viernes, 22 de febrero de 2019

Rheumatoid Arthritis History

Rheumatoid Arthritis History

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Rheumatoid Arthritis History

Arthritis and diseases of the joints have been plaguing mankind since ancient times. In around 1500 BC the Ebers Papyrus described a condition that is similar to rheumatoid arthritis. This is probably the first reference to this disease.
There is evidence of rheumatoid arthritis in the Egyptian mummies as found in several studies. G. Elliot in his studies found that rheumatoid arthritis was a prevalent disease among Egyptians.
In the Indian literature, Charak Samhita (written in around 300 – 200 BC) also described a condition that describes pain, joint swelling and loss of joint mobility and function. Hippocrates described arthritis in general in 400 BC. He however did not describe specific types of arthritis. Galen between 129 and 216 AD introduced the term rheumatismus.
Paracelsus (1493-1511) suggested that substances that could not be passed in urine got stored and collected in the body especially in the joints and this caused arthritis. Ayurveda in ancient Indian medicine also considered arthritis as one of the Vata. Practitioners attributed rheumatic disorders to humors (rheuma).
Thomas Sydenham first described a disabling form of chronic arthritis that was described later by Beauvais in 1880. Brodie went on to show the progressive nature of this disease and found how rheumatoid arthritis affected the tendon sheaths and sacs of synovium in the joints. He found how there was synovial inflammation or synovitis and cartilage damage associated with rheumatoid arthritis.

History of the terms rheumatoid arthritis, rheumatology and rheumatologist

A B Garrod in 1858 named the disease rheumatoid arthritis replacing the old terms arthritis deformans and rheumatic gout. He is thus credited to make a distinction between rheumatoid arthritis and osteoarthritis and gout.
Appearance of rheumatoid arthritis affected joints was first described by Bannatyne (1896). It was in 1940 that Camroe coined the term rheumatologist and the term rheumatology was coined by Hollander in 1949.
In 1932 the International Committee on Rheumatism was formed. It later became American Rheumatism Association and then American College of Rheumatology.

History of treatment of rheumatoid arthritis

In the olden days treatments for rheumatoid arthritis included bloodletting and leeching. In the Far East developed practises of acupuncture, acupressure, moxibustion (use of heat), cupping etc. were used.
After several failed treatments that did not improve the condition of the patients, came the use of heavy metals in treatment of many diseases including rheumatoid arthritis. Gold, bismuth, arsenic and copper salts were used with varying rates of success. Gold however has shown success over years of use and is still a part of Disease Modifying Antirheumatic drugs (DMARDs). DMARDs are widely used in treatment of Rheumatoid arthritis.

History of pain relief

Pain relief was achieved using plant extracts of Willow bark and leaves. These contained salicin. Hippocrates, Galen used Willow extracts to treat pain of rheumatoid arthritis and other forms of arthritis.
In 1929 Leroux identifies Salicylic acid as the active substance that eased pain. In 1853, acetyl salicylic acid (aspirin) was synthesized by Gerhardt. Thereafter beginning with phenylbutazone in 1949 several other non steroidal anti-inflammatiory agents came into being.

History of Disease Modifying Anti-rheumatic drugs (DMARDs)

Payne in 1895 was the first to suggest the use of quinine to treat lupus erythematosus and rheumatic diseases. In 1957 Baguall used chloroquine and now hydroxychloroquine is still part of the DMARDs.
In 1940’s sulphasalazine was developed as an anti-inflammatory and still forms part of DMARDs. In 1949 Philip Hench and Edward Kendall first showed the successful use of cortisone in autoimmune diseases including rheumatoid arthritis.
Methotrexate was first synthesized in 1950’s as a folate antogonist to treat leukaemia. It was not until 1980’s that the role of methotrexate in rheumatoid arthritis was discovered. It still forms part of the DMARDs.

Anti-TNF antibodies

Monocyte derived tumour necrosis (TNF) factor was first identified for its role in the pathogenesis of rheumatoid arthritis in 1975. In 1993 Anti-TNF antibodies were shown to be effective in the treatment of patients with rheumatoid arthritis.

Further Reading

Last Updated: Aug 23, 2018

Psoriatic Arthritis vs Rheumatoid Arthritis

Psoriatic Arthritis vs Rheumatoid Arthritis

News-Medical

Psoriatic Arthritis vs Rheumatoid Arthritis

Both psoriatic arthritis (PsA) and rheumatoid arthritis (RA) are inflammatory joint conditions with a wide variability of clinical features, and both may involve multiple systems of the body. Both may affect the eyes, the skin, the joints, and the cardiovascular system. However, their differences go deeper and they require different treatments with a clear divergence in the expected response to various specific modes of therapy and prognosis.

Clinical Similarities

The diseases are similar in that patients with both conditions complain of joint pain, swelling and tenderness over the proximal interphalangeal joints of the fingers and the metacarpophalangeal joints (in 70% and 80% of PsA and RA respectively). The microscopy often shows symmetrical involvement of the synovial membrane in both cases, though asymmetrical joint involvement is also common in PsA.


Fundamental Differences

PsA and RA show deep underlying differences, such as:
Distribution
PsA is an inflammatory disease affecting a few joints of the spine, the sacroiliac joints, and the peripheral skeleton; RA characteristically shows peripheral joint involvement.
Clinical course
PsA typically has a less severe clinical picture than RA, but axial skeletal involvement including sacroiliac arthritis with a strong resemblance to ankylosing spondylitis is typical. Thus it is a spondyloarthropathy. DIP arthritis is characteristic in PsA, seen in 20-60% of patients.


Type of Bone Erosion

The type of bone lesion in PsA is a cortical erosion of significant size with indistinct margins, often just outside the joint surface of the bone with evidence of new bone formation, whereas the RA lesion is well-defined and located at the joint margin.

Presence of Enthesitis

PsA is characterized by enthesitis leading to entheseal osteogenesis with synovitis, compared to synovitis alone in RA as seen with MRI and micro-CT scanning.

Pathogenesis

The pathogenesis of the conditions is distinct, with PsA being part of the seronegative spondyloarthropathies, while RA shows the presence of rheumatoid factor (RF) or anti-citrullinated protein antibodies (ACPA) in circulation.

Inflammatory Markers

Systemic inflammatory response measured by the ESR or CRP rate is much less in PsA compared to RA. PsA is thus considered to be possibly an autoinflammatory disease due to inflammasome disturbance, while RA is an autoimmune disease.

Microscopy

The synovial tissue obtained by biopsy in PsA shows villous structures infiltrated by mononuclear cells and heavy angiogenesis, with increased expression of vascular endothelial growth factor (VEGF), angiopoietin 2 and basic fibroblast growth factor (BFGF). The blood vessels are thickened and the endothelial cells are swollen. The network is formed of elongated and tortuous vessels indicating that cells from existing vessels have proliferated, while in RA actual neovascularization occurs to form a branching network.

Vascular Proliferation

New vessels are actively formed within the synovial membrane of affected joints early in the course of the disease in PsA but later in the disease in RA.

Type of Cellular Infiltrate

T-lymphocyte infiltration is more common in PsA while RA shows a more prominent cellular infiltrate composed of both T and B cells with more marked synovial lining cell hyperplasia.

HLA Typing

Genetic testing shows an increased propensity to PsA in patients with the HLA Cw6 and HLA B27 with the IL23 receptor, but to RA in patients with HLA DRB1.

Therapeutic Response

Both PsA and RA respond to conventional DMARDs but TNF inhibitors induce remission in 60% of patients with PsA compared to 44% in RA. These drugs inhibit bone damage and relieve spinal symptoms as well as nail disease and dactylitis, which are seen in 25% and 20% of PsA patients, respectively. The spinal effect indicates that TNF inhibitors are best used early in PsA rather than DMARDs.
Other monoclonal antibodies directed against other molecules such as CD20 are effective in RA but not PsA because of the lack of autoimmune phenomena in the latter.
A fusion molecule targeting CTLA-4 (cytotoxic T-lymphocyte-associated protein 4) is equally effective in both conditions, indicating that the downregulation of activated T cells is important in relieving both these diseases.

Prognosis

The prognosis is usually better with PsA.

Conclusion

While PsA and RA appear to have many similarities, these are more superficial than their differences, which embrace the clinical picture, the immunological changes, and cellular and molecular phenomena. These are particularly obvious in relation to the autoimmune phenomena, vascular changes in the synovium and pattern of joint inflammation and new bone formation. The final differences are with respect to the specific therapy of each of these conditions.

Further Reading

Last Updated: Aug 23, 2018

Rheumatoid Arthritis and Vitamin D

Rheumatoid Arthritis and Vitamin D

News-Medical

Rheumatoid Arthritis and Vitamin D

by Lana Barhum
Research finds a majority of people with rheumatoid arthritis (RA) are also vitamin D deficient and deficiency may worsen RA symptom severity. The most common causes of vitamin D deficiency in rheumatoid arthritis patients are insufficient intake of vitamin D from food sources, limited exposure to sunlight, and having a disorder that limits the body’s ability to absorb vitamin D in the body.
Vitamin D. source and synthesis, UVB radiation illustration
Vitamin D metabolism diagram.

Vitamin D benefits RA patients

Vitamin D deficiency has been strongly associated with disabling symptoms among those with rheumatoid arthritis, this according to a 2012 Greek study reported in Therapeutic Advances in Endocrinology and Metabolism. This is may be due to the fact that RA can affect the body’s ability to absorb vitamin D from the foods we take in, and when vitamin D levels are low, RA symptoms and pain may worsen.
Taking in more vitamin D - thrugh supplements and increased exposure to sunlight - can help to reduce inflammation, strengthen bone cartilage, and minimize pain and risk for disability. Vitamin D supplements can also help to alleviate other symptoms of arthritic conditions.

Vitamin D prevention and risk for RA

A 2004 study, with results published in Arthritis & Rheumatism, supports the idea that vitamin D plays an important role in preventing RA. The study looked at about 30,000 women between the ages of 55-69 years who did not have a history of RA.
After 11 years of follow-up with the women, including checking vitamin D levels, 152 cases of RA were confirmed. The researchers' findings were suggestive of an increased risk for RA in older women with lower vitamin D levels but researchers agreed the results were only preliminary.
Newer studies have disputed the claim that low vitamin D levels increase the risk for developing RA. A 2011 review in Seminars in Arthritis and Rheumatism looked at several studies examining the relationship between RA and vitamin D. The researchers reported they were not able to point to enough evidence to confirm low vitamin D is a risk factor for developing RA.

Deficiency in RA patients

A study out of the Albert Einstein University of Medicine of Yeshiva University in New York City, found that people who take corticosteroid medications are twice as likely to become vitamin D deficient, compared to those who don’t take them.
Corticosteroid medications, such as prednisone, prescribed to reduce inflammation in RA patients, can reduce calcium absorption and impair vitamin D metabolism. Other RA medications, such as Hydroxychloroquine and immunosuppressants are also linked to malabsorption of vitamin D. If you are taking these medications to treat RA symptoms and pain, it is important to have your levels checked regularly.
These is also an increased risk for RA patients who are restricted from going outside due to mobility issues and disability, live in parts of the world where sunlight is limited during the winter months, have dark skin, or who frequently wear clothing covering most of the body.

Symptoms and tests for vitamin D deficiency

Symptoms of vitamin D deficiency for patients with RA include worsening pain, depression, weak bones, fatigue, and difficulty concentrating. It takes one simple blood test to get your levels tested. A 25-hydoxy vitamin D test can tell your doctor if your vitamin D level is deficient or if you are at risk due to lower levels.
The 25-hydoxy test measures vitamin D levels in blood as nanograms per milliliter (ng/mL). Normal levels of vitamin D are between 30-40 ng/mL. Deficiency is a level less than 20 ng/mL, while toxic levels are anything greater than 150 ng/mL.

Managing vitamin D levels

When vitamin D levels are normal, RA symptoms and pain and overall health are improved. The National Institutes of Health recommends a dietary allowance of 600 international units (IUs) per day of vitamin D. People who are deficient need more and may benefit from taking 1-2,000 IUs per day.
Patients who have been diagnosed with severe deficiency, or who have certain health conditions, may take a 50,000 IUs prescribed dose, over a longer period of time, i.e., twice a week. Too much vitamin D can cause toxicity, resulting in serious health issues.
According to the Vitamin D Council, patients are most likely to develop toxicity if they take more than 40,000 international units of vitamin D everyday for more than three months. Talk to your doctor before taking any high doses of vitamin D.
The sun is your best source for vitamin D but you shouldn’t sit in the sun for longer than 30 minutes per day without adequate protection, such as sun creams and screens. You can also acquire vitamin D from the foods you eat. Fatty fish, such as salmon and tuna, fish liver oils, vitamin D fortified milk and eggs are good vitamin D sources.

Further Reading

Last Updated: Aug 23, 2018

Causes of Hand Pain

Causes of Hand Pain

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Causes of Hand Pain

There are various possible causes of hand pain, including injury to the hand, autoimmune conditions, arthritic conditions and damage to the nerves or tendons that serve the hands. The most common causes of hand pain are described in more detail in this article.

Fractures, dislocation or injury

A fracture or dislocation of one of the bones in the hand is a common cause of hand pain. This is usually associated with severe pain, and often there is inflammation and tenderness in the area. In most cases, patients with a fracture or dislocation of the hand will know the cause of the pain as there will be a particular incident that caused the injury.
Hand fracture x-ray
X-ray showing fracture of middle finger.

Gout

Gout is a type of arthritis that involves the formation of monosodium urate crystals in the body, due to the accumulation of excessive uric acid in the bloodstream. When these crystals are formed near or inside the joints of the fingers or wrist, they can cause severe hand pain.

Carpal tunnel syndrome

Carpal tunnel syndrome involves compression of the nerve that carries messages of sensation and movement to the hand. This can lead to sensations of pain, numbness, or tingling in the hands and fingers. In most cases the thumb, index finger, middle finger and ring finger, are affected. It tends to develop gradually and is often worse at night-time.


Osteoarthritis

Hand pain can be caused by osteoarthritis, which is a condition involving inflammation, swelling and bending of the joints. It can affect any joint in the body and commonly affects the joints at the middle and end of the fingers and the base of the thumb, leading to pain in these areas. Some patients may also develop a bump at the base of the thumb, which can be particularly painful during activities that involve the hands, such as writing.

Rheumatoid arthritis

Rheumatoid arthritis is an autoimmune disease that involves the destruction of the cells that line and support the joints, which can lead to pain and inflammation in the hands. Hand pain caused by rheumatoid arthritis is often described as throbbing or aching and is usually worse in the morning, or when the joints have been inactive for an extended period of time.

Lupus

Lupus is an autoimmune disease that can lead to inflammation and destruction of the joints in the wrist and fingers, which can lead to hand pain.

Ganglion

A ganglion that develops close to a joint or tendon in the hands can cause pain in the area. In such cases, a small lump develops under the skin that is composed of encapsulated synovial fluid. This fluid is a viscous clear liquid that is secreted inside the joint cavities of synovial joints. It usually provides lubrication and cushioning to the joints. Ganglions most frequently develop on the wrists, hands, and fingers, causing hand pain.
Ganglion
Ganglion cyst on the back of hand.

Stenosing tenosynovitis

Stenosing tenosynovitis, also known as trigger finger, is a condition that involves clicking or locking of a tendon when the connected finger or thumb is moved towards the palm. This can cause pain and stiffness in the hand, usually at the base of the finger that is affected.

Tenosynovitis

Hand pain may sometimes be caused by tenosynovitis, which is a condition that involves inflammation of the fibrous sheath surrounding a tendon in the body, such as those that occur in the wrist or the fingers.

De Quervain’s disease

De Quervain’s disease is a condition that involves swelling and thickening of the sheath that surrounds the tendons of the thumb near the wrist. This can cause pain in the thumb, wrist and hand. It differs from tenosynovitis in that it is not caused by inflammation.

Raynaud’s phenomenon

Raynaud’s phenomenon is a condition that is brought about by the narrowing of the blood vessels that supply the peripheral areas of the body, such as the hands. This effect is worsened when the person is exposed to cold temperatures or stress. It can lead to discoloration, numbness, and pain in the hands.

References

  1. http://www.arthritis.org/about-arthritis/where-it-hurts/wrist-hand-and-finger-pain/causes/hand-wrist-arthritis.php
  2. http://www.arthritis.org/about-arthritis/where-it-hurts/wrist-hand-and-finger-pain/causes/hand-wrist-injury.php
  3. http://www.nhs.uk/conditions/hand-pain/Pages/Introduction.aspx
  4. https://www.healthlinkbc.ca/health-topics/handp
  5. http://my.clevelandclinic.org/health/diseases_conditions/hic_Arthritis/hic_Arthritis_of_the_Hand_and_Wrist

Further Reading

Last Updated: Aug 23, 2018

Rheumatoid Arthritis Skin Problems

Rheumatoid Arthritis Skin Problems

News-Medical

Rheumatoid Arthritis Skin Problems

Rheumatoid arthritis (RA) is a systemic autoimmune illness. It is the result of the body’s immune system producing antibodies against its own antigens, causing damage to the target organs. Like most other autoimmune diseases, RA occurs three times more often in women as compared to men.
Symptoms of RA include chronic progressive joint pain, severe joint inflammation and in many cases, total loss of joint function.
Most cases of RA show symmetrical joint involvement. The pain of RA is typically worse on waking. RA, in contrast to osteoarthritis, which also causes joint inflammation and pain, causes symptoms in a host of organs than just the joints.
RA is thus associated with a number of skin conditions highlighted below. In general, the severity of skin involvement indicates to which form the RA belongs:

Rheumatoid Nodules (Subcutaneous Nodules)

These are the most common dermatological manifestation of RA, affecting up to one-fifth of patients with RA. These firm subcutaneous nodules of tissue arise most frequently over joints affected by RA. Therefore, they are most commonly found over the elbow, finger, or behind the heel. More rarely, nodules may develop on the vocal cords and in the lungs. These nodules are generally non-tender and painless. It is uncommon that the patient experiences pain related to the nodules, and in the rarest of situations does the skin over the nodule show signs of infection or ulceration.
Small nodules are usually not treated. Larger ones may be treated with corticosteroid injections into the lesions, or with anti-rheumatic drugs. If a nodule is painful or infected, as may occur when it is subjected to friction or repeated trauma, it may require surgical excision.

Rheumatoid Vasculitis

Approximately 1 in 100 people with RA show signs of rheumatoid vasculitis (RV). It is an uncommon complication of RA, therefore. Yet, in a few patients, the presence of subcutaneous nodules indicates RV.
This is a complication seen most typically in severe and long-standing RA. It refers to the inflammation of blood vessels in the skin along with joint inflammation. The vessels most commonly affected in this manner are those that supply blood to the nerves and to numerous organs, in addition to the skin. RV can thus impact the peripheral nervous system, the blood vessels that supply the extremities (fingers and toes), causing a pitted appearance, redness, or sores that form on the fingertips and around the nails. In more serious cases it may even cause digital ischemia. In some patients with RA, it may affect larger vessels. In these individuals, sensitive rashes may form on  areas such as the legs. More alarming manifestations include the formation of ulcers which have the potential to become infected, or the appearance of scleritis, namely, inflammation of the white part of the eye.

Pharmaceutical Side Effects

Many of the skin conditions that are seen in RA sufferers are caused by the prescription medications that they take to ease symptoms or control the disease.
Skin rashes are a common manifestation of RA. They may be a sign of an allergic reaction to a drug. Following the assessment of the type of rash and its severity, it may be necessary to lower the dosage of a prescribed medication, or even to stop it entirely.  In some cases, the administration of anti-histamines or corticosteroids may be required to arrest the cutaneous drug reaction.
Some drugs which may be responsible for such skin rashes include:
  • Celecoxib
  • Ibuprofen
  • Minocycline
  • Naproxen

References

Further Reading

Last Updated: Aug 23, 2018