Miltefosine effectively modulates the cytokine milieu in Indian post kala-azar dermal leishmaniasis.

BACKGROUND: The increasing incidence of unresponsiveness to antimonials in leishmaniasis prompted the use of newer drugs such as miltefosine. Miltefosine influences macrophage effector functions, but its effect on patients with post kala-azar dermal leishmaniasis (PKDL) has not been evaluated. METHODOLOGY: The immunomodulatory activity of miltefosine was evaluated in patients with PKDL by studying the expression of activation markers (CD14 and CD16) and costimulatory molecules (CD80 and CD86) on circulating monocytes, levels of pro-inflammatory cytokines (tumor necrosis factor α, interleukin 6, interleukin 1ß, and interleukin 8) and anti-inflammatory cytokines (interleukin 10, transforming growth factor ß, interleukin 4, and interleukin 13) in serum and peripheral blood mononuclear cell culture supernatants, and serum nitrite and arginase activity. RESULTS: Miltefosine on circulating monocytes upregulated expression of CD16 and CD86 and reduced that of CD14. Miltefosine also induced a significant increase in circulating levels of pro-inflammatory cytokines with a concomitant decrease in anti-inflammatory cytokines. Its macrophage activating potential was evidenced by its ability to decrease serum arginase activity and increase serum nitrite. CONCLUSIONS: Miltefosine increased the proportion of monocytes that have a pro-inflammatory phenotype, which was accompanied by an enhanced secretion of pro-inflammatory cytokines and increased levels of serum nitrite. The decrease in anti-inflammatory cytokine levels and serum arginase activity collectively indicated that miltefosine triggered a robust T-helper 1 response that facilitated parasite elimination.

Pilomatrixoma.

Clinical and histopathological features of two cases of pilomatrixoma are reported. The tumour in each case was slow-growing, asymptomatic and at the same site. Histopathology showed classical eosinophilic ghost cell, surrounded by basophilic cells, along with areas of calcification and keratinization.

Comparative evaluation of clindamycin phosphate 1% and clindamycin phosphate 1% with nicotinamide gel 4% in the treatment of acne vulgaris.

Eighty patients with moderate acne vulgaris were enrolled from out-patient department for the comparative evaluation of clindamycin phosphate 1% and clindamycin phosphate 1% with nicotinamide gel 4%. In group I forty patients were given clindamycin phosphate 1% alone.ln group II forty patients were given clindamycin phosphate 1% and nicotinamide gel 4% in combination. The study did not show any added advantage of clindamycin phosphate 1% in combination with nicotinamide gel 4% over clindamycin phosphate 1% alone.

The efficacy of low-dose oral corticosteroids in the treatment of vitiligo patient.

Autoimmunity is one of the most probable pathogenesis of vitiligo. Systemic corticosteroids may arrest the progression of vitiligo and lead to repigmentation by suppressing immunity. The clinical efficacy of low-dose oral corticosteroids was assessed to minimize the side-effects in actively spreading vitiligo patients. One hundred (100) patients with vitiligo were evaluated. The patients took daily doses of oral prednisolone (0.3 mg/kg body weight) initially as a single oral dose after breakfast for the first 2 months. The dosage was then reduced to half the initial dose during the 3rd month and was halved again for the 4th and final month. After 4 months of treatment, 76% showed repigmentation while the arrest of progression (both repigmentation and stationary) was noted in 90% of patients. Male sex, and patients under 15 years of age showed pronounced repigmentation with statistical significance. According to this study low-dose oral prednisolone is an effective method in preventing progression and inducing repigmentation of fast-spreading vitiligo without the associated serious side-effects.