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Systemic Lupus Erythematosus

Also indexed as: Discoid Lupus Erythematosus, DLE, Lupus, SLE

Illustration

A butterfly-shaped rash on the face may be the first visible sign of lupus. While causes of this autoimmune disease are not clear, treatments do exist. According to research or other evidence, the following self-care steps may be helpful:

What you need to know

  • Get more omega-3s
  • Reduce lupus-related inflammation by frequently eating foods rich in omega-3s, such as flaxseed and fatty fish; take up to 20 grams a day of fish oil under a doctor’s supervision
  • Discover DHEA
  • Under your healthcare provider’s supervision, take up to 200 mg a day of the hormone dehydroepiandrosterone to improve lupus symptoms
  • Uncover food sensitivities
  • Work with a knowledgeable health professional to find out if certain foods aggravate your condition

These recommendations are not comprehensive and are not intended to replace the advice of your doctor or pharmacist. Continue reading the full lupus article for more in-depth, fully-referenced information on medicines, vitamins, herbs, and dietary and lifestyle changes that may be helpful.

About lupus

Systemic lupus erythematosus (SLE) is an autoimmune illness that causes a characteristic butterfly-shaped rash on the face accompanied by inflammation of connective tissue, particularly joints, throughout the body. In autoimmune diseases, the immune system attacks the body instead of protecting it. Kidney, lung, and vascular damage are potential problems resulting from SLE.

The cause of SLE is unknown, though 90% of cases occur in women of childbearing age. Several drugs, such as procainamide, hydralazine, methyldopa, and chlorpromazine, may create SLE-like symptoms. Environmental pollution and industrial emissions were associated with an increased risk of SLE in one study.1 In one reported case, zinc supplementation appears to have aggravated drug-induced SLE.2 Ultraviolet radiation from sun exposure is a commonly recognized trigger of the skin manifestations of lupus.3 Some environmental chemicals such as hydrazine4 and food dyes such as tartrazine5 may be environmental triggers of SLE in susceptible people.

Risk factors include a family history of SLE, other collagen diseases or asthma,6 menstrual irregularity,7 beginning menstruation at age 15 or later,8 exposure to toxic chemicals,9 and low blood levels of antioxidant nutrients, such as vitamin A and vitamin E, or beta-carotene.10 Free radicals are thought to promote SLE.11

Discoid lupus erythematosus (DLE) is a milder form of lupus that affects the skin. Like SLE, it’s not known what causes DLE, though sun exposure may trigger the first outbreak. DLE is most common among women in their thirties.

Product ratings for systemic lupus erythematosus

Science Ratings Nutritional Supplements Herbs
2Stars

DHEA

Fish oil (EPA/DHA)

Tripterygium wilfordii

1Star

Pantothenic acid

Vitamin E

Astragalus

3Stars Reliable and relatively consistent scientific data showing a substantial health benefit.
2Stars Contradictory, insufficient, or preliminary studies suggesting a health benefit or minimal health benefit.
1Star For an herb, supported by traditional use but minimal or no scientific evidence. For a supplement, little scientific support and/or minimal health benefit.

What are the symptoms?

Symptoms include decreased energy, weakness, fever, nausea, diarrhea, muscle and joint pain, chest pain, bruising, loss of appetite, weight loss, and a red, butterfly-shaped rash across the nose and cheeks. In addition, people with SLE may have symptoms of mouth sores, joint swelling, hair loss, changes in personality, seizures, and a coin-shaped, red skin rash elsewhere on the body that is aggravated by sunlight. Kidney, lung, and blood-vessel damage are potentially life-threatening manifestations of SLE.

Medical options

Prescription drug treatment includes cortisone-like drugs, such as prednisone (Deltasone®, Orasone®), methylprednisolone (Medrol®), and dexamethasone (Decadron®); the hormone dehydroepiandrosterone (DHEA); immunosuppressants, such as azathioprine (Imuran®), chlorambucil (Leukeran®), cyclosporine (Sandimmune®), methotrexate (Rheumatrex®), and cyclophosphamide (Cytoxan®); and the antimalarial drugs hydroxychloroquine (Plaquenil®) and chloroquine (Aralen®). Miscellaneous agents, such as danazol and dapsone might also benefit individuals with lupus. The goal of therapy is to suppress symptoms and relieve discomfort.

Dietary changes that may be helpful

An isolated case of someone with SLE improving significantly after the introduction of a vegetarian diet has been reported.12 In Japan, women who frequently ate fatty meats, such as beef and pork, were reported to be at higher risk for SLE compared with women eating little of these foods.13 Consuming fewer calories, less fat, and foods low in phenylalanine and tyrosine (prevalent in high protein foods, such as meat and dairy) might be helpful, according to animal and preliminary human studies.14

Foods high in omega-3 fatty acids, such as fish and flaxseed, may decrease lupus-induced inflammation. In one preliminary trial, nine people with kidney damage due to SLE were fed increasing amounts of flaxseed for a total of 12 weeks.15 After examining the results, researchers concluded that 30 grams per day was the optimal intake for improving kidney function, decreasing inflammation, and reducing atherosclerotic development. Flaxseeds also contain antioxidants, potentially helpful to those with SLE.16

To date, all studies on fish oil have used supplements and not fish (see below). Nonetheless, many doctors recommend that SLE patients eat several servings of fatty fish each week.

Spanish researchers discovered that people with SLE tend to have more allergies, including food allergies, than do healthy people or even people with other autoimmune diseases.17 While one study reported that drinking milk was associated with a decrease in SLE risk,18 other investigations point to both beef19 and dairy20 as foods that might trigger allergic reactions in some people with SLE. Casein, the main protein in cow’s milk, has immune-stimulating properties.21 This might explain why some people with SLE have been reported to be intolerant of milk products. Although there are several published case reports of patients with SLE showing clinical improvement after avoiding allergenic foods, additional research is needed to determine the importance of allergies as a cause of SLE. People with SLE who wish to explore whether allergies are contributing to their condition should consult a doctor.

Alfalfa seeds and sprouts contain the amino acid L-canavanine, which provokes a lupus-like condition in monkeys22 and possibly humans.23 For this reason, some doctors recommend that people with SLE should avoid these foods. Cooking alfalfa seeds has been reported to erase this effect.24

Lifestyle changes that may be helpful

In preliminary research, smoking has been linked to significantly increased risk of developing SLE, while drinking alcohol has been associated with a decrease in risk.25 The importance of these associations remains unclear, though an increased risk for many other diseases has been definitively linked to excessive consumption of alcohol.

Vitamins that may be helpful

Low blood levels of the hormone DHEA and the related compound DHEA-sulfate have been associated with more severe symptoms in people with SLE.26 Preliminary trials have suggested that 50 to 200 mg per day DHEA improved symptoms in people with SLE.27 28 One double-blind trial of women with mild to moderate SLE found that 200 mg of DHEA per day improved symptoms and allowed a greater decrease in prednisone use,29 but a similar trial in women with severe SLE found only insignificant benefits.30

Experts have concerns about the use of DHEA, particularly because there are no long-term safety data. Side effects at high intakes (50 to 200 mg per day) in one 12-month trial included acne (in over 50% of people), increased facial hair (18%), and increased perspiration (8%). Less common problems reported with DHEA supplementation were breast tenderness, weight gain, mood alteration, headache, oily skin, and menstrual irregularity.31

High amounts of DHEA have caused cancer in animals.32 33 Although anticancer effects of DHEA have also been reported,34 they involve trials using animals that do not process DHEA the way humans do, so these positive effects may have no relevance for people. Links have begun to appear between higher DHEA levels and risks of prostate cancer in humans.35 At least one person with prostate cancer has been reported to have had a worsening of his cancer despite feeling better while taking very high amounts (up to 700 mg per day) of DHEA.36 While younger women with breast cancer may have low levels of DHEA, postmenopausal women with breast cancer appear to have high levels of DHEA, which has researchers concerned.37 These cancer concerns make sense because DHEA is a precursor to testosterone (linked to prostate cancer) and estrogen (linked to breast cancer). Until more is known, it would be prudent for people with breast or prostate cancer or a family history of these conditions to avoid supplementing with DHEA. Preliminary evidence has also linked higher DHEA levels to ovarian cancer in women.38

Some doctors recommend that people taking DHEA have liver enzymes measured routinely. Anecdotes of DHEA supplementation (of at least 25 mg per day) leading to heart arrhythmias have appeared.39 At only 25 mg per day, DHEA has lowered HDL cholesterol while increasing insulin-like growth factor (IGF).40 Decreasing HDL could increase the risk of heart disease. Increasing IGF might increase the risk of breast cancer.

The omega-3 fatty acids in fish oil—eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)—decrease inflammation. Supplementation with EPA and DHA has prevented autoimmune lupus in animal research.41 In a double-blind trial, 20 grams of fish oil daily combined with a low-fat diet led to improvement in 14 of 17 people with SLE in 12 weeks.42 Smaller amounts of fish oil have led to only temporary improvement in another double-blind trial.43 People wishing to take such a large amount of fish oil should first consult with a doctor.

Antioxidant levels have been reported to be low in people with SLE, though this finding was not statistically significant in one trial.44 When animals are fed antioxidant-deficient diets, they develop a condition similar to SLE; supplementation with antioxidants, such as vitamin C, vitamin E, beta-carotene, and selenium, has helped animals with existing SLE.45 It remains unclear whether antioxidant supplementation would have a positive effect on people with SLE.

Some preliminary evidence suggests that vitamin E might help people with discoid lupus erythematosus (DLE). Two doctors reported good to excellent results by giving 800–2,000 IU of vitamin E per day to eight people with DLE.46 47 According to these physicians, lower amounts of vitamin E did not work as well. In another small trial, vitamin E, also given in high amounts, had no effect.48 Unlike with DLE, there appear to be no reports on the effects of vitamin E in people with SLE.

In one preliminary report, 250,000 IU beta-carotene per day cleared up all facial rashes in as little as one week for three people with DLE.49 However, another study involving 26 people (19 with DLE and seven with SLE) found that using an even higher intake (400,000 IU per day) for an average of five and a half months was ineffective.50 Research has not yet supported the use of beta-carotene for people with SLE.

Preliminary research suggests that pantothenic acid, when taken together with vitamin E, may help those with DLE. In one trial, taking 10 to 15 grams of pantothenic acid per day with 1,500 to 3,000 IU of vitamin E per day for as long as 19 months helped 67 people with DLE.51 Pantothenic acid by itself for shorter periods of time in lower amounts has been reported to fail.52 The amounts of pantothenic acid and vitamin E used in the first trial are very high and should not be taken without the supervision of a physician.

In a preliminary study, supplementation with pycnogenol was said to be beneficial in a small group of people with SLE.53 However, in this study, the pycnogenol and placebo groups were not comparable; moreover, according to some criteria, the placebo group actually fared better than the treatment group. Until a better designed study is performed, pycnogenol cannot be recommended as a treatment for lupus.

Are there any side effects or interactions?
Refer to the individual supplement for information about any side effects or interactions.

Herbs that may be helpful

Preliminary evidence indicates that some Chinese herbs may help those with SLE. In one preliminary trial, a formula composed of 17 Chinese herbs was given to people with SLE.54 Of the people who were also taking cortisone, 92% improved, but 85% of those taking the herbs alone also benefited. People with SLE-induced kidney damage given a combination of conventional drugs plus a Chinese herbal formula for six months did significantly better than those given the drugs alone.55 Various Chinese herbs have prolonged survival in animals with SLE.56

One of these Chinese herbs, Tripterygium wilfordii, is thought to benefit those with SLE or DLE by both suppressing immune function and acting as an anti-inflammatory agent. When people with DLE took 30 to 45 grams of tripterygium per day for two weeks in a preliminary trial, most experienced some degree of improvement, including reduction or disappearance of skin rashes.57 Skin rashes in eight people completely cleared up, while in ten people over 50% of the rash improved.

A preliminary trial gave the same dose of tripterygium to people with SLE. 58 After one month, 54% experienced relief from symptoms such as joint pain and malaise.

Use of the crude tripterygium herb is not recommended, and people interested in using it should work with their doctor to obtain the specially prepared and standardized extracts used in clinical studies. Because of potential side effects, people with SLE or DLE should consult with a doctor experienced in herbal medicine before using this herb. In the first two studies summarized, less than 8% of women with DLE and approximately one-third of women with SLE experienced amenorrhea (cessation of menstruation) after taking tripterygium. Other side effects ranged from stomach upset or pain, to nausea, loss of appetite, dizziness, and increased facial coloring. Both studies found that these effects subsided with time once people stopped using the herb. However, some reports have found more serious side effects and even death with use of tripterygium.59 Pregnant women should not use the herb.

Finally, a report suggests that long-term use (over five years) of tripterygium significantly reduced bone density in women taking it to treat lupus.60 While this loss of bone density was less severe than that found with long-term use of prednisone, lupus patients should have their bone density checked at yearly intervals by their doctor when using the herb.

One Chinese preliminary trial also found that astragalus could decrease overactive immune function in people with systemic lupus erythematosus.61 However, much more research is needed to know whether astragalus is safe in lupus or any other autoimmune disease.

Are there any side effects or interactions?
Refer to the individual herb for information about any side effects or interactions.

References:

1. Kardestuncer T, Frumkin H. Systemic lupus erythematosus in relation to environmental pollution: an investigation in an African-American community in North Georgia. Arch Environ Health 1997;52:85–90.

2. Fjellner B. Drug-induced lupus erythematosus aggravated by oral therapy. Acta Derm Venereol 1979;59:368–70.

3. Millard TP, Hawk JL, McGregor JM. Photosensitivity in lupus. Lupus 2000;9:3–10 [review].

4. Reidenberg MM, Durant PJ, Harris RA, et al. Lupus erythematosus-like disease due to hydrazine. Am J Med 1983;75:365–70.

5. Pereyo N. Hydrazine derivatives and induction of systemic lupus erythematosus. J Am Acad Dermatol 1986;14:514–5 [letter].

6. Nagata C, Fuyita, Iwata H, et al. Systemic lupus erythematosus: a case-control epidemiologic study in Japan. Int J Dermatol 1995;34:333–7.

7. Minami Y, Sasaki Ti, Komatsu S, et al. Female systemic lupus erythematosus in Miyagi Prefecture, Japan: a case-control study of dietary and reproductive factors. Tohoku J Exp Med 1993;169:245–52.

8. Nagata C, Fuyita, Iwata H, et al. Systemic lupus erythematosus: a case-control epidemiologic study in Japan. Int J Dermatol 1995;34:333–7.

9. Kardestuncer T, Frumkin H. Systemic lupus erythematosus in relation to environmental pollution: an investigation in an African-American community in North Georgia. Arch Environ Health 1997;52:85–90.

10. Comstock GW, Burke AE, Hoffman SC, et al. Serum concentrations of alpha-tocopherol, beta-carotene, and retinol preceding the diagnosis of rheumatoid arthritis and systemic lupus erythematosus. Ann Rheum Dis 1997;56:323–35.

11. Nagata C, Fuyita, Iwata H, et al. Systemic lupus erythematosus: a case-control epidemiologic study in Japan. Int J Dermatol 1995;34:333–7.

12. Shigemasa C, Tanaka T, Mashiba H. Effect of vegetarian diet on systemic lupus erythematosus. Lancet 1992;339:1177 [letter].

13. Minami Y, Sasaki Ti, Komatsu S, et al. Female systemic lupus erythematosus in Miyagi Prefecture, Japan: a case-control study of dietary and reproductive factors. Tohoku J Exp Med 1993;169:245–52.

14. Corman LC. The role of diet in animal models of systemic lupus erythematosus: possible implications for human lupus. Semin Arthritis Rheum 1985;15:61–9 [review].

15. Clark WF, Parbtani A, Huff MW, et al. Flaxseed: a potential treatment for lupus nephritis. Kidney Int 1995;48:475–80.

16. Prasad K. Hydroxyl radical-scavenging property of secoisolariciresinol diglucoside (SDG) isolated from flax-seed. Mol Cell Biochem 1997;168:117–23.

17. Diumenjo MS, Lisanti M, Valles R, Rivero I. Allergic manifestations of systemic lupus erythematosus. Allergol Immunopathol (Madr) 1985;13:323–6 [in Spanish].

18. Nagata C, Fuyita, Iwata H, et al. Systemic lupus erythematosus: a case-control epidemiologic study in Japan. Int J Dermatol 1995;34:333–7.

19. Carr RI, Tilley D, Forsyth S, et al. Failure of oral tolerance in (NZB X NZW)F1 mice is antigen specific and appears to parallel antibody patterns in human systemic lupus erythematosus (SLE). Clin Immunol Immunopathol 1987;42:298–310.

20. Rutkowska-Sak L, Legatowicz-Koprowska M, Ryzko J, Socha J. Changes in the gastrointestinal system of children with inflammatory systemic connective tissue diseases. Pediatr Pol 1995;70:235–41 [in Polish].

21. Carr R, Forsyth S, Sadi D. Abnormal responses to ingested substances in murine systemic lupus erythematosus: apparent effect of a casein-free diet on the development of systemic lupus erythematosus in NZB/W mice. J Rheumatol 1987;14 (suppl 13):158–65.

22. Bardana EJ Jr, Malinow MR, Houghton DC, et al. Diet-induced systemic lupus erythematosus (SLE) in primates. Am J Kidney Dis 1982;1:345–52.

23. Roberts JL, Hayashi JA. Exacerbation of SLE associated with alfalfa ingestion. N Engl J Med 1983;308(22):1361 [letter].

24. Malinow MR, McLaughlin P, Bardana EJ Jr, Craig S. Elimination of toxicity from diets containing alfalfa seeds. Food Chem Toxicol 1984;22:583–7.

25. Hardy CJ, Palmer BP, Muir KR, et al. Smoking history, alcohol consumption, and systemic lupus erythematosus: a case-control study. Ann Rheum Dis 1998;57:451–5.

26. Barry NN, McGuire JL, van Vollenhoven RF. Dehydroepiandrosterone in systemic lupus erythematosus: relationship between dosage, serum levels, and clinical response. J Rheumatol 1998;25:2352–6.

27. Van Vollenhoven RF, Morabito LM, Engleman EG, McGuire JL. Treatment of systemic lupus erythematosus with dehyroepiandrosterone: 50 patients treated up to 12 months. J Rheumatol 1998;25:285–9.

28. Van Vollenhoven RF, Engleman EG, McGuire JL. An open study of dehydroepiandrosterone in systemic lupus erythematosus. Arthritis Rheum 1994;37:1305–10.

29. Van Vollenhoven RF, Engleman EG, McGuire JL. Dehydroepiandrosterone in systemic lupus erythematosus. Results of a double-blind, placebo-controlled, randomized clinical trial. Arthritis Rheum 1995;38:1826–31.

30. Van Vollenhoven RF, Park JL, Genovese MC, et al. A double-blind, placebo-controlled, clinical trial of dehydroepiandrosterone in severe systemic lupus erythematosus. Lupus 1999;8:181–7.

31. van Hollenhoven RF, Morabito LM, Engleman EG, McGuire JL. Treatment of systemic lupus erythematosus with dehydroepiandrosterone: 50 patients treated up to 12 months. J Rheumatol 1998;25:285–9.

32. Orner GA, Mathews C, Hendricks JD, et al. Dehydroepiandrosterone is a complete hepatocarcinogen and potent tumor promoter in the absence of peroxisome proliferation in rainbow trout. Carcinogenesis 1995;16:2893–8.

33. Metzger C, Mayer D, Hoffmann H, et al. Sequential appearance and ultrastructure of amphophilic cell foci, adenomas, and carcinomas in the liver of male and female rats treated with dehydroepiandrosterone. Taxicol Pathol 1995;23:591–605.

34. Schwartz AG. Inhibition of spontaneous breast cancer formation in female C3H (A vy/a) mice by long-term treatment with dehydroepiandrosterone. Cancer Res 1979;39:1129–32.

35. McNeil C. Potential drug DHEA hits snags on way to clinic. J Natl Cancer Inst 1997;89:681–3.

36. Jones JA, Nguyen A, Strab M, et al. Use of DHEA in a patient with advanced prostate cancer: a case report and review. Urology 1997;50:784–8.

37. Zumoff B, Levin J, Rosenfeld RS, et al. Abnormal 24-hr mean plasma concentrations of dehydroisoandrosterone and dehydroisoandrosterone sulfate in women with primary operable breast cancer. Cancer Res 1981;41:3360–3.

38. Skolnick AA. Scientific verdict still out on DHEA. JAMA 1996;276:1365–7 [review].

39. Sahelian R. New supplements and unknown, long-term consequences. Am J Natural Med 1997;4:8 [editorial].

40. Casson PR, Santoro N, Elkind-Hirsch K, et al. Postmenopausal dehydroepiandrosterone administration increases free insulin-like growth factor-I and decreases high-density lipoprotein: a six-month trial. Fertil Steril 1998;70:107–10.

41. Kelley VE, Ferretti A, Izui S, Strom TB. A fish oil diet rich in eicosapentaenoic acid reduces cyclooxygenase metabolites, and suppresses lupus in MRL-1pr mice. J Immunol 1985;134:2914–9.

42. Walton AJE, Snaith ML, Locniskar M, et al. Dietary fish oil and the severity of symptoms in patients with systemic lupus erythematosus. Ann Rheum Dis 1991;50:463–6.

43. Westberg G, Tarkowski A. Effect of MaxEPA in patients with SLE. Scand J Rheumatology 1990;19:137–43.

44. Comstock GW, Burke AE, Hoffman SC, et al. Serum concentrations of alpha-tocopherol, beta-carotene, and retinol preceding the diagnosis of rheumatoid arthritis and systemic lupus erythematosus. Ann Rheum Dis 1997;56:323–35.

45. Weimann BJ, Weiser H. Effects of antioxidant vitamins C, E, and beta-carotene on immune functions in MRL/lpr mice and rats. Ann N Y Acad Sci 1992;669:390–2.

46. Ayres S Jr, Mihan R. Is vitamin E involved in the autoimmune mechanism? Cutis 1978;21:321–5.

47. Ayres S Jr, Mihan R. Lupus erythematosus and vitamin E: an effective and nontoxic therapy. Cutis 1979;23:49–54.

48. Yell JA, Burge S, Wojnarowska F. Vitamin E and discoid lupus erythematosus. Lupus 1992;1:303–5.

49. Newbold PC. Beta-carotene in the treatment of discoid lupus erythematosus. Br J Dermatol 1976;95:100–1.

50. Dubois EL, Patterson C. Ineffectiveness of beta-carotene in lupus erythematosus JAMA 1976;236:138–9 [letter].

51. Welsh AL. Lupus erythematosus: Treatment by combined use of massive amounts of pantothenic acid and vitamin E. Arch Dermatol Syphilol 1954;70:181–98.

52. Cochrane T, Leslie G. The treatment of lupus erythematosus with calcium pantothenate and panthenol. J Invest Dermatol 1952;18:365–7.

53. Stefanescu M, Matache C, Onu A, et al. Pycnogenol efficacy in the treatment of systemic lupus erythematosus patients. Phytother Res 2001;15:698–704.

54. Wang ZY. Clinical and laboratory studies of the effect of an antilupus pill on systemic lupus erythematosus. Chung His I Chieh Ho Tsa Chih 1989;9:452,465–8 [in Chinese].

55. Ruan J, Ye RG. Lupus nephritis treated with impact therapy of cyclophosphamide and traditional Chinese medicine. Chung Kuo Chung His I Chieh Ho Tsa Chih 1994;14:260, 276–8 [in Chinese].

56. Chen JR, Yen JH, Lin CC, et al. The effects of Chinese herbs on improving survival and inhibiting anti-ds DNA antibody production in lupus mice. Am J Chin Med 1993;21:257–62.

57. Wanzhang Q. Clinical observations on Tripterygium wilfordii in the treatment of 26 cases of discoid lupus erythematosus. J Trad Chin Med 1983;3:131–2.

58. Wanzhang Q. Tripterygium wilfordii hook F. in systemic lupus erythematosus. Report of 103 cases. Chin Med J 1981;94:827–34.

59. Chou WC, Wu CC, Yang PC, Lee YT. Hypovolemic shock and mortality after ingestion of Tripterygium wilfordii hook F: a case report. Int J Cardiol 1995;49:173–7.

60. Huang L, Feng S, Wang H. Decreased bone mineral density in female patients with systemic lupus erythematosus after long-term administration of Tripterygium wilfordii Hook. F. Chinese Med J 2000;113:159–61.

61. Klepser T, Nisly N. Astragalus as an adjunctive therapy in immunocompromised patients. Alt Med Alert 1999;Nov:125–8 [review].

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