Check for infection with frequent atopic dermatitis flares.
In many patients, the flares are due simply to severe disease. But Dr. Berger looks for secondary infection as well as four other factors to find opportunities to intervene. He listed the five factors in descending order: noncompliance (for example, the patient is tired of taking medications, leading to a flare); secondary infection; photosensitivity; allergic or contact dermatitis; or conversion to cutaneous T-cell lymphoma.
Of the five factors, infection is where most of the action is when sleuthing the cause of atopic dermatitis flares, said Dr. Berger, professor of clinical dermatology at the University of California, San Francisco. Infection is "an axis of atopic dermatitis that we tend to undertreat," he said.
He described a typical case: a 47-year-old man with moderate to severe chronic atopic dermatitis who had a 3-week-long severe flare of disease at presentation. He had extensive excoriations, redness, focal erosions, and crusts. He had been on and off systemic steroids to treat atopic dermatitis flares several times in the past.
When you see crusts or erosions, get cultures. This patient's culture grew methicillin-resistant Staphylococcus aureus (MRSA) even though he had no association with traditional avenues for exposure to MRSA such as intravenous drug use or stays in a hospital, nursing home, or prison, he said.
Doxycycline is recommended by infectious disease specialists as the first choice for treating MRSA because 95% of MRSA strains will be sensitive to the drug. Minocycline is an alternative, but is a bit more expensive, he said.
Second choice for treatment would be trimethoprim-sulfamethoxazole (TMP/SMZ), except in patients with AIDS, who are almost guaranteed to have a strain of MRSA resistant to TMP/SMZ, Dr. Berger said.
He adds rifampin to one of these drug choices for a better shot at success with combination therapy. He usually prescribes doxycycline 100 mg b.i.d, for 10 days plus rifampin 600 mg/day for 5 days to treat atopic dermatitis flares related to MRSA.
Clindamycin also can be a good therapeutic option, but if the culture produced bacteria resistant to erythromycin, the MRSA will have a gene for inducing resistance to clindamycin. These patients will start to improve on clindamycin only to relapse.
Linezolid also is an option "if your patient is Bill Gates," because it's extremely expensive, Dr. Berger said. Don't use macrolides or cephalosporins, because of high rates of resistance in MRSA. Avoid quinolones, because the infection tends to recur, leading to overuse of these drugs, he added.
Dr. Berger's MRSA patient improved dramatically on doxycycline-rifampin combination therapy but returned 1 month later with another flare and cultures again showing MRSA. Dr. Berger sent him home with a repeat prescription and a swab to get samples from his girlfriend's nose and groin. Cultures showed that the girlfriend carried MRSA and infected the patient.
"When the axis is along infection and patients reflare, I look into family members and close contacts," and treat them, he said. "That stabilizes their disease."
In similar situations, be sure to ask if the female partner uses oral contraceptives, because rifampin will interfere with the pills" effectiveness, he cautioned. Dr. Berger treated the patient's girlfriend with doxycycline and mupirocin (instead of rifampin). The patient's atopic dermatitis now is stable, and he has stopped intermittent systemic steroids because his flares have ended.
San Francisco Bureau
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|Title Annotation:||Skin Disorders|
|Publication:||Family Practice News|
|Date:||Mar 15, 2005|
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