Twelve patients with 16 leg ulcers, existing for at least 3 months and not responsive to conventional inpatient therapy of at least 3 weeks, were treated with repeated applications of cultured allogenic keratinocyte sheets. A marked decrease in size was seen in all ulcers but 2. Complete closure of the ulcer was seen in 62% of the ulcers within 8 weeks. Healing was due to enhanced granulation and increased epithelialization, starting from the periphery of the wound. This edge effect suggests that the epidermal allografts act by stimulation of migration and/or multiplication of the acceptor’s keratinocytes, rather than by take of the allograft.
We studied the effect of 2 months of treatment with budesonide (BUD) (Pulmicort), an inhaled corticosteroid, on the bronchial hyperresponsiveness to house-dust mite antigen (BHR-HDM) and to histamine (BHR-H). We also investigated whether BUD started 20 to 24 h after the development of a late asthmatic reaction (LAR) would influence the antigen-induced increase in nonspecific bronchial hyperresponsiveness to BHR-H. Thirty-one children with mild asthma who were atopic to HDM were randomized double blind into two parallel groups. Fifteen patients inhaled 0.2 mg BUD three times a day. Sixteen inhaled placebo in a similar way. Treatment began 20 to 24 h after antigen exposure and continued for 2 months. BHR-H and BHR-HDM were measured prior to and at the end of treatment. BHR-H was also determined 3 days after each antigen provocation. In the children receiving BUD, mean BHR-H and mean BHR-HDM were decreased approximately twofold after 2 months. No increase in BHR-H was observed after 3 days in the BUD group, irrespective of whether a LAR occurred. In patients in whom BUD treatment was withheld after the second antigen provocation, the protective effect of BHR-H was abolished. We conclude that 2 months of treatment with an inhaled corticosteroid causes a decrease in BHR-H and BHR-HDM. When an inhaled corticosteroid is administered 20 to 24 h after antigen provocation, It may protect against the antigen-induced increase in BHR-H. After treatment is discontinued, the protective effect wears off rapidly.
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