When an earthquake is about to take place, something happens in nature that prefigures the coming cataclysm. Dogs howl, cats climb trees, and birds stop singing. Whatever it is that signals these other members of the animal kingdom, man alone remains oblivious to the warning, either because he can’t detect it, or because he doesn’t recognize its meaning. Nature provides similar advance notice of the advent of diseases. Over the years, it has become clear that there is a forerunner to the development of acute rheumatoid arthritis, and in taking histories and treating patients, I have learned to become suspicious when certain symptoms are mentioned.
The most important of all antecedents to the rheumatoid explosion, the first development symptom on which one can most reliably base the suspicion that rheumatoid arthritis is about to happen, is unexplained fatigue; it precedes almost every case I have ever treated, sometimes coming on a year before there is any particular discomfort in the joints.
The fatigue will be serious enough that the patient goes to the doctor, but the doctor doesn’t know what he is looking for and as a rule he doesn’t find anything. He tells the patient that he or she is working too hard or is under too much stress. Another gambit is to ask the patient’s age, and then to suggest that when one gets to that point in life—whatever point it happens to be—one naturally slows down a bit. That way, the doctor can sound profound at the same time as he admits his ignorance, which is precisely the posture favored by most physicians when they haven’t the foggiest idea what’s happening.
The patient starts to become anxious; feeling tired and poorly is bad enough, but not knowing why is worse. Perhaps there is something else going on. Or perhaps, as the doctor seems to suggest, the patient expects too much from life or is not altogether balanced psychologically. People who are tired are also down emotionally, so these suggestions fall on fertile soil.
Sometimes the fatigue is accompanied by anemia, and the physician usually jumps at the chance to connect the two as effect and cause. And when he finds that the anemia doesn’t respond to iron or vitamin B-12 or folic acid or liver or to any of the things that ordinarily tend to raise the blood count, the common stratagem is to blame the intransigence of the anemia on the patient’s peculiar nature, which, in turn, adds to the patient’s anxiety. Stress has been clearly identified as an accelerator of the disease process, so by now the doctor has become a part of the problem.
When the next symptom emerges, it is usually a troublesome joint. The common reaction at this point is for the doctor to diagnose it as a sprain, and when the patient can’t recall any event that might explain such a result, the doctor blames it on the patient’s faulty memory. The diagnosis seems to be vindicated when the joint pain subsides and disappears, as usually happens with these first small warning shots before the arthritis explodes.
We have found that when a patient first complains of fatigue, especially if there is any connection with joint complaints, a test of blood for mycoplasma antibodies will produce positive results. Moreover, many patients will display these results for mycoplasma antibodies when nothing else shows. I have reached the conclusion, through long experience in following thousands of such patients, that even in the absence of any other indicator, signs of mycoplasmas in the blood are a guarantee that the patient is eventually going to develop either rheumatoid arthritis or some other disease of the connective tissue unless treatment is started. And I have learned not to wait.
At this stage it is also possible to gain supporting evidence by going back into the patient’s history. Many have had periods of fatigue before, and some can recall times when they were also suffering from depression, although most people have never spoken of the depression to anyone or looked at it from the viewpoint that it might be a symptom of something else. There is a certain amount of risk in admitting to either fatigue or depression, and most people would rather accept these symptoms as normal parts of growing up than take that risk in bringing them out for examination. I suspect that in most such cases, the fatigue and depression go back to early childhood.
Of course there are other disorders that can explain fatigue—such as mononucleosis, infectious hepatitis, or low thyroid function—and these should be on the physician’s list of things to eliminate. But once they have been ruled out, the doctor should be suspicious of early rheumatoid disease, and not write it off as an emotional imbalance. This is particularly important because at the time the fatigue develops, the patient is also usually more tense and nervous. These traits may owe to natural worry about a symptom that cannot be explained, or they may be symptoms in themselves, as we know them to be at later stages of rheumatoid disease.
Many other psychological factors can appear in this early syndrome of arthritis: irritability, reduced mental acuity, slower motor skills, shorter attention span, hesitancy, and loss of confidence. These can be bothersome to anybody, but they are particularly frightening to older people, who often interpret them as early signs of senility or Alzheimer’s disease.
Some pre-arthritics are extraordinarily sensitive to cold. I had one patient arrive in my office wearing a fur coat on a hot summer day. Others can be overly sensitive to heat. An impaired thermostat in either direction is a warning sign.
When the actual rheumatoid aspect finally shows itself, it is most commonly first seen in the small joints of the hands, feet, and ankles, although not always by any means. Regardless of where it begins, the real key to early rheumatoid disease is its migratory nature; it is an elusive Gypsy. Many people are misled by that nomadic feature into the belief that once it has left a particular area, it has cleared up. But it always comes back, becoming progressively more constant and more fixed.
From a treatment point of view, once the disease starts becoming localized, it is getting more serious. The migratory phase, before the body has started to encase the infectious agent inside its defensive walls of scars and inflammation, is considerably simpler to get at.
That is pretty much the way rheumatoid arthritis starts. In some cases it can tarry at one or another of these stages for months or even a few years, slight, insidious, mistaken for something else, often simply tolerated and ignored. In other cases it can explode overnight with a violence that leaves its victim suffering agonies in every joint.
It is interesting that people who experience an explosive onset often go into remission for a couple of years. Their immune systems have been shaken up to fight back hard, and protect them for a period following the attack. This action and reaction portrays a typical infectious process, and even when the arthritis finally returns after that kind of a start, it is frequently more responsive to treatment than the kind that seems to creep into the system a little bit at a time.
Viral pneumonia is a good prototype for what happens when a mycoplasma infection becomes fixed around a certain area. In the lung, the disease produces sections of what look like nodules of granulation material, inflamed tissues that are apparently fixed around the infectious organism and remain in position for months, producing the characteristic cough of the disease. I visualize the same thing happening in the joints, although it’s a lot harder to see there; we seldom biopsy joint tissue, although doctors used to, because we have found that rheumatoid arthritis tends to produce excessive scars where the mycoplasmas cluster, and the biopsy produces more pain than the information is worth.
The physician has to pay careful attention to the body’s defense mechanism as one of the primary aspects of the treatment of rheumatoid arthritis. He has to let the body do as much as it can to suppress the agents that cause the arthritis. That means carefully reducing the barriers which the body erects around the mycoplasmas so that they can be effectively purged without stimulating the production of the toxins that characterize the allergic flareup.
The doctor starts this process on first seeing the patient by giving some simple anti-inflammatory remedy such as aspirin, Bufferin, Ecotrin, or the like, the choice depending on how the patient’s stomach responds; this assumes the disease is a fresh, new case and not severe. (I must admit that only about 5 percent of the patients in my own practice are in this category; as a rule, by the time a patient gets as far as the Arthritis Institute, the disease is pretty well advanced.) The purpose in using these mild anti-inflammatories is not to treat symptoms, but rather to permit the body to get through its own barriers. If the aspirin doesn’t do the job, the doctor goes on to the encids: Clinoril, Naprosyn, Meclomen, Tolectin, Nalfon, Motrin, or similar drugs.
The doctor has to be continuously mindful of the mechanism, and not the symptoms, when he is treating the disease. This calls for a clear understanding of a very complex process (described in detail in Chapter 18) and a certain degree of tough-mindedness. The physician’s main responsibility is to relieve the disease, not just to make the patient feel better without regard for what happens next.