treatment for rheumatoid arthritis

Clinical History

A 73-year-old woman comes into the clinic in the afternoon. She complains that all her hand and foot joints are painful. Most of her hand joints and foot joints are red, warm and swollen. On the back of her right hand, there is a 1.3 cm diameter red nodule. She says that when she wake up in the morning, her hands and feet are very stiff, and she couldn't move them a lot until about an hour later, but elbows and knees are okay. She says her mouth is always dry and feels weak all day. Because of the dexterity problem, she is not willing to brush her tooth as often, and has bad oral hygiene.

Investigations

Physical appearance

Her hand joints are stiff. Little movement can occur. The joints are also red, swollen and warm

Her foot joints are also swollen and stiff.

There is a nodule on your right hand

Radiology

Radiology results of the patient's hand joints

Articular plates are destroyed.

Multiple finger joints are involved.

Affected joints are bilateral and symmetrical.

Blood test

Rheumatoid factor is positive.

Anti-citrullinated protein antibodies is positive.

Anti-CCP (cyclic citrullinated peptide) test and theAnti-MCVassay are positive.

Antibody against double stranded DNA is negative.

Discussion with clinico-pathological correlations and prognosis

This woman is diagnosed with rheumatoid arthritis.

Etiology

The etiology of the disease is not entirely known, but it is suspected that the patients are mostly genetically dispositional. Those genes include HLA-DR4 and its related MHC II, and T cell protein PTPN22 gene. One of the most suspected triggers of the disease are microbial infections. The hypothesis suggests that after a patient is infected by certain microbial, humeral immune system is activated, antibodies are produced against the infecting microbial. However, there is a cross-link in between infectious molecule and articular joint tissue. The antibodies start to attack patients' own tissue and become an auto-immune disease. The suspected triggering microbials include Epstein-Barr virus, Human Herpes virus 6, Mycroplasma, Erysipelothrix, parvovirus B19 and rubella. After the triggering microbials are eliminated, the antibody producing B cells persist to exist and start to attack small joints which contain tissues resemble the molecules on the triggering microbials. Those affected small joints are filled with macrophages that's activated by IgG

Pannus which are granulation tissue at the side of the synovial lining start to cover and eat away the articulate cartilage. Rise bodies are also in some of the cases.

Differential diagnosis

Rheumatoid arthritis is different from osteoarthritis, the latter one usually happens on big joints like knee joints and non-bilateral. Immune response is not involved, so rheumatoid factor will not be found.

Systematic Lupus sometimes resembles RA, but blood test will show anti double stranded DNA positive.

Treatment

There is currently no cure for rheumatoid arthritis. Different medicine and therapies are used to reduce the syndrome and modify the progression of the disease.

Non-steroidal anti-inflammatory drugs are widely used to control the inflammation of the joints. They are also used as analgesics. Examples are Aspirin and Advil. Their side effects include bleeding and mucosal ulcers. Analgesicsa are often used in combination with NSAIDs to reduce the joint pains. Glucocorticoids(prednisone) are used to effectively reduce the immune response against the joints. But the problem with it is long-term immune suppression and adrenal suppression. Moon-face and buffalo hump also present in long-term glucocorticoid users.

Many cytokine blockers are used to reduce immune responses. They include tumor necrosis factor alpha blockers, interleukin 6 blockers, and interleukin 1 blockers. Their usage associates with suppressed immune response to other infectious diseases.

Cytotoxic drugs, for example cylcophosphamide, are occasionally used in severe patients. They are well known for bone marrow toxicity and cause liver damages.

Complications

Chronic inflammation can affect other organ systems.

Rheumatoid arthritis patients are more likely to get arthrosclerosis due to high concentration of inflammatory mediators in the blood stream. Thus those patients are more likely to get ischemic heart disease, myocardial infarction, endocarditis and pericarditis.

Lung nodules, pulmonary effusions, and lung fibrosis are known to be caused by rheumatoid arthritis and its therapies.

Antibody and rheumatoid factors deposition inside the kidney will cause renal amyloidosis, which ultimately leads to renal failure. Some drugs might cause nephropathy.

Anemia is also likely to happen because of the toxicity of the cytotoxic drugs, which is toxic to the bone marrow and blood cell productions.

Because of inflammatory mediator and possibly glucocorticoid, it will also cause osteoporosis in patients

Prognosis

The outcome of the disease is highly variable, 10% of the patients will experience reemission after one to two years. 10% of the patients will become severely disabled. The life spans of the patients will be expected to be ten to fifteen years shorter

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