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1.
Drug Res (Stuttg) ; 65(3): 119-24, 2015 Mar.
Article in English | MEDLINE | ID: mdl-24623031

ABSTRACT

Leishmania major is resistant to the traditional treatments in many parts of the world. PgpA, a member of (ABC) transporter superfamily, has been identified in Leishmania involved in antimony resistance. Silymarin can inhibit PgpA. The aim of this study was to determine the effect of combined therapy with glucantime and silymarin on Cutaneous Leishmaniasis. The effects of silymarin on response of L. major to glucantime were evaluated with amastigote macrophage and mice model of leishmaniasis. Immediately after injection in mice inoculated into footpads with L. major amastigote, systemic treatment was performed and the size of footpad swelling was measured twice a week. 4 and 8 weeks after the beginning of the treatment, splenic parasite burden was done. Silymarin showed no significant effect on the response of L. major promastigotes to glucantime. 2 formulations (glucantime 25 µm with silymarin 25 µm or 12.5 µm) reduced cell death in amastigote assays. The effect of silymarin on footpad swelling was detected when the combination of low-dose glucantime (20 mg/kg) with 25-50 mg/kg silymarin (especially 50 mg/kg) were used at day 22 of post infection (P<0.05). According to the parasite burden data, use of silymarin in the presence of different doses of glucantime, did not show significant effect compared to glucantime alone. The results of this study suggest that silymarin in conjunction with glucantime may have benefit effects in murine model of cutaneous leishmaniasis.


Subject(s)
Leishmania major/drug effects , Leishmaniasis, Cutaneous/drug therapy , Meglumine/pharmacology , Organometallic Compounds/pharmacology , Silymarin/pharmacology , Animals , Drug Therapy, Combination/methods , Macrophages/drug effects , Meglumine Antimoniate , Mice , Mice, Inbred BALB C
2.
Ecancermedicalscience ; 7: 289, 2013.
Article in English | MEDLINE | ID: mdl-23390454

ABSTRACT

Adrenocortical tumour is rare in children. We report on a female infant with adrenocortical carcinoma presenting with pseudoprecocious puberty at the age of two. She had a history of gradually increasing public hair growth after birth. Physical examination showed signs of virilisation such as pubic hair growth and hirsutism with evidence of facial hair growth. On biochemical evaluation, DHEA-S, 17-OH progesterone, and testosterone levels were elevated. An abdominopelvic spiral computed tomography (CT) scan with intravenous contrast identified a well-defined heterogeneously enhanced mass with areas of necrosis in the right adrenal gland and downward displacement of the underlying kidney. There was no evidence of distant metastasis on CT imaging. An exploratory laparotomy was performed in which a large, haemorrhagic and necrotic mass in the right adrenal gland with pressure effect on right liver lobe and signs of thrombosis in the inferior vena cava was detected. Pathologic examination confirmed the adrenocortical carcinoma. She received eight cycles of adjuvant chemotherapy with Carboplatin, Etoposide, and Doxorubicin regimens and underwent follow-up visits thereafter in which no sign of recurrence was observed. In conclusion, adrenocortical carcinomas are rare in children, but they should be considered in any child presenting with signs of pseudoprecocious puberty.

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