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Common triggers for lupus | Lupus Foundation of America
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Viruses and infections In addition to looking at chemicals and other substances in the environment, researchers have homed in on a possible lupus-virus link. Identifying your environmental triggers As with solvents, the research on triggers of flares is incomplete. Was this resource helpful? Yes No. Understanding lupus. Get lupus resources and updates.
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Sign Up for Emails. Tell Your Story. Media Relations. Contact Us. Annual Report. National Lupus Partners Network. In English En Español. Common triggers for lupus.References 1. Antimalarials are recommended as first-line systemic therapy for CLE and SLE, given their effectiveness in prevention and treatment of symptoms such as photosensitivity, acute malar rash, discoid lupus erythematosus DLE, oral ulcers, alopecia, arthritis, pleuritis, and pericarditis.
The following are common environmental triggers: Ultraviolet rays from the sun or from fluorescent light bulbs Sulfa drugs, which make a person more sensitive to the sun, such as: Bactrim® and Septra® trimethoprim-sulfamethoxazole ; sulfisoxazole Gantrisin® ; tolbutamide Orinase® ; sulfasalazine Azulfidine® ; diuretics Sun-sensitizing tetracycline drugs such as minocycline Minocin® Penicillin or other antibiotic drugs such as: amoxicillin Amoxil® ; ampicillin Ampicillin Sodium ADD-Vantage® ; cloxacillin Cloxapen® An infection, a cold or a viral illness An injury, particularly traumatic injury Emotional stress, such as a divorce, illness, death in the family, or other life complications Anything that causes stress to the body, such as surgery, physical harm, pregnancy, or giving birth Exhaustion.
More resources for people with lupus. Was this resource helpful? Yes No. Living with lupus, I have lupus, I'm newly diagnosed. Medically reviewed: July 18, Get lupus resources and updates. Subscribe to our emails. Close Choose a chapter. Lupus Foundation of America. UV light induces pro-inflammatory cytokines, chemokines, and adhesion molecules that eventually lead to tissue injury. There are no autoantibodies associated with LET, and ANA titers tend to be low or nonexistent in this patient population.
Overall, the complex inflammatory cascade of necrosis, apoptosis, autoantibodies, T and B cells, and vascular changes leads to the development of CLE. Nonetheless, laboratory studies to evaluate for SLE are warranted, but should be symptom directed in an otherwise healthy patient.
Symptoms of arthralgias, discoid lesions, malar rash, oral ulcers, serositis, and arthritis, as well as hematologic, neurologic, and renal involvement would warrant concern for SLE. This is also a more cost-effective way to use specific autoantibody tests. LET is extremely photosensitive, and thus sun avoidance and protection with the use of broad-spectrum sunscreens, to cover UVB and UVA spectrum, is necessary.
This ideally includes sunscreens with helioplex, mexoryl, or physical blockers titanium dioxide, zinc oxide. A sun protection factor of at least 60 should be applied daily to all sun-exposed areas.
With appropriate sun protection, some LET lesions may resolve spontaneously. Patients with LET should be counseled on smoking cessation. Topical therapy with topical steroids can be initiated as first-line therapy, with or without topical calcineurin inhibitors.
Topical steroid should be tried for weeks in patients with mild skin disease prior to starting systemic therapies. Lower strength topical steroids Class V or VI may be used on the face.
Topical calcineurin inhibitors have been shown to be effective in some CLE subsets, and offer a decreased risk of telangiectasia development compared to topical steroids. Combining topical steroids and calcineurin inhibitors may provide an added benefit. For refractory or multiple lesions, antimalarial agents are highly effective. Antimalarials are recommended as first-line systemic therapy for CLE and SLE, given their effectiveness in prevention and treatment of symptoms such as photosensitivity, acute malar rash, discoid lupus erythematosus DLE, oral ulcers, alopecia, arthritis, pleuritis, and pericarditis.
As mentioned earlier, the vast majority of patients with LET respond to antimalarial therapy. Hydroxychloroquine is the treatment of choice over chloroquine, given its lower ocular toxicity risk. Typically, hydroxychloroquine is started at mgmg a day. To avoid ocular toxicity, the daily dose should not exceed 6.
Antimalarials take months for improvement to be noticed and up to 6 months for a c.
1 komentara na“Tumid lupus triggers”
Although uncommon, TLE may present with a Blaschkoid