LUPUS ERYTHEMATOSIS (SLE)
Consultant: Edward M. Lichten, M.D., P.C.
Director, Headache Institute for Women
180 East Brown Street ‘2’
Birmingham, Michigan 48009
Telephone: (248) 593.9999
Email: firstname.lastname@example.orgSample Text
Lupus erythematosis is a gender-specific disease. The female to male ratio is as high as 10:1. The cause of this disparity in sexes is as yet unexplained. Human and animal studies confirm that hormones play a most significant roles in this difference in susceptibility.
Lupus is an autoimmune disease. This means there is a failure of the body’s normal mechanism of not attacking its own tissue. Patients with lupus report feeling “like their foot is on the accelerator and the brake of the car at the same time." Their body’s consume vast amounts of energy repairing its own ongoing damage of tissue. This disease is most often of long durations with chronic fatigue as the most consistent finding. Lupus can cause death by its destruction of lung, kidney, liver and brain tissue.
Hormones and Disease:
All tissues in a person’s body respond to hormones. Except thyroid, all major hormones are derived from cholesterol. The major pathway is cholesterol to pregnenolone to dihydroepiandosterone(DHEA) to androstenedione to testosterone. In women, the vast majority of testosterone is converted to estradiol. For men, a significant amount of testosterone is converted to dihydrotestosterone, a super potent anabolic steroid.
Sex hormones have the strongest influence on growth and repair in the human body. For women the primary hormone is estrogen which is key to reproduction. But women’s natural testosterone is a strong influence for muscle and bone growth and for her interest in reproduction.
Interestingly, researchers in animals and humans are reporting that testosterone can reduce the body’s inflammatory response. There are reports that the inflammatory states of Crohn’s disease, rheumatoid arthritis, diabetes vaculitis and now Lupus erythematosis may improve when treated with anabolic steroids (testosterone, DHEA and human growth hormone). This benefits of anabolic steroid therapy are, therefore, not limited only to men. It now seems that for these diseases, testosterone works well for women too.
One of the first medical publications to report the beneficial effects of anabolic steroids on Lupus erythematosis was performed at Stanford University Medical Center under the direction of JL McGuire, M.D.  He reported in 1995 that DHEA, an over-the-counter hormone, was able to decrease proteinuria and fatigue symptoms in female lupus patients. In a follow-up study in by his associate van Vollenhoven, they confirmed the beneficial effects of DHEA in both premenopausal and menopausal women followed for one year.
Van Vollenhoven reported that “the weakly androgenic adrenal steroid dehydro- epiandrosterone (DHEA) raised not only DHEA and DHEA-S levels, but also the level of testosterone. His patients showed a decrease in disease activity measured by the SLE Disease Activity Index score, patient global assessment and physician global assessment over the entire year. Other than mild acne, there were no complaints.
Lahita took a different look at lupus erythematosis in women. She questioned whether women with lupus had a deficiency in their normal production and utilization of testosterone. Following up from the mice studies, Lahita found elevated tesosterone oxidation at C-17 in females with Lupus. She then proceeded to measure anabolic steroids in 42 lupus patients. The results show that levels of all androgens were suppressed: testosterone, androsteinedione, DHEA and DHEA-S. The lowest levels of androgens were found in those individuals with the worst disease. The author suggests that “future therapeutic regimens (will be) based on male hormone replacement."
Folomeev finds another defect in endocrine balance in SLE patients. He documents an acceleration of the testosterone to estradiol conversion. There is a tendency toward an increase in aromatase activity in healthy SLE patients when compared to controls. Interestingly, “among SLE patients the aromatase activity varied inversely with the disease activity. Patients with SLE had decreased androgen and increased estrogen levels. Aromatase activity in SLE patients had significant direct correlation with estrogen levels. These data suggest that abnormal regulation of aromatase activity may partially explain the abnormalities of estrogen synthesis in SLE." These patients are relatively testosterone deficient.
Treatment protocols with testosterone in human subjects is antidotal. The animal studies report sometimes dramatic results. Van Griensven documents that testosterone-decanoate reduced significantly the development of albuminuria in females(mice) in a line of mice who develop lupus. In contrast, giving 17 beta-ethinyloestradiol will have no effects on the disease development but will worsen the amount of autoantibodies against renal tissue. “Our findings confirm earlier observations, in that testsoterone-decanoate is shown to be an inhibitory compound, whereas 17 beta-ethinyloestradiol has stimulating properties in autoantibodies."
In our medical practice, we carefully evaluate the levels of anabolic steroid hormones. If the levels of DHEA-sulfate is less than 100ng/ml we supplement first with oral DHEA. The dosage is 10 to 25 mg in the morning and afternoon. For more severe disease, we increase the DHEA to 50 mg twice daily with an upper limit of 300mg twice daily. The only side effects maybe facial hair and acne. These are much less severe if spirolactone, 50mg is prescribed once to three tablets twice daily. Some note improvement of acne with the herb Saw Palmetto 120mg twice daily also.
Secondly, we add injectable testosterone in the form of Deca-Durabolin 100mg every 2 to 4 weeks for its strong anti-inflammatory effect. If cost is a factor, testosterone cyprionate is used. Many of my patients prefer the testosterone pellets because they need return only 2 to 3 times per years. It is just a question of preference and realized results.
Lastly, we measure human growth hormone. As the cost is $600 per month, few individuals are able to afford this treatment. Normal levels are greater than 200 MIU/ml but I have seen levels below 100 mIU/ml in many patients. Replacement therapy involves daily subcutaneous injections. The three listed anabolic hormones are synergetic an should be taken concurrently. We also promote a gluten-free diet and a diet to minimize exposure to yeast in food. Conclusion: New findings in animal and human studies point to a defect in testosterone production in the affected female who suffers from lupus. Until we are able to change the genetic makeup of these individuals, the most promising therapy might be anabolic therapy with DHEA, testosterone and human growth hormone replacement. When hormonal therapy is used to treat medical diseases, we call this “Gender-Specific Medicine."
For more information about Gender-Specific Medicine, explore the other articles listed in the column on the left of the screen. For a copy of the CD-ROM entitled “Gender-Specific Medicine" click on Order CD_ROM Book below.
References: 1. Van Griensven M, Bergijk EC, Baelde JJ, De Heer E, Bruijn JA. Differnetial effects of sex hormones on autoantibody production and proteinurua in chronic graft-versus-host disease-induced experimental lupus nephritis. Clinical Exp Immunology 107(2):254-260 1997.
2. Barry NN, Van Vollenhoven RF, McGuire JL. Dehydroeiandrosterone in systemic lupus erythematosis: relationship between dosage, serum levels, and clinical response. J Rheumatology 1998:25(12):2352-6.
3. Van Vollenhoven RF, Morabiot LM, Engleman EG, McGuire JL. Treatment of systemic lupus erythematosis with dehydroepinadrosterone: 50 patients treated up to 12 months. J Rheumatology 1998;25(2):285-9.
4. Lahita RG, Bradlow HL, Ginzler E, Pang S, New M. Low plasma androgens in women with systemic lupus erythematosis. Arthritis Rheumatology 1987;30(3):241-8
5.Folomeev M, Dougados M, Beaune J, Kouyoumdjian JC, Nahoul K, Amor B, Alekberova Z. Plasma sex hormones and aromatase activity in tusses of patients with systemic lupus erythematosis. Lupus 1992;1(3):191-5
The information in this newsletter does not dictate an exclusive course of treatment or procedure to be followed and should not be construed as excluding other acceptable methods of practice.
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Installed: March 14, 2000