(lithaemia) n. the presence in the blood of an abnormally high concentration of uric acid. See gout.
BURSITIS, TENDINITIS and non-speci?c back pain (see BACKACHE).
Osteoarthritis (OA) rarely starts before 40, but by the age of 80 affects 80 per cent of the population. There are structural and functional changes in the articular cartilage, as well as changes in the collagenous matrix of tendons and ligaments. OA is not purely ‘wear and tear’; various sub-groups have a genetic component. Early OA may be precipitated by localised alteration in anatomy, such as a fracture or infection of a joint. Reactive new bone growth typically occurs, causing sclerosis (hardening) beneath the joint, and osteophytes – outgrowths of bone – are characteristic at the margins of the joint. The most common sites are the ?rst metatarsal (great toe), spinal facet joints, the knee, the base of the thumb and the terminal ?nger joints (Heberden’s nodes).
OA has a slow but variable course, with periods of pain and low-grade in?ammation. Acute in?ammation, common in the knee, may result from release of pyrophosphate crystals, causing pseudo-gout.
Urate gout results from crystallisation of URIC ACID in joints, against a background of hyperuricaemia. This high concentration of uric acid in the blood may result from genetic and environmental factors, such as excess dietary purines, alcohol or diuretic drugs.
In?ammatory arthritis is less common than OA, but potentially much more serious. Several types exist, including: SPONDYLARTHRITIS This affects younger men, chie?y involving spinal and leg joints. This may lead to in?ammation and eventual ossi?cation of the enthesis – that is, where the ligaments and tendons are inserted into the bone around joints. This may be associated with disorders in other parts of the body: skin in?ammation (PSORIASIS), bowel and genito-urinary in?ammation, sometimes resulting in infection of the organs (such as dysentery). The syndromes most clearly delineated are ankylosing spondylitis (see SPINE AND SPINAL CORD, DISEASES AND INJURIES OF), psoriatic or colitic spondylitis, and REITER’S SYNDROME. The diagnosis is made clinically and radiologically; no association has been found with autoantibodies (see AUTOANTIBODY). A particularly clear gene locus, HLA B27, has been identi?ed in ankylosing spondylitis. Psoriasis can be associated with a characteristic peripheral arthritis.
Systemic autoimmune rheumatic diseases (see AUTOIMMUNE DISORDERS). RHEUMATOID ARTHRITIS (RA) – see also main entry. The most common of these diseases. Acute in?ammation causes lymphoid synovitis, leading to erosion of the cartilage, associated joints and soft tissues. Fibrosis follows, causing deformity. Autoantibodies are common, particularly Rheumatoid Factor. A common complication of RA is Sjögren’s syndrome, when in?ammation of the mucosal glands may result in a dry mouth and eyes. SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) and various overlap syndromes occur, such as systemic sclerosis and dermatomyositis. Autoantibodies against nuclear proteins such as DNA lead to deposits of immune complexes and VASCULITIS in various tissues, such as kidney, brain, skin and lungs. This may lead to various symptoms, and sometimes even to organ failure.
Infective arthritis includes: SEPTIC ARTHRITIS An uncommon but potentially fatal disease if not diagnosed and treated early with approriate antibiotics. Common causes are TUBERCLE bacilli and staphylococci (see STAPHYLOCOCCUS). Particularly at risk are the elderly and the immunologically vulnerable, such as those under treatment for cancer, or on CORTICOSTEROIDS or IMMUNOSUPPRESSANT drugs. RHEUMATIC FEVER Now rare in western countries. Resulting from an immunological reaction to a streptococcal infection, it is characterised by migratory arthritis, rash and cardiac involvement.
Other infections which may be associated with arthritis include rubella (German measles), parvovirus and LYME DISEASE.
Treatment Septic arthritis is the only type that can be cured using antibiotics, while the principles of treatment for the others are similar: to reduce risk factors (such as hyperuricaemia); to suppress in?ammation; to improve function with physiotherapy; and, in the event of joint failure, to perform surgical arthroplasty. NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS) include aspirin, paracetamol and many recently developed ones, such as the proprionic acid derivatives IBUPROFEN and naproxen, along with other drugs that have similar properties such as PIROXICAM. They all carry a risk of toxicity, such as renal dysfunction, or gastrointestinal irritation with haemorrhage. Stronger suppression of in?ammation requires corticosteroids and CYTOTOXIC drugs such as azathioprine or cyclophosphamide. Recent research promises more speci?c and less toxic anti-in?ammatory drugs, such as the monoclonal antibodies like in?iximab. An important treatment for some osteoarthritic joints is surgical replacement of the joints.... joints, diseases of
It is a sign of hyperuricaemia, which accompanies gout.... tophus
When uric acid excretion is disrupted, for example by kidney disease, it may result in hyperuricaemia.... uric acid
days and often recur. They are sometimes accompanied by fever. Gout may be associated with kidney stones (see calculus, urinary tract), and affects 10 times more men than women. In men, it occurs any time after puberty; in women it usually occurs after the menopause. The condition tends to run in families.
The diagnosis is confirmed by tests on blood or fluid from the affected joint to measure uric acid levels. Pain and inflammation can usually be controlled by nonsteroidal anti-inflammatory drugs or colchicine. If these are ineffective, a corticosteroid may be injected into the joint. Long-term treatment with drugs such as allopurinol or probenecid can stop or reduce the frequency of attacks.... gout
hyperuricaemia An abnormally high level of uric acid in the blood. Hyperuricaemia may lead to gout due to the deposition of uric acid crystals in the joints; it may also cause kidney stones (see calculus, urinary tract) and tophus.
Hyperuricaemia may be caused by an inborn error of metabolism (see metabolism, inborn errors of), by the rapid destruction of cells in a disease such as leukaemia, or by medication that reduces the excretion of uric acid by the kidneys, such as diuretic drugs. Large amounts of purine in the diet may also cause hyperuricaemia.
Drugs such as allopurinol or sulfinpyrazone are prescribed for the duration of the patient’s life. Purine-rich foods should be avoided.... hypertrichosis
Congenital abnormalities, such as horseshoe kidney, are fairly common and usually harmless. Serious inherited disorders include polycystic kidney disease (see kidney, polycystic), Fanconi’s syndrome, and renal tubular acidosis.
Blood vessels in the kidneys can be damaged by shock, haemolytic–uraemic syndrome, polyarteritis nodosa, diabetes mellitus, and systemic lupus erythematosus. The filtering units may be inflamed (see glomerulonephritis). Allergic reactions to drugs, prolonged treatment with analgesic drugs, and some antibiotics can damage kidney tubules. Noncancerous kidney tumours are rare, as is kidney cancer. Metabolic disorders, such as hyperuricaemia, may cause kidney stones (see calculus, urinary tract). Infection of the kidney is called pyelonephritis. Hydronephrosis is caused by urinary tract obstruction. In crush syndrome, kidney function is disrupted by proteins released into the blood from damaged muscle. Hypertension can be a cause and an effect of kidney damage. The most obvious symptom of acute kidney failure is usually oliguria (reduced volume of urine). This leads to a build-up of urea and other waste products in the blood and tissues, which may cause drowsiness, nausea, and breathlessness. Symptoms of chronic kidney failure develop more gradually and may include nausea, loss of appetite, and weakness. If acute kidney failure is due to sudden reduction in blood flow, blood volume and pressure can be brought back to normal by saline intravenous infusion or blood transfusion. Surgery may be needed to remove an obstruction in the urinary tract. Acute kidney disease may be treated with corticosteroid drugs. Treatment may also involve diuretic drugs and temporary dialysis (artificial purification of the blood). A high-carbohydrate, lowprotein diet with controlled fluid and salt intake is important for both types of kidney failure. Chronic kidney failure may progress over months or years towards end-stage kidney failure, which is life-threatening. At this stage, longterm dialysis or a kidney transplant is the only effective treatment.... kidney disorders
Health Encyclopedia