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Sjogren’s syndrome

Alternative Names: Mikulicz disease” and “Sicca syndrome

Definition:
Sjögren’s syndrome (SHOW-grins)is a systemic autoimmune disease in which immune cells attack and destroy the exocrine glands  that produce tears and saliva.In some cases, other organs of the body are also affected, including the:
•Kidneys
•Liver
•Pancreas
•Lungs
•Blood vessels
•Brain

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It is named after Swedish ophthalmologist Henrik Sjögren (1899–1986), who first described it.

Nine out of ten Sjögren’s patients are women  and the average age of onset is late 40s, although Sjögren’s occurs in all age groups in both women and men. It is estimated to strike as many as 4 million people in the United States alone, making it the second most common autoimmune rheumatic disease.

Sjogren’s syndrome may be classified as primary or secondary. Primary Sjogren’s syndrome occurs alone; secondary Sjogren’s syndrome is seen alongside another disease, such as rheumatoid arthritis and systemic lupus erythematosis (SLE).

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The disorder should not be confused with the Sjögren–Larsson syndrome, which was also denoted T. Sjögren syndrome in early studies.

Symptoms:
There are many different symptoms of Sjogren’s. However, not everyone experiences the same ones or to the same degree.
The characteristic dryness of Sjogren’s means the eyes often feel very uncomfortable and may burn, itch or feel gritty. Mouth dryness makes talking, chewing and swallowing difficult.

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Other symptoms include:

•A sore or cracked tongue
•Dry nose and skin
•Digestive problems
•Joint pains
•Fatigue
•Dental problems are more likely (because of the lack of saliva)
As is often the case with any long-term condition, a person’s quality of life may be adversely affected. This may result in depression and make social life, work and relationships more difficult to maintain and enjoy.

Sjogren’s is also associated with an increased risk of miscarriage, Raynauds phenomenom and adverse reactions to medication such as antibiotics.

Causes:
Sjogren’s syndrome is an autoimmune disorder. This means that your immune system mistakenly attacks your body’s own cells and tissues.

Scientists aren’t certain why some people develop Sjogren’s syndrome and others don’t. Certain genes put people at higher risk for the disorder, but it appears that a triggering mechanism — such as infection with a particular virus or strain of bacteria — is also necessary.

In Sjogren’s syndrome, your immune system first targets the moisture-secreting glands of your eyes and mouth. But it can also damage other parts of your body, such as your:

*Joints
*Thyroid
*Kidneys
*Liver
*Lungs
*Skin
*Nerves
Risk Factors:
Although anyone can develop Sjogren’s syndrome, it typically occurs in people with one or more known risk factors. These include:

*Age. Sjogren’s syndrome is usually diagnosed in people older than 40.
*Sex. Women are much more likely to have Sjogren’s syndrome.
*Rheumatic disease. It’s common for people who have Sjogren’s syndrome to also have a rheumatic disease — such as rheumatoid arthritis or lupus.

Complications:
The most common complications of Sjogren’s syndrome involve your eyes and mouth.

*Dental cavities. Because saliva helps protect the teeth from the bacteria that cause cavities, you’re more prone to developing cavities if your mouth is dry.

*Yeast infections. People with Sjogren’s syndrome are much more likely to develop oral thrush, a yeast infection in the mouth.

*Vision problems. Dry eyes can lead to light sensitivity, blurred vision and corneal ulcers.

Less common complications may affect your:

*Lungs, kidneys or liver. Inflammation may cause pneumonia, bronchitis or other problems in your lungs; may lead to problems with kidney function; and may cause hepatitis or cirrhosis in your liver.

*Unborn baby. If you’re a woman with Sjogren’s syndrome and you plan to become pregnant, talk with your doctor about being tested for certain autoantibodies that may be present in your blood. In rare cases, these antibodies have been associated with heart problems in newborns

*Lymph nodes. A small percentage of people with Sjogren’s syndrome develop cancer of the lymph nodes (lymphoma).

*Nerves. You may develop numbness, tingling and burning in your hands and feet (peripheral neuropathy).

Diagnosis:
Diagnosing Sjögren’s syndrome is complicated by the range of symptoms a patient may manifest, and the similarity between symptoms of Sjögren’s syndrome and those of other conditions. Nevertheless, the combination of several tests can lead to a diagnosis of Sjögren’s syndrome.

Blood tests can be done to determine if a patient has high levels of antibodies that are indicative of the condition, such as anti-nuclear antibody (ANA) and rheumatoid factor (because SS frequently occurs secondary to rheumatoid arthritis), which are associated with autoimmune diseases. Typical Sjögren’s syndrome ANA patterns are SSA/Ro and SSB/La, of which SSB/La is far more specific; SSA/Ro is associated with numerous other autoimmune conditions but are often present in Sjögren’s.

Schirmer’s test measures the production of tears: a strip of filter paper is held inside the lower eyelid for five minutes, and its wetness is then measured with a ruler. Producing less than five millimeters of liquid is usually indicative of Sjögren’s syndrome. However, lacrimal function declines with age or may be impaired from other medical conditions. An alternative test is nonstimulated whole saliva flow collection, in which the patient spits into a test tube every minute for 15 minutes. A resultant collection of less than 1.5 mL is considered a positive result. It takes longer to perform than Schirmer’s test, but does not require special equipment.

A slit-lamp examination can reveal dryness on the surface of the eye. Salivary gland function can be tested by collecting saliva and determining the amount produced in a five minute period. A lip biopsy can reveal lymphocytes clustered around salivary glands, and damage to these glands due to inflammation.

Ultrasound examination of the salivary glands is the simplest confirmatory test and has the added advantage of being non-invasive with no complications. The parenchyma of the gland demonstrates multiple, small-2-6 mm hypoechoic lesions which are representations of the lymphocytic infiltrates. Often sialectasis with calculi are demonstrated if the disease is advanced. The sonographic findings have excellent symptom correlation. The other advantage of ultrasound is that complications of the disease such as extra-nodal lymphomas can often be detected as larger 1–4 cm hypoechoic intra-parenchymal masses.

There is also a radiological procedure which is a reliable and accurate test for Sjögren’s syndrome. A contrast agent is injected into the parotid duct, which opens from the cheek into the vestibule of the mouth opposite the neck of the upper second molar tooth. Widespread puddling of the injected contrast scattered throughout the gland indicates Sjögren’s syndrome.

The Revised Classification Criteria for Sjögren’s Syndrome requires the presence of signs, symptoms, and lab findings.

Patient-reported symptoms must include both ocular symptoms, such as daily, persistent, troublesome dry eyes for more than three months, and oral symptoms, such as needing to drink water to swallow food.

Objective evidence of eye involvement relies on Schirmer’s test and the Rose bengal score (or similar). Histopathology studies should show focal lymphocytic sialadenitis. Objective evidence of salivary gland involvement is tested through ultrasound examinations, the level of unstimulated whole salivary flow, a parotid sialography, or salivary scintigraphy. Autoantibodies against Ro (SSA) and/or La (SSB) antigens are also expected.

SS can be excluded from people with past head and neck radiation therapy, hepatitis C infection, Acquired immunodeficiency syndrome (AIDS), pre-existing lymphoma, sarcoidosis, graft-versus-host disease, and use of anticholinergic drugs (since a time shorter than four times the life of the drug).

Treatment:
It’s not possible to prevent Sjogren’s syndrome and there’s no cure, but treatments can help to relieve many of the symptoms. Treatment varies depending on which parts of the body are affected and may include:

•Artificial tears to help with dry eyes
•Saliva stimulants and mouth lubricants for dry mouth
•Anti-inflammatory medication for joint or muscle pain
•Corticosteroids or immunosuppressive drugs for lung, kidney, blood vessel or nervous system problems

Lifestyle and home remedies:

Many symptoms of Sjogren’s syndrome respond well to self-care measures.

To relieve dry eyes:

*Use artificial tears, an eye lubricant or both. Artificial tears (in eyedrop form) and eye lubricants (in eyedrop, gel or ointment form) help relieve the discomfort of dry eyes. Both types of product are available over-the-counter. You don’t have to apply eye lubricants as often as artificial tears. Because of their thicker consistency, though, eye lubricants can blur your vision and collect on your eyelashes. Your doctor may recommend artificial tears without preservatives because the preservatives can be irritating for people with dry eye syndrome.

* Increase humidity. Increasing the indoor humidity and reducing your exposure to blowing air may help keep your eyes from getting uncomfortably dry. For example, avoid sitting in front of a fan or air-conditioning vent, and wear goggles or protective eyewear when you go outdoors.

To help with dry mouth:

*Increase  fluid intake. Drinking lots of fluids, particularly water, helps to reduce dry mouth.

*Stimulate saliva flow. Sugarless gum or hard candies can boost saliva flow. Because Sjogren’s syndrome increases your risk of dental cavities, limit sweets, especially between meals. Lemon juice in water can also help stimulate saliva flow.

*Try artificial saliva. Saliva replacement products often work better than plain water because they contain a lubricant that helps your mouth stay moist longer. These products may come as a spray or lozenge.

*Use nasal saline spray. A nasal saline spray can help moisturize and clear nasal passages so you can breathe freely through your nose. A dry, stuffy nose can increase mouth breathing.

Oral health:

Dry mouth increases your risk of dental cavities and tooth loss. The following precautions may help prevent those types of problems.

*Brush your teeth and floss after every meal.

*Schedule regular dental appointments, at least every six months.

*Use daily topical fluoride treatments and antimicrobial mouthwashes.

Other areas of dryness:

If dry skin is a problem, avoid hot water when you bathe and shower. Pat your skin — don’t rub — with a towel and apply moisturizer when your skin is still damp. Use rubber gloves when doing dishes or housecleaning. Vaginal moisturizers and lubricants help women who experience vaginal dryness.

Prognosis:
Sjögren’s can damage vital organs of the body with symptoms that may plateau or worsen, but the disease does not go into remission as with other autoimmune diseases. Some people may experience only the mild symptoms of dry eyes and mouth, while others have symptoms of severe disease. Many patients are able to treat problems symptomatically. Others are forced to cope with blurred vision, constant eye discomfort, recurrent mouth infections, swollen parotid glands, hoarseness, and difficulty in swallowing and eating. Debilitating fatigue and joint pain can seriously impair quality of life. Some patients can develop renal involvement (autoimmune tubulointerstitial nephritis) leading to proteinuria, urinary concentrating defect and distal renal tubular acidosis.

Patients with Sjögren’s syndrome have a higher rate of non-Hodgkin lymphoma compared to both patients with other autoimmune diseases and healthy people.  About 5% of patients with Sjögren’s syndrome will develop some form of lymphoid malignancy. Patients with severe cases are much more likely to develop lymphomas than patients with mild or moderate cases. The most common lymphomas are salivary extranodal marginal zone B cell lymphomas (MALT lymphomas in the salivary glands)   and diffuse large B-cell lymphoma.

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://halter4sen.org/wp-content/uploads/2011/09/sjogren_syndrome.jpg
http://en.wikipedia.org/wiki/Sj%C3%B6gren’s_syndrome
http://www.mayoclinic.com/health/sjogrens-syndrome/DS00147
http://www.bbc.co.uk/health/physical_health/conditions/sjogrensyndrome1.shtml
http://pubs.acs.org/subscribe/archive/mdd/v05/i04/html/04disease.html

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Silicosis

Alternative Names:Potter’s rot,  Acute silicosis; Chronic silicosis; Accelerated silicosis; Progressive massive fibrosis; Conglomerate silicosis; Silicoproteinosis

Definition:
Silicosis is a respiratory disease caused by breathing in (inhaling) silica dust. It is an occupational lung disease that develops over time when dust that contains silica is inhaled into the lungs. Other examples of occupational lung disease include coalworker’s pneumoconiosis and asbestosis.

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The name silicosis (from the Latin silex, or flint) was originally used in 1870 by Achille Visconti (1836-1911), prosector in the Ospedale Maggiore of Milan. The recognition of respiratory problems from breathing in dust dates to ancient Greeks and Romans. Agricola, in the mid-16th century, wrote about lung problems from dust inhalation in miners. In 1713, Bernardino Ramazzini noted asthmatic symptoms and sand-like substances in the lungs of stone cutters. With industrialization, as opposed to hand tools, came increased production of dust. The pneumatic hammer drill was introduced in 1897 and sandblasting was introduced in about 1904, both significantly contributing to the increased prevalence of silicosis.

Classification:
Classification of silicosis is made according to the disease’s severity (including radiographic pattern), onset, and rapidity of progression. These include:

Chronic simple silicosis
Usually resulting from long-term exposure (10 years or more) to relatively low concentrations of silica dust and usually appearing 10–30 years after first exposure. This is the most common type of silicosis. Patients with this type of silicosis, especially early on, may not have obvious signs or symptoms of disease, but abnormalities may be detected by x-ray. Chronic cough and exertional dyspnea are common findings. Radiographically, chronic simple silicosis reveals a profusion of small (<10 mm in diameter) opacities, typically rounded, and predominating in the upper lung zones.

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Accelerated silicosis
Silicosis that develops 5–10 years after first exposure to higher concentrations of silica dust. Symptoms and x-ray findings are similar to chronic simple silicosis, but occur earlier and tend to progress more rapidly. Patients with accelerated silicosis are at greater risk for complicated disease, including progressive massive fibrosis (PMF).

Complicated silicosis
Silicosis can become “complicated” by the development of severe scarring (progressive massive fibrosis, or also known as conglomerate silicosis), where the small nodules gradually become confluent, reaching a size of 1 cm or greater. PMF is associated with more severe symptoms and respiratory impairment than simple disease. Silicosis can also be complicated by other lung disease, such as tuberculosis, non-tuberculous mycobacterial infection, and fungal infection, certain autoimmune diseases, and lung cancer. Complicated silicosis is more common with accelerated silicosis than with the chronic variety.
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Acute silicosis
Silicosis that develops a few weeks to 5 years after exposure to high concentrations of respirable silica dust. This is also known as silicoproteinosis. Symptoms of acute silicosis include more rapid onset of severe disabling shortness of breath, cough, weakness, and weight loss, often leading to death. The x-ray usually reveals a diffuse alveolar filling with air bronchograms, described as a ground-glass appearance, and similar to pneumonia, pulmonary edema, alveolar hemorrhage, and alveolar cell lung cancer.

Symptoms:
Because chronic silicosis is slow to develop, signs and symptoms may not appear until years after exposure. Signs and symptoms include:

*Dyspnea (shortness of breath) exacerbated by exertion

*Cough, often persistent and sometimes severe

*Fatigue

*Tachypnea (rapid breathing) which is often labored

*Loss of appetite and weight loss

*Chest pain

*Fever

*Gradual dark shallow rifts in nails eventually leading to cracks as protein fibers within nail beds are destroyed.

In advanced cases, the following may also occur:

*Cyanosis (blue skin)

*Cor pulmonale (right ventricle heart disease)

*Respiratory insufficiency

Patients with silicosis are particularly susceptible to tuberculosis (TB) infection—known as silicotuberculosis. The reason for the increased risk—3 fold increased incidence—is not well understood. It is thought that silica damages pulmonary macrophages, inhibiting their ability to kill mycobacteria. Even workers with prolonged silica exposure, but without silicosis, are at a similarly increased risk for TB.

Pulmonary complications of silicosis also include Chronic Bronchitis and airflow limitation (indistinguishable from that caused by smoking), non-tuberculous Mycobacterium infection, fungal lung infection, compensatory emphysema, and pneumothorax. There are some data revealing an association between silicosis and certain autoimmune diseases, including nephritis, Scleroderma, and Systemic Lupus Erythematosus, especially in acute or accelerated silicosis.

In 1996, the International Agency for Research on Cancer (IARC) reviewed the medical data and classified crystalline silica as “carcinogenic to humans.” The risk was best seen in cases with underlying silicosis, with relative risks for lung cancer of 2-4. Numerous subsequent studies have been published confirming this risk. In 2006, Pelucchi et al. concluded, “The silicosis-cancer association is now established, in agreement with other studies and meta-analysis

Causes:
Silica in crystalline form is toxic to the lining of the lungs. When the two come into contact, a strong inflammatory reaction occurs. Over time this inflammation causes the lung tissue to become irreversibly thickened and scarred – a condition known as fibrosis.

Common sources of crystalline silica dust include:

•Sandstone
•Granite
•Slate
•Coal
•Pure silica sand

People who work with these materials, as well as foundry workers, potters and sandblasters, are most at risk. Other forms of silica, such as glass, are less of a health risk as they aren’t as toxic to the lungs.

Men tend to be affected more often than women, as they are more likely to have been exposed to silica.

Risk Factors:
Silicosis is most commonly diagnosed in people over 40, as it usually takes years of exposure before the gradually progressive lung damage becomes apparent.

There are now fewer than 100 new cases of silicosis diagnosed each year in the UK. This is mostly the result of better working practices, such as wet drilling, appropriate ventilation, dust-control facilities, showers and the use of face masks. Many foundries are also replacing silica sand with synthetic materials.

With these measures and an increased awareness of the risks of silica exposure, the number of cases should fall even further in the future.

When silicosis is suspected, a chest x-ray will look for any damaged areas of the lungs to confirm the diagnosis. Lung function tests are often performed to assess the amount of damage the lungs have suffered and to guide treatment.

Possible Complications:
•Connective tissue disease, including rheumatoid arthritis, scleroderma (also called progressive systemic sclerosis), and systemic lupus erythematosus
•Lung cancer
•Progressive massive fibrosis
•Respiratory failure
•Tuberculosis

You may click to see the pictures:    ->(1) Simple  silicosis    :   (2)  Complicated silicosis    :(3) Silicosis.ILO Classification 2-2 R-R  :

Diagnosis:
There are three key elements to the diagnosis of silicosis. First, the patient history should reveal exposure to sufficient silica dust to cause this illness. Second, chest imaging (usually chest x-ray) that reveals findings consistent with silicosis. Third, there are no underlying illnesses that are more likely to be causing the abnormalities. Physical examination is usually unremarkable unless there is complicated disease. Also, the examination findings are not specific for silicosis. Pulmonary function testing may reveal airflow limitation, restrictive defects, reduced diffusion capacity, mixed defects, or may be normal (especially without complicated disease). Most cases of silicosis do not require tissue biopsy for diagnosis, but this may be necessary in some cases, primarily to exclude other conditions.

For uncomplicated silicosis, chest x-ray will confirm the presence of small (< 10 mm) nodules in the lungs, especially in the upper lung zones. Using the ILO classification system, these are of profusion 1/0 or greater and shape/size “p”, “q”, or “r”. Lung zone involvement and profusion increases with disease progression. In advanced cases of silicosis, large opacity (> 1 cm) occurs from coalescence of small opacities, particularly in the upper lung zones. With retraction of the lung tissue, there is compensatory emphysema. Enlargement of the hilum is common with chronic and accelerated silicosis. In about 5-10% of cases, the nodes will calcify circumferentially, producing so-called “eggshell” calcification. This finding is not pathognomonic (diagnostic) of silicosis. In some cases, the pulmonary nodules may also become calcified.

A computed tomography or CT scan can also provide a mode detailed analysis of the lungs, and can reveal cavitation due to concomitant mycobacterial infection.

Treatment:
Silicosis is an irreversible condition with no cure.  Treatment options currently focus on alleviating the symptoms and preventing complications. These include:

*Stopping further exposure to silica and other lung irritants, including tobacco smoking.

*Cough suppressants.

*Antibiotics for bacterial lung infection.

*TB prophylaxis for those with positive tuberculin skin test or IGRA blood test.

*Prolonged anti-tuberculosis (multi-drug regimen) for those with active TB.

*Chest physiotherapy to help the bronchial drainage of mucus.

*Oxygen administration to treat hypoxemia, if present.

*Bronchodilators to facilitate breathing.

*Lung transplantation to replace the damaged lung tissue is the most effective treatment, but is associated with severe risks of its own.

*For acute silicosis, Whole-lung lavage (see Bronchoalveolar lavage) may alleviate symptoms, but does not decrease overall mortality.

Experimental treatments include:

*Inhalation of powdered aluminium, d-penicillamine and polyvinyl pyridine-N-oxide.

*Corticosteroid therapy.

*The herbal extract tetrandine may slow progression of silicosis.

Support Groups:
Joining a support group where you can meet other people with silicosis or related diseases can help you understand your disease and adapt to its treatments.

Prognosis:
The outcome varies depending on the amount of damage to the lungs.

Prevention:
The best way to prevent silicosis is to identify work-place activities that produce respirable crystalline silica dust and then to eliminate or control the dust (“primary prevention”). Water spray is often used where dust emanates. Dust can also be controlled through dry air filtering.

Following observations on industry workers in Lucknow (India), experiments on rats found that jaggery (a traditional sugar) had a preventive action against silicosis.

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/Silicosis
http://www.nlm.nih.gov/medlineplus/ency/article/000134.htm
http://www.smianalytical.com/dust-sampling/what-is-silicosis.html
http://www.bbc.co.uk/health/physical_health/conditions/silicosis1.shtml

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Glomerulonephritis

Alternative Names: Glomerulonephritis – chronic; Chronic nephritis; Glomerular disease; Necrotizing glomerulonephritis; Glomerulonephritis – crescentic; Crescentic glomerulonephritis; Rapidly progressive glomerulonephritis

Definition:
Glomerulonephritis is a type of kidney disease in which the part of your kidneys that helps filter waste and fluids from the blood is damaged.

It is an inflammation of the tiny filters in your kidneys (glomeruli). Glomeruli remove excess fluid, electrolytes and waste from your bloodstream and pass them into your urine.


You may click to see the picture

The inflammation can be caused by many different conditions. but is usually due to an overactivity of the immune system.

Glomerulonephritis can be acute — a sudden attack of inflammation — or chronic — coming on gradually.

If glomerulonephritis occurs on its own, it’s known as primary glomerulonephritis. If another disease, such as lupus or diabetes, is the cause, it’s called secondary glomerulonephritis. If severe or prolonged, the inflammation associated with glomerulonephritis can damage your kidneys. Treatment depends on the type of glomerulonephritis you have.

Symptoms:
There are seven different types of glomerulonephritis, that present in very different ways. For some types, symptoms can include ankle swelling that develops over months or years. For others, shortness-of-breath over days or weeks (due to water in the lungs) causing a rapid onset of kidney failure.

The outlook is also variable, from complete recovery with no treatment, to end-stage renal failure (ESRF), requiring dialysis and/or a transplant. Some types of glomerulonephritis can return in a transplant.

The various symptoms of the different types also include:
*Swelling of the face, eyes and legs
*Reduction in urine volume
*Dark urine (containing blood which may not be visible)
*Headaches and visual disturbances
*Drowsiness
*Tiredness and general malaise (feeling ill)
*Nausea
*Loss of appetite
*Rashes and itchy skin
*Pink or cola-colored urine from red blood cells in your urine (hematuria)
*Foamy urine due to excess protein (proteinuria)
*High blood pressure (hypertension)
*Fluid retention (edema) with swelling evident in your face, hands, feet and abdomen
*Fatigue from anemia or kidney failure

Tests for the condition show protein, blood cells, and kidney cells in the urine, while a high concentration of the body’s waste products (such as urea and creatinine) may be found in the blood.

Swabs of the throat may show there’s been a streptococcal infection, while blood tests may be used to check for antibodies to streptococci or other infections, or signs of an abnormal immune response.

All patients will need a kidney biopsy (removal of a piece of kidney with a needle) to make a definite diagnosis.

Sometimes when there are no symptoms, the problem is picked up by a routine blood test, or during investigation of high blood pressure

Causes:
Primary causes are ones which are intrinsic to the kidney, whilst secondary causes are associated with certain infections (bacterial, viral or parasitic pathogens), drugs, systemic disorders (SLE, vasculitis) or diabetes.

Glomerulonephritis may be caused by specific problems with the body’s immune system. Often, the precise cause of glomerulonephritis is unknown.

Damage to the glomeruli causes blood and protein to be lost in the urine.

The condition may develop quickly, with loss of kidney function occurring over weeks and months (called rapidly progressive glomerulonephritis).

In about a quarter of people with chronic glomerulonephritis there is no history of kidney disease and the disorder first appears as chronic renal failure.

Risk Factors:
The following increase your risk of developing this condition:
•History of cancer
•Blood or lymphatic system disorders
•Exposure to hydrocarbon solvents
•Infections such as strep infections, viruses, heart infections,or abscesses
•Diabetes
Many conditions are known to cause or increase the risk for glomerulonephritis, including:
•Focal segmental glomerulosclerosis
•Goodpasture syndrome
•Membranoproliferative GN
•IgA nephropathy
•Lupus nephritis or Henoch-Schonlein purpura
•Anti-glomerular basement membrane antibody disease
•Blood vessel diseases such as vasculitis or polyarteritis
•Amyloidosis

In most cases, no cause is found. Though in a few patients, they may be ‘set off’ by an infection or a cancer. Post-streptococcal glomerulonephritis is now extremely rare

There is also a very serious type called ’rapidly progressive glomerulonephritis’ (RPGN), which can follow a flu-like illness in the month before symptoms start in 50 per cent of patients. This can cause kidney failure in days or weeks and can be linked to bleeding from the lungs, causing blood to be coughed up.

Diagnosis:
Specific signs and symptoms may suggest glomerulonephritis, but the condition often comes to light when a routine urinalysis is abnormal. Because symptoms develop gradually, the disorder may be discovered when there is an abnormal urinalysis during a routine physical or examination for unrelated disorders.

Glomerulonephritis can cause high blood pressure. It may only be discovered as a cause of high blood pressure that is difficult to control.

Laboratory tests may reveal anemia or show signs of reduced kidney functioning. A kidney biopsy confirms the diagnosis.

Later, signs of chronic kidney failure may be seen, including swelling (edema), polyneuropathy, and signs of fluid overload, including abnormal heart and lung sounds.

Imaging tests that may be done include:
•Abdominal CT scan
•Abdominal ultrasound
•Chest x-ray
•IVP

Urinalysis and other urine tests include:
•Examination of the urine under a microscope
•Creatinine clearance
•Total protein
•Uric acid, urine
•Urine concentration test
•Urine creatinine
•Urine protein
•Urine RBC
•Urine specific gravity

This disease may also affect the results of the following blood tests:
•Albumin
•Anti-glomerular basement membrane antibody test
•Anti-neutrophil cytoplasmic antibodies (ANCAs)
•BUN and creatinine
•Complement component 3
•Complement levels

Treatment:
Treatment varies depending on the cause of the disorder, and the type and severity of symptoms. High blood pressure may be difficult to control, and it is generally the most important aspect of treatment.

Medicines that may be prescribed include:
•Blood pressure medications are often needed to control high blood pressure. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are most commonly prescribed.
•Corticosteroids may relieve symptoms in some cases.
•Medications that suppress the immune system may also be prescribed, depending on the cause of the condition.

A procedure called plasmapheresis may be used for some cases of glomerulonephritis due to immune-related causes. The fluid part of the blood containing antibodies is removed and replaced with intravenous fluids or donated plasma (without antibodies). Removing antibodies may reduce inflammation in the kidney tissues.

Dietary restrictions on salt, fluids, protein, and other substances may be recommended.

Persons with this condition should be closely watched for signs that they are developing kidney failure. Dialysis or a kidney transplant may eventually be necessary.

Lifestyle and home remedies:-
Your doctor may recommend lifestyle changes, including:

*Restricting salt intake to prevent or minimize fluid retention, swelling and hypertension

*Cutting back on protein and potassium consumption to slow the buildup of wastes in your blood

*Maintaining a healthy weight

*Controlling your blood sugar level if you have diabetes

Possible Complications:
•Nephrotic syndrome
•Acute nephritic syndrome
•Chronic kidney failure
•End-stage kidney disease
•Hypertension
•Malignant hypertension
•Fluid overload — congestive heart failure, pulmonary edema
•Chronic or recurrent urinary tract infection
•Increased susceptibility to other infections
•Hyperkalemia

Prognosis:
Glomerulonephritis may be a temporary and reversible condition, or it may get worse. Progressive glomerulonephritis may lead to chronic kidney failure and end-stage kidney disease.

If you have nephrotic syndrome and it can be controlled, other symptoms may also be controlled. If it can’t be controlled, end-stage kidney disease may result.

Prevention:
There is no specific way to prevent most cases of glomerulonephritis. Some cases may be prevented by avoiding or limiting exposure to organic solvents, mercury, and nonsteroidal anti-inflammatory drugs (NSAIDs).

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/in_depth/kidneys/glomerulonephritis1.shtml
http://www.nlm.nih.gov/medlineplus/ency/article/000484.htm
http://www.mayoclinic.com/health/glomerulonephritis/DS00503
http://en.wikipedia.org/wiki/Glomerulonephritis

http://www.marvistavet.com/html/body_glomerulonephritis.html

http://www.butler.org/body.cfm?id=125&chunkiid=96731

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Tea Associated With Increased Risk of Rheumatoid Arthritis in Women

According to a study, women who drink tea have an increased risk of developing rheumatoid arthritis compared with those who drink none (p=0.04). Further results from the same study showed no correlation between the amount of coffee consumption and rheumatoid arthritis incidence (p=0.16).

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The results of the US based longitudinal cohort study involving 76,643 women showed a positive association of incident rheumatoid arthritis in tea drinkers with an increasing Hazard Ratio (HR) observed alongside tea consumption (p=0.03). Consuming any amount of tea carried a significant risk of developing rheumatoid arthritis (HR 1.40 (95%CI 1.01-1.93) p=0.04) and women who drank ?4 cups of tea per day had an increased risk of developing rheumatoid arthritis compared to those who drank none (HR 1.78 (95%CI 0.83-3.82)). An analysis of the method of preparation of coffee (filtered vs unfiltered) and presence or lack of caffeine in the beverage did not show any significant associations with rheumatoid arthritis or Systemic Lupus Erythematosus (SLE, an autoimmune disease in which the immune system harms the body’s own healthy cells and tissues) (rheumatoid arthritis: filtered p=0.08, unfiltered p=0.38, SLE: filtered p=0.74, unfiltered p=0.97). No increase was shown in the risk of developing rheumatoid arthritis in participants who drank coffee compared to those that did not (rheumatoid arthritis: HR 1.09 (95%CI 0.77-1.54 p=0.63).

“We set out to determine whether tea or coffee consumption, or the method of preparation of the drinks was associated with an increased risk of rheumatoid arthritis or SLE – it is surprising that we saw such differences in results between tea and coffee drinkers,” said Professor Christopher Collins. “This does make us wonder what it is in tea, or in the method of preparation of tea that causes the significant increase in risk of developing rheumatoid arthritis.”

Data on women aged 50-79 were taken from the Women’s Health Initiative Observational Study database (a major 15-year research program to address the most common causes of death, disability and poor quality of life in postmenopausal women) where participants completed a self-administered questionnaire providing information on daily consumption of coffee and tea.

The relationships between drinking tea and coffee and the risk of rheumatoid arthritis or SLE were assessed in age-adjusted models and in multivariate Cox proportional hazard models (a statustical approach to estimating survival data). At three years follow up, the diagnosis of incident rheumatoid arthritis was determined using self-reporting and respondent’s feedback on use of disease modifying anti-rheumatic drugs (DMARDS). The variables studied in the rheumatoid arthritis population were also investigated in women with SLE, but no significant associations were found.

“These are very interesting findings and we hope that additional research will investigate this topic further. We do assert the need for caution in the interpretation of these findings as no strong causation effect has been confirmed, and encourage patients with rheumatic diseases to consult their physician before making any significant changes to their diet or caffeine intake” said Professor Paul Emery, President of European League Against Rheumatism.


Source:
Elements4Health.June18.2010

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Raynaud’s disease


Definition:-

Raynaud’s disease is a condition that causes some areas of your body — such as your fingers, toes, tip of your nose and your ears — to feel numb and cool in response to cold temperatures or stress. In Raynaud’s disease, smaller arteries that supply blood to your skin narrow, limiting blood circulation to affected areas.

Click to see the pictures of  Raynaud’s  diseas

Raynaud’s disease (also known as “Primary Raynaud’s phenomenon” where the phenomenon is idiopathic, and Raynaud’s syndrome (secondary Raynaud’s), where it is caused by some other instigating factor. Measurement of hand-temperature gradients is one tool used to distinguish between the primary and secondary forms.

It is possible for the primary form to progress to the secondary form.

Symptoms:-
Raynaud’s disease is more than simply having cold hands and cold feet, and it’s not the same as frostbite. Signs and symptoms of Raynaud’s depend on the frequency, duration and severity of the blood vessel spasms that underlie the disorder.

The list of signs and symptoms mentioned in various sources for Raynaud’s phenomenon includes the 51 symptoms listed below:

•Symptoms usually affect fingers, toes, nose, lips or earlobes
•Skin color changes
•Skin whiteness then blueness then redness
•Cold sensitivity
•Pallor (whiteness)
•Cyanosis (blueness)
•Redness (rubor)
•Finger symptoms
*Finger color changes
*Finger pallor
*Finger tingling
*Finger redness
*Finger numbness
*Finger sensitivity
*Finger pain

•Toe symptoms

*Toe color changes
*Toe numbness
*Toe redness
*Toe pallor
*Toe sensitivity
*Toe pain

•Nose symptoms
*Nose color changes
*Nose numbness
*Nose redness
*Nose pallor
*Nose sensitivity
*Nose pain

•Earlobe symptoms
*Earlobe color changes
*Earlobe numbness
*Earlobe redness
*Earlobe pallor
*Earlobe pain
•Lip symptoms

*Lip color changes
*Lip numbness
*Lip redness
*Lip pallor
*Lip sensitivity
*Lip pain

•Episodic attacks – lasting minutes or hours
•Small blood vessel constriction (vasospastic attacks)
•Symmetric symptoms – usually both hands or both feet rather than just one
•Both hands and both feet – primary Raynaud’s affects all 4; secondary Raynaud’s typically affects either hands or feet but not both.

•Other areas affected – hands and feet most common but others are possible
*Nose symptoms
*Lips symptoms
*Ear lobes symptoms

Causes:-
Doctors don’t completely understand the cause of Raynaud’s attacks, but blood vessels in the hands and feet appear to overreact to cold temperatures or stress:

*Cold temperatures. When your body is exposed to cold temperatures, your extremities lose heat. Your body slows down blood supply to your fingers and toes to preserve your body’s core temperature. Your body specifically reduces blood flow by narrowing the small arteries under the skin of your extremities. In people with Raynaud’s, this normal response is exaggerated.
*Stress. Stress causes a similar reaction to cold in the body, and likewise the body’s response may be exaggerated in people with Raynaud’s.


Blood vessels in spasm
:
With Raynaud’s, arteries to your fingers and toes go into what’s called vasospasm. This narrows your vessels dramatically and temporarily limits blood supply. Over time, these same small arteries may also thicken slightly, further limiting blood flow. The result is that affected skin turns a pale and dusky color due to the lack of blood flow to the area. Once the spasms go away and blood returns to the area, the tissue may turn red before returning to a normal color.

Cold temperatures are most likely to trigger an attack. Exposure to cold can be as simple as putting your hands under a faucet of running cold water, taking something out of the freezer or exposure to cold air. For some people, exposure to cold temperatures isn’t necessary. Emotional stress alone can cause an episode of Raynaud’s.

Raynaud’s may be partly an inherited disorder.

In extreme cases, the secondary form can progress to necrosis or gangrene of the fingertips.

Raynaud’s phenomenon is an exaggeration of vasomotor responses to cold or emotional stress. More specifically, it is a hyperactivation of the sympathetic system causing extreme vasoconstriction of the peripheral blood vessels, leading to tissue hypoxia. Chronic, recurrent cases of Raynaud phenomenon can result in atrophy of the skin, subcutaneous tissues, and muscle. In rare cases it can cause ulceration and ischemic gangrene.

It is important to distinguish Raynaud’s disease from syndrome. In order to diagnose these two forms of Raynaud’s, a doctor may look for signs of arthritis or vasculitis, and may conduct a number of laboratory tests.

Primary Raynaud’s (disease):
Raynaud’s disease, or “Primary Raynaud’s”, is diagnosed if the symptoms are idiopathic, that is, they occur by themselves and not in association with other diseases. Some refer to Primary Raynaud’s disease as “being allergic to coldness”. It often develops in young women in their teens and early adulthood. Primary Raynaud’s is thought to be at least partly hereditary, although specific genes have not yet been identified.

Smoking worsens frequency and intensity of attacks, and there is a hormonal component. Caffeine also worsens the attacks. Sufferers are more likely to have migraine and angina than controls.

Secondary Raynaud’s (syndrome)
:
Raynaud’s syndrome, or “Secondary Raynaud’s”, occurs secondary to a wide variety of other conditions. Secondary Raynaud’s has a number of associations:

Connective tissue disorders:
*scleroderma
*systemic lupus erythematosus
*rheumatoid arthritis
*Sjögren’s syndrome
*dermatomyositis
*polymyositis
*mixed connective tissue disease

*cold agglutinin disease

*Ehlers-Danlos Syndrome

Eating disorders
*anorexia nervosa

Obstructive disorders :
*atherosclerosis
*Buerger’s disease
*Takayasu’s arteritis
*subclavian aneurysms
*thoracic outlet syndrome


Drugs
:
*Beta-blockers
*cytotoxic drugs – particularly chemotherapeutics and most especially *bleomycin
*ciclosporin
*ergotamine
*sulfasalazine
*anthrax vaccines whose primary ingredient is the Anthrax Protective Antigen


Occupation
:
*jobs involving vibration, particularly drilling
*exposure to vinyl chloride, mercury
*exposure to the cold (e.g. by working packing frozen food)


Others
:
*hypothyroidism
*cryoglobulinemia
*malignancy
*reflex sympathetic dystrophy
*carpal tunnel syndrome
*Magnesium Deficiency
*Erythromelalgia, (the opposite of Raynaud’s, with hot and warm extremities) often co-exists in patients with Raynaud’s)
It is important to realize that Raynaud’s can herald these diseases by periods of more than 20 years in some cases, making it effectively their first presenting symptom. This can be the case in the CREST syndrome, of which Raynaud’s is a part.

Patients with Secondary Raynaud’s can also have symptoms related to their underlying diseases. Raynaud’s phenomenon is the initial symptom that presents for 70% of patients with scleroderma, a skin and joint disease.

Raynaud’s phenomenon which is limited to one hand (or to one foot) is referred to as Unilateral Raynaud’s. This is an uncommon form, and it is always secondary to local or regional vascular disease. It commonly progresses within several years to affect other limbs as the vascular disease progresses.

Risk factors:-
Risk factors for primary Raynaud’s include:

*Your gender.
Primary Raynaud’s affects women more than men.
*Your age. Although anyone can develop the condition, primary Raynaud’s often begins between the ages of 15 and 30.
*Where you live. The disorder is also more common in people who live in colder climates.
*Your family history. Additionally, a family history appears to increase your risk of primary Raynaud’s. About one-third of people with primary Raynaud’s have a first-degree relative — a parent, sibling or child — with the disorder.

Risk factors for secondary Raynaud’s include:


*Associated diseases.
These include conditions such as scleroderma and lupus.

*Certain occupations. People in occupations that cause repetitive trauma, such as workers who operate tools that vibrate, also may be more vulnerable to secondary Raynaud’s.

*Exposure to certain substances.
Smoking, medications that affect the blood vessels and exposure to chemicals such as vinyl chloride are associated with an increased risk of Raynaud’s.
Complications:
If Raynaud’s is severe — which is rare — blood circulation to your fingers or toes could permanently diminish, causing deformities of your fingers or toes.

If an artery to an affected area becomes blocked completely, sores (skin ulcers) or dead tissue (gangrene) may develop. Ulcers and gangrene can be difficult to treat.

Diagnosis:-
Examinations & Tests:
To diagnose Raynaud’s, your doctor will ask detailed questions about your symptoms and medical history and conduct a physical examination. Your doctor may also run tests to rule out other medical problems that may cause similar signs and symptoms, such as a pinched nerve.

Your doctor may perform a simple test called a cold-stimulation test during your office visit. This test may involve placing your hands in cool water or exposing you to cold air, to trigger an episode of Raynaud’s.

A careful medical history will often reveal whether the condition is primary or secondary. Once this has been established, an examination is largely to identify or exclude possible secondary causes.

Digital artery pressure: pressures are measured in the arteries of the fingers before and after the hands have been cooled. A decrease of at least 15 mmHg is diagnostic (positive).

Doppler ultrasound: to assess blood flow.

Full blood count: this can reveal a normocytic anaemia suggesting the anaemia of chronic disease or renal failure.

Blood test for urea and electrolytes:
this can reveal renal impairment.
Thyroid function tests: this can reveal hypothyroidism.
An autoantibody screen, tests for rheumatoid factor, Erythrocyte sedimentation rate and C-reactive protein, which may reveal specific causative illnesses or a generalised inflammatory process.
Nail fold vasculature: this can be examined under the microscope

Sorting out primary vs. secondary Raynaud’s
:
To distinguish between primary and secondary Raynaud’s, your doctor may perform an in-office test called nail fold capillaroscopy. During the test, the doctor examines your nail fold — the skin at the base of your fingernail — under a microscope. Tiny blood vessels (capillaries) near the nail fold that are enlarged or deformed may indicate an underlying disease. However, some secondary diseases can’t be detected by this test.

If your doctor suspects that another condition, such as an autoimmune or connective tissue disease, underlies Raynaud’s, he or she may order blood tests, such as:

*Antinuclear antibodies test. A positive test for the presence of these antibodies — produced by your immune system — indicates a stimulated immune system and is common in people who have connective tissue diseases or other autoimmune disorders.

*Erythrocyte sedimentation rate. This blood test determines the rate at which red blood cells settle to the bottom of a tube in the space of an hour. A faster than normal rate may signal an underlying inflammatory or autoimmune disease. Autoimmune diseases are commonly associated with secondary Raynaud’s.
There’s no single blood test to diagnose Raynaud’s. Your doctor may order other tests, such as those that rule out diseases of the arteries, to help pinpoint a disease or condition that may be associated with Raynaud’s.

Modern Treatments and drugs:-

Treatment options are dependent on the type of Raynaud’s present. Raynaud’s syndrome is treated primarily by addressing the underlying cause, but includes all options for Raynaud’s disease as well. Treatment of primary Raynaud’s focuses on avoiding triggers.

General care:
*Avoid environmental triggers, e.g. cold, vibration, etc. Emotional stress is another recognized trigger; although the various sources of stress can not all be avoided, it is possible to learn healthier, more effective ways of dealing with them, which will reduce stress and its damaging physical effects overall.

*Keep your hands, feet and head warm—especially your fingers, toes, ears and nose—by wearing mittens, insulated footwear, a ski mask; by using hand and foot warmers, etc.

*Quit smoking.

*Avoid caffeine and other stimulants and vasoconstrictors that have not been prescribed to you by your doctor. Read product labels; caffeine is found not only in coffee and tea, stay-awake pills, many soft drinks and candies, but also in some cosmetics, soaps and shampoos(reference needed).

  • Exercise. Your doctor may encourage you to exercise regularly, particularly if you have primary Raynaud’s. Exercise can increase circulation, among other health benefits.
  • Control stress. Because stress may trigger an attack, learning to recognize and avoid stressful situations may help control the number of attacks.

*Make sure all your doctors know about all the medicines you take and about all the OTC remedies you use, especially hormones and drugs that regulate hormones, such as hormonal contraception, so that these professionals can make an assessment of your chemical regimen and make any changes that may be indicated. Contraception which is low in estrogen is preferable, and the progesterone only pill is often prescribed for women with Raynaud’s.

*If you are diabetic, follow your diabetes treatment plan.

Emergency measures:
*If white finger (Raynaud’s) occurs unexpectedly and a source of warm water is available, allow tepid to slightly warm water to run over the affected digits while you gently massage the area. Continue this process until the white area returns to its normal, healthy color.

*If triggered by exposure in a cold environment, and no warm water is available, place the affected digits in a warm body cavity – arm pit, crotch, or even in the mouth. Keep the affected area warm at least until the whiteness returns to its normal, healthy color. Get out of the cold as soon as possible.

Drug therapy
:
*Treatment for Raynaud’s phenomenon may include prescription medicines that dilate blood vessels, such as calcium channel blockers (nifedipine) or diltiazem.  It has the usual common side effects of headache, flushing, and ankle edema; but these are not typically of sufficient severity to require cessation of treatment.

*There is some evidence that Angiotensin II receptor antagonists (often Losartan) reduce frequency and severity of attacks,and possibly better than nifedipine.

*Alpha-1 adrenergic blockers such as prazosin can be used to control Raynaud’s vasospasms under supervision of a health care provider.

*In a study published in the November 8, 2005 issue of Circulation, sildenafil (Viagra) improved both microcirculation and symptoms in patients with secondary Raynaud’s phenomenon resistant to vasodilatory therapy. The authors, led by Dr Roland Fries (Gotthard-Schettler-Klinik, Bad Schönborn, Germany), report: “In the present study, capillary blood flow was severely impaired and sometimes hardly detectable in patients with Raynaud’s phenomenon. Sildenafil led to a more than 400% increase of flow velocity.”

*Fluoxetine, a selective serotonin reuptake inhibitor, and other antidepressant medications may reduce the frequency and severity of episodes if caused mainly by psychological stress.

Surgical Intervention
:
*In severe cases, a sympathectomy   procedure can be performed. Here, the nerves that signal the blood vessels of the fingertips to constrict are surgically cut. Microvascular surgery of the affected areas is another possible therapy. Infusions of prostaglandins, e.g. prostacyclin, may be tried, with amputation in exceptionally severe cases.

*A more recent treatment for severe Raynaud’s is the use of Botox. The 2009 article studied 19 patients ranging in age from 15 to 72 years with severe Raynaud’s phenomenon of which 16 patients (84%) reported pain reduction at rest. 13 patients reported immediate pain relief, 3 more had gradual pain reduction over 1-2 months. All 13 patients with chronic finger ulcers healed within 60 days. Only 21% of the patients required repeated injections. A 2007 article describes similar improvement in a series of 11 patients. All patients had significant relief of pain.

Sometimes in cases of severe Raynaud’s, approaches other than medications may be a treatment option:

*Nerve surgery
. Nerves called sympathetic nerves in your hands and feet control the opening and narrowing of blood vessels in your skin. Sometimes it’s necessary in cases of severe Raynaud’s to cut these nerves to interrupt their exaggerated response. Through small incisions in the affected hands or feet, a doctor strips away these tiny nerves around the blood vessels. The surgery, called sympathectomy, may reduce the frequency and duration of attacks, but it’s not always successful.
*Chemical injection. Doctors can inject chemicals to block sympathetic nerves in affected hands or feet. You may need to have the procedure repeated if symptoms return or persist.
*Amputation. Sometimes, doctors need to remove tissue damaged from a lack of blood supply. This may include amputating a finger or toe affected by Raynaud’s in which the blood supply has been completely blocked and the tissue has developed gangrene. But this is rare.


Alternative and Experimental (Research) Approaches
:-
Lifestyle changes and supplements that encourage better circulation may be effective alternatives for managing Raynaud’s. If  one is interested, may talk to the doctor about:

*Biofeedback. Biofeedback — using your mind to control body temperature — may help decrease the severity and frequency of attacks. Biofeedback includes guided imagery to increase the temperature of hands and feet, deep breathing and other relaxation exercises. Your doctor may be able to suggest a therapist who can help you learn biofeedback techniques. Books and tapes also are available on the subject.

*Niacin. Niacin, also known as vitamin B-3, causes blood vessels to dilate, increasing blood flow to skin. Niacin supplements may be useful in treating Raynaud’s, although niacin supplements may have side effects.
*The extract of the Ginkgo biloba leaves (Egb 761, 80 mg) may reduce frequency of attacks.

*Two separate gels combined on the fingertip (somewhat like two-part epoxy, they cannot be combined before use because they will react) increased blood flow in the fingertips by about three times. One gel contained 5% sodium nitrite and the other contained 5% ascorbic acid. The milliliter of combined gel covered an area of ~3 cm². The gel was wiped off after a few seconds.

*Piracetam, a nootropic drug, can be useful as a long-term treatment for vasospastic disorders.

*Arginine, which increase nitrous oxide acts as a vasodilator

*Milder cases of Raynaud’s can often be addressed by biofeedback[23] or other techniques to help control involuntary body functions like skin temperature.

*Fish oil supplements which contain long-chain omega-3 fatty acids may help to control symptoms of primary Raynaud’s. There are few studies in the medical literature dealing with this subject. However, in one 1989 controlled, double-blinded study of 32 patients, consumption of roughly 6.5 grams of long chain omega-3 fatty acids in the form of fish oil significantly increased the time to onset or entirely prevented symptoms in response to cold in patients with primary Raynaud’s. Lower doses of fish oil such as may be commonly available from commercial vendors have not been studied and may not be as effective.

Coping with the stress and nuisance of Raynaud’s takes patience and effort. Work with your doctor to manage your condition and maintain a positive attitude. The majority of people with Raynaud’s respond to 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.


Rersources:
http://en.wikipedia.org/wiki/Raynaud’s_phenomenon
http://www.mayoclinic.com/health/raynauds-disease/DS00433/DSECTION=lifestyle-and-home-remedies
http://www.wrongdiagnosis.com/r/raynauds_phenomenon/symptoms.htm
http://www.myfootshop.com/detail.asp?Condition=Raynauds%20Disease.

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