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The efficacy and safety of 3 regimens of liposomal amphotericin B (AmBisome) in the treatment of Indian visceral leishmaniasis were compared in a prospective open randomized trial. Thirty parasitologically confirmed patients were randomly divided into 3 equal treatment groups; group 1 received AmBisome 2mg/kg on days 1, 2, 3, 4, 5, 6, and 10 (total dose 14 mg/kg); group 2 received AmBisome 2 mg/kg on days 1, 2, 3, 4, and 10 (total dose 10 mg/kg); group 3 received the same dosage on 1, 5 and 10 (total dose 6 mg/kg). Clinical cure resulted in all patients by day 24. Haemoglobin, white blood cell count, body weight and serum albumin level improved on day 24 and became normal by day 180. No patient relapsed within 12 months of follow-up. Side effects were minimal. One patient in group 2 died after 2 months from an unrelated disease. Liposomal amphotericin B is a promising new drug which is highly efficacious in the treatment of Indian kala-azar and produces minimal toxicity.

We have previously demonstrated raised levels of IgG and IgA antibody to the mycobacterial 65-kDa heat shock protein (hsp) in the sera of patients with rheumatoid arthritis (RA). We have now attempted to determine whether this phenomenon is specific for RA, and whether it is seen only with the mycobacterial homologue of this particular hsp gene family. We therefore screened antibody levels to the mycobacterial and Escherichia coli hsp 65, and the mycobacterial, E. coli, and human hsp70, in sera from RA, systemic lupus erythematosus (SLE), tuberculosis (TB), ankylosing spondylitis (AS), Crohn's disease, and control donors. RA sera show the greatest increase in IgA binding to the mycobacterial hsp65, but no increase in IgA binding to the E. coli homologue. Similarly, only RA and TB sera show increased IgG binding to the mycobacterial hsp65, and we have shown previously that the titre is greater in RA. In contrast, the use of mycobacterial and E. coli hsp70 preparations as control bacterial hsp gene products has shown that RA patients do not differ from TB or SLE patients in their antibody binding to these proteins. Moreover, neither IgA nor IgG antibody to the human hsp70 in RA sera were higher than in TB, and the IgA binding was not higher than in SLE. These findings suggest that elevated IgG antibody levels to the mycobacterial hsp65 shows some disease specificity, and further studies with the human homologue and at the T-cell level are required.

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