Different Types of Arthritis and Its Homeopathic Management by Dr Mujeeb Rehuman

Arthritis is a group of conditions involving damage to the joints of the body. Arthritis is the leading cause of disability in people older than fifty-five years.

There are different forms of arthritis; each has a different cause. The most common form of arthritis, Osteoarthritis (degenerative joint disease) is a result of trauma to the joint, infection of the joint, or age. Emerging evidence suggests that abnormal anatomy might contribute to the early development of osteoarthritis.

Other arthritis forms are Rheumatoid arthritis and Psoriatic arthritis, autoimmune diseases in which the body attacks itself. Septic arthritis is caused by joint infection.

Gouty arthritis is caused by deposition of uric acid crystals in the joint, causing inflammation. There is also an uncommon form of gout caused by the formation of rhomboid crystals of calcium pyrophosphate. This gout is known as Pseudogout.

HISTORY AND PHYSICAL EXAMINATION

All arthritides feature pain. Pain patterns may differ depending on the arthritides and the location. Rheumatoid arthritis is generally worse in the morning and associated with stiffness; in the early stages, patients often have no symptoms after a morning shower. In the aged and children, pain might not be the main presenting feature; the aged patient simply moves less, the infantile patient refuses to use the affected limb.

Elements of the history of the disorder guide diagnosis. Important features are speed and time of onset, pattern of joint involvement, symmetry of symptoms, early morning stiffness, tenderness, gelling or locking with inactivity, aggravating and relieving factors, and other systemic symptoms. Physical examination may confirm the diagnosis, or may indicate systemic disease. Radiographs are often used to follow progression or assess severity in a more quantitative manner.

Extra articular features

cutaneous nodules

cutaneous vasculitic lesions

lymphadenopathy

oedema

ocular inflammation

urethritis

tenosynovitis (tendon sheath effusions)

bursitis (swollen bursa)

diarrhea

orogenital ulceration

OSTEOARTHRITIS(OA)

Osteoarthritis (OA, also known as degenerative arthritis, degenerative joint disease), is a clinical syndrome in which low-grade inflammation results in pain in the joints, caused by abnormal wearing of the cartilage that covers and acts as a cushion inside joints and destruction or decrease of synovial fluid that lubricates those joints. As the bone surfaces become less well protected by cartilage, the patient experiences pain upon weight bearing, including walking and standing. Due to decreased movement because of the pain, regional muscles may atrophy, and ligaments may become more lax.

"Osteoarthritis" is derived from the Greek word "osteo", meaning "of the bone", "arthro", meaning "joint", and "itis", meaning inflammation, although many sufferers have little or no inflammation... A common misconception is that OA is due solely to wear and tear, due to the fact that OA typically is not present in younger people. However, while age is correlated with OA incidence, this merely illustrates that OA is a process that takes time to develop. There is usually an underlying cause for OA, in which case it is described as secondary OA. If no underlying cause can be identified it is described as primary OA. "Degenerative arthritis" is often used as a synonym for OA, but the latter involves both degenerative and regenerative changes.

Causes

Although it commonly arises from trauma, osteoarthritis often affects multiple members of the same family, suggesting that there is hereditarysusceptibility to this condition. A number of studies have shown that there is a greater prevalence of the disease between siblings and especially identical twins, indicating a hereditary basis . Up to 60% of OA cases are thought to result from genetic factors. Researchers are also investigating the possibility of allergies, infections, or fungi as a cause.

Signs and Symptoms

The main symptom is acute pain, causing loss of ability and often stiffness. "Pain" is generally described as a sharp ache, or a burning sensation in the associated muscles and tendons. OA can cause a crackling noise (called "crepitus") when the affected joint is moved or touched, and patients may experience muscle spasm and contractions in the tendons. Occasionally, the joints may also be filled with fluid. Humid weather increases the pain in many patients.

OA commonly affects the hips, feet, spine, and the large weight bearing joints, such as the hips and knees, although in theory, any joint in the body can be affected. As OA progresses, the affected joints appear larger, are stiff and painful, and usually feel worse, the more they are used throughout the day, thus distinguishing it from rheumatoid arthritis.

In smaller joints, such as at the fingers, hard bony enlargements, called Heberden's nodes (on the distal interphalangeal joints) and/orBouchard's nodes (on the proximal interphalangeal joints), may form, and though they are not necessarily painful, they do limit the movement of the fingers significantly. OA at the toes leads to the formation of bunions, rendering them red or swollen. OA is the most common cause of water on the knee, an accumulation of excess fluid in or around the knee joint.

Types of OA

Primary

This type of OA is a chronic degenerative disorder related to but not caused by aging, as there are people well into their nineties who have no clinical or functional signs of the disease. As a person ages, the water content of the cartilage decreases due to a reduced proteoglycan content, thus causing the cartilage to be less resilient. Without the protective effects of the proteoglycans, the collagen fibers of the cartilage can become susceptible to degradation and thus exacerbate the degeneration. Inflammation of the surroundingjoint capsule can also occur, though often mild (compared to that which occurs in rheumatoid arthritis). This can happen as breakdown products from the cartilage are released into the synovial space, and the cells lining the joint attempt to remove them. New bone outgrowths, called "spurs" or osteophytes, can form on the margins of the joints, possibly in an attempt to improve the congruence of the articular cartilage surfaces. These bone changes, together with the inflammation, can be both painful and debilitating.

Secondary

This type of OA is caused by other factors but the resulting pathology is the same as for primary OA:

§  Congenital disorders, such as:

§  Congenital hip luxation

§  People with abnormally-formed joints (e.g. hip dysplasia (human)) are more vulnerable to OA, as added stress is specifically placed on the joints whenever they move. [However, recent studies have shown that double-jointedness may actually protect the fingers and hand from osteoarthritis.]

§  Cracking joints—the evidence is weak at best that this has any connection to arthritis.

§  Diabetes.

§  Inflammatory diseases (such as Perthes' disease), (Lyme disease), and all chronic forms of arthritis (e.g. costochondritis, gout, and rheumatoid arthritis). In gout, uric acid crystals cause the cartilage to degenerate at a faster pace.

§  Injury to joints, as a result of an accident.

§  A joint infection, e.g. from an injury.

§  Hormonal disorders.

§  Ligamentous deterioration or instability may be a factor.

§  Obesity. Obesity puts added weight on the joints, especially the knees.

§  Sports injuries, or similar injuries from exercise or work. Certain sports, such as running or football, put undue pressure on the knee joints. Injuries resulting in broken ligaments can lead to instability of the joint and over time to wear on the cartilage and eventually osteoarthritis.

§  Pregnancy

§  Alkaptonuria

§  Hemochromatosis and Wilson's disease

Diagnosis

Diagnosis is normally done through x-rays. This is possible because loss of cartilage, subchondral ("below cartilage") sclerosis, subchondralcysts from synovial fluid entering small microfractures under pressure, narrowing of the joint space between the articulating bones, and bone spur formation (osteophytes) - from increased bone turnover in this inflammatory condition, show up clearly on x-rays. Plain films, however, often do not correlate well with the findings of physical examination of the affected joints.

With or without other techniques, such as MRI (magnetic resonance imaging), arthrocentesis and arthroscopy, diagnosis can be made by a careful study of the duration, location, the character of the joint symptoms, and the appearance of the joints themselves. As yet, there are no methods available to detect OA in its early and potentially treatable stages.

In 1990, the College of Rheumatology, using data from a multi-center study, developed a set of criteria for the diagnosis of hand osteoarthritis based on hard tissue enlargement and swelling of certain joints. These criteria were found to be 92% sensitive and 98%specific for hand osteoarthritis versus other entities such as rheumatoid arthritis and spondyloarthropities.

Related pathologies whose names may be confused with osteoarthritis include pseudo-arthrosis. This is derived from the Greek words pseudo, meaning "false", and arthrosis, meaning "joint." Radiographic diagnosis results in diagnosis of a fracture within a joint, which is not to be confused with osteoarthritis which is a degenerative pathology affecting a high incidence of distal phalangeal joints of female patients.

RHEUMATOID ARTHRITIS (RA)

Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disorder that causes the immune systemto attack the joints, where it causes inflammation (arthritis) and destruction. It can also damage some organs, such as the lungs and skin. It can be a disabling and painful condition, which can lead to substantial loss of functioning and mobility. It is diagnosed with blood tests (especially a test calledrheumatoid factor) and X-rays. Diagnosis and long-term management are typically performed by arheumatologist, an expert in the diseases of joints and connective tissues.

The name is based on the term "rheumatic fever", an illness which includes joint pain and is derived from the Greek word rheumatos ("flowing"). The suffix-oid  ("resembling") gives the translation as joint inflammation that resembles rheumatic fever.

Signs and Symptoms

While rheumatoid arthritis primarily affects joints, problems involving all other organs of the body are known to occur. Extra-articular ("outside the joints") manifestations occur in about 15% of individuals with rheumatoid arthritis. It can be difficult to determine whether disease manifestations are directly caused by the rheumatoid process itself, or from side effects of the medications commonly used to treat it - for example, lung fibrosis from methotrexate, or osteoporosis from corticosteroids.

Joints

The arthritis of rheumatoid arthritis is due to synovitis, which is inflammation of the synovial membrane that covers the joint. Joints become red, swollen, tender and warm, and stiffness prevents their use. By definition, RA affects multiple joints (it is a polyarthritis). Most commonly, small joints of the hands, feet and cervical spine are affected, but larger joints like the shoulder and knee can also be involved, differing per individual. Eventually, synovitis leads to erosion of the joint surface, causing deformity and loss of function.

Inflammation in the joints manifests itself as a soft, "doughy" swelling, causing pain and tenderness to palpation and movement, a sensation of localized warmth, and restricted movement. Increased stiffness upon waking is often a prominent feature and may last for more than an hour. These signs help distinguish rheumatoid from non-inflammatory diseases of the joints such as osteoarthritis (sometimes referred to as the "wear-and-tear" of the joints). In RA, the joints are usually affected in a fairly symmetrical fashion although the initial presentation may be asymmetrical.

As the pathology progresses the inflammatory activity leads to erosion and destruction of the joint surface, which impairs their range of movement and leads to deformity. The fingers are typically deviated towards the little finger (ulnar deviation) and can assume unnatural shapes. Common deformities in rheumatoid arthritis are the Boutonniere deformity (Hyperflexion at the proximal interphalangeal joint with hyperextension at the distal interphalangeal joint), swan neck deformity (Hyperextension at the proximal interphalangeal joint, hyperflexion at the distal interphalangeal joint). The thumb may develop a "Z-thumb" deformity with fixed flexion and subluxation at the metacarpophalangeal joint, and hyperextension at the IP joint.

Skin

The rheumatoid nodule is the cutaneous (strictly speaking subcutaneous) feature most characteristic of rheumatoid arthritis. The initial pathologic process in nodule formation is unknown but is thought to be related to small-vessel inflammation. The mature lesion (a part of an organ or tissue which has been damaged) is defined by an area of central necrosis surrounded by palisading macrophages and fibroblasts and a cuff of cellular connective tissue and chronic inflammatory cells. The typical rheumatoid nodule may be a few millimetres to a few centimetres in diameter and is usually found over bony prominences, such as the olecranon, the calcaneal tuberosity, the metacarpophalangeal joints, or other areas that sustain repeated mechanical stress. Nodules are associated with a positive RF titer and severe erosive arthritis. Rarely, they can occur in internal organs.

Several forms of vasculitis are also cutaneous manifestations associated with rheumatoid arthritis. A benign form occurs as microinfarcts around the nailfolds. More severe forms include livedo reticularis, which is a network (reticulum) of erythematous to purplish discoloration of the skin due to the presence of an obliterative cutaneous capillaropathy.

Other, rather rare, skin associated symtoms include:

§  pyoderma gangrenosum, a necrotizing, ulcerative, noninfectious neutrophilic dermatosis.

§  Sweet's syndrome, a neutrophilic dermatosis usually associated with myeloproliferative disorders

§  drug reactions

§  erythema nodosum

§  lobular panniculitis

§  atrophy of digital skin

§  palmar erythema

§  diffuse thinning (rice paper skin), and skin fragility (often worsened by corticosteroid use).

Lungs

Fibrosis of the lungs is a recognised response to rheumatoid disease. It is also a rare but well recognised consequence of therapy (for example with methotrexate and leflunomide). Caplan's syndrome describes lung nodules in individuals with rheumatoid arthritis and additional exposure to coal dust. Pleural effusions are also associated with rheumatoid arthritis.

Kidneys

Renal amyloidosis can occur as a consequence of chronic inflammation. Rheumatoid vasculitis is a rare cause of glomerular disease in the kidney. Treatment with Penicillamine and gold salts are recognized causes of membranous nephropathy

Heart and blood vessels

People with rheumatoid arthritis are more prone to atherosclerosis, and risk of myocardial infarction (heart attack) and stroke is markedly increased. Other possible complications that may arise include: pericarditis, endocarditis, left ventricular failure, valvulitis andfibrosis

Other Features

Ocular

Keratoconjunctivitis sicca (dry eyes), scleritis, episcleritis and scleromalacia.

Gastrointestinal and hematological

Felty syndrome, anemia, thrombocytosis.

Neurological

Peripheral neuropathy and mononeuritis multiplex may occur. The most common problem is carpal tunnel syndrome due to compression of the median nerve by swelling around the wrist. Atlanto-axial subluxation can occur, owing to erosion of the odontoid process and or/transverse ligaments in the cervical spine's connection to the skull. Such an erosion (>3mm) can give rise to vertebrae slipping over one another and compressing the spinal cord. Clumsiness is initially experienced, but without due care this can progress to quadriplegia.

Constitutional symptoms

Constitutional symptoms including fatigue, low grade fever, malaise, morning stiffness, loss of appetite and loss of weight are common systemic manifestations seen in patients with active rheumatoid arthritis.

Vasculitis

Vasculitis in rheumatoid arthritis is common. It typically presents as vasculitic nailfold infarcts.

Osteoporosis

Osteoporosis classically occurs in RA around inflamed joints. It is postulated to be partially caused by inflammatory cytokines.

Lymphoma

The incidence of lymphoma is increased in RA as it is in most autoimmune conditions

Diagnosis

X-rays

X-rays of the hands and feet are generally performed in people with a polyarthritis. In rheumatoid arthritis, these may not show any changes in the early stages of the disease, but in more advanced cases demonstrates erosions and bone resorption. X-rays of other joints may be taken if symptoms of pain or swelling occur in those joints

Blood tests

When RA is clinically suspected, immunological studies are required, such as testing for the presence of rheumatoid factor (RF, a specific antibody). A negative RF does not rule out RA; rather, the arthritis is called seronegative. This is the case in 69% of patients. During the first year of illness, rheumatoid factor is frequently negative. 80% of these individuals eventually convert to seropositive status. RF is also seen in other illnesses, for example Sjögren's syndrome, and in approximately 10% of the healthy population, therefore the test is not very specific.

Because of this low specificity, a new serological test has been developed, which tests for the presence of so called anti-citrullinated protein antibodies (ACPAs). Like RF, this test is positive in only a proportion (67%) of all RA cases, but is rarely positive if RA is not present, giving it a specificity of around 95%. In addition, ACPAs can sometimes be detected in early stages of the disease, even before onset of clinical disease. Currently, the most common test for ACPAs is the anti-CCP (cyclic citrullinated peptide) test.

Also, several other blood tests are usually done to allow for other causes of arthritis, such as lupus erythematosus. The erythrocyte sedimentation rate (ESR), C-reactive protein, full blood count, renal function, liver enzymes and other immunological tests (e.g. antinuclear antibody/ANA) are all performed at this stage. Elevated ferritin levels can reveal hemochromatosis, a mimic RA, or be a sign of Still's diseasea seronegative, usually juvenile, variant of rheumatoid.

Diagnostic criteria

The American College of Rheumatology has defined (1987) the following criteria for the classification of rheumatoid arthritis:

§  Morning stiffness of >1 hour most mornings for at least 6 weeks.

§  Arthritis and soft-tissue swelling of >3 of 14 joints/joint groups, present for at least 6 weeks

§  Arthritis of hand joints, present for at least 6 weeks

§  Symmetric arthritis, present for at least 6 weeks

§  Subcutaneous nodules in specific places

§  Rheumatoid factor at a level above the 95th percentile

§  Radiological changes suggestive of joint erosion

At least four criteria have to be met for classification as RA. These criteria are not intended for the diagnosis for routine clinical care; they were primarily intended to categorize research. For example: one of the criteria is the presence of bone erosion on X-Ray. Prevention of bone erosion is one of the main aims of treatment because it is generally irreversible. To wait until all of the ACR criteria for rheumatoid arthritis are met may sometimes result in a worse outcome. Most sufferers and rheumatologists would agree that it would be better to treat the condition as early as possible and prevent bone erosion from occurring, even if this means treating people who don't fulfill the ACR criteria. The ACR criteria are, however, very useful for categorising established rheumatoid arthritis, for example for epidemiological purposes

Differential diagnosis

Several other medical conditions can resemble RA, and usually need to be distinguished from it at the time of diagnosis:

§  Crystal induced arthritis (gout, and pseudogout) - usually involves particular joints and can be distinguished with aspiration of joint fluid if in doubt

§  Osteoarthritis - distinguished with X-rays of the affected joints and blood tests

§  Systemic lupus erythematosus (SLE) - distinguished by specific clinical symptoms and blood tests (antibodies against double-stranded DNA)

§  One of the several types of psoriatic arthritis resembles RA - nail changes and skin symptoms distinguish between them

§  Lyme disease causes erosive arthritis and may closely resemble RA - it may be distinguished by blood test in endemic areas

§  Reactive arthritis (previously Reiter's disease) - asymmetrically involves heel, sacroiliac joints, and large joints of the leg. It is usually associated with urethritis, conjunctivitis, iritis, painless buccal ulcers, and keratoderma blennorrhagica.

§  Ankylosing spondylitis - this involves the spine and is usually diagnosed in males, although a RA-like symmetrical small-joint polyarthritis may occur in the context of this condition.

Rarer causes that usually behave differently but may cause joint pains:

§  Sarcoidosis, amyloidosis, and Whipple's disease can also resemble RA.

§  Hemochromatosis may cause hand joint arthritis.

§  Acute rheumatic fever can be differentiated from RA by a migratory pattern of joint involvement and evidence of antecedent streptococcalinfection. Bacterial arthritis (such as streptococcus) is usually asymmetric, while RA usually involves both sides of the body symmetrically.

§  Gonococcal arthritis (another bacterial arthritis) is also initially migratory and can involve tendons around the wrists and ankles.

GOUT

Gout (metabolic arthritis) is a disease created by a buildup of uric acid. In this condition, crystals of monosodium urate or uric acid are deposited on the articular cartilage of joints, tendons and surrounding tissues. These crystals cause inflammation and pain, both severe. If unchecked, the crystals form tophi, which can cause significant tissue damage. Gout results from a combination of elevated concentrations of uric acid and and overall acidity in the bloodstream. In isolation, neither elevated uric acid (hyperuricemia) nor acidity is normally sufficient to cause gout.

Signs and symptoms

Gout is characterized by excruciating, sudden, unexpected, burning pain, as well as swelling, redness, warmth, and stiffness in the affected joint. This occurs commonly in men in their toes but can appear in other parts of the body and affects women as well. Low-grade fever may also be present. The patient usually suffers from two sources of pain. The crystals inside the joint cause intense pain whenever the affected area is moved. The inflammation of the tissues around the joint also causes the skin to be swollen, tender and sore if it is even slightly touched. For example, a blanket or even the lightest sheet draping over the affected area could cause extreme pain.

Gout usually attacks the big toe (approximately 75 percent of first attacks); however, it also can affect other joints such as the ankle, heel, instep, knee, wrist, elbow, fingers, and spine. In some cases, the condition may appear in the joints of small toes that have become immobile due to impact injury earlier in life, causing poor blood circulation that leads to gout.

Patients with long-standing hyperuricemia (see below) can have uric acid crystal deposits called tophi(singular: tophus) in other tissues such as the helix of the ear. Elevated levels of uric acid in the urine can lead to uric acid crystals precipitating in the kidneys or bladder, forming uric acid kidney stones.

Pathophysiology

Gout occurs when crystals of uric acid, in the form of mono-sodium urate, precipitate on the articular cartilage of joints, on tendons, and in the surrounding tissues. Uric acid is a normal component ofblood serum. Uric acid is more likely to form into crystals when there is hyperuricemia, although hyperuricemia is 10 times more common without clinical gout than with it. Gout can also occur when serum uric acid is normal, and when it is abnormally low (hypouricemia). Paradoxically, acute attacks of gout can occur together with a sudden decrease in serum uric acid, such as due to use of drugs (uricosurics, xanthine oxidase inhibitors), or total parenteral nutrition. However, correlation does not imply causation. The sudden decrease may be a consequence of abrupt formation of crystals (removing uric acid from the serum), rather than a cause.

Regardless of the serum concentration of uric acid, precipitation of uric acid is markedly enhanced when the blood pH is low (acidosis). A similar pH-sensitive effect occurs in urine, contributing touric acid nephrolithiasis.

Uric acid is a product of purine metabolism, and in humans is normally excreted in the urine. Purinesare generated by the body via breakdown of cells in normal cellular turnover, and also are ingested as part of a normal diet. The kidneys are responsible for approximately two-third of uric acid excretion, with the gut responsible for the rest.

Causes

Gout may be primary (including idiopathic), or secondary to (a complication of) another condition.

Primary gout

The high levels of uric acid in the blood are caused by protein rich foods. Alcohol intake often causes acute attacks of gout and hereditary factors may contribute to the elevation of uric acid. Typically, persons with gout are obese, predisposed to diabetes and hypertension, and at higher risk of heart disease. Gout is more common in affluent societies due to a diet rich in proteins, fat, and alcohol. When it follows as a consequence of other health conditions such as renal failure, it is often regardless of the person's lifestyle. Lin, et al have statistical evidence linking gout to lead poisoning, and lead level in the body is significantly correlated with urate excretion and gout. It is known that lead sugarwas used to sweeten wine, and that chronic lead poisoning is a cause of gout, and condition is then known as saturnine gout, because of its association with lead (Saturnus was the alchemists' term for the metal lead).

Diuretics (particularly thiazide diuretics) have traditionally been blamed for precipitating attacks of gout because they compete at the same transporter, but a Dutch case-control study from 2006 appears to cast doubt on this conclusion.

Secondary gout

Secondary gout is a complication of another medical conditions. Medical conditions that commonly result in gout include:

§  Metabolic syndrome (combining obesity and hyperuricemia)

§  Leukemia

§  Inborn errors of purine-pyrimidine metabolism

Gout also can develop as co-morbidity of other diseases, including polycythaemia, intake of cytotoxics, obesity, diabetes, hypertension, renaldisorders, and hemolytic anemia.

Diagnosis

Clinically, gout can be hard to distinguish from several other conditions, including chondrocalcinosis. Chondrocalcinosis is a very similar disease, caused by deposition of calcium pyrophosphate rather than uric acid.

Hyperuricemia is a common feature of gout, so its presence supports a diagnosis of gout. However, gout can occur without hyperuricemia. Hyperuricemia is defined as a plasma urate (uric acid) level greater than 420 μmol/L (7.0 mg/dL) in males, or 380 μmol/L in females. However, a high uric acid level does not necessarily mean a person will develop gout. Urate is within the normal range in up to two-thirds of cases. If gout is suspected, the serum urate test should be repeated once the attack has subsided. Other blood tests commonly performed are full blood count, electrolytes, renal function, thyroid function tests and erythrocyte sedimentation rate (ESR). This helps to exclude other causes ofarthritis, most notably septic arthritis, and to investigate any underlying cause for the hyperuricaemia.

A definitive diagnosis of gout is from light microscopy of fluid aspirated from the joints (this test may be difficult to perform) to demonstrateintracellular monosodium urate crystals in synovial fluid polymorphonuclear leukocytes. The urate crystal is identified by strong negativebirefringence under polarised microscopy and its needle-like morphology. A trained observer does better in distinguishing them from other crystals.

Pseudo gout

Calcium pyrophosphate deposition disease (CPPD) is a rheumatologic disorder with varied clinical manifestations due to precipitation of calcium pyrophosphate dihydrate crystals in the connective tissues. It is more commonly known by alternative names that specify certain clinical or radiographic findings, although neither is synonymous with CPPD. Pseudogout refers to the clinically evident acute synovitiswith red, tender, and swollen joints that may resemble gouty arthritis (a similar condition with joint deposition of monosodium urate crystals). Chondrocalcinosison the other hand, refers to the radiographic evidence of calcification in hyaline and/or fibrocartilage. Pyrophosphate arthropathy is a term that may refer to either of the above. Statistically, the interphalangeal joints are the most commonly affected.

CPDD crystal deposition disease is a polyarticular arthritis (i.e. it leads to an inflammation of several joints in the body), although it can initially present as monoarticular (i.e. confined to just one joint). CPDD crystals tend to form within articular tissues. Although, in theory, any joint may be affected, the knees, wrists, and hips are the statistically the most commonly attributed areas. In rare case, pseuogout may affect the spinal canal and cause myelopathy. The exact pathology of CPDD is unknown, although increased adenosine triphosphate (the molecule used as energy currency in all animals) breakdown, which results in increased pyrophosphate levels in joints, is thought to be a method of crystal development. There is some recent evidence suggesting that the gene ANKH is involved in crystal-related inflammatory reactions and inorganic phosphate transport.

Signs and Symptoms

Patients usually present with inflammation of one or more joints often resulting in pain in the affected joint(s). Hyperparathyroidism,hemochromatosis, hypophosphatemia and renal osteodystrophy are often also associated with chondrocalcinosis. In some cases, traumaticarthritis has resulted in chondrocalcinosis. In general, the white blood cell count is raised. Rarely, patients may also present with signs ofcarpal tunnel syndrome.

Diagnosis

Radiography has a large role to play in the diagnosis of chondrocalcinosis with radiographs, CT scans, MRIs, ultrasound and nuclear medicineall having a part. CT scans and MRIs show calcific masses (usually within the ligamentum flavum or joint capsule) however radiography is more successful. As with most conditions, chondrocalcinosis can present with similarity to other diseases such as Ankylosing spondylitis orGout.

JUVENILE IDIOPATHIC ARTHRITIS (JIA)

Juvenile idiopathic arthritis (JIA), formerly known as juvenile rheumatoid arthritis (JRA), is the most common form of persistent arthritis in children.

JIA is sometimes referred to as juvenile chronic arthritis (JCA), a term that is not precise as JIA does not encompass all forms of chronic childhood arthritis.Arthritis is the inflammation of the synovium (the lining tissues) of a joint.

JIA is a subset of arthritis seen in childhood, which may be transient and self-limited or chronic. It differs significantly from arthritis commonly seen in adults (osteoarthritis, rheumatoid arthritis), and other types of arthritis that can present in childhood which are chronic conditions (e.g. psoriatic arthritis and ankylosing spondylitis).

Etiology

The cause of JIA, as the word idiopathic suggests, is unknown and currently an area of active research. Current understanding of JIA suggests that it arises in a genetically susceptible individual due to environmental factors.

Symptoms

Symptoms of JIA are often non-specific initially, and include lethargy, reduced physical activity, and poor appetite (often due to medication). The first manifestation, particularly in young children, may be limping. Children may also become quite ill, presenting with flu-like syptoms that persist. The cardinal clinical feature is persistent swelling of the affected joint(s), which commonly include the knee,ankle, wrist and small joints of the hands and feet. Swelling may be difficult to detect clinically, especially for joints such as those of the spine,sacroiliac joints, shoulder, hip and jaw, where imaging techniques such as ultrasound or MRI are very useful.

Pain is an important feature of JIA, but young children may have difficulty in communicating this symptom. Late effects of arthritis include joint contracture (stiff, bent joint) and joint damage. Children with JIA vary in the degree to which they are affected by particular symptoms.

Types of JIA

The 3 major types of JIA are oligoarticular JIA, polyarticular JIA and systemic JIA.

JIA

Oligoarticular JIA

Polyarticular JIA

Systemic JIA

 

 

Oligoarticular (pauciarticular) JIA

Oligoarticular (or pauciarticular) JIA affects 4 or fewer joints in the first 6 months of illness. Oligo means few. It was previously known as pauciarticular JIA. Patients with oligoarticular JIA are more often ANA positive, when compared to other types of JIA.

Polyarticular JIA

Affecting 5 or more joints in the first 6 months of disease. This subtype can include the affect of the neck and jaw as well as the small joints usually affected. This type of JIA is more common in small girls to that of boys.

Systemic JIA (Still's Disease)

Is characterized by arthritis, fever and a salmon pink rash. Systemic JIA can be challenging to diagnose because the fever and rash come and go. It affects males and females equally, unlike the other two subtypes of JIA. Systemic JIA may have internal organ involvement and lead to serositis (e.g. pericarditis).

Onset

JIA occurs in both sexes. Symptoms onset is frequently dependent on the subtype of JIA (see Types of JIA) and is from the pre-school years to the early teenage years.

Extra articular manifestations

1. Eye disease: JIA is associated with inflammation in the front of the eye (chronic anterior uveitis). This complication may not have any symptoms and can be detected by an experienced ophthalmologist using a slit lamp. Most children with JIA are enrolled in a regular slit lamp screening program, as poorly controlled chronic anterior uveitis may result in permanent eye damage, including blindness.

2. Growth disturbance: Children with JIA may have reduced overall rate of growth, especially if the disease involves many joints or other body systems. Paradoxically, individually affected large joints (such as the knee) may grow faster, due to inflammation - induced, increased blood supply to the bone growth plates situated near the joints.

STILL'S DISEASE

Still's disease is a form of juvenile idiopathic arthritis, characterized by high spiking fevers and transientrashes, named after the English physician Sir George Frederic Still (1861-1941). The disease was first discovered in children, but now it is also known to occur, less commonly, in adults in whom it is referred to as adult-onset Still's disease (AOSD) described by another English physician, Bywaters in 1971 (the same author is famous for the crush syndrome). The Irish writer William Wall is a well-known sufferer of the disease.

There are several theories about the cause of Still's disease. It has been suggested it may be caused by amicrobacterial infection. However, the cause of Still's disease remains unknown. The pathogenesis of the disease is more likely to be autoimmune.

Symptoms

Patients with Still's disease usually have systemic symptoms. Usual symptoms include:

§  Waves of high fevers that rise to 40 °C (104 °F) which may be accompanied by extreme fatigue

§  A faint transient non-itching salmon-colored skin rash can also be observed

§  Flu-like pain throughout the body

§  Muscle pain

§  Severe joint pain and joint damage

Diagnosis

Because the disease presents in many different ways, diagnosis is difficult. It is often a laborious process consisting of the elimination of other diseases. It is diagnosed on a basis of clinical features of the illness, with the results of a number of common tests combined. Persistent arthritis (lasting at least 6 weeks) is frequently a symptom. A rash is frequently visible on the body, and the patients usually suffer from high, spiking fevers. Blood tests frequently indicate elevated white blood cell counts, suggesting there is serious inflammation. Also, low red blood cell counts (anemia) are common. Typically, elevated blood tests indicate in high sedimentation rates, an indicator of inflammation. Other indicators of inflammation may also be elevated, including CRP (c-reactive protein) and ferritin levels. However, the classic blood tests forrheumatoid arthritis and systemic lupus erythematosus are usually negative. A new important marker of AOSD is the glycosylated ferritin: the percentage of this form of the protein is often below the 50% of the total during the flare of the disease and often during the remission phases.

ANKYLOSING SPONDYLITIS 

Ankylosing spondylitis (AS; previously known as Bechterew's disease, Bechterew syndrome, Marie Strümpell disease and a form of Spondyloarthritis) is a chronic, painful, degenerative inflammatoryarthritis primarily affecting spine and sacroiliac joints, causing eventual fusion of the spine; it is a member of the group of the autoimmune spondyloarthropathies with a strong genetic predisposition. Complete fusion results in a complete rigidity of the spine, a condition known as bamboo spine.

Signs and Symptoms

The typical patient is young, of 20 to 40 years of age, with chronic pain and stiffness in the lower part of the spine, often with sciatic pain. Usually pain worsen with rest, and improves with physical activity, although exercise during active phases of the disease may severely limit movements. Men are affected more than women by a ratio about of 3:1. In 40% of cases, ankylosing spondylitis is associated withiridocyclitis causing eye pain and photophobia (increased sensitivity to light). Other common symptoms are recurring mouth ulcers (aphthae) and fatigue.

Typical prodromes (early symptoms) may occur at a very young age (e.g., 3 years old), when the patient may experience recurring painful joints (e.g. knees, elbows) commonly misinterpreted as simple rheumatism.AS is also associated with ulcerative colitis, Crohn's disease, psoriasis, and Reiter's disease.

Diagnosis

There is no direct test to diagnose AS. A clinical examination and X-ray studies of the spine, which show characteristic spinal changes and sacroiliitis, are the major diagnostic tools. A drawback of X-ray diagnosis is that signs and symptoms of AS have usually been established as long as 8-10 years prior to X-ray-evident changes occurring on a plain film X-ray, which means a delay of as long as 10 years before adequate therapies can be introduced. Options for more accurate (and much earlier) diagnosis are tomography and magnetic resonance imaging of the sacroiliac joints. The Schober's test is a useful clinical measure of flexion of the lumbar spine performed during examination.

During acute inflammatory periods, AS patients will usually show an increase in the blood concentration of C-reactive protein (CRP) and an increase in the erythrocyte sedimentation rate (ESR).

Variations of the HLA-B gene increase the risk of developing ankylosing spondylitis, although it is not a diagnostic test. Those with the HLA-B27 variant are at a higher risk than the general population of developing the disorder. HLA-B27, demonstrated in a blood test, is occasionally used as a diagnostic but does not distinguish AS from other diseases and is therefore not of real diagnostic value. Over 95% of people that have been diagnosed with AS are HLA-B27 positive, although this ratio varies from population to population (only 50% of African American patients with AS possess HLA-B27, and it is close to 80% among AS patients from Mediterranean countries). In early onset disease HLA-B7/B*2705 heterozygotes exhibited the highest risk for disease.

Prognosis

AS can range from mild to progressively debilitating and from medically controlled to refractive. Unattended cases of AS normally lead to knee pain and may be accompanied by dactylitis or enthesitis, which may result in a misdiagnosis of normal rheumatism. In a long-term undiagnosed period, osteopenia or osteoporosis of the AP spine may occur, causing eventual compression fractures and a back "hump" if untreated. Typical signs of progressed AS are the visible formation of syndesmophytes on X-rays and abnormal bone outgrowths similar to osteophytes affecting the spine. The fusion of the vertebrae paresthesia is a complication due to the inflammation of the tissue surrounding nerves.

Organs commonly affected by AS, other than the axial spine and other joints, are the heart, lungs, colon, and kidney. Other complications areaortic regurgitation, Achilles tendinitis, AV node block and amyloidosis. Owing to lung fibrosis, chest X-rays may show apical fibrosis whilepulmonary function testing may reveal a restrictive lung defect. Very rare complications involve neurologic conditions such as the cauda equina syndrome.

MEDICINAL MANAGEMENT

Rhus toxicodendron

From the earliest homoeopathic times Rhus has been the great rheumatic remedy of the school, comparing only with Bryonia; and the difference between these remedies must be repeated once more.

Rhus
Restlessness and desire to move about continually, on account of the relief it to the aches and pains.

Bryonia 
Disposition to keep perfectly still, since moving causes an aggravation of of all aches and yet sometimes pains force patient to move .

Rhus 
Suitable especially to rheumatism affecting fibrous tissues, sheaths of muscles etc., Rheumatism from exposure to wet when overheated and perspiring.

Bryonia
Suitable to rheumatism of the joints and of muscular tissues itself. This is not especially the case with Bryonia, though a Bryonia rheumatism from these causes.
All Rhus rheumatic symptoms are relieved by motion. They are worse from sitting and worse from rising from a sitting position, or on first commencing to move; continued motion, however, relieves. Warmth also relieves the Rhus rheumatism. Damp weather and the approach of storms aggravate. Cold also aggravates. Rhododendron is similar, in that change of weather aggravates. The character of the Rhus pains is first a stiffness and soreness. there are also tearing pains,drawing, paralyzed sensations and even stitches. The sudden pain in the back known as "crick" is met well with Rhus. Rhus has an especial affinity for the deep muscles of the back. It is perhaps the most often indicated of any remedy in lumbago. It is also, it may be mentioned in passing, a remedy for the effects of overexertion such as sprains, wrenches, etc., being to fibrous tissues what Arnica is to the softer structures. The rheumatism keeling for Rhus may appear in any part ;of the body; the lower extremities seem to have suffered most in the provers. The great keynotes of Rhus are the following: 1. Relief from continued motion; the lumbago, however, being sometimes worse from motion. 2. The stiffness and soreness. 3. The aggravation when first beginning to move.4. The aggravation from damp weather and cold. cold air is not tolerated; it seems to make the skin painful. 5. The relief of all the symptoms by warmth. Rhus will not cure every case of rheumatism, but it will cure a good many.

Bryonia

The rheumatism of Bryonia attacks the joints themselves, producing articular rheumatism, and it also inflames the muscle tissue, causing muscular rheumatism. The muscles are sores and swollen, and the joints are violently inflamed, red, swollen, shiny,l and very hot. The pains are sharp,stitching or cutting in character, and the great feature of the drug should always be present, namely the aggravation from the slightest motion. Touch and pressure also aggravate. There is but little tendency for the rheumatism of Bryonia to shift about like that of Pulsatilla or Kalmia. It is not liable to be mistaken for any other remedy. Ledum has some points of similarity. It would come in in articular rheumatism, where there is a scanty effusion, while Bryonia tends to copious exudation. Bryonia seems to suit well the acid condition of the blood, which gives rise to rheumatism; it has a sour sweat; also, Kali carbonicum has stitching pains, but absence of fever will distinguish it from Bryonia. Bryonia, Ledum, Nux and Colchicum are the four chief remedies having aggravation from motion. General constitutional symptoms will most likely be present in cases calling for Bryonia. Excessive tenderness of the soles of the feet in rheumatism may suggest antimonium crudum.

Causticum

This remedy resembles Rhus quite closely in many respects. The following are some of the differences:

Causticum
The restlessness of this remedy occurs only at night. Rheumatism caused by dry, cold frosty air. Pains impel constant motion, which does not relieve.

Rhus
Restlessness all the time. Rheumatism from damp wet weather. Motion relieves the patient temporarily. The symptoms calling for Causticum are a stiffness of the joints. The tendons seem shortened and the limbs are drawn out of shape. It is a sort ;of rheumatoid arthritis. As with Rhus, there is relief from warmth. There are drawing muscular pains sand soreness of the parts o;f which the patient lies. It has been found useful in rheumatism about the articulations of the jaw. Rhus has a cracking of the lower jaw when chewing. Colocynth has a stiffness about the joints and is also a useful remedy in articular rheumatism. Causticum, like Guaiacum and Ledum, has gouty concretions in the joints. There is much weakness and trembling with Causticum, as with all the preparations of potash, and it is ;of little use in arthritic troubles if fever be present. Weakness of the ankle-joint, contracted tendons, and a sprained feeling in the hip-joints are some of its important symptoms.

Ledum

Ledum is one of our best remedies for rheumatism ands gout, especially the latter. The great symptom which has always been regarded as the distinctive characteristic is the direction the pains takes, namely, going from below upwards. Like Caulophyllum and some others, Ledum seems to haves a predilection for the smaller joints. Nodes form in them and the pains travel up the limbs. The pains are made worse from the warmth of the bed. the effusion into the joints is scanty and it soon hardens and forms the nodosities above mentioned. Ledum, like Colchicum, causes acute, tearing pains in the joints; weakness of the limbs and numbness and coldness of the surface. Kalmia also has pains which travel upwards, but the character of the pains will distinguish. It may also be mentioned that Ledum is an excellent remedy in erythema nodosum, which is of rheumatic origin. Ledum produces and cures in certain cases an obstinate swelling of the feet. Wine aggravates all the symptoms of this drug. The characteristics of
Ledum may be thus summed up: 1. Upward extension of the pains 2. Tendency to the formation of nodes in the small joints. 3. Aggravation ;by the warmth ;of the bed. 4. Aggravation by motion. It is useful, too, after the abuse of Colchicum in large doses.

Pulsatilla

Pulsatilla is usually brought prominently to mind when there is a tendency for the rheumatism to shift about, wandering rheumatic pains being one of its red strings. But other remedies have this symptom also, prominent among them being Kalmia, Bryonia, Colchicum, Sulphur, Kali bichromicum and that member of the tissue family most resembling Pulsatilla, namely, Kali sulphuricum. There is little trouble in distinguishing Pulsatilla from any or all of these remedies by its general symptoms. Kali sulphuricum, however, will give the most trouble, but it is not a well-proven remedy and need only be thought of to try when Pulsatilla seems the remedy yet fails. Other characteristics of the Pulsatilla rheumatism are the aggravation from warmth, aggravation in the evening, and the relief from cold. The knee, ankle and tarsal joints are the most usual seat of the trouble when Pulsatilla is indicated. There is, too a restlessness with the remedy, the pains are so severe that the patient is compelled to moves, and slow, easy motion relieves, as also with Lycopodium and Ferrum. A prominent use for Pulsatilla is in gonorrhoeal rheumatism. The joints are swollen and the pains are sharp and stinging, with a feeling of subcutaneous ulceration. Kali bichromicum is also a remedy for gonorrhoeal rheumatism, as well as for wandering rheumatic pains; it has relief in a warm room, which at once distinguishes it from Pulsatilla. Thuja is another remedy for gonorrhoeal rheumatism. Rheumatism dependent on disturbance of the liver or stomach is apt to find its remedy in Pulsatilla.

Kalmia

Kalmia is another of the remedies which have wandering rheumatic pains, and it is especially useful in rheumatism affecting the chest, or when rheumatism or gout shifts from the joints to the heart, driven there perhaps by external applications. It also has tearing pains in the legs, without swelling, without fever, but with great weakness, and in this symptom of weakness it resembles colchicum. The pains about the chest in Kalmia cases shoot down into the stomach and abdomen. The muscles of the neck are sore and the back is lames. Hering says that the rheumatism of Kalmia "generally goes from the upper to the lower parts," while Farrington says, "the Kalmia rheumatism, like that of Ledum, almost always travels upwards." At any rate, the rheumatic pains are mostly in the upper parts of the arms and lower parts of the legs; and are worse when going to sleep. Inflammatory rheumatism, shifting from joint to joint, with tendency to attack the heart, high fever, excruciating pains, which, of course, are made worse by motion, will be benefited by Kalmia. In valvular deposits Kalmia and Lithium carbonicum are our foremost drugs. The Rhododendron family, furnishes us another useful rheumatic remedy, besides Ledum and Kalmia, which is Rhododendron itself. Its great keynote is its susceptibility to changes in the weather, "barometer pains,"and its pains, like Rhus, are worse during rest. It is especially adapted to rheumatism of the smaller joints, as we have already seem Ledum to be. Although Kalmia has some action on the smaller joints, it is in a less degree than Ledum or Rhododendron. Dulcamara is a prominent remedy for rheumatism, made worse by sudden changes in the weather, especially when cold and damp.

Cimicifuga

Another example of family relationship in rheumatic troubles may be found in the ranunculaceae family. Aconite is often a useful remedy in the first stage of rheumatic fever; it is homoeopathic, not only to the fever, but to the local affections caused by the rheumatic poison. It is in many cases a specific antidote to the whole condition. Dr.Jousset insists upon the efficacy of Aconite tincture in acute rheumatic fever. Pulsatilla we have already seen. Ranunculus bulbosus is especially useful in rheumatism of the muscles of the chest and trunk. There is a great deal of soreness, the muscles have a bruised feeling, and changeable, damp weather aggravates. Cimicifuga is a rheumatic remedy; its chief symptom is great aching in the muscles, and this right in the fleshy part of the muscles, the belly of the muscles rather than the extremities. It is also prone to occur in the large muscles of the trunk rather than the small muscles of the extremities, here resembling Nux vomica. It differs from Rhus by not acting on fibrous structures, being rather a remedy for muscular rheumatism. Rheumatism in the muscles, coming on suddenly and of great severity, worse at night and in wet and windy weather, will find its remedy in Cimicifuga. Actaea spicata, another of the same family, on the contrary, acts on the small joints of the hands and feet; the joints ache and swell while the patient is walking. Under Cimicifuga there is great restlessness, but motion aggravates. Caulophyllum, so similar in many other ways, differs from Cimicifuga in having rheumatism of the metacarpal and phalangeal articulations of the hand.

Colchicum

Although usually thought of in gout, Colchicum is no mean remedy in rheumatism. It has a special affinity for fibrous tissues, tendons, aponeuroses, ligaments,and periosteum. It has also shifting rheumatism like Kalmia, Pulsatilla, etc., The pains are worse in the evening; the slightest motion aggravates; the patient is irritable; the pain seems unbearable. Sometimes it is useful when the rheumatism attacks the chest, with pains about the heart and a sensation as if the heart were squeezed by a tight bandage. There is great evening aggravation; the joints are swollen and dark red. Colchicum is especially useful for rheumatic affections in debilitated persons those who ares weak-weakness being the characteristic. It is a remedy too, for the smaller joints. As we have already seen,m there are a number of remedies affecting the smaller joints of the hands and feet, such as Actaea spicata, Caulophyllum, Ledum and Rhododendron. And there are ad few more: Benzoic acid has rheumatism of the small joints,gouty nodosities, weeping sinews, cracking in joints, gouty nodosities with great characteristic accompaniment of extremely offensive urine. Ammonium phosphoricum has nodes and concretions in the joints. Lithium carbonicum also has rheumatism of the finger joints, with tendency to heart complications and it must be compared with Kalmia, Ledum and Benzoic acid in this respect; it has rheumatic soreness about the heart; recurring attacks also indicate it. Viola odorata and Ruta have rheumatism of the wrists. It is finally well to remember that Colchicum is rarely indicated early in rheumatism but later when the patient is weak and exhausted, it may do good work.

Sanguinaria

Sanguinaria inflames muscular tissue, giving a picture of acute muscular rheumatism. The muscles are sore and stiff, with flying erratic pains in them or stitching. The muscles of the back and neck are especially affected by it. The chief field of usefulness of the remedy seems to be in rheumatism affecting the right deltoid muscle. It is described as a rheumatic pain in the right arm and shoulder, worse at night or on turning in bed. It is so severe that the patient cannot raise the arm. Magnesia carbonica is similar in having rheumatism in the right shoulder, rheumatic pains better from warmth and worse in bed. Ferrum has a paralytic tearing pain in the shoulder and muscles of the upper arm so that raising the arm is impossible; but it gradually disappears on gentle motion. Although Farrington says it is especially adapted to the left deltoid muscle, most of the symptoms point to the right shoulder. Nux moschata, however, affects the left deltoid muscle. Ferrum phosphoricum is a very useful remedy in rheumatism of the shoulders, especially the right shoulder. Urtica urens has cured obstinate case of deltoid rheumatism in 10-drop doses of the tincture. It is thought this drug has the power to dissolve deposits of urates in the muscles.

Phytolacca

The sphere of Phytolacca seems to be where there is a syphilitic taint. It is particularly useful in pains below the elbows and knees. There is stiffness and lameness of the muscles; the pains seem to fly about, are worse at night and are especially aggravated by damp weather. Rheumatic affections of the sheaths ;of the nerves; periosteal rheumatism or rheumatism of the fibrous tissues often is benefited by Phytolacca. Rheumatism of the shoulder and arms, especially in syphilitic cases, may call for this remedy. It cured a case of right deltoid rheumatism of twenty-seven years'standing.