History Taking and Interpretation in a Patient with Arthritis

History taking is the most important skill needed in rheumatology. Obtaining a good rheumatology history involves the art of medicine as much as its science. This section is about the importance of good history taking and about the systematic steps of a good history taking.

Topics:
The importance of history taking and interpretation in rheumatology
What is arthritis
Steps of history taking from a patient with arthritis

The importance of history taking and interpretation in rheumatology:
History taking is the most important skill needed in rheumatology. Obtaining a good rheumatology history involves the art of medicine as much as its science. However, it is very difficult both to teach and to learn the central art of history taking, which probably depends more on experience than does any other aspect of medical practice. When junior physicians complain that patients do not tell them the same facts as they reveal to the senior consultants, they are exposing their inability to take a good history. A good history can be a powerful therapeutic experience for the patient, as well as provide the physician with some 80% of the diagnostic information required. History taking involves an initial (patient-centered) listening phase which is a therapeutic process in itself and a second (physician-centered) interrogative phase which enables the physician to sort out the nature of the problem (diagnosis) and decide on any further course of action that might need to be taken. The physician needs to learn about the major presenting symptoms, the chronology of the disorder and its impact on the patient and the people around the patient, as well as ancillary information such as past and family history and involvement of other systems. At the same time, patients must have the opportunity to voice the problems that matter most to them.

Most physicians think that they are good at communicating with their patients, but surveys of the patients themselves disagree: all physicians should be prepared to be critical of their technique when interviewing patients and to spend more time learning the key skill involved in communication.

It is important to note that acute symptoms, whether mono- or polyarticular, may represent musculoskeletal emergencies. Such emergency conditions include infection (septic arthritis, subacute bacterial endocarditis, osteomyelitis, necrotizing fasciitis), systemic vasculitis, acute myelopathy or cervical cord compression, fracture, deep vein thrombosis, compartment syndromes and tumor. Delayed diagnosis may lead to permanent disability or death. Thus, it is very important that these conditions be excluded before proceeding with evaluation of the major diagnostic possibilities.

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What is arthritis:
Arthritis is joint inflammation. Arthritis may involve a single joint (monoarthritis) or it may involve 2-4 joints (oligoarthritis) or it may involve more than 4 joints (polyarthritis).

Clinically: Pain in the joint(s) that is accompanied by objective signs of joint inflammation. The most common sign is swelling (effusion). Joint pain causes limitation of both active and passive movements. It is important to differentiate between mechanical and inflammatory types of pain. Mechanical pain is increased with activity and is relieved by rest and is not associated with morning stiffness more than 30 minutes. Inflammatory pain, on the other hand, is increased with rest and is relieved to some extent by moderate activity. It is associated with morning stiffness more than 30 minutes.

Redness and hotness of the joint may also be seen in conditions characterized by pretty aggressive and acute inflammation as septic arthritis, gout, acute rheumatic fever and palindromic rheumatism.

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STEPS IN HISTORY TAKING FROM A PATIENT WITH ARTHRITIS ENUMERATED:

 I. Identifying data:

1. Age and sex

2. Race

3. Residence and occupation

II. Present history:

A. Pattern recognition:

1. Mode of onset

2. Duration of symptoms

3. Number of joints affected

4. Symmetry

5. Regions or joints affected

6. Pattern of sequence of joint involvement

7. Quality and severity of symptoms

8. The setting in which symptoms occurred

9. Factors that aggravate and ameliorate symptoms

10. Associated manifestations

B. Diet, special habits

C. Relevant data from the patient’s chart

D. Drugs

III. Past history

IV. Family history

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Now we start…

I. IDENTIFYING DATA

I. IDENTIFYING DATA/1. AGE AND SEX

“As a rule, it is important to note that infection can occur in all age groups of either sex.”

CHILDREN:

Some rheumatic diseases may (or may not) start in childhood and continue to adulthood. In fact, a significant fraction of adults with rheumatic diseases have the onset of their disease in childhood. Up to one fifth of all patients with systemic lupus or dermatomyositis/polymyositis have the onset of their disease before age 16 years. Other diseases include spondyloarthropathies and rheumatoid arthritis.

Some rheumatic diseases occur almost exclusively in those under 16 years of age. Included in this category are juvenile rheumatoid arthritis, acute rheumatic fever and some vasculitides (Henoch Schonlein purpura and Kawasaki disease).

Certain rheumatic diseases almost never occur in childhood. Included in this group are gout, calcium pyrophosphate deposition disease (CPPD disease), polymyalgia rheumatica and primary osteoarthritis.

Many of the rheumatic diseases of childhood have characteristic ages of onset so that consideration of the age of the child at the onset of symptoms can be of value in diagnosis. For this purpose, four age groups can be considered:

The neonatal period: Three rare syndromes occur. These are neonatal lupus syndromes, neonatal onset multisystem inflammatory disease (NOMID, also called chronic infantile neurological, cutaneous and articular syndrome-CINCA) and infantile sarcoidosis. In addition, septic arthritis may occur in the neonate.

Early childhood (from 1-4 years): early type of oligoarticular juvenile chronic arthritis, juvenile psoriatic arthritis, Kawasaki disease and septic arthritis.

Mid childhood (5-11 years): polyarticular juvenile chronic arthritis, late type of oligoarticular juvenile chronic arthritis (juvenile ankylosing spondylitis), juvenile dermatomyositis begin to be seen. Henoch Schonlein purpura and polyarteritis nodosa have their peak frequencies.

Late childhood (above 11 years) and teenage years: Juvenile ankylosing spondylitis (in boys) and systemic lupus erythematosus (in girls) show a marked increase in incidence. The rare vasculitic syndromes such as Wegener’s granulomatosis and Takayasu’s arteritis occur.

Important Notes:

The systemic type of JRA can have its onset at any age during childhood.

In a child with acute onset of monoarthritis, the initial differential diagnosis should include:

Infection (septic arthritis and/or osteomyelitis)

Trauma (accidental or non-accidental)

Malignancy (leukemia and neuroblastoma).

In a child with chronic monoarthritis, the differential diagnosis includes:

1. Oligoarticular JRA

2. A seronegative spondyloarthropathy or one of the related disorders as coeliac disease (CD) which occurs in mid-late childhood, monoarthritis may antedate clinical bowel involvement; diagnosed by antigliadin and anti-endomysium antibodies; it is recommended that the possibility of CD be considered in any child with arthritis of unclear origin; gluten-free diet results in persistent remission of arthritis.

3. In addition, a number of uncommon disorders should also be included as intra-articular hemangiomas, synovial chondromatosis, villonodular synovitis, lipomatosis arborescens, osteoid osteomas, osteochondritis disssecans (especially at the knee) and discoid meniscus.

Influence of sex in children:

The most striking differential sex ratios are seen in the predominance of juvenile ankylosing spondylitis (spondyloarthropathis in general) in boys and of systemic lupus in girls although in the later disease, the ratio is closer to unity in the very young.

Oligoarticular juvenile chronic arthritis, especially when accompanied by uveitis, is much more common in girls than in boys.

Vasculitides are more common in boys than in girls.

Systemic onset juvenile chronic arthritis occurs with equal frequency in both sexes.

YOUNG AND MIDDLE-AGED ADULTS:

Men aged 25-50: Reiter’s, ankylosing, gonococcal arthritis, gout, internal derangement, osteoarthritis, hemochromatosis.

Women aged 25-50: Systemic lupus, rheumatoid arthritis, fibromyalgia, benign hypermobile syndrome, osteoarthritis.

OLDER ADULTS:

There are diseases that are not seen as new onset disease among older people. These include Reiter’s disease, Still’s disease and ankylosing spondylitis. By contrast, there are diseases that occur almost exclusively in the older population. These include primary osteoarthritis, polymyalgia rheumatica, giant cell arteritis, Sjogren’s syndrome and CPPD disease.

Equally important in geriatric rheumatology is the fact that musculoskeletal symptoms occurring in the older age group may reflect a wide variety of conditions, many of them with serious implications which are not usually regarded as falling within the constellation of rheumatic disease. Examples include carcinomatosis, multiple myeloma, hyperthyroidism, myxedema and a variety of neurological entities including Parkinson’s disease and Alzheimer’s disease. Differential diagnosis requires a broad understanding of many aspects of clinical medicine including ones that fall outside the frame of reference of traditional rheumatology.

Diseases that are more common in males:

Ankylosing spondylitis

Churg Strauss: 15-70 years, mean 38 years. Males twice as common as females.

Gout

Pancreatic arthropathy

Polyarteritis nodosa: Males twice as common as females.

Primary amyloidosis: middle age and elderly, mean age at diagnosis 55 years. More in men. More in whites.

Reiter’s disease: young men: the most common cause of inflammatory arthritis of the lower extremities in young men. Twenty times more frequent in men.

Rheumatoid vasculitis: middle-aged male with a long standing RA.

Wegener’s granulomatosis: 3 months-75 years, peak 30s-40s. Slight male predominance.

Whipple’s: middle aged whites, may be familial. More in men.

Diseases that are more common in females:

By pass arthritis dermatitis: within 1 year of the operation. Three times more common in women.

Collagenous colitis: mid fifties. More in women.

Felty’s syndrome: in whites who have had RA for more than 10 years. Two thirds are women.

Henoch Schonlein purpura: More in winter and early spring. 4-11 years, any age.

Hypocomplementemic vasculitis: young adults

Mixed connective tissue disease

Mixed cryoglobulinemia: Middle age. More in women.

Multicentric reticulohistocytosis: 11-71 years, mean age 30 years. Slight female predominance.

Rheumatoid arthritis: 3 times more common in females

Sjogren’s syndrome

Systemic lupus erythematosus

Systemic sclerosis

Takayasu arteritis: 10-30 years, children and young women.

Temporal arteritis: 50 years and above, mean age 70 years. Females twice as common as males.

Examples of diseases that show an equal sex distribution include psoriatic arthritis.

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I. IDENTIFYING DATA/2. RACE

Whites: Ankylosing spondylitis, Whipple’s disease.

Blacks: Sickle cell disease

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I. IDENTIFYING DATA/3. RESIDENCE AND OCCUPATION

These are more likely to be related to infectious diseases (reference here is made to residents of Middle East).

Residence in Fayoum (Egypt): leprosy

Residence in Saudia Arabia should raise the suspicion of Medina worm infection.

A farmer or gardener exposed to soil may have sporotrichosis.

Butchers and farmers may get infected with Coxiella Burnetti (Q fever), brucella.

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II. PRESENT HISTORY

A. Pattern recognition:

B. Diet, special habits

C. Relevant data from the patient’s chart

II. PRESENT HISTORY/A. PATTERN RECOGNITION

A. PATTERN RECOGNITION

1. Mode of onset

2. Duration of symptoms

3. Number of joints affected

4. Symmetry

5. Regions or joints affected

6. Pattern of sequence of joint involvement

7. Quality and severity of symptoms

8. The setting in which symptoms occurred

9. Factors that aggravate and ameliorate symptoms

10. Associated manifestations

II. PRESENT HISTORY/ A. PATTERN RECOGNITION/1. MODE OF ONSET

Hyper-acute onset of pain with peak intensity reached within seconds to minutes:

Fracture, internal derangement.

Acute onset of pain with peak intensity reached within hours to a few days:

Bacterial arthritis, viral arthritis (e.g. parvovirus 19 and rubella), acute rheumatic fever, reactive arthritis, palindromic rheumatism, crystal-induced arthritis (the best example being nocturnal attacks of gout), elderly onset RA (acute monoarthritis of the large joints with slow and incomplete remissions)

Insidious onset of pain with peak intensity reached gradually over several weeks to months:

Juvenile rheumatoid arthritis (oligo and polyarticular types), rheumatoid arthritis, osteoarthritis, psoriatic arthritis, hypertrophic osteoarthropathy, mycobacterial and fungal arthritis, most cases of neuropathic arthropathy (Charcot’s joints), tumors, infiltrative diseases.

Note:

It is important to note that variations may occur and the same disorder may have a sudden onset in some patients and a gradual onset in others. Rheumatoid arthritis, for example, may present as an acute polyarthritis (especially in the elderly) and psoriatic arthropathy as an acute monoarthritis resembling gout, whereas in most cases both disorders begin insidiously.

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II. PRESENT HISTORY/ A. PATTERN RECOGNITION/2. DURATION OF SYMPTOMS

Self-limiting disorders are those disorders in which the arthritis lasts less than 4-6 weeks.

In self-limiting arthritic disorders, the duration of symptoms and signs may be a valuable discriminating feature.

Examples:

Episodes of palindromic rheumatism disappear within hours to several days.

Attacks of rheumatic fever arthritis never last more than 5-6 days in any individual joint.

Early episodes of monoarticular gout tend to subside spontaneously after 3-10 days and resolution is complete.

Acute or subacute attacks of CPPD disease (pseudogout) may last from 2-3 days to 3-4 weeks.

Chronic disorders are those disorders where the arthritis lasts longer than 6 weeks.

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A. PATTERN RECOGNITION/3. NUMBER OF JOINTS AFFECTED

THE CLINICAL PATTERN MAY BE MONOARTICULAR, POLYARTICULAR OR OLIGOARTICULAR.

MONOARTHRITIS: This is the involvement of a single joint. Although almost any individual arthropathy may begin as monoarthritis, the initial pattern of some disorders is characteristically monoarticular regardless of the subsequent course.

Chronic monoarthritis is often the presenting feature of a variety of joint disorders. Histologic elucidation may be necessary to make the correct diagnosis. In a substantial number of patients, however, the cause remains undetermined.

CAUSES OF MONOARTHRITIS: With rare exceptions, any disorder is capable of presenting initially as monoarthritis.

Diseases that are usually monoarticular:

Congenital: Congenital hip dysplasia

Traumatic: Internal derangement, stress fracture with effusion in adjacent joint, osteochondritis dissecans, loose body, slipped capital femoral epiphysis

Inflammatory: Pauciarticular JRA, palindromic rheumatism, crystal-induced, sometimes seronegative spondyloarthropathies

Infectious: bacterial, fungal, TB, viral (AIDS), osteomyelitis (sympathetic effusion).

Neoplastic: Osteoid osteoma, Synovial osteochondromatosis, pigmented villonodular synovitis (PVNS), synovioma, osteogenic sarcoma, neuroblastoma, metastasis, leukemia, lymphoma.

Infiltrative: one type of chronic sarcoidosis

Miscellaneous: Acute coagulopathy, hemoglobinopathy, osteonecrosis, Paget’s involving joint, neuropathic, reflex sympathetic dystrophy, intermittent hydrathrosis, neurofibromatosis, pancreatic fat necrosis, familial Mediterranean fever (FMF), foreign body synovitis, sea urchin spine synovitis, plant thorn synovitis, Gaucher’s disease, transient osteoporosis

Notes:

Single red hot joint in RA: Owing to the frequency of the underlying disease, it should be remembered that the uncommon occurrence of a red hot joint in the context of RA may be due to superimposed septic arthritis and not to the disease process itself.

Monoarthritis in SLE: The occurrence of monoarthritis in a patient with SLE suggests infection or osteonecrosis.

Hemoglobinopathies (sickle cell arthritis): Arthritic pain, swelling and effusion may be related to periarticular infarction or gouty arthritis. The arthritis usually responds to nonsteroidal anti-inflammatory drugs. Bone infarction and osteonecrosis may occur. Excruciating pain due to bone infarction, the hand-foot syndrome or dactylitis, is the most common initial symptoms of sickle cell disease, occurring in 40 percent of patients overall and 50 percent of children who became symptomatic before age two. It is important to distinguish this syndrome, which resolves spontaneously, from osteomyelitis with nuclear medicine scintigraphy or magnetic resonance imaging (MRI). Osteomyelitis: There is an increased incidence of osteomyelitis in patients with sickle cell anemia resulting from infection of infarcted bone.

Paget’s disease: Pain may arise either directly from a pagetic lesion or, more often, from complications indirectly caused by the abnormal bone, including degenerative arthritis, nerve impingement, or osteosarcoma.

OLIGOARTHRITIS: This is the involvement of 2 to 4 joints.

In general, some of the rheumatic disorders manifesting as monoarthritis may also be oligoarticular. Example: oligoarticular JRA and Coagulopathy. At the same time, many of the rheumatic disorders manifesting as polyarthritis may also be oligoarticular

Despite this overlap, there are instances in which involvement of two or three joints rather than one may significantly narrow the diagnostic spectrum.

Example 1: lower limb oligoarthritis especially of the knees and ankles in an asymmetric fashion is reminiscent of reactive arthritis.

Example 2: an asymmetric oligoarthritis affecting DIP and PIP and MCP joints characterizes a common subgroup of patients with psoriatic arthropathy.

POLYARTHRITIS: This is the involvement of more than 4 joints. A wide variety of inflammatory and non-inflammatory disorders, both common and uncommon may present as polyarthritis. Examples include:

Diseases that are often polyarticular:

Inflammatory: Rheumatoid arthritis, JRA (polyarticular and Still’s), adult Still’s, Sjogren’s, SLE and other CT diseases, seronegative spondyloarthropathies and related disorders, calcium pyrophosphate deposition disease, ca oxalate deposition disease, Vasculitides (Henoch Shonlein Purpura, Bechet’s, PAN, Wegner’s, Takayasu, temporal arteritis, PMR), Pseudovasculitic syndromes (MCES, SABE), Erythema nodosum, pyoderma gangrenosum, serum sickness (HBV, Rubella), relapsing polychondritis.

Infectious: bacterial (neisserial gonorrhea, brucellosis, mycoplasma), viral (Parvovirus, AIDS), Lyme disease, spirochetal (leprosy), fungal (candida in immunocompromised subjects)

Neoplastic: Paraneoplastic syndromes (HPO, carcinoma polyarthritis and Jaccoud’s arthropathy), metastasis, leukemia, lymphoma

Infiltrative: Sarcoidosis, Chondrocalcinosis-like syndromes (Hemochromatosis, Ochronosis, Wilson’s), amyloidosis with MM, Gaucher’s disease

Miscellaneous:

Degenerative: Osteoarthritis, DISH

Years of build up: Dialysis arthropathy, chronic articular hemorrhage (Coagulopathy)

Endocrinal: hyperparathyroidism, hypothyroidism, acromegaly

Metabolic: Hyperlipidemias types II & IV

Bone diseases: multiple epiphyseal dysplasia

Skin conditions: acne fulminans, Sweet’s syndrome, angioedema

Drug-related: pseudorheumatism, anthracyclines, penicillamine

MRH, HPO, FMF, Immunodeficiency syndromes, Sea urchin spine synovitis

Notes:

Arthritis in Bechet’s: A nonerosive, asymmetric, usually nondeforming oligoarthritis occurs in about one-half of patients with Behcet’s disease, particularly during exacerbations of illness. The arthritis most commonly affects the medium and large joints, including the knee, ankle, and wrist; inflammation is evident on synovial fluid and biopsy specimens. Pseudopodagra has also been described in these patients. Sacroiliitis may occur, particularly in patients with HLA-B27).

Temporal arteritis: Musculoskeletal symptoms, in addition to those of PMR, have been observed in patients with GCA. In a cohort of 128 patients, for example, peripheral synovitis, distal extremity swelling with pitting edema, swelling without pitting edema, tenosynovitis, and carpal tunnel syndrome developed in 23, 13, 5, 6, and 2 patients, respectively. The onset of most symptoms occurred within two years of the initial diagnosis.

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II. PRESENT HISTORY/ A. PATTERN RECOGNITION/4. SYMMETRY

Symmetrical arthritis: occurs in rheumatoid arthritis that happens to be the classic example of symmetric arthritis. However, symmetry is not necessarily strict in the hands: the same MCP or PIP joint may not be equally affected in both extremities of RA patients especially in early disease.

Other examples of symmetrical arthritis include:

Inflammatory:

From the RA family: JRA (systemic and polyarticular types), Adult onset Still’s disease, Sjogren’s

Other CT diseases: SLE, MCTD, SSc, PM/DM, Adult onset rheumatic fever, Polymyalgia rheumatica

Erosive inflammatory osteoarthritis, CPPD disease (pseudo-RA type), Milwaukee shoulder

Infectious:

Viral arthritis especially parvovirus arthritis, Lyme disease

Infiltrative:

Sarcoid arthritis (acute type), Amyloid arthropathy, Hemochromatosis arthropathy

Neoplastic:

Jaccoud’s arthritis, Hypertorphic osteoarthropathy

Endocrinal:

Myxedematous arthropathy

Asymmetrical arthritis:

Inflammatory:

Seronegatives (e.g. reactive arthritis, oligoarticular psoriatic arthritis)

From the RA family: pauciarticular juvenile rheumatoid arthritis, palindromic rheumatism

Oligoarticular or polyarticular gout, CPPD disease (pseudogout type)

Infectious:

bacterial arthritis and bacterial endocarditis.

Notes:

Every patient with a symmetric disorder may have an initial asymmetric phase.

Most asymmetric arthritides may be or are characteristically initially monoarticular.

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II. PRESENT HISTORY/ A. PATTERN RECOGNITION/5. REGIONS OR JOINTS AFFECTED

Axial involvement:

Axial structures include, apart from the spine, centrally located joints such as the sacroiliac, sternoclavicular, manubriosternal and the rest of the chest wall and sometimes shoulders and hips. In the presence of peripheral arthritis, one of the most important clues is to determine whether there is concomitant axial involvement or not. While some rheumatic disorders rarely affect the axial segments, a combined pattern is often seen in others.

Examples:

Inflammatory:

Seronegative spondyloarthropathies.

Polyarticular and systemic onset JRA as well as adult onset Still’s disease that commonly affect the apophyseal joints of the cervical spine in addition to peripheral joints.

Rheumatoid arthritis: involvement of the cervical spine structures is common, whereas the dorsal and lumbar segments are spared. Persistent pain in these areas should raise the suspicion of insufficiency fractures of the spine, sacrum or iliac bones.

Tuberculosis: affects the spine in addition to large peripheral joints as knees and hips. Midtarsal joints’ involvement has been reported.

The SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis and osteitis).

Non-inflammatory:

Degenerative:

Osteoarthritis of the spine that often coexists with appendicular involvement.

Diffuse idiopathic skeletal hyperostosis.

Endocrinal:

Acromegalic arthropathy: Hypermobility of the spine. Also, involvement of large and small peripheral joints may occur in as many as 75% of patients. It may be monoarticular or polyarticular. The knees, shoulders, hips, or hands are more commonly affected; the elbows and ankles are involved less frequently.

Infiltrative:

Ochronosis

Miscellaneous:

Spondyloepiphyseal dysplasia.

Peripheral involvement:

Affection of certain joints is closely associated with the early phases of certain diseases. Consequently, their involvement often facilitates the diagnostic process.

Joints commonly involved and commonly spared in selected rheumatic diseases:

Rheumatoid arthritis:

Involved: Wrist, MCP, PIP, elbow, glenohumeral, cervical spine, hip, knee, ankle, tarsal, MTP.

Spared: Thoracolumbar spine

Osteoarthritis:

Involved: First CMC, PIP, DIP, Cervical spine, thoracolumbar spine, hip, knee, First MTP, toe IPs.

Spared: MCP, Wrist, elbow, glenohumeral, ankle, tarsal

Reiter’s disease:

Involved: Knee, ankle, tarsal, MTP, toe IPs, elbow, axial

Psoriatic arthritis:

Involved: Knee, ankle, MTP, toe IPs, wrist, MCP, PIP, DIP, axial

Enteropathic arthritis:

Involved: knee, ankle, elbow, shoulder, MCP, PIP, wrist, axial

Sarcoidosis:

Involved: Ankle, knee

Hemochromatosis:

Involved: MCP, wrist, knee, hip, feet, shoulder

Spared: Axial

Polyarticular gout:

Involved: First MTP, instep, heel, ankle, knee

CPPD:

Involved: Knee, wrist, shoulder, ankle, MCP, PIP, DIP, hip, elbow.

Spared: Axial

Gonococcal arthritis:

Involved: Knee, wrist, ankle, PIP, DIP

Spared: Axial

Sporotrichosis:

Involved: Hand

IV drug users:

Involved: Septic Sternoclavicular arthritis

Other examples:

1. Hypothyroidism: Myxedema arthropathy occurs in one third of hypothyroid patients. The arthritis is usually bilateral, most often affecting the knees; the ankles, metacarpophalangeal joints, and small joints of the hands and feet are less frequently involved. The increased intra-articular viscid fluid is reflected in a sluggish “bulge” sign.

2. Hyperparathyroidism: interphalangeal, metacarpophalangeal, carpal, and acromioclavicular joints. Bone erosions may occur in juxta-articular sites in these joints. These lesions can be found in the absence of subperiosteal resorption, can be symmetric, and can be associated with morning stiffness, thus mimicking RA. Several features distinguish parathyroid disorders: (1) the erosions may have a shaggy appearance; (2) they often occur at the distal interphalangeal joints and spare the proximal interphalangeal joints; (3) joint-space narrowing in association with these erosions is uncommon because parathyroid hormone does not directly induce inflammatory synovitis or cartilage dissolution; and (4) concurrent articular calcification is common.

3. Diabetic neuroarthropathy: As a consequence of sensory neuropathy, severe ar-thropathy with Charcot-like changes develops in approximately 0.1% of patients with long-standing diabetes. The tarsometatarsal and metatarsophalangeal joints are by far the most common sites of involvement. Changes may rarely affect joints above the ankle. A combination of microfragmentation from trauma, ischemia from small blood vessel disease, and superimposed infection can contribute to the clinical and radiographic changes of neuroarthropathy. All patients with diabetic neuroarthropathy have peripheral neuropathy. Unstable gait may be seen in diabetic neuroarthropathy of the tarsometatarsal and metatarsophalangeal joints. This is because, in advanced disease, the longitudinal arch of the foot collapses, leading to an unstable gait and a “rocker-sole” appearance. Ulcerations and plantar callosites occur over hypoesthetic pressure points.

4. Cushing’s syndrome: A polyarthropathy associated with Cushing’s disease has been reported.

5. Hyperlipoproteinemias: Type II homozygous hyperlipoproteinemia: Large joint migratory polyarthritis. Type II heterozygous hyperlipoproteinemia: recurrent migratory polyarthritis involving knees, other large joints and to a lesser extent small joints OR monoarthritis involving the knee or great toe (NB: fever may accompany the arthritis). Type IV hyperlipoproteinemia: an asymmetric oligoarthritis involving small and large joints appearing in middle aged patients and lasting a few days to weeks.

NB: The arthritis in type II hyperlipoproteinemia resembles that of rheumatic fever: migratory arthritis / sudden onset / lasts for a few days (but may last up to 2 weeks) / involved joints can be warm, erythematous, swollen and tender / no joint damage occurs / patients have a high ESR and a falsely elevated ASOT and, in some cases, aortic valvular disease secondary to atherosclerosis / several attacks occur in a year.

NB: Joint fluid in hyperlipidemic arthritis is non-inflammatory with few or no crystals.

6. HCV arthritis: wrists and small joints of the hands. It is sometimes difficult to differentiate from rheumatoid arthritis.

7. HCV-cryoglobulinemic arthritis: an intermittent, mono or oligoarticular, nondestructive arthritis affecting large and medium sized joints.

8. Polymyalgia rheumatica: Clinical synovitis is most frequently noted in the knees, wrists and sternoclavicular joints. Joint effusions have WBC counts that range between 1000 and 20,000 cells/mm.

9. Hypermobility syndrome: traumatic arthritis, synovitis and effusions, juvenile episodic synovitis. Also arthrlagias, TMJ dysfunction.

10. Osteoid osteoma: ankle, subtalar, elbow.

11. Neurofibromatosis: plexiform neurofibromatosis around the ankle in children may present with a picture very similar to chronic monoarthritis. Also, osteoid osteoma which, in the author’s experience, has been present in a child with neurofibromatosis may present as monoarthritis.

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II. PRESENT HISTORY/ A. PATTERN RECOGNITION/6. PATTERN OF SEQUENCE OF JOINT INVOLVEMENT

Clinical involvement of joints may follow three major patterns: additive, migratory and intermittent:

Additive: refers to the involvement of more joints while the previous joints remain symptomatic. This is a rather non-specific pattern. Polyarticular osteoarthritis (OA) and rheumatoid arthritis (RA) are typical examples of this progressive sequence.

Migratory: means that the process ceases or abates in one joint while simultaneously or immediately after starts in a previously normal joint.

Examples include:

Inflammatory: Rheumatic fever, Whipple’s disease

Infectious: Gonococcal arthritis (associated with tenosynovitis)

Infiltrative: acute sarcoid arthritis (sometimes)

Metabolic: Arthritis of hyperlipoproteinemia

Early Lyme disease

Note: It is important to note that the monoarthritis that some patients may present with may actually be part of a migratory disease.

Intermittent: means there is complete remission of symptoms and signs until the next recurrence in the same or other joint. No evidence of active disease or residual signs can be detected during the inter-attack intervals.

Examples include:

Palindromic rheumatism

Intermittent hydrathrosis

Crystal induced arthritis as gout, CPPD (pseudo-gout type)

Familial Mediterranean fever: acute, self-limited large joint monoarthritis (most often affecting the knee or hip). Rarely, a more protracted arthritis may occur.

ALSO:

Inflammatory:

From RA family: Adult onset Still’s disease may also run a polycyclic clinical course

CT diseases: Patients with SLE also often show complete resolution of synovitis (commonly polyarthritis) and follow a discontinuous pattern of arthropathy.

HCV-cryoglobulinemic arthritis: intermittent non-destructive mono- or oligoarthritis.

Seronegatives: Reiter’s syndrome

Other:

Early phases of erosive inflammatory osteoarthritis

Endocrinal:

Early phase of acromegalic arthropathy. Some patients develop intermittent painful effusions lasting weeks or months. Less commonly, patients complain initially of joint pain and morning stiffness. This presentation, together with the elevated erythrocyte sedimentation rate seen in some patients, can cause confusion with rheumatoid arthritis (RA).

Metabolic:

Hyperlipoproteinemia: Recurrent attacks of migratory polyarthritis in 50% of patients with type II hyperlipoproteinemia heterozygous type. They are self-limited lasting several days to 2 weeks. The inflammation may be mild or severe resembling rheumatic fever or episodes of gout.

Note: In case of intermittent pattern, it is important to inquire about the location of the previous attacks. For example, previous acute attacks that resolved spontaneously in the same joint suggest crystal deposition diseases while previous acute attacks that resolved spontaneously in other joints suggest palindromic rheumatism.

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II. PRESENT HISTORY/ A. PATTERN RECOGNITION/7. QUALITY AND SEVERITY OF PAIN

Quality of pain:

Burning pain especially at night or pain described as electric shock-like or shooting: suspect neuropathic origin rather than arthritis e.g. entrapment.

Pain described as severe aching sensation: may originate in the joints

An attack of pain that begins in the middle of the night with a pricking sensation in the great toe which quickly builds up into an intolerable burning pain: typical gouty podagra.

Throbbing pain: may be vascular.

Note:

However, neither the adjectives that the patients use to describe their pain nor their assessment of its severity is generally of great diagnostic value.

Severity of pain:

Severe pain with joint dysfunction following a minor trauma: Osteochondritis dissecans

Severe pain with moderate physical findings: SLE, FMF, leukemia.

Mild pain with impressive physical findings: Neuroarthropathy

Extreme description of pain: central pain where there is perception of pain with no evident external causes. However it is important to consider that sometimes some individuals or groups of individuals tend to use these extreme terms out of a sense of frustration or anxiety or because of ethnic variation and risk being labeled as neurotic because of them when the presence of organic disease may be missed

Note:

When history reveals long-standing symptoms in a joint, it is important to distinguish exacerbations of pre-existing disease (e.g. worsening of degenerative joint disease with excessive use) from a second superimposed process (e.g. infection).

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II. PRESENT HISTORY/ A. PATTERN RECOGNITION/8. THE SETTING IN WHICH IT OCCURRED

Hospitalized patients: acute gout, pseudogout and infection. These patients are often middle-aged or elderly, the primary age range for the crystalline arthropathies, In addition, they often have hospitalization-related risk factors known to provoke gout or pseudogout attacks: trauma, surgery, hemorrhage, infection, or medical stress such as renal failure, myocardial infarction and stroke. One must also be very careful to exclude infection in these patients.

Postpartum period: onset or flare of RA.

Penetrating trauma: Infection.

Recent upper respiratory tract infection: Henoch Shonlein purpura, post streptococcal reactive arthritis (most patients “children” only have mild pharyngitis by history).

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II. PRESENT HISTORY/ A. PATTERN RECOGNITION/9. FACTORS THAT AGGRAVATE OR RELIEVE SYMPTOMS

FACTORS THAT AGGRAVATE SYMPTOMS:

Pain that worsens with activity: mechanical causes or non-inflammatory causes.

Pain that worsens at night and with rest: inflammatory causes.

Constant severe pain, present throughout the day and night and not affected by or linked to anything might be due to a bone disorder but can also be functional.

Pain that increases with limb dependency: Hypertrophic osteoarthropathy.

Pain that increases with limb elevation: ischemia.

Pain that comes or increases with alcohol: Gout, hypertrophic osteoarthropathy

FACTORS THAT AMELIORATE SYMPTOMS:

Morning stiffness and gelling that improves with motion: inflammatory arthritis.

Joint pain that improves with rest: mechanical causes.

Aspirin: dramatically relieves the pain of osteoid osteoma (OO). It is suggested that synovitis in OO is secondary to prostaglandin secretion by the tumor.

Limb elevation: Improves the pain of hypertrophic osteoarthropathy.

Examples of inflammatory arthropathies include:

Rheumatoid arthritis and its variants

CT diseases

Seronegative spondyloarthropathies & related disorders as SAPHO syndrome

Crystal arthritis

Infectious arthritis

Examples of non-inflammatory arthropathies include:

Degenerative and related disorders:

Osteoarthritis

Epiphyseal dysplasia

Familial hypertrophic synovitis (CAC syndrome)

Endocrinal arthropathies:

Hypothyroidism: Myxedema arthropathy (noninflammatory viscous effusions with leukocytic counts less than 1000/mm3. Inflammation is neither common nor severe, with minimal pain and tenderness and only slight warmth and erythema).

Acromegalic arthropathy: proliferation of articular and periarticular structures, with osteophytosis and degenerative changes of the articular cartilage.

Hyperparathyroidism

Metabolic:

Hyperlipoproteinemia arthropathy

Infiltrative:

Ochronosis

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II. PRESENT HISTORY/ A. PATTERN RECOGNITION/10. ASSOCIATED OTHER MUSCULOSKELETAL MANIFESTATIONS

Presence of redness:

Although redness may occur in any acute arthritis regardless of the etiology, its presence is more often suggestive of infections as bacterial and neisserial (which may be preceded by transient polyarticular disease), crystal arthritis (gout, pseudogout, hydroxyapatite as acute calcific periarthritis), acute rheumatic fever, psoriatic arthritis, reactive arthritis and palindromic rheumatism.

The presence of erythema implies associated periarticular inflammation.

Sausage digits:

Psoriatic arthritis

Periarthritis:

Acute sarcoidosis: sometimes is a polyperiarthritis rather than polyarthritis

Hyperlipidemic arthritis is considered to be an inflammatory periarthritis or peritendinitis

Palindromic rheumatism, sometimes inflammation is beside, rather than, in the joint.

Hypermobility:

Hypermobility syndrome

Hyperparathyroidism: more prominent in the lumbar spine.

Hypothyroidism: Ligamentous laxity occurs in approximately one third of patients with myxedema.

Early phase of acromegalic arthropathy. Hypermobility is especially prominent in the spine. This striking finding may be a key in distinguishing between this and other spinal disorders. Loss of motion, on the other hand, characterizes the late phase of the disease. Palpable dorsal phalangeal ridging just distal to the proximal interphalangeal joints and pronounced degree of joint crepitation attributed to cartilaginous thickening and joint hypermobility may also be seen in acromegalic arthropathy.

Occurrence of skin desquamation when inflammation declines:

Suggests acute gouty monoarthritis.

Puffy hands:

Hypothyroidism

RS3PE (remitting symmetrical seronegative synovitis with pitting edema)

Thickening of periarticular tissues:

1. Hypothyroidism: myxedema arthropathy

2. Acromegalic arthropathy: Thickened synovium and periarticular tissues may have a swollen appearance, but effusions are relatively rare.

Periarticular hyperesthesia:

Type IV hyperlipoproteinemia

Vasculitis (if hyperesthesia is in feet for example)

Unequal leg girth:

Neurofibromatosis (also associated with pes cavus, spinal bifida).

Muscle cramps:

Hypothyroidism

Acromegaly

Dorsal kyphosis:

Hyperparathyroidism: secondary to ligament laxity (associated with anterior bowing of the sternum).

Acromegaly: dorsal kyphosis is frequently observed, possibly secondary to the barrel-chest deformity related to rib elongation.

Variable pain in hands and feet (+/-digital clubbing and local signs of inflammation):

Hypertrophic osteoarthropathy, acquired pachydermoperiostosis

Acromegaly (widening of the distal ungual tufts in acromegaly may lead to an appearance of the hands similar to that of clubbing) and thyroid acropachy.

Recurrent traumatic soft tissue injuries or recurrent fractures:

Benign hypermobile syndrome: recurrent bruising, sprains, meniscus tears, acute or recurrent dislocations/subluxations of the: shoulder, patella, metacarpophalangeal joint, temporomandibular joint.

Important Notes:

Systemic versus local nature of disease: It is important to differentiate systemic from local nature of the disease that is being dealt with. If there is suspicion of a systemic disease, a full systematic medical inquiry must be embarked upon and any significant symptoms or signs noted. Systemic disease is suggested by the patient looking ill, weight loss, dysnea, fever, neuropathy, lymphadenopathy, splenomegaly, rash, anemia, raised ESR or CRP and abnormal urinalysis.

However, even if the problem appears to be localized, one must be conscious of the fact that systemic diseases (rheumatic and non-rheumatic) often present with local symptoms. Examples of these include:

Weight loss and bone pain in multiple myeloma or secondary tumor.

Carpal tunnel syndrome in acromegaly, hypothyroidism and amyloid.

Vasculitis (polyarteritis nodosa) in hepatitis B.

Chronic synovitis with bowel problems in inflammatory bowel disease.

Stiff fingers and shoulder pain in diabetic cheiroarthropathy.

Nevertheless, localized problems may sometimes be multifocal suggesting a generalized disorder as in case of polytendinitis and bursitis.

It is important to always be wary of the diagnosis of diffuse or focal osteoarthritis as the cause of symptoms even when there may be supporting radiographic evidence. Although this condition may be present, yet it may not be the predominant cause of symptoms as in the case of rheumatoid arthritis or gout on top of osteoarthritis.

HEURISTICS IN PATTERN RECOGNITION:

Acute onset of large joint monoarthritis in a young girl should be considered to be oligoarticular JRA unless there is evidence of infection.

At any age during childhood and in either sex, a pattern of scattered, asymmetrical, large and small joint oligoarthritis or limited polyarthritis suggests the possibility juvenile psoriatic arthritis.

Oligoarthritis of large joints of the lower extremity in an older boy suggests a seronegative spondyloarthropathy, most likely ankylosing spondylitis.

The presence of enthesitis with arthritis indicates the likely presence of seronegative enthesitis and arthritis syndrome (SEA) and the probable later development of ankylosing spondylitis.

The onset of polyarthritis in a teenage girl should suggest the possibility of systemic lupus as well as polyarticular juvenile rheumatoid arthritis.

Isolated hip joint arthritis may be caused by toxic synovitis, Legg-Calve Perthe’s disease, a slipped capital femoral epiphysis, or less likely, by chronic inflammatory arthritis, probably ankylosing spondylitis.

In a child presenting with acute onset of fever and painful arthritis that is presumed to be septic but with negative cultures, the possibility of post-streptococcal reactive arthritis should be considered. The arthritis may be migratory, additive or monoarthritis.

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II. PRESENT HISTORY/ B. DIET, TOBACCO, ALCOHOL, SLEEP PATTERN, OTHER

Cigarette smoking: Beurger’s disease, rheumatoid vasculitis (in a long-standing disease in a middle aged male).

Alcohol: Hyperlipoproteinemia, hyperuricemia that may lead to gout, osteonecrosis, infection, pancreatic arthropathy (one half to two-thirds of cases have a history of alcoholism causing pancreatitis), scurvy (scurvy also occurs in food faddists, infants fed exclusively on cow’s milk formula)

Intravenous drug abuse: Infection.

Goat milk: Brucellosis

Diet containing gluten: arthritis of celiac disease.

Perversion to sweet tasting foods: diabetes mellitus.

Contact with dogs and cats: parasites as visceral larva migrans.

Disturbed sleep pattern: fibromyalgia, functional disorder, inflammatory disease

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II. PRESENT HISTORY/ C. RELEVANT DATA FROM THE PATIENT’S CHART

THESE MAY PROVIDE A CLUE TO THE CAUSE OF THE RHEUMATIC PROBLEMS IN ONE OF THE FOLLOWING WAYS:

A. RHEUMATIC DISEASE IS CAUSED BY A CONCOMITANT DISORDER:

GENERAL:

Presence of a septic focus: infectious arthritis.

Immunodeficiency: infectious arthritis.

History of any recent GI or urinary tract infection: reactive arthritis

ENDOCRINE AND METABOLIC:

Diabetes mellitus: infectious arthritis, neuroarthropathy, patients are more prone to RA, hyperuricemia, scleredema, osteonecrosis, hyperlipoproteinemia (may lead to monoarthritis for example of the dorsum of the foot: MTPs). Some clinical features in diabetes suggest secondary Sjogren’s syndrome. Diabetes can cause limited joint mobility

Type B insulin-resistant diabetes mellitus secondary to insulin-receptor antibodies: has been associated with multiple rheumatic complaints suggestive of systemic lupus erythematosus, Sjogren’s syndrome, or progressive systemic sclerosis. In one study, fourteen such patients developed features of an autoimmune disease; 8 of the 14 met the American Rheumatism Association criteria for systemic lupus erythematosus, and 4 developed glomerulonephritis histologically consistent with lupus nephritis. Thus, whenever a patient has extremely insulin-resistant diabetes mellitus and features of a systemic rheumatic disease, the possibility of circulating antibodies to insulin receptors should be considered.

Hyperlipidemia: gout, osteonecrosis in addition to arthritis of hyperlipidemia.

Atherosclerosis: Multiple cholesterol embolization syndrome

Hemochromatosis: Chondrocalcinosis, infection with Listeria monocytogenes

Hyperparathyroidism: gout, pseudogout in addition to hyperparathyroid arthropathy

Hypothyroidism: Hyperlipoproteinemia, hyperuricemia and gout, CPPD, epiphyseal dysplasia. Also myopathy and myotonia.

Hyperthyroidism: Thyroid acropachy, periostitis (LATS), myopathy, myasthenia, periodic paralysis.

Pancreatic disease: pancreatic arthropathy

HEMATOLOGICAL:

Hemoglobinopathy: osteonecrosis, infection.

Bleeding diathesis: Hemarthrosis as in hemophilia.

RENAL:

Renal failure: crystal arthritis, infection.

HEPATIC:

Hepatitis B virus: Polyarteritis nodosa.

Hepatitis C virus: HCV arthritis, cryoglobulinemic arthritis.

Primary biliary cirrhosis: Osteomalacia.

MUSCULOSKELETAL:

Long standing RA: Rheumatoid vasculitis, Felty’s syndrome.

B. RHEUMATIC DISEASE IS CAUSED BY THE TREATMENT OF THE DISORDER:

Bronchial asthma: previous treatment with steroids: osteonecrosis.

Hypertension: thiazides: hyperuricemia, hyperlipoproteinemia

Epilepsy: on an anti-epileptic drug (as Epanutin) that can induce lupus and that can cause osteomalacia

C. RHEUMATIC DISORDER AND A CONCOMITANT DISORDER TOGETHER FORM PART OF A THIRD DIAGNOSIS:

GENERAL:

Recurrent infections: Felty’s syndrome.

Inguinal hernia: cutis laxa.

ENDOCRINE AND METABOLIC:

Atherosclerosis: hyperlipoproteinemia.

Diabetes mellitus: Hemochromatosis.

Gynecomastia: Hemochromatosis, pachydermoperiostiosis, POEMS

Addison’s disease: Antiphospholipid syndrome (causing venous thrombosis of the supra-renal gland).

Nephrogenic diabetes insipidus: Amyloidosis.

Pituitary diabetes insipidus: Wegener’s granulomatosis, sarcoidosis, eosinophilic granuloma, hemochromatosis.

Hypogonadism: Hemochromatosis (causing pituitary dysfunction).

Pancreatic disease: systemic sclerosis, SLE, hyperlipoproteinemia

RESPIRATORY

Chronic sinusitis: Wegener’s granulomatosis.

Bronchial asthma: Churg Strauss vasculitis.

Positive tuberculin test: tuberculous arthritis.

CARDIOVASCULAR:

Hypertension: SLE with renal affection, Vasculitis, Paget’s, amyloidosis.

Ischemic heart disease: Vasculitis, hemochromatosis, sarcoidosis, hyper or hypothyroidism

RENAL:

Renal tubular acidosis: Sjogren’s (can cause osteomalacia).

Urinary lithiasis: Gout, Ca oxalate crystal deposition disease, inflammatory bowel disease, Sjogren’s.

HEPATIC:

Primary biliary cirrhosis: CREST

NEUROLOGICAL:

Multiple sclerosis: Occasional co-incident occurrence with AS, with relapsing polychondritis

Epilepsy: SLE

Pseudodementia: Whipple’s disease.

In children: neurodevelopmental disabilities and psychomotor retardation: scurvy

OTOLARYNGEOLOGICAL:

Hearing troubles: Behcet’s disease, Cogan’s syndrome, relapsing polychondritis (causes stenosis of the external auditory canal as well as vasculitis of the internal auditory artery), hypothyroidism, acromegaly, Paget’s disease, Wegener’s

REPRODUCTIVE:

Pelvic inflammatory disease: Reiter’s disease.

Menstrual troubles: Menorrhagia: hypothyroidism.

MUSCULOSKELETAL:

Recurrent fractures: osteogenesis imperfecta, Idiopathic juvenile osteoporosis

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II. PRESENT HISTORY/ D. DRUGS

The efficacy of a drug may be a valuable diagnostic clue to diagnosis as in dramatic response of polymyalgia rheumatica to steroids.

At the same time, drugs themselves can be the cause of the problem as in drug-induced lupus.

PAST MEDICATIONS

Anti-tuberculous drugs: tuberculous arthritis

Prolonged courses of corticosteroids: osteonecrosis.

CURRENT MEDICATIONS

Corticosteroids: Infection, osteonecrosis, hyperlipoproteinemia

Immunosuppressives: infection.

Anticoagulants: hemarthrosis.

Start of replacement therapy for hypothyroidism: gout

Thiazides: hyperlipoproteinemia, hyperuricemia.

Epanutin: Osteomalacia, drug-induced lupus.

Oral contraceptives: SLE, deep vein thrombosis, hyperlipidemia

Beta-blockers: hyperlipoproteinemia

Quinolones: Tenosynovitis.

Minocin (for treatment of acne): Drug induced lupus

Isotrenetoin: may cause arthritis (monoarthritis).

Interferon alpha: IFN induced arthritis (IFN may be implicated in the induction of autoimmune phenomenon).

Anti-thyroid drugs: The administration of antithyroid drugs may be followed by syndromes resembling either RA or systemic lupus erythematosus, especially in children

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III. PAST HISTORY

ILLNESSES, ACCIDENTS AND INJURIES, OPERATIONS, JOINT OVERUSE OR DAMAGE

Past history of tuberculosis: Tuberculous arthritis.

Joint prosthesis: infection.

Joint damage or overuse: Traumatic arthritis, Osteoarthritis.

Thyroid disease: hypothyroidism: following treatment of hyperthyroidism

Intestinal by pass: Bypass arthritis dermatitis, cryoglobulinemia.

An attack of unexplained epilepsy: lupus.

A swollen ankle or knee in childhood in a young man now presenting with back pain: ankylosing spondylitis.

Hypermobility: FMS, predisposition to OA

Blood transfusion: Hepatitis B infection (rarely presents as a monoarthritis), Hepatitis C infection.

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IV. FAMILY HISTORY

A positive family history of: Rheumatoid arthritis, one of the seronegative spondyloarthropathies, gout, hemophilia.

Of stroke or myocardial infarction before age 55: Hyperlipidemia.

Heart disease: Hemochromatosis, hyperlipoproteinemia

Hyperlipoproteinemia: Deep vein thrombosis, hyperlipoproteinemic arthritis.

Neuropathy: Amyloidosis

Fractures: may occur repeatedly in patients with osteogenesis imperfecta.

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