Chapter two
RHEUMATIC DISORDERS
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Chapter twoRHEUMATIC DISORDERS |
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What are they?
A short anatomy lesson
The immune system
"Oh yes, dear, you've got rheumatism, have you? Fancy, and at your age, too. Well, I know all about it. I get twinges meself", says one Older Dear, with 'odd twinges', to one Younger Dear who has RA and knows only too well that the two experiences are poles apart. Symptoms and treatment differ enormously.
The words 'arthritis' and 'rheumatism' are used very loosely. People tend to use 'arthritis' for any joint trouble, and 'rheumatism' for vague aches and pains and muscle twinges. Correctly used, 'arthritis' literally means 'inflammation of the joint' ('arthron' = joint, '-itis' = inflammation, as in 'tonsillitis' for instance). 'Rheumatism' is too vague a term to be used medically.
Medical experts prefer the general term 'rheumatic diseases', or 'rheumatic disorders'. They also talk about 'disorders of the musculo-skeletal system' or 'locomotor system' (the body's 'movement' system), though other body systems and organs can be involved in rheumatic disorders too. The general medical term actually covers some 200 very different conditions.
Some people experience a rheumatic disorder as just a slight, temporary nuisance. For others it may mean a lifetime of misery. For just a few, very few people, some rare types of rheumatic disorder and complications can even be fatal. For most of us YPAs, though, it means a sort of switchback existence of ups and downs — sometimes black periods of utter misery but good and better times too. More detail in chapter 3 about some individual rheumatic disorders. For now, here's a brief summary of the main groups.
Rheumatic disorders account for 23% of all attendances in family doctor practices and 65 million working days being lost annually. That's even before you start thinking about their physical, social and emotional consequences (which this book will do). They can affect anyone, at any age, even babies. Some are more common in men than women (eg AS, gout, Reiter's syndrome), or vice versa (eg RA, lupus).
"Approximately five per cent of persons between the ages of 16 and 44 years have a rheumatic disorder, compared with 23 per cent for persons between 45 and 64, and 41 per cent of those aged 65 years and older."
(ARC's Arthritis and Rheumatism in the Eighties, 1986)
Numerically speaking, most people with arthritis are over 50 and have osteoarthritis (OA). Books and information about arthritis usually focus on this age group. Older OA usually affects one, or just a few joints. Not a true picture for younger people with arthritis. So in this book, and when I use the term 'arthritis' loosely, I'm referring to the forms more common to our age group, like RA, AS, JIA, and psoriatic arthritis.
As there are so many different conditions classified as rheumatic disorders, there can be no one cause or no one cure for 'arthritis', as such. The cause of rheumatic fever, which used to be one of the commonest serious diseases of childhood, is now known. Not so for disorders like RA and AS, yet, so for those there's no instant cure either, not yet, anyway. However there is plenty of research going on, and while we wait for a cure treatments are constantly improving. Chronic gout, for instance, is now fully controllable with a drug called allopurinol. (Look too at chapter 4, for more on the topic of no-cure-yet.)
Better understanding of our disorders means they can be better treated and 'managed'. Keep up-to-date with research by getting ARC's Arthritis Today magazine, or visiting ARC's website: www.arc.org.uk. It's thought that the cause or causes of something like RA, AS, lupus or Reiter's may be a particular 'jackpot' combination of factors. We may perhaps have a genetic predisposition which alone does nothing unless and until it's combined with one or more trigger factors — perhaps infection by a bacteria or virus (though the disorders themselves are not infectious or contagious), perhaps something environmental, perhaps something hormonal. It's even possible the same condition may have different causes in different people.
Whatever the cause, in inflammatory arthritis the body develops an 'auto-immune' reaction, a sort of allergic reaction to bits of itself. Instead of your immune system defending your body against foreign invaders it mistakenly (and painfully) turns on itself. More about the immune system in a moment.
As rheumatic disorders are mainly disorders of the musculo-skeletal system, learning a little about the system's bits and pieces will help you understand not only what's gone wrong, but also why and how different treatments work. For instance:
Any of the bones and joints of the musculo-skeletal system and/or the body tissues in and around them, like muscles, tendons, bursae, blood vessels, skin, can be affected. It just depends which particular disorder has chosen you as its victim.
But even then, no two experiences of the same rheumatic disorder are exactly the same. Even the same disorder in the same individual can change mysteriously from hour to hour or day to day or month to month. Remember that does mean things can and do get unexpectedly better as well as unexpectedly worse.
Bones (some 206 of them!) form the body's framework. Bones connect with each other at joints. Not all joints move, but those that do are called synovial joints. Joints are connected, stabilised, and moved by soft tissue (muscles, tendons, ligaments). Next time you cook a chicken, look first at the joints and how they move and fit together. Joints in the back have a different structure from synovial joints.
A synovial joint is enclosed in a joint capsule, lined with a fine skin-like synovial membrane (or synovium). This contains synovial fluid, which lubricates the joint, like oil (though it's much more complex). Fluid increases in an inflamed joint, causing swelling.
The surface of each adjoining bone in the joint capsule is covered by a white shiny rubbery substance called articular cartilage (not the same as cartilages removed from knee joints). Synovial fluid pumps in and out of its fine sponge-like surface as the joint moves or rests. The cartilage contains no nerves to act as pain-transmitters. That's why symptoms of early OA, which starts in the cartilage, tend to be stiffness, rather than pain. But when a rheumatic disorder starts elsewhere, eg in the bone, or synovial membrane (as in RA), pain is a much earlier symptom, because these bits have a rich nerve and blood supply.
Muscles which move bones and joints are called skeletal muscles. Some are attached directly to the bone, while others are attached by extra strong fibrous bands or cords called tendons. When muscles contract, joints move. Some tendons run through sliding tunnels which are lined by a sheath of the same type of synovial membrane as the joint capsule, and can similarly become inflamed (tenosynovitis) and possibly damaged.
Tendons can be displaced sideways, pulling bones (eg finger joints) in the wrong direction. Sometimes in RA a tendon can become so weak that it breaks, and the attached muscle and joint no longer work properly, leading to a 'dropped finger' appearance. Special splints may be used to encourage the tendon to heal. (Although my fingers have 'dropped' so I can't straighten them, after several years in remission they have regained remarkable strength.)
Muscles can be very strong, those in your thighs, for instance - the quadriceps muscles or 'quads' physios are so fond of. Weak quads make life really difficult, but simple exercises can keep them strong. Each muscle fibre receives 'relax' and 'contract' signals via the nervous system, is fed with oxygen and other energy-producing substances (eg glycogen) through the blood, and produces waste products (like lactic acid).
Doctors and physios sometimes talk about muscles going into spasm. The muscles tighten, to try to prevent a painful joint moving. In an arthritic knee for instance this means you tend to walk with the knee slightly bent. Unfortunately the muscles are then in danger of weakening and wasting, leading to greatly increased pressure within the knee as it bears weight, and increasing the danger of joint damage and deformity.
The first step in counteracting this is treatment with painkillers and heat or cold to relieve the pain. Then you can, coached by your physio, work on strengthening the weakened muscles. Stronger muscles help prevent possible damage and deformity. In the prolapsed disc ('slipped' disc) of backache, bedrest aims to relax the back muscles which are in painful spasm, and aims to protect the displaced disc tissues.
Ligaments are another part of the musculo-skeletal system. They hold together bones, cartilage, and other parts of the body. A bursa is a sort of protective cushion of body tissue, which lies between a tendon and and a bone, or between other moving parts. It's lined with a membrane like the synovial membrane, and can become inflamed and painful (bursitis) in disorders like housemaid's knee.
That's a brief picture of the main musculo-skeletal bits and pieces. Different disorders affect different bits in different ways. Gout, for instance, is an inflammatory arthritis in which 'urate' crystals are deposited in and around the joints, resulting in excruciatingly painful inflammation, if left untreated. In OA it's the joint cartilage (insensitive to pain) which is first affected, and pain follows later as pain-sensitive bits like the bone become involved.
RA on the other hand starts in the very pain-sensitive synovial membrane, which becomes inflamed and swollen, and can lead to thinning and destruction of the smooth cartilage and bone. Synovial fluid increases and swells the joint, stretching the stabilising ligaments and tendons, leading to weakness and possible deformity if left untreated. AS usually starts in the bones of the lower back, with inflammation of the 'enthesis', the place where muscle is attached to the bone. 'Soft tissue' disorders affect body tissues around the joint rather than the joint itself. For more about:
This is the body's internal self-defence system. Abnormalities with the way it works are closely linked with many rheumatic disorders. Normally it works well. The body's natural reaction is to fight anything it identifies as foreign. For instance it responds to a first attack of measles or other invader infection by producing antibodies, to fight and conquer the infection, the antigen. Some of these antibodies remain in the body ready to leap into action again at the first sign of any repeat infection and quash it at once. Vaccines are a way of artificially stimulating antibody production, to protect the body against infections, and confer immunity.
Many rheumatic disorders, for instance RA and lupus, are described as auto-immune disorders ('autos' = self, in Greek). Instead of beneficially fighting a foreign invader, the body for some unknown reason mistakenly over-reacts and fights its own tissue, causing damage. (You might have noticed that the full name for the illness 'AIDS' is 'auto-immune deficiency syndrome'. AIDS is not a rheumatic disorder but an entirely different type of auto-immune disorder where the immune system weakens and ultimately gives up fighting completely.)
Blood tests tell the experts something about past or present fighting inside the body by its immune system. All sorts of different antibodies (or 'immune complexes') may be identified. One of these is the rheumatoid factor, discovered in 1940, found in some but by no means all, people with RA. Having the factor doesn't automatically mean you'll get RA. Masses of people with rheumatoid factor never develop RA.
So by itself the rheumatoid factor doesn't tell us much about why someone does or doesn't develop RA. It may be only one of a particular 'fruit-machine' combination of environmental, physical, infectious or possibly genetic factors which trigger release of the unwanted 'jackpot'. It's even possible that the same disorder may have different causes in different people. Researchers are working hard to unravel these mysteries.
Similarly, the LE cell test used for people with lupus (SLE) isn't positive in everyone with lupus though another more recently developed test, for anti-DNA antibodies, does give a positive response for practically everyone with lupus. In lupus various auto-antibodies circulate in the blood, and can cause problems wherever they end up, eg rashes in the skin, damage to blood vessels, or trouble in the kidney, lungs, joints, and occasionally the brain.
HLAs are another bit of the immune system. An HLA (Human Leucocyte Antigen) is a sort of biological trademark in our genes, which helps an individual immune system to distinguish between what is or isn't part of the body for which it is responsible. We each have only eight out of a vast range of possible HLAs. Someone needing a kidney transplant needs to find a kidney with a perfect or almost perfect match of HLAs, to avoid it being rejected by the immune system. Identical combinations are hard to find. HLA incompatibility is similar to blood group incompatibility, where a bodyful of, say, blood group A will reject an infusion of blood group B.
Someone with AS may read that over 90% of people with AS have HLA B27, though it's present in only about 7% of the general population. People with Reiter's syndrome also usually have HLA B27. Many other disorders are associated with a particular HLA. HLA DR4, for instance, is found in 70% of people with RA, but in only 25% of the general population.
Immunosuppressives are sometimes used to treat severe problems in rheumatic disorders. They suppress activity in the immune system, and hopefully any harmful auto-immune activity. Unfortunately they also lower or suppress beneficial immune activity, putting the body at risk of attack by outside infections. That's why they're only used with the utmost care and caution by doctors.
Two books written to explain the immune system to the layperson: The Body at War (Unwin, 1989), by Professor John Dwyer (Australian), and Friendly Fire: Explaining Autoimmune Disease (OUP, 1995) by Professor David Isenberg (University College, London).