with improvement occurring in the late teens and continuing into adulthood.

Clacification
Tics are sudden, repetitive, stereotyped, nonrhythmic movements (motor tics) and utterances (phonic tics) that involve discrete muscle groups.[8] Motor tics are movement-based tics, while phonic tics are involuntary sounds produced by moving air through the nose, mouth, or throat.

Tourette’s is one of several tic disorders, which are classified by the Diagnostic and Statistical Manual of Mental Disorders (DSM) according to type (motor or phonic tics) and duration (transient or chronic). Transient tic disorder consists of multiple motor tics, phonic tics or both, with a duration between four weeks and twelve months. Chronic tic disorder is either single or multiple, motor or phonic tics (but not both), which are present for more than a year. Tourette’s is diagnosed when multiple motor tics, and at least one phonic tic, are present for more than a year. Tic disorders are defined similarly by the World Health Organization (International Statistical Classification of Diseases and Related Health Problems, ICD-10 codes).

Although Tourette’s is the more severe expression of the spectrum of tic disorders, most cases are mild. The severity of symptoms varies widely among people with Tourette’s, and mild cases may be undetected

Symptoms:
Tics — sudden, brief, intermittent movements or sounds — are the hallmark sign of Tourette syndrome. Symptoms range from mild to severe and debilitating.

Tics are classified as either:
*Simple tics, which are sudden, brief and repetitive and involve a limited number of muscle groups

*Complex tics, which are distinct, coordinated patterns of movements involving several muscle groups

Tics involving movement (motor tics) — often facial tics, such as blinking — usually begin before vocal tics do. But the spectrum of tics that people experience is diverse, and there’s no typical case.

Some of the more common tics seen in Tourette syndrome
Motor tics:-

Simple tics:
*Eye blinking
*Head jerking
*Shoulder shrugging
*Eye darting
*Finger flexing
*Sticking the tongue out

Complex tics :
*Touching the nose
*Touching other people
*Smelling objects
*Obscene gestures
*Flapping the arms
*Hopping

Vocal tics:-

Simple tics :
*Hiccuping
*Yelling
*Throat clearing
*Barking

Complex tics :
*Using different voice intonations
*Repeating one’s own words or phrases
*Repeating others’ words or phrases
*Using expletives

Tics can vary in type, frequency and severity over time. They may worsen during periods of stress and anxiety, fatigue, illness, or excitement. They can occur during sleep. You’ll likely experience an urge, called a premonitory urge, before the onset of motor or vocal tics. A premonitory urge is an uncomfortable bodily sensation, such as an itch, a tingle or tension. Expression of the tic brings relief.

Different tics may develop over time. Tourette symptoms are usually at their worst during the teenage years and sometimes improve during the transition to adulthood.

With great effort, some people with Tourette syndrome can sometimes temporarily stop a tic or hold back tics until they find a place where it’s less disruptive to express them.

 

Causes:
The exact cause of Tourette’s is unknown, but it is well established that both genetic and environmental factors are involved. Genetic studies have shown that the overwhelming majority of cases of Tourette’s are inherited, although the exact mode of inheritance is not yet known, and no gene has been identified. In some cases, Tourette’s is sporadic, that is, it is not inherited from parents. In other cases, tics are associated with disorders other than Tourette’s, a phenomenon known as tourettism.

A person with Tourette’s has about a 50% chance of passing the gene(s) to one of his or her children, but Tourette’s is a condition of variable expression and incomplete penetrance. Thus, not everyone who inherits the genetic vulnerability will show symptoms; even close family members may show different severities of symptoms, or no symptoms at all. The gene(s) may express as Tourette’s, as a milder tic disorder (transient or chronic tics), or as obsessive–compulsive symptoms without tics. Only a minority of the children who inherit the gene(s) have symptoms severe enough to require medical attention. Gender appears to have a role in the expression of the genetic vulnerability: males are more likely than females to express tics.

Non-genetic, environmental, infectious, or psychosocial factors—while not causing Tourette’s—can influence its severity. Autoimmune processes may affect tic onset and exacerbation in some cases. In 1998, a team at the US National Institute of Mental Health proposed a hypothesis that both obsessive–compulsive disorder (OCD) and tic disorders may arise in a subset of children as a result of a poststreptococcal autoimmune process. Children who meet five diagnostic criteria are classified, according to the hypothesis, as having Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections (PANDAS).  This contentious hypothesis is the focus of clinical and laboratory research, but remains unproven.

The exact mechanism affecting the inherited vulnerability to Tourette’s has not been established, and the precise etiology is unknown. Tics are believed to result from dysfunction in cortical and subcortical regions, the thalamus, basal ganglia and frontal cortex. Neuroanatomic models implicate failures in circuits connecting the brain’s cortex and subcortex, and imaging techniques implicate the basal ganglia and frontal cortex.

Some forms of OCD may be genetically linked to Tourette’s. A subset of OCD is thought to be etiologically related to Tourette’s and may be a different expression of the same factors that are important for the expression of tics.   The genetic relationship of ADHD to Tourette syndrome, however, has not been fully established

Risk factors
Having a family history of Tourette syndrome or other tic disorders may increase the risk of developing Tourette syndrome.

Complication:
People with Tourette syndrome have a normal life span and often lead a healthy, active life. However, having Tourette syndrome may increase the risk of learning, behavioral and social challenges, which can mar self-image.

In addition, having Tourette syndrome means you’re likely to have other related conditions, such as:

*Attention-deficit/hyperactivity disorder (ADHD)

*Obsessive-compulsive disorder

*Learning disabilities

*Sleep disorders

*Depression

*Anxiety disorders

Diagnosis:
According to the revised fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), Tourette’s may be diagnosed when a person exhibits both multiple motor and one or more vocal tics (although these do not need to be concurrent) over the period of a year, with no more than three consecutive tic-free months. The previous DSM-IV included a requirement for “marked distress or significant impairment in social, occupational or other important areas of functioning”, but this requirement was removed in the most recent update of the manual, in recognition that clinicians see patients who meet all the other criteria for Tourette’s, but do not have distress or impairment.[44] The onset must have occurred before the age of 18, and cannot be attributed to the “direct physiological effects of a substance or a general medical condition”. Hence, other medical conditions that include tics or tic-like movements—such as autism or other causes of tourettism—must be ruled out before conferring a Tourette’s diagnosis.

There are no specific medical or screening tests that can be used in diagnosing Tourette’s; it is frequently misdiagnosed or underdiagnosed, partly because of the wide expression of severity, ranging from mild (the majority of cases) or moderate, to severe (the rare, but more widely-recognized and publicized cases). Coughing, eye blinking and tics that mimic asthma are commonly misdiagnosed.

The diagnosis is made based on observation of the individual’s symptoms and family history, and after ruling out secondary causes of tic disorders. In patients with a typical onset and a family history of tics or obsessive–compulsive disorder, a basic physical and neurological examination may be sufficient.

There is no requirement that other comorbid conditions (such as ADHD or OCD) be present, but if a physician believes that there may be another condition present that could explain tics, tests may be ordered as necessary to rule out that condition. An example of this is when diagnostic confusion between tics and seizure activity exists, which would call for an EEG, or if there are symptoms that indicate an MRI to rule out brain abnormalities.  TSH levels can be measured to rule out hypothyroidism, which can be a cause of tics. Brain imaging studies are not usually warranted. In teenagers and adults presenting with a sudden onset of tics and other behavioral symptoms, a urine drug screen for cocaine and stimulants might be necessary. If a family history of liver disease is present, serum copper and ceruloplasmin levels can rule out Wilson’s disease. Most cases are diagnosed by merely observing a history of tics.

Secondary causes of tics (not related to inherited Tourette syndrome) are commonly referred to as tourettism. Dystonias, choreas, other genetic conditions, and secondary causes of tics should be ruled out in the differential diagnosis for Tourette syndrome.  Other conditions that may manifest tics or stereotyped movements include developmental disorders, autism spectrum disorders, and stereotypic movement disorder;  Sydenham’s chorea; idiopathic dystonia; and genetic conditions such as Huntington’s disease, neuroacanthocytosis, Hallervorden-Spatz syndrome, Duchenne muscular dystrophy, Wilson’s disease, and tuberous sclerosis. Other possibilities include chromosomal disorders such as Down syndrome, Klinefelter’s syndrome, XYY syndrome and fragile X syndrome. Acquired causes of tics include drug-induced tics, head trauma, encephalitis, stroke, and carbon monoxide poisoning. The symptoms of Lesch-Nyhan syndrome may also be confused with Tourette syndrome. Most of these conditions are rarer than tic disorders, and a thorough history and examination may be enough to rule them out, without medical or screening tests
Treatment:
There’s no cure for Tourette syndrome. Treatment is intended to help control tics that interfere with everyday activities and functioning. When tics aren’t severe, treatment may be unnecessary.

Medications:
No medication is helpful to everyone with Tourette syndrome, none completely eliminates symptoms, and they all have side effects to be weighed against the benefits. However, some medications can be used to help control or minimize tics or to control symptoms of related conditions, such as attention-deficit/hyperactivity disorder (ADHD) or obsessive-compulsive disorder (OCD). These may include:

*Drugs that block or deplete the neurotransmitter dopamine in the brain, such as fluphenazine or pimozide (Orap). Used to control tics, these medications may have side effects such as weight gain and a dulling of the mind.

*Botulinum Toxin Type A (Botox) injections. For simple or vocal tics, an injection into the affected muscle may help relieve the tic.

*Stimulant medications, such as methylphenidate (Concerta, Ritalin, others) and dextroamphetamine (Dexedrine, others). These are used to help increase attention and concentration for people with ADHD.

*Central adrenergic inhibitors, such as clonidine (Catapres) or guanfacine (Tenex). Typically prescribed for high blood pressure, these drugs may help control behavioral symptoms, such as impulse control problems and rage attacks. Side effects may include sleepiness.

*Antidepressants, such as fluoxetine (Prozac, Sarafem, others). These may help control the symptoms of OCD.

Therapies
*Psychotherapy. Psychotherapy can be helpful for two reasons. It can help with accompanying problems, such as ADHD, obsessions, depression and anxiety. Therapy can also help people cope with Tourette syndrome.

*Deep brain stimulation. For debilitating tics that don’t respond to other treatment, deep brain stimulation (DBS) may help. DBS consists of implanting a battery-operated medical device (neurostimulator) in the brain to deliver electrical stimulation to targeted areas that control movement. Further research is needed to determine whether DBS is beneficial for people with Tourette syndrome.

 

Prognosis:
Tourette syndrome is a spectrum disorder—its severity ranges over a spectrum from mild to severe. The majority of cases are mild and require no treatment. In these cases, the impact of symptoms on the individual may be mild, to the extent that casual observers might not know of their condition. The overall prognosis is positive, but a minority of children with Tourette syndrome have severe symptoms that persist into adulthood. A study of 46 subjects at 19 years of age found that the symptoms of 80% had minimum to mild impact on their overall functioning, and that the other 20% experienced at least a moderate impact on their overall functioning. The rare minority of severe cases can inhibit or prevent individuals from holding a job or having a fulfilling social life. In a follow-up study of thirty-one adults with Tourette’s, all patients completed high school, 52% finished at least two years of college, and 71% were full-time employed or were pursuing higher education.

Regardless of symptom severity, individuals with Tourette’s have a normal life span. Although the symptoms may be lifelong and chronic for some, the condition is not degenerative or life-threatening. Intelligence is normal in those with Tourette’s, although there may be learning disabilities. Severity of tics early in life does not predict tic severity in later life, and prognosis is generally favorable, although there is no reliable means of predicting the outcome for a particular individual. The gene or genes associated with Tourette’s have not been identified, and there is no potential “cure”. A higher rate of migraines than the general population and sleep disturbances are reported.

Several studies have demonstrated that the condition in most children improves with maturity. Tics may be at their highest severity at the time that they are diagnosed, and often improve with understanding of the condition by individuals and their families and friends. The statistical age of highest tic severity is typically between eight and twelve, with most individuals experiencing steadily declining tic severity as they pass through adolescence. One study showed no correlation with tic severity and the onset of puberty, in contrast with the popular belief that tics increase at puberty. In many cases, a complete remission of tic symptoms occurs after adolescence. However, a study using videotape to record tics in adults found that, although tics diminished in comparison with childhood, and all measures of tic severity improved by adulthood, 90% of adults still had tics. Half of the adults who considered themselves tic-free still displayed evidence of tics.

It is not uncommon for the parents of affected children to be unaware that they, too, may have had tics as children. Because Tourette’s tends to subside with maturity, and because milder cases of Tourette’s are now more likely to be recognized, the first realization that a parent had tics as a child may not come until their offspring is diagnosed. It is not uncommon for several members of a family to be diagnosed together, as parents bringing children to a physician for an evaluation of tics become aware that they, too, had tics as a child.

Children with Tourette’s may suffer socially if their tics are viewed as “bizarre”. If a child has disabling tics, or tics that interfere with social or academic functioning, supportive psychotherapy or school accommodations can be helpful.  Because comorbid conditions (such as ADHD or OCD) can cause greater impact on overall functioning than tics, a thorough evaluation for comorbidity is called for when symptoms and impairment warrant.

A supportive environment and family generally gives those with Tourette’s the skills to manage the disorder.  People with Tourette’s may learn to camouflage socially inappropriate tics or to channel the energy of their tics into a functional endeavor. Accomplished musicians, athletes, public speakers, and professionals from all walks of life are found among people with Tourette’s. Outcomes in adulthood are associated more with the perceived significance of having severe tics as a child than with the actual severity of the tics. A person who was misunderstood, punished, or teased at home or at school will fare worse than children who enjoyed an understanding and supportive environment

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/Tourette_syndrome
http://www.mayoclinic.com/health/tourette-syndrome/DS00541

http://www.sfn.org/index.aspx?pagename=brainBriefings_tourette#full

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Herbs & Plants

Swertia Radiata

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Botanical Name : Swertia radiata
Family: Gentianaceae
Genus: Frasera
Species: F. speciosa
Kingdom: Plantae
Order: Gentianales

Synonims:Frasera speciosa

Common Name :Cebadilla,Monument plant, Elkweed, and Deer’s ears.Green Gentian

Habitat : It is native to the western United States, where it grows in mountain forests, woodlands, and meadows. the northwestern United States, where it grows in open areas in mountain habitat.

Description:
It is a perennial herb growing from a woody base surrounded by rosettes of large leaves that measure up to 50 centimeters long by 15 wide. It produces a single erect stem which can reach two meters in height. The stem bears whorls of lance-shaped, pointed leaves smaller than those at the base. The plant is monocarpic, growing for several years and only flowering once before it dies. Flowering is synchronized among plants in a given area, with widespread, picturesque blooms occurring periodically. The inflorescence is a tall, erect panicle with flowers densely clustered at the top and then spread out in interrupted clusters below. Each flower has a calyx of four pointed sepals and a corolla of four pointed lobes each one to two centimeters long. The corolla is yellow-green with purple spots and each lobe has two fringed nectary pits at the base. There are four stamens tipped with large anthers and a central ovary.

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Cultivation: Requires a moist but well-drained position and a stony peaty soil. Requires an acidic soil. A very ornamental plant.

Propagation: Seed – sow spring in a greenhouse. When they are large enough to handle, prick the seedlings out into individual pots and grow them on in the greenhouse for at least their first winter. Plant them out into their permanent positions in late spring or early summer, after the last expected frosts. Division in late winter

Edible Uses:  Root. It has been reported that the N. American Indians ate the fleshy root of this plant, but caution is advised since the roots of closely related plants are used medicinally as emetics and cathartics. See the notes above on toxicity.

Medicinal Uses;
An infusion of the dried, powdered leaves, or the root, has been used in the treatment of diarrhea. A cooled decoction of the roots has been used in the treatment of asthma, colds, digestive complaints etc. An infusion of the plant has been used as a contraceptive.  Primarily a medicine for the digestive tract.  Similar to Gentian in its effect, it is more energetic and irritating.  A stimulant to stomach and small intestinal secretions and contractions, it makes a bitter tonic especially useful for the elderly. The dried root is powdered, 6-8 tablespoons added to a pint of brandy and it is steeped for at least a week; a tablespoon is taken before meals.  A pinch of the powder in sweetened water has a similar effect.  One-half to one teaspoon of the root powder boiled in water will act as a laxative-cathartic.  More than a teaspoon can act as an irritant to the large intestine, and in any respect, Cebadilla should be used as a laxative only occasionally.  The root can also serve as a fungicide for athlete’s foot and the like.  Sometimes effective as a tincture for ringworm, but care should be taken when used on children it can irritate the skin.  In New Mexico the powdered root is melted in lard and applied on the scalp to kill lice or rubbed on the legs to kill scabies.

Other Uses:…..Parasiticide...….The root, when ground into a powder and then mixed with oil, has been used as a parasiticide in order to kill lice.

Known Hazards :  When used medicinally, large doses of the powdered root have proved fatal.

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/Frasera_speciosa
http://www.herbnet.com/Herb%20Uses_C.htm
http://www.worldbotanical.com/swertia.htm

http://www.yosemitehikes.com/wildflowers/monument-plant/monument-plant.htm

http://www.pfaf.org/user/Plant.aspx?LatinName=Frasera+speciosa

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Ailmemts & Remedies

Multiple Myeloma

Alternative Name :Plasma cell myeloma or Kahler’s disease

Definition:
Multiple myeloma is a type of cancer. Cancer is a group of many related diseases. Myeloma is a cancer that starts in plasma cells, a type of white blood cell. It’s the most common type of plasma cell cancer.

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Multiple myeloma (from Greek myelo-, bone marrow), a type of white blood cell normally responsible for the production of antibodies. Collections of abnormal cells accumulate in bones, where they cause bone lesions, and in the bone marrow where they interfere with the production of normal blood cells. Most cases of myeloma also feature the production of a paraprotein, an abnormal antibody that can cause kidney problems and interferes with the production of normal antibodies leading to immunodeficiency. Hypercalcemia (high calcium levels) is often encountered

Health problems caused by multiple myeloma can affect your bones, immune system, kidneys and red blood cell count.

If some one has multiple myeloma but don’t have symptoms,the doctors may just monitor his or her condition. If experiencing symptoms, a number of treatments are available to help control multiple myeloma.

The disease develops in 1–4 per 100,000 people per year. It is more common in men, and is twice as common in blacks as it is in whites. With conventional treatment, the prognosis is 3–4 years, which may be extended to 5–7 years or longer with advanced treatments. Multiple myeloma is the second most common hematological malignancy (13%) and constitutes 1% of all cancers.

Signs and symptoms:
Because many organs can be affected by myeloma, the symptoms and signs vary greatly. A mnemonic sometimes used to remember the common tetrad of multiple myeloma is CRAB: C = Calcium (elevated), R = Renal failure, A = Anemia, B = Bone lesions. Myeloma has many possible symptoms, and all symptoms may be due to other causes. They are presented here in decreasing order of incidence.

Bone pain
Myeloma bone pain usually involves the spine and ribs, and worsens with activity. Persistent localized pain may indicate a pathological bone fracture. Involvement of the vertebrae may lead to spinal cord compression. Myeloma bone disease is due to the overexpression of Receptor Activator for Nuclear Factor ? B Ligand (RANKL) by bone marrow stroma. RANKL activates osteoclasts, which resorb bone. The resultant bone lesions are lytic in nature and are best seen in plain radiographs, which may show “punched-out” resorptive lesions (including the “pepper pot” appearance of the skull on radiography). The breakdown of bone also leads to release of calcium into the blood, leading to hypercalcemia and its associated symptoms.

Infection
The most common infections are pneumonias and pyelonephritis. Common pneumonia pathogens include S. pneumoniae, S. aureus, and K. pneumoniae, while common pathogens causing pyelonephritis include E. coli and other gram-negative organisms. The greatest risk period for the occurrence of infection is in the initial few months after the start of chemotherapy. The increased risk of infection is due to immune deficiency resulting from diffuse hypogammaglobulinemia, which is due to decreased production and increased destruction of normal antibodies. A selected group of patients may benefit from replacement immunoglobulin therapy to reduce the risk of infection.

Renal failure
Renal failure may develop both acutely and chronically. It is commonly due to hypercalcemia (see above). It may also be due to tubular damage from excretion of light chains, also called Bence Jones proteins, which can manifest as the Fanconi syndrome (type II renal tubular acidosis). Other causes include glomerular deposition of amyloid, hyperuricemia, recurrent infections (pyelonephritis), and local infiltration of tumor cells.

Anemia
The anemia found in myeloma is usually normocytic and normochromic. It results from the replacement of normal bone marrow by infiltrating tumor cells and inhibition of normal red blood cell production (hematopoiesis) by cytokines.

Neurological symptoms
Common problems are weakness, confusion and fatigue due to hypercalcemia. Headache, visual changes and retinopathy may be the result of hyperviscosity of the blood depending on the properties of the paraprotein. Finally, there may be radicular pain, loss of bowel or bladder control (due to involvement of spinal cord leading to cord compression) or carpal tunnel syndrome and other neuropathies (due to infiltration of peripheral nerves by amyloid). It may give rise to paraplegia in late presenting cases.

Causes:
Although the exact cause isn’t known, doctors do know that multiple myeloma begins with one abnormal plasma cell in our bone marrow — the soft, blood-producing tissue that fills in the center of most of our bones.

Normal blood cells
Most blood cells develop from cells in the bone marrow called stem cells. Bone marrow is the soft material in the center of most bones.

Stem cells mature into different types of blood cells. Each type has a special job:

*White blood cells help fight infection. There are several types of white blood cells.

*Red blood cells carry oxygen to tissues throughout the body.

*Platelets help form blood clots that control bleeding.

Plasma cells are white blood cells that make antibodies. Antibodies are part of the immune system. They work with other parts of the immune system to help protect the body from germs and other harmful substances. Each type of plasma cell makes a different antibody.

Myeloma cells
Myeloma, like other cancers, begins in cells. In cancer, new cells form when the body doesn’t need them, and old or damaged cells don’t die when they should. These extra cells can form a mass of tissue called a growth or tumor.

Myeloma begins when a plasma cell becomes abnormal. The abnormal cell divides to make copies of itself. The new cells divide again and again, making more and more abnormal cells. These abnormal plasma cells are called myeloma cells.

In time, myeloma cells collect in the bone marrow. They may damage the solid part of the bone. When myeloma cells collect in several of your bones, the disease is called “multiple myeloma.” This disease may also harm other tissues and organs, such as the kidneys.

Myeloma cells make antibodies called M proteins and other proteins. These proteins can collect in the blood, urine, and organs.
click to see the picture.

..Normal plasma cells help protect the body from germs and other harmful substances.

click to see picture.

…Myeloma cell (abnormal plasma cell) making M proteins.

Risk Factors:
Multiple myeloma isn’t contagious. Most people who develop multiple myeloma have no clearly identifiable risk factors for the disease.

Some factors that may increase your risk of multiple myeloma include:

*Age. Multiple myeloma is most common in people over 65, affecting men more than women. It rarely occurs in young people.

*Sex. Men are more likely to develop the disease than are women.

*Race. Blacks are about twice as likely to develop multiple myeloma as are whites.History of a monoclonal gammopathy of undetermined significance. Every year 1 percent of the people with MGUS in the United States develop multiple myeloma.

*Obesity. Your risk of multiple myeloma is increased if you’re overweight or obese.

Other factors that may increase your risk of developing multiple myeloma include exposure to radiation and working in leather or rubber manufacturing or the petrol industry, obesity and radiation exposure may increase the risk of multiple myeloma.

Diagnosis:
Doctors sometimes find multiple myeloma after a routine blood test. More often, doctors suspect multiple myeloma after an x-ray for a broken bone. Usually though, patients go to the doctor because they are having other symptoms.

To find out whether such problems are from multiple myeloma or some other condition, your doctor may ask about your personal and family medical history and do a physical exam. Your doctor also may order some of the following tests:

*Blood tests: The lab does several blood tests:

…#Multiple myeloma causes high levels of proteins in the blood. The lab checks the levels of many different proteins, including M protein and other immunoglobulins (antibodies), albumin, and beta-2-microglobulin.

…#Myeloma may also cause anemia and low levels of white blood cells and platelets. The lab does a complete blood count to check the number of white blood cells, red blood cells, and platelets.

…#The lab also checks for high levels of calcium.

…#To see how well the kidneys are working, the lab tests for creatinine.

*Urine tests: The lab checks for Bence Jones protein, a type of M protein, in urine. The lab measures the amount of Bence Jones protein in urine collected over a 24-hour period. If the lab finds a high level of Bence Jones protein in your urine sample, doctors will monitor your kidneys. Bence Jones protein can clog the kidneys and damage them.

*X-rays: You may have x-rays to check for broken or thinning bones. An x-ray of your whole body can be done to see how many bones could be damaged by the myeloma.

*Biopsy: Your doctor removes tissue to look for cancer cells. A biopsy is the only sure way to know whether myeloma cells are in your bone marrow. Before the sample is taken, local anesthesia is used to numb the area. This helps reduce the pain. Your doctor removes some bone marrow from your hip bone or another large bone. A pathologist uses a microscope to check the tissue for myeloma cells.

There are two ways your doctor can obtain bone marrow. Some people will have both procedures during the same visit:

...#Bone marrow aspiration: The doctor uses a thick, hollow needle to remove samples of bone marrow.
...#Bone marrow biopsy: The doctor uses a very thick, hollow needle to remove a small piece of bone and bone marrow.

Staging and classification:
These tests can help confirm whether you have multiple myeloma or another condition. If tests indicate you have multiple myeloma, the results from these tests allow your doctor to classify your disease as stage 1, stage 2 or stage 3. People with stage 3 myeloma are more likely to have one or more signs of advanced disease, including greater numbers of myeloma cells and kidney failure.

Treatment:
Treatment for multiple myeloma is focused on disease containment and suppression. If the disease is completely asymptomatic (i.e. there is a paraprotein and an abnormal bone marrow population but no end-organ damage), treatment may be deferred.

In addition to direct treatment of the plasma cell proliferation, bisphosphonates (e.g. pamidronate or zoledronic acid) are routinely administered to prevent fractures and erythropoietin to treat anemia.

Initial therapy
Initial treatment of multiple myeloma depends on the patient’s age and comorbidities. In recent years, high-dose chemotherapy with hematopoietic stem-cell transplantation has become the preferred treatment for patients under the age of 65. Prior to stem-cell transplantation, these patients receive an initial course of induction chemotherapy. The most common induction regimens used today are thalidomide–dexamethasone, bortezomib based regimens, and lenalidomide–dexamethasone.  Autologous stem cell transplantation (ASCT), the transplantation of a patient’s own stem cells after chemotherapy, is the most common type of stem cell transplantation for multiple myeloma. It is not curative, but does prolong overall survival. Allogeneic stem cell transplantation, the transplantation of a healthy person’s stem cells into the affected patient, has the potential for a cure, but is only available to a small percentage of patients. Furthermore, there is a 5-10% treatment-associated mortality rate.

Patients over age 65 and patients with significant concurrent illness often cannot tolerate stem cell transplantation. For these patients, the standard of care has been chemotherapy with melphalan and prednisone. Recent studies among this population   suggest improved outcomes with new chemotherapy regimens. Treatment with bortezomib, melphalan and prednisone had an estimated overall survival of 83% at 30 months, lenalidomide plus low-dose dexamethasone an 82% survival at 2 years and melphalan, prednisone and lenalidomide had a 90% survival at 2 years. Head-to-head studies comparing these regimens have not been performed.

A 2009 review noted “Deep venous thrombosis and pulmonary embolism are the major side effects of thalidomide and lenalidomide. Lenalidomide causes more myelosuppression, and thalidomide causes more sedation. Peripheral neuropathy and thrombocytopenia are major side effects of bortezomib.”

Treatment of related hyperviscosity syndrome may be required to prevent renal failure

Maintenance therapy
Sometimes after the initial treatment an ongoing maintenance therapy is offered. A 2009 review of maintenance therapy concluded “In younger patients, post-ASCT maintenance therapy with thalidomide appears to increase tumor burden reduction further, which translates in[to] prolonged PFS (progression free survival).”

Another 2009 review stated “the role of maintenance therapy with thalidomide, lenalidomide, or bortezomib for patients with multiple myeloma is not definitively established; such therapy should be performed only in the context of a clinical trial.”

Relapse
The natural history of myeloma is of relapse following treatment. Depending on the patient’s condition, the prior treatment modalities used and the duration of remission, options for relapsed disease include re-treatment with the original agent, use of other agents (such as melphalan, cyclophosphamide, thalidomide or dexamethasone, alone or in combination), and a second autologous stem cell transplant.

Later in the course of the disease, “treatment resistance” occurs. This may be a reversible effect,  and some new treatment modalities may re-sensitize the tumor to standard therapy. For patients with relapsed disease, bortezomib (or Velcade) is a recent addition to the therapeutic arsenal, especially as second line therapy, since 2005. Bortezomib is a proteasome inhibitor. Finally, lenalidomide (or Revlimid), a less toxic thalidomide analog, is showing promise for treating myeloma.

Renal failure in multiple myeloma can be acute (reversible) or chronic (irreversible). Acute renal failure typically resolves when the calcium and paraprotein levels are brought under control. Treatment of chronic renal failure is dependent on the type of renal failure and may involve dialysis.

Prognosis:
The International Staging System can help to predict survival, with a median survival of 62 months for stage 1 disease, 45 months for stage 2 disease, and 29 months for stage 3 disease.

Cytogenetic analysis of myeloma cells may be of prognostic value, with deletion of chromosome 13, non-hyperdiploidy and the balanced translocations t(4;14) and t(14;16) conferring a poorer prognosis. The 11q13 and 6p21 cytogenetic abnormalities are associated with a better prognosis.

Prognostic markers such as these are always generated by retrospective analyses, and it is likely that new treatment developments will improve the outlook for those with traditionally “poor-risk” disease.

SNP array karyotyping can detect copy number alterations of prognostic significance that may be missed by a targeted FISH panel. In MM, lack of a proliferative clone makes conventional cytogenetics informative in only ~30% of cases.

1.Virtual karyotyping identified chromosomal abnormalities in 98% of MM cases

2.del(12p13.31)is an independent adverse marker

3.amp(5q31.1) is a favorable marker

4.The prognostic impact of amp(5q31.1) over-rides that of hyperdiploidy and also identifies patients who greatly benefit from high-dose therapy.

Array-based karyotyping cannot detect balanced translocations, such as t(4;14) seen in ~15% of MM. Therefore, FISH for this translocation should also be performed if using SNP arrays to detect genome-wide copy number alterations of prognostic significance in MM.

The prognoses for patients with multiple myeloma, as those with other diseases, are not the same for everyone. The average age of onset is 70 years. Older patients often are experiencing other serious diseases, which affect survival. Younger patients might have much longer survival rates.

Some myeloma centers now employ genetic testing, which they call a “gene array.” By examining DNA oncologists can determine if patients are high risk or low risk. Myeloma patients identified as high risk are at high risk of having the cancer return more quickly following treatment. Low risk patients are at low risk of having the cancer return quickly following treatment.

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/Multiple_myeloma
http://www.bbc.co.uk/health/physical_health/conditions/in_depth/cancer/myeloma1.shtml
http://www.mayoclinic.com/health/multiple-myeloma/DS00415
http://www.medicinenet.com/multiple_myeloma/article.htm
http://www.nature.com/nrc/journal/v2/n12/fig_tab/nrc952_F5.html

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Categories
Ailmemts & Remedies

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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