sábado, 12 de abril de 2008

Mais um dia...

A Cláudia hoje iniciou o ciclo com ciclofosfamida.
Hoje o processo foi mais lento. Em vez de ser em duas horas, foi em 6 horas e mais diluído. Sempre acompanhada pela equipa medica que a está seguir para verificar se não fazia reacção alérgica como da primeira vez.
Ás 19 horas estava quase acabar o ciclo, e não tinha marcas de reacção, falamos há bocado pelo telefone e também não tinha sinais de reacção, contudo, vamos aguardar por amanha e verificar como está…

Vamos aguardar!

Marco de canaveses, 12 de Abril

Tony Madureira

3 comentários:

msilva disse...

Lupus erythematosus - The food factor
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).

In: http://www.wddty.com/03363800371963609773/lupus-erythematosus-the-food-factor.html

msilva disse...

Lupus erythematosus
Q:I have systemic lupus erythematosus (SLE) and would be interested to know of alternative therapy, if possible. I was diagnosed in 1989 when I had my gallbladder removed. I had problems all along until 18 months ago when I had a massive flare up i

I'd also be interested in your comments on my medication, which includes cyclophosphamide, prednisolone, ranitidine, nifedipine, frusemide and carbamazepine (the latter because I suffer from petit mal epilepsy). What alarms me is that all the tablets say they should not be taken with kidney impairment, which I have. It was suggested that I may live five years. I'm 46. Well, I think if I don't die from lupus, I'll die from the medicine. U J S, Newcastle-on-Tyne...

A:As you know, SLE is an auto immune disease, in which the immune system begins to attack the body's own cells. There is much that medicine doesn't know about this condition for instance, what causes it or even how to devise a test to definitely diagnose it.

In most cases, diagnosis is made on the basis of a collection of symptoms: arthritic like joint and muscle pain, swelling of hands and feet, a red rough "wolverine" rash over the skin hence the name, which means, literally "red wolf".

In some cases, the disease can progress to attack the kidneys and central nervous system. Although the treatment and diagnosis of the disease hasn't changed much in 10 years, we do know that certain things such as ultraviolet light, hormones (such as the Pill) and infections can cause a flare up. Luckily, the arthritis accompanying SLE is rarely permanently crippling and the rashes can heal without scarring.

In the 1970s the late American medical critic Dr Robert Mendelsohn called SLE one of the most important of the modern iatrogenic (doctor produced) diseases (The People's Doctor, vol 5 no 2). He identified a number of drugs which can precipitate lupus. Significantly, in your case, these include drugs to control epilepsy, such as carbamazapine the drug you are taking. Phenytoin, methsuximide and ethosuximide also may bring on SLE. If you were taking an anti convulsant before your symptoms of SLE started, it is possible that one of those drugs triggered (or worsened) the disease.

Other drugs which can cause lupus include antihypertensives such as methyldopa drugs, those for irregular heartbeat like procainamide hydrochloride, the anti tuberculosis drug isoniazid, anti psychotic drugs such as chlorpromazine, certain antibiotics like penicillin, streptomycin and tetracycline, phenelzine sulfate, for anxious and depressed patients, or the antihypertensive hydralazine hydrochloride.

Conventional treatment assumes that lupus can't really be cured, and so seeks to suppress symptoms and control them through maintenance therapy. The mainstay of treatment is steroids, such as prednisone or prednisolone whose anti inflammatory affects control many of the more obvious symptoms.

According to a review of lupus treatment in the British Medical Journal (11 September 1993), Patrick Venables, senior lecturer at the Kennedy Institute of Rheumatology in London, says that in the 1970s and 1980s it became fashionable to give high doses of intravenous prednisolone in a "pulsed" way to avoid cumulative side effects from steroids (everything from osteoporosis and diabetes to an increased likelihood of infections, and even sudden death).

However, several studies, he said, showed no difference in terms of effect on kidney function between the two groups and no long term benefit.

Cyclophosphamide is a powerful cytotoxic drug used to treat leukemia and some forms of cancer. It acts as an immunosuppressant to stop the body from rejecting transplant drugs and is given in cases of severe rheumatoid arthritis. Recently, these sorts of drugs have been flavour of the month in treating autoimmune diseases.

According to Venables, it can be of some benefit in kidney lupus, but its use is often cut short by almost invariable side effects. These include nausea, and vomiting, hair loss, an early menopause in women and permanent sterility in men, bladder cancer, cystitis and bone marrow suppression.

It has been found, says Venables, that pulsed intravenous treatment and the concurrent use of the drug mensa can help to avoid some of these side effects.

In reviewing treatment of SLE, Venables says in essence that although more people with lupus are surviving the disease, an increased number are now suffering from the side effects of the drugs. Hence, the emphasis now is in trying to modify current regimens to cut down the number of problems caused by the treatment itself.

You rightfully say that the cocktail of powerful drugs should not be used in people with kidney damage. Presumably you are taking the nifedipine, an antihypertensive, and frusemide, a powerful diuretic, for hypertension, and ranitidine (Zantac) for peptic ulcers or disturbance of stomach function.

As you say, the main worry is that all of these drugs aren't supposed to be given to someone with kidney impairment.

The first thing you might do is to investigate with your doctor whether your SLE could have been caused or exacerbated by your anti convulsant drugs.

Ask your doctor to change to a milder anti convulsant drug or see if you can lower the dose or be weaned off it altogether. This alone may help your symptoms.

You might also wish to have a session with him in which you review the potential for kidney damage of all these drugs and try to cut out any which aren't essential. For instance, is it absolutely necessary to have the cyclophosphamide, clearly the most potent? Is it at all possible to simply stick to a low dose of steroids?

Also clarify why are you being given the other drugs. Do they have a legitimate function in controlling your disease or are they only there to combat side effects of your other medication?

As for an alternative approach, Dr Jonathan Brostoff, honorary consultant physician at the Middlesex Hospital Medical School and a leading international authority on food allergy and the immune system, is one of a number of medics who believe that SLE is aggravated and possibly even caused by food intolerance. He finds that some of his patients with SLE do much better if a classic elimination diet is tried on them and they are subsequently treated for reactions to food or other environmental chemicals.

You may wish to try this approach with a very experienced doctor like Brostoff, who can see if the dietary method will halt SLE sufficiently for you to quit some of the drugs.

In:
http://www.wddty.com/03363800370655783779/lupus-erythematosus.html

Tony Madureira disse...

Boa tarde,

Muito obrigado pelo teu contributo.
Peço-te para divulgar este blogue sempre que puderes.
Pretendemos que seja um local de informaçao para quem tem lúpus. As pessoas a quem é diagnostica esta doença ficam á deriva. Se ouvirem e trocaremm ideias com quem já passou pela mesma experiencia pode ser muito importante.

mais uma vez muito obrigado.

Abraço.