Forty years ago, if you were diagnosed as having lupus, otherwise known as systemic lupus erythematosus (SLE), the prognosis would not have been good. Odds were that you would have a 50/50 chance of dying within five years. Today doctors are most lik
Lupus is a baffling disorder with a multitude of symptoms and a different pathogenesis in each individual. Diagnosing this disorder, which affects nine times more women than men, can be difficult.
Although the general consensus is that it affects around 1 in 1000 people in Europe and America, recent research shows that it is underdiagnosed and that rates may be double what we have previously assumed (Lancet, 1996; 347: 367-9).
Lupus is an autoimmune disease which causes inflammation of the connective tissue, in particular of the membranes around the joints (with symptoms similar to those of rheumatoid arthritis) and around such organs as the lungs, kidneys and heart. Its most well known characteristic, however, is a red rash on the cheeks. In some cases this rash may spread to the entire upper body.
The less common form of lupus, discoid lupus erythematosus (DLE) presents as a red, scaly rash on the face the “wolf mask” from which lupus derives its name. DLE can remain static or it can turn into SLE the most common and severe form of lupus. When this happens the body begins to form antibodies against itself, causing inflammation, tissue damage and pain. Lupus can affect virtually any organ or system within the body and it can be life threatening.
The criteria for diagnosing lupus has not been revised since 1982 (Arthritis Rheum, 1982; 25: 1271-7), which may account for so many cases going undetected. When a physician is attempting to diagnose lupus, one of the first things he will check will be the patient’s levels of anti nuclear antibodies (ANA). Some 95 per cent of lupus sufferers will have raised ANA (Rheum Dis Clin North Am, 1990; 16:617-39). ANA is common in other rheumatic diseases and in autoimmune liver and thyroid diseases. It is also present in around 2 per cent of the population without producing symptoms (Adv Immunol, 1989; 44: 93-151). There will also be a higher level of foreign DNA (Arthritis Rheum, 1990; 33: 634-43). In fact, SLE patients produce a large number of antibodies and, depending on which are present, physicians can predict with some certainty how the disease will develop (Clin Exp Immunol, 1985; 62: 337-45; J Clin Immunol, 1991; 11: 297-316).
What confounds doctors is what causes the immune system to go haywire in the first place. As with so many autoimmune disorders, doctors’ bewilderment leads them to assume that SLE can’t be cured and so they concern themselves more with what can be done to suppress and control symptoms. Because SLE patients can have a wide variety of symptoms, often it is treated in a rather haphazard way with courses, cocktails even, of drugs in the hopes that one of them will do the trick.
What this means is that, although more people are surviving SLE, they are at best living with a vastly decreased quality of life, and at worst, trading the risk of death from lupus for the risk of death from the drugs used to control it. For instance, one of the most common treatments is steroids, such as prednisone or prednisolone, to suppress the action of the immune system. These are given either as creams or in pill form. The side effects of steroids are wide ranging and too serious to use on a just in case basis. At one end of the spectrum they include weight gain, puffiness in your face and easy bruising. At the other extreme patients will suffer osteoporosis (Ann Int Med, Nov 15, 1993; Clin Pharm, 1993; 25(2): 126-35), muscle wastage (Euro Respir J, 1992; 5(8): 997-1003; Pol Tygo Lekar, 1989; 44(27): 6324), cataracts (Dermatol Clin, 1992; 10: 505-12; Surv Opthamol, 1986; 31: 2602) diabetes, hypertension and increased susceptibility to infection.
Studies have shown that steroids can cause permanent damage after just a single dose, and may actually cause further damage to a individual’s already fragile immune system (see WDDTY, 1996; 7(2): 1-3, 11-12).
There are dangers in other drugs used to treat SLE. Cyclosporin, an immunosupressant usually used to stop rejection of transplanted organs, can cause kidney dysfunction, high blood pressure and stomach problems; anti malaria drugs such as chloroquine and hydroxychloroquine have been found, mostly by trial and error, to exert some beneficial effects on the arthritic symptoms associated with SLE. But their most common side effect is visual impairment, which can occur in doses above 6 mg per day (Arthritis Rheum, 1979; 22: 832). Other side effects include tinnitus, insomnia, hyperactivity and anemia. Another immunosuppressant, methotrexate, can cause stomach complaints and nausea as well as damage to the liver and lungs (Ann Rheum Dis, 1990; 49: 25-7). Death can occur in high doses, especially if the patient is taking daily, instead of weekly doses (Drugs and Therapeutics Bulletin, 1993; 31: 18). The side effects of these drugs are so severe that they should only be used in extreme cases where the patient’s life is under threat.
By concentrating on suppressing and managing symptoms, it seems that medicine is missing some important clues about where SLE may come from. Medicine believes that SLE can be organic, originating within the individual’s body, triggered by toxins or genetic predisposition. But it can also be iatrogenic, caused by many different medicines given to treat other, unrelated disorders (Science, 1994; 266: 810-13). There are, in fact, more than 80 different drugs which can cause lupus.
For instance an attack of SLE can be brought about by the use of procainamide (used to treat heart arythmias), propylthiouracil (an antithyroid), trimethadione (an antituberculosis drug), hydralazine (a vasodilator) or even the tetanus vaccine.
The over consumption of antibiotics, particularly those containing sulphonamide (Septra, Septrin, cotrimoxazole) to treat viruses such as those associated with colds or flu (for which they are almost always totally ineffective) has been shown to damage the immune system and is very commonly associated with bringing on an attack of lupus.
Women who have SLE have been shown to have very low levels of testosterone, apparently because their bodies break down the hormone more rapidly than others (Arthritis Rheum, 1994; 26: 1517-21). Patients of both sexes may also have elevated levels of prolactin (J Rheumatol, 1993; 20: 1095-100). Because of this, women with SLE are increasingly given hormone therapy, though there is little evidence that it is effective (Arth Rheum, 1985; 28: 1243-50; Ann Rheum Dis, 1991; 50: 897-8). What has been demonstrated, though, is that putting women on high doses of estrogen (such as those contained in some birth control pills) can both produce SLE like symptoms and aggravate existing SLE (Scan J Rheumatol, 1991; 20: 427-33).
The lupus induced by medicines has a slightly different character to other forms of lupus (Rheum Dis Clin North Am, 1994; 20: 6186), which are 10 times more common. Once medication is stopped, SLE symptoms can disappear within four to six weeks. But harmful antibodies can remain in the system for as long as a year (N Eng J Med, 1994; 330: 1871-9).
Where does lupus come from? Research has turned up an intriguing possible link with the menstrual cycle. In the 1980s a maverick UCLA scientist named Patrick Schlievert was trying to convince the Centers for Disease Control (CDC) in America that a new strain of Staphylococcus aureus was producing a lethal toxin which was leading to Toxic Shock syndrome (TSS). It took years for the CDC to officially recognize the Toxic Shock Syndrome Toxin-1 (TSST-1) and admit that tampons weren’t the cause of TSS, but simply the growth medium for a particularly deadly bug which, once a woman was infected, acted like a time bomb inside her. A first exposure to the virus produced flu like symptoms and sensitized the immune system. Although the woman would recover from the illness, the Staph virus would remain in her vagina, where its population would surge, feeding on the nutrient rich menstrual blood and endometrial tissue, resulting in TSS.
A byproduct of his research, however, was the discovery that, of the women who survived TSS, a substantial proportion developed autoimmune disorders: 11 of the 123 women in one survey developed lupus and a further 40 per cent had early symptoms of arthritis a striking finding considering that most TSS sufferers were under the age of 35 (J Infec Dis, 1981; 143: 509-16; Ann Int Med, 1982; 96: 982-6; see also The Coming Plague, Laurie Garrett, Penguin, 1994). But not all women infected with the
Staph a. virus develop TSS. The question is, is there a population of women walking around with more subtle self destruction taking place inside of them which is linked to the virus?
There are other theories as well. In America, Dr. William Crook has suggested that chronic intestinal yeast infections can promote a wide range of illnesses, from fatigue, depression, and bloating to more serious diseases such as lupus. The theory is that the yeast germ, known as Candida albicans, produces toxins which are absorbed from the gastrointestinal tract into the body. These toxins are thought to provoke either autoimmune reactions or other adverse effects. (Nutrition and Healing, 1995; 2(12): 1, l0-11). Treatment with an anti-candida diet (see box p5) has been shown to reduce levels of anti nuclear antibodies (ANA), the cells which attack the body.
The link between food allergy and lupus is another fruitful avenue for exploration, according to the copious anecdotal evidence to date. In one report a child with lupus was found to have antibodies to milk. Symptoms vanished when he eliminated milk from his diet, and returned when he drank milk on a further two occasions (J Pedia, 1974; 84:59-647). In a study from Australia, four patients with lupus had marked symptom relief after following a programme that included nutritional supplements and avoiding allergenic foods. In addition to a reduction in symptoms, their ANA levels became normal (Int Clin Nutr Rev, 1985; 5(4): 166-76).