A 35-year-old subpolar lepromatous leprosy patient had completed 24 months WHO/MDT/MB, then followed by the 2nd regimen composed of diaphenylsulfone and minocycline (MINO). Ten months later from the 2nd regimen, he developed type 1 leprosy reaction (T1R) having facial nerve paresis. Another 1 month later, several lesions of leukoderma acquisitum centrifugum (halo nevus) were noticed with some other depigmented lesions. On the pathological examination, nevus cell nests were intermingled with foamy macrophages, accompanied with inflammatory lymphocytes. Macrophages were positively stained with mycobacterium leprae specific anti-phenolic glycolipid-I antibody. During T1R, foamy macrophages and coexisted nevus cells should have been severely attacked. The destruction of nevus cells is supposed to trigger the immune response leading to the leukoderma. On the other hand, some components released from injured nerve tissues, that have common antigenicity with melanin-forming cells, also might have participated in the appearance of leukoderma. MINO-related autoimmunity seemed not to be involved in this case, based on the clinical course.
Two relapsed cases of leprosy having drug resistance related mutations to diaphenylsulfone, rifampicin and new quinolone (NQ) are presented. Case 1 was prescribed ofloxacin in the past with unknown purpose and that was supposed to have led to NQ-resistance. Case 2 had high bacterial load for more than 10 years having no effective chemotherapy. Then eventually, multi-drug-resistance must have developed. These 2 cases were treated with CAM, MINO, CLF and completely cured without newly developed disability since our first examination. There is no guide line of chemotherapy for the cases of resistance to these 3 drugs. Then therapeutic regimen should be discussed more. During the clinical course of case 1, we observed good correlation between the decrease of PGL-I titer and reversal reaction.
Past histories of these 2 cases explain that the benefit of advanced medicine was not available in some sanatorium, even when the WHO’s MDT had been adopted worldwide. Under the leprosy segregation law, the treatment of leprosy itself had been confined in sanatoria for a long time.
Both cases have completed treatment in outpatient care without taking long-term absence from their occupations. Originally, leprosy should have been treated in the community-based medical institutions.
In Hawaii the epidemic of leprosy began in the middle of the nineteenth century. In response, the Kingdom of Hawai’i government decided to isolate it as a public health policy in 1865, began treatment of patients using Kalawaw of Molokai as a medical treatment area. The patient’s findings were made by snitching and arrest and sent to Molokai without mercy. Originally, the government aimed for agricultural colonies self-sufficient in patients in Karawawo, but due to geographical characteristics and lack of budget, the agricultural colony concept failed and Karawawo became a lawless zone, causing many confusion. In 1873 Father Damian went to Karawawo, started salvation of the patient, also served as negotiator with the government, confusion was settled. Thereafter, security was secured for Kalaowo by the increase of leprosy measures expenses, the establishment of a security system, etc., and the sanatoria spread to neighboring Kala Papa, and in the process of expansion and system development and the involvement of the United States absolute isolation policy developed.