Abstract:
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Background: Post kala-azar dermal leishmaniasis (PKDL) is a
cutaneous form of disease that develops at variable times
after individuals have received treatment for clinical visceral
leishmaniasis (VL). The study aimed to investigate the possible
role of interleukin 10 (IL-10) and development of PKDL.
Methods: 77 families composed of 41 complete case-parent
trios and 36 case-parent pairs from the Masalit ethnic
group were genotyped for 3 IL10 promoter polymorphisms:
-1082A/G, -819C/T and -592C/A. Results: Single point analysis
using the transmission disequilibrium test showed no evidence
of association between any of these IL10 promoter
single nucleotide polymorphisms (SNPs) and development
of PKDL. Haplotype analysis performed using TRANSMIT
showed borderline significance between PKDL and the haplotype
AA across -592C/A and -1082A/G (p = 0.053). Haplotypes
GCC (0.33) and ATA (0.30) were the common haplotypes
in this Sudanese population. Allele frequencies for the
3 SNPs differed significantly in Sudan compared to other African
(Gambian, Malawian, YRI) populations.
Conclusion:In Sudan post kala-azar dermal leishmaniasis (PKDL)
is a known complication of visceral leishmaniasis (VL)
caused by Leishmania donovani and occurs in some patients
after treatment and cure of VL. PKDL occurs with
a frequency of 56–62%, usually after a latent phase from
months to years [1, 2] . Clinical characterization of the disease
was previously described [3] . Experimental studies
indicate that interleukin 10 (IL-10) plays an important
regulatory role in the progression of VL. IL-10 was the
most prominent cytokine in PKDL lesions [4] with high
levels also observed in plasma [5] . However, interferon-
(IFN- ) was also seen in all lesions [4] and was detected
in keratinocytes and/or sweat glands of patients who developed
PKDL. In response to leishmanial antigens, peripheral
blood mononuclear cells from most Sudanese
PKDL patients proliferate and produce IFN- and IL-10
[4, 5] . Silva et al. (1992) postulated that the presence of IL-
10 in the skin lesions could block the action of IFN |