Fig 1.
Flow chart of inclusion and exclusion criteria.
Fig 2.
Agarose gel electrophoresis Representative RFLP pattern to distinguish Bsm I, FOK I, Apa I, Taq I polymorphism.
A. FOK I polymorphism: Lane 1 DNA ladder and lanes 2–7 patients’ samples, the TT (495 bp and 245 bp), Tt (495 bp, 290 bp, 245 bp, and 205 bp) and tt (290 bp, 245 bp, and 205 bp) genotypes. B. Bsm I polymorphism: Lane 1 DNA ladder and lanes 2–8 patients’ samples, BB (850 bp), Bb (850, 650, 200 bp), and bb (650, 200 bp) alleles. C. Apa I polymorphism: Lane 1 DNA ladder and lanes 2–16 patients’ samples the AA (740 bp), Aa (740 bp, 515 bp, and 225 bp), and aa (515 bp and 225 bp) genotypes. D. Taq I polymorphism: Lane 1 DNA ladder and lanes 2–10 patients’ samples the TT (495 bp and 245 bp), Tt (495 bp, 290 bp, 245 bp, and 205 bp) and tt (290 bp, 245 bp, and 205 bp) genotypes.
Fig 3.
Clinical and skin smear spectrum of cutaneous leishmaniasis.
A-Papular cutaneous lesion on the tip of the nose for a 10-year-old patient. B-Ulcerated plaque measuring 2.2cm in diameter on the upper limb, in a 33-year-old female patient. C- Crusted nodular lesion on the upper limb in a 29-year-old male patient. D. Skin smear lesion stained with Giemsa stain demonstrating amastigotes inside and outside the macrophages.
Table 1.
Epidemiological and clinical data of the studied participants.
Fig 4.
Histopathology of cutaneous leishmaniasis (H&E stain).
A- The histopathological changes seen in the epidermis of the CL skin lesion, there are mixed inflammatory cell infiltrates including plasma cells, lymphocytes, and macrophages with intracellular Leishman-Donovan bodies (100x). B- The histopathology sections of the skin biopsy with a high Ridley parasitic index in CL “white arrows” (+4 Ridley parasitic index) (200x). C- The histopathology of CL lesion with low Ridley parasitic index in a CL patient with a history of vitamin D therapy “green arrow” (+2 Ridley parasitic index) (200x).
Table 2.
Vitamin D levels and categories among the studied participants.
Table 3.
Genotypes and allele frequencies for vitamin D receptor (VDR) BsmI, ApaI, TaqI, and FokI in patients with cutaneous leishmaniasis and control subjects.
Table 4.
The haplotype frequencies of the studied four vitamin D receptor gene polymorphisms in patients with cutaneous leishmaniasis (CL) and controls.
Table 5.
Serum levels of vitamin D according to vitamin D receptor genotypes among patients with cutaneous leishmaniasis with no history of vitamin D therapy.
Table 6.
The Ridley parasitic load index (RPI) according to vitamin D receptor genotypes among patients with cutaneous leishmaniasis with no history of vitamin D therapy.
Fig 5.
Showed a highly significant negative correlation between Ridhley parasitic index and vitamin D levels (r62 = -0.53, p < 0.001).
Fig 6.
Showed a highly significant negative correlation between the size of the lesions and vitamin D levels (r2 = -0.49, p < 0.001).