02423nas a2200325   4500000000100000008004100001260001600042653002100058653001100079653002100090653002400111653002500135653001400160653002500174653000900199653001600208653001700224653003200241100001600273700001600289700001400305700001400319700001300333245012500346856007600471300001200547490000800559520151600567022001402083       1992                            d  c1992 Jun 0110aErythema Nodosum10aHumans10aInterferon-gamma10aLeprosy, Borderline10aLeprosy, lepromatous10aMonocytes10aRecombinant Proteins10aSkin10aThalidomide10aTime Factors10aTumor Necrosis Factor-alpha1 aSampaio E P1 aMoreira A L1 aSarno E N1 aMalta A M1 aKaplan G00aProlonged treatment with recombinant interferon gamma induces erythema nodosum leprosum in lepromatous leprosy patients.  uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2119233/pdf/je17561729.pdf  a1729-370 v1753 a<p>10 patients with borderline and lepromatous leprosy were selected for a prolonged trial with recombinant interferon gamma (rIFN-gamma). Patients received 30 micrograms intradermally for six injections over a 9-d period, and then either 100 micrograms intradermally every 1 mo for 10 mo or every 2 wk for 5 mo (total, 1.2 mg). Erythema nodosum leprosum (ENL) was induced in 60% of the patients within 6-7 mo, as compared with an incidence of 15% per year with multiple drug therapy alone. The mean whole-body reduction in bacterial index over the first 6 mo was 0.9 log units. Cutaneous induration at the intradermal injection sites of greater than or equal to 15 mm predicted the development of a subsequent reactional state. Monocytes obtained from patients receiving the lymphokine demonstrated an increased respiratory burst and a 2.5-5.1-fold increase in tumor necrosis factor alpha (TNF-alpha) secretion in response to agonists. Patients in ENL had an even higher release of TNF-alpha from monocytes as well as high levels of TNF-alpha in the plasma (mean, 2,000 pg/ml). Thalidomide therapy was required to treat the systemic manifestations of ENL. Control of toxic symptoms with thalidomide was associated with a 50-80% reduction in agonist-stimulated monocyte TNF-alpha secretion. IFN-gamma enhanced the monocyte release of TNF-alpha by 3-7.5-fold (agonist dependent) when added to patient's cells in vitro, and this could be suppressed by the in vitro addition of 10 micrograms/ml of thalidomide.</p>  a0022-1007